FN Thomson Reuters Web of Science™ VR 1.0 PT J AU FISCHMAN, AJ STRAUSS, HW AF FISCHMAN, AJ STRAUSS, HW TI CLINICAL PET - A MODEST PROPOSAL SO JOURNAL OF NUCLEAR MEDICINE LA English DT Note ID POSITRON EMISSION TOMOGRAPHY; CORONARY-ARTERY DISEASE; MYOCARDIAL BLOOD-FLOW; QUANTITATIVE MEASUREMENT; COMPUTED-TOMOGRAPHY; N-13 AMMONIA; PERFUSION; TUMORS; RUBIDIUM-82; METASTASES C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP STRAUSS, HW (reprint author), ROOM 5406,MGH E BLDG,149 13TH ST,BOSTON,MA 02129, USA. NR 52 TC 6 Z9 6 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 1991 VL 32 IS 12 BP 2351 EP 2355 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GU534 UT WOS:A1991GU53400038 PM 1744727 ER PT J AU STRAUSS, HW AF STRAUSS, HW TI THE JOY OF THE QUEST SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material RP STRAUSS, HW (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 1991 VL 32 IS 12 BP A3 EP A3 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GU534 UT WOS:A1991GU53400001 ER PT J AU AMBROSINO, DM BLACK, CM PLIKAYTIS, BD REIMER, CB LEE, MC EVATT, BL CARLONE, GM AF AMBROSINO, DM BLACK, CM PLIKAYTIS, BD REIMER, CB LEE, MC EVATT, BL CARLONE, GM TI IMMUNOGLOBULIN-G SUBCLASS VALUES IN HEALTHY BLACK-AND-WHITE CHILDREN SO JOURNAL OF PEDIATRICS LA English DT Article ID HEMOPHILUS-INFLUENZAE DISEASE; IMPAIRED ANTIBODY-RESPONSE; IGG SUBCLASSES; B DISEASE; DEFICIENCY; INFECTIONS; POLYSACCHARIDE; EPIDEMIOLOGY; POPULATION; RECURRENT AB To determine whether IgG subclass concentrations differed between healthy black and white children, we measured IgG1, IgG2, IgG3, and IgG4 immunoglobulins by enzyme-linked immunosorbent assay in sera from 246 black children aged 6 to 42 months. We then compared these values with the normal values established for 664 white children aged 6 to 60 months. The IgG1, IgG2, and IgG4 subclass concentrations of the black children were lower than those for white children; many of the values were below the 95% confidence limits established for white children: 46 (19%) of 246 IgG2 values and 19 (8%) of 246 IgG4 values for black children were below the normal limits. We compared the geometric mean values for black and white children, as determined for each 6-month age grouping between 6 and 42 months of age; 367 of the 664 white children were less than 42 months of age and were included in this analysis. The geometric mean values for IgG1, IgG2, and IgG4 levels were consistently lower for black children than for white children. The differences were significant for IgG1 subclass values of those children older than 24 months and for IgG2 and IgG4 values of those children older than 18 months. No consistent differences were noted for IgG3 subclass values. We conclude that young black children have lower IgG1, IgG2, and IgG4 serum concentrations than are found in white children. If normal IgG values for white children are used, healthy black children may be erroneously classified as IgG subclass deficient. The mechanism and biologic relevance of these population differences need to be evaluated. C1 CTR DIS CONTROL, MOLEC BIOL LAB, BLDG 1, ROOM 1260, A36, ATLANTA, GA 30333 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, INFECT DIS LAB, BOSTON, MA 02115 USA. RP CARLONE, GM (reprint author), CTR DIS CONTROL, MOLEC BIOL LAB, BLDG 1, ROOM 1260, A36, ATLANTA, GA 30333 USA. FU NIAID NIH HHS [AI29623, AI24659] NR 29 TC 18 Z9 18 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD DEC PY 1991 VL 119 IS 6 BP 875 EP 879 DI 10.1016/S0022-3476(05)83036-7 PG 5 WC Pediatrics SC Pediatrics GA GV185 UT WOS:A1991GV18500005 PM 1960601 ER PT J AU FISCHMAN, AJ ALPERT, NM LIVNI, E RAY, S SINCLAIR, I ELMALEH, DR WEISS, S CORREIA, JA WEBB, D LISS, R STRAUSS, HW RUBIN, RH AF FISCHMAN, AJ ALPERT, NM LIVNI, E RAY, S SINCLAIR, I ELMALEH, DR WEISS, S CORREIA, JA WEBB, D LISS, R STRAUSS, HW RUBIN, RH TI PHARMACOKINETICS OF F-18 LABELED FLUCONAZOLE IN RABBITS WITH CANDIDAL INFECTIONS STUDIED WITH POSITRON EMISSION TOMOGRAPHY SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID CEREBROSPINAL-FLUID; PENETRATION; HUMANS; PERFORMANCE; HYPOTHESIS; TRIAZOLES; PROFILE; SYSTEM; DRUG AB [4-F-18]Fluconazole was used to measure the pharmacokinetics of fluconazole in normal and infected animals. The biodistribution of fluconazole was determined after administration of the F-18-tracer with/without a pharmacological dose of unlabeled drug by radioactivity measurements on excised tissues. In normal rabbits and rabbits with candidal infection of the thigh, tissue concentrations of drug were determined by serial positron emission tomographic imaging. In rats, coinjection of tracer quantities of [4-F-18]fluconazole with a pharmacological dose of unlabeled drug resulted in a relatively uniform distribution of radioactivity in most organs, whereas, when the F-18-tracer was injected alone, spleen, muscle and heart accumulation was decreased and liver accumulation was increased. In rabbits, this effect was less pronounced. Early accumulation of [4-F-18]fluconazole was greater in infected muscle. The areas under the 2-hr uptake curves were 4.30 and 6.05-mu-g.hr.ml-1 for normal and infected tissue. A mathematical model was used to summarize the kinetics of fluconazole in normal and infected muscle. The model hypothesizes that fluconazole is compartmentalized in blood and tissue, with rate constants describing the transition between compartments. Direct measurement of the partition coefficient of fluconazole in muscle and predictions of the kinetic model were in close agreement, suggesting that fluconazole enters muscle via a passive transport mechanism. Transport rates of fluconazole, into (K(in)) and out of tissue (K(out)), were increased in infected compared with normal muscle, possibly due to increased capillary permeability (K(in): 0.064 +/- 0.001 vs. 0.0270 +/- 0.0002, K(out): 0.063 +/- 0.002 vs. 0.035 +/- 0.001). 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 02115. PFIZER LTD,CENT RES,SANDWICH,KENT,ENGLAND. PFIZER INC,ROERIG MED DEPT,NEW YORK,NY. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02115. RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 26 TC 22 Z9 23 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD DEC PY 1991 VL 259 IS 3 BP 1351 EP 1359 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GW107 UT WOS:A1991GW10700057 PM 1762083 ER PT J AU DEPAOLA, PF AF DEPAOLA, PF TI REACTION PAPER - THE USE OF TOPICAL AND SYSTEMIC FLUORIDES IN THE PRESENT ERA SO JOURNAL OF PUBLIC HEALTH DENTISTRY LA English DT Article; Proceedings Paper CT SYMP AT THE 1990 ANNUAL MEETING OF THE AMERICAN ASSOC OF PUBLIC HEALTH DENTISTRY - APPROPRIATE USES OF FLUORIDE : CONSIDERATIONS FOR THE 90S CY OCT 10-13, 1990 CL BOSTON, MA SP AMER ASSOC PUBLIC HLTH DENT ID TEETH AB Systemic fluoride may enhance the resistance of the tooth by way of (1) an alteration in tooth morphology, and (2) a conversion of the hydroxyapatitic mineral to a fluoridated state with an attendant reduction in solubility and an enhancement of the remineralization phase of the caries process. It has been reported by a number of investigators, although it is not universally accepted, that the posterior teeth from fluoridated areas have a distinct morphology that is less susceptible to caries attack. Fluorapatite and hydroxyapatite do not differ appreciably with respect to the amount of mineral that dissolves at a specified concentration of acid. However, if solubility is considered as a function of pH at equilibrium, i.e., the final pH after the dissolution products have entered the solvent-a model more akin to the in vivo situation-hydroxyapatite is the conspicuously more soluble of the two minerals. In this connection, epidemiologic data suggest that children with unusually high levels of surface enamel fluoride have little or no caries. This observation is consistent with the finding that the solubility of solid apatite solutions with varying degrees of fluoride substitution was inversely related to fluoride content, with minimal solubility at 0.5 substitution, a value observed in natural teeth at the very outermost surface of the enamel. Evidence of a preeruptive effect of fluoride has also been shown in field studies in which subjects had reduced levels of caries with fluoride exposure in childhood only. RP DEPAOLA, PF (reprint author), FORSYTH DENT CTR,DEPT CLIN TRIALS & EXPERIMENTAT,140 FENWAY,BOSTON,MA 02115, USA. NR 16 TC 9 Z9 9 U1 1 U2 2 PU AAPHD NATIONAL OFFICE PI RICHMOND PA J PUBLIC HEALTH DENT 10619 JOUSTING LANE, RICHMOND, VA 23235 SN 0022-4006 J9 