FN Thomson Reuters Web of Science™ VR 1.0 PT J AU MENDEZ, MF AF MENDEZ, MF TI THE NEUROPSYCHIATRIC ASPECTS OF BOXING SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Article DE BOXING; PUGILISM; DEMENTIA PUGILISTICA; PUNCH DRUNK; HEAD TRAUMA; CHRONIC TRAUMATIC ENCEPHALOPATHY; CLOSED HEAD INJURY; CONCUSSION; POST-CONCUSSION SYNDROME ID CHRONIC BRAIN-DAMAGE; ACTIVE AMATEUR BOXERS; DEMENTIA-PUGILISTICA; HEAD-INJURY; NEUROFIBRILLARY TANGLES; ALZHEIMERS-DISEASE; PROFESSIONAL BOXERS; COMPUTED-TOMOGRAPHY; LEAD; CT AB Objective: To review the neuropsychiatry of boxing. Method: This update considers the clinical, neuropsychological, diagnostic, neurobiological, and management aspects of boxing-related brain injury. Results: Professional boxers with multiple bouts and repeated head blows are prone to chronic traumatic encephalopathy (CTE). Repeated head blows produce rotational acceleration of the brain, diffuse axonal injury, and other neuropathological features. CTE includes motor changes such as tremor, dysarthria, and parkinsonism; cognitive changes such as mental slowing and memory deficits; and psychiatric changes such as explosive behavior, morbid jealousy, pathological intoxication, and paranoia. Screening with neuropsychological tests and neuroimaging may help predict those boxers at risk for CTE. Conclusions: Boxing results in a spectrum of CTE ranging from mild, nonprogressive motor changes to dementia pugilistica. Recent emphasis on safety in the ring, rehabilitation techniques, and other interventions do not eliminate the risk for CTE. For this reason, there is an active movement to ban boxing. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. RP MENDEZ, MF (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,NEUROBEHAV UNIT 691116AF,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 75 TC 73 Z9 74 U1 1 U2 12 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 1995 VL 25 IS 3 BP 249 EP 262 DI 10.2190/CUMK-THT1-X98M-WB4C PG 14 WC Psychiatry SC Psychiatry GA TF010 UT WOS:A1995TF01000003 PM 8567192 ER PT J AU ALDERTON, MR KOROLIK, V COLOE, PJ DEWHIRST, FE PASTER, BJ AF ALDERTON, MR KOROLIK, V COLOE, PJ DEWHIRST, FE PASTER, BJ TI CAMPYLOBACTER HYOILEI SP-NOV, ASSOCIATED WITH PORCINE PROLIFERATIVE ENTERITIS SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID ILEAL SYMBIONT INTRACELLULARIS; ENTEROPATHY; REPRODUCTION; BACTERIUM; ILEITIS; STRAIN; RNA AB Campylobacter hyoilei sp, nov, is the name proposed for an organism formerly described as strain RMIT 32A(T) (T = type strain) and a group of similar bacteria isolated from intestinal lesions of pigs with proliferative enteritis. The phenotypic characteristics of these organisms indicated that they are closely related to each other and are not strains of other Campylobacter spp, commonly isolated from pigs, The results of probing of ClaI-, EcoRV-, or BglII-cleaved genomic DNAs from C. hyoilei strains with a radiolabeled DNA probe that distinguishes between Campylobacter jejuni and Campylobacter coli indicated that C, hyoilei and C, coli are closely related, However, the 16S rRNA sequence of the reference strain of C. hyoilei, RMIT 32A(T), was four bases different from the 16S rRNA sequence of C. jejuni CCUG 11284(T) and five bases different from the 16S rRNA sequence of C. jejuni subsp. doylei CCUG 24567(T), suggesting that C, hyoilei is more closely related to C. jejuni than to C. coli. Hybridization between DNA from C, hyoilei type strain RMIT 32A and DNAs from selected type and reference strains of other Campylobacter species and subspecies, including C. jejuni, C. jejuni subsp. doylei, C. coli, Campylobacter mucosalis, and Campylobacter hyointestinalis, as well as the other C. hyoilei strains (the RMIT 32A(T)-like isolates), revealed that high levels of DNA hybridization (>70%) occurred only between the reference strain and other strains of C. hyoilei. C1 ROYAL MELBOURNE INST TECHNOL,DEPT APPL BIOL & BIOTECHNOL,MELBOURNE,VIC 3001,AUSTRALIA. FORSYTH DENT CTR,BOSTON,MA 02115. FU NIDCR NIH HHS [DE-08303, DE-04881] NR 24 TC 37 Z9 38 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1995 VL 45 IS 1 BP 61 EP 66 PG 6 WC Microbiology SC Microbiology GA QB873 UT WOS:A1995QB87300011 PM 7857809 ER PT J AU DEFOSSE, DL JOHNSON, RC PASTER, BJ DEWHIRST, FE FRASER, GJ AF DEFOSSE, DL JOHNSON, RC PASTER, BJ DEWHIRST, FE FRASER, GJ TI BREVINEMA-ANDERSONII GEN-NOV, SP-NOV, AND INFECTIOUS SPIROCHETE ISOLATED FROM THE SHORT-TAILED SHREW (BLARINA-BREVICAUDA) AND THE WHITE-FOOTED MOUSE (PEROMYSCUS-LEUCOPUS) SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID BORRELIA-BURGDORFERI; LYME-DISEASE; RNA; SEQUENCE AB A spirochete which infects short-tailed shrews (Blarina brevicauda) and white-footed mice (Peromyscus leucopus) has been shown previously to be ultrastructurally and serologically distinct from other spirochetes. Two of the original isolates from Connecticut and Minnesota and 16 new isolates obtained from shrews captured in Minnesota were characterized phenotypically and genetically in this study, A comparative analysis of the 16S rRNA sequences of two shrew isolates and one mouse isolate and the 16S rRNA sequences of 16 other spirochetes and Escherichia coli revealed that these organisms exhibited low levels of similarity (range of similarity values, 73.9 to 77.8%; average level of similarity, 74.7%). The shrew and mouse isolates which we examined formed a deeply branching subgroup that was clearly distinct from the other genera of spirochetes examined, These and other results indicated that the new spirochetes represent a unique taxon in the order Spirochaetales. Accordingly, we propose that they should be classified as members of a new genus, Brevinema, The three strains of Brevinema which we examined had 16S rRNA sequences that were nearly identical, We also compared these isolates by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis, fatty acid and enzyme analyses, restriction endonuclease analysis, and Southern hybridization and found that the levels of genetic and phenotypic homogeneity among the strains were very high, We concluded that the isolates which we examined were members of a single species, for which we propose the name Brevinema andersonii, The type strain of Brevinema andersonii is CT11616 (= ATCC 43811). The guanine-plus-cytosine content of the DNA of this species was determined to be 34 to 36 mol% by the thermal denaturation method. C1 FORSYTH DENT CTR,BOSTON,MA 02115. RP DEFOSSE, DL (reprint author), UNIV MINNESOTA,DEPT MICROBIOL,420 DELAWARE ST SE,BOX 196 UMHC,MINNEAPOLIS,MN 55455, USA. FU NIAMS NIH HHS [AR 34744]; NIDCR NIH HHS [DE-10374, DE-08303] NR 22 TC 16 Z9 16 U1 1 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1995 VL 45 IS 1 BP 78 EP 84 PG 7 WC Microbiology SC Microbiology GA QB873 UT WOS:A1995QB87300013 PM 7857811 ER PT J AU VANDAMME, P DANESHVAR, MI DEWHIRST, FE PASTER, BJ KERSTERS, K GOOSSENS, H MOSS, CW AF VANDAMME, P DANESHVAR, MI DEWHIRST, FE PASTER, BJ KERSTERS, K GOOSSENS, H MOSS, CW TI CHEMOTAXONOMIC ANALYSES OF BACTEROIDES-GRACILIS AND BACTEROIDES-UREOLYTICUS AND RECLASSIFICATION OF B-GRACILIS AS CAMPYLOBACTER-GRACILIS COMB-NOV SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID NON-GONOCOCCAL URETHRITIS; POLYACRYLAMIDE-GEL-ELECTROPHORESIS; FATTY-ACID COMPOSITION; NUMERICAL-ANALYSIS; WOLINELLA-RECTA; EIKENELLA-CORRODENS; PERIODONTAL-DISEASE; GENUS BACTEROIDES; PROTEIN-PATTERNS; CONCISUS AB The cellular fatty acids, respiratory quinones, and proteins of the generically misnamed taxa Bacteroides gracilis and Backteroides ureolyticus were analyzed and compared with the corresponding chemotaxonomic features of their closest relatives, the campylobacters. Our results and previously published data for genotypic and phenotypic characteristics were used in a polyphasic approach to reconsider the classification of these organisms. We transfer B. gracilis to the genus Campylobacter as Campylobacter gracilis comb. nov. B. ureolyticus can be considered a campylobacter on genotypic grounds; in contrast, the proteolytic metabolism and fatty acid components of this taxon exclude it from the genus Campylobacter. We prefer to consider this taxon a species incertae sedis pending the isolation and characterization of additional B. ureolyticus-like bacteria. C1 CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV BACTERIAL & MYCOT DIS,ATLANTA,GA 30333. FORSYTH DENT CTR,DEPT MOLEC GENET,BOSTON,MA 02115. RP VANDAMME, P (reprint author), STATE UNIV GHENT,MICROBIOL LAB,KL LEDEGANCKSTR 35,B-9000 GHENT,BELGIUM. RI Vandamme, Peter/B-7967-2009; OI Vandamme, Peter/0000-0002-5581-7937 NR 48 TC 57 Z9 57 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1995 VL 45 IS 1 BP 145 EP 152 PG 8 WC Microbiology SC Microbiology GA QB873 UT WOS:A1995QB87300025 PM 7857794 ER PT B AU SANDERSON, IR WALKER, WA AF SANDERSON, IR WALKER, WA BE deWeck, AL Sampson, HA TI Uptake and transport of macromolecules by the intestine SO INTESTINAL IMMUNOLOGY AND FOOD ALLERGY SE NESTLE NUTRITION WORKSHOP SERIES LA English DT Proceedings Paper CT 34th Nestle Nutrition Workshop - Intestinal Immunology and Food Allergy CY JUN 21-23, 1993 CL VERSAILLES, FRANCE SP Nestle Nutr Serv RP HARVARD UNIV,CHILDRENS HOSP,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02129, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 BN 0-7817-0250-X J9 NESTLE NUTR WORKS SE PY 1995 VL 34 BP 19 EP 36 PG 18 WC Allergy; Food Science & Technology; Immunology; Nutrition & Dietetics SC Allergy; Food Science & Technology; Immunology; Nutrition & Dietetics GA BD27E UT WOS:A1995BD27E00002 ER PT J AU Baruchel, S Bernstein, M Whitehead, VM Devine, S Bell, B Dubowy, R Grier, H Kretschmar, C Langevin, AM Vietti, T AF Baruchel, S Bernstein, M Whitehead, VM Devine, S Bell, B Dubowy, R Grier, H Kretschmar, C Langevin, AM Vietti, T TI A Phase I study of acivicin in refractory pediatric solid tumors - A Pediatric Oncology Group study SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE brain tumor; glutamine; glutathione; Phase I study ID CLINICAL-TRIALS; LUNG-CANCER; GLUTATHIONE; CELLS; PHARMACOKINETICS; TRANSPEPTIDASE; INHIBITION; GLUTAMINE; AT-125; PLASMA AB Forty-two patients with progressive solid tumors and brain tumors were entered in this Phase I study pf the glutamine antagonist acivicin given intravenously over thirty minutes daily for five days. The major toxicities encountered were myelosuppression and central nervous system toxicity (nightmares and somnolence). The maximum tolerated dosage on this schedule was 26 mg/M(2) daily for five days. Six patients including three patients with brain tumor had stable disease. C1 MCGILL UNIV, MONTREAL, PQ 30322, CANADA. EMORY UNIV, ATLANTA, GA USA. SUNY SYRACUSE, SYRACUSE, NY 02115 USA. DANA FARBER CANC INST, BOSTON, MA USA. BOSTON FLOATING HOSP INFANTS & CHILDREN, BOSTON, MA USA. UNIV TEXAS HLTH SCI CTR SAN ANTONIO, SAN ANTONIO, TX USA. WASHINGTON UNIV, SCH MED, ST LOUIS, MO USA. FU NCI NIH HHS [CA-20549, CA-28383, CA-33587] NR 24 TC 8 Z9 8 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1995 VL 13 IS 3 BP 211 EP 216 DI 10.1007/BF00873802 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA UD850 UT WOS:A1995UD85000005 PM 8729948 ER PT J AU Witte, RS Leong, T Ernstoff, MS Krigel, RL Oken, MM Harris, J Tormey, DC Trump, DL AF Witte, RS Leong, T Ernstoff, MS Krigel, RL Oken, MM Harris, J Tormey, DC Trump, DL TI A phase II study of interleukin-2 with and without beta-interferon in the treatment of advanced renal cell carcinoma SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE renal cell carcinoma; interleukin-2; beta-interferon ID CANCER; TRIAL AB Background. Biologic response modifiers have activity in renal cell carcinoma. The combination of interleukin-2 (IL-2) and beta-interferon (B-IFN) is synergistic in vitro. This trial was initiated to determine the efficacy of IL-2 alone and with B-IFN in advanced RCC. Methods. Ambulatory patients with advanced RCC were randomly allocated to either IL-2 6 x 10(6) units/M(2) intravenously (IV) three days a week for four weeks or IL-25 x 10(6) units/M(2)-IV plus B-IFN 6 x 10(6) units/M(2)-IV three days a week for 4 weeks. This induction phase was followed by a maintenance phase of the same drugs and doses administered for two weeks out of every four. Results. 84 patients were entered onto this phase II trial with 75 considered eligible for response and survival. Toxicity is reported for the 81 patients on whom data was received, irrespective of eligibility. The overall response rate (RR) was 9.3% (7/75). Of the 3 responses in the IL-2 arm (RR = 8.3%), one was a complete response. 4 patients in the IL-2 + B-IFN arm (RR = 10.3%) achieved a partial response. Median survival was estimated to be 8.4 months for patients given IL-2 and 8.0 months for patients given the IL-2 and B-IFN combination. Multivariate analysis of survival data identified initial performance status, metastases of > 1 site, and weight loss as being important prognostic factors for survival. There were 2 lethal and 3 life threatening toxicities with the IL-2 treatment. While there were no lethal toxicities on the combination arm, there were 4 life threatening toxicities. Conclusions. The results of this study indicate that further investigation of IL-2 with or without B-IFN at this dose and schedule as treatments for renal cell carcinoma is probably not warranted. C1 DANA FARBER CANC INST,BOSTON,MA 02115. DARTMOUTH HITCHCOCK MED CTR,LEBANON,NH. LANENKAU HOSP CANC TREATMENT CTR,WYNNEWOOD,PA. ABBOTT NW HOSP,VIRGINIA PIPER CANC INST,MINNEAPOLIS,MN. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. AMC,CANC RES CTR,DENVER,CO. UNIV PITTSBURGH,MED CTR,PITTSBURGH CANC INST,PITTSBURGH,PA. RP Witte, RS (reprint author), GUNDERSON CLIN LTD,1836 S AVE,LA CROSSE,WI 54601, USA. FU NCI NIH HHS [CA18653, CA23318, CA21076] NR 17 TC 5 Z9 4 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1995 VL 13 IS 3 BP 241 EP 247 DI 10.1007/BF00873807 PG 7 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA UD850 UT WOS:A1995UD85000010 PM 8729953 ER PT J AU Pazdur, R Meropol, NJ Casper, ES Fuchs, C Douglass, HO Vincent, M Abbruzzese, JL AF Pazdur, R Meropol, NJ Casper, ES Fuchs, C Douglass, HO Vincent, M Abbruzzese, JL TI Phase II trial of ZD1694 (Tomudex(TM)) in patients with advanced pancreatic cancer SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE Tomudex(TM); thymidylate synthase inhibitor; pancreatic carcinoma AB Background: Currently available therapies for advanced pancreatic cancer offer only palliative benefits, and patients with this disease have a poor prognosis. We undertook a phase II trial of ZD 1694 (Tomudex(TM)), a quinazoline folate analogue that is a potent and selective thymidylate synthase inhibitor, to determine this analogue's efficacy and safety in patients with advanced pancreatic adenocarcinoma. Patients and methods: ZD1694, 3.0 mg/m(2), was administered to 42 adult patients with pancreatic adenocarcinoma as a 15-minute intravenous infusion every 3 weeks for up to 6 doses. Objective tumor response was assessed every 6 weeks; clinical examinations, adverse event assessments, and clinical laboratory tests were performed every 3 weeks. Results: ZD 1694 produced an overall response rate of 5% (95% confidence limits [CI], 1% to 16%) in the study group. Of 42 patients, 2 (5%) had a partial response, 12 (29%) had stable disease, 21 (50%) had disease progression, and 5 (11%) could not be evaluated for response. Grade 3 vomiting, grades 3 and 4 fever, grade 3 leukopenia, grade 4 thrombocytopenia, and grades 3 and 4 liver function elevations were reported. Toxic effects with ZD1694 were reversible and manageable. Conclusions: ZD1694 has an acceptable safety profile but limited activity in patients with advanced pancreatic cancer. C1 ROSWELL PK CANC INST,BUFFALO,NY. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. DANA FARBER CANC INST,BOSTON,MA 02115. LONDON REG CANC CTR,LONDON,ON N6A 4L6,CANADA. RP Pazdur, R (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,DIV MED,BOX 92,1515 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 7 TC 4 Z9 4 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1995 VL 13 IS 4 BP 355 EP 358 DI 10.1007/BF00873144 PG 4 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA VB110 UT WOS:A1995VB11000012 ER PT J AU SHOKRAVI, MT MARCUS, DM ALROY, J EGAN, K SAORNIL, MA ALBERT, DM AF SHOKRAVI, MT MARCUS, DM ALROY, J EGAN, K SAORNIL, MA ALBERT, DM TI VITAMIN-D INHIBITS ANGIOGENESIS IN TRANSGENIC MURINE RETINOBLASTOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE RETINOBLASTOMA; VITAMIN-D3 COMPOUNDS; TRANSGENIC MICE; ANGIOGENESIS ID TUMOR ANGIOGENESIS; CORPUS-LUTEUM; CELL-GROWTH; 1,25-DIHYDROXYVITAMIN-D3; PROLIFERATION; NEOVASCULARIZATION; DIFFERENTIATION; RECEPTORS; CARCINOMA; INDUCTION AB Purpose. Vitamin D compounds have been shown to inhibit tumor growth in a transgenic retinoblastoma murine model. The mechanism of action has not been defined clearly, although an antiangiogenic action has been proposed. Methods. Transgenic retinoblastoma mice received high (0.05 mu g) and low (0.025 mu g) doses of vitamin D3 by intraperitoneal injection 5 times per week for 5 weeks. Control animals were injected with mineral oil vehicle atone. At 5 months of age, the animals were killed and eyes were enucleated and processed for light microscopy. Paraffin-embedded sections were stained with an immunoperoxidase stain (GSI) specific for mammalian vascular endothelium. Sections were graded by a single masked reviewer, and intraobserver reliability was assessed. Mean vessel counts were made for each group. Results,The high-dose group had the lowest mean vessel count (8.5), followed by the low-dose group (10.1). The control group had the highest mean vessel count (14.1). Vitamin D-treated animals (high- and low-dose groups combined) had significantly fewer vessels (P = 0.001) than untreated controls. Conclusions. These results support the hypothesis that inhibition of angiogenesis is a mechanism of action for vitamin D in the transgenic retinoblastoma mouse model. C1 UNIV WISCONSIN,SCH MED,DEPT OPHTHALMOL & VISUAL SCI,MADISON,WI 53792. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA. TUFTS UNIV,SCH MED,DEPT PATHOL,BOSTON,MA. TUFTS UNIV,SCH VET MED,BOSTON,MA. MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA. UNIV VALLADOLID,VALLADOLID,SPAIN. UNIV WISCONSIN,SCH MED,DEPT OPHTHALMOL & VISUAL SCI,MADISON,WI. FU NEI NIH HHS [EY01917] NR 39 TC 64 Z9 65 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 1995 VL 36 IS 1 BP 83 EP 87 PG 5 WC Ophthalmology SC Ophthalmology GA QC195 UT WOS:A1995QC19500014 PM 7529753 ER PT J AU STRISSEL, KJ RINEHART, WB FINI, ME AF STRISSEL, KJ RINEHART, WB FINI, ME TI A CORNEAL EPITHELIAL INHIBITOR OF STROMAL CELL COLLAGENASE SYNTHESIS IDENTIFIED AS TGF-BETA-2 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE TRANSFORMING GROWTH FACTOR-BETA; INTERLEUKIN-L RECEPTOR ANTAGONIST; COLLAGENASE; EPITHELIUM; CORNEA ID GROWTH-FACTOR-BETA; INTERLEUKIN-1 RECEPTOR ANTAGONIST; RHEUMATOID SYNOVIAL-CELLS; TGF-BETA; METALLOPROTEINASE EXPRESSION; MATRIX METALLOPROTEINASES; EXTRACELLULAR-MATRIX; RABBIT CORNEA; MESSENGER-RNA; AQUEOUS-HUMOR AB Purpose. To determine the molecular mechanisms whereby substances released by corneal epithelial cells act to inhibit the elaboration of collagenolytic activity by corneal stromal cells and to determine whether inhibitory activity might be mediated by interleukin-1 receptor antagonist (IL-1ra) or transforming growth factor (TGF)-beta. Methods. Conditioned media were generated from primary cultures of rabbit corneal epithelial cells, from passaged cultures of rabbit corneal stromal fibroblasts, and from cells of the rabbit corneal epithelial cell, line, SIRC. Pure populations of stromal cells were isolated from rabbit cornea and used directly for bioassay of the conditioned media to detect substances that inhibit collagenase synthesis. The mink lung epithelial cell line, Mv1Lu, was used for bioassay of TGF-beta-like activity. The addition of specific neutralizing antisera to bioassays allowed an assessment of the contribution of each isoform to the net regulatory activity. Reverse transcription-polymerase chain reaction and Northern blot analysis were employed to detect the presence of IL-1ra or TGF-beta mRNA species in cells from cultures used to generate conditioned media. Results. Both stimulatory and inhibitory substances that regulate the synthesis of stromal cell collagenase are released by corneal epithelial cells in primary culture. In contrast, only stimulatory activity is produced by corneal fibroblasts or SIRCs. MRNAs for a TGF-beta isoform, TGF-beta 2, and IL-1ra were identified in epithelial cells. Stromal fibroblasts also expressed TGF-beta 2 mRNA, but no evidence was found for expression of TGF-beta 3 mRNA in any of the three cell types. TGF-beta 2 is released by epithelial cells in both active and latent forms. This cytokine mediates the major portion of the net inhibitory activity against stromal cell collagenase synthesis produced by corneal epithelial cells. Conclusions. This study demonstrates the expression of TGF-beta 2 and IL-1ra by corneal epithelial cells in culture. It is the TGF-beta 2 that acts as the major inhibitor of collagenase synthesis by corneal stromal cells in culture. However, IL-1ra and TGF-beta 2 are likely to play important roles in epithelial-mesenchymal interactions regulating corneal development, homeostatic maintenance, and repair. C1 MASSACHUSETTS GEN HOSP,HARVARD CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. FU NEI NIH HHS [R01 EY08408, R01 EY09828]; NIAMS NIH HHS [T32-AR07098] NR 57 TC 46 Z9 47 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 1995 VL 36 IS 1 BP 151 EP 162 PG 12 WC Ophthalmology SC Ophthalmology GA QC195 UT WOS:A1995QC19500022 PM 7822142 ER PT J AU Silva, JA Leong, GB Tekell, JL Bowden, CL AF Silva, JA Leong, GB Tekell, JL Bowden, CL TI Visual perceptual disturbances in delusional misidentification SO ISRAEL JOURNAL OF PSYCHIATRY AND RELATED SCIENCES LA English DT Article ID CAPGRAS SYNDROME; DISORDER; SELF AB The delusional misidentification syndromes can involve physical misidentification. Delusional misidentification of the physical make-up of the self shares delusional dysmorphic symptoms with delusional disorder of the somatic type. In this article, we discuss how the study of delusional and perceptual symptoms in delusional misidentification syndromes may lead to a better understanding of the delusional dysmorphic process. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA 90073. RP Silva, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 20 TC 0 Z9 0 U1 0 U2 0 PU GEFEN PUBL HOUSE LTD PI JERUSALEM PA PO BOX 6056, JERUSALEM 91060, ISRAEL SN 0333-7308 J9 ISRAEL J PSYCHIAT JI Isr. J. Psychiatr. Relat. Sci. PY 1995 VL 32 IS 4 BP 286 EP 290 PG 5 WC Psychiatry SC Psychiatry GA TQ656 UT WOS:A1995TQ65600014 PM 8641858 ER PT J AU Caliendo, A Savara, A An, D Kaplan, J DAquila, R AF Caliendo, A Savara, A An, D Kaplan, J DAquila, R TI Zidovudine-resistance mutations increase replication in drug-free PBMC stimulated after infection SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1995 VL 10 SU 3 BP 4 EP 4 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UC138 UT WOS:A1995UC13800005 ER PT J AU Sylvester, A Caliendo, A An, D Savara, A Byington, R Strick, D Lillaney, R Sutton, L Sepkowitz, K Fischl, M Simon, G Lalezari, J Mitsuyasu, R DAquila, R AF Sylvester, A Caliendo, A An, D Savara, A Byington, R Strick, D Lillaney, R Sutton, L Sepkowitz, K Fischl, M Simon, G Lalezari, J Mitsuyasu, R DAquila, R TI HIV-1 resistance mutations and plasma RNA during zidovudine plus zalcitabine combination therapy SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NEW YORK HOSP,NEW YORK,NY 10021. UNIV MIAMI,MIAMI,FL 33152. WASHINGTON UNIV,ST LOUIS,MO. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1995 VL 10 SU 3 BP 47 EP 47 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UC138 UT WOS:A1995UC13800048 ER PT J AU FRIBORG, J LADHA, A GOTTLINGER, H HASELTINE, WA COHEN, EA AF FRIBORG, J LADHA, A GOTTLINGER, H HASELTINE, WA COHEN, EA TI FUNCTIONAL-ANALYSIS OF THE PHOSPHORYLATION SITES ON THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 VPU PROTEIN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV; SYNCYTIUM FORMATION; VIRAL RELEASE; VPU ID HTLV-III/LAV ENVELOPE; ENDOPLASMIC-RETICULUM; CYTOPLASMIC DOMAIN; CD4; GLYCOPROTEIN; HIV-1; DEGRADATION; GENE; RETROVIRUSES; MATURATION AB The human immunodeficiency virus type 1 (HIV-1)-encoded nu pu product is a small class 1 integral membrane protein that is phosphorylated by the ubiquitous casein kinase II (CKII) in HIV-1-infected cells. The Vpu protein facilitates the release of budding virions from the surface of infected cells and delays the rate of syncytium formation. In this study, we investigated the role of phosphorylation in the biological activity of Vpu. Our results show that phosphorylation of Vpu occurs on serine residues at positions 52 and 56 located in st highly conserved dodecapeptide sequence. Mutation of either Ser 56, or both Ser 52 and Ser 56 impaired the ability of Vpu to delay the rate of syncytium formation while retaining virion release activity at levels comparable to nu pu(+) proviruses. Flow cytometry analysis indicates that the relative amounts of envelope glycoprotein gp120 expressed at the surface of cells transfected with these nu pu mutant proviruses was two- to threefold greater than that observed on cells transfected with a nu pu(+) provirus. This increased expression of gp120 at the cell surface may explain the more rapid onset of syncytium formation observed in cell transfected with nu pu mutant proviruses. These results suggest that Vpu-facilitated virion release and delayed cytopathic effect are the consequence of two distinct functional activities of the protein. C1 UNIV MONTREAL,FAC MED,DEPT MICROBIOL & IMMUNOL,RETROVIROL HUMAINE LAB,MONTREAL,PQ H3C 3J7,CANADA. DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA. FU NIAID NIH HHS [AI34267] NR 41 TC 67 Z9 67 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN 1 PY 1995 VL 8 IS 1 BP 10 EP 22 PG 13 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA QA526 UT WOS:A1995QA52600004 PM 8548340 ER PT J AU SPRINGER, SA GASTFRIEND, DR AF SPRINGER, SA GASTFRIEND, DR TI A PILOT-STUDY OF FACTORS ASSOCIATED WITH RESILIENCE TO SUBSTANCE-ABUSE IN ADOLESCENT SONS OF ALCOHOLIC FATHERS SO JOURNAL OF ADDICTIVE DISEASES LA English DT Article ID LIFE-EVENTS; CHILDREN; SCALE; DRUG; DISORDER; PARENTS AB This pilot study evaluated the association between substance abuse outcome and putative protective factors in sons of alcoholic fathers. A battery of questionnaires was anonymously self-administered to 24 sons of alcoholic fathers ages 16-19 years to identify relationships between alcohol and/or drug abuse and factors hypothesized to be related to parental alcoholism Of the 24 subjects, 13 were categorized through self-identification and self-report screening measures as having alcohol and/or drug problems and 11 were categorized as not having substance abuse problems. Boys without substance problems: (1) had significantly higher maternal occupational status (p = .01); (2) experienced more good life events (p < .001), and (3) had a more internally oriented locus of control (p < .001). Good events and internal locus of control were highly correlated with each other (r = .620, p < .01). The fact that these preliminary findings are consistent with other literature despite marked methodologic and sample differences indicates that these putative components of resilience are robust and deserve further study towards improved substance abuse prevention in those at high risk. C1 MASSACHUSETTS GEN HOSP,ADDICT SERV,BOSTON,MA 02114. HARVARD UNIV,DEPT PSYCHOL,BOSTON,MA. NR 25 TC 7 Z9 7 U1 1 U2 2 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1995 VL 14 IS 2 BP 53 EP 66 DI 10.1300/J069v14n02_06 PG 14 WC Substance Abuse SC Substance Abuse GA RT835 UT WOS:A1995RT83500006 PM 8541360 ER PT J AU COMPTON, PA LING, W CHARUVASTRA, VC WESSON, DR AF COMPTON, PA LING, W CHARUVASTRA, VC WESSON, DR TI BUPRENORPHINE AS A PHARMACOTHERAPY FOR COCAINE ABUSE - A REVIEW OF THE EVIDENCE SO JOURNAL OF ADDICTIVE DISEASES LA English DT Review ID RHESUS-MONKEYS; OPIOID DEPENDENCE; METHADONE-MAINTENANCE; WITHDRAWAL; DETOXIFICATION; ANTAGONISTS; ADDICTS; TRIAL AB The partial mu-opiate agonist, buprenorphine, is the subject of recent evaluation as a potential pharmacotherapy for cocaine dependence. This paper reviews the extant preclinical and clinical evidence of buprenorphine effectiveness in treating cocaine abuse, including data from our large methadone comparison trial and a smaller buprenorphine dose ranging study. Although buprenorphine appears to reduce cocaine self-administration in studies of non-opiate dependent animals, clinical evidence for the same response in opiate addicts abusing cocaine has not been demonstrated. Further efficacy trials should await preclinical demonstrations of effectiveness in samples with opiate and cocaine exposure. C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT PSYCHIAT,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA. SUMMIT MED CTR,OAKLAND,CA. RP COMPTON, PA (reprint author), LOS ANGELES ADDICT TREATMENT RES CTR,10350 SANTA MONICA BLVD,SUITE 340,LOS ANGELES,CA 90025, USA. FU NIDA NIH HHS [DA 06082] NR 56 TC 18 Z9 18 U1 2 U2 3 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1995 VL 14 IS 3 BP 97 EP 114 DI 10.1300/J069v14n03_07 PG 18 WC Substance Abuse SC Substance Abuse GA TC347 UT WOS:A1995TC34700007 PM 8555282 ER PT J AU LEAF, DA MACRAE, H AF LEAF, DA MACRAE, H TI VALIDITY OF 2 INDIRECT MEASURES OF ENERGY-EXPENDITURE DURING WALKING IN THE ELDERLY SO JOURNAL OF AGING AND PHYSICAL ACTIVITY LA English DT Article DE PHYSICAL ACTIVITY; KILOCALORIE EXPENDITURE; EXERCISE ID PHYSICAL-ACTIVITY; RUNNING ECONOMY; EXERCISE; OLD AB The purpose of this study was to examine the criterion-related validity of two indirect measures of energy expenditure (EE): American College of Sports Medicine (ACSM) predictive equations, and estimated EE based on the Caltrac accelerometer. These measures were compared in 20 community-dwelling older men and women (mean age 71 years). The strength of the relationships among major determinants of EE during self-selected speeds of treadmill and outdoor walking was also examined. EE measured by respiratory gas analysis during an exercise stress test was highly correlated with ACSM predictive equations and poorly correlated with Caltrac. Multivariate regression equations were established to evaluate the ability of independent variables-body weight and height, age, and preferred treadmill walking speed-to predict EE (dependent variable). It was concluded that the ACSM predictive equations are suitable for use in elderly individuals, and that the apparent differences in the relationships between treadmill and outdoor walking speeds on EE deserve further investigation. C1 PEPPERDINE UNIV,DEPT SPORTS MED,MALIBU,CA 90263. RP LEAF, DA (reprint author), UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073, USA. NR 25 TC 2 Z9 2 U1 1 U2 5 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST BOX 5076, CHAMPAIGN, IL 61820-5076 SN 1063-8652 J9 J AGING PHYS ACTIV JI J. Aging Phys. Act. PD JAN PY 1995 VL 3 IS 1 BP 97 EP 106 PG 10 WC Geriatrics & Gerontology; Gerontology; Sport Sciences SC Geriatrics & Gerontology; Sport Sciences GA QA358 UT WOS:A1995QA35800007 ER PT J AU BORNSCHEIN, S BLOCH, KJ MCKOOL, BT WONG, JT AF BORNSCHEIN, S BLOCH, KJ MCKOOL, BT WONG, JT TI CHRONIC ERYTHRODERMA WITH EOSINOPHILIC INFILTRATE COMPLICATING INTRAVENOUS IMMUNOGLOBULIN (IVIG) INFUSION SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. 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 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1995 VL 95 IS 1 BP 283 EP 283 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA QE854 UT WOS:A1995QE85400569 ER PT J AU HALES, CA MUSTO, S HUTCHISON, WG MAHONEY, E AF HALES, CA MUSTO, S HUTCHISON, WG MAHONEY, E TI BW-755C DIMINISHES SMOKE-INDUCED PULMONARY-EDEMA SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE LEUKOTRIENES; ADULT RESPIRATORY DISTRESS SYNDROME; LUNG LYMPH ID INHALATION INJURY; LUNG INJURY; SYNTHETIC SMOKE; SULFIDOPEPTIDE LEUKOTRIENES; PATHO-PHYSIOLOGY; SHEEP; THROMBOXANE; CYCLOOXYGENASE; INHIBITORS; MORTALITY AB Pulmonary edema following smoke inhalation is due to the chemical toxins in smoke and not to the heat. We have shown that acrolein, a common component of smoke, induces pulmonary edema, perhaps via release of leukotrienes. We, therefore, hypothesized that acrolein, a component of smoke from burning cotton, might have a major role in producing pulmonary edema in sheep after cotton smoke inhalation and that BW-755C, a combined cyclo- and lipoxygenase inhibitor, would prevent the edema, whereas indomethacin, a cyclooxygenase inhibitor, would not. In control anesthetized sheep (n = 7), 128 breaths of cotton smoke induced no change in pulmonary arterial pressure but induced increases (P < 0.05) in pulmonary lymph flow from 4.4 +/- 0.8 (SE) to 15 +/- 2.7 ml/h, lymph protein flux from 0.25 +/- 0.08 to 0.80 +/- 0.16 g/h, and blood-corrected wet-to-dry weight ratios from a normal value of 3.8 +/- 0.07 (n = 9) to 4.5 +/- 0.18. Indomethacin (n = 6) did not significantly prevent these changes, whereas BW-755C decreased lung lymph flow change from 5 +/- 1 to 7 +/- 2 ml/h (P = NS), lymph protein flux from 0.25 +/- 0.08 to 0.35 +/- 0.1 g/h (P = NS), and weight-to-dry ratio from normal to 3.9 +/- 2.1 (P = NS). These data suggest leukotrienes may have a role in producing cotton smoke-induced noncardiogenic pulmonary edema. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP HALES, CA (reprint author), MASSACHUSETTS GEN HOSP,SHRINERS BURN INST,DEPT MED,PULM & CRIT CARE UNIT,32 FRUIT ST,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-36829] NR 31 TC 12 Z9 13 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JAN PY 1995 VL 78 IS 1 BP 64 EP 69 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA QC301 UT WOS:A1995QC30100011 PM 7713845 ER PT J AU BRIDGES, AJ AF BRIDGES, AJ TI RHEUMATIC DISORDERS IN PATIENTS WITH SILICONE IMPLANTS - A CRITICAL-REVIEW SO JOURNAL OF BIOMATERIALS SCIENCE-POLYMER EDITION LA English DT Review DE RHEUMATIC DISEASE; SCLERODERMA; MYOSITIS; CONNECTIVE TISSUE DISEASE; SILICONE ID CONNECTIVE-TISSUE DISEASE; GEL BREAST IMPLANTS; SYSTEMIC-SCLEROSIS; AUGMENTATION MAMMOPLASTY; REVISED CRITERIA; SCLERODERMA; WOMEN; CLASSIFICATION; DERMATOMYOSITIS; AUTOANTIBODIES AB More than 1000 patients with rheumatic disorders and silicone implants have been reported. In this review, the clinical features of patients with scleroderma, inflammatory myositis, systemic lupus erythematosus and silicone implants are discussed. The clinical features of the most common rheumatic disorder associated with silicone implants, the ''Silicone Implant Associated Syndrome'', are introduced. In addition, other local regional, and neurologic disorders associated with silicone implants are discussed. This comprehensive clinical review provides the clinician with information regarding the common symptoms, signs and laboratory features of rheumatic disorders of patients with silicone implants. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,CLIN IMMUNOL LAB,MADISON,WI 53706. RP BRIDGES, AJ (reprint author), UNIV WISCONSIN,SCH MED,RHEUMATOL SECT,MADISON,WI 53706, USA. NR 50 TC 19 Z9 20 U1 0 U2 0 PU VSP BV PI ZEIST PA PO BOX 346, 3700 AH ZEIST, NETHERLANDS SN 0920-5063 J9 J BIOMAT SCI-POLYM E JI J. Biomater. Sci.-Polym. Ed. PY 1995 VL 7 IS 2 BP 147 EP 157 PG 11 WC Engineering, Biomedical; Materials Science, Biomaterials; Polymer Science SC Engineering; Materials Science; Polymer Science GA QZ524 UT WOS:A1995QZ52400006 PM 7654629 ER PT J AU SANCHEZ, CP GOODMAN, WG BRANDLI, D GOLDENHERSH, M MURRAY, C CARLTON, E HAHN, T SALUSKY, IB AF SANCHEZ, CP GOODMAN, WG BRANDLI, D GOLDENHERSH, M MURRAY, C CARLTON, E HAHN, T SALUSKY, IB TI SKELETAL RESPONSE TO RECOMBINANT HUMAN GROWTH-HORMONE (RHGH) IN CHILDREN TREATED WITH LONG-TERM CORTICOSTEROIDS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID JUVENILE CHRONIC ARTHRITIS; FACTOR-I; LINEAR GROWTH; BONE TURNOVER; GH DEFICIENCY; SERUM; SOMATOMEDIN; 1,25-DIHYDROXYVITAMIN-D; PROLIFERATION; RETARDATION AB Corticosteroid therapy causes osteopenia and growth retardation in children; such changes are associated with diminished rates of bone formation and turnover. Since growth hormone activates bone remodeling, the biochemical and skeletal responses to rhGH were evaluated in four pediatric patients, aged 12.8 +/- 3 years, with long-term corticosteroid use (5 +/- 2 years). Recombinant human growth hormone (rhGH), 0.125 mg/kg, was given 3 times/week by subcutaneous injection for 12 months. Iliac crest bone biopsies were obtained after double tetracycline labeling before and at the end of rhGH therapy; serum levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone (intact), 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D-3, osteocalcin (BGP), and insulin-like growth factor-1 (IGF-1) were measured every 3 months during the treatment period. The average dose of prednisone was 0.24 +/- 0.05 mg/kg/day initially, and this did not change during the study. Serum calcium, phosphorus, alkaline phosphatase, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D-3, and BGP were unchanged during the rhGH therapy, but the serum IGF-1 level increased by 71%, p < 0.01. Eroded bone perimeter and cancellous bone area did not change significantly during rhGH therapy. Bone formation rates rose from 423 +/- 475 to 781 +/- 407 mu m(2)/mm(2)/day, p < 0.05, and the length of double tetracycline-labeled bone perimeter increased by 85%, p < 0.05. The bone formation rate in the growth hormone group exceeded the values of an age-matched reference group (14.3 +/- 3 years), 780 +/- 407 mu m(2)/mm(2)/day versus 411 +/- 479 mu m(2)/mm(2)/day,p < 0.05. Thus, rhGH therapy increases osteoblastic activity, bone formation, and possibly bone turnover despite continued and prolonged corticosteroid administration in children. C1 NICHOLS INST,SAN JUAN CAPISTRANO,CA. W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. FU NCRR NIH HHS [RR-00865]; NIDDK NIH HHS [DK-35423] NR 39 TC 28 Z9 29 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JAN PY 1995 VL 10 IS 1 BP 2 EP 6 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PZ869 UT WOS:A1995PZ86900002 PM 7747627 ER PT J AU WRIGHT, NM RENAULT, J HOLLIS, B BELL, NH KEY, LL AF WRIGHT, NM RENAULT, J HOLLIS, B BELL, NH KEY, LL TI EFFECT OF GROWTH-HORMONE ON BONE - BONE-MINERAL DENSITY, TRABECULAR BONE VOLUME, AND ALKALINE-PHOSPHATASE IMPROVE OR ARE RESTORED IN THE DWARF RAT TREATED WITH GROWTH-HORMONE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID OSTEOBLAST-LIKE CELLS; FACTOR-I; MEN; ABSORPTIOMETRY; DEFICIENCY; THERAPY; PUBERTY AB Studies were performed to determine whether serum total alkaline phosphatase (SAP), an index of bone formation; body weight; total body bone mineral density (BMD), measured by dual-energy X-ray absorptiometry; and tibial trabecular bone volume (TBV), measured by histomorphometry, are reduced in a-week-old female sexually immature Lewis dwarf (dw/dw) rats (DW-CT, n = 9) with isolated growth hormone (GH) deficiency and, if so, whether recombinant human GH (rhGH), 200 mu g/day subcutaneously for 4 weeks (DW-GH, n = 7), restores them. Studies were also performed to determine if 30% dietary restriction in 2-week-old female Lewis rats (LW-DR, n = 11) alters SAP, body weight, total BMD), or TBV compared with pair-fed controls (LW-CT, n = 7) given an ad libitum diet. Mean SAP (91 +/- 5 versus 109 +/- 5 U/l), body weight (102 +/- 11 versus 140 +/- 10 g), total BMD (88.5 +/- 0.3 versus 101.4 +/- 2.0 mg/cm(2)), and TBV (19.0 +/- 1.0 versus 27.0 +/- 1.4%) were significantly lower in DW-CT than in LW-CT animals,p < 0.05. In DW-GH, rhGH significantly increased mean SAP (130 +/- 7 U/l), bodyweight (133 +/- 10 g), total BMD (92.7 +/- 1.3), and TBV (24.0 +/- 1.9) compared with DW-CT animals. Compared with LW-CT rats, mean body weight and TBV were not different, but mean SAP was significantly higher (p < 0.01) and mean total BMD was significantly lower (p < 0.003) in DW-GH rats. In LW-DR compared with LW-CT animals, dietary restriction significantly reduced mean body weight (p < 0.05) but did not alter mean SAP, total BMD, or TBV. Thus, body weight, SAP, total BMD, and TBV were lower in DW-CT than in LW-CT rats. In the dose administered, SAP is markedly increased and reductions in body weight, total BMD, and TBV are completely or partially restored by treatment with rhGH in young female rats caused by isolated GH deficiency. Dietary restriction in young female rats with intact secretion of GH prevents weight gain but does not alter SAP, total BMD, or TBV compared with animals fed ad libitum. C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29425. RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC. RP WRIGHT, NM (reprint author), MED UNIV S CAROLINA,DEPT PEDIAT,DIV ENDOCRINOL,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. NR 27 TC 17 Z9 17 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JAN PY 1995 VL 10 IS 1 BP 127 EP 131 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PZ869 UT WOS:A1995PZ86900016 PM 7747619 ER PT J AU PEI, Y HERCZ, G GREENWOOD, C SEGRE, G MANUEL, A SAIPHOO, C FENTON, S SHERRARD, D AF PEI, Y HERCZ, G GREENWOOD, C SEGRE, G MANUEL, A SAIPHOO, C FENTON, S SHERRARD, D TI RISK-FACTORS FOR RENAL OSTEODYSTROPHY - A MULTIVARIANT ANALYSIS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID AMBULATORY PERITONEAL-DIALYSIS; PARATHYROID-HORMONE; BONE-DISEASE; DIABETES-MELLITUS; ALUMINUM; FAILURE; UREMIA; HYPERCALCEMIA; OSTEOMALACIA; HEMODIALYSIS AB To assess the risk factors associated with renal osteodystrophy, we examined the database of 256 patients who were prospectively studied in three Toronto dialysis centers between October of 1987 and 1989, The potential risk factors examined included age, sex, type and duration of dialysis, type and dose of phosphate binders, vitamin D treatment, and history of diabetes mellitus, renal allograft failure, parathyroidectomy, and bilateral nephrectomy, AH patients had undergone a bone biopsy and were categorized into one of four disease groupings: (1) osteitis fibrosa and mixed bone disease, (2) aluminum bone disease, (3) mild bone disorder, and (4) aplastic bone disorder. The mean (+/- SD) age of the patients at bone biopsy was 57 +/- 15 years, and 62% were men, Forty-five percent of patients were treated by hemodialysis and 55% by peritoneal dialysis, The mean duration of dialysis was 4 +/- 4 years, Twenty-five percent were also diabetic, The most common disorder was the aplastic (or ''adynamic'') bone disorder, found in 34% of patients, Aluminum bone disease was found in 27%, osteitis fibrosa or mixed bone disease in 27%, and mild bone disorder in 12% of patients, Cumulative intake of aluminum gels was associated with aluminum bone disease, whereas peritoneal dialysis with supraphysiologic calcium concentrations, ingestion of calcium carbonate, and diabetes mellitus were associated with both mild bone disorder and aplastic bone disorder, These three latter risk factors may be important in predisposing patients to a low bone turnover state through modulation of parathyroid hormone secretion, Thus, recent increases in the frequencies of these risk factors in dialysis patients are associated with a high prevalence of aplastic bone disorder. The clinical significance of this bone disorder remains to be defined. C1 UNIV TORONTO,TORONTO HOSP,DIV NEPHROL,TORONTO,ON,CANADA. UNIV TORONTO,TORONTO HOSP,DEPT MED,TORONTO,ON,CANADA. UNIV TORONTO,WELLESLEY HOSP,TORONTO,ON M4Y 1J3,CANADA. UNIV TORONTO,MT SINAI HOSP,SAMUEL LUNENFELD RES INST,TORONTO,ON M5G 1X5,CANADA. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. UNIV TORONTO,SUNNYBROOK SINAI HOSP,TORONTO,ON,CANADA. VET ADM MED CTR,SEATTLE,WA 98108. NR 36 TC 111 Z9 112 U1 0 U2 3 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JAN PY 1995 VL 10 IS 1 BP 149 EP 156 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA PZ869 UT WOS:A1995PZ86900019 PM 7747622 ER PT J AU Scully, RE AF Scully, RE TI Pathology of ovarian cancer precursors SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT Conference on Prospects for Chemoprevention of Cancers of the Cervix, Endometrium and Ovary - Surrogate Endpoints and Design of Clinical Trials CY FEB 01-05, 1995 CL OXNARD, CA SP NCI, Div Canc Prevent & Control DE carcinoma; ovary; pathology; precursor lesions; surface epithelium ID EPITHELIAL TUMORS; NEOPLASMS; MARKERS; BENIGN AB Ninety percent of ovarian cancers in the Western world are epithelial cancers derived from the surface epithelium of the ovary and its inclusion cysts. The so-called surface epithelium is mesothelium that comes to resemble epithelium as it is reflected over the surfaces of the ovaries. At various ages, but particularly in women in the reproductive, menopausal, and postmenopausal age groups, this epithelium migrates into the ovarian stroma to form inclusion cysts. These cysts probably result from a dynamic interplay of surface epithelium and underlying ovarian stroma, but can also develop as a result of periovarian adhesions. There is abundant evidence that their formation is not related to repair of ovulation. It is generally accepted that benign and malignant ovarian epithelial tumors arise from surface epithelium and its cystic derivatives because they both, but particularly the latter, have a potential to differentiate into epithelia similar to those of normal mullerian derivation (tubal, endometrial, and endocervical epithelia) and their tumors resemble those of the fallopian tube, endometrium, and endocervix. Also, both intraepithelial carcinomas and precarcinomatous lesions can be observed in the surface epithelium and its cystic derivatives. These carcinomas may arise de novo or as a transformation of pre-existing benign tumors and non-neoplastic lesions of similar derivation. Surface epithelial inclusion cysts have a greater propensity to undergo neoplasia than does the surface epithelium itself. This difference has been recognized for many years because most epithelial ovarian tumors are intraparenchymal, rather than being located on the ovarian surface. More recent evidence includes the immunohistochemical demonstration of various ovarian carcinoma antigens far more frequently in inclusion cyst epithelium than in surface epithelium; and the much more frequent presence of tubal metaplasia in the cyst epithelium than in the surface epithelium. Tubal metaplasia is encountered in non-neoplastic ovaries contralateral to ovarian carcinomas two to three times as frequently as in control ovaries, suggesting that the metaplastic epithelium is more prone to the development of carcinoma that non-metaplastic epithelium. Carcinoma precursors occur in the ovary, as in the cervix and endometrium, but have been reported only rarely because they are easily overlooked and have not been searched for by pathologists. (C) 1995 Wiley Liss, Inc. RP Scully, RE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 23 TC 21 Z9 22 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1995 SU 23 BP 208 EP 218 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TQ519 UT WOS:A1995TQ51900028 ER PT J AU ANDERSON, KC AF ANDERSON, KC TI AUTOLOGOUS PERIPHERAL-BLOOD PROGENITOR-CELL TRANSPLANTATION SO JOURNAL OF CLINICAL APHERESIS LA English DT Article; Proceedings Paper CT 16th Annual Meeting of the American-Society-for-Apheresis CY MAR 23-25, 1995 CL SAN DIEGE, CA SP Amer Soc Apheresis DE HEMATOPOIETIC STEM CELL GRAFTING; CD34(+) CELLS; ADOPTIVE IMMUNOTHERAPY; GENE THERAPY ID COLONY-STIMULATING FACTOR; HEMATOPOIETIC GROWTH-FACTORS; HIGH-DOSE CHEMOTHERAPY; UMBILICAL-CORD BLOOD; BONE-MARROW; GRANULOCYTE-MACROPHAGE; STEM-CELLS; CD34+ CELLS; MONONUCLEAR-CELLS; MULTIPLE-MYELOMA AB Harvesting of autologous peripheral blood stem cells (PBSCs) has been facilitated by using currently available, efficient apheresis technology at the time of rebound from chemotherapy while patients are receiving recombinant growth factors, i.e., granulocyte (G) or granulocyte-macrophage (GM) colony stimulating factor (CSF). Ideally pheresis should be done before patients have had extensive stem cell toxins, i.e., alkylating agents or nitrosoureas. This strategy has facilitated the use of high dose chemoradiotherapy given as a single regimen or in a divided dose for patients with solid tumors or hematologic malignancies and results in more rapid engraftment than bone marrow transplantation (BMT). Although there are no assays which measure repopulating stem cells, enumeration of CD34(+) cells within PBSCs is a direct and rapid assay which provides an index of both early and late long-term reconstitutive capacity, since it correlates with colony-forming unit (CFU)-GMs, as well as pre-progenitor or delta assays and long-term culture-initiating cells (LTC-IC). A threshold of greater than or equal to 2 x 10(6) CD34(+) cells/kg recipient body weight has been reported to be required for engraftment, but may vary depending upon the clinical setting. Strategies for mobilization of normal PBSCs also increase tumor cell contamination within PB in the setting of both hematologic malignancies and solid tumors, but the significance of these tumor cells in terms of patient outcome is unclear. Recently isolation of CD34(+) cells from PBSCs has been done using magnetic beads or immunoabsorption on columns or rigid plates in order to enrich for normal hematopoietic progenitors and potentially decrease tumor cell contamination. As for other cellular blood components, standards have been developed to assure efficient collection and processing, thawing, and reinfusion, and to maintain optimal PBPC viability. Finally, future directions of clinical research include expansion of hematopoietic progenitor cells ex vivo; use of umbilical cord or placenta as rich sources of progenitor cells; syngeneic hematopoietic stem cell transplantation; related and unrelated allogeneic hematopoietic stem cell transplantation; treatment of infections, i.e., Epstein Barr virus, or tumor relapse after allogeneic BMT using donor PBSC infusions; and gene therapy approaches. (C) 1995 Wiley-Liss, Inc. C1 DANA FARBER CANC INST,DEPT MED ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. RP ANDERSON, KC (reprint author), DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA50947] NR 60 TC 7 Z9 7 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0733-2459 J9 J CLIN APHERESIS JI J. Clin. Apheresis PY 1995 VL 10 IS 3 BP 131 EP 138 DI 10.1002/jca.2920100307 PG 8 WC Hematology SC Hematology GA TC821 UT WOS:A1995TC82100005 PM 8582895 ER PT J AU SOIFFER, RJ ALYEA, EP RITZ, J AF SOIFFER, RJ ALYEA, EP RITZ, J TI IMMUNOMODULATORY EFFECTS OF DONOR LYMPHOCYTE INFUSIONS FOLLOWING ALLOGENEIC BONE-MARROW TRANSPLANTATION SO JOURNAL OF CLINICAL APHERESIS LA English DT Article; Proceedings Paper CT 16th Annual Meeting of the American-Society-for-Apheresis CY MAR 23-25, 1995 CL SAN DIEGE, CA SP Amer Soc Apheresis DE GRAFT-VERSUS-LEUKEMIA; DONOR LYMPHOCYTES; BONE MARROW TRANSPLANT ID VERSUS-HOST DISEASE; CHRONIC MYELOGENOUS LEUKEMIA; CHRONIC MYELOID-LEUKEMIA; T-CELL DEPLETION; LEUKOCYTE INFUSIONS; CHRONIC PHASE; GRAFT; RELAPSE; IMMUNOTHERAPY; TRANSFUSION AB Recently, donor lymphocyte infusions have been successfully used to treat patients with CML who have relapsed following allogeneic bone marrow transplantation (BMT). Responses can be achieved in more than 60-70% of patients with stable phase CML without the need for the additional high dose cytotoxic chemotherapy that would accompany a second transplant procedure. The clinical and molecular remissions induced by this approach are a clear demonstration of graft-versus-leukemia (GVL) activity. Although undoubtedly donor lymphocyte infusions are safer than a second BMT, they are associated with toxicities stemming from graft-versus-host disease (GVHD) and pancytopenia. In this review, the immunomodulatory mechanisms underlying the GVL activity of donor allogeneic lymphocytes infusions are presented. Unresolved issues regarding lymphocyte administration are discussed as well as potential ways to limit complications due to GVHD and pancytopenia. New potential applications of this immunotherapeutic approach for treatment of infectious disease and non-hematologic malignancies will be presented. (C) 1995 Wiley-Liss, Inc. RP SOIFFER, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 NR 36 TC 4 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0733-2459 J9 J CLIN APHERESIS JI J. Clin. Apheresis PY 1995 VL 10 IS 3 BP 139 EP 143 DI 10.1002/jca.2920100308 PG 5 WC Hematology SC Hematology GA TC821 UT WOS:A1995TC82100006 PM 8582896 ER PT J AU Vamvakas, EC Pineda, AA Weinshenker, BG AF Vamvakas, EC Pineda, AA Weinshenker, BG TI Meta-analysis of clinical studies of the efficacy of plasma exchange in the treatment of chronic progressive multiple sclerosis SO JOURNAL OF CLINICAL APHERESIS LA English DT Article DE multiple sclerosis; disability status scale; course; progression; plasmapheresis; therapeutic plasma exchange; meta-analysis ID NATURAL-HISTORY; THERAPEUTIC TRIALS; PLASMAPHERESIS; CYCLOPHOSPHAMIDE; IMMUNOSUPPRESSION AB OBJECTIVE: To examine the hypothesis that addition of therapeutic plasma exchange (TPEX) to an immunosuppressive drug regimen increases that regimen's efficacy to halt the progression of chronic progressive multiple sclerosis (CPMS). METHODS: The literature was searched for prospective controlled clinical trials evaluating the efficacy of TPEX in CPMS. Six studies were eligible for meta-analysis. Their results were combined, using Cochran's and Pete's methods. Three outcome measures were studied: 1) the change in Kurtzke's disability status scale (DSS) scores, 2) the relative odds of neurologic decline by 1 or more DSS grades, and 3) the relative odds of neurologic improvement by 1 or more DSS grades, in the treatment versus the comparison group of patients. Reported results of neurologic evaluations at 6, 12, 24, and 36 months of follow-up were analyzed separately. RESULTS: TPEX significantly (P < .05) reduced the proportion of patients who experienced neurologic decline (by 1 or more DSS grades) at 12 months of follow-up (relative odds of decline = 0.441, 95% confidence interval = 0.210-0.929). CONCLUSIONS: There is a need for further clinical research into the possibility of a beneficial effect of TPEX in patients with CPMS likely to experience neurologic decline over the ensuring 12 months. Targeting treatment to a particular subgroup of CPMS patients may be necessary for TPEX to prove effective. (C) 1995 Wiley-Liss, Inc. C1 MAYO CLIN,DIV TRANSFUS MED,ROCHESTER,MN. MAYO CLIN,DEPT NEUROL,ROCHESTER,MN. RP Vamvakas, EC (reprint author), MASSACHUSETTS GEN HOSP,BLOOD TRANSFUS SERV,GRJ-224,BOSTON,MA 02114, USA. NR 42 TC 20 Z9 20 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 0733-2459 J9 J CLIN APHERESIS JI J. Clin. Apheresis PY 1995 VL 10 IS 4 BP 163 EP 170 DI 10.1002/jca.2920100402 PG 8 WC Hematology SC Hematology GA TN257 UT WOS:A1995TN25700001 PM 8770707 ER PT J AU VADAKEKALAM, J STAMOS, T SHENKER, Y AF VADAKEKALAM, J STAMOS, T SHENKER, Y TI SOMETIMES THE HOOVES DO BELONG TO ZEBRAS - AN UNUSUAL CASE OF HYPOPITUITARISM SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR, MED SERV, ENDOCRINOL SECT, MADISON, WI 53705 USA. UNIV WISCONSIN, DEPT MED, ENDOCRINOL SECT, MADISON, WI 53792 USA. NR 9 TC 5 Z9 5 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1995 VL 80 IS 1 BP 17 EP 20 DI 10.1210/jc.80.1.17 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QC590 UT WOS:A1995QC59000004 PM 7829607 ER PT J AU WEISS, RE SUNTHORNTHEPVARAKUL, T ANGKEOW, P MARCUSBAGLEY, D COX, N ALPER, CA REFETOFF, S AF WEISS, RE SUNTHORNTHEPVARAKUL, T ANGKEOW, P MARCUSBAGLEY, D COX, N ALPER, CA REFETOFF, S TI LINKAGE OF FAMILIAL DYSALBUMINEMIC HYPERTHYROXINEMIA TO THE ALBUMIN GENE IN A LARGE AMISH KINDRED SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID EUTHYROID THYROXINE EXCESS; HORMONE-BINDING PROTEIN; INCREASED AFFINITY; SERUM ABNORMALITY; VARIANT; IODOTHYRONINES; POLYMORPHISMS