FN Thomson Reuters Web of Science™ VR 1.0 PT J AU ROYALL, DR MAHURIN, RK CORNELL, J AF ROYALL, DR MAHURIN, RK CORNELL, J TI BEDSIDE ASSESSMENT OF FRONTAL DEGENERATION - DISTINGUISHING ALZHEIMERS-DISEASE FROM NON-ALZHEIMERS CORTICAL DEMENTIA SO EXPERIMENTAL AGING RESEARCH LA English DT Article ID COGNITIVE IMPAIRMENT; FEATURES AB Two instruments, the Executive Interview (EXIT) and the Qualitative Evaluation of Dementia (QED), that are useful in the evaluation of frontal system failure are discussed. The ability of these instruments to discriminate frontal-type dementia (FTD) from Alzheimer's disease (AD) and the dementia of major depression (DMD) was examined in 100 consecutive elderly dementia patients presenting to a multidisciplinary geriatric clinic. All groups showed executive impairment by the EXIT, and 46% of the FTD patients were found to be unimpaired by the Mini-Mental State Examination (MMSE). The AD and FTD groups differed significantly from the DMD group on the QED. The QED alone could not distinguish AD from FTD cases. However, mapping of scores against MMSE (errors) scores revealed that AD and FTD follow very different regression lines. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT PSYCHIAT,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT MED,SAN ANTONIO,TX. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 20 TC 47 Z9 47 U1 1 U2 1 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0361-073X J9 EXP AGING RES JI Exp. Aging Res. PD APR-JUN PY 1994 VL 20 IS 2 BP 95 EP 103 DI 10.1080/03610739408253956 PG 9 WC Geriatrics & Gerontology; Psychology SC Geriatrics & Gerontology; Psychology GA NE556 UT WOS:A1994NE55600002 PM 8020544 ER PT J AU SEONG, SC MATSUMURA, T LEE, FY WHELAN, MC LI, XQ TRIPPEL, SB AF SEONG, SC MATSUMURA, T LEE, FY WHELAN, MC LI, XQ TRIPPEL, SB TI INSULIN-LIKE GROWTH-FACTOR-I REGULATION OF SWARM RAT CHONDROSARCOMA CHONDROCYTES IN CULTURE SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID MULTIPLICATION-STIMULATING ACTIVITY; ARTICULAR-CARTILAGE EXPLANTS; SOMATOMEDIN-C; PROTEOGLYCAN BIOSYNTHESIS; COLLAGEN-SYNTHESIS; BOVINE SERUM; IGF-I; PROTEIN; HORMONE; FETAL AB Insulin-like growth factor I (IGF-I) is anabolic for chondrocytes and is thought to be important in regulating such normal cartilaginous tissues as the epiphyseal growth plate. In the present studies, we have investigated the role of IGF-I in the regulation of neoplastic cartilage. Chondrocytes cultured from a transplantable rat chondrosarcoma were analyzed for responsiveness to IGF-I with respect to DNA and glycosaminoglycan synthesis as determined by labeling with radioactive thymidine and sulfate, respectively. Stimulation of [H-3]- thymidine and [S-35]sulfate incorporation by IGF-I was two to four times that in serum-free controls, with half-maximal stimulation at 1 X 10(-9) M. The efficacy of IGF-I was approximately one-half of that of serum in stimulating [H-3]thymidine incorporation and was comparable to that of serum for [S-35]sulfate incorporation. When Swarm rat chondrosarcoma chondrocytes were cultured in the presence of IGF-I and exposed to graded concentrations of anti-IGF-I antibody, [H-3]thymidine incorporation and [S-35]sulfate incorporation were attenuated in a dose-dependent fashion to 29 and 25% of antibody-free controls, respectively. Nonspecific antibody not raised against IGF-I was not inhibitory. These observations suggest that the majority of IGF-I action on these cells is susceptible to immunoinhibition. To estimate the contribution of IGF-I to the regulation of these cells by serum, Swarm rat chondrosarcoma chondrocytes were cultured with graded concentrations of either calf serum or fetal calf serum in the presence of anti-IGF-I antibody, nonspecific antibody, or no other additives. Specific antibody attenuated the effect of calf serum on both [H-3]thymidine and [S-35]sulfate incorporation with overall inhibition of 52% (P < 0.01) and 48% (P < 0.001), respectively. Nonspecific antibody superimposed small, variably stimulatory or inhibitory effects on those of calf serum. When chondrosarcoma chondrocytes were incubated with fetal calf serum, anti-IGF-I antibody exerted a minimal inhibitory effect, reducing both [H-3]thymidine and [S-35]sulfate incorporation by less than 25%. The immunoinhibition of both pre- and postnatal serum could be overcome in a dose-dependent fashion by increasing serum concentrations. These results suggest that the factors influencing Swarm rat chondrosarcoma chondrocytes may be developmentally regulated and that the contribution of IGF-I to the action of serum increases between fetal and postnatal life. These data support the hypothesis that chondrosarcoma is a somatomedin-responsive neoplasm and suggest that this tumor may be susceptible to interventions directed toward mechanisms that block insulin-like growth factor action. (C) 1994 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Seong, Sang Cheol/J-5514-2012 NR 55 TC 13 Z9 14 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD APR PY 1994 VL 211 IS 2 BP 238 EP 244 DI 10.1006/excr.1994.1083 PG 7 WC Oncology; Cell Biology SC Oncology; Cell Biology GA NE897 UT WOS:A1994NE89700009 PM 8143769 ER PT J AU WONG, J WANG, N MILLER, JW SCHUMAN, JS AF WONG, J WANG, N MILLER, JW SCHUMAN, JS TI MODULATION OF HUMAN FIBROBLAST ACTIVITY BY SELECTED ANGIOGENESIS INHIBITORS SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE BETA-CYCLODEXTRIN TETRADECASULFATE (BCD-TDS); AGM-1470; ANGIOGENESIS INHIBITORS; TENONS FIBROBLASTS; CELL CULTURE ID ENDOTHELIAL-CELLS; HEPARIN FRAGMENT; GROWTH; NEOVASCULARIZATION; 5-FLUOROURACIL; PROLIFERATION; MITOMYCIN; INVITRO; SURGERY; SHAPE C1 TUFTS UNIV,NEW ENGLAND MED CTR HOSP,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,LASER RES CTR,RETINA SERV,BOSTON,MA 02114. RI Schuman, Joel/K-7304-2012 OI Schuman, Joel/0000-0002-8885-3766 NR 24 TC 36 Z9 38 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD APR PY 1994 VL 58 IS 4 BP 439 EP 451 DI 10.1006/exer.1994.1037 PG 13 WC Ophthalmology SC Ophthalmology GA NK169 UT WOS:A1994NK16900008 PM 7523160 ER PT J AU NEBEN, S DONALDSON, D SIEFF, C MAUCH, P BODINE, D FERRARA, J YETZALDAPE, J TURNER, K AF NEBEN, S DONALDSON, D SIEFF, C MAUCH, P BODINE, D FERRARA, J YETZALDAPE, J TURNER, K TI SYNERGISTIC EFFECTS OF INTERLEUKIN-11 WITH OTHER GROWTH-FACTORS ON THE EXPANSION OF MURINE HEMATOPOIETIC PROGENITORS AND MAINTENANCE OF STEM-CELLS IN LIQUID CULTURE SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE INTERLEUKIN-11; STEM CELLS; STEEL FACTOR; HEMATOPOIESIS ID MEDIATED GENE-TRANSFER; C-KIT; INVITRO; PROLIFERATION; LIGAND; MICE; IDENTIFICATION; SURVIVAL; CYTOKINE; NUMBER AB The effect of interleukin-11 (IL-11), alone and in combination with other hematopoietic growth factors, was studied in liquid suspension cultures of murine bone marrow. Stem and progenitor cell contents of input bone marrow 2 days after 5-fluorouracil (5-FU) treatment (FU(2d)BM) and lineage-depleted, Sca-1-positive FU(2d)BM (Lid(-)Sca(+)FU(2d)BM) were compared with output values obtained after 6 days in different growth factor combinations. Stem and progenitor cell recoveries were measured by long-term in vivo competitive repopulation, spleen colony-forming unit (CFU-S), and in vitro limiting dilution long-term bone marrow culture (cobblestone area-forming cell [CAFC]) assays. IL-11, IL-3, IL-6, and Steel factor (SF) were tested separately and in combinations of two, three, and four factors. IL-11 was incapable of maintaining the survival of stem or progenitor cells as a single agent but synergized with either IL-3 or SF to expand progenitor cell output in cultures of FU(2d)BM. IL-11 greatly enhanced progenitor cell expansion from FU(2d)BM when added to two- and three-factor combinations of SF, IL-3, and IL6, The recovery of long-term repopulating ability was enhanced four-fold by incubation in SF plus IL-11 compared to SF alone. IL-11 in combination with SF, IL-3, and IL-6 stimulated a 24,000-fold expansion of progenitor cells from stem cell-enriched Lin(-)Sca(+)FU(2d)BM, Overall, the results indicate that IL-11 is a potent synergistic factor for stem cell proliferation and expansion of progenitors in liquid culture. C1 DANA FARBER CANC INST,DIV PEDIAT HEMATOL & ONCOL,BOSTON,MA. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. RP NEBEN, S (reprint author), GENET INST INC,87 CAMBRIDGEPK DR,CAMBRIDGE,MA 02140, USA. NR 43 TC 50 Z9 52 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD APR PY 1994 VL 22 IS 4 BP 353 EP 359 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA NE560 UT WOS:A1994NE56000003 PM 8150033 ER PT J AU WULLNER, U PAKZABAN, P BROWNELL, AL HANTRAYE, P BURNS, L SHOUP, T ELMALEH, D PETTO, AJ SPEALMAN, RD BROWNELL, GL ISACSON, O AF WULLNER, U PAKZABAN, P BROWNELL, AL HANTRAYE, P BURNS, L SHOUP, T ELMALEH, D PETTO, AJ SPEALMAN, RD BROWNELL, GL ISACSON, O TI DOPAMINE TERMINAL LOSS AND ONSET OF MOTOR SYMPTOMS IN MPTP-TREATED MONKEYS - A POSITRON EMISSION TOMOGRAPHY STUDY WITH C-11 CFT SO EXPERIMENTAL NEUROLOGY LA English DT Note ID IDIOPATHIC PARKINSONS-DISEASE; RHESUS-MONKEY; BRAIN; PRIMATE; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; PATTERN; PUTAMEN; MODEL; PET AB We studied the time course of dopamine (DA) terminal loss in three macaca fascicularis injected with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) intravenously every 10-14 days for up to 389 days. Striatal DA terminal loss was monitored in vivo by positron emission tomography using C-11-CFT (WIN 35,428), a cocaine derivative that labels the DA transporter. The C-11-CFT uptake rate constant in the striatum of MPTP-treated monkeys decreased exponentially over time, with the putamen significantly more affected than the caudate. Spontaneous locomotor activity decreased in parallel with the decline of the C-11-CFT uptake rate; however, overt parkinsonian signs appeared only after the C-11-CFT uptake rate had declined to about 30% of the pretreatment values. We conclude that a long-term intermittent mode of administration of MPTP can lead to a pattern of terminal loss that closely resembles idiopathic Parkinson disease. (C) 1994 Academic Press, Inc. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,SOUTHBOROUGH,MA 01772. NEW ENGLAND REG PRIMATE RES CTR,DIV BEHAV BIOL,SOUTHBOROUGH,MA 01772. RP WULLNER, U (reprint author), MCLEAN HOSP,NEUROREGENERAT LABS,115 MILL ST,BELMONT,MA 02178, USA. FU NIMH NIH HHS [MH14275]; NINDS NIH HHS [NS29178, NS30064] NR 22 TC 37 Z9 37 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD APR PY 1994 VL 126 IS 2 BP 305 EP 309 DI 10.1006/exnr.1994.1069 PG 5 WC Neurosciences SC Neurosciences & Neurology GA NM716 UT WOS:A1994NM71600017 PM 7925829 ER PT J AU FRUMAN, DA BURAKOFF, SJ BIERER, BE AF FRUMAN, DA BURAKOFF, SJ BIERER, BE TI IMMUNOPHILINS IN PROTEIN-FOLDING AND IMMUNOSUPPRESSION SO FASEB JOURNAL LA English DT Article DE CYCLOSPORINE A; CYCLOPHILIN; FK506; RAPAMYCIN; FKBP; CALCINEURIN ID CIS-TRANS-ISOMERASE; CALCINEURIN PHOSPHATASE-ACTIVITY; RAPAMYCIN-BINDING-PROTEIN; CYCLOPHILIN MULTIGENE FAMILY; P70 S6 KINASE; CYCLOSPORINE-A; SACCHAROMYCES-CEREVISIAE; FK506-BINDING PROTEIN; YEAST CYCLOPHILIN; LYMPHOCYTES-T AB Lymphocyte activation requires the transmission of signals from molecules at the plasma membrane to nuclear signals that regulate gene expression. In recent years, several immunosuppressive compounds have been used as probes to identify important and potentially novel molecules involved in lymphocyte signal transduction processes. The immunosuppressants cyclosporin A (CsA), FK506, and rapamycin have been studied in particular detail. Two distinct classes of immunosuppressant binding proteins have been identified, and collectively termed immunophilins. The cyclophilin family of immunophilins binds CsA, whereas the FK506-binding protein (FKBP) family binds FK506 and rapamycin. This review will discuss both the endogenous functions of immunophilins as well as their roles in mediating immunosuppression. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DIV MED SCI,COMM IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 89 TC 212 Z9 219 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 1 PY 1994 VL 8 IS 6 BP 391 EP 400 PG 10 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH250 UT WOS:A1994NH25000005 PM 7513288 ER PT J AU BHATTA, N ISAACSON, K BHATTA, KM ANDERSON, RR SCHIFF, I AF BHATTA, N ISAACSON, K BHATTA, KM ANDERSON, RR SCHIFF, I TI COMPARATIVE-STUDY OF DIFFERENT LASER SYSTEMS SO FERTILITY AND STERILITY LA English DT Article DE LASERS; LASER PHYSICS; LASER-TISSUE INTERACTION; LASER DELIVERY SYSTEM ID PHOTORADIATION THERAPY; PHOTODYNAMIC THERAPY; ARGON-LASER; ENDOMETRIAL ABLATION; YAG LASER; PHASE-I; TISSUE; TUMORS; REANASTOMOSIS; LAPAROSCOPY AB Objective: To review lasers, laser physics, laser-tissue interaction, delivery systems, and their clinical applications relevant to gynecology. Settings: Gynecological Service at Massachusetts General Hospital (MGH) and MGH Laser Center. Interventions: None. Design: Laser literature review and personal experiences of the authors were used to prepare this manuscript. Conclusions: Lasers have been used in gynecologic practice for cutting and coagulating pur poses. Photodynamic therapy has been used clinically for malignant conditions and is being investigated for dysplastic lesions of the lower genital tract and for endometrial ablation. Laser welding has potential, but further work is required in this field before it finds a clinical application. The main lasers used in gynecology are CO2, neodymium-yttrium aluminum garnet (Nd:YAG), and potassium tatanyl-phosphate-doubled Nd:YAG. Pulsed Ho:YAG laser looks promising, as does diode lasers. Holmium-yttrium aluminum garnet and diode lasers will be soon available commercially. Improvements in delivery systems have increased user friendliness, and more developments in this area are anticipated, for example, a fiber-optic delivery system for CO2 lasers. We believe that enhanced understanding of laser technology will provide unique applications for development in gynecology. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 50 TC 22 Z9 22 U1 1 U2 1 PU AMER SOC REPRODUCTIVE MEDICINE PI BIRMINGHAM PA 1209 MONTGOMERY HIGHWAY, BIRMINGHAM, AL 35216-2809 SN 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD APR PY 1994 VL 61 IS 4 BP 581 EP 591 PG 11 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA NE515 UT WOS:A1994NE51500001 PM 8150095 ER PT J AU BABYATSKY, MW THIM, L PODOLSKY, DK AF BABYATSKY, MW THIM, L PODOLSKY, DK TI TREFOIL PEPTIDES PROTECT AGAINST ETHANOL AND INDOMETHACIN-INDUCED GASTRIC INJURY IN RATS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NERPC,CTR STUDY INFLAMMATORY BOWL DIS,BOSTON,MA 02114. BIOSCI NOVO RES INST,COPENHAGEN,DENMARK. NR 0 TC 6 Z9 6 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A43 EP A43 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90900166 ER PT J AU CHUNG, DC BRAND, SJ TILLOTSON, LG AF CHUNG, DC BRAND, SJ TILLOTSON, LG TI REGULATION OF GASTRIN GENE-EXPRESSION BY A NOVEL HOMEODOMAIN FACTOR AND SP1 SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GI UNIT,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A803 EP A803 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903196 ER PT J AU CHUNG, RT NEW, TN DIENSTAG, JL KAPLAN, LM AF CHUNG, RT NEW, TN DIENSTAG, JL KAPLAN, LM TI HEPATITIS-C VIRUS CIRCULATES IN THE CEREBROSPINAL-FLUID OF INFECTED INDIVIDUALS BUT DOES NOT CAUSE MENINGITIS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A876 EP A876 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903486 ER PT J AU DARMOUL, D WANG, A OUELLETTE, AJ AF DARMOUL, D WANG, A OUELLETTE, AJ TI DIFFERENTIAL EXPRESSION OF CRYPTDIN GENES DURING CRYPT ONTOGENY AND ALONG THE LONGITUDINAL AXIS OF MOUSE SMALL-INTESTINE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,SHRINERS BURN INST,SURG SERV,BOSTON,MA 02114. NR 1 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A603 EP A603 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902397 ER PT J AU DIGNASS, A PODOLSKY, D RACHMILEWITZ, D AF DIGNASS, A PODOLSKY, D RACHMILEWITZ, D TI NITRIC-OXIDE GENERATION BY INTESTINAL EPITHELIAL-CELLS IS STIMULATED BY CYTOKINES AND BACTERIAL-ENDOTOXIN SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR INFLAMMATORY BOWEL DIS,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A673 EP A673 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902677 ER PT J AU DIGNASS, A LYNCHDEVANEY, K KINDON, H THIM, L PODOLSKY, DK AF DIGNASS, A LYNCHDEVANEY, K KINDON, H THIM, L PODOLSKY, DK TI TREFOIL PEPTIDES PROMOTE EPITHELIAL RESTITUTION THROUGH A TGF-BETA-INDEPENDENT PATHWAY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NERPRC,CTR STUDY INFLAMMATORY BOWEL DIS,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A673 EP A673 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902675 ER PT J AU DIGNASS, AU TSUNEKAWA, S PODOLSKY, DK AF DIGNASS, AU TSUNEKAWA, S PODOLSKY, DK TI FIBROBLAST GROWTH-FACTORS MODULATE INTESTINAL EPITHELIAL-CELL GROWTH AND MIGRATION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR STUDY INFLAMMATORY BOWEL DIS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A603 EP A603 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902400 ER PT J AU FOITZIK, T FERNANDEZDELCASTILLO, C WARSHAW, AL KLAR, E RATTNER, DW AF FOITZIK, T FERNANDEZDELCASTILLO, C WARSHAW, AL KLAR, E RATTNER, DW TI ALCOHOL IMPAIRS PANCREATIC OXYGENATION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. DEPT SURG,HEIDELBERG,GERMANY. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A292 EP A292 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901158 ER PT J AU FRICK, TW MITHOFER, K FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL AF FRICK, TW MITHOFER, K FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL TI INTRACELLULAR TRYPSINOGEN ACTIVATION IS ASSOCIATED WITH ELEVATED EXTRACELLULAR CALCIUM, BUT NOT SUPRAMAXIMAL CERULEIN STIMULATION IN RAT PANCREATIC ACINI SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. UNIV HOSP ZURICH,DEPT SURG,CH-8091 ZURICH,SWITZERLAND. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A293 EP A293 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901160 ER PT J AU FRICK, TW FERNANDEZDELCASTILLO, C MITHOFER, K RATTNER, DW WARSHAW, AL AF FRICK, TW FERNANDEZDELCASTILLO, C MITHOFER, K RATTNER, DW WARSHAW, AL TI TRYPSINOGEN ACTIVATION IS ACCELERATED BY CALCIUM SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A292 EP A292 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901159 ER PT J AU GILBERT, RJ FLAHERTY, RF SELTZER, S WEISSKOFF, R AF GILBERT, RJ FLAHERTY, RF SELTZER, S WEISSKOFF, R TI SPATIOTEMPORAL ASSESSMENT OF VOCAL CORD MOTION DURING DEGLUTITION BY ULTRAFAST MAGNETIC-RESONANCE-IMAGING (MRI) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ST ELIZABETH HOSP,WASHINGTON,DC 20032. MASSACHUSETTS GEN HOSP,NMR IMAGING CTR,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A503 EP A503 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902001 ER PT J AU HOECKER, M ZHANG, Z CHULAK, MB WANG, TC AF HOECKER, M ZHANG, Z CHULAK, MB WANG, TC TI THE HISTIDINE-DECARBOXYLASE PROMOTER IS REGULATED BY GASTRIN IN GASTRIC-CANCER CELL-LINES SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A815 EP A815 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903243 ER PT J AU JACOBY, RF MARSHALL, DJ SCHLACK, S HARMS, B LOVE, RR AF JACOBY, RF MARSHALL, DJ SCHLACK, S HARMS, B LOVE, RR TI DNA-REPLICATION ERRORS DURING ADENOMA TO CARCINOMA PROGRESSION IN HNPCC SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT HUMAN ONCOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI 53706. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A398 EP A398 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901580 ER PT J AU LEWIS, JD DAVIES, JK GRUTZENDLER, J KAPLAN, LM AF LEWIS, JD DAVIES, JK GRUTZENDLER, J KAPLAN, LM TI FUNCTIONAL ISOFORMS OF THE TRKC NEUROTROPHIN-3 RECEPTOR ARE PREFERENTIALLY EXPRESSED IN THE DEVELOPING RAT ENTERIC NERVOUS-SYSTEM SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR STUDY IBD,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. RI Grutzendler, Jaime/F-3691-2010 NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A821 EP A821 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903268 ER PT J AU MITHOFER, K FRICK, TW FERNANDEZDELCASTILLO, C LEWANDROWSKI, KB BASSI, DG RATTNER, DW WARSHAW, AL AF MITHOFER, K FRICK, TW FERNANDEZDELCASTILLO, C LEWANDROWSKI, KB BASSI, DG RATTNER, DW WARSHAW, AL TI EVIDENCE FOR ECTOPIC TRYPSINOGEN ACTIVATION IN HYPERCALCEMIA-INDUCED PANCREATITIS IN THE RAT SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A1040 EP A1040 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90904137 ER PT J AU MORALES, V DASS, C POLISCHUK, J RUSSELL, G MIZOGUCHI, A BHAN, A BLUMBERG, R AF MORALES, V DASS, C POLISCHUK, J RUSSELL, G MIZOGUCHI, A BHAN, A BLUMBERG, R TI CLONING AND CHARACTERIZATION OF A NOVEL INTESTINAL EPITHELIAL-CELL (IEC) LIGAND FOR T-CELLS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A738 EP A738 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902937 ER PT J AU NAKAGAWA, H ZUCKERBERG, L TOGAWA, K YANG, WI NISHIHIRA, T RUSTGI, AK AF NAKAGAWA, H ZUCKERBERG, L TOGAWA, K YANG, WI NISHIHIRA, T RUSTGI, AK TI CYCLIN-D1 ONCOGENE OVEREXPRESSION AND AMPLIFICATION IN ESOPHAGUS SQUAMOUS-CELL CARCINOMA SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. TOHOKU UNIV,DEPT SURG,SENDAI,MIYAGI 980,JAPAN. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A419 EP A419 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901666 ER PT J AU OGUCHI, S WALKER, WA SANDERSON, IR AF OGUCHI, S WALKER, WA SANDERSON, IR TI GROWTH-FACTORS MODULATE INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEINS IN HUMAN INTESTINAL EPITHELIAL-CELLS DURING DIFFERENTIATION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,DEV GASTROENTEROL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A624 EP A624 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902482 ER PT J AU RALL, CJN GRAEMECOOKE, F BEAUCHAMP, R YANDELL, DW RUSTGI, AK AF RALL, CJN GRAEMECOOKE, F BEAUCHAMP, R YANDELL, DW RUSTGI, AK TI P53 TUMOR-SUPPRESSOR GENE-MUTATIONS AND PROTEIN OVEREXPRESSION IN PANCREATIC DUCTAL ADENOCARCINOMAS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A431 EP A431 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901711 ER PT J AU RUSTGI, AK TOGAWA, K AF RUSTGI, AK TOGAWA, K TI MITOGEN ACTIVATING PROTEIN (MAP) KINASE INCREASES C-MYC TRANSCRIPTIONAL ACTIVATION IN CACO2 CELLS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A435 EP A435 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901728 ER PT J AU SANDERSON, IR DAMBROSE, M AF SANDERSON, IR DAMBROSE, M TI A NUCLEAR FACTOR THAT BINDS THE INVARIANT CHAIN PROMOTER IS PRESENT IN THE SMALL-INTESTINAL EPITHELIUM OF MICE WEANED ONTO CHOW BUT NOT IN MICE WEANED ONTO AN ELEMENTAL DIET SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEV GASTROENTEROL LAB,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A631 EP A631 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902511 ER PT J AU SINGARAM, C SWEET, MA SNIPES, RL GAUMNITZ, EA AF SINGARAM, C SWEET, MA SNIPES, RL GAUMNITZ, EA TI COLONIC PEPTIDERGIC MUCOSAL INNERVATION IN CONSTIPATION PREDOMINANT IRRITABLE-BOWEL-SYNDROME (IBS) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A567 EP A567 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902253 ER PT J AU TILLOTSON, LG BRAND, SJ AF TILLOTSON, LG BRAND, SJ TI IDENTIFICATION AND CLONING OF A NOVEL TRANSCRIPTION FACTOR THAT EXHIBITS SEQUENCE-SPECIFIC BINDING TO THE HUMAN GASTRIN PROMOTER SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GI UNIT,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A846 EP A846 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903365 ER PT J AU TOGAWA, K RUSTGI, AK AF TOGAWA, K RUSTGI, AK TI A NOVEL HUMAN PAPILLOMAVIRUS GENOTYPE IS ASSOCIATED WITH ESOPHAGUS SQUAMOUS-CELL CARCINOMA SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A445 EP A445 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901768 ER PT J AU TOSKES, PP FORSMARK, CE DEMEO, MT PRINZ, RA OWYANG, C SOUDAH, H DIMAGNO, EP NEALON, WH VINAYEK, R BANKS, PA ADAMS, D WARSHAW, A KATKOV, W AF TOSKES, PP FORSMARK, CE DEMEO, MT PRINZ, RA OWYANG, C SOUDAH, H DIMAGNO, EP NEALON, WH VINAYEK, R BANKS, PA ADAMS, D WARSHAW, A KATKOV, W TI AN OPEN-LABEL TRIAL OF OCTREOTIDE FOR THE PAIN OF CHRONIC-PANCREATITIS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV FLORIDA,GAINESVILLE,FL 32611. LOYOLA UNIV,MED CTR,CHICAGO,IL 60611. UNIV MICHIGAN,ANN ARBOR,MI 48109. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77550. UNIV MARYLAND,COLLEGE PK,MD 20742. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MED UNIV S CAROLINA,CHARLESTON,SC 29425. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A326 EP A326 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901293 ER PT J AU TSUNEKAWA, S MURGUE, B ROSENBERG, I DEBEAUMONT, M PODOLSKY, DK AF TSUNEKAWA, S MURGUE, B ROSENBERG, I DEBEAUMONT, M PODOLSKY, DK TI A NOVEL FIBROBLAST GROWTH-FACTOR RECEPTOR EXPRESSED IN HUMAN COLONIC CELLS IS THE PRODUCT OF ALTERNATIVE SPLICING OF FGFR3 GENE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. NR 0 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A635 EP A635 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902527 ER PT J AU SOLNICAKREZEL, L SCHIER, AF DRIEVER, W AF SOLNICAKREZEL, L SCHIER, AF DRIEVER, W TI EFFICIENT RECOVERY OF ENU-INDUCED MUTATIONS FROM THE ZEBRAFISH GERMLINE SO GENETICS LA English DT Article ID ETHYL-N-NITROSOUREA; RECESSIVE LETHAL MUTATIONS; DNA ADDUCT FORMATION; DROSOPHILA-MELANOGASTER; LOCUS MUTATIONS; LARVAL CUTICLE; ZYGOTIC LOCI; BRACHYDANIO-RERIO; CELL MUTAGENESIS; ORYZIAS-LATIPES AB We studied the efficiency with which two chemical mutagens, ethyl methanesulfonate (EMS) and N-ethyl-N-nitrosourea (ENU) can induce mutations at different stages of spermatogenesis in zebrafish (Brachydanio rerio). Both EMS and ENU induced mutations at high rates in post-meiotic germ cells, as indicated by the incidence of F-1 progeny mosaic for the albino mutation. For pre-meiotic germ cells, however, only ENU was found to be an effective mutagen, as indicated by the frequencies of non-mosaic mutant progeny at four different pigmentation loci. Several mutagenic regimens that varied in either the number of treatments or the concentration of ENU were studied to achieve an optimal ratio between the mutagenicity and toxicity. For the two most mutagenic regimens: 4 X 1 hr in 3 mM ENU and 6 X 1 hr in 3 mM ENU, the minimum estimate of frequencies of independent mutations per locus per gamete was 0.9-1.3 X 10(-3). We demonstrate that embryonic lethal mutations induced with ENU were transmitted to offspring and that they could be recovered in an F-2 screen. An average frequency of specific-locus mutations of 1.1 x 10(-3) corresponded to approximately 1.7 embryonic lethal mutations per single mutagenized genome. The high rates of mutations achievable with ENU allow for rapid identification of large numbers of genes involved in a variety of aspects of zebrafish development. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP SOLNICAKREZEL, L (reprint author), MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129, USA. FU NICHD NIH HHS [HD29761] NR 66 TC 337 Z9 350 U1 2 U2 13 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 SN 0016-6731 J9 GENETICS JI Genetics PD APR PY 1994 VL 136 IS 4 BP 1401 EP 1420 PG 20 WC Genetics & Heredity SC Genetics & Heredity GA NB821 UT WOS:A1994NB82100018 PM 8013916 ER PT J AU GAJEWSKI, WH FULLER, AF PASTELLEY, C FLOTTE, TJ BELL, DA AF GAJEWSKI, WH FULLER, AF PASTELLEY, C FLOTTE, TJ BELL, DA TI PROGNOSTIC-SIGNIFICANCE OF DNA CONTENT IN EPITHELIAL OVARIAN-CANCER SO GYNECOLOGIC ONCOLOGY LA English DT Article ID TRANSITIONAL CELL-CARCINOMA; FLOW-CYTOMETRY; SURVIVAL; TUMOR AB The prognostic significance of cellular DNA content of epithelial ovarian cancer as determined by flow-cytometric analysis of paraffin-embedded tumor blocks was investigated in 87 patients. Seventy-five percent of tumors were DNA aneuploid and 25% were DNA diploid. The survival at median follow-up for patients with DNA diploid tumors (68%) was significantly longer than for DNA aneuploid tumors (49%; P = 0.003). The other prognostic factors which significantly affected survival were stage (P < 0.0001), tumor grade (P < 0.006), and residual disease at completion of initial surgery (P = 0.0005). When patients were separated into low-stage and advanced-stage disease, DNA content was a significant prognostic variable for survival in Stage I and II patients (P = 0.05). In Stage III and IV patients, DNA content had no independent prognostic significance. There were 33 patients who underwent second-look surgery. Seven of 15 patients (47%) with negative second-look surgery were DNA aneuploid, whereas 17 of 18 patients (94%) with positive second-look surgery were DNA aneuploid. Therefore, there was a much higher likelihood of positive second-look in the DNA aneuploid group (17/24) compared to the DNA diploid group (1/9) (P = 0.003). In addition for those patients with negative second-look surgery, none (0/8) of the DNA diploid tumors recurred; however, 3 of 7 (43%) of the DNA aneuploid tumors recurred and died. Cox proportional/hazards analysis showed that DNA content is an independent prognostic factor for survival in epithelial ovarian cancer. Aneuploid DNA content in ovarian tumors is also correlated with more aggressive biologic behavior, and therefore, a worse clinical course. (C) 1994 Academic Press, Inc. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP GAJEWSKI, WH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV GYNECOL ONCOL,BOSTON,MA 02114, USA. NR 26 TC 26 Z9 26 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD APR PY 1994 VL 53 IS 1 BP 5 EP 12 DI 10.1006/gyno.1994.1078 PG 8 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA NL952 UT WOS:A1994NL95200002 PM 8175021 ER PT J AU SHIOTA, G WANG, TC NAKAMURA, T SCHMIDT, EV AF SHIOTA, G WANG, TC NAKAMURA, T SCHMIDT, EV TI HEPATOCYTE GROWTH-FACTOR IN TRANSGENIC MICE - EFFECTS ON HEPATOCYTE GROWTH, LIVER-REGENERATION AND GENE-EXPRESSION SO HEPATOLOGY LA English DT Article ID ADULT-RAT HEPATOCYTES; C-MYC-GENE; SCATTER FACTOR; PARTIAL-HEPATECTOMY; MET PROTOONCOGENE; PROTEIN-SYNTHESIS; ALBUMIN GENE; FACTOR-ALPHA; CELL-CYCLE; IDENTIFICATION AB Attention has recently been focused on hepatocyte growth factor as a major candidate factor in liver regeneration because it is the most potent known mitogen for hepatocytes in vitro. However, hepatocyte growth factor also displays diverse activities in vitro as scatter factor, as an epithelial morphogen, as a pluripotent mitogen and as a growth inhibitor. Consequently, we developed transgenic mice that expressed hepatocyte growth factor under the control of albumin regulatory sequences to examine its in vivo role in hepatocyte growth. Hepatocytes of these mice expressed increased levels of hepatocyte growth factor as an autocrine growth factor. Hepatocyte growth factor was a potent stimulus for liver repair; the livers of hepatocyte growth factor-transgenic mice recovered completely in half the time needed for their normal siblings after partial hepatectomy. This transgenic model also enabled us to study the chronic effects of hepatocyte growth factor expression. During several months of observation, the labeling index of hepatocytes in albumin-hepatocyte growth factor mice was doubled, and liver DNA content was increased compared with that in wild-type mice. To identify intermediate signaling pathways for hepatocyte growth factor that might regulate this increased growth response, we examined transgenic mice for changes in expression of genes that are known to be regulated during liver regeneration. We found that levels of c-myc and c-jun mRNA were increased in the hepatocyte growth factor-transgenic mice. In additional experiments the increased c-myc expression was the consequence of increased transcription rates as seen in nuclear run-on and myc-CAT reporter gene experiments. We conclude that hepatocyte growth factor increases growth and repair processes when expressed for long periods in the liver and that c-myc and c-jun may be important intermediaries in the hepatocyte growth response caused by hepatocyte growth factor. C1 MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. KYUSHU UNIV,FAC SCI,DEPT BIOL,FUKUOKA 812,JAPAN. FU NIDDK NIH HHS [DK01937, DK34854] NR 59 TC 148 Z9 150 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1994 VL 19 IS 4 BP 962 EP 972 DI 10.1016/0270-9139(94)90297-6 PG 11 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ND702 UT WOS:A1994ND70200022 PM 8138271 ER PT J AU AFTRING, RP FREEMAN, MW AF AFTRING, RP FREEMAN, MW TI OF MICE, MEN AND CHOLESTEROL SO HEPATOLOGY LA English DT Note ID LOW-DENSITY-LIPOPROTEIN; GENE-THERAPY; HYPERCHOLESTEROLEMIA RP AFTRING, RP (reprint author), MASSACHUSETTS GEN HOSP,LIPID METAB UNIT,BOSTON,MA 02114, USA. NR 7 TC 0 Z9 0 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1994 VL 19 IS 4 BP 1054 EP 1056 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ND702 UT WOS:A1994ND70200035 PM 8138246 ER PT J AU SHIOTA, G OKANO, J KITANO, M KAWASAKI, H SCHMIDT, EV NAKAMURA, T AF SHIOTA, G OKANO, J KITANO, M KAWASAKI, H SCHMIDT, EV NAKAMURA, T TI SIGNIFICANCE OF HEPATOCYTE GROWTH-FACTOR (HGF) IN LIVER-REGENERATION - FROM BASIC AND CLINICAL POINTS-OF-VIEW SO HEPATOLOGY LA English DT Meeting Abstract C1 TOTTORI UNIV,DEPT MED 2,YONAGO,TOTTORI 683,JAPAN. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. OSAKA UNIV,DEPT TUMOR BIOCHEM,SUITA,OSAKA 565,JAPAN. NR 1 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1994 VL 19 IS 4 BP I123 EP I123 DI 10.1016/0270-9139(94)90658-0 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ND702 UT WOS:A1994ND70200377 ER PT J AU CHEN, JZ STEWART, V SPYROU, G HILBERG, F WAGNER, EF ALT, FW AF CHEN, JZ STEWART, V SPYROU, G HILBERG, F WAGNER, EF ALT, FW TI GENERATION OF NORMAL T-LYMPHOCYTES AND B-LYMPHOCYTES BY C-JUN DEFICIENT EMBRYONIC STEM-CELLS SO IMMUNITY LA English DT Article ID ANTIGEN RECEPTOR; TRANSGENIC MICE; CYCLOSPORINE-A; NUCLEAR FACTOR; NULL MUTATION; ES CELLS; INTERLEUKIN-2; FOS; TRANSCRIPTION; PROTEIN AB To determine the potential roles of c-jun in lymphocyte development, we generated somatic chimeric mice by injecting homozygous c-jun mutant embryonic stem (ES) cells into blastocysts from recombination activating gene-2 (RAG-2)-deficient mice. Chimeric mice had poor restoration of thymocytes, but contained substantial numbers of mature T and a lymphocytes in the periphery. Stimulation of c-jun(-/-) 8 cells resulted in normal levels of proliferation and immunoglobulin secretion. Likewise, stimulation of c-jun(-/-) T cells resulted in essentially normal levels of IL-2R alpha expression, IL-2 secretion, and proliferation. We further showed that the relatively normal activation responses of the c-jun(-/-) T cells probably results from the fact that other members of the Jun family contribute to the bulk of the activator protein-1 (AP-1) complexes in normal T cells and, as a result, AP-1 complexes are found at relatively normal levels in c-jun(-/-) T cells. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RES INST MOLEC PATHOL,A-1030 VIENNA,AUSTRIA. KAROLINSKA INST,MED NOBLE INST,BIOCHEM LAB,INST MED BIOCHEM & BIOPHYS,S-17177 STOCKHOLM,SWEDEN. RP CHEN, JZ (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,HOWARD HUGHES MED INST,DEPT GENET,BOSTON,MA 02115, USA. RI Wagner, Erwin/G-9637-2012 OI Wagner, Erwin/0000-0001-7872-0196 FU NCI NIH HHS [CA42335]; NIAID NIH HHS [AI20047, U01 AI31541] NR 35 TC 59 Z9 59 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD APR PY 1994 VL 1 IS 1 BP 65 EP 72 DI 10.1016/1074-7613(94)90010-8 PG 8 WC Immunology SC Immunology GA PK154 UT WOS:A1994PK15400008 PM 7889400 ER PT J AU MCKNIGHT, AJ SHEA, CM WIENS, GR RIMM, IJ ABBAS, AK AF MCKNIGHT, AJ SHEA, CM WIENS, GR RIMM, IJ ABBAS, AK TI DIFFERENTIATION OF V-BETA-8.2(+) CD4(+) T-CELLS INDUCED BY A SUPERANTIGEN - ROLES OF ANTIGEN-PRESENTING CELLS AND CYTOKINES SO IMMUNOLOGY LA English DT Article ID CHAIN TRANSGENIC MICE; LYMPHOCYTES-T; LYMPHOKINE SECRETION; B-CELLS; MONOCLONAL-ANTIBODY; MEDIATED IMMUNITY; TH2 CLONES; HELPER; RECEPTOR; SUBSETS AB The activation and subsequent differentiation of naive CD4(+) T cells into functionally distinct effector cells is a vital step in the generation of an effective immune response to protein antigens. To analyse the development of effector T cells following the activation of resting, naive CD4(+) T cells, we have utilized a transgenic mouse model in which the majority of T cells express a common T-cell receptor V beta molecule. The resting T cells were purified and stimulated in vitro with staphylococcal enterotoxin B, in the presence of accessory cells expressing class II major histocompatibility complex (MHC) molecules. We found that the cells which developed from these primary cultures were capable of producing varying levels of interleukin-2 (IL-2), IL-4 and interferon-gamma (IFN-gamma) following restimulation with anti-V beta 8 antibody, irrespective of whether B cells or macrophages/dendritic cells were the accessory cells in the primary cultures. The addition of IL-4 during primary stimulation enhanced the differentiation of IL-4-producing cells and suppressed the expansion of IFN-gamma-producing cells, especially when B cells were the antigen-presenting cells (APC). Neutralization of endogenously produced IL-1, even in the presence of exogenous IL-4, did not inhibit the differentiation of IL-4-producing T cells. Strikingly, IL-10 completely suppressed the development of effector T cells when adherent macrophages/dendritic cells were utilized as accessory cells in the primary cultures, but had minimal effect in the presence of B cells. IFN-gamma suppressed the generation of IL-4-producing cells, presumably by inhibiting their expansion following primary activation. Finally, in vitro-generated IL-4-producing T cells were the most potent helpers for B lymphocytes. Thus, exogenous cytokines alter the patterns of T-cell differentiation in vitro, and the effects of cytokines vary depending on the types of accessory cells present during initial T-cell activation. C1 HARVARD UNIV,SCH MED,BOSTON,MA. CHILDRENS HOSP,DANA FARBER CANC INST,DEPT PEDIAT,DIV PEDIAT ONCOL,BOSTON,MA 02115. RP MCKNIGHT, AJ (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV IMMUNOL RES,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI25022] NR 38 TC 7 Z9 7 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD APR PY 1994 VL 81 IS 4 BP 513 EP 520 PG 8 WC Immunology SC Immunology GA ND746 UT WOS:A1994ND74600005 PM 7913692 ER PT J AU REISER, H SCHNEEBERGER, EE AF REISER, H SCHNEEBERGER, EE TI THE COSTIMULATORY MOLECULE B7 IS EXPRESSED IN THE MEDULLARY REGION OF THE MURINE THYMUS SO IMMUNOLOGY LA English DT Article ID T-CELL ACTIVATION; LYMPHOCYTES-T; MONOCLONAL-ANTIBODIES; ANTIGEN PROVIDES; IL-2 PRODUCTION; MESSENGER-RNA; CD28; SIGNAL; CTLA-4; INTERLEUKIN-2 AB Several laboratories, including our own, have previously shown that the B7 antigen, a glycoprotein expressed on activated B cells, macrophages and dendritic cells, can provide a potent costimulatory signal for peripheral murine T lymphocytes. In the present report we have analysed the expression and function of B7 in the murine thymus. The expression of B7 was demonstrated histochemically. B7-expressing cells were present in the thymic medulla but virtually absent from the cortex. Further analysis by immunofluorescence and flow fluorocytometry revealed that the B7-positive cells also expressed major histocompatibility complex (MHC) class II molecules. Both epithelial and dendritic cells expressed the B7 antigen. Finally, although we have demonstrated expression of mB7 in the murine thymus, we have been unable to detect a function for this antigen in this organ. The implications of these findings are discussed. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP REISER, H (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-36781]; NIAID NIH HHS [AI-33679] NR 38 TC 26 Z9 27 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD APR PY 1994 VL 81 IS 4 BP 532 EP 537 PG 6 WC Immunology SC Immunology GA ND746 UT WOS:A1994ND74600007 PM 7518793 ER PT J AU CALIA, KE MURTAGH, M FERRARO, MJ CALDERWOOD, SB AF CALIA, KE MURTAGH, M FERRARO, MJ CALDERWOOD, SB TI COMPARISON OF VIBRIO-CHOLERAE O139 WITH VIBRIO-CHOLERAE O1 CLASSICAL AND EL-TOR BIOTYPES SO INFECTION AND IMMUNITY LA English DT Note ID TRANSCRIPTIONAL REGULATION; CLONING; GENE AB Vibrio cholerae O139 is a recently identified non-O1 V. cholerae strain responsible for outbreaks of epidemic cholera in India, Bangladesh, and Thailand in the past 2 years. Other workers have demonstrated the presence of the cholera toxin genetic element in V. cholerae O139, unlike the situation for other non-O1 V. cholerae strains. We sought to compare further this strain with strains of V. cholerae O1, classical and El Tor biotypes, by classic microbiologic methods, Southern blot analysis for restriction fragment length polymorphisms with probes for iron-regulated genes of V. cholerae O1, and comparisons of outer membrane protein profiles. Our results were similar for V. cholerae O139 and the El Tor biotype of V. cholerae O1, with the exception of the constitutive expression in V. cholerae O139 of OmpS, an outer membrane protein that was maltose inducible in comparison strains of V. cholerae O1. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CLIN MICROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NIAID NIH HHS [AI34968] NR 19 TC 48 Z9 50 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1994 VL 62 IS 4 BP 1504 EP 1506 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NC074 UT WOS:A1994NC07400056 PM 7510671 ER PT J AU LI, SC ROTHMAN, PB ZHANG, J CHAN, C HIRSH, D ALT, FW AF LI, SC ROTHMAN, PB ZHANG, J CHAN, C HIRSH, D ALT, FW TI EXPRESSION OF I-MU - C-GAMMA HYBRID GERMLINE TRANSCRIPTS SUBSEQUENT TO IMMUNOGLOBULIN HEAVY-CHAIN CLASS SWITCHING SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE CLASS SWITCHING; HEAVY CHAIN; IMMUNOGLOBULIN ID IGH ENHANCER REGION; CIRCULAR DNA; B-CELLS; NUCLEOTIDE-SEQUENCES; INTERFERON-GAMMA; RECOMBINATION; LINE; EPSILON; MOUSE; REARRANGEMENT AB Germline C-H transcripts initiate from a non-coding I exon and terminate downstream of the associated C-H exons. Ig heavy chain class switch recombination from the VDJ - C-mu gene to particular downstream C-H genes appears to be regulated by a process that involves mitogen and/or cytokine induction of germline C-H transcripts from the downstream genes. We have examined the expression of germline C-mu transcripts (I-mu,- C-mu, transcripts) in splenic B cells and pre-a cell lines after cytokine and mitogen stimulation. In contrast to the expression of the germline transcripts from downstream C-H genes, expression of germline C-mu transcripts was constitutive and unaffected by mitogen and cytokine treatment. After a primary switch recombination event, the germline I-mu promoter, which is now associated with a downstream C-H gene, continues to be active-leading to the generation of a novel germline transcript consisting of the I-mu exon spliced to the C-H exons of the switched C-H gene. We discuss the potential role of the expression of hybrid I-mu-containing transcripts in the class switch process. We also describe a novel and sensitive assay, based on the detection of the hybrid I-mu-containing transcripts, that allows detection of class switch recombination events even in heterogeneous populations of cells. C1 DEPT MICROBIOL & MED,NEW YORK,NY 10032. DEPT BIOCHEM,NEW YORK,NY 10032. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RP LI, SC (reprint author), DEPT PEDIAT,630 W 168TH ST,NEW YORK,NY 10032, USA. FU NIAID NIH HHS [AI-31541, AI-20087]; NIGMS NIH HHS [GM 37823] NR 42 TC 58 Z9 58 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD APR PY 1994 VL 6 IS 4 BP 491 EP 497 DI 10.1093/intimm/6.4.491 PG 7 WC Immunology SC Immunology GA NF242 UT WOS:A1994NF24200001 PM 8018590 ER PT J AU MCCARTHY, MK GOFF, DC BAER, L CIOFFI, J HERZOG, DB AF MCCARTHY, MK GOFF, DC BAER, L CIOFFI, J HERZOG, DB TI DISSOCIATION, CHILDHOOD TRAUMA, AND THE RESPONSE TO FLUOXETINE IN BULIMIC PATIENTS SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Article ID EATING DISORDERS; SEXUAL ABUSE; ANOREXIA-NERVOSA; PERSONALITY-DISORDER; PHYSICAL ABUSE; WOMEN; INCEST AB Histories of childhood trauma have been reported previously in bulimic subjects but no study to date has assessed how these experiences may affect response to fluoxetine. Thirty outpatient subjects in a placebo-controlled trial of 60 mg of fluoxetine for the treatment of bulimia nervosa completed the Dissociative Experiences Scale and a self-report instrument assessing trauma. Response to treatment was measured with the Hamilton Depression Scale-17 (HAMD-17), the CGI, the PGI, and the change in number of binges per day. Subjects taking fluoxetine with histories of physical abuse showed a significantly greater drop in HAMD-17 scores than those without such histories. No relationship between a reported history of abuse and the response of binging to fluoxetine was found. A history of abuse does not appear to predict the response of binging to fluoxetine but may predict a greater response of nonspecific symptoms like depression. (C) 1994 by John Wiley & Sons, Inc. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CORNELL UNIV,MED CTR,COLL MED,NEW YORK,NY 10021. RP MCCARTHY, MK (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 31 TC 17 Z9 17 U1 2 U2 3 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0276-3478 J9 INT J EAT DISORDER JI Int. J. Eating Disord. PD APR PY 1994 VL 15 IS 3 BP 219 EP 226 DI 10.1002/1098-108X(199404)15:3<219::AID-EAT2260150304>3.0.CO;2-F PG 8 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA NC977 UT WOS:A1994NC97700002 PM 8199601 ER PT J AU YOUNG, RH JACKSON, A WELLS, M AF YOUNG, RH JACKSON, A WELLS, M TI OVARIAN METASTASIS FROM THYROID-CARCINOMA 12 YEARS AFTER PARTIAL THYROIDECTOMY MIMICKING STRUMA OVARII - REPORT OF A CASE SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Note DE OVARY; METASTASIS; THYROID; CARCINOMA ID DISTANT METASTASES AB A 29-year-old woman experienced abdominal swelling 12 years after undergoing partial thyroidectomy for follicular carcinoma of the thyroid with vascular invasion and 6 months after a right cerebral tumor that had caused hemiplegia had been excised. Laparotomy disclosed a solid and cystic right ovarian tumor, 17 cm in greatest dimension, and a 12-cm tumor of the right adrenal gland. Microscopic examination showed a malignant tumor of the thyroid follicular type with frequent mitotic figures; other teratomatous elements were absent. Because of the interval since the thyroid cancer, the diagnosis of a malignant struma ovarii was initially considered. The patient rapidly developed widespread metastatic disease and died, supporting the interpretation that the ovarian tumor was a metastasis from the thyroid neoplasm. This case illustrates that when other teratomatous elements are not identified, the diagnosis of malignant struma ovarii should be made only when the possibility of spread from a prior thyroid neoplasm, possibly one treated many years previously, has been excluded. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. SCARBOROUGH GEN HOSP,DEPT PATHOL,SCARBOROUGH,N YORKSHIRE,ENGLAND. UNIV LEEDS,LEEDS LS2 9JT,W YORKSHIRE,ENGLAND. RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 19 TC 40 Z9 42 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1994 VL 13 IS 2 BP 181 EP 185 DI 10.1097/00004347-199404000-00012 PG 5 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA NB461 UT WOS:A1994NB46100012 PM 8005740 ER PT J AU CHANG, MP YAMAGUCHI, DT YEH, M TAYLOR, AN NORMAN, DC AF CHANG, MP YAMAGUCHI, DT YEH, M TAYLOR, AN NORMAN, DC TI MECHANISM OF THE IMPAIRED T-CELL PROLIFERATION IN ADULT-RATS EXPOSED TO ALCOHOL IN-UTERO SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article ID HUMAN LYMPHOCYTE-T; MEDIATED SIGNAL TRANSDUCTION; CYTOSOLIC FREE CALCIUM; INTERLEUKIN-2 RECEPTOR; FETAL ALCOHOL; TYROSINE PHOSPHORYLATION; ANTIGEN RECEPTOR; PRENATAL ETHANOL; BETA-CHAIN; ACTIVATION AB Although attempts have been made to assess the effect of ethanol on the immune responses in individuals with fetal alcohol syndrome, there is no consensus as to the effect of ethanol on the immune system. Evidence that fetal alcohol-exposed (FAE) humans and animals have diminished proliferative response of T-cells to mitogenic lectins is well established. However, little is known about the mechanism of a toxic effect of ethanol on T-cell growth. Thus, a rat model was used to delineate the mode of ethanol action on T-cell proliferation. We found that the diminished T-cell proliferation in young adult FAE rats was due to a decreased responsiveness to interleukin 2 (IL2), but not to an impaired production of IL2 and expression of IL2 receptors (IL2R). Furthermore, the decreased proliferative response did not result from the presence of an excessive suppressor T-cell activity. Measurements of [Ca+2](i) and T-cell proliferation were concurrently performed in batches of cells from the same animals. It was demonstrated that an increase in [Ca+2](i) induced by Concanavalin A (Con A) in T-cells from FAE rats was not impaired, although the T-cell proliferation induced by Con A was significantly diminished. The results of the IL2-binding study showed that the K-d values and the number of both high- and low-affinity IL2R binding sites on the T-cells of FAE rats were comparable to those of pair-, or chow-fed rats. Finally, the results of the kinetics and rate of the internalization of IL2 showed that (1) the amount of the internalized IL2 was significantly reduced in T-cells from FAE rats, and (2) the half-time (t(1/2)) for dissociation of IL2 from the receptors in the T-cells from FAE rats was also greater than that of the control rats. These results taken together indicate that ethanol suppresses T-cell proliferation by interfering with events following the IL2 - IL2R interaction. C1 W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH RES DIV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT ANAT & CELL BIOL,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90073. RP CHANG, MP (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,CTR GERIATR RES EDUC & CLIN,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 53 TC 16 Z9 17 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PD APR PY 1994 VL 16 IS 4 BP 345 EP 357 PG 13 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA NG597 UT WOS:A1994NG59700010 PM 8045674 ER PT J AU NAPOLITANO, A LOWELL, BB DAMM, D LEIBEL, RL RAVUSSIN, E JIMERSON, DC LESEM, MD VANDYKE, DC DALY, PA CHATIS, P WHITE, RT SPIEGELMAN, BM FLIER, JS AF NAPOLITANO, A LOWELL, BB DAMM, D LEIBEL, RL RAVUSSIN, E JIMERSON, DC LESEM, MD VANDYKE, DC DALY, PA CHATIS, P WHITE, RT SPIEGELMAN, BM FLIER, JS TI CONCENTRATIONS OF ADIPSIN IN BLOOD AND RATES OF ADIPSIN SECRETION BY ADIPOSE-TISSUE IN HUMANS WITH NORMAL, ELEVATED AND DIMINISHED ADIPOSE-TISSUE MASS SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE ADIPSIN; OBESITY ID COMPLEMENT FACTOR-D; GENE-EXPRESSION; MESSENGER-RNA; GLYCEROPHOSPHATE DEHYDROGENASE; OBESITY; PATHWAY; INSULIN; CELLS; MICE AB Adipsin, which is identical to complement factor D, is synthesized by fat cells, circulates in the bloodstream and is profoundly deficient in mice with genetic and hypothalamic obesity. With the recent cloning of human adipsin, a quantitative human immunoassay has been developed. In the present study, we measured adipsin blood concentrations in humans with increased and decreased adipose stores as well as adipsin secretion by adipose tissue obtained from lean and obese individuals. The results demonstrate that adipsin is released by human adipose tissue fragments as has previously been shown in mice, and that, in contrast to obese mice, blood adipsin concentrations were not reduced in the obese humans tested in this study. We also observed that blood adipsin concentrations can vary as a function of feeding or adiposity, in that they tend to be mildly elevated in obese individuals or mildly reduced in individuals with total lipo-atrophy, cachexia related to AIDS and anorexia nervosa. Thus, the circulating concentration of adipsin tends to correlate positively with degree of adiposity. Clearly, no deficiency in blood adipsin concentrations or adipsin secretion by adipose tissue was observed in the obese individuals studied. C1 BETH ISRAEL HOSP,DEPT MED,DIV ENDOCRINOL,BOSTON,MA 02215. BETH ISRAEL HOSP,DEPT MED,DIV INFECT DIS,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA. SCIOS NOVA INC,MT VIEW,CA. ROCKEFELLER UNIV,HUMAN BEHAV & METAB LAB,NEW YORK,NY 10021. NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. UNIV TEXAS,SCH MED,DEPT PSYCHIAT,HOUSTON,TX. UNIV IOWA,HOSP SCH,DEPT PEDIAT,DIV DEV DISABIL,IOWA CITY,IA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 30583, 2 P30 DK 26687-12, 5 F32 DK08525-02] NR 22 TC 56 Z9 57 U1 0 U2 4 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD APR PY 1994 VL 18 IS 4 BP 213 EP 218 PG 6 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA NE982 UT WOS:A1994NE98200005 PM 8044195 ER PT J AU FRICK, TW WIEGAND, D BIMMLER, D FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL AF FRICK, TW WIEGAND, D BIMMLER, D FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL TI A RAT MODEL TO STUDY HYPERCALCEMIA-INDUCED ACUTE-PANCREATITIS SO INTERNATIONAL JOURNAL OF PANCREATOLOGY LA English DT Article DE ACUTE PANCREATITIS; CHEMICALLY INDUCED PANCREATITIS; HYPERCALCEMIA; PANCREATITIS ETIOLOGY; PANCREATITIS PATHOGENESIS; EXPERIMENTAL PANCREATITIS; CALCIUM ID GUINEA-PIG PANCREAS; ACINAR CELL; PLASMA-MEMBRANE; CALCIUM; ULTRASTRUCTURE; SECRETAGOGUE; STIMULATION; SECRETION; DISCHARGE; PROTEIN AB Hypercalcemia causes acute pancreatitis in humans, a phenomenon reproduced experimentally in cats and guinea pigs. Because the rat is the most frequently used animal for the study of experimental pancreatitis, the present studies were performed to evaluate the effects of hypercalcemia in the rat. In in vitro studies, pancreatic lobules were prepared from fasted Wistar rats (200-250 g) and incubated in HEPES bicarbonate-buffered medium (pH 7.4) containing 0, 0.6, 1.2, 2.5, 5, and 10 mM CaCl2 with or without carbachol 10(-6)M. Amylase was measured in the medium after 30 min to 3 h, and expressed as percent of total amylase. In in vivo studies, fasted male Wistar rats (300-400 g) received calcium (CaCl2; 0.6 mmol/kgh) into the tail vein for 12 h. Control animals received NaCl 0.9% infusion. Histologic slides (H&E-stained) were evaluated in a blinded fashion. Pancreatic lobules showed a higher basal amylase output when incubated in higher calcium medium. The largest, significant difference (2.6-fold) was between 0.6 and 5 mM medium CaCl2 (p < 0.05). Carbachol-stimulated amylase release was again higher with increasing medium calcium with the most pronounced difference (1.3-fold) between 0.6 and 2.5 mM CaCl2 (p < 0.05). In vivo calcium-treated animals showed accumulation of zymogen granules in the cytoplasm, cytoplasmic vacuolization, focal acinar cell depolarization, acinar necrosis, and edema. Calcium causes amylase release from rat pancreatic lobules in vitro. Higher medium calcium levels both significantly increase amylase release from unstimulated and carbachol stimulated lobules. Twelve-hour in vivo calcium infusion leads to accumulation of zymogen granules in acinar cells and acinar injury. These findings are consistent with pancreatitis evolving from calcium-induced hypersecretion to a secretion block lesion in the rat. C1 UNIV ZURICH HOSP,CH-8091 ZURICH,SWITZERLAND. RP FRICK, TW (reprint author), MASSACHUSETTS GEN HOSP,CTR WANG AMBULATORY CARE,DEPT SURG,SUITE 336,BOSTON,MA 02114, USA. NR 22 TC 12 Z9 12 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0169-4197 J9 INT J PANCREATOL JI Int. J. Pancreatol. PD APR PY 1994 VL 15 IS 2 BP 91 EP 96 PG 6 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA NJ710 UT WOS:A1994NJ71000002 PM 7520926 ER PT J AU DEWHIRST, FE CHEN, CKC PASTER, BJ ZAMBON, JJ AF DEWHIRST, FE CHEN, CKC PASTER, BJ ZAMBON, JJ TI PHYLOGENY OF SPECIES IN THE FAMILY NEISSERIACEAE ISOLATED FROM HUMAN DENTAL PLAQUE AND DESCRIPTION OF KINGELLA-ORALE SP-NOV (VOL 43, PG 490, 1993) SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Correction, Addition C1 SUNY BUFFALO,SCH DENT MED,DEPT ORAL BIOL & PERIODONTOL,BUFFALO,NY 14214. RP DEWHIRST, FE (reprint author), FORSYTH DENT CTR,DEPT MOLEC GENET,140 FENWAY,BOSTON,MA 02115, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 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 APR PY 1994 VL 44 IS 2 BP 376 EP 376 PG 1 WC Microbiology SC Microbiology GA NE811 UT WOS:A1994NE81100035 ER PT J AU LI, TS ADAMIAN, M ROOF, DJ BERSON, EL DRYJA, TP ROESSLER, BJ DAVIDSON, BL AF LI, TS ADAMIAN, M ROOF, DJ BERSON, EL DRYJA, TP ROESSLER, BJ DAVIDSON, BL TI IN-VIVO TRANSFER OF A REPORTER GENE TO THE RETINA MEDIATED BY AN ADENOVIRAL VECTOR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE ADENOVIRAL VECTOR; VIRAL TRANSDUCTION; GENE TRANSFER; GENE THERAPY; RETINITIS PIGMENTOSA ID HERPES-SIMPLEX VIRUS; RHODOPSIN GENE; MESSENGER-RNA; ONE FORM; PIGMENTOSA; EXPRESSION; INVIVO; DEGENERATION; CELLS; DNA AB Purpose. The ability of replication-deficient adenovirus to mediate gene transfer to retinal cells was evaluated. Methods. A replication-deficient adenoviral vector, AdCMV beta A.ntlacZ, which contains the bacterial beta-galactosidase (lacZ) reporter gene, was injected into the subretinal space of normal, rd, and rds strains of mice at various ages. The efficiency and duration of transgene expression were assessed by histochemical examination and transmission electron microscopy. Results. AdCMV beta A.ntlacZ was effective in mediating gene transfer to the retinal pigment epithelial cells, rod and cone photoreceptor cells, and cells in the inner nuclear layer of the retina for periods of up to 1 month. Gene transfer to retinal pigment epithelial cells occurred at much lower viral titers than was required for gene transfer to photoreceptor cells. The extent to which photoreceptor cells could be transduced varied with the age of the animals and the conditions of the photoreceptor cells: greater numbers of photoreceptor cells were transduced in 5- to 7-day-old pups and in mice at the initial stages of photoreceptor degeneration than in normal adult mice. No evidence of gross pathogenic effects or viremia in recipient mice was observed. Conclusions. Replication-deficient adenovirus mediates transfer and expression of a foreign gene in retinal pigment epithelial and photoreceptor cells. Gene transfer to photoreceptor cells is enhanced in developing retinas or at the predegenerate stage of photoreceptors in genetically programmed retinal degeneration. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,ANN ARBOR,MI 48109. NR 23 TC 164 Z9 169 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD APR PY 1994 VL 35 IS 5 BP 2543 EP 2549 PG 7 WC Ophthalmology SC Ophthalmology GA NG609 UT WOS:A1994NG60900018 PM 8163343 ER PT J AU BRINK, JA KAMMER, B MUELLER, PR PRIEN, EL FERRUCCI, JT AF BRINK, JA KAMMER, B MUELLER, PR PRIEN, EL FERRUCCI, JT TI DISSOLUTION OF CALCIFIED GALLSTONES .1. CORRELATION OF IN-VITRO DISSOLUTION KINETICS IN METHYL TERT-BUTYL ETHER WITH PATTERNS OF CALCIFICATION BY COMPUTED-TOMOGRAPHY SO INVESTIGATIVE RADIOLOGY LA English DT Article DE CHOLELITHIASIS; COMPUTED X-RAY TOMOGRAPHY; METHYL TERT-BUTYL ETHER; CALCIFIED GALLSTONES; KINETICS ID INVITRO DISSOLUTION; CT; SOLVENTS; INVIVO AB RATIONALE AND OBJECTIVES. The authors evaluated the relationship between stone computed tomography (CT) attenuation patterns and the kinetics of dissolution with methyl tert-butyl ether (MTBE). METHODS. Single moderately and heavily calcified gallstones from 40 patients were selected from a gallstone library and classified for pattern of calcification by in vitro CT scan (dense, rim, core, and laminated). Each stone was placed in a 10-mL aliquot of MTBE for 24 hours. Stone residue was blotted dry and weighed at 8, 16, and 24 hours. Results were normalized with respect to stone size. RESULTS. Only 1 of 40 (4%) specimens dissolved to particulate matter that was smaller than 2 mm. All (6 of 6) stones that were densely calcified showed virtually no dissolution. The rate of gallstone dissolution varied temporally within the rim, core, and laminated stone categories and was related to the composition of the layer exposed to the solvent at any given time. CONCLUSION. The success and rate of dissolution may be predicted by the pattern of calcification as determined by computed tomography (CT). C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,BOSTON,MA. NR 16 TC 2 Z9 2 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD APR PY 1994 VL 29 IS 4 BP 448 EP 453 DI 10.1097/00004424-199404000-00011 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NL695 UT WOS:A1994NL69500009 PM 8034451 ER PT J AU KAMMER, B BRINK, JA KNOEFEL, WT MUELLER, PR PRIEN, EL FERRUCCI, JT AF KAMMER, B BRINK, JA KNOEFEL, WT MUELLER, PR PRIEN, EL FERRUCCI, JT TI DISSOLUTION OF CALCIFIED GALLSTONES .2. EVALUATION OF EDETIC ACID PREPARATIONS FOR DISSOLUTION OF RESIDUE AFTER IN-VITRO METHYL TERT-BUTYL ETHER TREATMENT SO INVESTIGATIVE RADIOLOGY LA English DT Article DE GALLBLADDER; CALCULI; CHEMICAL THERAPY; COMPUTED TOMOGRAPHY; RADIOGRAPHY ID CALCIUM BILIRUBINATE; GALLBLADDER; STONES; INVITRO; BROWN AB RATIONALE AND OBJECTIVES. The authors assessed the potential of edetic acid (EDTA) preparations to dissolve the residue of calcified gallstones partially treated with methyl tert-butyl ether (MTBE). METHODS. Nineteen triplets (57 gallstones) were submitted to dissolution in EDTA, urea-EDTA, and an MTBE control for 48 hours after initial partial dissolution in MTBE for 24 hours. Results were compared with findings at specimen computed tomography and crystallographic analysis. All data were corrected for differences in stone size. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT RADIOL, BOSTON, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT SURG, BOSTON, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, MED SERV, BOSTON, MA USA. NR 16 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD APR PY 1994 VL 29 IS 4 BP 454 EP 458 DI 10.1097/00004424-199404000-00012 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NL695 UT WOS:A1994NL69500010 PM 8034452 ER PT J AU MOORE, JP CAO, YZ CONLEY, AJ WYATT, R ROBINSON, J GORNY, MK ZOLLAPAZNER, S HO, DD KOUP, RA AF MOORE, JP CAO, YZ CONLEY, AJ WYATT, R ROBINSON, J GORNY, MK ZOLLAPAZNER, S HO, DD KOUP, RA TI STUDIES WITH MONOCLONAL-ANTIBODIES TO THE V3 REGION OF HIV-1 GP120 REVEAL LIMITATIONS TO THE UTILITY OF SOLID-PHASE PEPTIDE BINDING ASSAYS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE MONOCLONAL ANTIBODIES; V3-PEPTIDE; SOLID-PHASE PEPTIDE BINDING ASSAY ID VIRUS TYPE-1 GP120; ENVELOPE GLYCOPROTEIN; CD4 BINDING; NEUTRALIZATION; DOMAIN; EPITOPE; STRAIN; SITE AB Using human monoclonal antibodies (HuMAbs) r(1)-447 (L-736,523) and 19b to the V3 region of HIV-1 gp120, we have explored epitope presentation on V3-peptides and on the corresponding gp120 proteins. HuMAb r(1)-447 binds strongly to the MN and SF-2 peptides and gp120 proteins. In contrast, while this HuMAb binds equally avidly to both the HxB2 and the BRU/BH10 peptides, it binds but weakly to the HxB2 V3 loop on gp120 and fails to bind at all to BH10 gp120. Thus, the solid-phase peptide binding assay can falsely predict reactivity of an MAb with a gp120 protein. Conversely, HuMAb 19b fails to bind to a peptide from the V3 loop of HIV-1 AD-6 in solid-phase assays, but binds to the same peptide in solution and also to AD-6 gp120. Thus, the solid-phase peptide binding assay can fail to predict reactivity of an MAb with a gp120 protein. Furthermore, serum antibodies from individual AD-6 do not react well with the AD-6 V3-peptide in a solid-phase assay, but react strongly with the corresponding MN V3-peptide. On the basis of peptide binding assays, we had assumed that the AD-6 virus was ''MN-like'' with a prototypic North American/European subtype B GPGR motif at the crown of the V3 loop. However, direct sequencing demonstrates that the AD-6 V3 loop contains a variant GPGK motif. This highlights a limitation of V3-peptide-based assays for serotyping viruses. C1 DEPT VET AFFAIRS,NEW YORK,NY. MERCK SHARP & DOHME LTD,RES LABS,W POINT,PA. DANA FARBER CANC INST,BOSTON,MA. UNIV CONNECTICUT,DEPT PEDIAT,STORRS,CT. RP MOORE, JP (reprint author), NYU,SCH MED,AARON DIAMOND AIDS RES CTR,455 1ST AVE,NEW YORK,NY 10016, USA. FU NIAID NIH HHS [AI 32424, 1 P30 AI27742-04] NR 24 TC 26 Z9 26 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD APR PY 1994 VL 7 IS 4 BP 332 EP 339 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NC775 UT WOS:A1994NC77500003 PM 7510807 ER PT J AU POLLACK, MH OTTO, MW SACHS, GS LEON, A SHEAR, MK DELTITO, JA KELLER, MB ROSENBAUM, JF AF POLLACK, MH OTTO, MW SACHS, GS LEON, A SHEAR, MK DELTITO, JA KELLER, MB ROSENBAUM, JF TI ANXIETY PSYCHOPATHOLOGY PREDICTIVE OF OUTCOME IN PATIENTS WITH PANIC DISORDER AND DEPRESSION TREATED WITH IMIPRAMINE, ALPRAZOLAM AND PLACEBO SO JOURNAL OF AFFECTIVE DISORDERS LA English DT Article DE PANIC DISORDER; DEPRESSION; ALPRAZOLAM; IMIPRAMINE; PLACEBO ID FOLLOW-UP; AGORAPHOBIA; EFFICACY; ATTACKS AB This study examines clinical predictors of outcome for patients with panic disorder and depression in a 16 week, placebo-controlled trial of alprazolam and imipramine (n = 126). Baseline global severity of illness and phobic avoidance were differentially predictive of acute response to treatment. Patients in the mild to moderate range of global distress experienced smaller degrees of improvement on alprazolam than on imipramine at week 4. At endpoint, the relative effectiveness of the active medication versus placebo was diminished in patients with higher levels of phobic avoidance. This relationship was not evident for completers, suggesting that the adverse effects of avoidance on outcome after sustained treatment was reduced. C1 NEW YORK HOSP,CORNELL MED CTR,DEPT PSYCHIAT,NEW YORK,NY 10021. WESTERN PSYCHIAT INST & CLIN,ANXIETY DISORDERS PROGRAM,PITTSBURGH,PA. CORNELL UNIV,COLL MED,ANXIETY & MOODS DISORDERS PROGRAM,WORCESTER,MA. BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. RP POLLACK, MH (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,ANXIETY DISORDERS PROGRAM,BOSTON,MA 02114, USA. FU NIMH NIH HHS [R01 MH025478] NR 18 TC 28 Z9 28 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0327 J9 J AFFECT DISORDERS JI J. Affect. Disord. PD APR PY 1994 VL 30 IS 4 BP 273 EP 281 DI 10.1016/0165-0327(94)90134-1 PG 9 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NG221 UT WOS:A1994NG22100004 PM 8014326 ER PT J AU KASPI, SP OTTO, MW POLLACK, MH EPPINGER, S ROSENBAUM, JF AF KASPI, SP OTTO, MW POLLACK, MH EPPINGER, S ROSENBAUM, JF TI PREMENSTRUAL EXACERBATION OF SYMPTOMS IN WOMEN WITH PANIC DISORDER SO JOURNAL OF ANXIETY DISORDERS LA English DT Article ID MENSTRUAL-CYCLE; ANXIETY; ATTACKS AB Women with panic disorder commonly report a premenstrual worsening of panic symptoms, but to date this report has not been confirmed in prospective trials. The present study investigated fluctuations in panic symptomatology across the menstrual cycle, with particular attention to the discrepancies between retrospective and prospective studies. Ninety-four women with panic disorder reported their history of premenstrual symptoms of panic, and 24 of these patients completed prospective diaries comprising two full menstrual cycles. Similar to previous studies, 41% of the sample provided a retrospective report of premenstrual worsening of panic symptoms. Unlike previous investigations, a significant increase in panic frequency during the premenstruum was found in our prospective study, with 50% of subjects reporting at least a 100% increase in panic frequency. Women who experienced negative mood premenstrually were more likely to accurately report exacerbation of panic symptoms during the premenstruum. C1 MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC-815,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 20 TC 40 Z9 40 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6185 J9 J ANXIETY DISORD JI J. Anxiety Disord. PD APR-JUN PY 1994 VL 8 IS 2 BP 131 EP 138 DI 10.1016/0887-6185(94)90011-6 PG 8 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA NJ548 UT WOS:A1994NJ54800003 ER PT J AU BADR, MS SKATRUD, JB DEMPSEY, JA AF BADR, MS SKATRUD, JB DEMPSEY, JA TI EFFECT OF CHEMORECEPTOR STIMULATION AND INHIBITION ON TOTAL PULMONARY RESISTANCE IN HUMANS DURING NREM SLEEP SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE HYPOXIA; HYPOCAPNIA; UPPER AIRWAY PATENCY ID UPPER AIRWAY-RESISTANCE; RESPIRATORY DRIVE; NORMAL MEN; HYPERCAPNIA; HYPOXIA; COLLAPSIBILITY; HYPOGLOSSAL; OBSTRUCTION; RESPONSES; MECHANICS AB We investigated the effect of chemoreceptor stimulation and inhibition on total pulmonary resistance (RL) during non-rapid-eye-movement (NREM) sleep in healthy subjects. Chemoreceptor stimulation was accomplished with brief isocapnic hypoxia (n = 8). Minute ventilation increased to 150% of room air control. RL at peak inspiratory flow decreased to 66% of room air control. Resistive pressure-inspiratory flow plots demonstrated lower resistive pressures for a given inspiratory flow. Chemoreceptor inhibition was accomplished by abruptly terminating brief hypocapnic hypoxia with 100% O-2 (n = 7). Minute ventilation decreased to 63% of room air control. RL calculated at peak inspiratory or fixed flow did not change significantly, and pressure-flow plots at nadir ventilation showed no systematic change from room air control. We conclude that I) hypoxic chemoreceptor stimulation is associated with decreased RL and enhancement of pressure-flow relationships, suggesting increased upper airway caliber; 2) upper airway patency is not compromised during periods of low ventilatory drive in normal subjects; and 3) upper airway dilating muscles and thoracic pump muscles are optionally coordinated with increased and decreased ventilatory drive. C1 UNIV WISCONSIN,SCH MED,WILLIAM S MIDDLETON MEM VET ADM HOSP,MED SERV,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT MED,JOHN RANKIN LAB PREVENT MED,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PREVENT MED,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. FU NHLBI NIH HHS [NHLBI 42242, NHLBI HL-02588] NR 34 TC 30 Z9 30 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 APR PY 1994 VL 76 IS 4 BP 1682 EP 1692 PG 11 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA NG707 UT WOS:A1994NG70700042 PM 8045848 ER PT J AU CLOHISY, DR MANKIN, HJ AF CLOHISY, DR MANKIN, HJ TI OSTEOARTICULAR ALLOGRAFTS FOR RECONSTRUCTION AFTER RESECTION OF A MUSCULOSKELETAL TUMOR IN THE PROXIMAL END OF THE TIBIA SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID BONE-TUMORS; ARTHRODESIS; GRAFTS AB An osteoarticular allograft was used to reconstruct a skeletal deficiency in sixteen patients after resection of a tumor in the proximal end of the tibia. The status of each allograft and the condition of each involved limb were evaluated an average of nine years (range, six to fourteen years) postoperatively. The status of the allograft was evaluated according to the survival of the allograft and the occurrence of complications. Of the original sixteen allografts, seven were removed: six, between two and five years after the reconstruction and one, seven years after the reconstruction. A second reconstruction with use of an allograft was performed in five of the seven patients. Fifteen complications occurred in association with eleven of the original sixteen allografts. These included fracture of the allograft (five patients), subchondral collapse (five patients), infection (two patients), non-union (two patients), and instability of the joint (one patient). At the latest follow-up examination, nine patients had retained the original allograft, five had had a second allograft procedure, and two had had an above-the-knee amputation. The most recent result was rated excellent or good in eleven patients and fair or a failure in five, with use of the system of Mankin et al. It was rated good or excellent in nine patients and fair, poor, or a failure in six, and it was not rated in one patient who had died, according to the system of the Musculoskeletal Tumor Society. Finally, the result was rated good or excellent in twelve patients and a failure in three, and it was not rated in the patient who had died, on the basis of the system of The Hospital for Special Surgery. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. RP CLOHISY, DR (reprint author), UNIV MINNESOTA HOSP & CLIN,DEPT ORTHOPED SURG,420 DELAWARE ST,SE,BOX 189,MINNEAPOLIS,MN 55455, USA. NR 21 TC 92 Z9 95 U1 1 U2 2 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD APR PY 1994 VL 76A IS 4 BP 549 EP 554 PG 6 WC Orthopedics; Surgery SC Orthopedics; Surgery GA NG212 UT WOS:A1994NG21200009 PM 8150822 ER PT J AU WUCHERPFENNIG, AL LI, YP STETLERSTEVENSON, WG ROSENBERG, AE STASHENKO, P AF WUCHERPFENNIG, AL LI, YP STETLERSTEVENSON, WG ROSENBERG, AE STASHENKO, P TI EXPRESSION OF 92 KD TYPE-IV COLLAGENASE GELATINASE-B IN HUMAN OSTEOCLASTS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID BONE-RESORBING AGENTS; CYSTEINE-PROTEINASES; CATHEPSIN-B; RESORPTION; CELLS; TISSUE; METALLOPROTEINASES; INHIBITORS; PROCOLLAGENASE; LOCALIZATION AB The digestion of type I collagen is an essential step in bone resorption. It is well established that osteoclasts solubilize the mineral phase of bone during the resorptive process, but the mechanism by which they degrade type I collagen, the major proteinaceous component of bone, is controversial. Differential screening of a human osteoclastoma cDNA library was performed to characterize genes specifically expressed in osteoclasts. A large number of cDNA clones obtained by this procedure were found to represent 92 kD type IV collagenase (gelatinase B; MMP-9, EC 3.4.24.35), as well as tartrate-resistant acid phosphatase. In situ hybridization localized mRNA for gelatinase B to multinucleated giant cells in human osteoclastomas. Gelatinase B immunoreactivity was demonstrated in giant cells from eight of eight osteoclastomas, osteoclasts in normal bone, and osteoclasts of Paget's disease by use of a polyclonal antiserum raised against a synthetic gelatinase B peptide. In contrast, no immunoreactivity for 72 kD type IV collagenase (gelatinase A; MMP-2, EC 3.4.24.24), which is the product of a separate gene, was detected in osteoclastomas or normal osteoclasts. We propose that the 92 kD type IV collagenase/gelatinase B plays an important role in the resorption of collagen during bone remodeling. C1 NCI,DEPT PATHOL,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP WUCHERPFENNIG, AL (reprint author), FORSYTH RES INST,DEPT CYTOKINE BIOL,140 FENWAY,BOSTON,MA 02115, USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 FU NIDCR NIH HHS [DE 05590, DE 07378] NR 48 TC 109 Z9 113 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD APR PY 1994 VL 9 IS 4 BP 549 EP 556 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ND159 UT WOS:A1994ND15900014 PM 8030443 ER PT J AU TONG, HS SAKAI, DD SIMS, SM DIXON, SJ YAMIN, M GOLDRING, SR SNEAD, ML MINKIN, C AF TONG, HS SAKAI, DD SIMS, SM DIXON, SJ YAMIN, M GOLDRING, SR SNEAD, ML MINKIN, C TI MURINE OSTEOCLASTS AND SPLEEN-CELL POLYKARYONS ARE DISTINGUISHED BY MESSENGER-RNA PHENOTYPING SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID RESISTANT ACID-PHOSPHATASE; BONE-MARROW CULTURES; TARTRATE-RESISTANT; RAT BONE; IDENTIFICATION; OSTEOPONTIN; CALCITONIN; MARKER; DNA; DIFFERENTIATION AB To probe osteoclast gene expression, we combined the techniques of cell microisolation and RT-PCR to develop a novel and sensitive method for the isolation and mRNA phenotyping of small numbers of authentic osteoclasts and spleen cell polykaryons. Using this method we report (1) direct evidence for the presence of calcitonin receptor mRNA in osteoclasts, (2) confirmation of the recent finding of osteopontin mRNA in osteoclasts, and (3) demonstration that the specific expression of mRNA for tartrate-resistant acid phosphatase, carbonic anhydrase II, calcitonin receptor, and osteopontin enable one to distinguish the osteoclast from the morphologically similar and developmentally related spleen cell polykaryon. We also show that mRNA associated with the osteoblast phenotype, such as alkaline phosphatase, osteocalcin, and type I collagen, are absent in osteoclasts. This is the first report in which such an approach has been used successfully to distinguish the mRNA expression pattern of an authentic osteoclast from a macrophage polykaryon, and as such it should provide an important new tool for evaluating the results of various cell culture model systems designed to examine the origin and ontogeny of osteoclasts. Our results also indicate that these procedures can be used as an alternative to in situ hybridization methods for the cell-specific localization of specific MRNA in a mixed cell preparation and for colocalization of multiple mRNA species to a single cell type. C1 UNIV SO CALIF,SCH DENT,UNIV PK MC0641,LOS ANGELES,CA 90089. UNIV SO CALIF,DIV MOLEC BIOL,LOS ANGELES,CA 90089. UNIV WESTERN ONTARIO,DEPT PHYSIOL,LONDON N6A 3K7,ONTARIO,CANADA. UNIV WESTERN ONTARIO,DIV ORAL BIOL,LONDON N6A 3K7,ONTARIO,CANADA. MASSACHUSETTS GEN HOSP,ARTHRIT UNIT,BOSTON,MA 02114. RI Dixon, S./G-3657-2013; Sims, Stephen/G-4510-2013 OI Dixon, S./0000-0001-9162-1686; FU NIAMS NIH HHS [AR40176]; NIDCR NIH HHS [DE08678, DE09965] NR 33 TC 40 Z9 42 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD APR PY 1994 VL 9 IS 4 BP 577 EP 584 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ND159 UT WOS:A1994ND15900017 PM 8030446 ER PT J AU VONDERHEIDE, RH TEDDER, TF SPRINGER, TA STAUNTON, DE AF VONDERHEIDE, RH TEDDER, TF SPRINGER, TA STAUNTON, DE TI RESIDUES WITHIN A CONSERVED AMINO-ACID MOTIF OF DOMAIN-1 AND DOMAIN-4 OF VCAM-1 ARE REQUIRED FOR BINDING TO VLA-4 SO JOURNAL OF CELL BIOLOGY LA English DT Article ID CELL-ADHESION MOLECULE-1; HUMAN ENDOTHELIAL-CELLS; VERSUS-HOST DISEASE; MONONUCLEAR LEUKOCYTE ADHESION; FIBROBLAST-LIKE SYNOVIOCYTES; TUMOR-NECROSIS-FACTOR; HUMAN-B-CELLS; VASCULAR ENDOTHELIUM; COUNTER-RECEPTOR; INTEGRIN VLA-4 AB Vascular cell adhesion molecule 1 (VCAM-1), a member of the Ig superfamily originally identified on activated endothelium, binds to the integrin very late antigen-4 (VLA-4), also known as alpha4beta1 or CD49d/CD29, to support cell-cell adhesion. Studies based on cell adhesion to two alternatively spliced forms of VCAM-1 or to chimeric molecules generated from them and intercellular adhesion molecule-1 (ICAM-1) have demonstrated two VLA-4 binding sites on the predominate form of VCAM-1. Here, we studied VLA-4-dependent adhesion of the lymphoid tumor cell line Ramos to cells expressing wild type and mutant forms of VCAM-1. Results based on domain deletion mutants demonstrated the existence and independence of two VLA-4-binding sites located in the first and fourth domains of VCAM-1. Results based on amino acid substitution mutants demonstrated that residues within a linear sequence of six amino acids found in both domain 1 and 4 were required for VLA-4 binding to either domain. Five of these amino acids represent a conserved motif also found in ICAM domains. We propose that integrin binding to these Ig-like domains depends on residues within this conserved motif. Specificity of integrin binding to Ig-like domains may be regulated by a set of nonconserved residues distinct from the conserved motif. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA-54464]; NHLBI NIH HHS [P01-HL48675]; PHS HHS [A126872] NR 66 TC 157 Z9 159 U1 1 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1994 VL 125 IS 1 BP 215 EP 222 DI 10.1083/jcb.125.1.215 PG 8 WC Cell Biology SC Cell Biology GA NE036 UT WOS:A1994NE03600018 PM 7511143 ER PT J AU PASQUALINI, R HEMLER, ME AF PASQUALINI, R HEMLER, ME TI CONTRASTING ROLES FOR INTEGRIN-BETA(1) AND INTEGRIN-BETA(5) CYTOPLASMIC DOMAINS IN SUBCELLULAR-LOCALIZATION, CELL-PROLIFERATION, AND CELL-MIGRATION SO JOURNAL OF CELL BIOLOGY LA English DT Article ID PROTEIN-TYROSINE PHOSPHORYLATION; GLYCOPROTEIN-IIB-IIIA; FIBRONECTIN RECEPTOR; BETA-SUBUNIT; T-CELLS; EXTRACELLULAR-MATRIX; SIGNAL TRANSDUCTION; ENDOTHELIAL-CELLS; INTRACELLULAR PH; GENE-EXPRESSION AB To carry out a detailed comparison of the roles of integrin beta1 and beta5 cytoplasmic domains, we expressed both wild type beta1 and chimeric beta1/5 constructs in CHO cells. In the latter, the cytoplasmic domain of beta1 was replaced with that of beta5. The human beta1 and beta1/5 constructs appeared at similar levels at the cell surface (mostly as alpha5beta1 heterodimers) and contributed equally to CHO cell adhesion to fibronectin. However, beta1 but not beta1/5 localized to focal adhesion-like structures when CHO cells were spread on fibronectin. Furthermore, only the beta1-CHO cells showed increased proliferation in response to fibronectin plus an integrin-activating anti-beta1 antibody, and showed increased appearance of P-12-labeled protein (p90) that correlated with proliferation. In sharp contrast, the beta1/5-CHO cells were notably more migratory than beta1-CHO cells in a transwell haptotactic migration assay. These results indicate that the beta1 and beta5 integrin subunit cytoplasmic domains can translate similar adhesive information into highly contrasting subsequent events. Thus, we have established that ''inside-out'' and ''outside-in'' integrin signaling pathways are regulated by fundamentally distinct mechanisms. In addition, we suggest that the same properties of the beta1 cytoplasmic domain that promote recruitment to visible focal adhesion-like structures may also be conducive to cell proliferation. Conversely, the properties of the beta5 tail that make it less likely to localize into focal adhesion-like structures may contribute to enhanced cell migration. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,ROOM M-613,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA42368] NR 88 TC 93 Z9 93 U1 1 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1994 VL 125 IS 2 BP 447 EP 460 DI 10.1083/jcb.125.2.447 PG 14 WC Cell Biology SC Cell Biology GA NF965 UT WOS:A1994NF96500019 PM 7512969 ER PT J AU PARDEE, AB AF PARDEE, AB TI MULTIPLE MOLECULAR-LEVELS OF CELL-CYCLE REGULATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE REGULATION; CELL CYCLE; CANCER; TRANSCRIPTION; TRANSLATION; PROTEIN MODIFICATION ID MESSENGER-RNA; PROTEIN; KINASE; DNA; TRANSLATION; COMPLEX; GROWTH AB The objective of this brief review is to stress the importance of multiple levels of molecular regulation of complex processes such as cell growth and to illustrate their derangements as they occur in cancer cells. One major research emphasis today is the regulation of transcription by binding of transactivating proteins to promoter motifs. Another focus is on the multiple roles of protein phosphorylations in signal transduction pathways. Evidence is strong, however, that major controls exist at numerous other molecular levels as well (Fig. 1). These include pre-mRNA processing, pre-mRNA degradation, mRNA degradation, control of translation, permanent protein modifications, protein degradation, reversible covalent protein alterations, noncovalent interactions with small molecules and with other proteins, and effects of relocations into cell compartments. These controls are exhibited in all biological processes. A few illustrative examples are briefly discussed, which come mainly from our researches in the area of cell cycle regulation and its derangement in cancer. (C) 1994 Wiley-Liss, Inc. RP PARDEE, AB (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM 24571] NR 37 TC 26 Z9 26 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR PY 1994 VL 54 IS 4 BP 375 EP 378 DI 10.1002/jcb.240540403 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ND155 UT WOS:A1994ND15500002 PM 8014185 ER PT J AU LAN, SP RYAN, CM ADAMS, KM GRANT, I HEATON, RK RAND, LI JACOBSON, AM NATHAN, DM CLEARY, PA AF LAN, SP RYAN, CM ADAMS, KM GRANT, I HEATON, RK RAND, LI JACOBSON, AM NATHAN, DM CLEARY, PA TI A SCREENING ALGORITHM TO IDENTIFY CLINICALLY SIGNIFICANT CHANGES IN NEUROPSYCHOLOGICAL FUNCTIONS IN THE DIABETES CONTROL AND COMPLICATIONS TRIAL SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Article ID OBSTRUCTIVE PULMONARY-DISEASE; HYPOGLYCEMIA; IMPAIRMENT; MELLITUS; COMPLEX; AIDS AB Neuropsychological (NP) evaluations provide an accepted means of monitoring safety in multi-center long-term medical trials. However, using neuropsychologists to review test protocols and rate level of clinical impairment can be a costly and logistically complex undertaking. To facilitate that process, the DCCT Research Group developed a computerized screening strategy that utilized statistical models to identify individuals with possible cognitive deterioration. Two hundred and eight subjects with insulin-dependent diabetes mellitus were assessed twice, 2 years apart, with an extensive battery of NP tests, and the results were rated by expert clinicians. Multiple logistic regression was used to develop a statistical model to predict clinically significant NP worsening (as determined by clinical raters) on the basis of changes in scores (year 2 - baseline) derived from the actual tests. A subsequent performance evaluation with an additional 1087 subjects demonstrated that the computerized algorithm was highly successful in identifying individuals with significantly worsened NP performance. Despite a high false positive rate, the algorithm can achieve an 80-90% reduction in the number of cases requiring evaluation by expert neuropsychologists. C1 GEORGE WASHINGTON UNIV, CTR BIOSTAT, DEPT STAT COMP & INFORMAT SYST, ROCKVILLE, MD USA. UNIV PITTSBURGH, SCH MED, WESTERN PSYCHIAT INST & CLIN, PITTSBURGH, PA USA. VET ADM MED CTR, PSYCHOL SERV, ANN ARBOR, MI USA. VET ADM MED CTR, DEPT PSYCHIAT, SAN DIEGO, CA USA. UNIV CALIF SAN DIEGO, DEPT PSYCHIAT, SAN DIEGO, CA 92103 USA. JOSLIN DIABET CTR, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, DEPT PSYCHIAT, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, DIABET UNIT, BOSTON, MA 02114 USA. RI Zinman, Bernard/E-7266-2013 NR 32 TC 6 Z9 6 U1 0 U2 1 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1380-3395 EI 1744-411X J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD APR PY 1994 VL 16 IS 2 BP 303 EP 316 DI 10.1080/01688639408402640 PG 14 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA NG556 UT WOS:A1994NG55600014 ER PT J AU YOSHIMURA, M PEKARY, AE PANG, XP BERG, L GOODWIN, TM HERSHMAN, JM AF YOSHIMURA, M PEKARY, AE PANG, XP BERG, L GOODWIN, TM HERSHMAN, JM TI THYROTROPIC ACTIVITY OF BASIC ISOELECTRIC FORMS OF HUMAN CHORIONIC-GONADOTROPIN EXTRACTED FROM HYDATIDIFORM MOLE TISSUES SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID STIMULATOR; VARIANTS; CELLS AB hCG is known to have thyroid-stimulating activity and may cause hyperthyroidism in patients with trophoblastic diseases. hCG occurs in normal and molar pregnancy with breaks or nicks in the alpha- or beta-subunit peptide linkage and with substantial heterogeneity in the composition and degree of branching within the oligosaccharide side-chains. The bioactivity of hCG is markedly influenced by these structural variations. We purified hCG from five hydatidiform moles, using chromatofocusing separation after gel filtration. The hCG molecules were fractionated according to their isoelectric points, with a linear pH gradient from 3.2-6.1 and a final 1.0 mol/L NaCl step elution. The hCG immunoreactivity of each fraction was measured by RIA, and the thyroid-stimulating activity of hCG was determined by means of the cAMP response in Chinese hamster ovary cells expressing functional human TSH receptors (Chinese hamster ovary-JP09 cells). The chromatofocusing profile showed that hCG from the moles was eluted in six or seven major peaks at pH 6.1, 5.5, 5.3, 4.8, 3.8, and 3.2 and with 1.0 mol/L NaCl, whereas hCG extracted from serum of hydatidiform moles and standard hCG preparation CR-127 extracted from pregnancy urine showed only small peaks at pH greater than 5.3. Each fraction increased cAMP production significantly in Chinese hamster ovary-JP09 cells. The relative bioactivity/immunoreactivity, represented as the ratio of cAMP/hCG (picomoles per IU), was significantly higher in basic components (pI 6.1, 6.2 +/- 1.2; pI 5.5, 4.4 +/- 2.7; pI 5.3, 5.8 +/- 0.3) than in hCG CR-127 (bioactivity/immunoreactivity, 0.42; P < 0.05). The difference in pI of each hCG isoform was attributable to the extent of sialylation; basic hCG isoforms contained less sialic acid by immunological detection using lectins. These results indicate that isoforms of hCG with more thyrotropic activity were produced by trophoblastic tissues in patients with hydatidiform mole. We speculate that these isoforms of hCG may be responsible for the hyperthyroidism in some patients with hydatidiform moles. C1 W LOS ANGELES VET AFFAIRS MED CTR, ENDOCRINOL RES LAB, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90073 USA. UNIV SO CALIF, SCH MED, DEPT OBSTET & GYNECOL, LOS ANGELES, CA 90033 USA. NR 27 TC 47 Z9 47 U1 0 U2 2 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 APR PY 1994 VL 78 IS 4 BP 862 EP 866 DI 10.1210/jc.78.4.862 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NF021 UT WOS:A1994NF02100013 PM 8157712 ER PT J AU ZHU, JG LEON, SP BEGGS, AH BUSQUE, L GILLILAND, DG BLACK, PM AF ZHU, JG LEON, SP BEGGS, AH BUSQUE, L GILLILAND, DG BLACK, PM TI HUMAN PITUITARY-ADENOMAS SHOW NO LOSS OF HETEROZYGOSITY AT THE RETINOBLASTOMA GENE LOCUS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID X-CHROMOSOME INACTIVATION; CUSHINGS-DISEASE; ADENYLYL CYCLASE; CLONAL ORIGIN; DNA-SEQUENCE; TUMORS; MUTATIONS; PROTEIN; POLYMORPHISMS; GS AB The retinoblastoma tumor suppressor gene (RB1) is inactivated in hereditary and sporadic forms of retinoblastoma as well as in a number of other sporadic tumors. The majority of human pituitary tumors have been shown to be monoclonal neoplasms, suggesting that 1 or more somatic mutations are involved in the clonal expansion of a single progenitor cell. Recently, a high percentage of transgenic mice containing a disrupted RB1 allele have been shown to develop pituitary tumors. To investigate whether RB1 inactivation contributes to the development of human pituitary adenomas, we searched for loss of heterozygosity (LOH) within the RB1 gene locus in a variety of human pituitary adenomas. We screened 34 adenomas for LOH using a polymerase chain reaction (PCR)-based microsatellite polymorphic marker at the RB1 gene locus. In addition, a variable number of tandem repeat markers from within the RB1 gene was also used to search for LOH in 14 tumors. We found no LOH or microsatellite instability at the RB1 locus in any of the informative cases (30 of 34). Additionally, we showed that 4 representative adenomas from female patients are monoclonal in origin using a PCR-based clonality analysis assay. We conclude that the RB1 gene shows no LOH in a variety of human pituitary adenomas and that PCR-based microsatellite markers can serve as a useful tool for LOH analysis in human pituitary tumors. C1 BRIGHAM & WOMENS HOSP, BRAIN TUMOR RES CTR, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DIV HEMATOL ONCOL, BOSTON, MA 02115 USA. CHILDRENS HOSP, DIV GENET, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. CHILDRENS HOSP, DEPT NEUROSURG, BOSTON, MA 02115 USA. RP ZHU, JG (reprint author), BRIGHAM & WOMENS HOSP, NEUROSURG LABS, 221 LONGWOOD AVE, ROOM 121, BOSTON, MA 02115 USA. OI Beggs, Alan/0000-0001-8818-0568 NR 42 TC 73 Z9 76 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1994 VL 78 IS 4 BP 922 EP 927 DI 10.1210/jc.78.4.922 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NF021 UT WOS:A1994NF02100023 PM 8157722 ER PT J AU SCHENKER, S BAY, M AF SCHENKER, S BAY, M TI DRUG DISPOSITION AND HEPATOTOXICITY IN THE ELDERLY SO JOURNAL OF CLINICAL GASTROENTEROLOGY LA English DT Article DE HEPATOTOXICITY; DRUG DISPOSITION; ELDERLY ID AGE-RELATED-CHANGES; ANTIOXIDANT ENZYMES; DIETARY RESTRICTION; LIVER-DISEASE; RAT-LIVER; EXPRESSION; INJURY; METABOLISM AB Overall, the aged liver seems to function remarkably well in the elderly. Decreased drug disposition is selective and modest and there is no compelling evidence of greater susceptibility to drug-induced or other types of injury. Drug-drug interactions and concurrent derangements accompanying advanced age may, however, contribute to adverse drug effects. Still, the aged, consume about three times as many therapeutic agents as other people. Most of these are metabolized in the liver before excretion. With increasing age, hepatic blood flow falls and so does hepatic volume. Moreover, binding of some agents normally carried on albumin may decrease. In contrast, increasing age has relatively modest effects on hepatic drug metabolism and these are highly selective. In the healthy aged, hepatic drug elimination is only modestly, if at all, impaired and this is likely to especially affect agents dependent on liver blood flow. Other factors that affect drug elimination in the aged are drug-drug interaction and the frailty and functional impairment of many elderly, as a result of poor diet, infection, multiple hospitalizations, or other events. Decreased host defense systems in the aged liver may lead to decreased adaptation to stress and slower regeneration after injury. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP SCHENKER, S (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL & NUTR,7703 FLOYD CURL,SAN ANTONIO,TX 78284, USA. FU NIAAA NIH HHS [R01 AA07514] NR 40 TC 14 Z9 14 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-0790 J9 J CLIN GASTROENTEROL JI J. Clin. Gastroenterol. PD APR PY 1994 VL 18 IS 3 BP 232 EP 237 DI 10.1097/00004836-199404000-00013 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NE689 UT WOS:A1994NE68900012 PM 8034922 ER PT J AU ALPER, SL STUARTTILLEY, A SIMMONS, CF BROWN, D DRENCKHAHN, D AF ALPER, SL STUARTTILLEY, A SIMMONS, CF BROWN, D DRENCKHAHN, D TI FODRIN-ANKYRIN CYTOSKELETON OF CHOROID-PLEXUS PREFERENTIALLY COLOCALIZES WITH APICAL NA+K+-ATPASE RATHER THAN WITH BASOLATERAL ANION-EXCHANGER AE2 SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CHOROID PLEXUS; EPITHELIAL POLARITY; ANION EXCHANGER 2; SODIUM-POTASSIUM ADENOSINE TRIPHOSPHATASE; CYTOSKELETON ID ADHESION MOLECULE UVOMORULIN; NA+,K+-ATPASE ALPHA-SUBUNIT; CANINE KIDNEY-CELLS; EPITHELIAL-CELLS; SUBCELLULAR-LOCALIZATION; INTERCALATED CELLS; PLASMA-MEMBRANE; BRUSH-BORDER; EXPRESSION; POLARITY AB A unique feature of the choroid plexus as a single-layer epithelium is its localization of Na+K+-ATPase at its apical (lumenal) surface. In contrast, a band 3 (AE1)-related anion exchanger protein has been localized to the basolateral surface of the choroid plexus. Both Na+K+-ATPase and AE1 in other tissues have been shown to bind via ankyrin to the spectrin-actin-based membrane cytoskeleton. Since linkage of integral membrane proteins to the membrane cytoskeleton is important for their restriction to specialized domains of the cell surface, we investigated the polarity of the choroid plexus membrane cytoskeleton. We developed isoform-specific antibodies to confirm the identity of choroid plexus band 3-related polypeptide as AE2. We demonstrated that ankyrin, fodrin/spectrin, actin, myosin, and cr-actinin are predominantly apical in choroid plexus and preferentially colocalize with apical Na+K+-ATPase rather than with basolateral anion exchanger AE2. Colchicine administration did not alter the polarity of apical cytoskeletal and transport proteins or basolateral AE2 in choroid plexus, suggesting that biosynthetic targeting of these proteins is not microtubule dependent. In choroid plexus papilloma, Na+K+-ATPase and AE2 were decreased in amount and failed to preserve their polarized distributions. C1 BETH ISRAEL HOSP,RENAL UNIT,BOSTON,MA 02215. CHILDRENS HOSP,DIV NEONATOL,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02215. UNIV WURZBURG,INST ANAT,D-97070 WURZBURG,GERMANY. RP ALPER, SL (reprint author), BETH ISRAEL HOSP,MOLEC MED UNIT,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK-43495] NR 54 TC 94 Z9 94 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1994 VL 93 IS 4 BP 1430 EP 1438 DI 10.1172/JCI117120 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF562 UT WOS:A1994NF56200013 PM 8163647 ER PT J AU MONTANA, E BONNERWEIR, S WEIR, GC AF MONTANA, E BONNERWEIR, S WEIR, GC TI TRANSPLANTED BETA-CELL RESPONSE TO INCREASED METABOLIC DEMAND - CHANGES IN BETA-CELL REPLICATION AND MASS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE DIABETES; ISLET TRANSPLANTATION; BETA CELL GROWTH; BETA CELL MASS; PANCREATECTOMY ID OBESE-HYPERGLYCEMIC MICE; MOUSE PANCREATIC-ISLETS; INSULIN-SECRETION; DIABETIC-PATIENTS; DNA-REPLICATION; GROWTH; IMPLANTATION; GLUCOSE; RAT; PROLIFERATION AB We determined the capacity of transplanted beta cells to modify their replication and mass when stimulated by changes in metabolic demand. Five groups of Lewis rats were studied: group 1 (Tx-Px) had a 95% pancreatectomy 14 d after transplantation of 500 islets; group 2 (Px-Tx) had a 95% pancreatectomy 14 d before transplantation of 500 islets; group 3 (Tx) was transplanted with 500 islets; group 4 (Px) had a 95% pancreatectomy; and group 5 (normal) was neither transplanted nor pancreatectomized. Blood glucose was normal in Tx-Px and Tx groups at all times. Px-Tx and Pr groups developed severe hyperglycemia after pancreatectomy that was corrected in Px-Tx group in 83% of rats 28 d after transplantation. Replication of transplanted beta cells increased in Tx-Px (1.15+/-0.12%) and Px-Tx (0.85+/-0.12%) groups, but not in Tx group (0.64+/-0.07%) compared with normal pancreatic beta cells (0.38+/-0.05%) (P < 0.001). Mean beta cell size increased in Tx-Px (311+/-14 mu m(2)) and Px-Tx (328+/-13 mu m(2)) groups compared with Tx (252+/-12 mu m(2)) and normal (239+/-9 mu m(2)) groups (P ( 0.001). Transplanted beta cell mass increased in Tx-Px (1.87+/-0.51 mg) and Px-Tx (1.55+/-0.21 mg) groups compared with Tx group (0.78+/-0.17 mg) (P < 0.05). In summary, changes in transplanted beta cells prevented the development of hyperglycemia in Tx-Px rats. Transplanted beta cells responded to increased metabolic demand increasing their beta cell mass. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02215. FU NIDDK NIH HHS [DK-35449, DK-36836] NR 33 TC 72 Z9 72 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1994 VL 93 IS 4 BP 1577 EP 1582 DI 10.1172/JCI117137 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF562 UT WOS:A1994NF56200030 PM 8163660 ER PT J AU HARRIS, JR GELMAN, R AF HARRIS, JR GELMAN, R TI WHAT HAVE WE LEARNED ABOUT RISK-FACTORS FOR LOCAL RECURRENCE AFTER BREAST-CONSERVING SURGERY AND IRRADIATION SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID RANDOMIZED TRIAL; CONSERVATION THERAPY; TUMOR RECURRENCE; CANCER; MASTECTOMY; AGE; LUMPECTOMY; CARCINOMA; SURVIVAL C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA. RP HARRIS, JR (reprint author), HARVARD UNIV,BETH ISRAEL HOSP,CTR RADIAT THERAPY,SCH MED,DANA FARBER CANC INST,BOSTON,MA, USA. NR 23 TC 16 Z9 16 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 APR PY 1994 VL 12 IS 4 BP 647 EP 649 PG 3 WC Oncology SC Oncology GA NG395 UT WOS:A1994NG39500001 PM 8151312 ER PT J AU WILLETT, CG WARLAND, G CHEEK, R COEN, J EFIRD, J SHELLITO, PC COMPTON, CC AF WILLETT, CG WARLAND, G CHEEK, R COEN, J EFIRD, J SHELLITO, PC COMPTON, CC TI PROLIFERATING CELL NUCLEAR ANTIGEN AND MITOTIC-ACTIVITY IN RECTAL-CANCER - PREDICTOR OF RESPONSE TO PREOPERATIVE IRRADIATION SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID DNA POLYMERASE-DELTA; PARAFFIN SECTIONS; GROWTH FRACTION; MONOCLONAL-ANTIBODIES; RADIATION-THERAPY; AUXILIARY PROTEIN; EMBEDDED TISSUES; CYCLIN PCNA; EXPRESSION; CARCINOMA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT GEN SURG,BOSTON,MA. NR 20 TC 33 Z9 33 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 APR PY 1994 VL 12 IS 4 BP 679 EP 682 PG 4 WC Oncology SC Oncology GA NG395 UT WOS:A1994NG39500006 PM 7908689 ER PT J AU SCHORIN, MA BLATTNER, S GELBER, RD TARBELL, NJ DONNELLY, M DALTON, V COHEN, HJ SALLAN, SE AF SCHORIN, MA BLATTNER, S GELBER, RD TARBELL, NJ DONNELLY, M DALTON, V COHEN, HJ SALLAN, SE TI TREATMENT OF CHILDHOOD ACUTE LYMPHOBLASTIC-LEUKEMIA - RESULTS OF DANA-FARBER-CANCER-INSTITUTE CHILDRENS-HOSPITAL ACUTE LYMPHOBLASTIC-LEUKEMIA CONSORTIUM PROTOCOL-85-01 SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CENTRAL NERVOUS-SYSTEM; THERAPY; ASPARAGINASE; METHOTREXATE; EXPERIENCE; INDUCTION; INFANTS C1 DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA. CHILDRENS HOSP,DEPT RADIAT ONCOL,BOSTON,MA. CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA. JOINT CTR RADIAT ONCOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA. OCHSNER MED INST,DEPT PEDIAT,NEW ORLEANS,LA. MAINE MED CTR,DEPT PEDIAT,PORTLAND,ME. UNIV ROCHESTER,MED CTR,DEPT PEDIAT,ROCHESTER,NY. UNIV ROCHESTER,MED CTR,CTR CANC,ROCHESTER,NY. FU NCI NIH HHS [CA 06516, CA 34183] NR 21 TC 155 Z9 157 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 APR PY 1994 VL 12 IS 4 BP 740 EP 747 PG 8 WC Oncology SC Oncology GA NG395 UT WOS:A1994NG39500015 PM 8151317 ER PT J AU BENNETT, JM TROXEL, AB GELMAN, R FALKSON, G DREICER, R TORMEY, DC RUSHING, D COCCIAPORTUGAL, MD AF BENNETT, JM TROXEL, AB GELMAN, R FALKSON, G DREICER, R TORMEY, DC RUSHING, D COCCIAPORTUGAL, MD TI MYELODYSPLASTIC SYNDROME AND ACUTE MYELOID-LEUKEMIA SECONDARY TO MITOLACTOL TREATMENT IN PATIENTS WITH BREAST-CANCER SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter C1 HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV PRETORIA,PRETORIA 0002,SOUTH AFRICA. UNIV IOWA,IOWA CITY,IA. AMC CANC RES CTR,DENVER,CO. MARSHFIELD CLIN FDN MED RES & EDUC,MARSHFIELD,WI 54449. RP BENNETT, JM (reprint author), UNIV ROCHESTER,CTR CANC,ROCHESTER,NY, USA. NR 1 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 APR PY 1994 VL 12 IS 4 BP 874 EP 875 PG 2 WC Oncology SC Oncology GA NG395 UT WOS:A1994NG39500031 PM 8151329 ER PT J AU HARRIS, NL AF HARRIS, NL TI MANTLE CELL LYMPHOMA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter ID GERMINAL-CENTER; MALIGNANT-LYMPHOMAS RP HARRIS, NL (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 17 TC 5 Z9 5 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 APR PY 1994 VL 12 IS 4 BP 876 EP 877 PG 2 WC Oncology SC Oncology GA NG395 UT WOS:A1994NG39500033 PM 8151331 ER PT J AU SHIVDASANI, RA PINKUS, GS AF SHIVDASANI, RA PINKUS, GS TI MANTLE CELL LYMPHOMA - REPLY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. RP SHIVDASANI, RA (reprint author), DANA FARBER CANC INST,BOSTON,MA, USA. NR 5 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 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1994 VL 12 IS 4 BP 877 EP 877 PG 1 WC Oncology SC Oncology GA NG395 UT WOS:A1994NG39500034 ER PT J AU CENTORRINO, F BALDESSARINI, RJ KANDO, JC FRANKENBURG, FR VOLPICELLI, SA FLOOD, JG AF CENTORRINO, F BALDESSARINI, RJ KANDO, JC FRANKENBURG, FR VOLPICELLI, SA FLOOD, JG TI CLOZAPINE AND METABOLITES - CONCENTRATIONS IN SERUM AND CLINICAL FINDINGS DURING TREATMENT OF CHRONICALLY PSYCHOTIC-PATIENTS SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Note ID DRUG-DRUG INTERACTIONS; PLASMA-LEVELS; CHLORPROMAZINE; PHARMACOKINETICS; SCHIZOPHRENIA; VARIABLES; SEIZURES; THERAPY; GENDER; SCALE AB Clozapine (CLZ) and metabolites norclozapine and clozapine-N-oxide were assayed with a new, sensitive (2 pmol), and selective method in 68 serum samples from 44 psychotic subjects, 20 to 54 years old, ill 16 years, and treated with CLZ for 2.2 years (currently at 294 mg, 3.4 mg/kg daily). CLZ levels averaged 239 ng/ml (0.73 muM; 92 ng/ml per mg/kg dose) or 48% of total analytes (norclozapine = 41% [91% of CLZ] and clozapine-N-oxide = 11%); metabolite and CLZ levels were highly correlated (r(s) = 0.9), and CLZ levels varied with daily dose (r(s) = 0.7). Sampling twice yielded similar within-subject analyte levels (r = 0.8 to 0.9; difference = 24% to 33%). Range and variance narrowed when levels were expressed per weight-corrected dose (ng/ml per mg/kg). Levels per dose were 40% higher in nonsmoking women than men, despite a 60% lower milligram per kilogram dose in women, and did not vary by diagnosis or age in this limited sample. Fluoxetine increased serum CLZ analytes by 60%; valproate had less effect. Patients rated treatment very positively; observer-assessed benefits typically were more moderate. Common late side effects were sialorrhea (80%), excess sedation (58%), obesity (55% > 200 lb), mild tachycardia (51%), constipation (32%), and enuresis (27%); there were no seizures or leukopenia. There was little evident relationship of drug dose or serum level to current clinical measures or side effect risks. C1 HARVARD UNIV,SCH MED,DEPT HUMAN ANAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MCLEAN HOSP,DEPT PHARM,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,CLIN CHEM LAB,BOSTON,MA 02114. RP CENTORRINO, F (reprint author), MCLEAN HOSP,MAILMAN RES CTR,BIPOLAR & PSYCHOT DISORDERS PROGRAM,115 MILL ST,BELMONT,MA 02178, USA. FU NIMH NIH HHS [MH-31154] NR 56 TC 116 Z9 118 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1994 VL 14 IS 2 BP 119 EP 125 PG 7 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA NC590 UT WOS:A1994NC59000006 PM 8195452 ER PT J AU LABBATE, LA SACHS, GS AF LABBATE, LA SACHS, GS TI PHOTOTHERAPY-INDUCED HOT FLUSHES SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Letter C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. RP LABBATE, LA (reprint author), WALTER REED ARMY MED CTR,DEPT PSYCHIAT,WASHINGTON,DC 20307, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1994 VL 14 IS 2 BP 151 EP 151 DI 10.1097/00004714-199404000-00015 PG 1 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA NC590 UT WOS:A1994NC59000015 PM 8195461 ER PT J AU BALL, SG OTTO, MW POLLACK, MH ROSENBAUM, JF AF BALL, SG OTTO, MW POLLACK, MH ROSENBAUM, JF TI PREDICTING PROSPECTIVE EPISODES OF DEPRESSION IN PATIENTS WITH PANIC DISORDER - A LONGITUDINAL-STUDY SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY LA English DT Article ID MAJOR DEPRESSION; SOCIAL PHOBIA; FOLLOW-UP; RECURRENCE; RECOVERY; VALIDITY; BEHAVIOR; RELAPSE AB This study used a naturalistic, longitudinal study to examine predictors of the emergence of major depression among 90 nondepressed patients with panic disorder who were followed for a 2-year period. Twenty-four percent of the sample experienced a major depressive episode during the study period. Adequacy and type of medication treatment were not associated with decreased risk. Past history of major depression was associated with a greater risk for a prospective episode. The degree of assertiveness, presence of comorbid generalized anxiety disorder, and severity of agoraphobia were each significant predictors of the occurrence of depression when considered alone and when the influence of past history of depression was statistically controlled. The implications of these findings for the clinical management of patients with panic disorder are discussed. C1 MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIMH NIH HHS [MH 19600] NR 33 TC 46 Z9 47 U1 1 U2 3 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0022-006X J9 J CONSULT CLIN PSYCH JI J. Consult. Clin. Psychol. PD APR PY 1994 VL 62 IS 2 BP 359 EP 365 DI 10.1037//0022-006X.62.2.359 PG 7 WC Psychology, Clinical SC Psychology GA NF750 UT WOS:A1994NF75000019 PM 8201074 ER PT J AU BENNETT, J DRETLER, SP SELENGUT, J ORMEJOHNSON, WH AF BENNETT, J DRETLER, SP SELENGUT, J ORMEJOHNSON, WH TI IDENTIFICATION OF THE CALCIUM-BINDING PROTEIN CALGRANULIN IN THE MATRIX OF STRUVITE STONES SO JOURNAL OF ENDOUROLOGY LA English DT Article ID POLYACRYLAMIDE-GEL ELECTROPHORESIS; GAMMA-CARBOXYGLUTAMIC ACID; MYELOMONOCYTIC ANTIGEN L1; CYSTIC-FIBROSIS; CRYSTAL-GROWTH; HUMAN-TISSUES; DIFFERENTIATION; INHIBITORS; EXPRESSION AB The identification of calcium-binding proteins in urine and kidney stones has led to a closer look at the role of matrix proteins in urolithiasis. We analyzed five struvite stones for protein content and identified two bands (8 and 14 KDa) that were confirmed by gel electrophoresis and amino acid sequencing to be calgranulin. This protein, which is known by several other names, has bacteriostatic antifungal activity. Its role in the formation of struvite stones warrants further investigation. C1 MIT,DEPT CHEM,CAMBRIDGE,MA 02139. RP BENNETT, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT UROL,15 PARKHAM ST,SUITE 486,BOSTON,MA 02114, USA. NR 22 TC 12 Z9 12 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0892-7790 J9 J ENDOUROL JI J. Endourol. PD APR PY 1994 VL 8 IS 2 BP 95 EP 98 DI 10.1089/end.1994.8.95 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA NL788 UT WOS:A1994NL78800002 PM 8061680 ER PT J AU DUBEY, DP ALPER, CA MIRZA, NM AWDEH, Z YUNIS, EJ AF DUBEY, DP ALPER, CA MIRZA, NM AWDEH, Z YUNIS, EJ TI POLYMORPHIC HH GENES IN THE HLA-B(C) REGION CONTROL NATURAL-KILLER-CELL FREQUENCY AND ACTIVITY SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; INHERITED STRUCTURAL POLYMORPHISM; NK-CELLS; MARROW GRAFTS; ALLOANTIGEN RECOGNITION; PEMPHIGUS-VULGARIS; JEWISH PATIENTS; CYTO-TOXICITY; TARGET-CELLS; RESISTANCE AB We demonstrated earlier that individuals homozygous for conserved major histocompatibility complex (MHC)-wended haplotypes have low natural killer (NK) activity as measured by cytolysis of the K562 tumor cell line. In the present study, we investigated the segregation and MHC linkage of NK activity in families in which MHC haplotypes of human histocompatibility leukocyte antigens (HLA)-A, -C, and -B, complotype, and DR specificities are known. In two informative families, low activity was inherited as a recessive trait linked to the MHC. By using individuals homozygous for specific fragments of extended haplotypes or for HLA-B alleles, we found that the HLA-C and -B and not the complotype or HLA-DR region contains genes controlling NK activity. The majority of the unrelated individuals with low NK activity were homozygous or doubly heterozygous for HLA-B7 (Cw7), B8 (Cw7), B44 (Cw5), B18, or B57 (Cw6). Thus, these alleles form one complementation group designated NKB1. Another less frequent group, NKB2, was also identified, and consisted of individuals homozygous for B35 (Cw4). NK activity was correlated with the number of circulating NK (CD16+CD56+) cells. Individuals homozygous for the NKB complementation groups have fewer circulating NK cells than individuals heterozygous for these alleles and alleles of other complementation groups, possibly explaining the low activity of cells in these subjects. These findings suggest that during the maturation of NK cells there is NK cellular deletion in donors homozygous for NKB genes resulting in low NK cell numbers and activity. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP DUBEY, DP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [2P30 CA06516]; NIAID NIH HHS [AI-14157, AI-26817] NR 53 TC 23 Z9 23 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1994 VL 179 IS 4 BP 1193 EP 1203 DI 10.1084/jem.179.4.1193 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA NC777 UT WOS:A1994NC77700013 PM 8145038 ER PT J AU KALAMS, SA JOHNSON, RP TROCHA, AK DYNAN, MJ NGO, HS DAQUILA, RT KURNICK, JT WALKER, BD AF KALAMS, SA JOHNSON, RP TROCHA, AK DYNAN, MJ NGO, HS DAQUILA, RT KURNICK, JT WALKER, BD TI LONGITUDINAL ANALYSIS OF T-CELL RECEPTOR (TCR) GENE USAGE BY HUMAN IMMUNODEFICIENCY VIRUS-1 ENVELOPE-SPECIFIC CYTOTOXIC T-LYMPHOCYTE CLONES REVEALS A LIMITED TCR REPERTOIRE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID POLYMERASE CHAIN-REACTION; VARIABLE REGION GENES; CYTO-TOXIC RESPONSES; MYELIN BASIC-PROTEIN; BETA-CHAIN; CHORIOMENINGITIS VIRUS; ANTIGEN RECEPTOR; FINE SPECIFICITY; ALPHA-CHAIN; SEROPOSITIVE INDIVIDUALS AB Human immunodeficiency virus 1 (HIV-1) infection is associated with a vigorous cellular immune response that allows detection of cytotoxic T lymphocyte (CTL) activity using freshly isolated peripheral blood mononuclear cells (PBMC). Although restricting class I antigens and epitopes recognized by HIV-1-specific CTL have been defined, the effector cells mediating this vigorous response have been characterized less well. Specifically, no studies have addressed the breadth and duration of response to a defined epitope. In the present study, a longitudinal analysis of T cell receptor (TCR) gene usage by CTL clones was performed in a seropositive person using TCR gene sequences as a means of tracking responses to a well-defined epitope in the glycoprotein 41 transmembrane protein. 10 CTL clones specific for this human histocompatibility leukocyte antigen-B14-restricted epitope were isolated at multiple time points over a 31-mo period. All clones were derived from a single asymptomatic HIV-1-infected individual with a vigorous response to this epitope that was detectable using unstimulated PBMC. polymerase chain reaction amplification using Valpha and Vbeta family-specific primers was performed on each clone, followed by DNA sequencing of the V-D-J regions. All 10 clones utilized Valpha14 and Vbeta4 genes. Sequence analysis of the TCR-alpha revealed the first nine clones isolated to also be identical at the nucleotide level. The TCR-alpha junctional region sequence of the tenth clone was identical to the junctional region sequences of the other nine, but this clone utilized distinct Dbeta and Jbeta gene segments. This study provides evidence that the observed high degree of HIV-1-specific CTL activity may be due to monoclonal or oligoclonal expansion of specific effector cells, and that progeny of a particular CTL clone may persist for prolonged periods in vivo in the presence of a chronic productive viral infection. The observed limited TCR diversity against an immunodominant epitope may limit recognition of virus variants with mutations in regions interacting with the TCR, thereby facilitating immune escape. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP KALAMS, SA (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,GRAY 5,BOSTON,MA 02114, USA. RI Yang, Chen/G-1379-2010 FU NIAID NIH HHS [AI-30914, AI-28568, AI-33327] NR 69 TC 217 Z9 217 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1994 VL 179 IS 4 BP 1261 EP 1271 DI 10.1084/jem.179.4.1261 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA NC777 UT WOS:A1994NC77700020 PM 8145043 ER PT J AU ZHENG, G BACHINSKY, DR STAMENKOVIC, I STRICKLAND, DK BROWN, D ANDRES, G MCCLUSKEY, RT AF ZHENG, G BACHINSKY, DR STAMENKOVIC, I STRICKLAND, DK BROWN, D ANDRES, G MCCLUSKEY, RT TI ORGAN DISTRIBUTION IN RATS OF 2 MEMBERS OF THE LOW-DENSITY-LIPOPROTEIN RECEPTOR GENE FAMILY, GP330 AND LRP/ALPHA-2MR, AND THE RECEPTOR-ASSOCIATED PROTEIN (RAP) SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article DE GLYCOPROTEIN 330 (GP330); LOW-DENSITY LIPOPROTEIN RECEPTOR-RELATED PROTEIN/ALPHA-2-MACROGLOBULIN RECEPTOR (LRP/ALPHA-2MR); RECEPTOR-ASSOCIATED PROTEIN (RAP); IMMUNOHISTOCHEMISTRY ID BRUSH-BORDER ANTIGENS; HEYMANN NEPHRITIS ANTIGEN; ALPHA-2-MACROGLOBULIN RECEPTOR; MONOCLONAL-ANTIBODIES; LDL-RECEPTOR; ULTRASTRUCTURAL-LOCALIZATION; MEMBRANE GLYCOPROTEIN; CEREBROSPINAL-FLUID; HIGH-AFFINITY; HUMAN-KIDNEY AB We investigated immunohistochemically the distribution in rats of the homologous proteins gp330 and the LDL receptor-related protein (LRP/alpha 2MR), and a receptor-associated protein (RAP), and the sites to which soluble exogenous RAP binds. We found gp330 in a restricted group of epithelial cells, including renal proximal tubule cells, podocytes, Type II pneumocytes, cells of the parathyroid, thyroid, epididymis, lining of the uterus, ependyma, retina, ciliary body, yolk sac, and placenta. In these cells gp330 was detected mainly at the cell surface, except for parathyroid and retinal epithelial cells, where diffuse cell staining was found. LRP/alpha 2MR was widely distributed in interstitial cells, notably in fibroblasts and macrophages, and was also present in a selected group of epithelial or specialized cells, including hepatocytes, adrenal cortical cells, follicular cells of the ovary, cells of the choroid plexus, ciliary body, mesangial cells, and some neurons. In certain cells, notably hepatocytes and adrenal cortical cells, LRP/alpha 2MR was detected mainly on the surface, but in others, including macrophages, fibroblasts, and epithelial cells of the choroid plexus and ciliary body, staining throughout the cell was seen. The only cells that clearly expressed both LRP/alpha 2MR and gp330 were retinal and ciliary epithelial cells. RAP was found in intracellular vesicles in all cells that expressed gp330 or LRP/alpha 2MR. RAP was not definitely detected on the cell surface. Binding sites for RAP were found on the surface of those cells with surface gp330 or LRP, and also throughout the cytoplasm in cells with diffuse cellular LRP/alpha 2MR or gp330. Because of their different locations, we conclude that gp330 and LRP/alpha 2MR serve distinct functions in vivo, despite similarities in ligand-binding properties observed in vitro. Since RAP is found largely within cells, its major physiological function may be concerned with intracellular assembly or trafficking of the receptors to which it binds. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. AMER RED CROSS,BIOCHEM LAB,ROCKVILLE,MD 20855. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA. FU NCI NIH HHS [R01 CA55735-02]; NIDDK NIH HHS [DK36807-23, DK42956] NR 56 TC 276 Z9 282 U1 0 U2 2 PU HISTOCHEMICAL SOC INC PI NEW YORK PA MT SINAI MEDICAL CENTER 19 EAST 98TH ST SUTIE 9G, NEW YORK, NY 10029 SN 0022-1554 J9 J HISTOCHEM CYTOCHEM JI J. Histochem. Cytochem. PD APR PY 1994 VL 42 IS 4 BP 531 EP 542 PG 12 WC Cell Biology SC Cell Biology GA NA326 UT WOS:A1994NA32600011 PM 7510321 ER PT J AU ERNST, CA ZHANG, YJ HANCOCK, PR RUTLEDGE, BJ CORLESS, CL ROLLINS, BJ AF ERNST, CA ZHANG, YJ HANCOCK, PR RUTLEDGE, BJ CORLESS, CL ROLLINS, BJ TI BIOCHEMICAL AND BIOLOGIC CHARACTERIZATION OF MURINE MONOCYTE CHEMOATTRACTANT PROTEIN-1 - IDENTIFICATION OF 2 FUNCTIONAL DOMAINS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SMOOTH-MUSCLE CELLS; ACTIVATING FACTOR; CHEMOTACTIC PROTEIN-1; ENDOTHELIAL-CELLS; CYTOKINE FAMILY; LYMPHOCYTES-T; GROWTH-FACTOR; JE GENE; EXPRESSION; GLYCOPROTEINS AB Monocyte chemoattractant protein-1 (MCP-1) is a member of the chemokine-beta (or C-C) family of cytokines. Murine MCP-1, first identified as the JE gene, differs from human MCP-1 in molecular size and extent of glycosylation. We have used Chinese hamster ovary cells to express recombinant murine MCP-1 and find that its predominant form is a microheterogeneous protein of M(r) approximate to 25,000. Most of MCP-1's microheterogeneity is due to variable amounts of sialic acid that are terminally attached to a constant number of O-linked oligosaccharide chains per molecule. This carbohydrate, along with a small amount of N-linked carbohydrate, accounts for 50% of the apparent molecular size of murine MCP-1 and is not required for in vitro monocyte chemoattractant activity. Mutational analysis shows that most of the carbohydrate is added to a 49-amino acid C-terminal domain that is not present in human MCP-1 and is not required for in vitro biologic activity, suggesting that murine MCP-1 consists of an N-terminal domain containing monocyte chemoattractant activity and a heavily glycosylated C-terminal domain of as yet unknown function. MCP-1 produced in COS cells contains a small amount of Sulfate, but Chinese hamster ovary-produced MCP-1 does not. The absence of sulfate does not alter MCP-1's in vitro chemoattractant properties. In vitro, highly purified murine MCP-1 attracts monocytes, but not neutrophils, with a specific activity similar to human MCP-1 (EC(50) approximate to 0.5 nM). Equilibrium binding experiments with human monocytes reveal the presence of approximate to 3000 binding sites per cell with a K-d of 0.77 nM. In vivo, injection of up to 1 mu g murine MCP-1; in a variety of murine strains induces the appearance of a sparse mixed inflammatory infiltrate. The disparity between MCP-1's in vitro and in vivo effects suggests that other factors may be required to elicit a full-blown monocyte chemotactic response to MCP-1 in vivo. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,BRIGHAMS & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA53091] NR 38 TC 77 Z9 79 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1994 VL 152 IS 7 BP 3541 EP 3549 PG 9 WC Immunology SC Immunology GA NC609 UT WOS:A1994NC60900032 PM 8144933 ER PT J AU REMOLDODONNELL, E PARENT, D AF REMOLDODONNELL, E PARENT, D TI 2 PROTEOLYTIC PATHWAYS FOR DOWN-REGULATION OF THE BARRIER MOLECULE CD43 OF HUMAN NEUTROPHILS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID WISKOTT-ALDRICH SYNDROME; LYMPHOCYTE SURFACE SIALOGLYCOPROTEIN; AMYLOID PRECURSOR PROTEIN; T-CELL ACTIVATION; SIALOPHORIN CD43; MONOCLONAL-ANTIBODY; LEUKOCYTE ADHESION; HUMAN-PLASMA; EXPRESSION; IDENTIFICATION AB CD43, an anionic rod-like mucin molecule on white blood cells, is thought to provide a barrier that prevents interactions of other surface molecules and acts as negative regulator of cell function. As a correlate, CD43 is expected to be altered or down-regulated when blood cells are functionally activated. This study examines CD43 of blood neutrophils before and after treatment with known activating agents. Flow cytometry indicated that PMA and A23187, and to a much lesser extent, FMLP and IL-8, decrease neutrophil expression of CD43. Two separate mechanisms were identified for CD43 down-regulation. Both are proteolytic processes. PMA-induced down- regulation is a rapid process involving proteolysis at a minimum of two sites, one within the N-terminal distal region recognized by mAbs and the other at a membrane-proximal site. The PMA-induced protease, cd43'ase, is characterized by insensitivity to DFP, TLCK, leupeptin, pepstatin, and 1,10 phenanthroline (<5 mM). PMA-induced CD43 down-regulation is extensive but never complete, terminating at similar to 10 min after down-regulating 65 to 85% of molecules, and thereby converting neutrophils from dense to sparse CD43 expression. The second CD43 down-regulation mechanism, although likely a regulated event in vivo, occurred slowly in this study in neutrophils incubated without additives; the process is not affected by PMA, involves the action of a DFP-sensitive protease, releases N-terminal mAb-reactive fragments of 52 kDa or 40 kDa and can be mimicked by exogenous neutrophil elastase. The complexity and apparent tight regulation described here for the two down-regulatory mechanisms are consistent with an important role for CD43 in preventing or dampening cell surface interactions of blood neutrophils. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP REMOLDODONNELL, E (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI29880] NR 42 TC 55 Z9 55 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1994 VL 152 IS 7 BP 3595 EP 3605 PG 11 WC Immunology SC Immunology GA NC609 UT WOS:A1994NC60900038 PM 7511653 ER PT J AU BEISSERT, S GRABBE, S BRUVERS, S GRANSTEIN, RD AF BEISSERT, S GRABBE, S BRUVERS, S GRANSTEIN, RD TI INTERLEUKIN-10 (IL-10) INHIBITS THE FUNCTIONAL MATURATION OF LANGERHANS CELLS (LC) FOR EFFECTIVE PRESENTATION OF TUMOR-ASSOCIATED ANTIGENS (TAA) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 526 EP 526 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600038 ER PT J AU COMPTON, CC NADIRE, K WARLAND, G LANDRY, DB AF COMPTON, CC NADIRE, K WARLAND, G LANDRY, DB TI EPIDERMAL LANGERHANS CELL-POPULATION DENSITIES AND HIV EXPRESSION OVER AN 8-YEAR PERIOD FROM THE TIME OF INFECTION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 543 EP 543 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600142 ER PT J AU GERECKE, D PULKKINEN, L CHRISTIANO, AM BURGESON, RE UITTO, J AF GERECKE, D PULKKINEN, L CHRISTIANO, AM BURGESON, RE UITTO, J TI CLONING OF THE COMPLETE KALININ B1 CDNA (LAMBIK) AND IDENTIFICATION OF A PREMATURE TERMINATION CODON MUTATION IN A PATIENT WITH JUNCTIONAL EPIDERMOLYSIS-BULLOSA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CBRC,BOSTON,MA. JEFFERSON MED COLL,PHILADELPHIA,PA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 544 EP 544 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600146 ER PT J AU ASAHINA, A HOSOI, J GRANSTEIN, RD AF ASAHINA, A HOSOI, J GRANSTEIN, RD TI INHIBITION OF THE INDUCTION OF CONTACT HYPERSENSITIVITY (CHS) BY CALCITONIN-GENE-RELATED PEPTIDE (CGRP) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 546 EP 546 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600157 ER PT J AU AYEHUNIE, S GROVES, RW BRUZZESE, AM KUPPER, TS LANGHOFF, E AF AYEHUNIE, S GROVES, RW BRUZZESE, AM KUPPER, TS LANGHOFF, E TI PRODUCTIVE INFECTION OF T-CELLS BY HIV-1 IS EFFICIENTLY MEDIATED BY LANGERHANS CELLS AND BLOOD DENDRITIC CELLS IN-VITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV DERMATOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 546 EP 546 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600160 ER PT J AU LUCCHINA, LC KOLLIAS, N PHILLIPS, SB MUCCINI, JA FORREST, M STILLER, MJ TRANCIK, RJ DRAKE, LA AF LUCCHINA, LC KOLLIAS, N PHILLIPS, SB MUCCINI, JA FORREST, M STILLER, MJ TRANCIK, RJ DRAKE, LA TI QUANTITATIVE-EVALUATION OF NONINFLAMMATORY ACNE WITH FLUORESCENT PHOTOGRAPHY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA. UPJOHN CO,KALAMAZOO,MI 49001. NR 0 TC 8 Z9 8 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 560 EP 560 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600243 ER PT J AU COHENGOIHMAN, C KOLLIAS, N FORREST, M STILLER, M DRAKE, LA AF COHENGOIHMAN, C KOLLIAS, N FORREST, M STILLER, M DRAKE, LA TI FLUORESCENCE PHOTOGRAPHY (FP) IN THE ASSESSMENT OF HYPERPIGMENTATION OF PHOTODAMAGED SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 568 EP 568 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600289 ER PT J AU YOSHINAGA, IG MIHM, MC BYERS, HR AF YOSHINAGA, IG MIHM, MC BYERS, HR TI ROLE OF EXTRACELLULAR MAGNESIUM AND CALCIUM IN THE ALPHA-2-BETA-1-MEDIATED MELANOMA CELL-MIGRATION ON TYPE-IV COLLAGEN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 573 EP 573 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600320 ER PT J AU KADUNCE, DP JORGENSEN, CM SCHMIDT, LA LI, HL MORGAN, JR PETERSON, MJ KWAN, MK KRUEGER, GG AF KADUNCE, DP JORGENSEN, CM SCHMIDT, LA LI, HL MORGAN, JR PETERSON, MJ KWAN, MK KRUEGER, GG TI AN IN-VIVO ASSESSMENT OF LONG-TERM SURVIVAL OF GENETICALLY-MODIFIED HUMAN FIBROBLASTS CLONED FOR EXPRESSION OF LAC-Z SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV UTAH,CTR HLTH SCI,DIV DERMATOL,SURG SERV,SALT LAKE CITY,UT 84112. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 578 EP 578 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600353 ER PT J AU AKASAKA, T VANLEEUWEN, RL YOSHINAGA, IG MIHM, MC BYERS, HR AF AKASAKA, T VANLEEUWEN, RL YOSHINAGA, IG MIHM, MC BYERS, HR TI EXPRESSION AND DISTRIBUTION OF FOCAL ADHESION KINASE (P125FAK) IN MELANOMA CELL-LINES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 579 EP 579 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600354 ER PT J AU ARBISER, JL VANLEEUWEN, RL FLINT, A BYERS, HR AF ARBISER, JL VANLEEUWEN, RL FLINT, A BYERS, HR TI CYTOTOXICITY OF CLIOQUINOL TOWARDS HUMAN-MELANOMA CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 598 EP 598 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600469 ER PT J AU VANLEEUWEN, RL ARBISER, JL VERMEER, BJ BRUIJN, JA BYERS, HR AF VANLEEUWEN, RL ARBISER, JL VERMEER, BJ BRUIJN, JA BYERS, HR TI CURCUMIN BLOCKS PHORBOL ESTER-INDUCED SPREADING OF HUMAN-MELANOMA CELLS IN-VITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. LEIDEN UNIV,DEPT DERMATOL & PATHOL,LEIDEN,NETHERLANDS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 598 EP 598 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600471 ER PT J AU RIORDAN, AT STILLER, MJ COHEN, L FLOOD, JG PHILLIPS, SB NAIDOO, U DRAKE, LA AF RIORDAN, AT STILLER, MJ COHEN, L FLOOD, JG PHILLIPS, SB NAIDOO, U DRAKE, LA TI PHARMACOKINETIC EVALUATION OF TOPICAL DOXEPIN IN PATIENTS WITH ATOPIC-DERMATITIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 600 EP 600 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600485 ER PT J AU LUCCHINA, LC BUA, DP DOMANKEVITZ, Y SILVER, GM SHERIDAN, RL NISHIOKA, NS AF LUCCHINA, LC BUA, DP DOMANKEVITZ, Y SILVER, GM SHERIDAN, RL NISHIOKA, NS TI HIGH-POWER CO2-LASER ABLATION AND SPLIT-THICKNESS GRAFTING OF BURN WOUNDS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 602 EP 602 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600493 ER PT J AU KOLLIAS, N DRAKE, LA AF KOLLIAS, N DRAKE, LA TI THE SPECTROSCOPIC CHARACTERISTICS OF CUTANEOUS VASCULAR REACTIONS - UVB INDUCED ERYTHEMA, OCCLUSION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PHOTOMED LABS,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 608 EP 608 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600532 ER PT J AU YUNIS, JJ MOBINI, N ALHANDRO, R FOSTER, CS AHMED, AR AF YUNIS, JJ MOBINI, N ALHANDRO, R FOSTER, CS AHMED, AR TI COMPARISON OF MHC CLASS-II GENES IN PATIENTS WITH ORAL PEMPHIGOID ONLY AND OCULAR CICATRICIAL PEMPHIGOID SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02118. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 609 EP 609 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600535 ER PT J AU NISHIYAMA, T MCDONOUGH, AM BRUNS, R BURGESON, RE AF NISHIYAMA, T MCDONOUGH, AM BRUNS, R BURGESON, RE TI CONTRIBUTION OF THE DERMAL-EPIDERMAL INTERACTIONS TO DEPOSITION AND ASSEMBLY OF BASEMENT-MEMBRANE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HARVARD CUTENEOUS BIOL RES CTR,BOSTON,MA. RI Nishiyama, Toshio/C-5434-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 622 EP 622 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600616 ER PT J AU MAYTIN, EV HABENER, JF AF MAYTIN, EV HABENER, JF TI INDUCTION OF EXPRESSION OF THE TRANSCRIPTION FACTORS C/EBP-ALPHA, C/EBP-BETA, AND CHOP-10 DURING CALCIUM-INDUCED DIFFERENTIATION OF BALB/MK KERATINOCYTES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 623 EP 623 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600621 ER PT J AU WOLFE, JT CHOOBACK, L FINN, DT BENOIT, BM JAWORSKY, C ROOK, AH LESSIN, SR AF WOLFE, JT CHOOBACK, L FINN, DT BENOIT, BM JAWORSKY, C ROOK, AH LESSIN, SR TI LARGE-CELL TRANSFORMATION (LCT) IN CUTANEOUS T-CELL LYMPHOMA (CTCL) - DEMONSTRATION OF A SINGLE NEOPLASTIC T-CELL CLONE EXPRESSING THE IDENTICAL T-CELL RECEPTOR (TCA) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV PENN,DEPT DERMATOL,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 623 EP 623 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600623 ER PT J AU KONDO, S KONO, T PASTORE, S MAK, TW BEISSERT, S GRANSTEIN, R SAUDER, DN AF KONDO, S KONO, T PASTORE, S MAK, TW BEISSERT, S GRANSTEIN, R SAUDER, DN TI CD4 AND CD8 REQUIRED FOR OPTIMAL SENSITIZATION AND ELICITATION OF ALLERGIC CONTACT-DERMATITIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV TORONTO,DIV DERMATOL,TORONTO,ON,CANADA. UNIV TORONTO,DEPT BIOPHYS,TORONTO,ON,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 629 EP 629 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600654 ER PT J AU KIM, JJ MODLIN, RL MOU, RL DUBINETT, S TOMONO, S UYEMURA, K AF KIM, JJ MODLIN, RL MOU, RL DUBINETT, S TOMONO, S UYEMURA, K TI IL-10 PRODUCTION BY BASAL-CELL CARCINOMA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,DIV DERMATOL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 633 EP 633 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600678 ER PT J AU HIBINO, T TAKAHASHI, T LEUTHARDT, D GOETINCK, PF AF HIBINO, T TAKAHASHI, T LEUTHARDT, D GOETINCK, PF TI INVOLVEMENT OF UROKINASE PLASMINOGEN-ACTIVATOR (UPA) IN KERATINOCYTE PROLIFERATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. SHISEIDO RES CTR,YOKOHAMA,KANAGAWA,JAPAN. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 641 EP 641 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600730 ER PT J AU LIN, GC KOLLIAS, N GILLIES, R ANDERSSON, RR DOUKAS, AG AF LIN, GC KOLLIAS, N GILLIES, R ANDERSSON, RR DOUKAS, AG TI ACTION SPECTRUM OF IMMEDIATE CHANGES IN THE TRYPTOPHAN FLUORESCENCE OF HUMAN SKIN UPON UV IRRADIATION IN-VIVO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 651 EP 651 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600787 ER PT J AU BILSLAND, CAG SPRINGER, TA AF BILSLAND, CAG SPRINGER, TA TI CLONING AND EXPRESSION OF THE CHICKEN CD18 CDNA SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE LFA-1; CHICKEN CD18 CDNA; LEUKOCYTE INTEGRINS ID LEUKOCYTE ADHESION DEFICIENCY; MACROPHAGE DIFFERENTIATION ANTIGEN; CELL-SURFACE EXPRESSION; INTEGRIN BETA-SUBUNIT; CYTOPLASMIC DOMAIN; COUNTER-RECEPTOR; MONOCLONAL-ANTIBODIES; P150,95 GLYCOPROTEINS; MOLECULE ICAM-1; IMMUNE-SYSTEM AB The leukocyte integrins play a critical role in a number of cellular adhesive interactions during the immune response. We describe here the isolation and characterization of the chicken beta 2 (CD18) subunit, common to the leukocyte integrin family. The deduced 748-amino-acid sequence reveals a transmembrane protein with 65% and 64% identity with its human and murine homologues, respectively. The chicken beta 2 can associate on the cell surface with the human alpha subunit of LFA-1 and yields a hybrid molecule capable of binding to purified ICAM-1 and ICAM-3. C1 HARVARD UNIV,CTR BLOOD RES,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA. FU NCI NIH HHS [CA31798] NR 43 TC 13 Z9 13 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 APR PY 1994 VL 55 IS 4 BP 501 EP 506 PG 6 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA NE677 UT WOS:A1994NE67700012 PM 7908319 ER PT J AU SCHAFER, U HARHAMMER, R BOOMGAARDEN, M SOHR, R OTT, T HENKLEIN, P REPKE, H AF SCHAFER, U HARHAMMER, R BOOMGAARDEN, M SOHR, R OTT, T HENKLEIN, P REPKE, H TI BINDING OF CHOLECYSTOKININ-8 (CCK-8) PEPTIDE DERIVATIVES TO CCK(A) AND CCK(B) RECEPTORS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE CHOLECYSTOKININ; CHOLECYSTOKININ-8 DERIVATIVES; CHOLECYSTOKININ RECEPTORS; RADIOLIGAND BINDING; RAT PANCREAS; GUINEA PIG CORTEX ID BIOLOGICAL-ACTIVITY; ANTAGONISTS; BRAIN; ANALOGS; POTENT; OCTAPEPTIDE; MEMBRANES; MK-329; SITES AB The structural requirements for the selective binding of cholecystokinin-8 (CCK-8)-related peptides to peripheral (CCK(A)) receptors are not sufficiently understood. In this study, the interaction of a series of newly shortened analogues of CCK-8 with both receptor subtypes was analyzed by displacement studies using [H-3]-CCK-8 and I-125-Bolton-Hunter (BH)-CCK-8 as radioligands. The pentapeptide derivative of CCK-8, succinyl-Tyr (SO3H)-Met-Gly-Trp-Met-phenethylamide, was found to bind selectively with high affinity to the CCK(A) receptor. The replacement of Met28 and/or Met31 by norleucine and of L-Trp30) by its D-analogue had no significant effect on the binding properties of the peptide. Further C-terminal shortening resulted in a drastic loss of affinity and selectivity of the CCK receptor binding. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP SCHAFER, U (reprint author), HUMBOLDT UNIV BERLIN,FAC MED CHARITE,INST PHARMACOL & TOXICOL,PF 140,D-10098 BERLIN,GERMANY. NR 29 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD APR PY 1994 VL 62 IS 4 BP 1426 EP 1431 PG 6 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NB403 UT WOS:A1994NB40300024 PM 8133271 ER PT J AU GABRIEL, SM BIERER, LM DAVIDSON, M PUROHIT, DP PERL, DP HAROTUNIAN, V AF GABRIEL, SM BIERER, LM DAVIDSON, M PUROHIT, DP PERL, DP HAROTUNIAN, V TI GALANIN-LIKE IMMUNOREACTIVITY IS INCREASED IN THE POSTMORTEM CEREBRAL-CORTEX FROM PATIENTS WITH ALZHEIMERS-DISEASE SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE ALZHEIMERS DISEASE; GALANIN; DEMENTIA; NEUROPEPTIDES; NEURODEGENERATION ID CENTRAL-NERVOUS-SYSTEM; NITRIC-OXIDE SYNTHASE; NEURONAL NADPH DIAPHORASE; BASAL FOREBRAIN COMPLEX; ACETYLCHOLINE-RELEASE; CHOLINERGIC NEURONS; NEUROPEPTIDE-Y; SPINAL-CORD; PHOSPHOINOSITIDE TURNOVER; HUNTINGTONS-DISEASE AB Galanin is a peptide that is associated with cholinergic neurons of the basal forebrain and, thus, of interest for the neuropathology of Alzheimer's disease. In the present study, human galanin-like immunoreactivity was measured in postmortem human cerebral cortical tissues by using a homologous radioimmunoassay. In an initial study, six cerebral cortical regions were evaluated from nine elderly controls, 13 neuropathologically verified Alzheimer's disease patients, and 19 elderly schizophrenics. A significant 65% increase in galanin was found in frontal cortex Brodmann area 8 of Alzheimer's disease patients compared with controls. In contrast, cerebral cortical tissues from elderly schizophrenics were not different from those from elderly controls in any region. In a second study, 10 cerebral cortical regions were evaluated from 50 neuropathologically verified Alzheimer's disease patients and nine elderly controls. Concentrations of galanin were increased significantly 26-61% in six of 10 cerebral cortical regions examined (Brodmann areas F8, F44, T20, T21, T36, and P22). Purification of brain extracts by size-exclusion Sephadex G-50 chromatography revealed that human galanin-like immunoreactivity eluted in two peaks of different molecular weights. These studies reveal increased concentrations of galanin in the cerebral cortex of Alzheimer's disease, similar to previous findings in basal forebrain tissue. Because galanin inhibits cholinergic neurotransmission, these findings may have important implications in the understanding of Alzheimer's disease neuropathology and associated cognitive deficits. RP GABRIEL, SM (reprint author), BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIA NIH HHS [NIA AG02219, NIA AG05138, NIA AG00408] NR 57 TC 52 Z9 52 U1 0 U2 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD APR PY 1994 VL 62 IS 4 BP 1516 EP 1523 PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NB403 UT WOS:A1994NB40300036 PM 7510783 ER PT J AU KANG, I LINDQUIST, DG KINANE, TB ERCOLANI, L PRITCHARD, GA MILLER, LG AF KANG, I LINDQUIST, DG KINANE, TB ERCOLANI, L PRITCHARD, GA MILLER, LG TI ISOLATION AND CHARACTERIZATION OF THE PROMOTER OF THE HUMAN GABA(A) RECEPTOR ALPHA-1-SUBUNIT GENE SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE GABA(A) ALPHA-1 SUBUNIT; PROMOTER; BENZODIAZEPINE ID SUBUNIT MESSENGER-RNAS; DOWN-REGULATION; A RECEPTOR; RAT-BRAIN; CELLS AB The GABA(A) receptor, as assessed by ligand binding and chloride flux measurement in vivo and in vitro, is down-regulated in response to chronic benzodiazepine exposure. The mRNA levels of the alpha1 and gamma2 subunits of the receptor are also reduced. We have isolated the promoter of the gene encoding the alpha1 subunit of the GABA(A) receptor to elucidate the regulatory mechanism of its expression. A DNA segment 650 bp long has been isolated that includes 151 bp of untranslated 5' end of the cDNA sequence and 500 bp of potential promoter-enhancer region. The transcriptional activity of this DNA segment linked to the firefly luciferase gene showed a strong orientation specificity. The promoter activity was localized to a 60-bp segment by deletion mapping. Mobility shift binding assay results suggest that this segment may interact with one or more factors in HeLa cell nuclear extracts to form a transcriptional complex. Primary cultures of embryonic chick cortical cells transfected with the promoter-luciferase construct were treated chronically with lorazepam. Transcriptional activity of this promoter construct was strongly repressed by chronic administration of lorazepam. C1 MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02114 USA. RP KANG, I (reprint author), TUFTS UNIV, SCH MED, DEPT PHARMACOL & EXPTL THERAPEUT, 136 HARRISON AVE, BOSTON, MA 02111 USA. FU NIDA NIH HHS [DA-05258]; NIMH NIH HHS [MH-47598] NR 24 TC 31 Z9 31 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD APR PY 1994 VL 62 IS 4 BP 1643 EP 1646 PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NB403 UT WOS:A1994NB40300052 PM 8133292 ER PT J AU STRITTMATTER, SM FISHMAN, MC ZHU, XP AF STRITTMATTER, SM FISHMAN, MC ZHU, XP TI ACTIVATED MUTANTS OF THE ALPHA-SUBUNIT OF G(0) PROMOTE AN INCREASED NUMBER OF NEURITES PER CELL SO JOURNAL OF NEUROSCIENCE LA English DT Article DE GTP-BINDING PROTEINS; NEURONAL GROWTH CONE; G(0) NEURITE OUTGROWTH; SIGNAL TRANSDUCTION; ONCOGENIC MUTATIONS; AXONAL GROWTH; PC12 CELLS; NEUROBLASTOMA CELLS ID NEURONAL GROWTH CONE; NEUROBLASTOMA-CELLS; ADENYLYL CYCLASE; G-PROTEINS; GAP-43; MUTATIONS; STIMULATION; MORPHOLOGY; RETRACTION; RECEPTORS AB The high concentration of the GTP-binding protein G(o) in the neuronal growth cone suggests that G(o) activation state may alter neurite outgrowth. We find that activation of pertussis toxin-sensitive G-proteins by mastoparan increases neurite outgrowth from neuroblastoma cells. To examine G(o) activation specifically, point mutations homologous to activating, oncogenic mutations in alpha a(i2) and alpha(s) were introduced into the alpha subunit of G(o). The stability of the alpha(o), mutants to tryptic digestion confirms that they are activated. When expressed in PC12 or N1E-115 cells, activated alpha(o), doubles total neurite length per cell, primarily by increasing the number of neurites per cell. The growth cones of cells expressing activated alpha(o) are narrower than control growth cones. Expression of wild-type alpha(o) or the activated alpha subunits of other G-proteins did not affect total neurite length per cell. Thus, factors that lead to activation of G(o) can modulate neurite number per cell. C1 MASSACHUSETTS GEN HOSP,DEPT BIOL LAB,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02129. OI Strittmatter, Stephen/0000-0001-8188-3092 NR 46 TC 77 Z9 77 U1 0 U2 0 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1994 VL 14 IS 4 BP 2327 EP 2338 PG 12 WC Neurosciences SC Neurosciences & Neurology GA NF026 UT WOS:A1994NF02600038 PM 8158271 ER PT J AU DESALLES, AAF MANCHOLA, I AF DESALLES, AAF MANCHOLA, I TI CO2 REACTIVITY IN ARTERIOVENOUS-MALFORMATIONS OF THE BRAIN - A TRANSCRANIAL DOPPLER ULTRASOUND STUDY SO JOURNAL OF NEUROSURGERY LA English DT Article DE ULTRASOUND; ANGIOGRAPHY; ARTERIOVENOUS MALFORMATION; BLOOD FLOW VELOCITY; HYPOCAPNIA ID MIDDLE CEREBRAL-ARTERY; BLOOD-FLOW VELOCITY; PRESSURE; CIRCULATION; VALIDATION; EXCISION; AVMS AB Arteriovenous malformations (AVM's) are congenital tangles of vessels that have a high blood flow through a low-resistance nidus. The vessels in the nidus may lack normal vasoreactivity in response to changes in PaCO2 or perfusion pressure (autoregulation). Arteriovenous malformation hemodynamics have been assessed based on the response of AVM feeding arteries to hypocapnia. Twenty-five AVM patients, aged 34 +/- 11 years (mean +/- standard deviation), were admitted to the Massachusetts General Hospital for proton-beam radiation therapy. Fourteen healthy volunteers aged 30 +/- 7 years served as control subjects. Angiograms with calibrated markers permitting magnification correction were available for all patients. The limits of the middle cerebral artery, as determined by transcranial Doppler ultrasonography, were compared to measurements made on the angiograms. Hyperventilation was induced at a rate set by a metronome. Fixed bilateral Doppler probes allowed almost simultaneous sampling of two vessels. Volunteer control subjects were hyperventilated in two steps. The two PaCO2 step decreases were significant (mean resting PaCO2 40.6 +/- 3.5 mm Hg, Step 1 level 29.4 +/- 3.5 mm Hg and Step 2 level 23.8 +/- 3.5 mm Hg; p < 0.01). These decreases induced a significant decrease in mean now velocity (V-m) and an increase in the pulsatility index (p < 0.001). Mean carbon dioxide reactivity (%Delta V-m/Delta PaCO2) was 2.74 +/- 1.0 for Step 1 and 1.44 +/- 1.8 for Step 2 (p < 0.003). The mean PaCO2 decrease in patients was from 39.5 +/- 4.0 mm Hg to 27.0 +/- 3.5 mm Hg. Carbon dioxide reactivity was 0.92 +/- 1.12 for feeding vessels and 2.59 +/- 1.78 for nonfeeding vessels (p < 0.001). Transcranial Doppler ultrasound and angiographic depth measurements correlated well. Hyperventilation induced significantly more hemodynamic changes in control and nonfeeding middle cerebral arteries than in feeding vessels. Impaired CO2 reactivity may help to identify AVM feeding vessels as well as the relative magnitude of the flow provided to the malformation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA. RP DESALLES, AAF (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DIV NEUROSURG,300 UCLA MED PLAZA,SUITE B-212,LOS ANGELES,CA 90024, USA. NR 30 TC 29 Z9 29 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD APR PY 1994 VL 80 IS 4 BP 624 EP 630 DI 10.3171/jns.1994.80.4.0624 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA NC826 UT WOS:A1994NC82600004 PM 7908692 ER PT J AU KABAN, LB AF KABAN, LB TI EFFECT OF FREEZE-DRIED POLY-L-LACTIC ACID DISKS MIXED WITH BONE MORPHOGENETIC PROTEIN ON THE HEALING OF RAT SKULL DEFECTS - DISCUSSION SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY LA English DT Discussion RP KABAN, LB (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 6 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 0278-2391 J9 J ORAL MAXIL SURG JI J. Oral Maxillofac. Surg. PD APR PY 1994 VL 52 IS 4 BP 392 EP 392 DI 10.1016/0278-2391(94)90444-8 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ND819 UT WOS:A1994ND81900012 ER PT J AU KNIBBE, MA LEWIS, ES ROBINSON, ML KELLY, JP AF KNIBBE, MA LEWIS, ES ROBINSON, ML KELLY, JP TI SUBMUCOSAL NODULE OF THE LOWER LIP ASSOCIATED WITH PIGMENTED NECK MACULES SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY LA English DT Article C1 UNIV CINCINNATI,MED CTR,DIV ORAL & MAXILLOFACIAL SURG,CINCINNATI,OH 45267. HARVARD UNIV,SCH DENT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 6 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 0278-2391 J9 J ORAL MAXIL SURG JI J. Oral Maxillofac. Surg. PD APR PY 1994 VL 52 IS 4 BP 402 EP 405 DI 10.1016/0278-2391(94)90449-9 PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ND819 UT WOS:A1994ND81900017 PM 8133374 ER PT J AU JACOX, AK CARR, DB PAYNE, R AF JACOX, AK CARR, DB PAYNE, R TI POLICY ISSUES RELATED TO CLINICAL-PRACTICE GUIDELINES - PREFACE SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,DIV PAIN MANAGEMENT,BOSTON,MA 02114. MD ANDERSON CANC CTR,PAIN & SYMPTOM MANAGEMENT SECT,HOUSTON,TX. RP JACOX, AK (reprint author), JOHNS HOPKINS UNIV,BALTIMORE,MD 21218, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0885-3924 J9 J PAIN SYMPTOM MANAG JI J. Pain Symptom Manage. PD APR PY 1994 VL 9 IS 3 BP 143 EP 145 DI 10.1016/0885-3924(94)90122-8 PG 3 WC Health Care Sciences & Services; Medicine, General & Internal; Clinical Neurology SC Health Care Sciences & Services; General & Internal Medicine; Neurosciences & Neurology GA NH272 UT WOS:A1994NH27200001 PM 7516954 ER PT J AU BUDIMANMAK, E ROACH, KE STUCK, R SPENCER, F POLIZOS, T CONRAD, KJ AF BUDIMANMAK, E ROACH, KE STUCK, R SPENCER, F POLIZOS, T CONRAD, KJ TI RADIOGRAPHIC MEASUREMENT OF HALLUX-VALGUS IN THE RHEUMATOID ARTHRITIC FOOT SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE RADIOGRAPHS; HALLUX VALGUS ID OBSERVER AB Objective. To develop a method which is objective and quantifiable, as well as reliable and valid for measuring the severity and progression of hallux valgus deformity (HVD). HVD is defined as an increase in the hallux abductus angle (HAA). Methods. HAA drawn on plain anterioposterior radiographs of the foot was measured in 94 patients with rheumatoid arthritis. The intra and interrater reliability were analyzed. Results. Findings were significant with interclass correlation coefficients ranging from 0.9 to 0.99. Detection of changes in HAA using this method were comparable to the judgment of a panel of experienced clinicians. Conclusion. This method is useful in detecting progression of HVD. C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,MIDWEST HLTH SERV RES & DEV,HINES,IL 60141. US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,MIDWEST HLTH SERV RES & DEV,FIELD PROGRAM,HINES,IL 60141. RP BUDIMANMAK, E (reprint author), US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,MIDWEST HLTH SERV RES & DEV,HINES,IL 60141, USA. NR 13 TC 5 Z9 5 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD APR PY 1994 VL 21 IS 4 BP 623 EP 626 PG 4 WC Rheumatology SC Rheumatology GA NG016 UT WOS:A1994NG01600008 PM 8035383 ER PT J AU BLACKBURN, WD BERNREUTER, WK ROMINGER, M LOOSE, LL AF BLACKBURN, WD BERNREUTER, WK ROMINGER, M LOOSE, LL TI ARTHROSCOPIC EVALUATION OF KNEE ARTICULAR-CARTILAGE - A COMPARISON WITH PLAIN RADIOGRAPHS AND MAGNETIC-RESONANCE-IMAGING SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE ARTHROSCOPY; MAGNETIC RESONANCE IMAGING; OSTEOARTHRITIS ID OSTEO-ARTHRITIS; HYALINE CARTILAGE; MR; OSTEOARTHRITIS; JOINT; DEGENERATION; SEVERITY; DEFECTS AB Objective. To compare radiographic, magnetic resonance imaging (MRT), and outpatient direct arthroscopic evaluation of cartilage in patients with osteoarthritis (OA) of the knee. Methods. Thirty-three patients with OA of the knee were evaluated by plain weight bearing radiographs and arthroscopy using a 1.9 mm arthroscope under local anesthesia. Sixteen of these patients also had MRI of the knee performed. Knee compartments were evaluated using AP weight bearing and lateral radiographs of the knee. MRI and outpatient arthroscopic grading of cartilage were performed within 2 weeks of the plain radiographs. The MRI and arthroscopic evaluations were performed independently and were graded without knowledge of the other. Results. In patients in whom plain radiographs, MRI, and arthroscopy were compared, the plain radiographs and MRI significantly underestimated the extent of cartilage abnormalities. There was a moderate correlation between imaged cartilage scores and the arthroscopy scores (Pearson correlation coefficient = 0.40). The arthroscopic scores were reproducible with good intra and interobserver reliability. The arthroscopic procedure was well tolerated and actually preferred over the MRI by the majority of patients. No significant complications were noted as a result of arthroscopy. Conclusions. Our results indicate that outpatient arthroscopic evaluation is a useful method in evaluating surface cartilage abnormalities and is more sensitive in detecting these abnormalities than either plain radiographs or MRI. Outpatient arthroscopic evaluation of cartilage appears to be a safe, sensitive, and a well tolerated tool for evaluating patients with OA of the knee and may prove to be particularly useful in evaluating response to therapeutic interventions. C1 UNIV ALABAMA,DEPT RADIOL,BIRMINGHAM,AL. UNIV ALABAMA,DIV CLIN IMMUNOL & RHEUMATOL,BIRMINGHAM,AL. PFIZER INC,DIV CENT RES,GROTON,CT 06340. RP BLACKBURN, WD (reprint author), BIRMINGHAM VET AFFAIRS MED CTR,RES SERV 151F,700 19TH ST S,BIRMINGHAM,AL 35233, USA. NR 25 TC 78 Z9 80 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD APR PY 1994 VL 21 IS 4 BP 675 EP 679 PG 5 WC Rheumatology SC Rheumatology GA NG016 UT WOS:A1994NG01600019 PM 8035392 ER PT J AU MORENO, PR JANG, IK NEWELL, JB BLOCK, PC PALACIOS, IF AF MORENO, PR JANG, IK NEWELL, JB BLOCK, PC PALACIOS, IF TI THE ROLE OF PERCUTANEOUS AORTIC BALLOON VALVULOPLASTY IN PATIENTS WITH CARDIOGENIC-SHOCK AND CRITICAL AORTIC-STENOSIS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID VALVE-REPLACEMENT; HEART-FAILURE; RESISTANCE; DETERMINANTS; IMPROVEMENT AB Objectives. The goal of this study was to evaluate the role of percutaneous aortic valvuloplasty in patients with cardiogenic shock due to severe aortic stenosis and associated major comorbid conditions and to establish predictors of survival. Background. The prognosis for patients in cardiogenic shock with severe aortic stenosis is poor. Aortic valve replacement can be lifesaving, but the presence of multiorgan failure precludes these patients from operation. Percutaneous aortic balloon valvuloplasty has been used in these patients with short-term improve ment and could be an alternative therapeutic option. Methods. Of 310 patients undergoing percutaneous aortic balloon valvuloplasty, 21 were in cardiogenic shock and were included in this study. All 21 patients had associated major comorbid conditions at the time of presentation. Results. After percutaneous aortic balloon valvuloplasty, systolic aortic pressure increased from 77 +/- 3 (mean +/- SEM) to 116 +/- 8 mm Hg (p = 0.0001); aortic valve area increased from 0.48 +/- 0.04 to 0.84 +/- 0.06 cm(2) (p = 0.0001); and cardiac index increased from 1.84 +/- 0.13 to 2.24 +/- 0.15 liters/min per m(2) (p = 0.06). Nine patients died in the hospital, two during the procedure and seven after successful percutaneous aortic balloon valvuloplasty (five from multiorgan failure). Five patients had vascular complications. Stroke, cholesterol emboli and aortic regurgitation requiring aortic valve replacement occurred in one patient each. Twelve patients (57%) survived and were followed up for 15 +/- 6 months; five patients subsequently died. The Kaplan-Meier survival curve showed a 38 +/- 11% survival rate at 27 months. The only predictor for longer survival rate was the postprocedure cardiac index. Conclusions. 1) Emergency percutaneous aortic balloon valvuloplasty can be performed successfully as a lifesaving procedure. 2) Morbidity and mortality remain high despite successful percutaneous aortic balloon valvuloplasty. 3) For nonsurgical candidates, percutaneous aortic balloon valvuloplasty may be the only therapeutic alternative. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 22 TC 47 Z9 47 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1994 VL 23 IS 5 BP 1071 EP 1075 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PH371 UT WOS:A1994PH37100012 PM 8144770 ER PT J AU EAGLE, KA RIHAL, CS FOSTER, ED MICKEL, MC GERSH, BJ AF EAGLE, KA RIHAL, CS FOSTER, ED MICKEL, MC GERSH, BJ TI LONG-TERM SURVIVAL IN PATIENTS WITH CORONARY-ARTERY DISEASE - IMPORTANCE OF PERIPHERAL VASCULAR-DISEASE SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID INTERMITTENT CLAUDICATION; FRAMINGHAM; MORTALITY AB Objectives. The purpose of this study was to determine the importance of peripheral arterial disease in predicting longterm survival in patients with clinically evident coronary artery disease. Background. Patients in the Coronary Artery Surgery Study (CASS) Registry were followed up for >10 Sears. Methods. Survival in 2,296 patients with peripheral arterial disease was compared with that of 13,953 patients without peripheral arterial disease using Kaplan-Meier survival curves. All patients had known stable coronary artery disease. Clinical, electrocardiographic (ECG), chest X-ray film and catheterization variables of the two groups were compared using the chi-square statistic or the two-sample t test. The independent effect of peripheral arterial disease (as well as other variables) on mortality was determined utilizing a Cox proportional hazards model. Results. Patients with peripheral vascular disease were more Likely to have hypertension, diabetes, family history of coronary artery disease, previous angina or myocardial infarction, previous coronary bypass surgery or to have smoked, They also had a higher incidence of congestive heart failure, ECG abnormality and modestly increased frequency of three-vessel disease. Independent correlates of long term mortality for the entire cohort included age, smoking, diabetes, number of diseased coronary vessels, left ventricular function, hypertension, pulmonary disease, anginal class, previous myocardial infarction and peripheral vascular disease (all p < 0.001). At any point in time, patients with peripheral vascular disease had a 25% greater likelihood of mortality than patients without peripheral vascular disease (multivariate chi-square 25.83, hazard ratio 1.25, 9.5% confidence interval 1.15 to 1.36, p < 0.0001). Conclusions. Peripheral vascular disease is a strong, independent predictor of long term mortality in patients with stable coronary artery disease. Aggressive attempts at secondary disease prevention are warranted in this high risk group. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. UNIV WASHINGTON,CASS,CTR COORDINATING,SEATTLE,WA 98195. RP EAGLE, KA (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,CARDIAC UNIT,SUITE 469,15 PARKMAN ST,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [5-R01-HL38941] NR 10 TC 138 Z9 140 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1994 VL 23 IS 5 BP 1091 EP 1095 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PH371 UT WOS:A1994PH37100016 PM 8144774 ER PT J AU HENDRICKS, KM WILLIAMS, E STOKER, TW SCHOENFELD, DA WALKER, WA KLEINMAN, RE AF HENDRICKS, KM WILLIAMS, E STOKER, TW SCHOENFELD, DA WALKER, WA KLEINMAN, RE TI DIETARY-INTAKE OF ADOLESCENTS WITH CROHNS-DISEASE SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Note ID INFLAMMATORY BOWEL-DISEASE; GROWTH FAILURE; CHILDREN; METABOLISM; DRUG; ZINC; IRON C1 BOSTON UNIV,SARGENT COLL ALLIED HLTH PROFESS,DIV NUTR,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,GEN CLIN RES CTR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR BIOSTAT,BOSTON,MA 02114. RP HENDRICKS, KM (reprint author), HARVARD UNIV,SCH MED,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02115, USA. NR 28 TC 7 Z9 7 U1 0 U2 1 PU AMER DIETETIC ASSN PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD APR PY 1994 VL 94 IS 4 BP 441 EP 444 DI 10.1016/0002-8223(94)90102-3 PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA NE705 UT WOS:A1994NE70500016 PM 8144814 ER PT J AU MULROW, CD GERETY, MB CORNELL, JE LAWRENCE, VA KANTEN, DN AF MULROW, CD GERETY, MB CORNELL, JE LAWRENCE, VA KANTEN, DN TI THE RELATIONSHIP BETWEEN DISEASE AND FUNCTION AND PERCEIVED HEALTH IN VERY FRAIL ELDERS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article; Proceedings Paper CT Southern-Section of the Society-of-General-Internal-Medicine Meeting CY JAN, 1993 CL NEW ORLEANS, LA SP SOC GEN INTERNAL MED, SO SECT ID PRIMARY CARE PATIENTS; COMORBIDITY; VALIDATION; OUTCOMES; SEVERITY; IMPACT; INDEX AB Objective: To study associations between disease and observed function and self-perceived health in very frail elders. Design and Setting: Cross-sectional survey of nine nursing homes in San Antonio, TX. Participants: 194 elderly long-stay nursing home residents dependent in at least two ADLs and without severe cognitive impairment. Measures: Burden of disease (BOD) was chart abstracted using a standardized protocol that assessed types and severities of 59 categorizations of chronic and acute medical conditions. Observed function and self-perceived health status were assessed independently by the Katz Activities of Daily Living scale (ADL) and the Sickness Impact Profile (SIP), respectively. Results: Summary BOD scores had a low, but statistically significant, univariate correlation with ADL scores (r = 0.21, P = 0.003) and no significant correlation with SIP scores (R = -0.008). Multiple linear regression analyses, including the 24 most frequent disease categories, showed that disease explained significant amounts of ADL (r2 = 0.25, P = 0.001) and borderline significant amounts of SIP (r2 = 0.16, P = 0.11). Models including both disease and sociodemographic, cognitive, and affective variables showed disease added significant incremental explanation beyond the other factors to ADL (incremental r2 = 0.14, P = 0.04), but not to SIP (incremental r2 = 0.08, P > 0.10). Conclusions: Disease, observed function, and self-perceived health status are separate, but interrelated entities, with disease having a stronger relationship to observed function than self-perceived health. Comprehensive assessment of frail elders may need to include all three areas, and studies that focus on one area should take into account the other two as potential important covariates. C1 UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. RP MULROW, CD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,GERIATR RES EDUC & CLIN CTR,AMBULATORY CARE 11C,SAN ANTONIO,TX 78284, USA. FU NIA NIH HHS [NIA UO1AG09117-01] NR 35 TC 57 Z9 60 U1 1 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 1994 VL 42 IS 4 BP 374 EP 380 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA NE417 UT WOS:A1994NE41700003 PM 8144821 ER PT J AU BROWN, D STOW, JL AF BROWN, D STOW, JL TI MOVING THINGS AROUND - THE STRUCTURAL BASIS OF INTRACELLULAR PROTEIN TRAFFICKING - NOVEMBER 17-20, 1993 CHATHAM-BARS-INN, CHATHAM, MA SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP BROWN, D (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114, USA. 