J PUBLIC HEALTH DENT JI J. Public Health Dent. PD WIN PY 1991 VL 51 IS 1 BP 48 EP 52 DI 10.1111/j.1752-7325.1991.tb02174.x PG 5 WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health GA FA385 UT WOS:A1991FA38500007 PM 2027102 ER PT J AU BARDIN, T SCHUMACHER, HR AF BARDIN, T SCHUMACHER, HR TI SHOULD WE TREAT POSTVENEREAL REITERS-SYNDROME BY ANTIBIOTICS SO JOURNAL OF RHEUMATOLOGY LA English DT Editorial Material ID CHLAMYDIA-TRACHOMATIS INFECTIONS; REACTIVE ARTHRITIS; DISEASE C1 UNIV PENN,SCH MED,RHEUMATOL SECT,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,PHILADELPHIA,PA 19104. HOP LARIBOISIERE,CTR VIGGO PETERSEN,RHUMATOL CLIN,F-75475 PARIS 10,FRANCE. NR 30 TC 16 Z9 16 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 DEC PY 1991 VL 18 IS 12 BP 1780 EP 1782 PG 3 WC Rheumatology SC Rheumatology GA HA099 UT WOS:A1991HA09900003 PM 1795310 ER PT J AU ROSENBEK, JC ROBBINS, J FISHBACK, B LEVINE, RL AF ROSENBEK, JC ROBBINS, J FISHBACK, B LEVINE, RL TI EFFECTS OF THERMAL APPLICATION ON DYSPHAGIA AFTER STROKE SO JOURNAL OF SPEECH AND HEARING RESEARCH LA English DT Article DE DYSPHAGIA; THERMAL APPLICATION; STROKE; REHABILITATION C1 UNIV WISCONSIN,SCH MED,DEPT NEUROL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP ROSENBEK, JC (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 21 TC 52 Z9 56 U1 0 U2 1 PU AMER SPEECH-LANG-HEARING ASSN PI ROCKVILLE PA 10801 ROCKVILLE PIKE RD, ROCKVILLE, MD 20852-3279 SN 0022-4685 J9 J SPEECH HEAR RES JI J. Speech Hear. Res. PD DEC PY 1991 VL 34 IS 6 BP 1257 EP 1268 PG 12 WC Language & Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA GU526 UT WOS:A1991GU52600004 PM 1787707 ER PT J AU MUNFAKH, NA STEINBERG, JB TITUS, JS DENENBERG, AG OKEEFE, DD DAGGETT, WM GEFFIN, GA AF MUNFAKH, NA STEINBERG, JB TITUS, JS DENENBERG, AG OKEEFE, DD DAGGETT, WM GEFFIN, GA TI PROTECTION OF THE HYPERTROPHIED MYOCARDIUM BY CRYSTALLOID CARDIOPLEGIA SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 1990 ANNUAL MEETING OF THE ASSOC FOR ACADEMIC SURGERY CY NOV 14-17, 1990 CL HOUSTON, TX SP ASSOC ACAD SURG ID LEFT-VENTRICULAR HYPERTROPHY; VALVULAR AORTIC-STENOSIS; BLOOD-FLOW; PRESERVATION; CALCIUM; HEART; ISCHEMIA; INJURY; ARREST; REPLACEMENT C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP MUNFAKH, NA (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL 12322] NR 37 TC 9 Z9 9 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD DEC PY 1991 VL 51 IS 6 BP 447 EP 456 DI 10.1016/0022-4804(91)90163-G PG 10 WC Surgery SC Surgery GA GP885 UT WOS:A1991GP88500001 PM 1834890 ER PT J AU EMANUEL, L AF EMANUEL, L TI THE HEALTH-CARE DIRECTIVE - LEARNING HOW TO DRAFT ADVANCE CARE DOCUMENTS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID LIFE-SUSTAINING TREATMENT; PREFERENCES; PHYSICIANS; ATTITUDES C1 MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BOSTON,MA 02114. RP EMANUEL, L (reprint author), HARVARD UNIV,SCH MED,DIV MED ETH,BOSTON,MA 02115, USA. NR 17 TC 43 Z9 43 U1 0 U2 1 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 DEC PY 1991 VL 39 IS 12 BP 1221 EP 1228 PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA GT521 UT WOS:A1991GT52100013 PM 1960367 ER PT J AU SZERLIP, H PALEVSKY, P COX, M BLAZERYOST, B AF SZERLIP, H PALEVSKY, P COX, M BLAZERYOST, B TI RELATIONSHIP OF THE ALDOSTERONE-INDUCED PROTEIN, GP70, TO THE CONDUCTIVE NA+ CHANNEL SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article DE RENAL EPITHELIAL NA+ TRANSPORT; SODIUM CHANNEL; TOAD URINARY BLADDER (BUFO-MARINUS); GLYCOPROTEINS ID EPITHELIAL SODIUM-CHANNEL; MARINUS URINARY BLADDERS; TOAD BLADDER; HORMONAL-REGULATION; SUBUNIT; PUMP; PERMEABILITY; LOCALIZATION; SPECIFICITY; TRANSPORT AB Although one of the primary effects of aldosterone is to increase apical membrane Na+ conductance, as yet none of the proteins induced by the hormone in renal epithelia have been shown to be related to the conductive Na+ channel. Because the toad urinary bladder aldosterone-induced glycoprotein, GP70, has recently been localized to the apical surface of this Na+ transporting epithelium, whether GP70 is associated with the Na+ channel was examined. The specilicities of a monoclonal antibody used to characterize GP70 (mAb 20) and a polyclonal antibody raised against the purified bovine renal papillary Na+ channel (anti-CH) were compared: GP70 was specifically immunoprecipitated by both mAb 20 and anti-CH. Moreover, the sodium dodecyl sulfate-polyacrylamide gel electrophoresis profile of mAb 20 purified toad urinary bladder membrane preparations was similar to those reported for bovine and A6 cell Na+ channels. Under nonreducting conditions, a single, very large protein was evident; reduction yielded GP70, a 140-kd polypeptide, and a number of minor bands. Interestingly, only GP70 was induced by aldosterone. Thus, GP70 appears to be associated with the toad urinary bladder conductive Na+ channel; whether GP70 is an integral subunit of the channel or whether it functions as a regulatory moiety remains to be determined. Whatever the case, because GP70 is induced by aldosterone, it likely has a central role in Na+ channel modulation. C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. RP SZERLIP, H (reprint author), VET AFFAIRS MED CTR,MED SERV 3,DEPT MED,RENAL ELECTROLYTE SECT,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 31 TC 14 Z9 14 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 DEC PY 1991 VL 2 IS 6 BP 1108 EP 1114 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA GV914 UT WOS:A1991GV91400008 PM 1663799 ER PT J AU YUCEL, EK FILLMORE, DJ KNOX, TA WALTMAN, AC AF YUCEL, EK FILLMORE, DJ KNOX, TA WALTMAN, AC TI SONOGRAPHIC MEASUREMENT OF ABDOMINAL AORTIC DIAMETER - INTEROBSERVER VARIABILITY SO JOURNAL OF ULTRASOUND IN MEDICINE LA English DT Article ID ANEURYSMS; ULTRASOUND AB Twenty-eight patients undergoing sonographic evaluation of the abdominal aorta were examined by two separate observers. Three measurements were obtained from each patient: the anteroposterior diameter from an axial image (APA), the right-left diameter from an axial image (RLA), and the anteroposterior diameter from a longitudinal image (APL). Calculation of the interobserver variability gave the following results (in mm): APL, 2.22; APA, 2.53; and RLA, 2.84. The calculated 95% confidence intervals for a single measurement (in mm) were APL, 4.35; APA, 4.94; and RLA, 5.58. C1 NEW ENGLAND MED CTR HOSP,DEPT MED,BOSTON,MA 02111. RP YUCEL, EK (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 7 TC 27 Z9 27 U1 0 U2 0 PU AMER INST ULTRASOUND MEDICINE PI LAUREL PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906 SN 0278-4297 J9 J ULTRAS MED JI J. Ultrasound Med. PD DEC PY 1991 VL 10 IS 12 BP 681 EP 683 PG 3 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA GW580 UT WOS:A1991GW58000007 PM 1766039 ER PT J AU BACHOR, R SHEA, CR BELMONTE, SJ HASAN, T AF BACHOR, R SHEA, CR BELMONTE, SJ HASAN, T TI FREE AND CONJUGATED CHLORIN-E6 IN THE PHOTODYNAMIC THERAPY OF HUMAN BLADDER-CARCINOMA CELLS SO JOURNAL OF UROLOGY LA English DT Article DE BLADDER NEOPLASMS; PHOTO-CHEMO-THERAPY ID TUMOR; CANCER; PORPHYRIN; AGENTS AB Photodynamic therapy is an experimental modality for treatment of superficial bladder cancer, and consists of the administration of a photosensitizer and subsequent tumor-irradiation with light. Presently hematoporphyrin derivative (HPD) is the only photosensitizer in experimental clinical use in the United States. Because of the high nonspecific phototoxicity of HPD, new methods of photosensitization have been sought. In this study we compared chlorin e6, free and conjugated to 1-mu-m.-diameter latex microspheres. Phototoxicity was evaluated on MGH-U1 cells derived from a human bladder carcinoma. MGH-U1 cells were preincubated for 18 hours either with free Ce6 (0.43-mu-M) or Ce6-microspheres (0.43-mu-M equivalent in Ce6) and irradiated with an argon-laser-pumped dye laser emitting at 659 nm., over the radiant-exposure range of 5-50 J/cm.2 At 24 hours after light exposure the cells were observed microscopically for morphological alteration and evaluated for cell death by trypan blue exclusion. Cultures incubated with Ce6-microspheres and subsequently irradiated showed morphologic evidence of cell damage, apparent after irradiation with five J/cm.2 and a light dose dependent decrease in cell survival. In contrast, cells incubated with free Ce6 at the same concentration of 0.43-mu-M and subsequently irradiated demonstrated neither detectable morphologic alteration nor change in cell survival. Only cells preincubated with free Ce6 at higher concentration showed morphologic changes. Thus, Ce6-microsphere conjugate was much more efficient at inducing photodynamic destruction of bladder carcinoma cells than was free Ce6. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. RP BACHOR, R (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT UROL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [2 RO1-AR23595] NR 28 TC 14 Z9 14 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD DEC PY 1991 VL 146 IS 6 BP 1654 EP 1658 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA GR667 UT WOS:A1991GR66700061 PM 1942362 ER PT J AU CASAZ, P SUNDSETH, R HANSEN, U AF CASAZ, P SUNDSETH, R HANSEN, U TI TRANSACTIVATION OF THE SIMIAN VIRUS-40 LATE PROMOTER BY LARGE T-ANTIGEN REQUIRES BINDING-SITES FOR THE CELLULAR TRANSCRIPTION FACTOR TEF-1 SO JOURNAL OF VIROLOGY LA English DT Article ID SV40 LATE PROMOTER; UBIQUITOUS NUCLEAR PROTEINS; LARGE TUMOR-ANTIGEN; GENE-EXPRESSION; ENHANCER FUNCTION; SEQUENCE MOTIFS; DNA; INVITRO; STIMULATION; INDUCTION AB Simian virus 40 (SV40) T antigen stimulates the level of transcription from several RNA polymerase II promoters, including the SV40 late promoter. The mechanism of trans activation appears to be indirect since binding of T antigen to specific DNA sequences is not required. However, specific promoter elements that respond to T antigen have not previously been defined. We identified DNA sequences from the SV40 late promoter whose ability to stimulate transcription is induced by the expression of T antigen. In particular, the Sph I + II motifs of the SV40 enhancer can confer T-antigen inducibility to the normally uninducible herpes simplex virus thymidine kinase gene promoter when multiple copies of the sequence are inserted 5' of the transcription initiation site and TATA sequence. Binding sites for the cellular transcription factor TEF-1 and octamer binding proteins are contained within the Sph I + II motifs, as well as at other positions in the SV40 promoter. To study the role of individual protein-binding sites in trans activation by T antigen, mutations were constructed in various TEF-1 and octamer protein-binding sites of the SV40 late promoter. These mutations did not significantly affect basal promoter activity. However, mutation of all three TEF-1 sites prevented detectable activation by T antigen. DNase I footprinting of the mutated promoters with purified proteins demonstrated that inducibility by T antigen correlated with binding affinity of TEF-1 for the DNA and not with binding affinity of an octamer binding protein. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,EUKARYOT TRANSCRIPT LAB,COMM VIROL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NCI NIH HHS [T32 CA09361] NR 51 TC 25 Z9 25 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 DEC PY 1991 VL 65 IS 12 BP 6535 EP 6543 PG 9 WC Virology SC Virology GA GP878 UT WOS:A1991GP87800019 PM 1658359 ER PT J AU BAND, V DECAPRIO, JA DELMOLINO, L KULESA, V SAGER, R AF BAND, V DECAPRIO, JA DELMOLINO, L KULESA, V SAGER, R TI LOSS OF P53 PROTEIN IN HUMAN PAPILLOMAVIRUS TYPE-16 E6-IMMORTALIZED HUMAN MAMMARY EPITHELIAL-CELLS SO JOURNAL OF VIROLOGY LA English DT Article ID RETINOBLASTOMA SUSCEPTIBILITY GENE; PRIMARY HUMAN KERATINOCYTES; T-ANTIGEN; HUMAN-FIBROBLASTS; PRODUCT; SV40; GROWTH; IDENTIFICATION; TRANSFORMATION; DNA AB We have shown previously that introduction of the human papillomavirus type 16 (HPV16) or HPV18 genome into human mammary epithelial cells induces their immortalization. These immortalized cells have reduced growth factor requirements. We report here that transfection with a single HPV16 gene E6 is sufficient to immortalize these cells and reduce their growth factor requirements. The RB protein is normal in these cells, but the p53 protein is sharply reduced, as shown by immunoprecipitation with anti-p53 antibody (pAB 421). We infer that the E6 protein reduces the p53 protein perhaps by signalling its destruction by the ubiquitin system. The HPV-transforming gene E7 was unable to immortalize human mammary epithelial cells. Thus, cell-specific factors may determine which viral oncogene plays a major role in oncogenesis. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV NEOPLAST DIS MECHANISMS,BOSTON,MA 02115. FU NCI NIH HHS [CA39814] NR 35 TC 174 Z9 176 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 DEC PY 1991 VL 65 IS 12 BP 6671 EP 6676 PG 6 WC Virology SC Virology GA GP878 UT WOS:A1991GP87800035 PM 1658367 ER PT J AU VIRGIN, HW MANN, MA FIELDS, BN TYLER, KL AF VIRGIN, HW MANN, MA FIELDS, BN TYLER, KL TI MONOCLONAL-ANTIBODIES TO REOVIRUS REVEAL STRUCTURE-FUNCTION-RELATIONSHIPS BETWEEN CAPSID PROTEINS AND GENETICS OF SUSCEPTIBILITY TO ANTIBODY ACTION SO JOURNAL OF VIROLOGY LA English DT Article ID CELL-ATTACHMENT PROTEIN; TEMPERATURE-SENSITIVE PHENOTYPE; NUCLEOTIDE-SEQUENCE; TYPE-3 REOVIRUS; 3 SEROTYPES; EXTRAGENIC SUPPRESSION; GENOME SEGMENTS; NEONATAL MICE; S1 GENES; SIGMA-1 AB Thirteen newly isolated monoclonal antibodies (MAbs) were used to study relationships between reovirus outer capsid proteins sigma-3, mu-1c, and lambda-2 (core spike) and the cell attachment protein sigma-1. We focused on sigma-1-associated properties of serotype specificity and hemagglutination (HA). Competition between MAbs revealed two surface epitopes on mu-1c that were highly conserved between reovirus serotype 1 Lang (T1L) and serotype 3 Dearing (T3D). There were several differences between T1L and T3D sigma-3 epitope maps. Studies using T1L x T3D reassortants showed that primary sequence differences between T1L and T3D sigma-3 proteins accounted for differences in sigma-3 epitope maps. Four of 12 non-sigma-1 MAbs showed a serotype-associated pattern of binding to 25 reovirus field isolates. Thus, for reovirus field isolates, different sigma-1 proteins are associated with preferred epitopes on other outer capsid proteins. Further evidence for a close structural and functional interrelationship between sigma-3/mu-1c and sigma-1 included (i) inhibition by sigma-3 and mu-1c MAbs of sigma-1-mediated HA, (ii) enhancement of sigma-1-mediated HA by proteolytic cleavage of sigma-3 and mu-1c, and (iii) genetic studies demonstrating that sigma-1 controlled the capacity of sigma-3 MAbs to inhibit HA. These data suggest that (i) epitopes on sigma-3 and mu-1c lie in close proximity to sigma-1 and that MAbs to these epitopes can modulate sigma-1-mediated functions, (ii) these spatial relationships have functional significance, since removal of sigma-3 and/or cleavage of mu-1c to sigma can enhance sigma-1 function, (iii) in nature, the sigma-1 protein places selective constraints on the epitope structure of the other capsid proteins, and (iv) viral susceptibility to antibody action can be determined by genes other than that encoding an antibody's epitope. C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. OI Tyler, Kenneth/0000-0003-3294-5888 FU NIAID NIH HHS [K11 AI00610]; NINDS NIH HHS [2 P50 NS16998] NR 51 TC 106 Z9 108 U1 1 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD DEC PY 1991 VL 65 IS 12 BP 6772 EP 6781 PG 10 WC Virology SC Virology GA GP878 UT WOS:A1991GP87800047 PM 1719233 ER PT J AU FARNET, CM HASELTINE, WA AF FARNET, CM HASELTINE, WA TI CIRCULARIZATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 DNA INVITRO SO JOURNAL OF VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; HOMOLOGOUS RECOMBINATION; MAMMALIAN-CELLS; RETROVIRAL DNA; RESTRICTION ENDONUCLEASE; NUCLEOTIDE-SEQUENCE; TRANSFECTED DNA; VIRAL-DNA; INTEGRATION; EXPRESSION AB Linear viral DNA present in cytoplasmic extracts of cells newly infected with human immunodeficiency virus type 1 can be induced to form 1-LTR and 2-LTR circles by incubation of the extracts in the presence of added nucleoside triphosphates. No circular DNA forms are detected when extracts are incubated in the absence of added nucleoside triphosphates. Restriction enzyme analysis and polymerase chain reaction analysis with selected primers, as well as DNA sequence analysis of the polymerase chain reaction analysis with selected primers, as well as DNA sequence analysis of the polymerase chain reaction products, show that most of the 2-LTR circles are the result of autointegration reactions, while 1-LTR circles result from recombination between the long terminal repeats on the linear viral DNA. In addition, a small amount of simple 2-LTR circles, formed by end-to-end joining of the linear viral DNA, is formed in vitro. Integration of the linear viral DNA into heterologous DNA competes effectively with the formation of 2-LTR circles by autointegration. However, concentrations of target DNA which completely block autointegration have no effect on the formation of 1-LTR circles or simple 2-LTR circles. Factors present in extracts of uninfected cells can mediate the formation of 1-LTR circles and simple 2-LTR circles from purified deproteinated linear viral DNA, indicating that viral proteins are not necessary for the formation of these two types of circular viral DNA. These experiments demonstrate that all the transformations of linear viral DNA which occur in the nuclei of cells infected with human immunodeficiency virus type 1 can be reproduced in vitro. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,COMM VIROL,BOSTON,MA 02115. OI Farnet, Chris/0000-0003-4927-198X FU NIAID NIH HHS [UOI AI 24845] NR 34 TC 97 Z9 99 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 DEC PY 1991 VL 65 IS 12 BP 6942 EP 6952 PG 11 WC Virology SC Virology GA GP878 UT WOS:A1991GP87800065 PM 1834863 ER PT J AU FLEMINGTON, EK GOLDFELD, AE SPECK, SH AF FLEMINGTON, EK GOLDFELD, AE SPECK, SH TI EFFICIENT TRANSCRIPTION OF THE EPSTEIN-BARR-VIRUS IMMEDIATE-EARLY BZLF1 AND BRLF1 GENES REQUIRES PROTEIN-SYNTHESIS SO JOURNAL OF VIROLOGY LA English DT Note ID DNA-BINDING SPECIFICITY; EARLY ANTIGEN; DISRUPTS LATENCY; LEUCINE ZIPPER; P3HR-1 CELLS; RAJI CELLS; C-FOS; PROMOTER; EBV; EXPRESSION AB The Epstein-Barr virus BRLF1 and BZLF1 genes appear to be the first viral genes transcribed upon induction of the Epstein-Barr virus lytic cycle. Both gene products activate transcription of other viral genes, thereby initiating the lytic cascade. Among the viral antigens expressed upon induction of the lytic cycle, the product of the BZLF1 gene is unique in its ability to disrupt viral latency; thus, expression of this gene is both necessary and sufficient for triggering the viral lytic cascade. Moreover, transcription initiation from both the BRLF1 and BZLF1 promoters can be activated by the BZLF1 gene product. The latter results suggest a two-step model for induction of the viral lytic cycle in which the initial signal leads to low-level transcription of the BZLF1 gene, followed by upregulation of transcription by the BZLF1 gene product. In this report we demonstrate that efficient transcription from the BRLF1 and BZLF1 promoters after anti-immunoglobulin induction of the lytic cycle, in a synchronous induction system, is dependent on de novo protein synthesis. These data support the two-step induction model in which synthesis of BZLF1 protein is required to activate expression of the BRLF1 and BZLF1 genes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [5 R01 CA43143] NR 40 TC 69 Z9 70 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 DEC PY 1991 VL 65 IS 12 BP 7073 EP 7077 PG 5 WC Virology SC Virology GA GP878 UT WOS:A1991GP87800088 PM 1658397 ER PT J AU ZEITELS, SM DOMANOWSKI, GF VINCENT, ME MALHOTRA, C VAUGHAN, CW AF ZEITELS, SM DOMANOWSKI, GF VINCENT, ME MALHOTRA, C VAUGHAN, CW TI A MODEL FOR MULTIDISCIPLINARY DATA-COLLECTION FOR CERVICAL METASTASIS SO LARYNGOSCOPE LA English DT Article ID ORAL CAVITY; COMPUTED-TOMOGRAPHY; NECK DISSECTION; EPIDERMOID CARCINOMA; LYMPH-NODES; CANCER; MANAGEMENT; OROPHARYNX; RATIONALE; DISEASE AB A system for multidisciplinary data collection for metastatic neck disease is discussed. Information from 87 neck dissections and 3218 lymph nodes is reported to illustrate the strength of the model. Clinical (endoscopic) assessment under general anesthesia, surgical assessment during the neck dissection, and radiographic (computed tomographic scan) assessment were compared with the pathological evaluation. All disciplines stratified the necks by region and node size. This model provides an effective stratagem for multi-institutional studies. C1 BOSTON VET AFFAIRS MED CTR,OTOLARYNGOL SECT,BOSTON,MA. BOSTON VET AFFAIRS MED CTR,RADIOL SECT,BOSTON,MA. BOSTON UNIV,SCH MED,BOSTON,MA 02118. TUFTS UNIV,SCH MED,BOSTON,MA 02111. BOSTON VET AFFAIRS MED CTR,PATHOL SECT,BOSTON,MA. RP ZEITELS, SM (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOL & LARYNGOL,243 CHARLES ST,BOSTON,MA 02110, USA. NR 17 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD DEC PY 1991 VL 101 IS 12 BP 1313 EP 1317 PN 1 PG 5 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA HC472 UT WOS:A1991HC47200010 PM 1766302 ER PT J AU WEISSLEDER, R AF WEISSLEDER, R TI TARGET-SPECIFIC SUPERPARAMAGNETIC MR CONTRAST AGENTS SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article; Proceedings Paper CT WORKSHOP ON CONTRAST ENHANCED MAGNETIC RESONANCE CY MAY 23-25, 1991 CL NAPA, CA SP SOC MAGNET RESONANCE MED, ADV MAGNET, BERLEX, BRACCO, GE, GEURBET, EASTMAN KODAK, NYCOMED, SQUIBB, STERLING WINTHROP ID IRON-OXIDE PARTICLES; ASIALOGLYCOPROTEIN RECEPTORS; MAGNETIC SEPARATION; LIVER; MICROSPHERES; HEPATOCYTE; SPLEEN; TUMORS; CELLS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WEISSLEDER, R (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,MR PHARMACEUT PROGRAM,MGH NMR CTR,BOSTON,MA 02114, USA. NR 37 TC 16 Z9 17 U1 0 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD DEC PY 1991 VL 22 IS 2 BP 209 EP 212 DI 10.1002/mrm.1910220209 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GV211 UT WOS:A1991GV21100007 PM 1812348 ER PT J AU WOLF, GL ROGOWSKA, J AF WOLF, GL ROGOWSKA, J TI CONTRAST AGENTS FOR FAST IMAGING SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article; Proceedings Paper CT WORKSHOP ON CONTRAST ENHANCED MAGNETIC RESONANCE CY MAY 23-25, 1991 CL NAPA, CA SP SOC MAGNET RESONANCE MED, ADV MAGNET, BERLEX, BRACCO, GE, GEURBET, EASTMAN KODAK, NYCOMED, SQUIBB, STERLING WINTHROP ID BLOOD-FLOW RP WOLF, GL (reprint author), MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 12 TC 6 Z9 6 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD DEC PY 1991 VL 22 IS 2 BP 268 EP 272 DI 10.1002/mrm.1910220222 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GV211 UT WOS:A1991GV21100016 PM 1812357 ER PT J AU BRADY, TJ COHEN, MS WEISSKOFF, RM ROSEN, BR AF BRADY, TJ COHEN, MS WEISSKOFF, RM ROSEN, BR TI EQUIPMENT REQUIREMENTS TO FACILITATE CONTRAST-ENHANCED MR IMAGING SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article; Proceedings Paper CT WORKSHOP ON CONTRAST ENHANCED MAGNETIC RESONANCE CY MAY 23-25, 1991 CL NAPA, CA SP SOC MAGNET RESONANCE MED, ADV MAGNET, BERLEX, BRACCO, GE, GEURBET, EASTMAN KODAK, NYCOMED, SQUIBB, STERLING WINTHROP ID INTRAVOXEL INCOHERENT MOTION; FLIP-ANGLE PULSES; MAGNETIC-RESONANCE; IRON-OXIDE; NMR; PERFUSION; FLOW C1 HARVARD UNIV,SCH MED,CHARLESTON,MA 02129. RP BRADY, TJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,CTR NUCL MAGNET RESONANCE,BOSTON,MA 02129, USA. RI Cohen, Mark/C-6610-2011 OI Cohen, Mark/0000-0001-6731-4053 NR 21 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD DEC PY 1991 VL 22 IS 2 BP 273 EP 279 DI 10.1002/mrm.1910220223 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GV211 UT WOS:A1991GV21100017 PM 1812358 ER PT J AU ROSEN, BR BELLIVEAU, JW ARONEN, HJ KENNEDY, D BUCHBINDER, BR FISCHMAN, A GRUBER, M GLAS, J WEISSKOFF, RM COHEN, MS HOCHBERG, FH BRADY, TJ AF ROSEN, BR BELLIVEAU, JW ARONEN, HJ KENNEDY, D BUCHBINDER, BR FISCHMAN, A GRUBER, M GLAS, J WEISSKOFF, RM COHEN, MS HOCHBERG, FH BRADY, TJ TI SUSCEPTIBILITY CONTRAST IMAGING OF CEREBRAL BLOOD-VOLUME - HUMAN-EXPERIENCE SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article; Proceedings Paper CT WORKSHOP ON CONTRAST ENHANCED MAGNETIC RESONANCE CY MAY 23-25, 1991 CL NAPA, CA SP SOC MAGNET RESONANCE MED, ADV MAGNET, BERLEX, BRACCO, GE, GEURBET, EASTMAN KODAK, NYCOMED, SQUIBB, STERLING WINTHROP ID POSITRON-EMISSION TOMOGRAPHY; HUMAN VISUAL-CORTEX; MEAN TRANSIT TIME; FLOW; GLIOMAS; PET C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROONCOL SERV,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,CTR NUCL MAGNET RESONANCE,BOSTON,MA 02129. RP ROSEN, BR (reprint author), MASSACHUSETTS GEN HOSP,CTR NUCL MAGNET RESONANCE,BLDG 149,13TH ST,CHARLESTON,MA 02129, USA. RI Kennedy, David/H-3627-2012; Cohen, Mark/C-6610-2011 OI Cohen, Mark/0000-0001-6731-4053 NR 33 TC 220 Z9 223 U1 0 U2 7 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD DEC PY 1991 VL 22 IS 2 BP 293 EP 299 DI 10.1002/mrm.1910220227 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GV211 UT WOS:A1991GV21100020 PM 1812360 ER PT J AU STARK, DD AF STARK, DD TI PHYSIOLOGICAL PRINCIPLES FOR THE DESIGN OF HEPATIC CONTRAST AGENTS SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article; Proceedings Paper CT WORKSHOP ON CONTRAST ENHANCED MAGNETIC RESONANCE CY