AB Familial dysalbuminemic hyperthyroxinemia (FDH) is the most common cause of inherited euthyroid hyperthyroxinemia in Caucasians. Transmitted as an autosomal dominant trait, it is always associated with high serum total T-4 (TT4) and more rarely with elevated total T-3 (TT3) and/or rT(3) (TrT(3)) concentrations. Free T-4, by dialysis, and TSH levels are normal, suggesting the presence of a T-4-binding protein abnormality. The abnormal serum T-4 carrier shares some physical and immunological properties with albumin, suggesting that it may be albumin itself. Here we show linkage between FDH and the albumin gene in a large Amish family of Swiss descent, using as markers a SacI polymorphism in the coding sequence of the albumin gene and the group-specific component (Gc) gene, located less than 1 centimorgan from the albumin gene. Blood samples were obtained from 160 members of this kindred, and 22 had FDH identified by the pattern of T-4 binding to serum proteins separated by isoelectric focusing. Serum TT4 values were above the normal range in all subjects expressing the FDH phenotype, and TrT(3) levels were above the normal range in only one half. TT4 concentrations correlated positively with TrT(3) and TT3. All TT3 values were, however, within the normal range. Free T-4 and TSH levels were normal, confirming the euthyroid state in these subjects. FDH was associated with the albumin SacI(+)/Gc 1S haplotype, yielding a LOD (logarithm of the odds ratio) score of 5.53, with a recombination frequency of O. These data provide strong support that a variant albumin is the cause of FDH in this kindred. C1 UNIV CHICAGO, DEPT PEDIAT, CHICAGO, IL 60637 USA. UNIV CHICAGO, JOSEPH P KENNEDY JR MENTAL RETARDAT RES CTR, CHICAGO, IL 60637 USA. CTR BLOOD RES, BOSTON, MA 02115 USA. RP WEISS, RE (reprint author), UNIV CHICAGO, DEPT MED, ENDOCRINOL SECT, MC 3090, 5841 S MARYLAND AVE, CHICAGO, IL 60637 USA. FU NIAID NIH HHS [AI-14157]; NIDDK NIH HHS [DK-02081, DK-15070] NR 36 TC 9 Z9 9 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1995 VL 80 IS 1 BP 116 EP 121 DI 10.1210/jc.80.1.116 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QC590 UT WOS:A1995QC59000020 PM 7829599 ER PT J AU ALEXANDER, JM SWEARINGEN, B TINDALL, GT KLIBANSKI, A AF ALEXANDER, JM SWEARINGEN, B TINDALL, GT KLIBANSKI, A TI HUMAN PITUITARY-ADENOMAS EXPRESS ENDOGENOUS INHIBIN SUBUNIT AND FOLLISTATIN MESSENGER RIBONUCLEIC-ACIDS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID GONADOTROPIN-RELEASING-HORMONE; ACTIVIN-BINDING PROTEIN; GROWTH FACTOR-BETA; RAT PITUITARY; CELLS INVITRO; PROLIFERATION; BIOSYNTHESIS; SECRETION; CULTURES AB Specific factors involved in the pathogenesis of tumors that stimulate clonal human pituitary adenoma cell proliferation remain unknown. An important question regarding the pathogenesis of human pituitary tumors is whether they synthesize autocrine regulatory factors that regulate both hormone biosynthesis and neoplastic growth. Activin and inhibin are both comprised of inhibin subunits and have diverse regulatory roles as growth and differentiation factors in normal and neoplastic tissue. Activin stimulates FSH beta messenger ribonucleic acid (mRNA) biosynthesis and FSH secretion, and these effects are down-regulated in normal gonadotrophs by the endogenous glycoprotein follistatin. In addition to its effects on gonadotrophs, activin modulates hormone secretion by somatotroph and corticotroph cell lines. It is not known whether human neoplastic pituitary tissue synthesizes inhibin subunits or follistatin or whether their expression is cell type specific. We investigated whether alpha-, beta A-, and beta B-inhibin subunit and follistatin mRNAs could be detected in 27 human pituitary adenomas [clinically nonfunctioning (n = 11), somatotroph (n = 5), corticotroph (n = 5), and lactotroph (n = 6)] using reverse transcriptase-polymerase chain reaction techniques. Twentysix of the tumors contained mRNAs encoding one or more inhibin subunits. beta-Inhibin mRNA was the most prevalent (81% of tumors), followed by beta A-inhibin (59% of tumors) and alpha-inhibin (52% of tumors). Endogenous alpha-, beta A-, and beta B-inhibin subunit mRNA synthesis was also examined in normal human pituitary and testicular complementary DNA libraries, and all subunit mRNAs were detected. In contrast to the widespread expression of inhibin subunits in pituitary tumors, follistatin mRNA was detected in a subset of nonfunctioning tumors (54%) as well as in control normal human pituitary and testicular complementary DNA libraries. Tumor-specific follistatin biosynthesis was not observed in other pituitary tumor subtypes. These data are the first to demonstrate that 1) endogenous inhibin subunits are synthesized in human pituitary adenomas of all known secretory phenotypes as well as normal pituitary tissue; and 2) follistatin gene expression in pituitary adenomas is specific to clinically nonfunctioning or gonadotropin subunit-producing tumors. The characterization of inhibin subunit and follistatin biosynthesis by human pituitary tumors will be important in investigating their potential roles in regulating both tumor phenotype and cell proliferation. C1 MASSACHUSETTS GEN HOSP, DEPT MED, NEUROENDOCRINE UNIT, JACKSON 1021, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, NEUROSURG SERV, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. EMORY UNIV, SCH MED, DEPT NEUROSURG, ATLANTA, GA 30322 USA. FU NIADDK NIH HHS [R32-AM-07028-16]; NIDDK NIH HHS [DK-40947] NR 33 TC 33 Z9 33 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1995 VL 80 IS 1 BP 147 EP 152 DI 10.1210/jc.80.1.147 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QC590 UT WOS:A1995QC59000024 PM 7829603 ER PT J AU WEIR, GC AF WEIR, GC TI GLUCAGON-LIKE PEPTIDE-1 (GLP-1) - A PIECE OF THE INCRETIN PUZZLE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Editorial Material RP WEIR, GC (reprint author), JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 6 TC 6 Z9 6 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1995 VL 95 IS 1 BP 1 EP 1 DI 10.1172/JCI117625 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QA882 UT WOS:A1995QA88200002 PM 7814603 ER PT J AU LI, HM FREEMAN, MW LIBBY, P AF LI, HM FREEMAN, MW LIBBY, P TI REGULATION OF SMOOTH-MUSCLE CELL SCAVENGER RECEPTOR EXPRESSION IN-VIVO BY ATHEROGENIC DIETS AND IN-VITRO BY CYTOKINES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE SCAVENGER RECEPTOR; SMOOTH MUSCLE CELLS; ATHEROSCLEROSIS; RABBIT; BALLOON INJURY ID LOW-DENSITY-LIPOPROTEIN; HUMAN ATHEROSCLEROTIC LESIONS; LEUKOCYTE ADHESION MOLECULE; HUMAN CAROTID ARTERIES; FOAM CELLS; INTERFERON-GAMMA; GENE-EXPRESSION; MESSENGER-RNA; IMMUNOCYTOCHEMICAL ANALYSIS; CHOLESTEROL DEPOSITION AB Scavenger receptor (ScR)-mediated uptake of modified lipoproteins may contribute to the transformation of smooth muscle cells into lipid-laden foam cells during atherogenesis. This study examined the in vivo expression of ScRs in aortas, with or without balloon injury, taken from hypercholesterolemic or normocholesterolemic rabbits. Numerous intimal cells in the rabbit aortic lesions expressed ScRs as detected by immunocytochemical staining with a goat anti-rabbit ScR antibody. Single immunostaining for cell identification markers in serial sections, as well as double staining, confirmed the expression of ScRs by both intimal smooth muscle cells and macrophages. To explore potential inducers of ScR expression by smooth muscle cells in vivo, we studied the regulation of ScR expression in vitro by cytokines known to be present in atherosclerotic lesions. Tumor necrosis factor-alpha (TNF-alpha) or interferon-gamma (IFN-gamma) increased ScR mRNA levels, protein expression, and AcLDL degradative activity in cultured rabbit aortic smooth muscle cells. The induction of ScR expression in intimal smooth muscle cells in vivo could be a useful marker of smooth muscle cell activation during atherogenesis and may contribute to foam cell formation by this cell type following balloon injury and/ or hypercholesterolemia. Cytokines, such as TNF-alpha or IFN-gamma, may stimulate some of the phenotypic changes that characterize the alteration in gene expression of intimal smooth muscle cells in rabbit atherosclerotic lesions. C1 MASSACHUSETTS GEN HOSP,DEPT MED,LIPID METAB UNIT,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV VASC RES,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOVASC,VASC MED & ATHEROSCLEROSIS UNIT,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-47840, HL-45098, P0-1-HL-48743] NR 55 TC 154 Z9 161 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1995 VL 95 IS 1 BP 122 EP 133 DI 10.1172/JCI117628 PG 12 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QA882 UT WOS:A1995QA88200018 PM 7814605 ER PT J AU TAKAHASHI, S GOLDRING, S KATZ, M HILSENBECK, S WILLIAMS, R ROODMAN, GD AF TAKAHASHI, S GOLDRING, S KATZ, M HILSENBECK, S WILLIAMS, R ROODMAN, GD TI DOWN-REGULATION OF CALCITONIN RECEPTOR MESSENGER-RNA EXPRESSION BY CALCITONIN DURING HUMAN OSTEOCLAST-LIKE CELL-DIFFERENTIATION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE POLYMERASE CHAIN REACTION; CALCITONIN ESCAPE; HUMAN MARROW CULTURES; CELL DIFFERENTIATION; GENE EXPRESSION ID BONE-MARROW CULTURES; MULTINUCLEATED CELLS; SALMON-CALCITONIN; ADENYLATE-CYCLASE; RIBONUCLEIC-ACID; DOWN-REGULATION; RESORPTION; RAT; LINE; INVITRO AB Calcitonin inhibits both osteoclast formation and bone resorption, and is a primary treatment for patients with hypercalcemia and increased bone turnover. However, the clinical utility of calcitonin is limited because patients become refractory to calcitonin after several days (the calcitonin ''escape phenomenon''). The molecular basis for calcitonin ''escape'' is unclear. To determine the regulatory mechanisms controlling calcitonin receptor (CTR) expression in osteoclasts and their precursors, we treated immature mononuclear precursors for human osteoclast-like multinucleated cells (MNC) formed in vitro with 1,25-(OH)(2)D-3, to induce their differentiation to committed mononuclear precursors, and mature multinucleated osteoclasts, and used reverse transcriptase (RT)-PCR to assess expression of CTR mRNA in both committed mononuclear precursors and MNC. The PCR fragment produced was cloned and sequenced to confirm that it was derived from CTR mRNA. CTR mRNA expression was detected in mononuclear MNC precursors after 7 d of 1,25-(OH)(2)D-3 treatment. It was also present in osteoclast-like MNC and highly purified giant cells from osteoclastomas, but not in monocytes or macrophage polykaryons formed in vitro. Calcitonin markedly decreased CTR but not actin mRNA expression in giant cells and MNC after 12 h, and removal of calcitonin restored CTR mRNA expression. Similarly, calcitonin decreased calcitonin-induced adenylate cyclase activity. These data suggest: (a) downregulation of CTR gene expression by calcitonin may in part explain the calcitonin ''escape phenomenon'' and (b) expression of CTR mRNA occurs in mononuclear osteoclast precursors within 7 d after exposure to 1,25-(OH)(2)D-3. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. VET ADM MED CTR,SAN ANTONIO,TX 78284. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FU NIADDK NIH HHS [AM-35188]; NIAMS NIH HHS [AR-39539, AR-41336] NR 42 TC 88 Z9 91 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1995 VL 95 IS 1 BP 167 EP 171 DI 10.1172/JCI117634 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QA882 UT WOS:A1995QA88200023 PM 7814611 ER PT J AU SHERIDAN, RL PRELACK, KM PETRAS, LM SZYFELBEIN, SK TOMPKINS, RG AF SHERIDAN, RL PRELACK, KM PETRAS, LM SZYFELBEIN, SK TOMPKINS, RG TI INTRAOPERATIVE REFLECTANCE OXIMETRY IN BURN PATIENTS SO JOURNAL OF CLINICAL MONITORING LA English DT Article AB Objective. Transmission oximetry sites for intraoperative monitoring are frequently difficult to find in burn patients, as standard transmission oximetry sites are often burned or contained within the operative field. The objective of this study was to determine if reflectance oximetry is of potential value in monitoring this group of patients. Methods. A total of 16 operative procedures in a group of acutely burned adult and pediatric patients with an average age of 9.7 years (range, 10 months to 37 years), average burn size of 42% of the body surface (range, 15% to 94%), and average weight of 34.2. kg (range, 9 to 100 kg) were done with simultaneous transmission and reflectance oximetry monitoring. Results. During these 16 procedures in a diverse group of acutely burned adult and pediatric patients, there was no significant difference in saturations derived from transmission and reflectance oximetry probes. In smaller children, adequate signal for reflectance probe monitoring was often detected in hyperemic sites, such as healed partial thickness burn. Conclusions. This is the first published report documenting both the clinical use of the reflectance oximetry in burn patients and the clinical use of the Nellcor Oxisensor II RS-10 reflectance oximetry probe (Nellcor Corporation, Hayward, CA). This technique can facilitate the intraoperative monitoring of acutely burned adult and pediatric patients in whom standard transmission oximetry sites are difficult to find. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA. RP SHERIDAN, RL (reprint author), SHRINERS BURN INST,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 0 TC 5 Z9 5 U1 2 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0748-1977 J9 J CLIN MONITOR JI J. Clin. Monit. PD JAN PY 1995 VL 11 IS 1 BP 32 EP 34 DI 10.1007/BF01627417 PG 3 WC Anesthesiology SC Anesthesiology GA QC788 UT WOS:A1995QC78800007 PM 7745451 ER PT J AU KANNER, AM RAMIREZ, L JONES, JC AF KANNER, AM RAMIREZ, L JONES, JC TI THE UTILITY OF PLACING SPHENOIDAL ELECTRODES UNDER THE FORAMEN OVALE WITH FLUOROSCOPIC GUIDANCE SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY LA English DT Article DE SPHENOIDAL ELECTRODES; FLUOROSCOPY; ANTEROTEMPORAL SPIKES; FORAMEN OVALE; TEMPORAL LOBECTOMY ID TEMPORAL SPIKES; LOCALIZATION; EEG; EPILEPSY; SEIZURES AB Although sphenoidal electrodes are widely used to detect epileptiform activity, there is no agreement on an optimal target to which electrodes should be aimed. The purpose of this study was to determine whether fluoroscopic guidance is a reliable method for placing electrodes directly below the foramen ovale and whether such positioning enhances their capacity to detect epileptiform activity when compared to similar electrodes placed blindly into the infratemporal fossa. We examined the surface/sphenoidal EEG recordings of 17 patients with intractable partial seizures of anterotemporal origin, after fluoroscopically placed sphenoidal electrodes (FPSE) had been inserted to lie just below the foramen ovale. A criterion for eligibility was a previous prolonged video/EEG monitoring with blindly placed sphenoidal electrodes (BPSE) that failed to detect seizures with a focal onset, No blindly placed electrode, for which there was radiographic documentation, reached the foramen ovale. Fluoroscopic guidance assured accurate targeting. FPSE detected a unilateral anterotemporal interictal focus in four patients in whom BPSE had failed to record any interictal spikes and detected bitemporal independent interictal foci in one patient in whom BPSE had identified only unilateral spikes. In nine other patients, the spike count obtained with FPSE recordings increased by >100% when compared to that obtained with BPSE recordings. FPSE recorded seizures with an anterotemporal focal onset pattern in 10 patients in whom BPSE had recorded seizures with a regional, lateralized, or nonlocalized onset pattern. In nine of these 10 patients, this was adequate to recommend surgery and avoid invasive monitoring. Fluoroscopic guidance assures accurate targeting of the foramen ovale. When compared to BPSE, FPSE resulted in better detection of interictal and ictal epileptiform activity of mesial-basal-temporal origin. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT NEUROL,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT NEUROSURG,MADISON,WI. UNIV WISCONSIN,HOSP & CLIN,SCH MED,MADISON,WI 53792. NR 16 TC 31 Z9 31 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0736-0258 J9 J CLIN NEUROPHYSIOL JI J. Clin. Neurophysiol. PD JAN PY 1995 VL 12 IS 1 BP 72 EP 81 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA PY513 UT WOS:A1995PY51300008 PM 7896912 ER PT J AU CHIAPPA, KH CROS, D KIERS, L TRIGGS, W CLOUSTON, P FANG, JJ AF CHIAPPA, KH CROS, D KIERS, L TRIGGS, W CLOUSTON, P FANG, JJ TI CROSSED INHIBITION IN THE HUMAN MOTOR SYSTEM SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY LA English DT Article DE MOTOR EVOKED POTENTIAL; FACILITATION; INHIBITION ID TRANSCRANIAL MAGNETIC STIMULATION; ELECTRICAL-STIMULATION; BRAIN-STIMULATION; CORTICAL EXCITABILITY; INTACT MAN; CORTEX STIMULATION; CORPUS-CALLOSUM; NERVOUS-SYSTEM; SILENT PERIOD; AWAKE MONKEY AB We used transcranial magnetic stimulation in humans to investigate the effect of focal unilateral stimulation of the motor cortex on the function of the contralateral motor cortex. Surface-recorded, rectified, averaged electromyography (EMG) showed relative silent periods in small hand muscles at 35-64 and 123-158 ms following ipsilateral cortical stimulation over the hand area. The first inhibitory phase started Il ms after the minimum corticospinal conduction time from the contralateral cortex, appropriate for transcallosal conduction. Foot muscles (with focal stimulation over the ipsilateral hand area) also showed silent periods at 61-104 ms, indicating a marked spread of the inhibitory effect throughout the opposite motor cortex. H-reflex studies in the upper limb showed that this inhibitory effect was not mediated at the level of the alpha motoneuron. Single motor unit peristimulus time histogram studies in upper limb muscles showed inhibition similar to that seen in the surface recordings and no evidence of excitation following ipsilateral motor cortex stimulation, Transcranial magnetic stimulation performed with large circular coils centered at the vertex activates both excitatory and inhibitory processes bilaterally so that focal unilateral stimulation is preferable in detailed studies of motor system physiology. RP CHIAPPA, KH (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,CLIN NEUROPHYSIOL LAB,EEG LAB,BOSTON,MA 02114, USA. NR 77 TC 25 Z9 25 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0736-0258 J9 J CLIN NEUROPHYSIOL JI J. Clin. Neurophysiol. PD JAN PY 1995 VL 12 IS 1 BP 82 EP 96 PG 15 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA PY513 UT WOS:A1995PY51300009 PM 7896913 ER PT J AU BAJORIN, DF NICHOLS, CR SCHMOLL, HJ KANTOFF, PW BOKEMEYER, C DEMETRI, GD EINHORN, LH BOSL, GJ AF BAJORIN, DF NICHOLS, CR SCHMOLL, HJ KANTOFF, PW BOKEMEYER, C DEMETRI, GD EINHORN, LH BOSL, GJ TI RECOMBINANT HUMAN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR AS AN ADJUNCT TO CONVENTIONAL-DOSE IFOSFAMIDE-BASED CHEMOTHERAPY FOR PATIENTS WITH ADVANCED OR RELAPSED GERM-CELL TUMORS - A RANDOMIZED TRIAL SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CANCER-CENTER EXPERIENCE; INDUCED MYELOSUPPRESSION; SALVAGE CHEMOTHERAPY; CISPLATIN; ETOPOSIDE; THERAPY; PLUS; RISK AB Purpose: Ifosfamide-containing therapy with cisplatin plus either etoposide (VIP) or vinblastine (VeIP) can cure of patients with relapsed germ cell tumors (GCTs), but results in substantial myelotoxicity. This study sought to assess the impact of recombinant human granulocyte macrophage colony-stimulating factor (rhGM-CSF) on the severity of neutropenia and incidence of infectious complications in patients who receive ifosfamide-based chemotherapy for GCT. Patients and Methods: One hundred and four assessable GCT patients from 20 centers were randomized to receive rhGM-CSF with either cycles 1 and 2 or cycles 3 and 4 of chemotherapy. Standard doses of VIP or VeIP were used. Efficacy data were analyzed using a parallel design for cycles 1 and 2 before the crossover. Results: Fewer clinically relevant infections occurred in rhGM-CSF patients (13 of 55, 24%) versus observation patients (22 of 49, 45%) in cycle 1 (P = .01). Decreases were observed in infections during neutropenia (22% v 43%, P = .03), infections requiring intravenous antibiotics (20% v 43%, P = .01), and any infection irrespective of severity (29% v 55%, P = .01) in cycle 1. However, there were no significant differences among the treatment arms in cycle 2 in the proportion of clinically relevant infections (P = .23), infections associated with neutropenia (P = .11), infections requiring antibiotics (P = .22), or any infection (P = .65). rhGM-CSF was discontinued in 14% of cycles because of toxicity related to the growth factor. Conclusion: rhGM-CSF reduced the incidence of infections in the first cycle of chemotherapy, but no benefit beyond the initial chemotherapy cycle was evident. Based on the limited clinical impact and the high incidence of rhGM-CSF-related toxicity that required growth factor discontinuation, the routine administration of rhGM-CSF to prevent neutropenia and infection after ifosfamide-based chemotherapy for GCT patients is not recommended. C1 MEM SLOAN KETTERING CANC CTR,DEPT MED,DIV SOLID TUMOR ONCOL,GENITOURINARY ONCOL SERV,NEW YORK,NY 10021. CORNELL UNIV,COLL MED,DEPT MED,NEW YORK,NY. INDIANA UNIV,DIV MED ONCOL,INDIANAPOLIS,IN 46204. HANNOVER MED SCH,DEPT HEMATOL & ONCOL,W-3000 HANNOVER,GERMANY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. NR 23 TC 31 Z9 32 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1995 VL 13 IS 1 BP 79 EP 86 PG 8 WC Oncology SC Oncology GA QA325 UT WOS:A1995QA32500013 PM 7799046 ER PT J AU WHITTINGTON, R NEUBERG, D TESTER, WJ BENSON, AB HALLER, DG AF WHITTINGTON, R NEUBERG, D TESTER, WJ BENSON, AB HALLER, DG TI PROTRACTED INTRAVENOUS FLUOROURACIL INFUSION WITH RADIATION-THERAPY IN THE MANAGEMENT OF LOCALIZED PANCREATICOBILIARY CARCINOMA - A PHASE-I EASTERN-COOPERATIVE-ONCOLOGY-GROUP TRIAL SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID 5-FLUOROURACIL AB Purpose: The purpose of this study was to determine the maximum-tolerated dose (MTD) of fluorouracil (5-FU) administered os a protracted intravenous (IV) infusion with concurrent radiation in patients with pancreaticobiliary carcinoma. Methods: Twenty five patients with recurrent, residual, or unresectable carcinoma of the pancreas or biliary tract were treated on ct phase I trial of protracted IV infusions of 5-FU, beginning at 200 mg/m(2)/d, concurrent with radiation therapy (59.4 Gy in 33 fractions over 6 to 7 weeks). Chemotherapy began on the first day of radiation and continued through the entire course of treatment. After each cohort of five patients held been treated and observed, the daily dose was escalated in 25-mg/m(2) increments until dose-limiting toxicity was encountered. An additional cohort of five patients was treated at the MTD. Clinical examination and computed tomography (CT) were used to evaluate response and patterns of progression. Results: The MTD of 5-FU was 250 mg/m(2)/d. The dose-limiting toxicity was oral mucositis. The median survival duration of all patients treated was 11.9 months and the 5-year survival rate was 19%. Eleven of 25 patients remain free of local progression and four patients are without evidence of progression at 18+, 18+, 34+, and 44+ months following treatment. Conclusion: Concurrent radiation with protracted 5-FU infusion at 250 mg/m(2)/d is well tolerated and shows evidence of activity against rumors of the pancreas and biliary system. (C) 1995 by American Society of Clinical Oncology. C1 UNIV PENN,SCH MED,PHILADELPHIA,PA. DANA FARBER CANC INST,DIV BIOSTAT,EASTERN COOPERAT ONCOL GRP,STAT OFF,BOSTON,MA. ALBERT EINSTEIN MED CTR,PHILADELPHIA,PA. NORTHWESTERN UNIV,SCH MED,DEPT MED,DIV HEMATOL ONCOL,CHICAGO,IL 60611. FU NCI NIH HHS [CA23318, CA15488, CA21115] NR 14 TC 114 Z9 117 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1995 VL 13 IS 1 BP 227 EP 232 PG 6 WC Oncology SC Oncology GA QA325 UT WOS:A1995QA32500030 PM 7799024 ER PT J AU LEW, MA KEHOE, K RITZ, J ANTMAN, KH NADLER, L KALISH, LA FINBERG, R AF LEW, MA KEHOE, K RITZ, J ANTMAN, KH NADLER, L KALISH, LA FINBERG, R TI CIPROFLOXACIN VERSUS TRIMETHOPRIM-SULFAMETHOXAZOLE FOR PROPHYLAXIS OF BACTERIAL-INFECTIONS IN BONE-MARROW TRANSPLANT RECIPIENTS - A RANDOMIZED, CONTROLLED TRIAL SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ACUTE NONLYMPHOCYTIC LEUKEMIA; PLACEBO-CONTROLLED TRIAL; GRAM-NEGATIVE SEPSIS; TRIMETHOPRIM-SULFAMETHOXAZOLE; GRANULOCYTOPENIC PATIENTS; CO-TRIMOXAZOLE; NEUTROPENIC PATIENTS; DOUBLE-BLIND; SELECTIVE DECONTAMINATION; ANTIBIOTIC-PROPHYLAXIS AB Purpose: To compare the efficacy and safety of ciprofloxacin (CIP) and trimethoprim/sulfamethoxazole (TMS) for the prevention of bacteriol infections in patients who received bone marrow transplantation (BMT) for the treatment of solid and hematopoietic neoplasms. Patients and Methods: Adult inpatients about to undergo BMT for lymphoma, leukemia, or solid tumors were enrolled onto a prospective, randomized, double-blinded, controlled trial that compared CIP (750 mg orally twice per day) with TMS (160 mg trimethoprim and 800 mg sulfamethoxazole orally twice per day). Subjects were stratified before randomization according to tumor and BMT type. Prophylaxis was begun within 96 hours of initiation of the BMT preparative regimen and continued until the onset of fever, signs or symptoms of infection, serious adverse effects, or recovery of the absolute granulocyte count (AGC) to greater than or equal to 400/mu L. Results: Seventy-five CIP recipients and 71 TMS recipients were assessable for efficacy. No difference was noted between the two groups in occurrence of fever during neutropenia, time to onset of first fever, or overall infection rates. Ten bacteremias occurred in CIP recipients versus six in TMS recipients (P = .43). Ten episodes of Clostridium difficile enterocolitis occurred in TMS recipients versus no episodes in CIP recipients (P = .001). Four infections caused by gram-negative bacilli, including one bacteremia, occurred in TMS recipients versus none in CIP recipients (P = .06). No differences were noted in the incidence of rash or organ toxicity. TMS recipients had ranger durations of granulocytopenia at AGC levels less than or equal to 500/mu L and less than or equal to 100/mu L than did CIP recipients (P = .08 for both comparisons). Mean peak and trough serum levels of CIP decreased significantly between weeks 1 and 2 of prophylaxis. Conclusion: CIP and TMS were equally safe and effective in the prevention of bacterial infections in BMT patients when the overall infection rate was used as the principal end point. TMS prophylaxis was associated with a higher incidence of C difficile enterocolitis and infections caused by gram-negative bacilli, as well as a trend toward prolongation of granulocytopenia. (C) 1995 by American Society of Clinical Oncology. C1 DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. RI Finberg, Robert/E-3323-2010; Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA 06516, CA 13849]; NIAID NIH HHS [AI129530] NR 78 TC 77 Z9 77 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1995 VL 13 IS 1 BP 239 EP 250 PG 12 WC Oncology SC Oncology GA QA325 UT WOS:A1995QA32500032 PM 7799026 ER PT J AU PATTERSON, WB EMANUEL, EJ AF PATTERSON, WB EMANUEL, EJ TI THE ELIGIBILITY OF WOMEN FOR CLINICAL RESEARCH TRIALS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Discussion C1 DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,BOSTON,MA 02115. SUNY HLTH SCI CTR,DIV HUMANIT MED,BROOKLYN,NY 11203. NR 6 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1995 VL 13 IS 1 BP 293 EP 299 PG 7 WC Oncology SC Oncology GA QA325 UT WOS:A1995QA32500038 PM 7799033 ER PT J AU MCCALL, WV MANN, SC SHELP, FE CAROFF, SN AF MCCALL, WV MANN, SC SHELP, FE CAROFF, SN TI FATAL PULMONARY-EMBOLISM IN THE CATATONIC SYNDROME - 2 CASE-REPORTS AND A LITERATURE-REVIEW SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID NEUROLEPTIC MALIGNANT SYNDROME; AMOBARBITAL INTERVIEW; LETHAL CATATONIA; BENZODIAZEPINES; STATES; STUPOR; MUTISM; DEATH; ECT AB Background: Catatonia is associated with excess early mortality when it is unrecognized or inadequately treated. The characteristics of the lethal catatonia subtype are now well described, but the excess mortality of the remaining patients with catatonic syndrome, particularly from pulmonary embolism, appears to be inadequately recognized. The fatal risk of the catatonic Syndrome is reviewed. Method: Two new case reports of sudden death from pulmonary embolism in catatonic syndrome are presented. The world literature on morbidity, mortality, and pulmonary embolism in catatonia was reviewed by a search of MEDLINE and PsychInfo from 1966 to the present. Additional older references were discovered by screening bibliographies from articles produced by the searches. Results: Twenty cases of autopsy-confirmed pulmonary embolism were found in patients with catatonic syndrome. Catatonic patients were more likely to die of pulmonary embolism and die earlier than patients with other types of schizophrenia. Death from pulmonary embolism did not occur until after the second week of catatonic symptoms and often occurred without warning. Conclusion: Risk of a fatal pulmonary embolism is inherent in persistent catatonic symptoms and may explain the observed excess early mortality. Prompt resolution of the catatonic syndrome with benzodiazepines, barbiturates, or electroconvulsive therapy is the best way to reduce risk of pulmonary embolism. The prophylactic value of physical therapy or anticoagulation merits further investigation. Despite the absence of controlled trials of treatment effectiveness, the catastrophic outcome of acute pulmonary embolism warrants early and vigorous intervention in catatonic patients. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. UNITED BEHAV SERV,RICHMOND,VA. RP MCCALL, WV (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PSYCHIAT & BEHAV MED,MED CTR BLVD,WINSTON SALEM,NC 27157, USA. NR 50 TC 52 Z9 53 U1 0 U2 1 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JAN PY 1995 VL 56 IS 1 BP 21 EP 25 PG 5 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA QE919 UT WOS:A1995QE91900004 PM 7836335 ER PT J AU BLAIS, MA NORMAN, DK QUINTAR, B HERZOG, DB AF BLAIS, MA NORMAN, DK QUINTAR, B HERZOG, DB TI THE EFFECT OF ADMINISTRATION METHOD - A COMPARISON OF THE RAPAPORT AND EXNER RORSCHACH SYSTEMS SO JOURNAL OF CLINICAL PSYCHOLOGY LA English DT Article AB This study compared two Rorschach administration methods across a number of test variables. With a within-subjects, counter-balanced design, 20 female subjects randomly received either an initial Rapaport (Rapaport, Gill, & Schafer, 1968) or an Exner (Exner, 1974, 1986) Rorschach administration. Results showed that the Exner administration produced significantly more Color (C), Shading (Shd), and Blend (B) responses than did the Rapaport administration. Intersystem differences were most prominent on the first presentation of the two administrations. The first Exner administration produced significantly more C, Shd, and Blend responses than did the first Rapaport administration. Findings are discussed in light of their clinical implications, limitations in the experimental design, and suggestions for improving future research. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. NOVA UNIV,FT LAUDERDALE,FL 33314. RP BLAIS, MA (reprint author), MASSACHUSETTS GEN HOSP,BULFINCH 5,BOSTON,MA 02114, USA. NR 19 TC 6 Z9 6 U1 0 U2 0 PU CLINICAL PSYCHOLOGY PUBL CO PI BRANDON PA 4 CONANT SQUARE, BRANDON, VT 05733 SN 0021-9762 J9 J CLIN PSYCHOL JI J. Clin. Psychol. PD JAN PY 1995 VL 51 IS 1 BP 100 EP 107 DI 10.1002/1097-4679(199501)51:1<100::AID-JCLP2270510116>3.0.CO;2-A PG 8 WC Psychology, Clinical SC Psychology GA QL983 UT WOS:A1995QL98300015 PM 7782463 ER PT J AU BHALLA, M SHEPARD, JO NAKAMURA, K KAZEROONI, EA AF BHALLA, M SHEPARD, JO NAKAMURA, K KAZEROONI, EA TI DUAL KV CT TO DETECT CALCIFICATION IN SOLITARY PULMONARY NODULE SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE COMPUTED TOMOGRAPHY, TECHNIQUES; LUNGS, NEOPLASMS; ATTENUATION VALUES ID ENERGY CT; QUANTIFICATION; CALCIUM AB Objective: At the high kVp values used in CT scanning, almost all interactions in soft tissues occur by Compton scattering. By lowering the kVp close to the k-edge of calcium, beam attenuation by calcium will be greater and will be reflected as an increase in density reading (DR). The presence of calcification in solitary pulmonary nodules (SPNs), and thus an implied benign etiology, is currently being diagnosed on CT by using reference phantoms. We explored the possibility of utilizing low kVp (i.e., 80 kVp) to detect the presence of such calcification in SPNs, thus obviating the need for expensive and cumbersome reference phantoms. Materials and Methods: We first tested this phenomenon of photoelectric interaction by CT and its effect on DRs by scanning various dilutions of calcium bicarbonate solution at the standard 140 kVp and at a lower, 80 kVp, setting. After confirming the hypothesis, we conducted a prospective clinical study of 27 consecutive SPNs and scanned them at 140 and 80 kVp to detect the presence of calcification by measuring their DRs at both kVp values. Results: All calcium solutions showed an increase in DR on the 80 kVp scan. Of the 27 nodules, 11 (41%) showed an increase in DR, suggesting the presence of calcification: 10 (91%) were benign, and 1 (9%) was malignant. Conclusion: Our study demonstrates that dual kVp CT could be reliably used to identify calcifications in SPNs, very similar to the use of the reference phantoms currently being applied for the purpose. RP BHALLA, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 16 TC 15 Z9 17 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD JAN-FEB PY 1995 VL 19 IS 1 BP 44 EP 47 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QC326 UT WOS:A1995QC32600008 PM 7822546 ER PT J AU GAZELLE, GS GAA, JC SAINI, S SHELLITO, P AF GAZELLE, GS GAA, JC SAINI, S SHELLITO, P TI STAGING OF COLON-CARCINOMA USING WATER ENEMA CT SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE GASTROINTESTINAL TRACT, NEOPLASMS; COLON, NEOPLASMS; COMPUTED TOMOGRAPHY ID CONTRAST-MEDIUM AB Objective: To determine the accuracy of water enema CT (WECT) for staging colon carcinoma. Materials and Methods: Thirty patients with colon cancer, diagnosed by barium enema andior colonoscopy, underwent preoperative WECT. Dynamic contrast enhanced CT studies were performed after rectal administration of less than or equal to 2 L lukewarm tap water. Images were prospectively analyzed for depth of tumor invasion, nodal involvement, and distant metastases by investigators blinded to the results of barium enema and colonoscopy. SurgicaIipathologic proof was obtained in all cases Results: Using WECT, 23 of 30 patients were correctly staged. Correct staging occurred in 2 of 2 patients with Stage A, 3 of 3 patients with Stage B1, 6 of 9 patients with Stage B2, 1 of 2 patients with Stage C1, 5 of 8 patients with Stage C2, and 6 of 6 patients with Stage D tumors. Of the patients incorrectly staged, 3 were understaged and 3 were overstaged; all were due to errors in predicting lymph node involvement. Sensitivity and specificity for evaluating nodal involvement were 60 and 79%, respectively. Conclusions: Water enema CT allows for accurate depiction and staging of colon carcinoma. Aqueous distention of the colon avoids artifacts seen with positive contrast agents yet allows accurate evaluation of the bowel wall and pericolonic structures. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. RP GAZELLE, GS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 8 TC 61 Z9 70 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD JAN-FEB PY 1995 VL 19 IS 1 BP 87 EP 91 DI 10.1097/00004728-199501000-00017 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QC326 UT WOS:A1995QC32600017 PM 7822556 ER PT J AU PROVENZALE, JM HACEINBEY, L TAVERAS, JM AF PROVENZALE, JM HACEINBEY, L TAVERAS, JM TI INTERNAL CAROTID-ARTERY DISSECTION ASSOCIATED WITH PITUITARY APOPLEXY - MR FINDINGS SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Note DE ARTERIES, DISSECTION; PITUITARY, ABNORMALITIES; MAGNETIC RESONANCE IMAGING ID HEMORRHAGE; ADENOMAS; NECK AB Pituitary apoplexy almost invariably occurs following hemorrhage into a pituitary neoplasm. We report a case in which pituitary apoplexy occurred in the setting of, and probably secondary to, dissection of the internal carotid artery. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP PROVENZALE, JM (reprint author), DUKE UNIV,MED CTR,DEPT RADIOL,BOX 3808,DURHAM,NC 27710, USA. NR 14 TC 8 Z9 8 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD JAN-FEB PY 1995 VL 19 IS 1 BP 150 EP 152 DI 10.1097/00004728-199501000-00031 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QC326 UT WOS:A1995QC32600031 PM 7822536 ER PT J AU YASKELL, T MENGSHOEL, K KASHKET, S AF YASKELL, T MENGSHOEL, K KASHKET, S TI EFFECT OF SODIUM MONOFLUOROPHOSPHATE DURING SUCROSE-INDUCED INTRAORAL DEMINERALIZATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 15 EP 15 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800026 ER PT J AU PROSTAK, K LEES, S AF PROSTAK, K LEES, S TI RELATION BETWEEN MINERAL AND ORGANIC-COMPONENTS OF MINERALIZED COLLAGEN SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 1 U2 2 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 24 EP 24 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800098 ER PT J AU BACHIMAN, R TAVARES, M KENT, R LEGEROS, J BIVONA, P GAO, W GALVIS, D AF BACHIMAN, R TAVARES, M KENT, R LEGEROS, J BIVONA, P GAO, W GALVIS, D TI CARIES PREVALENCE IN ASIAN-AMERICAN ADULTS IN NEW-YORK-CITY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NYU,COLL DENT,NEW YORK,NY 10003. FORSYTH DENT CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 44 EP 44 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800260 ER PT J AU LI, Y CHEN, W STASHENKO, P AF LI, Y CHEN, W STASHENKO, P TI RETINOIC ACID EXERTS DIFFERENTIATION STAGE-DEPENDENT INHIBITION OF BONE-FORMATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 51 EP 51 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800315 ER PT J AU TELES, R WANG, CY ALT, F SOCRANSKY, S TANNER, A STASHENKO, P AF TELES, R WANG, CY ALT, F SOCRANSKY, S TANNER, A STASHENKO, P TI DEVELOPMENT OF A SCID MOUSE MODEL OF PERIAPICAL PATHOGENESIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HSDM,FORSYTH DENT CTR,BOSTON,MA. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 57 EP 57 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800361 ER PT J AU KASHKET, S ZHANG, J VANHOUTE, J AF KASHKET, S ZHANG, J VANHOUTE, J TI ACCUMULATION OF SHORT-CHAIN CARBOXYLIC-ACIDS IN RETAINED FOOD PARTICLES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 79 EP 79 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800537 ER PT J AU BELCHER, JC DEWHIRST, FE PASTER, BJ FRASER, GJ LOPMAN, J VANHOUTE, J AF BELCHER, JC DEWHIRST, FE PASTER, BJ FRASER, GJ LOPMAN, J VANHOUTE, J TI PHYLOGENETIC DIVERSITY OF LOW-PH NON-MUTANS STREPTOCOCCI BY 16S RIBOSOMAL-RNA SEQUENCE-ANALYSIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 93 EP 93 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800652 ER PT J AU COSTELLO, KA SONIS, ST AF COSTELLO, KA SONIS, ST TI ALPHA-HEMOLYTIC STREPTOCOCCAL INFECTION IN GRANULOCYTOPENIC CANCER-PATIENTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 99 EP 99 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800694 ER PT J AU HOUSER, BE ALDER, ME MCANEAR, JT AF HOUSER, BE ALDER, ME MCANEAR, JT TI DENSITY VARIATIONS OF AUTOLOGOUS BONE-GRAFTS ADJACENT TO DENTAL IMPLANTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HSC,SAN ANTONIO,TX 78285. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 111 EP 111 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800794 ER PT J AU ALEXANDER, M LI, YP YELICK, P WUCHERPFENNIG, A CHEN, W STASHENKO, P AF ALEXANDER, M LI, YP YELICK, P WUCHERPFENNIG, A CHEN, W STASHENKO, P TI CHARACTERIZATION OF THE REGULATORY REGION OF A NOVEL OSTEOCLAST CATHEPSIN SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. HSDM,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 118 EP 118 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800849 ER PT J AU KHURANA, P LEE, J SRITHAVAJ, T AKINTOYE, S SYNENSKI, M BIVONA, P HAY, DI SPIELMAN, AI AF KHURANA, P LEE, J SRITHAVAJ, T AKINTOYE, S SYNENSKI, M BIVONA, P HAY, DI SPIELMAN, AI TI SALIVARY ADHESION-PROMOTING PROTEIN - IMMUNOREACTIVE PATTERN AND ETHNICITY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NYU,COLL DENT,NEW YORK,NY 10003. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 122 EP 122 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800881 ER PT J AU SMITH, DJ KING, WF TAUBMAN, MA AF SMITH, DJ KING, WF TAUBMAN, MA TI SYNTHESIS, CELLULAR-DISTRIBUTION AND IMMUNOGENICITY OF STREPTOCOCCUS-MUTANS GLUCAN BINDING-PROTEIN (GBP59) SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. NR 0 TC 3 Z9 5 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 123 EP 123 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800888 ER PT J AU GORTON, J SOCRANSKY, S AF GORTON, J SOCRANSKY, S TI PERIODONTAL PATHOGENS IN PUERTO-RICAN HIV+ SUBJECTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH DENT,CAMBRIDGE,MA 02138. FORSYTH DENT CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 128 EP 128 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800928 ER PT J AU NIEDERMAN, R BUYLEBODIN, T LU, BY NALEWAY, U ROBINSON, P AF NIEDERMAN, R BUYLEBODIN, T LU, BY NALEWAY, U ROBINSON, P TI SHORT-CHAIN CARBOXYLIC-ACIDS IN GCF, CLINICAL AND INFLAMMATORY RELATIONSHIPS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 ADA,CHICAGO,IL. FORSYTH DENT CTR,BOSTON,MA 02115. NORTHWESTERN UNIV,CHICAGO,IL 60611. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 131 EP 131 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800955 ER PT J AU ZHANG, J KASHKET, S NIEDERMAN, R AF ZHANG, J KASHKET, S NIEDERMAN, R TI FOOD-INDUCED ELEVATION OF GINGIVAL TEMPERATURE AND NEUTROPHIL EMIGRATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 131 EP 131 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00800952 ER PT J AU TAVARES, M BACHIMAN, R GALVIS, D KENT, R LEGEROS, J BIVONA, P GAO, W AF TAVARES, M BACHIMAN, R GALVIS, D KENT, R LEGEROS, J BIVONA, P GAO, W TI THE PERIODONTAL PROFILE OF ASIAN-AMERICAN ADULTS IN NEW-YORK-CITY SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NYU,COLL DENT,NEW YORK,NY 10003. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 145 EP 145 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801067 ER PT J AU YELICK, PC NEUHASS, S DRIEVER, W STASHENKO, P AF YELICK, PC NEUHASS, S DRIEVER, W STASHENKO, P TI CRANIOFACIAL DEVELOPMENT IN NORMAL AND MUTANT ZEBRAFISH SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 148 EP 148 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801087 ER PT J AU WANG, CY TELES, R MARKS, S STASHENKO, P AF WANG, CY TELES, R MARKS, S STASHENKO, P TI EFFECT OF OSTEOCLAST DEFICIENCY ON PERIAPICAL BONE-RESORPTION IN TL/TL RATS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA 01605. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 161 EP 161 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801189 ER PT J AU SAUNDERS, MJ PAUNOVICH, ED CORNELL, JE AF SAUNDERS, MJ PAUNOVICH, ED CORNELL, JE TI ORAL HEALTH QUALITY-OF-LIFE INVENTORY - DEVELOPMENT AND VALIDATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,RCOHA,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 168 EP 168 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801246 ER PT J AU MCANEAR, JT SAUNDERS, MJ VENUS, CA CHAMBERLAIN, CK SMITH, C AF MCANEAR, JT SAUNDERS, MJ VENUS, CA CHAMBERLAIN, CK SMITH, C TI BITE FORCE FOLLOWING OSSEOINTEGRATED MAXILLARY BONE-GRAFTS AND IMPLANTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 170 EP 170 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801264 ER PT J AU FINKELMAN, RD HILL, EL MITLAK, BH MARTIN, RB LI, J LYNCH, SE AF FINKELMAN, RD HILL, EL MITLAK, BH MARTIN, RB LI, J LYNCH, SE TI SYSTEMIC PDGF+/- ALENDRONATE INCREASES BONE-DENSITY IN OVX RATS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 INST MOLEC BIOL INC,WORCESTER,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,BOSTON,MA 02115. UNIV CALIF DAVIS,DAVIS,CA 95616. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 172 EP 172 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801276 ER PT J AU HAFFAJEE, AD SMITH, C DIBART, S CUGINI, MA SOCRANSKY, SS AF HAFFAJEE, AD SMITH, C DIBART, S CUGINI, MA SOCRANSKY, SS TI THE PREVALENCE OF SUBGINGIVAL TAXA USING CHECKERBOARD DNA-DNA HYBRIDIZATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 1 U2 2 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 173 EP 173 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801291 ER PT J AU SAKELLARI, D TAUBMAN, MA SOCRANSKY, SS AF SAKELLARI, D TAUBMAN, MA SOCRANSKY, SS TI QUANTITATION OF SERUM ANTIBODY TO SUBGINGIVAL SPECIES USING CHECKERBOARD IMMUNOBLOTTING SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. RI SAKELLARI, DIMITRA/F-3299-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 173 EP 173 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801287 ER PT J AU SOCRANSKY, SS SMITH, C DIBART, S CUGINI, MA HAFFAJEE, AD AF SOCRANSKY, SS SMITH, C DIBART, S CUGINI, MA HAFFAJEE, AD TI COMPARISON OF CHECKERBOARD AND COLONY LIFT DNA-DNA HYBRIDIZATION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 1 U2 3 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 174 EP 174 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801292 ER PT J AU DOBECK, JM SKOBE, Z HEELEY, JD SMITH, C SOCRANSKY, SS AF DOBECK, JM SKOBE, Z HEELEY, JD SMITH, C SOCRANSKY, SS TI DNA HYBRIDIZATION TO IDENTIFY BACTERIA IN HISTOLOGICAL SECTIONS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 197 EP 197 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801481 ER PT J AU MACHUCH, PJ TANNER, A MAIDEN, MFJ AF MACHUCH, PJ TANNER, A MAIDEN, MFJ TI CAMPYLOBACTER SPECIES FROM SUBGINGIVAL SITES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 198 EP 198 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801486 ER PT J AU KAWAI, T TAUBMAN, MA EASTCOTT, JW SMITH, DJ AF KAWAI, T TAUBMAN, MA EASTCOTT, JW SMITH, DJ TI MHC CLASS-II ANTIGEN ON RAT GINGIVAL FIBROBLASTS DETECTED BY CELLULAR ELISA SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 202 EP 202 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801521 ER PT J AU STERN, D SENGER, D ASHKAR, S GLIMCHER, MJ SAAVEDRA, R AF STERN, D SENGER, D ASHKAR, S GLIMCHER, MJ SAAVEDRA, R TI LOCALIZATION OF OSTEOPONTIN AND BETA-3-INTEGRIN RECEPTOR IN HUMAN GINGIVAL EPITHELIUM SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DEPT ORTHOPAED RES,BOSTON,MA 02115. FORSYTH DENT CTR,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT PATHOL,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 202 EP 202 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801523 ER PT J AU TAKEICHI, O TAUBMAN, MA HABER, J SMITH, DJ MORO, I AF TAKEICHI, O TAUBMAN, MA HABER, J SMITH, DJ MORO, I TI CYTOKINE PROFILES OF CD4 AND CD8 T-CELLS ISOLATED FROM ADULT PERIODONTITIS GINGIVAE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TUFTS UNIV,FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02111. NIHON UNIV,TOKYO 101,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 205 EP 205 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801542 ER PT J AU TANNER, A MACUCH, PJ MAIDEN, MFJ MURRAY, L CUGINI, MA AF TANNER, A MACUCH, PJ MAIDEN, MFJ MURRAY, L CUGINI, MA TI CLINICAL AND MICROBIAL CHARACTERISTICS OF HEALTH, GINGIVITIS, AND INITIAL PERIODONTITIS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 225 EP 225 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801702 ER PT J AU COLOMBO, AP SAKELLARI, D HAFFAJEE, AD DIBART, S TAUBMAN, MA SOCRANSKY, SS AF COLOMBO, AP SAKELLARI, D HAFFAJEE, AD DIBART, S TAUBMAN, MA SOCRANSKY, SS TI SERUM ANTIBODY LEVEL IN REFRACTORY PERIODONTITIS SUBJECTS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. RI SAKELLARI, DIMITRA/F-3299-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 226 EP 226 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801711 ER PT J AU DIBART, S SOCRANSKY, SS HAFFAJEE, AD LAI, CH EFTIMIADI, C AF DIBART, S SOCRANSKY, SS HAFFAJEE, AD LAI, CH EFTIMIADI, C TI DETECTION OF BACTEROIDES-FORSYTHUS IN EPITHELIAL-CELLS FROM PERIODONTAL POCKETS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. UNIV PENN,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 226 EP 226 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801707 ER PT J AU EFTIMIADI, C SAKELLARI, D DIBART, S TAUBMAN, MA SOCRANSKY, SS AF EFTIMIADI, C SAKELLARI, D DIBART, S TAUBMAN, MA SOCRANSKY, SS TI DETECTION OF CREVICULAR FLUID ANTIBODY TO SUBGINGIVAL SPECIES USING CHECKERBOARD IMMUNOBLOTTING SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. RI SAKELLARI, DIMITRA/F-3299-2011 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 226 EP 226 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801708 ER PT J AU VENUS, CA CHAMBERLAIN, CK SAUNDERS, MJ MCANEAR, JT AF VENUS, CA CHAMBERLAIN, CK SAUNDERS, MJ MCANEAR, JT TI CHANGES IN SPEECH ARTICULATION FOLLOWING REMOVAL OF DENTURES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 226 EP 226 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801710 ER PT J AU OLSEN, J SALIH, M HARRISON, JL HERRERA, I LUTHER, MF LIFSCHITZ, MD KATZ, MS YEH, CK AF OLSEN, J SALIH, M HARRISON, JL HERRERA, I LUTHER, MF LIFSCHITZ, MD KATZ, MS YEH, CK TI EFFECTS OF FOOD RESTRICTION ON INTRACELLULAR CALCIUM SIGNALING IN PAROTID ACINAR-CELLS OF AGING RATS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UTHSCSA,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 229 EP 229 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801735 ER PT J AU BOYLAN, R BAMGBOYE, P FERRER, J HAFFAJEE, A MORENO, E CRAIG, R AF BOYLAN, R BAMGBOYE, P FERRER, J HAFFAJEE, A MORENO, E CRAIG, R TI PERIODONTAL-DISEASE RISK ASSESSMENT IN URBAN MINORITY POPULATIONS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NYUCD,NEW YORK,NY. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 232 EP 232 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801757 ER PT J AU JONES, JD WILLMANN, DE ARNOLD, R SAUNDERS, MJ AF JONES, JD WILLMANN, DE ARNOLD, R SAUNDERS, MJ TI ASSESSING RELIABILITY OF RETENTION AND STABILITY MEASUREMENTS IN EVALUATING COMPLETE DENTURES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,RCOHA,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 240 EP 240 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801824 ER PT J AU SMITH, DJ KING, WF MELVIN, JL TAUBMAN, MA AF SMITH, DJ KING, WF MELVIN, JL TAUBMAN, MA TI ORIGIN OF GLUCAN BINDING-PROTEIN (GBP99) AMONG ORAL STREPTOCOCCI THAT INITIALLY COLONIZE CHILDREN SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA. NR 0 TC 1 Z9 3 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 248 EP 248 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801889 ER PT J AU FRASER, GJ PASTER, BJ BELCHER, JC DEWHIRST, FE AF FRASER, GJ PASTER, BJ BELCHER, JC DEWHIRST, FE TI PHYLOGENY OF CULTIVABLE ORAL TREPONEMES FROM THE SMIBERT COLLECTION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 249 EP 249 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QA008 UT WOS:A1995QA00801893 ER PT J AU STASHENKO, P WANG, CY RILEY, E WU, Y OSTROFF, G NIEDERMAN, R AF STASHENKO, P WANG, CY RILEY, E WU, Y OSTROFF, G NIEDERMAN, R TI REDUCTION OF INFECTION-STIMULATED PERIAPICAL BONE-RESORPTION BY THE BIOLOGICAL RESPONSE MODIFIER PGG GLUCAN SO JOURNAL OF DENTAL RESEARCH LA English DT Article DE PERIAPICAL; BONE RESORPTION; BACTERIAL INFECTION; IMMUNOMODULATOR; LEUKOCYTES ID PERIODONTAL-DISEASE; LESIONS; RESISTANCE; ADJUVANT; CELLS AB Pulpal and periodontal diseases are bacterial infections which result in local connective tissue and bone destruction. Effective host resistance to these infections is primarily mediated by neutrophils and other phagocytic cells. PGG glucan (poly-beta 1-6-glucotriosyl-beta 1-3-glucopyranose glucan) is a biological response modifier which stimulates the production of neutrophils and upregulates their phagocytic and bactericidal activity. In the present studies, the effect of PGG glucan on infection-stimulated alveolar bone resorption was tested in an in vivo model. Periapical bone resorption was induced in Sprague-Dawley rats by surgical pulp exposure and subsequent infection from the oral environment. Animals were administered PGG glucan (0.5 mg/kg) or saline (control) subcutaneously the day before and on days 2, 4, 6, 9, 11, 13, 16, and 18 following the pulp exposure procedure. PGG glucan enhanced the number of circulating neutrophils and monocytes and increased neutrophil phagocytic activity approximately two-fold. PGG glucan-treated animals had significantly less infection-stimulated periapical bone resorption than control animals, as determined radiographically (-48.0%; p < 0.001) and by histomorphometry (-40.8% and -42.4% for first and second molars, respectively; p < 0.01). PGG glucan-treated animals also had less soft tissue destruction, as indicated by decreased pulpal necrosis. Only 3.3% of first molar pulps from PGG glucan-treated animals exhibited complete necrosis, as compared with 40.6% of pulps from controls. Finally, PGG glucan had no effect on either PTH- or IL-1-stimulated bone resorption in vitro. These findings support the concept that a biological response modifier which enhances endogenous antibacterial mechanisms in neutrophils can decrease infection-stimulated alveolar bone and soft tissue destruction in vivo. C1 FORSYTH DENT CTR,DEPT CELL BIOL,BOSTON,MA 02115. ALPHA BETA TECHNOL INC,WORCESTER,MA. RP STASHENKO, P (reprint author), FORSYTH DENT CTR,DEPT CYTOKINE BIOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-09018] NR 35 TC 34 Z9 37 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD JAN PY 1995 VL 74 IS 1 BP 323 EP 330 PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QK445 UT WOS:A1995QK44500006 PM 7876425 ER PT J AU SHANETZKY, B HORVITZ, D SMORODINSKY, N GANESHKUMAR, N WEISS, E AF SHANETZKY, B HORVITZ, D SMORODINSKY, N GANESHKUMAR, N WEISS, E TI COAGGREGATION WITH P-GINGIVALIS PK1924 SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA. TEL AVIV UNIV,SCH DENT MED,IL-69978 TEL AVIV,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 407 EP 407 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100053 ER PT J AU MASUNO, K WARAASWAPATI, N SOCRANSKY, S EGAL, M GENCO, C WAGNER, D MAYADAS, T HYNES, R NIEDERMAN, R AF MASUNO, K WARAASWAPATI, N SOCRANSKY, S EGAL, M GENCO, C WAGNER, D MAYADAS, T HYNES, R NIEDERMAN, R TI P-SELECTIN KNOCKOUT MOUSE SUSCEPTIBILITY TO PERIODONTAL-DISEASE SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 MIT,CTR BLOOD RES,CAMBRIDGE,MA 02139. MIT,MOREHOUSE SCH MED,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 419 EP 419 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100151 ER PT J AU NARA, Y MASEKI, T NAGAKURA, Y SHIZAKA, C DOGON, IL AF NARA, Y MASEKI, T NAGAKURA, Y SHIZAKA, C DOGON, IL TI MICROLEAKAGE AND INTERFACIAL SEM INVESTIGATION OF STANDARD AND MODIFIED ADHESIVE SYSTEMS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH DENT MED,FORSYTH DEN CTR,CAMBRIDGE,MA 02138. NIPPON DEN UNIV,TOKYO,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 428 EP 428 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100220 ER PT J AU ALI, RW MARTIN, L BAKKEN, V SKAUG, N SOCRANSKY, SS AF ALI, RW MARTIN, L BAKKEN, V SKAUG, N SOCRANSKY, SS TI ROBOTYPES OF PORPHYROMONAS-GINGIVALIS ISOLATES FROM 4 COUNTRIES SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV BERGEN,N-5007 BERGEN,NORWAY. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 466 EP 466 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100522 ER PT J AU GANESHKUMAR, N HAY, DI AF GANESHKUMAR, N HAY, DI TI IDENTIFICATION OF EXPORTED PROTEINS OF FUSOBACTERIUM-NUCLEATUM USING PHOA TRANSLATIONAL GENE FUSIONS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 466 EP 466 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100521 ER PT J AU TANAKA, M MARGOLIS, HC MORENO, EC AF TANAKA, M MARGOLIS, HC MORENO, EC TI RELEASE OF MINERAL IONS IN PLAQUE FOLLOWING ACID PRODUCTION SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TOKYO MED & DENT UNIV,TOKYO 113,JAPAN. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1995 VL 74 SI SI BP 473 EP 473 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT081 UT WOS:A1995QT08100581 ER PT J AU GRUPP, SA MITCHELL, RN SCHREIBER, KL MCKEAN, DJ ABBAS, AK AF GRUPP, SA MITCHELL, RN SCHREIBER, KL MCKEAN, DJ ABBAS, AK TI MOLECULAR MECHANISMS THAT CONTROL EXPRESSION OF THE B-LYMPHOCYTE ANTIGEN RECEPTOR COMPLEX SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID IG-BETA; CELL-SURFACE; T-CELL; IMMUNOGLOBULIN; ALPHA; PROTEIN; COMPONENTS; MB-1; GENE; IDENTIFICATION AB The B cell receptor for antigen (BCR) is a complex of membrane immunoglobulin (mig) and at least two other proteins, Ig alpha (mb-1) and Ig beta (B29). This complex promotes surface expression of the BCR and acts to transduce an activation signal. We have used a system of mu heavy chain constructs transfected into murine B cell lines to probe structure-function relationships in the BCR complex. One mutant mu chain, in which two polar transmembrane residues (Tyr(587), Ser(588)) are replaced with valine, fails to associate with Ig alpha and Ig beta and is incapable of transducing signals as a result of mig cross-linking. This mutant is expressed on the surface at high levels when transfected into a plasmacytoma line that lacks Ig alpha, whereas wild-type mu is retained in this cell line in the endoplasmic reticulum. pulse-chase and immunoprecipitation analyses indicate that the mutant is more rapidly released from calnexin than the wild-type mu. Further, transfection of Ig alpha into this Ig alpha-negative cell line allows release of the mu chain from calnexin and surface expression of the BCR. These results identify the transmembrane residues of Le heavy chain that control binding to calnexin and Ig alpha, and suggest that calnexin-dependent intracellular retention is an important control mechanism for expression of the BCR complex. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV IMMUNOL RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MAYO CLIN & MAYO FDN,DEPT IMMUNOL,ROCHESTER,MN 55905. RP GRUPP, SA (reprint author), DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-22802]; NIGMS NIH HHS [GM-47726] NR 28 TC 37 Z9 37 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 161 EP 168 DI 10.1084/jem.181.1.161 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200017 PM 7807000 ER PT J AU SCHNEIDER, H PRASAD, KVS SHOELSON, SE RUDD, CE AF SCHNEIDER, H PRASAD, KVS SHOELSON, SE RUDD, CE TI CTLA-4 BINDING TO THE LIPID KINASE PHOSPHATIDYLINOSITOL 3-KINASE IN T-CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID COSTIMULATORY SIGNAL; LYMPHOCYTES-T; CD28 RECEPTOR; ACTIVATION; ANTIGEN; EXPRESSION; MOLECULES; B7/BB1; LIGAND AB CTLA-4 is a T cell antigen that is structurally related to CD28 and serves as a high affinity ligand for the B cell antigen B7-1/2. Unlike CD28, the function of CTLA-4 is unclear, although reports have implicated the antigen in the costimulation of T cells. Recently, phosphatidylinositol 3-kinase (PI 3-kinase) has been implicated in the costimulatory function of CD28 by virtue of its ability to bind to a pYMNM motif within the cytoplasmic tail of the antigen. In this study, we show that CTLA-4 can also associate with PI 3-kinase as detected by lipid kinase analysis and immunoblotting with anti-p85 antiserum. High pressure liquid chromatographic separation of deacylated lipids showed the presence of a peak corresponding to PI-3-P. Anti-CTLA-4 ligation of the receptor induced a significant increase in the levels of precipitable PI 3-kinase activity. Peptide binding studies revealed that the NH2- and COOH-terminal SH2 domains of p85 bind the CTLA-4 cytoplasmic pYVKM motif with an affinity (ID50: 0.6 and 0.04 mu M), that is similar to CD28. CTLA-4 binding to PI 3-kinase provides further evidence that CTLA-4 is not an inert counterreceptor, but rather is coupled to an intracellular signaling molecule with the capacity to regulate cell growth. C1 DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU PHS HHS [R01 1206] NR 32 TC 131 Z9 133 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1995 VL 181 IS 1 BP 351 EP 355 DI 10.1084/jem.181.1.351 PG 5 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QA042 UT WOS:A1995QA04200035 PM 7807015 ER PT J AU ROYALL, DR MAHURIN, RK CORNELL, J AF ROYALL, DR MAHURIN, RK CORNELL, J TI EFFECT OF DEPRESSION ON DEMENTIA PRESENTATION - QUALITATIVE ASSESSMENT WITH THE QUALITATIVE EVALUATION OF DEMENTIA (QED) SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article ID MINI-MENTAL STATE; COGNITIVE IMPAIRMENT; ALZHEIMER TYPE; SUBCORTICAL DEMENTIA; BEDSIDE ASSESSMENT; SENILE DEMENTIA; DISEASE; PSEUDODEMENTIA; CRITERIA; FEATURES AB Two novel, bedsides, dementia assessment instruments, the Executive Interview (EXIT) and the Qualitative Evaluation of Dementia (QED) were used to examine the effects of DSM-III-R major depressive episodes on the clinical presentation of patients diagnosed with NINCDS ''possible'' AD. Intergroup comparisons were made of the various bedside cognitive measures given to 102 to 118 consecutive patients presenting to a university geriatric assessment clinic and consultation service. The assessment instruments used were: (1) the EXIT: a 15-minute, 25-item bedside interview for the assessment of executive control function (ECF); (2) the QED: a brief, clinically based checklist that operationalizes the approach of a geriatric psychiatrist to the qualitative assessment of dementing illnesses (when QED scores are mapped against EXIT scores, a qualitative picture of dementia typology emerges); and (3) the Mini-Mental State Exam (MMSE): a familiar bedside measure of cognitive function. Depressed and nondepressed patients differed significantly on the QED. There was no overlap in the QED scores of patients with probable AD versus those with depression. The QED discriminated between depressed and nondepressed patients with possible AD. Possible AD patients with depression could not be qualitatively distinguished from those with depression alone, although they could be discriminated by the EXIT. Only 44% of possible AD cases fall within the EXIT x QED 90% confidence limits for probable AD. No differences were found on either the QED or the MMSE between depressed non-AD patients and nondepressed patients exhibiting ''dementia with no cortical features.'' The MMSE was insensitive to cognitive impairment in non-AD cases. NINCDS ''possible'' AD is a qualitatively heterogeneous group. Depression alters the presentation of AD, with depressed Alzheimer's patients appearing qualitatively similar to other depressed patients, but with far more executive impairment. Patients with the ''dementia of depression'' cannot be qualitatively distinguished from those with subcortical dementias. The MMSE underestimates the level of executive cognitive impairment in qualitatively subcortical dementia. These distinctions can be made at the bedside through the combined use of the EXIT and the QED. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 55 TC 13 Z9 13 U1 4 U2 4 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON ST, PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD JAN PY 1995 VL 8 IS 1 BP 4 EP 11 PG 8 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA QE715 UT WOS:A1995QE71500002 PM 7710646 ER PT J AU DORFMAN, R WALTERS, K BURKE, P HARDIN, L KARANIK, T RAPHAEL, J SILVERSTEIN, E AF DORFMAN, R WALTERS, K BURKE, P HARDIN, L KARANIK, T RAPHAEL, J SILVERSTEIN, E TI OLD, SAD AND ALONE - THE MYTH OF THE AGING HOMOSEXUAL SO JOURNAL OF GERONTOLOGICAL SOCIAL WORK LA English DT Article ID DEPRESSIVE SYMPTOMS; SOCIAL SUPPORT; GAY AB This paper reports the findings of a survey of 108 elderly heterosexual and homosexual men and women in urban Central and Southern California. The purpose of the study was to test the assumption that elderly gay men and lesbians are more depressed and socially-isolated than their heterosexual cohort. The findings indicate that there are no significant differences between older heterosexuals and homosexuals in regard to depression and social support. However, the sources of social support vary with gay men and lesbians deriving significantly more support from friends, while heterosexual elderly derive more support from family. The findings suggest a need to redefine the concept of family to include ''friendship families.'' Future research which investigates the way in which these friendship families are created and maintained has the potential to benefit all elderly, especially those who have no biological families or whose biological families are unavailable for support. C1 W LOS ANGELES VET ADM,LOS ANGELES,CA. LOS ANGELES CTY DEPT CHILDRENS PROTECT SERV,LOS ANGELES,CA. MAPLE CTR,BEVERLY HILLS,CA. RP DORFMAN, R (reprint author), UNIV CALIF LOS ANGELES,DEPT SOCIAL WELFARE,LOS ANGELES,CA 90024, USA. NR 39 TC 34 Z9 34 U1 0 U2 1 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0163-4372 J9 J GERONTOL SOC WORK JI J. Gerontol. Soc. Work PY 1995 VL 24 IS 1-2 BP 29 EP 44 PG 16 WC Geriatrics & Gerontology; Social Work SC Geriatrics & Gerontology; Social Work GA TA219 UT WOS:A1995TA21900004 ER PT J AU KLOEN, P JENNINGS, CL GEBHARDT, MC SPRINGFIELD, DS MANKIN, HJ AF KLOEN, P JENNINGS, CL GEBHARDT, MC SPRINGFIELD, DS MANKIN, HJ TI TRANSFORMING GROWTH-FACTOR-BETA - POSSIBLE ROLES IN DUPUYTRENS CONTRACTURE SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Article AB Transforming growth factor-beta (TGF-beta) is a multifunctional polypeptide that stimulates extracellular matrix deposition and fibroblast proliferation. Because both these features characterize Dupuytren's contracture, we investigated a possible role for TGF-beta in the etiology of this disorder. We studied receptor expression for TGF-beta, effects of TGF-beta 1 on DNA-synthesis, and in vitro production of TGF-beta 1 and TCF-beta 2 in both normal and Dupuytren-derived fibroblasts. We also studied the effects of epidermal growth factor (ECF) on growth of the different cell types. TGF-beta receptor profiles were different between the two cell types, as were TGF-beta 1 and EGF-induced stimulation of cell growth. Both cell types secreted both active and latent TGF-beta. Our results suggest that growth factors such as TGF-beta and ECF may play a role in Dupuytren's contracture. RP KLOEN, P (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114, USA. NR 0 TC 37 Z9 38 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD JAN PY 1995 VL 20A IS 1 BP 101 EP 108 DI 10.1016/S0363-5023(05)80067-X PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA QD193 UT WOS:A1995QD19300022 PM 7722248 ER PT J AU ROSOWSKY, A MOTA, CE QUEENER, SF AF ROSOWSKY, A MOTA, CE QUEENER, SF TI SYNTHESIS AND ANTIFOLATE ACTIVITY OF 2,4-DIAMINO-5,6,7,8-TETRAHYDROPYRIDO[4,3-D]PYRIMIDINE ANALOGS OF TRIMETREXATE AND PIRITREXIM SO JOURNAL OF HETEROCYCLIC CHEMISTRY LA English DT Article ID PNEUMOCYSTIS-CARINII PNEUMONIA; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; GONDII DIHYDROFOLATE-REDUCTASE; LIPID-SOLUBLE ANTIFOLATE; TOXOPLASMA-GONDII; METHOTREXATE ANALOGS; INVITRO; POTENT; INVIVO; AIDS AB 2,4-Diamino-5,6,7,8-tetrahydropyrido[4,3-d]pyrimidines with di- and trimethoxyaralkyl substitution at the 6-position were synthesized from the N6-unsubstituted compound and appropriate aralkyl bromides in N,N-dimethylformamide solution containing a catalytic amount of sodium iodide. An improved method of preparation of 2,4-diamino-5,6,7,8-tetrahydropyrido[4,3-d]pyrimidine from 2-amino-6-benzyl-5,6,7,8-tetrahydropyrido[4,3-d]pyrimidin-4(3H)-one was also developed, in which N2 was protected by reaction with pivalic anhydride and the resulting product was subjected consecutively to reaction with 4-chloro-phenylphosphorodichloridate and 1,2,4-triazole, ammonolysis to replace the 4-imidazolido group and remove the N2-pivaloyl group, and catalytic hydrogenolysis to remove the 6-benzyl group. In assays of the ability of the products to inhibit dihydrofolate reductase from Pneumocystis carinii, and Toxoplasma gondii, and rat liver the most active of the compounds tested was 2,4-diamino-6-(2'-!romo-3',4',5'-trimethoxybenzyl)-5,6,7,8-tetrahydropyrido[4,3-d]pyrimidine. The concentration of this compound needed to inhibit enzyme activity by 50% was 0.51 muM against the P. carinii enzyme, 0.09 muM against the T. gondii enzyme, and 0.35 muM against the rat enzyme. Thus, there was selectivity of binding to T. gondii enzyme, but not P. carinii enzyme, relative to rat enzyme. 2',5'-Dimethoxybenzyl analogues were less active than the corresponding 3',4',5'-trimethoxybenzyl analogues, and compounds with a CH2CH2 or CH2CH2CH2 bridge were less active than those with a CH2 bridge. 2,4-Diamino-6-(2'-bromo-3',4',5'-trimethoxybenzyl)-5,6,7,8-tetrahydropyriod[4,3-d]pyrimidine showed greater selectivity than trimetrexate or piritrexim for the P. carinii and T. gondii enzyme, but was less selective than trimethoprim or pyrimethamine. However its molar potency against both enzymes was greater than that of trimethoprim, the antifolate most commonly used, in combination with sulfamethoxazole, for initial treatment of opportunistic P. carinii and T. gondii infections in patients with AIDS and other disorders of the immune system. C1 INDIANA UNIV,SCH MED,DEPT PHARMACOL & TOXICOL,INDIANAPOLIS,IN 46202. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP ROSOWSKY, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 46 TC 55 Z9 56 U1 0 U2 0 PU HETERO CORPORATION PI TAMPA PA BOX 20285, TAMPA, FL 33622-0285 SN 0022-152X J9 J HETEROCYCLIC CHEM JI J. Heterocycl. Chem. PD JAN-FEB PY 1995 VL 32 IS 1 BP 335 EP 340 PG 6 WC Chemistry, Organic SC Chemistry GA QH746 UT WOS:A1995QH74600055 ER PT J AU LUZURIAGA, K HOLMES, D HEREEMA, A WONG, J PANICALI, DL SULLIVAN, JL AF LUZURIAGA, K HOLMES, D HEREEMA, A WONG, J PANICALI, DL SULLIVAN, JL TI HIV-1-SPECIFIC CYTOTOXIC T-LYMPHOCYTE RESPONSES IN THE FIRST YEAR OF LIFE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; RESPIRATORY SYNCYTIAL VIRUS; CEREBROSPINAL-FLUID; INFECTED CHILDREN; PERIPHERAL-BLOOD; HIV-1; CELLS; INFANTS; INDIVIDUALS; COMPLEX AB HIV-1-specific CTL responses were prospectively evaluated in infants born to HIV-1-seropositive women to assess the capability of the young infant to generate HIV-1-specific CTL and to examine the potential role of HIV-1-specific CTL in the pathogenesis of vertical infection. Our results indicate that some young infants, and even the fetus, seem to be capable of generating virus-specific CTL responses. The detection of HIV-1-specific CTL responses varied among infants, however, with respect to timing, HIV-1 gene product recognition, and the magnitude of detectable responses; HIV-1-specific CTL responses were uncommonly detected in the first few months of life. The less consistent detection of HIV-specific CTL in early infancy contrasts with reports of the detection of HIV-1-specific CTL soon after primary infection in adults. HIV-1-specific CTL were not detected in any uninfected infants born to HIV-1-seropositive women. This description of HIV-1-specific CTL in infants may have important implications for understanding the pathogenesis of vertical HIV-1 infection and for the development of a vaccine to interrupt vertical infection. C1 UNIV MASSACHUSETTS,SCH MED,PROGRAM MOLEC MED,WORCESTER,MA 01605. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. THERION BIOL,CAMBRIDGE,MA 02142. RP LUZURIAGA, K (reprint author), UNIV MASSACHUSETTS,SCH MED,DEPT PEDIAT,SUITE 318,BIOTECH 2,373 PLANTAT ST,WORCESTER,MA 01605, USA. FU NIAID NIH HHS [AI 26507, AI 32391, AI 82507] NR 37 TC 122 Z9 123 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1995 VL 154 IS 1 BP 433 EP 443 PG 11 WC Immunology SC Immunology GA PY218 UT WOS:A1995PY21800044 PM 7995957 ER PT J AU ENGLUND, JA GLEZEN, WP TURNER, C HARVEY, J THOMPSON, C SIBER, GR AF ENGLUND, JA GLEZEN, WP TURNER, C HARVEY, J THOMPSON, C SIBER, GR TI TRANSPLACENTAL ANTIBODY TRANSFER FOLLOWING MATERNAL IMMUNIZATION WITH POLYSACCHARIDE AND CONJUGATE HAEMOPHILUS-INFLUENZAE TYPE-B VACCINES SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HEMOPHILUS-INFLUENZAE; CAPSULAR POLYSACCHARIDE; IGG SUBCLASS; INFECTIONS; CHILDREN; INFANTS; TETANUS; EPIDEMIOLOGY; PREVENTION; MENINGITIS AB Passive transfer of antibody to infants born to women immunized during the third trimester of pregnancy with a Haemophilus influenzae type b (Hib) vaccine (PRP polysaccharide or Hib conjugates PRP-D or HbOC) was studied in 50 mothers and infants and 47 nonimmunized mother-infant pairs. Geometric mean total PRP antibody by RIA was 1.2 mu g/mL at delivery in unimmunized women and 21, 149, and 171 mu g/mL in women who received PRP, PRP-D, and HbOC, respectively. Mean cord PRP antibody levels were 0.29, 3.0, 17.5, and 29.3 mu g/mL for the corresponding groups. Postimmunization and cord PRP antibody levels were higher after maternal immunization with conjugate vaccines than with PRP vaccine (P <.01). PRP Ige1 subclass was transmitted more efficiently than IgG2 (56% vs, 35%, P <.01). The proportion of anti-PRP IgG transmitted from immunized mothers to infants correlated with time between immunization and delivery. Administration of PRP conjugate vaccines to women during pregnancy resulted in higher levels of PRP antibodies in infants than did polysaccharide or no vaccine. C1 BAYLOR COLL MED,DEPT PEDIAT,HOUSTON,TX 77030. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ENGLUND, JA (reprint author), BAYLOR COLL MED,DEPT MICROBIOL & IMMUNOL,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. FU NIAID NIH HHS [AI-15126, AI-18125, AI-25135] NR 25 TC 69 Z9 72 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1995 VL 171 IS 1 BP 99 EP 105 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA PZ873 UT WOS:A1995PZ87300015 PM 7798688 ER PT J AU Shenkar, R Cohen, AJ Vestweber, D Miller, YE Tuder, R Abraham, E AF Shenkar, R Cohen, AJ Vestweber, D Miller, YE Tuder, R Abraham, E TI Hemorrhage and resuscitation alter the expression of ICAM-1 and P-selectin in mice SO JOURNAL OF INFLAMMATION LA English DT Article DE inflammatory lung injury; blood loss; trauma; neutrophil infiltration; cell trafficking ID INTERCELLULAR-ADHESION MOLECULE-1; RESPIRATORY-DISTRESS SYNDROME; TUMOR-NECROSIS-FACTOR; HUMAN-ENDOTHELIAL-CELLS; GROWTH-FACTOR-BETA; WEIBEL-PALADE BODIES; OXYGEN-TOXICITY; FACTOR-ALPHA; LUNG INJURY; GMP-140 AB Acute inflammatory lung injury is a common clinical occurrence following blood loss and trauma, and is characterized by massive neutrophil infiltration into the lung. In order to better examine cell trafficking that may contribute to lung injury in this setting, we investigated in vivo mRNA levels and immunohistochemically determined expression of the adhesion molecules P-selectin and the intercellular adhesion molecule (ICAM)-1 in murine lungs over the 3-day period following hemorrhage and resuscitation. Significant increases in P-selectin mRNA levels were present in lungs obtained 3 days after hemorrhage. ICAM-1 mRNA levels were significantly increased 6 and 72 hr after hemorrhage. Immunohistochemical staining for P-selectin was enhanced on pulmonary vascular endothelium in all visible vessels at 6, 24, and 72 hr after hemorrhage. ICAM-1 immunoreactivity was significantly increased on the alveolar epithelium at 6 and 72 hr post-hemorrhage. These results suggest that increased expression of adhesion molecules in the lung at early post-hemorrhage timepoints may contribute to neutrophil infiltration into the lungs and the frequent development of acute lung injury following blood loss and trauma. (C) 1995 Wiley-Liss, Inc. C1 UNIV COLORADO,HLTH SCI CTR,DIV PULM SCI & CRIT CARE MED,DENVER,CO 80262. MAX PLANCK INST IMMUNBIOL,SPEMAN LABS,FREIBURG ZAHRINGER,GERMANY. DENVER VET AFFAIRS MED CTR,DENVER,CO. OI Vestweber, Dietmar/0000-0002-3517-732X FU NCI NIH HHS [P50 CA 58187]; NHLBI NIH HHS [HL 50284, R01 HL 45745] NR 53 TC 15 Z9 15 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 1078-7852 J9 J INFLAMM JI J. Inflamm. PY 1995 VL 45 IS 4 BP 248 EP 259 PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Hematology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Hematology; Immunology GA TT108 UT WOS:A1995TT10800003 PM 8867669 ER PT J AU SHIH, VE STEWART, B AF SHIH, VE STEWART, B TI ORGAN DONATION BY A MAPLE-SYRUP-URINE-DISEASE PATIENT SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Note C1 MASSACHUSETTS GEN HOSP,TRANSPLANT UNIT,BOSTON,MA 02129. RP SHIH, VE (reprint author), MASSACHUSETTS GEN HOSP,AMINO ACID DISORDER UNIT,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1995 VL 18 IS 3 BP 367 EP 367 DI 10.1007/BF00710437 PG 1 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA RM491 UT WOS:A1995RM49100022 PM 7474912 ER PT J AU KANE, KS MAYTIN, EV AF KANE, KS MAYTIN, EV TI ULTRAVIOLET-B-INDUCED APOPTOSIS OF KERATINOCYTES IN MURINE SKIN IS REDUCED BY MILD LOCAL HYPERTHERMIA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE HEAT SHOCK; STRESS RESPONSE; UV LIGHT; APOPTOSIS ID PROGRAMMED CELL-DEATH; HEAT-SHOCK RESPONSE; EPIDERMAL-KERATINOCYTES; SUNBURN CELL; MOUSE SKIN; LIGHT; DAMAGE; PROTEIN; STRESS; UV AB Two components of sunlight, ultraviolet (UV)B(290-320 nm) and infrared (greater than 700 nm), each cause damage to the skin, However, we recently identified a protective response in which heat reduces UVB-induced killing of cultured keratinocytes. Here, this investigation is extended to the living epidermis. The effects of hyperthermic preconditioning upon UVB-induced apoptosis were studied morphologically with hematoxylin and eosin staining, and biochemically with TUNEL (terminal deoxynucleotide transferase nick-end labeling) to measure endonucleolytic cleavage of DNA in situ. Anesthetized SKH-1 hairless mice were exposed to UVB light (0 to 120 mJ/cm(2)), after which their skin was biopsied at 24 h and paraffin sections were stained with hematoxylin and eosin or with TUNEL, Apoptotic keratinocytes were found to increase after UVB in a dose-related manner, In contrast, if one flank of the mouse was pretreated at 40 degrees C for 1 h and both flanks subsequently were UVB-irradiated at 6 h, the resulting formation of apoptotic cells was reduced twofold or more in the heated flank. Protection appeared by 3 h, reached a maximum at 6 h, and disappeared by 12 h, In summary, heat induces a transient protective effect that reduces UVB-mediated death of keratinocytes in skin at physiologically attainable doses of heat and UVB. C1 MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 46 TC 70 Z9 72 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JAN PY 1995 VL 104 IS 1 BP 62 EP 67 DI 10.1111/1523-1747.ep12613497 PG 6 WC Dermatology SC Dermatology GA QA158 UT WOS:A1995QA15800013 PM 7798642 ER PT J AU KINASHI, T STPIERRE, Y SPRINGER, TA AF KINASHI, T STPIERRE, Y SPRINGER, TA TI EXPRESSION OF GLYCOPHOSPHATIDYLINOSITOL-ANCHORED AND GLYCOPHOSPHATIDYLINOSITOL-NONANCHORED ISOFORMS OF VASCULAR CELL-ADHESION MOLECULE-1 IN MURINE STROMAL AND ENDOTHELIAL-CELLS SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE CELL-CELL ADHESION; TUMOR NECROSIS FACTOR ALPHA; VERY LATE ANTIGEN-4; CD49D/CD29; CD106 ID COUNTER-RECEPTOR; INTEGRIN VLA-4; BINDING-SITE; SPLICED DOMAIN; CLONING; LYMPHOCYTES; MEMBRANE; VCAM-1; LFA-3; IDENTIFICATION AB Monoclonal antibodies to murine vascular cell adhesion molecule-1 (VCAM-1, CD106) revealed not only the expected VCAM-1 molecule with an apparent molecular weight of 100 kDa, but also a molecule with a smaller size of 46 kDa in stromal cells and stimulated endothelial cells. Peptide mapping suggested the 46 kDa and 100 kDa proteins were closely related. The 46 kDa, but not 100 kDa protein, was cleaved from the cell surface with phosphatidylinositol-specific phospholipase C (PI-PLC), showing that the 46 kDa protein was a GPI-linked molecule. The 46 kDa and 100 kDa isoforms of VCAM-1 were shown to be N-glycosylated, have similar kinetics of biosynthesis, and to be partially shed from the cell surface with a slight reduction of size. TNF-alpha induced both isoforms of VCAM-1 with a similar time course of appearance on the surface of endothelial cells. The relative amounts of the 46 kDa and 100 kDa isoforms depended on the cell type examined. The GPI-anchored isoform is functionally important, because on a cell on which it was expressed almost as well as the 100 kDa isoform, treatment with PI-PLC reduced VLA-4-dependent conjugate formation. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. FU NHLBI NIH HHS [HL48675]; NIDDK NIH HHS [DK45104] NR 34 TC 25 Z9 25 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD JAN PY 1995 VL 57 IS 1 BP 168 EP 173 PG 6 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA QC581 UT WOS:A1995QC58100023 PM 7530279 ER PT J AU NETSCHER, DT WALKER, LE WEIZER, G THORNBY, J WIGODA, P BOWEN, D AF NETSCHER, DT WALKER, LE WEIZER, G THORNBY, J WIGODA, P BOWEN, D TI A REVIEW OF 198 PATIENTS (389 IMPLANTS) WHO HAD BREAST IMPLANTS REMOVED SO JOURNAL OF LONG-TERM EFFECTS OF MEDICAL IMPLANTS LA English DT Article DE BREAST IMPLANTS; RUPTURE RATE; FACTORS ASSOCIATED WITH RUPTURE ID CAPSULAR CONTRACTURE; AUGMENTATION MAMMAPLASTY; SILICONE GEL; PROSTHESES; DISEASE; RUPTURE; SAFETY AB Because of the large number of women now returning to their plastic surgeons with concerns about their breast implants many years after surgery, we are afforded an ideal opportunity to evaluate these patients over the long-term. This study reviewed 198 patients (389 implants) who underwent explantation by two surgeons over a 2-year period, correlating prosthesis type, location, and length of time since implantation with two adverse endpoints, implant rupture and symptomatic capsular contracture. Significant findings included a relatively high rate of implant rupture in patients whose implants had been in place over 20 years, an increased incidence of both symptomatic capsular contracture and implant rupture in single lumen gel implants and a positive correlation between severity of capsular contracture and implant rupture. C1 BAYLOR COLL MED,HOUSTON,TX 77030. DEPT VET AFFAIRS MED CTR,HOUSTON,TX 77030. UNIV TEXAS,SOUTHWESTERN MED CTR,DALLAS,TX 75235. RP NETSCHER, DT (reprint author), BAYLOR COLL MED,DIV PLAST SURG,6560 FANNIN,SUITE 800,HOUSTON,TX 77030, USA. NR 21 TC 12 Z9 12 U1 0 U2 0 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, STE 1202, NEW YORK, NY 10016-7892 SN 1050-6934 J9 J LONG-TERM EFF MED JI J. Long-Term Eff. Med. Implants PY 1995 VL 5 IS 1 BP 11 EP 18 PG 8 WC Engineering, Biomedical; Medicine, Research & Experimental; Orthopedics; Pathology SC Engineering; Research & Experimental Medicine; Orthopedics; Pathology GA TF738 UT WOS:A1995TF73800002 PM 10163505 ER PT J AU Xu, YY Bhavani, K Wands, JR delaMonte, SM AF Xu, YY Bhavani, K Wands, JR delaMonte, SM TI Insulin-induced differentiation and modullation of neuronal thread protein expression in primitive neuroectodermal tumor cells is linked to phosphorylation of insulin receptor substrate-1 SO JOURNAL OF MOLECULAR NEUROSCIENCE LA English DT Article DE neuronal thread protein; primitive neuroectodermal tumor cells; insulin; central nervous system; insulin receptor substrate-1; insulin receptor; signal transduction ID NERVE GROWTH-FACTOR; HEPATOCYTE DNA-SYNTHESIS; CULTURED FETAL NEURONS; C-FOS TRANSCRIPTION; ALZHEIMERS-DISEASE; FACTOR-II; NEURITE FORMATION; SIGNAL TRANSDUCTION; SECRETORY PROTEIN; TYROSINE KINASES AB Neuronal thread proteins (NTPs) are a family of developmentally regulated molecules expressed in central nervous system (CNS) neurons and primitive neuroectodermal tumor (PNET) cell lines. NTP gene expression is modulated with DNA synthesis, neuritic sprouting, and neuronal differentiation. The present study explores the mechanism of insulin modulation of NTP gene expression during neuronal differentiation using PNET cell lines of CNS origin. PNET2 cells underwent neuronal differentiation with neurite outgrowth coupled with transient up-regulation of several species of NTP. In contrast, PNET1 cells failed to differentiate in response to insulin stimulation, although insulin receptors were more abundant than in PNET2 eels. Analysis of the insulin-mediated signal transduction pathway demonstrated that the lack of insulin responsiveness in PNET1 cells was primarily caused by impaired insulin-mediated tyrosyl phosphorylation of the insulin receptor substrate-1 (IRS-1). Correspondingly, the association between phosphatidyl-inositol 3 (PI3) kinase and phosphorylated IRS-1 was reduced in PNET1 compared with PNET2 eels. In contrast, the levels of IRS-1 protein were similar in PNETI and PNET2 cells, and expression of the insulin receptor beta subunit (Ir beta) and insulin-mediated tyrosyl phosphorylation of the Ir beta were greater in PNET1 than PNET2 cells. The findings suggest that insulin effected neuronal differentiation and modulation of NTP gene expression in PNET cells utilizes a signal transduction cascade that requires tyrosyl phosphorylation of IRS-1. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CANC CTR,DEPT MED,DIV NEUROPATHOL,BOSTON,MA 02114. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-02666]; NINDS NIH HHS [NS-29793] NR 65 TC 11 Z9 12 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0895-8696 J9 J MOL NEUROSCI JI J. Mol. Neurosci. PY 1995 VL 6 IS 2 BP 91 EP 108 DI 10.1007/BF02736769 PG 18 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA TP689 UT WOS:A1995TP68900002 PM 8746448 ER PT J AU FAVA, M NOLAN, S KRADIN, R ROSENBAUM, J AF FAVA, M NOLAN, S KRADIN, R ROSENBAUM, J TI GENDER DIFFERENCES IN HOSTILITY AMONG DEPRESSED AND MEDICAL OUTPATIENTS SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID SEX-DIFFERENCES; ANGER ATTACKS; EXPRESSION; FLUOXETINE; DISEASE; SCALE AB We assessed possible gender differences in state and trait hostility in a large sample of depressed outpatients and in a group of medical outpatients. We administered the Cook and Medley Hostility Scale, measuring trait hostility and aggressiveness, and the Symptom Questionnaire, including a state measure of irritability and hostility, to 218 depressed outpatients and 51 medical outpatients. There was a statistically significant positive correlation between severity of depression and our state measure of hostility, and a weak, although statistically significant, relationship between severity of depression and total score of our trait measure of hostility. Among depressed outpatients, trait hostility was greater in men than in women, while no significant gender difference was observed in state hostility. Among medical outpatients, the state hostility scale scores were significantly higher in men than in women. These gender differences in both groups remained significant even after adjusting for severity of depression. Thus, it appears that men with depression tend to have higher scores than women on state and trait measures of hostility, suggesting that men may be at greater risk than women of developing patterns of pathologic aggression and hostile behavior. RP FAVA, M (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT ACC 815,DEPRESS RES PROGRAM,BOSTON,MA 02114, USA. NR 20 TC 31 Z9 32 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD JAN PY 1995 VL 183 IS 1 BP 10 EP 14 DI 10.1097/00005053-199501000-00003 PG 5 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QB802 UT WOS:A1995QB80200002 PM 7807063 ER PT J AU GOLOMB, M FAVA, M ABRAHAM, M ROSENBAUM, JF AF GOLOMB, M FAVA, M ABRAHAM, M ROSENBAUM, JF TI THE RELATIONSHIP BETWEEN AGE AND PERSONALITY-DISORDERS IN DEPRESSED OUTPATIENTS SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Note C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,DEPRESS RES PROGRAM,BOSTON,MA 02114. FU NIMH NIH HHS [R0-1, MH4-8483-03] NR 7 TC 7 Z9 7 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD JAN PY 1995 VL 183 IS 1 BP 43 EP 44 DI 10.1097/00005053-199501000-00008 PG 2 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QB802 UT WOS:A1995QB80200007 PM 7807069 ER PT J AU WILENS, TE BIEDERMAN, J MICK, E SPENCER, TJ AF WILENS, TE BIEDERMAN, J MICK, E SPENCER, TJ TI A SYSTEMATIC ASSESSMENT OF TRICYCLIC ANTIDEPRESSANTS IN THE TREATMENT OF ADULT ATTENTION-DEFICIT HYPERACTIVITY DISORDER SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Note ID CHILDREN; DESIPRAMINE C1 HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA. RP WILENS, TE (reprint author), MASSACHUSETTS GEN HOSP,CONSOLIDATED DEPT PSYCHIAT,PEDIAT PSYCHOPHARMACOL UNIT,ACC 725,BOSTON,MA 02114, USA. OI Mick, Eric/0000-0001-8505-8145 FU NIMH NIH HHS [MH-41314] NR 16 TC 58 Z9 59 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD JAN PY 1995 VL 183 IS 1 BP 48 EP 50 DI 10.1097/00005053-199501000-00010 PG 3 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QB802 UT WOS:A1995QB80200009 PM 7807071 ER PT J AU MONTOYA, ID HAERTZEN, C HESS, JM COVI, L FUDALA, PJ JOHNSON, RE GORELICK, DA AF MONTOYA, ID HAERTZEN, C HESS, JM COVI, L FUDALA, PJ JOHNSON, RE GORELICK, DA TI COMPARISON OF PSYCHOLOGICAL SYMPTOMS BETWEEN DRUG-ABUSERS SEEKING AND NOT SEEKING TREATMENT SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Note ID COCAINE ABUSERS; PSYCHOPATHOLOGY; ADDICTS C1 UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. RP MONTOYA, ID (reprint author), NIDA,INTRAMURAL RES PROGRAM,POB 5180,BALTIMORE,MD 21224, USA. FU Intramural NIH HHS [Z99 DA999999] NR 16 TC 5 Z9 6 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD JAN PY 1995 VL 183 IS 1 BP 50 EP 53 DI 10.1097/00005053-199501000-00011 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QB802 UT WOS:A1995QB80200010 PM 7807072 ER PT J AU SALKOVIC, M SABOLIC, I LACKOVIC, Z AF SALKOVIC, M SABOLIC, I LACKOVIC, Z TI STRIATAL DOPAMINERGIC D-1 AND D-2 RECEPTORS AFTER INTRACEREBROVENTRICULAR APPLICATION OF ALLOXAN AND STREPTOZOCIN IN RAT SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Article DE DOPAMINERGIC RECEPTORS; G-PROTEINS; STRIATUM; ALLOXAN; STREPTOZOCIN ID G-PROTEIN LEVELS; DIABETIC RATS; ADENYLATE-CYCLASE; ADP-RIBOSYLATION; NERVOUS-SYSTEM; BRAIN; EXPRESSION; MEMBRANES; BINDING; ANTIBODIES AB Intracerebroventricular application of low, nondiabetogenic doses (500 mu g kg(-1)) of alloxan and streptozocin is followed by alterations of the dopaminergic system in rat striatum. In this brain region the dopamine content significantly increased, while the density of dopaminergic D-1 receptors significantly decreased seven days after the intracerebroventricular application of betacytotoxics, as compared with the control group. The density of dopaminergic D-2 receptors in striatum remained unchanged. Dopaminergic D-1 and D-2 receptors operate through signalling mechanism of G proteins, but no changes of G(s) and G(i) proteins content have been found in rat striatum after the intracerebroventricular application of betacytotoxics. As intracerebroventricular, nondiabetogenic administration of betacytotoxics produces changes of the striatal dopamine content and D-1 receptor density similar to that produced by peripheral, diabetogenic administration of these drugs, the effect might be related not solely to pancreatic beta cells damage, but to alterations of the brain insulin system, as well. C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. RP SALKOVIC, M (reprint author), UNIV ZAGREB,SCH MED,DEPT PHARMACOL,MOLEC NEUROPHARMACOL LAB,SALATA 11,ZAGREB 41000,CROATIA. NR 28 TC 13 Z9 13 U1 0 U2 3 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1995 VL 100 IS 2 BP 137 EP 145 DI 10.1007/BF01271536 PG 9 WC Neurosciences SC Neurosciences & Neurology GA QY853 UT WOS:A1995QY85300006 PM 8962683 ER PT J AU HIESIGER, EM GREEN, SB SHAPIRO, WR BURGER, PC SELKER, RG MAHALEY, MS RANSOHOFF, J VANGILDER, JC MEALEY, J ROBERTSON, JT HOCHBERG, FH YOUNG, RF AF HIESIGER, EM GREEN, SB SHAPIRO, WR BURGER, PC SELKER, RG MAHALEY, MS RANSOHOFF, J VANGILDER, JC MEALEY, J ROBERTSON, JT HOCHBERG, FH YOUNG, RF TI RESULTS OF A RANDOMIZED TRIAL COMPARING INTRAARTERIAL CISPLATIN AND INTRAVENOUS PCNU FOR THE TREATMENT OF PRIMARY BRAIN-TUMORS IN ADULTS - BRAIN-TUMOR COOPERATIVE GROUP TRIAL 8420A SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE GLIOMA; INTRAARTERIAL CISPLATIN; PCNU; RANDOMIZED TRIAL ID MALIGNANT GLIOMA; POSTOPERATIVE TREATMENT; ANAPLASTIC GLIOMAS; RADIOTHERAPY; INTRAARTERIAL; CHEMOTHERAPY; BCNU; CIS-DIAMMINEDICHLOROPLATINUM(II); INFUSION; SURGERY AB Purpose: To test the efficacy of intra-arterial (IA) cisplatin versus intravenous (IV) PCNU for treating primary brain tumors, in a randomized trial (Brain Tumor Cooperative Group [BTCG] Trial 8420A). Methods: 311 adult patients (ages 19-79 years; median 45) with supratentorial tumors (confirmed histologically) were randomized by nine participating institutions. Patients were required to have completed radiotherapy (4500-6020 cGy to the tumor bed) before randomization. Patients were stratified as either nonprogressive (clinically and radiologically stable) or progressive. Results were analyzed for the 311 patients in the randomized population (RP), and for the 281 patients in the Valid Study Group (VSG) meeting protocol eligibility requirements. 56% of patients in the VSG had glioblastoma multiforme, 33% had other malignant glioma, and 11% had low-grade glioma. 64% were stratified as progressive. 12% had received prior chemotherapy. Results: The group randomized to PCNU had the longer survival (p = 0.06 for the RP, p = 0.07 for the VSG). In the VSG, median survival was 10 months for the cisplatin group, 13 months for the PCNU group. The difference between treatment groups was significant (p less than or equal to 0.02) when adjusted for important prognostic factors. PCNU lead to greater hematotoxicity; cisplatin lead to greater renal toxicity and some ototoxicity. Some cisplatin patients experienced complications associated with IA administration, including six cases of encephalopathy. Conclusion: The trial showed a survival advantage to the group randomized to PCNU, although the difference was modest. Coupled with previous BTCG results, these trials suggest that PCNU is an active drug for brain tumors. C1 NCI,BETHESDA,MD 20892. NYU,MED CTR,NEW YORK,NY 10016. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. DUKE UNIV,MED CTR,DURHAM,NC 27706. UNIV PITTSBURGH,MONTEFIORE HOSP,PITTSBURGH,PA 15213. UNIV N CAROLINA,CHAPEL HILL,NC 27599. UNIV IOWA,IOWA CITY,IA 52242. INDIANA UNIV,BLOOMINGTON,IN 47405. UNIV TENNESSEE,KNOXVILLE,TN 37996. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV CALIF IRVINE,IRVINE,CA 92717. FU NCI NIH HHS [CA 36005, CA 36047, CA 36014] NR 33 TC 22 Z9 23 U1 1 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1995 VL 25 IS 2 BP 143 EP 154 DI 10.1007/BF01057758 PG 12 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA RU192 UT WOS:A1995RU19200007 PM 8543970 ER PT J AU JELLINGER, KA PAULUS, W AF JELLINGER, KA PAULUS, W TI PRIMARY CENTRAL-NERVOUS-SYSTEM LYMPHOMAS - NEW PATHOLOGICAL DEVELOPMENTS SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article; Proceedings Paper CT Satellite Symposium on Brain Tumors CY SEP 24-25, 1994 CL OTTAWA, CANADA SP Canadian Assoc Neuropathologists DE CNS MALIGNANT LYMPHOMAS; CLASSIFICATION; IMMUNOPHENOTYPING; EPSTEIN-BARR VIRUS GENOME; ONCOGENES; ADHESION MOLECULES ID NON-HODGKINS-LYMPHOMA; ADHESION MOLECULES; EXPRESSION; METASTASIS; INVASION; INTEGRIN; CELLS AB Primary central nervous system lymphomas (PCNSL) show increased incidence both in immunocompromised high-risk groups and in the general population. They are extranodal diffuse non-Hodgkin's lymphomas with a morphology similar to systemic lymphomas, but differ in their biological and molecular behaviour. The majority are large B-cell variants of high-grade malignancy; low-grade subtypes and T-cell lymphomas are rare; up to 50% remain unclassified according to the New Working Formulation and updated Kiel classification. Monoclonality of immunoglobulin receptor gene rearrangement can be diagnostically useful. The pathogenesis of PCNSL is obscure. Epstein-Barr virus (EBV) genome/proteins expression in two-thirds of HIV-related PCNSL but only in 15% of those in immunocompetent patients suggest different EBV latency stages in both types; human herpesvirus type 6 does not appear to play a pathogenic role. Comparison of expression patterns of integrin chains and adhesion molecules are very similar for PCNSL and nodal lymphomas suggesting that they are not selective mediators of lymphoma cell homing to the brain. In HIV-negative PCNSL they appear not to be influenced by EBV. Studies of protooncogenes (bcl-1 and bcl-2 genes) revealed no rearrangement in PCNSL, suggesting that they are not involved in the pathogenesis of PCNSL that probably do not differ cytogenetically from nodal B-cell lymphomas. Since most of the currently known molecular parameters are probably not the primary pathogenic events, the molecular genetics and pathogenesis of PCNSL are still to be elucidated. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. RP JELLINGER, KA (reprint author), LAINZ HOSP,LUDWIG BOLTZMANN INST CLIN NEUROBIOL,WOLKERSBERGENSTR,A-1130 VIENNA,AUSTRIA. NR 23 TC 79 Z9 83 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1995 VL 24 IS 1 BP 33 EP 36 DI 10.1007/BF01052655 PG 4 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA RJ055 UT WOS:A1995RJ05500007 PM 8523072 ER PT J AU PAULUS, W TONN, JC AF PAULUS, W TONN, JC TI INTERACTIONS OF GLIOMA-CELLS AND EXTRACELLULAR-MATRIX SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article; Proceedings Paper CT Satellite Symposium on Brain Tumors CY SEP 24-25, 1994 CL OTTAWA, CANADA SP Canadian Assoc Neuropathologists DE ASTROCYTOMA; EXTRACELLULAR MATRIX; GLIOBLASTOMA; INFILTRATION; INTEGRINS; INVASION ID HUMAN BRAIN; INTEGRIN; EXPRESSION; MOLECULES; RECEPTORS; MIGRATION AB The communication between tumor cells and extracellular matrix (ECM) is responsible for clinically important features of malignant gliomas, such as cerebral invasion and leptomeningeal spread. The synthesis of ECM components, ECM-degrading activities and ECM receptors as well as the interaction between ECM components and their receptors represents the molecular basis for these processes. Recent studies have shown that proteases and integrins, the major group of ECM receptors, may be over-expressed by astrocytic tumor cells. Furthermore, integrins and the hyaluronate receptor CD44 have been found to be involved in adhesion and basement membrane invasion of glioma cells. Critical issues which are poorly understood so far include the ECM composition of the normal human brain and of brain tumors, the function of individual ECM components and receptors in a neuro-oncological context, and the molecular processes mediating the diffuse invasion of glioma cells into the brain. C1 UNIV WURZBURG,INST PATHOL,W-8700 WURZBURG,GERMANY. UNIV WURZBURG,DEPT NEUROSURG,W-8700 WURZBURG,GERMANY. RP PAULUS, W (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 25 TC 32 Z9 32 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1995 VL 24 IS 1 BP 87 EP 91 DI 10.1007/BF01052664 PG 5 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA RJ055 UT WOS:A1995RJ05500016 PM 8523081 ER PT J AU BASHIR, RM HOCHBERG, FH WEI, MX AF BASHIR, RM HOCHBERG, FH WEI, MX TI EPSTEIN-BARR-VIRUS AND BRAIN LYMPHOMAS SO JOURNAL OF NEURO-ONCOLOGY LA English DT Review DE EPSTEIN-BARR VIRUS; CNS LYMPHOMA; PRIMARY BRAIN LYMPHOMA ID CENTRAL-NERVOUS-SYSTEM; IMMUNE-DEFICIENCY-SYNDROME; INTRACRANIAL MALIGNANT-LYMPHOMAS; RETICULUM-CELL SARCOMA; NON-HODGKIN LYMPHOMA; INSITU HYBRIDIZATION; PHOSPHORAMIDE MUSTARD; NASOPHARYNGEAL CARCINOMA; IMMUNODEFICIENCY-VIRUS; TRANSPLANT RECIPIENTS C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,MOLEC NEUROGENET LAB,BOSTON,MA. RP BASHIR, RM (reprint author), UNIV NEBRASKA,MED CTR,DIV NEUROL,600 S 42ND ST,OMAHA,NE 68198, USA. NR 117 TC 5 Z9 5 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1995 VL 24 IS 2 BP 195 EP 205 DI 10.1007/BF01078490 PG 11 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA RJ117 UT WOS:A1995RJ11700007 PM 7562007 ER PT J AU DIRVEN, CMF TUERLINGS, J MOLENAAR, WM GO, KG LOUIS, DN AF DIRVEN, CMF TUERLINGS, J MOLENAAR, WM GO, KG LOUIS, DN TI GLIOBLASTOMA-MULTIFORME IN 4 SIBLINGS - A CYTOGENETIC AND MOLECULAR-GENETIC STUDY SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE BRAIN TUMORS; FAMILIAL GLIOMAS; GLIOBLASTOMA MULTIFORME; INHERITABLE SYNDROMES; MTS1 GENE; P53 MUTATION ID FAMILIAL GLIOMA; P53 GENE; ASTROCYTOMA; TUMORS; CANCER AB The familial occurrence of gliomas, in the absence of well-defined neurological tumor syndromes such as the neurofibromatoses, is uncommon, We present a family of ten children in which the four eldest suffered from gliomas. Three of these siblings had histologically verified glioblastoma multiforme, and one patient also had an intestinal non-Hodgkin's lymphoma, but there were no stigmata or family history of a neurological tumor syndrome. Cytogenetic studies of the proband revealed a normal karyotype. Molecular genetic analysis of the proband's glioblastoma revealed two mutations in the p53 tumor suppressor gene, but these were not present in the germline DNA, mutations were not detected in the MTS1 gene in the tumors or in the germline DNA. These findings suggest that a genetic factor may be responsible for the clustering of glial tumors in this family, but it is unlikely that the genetic alteration is mutation of the p53 gene. The data are discussed in light of the literature on familial brain tumors. C1 UNIV GRONINGEN HOSP,DEPT PATHOL,9700 RB GRONINGEN,NETHERLANDS. UNIV NIJMEGEN HOSP,DEPT HUMAN GENET,6500 HB NIJMEGEN,NETHERLANDS. MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP DIRVEN, CMF (reprint author), UNIV GRONINGEN HOSP,DEPT NEUROSURG,OOSTERSINGEL 59,POB 30001,9700 RB GRONINGEN,NETHERLANDS. FU NCI NIH HHS [CA 57683] NR 47 TC 15 Z9 15 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1995 VL 24 IS 3 BP 251 EP 258 DI 10.1007/BF01052841 PG 8 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA RM510 UT WOS:A1995RM51000005 PM 7595755 ER PT J AU BUSH, AI MOR, RD ROSENKRANZ, K RODES, L TANZI, RE AF BUSH, AI MOR, RD ROSENKRANZ, K RODES, L TANZI, RE TI THE ROLE OF CEREBRAL ZINC-METABOLISM IN ALZHEIMERS-DISEASE A-BETA-AMYLOIDOSIS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GENET & AGING UNIT,BOSTON,MA 02029. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,CHARLESTWN,MA 02129. RI Bush, Ashley/A-1186-2007 OI Bush, Ashley/0000-0001-8259-9069 NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S9 EP S9 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100034 ER PT J AU CHEN, JF FINK, JS AF CHEN, JF FINK, JS TI ANTISENSE OLIGONUCLEOTIDES TO A2A ADENOSINE RECEPTOR INHIBIT ADENOSINE AGONIST-INDUCED CATALEPSY IN RATS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S26 EP S26 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100099 ER PT J AU KIM, TW TANZI, RE WASCO, W AF KIM, TW TANZI, RE WASCO, W TI SYNAPTIC LOCALIZATION OF AMYLOID PRECURSOR-LIKE PROTEIN-2 (APLP2), A HOMOLOG OF THE ALZHEIMER-ASSOCIATED AMYLOID-BETA PROTEIN-PRECURSOR, IN HUMAN CEREBRAL-CORTEX SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GENET & AGING LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S8 EP S8 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100029 ER PT J AU TSAI, G GOFF, DC CHANG, RW COYLE, JT AF TSAI, G GOFF, DC CHANG, RW COYLE, JT TI INCREASED GLUTAMATERGIC TRANSMISSION AND OXIDATIVE STRESS IN TARDIVE-DYSKINESIA SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,MOLEC & DEV NEUROSCI LAB,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1995 VL 65 SU S BP S76 EP S76 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA RC601 UT WOS:A1995RC60100298 ER PT J AU SCHWAGERL, AL MOHAN, PS CATALDO, AM VONSATTEL, JP KOWALL, NW NIXON, RA AF SCHWAGERL, AL MOHAN, PS CATALDO, AM VONSATTEL, JP KOWALL, NW NIXON, RA TI ELEVATED LEVELS OF THE ENDOSOMAL-LYSOSOMAL PROTEINASE CATHEPSIN-D IN CEREBROSPINAL-FLUID IN ALZHEIMER-DISEASE SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE CATHEPSIN D; ALZHEIMER DISEASE; VENTRICULAR CSF; LYSOSOMAL HYDROLASES ID AMYLOID PRECURSOR PROTEIN; SENILE PLAQUES; BRAIN; DEGRADATION; MELANOMAS; SYSTEM AB Lysosomal hydrolases are normally intracellular enzymes but are abundant extracellularly within senile plaques in Alzheimer disease and in other conditions where beta-amyloid accumulates. To examine whether acid hydrolases released from abnormal hydrolase-laden neurons are detectable in CSF, we measured levels of the major aspartic proteinase of lysosomes, cathepsin D (Cat D), in Ventricular CSF collected after death from 30 patients with Alzheimer disease, 14 patients with Huntington disease, and seven patients with other neurodegenerative diseases. The levels of Cat D-immunoreactive protein, expressed as micrograms per milliliter of protein, determined by western blot immunoassay using a polyclonal antiserum against human brain Cat D, were more than fourfold higher in the Alzheimer patients than in the other patient groups (p < 0.0005). Cat D activity, assayed separately against [C-14]methemoglobin at pH 3.2, was also significantly elevated but less than Cat D content. The tower specific activity of Cat D in Alzheimer CSF therefore indicated that the abnormally accumulated Cat D included a high proportion of inactive enzyme. These results indicate that abnormal Cat D release from affected neurons into the extracellular space is an active, ongoing process in Alzheimer brain. In addition, the levels of this enzyme and possibly other lysosomal hydrolases in CSF may prove to be useful biological markers of Alzheimer disease. C1 HARVARD UNIV,MCLEAN HOSP,SCH MED,MOLEC NEUROSCI LABS,BELMONT,MA 02178. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BELMONT,MA 02178. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BELMONT,MA 02178. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. VET ADM MED CTR,BEDFORD,MA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NIA NIH HHS [AG10916]; NIMH NIH HHS [MH 31862] NR 21 TC 58 Z9 59 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1995 VL 64 IS 1 BP 443 EP 446 PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA PX199 UT WOS:A1995PX19900052 PM 7798944 ER PT J AU Syndulko, K Woldanski, A Baumhefner, RW Tourtellotte, WW AF Syndulko, K Woldanski, A Baumhefner, RW Tourtellotte, WW TI Preliminary evaluation of lowering tympanic temperature for the symptomatic treatment of multiple sclerosis SO JOURNAL OF NEUROLOGIC REHABILITATION LA English DT Article DE multiple sclerosis; cooling; symptomatic treatment; cooling garment ID SEVERITY; SCALE; HEAD AB Objective: Two pilot studies were designed to assess the effects of acute cooling in the laboratory (experiment one) and daily home cooling (experiment two) on objective indices of MS impairment and disability. Methods: Experiment one was a single group, repeated measures design in which nine MS outpatients with a history of heat lability were tested for immediate effects of lowering tympanic temperature in the laboratory. Subjects were tested under three experimental conditions separated by about one week: cooling with each of two cooling garments (the Life Support Systems, Inc., Mark VII MicroClimate System(TM) and the SteeleVest(TM) Body Cooling System) and no cooling. Experiment two was a prospective, unblinded, parallel group study in which twelve chronic progressive MS outpatients with a history of heat lability entered a six-week cooling protocol. Subjects used a cooling suit at home to lower body temperature two times per day. Five additional MS patients were in a non-cooling control group. In both experiments subjects were evaluated by clinical, neuroperformance, and quality of life indices, and were tested with a reduced battery of indices immediately before and after cooling on their weekly visit to the laboratory. Results: In experiment one, significant temperature decreases (mean 0.6 degrees C) were achieved with both cooling garments, but no statistically significant change in performance post-cooling was found on any test measure. In experiment: two, eight out of twelve subjects reported reduced fatigue and improved ability to ambulate immediately after and up to two to three hours after cooling. There was a significant immediate post-cooling (non-cumulative) improvement on tandem gait and standing balance. Additionally, seven subjects reported long-term improvements in quality of life over the cooling weeks. No statistically significant cumulative effect of cooling was found on objective indices of motor and cognitive function. Conclusions: The results provided weak subjective support for both acute and cumulative effects of cooling. A placebo effect cannot be ruled out. The study raised important questions regarding development of an appropriate sham cooling procedure, measurement of core temperature changes, and other design issues in evaluating cooling in MS patients. C1 W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. NR 27 TC 11 Z9 11 U1 1 U2 1 PU DEMOS PUBLICATIONS PI NEW YORK PA 386 PARK AVE S STE 201, NEW YORK, NY 10016-8804 SN 0888-4390 J9 J NEUROL REHABIL JI J. Neurol. Rehabil. PY 1995 VL 9 IS 4 BP 205 EP 215 PG 11 WC Clinical Neurology; Rehabilitation SC Neurosciences & Neurology; Rehabilitation GA VP017 UT WOS:A1995VP01700004 ER PT J AU HARR, SD SIMONIAN, NA HYMAN, BT AF HARR, SD SIMONIAN, NA HYMAN, BT TI FUNCTIONAL ALTERATIONS IN ALZHEIMERS-DISEASE - DECREASED GLUCOSE-TRANSPORTER-3 IMMUNOREACTIVITY IN THE PERFORANT PATHWAY TERMINAL ZONE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE ALZHEIMERS DISEASE; CEREBRAL METABOLISM; GLUCOSE TRANSPORT; HIPPOCAMPAL FORMATION; IMMUNOHISTOCHEMISTRY ID BLOOD-BRAIN-BARRIER; INSITU HYBRIDIZATION; CYTOCHROME-OXIDASE; PRIMARY CULTURES; GENE-EXPRESSION; MESSENGER-RNA; GLIAL-CELLS; GLUT3; PATTERN; RAT AB Positron emission tomography (PET) studies measuring glucose utilization have demonstrated cerebral hypometabolism in Alzheimer's disease (AD). The anatomic and biochemical basis for this observation remains unknown. We have examined the distribution in the hippocampal formation of the neuron-specific glucose transporter 3 (Glut3) protein. Using quantitative immunohistochemistry, we find a large reduction (49.5%) in Glut3 immunoreactivity in the outer portion of the molecular layer of the dentate gyrus in AD brains. This region corresponds to the terminal zone of the perforant pathway, whose cells of origin in layer II of the entorhinal cortex are selectively destroyed in AD. Because glucose uptake reflects metabolic demand, these results suggest a decrement of functional activity in the deafferented dentate gyrus granule cells. Generalizing from this observation, decreased glucose uptake seen on PET studies may reflect, in part, decreased glucose transport and utilization in functionally deafferented cortical fields. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. FU NIA NIH HHS [AG08487, P01AG11337, P50AG05134] NR 45 TC 50 Z9 51 U1 0 U2 1 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD JAN PY 1995 VL 54 IS 1 BP 38 EP 41 DI 10.1097/00005072-199501000-00005 PG 4 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA QA879 UT WOS:A1995QA87900005 PM 7815078 ER PT J AU VONSATTEL, JPG AIZAWA, H GE, P DIFIGLIA, M MCKEE, AC MACDONALD, M GUSELLA, JF LANDWEHRMEYER, GB BIRD, ED RICHARDSON, EP HEDLEYWHYTE, ET AF VONSATTEL, JPG AIZAWA, H GE, P DIFIGLIA, M MCKEE, AC MACDONALD, M GUSELLA, JF LANDWEHRMEYER, GB BIRD, ED RICHARDSON, EP HEDLEYWHYTE, ET TI AN IMPROVED APPROACH TO PREPARE HUMAN BRAINS FOR RESEARCH SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE BRAIN BANKING; FREEZING ARTIFACTS; IN SITU HYBRIDIZATION; MESSENGER-RNA; NEUROPATHOLOGICAL EXAMINATION; POSTMORTEM BRAIN ID LEWY-BODY VARIANT; ALZHEIMERS-DISEASE; HUNTINGTONS-DISEASE; MESSENGER-RNA; PARKINSONS-DISEASE; CLINICAL-FEATURES; POST-MORTEM; TISSUE; DEMENTIA; SOMATOSTATIN AB We describe two protocols for preparing human brains collected for research and diagnosis. In both protocols, one half brain is processed for research and the other for neuropathological evaluation. Clinical, neuropathological and tissue mRNA retention data are used for sample categorization. In protocol 1, coronal, whole hemisphere slices cut at standardized landmarks are frozen with a cooling device at -90 degrees C, which yields discrete anatomical structures. In selected instances, small blocks of brain are frozen at -160 degrees C in liquid nitrogen vapor. Cooling device or liquid nitrogen vapor frozen samples are suitable for in situ hybridization, protein blotting or immunohistochemistry. Morphological freezing artifacts are minimal. In protocol 2, one half brain is frozen en bloc on dry ice; this tissue is suitable for regional evaluation of gene expression or neurochemistry. Morphological freezing artifacts are severe. In both protocols, the other half brain is fixed in formalin prior to sectioning and diagnostic evaluation. The standardized selection of paraffin blocks from each brain allows precise diagnoses to be established, including identification of dangerous infectious processes; moreover, it makes it possible to produce a set of uniformly selected blocks and slides for comparative studies. These protocols lead to standardized tissue preparation for research and reduce variables impairing interpretation and comparison of data. C1 MCLEAN HOSP,CTR BRAIN TISSUE RESOURCE,BELMONT,MA 02178. JAMES HOMER WRIGHT PATHOL LABS,CS KUBIK LAB NEUROPATHOL,BOSTON,MA. MASSACHUSETTS GEN HOSP,MASSACHUSETTS ALZHEIMER DIS RES CTR,BOSTON,MA. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA. RP VONSATTEL, JPG (reprint author), MASSACHUSETTS GEN HOSP E,CTR NEUROSCI,MOLEC NEUROPATHOL LAB,CNY 6,BLDG 149,BOSTON,MA 02129, USA. FU DS NIH HHS [NINCDS 31862]; NIA NIH HHS [2P50-AGO 5134-10]; NINDS NIH HHS [NS 16367] NR 76 TC 100 Z9 100 U1 0 U2 3 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD JAN PY 1995 VL 54 IS 1 BP 42 EP 56 PG 15 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA QA879 UT WOS:A1995QA87900006 PM 7815079 ER PT J AU KRAUS, JA KOOPMANN, J KASKEL, P MAINTZ, D BRANDNER, S SCHRAMM, J LOUIS, DN WIESTLER, OD VONDEIMLING, A AF KRAUS, JA KOOPMANN, J KASKEL, P MAINTZ, D BRANDNER, S SCHRAMM, J LOUIS, DN WIESTLER, OD VONDEIMLING, A TI SHARED ALLELIC LOSSES ON CHROMOSOMES 1P AND 19Q SUGGEST A COMMON ORIGIN OF OLIGODENDROGLIOMA AND OLIGOASTROCYTOMA SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE CHROMOSOME ARM 1P; CHROMOSOME ARM 19Q; LINEAGE; LOSS OF HETEROZYGOSITY; OLIGOASTROCYTOMA; OLIGODENDROGLIOMA ID BRAIN-TUMOR SPECIMENS; DINUCLEOTIDE REPEAT; GENE AMPLIFICATION; P53 MUTATIONS; HETEROZYGOSITY; GLIOMAS; ASTROCYTOMAS; PCR; POLYMORPHISM; LOCUS AB Loss of heterozygosity (LOH) in specific chromosomal regions, which are likely to harbor tumor suppressor genes, has been associated with human gliomas. In this study we have analyzed astrocytic and oligodendroglial tumors for LOH on chromosomes 1 and 19. By microsatellite analysis LOH was found on chromosome arm 1p in 6/15 oligodendrogliomas WHO grade II and III, 12/25 oligoastrocytomas WHO grade II and III, 6/79 glioblastomas WHO grade IV, 5/44 astrocytomas WHO grade II and III and 0/23 pilocytic astrocytomas WHO grade I. The high incidence of LOH on chromosome arm 1p in oligodendrogliomas and oligoastrocytomas indicates that a putative tumor suppressor gene in this region is involved in the formation of gliomas with oligodendroglial features. Furthermore, the frequent involvement of chromosome arm Ip in oligodendrogliomas and oligoastrocytomas, but not in astrocytomas, suggests that genetically oligoastrocytoma is more similar to oligodendroglioma than to astrocytoma. In order to support this hypothesis, oligodendroglial and astrocytic areas in three mixed oligoastrocytomas were examined differentially for LOH 1p and for LOH 19q, the second genetic region believed to be affected in these tumors. All three tumors had LOH of 1p and LOH of 19q in both areas of oligodendroglial and of astrocytic differentiation. These findings show that the astrocytic and oligodendroglial portions of oligoastrocytoma share molecular genetic features and probably are of monoclonal origin. C1 UNIV BONN KLINIKEN,INST NEUROPATHOL,D-53105 BONN,GERMANY. UNIV ZURICH HOSP,INST NEUROPATHOL,CH-8091 ZURICH,SWITZERLAND. UNIV BONN KLINIKEN,NEUROCHIRURG KLIN,D-53105 BONN,GERMANY. MASSACHUSETTS GEN HOSP,NEUROL SERV,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RI von Deimling, Andreas/F-7774-2013 OI von Deimling, Andreas/0000-0002-5863-540X NR 32 TC 282 Z9 287 U1 1 U2 2 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD JAN PY 1995 VL 54 IS 1 BP 91 EP 95 PG 5 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA QA879 UT WOS:A1995QA87900011 PM 7815084 ER PT J AU JELLINGER, KA PAULUS, W AF JELLINGER, KA PAULUS, W TI RECENT ADVANCES IN THE PATHOBIOLOGY OF PRIMARY CNS LYMPHOMAS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article; Proceedings Paper CT Symposium on Brain Research and Society CY SEP 21-24, 1995 CL BARCELONA, SPAIN C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. RP JELLINGER, KA (reprint author), LUDWIG BOLTZMANN INST CLIN NEUROBIOL,VIENNA,AUSTRIA. NR 19 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PY 1995 VL 54 SU S BP S63 EP S65 PG 3 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA RU716 UT WOS:A1995RU71600034 ER PT J AU NARULA, J TORCHILIN, VP PETROV, A KHAW, S TRUBETSKOY, VS ODONNELL, SM NOSSIFF, ND KHAW, BA AF NARULA, J TORCHILIN, VP PETROV, A KHAW, S TRUBETSKOY, VS ODONNELL, SM NOSSIFF, ND KHAW, BA TI IN-VIVO TARGETING OF ACUTE MYOCARDIAL-INFARCTION WITH NEGATIVE-CHARGE, POLYMER-MODIFIED ANTIMYOSIN ANTIBODY - USE OF DIFFERENT CROSS-LINKERS SO JOURNAL OF NUCLEAR CARDIOLOGY LA English DT Article DE POLYMER; RADIONUCLIDE IMAGING; PEPTIDE BOND; THIOETHER BOND; CHARGE-MODIFIED ANTIBODY; IMMUNOGLOBULINS; MYOSIN ID MONOCLONAL-ANTIBODY; PROTEINS; BINDING AB Background. Cell surfaces and intercellular matrixes contain acidic residues, making them negatively charged. Antibodies are basic, positively charged glycoproteins. Therefore the potential for nonspecific ionic interaction exists, which could increase the background activity. Modification of antibodies with negatively charge-modified polymers have been shown to reduce this nonspecific background activity. This study was performed to investigate the appropriateness of different cross-linkers used covalently to link the chelating negatively charge-modified polylysine to antimyosin Fab (AM-Fab). The cross-linking was performed through peptide (AM-I) or thioether (AM-II) bonds. The in vitro evaluation of the immunointegrity and the in vivo assessment were performed to investigate the potential for reduction of nontarget background activity. Furthermore, the role of the charge of the polymers (whether completely negatively charge modified by succinylation [AM-IIs] or only partially negatively charge modified [AM-IIns]) was also assessed. Methods and Results. All polymer-modified preparations (AM-I, AM-IIs, and AM-IIns) retained the immunoreactivities relative to the unmodified or conventional diethylenetriaminepentaacetic acid-coupled AM-Fab as assessed by radioimmunoassay or enzyme-linked immunosorbent assay. These polymer-modified preparations labeled with In-111 were assessed in 13 rabbits with acute experimental myocardial infarction. Acute infarcts were produced by 40 minutes of left anterior descending coronary artery occlusion followed by reperfusion. At between 10 and 30 minutes of reperfusion, 10.4 +/- 1.8 mBq In-111-AM-I (10 to 20 mu g; n = 7) or 11.4 +/- 2.3 mBq In-111-AM-II (n or ns) (20 to 25 mu g; n = 6) was administered intravenously. Gamma imaging was performed in the left lateral position and arterial blood samples were withdrawn serially for the next 3 hours. At the end of the final imaging session, AM-I uptake was determined to be 1.09% +/- 0.11% (mean percent injected dose per gram myocardium +/- SFM) in 20 infarcted myocardial segments from seven rabbits, compared with 0.031% +/- 0.003% in 20 normal myocardial segments (infarct/normal myocardial ratio 53.9 +/- 18.41). The mean percent injected dose of In-111-labeled thioether-linked AM-Fab preparations in nine infarcted myocardial segments from each group was 0.067% a 0.008% (infarct/normal myocardial ratio 9.0 +/- 1.5) and 0.144% +/- 0.011% (infarct/normal myocardial ratio 10.2 +/- 1.9) with AM-IIs in = 3) and AM-IIns (n = 3), respectively (p < 0.0001). The non-target organ distribution of the AM-I and AM-IIs was similar. AM-IIns preparation resulted in high non-target organ activities. Conclusions. This study shows that the charge of the antibody can be manipulated favorably by cross-linking with negatively charged polymers, which results in the reduced in vivo non-target organ activities. Charge modification does not adversely affect the apparent affinity of the antibody. However, the type of cross-linkers used may significantly influence the in vivo stability of the modified antibody preparations for target organ visualization. These data may find potential application in future clinical imaging protocols. C1 NORTHEASTERN UNIV,CTR DRUG TARGETING & ANAL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FU NCI NIH HHS [CA50505] NR 18 TC 7 Z9 7 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1071-3581 J9 J NUCL CARDIOL JI J. Nucl. Cardiol. PD JAN-FEB PY 1995 VL 2 IS 1 BP 26 EP 34 DI 10.1016/S1071-3581(05)80005-4 PG 9 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA QG220 UT WOS:A1995QG22000004 PM 9420759 ER PT J AU GEWIRTZ, H AF GEWIRTZ, H TI MYOCARDIAL CLEARANCE KINETICS OF TECHNETIUM-99M-TEBOROXIME FOLLOWING DIPYRIDAMOLE INJECTION SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID BLOOD-FLOW; TEBOROXIME RP GEWIRTZ, H (reprint author), MASSACHUSETTS GEN HOSP,VINCENT BURNHAM 3,32 FRUIT ST,BOSTON,MA 02114, USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JAN PY 1995 VL 36 IS 1 BP 119 EP 120 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA PZ710 UT WOS:A1995PZ71000028 PM 7799063 ER PT J AU ABRAHAMSSON, SO GELBERMAN, RH AMIEL, D WINTERTON, P HARWOOD, F AF ABRAHAMSSON, SO GELBERMAN, RH AMIEL, D WINTERTON, P HARWOOD, F TI AUTOGENOUS FLEXOR TENDON GRAFTS - FIBROBLAST ACTIVITY AND MATRIX REMODELING IN DOGS SO JOURNAL OF ORTHOPAEDIC RESEARCH LA English DT Article ID CROSS-LINKING; COLLAGEN AB To investigate rates of cellular proliferation and matrix turnover in autogenous flexor tendon grafts, hindlimb intrasynovial (flexor digitorum profundus) and extrasynovial (peroneus longus) tendons were placed within the synovial sheaths of the medial and lateral forepaw digits of 18 dogs and treated with controlled early passive motion. After the dogs had been killed, short-term culture and labeling in vitro were utilized to determine rates of DNA, proteoglycan, collagen, and noncollagen protein synthesis. Schiff base covalent collagen crosslink concentrations and total collagen and protein content also were evaluated at intervals through 6 weeks. Tendon grafts of extrasynovial origin showed greater rates of DNA synthesis and significantly elevated levels of proteoglycan, collagen, and noncollagen protein synthesis and Schiff base covalent collagen crosslink concentrations (dihydroxylysinonorleucine) compared with intrasynovial tendon grafts. It was not clear to what extent the increased activity in the extrasynovial graft was due to actual differences between the intrasynovial and extrasynovial tendons or to the responses of the connective tissue surrounding the extrasynovial tendon graft. Since both types of grafts demonstrated similar unaltered levels of collagen and protein content over time, these data suggest greater rates of matrix turnover in tendon grafts of extrasynovial origin than in those of intrasynovial origin. Coupled with previous findings showing increased cellular proliferation in extrasynovial tendon grafts, these data indicate that the process of translation to an intrasynovial environment necessitates a more active process of soft-tissue repair and remodeling when extrasynovial donor tendons are used. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. FU NIAMS NIH HHS [AR33097] NR 27 TC 27 Z9 27 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0736-0266 J9 J ORTHOPAED RES JI J. Orthop. Res. PD JAN PY 1995 VL 13 IS 1 BP 58 EP 66 DI 10.1002/jor.1100130110 PG 9 WC Orthopedics SC Orthopedics GA QG269 UT WOS:A1995QG26900009 PM 7853105 ER PT J AU JUPITER, JB RING, D ROSEN, H AF JUPITER, JB RING, D ROSEN, H TI COMPLICATIONS AND DIFFICULTIES OF MANAGEMENT OF NONUNION IN THE SEVERELY OBESE SO JOURNAL OF ORTHOPAEDIC TRAUMA LA English DT Article DE NONUNION; OBESITY AB Operative fixation of 22 nonunited fractures was undertaken in 21 obese patients. Eleven patients were women and 10 were men, with an average age of 46.3 years (range 25-74). The average body mass index in this group of patients was 37.9 kg/m(2) (range 33.2-57.1), Two patients were classified as morbidly obese and 19 as severely obese. The management of these patients proved to be fraught with difficulties related to their obesity. There were a number of occurrences believed to be related to poorly protective positioning and prolonged ischemic pressure under the patient's body weight during the administration of anesthetic, including a peroneal compartment syndrome, a gluteal compartment syndrome with sciatic nerve palsy, bilateral brachial plexus stretch injuries, an anterior interosseous nerve palsy, and the postoperative development of a patch of scalp alopecia. There were two wound separations and no episodes of thromboembolic disease. Sixteen nonunited fractures healed after the index procedure at an average time to healing of 5.6 months (range 2-14). Five nonunited fractures required a second procedure to gain union [average total time to healing 17 months (range 10-31)]. A single fracture remains ununited. Awareness of the unique technical demands and operative and anesthetic risks encountered when undertaking an operative procedure in a severely obese patient is imperative for the safe and successful treatment of orthopaedic surgical problems in these patients. C1 HARVARD UNIV,SCH MED,BOSTON,MA. HARVARD COMBINED ORTHOPAED RESIDENCY PROGRAM,BOSTON,MA. NYU,HOSP JOINT DIS ORTHOPAED INST,SCH MED,PROBLEM TRAUMA SERV,NEW YORK,NY. RP JUPITER, JB (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,ACC 527,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 0 TC 32 Z9 32 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0890-5339 J9 J ORTHOP TRAUMA JI J. Orthop. Trauma PY 1995 VL 9 IS 5 BP 363 EP 370 DI 10.1097/00005131-199505000-00001 PG 8 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA RW081 UT WOS:A1995RW08100001 PM 8537837 ER PT J AU SIMPSON, NS JUPITER, JB AF SIMPSON, NS JUPITER, JB TI DELAYED-ONSET OF FOREARM COMPARTMENT SYNDROME - A COMPLICATION OF DISTAL RADIUS FRACTURE IN YOUNG-ADULTS SO JOURNAL OF ORTHOPAEDIC TRAUMA LA English DT Article DE FOREARM COMPARTMENT SYNDROME; DISTAL RADIUS FRACTURE AB The signs and symptoms of elevated intracompartmental pressure in the volar forearm compartment developed on a delayed basis (range 18-54 h) in the absence of constricting casts or dressings in eight limbs after high-energy intraarticular fractures of the distal end of the radius. Intracompartment pressures averaged 80 mm Hg in the six limbs tested. Despite urgent decompression and fracture fixation with delayed wound closure, final functional outcomes were compromised in seven cases, reflecting the severity of the articular injuries, and poor in one case, in which a wrist fusion was later required. Lf potentially serious complications are to be prevented, careful observation of these patients, often for periods of 48 h, is important. Selective recording of forearm intracompartmental pressures may be advised in at-risk patients. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED TRAUMA SERV,BOSTON,MA 02114. NR 0 TC 18 Z9 18 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0890-5339 J9 J ORTHOP TRAUMA JI J. Orthop. Trauma PY 1995 VL 9 IS 5 BP 411 EP 418 DI 10.1097/00005131-199505000-00009 PG 8 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA RW081 UT WOS:A1995RW08100009 PM 8537845 ER PT J AU KRAMER, DL RODGERS, WB MANSFIELD, FL AF KRAMER, DL RODGERS, WB MANSFIELD, FL TI TRANSPEDICULAR INSTRUMENTATION AND SHORT-SEGMENT FUSION OF THORACOLUMBAR FRACTURES - A PROSPECTIVE-STUDY USING A SINGLE INSTRUMENTATION SYSTEM SO JOURNAL OF ORTHOPAEDIC TRAUMA LA English DT Article DE TRANSPEDICULAR INSTRUMENTATION; SHORT-SEGMENT FUSION; THORACOLUMBAR FRACTURES AB Eleven patients were prospectively treated with bilateral short-segment transpedicular instrumentation using the Posterior Segment Fixator (Ace Medical Co., Los Angeles, CA, U.S.A.) construct combined with posterolateral fusion using autogenous iliac crest bone graft for the treatment of thoracolumbar vertebral fractures. All patients were evaluated clinically, radiographically, and functionally for a minimum of 2 years (mean 33 months). Four of the 11 patients (36.3%) had breakage or disengagement of the caudad screws during this interval. During the follow-up period, the angle of kyphosis increased an average of 12.9 degrees. The loss of correction was greater in those patients in whom the instrumentation failed (22 degrees) than in those patients in whom it did not (7.7 degrees). Five of the patients (45.5%) had a progressive increase in the angle of kyphosis of 10 degrees or more. At follow-up, the average loss of anterior vertebral body height for all 11 patients was 14% when compared with the body height that had been attained at surgery. Six of these patients (54.5%) had 10% or more loss of anterior body height. Despite the high incidence of failure of the instrumentation, progressive increase in the angle of kyphosis, and progressive loss of anterior vertebral body height, there was no worsening in the patients' Frankel grade postoperatively. The high rate of hardware failure and major postoperative loss of fracture reduction associated with this construct suggest that posterior short-segment pedicle-screw instrumentation with the Posterior Segment Fixator was not adequate to ensure stabilization of thoracolumbar fractures in this small group of patients. Maintenance of post operative fracture reduction was the most consistent predictor of satisfactory functional outcome. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. NR 0 TC 72 Z9 94 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0890-5339 J9 J ORTHOP TRAUMA JI J. Orthop. Trauma PY 1995 VL 9 IS 6 BP 499 EP 506 DI 10.1097/00005131-199509060-00007 PG 8 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA TG680 UT WOS:A1995TG68000007 PM 8592263 ER PT J AU PLUMLEY, DA WATKINS, K BODE, BP PACITTI, AJ SOUBA, WW AF PLUMLEY, DA WATKINS, K BODE, BP PACITTI, AJ SOUBA, WW TI CYCLOOXYGENASE BLOCKADE ABROGATES THE ENDOTOXIN-INDUCED INCREASE IN NA+-DEPENDENT HEPATIC AMINO-ACID-TRANSPORT SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Article ID PLASMA-MEMBRANE VESICLES; RAT-LIVER; GLUTAMINE; SYSTEM; CELL AB Background: Endotoxemia is characterized by a marked increase in the uptake of amino acids by the liver, but the regulation of this response has not been fully elucidated. In the current study, we investigated the potential role of prostaglandins as mediators of this response. We examined the in vivo effects of the anti-inflammatory agent ketorolac, a cyclo-oxygenase inhibitor that blocks prostaglandin synthesis, on hepatic amino acid transport activity in endotoxin-treated rats. Methods: We assayed the activities of the Na+-dependent transport systems A and N in hepatic plasma membrane vesicles prepared from endotoxemic rats that were pretreated with ketorolac or vehicle. Hepatic plasma membrane vesicles were prepared by differential centrifugation, and the transport of [H-3]glutamine (system N) and [H-3] 2-methylamino-isobutyric acid (system A) was assayed. Hepatic plasma membrane vesicles were also prepared from normal rats that received prostaglandin E(2), and glutamine and MeAIB transport were measured. Results: Endotoxin treatment resulted in a twofold to threefold increase in Na+-dependent amino acid transport activity in hepatic plasma membrane vesicles secondary to an increase in the transport V-max, which was consistent with the appearance of increased numbers of corresponding transporter proteins in the hepatocyte plasma membrane. Pretreatment with ketorolac almost completely abrogated the endotoxin-induced increase in hepatic amino acid transport. Administration of prostaglandin E(2) to normal rats resulted in a statistically significant increase in glutamine and alanine transport by hepatic plasma membrane vesicles prepared from these animals. Conclusions: Prostaglandins play a key role in mediating the accelerated hepatic amino acid transport that occurs during endotoxemia. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. UNIV FLORIDA,COLL MED,DEPT SURG,SURG METAB LAB,GAINESVILLE,FL. UNIV FLORIDA,COLL MED,DEPT SURG,NUTR LAB,GAINESVILLE,FL. FU NCI NIH HHS [CA57690] NR 18 TC 11 Z9 12 U1 0 U2 0 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD JAN-FEB PY 1995 VL 19 IS 1 BP 9 EP 14 DI 10.1177/014860719501900109 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QA886 UT WOS:A1995QA88600003 PM 7658609 ER PT J AU BROTHERS, TE ROBISON, JG ELLIOTT, BM BOGGS, JM FRANKEL, AE WILLINGHAM, MC AF BROTHERS, TE ROBISON, JG ELLIOTT, BM BOGGS, JM FRANKEL, AE WILLINGHAM, MC TI UP-REGULATION OF B-FGF RECEPTOR EXPRESSION AFTER CAROTID BYPASS SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT Annual Symposium of the Association-of-Veterans-Administration-Surgeons CY MAY 05-07, 1994 CL RENO, NV SP ASSOC VET ADM SURGEONS ID FIBROBLAST GROWTH-FACTOR; SMOOTH-MUSCLE CELLS; INTIMAL HYPERPLASIA; ARTERIES; ATHEROSCLEROSIS; PREVENTION; RESTENOSIS; INJURY; GRAFT; TOXIN AB Basic fibroblast growth factor (b-FGF) appears to be an important positive modulator of the neointimal hyperplasia that occurs after prosthetic vascular graft implantation through its effects on vascular myointimal/smooth muscle cell migration and proliferation. The distribution and extent of b-FGF receptor (b-FGFR1) expression was compared using immunohistochemical techniques in normal porcine carotid arteries and at various times up to 6 weeks following implantation of small caliber prosthetic vascular grafts. At the time of graft harvest, specimens were infused with OCT medium at 100 mm Hg and rapidly frozen in liquid nitrogen. Transverse sections of the perianastomotic arterial tissues were labeled with primary mouse monoclonal antibody directed toward the extracellular domain of the receptor, followed by goat-anti mouse IgG and rabbit anti-goat IgG conjugated to horseradish peroxidase. The b-FGFR1-positive cells were identified by peroxidase activity within the Golgi complex of smooth muscle cells. Normal porcine carotid arteries showed no evidence of staining for b-FGFR1. However, at 6 weeks cells in the perianastomotic area clearly showed significant b-FGFR1 localization. Anti-muscle actin labeling confirmed these to be smooth muscle cells. The observed upregulation of b-FGFR1 expression supports the concept of positive feedback by cytokines as a contributing factor to the hyperplastic response of smooth muscle cells after prosthetic vascular graft implantation. This finding further supports a potential strategy to specifically target activated smooth muscle cells through use of mitotoxin therapy. (C) 1995 Academic Press, Inc. C1 MED UNIV S CAROLINA,MED CTR,DEPT MED,CHARLESTON,SC 29425. MED UNIV S CAROLINA,MED CTR,DEPT PATHOL,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29425. RP BROTHERS, TE (reprint author), MED UNIV S CAROLINA,MED CTR,DEPT SURG,CHARLESTON,SC 29425, USA. NR 26 TC 8 Z9 8 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD JAN PY 1995 VL 58 IS 1 BP 28 EP 32 DI 10.1006/jsre.1995.1005 PG 5 WC Surgery SC Surgery GA QD067 UT WOS:A1995QD06700005 PM 7830402 ER PT J AU GELLER, DA BIEDERMAN, J REED, ED SPENCER, T WILENS, TE AF GELLER, DA BIEDERMAN, J REED, ED SPENCER, T WILENS, TE TI SIMILARITIES IN RESPONSE TO FLUOXETINE IN THE TREATMENT OF CHILDREN AND ADOLESCENTS WITH OBSESSIVE-COMPULSIVE DISORDER SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE OBSESSIVE-COMPULSIVE DISORDER; FLUOXETINE; CHILDREN; ADOLESCENTS ID DOUBLE-BLIND; CLOMIPRAMINE TREATMENT; DESIPRAMINE; PLACEBO; TRIAL; ANTIDEPRESSANTS; PHENOMENOLOGY; EPIDEMIOLOGY; FLUVOXAMINE; TOURETTES AB Objective: Obsessive-compulsive disorder (OCD) is a relatively common disorder that frequently has its onset in childhood and is associated with substantial morbidity and dysfunction despite availability of new treatments. However, antiobsessional agents have not been systematically evaluated in young children and their effectiveness beyond the short term has not been well studied. The purpose of this study was to evaluate the usefulness of fluoxetine in the long-term treatment of both children and adolescents with OCD. Method: All pediatric patients with a DSM-III-R diagnosis of OCD who were treated with fluoxetine were ascertained from retrospective chart reviews of a pediatric psychopharmacology clinic. Response to treatment was evaluated by experienced clinicians using the Clinical Global Impression Scale. Results: Of 38 identified patients, 28 (74%) showed moderate to marked improvement of OCD symptoms on doses averaging 50 mg/day (1.0 mg/kg per day) over an average follow-up period of 19 months. Similar effects were observed in children and adolescents. Conclusion: Although limited by their retrospective nature, these findings indicate that fluoxetine may be effective in prepubertal children and that the effect can be sustained over time. C1 MCLEAN HOSP,JOINT PROGRAM PEDIAT PSYCHOPHARMACOL,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,JOINT PROGRAM PEDIAT PSYCHOPHARMACOL,BOSTON,MA 02114. NR 38 TC 53 Z9 53 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1995 VL 34 IS 1 BP 36 EP 44 DI 10.1097/00004583-199501000-00011 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA QD725 UT WOS:A1995QD72500012 PM 7860454 ER PT J AU WILENS, TE SPENCER, T BIEDERMAN, J WOZNIAK, J CONNOR, D AF WILENS, TE SPENCER, T BIEDERMAN, J WOZNIAK, J CONNOR, D TI COMBINED PHARMACOTHERAPY - AN EMERGING TREND IN PEDIATRIC PSYCHOPHARMACOLOGY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; CHILDREN; DESIPRAMINE; METHYLPHENIDATE; COMORBIDITY; CONDUCT C1 HARVARD UNIV,MCLEAN HOSP,SCH MED,BELMONT,MA 02178. UNIV MASSACHUSETTS,SCH MED,DIV CHILD PSYCHIAT,PEDIAT PSYCHOPHARMACOL CLIN,WORCESTER,MA 01605. RP WILENS, TE (reprint author), MASSACHUSETTS GEN HOSP,ORAL HLTH RES SERV,CLIN & RES PROGRAM PEDIAT PSYCHOPHARMACOL,ACC 725,BOSTON,MA 02114, USA. OI Connor, Daniel/0000-0002-7867-4094 NR 22 TC 69 Z9 69 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1995 VL 34 IS 1 BP 110 EP 112 DI 10.1097/00004583-199501000-00021 PG 3 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA QD725 UT WOS:A1995QD72500022 PM 7860450 ER PT J AU EMANUEL, LL AF EMANUEL, LL TI ADVANCE DIRECTIVES - DO THEY WORK SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID LIFE-SUSTAINING TREATMENT; ELDERLY PERSONS; LIVING WILLS; PREFERENCES; CARE; DECISIONS; PREDICTIONS; PROXIES; END AB Advance directives have been widely endorsed, and empiric work has taken place that can aid clinicians in the appropriate use of validated documents. This report reviews philosophic and methodologic issues and offers practical illustrations. Despite the evidence that advance directives can work, there are serious barriers to their actual use. Therefore, these barriers are evaluated and potential solutions suggested. C1 MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BOSTON,MA 02114. RP EMANUEL, LL (reprint author), HARVARD UNIV,SCH MED,DIV MED ETH,641 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 37 TC 18 Z9 18 U1 1 U2 3 PU ELSEVIER SCIENCE PUBL CO 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 JAN PY 1995 VL 25 IS 1 BP 35 EP 38 DI 10.1016/0735-1097(94)00339-R PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QL249 UT WOS:A1995QL24900012 PM 7798522 ER PT J AU FITZMAURICE, GM MOLENBERGHS, G LIPSITZ, SR AF FITZMAURICE, GM MOLENBERGHS, G LIPSITZ, SR TI REGRESSION-MODELS FOR LONGITUDINAL BINARY RESPONSES WITH INFORMATIVE DROP-OUTS SO JOURNAL OF THE ROYAL STATISTICAL SOCIETY SERIES B-METHODOLOGICAL LA English DT Article DE GENERALIZED ESTIMATING EQUATIONS; MAXIMUM LIKELIHOOD ESTIMATION; MISSING DATA; REPEATED MEASURES ID LIKELIHOOD AB This paper reviews both likelihood-based and non-likelihood (generalized estimating equations) regression models for longitudinal binary responses when there are drop-outs. Throughout, it is assumed that the regression parameters for the marginal expectations of the binary responses are of primary scientific interest. The association or time dependence between the responses is largely regarded as a nuisance characteristic of the data. The performance of the methods is compared, in terms of asymptotic bias, under misspecification of the association between the responses and the missing data mechanism or drop-out process. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA. LIMBURGS UNIV CENTRUM,DIEPENBEEK,BELGIUM. DANA FARBER CANC INST,BOSTON,MA. NR 24 TC 84 Z9 85 U1 1 U2 8 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0035-9246 J9 J ROY STAT SOC B MET JI J. R. Stat. Soc. Ser. B-Methodol. PY 1995 VL 57 IS 4 BP 691 EP 704 PG 14 WC Statistics & Probability SC Mathematics GA RU307 UT WOS:A1995RU30700004 ER PT J AU SHERIDAN, RL TOMPKINS, RG AF SHERIDAN, RL TOMPKINS, RG TI CULTURED AUTOLOGOUS EPITHELIUM IN PATIENTS WITH BURNS OF 90-PERCENT OR MORE OF THE BODY-SURFACE SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Article DE BURNS; EPITHELIUM; WOUNDS ID PROMPT ESCHAR EXCISION; FULL-THICKNESS; WOUND CLOSURE; KERATINOCYTES; AUTOGRAFTS; MORTALITY; CHILDREN; COVERAGE; CARE AB Objective: The increasing survival of patients with very large burns has driven an interest in innovative permanent wound closure techniques, one of which is the use of cultured autologous epithelium (CAE). To document our ability to achieve wound closure with CAE in patients with very large burns, we report our 19-month experience with this technology in five patients with burns of 90% or more of the body surface. Design: A retrospective review. Materials and Methods: Over a 19-month period five patients with burns in excess of 90% of the body surface had skin biopsies taken for epithelial culture. The clinical course of these five patients was reviewed in detail. Measurements and Main Results: These five patients had an average age of 11.5 years (range 7 months to 37 years), and an average total body surface area burn of 94% (range 90%-96%). Four of the five patients had inhalation injury. All wounds had vascularized allograft present at the time of CAE engraftment. Forty-five percent of the CAE was placed on vascularized allodermis and 55% on fascia (range on allodermis 20%-75%). Initial take of CAE was 51% (range 20%-80%). Delayed loss in percent of initial take averaged 60% (range 20%-100%). Delayed loss averaged 33% (range 20%-50%) when two patients who lost all of their CAE were excluded. Three patients had gram-negative bacteremia within 7 days of CAE placement, and two of these had 100% graft loss. Definitive closure rates with CAE averaged 7.5% (range 0%-15%) of the body surface, increasing to 12.5% (range 11.2%-15%) when two patients who lost all of their CAE are excluded. Conclusions: The initial enthusiasm for CAE has been tempered by demonstrations of low initial engraftment rates, graft fragility, delayed graft loss, and cost. Such liabilities become more tolerable as usable donor site decreases below 5% to 10% of the body surface. CAE can materially contribute to wound closure in patients with very extensive burns, but gram-negative sepsis is associated with complete graft loss. C1 MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP SHERIDAN, RL (reprint author), SHRINERS BURN INST,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 17 TC 52 Z9 59 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1079-6061 J9 J TRAUMA JI J. Trauma-Injury Inf. Crit. Care PD JAN PY 1995 VL 38 IS 1 BP 48 EP 50 DI 10.1097/00005373-199501000-00014 PG 3 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA QE914 UT WOS:A1995QE91400013 PM 7745657 ER PT J AU BROMLEY, B SHAMBERGER, RC BENACERRAF, B AF BROMLEY, B SHAMBERGER, RC BENACERRAF, B TI AN UNUSUAL OUTCOME FOR FETUS WITH GASTROCHISIS SO JOURNAL OF ULTRASOUND IN MEDICINE LA English DT Note C1 MASSACHUSETTS GEN HOSP,DEPT OBSTET & GYNECOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 5 TC 9 Z9 9 U1 0 U2 0 PU AMER INST ULTRASOUND MEDICINE PI LAUREL PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906 SN 0278-4297 J9 J ULTRAS MED JI J. Ultrasound Med. PD JAN PY 1995 VL 14 IS 1 BP 69 EP 72 PG 4 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA QB240 UT WOS:A1995QB24000014 PM 7707482 ER PT J AU DRETLER, SP AF DRETLER, SP TI INDWELLING URETERAL STENTS AS DEFINITIVE THERAPY FOR DISTAL URETERAL CALCULI - COMMENT SO JOURNAL OF UROLOGY LA English DT Editorial Material RP DRETLER, SP (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,DEPT UROL,BOSTON,MA 02114, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD JAN PY 1995 VL 153 IS 1 BP 36 EP 36 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA PW167 UT WOS:A1995PW16700014 ER PT J AU BARRY, MJ GIRMAN, CJ OLEARY, MP WALKERCORKERY, ES BINKOWITZ, BS COCKETT, ATK GUESS, HA HOLTGREWE, HL MCCONNELL, JD SIHELNIK, SA MCLEOD, M WINFIELD, HN WILLIAMS, R AF BARRY, MJ GIRMAN, CJ OLEARY, MP WALKERCORKERY, ES BINKOWITZ, BS COCKETT, ATK GUESS, HA HOLTGREWE, HL MCCONNELL, JD SIHELNIK, SA MCLEOD, M WINFIELD, HN WILLIAMS, R TI USING REPEATED-MEASURES OF SYMPTOM SCORE, UROFLOWMETRY AND PROSTATE-SPECIFIC ANTIGEN IN THE CLINICAL MANAGEMENT OF PROSTATE DISEASE SO JOURNAL OF UROLOGY LA English DT Article DE ANTIGENS, NEOPLASM; PROSTATIC NEOPLASMS; URODYNAMICS ID AMERICAN-UROLOGICAL-ASSOCIATION; HYPERPLASIA; VARIABILITY; MEN; TERM AB Measurements of American Urological Association symptom score, peak urine flow rate and prostate specific antigen (PSA) are often followed over time in urological management. However, their interpretation is confounded by within-patient variability due to chance. Data from 2 clinical trials are used to examine the magnitude of this variation. When these measures are repeated at a short interval variation is modest and might easily be misinterpreted as a true change in patient condition. For example, approximately 20% of patients might be expected to have a chance increase or decrease in symptom score by at least 4.9 points, in peak urine flow rate by at least 4.1 ml. per second or in PSA by at least 1.6 ng./ml. Clinicians can use these data to help interpret repeated measures of these variables in patients, and can consider obtaining paired measurements to decrease the effect of chance variation when they plan on following them over time. C1 BRIGHAM & WOMENS HOSP,DIV UROL,BOSTON,MA. UNIV ROCHESTER,SCH MED,DEPT UROL,ROCHESTER,NY. MERCK RES LABS,DEPT EPIDEMIOL,BLUE BELL,PA. MERCK RES LABS,DEPT BIOSTAT,BLUE BELL,PA. RP BARRY, MJ (reprint author), MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,BOSTON,MA, USA. FU AHRQ HHS [HS 06689, HS 06336, HS 08397] NR 20 TC 62 Z9 65 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD JAN PY 1995 VL 153 IS 1 BP 99 EP 103 DI 10.1097/00005392-199501000-00036 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA PW167 UT WOS:A1995PW16700037 PM 7526007 ER PT J AU Wood, CB Stern, DN AF Wood, C. B. Stern, D. N. TI THE FIRST PRISMATIC ENAMEL IN REPTILES AND MAMMALS LATEST EVIDENCE FOR PRISMS AS A SYNAPOMORPHY OF MAMMALIA SO JOURNAL OF VERTEBRATE PALEONTOLOGY LA English DT Meeting Abstract C1 [Wood, C. B.] Providence Coll, Nat Sci Program, Providence, RI 02918 USA. [Stern, D. N.] Forsyth Dent Ctr, EM Lab, Boston, MA 02118 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 530 CHESTNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA SN 0272-4634 EI 1937-2809 J9 J VERTEBR PALEONTOL JI J. Vertebr. Paleontol. PY 1995 VL 15 SU 3 SI SI BP 60A EP 61A PG 2 WC Paleontology SC Paleontology GA V32OC UT WOS:000208959500311 ER PT J AU ZHU, ZM SCHAFFER, PA AF ZHU, ZM SCHAFFER, PA TI INTRACELLULAR-LOCALIZATION OF THE HERPES-SIMPLEX VIRUS TYPE-1 MAJOR TRANSCRIPTIONAL REGULATORY PROTEIN, ICP4, IS AFFECTED BY ICP27 SO JOURNAL OF VIROLOGY LA English DT Article ID NF-KAPPA-B; TEMPERATURE-SENSITIVE MUTANTS; HUMAN IMMUNODEFICIENCY VIRUS; IMMEDIATE EARLY GENE-1; COMPLETE DNA-SEQUENCE; LONG UNIQUE REGION; MACROMOLECULAR-SYNTHESIS; MONOCLONAL-ANTIBODIES; ALPHA PROTEIN-ICP27; FUNCTIONAL DOMAINS AB Infected-cell protein 4 (ICP4) is the major transcriptional activator of herpes simplex virus (HSV) gene expression during productive infection. ICP0 has broad transactivating activity for all classes of HSV genes as well as cellular genes and genes of heterologous viruses. Together, the transactivating activities of ICP4 and ICP0 are synergistic. ICP27, which alone does not exhibit major transregulatory activity, is able to differentially activate and repress viral gene expression induced by ICP4 and ICP0. Thus, ICP27 plays a modulatory role in viral gene expression. In order to explore the functional relationships among ICP4, ICP0, and ICP27 in the regulation of viral gene expression, we have used indirect immunofluorescence to examine the intracellular localization of ICP4 in cells infected with wild-type virus or with mutant viruses that did not express functional forms of ICP0 or ICP27. Although ICP4 localized to both the nuclei and cytoplasm of cells infected with either the wild-type virus or an ICP0 null mutant virus, this protein was present exclusively in the nuclei of cells infected with an ICP27 null mutant virus, suggesting that ICP27 is able to inhibit the nuclear localization of ICP4 during virus infection. Transient expression assays with pairs of plasmids that express wild-type forms of ICP4 and ICP0 or of ICP4 and ICP27 demonstrated that ICP27 has a significant inhibitory effect on the nuclear localization of ICP4, confirming the observations made with the mutant-virus-infected cells. By using a plasmid expressing wild-type ICP4 and a series of ICP27 mutant plasmids in transient expression assays, the C-terminal half of ICP27 was shown to be required for its inhibitory effect on the nuclear localization of ICP4. In similar studies using a series of ICP4 mutant plasmids, the region of ICP4 responsive to wild-type ICP27 was mapped to the C-terminal portion of the molecule between amino acid residues 820 and 1029. The level of expression of ICP27 was shown to have a significant effect on the intracellular localization of ICP4 in transient assays. These findings are consistent with previous studies in which ICP27 was shown to have an inhibitory effect on the nuclear localization of ICP0 (Z. Zhu, W. Cai, and P. A. Schaffer J. Virol. 68:3027-3040, 1994). Thus, ICP27 has a significant inhibitory effect on the ability of the two major HSV type 1 (HSV-1) regulatory proteins to localize to the nucleus. Collectively, these findings indicate that cooperative regulation of HSV-1 gene expression may well involve intracellular compartmental constraints. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NCI NIH HHS [R37 CA20260] NR 63 TC 33 Z9 34 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 JAN PY 1995 VL 69 IS 1 BP 49 EP 59 PG 11 WC Virology SC Virology GA PW815 UT WOS:A1995PW81500006 PM 7983745 ER PT J AU BRAND, D SRINIVASAN, K SODROSKI, J AF BRAND, D SRINIVASAN, K SODROSKI, J TI DETERMINANTS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENTRY IN THE CDR2 LOOP OF THE CD4 GLYCOPROTEIN SO JOURNAL OF VIROLOGY LA English DT Article ID ENVELOPE GLYCOPROTEIN; SOLUBLE CD4; SYNCYTIUM FORMATION; MEMBRANE-FUSION; BINDING-SITE; MONOCLONAL-ANTIBODY; SYNTHETIC PEPTIDES; GP120-CD4 BINDING; ATOMIC-STRUCTURE; HIV-INFECTION AB Various roles for the viral receptor, CD4, have been proposed in facilitating human immunodeficiency virus type 1 (HIV-1) entry, including virion binding to the target cell and the induction of conformational changes in the viral envelope glycoproteins required for the membrane fusion reaction. Here, we compare the structural requirements in the CDR2-like loop of CD4 domain 1, the major contact site of the gp120 envelope glycoprotein, for gp120 binding and virus entry. For every CD4 mutant examined, the level of cell surface expression and the gp120 binding affinity were sufficient to explain the relative ability to function as a viral receptor. The decrease in relative infectibility associated with decreased gp120 binding affinity was more pronounced at lower cell surface CD4 concentrations. These results imply that both receptor density and affinity determine the efficiency of HIV-1 entry and that specific structures in the CD4 residues examined are probably not required for HIV-1 entry functions other than gp120 binding. C1 DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. FU NCI NIH HHS [CA06516]; NIAID NIH HHS [AI24845, AI28691] NR 54 TC 27 Z9 27 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1995 VL 69 IS 1 BP 166 EP 171 PG 6 WC Virology SC Virology GA PW815 UT WOS:A1995PW81500019 PM 7983707 ER PT J AU SHOTTON, C ARNOLD, C SATTENTAU, Q SODROSKI, J MCKEATING, JA AF SHOTTON, C ARNOLD, C SATTENTAU, Q SODROSKI, J MCKEATING, JA TI IDENTIFICATION AND CHARACTERIZATION OF MONOCLONAL-ANTIBODIES SPECIFIC FOR POLYMORPHIC ANTIGENIC DETERMINANTS WITHIN THE V2 REGION OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE GLYCOPROTEIN SO JOURNAL OF VIROLOGY LA English DT Article ID AMINO-ACID CHANGES; CD4 BINDING-SITE; CELL TROPISM; SYNCYTIUM FORMATION; MACROPHAGE TROPISM; SOLUBLE CD4; V3 DOMAIN; I GP120; NEUTRALIZATION; INFECTIVITY AB We have identified six monoclonal antibodies (MAbs) mapping to both linear and conformation-dependent epitopes within the V2 region of the human immunodeficiency virus type 1 clone HXB10. Three of the MAbs (12b, 66c, and 66a) were able to neutralize the molecular clones HXB10 and HXB2, with titers in the range of 9.5 to 20.0 mu g/ml. MAbs mapping to the crown of the V2 loop (12b, 60b, and 74) bound poorly to cell surface-expressed oligomeric gp120, suggesting an;explanation for the poor or negligible neutralizing activity of MAbs to this region. In contrast, MAbs 12b and 60b demonstrated good reactivity with recombinant gp120 in an enzyme-linked immunosorbent assay format, suggesting differential epitope exposure between the recombinant and native forms of gp120. Cross-competition analysis of these MAbs and additional V1V2 MAbs for gp120 binding enabled us td assign the MAbs to six groups (A to F). Selection of neutralization escape mutants with MAbs 10/76b and 11/68b, belonging to nonoverlapping competition groups, identified amino acid changes at residues 165 (I to T) and 185 (D to N), respectively. Interestingly, these escape variants remained sensitive to neutralization by the nonselecting V2 MAbs. All MAbs demonstrated good recognition of IIIB viral gp120 yet failed to neutralize nonclonal stocks of IIIB. In addition, MAbs 12b and 62c bound MN and RF viral gp120, respectively, yet failed to neutralize the respective isolates. Cloning and expression of a library of gp120 and V1V2 fragments from IIIB-, MN-, and RF-infected H9 cultures identified a number of polymorphic sites, resulting in antigenic variation and subsequent loss of V2 MAb recognition. In contrast, the V3 region from the clones of the same isolates showed no amino acid changes, suggesting that the V2 region is polymorphic in long-term-passaged laboratory isolates and may account for the reduced antibody recognition observed. C1 INST CANC RES,HYBRIDOMA UNIT,SUTTON SM2 5NG,SURREY,ENGLAND. CENT PUBL HLTH LAB,HEPATITIS & RETROVIRUS LAB,LONDON NW9 5HT,ENGLAND. UNIV READING,DEPT MICROBIOL,READING RG6 2AJ,BERKS,ENGLAND. CTR IMMUNOL MARSEILLE,F-13288 MARSEILLE,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. OI McKeating, Jane/0000-0002-7229-5886 FU NIAID NIH HHS [AI28691, AI31783] NR 40 TC 55 Z9 55 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 JAN PY 1995 VL 69 IS 1 BP 222 EP 230 PG 9 WC Virology SC Virology GA PW815 UT WOS:A1995PW81500026 PM 7527084 ER PT J AU RUDNICK, MR GOLDFARB, S WEXLER, L LUDBROOK, PA MURPHY, MJ HALPERN, EF HILL, JA WINNIFORD, M COHEN, MB VANFOSSEN, DB AF RUDNICK, MR GOLDFARB, S WEXLER, L LUDBROOK, PA MURPHY, MJ HALPERN, EF HILL, JA WINNIFORD, M COHEN, MB VANFOSSEN, DB TI NEPHROTOXICITY OF IONIC AND NONIONIC CONTRAST-MEDIA IN 1196 PATIENTS - A RANDOMIZED TRIAL SO KIDNEY INTERNATIONAL LA English DT Article ID ACUTE-RENAL-FAILURE; HIGH-RISK PATIENTS; LOW-OSMOLAR; RADIOCONTRAST AGENT; CARDIAC ANGIOGRAPHY; INSUFFICIENCY; DIATRIZOATE; DYSFUNCTION; NEPHROPATHY; IOPAMIDOL AB The incidence of nephrotoxicity occurring with the nonionic contrast agent, iohexol, and the ionic contrast agent, meglumine/sodium diatrizoate, was compared in 1196 patients undergoing cardiac angiography in a prospective, randomized, double-blind multicenter trial. Patients were stratified into four groups: renal insufficiency (RI), diabetes mellitus (DM) both absent (N = 364); RI absent, DM present (N = 318); RI present, DM absent (N = 298); and RI and DM both present (N = 216). Serum creatinine levels were measured at -18 to 24, 0, and 24, 48, and 72 hours following contrast administration. Prophylactic hydration was administered pre- and post-angiography. acute nephrotoxicity (increase in serum creatinine of greater than or equal to 1 mg/dl 48 to 72 hours post-contrast) was observed in 42 (7%) patients receiving diatrizoate compared to 19 (3%) patients receiving iohexol, P < 0.002. Differences in nephrotoxcity between the two contrast groups were confined to patients with RI alone or combined with DM. In a multivariate analysis, baseline serum creatinine, male gender, DM, volume of contrast agent, and RI were independently related to the risk of nephrotoxicity. Patients with RI receiving diatrizoate were 3.3 times as likely to develop acute nephrotoxcity compared to those receiving iohexol. Clinically severe adverse renal events were uncommon (N = 15) and did not differ in incidence between contrast groups (iohexol N = 6; diatrizoate N = 9). In conclusion, in patients undergoing cardiac angiography, only those with pre-existing RI alone or combined with DM are at higher risk for acute contrast nephrotoxicity. The incidence of acute nephrotoxicity in these high-risk patients is significantly less with the nonionic contrast media iohexol compared to the ionic contrast agent diatrizoate. C1 HOSP UNIV PENN,SCH MED,DIV NEPHROL,PHILADELPHIA,PA 19104. STANFORD UNIV HOSP,SCH MED,DEPT RADIOL,STANFORD,CA. WASHINGTON UNIV,BARNES HOSP,SCH MED,DIV CARDIOL,ST LOUIS,MO 63110. SANOFI WINTHROP PHARMACEUT,NEW YORK,NY. MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,BOSTON,MA. UNIV FLORIDA,SHANDS HOSP,COLL MED,DIV CARDIOL,GAINESVILLE,FL. UNIV IOWA HOSP & CLIN,DIV CARDIOL,IOWA CITY,IA. NEW YORK MED COLL,WESTCHESTER CTY MED CTR,DIV CARDIOL,VALHALLA,NY 10595. OHIO STATE UNIV HOSP,COLL MED,DIV CARDIOL,COLUMBUS,OH. RP RUDNICK, MR (reprint author), UNIV PENN,GRAD HOSP,SCH MED,DIV NEPHROL,NEPHROL SECT,PEPPER PAVIL 703,19TH & LOMBARD ST,PHILADELPHIA,PA 19146, USA. NR 36 TC 558 Z9 589 U1 2 U2 14 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1995 VL 47 IS 1 BP 254 EP 261 DI 10.1038/ki.1995.32 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA PZ597 UT WOS:A1995PZ59700032 PM 7731155 ER PT J AU BELL, DA YOUNG, RH SCULLY, RE AF BELL, DA YOUNG, RH SCULLY, RE TI OVARIAN DESMOPLASTIC IMPLANTS (AUTOIMPLANTATION) INVOLVING SEROUS BORDERLINE TUMORS - A MIMIC OF SEROUS CARCINOMA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A85 EP A85 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900506 ER PT J AU CENTENO, BA SOUTHERN, JF WARSHAW, AL LEWANDROWSKI, KB AF CENTENO, BA SOUTHERN, JF WARSHAW, AL LEWANDROWSKI, KB TI CYTOLOGICAL DIAGNOSIS OF PANCREATIC CYSTIC LESIONS - A PROSPECTIVE-STUDY OF 22 PERCUTANEOUS ASPIRATES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A38 EP A38 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900221 ER PT J AU DELAMONTE, SM BLOCH, KD AF DELAMONTE, SM BLOCH, KD TI ABERRANT EXPRESSION OF THE CONSTITUTIVE ENDOTHELIAL NITRIC-OXIDE SYNTHETASE (CDNOS) GENE IN ALZHEIMERS-DISEASE (AD) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A135 EP A135 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900802 ER PT J AU DELAMONTE, SM ZHAO, Y KRAGE, R ANDREWS, D HUTCHINS, GM KURNICK, JT WANDS, JR AF DELAMONTE, SM ZHAO, Y KRAGE, R ANDREWS, D HUTCHINS, GM KURNICK, JT WANDS, JR TI EXOCRINE PANCREATIC-ENZYME GENE-EXPRESSION IN ACTIVATED T-LYMPHOCYTES - POSSIBLE ROLE IN THE PATHOGENESIS OF MULTIPLE-SCLEROSIS (MS) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A135 EP A135 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900804 ER PT J AU DELAMONTE, SM XU, YY HUTCHINS, GM WANDS, JR AF DELAMONTE, SM XU, YY HUTCHINS, GM WANDS, JR TI DEVELOPMENTAL PATTERNS OF NEURONAL THREAD PROTEIN EXPRESSION IN DOWNS-SYNDROME SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A135 EP A135 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900803 ER PT J AU EICHHORN, JH CLEMENT, PB AF EICHHORN, JH CLEMENT, PB TI SERTOLIFORM ENDOMETRIAL ADENOCARCINOMA - A STUDY OF 3 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. VANCOUVER GEN HOSP,VANCOUVER,BC,CANADA. HLTH SCI CTR,VANCOUVER,BC,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A89 EP A89 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900526 ER PT J AU FALLON, JT MORENO, PR FALK, E PALACIOS, IF NEWELL, JB FUSTER, V AF FALLON, JT MORENO, PR FALK, E PALACIOS, IF NEWELL, JB FUSTER, V TI MACROPHAGE CONTENT OF RESTENOTIC CORONARY PLAQUES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. MT SINAI MED CTR,NEW YORK,NY 10029. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A32 EP A32 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900183 ER PT J AU FANBURG, JC SPIRO, IJ MANKIN, HJ ROSENBERG, AE AF FANBURG, JC SPIRO, IJ MANKIN, HJ ROSENBERG, AE TI INFILTRATIVE SUBCUTANEOUS MALIGNANT FIBROUS HISTIOCYTOMA - A NEWLY RECOGNIZED DISTINCT SUBSET OF AN OLD ENTITY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A5 EP A5 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900026 ER PT J AU FERRY, JA ZUKERBERG, LR FUNG, C HARRIS, NL AF FERRY, JA ZUKERBERG, LR FUNG, C HARRIS, NL TI OCULAR ADNEXAL LYMPHOMA - A STUDY OF 157 CASES WITH A HIGH-FREQUENCY OF MARGINAL ZONE B-CELL LYMPHOMA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A109 EP A109 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900650 ER PT J AU GAFFEY, MJ BOYD, JC WEISS, LM ZUCKERBERG, LR YANG, WI LEZZONI, JC WILLIAMS, ME AF GAFFEY, MJ BOYD, JC WEISS, LM ZUCKERBERG, LR YANG, WI LEZZONI, JC WILLIAMS, ME TI CYCLIN D1 (PRAD1) PROTEIN EXPRESSION IN HEAD AND NECK SQUAMOUS-CELL CARCINOMA (SCC) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV VIRGINIA HOSP,CHARLOTTESVILLE,VA. CITY HOPE NATL MED CTR,DUARTE,CA 91010. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A100 EP A100 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900596 ER PT J AU GAFFEY, MJ FRIERSON, HF MILLS, SE CLEMENT, PB SHASHI, V IEZZONI, JC GERSELL, DJ YOUNG, RH AF GAFFEY, MJ FRIERSON, HF MILLS, SE CLEMENT, PB SHASHI, V IEZZONI, JC GERSELL, DJ YOUNG, RH TI OVARIAN GRANULOSA-CELL TUMORS WITH BIZARRE NUCLEI (GCT-BN) - AN IMMUNOHISTOCHEMICAL AND FLUORESCENCE IN-SITU HYBRIDIZATION (FISH) STUDY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV VIRGINIA,CHARLOTTESVILLE,VA. VANCOUVER GEN HOSP,VANCOUVER,BC,CANADA. WASHINGTON UNIV,ST LOUIS,MO. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A90 EP A90 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900531 ER PT J AU HARRIST, TJ COSTA, JJ DEMETRI, GD DVORAK, AM HAYES, DF MERICA, EA MENCHACA, D GRINGERI, AJ GALLI, SJ AF HARRIST, TJ COSTA, JJ DEMETRI, GD DVORAK, AM HAYES, DF MERICA, EA MENCHACA, D GRINGERI, AJ GALLI, SJ TI RECOMBINANT HUMAN STEM-CELL FACTOR (SCF) (C-KIT LIGAND) PROMOTES MELANOCYTE HYPERPLASIA AND ACTIVATION IN-VIVO SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 BETH ISRAEL HOSP,DEPT PATHOL,BOSTON,MA 02215. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED ONCOL,BOSTON,MA 02115. AMGEN INC,THOUSAND OAKS,CA 91320. PATHOL SERV,CAMBRIDGE,MA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A48 EP A48 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900281 ER PT J AU HSI, ED ZUKERBERG, LR YANG, WI GOLDBLUM, JR ARNOLD, A AF HSI, ED ZUKERBERG, LR YANG, WI GOLDBLUM, JR ARNOLD, A TI CYCLIN D1 (PRAD1) EXPRESSION IN PARATHYROID ADENOMAS - AN IMMUNOHISTOCHEMICAL STUDY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV MICHIGAN,DEPT PATHOL,ANN ARBOR,MI 48109. CLEVELAND CLIN,DEPT PATHOL,CLEVELAND,OH 44106. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ENDOCRINE ONCOL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A54 EP A54 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900316 ER PT J AU MATSUBARA, O TAMURA, A OHDAMA, S MARK, EJ AF MATSUBARA, O TAMURA, A OHDAMA, S MARK, EJ TI THROMBOMODULIN OF ALVEOLAR-CAPILLARY ENDOTHELIUM IN DIFFUSE ALVEOLAR DAMAGE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 TOKYO MED & DENT UNIV,TOKYO,JAPAN. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A150 EP A150 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900890 ER PT J AU NGUYEN, PL ZUKERBERG, LR HARRIS, NL AF NGUYEN, PL ZUKERBERG, LR HARRIS, NL TI P53 AND BCL-2 PROTEIN EXPRESSION IN FOLLICULAR LYMPHOMAS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A118 EP A118 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900701 ER PT J AU NGUYEN, PL ROBERTSON, MJ RITZ, J HARRIS, NL AF NGUYEN, PL ROBERTSON, MJ RITZ, J HARRIS, NL TI EXPRESSION OF CD95 AND BCL-2 PROTEINS IN LOW-GRADE AND HIGH-GRADE NON-HODGKINS-LYMPHOMAS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. DANA FARBER CANC INST,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A118 EP A118 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900700 ER PT J AU NIELSEN, GP OLIVA, E YOUNG, RH ROSENBERG, AE DICKERSIN, GR SCULLY, RE AF NIELSEN, GP OLIVA, E YOUNG, RH ROSENBERG, AE DICKERSIN, GR SCULLY, RE TI ALVEOLAR SOFT PART SARCOMA OF THE FEMALE GENITAL-TRACT - A REPORT OF 9 CASES AND REVIEW OF THE LITERATURE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A94 EP A94 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900560 ER PT J AU OCONNELL, JX NANTHAKUMAR, S LOGAN, MP ROSENBERG, AE AF OCONNELL, JX NANTHAKUMAR, S LOGAN, MP ROSENBERG, AE TI OSTEOID OSTEOMA - THE RICHLY INNERVATED BONE-TUMOR SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 VANCOUVER GEN HOSP,VANCOUVER,BC,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A9 EP A9 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900050 ER PT J AU ODZE, R COMPTON, C HURLBUT, D AF ODZE, R COMPTON, C HURLBUT, D TI TREFOIL PEPTIDE (PS2, HSP), TGF-ALPHA AND EGF-R EXPRESSION IN MENETRIERS DISEASE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,DEACONESS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A66 EP A66 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900391 ER PT J AU OLIVA, E YOUNG, RH CLEMENT, PB BHAN, AK SCULLY, RE AF OLIVA, E YOUNG, RH CLEMENT, PB BHAN, AK SCULLY, RE TI CELLULAR BENIGN MESENCHYMAL TUMORS OF THE UTERUS - A COMPARATIVE MORPHOLOGIC AND IMMUNOHISTOCHEMICAL ANALYSIS OF 33 HIGHLY CELLULAR LEIOMYOMAS (CL) AND 7 ENDOMETRIAL STROMAL NODULES (ESN), 2 FREQUENTLY CONFUSED TUMORS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. UNIV BRITISH COLUMBIA,VANCOUVER GEN HOSP,DEPT PATHOL,VANCOUVER,BC V5Z 1M9,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A95 EP A95 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900562 ER PT J AU ONEILSMITH, K WITTENBERG, KH EFIRD, JT MANKIN, HJ BHAN, AK ROSENBERG, AE AF ONEILSMITH, K WITTENBERG, KH EFIRD, JT MANKIN, HJ BHAN, AK ROSENBERG, AE TI EWINGS-SARCOMA AND PERIPHERAL PRIMITIVE NEUROECTODERMAL TUMOR - A PROPOSAL FOR A STANDARDIZED CLASSIFICATION SCHEME BASED ON MORPHOLOGIC, IMMUNOHISTOCHEMICAL AND CLINICAL-FEATURES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A10 EP A10 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900052 ER PT J AU REID, A THOR, A EDGERTON, S TSAI, M WRIGHT, C OLEARY, T AF REID, A THOR, A EDGERTON, S TSAI, M WRIGHT, C OLEARY, T TI P53 ACCUMULATION AND MUTATION ARE INDEPENDENT PREDICTORS OF PROGNOSIS IN NODE-POSITIVE BREAST-CANCER SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A24 EP A24 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900135 ER PT J AU ROBBOY, SJ KRIGMAN, HR DONOHUE, J SCULLY, RE AF ROBBOY, SJ KRIGMAN, HR DONOHUE, J SCULLY, RE TI PROGNOSTIC INDEXES IN MALIGNANT STRUMA OVARII (MSO) - CLINICOPATHOLOGICAL ANALYSIS OF 36 PATIENTS WITH 20+-YEAR FOLLOW-UP SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DURHAM,NC. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A95 EP A95 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900566 ER PT J AU RUTGERS, JL BAERGEN, RN YOUNG, RH SCULLY, RE AF RUTGERS, JL BAERGEN, RN YOUNG, RH SCULLY, RE TI PLACENTAL SITE TROPHOBLASTIC TUMOR - A CLINICOPATHOLOGICAL STUDY OF 62 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. UNIV CALIF LOS ANGELES,HARBOR MED CTR,TORRANCE,CA 90509. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A96 EP A96 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900569 ER PT J AU ZERBINI, MCN TRIEGER, S GRIER, H HOLLISTER, C WEINBERG, DS CRISTOFANI, LM LATORRE, MRDO ALVES, VAF PEREZATAYDE, AR AF ZERBINI, MCN TRIEGER, S GRIER, H HOLLISTER, C WEINBERG, DS CRISTOFANI, LM LATORRE, MRDO ALVES, VAF PEREZATAYDE, AR TI PRIMARY MALIGNANT LIVER EPITHELIAL TUMORS IN CHILDREN - A STUDY OF DNA CONTENT AND PROLIFERATION MARKERS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV SAO PAULO,HOSP CLIN,SCH PUBL HLTH,BR-05508 SAO PAULO,BRAZIL. HARVARD UNIV,CHILDRENS HOSP,DANA FARBER CANC INST,BOSTON,MA. HARVARD UNIV,BRIGHAM & WOMENS HOSP,BOSTON,MA. RI Latorre, Maria/J-5780-2014; Zerbini, Maria Claudia/D-1586-2012 OI Latorre, Maria/0000-0002-5189-3457; Zerbini, Maria Claudia/0000-0002-7408-9816 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A145 EP A145 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900865 ER PT J AU ZUCKERBERG, L YANG, WI BENEDICT, W ARNOLD, A DYSON, N HARLOW, E HARRIS, N AF ZUCKERBERG, L YANG, WI BENEDICT, W ARNOLD, A DYSON, N HARLOW, E HARRIS, N TI EXPRESSION OF THE RETINOBLASTOMA PROTEIN IN LOW-GRADE B-CELL LYMPHOMA - RELATIONSHIP TO CYCLIN D1 (BCL-1) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1995 VL 72 IS 1 BP A125 EP A125 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA QD549 UT WOS:A1995QD54900741 ER PT J AU STOWELL, CP AF STOWELL, CP TI WHEN TO PULL THE TRIGGER - MAKING THE DECISION TO TRANSFUSE RED-BLOOD-CELLS SO LABORATORY MEDICINE LA English DT Article AB The decision to transfuse red blood cells cannot be made on the basis of a single parameter such ns the hemoglobin level. Making an intelligent decision about transfusion requires an understanding of the body's ability to respond to acute and chronic anemia, and an appreciation of the degree of risk that such anemia poses to patients with various concurrent medical problems. Based on this information, and a thorough evaluation of the patient's condition, a clinically sound decision can be made. Strategies for making the decision to transfuse patients with acute and chronic anemia are described. This is the fourth article in a four-part CE Update series on blood banking. Other articles focused on ensuring quality during intraoperative blood salvage, blood substitutes, and electronic crossmatch. RP STOWELL, CP (reprint author), MASSACHUSETTS GEN HOSP,BLOOD TRANSFUS SERV,GRJ 212,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC CLIN PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON ST, CHICAGO, IL 60612 SN 0007-5027 J9 LAB MED JI Lab. Med. PD JAN PY 1995 VL 26 IS 1 BP 55 EP 62 PG 8 WC Medical Laboratory Technology SC Medical Laboratory Technology GA QA177 UT WOS:A1995QA17700026 ER PT B AU FLOTTE, TJ LEE, S ZHANG, H MCAULIFFE, D DOUKI, T DOUKAS, A AF FLOTTE, TJ LEE, S ZHANG, H MCAULIFFE, D DOUKI, T DOUKAS, A BE Jacques, SL Katzir, A TI LASER-INDUCED STRESS TRANSIENTS - APPLICATIONS FOR MOLECULAR DELIVERY SO LASER-TISSUE INTERACTION VI, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Laser-Tissue Interaction VI Conference CY FEB 06-09, 1995 CL SAN JOSE, CA SP Soc Photo Opt Instrumentat Engineers DE LASER; PRESSURE; GENE THERAPY; CANCER THERAPY; GENETIC VECTORS C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 12 Z9 12 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1738-6 J9 P SOC PHOTO-OPT INS PY 1995 VL 2391 BP 202 EP 207 DI 10.1117/12.209883 PG 6 WC Engineering, Biomedical; Optics SC Engineering; Optics GA BD32D UT WOS:A1995BD32D00020 ER PT B AU LIN, CP KELLY, MW AF LIN, CP KELLY, MW BE Jacques, SL Katzir, A TI ULTRAFAST TIME-RESOLVED IMAGING OF STRESS TRANSIENT AND CAVITATION FROM SHORT PULSED LASER IRRADIATED MELANIN PARTICLES SO LASER-TISSUE INTERACTION VI, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Laser-Tissue Interaction VI Conference CY FEB 06-09, 1995 CL SAN JOSE, CA SP Soc Photo Opt Instrumentat Engineers DE MELANIN; MICROPARTICLES; STRESS TRANSIENT; SHOCK WAVES; CAVITATION; RETINAL INJURY; PHOTOACOUSTIC EFFECTS C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 14 Z9 14 U1 0 U2 2 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1738-6 J9 P SOC PHOTO-OPT INS PY 1995 VL 2391 BP 294 EP 299 DI 10.1117/12.209895 PG 6 WC Engineering, Biomedical; Optics SC Engineering; Optics GA BD32D UT WOS:A1995BD32D00030 ER PT B AU ADILI, F VANEPS, RGS LAMURAGLIA, GM AF ADILI, F VANEPS, RGS LAMURAGLIA, GM BE Anderson, RR Katzir, A TI Local delivery of photosensitizing drugs in arteries: A novel approach to photodynamic therapy for the prevention of intimal hyperplasia SO LASERS IN SURGERY: ADVANCED CHARACTERIZATION, THERAPEUTICS, AND SYSTEMS V, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Lasers in Surgery: Advanced Characterization, Therapeutics, and Systems V CY FEB 04-06, 1995 CL SAN JOSE, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS DE PHOTODYNAMIC THERAPY; COMMON CAROTID ARTERY; LOCAL DELIVERY; INTIMAL HYPERPLASIA; BENZPORPHYRIN DERIVATIVE; BALLOON-INJURY C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV VASC SURG,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1742-4 J9 P SOC PHOTO-OPT INS PY 1995 VL 2395 BP 402 EP 408 DI 10.1117/12.209126 PG 7 WC Optics; Surgery SC Optics; Surgery GA BD11K UT WOS:A1995BD11K00057 ER PT J AU SCHMIDTERFURTH, U HASAN, T SCHOMACKER, K FLOTTE, T BIRNGRUBER, R AF SCHMIDTERFURTH, U HASAN, T SCHOMACKER, K FLOTTE, T BIRNGRUBER, R TI IN-VIVO UPTAKE OF LIPOSOMAL BENZOPORPHYRIN DERIVATIVE AND PHOTOTHROMBOSIS IN EXPERIMENTAL CORNEAL NEOVASCULARIZATION SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE BENZOPORPHYRIN DERIVATIVE; OCULAR PHOTOTHROMBOSIS; LIPOSOMES; CORNEA; NEOVASCULARIZATION ID LOW-DENSITY LIPOPROTEIN; PHOTODYNAMIC THERAPY; LASER PHOTOCOAGULATION; PHOTOCHEMICAL INITIATION; VASCULAR OCCLUSION; LIPID KERATOPATHY; ENDOTHELIAL-CELLS; FEEDER VESSELS; THROMBOSIS; HEMATOPORPHYRIN AB Background and Objective: Photodynamic therapy (PDT) has been used successfully to occlude neovascularizations experimentally. We evaluated the vasoocclusive potential of benzoporphyrin derivative (BPD), a new photosensitizer currently in clinical trials. Since liposomally formulated BPD strongly binds to endogenous low density lipoproteins (LDL) after i.v. injection, LDL act as carrier to deliver BPD preferentially 60 proliferating endothelial cells. Study Design/Materials and Methods: Corneal neovascularizations in rabbits were used as model. Time-dependent uptake and retention of liposomal BPD were measured in vivo by monitoring the laser-induced fluorescence (LIF). Photothrombosis was induced using a dye laser emitting at 692 nm. Results: A maximal BPD concentration was measured at 60-90 minutes postinjection determining the optimal time interval for treatment. Exposures as low as 10 J/cm(2) allowed complete and irreversible neovascular occlusion as documented angiographically. Histology revealed selective endothelial damage, adjacent corneal stroma, or iris vessels, remained intact. Identical results were obtained using BPD directly complexed with LDL suggesting use of a LDL-mediated pathway. Conclusion: We suggest BPD-PDT for a selective treatment of neovascular diseases. (C) 1995 Wiley-Liss, Inc. C1 UNIV LUBECK,MED LASERZENTRUM LUBECK,D-23562 LUBECK,GERMANY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA. RP SCHMIDTERFURTH, U (reprint author), UNIV LUBECK,AUGENKLIN MED,RATZEBURGER ALLEE 160,D-23562 LUBECK,GERMANY. RI Birngruber, Reginald/Q-2342-2016 NR 39 TC 74 Z9 76 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 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1995 VL 17 IS 2 BP 178 EP 188 DI 10.1002/lsm.1900170207 PG 11 WC Dermatology; Surgery SC Dermatology; Surgery GA RW607 UT WOS:A1995RW60700006 PM 8569414 ER PT J AU NISHIOKA, NS AF NISHIOKA, NS TI APPLICATIONS OF LASERS IN GASTROENTEROLOGY SO LASERS IN SURGERY AND MEDICINE LA English DT Review DE ENDOSCOPY; OPTICAL DIAGNOSTICS; PHOTODYNAMIC THERAPY ID INDUCED FLUORESCENCE SPECTROSCOPY; BILE-DUCT STONES; BLEEDING PEPTIC-ULCERS; YAG LASER; PHOTODYNAMIC THERAPY; CONTROLLED TRIAL; BILIARY CALCULI; ENDOSCOPIC ND; ARGON-LASER; PHOTOCOAGULATION AB In this article the clinical uses of lasers in gastroenterology are reviewed. The endoscopic delivery of light for therapeutic as well as diagnostic purposes is discussed. Current research directions in the field are also indicated where appropriate. (C) 1995 Wiley-Liss, Inc. C1 HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02114 USA. RP NISHIOKA, NS (reprint author), MASSACHUSETTS GEN HOSP, MED SERV, GASTROINTESTINAL UNIT, BHX 630, 55 FRUIT ST, BOSTON, MA 02114 USA. NR 46 TC 8 Z9 8 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0196-8092 EI 1096-9101 J9 LASER SURG MED JI Lasers Surg. Med. PY 1995 VL 16 IS 3 BP 205 EP 214 DI 10.1002/lsm.1900160302 PG 10 WC Dermatology; Surgery SC Dermatology; Surgery GA QU338 UT WOS:A1995QU33800001 PM 7791494 ER PT J AU GLATT, CR AF GLATT, CR TI ANCIENT ZIONISM - THE BIBLICAL ORIGINS OF THE NATIONAL IDEA - ERLICH,A SO LIBRARY JOURNAL LA English DT Book Review RP GLATT, CR (reprint author), PHILADELPHIA VA MED CTR,PHILADELPHIA,PA, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 SN 0363-0277 J9 LIBR J JI Libr. J. PD JAN PY 1995 VL 120 IS 1 BP 107 EP 107 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA QC391 UT WOS:A1995QC39100139 ER PT J AU PFLEIDERER, B GARRIDO, L AF PFLEIDERER, B GARRIDO, L TI MIGRATION AND ACCUMULATION OF SILICONE IN THE LIVER OF WOMEN WITH SILICONE GEL-FILLED BREAST IMPLANTS SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE SILICONE MIGRATION; BREAST PROSTHESES; LIVER; H-1 MAGNETIC RESONANCE SPECTROSCOPY ID MAGNETIC-RESONANCE SPECTROSCOPY; LOCALIZED PROTON SPECTROSCOPY; AUGMENTATION MAMMAPLASTY; INVIVO; RAT; DISEASE; MOTION AB H-1 NMR localized spectroscopy (STEAM), combined with echocardiography (EGG), respiratory gating, and water and fat suppression, was used to quantify silicone concentrations in the liver of women with silicone gel-filled breast implants. Localized spectroscopy was performed on 15 patients with silicone gel-filled breast prostheses and on eight volunteers with no implants. The H-1 spectra in the liver of patients showed silicone resonances from 0.3 to -0.8 ppm, attributable to protons in the methyl groups of silicone. The presence of silicone in the liver could first be detected 3-4 years after breast prostheses implantation. No correlation between silicone concentrations and implantation times was observed, However, our results indicated that silicone concentrations may reflect implant integrity: detectable silicone concentrations in the liver appeared to be higher when the implants were ruptured than when the implants appeared intact. Moreover, new resonances in the range of -2.6 to -4 ppm were observed in most patients after long-term implantation, As these species increase with implantation time, the new resonances may reflect chemically changed silicone (paramagnetically shifted silicon complexes bound to iron) accumulated over time, The sensitivity of H-1 NMR localized spectroscopy is sufficient to detect silicon concentrations as low as 0.20 mM. Results from one patient whose implants had been removed 14 months prior to the NMR examination showed no detectable silicone in the liver, indicating that it may have been excreted via bile or degraded to silica and high coordinated silicon complexes. Quantitative H-1 localized spectroscopy of the liver in women with silicone gel-filled breast implants may provide valuable information concerning silicone accumulation and degradation in vivo, as well as about the kinetics of its elimination from the body after implant removal. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP PFLEIDERER, B (reprint author), MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,BIOMAT LAB,149 13TH ST,BOSTON,MA 02129, USA. RI Garrido, Leoncio/K-3092-2014 OI Garrido, Leoncio/0000-0002-7587-1260 FU NCI NIH HHS [R01 CA 59651-01AL] NR 35 TC 40 Z9 40 U1 2 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD JAN PY 1995 VL 33 IS 1 BP 8 EP 17 DI 10.1002/mrm.1910330103 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA PZ808 UT WOS:A1995PZ80800002 PM 7891539 ER PT J AU HARIKA, L WEISSLEDER, R POSS, K ZIMMER, C PAPISOV, MI BRADY, TJ AF HARIKA, L WEISSLEDER, R POSS, K ZIMMER, C PAPISOV, MI BRADY, TJ TI MR LYMPHOGRAPHY WITH A LYMPHOTROPIC T-1-TYPE MR CONTRAST AGENT - GD-DTPA-PGM SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE MRI; CONTRAST AGENT; POLYMER; MACROMOLECULE ID RELAXATION-TIMES AB A model system of a paramagnetic lymphotropic MR contrast agent (Gd-DTPA labeled polyglucose associated macrocomplex, PGM) for T-1-weighted MR imaging of lymph nodes in rats and rabbits was evaluated, Pharmacokinetic (tissue accumulation) and MR imaging data (optimal dose and timing parameters) were obtained in normal rats (n = 88) after subcutaneous (SC) injection of paramagnetic, radiolabeled [111In]Gd-DTPA-PGM. A rabbit model of lymph node metastases (n = 8) was ultimately used to demonstrate the potential of MR imaging with Gd-DTPA-PGM for nodal tumor detection, Maximum concentrations of Gd-DTPA-PGM were found in popliteal and paraaortic lymph nodes within 24 h after SC administration, and highest lymph node SNR values were obtained by MR imaging at this time point. The optimum imaging dose was 6-12 mu mol Gd/kg. Tumor-lymph node contrast increased from 0.0 +/- 1.2 precontrast to 19.2 +/- 6.5 (spoiled gradient echo sequence, TR 50/TE 7/flip angle 60 degrees) postcontrast and conspicuity of nodal metastases was improved, Gd-DTPA-PGM accumulates in lymph nodes after SC administration and significantly enhances lymph node signal intensity of normal animals but not metastatic lymph nodes. C1 MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,MR PHARMACEUT PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. FU NCI NIH HHS [R01 CA 59649-01] NR 10 TC 58 Z9 61 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD JAN PY 1995 VL 33 IS 1 BP 88 EP 92 DI 10.1002/mrm.1910330113 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA PZ808 UT WOS:A1995PZ80800012 PM 7891541 ER PT J AU TRUETT, GE JACOB, HJ MILLER, J DROUIN, G BAHARY, N SMOLLER, JW LANDER, ES LEIBEL, RL AF TRUETT, GE JACOB, HJ MILLER, J DROUIN, G BAHARY, N SMOLLER, JW LANDER, ES LEIBEL, RL TI GENETIC-MAP OF RAT CHROMOSOME-5 INCLUDING THE FATTY (FA) LOCUS SO MAMMALIAN GENOME LA English DT Article ID MOUSE; OBESITY; NORVEGICUS; CLUSTER; DB AB Thirteen loci, including the obesity gene fatty (fa), were incorporated into a linkage map of rat Chromosome (Chr) 5. These loci were mapped in obese (fa/fa) progeny of a cross between BN x 13M-fal+ F-1 animals. Obese rats were scored for BN and 13M alleles at four loci (Ifna, D1S85h, C8b, and Lck1) by restriction fragment length polymorphisms and at eight additional loci (Glut1, Sv4j2, R251, R735, R980, R252, R371, and R1138) by simple sequence length polymorphisms (SSLP). The resulting map spans 67.3 cM of Chr 5, presenting nine previously unmapped loci and one locus (Lck1) previously assigned to Chr 5 by use of somatic cell hybrid lines. Seven of the eight SSLP loci are newly identified; the SSLP linkage group alone spans 56.8 cM. The order of the loci is Sv4j2-R251-R735-R980-R1138-Ifna-fa-D1S85h-C8b(Glut1-R252-R371)-Lck1. One locus, D1S85h, was found to lie only 0.4 cM from fa, close enough to serve as a reliable marker for the prediction of phenotype from genotype, and will be useful also for studies on the development of obesity in the fatty rat. C1 ROCKEFELLER UNIV,HUMAN BEHAV & METAB LAB,NEW YORK,NY 10021. WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. HARVARD UNIV,BETH ISRAEL HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. RP TRUETT, GE (reprint author), PENNINGTON BIOMED RES CTR,6400 PERKINS RD,BATON ROUGE,LA 70808, USA. FU NICHD NIH HHS [HD-28047]; NIDDK NIH HHS [5P30-DK-26687, DK-41096] NR 37 TC 20 Z9 20 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD JAN PY 1995 VL 6 IS 1 BP 25 EP 30 DI 10.1007/BF00350889 PG 6 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA QB671 UT WOS:A1995QB67100005 PM 7719022 ER PT B AU ANDERSON, KC AF ANDERSON, KC BE Lasky, LC Warkentin, PI TI MALIGNANT CELL PURGING - MONOCLONAL ANTIBODIES SO MARROW AND STEM CELL PROCESSING FOR TRANSPLANTATION LA English DT Proceedings Paper CT Conference on Marrow and Stem Cell Processing for Transplantation CY MAR 07-09, 1993 CL TAMPA, FL SP AMER ASSOC BLOOD BANKS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BLOOD COMPONENT LAB,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 BN 1-56395-042-1 PY 1995 BP 103 EP 122 PG 20 WC Cell Biology; Hematology; Transplantation SC Cell Biology; Hematology; Transplantation GA BD11B UT WOS:A1995BD11B00007 ER PT J AU MCHORNEY, CA WARE, JE AF MCHORNEY, CA WARE, JE TI CONSTRUCTION AND VALIDATION OF AN ALTERNATE FORM GENERAL MENTAL-HEALTH SCALE FOR THE MEDICAL OUTCOMES STUDY SHORT-FORM 36-ITEM HEALTH SURVEY SO MEDICAL CARE LA English DT Article DE HEALTH STATUS ASSESSMENT; MENTAL HEALTH; ALTERNATE FORMS; RELIABILITY; INSTRUMENT DEVELOPMENT ID QUALITY-OF-LIFE; FUNCTIONAL STATUS; RANDOMIZED TRIAL; SURVEY SF-36; PRIMARY CARE; VALIDITY; INSTRUMENT; RELIABILITY; PROFILE; IMPACT AB Alternate-form health measures are useful for clinical trials or health services research requiring repeated administrations over a short interval of time. Further, by using alternate-form methodology, they can be utilized to estimate score reliability. Data from the Medical Outcomes Study were used to evaluate five alternate forms of the Short-Form 36-Item Health Survey (SF-36) general mental health scale (MHI-5). Well-established psychometric criteria were used to select the best alternate form and to estimate the reliability of the MHI-5 using the alternate-form methodology. Although a considerable degree of comparability across the five alternate forms was observed for criteria pertaining to estimates of item-internal consistency and reliability, distributional characteristics of scales, tests of empirical validity, and score equivalence at the individual level, we recommend one alternate form that satisfied all evaluation criteria and did so better than any other alternate form. Using the alternate-form methodology of estimating reliability, results suggest that the internal-consistency method underestimates the reliability of the MHI-5 by 3%. The methodology presented here should prove useful to others interested in constructing and evaluating alternate forms, and the alternate form recommended here (MHI-5AF) should prove useful across many health status assessment applications. C1 UNIV WISCONSIN, SCH MED, DEPT PREVENT MED, MADISON, WI USA. TUFTS UNIV NEW ENGLAND MED CTR, INST HLTH, BOSTON, MA 02111 USA. RP MCHORNEY, CA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR, HLTH SERV RES & DEV FIELD PROGRAM, 2500 OVERLOOK TERRACE, MADISON, WI 53705 USA. NR 49 TC 123 Z9 125 U1 2 U2 7 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD JAN PY 1995 VL 33 IS 1 BP 15 EP 28 DI 10.1097/00005650-199501000-00002 PG 14 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA QB423 UT WOS:A1995QB42300002 PM 7823644 ER PT J AU STOVALL, M BALCKWELL, CR CUNDIFF, J NOVACK, DH PALTA, JR WAGNER, LK WEBSTER, EW SHALEK, RJ AF STOVALL, M BALCKWELL, CR CUNDIFF, J NOVACK, DH PALTA, JR WAGNER, LK WEBSTER, EW SHALEK, RJ TI FETAL DOSE FROM RADIOTHERAPY WITH PHOTON BEAMS - REPORT OF AAPM-RADIATION-THERAPY-COMMITTEE TASK GROUP NO-36 SO MEDICAL PHYSICS LA English DT Article DE RADIATION THERAPY; FETUS ID X-RAY-EXPOSURE; CHILDHOOD-CANCER; SECONDARY RADIATION; TREATMENT FIELD; IRRADIATION; ACCELERATORS; TWINS; RISK; NEUTRONS; EMBRYOS C1 MAYO CLIN & MAYO FDN,DEPT THERAPEUT RADIOL,ROCHESTER,MN 55905. OAKMORE MED PHYS,OAKLAND,CA 94602. THOMAS JEFFERSON UNIV,BODINE CTR CANC TREATMENT,DEPT RADIAT THERAPY,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,BODINE CTR CANC TREATMENT,DEPT NUCL MED,PHILADELPHIA,PA 19107. UNIV TEXAS,SCH MED,DEPT RADIOL,HOUSTON,TX 77030. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP STOVALL, M (reprint author), UNIV TEXAS,MD ANDERSON CANCER CTR,DEPT RADIAT PHYS,HOUSTON,TX 77030, USA. NR 49 TC 195 Z9 197 U1 1 U2 5 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0094-2405 J9 MED PHYS JI Med. Phys. PD JAN PY 1995 VL 22 IS 1 BP 63 EP 82 DI 10.1118/1.597525 PG 20 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QC862 UT WOS:A1995QC86200010 PM 7715571 ER PT B AU Kollias, N AF Kollias, N BE Zeise, L Chedekel, MR Fitzpatrick, TB TI The spectroscopy of human melanin pigmentation SO MELANIN: ITS ROLE IN HUMAN PHOTOPROTECTION LA English DT Proceedings Paper CT Symposium on Melanin - Its Role in Human Photoprotection CY MAR 11-12, 1994 CL WASHINGTON, DC SP Adv Polym Syst Inc, Lancaster Grp, Biosource Genet Corp, DUSA Pharm Inc, Estee Lauder C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 27 Z9 27 U1 0 U2 3 PU VALDENMAR PUBLISHING CO PI OVERLAND PK PA 9812 W 121ST TERRACE, OVERLAND PK, KS 66213-1677 BN 0-9632105-2-1 PY 1995 BP 31 EP 38 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Dermatology SC Biochemistry & Molecular Biology; Cell Biology; Dermatology GA BE87M UT WOS:A1995BE87M00004 ER PT B AU Pathak, MA AF Pathak, MA BE Zeise, L Chedekel, MR Fitzpatrick, TB TI Functions of melanin and protection by melanin SO MELANIN: ITS ROLE IN HUMAN PHOTOPROTECTION LA English DT Proceedings Paper CT Symposium on Melanin - Its Role in Human Photoprotection CY MAR 11-12, 1994 CL WASHINGTON, DC SP Adv Polym Syst Inc, Lancaster Grp, Biosource Genet Corp, DUSA Pharm Inc, Estee Lauder C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 26 Z9 26 U1 0 U2 0 PU VALDENMAR PUBLISHING CO PI OVERLAND PK PA 9812 W 121ST TERRACE, OVERLAND PK, KS 66213-1677 BN 0-9632105-2-1 PY 1995 BP 125 EP 134 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Dermatology SC Biochemistry & Molecular Biology; Cell Biology; Dermatology GA BE87M UT WOS:A1995BE87M00014 ER PT B AU Fitzpatrick, TB Bolognia, JL AF Fitzpatrick, TB Bolognia, JL BE Zeise, L Chedekel, MR Fitzpatrick, TB TI Human melanin pigmentation: Role in pathogenesis of cutaneous melanoma SO MELANIN: ITS ROLE IN HUMAN PHOTOPROTECTION LA English DT Proceedings Paper CT Symposium on Melanin - Its Role in Human Photoprotection CY MAR 11-12, 1994 CL WASHINGTON, DC SP Adv Polym Syst Inc, Lancaster Grp, Biosource Genet Corp, DUSA Pharm Inc, Estee Lauder C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CAMBRIDGE,MA 02138. NR 0 TC 10 Z9 11 U1 0 U2 0 PU VALDENMAR PUBLISHING CO PI OVERLAND PK PA 9812 W 121ST TERRACE, OVERLAND PK, KS 66213-1677 BN 0-9632105-2-1 PY 1995 BP 177 EP 182 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Dermatology SC Biochemistry & Molecular Biology; Cell Biology; Dermatology GA BE87M UT WOS:A1995BE87M00019 ER PT B AU Kollias, N AF Kollias, N BE Zeise, L Chedekel, MR Fitzpatrick, TB TI Melanin and non-melanin photoprotection SO MELANIN: ITS ROLE IN HUMAN PHOTOPROTECTION LA English DT Proceedings Paper CT Symposium on Melanin - Its Role in Human Photoprotection CY MAR 11-12, 1994 CL WASHINGTON, DC SP Adv Polym Syst Inc, Lancaster Grp, Biosource Genet Corp, DUSA Pharm Inc, Estee Lauder C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU VALDENMAR PUBLISHING CO PI OVERLAND PK PA 9812 W 121ST TERRACE, OVERLAND PK, KS 66213-1677 BN 0-9632105-2-1 PY 1995 BP 233 EP 237 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Dermatology SC Biochemistry & Molecular Biology; Cell Biology; Dermatology GA BE87M UT WOS:A1995BE87M00026 ER PT J AU HILDEBRANDT, N CAPLAN, D SOKOL, S TORREANO, L AF HILDEBRANDT, N CAPLAN, D SOKOL, S TORREANO, L TI LEXICAL FACTORS IN THE WORD-SUPERIORITY EFFECT SO MEMORY & COGNITION LA English DT Article ID LETTER IDENTIFICATION; RECOGNITION; PERCEPTION; MODEL AB In the Reicher-Wheeler paradigm, fluent readers can identify letters better when they appear in a word than when they appear in either a pronounceable pseudoword (a lexicality effect) or a single letter (a word-letter effect). It was predicted that if both of these effects involve a lexical factor, then adult acquired dyslexic subjects whose deficit prevents access to visual word form should show disruptions of the normal effects on the Reicher-Wheeler task. The results were that dyslexic subjects as well as matched control subjects showed a lexicality effect; however, while the control subjects showed a normal word-letter effect, the dyslexic subjects showed a reverse letter-superiority effect. Both effects, however, showed a systematic variation: As performance on lexical decision improved, the subjects' performance on words in the Reicher-Wheeler task was better than that for all the other conditions. These subject correlations were replicated by using data from a second lexical decision experiment, which utilized the same words and pseudowords that were used in the Reicher-Wheeler task. In addition, an item analysis showed that the words that the subjects had discriminated correctly in lexical decision showed a significant advantage over those that they had not, as well as an improvement relative to the other conditions. These results suggest that there is a lexical factor underlying the lexicality and word-letter effects, and it is proposed that the abnormal letter-superiority effect can be accounted for as the manifestation of other competing factors. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HILDEBRANDT, N (reprint author), MASSACHUSETTS GEN HOSP,NEUROPSYCHOL LAB,VBK 827,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC00462] NR 30 TC 8 Z9 9 U1 1 U2 4 PU PSYCHONOMIC SOC INC PI AUSTIN PA 1710 FORTVIEW RD, AUSTIN, TX 78704 SN 0090-502X J9 MEM COGNITION JI Mem. Cogn. PD JAN PY 1995 VL 23 IS 1 BP 23 EP 33 DI 10.3758/BF03210554 PG 11 WC Psychology, Experimental SC Psychology GA QD504 UT WOS:A1995QD50400003 PM 7885263 ER PT J AU KREUZ, RJ DEWS, S AF KREUZ, RJ DEWS, S TI SPECIAL ISSUE - NONLITERAL LANGUAGE - PROCESSING AND USE SO METAPHOR AND SYMBOLIC ACTIVITY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA. RP KREUZ, RJ (reprint author), MEMPHIS STATE UNIV,DEPT PSYCHOL,MEMPHIS,TN 38152, USA. NR 0 TC 1 Z9 1 U1 1 U2 1 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0885-7253 J9 METAPHOR SYMB ACT JI Metaphor Symb. Act. PY 1995 VL 10 IS 1 BP 1 EP 2 DI 10.1207/s15327868ms1001_1 PG 2 WC Language & Linguistics; Psychology, Experimental SC Linguistics; Psychology GA QU408 UT WOS:A1995QU40800001 ER PT J AU DEWS, S WINNER, E AF DEWS, S WINNER, E TI MUTING THE MEANING - A SOCIAL FUNCTION OF IRONY SO METAPHOR AND SYMBOLIC ACTIVITY LA English DT Article ID METAPHOR COMPREHENSION; INDIRECT REQUESTS; LANGUAGE; IDIOMS AB According to the tinge hypothesis, the evaluative tone of the literal meaning of ironic utterances automatically colors the hearer's perception of the intended meaning. In Experiment 1, participants read short stories that end with either a literal or an ironic insult. Ironic insults are rated as less critical than literal insults, and the ironic speaker is rated as less annoyed than the literal speaker. In addition, the speaker-target relationship is affected less negatively when the insult is delivered ironically rather than literally. These results are obtained regardless of whether the addressee or a third person is the target of the remark and regardless of whether the story characters know one another or have just met. In Experiment 2, participants read similar short stories that end with either a literal or ironic compliment. Results mirror those of Experiment 1. Ironic compliments are rated as less praising than literal compliments, and the ironic speaker is rated as less pleased than the literal speaker. The speaker-target relationship is affected less positively when the compliment is ironic than when it is literal. As in Experiment 1, these results are obtained regardless of addressee or familiarity of the story characters. The results from these two experiments support the tinge hypothesis by demonstrating that irony mutes the criticism or praise conveyed by literal language. C1 BOSTON COLL,DEPT PSYCHOL,BOSTON,MA. HARVARD PROJECT ZERO,CAMBRIDGE,MA. RP DEWS, S (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 22 TC 103 Z9 104 U1 0 U2 15 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0885-7253 J9 METAPHOR SYMB ACT JI Metaphor Symb. Act. PY 1995 VL 10 IS 1 BP 3 EP 19 DI 10.1207/s15327868ms1001_2 PG 17 WC Language & Linguistics; Psychology, Experimental SC Linguistics; Psychology GA QU408 UT WOS:A1995QU40800002 ER PT J AU Lewis, JA Fleming, JT AF Lewis, JA Fleming, JT TI Basic culture methods SO METHODS IN CELL BIOLOGY, VOL 48 SE METHODS IN CELL BIOLOGY LA English DT Review ID NEMATODE CAENORHABDITIS-ELEGANS; PHENOTYPIC CHARACTERIZATION; MUTANTS; MYOSINS; TEMPERATURE; CUTICLE; PROTEIN; MUSCLE; DNA C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT HEMATOL ONCOL,BOSTON,MA 02114. RP Lewis, JA (reprint author), UNIV TEXAS,DIV LIFE SCI,SAN ANTONIO,TX 78249, USA. FU NIGMS NIH HHS [GM-08194] NR 35 TC 288 Z9 295 U1 2 U2 10 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0091-679X J9 METHOD CELL BIOL PY 1995 VL 48 BP 3 EP 29 PG 27 WC Biochemical Research Methods; Cell Biology; Developmental Biology SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology GA BE40R UT WOS:A1995BE40R00001 PM 8531730 ER PT J AU Sheen, J AF Sheen, J TI Methods for mesophyll and bundle sheath cell separation SO METHODS IN CELL BIOLOGY, VOL 49 SE METHODS IN CELL BIOLOGY LA English DT Review ID GREENING MAIZE LEAVES; DIFFERENTIAL EXPRESSION; C-4 PHOTOSYNTHESIS; GENE-EXPRESSION; PHOSPHOENOLPYRUVATE CARBOXYLASE; PHOTOSYSTEM-II; LEAF MESOPHYLL; C4 PLANTS; ZEA-MAYS; CHLOROPLASTS C1 MASSACHUSETTS GEN HOSP,DEPT BIOL MOLEC,BOSTON,MA 02114. RP Sheen, J (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114, USA. NR 25 TC 17 Z9 18 U1 2 U2 9 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0091-679X J9 METHOD CELL BIOL PY 1995 VL 49 BP 305 EP 314 DI 10.1016/S0091-679X(08)61462-4 PG 10 WC Biochemical Research Methods; Plant Sciences; Cell Biology SC Biochemistry & Molecular Biology; Plant Sciences; Cell Biology GA BE40S UT WOS:A1995BE40S00021 PM 8531764 ER PT J AU Reuber, TL Ausubel, FM AF Reuber, TL Ausubel, FM TI Differential mRNA display SO METHODS IN CELL BIOLOGY, VOL 49 SE METHODS IN CELL BIOLOGY LA English DT Review ID MESSENGER-RNA RP Reuber, TL (reprint author), MASSACHUSETTS GEN HOSP,DEPT BIOL MOLEC,BOSTON,MA 02114, USA. NR 4 TC 7 Z9 7 U1 0 U2 5 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0091-679X J9 METHOD CELL BIOL PY 1995 VL 49 BP 431 EP 440 DI 10.1016/S0091-679X(08)61471-5 PG 10 WC Biochemical Research Methods; Plant Sciences; Cell Biology SC Biochemistry & Molecular Biology; Plant Sciences; Cell Biology GA BE40S UT WOS:A1995BE40S00030 PM 8531774 ER PT J AU Galbraith, DW Lambert, GM Grebenok, RJ Sheen, J AF Galbraith, DW Lambert, GM Grebenok, RJ Sheen, J TI Flow cytometric analysis of transgene expression in higher plants: Green-fluorescent protein SO METHODS IN CELL BIOLOGY, VOL 50 SE METHODS IN CELL BIOLOGY LA English DT Review C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP Galbraith, DW (reprint author), UNIV ARIZONA,DEPT PLANT SCI,TUCSON,AZ 85721, USA. NR 19 TC 32 Z9 32 U1 2 U2 7 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0091-679X J9 METHOD CELL BIOL PY 1995 VL 50 BP 3 EP 14 DI 10.1016/S0091-679X(08)61018-3 PG 12 WC Biochemical Research Methods; Plant Sciences; Cell Biology SC Biochemistry & Molecular Biology; Plant Sciences; Cell Biology GA BE40T UT WOS:A1995BE40T00001 PM 8531802 ER PT J AU STOECKLE, JD AF STOECKLE, JD TI THE CITADEL CANNOT HOLD - TECHNOLOGIES GO OUTSIDE THE HOSPITAL, PATIENTS AND DOCTORS TOO SO MILBANK QUARTERLY LA English DT Article AB Use of the acute hospital has markedly decreased over the past four decades for various reasons: the decentralization of diagnostic treatment technologies to out-of-hospital sites; the clinical substitutions of quick diagnostic testing of the ambulatory patient for the longer diagnostic testing of the hospitalized patient; the diminished use of hospital bed rest and the expanded use of exercise for treatment; the corporate organization of hospital work that emphasizes efficiency; and the group practice organization of generalists and specialists that avoids hospital use for the diagnosis of complex disorders in ambulatory patients. A smaller domain for hospital bed care and renewed attention to chronic disease and prevention in the community diminish the hold of the acute hospital on care. The evolution of more collaborative, decentralized arrangements promises to be a positive development for community care. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP STOECKLE, JD (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,PRIMARY CARE PROGRAM,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 44 TC 12 Z9 13 U1 0 U2 1 PU BLACKWELL PUBLISHERS PI CAMBRIDGE PA 238 MAIN STREET, CAMBRIDGE, MA 02142 SN 0887-378X J9 MILBANK Q JI Milbank Q. PY 1995 VL 73 IS 1 BP 3 EP 17 DI 10.2307/3350311 PG 15 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA QN030 UT WOS:A1995QN03000001 PM 7898407 ER PT J AU POTTS, JT AF POTTS, JT TI NONTRADITIONAL ACTIONS OF PARATHYROID-HORMONE - AN OVERVIEW SO MINERAL AND ELECTROLYTE METABOLISM LA English DT Article; Proceedings Paper CT 3rd International Conference on New Actions of Parathyroid Hormone CY APR 18-21, 1994 CL KYOTO, JAPAN DE HORMONE ACTION; PTH; PTH RECEPTOR; PTHRP; PTH/PTHRP RECEPTOR STRUCTURE ID RECEPTOR; EXPRESSION; CLONING; PEPTIDE C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP POTTS, JT (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,FRUIT ST,BOSTON,MA 02114, USA. NR 12 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-0392 J9 MINER ELECTROL METAB JI Miner. Electrolyte Metab. PD JAN-JUN PY 1995 VL 21 IS 1-3 BP 9 EP 12 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA RG689 UT WOS:A1995RG68900002 PM 7565471 ER PT J AU LEE, KC DEEDS, JD CHIBA, S SEGRE, GV AF LEE, KC DEEDS, JD CHIBA, S SEGRE, GV TI PARATHYROID-HORMONE INDUCES SEQUENTIAL C-FOS EXPRESSION IN BONE-CELLS IN-VIVO - A MODEL FOR INTERCELLULAR COMMUNICATION IN BONE SO MINERAL AND ELECTROLYTE METABOLISM LA English DT Article; Proceedings Paper CT 3rd International Conference on New Actions of Parathyroid Hormone CY APR 18-21, 1994 CL KYOTO, JAPAN DE CELL-CELL COMMUNICATION; C-FOS; IN SITU HYBRIDIZATION; PARATHYROID HORMONE ID MESSENGER-RNA RP LEE, KC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ENDOCRINE UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK11794, DK47237] NR 4 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-0392 J9 MINER ELECTROL METAB JI Miner. Electrolyte Metab. PD JAN-JUN PY 1995 VL 21 IS 1-3 BP 120 EP 122 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA RG689 UT WOS:A1995RG68900022 PM 7565431 ER PT J AU SEGRE, GV DEEDS, JD LEE, KC AF SEGRE, GV DEEDS, JD LEE, KC TI EXPRESSION OF PARATHYROID HORMONE-RELATED PEPTIDE AND ITS RECEPTOR MESSENGER-RNAS DURING FETAL DEVELOPMENT OF RATS SO MINERAL AND ELECTROLYTE METABOLISM LA English DT Article; Proceedings Paper CT 3rd International Conference on New Actions of Parathyroid Hormone CY APR 18-21, 1994 CL KYOTO, JAPAN DE FETAL DEVELOPMENT; PARATHYROID HORMONE (PTH)-RELATED PEPTIDE; PTH/PTHR RECEPTORS ID HYPERCALCEMIA; CLONING RP SEGRE, GV (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ENDOCRINE UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK47237, DK11794] NR 9 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-0392 J9 MINER ELECTROL METAB JI Miner. Electrolyte Metab. PD JAN-JUN PY 1995 VL 21 IS 1-3 BP 129 EP 132 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA RG689 UT WOS:A1995RG68900024 PM 7565433 ER PT J AU KRONENBERG, HM AF KRONENBERG, HM TI DISRUPTION OF THE PARATHYROID HORMONE-RELATED PEPTIDE GENE SO MINERAL AND ELECTROLYTE METABOLISM LA English DT Article; Proceedings Paper CT 3rd International Conference on New Actions of Parathyroid Hormone CY APR 18-21, 1994 CL KYOTO, JAPAN DE BONE DEVELOPMENT; GROWTH PLATE CARTILAGE; PARATHYROID HORMONE RELATED PEPTIDE ID EMBRYONIC CHICK; GROWTH; EXPRESSION; RAT C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP KRONENBERG, HM (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,WELLMAN 5,BOSTON,MA 02114, USA. NR 7 TC 2 Z9 2 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-0392 J9 MINER ELECTROL METAB JI Miner. Electrolyte Metab. PD JAN-JUN PY 1995 VL 21 IS 1-3 BP 140 EP 142 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA RG689 UT WOS:A1995RG68900026 PM 7565436 ER PT J AU IIDAKLEIN, A GUO, J DRAKE, MT KRONENBERG, HM ABOUSAMRA, AB BRINGHURST, FR SEGRE, GV AF IIDAKLEIN, A GUO, J DRAKE, MT KRONENBERG, HM ABOUSAMRA, AB BRINGHURST, FR SEGRE, GV TI STRUCTURAL REQUIREMENTS OF PARATHYROID-HORMONE PARATHYROID HORMONE-RELATED PEPTIDE RECEPTORS FOR PHOSPHOLIPASE-C ACTIVATION AND REGULATION OF PHOSPHATE-UPTAKE SO MINERAL AND ELECTROLYTE METABOLISM LA English DT Article; Proceedings Paper CT 3rd International Conference on New Actions of Parathyroid Hormone CY APR 18-21, 1994 CL KYOTO, JAPAN DE ADENYLYL CYCLASE; CT PROTEINS; PHOSPHOLIPASE C; PI UPTAKE; PTH/PTHRP RECEPTOR ID EXPRESSION CLONING; MOLECULAR-CLONING; POLYPEPTIDE RP IIDAKLEIN, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ENDOCRINE UNIT,BLOSSOM ST,BOSTON,MA 02114, USA. OI Abou-Samra, Abdul/0000-0001-8735-1142 NR 16 TC 8 Z9 8 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-0392 J9 MINER ELECTROL METAB JI Miner. Electrolyte Metab. PD JAN-JUN PY 1995 VL 21 IS 1-3 BP 177 EP 179 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA RG689 UT WOS:A1995RG68900034 PM 7565444 ER PT J AU Reers, M Smiley, ST MottolaHartshorn, C Chen, A Lin, M Chen, LB AF Reers, M Smiley, ST MottolaHartshorn, C Chen, A Lin, M Chen, LB TI Mitochondrial membrane potential monitored by JC-1 dye SO MITOCHONDRIAL BIOGENESIS AND GENETICS, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID LIVING CELLS; AGBR SURFACES; RHODAMINE-123; CARBOCYANINE; EQUILIBRIA; CYANINES RP Reers, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 24 TC 400 Z9 410 U1 6 U2 37 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 260 BP 406 EP 417 DI 10.1016/0076-6879(95)60154-6 PG 16 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA BE40M UT WOS:A1995BE40M00029 PM 8592463 ER PT S AU Kazemi, H Burton, MD AF Kazemi, H Burton, MD BE Semple, SJG Adams, L Whipp, BJ TI Role of acetylcholine as an essential neurotransmitter in central respiratory drive SO MODELING AND CONTROL OF VENTILATION SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT London Conference on Modeling and Control of Ventilation (LCMCV) CY SEP 17-20, 1994 CL EGHAM, ENGLAND ID VENTILATION; ACID RP Kazemi, H (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. NR 12 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45180-8 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 393 BP 29 EP 32 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA BE85H UT WOS:A1995BE85H00006 PM 8629499 ER PT J AU KOMINATO, Y GALSON, DL WATERMAN, WR WEBB, AC AURON, PE AF KOMINATO, Y GALSON, DL WATERMAN, WR WEBB, AC AURON, PE TI MONOCYTE EXPRESSION OF THE HUMAN PROINTERLEUKIN 1-BETA GENE (IL1B) IS DEPENDENT ON PROMOTER SEQUENCES WHICH BIND THE HEMATOPOIETIC TRANSCRIPTION FACTOR SPI-1/PU.1 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HUMAN INTERLEUKIN-1-BETA GENE; PU.1 REGULATES EXPRESSION; ACTIVATION DOMAIN; ENHANCER ACTIVITY; NUCLEAR FACTOR; DNA-SEQUENCE; C-FOS; SITE; PROTEIN; PROTOONCOGENE AB Interleukin-1 beta (IL-1 beta) is produced primarily by stimulated monocytes, suggesting that the IL1B gene, which codes for this protein, depends upon at least one cell-type-specific factor. Our previous characterization of the IL1B promoter indicated that the region between -131 and +12 is sufficient to direct cell-type-specific expression of a reporter gene (F. Shirakawa, K. Saito, C. A. Bonagura, D. L. Galson, M. J. Fenton, A. C. Webb, and P. E. Auron, Mel. Cell. Biol. 13:1332-1344, 1993). We now show that a sequence located between positions -50 and -39 of the IL1B promoter binds the tissue-restricted Ets domain transcription factor Spi-1/PU.1 (Spi-1). Mutation of this site abrogates binding of this factor and reduces the ability of the IL1B promoter to function in macrophages. A second Spi-1 binding site located between positions -115 and -97 also is required for maximal IL1B promoter activity in the presence of the proximal Spi-1 binding site. In addition, an activation domain-deficient Spi-1 expression vector acts as a dominant-negative inhibitor of reporter gene expression in a monocyte cell line. Finally, the IL1B promoter, which is inactive in Spi-1-deficient HeLa cells, is activated in these cells by cotransfection with a Spi-1 expression vector. Thus, the cell-type-specific expression of the IL1B promoter appears to be dependent on the binding of Spi-1. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. WELLESLEY COLL,DEPT BIOL SCI,WELLESLEY,MA 02181. RI Galson, Deborah/E-9370-2010 OI Galson, Deborah/0000-0002-2045-8807 FU NIAID NIH HHS [R01 AI27850] NR 40 TC 64 Z9 64 U1 0 U2 6 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 JAN PY 1995 VL 15 IS 1 BP 58 EP 68 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PX953 UT WOS:A1995PX95300008 PM 7799967 ER PT J AU FRETER, RR ALBERTA, JA LAM, KK STILES, CD AF FRETER, RR ALBERTA, JA LAM, KK STILES, CD TI A NEW PLATELET-DERIVED GROWTH FACTOR-REGULATED GENOMIC ELEMENT WHICH BINDS A SERINE THREONINE PHOSPHOPROTEIN MEDIATES INDUCTION OF THE SLOW IMMEDIATE-EARLY GENE MCP-1 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SERUM RESPONSE ELEMENT; C-FOS PROMOTER; MULTIPLE SEQUENCE ELEMENTS; FACTOR-INDUCIBLE GENE; TRANSCRIPTION FACTOR; 3T3 CELLS; PROTO-ONCOGENE; CYCLIC-AMP; IDENTIFICATION; RNA AB The MCP-1 chemokine gene belongs to a cohort of immediate-early genes that are induced with slower kinetics than c-fos. In this study, we identified a cluster of four platelet-derived growth factor (PDGF)-responsive elements within a 240-bp enhancer found in the distal 5' flanking MCP-1 sequences. Two of the elements bind one or more forms of the transcription factor NF-kappa B. We focused on the other two elements which are hitherto unreported, PDGF-regulated genomic motifs. One of these novel elements, detected as a 28-mer by DNase I footprinting, restores PDGF inducibility when added in two copies to a 5' truncated MCP-1 gene. A single copy of the second novel element, a 27-mer, restores PDGF inducibility to a 5' truncated MCP-1 gene. The 27-base element interacts with a PDGP-activated serine/threonine phosphoprotein that is detected only within the nucleus of PDGF-treated 3T3 cells. DNA binding of this phosphoprotein is activated by PDGF treatment with slow kinetics that match the time course of MCP-1 gene expression, and activation is not inhibited by cycloheximide. PDGP-activated binding to the 27-mer is shown to involve a single 30-kDa protein by UV-cross-linking analysis. C1 HARVARD UNIV,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,DIV CLIN ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. FU NCI NIH HHS [CA22042]; NIGMS NIH HHS [5 F32 GM14091] NR 52 TC 35 Z9 35 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 JAN PY 1995 VL 15 IS 1 BP 315 EP 325 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PX953 UT WOS:A1995PX95300036 PM 7799939 ER PT J AU TONTONOZ, P HU, ED DEVINE, J BEALE, EG SPIEGELMAN, BM AF TONTONOZ, P HU, ED DEVINE, J BEALE, EG SPIEGELMAN, BM TI PPAR-GAMMA-2 REGULATES ADIPOSE EXPRESSION OF THE PHOSPHOENOLPYRUVATE CARBOXYKINASE GENE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ENHANCER-BINDING-PROTEIN; HORMONE RECEPTOR SUPERFAMILY; ACID RESPONSE ELEMENT; RETINOIC ACID; TRANSGENIC MICE; ADIPOCYTE DIFFERENTIATION; THYROID-HORMONE; 3T3 CELLS; TRANSCRIPTION; IDENTIFICATION AB Phosphoenolpyruvate carboxykinase (PEPCK) is expressed at high levels in liver, kidney, acid adipose tissue. This enzyme catalyzes the rate-limiting step in hepatic and renal gluconeogenesis and adipose glyceroneogenesis. The regulatory factors important for adipose expression of the PEPCK gene are not well defined. Previous studies with transgenic mice established that the region between bp -2086 and -888 is required for expression in adipose tissue but not for expression in liver or kidney tissue. We show here that a DNA fragment containing this region can function as an enhancer and direct differentiation-dependent expression of a chloramphenicol acetyltransferase gene from a heterologous promoter in cultured 3T3-F442A preadipocytes and adipocytes. We further demonstrate that the adipocyte-specific transcription factor PPAR gamma 2, previously identified as a regulater of the adipocyte P2 enhancer, binds in a heterodimeric complex with RXR alpha to the PEPCK 5'-flanking region at two sites, termed PCK1 (bp -451 to -439) and PCK2 (bp -999 to -987). Forced expression of PPAR gamma 2 and RXR alpha activates the PEPCK enhancer in non-adipose cells. This activation is potentiated by peroxisome proliferators and fatty acids but not by 9-cis retinoic acid. Mutation of the PPAR gamma 2 binding site (PCK2) abolishes both the activity of the enhancer in adipocytes and its ability to be activated by PPAR gamma 2 and RXR alpha. These results establish a role for PPAR gamma 2 in the adipose expression of the PEPCK gene and suggest that this factor functions as a coordinate regulator of multiple adipocyte-specific genes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. TEXAS TECH UNIV,SCH MED,DEPT BIOCHEM & CELL BIOL,LUBBOCK,TX 79430. OI Beale, Elmus/0000-0002-7758-0600 FU NICHD NIH HHS [T32 HD07271]; NIDDK NIH HHS [DK31405]; NIGMS NIH HHS [T32 GM007753, T32 GM07753] NR 44 TC 450 Z9 464 U1 3 U2 10 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 JAN PY 1995 VL 15 IS 1 BP 351 EP 357 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PX953 UT WOS:A1995PX95300040 PM 7799943 ER PT J AU VALLEJO, M GOSSE, ME BECKMAN, W HABENER, JF AF VALLEJO, M GOSSE, ME BECKMAN, W HABENER, JF TI IMPAIRED CYCLIC-AMP-DEPENDENT PHOSPHORYLATION RENDERS CREB A REPRESSOR OF C/EBP-INDUCED TRANSCRIPTION OF THE SOMATOSTATIN GENE IN AN INSULINOMA CELL-LINE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ELEMENT-BINDING-PROTEIN; CAMP RESPONSE ELEMENT; PANCREATIC-ISLET CELLS; PHOSPHOENOLPYRUVATE CARBOXYKINASE GTP; CATALYTIC SUBUNIT; KINASE-A; STIMULATED TRANSCRIPTION; REGULATORY SUBUNIT; NUCLEAR-PROTEIN; LEUCINE ZIPPER AB Transcription factor CREB regulates cyclic AMP (cAMP)-dependent gene expression by binding to and activating transcription from cAMP response elements (CREs) in the promoters of target genes. The transcriptional transactivation functions of CREB are activated by its phosphorylation by cAMP-dependent protein kinase A (PKA). In studies of many different phenotypically distinct cells, the CRE of the somatostatin gene promoter is a prototype of a highly cAMP-responsive element regulated by CREB. We now report on a somatostatin-producing rat insulinoma cell line, RIN-1027-B2, in which transcription from the somatostatin gene promoter is paradoxically repressed by CREB. We find that CREB fails to transactivate a CRE-containing somatostatin-chloramphenicol acetyltransferase reporter even when coexpressed with the catalytic subunit of PKA. CAAT box/enhancer-binding protein beta (C/EBP beta) and C/EBP-related activating transcription factor bind to the CRE in the promoter of the somatostatin gene and transactivate transcription. CREB binds competitively with C/EBP beta to the somatostatin CRE in vitro and represses C/EBP beta-induced transcription of the CRE-containing somatostatin-chloramphenicol acetyltransferase reporter. The lack of CREB-mediated transcriptional stimulation is due to the presence of a heat-stable inhibitor of PKA that prevents activation of PKA and subsequent CREB phosphorylation in the nucleus. These findings indicate that dephosphorylated CREB is a negative regulator of C/EBP-activated transcription of the somatostatin gene promoter in RIN-1027-B2 cells. RP VALLEJO, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK30834, DK30457] NR 61 TC 32 Z9 34 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 JAN PY 1995 VL 15 IS 1 BP 415 EP 424 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PX953 UT WOS:A1995PX95300047 PM 7799950 ER PT J AU STEPP, JD PELLICENAPALLE, A HAMILTON, S KIRCHHAUSEN, T LEMMON, SK AF STEPP, JD PELLICENAPALLE, A HAMILTON, S KIRCHHAUSEN, T LEMMON, SK TI A LATE GOLGI SORTING FUNCTION FOR SACCHAROMYCES-CEREVISIAE APM1P, BUT NOT FOR APM2P, A 2ND YEAST CLATHRIN AP MEDIUM CHAIN-RELATED PROTEIN SO MOLECULAR BIOLOGY OF THE CELL LA English DT Article ID RECEPTOR-MEDIATED ENDOCYTOSIS; COATED VESICLE PROTEINS; FACTOR-II RECEPTOR; PLASMA-MEMBRANE; HEAVY-CHAIN; ASSEMBLY POLYPEPTIDES; SHUTTLE VECTORS; BETA-ADAPTIN; MONOCLONAL-ANTIBODIES; SECRETORY PATHWAY AB Mammalian clathrin-associated protein (AP) complexes, AP-1 (trans-Golgi network) and AP-2 (plasma membrane), are composed of two large subunits of 91-107 kDa, one medium chain (mu) of 47-50 kDa and one small chain (sigma) of 17-19 kDa. Two veast genes, APM1 and APM2, have been identified that encode proteins related to AP mu chains. APM1, whose sequence was reported previously, codes for a protein of 54 kDa that has greatest similarity to the mammalian 47-kDa mu 1 chain of AP-1. APM2 encodes an AP medium chain-related protein of 605 amino acids (predicted molecular weight of 70 kDa) that is only 30-33% identical to the other family members. In yeast containing a normal clathrin heavy chain gene (CHC1), disruptions of the APM genes, singly or in combination, had no detectable phenotypic consequences. However, deletion of APM1 greatly enhanced the temperature-sensitive growth phenotype and the a-factor processing defect displayed by cells carrying a temperature-sensitive allele of the clathrin heavy chain gene. In contrast, deletion of APM2 caused no synthetic phenotypes with clathrin mutants. Biochemical analysis indicated that Apm1p and Apm2p are components of distinct high molecular weight complexes. Apm1p, Apm2p, and clathrin cofractionated in a discrete reside population, and the association of Apm1p with the vesicles was disrupted in CHC1 deletion strains. These results suggest that Apm1p is a component of an AP-1-like complex that participates with clathrin in sorting at the trans-Golgi in yeast. We propose that,Apm2p represents a new class of AP-medium chain-related proteins that may be involved in a nonclathrin-mediated vesicular transport process in eukaryotic cells. C1 CASE WESTERN RESERVE UNIV, SCH MED, DEPT MOLEC BIOL & MICROBIOL, CLEVELAND, OH 44106 USA. HARVARD UNIV, SCH MED, CTR BLOOD RES, BOSTON, MA 02115 USA. FU NIA NIH HHS [AG-00105] NR 87 TC 72 Z9 74 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA SN 1059-1524 EI 1939-4586 J9 MOL BIOL CELL JI Mol. Biol. Cell PD JAN PY 1995 VL 6 IS 1 BP 41 EP 58 PG 18 WC Cell Biology SC Cell Biology GA QT650 UT WOS:A1995QT65000004 PM 7749194 ER PT J AU ROTENBERG, SA HUANG, MH ZHU, JW SU, LH RIEDEL, H AF ROTENBERG, SA HUANG, MH ZHU, JW SU, LH RIEDEL, H TI DELETION ANALYSIS OF PROTEIN-KINASE-C INACTIVATION BY CALPHOSTIN-C SO MOLECULAR CARCINOGENESIS LA English DT Article DE INHIBITION; MUTANT PROTEINS; PKC ISOFORMS ID REGULATORY DOMAIN; EXPRESSION; CONTAINS; CALCIUM; YEAST; INHIBITION; SEQUENCE; ZINC AB Protein kinase C (PKC) undergoes specific inactivation by nanomolar concentrations of calphostin C. Both PKC-alpha (a Ca2+-dependent conventional isoform) and PKC-epsilon (a Ca2+-independent novel isoform) are similarly inactivated by calphostin C (75-100 nM produced 50% inhibition), suggesting that inactivation requires a site common to both classes of PKC. We therefore performed studies to identify a critical region in the regulatory domain of PKC-alpha required for inactivation by calphostin C. A series of N-terminal-truncation mutants of bovine PKC-alpha expressed in Saccharomyces cerevisiae was tested with 500 nM calphostin C, a concentration sufficient to inactivate wild-type PKC-alpha by 80-90%. This concentration was as effective with mutant proteins containing deletions of up to 91 amino acid (aa) residues from the amino terminus (ND91), whereas a mutant protein truncated by 140 aa (ND140) was inactivated by only 20%. These findings imply that the aa sequence 92-140 is a structural determinant of PKC-alpha inactivation by calphostin C. This sequence contains one of the phorbol ester-binding sites (aa 102-144), which is highly conserved among most PKC isoforms including PKC-epsilon. In addition to aa 92-140, PKC-stimulating cofactors (phosphatidylserine, phorbol ester, and Ca2+) are required for inactivation by calphostin C even in the case of PKC muta nts that do not require these cofactors for enzymatic activity. These results suggest that cofactors provide a template that is required for productive interaction of PKC and the inhibitor. The significance of the proposed proximity effect to calphostin C action is discussed. (C) 1995 Wiley-Liss, Inc. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,MOLEC BIOL SECT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ROTENBERG, SA (reprint author), CUNY QUEENS COLL,DEPT CHEM & BIOCHEM,65-30 KISSENA BLVD,FLUSHING,NY 11367, USA. NR 35 TC 45 Z9 45 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD JAN PY 1995 VL 12 IS 1 BP 42 EP 49 DI 10.1002/mc.2940120107 PG 8 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA QQ422 UT WOS:A1995QQ42200006 PM 7529505 ER PT J AU MAINS, RE MILGRAM, SL KEUTMANN, HT EIPPER, BA AF MAINS, RE MILGRAM, SL KEUTMANN, HT EIPPER, BA TI THE NH2-TERMINAL PROREGION OF PEPTIDYLGLYCINE ALPHA-AMIDATING MONOOXYGENASE FACILITATES THE SECRETION OF SOLUBLE-PROTEINS SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID MICROINJECTED XENOPUS OOCYTES; PROHORMONE CONVERTASES PC1; ENDOPLASMIC-RETICULUM; INTRACELLULAR-TRANSPORT; CARBOXYPEPTIDASE-E; SUBTILISIN FAMILY; PROCESSING ENZYME; TERMINAL DOMAIN; HUMAN PRORENIN; CELLS AB A highly conserved ten amino acid proregion separates the peptidylglycine alpha-hydroxylating monooxygenase (PHM) domain of the bifunctional peptidylglycine alpha-amidating monooxygenase (PAM) protein from the NH2-terminal signal peptide; propeptides with amino acid sequences similar to the PAM proregion have been identified in other secreted proteins, In AtT-20 cells, but not in human embryonic kidney (hEK)-293 cells, an endogenous endoprotease acting at a site distal to the trans-Golgi network efficiently removes the propeptide from stably transfected monofunctional PHM (PHMs). We constructed a mutant PHM protein (Delta ProPHMs) in which the proregion was deleted and the signal peptide joined directly to the monooxygenase domain. Newly synthesized, enzymatically active Delta ProPHMs was secreted from both AtT-20 cells and hEK-293 cells more slowly than PHMs, In endocrine cells, the proregion was not required for storage in regulated secretory granules. We transferred the PAM proregion to prohormone convertase 2 (PC2), another soluble constituent of secretory granules, to determine whether the effect of the proregion were transferrable. In both AtT-20 cells and hEK-293 cells, the PAM/PC2 fusion molecule was able to exit the endoplasmic reticulum more rapidly than PC2. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,BALTIMORE,MD 21205. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. RP MAINS, RE (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,725 N WOLFE ST,BALTIMORE,MD 21205, USA. FU NIDDK NIH HHS [DK-32948]; NIGMS NIH HHS [GM-15293] NR 78 TC 20 Z9 20 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD JAN PY 1995 VL 9 IS 1 BP 3 EP 13 DI 10.1210/me.9.1.3 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QF725 UT WOS:A1995QF72500001 PM 7760848 ER PT J AU SEOL, WG CHOI, HS MOORE, DD AF SEOL, WG CHOI, HS MOORE, DD TI ISOLATION OF PROTEINS THAT INTERACT SPECIFICALLY WITH THE RETINOID-X RECEPTOR - 2 NOVEL ORPHAN RECEPTORS SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID THYROID-HORMONE RECEPTOR; NUCLEAR RECEPTOR; TRANSCRIPTIONAL ACTIVATION; HOMODIMER FORMATION; RESPONSE ELEMENT; ACID RECEPTORS; BINDING DOMAIN; DIRECT REPEAT; RXR; GENE AB We have used a yeast genetic system to isolate cDNAs encoding proteins that specifically interact with the ligand-binding domain of human retinoid X receptor-alpha (RXR alpha). A number encoded portions of two known RXR heterodimer partners, the retinoic acid receptor (RAR) and the peroxisome proliferator activated receptor. Of four additional RXR-interacting proteins (Rips) selected for further study two, RIP14 and RIP15, are previously unidentified orphan members of the nuclear receptor superfamily. Two others, RIP110 and RIP13, do not show significant similarities to previously reported proteins. RIP110 interacts with LexA-RXR only in yeast cells grown in the presence of the RXR ligand 9-cis-RA, while the interaction of the four receptor superfamily members and RIP13 is unaffected by the presence or absence of 9-cis-RA. RIP110 and RIP13 also interact in yeast with several other members of the receptor superfamily, but RIP14 and RIP15 interact only with RXR. Analysis of larger cDNA clones demonstrates that there are at least two isoforms of RIP14 that differ in the N-terminal (A and B) and hinge (D) domains. Northern blot analysis indicates that RIP14 is expressed specifically in liver and kidney, while RIP15 is expressed in every tissue tested. Both RIP14 and 15 bind as heterodimers with RXR to the RA response element (RARE) from the promoter of the RAR beta 2 isoform (the beta RARE), and RIP14 and RXR heterodimers also bind the ecdysone response element from the Drosophila heat shock protein 27 promoter. Both heterodimers also bind to several synthetic RAREs and other elements. In cotransfections, neither RIP14 nor RIP15 trans-activates a reporter containing multiple copies of the beta RARE under any of a variety of conditions, suggesting that their activities are dependent on the binding of as yet unidentified specific ligands or on activation by other processes. C1 MASSACHUSETTS GEN HOSP, DEPT MOLEC BIOL, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK-43382] NR 47 TC 267 Z9 277 U1 0 U2 9 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD JAN PY 1995 VL 9 IS 1 BP 72 EP 85 DI 10.1210/me.9.1.72 PG 14 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QF725 UT WOS:A1995QF72500008 PM 7760852 ER PT J AU CHEN, ZH SAGER, R AF CHEN, ZH SAGER, R TI DIFFERENTIAL EXPRESSION OF HUMAN TISSUE FACTOR IN NORMAL MAMMARY EPITHELIAL-CELLS AND IN CARCINOMAS SO MOLECULAR MEDICINE LA English DT Article ID ENDOTHELIAL-CELLS; MESSENGER-RNA; GROWTH; GENE; HEMOSTASIS; INDUCTION; MONOCYTES; DISPLAY; IDENTIFICATION; PROCOAGULANT AB Background: Tissue factor (TF) is a glycoprotein which binds factor VIIa. The TF-VIIa complex serves as a potent initiator of the coagulation pathways. TF, an immediate early gene, may also play a role in cell growth. Expression of TF was correlated with some types of cancers. Materials and Methods: Normal, immortalized, and tumor human mammary epithelial cells were used in the experiments. The differential display (DD) technique was used to identify genes differentially expressed in the cells. TF expression patterns were examined by Northern blot analysis, immunofluorescence staining of cultured cells, and immunohistochemical staining in human cryostat sections. Results: In a 5-way display, an amplified polymerase chain reaction (PCR) product was found in normal and immortalized human mammary epithelial cells but not in the breast cancer cells. The PCR fragment was cloned and sequenced. The result showed that the fragment was identical to human tissue factor. Northern blot analysis showed that expression level of tissue factor mRNA remained high in growing, quiescent, and senescent normal mammary epithelial cells. Immunofluorescence staining also confirmed tissue factor expression pattern in the cell lines tested. Immunohistochemical staining showed that tissue factor was expressed in the normal luminal and myoepithelial cells of some ducts but not others. No staining was observed in invasive carcinoma cells. However, myo epithelial cell staining was seen in some residual ductal structures in invasive tumors. Conclusions: This study shows the use of DD to reveal the loss of TF expression pattern in human breast cancer cell lines. Immunohistochemical staining results showed breast carcinoma cells expressed little TF, if any, suggesting that TF is not required for breast tumor cell invasion. The results also indicated that TF expression was independent of the proliferation status of the expressing cells. The expression pattern of TF may be a meaningful marker in the development of breast cancer. C1 DANA FARBER CANC INST,DIV CANC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. NR 34 TC 26 Z9 26 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 1076-1551 J9 MOL MED JI Mol. Med. PD JAN PY 1995 VL 1 IS 2 BP 153 EP 160 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA QX599 UT WOS:A1995QX59900006 PM 8529094 ER PT J AU SHIMA, DT ADAMIS, AP FERRARA, N YEO, KT YEO, TK ALLENDE, R FOLKMAN, J DAMORE, PA AF SHIMA, DT ADAMIS, AP FERRARA, N YEO, KT YEO, TK ALLENDE, R FOLKMAN, J DAMORE, PA TI HYPOXIC INDUCTION OF ENDOTHELIAL-CELL GROWTH-FACTORS IN RETINAL CELLS - IDENTIFICATION AND CHARACTERIZATION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF) AS THE MITOGEN SO MOLECULAR MEDICINE LA English DT Article ID PIGMENT EPITHELIAL-CELLS; PERMEABILITY FACTOR; FACTOR FAMILY; ANGIOGENESIS FACTOR; GENE-EXPRESSION; TUMOR; BFGF; SECRETION; INVITRO; INVIVO AB Background: New vessel,growth is often associated with ischemia, and hypoxic tissue has been identified as a potential source of angiogenic factors. In particular, ischemia is associated with the development of neovascularization in a number of ocular pathologies. For this reason, we have studied the induction of endothelial cell mitogens by hypoxia in retinal cells. Materials and Methods: Human retinal pigment epithelium (hRPE) were grown under normoxic and hypoxic conditions and examined for the production of endothelial mitogens. Northern analysis, biosynthetic labeling and immunoprecipitation, and ELISA were used to assess the levels of vascular endothelial growth factor/vascular permeability factor (VEGF) and basic fibroblast growth factor (bFGF), two endothelial cell mitogens and potent angiogenic factors. Soluble receptors for VEGF were employed as competitive inhibitors to determine the contribution of the growth factor to the hypoxia-stimulated mitogen production. Results: Following 6-24 hr of hypoxia, confluent and growing cultures of hRPE increase their levels of VEGF mRNA and protein synthesis. Biosynthetic labeling studies and RT-PCR analysis indicate that the cells secrete VEGF(121) and VEGF(165), the soluble forms of the angiogenic factor. In contrast, hRPE cultured under hypoxic conditions show reduced steady-state levels of basic fibroblast growth factor (bFGF) mRNA and decreased bFGF protein synthesis. Unlike VEGF, bFGF is not found in conditioned media of hRPE following 24 hr of hypoxia. Using a soluble high-affinity VEGF receptor as a competitive inhibitor of VEGF, we demonstrate that a VEGF-like activity is the sole hypoxia-inducible endothelial mitogen produced by cultured hRPE. Conclusions: From this comparison we conclude that hRPE do not respond to hypoxia with a general, nonspecific increase in the overall levels of growth factors, as is seen during cell wounding responses or serum stimulation. The physiological relevance of data from this in vitro model are affirmed by separate studies in an animal model of retinal ischemia-induced ocular neovascularization (1) in which retina-derived VEGF levels have been shown to correlate spatio-temporally with the onset of angiogenesis. Taken together, these data support the hypothesis that the induction of VEGF by hypoxia mediates the rapid, initial angiogenic response to retinal ischemia. C1 CHILDRENS HOSP, DEPT SURG, SURG RES LAB, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, PROGRAM CELL & DEV BIOL, BOSTON, MA 02115 USA. MASSACHUSETTS EYE & EAR INFIRM, DEPT OPHTHALMOL, BOSTON, MA 02114 USA. GENENTECH INC, DEPT CARDIOVASC RES, S SAN FRANCISCO, CA 94080 USA. BETH ISRAEL HOSP, DEPT PATHOL, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, DEPT CELL BIOL, BOSTON, MA USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA45548]; NEI NIH HHS [EY00325, EY05985] NR 55 TC 235 Z9 244 U1 0 U2 2 PU FEINSTEIN INST MED RES PI MANHASSET PA 350 COMMUNITY DR, MANHASSET, NY 11030 USA SN 1076-1551 EI 1528-3658 J9 MOL MED JI Mol. Med. PD JAN PY 1995 VL 1 IS 2 BP 182 EP 193 PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA QX599 UT WOS:A1995QX59900009 PM 8529097 ER PT J AU WOOD, SC TONNER, PH DEARMENDI, AJ BUGGE, B MILLER, KW AF WOOD, SC TONNER, PH DEARMENDI, AJ BUGGE, B MILLER, KW TI CHANNEL INHIBITION BY ALKANOLS OCCURS AT A BINDING-SITE ON THE NICOTINIC ACETYLCHOLINE-RECEPTOR SO MOLECULAR PHARMACOLOGY LA English DT Article ID LIGAND-BINDING; POSTSYNAPTIC MEMBRANES; GENERAL-ANESTHESIA; ALPHA-SUBUNIT; TORPEDO; AGONIST; QUINACRINE; VESICLES; PROTEIN AB The mechanism by which normal alkanols longer than ethanol inhibit cation flux through the transient open state of the nicotinic acetylcholine receptor (nAcChoR) is unknown. They might act nonspecifically either by perturbing the lipid bilayer or by binding to many low affinity sites. Alternatively, they might act in a mutually exclusive manner at a well defined site on the protein. To address this problem, a rapid assay of agonist-induced Rb-86(+) efflux from nAcChoR-rich Torpedo membrane vesicles was used that enabled the anesthetic-induced inhibition to be measured on a millisecond time scale, under conditions where the concentration of all ligands was raised in tl msec, thereby avoiding complications due to desensitization. By measuring the inhibition constant of one agent as a function of the fixed concentration of a second agent, it is possible to distinguish between nonspecific action and mutually exclusive action. Our data are inconsistent with the hypothesis that 1-octanol and 1-heptanol act in a nonspecific manner, but they are consistent with the hypothesis that these two alkanols act in a mutually exclusive manner at a well defined site. The data suggest that the alkanols sterically compete for the site, but experimental limitations prevented a less plausible model, in which there is a strong negative allosteric interaction between separate octanol and heptanol sites, from being ruled out. Should the latter interaction occur, the data indicate that occupation of one alkanol site would decrease the affinity of the other by about 50-fold. The local anesthetic procaine is known to act in a mutually exclusive manner with the agonist self-inhibition site. We found that octanol and procaine acted at separate sites, which exhibited a negative heterotrophic interaction such that octanol reduced the affinity of procaine 6-fold. We conclude that octanol and heptanol inhibit cation flux through the channel of the nAcChoR by binding to a site (or a set of sites of equal affinity) whose location is distinct from, but allosterically coupled to, the agonist self-inhibition site. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. FU NIGMS NIH HHS [GM15904] NR 39 TC 46 Z9 47 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JAN PY 1995 VL 47 IS 1 BP 121 EP 130 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QE167 UT WOS:A1995QE16700015 PM 7530805 ER PT J AU TODRES, ID NOVISKI, N AF TODRES, ID NOVISKI, N TI FLEXIBLE FIBEROPTIC BRONCHOSCOPY - A PRACTICAL GUIDE TO EXAMINING INFANTS AND CHILDREN SO MOUNT SINAI JOURNAL OF MEDICINE LA English DT Article ID TOPICAL ANESTHESIA C1 HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PEDIAT INTENS CARE UNIT,BOSTON,MA 02115. RP TODRES, ID (reprint author), MASSACHUSETTS GEN HOSP,NEONATAL INTENS CARE UNIT,BOSTON,MA 02114, USA. NR 12 TC 2 Z9 2 U1 0 U2 0 PU MOUNT SINAI HOSPITAL PI NEW YORK PA BOX 1094 ONE GUSTAVE L LEVY PLACE ATTN: CIRCULATION ASST, NEW YORK, NY 10029-6574 SN 0027-2507 J9 MT SINAI J MED JI Mt. Sinai J. Med. PD JAN PY 1995 VL 62 IS 1 BP 36 EP 40 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA QK540 UT WOS:A1995QK54000007 PM 7739584 ER PT B AU Kitz, RJ AF Kitz, RJ BE Fukushima, K Ochiai, R TI Anticholinesterase agents: An odyssey SO MUSCLE RELAXANTS: PHYSIOLOGIC AND PHARMACOLOGIC ASPECTS LA English DT Proceedings Paper CT 5th International Neuromuscular Meeting CY NOV 17-20, 1994 CL TOKYO, JAPAN C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG PI TOKYO PA 37-3, HONGO 3-CHOME BONKYO-KU, TOKYO 113, JAPAN BN 4-431-70168-0 PY 1995 BP 330 EP 331 PG 2 WC Anesthesiology; Pharmacology & Pharmacy SC Anesthesiology; Pharmacology & Pharmacy GA BF38J UT WOS:A1995BF38J00048 ER PT B AU Yang, HS Goudsouzian, NG Martyn, JAJ AF Yang, HS Goudsouzian, NG Martyn, JAJ BE Fukushima, K Ochiai, R TI The sensitivity of the neonatal rat to mivacurium relative to mature rats SO MUSCLE RELAXANTS: PHYSIOLOGIC AND PHARMACOLOGIC ASPECTS LA English DT Proceedings Paper CT 5th International Neuromuscular Meeting CY NOV 17-20, 1994 CL TOKYO, JAPAN C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG PI TOKYO PA 37-3, HONGO 3-CHOME BONKYO-KU, TOKYO 113, JAPAN BN 4-431-70168-0 PY 1995 BP 390 EP 390 PG 1 WC Anesthesiology; Pharmacology & Pharmacy SC Anesthesiology; Pharmacology & Pharmacy GA BF38J UT WOS:A1995BF38J00091 ER PT J AU JACOB, HJ BROWN, DM BUNKER, RK DALY, MJ DZAU, VJ GOODMAN, A KOIKE, G KREN, V KURTZ, T LERNMARK, A LEVAN, G MAO, YP PETTERSSON, A PRAVENEC, M SIMON, JS SZPIRER, C SZPIRER, J TROLLIET, MR WINER, ES LANDER, ES AF JACOB, HJ BROWN, DM BUNKER, RK DALY, MJ DZAU, VJ GOODMAN, A KOIKE, G KREN, V KURTZ, T LERNMARK, A LEVAN, G MAO, YP PETTERSSON, A PRAVENEC, M SIMON, JS SZPIRER, C SZPIRER, J TROLLIET, MR WINER, ES LANDER, ES TI A GENETIC-LINKAGE MAP OF THE LABORATORY RAT, RATTUS-NORVEGICUS SO NATURE GENETICS LA English DT Article ID TISSUE-SPECIFIC EXPRESSION; ENCODING GENE; MOUSE; HYPERTENSION; ORGANIZATION; SEQUENCES; MUTATION; RECEPTOR; FAMILY AB We report the construction of the first complete genetic linkage map of the laboratory rat. By testing 1171 simple sequence length polymorphisms (SSLPs), we have identified 432 markers that show polymorphisms between the SHR and BN rat strains and mapped them in a single (SHR x BN) F-2 intercross. The loci define 21 large linkage groups corresponding to the 21 rat chromosomes, together with a pair of nearby markers on chromosome 9 that are not linked to the rest of the map. Because 99.5% of the markers fall into one of the 21 large linkage groups, the maps appear to cover the vast majority of the rat genome. The availability of the map should facilitate whole genome scans for genes underlying qualitative and quantitative traits relevant to mammalian physiology and pathobiology. C1 MIT,WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA. STANFORD UNIV,CARDIOVASC RES CTR,PALO ALTO,CA. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. GOTHENBURG UNIV,GOTHENBURG,SWEDEN. KAROLINSKA INST,DEPT MOLEC MED,STOCKHOLM,SWEDEN. FREE UNIV BRUSSELS,BRUSSELS,BELGIUM. CHARLES UNIV,DEPT BIOL,PRAGUE,CZECH REPUBLIC. ACAD SCI CZECH REPUBL,INST PHYSIOL,PRAGUE,CZECH REPUBLIC. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. RP JACOB, HJ (reprint author), MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA, USA. RI Pravenec, Michal/B-1666-2012; Kren, Vladimir/H-8461-2014 NR 49 TC 422 Z9 429 U1 0 U2 14 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD JAN PY 1995 VL 9 IS 1 BP 63 EP 69 DI 10.1038/ng0195-63 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA PZ913 UT WOS:A1995PZ91300016 PM 7704027 ER PT B AU PRALONG, FP FINKELSTEIN, JS CROWLEY, WF AF PRALONG, FP FINKELSTEIN, JS CROWLEY, WF BE Plant, TM Lee, PA TI Sex steroid control of gonadotropin secretion in the human male: Lessons from the human models of normal and gonadotropin-releasing hormone-deficient men SO NEUROBIOLOGY OF PUBERTY SE ENDOCRINE UPDATES LA English DT Proceedings Paper CT 4th International Conference on the Control of the Onset of Puberty CY SEP 29-OCT 01, 1994 CL PITTSBURGH, PA SP Univ Pittsburgh Med Ctr, Univ Pittsburgh Sch Med, Magee Womens Hosp, Childrens Hosp Pittsburgh, TAP Pharm Inc, Roberts Labs Inc, Genentech Inc, Eli Lilly & Co, Bristol Myers Squibb Co, Kabi Pharmacia Inc, Serono Labs Inc C1 MASSACHUSETTS GEN HOSP,DEPT MED,REPROD ENDOCRINE UNIT,BOSTON,MA 02146. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOCIETY ENDOCRINOLOGY PI BRISTOL PA 17/18 THE COURTYARD, WOODLANDS ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ BN 1-898099-06-5 J9 ENDOCRIN UPDAT PY 1995 BP 217 EP 227 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BD69L UT WOS:A1995BD69L00018 ER PT B AU BOEPPLE, PA MANSFIELD, MJ CRAWFORD, JD CRIGLER, JF BLIZZARD, RM CROWLEY, WF AF BOEPPLE, PA MANSFIELD, MJ CRAWFORD, JD CRIGLER, JF BLIZZARD, RM CROWLEY, WF BE Plant, TM Lee, PA TI Completion of growth and puberty in girls with central precocious puberty following long-term GnRH agonist-induced pituitary-gonadal suppression SO NEUROBIOLOGY OF PUBERTY SE ENDOCRINE UPDATES LA English DT Proceedings Paper CT 4th International Conference on the Control of the Onset of Puberty CY SEP 29-OCT 01, 1994 CL PITTSBURGH, PA SP Univ Pittsburgh Med Ctr, Univ Pittsburgh Sch Med, Magee Womens Hosp, Childrens Hosp Pittsburgh, TAP Pharm Inc, Roberts Labs Inc, Genentech Inc, Eli Lilly & Co, Bristol Myers Squibb Co, Kabi Pharmacia Inc, Serono Labs Inc C1 MASSACHUSETTS GEN HOSP,PEDIAT UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SOCIETY ENDOCRINOLOGY PI BRISTOL PA 17/18 THE COURTYARD, WOODLANDS ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ BN 1-898099-06-5 J9 ENDOCRIN UPDAT PY 1995 BP 327 EP 334 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BD69L UT WOS:A1995BD69L00028 ER PT J AU RIZZO, JF AF RIZZO, JF TI ADENOSINE-TRIPHOSPHATE DEFICIENCY - A GENRE OF OPTIC NEUROPATHY SO NEUROLOGY LA English DT Article ID CLINICAL MANIFESTATIONS; GANGLION-CELLS; 11778 MUTATION; METABOLIC-RATE; RABBIT RETINA; HEREDITARY; NEUROTOXICITY; BRAIN; PEDIGREES; AMBLYOPIA AB Purpose: To offer clinical evidence that deficiency of vitamin B-12 may adversely affect the neuronal function of patients who also have the 14,484 mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy (LHON). Methods: A case of a 27-year-old man with vitamin B-12 deficiency and the 14,484 mitochondrial DNA mutation is presented and the literature on causes of some metabolic optic neuropathies reviewed. Results: Visual loss and neurologic symptoms of vitamin B-12 deficiency occurred together, at a time when the level of vitamin B-12 was subnormal. Vision and other sensory functions began to improve within 2 months of vitamin therapy, and normal vision eventually was restored. Conclusions: The relatively prompt improvement and the eventual complete recovery of vision following vitamin replacement therapy suggest that; the subnormal level of vitamin B-12 precipitated visual loss. Given the clinical similarities of subnormal vitamin B-12, LHON, and nutritional/tobacco amblyopia, deficiency of adenosine triphosphate might be a unifying etiology for several types of optic neuropathy. This energy hypothesis provides a theoretical basis for the enigmatic phenomena of centrocecal scotomata and recovery of visual function after prolonged blindness. C1 HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. RP RIZZO, JF (reprint author), MASSACHUSETTS EYE & EAR INFIRM,NEUROOPHTHALMOL SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 69 TC 41 Z9 41 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1995 VL 45 IS 1 BP 11 EP 16 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA QB886 UT WOS:A1995QB88600003 PM 7824099 ER PT J AU PARBOOSINGH, JS ROULEAU, GA MENINGER, V MCKENNAYASEK, D BROWN, RH FIGLEWICZ, DA AF PARBOOSINGH, JS ROULEAU, GA MENINGER, V MCKENNAYASEK, D BROWN, RH FIGLEWICZ, DA TI ABSENCE OF MUTATIONS IN THE MN SUPEROXIDE-DISMUTASE OR CATALASE GENES IN FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS SO NEUROMUSCULAR DISORDERS LA English DT Article DE FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS (FALS); MN SUPEROXIDE DISMUTASE (SOD2); CATALASE; MUTATION ANALYSIS; SSCA ID MANGANESE; LINKAGE; LOCUS AB Familial amyotrophic lateral sclerosis (FALS) is an autosomal dominant, adult onset, neurological disorder caused by the degeneration of motor neurons of the cortex, brainstem and spinal cord. Recently, the defective gene in some FALS families was identified as the Cu/Zn superoxide dismutase (SOD1) gene. However, SOD1 mutations are present in approximately 20% of patients with FALS. We have tested the genes of two more free radical detoxifying enzymes, Mn superoxide dismutase (SOD2) and catalase by single strand conformation analysis (SSCA) for mutations in the remaining FALS cases. No mutations were found in the catalase enzyme in 73 unrelated FALS cases; mutations were not detected in the 66% of the SOD2 gene analyzed. FALS does not appear to be caused by mutations in the SOD2 nor the catalase genes. C1 MONTREAL GEN HOSP,RES INST,CTR RES NEUROSCI,MONTREAL,PQ H3G 1A4,CANADA. MCGILL UNIV,CTR RES NEUROSCI,MONTREAL,PQ H3A 2T5,CANADA. HOP HOTEL DIEU,CTR SLA,PARIS,FRANCE. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DAY NEUROMUSCULAR LAB,BOSTON,MA. UNIV ROCHESTER,MED CTR,DEPT NEUROL,ROCHESTER,NY 14642. NR 16 TC 15 Z9 15 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-8966 J9 NEUROMUSCULAR DISORD JI Neuromusc. Disord. PD JAN PY 1995 VL 5 IS 1 BP 7 EP 10 DI 10.1016/0960-8966(94)E0022-Z PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA QE055 UT WOS:A1995QE05500002 PM 7719145 ER PT S AU Schulz, JB Beal, MF AF Schulz, JB Beal, MF BE Trembly, B Slikker, W TI Neuroprotective effects of free radical scavengers and energy repletion in animal models of neurodegenerative disease SO NEUROPROTECTIVE AGENTS: CLINICAL AND EXPERIMENTAL ASPECTS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 2nd International Conference on Neuroprotective Agents - Clinical and Experimental Aspects CY JUL 31-AUG 03, 1994 CL LAKE GEORGE, NY SP FDA, Natl Ctr Toxicol Res, Jefferson, Arkansas, Dept Vet Affairs Med Ctr, Togus, Maine ID TOXIN 3-NITROPROPIONIC ACID; BUTYL-ALPHA-PHENYLNITRONE; EXCITOTOXIC LESIONS; SUPEROXIDE-DISMUTASE; CEREBELLAR NEURONS; INDUCED INJURY; 1-METHYL-4-PHENYLPYRIDINIUM; NEUROTOXICITY; BRAIN; MPP+ C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Schulz, Jorg/D-9786-2012 OI Schulz, Jorg/0000-0002-8903-0593 NR 56 TC 16 Z9 18 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-945-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 765 BP 100 EP 110 DI 10.1111/j.1749-6632.1995.tb16565.x PG 11 WC Neurosciences; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA BE39D UT WOS:A1995BE39D00009 PM 7486598 ER PT J AU WILLINGHAM, DB TREADWELL, JR KOROSHETZ, WJ BENNETT, JP AF WILLINGHAM, DB TREADWELL, JR KOROSHETZ, WJ BENNETT, JP TI COMPARISON OF HUNTINGTONS-DISEASE AND PARKINSONS-DISEASE PATIENTS USE OF ADVANCE INFORMATION SO NEUROPSYCHOLOGY LA English DT Article ID CHOICE REACTION-TIME; SEQUENTIAL MOVEMENTS; INTENDED DIRECTION; PREFRONTAL CORTEX; BASAL GANGLIA; MOTOR; ATTENTION; PERFORMANCE; EXECUTION; MONKEY AB Neurologically intact subjects respond more quickly in a choice response time (CRT) task if they are told beforehand which signal will appear. Previous studies with Parkinson's disease (PD) patients are equivocal as to whether patients benefit from such cues. This experiment provided several convergent measures of the use of advance information in the motor responses of PD patients and also compared their performance to patients with striatal atrophy due to Huntington's disease (HD). Nine early PD patients, 8 early HD patients, 5 moderate HD patients, and 16 neurologically intact control subjects performed a simple response time (SRT) task and 3 CRT tasks: 1 without a cue as to where the GO signal would appear, 1 with a cue subjects watched, and 1 with a cue to which subjects responded. PD patients and HD patients showed a benefit in response times equal to that of control subjects in all conditions. C1 MASSACHUSETTS GEN HOSP,HUNTINGTONS DIS CTR,BOSTON,MA. WASHINGTON UNIV,DEPT PSYCHOL,ST LOUIS,MO 63130. UNIV VIRGINIA,DEPT NEUROL,CHARLOTTESVILLE,VA 22908. RP WILLINGHAM, DB (reprint author), UNIV VIRGINIA,DEPT PSYCHOL,GILMER HALL,CHARLOTTESVILLE,VA 22903, USA. NR 44 TC 12 Z9 12 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0894-4105 J9 NEUROPSYCHOLOGY JI Neuropsychology PD JAN PY 1995 VL 9 IS 1 BP 39 EP 46 PG 8 WC Psychology, Clinical; Neurosciences; Psychology SC Psychology; Neurosciences & Neurology GA RF680 UT WOS:A1995RF68000004 ER PT J AU SAPP, E GE, P AIZAWA, H BIRD, E PENNEY, J YOUNG, AB VONSATTEL, JP DIFIGLIA, M AF SAPP, E GE, P AIZAWA, H BIRD, E PENNEY, J YOUNG, AB VONSATTEL, JP DIFIGLIA, M TI EVIDENCE FOR A PREFERENTIAL LOSS OF ENKEPHALIN IMMUNOREACTIVITY IN THE EXTERNAL GLOBUS-PALLIDUS IN LOW-GRADE HUNTINGTONS-DISEASE USING HIGH-RESOLUTION IMAGE-ANALYSIS SO NEUROSCIENCE LA English DT Article ID SUBSTANCE-P; METHIONINE-ENKEPHALIN; MET-ENKEPHALIN; SPINY NEURONS; BASAL GANGLIA; BRAIN; RAT; RECEPTORS; TISSUES; CHOREA AB Previous studies have shown that in advanced cases of Huntington's disease, enkephalin-immunoreactive striatal projections to the external globus pallidus may be more affected than substance P-containing striatal projections to the inner segment of the pallidum [Reiner A. et al. (1988) Proc. natn. Acad. Sci. U.S.A. 85, 5733-5737]. Other immunohistochemical [Ferrante R. J. ct al. (1990) Sec. Neurosci. Abstr. 16, 1120] and neurochemical observations [Storey E. and Beal M. F. (1993) Brain 116, 1201-1222] suggest no difference in the loss of these peptide-containing pathways in Huntington's disease. In view of the potential significance of this issue for understanding the neuropathological process in Huntington's disease, we examined the globus pallidus in control and Huntington's disease brains, using a quantitative approach which involved high resolution image analysis of 7 mu m frozen sections to determine the overall density of peptide-immunoreactive terminals. Results showed that in the controls there was no significant difference between the density of enkephalin- and substance P-immunoreactive terminals in the external and internal globus pallidus, respectively. In all Huntington's disease brains, including grade 1 cases, enkephalin-immunoreactive terminals in the external globus pallidus were significantly reduced compared to substance P-positive boutons in the internal segment of the adjacent section. In comparison to controls, enkephalin immunoreactivity in all Huntington's disease cases was significantly lower; substance P-immunoreactive terminals in the internal globus pallidus were significantly lower than controls in some of the grade 2 cases and in the grade 3 cases. Our results using a method of analysis different from previous studies support the earlier findings of Reiner el al., that in Huntington's disease the striatopallidal pathway containing immunoreactive enkephalin is affected to a greater extent than the projection containing substance P. Moreover, the additional finding in this study that enkephalin and substance P projections differ markedly in the grade I cases strongly suggests that the alterations in the enkephalin pathway signal a relatively early event in the neuropathological process in Huntington's disease. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NINDS NIH HHS [NS16367] NR 21 TC 110 Z9 112 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 JAN PY 1995 VL 64 IS 2 BP 397 EP 404 DI 10.1016/0306-4522(94)00427-7 PG 8 WC Neurosciences SC Neurosciences & Neurology GA QB159 UT WOS:A1995QB15900009 PM 7535402 ER PT J AU SWEARINGEN, B JOSEPH, M CHENEY, M OJEMANN, RG AF SWEARINGEN, B JOSEPH, M CHENEY, M OJEMANN, RG TI A MODIFIED TRANSFACIAL APPROACH TO THE CLIVUS SO NEUROSURGERY LA English DT Article DE CLIVUS; CRANIAL BASE SURGERY; TRANSCLIVAL APPROACH ID UPPER CERVICAL-SPINE; SKULL-BASE TUMORS; SURGICAL-MANAGEMENT; TRANSORAL APPROACH; TRANSPALATAL APPROACH; EXTENDED MAXILLOTOMY; CRANIAL BASE; EXPERIENCE; CHORDOMA; EXPOSURE AB ANTERIOR APPROACHES TO the clivus must provide excellent visualization of the lesion, give adequate access for dural repair, and be cosmetically acceptable. Most current approaches enter through the nasopharynx or oropharynx, with either palatal, maxillary, or mandibular splitting for greater exposure. We have modified the transfacial approach described by others, which provides excellent access to the clivus along its rostrocaudal extent. A lateral rhinotomy incision is used and carried along the base of the right alae nasi and columella. The nasal bones are osteotomized bilaterally, and the nose is rotated on a pedicle flap, thus opening the entire nasal cavity to view. The septum and medial maxillary walls are removed. This provides excellent visualization of the ethmoid, sphenoid, posterior nasopharynx, and upper oropharynx. At the conclusion of the procedure, the nasal incision is closed, with good cosmesis. A case of recurrent chordoma of the middle and lower clivus is presented to exemplify this technique. The approach has since been used to approach clivus tumors and midline aneurysms of the vertebrobasilar system. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA. RP SWEARINGEN, B (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,ACC 331,BOSTON,MA 02114, USA. NR 30 TC 22 Z9 24 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD JAN PY 1995 VL 36 IS 1 BP 101 EP 104 PG 4 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA QA101 UT WOS:A1995QA10100035 PM 7708145 ER PT J AU COSGROVE, GR RAUCH, SL AF COSGROVE, GR RAUCH, SL TI PSYCHOSURGERY SO NEUROSURGERY CLINICS OF NORTH AMERICA LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; FOLLOW-UP; ABNORMALITIES; CINGULOTOMY AB Surgical treatment of psychiatric disease can be helpful in certain patients with severe, disabling and treatment refractory major affective disorders, obsessive compulsive disorders, and chronic anxiety states. Psychosurgical treatment should be carried out by an expert multidisciplinary team with experience in these disorders. Surgery should be considered as one part of an entire treatment plan and must be followed by an appropriate psychiatric rehabilitation program. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP COSGROVE, GR (reprint author), MASSACHUSETTS GEN HOSP,15 PARKMAN ST,ACC SUITE 331,BOSTON,MA 02114, USA. NR 64 TC 53 Z9 53 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1042-3680 J9 NEUROSURG CLIN N AM JI Neurosurg. Clin. N. Am. PD JAN PY 1995 VL 6 IS 1 BP 167 EP 176 PG 10 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA QX550 UT WOS:A1995QX55000013 PM 7696872 ER PT B AU OGAWA, M HIRAYAMA, F AF OGAWA, M HIRAYAMA, F BE Mihich, E Metcalf, D TI Cytokine regulation of lymphohemopoietic progenitors SO NORMAL AND MALIGNANT HEMATOPOIESIS: NEW ADVANCES SE PEZCOLLER FOUNDATION SYMPOSIA LA English DT Proceedings Paper CT 6th Pezcoller Symposium on Normal and Malignant Hematopoiesis - New Advances CY JUN 29-JUL 01, 1994 CL ROVERETO, ITALY SP Pezcoller Fdn C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. NR 0 TC 6 Z9 6 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45136-0 J9 PEZ FDN SYM PY 1995 VL 6 BP 11 EP 14 PG 4 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Medicine, Research & Experimental; Microbiology SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Research & Experimental Medicine; Microbiology GA BE24B UT WOS:A1995BE24B00002 ER PT B AU ECKNER, R ARANY, Z LIVINGSTON, DM AF ECKNER, R ARANY, Z LIVINGSTON, DM BE Mihich, E Metcalf, D TI A family of high molecular weight proteins active in differentiation and growth control SO NORMAL AND MALIGNANT HEMATOPOIESIS: NEW ADVANCES SE PEZCOLLER FOUNDATION SYMPOSIA LA English DT Proceedings Paper CT 6th Pezcoller Symposium on Normal and Malignant Hematopoiesis - New Advances CY JUN 29-JUL 01, 1994 CL ROVERETO, ITALY SP Pezcoller Fdn C1 DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45136-0 J9 PEZ FDN SYM PY 1995 VL 6 BP 89 EP 100 PG 12 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Medicine, Research & Experimental; Microbiology SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Research & Experimental Medicine; Microbiology GA BE24B UT WOS:A1995BE24B00009 ER PT B AU BOUSSIOTIS, VA FREEMAN, GJ GRIBBEN, JG NADLER, LM AF BOUSSIOTIS, VA FREEMAN, GJ GRIBBEN, JG NADLER, LM BE Mihich, E Metcalf, D TI Induction of alloantigen specific T cell anergy by inhibition of the B7: CD28 pathway SO NORMAL AND MALIGNANT HEMATOPOIESIS: NEW ADVANCES SE PEZCOLLER FOUNDATION SYMPOSIA LA English DT Proceedings Paper CT 6th Pezcoller Symposium on Normal and Malignant Hematopoiesis - New Advances CY JUN 29-JUL 01, 1994 CL ROVERETO, ITALY SP Pezcoller Fdn C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45136-0 J9 PEZ FDN SYM PY 1995 VL 6 BP 205 EP 218 PG 14 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Medicine, Research & Experimental; Microbiology SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Research & Experimental Medicine; Microbiology GA BE24B UT WOS:A1995BE24B00016 ER PT B AU HURFORD, RK GOILLOT, E TEPPER, RI AF HURFORD, RK GOILLOT, E TEPPER, RI BE Mihich, E Metcalf, D TI Novel strategies for cancer treatment through modulation of proimmune and proinflammatory cytokines SO NORMAL AND MALIGNANT HEMATOPOIESIS: NEW ADVANCES SE PEZCOLLER FOUNDATION SYMPOSIA LA English DT Proceedings Paper CT 6th Pezcoller Symposium on Normal and Malignant Hematopoiesis - New Advances CY JUN 29-JUL 01, 1994 CL ROVERETO, ITALY SP Pezcoller Fdn C1 MASSACHUSETTS GEN HOSP,CTR CANC,TUMOR BIOL LAB,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45136-0 J9 PEZ FDN SYM PY 1995 VL 6 BP 219 EP 234 PG 16 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Medicine, Research & Experimental; Microbiology SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Hematology; Research & Experimental Medicine; Microbiology GA BE24B UT WOS:A1995BE24B00017 ER PT J AU BABICH, JW FISCHMAN, AJ AF BABICH, JW FISCHMAN, AJ TI EFFECT OF CO-LIGAND ON THE BIODISTRIBUTION OF TC-99M-LABELED HYDRAZINO NICOTINIC-ACID DERIVATIZED CHEMOTACTIC PEPTIDES SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article ID IMAGING FOCAL SITES; BACTERIAL-INFECTION; RATS; LEUKOCYTES; ANALOGS AB Hydrazinonicotinamide (HYNIC) derivatized chemotactic peptides radiolabeled with Tc-99m- (via Tc-99m-glucoheptonate) have been demonstrated to be useful for infection imaging [J. Nucl. Med. 34, 1964-1974 (1993)]. Since HYNIC can occupy only two sites of the technetium co-ordination sphere, the labeled product most probably contains additional ligands. Thus we hypothesized that glucoheptonate serves this role by acting as a '''co-ligand'''. Due to the low molecular weight of the chemotactic peptides, the ''co-ligand'' used for technetium labeling could have profound effects on biodistribution. To evaluate this possibility, we measured the biodistribution of Tc-99m-labeled For-MLFK-HYNIC radiolabeled using four different ''co-ligand''s: glucarate, glucoheptonate, mannitol and glucamine, providing a small series of hydroxyl-backbone ligands which differ in the number and type of ionizable functional groups present. Each preparation was injected into groups of 6 rats (similar to 10 mu Ci/rat) and biodistribution was determined at 5, 30, 60 and 120 min. Although small differences in biodistribution were detected in most tissues, the most prominent differences (P <0.01) were observed in lung (glucoheptonate, glucarate > mannitol >> glucamine), liver (glucarate, glucoheptonate, mannitol >> glucamine), kidney (mannitol > glucarate, glucoheptonate, glucamine), spleen (glucarate >> glucoheptonate, mannitol >> glucamine) and GI-tract (glucarate, glucamine >> gluco-heptonate >> mannitol). These results provide support for the ''co-ligand'' hypothesis and indicate that the nature of the ''co-ligand'' can have profound effects on biodistribution. Although radiolabeling using glucamine as the ''co-ligand'' results in the lowest concentrations of radioactivity in most organs, the extremely low concentration of mannitol-labeled peptide in the GI-tract suggests that this may be the ''co-ligand'' of choice for most applications. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 13 TC 102 Z9 103 U1 0 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD JAN PY 1995 VL 22 IS 1 BP 25 EP 30 DI 10.1016/0969-8051(94)00081-T PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QJ044 UT WOS:A1995QJ04400004 PM 7735166 ER PT J AU LIVNI, E BABICH, JW DESAI, MC GODEK, DM WILKINSON, RA RUBIN, RH FISCHMAN, AJ AF LIVNI, E BABICH, JW DESAI, MC GODEK, DM WILKINSON, RA RUBIN, RH FISCHMAN, AJ TI SYNTHESIS OF A C-11 LABELED NK1 RECEPTOR-LIGAND FOR PET STUDIES SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article ID SUBSTANCE-P ANTAGONIST; CENTRAL NERVOUS-SYSTEM; NONPEPTIDE ANTAGONIST; INFLAMMATION; RECOGNITION; ACTIVATION; DISCOVERY; CP-96,345; NEURONS AB Changes in substance P (SP) receptor concentration have been implicated in neuropsychiatric disorders, Parkinson's disease, arthritis, inflammatory bowel disease and asthma. Since, SP and peptide analogs are rapidly metabolized and do not penetrate into the CNS, they are not useful for PET. Recently, a non-peptide SP antagonist, (+)-(2S,3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine(CP-99,994) was developed. As a prelude to PET studies, this compound was radiolabeled with C-11 and biodistribution was determined in hamsters. CP-99,994 was radiolabeled by methylation of tert-Boc, desmethyl CP-99,994 with (CH3I)-C-11 followed by deprotection and HPLC purification. The time required for the synthesis was 40 min from the end of bombardment. Radiochemical purity of the final product was >95% and specific activity was routinely >1000 mCi/mu mol [EOS]. The biodistribution of C-11-CP-99,994 was determined in groups of six Syrian hamsters at 5 and 30 min after injection. The results of these studies demonstrated that significant concentrations (%ID/g +/- SEM) of CP-99,994 accumulate in most tissues of the hamster. The highest levels of drug were detected in the lung: 21.04 +/- 1.26 (5 min) and 13.49 +/- 1.71 (30 min). Brain accumulation was: 1.44 +/- 0.06 (5 min), 1.32 +/- 0.05 (30 min). These results indicate that C-11-CP-99,994 can be prepared in high purity and specific activity. This new radiopharmaceutical may be useful for studying both central and peripheral SP receptors by PET. C1 MASSACHUSETTS GEN HOSP, DEPT RADIOL, DIV NUCL MED, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, MED SERV, CLIN INVEST PROGRAM, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT RADIOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02114 USA. PFIZER INC, DIV CENT RES, GROTON, CT 06340 USA. NR 29 TC 8 Z9 8 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 JAN PY 1995 VL 22 IS 1 BP 31 EP 36 DI 10.1016/0969-8051(94)00080-4 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QJ044 UT WOS:A1995QJ04400005 PM 7735167 ER PT J AU SHIPP, TD BROMLEY, B HORNBERGER, LK NADEL, A BENACERRAF, BR AF SHIPP, TD BROMLEY, B HORNBERGER, LK NADEL, A BENACERRAF, BR TI LEVOROTATION OF THE FETAL CARDIAC AXIS - A CLUE FOR THE PRESENCE OF CONGENITAL HEART-DISEASE SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID ECHOCARDIOGRAPHY; POSITION AB Objective: To evaluate the use of the cardiac axis within the chest for the prenatal detection of congenital heart defects. Methods: We reviewed retrospectively the sonographic findings of all fetuses scanned between 17 and 40 weeks' gestation and diagnosed prenatally as having heart defects. The cardiac diagnoses were confirmed postnatally. The control group consisted of 75 consecutive fetuses with normal fetal surveys and newborn follow-up examinations. The cardiac axes were measured retrospectively using an image of the four-chamber view of the heart and measuring the angle between the interventricular septum and a line bisecting the chest. Mean and standard deviations (SDs) of the axis measurements in normal and abnormal fetuses were compared by Student t test. Results: The 75 fetuses with heart defects diagnosed by prenatal sonogram had a mean cardiac axis of 56 +/- 13 degrees, compared with 43 +/- 7 degrees in normal fetuses (P < .001). Using 57 degrees (two SDs above the mean for normal fetuses) as the upper limit of normal, 33 of 75 (44%) abnormal fetuses versus none of 75 normal fetuses were identified. The frequency of cardiac rotation was greater in fetuses with truncus arteriosus, Ebstein's anomaly, pulmonic stenosis, coarctation of the aorta, and tetralogy of Fallot. Conclusion: The presence of a cardiac axis exceeding 57 degrees in the fetal chest is associated with a substantial risk of congenital heart defects. The finding of an abnormal axis should prompt further evaluation of the fetal heart. C1 BRIGHAM & WOMENS HOSP,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV CARDIOL,BOSTON,MA 02115. NR 8 TC 36 Z9 40 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD JAN PY 1995 VL 85 IS 1 BP 97 EP 102 DI 10.1016/0029-7844(94)00328-B PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA PX706 UT WOS:A1995PX70600021 PM 7800334 ER PT J AU Silverman, PR Weiner, A ELAd, N AF Silverman, PR Weiner, A ELAd, N TI Parent-child communication in bereaved Israeli families SO OMEGA-JOURNAL OF DEATH AND DYING LA English DT Article AB The nature of surviving parent-child communication in bereaved Israeli families is examined in terms of the culture of Israeli society. Concern is with the way the culture frames the parent-child relationship in the period shortly after the death. Twenty-three surviving parents and their forty-three children between ages of six and sixteen were interviewed four months after the death. Both parents and children seemed concerned with protecting each other from the pain and sadness associated with the loss. Two types of families were identified. In the open family, language is used to console and inform. Parents see themselves as able to respond to their child(ren)'s needs. Less open families used language to influence the child to avoid their feelings and confronting the death. These surviving parents often saw the deceased as the competent family caregiver. C1 UNIV HAIFA,SCH SOCIAL WORK,IL-31999 HAIFA,ISRAEL. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CAMBRIDGE,MA 02138. NR 22 TC 6 Z9 6 U1 0 U2 1 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0030-2228 J9 OMEGA-J DEATH DYING JI Omega-J. Death Dying PY 1995 VL 31 IS 4 BP 275 EP 293 PG 19 WC Psychology, Multidisciplinary; Social Sciences, Biomedical SC Psychology; Biomedical Social Sciences GA TP852 UT WOS:A1995TP85200003 ER PT J AU KREK, W DECAPRIO, JA AF KREK, W DECAPRIO, JA TI CELL SYNCHRONIZATION SO ONCOGENE TECHNIQUES SE METHODS IN ENZYMOLOGY LA English DT Review ID RETINOBLASTOMA SUSCEPTIBILITY GENE; PHOSPHORYLATION; CYCLE; KINASE; DEPHOSPHORYLATION; EXPRESSION; ACTIVATION; INHIBITOR; PRODUCT; PROTEIN C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KREK, W (reprint author), DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 23 TC 78 Z9 80 U1 0 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 254 BP 114 EP 124 PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE08E UT WOS:A1995BE08E00007 PM 8531680 ER PT J AU LIANG, P BAUER, D AVERBOUKH, L WARTHOE, P ROHRWILD, M MULLER, H STRAUSS, M PARDEE, AB AF LIANG, P BAUER, D AVERBOUKH, L WARTHOE, P ROHRWILD, M MULLER, H STRAUSS, M PARDEE, AB TI ANALYSIS OF ALTERED GENE-EXPRESSION BY DIFFERENTIAL DISPLAY SO ONCOGENE TECHNIQUES SE METHODS IN ENZYMOLOGY LA English DT Review ID MAMMARY EPITHELIAL-CELLS; ARBITRARY PRIMERS; MESSENGER-RNAS; TUMOR; CANDIDATE; PCR; IDENTIFICATION; CLONING; GROWTH C1 HUMBOLDT UNIV BERLIN,MAX DELBRUCK CTR MOLEC MED,MAX PLANCK SOC,D-13122 BERLIN,GERMANY. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. DANISH CANC SOC,DIV CANC BIOL,DK-2100 COPENHAGEN,DENMARK. RP LIANG, P (reprint author), DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115, USA. OI Muller, Heiko/0000-0001-9873-3146 NR 22 TC 104 Z9 117 U1 0 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 254 BP 304 EP 321 PG 18 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE08E UT WOS:A1995BE08E00020 PM 8531695 ER PT J AU CEPKO, C RYDER, EF AUSTIN, CP WALSH, C FEKETE, DM AF CEPKO, C RYDER, EF AUSTIN, CP WALSH, C FEKETE, DM TI LINEAGE ANALYSIS USING RETROVIRUS VECTORS SO ONCOGENE TECHNIQUES SE METHODS IN ENZYMOLOGY LA English DT Review ID PACKAGING CELL-LINE; CEREBRAL-CORTEX; GENE-TRANSFER; HIGH-TITER; ALKALINE-PHOSPHATASE; COMMON PROGENITOR; NEURONAL CLONES; MIGRATION; RETINA; DISPERSION C1 BOSTON COLL,DEPT BIOL,BOSTON,MA. BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP CEPKO, C (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115, USA. RI Fekete, Donna/B-9170-2009 OI Fekete, Donna/0000-0003-0662-0246 NR 41 TC 34 Z9 34 U1 0 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 254 BP 387 EP 419 PG 33 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE08E UT WOS:A1995BE08E00025 PM 8531701 ER PT J AU SHAMAH, SM STILES, CD AF SHAMAH, SM STILES, CD TI TRANSDOMINANT NEGATIVE MUTATIONS SO ONCOGENE TECHNIQUES SE METHODS IN ENZYMOLOGY LA English DT Review ID GROWTH-FACTOR RECEPTOR; SIS GENE-PRODUCT; TYROSINE KINASE-ACTIVITY; PDGF BETA-RECEPTOR; THYROID-HORMONE; SIGNAL-TRANSDUCTION; AUTOCRINE TRANSFORMATION; CELLULAR-TRANSFORMATION; ONCOGENE PRODUCT; B-CHAIN C1 DANA FARBER CANC INST,BOSTON,MA 02115. RP SHAMAH, SM (reprint author), HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115, USA. NR 58 TC 5 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 254 BP 565 EP 576 PG 12 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE08E UT WOS:A1995BE08E00038 PM 8531715 ER PT J AU BLACKWELL, TK AF BLACKWELL, TK TI SELECTION OF PROTEIN-BINDING SITES FROM RANDOM NUCLEIC-ACID SEQUENCES SO ONCOGENE TECHNIQUES SE METHODS IN ENZYMOLOGY LA English DT Review ID STRANDED-DNA MOLECULES; CYCLIC AMPLIFICATION; MYC PROTEINS; RNA LIGANDS; INVITRO; SPECIFICITY; RECOGNITION; COMPLEXES; ENHANCER; TARGETS C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP BLACKWELL, TK (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM50900] NR 30 TC 16 Z9 16 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 254 BP 604 EP 618 PG 15 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE08E UT WOS:A1995BE08E00041 PM 8531718 ER PT J AU TEICHER, BA DUPUIS, NP ROBINSON, MF EMI, Y GOFF, DA AF TEICHER, BA DUPUIS, NP ROBINSON, MF EMI, Y GOFF, DA TI ANTIANGIOGENIC TREATMENT (TNP-470/MINOCYCLINE) INCREASES TISSUE-LEVELS OF ANTICANCER DRUGS IN MICE BEARING LEWIS-LUNG-CARCINOMA SO ONCOLOGY RESEARCH LA English DT Article DE ANTIANGIOGENIC AGENTS; TNP-470; MINOCYCLINE; TISSUE DRUG LEVELS ID ANGIOGENESIS INHIBITOR TNP-470; 4 PLATINUM COMPLEXES; TUMOR-GROWTH; CANCER THERAPIES; CELL-LINES; IN-VITRO; AGM-1470; INVIVO; MINOCYCLINE; INVITRO AB Although the antiangiogenic agent TNP-470 does not, in general, increase the cytotoxicity of anticancer therapies in cell culture, the antiangiogenic agents TNP-470 and minocycline individually and especially in combination have been shown to increase the tumor growth delay produced by several standard cytotoxic therapies in the Lewis lung carcinoma. In an effort to understand the mechanism by which the antiangiogenic agent combination TNP-470/minocycline potentiates the antitumor activity of cytotoxic therapeutic agents in vivo, the biodistribution of [C-14]-cyclophosphamide and cis-diamminedichloroplatinum(II) was determined 6 h after cytotoxic drug administration in animals bearing Lewis lung carcinoma pretreated with TNP-470/minocycline and in animals without pretreatment. Higher levels of C-14 and platinum were found in 9 tissues (including tumor) except blood in animals pretreated with TNP-470/minocycline, The increased drug levels in the tumors may be sufficient to account for the increased tumor growth delays observed previously. DNA alkaline elution of tumors from animals pretreated with TNP-470/minocycline showed increased DNA cross-linking by both cyclophosphamide and cis-diamminedichloroplatinum(II). The possible implications of these results are discussed. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [P01-CA38493, P01-CA19589]; PHS HHS [P01-31303] NR 34 TC 49 Z9 51 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0965-0407 J9 ONCOL RES JI Oncol. Res. PY 1995 VL 7 IS 5 BP 237 EP 243 PG 7 WC Oncology SC Oncology GA RP616 UT WOS:A1995RP61600004 PM 8534929 ER PT J AU IGARASHI, H YOSHIDA, A TANAKA, K CHENG, HM AF IGARASHI, H YOSHIDA, A TANAKA, K CHENG, HM TI CHANGES IN LENS ORGANOPHOSPHATE METABOLITES IN RESPONSE TO ENDOTOXIN-INDUCED UVEITIS SO OPHTHALMIC RESEARCH LA English DT Article DE LENS; ADENOSINE TRIPHOSPHATE; CHOLINE PHOSPHATE; INORGANIC PHOSPHATE; EXPERIMENTAL UVEITIS; ENDOTOXIN; NUCLEAR MAGNETIC RESONANCE ID SPECTROSCOPY; LIVER AB Uveitis was induced in rats by endotoxin administration. The temporal correlation between ocular inflammatory reaction and lens metabolic change was examined. The levels of lens phosphate compounds, adenosine triphosphate (ATP), choline phosphate (CP), and inorganic phosphate (Pi), were measured using P-31-nuclear magnetic resonance (NMR) spectroscopy. Anterior chamber inflammation reaction appeared 12 h after administration, peaked at 24 h, and disappeared by 72 h. Concurrent with the active inflammation, lens Pi increased significantly 22 +/- 17% (p < 0.05) and 23 +/- 15% (p < 0.05), 12 and 24 h after administration, respectively, and returned to normal while the inflammation abated. No significant changes were observed in CP and ATP levels in the lens during the course of inflammation. The time course of the inflammation appeared closely related to the change in Pi level, which may be part of the protective mechanism of the Lens against inflammation. C1 ASAHIKAWA MED COLL,DEPT OPHTHALMOL,ASAHIKAWA,HOKKAIDO,JAPAN. ASAHIKAWA MED COLL,CENT LAB RES & EDUC,ASAHIKAWA,HOKKAIDO,JAPAN. RP IGARASHI, H (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 29 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0030-3747 J9 OPHTHALMIC RES JI Ophthalmic Res. PD JAN-FEB PY 1995 VL 27 IS 1 BP 12 EP 17 PG 6 WC Ophthalmology SC Ophthalmology GA QU800 UT WOS:A1995QU80000002 PM 7596554 ER PT B AU BERGER, JW KIM, SH LAMARCHE, KJ DAMICO, DJ TALAMO, JH AF BERGER, JW KIM, SH LAMARCHE, KJ DAMICO, DJ TALAMO, JH BE Parel, JM Ren, QS Joos, KM Katzir, A TI ER YAG LASER DRILLING OF CATARACTOUS LENS - PREDICTING THE ABLATION RATE WITH A SIMPLE MODEL SO OPHTHALMIC TECHNOLOGIES V, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Ophthalmic Technologies V Conference CY FEB 04-05, 1995 CL SAN JOSE, CA SP Soc Photo Opt Instrumentat Engineers DE ERBIUM; LENS; CATARACT; INFRARED; ABLATION; MODELING; LASER C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTALMOL,LASER RES LAB,BOSTON,MA 02114. NR 0 TC 10 Z9 10 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1740-8 J9 P SOC PHOTO-OPT INS PY 1995 VL 2393 BP 148 EP 159 DI 10.1117/12.209840 PG 12 WC Ophthalmology; Optics SC Ophthalmology; Optics GA BD19Q UT WOS:A1995BD19Q00022 ER PT J AU WARD, JB NIFFENEGGER, AS LAVIN, CW ACQUADRO, MA AHERN, DK SMITH, PV MCKEOWN, CA AF WARD, JB NIFFENEGGER, AS LAVIN, CW ACQUADRO, MA AHERN, DK SMITH, PV MCKEOWN, CA TI THE USE OF PROPOFOL AND MIVACURIUM ANESTHETIC TECHNIQUE FOR THE IMMEDIATE POSTOPERATIVE ADJUSTMENT OF SUTURES IN STRABISMUS SURGERY SO OPHTHALMOLOGY LA English DT Article ID OCULOCARDIAC REFLEX AB Purpose: Adjustable suture techniques have become increasingly popular over the last decade and may reduce the re-operation rate after strabismus surgery. The adjustment usually is made in the hospital or office 5 to 24 hours after surgery, when the patient has fully recovered from general anesthesia. The ability to perform suture adjustment in the operating room, immediately after completion of surgery, would be an attractive alternative with respect to patient monitoring, sterility, comfort, and timing. The purpose of this study is to compare the alignment of patients in the operating room adjusted immediately after surgery with their alignment the morning after surgery. Methods: Patients with strabismus who have good vision in each eye and who were judged to be appropriate candidates for adjustable sutures were invited to enroll in a study using propofol and mivacurium total intravenous anesthetic technique. Patients underwent strabismus surgery in which one or more muscles were placed on adjustable sutures. Immediately after extubation, these patients were awakened in the operating room, assisted in sitting upright, and asked to fixate on a 20/400 Snellen E target on the operating room walt. Sutures were adjusted, when necessary, to obtain the desired postoperative alignment. Prism and alternate cover measurements, taken after the sutures were permanently tied, were compared with measurements taken the morning after surgery. Results: Twenty-nine patients qualified for inclusion. Measurements of horizontal and vertical alignment in the operating room were all within 12 prism diopters (PD) of the measurements taken 18 to 24 hours after surgery (mean variation, 4 PD horizontally and 2 PD diopters vertically). The measured deviation changed less than or equal to 6 PD horizontally in 78% of patients and less than or equal to 3 PD vertically in 70% of patients. Conclusion: For some adult patients with strabismus, a total intravenous general anesthesia technique using an infusion of propofol and mivacurium may provide the opportunity for accurate suture adjustment in the operating room, immediately after completion of surgery. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 13 TC 18 Z9 18 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD JAN PY 1995 VL 102 IS 1 BP 122 EP 128 PG 7 WC Ophthalmology SC Ophthalmology GA QB558 UT WOS:A1995QB55800025 PM 7831026 ER PT J AU POWER, WJ RODRIGUEZ, A NEVES, RA LANE, L FOSTER, CS AF POWER, WJ RODRIGUEZ, A NEVES, RA LANE, L FOSTER, CS TI DISEASE RELAPSE IN PATIENTS WITH OCULAR MANIFESTATIONS OF WEGENER GRANULOMATOSIS SO OPHTHALMOLOGY LA English DT Article ID SOLUBLE INTERLEUKIN-2 RECEPTOR; CYTOPLASMIC ANTIBODY TITER; RHEUMATOID-ARTHRITIS; PERIPHERAL-BLOOD; AUTOANTIBODIES; ASSOCIATION; VASCULITIS; SERUM; GLOMERULONEPHRITIS; EXPERIENCE AB Purpose: To evaluate possible factors associated with disease relapse in patients with ocular manifestations of Wegener granulomatosis. Methods: Eight patients with ocular manifestations of Wegener granulomatosis were longitudinally followed for a mean period of 34 months. Serial antineutrophil cytoplasmic antibody (ANCA) levels were determined on all patients. Results: All eight patients had either scleritis alone or scleritis combined with peripheral ulcerative keratitis. Clinical disease remission was achieved in all patients using immunosuppressive chemotherapy. Five patients had subsequent relapse after treatment withdrawal. The serum ANCA level had failed to revert to normal during remission in four of the five patients who had had relapses. The ANCA levels for all three patients who remained in remission without therapy converted to normal. There was no significant difference in the initial serum ANCA level (P = 0.35) or the mean cumulative cyclophosphamide dose (P = 0.13) between those who had a relapse and those who did not. Conclusion: Failure of ANCA titers to revert to normal levels may be associated with the potential for relapse in patients with ocular manifestations of Wegener granulomatosis. C1 MASSACHUSETTS GEN HOSP,DEPT OPHTHALMOL,IMMUNOL & UVEITIS SERV,BOSTON,MA 02114. NR 32 TC 23 Z9 24 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD JAN PY 1995 VL 102 IS 1 BP 154 EP 160 PG 7 WC Ophthalmology SC Ophthalmology GA QB558 UT WOS:A1995QB55800030 PM 7831031 ER PT B AU Finkelstein, JS AF Finkelstein, JS BE Baird, DT Schutz, G Krattenmacher, R TI Androgen action on the bone SO ORGAN-SELECTIVE ACTIONS OF STEROID HORMONES SE ERNST SCHERING RESEARCH FOUNDATION WORKSHOP LA English DT Proceedings Paper CT Ernst-Schering-Research-Foundation 16th Workshop on Organ-Selective Actions of Steroid Hormones CY MAY 17-19, 1995 CL BERLIN, GERMANY SP Ernst Schering Res Fdn C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SPRINGER-VERLAG BERLIN PI BERLIN 33 PA HEIDELBERGER PLATZ 3, W-1000 BERLIN 33, GERMANY BN 3-540-60338-7 J9 E SCHERING RES FDN W PY 1995 VL 16 BP 121 EP 136 PG 16 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA BE91J UT WOS:A1995BE91J00007 ER PT B AU SYKES, M AF SYKES, M BE Touraine, JL Traeger, J Betuel, H Dubernard, JM Revillard, JP Dupuy, C TI Xenochimerism and tolerance SO ORGAN SHORTAGE: THE SOLUTIONS SE TRANSPLANTATION AND CLINICAL IMMUNOLOGY (SYMPOSIA FOUNDATION MARCEL MERIEUX) LA English DT Proceedings Paper CT 26th Conference on Transplantation and Clinical Immunology CY JUN 13-15, 1994 CL LYON, FRANCE SP Fdn Marcel Merieux, Univ Claude Bernard Lyon I C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-3179-6 J9 TRANSP CL IMMUN SFMM PY 1995 VL 26 BP 301 EP 308 PG 8 WC Immunology; Transplantation SC Immunology; Transplantation GA BD52Y UT WOS:A1995BD52Y00039 ER PT S AU SAAVEDRA, RA KIMBRO, SK STERN, DN SCHNUER, J ASHKAR, S GLIMCHER, MJ LJUBETIC, CI AF SAAVEDRA, RA KIMBRO, SK STERN, DN SCHNUER, J ASHKAR, S GLIMCHER, MJ LJUBETIC, CI BE Denhardt, DT Butler, WT Chambers, AF Senger, DR TI GENE-EXPRESSION AND PHOSPHORYLATION OF MOUSE OSTEOPONTIN SO OSTEOPONTIN: ROLE IN CELL SIGNALLING AND ADHESION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Osteopontin - Role in Cell Signalling and Adhesion CY OCT 21-23, 1994 CL NEW BRUNSWICK, NJ SP New York Acad Sci ID RAT-KIDNEY CELLS; DEVELOPMENTAL EXPRESSION; SECRETED PHOSPHOPROTEIN; ESCHERICHIA-COLI; NEOPLASTIC TRANSFORMATION; PHYSIOLOGICAL-PROPERTIES; NONPHOSPHORYLATED FORMS; TUMOR PROMOTER; BONE; SEQUENCE C1 HARVARD UNIV,SCH MED,DEPT ORTHOPAED SURG,BOSTON,MA 02115. FORSYTH DENT CTR,BOSTON,MA 02115. RP SAAVEDRA, RA (reprint author), CHILDRENS HOSP,ENDERS PEDIAT RES CTR,STUDY SKELETAL DISORDERS & REHAB LAB,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIAMS NIH HHS [P01AR34078, T32AR07112, IR29AR41046]; NIMHD NIH HHS [P20 MD000175] NR 36 TC 5 Z9 5 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-939-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 760 BP 35 EP 43 DI 10.1111/j.1749-6632.1995.tb44618.x PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics GA BD12E UT WOS:A1995BD12E00005 PM 7540379 ER PT S AU CANTOR, H AF CANTOR, H BE Denhardt, DT Butler, WT Chambers, AF Senger, DR TI THE ROLE OF ETA-1/OSTEOPONTIN IN THE PATHOGENESIS OF IMMUNOLOGICAL DISORDERS SO OSTEOPONTIN: ROLE IN CELL SIGNALLING AND ADHESION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Osteopontin - Role in Cell Signalling and Adhesion CY OCT 21-23, 1994 CL NEW BRUNSWICK, NJ SP New York Acad Sci ID SYSTEMIC LUPUS-ERYTHEMATOSUS; B-CELL ACTIVATION; CD4+ T-CELLS; MURINE AUTOIMMUNE-DISEASE; SECRETED PHOSPHOPROTEIN; NEOPLASTIC TRANSFORMATION; INTERFERON-GAMMA; MICE; OSTEOPONTIN; IMMUNODEFICIENCY RP CANTOR, H (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,IMMUNOPATHOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. NR 41 TC 21 Z9 22 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-939-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 760 BP 143 EP 150 DI 10.1111/j.1749-6632.1995.tb44626.x PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics GA BD12E UT WOS:A1995BD12E00013 PM 7785892 ER PT S AU KLEINMAN, JG WORCESTER, EM BESHENSKY, AM SHERIDAN, AM BONVENTRE, JV BROWN, D AF KLEINMAN, JG WORCESTER, EM BESHENSKY, AM SHERIDAN, AM BONVENTRE, JV BROWN, D BE Denhardt, DT Butler, WT Chambers, AF Senger, DR TI UP-REGULATION OF OSTEOPONTIN EXPRESSION BY ISCHEMIA IN RAT-KIDNEY SO OSTEOPONTIN: ROLE IN CELL SIGNALLING AND ADHESION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Osteopontin - Role in Cell Signalling and Adhesion CY OCT 21-23, 1994 CL NEW BRUNSWICK, NJ SP New York Acad Sci C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RENAL UNIT,BOSTON,MA 02129. RP KLEINMAN, JG (reprint author), MED COLL WISCONSIN,VA MED CTR,DIV NEPHROL,MILWAUKEE,WI 53295, USA. NR 5 TC 45 Z9 46 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-939-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 760 BP 321 EP 323 DI 10.1111/j.1749-6632.1995.tb44647.x PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics GA BD12E UT WOS:A1995BD12E00034 PM 7785909 ER PT S AU STERN, DN GLIMCHER, MJ SAAVEDRA, RA AF STERN, DN GLIMCHER, MJ SAAVEDRA, RA BE Denhardt, DT Butler, WT Chambers, AF Senger, DR TI LOCALIZATION OF OSTEOPONTIN DURING MOUSE DEVELOPMENT SO OSTEOPONTIN: ROLE IN CELL SIGNALLING AND ADHESION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Osteopontin - Role in Cell Signalling and Adhesion CY OCT 21-23, 1994 CL NEW BRUNSWICK, NJ SP New York Acad Sci ID EXPRESSION; BONE; RAT; OSTEOCALCIN; PROTEIN; TISSUES; INVITRO C1 FORSYTH DENT CTR,BOSTON,MA 02115. RP STERN, DN (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,ENDERS PEDIAT RES CTR,STUDY SKELETAL DISORDERS LAB,BOSTON,MA 02115, USA. FU NIAMS NIH HHS [P01AR34078, T32ARO7112 (DNS), IR29AR41046] NR 10 TC 5 Z9 5 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-939-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 760 BP 367 EP 370 DI 10.1111/j.1749-6632.1995.tb44659.x PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics GA BD12E UT WOS:A1995BD12E00046 PM 7785919 ER PT J AU WALL, C RAUCH, SD AF WALL, C RAUCH, SD TI PERILYMPH FISTULA PATHOPHYSIOLOGY SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article; Proceedings Paper CT Conference on Clinical Applications of Vestibular Science CY FEB 12-13, 1994 CL UNIV CALIF LOS ANGELES, LOS ANGELES, CA SP NIH, NATL INST DEAFNESS & OTHER COMMUN DISORDERS HO UNIV CALIF LOS ANGELES ID CEREBROSPINAL-FLUID; GEL ELECTROPHORESIS; BETA-2-TRANSFERRIN; IDENTIFICATION; DIAGNOSIS; TESTS AB A great deal of the controversy associated with perilymph fistula is due to the lack of a sensitive, specific way of detecting and thus diagnosing one. The existing subjective, clinical observations need to be replaced with an objective, scientific methodology having higher specificity and sensitivity for the detection of perilymph fistula. Three detection methods presently under development are presented here. One uses a miniendoscope to observe the middle ear. This procedure is less traumatic than inspection with tympanotomy. Thus it is less likely to create artifacts that can be mistaken for a fistula leakage. The ''yes-no'' observation decision is to be replaced with ct graded quantitative measure. The second method concentrates on detected leakage from inner to middle ear. PS-Transferrin, a unique endogenous substance found in perilymph and cerebrospinal fluid, can be detected with one- or two-dimensional gel electrophoresis and immunoblotting. The third method is a system identification fistula test. It measures a change in a physiologic response that is caused by the presence of the fistula. Classic biophysical models of the vestibular end organs can be used to predict the dynamics of responses to systems identification stimuli. RP WALL, C (reprint author), MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114, USA. NR 44 TC 14 Z9 15 U1 0 U2 1 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 JAN PY 1995 VL 112 IS 1 BP 145 EP 153 DI 10.1016/S0194-5998(95)70314-4 PG 9 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA QB553 UT WOS:A1995QB55300017 PM 7816449 ER PT J AU NADOL, JB AF NADOL, JB TI VESTIBULAR NEURITIS SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article; Proceedings Paper CT Conference on Clinical Applications of Vestibular Science CY FEB 12-13, 1994 CL UNIV CALIF LOS ANGELES, LOS ANGELES, CA SP NIH, NATL INST DEAFNESS & OTHER COMMUN DISORDERS HO UNIV CALIF LOS ANGELES ID NEURONITIS; VERTIGO; EAR AB Because the cause of vestibular neuritis is unknown, this disorder is best understood as a constellation of characteristic clinical symptoms and signs. The differential diagnosis includes peripheral otologic disorders, including Meniere's disease, perilymph fistula, and vestibular atelectasis; and central disorders, including vascular insufficiency, acoustic neuroma, migraine equivalent, paraneoplastic syndrome, metastatic carcinoma, and multiple sclerosis. The site of lesion, as evaluated by clinical signs and symptoms, is controversial because concomitant central nervous system abnormalities have been described. The histopathology of temporal bones from persons who in life had symptoms characteristic of vestibular neuritis demonstrates degeneration of branches of the vestibular nerve and the neuroepithelium of vestibular end organs. Possible causes of vestibular neuritis include viral or other infectious agents and vascular or immune-mediated disorders. The natural history of this disorder is variable. In some patients complete recovery of acute signs and symptoms, including loss of vestibular response, is seen, whereas in others permanent changes have been reported. Initial treatment is generally symptomatic only. Patients with poor recovery may benefit from vestibular rehabilitation or, occasionally, from surgical intervention. The elucidation of the pathogenesis of vestibular neuritis and the development of logical guidelines for individual rehabilitation are needed. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA. RP NADOL, JB (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 46 TC 51 Z9 57 U1 1 U2 8 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 JAN PY 1995 VL 112 IS 1 BP 162 EP 172 DI 10.1016/S0194-5998(95)70316-0 PG 11 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA QB553 UT WOS:A1995QB55300019 PM 7816452 ER PT B AU KOCHEVAR, IE AF KOCHEVAR, IE BE Dubertret, L Santus, R Morliere, P TI Photochemical and radical induced damage to proteins and lipids SO OZONE SUN CANCER: MOLECULAR AND CELLULAR MECHANISMS PREVENTION LA English DT Proceedings Paper CT International Symposium on Ozone Sun Cancer - Molecular and Cellular Mechanisms Prevention CY MAY 17-20, 1994 CL PARIS, FRANCE SP Minist Environm, Paris, INSERM, Museum Natl Hist Nat, European & French Soc Photobiol, Fdn Rene Touraine C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS INSERM PI PARIS PA 101 RUE DE TOLBIAC, 75654 PARIS, FRANCE BN 2-85598-582-X PY 1995 BP 47 EP 50 PG 4 WC Oncology SC Oncology GA BD54T UT WOS:A1995BD54T00009 ER PT B AU KOLLIAS, N AF KOLLIAS, N BE Dubertret, L Santus, R Morliere, P TI Aspects of photoprotection by epidermal melanin pigmentation at the molecular, cellular and organ levels: A review SO OZONE SUN CANCER: MOLECULAR AND CELLULAR MECHANISMS PREVENTION LA English DT Proceedings Paper CT International Symposium on Ozone Sun Cancer - Molecular and Cellular Mechanisms Prevention CY MAY 17-20, 1994 CL PARIS, FRANCE SP Minist Environm, Paris, INSERM, Museum Natl Hist Nat, European & French Soc Photobiol, Fdn Rene Touraine C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 1 U2 2 PU EDITIONS INSERM PI PARIS PA 101 RUE DE TOLBIAC, 75654 PARIS, FRANCE BN 2-85598-582-X PY 1995 BP 187 EP 198 PG 12 WC Oncology SC Oncology GA BD54T UT WOS:A1995BD54T00032 ER PT J AU GOUDSOUZIAN, NG AF GOUDSOUZIAN, NG TI REPORT ON THE FIRST JOINT MEETING OF THE SOCIETY-OF-PEDIATRIC-ANESTHESIA AND THE AMERICAN-ACADEMY-OF-PEDIATRICS, FEBRUARY 17-19, 1995, PHOENIX, ARIZONA, USA SO PAEDIATRIC ANAESTHESIA LA English DT Editorial Material RP GOUDSOUZIAN, NG (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARNETTE-BLACKWELL S A PI PARIS PA 1, RUE DE LILLE, 75007 PARIS, FRANCE SN 1155-5645 J9 PAEDIATR ANAESTH JI Paediatr. Anaesth. PY 1995 VL 5 IS 5 BP 330 EP 330 DI 10.1111/j.1460-9592.1995.tb00317.x PG 1 WC Anesthesiology; Pediatrics SC Anesthesiology; Pediatrics GA RU273 UT WOS:A1995RU27300014 ER PT S AU HOSLER, BA BROWN, RH AF HOSLER, BA BROWN, RH BE Serratrice, GT Munsat, TL TI COPPER/ZINC SUPEROXIDE-DISMUTASE MUTATIONS AND FREE-RADICAL DAMAGE IN AMYOTROPHIC-LATERAL-SCLEROSIS SO PATHOGENESIS AND THERAPY OF AMYOTROPHIC LATERAL SCLEROSIS SE ADVANCES IN NEUROLOGY LA English DT Article; Proceedings Paper CT Conference on Pathogenesis and Therapy of Amyotrophic Lateral Sclerosis CY OCT 28-29, 1994 CL MARSEILLE, FRANCE ID MITOCHONDRIAL ENERGY-METABOLISM; MOTOR-NEURON DISEASE; GENE; PATHOLOGY; DEFECTS RP HOSLER, BA (reprint author), MASSACHUSETTS GEN HOSP EAST,DEPT NEUROL,BOSTON,MA 02129, USA. FU NINDS NIH HHS [1P01NS31248, NS31248-01] NR 24 TC 12 Z9 12 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA E WASHINGTON SQ, PHILADELPHIA, PA 19105 SN 0091-3952 BN 0-7817-0333-6 J9 ADV NEUROL JI Adv.Neurol. PY 1995 VL 68 BP 41 EP 46 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA BE25C UT WOS:A1995BE25C00005 PM 8787241 ER PT J AU OLSTAD, OK JEMTLAND, R LOSETH, OP BRINGHURST, FR GAUTVIK, KM AF OLSTAD, OK JEMTLAND, R LOSETH, OP BRINGHURST, FR GAUTVIK, KM TI EXPRESSION AND CHARACTERIZATION OF A RECOMBINANT HUMAN PARATHYROID-HORMONE PARTIAL AGONIST WITH ANTAGONISTIC PROPERTIES - GLY-HPTH(-1-]+84) SO PEPTIDES LA English DT Article DE RECOMBINANT PARATHYROID HORMONES; RECOMBINANT PTH/PTHRP RECEPTOR; CAMP RESPONSE; ANTAGONISM ID OSTEO-SARCOMA CELLS; PROTEIN-KINASE-C; ESCHERICHIA-COLI; RECEPTOR-BINDING; SACCHAROMYCES-CEREVISIAE; BIOLOGICAL-ACTIVITY; PEPTIDE; BONE; ACTIVATION; MEMBRANES AB We have produced and characterized a hPTH analogue with an amino-terminal extension of glycine, Gly-hPTH(-1-->+84) (denoted Gly-hPTH). The hormone analogue was synthesized in E. coli strain BJ5183 transformed with the expression plasmid pKKPTH, extracted from the bacterial pellet and purified by reverse-phase high performance liquid chromatography. Its chemical nature, as determined by amino acid composition analysis, N-terminal amino acid analysis, and mass spectrometry, showed the 9480-Da Gly-hPTH as the predominant species. Because f-Met-Gly-hPTH was the expected form encoded by the plasmid construct, the results indicate that the f-Met residue was efficiently removed from the precurser form. The following functional characteristics of Gly-hPTH were demonstrated. 1) In cells transfected with the human PTH/PTHrP receptor, the receptor binding affinity was reduced threefold compared to the authentic hPTH(1-84) produced by Saccharomyces cerevisiae (apparent K(d)s: 8.4 and 2.7 nM, respectively). 2) Using the same cells, Gly-hPTH showed 27-fold reduced potency compared to hPTH(1-84) in stimulating intracellular cAMP production (EC(50): 32 and 1.2 nM, respectively). 3) Gly-hPTH demonstrated an tagonist activity by reducing hPTH-induced cAMP production by 33 +/- 5% (mean +/- SD) when tested at a 1:1 molar ratio. In these studies the recombinant authentic hPTH(1-84) was used as standard for comparisons, and it showed an equal receptor binding affinity and cAMP production as the chemically synthesized peptide [Nle(8.18),Tyr(34)]bovinePTH(1-34)-NH2. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114. RP OLSTAD, OK (reprint author), UNIV OSLO,INST MED BIOCHEM,POB 1112 BLINDERN,N-0317 OSLO,NORWAY. NR 51 TC 2 Z9 4 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0196-9781 J9 PEPTIDES JI Peptides PY 1995 VL 16 IS 6 BP 1031 EP 1037 DI 10.1016/0196-9781(95)00069-V PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA RU938 UT WOS:A1995RU93800006 PM 8532584 ER PT J AU KATO, K MARTINEZ, V STPIERRE, S TACHE, Y AF KATO, K MARTINEZ, V STPIERRE, S TACHE, Y TI CGRP ANTAGONISTS ENHANCE GASTRIC-ACID SECRETION IN 2-H PYLORUS-LIGATED RATS SO PEPTIDES LA English DT Article DE CGRP; CGRP(8-37); CGRP ANTIBODY; GASTRIC ACID SECRETION; PYLORUS LIGATION; PENTAGASTRIN ID GENE-RELATED PEPTIDE; THYROTROPIN-RELEASING-HORMONE; SENSORY NEURONS; MONOCLONAL-ANTIBODY; CALCITONIN; CAPSAICIN; INHIBITION; STOMACH; IMMUNONEUTRALIZATION; AFFERENT AB The influence of calcitonin gene-related peptide (CGRP) antagonists on gastric acid secretion was investigated in rats. Intravenous injection of the CGRP receptor antagonist, CGRP(8-37)(128 nmol/kg) or the CGRP antibody #4901 (4.8 mg/kg, IV) completely prevented alpha-CGRP (3.9 nmol/kg/h)-induced inhibition of acid response to pentagastrin in urethane-anesthetized rats with gastric fistula. CGRP antibody (4.8 mg/kg, IV) increased by 93% gastric acid secretion in conscious rats with pylorus ligation for 2 h. CGRP(8-37) (128 nmol/kg, IV) also enhanced the acid response measured 2 h after pylorus ligation in conscious rats and in urethane-anesthetized rats infused with pentagastrin by 91% and 56%, respectively. These results suggest that endogenous CGRP attenuates the gastric acid response measured 2 h after pylorus ligation. C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CTR ULCER RES & EDUC,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90073. UNIV QUEBEC,INST NATL RECH SCI SANTE,POINTE CLAIRE,PQ H9R 1G6,CANADA. RI Martinez, Vicente/N-1189-2014 FU NIDDK NIH HHS [DK-41301, DK-30110]; NIMH NIH HHS [MH-00663] NR 38 TC 23 Z9 23 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0196-9781 J9 PEPTIDES JI Peptides PY 1995 VL 16 IS 7 BP 1257 EP 1262 DI 10.1016/0196-9781(95)02004-G PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA TA633 UT WOS:A1995TA63300014 PM 8545247 ER PT J AU MILLER, M HAROUTUNIAN, V WILTSHIRECLEMENT, M AF MILLER, M HAROUTUNIAN, V WILTSHIRECLEMENT, M TI ALTERED ALERTNESS OF VASOPRESSIN-SECRETING TRANSGENIC MICE SO PEPTIDES LA English DT Article DE ADH; AVP; BEHAVIOR; EMOTIONALITY; LEARNING; MEMORY; TRANSGENIC MICE; VASOPRESSIN ID DEFICIENT BRATTLEBORO RAT; BRIGHTNESS-DISCRIMINATION; BEHAVIOR; OXYTOCIN; MEMORY; REVERSAL; PEPTIDES; GENE AB We evaluated behavior and cognitive performance in a line of transgenic mice that overexpress the rat gene for vasopressin. Open field testing revealed greatest habituation in homozygous mice. Passive avoidance performance indicated equal learning and memory ability of transgenic compared to normal mice. Drinking behavior following exposure to 10% sucrose solution suggested diminished neophobia in homozygous mice. These observations are consistent with enhanced attention and alertness in the transgenic animals and support prior observations on the effects of vasopressin on behavior and cognitive function. C1 CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029. BRONX VET AFFAIRS MED CTR,NEW YORK,NY 10029. RP MILLER, M (reprint author), CUNY MT SINAI SCH MED,DEPT GERIATR & ADULT DEV,BOX 1070,1 GUSTAVE L LEVY PL,NEW YORK,NY 10029, USA. NR 29 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0196-9781 J9 PEPTIDES JI Peptides PY 1995 VL 16 IS 8 BP 1329 EP 1333 DI 10.1016/0196-9781(95)02047-0 PG 5 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA TK330 UT WOS:A1995TK33000002 PM 8745040 ER PT J AU Calder, AJ Young, AW Perrett, DI Etcoff, N Rowland, D AF Calder, A. J. Young, A. W. Perrett, D. I. Etcoff, N. Rowland, D. TI Perception of morphed facial expressions is categorical, not continuous SO PERCEPTION LA English DT Meeting Abstract C1 [Young, A. W.] MRC, Appl Psychol Unit, Cambridge CB2 2EF, England. [Calder, A. J.] Univ Durham, Sci Labs, Dept Psychol, Durham DH1 3LE, England. [Perrett, D. I.; Rowland, D.] Univ St Andrews, Dept Psychol, St Andrews KY16 9JU, Fife, Scotland. [Etcoff, N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02116 USA. [Etcoff, N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA 02116 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 1995 VL 24 SU S BP 73 EP 74 PG 2 WC Ophthalmology; Psychology; Psychology, Experimental SC Ophthalmology; Psychology GA V17AM UT WOS:000207910100220 ER PT J AU Bricolo, E Mendola, JD Cole, AJ Cosgrove, GR Corkin, S Bulthoff, HH AF Bricolo, E. Mendola, J. D. Cole, A. J. Cosgrove, G. R. Corkin, S. Buelthoff, H. H. TI Impairment of immediate visual recognition after unilateral temporal lobectomy SO PERCEPTION LA English DT Meeting Abstract C1 [Bricolo, E.; Mendola, J. D.; Corkin, S.] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA. [Bricolo, E.; Mendola, J. D.; Corkin, S.] MIT, Clin Res Ctr, Cambridge, MA 02139 USA. [Cole, A. J.; Cosgrove, G. R.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. [Cole, A. J.; Cosgrove, G. R.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA. [Buelthoff, H. H.] Max Planck Inst Biol Kybernet, D-72076 Tubingen, Germany. EM emanuela@ai.mit.edu RI Bulthoff, Heinrich/J-6579-2012 OI Bulthoff, Heinrich/0000-0003-2568-0607 NR 0 TC 0 Z9 0 U1 0 U2 0 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 1995 VL 24 SU S BP 113 EP 114 PG 2 WC Ophthalmology; Psychology; Psychology, Experimental SC Ophthalmology; Psychology GA V17AM UT WOS:000207910100337 ER PT J AU EJAZ, AA MCSHANE, AP GANDHI, VC LEEHEY, DJ ING, TS AF EJAZ, AA MCSHANE, AP GANDHI, VC LEEHEY, DJ ING, TS TI HYPOMAGNESEMIA IN CONTINUOUS AMBULATORY PERITONEAL-DIALYSIS PATIENTS DIALYZED WITH A LOW-MAGNESIUM PERITONEAL-DIALYSIS SOLUTION SO PERITONEAL DIALYSIS INTERNATIONAL LA English DT Article DE HYPOMAGNESEMIA; MAGNESIUM AB Objective: Previous studies have shown a decrease in serum magnesium (Mg) concentration when continuous ambulatory peritoneal dialysis (CAPD) patients previously maintained on a 1.0 - 1.2 mEq/L Mg peritoneal dialysis solution (PDS) were dialyzed with a 0.5 mEq/L Mg PDS. However, the prevalence of hypomagnesemia in CAPD patients dialyzed with low-Mg PDS is unknown. Design: A retrospective study to determine the prevalence of hypomagnesemia and the factors associated with its occurrence in CAPD patients dialyzed using a 0.5 mEq/L Mg PDS. Setting: A CAPD unit in a large Veterans Affairs Hospital. Patients: All our CAPD patients (33) enrolled over a 52-month period. Results: All patients had serum magnesium levels higher than 1.25 mEq/L prior to use of low-Mg PDS, Hypomagnesemia (serum Mg <1.25 mEq/L) developed in 21/33 patients (64%) when a 0.5 mEq/L Mg PDS was employed. Hypomagnesemia developed a mean of 8.2 months after beginning treatments. The duration of dialysis and the number of episodes of peritonitis did not differ between patients with and those without hypomagnesemia. Serum albumin levels were significantly lower in patients with hypomagnesemia (2.5+/-0.12 g/dL vs 3.2+/-0.12, p <0.01). Magnesium supplements were given to 13 patients; following this therapy, serum magnesium values became normal. Conclusions: CAPD patients dialyzed with a 0.5 mEq/L Mg PDS may develop a considerable fall in serum magnesium level and may require magnesium supplements in order to restore normal serum values. C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,DEPT MED,HINES,IL 60141. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. NR 28 TC 30 Z9 30 U1 0 U2 0 PU MULTIMED INC PI TORONTO PA 1120 FINCH AVE WEST SUITE 601, TORONTO ON M3J 3H7, CANADA SN 0896-8608 J9 PERITON DIALYSIS INT JI Perit. Dial. Int. PY 1995 VL 15 IS 1 BP 61 EP 64 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA QH586 UT WOS:A1995QH58600011 PM 7734563 ER PT B AU GOITEIN, M AF GOITEIN, M BE Kogelnik, HD TI Lessons to be learned from proton beam therapy SO PROGRESS IN RADIO-ONCOLOGY V LA English DT Proceedings Paper CT 5th International Meeting on Progress in Radio-Oncology (ICRO/OGRO 5) CY MAY 10-14, 1995 CL SALZBURG, AUSTRIA SP Austria Soc Radio Oncol Radiobiol & Med Radiophys, Austria Int Club Radio Oncologists C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MONDUZZI EDITORE PI 40128 BOLOGNA PA VIA FERRARESE 119/2, 40128 BOLOGNA, ITALY BN 88-323-0510-2 PY 1995 BP 667 EP 672 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA BD79Z UT WOS:A1995BD79Z00102 ER PT J AU SZOSTAK, JW BARTEL, DP WILSON, C LORSCH, J CHAPMAN, K AF SZOSTAK, JW BARTEL, DP WILSON, C LORSCH, J CHAPMAN, K TI SEARCHING RNA SEQUENCE SPACE FOR NEW RIBOZYMES SO PROTEIN ENGINEERING LA English DT Article; Proceedings Paper CT 1995 Miami Bio/Technology Winter Symposium - Advances in Gene Technology: Protein Engineering and Structural Biology CY FEB 04-09, 1995 CL MIAMI, FL SP Univ Miami, Nature Publishing Co RP SZOSTAK, JW (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PY 1995 VL 8 SU S BP 3 EP 3 PG 1 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA RL742 UT WOS:A1995RL74200006 ER PT J AU OKIN, RL BORUS, JF BAER, L JONES, AL AF OKIN, RL BORUS, JF BAER, L JONES, AL TI LONG-TERM OUTCOME OF STATE-HOSPITAL PATIENTS DISCHARGED INTO STRUCTURED COMMUNITY RESIDENTIAL SETTINGS SO PSYCHIATRIC SERVICES LA English DT Article ID SEVERE MENTAL-ILLNESS; FOLLOW-UP; REVOLVING DOOR; 1ST ADMISSIONS; SCHIZOPHRENIA; PROGNOSIS; METHODOLOGY; RECIDIVISM; PREDICTION; COHORT AB Objective: This longitudinal study examined various dimensions of the lives of patients with chronic mental illness immediately before and again several years after their discharge from a state hospital into well-staffed structured community residential settings. Methods: Fifty-three patients with chronic mental illness and long histories of hospitalization were evaluated shortly before their state hospital discharge using a comprehensive structured assessment of nine dimensions of functioning and symptomatology. A follow-up assessment was undertaken a mean of 7.5 years after discharge into four structured group home settings. Results: At follow-up, 57 percent of the patients continued to live in structured community residential settings, 28 percent had moved on to independent living, and 16 percent had returned to an institutional setting. Fifty-five percent needed hospital readmission, but the total sample spent only I I percent of the time after discharge in the hospital. At follow-up, patients showed significant improvements in cognitive and social functioning, and 94 percent expressed a preference for life in the community. Conclusions: Many patients discharged to structured community residential settings seem to prefer them to the state hospital, are able to graduate to independent settings, and show improvement in important dimensions of functioning after several years in the community. Other dimensions seem resistant to change despite the structure and support afforded by residential settings. C1 SAN FRANCISCO GEN HOSP,SAN FRANCISCO,CA 94110. HARVARD UNIV,SCH MED,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT PSYCHIAT,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,COMP UNIT,BOSTON,MA 02114. RHODE ISL DEPT HLTH,PROVIDENCE,RI. RP OKIN, RL (reprint author), UNIV CALIF SAN FRANCISCO,DEPT PSYCHIAT,SAN FRANCISCO,CA 94143, USA. RI McCarthy, Jodie/B-5760-2012 NR 28 TC 35 Z9 36 U1 2 U2 3 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1075-2730 J9 PSYCHIATR SERV JI Psychiatr. Serv. PD JAN PY 1995 VL 46 IS 1 BP 73 EP 78 PG 6 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA QL268 UT WOS:A1995QL26800015 PM 7895127 ER PT J AU WORTHINGTON, J FAVA, M DAVIDSON, K ALPERT, J NIERENBERG, AA ROSENBAUM, JF AF WORTHINGTON, J FAVA, M DAVIDSON, K ALPERT, J NIERENBERG, AA ROSENBAUM, JF TI PATTERNS OF IMPROVEMENT IN DEPRESSIVE SYMPTOMS WITH FLUOXETINE TREATMENT SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article DE DEPRESSION; IMPROVEMENT; FLUOXETINE; TREATMENT RESPONSE; NEUROVEGETATIVE ID AMITRIPTYLINE AB By definition, patients who respond to antidepressant treatment show significant improvements in most, if not all, of their depressive symptoms. We assessed the patterns of change in depressed outpatients treated openly with fluoxetine 20 mg/day for 8 weeks. We studied 62 depressed outpatients with major depressive disorder who showed full response following fluoxetine treatment. Analysis of the data revealed that the symptoms that tended to improve relatively early during treatment were suicidal ideation, excessive guilt, and lack of appetite. Our tentative conclusion from this pilot study was that symptom improvement tends to occur in both cognitive and neurovegetative areas early in treatment as well as later. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP WORTHINGTON, J (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,DEPRESS RES PROGRAM,WAC-815,15 PARKMAN ST,BOSTON,MA 02114, USA. OI Alpert, Jonathan/0000-0002-4332-908X FU NIMH NIH HHS [MH-48483] NR 14 TC 26 Z9 26 U1 0 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1995 VL 31 IS 2 BP 223 EP 226 PG 4 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA TF595 UT WOS:A1995TF59500005 PM 7491372 ER PT J AU SHEAR, MK LEON, AC POLLACK, MH ROSENBAUM, JF KELLER, MB AF SHEAR, MK LEON, AC POLLACK, MH ROSENBAUM, JF KELLER, MB TI PATTERN OF PLACEBO-RESPONSE IN PANIC DISORDER SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article DE PLACEBO; PANIC DISORDER; PHARMACOTHERAPY; DEPRESSION; REMISSION ID TERM TREATMENT; ALPRAZOLAM; IMIPRAMINE; AGORAPHOBIA AB This study characterizes the pattern of placebo response in depressed panic disorder patients who participated in a randomized clinical trial, We compared placebo-treated subjects whose panic attacks remitted, with those whose attacks did not remit, and with remitting and nonremitting subjects treated with active medication. Seventy-one subjects who mat criteria for panic disorder and for a concurrent depressive diagnosis (major depression, dysthymia, or depressive disorder not otherwise specified [NOS]) were treated with either imipramine (n=36) or alprazolam (n=35), and 28 patients were treated with placebo. Sixteen placebo-treated and 40 medication-treated patients were panic free at Week 8. Placebo panic remitters were significantly more ill than active-medication remitters on all measures, In contrast, subjects who achieved panic remission on placebo showed no difference on other clinical measures from active medication nonremitters, and little difference from placebo nonremitters. Results support the need for assessment of all core panic disorder symptoms in determining treatment efficacy and in considerations of response and remission. C1 CORNELL UNIV MED COLL,DEPT PSYCHIAT,DEPT BIOSTAT PSYCHIAT,NEW YORK,NY. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DIV OUTPATIENT PSYCHIAT,BOSTON,MA 02114. BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. RP SHEAR, MK (reprint author), UNIV PITTSBURGH,WESTERN PSYCHIAT INST & CLIN,DEPT PSYCHIAT,3811 OHARA ST,PITTSBURGH,PA 15213, USA. FU NIMH NIH HHS [R01 MH051415] NR 19 TC 15 Z9 15 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1995 VL 31 IS 2 BP 273 EP 278 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA TF595 UT WOS:A1995TF59500012 PM 7491379 ER PT J AU Nelson, JC Docherty, JP Henschen, GM Kasper, S Nierenberg, AA Ward, NG AF Nelson, JC Docherty, JP Henschen, GM Kasper, S Nierenberg, AA Ward, NG TI International psychopharmacology algorithm project report .C. Algorithms for the treatment of subtypes of unipolar major depression SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article C1 NATL MED ENTERPRISES INC,WASHINGTON,DC. GREENSBORO PSYCHIAT CTR,GREENSBORO,NC. UNIV VIENNA,A-1010 VIENNA,AUSTRIA. MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. UNIV WASHINGTON,SEATTLE,WA 98195. RP Nelson, JC (reprint author), YALE UNIV,NEW HAVEN,CT, USA. NR 0 TC 17 Z9 17 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1995 VL 31 IS 3 BP 475 EP 482 PG 8 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA TR743 UT WOS:A1995TR74300005 PM 8668752 ER PT J AU Jobson, KO Davidson, JRT Lydiard, RB McCann, UD Pollack, MH Rosenbaum, JF AF Jobson, KO Davidson, JRT Lydiard, RB McCann, UD Pollack, MH Rosenbaum, JF TI International psychopharmacology algorithm project report .D. Algorithm for the treatment of panic disorder with agoraphobia SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article C1 DUKE UNIV,MED CTR,DURHAM,NC. MED UNIV S CAROLINA,CHARLESTON,SC 29425. NIMH,INTRAMURAL RES PROGRAM,BIOL PSYCHIAT BRANCH,UNIT ANXIETY & AFFECT DISORDERS,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. RP Jobson, KO (reprint author), TENNESSEE PSYCHIAT & PSYCHOPHARMACOL CLIN,KNOXVILLE,TN, USA. NR 0 TC 15 Z9 15 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1995 VL 31 IS 3 BP 483 EP 485 PG 3 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA TR743 UT WOS:A1995TR74300006 PM 8668753 ER PT J AU Jefferson, JW Altemus, M Jenike, MA Pigott, TA Stein, DJ Griest, JH AF Jefferson, JW Altemus, M Jenike, MA Pigott, TA Stein, DJ Griest, JH TI International psychopharmacology algorithm project report .E. Algorithm for the treatment of obsessive-compulsive disorder (OCD) SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article C1 FDN HLTH RES & EDUC,MADISON,WI. NIMH,INTRAMURAL RES PROGRAM,CLIN NEUROPHARMACOL BRANCH,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,BOSTON,MA. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77550. UNIV STELLENBOSCH,TYGERBERG 7505,SOUTH AFRICA. RP Jefferson, JW (reprint author), UNIV WISCONSIN,MADISON,WI 53706, USA. RI Stein, Dan/A-1752-2008 OI Stein, Dan/0000-0001-7218-7810 NR 0 TC 10 Z9 11 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1995 VL 31 IS 3 BP 487 EP 490 PG 4 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA TR743 UT WOS:A1995TR74300007 PM 8668754 ER PT J AU JACOBSON, AM AF JACOBSON, AM TI HEALTH-CARE SEEKING BEHAVIOR - IMPLICATIONS FOR THE PRIMARY-CARE PHYSICIAN SO PSYCHOSOMATIC MEDICINE LA English DT Editorial Material RP JACOBSON, AM (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK27845, DK24315] NR 5 TC 3 Z9 3 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0033-3174 J9 PSYCHOSOM MED JI Psychosom. Med. PD JAN-FEB PY 1995 VL 57 IS 1 BP 48 EP 49 PG 2 WC Psychiatry; Psychology; Psychology, Multidisciplinary SC Psychiatry; Psychology GA QE074 UT WOS:A1995QE07400007 PM 7732158 ER PT J AU LITTMAN, AB AF LITTMAN, AB TI USE OF SEROTONERGIC (5-HT) AGENTS IN THE TREATMENT OF PATIENTS WITH CORONARY-ARTERY DISEASE (CAD) SO PSYCHOSOMATIC MEDICINE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0033-3174 J9 PSYCHOSOM MED JI Psychosom. Med. PD JAN-FEB PY 1995 VL 57 IS 1 BP 58 EP 58 PG 1 WC Psychiatry; Psychology; Psychology, Multidisciplinary SC Psychiatry; Psychology GA QE074 UT WOS:A1995QE07400017 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI THE BODY SPEAKS - THERAPEUTIC DIALOGS FOR MIND-BODY PROBLEMS - GRIFFITH,JL, GRIFFITH,MG SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GREENBERG, DB (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JAN-FEB PY 1995 VL 36 IS 1 BP 78 EP 79 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA PZ733 UT WOS:A1995PZ73300013 ER PT J AU FALK, W AF FALK, W TI DEMENTIA - PRESENTATIONS, DIFFERENTIAL-DIAGNOSIS AND NOSOLOGY - OLGA,V, EMERY,B, OXMAN,TE SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FALK, W (reprint author), MASSACHUSETTS GEN HOSP,BGERIATR NEUROBEH CLIN,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JAN-FEB PY 1995 VL 36 IS 1 BP 79 EP 80 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA PZ733 UT WOS:A1995PZ73300014 ER PT J AU KEUTHEN, NJ OSULLIVAN, RL RICCIARDI, JN SHERA, D SAVAGE, CR BORGMANN, AS JENIKE, MA BAER, L AF KEUTHEN, NJ OSULLIVAN, RL RICCIARDI, JN SHERA, D SAVAGE, CR BORGMANN, AS JENIKE, MA BAER, L TI THE MASSACHUSETTS-GENERAL-HOSPITAL (MGH) HAIRPULLING SCALE .1. DEVELOPMENT AND FACTOR-ANALYSES SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Article DE HAIRPULLING; TRICHOTILLOMANIA; SELF-REPORT SCALE ASSESSMENT ID OBSESSIVE-COMPULSIVE SCALE; TRICHOTILLOMANIA AB We developed the MGH Hairpulling Scale to provide a brief, self-report instrument for assessing repetitive hairpulling. Seven individual items, rated for severity from 0 to 4, assess urges to pull, actual pulling, perceived control, and associated distress. We administered the scale to 119 consecutive patients with chronic hairpulling. Statistical analyses indicate that the seven items form a homogenous scale for the measurement of severity in this disorder. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP KEUTHEN, NJ (reprint author), MASSACHUSETTS GEN HOSP EAST,OBSESS COMPULS DISORDERS CLIN & RES UNIT,149 13TH ST,BOSTON,MA 02129, USA. RI Citations, TLC SAB/C-4006-2011 NR 8 TC 166 Z9 167 U1 3 U2 7 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1995 VL 64 IS 3-4 BP 141 EP 145 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA TK038 UT WOS:A1995TK03800004 PM 8657844 ER PT J AU ALPERT, JE UEBELACKER, LA MCLEAN, NE ABRAHAM, M ROSENBAUM, JF FAVA, M AF ALPERT, JE UEBELACKER, LA MCLEAN, NE ABRAHAM, M ROSENBAUM, JF FAVA, M TI THE MINI-MENTAL-STATE-EXAMINATION AMONG ADULT OUTPATIENTS WITH MAJOR DEPRESSIVE DISORDER SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Article DE NEUROPSYCHIATRIC TESTING; DEPRESSION; MINI MENTAL STATE EXAMINATION; COGNITION; FLUOXETINE AB One hundred forty-eight patients, ages 18-65, with major depression were administered the Mini-Mental State Examination (MMSE) prior to 8 weeks of treatment with fluoxetine; 75 of these patients were readministered the MMSE following treatment. MMSE scores were not related to pretreatment severity of depression or to reported concentration problems and were not predicitve of antidepressant response. Non- and partial responders had lower posttreatment MMSE scores than responders, men had lower posttreatment scores than women, and subjects over 50 had lower pretreatment scores than younger subjects, although in all cases, the magnitude of the differences was small and unlikely to be clinically important. Our results suggest that while the MMSE has been shown to be useful among geriatric and other depressed inpatients, it is not a sensitive indicator of depression severity, concentration problems, or likelihood of treatment response among otherwise healthy adults with major depression in an outpatient setting. RP ALPERT, JE (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT WACC 815,DEPRESS RES PROGRAM,15 PARKMAN ST,BOSTON,MA 02114, USA. OI Alpert, Jonathan/0000-0002-4332-908X FU NIMH NIH HHS [5 R01 MH48403-03] NR 7 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1995 VL 63 IS 3-4 BP 207 EP 211 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA QY565 UT WOS:A1995QY56500012 PM 7624468 ER PT B AU SPITZER, TR AF SPITZER, TR BE Dubois, AA King, GL Livengood, DR TI CLINICAL ASPECTS OF IRRADIATION-INDUCED ALIMENTARY TRACT INJURY SO RADIATION AND THE GASTROINTESTINAL TRACT LA English DT Proceedings Paper CT International Symposium on Radiation and the Gastrointestinal Trace CY SEP 16-17, 1993 CL BETHESDA, MD SP ARMED FORCES RADIOBIOL RES INST, UNIFORMED SERV UNIV HLTH SCI C1 MASSACHUSETTS GEN HOSP,BONE MARROW TRANSPLANT PROGRAM,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-8493-7667-X PY 1995 BP 3 EP 19 PG 17 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA BC67T UT WOS:A1995BC67T00001 ER PT B AU FLYNN, DF MIHALAKIS, I MAUCERI, T PINS, MR AF FLYNN, DF MIHALAKIS, I MAUCERI, T PINS, MR BE Dubois, AA King, GL Livengood, DR TI GASTROINTESTINAL SYNDROME AFTER ACCIDENTAL OVEREXPOSURE DURING RADIOTHERAPY SO RADIATION AND THE GASTROINTESTINAL TRACT LA English DT Proceedings Paper CT International Symposium on Radiation and the Gastrointestinal Trace CY SEP 16-17, 1993 CL BETHESDA, MD SP ARMED FORCES RADIOBIOL RES INST, UNIFORMED SERV UNIV HLTH SCI C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-8493-7667-X PY 1995 BP 225 EP 234 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA BC67T UT WOS:A1995BC67T00017 ER PT B AU HELD, KD AF HELD, KD BE Fuciarelli, AF Zimbrick, JD TI Use of chemical agent radiation modifiers as probes for mechanisms of radiation damage SO RADIATION DAMAGE IN DNA: STRUCTURE/FUNCTION RELATIONSHIPS AT EARLY TIMES LA English DT Proceedings Paper CT International Workshop on Radiation Damage in DNA - Structure/Function Relationships at Early Times CY OCT 01-06, 1994 CL GLENEDEN BEACH, OR SP Rad Res Soc, Dept Energy, NCI, Battelle, Pacific NW Labs, Life Sci Ctr, Beckman Instruments Inc, Hewlett Packard Inc C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BATTELLE PRESS PI COLUMBUS PA 505 KING AVE, COLUMBUS, OH 43201 BN 0-935470-90-5 PY 1995 BP 357 EP 376 PG 20 WC Biochemistry & Molecular Biology; Biophysics; Chemistry, Medicinal; Chemistry, Organic; Physics, Condensed Matter; Radiology, Nuclear Medicine & Medical Imaging SC Biochemistry & Molecular Biology; Biophysics; Pharmacology & Pharmacy; Chemistry; Physics; Radiology, Nuclear Medicine & Medical Imaging GA BE26M UT WOS:A1995BE26M00037 ER PT J AU BOLAND, GW GOLDBERG, MA LEE, MJ MAYOSMITH, WW DIXON, J MCNICHOLAS, MM MUELLER, PR AF BOLAND, GW GOLDBERG, MA LEE, MJ MAYOSMITH, WW DIXON, J MCNICHOLAS, MM MUELLER, PR TI INDETERMINATE ADRENAL MASS IN PATIENTS WITH CANCER - EVALUATION AT PET WITH 2-[F-18]-FLUORO-2-DEOXY-D-GLUCOSE SO RADIOLOGY LA English DT Article DE ADRENAL GLAND, NEOPLASMS,; ADRENAL GLAND, RADIONUCLIDE STUDIES; EMISSION CT (ECT) ID POSITRON EMISSION TOMOGRAPHY; CELL LUNG-CARCINOMA; COMPUTED-TOMOGRAPHY; COLORECTAL TUMORS; CHEMICAL-SHIFT; MR; DIAGNOSIS; BIOPSY; FLUORINE-18-FLUORODEOXYGLUCOSE; DIFFERENTIATION AB PURPOSE: To evaluate the ability of positron emission tomography (PET) to characterize adrenal masses in patients with cancer. MATERIALS AND METHODS: Twenty-four adrenal masses (size range, 1.5-10.0 cm [mean, 2.8 cm]) in 20 patients (13 men and seven women) with cancer (lung [n = 10], colon [n = 3], lymphoma [n = 3], miscellaneous [n = 4]) were evaluated. PET was performed in fasting patients 45 minutes after infusion of 5-10 mCi (185-370 MBq) of 2-[fluorine-18]-fluoro-2-deoxy-D-glucose (FDG). PET images were correlated with findings at computed tomography (CT), surgery, and/or percutaneous biopsy. RESULTS: Fourteen adrenal masses were proved malignant at surgery fn = 4), biopsy (n = 7), or follow-up (n = 3). Ten lesions were proved benign at biopsy (n = 4) or follow-up CT (n = 6). PET helped correct differentiation of benign from malignant adrenal lesions in all patients. A statistically significant difference (P < .001) was seen between mean tumor-to-background ratios for malignant (mean, 7.4; range, 2.9-16.6; median, 6.9) versus benign (mean, 0.8; range, 0.2-1.2; median, 0.6) adrenal lesions. CONCLUSION: PET helped correct differentiation of benign from malignant adrenal lesions. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 36 TC 169 Z9 176 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JAN PY 1995 VL 194 IS 1 BP 131 EP 134 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA PX684 UT WOS:A1995PX68400026 PM 7997539 ER PT S AU Ravichandran, KS Pratt, JC Sawasdikosol, S Irie, HY Burakoff, SJ AF Ravichandran, KS Pratt, JC Sawasdikosol, S Irie, HY Burakoff, SJ BE Naor, D DeMeyts, P Feldmann, M Schlessinger, J TI Coreceptors and adapter proteins in T-cell signaling SO RECEPTOR ACTIVATION BY ANTIGENS, CYTOKINES, HORMONES, AND GROWTH FACTORS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Receptor Activation by Antigens, Cytokines, Hormones, and Growth Factors CY OCT 21-25, 1994 CL ORLANDO, FL SP New York Acad Sci ID TYROSINE KINASE P56LCK; AMINO-TERMINAL DOMAIN; CROSS-LINKING; ANTIGEN RECEPTOR; PHYSICAL ASSOCIATION; LYMPHOCYTES-T; BINDING-SITE; POSITIVE SELECTION; CYTOPLASMIC DOMAIN; CD4 RECEPTOR C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP Ravichandran, KS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 91 TC 6 Z9 6 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-951-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 766 BP 117 EP 133 DI 10.1111/j.1749-6632.1995.tb26656.x PG 17 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BE40J UT WOS:A1995BE40J00014 PM 7486649 ER PT S AU Wang, DZ McCaffrey, PG Rao, A AF Wang, DZ McCaffrey, PG Rao, A BE Naor, D DeMeyts, P Feldmann, M Schlessinger, J TI The cyclosporin-sensitive transcription factor NFATp is expressed in several classes of cells in the immune system SO RECEPTOR ACTIVATION BY ANTIGENS, CYTOKINES, HORMONES, AND GROWTH FACTORS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Receptor Activation by Antigens, Cytokines, Hormones, and Growth Factors CY OCT 21-25, 1994 CL ORLANDO, FL SP New York Acad Sci ID ACTIVATED T-CELLS; FACTOR-ALPHA GENE; NUCLEAR FACTOR; MAST-CELL; FK506; PROMOTER; BINDING; PROTEIN; COMPLEX; IDENTIFICATION C1 DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,COMM IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA42471]; NIGMS NIH HHS [GM46227] NR 46 TC 47 Z9 47 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-951-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 766 BP 182 EP 194 DI 10.1111/j.1749-6632.1995.tb26661.x PG 13 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BE40J UT WOS:A1995BE40J00019 PM 7486655 ER PT S AU Ravichandran, KS Lorenz, U Shoelson, SE Burakoff, SJ AF Ravichandran, KS Lorenz, U Shoelson, SE Burakoff, SJ BE Naor, D DeMeyts, P Feldmann, M Schlessinger, J TI Interaction of Shc with Grb2 regulates the Grb2 association with mSOS SO RECEPTOR ACTIVATION BY ANTIGENS, CYTOKINES, HORMONES, AND GROWTH FACTORS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Receptor Activation by Antigens, Cytokines, Hormones, and Growth Factors CY OCT 21-25, 1994 CL ORLANDO, FL SP New York Acad Sci ID RECEPTOR TYROSINE KINASES; RAS; DOMAINS C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP Ravichandran, KS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 7 TC 15 Z9 15 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-951-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 766 BP 202 EP 203 DI 10.1111/j.1749-6632.1995.tb26663.x PG 2 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BE40J UT WOS:A1995BE40J00021 PM 7486657 ER PT S AU Kyriakis, JM Woodgett, JR Avruch, J AF Kyriakis, JM Woodgett, JR Avruch, J BE Naor, D DeMeyts, P Feldmann, M Schlessinger, J TI The stress-activated protein kinases - A novel ERK subfamily responsive to cellular stress and inflammatory cytokines SO RECEPTOR ACTIVATION BY ANTIGENS, CYTOKINES, HORMONES, AND GROWTH FACTORS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Receptor Activation by Antigens, Cytokines, Hormones, and Growth Factors CY OCT 21-25, 1994 CL ORLANDO, FL SP New York Acad Sci ID SIGNAL-TRANSDUCTION PATHWAY; DNA-BINDING ACTIVITY; C-JUN; MAP KINASE; PHOSPHORYLATION; INSULIN; DOMAIN; MECHANISM C1 MASSACHUSETTS GEN HOSP EAST,DIABET RES LAB,BOSTON,MA 02129. PRINCESS MARGARET HOSP,ONTARIO CANC INST,DIV CELL & MOLEC BIOL,TORONTO,ON M4X 1K9,CANADA. RI Woodgett, Jim/F-1087-2010 OI Woodgett, Jim/0000-0003-3731-5797 NR 48 TC 59 Z9 59 U1 0 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-951-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 766 BP 303 EP 319 DI 10.1111/j.1749-6632.1995.tb26683.x PG 17 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BE40J UT WOS:A1995BE40J00041 PM 7486678 ER PT S AU Myers, MG Cheatham, B Fisher, TL Jachna, BR Kahn, CR Backer, JM White, MF AF Myers, MG Cheatham, B Fisher, TL Jachna, BR Kahn, CR Backer, JM White, MF BE Naor, D DeMeyts, P Feldmann, M Schlessinger, J TI Common and distinct elements in insulin and PDGF signaling SO RECEPTOR ACTIVATION BY ANTIGENS, CYTOKINES, HORMONES, AND GROWTH FACTORS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Receptor Activation by Antigens, Cytokines, Hormones, and Growth Factors CY OCT 21-25, 1994 CL ORLANDO, FL SP New York Acad Sci ID GROWTH-FACTOR RECEPTOR; TYROSINE KINASE-ACTIVITY; AFFINITY PHOSPHOTYROSYL PEPTIDE; GTPASE-ACTIVATING PROTEIN; PHOSPHATIDYLINOSITOL 3-KINASE; BETA-SUBUNIT; SH3 DOMAINS; FACTOR-I; PHOSPHORYLATION SITES; HEMATOPOIETIC-CELLS C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,PROGRAM CELL & DEV BIOL,BOSTON,MA 02215. ALBERT EINSTEIN COLL MED,DEPT MOLEC PHARMACOL,NEW YORK,NY. FU NIDDK NIH HHS [DK 43828, DK 38712] NR 70 TC 10 Z9 10 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-951-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 766 BP 369 EP 387 DI 10.1111/j.1749-6632.1995.tb26687.x PG 19 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism; Immunology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BE40J UT WOS:A1995BE40J00045 PM 7486683 ER PT J AU HAUG, CE LOPEZ, IA MOORE, RH RUBIN, RH TOLKOFFRUBIN, N DECARETTA, NP COLVIN, RB COSIMI, AB RABITO, CA AF HAUG, CE LOPEZ, IA MOORE, RH RUBIN, RH TOLKOFFRUBIN, N DECARETTA, NP COLVIN, RB COSIMI, AB RABITO, CA TI REAL-TIME MONITORING OF RENAL-FUNCTION DURING ISCHEMIC-INJURY IN THE RHESUS-MONKEY SO RENAL FAILURE LA English DT Article DE ACUTE TUBULAR NECROSIS; GLOMERULAR FILTRATION RATE; KIDNEY TRANSPLANTATION; PROLIFERATING CELL NUCLEAR ANTIGEN; RADIOISOTOPE CLEARANCE AB The presence of delayed graft function (DGF) following cadaver donor renal transplantation is associated with inferior graft survival as well as decreased patient survival. Delay in onset of function eliminates a valuable indicator of allograft viability, which is not easily replaced by standard diagnostic procedures. The purpose of this study was to demonstrate that a new clearance technique could be used to measure renal function minute to minute and under conditions similar to those observed in humans in the immediate posttransplantation period. A monkey model was used to provide controlled conditions. Increasing levels of ischemic injury were produced in 12 Rhesus monkeys by renal hilum cross-clamping. Real-rime measurements of glomerular filtration rate (GFR) were obtained from the rate of clearance of the extracellular fluid of the GFR agent Tc-99m-DTPA, as measured with a specially designed external radioactivity counting device called the ambulatory renal monitor or ARM. GFR was measured every 2-5 min as the slope (k) of the log of activity measured minute to minute versus time. GFR measurements were correlated with blood urea nitrogen (BUN), plasma creatinine (Cr), routine light microscopy, and measurement of proliferating cell nuclear antigen (PCNA), a marker of cell proliferation. Large changes in renal function due to ischemia or ureteral obstruction were observed within minutes. In addition, the rate constant on Day I was predictive of peak serum Cr (R = -0.86, R(2) =.74, p =.0001). Acute tubular necrosis (ATN) resolution was reflected more quickly when using the rare constant (Day I) than when using either BUN or plasma Cr (Day 3-4). Because of renal functional reserve, BUN and plasma Cr were relatively insensitive indicators of mild to moderate reductions in GI;R as compared with the rare constant. We conclude that ARM is a simple method which provides an accurate, near real-time GFR readout with potential applications not only for the clinical management of patients with DGF, but also as a research tool in acute renal failure (ARF). C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. FU NHLBI NIH HHS [P01-HL 18646] NR 0 TC 8 Z9 8 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0886-022X J9 RENAL FAILURE JI Ren. Fail. PY 1995 VL 17 IS 5 BP 489 EP 502 DI 10.3109/08860229509037614 PG 14 WC Urology & Nephrology SC Urology & Nephrology GA RW059 UT WOS:A1995RW05900002 PM 8570862 ER PT B AU GROWDON, JH AF GROWDON, JH BE Iqbal, K Mortimer, JA Winblad, B Wisniewski, HM TI Advances in the diagnosis of Alzheimer's disease SO RESEARCH ADVANCES IN ALZHEIMER'S DISEASE AND RELATED DISORDERS LA English DT Proceedings Paper CT 4th International Conference on Alzheimers Disease and Related Disorders CY JUL 29-AUG 03, 1994 CL MINNEAPOLIS, MN RP MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, WEST SUSSEX, ENGLAND PO19 1UD BN 0-471-95236-2 PY 1995 BP 139 EP 153 PG 15 WC Clinical Neurology SC Neurosciences & Neurology GA BD06G UT WOS:A1995BD06G00016 ER PT B AU WEST, HL REBECK, GW GROWDON, JH HYMAN, BT AF WEST, HL REBECK, GW GROWDON, JH HYMAN, BT BE Iqbal, K Mortimer, JA Winblad, B Wisniewski, HM TI Apolipoprotein E4 affects neuropathology but not clinical progression in Alzheimer's disease SO RESEARCH ADVANCES IN ALZHEIMER'S DISEASE AND RELATED DISORDERS LA English DT Proceedings Paper CT 4th International Conference on Alzheimers Disease and Related Disorders CY JUL 29-AUG 03, 1994 CL MINNEAPOLIS, MN RP MASSACHUSETTS GEN HOSP,NEUROL SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, WEST SUSSEX, ENGLAND PO19 1UD BN 0-471-95236-2 PY 1995 BP 363 EP 370 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA BD06G UT WOS:A1995BD06G00040 ER PT B AU HYMAN, BT WEST, HL GOMEZISLA, T MUI, S AF HYMAN, BT WEST, HL GOMEZISLA, T MUI, S BE Iqbal, K Mortimer, JA Winblad, B Wisniewski, HM TI Quantitative neuropathology in Alzheimer's disease: Neuronal loss in high-order association cortex parallels dementia SO RESEARCH ADVANCES IN ALZHEIMER'S DISEASE AND RELATED DISORDERS LA English DT Proceedings Paper CT 4th International Conference on Alzheimers Disease and Related Disorders CY JUL 29-AUG 03, 1994 CL MINNEAPOLIS, MN RP MASSACHUSETTS GEN HOSP,NEUROL SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 10 Z9 10 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, WEST SUSSEX, ENGLAND PO19 1UD BN 0-471-95236-2 PY 1995 BP 453 EP 460 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA BD06G UT WOS:A1995BD06G00049 ER PT B AU WASCO, W GURUBHAGAVATULA, S TANZI, RE AF WASCO, W GURUBHAGAVATULA, S TANZI, RE BE Iqbal, K Mortimer, JA Winblad, B Wisniewski, HM TI Molecular characterization of the members of the APP-like gene family SO RESEARCH ADVANCES IN ALZHEIMER'S DISEASE AND RELATED DISORDERS LA English DT Proceedings Paper CT 4th International Conference on Alzheimers Disease and Related Disorders CY JUL 29-AUG 03, 1994 CL MINNEAPOLIS, MN RP HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GENET AGING LAB,149 13TH ST,BOSTON,MA 02129, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, WEST SUSSEX, ENGLAND PO19 1UD BN 0-471-95236-2 PY 1995 BP 657 EP 667 PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA BD06G UT WOS:A1995BD06G00071 ER PT J AU SANDBERG, MA GAUDIO, AR AF SANDBERG, MA GAUDIO, AR TI SLOW PHOTOSTRESS RECOVERY AND DISEASE SEVERITY IN AGE-RELATED MACULAR DEGENERATION SO RETINA-THE JOURNAL OF RETINAL AND VITREOUS DISEASES LA English DT Article AB Purpose: To determine whether photostress recovery time varies with severity of disease in age-related macular degeneration. Methods: Photostress recovery time, visual acuity, and foveal retinal pigment epithelial atrophy were evaluated for the fellow eyes of 133 patients with unilateral neovascular agerelated macular degeneration. Recovery times were measured by a method that flashed letters on a computer screen in random order before and after a 10 second bleach. Results: Recovery times were delayed in 62% of the patients (including 47% of those with normal visual acuity), ranged up to 6 times the normal limit, and increased with advancing age (P < 0.0001). Photostress recovery time was inversely correlated with visual acuity (P < 0.0001) and longer in eyes with Visible atrophy than in eyes without atrophy (P = 0.0007). Significant relationships between these two pairs of measures were also found after controlling for age. Conclusion: These findings support previous evidence that the time for visual recovery after exposure to a glare source is commonly slowed in age-related macular degeneration even among patients with normal visual acuity and further show that it can vary with age and extent of disease. RP SANDBERG, MA (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY08398] NR 0 TC 32 Z9 32 U1 0 U2 6 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0275-004X J9 RETINA-J RET VIT DIS JI Retin.-J. Retin. Vitr. Dis. PY 1995 VL 15 IS 5 BP 407 EP 412 PG 6 WC Ophthalmology SC Ophthalmology GA TB891 UT WOS:A1995TB89100006 PM 8594633 ER PT J AU Friedman, ES DAmico, DJ AF Friedman, ES DAmico, DJ TI Vitrectomy alone for the management of uncomplicated recurrent retinal detachments SO RETINA-THE JOURNAL OF RETINAL AND VITREOUS DISEASES LA English DT Article DE pneumatic; recurrent retinal detachment; scleral buckle revision; vitrectomy techniques; vitreous surgery AB Background: The role of vitrectomy for the treatment of uncomplicated recurrent retinal detachments has not been defined clearly. The authors report their experience with vitrectomy alone for the management of such cases. Methods: Pars plana vitrectomy with internal subretinal fluid drainage and long-term tamponade was performed on nine patients with uncomplicated recurrent retinal detachments after primary scleral buckling surgery. The duration of follow-up was a minimum of 6 months (mean, 39 months). Results: Anatomic success was achieved after the initial reoperation in seven eyes (78%). The overall success rate was 89%. The visual acuity was 20/30 or better in three patients, 20/40 to 20/80 in three patients, and 20/200 in two patients. Complications included progressive nuclear sclerosis and macular pucker. Conclusion: Vitrectomy is effective and may have advantages over other methods for the management of uncomplicated recurrent retinal detachments. C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. NR 0 TC 11 Z9 12 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0275-004X J9 RETINA-J RET VIT DIS JI Retin.