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 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD APR PY 1994 VL 4 IS 10 BP 1827 EP 1831 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA NJ332 UT WOS:A1994NJ33200012 ER PT J AU MISRA, AK MISHRA, SK EIGEN, AC TOURTELLOTTE, WW AF MISRA, AK MISHRA, SK EIGEN, AC TOURTELLOTTE, WW TI SUCCESSFUL IMMUNOSUPPRESSIVE THERAPY FOR HTLV-I-ASSOCIATED MYELOPATHY SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article DE HTLV-I ASSOCIATED MYELOPATHY (HAM); IMMUNOSUPPRESSION; CYCLOPHOSPHAMIDE; PREDNISONE ID VIRUS TYPE-I AB We report here a patient with HTLV-I associated myelopathy (HAM), who showed remarkable improvement clinically and immunologically with combined cyclophosphamide and prednisone therapy. C1 DEPT VET AFFAIRS OUTPATIENT CLIN,SCH MED,NEUROL SERV 752-127,351 E TEMPLE ST,LOS ANGELES,CA 90012. W LOS ANGELES DEPT VET AFFAIRS MED CTR,NEUROL SERV,LOS ANGELES,CA. UNIV SO CALIF,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90033. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. NR 7 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD APR PY 1994 VL 122 IS 2 BP 155 EP 156 DI 10.1016/0022-510X(94)90293-3 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA ND187 UT WOS:A1994ND18700006 PM 8021699 ER PT J AU WATKINS, KT DUDRICK, PS COPELAND, EM SOUBA, WW AF WATKINS, KT DUDRICK, PS COPELAND, EM SOUBA, WW TI INTERLEUKIN-6 AND DEXAMETHASONE WORK COORDINATELY TO AUGMENT HEPATIC AMINO-ACID-TRANSPORT SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Article; Proceedings Paper CT 53rd Annual Session of the American-Association-for-the-Surgery-of-Trauma CY SEP 23-25, 1993 CL NEW ORLEANS, LA SP AMER ASSOC SURG TRAUMA ID TUMOR-NECROSIS-FACTOR; PLASMA-MEMBRANE VESICLES; RAT HEPATOCYTES; ARGININE TRANSPORT; GENE-EXPRESSION; METABOLISM; GLUTAMINE; LIVER; CELLS; STIMULATE AB The in vivo effects of interleukin-6 (IL-6) and dexamethasone (Dex) on amino acid transport in rat liver were studied employing hepatic plasma membrane vesicles (HPMVs). Adult rats were treated with Dex (0.5 mg/kg) and subsequently with varying concentrations if IL-6 (10, 50, or 150 mu g/kg). The HPMVs were prepared by Percoll density gradient centrifugation. The activities of System A, System N, and System y(+) transport proteins were evaluated by tritiated uptake of their respective amino acids (methyl-aminoisobutyric acid [MeAIB], glutamine, and arginine). System A activity was increased in response to low doses of IL-6. Dex alone increased System A and had an additive effect to enhance transport in response to IL-6. System N was stimulated by higher doses of IL-6 in a dose-dependent manner. Dexamethasone had no effect by itself on System N activity but worked synergistically to enhance the effect of IL-6 even at low doses. System y(+) activity was increased by Dex but IL-6 did not alter arginine transport. Kinetic analysis of the increases in System A and N showed the increases to be related to an increase in the V-max (maximal transport velocity) for the carrier with no significant change in K-m, carrier affinity. We conclude that IL-6 and glucocorticoids work in a coordinated fashion to enhance hepatic amino acid uptake. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02114. UNIV FLORIDA,COLL MED,DEPT SURG,SURG METAB & NUTR LAB,GAINESVILLE,FL. HARVARD UNIV,SCH MED,BOSTON,MA. FU NCI NIH HHS [CA 45327, T32-CA09605-03] NR 27 TC 17 Z9 17 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 Infect. Crit. Care PD APR PY 1994 VL 36 IS 4 BP 523 EP 528 DI 10.1097/00005373-199404000-00011 PG 6 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA NG222 UT WOS:A1994NG22200011 PM 8158714 ER PT J AU DRETLER, SP AF DRETLER, SP TI URETEROSCOPIC FRAGMENTATION FOLLOWED BY EXTRACORPOREAL SHOCK-WAVE LITHOTRIPSY - A TREATMENT ALTERNATIVE FOR SELECTED LARGE OR STAGHORN CALCULI SO JOURNAL OF UROLOGY LA English DT Article DE EXTRACORPOREAL SHOCKWAVE LITHOTRIPSY; KIDNEY CALCULI; URINARY CALCULI ID NEPHROLITHOTOMY; MONOTHERAPY AB Ureterorenoscopic fragmentation followed by extracorporeal shock wave lithotripsy (ESWL*) is proposed as an addition to the alternatives of percutaneous nephrostolithotomy alone or with ESWL, or ESWL monotherapy for treatment of large (greater than 500 mm.(2)) or staghorn calculi. Six patients who failed percutaneous tube placement and 2 additional patients, all of whom had fragile-appearing, large volume (greater than 500 mm.(2)) renal calculi, were treated by primary ureteroscopy with semirigid or flexible instruments, fragmentation of the stone with the pulsed dye laser, ureteral stenting and subsequent ESWL. There were 2 instances of acute pyelonephritis and 2 of steinstrasse. A total of 2.76 procedures was performed per patient and the average anesthesia time was 160 minutes (excluding ESWL). Median hospitalization was 3.5 days (average 7.5). Of the 8 patients 7 became stone-free. One patient has sterile urine and a residual fragment smaller than 5 mm. All patients have been followed for 1 year and there have been no recurrences. The properly selected patient for ureterorenoscopic fragmentation followed by ESWL is one with a fragile calculus of moderate volume without strictured infundibula or significantly dilated calices. RP DRETLER, SP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,KIDNEY STONE CTR,BOSTON,MA, USA. NR 6 TC 12 Z9 13 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 APR PY 1994 VL 151 IS 4 BP 842 EP 846 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA NA970 UT WOS:A1994NA97000004 PM 8126806 ER PT J AU SPITKOVSKY, D STEINER, P LUKAS, J LEES, E PAGANO, M SCHULZE, A JOSWIG, S PICARD, D TOMMASINO, M EILERS, M JANSENDURR, P AF SPITKOVSKY, D STEINER, P LUKAS, J LEES, E PAGANO, M SCHULZE, A JOSWIG, S PICARD, D TOMMASINO, M EILERS, M JANSENDURR, P TI MODULATION OF CYCLIN GENE-EXPRESSION BY ADENOVIRUS E1A IN A CELL-LINE WITH E1A-DEPENDENT CONDITIONAL PROLIFERATION SO JOURNAL OF VIROLOGY LA English DT Article ID E2F TRANSCRIPTION FACTOR; RETINOBLASTOMA PROTEIN; G1 PHASE; PRODUCT; BINDING; ASSOCIATION; CDK2; PROMOTERS; PREVENTS; RECEPTOR AB To investigate how adenovirus ELA controls cell proliferation,,fe have fused E1A to the hormone-binding domain of the human estrogen receptor (ER) and introduced the E1A-ER chimeric gene together with an activated ras gene into primary rat embryo fibroblasts. Cell lines derived from this transfection proliferate in an estrogen-dependent manner. Estrogen-dependent activation of E1A-ER led to a rapid induction of both cyclin E and cyclin A gene expression. In contrast, levels of cyclin D1 were strongly reduced by activation of E1A-ER. Similar changes in cyclin gene expression mere observed when primary human fibroblasts were infected with wild-type adenovirus and when adenovirus E1A was stably expressed in NIH 3T3 cells. Our findings suggest that activation of cyclin A and E, but not D1, gene expression by E1A precedes and may be responsible for E1A-dependent cell proliferation. In contrast, we found that quantitative disruption of complexes between the E2F transcription factor and the retinoblastoma protein is not required for E1A-dependent S-phase entry. C1 DEUTSCH KREBSFORSCHUNGSZENTRUM,ABT 620,D-69120 HEIDELBERG,GERMANY. ZENTRUM MOLEK BIOL HEIDELBERG,D-69120 HEIDELBERG,GERMANY. DANISH CANC SOC,RES CTR,DIV CANC BIOL,DK-2100 COPENHAGEN,DENMARK. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. MITOTIX,CAMBRIDGE,MA 02139. UNIV GENEVA,DEPT BIOL CELLULAIRE,CH-1211 GENEVA 4,SWITZERLAND. IMPERIAL CANC RES FUND,TUMOR VIRUS GRP,CAMBRIDGE CB2 1QP,ENGLAND. NR 47 TC 60 Z9 60 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2206 EP 2214 PG 9 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700020 PM 8139005 ER PT J AU SOSA, MAG ROSAS, DH DEGASPERI, R MORITA, E HUTCHISON, MR RUPRECHT, RM AF SOSA, MAG ROSAS, DH DEGASPERI, R MORITA, E HUTCHISON, MR RUPRECHT, RM TI NEGATIVE REGULATION OF THE 5' LONG TERMINAL REPEAT (LTR) BY THE 3' LTR IN THE MURINE PROVIRAL GENOME SO JOURNAL OF VIROLOGY LA English DT Article ID LEUKOSIS VIRUS-DNA; LEUKEMIA-VIRUS; PROMOTER INSERTION; AVIAN RETROVIRUSES; ENHANCER REGION; PLUS STRAND; GENE; TRANSCRIPTION; ACTIVATION; SEQUENCES AB To assess the influence of the 3' long terminal repeat (LTR) on the promoter/enhancer activity of the 5' LTR, a set of isogenic retroviral vectors differing only in the U3 region of the 3' LTR was constructed. These U3 elements were derived from viruses with different tissue tropism. The 5' LTR originated from Moloney murine leukemia virus and directed the transcription of a reporter gene (chloramphenicol acetyltransferase [CAT] gene), giving rise to plasmids of the general configuration LTR-CAT-LTR'. Following transfection of these chimeric constructs into various cell types, the CAT activity in a given cell line was inversely related to the activity of the downstream U3 region when used in a single-LTR construct in that cell type, indicating negative regulation of the 5' LTR by the chimeric 3' LTR'. Our data indicate that a highly active 3' LTR interferes with gene expression from the 5' LTR. Potential mechanisms for this down-regulation are discussed. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 53 TC 10 Z9 10 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2662 EP 2670 PG 9 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700067 ER PT J AU SCHLANGER, LE KLEYMAN, TR LING, BN AF SCHLANGER, LE KLEYMAN, TR LING, BN TI K+-SPARING DIURETIC ACTIONS OF TRIMETHOPRIM - INHIBITION OF NA+ CHANNELS IN A6 DISTAL NEPHRON CELLS SO KIDNEY INTERNATIONAL LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; POTASSIUM CHANNELS; THERAPY; HYPERKALEMIA AB Hyperkalemia complicates trimethoprim-sulfamethoxazole (TMP-SMX) therapy in over 20% of HIV-infected patients. TMP is a heterocyclic weak base, similar to amiloride, a ''K+-sparing'' diuretic and Na+ channel blocker. Apical TMP is known to inhibit amiloride-sensitive short circuit current in A6 cells, a tissue culture model for mammalian cortical collecting tubule principal cells [1]. We used cell-attached patch clamp techniques to investigate the effect of TMP on the 4 pS, highly selective Na+ channel in the apical membrane of A6 cells grown on permeable supports in the presence of 1.5 mu M aldosterone. Baseline channel activity at resting membrane potential, measured as NPo (N of channels x open probability), was 1.09 +/- 0.50 (N = 18). NPo (0.92 +/- 0.38; N = 9) was unchanged when 10(-3) M TMP was added to the basolateral bath for 30 minutes. However, apical exposure with pipettes containing 10(-3) or 10(-5) M TMP reduced NPo approximate to tenfold (0.12 +/- 0.08; N = 7 and 0.18 +/- 0.14; N = 12, respectively). Kinetic analysis revealed the appearance of a new closed state after apical TMP treatment. Another group of A6 cells were pretreated with 10(-3) M apical TMP for 30 minutes prior to patching with pipettes filled with TMP-free saline. NP, progressively rose from 0.07 +/- 0.09 to 0.87 +/- 0.23 (N = 5) as the residual TMP was diluted within the pipette. Apical or basolateral pretreatment (30 min) with 10(-3) M SMX did not change Na+ channel activity. In conclusion, in A6 distal nephron cells: (1) TMP reversibly blocks highly selective Na+ channels; (2) direct interaction with the outer channel pore is required since inhibition was observed with apical, but not basolateral TMP; (3) the SMX component of TMP-SMX preparations has no direct effect on Na+ channel activity; (4) This K+-sparing diuretic effect likely contributes to the hyperkalemia associated with TMP therapy in HIV-infected patients. C1 EMORY UNIV,SCH MED,DEPT MED,DIV RENAL,ATLANTA,GA 30322. VET AFFAIRS MED CTR,ATLANTA,GA 30033. UNIV PENN,DEPT MED,DIV RENAL & ELECTROLYTE,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. FU NIDDK NIH HHS [T32-DK07656, K08-DK02111, R01-DK37963] NR 25 TC 37 Z9 38 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD APR PY 1994 VL 45 IS 4 BP 1070 EP 1076 DI 10.1038/ki.1994.143 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA NB502 UT WOS:A1994NB50200016 PM 8007576 ER PT J AU HASNAIN, Q MACDONALD, G HAUPERT, GT AF HASNAIN, Q MACDONALD, G HAUPERT, GT TI METABOLISM OF URIDINE IN EXPANDED EXTRACELLULAR VOLUME STATES SO KIDNEY INTERNATIONAL LA English DT Meeting Abstract C1 PRINCE HENRY HOSP,SCH MED,DEPT NEPHROL,LITTLE BAY,NSW 2036,AUSTRALIA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD APR PY 1994 VL 45 IS 4 BP 1265 EP 1266 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA NB502 UT WOS:A1994NB50200094 ER PT J AU BARNES, JL HEVEY, KA HASTINGS, RR BOCANEGRA, RA AF BARNES, JL HEVEY, KA HASTINGS, RR BOCANEGRA, RA TI MESANGIAL CELL-MIGRATION PRECEDES PROLIFERATION IN HABU SNAKE VENOM-INDUCED GLOMERULAR INJURY SO LABORATORY INVESTIGATION LA English DT Article DE PLATELETS; GLOMERULONEPHRITIS; CELL PROLIFERATION ID EXTRACELLULAR-MATRIX COMPONENTS; PLATELET SECRETORY PROTEINS; IMMUNE-COMPLEX NEPHRITIS; GROWTH-FACTOR; EXPRESSION; RAT; GLOMERULONEPHRITIS; ANTIBODIES; LESIONS; ACTIN AB BACKGROUND: Mesangial cells migrate in response to platelet released products in vitro (Am J Pathol 1991;138:859). Cell migration, in addition to proliferation might play a role in cell remodeling during the course of proliferative glomerular disease. EXPERIMENTAL DESIGN: In this study, we examined mesangial cell migration in vivo in a platelet-dependent model of proliferative glomerulonephritis induced by Habu snake venom. Mesangial cell migration was assessed by phenotypic identification and temporal location of mesangial cells within glomerular lesions in serial time studies from 8 to 48 hours after Habu snake venom. Autoradiography of [H-3]thymidine incorporation into cells was employed to identify and temporally separate cell division and proliferation from cell motility and other related events. RESULTS: Early (8-hour) lesions consisted of microaneurysms devoid of mesangial cells. By 24 hours, glomeruli showed mesangial cells at the margins of lesions adjacent to intact glomerular tufts, followed by the presence of clusters of cells at 30 and 36 hours. By 48 hours, most lesions were filled with proliferating mesangial cells. Cells containing [H-3]thymidine were rarely observed until 30 hours, at which point they were found in advanced lesions. Marginating cells did not contain [H-3]thymidine, suggesting that the location of these cells was not related to cell division but rather to migration. Platelet depletion eliminated platelets from lesions and substantially retarded mesangial cell migration into glomerular lesions indicating mesangial cell migration is, in part, dependent on platelets or their secretory products. CONCLUSIONS: These studies show that mesangial cells can migrate in vivo and suggest that cell migration is an important early step in cell redistribution and remodeling during glomerular injury in this model of proliferative glomerulonephritis. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RHODE ISL HOSP,DEPT PATHOL,PROVIDENCE,RI 02902. RP BARNES, JL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [NIDDK DK37859] NR 32 TC 34 Z9 34 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 APR PY 1994 VL 70 IS 4 BP 460 EP 467 PG 8 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA NK099 UT WOS:A1994NK09900004 PM 8176886 ER PT J AU PANG, XP YOSHIMURA, M WANG, JY DUBINETT, SM AF PANG, XP YOSHIMURA, M WANG, JY DUBINETT, SM TI TNF-ALPHA-INDUCED ANTIPROLIFERATION IS NOT DEPENDENT ON THE AUTOCRINE ACTION OF TGF-BETA-1 IN A THYROID-CANCER SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR-BETA; FACTOR-KAPPA-B; PROGNOSTIC FACTORS; CELLS; PAPILLARY; CARCINOMA; INHIBITOR AB The autocrine inhibitory action of transforming growth factor-beta 1 (TGF-beta 1) may play an important role in maintaining the normal state of thyroid follicular epithelial cells. Deficiency of this regulatory mechanism has been implicated in the pathogenesis of nontoxic nodular goiter and thyroid epithelial cell cancer. Tumor necrosis factor-alpha (TNF-alpha) has an antiproliferative action in a human papillary thyroid carcinoma cell line, NP-PTC cells, through a receptor-mediated mechanism. In the present work, we studied the antiproliferative action of TNF-alpha. and TGF-beta 1 in NP-PTC cells. TNF-alpha induced TGF-beta 1 mRNA and secretion of the latent form of TGF-beta 1. Both TNF-alpha and TGF-beta 1 inhibited the proliferation of NP-PTC cells. A neutralizing antibody specific to human TGF-beta 1 blocked the antiproliferative action of TGF-beta 1 on NP-PTC cells, but it failed to block TNF-alpha-induced antiproliferation. Further, TNF-alpha and TGF-beta 1 acted synergistically to inhibit NP-PTC cell proliferation. The results show that both TNF-alpha and TGF-beta 1 inhibit the proliferation of NP-PTC cells. However, the actions of TGF-beta 1 and TNF-alpha differ in NP-PTC cells; TNF-alpha activates nuclear factor kappa B (NF-kappa B) and TGF-beta 1 does not. Although TNF-alpha induced TGF-beta 1 mRNA and secretion of the latent form of TGF-beta 1, the antiproliferative action of TNF-alpha is not dependent on the autocrine action of TGF-beta 1 in NP-PTC cells. C1 W LOS ANGELES VET AFFAIRS MED CTR,IMMUNOL PULM LAB,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90073. RP PANG, XP (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,ENDOCRINE RES LAB,BLDG 114,ROOM 200,LOS ANGELES,CA 90073, USA. NR 24 TC 8 Z9 9 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0277-6766 J9 LYMPHOKINE CYTOK RES JI Lymphokine Cytokine Res. PD APR PY 1994 VL 13 IS 2 BP 93 EP 97 PG 5 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA NL491 UT WOS:A1994NL49100005 PM 8061120 ER PT J AU BURGESON, RE CHIQUET, M DEUTZMANN, R EKBLOM, P ENGEL, J KLEINMAN, H MARTIN, GR MENEGUZZI, G PAULSSON, M SANES, J TIMPL, R TRYGGVASON, K YAMADA, Y YURCHENCO, PD AF BURGESON, RE CHIQUET, M DEUTZMANN, R EKBLOM, P ENGEL, J KLEINMAN, H MARTIN, GR MENEGUZZI, G PAULSSON, M SANES, J TIMPL, R TRYGGVASON, K YAMADA, Y YURCHENCO, PD TI A NEW NOMENCLATURE FOR THE LAMININS SO MATRIX BIOLOGY LA English DT Note DE LAMININ; NOMENCLATURE AB The authors have adopted a new nomenclature for the laminins. They are numbered with arabic numeral in the order discovered. The previous A, B1 and B2 chains, and their isoforms, are alpha, beta and gamma and respectively, followed by an arabic numeral to identify the isoform. For example, the first laminin identified from the Engelbreth-Holm-Swarm tumor is laminin-1 with the chain composition alpha 1 beta 1 gamma 1.. The genes for these chains are LAMA1, LAMB1 and LAMC1, respectively. C1 MAX PLANCK INST BIOCHEM,D-82152 MARTINSRIED,GERMANY. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA. UNIV BASEL,BIOCTR,CH-4056 BASEL,SWITZERLAND. UNIV REGENSBURG,DEPT BIOCHEM MICROBIOL & GENET,W-8400 REGENSBURG,GERMANY. UNIV UPPSALA,DEPT ANIM PHYSIOL,UPPSALA,SWEDEN. NIDR,BETHESDA,MD 20892. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. UNIV NICE,RECH DERMATOL LAB,NICE,FRANCE. UNIV BERN,ME MULLER INST BIOMECH,BERN,SWITZERLAND. WASHINGTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,ST LOUIS,MO 63110. UNIV OULU,BIOCTR OULU,OULU,FINLAND. UNIV OULU,DEPT BIOCHEM,OULU,FINLAND. ROBERT WOOD JOHNSON MED SCH,DEPT PATHOL,PISCATAWAY,NJ. NR 1 TC 690 Z9 696 U1 2 U2 12 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0945-053X J9 MATRIX BIOL JI Matrix Biol. PD APR PY 1994 VL 14 IS 3 BP 209 EP 211 DI 10.1016/0945-053X(94)90184-8 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NK840 UT WOS:A1994NK84000002 PM 7921537 ER PT J AU ASHTON, CM KUYKENDALL, DH WRAY, NP AF ASHTON, CM KUYKENDALL, DH WRAY, NP TI MISCLASSIFICATION OF PATIENTS CAN AFFECT GROUP QUALITY OF CARE SCORES SO MEDICAL CARE LA English DT Letter RP ASHTON, CM (reprint author), DEPT VET AFFAIRS MED CTR,HOUSTON CTR QUAL CARE & UTILIZAT STUDIES,HOUSTON,TX, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD APR PY 1994 VL 32 IS 4 BP 405 EP 405 DI 10.1097/00005650-199404000-00009 PG 1 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA NE246 UT WOS:A1994NE24600009 PM 8139305 ER PT J AU ASCH, DA BARON, J HERSHEY, JC KUNREUTHER, H MESZAROS, J RITOV, I SPRANCA, M AF ASCH, DA BARON, J HERSHEY, JC KUNREUTHER, H MESZAROS, J RITOV, I SPRANCA, M TI OMISSION BIAS AND PERTUSSIS VACCINATION SO MEDICAL DECISION MAKING LA English DT Article DE BEHAVIORAL SCIENCES; DECISION MAKING; DECISION THEORY; ETHICS; HEALTH POLICY; JUDGMENT; PERTUSSIS VACCINE; PROBABILITY; PSYCHOLOGY; PUBLIC HEALTH; RISK; VACCINATION; WHOOPING COUGH ID ENCEPHALOPATHY; VACCINES; CHOICE AB Background: Several laboratory studies have suggested that many people favor potentially harmful omissions over less harmful acts. The authors studied the role of this omission bias in parents' decisions whether to vaccinate their children against pertussis. Methods: Two hundred mail surveys were sent to subscribers to a magazine that had published articles favoring and opposing pertussis vaccination. Subjects were asked about their beliefs about the vaccine and the disease, and whether they had vaccinated their own children or planned to, and they were given test items to identify omission bias in their reasoning. Results: One hundred and three subjects (52%) responded to the survey. Respondents who reported they did not or would not allow their children to be vaccinated (n = 43; 41%) were more likely to believe that vaccinating was more dangerous than not vaccinating (p < 0.001). They were also more likely to exhibit omission bias (p = 0.004), holding constant their stated beliefs about the danger of the vaccine. Conclusions: Omission bias plays a role in decisions not to vaccinate with pertussis vaccine, beyond the role played by belief about the risk of vaccination. C1 PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. UNIV PENN,SCH ARTS & SCI,DEPT PSYCHOL,PHILADELPHIA,PA 19104. UNIV PENN,WHARTON SCH,PHILADELPHIA,PA 19104. UNIV PENN,WHARTON RISK & DECIS PROC CTR,PHILADELPHIA,PA 19104. UNIV PENN,LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA 19104. RP ASCH, DA (reprint author), UNIV PENN,SCH MED,DIV GEN INTERNAL MED,PHILADELPHIA,PA 19104, USA. NR 23 TC 91 Z9 91 U1 3 U2 11 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 0272-989X J9 MED DECIS MAKING JI Med. Decis. Mak. PD APR-JUN PY 1994 VL 14 IS 2 BP 118 EP 123 DI 10.1177/0272989X9401400204 PG 6 WC Health Care Sciences & Services; Medical Informatics SC Health Care Sciences & Services; Medical Informatics GA NG124 UT WOS:A1994NG12400004 PM 8028464 ER PT J AU LINTON, D DEWHIRST, FE CLEWLEY, JP OWEN, RJ BURNENS, AP STANLEY, J AF LINTON, D DEWHIRST, FE CLEWLEY, JP OWEN, RJ BURNENS, AP STANLEY, J TI 2 TYPES OF 16S RIBOSOMAL-RNA GENE ARE FOUND IN CAMPYLOBACTER-HELVETICUS - ANALYSIS, APPLICATIONS AND CHARACTERIZATION OF THE INTERVENING SEQUENCE FOUND IN SOME STRAINS SO MICROBIOLOGY-UK LA English DT Article DE CAMPYLOBACTER HELVETICUS; 16S RIBOSOMAL-RNA GENE; INTERVENING SEQUENCE; PHYLOGENETIC ANALYSIS; MOLECULAR SUBTYPING ID RIBOSOMAL-RNA GENE; UPSALIENSIS; JEJUNI; COLI AB In the recently described species Campylobacter helveticus, two sizes of PCR amplicon were detected with primers homologous to conserved regions of the 16S rRNA gene. A conventionally sized gene was sequenced from the type strain, NCTC 12470, placing the new species as phylogenetically related to C. upsaliensis and the thermotolerant campylobacters. This nucleotide sequence enabled PCR primers to be designed for use in rapid molecular identification of C. helveticus and its closest phylogenetic relative, C. upsaliensis. When this assay was employed to characterize 22 'C. upsaliensis-like' isolates, twelve were identified as C. helveticus and nine as C. upsaliensis, in agreement with data obtained with a C. helveticus-specific DNA probe. A 550 bp amplicon internal to the 16S rRNA gene of C. helveticus was used to determine restriction fragment length polymorphisms (RFLPs) in genomic Southern blots, confirming that the copy number of the C. helveticus gene was three, and identifying nine 16S rRNA gene profiles. In 5/12 C. helveticus isolates identified by PCR, an enlarged amplicon was detected. The enlarged 16S rRNA gene of one of these strains, NCTC 12838, was sequenced and shown to contain an atypical intervening sequence (IVS) of 148 nucleotides. The position and size of such an IVS was inferred in the other four isolates by PCR with primers 5' and 3' to its position in NCTC 12838. This is a first report of an IVS in the 16S rRNA gene of a eubacterium. C1 CENT PUBL HLTH LAB,NATL COLLECT TYPE CULTURES,LONDON NW9 5HT,ENGLAND. CENT PUBL HLTH LAB,DIV VIRUS REFERENCE,LONDON NW9 5HT,ENGLAND. FORSYTH DENT CTR,DEPT MOLEC GENET,BOSTON,MA 02115. UNIV BERN,INST VET BACTERIOL,SWISS NATL REFERENCE LAB FOODBORNE DIS,CH-3012 BERN,SWITZERLAND. NR 26 TC 49 Z9 49 U1 0 U2 1 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 1350-0872 J9 MICROBIOL-UK JI Microbiology-(UK) PD APR PY 1994 VL 140 BP 847 EP 855 PN 4 PG 9 WC Microbiology SC Microbiology GA NF904 UT WOS:A1994NF90400020 PM 7516795 ER PT J AU BHARGAVA, V THOR, A DENG, GR LJUNG, BM MOORE, DH WALDMAN, F BENZ, C GOODSON, W CHEW, K SMITH, HS AF BHARGAVA, V THOR, A DENG, GR LJUNG, BM MOORE, DH WALDMAN, F BENZ, C GOODSON, W CHEW, K SMITH, HS TI THE ASSOCIATION OF P53 IMMUNOPOSITIVITY WITH TUMOR PROLIFERATION AND OTHER PROGNOSTIC INDICATORS IN BREAST-CANCER SO MODERN PATHOLOGY LA English DT Article DE P53 IMMUNOPOSITIVITY; BREAST CARCINOMA; TUMOR PROLIFERATION ID WILD-TYPE; SUPPRESSOR GENES; POOR PROGNOSIS; EXPRESSION; OVEREXPRESSION; P53-PROTEIN; MUTATIONS; PROTEIN; BENIGN; INSITU AB Abnormal accumulation of the p53 tumor suppressor gene product was analyzed in 198 primary invasive human breast carcinomas. In 47 of these cases, single-strand conformational polymorphism was used to detect mutations in the highly conserved exons 5-9 of the gene. Mutations as determined by single-strand conformational polymorphism were found in 15 of 15 strongly immunopositive cases (100%) and 3 of 23 immunonegative cases (13%). There were also nine cases with <1% immunopositive cells (borderline immunopositivity); p53 mutations were detected in seven of these cases. The results suggest that p53 immunopositivity is a highly specific, albeit somewhat insensitive surrogate for p53 mutations. p53 accumulation, detected by immunohistochemical methods using antibody PAb 1801, was noted in 29.8% of the cases and was associated with estrogen receptor (ER) negativity (P = 0.0003), progesterone receptor (PR) negativity (P = 0.008), and high histological grade (P = 0.037) by univariate analysis. Incorporation of bromodeoxyuridine was used to determine the percentage of cells synthesizing DNA (proliferative fraction). When bromodeoxyuridine was administered either in vivo (n = 93) or in vitro (n = 79), p53 accumulation was only marginally related to proliferative fraction (P = 0.067 by chi(2); P = 0.055 by Mann-Whitney). When tumors were segregated by ER status, the aforementioned associations of p53 immunopositivity with PR negativity, high histological grade, and increased proliferation rate lost their significance. p53 accumulation did not correlate with tumor size, clinical stage, axillary node metastases, or age at diagnosis. Three of ten exclusively intraductal carcinomas (two of which were of the comedo type) were immunopositive for p53. There was complete concordance between p53 immunopositivity of primary invasive lesions and concurrent lymph node metastases (24 cases examined). These observations suggest that p53 mutations usually are acquired at a stage in malignant progression prior to invasive carcinoma. Additionally, the fact that immunohistochemistry detected the majority of tumors with p53 mutations suggests that missense mutations leading to an altered gene product, rather than nonsense mutations, are the most frequent form of p53 alterations in breast cancer. C1 CALIFORNIA PACIFIC MED CTR,GERALDINE BRUSH CANC RES INST,SAN FRANCISCO,CA 94115. UNIV CALIF SAN FRANCISCO,DEPT PATHOL,SAN FRANCISCO,CA. UNIV CALIF SAN FRANCISCO,DEPT SURG,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. LAWRENCE LIVERMORE NATL LAB,DIV BIOMED SCI,LIVERMORE,CA 94550. FU NCI NIH HHS [P01 CA44768] NR 31 TC 49 Z9 49 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD APR PY 1994 VL 7 IS 3 BP 361 EP 368 PG 8 WC Pathology SC Pathology GA NK273 UT WOS:A1994NK27300014 PM 8058709 ER PT J AU GOLDBERG, DE STUART, J KOERNER, FC AF GOLDBERG, DE STUART, J KOERNER, FC TI PROGESTERONE-RECEPTOR DETECTION IN PARAFFIN SECTIONS OF HUMAN BREAST CANCERS BY AN IMMUNOPEROXIDASE TECHNIQUE INCORPORATING MICROWAVE-HEATING SO MODERN PATHOLOGY LA English DT Article DE PROGESTERONE RECEPTOR; IMMUNOPEROXIDASE STAINING; DEXTRAN-COATED CHARCOAL ASSAY; MICROWAVE HEATING ID ESTROGEN AB We sought to establish an easily interpretable and highly sensitive immunohistochemical method for detecting progesterone receptor protein in formalin-fixed, paraffin-embedded samples of breast carcinomas. Beginning with a conventional immunoperoxidase staining procedure, we incorporated microwave heating to compensate for the effects of conventional fixation and processing and then applied the method to 90 samples of primary breast carcinomas. We used the results of hormone binding assays as true values to establish the sensitivity, specificity, positive predictive value, and negative predictive value of the staining method. Our technique yielded good preservation of morphological detail and low nonspecific staining of background tissue. Comparisons of the results of staining and biochemical assays revealed that this progesterone receptor immunostaining procedure shows high sensitivity and acceptable specificity. We believe its performance characteristics make reliable study of small specimens and archival material possible. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT GYNECOL,BOSTON,MA 02114. NORTHEASTERN UNIV,BOUVE COLL PHARM & HLTH SCI,BOSTON,MA 02115. NR 13 TC 19 Z9 19 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD APR PY 1994 VL 7 IS 3 BP 401 EP 406 PG 6 WC Pathology SC Pathology GA NK273 UT WOS:A1994NK27300021 PM 8058716 ER PT J AU BARBER, DL DEMARTINO, JC SHOWERS, MO DANDREA, AD AF BARBER, DL DEMARTINO, JC SHOWERS, MO DANDREA, AD TI A DOMINANT-NEGATIVE ERYTHROPOIETIN (EPO) RECEPTOR INHIBITS EPO-DEPENDENT GROWTH AND BLOCKS F-GP55-DEPENDENT TRANSFORMATION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PROTEIN TYROSINE PHOSPHORYLATION; COLONY-STIMULATING FACTOR; VIRUS GP55 GLYCOPROTEIN; SIGNAL TRANSDUCTION; CYTOPLASMIC REGION; ERYTHROLEUKEMIA-CELLS; EXTRACELLULAR DOMAIN; ACTIVATION; EXPRESSION; HORMONE AB The erythropoietin receptor (EPO-R), a member of the cytokine receptor superfamily, can be activated to signal cell growth by binding either EPO or F-gp55, the Friend spleen focus-forming virus glycoprotein. Activation by F-gp55 results in constitutive EPO-R signalling and the first stage of Friend virus-induced erythroleukemia. We have generated a truncated form of the EPO-R polypeptide [EPO-R(T)] which lacks the critical cytoplasmic signal-transducing domain of the EPO-R required for EPO- or F-gp55-induced cell growth. EPO-R(T) specifically inhibited the EPO-dependent growth of EPO-R-expressing Ba/F3 cells without changing the interleukin-3-dependent growth of these cells. In addition, Ba/F3 cells that coexpressed wild-type EPO-R and EPO-R(T) were resistant to transformation by F-gp55 despite efficient expression of the F-gp55 transforming oncoprotein in infected cells. EPO-R(T) inhibited the EPO-dependent tyrosine phosphorylation of wild-type EPO-R, the tyrosine kinase (JAK2), and the SH2 adaptor protein (Shc). In conclusion, the EPO-R(T) polypeptide is a dominant negative polypeptide which specifically interferes with the early stages of EPO-R-mediated signal transduction and which prevents Friend virus transformation of erythroblasts. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. FU NIDDK NIH HHS [R01 DK 43889-01] NR 45 TC 53 Z9 53 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1994 VL 14 IS 4 BP 2257 EP 2265 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NC057 UT WOS:A1994NC05700004 PM 8139531 ER PT J AU DABROWSKI, CE CARMILLO, PJ SCHAFFER, PA AF DABROWSKI, CE CARMILLO, PJ SCHAFFER, PA TI CELLULAR PROTEIN INTERACTIONS WITH HERPES-SIMPLEX VIRUS TYPE-1 ORIS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ORIGIN-BINDING-PROTEIN; DNA-REPLICATION; FUNCTIONAL-ANALYSIS; GENE-PRODUCTS; VIRAL ORIGIN; UL9 PROTEIN; SEQUENCE; IDENTIFICATION; CLONING; SITES AB The herpes simplex virus type 1 (HSV-1) origin of DNA replication, oriS, contains an AT-rich region and three highly homologous sequences, sites I, II, and III, identified as binding sites for the HSV-1 origin-binding protein (OBP). In the present study, interactions between specific oriS DNA sequences and proteins in uninfected cell extracts were characterized. The formation of one predominant protein-DNA complex, M, was demonstrated in gel shift assays following incubation of uninfected cell extracts with site I DNA. The cellular protein(s) that comprises complex M has been designated origin factor I (OF-I). The OF-I binding site was shown to partially overlap the OBP binding site within site I. Complexes with mobilities indistinguishable from that of complex M also formed with site II and III DNAs in gel shift assays. oriS-containing plasmid DNA mutated in the OF-I binding site exhibited reduced replication efficiency in transient assays, demonstrating a role for this site in oriS function. The OF-I binding site is highly homologous to binding sites for the cellular CCAAT DNA-binding proteins. The binding site for the CCAAT protein CP2 was found to compete for OF-I binding to site I DNA. These studies support a model involving the participation of cellular proteins in the initiation of HSV-1 DNA synthesis at oriS. 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 [CA08749]; NIAID NIH HHS [R01 AI28537] NR 53 TC 32 Z9 32 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1994 VL 14 IS 4 BP 2545 EP 2555 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NC057 UT WOS:A1994NC05700034 PM 8139557 ER PT J AU BOTTINGER, EP SHELLEY, CS FAROKHZAD, OC ARNAOUT, MA AF BOTTINGER, EP SHELLEY, CS FAROKHZAD, OC ARNAOUT, MA TI THE HUMAN BETA-2 INTEGRIN CD18 PROMOTER CONSISTS OF 2 INVERTED ETS CIS-ELEMENTS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID TRANSCRIPTION FACTOR; GENE FAMILY; C-FOS; PRE-B; REGULATED EXPRESSION; MOLECULAR-CLONING; RESPONSE ELEMENT; INDUCIBLE GENE; BINDING SITES; ADHESION AB To define the minimal promoter responsible for expression of CD18 in myeloid and lymphoid cells, we generated 5' and 3' deletion constructs of a-segment extending 785 bp upstream and 19 bp downstream of a major transcription start site and determined their effects on driving expression of the luciferase reporter gene in transfected hematopoietic cell lines. A region extending from nucleotides (nt) -302 to +19 was sufficient for cell-restricted and phorbol ester-inducible expression. DNase I footprinting of this region revealed two adjacent protected segments extending from nt -81 to -68 (box A) and -55 to - 41 (box B). When a construct of 47 nt in length containing box A and box B and lacking other 3' or 5' elements was cloned into a promoterless vector, it conferred tissue-specific and phorbol ester-inducible expression. Gel retardation revealed that the protein components of two major protein-DNA complexes that form on both box A and box B and are required for transcriptional activation are members of the Ets oncoprotein family; one is related to the GA-binding protein (GABP), and the other is related to PU.1/Spi-1. The minimal CD18 promoter, lacking TATA, CAAT, and initiator elements and consisting primarily of Ets repeats, may exemplify an emerging class of promoters with which the concerted binding of Ets factors is necessary and sufficient to mediate transcriptional activation through direct recruitment of the basal transcription machinery. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,LEUKOCYTE BIOL & INFLAMMAT PROGRAM,BOSTON,MA 02129. FU NIAID NIH HHS [P01 AI-28465] NR 71 TC 89 Z9 89 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1994 VL 14 IS 4 BP 2604 EP 2615 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NC057 UT WOS:A1994NC05700040 PM 7511209 ER PT J AU SONGYANG, Z SHOELSON, SE MCGLADE, J OLIVIER, P PAWSON, T BUSTELO, XR BARBACID, M SABE, H HANAFUSA, H YI, T REN, R BALTIMORE, D RATNOFSKY, S FELDMAN, RA CANTLEY, LC AF SONGYANG, Z SHOELSON, SE MCGLADE, J OLIVIER, P PAWSON, T BUSTELO, XR BARBACID, M SABE, H HANAFUSA, H YI, T REN, R BALTIMORE, D RATNOFSKY, S FELDMAN, RA CANTLEY, LC TI SPECIFIC MOTIFS RECOGNIZED BY THE SH2 DOMAINS OF CSK, 3BP2, FPS FES, GRB-2, HCP, SHC, SYK, AND VAV SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PHOSPHATIDYLINOSITOL KINASE-ACTIVITY; GROWTH-FACTOR RECEPTORS; PHOSPHOLIPASE-C-GAMMA; PDGF BETA-RECEPTOR; MIDDLE T-ANTIGEN; MOLECULAR-CLONING; TYROSINE KINASE; SIGNAL TRANSDUCTION; BINDING-SITE; EGF RECEPTOR AB Src homology 2 (SH2) domains provide specificity to intracellular signaling by binding to specific phosphotyrosine (phospho-Tyr)-containing sequences. We recently developed a technique using a degenerate phosphopeptide library to predict the specificity of individual SH2 domains (src family members, Abl, Nck, Sem5, phospholipase C-gamma, p85 subunit of phosphatidylinositol-3-kinase, and SHPTP2 (Z. Songyang, S. E. Shoelson, M. Chaudhuri, G. Gish, T. Pawson, W. G. Haser, F. King, T. Roberts, S. Ratnofsky, R. J. Lechleider, B. G. Neel, R. B. Birge, J. E. Fajardo, M. M. Chou, H. Hanafusa, B. Schaffhausen, and L. C. Cantley, Cell, 72:767-778, 1993). We report here the optimal recognition motifs for SH2 domains from GRB-2, Drk, Csk, Vav, fps/fes, SHC, Syk (carboxy-terminal SH2), 3BP2, and HCP (amino-terminal SH2 domain, also called PTP1C and SHPTP1). As predicted, SH2 domains from proteins that fall into group I on the basis of a Phe or Tyr at the betaD5 position (GRB-2, 3BP2, Csk, fps/fes, Syk C-terminal SH2) select phosphopeptides with the general motif phospho-Tyr-hydrophilic (residue)-hydrophilic (residue)-hydrophobic (residue). The SH2 domains of SHC and HCP (group III proteins with Ile, Leu, or Cys at the betaD5 position) selected the general motif phospho-Tyr-hydrophobic-Xxx-hydrophobic, also as predicted. Vav, which has a Thr at the betaD5 position, selected phospho-Tyr-Met-Glu-Pro as the optimal motif. Each SH2 domain selected a unique optimal motif distinct from motifs previously determined for other SH2 domains. These motifs are used to predict potential sites in signaling proteins for interaction with specific SH2 domain-containing proteins. The Syk SH2 domain is predicted to bind to Tyr-hydrophilic-hydrophilic-Leu/Ile motifs like those repeated at 10-residue intervals in T- and B-cell receptor-associated proteins. SHC is predicted to bind to a subgroup of these same motifs. A structural basis for the association of Csk with Src family members is also suggested from these studies. C1 HARVARD UNIV, SCH MED,DEPT CELL BIOL,WARREN ALPERT 152, 200 LONGWOOD AVE, BOSTON, MA 02115 USA. BETH ISRAEL HOSP, DEPT MED, BOSTON, MA 02215 USA. BRIGHAM & WOMENS HOSP, DEPT MED, BOSTON, MA 02115 USA. BRISTOL MYERS SQUIBB, PHARMACEUT RES INST, PRINCETON, NJ 08543 USA. CLEVELAND CLIN FDN, RES INST, DEPT CANC BIOL, CLEVELAND, OH 44195 USA. UNIV MARYLAND, SCH MED, DEPT MICROBIOL & IMMUNOL, BALTIMORE, MD 21201 USA. BASF BIORES CORP, WORCESTER, MA 01605 USA. UNIV MARYLAND, INST BIOTECHNOL, CTR MED BIOTECHNOL, BALTIMORE, MD 21201 USA. TUFTS UNIV, SCH MED, DEPT PHYSIOL, BOSTON, MA 02111 USA. JOSLIN DIABET CTR, DIV RES, BOSTON, MA 02115 USA. MT SINAI HOSP, SAMUEL LUNENFELD RES INST, DIV MOLEC & DEV BIOL, TORONTO M5G 1X5, ONTARIO, CANADA. ROCKEFELLER UNIV, NEW YORK, NY 10021 USA. RI Sabe, Hisataka/A-4066-2012; Pawson, Tony/E-4578-2013; Cantley, Lewis/D-1800-2014 OI Cantley, Lewis/0000-0002-1298-7653 NR 54 TC 846 Z9 850 U1 1 U2 23 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 EI 1098-5549 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1994 VL 14 IS 4 BP 2777 EP 2785 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NC057 UT WOS:A1994NC05700055 PM 7511210 ER PT J AU LIPTON, SA AF LIPTON, SA TI HIV-RELATED NEURONAL INJURY - POTENTIAL THERAPEUTIC INTERVENTION WITH CALCIUM-CHANNEL ANTAGONISTS AND NMDA ANTAGONIST SO MOLECULAR NEUROBIOLOGY LA English DT Article; Proceedings Paper CT Symposium on Transmissible and Nontransmissible Neurodegenerative Disorders CY FEB 28-MAR 05, 1993 CL OCHO RIOS, JAMAICA SP INT BRAIN RES ORG, UNIV GOTEBORG, UNIV WEST INDIES DE NMDA RECEPTOR; EXCITOTOXICITY; AIDS DEMENTIA; FREE RADICALS ID METHYL-D-ASPARTATE; PLATELET-ACTIVATING-FACTOR; TUMOR-NECROSIS-FACTOR; RECEPTOR-MEDIATED NEUROTOXICITY; IMMUNODEFICIENCY-VIRUS TYPE-1; REDOX MODULATORY SITE; VASOACTIVE-INTESTINAL-PEPTIDE; PRIMARY CORTICAL CULTURES; AMINO-ACID NEUROTOXICITY; ENVELOPE PROTEIN GP120 AB Perhaps as many as 25-50% of adult patients and children with acquired immunodeficiency syndrome (AIDS) eventually suffer from neurological manifestations, including dysfunction of cognition, movement, and sensation. How can human immunodeficiency virus type 1 (HIV-1) result in neuronal damage if neurons themselves are for all intents and purposes not infected by the virus? This article reviews a series of experiments leading to a hypothesis that accounts at least in part for the neurotoxicity observed in the brains of AIDS patients. There is growing support for the existence of HIV- or immune-related toxins that lead indirectly to the injury or demise of neurons via a potentially complex web of interactions among macrophages (or microglia), astrocytes, and neurons. HIV-infected monocytoid cells (macrophages, microglia, or monocytes), after interacting with astrocytes, secrete eicosanoids, i.e., arachidonic acid and its metabolites, including platelet-activating factor. Macrophages activated by HIV-1 envelope protein gp120 also appear to release arachidonic acid and its metabolites. In addition, interferon-gamma (IFN-gamma) stimulation of macrophages induces release of the glutamate-like agonist, quinolinate. Furthermore, HIV-infected macrophage production of cytokines, including TNF-alpha and IL1-beta, contributes to astrogliosis. A final common pathway for neuronal susceptibility appears to be operative, similar to that observed in stroke, trauma, epilepsy, neuropathic pain, and several neurodegenerative diseases, possibly including Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This mechanism involves the activation of voltage-dependent Ca2+ channels and N-methyl-D-aspartate (NMDA) receptor-operated channels, and, therefore, offers hope for future pharmacological intervention. This article focuses on clinically tolerated calcium channel antagonists and NMDA antagonists with the potential for trials in humans with AIDS dementia in the near future. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP LIPTON, SA (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115, USA. FU NEI NIH HHS [EY05477, EY09024]; NICHD NIH HHS [HD29587] NR 135 TC 85 Z9 86 U1 1 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0893-7648 J9 MOL NEUROBIOL JI Mol. Neurobiol. PD APR-JUN PY 1994 VL 8 IS 2-3 BP 181 EP 196 DI 10.1007/BF02780669 PG 16 WC Neurosciences SC Neurosciences & Neurology GA PD120 UT WOS:A1994PD12000014 PM 7999315 ER PT J AU CATANIA, MV DESOCARRAZ, H PENNEY, JB YOUNG, AB AF CATANIA, MV DESOCARRAZ, H PENNEY, JB YOUNG, AB TI METABOTROPIC GLUTAMATE-RECEPTOR HETEROGENEITY IN RAT-BRAIN SO MOLECULAR PHARMACOLOGY LA English DT Article ID AMINO-ACID RECEPTOR; AMYGDALA PYRIFORM CORTEX; CENTRAL-NERVOUS-SYSTEM; MEDIATED POLYPHOSPHOINOSITIDE HYDROLYSIS; INOSITOL PHOSPHOLIPID-METABOLISM; BINDING-SITES; PHOSPHOINOSITIDE HYDROLYSIS; SIGNAL TRANSDUCTION; HIPPOCAMPAL-NEURONS; PURKINJE-CELLS AB Metabotropic glutamate receptors (mGluRs) are G protein-linked receptors that operate through the formation of different second messengers. Utilizing quantitative autoradiographic techniques, we have characterized [H-3]glutamate binding to mGluRs in discrete regions of adult rat brain. [H-3]Glutamate binding, in the presence of high concentrations of alpha-amino-3-hydroxymethyl-4-isoxazolepropionic acid (10 mu M), N-methyl-D-aspartate (100 mu M), and 2.5 mM calcium chloride (CaCl2), was saturable. Scatchard plots were linear in all regions examined and revealed similar affinity constants of about 500 nM. The largest number of sites was found in the outer cerebral cortical layers (10 pmol/mg of protein). [H-3]Glutamate binding was displaced by quisqualate, trans-1-amino-1,3-cyclopentane dicarboxylic acid (t-ACPD) (racemic mixture), and (1S,3R)-ACPD but not by (1R,3S)-ACPD. The guanine nucleotide analogue guanosine-5'-O-(3-thio) triphosphate (100 mu M) reduced the binding by affecting the affinity but not the total number of sites, as predicted for G protein-coupled receptor sites. Quisqualate displacement curves were always biphasic and resolved two binding sites, with K-i values in the low nanomolar (15 nM) and micromolar (63 mu M) ranges. (1S,3R)-ACPD displaced [H-3]glutamate binding both in the absence and in the presence of 2.5 mu M quisqualate, suggesting that both high and low affinity quisqualate sites are linked to mGluRs. (1S,3R)-ACPD competition curves were broad (Hill coefficient = 0.73) but monophasic under both conditions, with K-i values in the micromolar range (14-116 mu M), suggesting that (1S,3R)-ACPD acts on the two quisqualate sites with similar apparent affinities. The regional distributions of the two sites were different. The highest levels of the high affinity quisqualate binding site were found in the cerebellar molecular layer. The highest levels of the low affinity quisqualate binding sites were found in the outer cerebral cortex. The pharmacological profile and regional distribution suggest that the high and low affinity quisqualate-sensitive components of [H-3]glutamate binding sites might correspond to the mGluR1/mGluR5 and mGluR2/mGluR3 subgroups of cloned mGluRs, respectively. C1 MASSACHUSETTS GEN HOSP, DEPT NEUROL, NEUROL SERV, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. RI Catania, Maria Vincenza/E-2627-2017 OI Catania, Maria Vincenza/0000-0002-9329-8517 FU NIA NIH HHS [AG08671]; NINDS NIH HHS [NS19613] NR 65 TC 40 Z9 41 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 APR PY 1994 VL 45 IS 4 BP 626 EP 636 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NH460 UT WOS:A1994NH46000009 PM 8183241 ER PT J AU RHEE, MS GALIVAN, J WRIGHT, JE ROSOWSKY, A AF RHEE, MS GALIVAN, J WRIGHT, JE ROSOWSKY, A TI BIOCHEMICAL-STUDIES ON PT523, A POTENT NONPOLYGLUTAMATABLE ANTIFOLATE, IN CULTURED-CELLS SO MOLECULAR PHARMACOLOGY LA English DT Article ID THYMIDYLATE SYNTHASE INHIBITOR; FOLYLPOLYGLUTAMATE SYNTHETASE-ACTIVITY; RAT HEPATOMA-CELLS; DIHYDROFOLATE-REDUCTASE; METHOTREXATE ANALOGS; LEUKEMIA-CELLS; 5,10-DIDEAZATETRAHYDROFOLIC ACID; FOLATE ANTAGONISTS; GROWTH-INHIBITION; ANTI-FOLATE AB Studies on the mode of action of PT523 [N-alpha-(4-amino-4-deoxypteroyl)-N delta-hemiphthaloyl-L-ornithine], a potent nonpolyglutamatable antifolate, were carried out in sensitive and resistant H35 rat hepatoma cell lines in culture, to compare it with other antifolates, including three dihydrofolate reductase (DHFR) inhibitors, i.e., methotrexate (MTX), gamma-fluoro-MTX, and trimetrexate (TMQ), two thymidylate synthase inhibitors, i.e., N-10-propargyl-5,8-dideazafolate (PDDF) and 2-desamino-2-methyl-N-10-propargyl-5,8-dideazafolate (dmPDDF), and the glycinamide ribonucleotide formyltransferase inhibitor 5,10-dideaza-5,6,7,8-tetrahydrofolate. PT523 was the most active compound in this group against the parental H35 cells, with an IC50 ranging from 2.5 nM for 72 hr of treatment to 0.21 mu M for 2 hr of treatment. Sublines resistant to MTX by virtue of a transport defect or a combination of defective transport and increased DHFR activity were resistant to PT523 and MTX but not to PDDF, whereas sublines resistant to fluoropyrimidines by virtue of increased thymidylate synthase activity were resistant to PDDF but not to PT523, TMQ, or MTX. Inhibition of H35 cell growth by PT523 was associated with a concentration- and time-related decrease in de novo dTMP and purine biosynthesis. Growth inhibition by PT523, MTX, and TMQ was prevented by leucovorin or a combination of thymidine (dThd) and hypoxanthine but not by dThd or hypoxanthine alone; in contrast, growth inhibition by dmPDDF was prevented by dThd alone. Intracellular reduced folate polyglutamate pools were markedly altered by PT523 treatment, with the most pronounced effect being an increase in 7,3-dihydrofolate mono- and polyglutamates and a decrease in 5,10-methylene-5,6,7,8-tetrahydrofolate mono- and polyglutamates, 5,6,7,8-tetrahydrofolate mono- and polyglutamates, and 10-formyl-5,6,7, 8-tetrahydrofolate mono- and polyglutamates. This pattern was qualitatively similar to that observed with MTX and TMQ but different from that observed with dmPDDF or 5,10-dideaza-5,6,7,8-tetrahydrofolate, which resulted in little or no change in the folate species. Uptake of [H-3]MTX and [H-3]folinic acid, but not [H-3]folic acid, by H35 cells was inhibited in a dose-related manner by PT523, suggesting that penetration of the cell probably involves, at least in part, active transport by the MTX/reduced folate carrier. To determine whether the potent cellular effects of PT523 might be due to chemical or enzymic cleavage to N-alpha-(4-amino-4-deoxypteroyl)-L-ornithine, a potent inhibitor of folylpolyglutamate synthetase, the formation of [H-3]MTX polyglutamates in CCRF-CEM lymphoblasts pulsed with [H-3]MTX after preincubation with PT523 was examined. The MTX polyglutamate profile was not markedly altered by PT523 treatment, suggesting that inhibition of DNA precursor synthesis and cell growth is not due to any significant perturbation of cellular folylpolyglutamate synthetase activity. The results of these studies support the view that cell growth inhibition by PT523 is due to DHFR inhibition. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,ALBANY,NY 12201. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. FU NCI NIH HHS [CA25933, CA25394, CA46126] NR 41 TC 30 Z9 30 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 1994 VL 45 IS 4 BP 783 EP 791 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NH460 UT WOS:A1994NH46000029 PM 7514264 ER PT J AU BEDNAR, MM FANBURG, JC ANDERSON, ML RAYMOND, SJ DOOLEY, RH GROSS, CE AF BEDNAR, MM FANBURG, JC ANDERSON, ML RAYMOND, SJ DOOLEY, RH GROSS, CE TI COMPARISON OF TRIPHENYLTETRAZOLIUM DYE WITH LIGHT-MICROSCOPIC EVALUATION IN A RABBIT MODEL OF ACUTE CEREBRAL-ISCHEMIA SO NEUROLOGICAL RESEARCH LA English DT Article DE 2,3,5-TRIPHENYLTETRAZOLIUM CHLORIDE; LIGHT MICROSCOPIC EVALUATION; ISCHEMIA; INFARCTION ID THROMBOEMBOLIC STROKE; BRAIN INFARCTS; CHLORIDE TTC; INJURY; STAIN AB The present study was performed to compare brain infarct size assessment by routine histology (haematoxylin and eosin) and by 2,3,5-triphenyltetrazolium chloride staining techniques. New Zealand white rabbits were subjected to autologous clot embolization to the anterior circulation of the brain. After a study period of 7-8 h the brains were harvested and serially sectioned in the coronal plane. Brain slices were then immersed in a 1% triphenyltetrazolium chloride dye. Following visualization oi the infarcted region, the brains were immediately placed in 10% formalin and later prepared for histologic evaluation by routine haematoxylin and eosin. The two methods were compared for their ability to estimate infarct size by an independent observer. There was excellent correlation between the two methodologies; infarct sizes of 57.4 +/- 5.0% versus 55.9 +/- 5.4% (mean +/- SEM, p < 0.007, r = 0.73, n = 12; expressed as percentage of the hemisphere infarcted) were noted for light microscopic evaluation versus triphenyltetrazolium chloride staining, respectively. It is concluded that triphenyltetrazolium chloride staining is an acceptable method for delineating brain infarct size in this rabbit model of thromboembolic stroke. The relative ease of infarct size determination with this technique suggests its more widespread use in similar models. C1 UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. UNIV MINNESOTA,SCH MED,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. RP BEDNAR, MM (reprint author), UNIV VERMONT,VERMONT CTR VASC RES,DIV NEUROSURG,GIVEN E309,BURLINGTON,VT 05405, USA. FU NINDS NIH HHS [1-R55-NS708-01A1, 1-R29-NS31008-02] NR 16 TC 19 Z9 19 U1 0 U2 0 PU FOREFRONT PUBL GROUP PI LONDON PA MONOMARK HOUSE 27 OLD GLOUCESTER STREET, LONDON, ENGLAND WC1N 3XX SN 0161-6412 J9 NEUROL RES JI Neurol. Res. PD APR PY 1994 VL 16 IS 2 BP 129 EP 132 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NF694 UT WOS:A1994NF69400014 PM 7519330 ER PT J AU OKEN, BS KISHIYAMA, SS KAYE, JA HOWIESON, DB AF OKEN, BS KISHIYAMA, SS KAYE, JA HOWIESON, DB TI ATTENTION-DEFICIT IN ALZHEIMERS-DISEASE IS NOT SIMULATED BY AN ANTICHOLINERGIC/ANTIHISTAMINERGIC DRUG AND IS DISTINCT FROM DEFICITS IN HEALTHY AGING SO NEUROLOGY LA English DT Article; Proceedings Paper CT 45th Annual Meeting of the American-Academy-of-Neurology CY APR, 1993 CL NEW YORK, NY SP AMER ACAD NEUROL ID MINI-MENTAL-STATE; SENILE DEMENTIA; DIVIDED ATTENTION; VISUAL-ATTENTION; AGE-DIFFERENCES; HUMAN-MEMORY; TIME COURSE; SCOPOLAMINE; HYPERSENSITIVITY; SENSITIVITY AB Objective. To evaluate attention deficit in Alzheimer's disease (AD) and its relationship to attention deficits associated with aging and with medications altering alertness. Methods, Ten patients with probable AD, 10 healthy old controls, and 15 young controls performed a covert orienting of spatial attention task. Young controls performed the task an additional time after ingestion of diphenhydramine 1 mg/kg. Reaction times were obtained following valid, neutral, and invalid cues. Results. In all groups, the reaction times were shortest for the validly cued stimuli and longest for the invalidly cued stimuli. Additionally, the AD patients performed disproportionately worse following the invalid cue than did the control groups. Young controls given diphenhydramine had decreased subjective alertness, performed worse than they did before drug but better than the old controls or AD patients, and had no disproportionate impairment with the invalid cue. Conclusions, AD patients have disproportionate problems shifting spatial attention compared with age-matched controls. Impaired attentional performance in AD cannot be simulated in young subjects by ingestion of a combined antihistamine/anticholinergic agent at a dose sufficient to produce significant changes in alertness. C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP OKEN, BS (reprint author), OREGON HLTH SCI UNIV,DEPT NEUROL,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. OI Kaye, Jeffrey/0000-0002-9971-3478 FU NIA NIH HHS [1P30 AG08017, R01 AG08714] NR 58 TC 43 Z9 44 U1 1 U2 3 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1994 VL 44 IS 4 BP 657 EP 662 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA NG065 UT WOS:A1994NG06500013 PM 8164820 ER PT J AU BYLSMA, FW FOLSTEIN, MF DEVANAND, DP RICHARDS, M BELLO, J ALBERT, M STERN, Y AF BYLSMA, FW FOLSTEIN, MF DEVANAND, DP RICHARDS, M BELLO, J ALBERT, M STERN, Y TI DELUSIONS AND PATTERNS OF COGNITIVE IMPAIRMENT IN ALZHEIMERS-DISEASE SO NEUROPSYCHIATRY NEUROPSYCHOLOGY AND BEHAVIORAL NEUROLOGY LA English DT Article DE DELUSION; COGNITION; ALZHEIMERS DISEASE ID NEUROPSYCHIATRIC ASPECTS; EXTRAPYRAMIDAL SIGNS; SENILE DEMENTIA; PSYCHOSIS; PSYCHOPATHOLOGY; DEPRESSION; SCALE AB Cognitive correlates of delusions were examined in 180 probable Alzheimer's disease (AD) patients. Deluded (n = 45) and nondeluded (n = 135) AD patients were equally demented, but deluded patients had relatively preserved attention and worse confrontation naming. In an independent sample of AD patients, the finding of better attention in deluded patients was replicated but the naming difference, although in the expected direction. failed to reach significance. Preserved attention and poor naming may be important for the development of delusions in AD patients. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT NEUROL & PSYCHIAT,NEW YORK,NY 10032. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP BYLSMA, FW (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,MEYER 218,600 N WOLFE ST,BALTIMORE,MD 21205, USA. NR 37 TC 21 Z9 21 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0894-878X J9 NEUROPSY NEUROPSY BE JI Neuropsychiatr. Neuropsychol. Behav. Neurol. PD APR PY 1994 VL 7 IS 2 BP 98 EP 103 PG 6 WC Clinical Neurology; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA NJ804 UT WOS:A1994NJ80400003 ER PT J AU LEON, SP ZHU, JG BLACK, PM AF LEON, SP ZHU, JG BLACK, PM TI GENETIC ABERRATIONS IN HUMAN BRAIN-TUMORS SO NEUROSURGERY LA English DT Review DE BRAIN NEOPLASMS; CYTOGENETICS; MOLECULAR GENETICS; ONCOGENES; TUMOR SUPPRESSOR GENES ID EPIDERMAL GROWTH-FACTOR; FACTOR RECEPTOR GENE; MALIGNANT HUMAN GLIOMAS; CENTRAL-NERVOUS-SYSTEM; PRIMITIVE NEUROECTODERMAL TUMORS; POLYMERASE CHAIN-REACTION; HUMAN PITUITARY-TUMORS; HUMAN GLIOBLASTOMA-MULTIFORME; HUMAN GLIAL TUMORS; SUPPRESSOR GENES AB OVER THE LAST decade, much has been learned about the genetic changes that occur in human neoplasia and how they contribute to the neoplastic state. Oncogenes and tumor suppressor genes have been identified, and many powerful molecular genetic techniques have emerged. Brain tumors have been intensively studied as part of this process. Specific and recurring genetic alterations have been identified and are associated with specific tumor types. In astrocytomas, for example, losses of genetic material on chromosomes 10 and 17 and amplification of the epidermal growth factor receptor gene seem important in pathogenesis, with the loss of chromosome 10 and the amplification of epidermal growth factor receptor being strongly associated with glioblastoma multiforme. Meningiomas, on the other hand, have usually lost part or all of chromosome 22. Brain tumors also express growth factors and growth factor receptors that may be important in promoting tumor growth and angiogenesis. These include epidermal growth factor, transforming growth factor-alpha, platelet-derived growth factor, the fibroblast growth factors, and vascular endothelial growth factor. In this article, we review the genetic aberrations that occur in the major types of brain tumors, including glial tumors, meningiomas, acoustic neuromas, medulloblastomas, primitive neuroectodermal tumors, and pituitary tumors. Wherever possible, clinical correlations have been made concerning the prognostic and therapeutic implications of specific aberrations. We also provide some background about the cytogenetic and molecular genetic techniques that have contributed to the description and understanding of these alterations and speculate as to some clinical and basic science issues that might be explored in the future. C1 BRIGHAM & WOMENS HOSP, NEUROSURG LABS, 75 FRANCIS ST, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, CTR BRAIN TUMOR, BOSTON, MA 02115 USA. CHILDRENS HOSP MED CTR, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT SURG, BOSTON, MA 02115 USA. NR 214 TC 72 Z9 73 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD APR PY 1994 VL 34 IS 4 BP 708 EP 722 PG 15 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA NC633 UT WOS:A1994NC63300061 PM 8008171 ER PT J AU CARLSON, KJ MILLER, BA FOWLER, FJ AF CARLSON, KJ MILLER, BA FOWLER, FJ TI THE MAINE-WOMENS-HEALTH-STUDY .1. OUTCOMES OF HYSTERECTOMY SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID TOTAL ABDOMINAL HYSTERECTOMY; VAGINAL HYSTERECTOMY; UNITED-STATES AB Objective: To assess the effect of hysterectomy for nonmalignant conditions on symptoms and quality of life and to identify adverse effects 1 year after surgery. Methods: The Maine Women's Health Study was a prospective cohort study of 418 women ages 25-50 years undergoing hysterectomy for any nonmalignant condition. Patients recruited from the practices of 63 physicians performing hysterectomy throughout Maine were interviewed at the time of surgery and 3, 6, and 12 months later. Clinical and hospitalization data were obtained from physician reports and from a statewide hospital discharge data base. The primary outcomes of interest were symptom relief, changes in quality of life, and the development of new symptoms or problems during the year following surgery. Results: The most frequent indications for hysterectomy were leiomyomas (35%), abnormal bleeding (22%), and chronic pelvic pain (18%). For these indications, hysterectomy resulted in marked improvements in a range of symptoms, including pelvic pain, urinary symptoms, fatigue, psychological symptoms, and sexual dysfunction. Significant improvements in scores for indices of mental health, general health, and activity were evident at 6 months and sustained at 1 year. New problems after hysterectomy (measured in those free of the symptom preoperatively) included hot flashes (13%), weight gain (12%), depression (8%), and lack of interest in sex (7%). Conclusions: Hysterectomy is highly effective for relief of symptoms associated with common nonmalignant gynecologic conditions. Symptom relief following hysterectomy is associated with a marked improvement in quality of life. New problems are reported after hysterectomy by a limited number of women. C1 MAINE MED ASSESSMENT FDN,PORTLAND,ME. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV MASSACHUSETTS,CTR SURVEY RES,BOSTON,MA 02125. RP CARLSON, KJ (reprint author), MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,50 STANIFORD ST,9TH FLOOR,BOSTON,MA 02114, USA. FU AHRQ HHS [R01 HS06121] NR 44 TC 306 Z9 313 U1 3 U2 8 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD APR PY 1994 VL 83 IS 4 BP 556 EP 565 PG 10 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA ND231 UT WOS:A1994ND23100012 PM 8134066 ER PT J AU CARLSON, KJ MILLER, BA FOWLER, FJ AF CARLSON, KJ MILLER, BA FOWLER, FJ TI THE MAINE-WOMENS-HEALTH-STUDY .2. OUTCOMES OF NONSURGICAL MANAGEMENT OF LEIOMYOMAS, ABNORMAL BLEEDING, AND CHRONIC PELVIC PAIN SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID HYSTERECTOMY AB Objective: To assess the effect of nonsurgical management of leiomyomas, abnormal uterine bleeding, and chronic pelvic pain on symptoms and quality of life. Methods: We performed a prospective cohort study of women receiving nonsurgical management (n = 380) or hysterectomy (n = 311) for leiomyomas, abnormal uterine bleeding, or chronic pelvic pain. Patients recruited from the practices of 63 physicians throughout Maine were interviewed at the outset of treatment and 3, 6, and 12 months later. The principal outcome measures were frequency and severity of physical and psychological symptoms, and quality of life as measured by validated indices of mental and general health and physical activity. Results: Medical therapy for abnormal bleeding and chronic pelvic pain produced significant improvements in symptoms and quality of life. However, almost one-quarter of patients initially treated nonsurgically subsequently underwent hysterectomy; of patients continuing nonsurgical therapy, 25% with abnormal bleeding and 50% with chronic pelvic pain reported substantial levels of symptoms after 1 year. There were no significant changes in symptoms and quality of life in patients treated nonsurgically for leiomyomas. New problems including tiredness, hot flashes, weight gain, and depression developed in 10% or less of women who did not report these symptoms preoperatively. A logistic regression analysis controlling for age, reproductive history, and severity of symptoms showed that hysterectomy was the factor most highly correlated with a positive outcome at 1 year for all three conditions. Conclusions: Many women with leiomyomas, abnormal bleeding, and chronic pelvic pain report improved symptoms over time with nonsurgical management. Hysterectomy remains an important alternative when conservative treatment fails. C1 MAINE MED ASSESSMENT FDN,PORTLAND,ME. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV MASSACHUSETTS,CTR SURVEY RES,BOSTON,MA 02125. RP CARLSON, KJ (reprint author), MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,50 STANIFORD ST,9TH FLOOR,BOSTON,MA 02114, USA. FU AHRQ HHS [R01 HS06121] NR 10 TC 127 Z9 129 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD APR PY 1994 VL 83 IS 4 BP 566 EP 572 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA ND231 UT WOS:A1994ND23100013 PM 8134067 ER PT J AU SOPARKAR, CNS PATRINELY, JR CUAYCONG, MJ DAILEY, RA KERSTEN, RC RUBIN, PAD LINBERG, JV HOWARD, GR DONOVAN, DT MATOBA, AY HOLDS, JB AF SOPARKAR, CNS PATRINELY, JR CUAYCONG, MJ DAILEY, RA KERSTEN, RC RUBIN, PAD LINBERG, JV HOWARD, GR DONOVAN, DT MATOBA, AY HOLDS, JB TI THE SILENT SINUS - A CAUSE OF SPONTANEOUS ENOPHTHALMOS SO OPHTHALMOLOGY LA English DT Article ID MAXILLARY SINUS; OPHTHALMIC MANIFESTATIONS; MUCOCELES; ANTRUM; CYSTS AB Purpose: Spontaneous enophthalmos and hypoglobus, in the absence of other symptoms and unrelated to trauma or surgery, may be alarming to both physician and patient. The authors describe the clinicopathologic features of a benign syndrome (''silent sinus syndrome'') with this constellation of features and discuss the possible pathophysiology. Methods: A multicenter retrospective search for similar clinical cases was performed. All clinical records, computed tomographs, and pathology reports for each case were reviewed at one center. A literature search for similar cases also was conducted. Results: Nineteen cases of a new syndrome are presented. This syndrome affects individuals at approximately the fourth decade of life (average age, 36 years; range, 29-46 years); is characterized by bone resorption and remodeling of the orbital floor due to otherwise asymptomatic maxillary sinus disease; is associated with ipsilateral maxillary sinus hypoplasia; and is not fully explained by any previously described, classic cystic lesion of the maxillary antrum. Conclusion: Enophthalmos and hypoglobus unassociated with prior trauma, surgery, or other symptoms may represent ''silent sinus syndrome,'' which is ipsilateral maxillary sinus hypoplasia and orbital floor resorption. C1 BAYLOR COLL MED,CULLEN EYE INST,DEPT OPHTHALMOL,HOUSTON,TX 77030. OREGON HLTH SCI UNIV,DEPT OPHTHALMOL,PORTLAND,OR. UNIV CINCINNATI,MED CTR,DEPT OPHTHALMOL,CINCINNATI,OH 45267. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. W VIRGINIA UNIV,CTR EYE,MORGANTOWN,WV. MED UNIV S CAROLINA,STORM EYE INST,CHARLESTON,SC 29425. BAYLOR COLL MED,DEPT OTOLARYNGOL,HOUSTON,TX. ST LOUIS UNIV,MED CTR,BETHESDA EYE INST,ST LOUIS,MO. NR 21 TC 106 Z9 114 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD APR PY 1994 VL 101 IS 4 BP 772 EP 778 PG 7 WC Ophthalmology SC Ophthalmology GA NF504 UT WOS:A1994NF50400031 PM 8152774 ER PT J AU SMITH, DJ VANHOUTE, J KENT, R TAUBMAN, MA AF SMITH, DJ VANHOUTE, J KENT, R TAUBMAN, MA TI EFFECT OF ANTIBODY IN GINGIVAL CREVICULAR FLUID ON EARLY COLONIZATION OF EXPOSED ROOT SURFACES BY MUTANS-STREPTOCOCCI SO ORAL MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE IGG; GINGIVAL CREVICULAR FLUID; MUTANS-STREPTOCOCCI; ROOT CARIES ID LOCAL PASSIVE-IMMUNIZATION; DENTAL-CARIES; ORAL MICROORGANISMS; MONOCLONAL-ANTIBODIES; PURIFIED PROTEIN; ANTIGEN; SERUM; ASSOCIATION; RESPONSES; IGG AB The effect of antibody to Streptococcus mutans in gingival crevicular fluid (GCF) on the recolonization of cleaned buccal root surface sites by indigenous mutans streptococci was studied. Seven subjects (mean age=64 years) were selected from a population of 28 on the basis of the presence of appropriate sites with and without detectable immunoglobulin G (IgG) antibody in GCF to formalin-killed S. mutans and adequate levels of mutans streptococci in saliva available for root surface recolonization. Root surfaces exposed to GCF that did or did not contain antibody were then cleaned and sampled for residual plaque organisms (total cultivable flora and mutans streptococci) directly after cleaning (time 0) as well as 24 h later. One subject failed to recolonize at 24 h at any (antibody-positive or antibody-negative) experimental site. For each of the remaining 6 subjects, the mean levels of mutans streptococci (mean percentage of total flora) were lower at sites with IgG antibody to S. mutans in GCF than at antibody-negative sites in the same subject. In each of the 6 subjects, the site with the highest recolonization level was antibody-negative. Comparison based on intra-subject randomization of sites suggested diminished recolonization of mutans streptococci at sites with antibody 24 h after cleaning. The results support the idea that antibody in GCF can modify the early colonization of gingival root surface areas by potentially cariogenic plaque bacteria such as mutans streptococci. C1 FORSYTH DENT CTR,DEPT MICROBIOL,BOSTON,MA 02115. FORSYTH DENT CTR,DEPT BIOSTAT,BOSTON,MA 02115. RP SMITH, DJ (reprint author), FORSYTH DENT CTR,DEPT IMMUNOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-07009] NR 30 TC 9 Z9 11 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0055 J9 ORAL MICROBIOL IMMUN JI Oral Microbiol. Immunol. PD APR PY 1994 VL 9 IS 2 BP 65 EP 69 DI 10.1111/j.1399-302X.1994.tb00036.x PG 5 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology GA ND219 UT WOS:A1994ND21900001 PM 8008431 ER PT J AU BIELAMOWICZ, S BERKE, GS WATSON, D GERRATT, BR KREIMAN, J AF BIELAMOWICZ, S BERKE, GS WATSON, D GERRATT, BR KREIMAN, J TI EFFECTS OF RLN AND SLN STIMULATION ON GLOTTAL AREA SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID VOICE; PHONATION; FEMALE; INVIVO; LARYNX; FLOW AB In vivo canine experiments have demonstrated that vocal fold stiffness varies proportionately with changing levels of recurrent laryngeal nerve (RLN) and superior laryngeal nerve (SLN) stimulation. This study evaluated the morphologic changes in the glottis at varying levels of nerve stimulation and the presumed effects on laryngeal air particle velocity. Stroboscopic data from the in vivo canine model of phonation were examined under varying conditions of RLN and SLN stimulation. Computerized analysis of stroboscopic images was used to reconstruct the glottal area vs. time waveforms. As RLN stimulation increased, glottal area per cycle decreased (p < 0.05). However, as SLN stimulation increased, glottal area per cycle increased (p < 0.05). These results support the hypothesis that increasing RLN stimulation at similar levels of SLN stimulation produces an increase in air particle velocity, whereas an increase in SLN stimulation causes a decrease in air particle velocity. C1 UNIV CALIF LOS ANGELES,MED CTR,DIV HEAD & NECK SURG,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DIV HEAD & NECK SURG,LOS ANGELES,CA. OI Kreiman, Jody/0000-0002-5360-1729 NR 20 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 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD APR PY 1994 VL 110 IS 4 BP 370 EP 380 PG 11 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA NG807 UT WOS:A1994NG80700003 PM 8170680 ER PT J AU GOEBEL, JA HANSON, JM FISHEL, DG FURMAN, JM HAMID, MA HONRUBIA, V PETERKA, R SHEPARD, NT STOCKWELL, CW WALL, C AF GOEBEL, JA HANSON, JM FISHEL, DG FURMAN, JM HAMID, MA HONRUBIA, V PETERKA, R SHEPARD, NT STOCKWELL, CW WALL, C TI INTERLABORATORY VARIABILITY OF ROTATIONAL CHAIR TEST-RESULTS SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article AB Test-retest reliability of rotational chair testing for a single facility has previously been examined by others. The actual data analysis methods, however, have received far less attention. The variety of both hardware and software currently used theoretically may affect the results for a given subject tested at different facilities. The purposes of this study were, first, to quantify the amount of variability in the analysis of identical raw data files at multiple rotational chair testing facilities by using automated analysis; second, to evaluate the effect of operator intervention on the analysis; and third, to identify possible sources of variability. Raw data were collected from 10 normal subjects at 0.05 Hz and 0.5 Hz (50 degrees per second peak velocity). Diskettes containing raw electro-oculogram data files were then distributed to eight participating laboratories for analysis by two methods: (I) using automated analysis algorithms and (2) using the same algorithms but allowing operator intervention into the analysis. Response parameters calculated were gain and phase (re: velocity). The SD of gain values per subject for automated analysis ranged from 0.01 to 0.32 gain units and of phase values from 0.4 to 13.7 degrees. For analysis with operator intervention, the SD of gain values ranged from 0.02 to 0.10 gain units and of phase values from 0.4 to 4.4 degrees. The difference between automated analysis and analysis with operator intervention was significant for gain calculations (p < 0.02) but not for phase calculations (p > 0.05). This study demonstrates significant variability in automated analysis of rotational chair raw data for gain and phase. Operator intervention into the analysis significantly reduces variability for gain but not for phase. C1 UNIV PITTSBURGH,PITTSBURGH,PA. CLEVELAND CLIN FDN,CLEVELAND,OH 44195. UNIV CALIF LOS ANGELES,HOSP & CLIN,LOS ANGELES,CA. GOOD SAMARITAN HOSP,PORTLAND,OR. UNIV MICHIGAN,MED CTR,ANN ARBOR,MI. PROVIDENCE HOSP,GROSSE POINTE,MI. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RP GOEBEL, JA (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,VESTIBULAR & OCULOMOTOR LAB,ST LOUIS,MO 63110, USA. NR 5 TC 5 Z9 5 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD APR PY 1994 VL 110 IS 4 BP 400 EP 405 PG 6 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA NG807 UT WOS:A1994NG80700008 ER PT J AU SONG, SL BILITCH, M FURMAN, S GROSS, J FRAME, R JOHNSTON, D PARSONNET, V ROTHBART, ST ZIMMERMAN, J KAWANISHI, DT PERRY, GY HASHIMOTO, KK BUCKINGHAM, TA GOLDIN, MD STALLER, BJ DENKER, ST LIPTON, IH CASTLE, LW SHEWCHIK, JM HARTHORNE, JW RUSKIN, JN GARAN, H MCGOVERN, BA GRIFFIN, JC SCHEINMAN, MM LESH, MD DORIAN, P NEWMAN, D DENES, P DAHL, W SAKSENA, S KROL, RB FOGOROS, RN AF SONG, SL BILITCH, M FURMAN, S GROSS, J FRAME, R JOHNSTON, D PARSONNET, V ROTHBART, ST ZIMMERMAN, J KAWANISHI, DT PERRY, GY HASHIMOTO, KK BUCKINGHAM, TA GOLDIN, MD STALLER, BJ DENKER, ST LIPTON, IH CASTLE, LW SHEWCHIK, JM HARTHORNE, JW RUSKIN, JN GARAN, H MCGOVERN, BA GRIFFIN, JC SCHEINMAN, MM LESH, MD DORIAN, P NEWMAN, D DENES, P DAHL, W SAKSENA, S KROL, RB FOGOROS, RN TI PERFORMANCE OF IMPLANTABLE CARDIAC-RHYTHM MANAGEMENT DEVICES SO PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY LA English DT Article C1 MONTEFIORE MED CTR,BRONX,NY. NEWARK BETH ISRAEL MED CTR,PACEMAKER CTR INC,NEWARK,NJ. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL. ST LUKES HOSP,MILWAUKEE,WI. TORONTO HOSP,TORONTO,ON,CANADA. CLEVELAND CLIN FDN,CLEVELAND,OH. MASSACHUSETTS GEN HOSP,BOSTON,MA. UNIV CALIF SAN FRANCISCO,MOFFITT HOSP,SAN FRANCISCO,CA. ST MICHAELS HOSP,TORONTO,ON,CANADA. ST PAUL RAMSEY MED CTR,ST PAUL,MN. EASTERN HEART INST,PASSAIC,NJ. ALLEGHENY GEN HOSP,PITTSBURGH,PA 15212. RP SONG, SL (reprint author), UNIV SO CALIF,SCH MED,CTR PACEMAKER,LOS ANGELES,CA 90089, USA. NR 2 TC 31 Z9 31 U1 0 U2 2 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 0147-8389 J9 PACE JI PACE-Pacing Clin. Electrophysiol. PD APR PY 1994 VL 17 IS 4 BP 692 EP 708 DI 10.1111/j.1540-8159.1994.tb02410.x PN 1 PG 17 WC Cardiac & Cardiovascular Systems; Engineering, Biomedical SC Cardiovascular System & Cardiology; Engineering GA NG786 UT WOS:A1994NG78600019 PM 7516555 ER PT J AU POREMBA, C YANDELL, DW SPIRO, IJ HEIDL, G BOCKER, W DOCKHORNDWORNICZAK, B AF POREMBA, C YANDELL, DW SPIRO, IJ HEIDL, G BOCKER, W DOCKHORNDWORNICZAK, B TI VARIABLE NUMBER TANDEM REPEATS (VNTR) AS GENETIC-MARKERS - METHODOLOGY AND APPLICATION IN DIAGNOSTIC PATHOLOGY SO PATHOLOGE LA German DT Article DE VARIABLE NUMBER TANDEM REPEATS; MOLECULAR GENETIC MARKERS; POLYMERASE CHAIN REACTION; SINGLE STRAND CONFORMATION POLYMORPHISM ID POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDERS; RENAL-ALLOGRAFT RECIPIENT; POLYMORPHISM; LYMPHOMA; DNA AB Variable number tandem repeats (VNTR) are highly polymorphic DNA sequences which can be used as genetic markers in different fields of medicine. In this report, we describe the methodology of VNTR in diagnostic molecular pathology, using a rapid, DNA-based approach involving polymerase chain reaction (PCR) amplification and electrophoresis of highly polymorphic DNA satellite sequences. As concrete examples of the application of this approach, we present two case reports: 1. A B-cell lymphoma of the porta hepatis developed in a 54-year-old man 4.5 months after orthotopic liver transplantation for liver failure due to chronic hepatitis C infection. Using DNA polymorphisms as genetic markers, we showed that the tumor was of donor origin. This finding may be important for the patient's subsequent management. 2. An immature teratoma of the left ovary was found during delivery by cesarean section in a 27-year-old woman. The female newborn survived for 9 weeks and then died from central dysregulation because of an intracranial immature teratoma. Because the synchronous tumors were of similar histology, clonal origin in maternal tissues and metastatic spread were initially suspected. Analysis of highly polymorphic DNA markers clearly indicated that the teratoma carried by the child was of independent genetic origin from the mother's tumor. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. INST PATHOL,SIEGEN,GERMANY. RP POREMBA, C (reprint author), UNIV MUNSTER,GERHARD DOMAGK INST PATHOL,D-48149 MUNSTER,GERMANY. NR 18 TC 2 Z9 2 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0172-8113 J9 PATHOLOGE JI Pathologe PD APR PY 1994 VL 15 IS 2 BP 113 EP 118 DI 10.1007/s002920050033 PG 6 WC Pathology SC Pathology GA NF479 UT WOS:A1994NF47900006 PM 8197067 ER PT J AU SCHUNIOR, A MULLENIX, PJ ZENGEL, AE LANDY, H HOWES, A TARBELL, NJ AF SCHUNIOR, A MULLENIX, PJ ZENGEL, AE LANDY, H HOWES, A TARBELL, NJ TI RADIATION EFFECTS ON GROWTH ARE ALTERED IN RATS BY PREDNISOLONE AND METHOTREXATE SO PEDIATRIC RESEARCH LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; HORMONE-RELEASING FACTOR; LONG-TERM SURVIVORS; HEAD-IRRADIATED RAT; ACUTE LYMPHOCYTIC-LEUKEMIA; NERVOUS-SYSTEM THERAPY; CATCH-UP GROWTH; CRANIAL IRRADIATION; CHILDHOOD LEUKEMIA; SEXUAL DIMORPHISM AB CNS therapy for childhood leukemia has adverse effects upon growth and cognition. The cause of these deficits is unknown. In a rat model, we determined which agent, or combination of agents, in CNS therapy affected growth. Young Sprague-Dawley rats were exposed to cranial irradiation (1000 cGy), methotrexate (2 or 4 mg/kg, intraperitoneally), or prednisolone (18 or 36 mg/kg, intraperitoneally) alone or in two- or three-agent combinations. Matched control groups received appropriate sham radiation, intraperitoneal saline, or both. Body weight was recorded from 14 through 150 d of age. After the rats were killed at 150 d, body length was recorded and the head and left femur were removed to determine body and craniofacial proportions. Cranial irradiation alone, but not methotrexate or prednisolone alone, stunted growth permanently and altered craniofacial proportions. When these agents were combined, methotrexate and prednisolone modified the growth response to cranial irradiation. Methotrexate given before cranial irradiation prevented radiation stunting in males. This protection was lost when the dose of methotrexate was increased, when prednisolone was added to the combination, or when females were studied. The protection in males was effective against both growth and behavioral deficits. These results indicate that the physical and behavioral side effects of CNS therapy are better understood in the context of dose, sex, and interactions of the agents. C1 FORSYTH RES INST,DEPT TOXICOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT RADIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,CTR MED,DEPT ENDOCRINOL,BOSTON,MA 02115. FU NCI NIH HHS [CA53858] NR 40 TC 11 Z9 11 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP 416 EP 423 PN 1 PG 8 WC Pediatrics SC Pediatrics GA NG778 UT WOS:A1994NG77800006 PM 8047378 ER PT J AU ANAND, KJS CLANCY, GT AF ANAND, KJS CLANCY, GT TI CREATING A PROSPECTIVE DATABASE FOR NEONATAL ANALGESIC PRACTICES - PRELIMINARY-RESULTS FROM EARLY RESPONDERS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 EMORY UNIV,SCH MED,ATLANTA,GA 30322. EMORY UNIV,EGLESTON CHILDRENS HOSP,ATLANTA,GA 30322. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A212 EP A212 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901252 ER PT J AU BABA, TW KOCH, JA GREENE, MF WYAND, MS PENNINCK, D RUPRECHT, RM AF BABA, TW KOCH, JA GREENE, MF WYAND, MS PENNINCK, D RUPRECHT, RM TI ORAL INFECTION OF NEONATAL RHESUS-MONKEYS WITH CELL-FREE SIMIAN IMMUNODEFICIENCY VIRUS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,JOINT PROGRAM NEONATOL,BOSTON,MA 02115. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A293 EP A293 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901738 ER PT J AU BERGELSON, JM STJOHN, N FINBERG, RW AF BERGELSON, JM STJOHN, N FINBERG, RW TI ECHOVIRUS-1 AND EXTRACELLULAR-MATRIX PROTEINS BIND TO THE I-DOMAIN OF THE INTEGRIN VLA-2 SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A174 EP A174 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901027 ER PT J AU JUBINSKY, P LAURIE, A SHIKAMA, Y NATHAN, D SIEFF, C AF JUBINSKY, P LAURIE, A SHIKAMA, Y NATHAN, D SIEFF, C TI FUNCTIONAL MONOCLONAL-ANTIBODIES AGAINST THE HUMAN GM-CSF RECEPTOR ALPHA-SUBUNIT SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A162 EP A162 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900959 ER PT J AU JUNG, FF PROVOOST, AP BOUYOUNES, B INGELFINGER, JR AF JUNG, FF PROVOOST, AP BOUYOUNES, B INGELFINGER, JR TI UP-REGULATION OF THE CIRCULATING AND INTRARENAL RENIN-ANGIOTENSIN SYSTEM IN THE YOUNG FAWN-HOODED (FH) RAT SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ERASMUS UNIV ROTTERDAM,3000 DR ROTTERDAM,NETHERLANDS. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A274 EP A274 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901628 ER PT J AU MOLRINE, D GEORGE, S TARBELL, N MAUCH, P DILLER, L NEUBERG, D SHAMBERGER, R ANDERSON, E PHILLIPS, N KINSELLA, K AMBROSINO, D AF MOLRINE, D GEORGE, S TARBELL, N MAUCH, P DILLER, L NEUBERG, D SHAMBERGER, R ANDERSON, E PHILLIPS, N KINSELLA, K AMBROSINO, D TI ANTIBODY-RESPONSE TO POLYSACCHARIDE (PS)-CONJUGATE VACCINES FOLLOWING TREATMENT FOR HODGKINS-DISEASE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. ST LOUIS UNIV,MED CTR,ST LOUIS,MO 63103. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A189 EP A189 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901114 ER PT J AU MOLRINE, DC GUINAN, EC PARSONS, SK WEINSTEIN, HJ ANTIN, JH WHEELER, C PHILLIPS, NR KINSELLA, K DEANS, K GEORGE, S AMBROSINO, DM AF MOLRINE, DC GUINAN, EC PARSONS, SK WEINSTEIN, HJ ANTIN, JH WHEELER, C PHILLIPS, NR KINSELLA, K DEANS, K GEORGE, S AMBROSINO, DM TI ANTIBODY-RESPONSES TO MULTIPLE DOSES OF A POLYSACCHARIDE (PS)-CONJUGATE VACCINE POST BONE-MARROW TRANSPLANTATION SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A189 EP A189 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901115 ER PT J AU SIBER, GR THOMPSON, C DHALLA, M CROLL, L CROLL, J GLEZEN, WP SANTOSHAM, M AF SIBER, GR THOMPSON, C DHALLA, M CROLL, L CROLL, J GLEZEN, WP SANTOSHAM, M TI MATERNAL IMMUNIZATION WITH HAEMOPHILUS-INFLUENZAE TYPE-B (HIB) VACCINES BEFORE PREGNANCY SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 IHS,MATERNAL IMMUNIZAT GRP,SACATOR,AZ. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BAYLOR COLL MED,HOUSTON,TX 77030. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A196 EP A196 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901159 ER PT J AU SUARA, RO MULHOLLAND, KE GLEZEN, WP NJIE, J SIBER, GR ANWARUDDIN, R THOMPSON, C DIANAN, L ROBERTON, D GREENWOOD, BM AF SUARA, RO MULHOLLAND, KE GLEZEN, WP NJIE, J SIBER, GR ANWARUDDIN, R THOMPSON, C DIANAN, L ROBERTON, D GREENWOOD, BM TI MATERNAL IMMUNIZATION WITH HAEMOPHILUS-INFLUENZAE TYPE-B PRP-T CONJUGATE VACCINE IN THE GAMBIA, WEST-AFRICA SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 BAYLOR COLL MED,HOUSTON,TX 77030. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. ADELAIDE CHILDRENS HOSP INC,ADELAIDE,SA 5006,AUSTRALIA. MRC LABS,BANTUL,GAMBIA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A122 EP A122 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900718 ER PT J AU VELINOY, M SLAUGENHAUPT, S STOILOV, I SCOTT, C GUSELLA, J TSIPOURAS, P AF VELINOY, M SLAUGENHAUPT, S STOILOV, I SCOTT, C GUSELLA, J TSIPOURAS, P TI THE ACHONDROPLASIA GENE MAPS TO THE TELOMERIC REGION OF CHROMOSOME-4P SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV CONNECTICUT,CTR HLTH,DEPT PEDIAT,FARMINGTON,CT 06032. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. ALFRED I DUPONT INST,DIV MOLEC GENET,WILMINGTON,DE 19899. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A155 EP A155 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900912 ER PT J AU WHARTON, R LEVINE, K BUKA, S PERRIN, J AF WHARTON, R LEVINE, K BUKA, S PERRIN, J TI PARENTAL WISHES REGARDING PARTICIPATION IN CRITICAL HEALTH-CARE PLANNING FOR CHILDREN WITH DISABILITIES SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. CHILDRENS SERV,BOSTON,MA. RI Buka, Stephen/H-7335-2014 OI Buka, Stephen/0000-0002-8578-9308 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A47 EP A47 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900269 ER PT J AU ZHENG, QJ RHOADS, DB MINK, K OSATHANONDH, R LEVITSKY, LL AF ZHENG, QJ RHOADS, DB MINK, K OSATHANONDH, R LEVITSKY, LL TI GLUCOSE-TRANSPORTER 1 (GLUT1) AND 2 (GLUT2) MESSENGER-RNAS ARE NOT REGULATED BY GLUCOSE IN HUMAN FETAL HEPATOCYTES (HFH) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CHILDRENS SERV & LAB TUMOR BIOL,GL UNIT & CANCER CTR,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT OBSTET GYNECOL & REPROD BIOL,BOSTON,MA 02115. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A210 EP A210 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901240 ER PT J AU HALL, CB GRANOFF, DM GROMISCH, DS HALSEY, NA KOHL, S MARCUSE, EK MARKS, MI NANKERVIS, GA PICKERING, LK SCOTT, GB STEELE, RW YOGEV, R PETER, G BART, KJ BROOME, C HARDEGREE, MC JACOBS, RF MACDONALD, NE ORENSTEIN, WA RABINOVICH, NR SIBER, G FINLAYSON, J WATSON, JC AF HALL, CB GRANOFF, DM GROMISCH, DS HALSEY, NA KOHL, S MARCUSE, EK MARKS, MI NANKERVIS, GA PICKERING, LK SCOTT, GB STEELE, RW YOGEV, R PETER, G BART, KJ BROOME, C HARDEGREE, MC JACOBS, RF MACDONALD, NE ORENSTEIN, WA RABINOVICH, NR SIBER, G FINLAYSON, J WATSON, JC TI RECOMMENDED TIMING OF ROUTINE MEASLES IMMUNIZATION FOR CHILDREN WHO HAVE RECENTLY RECEIVED IMMUNE GLOBULIN PREPARATIONS SO PEDIATRICS LA English DT Article ID ANTIBODY-RESPONSE; VACCINE; POLIOVIRUS; EFFICACY; INFANTS C1 CANADIAN PAEDIAT SOC,OTTAWA,ON,CANADA. AMER ACAD PEDIAT,COMM INFECT DIS,EVANSTON,IL 60204. CTR DIS CONTROL & PREVENT,ATLANTA,GA. US FDA,BETHESDA,MD 20014. AMER THORAC SOC,NEW YORK,NY. NIH,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 17 TC 5 Z9 6 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD APR PY 1994 VL 93 IS 4 BP 682 EP 685 PG 4 WC Pediatrics SC Pediatrics GA ND363 UT WOS:A1994ND36300030 ER PT J AU HERBERT, V AF HERBERT, V TI FOLATE SUPPLEMENTS SHOULD BE APPROPRIATELY LABELED TO PROTECT CONSUMERS SO PEDIATRICS LA English DT Letter C1 BRONX VET AFFAIRS MED CTR,BRONX,NY 10468. RP HERBERT, V (reprint author), MT SINAI MED CTR,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 3 TC 3 Z9 3 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD APR PY 1994 VL 93 IS 4 BP 694 EP 695 PG 2 WC Pediatrics SC Pediatrics GA ND363 UT WOS:A1994ND36300037 PM 8155182 ER PT J AU VITKIN, IA WOOLSEY, J WILSON, BC ANDERSON, RR AF VITKIN, IA WOOLSEY, J WILSON, BC ANDERSON, RR TI OPTICAL AND THERMAL CHARACTERIZATION OF NATURAL (SEPIA-OFFICINALIS) MELANIN SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID PULSED PHOTOTHERMAL RADIOMETRY; DIFFUSIVITY; ABSORBER; SPECTRUM AB The optical properties and the thermal diffusivity of natural cuttlefish (Sepia officinalis) melanin have been measured. The optical absorption and scattering properties of melanin particles were determined at 580 nm and 633 nm, using photometric and photothermal techniques. For the photometric studies, the absorption and the transport scattering coefficients were determined from the measurements of diffuse reflectance and transmittance. The scattering anisotropy was obtained from an additional measurement of the total attenuation coefficient and independently obtained by goniometry. For photothermal studies, pulsed photothermal radiometry was used to deduce the absorption and transport scattering coefficients via a model based on optical diffusion theory. Pulsed photothermal radiometry was also used to provide the thermal diffusivity of solid melanin pressed pellets. C1 MCMASTER UNIV, DEPT PHYS, HAMILTON L8V 1C3, ON, CANADA. PRINCESS MARGARET HOSP, ONTARIO CANC INST, DEPT CLIN PHYS, TORONTO M4X 1K9, ON, CANADA. MASSACHUSETTS GEN HOSP, WELLMAN LABS PHOTOMED, BOSTON, MA 02114 USA. RP VITKIN, IA (reprint author), HAMILTON REG CANC CTR, 699 CONCESS ST, HAMILTON L8V 1C3, ON, CANADA. RI Vitkin, Alex/I-8166-2012 FU NIAMS NIH HHS [AR-25395] NR 25 TC 70 Z9 72 U1 0 U2 11 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0031-8655 EI 1751-1097 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD APR PY 1994 VL 59 IS 4 BP 455 EP 462 DI 10.1111/j.1751-1097.1994.tb05064.x PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NK213 UT WOS:A1994NK21300012 PM 8022888 ER PT J AU TAKAHASHI, LK AF TAKAHASHI, LK TI STIMULUS-CONTROL OF BEHAVIORAL-INHIBITION IN THE PREWEANLING RAT SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE PREWEANLING RATS; BEHAVIORAL INHIBITION; ULTRASONIC VOCALIZATION; FREEZING; DEVELOPMENT; CONSPECIFIC THREAT; SOCIAL ISOLATION; CONSPECIFIC ODORS ID OLFACTORY CUES; ANTIPREDATOR BEHAVIOR; DEFENSIVE BEHAVIORS; ALARM CALLS; RESPONSES; PREDATOR; VOCALIZATIONS; FLOCKS; RECOGNITION; NORVEGICUS AB Previous studies demonstrate that 14-day-old rats reduce their emission of ultrasonic vocalizations and freeze when exposed to an unfamiliar adult male rat. This study sought to identify the stimulus characteristics of conspecific males that potentiate the display of behavioral inhibition. In Experiment 1, day 14 rats were isolated from the nest and exposed to either an unfamiliar prepubescent male rat or an unfamiliar adult male rat. Pups exposed to the unfamiliar adult male rat exhibited significantly elevated levels of freezing and reduced their emission of ultrasounds. In Experiment 2, pups were exposed to either a familiar or an unfamiliar adult male rat. Although several pups exposed to the familiar adult male rat exhibited freezing, pups tested with the unfamiliar adult rat showed a reliably higher duration of freezing and made fewer vocalizations. Results suggest that neither the unfamiliar factor nor cues associated with male adulthood are sufficient to account for the occurrence of behavioral inhibition when presented separately. However, the combination of unfamiliarity and adult male stimuli are highly potent stimulus features that elicit behavioral inhibition in preweanling rats. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53792. RP TAKAHASHI, LK (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIMH NIH HHS [NIMH MH-43986] NR 49 TC 36 Z9 36 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD APR PY 1994 VL 55 IS 4 BP 717 EP 721 DI 10.1016/0031-9384(94)90050-7 PG 5 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA NA800 UT WOS:A1994NA80000018 PM 8190800 ER PT J AU CHEN, NT GLOWACKI, J BUCKY, LP HONG, HZ KIM, WK YAREMCHUK, MJ AF CHEN, NT GLOWACKI, J BUCKY, LP HONG, HZ KIM, WK YAREMCHUK, MJ TI THE ROLES OF REVASCULARIZATION AND RESORPTION ON ENDURANCE OF CRANIOFACIAL ONLAY BONE-GRAFTS IN THE RABBIT SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID FIXATION AB A total of 32 New Zealand white rabbits underwent subperiosteal implantation of fresh autogenous unicortical calvarial and iliac crest grafts on their snouts with microscrew rigid fixation. After 3 and 10 days, vascularity was assessed by latex casting, and osteoclastic activity was determined by histochemical staining for tartrate-resistant acid phosphatase. After 10 days, volumetric analysis and tartrate-resistant acid phosphatase staining were performed on six animals. The calvarial grafts demonstrated greater volume maintenance than the iliac bone (72 percent versus 32 percent, p < 0.025). There were significantly greater osteoclastic activity and revascularization in the cancellous portion of calvarial and iliac crest bone grafts by the 1Oth day of onlay grafting. Minimal activities were present at the cortical bone. Because calvarial grafts contain more cortical bone, its superior volume maintenance can be understood by the architectural influence on revascularization and resorption. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV PLAST & RECONSTRUCT SURG,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 11 TC 83 Z9 84 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD APR PY 1994 VL 93 IS 4 BP 714 EP 722 DI 10.1097/00006534-199404000-00009 PG 9 WC Surgery SC Surgery GA NA964 UT WOS:A1994NA96400009 PM 7510892 ER PT J AU FIALA, TGS PAIGE, KT DAVIS, TL CAMPBELL, TA ROSEN, BR YAREMCHUK, MJ AF FIALA, TGS PAIGE, KT DAVIS, TL CAMPBELL, TA ROSEN, BR YAREMCHUK, MJ TI COMPARISON OF ARTIFACT FROM CRANIOMAXILLOFACIAL INTERNAL-FIXATION DEVICES - MAGNETIC-RESONANCE-IMAGING SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID METALLIC IMPLANTS; POTENTIAL HAZARDS; MR; SAFETY; STENTS; FIELDS AB This study compares artifact from craniomaxillofacial internal fixation devices in magnetic resonance images and examines heating and magnetic deflection effects on these devices. Stainless steel wires, microfixation plates of vitallium and titanium, and minifixation and mandibular reconstruction plates of stainless steel, vitallium, and titanium were evaluated. The plates were mounted on a dry skull and submerged in dilute copper sulfate solution. All images were obtained in duplicate by two independent, nonblinded teams of observers with a 1.5-T Signa magnetic resonance system. Each team ranked artifact size for each material by computerized measurement. The rank order of artifact size for each material within each fixation system group and between fixation groups was identical between the two teams. Bath and plate temperatures were recorded before and after imaging. Artifact production was related to hardware size and composition. Titanium hardware caused the least amount of ''blackhole'' artifact. Vitallium and stainless steel fixation devices of similar size produced significantly more artifact. No significant heating or magnetic deflection effects were seen with any of the fixation devices. C1 MASSACHUSETTS GEN HOSP,WANG AMBULATORY CARE CTR,DEPT SURG,DIV PLAST SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,BOSTON,MA. NR 17 TC 37 Z9 38 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD APR PY 1994 VL 93 IS 4 BP 725 EP 731 DI 10.1097/00006534-199404000-00011 PG 7 WC Surgery SC Surgery GA NA964 UT WOS:A1994NA96400011 PM 8134430 ER PT J AU VEDDER, NB BUCKY, LP RICHEY, NL WINN, RK MAY, JW AF VEDDER, NB BUCKY, LP RICHEY, NL WINN, RK MAY, JW TI IMPROVED SURVIVAL RATES OF RANDOM FLAPS IN RABBITS WITH A MONOCLONAL-ANTIBODY THAT BLOCKS LEUKOCYTE ADHERENCE SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID OXYGEN-FREE-RADICALS; NO-REFLOW PHENOMENON; ISLAND SKIN FLAPS; PENTOXIFYLLINE; INJURY; GLYCOPROTEIN; REPERFUSION; INHIBITION; FAILURE; SHOCK AB To examine the role of neutrophil adhesiveness in the tissue injury involving the ischemic ''at risk'' area of random flaps, we used the monoclonal antibody 60.3, which binds selectively to the primary neutrophil adherence-mediating glycoprotein CD18 in a random cutaneous flap model. Control animals that had flaps elevated and replaced (n = 12) had a mean distal necrosis of 31.9 +/- 9.3 percent of the total flap surface area. Treatment with monoclonal antibody 60.3 (n = 12) reduced distal necrosis to 10.6 +/-7.5 percent (p < 0.005). Inhibiting inosculation by interposing a thin silicone sheet decreased distal flap survival; however, the protective effect of monoclonal antibody 60.3 on improving flap survival was unchanged. Control isolated flaps (n = 13) had a mean distal necrosis of 49.0 +/- 15. 5 percent compared with 22.2 +/- 5.6 percent for the antibody-treated (n = 8) isolated flaps (p < 0.05). We conclude that increased neutrophil adhesiveness plays an important role in the tissue injury involving the ischemic ''at risk'' area of random flaps and that transient, specific inhibition of leukocyte adherence by monoclonal antibody 60.3 improves the distal survival of random flaps in this model. Moreover, we conclude that ''graft inosculation'' contributes to ''flap'' survival in this model; however, conclusions regarding the effect of treatment are not altered by blocking inosculation. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV PLAST SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,DIV PLAST SURG,BOSTON,MA 02115. RP VEDDER, NB (reprint author), UNIV WASHINGTON,HARBORVIEW MED CTR,DEPT SURG,DIV PLAST SURG,ZA-16,SEATTLE,WA 98104, USA. FU NCRR NIH HHS [RR05432]; NIGMS NIH HHS [GM42686] NR 27 TC 38 Z9 40 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD APR PY 1994 VL 93 IS 5 BP 1035 EP 1040 DI 10.1097/00006534-199404001-00020 PG 6 WC Surgery SC Surgery GA ND658 UT WOS:A1994ND65800020 PM 7907798 ER PT J AU LESLIE, CA DUBEY, DP AF LESLIE, CA DUBEY, DP TI INCREASED PGE2 FROM HUMAN MONOCYTES ISOLATED IN THE LUTEAL-PHASE OF THE MENSTRUAL-CYCLE - IMPLICATIONS FOR IMMUNITY SO PROSTAGLANDINS LA English DT Correction, Addition ID SYSTEMIC LUPUS-ERYTHEMATOSUS; SYNTHASE CYCLOOXYGENASE; MONOCLONAL-ANTIBODIES; GONADAL-STEROIDS; CANDIDA-ALBICANS; MESSENGER-RNA; CELL-ACTIVITY; PROSTAGLANDINS; PROGESTERONE; MACROPHAGES AB The reproductive hormones are implicated in the well documented sexual dimorphism in cellular and immune responses. Prostaglandins (PGs) are mediators of the immune response with their concentration and relative amounts being pivotal to their impact. In resident peritoneal macrophages isolated from mice we had previously noted that the cells from females synthesized significantly more PG than males. In these experiments we investigated whether PG metabolism in the human monocyte was influenced by gender and by stage of the menstrual cycle, Monocytes isolated from the female and activated in vitro with LPS produced on average significantly more PG into the medium than the males. Among females, significantly more PG was found in the medium from cells isolated during the luteal phase of the cycle than during the early follicular phase. It was also in this luteal phase in which the female differed substantially from males. We suggest that the in vivo hormonal changes associated with the menstrual cycle modulate monocyte synthesis of PG and other immune modulators such as interleukin-1 (lL-1). This could be a key to understanding differences in vulnerability between males and females as well as within phases of the cycle, to immune and inflammatory insult. C1 BOSTON UNIV,SCH MED,DEPT BIOCHEM,BOSTON,MA 02118. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA 02115. RP LESLIE, CA (reprint author), EDITH NOURSE ROGERS MEM VET ADM HOSP,200 SPRINGS RD,BEDFORD,MA 01730, USA. NR 47 TC 1 Z9 1 U1 1 U2 1 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0090-6980 J9 PROSTAGLANDINS JI Prostaglandins PD APR PY 1994 VL 47 IS 4 BP 267 EP 280 DI 10.1016/0090-6980(94)90022-1 PG 14 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NG611 UT WOS:A1994NG61100001 ER PT J AU ABE, K KAKIUCHI, M SHIMADA, Y AF ABE, K KAKIUCHI, M SHIMADA, Y TI EPIDURAL BLOOD-FLOW DURING PROSTAGLANDIN-E(1) OR TRIMETHAPHAN INDUCED HYPOTENSION SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID SPINAL-CORD; ANESTHESIA; FUSION AB To evaluate the effect of prostaglandin E1 (PGE1) or trimethaphan (TMP) induced hypotension on epidural blood flow (EBF) during spinal surgery, EBF was measured using the heat clearance method in 30 patients who underwent postero-lateral interbody fusion under isoflurane anaesthesia. An initial dose of 0.1 mug.kg-1.min-1 of PGE1 (15 patients), or 10 mug.kg-1.min-1 of TMP (15 patients) was administered intravenously after the dural opening and the dose was adjusted to maintain the mean arterial blood pressure (MAP) at about 60 mmHg. The hypotensive drug was discontinued at the completion of the operative procedure. After starting PGE1 or TMP, MAP and rate pressure product (RPP) decreased significantly compared with preinfusion values (P < 0.01), and the degree of hypotension due to PGE1 remained constant until 60 min after its discontinuation. Heart rate (HR) did not change in either group. EBF did not change during PGE1 infusion whereas in the TMP group, EBF decreased significantly at 30 min and 60 min after the start of TMP (preinfusion: 45.9 +/- 13.9 ml/100 g/min. 30 min: 32.3 +/- 9.9 ml/100 g/min (P < 0.05). 60 min: 30 +/-7.5 ml/100 g/min (P < 0.05). These results suggest that PGE1 may be preferable to TMP for hypotensive anaesthesia in spinal surgery because TMP decreased EBF. C1 NAGOYA UNIV,SCH MED,DEPT ANAESTHESIA,NAGOYA,AICHI 466,JAPAN. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. RP ABE, K (reprint author), NAGOYA UNIV,SCH MED,OSAKA POLICE HOSP,DEPT ANAESTHESIA & ORTHOPAED SURG,NAGOYA,AICHI 466,JAPAN. NR 23 TC 2 Z9 2 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0952-3278 J9 PROSTAG LEUKOTR ESS JI Prostaglandins Leukot. Essent. Fatty Acids PD APR PY 1994 VL 50 IS 4 BP 199 EP 202 DI 10.1016/0952-3278(94)90145-7 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA ND783 UT WOS:A1994ND78300008 PM 8022855 ER PT J AU ARONEN, HJ GAZIT, IE LOUIS, DN BUCHBINDER, BR PARDO, FS WEISSKOFF, RM HARSH, GR COSGROVE, GR HALPERN, EF HOCHBERG, FH ROSEN, BR AF ARONEN, HJ GAZIT, IE LOUIS, DN BUCHBINDER, BR PARDO, FS WEISSKOFF, RM HARSH, GR COSGROVE, GR HALPERN, EF HOCHBERG, FH ROSEN, BR TI CEREBRAL BLOOD-VOLUME MAPS OF GLIOMAS - COMPARISON WITH TUMOR GRADE AND HISTOLOGIC-FINDINGS SO RADIOLOGY LA English DT Article DE BRAIN NEOPLASMS; MAGNETIC RESONANCE (MR), ECHO PLANAR; MAGNETIC RESONANCE (MR), VASCULAR STUDIES; MAGNETIC RESONANCE (MR), VOLUME MEASUREMENT ID POSITRON EMISSION TOMOGRAPHY; BRAIN-TUMORS; GD-DTPA; CONTRAST; MR; SUSCEPTIBILITY; ASTROCYTOMAS; FLOW; NMR; ANGIOGENESIS AB PURPOSE: To assess the utility of magnetic resonance (MR) cerebral blood volume (CBV) maps in the evaluation of gliomas. MATERIALS AND METHODS: CBV maps from 19 patients with histologically proved gliomas were calculated from dynamic MR image sets acquired with echo-planar spin-echo imaging after intravenous injection of gadolinium-based contrast material. RESULTS: The maximum CBV varied from 0.82 to 5.40 in the high-grade group (n = 13) and from 1.01 to 1.21 in the low-grade group (n = 6). The difference was statistically significant. Maximum CBV was associated with mitotic activity and vascularity, but not with cellular atypia, endothelial proliferation, necrosis, or cellularity. CONCLUSION: MR CBV maps provided diagnostic information not available with conventional MR imaging in six cases and offers a functional parameter for assessing glioma grade and regions of focal activity. C1 MASSACHUSETTS GEN HOSP,MGH NMR CTR,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,MGN NMR CTR,DEPT RADIOTHERAPY,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,MGH NMR CTR,DEPT NEUROSURG,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,MGH NMR CTR,DEPT NEUROL,BOSTON,MA 02129. RP ARONEN, HJ (reprint author), MASSACHUSETTS GEN HOSP,MGH NMR CTR,DEPT RADIOL,BOSTON,MA 02129, USA. FU NCI NIH HHS [P01-CA48729, R01-CA40303]; NHLBI NIH HHS [R01-HL39810] NR 46 TC 609 Z9 647 U1 1 U2 17 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD APR PY 1994 VL 191 IS 1 BP 41 EP 51 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NB685 UT WOS:A1994NB68500009 PM 8134596 ER PT J AU BOLAND, GW LEE, MJ CATS, AM GAA, JA SAINI, S MUELLER, PR AF BOLAND, GW LEE, MJ CATS, AM GAA, JA SAINI, S MUELLER, PR TI ANTIBIOTIC-INDUCED DIARRHEA - SPECIFICITY OF ABDOMINAL CT FOR THE DIAGNOSIS OF CLOSTRIDIUM-DIFFICILE DISEASE SO RADIOLOGY LA English DT Article DE ANTIBIOTICS; COLITIS, PSEUDOMEMBRANOUS; COLON, DISEASES ID PSEUDO-MEMBRANOUS COLITIS; PSEUDOMEMBRANOUS COLITIS AB PURPOSE: To evaluate the specificity of abdominal computed tomography (CT) in the diagnosis of Clostridium difficile disease. MATERIALS AND METHODS: The authors retrospectively reviewed CT scans of 64 patients with C difficile disease and 30 control subjects with diarrhea and negative findings for C difficile disease at stool tests. RESULTS: Colon wall thickening (range, 4-22 mm; mean, 11.7 mm; median, 11 mm) was seen in 39 patients (61%) with C difficile disease. Other findings included focal colon wall thickening (n = 28) and pancolonic thickening (n = 11). Two patients had only right-sided and transverse colon involvement. CT-specific diagnostic features of C difficile disease, such as nodular haustral thickening or the accordion pattern, were present in 17% of patients. No colonic abnormality was detected in 25 patients (39%). Seven of the 30 (23%) control subjects had colon wall thickening. Six of those seven subjects were subsequently determined to have ischemic colitis. The sensitivity of CT in the detection of colon abnormalities in patients with C difficile disease was 85%, and the specificity was 48%. CONCLUSION: Specific CT features of C difficile disease are uncommon. A considerable number of patients (39%) with C difficile disease have normal abdominal CT scans. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 12 TC 45 Z9 46 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 APR PY 1994 VL 191 IS 1 BP 103 EP 106 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NB685 UT WOS:A1994NB68500020 PM 8134552 ER PT J AU PRINCE, MR AF PRINCE, MR TI GADOLINIUM-ENHANCED MR AORTOGRAPHY SO RADIOLOGY LA English DT Article DE AORTA, MR; MAGNETIC RESONANCE (MR), CONTRAST ENHANCEMENT; MAGNETIC RESONANCE (MR), VASCULAR STUDIES ID GADOPENTETATE DIMEGLUMINE; ARTERY STENOSIS; ANGIOGRAPHY; CONTRAST; BRAIN AB PURPOSE: To evaluate the potential for preferential arterial enhancement at magnetic resonance (MR) aortography with an intravenous infusion of paramagnetic contrast material. MATERIALS AND METHODS: Gadolinium chelates were administered intravenously (0.2 mmol/kg) during three-dimensional MR imaging (1.5 T) in 125 patients (77 male and 48 female patients, aged 4-86 years [mean, 66 years]) with suspected aorta or aortic branch vessel disease. RESULTS: Infusion for the duration of the MR acquisition resulted in significant preferential arterial enhancement without the confounding effects of excessive venous or background-tissue enhancement (P < 10(-5)). Angiographic or surgical correlation in 48 patients revealed an 88% sensitivity and a 97% specificity for detection of stenoses or occlusions and a 100% sensitivity and a 100% specificity for detection of aortic or iliac artery aneurysms. CONCLUSION: Preferential arterial enhancement is possible at MR aortography with an intravenous infusion of paramagnetic contrast material. C1 UNIV MICHIGAN HOSP,DEPT RADIOL,ANN ARBOR,MI 48109. RP PRINCE, MR (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114, USA. RI Prince, Martin/S-6850-2016 FU NHLBI NIH HHS [HL46384] NR 26 TC 650 Z9 660 U1 0 U2 11 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD APR PY 1994 VL 191 IS 1 BP 155 EP 164 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NB685 UT WOS:A1994NB68500031 PM 8134563 ER PT J AU HUNCHAREK, M AF HUNCHAREK, M TI PLEURAL MESOTHELIOMA IN A CIGARETTE FILTER FACTORY-WORKER SO SCANDINAVIAN JOURNAL OF WORK ENVIRONMENT & HEALTH LA English DT Note DE ASBESTOS; CROCIDOLITE; MESOTHELIOMA ID EPIDEMIOLOGY; RISK AB The incidence of pleural mesothelioma is increasing. Over the past two decades many new occupational and nonoccupational risk groups have been identified. This paper reports a case of pleural mesothelioma in an office worker employed in a cigarette filter factory. Both secondary occupational and domestic asbestos exposure may have occurred. Only one prior report describes the potential asbestos health risks of this occupational group. RP HUNCHAREK, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 7 TC 1 Z9 1 U1 1 U2 1 PU SCAND J WORK ENV HEALTH PI HELSINKI PA TOPELIUKSENKATU 41A, SF-00250 HELSINKI, FINLAND SN 0355-3140 J9 SCAND J WORK ENV HEA JI Scand. J. Work Environ. Health PD APR PY 1994 VL 20 IS 2 BP 146 EP 147 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NL141 UT WOS:A1994NL14100011 PM 8079137 ER PT J AU GARNICK, MB AF GARNICK, MB TI THE DILEMMAS OF PROSTATE-CANCER SO SCIENTIFIC AMERICAN LA English DT Article C1 GENET INST INC,CLIN DEV,CAMBRIDGE,MA. RP GARNICK, MB (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CAMBRIDGE,MA 02138, USA. NR 6 TC 32 Z9 32 U1 0 U2 0 PU SCI AMERICAN INC PI NEW YORK PA 415 MADISON AVE, NEW YORK, NY 10017 SN 0036-8733 J9 SCI AM JI Sci.Am. PD APR PY 1994 VL 270 IS 4 BP 72 EP & PG 0 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NB548 UT WOS:A1994NB54800018 PM 8178117 ER PT J AU FISCHMAN, AJ BABICH, JW RUBIN, RH AF FISCHMAN, AJ BABICH, JW RUBIN, RH TI INFECTION IMAGING WITH TC-99M-LABELED CHEMOTACTIC PEPTIDE ANALOGS SO SEMINARS IN NUCLEAR MEDICINE LA English DT Article ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; BACTERIAL-INFECTION; FOCAL SITES; POLYCLONAL IGG; RECEPTOR; NEUTROPHILS; CHEMOATTRACTANTS; INFLAMMATION; LESIONS; RABBIT C1 MASSACHUSETTS GEN HOSP,MED SERV,CLIN INVEST PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 43 TC 59 Z9 60 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0001-2998 J9 SEMIN NUCL MED JI Semin. Nucl. Med. PD APR PY 1994 VL 24 IS 2 BP 154 EP 168 DI 10.1016/S0001-2998(05)80229-6 PG 15 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NF843 UT WOS:A1994NF84300007 PM 8023171 ER PT J AU RUBIN, RH FISCHMAN, AJ AF RUBIN, RH FISCHMAN, AJ TI THE USE OF RADIOLABELED NONSPECIFIC IMMUNOGLOBULIN IN THE DETECTION OF FOCAL INFLAMMATION SO SEMINARS IN NUCLEAR MEDICINE LA English DT Article ID INTRA-ABDOMINAL ABSCESSES; MONOCLONAL ANTIGRANULOCYTE ANTIBODY; POLYCLONAL HUMAN-IMMUNOGLOBULIN; VASCULAR GRAFT INFECTION; COMPUTED-TOMOGRAPHY; LEUKOCYTE SCINTIGRAPHY; IN-111; DIAGNOSIS; IGG; SITES C1 MASSACHUSETTS GEN HOSP,HARVARD MIT DIV HLTH SCI & TECHNOL,CTR EXPTL PHARMACOL & THERAPEUT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. NR 44 TC 31 Z9 31 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0001-2998 J9 SEMIN NUCL MED JI Semin. Nucl. Med. PD APR PY 1994 VL 24 IS 2 BP 169 EP 179 DI 10.1016/S0001-2998(05)80230-2 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NF843 UT WOS:A1994NF84300008 PM 8023172 ER PT J AU MOSKOWITZ, MA DALKARA, T AF MOSKOWITZ, MA DALKARA, T TI NITRIC-OXIDE SYNTHASE INHIBITION REDUCES CAUDATE INJURY FOLLOWING TRANSIENT FOCAL ISCHEMIA IN CATS SO STROKE LA English DT Article RP MOSKOWITZ, MA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114, USA. NR 2 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 APR PY 1994 VL 25 IS 4 BP 885 EP 885 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA ND342 UT WOS:A1994ND34200027 ER PT J AU BADIMON, JJ WENG, D CHESEBRO, JH FUSTER, V BADIMON, L AF BADIMON, JJ WENG, D CHESEBRO, JH FUSTER, V BADIMON, L TI PLATELET DEPOSITION INDUCED BY SEVERELY DAMAGED VESSEL WALL IS INHIBITED BY A BOROARGININE SYNTHETIC PEPTIDE WITH ANTITHROMBIN ACTIVITY SO THROMBOSIS AND HAEMOSTASIS LA English DT Article ID DEEP ARTERIAL INJURY; COLLAGEN TYPE-I; THROMBIN; MODEL; HEPARIN; HIRUDIN; THERAPY; EXVIVO; BLOOD; PIG AB Thrombin plays a key role in platelet activation and thrombosis. Specific inhibition of thrombin appears to be one of the best approaches to prevent thrombus formation. We have studied the effects of a synthetic alpha-aminoboronic acid derivative - [Ac, (D) Phe-Pro-Boro-Arg-Hydrocloric acid] - on platelet deposition on severely damaged arterial wall. Platelet deposition was evaluated under well characterized rheological conditions in an original perfusion chamber and detected by autologous In-111-labeled platelets. The study was performed ''in vivo'' in a porcine model of arterial thrombosis triggered by severely damaged vessel wall at blood flow conditions mimicking mild stenosis (1690 s(-1)) and patent (212 s(-1)) vessels. In addition, ex-vivo platelet aggregation activity was evaluated by whole blood impedance aggregometry using collagen, ADP and thrombin as agonists. The synthetic alpha-aminoboronic peptide was intravenously administered as a bolus followed by continuous infusion. Ex vivo thrombin-induced whole blood platelet aggregation was totally abolished, while ADP- and Collagen-induced whole blood platelet aggregation was not modified. The effects of the synthetic antithrombin on platelet deposition were evaluated in native blood (non-anticoagulated) conditions and in combination with heparin. Under both experimental conditions, the synthetic peptide significantly inhibited platelet deposition at local flow conditions of both high (1690 s(-1)) and low (212 s(-1)) shear rates. Our results suggest that specific inhibition of locally generated thrombin might be a good strategy to prevent platelet dependent arterial thrombus formation independently of the local flow shear rate of the area at risk. C1 HOSP SANT PAU,CSIC,CARDIOVASC RES UNIT,BARCELONA,SPAIN. HOSP SANT PAU,CSIC,CID FDN,BARCELONA,SPAIN. RP BADIMON, JJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,JACKSON BLDG,ROOM 13-28,BOSTON,MA 02114, USA. RI BADIMON, LINA/O-4711-2014; Fuster, Valentin/H-4319-2015 OI BADIMON, LINA/0000-0002-9162-2459; Fuster, Valentin/0000-0002-9043-9986 FU NHLBI NIH HHS [HL-38933] NR 19 TC 19 Z9 19 U1 0 U2 1 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD APR PY 1994 VL 71 IS 4 BP 511 EP 516 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA NE465 UT WOS:A1994NE46500019 PM 8052972 ER PT J AU UCHIYAMA, H ANDERSON, KC AF UCHIYAMA, H ANDERSON, KC TI CELLULAR ADHESION MOLECULES SO TRANSFUSION MEDICINE REVIEWS LA English DT Article ID NON-HODGKINS-LYMPHOMA; MARROW STROMAL CELLS; FUNCTION-ASSOCIATED ANTIGEN-1; MONONUCLEAR LEUKOCYTE ADHESION; HEMATOPOIETIC STEM-CELLS; HUMAN BONE-MARROW; HOMING RECEPTOR; PLASMA-CELLS; ICAM-1 CD54; ENDOTHELIAL-CELLS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA50947] NR 81 TC 17 Z9 19 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0887-7963 J9 TRANSFUS MED REV JI Transf. Med. Rev. PD APR PY 1994 VL 8 IS 2 BP 84 EP 95 DI 10.1016/S0887-7963(94)70101-2 PG 12 WC Hematology SC Hematology GA NU481 UT WOS:A1994NU48100001 PM 8003858 ER PT J AU MONTANA, E BONNERWEIR, S WEIR, GC AF MONTANA, E BONNERWEIR, S WEIR, GC TI TRANSPLANTED BETA-CELL REPLICATION AND MASS INCREASE AFTER 95-PERCENT PANCREATECTOMY SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 4th International Congress on Pancreas and Islet Transplantation CY JUN 27-30, 1993 CL AMSTERDAM, NETHERLANDS SP BAYER NEDERLAND, BAYER AG, BOEHRINGER MANNHEIM CORP, CILAG NV SA, DU PONT PHARMA, ELI LILLY, HOECHST AG, INST RECH INT SERVIER, JOHNSON & JOHNSON, KLM ROYAL DUTCH AIRLINES, NOVO NORDISK FARMA BV, SYNTEX BV C1 JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-35449, DK-36836] NR 2 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1994 VL 26 IS 2 BP 657 EP 657 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA NH683 UT WOS:A1994NH68300151 PM 7909632 ER PT J AU KLAHR, S LEVEY, AS BECK, GJ CAGGIULA, AW HUNSICKER, L KUSEK, JW STRIKER, G BUCKALEW, V BURKART, J FURBERG, C FELTS, J MOORE, M ROCCO, H DOLECEK, T WARREN, S BEARDEN, B STARKEY, C HARVEY, J POOLE, D DAHLQUIST, S DOROSHENKO, L BRADHAM, K WEST, D AGOSTINO, J COLE, L BAKER, B HAIRSTON, K BURGOYNE, S LAZARUS, J STEINMAN, T SEIFTER, J DESMOND, M FIORENZO, M CHIAVACCI, A METALIDES, T KORZECRAMIREZ, D GOULD, S PICKETT, V PORUSH, J FAUBERT, P SPITALEWITZ, S FAUBERT, J ZIMMER, G SAUM, D BLOCK, M WOEL, J ROSE, M DENNIS, V SCHWAB, S MINDA, S CONDON, S JENKS, B ECKARD, L GEDON, G MITCH, W MARONI, B ENGLAND, B SOUCIE, J PEDERSEN, M AKPELE, L CALLAHAN, P HALL, B SHELTON, S BOSCH, J HABWE, V CULBERTSON, B STACKDUNNE, M HANKEY, M ONEILL, S WITZMANN, K GOLDMAN, C JONES, T BOYLE, D SALMON, L KOPPLE, J ADLER, S HIRSCHBERG, R DICHIRO, J SNIDER, K DEVINE, W MCKAY, S MCDONALD, J CARTER, J NELSON, W LEVEY, A COGGINS, C DWYER, J MCLAUGHLIN, M GRONICH, J KING, A STOLLAR, C RAIZMAN, D CASTALDO, L DESIMONE, D EFSTATHION, A YONKER, K FINE, J SAUL, N HUGGINS, N MARTIN, A BALDI, S MOLESKE, C SHEEHAN, K FURLONG, D HEBERT, L NAHMAN, N DRIVER, V COSIO, M HARTMAN, J LEVY, C LONDERGAN, D GILLIGAN, M BECKMAN, T SMITH, E ZACHRICH, D TISHER, C PETERSON, J WINGO, C FINLAY, R PARRIS, E IVEY, G GREGORY, P HOFFINGER, R GARCIA, D PRESTON, C BERTOLATUS, J LIM, V SNETSELAAR, L WELCH, B BROOKS, L HOLLINGER, D LICHTY, I MUELLER, D EASTIN, S TANNA, A STEELE, J RIECK, K BOURGOIGNIE, J ROTH, D GREEN, D BUTCHER, C MERRILL, D DEVELASCO, A GARCON, M ROJAS, C ZARAGOZA, M BARTON, S MASSRY, S AKMAL, M FADDA, G SMORGORZERSKI, M KIEFER, S RAUCH, S EYERMAN, M KIGAWA, L RICHARDSON, A LIFSCHITZ, M KUNAU, R NOLAN, C GOUGE, S BAKRIS, G HURA, C YOUNG, E ARMES, C WARNER, C TANSEY, A FLORES, M DELEA, C TESCHAN, P HAKIM, R BREYER, J SCHULMAN, G ROGERS, N POWERS, S MCLEROY, S FISCHER, S DEERE, M CUTLER, E KUSEK, J AGODOA, L ANDERSON, A BECK, G WILLIAMS, G GASSMAN, J GREENE, T SCHLUCHTER, M BERG, R BROWN, M CHU, L DRABIK, M FATICA, K KNUTH, T LAMBDIN, K LEATHERMAN, J MCPHERSON, J MIDCALF, V MOORE, B PARANANDI, L PEARCE, G SWINDERMAN, D WANG, S WEBB, L YANCHAR, K CAGGIULA, A MILAS, N YAMAMOTO, M AMOROSO, W AVERBACH, F COYNE, T GILLIS, B JONES, F MAURER, E MEEHAN, R NAUJELIS, J OLSON, M SCHERCH, L STANO, E STEGINK, L BRUMMEL, M LUDWIG, B VANLENTE, F WALETZKY, J ERDEI, L SOUTH, C SPAGNOLA, C OLAUGHLIN, C PROUDFIT, W UNDERWOOD, D HALL, P ROLIN, H PEXA, D JONES, E BASCH, M CHUMLEA, W DOLLIFF, G KAPLAN, R WING, R DAMICO, G DIRKS, J GRANTHAM, J HARPER, A PETERS, K STEIN, J PELLEGRINO, E VANYPERSELE, C BAIN, R GRIZZLE, J HAWKINS, C HOLLIDAY, M LUKE, R MYERS, B RUDMAN, D WHELTON, P YOUNG, D YOUNG, V AF KLAHR, S LEVEY, AS BECK, GJ CAGGIULA, AW HUNSICKER, L KUSEK, JW STRIKER, G BUCKALEW, V BURKART, J FURBERG, C FELTS, J MOORE, M ROCCO, H DOLECEK, T WARREN, S BEARDEN, B STARKEY, C HARVEY, J POOLE, D DAHLQUIST, S DOROSHENKO, L BRADHAM, K WEST, D AGOSTINO, J COLE, L BAKER, B HAIRSTON, K BURGOYNE, S LAZARUS, J STEINMAN, T SEIFTER, J DESMOND, M FIORENZO, M CHIAVACCI, A METALIDES, T KORZECRAMIREZ, D GOULD, S PICKETT, V PORUSH, J FAUBERT, P SPITALEWITZ, S FAUBERT, J ZIMMER, G SAUM, D BLOCK, M WOEL, J ROSE, M DENNIS, V SCHWAB, S MINDA, S CONDON, S JENKS, B ECKARD, L GEDON, G MITCH, W MARONI, B ENGLAND, B SOUCIE, J PEDERSEN, M AKPELE, L CALLAHAN, P HALL, B SHELTON, S BOSCH, J HABWE, V CULBERTSON, B STACKDUNNE, M HANKEY, M ONEILL, S WITZMANN, K GOLDMAN, C JONES, T BOYLE, D SALMON, L KOPPLE, J ADLER, S HIRSCHBERG, R DICHIRO, J SNIDER, K DEVINE, W MCKAY, S MCDONALD, J CARTER, J NELSON, W LEVEY, A COGGINS, C DWYER, J MCLAUGHLIN, M GRONICH, J KING, A STOLLAR, C RAIZMAN, D CASTALDO, L DESIMONE, D EFSTATHION, A YONKER, K FINE, J SAUL, N HUGGINS, N MARTIN, A BALDI, S MOLESKE, C SHEEHAN, K FURLONG, D HEBERT, L NAHMAN, N DRIVER, V COSIO, M HARTMAN, J LEVY, C LONDERGAN, D GILLIGAN, M BECKMAN, T SMITH, E ZACHRICH, D TISHER, C PETERSON, J WINGO, C FINLAY, R PARRIS, E IVEY, G GREGORY, P HOFFINGER, R GARCIA, D PRESTON, C BERTOLATUS, J LIM, V SNETSELAAR, L WELCH, B BROOKS, L HOLLINGER, D LICHTY, I MUELLER, D EASTIN, S TANNA, A STEELE, J RIECK, K BOURGOIGNIE, J ROTH, D GREEN, D BUTCHER, C MERRILL, D DEVELASCO, A GARCON, M ROJAS, C ZARAGOZA, M BARTON, S MASSRY, S AKMAL, M FADDA, G SMORGORZERSKI, M KIEFER, S RAUCH, S EYERMAN, M KIGAWA, L RICHARDSON, A LIFSCHITZ, M KUNAU, R NOLAN, C GOUGE, S BAKRIS, G HURA, C YOUNG, E ARMES, C WARNER, C TANSEY, A FLORES, M DELEA, C TESCHAN, P HAKIM, R BREYER, J SCHULMAN, G ROGERS, N POWERS, S MCLEROY, S FISCHER, S DEERE, M CUTLER, E KUSEK, J AGODOA, L ANDERSON, A BECK, G WILLIAMS, G GASSMAN, J GREENE, T SCHLUCHTER, M BERG, R BROWN, M CHU, L DRABIK, M FATICA, K KNUTH, T LAMBDIN, K LEATHERMAN, J MCPHERSON, J MIDCALF, V MOORE, B PARANANDI, L PEARCE, G SWINDERMAN, D WANG, S WEBB, L YANCHAR, K CAGGIULA, A MILAS, N YAMAMOTO, M AMOROSO, W AVERBACH, F COYNE, T GILLIS, B JONES, F MAURER, E MEEHAN, R NAUJELIS, J OLSON, M SCHERCH, L STANO, E STEGINK, L BRUMMEL, M LUDWIG, B VANLENTE, F WALETZKY, J ERDEI, L SOUTH, C SPAGNOLA, C OLAUGHLIN, C PROUDFIT, W UNDERWOOD, D HALL, P ROLIN, H PEXA, D JONES, E BASCH, M CHUMLEA, W DOLLIFF, G KAPLAN, R WING, R DAMICO, G DIRKS, J GRANTHAM, J HARPER, A PETERS, K STEIN, J PELLEGRINO, E VANYPERSELE, C BAIN, R GRIZZLE, J HAWKINS, C HOLLIDAY, M LUKE, R MYERS, B RUDMAN, D WHELTON, P YOUNG, D YOUNG, V TI THE EFFECTS OF DIETARY-PROTEIN RESTRICTION AND BLOOD-PRESSURE CONTROL ON THE PROGRESSION OF CHRONIC RENAL-DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID LONGITUDINAL DATA; INSUFFICIENCY; FAILURE; TRIAL AB Background. Restricting protein intake and controlling hypertension delay the progression of renal disease in animals. We tested these interventions in 840 patients with various chronic renal diseases. C1 NIDDKD,BETHESDA,MD 20892. WASHINGTON UNIV,MED CTR,ST LOUIS,MO. UNIV PITTSBURGH,PITTSBURGH,PA. UNIV IOWA HOSP & CLIN,IOWA CITY,IA. BOWMAN GRAY SCH MED,WINSTON SALEM,NC. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. BROOKDALE HOSP MED CTR,BROOKLYN,NY. DUKE UNIV,SCH MED,DURHAM,NC. EMORY UNIV,ATLANTA,GA 30322. GEORGE WASHINGTON UNIV,WASHINGTON,DC. HARBOR UCLA MED CTR,TORRANCE,CA. TUFTS UNIV NEW ENGLAND MED CTR,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. OHIO STATE UNIV,COLUMBUS,OH 43210. UNIV FLORIDA,GAINESVILLE,FL. UNIV IOWA HOSP & CLIN,IOWA CITY,IA 52242. UNIV MIAMI,CORAL GABLES,FL 33124. JACKSON MEM HOSP,MED CTR,MIAMI,FL. UNIV SO CALIF,LOS ANGELES,CA. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. VANDERBILT UNIV,MED CTR,NASHVILLE,TN. HLTH CARE FINANCING ADM,SEATTLE,WA. UNIV PITTSBURGH,CTR NUTR COORDINATING,PITTSBURGH,PA. UNIV IOWA,CENT AMINO ACID LAB,IOWA CITY,IA. CLEVELAND CLIN FDN,CENT BIOCHEM LAB,CLEVELAND,OH. CLEVELAND CLIN FDN,CENT GLOMERULAR FILTRAT RATE LAB,CLEVELAND,OH. CLEVELAND CLIN FDN,CTR DRUG DISTRIBUT,CLEVELAND,OH. CLEVELAND CLIN FDN,CENT ELECTROCARDIOG LAB,CLEVELAND,OH. RP KLAHR, S (reprint author), CLEVELAND CLIN FDN,MDRD STUDY DATA COORDINATING CTR,DEPT BIOSTAT & EPIDEMIOL,P88,CLEVELAND,OH 44195, USA. NR 28 TC 1393 Z9 1424 U1 4 U2 34 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 31 PY 1994 VL 330 IS 13 BP 877 EP 884 DI 10.1056/NEJM199403313301301 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA NC608 UT WOS:A1994NC60800001 PM 8114857 ER PT J AU ANDERSON, KC DZIECZKOWSKI, J SHEPARD, JAO BLOCH, KJ AF ANDERSON, KC DZIECZKOWSKI, J SHEPARD, JAO BLOCH, KJ TI A 62-YEAR-OLD MAN WITH EPISTAXIS, CONFUSION, RENAL-FAILURE, AND BILATERAL CENTRAL-RETINAL-VEIN THROMBOSIS - MULTIPLE-MYELOMA, IGG3-KAPPA LIGHT-CHAIN, WITH HYPERVISCOSITY SYNDROME AND TYPE-I CRYOGLOBULINEMIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ANDERSON, KC (reprint author), DANA FARBER CANC INST,BLOOD COMPONENT LAB,BOSTON,MA 02115, USA. NR 22 TC 7 Z9 7 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 31 PY 1994 VL 330 IS 13 BP 920 EP 927 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA NC608 UT WOS:A1994NC60800009 ER PT J AU JOSEPH, PM TIERNEY, M AF JOSEPH, PM TIERNEY, M TI CASE-45-1993 - ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP JOSEPH, PM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 31 PY 1994 VL 330 IS 13 BP 941 EP 941 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA NC608 UT WOS:A1994NC60800031 ER PT J AU SWARTZ, MN AF SWARTZ, MN TI HOSPITAL-ACQUIRED INFECTIONS - DISEASES WITH INCREASINGLY LIMITED THERAPIES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article; Proceedings Paper CT Colloquium on Changes in Human Ecology and Behavior: Effects on Infectious Diseases CY SEP 27-28, 1993 CL NATL ACAD SCI, WASHINGTON, DC HO NATL ACAD SCI ID RESISTANT STAPHYLOCOCCUS-AUREUS; COAGULASE-NEGATIVE STAPHYLOCOCCI; SPECTRUM BETA-LACTAMASES; ENTEROCOCCUS-FAECALIS; NOSOCOMIAL INFECTION; UNITED-STATES; ANTIMICROBIAL RESISTANCE; STREPTOCOCCUS-FAECALIS; HIGH-LEVEL; VANCOMYCIN AB About 5% of patients admitted to acute-care hospitals acquire nosocomial infections. A variety of factors contribute: increasing age of patients; availability, for treatment of formerly untreatable diseases, of extensive surgical and intensive medical therapies; and frequent use of antimicrobial drugs capable of selecting a resistant microbial flora. Nosocomial infections due to resistant organisms have been a problem ever since infections due to penicillinase-producing Staphylococcus aureus were noted within a few years of the introduction of penicillin. By the 1960s aerobic Gram-negative bacilli had assumed increasing importance as nosocomial pathogens, and many strains were resistant to available antimicrobials. During the 1980s the principal organisms causing nosocomial bloodstream infections were coagulase-negative staphylococci, aerobic Gram-negative bacilli, S. aureus, Candida spp., and Enterococcus spp. Coagulase-negative staphylococci and S. aureus are often methicillin-resistant, requiring parenteral use of vancomycin. Prevalence of vancomycin resistance among enterococcal isolates from patients in intensive care units has increased, likely due to increased use of this drug. Plasmid-mediated gentamicin resistance in up to 50% of enterococcal isolates, along with enhanced penicillin resistance in some strains, leaves few therapeutic options. The emergence of Enterobacteriaceae with chromosomal or plasmid-encoded extended spectrum beta-lactamases presents a world-wide problem of resistance to third generation cephalosporins. Control of these infections rests on (1) monitoring infections with such resistant organisms in an ongoing fashion, (ii) prompt institution of barrier precautions when infected or colonized patients are identified, and (iii) appropriate use of antimicrobials through implementation of antibiotic control programs. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SWARTZ, MN (reprint author), HARVARD UNIV,SCH MED,DEPT MED,FRUIT ST,BOSTON,MA 02115, USA. NR 60 TC 195 Z9 204 U1 0 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2420 EP 2427 DI 10.1073/pnas.91.7.2420 PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200009 PM 8146133 ER PT J AU PRASAD, KVS CAI, YC RAAB, M DUCKWORTH, B CANTLEY, L SHOELSON, SE RUDD, CE AF PRASAD, KVS CAI, YC RAAB, M DUCKWORTH, B CANTLEY, L SHOELSON, SE RUDD, CE TI T-CELL ANTIGEN CD28 INTERACTS WITH THE LIPID KINASE PHOSPHATIDYLINOSITOL 3-KINASE BY A CYTOPLASMIC TYR(P)-MET-XAA-MET MOTIF SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID POINT MUTATION; LYMPHOCYTES-T; RECEPTOR; CD4; MITOGENESIS; CLONES; P56LCK; CTLA-4; SH2 AB The T-cell antigen CD28 provides a costimulatory signal that is required for T-cell proliferation. T-cell receptor zeta/CD3 engagement without CD28 ligation leads to a state of nonresponsiveness/anergy, thereby implicating CD28 in the control of peripheral tolerance to foreign antigens or tumors. A key unresolved question has concerned the mechanism by which CD28 generates intracellular signals. Phosphatidylinositol 3-kinase (PI 3-kinase) is a lipid kinase with Src-homology 2 (SH2) domain(s) that binds to the platelet-derived growth factor receptor (PDGF-R), an interaction that is essential for signaling by growth factor. In this study, we demonstrate that CD28 binds to PI 3-kinase by means of a Y(P)MXM motif within its cytoplasmic tail. CD28-associated PI 3-kinase was detected by lipid kinase and HPLC analysis as well as by reconstitution experiments with baculoviral-expressed p85 subunit of PI 3-kinase. CD28 bound directly to the p85 subunit without the need for the associated p110 subunit. Site-directed mutagenesis and peptide competition analysis using Y(P)MXM-containing peptides showed that PI 3-kinase bound to a Y(P)MXM motif within the CD28 cytoplasmic tail (residues 191-194). Mutation of the Y191 within the motif resulted in a complete loss of binding, while mutation of M194 caused partial loss of binding. Binding analysis showed that the CD28 Y(P)MXM motif bound to the p85 C- and N-terminal SH2 domains with an affinity comparable to that (observed for PDGF-R and insulin receptor substrate 1. In terms of signaling, CD28 ligation induced a dramatic increase in the recruitment and association of PI 3-kinase with the receptor. CD28 is likely to use PI 3-kinase as the second signal leading to T-cell proliferation, an event with implications for anergy and peripheral T-cell tolerance. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. JOSLIN DIABET FDN INC,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02115. RI Cantley, Lewis/D-1800-2014 OI Cantley, Lewis/0000-0002-1298-7653 FU NIGMS NIH HHS [R01 GM041890] NR 36 TC 256 Z9 259 U1 0 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2834 EP 2838 DI 10.1073/pnas.91.7.2834 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200092 PM 8146197 ER PT J AU POWELSON, JA KNOWLES, RW DELMONICO, FL KAWAI, T MOURAD, G PFEFFER, FI COLVIN, RB COSIMI, AB AF POWELSON, JA KNOWLES, RW DELMONICO, FL KAWAI, T MOURAD, G PFEFFER, FI COLVIN, RB COSIMI, AB TI CDR-GRAFTED OKT4A MONOCLONAL-ANTIBODY IN CYNOMOLGUS RENAL-ALLOGRAFT RECIPIENTS SO TRANSPLANTATION LA English DT Article; Proceedings Paper CT 19th Annual Meeting of the American-Society-of-Transplant-Surgeons CY MAY 19-21, 1993 CL HOUSTON, TX SP AMER SOC TRANSPLANT SURGEONS ID T-CELL SUBSET; CARDIAC ALLOGRAFTS; HUMANIZED OKT4A; INDUCTION; THERAPY; TOLERANCE; IMMUNOSUPPRESSION; THYMOCYTES; REJECTION; SURVIVAL AB In an attempt to improve therapeutic efficacy and limit antimurine responses to the IgG2a monoclonal antibody OKT4A, humanized complementarity determining region (CDR)-grafted OKT4A mAbs (IgG1 and IgG4 isotypes) were developed from the murine molecule. Preclinical evaluation was undertaken in 12 cynomolgus renal allograft recipients (IgG1, n=7; IgG4, n=5). Control animals received either no therapy (n=2) or OKT3 (n=2). The mAbs were given as a single 10-mg/kg bolus on the day of transplantation or as multiple 1-mg/kg doses. Mean allograft survival (+/-SEM) was 9+/-0.7 days in control animals; 45.2+/-6.0 days, P=0.002 (single dose, n=5), and 39+/-5.0 days, P=0.053, (multiple doses, n=2) in IgG1-treated animals; and 35.3+/-7.2 days, P=0.034, (single dose, n=3) and 15.5+/-6.5 days, P=.251 (multiple doses, n=2) in IgG4-treated animals. Whereas IgG4-treated animals showed coating of peripheral blood CD4+ T cells, significant CD4+ T cell depletion was observed in IgG1-treated animals. These results confirm the retained immunosuppressive efficacy of hilmanized OKT4A antibodies. In contrast to murine mAbs, the use of these agents would not preclude sequential treatment with mAbs directed against different epitopes. The fact that rejection can occur despite peripheral blood CD4+ cell depletion suggests that indefinite control of allograft rejection in primates may require more intensive therapy than has proved effective in rodent models. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GEN SURG SERV,TRANSPLANTAT UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RW JOHNSON PHARMACEUT RES INST,RARITAN,NJ. FU NHLBI NIH HHS [P01-HL-18646] NR 30 TC 21 Z9 21 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 27 PY 1994 VL 57 IS 6 BP 788 EP 793 DI 10.1097/00007890-199403270-00002 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA ND846 UT WOS:A1994ND84600002 PM 7908767 ER PT J AU ROSENGARD, BR FISHBEIN, JM GIANELLO, P OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K HILL, GS SACHS, DH AF ROSENGARD, BR FISHBEIN, JM GIANELLO, P OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K HILL, GS SACHS, DH TI RETRANSPLANTATION IN MINIATURE SWINE - LACK OF A REQUIREMENT FOR GRAFT ADAPTATION FOR MAINTENANCE OF SPECIFIC RENAL-ALLOGRAFT TOLERANCE SO TRANSPLANTATION LA English DT Article; Proceedings Paper CT 19th Annual Meeting of the American-Society-of-Transplant-Surgeons CY MAY 19-21, 1993 CL HOUSTON, TX SP AMER SOC TRANSPLANT SURGEONS ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-I; KIDNEY ALLOGRAFTS; TRANSPLANTATION; REJECTION; SURVIVAL; ANTIGEN; RAT; SUPPRESSION; MECHANISM AB In miniature swine, one-haplotype class I disparate renal allografts are accepted without exogenous immunosuppression by approximately 35% of recipients. Alternatively, transplants bearing a two-haplotype class I mismatch are always rejected acutely. However, long-term acceptance in the latter animals can be achieved uniformly with a 12-day course of cyclosporine. In vitro studies of recipient cell-mediated lymphocytotoxicity responses have shown donor-specific cytotoxic T lymphocyte clones in tolerant animals, suggesting that tolerance may be a local phenomenon or a central phenomenon activated in the milieu of the graft. Six animals were retransplanted with kidneys MHC-matched to their original allograft to determine whether (1) tolerance is a central phenomenon; (2) host tolerance can be broken with a fresh challenge of donor antigen and antigen-presenting cells; and (3) graft adaptation is required for maintenance of tolerance. Four of the retransplanted animals had been spontaneous acceptors of one-haplotype class I-disparate grafts and two had been rendered tolerant to two-haplotype class I-mismatched kidneys with CsA induction. All six explanted allografts showed no histological evidence of rejection and all six retransplants were accepted without exogenous immunosuppression. These findings suggest that in miniature swine tolerance of class I-disparate kidneys is a stable, centrally mediated phenomenon that cannot be broken with a challenge of fresh donor antigen and donor-type APCs. Furthermore, successful retransplantation without immunosuppression in animals receiving CsA induction therapy for their first transplant suggests that graft adaptation is not necessary for the maintenance of tolerance. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. FU NHLBI NIH HHS [HL-18646]; NIAID NIH HHS [AI-31156] NR 26 TC 12 Z9 12 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 27 PY 1994 VL 57 IS 6 BP 794 EP 799 DI 10.1097/00007890-199403270-00003 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA ND846 UT WOS:A1994ND84600003 PM 8154022 ER PT J AU GRITSCH, HA GLASER, RM EMERY, DW LEE, LA SMITH, CV SABLINSKI, T ARN, JS SACHS, DH SYKES, M AF GRITSCH, HA GLASER, RM EMERY, DW LEE, LA SMITH, CV SABLINSKI, T ARN, JS SACHS, DH SYKES, M TI THE IMPORTANCE OF NONIMMUNE FACTORS IN RECONSTITUTION BY DISCORDANT XENOGENEIC HEMATOPOIETIC-CELLS SO TRANSPLANTATION LA English DT Article; Proceedings Paper CT 19th Annual Meeting of the American-Society-of-Transplant-Surgeons CY MAY 19-21, 1993 CL HOUSTON, TX SP AMER SOC TRANSPLANT SURGEONS ID SEVERE COMBINED IMMUNODEFICIENCY; COMBINED IMMUNE-DEFICIENCY; NATURAL-KILLER-CELLS; SCID-HU MOUSE; MAJOR HISTOCOMPATIBILITY COMPLEX; MARROW GRAFT-REJECTION; HUMAN PERIPHERAL-BLOOD; HUMAN BONE-MARROW; MONOCLONAL-ANTIBODIES; T-CELLS AB Bone marrow transplantation has been shown to induce donor-specific tolerance in rodent models. This approach could potentially be applied to xenotransplantation across discordant species barriers. To evaluate host factors resisting hematopoietic cell engraftment, we have developed two model systems utilizing the combination of swine into severe combined immunodeficient (SCID) mice. SCID mice lack functional B and T lymphocytes, and can therefore be used to evaluate nonimmune factors resisting marrow engraftment, and for adoptive transfer studies to test the role of immune cells and antibodies. First we transplanted swine bone marrow cells into SCID mice conditioned with whole-body irradiation (4 Gy). For nine weeks following the intravenous administration of 10(8) swine bone marrow cells, up to 3.8% of peripheral blood leukocytes were of swine origin, as determined by flow cytometry (FCM). These cells were all of the myeloid lineage. Swine IgG was also detectable in the serum for up to 14 weeks. The bone marrow of the reconstituted mice contained low percentages of swine myeloid cells, and swine myeloid progenitors could be detected for up to 20 weeks after bone marrow transplantation. In a second model, we grafted thymus and liver tissue from 45-69-day-old swine fetuses under the kidney capsule of 4 Gy-irradiated SCID mice. A suspension containing 10(8) swine fetal liver cells (FLC) was also administered i.p. Long-term repopulation with swine T cells was observed, with up to 1.5% swine T cells detected in the WBC, peritoneum, and spleen for at least 5.5 months postgrafting. These T cells expressed either CD4 or CD8, whereas up to 17.6% of cells in the thymic grafts expressed both CD4 and CD8. The i.p. FLC suspension was required for optimal long-term graft maintenance. Our studies show that (1) low level myeloid and B lymphocyte reconstitution can be achieved by transferring adult swine BMC to irradiated SCID recipients; (2) swine myeloid progenitors were detectable long-term in BMC of these mice, suggesting that stem cell engraftment was achieved; and (3) T cell reconstitution of SCID mice by swine progenitors requires cotransplantation of a swine stromal environment, as is provided by fetal swine thymus/liver grafts. We conclude that nonimmune factors such as those provided by species-specific stromal environments are important for reconstitution of some lineages by discordant hematopoietic stem cells. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,TRANSPLANTAT BIOL RES CTR,MGH E,BOSTON,MA 02129. BIOTRANSPLANT INC,BOSTON,MA 02129. FU NHLBI NIH HHS [NHLBI HL 46532] NR 66 TC 55 Z9 59 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 27 PY 1994 VL 57 IS 6 BP 906 EP 917 DI 10.1097/00007890-199403270-00024 PG 12 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA ND846 UT WOS:A1994ND84600024 PM 7908768 ER PT J AU ROTEM, A TONER, M BHATIA, S FOY, BD TOMPKINS, RG YARMUSH, ML AF ROTEM, A TONER, M BHATIA, S FOY, BD TOMPKINS, RG YARMUSH, ML TI OXYGEN IS A FACTOR DETERMINING IN-VITRO TISSUE ASSEMBLY - EFFECTS ON ATTACHMENT AND SPREADING OF HEPATOCYTES SO BIOTECHNOLOGY AND BIOENGINEERING LA English DT Article DE HEPATOCYTES; OXYGEN; ARTIFICIAL LIVER; BIOARTIFICIAL ORGANS ID CULTURE AB Many recent studies related to the development of bioartificial liver devices have utilized hepatocytes cultured within devices of various geometries. Because hepatocytes are anchorage-dependent cells, they need to attach and spread onto the extracellular matrix to be able to function, a process that requires energy. Thus, it is important to deliver enough oxygen to hepatocytes contained within bioartificial liver devices during the early phase of cellular organization while the cells interact with the extracellular matrix. In this study, we investigated the effect of oxygen on the attachment and spreading of hepatocytes. Increasing the gas phase oxygen from 0 to 160 mmHg resulted in an increase in the percentage of cells attaching from 43.0 +/- 5.8% to 103.6 +/- 29%, 1 h after seeding. In a similar manner, increasing the gas phase oxygen from 0 to 160 mmHn resulted in an Increase of the projected surface area from 310 +/- 35 to 827 +/- 127 mu m(2), 24 h after seeding. Furthermore, the partial pressure of oxygen at the cell level was estimated using a diffusion-reaction model. The model indicated that a cell surface oxygen partial pressure of 0.064 mmHg was required for the half-maximal (K-m(a)) attachment of hepatocytes to collagen-based substrate. On the other hand, the K-m(s) value of the spreading process was predicted to be 0.13 mmHg. The results of this study demonstrate the importance of oxygen during the initial stages of attachment and spreading of hepatocytes, and it has important implications in the design of hepatocytebased bioartificial liver devices. (C) 1994 John wiley & Sons, Inc. C1 RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08855. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,SHRINERS BURNS INST,BOSTON,MA 02114. NR 17 TC 70 Z9 70 U1 0 U2 4 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3592 J9 BIOTECHNOL BIOENG JI Biotechnol. Bioeng. PD MAR 25 PY 1994 VL 43 IS 7 BP 654 EP 660 DI 10.1002/bit.260430715 PG 7 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA MY102 UT WOS:A1994MY10200014 PM 18615765 ER PT J AU FOY, BD TONER, M TOMPKINS, RG YARMUSH, ML AF FOY, BD TONER, M TOMPKINS, RG YARMUSH, ML TI ENGINEERING ORGAN PERFUSION PROTOCOLS - NMR ANALYSIS OF HEPATOCYTE ISOLATION FROM PERFUSED-RAT-LIVER SO BIOTECHNOLOGY AND BIOENGINEERING LA English DT Article DE HEPATOCYTE; MAGNETIC RESONANCE; ARTIFICIAL LIVER; PERFUSION ID NUCLEAR-MAGNETIC-RESONANCE; PERCOLL CENTRIFUGATION; PARENCHYMAL-CELLS; MOUSE-LIVER; HIGH-YIELD; P-31; C-13; METABOLISM; DISPERSION; CULTURES AB The development and use of an extracorporeal liver support device depends upon the isolation of a large number of viable, functioning hepatocytes from whole or partial livers. Current practice, however, produces nonoptimal yields, given that a large percentage of hepatocytes initially presented are not successfully isolated. The normal hepatocyte isolation protocol consists of sequential perfusion with calcium chelating and collagenase buffers, and then separation of viable hepatocytes from non-viable and nonparenchymal cells, usually on the basis of cell density. In order to improve understanding regarding the metabolic and perfusion state of the liver during this perfusion protocol, ATP, pH, and tissue perfusion were evaluated using nuclear magnetic resonance (NMR). Perfusion with calcium chelating buffer was found to have minimal effect on the metabolic and perfusion parameters, whereas subsequent perfusion with collagenase buffer produced large declines in ATP, pH, and homogeneity of perfusion within 3 min. Perfusion with calcium-chelating buffer alone, or perfusion with calcium chelating buffer followed by a short period of ischemia to mimic the perfusion disruption of collagenase, did not produce the same decline in metabolic parameters. This NMR data suggested that enhancing the early perfusion and penetration of collagenase or prolonging the nontoxic calcium-chelation step may improve the yield and/or functionality of isolated cells. Therefore, several altered perfusion protocols were evaluated in terms of yield of viable parenchymal hepatocytes and hepatocyte albumin production. Although increasing the perfusion flow rate and initial perfusion with inactive (cold) collagenase did not produce significant improvements when compared with the control protocol (control cell yield 226 +/- 42 x 10(6) viable hepatocytes for 10- to 14-week-old female Lewis rat), prolonging and enhancing the calcium-chelating perfusion step or increasing the collagenase concentration did yield a significantly great number of viable parenchymal hepatocytes (393 - 44 and 328 +/- 39 x 106 viable hepatocytes, respectively) with no change in albumin production per seeded viable cell. (C) 1994 John Wiley and Sons, Inc. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA 02114. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. NR 41 TC 2 Z9 2 U1 0 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3592 J9 BIOTECHNOL BIOENG JI Biotechnol. Bioeng. PD MAR 25 PY 1994 VL 43 IS 7 BP 661 EP 672 DI 10.1002/bit.260430716 PG 12 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA MY102 UT WOS:A1994MY10200015 PM 18615766 ER PT J AU DULIC, V KAUFMANN, WK WILSON, SJ TLSTY, TD LEES, E HARPER, JW ELLEDGE, SJ REED, SI AF DULIC, V KAUFMANN, WK WILSON, SJ TLSTY, TD LEES, E HARPER, JW ELLEDGE, SJ REED, SI TI P53-DEPENDENT INHIBITION OF CYCLIN-DEPENDENT KINASE-ACTIVITIES IN HUMAN FIBROBLASTS DURING RADIATION-INDUCED G1 ARREST SO CELL LA English DT Article ID WILD-TYPE P53; RETINOBLASTOMA GENE-PRODUCT; HUMAN CELL-CYCLE; ATAXIA-TELANGIECTASIA; PROTEIN-KINASE; FISSION YEAST; S-PHASE; TYROSINE PHOSPHORYLATION; SACCHAROMYCES-CEREVISIAE; IONIZING-RADIATION AB Gamma-irradiation of human diploid fibroblasts in the G1 interval caused arrest of the cell cycle prior to S phase. This cell cycle block was correlated with a lack of activation of both cyclin E-Cyclin-dependent kinase 2 (Cdk2) and cyclin A-Cdk2 kinases and depended on wild-type p53. Although the accumulation of cyclin A was strongly inhibited in gamma-irradiated cells, cyclin E accumulated and bound Cdk2 at normal levels but remained in an inactive state. We found that both whole-cell lysates and inactive cyclin E-Cdk2 complexes prepared from irradiated cells contained an activity capable of inactivating cyclin E-Cdk2 complexes. The protein responsible for this activity was shown to be p21CIP1/WAF1, recently described as a p53-inducible Cdk inhibitor. Our data suggest a model in which ionizing radiation confers G1 arrest via the p53-mediated induction of a Cdk inhibitor protein. C1 SCRIPPS RES INST, DEPT MOLEC BIOL MB7, LA JOLLA, CA 92037 USA. UNIV N CAROLINA, LINEBERGER COMPREHENS CANC CTR, CHAPEL HILL, NC 27599 USA. MASSACHUSETTS GEN HOSP, CTR CANC, MOLEC ONCOL LAB, BOSTON, MA 02129 USA. BAYLOR COLL MED, INST MOLEC GENET, VERNA & MARRS MCLEAN DEPT BIOCHEM, HOUSTON, TX 77030 USA. BAYLOR COLL MED, INST MOLEC GENET, HOWARD HUGHES MED INST, HOUSTON, TX 77030 USA. OI Dulic, Vjekoslav/0000-0003-1201-3901 FU NCI NIH HHS [CA42765, CA55339]; NIGMS NIH HHS [GM46006] NR 81 TC 1373 Z9 1394 U1 5 U2 28 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 25 PY 1994 VL 76 IS 6 BP 1013 EP 1023 DI 10.1016/0092-8674(94)90379-4 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ND246 UT WOS:A1994ND24600008 PM 8137420 ER PT J AU LOH, C ROMEO, C SEED, B BRUDER, JT RAPP, U RAO, A AF LOH, C ROMEO, C SEED, B BRUDER, JT RAPP, U RAO, A TI ASSOCIATION OF RAF WITH THE CD3 DELTA-CHAIN AND GAMMA-CHAIN OF THE T-CELL RECEPTOR-CD3 COMPLEX SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-TYROSINE KINASE; SERINE-THREONINE KINASE; PDGF BETA-RECEPTOR; ANTIGEN RECEPTOR; GROWTH-FACTOR; SIGNAL TRANSDUCTION; ZETA-CHAIN; PHOSPHOLIPASE-C; MONOCLONAL-ANTIBODY; BINDING-SITE AB Protein kinases and phosphatases play an important role in signal transduction. In the T cell, activation via the T cell receptor-CD3 complex results in rapid tyrosine phosphorylation of proteins, as well as subsequent increases in serine/threonine phosphorylation. The Raf serine/threonine kinase has been implicated in many receptor signaling pathways, including those of platelet-derived growth factor, epidermal growth factor, insulin, and interleukin-2 receptors. We show here that Raf is associated with the T cell receptor-CD3 complex in unstimulated murine T cells. Using a COS cell expression system, we show that a hypophosphorylated form of Raf specifically associates with the CD3 gamma and delta chains but not with the CD3 epsilon or zeta chains. These results suggest that Raf mediates signal transduction from the gamma and delta chains of the T cell receptor-CD3 complex, analogous to the role played by ZAP-70 in signal transduction mediated by the zeta chain. C1 DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. FU NIAID NIH HHS [AI27849]; NIGMS NIH HHS [GM46227] NR 62 TC 11 Z9 11 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1994 VL 269 IS 12 BP 8817 EP 8825 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB411 UT WOS:A1994NB41100033 PM 8132616 ER PT J AU DANDREA, AD FLIER, J MOSES, A LOWELL, B MONROE, MJ AF DANDREA, AD FLIER, J MOSES, A LOWELL, B MONROE, MJ TI SEMINARS IN MEDICINE OF THE BETH-ISRAEL-HOSPITAL, BOSTON - CYTOKINE RECEPTORS IN CONGENITAL HEMATOPOIETIC DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID COLONY-STIMULATING FACTOR; LARON-TYPE DWARFISM; ACUTE MYELOBLASTIC-LEUKEMIA; HUMAN GROWTH-HORMONE; ERYTHROPOIETIN RECEPTOR; IL-2 RECEPTOR; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION; CYTOPLASMIC REGION; LINEAR GROWTH C1 DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. RP DANDREA, AD (reprint author), DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 55 TC 21 Z9 22 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 24 PY 1994 VL 330 IS 12 BP 839 EP 846 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA NB803 UT WOS:A1994NB80300007 PM 8114837 ER PT J AU KAUFMAN, DS SHIPLEY, WU HENEY, NM ALTHAUSEN, AF AF KAUFMAN, DS SHIPLEY, WU HENEY, NM ALTHAUSEN, AF TI BLADDER PRESERVATION AFTER TREATMENT OF INVASIVE BLADDER-CANCER - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP KAUFMAN, DS (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 4 TC 1 Z9 1 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 24 PY 1994 VL 330 IS 12 BP 867 EP 868 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA NB803 UT WOS:A1994NB80300030 ER PT J AU BREWER, TF FELSENSTEIN, D WILSON, ME AF BREWER, TF FELSENSTEIN, D WILSON, ME TI FURUNCULAR MYIASIS - ALTERNATIVES TO BACON THERAPY - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter C1 MT AUBURN HOSP,CAMBRIDGE,MA. RP BREWER, TF (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA, USA. NR 4 TC 2 Z9 2 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 23 PY 1994 VL 271 IS 12 BP 901 EP 902 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA NA743 UT WOS:A1994NA74300012 ER PT J AU BOWDEN, CL BRUGGER, AM SWANN, AC CALABRESE, JR JANICAK, PG PETTY, F DILSAVER, SC DAVIS, JM RUSH, AJ SMALL, JG GARZATREVINO, ES RISCH, SC GOODNICK, PJ MORRIS, DD AF BOWDEN, CL BRUGGER, AM SWANN, AC CALABRESE, JR JANICAK, PG PETTY, F DILSAVER, SC DAVIS, JM RUSH, AJ SMALL, JG GARZATREVINO, ES RISCH, SC GOODNICK, PJ MORRIS, DD TI EFFICACY OF DIVALPROEX VS LITHIUM AND PLACEBO IN THE TREATMENT OF MANIA SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID AFFECTIVE-DISORDERS; BIPOLAR DISORDER; DOUBLE-BLIND; FOLLOW-UP; VALPROATE; ILLNESS; CARBAMAZEPINE; ALCOHOL; STATES; SODIUM AB Objective.-To compare the effectiveness of divalproex sodium with that of lithium and placebo in patients with acute mania. Design.-Randomized, double-blind, parallel-group study of treatment outcomes in patients with manic-depressive illness. Patients.-A total of 179 hospitalized, acutely manic patients meeting the Research Diagnostic Criteria for manic disorder, approximately half of whom had been nonresponsive to lithium previously, were studied at nine university-affiliate hospitals. Interventions.-After a minimum 3-day washout period, random assignment for 21 days to divalproex, lithium, or placebo in a 2:1:2 ratio. Dosage of divalproex and lithium was increased if tolerated to a target concentration of 1041 mu mol/L (150 mu g/ mL) or 1.5 mmol/L (conventionally expressed as milliequivalents per liter), respectively. Main Outcome Measures.-Primary outcome measures were changes in the Mania Rating scale derived from the Schedule for Affective Disorders and Schizophrenia. Results.-lntent-to-treat analysis for efficacy was based on data from 68, 35, and 73 patients in the divalproex, lithium, and placebo groups, respectively. Groups were initially comparable except that all eight patients with four or more manic episodes in the previous year were in the divalproex group. In 30%, 33%, and 51% of the above groups, treatment was prematurely terminated due to lack of efficacy, with fewer premature terminations from divalproex than placebo (P=.017). The proportions of patients improving at least 50% were higher for divalproex and lithium groups than for the placebo group: 48% for divalproex (P=.004) and 49% for lithium (P=.025) vs 25% for placebo. Divalproex was as effective in rapid-cycling manic patients as in other patients. Conclusions.-Both divalproex and lithium were significantly more effective than placebo in reducing the symptoms of acute mania. The efficacy of divalproex appears to be independent of prior responsiveness to lithium. C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX USA. ABBOTT LABS, CLIN RES SECT, N CHICAGO, IL USA. UNIV TEXAS, SCH MED, DEPT PSYCHIAT, HOUSTON, TX USA. CASE WESTERN RESERVE UNIV, SCH MED, DEPT PSYCHIAT, CLEVELAND, OH 44106 USA. ILLINOIS STATE PSYCHIAT INST, CHICAGO, IL USA. UNIV ILLINOIS, DEPT PSYCHIAT, CHICAGO, IL 60612 USA. VET AFFAIRS MED CTR, DALLAS, TX USA. UNIV TEXAS, SW MED CTR, DEPT PSYCHIAT, DALLAS, TX USA. INDIANA UNIV, SCH MED, DEPT PSYCHIAT, INDIANAPOLIS, IN 46202 USA. EMORY UNIV, SCH MED, DEPT PSYCHIAT, ATLANTA, GA 30322 USA. UNIV MIAMI, DEPT PSYCHIAT, CORAL GABLES, FL USA. RP BOWDEN, CL (reprint author), UNIV TEXAS, HLTH SCI CTR, DEPT PSYCHIAT, DIV BIOL PSYCHIAT, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. OI Rush, Augustus/0000-0003-2004-2382 NR 45 TC 741 Z9 752 U1 2 U2 22 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0098-7484 EI 1538-3598 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 23 PY 1994 VL 271 IS 12 BP 918 EP 924 DI 10.1001/jama.271.12.918 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA NA743 UT WOS:A1994NA74300027 PM 8120960 ER PT J AU MCBRIDE, R CHESEBRO, JH WIEBERS, DO HOLLAND, AE LINKER, S BARDSLEY, WT KOPECKY, S LITIN, SC MEISSNER, I ZERBE, DM FLAKER, GC WEBEL, R NOLTE, B STEVENSON, P BYER, J JENKINS, JS WRIGHT, W ANDERSON, DC ASINGER, RW NEWBURG, SM BUNDLIE, SR FARMER, CC KOLLER, RL HAUGLAND, JM NANCE, MA TARREL, RM DUNBAR, DN JORGENSEN, CR SHARKEY, SW LEONARD, ADS KANTER, MC SOLOMON, DH ZABALGOITIA, M MCANULTY, JH MARCHANT, C COULL, BM KELLEY, RE CHAHINE, R PALERMO, M TEIXEIRO, P FELDMAN, G HAYWARD, A MACMILLAN, K GANDARA, E ANDERSON, W BLANK, N STRAUSS, R FEINBERG, WM VOLD, BK KERN, KB APPLETON, C BRUCK, D DORR, S DITTRICH, HC ROTHROCK, JF KERRIDGE, C LOGAN, WR HAMILTON, WP GREEN, BJ BACON, RS HELGASON, CM KONDOS, GT HOFF, J MCRAE, RP HALPERIN, JL ROTHLAUF, EB WEINBERGER, JM GOLDMAN, ME MILLER, VT HOCKERSMITH, CJ COHEN, BA JANOSIK, DL CADELL, DJ KELLERMAN, L GOMEZ, CR LABOVITZ, AJ ROTHBART, RM BAILEY, GH BURKHARDT, C HORWITZ, L BLACKSHEAR, JL WEAVER, L BAKER, V LEE, G LANE, G RUBINO, F SAFFORD, R KRONMAL, RA PEARCE, LA FLETCHER, KA NASCO, E HART, RG SHERMAN, DG TALBERT, RL DACY, TL HERBERLING, PA AF MCBRIDE, R CHESEBRO, JH WIEBERS, DO HOLLAND, AE LINKER, S BARDSLEY, WT KOPECKY, S LITIN, SC MEISSNER, I ZERBE, DM FLAKER, GC WEBEL, R NOLTE, B STEVENSON, P BYER, J JENKINS, JS WRIGHT, W ANDERSON, DC ASINGER, RW NEWBURG, SM BUNDLIE, SR FARMER, CC KOLLER, RL HAUGLAND, JM NANCE, MA TARREL, RM DUNBAR, DN JORGENSEN, CR SHARKEY, SW LEONARD, ADS KANTER, MC SOLOMON, DH ZABALGOITIA, M MCANULTY, JH MARCHANT, C COULL, BM KELLEY, RE CHAHINE, R PALERMO, M TEIXEIRO, P FELDMAN, G HAYWARD, A MACMILLAN, K GANDARA, E ANDERSON, W BLANK, N STRAUSS, R FEINBERG, WM VOLD, BK KERN, KB APPLETON, C BRUCK, D DORR, S DITTRICH, HC ROTHROCK, JF KERRIDGE, C LOGAN, WR HAMILTON, WP GREEN, BJ BACON, RS HELGASON, CM KONDOS, GT HOFF, J MCRAE, RP HALPERIN, JL ROTHLAUF, EB WEINBERGER, JM GOLDMAN, ME MILLER, VT HOCKERSMITH, CJ COHEN, BA JANOSIK, DL CADELL, DJ KELLERMAN, L GOMEZ, CR LABOVITZ, AJ ROTHBART, RM BAILEY, GH BURKHARDT, C HORWITZ, L BLACKSHEAR, JL WEAVER, L BAKER, V LEE, G LANE, G RUBINO, F SAFFORD, R KRONMAL, RA PEARCE, LA FLETCHER, KA NASCO, E HART, RG SHERMAN, DG TALBERT, RL DACY, TL HERBERLING, PA TI WARFARIN VERSUS ASPIRIN FOR PREVENTION OF THROMBOEMBOLISM IN ATRIAL-FIBRILLATION - STROKE PREVENTION IN ATRIAL-FIBRILLATION-II STUDY SO LANCET LA English DT Article ID COMPLICATIONS; THERAPY AB Warfarin is an established treatment for prevention of ischaemic stroke in patients with atrial fibrillation, but the value of this agent relative to aspirin is unclear. In the first Stroke Prevention in Atrial Fibrillation (SPAF-I) study, direct comparison of warfarin with aspirin was limited by the small number of thromboembolic events. SPAF-II aims to address this issue and also to assess the differential effects of the two treatments according to age. We compared warfarin (prothrombin time ratio 1.3-1.8, international normalised ratio 2.0-4.5) with aspirin 325 mg daily for prevention of ischaemic stroke and systemic embolism (primary events) in two parallel randomised trials involving 715 patients aged 75 years or less and 385 patients older than 75; we sought reductions in the absolute rate of primary events by warfarin compared with aspirin of 2% per year and 4% per year, respectively. In the younger patients, warfarin decreased the absolute rate of primary events by 0.7% per year (95% Cl - 0.4 to 1.7). The primary event rate per year was 1.3% with warfarin and 1.9% with aspirin (relative risk [RR] 0.67, p = 0.24). The absolute rate of primary events in low-risk younger patients (without hypertension, recent heart failure, or previous thromboembolism) on aspirin was 0.5% per year (95% Cl 0.1 to 1.9). Among older patients, warfarin decreased the absolute rate of primary events by 1.2% per year (95% Cl - 1.7 to 4.1). The primary event rate per year was 3.6% with warfarin and 4.8% with aspirin (RR 0.73, p = 0.39). In this older group, the rate of all stroke with residual deficit (ischaemic or haemorrhagic) was 4.3% per year with aspirin and 4.6% per year with warfarin (RR 1.1). Warfarin may be more effective than aspirin for prevention of ischaemic stroke in patients with atrial fibrillation, but the absolute reduction in stroke rate by warfarin is small. Younger patients without risk factors had a low rate of stroke when treated with aspirin. In older patients the rate of stroke (ischaemic and haemorrhagic) was substantial, irrespective of which agent was given. Patient age and the inherent risk of thromboembolism should be considered in the choice of antithrombotic prophylaxis for patients with atrial fibrillation. C1 MAYO CLIN & MAYO FDN, ROCHESTER, MN USA. UNIV MISSOURI, COLUMBIA, MO USA. HENNEPIN CTY MED CTR, MINNEAPOLIS, MN USA. ABBOTT NW HOSP, MINNEAPOLIS, MN USA. PARK NICOLLET MED CTR, MINNEAPOLIS, MN USA. UNIV TEXAS, HLTH SCI CTR, SAN ANTONIO, TX USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. OREGON HLTH SCI UNIV, PORTLAND, OR 97201 USA. UNIV MIAMI, SCH MED, MIAMI, FL USA. KAISER PERMANENTE CTR HLTH RES, PORTLAND, OR USA. UNIV ARIZONA, COLL MED, TUCSON, AZ USA. UNIV CALIF SAN DIEGO, MED CTR, SAN DIEGO, CA 92103 USA. ST JOHNS MERCY MED CTR, ST LOUIS, MO USA. UNIV CHICAGO, COLL MED, CHICAGO, IL 60637 USA. UNIV ILLINOIS, COLL MED, PEORIA, IL 61656 USA. MT SINAI MED CTR, NEW YORK, NY 10029 USA. NORTHWESTERN UNIV, SCH MED, CHICAGO, IL USA. ST LOUIS UNIV, MED CTR, ST LOUIS, MO USA. UNIV COLORADO, SCH MED, DENVER, CO USA. MAYO CLIN, JACKSONVILLE, FL USA. UNIV WASHINGTON, SEATTLE, WA USA. RP MCBRIDE, R (reprint author), STAT & EPIDEMIOL RES CORP, 1107 NE 45TH ST, SUITE 520, SEATTLE, WA 98105 USA. NR 20 TC 609 Z9 616 U1 0 U2 10 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0140-6736 EI 1474-547X J9 LANCET JI Lancet PD MAR 19 PY 1994 VL 343 IS 8899 BP 687 EP 691 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA NB809 UT WOS:A1994NB80900006 ER PT J AU ALAGAR, R ALHIMYARY, A SYSTROM, D KAZEMI, H AF ALAGAR, R ALHIMYARY, A SYSTROM, D KAZEMI, H TI PULMONARY MEAN TRANSIT-TIME (MTT) AS A NONINVASIVE MARKER OF EXERCISE-INDUCED PULMONARY-HYPERTENSION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A917 EP A917 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701923 ER PT J AU BERK, DA YUAN, F LEUNIG, M JAIN, RK AF BERK, DA YUAN, F LEUNIG, M JAIN, RK TI MEASUREMENT OF IN-VIVO BINDING-KINETICS WITH FLUORESCENCE PHOTOBLEACHING SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RI Berk, David/A-4863-2012 OI Berk, David/0000-0002-3855-6886 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1034 EP A1034 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702588 ER PT J AU CARLBERG, KA GWOSDOW, AR ALVIN, BL AF CARLBERG, KA GWOSDOW, AR ALVIN, BL TI EXERCISE IN PREGNANT RATS INCREASES CORTICOSTERONE (CORT) CONCENTRATION IN MOTHERS AND FETUSES SO FASEB JOURNAL LA English DT Meeting Abstract C1 EASTERN WASHINGTON UNIV,CHENEY,WA 99004. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A791 EP A791 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701199 ER PT J AU CONLON, K OSBORNE, J MORIMOTO, C YOUNG, H ORTALDO, J AF CONLON, K OSBORNE, J MORIMOTO, C YOUNG, H ORTALDO, J TI COMPARISON OF LYMPHOKINE SECRETION AND LYMPHOKINE MESSENGER-RNA EXPRESSION IN THE CD45RA+ AND CD45RO+ SUBSETS OF HUMAN PERIPHERAL-BLOOD CD4+ AND CD8+ LYMPHOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 PRI,DYNCORP,BCDP,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. PRI,DYNCORP,BRMP,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. HARVARD UNIV,DANA FARBER CANC INST,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A999 EP A999 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702393 ER PT J AU CRUMP, AL GRUSBY, MJ GLIMCHER, LH CANTOR, H AF CRUMP, AL GRUSBY, MJ GLIMCHER, LH CANTOR, H TI MECHANISM OF INTRATHYMIC COMMITMENT TO THE CD4 AND CD8 LINEAGES SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOPATHOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A740 EP A740 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700900 ER PT J AU DELLIAN, M ABELS, C KUHNLE, GEH GOETZ, AE AF DELLIAN, M ABELS, C KUHNLE, GEH GOETZ, AE TI RAPID ONSET OF TUMOR ISCHEMIA FOLLOWING PHOTODYNAMIC THERAPY SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV MUNICH,INST SURG RES,W-8000 MUNICH 2,GERMANY. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1037 EP A1037 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702606 ER PT J AU DUBEY, DP MIRZA, NM ZAHARIAN, BI YUNIS, EJ AF DUBEY, DP MIRZA, NM ZAHARIAN, BI YUNIS, EJ TI REGULATION OF NK ACTIVITY BY A GENE OF CHROMOSOME-4 IN MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV IMMUNOGENET,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A987 EP A987 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702322 ER PT J AU DUPONTVERSTEEGDEN, EE MCCARTER, RJM KATZ, MS AF DUPONTVERSTEEGDEN, EE MCCARTER, RJM KATZ, MS TI PULMONARY-FUNCTION IS DECREASED IN MDX MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 UT,HLTH SCI CTR,DEPT PHYSIOL,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 FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A901 EP A901 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701830 ER PT J AU FURLONG, S THIBAULT, K SAMIA, J ROSE, R FISHMAN, J AF FURLONG, S THIBAULT, K SAMIA, J ROSE, R FISHMAN, J TI LIPIDS CHARACTERISTIC OF FUNGI IN PNEUMOCYSTIS-CARINII SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,DIV PULM MED,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A908 EP A908 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701871 ER PT J AU GAZIT, Y BERK, D LEUNIG, M BAXTER, LT JAIN, RK AF GAZIT, Y BERK, D LEUNIG, M BAXTER, LT JAIN, RK TI FRACTAL ANALYSIS OF 2-DIMENSIONAL TUMOR AND NORMAL VASCULAR NETWORKS AND ITS IMPLICATIONS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MIT,DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Berk, David/A-4863-2012 OI Berk, David/0000-0002-3855-6886 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1040 EP A1040 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702627 ER PT J AU GRANT, EP MICHALEK, MT ROCK, KL AF GRANT, EP MICHALEK, MT ROCK, KL TI UBIQUITIN AND THE 26S PROTEASOME ARE INVOLVED IN MHC CLASS-I ANTIGEN PRESENTATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A741 EP A741 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700908 ER PT J AU HAYES, LL MAYOR, SE FERRANTI, TJ ERICKSON, JE ODONNELL, MA CLINTON, SK AF HAYES, LL MAYOR, SE FERRANTI, TJ ERICKSON, JE ODONNELL, MA CLINTON, SK TI ANTITUMOR AND ANTIMETASTATIC EFFECTS OF INTERLEUKIN-12 (IL-12) IN THE MBT-2 MURINE BLADDER-CANCER MODEL SO FASEB JOURNAL LA English DT Meeting Abstract C1 GENET INST INC,CAMBRIDGE,MA 02140. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A772 EP A772 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701088 ER PT J AU HERBERT, V SHAW, S JAYATILLEKE, E AF HERBERT, V SHAW, S JAYATILLEKE, E TI VITAMIN-C SUPPLEMENTS ARE HARMFUL TO LETHAL FOR THE OVER 10-PERCENT OF AMERICANS WITH HIGH IRON STORES SO FASEB JOURNAL LA English DT Meeting Abstract C1 MT SINAI VA MED CTR,NEW YORK,NY 10468. BRONX VET ADM MED CTR,NEW YORK,NY 10468. NR 3 TC 8 Z9 8 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A678 EP A678 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700541 ER PT J AU HOBBS, SK CIMA, LG NUGENT, M LEUNIG, M JAIN, RK AF HOBBS, SK CIMA, LG NUGENT, M LEUNIG, M JAIN, RK TI MATHEMATICAL-MODEL AND IN-VITRO CHARACTERIZATION OF A BFGF CONTROLLED-RELEASE DEVICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MIT,DEPT CHEM ENGN,CAMBRIDGE,MA 02139. BOSTON UNIV,SCH MED,SCH MED,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,STEELE LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1043 EP A1043 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702643 ER PT J AU KANG, C HARIHARAN, K NARA, P SODROSKI, J MOORE, J AF KANG, C HARIHARAN, K NARA, P SODROSKI, J MOORE, J TI SOLUBLE CD4-GP120 COMPLEX PREFERENTIALLY INDUCES NEUTRALIZING ANTI-GP120 ANTIBODIES DIRECTED TO THE CONFORMATIONAL DEPENDENT EPITOPES SO FASEB JOURNAL LA English DT Meeting Abstract C1 IDEC PHARMACEUT CORP,SAN DIEGO,CA 92121. NCI,VIRUS BIOL UNIT,FREDERICK,MD 21701. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. DEPT CANC BIOL,BOSTON,MA. AARON DIAMOND AIDS RES CTR,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A961 EP A961 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702177 ER PT J AU KLICKSTEIN, LB DEFOUGEROLLES, LB YORK, AR SPRINGER, TA AF KLICKSTEIN, LB DEFOUGEROLLES, LB YORK, AR SPRINGER, TA TI LOCALIZATION OF THE LFA-1 BINDING-SITE ON ICAM-3 (CD50) SO FASEB JOURNAL LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1013 EP A1013 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702474 ER PT J AU KOVACSOVICSBANKOWSKI, M ROCK, KL AF KOVACSOVICSBANKOWSKI, M ROCK, KL TI CHARACTERIZATION OF THE EXOGENOUS ANTIGEN MHC CLASS-I PRESENTATION PATHWAY SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A991 EP A991 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702348 ER PT J AU LEU, AJ BERK, DA YUAN, F JAIN, RK AF LEU, AJ BERK, DA YUAN, F JAIN, RK TI FLOW VELOCITY IN LYMPH CAPILLARIES OF THE SKIN MEASURED IN A NEW MODEL USING THE TAIL OF THE NUDE-MOUSE SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114. RI Berk, David/A-4863-2012 OI Berk, David/0000-0002-3855-6886 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1048 EP A1048 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702674 ER PT J AU MICHAELEK, MT GRANT, EP ROCK, KL AF MICHAELEK, MT GRANT, EP ROCK, KL TI UBIQUITIN-DEPENDENT AND INDEPENDENT PROTEOLYTIC PATHWAYS FOR MHC CLASS I-RESTRICTED PRESENTATION OF OVALBUMIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A747 EP A747 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700944 ER PT J AU MIRZA, NM WEBER, GF DUBEY, DP CANTOR, H YUNIS, EJ AF MIRZA, NM WEBER, GF DUBEY, DP CANTOR, H YUNIS, EJ TI AGE-DEPENDENT DEFECT IN SIGNAL-TRANSDUCTION IN MURINE T-CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET & IMMUNOPATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A783 EP A783 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701150 ER PT J AU MUNN, LL MELDER, RJ JAIN, RK AF MUNN, LL MELDER, RJ JAIN, RK TI LYMPHOCYTE ADHESION TO ENDOTHELIAL MONOLAYERS UNDER DEFINED SHEAR-STRESS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. RI Munn, Lance/L-3950-2016 OI Munn, Lance/0000-0003-0698-7232 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1052 EP A1052 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702699 ER PT J AU NANJI, AA ZHAO, S SADRZADEH, SMH KHETTRY, U TAHAN, S WAXMAN, DJ AF NANJI, AA ZHAO, S SADRZADEH, SMH KHETTRY, U TAHAN, S WAXMAN, DJ TI MARKEDLY ENHANCED CYTOCHROME-P450 2E1 INDUCTION AND LIPID-PEROXIDATION IS ASSOCIATED WITH SEVERE LIVER-INJURY IN FISH-OIL ETHANOL-FED RATS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOL PHARMACOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A896 EP A896 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701800 ER PT J AU NICKELEIT, V ZAGACHIN, L ANDRES, G PETERS, J HYNES, R COLVIN, R AF NICKELEIT, V ZAGACHIN, L ANDRES, G PETERS, J HYNES, R COLVIN, R TI EMBRYONIC TYPE EIII-B FIBRONECTIN IS SYNTHESIZED AND DEPOSITED IN CRESCENTS IN AUTOIMMUNE GLOMERULONEPHRITIS IN THE RAT SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A872 EP A872 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701665 ER PT J AU RODBERG, G SURMAN, O KRADIN, R AF RODBERG, G SURMAN, O KRADIN, R TI EPINEPHRINE AUGMENTS LYMPHOCYTE TRAFFIC TO THE LUNG SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM UNIT,BOSTON,MA 02214. MASSACHUSETTS GEN HOSP,IMMUNOPATHOL UNIT,BOSTON,MA 02214. MASSACHUSETTS GEN HOSP,PSYCHOPHARMACOL UNIT,BOSTON,MA 02214. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1006 EP A1006 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702434 ER PT J AU SHEN, YT FALLON, JT DOWNEY, JM VATNER, SF AF SHEN, YT FALLON, JT DOWNEY, JM VATNER, SF TI SUPEROXIDE-DISMUTASE FAILS TO PROTECT ISCHEMIC MYOCARDIUM IN CONSCIOUS PIGS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. UNIV SO ALABAMA,DEPT MED PHYSIOL,MOBILE,AL 36688. NR 0 TC 0 Z9 0 U1 0 U2 4 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A831 EP A831 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701423 ER PT J AU TREPPO, S MIJAILOVICH, S HALES, CA VENEGAS, J AF TREPPO, S MIJAILOVICH, S HALES, CA VENEGAS, J TI CONTRIBUTION OF GRAVITY TO THE HETEROGENEITY OF PULMONARY PERFUSION (Q), VENTILATION (VA) AND VA/Q SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A691 EP A691 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700619 ER PT J AU VENEGAS, J TREPO, S MIJAILOVICH, S ZAPOL, W HALES, C AF VENEGAS, J TREPO, S MIJAILOVICH, S ZAPOL, W HALES, C TI EFFECTS OF INHALED NO IN THE SPATIAL HETEROGENEITY OF PULMONARY PERFUSION (Q), VENTILATION (VA) AND VA/Q SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A691 EP A691 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700617 ER PT J AU VILLANUEVA, POF REISER, H STADECKER, MJ AF VILLANUEVA, POF REISER, H STADECKER, MJ TI THE REGULATION OF T-HELPER CELL RESPONSES BY IL-10 AND ACCESSORY CELL COSTIMULATORY MOLECULES IN EXPERIMENTAL MURINE SCHISTOSOMIASIS SO FASEB JOURNAL LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A973 EP A973 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702243 ER PT J AU WANG, IH MA, I GUO, YI SY, MS BIGBY, M AF WANG, IH MA, I GUO, YI SY, MS BIGBY, M TI IN-VIVO TREATMENT WITH ANTI-ICAM-1 AND ANTI-LFA-1 ANTIBODIES INHIBITS CONTACT SENSITIZATION INDUCED MIGRATION OF EPIDERMAL LANGERHANS CELLS TO REGIONAL LYMPH-NODES SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02129. NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A981 EP A981 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702287 ER PT J AU WANG, W ZHOU, T MOUNTZ, JD AF WANG, W ZHOU, T MOUNTZ, JD TI BOTH CD3 AND FAS SIGNALS ARE REQUIRED TO INDUCE DELETION OF CD4+ CD8+ THYMOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 BIRMINGHAM VAMC,BIRMINGHAM,AL 35294. UNIV ALABAMA,BIRMINGHAM,AL 35294. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A740 EP A740 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700901 ER PT J AU WONG, JT MACLEAN, JA COLVIN, RB AF WONG, JT MACLEAN, JA COLVIN, RB TI ANTI-CD3 - ANTI-IL2 RECEPTOR (CD3,25) BISPECIFIC MONOCLONAL-ANTIBODY (BSMAB) - PREVENTION OF DIABETES IN NONOBESE DIABETIC (NOD) MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A967 EP A967 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702209 ER PT J AU IMBALZANO, AN ZARET, KS KINGSTON, RE AF IMBALZANO, AN ZARET, KS KINGSTON, RE TI TRANSCRIPTION FACTOR (TF) IIB AND TFIIA CAN INDEPENDENTLY INCREASE THE AFFINITY OF THE TATA-BINDING PROTEIN FOR PNA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RNA POLYMERASE-II; PREINITIATION COMPLEX; ACTIVATION DOMAIN; BASIC REPEAT; BOX FACTOR; INITIATION; DNA; MECHANISM; IDENTIFICATION; SEQUENCES AB The general transcription factors (TF) IIB and TFIIA are the first factors to associate with the TATA-binding protein (TBP) during formation of a transcription initiation complex on RNA polymerase II promoters. DNase I footprint titration was used to measure the effects of TFIIB and TFIIA on binding of TBP to a consensus TATA box. Under reaction conditions optimized for TBP.DNA complex formation, the presence of TFIIB increased affinity of TBP for the TATA box by 2.5-fold, while TFIIA had no effect. When TBP binding conditions were suboptimal, both TFIIB and TFIIA independently increased TBP affinity by approximately 10-fold. Therefore both TFIIB and TFIIA have the intrinsic ability to directly increase the affinity of TBP for the TATA box. We suggest that this property of TFIIA and TFIIB may increase the range of conditions under which high affinity TBP.DNA interactions can occur and may therefore favor the formation of the preinitiation complex. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. BROWN UNIV,BIOCHEM SECT,PROVIDENCE,RI 02912. FU NIGMS NIH HHS [GM48405] NR 42 TC 88 Z9 89 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 18 PY 1994 VL 269 IS 11 BP 8280 EP 8286 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB409 UT WOS:A1994NB40900068 PM 8132551 ER PT J AU CONDORELLI, G BUENO, R SMITH, RJ AF CONDORELLI, G BUENO, R SMITH, RJ TI 2 ALTERNATIVELY SPLICED FORMS OF THE HUMAN INSULIN-LIKE GROWTH-FACTOR-I RECEPTOR HAVE DISTINCT BIOLOGICAL-ACTIVITIES AND INTERNALIZATION KINETICS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID JUXTAMEMBRANE REGION; SIGNAL TRANSDUCTION; KINASE-ACTIVITY; PROTEIN; EXPRESSION; MUSCLE; IRS-1 AB Two alternatively spliced human insulin-like growth factor I (IGF I) receptor mRNA transcripts have been described that differ by three nucleotides (CAG) starting at position 2829. This results in an amino acid coding sequence change from Thr-Gly to Arg in the extracellular portion of the receptor beta subunit. To investigate the functional significance of this sequence difference, we obtained full-length cDNAs for the CAG+ and CAG- receptor forms, transfected CHO cells, and isolated multiple clones expressing approximately equal numbers of receptors (0.57-0.73 x 10(6) receptors/cell). The two receptors bound IGF I with similar affinity (K-d similar to 1.7 nM), but the CAG- form exhibited an approximately 2-fold increase in IGF I stimulation of receptor autophosphorylation, insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, thymidine incorporation, and IRS-1-associated phosphatidylinositol 3-kinase activity. In contrast to its higher signaling activity, the rate of receptor mediated internalization of IGF I by the CAG-receptor was decreased by 50% in comparison with the CAG+ receptor. We conclude that proteins corresponding to the two alternatively spliced human IGF I receptor transcripts are biologically active, but have distinct signaling properties. These experiments further indicate a previously unrecognized role for the extramembranous portion of the beta subunit in receptor signaling and internalization. C1 JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. OI condorelli, gerolama/0000-0003-0177-8829 FU NIDDK NIH HHS [DK43038]; NIGMS NIH HHS [GM07560]; PHS HHS [36836] NR 30 TC 52 Z9 53 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 18 PY 1994 VL 269 IS 11 BP 8510 EP 8516 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB409 UT WOS:A1994NB40900102 PM 7510688 ER PT J AU ETCOFF, NL AF ETCOFF, NL TI PSYCHOLOGY - BEAUTY AND THE BEHOLDER SO NATURE LA English DT Editorial Material ID ATTRACTIVE FACES RP ETCOFF, NL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,NEUROPSYCHOL LAB,BOSTON,MA 02114, USA. NR 12 TC 23 Z9 24 U1 1 U2 10 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 17 PY 1994 VL 368 IS 6468 BP 186 EP 187 DI 10.1038/368186a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NA870 UT WOS:A1994NA87000025 PM 8145814 ER PT J AU BRONNER, CE BAKER, SM MORRISON, PT WARREN, G SMITH, LG LESCOE, MK KANE, M EARABINO, C LIPFORD, J LINDBLOM, A TANNERGARD, P BOLLAG, RJ GODWIN, AR WARD, DC NORDENSKJOLD, M FISHEL, R KOLODNER, R LISKAY, RM AF BRONNER, CE BAKER, SM MORRISON, PT WARREN, G SMITH, LG LESCOE, MK KANE, M EARABINO, C LIPFORD, J LINDBLOM, A TANNERGARD, P BOLLAG, RJ GODWIN, AR WARD, DC NORDENSKJOLD, M FISHEL, R KOLODNER, R LISKAY, RM TI MUTATION IN THE DNA MISMATCH REPAIR GENE HOMOLOG HMLH1 IS ASSOCIATED WITH HEREDITARY NONPOLYPOSIS COLON-CANCER SO NATURE LA English DT Article ID SACCHAROMYCES-CEREVISIAE; NUCLEOTIDE-SEQUENCE; STREPTOCOCCUS-PNEUMONIAE; SALMONELLA-TYPHIMURIUM; INSITU HYBRIDIZATION; PMS1; MUTL; HEXB AB THE human DNA mismatch repair gene homologue, hMSH2, on chromosome 2p is involved in hereditary non-polyposis colon cancer (HNPCC)(1,2). On the basis of linkage data, a second HNPCC locus was assigned to chromosome 3p21-23 (ref. 3). Here we report that a human gene encoding a protein, hMLH1 (human MutL homologue), homologous to the bacterial DNA mismatch repair protein MutL, is located on human chromosome 3p21.3-23. We propose that hMLH1 is the HNPCC gene located on 3p because of the similarity of the hMLH1 gene product to the yeast DNA mismatch repair protein, MLH1(4,5), the coincident location of the hMLH1 gene and the HNPCC locus on chromosome 3, and hMLH1 missense mutations in affected individuals from a chromosome 3-linked HNPCC family. C1 OREGON HLTH SCI UNIV,DEPT MOLEC & MED GENET,PORTLAND,OR 97201. DANA FARBER CANC INST,MOLEC BIOL CORE FACIL,BOSTON,MA 02115. YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT MOLEC BIOPHYS & BIOCHEM,NEW HAVEN,CT 06510. UNIV VERMONT,MARKEY CTR MOLEC GENET,DEPT MICROBIOL & MOLEC GENET,BURLINGTON,VT 05405. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. KAROLINSKA HOSP,DEPT MOLEC MED,S-17176 STOCKHOLM,SWEDEN. NR 30 TC 1708 Z9 1746 U1 4 U2 79 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 17 PY 1994 VL 368 IS 6468 BP 258 EP 261 DI 10.1038/368258a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NA870 UT WOS:A1994NA87000060 PM 8145827 ER PT J AU LENDERKING, WR GELBER, RD COTTON, DJ COLE, BF GOLDHIRSCH, A VOLBERDING, PA TESTA, MA AF LENDERKING, WR GELBER, RD COTTON, DJ COLE, BF GOLDHIRSCH, A VOLBERDING, PA TESTA, MA TI EVALUATION OF THE QUALITY-OF-LIFE ASSOCIATED WITH ZIDOVUDINE TREATMENT IN ASYMPTOMATIC HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID PLACEBO-CONTROLLED TRIAL; ADJUSTED SURVIVAL ANALYSIS; AIDS-RELATED COMPLEX; OF-LIFE; HIV-INFECTION; BREAST-CANCER; DOUBLE-BLIND; THERAPY; AZT AB Background. Zidovudine therapy is recommended for asymptomatic patients infected with the human immunodeficiency virus (HIV) who have fewer than 500 CD4+ cells per cubic millimeter. An analysis of the quality of life associated with therapy that integrated both the effects of adverse events and the benefits of delayed disease progression might influence this recommendation. Methods. We applied a survival analysis adjusted for the quality of life to data from a randomized trial conducted by the AIDS Clinical Trials Group, The trial compared treatment with 500 mg of zidovudine per day, 1500 mg of zidovudine per day, and placebo (Protocol 019) in 1338 asymptomatic HIV-infected patients. Results. The average time with neither a progression of disease nor an adverse event (symptom or laboratory finding) was 15.7, 15.6, and 14.8 months for patients receiving placebo, 500 mg of zidovudine, and 1500 mg of zidovudine, respectively. The incidence of severe symptoms was 13.8 percent in the placebo group, 15.2 percent in the 500-mg group, and 19.9 percent in the 1500-mg group (P = 0.038). After 18 months, the 500-mg group gained an average of 0.5 month without disease progression, as compared with the placebo group, but had severe adverse events an average of 0.6 month sooner. The 500-mg group had more quality-of-life-adjusted time than the placebo group only if the time lived after the progression of disease was considered by a patient to have less value than the time after the occurrence of a severe symptom. Conclusions. For asymptomatic patients treated with 500 mg of zidovudine, a reduction in the quality of life due to severe side effects of therapy approximately equals the increase in the quality of life associated with a delay in the progression of HIV disease. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. SAN FRANCISCO GEN HOSP,SAN FRANCISCO,CA 94110. RP LENDERKING, WR (reprint author), HARVARD UNIV,SCH PUBL HLTH,CTR STAT DATA & ANAL,DEPT BIOSTAT AIDS CLIN TRIALS GRP,BOSTON,MA 02115, USA. RI Cole, Bernard/I-3775-2012 FU AHRQ HHS [R01 HS07767-01]; PHS HHS [N0-A1-95030] NR 20 TC 129 Z9 129 U1 1 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 17 PY 1994 VL 330 IS 11 BP 738 EP 743 DI 10.1056/NEJM199403173301102 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA NA742 UT WOS:A1994NA74200002 PM 7906386 ER PT J AU CRYNS, VL THOR, A XU, HJ HU, SX WIERMAN, ME VICKERY, AL BENEDICT, WF ARNOLD, A AF CRYNS, VL THOR, A XU, HJ HU, SX WIERMAN, ME VICKERY, AL BENEDICT, WF ARNOLD, A TI LOSS OF THE RETINOBLASTOMA TUMOR-SUPPRESSOR GENE IN PARATHYROID CARCINOMA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID SUSCEPTIBILITY GENE; CELL-CYCLE; EXPRESSION; PROTEIN; CANCER; POLYMORPHISMS; PROGRESSION; DIAGNOSIS; FEATURES; SEQUENCE AB Background. The origin and molecular pathogenesis of parathyroid carcinoma are unknown. This life-threatening cause of primary hyperparathyroidism cannot be reliably distinguished from its benign counterpart on the basis of histopathological features alone. Because the PRAD1, or cyclin D1, gene, a cell-cycle regulator, has been implicated in a subgroup of benign parathyroid tumors, we examined the possibility that another cell-cycle regulator with possible functional links to PRAD1, the retinoblastoma tumor-suppressor gene (RB), might be involved in the molecular pathogenesis of parathyroid carcinoma. Methods. Parathyroid carcinomas from 9 patients and adenomas from 21 were studied for evidence of tumor-specific loss of RB gene DNA (allelic loss) by analysis of four DNA polymorphisms and for evidence of altered expression of RB protein by immunohistochemical staining. Results. All of 11 specimens from 5 patients with parathyroid carcinoma and informative DNA patterns and 1 of 19 specimens from 19 patients with parathyroid adenoma and informative DNA patterns lacked an RB allele. Fourteen of 16 specimens (88 percent) from the nine patients with carcinoma had abnormal expression of RB protein (a complete or predominant absence of nuclear staining for the protein). None of the 19 adenomas, including the tumor with loss of an RB allele, had unequivocally abnormal staining for RB protein. Conclusions. Inactivation of the RB gene is common in parathyroid carcinoma and is likely to be an important contributor to its molecular pathogenesis. The presence of such inactivation may help to distinguish benign from malignant parathyroid disease and may have useful diagnostic, prognostic, and therapeutic implications. C1 MASSACHUSETTS GEN HOSP,DEPT MED,ENDOCRINE ONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. BAYLOR COLL MED,CTR BIOTECHNOL,THE WOODLANDS,TX 77381. VET AFFAIRS MED CTR,ENDOCRINOL SECT,DENVER,CO. UNIV COLORADO,HLTH SCI CTR,DENVER,CO. FU NCI NIH HHS [1F32 CA-0938101, 1K08 CA-01752-01A1]; NIDDK NIH HHS [5T32 DK-0702817] NR 35 TC 205 Z9 209 U1 0 U2 4 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 17 PY 1994 VL 330 IS 11 BP 757 EP 761 DI 10.1056/NEJM199403173301105 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA NA742 UT WOS:A1994NA74200005 PM 7906387 ER PT J AU HENSON, JW AF HENSON, JW TI CASE-43-1993 - OCCIPITAL MASS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP HENSON, JW (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02129, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 17 PY 1994 VL 330 IS 11 BP 793 EP 793 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA NA742 UT WOS:A1994NA74200027 ER PT J AU CASALE, PN FIFER, MA GRAHAM, RM PALACIOS, IF AF CASALE, PN FIFER, MA GRAHAM, RM PALACIOS, IF TI RELATION OF ATRIAL PRESSURE AND PLASMA-LEVEL OF ATRIAL-NATRIURETIC-FACTOR IN CARDIAC-TAMPONADE SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Note ID PEPTIDE; RELEASE; PERICARDIOCENTESIS; ELEVATION; RESPONSES; HORMONE; STRETCH; DOGS C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. NR 20 TC 3 Z9 3 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAR 15 PY 1994 VL 73 IS 8 BP 610 EP 613 DI 10.1016/0002-9149(94)90346-8 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NB935 UT WOS:A1994NB93500020 PM 8147312 ER PT J AU GROSS, FJ TINGEY, D EPSTEIN, DL AF GROSS, FJ TINGEY, D EPSTEIN, DL TI INCREASED PREVALENCE OF OCCLUDABLE ANGLES AND ANGLE-CLOSURE GLAUCOMA IN PATIENTS WITH PSEUDOEXFOLIATION SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID EXFOLIATION SYNDROME AB The association between angle-closure glaucoma and pseudoexfoliation is controversial. We retrospectively studied the angle configurations of 54 patients with pseudoexfoliation and found gonioscopically occludable angles in five cases (9.3%). We also analyzed the data from several large studies of pseudoexfoliation patients and found an increased prevalence of acute angle-closure glaucoma in this group. These data suggest that pseudoexfoliation patients may represent a high-risk population for the development of angle-closure glaucoma. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 11 TC 36 Z9 42 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD MAR 15 PY 1994 VL 117 IS 3 BP 333 EP 336 PG 4 WC Ophthalmology SC Ophthalmology GA MZ314 UT WOS:A1994MZ31400007 PM 8129006 ER PT J AU CHEN, G WAXMAN, DJ AF CHEN, G WAXMAN, DJ TI ROLE OF CELLULAR GLUTATHIONE AND GLUTATHIONE-S-TRANSFERASE IN THE EXPRESSION OF ALKYLATING AGENT CYTOTOXICITY IN HUMAN BREAST-CANCER CELLS SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE ALKYLATING AGENTS; DRUG RESISTANCE; DRUG SENSITIVITY; REDUCED GLUTATHIONE; GLUTATHIONE S-TRANSFERASE; MCF-7 CELLS ID MELPHALAN CYTO-TOXICITY; L-PHENYLALANINE MUSTARD; HUMAN-MELANOMA CELLS; HUMAN-LEUKEMIA-CELLS; ETHACRYNIC-ACID; BUTHIONINE SULFOXIMINE; DRUG-RESISTANT; CROSS-LINKING; CISPLATIN RESISTANCE; PLATINUM COMPOUNDS AB Glutathione (GSH) and glutathione S-transferases (GSTs) play an important role in the protection of cells against toxic effects of many electrophilic drugs and chemicals. Modulation of cellular GSH and/or GST activity levels provides a potentially useful approach to sensitizing tumor cells to electrophilic anti-cancer drugs. In this study, we describe the interactions of four representative alkylating agents (AAs), melphalan, 4-hydroperoxy-cyclophosphamide (4HC), an activated form of cyclophosphamide, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), and cisplatin, with GSH and GST in the human breast cancer cell line MCF-7. Depletion of cellular GSH pools by approximately 80% by treatment of the cells with the GSH synthesis inhibitor buthionine sulfoximine (BSO) sensitized the tumor cells to each AA to a different extent, with dose-modifying factors of 2.39, 2.21, 1.64, and 1.27 observed for melphalan, 4HC, cisplatin, and BCNU, respectively. Treatment of the cells with the GST inhibitor ethacrynic acid (EA) failed to show any significant effects on the cytotoxicity of these AAs. However, EA did potentiate the cytotoxicity of melphalan when given in combination with BSO, an effect that may be due to a more complete depletion of cellular GSH levels by the combined modulator treatment. Following a 1-hr exposure to cytotoxic-equivalent concentrations of these AAs, GSH levels decreased substantially in the case of 4HC and BCNU, but increased by 30-50% in the case of cisplatin and melphalan. BSO pretreatment largely blocked this effect of cisplatin and melphalan on cellular GSH, while it further enhanced the GSH-depleting activity of both 4HC and BCNU. On the basis of these results, it is concluded that (a) GSH affects the cytotoxicity of different AAs to different extents, (b) basal GST expression in MCF-7 cells does not play a major role in AA metabolism, (c) EA can potentiate the enhancing effect of BSO on melphalan cytotoxicity in MCF-7 cells, and (d) depletion of cellular GSH by pretreatment with BCNU or cyclophosphamide may correspond to a useful strategy for enhancing the anti-tumor activity of other AAs given in a sequential combination. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 57 TC 67 Z9 67 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 15 PY 1994 VL 47 IS 6 BP 1079 EP 1087 DI 10.1016/0006-2952(94)90420-0 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NC158 UT WOS:A1994NC15800019 PM 8147907 ER PT J AU FARAONE, SV BIEDERMAN, J MILBERGER, S AF FARAONE, SV BIEDERMAN, J MILBERGER, S TI AN EXPLORATORY-STUDY OF ADHD AMONG 2ND-DEGREE RELATIVES OF ADHD CHILDREN SO BIOLOGICAL PSYCHIATRY LA English DT Article DE ATTENTION DEFICIT HYPERACTIVITY DISORDER; FAMILY STUDY; 2ND-DEGREE RELATIVES ID ATTENTION-DEFICIT DISORDER; HYPERACTIVE-CHILDREN; CONDUCT DISORDER; FAMILIAL ASSOCIATION; RISK-FACTORS; PARENTS; PSYCHOPATHOLOGY; GIRLS; TWIN AB Family-genetic studies consistently show that attention deficit hyperactivity disorder (ADHD) aggregates in nuclear families. Little is known about the aggregation of ADHD in second-degree relatives. We examined the prevalence of ADHD in second-degree relatives of 140 ADHD probands and 120 normal controls. Information pertinent to the diagnosis of ADHD in second-degree relatives was collected from the probands' parents. The second-degree relatives of ADHD probands were at increased risk for ADHD compared with the second-degree relatives of normal control probands. These risks were greatest when the second-degree relative was biologically related to an ADHD parent of an ADHD proband. Consistent with the greater prevalence of ADHD among boys compared with girls, grandfathers were at greater risk than grandmothers and uncles were at greater risk than aunts. Our results support the usefulness of ascertaining information from second-degree relatives in studies evaluating the genetic epidemiology of ADHD. If confirmed, such studies may help clarify the mechanism of familial transmission of ADHD. C1 MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT ACC 725,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,MASSACHUSETTS MENTAL HLTH CTR,BOSTON,MA 02115. BROCKTON W ROXBURY VET AFFAIRS MED CTR,BROCKTON,MA. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [R01 MH-41314-01A2] NR 32 TC 51 Z9 51 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1994 VL 35 IS 6 BP 398 EP 402 DI 10.1016/0006-3223(94)90006-X PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NF092 UT WOS:A1994NF09200006 PM 8018786 ER PT J AU GULLEY, ML EAGAN, PA QUINTANILLAMARTINEZ, L PICADO, AL SMIR, BN CHILDS, C DUNN, CD CRAIG, FE WILLIAMS, JW BANKS, PM AF GULLEY, ML EAGAN, PA QUINTANILLAMARTINEZ, L PICADO, AL SMIR, BN CHILDS, C DUNN, CD CRAIG, FE WILLIAMS, JW BANKS, PM TI EPSTEIN-BARR-VIRUS DNA IS ABUNDANT AND MONOCLONAL IN THE REED-STERNBERG CELLS OF HODGKINS-DISEASE - ASSOCIATION WITH MIXED CELLULARITY SUBTYPE AND HISPANIC AMERICAN ETHNICITY SO BLOOD LA English DT Article ID POLYMERASE CHAIN-REACTION; INSITU HYBRIDIZATION; VIRAL GENOMES; SAN-ANTONIO; EBV; LYMPHOMA; EXPRESSION; GENE; SIBLINGS; TISSUE C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. INST NACL NUTR,DEPT PATOL,THALPAN,DF,MEXICO. HOSP SAN JUAN DIOS,DEPT PATOL,SAN JOSE,COSTA RICA. SW TEXAS METHODIST HOSP,SAN ANTONIO,TX. WILFORD HALL USAF MED CTR,SAN ANTONIO,TX 78236. RP GULLEY, ML (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU AHRQ HHS [U01-HS07397]; NCI NIH HHS [K08-CA01615] NR 51 TC 104 Z9 105 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 1994 VL 83 IS 6 BP 1595 EP 1602 PG 8 WC Hematology SC Hematology GA NA491 UT WOS:A1994NA49100021 PM 8123850 ER PT J AU NEUBAUER, A DODGE, RK GEORGE, SL DAVEY, FR SILVER, RT SCHIFFER, CA MAYOR, RJ BALL, ED WURSTERHILL, D BLOOMFIELD, CD LIU, ET AF NEUBAUER, A DODGE, RK GEORGE, SL DAVEY, FR SILVER, RT SCHIFFER, CA MAYOR, RJ BALL, ED WURSTERHILL, D BLOOMFIELD, CD LIU, ET TI PROGNOSTIC IMPORTANCE OF MUTATIONS IN THE RAS PROTOONCOGENES IN DE-NOVO ACUTE MYELOID-LEUKEMIA SO BLOOD LA English DT Article ID GENE-MUTATIONS; MYELOGENOUS LEUKEMIA; PROTOONCOGENES; CARCINOGENESIS; ACTIVATION; CELLS C1 UNIV N CAROLINA,LINEBERGER CANC RES CTR,DEPT MED,DIV HEMATOL & ONCOL,CHAPEL HILL,NC 27599. UNIV N CAROLINA,LINEBERGER CANC RES CTR,CURRICULUM GENET,CHAPEL HILL,NC. DUKE UNIV,CTR STAT,CANC & LEUKEMIA GRP B,DURHAM,NC. SYRACUSE UNIV,SYRACUSE,NY. CORNELL UNIV,NEW YORK HOSP,MED CTR,DEPT MED,NEW YORK,NY. UNIV MARYLAND,CTR CANC,BALTIMORE,MD 21201. DANA FARBER CANC INST,BOSTON,MA. UNIV PITTSBURGH,DEPT MED,PITTSBURGH,PA. DARTMOUTH COLL,SCH MED,DEPT PATHOL,HANOVER,NH. ROSWELL PK CANC INST,BUFFALO,NY. RI Liu, Edison/C-4141-2008 FU NCI NIH HHS [CA47545-04, CA-37027, R01-CA49240-03] NR 32 TC 159 Z9 161 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 1994 VL 83 IS 6 BP 1603 EP 1611 PG 9 WC Hematology SC Hematology GA NA491 UT WOS:A1994NA49100022 PM 8123851 ER PT J AU WONG, TY SUSTER, S NOGITA, T DUNCAN, LM DICKERSIN, RG MIHM, MC AF WONG, TY SUSTER, S NOGITA, T DUNCAN, LM DICKERSIN, RG MIHM, MC TI CLEAR-CELL ECCRINE CARCINOMAS OF THE SKIN - A CLINICOPATHOLOGICAL STUDY OF 9 PATIENTS SO CANCER LA English DT Article DE SWEAT GLAND CARCINOMA; SKIN ADNEXAL NEOPLASMS; CLEAR CELL NEOPLASM; ECCRINE CARCINOMA ID SWEAT GLAND TUMORS; CARCINOEMBRYONIC ANTIGEN; IMMUNOHISTOCHEMISTRY; HIDRADENOMA; SPIRADENOMA; NEOPLASMS; PROTEIN AB Background. Sweat gland carcinomas with clear cell features are extremely rare neoplasms, with few well documented cases reported in the literature. Methods. Data on nine patients with malignant eccrine adnexal neoplasms characterized by a prominent clear cell neoplastic component were studied. Immunohistochemical stains with a panel of antibodies against epithelial, stromal, and neural antigens were performed on five tumors and electron microscopic examination of one. Results. The tumors showed a spectrum of histologic features and growth patterns that ranged from well differentiated, low grade malignant neoplasms to poorly differentiated, highly aggressive, recurrent, and metastasizing tumors. All tumors contained a varied proportion of cells with abundant clear cytoplasm, similar to those seen in a group of benign eccrine adnexal neoplasms that have been variously designated as clear cell hidradenoma, nodular hidradenoma, clear cell myoepithelioma, and eccrine acrospiroma. Immunohistochemical stains on five tumors and ultrastructural examination in one were consistent with eccrine differentiation. Clinical follow-up of eight patients showed local recurrence in six, followed by metastases in three, despite local excision, radiation, and chemotherapy. Criteria for differentiating these tumors from their benign counterparts and from other types of malignant adnexal neoplasms and metastatic lesions are presented. Conclusions. The findings indicate that clear cell eccrine carcinomas comprise a heterogeneous group of lesions that may range from locally recurring, low grade well differentiated tumors to highly aggressive, high grade tumors with a definite potential for uncontrollable local recurrence and metastasis. Wide surgical excision is recommended as the primary treatment for such neoplasms. C1 MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. MT SINAI MED CTR,DEPT PATHOL,MIAMI BEACH,FL. UNIV MIAMI,SCH MED,MIAMI BEACH,FL. RI Duncan, Lyn/E-9878-2013 NR 32 TC 54 Z9 56 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 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1994 VL 73 IS 6 BP 1631 EP 1643 DI 10.1002/1097-0142(19940315)73:6<1631::AID-CNCR2820730615>3.0.CO;2-7 PG 13 WC Oncology SC Oncology GA NA319 UT WOS:A1994NA31900014 PM 7512435 ER PT J AU VONDEIMLING, A BENDER, B JAHNKE, R WAHA, A KRAUS, J ALBRECHT, S WELLENREUTHER, R FASSBENDER, F NAGEL, J MENON, AG LOUIS, DN LENARTZ, D SCHRAMM, J WIESTLER, OD AF VONDEIMLING, A BENDER, B JAHNKE, R WAHA, A KRAUS, J ALBRECHT, S WELLENREUTHER, R FASSBENDER, F NAGEL, J MENON, AG LOUIS, DN LENARTZ, D SCHRAMM, J WIESTLER, OD TI LOCI ASSOCIATED WITH MALIGNANT PROGRESSION IN ASTROCYTOMAS - A CANDIDATE ON CHROMOSOME 19Q SO CANCER RESEARCH LA English DT Note ID DINUCLEOTIDE REPEAT POLYMORPHISM; GENE AMPLIFICATION; SHORT ARM; DELETIONS; OLIGODENDROGLIOMAS; HETEROZYGOSITY; ALLELOTYPE; GLIOMAS; TUMORS; PCR AB WHO grades II, and III astrocytomas frequently exhibit loss of genetic material on chromosomes 9p, 11p, 17p, 19q, and 22q, indicating that these chromosomal regions harbor tumor suppressor genes involved in the pathogenesis of astrocytic neoplasms. The present study was conducted to examine whether these genetic regions are involved in the process of malignant progression from astrocytoma WHO grade II (A TT) to anaplastic astrocytoma WHO grade III (A III). We have analyzed 44 astrocytomas, i.e., 18 A II and 26 A III for loss of heterozygosity (LOH) on chromosomes 1p, 1q, 9p, 9q, 10p, 10q, 11p, 13q, 17p, 19p, 19a, and 22q and for amplification of the epidermal growth factor receptor gene. A polymerase chain reaction-based assay with microsatellite repeat sequences was used for the detection of polymorphisms on silver-stained polyacrylamide gels. LOH on 9p was seen in 1 of 18 (6%) informative cases of A II and 4 of 24 (17%) informative cases of A III. LOH on 17p was observed in 9 of 17 (53%) informative cases of A II and 15 of 26 (58%) informative cases of A III. LOH on 19q was detected in 2 of 18 (11%) informative cases of A ZI and in 12 of 26 (46%) informative cases of A III. The association of LOH on 19q with anaplasia in astrocytoma was significant (P = 0.015). Amplification of the epidermal growth factor receptor gene was not detected in A II or A III. These data suggest that a putative tumor suppressor gene on the long arm of chromosome 19 is a candidate for a gene associated with tumor progression in astrocytic gliomas. C1 UNIV CINCINNATI,DEPT MOLEC GENET BIOCHEM & MICROBIOL,CINCINNATI,OH 45267. MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02129. NEUROCHIRURG KLIN KOLN MERHEIM,D-51109 COLOGNE,GERMANY. UNIV BONN,NEUROCHIRURG KLIN,D-53105 BONN,GERMANY. RP VONDEIMLING, A (reprint author), UNIV BONN KLINIKEN,INST NEUROPATHOL,SIGMUND FREUD STR 25,D-53105 BONN,GERMANY. RI von Deimling, Andreas/F-7774-2013 OI von Deimling, Andreas/0000-0002-5863-540X NR 38 TC 83 Z9 83 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1994 VL 54 IS 6 BP 1397 EP 1401 PG 5 WC Oncology SC Oncology GA NA887 UT WOS:A1994NA88700002 PM 8137236 ER PT J AU SALA, A NICOLAIDES, NC ENGELHARD, A BELLON, T LAWE, DC ARNOLD, A GRANA, X GIORDANO, A CALABRETTA, B AF SALA, A NICOLAIDES, NC ENGELHARD, A BELLON, T LAWE, DC ARNOLD, A GRANA, X GIORDANO, A CALABRETTA, B TI CORRELATION BETWEEN E2F-1 REQUIREMENT IN THE S-PHASE AND E2F-1 TRANSACTIVATION OF CELL CYCLE-RELATED GENES IN HUMAN-CELLS SO CANCER RESEARCH LA English DT Note ID TRANSCRIPTION FACTOR-E2F; BINDING PROTEIN; CDC2 GENE; EXPRESSION; MYB; ACTIVATION; IDENTIFICATION; COMPONENT; PROMOTER; COMPLEX AB The mammalian nuclear protein E2F-1 has recently been cloned based on its ability to bind the retinoblastoma protein. To determine whether E2F-1 plays a role in the control of the cell proliferation, we introduced an inducible construct expressing an E2F-1 antisense RNA into the human glioblastoma T98G cell line and assessed DNA synthesis during the cell cycle. Expression of the antisense transcripts during the G(1)-S transition resulted in a marked delay in the completion of DNA synthesis. Band-shift analysis of bacterially produced E2F-1 showed that this protein bound to the promoters of human DNA polymerase-alpha, cyclin D1, and c-myb but not to the cdc2 gene promoter. E2F-1 also transactivated the bound promoters in transient transfection assays. These results suggest a major role for E2F-1 in the control of cell cycle progression via transcriptional regulation of proliferation-associated genes. C1 THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19107. MASSACHUSETTS GEN HOSP,ENDOCRINE ONCOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. TEMPLE UNIV,FELS INST CANC RES & MOLEC BIOL,PHILADELPHIA,PA 19140. TEMPLE UNIV,DEPT PATHOL & BIOCHEM,PHILADELPHIA,PA 19140. RI sala, arturo/C-4959-2008; Giordano, Antonio/F-1927-2010 OI Giordano, Antonio/0000-0002-5959-016X FU NCI NIH HHS [CA55909] NR 34 TC 79 Z9 79 U1 0 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1994 VL 54 IS 6 BP 1402 EP 1406 PG 5 WC Oncology SC Oncology GA NA887 UT WOS:A1994NA88700003 PM 8137237 ER PT J AU KHARBANDA, S SALEEM, A DATTA, R YUAN, ZM WEICHSELBAUM, R KUFE, D AF KHARBANDA, S SALEEM, A DATTA, R YUAN, ZM WEICHSELBAUM, R KUFE, D TI IONIZING-RADIATION INDUCES RAPID TYROSINE PHOSPHORYLATION OF P34(CDC2) SO CANCER RESEARCH LA English DT Note ID CELL-CYCLE; SCHIZOSACCHAROMYCES-POMBE; SACCHAROMYCES-CEREVISIAE; DNA DAMAGE; RAD9 GENE; KINASE; MECHANISM; MITOSIS; P34CDC2; ARREST AB Eukaryotic cells respond to ionizing radiation exposure with cell cycle arrest. However, little is known about the signaling mechanisms responsible for this effect. The present work has asked whether ionizing radiation exposure is associated with changes in phosphorylation of proteins in HL-60 myeloid leukemia cells. The results demonstrate increased tyrosine phosphorylation of a M(r) 34,000 substrate. This effect was detectable at 1 to 10 min after irradiation and was induced by doses of 50 to 500 cGy. Immunoprecipitation studies further suggest that this substrate is the serine/threonine p34(cdc2) protein kinase. Since p34(cdc2) is required for entry into mitosis, these findings support the posttranslational modification of a cell cycle regulatory protein in the response to ionizing radiation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. UNIV CHICAGO,PRITZKER SCH MED,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. FU NCI NIH HHS [CA55241] NR 22 TC 96 Z9 98 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1994 VL 54 IS 6 BP 1412 EP 1414 PG 3 WC Oncology SC Oncology GA NA887 UT WOS:A1994NA88700005 PM 8137239 ER PT J AU SUN, XC WONG, JR SONG, KL HU, JL GARLID, KD CHEN, LB AF SUN, XC WONG, JR SONG, KL HU, JL GARLID, KD CHEN, LB TI AA1, A NEWLY SYNTHESIZED MONOVALENT LIPOPHILIC CATION, EXPRESSES POTENT IN-VIVO ANTITUMOR-ACTIVITY SO CANCER RESEARCH LA English DT Article ID MULTIDRUG-RESISTANCE GENE; RAT-LIVER MITOCHONDRIA; LIGHT-SCATTERING; CARCINOMA-CELLS; HUMAN-TUMORS; RHODAMINE-123; ACCUMULATION; MEMBRANE; PHOTOCHEMOTHERAPY; CONTRACTION AB Certain lipophilic cations have been reported to display anticarcinoma activities because of their selective uptake and retention by mitochondria of cancer tells. Thus, these agents may comprise a unique class of agents directed against carcinoma. After screening more than 1000 lipophilic cations, we found that the monovalent lipophilic cation, 2,6-bis(4-aminophenyl)-4-[4-(dimethylamino)phenyl]thiop chloride (AA1), displayed remarkable anticarcinoma activity both in vitro and in vivo. Unlike most other lipophilic cations, AA1 is stable and displays minimal light sensitivity. In vitro testing showed that AA1 was 10 times more toxic to the carcinoma cell line CX-1 than to the normal epithelial cell line CV-1. In vivo animal experiments showed that AA1 significantly prolonged the survival of mice implanted with tumors. For C57BL x DBA/2 F-1 mice implanted with the mouse bladder carcinoma cell line, MB49, the treated:control ratio was 344%. For Swiss nu/nu mice implanted i.p. with the human melanoma cell line, LOX, the treated:control ratio was 341%. The most significant observation was obtained with Swiss nu/nu mice that were implanted i.p. with the human ovarian cell line, OVCAR-III. The treated:control ratio in this situation was greater than 450%. In all these tumor models, AA1 produced minimal toxicities. AA1 exhibited little inhibition of electron transport in isolated rat liver mitochondria; however, it inhibited mitochondrial ATPase with 50% inhibitory concentration of 6 mu M. Compared with previously reported anticarcinoma lipophilic cations such as rhodamine 123 and dequalinium chloride, AA1 appeared to display more effective in vivo anticarcinoma activity. Thus, AA1 could be considered for further clinical development as a candidate for anticarcinoma chemotherapy. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MED COLL OHIO,DEPT PHARMACOL,TOLEDO,OH 43614. NR 34 TC 76 Z9 78 U1 0 U2 6 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1994 VL 54 IS 6 BP 1465 EP 1471 PG 7 WC Oncology SC Oncology GA NA887 UT WOS:A1994NA88700015 PM 8137249 ER PT J AU ARA, G KUSUMOTO, T KORBUT, TT CULLERELUENGO, F TEICHER, BA AF ARA, G KUSUMOTO, T KORBUT, TT CULLERELUENGO, F TEICHER, BA TI CIS-DIAMMINEDICHLOROPLATINUM(II) RESISTANT HUMAN TUMOR-CELL LINES ARE COLLATERALLY SENSITIVE TO PTCL4(RH-123)(2) - EVIDENCE FOR MITOCHONDRIAL INVOLVEMENT SO CANCER RESEARCH LA English DT Article ID HUMAN OVARIAN-CARCINOMA; ALKYLATING AGENT RESISTANCE; ENHANCED DNA-REPAIR; LIVING CELLS; ANTICANCER DRUGS; CROSS-RESISTANCE; LEUKEMIA-CELLS; RHODAMINE 123; INVITRO; ACCUMULATION AB Three human tumor cell lines made resistant to cis-diamminedichloroplatinum(II) (CDDP), SCC-25/CP, MCF-7/CP, and C13, are more sensitive to rhodamine-123 [tetrachloroplatinum(II)] [(PtCl4(Rh-123)(2)] than are the corresponding parental cell lines. The CDDP-resistant cells have higher intracellular concentrations of PtCl4(Rh-123)(2) for the same exposure than do the parent cells. Each of the CDDP-resistant cell lines has an increased level of cytochrome c oxidase activity compared with the parent cell lines, indicating that the resistant cells have greater mitochondrial mass or activity than the parent cells. In fact, there was a linear correlation between the increase in cytochrome c oxidase activity and the increased sensitivity to PtCl4(Rh-123)(2) in the CDDP-resistant lines. Exposure of the cells to each of the mitochondrial effecters, chloramphenicol, FCCP, oligomycin, or antimycin prior to and during exposure to CDDP or PtCl4-(Rh-123)(2) had variable effects on the cytotoxicity of the platinum complexes in the parental lines. However, there was a consistent decrease in the cytotoxicity of PtCl4(Rh-123)(2) in the CDDP-resistant cells in the presence of the mitochondrial effecters such that, in some cases, the CDDP-resistant lines were now less responsive to PtCl4(Rh-123)(2) than were the parent cell lines. These studies indicate that mitochondrial alterations may be an important component of CDDP resistance in these cell lines and that PtCl4(Rh-123)(2) mag represent a prototype platinum complex useful in the treatment of CDDP resistant tumors. C1 DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [R01-CA47379, R01-CA50174] NR 58 TC 27 Z9 27 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1994 VL 54 IS 6 BP 1497 EP 1502 PG 6 WC Oncology SC Oncology GA NA887 UT WOS:A1994NA88700020 PM 8137254 ER PT J AU BAXTER, LT ZHU, H MACKENSEN, DG JAIN, RK AF BAXTER, LT ZHU, H MACKENSEN, DG JAIN, RK TI PHYSIOLOGICALLY-BASED PHARMACOKINETIC MODEL FOR SPECIFIC AND NONSPECIFIC MONOCLONAL-ANTIBODIES AND FRAGMENTS IN NORMAL-TISSUES AND HUMAN TUMOR XENOGRAFTS IN NUDE-MICE SO CANCER RESEARCH LA English DT Article ID BINDING-SITE BARRIER; CARCINOEMBRYONIC ANTIGEN; SOLID TUMORS; INTERSTITIAL PRESSURE; PERIVASCULAR DISTRIBUTION; NEOPLASTIC TISSUES; TRANSPORT; FLUID; MACROMOLECULES; AFFINITY AB A physiologically based pharmacokinetic model to describe the biodistribution of a specific monoclonal antibody IgG1 (ZCE025) and its fragments (F(ab')(2) and Fab) and of a nonspecific IgG1 (MOPC21) in normal tissues and a human colon carcinoma xenograft (T380) in nude mice is developed. The model simulates the experimental data on the concentration of these four macromolecules in plasma, urine, heart, lung, liver, kidney, spleen, bone, muscle, skin, GI tract, and tumor. This is the first such model for macromolecules with specific binding. A two-pore formalism for transcapillary solute exchange is used which avoids the oversimplifications of unidirectional transport or a single effective permeability coefficient. Comparison of the model with our biodistribution data shows that: (a) a physiologically based pharmacokinetic model for specific and nonspecific antibodies is able to explain experimental data using as few adjustable parameters as possible; (b) for antibodies and fragments, the tumor itself has no significant influence on the pharmacokinetics in normal tissues; and (c) the two-pore formalism for transcapillary exchange describes the data better than a single-pore model without introducing extra adjustable parameters. Sensitivity analysis shows that the lymph flow rate and transvascular fluid recirculation rate are important parameters for the uptake of antibodies, while for the retention of specific antibodies, extravascular binding is the key parameter. A single-pore model could also obtain a good fit between model and data by adjusting two parameters; however, the estimated permeability was 1000 times higher than with the two-pore model, and the binding affinity was such that approximately five times more material was bound than free in the extravascular space for nonspecific antibody. Setting the binding affinity to zero or reducing the value of the permeability-surface area product did not allow a good fit, even when the lymph flow rate was varied. The present model may be useful in scaling up antibody pharmacokinetics from mouse to man. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MIT,RADIOL SCI PROGRAM,CAMBRIDGE,MA 02139. HYBRITECH INC,SAN DIEGO,CA 92121. RP BAXTER, LT (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,STEELE LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-49792] NR 48 TC 139 Z9 141 U1 0 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1994 VL 54 IS 6 BP 1517 EP 1528 PG 12 WC Oncology SC Oncology GA NA887 UT WOS:A1994NA88700024 PM 8137258 ER PT J AU GUO, YJ MA, J WANG, JH CHE, XY NARULA, J BIGBY, M WU, MC SY, MS AF GUO, YJ MA, J WANG, JH CHE, XY NARULA, J BIGBY, M WU, MC SY, MS TI INHIBITION OF HUMAN-MELANOMA GROWTH AND METASTASIS IN-VIVO BY ANTI-CD44 MONOCLONAL-ANTIBODY SO CANCER RESEARCH LA English DT Article ID LYMPHOCYTE HOMING RECEPTOR; CELL-LINES; PROTEOGLYCAN CORE; CD44; EXPRESSION; SURFACE; ANTIGEN; PGP-1; DISTINCT; BINDING AB CD44 is a M(r) 90,000 surface glycoprotein believed to be involved in cell adhesion and migration. We investigated the role of CD44 in tumor grow th and metastasis using human melanoma cell lines SMMU-1 and SMMU-2. Both SMMU-1 and SMMU-2 form tumors in the s.c. tissues when injected s.c. in SCID mice but only SMMU-2 metastasizes. Approximately one-half of SCID mice receiving injections of SMMU-2 s.c. develop metastatic tumors. SMMU-2 but not SMMU-1 expresses high levels of the hematopoietic form of CD44 and binds fluorescence-conjugated hyaluronic acid in vitro. GKW.A3 is a monoclonal antibody specific for human CD44 that can completely inhibit the binding of hyaluronic acid to SMMU-2 tumor cells in vitro. Moreover, in vivo injection of GKW.A3 inhibited the growth and metastatic potential of SMMU-2 tumor cells. Administration of GKW.A3 i.v. 1 week after s.c. tumor injection did not inhibit local tumor development but inhibited the formation of metastatic tumors and prolonged animal survival. Therefore, interactions between CD44 on tumor cells and its ligands in vivo may be necessary for tumor growth and metastasis. C1 CHANGHAI HOSP,INST HEPATOBILIARY SURG,SHANGHAI 200433,PEOPLES R CHINA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. RP GUO, YJ (reprint author), CASE WESTERN RESERVE UNIV,SCH MED,INST PATHOL,DEPT PATHOL,BIOMED RES BLDG,ROOM 947,CLEVELAND,OH 44106, USA. FU NIAID NIH HHS [R0-1 AI-277740]; NIAMS NIH HHS [AR-38018, AR39795] NR 36 TC 146 Z9 151 U1 1 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1994 VL 54 IS 6 BP 1561 EP 1565 PG 5 WC Oncology SC Oncology GA NA887 UT WOS:A1994NA88700031 PM 7511044 ER PT J AU CHEN, YY WANG, LC HUANG, MS ROSENBERG, N AF CHEN, YY WANG, LC HUANG, MS ROSENBERG, N TI AN ACTIVE V-ABL PROTEIN-TYROSINE KINASE BLOCKS IMMUNOGLOBULIN LIGHT-CHAIN GENE REARRANGEMENT SO GENES & DEVELOPMENT LA English DT Article DE V-ABL; PROTEIN TYROSINE KINASE; IMMUNOGLOBULIN GENE REARRANGEMENT; RAG GENES ID MURINE LEUKEMIA-VIRUS; NF-KAPPA-B; V(D)J RECOMBINATION; CELL LINES; LYMPHOID-CELLS; LYMPHOCYTES-B; EXPRESSION; SEGMENTS; BCL-2; TRANSCRIPTION AB Lymphoid cells transformed by Abelson murine leukemia virus have provided one of the classic models for study of early B-cell development and immunoglobulin rearrangement. Most of these cells have rearranged their heavy-chain locus but not their light chain genes, suggesting that an active v-abl protein interferes with this differentiation step. To test this hypothesis, light-chain gene structure was examined in pre-B cells transformed by temperature-sensitive mutants of the Abelson virus and in derivatives that survive at the nonpermissive temperature because they express a human BCL-2 gene. Our studies reveal that inactivation of the v-abl protein tyrosine kinase triggers high-frequency rearrangement of kappa and lambda light-chain genes. These events are accompanied by marked increases in the expression of RAG-1 and RAG-2 RNAs. These increases occur in the absence of protein synthesis but are dependent on inactivation of the v-abl protein tyrosine kinase. As documented in the accompanying paper (Klug et al., this issue), an active v-abl protein also suppresses the activity of NF-kappaB/rel and expression controlled by the kappa intron enhancer. Together these data demonstrate that the v-abl protein specifically interferes with light-chain gene rearrangement by suppressing at least two pathways essential for this stage of B-cell differentiation and suggest that tyrosine phosphorylation is important in regulating RAG gene expression. C1 TUFTS UNIV,SCH MED,GRAD PROGRAM IMMUNOL,BOSTON,MA 02111. TUFTS UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02111. TUFTS UNIV,SCH MED,DEPT MOLEC BIOL & MICROBIOL,BOSTON,MA 02111. CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [CA24220, CA09172] NR 52 TC 126 Z9 126 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD MAR 15 PY 1994 VL 8 IS 6 BP 688 EP 697 DI 10.1101/gad.8.6.688 PG 10 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA ND121 UT WOS:A1994ND12100005 PM 7926759 ER PT J AU MACCOLLIN, M PETERFREUND, R MACDONALD, M FINK, JS GUSELLA, J AF MACCOLLIN, M PETERFREUND, R MACDONALD, M FINK, JS GUSELLA, J TI MAPPING OF A HUMAN-A2A ADENOSINE RECEPTOR (ADORA2) TO CHROMOSOME-22 SO GENOMICS LA English DT Note ID MOLECULAR-CLONING C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BLDG 149,13TH ST,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02129. FU NHGRI NIH HHS [HG00317]; NIDA NIH HHS [DA07496] NR 11 TC 30 Z9 30 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR 15 PY 1994 VL 20 IS 2 BP 332 EP 333 DI 10.1006/geno.1994.1181 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NB820 UT WOS:A1994NB82000033 PM 8020991 ER PT J AU DAMICO, DJ BRAZITIKOS, PD BERNAL, MT AF DAMICO, DJ BRAZITIKOS, PD BERNAL, MT TI EXPERIMENTAL SURGICAL APPROACHES WITH THE ERBIUM-YAG LASER - TRANSECTION OF ELEVATED VITREOUS MEMBRANES AND CREATION OF RETINOTOMIES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,RETINA SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,LASER RES LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1261 EP 1261 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500029 ER PT J AU DELAMAZA, MS AYLIFFE, W FOSTER, CS AF DELAMAZA, MS AYLIFFE, W FOSTER, CS TI IMMUNOHISTOCHEMICAL STUDY OF CONJUNCTIVA FROM PATIENTS WITH KERATOCONJUNCTIVITIS SICCA DUE TO GRAFT-VERSUS-HOST DISEASE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV BARCELONA,HOSP CLIN,DEPT OPHTHALMOL,BARCELONA 7,SPAIN. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1290 EP 1290 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500171 ER PT J AU LANE, L MERAYO, JM DUTT, JE ZHAO, TZ FOSTER, CS AF LANE, L MERAYO, JM DUTT, JE ZHAO, TZ FOSTER, CS TI CYTOKINE EXPRESSION IN A NEW MURINE MODEL MIMICKING HUMAN ALLERGIC CONJUNCTIVITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1292 EP 1292 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500187 ER PT J AU MERAYOLLOVES, J DUTT, J ZHAO, T FOSTER, CS AF MERAYOLLOVES, J DUTT, J ZHAO, T FOSTER, CS TI CONJUNCTIVAL CYTOKINE EXPRESSION IN A MURINE MODEL OF OCULAR ALLERGY AFTER TOPICAL TREATMENT WITH NEDOCROMIL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1292 EP 1292 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500184 ER PT J AU WALLER, SG LAMARCHE, K TALAMO, JH AF WALLER, SG LAMARCHE, K TALAMO, JH TI MODIFICATION OF ASTIGMATIC KERATOTOMY EFFECT WITH COLLAGEN IMPLANTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1296 EP 1296 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500203 ER PT J AU ARRUNATEGUICORREA, VR FOSTER, CS AF ARRUNATEGUICORREA, VR FOSTER, CS TI THE ROLE OF IL-6 IN EXPERIMENTAL HERPES-SIMPLEX-KERATITIS (HSK) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,RHOADS MOLEC IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1332 EP 1332 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500353 ER PT J AU FOSTER, CS PEDROZASERES, M MERAYOLLOVES, J ARRUNATEGUICORREA, VR AF FOSTER, CS PEDROZASERES, M MERAYOLLOVES, J ARRUNATEGUICORREA, VR TI DIVERSE T-CELL RECEPTOR V-BETA GENE-EXPRESSION IN EXPERIMENTAL HERPES-SIMPLEX-VIRUS-RETINITIS (HSR) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,RHOADS MOLEC IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1333 EP 1333 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500355 ER PT J AU BERRIOS, RR CHI, TSK NETLAND, PA AF BERRIOS, RR CHI, TSK NETLAND, PA TI VARIATION OF OPTIC-NERVE HEAD TOPOGRAPHY MEASUREMENTS DURING THE CARDIAC CYCLE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1348 EP 1348 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500431 ER PT J AU TAKAMOTO, T NETLAND, PA SCHWARTZ, B AF TAKAMOTO, T NETLAND, PA SCHWARTZ, B TI COMPARISON OF MEASUREMENTS OF OPTIC DISC CUP BY GLAUCOMA-SCOPE AND STEREOPHOTOGRAMMETRY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. TUFTS UNIV,SCH MED,BOSTON,MA 02111. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1348 EP 1348 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500432 ER PT J AU KAUFMAN, AH NOURI, M PETERS, JH HYNES, RO DUTT, JE COLVIN, RB FOSTER, CS AF KAUFMAN, AH NOURI, M PETERS, JH HYNES, RO DUTT, JE COLVIN, RB FOSTER, CS TI FIBRONECTIN ISOFORM IMMUNOFLUORESCENCE IN NORMAL AND EPITHELIAL SCRAPE WOUNDED RAT CORNEAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV CINCINNATI,CINCINNATI,OH 45221. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1352 EP 1352 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500448 ER PT J AU SAMY, CN LUI, CJ KAISER, PK LIPTON, SA DREYER, EB AF SAMY, CN LUI, CJ KAISER, PK LIPTON, SA DREYER, EB TI TOXICITY OF CHRONIC GLUTAMATE ADMINISTRATION TO THE RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1361 EP 1361 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500494 ER PT J AU CIULLA, TA MOULTON, R OBEROI, A MILLER, JW AF CIULLA, TA MOULTON, R OBEROI, A MILLER, JW TI CENTRAL RETINAL ARTERY-OCCLUSION IN RABBIT EYES, A REALISTIC ANIMAL-MODEL USING HUMAN ATHEROMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1375 EP 1375 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500569 ER PT J AU MANN, J EDELL, D RIZZO, JF RAFFEL, J WYATT, JL AF MANN, J EDELL, D RIZZO, JF RAFFEL, J WYATT, JL TI DEVELOPMENT OF A SILICON RETINAL IMPLANT - MICROELECTRONIC SYSTEM FOR WIRELESS TRANSMISSION OF SIGNAL AND POWER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MIT,LINCOLN LAB,LEXINGTON,MA 02173. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. NR 0 TC 4 Z9 4 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1380 EP 1380 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500591 ER PT J AU NARAYANAN, MV RIZZO, JF EDELL, D WYATT, JL AF NARAYANAN, MV RIZZO, JF EDELL, D WYATT, JL TI DEVELOPMENT OF A SILICON RETINAL IMPLANT - CORTICAL EVOKED-POTENTIALS FOLLOWING FOCAL STIMULATION OF THE RABBIT RETINA WITH LIGHT AND ELECTRICITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. MIT,LINCOLN LAB,LEXINGTON,MA 02173. NR 0 TC 12 Z9 12 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1380 EP 1380 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500589 ER PT J AU WYATT, JL RIZZO, JF GRUMET, A EDELL, D JENSEN, RJ AF WYATT, JL RIZZO, JF GRUMET, A EDELL, D JENSEN, RJ TI DEVELOPMENT OF A SILICON RETINAL IMPLANT - EPIRETINAL STIMULATION OF RETINAL GANGLION-CELLS IN THE RABBIT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. MIT,LINCOLN LAB,LEXINGTON,MA 02173. SO COLL OPTOMETRY,MEMPHIS,TN. NR 0 TC 20 Z9 20 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1380 EP 1380 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500590 ER PT J AU PANIGRAHY, D RUPNICK, MA MELBY, JC ADAMIS, AP AF PANIGRAHY, D RUPNICK, MA MELBY, JC ADAMIS, AP TI MODULATION OF INTRAOCULAR-PRESSURE BY ALDOSTERONE AND SPIRONOLACTONE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. BOSTON UNIV HOSP,SCH MED,DEPT ENDOCRINOL,BOSTON,MA 02218. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1388 EP 1388 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500620 ER PT J AU DREYER, EB CHATURVEDI, N GROSSKREUTZ, CL BARNSTABLE, CJ LIU, CJ AF DREYER, EB CHATURVEDI, N GROSSKREUTZ, CL BARNSTABLE, CJ LIU, CJ TI EXPRESSION OF THY-1 ANTIGEN IN THE RAT RETINA DURING POSTNATAL-DEVELOPMENT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. YALE UNIV,DEPT VISUAL SCI,NEW HAVEN,CT 06520. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1403 EP 1403 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500681 ER PT J AU BHISTIKUL, RB DREYER, EB AF BHISTIKUL, RB DREYER, EB TI A PROSPECTIVE ANALYSIS OF ANTERIOR SEGMENT CHANGES AT ONE-YEAR AFTER MITOMYCIN-C OR 5-FLUOROURACIL SUPPLEMENTED TRABECULECTOMY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,GLAUCOMA CONSULTAT SERV,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1427 EP 1427 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500794 ER PT J AU WEST, JA STRISSEL, KJ GIRARD, MT FINI, ME AF WEST, JA STRISSEL, KJ GIRARD, MT FINI, ME TI ENDOGENOUSLY PRODUCED INTERLEUKIN-1-ALPHA MEDIATES COLLAGENASE SYNTHESIS BY CORNEAL FIBROBLASTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT DERMATOL,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1457 EP 1457 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500943 ER PT J AU FINI, ME BARTLETT, JD MATSUBARA, M MODY, MK RINEHART, WT GIRARD, MT RAINVILLE, M AF FINI, ME BARTLETT, JD MATSUBARA, M MODY, MK RINEHART, WT GIRARD, MT RAINVILLE, M TI GELATINASE B-GENE EXPRESSION IS REGULATED BY TRANSCRIPTION FACTOR AP-2 - A TARGET FOR THERAPY OF CORNEAL ULCERS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1458 EP 1458 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500945 ER PT J AU STRISSEL, KJ RINEHART, WB FINI, ME AF STRISSEL, KJ RINEHART, WB FINI, ME TI EPITHELIAL INHIBITOR(S) OF STROMAL COLLAGENASE SYNTHESIS IN RABBIT CORNEA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1458 EP 1458 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500947 ER PT J AU HUANG, SH MOSES, MA WIEDERSCHAIN, DG ADAMIS, AP AF HUANG, SH MOSES, MA WIEDERSCHAIN, DG ADAMIS, AP TI IDENTIFICATION AND CHARACTERIZATION OF MATRIX METALLOPROTEINASE INHIBITORS IN BOVINE AQUEOUS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,MED CTR,SCH MED,DEPT SURG,SURG RES LAB,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1459 EP 1459 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500951 ER PT J AU SHANKER, R HENG, J KAISER, PK DREYER, EB AF SHANKER, R HENG, J KAISER, PK DREYER, EB TI THE CASE FOR MONOMERIC THY-1, THE UBIQUITOUS NEURONAL GLYCOPROTEIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1467 EP 1467 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500995 ER PT J AU CEISLER, EJ SPORN, C PAGLINAUAN, C WIGGS, JL AF CEISLER, EJ SPORN, C PAGLINAUAN, C WIGGS, JL TI INHERITANCE OF PSEUDOEXFOLIATION - EVIDENCE FOR AUTOSOMAL-DOMINANT TRANSMISSION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1471 EP 1471 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501011 ER PT J AU PAGLINAUAN, C SPORN, C HAINES, JL WIGGS, JL AF PAGLINAUAN, C SPORN, C HAINES, JL WIGGS, JL TI GENETIC EXCLUSION OF PIGMENTARY DISPERSION SYNDROME FROM CHROMOSOME-1Q21-Q31 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1471 EP 1471 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501009 ER PT J AU ROSENFELD, PJ HAHN, LB MILLER, S SANDBERG, MA DRYJA, TP BERSON, EL AF ROSENFELD, PJ HAHN, LB MILLER, S SANDBERG, MA DRYJA, TP BERSON, EL TI A RHODOPSIN SPLICE-SITE MUTATION - RECESSIVE OR DOMINANT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB,BOSTON,MA 02114. NR 2 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1478 EP 1478 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501035 ER PT J AU SANDBERG, MA WEIGELDIFRANCO, C DRYJA, TP BERSON, EL AF SANDBERG, MA WEIGELDIFRANCO, C DRYJA, TP BERSON, EL TI ERG AMPLITUDE AND VISUAL-FIELD AREA CORRELATE WITH CATEGORIES OF RHODOPSIN MUTATIONS CAUSING DOMINANT RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1478 EP 1478 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501036 ER PT J AU KIM, SK HAINES, JL BERSON, EL DRYJA, TP AF KIM, SK HAINES, JL BERSON, EL DRYJA, TP TI NONALLELIC HETEROGENEITY IN AUTOSOMAL-DOMINANT RETINITIS-PIGMENTOSA WITH REDUCED PENETRANCE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1479 EP 1479 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501039 ER PT J AU ROOF, DJ ADAMIAN, M HAYES, A AF ROOF, DJ ADAMIAN, M HAYES, A TI ANALYSIS OF GENE-FUNCTION BY THE USE OF TRANSGENIC ANIMALS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1480 EP 1480 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501043 ER PT J AU CHATURVEDI, N DREYER, EB AF CHATURVEDI, N DREYER, EB TI EFFECT OF NITRATES ON GLAUCOMATOUS VISUAL-LOSS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,GLAUCOMA CONSULTAT SERV,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1484 EP 1484 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501060 ER PT J AU KRAMER, M MILLER, JW MICHAUD, N MOULTON, R OBEROI, A FLOTTE, T HASAN, T GRAGOUDAS, ES AF KRAMER, M MILLER, JW MICHAUD, N MOULTON, R OBEROI, A FLOTTE, T HASAN, T GRAGOUDAS, ES TI PHOTODYNAMIC THERAPY (PDT) OF EXPERIMENTAL CHOROIDAL NEOVASCULARIZATION (CNV) USING LIPOSOMAL BENZOPORPHYRIN DERIVATIVE MONOACID (BPD-MA) - REFINEMENT OF DOSIMETRY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1503 EP 1503 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501142 ER PT J AU REMULLA, JFC GAUDIO, AR MILLER, S SANDBERG, MA AF REMULLA, JFC GAUDIO, AR MILLER, S SANDBERG, MA TI FOVEAL CONE ELECTRORETINOGRAMS IN AGE-RELATED MACULAR DEGENERATION WITH DELAYED CHOROIDAL PERFUSION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract ID BRUCH MEMBRANE CHANGE C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1503 EP 1503 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501141 ER PT J AU HAIMOVICI, R CIULLA, TA FLOTTE, T MILLER, JW HASAN, T SCHOMACKER, KT GRAGOUDAS, ES AF HAIMOVICI, R CIULLA, TA FLOTTE, T MILLER, JW HASAN, T SCHOMACKER, KT GRAGOUDAS, ES TI LOCALIZATION OF ROSE-BENGAL CASPC, AND CHLORIN E6 IN THE RABBIT EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1505 EP 1505 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501154 ER PT J AU KAISER, PK GONZALEZ, VH THEODOSSIADIS, PG GRAGOUDAS, ES MILLER, J AF KAISER, PK GONZALEZ, VH THEODOSSIADIS, PG GRAGOUDAS, ES MILLER, J TI IMPORTANCE OF TIME-INTERVAL BETWEEN INDOCYANINE GREEN-DYE ADMINISTRATION AND DIODE-LASER TRANSPUPILLARY CHOROIDAL VESSEL PHOTOCOAGULATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1506 EP 1506 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501162 ER PT J AU RIZZO, JF SOCHA, M EDELL, D ANTKOWIAK, B BROCK, D AF RIZZO, JF SOCHA, M EDELL, D ANTKOWIAK, B BROCK, D TI DEVELOPMENT OF A SILICON RETINAL IMPLANT - SURGICAL METHODS AND MECHANICAL DESIGN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. MIT,LINCOLN LAB,LEXINGTON,MA 02173. MIT,CAMBRIDGE,MA 02139. DRAPER LABS,CAMBRIDGE,MA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1535 EP 1535 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501307 ER PT J AU FRIEDMAN, ES DAMICO, DJ AF FRIEDMAN, ES DAMICO, DJ TI VITRECTOMY ALONE FOR THE MANAGEMENT OF UNCOMPLICATED RECURRENT RETINAL-DETACHMENT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,RETINA SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1539 EP 1539 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501329 ER PT J AU DUNYA, IM REMULLA, HD BILYK, JR RUBIN, PAD AF DUNYA, IM REMULLA, HD BILYK, JR RUBIN, PAD TI THE USE OF CALIBRATED GOLD WEIGHTS TO ANALYZE HERINGS LAW ON LEVATOR PALPEBRAE-SUPERIORIS MUSCLE FUNCTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1547 EP 1547 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501370 ER PT J AU MEHTA, M LASHKARI, K HIROSE, T MASKATI, QB TALWAR, I CHENG, HM AF MEHTA, M LASHKARI, K HIROSE, T MASKATI, QB TALWAR, I CHENG, HM TI MR-IMAGING OF FREE-WATER MOVEMENT IN NORMAL AND GLAUCOMATOUS EYES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 SCHEPENS EYE RES INST,DEPT CLIN RES,BOSTON,MA. HARVARD UNIV,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. RETINA ASSOCIATES,BOSTON,MA. BOMBAY HOSP & MED RES CTR,BOMBAY,INDIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1557 EP 1557 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501411 ER PT J AU JENKINS, C ATHAN, E JAKOBIEC, F KNOWLES, DM AF JENKINS, C ATHAN, E JAKOBIEC, F KNOWLES, DM TI MOLECULAR CHARACTERIZATION OF PRIMARY OCULAR ADNEXAL MALIGNANT-LYMPHOMAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT PATHOL,NEW YORK,NY 10032. MASSACHUSETTS GEN HOSP,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1566 EP 1566 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501447 ER PT J AU LATINA, MA PARK, CH AF LATINA, MA PARK, CH TI SELECTIVE TARGETING OF TRABECULAR MESHWORK CELLS BY LASER IRRADIATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SCHEPENS EYE RES INST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1574 EP 1574 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501479 ER PT J AU BRAZITIKOS, PD BERNAL, MT DAMICO, DJ AF BRAZITIKOS, PD BERNAL, MT DAMICO, DJ TI EPIRETINAL MEMBRANE SURGERY WITH THE ERBIUM-YAG LASER - RESULTS IN FLUID, AIR, AND PERFLUOROOCTANE MEDIA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,RETINA SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,LASER RES LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1580 EP 1580 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501500 ER PT J AU CUMMINS, DR BURSELL, SE CLERMONT, AC TAGGART, JJ KING, GL AF CUMMINS, DR BURSELL, SE CLERMONT, AC TAGGART, JJ KING, GL TI THE EFFECT OF INTRAVITREAL ANGIOTENSIN-II ON RETINAL VASCULAR FLOW SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1589 EP 1589 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501542 ER PT J AU MARCUS, DM LASUDRY, JGH ALUBAIDI, MR BAEHR, W OVERBEEK, PA FONT, RL ALBERT, DM AF MARCUS, DM LASUDRY, JGH ALUBAIDI, MR BAEHR, W OVERBEEK, PA FONT, RL ALBERT, DM TI TRILATERAL TUMORS IN TRANSGENIC MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. UNIV WISCONSIN,DEPT OPHTHALMOL,MADISON,WI 53706. BAYLOR COLL MED,DEPT OPHTHALMOL & CELL BIOL,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1612 EP 1612 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501661 ER PT J AU LASHKARI, K HIROSE, T MCMEEL, JW PFLEIDERER, B XIONG, J IGARASHI, H CHENG, HM AF LASHKARI, K HIROSE, T MCMEEL, JW PFLEIDERER, B XIONG, J IGARASHI, H CHENG, HM TI PROTON NMR ANALYSIS AND IMAGING OF INTRAOCULAR FLUIDS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 SCHEPENS EYE RES INST,DEPT CLIN RES,BOSTON,MA. HOWE LAB OPHTHALMOL,BOSTON,MA. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RETINA ASSOCIATES,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1614 EP 1614 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501671 ER PT J AU NETLAND, PA YE, H STREETEN, BW HERNANDEZ, MR AF NETLAND, PA YE, H STREETEN, BW HERNANDEZ, MR TI ELASTOSIS OF THE LAMINA-CRIBROSA IN PSEUDOEXFOLIATION SYNDROME WITH GLAUCOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. SCHEPENS EYE RES INST,BOSTON,MA. SYRACUSE UNIV,HLTH SCI CTR,DEPT PATHOL,SYRACUSE,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1646 EP 1646 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501815 ER PT J AU MCMILLEN, JJ AF MCMILLEN, JJ TI PLANNED DISPOSAL OF EMERGENCY ROOM DIAGNOSTIC AND THERAPEUTIC MEDICATIONS - AN EVALUATION OF EFFICACY IN PREVENTING CONTAMINATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1671 EP 1671 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501924 ER PT J AU LEE, PP KOWAL, VO MEAD, MD MCDONNELL, PJ AF LEE, PP KOWAL, VO MEAD, MD MCDONNELL, PJ TI OUTCOMES IN COMMUNITY-ACQUIRED CORNEAL ULCERS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 DOHENY EYE INST,LOS ANGELES,CA. WILLS EYE HOSP & RES INST,PHILADELPHIA,PA 19107. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1675 EP 1675 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501944 ER PT J AU AKOVA, Y DUTT, JE RODRIGUEZ, A FOSTER, CS AF AKOVA, Y DUTT, JE RODRIGUEZ, A FOSTER, CS TI THE ROLE OF T-LYMPHOCYTES IN THE PATHOGENESIS OF MURINE HERPES-SIMPLEX KERATITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1679 EP 1679 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501962 ER PT J AU HEILIGENHAUS, A FOSTER, CS AF HEILIGENHAUS, A FOSTER, CS TI IMMUNOPATHOLOGICAL STUDY OF T-CELL SUBSETS IN MURINE HSV-1 KERATITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 DEPT OPHTHALMOL,ESSEN,GERMANY. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1679 EP 1679 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501963 ER PT J AU PEDROZASERES, M GOEI, S ARRUNATEGUICORREA, V FOSTER, CS AF PEDROZASERES, M GOEI, S ARRUNATEGUICORREA, V FOSTER, CS TI TCR-V-BETA EXPRESSION IN A MURINE MODEL OF HERPES-SIMPLEX KERATITIS (HSK) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,HILLES 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1679 EP 1679 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501964 ER PT J AU RODRIGUEZ, A CRUMP, A CANTOR, H FOSTER, CS AF RODRIGUEZ, A CRUMP, A CANTOR, H FOSTER, CS TI IGH-1(B) IGG2A IMMUNOGLOBULIN-(IG) RENDERS C.AL-20 SUSCEPTIBLE MICE RESISTANT TO HERPES-SIMPLEX STROMAL KERATITIS (HSK) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,HILLES IMMUNOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1680 EP 1680 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501967 ER PT J AU NEVES, R RODRIGUEZ, A BERRA, A VANROOIJEN, N FOSTER, CS AF NEVES, R RODRIGUEZ, A BERRA, A VANROOIJEN, N FOSTER, CS TI THE ROLE OF MACROPHAGES (MO) IN HSV-1 INDUCED CHORIORETINITIS IN BALB/C MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. FREE UNIV AMSTERDAM,DEPT CELL BIOL HISTOL,1007 MC AMSTERDAM,NETHERLANDS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1682 EP 1682 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501979 ER PT J AU FILIPEC, M CINTRON, C KUBLIN, C FOSTER, CS AF FILIPEC, M CINTRON, C KUBLIN, C FOSTER, CS TI PROTEOGLYCAN CHANGES IN CICATRICIAL CONJUNCTIVITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 CHARLES UNIV,DEPT OPHTHALMOL 2,CS-11636 PRAGUE 1,CZECH REPUBLIC. SCHEPENS EYE RES INST,BOSTON,MA. MASSACHUSETTS EYE & EAR INFIRM,HILES IMMUNOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1691 EP 1691 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502024 ER PT J AU DUTT, JE FOSTER, CS AF DUTT, JE FOSTER, CS TI CYTOKINE PRODUCTION IN THE CONJUNCTIVA OF PATIENTS WITH OCULAR CICATRICIAL PEMPHIGOID SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1692 EP 1692 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502025 ER PT J AU FINKELSTEIN, M AF FINKELSTEIN, M TI FACTORS ASSOCIATED WITH PROTECTIVE EYEWEAR USE DURING SQUASH SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1699 EP 1699 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502063 ER PT J AU LI, T BERSON, EL DRYJA, TP ROESSLER, BJ DAVIDSON, BL AF LI, T BERSON, EL DRYJA, TP ROESSLER, BJ DAVIDSON, BL TI IN-VIVO GENE-TRANSFER TO NORMAL AND RD MOUSE RETINAS MEDIATED BY ADENOVIRAL VECTORS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB,BOSTON,MA 02114. UNIV MICHIGAN,DEPT RHEUMATOL,ANN ARBOR,MI 48109. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1716 EP 1716 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502147 ER PT J AU MCGEE, TL LIN, D BERSON, EL DRYJA, TP AF MCGEE, TL LIN, D BERSON, EL DRYJA, TP TI DEFECTS IN THE ROD CGMP-GATED CHANNEL GENE IN PATIENTS WITH RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB,BOSTON,MA 02114. NR 0 TC 14 Z9 15 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1716 EP 1716 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502150 ER PT J AU KAJIWARA, K CHRISTEN, W SEDDON, JM DRYJA, TP AF KAJIWARA, K CHRISTEN, W SEDDON, JM DRYJA, TP TI SCREEN FOR MUTATIONS IN THE HUMAN RDS/PERIPHERIN GENE IN PATIENTS WITH AGE-RELATED MACULAR DEGENERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,HOWE LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,EPIDEMIOL UNIT,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1717 EP 1717 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502151 ER PT J AU PAWLYK, BS LI, T FRANSON, WK DRYJA, TP BERSON, EL AF PAWLYK, BS LI, T FRANSON, WK DRYJA, TP BERSON, EL TI DEFINING THE EXPRESSION THRESHOLD OF A NORMAL HUMAN OPSIN GENE THAT LEADS TO PHOTORECEPTOR DEGENERATION IN TRANSGENIC MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1717 EP 1717 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502153 ER PT J AU KHANI, SC ABITBOL, M POLANS, AS ZHOU, J ASSONBATRES, MA PALCZEWSKI, K DRYJA, TP AF KHANI, SC ABITBOL, M POLANS, AS ZHOU, J ASSONBATRES, MA PALCZEWSKI, K DRYJA, TP TI THE NUCLEOTIDE-SEQUENCE OF HUMAN RHODOPSIN KINASE CDNA AND THE CHROMOSOMAL LOCALIZATION OF THE GENE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. GOOD SAMARITAN HOSP,INST NEUROL SCI,PORTLAND,OR 97210. UNIV WASHINGTON,DEPT OPHTHALMOL,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1718 EP 1718 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502157 ER PT J AU MCLAUGHLIN, ME EHRHART, TL SANDBERG, MA BERSON, EL DRYJA, TP AF MCLAUGHLIN, ME EHRHART, TL SANDBERG, MA BERSON, EL DRYJA, TP TI MUTATIONS IN THE BETA-SUBUNIT OF ROD PHOSPHODIESTERASE IN PATIENTS WITH AUTOSOMAL RECESSIVE RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract ID GENE C1 HARVARD UNIV,SCH MED,HOWE LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BERMAN GUND LAB,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 2 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1718 EP 1718 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502158 ER PT J AU NISHIO, Y AIELLO, LP AIELLO, LM KING, GL AF NISHIO, Y AIELLO, LP AIELLO, LM KING, GL TI GLUCOSE-INDUCED GENES IN BOVINE RETINAL ENDOTHELIAL-CELLS IDENTIFIED BY MESSENGER-RNA DIFFERENTIAL DISPLAY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1720 EP 1720 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502167 ER PT J AU HOWARD, MA HU, LK GONZALEZ, VH GRAGOUDAS, ES YOUNG, LHY AF HOWARD, MA HU, LK GONZALEZ, VH GRAGOUDAS, ES YOUNG, LHY TI PHOTODYNAMIC THERAPY (PDT) OF PIGMENTED CHOROIDAL MELANOMA USING A LIPOSOMAL PREPARATION OF BENZOPORPHYRIN DERIVATIVE (BPD) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1722 EP 1722 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502176 ER PT J AU POWER, WJ KAUFMAN, AH ARRUNATEGUICORREA, V FOSTER, CS AF POWER, WJ KAUFMAN, AH ARRUNATEGUICORREA, V FOSTER, CS TI EXPRESSION OF COLLAGEN TYPE-I, TYPE-III, TYPE-IV AND TYPE-V IN RAT CORNEA FOLLOWING EXCIMER-LASER KERATECTOMY - ANALYSIS BY SEMIQUANTITATIVE PCR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RHOADS MOLEC IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1724 EP 1724 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502182 ER PT J AU PIERCE, EA FOLEY, E SULLIVAN, R SMITH, LEH AF PIERCE, EA FOLEY, E SULLIVAN, R SMITH, LEH TI VASCULAR ENDOTHELIAL GROWTH-FACTOR MESSENGER-RNA EXPRESSION IN A MOUSE MODEL OF OXYGEN-INDUCED PROLIFERATIVE RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT OPHTHALMOL,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1733 EP 1733 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502218 ER PT J AU LUCARELLI, MJ WIGGS, JL AF LUCARELLI, MJ WIGGS, JL TI PERIPAPILLARY CHORIORETINAL ATROPHY IN PSEUDOEXFOLIATION GLAUCOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1746 EP 1746 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502271 ER PT J AU BERNAL, MT MILLER, JW DAMICO, DJ FOLKMAN, J YEO, KT YEO, TK ADAMIS, AP AF BERNAL, MT MILLER, JW DAMICO, DJ FOLKMAN, J YEO, KT YEO, TK ADAMIS, AP TI VASCULAR-PERMEABILITY FACTOR VASCULAR ENDOTHELIAL GROWTH-FACTOR (VPF/VEGF) LEVELS ARE ELEVATED IN THE VITREOUS OF PATIENTS WITH PROLIFERATIVE DIABETIC-RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT PATHOL,BOSTON,MA 02215. 