MAY 23-25, 1991 CL NAPA, CA SP SOC MAGNET RESONANCE MED, ADV MAGNET, BERLEX, BRACCO, GE, GEURBET, EASTMAN KODAK, NYCOMED, SQUIBB, STERLING WINTHROP ID PULSE SEQUENCE OPTIMIZATION; GADOLINIUM-DTPA; LIVER-CANCER; BIODISTRIBUTION; RELAXATION; PARTICLES; TISSUE RP STARK, DD (reprint author), MASSACHUSETTS GEN HOSP,32 FRUIT ST,BOSTON,MA 02114, USA. NR 32 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD DEC PY 1991 VL 22 IS 2 BP 324 EP 328 DI 10.1002/mrm.1910220234 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GV211 UT WOS:A1991GV21100025 PM 1812365 ER PT J AU LAUFFER, RB AF LAUFFER, RB TI TARGETED RELAXATION ENHANCEMENT AGENTS FOR MRI SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article; Proceedings Paper CT WORKSHOP ON CONTRAST ENHANCED MAGNETIC RESONANCE CY MAY 23-25, 1991 CL NAPA, CA SP SOC MAGNET RESONANCE MED, ADV MAGNET, BERLEX, BRACCO, GE, GEURBET, EASTMAN KODAK, NYCOMED, SQUIBB, STERLING WINTHROP ID IONS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LAUFFER, RB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,NUCL MAGNET RESONANCE SECT,BOSTON,MA 02114, USA. NR 16 TC 58 Z9 60 U1 4 U2 7 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD DEC PY 1991 VL 22 IS 2 BP 339 EP 342 DI 10.1002/mrm.1910220237 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GV211 UT WOS:A1991GV21100028 PM 1812368 ER PT J AU KWONG, KK XIONG, J KUAN, WP CHENG, HM AF KWONG, KK XIONG, J KUAN, WP CHENG, HM TI MEASUREMENT OF WATER-MOVEMENT IN THE RABBIT EYE INVIVO USING H217O SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article ID INSTANT IMAGES; BODY; MR C1 HARVARD UNIV,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR NUCL MAGNET RESONANCE,BOSTON,MA 02129. RP CHENG, HM (reprint author), HARVARD UNIV,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02115, USA. FU NCRR NIH HHS [RR03264] NR 24 TC 9 Z9 9 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD DEC PY 1991 VL 22 IS 2 BP 443 EP 450 DI 10.1002/mrm.1910220252 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GV211 UT WOS:A1991GV21100040 PM 1812378 ER PT J AU EAGLE, KA MULLEY, AG FIELD, TS SKATES, S BERO, G CLARK, CE SEXTON, JO REDER, VA BERRIGAN, G PROCACCINI, J THIBAULT, GE AF EAGLE, KA MULLEY, AG FIELD, TS SKATES, S BERO, G CLARK, CE SEXTON, JO REDER, VA BERRIGAN, G PROCACCINI, J THIBAULT, GE TI VARIATION IN INTENSIVE-CARE UNIT PRACTICES IN 2 COMMUNITY HOSPITALS SO MEDICAL CARE LA English DT Note C1 MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. RP EAGLE, KA (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,GEN INTERNAL MED UNIT,BULFINCH 1,BOSTON,MA 02114, USA. NR 13 TC 4 Z9 4 U1 2 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD DEC PY 1991 VL 29 IS 12 BP 1237 EP 1245 DI 10.1097/00005650-199112000-00006 PG 9 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA GV206 UT WOS:A1991GV20600006 PM 1745081 ER PT J AU TRODAHL, JN AF TRODAHL, JN TI DENTIST DISCRIMINATION SO MILITARY MEDICINE LA English DT Letter C1 US DEPT VET AFFAIRS,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASSN MILITARY SURG US PI BETHESDA PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0026-4075 J9 MIL MED JI Milit. Med. PD DEC PY 1991 VL 156 IS 12 BP A12 EP A12 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA GV758 UT WOS:A1991GV75800005 ER PT J AU RAVID, K DOI, T BEELER, DL KUTER, DJ ROSENBERG, RD AF RAVID, K DOI, T BEELER, DL KUTER, DJ ROSENBERG, RD TI TRANSCRIPTIONAL REGULATION OF THE RAT PLATELET FACTOR 4 GENE - INTERACTION BETWEEN AN ENHANCER SILENCER DOMAIN AND THE GATA SITE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DNA-BINDING PROTEIN; HUMAN MEGAKARYOCYTES; EXPRESSION; CELLS; RECEPTOR; MARKER AB We used various segments of the 5' upstream region of the rat platelet factor 4 (PF4) gene coupled to the human growth hormone gene and heterologous promoters to identify domains which are critical for tissue-specific expression. Transient expression experiments with rat bone marrow cells and other cell lines revealed a complex interplay between a core promoter domain from -97 to the transcriptional start site and an enhancer/silencer domain from -448 to -112. The core promoter contains a GATA site at -31 to -28 whose mutation to TATA or AATA decreases tissue specificity and moderately affects expression in megakaryocytes as well as a positively acting subdomain from -97 to -83 whose removal decreases overall transcription without affecting tissue specificity. The enhancer/silencer domain possesses three positively acting subdomains from -380 to -362, -270 to -257, and -137 to -120 as well as a negatively acting subdomain at -184 to -151 which is able to reduce overall transcription but has no effect on tissue specificity. The subdomain from -380 to -362 is most critical in restricting gene expression driven either by the PF4 promoter or by a heterologous promoter to the megakaryocytic lineage. The subdomains from -270 to -257 and -137 to -120 function together with the subdomain from -380 to -362 to somewhat increase tissue specificity. Simultaneous mutation of the GATA site and deletion of either the whole enhancer/silencer domain or the subdomain from -380 to -362 or -137 to -120 reduce transcription in megakaryocytes by 10- to 30-fold. On the basis of the above-described results, we propose that the megakaryocyte-specific enhancer/silencer domain and the GATA site are responsible for high-level expression of the PF4 gene in a lineage-specific manner. C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. BETH ISRAEL HOSP,BOSTON,MA 02215. FU NHLBI NIH HHS [HL39753] NR 40 TC 128 Z9 130 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 DEC PY 1991 VL 11 IS 12 BP 6116 EP 6127 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GQ932 UT WOS:A1991GQ93200038 PM 1944279 ER PT J AU SUN, H DAWSON, D SZOSTAK, JW AF SUN, H DAWSON, D SZOSTAK, JW TI GENETIC AND PHYSICAL ANALYSES OF SISTER CHROMATID EXCHANGE IN YEAST MEIOSIS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DOUBLE-STRAND BREAKS; SACCHAROMYCES-CEREVISIAE; MEIOTIC RECOMBINATION; CHROMOSOME SEGREGATION; INITIATION SITE; DNA GYRASE; CONVERSION; MINICHROMOSOMES; SYNAPSIS; PLASMIDS AB We have used nonessential circular minichromosomes to monitor sister chromatid exchange during yeast meiosis. Genetic analysis shows that a 64-kb circular minichromosome undergoes sister chromatid exchange during 40% of meioses. This frequency is not reduced by the presence of a homologous linear minichromosome. Furthermore, sister chromatid exchange can be stimulated by the presence of a 12-kb ARG4 DNA fragment, which contains initiation sites for meiotic gene conversion. Using physical analysis, we have directly identified a product of sister chromatid exchange: a head-to-tail dimer form of a circular minichromosome. This dimer form is absent in a rad50S mutant strain, which is deficient in processing of the ends of meiosis-specific double-stranded breaks into single-stranded DNA tails. Our studies suggest that meiotic sister chromatid exchange is stimulated by the same mechanism as meiotic homolog exchange. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. NR 42 TC 8 Z9 8 U1 2 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 1991 VL 11 IS 12 BP 6328 EP 6336 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GQ932 UT WOS:A1991GQ93200059 PM 1944292 ER PT J AU DICKSTEIN, R SCHEIRER, DC FOWLE, WH AUSUBEL, FM AF DICKSTEIN, R SCHEIRER, DC FOWLE, WH AUSUBEL, FM TI NODULES ELICITED BY RHIZOBIUM-MELILOTI HEME MUTANTS ARE ARRESTED AT AN EARLY STAGE OF DEVELOPMENT SO MOLECULAR & GENERAL GENETICS LA English DT Article DE LEGHEMOGLOBIN; SYMBIOSIS; NITROGEN FIXATION; NODULINS ID SOYBEAN ROOT-NODULES; AMINOLEVULINIC-ACID SYNTHETASE; GENE-EXPRESSION; AUXOTROPHIC MUTANTS; ALFALFA NODULES; LEGHEMOGLOBIN; EXOPOLYSACCHARIDE; DIFFERENTIATION; NODULATION; SYMBIOSIS AB Heme-deficient mutants of Rhizobium and Bradyrhizobium have been found to exhibit diverse phenotypes with respect to symbiotic interactions with plant hosts. We observed that R. meliloti hemA mutants elicit nodules that do not contain intracellular bacteria; the nodules contain either no infection threads ("empty" nodule phenotype) or aberrant infection threads that failed to release bacteria (Bar- phenotype). These mutant nodules expressed nodulin genes associated with nodules arrested at an early stage of development, including ENOD2, Nms-30, and four previously undescribed nodulin genes. These nodules also failed to express any of six late nodulin genes tested by hybridization, including leghemoglobin, and twelve tested by in vitro translation product analysis which are not yet correlated with specific cloned genes. We observed that R. meliloti leucine and adenosine auxotrophs induced invaded Fix- nodules that expressed late nodulin genes, suggesting that it is not auxotrophy per se that causes the hemA mutants to elicit Bar- or empty nodules. Because R. meliloti hema mutants elicit nodules that do not contain intracellular bacteria, it is not possible to decide whether or not the Fix- phenotype of these nodules is a direct consequence of the failure of R. to supply the heme moiety of hololeghemoglobin. Our results demonstrate the importance of establishing the stage in development at which a mutant nodule is arrested before conclusions are drawn about the role of small metabolite exchange in the symbiosis. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NORTHEASTERN UNIV,DEPT BIOL,BOSTON,MA 02115. DREXEL UNIV,DEPT BIOSCI & BIOTECHNOL,PHILADELPHIA,PA 19104. RP DICKSTEIN, R (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114, USA. NR 38 TC 43 Z9 43 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD DEC PY 1991 VL 230 IS 3 BP 423 EP 432 DI 10.1007/BF00280299 PG 10 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA GV590 UT WOS:A1991GV59000011 PM 1766439 ER PT J AU ASSAD, JA SHEPHERD, GMG COREY, DP AF ASSAD, JA SHEPHERD, GMG COREY, DP TI TIP-LINK INTEGRITY AND MECHANICAL TRANSDUCTION IN VERTEBRATE HAIR-CELLS SO NEURON LA English DT Article ID MECHANOELECTRICAL TRANSDUCTION; GUINEA-PIG; STEREOCILIA; ADAPTATION; BUNDLE; SELECTIVITY; DEPENDENCE; CHANNELS; STIMULATION; MEMBRANE AB An attractive hypothesis for hair-cell transduction is that fine, filamentous "tip links" pull directly on mechanically sensitive ion channels located dt the tips of the stereocilia. We tested the involvement of tip links in the transduction process by treating bundles with a BAPTA-buffered, low-Ca2+ saline (10(-9) M). BAPTA abolished the transduction current in a few hundred milliseconds. BAPTA treatment for a few seconds eliminated the tip links observed by either scanning or transmission electron microscopy. BAPTA also eliminated the voltage-dependent movement and caused a positive bundle displacement of 133 nm, in quantitative agreement with a model for regulation of tension. We conclude that tip links convey tension to the transduction channels of hair cells. C1 HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HOWARD HUGHES MED INST,NEUROSCI GRP,COCONUT GROVE,FL 33133. RI Shepherd, Gordon/F-2679-2010; OI Corey, David/0000-0003-4497-6016 FU NIDCD NIH HHS [DC-00304] NR 32 TC 299 Z9 305 U1 2 U2 16 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD DEC PY 1991 VL 7 IS 6 BP 985 EP 994 DI 10.1016/0896-6273(91)90343-X PG 10 WC Neurosciences SC Neurosciences & Neurology GA GY438 UT WOS:A1991GY43800011 PM 1764247 ER PT J AU RORDORF, G KOROSHETZ, WJ BONVENTRE, JV AF RORDORF, G KOROSHETZ, WJ BONVENTRE, JV TI HEAT-SHOCK PROTECTS CULTURED NEURONS FROM GLUTAMATE TOXICITY SO NEURON LA English DT Article ID TRANSIENT ISCHEMIA; HYPERTHERMIA PROTECTS; STRIATAL CULTURES; GENE-EXPRESSION; BINDING-PROTEIN; HSP70; RAT; CELLS; INDUCTION; RECEPTOR AB Expression of heat shock proteins (HSPs) occurs in brain after ischemia and status epilepticus. We report that induction of the heat shock response in cortical cultures protects neurons from glutamate-induced excitotoxicity. Cultures heated to 42.2-degrees-C for 20 min showed an overall decrease in protein synthesis but an increase in the synthesis of approximately 72 and approximately 85 kd proteins and in the levels of HSP70 mRNA. Heat shock inhibited excitotoxicity in cells exposed to glutamate at 3 or 24 hr following heat exposure, but not when the interval between heat and glutamate exposure was shortened to 15 min or lengthened to 48 hr. Protection due to heat shock required new protein synthesis, since it did not occur when protein or RNA synthesis inhibitors were added. By ameliorating excitotoxic processes, HSPs may attenuate brain injury in certain pathologic conditions. C1 MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP RORDORF, G (reprint author), MASSACHUSETTS GEN HOSP,STROKE RES CTR,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK39773]; NINDS NIH HHS [NS10828] NR 45 TC 185 Z9 192 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD DEC PY 1991 VL 7 IS 6 BP 1043 EP 1051 DI 10.1016/0896-6273(91)90348-4 PG 9 WC Neurosciences SC Neurosciences & Neurology GA GY438 UT WOS:A1991GY43800016 PM 1722411 ER PT J AU BAGGERLY, J AF BAGGERLY, J TI SENSORY PERCEPTUAL PROBLEMS FOLLOWING STROKE - THE INVISIBLE DEFICITS SO NURSING CLINICS OF NORTH AMERICA LA English DT Article C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 14 TC 1 Z9 1 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0029-6465 J9 NURS CLIN N AM JI Nurs. Clin. North Am. PD DEC PY 1991 VL 26 IS 4 BP 997 EP 1005 PG 9 WC Nursing SC Nursing GA LA138 UT WOS:A1991LA13800018 PM 1945951 ER PT J AU BILLER, BMK COUGHLIN, JF SAXE, V SCHOENFELD, D SPRATT, DI KLIBANSKI, A AF BILLER, BMK COUGHLIN, JF SAXE, V SCHOENFELD, D SPRATT, DI KLIBANSKI, A TI OSTEOPENIA IN WOMEN WITH HYPOTHALAMIC AMENORRHEA - A PROSPECTIVE-STUDY SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; BONE-MINERAL CONTENT; POSTMENOPAUSAL WOMEN; BODY-COMPOSITION; DENSITY; OSTEOPOROSIS; PREVALENCE; SECRETION; SPINE; MASS AB Hypothalamic amenorrhea, a common disorder associated with abnormalities in gonadotropin pulsatility and subsequent estrogen deficiency, is usually transient, and treatment indications are unclear unless fertility is desired. To determine whether this disorder is associated with progressive bone loss, we studied 24 women with primary or secondary amenorrhea related to stress or simple weight loss, compared with 31 normal women of the same age. Amenorrhea women had significantly lower (P = .01) body fat (26.4 +/- 7.3 versus 30.6 +/- 4.7%) and higher (P = .0001) urine free cortisol levels (250 +/- 100 versus 140 +/- 50 nmol/day) than normals. Trabecular bone density in women with hypothalamic amenorrhea as assessed by spinal computed tomography was significantly (P = .001) lower than in normals (140.2 +/- 27.3 versus 175.1 +/- 24.6 mg K2HPO4/mL, respectively). Twenty of the 24 amenorrheic women had initial spinal bone density below the mean in normals, and in eight it was 2 standard deviations or more below the normal mean. Initial bone density correlated negatively with duration of amenorrhea (r = -0.489, P = .02) and positively with serum free testosterone levels (r = 0.517, P = .02). Prospective evaluation showed a decline in spinal bone density in those who were amenorrheic for fewer than 5 years. The slope of change in bone density correlated with initial weight, percent deal body weight, and percent body fat (R2 = 0.597, P = .0003; R2 = 0.549, P = .0007; and R2 = 0.618, P = .0002, respectively). We conclude that in women with hypothalamic amenorrhea: 1) Trabecular osteopenia is common; 2) the greatest risk of progressive bone loss occurs early after the onset of amenorrhea; 3) low levels of androgens may play a role in the development of osteopenia; 4) low indices of body mass predict higher risk for declining bone density; and 5) prolonged amenorrhea can occur. These findings may have implications about the benefit and timing of gonadal steriod replacement in hypothalamic amenorrhea. C1 MASSACHUSETTS GEN HOSP,GEN CLIN RES CTR,BOSTON,MA 02114. MAINE MED CTR,PORTLAND,ME 04102. RP BILLER, BMK (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,NEUROENDOCRINE UNIT,ACC 730,BOSTON,MA 02114, USA. FU NCRR NIH HHS [RR-01066]; NICHD NIH HHS [HD-21204]; NIDDK NIH HHS [F32DK08330] NR 36 TC 56 Z9 58 U1 1 U2 3 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 DEC PY 1991 VL 78 IS 6 BP 996 EP 1001 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA GR679 UT WOS:A1991GR67900002 PM 1945230 ER PT J AU HAASE, VH SNIJDERS, AJ COOKE, SM TENG, MN KAUL, D LEBEAU, MM BRUNS, GAP BERNARDS, A AF HAASE, VH SNIJDERS, AJ COOKE, SM TENG, MN KAUL, D LEBEAU, MM BRUNS, GAP BERNARDS, A TI ALTERNATIVELY SPLICED LTK MESSENGER-RNA IN NEURONS PREDICTS A RECEPTOR WITH A LARGER PUTATIVE EXTRACELLULAR DOMAIN SO ONCOGENE LA English DT Article ID GROWTH-FACTOR RECEPTOR; ACUTE PROMYELOCYTIC LEUKEMIA; TYROSINE KINASE; SEVENLESS PROTEIN; TISSUE; GENES; IDENTIFICATION; LYMPHOCYTES; EXPRESSION; BRAIN AB Ltk is a new member of the ros/insulin receptor family of tyrosine kinases that is expressed in murine B-lymphocyte precursors and forebrain neurons. We previously reported that lymphoid ltk cDNAs predict a 69kDa transmembrane glycoprotein, which uses a CUG translational start codon and has a 110 amino acid putative extracellular domain. We now show that the predominant ltk mRNA in brain is alternatively spliced and predicts a protein with a substantially larger extracellular part. The human ltk gene maps to chromosome 15, bands q13-21, a region containing the breakpoint of a recurring chromosomal abnormality in B-cell non-Hodgkin lymphomas. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC GENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02129. UNIV CHICAGO,HEMATOL ONCOL SECT,CHICAGO,IL 60637. CHILDRENS HOSP MED CTR,DIV GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RI Teng, Michael/I-5006-2012; Haase, Volker Hans/A-6758-2013 OI Teng, Michael/0000-0002-0722-3659; Haase, Volker Hans/0000-0002-7051-8994 FU NCI NIH HHS [CA 42557] NR 29 TC 8 Z9 11 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD DEC PY 1991 VL 6 IS 12 BP 2319 EP 2325 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA GX735 UT WOS:A1991GX73500021 PM 1662793 ER PT J AU CHENG, HM AF CHENG, HM TI MAGNETIC-RESONANCE-IMAGING OF THE HUMAN EYE INVIVO SO OPTOMETRY AND VISION SCIENCE LA English DT Article DE MAGNETIC RESONANCE IMAGING; HUMAN EYE; MORPHOLOGY; MORPHOMETRY; SUBRETINAL HEMORRHAGE; OCULAR MELANOMA; REFRACTIVE ERROR; NANOPHTHALMOS AB Because of the broad range of Tl (longitudinal relaxation time), T2 (transverse relaxation time), and proton density of the component tissues in the eye, proton magnetic resonance imaging (MRI) can provide ocular images of high contrast. The use of surface coils further enhances the signal-to-noise (S/N) ratio and shortens the image acquisition time to 1 to 6 min. High-resolution MR images of the eye therefore can be acquired readily and routinely. At present, with conventional spin-echo imaging, the in-plane resolution of MR images can be as high as (but not limited to) 0.3 x 0.3 mm with a 3-mm slice thickness. MRI can be used to detect and differentiate ocular lesions and to determine the ocular shape and measure ocular dimensions such as tissue thickness, curvature, and volume. RP CHENG, HM (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY07620] NR 0 TC 9 Z9 10 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1040-5488 J9 OPTOMETRY VISION SCI JI Optom. Vis. Sci. PD DEC PY 1991 VL 68 IS 12 BP 976 EP 980 DI 10.1097/00006324-199112000-00013 PG 5 WC Ophthalmology SC Ophthalmology GA GV710 UT WOS:A1991GV71000013 PM 1787959 ER PT J AU SIEVERS, TD YEE, JD FOLEY, ME BLANDING, PJ BERDE, CB AF SIEVERS, TD YEE, JD FOLEY, ME BLANDING, PJ BERDE, CB TI MIDAZOLAM FOR CONSCIOUS SEDATION DURING PEDIATRIC ONCOLOGY PROCEDURES - SAFETY AND RECOVERY PARAMETERS SO PEDIATRICS LA English DT Article DE MIDAZOLAM; PEDIATRIC; CANCER; SEDATION; PROCEDURES ID BENZODIAZEPINE ANTAGONIST; INTRAVENOUS SEDATION; MEDICAL PROCEDURES; CHILDREN; DIAZEPAM; ANESTHESIA; PREMEDICATION; OUTPATIENTS; RO-15-1788; DENTISTRY AB Multiple bone marrow aspirations or biopsies and lumbar punctures are a necessary part of the diagnosis and treatment of many pediatric cancer patients. Pharmacologic sedation may decrease the distress associated with these procedures. Midazolam (MDZ, Versed) is a water-soluble, rapid-onset, short-duration benzodiazepine that has not been studied widely in children. We prospectively evaluated safety and recovery parameters for intravenous MDZ used for conscious sedation by oncologists (without an anesthesiologist in attendance) for 70 procedures (bone marrow aspirations, lumbar punctures, or bone marrow aspirations plus lumbar punctures) in 24 ambulatory pediatric cancer patients, aged 1.5 to 15.5 years. MDZ was used alone or in combination with morphine or fentanyl. Respiratory rate, oxygen saturation, blood pressure, and heart rate were monitored. Sedation, anxiolysis, and recovery were assessed with a behavior score and a modified recovery room discharge score. Restraint was not required in 45% of the procedures. In no case was a respiratory rate < 12 observed. In nine procedures (13%), an oxygen saturation less-than-or-equal-to 90 occurred, all within 10 minutes after the last dose of MDZ. Ten procedures (14%) required verbal stimulation to take deeper breaths. Two patients did not respond immediately to verbal stimulation and received face-mask oxygen. Hypoxemia was not correlated with opioid use. Hypoxemia appears to be related to total MDZ dose and may occur with normal respiratory rates; all cases resolved with verbal stimulation or face-mask oxygen without specific airway maneuvers or assisted ventilation. Heart rate and blood pressure remained stable in all 70 procedures. In all 70 procedures a satisfactory discharge score was achieved by 60 minutes after the last dose of MDZ. Full or partial amnesia was reported in 90% of the procedures. No long-term adverse effects were reported on follow-up. Midazolam appeared to offer effective sedation and amnesia in children undergoing bone marrow aspirations or lumbar punctures. Safe administration requires constant observation, use of pulse oximetry, and availability of supplemental oxygen and resuscitation equipment because significant hypoxemia can occur in patients breathing room air. A recovery period of 60 minutes appeared to be adequate. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PHARM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. CHILDRENS HOSP,DEPT MED,BUFFALO,NY 14222. CHILDRENS HOSP,DEPT ANESTHESIA,BUFFALO,NY 14222. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP SIEVERS, TD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT NURSING,PEDIAT ONCOL CLIN,BOSTON,MA 02115, USA. NR 25 TC 88 Z9 90 U1 0 U2 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD DEC PY 1991 VL 88 IS 6 BP 1172 EP 1179 PG 8 WC Pediatrics SC Pediatrics GA GU883 UT WOS:A1991GU88300014 PM 1956734 ER PT J AU BHATIA, V WOLFSDORF, JI AF BHATIA, V WOLFSDORF, JI TI SEVERE HYPOGLYCEMIA IN YOUTH WITH INSULIN-DEPENDENT DIABETES-MELLITUS - FREQUENCY AND CAUSATIVE FACTORS SO PEDIATRICS LA English DT Article DE SEVERE HYPOGLYCEMIA; INSULIN-DEPENDENT DIABETES-MELLITUS (IDDM); CHILDREN AND ADOLESCENTS; INSULIN TREATMENT ID DEFECTIVE GLUCOSE COUNTERREGULATION; SYMPTOMATIC HYPOGLYCEMIA; INTENSIVE THERAPY; WARNING SYMPTOMS; PORCINE INSULIN; INFUSION; CHILDREN; IDDM; (UN)AWARENESS; UNAWARENESS AB Hypoglycemia is the most common acute complication of insulin-dependent diabetes mellitus, yet data are sparse concerning its frequency and the factors that predispose children and adolescents to its occurrence. This study was undertaken, during a 2-year period, to determine the frequency of severe hypoglycemia and to identify its causative factors in 196 youth with insulin-dependent diabetes mellitus (mean age and duration of diabetes, 13.5 +/- 4.3 and 4.8 +/- 3.2 years, respectively) treated conventionally. The mean daily insulin dose was 0.85 +/- 0.23 U/kg, and 92% of patients received insulin twice daily. Severe hypoglycemia occurred at least once in 2 years in 29 of 196 (14.8%) patients, of whom 9 (31%) had two or more episodes. The mean level of glycosylated hemoglobin closest to the event was significantly lower than that of patients who did not have severe hypoglycemia, 10.6 +/- 1.8 vs 11.4 +/- 2.0, P < .02; however, the mean insulin dose, 0.88 +/- 0.19 vs 0.85 +/- 0.23 U/kg every 24 hours, was similar. Severe hypoglycemia occurred with equal frequency during waking and sleeping, and it was not related to the species of insulin used. The use of human insulin, per se, did not increase the risk of severe hypoglycemia. Asymptomatic hypoglycemia was reported significantly more often in those who experienced severe hypoglycemia, 24% vs 8%, P = .01. Severe hypoglycemia was common (12.2 episodes per 100 patient-years), and symptomatic hypoglycemia universal in youth with insulin-dependent diabetes mellitus treated with conventional insulin therapy. Approximately two thirds of episodes were attributable to lapses in the application of basic principles of diabetes self-care. C1 JOSLIN DIABET CTR, DEPT PEDIAT, 1 JOSLIN PL, BOSTON, MA 02215 USA. RP WOLFSDORF, JI (reprint author), JOSLIN DIABET CTR, DEPT PEDIAT, 1 JOSLIN PL, BOSTON, MA 02215 USA. NR 39 TC 39 Z9 39 U1 0 U2 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 EI 1098-4275 J9 PEDIATRICS JI Pediatrics PD DEC PY 1991 VL 88 IS 6 BP 1187 EP 1193 PG 7 WC Pediatrics SC Pediatrics GA GU883 UT WOS:A1991GU88300016 PM 1956736 ER PT J AU SIEVER, LJ KAHN, RS LAWLOR, BA TRESTMAN, RL LAWRENCE, TL COCCARO, EF AF SIEVER, LJ KAHN, RS LAWLOR, BA