-J. Retin. Vitr. Dis. PY 1995 VL 15 IS 6 BP 469 EP 474 PG 6 WC Ophthalmology SC Ophthalmology GA TL846 UT WOS:A1995TL84600002 PM 8747439 ER PT B AU Parrish, JA Osborn, LR AF Parrish, JA Osborn, LR BE Grundfest, WS TI Better, less expensive health care: Technological opportunities and the organizational challenge SO ROLE OF TECHNOLOGY IN THE COST OF HEALTH CARE: PROVIDING THE SOLUTIONS: HEALTH CARE TECHNOLOGY POLICY II SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Health Care Technology Policy II - the Role of Technology in the Cost of Health Care: Providing the Solutions CY MAY 10-12, 1995 CL ARLINGTON, VA SP Soc Photo Opt Instrumentat Engineers, Whitaker Fdn, NIST, Adv Technol Programs, Cedars Sinai Medallions Charitable Fund, Hamamatsu Corp, Mayo Clin, IEEE, Engn Med & Biol Soc DE healthcare; technology; procedural medicine; minimally invasive therapy; strategic alliance; lasers; endoscopy; imaging; minimally invasive surgery; center of excellence C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1856-0 J9 P SOC PHOTO-OPT INS PY 1995 VL 2499 BP 12 EP 22 PG 11 WC Computer Science, Information Systems; Optics SC Computer Science; Optics GA BE37N UT WOS:A1995BE37N00002 ER PT J AU SCHUMACHER, HR AF SCHUMACHER, HR TI MICROVASCULAR PERMEABILITY AND THE EFFECTS OF JOINT MOTION SO SCANDINAVIAN JOURNAL OF RHEUMATOLOGY LA English DT Article; Proceedings Paper CT 6th Bertine Koperberg Conference - Chronic Arthritis: Why the Joints CY APR 28-30, 1994 CL NIJMEGEN, NETHERLANDS ID RHEUMATOID-ARTHRITIS; PRESSURE CHANGES; EXERCISE; SYNOVIUM; KNEE C1 UNIV PENN,SCH MED,DEPT MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. RP SCHUMACHER, HR (reprint author), VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 27 TC 0 Z9 0 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0300-9742 J9 SCAND J RHEUMATOL JI Scand. J. Rheumatol. PY 1995 SU 101 BP 17 EP 20 PG 4 WC Rheumatology SC Rheumatology GA QW129 UT WOS:A1995QW12900003 ER PT J AU SCHUMACHER, HR AF SCHUMACHER, HR TI HOW MICROORGANISMS ARE HANDLED TO LOCALIZE TO JOINTS AND WITHIN JOINTS SO SCANDINAVIAN JOURNAL OF RHEUMATOLOGY LA English DT Article; Proceedings Paper CT 6th Bertine Koperberg Conference - Chronic Arthritis: Why the Joints CY APR 28-30, 1994 CL NIJMEGEN, NETHERLANDS ID RHEUMATOID-ARTHRITIS; SYNOVIAL-MEMBRANE; BORRELIA-BURGDORFERI; COLLAGENOUS TISSUES; KNEE JOINTS; IDENTIFICATION; DESTRUCTION; MECHANISM; DISEASE; BIOPSY C1 UNIV PENN,SCH MED,DEPT MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. RP SCHUMACHER, HR (reprint author), VET AFFAIRS MED CTR,CTR ARTHRIT IMMUNOL,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 36 TC 0 Z9 0 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0300-9742 J9 SCAND J RHEUMATOL JI Scand. J. Rheumatol. PY 1995 SU 101 BP 199 EP 202 PG 4 WC Rheumatology SC Rheumatology GA QW129 UT WOS:A1995QW12900033 ER PT J AU IVERSEN, P MADSEN, PO CORLE, DK AF IVERSEN, P MADSEN, PO CORLE, DK TI RADICAL PROSTATECTOMY VERSUS EXPECTANT TREATMENT FOR EARLY CARCINOMA OF THE PROSTATE - 23-YEAR FOLLOW-UP OF A PROSPECTIVE RANDOMIZED STUDY SO SCANDINAVIAN JOURNAL OF UROLOGY AND NEPHROLOGY LA English DT Article DE RADICAL PROSTATECTOMY; EXPECTANT TREATMENT; EARLY CARCINOMA OF THE PROSTATE ID STAGE-I; CANCER; MANAGEMENT; SURVIVAL; IMPACT; RISK AB In a study by the Veterans Administration Cooperative Urological Research Group (VACURG),142 patients with localized prostate cancer, VACURG stage I and II, were randomized between radical prostatectomy plus placebo versus placebo alone as initial treatment. 111 patients were evaluable for treatment comparison. Median follow-up for survival is 23 years. The prognostic value of Gleason histologic grading was confirmed. A difference in overall survival in favor of radical prostatectomy was observed in stage I patients. However, after adjustment for imbalance in age distribution, no statistically significant differences in survival could be demonstrated in either stage or in both stages combined. The results are discussed considering the small sample size and the limited statistical power of the study. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SECT,MADISON,WI 53705. UNIV COPENHAGEN,RIGSHOSP,DEPT UROL,DK-2100 COPENHAGEN,DENMARK. UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI. NCI,DIV CANC CONTROL,BETHESDA,MD 20892. NR 34 TC 0 Z9 0 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5599 J9 SCAND J UROL NEPHROL JI Scand. J. Urol. Nephrol. PY 1995 SU 172 BP 65 EP 72 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA RX700 UT WOS:A1995RX70000013 ER PT J AU DRESCHER, P RAUCH, D KNES, JM MADSEN, PO AF DRESCHER, P RAUCH, D KNES, JM MADSEN, PO TI CONTRAST-MEDIUM INDUCED RENAL VASOCONSTRICTION, ROLE OF ALPHA-RECEPTORS SO SCANDINAVIAN JOURNAL OF UROLOGY AND NEPHROLOGY LA English DT Article DE RENAL ARTERY; RADIOCONTRAST MEDIUM; ALPHA(1) RECEPTORS ID SUBTYPES; ARTERIES; RABBIT; NEPHROTOXICITY; INSUFFICIENCY; ADRENOCEPTORS; DIATRIZOATE; AGONISTS; SAFETY; DOGS AB Standard imaging techniques for evaluation of renal and renovascular disease require the application of radiocontrast medium. The use of high osmolar, ionic radio contrast medium is however associated with adverse effects including acute renal insufficiency. Renal vasoconstriction seems to play an important role in the pathomechanism of this side effect. The cellular mechanisms however remain unsolved. Alpha1 - adrenoceptors and their subtypes are the crucial link between sympathetic stimulation and renal vasoconstriction. We investigated the role of alpha(1)-receptors and the alpha(1A) and alpha(1B) subtypes in the renal artery and in sodium/meglumine diatrizoate induced renal artery smooth muscle contraction. Alpha1-receptor induced rabbit renal artery contraction was produced by stimulation with the specific agonist phenylephrine which was antagonized dose-dependently and reversibly by the alpha(1A)-blockers prazosin, terazosin and YM 617. The alpha(1A)-receptor was the prevalent receptor subtype in rabbit renal artery. This was identified by applying the specific alpha(1A)-receptor antagonist 5-methylurapidil and the irreversible alpha(1B)-receptor antagonist chloroethylclonidine. These two inhibited the PE induced contraction by 96% and 66%,respectively. Sodium/meglumine diatrizoate elicited renal artery contraction at 25% of the phenylephrine control. This contraction was not influenced by alpha(1)-blockers indicating the absence of an alpha(1)-receptor mediated process. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SECT,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI. RP DRESCHER, P (reprint author), MED COLL WISCONSIN,DEPT RADIOL,MILWAUKEE,WI 53226, USA. NR 40 TC 0 Z9 0 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5599 J9 SCAND J UROL NEPHROL JI Scand. J. Urol. Nephrol. PY 1995 SU 172 BP 103 EP 108 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA RX700 UT WOS:A1995RX70000018 ER PT J AU AMIN, F DAVIDSON, M KAHN, RS SCHMEIDLER, J STERN, R KNOTT, PJ APTER, S AF AMIN, F DAVIDSON, M KAHN, RS SCHMEIDLER, J STERN, R KNOTT, PJ APTER, S TI ASSESSMENT OF THE CENTRAL DOPAMINERGIC INDEX OF PLASMA HVA IN SCHIZOPHRENIA SO SCHIZOPHRENIA BULLETIN LA English DT Article ID HOMOVANILLIC-ACID CONCENTRATION; NORADRENERGIC NEURONAL-ACTIVITY; CATECHOLAMINE METABOLITES; DEAMINATED METABOLITES; NEUROLEPTIC TREATMENT; CEREBROSPINAL-FLUID; URINARY-EXCRETION; HUMAN-BRAIN; DEBRISOQUIN; RAT AB Under fasting conditions, the dopamine (DA) metabolite homovanillic acid (HVA) in plasma originates mainly from central DA neurons or from central and peripheral noradrenergic (NA) neurons. The latter source contributes, in addition to HVA, the norepinephrine metabolites, for example, 3-methoxy-4-hydroxyphenylglycol (MHPG). It has been shown in primates that the association between HVA and MHPG in plasma or urine under varying rates elf NA metabolism can be used to obtain an estimate of the central DA neuronal contribution of HVA to plasma or urine. This estimate is called the central dopaminergic index (CDI). Two studies presented here examine the applicability of this model in schizophrenia patients. The results were consistent with the proposed model and suggested that only about 30 percent of the total plasma HVA concentrations in our patients were derived from central DA neurons. A convenient modification of this model is proposed for future studies. Since the CDI of plasma HVA is not likely to be confounded by NA activity, this tool may prove useful in disentangling the roles played by the DA and NA systems in schizophrenia. C1 BAYLOR COLL MED,HOUSTON,TX. CUNY MT SINAI SCH MED,DEPT PSYCHIAT,DIV CLIN RES,NEW YORK,NY. UNIV UTRECHT HOSP,DEPT PSYCHIAT,UTRECHT,NETHERLANDS. CUNY MT SINAI SCH MED,DEPT BIOMATH SCI,NEW YORK,NY. RP AMIN, F (reprint author), HOUSTON VET AFFAIRS MED CTR,PSYCHIAT SERV,RM 6C-316,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 60 TC 37 Z9 38 U1 1 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1995 VL 21 IS 1 BP 53 EP 66 PG 14 WC Psychiatry SC Psychiatry GA QK967 UT WOS:A1995QK96700006 PM 7770741 ER PT J AU DASSORI, AM MILLER, AL SALDANA, D AF DASSORI, AM MILLER, AL SALDANA, D TI SCHIZOPHRENIA AMONG HISPANICS - EPIDEMIOLOGY, PHENOMENOLOGY, COURSE, AND OUTCOME SO SCHIZOPHRENIA BULLETIN LA English DT Article ID MENTAL-HEALTH-SERVICES; ETHNIC-MINORITY GROUPS; PSYCHIATRIC-DISORDERS; LIFETIME PREVALENCE; EXPRESSED EMOTION; SYMPTOMS; INSTRUMENT; LANGUAGE; FAMILIES; ILLNESS AB A number of studies point to the influence of culture and ethnicity on the presentation and course of schizophrenia. In general, a relatively powerful influence of environmental factors is identified. This article reviews the literature on schizophrenia among Hispanics in the United States and uses the results of this review as a basis for identifying directions for future study. Research is divided into three major areas: epidemiology, phenomenology, and illness course and outcome. Ethnic comparisons suggest similar prevalence rates of schizophrenia. However, differences in illness phenomenology between certain subgroups of Hispanics are also observed. Moreover, culture can affect various aspects of the illness process, including illness definition, help-seeking behavior, response to treatment, and posttreatment adjustment. Proposed guidelines to direct future research ventures include (1) better delineation of the sociocultural attributes of the group under study, (2) validation of assessment instruments across ethnic groups, (3) use of innovative approaches to assess incidence and prevalence, (4) incorporation of qualitative methodology, (5) use of illness behavior models to provide a conceptual framework to guide investigations, and (6) integration of cross-cultural and biological studies. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. SAN ANTONIO STATE HOSP,SAN ANTONIO,TX. RP DASSORI, AM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 53 TC 15 Z9 16 U1 4 U2 5 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1995 VL 21 IS 2 BP 303 EP 312 PG 10 WC Psychiatry SC Psychiatry GA QX822 UT WOS:A1995QX82200015 PM 7631176 ER PT J AU DAVIDSON, M POWCHIK, P AF DAVIDSON, M POWCHIK, P TI COMMENTARY TO LATE-ONSET SCHIZOPHRENIA AND LATE PARAPHRENIA SO SCHIZOPHRENIA BULLETIN LA English DT Editorial Material AB The biological bases for late-life psychotic disorders are unknown. Thus, diverse clinical phenomenology that is often described by a single nominative may actually represent multiple biological abnormalities. Conversely, several differently named disorders may actually have similar biological substrates. Until there is a greater understanding of the biological underpinnings of such disorders, diagnostic nomenclature should not only be rigorously applied, but consistent across the scientific community. The review of the use of the term ''late paraphrenia'' by Riecher-Rossler et al. (1995, this issue) underscores the potential confusion of multiple nominatives, and their suggestion to abandon the term ''late paraphrenia'' in ICD-10 merits serious consideration. C1 MT SINAI SCH MED,NEW YORK,NY 10029. RP DAVIDSON, M (reprint author), BRONX VET AFFAIRS MED CTR,DIV CLIN RES,PSYCHIAT 116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1995 VL 21 IS 3 BP 355 EP 356 PG 2 WC Psychiatry SC Psychiatry GA RN381 UT WOS:A1995RN38100002 ER PT J AU GREENE, RW AF GREENE, RW TI STUDENTS WITH ADHD IN SCHOOL CLASSROOMS - TEACHER FACTORS RELATED TO COMPATIBILITY, ASSESSMENT, AND INTERVENTION SO SCHOOL PSYCHOLOGY REVIEW LA English DT Article ID ATTENTION-DEFICIT HYPERACTIVITY; BEHAVIORAL INTERVENTIONS; STIMULANT MEDICATION; CHILDREN; DISORDER; METHYLPHENIDATE; ACCEPTABILITY; PERFORMANCE; THERAPY; NORMALIZE AB Perhaps the most striking omission of school-based treatment outcome research for students with ADHD has been the examination of teacher factors that may have a significant bearing upon outcome. As a result, the conceptualization of ADHD and its treatment is incomplete. A perspective incorporating goodness-of-fit/systems theory may be a more adequate model from which to view interactions between students with ADHD and their teachers and a more predictive model from which to hypothesize anticipated treatment outcomes. Two compatibility issues are explored in some detail: teacher-treatment compatibility (i.e., the match between teacher characteristics and commonly recommended behavior management procedures) and teacher-student compatibility (i.e., the match between teacher characteristics and student characteristics). Potential teacher factors which might be important to consider in such compatibility equations are discussed, along with the implications of these variables for school-based assessment and intervention processes and future research. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP GREENE, RW (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,WACC-725,BOSTON,MA 02114, USA. NR 70 TC 15 Z9 16 U1 2 U2 7 PU NATL ASSN SCHOOL PSYCHOL PI HARRISONBURG PA JAMES MADISON UNIV DEPT PSYCHOL, HARRISONBURG, VA 22807 SN 0279-6015 J9 SCHOOL PSYCHOL REV JI Sch. Psychol. Rev. PY 1995 VL 24 IS 1 BP 81 EP 93 PG 13 WC Psychology, Educational SC Psychology GA RB998 UT WOS:A1995RB99800010 ER PT J AU BARNES, JL MILANI, S AF BARNES, JL MILANI, S TI IN-SITU HYBRIDIZATION IN THE STUDY OF THE KIDNEY AND RENAL DISEASES SO SEMINARS IN NEPHROLOGY LA English DT Review ID RECEPTOR GENE-EXPRESSION; LOCALLY RESTRICTED EXPRESSION; MOUSE EMBRYONIC-DEVELOPMENT; DEVELOPING EXCRETORY SYSTEM; MESSENGER-RIBONUCLEIC-ACID; HEPATOCYTE GROWTH-FACTOR; HUMAN-FETAL KIDNEY; PAIRED BOX GENE; INSITU HYBRIDIZATION; RAT-KIDNEY C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. UNIV FLORENCE,DEPT CLIN PATHOPHYSIOL,GASTROENTEROL UNIT,FLORENCE,ITALY. RP BARNES, JL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL FR,SAN ANTONIO,TX 78284, USA. OI milani, stefano/0000-0002-1337-9107 NR 175 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9295 J9 SEMIN NEPHROL JI Semin. Nephrol. PD JAN PY 1995 VL 15 IS 1 BP 9 EP 28 PG 20 WC Urology & Nephrology SC Urology & Nephrology GA QF380 UT WOS:A1995QF38000003 PM 7754257 ER PT J AU NEUSTADTER, LM WEISS, M AF NEUSTADTER, LM WEISS, M TI MEDICATION-INDUCED CHANGES OF BONE SO SEMINARS IN ROENTGENOLOGY LA English DT Article ID 13-CIS-RETINOIC ACID; EPIPHYSEAL; IFOSFAMIDE; FRACTURES; CHILDREN; THERAPY; RICKETS C1 ST CHRISTOPHERS MED CTR,PHILADELPHIA,PA. RP NEUSTADTER, LM (reprint author), HOSP UNIV PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. NR 33 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0037-198X J9 SEMIN ROENTGENOL JI Semin. Roentgenology PD JAN PY 1995 VL 30 IS 1 BP 88 EP 95 DI 10.1016/S0037-198X(05)80009-4 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QB954 UT WOS:A1995QB95400009 PM 7899887 ER PT J AU BARRY, MJ AF BARRY, MJ TI NATURAL-HISTORY OF CLINICALLY LOCALIZED PROSTATE-CANCER SO SEMINARS IN SURGICAL ONCOLOGY LA English DT Article DE PROSTATIC NEOPLASMS; PROGNOSIS; MORTALITY; RISK FACTORS; EPIDEMIOLOGY AB The natural history of clinically localized prostate cancer is controversial. However, the data that is available suggests outcomes are good for men with well and moderately differentiated disease, but relatively poor for men with poorly differentiated cancer. For example, in one synthesis of individual-patient level data from six series, ten-year prostate cancer-specific mortality for men with well, moderate, and poorly differentiated disease was estimated at 13%, 13%, and 66%, respectively. Tumor grade is the dominant predictor of prognosis. Few studies report on risks of morbidity due to local cancer progression; the data available suggest this risk is relatively low. Cancer-specific mortality figures overestimate the impact of disease among older men with competing causes of mortality. Given the available data on prognosis of men with localized prostate cancer not treated for cure, clinical trials designed to measure the effectiveness of aggressive therapy will need to be large. (C) 1995 Wiley-Liss, Inc. RP BARRY, MJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR MED PRACTICES EVALUAT,50 STANIFORD ST,9TH FLOOR,BOSTON,MA 02114, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 8756-0437 J9 SEMIN SURG ONCOL JI Semin. Surg. Oncol. PD JAN-FEB PY 1995 VL 11 IS 1 BP 3 EP 8 DI 10.1002/ssu.2980110103 PG 6 WC Oncology; Surgery SC Oncology; Surgery GA QE760 UT WOS:A1995QE76000002 PM 7754275 ER PT J AU MORAN, JS KAUFMAN, JA FELSENSTEIN, D AF MORAN, JS KAUFMAN, JA FELSENSTEIN, D TI SURVEY OF HEALTH-CARE PROVIDERS - WHO SEES PATIENTS NEEDING STD SERVICES AND WHAT SERVICES DO THEY PROVIDE SO SEXUALLY TRANSMITTED DISEASES LA English DT Note C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ABT ASSOCIATES INC,CAMBRIDGE,MA 02138. RP MORAN, JS (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR PREVENT SERV,DIV STD HIV PREVENT,ATLANTA,GA 30341, USA. NR 9 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0148-5717 J9 SEX TRANSM DIS JI Sex. Transm. Dis. PD JAN-FEB PY 1995 VL 22 IS 1 BP 67 EP 69 DI 10.1097/00007435-199501000-00011 PG 3 WC Infectious Diseases SC Infectious Diseases GA QC692 UT WOS:A1995QC69200011 PM 7709328 ER PT J AU CAI, H COOPER, GM AF CAI, H COOPER, GM TI INDUCIBLE EXPRESSION OF RAS N-17 DOMINANT INHIBITORY PROTEIN SO SMALL GTPASES AND THEIR REGULATORS, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID GENE C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP CAI, H (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 7 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 255 BP 230 EP 237 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE11X UT WOS:A1995BE11X00023 PM 8524106 ER PT J AU ZHANG, XF MARSHALL, MS AVRUCH, J AF ZHANG, XF MARSHALL, MS AVRUCH, J TI RAS-RAF COMPLEXES IN-VITRO SO SMALL GTPASES AND THEIR REGULATORS, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID KINASE C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,MED SERV,BOSTON,MA 02129. INDIANA UNIV,DEPT MED,DIV HEMATOL & ONCOL,INDIANAPOLIS,IN 46202. INDIANA UNIV,WALTHER ONCOL CTR,INDIANAPOLIS,IN 46202. HARVARD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,DEPT MED,DIABET UNIT,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,DEPT MED,MED SERV,BOSTON,MA 02129. RP ZHANG, XF (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,DIABET UNIT,BOSTON,MA 02129, USA. NR 10 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 255 BP 323 EP 331 PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE11X UT WOS:A1995BE11X00033 PM 8524118 ER PT J AU BLUMENFELD, A LUCENTE, DE TROFATTER, JA LERNER, T SLAUGENHAUPT, SA LIEBERT, CB MONAHAN, M HAINES, JL GUSELLA, JF BREAKEFIELD, XO PARYSEK, LM AF BLUMENFELD, A LUCENTE, DE TROFATTER, JA LERNER, T SLAUGENHAUPT, SA LIEBERT, CB MONAHAN, M HAINES, JL GUSELLA, JF BREAKEFIELD, XO PARYSEK, LM TI PERIPHERIN GENE IS LINKED TO KERATIN-18 GENE ON HUMAN-CHROMOSOME-12 SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Note ID EPIDERMOLYSIS-BULLOSA SIMPLEX; POLYMERASE CHAIN-REACTION; INTERMEDIATE FILAMENTS; LINKAGE MAP; LOCALIZATION; POLYMORPHISMS; CLUSTER; GENOME; MOUSE AB Peripherin is a neuron on-spectfic intermediate filament (IF) protein, found primarily in phylogenetically old regions of the nervous system. Whereas other neuronal IF genes have only two to three introns and are scattered in the genome, the peripherin gene (PRPH) has a complex intron-exon structure like nonneuronal IF genes that are clustered in tandem arrays, e.g., those encoding the keratins. We used a cosmid containing the human peripherin gene (PRPH) to determine its chromosomal location in relationship to nonneuronal IF genes. Using a rodent-human mapping panel, we localized the PRPH gene to human chromosome 12. Since a cluster of keratin genes maps to 12q12-13, polymorphic markers were developed for PRPH and for one of the keratin genes presumed to be in the cluster keratin 18 (KRT18). Both markers were typed in CEPH reference families. Pairwise and multipoint analyses of the CEPH data revealed that KRT18 is tightly linked to DNA markers D12S4, D12S22, D12S90, D12S96 and D12S103, which lie between D12S18 and D12S8, with odds greater than 1000:1. These markers are physically located at 12q11-13, thus supporting the fine localization of KRT18 in or near the group of type II keratins in this region. Furthermore, linkage analysis showed that the peripherin gene (PRPH) is tightly linked to KRT18 (($) over cap Z = 15.73, ($) over cap theta = 0.013), and therefore appears to be in close proximity to the cluster. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. UNIV CINCINNATI,DEPT ANAT & CELL BIOL,CINCINNATI,OH 45267. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00016]; NICHD NIH HHS [NICHD 25752]; NINDS NIH HHS [NS24279] NR 36 TC 6 Z9 7 U1 0 U2 3 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD JAN PY 1995 VL 21 IS 1 BP 83 EP 88 DI 10.1007/BF02255825 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA RF459 UT WOS:A1995RF45900008 PM 7541564 ER PT J AU LIPSITZ, SR PARZEN, M AF LIPSITZ, SR PARZEN, M TI SAMPLE-SIZE CALCULATIONS FOR NONRANDOMIZED STUDIES SO STATISTICIAN LA English DT Article DE COEFFICIENT OF DETERMINATION; OBSERVATIONAL STUDY; TREATMENT EFFECT AB References on sample size calculations for randomized studies with a continuous response are abundant. The sample size is usually calculated from a simple two-sample z-test. In fact, most introductory statistical books contain the calculations. Suppose that an investigator is interested in one main covariate, say a treatment covariate, in a non-randomized (or observational) study. In a non-randomized study, besides the treatment covariate, there are also other covariates that are used in a regression. The relationship between the main covariate and other covariates needs to be taken into account when calculating the necessary sample size for detecting a treatment effect. In this paper, we give a simple way to correct the usual sample size formulae (based on normal theory) to account for the relationships between the treatment covariate, the other covariates and the response; the relationships are accounted for by looking at various coefficients of determination. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. DANA FARBER CANC INST,BOSTON,MA. UNIV CHICAGO,CHICAGO,IL 60637. NR 3 TC 5 Z9 5 U1 0 U2 0 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0039-0526 J9 STATISTICIAN JI Statistician PY 1995 VL 44 IS 1 BP 81 EP 90 DI 10.2307/2348619 PG 10 WC Statistics & Probability SC Mathematics GA QN938 UT WOS:A1995QN93800010 ER PT J AU Myklebust, JB Cusick, JF Boerboom, LE Prieto, TE Khan, TA AF Myklebust, JB Cusick, JF Boerboom, LE Prieto, TE Khan, TA TI Vascular effects of spinal cord stimulation in the monkey SO STEREOTACTIC AND FUNCTIONAL NEUROSURGERY LA English DT Article DE spinal cord stimulation; microspheres; evoked potentials; sympathetic nervous system; monkey; peripheral vascular disease; regional blood flow ID DORSAL COLUMN STIMULATION; BLOOD-FLOW; ELECTRICAL-STIMULATION; DISEASE; EXTREMITIES; IMPROVEMENT AB Because of clinical reports suggesting beneficial effects of electrical stimulation in peripheral vascular disease, studies have been conducted in the monkey. Regional blood flow was measured prior to, during and following the application of electrical currents to the spinal cord. The flow measurements were made using radioactive microspheres. In addition, tissue temperatures and venous and arterial concentrations of epinephrine and norepinephrine were measured. The results show that electrical stimulation increases blood flow to the skin and muscle. It is hypothesized that the effect is due to sympathetic inactivation secondary to the application of electrical currents. C1 ZABLOCKI VET ADM MED CTR,MILWAUKEE,WI 53295. MARQUETTE UNIV,DEPT BIOMED ENGN,MILWAUKEE,WI 53233. MED COLL WISCONSIN,MILWAUKEE,WI 53226. US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,CTR REHABIL R&D,HINES,IL 60141. OI Myklebust, Joel/0000-0002-8709-9706 NR 28 TC 11 Z9 12 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1011-6125 J9 STEREOT FUNCT NEUROS JI Stereotact. Funct. Neurosurg. PY 1995 VL 64 IS 1 BP 32 EP 39 PG 8 WC Neurosciences; Neuroimaging; Surgery SC Neurosciences & Neurology; Surgery GA TK820 UT WOS:A1995TK82000004 PM 8751312 ER PT J AU JIANG, N FINKLESTEIN, SP DO, TY CADAY, CG CHARETTE, M CHOPP, M AF JIANG, N FINKLESTEIN, SP DO, TY CADAY, CG CHARETTE, M CHOPP, M TI DELAYED INTRAVENOUS ADMINISTRATION OF BASIC FIBROBLAST GROWTH-FACTOR (BFGF) REDUCES INFARCT VOLUME IN A MODEL OF FOCAL CEREBRAL-ISCHEMIA REPERFUSION SO STROKE LA English DT Meeting Abstract C1 HENRY FORD HOSP,DEPT NEUROL,DETROIT,MI 48202. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 5 Z9 5 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1995 VL 26 IS 1 BP 165 EP 165 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA PZ896 UT WOS:A1995PZ89600074 ER PT J AU HUANG, ZH HUANG, PL PANAHIAN, N DALKARA, T FISHMAN, MC MOSKOWITZ, MA AF HUANG, ZH HUANG, PL PANAHIAN, N DALKARA, T FISHMAN, MC MOSKOWITZ, MA TI EFFECTS OF FOCAL ISCHEMIA IN MICE DEFICIENT IN NEURONAL NITRIC-OXIDE SYNTHASE SO STROKE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1995 VL 26 IS 1 BP 168 EP 168 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA PZ896 UT WOS:A1995PZ89600092 ER PT J AU YOSHIDA, T WAEBER, C MOSKOWITZ, MA AF YOSHIDA, T WAEBER, C MOSKOWITZ, MA TI INDUCIBLE NITRIC-OXIDE SYNTHASE ACTIVITY IN FOCAL ISCHEMIA SO STROKE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. RI Waeber, Christian/A-8333-2009 OI Waeber, Christian/0000-0001-6078-0027 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1995 VL 26 IS 1 BP 179 EP 179 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA PZ896 UT WOS:A1995PZ89600156 ER PT S AU Cummings, JL AF Cummings, JL BE Grafman, J Holyoak, KJ Boller, F TI Anatomic and behavioral aspects of frontal-subcortical circuits SO STRUCTURE AND FUNCTIONS OF THE HUMAN PREFRONTAL CORTEX SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Workshop on Structure and Functions of the Human Prefrontal Cortex CY MAR 02-04, 1995 CL NEW YORK, NY SP New York Acad Sci ID OBSESSIVE-COMPULSIVE DISORDER; BASAL GANGLIA; PARKINSONS-DISEASE; RHESUS-MONKEY; STRIATOPALLIDAL SYSTEM; PARALLEL ORGANIZATION; THALAMIC INFARCTION; HUNTINGTONS-DISEASE; PREFRONTAL CORTEX; SECONDARY MANIA AB Five parallel circuits connect discrete regions of the frontal lobes with specific subregions of the striatum, globus pallidus, and thalamus. One circuit mediates motor function, another eye movements, and three of the circuits mediate cognitive, emotional, and motivational processes. The circuits serve as organizational axes integrating related information from widespread areas of the brain and mediating diverse behaviors. This review describes the anatomy of the circuits and the major transmitters present within the circuits. Circuit-specific behaviors (those that appear to be mediated exclusively by circuit structures) and circuit-related behaviors (those that involve both circuit and noncircuit structures) are discussed. Drugs that alter behavior through effects on the circuits are presented. The three circuits that are most relevant to understanding behavior are emphasized. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,BEHAV NEUROSCI SECT,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,REED NEUROL RES CTR,DEPT NEUROL,LOS ANGELES,CA 90024. FU NIA NIH HHS [AG 10123] NR 69 TC 225 Z9 228 U1 2 U2 7 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-991-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 769 BP 1 EP 13 DI 10.1111/j.1749-6632.1995.tb38127.x PG 13 WC Multidisciplinary Sciences; Neurosciences; Psychology SC Science & Technology - Other Topics; Neurosciences & Neurology; Psychology GA BE92F UT WOS:A1995BE92F00001 PM 8595019 ER PT J AU SOUBA, WW GAMELLI, RL LORBER, MI THOMPSON, JS KRON, IL TOMPKINS, RG HOYT, DB AF SOUBA, WW GAMELLI, RL LORBER, MI THOMPSON, JS KRON, IL TOMPKINS, RG HOYT, DB TI STRATEGIES FOR SUCCESS IN ACADEMIC SURGERY SO SURGERY LA English DT Article AB Background. A growing concern among university surgeons is a perceived threat to the traditional academician role. Factors that have led to this concern include (1) changes in reimbursement and patient referral patterns, both of which have resulted in reduced income; (2) mounting external pressure from the departmental chairperson/dean to generate professional fees; (3) pervasive ambiguity in the criteria for promotion and tenure; (4) intensified competition for research dollars in recent years; and (5) a perception that fellow academicians view surgeons as operating room technicians incapable of laboratory research. These cogent issues have the means to place academic goals in jeopardy. Potentially they lead to dissatisfaction, unhappiness, and eventual departure from academia. A healthy solution to the problem includes departmental recognition and reward for whichever primary role/s the academic surgeon embraces-clinical, educational, research, or administrative. Clear chairperson-faculty communication on the issues of expectation and reward is a key ingredient in the solution. Methods. A mail survey was conducted with chairpersons of surgical departments and academic surgeons addressing the issues of retention, promotion, and benefits. Results. Results revealed significant differences in perceptions, suggesting the need for improved communication between faculty and chairpersons and a team approach to help maintain academic viability in the future. Conclusions. When the quadruple threat can be mutually described as a departmental rather than individual quality, the joys and rewards of academic surgery can be considerable for faculty and chairpersons alike. C1 LOYOLA UNIV,MED CTR,SHOCK TRAUMA INST,MAYWOOD,IL 60153. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. YALE UNIV,SCH MED,NEW HAVEN,CT. UNIV NEBRASKA,MED CTR,OMAHA,NE. UNIV VIRGINIA,SCH MED,CHARLOTTESVILLE,VA 22908. UNIV CALIF SAN DIEGO,MED CTR,SAN DIEGO,CA 92103. NR 6 TC 25 Z9 25 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD JAN PY 1995 VL 117 IS 1 BP 90 EP 95 DI 10.1016/S0039-6060(05)80234-X PG 6 WC Surgery SC Surgery GA QB712 UT WOS:A1995QB71200014 PM 7809842 ER PT J AU OGILVY, CS CROWELL, RM HEROS, RC AF OGILVY, CS CROWELL, RM HEROS, RC TI SURGICAL-MANAGEMENT OF MIDDLE CEREBRAL-ARTERY ANEURYSMS - EXPERIENCE WITH TRANSSYLVIAN AND SUPERIOR TEMPORAL GYRUS APPROACHES SO SURGICAL NEUROLOGY LA English DT Article DE MIDDLE CEREBRAL ARTERY ANEURYSM; SUPERIOR TEMPORAL GYRUS APPROACH; SYLVIAN FISSURE APPROACH; INTRACRANIAL ANEURYSM AB BACKGROUND Middle cerebral artery (MCA) aneurysms are typically approached surgically using one of three basic techniques. The sylvian fissure can be opened in one of two ways; either from medial to lateral or from lateral to medial, Alternatively, an incision in the superior temporal gyrus with subpial resection can be used to expose the MCA branches and aneurysm neck. METHODS We reviewed 65 middle cerebral aneurysms in 62 patients operated on over a 5-year interval where a choice of operative approach was made based on preoperative evaluation of available radiological studies, RESULTS The superior temporal gyrus was used when intraparenchymal hematoma was present in the temporal lobe or when the length of the middle cerebral artery trunk was long (average length 2.44 +/- 0.41 SE cm), This approach was used in 20 operations on 22 aneurysms. The sylvian fissure approach was used in cases where the middle cerebral artery main trunk was short (1.32 +/- 0.41 SE cm) or the direction of the aneurysm was favorable. This approach was used in 38 operations. In 4 operations (5 aneurysms) we combined the two approaches to remove dot, obtain adequate exposure, and secure control of the proximal MCA, CONCLUSIONS In most cases of MCA aneurysms the decision as to which surgical approach to use is made preoperatively depending on the presence of intraparenchymal clot, size of aneurysm, direction of aneurysm, and length of the proximal middle cerebral artery. C1 UNIV MINNESOTA,DEPT NEUROSURG,MINNEAPOLIS,MN 55455. HARVARD UNIV,SCH MED,BOSTON,MA. RP OGILVY, CS (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 25 TC 14 Z9 18 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0090-3019 J9 SURG NEUROL JI Surg. Neurol. PD JAN PY 1995 VL 43 IS 1 BP 15 EP 22 DI 10.1016/0090-3019(95)80032-C PG 8 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA QQ091 UT WOS:A1995QQ09100009 PM 7701417 ER PT J AU OGILVY, CS CROWELL, RM HEROS, RC AF OGILVY, CS CROWELL, RM HEROS, RC TI SURGICAL-MANAGEMENT OF MIDDLE CEREBRAL-ARTERY ANEURYSMS - EXPERIENCE WITH TRANSSYLVIAN AND SUPERIOR TEMPORAL GYRUS APPROACHES - REPLY SO SURGICAL NEUROLOGY LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA. UNIV MINNESOTA,DEPT NEUROSURG,MINNEAPOLIS,MN 55455. RP OGILVY, CS (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0090-3019 J9 SURG NEUROL JI Surg. Neurol. PD JAN PY 1995 VL 43 IS 1 BP 24 EP 24 PG 1 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA QQ091 UT WOS:A1995QQ09100013 ER PT S AU NABOZNY, GH GRIFFITHS, MM RIMM, IJ LUTHRA, HS DAVID, CS AF NABOZNY, GH GRIFFITHS, MM RIMM, IJ LUTHRA, HS DAVID, CS BE Davis, MM Buxbaum, J TI EFFECT OF CONSTRAINED T-CELL RECEPTOR REPERTOIRES ON COLLAGEN-INDUCED ARTHRITIS IN T-CELL RECEPTOR V-BETA TRANSGENIC AND CONGENIC MICE SO T-CELL RECEPTOR USE IN HUMAN AUTOIMMUNE DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on T-Cell Receptor Use in Human Autoimmune Diseases CY APR 17-20, 1994 CL SAN DIEGO, CA SP Arthritis Fdn, New York Acad Sci ID ANTIBODIES C1 MAYO CLIN & MAYO GRAD SCH MED,DEPT RHEUMATOL,ROCHESTER,MN 55905. VET AFFAIRS MED CTR,RES SERV,SALT LAKE CITY,UT 84132. UNIV UTAH,DEPT MED,DIV RHEUMATOL,SALT LAKE CITY,UT 84132. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. RP NABOZNY, GH (reprint author), MAYO CLIN & MAYO GRAD SCH MED,DEPT IMMUNOL,200 1ST ST SW,ROCHESTER,MN 55905, USA. FU NIAMS NIH HHS [AR30752] NR 7 TC 0 Z9 0 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-915-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 756 BP 217 EP 220 DI 10.1111/j.1749-6632.1995.tb44516.x PG 4 WC Immunology; Multidisciplinary Sciences SC Immunology; Science & Technology - Other Topics GA BD46M UT WOS:A1995BD46M00040 PM 7645838 ER PT B AU SCHMID, P CONRAD, A SYNDULKO, K SINGER, EJ LI, XM TAO, GM HANDLEY, D FAHYCHANDON, B TOURTELLOTTE, WW AF SCHMID, P CONRAD, A SYNDULKO, K SINGER, EJ LI, XM TAO, GM HANDLEY, D FAHYCHANDON, B TOURTELLOTTE, WW BE Major, EO Levy, JA Schoenberg, D TI Techniques in PCR and PCR evaluation technology and its application to the study of cerebrospinal fluid in HIV disease SO TECHNICAL ADVANCES IN AIDS RESEARCH IN THE HUMAN NERVOUS SYSTEM LA English DT Proceedings Paper CT NIH Symposium on Technical Advances in AIDS Research in the Human Nervous System CY OCT 04-05, 1993 CL WASHINGTON, DC SP NIH C1 W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45000-3 PY 1995 BP 301 EP 316 PG 16 WC Infectious Diseases; Medicine, Research & Experimental; Neurosciences SC Infectious Diseases; Research & Experimental Medicine; Neurosciences & Neurology GA BD83E UT WOS:A1995BD83E00022 ER PT B AU KEITH, DA LEVINE, JD AF KEITH, DA LEVINE, JD BE Sessle, BJ Bryant, PS Dionne, RA TI REACTION PAPERS TO CHAPTERS 7-9 SO TEMPOROMANDIBULAR DISORDERS AND RELATED PAIN CONDITIONS SE PROGRESS IN PAIN RESEARCH AND MANAGEMENT LA English DT Proceedings Paper CT International Workshop on the Temporomandibular Disorders and Related Pain Conditions CY APR, 1994 CL HUNT VALLEY, MD SP NIH, NIDR, NIAMSD, OFF RES WOMENS HLTH, US FDA C1 MASSACHUSETTS GEN HOSP,DEPT ORAL & MAXILLOFACIAL SURG,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT ASSOC STUDY PAIN (IASP) PRESS PI SEATTLE PA 909 NE 43RD ST, SUITE 304, SEATTLE, WA 98105 BN 0-931092-09-4 J9 PROG PAIN RES MANAG PY 1995 VL 4 BP 151 EP 157 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA BD13F UT WOS:A1995BD13F00012 ER PT J AU ALEXANDER, JK AF ALEXANDER, JK TI AGE, ALTITUDE, AND ARRHYTHMIA SO TEXAS HEART INSTITUTE JOURNAL LA English DT Review DE AGE FACTORS; AGED; ALTITUDE; ANOXIA; ARRHYTHMIA; HYPOXIA; MOUNTAINEERING AB Continuous electrocardiographic recording by Holter monitor was carried out during a climb to 5,895 m by an unacclimatized 65-year-old man confirmed to be without cardiac disease on rigorous examination. During ascent, marked ventricular ectopy and multiple runs of left ventricular bigeminy developed in association with an increase in P-wave amplitude of lead V-2,V- and unchanged QT interval. With the diminished aerobic stress of descent, bigeminy disappeared, although premature ventricular complexes, apparently of right ventricular origin, remained increased throughout the climb. Arrhythmogenic mechanisms activated by prolonged exercise under hypoxic conditions are reviewed in relation to age. RP ALEXANDER, JK (reprint author), DEPT VET AFFAIRS MED CTR,CARDIOL SECT 111B,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU TEXAS HEART INST PI HOUSTON PA PO BOX 20345, HOUSTON, TX 77225-0345 SN 0730-2347 J9 TEX HEART I J JI Tex. Heart Inst. J. PY 1995 VL 22 IS 4 BP 308 EP 316 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA TH902 UT WOS:A1995TH90200006 PM 8605431 ER PT B AU JASTY, M BRAGDON, C BAL, BS HARRIS, WH AF JASTY, M BRAGDON, C BAL, BS HARRIS, WH BE Galante, JO Rosenberg, AG Callaghan, JJ TI ACETABULAR MODULARITY SO TOTAL HIP REVISION SURGERY SE BRISTOL-MYERS SQUIBB / ZIMMER ORTHOPAEDIC SYMPOSIUM SERIES LA English DT Proceedings Paper CT 8th Annual Bristol-Myers Squibb/Zimmer Orthopaedic Research Symposium - Current Concepts in Total Hip Revision Surgery CY NOV 19-21, 1993 CL CHICAGO, IL SP BRISTOL MYERS SQUIBB ZIMMER C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED SURG,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 BN 0-7817-0231-3 J9 BRIS MYER Z PY 1995 BP 73 EP 80 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA BC41R UT WOS:A1995BC41R00006 ER PT B AU HARRIS, WH AF HARRIS, WH BE Galante, JO Rosenberg, AG Callaghan, JJ TI IMPROVED LONG-TERM RESULTS OF FEMORAL FIXATION IN REVISION SURGERY USING MODERN CEMENTING SO TOTAL HIP REVISION SURGERY SE BRISTOL-MYERS SQUIBB / ZIMMER ORTHOPAEDIC SYMPOSIUM SERIES LA English DT Proceedings Paper CT 8th Annual Bristol-Myers Squibb/Zimmer Orthopaedic Research Symposium - Current Concepts in Total Hip Revision Surgery CY NOV 19-21, 1993 CL CHICAGO, IL SP BRISTOL MYERS SQUIBB ZIMMER C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ORTHOPAED BIOMECHAN LAB,HIP & IMPLANT UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 BN 0-7817-0231-3 J9 BRIS MYER Z PY 1995 BP 289 EP 294 PG 6 WC Orthopedics; Surgery SC Orthopedics; Surgery GA BC41R UT WOS:A1995BC41R00031 ER PT B AU JASTY, M HARRIS, WH AF JASTY, M HARRIS, WH BE Galante, JO Rosenberg, AG Callaghan, JJ TI CEMENTLESS ACETABULAR REVISIONS SO TOTAL HIP REVISION SURGERY SE BRISTOL-MYERS SQUIBB / ZIMMER ORTHOPAEDIC SYMPOSIUM SERIES LA English DT Proceedings Paper CT 8th Annual Bristol-Myers Squibb/Zimmer Orthopaedic Research Symposium - Current Concepts in Total Hip Revision Surgery CY NOV 19-21, 1993 CL CHICAGO, IL SP BRISTOL MYERS SQUIBB ZIMMER C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED SURG,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU RAVEN PRESS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 BN 0-7817-0231-3 J9 BRIS MYER Z PY 1995 BP 317 EP 323 PG 7 WC Orthopedics; Surgery SC Orthopedics; Surgery GA BC41R UT WOS:A1995BC41R00035 ER PT B AU HARRIS, WH RUBASH, HE AF HARRIS, WH RUBASH, HE BE Galante, JO Rosenberg, AG Callaghan, JJ TI DISCUSSION OF ACETABULAR REVISION SO TOTAL HIP REVISION SURGERY SE BRISTOL-MYERS SQUIBB / ZIMMER ORTHOPAEDIC SYMPOSIUM SERIES LA English DT Proceedings Paper CT 8th Annual Bristol-Myers Squibb/Zimmer Orthopaedic Research Symposium - Current Concepts in Total Hip Revision Surgery CY NOV 19-21, 1993 CL CHICAGO, IL SP BRISTOL MYERS SQUIBB ZIMMER C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 BN 0-7817-0231-3 J9 BRIS MYER Z PY 1995 BP 347 EP 350 PG 4 WC Orthopedics; Surgery SC Orthopedics; Surgery GA BC41R UT WOS:A1995BC41R00038 ER PT B AU BORTEN, K AF BORTEN, K BE Waegemann, CP TI Using an audit facility to protect patient data at the Massachusetts General Hospital SO TOWARD AN ELECTRONIC PATIENT RECORD '95, PROCEEDINGS, VOL 1 LA English DT Proceedings Paper CT 11th International Symposium on the Creation of Electronic Health Record Systems and Global Congress on Patient Cards CY MAR 14-19, 1995 CL ORLANDO, FL C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MEDICAL RECORDS INSTITUTE PI NEWTON PA 567 WALNUT ST, PO BOX 289, NEWTON, MA 02160 BN 0-9640667-5-0 PY 1995 BP 115 EP 120 PG 6 WC Computer Science, Information Systems; Health Policy & Services SC Computer Science; Health Care Sciences & Services GA BD54M UT WOS:A1995BD54M00029 ER PT J AU DZIECZKOWSKI, JS BARRETT, BB NESTER, D CAMPBELL, M COOK, J SUGRUE, M ANDERSEN, JW ANDERSON, KC AF DZIECZKOWSKI, JS BARRETT, BB NESTER, D CAMPBELL, M COOK, J SUGRUE, M ANDERSEN, JW ANDERSON, KC TI CHARACTERIZATION OF REACTIONS AFTER EXCLUSIVE TRANSFUSION OF WHITE CELL-REDUCED CELLULAR BLOOD COMPONENTS SO TRANSFUSION LA English DT Article ID CYTOMEGALO-VIRUS INFECTION; VERSUS-HOST DISEASE; CANCER RECURRENCE; YERSINIA-ENTEROCOLITICA; HLA ALLOIMMUNIZATION; REDUCTION FILTERS; RANDOMIZED TRIAL; PREVENTION; PLATELETS; LEUKOCYTE AB Background: Potential adverse effects of white cells (WBCs) within transfused cellular blood components include febrile nonhemolytic transfusion reactions (FNHTRs), alloimmunization, transmission of infectious diseases, transfusion-related acute lung injury, and immunomodulation. Although exclusive use of WBC-reduced components to prevent alloimmunization and cytomegalovirus transmission has been studied, the use of these components to avert FNHTR has not been examined. Study Design and Methods: Transfusion reactions (FNHTRs allergic reactions, and others) were characterized in recipients of 12,277 WBC-reduced single-donor apheresis platelets (SDAPs) and/or red cells (RBCs). Medical and laboratory evaluations for possible infectious and immunologic (alloimmunization) causes of each reaction were undertaken, and the benefit of further modification of components for the prevention of subsequent reactions was also evaluated. Results: Transfusion reactions occurred after 481 (3.92%) of 12,277 transfusions. Allergic reactions occurred more commonly after transfusion of SDAPs (3.69%) than of RBCs (0.51%). Conversely FNHTRs occurred more commonly after transfusion of RBCs (2.15%) than of SDAPs (1.58%). HLA antibodies were present in a posttransfusion sample from 27 (10.6%) of 255 patients; bacterial contamination was a possible cause of only 2 (0.42%) of 481 reactions. In patients with recurrent FNHTRs, further WBC reduction in components did not wholly prevent further FNHTRs. Conclusion: The incidence of FNHTRs and alloimmunization after exclusive transfusion of WBC-reduced RBCs and SDAPs was low. Further WBC reduction in components transfused to patients with a history of recurrent FNHTRs does not completely prevent subsequent reactions. C1 HARVARD UNIV,SCH MED,BLOOD COMPONENT LAB,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA. WAYNE STATE UNIV,SCH MED,DEPT PATHOL,DETROIT,MI. FU NCI NIH HHS [CA06516] NR 40 TC 49 Z9 51 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD JAN PY 1995 VL 35 IS 1 BP 20 EP 25 DI 10.1046/j.1537-2995.1995.35195090654.x PG 6 WC Hematology SC Hematology GA PY552 UT WOS:A1995PY55200005 PM 7998063 ER PT J AU GRIMES, RY NYARKO, SJ PULIDO, GA YANG, S WALKER, PG LEVINE, RA YOGANATHAN, AP AF GRIMES, RY NYARKO, SJ PULIDO, GA YANG, S WALKER, PG LEVINE, RA YOGANATHAN, AP TI ATRIAL INFLOW CAN ALTER REGURGITANT JET SIZE - IN-VITRO STUDIES SO ULTRASOUND IN MEDICINE AND BIOLOGY LA English DT Article DE MITRAL REGURGITATION; TRICUSPID REGURGITATION; PULMONARY VENOUS FLOW; COUNTERFLOW; COLOR DOPPLER FLOW MAPPING; REGURGITANT JETS; DIMENSIONAL ANALYSIS ID COLOR DOPPLER FLOW; MITRAL REGURGITATION; PULSED DOPPLER; NONINVASIVE QUANTIFICATION; TRICUSPID REGURGITATION; PULMONARY VEIN; ECHOCARDIOGRAPHY; MOMENTUM; VELOCITIES; MODEL AB Recent studies have attempted to predict the severity of regurgitant lesions from color Doppler jet size, which is a function of orifice momentum for free jets, Jets of mitral and tricuspid regurgitation, however, are opposed by flows entering the atria, Despite their low velocities, these counterflows may have considerable momentum that can limit jet penetration, The purpose of this study was to address the hypothesis that such counterflow fields influence regurgitant jet size, Steady flow was driven through 2.4- and 5.1-mm-diameter circular orifices at 2 to 6 m/s, At a constant orifice velocity and flow rate, the velocity of a uniform counterflow field was varied from 5 to 30 cm/s, Jet dimensions were measured by both fluorescent dye visualization and Doppler color flow mapping, The results showed that despite its relatively low velocities, counterflow dramatically curtailed jet length and area, Jet dimensions were functions of the ratio of jet to counterflow momentum, Thus, atrial inflow may participate in determining jet size and can alter the relation between jet size and lesion severity in mitral and tricuspid regurgitation. C1 GEORGIA INST TECHNOL,SCH MECH ENGN,ATLANTA,GA 30332. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC ULTRASOUND LAB,BOSTON,MA. RP GRIMES, RY (reprint author), GEORGIA INST TECHNOL,SCH CHEM ENGN,CARDIOVASC FLUID MECH LAB,ATLANTA,GA 30332, USA. FU NHLBI NIH HHS [HL38176, HL45485] NR 36 TC 7 Z9 7 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0301-5629 J9 ULTRASOUND MED BIOL JI Ultrasound Med. Biol. PY 1995 VL 21 IS 4 BP 459 EP 469 DI 10.1016/0301-5629(94)00138-4 PG 11 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA RA236 UT WOS:A1995RA23600004 PM 7571139 ER PT J AU BURLESON, AC NGUYEN, T FONTAINE, A LEVINE, RA YOGANATHAN, AP AF BURLESON, AC NGUYEN, T FONTAINE, A LEVINE, RA YOGANATHAN, AP TI A MODEL-BASED ON DIMENSIONAL ANALYSIS FOR NONINVASIVE QUANTIFICATION OF VALVULAR REGURGITATION UNDER CONFINED AND IMPINGING CONDITIONS - IN-VITRO PULSATILE FLOW VALIDATION SO ULTRASOUND IN MEDICINE AND BIOLOGY LA English DT Article DE VALVULAR REGURGITATION; CONFINED IMPINGING JETS; DIMENSIONAL ANALYSIS; DOPPLER ULTRASOUND; PEAK REGURGITANT FLOW RATE; IN VITRO FLOW MODEL ID MITRAL REGURGITATION; PULSED-DOPPLER; TRICUSPID REGURGITATION; ULTRASOUND; ECHOCARDIOGRAPHY; PRESSURE; INVITRO; INSUFFICIENCY; DIAGNOSIS; DISEASE AB A technique is proposed for the noninvasive quantification of regurgitant flows under confined and impinging conditions, Its use requires only the knowledge of the jet orifice velocity, receiving chamber diameter, orifice-to-end wall distance and any downstream jet centerline velocity at a known distance from the orifice, The technique is based on dimensional analysis and provides a prediction of peak regurgitant flow rates, To validate the technique, known physiologic pulsatile flows were pumped through 2- and 4-mm circular orifices at 70 to 150 beats/min, into two different receiving chambers of 51 and 88 mm in diameter. At each heart rate, the peak orifice velocity was varied from 2 to 5 m/s, and the orifice-to-end wall distance was varied from 30 to 93 mm. Centerline velocities were recorded by pulsed Doppler ultrasound and averaged over multiple beats. A dimensional analysis of the parameters of the study provided an equation relating normalized centerline velocity to orifice-to-end wall distance, chamber diameter and downstream location, Statistical modeling of the experimental data was performed to compute the constants involved in this equation, The estimated (i.e., predicted by the technique) peak regurgitant flow rates were found to fall within 10% of the actual values, when centerline velocities were measured over a range of centerline distances from six orifice diameters to 85% of the chamber length. Therefore, the proposed technique provides, for the first time, a quantitative method for calculating valvular regurgitant flow rates under confined and impinging conditions. C1 GEORGIA INST TECHNOL,SCH CHEM ENGN,CARDIOVASC FLUID MECH LAB,ATLANTA,GA 30332. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC ULTRASOUND LAB,BOSTON,MA. FU NHLBI NIH HHS [HL-45485] NR 44 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 0301-5629 J9 ULTRASOUND MED BIOL JI Ultrasound Med. Biol. PY 1995 VL 21 IS 7 BP 899 EP 911 DI 10.1016/0301-5629(95)00035-P PG 13 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA RQ775 UT WOS:A1995RQ77500005 PM 7491745 ER PT J AU DOUKAS, AG MCAULIFFE, DJ LEE, S VENUGOPALAN, V FLOTTE, TJ AF DOUKAS, AG MCAULIFFE, DJ LEE, S VENUGOPALAN, V FLOTTE, TJ TI PHYSICAL FACTORS INVOLVED IN STRESS-WAVE-INDUCED CELL INJURY - THE EFFECT OF STRESS GRADIENT SO ULTRASOUND IN MEDICINE AND BIOLOGY LA English DT Article DE ABLATION; PHOTOACOUSTICS; SHOCK WAVES; STRESS GRADIENT; CELL VIABILITY; MEMBRANE PERMEABILITY ID ENERGY SHOCK-WAVES; EXCIMER-LASER; INVITRO; PERMEABILITY; L1210-CELLS; IRRADIATION; EXPOSURE; DAMAGE; TUMORS; INVIVO AB We have studied the biological effects of ablation-induced stress waves in vitro. Mouse breast sarcoma cells (EMT-6) were exposed to stress waves that differed only in rise time, Two assays were used to determine cell injury: incorporation of tritiated thymidine (viability assay), and transmission electron microscopy (morphology assay), We present evidence that the rise time of stress waves can significantly modify cell viability and that cell injury correlates better with the stress gradient than peak stress. C1 HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. RP DOUKAS, AG (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,WEL 224 BOSTON,BOSTON,MA 02114, USA. NR 35 TC 58 Z9 60 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0301-5629 J9 ULTRASOUND MED BIOL JI Ultrasound Med. Biol. PY 1995 VL 21 IS 7 BP 961 EP 967 DI 10.1016/0301-5629(95)00027-O PG 7 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA RQ775 UT WOS:A1995RQ77500010 PM 7491750 ER PT S AU HOHMANN, EL OLETTA, CA MILLER, SI AF HOHMANN, EL OLETTA, CA MILLER, SI BE Chanock, RM Brown, F Ginsberg, HS Norrby, E TI PhoP-regulated expression of a model antigen in Salmonella typhimurium enhances immunogenicity SO VACCINES 95 - MOLECULAR APPROACHES TO THE CONTROL OF INFECTIOUS DISEASES SE VACCINES (COLD SPRING HARBOR LABORATORY PRESS) LA English DT Proceedings Paper CT 12th Annual Meeting on Molecular Approaches to the Control of Infectious Diseases CY OCT, 1994 CL COLD SPRING HARBOR, NY SP Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Boehringer Mannheim Corp, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, Du Pont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxco, Hoffman La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Tekeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU COLD SPRING HARBOR LABORATORY PRESS PI PLAINVIEW PA 10 SKYLINE DRIVE, PLAINVIEW, NY 11803-2500 SN 0899-4056 BN 0-87969-467-X J9 VACCINES PY 1995 BP 287 EP 292 PG 6 WC Immunology; Infectious Diseases; Medicine, Research & Experimental SC Immunology; Infectious Diseases; Research & Experimental Medicine GA BD72G UT WOS:A1995BD72G00045 ER PT J AU Habener, JF Miller, CP Vallejo, M AF Habener, JF Miller, CP Vallejo, M TI cAMP-dependent regulation of gene transcription by cAMP response element-binding protein and cAMP response element modulator SO VITAMINS AND HORMONES - ADVANCES IN RESEARCH AND APPLICATIONS, VOL 51 SE VITAMINS AND HORMONES-ADVANCES IN RESEARCH AND APPLICATIONS LA English DT Review ID PANCREATIC-ISLET CELLS; PHOSPHOENOLPYRUVATE CARBOXYKINASE GTP; STEROID-RECEPTOR SUPERFAMILY; LEUCINE ZIPPER PROTEINS; SCISSORS-GRIP MODEL; RAT GLUCAGON GENE; KINASE TYPE-II; CYCLIC-AMP; DNA-BINDING; FACTOR CREB C1 MASSACHUSETTS GEN HOSP,REPROD ENDOCRINOL UNIT,BOSTON,MA 02114. RP Habener, JF (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,LAB MOLEC ENDOCRINOL,BOSTON,MA 02114, USA. NR 195 TC 80 Z9 81 U1 2 U2 3 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0083-6729 J9 VITAM HORM PY 1995 VL 51 BP 1 EP 57 PG 57 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA BE46L UT WOS:A1995BE46L00001 PM 7483321 ER PT J AU WEISS, TW AF WEISS, TW TI IMPROVEMENTS IN VA HEALTH-SERVICES FOR WOMEN VETERANS SO WOMEN & HEALTH LA English DT Article; Proceedings Paper CT 12th Annual VA HSR&D Service Meeting CY APR, 1994 CL WASHINGTON, DC SP VA HSR&D ID FEMALE VETERANS AB Since the early 1980s, health care for women veterans in the Department of Veterans Affairs (VA) has improved considerably, although problems still remain. The lack of privacy for women at many VA facilities and the provision of incomplete physical examinations for women continue to be problematic issues. A 1992 congressional appropriation of $7.5 million has substantially increased the awareness of women veterans health care in the VA. This appropriation, from Public Law 102-585, Veterans Health Care Act of 1992, Title I-Women Veterans Health Programs, has allowed VA to expand services for women veterans. Using these funds, VA has established eight comprehensive women veterans health centers, 23 full-time women veterans coordinators, and four regional stress disorder teams. This paper describes these and other important new initiatives and discusses how they will serve as the foundation on which VA expands care for women within the context of a changing health care system. C1 BAYLOR COLL MED,HOUSTON,TX 77030. RP WEISS, TW (reprint author), HOUSTON VAMC,HOUSTON CTR QUAL CARE & UTILIZAT STUDIES,VA HSR&D FIELD PROGRAM,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 24 TC 14 Z9 14 U1 1 U2 1 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0363-0242 J9 WOMEN HEALTH JI Women Health PY 1995 VL 23 IS 2 BP 1 EP 12 DI 10.1300/J013v23n02_01 PG 12 WC Public, Environmental & Occupational Health; Women's Studies SC Public, Environmental & Occupational Health; Women's Studies GA TE921 UT WOS:A1995TE92100001 PM 8585222 ER PT J AU KLASSEN, H KLASSEN, MK HUNCHAREK, M AF KLASSEN, H KLASSEN, MK HUNCHAREK, M TI GROUP-B STREPTOCOCCAL MENINGITIS PRESENTING AS STROKE IN A NONDEBILITATED MAN SO YALE JOURNAL OF BIOLOGY AND MEDICINE LA English DT Article ID CHILDHOOD BACTERIAL-MENINGITIS; CEREBRAL INFARCTION; ADULTS; DISEASE; BACTEREMIA AB An unusual case of group B streptococcal meningitis in an adult is described. The evidence presented suggests that early vascular involvement during the meningitic process resulted in cerebral infarction, thereby explaining the patient's sudden deterioration and atypical presentation. C1 HARVARD UNIV,CAMBRIDGE HOSP,SCH MED,DEPT MED,CAMBRIDGE,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. NR 39 TC 3 Z9 3 U1 0 U2 0 PU YALE J BIOL MED INC PI NEW HAVEN PA 333 CEDAR ST, NEW HAVEN, CT 06510 SN 0044-0086 J9 YALE J BIOL MED JI Yale J. Biol. Med. PD JAN-APR PY 1995 VL 68 IS 1-2 BP 1 EP 6 PG 6 WC Biology; Medicine, General & Internal; Medicine, Research & Experimental SC Life Sciences & Biomedicine - Other Topics; General & Internal Medicine; Research & Experimental Medicine GA TK333 UT WOS:A1995TK33300001 PM 8748460 ER EF