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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1750 EP 1750 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502286 ER PT J AU YE, L HETH, CA AF YE, L HETH, CA TI IDENTIFICATION OF CALMODULIN-BINDING PROTEINS IN CULTURED RAT RETINAL-PIGMENT EPITHELIUM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1757 EP 1757 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502320 ER PT J AU SPURRMICHAUD, S LINDBERG, K TISDALE, A WATANABE, H FABRICANT, M KEUTMANN, H GIPSON, IK AF SPURRMICHAUD, S LINDBERG, K TISDALE, A WATANABE, H FABRICANT, M KEUTMANN, H GIPSON, IK TI CORNEAL EPITHELIUM EXPRESSES MORE THAN ONE MUCIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,SCHEPENS EYE RES INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,SCH OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BIOSURFACES TECHNOL,CAMBRIDGE,MA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1795 EP 1795 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502508 ER PT J AU HARRELL, JT EPPSTEIN, JA SAMUELS, MA KRANTZ, BS BURSELL, SE AF HARRELL, JT EPPSTEIN, JA SAMUELS, MA KRANTZ, BS BURSELL, SE TI DEVELOPMENT OF A HIGH-RESOLUTION SCANNING FLUOROPHOTOMETER WITH SCATTERING NORMALIZATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 SPECTRX INC,ATLANTA,GA. JOSLIN DIABET CTR,EYE UNIT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1810 EP 1810 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502582 ER PT J AU KRUPSKY, S FRIEDMAN, E LANE, AM OAK, SS FRIEDMAN, E GRAGOUDAS, ES AF KRUPSKY, S FRIEDMAN, E LANE, AM OAK, SS FRIEDMAN, E GRAGOUDAS, ES TI OCULAR BLOOD-FLOW IN AGE-RELATED MACULAR DEGENERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. HARVARD UNIV,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1817 EP 1817 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502602 ER PT J AU CLERMONT, AC HIGASHI, S KING, GL BURSELL, SE AF CLERMONT, AC HIGASHI, S KING, GL BURSELL, SE TI DIFFERENTIAL RESPONSIVENESS OF INSULIN-TREATMENT ON RETINAL HEMODYNAMICS IN DIABETIC RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1818 EP 1818 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502609 ER PT J AU WALD, H CLERMONT, AC AIELLO, LP MURTHA, T KING, GL AIELLO, LM BURSELL, SE AF WALD, H CLERMONT, AC AIELLO, LP MURTHA, T KING, GL AIELLO, LM BURSELL, SE TI INTENSIVE INSULIN THERAPY (DCCT PATIENTS) CAN NORMALIZE CHANGES IN RETINAL BLOOD-FLOW AND LOWER DIACYLGLYCEROL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1818 EP 1818 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502608 ER PT J AU SMITH, JA DREYER, EB MUKAI, S AF SMITH, JA DREYER, EB MUKAI, S TI IRIDOCORNEAL ABNORMALITIES IN CHILDREN WITH STICKLERS SYNDROME SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1851 EP 1851 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502753 ER PT J AU AIELLO, LP FERRARA, N KING, GL AF AIELLO, LP FERRARA, N KING, GL TI HYPOXIC REGULATION AND BIOACTIVITY OF VASCULAR ENDOTHELIAL GROWTH-FACTOR - CHARACTERIZATION IN RETINAL MICROVASCULAR PERICYTES AND PIGMENT EPITHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. GENENTECH INC,S SAN FRANCISCO,CA 94080. NR 0 TC 8 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1868 EP 1868 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502841 ER PT J AU HIGASHI, S ZHOU, ZH SHARUK, GS KING, GL AF HIGASHI, S ZHOU, ZH SHARUK, GS KING, GL TI INHIBITORY EFFECT OF INSULIN ON THE ENDOTHELIN-1 GENE-EXPRESSION IN CULTURED BOVINE PERICYTES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1871 EP 1871 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502854 ER PT J AU BERESTKA, JS KORNMEHL, EW LIN, S AF BERESTKA, JS KORNMEHL, EW LIN, S TI EARLY VISUAL RECOVERY AFTER PENETRATING KERATOPLASTY WITH ADJUSTABLE SINGLE CONTINUOUS SUTURE TECHNIQUE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1880 EP 1880 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502895 ER PT J AU PAVILACK, MA CHAVES, HV ELNER, VM KENYON, KR AF PAVILACK, MA CHAVES, HV ELNER, VM KENYON, KR TI ANTIBODIES TO ICAM-1 AND LFA-1 IN HIGH-RISK CORNEAL TRANSPLANTATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MICHIGAN,WK KELLOGG EYE CTR,ANN ARBOR,MI 48109. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. SCHEPENS EYE RES INST,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1896 EP 1896 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502968 ER PT J AU SMITH, SR DAMORE, PA DREYER, EB AF SMITH, SR DAMORE, PA DREYER, EB TI COMPARATIVE TOXICITY OF MITOMYCIN-C AND 5-FLUOROURACIL IN-VITRO SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,SURG RES LAB,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,GLAUCOMA CONSULTAT SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1899 EP 1899 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502979 ER PT J AU SAMIY, N PARK, SS RUOFF, K DAMICO, DJ BAKER, AS AF SAMIY, N PARK, SS RUOFF, K DAMICO, DJ BAKER, AS TI INTRAVITREAL STEROID IN THE TREATMENT OF PNEUMOCOCCAL ENDOPHTHALMITIS IN THE RABBIT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,INFECT DIS SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL & MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CLIN MICROBIOL LAB,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1910 EP 1910 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503026 ER PT J AU GANGADHAR, DV AHMED, U HANNINEN, LA LINDBERG, K KENYON, KR SHAMS, NBK AF GANGADHAR, DV AHMED, U HANNINEN, LA LINDBERG, K KENYON, KR SHAMS, NBK TI TRACKING TRANSPLANTED CORNEAL EPITHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 BIOSURFACE TECHNOL INC,CAMBRIDGE,MA. HARVARD UNIV,SCH MED,EYE SCHEPENS RES INST,IMMUNOL UNIT,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1912 EP 1912 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503035 ER PT J AU VITALE, AT PEDROZASERES, M ARRUNATEGUICORREA, V DIMEO, S FOSTER, CS COLVIN, RB AF VITALE, AT PEDROZASERES, M ARRUNATEGUICORREA, V DIMEO, S FOSTER, CS COLVIN, RB TI DIFFERENTIAL EXPRESSION OF ALTERNATIVELY SPLICED FIBRONECTIN IN NORMAL AND WOUNDED RAT CORNEAL STROMA AND EPITHELIUM - ANALYSIS BY POLYMERASE CHAIN-REACTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1979 EP 1979 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503355 ER PT J AU SHIMA, DT ADAMIS, AP DEUTSCH, U MILLER, JW DAMORE, PA AF SHIMA, DT ADAMIS, AP DEUTSCH, U MILLER, JW DAMORE, PA TI REGULATION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR IN HYPOXIC AND ISCHEMIC OCULAR-TISSUES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1995 EP 1995 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503418 ER PT J AU NOURI, M KAUFMAN, AH FOSTER, CS PULIAFITO, CA FERRARA, AH PETERS, JH HYNES, RO COLVIN, RB AF NOURI, M KAUFMAN, AH FOSTER, CS PULIAFITO, CA FERRARA, AH PETERS, JH HYNES, RO COLVIN, RB TI EIIIA, EIIIB, AND V-REGION FIBRONECTIN ISOFORM IMMUNOFLUORESCENCE FOLLOWING EXCIMER-LASER PHOTOKERATECTOMY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV CINCINNATI,CINCINNATI,OH 45221. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. TUFTS UNIV,MEDFORD,MA 02155. MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2015 EP 2015 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503499 ER PT J AU MILLER, S REMULLA, JFC SANDBERG, MA AF MILLER, S REMULLA, JFC SANDBERG, MA TI EFFECT OF LIGHT ATTENUATION ON THE FOVEAL CONE ERG IN NORMAL SUBJECTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2046 EP 2046 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503668 ER PT J AU KARDITSAS, SD SCHROEDER, AM ERICKSON, KA AF KARDITSAS, SD SCHROEDER, AM ERICKSON, KA TI THE EFFECT OF DIFFERENT DILUTIONS OF HEALON (SODIUM HYALURONATE) ON OUTFLOW FACILITY IN THE HUMAN EYE IN-VITRO SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2052 EP 2052 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503697 ER PT J AU SARFARAZI, F SCHROEDER, A ZHANG, X ERICKSON, K AF SARFARAZI, F SCHROEDER, A ZHANG, X ERICKSON, K TI INFLUENCE OF PGE2 ON OUTFLOW FACILITY IN THE HUMAN EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2053 EP 2053 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503707 ER PT J AU ZHANG, X SCHROEDER, A ERICKSON, K AF ZHANG, X SCHROEDER, A ERICKSON, K TI INFLUENCE OF VERAPAMIL AND EPINEPHRINE ON OUTFLOW FACILITY AND CYCLIC-AMP IN THE HUMAN EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2053 EP 2053 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503705 ER PT J AU SCHROEDER, A ERICKSON, K AF SCHROEDER, A ERICKSON, K TI CHOLINERGIC AGONISTS DO NOT INCREASE TRABECULAR OUTFLOW FACILITY IN THE HUMAN EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2054 EP 2054 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503710 ER PT J AU LEVIN, LA GRAGOUDAS, ES LESSELL, S AF LEVIN, LA GRAGOUDAS, ES LESSELL, S TI EFFECT OF PROTON-BEAM IRRADIATION ON OPTIC-NERVE ENDOTHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV WISCONSIN,DEPT OPHTHALMOL & VISUAL SCI,MADISON,WI 53706. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2058 EP 2058 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503725 ER PT J AU BERNSTEIN, PS CHOI, SY HO, YC RANDO, RR AF BERNSTEIN, PS CHOI, SY HO, YC RANDO, RR TI THE DETECTION OF NOVEL RETINOIC ACID-BINDING PROTEINS IN THE BOVINE RETINA USING PHOTOAFFINITY-LABELING SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RETINA SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2060 EP 2060 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503734 ER PT J AU CHI, TSK BERRIOS, RR NETLAND, PA AF CHI, TSK BERRIOS, RR NETLAND, PA TI HOLMIUM LASER SCLEROSTOMY VIA CORNEAL APPROACH WITH ADJUVANT TRANSCONJUNCTIVAL MITOMYCIN-C IN RABBITS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2067 EP 2067 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503760 ER PT J AU HART, L PINEDA, R GONZALEZ, VH THEODOSSIADIS, P GRAGOUDAS, ES YOUNG, LHY AF HART, L PINEDA, R GONZALEZ, VH THEODOSSIADIS, P GRAGOUDAS, ES YOUNG, LHY TI ESTABLISHMENT OF AN OCULAR MELANOMA RABBIT MODEL WITH EXTRASCLERAL EXTENSION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2084 EP 2084 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503828 ER PT J AU THIEME, H AIELLO, LP LIN, YW FEENER, EP IWAMOTO, M FERRARA, N KING, GL AF THIEME, H AIELLO, LP LIN, YW FEENER, EP IWAMOTO, M FERRARA, N KING, GL TI CHARACTERIZATION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR RECEPTORS IN RETINAL MICROVASCULAR ENDOTHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. GENENTECH INC,S SAN FRANCISCO,CA 94080. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2086 EP 2086 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503836 ER PT J AU BURSELL, SE CLERMONT, AC WALD, H PU, X AIELLO, LP KING, GL AIELLO, LM AF BURSELL, SE CLERMONT, AC WALD, H PU, X AIELLO, LP KING, GL AIELLO, LM TI CORRELATION BETWEEN DECREASED RETINAL BLOOD-FLOW AND INCREASED DIACYLGLYCEROL IN PATIENTS WITH EARLY DIABETES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2088 EP 2088 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503844 ER PT J AU TAKAGI, C BURSELL, SE CLEMONT, AC CUMMINS, DR TAKAGI, H KLETSKY, DL KING, GL AF TAKAGI, C BURSELL, SE CLEMONT, AC CUMMINS, DR TAKAGI, H KLETSKY, DL KING, GL TI REVERSAL OF ABNORMAL RETINAL HEMODYNAMICS IN DIABETIC RATS BY ACARBOSE, AN ALPHA-GLUCOSIDASE INHIBITOR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2088 EP 2088 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503843 ER PT J AU MESSMER, E RODRIGUEZ, A PEDROZASERES, M CALONGE, M AKOVA, YA DAMICO, D FOSTER, CS AF MESSMER, E RODRIGUEZ, A PEDROZASERES, M CALONGE, M AKOVA, YA DAMICO, D FOSTER, CS TI EPIDEMIOLOGIC AND ETIOLOGIC CHARACTERISTICS OF UVEITIS IN A TERTIARY CARE CENTER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL & UVEITIS SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RETINA SERV,BOSTON,MA 02114. RI Calonge, Margarita/K-2839-2014 OI Calonge, Margarita/0000-0001-8178-4836 NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2093 EP 2093 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503864 ER PT J AU STROH, EM MEHTA, M LYON, AT TREMPE, CL AF STROH, EM MEHTA, M LYON, AT TREMPE, CL TI OCULAR FINDINGS ASSOCIATED WITH MYCOBACTERIUM-TUBERCULOSIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 RETINA ASSOCIATES,BOSTON,MA. SCHEPENS EYE RES INST,BOSTON,MA. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. N SHORE UNIV HOSP,MANHASSET,NY 11030. NORTHWESTERN UNIV,COLL MED,CHICAGO,IL 60611. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2105 EP 2105 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503929 ER PT J AU GONZALEZ, VH THEODOSOADIS, P MCCLATCHEY, EA MUKAI, S AF GONZALEZ, VH THEODOSOADIS, P MCCLATCHEY, EA MUKAI, S TI RABBIT MODEL OF INTRAOCULAR RETINOBLASTOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2118 EP 2118 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503997 ER PT J AU PARK, SS GRAGOUDAS, ES YOUNG, LHY AF PARK, SS GRAGOUDAS, ES YOUNG, LHY TI EFFECT OF IMMUNOTHERAPY ON RATE OF METASTASIS IN MURINE MODEL OF OCULAR MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2119 EP 2119 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504000 ER PT J AU SCHMIDTERFURTH, U DIDDENS, H BAMBERG, M BIRNGRUBER, R HASAN, T AF SCHMIDTERFURTH, U DIDDENS, H BAMBERG, M BIRNGRUBER, R HASAN, T TI CARRIER-MEDIATED TARGETING IN PHOTODYNAMIC THERAPY OF RETINOBLASTOMA CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RI Birngruber, Reginald/Q-2342-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2119 EP 2119 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504004 ER PT J AU YOUNG, LHY HU, LK FLOTTE, TJ GRAGOUDAS, ES AF YOUNG, LHY HU, LK FLOTTE, TJ GRAGOUDAS, ES TI ACCUMULATION OF 2ND-GENERATION PHOTOSENSITIZERS IN OCULAR MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2119 EP 2119 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504001 ER PT J AU REGAN, S EGAN, KM WALSH, SM DREYER, E GRAGOUDAS, ES AF REGAN, S EGAN, KM WALSH, SM DREYER, E GRAGOUDAS, ES TI CORRELATES OF VISUAL-FIELD TEST-PERFORMANCE IN PATIENTS WITH UVEAL MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,GLAUCOMA SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2120 EP 2120 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504009 ER PT J AU WALSH, SM EGAN, KM REGAN, S GRAGOUDAS, ES AF WALSH, SM EGAN, KM REGAN, S GRAGOUDAS, ES TI DEVELOPMENT OF NEOVASCULAR GLAUCOMA AFTER PROTON-BEAM IRRADIATION FOR UVEAL MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2120 EP 2120 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504010 ER PT J AU BERGER, JW AF BERGER, JW TI RELEVANCE OF TRYPTOPHAN TRIPLET-STATES TO IN-SITU LENS PHOTOCHEMISTRY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,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 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2137 EP 2137 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504088 ER PT J AU HETH, CA MARESCALCHI, PA AF HETH, CA MARESCALCHI, PA TI INCREASING IP3 INCREASES ROS PHAGOCYTOSIS IN CULTURED RCS RAT RETINAL-PIGMENT EPITHELIUM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2140 EP 2140 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504104 ER PT J AU WIGGS, JL HAINES, JL PAGLINAUAN, C SPORN, C LOU, D AF WIGGS, JL HAINES, JL PAGLINAUAN, C SPORN, C LOU, D TI GENETIC-LINKAGE OF AUTOSOMAL-DOMINANT JUVENILE GLAUCOMA TO 1Q21-Q31 IN 3 AFFECTED PEDIGREES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2144 EP 2144 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504118 ER PT J AU TO, KW ADAMIAN, M JAKOBIEC, FA BERSON, EL AF TO, KW ADAMIAN, M JAKOBIEC, FA BERSON, EL TI CLINICAL AND HISTOPATHOLOGIC FEATURES OF CLUMPED PIGMENTARY RETINAL DEGENERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2159 EP 2159 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504177 ER PT J AU GROSSKREUTZ, CL KAISER, PK DREYER, EB AF GROSSKREUTZ, CL KAISER, PK DREYER, EB TI AN EVALUATION OF THE RISK OF GLAUCOMA SECONDARY TO INHALED STEROID USE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,GLAUCOMA CONSULT SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2179 EP 2179 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504268 ER PT J AU MCKEOWN, CA WARD, JB NIFFENEGGER, AS LAVIN, CW AHERN, DK ACQUADRO, MA AF MCKEOWN, CA WARD, JB NIFFENEGGER, AS LAVIN, CW AHERN, DK ACQUADRO, MA TI THE USE OF PROPOFOL AND MIVACURIUM ANESTHETIC TECHNIQUE FOR THE IMMEDIATE POSTOPERATIVE ADJUSTMENT OF SUTURES IN STRABISMUS SURGERY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2200 EP 2200 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504372 ER PT J AU NIFFENEGGER, AS WARD, JB LAVIN, CW AHEM, DK ACQUADRO, MA MCKEOWN, CA AF NIFFENEGGER, AS WARD, JB LAVIN, CW AHEM, DK ACQUADRO, MA MCKEOWN, CA TI LOW INCIDENCE OF NAUSEA AND VOMITING FOLLOWING GENERAL-ANESTHESIA FOR ADULT STRABISMUS SURGERY EMPLOYING CONTINUOUS INFUSIONS OF PROPOFOL, MIVACURIUM, AND ALFENTANIL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2200 EP 2200 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504373 ER PT J AU CHENG, HM CHENG, FY TANAKA, GH XIONG, J PFLEIDERER, B AF CHENG, HM CHENG, FY TANAKA, GH XIONG, J PFLEIDERER, B TI MANIPULATING RAT LENS METABOLISM WITH EXOGENOUS SUBSTRATES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 2208 EP 2208 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58504412 ER PT J AU GEWIRTZ, H FISCHMAN, AJ ABRAHAM, S GILSON, M STRAUSS, HW ALPERT, NM AF GEWIRTZ, H FISCHMAN, AJ ABRAHAM, S GILSON, M STRAUSS, HW ALPERT, NM TI POSITRON EMISSION TOMOGRAPHIC MEASUREMENTS OF ABSOLUTE REGIONAL MYOCARDIAL BLOOD-FLOW PERMITS IDENTIFICATION OF NONVIABLE MYOCARDIUM IN PATIENTS WITH CHRONIC MYOCARDIAL-INFARCTION SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; REPERFUSED CANINE MYOCARDIUM; LEFT-VENTRICULAR DYSFUNCTION; N-13 AMMONIA; OXYGEN-CONSUMPTION; F-18 DEOXYGLUCOSE; ISCHEMIA; ABNORMALITIES; THALLIUM; STENOSIS AB Objectives. This study tested the hypothesis that nonviable myocardium can be identified by quantitative measurements of regional myocardial blood flow obtained using positron emission tomography in conjunction with a mathematical model of nitrogen-13 (N-13) ammonia tracer kinetics. Background. Under steady state basal conditions there is a minimal level of blood flow required to sustain myocardial viability. Therefore, the hypothesis predicts that regions with flow below a certain threshold are likely to be composed primarily of scar. Methods. Studies were conducted in 26 patients with chronic myocardial infarction. Positron emission tomographic measurements of basal regional myocardial blood flow (N-13 ammonia) and fluorine 18 (F-18) fluorodeoxyglucose uptake were made and correlated with information about coronary anatomy and regional wall motion to assess myocardial viability. Results. In patients with chronic myocardial infarction, normal zone blood flow (0.81 +/- 0.32 ml/min per g [mean +/- SD]) was greater (p < 0.02) than that of border zones (0.59 +/- 0.29 ml/min per g), which in turn exceeded (p < 0.001) that of infarct zone flow (0.27 +/- 0.17 ml/min per g). Good correlation was noted between relative F-18 fluorodeoxyglucose uptake and relative regional myocardial blood flow in all zones (r = 0.63, p < 0.001). Mismatch between blood flow and F-18 fluorodeoxyglucose uptake, with a single exception, was not observed in any segment with blood how <0.25 ml/min per g. All dyskinetic segments (n = 5) also had blood flow <0.25 ml/min per g. In contrast, 43 of 45 myocardial segments (23 patients) with normal contraction or only mild hypokinesia had flow greater than or equal to 0.39 ml/min per g (average flow 0.78 +/- 0.35 ml/min per g). Conclusions. in patients with chronic myocardial infarction, myocardial viability is unlikely when basal regional myocardial blood flow is <0.25 ml/min per g. Average basal how in segments with normal or nearly normal wall motion is 0.78 +/- 0.35 ml/min per g. Thus, positron emission tomographic measurement of regional myocardial blood flow is helpful in identifying nonviable myocardium in these patients. C1 RHODE ISL HOSP,DEPT MED,DIV CARDIOL,PROVIDENCE,RI 02903. BROWN UNIV,SCH MED,PROVIDENCE,RI 02912. MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,NEW BRUNSWICK,NJ 08903. RP GEWIRTZ, H (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114, USA. FU NCI NIH HHS [NCI T32 CA09362-09A1] NR 31 TC 90 Z9 93 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 15 PY 1994 VL 23 IS 4 BP 851 EP 859 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PH370 UT WOS:A1994PH37000003 PM 8106689 ER PT J AU CHEN, CG RODRIGUEZ, L LETHOR, JP LEVINE, RA SEMIGRAN, MS FIFER, MA WEYMAN, AE THOMAS, JD AF CHEN, CG RODRIGUEZ, L LETHOR, JP LEVINE, RA SEMIGRAN, MS FIFER, MA WEYMAN, AE THOMAS, JD TI CONTINUOUS-WAVE DOPPLER-ECHOCARDIOGRAPHY FOR NONINVASIVE ASSESSMENT OF LEFT-VENTRICULAR DP/DT AND RELAXATION-TIME CONSTANT FROM MITRAL REGURGITANT SPECTRA IN PATIENTS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID MYOCARDIAL-INFARCTION; DIASTOLIC FUNCTION; PRESSURE; VALIDATION; MECHANISM; HEART AB Objectives. We previously demonstrated experimentally that the mitral regurgitant velocity spectrum can be used to estimate left ventricular pressure throughout systole and may provide a new noninvasive method for estimating maximal dP/dt and the relaxation time constant. This study was designed to test this method in patients. Background. The maximal first derivative of left ventricular pressure (dP/dt) and the time constant of left ventricular isovolumetric relaxation (tau) are important variables of left ventricular function, but the need for invasive measurement with high fidelity catheters has limited their use in clinical cardiology. Methods. Twelve patients with mitral regurgitation were studied. The Doppler mitral regurgitant velocity spectrum was recorded simultaneously with micromanometer left ventricular pressure tracings in all patients. The regurgitant velocity profiles were digitized and converted to ventriculoatrial (VA) pressure gradient curves using the simplified Bernoulli equation and differentiated into instantaneous dP/dt, The relaxation time constant (tau) was calculated assuming a zero pressure asymptote from catheter left ventricular pressure decay (tau(c)) and from the Doppler-derived VA gradient curve with corrections. Two methods were used to correct the Doppler gradient curve to better approximate the left ventricular pressure decay before calculating the relaxation time constant: 1) adding an arbitrary 10 mm Hg (tau(10)), and 2) adding the actual mean pulmonary capillary pressure (tau(LA)). Results. The Doppler derived maximal positive dP/dt (1,394 +/- 302 mm Hg/s [mean +/- SD]) correlated well (r = 0.91) with the catheter derived maximal dP/dt (1,449 +/- 307 mm Hg/s). Although the Doppler derived negative maximal dP/dt differed slightly from catheter measurement (1,014 +/- 289 vs. 1,195 +/- 354 mm Hg/s, p < 0.01), the correlation between Doppler and catheter measurements was similarly good (r = 0.89, p < 0.0001). The correlation between tau(10) and tau(c) was excellent (r = 0.93, p < 0.01), but the Doppler derived tau(10) (50.0 +/- 11.0 ms) slightly underestimated the catheter derived tau(c) (55.5 +/- 12.8 ms, p < 0.01). This slight underestimation could be corrected by adding the actual pulmonary capillary wedge pressure to the Doppler gradient curve. Conclusions. Doppler echocardiography provides an accurate and reliable method for estimating left ventricular maximal positive dP/dt, maximal negative dP/dt and the relaxation time constant (tau) in patients with mitral regurgitation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA. UNIV HAMBURG HOSP,DEPT CARDIOL,HAMBURG,GERMANY. CLEVELAND CLIN FDN,DEPT CARDIOL,CLEVELAND,OH 44195. NR 23 TC 40 Z9 42 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 15 PY 1994 VL 23 IS 4 BP 970 EP 976 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PH370 UT WOS:A1994PH37000019 PM 8106704 ER PT J AU EFRAT, S LEISER, M WU, YJ FUSCODEMANE, D EMRAN, OA SURANA, M JETTON, TL MAGNUSON, MA WEIR, G FLEISCHER, N AF EFRAT, S LEISER, M WU, YJ FUSCODEMANE, D EMRAN, OA SURANA, M JETTON, TL MAGNUSON, MA WEIR, G FLEISCHER, N TI RIBOZYME-MEDIATED ATTENUATION OF PANCREATIC BETA-CELL GLUCOKINASE EXPRESSION IN TRANSGENIC MICE RESULTS IN IMPAIRED GLUCOSE-INDUCED INSULIN-SECRETION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ANTISENSE RNA; BETA-CELL LINES; DIABETES; GLUCOSE PHOSPHORYLATION; GLUCOSE SENSING ID DIABETES-MELLITUS; GENE; ISLETS; RNA; PROMOTER; SEQUENCE; LIVER AB Phosphorylation of glucose to glucose 6-phosphate by glucokinase (GK; EC 2.7.1.2) serves as a glucose-sensing mechanism for regulating insulin secretion in beta cells. Recent findings of heterozygous GK gene mutations in patients with maturity-onset diabetes of the young (MODY), a form of type II (non-insulin-dependent) diabetes characterized by autosomal dominant inheritance, have raised the possibility that a decrease in beta-cell GK activity may impair the insulin secretory response of these cells to glucose. To generate an animal model for MODY we have expressed in transgenic mice a GK antisense RNA with a ribozyme element under control of the insulin promoter. Mice in two independent lineages had about 30% of the normal islet GK activity. Insulin release in response to glucose from in situ-perfused pancreas was impaired; however, the plasma glucose and insulin levels of the mice remained normal. These mice are likely to be predisposed to type II diabetes and may manifest increased susceptibility to genetic and environmental diabetogenic factors. They provide an animal model for studying the interaction of such factors with the reduced islet GK activity. C1 ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10461. JOSLIN DIABET CTR,BOSTON,MA 02215. VANDERBILT UNIV,SCH MED,DEPT MOLEC PHYSIOL & BIOPHYS,NASHVILLE,TN 37232. RP EFRAT, S (reprint author), ALBERT EINSTEIN COLL MED,DEPT MOLEC PHARMACOL,BRONX,NY 10461, USA. RI Magnuson, Mark/B-1335-2009 OI Magnuson, Mark/0000-0002-8824-6499 NR 25 TC 112 Z9 115 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1994 VL 91 IS 6 BP 2051 EP 2055 DI 10.1073/pnas.91.6.2051 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NC043 UT WOS:A1994NC04300018 PM 7510884 ER PT J AU TORRES, IP LEUNIG, M YUAN, F INTAGLIETTA, M JAIN, RK AF TORRES, IP LEUNIG, M YUAN, F INTAGLIETTA, M JAIN, RK TI NONINVASIVE MEASUREMENT OF MICROVASCULAR AND INTERSTITIAL OXYGEN PROFILES IN A HUMAN TUMOR IN SCID MICE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID BLOOD-FLOW; HYPOXIA; TENSION; TISSUES; PHOSPHORESCENCE; ANGIOGENESIS; CONVECTION; TRANSPORT; DIFFUSION; PRESSURE AB Simultaneous measurements of intravascular and interstitial oxygen partial pressure (PO2) in any tissue have not previously been reported, despite the importance of oxygen in health and in disease. This is due to the limitations of current techniques, both invasive and noninvasive. We have optically measured microscopic profiles of PO2 with high spatial resolution in subcutaneous tissue and transplanted tumors in mice by combining an oxygen-dependent phosphorescence quenching method and a transparent tissue preparation. The strengths of our approach include the ability to follow PO2 in the same location for several weeks and to relate these measurements to local blood flow and vascular architecture. Our results show that (i) PO2 values in blood vessels in well-vascularized regions of a human colon adenocarcinoma xenograft are comparable to those in surrounding arterioles and venules, (ii) carbogen (95% O-2/5% CO2) breathing increases microvascular PO2 in tumors, and (iii) in unanesthetized and anesthetized mice PO2 drops to hypoxic values at <200 mu m from isolated vessels but drops by <5 mmHg (1 mmHg = 133 Pa) in highly vascularized tumor regions. Our method should permit noninvasive evaluations of oxygen-modifying agents and offer further mechanistic information about tumor pathophysiology in tissue preparations where the surface of the tissue can be observed. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,STEELE LAB,BOSTON,MA 02114. RP TORRES, IP (reprint author), UNIV CALIF SAN DIEGO,INST BIOMED ENGN,DEPT APPL MECH & ENGN SCI,LA JOLLA,CA 92093, USA. RI Yuan, Fan/A-1287-2011; Leunig, Michael/E-7951-2017 OI Leunig, Michael/0000-0002-2036-5416 FU NCI NIH HHS [CA37239]; NHLBI NIH HHS [HL17421] NR 43 TC 108 Z9 109 U1 0 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1994 VL 91 IS 6 BP 2081 EP 2085 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NC043 UT WOS:A1994NC04300024 PM 8134352 ER PT J AU GUINAN, EC MOLRINE, DC ANTIN, JH LEE, MC WEINSTEIN, HJ SALLAN, SE PARSONS, SK WHEELER, C GROSS, W MCGARIGLE, C BLANDING, P SCHIFFMAN, G FINBERG, RW SIBER, GR BOLON, D WANG, M CARIATI, S AMBROSINO, DM AF GUINAN, EC MOLRINE, DC ANTIN, JH LEE, MC WEINSTEIN, HJ SALLAN, SE PARSONS, SK WHEELER, C GROSS, W MCGARIGLE, C BLANDING, P SCHIFFMAN, G FINBERG, RW SIBER, GR BOLON, D WANG, M CARIATI, S AMBROSINO, DM TI POLYSACCHARIDE CONJUGATE VACCINE RESPONSES IN BONE-MARROW TRANSPLANT PATIENTS SO TRANSPLANTATION LA English DT Article ID INFLUENZAE TYPE-B; IMPAIRED ANTIBODY-RESPONSE; NON-HODGKINS LYMPHOMA; CAPSULAR POLYSACCHARIDE; PNEUMOCOCCAL VACCINE; SUBCLASS DEFICIENCY; MONOCLONAL-ANTIBODY; IGG-SUBCLASS; HOST DISEASE; CHILDREN AB Bone marrow transplant patients have impaired responses to pure polysaccharide (PS) vaccines and are at an increased risk for disease caused by PS encapsulated pathogens such as Haemophilus influenzae type B (HIB) and Streptococcus pneumoniae. We immunized 35 BMT patients (21 allogeneic and 14 autologous) ages 2-45 years with pure PS pneumococcal (Pnu-imune 23), HIB-conjugate (HibTITER), and tetanus toroid vaccines. Patients were assigned to receive vaccines at either 12 and 24 months after transplantation or at 24 months only. Only 19% of all enrolled patients developed protective antibody concentrations (greater than or equal to 0.300 mu g antibody nitrogen/ml) to the 6 pneumococcal serotypes measured after the 24-month immunization. Poor response to pneumococcal vaccine was not different for the 2 study groups and was similar to previous studies. In contrast, HIB-coqjugate vaccine elicited protective concentrations of antibody (greater than or equal to 1.0 mu g/ml) in 56% of patients after 1 dose and in 80% after 2 doses. The group that received 2 doses of HIB-conjugate vaccine had a significantly higher geometric mean antibody concentration of 14.5 mu g/ml as compared with 1.43 mu g/ml for those receiving only 1 dose (P=0.012). Responses to tetanus toroid vaccine were similar to HIB-conjugate vaccine, with a booster response documented after the second dose. In summary 2 doses of HIB-coqjugate vaccine given at 12 and 24 months after transplantation produced protective antibody concentrations in 80% of patients. While the response to pure PS pneumococcal vaccine was poor, the results with HIB-coqjugate vaccine suggest that future pneumococcal conjugate vaccines may also benefit BMT patients. C1 DANA FABER CANC INST,DEPT PEDIAT ONCOL,INFECT DIS LAB,BOSTON,MA 02115. DANA FABER CANC INST,DEPT PHARM,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CHILDRENS HOSP,DIV HEMATOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CHILDRENS HOSP,DIV ONCOL,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02115. SUNY HLTH SCI CTR,DEPT MICROBIOL & IMMUNOL,BROOKLYN,NY 11203. FU NCI NIH HHS [CA39542]; NIAID NIH HHS [AI82699] NR 39 TC 89 Z9 91 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 15 PY 1994 VL 57 IS 5 BP 677 EP 684 DI 10.1097/00007890-199403150-00009 PG 8 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA NC190 UT WOS:A1994NC19000009 PM 8140632 ER PT J AU KLUMPP, TR FAIRCLOUGH, D RITZ, J SOIFFER, R AF KLUMPP, TR FAIRCLOUGH, D RITZ, J SOIFFER, R TI THE EFFECT OF MINOR ABO MISMATCHES ON THE INCIDENCE OF GRAFT-VERSUS-HOST DISEASE AFTER ALLOGENEIC BONE-MARROW TRANSPLANTATION SO TRANSPLANTATION LA English DT Letter C1 DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 NR 8 TC 7 Z9 7 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 15 PY 1994 VL 57 IS 5 BP 780 EP 780 DI 10.1097/00007890-199403150-00031 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA NC190 UT WOS:A1994NC19000031 PM 8140649 ER PT J AU BURTON, MD HITZIG, BM JOHNSON, DC AF BURTON, MD HITZIG, BM JOHNSON, DC TI VIABILITY OF THE NEONATAL RAT ISOLATED BRAIN-STEM PREPARATION BY P-31 MRS SO NEUROSCIENCE LETTERS LA English DT Article DE ISOLATED BRAIN-STEM; VIABILITY; NMR SPECTROSCOPY; PHOSPHATE; INTRACELLULAR PH ID MAGNETIC-RESONANCE SPECTROSCOPY; PHOSPHATE METABOLITE REGULATION; PARTIAL ISCHEMIA; MEASURED INVIVO; PH; PHOSPHORYLETHANOLAMINE; PHOSPHOMONOESTER AB The isolated brainstem-spinal axis from the neonatal rat is an established model for studying neuronal responses of the ventilatory control system, however, its viability has not been clearly established. We studied the brainstem-spinal axis from newborn rats at 8.5 T with P-31 NMR spectroscopy. The relative pattern of high energy phosphates (HEPs) was similar to that reported for the in vivo neonatal brain. The average pH(i) was 0.2 to 0.4 units less than the pH(i) for the in vivo neonatal brain. The HEPs and pH(i) were stable for 6 h, suggesting extended in vitro viability. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BURTON, MD (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. FU NCRR NIH HHS [RR-00995]; NHLBI NIH HHS [HL-43819] NR 14 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD MAR 14 PY 1994 VL 169 IS 1-2 BP 31 EP 34 DI 10.1016/0304-3940(94)90349-2 PG 4 WC Neurosciences SC Neurosciences & Neurology GA NC117 UT WOS:A1994NC11700008 PM 8047287 ER PT J AU BURKE, TR SMYTH, MS OTAKA, A NOMIZU, M ROLLER, PP CASE, RD SHOELSON, SE AF BURKE, TR SMYTH, MS OTAKA, A NOMIZU, M ROLLER, PP CASE, RD SHOELSON, SE TI FLUORINATED PHOSPHONOMETHYL PHENYLALANINE ANALOGS AS PHOSPHOTYROSYL MIMETICS IN SH2-BINDING PEPTIDES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,DCT,DTP,MED CHEM LAB,BETHESDA,MD 20892. HARVARD UNIV,JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 13 PY 1994 VL 207 BP 6 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA MY954 UT WOS:A1994MY95403314 ER PT J AU MYERS, AM WYRICK, SD BOOTH, RG OWENS, CE KULA, NS BALDESSARINI, RJ MAILMAN, RB AF MYERS, AM WYRICK, SD BOOTH, RG OWENS, CE KULA, NS BALDESSARINI, RJ MAILMAN, RB TI PHENYLAMINOTETRALINS AS LIGANDS FOR A NOVEL SIGMA-LIKE NEUROMODULATORY RECEPTOR SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 UNIV N CAROLINA,SCH PHARM,DIV MED CHEM & NAT PROD,CHAPEL HILL,NC 27599. HARVARD UNIV,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,BOSTON,MA 02114. UNIV N CAROLINA,SCH MED,BRAIN & DEV RES CTR,CHAPEL HILL,NC 27599. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 13 PY 1994 VL 207 BP 168 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA MY954 UT WOS:A1994MY95403475 ER PT J AU GAFFAR, A MORENO, EC GAMBOGI, RJ AFFLITTO, J AF GAFFAR, A MORENO, EC GAMBOGI, RJ AFFLITTO, J TI RELATIONSHIP BETWEEN CRYSTAL-GROWTH INHIBITION OF HA AND IN-VIVO ANTICALCULUS EFFECT SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 COLGATE PALMOLIVE CO,CTR TECHNOL,PISCATAWAY,NJ 08854. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 13 PY 1994 VL 207 BP 208 EP IEC PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA MY954 UT WOS:A1994MY95402750 ER PT J AU ROSENZWEIG, AC NORDLUND, P FREDERICK, CA LIPPARD, SJ AF ROSENZWEIG, AC NORDLUND, P FREDERICK, CA LIPPARD, SJ TI CRYSTAL-STRUCTURE OF THE HYDROXYLASE PROTEIN OF METHANE MONOOXYGENASE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 MIT,DEPT CHEM,CAMBRIDGE,MA 02139. UNIV STOCKHOLM,DEPT MOLEC BIOL,S-10691 STOCKHOLM,SWEDEN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 13 PY 1994 VL 207 BP 277 EP INOR PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA MY954 UT WOS:A1994MY95403038 ER PT J AU KEEGAN, AD NELMS, K WHITE, M WANG, LM PIERCE, JH PAUL, WE AF KEEGAN, AD NELMS, K WHITE, M WANG, LM PIERCE, JH PAUL, WE TI AN IL-4 RECEPTOR REGION CONTAINING AN INSULIN-RECEPTOR MOTIF IS IMPORTANT FOR IL4-MEDIATED IRS-1 PHOSPHORYLATION AND CELL-GROWTH SO CELL LA English DT Article ID STIMULATORY FACTOR-I; HUMAN INTERLEUKIN-4 RECEPTOR; SIGNAL TRANSDUCTION; FC-EPSILON; EXPRESSION CLONING; MOLECULAR-CLONING; B-CELLS; IDENTIFICATION; TRANSMISSION; SUPERFAMILY AB Interleukin-4 (IL-4) treatment of 32D cells overexpressing insulin receptor substrate 1 (IRS-1) causes prompt tyrosine phosphorylation of IRS-l. Transfection of truncation mutants of the human IL-4 (huIL-4) receptor into 32D-IRS-1 cells demonstrated that the region from amino acid 437-557 is important for IL-4 signaling. This region of the IL-4 receptor (IL-4R) contains the motif (488)PL-X4-NPXYXSXSD(502) (insulin/IL-4R [I4R]) found in the insulin and insulin-like growth factor 1 receptors. Mutation of Y497 to F yielded receptors that caused little or no IRS-1 phosphorylation in response to huIL-4 when expressed in 32D-IRS-1 cells. Most cell lines expressing Y497F also failed to proliferate in response to huIL-4. Furthermore, a glutathione-S-transferase fusion protein containing the I4R motif-bound IRS-1,tyrosine kinase(s), and other unidentified phosphoproteins with molecular sizes of 140, 80, and 55 kd. Thus, the central tyrosine of the I4R motif has a major role in IL-4-mediated signal transduction in 32D cells. C1 HARVARD UNIV,DEPT MED,JOSLIN DIABET CTR,BOSTON,MA 02215. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. RP KEEGAN, AD (reprint author), NIAID,IMMUNOL LAB,BETHESDA,MD 20892, USA. NR 43 TC 287 Z9 290 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 11 PY 1994 VL 76 IS 5 BP 811 EP 820 DI 10.1016/0092-8674(94)90356-5 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NA890 UT WOS:A1994NA89000007 PM 8124718 ER PT J AU BALDESSARINI, RJ KULA, NS ZONG, RS NEUMEYER, JL AF BALDESSARINI, RJ KULA, NS ZONG, RS NEUMEYER, JL TI RECEPTOR AFFINITIES OF APORPHINE ENANTIOMERS IN RAT-BRAIN TISSUE SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note DE ADRENOCEPTOR; APORPHINE; ANTIPSYCHOTIC; DOPAMINE RECEPTOR; PARTIAL AGONIST; RECEPTOR; 5-HT (5-HYDROXYTRYPTAMINE, SEROTONIN); STEREOISOMER ID DOPAMINE; BINDING AB R(-) and S(+) enantiomers of apomorphine, N-n-propylnorapomorphine and 11-hydroxy-N-n-propylnorapomorphine were screened for affinity at over 40 representative sites in rat brain tissue that included amine, purine, amino acid and peptide receptors, transporters, ion channels, and effector components; only dopamine receptors and alpha-adrenoceptors showed appreciable affinity that was quantified further. The aporphines showed R(-)> S(+) isomeric selectivity as well as D-2 > D-1 selectivity at dopamine receptors. While R(-) isomers preferred alpha(2)-adrenoceptors, S(+)-aporphines were alpha(1)-selective, with similar affinity at alpha(1)-adrenoceptors and dopamine D-2 receptors. Interactions of S(+)-aporphines at alpha(1)-adrenoceptors as well as dopamine D-2 receptors may contribute to their unusual behavioral properties. C1 MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,BELMONT,MA. HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. NORTHEASTERN UNIV,COLL PHARM & ALLIED HLTH PROFESS,MED CHEM SECT,BOSTON,MA. RES BIOCHEM INT,NATICK,MA. FU NIMH NIH HHS [NIMH MH-31154, NIMH MH-47370, NIMH MH-34006] NR 16 TC 29 Z9 29 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD MAR 11 PY 1994 VL 254 IS 1-2 BP 199 EP 203 DI 10.1016/0014-2999(94)90388-3 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NB717 UT WOS:A1994NB71700027 PM 7911429 ER PT J AU LI, CJ WANG, CL PARDEE, AB AF LI, CJ WANG, CL PARDEE, AB TI CAMPTOTHECIN INHIBITS TAT-MEDIATED TRANSACTIVATION OF TYPE-I HUMAN-IMMUNODEFICIENCY-VIRUS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID THYMIDINE KINASE PROMOTER; TRANS-ACTIVATOR GENE; KAPPA-B; T-CELLS; REPLICATION; TRANSCRIPTION; BINDING; EXPRESSION; RNA; INDUCTION AB Transcription of type I human immunodeficiency virus (HIV-I) is governed by the viral long terminal repeat (LTR). By using HTV-1 LTR-directed reporter gene systems, we found that the DNA topoisomerase I inhibitor camptothecin inhibits Tat-mediated transactivation of HIV-1 LTR. The 293.27.2 cells that carry a stably transfected HIV-1 LTR-directed lacZ gene expression vector (pNAZ) were used. Inhibitions of LTR were observed at camptothecin concentrations (IC50 about 0.03 mu m, which was an order of magnitude lower than for Ro 24-7429), which had minor effects on cell survival, expression of the cellular gene gro, or Rous sarcoma virus-directed chloramphenicol acetyltransferase (CAT) gene expression. Inhibition was also seen with RPMI 8402, which is a human CD4-positive lymphocyte line transiently transfected with a HIV-1 LTR-directed (CAT) gene. Experiments with HIV-1 LTR mutants suggest that transactivation response sequence but not NF-kappa B is responsible for the inhibition by camptothecin. The target for camptothecin may be a cellular factor that is important for the activation of HIV-1 LTR by Tat and thus may offer a potential target for therapy of HIV-1 infection. RP LI, CJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 50608] NR 36 TC 30 Z9 30 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 11 PY 1994 VL 269 IS 10 BP 7051 EP 7054 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA032 UT WOS:A1994NA03200002 PM 8125909 ER PT J AU TACCIOLI, GE CHENG, HL VARGHESE, AJ WHITMORE, G ALT, FW AF TACCIOLI, GE CHENG, HL VARGHESE, AJ WHITMORE, G ALT, FW TI A DNA-REPAIR DEFECT IN CHINESE-HAMSTER OVARY CELLS AFFECTS V(D)J RECOMBINATION SIMILARLY TO THE MURINE ACID MUTATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PRE-B CELLS; JUNCTIONAL SEQUENCES; RECEPTOR GAMMA; SCID MUTATION; GENES; MICE; MUTANTS; DEFICIENCY; RADIATION; SIGNAL AB Lymphocyte antigen receptor variable regions are encoded by gene segments that are assembled by the site-specific variable (diversity) joining (V(D)J) recombination process. We have assayed the V-3 Chinese hamster ovary cell line, which has a double-strand DNA break repair (dsbr) defect, for the ability to carry out V(D)J recombination following transfection of constructs that encode the RAG-1 and RAG-2 proteins necessary to confer V(D)J recombination activity to non-lymphoid cells. The V-3 cells had substantially impaired ability to undergo V(D)J recombination of transiently introduced test substrates. Although these cells can initiate V(D)J recombination by introducing endonucleolytic scissions at the junctions of V(D)J recombination signal sequences and the flanking coding sequences, they have a greatly impaired ability to rejoin the coding sequences. Detailed characterization of attempted coding joins recovered from these cells indicated that the V(D)J recombination defect in V-3 is similar in phenotype to the murine severe combined immunodeficient (scid) defect and quite distinct from that found in other Chinese hamster ovary dsbr mutant cell lines. Somatic cell complementation analyses between homozygous scid mutant fibroblasts and V-3 cells confirmed that these mutations fall into the same genetic complementation group. C1 HARVARD UNIV, CHILDRENS HOSP, SCH MED, HOWARD HUGHES MED INST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT GENET, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, CTR BLOOD RES, BOSTON, MA 02115 USA. ONTARIO CANC INST, TORONTO M4X 1K9, ON, CANADA. FU NIAID NIH HHS [AI20047] NR 29 TC 81 Z9 82 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 11 PY 1994 VL 269 IS 10 BP 7439 EP 7442 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA032 UT WOS:A1994NA03200065 PM 8125964 ER PT J AU MILLER, JB AF MILLER, JB TI DONT CALL US SO NATURE LA English DT Letter RP MILLER, JB (reprint author), MASSACHUSETTS GEN HOSP,NEUROMUSCULAR LAB,BOSTON,MA 02129, USA. OI Miller, Jeffrey/0000-0001-5273-2201 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 10 PY 1994 VL 368 IS 6467 BP 93 EP 93 DI 10.1038/368093c0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NA030 UT WOS:A1994NA03000026 PM 8139669 ER PT J AU GROSSBARD, ML HARRIS, NL BOLAND, GW CAREY, RW AF GROSSBARD, ML HARRIS, NL BOLAND, GW CAREY, RW TI A 37-YEAR-OLD WOMAN WITH THROMBOCYTOPENIA AND A PARAGASTRIC MASS AFTER TREATMENT FOR HODGKINS-DISEASE - HODGKINS-DISEASE, RECURRENT, INVOLVING STOMACH AND PARAGASTRIC LYMPH-NODES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID BONE-MARROW TRANSPLANTATION; PURPURA; CANCER; THERAPY; AUTOPSY; RISK C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP GROSSBARD, ML (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 32 TC 1 Z9 1 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 10 PY 1994 VL 330 IS 10 BP 698 EP 704 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA MY575 UT WOS:A1994MY57500008 ER PT J AU NADOL, JB AF NADOL, JB TI HEARING-LOSS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP NADOL, JB (reprint author), MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 10 PY 1994 VL 330 IS 10 BP 715 EP 715 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MY575 UT WOS:A1994MY57500022 ER PT J AU BOTFIELD, MC WEISS, MA AF BOTFIELD, MC WEISS, MA TI BIPARTITE DNA RECOGNITION BY THE HUMAN OCT-2 POU DOMAIN - POU(S)-SPECIFIC PHOSPHATE CONTACTS ARE ANALOGOUS TO THOSE OF BACTERIOPHAGE-LAMBDA REPRESSOR SO BIOCHEMISTRY LA English DT Note ID CATABOLITE GENE ACTIVATOR; CRYSTAL-STRUCTURE; OPERATOR COMPLEX; BINDING PROTEINS; IMMUNOGLOBULIN GENES; TRANSCRIPTION FACTOR; HOMEODOMAIN; RESOLUTION; SEQUENCE; SUGGESTS AB The POU motif defines a family of eukaryotic transcription factors broadly involved in tissue-specific gene expression and developmental regulation, The motif contains two DNA-binding domains: an N-terminal POU-specific domain (POUS) and C-terminal homeodomain (POUHD Surprisingly, POUS has recently been found to be similar in structure to helix-turn-helix (HTH) domains of phage repressor and Cro proteins [Assa-Munt, N., Mortishire-Smith, R., Aurora, R., Herr, W., and Wright, P. E. (1993) Cell 73, 193-205; Dekker, N., Cox, M., Boelens, R., Verrijzer, C. P., van der Vliet, P. C., and Kaptein, R. (1993) Nature 362, 852-855]. Because POUHD and POUS are expected to bind DNA differently, we have used ''methylphosphonate interference'' to investigate the alignment of their HTH elements in a specific DNA complex. This neutral phosphate analogue, originally developed for applications in antisense drug design [Miller, P. S., and Ts'o, P. O, P. (1987) Anti-Cancer Drug Des. 2, 117-128], is shown to provide a sensitive probe for sites of backbone-specific protein-DNA interaction. Inferred POUS-phosphate contacts are in striking accord with cocrystal structures of bacteriophage repressor and Cro proteins. Alignment of POUHD and POUS in successive major grooves in each case predicts unique HTH-adenine contacts. This prediction is verified using DNA base analogues to effect interchange of AT functional groups by the method of 2'-deoxyinosine/5-methyl-2'-deoxycytosine substitution [McLaughlin, L. W., Benseler, F., Graeser, E., Piel, N., and Scholtissek, S. (1987) Biochemistry 26, 7238-7245]. Our results strongly support the hypothesis that the DNA-binding properties of POUS are analogous to those of bacteriophage lambda repressor. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 55 TC 16 Z9 16 U1 1 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 8 PY 1994 VL 33 IS 9 BP 2349 EP 2355 DI 10.1021/bi00175a001 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MZ697 UT WOS:A1994MZ69700001 PM 8117693 ER PT J AU LIN, CW HANNA, M SZOSTAK, JW AF LIN, CW HANNA, M SZOSTAK, JW TI EVIDENCE THAT THE GUANOSINE SUBSTRATE OF THE TETRAHYMENA RIBOZYME IS BOUND IN THE ANTI CONFORMATION AND THAT N7 CONTRIBUTES TO BINDING SO BIOCHEMISTRY LA English DT Article ID CHEMICAL ALTERATIONS; MOLECULAR-STRUCTURE; PURINE NUCLEOSIDES; NUCLEIC-ACIDS; NUCLEOTIDES; ANALOGS; CRYSTAL; 8-BROMOADENOSINE; DEHYDROGENASE; GLYCOSYLATION AB The group I self-splicing introns are RNA enzymes that catalyze phosphodiester-exchange reactions. These ribozymes have a highly specific binding site for guanosine, a substrate for the first self-splicing reaction (Bass & Cech, 1984). The binding site for guanosine has been localized to a specific region of the ribozyme (Michel et al., 1989), but the conformation of the bound guanosine substrate remains unknown. Most analogs of guanosine with substituents at C8 have a preference for the syn conformation; however, some C8-substituted analogs have the potential to form a hydrogen bond between the C8 substituent and the 5'-hydroxyl that would stabilize the anti conformation; we have found that analogs with the potential to form such a hydrogen bond are more active substrates than those that cannot form such a hydrogen bond. These observations led us to test 8-5'-O-cycloguanosine, which is locked in the anti Conformation, and 8-(alpha-hydroxyisopropyl)guanosine, which is locked in the syn conformation; the former is active as a substrate, while the latter is inactive. These results strongly suggest that guanosine is bound to the ribozyme in the anti conformation and provide an additional constraint on structural models of this RNA enzyme. We have also examined a series of N7-substituted guanosine analogs; this position had previously been assumed to be unimportant for substrate binding since 7-methylguanosine is an excellent substrate. However, we have found that 7-deazaguanosine and 7-methyl-7-deazaguanosine are less active substrates than guanosine. We discuss several models for the role of N7 in guanosine binding. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 27 TC 11 Z9 11 U1 1 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 8 PY 1994 VL 33 IS 9 BP 2703 EP 2707 DI 10.1021/bi00175a045 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MZ697 UT WOS:A1994MZ69700045 PM 8117735 ER PT J AU DALLAS, SL PARKSNYDER, S MIYAZONO, K TWARDZIK, D MUNDY, GR BONEWALD, LF AF DALLAS, SL PARKSNYDER, S MIYAZONO, K TWARDZIK, D MUNDY, GR BONEWALD, LF TI CHARACTERIZATION AND AUTOREGULATION OF LATENT TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) COMPLEXES IN OSTEOBLAST-LIKE CELL-LINES - PRODUCTION OF A LATENT COMPLEX LACKING THE LATENT TGF-BETA-BINDING PROTEIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MOLECULAR-WEIGHT COMPLEX; MARFAN-SYNDROME; HUMAN-PLATELETS; BONE-FORMATION; MESSENGER-RNA; FACTOR-BETA-1; EXPRESSION; PRECURSOR; SEQUENCES; INVIVO AB We have previously shown that bone organ cultures produce large amounts of latent transforming growth factor beta (TGF beta), which lacks latent TGF beta-binding protein (LTBP). In this study we used the known osteoblastlike cell lines UMR-106, ROS 17/2.8, and MG63 as models to further examine latent TGF beta expression in bone. We found that the osteosarcoma cell line UMR-106 secreted latent TGF beta almost exclusively as a 100-kDa complex lacking LTBP. ROS 17/2.8 cells produced both the 100-kDa complex and also a 290-kDa complex containing the fibroblastic (190 kDa) form of LTBP. MG63 cells (like human foreskin fibroblasts) expressed almost exclusively the 290-kDa complex. To investigate the regulation of latent TGF beta complexes in bone cells we assessed the effects of TGF beta 1 treatment on expression of active and latent TGF beta. TGF beta 1 induced secretion of latent but not active TGF beta in all cell types examined. In human foreskin fibroblast cells, TGF beta 1 and LTBP mRNA were expressed concomitantly. In contrast, in osteosarcoma cell lines autoinduction of TGF beta 1 mRNA was associated with either a delayed increase or no change in LTBP mRNA In UMR-106 cells LTBP message was virtually undetectable. We postulate that the expression of different latent TGF beta forms by osteoblast-like cells may reflect their maturation states and that different latent TGF beta complexes may have different functions, for example as secretory forms or as matrix storage forms. C1 LUDWIG INST CANC RES,UPPSALA,SWEDEN. BRISTOL MYERS SQUIBB,SEATTLE,WA 98121. UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP DALLAS, SL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV ENDOCRINOL & METAB,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [DE-08569] NR 29 TC 135 Z9 139 U1 0 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 1994 VL 269 IS 9 BP 6815 EP 6822 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MZ503 UT WOS:A1994MZ50300088 PM 8120044 ER PT J AU TROPPMAIR, J BRUDER, JT MUNOZ, H LLOYD, PA KYRIAKIS, J BANERJEE, P AVRUCH, J RAPP, UR AF TROPPMAIR, J BRUDER, JT MUNOZ, H LLOYD, PA KYRIAKIS, J BANERJEE, P AVRUCH, J RAPP, UR TI MITOGEN-ACTIVATED PROTEIN-KINASE EXTRACELLULAR SIGNAL-REGULATED PROTEIN-KINASE ACTIVATION BY ONCOGENES, SERUM, AND 12-O-TETRADECANOYLPHORBOL-13-ACETATE REQUIRES RAF AND IS NECESSARY FOR TRANSFORMATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NIH 3T3 CELLS; MAP KINASE; XENOPUS OOCYTES; A-RAF; V-RAF; GROWTH; PHOSPHORYLATION; RECEPTOR; TRANSDUCTION; ONCOPROTEIN AB The protein kinase cascade Raf-MAPKK/MEK-MAPK/ERK connects protein tyrosine kinase receptors in the membrane with control of transcription factor activity in the nucleus. We have examined whether Raf is obligatory for activation of this cascade and whether this signaling pathway is relevant to transformation. By use of transient assays with epitope-tagged ERK-1 cDNA and a dominant inhibitory mutant of Raf-1 we found that serum and 12-O-tetradecanoylphorbol-13-acetate as well as representatives of three classes of oncogenes (protein tyrosine kinases abl/src, Ras, and protein serine/ threonine kinases mos/cot) were all Raf-dependent for stimulation of MAPK. All of the MAPK stimulating oncogenes were also activators of Raf kinase as judged by shift induction. It thus appears that there is little or no redundancy in pathways used by growth regulators for activation of MAPK/ERK. Furthermore, the ability to stimulate MAPK/ERK appears to be critical for transformation by oncogenic Raf-1 as ERK-1 and -2 synergized with v-raf in a focus induction assay on NIH3T3 cells and kinase dead mutants of ERK-2 were inhibitory. Raf/ERK synergism was also observed in transcriptional transactivation of the oncogene-response element in the polyoma enhancer. We conclude that this Raf signaling pathway, which connects to many upstream activators and downstream effecters, is essential for transformation by most oncogenes. C1 LAB VIRAL CARCINOGENESIS,VIRAL PATHOL SECT,FREDERICK,MD 21702. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02129. NR 54 TC 223 Z9 227 U1 2 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 1994 VL 269 IS 9 BP 7030 EP 7035 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MZ503 UT WOS:A1994MZ50300117 PM 8120067 ER PT J AU CLEELAND, CS GONIN, R HATFIELD, AK EDMONSON, JH BLUM, RH STEWART, JA PANDYA, KJ AF CLEELAND, CS GONIN, R HATFIELD, AK EDMONSON, JH BLUM, RH STEWART, JA PANDYA, KJ TI PAIN AND ITS TREATMENT IN OUTPATIENTS WITH METASTATIC CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CARE; PREVALENCE; BREAST; BLACK AB Background and Methods. Pain is often inadequately treated in patients with cancer. A total of 1308 outpatients with metastatic cancer from 54 treatment locations affiliated with the Eastern Cooperative Oncology Group rated the severity of their pain during the preceding week, as well as the degree of pain-related functional impairment and the degree of relief provided by analgesic drugs. Their physicians attributed the pain to various factors, described its treatment, and estimated the impact of pain on the patients' ability to function. We assessed the adequacy of prescribed analgesic drugs using guidelines developed by the World Health Organization, studied the factors that influenced whether analgesia was adequate, and determined the effects of inadequate analgesia on the patients' perception of pain relief and functional status. Results. Sixty-seven percent of the patients (871 of 1308) reported that they had had pain or had taken analgesic drugs daily during the week preceding the study, and 36 percent (475 of 1308) had pain severe enough to impair their ability to function. Forty-two percent of those with pain (250 of the 597 patients for whom we had complete information) were not given adequate analgesic therapy. Patients seen at centers that treated predominantly minorities were three times more likely than those treated elsewhere to have inadequate pain management. A discrepancy between patient and physician in judging the severity of the patient's pain was predictive of inadequate pain management (odds ratio, 2.3). Other factors that predicted inadequate pain management included pain that physicians did not attribute to cancer (odds ratio, 1.9), better performance status (odds ratio, 1.8), age of 70 years or older (odds ratio, 2.4), and female sex (odds ratio, 1.5). Patients with less adequate analgesia reported less pain relief and greater pain-related impairment of function. Conclusions. Despite published guidelines for pain management, many patients with cancer have considerable pain and receive inadequate analgesia. C1 UNIV WISCONSIN, CTR COMPREHENS CANC, MADISON, WI USA. DANA FARBER CANC INST, BOSTON, MA USA. CARLE CANC CTR, URBANA, IL USA. MAYO CLIN & MAYO FDN, ROCHESTER, MN USA. NYU MED CTR, NEW YORK, NY USA. UNIV ROCHESTER, CTR CANC, ROCHESTER, NY USA. RP CLEELAND, CS (reprint author), UNIV WISCONSIN, DEPT NEUROL, PAIN RES GRP, 1900 UNIV AVE, MADISON, WI 53705 USA. FU NCI NIH HHS [CA 21115, CA 26582, R01 CA026582] NR 33 TC 1189 Z9 1220 U1 4 U2 24 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 3 PY 1994 VL 330 IS 9 BP 592 EP 596 DI 10.1056/NEJM199403033300902 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MY573 UT WOS:A1994MY57300002 PM 7508092 ER PT J AU LIPTON, SA ROSENBERG, PA AF LIPTON, SA ROSENBERG, PA TI EXCITATORY AMINO-ACIDS AS A FINAL COMMON PATHWAY FOR NEUROLOGIC DISORDERS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID METHYL-D-ASPARTATE; RECEPTOR-MEDIATED NEUROTOXICITY; CALCIUM-CHANNEL ANTAGONISTS; CORTICAL CELL-CULTURE; SPINAL-CORD NEURONS; GLUTAMATE NEUROTOXICITY; NMDA-RECEPTOR; HIPPOCAMPAL-NEURONS; RAT-BRAIN; CEREBRAL-ISCHEMIA C1 CHILDRENS HOSP,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA. BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. RP LIPTON, SA (reprint author), CHILDRENS HOSP,HARVARD LONGWOOD NEUROL PROGRAM,300 LONGWOOD AVE,ENDERS BLDG,SUITE 361,BOSTON,MA 02115, USA. NR 90 TC 2131 Z9 2215 U1 7 U2 49 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 3 PY 1994 VL 330 IS 9 BP 613 EP 622 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA MY573 UT WOS:A1994MY57300007 PM 7905600 ER PT J AU RUSTGI, AK GRAEMECOOK, F AF RUSTGI, AK GRAEMECOOK, F TI 80-YEAR-OLD WOMAN WITH PERSISTENT GASTROINTESTINAL-BLEEDING AFTER RIGHT COLECTOMY - CHRONIC RADIATION ENTEROPATHY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID YERSINIA-ENTEROCOLITICA INFECTION; SURGICAL-MANAGEMENT; MEDICAL-MANAGEMENT; MALIGNANT-TUMORS; SMALL-INTESTINE; BOWEL-DISEASE; ENTERITIS; INJURY; TRACT; MANIFESTATIONS C1 HARVARD UNIV, SCH MED, BOSTON, MA USA. RP MASSACHUSETTS GEN HOSP, BOSTON, MA USA. NR 41 TC 1 Z9 1 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 3 PY 1994 VL 330 IS 9 BP 627 EP 632 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA MY573 UT WOS:A1994MY57300009 ER PT J AU EMANUEL, EJ BRETT, AS AF EMANUEL, EJ BRETT, AS TI MANAGED COMPETITION AND THE PATIENT-PHYSICIAN RELATIONSHIP - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID HEALTH-CARE; QUALITY C1 NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. RP EMANUEL, EJ (reprint author), DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 6 TC 1 Z9 1 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 3 PY 1994 VL 330 IS 9 BP 640 EP 641 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MY573 UT WOS:A1994MY57300018 ER PT J AU NATHAN, DM CROFFORD, OB LACHIN, JM AF NATHAN, DM CROFFORD, OB LACHIN, JM TI THE EFFECT OF INTENSIVE TREATMENT OF DIABETES-MELLITUS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 VANDERBILT UNIV, NASHVILLE, TN 37232 USA. GEORGE WASHINGTON UNIV, WASHINGTON, DC 20037 USA. RP NATHAN, DM (reprint author), MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 3 PY 1994 VL 330 IS 9 BP 642 EP 642 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA MY573 UT WOS:A1994MY57300022 ER PT J AU JAGOX, A CARR, DB PAYNE, R AF JAGOX, A CARR, DB PAYNE, R TI NEW CLINICAL-PRACTICE GUIDELINES FOR THE MANAGEMENT OF PAIN IN PATIENTS WITH CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article C1 MASSACHUSETTS GEN HOSP,CTR PAIN,DEPT ANESTHESIA,BOSTON,MA 02114. JOHNS HOPKINS UNIV,SCH NURSING,BALTIMORE,MD 21205. MD ANDERSON CANC CTR,HOUSTON,TX 77030. NR 17 TC 4 Z9 4 U1 0 U2 2 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 3 PY 1994 VL 330 IS 9 BP 651 EP 655 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MY573 UT WOS:A1994MY57300037 ER PT J AU KRIEG, M BILITZ, JM SRICHAI, MB REDMOND, RW AF KRIEG, M BILITZ, JM SRICHAI, MB REDMOND, RW TI EFFECTS OF STRUCTURAL MODIFICATIONS ON THE PHOTOSENSITIZING PROPERTIES OF DIALKYLCARBOCYANINE DYES IN HOMOGENEOUS AND HETEROGENEOUS SOLUTIONS SO BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS LA English DT Article DE HEAVY ATOM EFFECT; LIPOSOMES; PHOTOPHYSICS; PHOTOSENSITIZATION; SINGLET OXYGEN; CYANINE DYES ID SINGLET OXYGEN PRODUCTION; PHOTODYNAMIC-ACTION; MEROCYANINE 540; ACTION SPECTRA; CYANINE DYES; LIPOSOMES; PHOTOOXIDATION; MEMBRANES; MECHANISM; OXIDATION AB The photophysical characterization of structurally modified symmetric dialkylthiacarbocyanine dyes in homogeneous and biomimetic media is reported. The aim of the two specific structural modifications was to increase singlet oxygen production, hence enhancing the photosensitizing properties of these cyanine dyes. Specifically, (1) the sulfur was exchanged with selenium in order to enhance intersystem crossing via an internal heavy atom effect and (2) substituents of differing size were introduced into the meso-position of the polymethine chain to reduce photoisomerization. The result of incorporation of an internal heavy atom (selenium) into the structure of the dye yields the expected effect: this modification results in a 22-fold increase in the rate of intersystem crossing, but does not change the remaining competing deactivation rates of the first excited singlet state. As a consequence, singlet oxygen quantum yields increase from 0.001 to 0.014 in ethanol and from 0.006 to 0.08 in unilamellar liposomes. In the case of the meso-substituted thiacarbocyanine dyes, a significant reduction in photoisomerization is indeed observed. However, this modification drastically enhances internal conversion which then becomes the main deactivation pathway of the first excited singlet state. As a result, very small fluorescence and singlet oxygen quantum yields are obtained, e.g. 0.006 and 0.001, respectively, in ethanol. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RP KRIEG, M (reprint author), MED COLL WISCONSIN,MACC,FUND RES CTR,DEPT PEDIAT,MILWAUKEE,WI 53226, USA. FU NCI NIH HHS [NCI CA50733] NR 32 TC 31 Z9 32 U1 1 U2 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-4165 J9 BBA-GEN SUBJECTS JI Biochim. Biophys. Acta-Gen. Subj. PD MAR 2 PY 1994 VL 1199 IS 2 BP 149 EP 156 DI 10.1016/0304-4165(94)90110-4 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MZ858 UT WOS:A1994MZ85800007 PM 8123664 ER PT J AU COLDITZ, GA BREWER, TF BERKEY, CS WILSON, ME BURDICK, E FINEBERG, HV MOSTELLER, F AF COLDITZ, GA BREWER, TF BERKEY, CS WILSON, ME BURDICK, E FINEBERG, HV MOSTELLER, F TI EFFICACY OF BCG VACCINE IN THE PREVENTION OF TUBERCULOSIS - METAANALYSIS OF THE PUBLISHED LITERATURE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID IMMUNIZATION; INFECTION; OUTBREAK; INDIANS; TRIALS; LIFE AB Objective.-To quantify the efficacy of BCG vaccine against tuberculosis (TB). Data Sources.-MEDLINE with index terms BCG vaccine, tuberculosis, and human. Experts from the Centers for Disease Control and Prevention and the World Health Organization, among others, provided lists of all known studies. Study Selection.-A total of 1264 articles or abstracts were reviewed for details on BCG vaccination, concurrent vaccinated and unvaccinated groups, and SB outcome; 70 articles were reviewed in depth for method of vaccine allocation used to create comparable groups, equal surveillance and follow-up for recipient and concurrent control groups, and outcome measures of TB cases and/or deaths. Fourteen prospective trials and 12 case-control studies were included in the analysis. Data Extraction.-We recorded study design, age range of study population, number of patients enrolled, efficacy of vaccine, and items to assess the potential for bias in study design and diagnosis. At least two readers independently extracted data and evaluated validity. Data Synthesis.-The relative risk (RR) or odds ratio (OR) of TB provided the measure of vaccine efficacy that we analyzed. The protective effect was then computed by 1-RR or 1-OR. A random-effects model estimated a weighted average RR or OR from those provided by the trials or case-control studies. In the trials, the RR of TB was 0.49 (95% confidence interval [CI], 0.34 to 0.70) for vaccine recipients compared with nonrecipients (protective effect of 51%). In the case-control studies, the OR for TB was 0.50 (95% CI, 0.39 to 0.64), or a 50% protective effect. Seven trials reporting tuberculous deaths showed a protective effect from BCG vaccine of 71% (RR, 0.29; 95% CI, 0.16 to 0.53), and five studies reporting on meningitis showed a protective effect from BCG vaccine of 64% (OR, 0.36; 95% CI, 0.18 to 0.70). Geographic latitude of the study site and study validity score explained 66% of the heterogeneity among trials in a random-effects regression model. Conclusion.-On average, BCG vaccine significantly reduces the risk of TB by 50%. Protection is observed across many populations, study designs, and forms of TB. Age at vaccination did not enhance predictiveness of BCG efficacy. Protection against tuberculous death, meningitis, and disseminated disease is higher than for total TB cases, although this result may reflect reduced error in disease classification rather than greater BCG efficacy. C1 BRIGHAM & WOMENS HOSP,CHANNING LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. MT AUBURN HOSP,INFECT DIS UNIT,CAMBRIDGE,MA. RP COLDITZ, GA (reprint author), HARVARD UNIV,SCH PUBL HLTH,TECHNOL ASSESSMENT GRP,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 NR 70 TC 1201 Z9 1266 U1 18 U2 104 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 2 PY 1994 VL 271 IS 9 BP 698 EP 702 DI 10.1001/jama.271.9.698 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MX570 UT WOS:A1994MX57000032 PM 8309034 ER PT J AU NGUYEN, M WATANABE, H BUDSON, AE RICHIE, JP HAYES, DF FOLKMAN, J AF NGUYEN, M WATANABE, H BUDSON, AE RICHIE, JP HAYES, DF FOLKMAN, J TI ELEVATED LEVELS OF AN ANGIOGENIC PEPTIDE, BASIC FIBROBLAST GROWTH-FACTOR, IN THE URINE OF PATIENTS WITH A WIDE SPECTRUM OF CANCERS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID CELL CARCINOMA AB Background: Experimental evidence supports the hypothesis that the development of blood vessels is fundamental to the growth and metastasis of solid tumors. Elevated levels of the angiogenic peptide basic fibroblast growth factor (bFGF) have been significantly correlated with the status and extent of disease in bladder cancer. Purpose: We measured the bFGF levels in patients with cancer in organs other than the bladder to determine whether elevated levels accompany these cancers. Methods: Urine samples were collected from 950 patients having a wide variety of solid tumors, leukemia, or lymphoma and from a control group of 87 healthy volunteers and 198 patients with noncancer-related diseases, Levels of bFGF in samples prepared from the urine were measured using an enzyme bioassay. Results: Male control subjects had a median bFGF level of 151 pg/g and female control subjects a median of 237 pg/g, with a combined ''th percentile of 619 pg/g. An elevated level of bFGF was found in the urine of some of the patients with every type of tumor studied except cervical carcinoma. For example, patients with active local cancers had a median level of 312 pg/g. Those with active, metastatic cancers had a median level of 479 pg/g and a 90th percentile level of 14143 pg/g. After ''elevated'' was defined to mean higher than the 90th percentile level for controls, 31% of patients with local active and 47% of patients with metastatic active cancers showed elevated bFGF levels. Survival among cancer patients at the median follow-up time was 85%-88% for those with ''normal'' and 71%-72% for those with ''elevated'' urine bFGF levels. Implications: Our results suggest that bFGF in urine deserves further evaluation of its potential use as a monitor of therapy or as a predictor of outcome once a cancer has been diagnosed. C1 TAKEDA CHEM IND LTD,OSAKA 532,JAPAN. HARVARD UNIV,SCH MED,DEPT UROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BREAST EVALUAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG ANAT & CELLULAR BIOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP NGUYEN, M (reprint author), CHILDRENS HOSP MED CTR,HUNNEWELL 103,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [5T32CA0953506, CA3739509] NR 20 TC 410 Z9 413 U1 0 U2 2 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 2 PY 1994 VL 86 IS 5 BP 356 EP 361 DI 10.1093/jnci/86.5.356 PG 6 WC Oncology SC Oncology GA MX572 UT WOS:A1994MX57200013 PM 7508518 ER PT J AU ICHIMIYA, I ADAMS, JC KIMURA, RS AF ICHIMIYA, I ADAMS, JC KIMURA, RS TI IMMUNOLOCALIZATION OF NA+, K+-ATPASE, CA++-ATPASE, CALCIUM-BINDING PROTEINS, AND CARBONIC-ANHYDRASE IN THE GUINEA-PIG INNER-EAR SO ACTA OTO-LARYNGOLOGICA LA English DT Article DE IMMUNOHISTOCHEMISTRY; CALMODULIN; OSTEOPONTIN; SPIRAL LIGAMENT; ENDOLYMPHATIC SAC; GUINEA PIG ID CYTOCHEMICAL-LOCALIZATION; KIDNEY; NA+,K+-ATPASE; FIBROCYTES; TRANSPORT; NEURONS; STRIA AB The distribution of Na+, K+-ATPase, Ca++-ATPase, carbonic anhydrase, and calcium-binding proteins were investigated immunohistochemically in paraffin sections of guinea pig inner ears. Marginal cells of the stria vascularis, type II fibrocytes of the spiral ligament, and cells in supralimbal and suprastrial regions, were positive for Na+, K+-ATPase. Type I fibrocytes of the spiral ligament were positive for Ca++-ATPase, carbonic anhydrase, calmodulin and osteopontin. In the vestibular system, dark cells were positive for Na+, K+-ATPase. However, these cells and subepithelial fibrocytes were negative for Ca+-ATPase, carbonic anhydrase, and the calcium-binding proteins. In the endolymphatic sac, epithelial cells in intermediate and distal portions were positive for Na+, K+-ATPase, but the reaction was less than that in the stria. The same endolymphatic sac cells that were positive for Na+, K+-ATPase were also positive for Ca++-ATPase and calcium-binding proteins, but negative for carbonic anhydrase. The presence of Ca++-ATPase and calcium-binding proteins in the type I fibrocytes of the spiral ligament suggests that these cells are involved in mediating Ca++ regulation. Lower levels of Na+, K+-ATPase and the co-existence of Ca++-ATPase and calcium-binding proteins in the epithelial cells of the endolymphatic sac indicate that these cells have a distinctive role in ion transport that is different from that of the cells of the stria vascularis and vestibular dark cells. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. FU NIDCD NIH HHS [NIDCD R01 DC00073] NR 25 TC 83 Z9 88 U1 0 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6489 J9 ACTA OTO-LARYNGOL JI Acta Oto-Laryngol. PD MAR PY 1994 VL 114 IS 2 BP 167 EP 176 DI 10.3109/00016489409126037 PG 10 WC Otorhinolaryngology SC Otorhinolaryngology GA ND135 UT WOS:A1994ND13500010 PM 8203199 ER PT J AU SMALL, GW ROSENTHAL, M TOURTELLOTTE, WW AF SMALL, GW ROSENTHAL, M TOURTELLOTTE, WW TI CENTRAL-NERVOUS-SYSTEM IGG SYNTHESIS RATES IN ALZHEIMER-DISEASE - POSSIBLE DIFFERENCES IN EARLY-ONSET AND LATE-ONSET SUBGROUPS SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article DE IGG SYNTHESIS RATE; ALZHEIMER DISEASE; AGE AT ONSET ID MULTI-INFARCT DEMENTIA; BLOOD-BRAIN-BARRIER; CEREBROSPINAL-FLUID; OLIGOCLONAL BANDS; ALBUMIN; IMMUNOGLOBULIN; SERUM; AUTOANTIBODIES; ANTIBODIES; SCLEROSIS AB Central nervous system IgG synthesis rates were determined for 51 patients with autopsy-confirmed Alzheimer disease and 23 age-matched controls. Rates were no different between patients and controls when overall groups were compared. Age-at-dementia-onset data were available on 37 patients. Comparisons of 11 early-onset (<65 years of age) patients with 26 late-onset patients revealed significantly increased intrathecal IgG synthesis rates for the late-onset group. These results suggest that IgG synthesis may be a contributing pathogenic factor in a subgroup of patients with late-onset Alzheimer disease. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA USA. VET AFFAIRS MED CTR, CTR GERIATR RES EDUC & CLIN, SEPULVEDA, CA USA. FU NIA NIH HHS [NIA AG10123]; NIMH NIH HHS [NIMH 1R29 MH46424] NR 42 TC 8 Z9 8 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PD SPR PY 1994 VL 8 IS 1 BP 29 EP 37 DI 10.1097/00002093-199408010-00006 PG 9 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA MZ515 UT WOS:A1994MZ51500005 PM 8185879 ER PT J AU FREEMAN, GL HARRIS, MM GHIDONI, JJ PAGE, A CANTU, TL YOUNG, E AF FREEMAN, GL HARRIS, MM GHIDONI, JJ PAGE, A CANTU, TL YOUNG, E TI ANALYSIS OF MYOCARDIAL RESPONSE TO SIGNIFICANT WEIGHT-LOSS IN OBESE RATS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE CARDIAC MASS; MYOCARDIAL REGRESSION; OBESITY; ENERGY RESTRICTION ID SEMISTARVATION DIETS; LEFT-VENTRICLE; REDUCTION; HYPERTROPHY; CAPTOPRIL; SUDDEN; DEATH AB We evaluated cardiac response to weight loss induced by a very-low-energy (VLE) diet similar to commercially available protein-sparing diets. Such diets have been implicated in sudden death, and whether organ and tissue responses to them are untoward is not known. Rapid weight loss was induced in rats with weights ranging from obese to normal, and cardiac mass and myocardial histomorphometry were assessed. Over 3 wk body weight dropped from 544 +/- 12 to 417 +/- 21 g (P < 0.001). Heart weight was less in the VLE group than in obese controls (1246 +/- 115 vs 1625 +/- 179 mg, P < 0.001), as were the weights of the left ventricle (805 +/- 81 vs 1061 +/- 134 mg, P < 0.001) and right ventricle (198 +/- 27 vs 265 +/- 40 mg, P < 0.002). Reduction in heart weight was commensurate with loss of body weight (r = 0.89). Myocyte cross-sectional area was reduced in the VLE group (452.6 +/- 108.6 to 331.8 +/- 41.5 mu m(2), P < 0.05), with no structural abnormalities. We conclude that weight loss in the weight range studied is accompanied by proportional reduction in cardiac mass and myocyte size. Myocardial regression is not accompanied by myocyte dropout or edema, and likely represents a simple adaptation to reduced body size. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP FREEMAN, GL (reprint author), UNIV TEXAS,HLTH SCI CTR,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [5 RO1 DK35039-03] NR 29 TC 10 Z9 10 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD MAR PY 1994 VL 59 IS 3 BP 566 EP 571 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MZ669 UT WOS:A1994MZ66900004 PM 8116532 ER PT J AU WEINSTOCK, R LEONG, GB SILVA, JA AF WEINSTOCK, R LEONG, GB SILVA, JA TI COMPETENCE TO TERMINATE LIFE-SUSTAINING CARE - ETHICAL AND LEGAL CONSIDERATIONS SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article ID ADVANCE DIRECTIVES; HEALTH-CARE; CONSENT; DILEMMA; ORDERS AB Recent federal legislation requires that patients be provided with information about advance directives for terminating health care. Although the mental status of patients executing these directives is crucial, and states require competence to make such a directive, no clear criteria or mandated procedures exist to evaluate the patient's competence to make these decisions. No explicit criteria exist for competence of surrogates either. The authors propose guidelines for such competence determinations. They also consider psychiatric factors surrounding decisions to terminate life-sustaining care. Such decisions have particular importance for geriatric patients. Further research is needed to guide both physicians and policymakers in determining the frequency and types of psychiatric problems in such patients and resultant ''irrational'' decisions to die. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV,SAN ANTONIO,TX 78284. RP WEINSTOCK, R (reprint author), W LOS ANGELES VET ADM ADM CTR,PSYCHIAT SERV,116AC,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 36 TC 4 Z9 4 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1064-7481 J9 AM J GERIAT PSYCHIAT JI Am. J. Geriatr. Psychiatr. PD SPR PY 1994 VL 2 IS 2 BP 95 EP 106 PG 12 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA NF320 UT WOS:A1994NF32000002 PM 11652962 ER PT J AU ROYALL, DR MAHURIN, R AF ROYALL, DR MAHURIN, R TI QUALITATIVE DEMENTIA TYPES SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Letter C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1064-7481 J9 AM J GERIAT PSYCHIAT JI Am. J. Geriatr. Psychiatr. PD SPR PY 1994 VL 2 IS 2 BP 178 EP 179 PG 2 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA NF320 UT WOS:A1994NF32000015 ER PT J AU RUMBAUT, RE KROLL, MH GYORKEY, F SCHAFER, AI AF RUMBAUT, RE KROLL, MH GYORKEY, F SCHAFER, AI TI ACQUIRED PLATELET STORAGE POOL DEFICIENCY DUE TO SEVERE VALVULAR DISEASE CORRECTED BY PROSTHETIC VALVE-REPLACEMENT SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Letter ID AGGREGATION C1 BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030. HOUSTON VA MED CTR,HOUSTON,TX. RP RUMBAUT, RE (reprint author), BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030, USA. NR 4 TC 3 Z9 3 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD MAR PY 1994 VL 45 IS 3 BP 272 EP 273 DI 10.1002/ajh.2830450322 PG 2 WC Hematology SC Hematology GA MT449 UT WOS:A1994MT44900021 PM 8296805 ER PT J AU GARCIA, MJ LARAIA, PJ BOUCHER, CA AF GARCIA, MJ LARAIA, PJ BOUCHER, CA TI EXERCISE TL-201 IMAGING CHARACTERISTICS AND PROGNOSTIC VALUE IN PATIENTS WITH LEFT-BUNDLE-BRANCH BLOCK SO AMERICAN JOURNAL OF NONINVASIVE CARDIOLOGY LA English DT Article DE LEFT BUNDLE BRANCH BLOCK; THALLIUM EXERCISE TESTING; CORONARY DISEASE AB To determine the utility of exercise thallium-201 testing in patients with left bundle branch block (LBBB), we studied 61 consecutive patients referred to our laboratory from 1986 to 1989. We divided the patients into two groups for further analysis. Those with known coronary artery disease (CAD), documented either by cardiac catheterization or previous myocardial infarction, formed group I. Patients with no evidence of CAD formed grup II. Thirty-three of the 28 patients in group I had an abnormal thallium scan (87%) versus 7 of the 23 in group II (< 0.001). Although the number and location of the perfusion defects was similar in the patients with abnormal scans in either group, the proportion of severe defects was significantly higher in the patients in group I (21 vs. 5%) (p < 0.05), as well as the proportion of patients with increased thallium lung uptake (63 vs. 13%) (p < 0.001) and left ventricular (LV) cavity dilation (69 vs. 9%) (p < 0.001). We conclude that thallium exercise testing is useful evaluating patients with LBBB. Patients with 'isolated' LBBB have a low incidence of thallium perfusion abnormalities when compared to those with known CAD. The relative absence of severe perfusion defects and scan markers of exercise-induced LV dysfunction in this group correlated with a good clinical outcome. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0258-4425 J9 AM J NONINVAS CARD JI Am. J. Noninvas. Cardiol. PD MAR-APR PY 1994 VL 8 IS 2 BP 58 EP 62 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PA893 UT WOS:A1994PA89300002 ER PT J AU HUGHES, GB MOSCICKI, R BARNA, BP MARTIN, JES AF HUGHES, GB MOSCICKI, R BARNA, BP MARTIN, JES TI LABORATORY DIAGNOSIS OF IMMUNE INNER-EAR DISEASE SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article ID SENSORINEURAL HEARING-LOSS AB Immune inner ear disease is a relatively new and distinct clinical entity that produces unexplained, rapidly progressive, bilateral sensorineural hearing loss. The diagnosis is based on clinical manifestations, positive immune laboratory testing, and beneficial response to a trial of corticosteroids. Immune laboratory tests are used to confirm a presumptive clinical diagnosis. The two tests most commonly used are the lymphocyte transformation test and Western blot immune assay. The rationale behind these tests is presented, and the role they play in laboratory diagnosis of immune inner ear disease is discussed. C1 MASSACHUSETTS GEN HOSP,DEPT CLIN IMMUNOL & ALLERGY,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. CLEVELAND CLIN EDUC FDN,DEPT OTOLARYNGOL & COMMUNICAT DISORDERS,CLEVELAND,OH 44106. CLEVELAND CLIN EDUC FDN,DEPT CLIN PATHOL,CLEVELAND,OH 44106. NR 11 TC 33 Z9 33 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD MAR PY 1994 VL 15 IS 2 BP 198 EP 202 PG 5 WC Otorhinolaryngology SC Otorhinolaryngology GA MZ141 UT WOS:A1994MZ14100013 PM 8172301 ER PT J AU BUSABA, NY REBEIZ, EE SALMAN, SD THORNTON, AR WEST, C AF BUSABA, NY REBEIZ, EE SALMAN, SD THORNTON, AR WEST, C TI SIGNIFICANCE OF FALSE-POSITIVE AUDITORY BRAIN-STEM RESPONSE - A CLINICAL-STUDY SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article ID STEM RESPONSE; BELLS-PALSY; MULTIPLE-SCLEROSIS; NERVE; POTENTIALS; DISEASE AB Auditory brainstem response (ABR) is a good screening test for cerebellopontine angle (CPA) tumors and other retrocochlear diseases. The pathologic correlates of many cases with positive ABR remain unknown. A two-staged clinical study was performed to help us understand the significance of a false-positive ABR. In the first stage, data from 66 patients with abnormal ABR were reviewed. Nineteen patients had identifiable causes for the ABR abnormality, whereas 47 patients had no lesions identified. In the second phase of the study 21 of the 47 patients were re-evaluated with a minimum follow-up period of 1 year. A detailed interval history was obtained, and the work-up, including imaging studies, was repeated in an attempt to reach a diagnosis. One patient was found to have a CPA tumor, but for nine patients a definite final diagnosis could not be determined. The implications of abnormal ABR and normal initial imaging study are discussed, and a plan for the work-up of these patients is suggested. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. TUFTS UNIV NEW ENGLAND MED CTR,DEPT OTOLARYNGOL,BOSTON,MA 02111. RP BUSABA, NY (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114, USA. NR 18 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD MAR PY 1994 VL 15 IS 2 BP 233 EP 236 PG 4 WC Otorhinolaryngology SC Otorhinolaryngology GA MZ141 UT WOS:A1994MZ14100020 PM 8172308 ER PT J AU HYMAN, BT ELVHAGE, TE REITER, J AF HYMAN, BT ELVHAGE, TE REITER, J TI EXTRACELLULAR SIGNAL-REGULATED KINASES - LOCALIZATION OF PROTEIN AND MESSENGER-RNA IN THE HUMAN HIPPOCAMPAL-FORMATION IN ALZHEIMERS-DISEASE SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID PAIRED HELICAL FILAMENTS; TAU-PROTEIN; TYROSINE PHOSPHORYLATION; DEPENDENT KINASE; MAP KINASES; BRAIN; ACTIVATION; SEQUENCE; TANGLES; INSULIN AB MAP kinases (MAPK) are a family of serine/ threonine (Ser/Thr) kinases that link cell surface signals to changes in enzyme activity and gene expression. They are the products of the newly described gene family referred to as extracellular signal regulated kinases (ERKs). Moreover, MAPKs phosphorylate tau in vitro at Ser/Thr Proline sites, generating a multiply phosphorylated tate protein that is similar to the hyperphosphorylated tate found in Alzheimer neurofibrillary tangles (NFTs). We studied MAPK immunoreactivity and in situ hybridization patterns of the two major genes that comprise MAPK activity, ERK1 and ERK2, ill the human hippocampal formation. Our goal was to determine whether the pattern of ERK expression is consistent with the hypothesis that MAPKs contribute to NET formation. ERK1 mRNA is present in small amounts and confined primarily to dentate gyrus granule cells. ERK2 mRNA, by contrast, gives a much stronger hybridization signal and is present in dentate gyrus granule cells and pyramidal cells throughout all hippocampal subfields and adjacent temporal neocortex. Quantitative measures of ERK2 mRNA reveal that NFT-bearing neurons contain approximately 15% less ERK2 mRNA than nearest neighbors that do not contain NFT. NFT-bearing neurons contain approximately 25% less polyA mRNA, suggesting a relative preservation of ERK2 mRNA even in metabolically compromised cells. MAPK immunoreactivity (which represents both ERK1 and ERK2) is seen in neuronal soma, dendrites, axons, and in reactive astrocytes. lit Alzheimer's disease, neurons that contain NFTs are also MAPK immunoreactive, but neurons that contain the highest amounts of MAPK immunoreactivity are not necessarily vulnerable for NFT. MAPK immunoreactivity is present in the same neurons as NFT and in the same subcellular compartments as tau, supporting a role for MAPKs in tau phosphorylation in Alzheimer's disease. However, the presence of ERK immunoreactivity is not sufficient to predispose neurons to NFT formation. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP HYMAN, BT (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,WARREN 408,BOSTON,MA 02114, USA. FU NIA NIH HHS [AG08487] NR 38 TC 80 Z9 82 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD MAR PY 1994 VL 144 IS 3 BP 565 EP 572 PG 8 WC Pathology SC Pathology GA NA169 UT WOS:A1994NA16900018 PM 8129042 ER PT J AU BONADONNA, RC GROOP, LC SIMONSON, DC DEFRONZO, RA AF BONADONNA, RC GROOP, LC SIMONSON, DC DEFRONZO, RA TI FREE FATTY-ACID AND GLUCOSE-METABOLISM IN HUMAN AGING - EVIDENCE FOR OPERATION OF THE RANDLE CYCLE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE INSULIN; LIPID METABOLISM; SUBSTRATE COMPETITION ID INSULIN RESISTANCE; ELDERLY SUBJECTS; TURNOVER; OXIDATION; PLASMA; MEN; OBESITY; AGE; SENSITIVITY AB Free fatty acid and glucose metabolism in human aging: evidence for operation of the Randle cycle. Am. J. Physiol. 266 (Endocrinol. Metab. 29): E501-E509, 1994. - We assessed insulin effects on plasma free fatty acid (FFA) and glucose metabolism in seven elderly (71 +/- 2 yr) and in seven younger (21 +/- 1 yr) subjects matched for body weight and body mass index but not for percent body fat (32.4 +/- 3.8% in elderly vs. 20.4 +/- 3.5% in young, P < 0.05), by performing sequential euglycemic clamps at five insulin doses (0.6, 1.5, 3, 6, and 15 pmol.min(-1).kg(-1)) in combination with indirect calorimetry and [1-C-14]palmitate plus [3-H-3]glucose infusion. At baseline, plasma FFA concentration, turnover and oxidation, and total lipid oxidation were all increased in the elderly (897 +/- 107 vs. 412 +/- 50 mu mol/l and 11.2 +/- 1.4 vs. 5.14 +/- 0.86, 3.45 +/- 0.65 vs. 1.37 +/- 0.25, and 4.63 +/- 0.72 vs. 3.01 +/- 0.33 mu mol.min(-1).kg(-1) lean body mass, P < 0.05 for all comparisons), whereas glucose turnover was similar as a result of decreased glucose oxidation (8.2 +/- 1.4 vs. 13 +/- 1.9 mu mol.min(-1).kg(-1) lean body mass, P < 0.05) and increased glucose storage (6.6 +/- 1.4 vs. 1.7 +/- 1.3 mmol.min(-1).kg(-1) lean body mass, P < 0.05). At all insulin infusions, plasma FFA concentration, turnover and oxidation, and total lipid oxidation were higher in the elderly than in the younger group (P < 0.05). However, if normalized per fat mass, all FFA and lipid metabolic fluxes, both in the postabsorptive state and during hyperinsulinemia, were comparable in the two groups. Insulin-mediated inhibition of hepatic glucose production and stimulation of glucose storage were similar in the two groups, but glucose oxidation was lower in the elderly than in the young at all insulin concentrations tested (P < 0.05). Plasma FFA turnover rate and total lipid oxidation were negatively correlated with whole body glucose uptake and oxidation in the two groups (P < 0.05-0.01). Thus, in human aging, abnormalities in insulin regulation of FFA/lipid metabolism may be secondary to increased fat mass and substrate competition between fat and glucose and may play a role in determining a reduction in insulin-mediated glucose oxidation. C1 UNIV PISA,CNR,INST CLIN PHYSIOL,METAB UNIT,I-156100 PISA,ITALY. UNIV HELSINKI,DEPT MED 4,SF-00170 HELSINKI,FINLAND. UNIV TEXAS,HLTH SCI CTR,DIV DIABET,SAN ANTONIO,TX 78284. AUDIE L MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX 78284. FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK-24092] NR 39 TC 64 Z9 64 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1994 VL 266 IS 3 BP E501 EP E509 PN 1 PG 9 WC Physiology SC Physiology GA NF859 UT WOS:A1994NF85900058 PM 8166272 ER PT J AU KLEYMAN, TR ERNST, SA COUPAYEGERARD, B AF KLEYMAN, TR ERNST, SA COUPAYEGERARD, B TI ARGININE-VASOPRESSIN AND FORSKOLIN REGULATE APICAL CELL-SURFACE EXPRESSION OF EPITHELIAL NA+ CHANNELS IN A6 CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE AMILORIDE; ANTIDIURETIC HORMONE; ANTI-SODIUM CHANNEL ANTIBODY; BREFELDIN A ID BREFELDIN-A; SODIUM-TRANSPORT; HORMONAL-CONTROL; URINARY-BLADDER; LINE A6; ALDOSTERONE; MEMBRANE; PROTEINS; PHOSPHORYLATION; LOCALIZATION AB Both arginine vasopressin (AVP) and forskolin regulate vectorial Na+ transport across high-resistance epithelia by increasing the Na+ conductance of the apical membrane mediated by amiloride-sensitive Na+ channels. Pretreatment of A6 cells with brefeldin A partially inhibited the increase in Na+ transport in response to forskolin, suggesting recruitment of Na+ channels from an intracellular pool. The activation of Cl- secretion was not affected. Apical cell surface expression of Na+ channels was examined following activation of transepithelial Na+ transport across the epithelial cell line A6 by AVP or forskolin. Apical cell surface radioiodinated Na+ channels were immunoprecipitated to quantify the biochemical pool of Na+ channels at the apical plasma membrane and to determine whether an increment in the biochemical pool of Naf channels expressed at the apical cell surface is a potential mechanism by which AVP and forskolin increase apical membrane Na+ conductance. The activation of Na+ transport across A6 cells by AVP was accompanied by a significant increase in the biochemical pool of Na+ channels at the apical plasma membrane within 5 min after addition of hormone, which was sustained for at least 30 min. The increase in apical cell surface expression of Na+ channels was also observed 30 min after application of forskolin. No changes in the oligomeric subunit composition of the channel were noted. Brefeldin A inhibited the forskolin-stimulated increase in apical cell surface expression of Na+ channels. These results suggest that AVP and forskolin regulate Na+ transport, in part, via rapid recruitment of Na+ channels to the cell surface, perhaps from a pool of channels in the subapical cytoplasm. C1 UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. UNIV MICHIGAN,DEPT ANAT & CELL BIOL,ANN ARBOR,MI 48109. RP KLEYMAN, TR (reprint author), DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. FU NIDDK NIH HHS [DK-34933] NR 35 TC 74 Z9 74 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1994 VL 266 IS 3 BP F506 EP F511 PN 2 PG 6 WC Physiology SC Physiology GA NF861 UT WOS:A1994NF86100127 PM 8160801 ER PT J AU PORSA, E FREEMAN, GL HERLIHY, JT AF PORSA, E FREEMAN, GL HERLIHY, JT TI TACHYCARDIA HEART-FAILURE ALTERS RABBIT AORTIC SMOOTH-MUSCLE RESPONSIVENESS TO ANGIOTENSIN-II SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE POTASSIUM DEPOLARIZATION; CALCIUM; ISOPROTERENOL; PHENYLEPHRINE; VASCULAR SMOOTH MUSCLE ID CHRONIC SUPRAVENTRICULAR TACHYCARDIA; INOSITOL TRISPHOSPHATE; NOREPINEPHRINE; RECEPTORS; VASOCONSTRICTION; CALCIUM; CELLS; DOGS AB The effects of heart failure on the responsiveness of aortic smooth muscle tissue to various vasoactive agents were examined. Heart failure was induced in rabbits by sustained rapid ventricular pacing (400 beats/min) for 6-7 wk. After the rabbits were killed, strips of thoracic aorta were prepared and mounted in tissue baths. Responsiveness of these aortic strips to potassium depolarization and cumulative additions of vasoactive agents was determined. Aortic strips from control and tachycardia heart failure (THF) rabbits developed similar maximum forces to stimulation by potassium depolarization (0.77 +/- 0.08 vs. 0.96 +/- 0.16 kg/cm(2)), calcium chloride (0.71 +/- 0.09 vs. 0.88 +/- 0.06 kg/cm(2)), and phenylephrine (0.90 +/- 0.08 vs. 1.14 +/- 0.09 kg/cm(2)). The maximum relaxation to isoproterenol was also unaffected by THF (0.08 +/- 0.02 vs. 0.07 +/- 0.01 kg/cm(2)). In contrast, the maximum response of aortic strips from THF rabbits to angiotensin II was significantly lower than control (0.37 +/- 0.07 vs. 0.069 +/- 0.09 kg/cm(2)). With regard to aortic smooth muscle sensitivity, no differences in the concentrations at which 50% of the maximal response is achieved (EC(50)) were observed between THF and control strips for calcium chloride (0.10 +/- 0.01 vs. 0.16 +/- 0.04 mM), isoproterenol (51.5 +/- 13.5 vs. 51.0 +/- 5.4 nM), and phenylephrine (65.2 +/- 12.3 vs. 92.5 +/- 18.0 nM). However, THF was associated with a significant increase in the EC(50) value for angiotensin II response (2.03 +/- 0.25 vs. 0.58 +/- 0.05 nM). These results demonstrate that THF is associated with a specific and significant reduction in the sensitivity and maximal responsiveness of aortic smooth muscle to angiotensin II. THF-induced alterations in the characteristics of angiotensin II receptors may be responsible for these changes. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 30 TC 5 Z9 5 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1994 VL 266 IS 3 BP H1228 EP H1232 PN 2 PG 5 WC Physiology SC Physiology GA NF861 UT WOS:A1994NF86100049 ER PT J AU HITZIG, BM PERNG, WC BURT, T OKUNIEFF, P JOHNSON, DC AF HITZIG, BM PERNG, WC BURT, T OKUNIEFF, P JOHNSON, DC TI H-1-NMR MEASUREMENT OF FRACTIONAL DISSOCIATION OF IMIDAZOLE IN INTACT ANIMALS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ACID-BASE REGULATION; ALPHASTAT REGULATION; CARNOSINE; NEWT; INTRACELLULAR PH MEASUREMENT; P-31 NUCLEAR MAGNETIC RESONANCE; WHITE SKELETAL MUSCLE ID MAGNETIC-RESONANCE; ALPHASTAT HYPOTHESIS; TEMPERATURE; PH; CARNOSINE; MUSCLE AB The alphastat hypothesis states that intracellular acid-base status is regulated to maintain constancy of the fractional dissociation of intracellular protein and enzyme imidazole-histidine (alpha-imidazole). A major drawback of this theory has been the lack of a means to directly measure alpha-imidazole in intact animals. We developed a method for directly measuring alpha-imidazole in intact unanesthetized animals using H-1-nuclear magnetic resonance spectroscopy (NMR). We measured carnosine a-imidazole of white skeletal muscle from intact unanesthetized newts at three body temperatures (10, 20, and 30 degrees C). alpha-Imidazole remained constant, similar to 0.56, with alterations in body temperature, whereas intracellular pH (pH(i)) changed significantly (-0.015 U/degrees C), affirming the validity of the imidazole alphastat hypothesis for this tissue. This method was also used to determine the pK values of the imidazole moiety of carnosine and the imidazole moiety alone over a temperature (T) range 4-40 degrees C. The pK values of carnosine differed from those of imidazole, but the Delta pK/Delta T was the same. pH(i) was also determined using P-31- NMR and found to be the same as that calculated from carnosine alpha-imidazole values. Therefore Pi and carnosine share a similar pH(i) environment. We describe a novel technique to directly measure alpha-imidazole in intact tissue. C1 HARVARD UNIV,SCH MED,INST BIOMECH,DEPT PHYSIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED & RADIAT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. RP HITZIG, BM (reprint author), MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. NR 23 TC 17 Z9 17 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1994 VL 266 IS 3 BP R1008 EP R1015 PN 2 PG 8 WC Physiology SC Physiology GA NF861 UT WOS:A1994NF86100100 ER PT J AU OOKHTENS, M MITTUR, AV ERHART, NA AF OOKHTENS, M MITTUR, AV ERHART, NA TI CHANGES IN PLASMA GLUTATHIONE CONCENTRATIONS, TURNOVER, AND DISPOSAL IN DEVELOPING RATS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GLUTATHIONE; PLASMA; TURNOVER; KINETICS; DEVELOPMENT; AGING ID HEPATIC GLUTATHIONE; EFFLUX; LIVER; HEPATOCYTES; HOMEOSTASIS; INHIBITION; MECHANISM; STRESS; STATE; FORMS AB We have previously shown that sinusoidal reduced glutathione (GSH) efflux declines during development because of a declining maximum transport rate [Am. J. Physiol. 261 (Gastrointest. Liver Physiol. 24): G648-G656, 1991]. Because rat liver serves as the principal source of plasma GSH, we studied the response of plasma GSH to this declining inflow from liver. In immature (28- to 42-day) and mature (90- to 151-day) rats we injected tracer boluses of [S-35]GSH intravenously and collected arterial samples over a 0.75- to 8-mi:n interval while plasma GSH pool remained at steady state!. Concentrations and radioactivities of GSH, oxidized glutathione (GSSG), cysteine (CYSH), cystine (CYSS), and cysteine-glutathione disulfides (CYSSG) and the radioactivities of proteins were measured in plasma. Our results show the following changes in plasma concentrations (mu M): decreases in unbound (free) GSH (26.0 +/- 2.1 to 12.4 +/- 0.98; P < 0.001), total unbound GSH equivalents GSH + 2GSSG (29.1 +/- 2.1 to 15.3 +/- 1.2; P < 0.001), total reducible (unbound + bound) GSH (39.3 +/- 2.2 to 28.9 +/- 2.6; P < 0.025!, and free CYSH (57.6 +/- 8.5 to 29.9 +/- 4.0; P < 0.05); no changes in GSSG (1.57 +/- 0.27 vs. 1.47 +/- 0.41), CYSS (36.7 +/- 12 vs;. 43.4 +/- 17), and total unbound CYSH equivalents CYSH - 2CYSS (131 +/- 15 vs. 117 +/- 18); increases in total reducible (unbound + bound) CYSH (158 +/- 8.1 to 203 +/- 24; P < 0.05) and CYSSG (1.80 +/- 0.42 to 4.94 +/- 1.4 in IJ,M GSH equivalents; P < 0.05). A concurrent decline occurred in irreversible disposal rate (IDR) of plasma GSH from 38.5 +/- 4.9 to 16.4 +/- 1.4 nmol.min(-1).ml(-1) (P < 0.001) as determined by compartmental analysis of tracer data. This 57% decrease in IDR parallels a decrease of 53% in the inflow of GSH estimated by perfused livers (17.0 to 8.0 nmol.min(-1).ml plasma(-1)). However, perfused liver estimates do not match >44-49% of plasma IDR. Thus perfused liver appears to underestimate the true rate of sinusoidal GSH efflux taking place in vivo. Some earlier arteriovenous data and our present portal vein-to-hepatic vein difference measurements appear to corroborate this view. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES OUTPATIENT CLIN,RES SERV,LOS ANGELES,CA 90012. RP OOKHTENS, M (reprint author), UNIV SO CALIF,SCH MED,DEPT MED,DIV GASTROINTESTINAL & LIVER DIS,GI & LIVER RES L,LOS ANGELES,CA 90033, USA. FU NIA NIH HHS [AG-074667] NR 28 TC 22 Z9 22 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1994 VL 266 IS 3 BP R979 EP R988 PN 2 PG 10 WC Physiology SC Physiology GA NF861 UT WOS:A1994NF86100097 PM 8160895 ER PT J AU GREEN, MF HUGDAHL, K MITCHELL, S AF GREEN, MF HUGDAHL, K MITCHELL, S TI DICHOTIC-LISTENING DURING AUDITORY HALLUCINATIONS IN PATIENTS WITH SCHIZOPHRENIA SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID ACUTE PSYCHOTIC ILLNESS; CEREBRAL LATERALITY; FORCED-ATTENTION; TEMPORAL-LOBE; CHILDREN; RELIABILITY AB Objective: Auditory hallucinations are a serious problem for a large subgroup of psychotic patients who do not respond optimally to neuroleptic medication. It has been hypothesized that hearing imaginary voices involves the same physiological processes as those involved in hearing real voices, but this hypothesis has not been conclusively confirmed. Method: In this study a consonant-vowel version of the Dichotic Listening Test was used to assess the functional integration of the left hemisphere in hallucinating and nonhallucinating psychotic patients. The test was administered under three conditions: a nonforced attention condition, a condition in which attention was forced to the left ear, and one in which attention was forced to the right ear. Results: The nonhallucinating patients showed the normal right ear advantage, which indicates a left hemisphere superiority in the processing of linguistic stimuli. In contrast, the hallucinating patients showed no ear advantage, Neither group was able to modify its performance when instructed to attend to either the left or the right ear. A subgroup of patients was tested in both hallucinating and nonhallucinating states, but the ear asymmetry was not noticeably different between these states. Conclusions: The results suggest that auditory hallucinations are associated with abnormalities in left hemisphere functioning and that these abnormalities might not be limited to the time of the auditory hallucinations. It is hypothesized that a relatively enduring left hemisphere abnormality may leave some patients at risk for auditory hallucinations. C1 W LOS ANGELES VA MED CTR, LOS ANGELES, CA USA. UNIV BERGEN, DEPT MED & BIOL PSYCHOL, BERGEN, NORWAY. RP GREEN, MF (reprint author), UNIV CALIF LOS ANGELES, RES CTR, DEPT PSYCHIAT & BIOBEHAV SCI, BOX 6022, CAMARILLO, CA 93011 USA. FU NIMH NIH HHS [NIMH MH-4392, NIMH MH-30911] NR 28 TC 90 Z9 92 U1 0 U2 3 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAR PY 1994 VL 151 IS 3 BP 357 EP 362 PG 6 WC Psychiatry SC Psychiatry GA MY317 UT WOS:A1994MY31700006 PM 8109643 ER PT J AU BARSKY, AJ WOOL, C BARNETT, MC CLEARY, PD AF BARSKY, AJ WOOL, C BARNETT, MC CLEARY, PD TI HISTORIES OF CHILDHOOD TRAUMA IN ADULT HYPOCHONDRIACAL PATIENTS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID CHRONIC PELVIC PAIN; MEDICAL OUTPATIENTS; ILLNESS BEHAVIOR; SOMATIZATION; PREVALENCE; INCEST AB Objective: This study examined the childhood histories of trauma, parental attitudes toward health, and physical illness in hypochondriacal adults. Method: Sixty outpatients with DSM-III-R hypochondriasis and 60 nonhypochondriacal outpatients from the same general medical clinic were compared. All patients completed the Childhood Traumatic Events Scale and an eight-item questionnaire about childhood illness and health. Medical morbidity was assessed with a medical record audit. Results: Significantly more hypochondriacal than nonhypochondriacal patients reported traumatic sexual contact (28.6% versus 7.3%), physical violence (32.1% versus 7.3%), and major parental upheaval (28.6% versus 9.1%) before the age of 17. These differences remained statistically significant after sociodemographic differences between the groups were controlled for with multivariate regression analysis. The two groups did not differ in the age at which these traumas occurred or in the degree of trauma experienced. Significantly more hypochondriacal patients reported being sick as children and missing school for health reasons, but they did not differ in other measures of childhood illness and parental attitudes toward illness. The two group had similar levels of aggregate medical morbidity. Conclusions: Hypochondriacal adults recall more childhood trauma than do nonhypochondriacal patients, even after sociodemographic differences are controlled for. They also recall more childhood illness, although they are not currently more medically sick. C1 MASSACHUSETTS GEN HOSP, PSYCHIAT SERV, BOSTON, MA 02114 USA. RP BARSKY, AJ (reprint author), BRIGHAM & WOMENS HOSP, DIV PSYCHIAT, 75 FRANCIS ST, BOSTON, MA 02115 USA. FU NIMH NIH HHS [NIMH MH-40487] NR 37 TC 63 Z9 64 U1 2 U2 19 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X EI 1535-7228 J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAR PY 1994 VL 151 IS 3 BP 397 EP 401 PG 5 WC Psychiatry SC Psychiatry GA MY317 UT WOS:A1994MY31700013 PM 8109648 ER PT J AU GUCCIONE, AA FELSON, DT ANDERSON, JJ ANTHONY, JM ZHANG, YQ WILSON, PWF KELLYHAYES, M WOLF, PA KREGER, BE KANNEL, WB AF GUCCIONE, AA FELSON, DT ANDERSON, JJ ANTHONY, JM ZHANG, YQ WILSON, PWF KELLYHAYES, M WOLF, PA KREGER, BE KANNEL, WB TI THE EFFECTS OF SPECIFIC MEDICAL CONDITIONS ON THE FUNCTIONAL LIMITATIONS OF ELDERS IN THE FRAMINGHAM-STUDY SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID CORONARY HEART-DISEASE; UNITED-STATES ADULTS; DEPRESSIVE SYMPTOMS; HIP FRACTURE; RISK-FACTORS; DISABILITY; ARTHRITIS; COMMUNITY; HEALTH; PREDICTORS AB Objectives. The purpose of this study was to identify associations between specific medical conditions in the elderly and limitations in functional tasks; to compare risks of disability across medical conditions, controlling for age, sex, and comorbidity; and to determine the proportion of disability attributable to each condition. Methods. The subjects were 709 noninstitutionalized men and 1060 women of the Framingham Study cohort (mean age 73.7 +/- 6.3 years). Ten medical conditions were identified for study: knee osteoarthritis, hip fracture, diabetes, stroke, heart disease, intermittent claudication, congestive heart failure, chronic obstructive pulmonary disease, depressive symptomatology, and cognitive impairment. Adjusted odds ratios were calculated for dependence on human assistance in seven functional activities. Results. Stroke was significantly associated with functional limitations in all seven tasks; depressive symptomatology and hip fracture were associated with limitations in five tasks; and knee osteoarthritis, heart disease, congestive heart failure, and chronic obstructive pulmonary disease, were associated with limitations in four tasks each. Conclusions. In general, stroke, depressive symptomatology, hip fracture, knee osteoarthritis, and heart disease account for more physical disability in noninstitutionalized elderly men and women than other diseases. C1 BOSTON UNIV,SCH MED,ARTHRIT CTR,BOSTON,MA 02118. HARVARD UNIV,SCH MED,BOSTON,MA. BOSTON CITY HOSP,BOSTON,MA. UNIV BOSTON HOSP,BOSTON,MA 02118. FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. BOSTON UNIV,MED CTR,DEPT CLIN RES & PREVENT MED,BOSTON,MA 02215. BOSTON UNIV,SCH PUBL HLTH,PREVENT MED SECT,BOSTON,MA 02215. RP GUCCIONE, AA (reprint author), MASSACHUSETTS GEN HOSP,PHYS THERAPY SERV,15 PARKMAN ST,WAC 128,BOSTON,MA 02114, USA. FU NIA NIH HHS [NIA KO1AG00567, NIA RO1AG07861]; NIAMS NIH HHS [NIAMS P60AR20613] NR 36 TC 813 Z9 839 U1 3 U2 30 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD MAR PY 1994 VL 84 IS 3 BP 351 EP 358 DI 10.2105/AJPH.84.3.351 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NM618 UT WOS:A1994NM61800004 PM 8129049 ER PT J AU BERNARD, GR ARTIGAS, A BRIGHAM, KL CARLET, J FALKE, K HUDSON, L LAMY, M LEGALL, JR MORRIS, A SPRAGG, R COCHIN, B LANKEN, PN LEEPER, KV MARINI, J MURRAY, JF OPPENHEIMER, L PESENTI, A REID, L RINALDO, J VILLAR, J VANASBECK, BS DHAINAUT, JF MANCEBO, J MATTHAY, M MEYRICK, B PAYEN, D PERRET, C FOWLER, AA SCHALLER, MD HUDSON, LD HYERS, T KNAUS, W MATTHAY, R PINSKY, M BONE, RC BOSKEN, C JOHANSON, WG LEWANDOWSKI, K REPINE, J RODRIGUEZROISIN, R ROUSSOS, C ANTONELLI, MA BELOUCIF, S BIHARI, D BURCHARDI, H LEMAIRE, F MONTRAVERS, P PETTY, TL ROBOTHAM, J ZAPOL, W AF BERNARD, GR ARTIGAS, A BRIGHAM, KL CARLET, J FALKE, K HUDSON, L LAMY, M LEGALL, JR MORRIS, A SPRAGG, R COCHIN, B LANKEN, PN LEEPER, KV MARINI, J MURRAY, JF OPPENHEIMER, L PESENTI, A REID, L RINALDO, J VILLAR, J VANASBECK, BS DHAINAUT, JF MANCEBO, J MATTHAY, M MEYRICK, B PAYEN, D PERRET, C FOWLER, AA SCHALLER, MD HUDSON, LD HYERS, T KNAUS, W MATTHAY, R PINSKY, M BONE, RC BOSKEN, C JOHANSON, WG LEWANDOWSKI, K REPINE, J RODRIGUEZROISIN, R ROUSSOS, C ANTONELLI, MA BELOUCIF, S BIHARI, D BURCHARDI, H LEMAIRE, F MONTRAVERS, P PETTY, TL ROBOTHAM, J ZAPOL, W TI THE AMERICAN-EUROPEAN CONSENSUS CONFERENCE ON ARDS - DEFINITIONS, MECHANISMS, RELEVANT OUTCOMES, AND CLINICAL-TRIAL COORDINATION SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Editorial Material ID RESPIRATORY-DISTRESS SYNDROME; ICU PATIENTS; FAILURE; SYSTEM; PHYSIOLOGY; MORTALITY; SURVIVAL AB The acute respiratory distress syndrome (ARDS), a process of nonhydrostatic pulmonary edema and hypoxemia associated with a variety of etiologies, carries a high morbidity, mortality (10 to 90%), and financial cost. The reported annual incidence in the United States is 150,000 cases, but this figure has been challenged, and it may be different in Europe. Part of the reason for these uncertainties are the heterogeneity of diseases underlying ARDS and the lack of uniform definitions for ARDS. Thus, those who wish to know the true incidence and outcome of this clinical syndrome are stymied. The American-European Consensus Committee on ARDS was formed to focus on these issues and on the pathophysiologic mechanisms of the process. It was felt that international coordination between North America and Europe in clinical studies of ARDS was becoming increasingly important in order to address the recent plethora of potential therapeutic agents for the prevention and treatment of ARDS. C1 LATTER DAY ST HOSP,SALT LAKE CITY,UT. ST JOSEPHS HOSP,PARIS,FRANCE. HOSP PARIS,PARIS,FRANCE. UNIV PENN,PHILADELPHIA,PA. UNIV TENNESSEE,MEMPHIS,TN. UNIV MINNESOTA,MINNEAPOLIS,MN. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA. UNIV MANITOBA,WINNIPEG R3T 2N2,MB,CANADA. UNIV MILAN,MONZA,ITALY. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. UNIV TORONTO,TORONTO,ON,CANADA. VANDERBILT UNIV,SCH MED,NASHVILLE,TN 37212. UNIV LIEGE,LIEGE,BELGIUM. UNIV UTRECHT,UTRECHT,NETHERLANDS. HOP COCHIN,PARIS,FRANCE. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. UNIV LAUSANNE,LAUSANNE,SWITZERLAND. UNIV WASHINGTON,SEATTLE,WA. ST LOUIS UNIV,ST LOUIS,MO. GEORGE WASHINGTON UNIV,WASHINGTON,DC. UNIV PITTSBURGH,PITTSBURGH,PA. UNIV CALIF SAN DIEGO,SAN DIEGO,CA. RUSH MED COLL,CHICAGO,IL. NHLBI,DIV LUNG DIS,BETHESDA,MD. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,NEWARK,NJ 07103. UNIV COLORADO,HLTH SCI CTR,WEBB WARING INST BIOMED RES,DENVER,CO. HOSP CLIN BARCELONA,BARCELONA,SPAIN. EVANGELISMOS MED CTR,ATHENS,GREECE. UNIV ROME,ROME,ITALY. GUYS HOSP,LONDON,ENGLAND. UNIV GOTTINGEN,GOTTINGEN,GERMANY. MASSACHUSETTS GEN HOSP,BOSTON,MA. RP BERNARD, GR (reprint author), VANDERBILT UNIV,T-1219 MCN,NASHVILLE,TN, USA. FU NHLBI NIH HHS [NHLBI HL19153, NHLBI HL43167] NR 27 TC 3647 Z9 3962 U1 11 U2 74 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD MAR PY 1994 VL 149 IS 3 BP 818 EP 824 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NP719 UT WOS:A1994NP71900042 PM 7509706 ER PT J AU BENNETT, GL CHEW, FS AF BENNETT, GL CHEW, FS TI PULMONARY CARCINOID TUMORLETS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 5 TC 6 Z9 6 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAR PY 1994 VL 162 IS 3 BP 568 EP 568 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MY860 UT WOS:A1994MY86000015 PM 8109497 ER PT J AU DORSI, CJ KOPANS, DB AF DORSI, CJ KOPANS, DB TI THE AMERICAN-COLLEGE OF RADIOLOGYS MAMMOGRAPHY LEXICON - BARKING UP THE ONLY TREE SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP DORSI, CJ (reprint author), UNIV MASSACHUSETTS,MED CTR,DEPT RADIOL,55 LAKE AVE N,WORCESTER,MA 01655, USA. NR 1 TC 10 Z9 10 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAR PY 1994 VL 162 IS 3 BP 595 EP 595 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MY860 UT WOS:A1994MY86000021 PM 8109503 ER PT J AU DORFMAN, DM TO, K DICKERSIN, GR ROSENBERG, AE PILCH, BZ AF DORFMAN, DM TO, K DICKERSIN, GR ROSENBERG, AE PILCH, BZ TI SOLITARY FIBROUS TUMOR OF THE ORBIT SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE SOLITARY FIBROUS TUMOR; LOCALIZED FIBROUS MESOTHELIOMA; ORBIT ID BENIGN MESENCHYMAL TUMOR; MESOTHELIOMA; HEMANGIOPERICYTOMA; MYOFIBROBLASTOMA; PLEURA; REGION AB We report three cases of an orbital soft tissue lesion that fulfills the histologic, immunohistochemical, and electron microscopic criteria for solitary fibrous tumor, an entity previously described as a pleural tumor, but recently reported to occur in other locations. All three patients presented with proptosis. Two of the patients were cured by simple excision, and one patient had two recurrences, the last recurrence incompletely excised. The findings indicate that solitary fibrous tumor can occur in the orbit and, like solitary fibrous tumors of other anatomic sites, may behave in a nonaggressive or occasionally, locally aggressive fashion, with as yet no metastatic potential demonstrated in orbital lesions. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,DEPT PATHOL,BOSTON,MA 02114. BROWN UNIV,RHODE ISL HOSP,SCH MED,DEPT OPHTHALMOL & PATHOL,PROVIDENCE,RI 02903. PROVIDENCE VET ADM MED CTR,DEPT OPHTHALMOL & PATHOL,PROVIDENCE,RI. RP DORFMAN, DM (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 25 TC 154 Z9 159 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD MAR PY 1994 VL 18 IS 3 BP 281 EP 287 DI 10.1097/00000478-199403000-00008 PG 7 WC Pathology; Surgery SC Pathology; Surgery GA MZ331 UT WOS:A1994MZ33100008 PM 8116796 ER PT J AU BOHN, MJ KRANZLER, HR BEAZOGLOU, D STAEHLER, BA AF BOHN, MJ KRANZLER, HR BEAZOGLOU, D STAEHLER, BA TI NALTREXONE AND BRIEF COUNSELING TO REDUCE HEAVY DRINKING - RESULTS OF A SMALL CLINICAL-TRIAL SO AMERICAN JOURNAL ON ADDICTIONS LA English DT Article; Proceedings Paper CT Annual Meeting of the International Conference on Psychoneuroendocrinology CY AUG, 1992 CL MADISON, WI ID ALCOHOL DEPENDENCE; CONSUMPTION; POPULATION; STRATEGIES; MORPHINE AB Naltrexone (NTX) has been shown to be safe and effective in reducing relapses among alcoholics. Among nondependent heavy drinkers, who are more numerous in the general population than are alcohol-dependent drinkers, brief counseling has been shown to reduce alcohol consumption. The authors conducted a 6-week randomized study of the effects of adding 25-mg or 50-mg daily doses of NTX to brief counseling in 14 nondependent heavy drinkers. NTX was well-tolerated. Desire for alcohol, drinking frequency, frequency of heavy drinking, total alcohol consumption, and serum gamma-glutamyl transpeptidase all decreased significantly during treatment. A placebo-controlled trial is warranted to evaluate further the efficacy of NTX in this group of problem drinkers. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV CONNECTICUT,ALCOHOL RES CTR,FARMINGTON,CT 06030. RP BOHN, MJ (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. NR 28 TC 42 Z9 45 U1 1 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1055-0496 J9 AM J ADDICTION JI Am. J. Addict. PD SPR PY 1994 VL 3 IS 2 BP 91 EP 99 PG 9 WC Substance Abuse SC Substance Abuse GA NH408 UT WOS:A1994NH40800001 ER PT J AU PETERFREUND, RA NIVEN, RW KACMAREK, RM AF PETERFREUND, RA NIVEN, RW KACMAREK, RM TI SYRINGE-ACTUATED METERED-DOSE INHALERS - A QUANTITATIVE LABORATORY EVALUATION OF ALBUTEROL DELIVERY THROUGH NOZZLE EXTENSIONS SO ANESTHESIA AND ANALGESIA LA English DT Article ID MECHANICALLY VENTILATED PATIENTS; AEROSOL DELIVERY; EFFICIENCY; TUBES AB The metered dose inhaler (MDI) is a device that can be used to supply aerosolized bronchodilators to the tracheobronchial tree of patients requiring endotracheal intubation. Because direct actuation of the MDI into the breathing circuit is inefficient, a technique of extending the MDI nozzle with small-bore, long, intravenous catheters has been devised. To facilitate connecting the MDI to the extension and actuating the release of aerosol, insertion of the MDI cannister into the barrel of a large syringe attached to the Luer hub of the extension has been proposed but not quantitatively evaluated. The purpose of this study was to test, in a laboratory model, the performance of syringe-actuated MDIs attached to nozzle extensions. The deposition of the bronchodilator albuterol in the delivery device and distal to the extension was quantified spectrophotometrically. Maximum distal delivery of drug from nozzle extensions fashioned from small-bore (19-gauge) catheters was 80% of the actuated release. Loss of drug to the inner surface of the syringe plus extension varied inversely with the number of successive actuations. Syringes from two manufacturers in two sizes were compared and found to perform comparably. Syringes could be attached to the Luer connector of the secondary sampling channel of special pediatric-sized endotracheal tubes (ETTs) and the channels were evaluated as nozzle extensions, with distal delivery >80% as efficient as the 19-gauge intravenous catheter. We conclude that syringe actuation of MDIs through nozzle extensions is an efficient method for supplying the aerosol distal to the tip of the ETT. Luer-hubbed sampling lumina of specialized ETTs are also efficient nozzle extensions and may be convenient to use for enhanced delivery of aerosol in the clinical setting. C1 MASSACHUSETTS GEN HOSP,HARVARD MED SCH,DEPT ANAESTHESIA,BOSTON,MA. AMGEN INC,THOUSAND OAKS,CA. NR 13 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD MAR PY 1994 VL 78 IS 3 BP 554 EP 558 PG 5 WC Anesthesiology SC Anesthesiology GA NA403 UT WOS:A1994NA40300024 PM 8109777 ER PT J AU ACQUADRO, MA BORODIC, GE AF ACQUADRO, MA BORODIC, GE TI TREATMENT OF MYOFASCIAL PAIN WITH BOTULINUM-A TOXIN SO ANESTHESIOLOGY LA English DT Letter ID SPASMODIC TORTICOLLIS; BLEPHAROSPASM C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT ANESTHESIOL,PAIN MANAGEMENT UNIT,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. RP ACQUADRO, MA (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 6 TC 66 Z9 68 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAR PY 1994 VL 80 IS 3 BP 705 EP 706 DI 10.1097/00000542-199403000-00041 PG 2 WC Anesthesiology SC Anesthesiology GA NB247 UT WOS:A1994NB24700040 PM 8141474 ER PT J AU SPRUANCE, SL PAVIA, AT PETERSON, D BERRY, A POLLARD, R PATTERSON, TF FRANK, I REMICK, SC THOMPSON, M MACARTHUR, RD MOREY, GE RAMIREZRONDA, CH BERNSTEIN, BM SWEET, DE CRANE, L PETERSON, EA PACHUCKI, CT GREEN, SL BRAND, J RIOS, A DUNKLE, LM CROSS, A BROWN, MJ INGRAHAM, P GUGLIOTTI, R SCHINDZIELORZ, AH SMALDONE, L BECKER, T BIA, FJ BUJWIT, C DONABEDIAN, H EVANS, TG FIELLIN, M KAEMPFER, S OKEEFE, JP LIPTON, L MARK, RJ OTT, G REIMER, LG RIES, K WATERMAN, K WEST, MM AF SPRUANCE, SL PAVIA, AT PETERSON, D BERRY, A POLLARD, R PATTERSON, TF FRANK, I REMICK, SC THOMPSON, M MACARTHUR, RD MOREY, GE RAMIREZRONDA, CH BERNSTEIN, BM SWEET, DE CRANE, L PETERSON, EA PACHUCKI, CT GREEN, SL BRAND, J RIOS, A DUNKLE, LM CROSS, A BROWN, MJ INGRAHAM, P GUGLIOTTI, R SCHINDZIELORZ, AH SMALDONE, L BECKER, T BIA, FJ BUJWIT, C DONABEDIAN, H EVANS, TG FIELLIN, M KAEMPFER, S OKEEFE, JP LIPTON, L MARK, RJ OTT, G REIMER, LG RIES, K WATERMAN, K WEST, MM TI DIDANOSINE COMPARED WITH CONTINUATION OF ZIDOVUDINE IN HIV-INFECTED PATIENTS WITH SIGNS OF CLINICAL DETERIORATION WHILE RECEIVING ZIDOVUDINE - A RANDOMIZED, DOUBLE-BLIND CLINICAL-TRIAL SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS INFECTIONS; DIDANOSINE; ZIDOVUDINE; AIDS-RELATED COMPLEX; ACQUIRED IMMUNODEFICIENCY SYNDROME ID IMMUNODEFICIENCY-VIRUS INFECTION; 2',3'-DIDEOXYINOSINE; RESISTANCE; TYPE-1; AZT AB Objective: To determine the benefits of switching to didanosine compared with continuing zidovudine among patients infected with human immunodeficiency virus (HIV) who have previously used zidovudine and have signs of clinical deterioration. Design:Randomized, double-blind, two-armed, parallel, comparative clinical trial with a blinded, compassionate crossover provision at 12 weeks. Setting: Outpatient clinics at 19 tertiary care medical centers. Patients: 312 patients infected with HIV who had received zidovudine for 6 months or more, had CD4 cell counts of 300/mm(3) or less, and had signs of clinical deterioration within 12 weeks before study entry. Intervention: Peroral didanosine tablets (600 mg/d adjusted for weight, ''high dose'') or zidovudine capsules (600 mg/d). Measurements: Primary study end points were death, a new acquired immunodeficiency syndrome (AIDS)-defining event, or the combination of two new or recurrent HIV-related diagnoses with a 50% decrease in CD4 cells. Results: Switching to didanosine was associated with fewer end points than continuing zidovudine (relative risk [RR] for zidovudine:didanosine = 1.5; 95% Cl, 1.1 to 2.0). This benefit was consistent across subgroups of patients with either AIDS-related complex or AIDS and was most apparent among those with a CD4 count at entry of 100/mm(3) or more (RR = 2.2; Cl, 1.1 to 4.4). Conclusions: This study shows a positive treatment effect for switching from zidovudine to didanosine among patients with either AIDS-related complex or AIDS and validates the common practice of using clinical signs or a decrease in the CD4 count as an indication for changing therapy. C1 HOLY CROSS HOSP,SALT LAKE CITY,UT 84102. UNIV TEXAS,SW MED CTR DALLAS,DALLAS,TX 75235. UNIV ARIZONA,HLTH SCI CTR,INFECT DIS SECT,TUCSON,AZ 85724. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. YALE UNIV,SCH MED,NEW HAVEN,CT. UNIV PENN,IMMUNODEFICIENCY PROGRAM,PHILADELPHIA,PA 19104. ALBANY MED CTR,ALBANY,NY. AIDS RES CONSORTIUM ATLANTA,ATLANTA,GA. MED COLL OHIO,DEPT MED,TOLEDO,OH 43614. VET AFFAIRS MED CTR,SAN JUAN,PR 00927. MED COLL WISCONSIN,MILWAUKEE,WI 53226. UNIV KANSAS,SCH MED,WICHITA,KS 67214. VET AFFAIRS EDWARD HINES JR HOSP,INFECT DIS SECT,HINES,IL 60141. UNIV ARIZONA,HLTH SCI CTR,TUCSON,AZ 85724. HOME HLTH CARE SERV,RES INST,ORLANDO,FL. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,WALLINGFORD,CT 06492. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77555. HARPER GRACE HOSP,DETROIT,MI 48201. UNIV PUERTO RICO,SCH MED & AFFILIATED HOSP,SAN JUAN,PR. RP SPRUANCE, SL (reprint author), UNIV UTAH,HLTH SCI AIDS CTR,MC 4B322,50 N MED DR,SALT LAKE CITY,UT 84132, USA. NR 24 TC 72 Z9 72 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAR 1 PY 1994 VL 120 IS 5 BP 360 EP 368 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA MY497 UT WOS:A1994MY49700002 PM 7905722 ER PT J AU DAMORE, PA BROWN, RH KU, PT HOFFMAN, EP WATANABE, H ARAHATA, K ISHIHARA, T FOLKMAN, J AF DAMORE, PA BROWN, RH KU, PT HOFFMAN, EP WATANABE, H ARAHATA, K ISHIHARA, T FOLKMAN, J TI ELEVATED BASIC FIBROBLAST GROWTH-FACTOR IN THE SERUM OF PATIENTS WITH DUCHENNE MUSCULAR-DYSTROPHY SO ANNALS OF NEUROLOGY LA English DT Note C1 HARVARD UNIV,SCH MED,PROGRAM CELL & DEV BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CECIL B DAY LAB NEUROMUSCULAR RES,BOSTON,MA 02114. UNIV PITTSBURGH,SCH MED,DEPT MOLEC GENET & BIOCHEM,PITTSBURGH,PA 15261. TAKEDA CHEM CORP,OSAKA,JAPAN. NATL INST NEUROSCI,TOKYO,JAPAN. NATL HIGASHI SAITAMA HOSP,SAITAMA,JAPAN. RP DAMORE, PA (reprint author), CHILDRENS HOSP MED CTR,SURG RES LAB,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NEI NIH HHS [EY 05985] NR 13 TC 71 Z9 71 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD MAR PY 1994 VL 35 IS 3 BP 362 EP 365 DI 10.1002/ana.410350320 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NA805 UT WOS:A1994NA80500019 PM 8122890 ER PT J AU ISACSON, O AF ISACSON, O TI CLINICAL AND PRECLINICAL PET CORRELATES OF PARKINSONISM WITH C-11 WIN 35,428 SO ANNALS OF NEUROLOGY LA English DT Letter C1 MCLEAN HOSP,NEUROGENERAT LAB,BELMONT,MA 02178. RP ISACSON, O (reprint author), MASSACHUSETTS GEN HOSP,SERV NEUROL,MRC119,BELMONT,MA 02178, USA. NR 5 TC 3 Z9 3 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD MAR PY 1994 VL 35 IS 3 BP 377 EP 378 DI 10.1002/ana.410350328 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NA805 UT WOS:A1994NA80500027 PM 8122896 ER PT J AU SHAPIRO, CL HENDERSON, IC AF SHAPIRO, CL HENDERSON, IC TI LATE CARDIAC EFFECTS OF ADJUVANT THERAPY - TOO SOON TO TELL SO ANNALS OF ONCOLOGY LA English DT Editorial Material ID BREAST-CANCER; DOXORUBICIN; CARDIOTOXICITY; CYCLOPHOSPHAMIDE; METHOTREXATE; FLUOROURACIL C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. RP SHAPIRO, CL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 20 TC 10 Z9 10 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD MAR PY 1994 VL 5 IS 3 BP 196 EP 198 PG 3 WC Oncology SC Oncology GA ND130 UT WOS:A1994ND13000001 PM 8186167 ER PT J AU MAY, JW BUCKY, LP SOHONI, S EHRLICH, HP AF MAY, JW BUCKY, LP SOHONI, S EHRLICH, HP TI SMOOTH VERSUS TEXTURED EXPANDER IMPLANTS - A DOUBLE-BLIND-STUDY OF CAPSULE QUALITY AND DISCOMFORT IN SIMULTANEOUS BILATERAL BREAST RECONSTRUCTION PATIENTS SO ANNALS OF PLASTIC SURGERY LA English DT Article ID SILICONE TISSUE EXPANDER; HISTOLOGIC PROPERTIES; COLLAGEN LATTICES; EXPANSION; CONTRACTION; RABBIT AB Textured silicone expanders are alleged to be less painful in the filling process, to have less capsular contracture, and to stay in position better than smooth silicone expanders. To test these three hypotheses, 6 patients undergoing bilateral simultaneous expander implant placement for breast reconstruction after mastectomy were studied. In a double-blind fashion, after smooth and textured implant placement (one in each side) and initial wound healing, each patient was sequentially expanded with equal volumes of saline. In each patient, at each expansion, pressure data, discomfort scores, and implant placement measurements were made. At implant removal, smooth and textured capsule tissues were studied for collagen type content and ability to contract the patient's own fibroblast-populated collagen lattice. In 4 of 6 patients the smooth expander was associated with lower injection pressures and less discomfort. In all patients the expanders maintained their position, except in I patient whose smooth implant shifted laterally. The capsular collagen typing and fibroblast-populated collagen lattice studies demonstrated no difference between smooth and textured capsules. In this double-blind clinical study in simultaneous bilateral breast reconstruction patients we could not confirm the suggestion that textured silicone expanders produce less capsular contracture and cause less pain with injection. RP MAY, JW (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ACC-453,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 23 TC 11 Z9 12 U1 0 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0148-7043 J9 ANN PLAS SURG JI Ann. Plast. Surg. PD MAR PY 1994 VL 32 IS 3 BP 225 EP 233 DI 10.1097/00000637-199403000-00001 PG 9 WC Surgery SC Surgery GA NA340 UT WOS:A1994NA34000001 PM 8192380 ER PT J AU SCHOENTHALER, R PHILLIPS, TL CASTRO, J EFIRD, JT BETTER, A WAY, LW AF SCHOENTHALER, R PHILLIPS, TL CASTRO, J EFIRD, JT BETTER, A WAY, LW TI CARCINOMA OF THE EXTRAHEPATIC BILE-DUCTS - THE UNIVERSITY-OF-CALIFORNIA AT SAN-FRANCISCO EXPERIENCE SO ANNALS OF SURGERY LA English DT Article ID PROGNOSTIC FACTORS; BILIARY-TRACT; MANAGEMENT; RESECTION; CHOLANGIOCARCINOMA; RADIOTHERAPY; FAILURE; THERAPY; CANCER AB Objective The authors investigated the combined experience of a single institution in treating bile duct carcinoma during the modern era. Summary Background Data Bile duct carcinomas are notoriously difficult to cure, with locoregional recurrence the rule, even after radical resection. Adjuvant efforts have included various radiation modalities, with limited success. Recently, charged-particle radiotherapy has also been used in these patients. Methods The authors performed a retrospective chart analysis of 129 patients with bile duct adenocarcinomas treated between 1977 and 1987 through the University of California at San Francisco, including 22 patients treated at Lawrence Berkeley Laboratory with the charged particles helium and neon. The minimum follow-up was 5 years. Survival, outcome, and complication results were analyzed. Results Sixty-two patients were treated with surgery alone (S), 45 patients received conventional adjuvant x-ray radiotherapy (S + X), and 22 were treated with charged particles (S + CP). The median survival times were 6.5, 11, and 14 months, respectively, for the entire group, and 16, 16, and 23 months in patients treated with curative intent. There was a survival difference in patients undergoing total resection compared with debulking (p = 0.05) and minor resections (p = 0.0001). Patients with microscopic residual disease had increased median survival times when they were treated with adjuvant irradiation, most markedly after CP (p = 0.0005) but also with conventional X (p = 0.0109). Patients with gross residual disease had a less marked but still statistically significant extended survival (p = 0.05 for S + X and p = 0.0423 for S + CP) after irradiation. Conclusions The mainstay of bile duct carcinoma management was maximal surgical resection in these patients. Postoperative radiotherapy gave patients with positive microscopic margins a significant survival advantage and may be of value in selected patients with gross disease. C1 UNIV CALIF SAN FRANCISCO,DEPT RADIAT ONCOL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT SURG,SAN FRANCISCO,CA 94143. UNIV CALIF BERKELEY,BERKELEY,CA. RP SCHOENTHALER, R (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,COX BLDG,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA19138] NR 21 TC 92 Z9 97 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD MAR PY 1994 VL 219 IS 3 BP 267 EP 274 DI 10.1097/00000658-199403000-00006 PG 8 WC Surgery SC Surgery GA NA117 UT WOS:A1994NA11700006 PM 8147607 ER PT J AU ESPAT, NJ COPELAND, EM SOUBA, WW AF ESPAT, NJ COPELAND, EM SOUBA, WW TI ACCELERATED HEPATIC ARGININE TRANSPORT IN THE TUMOR-BEARING RAT SO ANNALS OF SURGICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 46th Annual Cancer Symposium of the Society-of-Surgical-Oncology CY MAR 18-21, 1993 CL LOS ANGELES, CA SP SOC SURG ONCOL DE ARGININE; HEPATIC TRANSPORT; AMINO ACIDS; CANCER ID PLASMA-MEMBRANE VESICLES; NECROSIS-FACTOR-ALPHA; AMINO-ACID-TRANSPORT; GLUTAMINE TRANSPORT; PROTEIN-SYNTHESIS; LIVER; CELLS; HEPATOCYTE; CACHECTIN; INVIVO AB Background: Arginine plays a pivotal role in regulating ureagenesis, polyamine biosynthesis, and nitric oxide production, metabolic pathways that may be stimulated in the liver of the tumor-bearing host. Normally, plasma arginine is excluded from the hepatocyte intracellular space by the low basal activity of its membrane transporter. We hypothesized that progressive malignant disease is associated with an increase in carrier-mediated arginine transport across the hepatocyte plasma membrane. Methods: Twenty-four adult Fischer 344 rats were implanted subcutaneously with fibrosarcomas (TBR) and were studied when the tumors were small [10 +/- 1% of body weight (BW)], medium-sized (15 +/- 1% of BW), and large (25 +/- 1% of BW). Groups of control rats (n = 24) were pair-fed to match carcass weights of the three TBR groups. Livers were excised, and hepatocyte plasma membrane vesicles (HPMVs) were prepared by Percoll density gradient centrifugation. Arginine transport by HPMVs was assayed by a rapid mixing/filtration technique. Vesicle purity and functionality were assessed by membrane enzyme marker enrichments and transportability into an osmotically active space. Results: Arginine uptake by HPMVs was mediated by both saturable carrier-mediated (System y+) and nonsaturable (diffusion) components. The time course of arginine uptake in HPMVs in the three groups showed similar equilibrium transport rates, indicating similar vesicle sizes. The presence of the growing tumor resulted in a 40-120% increase in System y+-mediated arginine transport in HPMVs. This response was dependent on tumor size and was due to a stimulation of carrier V(max), suggesting an increase in the number of functional System y+ carriers in the hepatocyte plasma membrane. The Na+-dependent transport of the System A analog MeAIB was also increased, but only in rats with large tumors. Conclusions: Tumor growth results in a progressive increase in hepatic arginine transport, a response mediated primarily by an increase in the activity of System y+. This accelerated transport may amplify the availability of arginine to support key arginine-dependent metabolic pathways in the hepatocyte. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02114. UNIV FLORIDA,COLL MED,DEPT SURG,GAINESVILLE,FL 32611. FU NCI NIH HHS [CA 45327] NR 25 TC 14 Z9 14 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1068-9265 J9 ANN SURG ONCOL JI Ann. Surg. Oncol. PD MAR PY 1994 VL 1 IS 2 BP 147 EP 156 DI 10.1007/BF02303559 PG 10 WC Oncology; Surgery SC Oncology; Surgery GA NM329 UT WOS:A1994NM32900012 PM 7834440 ER PT J AU SEYMOUR, C LEWIS, RG KIM, M GAGNON, DF FOX, JG DEWHIRST, FE PASTER, BJ AF SEYMOUR, C LEWIS, RG KIM, M GAGNON, DF FOX, JG DEWHIRST, FE PASTER, BJ TI ISOLATION OF HELICOBACTER STRAINS FROM WILD BIRD AND SWINE FECES SO APPLIED AND ENVIRONMENTAL MICROBIOLOGY LA English DT Article ID PYLORI INFECTION; SP-NOV; CAMPYLOBACTER; WATER; MUSTELAE; SURVIVAL AB We report the first isolations of Helicobacter strains from wild birds and swine. Genus-specific oligonueleotide probes identified nine Cape Cod isolates from gull, tern, house sparrow, and pig feces as Helicobacter spp. and not Campylobacter spp. Antibiotic sensitivity and urease tests distinguished three phenotypes. Strains examined rapidly lost culturability under simulated natural conditions. C1 BOSTON UNIV,SCH MED,DEPT MICROBIOL,BOSTON,MA 02118. MIT,PARSONS LAB HYDROL ENGN,CAMBRIDGE,MA 02139. MIT,DIV COMPARAT MED,CAMBRIDGE,MA 02139. FORSYTH DENT CTR,DEPT MOLEC GENET,BOSTON,MA 02115. FU NCRR NIH HHS [RR 01046]; NIDCR NIH HHS [DE 08303] NR 23 TC 36 Z9 38 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0099-2240 J9 APPL ENVIRON MICROB JI Appl. Environ. Microbiol. PD MAR PY 1994 VL 60 IS 3 BP 1025 EP 1028 PG 4 WC Biotechnology & Applied Microbiology; Microbiology SC Biotechnology & Applied Microbiology; Microbiology GA MZ137 UT WOS:A1994MZ13700039 PM 8161169 ER PT J AU HOLLIDAY, S ROMERO, J AF HOLLIDAY, S ROMERO, J TI ANTERIOR COMMUNICATING ARTERY (ACOA) ANEURYSM - A LONGITUDINAL CASE-STUDY EXAMINING THE EFFECTS OF PREEXISTING PSYCHIATRIC-ILLNESS AND MEDICATION EFFECTS OF THE ACOA SYNDROME SO ARCHIVES OF CLINICAL NEUROPSYCHOLOGY 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 PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6177 J9 ARCH CLIN NEUROPSYCH JI Arch. Clin. Neuropsychol. PD MAR-APR PY 1994 VL 9 IS 2 BP 141 EP 141 PG 1 WC Psychology, Clinical; Psychology SC Psychology GA NM848 UT WOS:A1994NM84800060 ER PT J AU SADEK, J JOHNSON, SA PAULSEN, JS SALMON, DP SWENSON, MP BUTTERS, N AF SADEK, J JOHNSON, SA PAULSEN, JS SALMON, DP SWENSON, MP BUTTERS, N TI DIFFERENTIATION OF HUNTINGTONS-DISEASE AND ALZHEIMERS-DISEASE - DISTINCT COGNITIVE PROFILES REMAIN IN ADVANCED ILLNESS SO ARCHIVES OF CLINICAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. US DEPT VET AFFAIRS,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6177 J9 ARCH CLIN NEUROPSYCH JI Arch. Clin. Neuropsychol. PD MAR-APR PY 1994 VL 9 IS 2 BP 179 EP 180 PG 2 WC Psychology, Clinical; Psychology SC Psychology GA NM848 UT WOS:A1994NM84800126 ER PT J AU KWIATKOWSKI, DJ SHORT, MP AF KWIATKOWSKI, DJ SHORT, MP TI TUBEROUS SCLEROSIS SO ARCHIVES OF DERMATOLOGY LA English DT Article ID POLYCYSTIC KIDNEY-DISEASE; GENETIC-HETEROGENEITY; DIAGNOSTIC-CRITERIA; LOCUS; LINKAGE; CHROMOSOME-9; SEIZURES; COMPLEX; ASSOCIATION; INVOLVEMENT AB Background and Design: Tuberous sclerosis (TS) is a genetic disease with prominent cutaneous and brain involvement whose clinical and molecular genetics are reviewed. Observations: Tuberous sclerosis is a systemic disorder (incidence one in 10 000) characterized by benign growths (hamartias and hamartomas) in multiple organ systems. Involvement of the brain can result in persistent seizures and mental retardation; skin involvement includes facial angiofibromas, subungual fibromas, hypomelanotic macules, forehead fibrous plaques, and Shagreen's patches. Approximately 60% of TS occurs as apparent sporadic cases. In families, it has autosomal dominant inheritance with high penetrance (approximately 95%), with careful clinical and radiologic evaluation. Genetic linkage analysis indicates that about half of all TS families show linkage to chromosome 9q34, and about half to chromosome 16p13. There are no distinguishing features in the two groups of families showing linkage to the two genomic regions, nor strong evidence for a third causative gene. Positional cloning efforts for both chromosomal regions have limited the region containing the gene to about 1 to 2 million bases. Conclusions: Identification of the two TS genes should illuminate the pathogenesis of TS and provide opportunities for genetic counseling, prenatal diagnosis, and therapeutic intervention. C1 MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. RP KWIATKOWSKI, DJ (reprint author), BRIGHAM & WOMENS HOSP, DIV EXPTL MED, 221 LONGWOOD AVE, BOSTON, MA 02115 USA. NR 55 TC 109 Z9 112 U1 1 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA SN 0003-987X EI 1538-3652 J9 ARCH DERMATOL JI Arch. Dermatol. PD MAR PY 1994 VL 130 IS 3 BP 348 EP 354 DI 10.1001/archderm.130.3.348 PG 7 WC Dermatology SC Dermatology GA ND877 UT WOS:A1994ND87700010 PM 8129414 ER PT J AU LUCARELLI, MJ ADAMIS, AP AF LUCARELLI, MJ ADAMIS, AP TI AVELLINO CORNEAL-DYSTROPHY SO ARCHIVES OF OPHTHALMOLOGY LA English DT Editorial Material RP LUCARELLI, MJ (reprint author), MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114, USA. NR 4 TC 10 Z9 10 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAR PY 1994 VL 112 IS 3 BP 418 EP 419 PG 2 WC Ophthalmology SC Ophthalmology GA NB947 UT WOS:A1994NB94700033 PM 8129670 ER PT J AU RYAN, CM BAILEY, SH CARTER, EA SCHOENFELD, DA TOMPKINS, RG AF RYAN, CM BAILEY, SH CARTER, EA SCHOENFELD, DA TOMPKINS, RG TI ADDITIVE EFFECTS OF THERMAL-INJURY AND INFECTION ON GUT PERMEABILITY SO ARCHIVES OF SURGERY LA English DT Article ID TUMOR NECROSIS FACTOR; INTESTINAL PERMEABILITY; BURN INJURY; HUMANS; SHOCK AB Objective: To determine the effects of burn size and burn wound infection on gut permeability to the macromolecule polyethylene glycol 3350 (PEG 3350; molecular weight, 3350 d). Design: Randomized, controlled study using 36 male Sprague-Dawley rats. Setting: Hospital research laboratory. Interventions: Animals received scald burns to 0%, 20%, or 35% of their total body surface area. Half of the animals in each group were infected with Pseudomonas aeruginosa. Main Outcome Measures: Gut permeability was measured using the intestinal absorption and renal excretion of enterally administered PEG 3350 and mannitol (molecular weight, 182 d). Results: There were dramatic increases in PEG 3350 excretion and in the PEG 3350/mannitol ratios (P=.0001 in both instances) that were seen in relation to burn size. Significant increases in PEG 3350 excretion and in the PEG 3350/mannitol ratios (P=.017 and P=.045, respectively) were also seen in animals in which infection was present. This was in addition to the effects of burn size already noted. Conclusions: A direct relationship between gut permeability and the extent of burn injury was found, which is consistent with the results from a previous study in humans. In addition, this study found that further separate increases in gut permeability occur in the presence of P aeruginosa in burn wound infections. C1 MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR BIOSTAT,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. FU NIGMS NIH HHS [T32 GM 07035, P50 GM 21700] NR 15 TC 17 Z9 17 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD MAR PY 1994 VL 129 IS 3 BP 325 EP 328 PG 4 WC Surgery SC Surgery GA NA520 UT WOS:A1994NA52000017 PM 8129610 ER PT J AU KISS, RG LU, HR ROSKAMS, T JANG, IK PLOW, EF GOLD, HK COLLEN, D AF KISS, RG LU, HR ROSKAMS, T JANG, IK PLOW, EF GOLD, HK COLLEN, D TI TIME-COURSE OF THE EFFECTS OF A SINGLE BOLUS INJECTION OF F(AB')(2) FRAGMENTS OF THE ANTIPLATELET GPIIB/IIIA ANTIBODY 7E3 ON ARTERIAL EVERSION GRAFT OCCLUSION, PLATELET-AGGREGATION, AND BLEEDING-TIME IN DOGS SO ARTERIOSCLEROSIS AND THROMBOSIS LA English DT Article DE ARTERIAL THROMBOSIS; ANTIPLATELET AGENTS; ANTI-GPIIB/IIIA ANTIBODY; ARTERIAL PATENCY ID ARG-GLY-ASP; GLYCOPROTEIN-IIB/IIIA RECEPTOR; ACUTE MYOCARDIAL-INFARCTION; PLASMINOGEN-ACTIVATOR; THROMBIN INHIBITION; MONOCLONAL-ANTIBODY; CANINE PREPARATION; UNSTABLE ANGINA; FACTOR BINDING; THROMBOLYSIS AB The time course of the effects of a single intravenous bolus injection of 10 mg/kg aspirin or 0.8 mg/kg F(ab'), fragments of the monoclonal antiplatelet glycoprotein IIb/IIIa receptor antibody 7E3 [7E3-F(ab')(2)] on arterial occlusion, platelet aggregation, and bleeding time was studied in 30 dogs with an everted (inside out) carotid arterial segment inserted into the femoral artery. In the absence of an antiplatelet agent, the eversion grafts occluded spontaneously with platelet-rich thrombus within 30 minutes. With aspirin, arterial occlusion persisting for 2 hours occurred in 5 of 10 dogs and cyclic occlusion and reflow in 4 animals; arterial occlusion was observed in all dogs at 24 hours. With 7E3-F(ab')(2), arterial patency persisted throughout a 2-hour observation period in all of 10 dogs and for 24 hours in 4 of the 10 dogs. Contralateral eversion grafting 24 hours after aspirin or 7E3-F(ab')(2) injection was associated with graft patency for 2 hours in 1 of 5 aspirin dogs and in 3 of 5 7E3-F(ab')(2) dogs; patency persisted for 24 hours. In dogs grafted 48 hours; after aspirin or 7E3-F(ab')(2) injection, patency at 24 hours was seen in 0 of 5 dogs given aspirin and 3 of 5 dogs given 7E3-F(ab')(2) The overall frequencies of arterial graft patency at 2, 24, 48, and 72 hours after study drug injection were significantly higher in the 7E3-F(ab')(2) groups than in the aspirin groups (P<.0005, n=10 in each group; P<.05, n=15; P<.005, n=15; and P=.05, n=5, respectively). ADP-induced ex vivo platelet aggregation was abolished after 7E3-F(ab')(2) injection with partial recovery (approximately 20%; P=.01 versus baseline) within 24 hours and complete recovery (P=not significant versus baseline) within 48 hours. Pathological examination of patent everted grafts revealed significant residual mural thrombus in all groups. Thus, 7E3-F(ab')(2) reduced platelet-rich arterial eversion graft thrombosis, and this effect persisted beyond normalization of bleeding time prolongation and inhibition of ex vivo platelet aggregation. Mural thrombus deposition still occurred with 7E3-F(ab')(2), but vascular occlusion was markedly reduced. C1 UNIV LEUVEN,CTR MOLEC & VASC BIOL,LOUVAIN,BELGIUM. UNIV LEUVEN,DEPT HISTOPATHOL,LOUVAIN,BELGIUM. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA. CLEVELAND CLIN FDN,CTR THROMBOSIS & VASC BIOL,CLEVELAND,OH. NR 47 TC 13 Z9 13 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1049-8834 J9 ARTERIOSCLER THROMB JI Arterioscler. Thromb. PD MAR PY 1994 VL 14 IS 3 BP 367 EP 374 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA NA955 UT WOS:A1994NA95500007 PM 8123640 ER PT J AU KISS, RG STASSEN, JM DECKMYN, H ROSKAMS, T GOLD, HK PLOW, EF COLLEN, D AF KISS, RG STASSEN, JM DECKMYN, H ROSKAMS, T GOLD, HK PLOW, EF COLLEN, D TI CONTRIBUTION OF PLATELETS AND THE VESSEL WALL TO THE ANTITHROMBOTIC EFFECTS OF A SINGLE BOLUS INJECTION OF FAB FRAGMENTS OF THE ANTIPLATELET GPIIB/IIIA ANTIBODY 7E3 IN A CANINE ARTERIAL EVERSION GRAFT PREPARATION SO ARTERIOSCLEROSIS AND THROMBOSIS LA English DT Article DE ARTERIAL THROMBOSIS; ANTIPLATELET AGENTS; ANTI-GPIIB/IIIA ANTIBODY; ARTERIAL PATENCY; VESSEL WALL PASSIVATION ID ACUTE MYOCARDIAL-INFARCTION; PLASMINOGEN-ACTIVATOR; F(AB')2 FRAGMENTS; INHIBITION; RECANALIZATION; STREPTOKINASE; ANGIOPLASTY; EXPRESSION; FIBRINOGEN; RECEPTOR AB The contribution of platelets and the vessel wall to the antithrombotic effects of a single intravenous bolus injection of 0.8 mg/kg Fab fragments of the monoclonal antiplatelet glycoprotein IIb/IIIa receptor antibody 7E3 (7E3-Fab), combined with continuous heparin anticoagulation (100 U/kg bolus and 50 U/kg per hour), was studied in a canine preparation consisting of an everted (inside out) carotid arterial segment that had been inserted into a transected femoral artery. In all 6 control dogs without antibody, persistent or transient eversion graft occlusion occurred during an initial 2-hour observation period, and 5 of the 6 grafts were occluded at 24 hours. In 6 dogs given 7E3-Fab 24 hours before receiving an everted carotid artery segment from a donor dog, cyclic occlusion and reflow occurred in all dogs, whereas the grafts were patent at the end of a 2-hour observation period in 5 of the 6 dogs (P=.056 versus control). When transferred back to the donor dogs, the patent eversion segments showed brief periods of cyclic occlusion and reflow within 2 hours in 3 of 5 dogs (P=.034 versus control), whereas all of the 5 eversion segments were patent at 24 hours (P<.005 versus control). When platelet concentrates (prepared 48 hours after injection of the antibody fragment from approximately 50% of the blood volume of the dogs given 7E3-Fab) were transfused into animals with eversion grafts 10 minutes before vessel clamp release, persistent or transient occlusion was observed within 2 hours in all 5 dogs (P=not significant versus control), but 4 of these 5 grafts were patent at 24 hours (P=.045 versus control). ADP-induced platelet aggregation and bleeding times remained normal throughout the eversion grafting experiments in all dogs. Thus, long-term or even short-term exposure of eversion grafts to platelets treated with 7E3-Fab conferred reduced thrombogenicity. C1 UNIV LEUVEN,CTR MOLEC & VASC BIOL,B-3000 LOUVAIN,BELGIUM. UNIV LEUVEN,DEPT HISTOPATHOL,LOUVAIN,BELGIUM. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA. CLEVELAND CLIN FDN,CTR THROMBOSIS & VASC BIOL,CLEVELAND,OH. RI Deckmyn, Hans/L-9434-2015 OI Deckmyn, Hans/0000-0003-3952-5501 NR 23 TC 23 Z9 23 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1049-8834 J9 ARTERIOSCLER THROMB JI Arterioscler. Thromb. PD MAR PY 1994 VL 14 IS 3 BP 375 EP 380 PG 6 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA NA955 UT WOS:A1994NA95500008 PM 8123641 ER PT J AU ALCANTARA, O REDDY, SV ROODMAN, GD BOLDT, DH AF ALCANTARA, O REDDY, SV ROODMAN, GD BOLDT, DH TI TRANSCRIPTIONAL REGULATION OF THE TARTRATE-RESISTANT ACID-PHOSPHATASE (TRAP) GENE BY IRON SO BIOCHEMICAL JOURNAL LA English DT Article ID LYMPHOBLASTOID T-CELLS; MESSENGER-RNA; TRANSFERRIN RECEPTOR; EXPRESSION; PROTEIN; INDUCTION; UTEROFERRIN; FERRITIN; PROGESTERONE; ISOENZYME AB Tartrate-resistant acid phosphatase (TRAP) was first identified in cells from patients with hairy cell leukaemia. Subsequently, it has been found in other leukaemias, B-lymphoblastoid cell lines, osteoclasts and subsets of normal lymphocytes, macrophages, and granulocytes. Recent data indicate that TRAP and porcine uteroferrin, a placental iron-transport protein, represent a single gene product. However, the intracellular role of TRAP is unknown. We used a full-length human placental TRAP cDNA probe to examine TRAP expression in human peripheral mononuclear cells (PMCs). TRAP mRNA increased 50-75-fold after 24 h in unstimulated PMC cultures. Cell-fractionation experiments indicated that monocytes were the main cell population accounting far increased TRAP mRNA transcripts, and this was confirmed by histochemical staining for TRAP enzyme activity. Because expression of other iron-binding and -transport proteins is controlled by iron availability, we examined the role of iron in regulating TRAP expression. Increase of TRAP mRNA transcripts in PMCs was inhibited by 50 mu M desferrioxamine, a potent iron chelator. The 5' flanking region of the TRAP gene was cloned from a mouse genomic library. In preliminary transient transfection experiments, it was determined that the 5'-flanking region of the TRAP gene contained iron-responsive elements. Therefore, a series of stably transfected HRE H9 cell lines was developed bearing genetic constructs containing various segments of the murine TRAP 5' promoter region driving a luciferase reporter gene. Treatment of transfectants with 100 mu g/ml iron-saturated human transferrin (FeTF) was performed to assess iron responsiveness of the constructs. Constructs containing a full-length TRAP promoter (comprising base pairs -1846 to +2) responded to FeTF with a 4-5-fold increase of luciferase activity whereas constructs containing only base pairs -363 to +2 of the TRAP promoter did not respond. Constructs containing 1240 or 881 bp of the TRAP promoter gave only a 1.5- to 2-fold increase of luciferase activity with FeTF. In all cases, increase of luciferase activity was blocked by desferrioxamine. Cells transfected with another luciferase construct driven by a simian virus 40 promoter did not show any increase of luciferase activity with FeTF. These data indicate that expression of TRAP is regulated by iron and that this regulation is exerted at the level of gene transcription. The transfection experiments also suggest that the region of the TRAP 5'-flanking sequence between base pairs - 1846 and - 1240 contains an iron regulatory element. C1 UNIV TEXAS,AUDIE L MURPHY VET ADM HOSP,HLTH SCI CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV HEMATOL,SAN ANTONIO,TX 78284. FU NIADDK NIH HHS [AM 35188]; NIAMS NIH HHS [AR 3539, AR 41336] NR 31 TC 32 Z9 32 U1 0 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD MAR 1 PY 1994 VL 298 BP 421 EP 425 PN 2 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA073 UT WOS:A1994NA07300026 PM 8135751 ER PT J AU XU, X QIN, XQ KANTROWITZ, ER AF XU, X QIN, XQ KANTROWITZ, ER TI PROBING THE ROLE OF HISTIDINE-372 IN ZINC-BINDING AND THE CATALYTIC MECHANISM OF ESCHERICHIA-COLI ALKALINE-PHOSPHATASE BY SITE-SPECIFIC MUTAGENESIS SO BIOCHEMISTRY LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; PHENOTYPIC SELECTION; ACTIVE-SITE; P-31; RESOLUTION; CD-113; NMR; PH AB In the X-ray structure of Escherichia coli alkaline phosphatase at 2.0-Angstrom resolution, His-372 was found only 3.8 Angstrom away from the zinc and forms a hydrogen-bonding interaction with Asp-327, a bidentate ligand of the zinc at the M1 site. However, His-372 does not directly interact with the zinc atom at the M1 site. In order to investigate the role of the side chain of His-372 in zinc binding and the catalytic mechanism of Escherichia coli alkaline phosphatase, site-directed mutagenesis was used to convert His-372 to alanine. The fact that the His-372-->Ala enzyme has similar zinc binding affinity as the wild-type enzyme indicates that His-372 is not involved in zinc binding at the M1 site. However, the altered kinetic behavior of the mutant enzyme compared to the wild-type enzyme suggests that the imidazole ring of His-372 plays an indirect role in the catalytic mechanism of the enzyme. The hydrolysis activity of the His-372-->Ala enzyme at pH 8.0 is 10-fold lower than that of the wild-type enzyme. In the presence of a phosphate acceptor at pH 8.0, the mutant enzyme is approximately 80% as active as the wild-type enzyme. Therefore, the His-372-->Ala mutation selectively enhances the transphosphorylation activity of the enzyme. The His-372-->Ala enzyme also exhibits 4- and 30-fold decreases in K-m as compared to the wild-type enzyme in 0.1 M MOPS buffer and 1.0 M Tris, buffer at pH 8.0, respectively. A change in the rate-determining step at pH 8.0 is also observed for the His-372-->Ala enzyme compared with the wild-type enzyme. The presence of a transient burst in the pre-steady-state kinetics of the His-372-->Ala enzyme indicates that breaking of the covalent phosphoserine bond is the rate-limiting step in the reaction. The lack of incorporation of [P-32]P-i into the His-372-->Ala enzyme at pH 8.0 suggests the presence of a stable intermediate during the transition from the enzyme-phosphate covalent complex to the enzyme-phosphate noncovalent complex. Taken together, these kinetic results suggest that the hydroxyl group coordinated to the zinc atom at the M1 site is a weaker nucleophile in the His-372-->Ala enzyme than in the wild-type enzyme. Therefore, the interaction between the side chain of His-372 and Asp-327 may be important for stabilizing the zinc hydroxyl which is the nucleophilic group that is responsible for the breakdown of the phosphoserine intermediate. C1 BOSTON COLL, DEPT CHEM, CHESTNUT HILL, MA 02167 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. FU NIGMS NIH HHS [GM42833] NR 46 TC 15 Z9 16 U1 1 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 1 PY 1994 VL 33 IS 8 BP 2279 EP 2284 DI 10.1021/bi00174a039 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MZ093 UT WOS:A1994MZ09300039 PM 8117685 ER PT J AU LIPSITZ, SR LAIRD, NM HARRINGTON, DP AF LIPSITZ, SR LAIRD, NM HARRINGTON, DP TI WEIGHTED LEAST-SQUARES ANALYSIS OF REPEATED CATEGORICAL MEASUREMENTS WITH OUTCOMES SUBJECT TO NONRESPONSE SO BIOMETRICS LA English DT Article DE MISSING AT RANDOM; MISSING COMPLETELY AT RANDOM; MISSING DATA MECHANISM; REPEATED MEASURES; WEIGHTED LEAST SQUARES ID CONTINGENCY-TABLES; MAXIMUM-LIKELIHOOD; LONGITUDINAL DATA; MISSING DATA AB In this paper, we describe a two-step weighted least squares method for analyzing repeated categorical outcomes when some individuals are not observed at all times of follow-up. Other weighted least squares methods for analyzing repeated measures data with missing responses have previously been proposed by Koch, Imrey, and Reinfurt (1972, Biometrics 28, 663-692) and Woolson and Clarke (1984, Journal of the Royal Statistical Society, Series A 147, 87-99). These methods give consistent estimators if the responses are missing completely at random, as discussed in Rubin (1976, Biometrika 63, 581-592). We propose a two-step method that will give consistent results under the weaker condition of missing at random, and compare it with the other two methods. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP LIPSITZ, SR (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI 24643]; NIGMS NIH HHS [GM 29745]; OID CDC HHS [CH 39929] NR 18 TC 19 Z9 19 U1 0 U2 1 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 1994 VL 50 IS 1 BP 11 EP 24 DI 10.2307/2533193 PG 14 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA NH265 UT WOS:A1994NH26500002 PM 8086595 ER PT J AU GRAY, RJ AF GRAY, RJ TI A BAYESIAN-ANALYSIS OF INSTITUTIONAL EFFECTS IN A MULTICENTER CANCER CLINICAL-TRIAL SO BIOMETRICS LA English DT Article DE CENSORED FAILURE TIME DATA; GIBBS SAMPLING; HIERARCHICAL MODELS; PROPORTIONAL HAZARDS ID GEOGRAPHIC-VARIATION; BREAST-CANCER; MODELS; INFERENCE AB This paper examines a Bayesian method for investigating the amount of institutional variation in a multicenter clinical trial with a censored failure time endpoint. A hierarchical structure is used to model the institutional effects in a proportional hazards model, with the posterior distributions calculated using Gibbs sampling. The methods are applied to data from a lung cancer trial conducted by the Eastern Cooperative Oncology Group. In this trial there appears to be substantial variation in the treatment effect across institutions. Although the reasons for this have not been identified, it would be possible to investigate this further through a detailed examination of the data from institutions with extreme effects. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RP GRAY, RJ (reprint author), DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-39929, CA-51962, CA-57253] NR 13 TC 56 Z9 57 U1 0 U2 3 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 1994 VL 50 IS 1 BP 244 EP 253 DI 10.2307/2533216 PG 10 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA NH265 UT WOS:A1994NH26500025 PM 8086608 ER PT J AU LIPSITZ, SR FITZMAURICE, GM ORAV, EJ LAIRD, NM AF LIPSITZ, SR FITZMAURICE, GM ORAV, EJ LAIRD, NM TI PERFORMANCE OF GENERALIZED ESTIMATING EQUATIONS IN PRACTICAL SITUATIONS SO BIOMETRICS LA English DT Article DE CORRELATED BINARY DATA; MARGINAL MODELS; REPEATED MEASURES; ROBUST VARIANCE ID BINARY DATA AB Moment methods for analyzing repeated binary responses have been proposed by Liang and Zeger (1986, Biometrika 73, 13-22), and extended by Prentice (1988, Biometrics 44, 1033-1048). In their generalized estimating equations (GEE), both Liang and Zeger (1986) and Prentice (1988) estimate the parameters associated with the expected value of an individual's vector of binary responses as well as the correlations between pairs of binary responses. In this paper, we discuss one-step estimators, i.e., estimators obtained from one step of the generalized estimating equations, and compare their performance to that of the fully iterated estimators in small samples. In simulations, we find the performance of the one-step estimator to be qualitatively similar to that of the fully iterated estimator. When the sample size is small and the association between binary responses is high, we recommend using the one-step estimator to circumvent convergence problems associated with the fully iterated GEE algorithm. Furthermore, we find the GEE methods to be more efficient than ordinary logistic regression with variance correction for estimating the effect of a time-varying covariate. C1 DANA FARBER CANC INST,BOSTON,MA. RP LIPSITZ, SR (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 8 TC 117 Z9 118 U1 3 U2 8 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 1994 VL 50 IS 1 BP 270 EP 278 DI 10.2307/2533218 PG 9 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA NH265 UT WOS:A1994NH26500027 PM 8086610 ER PT J AU BOLAND, LM JURMAN, ME YELLEN, G AF BOLAND, LM JURMAN, ME YELLEN, G TI CYSTEINES IN THE SHAKER K+ CHANNEL ARE NOT ESSENTIAL FOR CHANNEL ACTIVITY OR ZINC MODULATION SO BIOPHYSICAL JOURNAL LA English DT Article ID DNA-BINDING DOMAIN; POTASSIUM CHANNEL; TRANSCRIPTION FACTOR; SITE; INACTIVATION; COORDINATION; MUTAGENESIS; MECHANISMS; MUTATIONS; RESIDUES AB We investigated whether the cysteine residues in Shaker potassium (K+) channels are essential for activation and inactivation gating or for modulation of activation gating by external zinc (Zn2+). Mutants of the Shaker K+ channel were prepared in which all seven cysteine residues were replaced (C-less). These changes were made in both wild-type Shaker H4 channels and in a deletion mutant (Delta 6-46) lacking N-type (''fast'') inactivation. Replacement of all cysteines left most functional properties of the K+ currents unaltered. The most noticeable difference between the C-less and wild-type currents was the faster C-type inactivation of the C-less channel which could be attributed largely to the mutation of Cys(462). This is consistent with the effects of previously reported mutations of nearby residues in the S6 region. There were also small changes in the activation gating of C-less currents. Modulation by external Zn2+ of the voltage dependence and rate of activation gating is preserved in the C-less channels, indicating that none of the cysteines in the Shaker K+ channel plays an important role in Zn2+ modulation. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROBIOL,MOLEC PHYSIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02114. OI Yellen, Gary/0000-0003-4228-7866 FU NINDS NIH HHS [NS09272, NS29693, R01 NS029693] NR 25 TC 35 Z9 35 U1 0 U2 3 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD MAR PY 1994 VL 66 IS 3 BP 694 EP 699 PN 1 PG 6 WC Biophysics SC Biophysics GA MZ353 UT WOS:A1994MZ35300015 PM 8011900 ER PT J AU GIBSON, F LEHRACH, H BUCKLER, AJ BROWN, SDM NORTH, MA AF GIBSON, F LEHRACH, H BUCKLER, AJ BROWN, SDM NORTH, MA TI ISOLATION OF CONSERVED SEQUENCES FROM YEAST ARTIFICIAL CHROMOSOMES BY EXON AMPLIFICATION SO BIOTECHNIQUES LA English DT Note ID CDNA; SELECTION; LIBRARY; ELEMENT; CLONES; DNA AB Exon amplification is a technique designed to solve a central problem in mammalian molecular genetics-specifically, the isolation of genes from large regions of genomic DNA. This technique allows exons to be isolated from genomic DNA following the selective removal of introns by the eukaryotic splicing mechanism. It is a relatively rapid procedure and can theoretically be applied to test the coding potential of very long stretches of genomic DNA. In this paper we describe the application of exon amplification to a mouse yeast artificial chromosome (YAC) 175 kb in length. A number of potential coding sequences were amplified and two sequences were shown to be conserved across a wide variety of species representing potential genes. C1 IMPERIAL COLL SCI TECHNOL & MED,ST MARYS HOSP,SCH MED,DEPT BIOCHEM & MOLEC GENET,LONDON W2 1PG,ENGLAND. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 12 TC 6 Z9 6 U1 0 U2 2 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD MAR PY 1994 VL 16 IS 3 BP 453 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA429 UT WOS:A1994NA42900025 PM 8185919 ER PT J AU SHIPP, MA AF SHIPP, MA TI PROGNOSTIC FACTORS IN AGGRESSIVE NON-HODGKINS-LYMPHOMA - WHO HAS HIGH-RISK DISEASE SO BLOOD LA English DT Review ID LARGE-CELL LYMPHOMA; DIFFUSE HISTIOCYTIC LYMPHOMA; BONE-MARROW TRANSPLANTATION; SOUTHWEST-ONCOLOGY-GROUP; M-BACOD; B-CELL; COMBINATION CHEMOTHERAPY; MALIGNANT-LYMPHOMA; HOMING RECEPTOR; LNH-84 REGIMEN C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SHIPP, MA (reprint author), DANA FARBER CANC INST,DEPT MED,44 BINNEY ST,BOSTON,MA 02115, USA. NR 102 TC 207 Z9 214 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1994 VL 83 IS 5 BP 1165 EP 1173 PG 9 WC Hematology SC Hematology GA MZ289 UT WOS:A1994MZ28900002 PM 8118021 ER PT J AU LEE, I BOUCHER, Y DEMHARTNER, TJ JAIN, RK AF LEE, I BOUCHER, Y DEMHARTNER, TJ JAIN, RK TI CHANGES IN TUMOR BLOOD-FLOW, OXYGENATION AND INTERSTITIAL FLUID PRESSURE-INDUCED BY PENTOXIFYLLINE SO BRITISH JOURNAL OF CANCER LA English DT Article ID FLUOSOL-DA 20-PERCENT; HYPERTENSION; MACROMOLECULES; NICOTINAMIDE; TRANSPORT; CARCINOMA; NECROSIS; PHASE; RATS AB Pentoxifylline (PTX) has been shown to increase radiation damage to tumours and to decrease late radiation-induced injury to normal tissues. This tumour radiation sensitisation results from increased oxygen supply via improved tumour perfusion. We propose that the improved perfusion results from decreased viscous resistance and/or geometric resistance. The decreased flow resistance may be accompanied by a reduction in microvascular pressure (MVP). Since MVP is approximately equal to the interstitial fluid pressure (IFP), PTX should lead to a decrease in IFP. To test this hypothesis, we measured Po-2, laser Doppler flow (RBC flux) and IFP in FSaII murine tumours at two doses (PTX at 25 and 100 mg per kg body weight) which sensitise this tumour to X-irradiation. We found that 25 mg kg(-1) PTX was ineffective, but 100 mg kg(-1) PTX was effective in increasing the Po-2 of this tumour. PTX at 100 mg kg(-1) (i.p.) increased median Pot from 5 to 7 mmHg (P<0.05) within 2h, and decreased the fraction of Po-2 values <5mmHg from 65% to 45% (P<0.05). In support of our hypothesis, we found that with this dose of PTX, RBC Aux in the tumour centre increased significantly (n = 6, P<0.05) prior to an similar to 40% decrease (n = 13, P<0.05) in tumour interstitial fluid pressure (TIFP), without changes in mean arterial blood pressure (MABP). In conclusion, a single i.p. administration of PTX at 100 mg kg(-1) can increase oxygen availability in the tumour due to temporarily increased RBC flux in the tumour centre, where pretreatment flow is relatively low, and thus ameliorate hypoxia in tumour microregions. Second, PTX can lower the elevated TIFP without lowering the MABP. RP LEE, I (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [R35-CA-56591] NR 36 TC 66 Z9 67 U1 1 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD MAR PY 1994 VL 69 IS 3 BP 492 EP 496 DI 10.1038/bjc.1994.89 PG 5 WC Oncology SC Oncology GA NA001 UT WOS:A1994NA00100014 PM 8123479 ER PT J AU VANDERKOLK, BA FISLER, RE AF VANDERKOLK, BA FISLER, RE TI CHILDHOOD ABUSE AND NEGLECT AND LOSS OF SELF-REGULATION SO BULLETIN OF THE MENNINGER CLINIC LA English DT Article; Proceedings Paper CT 15th Annual Menninger Winter Psychiatry Conference CY MAR 07-12, 1993 CL PARK CITY, UT ID POSTTRAUMATIC-STRESS-DISORDER; BORDERLINE PERSONALITY-DISORDER; DISSOCIATIVE DISORDERS; RHESUS-MONKEYS; CHILDREN; SEPARATION; RESPONSES; VIOLENCE; BEHAVIOR; TRAUMA AB Secure attachments with caregivers play a critical role in helping children develop a capacity to modulate physiological arousal. Loss of ability to regulate the intensity of feelings and impulses is possibly the most far-reaching effect of trauma and neglect. It has been shown that most abused and neglected children develop disorganized attachment patterns. The inability to modulate emotions gives rise to a range of behaviors that are best understood as attempts at self-regulation. These include aggression against others, self-destructive behavior, eating disorders, and substance abuse. The capacity to regulate internal states affects both self-definition and one's attitude toward one's surroundings. Abused children often fail to develop the capacity to express specific and differentiated emotions: Their difficulty putting feelings into words interferes with flexible response strategies and promotes acting out. Usually, these behaviors coexist, which further complicates diagnosis and treatment. Affective dysregulation can be mitigated by safe attachments, secure meaning schemes, and pharmacological interventions that enhance the predictability of somatic responses to stress. The ability to create symbolic representations of terrifying experiences promotes taming of terror and desomatization of traumatic memories. RP VANDERKOLK, BA (reprint author), MASSACHUSETTS GEN HOSP,ERICH LINDEMANN MENTAL HLTH CTR,TRAUMA CLIN,25 STANIFORD ST,BOSTON,MA 02114, USA. NR 91 TC 163 Z9 163 U1 11 U2 37 PU MENNINGER FOUNDATION PI TOPEKA PA BOX 829, TOPEKA, KS 66601 SN 0025-9284 J9 B MENNINGER CLIN JI Bull. Menninger Clin. PD SPR PY 1994 VL 58 IS 2 BP 145 EP 168 PG 24 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA NL772 UT WOS:A1994NL77200002 PM 7519094 ER PT J AU ROSENBAUM, JF POLLOCK, RA AF ROSENBAUM, JF POLLOCK, RA TI THE PSYCHOPHARMACOLOGY OF SOCIAL PHOBIA AND COMORBID DISORDERS SO BULLETIN OF THE MENNINGER CLINIC LA English DT Article; Proceedings Paper CT Menninger Symposium on Fear of Humiliation: Integrated Treatment of Social Phobia and Comorbid Conditions, held during Annual of the American-Psychiatric-Association CY MAY 21-26, 1994 CL PHILADELPHIA, PA SP MENNINGER FDN, AMER PSYCHIAT ASSOC ID OBSESSIVE-COMPULSIVE DISORDER; R ANXIETY DISORDERS; PANIC DISORDER; MAJOR DEPRESSION; BEHAVIORAL-INHIBITION; CLONAZEPAM; PHENELZINE; CHILDREN; AGORAPHOBIA; FLUOXETINE AB The pharmacotherapy of social phobia includes agents from different classes with different mechanisms of action and has recently become the focus of more attention in the research community. The authors highlight drug treatments with reported efficacy, including: (1) certain antidepressants: monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and other antidepressants not yet available in the United States such as reversible inhibitors of MAO-A; (2) high-potency benzodiazepines; and (3) beta-adrenergic blocking drugs (mainly for performance anxiety). The frequent co-occurrence of social phobia with other psychiatric disorders often complicates patient management, treatment, and outcome. Rates of comorbidity, principles of pharmacotherapy for the comorbid condition, and the potential advantages and disadvantages of the aforementioned agents in social phobia patients suffering comorbid disorders are discussed. RP ROSENBAUM, JF (reprint author), MASSACHUSETTS GEN HOSP,15 PARKMAN ST,WACC 815,BOSTON,MA 02114, USA. NR 63 TC 12 Z9 12 U1 5 U2 6 PU MENNINGER FOUNDATION PI TOPEKA PA BOX 829, TOPEKA, KS 66601 SN 0025-9284 J9 B MENNINGER CLIN JI Bull. Menninger Clin. PD SPR PY 1994 VL 58 IS 2 SU A BP A67 EP A83 PG 17 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA NM496 UT WOS:A1994NM49600006 PM 7913851 ER PT J AU LO, SH CHEN, LB AF LO, SH CHEN, LB TI FOCAL ADHESION AS A SIGNAL-TRANSDUCTION ORGANELLE SO CANCER AND METASTASIS REVIEWS LA English DT Review DE FOCAL ADHESION; SIGNAL TRANSDUCTION ORGANELLE ID ROUS-SARCOMA VIRUS; PROTEIN-TYROSINE KINASE; PHOSPHOTYROSINE-CONTAINING PROTEINS; EPIDERMAL GROWTH-FACTOR; ACTIN-BINDING PROTEINS; CRK ONCOGENE PRODUCT; END-BOUND INSERTIN; SRC GENE-PRODUCT; CELL-ADHESION; ALPHA-ACTININ C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MAYER 840,44 BINNEY ST,BOSTON,MA 02115. NR 143 TC 94 Z9 96 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-7659 J9 CANCER METAST REV JI Cancer Metastasis Rev. PD MAR PY 1994 VL 13 IS 1 BP 9 EP 24 DI 10.1007/BF00690415 PG 16 WC Oncology SC Oncology GA MN723 UT WOS:A1994MN72300002 PM 8143347 ER PT J AU EWEN, ME AF EWEN, ME TI THE CELL-CYCLE AND THE RETINOBLASTOMA PROTEIN FAMILY SO CANCER AND METASTASIS REVIEWS LA English DT Review DE TUMOR SUPPRESSOR; RETINOBLASTOMA PROTEIN; P107; TRANSCRIPTION FACTOR-E2F; CYCLIN DEPENDENT KINASE; TRANSFORMING GROWTH FACTOR-BETA ID LARGE-T-ANTIGEN; SUSCEPTIBILITY GENE-PRODUCT; TRANSCRIPTION FACTOR E2F; SV40 LARGE-T; VIRUS-40 LARGE-T; TUMOR-SUPPRESSOR PROTEIN; ADENOVIRUS E1A PROTEINS; DNA-BINDING ACTIVITY; GROWTH-FACTOR-BETA; C-MYC AB Tumor formation results from alterations in the control of normal cell proliferation. To further our understanding of the molecular mechanisms underlying the deregulation of cell proliferation much attention, over the past decade, has been focused on the function of proto-oncogenes. Cellular oncogenes are thought to be growth promoting. More recently, a class of genes known as tumor suppressors have come under intense study. Tumor suppressors are largely thought to restrain cell proliferation. The retinoblastoma protein (Rb) is one of a growing list of tumor suppressors. Concurrent with the study of tumor suppressor genes has been a rapid increase in our understanding of the cell cycle at the molecular level. Rb and a related protein p107 are involved in the processes of cell proliferation and differentiation. Each functionally interacts with and affects the activity of the transcription factor E2F as well as other transcription factors involved in cell proliferation and differentiation. Additionally, Rb and p107 are modified by, and/or form specific complexes with, several elements of the basic cell cycle machinery. Specifically, Rb and p107 interact with and are modified by various cyclins and cyclin dependent kinases (cdk), some of which have been shown to be essential for cell cycle progression and in some cases their deregulation has been implicated in the development of cancer. This review will attempt to convey our current functional and mechanistic understanding of the biological roles Rb and p107 play in proliferation, development and differentiation. A knowledge of the interplay between these positive and negative regulators of cell proliferation and differentiation, noted above, is central to our understanding of human cancer. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP EWEN, ME (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 185 TC 173 Z9 176 U1 1 U2 6 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-7659 J9 CANCER METAST REV JI Cancer Metastasis Rev. PD MAR PY 1994 VL 13 IS 1 BP 45 EP 66 DI 10.1007/BF00690418 PG 22 WC Oncology SC Oncology GA MN723 UT WOS:A1994MN72300005 PM 8143345 ER PT J AU WILLIAMS, NG ROBERTS, TM AF WILLIAMS, NG ROBERTS, TM TI SIGNAL-TRANSDUCTION PATHWAYS INVOLVING THE RAF PROTOONCOGENE SO CANCER AND METASTASIS REVIEWS LA English DT Review DE RAF; PROTEIN KINASE; BACULOVIRUS; MAP KINASE ID NERVE GROWTH-FACTOR; COMPLETE CODING SEQUENCE; COLONY-STIMULATING FACTOR; SERINE THREONINE KINASE; MAP KINASE; C-RAF; TYROSINE PHOSPHORYLATION; B-RAF; REGULATED KINASES; V-RAF AB The raf genes encode for a family of cytoplasmic proteins (A-raf, B-raf and c-raf-1), with associated serine/threonine kinase activities. Raf-1 is an important mediator of signals involving cell growth, transformation and differentiation. It is activated in response to a wide variety of extracellular stimuli such as insulin, nerve growth factor (NGF), platelet derived-growth factor (PDGF), and in response to expression of oncogenes, v-src and v-ras, in a cell-specific manner. Recently, the first physiological substrate for Raf-1 protein kinase was identified. Raf-1 was found to phosphorylate and activate Mitogen-Activated Protein Kinase Kinase (MEK), an activator of MAP kinase, thus linking the Raf-1 signaling pathway with that of MAP kinase. Cell specific differences in signalling pathways involving Raf-1 and MAP kinase have also been discovered. Accumulating evidence indicates that membrane tyrosine kinases, ras, Raf-1, MEK and MAP kinase are interconnected via a complex network rather than via a linear pathway involving multiple substrates and feedback loops. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MAYER 856,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 98 TC 86 Z9 86 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-7659 J9 CANCER METAST REV JI Cancer Metastasis Rev. PD MAR PY 1994 VL 13 IS 1 BP 105 EP 116 DI 10.1007/BF00690421 PG 12 WC Oncology SC Oncology GA MN723 UT WOS:A1994MN72300008 PM 8143342 ER PT J AU TEICHER, BA KORBUT, TT MENON, K HOLDEN, SA ARA, G AF TEICHER, BA KORBUT, TT MENON, K HOLDEN, SA ARA, G TI CYCLOOXYGENASE AND LIPOXYGENASE INHIBITORS AS MODULATORS OF CANCER THERAPIES SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article ID LEWIS LUNG-CARCINOMA; GLUTATHIONE S-TRANSFERASES; CELL-LINES; PROSTAGLANDIN BIOSYNTHESIS; THROMBOXANE SYNTHESIS; TUMOR-METASTASIS; BINDING-SITES; MURINE TUMORS; DNA-SYNTHESIS; COLON CANCER AB Like many clinical non-small-cell lung cancers, the Lewis lung carcinoma produces prostaglandins. The Lewis lung carcinoma was used as a model of both primary and metastatic disease to assess the ability of cyclooxygenase inhibitors (mefenamic acid, diflunisal, sulindac, and indomethacin), the collagenase inhibitor minocycline, and the lipoxygenase inhibitor phenidone to act as modulators of cytotoxic cancer therapies. Although none of the single modulators given i.p. daily on days 4-18 altered tumor growth or the number of metastases found on day 20, modulator combinations consisting of minocycline/a cyclooxygenase inhibitor and, especially, of phenidone/a cyclooxygenase inhibitor resulted in modest tumor growth delay and a decreased number of lung metastases on day 20. The most effective modulators of cisplatin (CDDP) were phenidone/sulindac and phenidone/indomethacin, which led to 2.4- to 2.5-fold increases in the tumor growth delay produced by CDDP. The most effective modulations of cyclophosphamide resulted from administration of minocycline, minocycline/sulindac, or phenidone/sulindac and led to 2.0- to 2.1-fold increases in tumor growth delay by cyclophosphamide. The most effective modulators of melphalan produced 4.5- to 4.7-fold increases in tumor growth delay by the drug and were minocycline/sulindac, minocycline/mefenamic acid, and phenidone/sulindac. The most effective modulation of carmustine (BCNU) was obtained with minocycline/sulindac and minocycline/diflunisal leading to 2.8- to 3.1-fold increases in tumor growth delay by BCNU. Finally, the most effective modulation of radiation was obtained with minocycline/sulindac and phenidone/sulindac and resulted in 2.8- to 3.3-fold increases in tumor growth delay by radiation. The modulator combination that along with the cytotoxic therapies was most effective against metastatic disease was phenidone/mefenamic acid. There was no clear relationship between effective modulation of the cancer therapies and the degree of reduction in serum levels of prostaglandin E(2) and leukotriene B-4 by the agents in Lewis lung tumor bearing mice. 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-CA19589, P01-CA38493] NR 74 TC 43 Z9 45 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD MAR PY 1994 VL 33 IS 6 BP 515 EP 522 DI 10.1007/BF00686511 PG 8 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA NA059 UT WOS:A1994NA05900014 PM 8137463 ER PT J AU CINCOTTA, L FOLEY, JW MACEACHERN, T LAMPROS, E CINCOTTA, AH AF CINCOTTA, L FOLEY, JW MACEACHERN, T LAMPROS, E CINCOTTA, AH TI NOVEL PHOTODYNAMIC EFFECTS OF A BENZOPHENOTHIAZINE ON 2 DIFFERENT MURINE SARCOMAS SO CANCER RESEARCH LA English DT Article ID NECROSIS-FACTOR-ALPHA; MOUSE-TUMOR MODEL; NORMAL TISSUE; MALIGNANT-TUMORS; CELL-SURVIVAL; MAMMARY-TUMOR; CANCER-CELLS; THERAPY; OXYGEN; HEMATOPORPHYRIN AB The photochemotherapeutic properties of a novel benzophenothiazine, 5-ethylamino-9-diethylaminobenzo[alpha]phenothiazinium chloride, were assessed in vitro and in vivo against tao murine mammary sarcoma models (EMT-6 and RIF). Photodynamic therapy (PDT) of EMT-6 and RIF cells following a 30-min incubation with dye (0.4 mu g/ml) and a light dose of 3.3 J/cm(2) killed 87.0 and 99.6% of the cells, respectively. Over this same time period, RIF cells accumulate more than twice the amount of dye than the EMT-6 cell Line [7.54 +/- 0.17 (SD) versus 3.11 +/- 0.15 nmol/10(6) cells] which probably accounts for their increased sensitivity to PDT. Conversely, in vivo, the EMT-6 tumor accumulates 3 times more dye (34.66 +/- 2.16 mu g/g dry weight) than the RIF tumor (12.28 +/- 1.27 mu g of dye/g) 3 h post-s.c. injection of dye (15 mg/kg). A study of the concentration dependent uptake of dye (following s.c. injection) in the tumor and plasma of mice bearing the EMT-6 tumor indicated a nonlinear relationship for both compartments. Maximum tissue uptake of dye and discrimination between tumor and skin or muscle occur 3-8 h following s.c. injection of dye. The ratios of dye in the tumor to the dye in surrounding skin and gastrocnemius muscle 8 h following dye injection were 4:1 and 8:1, respectively. At 24 h after dye injection, the dye was not detectable by absorption spectroscopy in the tumor, skin, or muscle. Decreasing the fluence rate from 200 to 50 mW/cm(2) at a total light dose of 100 J/cm(2) optimized the PDT effect. At 3 h following s.c. administration of dye, PDT of EMT-6 (7.5 mg of dye/kg; 50 mW/cm(2); 100 J/cm(2)) and RIF tumors (15 mg dye/kg; 50 mW/cm(2); 150 J/cm(2)) resulted in 100 and 70% cures, respectively. Histology at 24 and 72 h post-PDT showed minimal or no damage to the surrounding tissue (skin) while 70-90% of the tumor cells were destroyed or damaged. Moreover, 50-60% of the tumor cells isolated and cultured immediately following PDT were found to be nonviable. Similarly, the administration of 60 mg 5-ethylamino-9-diethylaminabenzo[alpha]phenothiazinium chloride/kg also resulted in no damage to the skin 24 h following PDT. It is suggested that the redox properties of the dye coupled with the differing metabolic states of the tumor and skin, which increase the amount of photoactive, oxidized dye present in the tumor and decrease it in the skin, are responsible for this unique differential PDT effect. Histological and fluorescein dye exclusion data 24 and 72 h post-PDT indicated that there is minimal damage to the irradiated vasculature within and surrounding the tumor under conditions which lead to high cure rates. This correlates with the predominantly intracellular tumor localization of the dye, demonstrated by fluorescence microscopy, and the low levels of dye (54 ng/ml plasma) found in the plasma at the time of light exposure. Taken together, these results indicate a novel PDT effect in that direct tumor cell killing (without skin photosensitization) rather than destruction of the supporting vasculature is the primary mode of tumor irradication. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RP CINCOTTA, L (reprint author), ROWLAND INST SCI INC,100 EDWIN LANE BLVD,CAMBRIDGE,MA 02142, USA. NR 75 TC 68 Z9 71 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 1 PY 1994 VL 54 IS 5 BP 1249 EP 1258 PG 10 WC Oncology SC Oncology GA MZ092 UT WOS:A1994MZ09200023 PM 8118813 ER PT J AU DORMAN, RL KAUFMAN, JA LAMURAGLIA, GM AF DORMAN, RL KAUFMAN, JA LAMURAGLIA, GM TI DIGITAL EMBOLI FROM BRACHIAL-ARTERY FIBROMUSCULAR DYSPLASIA SO CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Note DE FIBROMUSCULAR DYSPLASIA; EMBOLUS; BRACHIAL ARTERIES; ANGIOGRAPHY AB A 64-year-old female presented with right digital artery emboli from biopsy-proven, angiographically typical, right brachial artery fibromuscular dysplasia (medial fibroplasia). Angiographic findings consistent with fibromuscular dysplasia were also found in the left brachial artery. The patient was treated with surgical excision of the abnormal right brachial artery segment and postoperative anticoagulation for 2 months. She remains asymptomatic at 22 months. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN SURG SERV,DIV VASC SURG,BOSTON,MA 02114. HARVARD UNIV,BOSTON,MA 02114. NR 0 TC 6 Z9 6 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0174-1551 J9 CARDIOVASC INTER RAD JI Cardiovasc. Interv. Radiol. PD MAR-APR PY 1994 VL 17 IS 2 BP 95 EP 98 PG 4 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA NA040 UT WOS:A1994NA04000006 PM 8013030 ER PT J AU KHARBANDA, S SALEEM, A HIRANO, M EMOTO, Y SUKHATME, V BLENIS, J KUFE, D AF KHARBANDA, S SALEEM, A HIRANO, M EMOTO, Y SUKHATME, V BLENIS, J KUFE, D TI ACTIVATION OF EARLY GROWTH-RESPONSE-1 GENE-TRANSCRIPTION AND PP90(RSK) DURING INDUCTION OF MONOCYTIC DIFFERENTIATION SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID S6 PROTEIN-KINASE; PROMYELOCYTIC LEUKEMIA-CELLS; SWISS 3T3 CELLS; C-FOS PROMOTER; OKADAIC ACID; SER/THR-PRO; PHOSPHORYLATION; EXPRESSION; PP90RSK; IDENTIFICATION AB The present work has studied mechanisms responsible for induction of early growth response 1 (EGR-1) gene expression during monocytic differentiation of U-937 myeloid leukemia cells. Differentiation of U-937 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA), an activator of the serine/threonine protein kinase C, was associated with transcriptional activation of EGR-1 promoter-reporter constructs. The ECR-1 promoter contains six CC(A/T)(6)GC (CArG) motifs. The two 5'-most distal CArG sequences conferred TPA inducibility. In contrast, there was little effect of TPA on ECR-1 transcription in a TPA-resistant U-937 cell variant, designated TUR. Treatment of both U-937 and TUR cells with okadaic acid, an inhibitor of serine/threonine protein phosphatases 1 and 2A, was associated with induction of monocytic differentiation and ECR-1 transcription through the 5'-most CArG element. Since these findings supported the involvement of serine/threonine protein phosphorylation in the regulation of ECR-1 expression, we studied activation of the 40S ribosomal protein 56 serine/threonine kinases, pp70(S6K) and pp90(rsk). Although both kinases participate in regulating cell growth, there was no detectable activation of pp70(S6K) during TPA- or okadaic acid-induced monocytic differentiation. Moreover, rapamycin, an inhibitor of pp70(S6K) activation, had no effect on induction of EGR-1 expression. In contrast, analysis of pp90(rsk) activity by phosphorylation of a peptide derived from S6 protein demonstrated stimulation of this kinase in TPA-treated U-937, and not TUR, cells. Okadaic acid treatment of both cell types was associated with activation of pp90(rsk). Since serum response factor interacts with CArG elements and is directly phosphorylated by pp90(rsk), the present findings suggest that activation of the pp90(rsk) cascade may contribute to induction of ECR-1 transcription and appearance of the differentiated monocytic phenotype. C1 BETH ISRAEL HOSP,DIV NEPHROL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. RP KHARBANDA, S (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA42802] NR 53 TC 19 Z9 19 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD MAR PY 1994 VL 5 IS 3 BP 259 EP 265 PG 7 WC Cell Biology SC Cell Biology GA MZ771 UT WOS:A1994MZ77100003 PM 8018558 ER PT J AU RUSSELL, GJ PARKER, CM CEPEK, KL BRENNER, MB BHAN, AK AF RUSSELL, GJ PARKER, CM CEPEK, KL BRENNER, MB BHAN, AK TI EVIDENCE FOR A STRUCTURAL DIFFERENCE IN THE CD7 POLYPEPTIDE ON HUMAN THYMOCYTES AND INTRAEPITHELIAL LYMPHOCYTES DEFINED BY A NEW MONOCLONAL-ANTIBODY, 3D9 SO CELLULAR IMMUNOLOGY LA English DT Article ID T-CELL RECEPTOR; CELIAC-DISEASE; HUMAN GUT; MUCOSAL LYMPHOCYTES; GAMMA-DELTA; ALPHA-BETA; ANTIGENS; EXPRESSION; BINDING; SUBPOPULATIONS AB Intestinal intraepithelial lymphocytes (IEL) represent a distinct subpopulation of lymphocytes located on or above the basement membrane and adjacent to the basolateral membrane of enterocytes. Thus IEL are strategically positioned to mediate a response to the uptake of foreign antigens or to the alteration of enterocytes by injury or infection. Because of their unique location, we hypothesized that IEL might selectively express specialized cell surface proteins important in their site-specific localization or function. To identify such proteins, we immunized mice with purified human IEL and identified one monoclonal antibody, 3D9, which was found to react with a majority of IEL but with very few lamina propria lymphocytes (LPL) and weakly with most peripheral blood lymphocytes (PBL). Evaluation of this antibody with two-dimensional gels demonstrated that it reacts with CD7, previously known as an early thymocyte differentiation antigen. Interestingly, unlike all other anti-CD7 monoclonal antibodies, 3D9 identified only occasional thymocytes by immunohistochemistry suggesting that CD7 is structurally different on IEL and thymocytes. However, the CD7 polypeptide immunoprecipitated from IEL and thymocytes appeared identical in SDS-PAGE mobility and in charge by two-dimensional gels, despite being recognized differently by monoclonal antibodies. These studies emphasize the expression of CD7 by IEL T cells and reveal the existence of an undefined structural difference between CD7 molecules on IEL compared to thymocytes. (C) 1994 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,DIV MED SCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02115. FU NIDDK NIH HHS [DK33506, DK43351, K08DK02010] NR 42 TC 4 Z9 4 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD MAR PY 1994 VL 154 IS 1 BP 153 EP 165 DI 10.1006/cimm.1994.1065 PG 13 WC Cell Biology; Immunology SC Cell Biology; Immunology GA MZ185 UT WOS:A1994MZ18500014 PM 7509727 ER PT J AU LEVINE, SM ANZUETO, A PETERS, JI CALHOON, JH JENKINSON, SG BRYAN, CL AF LEVINE, SM ANZUETO, A PETERS, JI CALHOON, JH JENKINSON, SG BRYAN, CL TI SINGLE-LUNG TRANSPLANTATION IN PATIENTS WITH SYSTEMIC-DISEASE SO CHEST LA English DT Article ID PRIMARY PULMONARY-HYPERTENSION AB Objective: To report functional results and survival in patients undergoing single lung transplantation (SLT) for pulmonary involvement associated with systemic disease or prior malignancy, criteria traditionally considered contraindications to SLT. Design: Case series. Setting: The University of Texas Health Science Center at San Antonio. Patients: Nine patients who have undergone SLT for end-stage lung disease: four patients with sarcoidosis; two patients with limited scleroderma; and three patients with prior malignancies (two with prior lymphoma and bleomycin-induced pulmonary fibrosis and one who received two bone marrow transplants for acute lymphocytic leukemia and subsequently developed chemotherapy-induced pulmonary fibrosis). Measurements: Pulmonary function testing, exercise oximetry, quantitative ventilation-perfusion lung scanning. Actuarial survival. Results: All patients had marked improvement in pulmonary function, exercise oximetry, and quantitative ventilation perfusion to the SLT. One patient with scleroderma died 90 days postoperatively from Pseudomonas pneumonia with a sepsis syndrome. One patient with sarcoidosis died 150 days postoperatively from disseminated aspergillosis. At autopsy, there was no evidence of recurrent fibrosis or sarcoidosis in the transplanted lungs in either of these two patients. The seven surviving patients have returned to work or school and are conducting all activities of daily living without pulmonary disability. The 1- and 2-year actuarial survival rates in these nine patients is 68.6 percent as compared with the 1- and e-year actuarial survival rates of 66.3 percent and 55.8 percent in the remainder of our SLT group as a whole (n=49). Despite pharmacologic immunosuppression, there is no evidence of recurrent malignancy in the 3 patients with prior malignancies. Conclusions: We conclude that carefully selected patients with end-stage lung involvement related to systemic disease or chemotherapy-induced fibrosis may benefit from SLT. C1 UNIV TEXAS,HLTH SCI CTR,DEPT SURG,DIV CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP LEVINE, SM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS,PULM DIS SECT 111B,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NHLBI NIH HHS [HL-32824] NR 13 TC 45 Z9 45 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAR PY 1994 VL 105 IS 3 BP 837 EP 841 DI 10.1378/chest.105.3.837 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NA618 UT WOS:A1994NA61800037 PM 7510601 ER PT J AU ANZUETO, A LEVINE, SM TILLIS, WP CALHOON, JH BRYAN, CL AF ANZUETO, A LEVINE, SM TILLIS, WP CALHOON, JH BRYAN, CL TI USE OF THE FLOW-VOLUME LOOP IN THE DIAGNOSIS OF BRONCHIAL STENOSIS AFTER SINGLE-LUNG TRANSPLANTATION SO CHEST LA English DT Note ID MANAGEMENT; REJECTION; GRAFT; LASER AB Bronchial complications, including stricture, stenosis, and/or anastomotic dehiscence, are a major cause of morbidity following single lung transplantation. This report describes a 19-year-old man with a diagnosis of end-stage pulmonary fibrosis secondary to prior chemotherapy for non-Hodgkins lymphoma who underwent single lung transplantation, The immunosuppressive regimen included cyclosporine, azathioprine, and methylprednisolone sodium succinate (Solu-Medrol) intravenously for six doses during the first 3 days postoperatively followed by oral prednisone. Sixteen weeks following transplantation, the patient complained of dyspnea. Spirometry revealed a decrease in FEF25-75 and the flow-volume curve demonstrated a bioconcave appearance. The now-volume loop showed a relatively high initial flow phase occurring over the first 2 to 3 s followed by a low-flow phase. The expiratory phase also showed the same characteristics. Bronchoscopy revealed 75 percent stenosis of the bronchial lumen to the transplanted lung. A transbronchial biopsy specimen obtained at that time was consistent with acute rejection. The patient was treated with a methylprednisolone bolus. A repeated bronchoscopy showed the persistence of stenosis distal to the anastomosis. The patient underwent several bronchoplastic balloon dilatations without complete resolution of the stenosis and a stainless steel mesh stent was placed. Repeated spirometry showed marked improvement of the FEF25-75 and normalization of the flow-volume loop. We conclude that the flow-volume loop curve is a noninvasive procedure that may help monitor the patency of the bronchial anastomoses following single lung transplantation. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,DIV CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. RP ANZUETO, A (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 14 TC 19 Z9 20 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAR PY 1994 VL 105 IS 3 BP 934 EP 936 DI 10.1378/chest.105.3.934 PG 3 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NA618 UT WOS:A1994NA61800058 PM 7510602 ER PT J AU ZAPOL, WM FALKE, KJ HURFORD, WE ROBERTS, JD AF ZAPOL, WM FALKE, KJ HURFORD, WE ROBERTS, JD TI INHALING NITRIC-OXIDE - A SELECTIVE PULMONARY VASODILATOR AND BRONCHODILATOR SO CHEST LA English DT Article; Proceedings Paper CT Thomas L Petty Aspen Lung Conference 36th Annual Meeting: Acute Lung Injury CY JUN 02-05, 1993 CL ASPEN, CO SP THOMAS L PETTY ASPEN LUNG CONF ID HYPERTENSION; NEWBORN C1 FREE UNIV BERLIN,ANASTHESIOL KLIN,W-1000 BERLIN,GERMANY. RP ZAPOL, WM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA, USA. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 FU NHLBI NIH HHS [HL-42397] NR 12 TC 20 Z9 21 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAR PY 1994 VL 105 IS 3 SU S BP S87 EP S91 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NF873 UT WOS:A1994NF87300020 PM 8131625 ER PT J AU FOITZIK, T FERNANDEZCASTILLO, C LEWANDROWSKI, KB RATTNER, DW HERFARTH, C WARSHAW, AL AF FOITZIK, T FERNANDEZCASTILLO, C LEWANDROWSKI, KB RATTNER, DW HERFARTH, C WARSHAW, AL TI TRYPSINOGEN ACTIVATION PEPTIDES IN ACUTE-PANCREATITIS - EXPERIMENTAL-DATA AND CLINICAL IMPLICATIONS SO CHIRURG LA German DT Article DE ACUTE PANCREATITIS; TRYPSINOGEN ACTIVATION PEPTIDES (TAP); ACINAR CELL NECROSIS ID ASSAY; MODEL; RAT C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FOITZIK, T (reprint author), UNIV HEIDELBERG,CHIRURG KLIN,KIRSCHNERSTR 1,D-69120 HEIDELBERG,GERMANY. NR 16 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0009-4722 J9 CHIRURG JI Chirurg PD MAR PY 1994 VL 65 IS 3 BP 186 EP 189 PG 4 WC Surgery SC Surgery GA ND500 UT WOS:A1994ND50000005 PM 8194402 ER PT J AU KIM, YH SOSASUAREZ, G TROUTON, TG ONUNAIN, SS OSSWALD, S MCGOVERN, BA RUSKIN, JN GARAN, H AF KIM, YH SOSASUAREZ, G TROUTON, TG ONUNAIN, SS OSSWALD, S MCGOVERN, BA RUSKIN, JN GARAN, H TI TREATMENT OF VENTRICULAR-TACHYCARDIA BY TRANSCATHETER RADIOFREQUENCY ABLATION IN PATIENTS WITH ISCHEMIC-HEART-DISEASE SO CIRCULATION LA English DT Article DE TACHYCARDIA; RADIOFREQUENCY; ABLATION; ISCHEMIA; HEART DISEASE ID PARKINSON-WHITE SYNDROME; CORONARY-ARTERY DISEASE; CATHETER ABLATION; MYOCARDIAL-INFARCTION; CONDUCTION; RESECTION; SURGERY; REENTRY AB Background Recurrent sustained ventricular tachycardia (VT) is not responsive to antiarrhythmic drugs in the majority of patients, who therefore need therapy with nonpharmacological methods. We evaluated prospectively the feasibility, safety, and efficacy of transcatheter radiofrequency (RF) ablation of VT in 21 selected patients with ischemic heart disease and VT. Methods and Results Twenty-one patients with ischemic heart disease and recurrent, drug-refractory VT documented by 12-lead ECG were selected who had sufficient hemodynamic tolerance of VT to undergo transcatheter mapping. Documented clinical VT was reproduced by programmed cardiac stimulation (PCS), and the site of origin was localized by a combination of techniques, including pace mapping, activation-sequence mapping, recordings of middiastolic potentials, and application of resetting and entrainment principles. RF current at 55 V was applied (3.8+/-3.1 applications per patient) for as long as 30 seconds at a time to target sites. Twenty-four distinct clinical VTs (mean cycle length, 445+/-52 milliseconds) were mapped and ablated in 21 patients. In 17 of 21 patients (81%), the procedure was acutely successful, and the target clinical VT could no longer be induced by PCS after the procedure, whereas in 4 patients, clinical VT remained inducible. By contrast, VTs with shorter cycle length and different QRS morphology than the ablated VT could still be induced by PCS in 12 of 21 patients. One patient died in intractable congestive heart failure 10 days after the procedure, and the remaining 20 are alive at the end of the follow-up period. The majority of the patients continued to be treated with at least one additional mode of antiarrhythmic therapy; 12 patients were still taking antiarrhythmic drugs, and 9 patients received an implantable cardioverter/defibrillator. During a mean follow-up period of 13.2+/-5.0 months, 9 of 20 patients (45%) had recurrent VT. In 4 patients, the recurrent VT was different than the previously ablated one. Clinical VT recurred in all 4 patients in whom RF ablation had been acutely unsuccessful. Four patients with recurrent VT underwent repeat RF ablation procedures that were acutely successful and had no further recurrence. Conclusions Transcatheter RF ablation is feasible but has only moderately high efficacy in a small, selected group of patients with ischemic heart disease and drug-refractory, highly frequent, hemodynamically tolerated, sustained VT, In the majority of the patients, this treatment technique is palliative rather than definitive, and many of the patients continue to require other methods of antiarrhythmic therapy. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA 02114. NR 24 TC 151 Z9 152 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1994 VL 89 IS 3 BP 1094 EP 1102 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA NA762 UT WOS:A1994NA76200021 PM 8124795 ER PT J AU SHARAF, AR NARULA, J NICOL, PD SOUTHERN, JF KHAW, BA AF SHARAF, AR NARULA, J NICOL, PD SOUTHERN, JF KHAW, BA TI CARDIAC SARCOPLASMIC-RETICULUM CALCIUM-ATPASE, AN AUTOIMMUNE ANTIGEN IN EXPERIMENTAL CARDIOMYOPATHY SO CIRCULATION LA English DT Article DE CARDIOMYOPATHY; SARCOPLASMIC RETICULUM; MYOCARDITIS; SARCOLEMMA; MYOCARDIAL CONTRACTION ID MONOCLONAL-ANTIBODY; SKELETAL-MUSCLE; MYOCARDITIS; TRANSPORT; CA2+-ATPASE; MEMBRANE; MYOSIN; MODEL; MICE; CA2+ AB Background Various myocardial cell surface and intracellular antigens have been associated with autoimmune myocarditis. Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Methods and Results Monoclonal antibody 4C11-20.21 (IgM class) specific for canine cardiac SR-ATPase (M(r) approximate to 110 kD) was generated by immunization of CAF1/J mice with dog heart sarcoplasmic reticulum. Antibody 4C11-20.21 inhibits 75% of the enzymatic activity of the cardiac SR-ATPase. This antibody also cross-reacts with the higher M(r) subunit of canine skeletal SR-ATPase, but the skeletal muscle SR-ATPase activity is unaffected. This antibody does not cross-react with sarcolemmal calcium ATPase (134 kD). Antibody 4C11-20.21 was used for affinity purification of cardiac muscle SR-ATPase, which did not contain sarcolemmal calcium ATPase antigen. Nine of 11 CAF1/J mice injected with purified canine cardiac SR-ATPase protein demonstrated myocardial lesions: 3 of 4 mice had occasional perivascular and/or interstitial mononuclear cell infiltrates after 3 weeks, 3 of 4 had borderline myocarditis after 6 weeks, and 3 of 3 had focal myocarditis after 12 weeks. No mononuclear infiltrates were seen in any other organ. To identify the independent effect of 4C11-20.21 antibody on cardiac muscle, 2x10(6) hybridoma cells producing the antibody were injected intraperitoneally into 12 severe combined immunodeficiency (SCID) mice. Eleven of 12 SCID mice showed variable cardiac myocyte degeneration without cellular infiltration between 8 and 19 days. Three control SCID mice, which received equivalent injections of hybridoma cells producing IgM anti-myosin light chain antibody, did not show any pathological lesions. Immunoperoxidase staining and/or immunoperoxidase transmission electron microscopy for detection of in vivo localization of 4C11-20.21 demonstrated staining of the subsarcolemmal myotubular system and focal staining of immediately adjacent sarcolemma in animals that received either 4C11-20.21 hybridoma cells or purified canine cardiac SR-ATPase antigen but not in controls. Immunofluorescence staining with goat anti-mouse C3 antibody revealed focal deposition of complement in the cardiac myocytes. Conclusions The time-dependent association between immunization with SR-ATPase antigen and the development of myocarditis in mice suggests that cardiac SR-ATPase constitutes one of several autoimmunogens capable of inducing autoimmune myocarditis. Besides antigenic specificity, since antibody to cardiac SR-ATPase also inhibits energy-dependent processes in the myocardium, it is reasonable to associate the pathological evidence of myonecrosis with the interference of calcium regulation, which controls myocardial contractility. C1 NORTHEASTERN UNIV,BOUVE COLL PHARM & HLTH SCI,BOSTON,MA 02115. AL-AZHAR UNIV,CAIRO,EGYPT. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 29 TC 14 Z9 15 U1 1 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1994 VL 89 IS 3 BP 1217 EP 1228 PG 12 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA NA762 UT WOS:A1994NA76200036 PM 8124810 ER PT J AU JOHNSON, TB KENT, RL BUBOLZ, BA MCDERMOTT, PJ AF JOHNSON, TB KENT, RL BUBOLZ, BA MCDERMOTT, PJ TI ELECTRICAL-STIMULATION OF CONTRACTILE ACTIVITY ACCELERATES GROWTH OF CULTURED NEONATAL CARDIOCYTES SO CIRCULATION RESEARCH LA English DT Article DE HYPERTROPHY; CARDIOCYTES; CONTRACTION; ELECTRICAL STIMULATION ID RIBOSOMAL-RNA SYNTHESIS; RAT CARDIAC MYOCYTES; ADULT FELINE CARDIOCYTES; HEART-CELLS; GENE-EXPRESSION; 2,3-BUTANEDIONE MONOXIME; MAMMALIAN MYOCARDIUM; PROTEIN-SYNTHESIS; MYOSIN SYNTHESIS; SKELETAL-MUSCLE AB An electrical stimulation system was designed to regulate synchronized contractile activity of neonatal rat cardiocytes and to examine the effects of mechanical contraction on cardiocyte growth. Continuous electrical stimulation at a pulse duration of 5 milliseconds and frequency of 3 Hz resulted in a time-dependent accumulation of cell protein that reached 34% above initial values, as measured by the protein-to-DNA ratio. The growth response did not occur using voltage amplitudes that were subthreshold for contraction and was independent of contraction frequencies set at greater than or equal to 0.5 Hz. The RNA-to-DNA ratio increased in parallel to cell protein, indicating that the capacity for protein synthesis was enhanced by contraction. Rates of 28S rRNA synthesis were accelerated twofold in contracting cardiocytes. By comparison, protein and RNA accumulation did not occur in electrically stimulated cardiocytes in which contraction was blocked by either 10 mu mol/L verapamil or by 5 mmol/L 2,3-butanedione monoxime, an inhibitor of actomyosin crossbridge cycling. Electrical stimulation of cardiocyte contraction did not enhance alpha-cardiac actin or myosin heavy chain (alpha+beta) mRNA transcript levels relative to 28S rRNA during the period of rapid growth that occurred over the first 48 hours. It is concluded that (1) electrical stimulation of contraction accelerates cardiocyte growth and RNA accumulation, (2) mechanical contraction is involved in regulating the growth of electrically stimulated cardiocytes, and (3) the levels of cu-actin and myosin heavy chain mRNA increase in proportion to rRNA during the growth of contracting cardiocytes. (Circ Res. 1994;74:448-459.) C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CARDIOL SECT,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT CELL BIOL & ANAT,CHARLESTON,SC. MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29425. GAZES CARDIAC RES INST,CHARLESTON,SC. NR 45 TC 40 Z9 40 U1 1 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD MAR PY 1994 VL 74 IS 3 BP 448 EP 459 PG 12 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA MZ583 UT WOS:A1994MZ58300010 PM 8118953 ER PT J AU ZHOU, SR HAN, Q LAGANKE, CC WHITAKER, JN AF ZHOU, SR HAN, Q LAGANKE, CC WHITAKER, JN TI COMPARISON OF PROPERTIES OF MURINE MONOCLONAL ANTIIDIOTYPIC ANTIBODIES GENERATED WITH IDIOTYPE-BEARING MONOCLONAL-ANTIBODIES TO MYELIN BASIC-PROTEIN PEPTIDES OR THEIR COMPLEMENTARY PEPTIDES SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID MESSENGER-RNA; IMMUNIZATION; IDIOTOPES; REGION AB The present study was undertaken to compare the features of monoclonal antibody (mAb) anti-idiotope (Id) induced by complementary peptides, synthesized on the basis of inverted hydropathy for a myelin basic protein (MBP) peptide, or by conventional methodology using Id-bearing antibodies to the same MBP peptide as immunogen. The six reagents studied consisted of mAbs reactive with MBP peptide acetyl 1-9 and MBP peptide 80-89 and anti-Id reagents against these two mAbs prepared by either the complementary peptide or the conventional approach. ELISA, immunoblotting, immunoinhibition of hybridoma cell production of Id-bearing mAb to MBP, and FACS indicated that the anti-Ids generated by either technique were similar although existing in a range reflecting biologic phenomena. mAbs anti-Id prepared by either method continued to show an IgM isotype preference, possibly related to technical considerations, and continued to recognize a cross-reactive Id on the K light chain of the mAbs to MBP peptides acetyl 1-9 and 80-89. There was no indication that the anti-Ids prepared by the complementary peptide approach were restrictive or selective in a manner different from those made by the conventional approach. (C) 1994 Academic Press, Inc. C1 UNIV ALABAMA,DEPT CELL BIOL,BIRMINGHAM,AL. UNIV ALABAMA,CTR NEUROIMMUNOL,BIRMINGHAM,AL. BIRMINGHAM VA MED CTR,NEUROL & RES SERV,BIRMINGHAM,AL 35294. RP ZHOU, SR (reprint author), UNIV ALABAMA,DEPT NEUROL,BIRMINGHAM,AL, USA. FU NINDS NIH HHS [NS 23240, NS 29719]; PHS HHS [T3207335] NR 23 TC 14 Z9 14 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD MAR PY 1994 VL 70 IS 3 BP 251 EP 259 DI 10.1006/clin.1994.1037 PG 9 WC Immunology; Pathology SC Immunology; Pathology GA MY664 UT WOS:A1994MY66400011 PM 7508836 ER PT J AU TEMPLE, HT SCULLY, SP OKEEFE, RJ ROSENTHAL, DI MANKIN, HJ AF TEMPLE, HT SCULLY, SP OKEEFE, RJ ROSENTHAL, DI MANKIN, HJ TI CLINICAL PRESENTATION OF ALVEOLAR SOFT-PART SARCOMA SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID HISTOGENESIS AB Alveolar soft-part sarcomas are rare and seldom considered in the differential diagnosis of a soft-tissue mass. Thus, early clinical recognition can be elusive. The authors have identified several clinical and radiographic features of alveolar soft-part sarcoma, emphasizing the importance of magnetic resonance imaging in the preoperative diagnostic and staging workup. Accurate diagnosis and treatment of this unusual tumor requires clinical suspicion and clinicopathologic correlation with appropriate radiographic studies. If the clinical or radiographic interpretation is equivocal, early biopsy is essential to differentiate alveolar soft-part sarcoma from arteriovenous malformation. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP TEMPLE, HT (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,GRAY 6,50 FRUIT ST,BOSTON,MA 02114, USA. NR 21 TC 16 Z9 16 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD MAR PY 1994 IS 300 BP 213 EP 218 PG 6 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MZ827 UT WOS:A1994MZ82700029 PM 8131338 ER PT J AU STEINBERG, BD GELBERMAN, RH AF STEINBERG, BD GELBERMAN, RH TI EVALUATION OF LIMB COMPARTMENTS WITH SUSPECTED INCREASED INTERSTITIAL PRESSURE - A NONINVASIVE METHOD FOR DETERMINING QUANTITATIVE HARDNESS SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID ARTICULAR-CARTILAGE; INDENTATION; DIAGNOSIS AB Six compartments in four dogs and three compartments in three anatomic specimen limbs were injected with plasma, and the intracompartmental interstitial pressure and hardness of the compartments were measured. Six patients suspected of having compartment syndromes were also studied. Of the compartments evaluated in the dog and anatomic specimen limbs, the average correlation coefficient between measurements with the two methods was 0.95 (range, 0.87 to 0.99). In six patients suspected of having compartment syndromes, the ratios of quantitative hardness of the injured to uninjured limbs closely matched the intracompartmental interstitial pressure measurement ratios (correlation coefficient, 0.95). All correlation coefficients were significant (F test, p < 0.05). There was a close correlation between the direct measurement of intracompartmental interstitial pressure, with the wick catheter and quantitative hardness in compartment syndrome models in dog and anatomic specimen limbs, and in patients suspected of having compartment syndromes. The determination of surface hardness of limb compartments, which appears accurate and reproducible, offers the advantages of being noninvasive and well suited for longer-term assessments of intracompartmental interstitial pressure. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. NR 11 TC 25 Z9 25 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD MAR PY 1994 IS 300 BP 248 EP 253 PG 6 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MZ827 UT WOS:A1994MZ82700034 PM 8131344 ER PT J AU GABRIELI, JDE KEANE, MM STANGER, BZ KJELGAARD, MM CORKIN, S GROWDON, JH AF GABRIELI, JDE KEANE, MM STANGER, BZ KJELGAARD, MM CORKIN, S GROWDON, JH TI DISSOCIATIONS AMONG STRUCTURAL-PERCEPTUAL, LEXICAL-SEMANTIC, AND EVENT-FACT MEMORY-SYSTEMS IN ALZHEIMER, AMNESIC, AND NORMAL SUBJECTS SO CORTEX LA English DT Article ID MONKEY VISUAL-CORTEX; HUNTINGTONS-DISEASE; FRAGMENT COMPLETION; PARKINSONS-DISEASE; CONTOUR PERCEPTION; SENILE DEMENTIA; EXPLICIT MEMORY; BASAL FOREBRAIN; RECOGNITION; IMPAIRMENT AB Patients with Alzheimer's disease (AD), patients with global amnesia (AMN), and normal control (NC) subjects received tests of recall and recognition, word-completion priming, and incomplete-picture priming. The AD and AMN patients had impaired recall and recognition. The AD patients, but not the AMN patients, had impaired word-completion priming. In contrast, the AD patients had intact incomplete-picture priming, a form of priming shown to be perceptual in normal subjects. These results provide neuropsychological evidence for a dissociation between two components of repetition priming, perceptual priming as measured with identification tasks and nonperceptual priming as measured with generation tasks. Preserverd perceptual priming in AD may be mediated by the occipital regions that are relatively spared in AD; compromised nonperceptual priming may be mediated by temporal regions that show dense neuropathological changes early in AD. C1 MIT,DEPT BRAIN & COGNIT SCI,BOSTON,MA. MIT,CLIN RES CTR,BOSTON,MA. NORTHWESTERN UNIV,DEPT PSYCHOL,EVANSTON,IL 60208. BOSTON UNIV,SCH MED,MEMORY DISORDERS RES CTR,BOSTON,MA 02118. BOSTON DEPT VET AFFAIRS,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. FU NCRR NIH HHS [M01RR00088]; NIA NIH HHS [5R37AG06605, 1P50AG05134] NR 96 TC 149 Z9 152 U1 1 U2 5 PU MASSON DIVISIONE PERIODICI PI MILAN PA VIA FRATELLI BRESSAN 2, 20126 MILAN, ITALY SN 0010-9452 J9 CORTEX JI Cortex PD MAR PY 1994 VL 30 IS 1 BP 75 EP 103 PG 29 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA NC258 UT WOS:A1994NC25800004 PM 8004991 ER PT J AU STERN, TA AF STERN, TA TI CONTINUOUS-INFUSION OF HALOPERIDOL IN AGITATED, CRITICALLY ILL PATIENTS SO CRITICAL CARE MEDICINE LA English DT Editorial Material DE HALOPERIDOL; AGITATION, PSYCHOMOTOR; SEDATION; BENZODIAZEPINES; CRITICAL ILLNESS RP STERN, TA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 10 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD MAR PY 1994 VL 22 IS 3 BP 378 EP 379 DI 10.1097/00003246-199403000-00002 PG 2 WC Critical Care Medicine SC General & Internal Medicine GA NA320 UT WOS:A1994NA32000002 PM 8124985 ER PT J AU BERTHIAUME, F EZZELL, RM TONER, M YARMUSH, ML TOMPKINS, RG AF BERTHIAUME, F EZZELL, RM TONER, M YARMUSH, ML TOMPKINS, RG TI TRANSPORT OF FLUORESCENT DEXTRANS ACROSS THE RAT ILEUM AFTER CUTANEOUS THERMAL-INJURY SO CRITICAL CARE MEDICINE LA English DT Article DE INTESTINAL PERMEABILITY; MACROMOLECULAR TRANSPORT; BURN INJURY; GUT; BACTERIAL INFECTION; CRITICAL ILLNESS; EPITHELIUM; DEXTRANS; FLUORESCENCE MICROSCOPY; INFECTION; SEPSIS ID SMALL INTESTINAL PERMEABILITY; GUT PERMEABILITY; EPITHELIAL-CELLS; ENDOTOXIN; TRAUMA; HYPERMETABOLISM; MACROMOLECULES; ABSORPTION; ISCHEMIA; INVITRO AB Objective: To determine the time course and spatial distribution of uptake of macromolecules in the small intestine of rats subjected to cutaneous thermal injury. Design: Prospective, controlled animal study. Subjects: Fifty-five female Sprague-Dawley (CD) rats subjected to scald burn injury covering 20% (small injury; n = 29) and 40% (large injury; n = 6) of the total body surface area between 3 and 72 hrs after injury. Animals subjected to sham injury (n = 20) were used as controls. Interventions: The intestine was cannulated near the distal ileum and incised 7 cm upstream. After perfusion with physiologic buffer, this intestinal loop was filled with the same buffer containing fluorescent-labeled dextrans (3 and 70 kilodaltons molecular weight) and Ligated 4 cm from the injection point. After a 2-hr incubation period, the tissues were fixed with paraformaldehyde and cryosections were examined by laser confocal microscopy. The mesentery was also observed by laser confocal microscopy during incubation with the permeability probes. The disappearance of fluorescence was studied after washing the dextran probes from the gut lumen. Measurements and Main Results: In small injuries, there was a transient uptake of the Q-kilodalton dextran by the epithelium in focal regions of the ileum with the effects seen between 7 and 21 hrs after injury. In large injuries, epithelial staining was visible within 3 hrs, and the marker was seen to translocate both to the lymphatics and the blood vessels of the mesentery. In comparison, the 70-kilodalton dextran was visible within the intercellular spaces. Little or no epithelial staining was seen in sham-injured animals. Conclusions: These results suggest that a transcellular pathway for the translocation of small macromolecules from the lumen to the mesentery can be activated after burn injury. The novel techniques described here will be useful to examine intestinal transport in various pathologic situations. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02115. SHRINERS BURN INST,BOSTON,MA 02114. FU NIGMS NIH HHS [P50 GM-21700]; PHS HHS [T32 07035] NR 35 TC 14 Z9 14 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD MAR PY 1994 VL 22 IS 3 BP 455 EP 464 DI 10.1097/00003246-199403000-00016 PG 10 WC Critical Care Medicine SC General & Internal Medicine GA NA320 UT WOS:A1994NA32000016 PM 7510222 ER PT J AU PALACIOS, IF AF PALACIOS, IF TI PERCUTANEOUS MITRAL BALLOON VALVOTOMY FOR PATIENTS WITH MITRAL-STENOSIS SO CURRENT OPINION IN CARDIOLOGY LA English DT Article AB This study reports the immediate outcome, in-hospital complications, and long-term clinical follow-up of patients undergoing percutaneous mitral balloon valvotomy. In most series, this procedure is reported to increase mitral valve area from less than 1.0 cm2 to at least 2.0 CM2. The most important predictor of the immediate outcome of percutaneous mitral valvotomy is the echocardiographic score. The best results with percutaneous mitral valvotomy occur in those patients with echocardiographic scores of 8 or less. Mortality and morbidity with percutaneous mitral valvotomy are low and similar to surgical commissurotomy. There is less than 1% mortality, a 0% to 3.1% incidence of thromboembolic episodes and stroke, a 1% to 5.2% incidence of severe mitral regurgitation, a 0.2% to 4.1% incidence of pericardial tamponade, and a 3% to 16% incidence of left-to-right shunt. Survival (83 +/- 6% vs 48 +/- 8%), survival with freedom from mitral valve surgery (58 +/- 5% vs 25 +/- 5%), and event-free survival (51 +/- 6% vs 22 +/- 5%) at 80-month follow-up was greater in patients with echocardiographic scores of 8 or less compared with those with scores greater than 8 (P<0.0001). Thus, the excellent immediate and long term results of percutaneous mitral valvotomy in patients with echocardiographic scores of 8 or less suggest that this procedure may be the treatment of choice in this group of patients. RP PALACIOS, IF (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC CATHETERIZAT LABS,BOSTON,MA 02114, USA. NR 0 TC 9 Z9 9 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0268-4705 J9 CURR OPIN CARDIOL JI Curr. Opin. Cardiol. PD MAR PY 1994 VL 9 IS 2 BP 164 EP 175 DI 10.1097/00001573-199403000-00005 PG 12 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NC267 UT WOS:A1994NC26700005 PM 8199382 ER PT J AU SUNDKVIST, G VELLOSO, LA KAMPE, O RABINOWE, SL IVARSSON, SA LILJA, B KARLSSON, FA AF SUNDKVIST, G VELLOSO, LA KAMPE, O RABINOWE, SL IVARSSON, SA LILJA, B KARLSSON, FA TI GLUTAMIC-ACID DECARBOXYLASE ANTIBODIES, AUTONOMIC NERVE ANTIBODIES AND AUTONOMIC NEUROPATHY IN DIABETIC-PATIENTS SO DIABETOLOGIA LA English DT Article DE AUTONOMIC NEUROPATHY; GLUTAMIC ACID DECARBOXYLASE ANTIBODIES; SYMPATHETIC NERVE ANTIBODIES; VAGAL NERVE ANTIBODIES; ISLET CELL ANTIBODIES ID ISLET CELL PROTEIN; HEART-RATE VARIABILITY; MELLITUS; TYPE-1; AUTOANTIBODIES; CHILDREN; DURATION; IDDM; CATECHOLAMINES; ASSOCIATION AB To clarify whether GAD-ab are associated with diabetic autonomic neuropathy and/or complement fixing antibodies against sympathetic ganglia, adrenal medulla, and vagus nerve, we examined 133 diabetic patients (95 with IDDM). GAD-ab were determined by a radioligand binding assay using in vitro expression of recombinant GAD-65 whereas sympathetic ganglia antibodies, adrenal medulla antibodies, vagus nerve, and ICA were evaluated by indirect immunofluorescence assays. Autonomic nerve function was evaluated by objective tests (heart rate reactions to deep breathing and to tilt). In the total material of 133 patients, GAD-ab were detected in 36 patients, all of whom had IDDM. The frequency of GAD-ab was similar (38 %) in IDDM patients with and without signs of autonomic neuropathy (21 of 55 vs 15 of 40). In addition, there were no significant associations between GAD-ab and autonomic nerve antibodies; GAD-ab were detected in 9 of 21 (43 %) of patients with and in 27 of 112 (24 %) of patients without sympathetic ganglia antibodies, in 5 of 15 (33 %) of patients with and 31 of 118 (26 %) without adrenal medulla antibodies, and in 5 of 15 (33 %) with and 31 of 118 (26 %) of patients without vagus nerve antibodies. The frequency of ICA, however, was significantly increased in patients with sympathetic ganglia antibodies compared with those without sympathetic ganglia antibodies (10 of 21 [48 %] vs 21 of 112 [19 %];p < 0.01). In conclusion, GAD-ab were neither associated with disturbed autonomic nerve function nor with antibodies against autonomic nerve structures. C1 UNIV HOSP UPPSALA,DEPT MED,UPPSALA,SWEDEN. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,IMMUNOL SECT,BOSTON,MA 02115. LUND UNIV,MALMO GEN HOSP,DEPT PEDIAT,S-21401 MALMO,SWEDEN. LUND UNIV,MALMO GEN HOSP,DEPT CLIN PHYSIOL,S-21401 MALMO,SWEDEN. RP SUNDKVIST, G (reprint author), LUND UNIV,MALMO GEN HOSP,DEPT MED,S-21401 MALMO,SWEDEN. FU PHS HHS [30987] NR 46 TC 27 Z9 27 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD MAR PY 1994 VL 37 IS 3 BP 293 EP 299 DI 10.1007/BF00398057 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NA160 UT WOS:A1994NA16000011 PM 8174844 ER PT J AU KEARSE, LA MANBERG, P DEBROS, F CHAMOUN, N SINAI, V AF KEARSE, LA MANBERG, P DEBROS, F CHAMOUN, N SINAI, V TI BISPECTRAL ANALYSIS OF THE ELECTROENCEPHALOGRAM DURING INDUCTION OF ANESTHESIA MAY PREDICT HEMODYNAMIC-RESPONSES TO LARYNGOSCOPY AND INTUBATION SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE BISPECTRAL ANALYSIS; POWER SPECTRUM; ELECTROENCEPHALOGRAPHY; ANESTHESIA; OPIOID; LARYNGOSCOPY ID EEG AB The use of electroencephalography as a measure of adequacy of anesthesia has achieved limited success. Our purpose was to determine whether the non-linear properties of the electroencephalogram (EEG) as defined by the bispectral index was a better predictor of autonomic responses to endotracheal intubation during opioid-based anesthesia than the linear statistical properties of the EEG formulated by power spectral analysis. Thirty-nine adults scheduled for elective non-cranial surgery had a continuous EEG recorded during induction of anesthesia and endotracheal intubation. Anesthesia consisted of thiopental and nitrous oxide in oxygen, followed by 1 of 5 randomized opioid dose regimens. The EEG was continuously recorded and blood pressure was measured every minute. All electroencephalographic parameters were derived for the 3 min before and after intubation and were compared to the blood pressure and heart rate responses. Responders were defined by 2 analyses: patients who had a 20% or greater increase (1) in blood pressure or (2) in heart rate to laryngoscopy. Responders and non-responders were compared using Student's unpaired t test, and differences due to dose regimens were examined with logistic regression. Based on the criterion for blood pressure change, there were 27 responders and 12 non-responders. Heart rate changes did not differentiate between the two groups. There was a significant difference between response groups as measured by the bispectral index which distinguished responders from non-responders independently of the amount of drug given. None of the variables of power spectral analysis accurately distinguished responder from non-responder. We conclude that the bispectral index of the EEG may accurately predict blood pressure responses in patients undergoing endotracheal intubation after induction of general anesthesia. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. RP KEARSE, LA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA & NEUROL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 25 TC 47 Z9 50 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD MAR PY 1994 VL 90 IS 3 BP 194 EP 200 DI 10.1016/0013-4694(94)90091-4 PG 7 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA ND221 UT WOS:A1994ND22100004 PM 7511501 ER PT J AU MILLER, CP MCGEHEE, RE HABENER, JF AF MILLER, CP MCGEHEE, RE HABENER, JF TI IDX-1 - A NEW HOMEODOMAIN TRANSCRIPTION FACTOR EXPRESSED IN RAT PANCREATIC-ISLETS AND DUODENUM THAT TRANSACTIVATES THE SOMATOSTATIN GENE SO EMBO JOURNAL LA English DT Article DE DNA BINDING; HOMEODOMAIN; PANCREATIC ISLET; SOMATOSTATIN GENE REGULATION; TRANSCRIPTIONAL ACTIVATION ID HOMEOBOX GENES; INSULIN-GENE; DNA-BINDING; CELL-LINES; RESPONSE ELEMENT; ENDOCRINE-CELLS; COMPLEX; ENHANCER; PROTEIN; MOUSE AB We describe the cloning from a rat islet somatostatin-producing cell line of a 1.4 kb cDNA encoding a new homeoprotein, IDX-1 (islet/duodenum homeobox-1), with close sequence similarity to the Drosophila melanogaster homeobox protein Antennapedia (Antp) and the Xenopus laevis endoderm-specific homeoprotein XlHbox8. Analyses of IDX-1 mRNA and protein in rat tissues show that IDX-1 is expressed in pancreatic islets and ducts and in the duodenum. In electrophoretic mobility shift assays ZDX-1 binds to three sites in the 5' flanking region of the rat somatostatin gene. In co-transfection experiments IDX-1 transactivates reporter constructs containing somatostatin promoter sequences, and mutation of the IDX-1 binding sites attenuates transactivation. Reverse transcription- polymerase chain reaction of islet RNA using degenerate amplimers for mRNAs encoding homeoproteins indicates that IDX-1 is the most abundant of 12 different Antp-like homeodomain mRNAs expressed in adult rat islets. The pattern of expression, relative abundance and transcriptional regulatory activity suggests that IDX-1 may be involved in the regulation of islet hormone genes and in cellular differentiation in the endocrine pancreas and the duodenum. C1 HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02114. RP MILLER, CP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK30457, DK30834] NR 64 TC 366 Z9 369 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD MAR 1 PY 1994 VL 13 IS 5 BP 1145 EP 1156 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NA288 UT WOS:A1994NA28800016 PM 7907546 ER PT J AU NANES, MS KUNO, H DEMAY, MB KURIAN, M HENDY, GN DELUCA, HF TITUS, L RUBIN, J AF NANES, MS KUNO, H DEMAY, MB KURIAN, M HENDY, GN DELUCA, HF TITUS, L RUBIN, J TI A SINGLE UP-STREAM ELEMENT CONFERS RESPONSIVENESS TO 1,25-DIHYDROXYVITAMIN D-3 AND TUMOR-NECROSIS-FACTOR-ALPHA IN THE RAT OSTEOCALCIN GENE SO ENDOCRINOLOGY LA English DT Article ID NF-KAPPA-B; BONE-FORMATION INVITRO; CELLS ROS 17/2.8; COLLAGEN-SYNTHESIS; INTERFERON-GAMMA; PRETRANSLATIONAL MECHANISM; DEOXYRIBONUCLEIC-ACID; MONOCLONAL-ANTIBODIES; PHENOTYPE SUPPRESSION; OSTEOSARCOMA CELLS AB Tumor necrosis factor-alpha (TNF alpha) is one of several autocrine/paracrine factors known to exert potent inhibitory effects on bone. We have shown that TNF alpha inhibition of 1,25-dihydroxyvitamin D-3 [1,25(OH)(2)D-3]-stimulated synthesis of the bone-specific protein osteocalcin (OC) occurs by decreasing steady state levels of OC mRNA, suggesting a pretranslational mechanism. In many genes, TNF alpha action is mediated by the transcription factor NF kappa B. Analysis of OC 5'-flanking DNA revealed a sequence structurally homologous to the previously described NF kappa B-binding site and, thus, a potential TNF alpha response element. Deletion analysis was performed to identify the sequences mediating the response to TNF alpha in osteoblastic ROS 17/2.8 cells by transient transfection with reporter constructs containing rat OC 5'-flanking DNA [chloramphenicol acetyltransferase (CAT)I that retained or deleted homologous NF kappa B sites or a previously defined 1,25-(OH)(2)D-3 response element (VDRE). Transfection with all reporter constructs resulted in low basal CAT activity, measured 72 h after transfection. 1,25-(OH)(2)D-3 stimulated CAT activity 2.8- to 4.5-fold in cells transfected with constructs that included the VDRE. TNF alpha inhibited 1,25-(OH)(2)D-3-stimulated, but not basal, CAT activity. Deletion analysis localized the effect of TNF alpha to a sequence between -522 and -306 relative to the OC transcription start site, an area that included the VDRE but deleted a homologous NF kappa B element. Transfection of cells with a heterologous reporter containing one copy of the OC VDRE inserted in correct orientation or two copies in inverse orientation was sufficient to confer a response to TNF alpha. Gel mobility shift analysis of DNA-nuclear protein interaction revealed that 1,25-(OH)(2)D-3 stimulated an increase in binding of nuclear proteins to an OC P-32-VDRE probe. Preincubation of nuclear extract with specific monoclonal antibodies confirmed that the proteins binding the VDRE included the vitamin D receptor and retinoid-X receptor. TNF alpha treatment of cells inhibited the 1,25-(OH)(2)D-3-stimulated increase in nuclear protein binding to the VDRE. These results suggest 1) the VDRE is sufficient to confer a response to the inhibitory effect of TNF alpha on 1,25-(OH)(2)D-3-stimulated rat OC gene transcription; 2) the action of TNF alpha does not require homologous NF kappa B response elements; and 3) the mechanism of TNF alpha inhibition of 1,25-(OH)(2)D-3-stimulated OC gene expression includes modulation of binding of the vitamin D receptor/retinoid-X receptor heterodimer to the VDRE. C1 MCGILL UNIV, CALCIUM RES LAB, MONTREAL H3A 1A1, PQ, CANADA. MCGILL UNIV, DEPT MED, MONTREAL H3A 1A1, PQ, CANADA. MCGILL UNIV, DEPT PHYSIOL, MONTREAL H3A 1A1, PQ, CANADA. ROYAL VICTORIA HOSP, MONTREAL H3A 1A1, PQ, CANADA. UNIV WISCONSIN, COLL AGR & LIFE SCI, MADISON, WI 53706 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, ENDOCRINE UNIT, BOSTON, MA 02114 USA. RP NANES, MS (reprint author), EMORY UNIV, SCH MED, VET AFFAIRS MED CTR, DIV ENDOCRINOL & METAB, MED SERV 111E, DECATUR, GA 30033 USA. FU NIDDK NIH HHS [R01-DK-36597] NR 61 TC 20 Z9 21 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 1994 VL 134 IS 3 BP 1113 EP 1120 DI 10.1210/en.134.3.1113 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MZ443 UT WOS:A1994MZ44300017 PM 8119149 ER PT J AU ARNOLD, A AF ARNOLD, A TI MOLECULAR MECHANISMS OF PARATHYROID NEOPLASIA SO ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA LA English DT Article ID GROWTH-FACTOR; CYCLIN-D; RETINOBLASTOMA PROTEIN; CENTROCYTIC LYMPHOMA; CANDIDATE ONCOGENE; PUTATIVE ONCOGENE; CHROMOSOME 11Q13; DEPENDENT KINASE; PRAD1/CYCLIN D1; ALLELIC LOSS RP ARNOLD, A (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE ONCOL LAB,JACKSON 1021,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA55909]; NIDDK NIH HHS [DK11794] NR 53 TC 19 Z9 19 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8529 J9 ENDOCRIN METAB CLIN JI Endocrinol. Metabol. Clin. North Amer. PD MAR PY 1994 VL 23 IS 1 BP 93 EP 107 PG 15 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NE023 UT WOS:A1994NE02300008 PM 7913032 ER PT J AU MITCHELL, JD LEE, R NEYA, K VLAHAKES, GJ AF MITCHELL, JD LEE, R NEYA, K VLAHAKES, GJ TI REDUCTION IN EXPERIMENTAL PERICARDIAL ADHESIONS USING A HYALURONIC-ACID BIOABSORBABLE MEMBRANE SO EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY LA English DT Article DE PERICARDIAL SUBSTITUTES; HYALURONIC ACID; PERICARDIAL ADHESIONS; REOPERATIVE CARDIAC SURGERY AB Various materials have been suggested for pericardial closure following cardiac surgery to limit postoperative adhesion formation. Unfortunately, these devices have caused difficulties with infection, calcification, and epicardial scar formation. A bioabsorbable membrane with a short in-vivo persistence time, acting as a barrier to adhesion formation until mesothelial healing occurs, might obviate many of these problems. We examined the efficacy of a bioabsorbable membrane containing hyaluronic acid in the prevention of experimental pericardial adhesions; hyaluronic acid solutions have been shown experimentally to reduce adhesions following abdominal, orthopedic and cardiac surgery. Eleven dogs underwent sternotomy and pericardiotomy followed by 2-h protocol of desiccation and abrasion of pericardial and epicardial surfaces. In five dogs, the epicardial surfaces were covered with the test material, followed by pericardial and sternotomy closure. Six dogs served as controls. All animals underwent resternotomy 8 weeks after surgery; intrapericardial adhesions were graded on a severity scale (0-4). The test animals (mean adhesion score 1.4 +/- 0.5) had either no adhesions or filmy, avascular adhesions easily taken down with blunt dissection. In contrast, dense adhesions were found in the control animals (mean score 3.2 +/- 0.4), frequently obscuring tissue planes and epicardial anatomy. Use of the bioabsorbable membrane significantly reduced adhesion formation (test vs control, P < 0.001, Mann-Whitney test). We conclude that a hyaluronic acid membrane reduces postoperative pericardial adhesions in this canine model, and that the use of a bioabsorbable barrier in the prevention of pericardial adhesions warrants further investigation. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 32 Z9 32 U1 1 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 1010-7940 J9 EUR J CARDIO-THORAC JI Eur. J. Cardio-Thorac. Surg. PD MAR PY 1994 VL 8 IS 3 BP 149 EP 152 DI 10.1016/1010-7940(94)90172-4 PG 4 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA NM463 UT WOS:A1994NM46300009 PM 8011349 ER PT J AU SLUSS, PM LEE, KE MATTOX, JH SMITH, PC GRAHAM, MC PARTRIDGE, AB AF SLUSS, PM LEE, KE MATTOX, JH SMITH, PC GRAHAM, MC PARTRIDGE, AB TI ESTRADIOL AND PROGESTERONE PRODUCTION BY CULTURED GRANULOSA-CELLS CRYOPRESERVED FROM IN-VITRO FERTILIZATION PATIENTS SO EUROPEAN JOURNAL OF ENDOCRINOLOGY LA English DT Article ID INVITRO FERTILIZATION; CLOMIPHENE CITRATE; LUTEAL CELLS; HORMONE; SECRETION; MODULATION; OVULATION; INDUCTION AB Gonadotropin-stimulated steroidogenesis was studied in cultured human granulosa-lutein cells obtained from patients undergoing procedures for in vitro fertilization. The impact of cryopreservation on cell function in vitro was studied. Granulosa cells obtained from in vitro fertilization patients were cultured in serum-supplemented medium or cryopreserved at -135 degrees C for 2-22 months. Fresh (unfrozen) cells (10(5)) produced estradiol at a rate of 1320 pmol/l (over 72 h) and progesterone at about 2500 nmol/l. Estradiol production by either fresh or cryopreserved granulosa cells in culture was unaffected by physiological concentrations of follicle-stimulating hormone (7 IU/l). Adding testosterone (10(-7) mol/l) to the medium increased estradiol secretion approximately sixfold. In contrast, progesterone production was not affected by follicle-stimulating hormone or testosterone. No significant differences were observed in cultures of cryopreserved granulosa cells compared to cultures of unfrozen cells with respect to estradiol secretion, the effects of follicle-stimulating hormone or testosterone on estradiol secretion, or progesterone production. Progesterone production by fresh and cryopreserved cells was stimulated by human chorionic gonadotropin. These data indicate that cryopreservation offers the potential to facilitate prospective studies utilizing large numbers of human granulosa-lutein cells in culture. C1 UNIV ROCHESTER,MED CTR,DEPT UROL,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT OBSTET & GYNECOL,ROCHESTER,NY 14642. MASSACHUSETTS GEN HOSP,REPROD ENDOCRINE UNIT,BOSTON,MA 02114. FU NICHD NIH HHS [HD19302, U54-HD29164] NR 22 TC 4 Z9 4 U1 0 U2 2 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0804-4643 J9 EUR J ENDOCRINOL JI Eur. J. Endocrinol. PD MAR PY 1994 VL 130 IS 3 BP 259 EP 264 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NK511 UT WOS:A1994NK51100010 PM 8156099 ER PT J AU SHERIDAN, RL HEGARTY, M TOMPKINS, RG BURKE, JF AF SHERIDAN, RL HEGARTY, M TOMPKINS, RG BURKE, JF TI ARTIFICIAL SKIN IN MASSIVE BURNS - RESULTS TO 10 YEARS SO EUROPEAN JOURNAL OF PLASTIC SURGERY LA English DT Article DE MASSIVE BURNS; ARTIFICIAL SKIN; FOLLOW-UP AB Artificial skin, applied as a completely synthetic bilaminate skin evolving into a completely biologic self-skin replacement, was initially used in 1980. It has been used in 121 patients to date, at the Massachusetts General Hospital and the Boston Unit of the Shriners Burns Institute with follow-up as long as ten years. This report describes the generally gratifying long-term results with the use of artificial skin in massive burns. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,DEPT SURG,SURG SERV,BOSTON,MA 02114. NR 0 TC 85 Z9 91 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0930-343X J9 EUR J PLAST SURG JI Eur. J. Plast. Surg. PD MAR PY 1994 VL 17 IS 2 BP 91 EP 93 PG 3 WC Surgery SC Surgery GA NG998 UT WOS:A1994NG99800009 ER PT J AU YANG, KD SHAIO, MF WANG, CL WU, NC STONE, RM AF YANG, KD SHAIO, MF WANG, CL WU, NC STONE, RM TI NEUROBLASTOMA CELL-MEDIATED LEUKOCYTE CHEMOTAXIS - LINEAGE-SPECIFIC DIFFERENTIATION OF INTERLEUKIN-8 EXPRESSION SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID TUMOR-NECROSIS-FACTOR; NEURO-BLASTOMA CELLS; RETINOIC ACID; MOLECULAR-CLONING; GAMMA-INTERFERON; GROWTH-FACTOR; INHIBITION; CYTOKINES; GENE; GLIOBLASTOMA AB To determine whether neural crest-derived neuroblastoma cells may release cytokines which regulate the function of leukocytes, we found that neuroblastoma (HTB-11) cells did not constitutionally express IL-1 beta, TNF alpha, or IL-8 mRNA. However, TNF alpha, which induced HTB-11 cells to differentiate to perineurium-like cells, induced expression of IL-8 mRNA in a dose- and time-dependent fashion. In contrast, pentoxifylline (1 mM), which promoted HTB-11 cells to differentiate to polygonal neuron-like cells, did not induce IL-8 mRNA expression. As determined by enzyme-linked immunoassay, high levels of IL-8 were detectable in the culture supernatants from TNF alpha-treated neuroblastoma cells, but not pentoxifylline-treated neuroblastoma cells (19.60 +/- 2.34 vs 0.10 +/- 0.06 ng/ml). Culture supernatants obtained from TNF alpha-treated neuroblastoma cells induced chemotaxis of neutrophils and lymphocytes that was significantly blocked by anti-IL-8 neutralizing antibodies. Detection of a leukocyte chemotactic factor was not observed in the culture supernatants from pentoxifylline-treated cells. These results suggest that neural crest-derived perineurium-like cells, but not neuron-like cells, may release a leukocyte chemotactic factor or factors such as IL-8 which could be involved in leukocyte recruitment seen in inflammatory diseases affecting peripheral nerves. (C) 1994 Academic Press, Inc. C1 NATL DEF MED CTR,DEPT PEDIAT,TAIPEI 107,TAIWAN. NATL DEF MED CTR,DEPT PARASITOL & TROP MED,TAIPEI 107,TAIWAN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. NR 34 TC 12 Z9 12 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD MAR PY 1994 VL 211 IS 1 BP 1 EP 5 DI 10.1006/excr.1994.1050 PG 5 WC Oncology; Cell Biology SC Oncology; Cell Biology GA MZ220 UT WOS:A1994MZ22000001 PM 8125147 ER PT J AU PAUL, SR HAYES, LL PALMER, R MORRIS, GE NEBEN, TY LOEBELENZ, J PEDNEAULT, G BROOKS, J BLUE, I MOORE, MAS MUENCH, M TURNER, KJ SCHAUB, R GOLDMAN, SJ WOOD, CR AF PAUL, SR HAYES, LL PALMER, R MORRIS, GE NEBEN, TY LOEBELENZ, J PEDNEAULT, G BROOKS, J BLUE, I MOORE, MAS MUENCH, M TURNER, KJ SCHAUB, R GOLDMAN, SJ WOOD, CR TI INTERLEUKIN-11 EXPRESSION IN DONOR BONE-MARROW CELLS IMPROVES HEMATOLOGICAL RECONSTITUTION IN LETHALLY IRRADIATED RECIPIENT MICE SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE INTERLEUKIN-11; RETROVIRUS MEDIATED GENE TRANSFER; BONE MARROW TRANSPLANTATION ID HEMATOPOIETIC PROGENITORS; MOLECULAR-CLONING; INHIBITORY FACTOR; GENE-TRANSFER; INVITRO; GROWTH; MURINE; LINE AB Lethally irradiated mice were transplanted with syngeneic bone marrow cells infected with a recombinant retrovirus vector containing the human interleukin-ll (hIL-11) cDNA under the control of the human cytomegalovirus (CMV) immediate early promoter. The hIL-11 RNA transcript from the vector was detected in the spleen and bone marrow of the recipient mice, and hIL-11 protein accumulated in their serum. The hematological reconstitution of these mice was compared with recipient mice rescued with bone marrow infected with the parental retrovirus vector not containing the hIL-11 cDNA. The hIL-11-expressing mice had an accelerated recovery of circulating platelets and red and white blood cells. Three months after the transplantation, bone marrow was harvested from the mice and used to rescue other lethally irradiated recipients. The hIL-11 mRNA and protein were also detected in these secondary recipients, and the mice showed improved hematological reconstitution relative to a control group. No abnormal cell proliferation or other histopathology was observed in the hIL-11-expressing mice. C1 GENET INST INC,CAMBRIDGE,MA 02140. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY. RI Muench, Marcus/C-5025-2009 OI Muench, Marcus/0000-0001-8946-6605 NR 29 TC 17 Z9 17 U1 0 U2 2 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD MAR PY 1994 VL 22 IS 3 BP 295 EP 301 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA MY677 UT WOS:A1994MY67700011 PM 8112427 ER PT J AU TANG, SS JUNG, F DIAMANT, D INGELFINGER, J AF TANG, SS JUNG, F DIAMANT, D INGELFINGER, J TI IMMORTALIZED RAT PROXIMAL TUBULE CELL-LINES EXPRESSING COMPONENTS OF THE RENIN-ANGIOTENSIN SYSTEM SO EXPERIMENTAL NEPHROLOGY LA English DT Note RP TANG, SS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT NEPHROL LAB,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL 43131, HL-48455] NR 0 TC 14 Z9 14 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-7782 J9 EXP NEPHROL JI Exp. Nephrol. PD MAR-APR PY 1994 VL 2 IS 2 BP 127 EP 127 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA NH188 UT WOS:A1994NH18800014 PM 8082004 ER PT J AU ANDERSON, P SORRELL, JM ACKERLY, M VIVIER, E AF ANDERSON, P SORRELL, JM ACKERLY, M VIVIER, E TI DEVELOPMENTAL REGULATION AND FUNCTIONAL-CHARACTERIZATION OF A NATURAL-KILLER CELL-SPECIFIC MUCIN-LIKE GLYCOPROTEIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A199 EP A199 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19601152 ER PT J AU CLINTON, SK BOSTWICK, DG MOORE, BJ GUGGER, ET WILLIAMS, AS ERDMAN, JW AF CLINTON, SK BOSTWICK, DG MOORE, BJ GUGGER, ET WILLIAMS, AS ERDMAN, JW TI CAROTENOIDS ARE FOUND IN THE HUMAN PROSTATE AT CONCENTRATIONS WHICH MODULATE CELLULAR FUNCTIONS IN-VITRO SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MAYO CLIN & MAYO FDN,DEPT PATHOL,ROCHESTER,MN 55905. UNIV ILLINOIS,DEPT FOOD SCI,DIV NUTR SCI,URBANA,IL 61801. NR 0 TC 1 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A423 EP A423 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19602445 ER PT J AU GONG, JL MCCARTHY, KM REISER, H SCHNEEBERGER, EE AF GONG, JL MCCARTHY, KM REISER, H SCHNEEBERGER, EE TI B7-1 EXPRESSION BY DENDRITIC CELLS (DC) IN MOUSE LUNG SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A513 EP A513 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19602972 ER PT J AU HATTORI, M YAMATO, E ITOH, N MATSUMOTO, E MACMURRAY, A SHIROISHI, T YOSHINO, M MORIWAKI, K AF HATTORI, M YAMATO, E ITOH, N MATSUMOTO, E MACMURRAY, A SHIROISHI, T YOSHINO, M MORIWAKI, K TI INTRA-MHC RECOMBINANT MICE FOR DISSECTING THE MHC REGIONS RESPONSIBLE FOR THE DEVELOPMENT OF DIABETES IN NOD MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 JOSLIN DIABET FDN INC,BOSTON,MA 02215. WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA. NATL INST GENET,MISHIMA,SHIZUOKA 411,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A518 EP A518 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19603000 ER PT J AU HERLIHY, JP GOLDSTEIN, DM VERMEULEN, MW JOSEPH, PM HALES, CA AF HERLIHY, JP GOLDSTEIN, DM VERMEULEN, MW JOSEPH, PM HALES, CA TI TISSUE DESTRUCTIVE POTENTIAL OF APOPTOTIC POLYMORPHONUCLEAR CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A420 EP A420 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19602430 ER PT J AU JOSEPH, PM JOHNSON, K HALES, CA AF JOSEPH, PM JOHNSON, K HALES, CA TI ACROLEIN ALTERS ACTIN STRESS FIBERS IN CULTURED PULMONARY-ARTERY ENDOTHELIAL-CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A148 EP A148 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19600859 ER PT J AU KRADIN, R SURMAN, O RODBERG, G AF KRADIN, R SURMAN, O RODBERG, G TI EPINEPHRINE AUGMENTS T-CELL RESPONSES TO ANTIGEN IN LOW RESPONDER MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,IMMUNOPATHOL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A481 EP A481 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19602784 ER PT J AU MIJAILOVICH, S TREPPO, S VENEGAS, J AF MIJAILOVICH, S TREPPO, S VENEGAS, J TI EFFECTS OF LUNG MOTION, TRACER KINETICS AND BLOOD-POOL CORRECTIONS ON PET IMAGING OF LUNGS IN NORMAL DOGS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A571 EP A571 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19603304 ER PT J AU NAKARAI, T STREULI, M ROBERTSON, MJ SMITH, KA RITZ, J AF NAKARAI, T STREULI, M ROBERTSON, MJ SMITH, KA RITZ, J TI IL-2 RECEPTOR-(R)GAMMA CHAIN EXPRESSION ON RESTING AND ACTIVATED LYMPHOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CORNELL UNIV,MED CTR,DEPT MED,NEW YORK,NY 10021. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A225 EP A225 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19601301 ER PT J AU RODRIGUEZ, A CRUMP, AL FOSTER, CS CANTOR, H AF RODRIGUEZ, A CRUMP, AL FOSTER, CS CANTOR, H TI ALLOTYPE-LINKED GENETIC SUSCEPTIBILITY TO AUTOIMMUNE-DISEASE MAY REFLECT MOLDING OF THE T-CELL REPERTOIRE BY IMMUNOGLOBULIN-DERIVED PROTEINS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,HILLES LAB IMMUNOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,IMMUNOPATHOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT OPHTHALMOL,IMMUNOPATHOL LAB,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A468 EP A468 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19602710 ER PT J AU RYAN, LK MAHONEY, E VERMEULEN, MW AF RYAN, LK MAHONEY, E VERMEULEN, MW TI LIPOPOLYSACCHARIDE ENDOTOXIN (LPS) STIMULATION OF TUMOR-NECROSIS-FACTOR (TNF) IN PRIMARY AND TRANSFORMED ALVEOLAR MACROPHAGES (AM) DERIVED FROM LPS-RESISTANT C3H/HEJ MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02129. NR 1 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A508 EP A508 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19602940 ER PT J AU SILVERMAN, ES GOSLANT, CE QUINN, DA BONVENTRE, JV JOSEPH, PM THOMPSON, BT HALES, CA AF SILVERMAN, ES GOSLANT, CE QUINN, DA BONVENTRE, JV JOSEPH, PM THOMPSON, BT HALES, CA TI SERUM STIMULATES NA+/H+ EXCHANGE IN HUMAN PULMONARY-ARTERY SMOOTH-MUSCLE CELLS BY INCREASING THE PK0.5 AND DECREASING THE HILL COEFFICIENT OF THE ALLOSTERIC INTERNAL MODIFIER SITE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,PULM CRIT CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. SHRINERS HOSP CRIPPLED CHILDREN,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A120 EP A120 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19600695 ER PT J AU SOTOARAPE, I BEAGLE, J BURTON, M KAZEMI, H AF SOTOARAPE, I BEAGLE, J BURTON, M KAZEMI, H TI ROLE OF CENTRAL GLUTAMATE ACID GABA AND SUBSTANCE-P IN THE BIPHASIC HYPOXIC VENTILATORY RESPONSE IN THE RAT SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 1994 VL 8 IS 4 BP A394 EP A394 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND196 UT WOS:A1994ND19602281 ER EF