TRESTMAN, RL LAWRENCE, TL COCCARO, EF TI CRITICAL ISSUES IN DEFINING THE ROLE OF SEROTONIN IN PSYCHIATRIC-DISORDERS .2. SO PHARMACOLOGICAL REVIEWS LA English DT Article; Proceedings Paper CT CONF ON SEROTONIN AND NEUROPSYCHIATRIC DISORDERS : IMPLICATIONS FOR THE DISCOVERY OF NEW PSYCHOTHERAPEUTIC AGENTS CY OCT 03, 1990 CL HERSHEY, PA SP HOECHST ROUSSEL PHARM ID OBSESSIVE-COMPULSIVE DISORDER; CSF 5-HYDROXYINDOLEACETIC ACID; MAJOR AFFECTIVE-DISORDERS; CONTROLLED CLINICAL-TRIAL; IMIPRAMINE BINDING-SITES; NUCLEUS RAPHE DORSALIS; CEREBROSPINAL-FLUID; ALZHEIMERS-DISEASE; NEURO-ENDOCRINE; PANIC DISORDER RP SIEVER, LJ (reprint author), MT SINAI MED SCH,BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,130 W KINGSBRIDGE,BRONX,NY 10469, USA. NR 184 TC 105 Z9 106 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-6997 J9 PHARMACOL REV JI Pharmacol. Rev. PD DEC PY 1991 VL 43 IS 4 BP 509 EP 525 PG 17 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GW852 UT WOS:A1991GW85200004 PM 1723206 ER PT J AU KREBS, DE EDELSTEIN, JE THORNBY, MA AF KREBS, DE EDELSTEIN, JE THORNBY, MA TI PROSTHETIC MANAGEMENT OF CHILDREN WITH LIMB DEFICIENCIES SO PHYSICAL THERAPY LA English DT Article DE AMPUTATIONS; CHILDREN PROSTHETICS; ORTHOTICS SPLINTS CASTS; GENERAL; PEDIATRICS; EQUIPMENT ID AMPUTATION AB Children with amputations present challenging management problems. Surgical management, prosthetic fitting options, and training regimens have progressed substantially over the past several decades. Clinicians should be familiar with the available technological options to provide children with amputations the best possible care. The plethora of small components available for lower- and upper-limb prostheses indicates the desirability of managing juvenile patients in an interdisciplinary, specialized clinical setting where the advantages and disadvantages of prosthetic options can be related to the particular needs and wishes of each young client and the client's family. Although prostheses are not anatomical avatars, careful appliance prescription and training, coordinated with the child's growth and developmental changes, can optimize the benefits the child derives from the prosthesis. C1 COLUMBIA UNIV,CLIN PHYS THERAPY,NEW YORK,NY 10032. NYU,SCH EDUC HLTH NURSING & ARTS PROFESS,DEPT PHYS THERAPY,NEW YORK,NY 10003. RP KREBS, DE (reprint author), MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,GRAD PROGRAM PHYS THERAPY,15 RIVER ST,BOSTON,MA 02018, USA. FU NIAMS NIH HHS [R01-AR40029] NR 63 TC 18 Z9 18 U1 1 U2 4 PU AMER PHYS THER ASSN PI ALEXANDRIA PA 1111 N FAIRFAX ST, ALEXANDRIA, VA 22314 SN 0031-9023 J9 PHYS THER JI Phys. Ther. PD DEC PY 1991 VL 71 IS 12 BP 920 EP 934 PG 15 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA GR799 UT WOS:A1991GR79900007 PM 1946626 ER PT J AU JUPITER, JB KOUR, AK PALUMBO, MD YAREMCHUK, MJ AF JUPITER, JB KOUR, AK PALUMBO, MD YAREMCHUK, MJ TI LIMB RECONSTRUCTION BY FREE-TISSUE TRANSFER COMBINED WITH THE ILIZAROV METHOD SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID MECHANICAL INDUCTION; OSTEOGENESIS; BONE AB In four complex cases of extremity reconstruction, we have been able to overcome the problems of combined bone and soft-tissue loss and length discrepancy by a combination of free-tissue transfer and the Ilizarov method of slow distraction. It is our observation that gradual distraction of a free tissue is a safe and viable procedure; the free tissue tolerates the pins of the circular external fixator well, and there is an equal degree of distraction and regeneration of the transferred free tissue and the native recipient tissue without evidence of wound dehiscence. Corticotomy through free tissue and in close proximity to vascularized bone is safe, with the subsequent bone regeneration not unlike that of normal bone. Manipulation by slow distraction does not appear to compromise the vasculature of the recipient bed for later microsurgical procedures or endanger the axial flow pattern of the transferred free tissue. C1 MASSACHUSETTS GEN HOSP,DEPT GEN SURG,DIV PLAST & RECONSTRUCT SURG,BOSTON,MA 02114. RP JUPITER, JB (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,5 WHITTIER PL,SUITE 102,BOSTON,MA 02114, USA. NR 20 TC 26 Z9 26 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 DEC PY 1991 VL 88 IS 6 BP 943 EP 951 DI 10.1097/00006534-199112000-00001 PG 9 WC Surgery SC Surgery GA GR655 UT WOS:A1991GR65500001 PM 1682964 ER PT J AU FERRUCCI, JT GANDINI, G REGGE, D RIGHI, D AF FERRUCCI, JT GANDINI, G REGGE, D RIGHI, D TI RADIOLOGIC APPROACHES SO PROBLEMS IN GENERAL SURGERY LA English DT Article AB Gallbladder and biliary duct stones can be safely managed by a variety of mechanical and radiologic interventional techniques. Wide choices in instrumentation, timing and number of treatment sessions allow the operator to tailor procedures for optimal results. RP FERRUCCI, JT (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114, USA. 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 0739-8328 J9 PROBL GEN SURG PD DEC PY 1991 VL 8 IS 4 BP 628 EP 649 PG 22 WC Surgery SC Surgery GA GR631 UT WOS:A1991GR63100014 ER PT J AU ZON, LI YOUSSOUFIAN, H MATHER, C LODISH, HF ORKIN, SH AF ZON, LI YOUSSOUFIAN, H MATHER, C LODISH, HF ORKIN, SH TI ACTIVATION OF THE ERYTHROPOIETIN RECEPTOR PROMOTER BY TRANSCRIPTION FACTOR GATA-1 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ERYTHROID CELLS; HEMATOPOIETIC GROWTH FACTOR; DNA-BINDING PROTEINS ID DNA-BINDING; MAMMALIAN-CELLS; EXPRESSION; CLONING; PROTEIN; MOUSE; GENE; SEQUENCE; LINEAGES; SITES AB Erythropoietin, a glycoprotein produced by the kidneys in response to anemia and hypoxia, is a major growth factor for cells of the erythroid lineage. Erythropoietin interacts with high-affinity cell surface receptors (EpoR) present on developing progenitors and is required for their survival. Previously we characterized the gene for EpoR and demonstrated that its promoter acts in a cell-specific manner. Here we show that the hematopoietic-specific transcription factor GATA-1 is necessary, and indeed is sufficient as the sole cell-restricted regulator, for activation of the EpoR promoter in fibroblast transfection assays. Hence, GATA-1, which participates in transcriptional control of the majority of erythroid-expressed genes, also acts on the promoter of an essential lineage-restricted receptor (EpoR). This central contribution of GATA-1 to EpoR promoter function provides a mechanism whereby a cell-restricted regulator may ensure the viability and subsequent maturation of progenitor cells during hematopoietic differentiation. C1 HOWARD HUGHES MED INST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. RP ZON, LI (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL02347, HL02277, 5PO1HL33262] NR 31 TC 181 Z9 182 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 DEC PY 1991 VL 88 IS 23 BP 10638 EP 10641 DI 10.1073/pnas.88.23.10638 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GT480 UT WOS:A1991GT48000055 PM 1660143 ER PT J AU ZON, LI MATHER, C BURGESS, S BOLCE, ME HARLAND, RM ORKIN, SH AF ZON, LI MATHER, C BURGESS, S BOLCE, ME HARLAND, RM ORKIN, SH TI EXPRESSION OF GATA-BINDING PROTEINS DURING EMBRYONIC-DEVELOPMENT IN XENOPUS-LAEVIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HEMATOPOIESIS; MESODERM; TRANSCRIPTION FACTOR; ERYTHROCYTES; ZINC-FINGER DOMAINS ID ERYTHROID TRANSCRIPTION FACTOR; GLOBIN GENE-EXPRESSION; DNA-BINDING; DEVELOPING MOUSE; SEQUENCE; CELLS; ALPHA; ACTIVATION; MESODERM; TADPOLE AB Proteins that recognize the core sequence GATA are important regulators of hematopoietic-specific gene transcription. We have characterized cDNAs encoding the Xenopus laevis homologues of three related transcription factors, designated GATA-1, -2, and -3. Comparative sequence analysis reveals strong conservation of the zinc-ringer DNA-binding domain among all vertebrate GATA-binding proteins. GATA-2 and GATA-3 polypeptides are homologous throughout their entire sequences, whereas GATA-1 sequence is conserved only in the region responsible for DNA binding. In Xenopus, RNAs encoding GATA-binding proteins are expressed in both larval and adult erythroid cells. GATA-1, -2, and -3 RNAs are first detectable in early gastrula (Nieuwkoop developmental stage 11). This is earlier than the appearance of the early larval alpha-T1 globin RNA (stage 15), beta-T1 globin RNA (stage 26), or blood island formation (stage 30). The expression of GATA-1, -2, and -3 in early development may signal an early commitment of mesoderm to form hematopoietic tissue. C1 HOWARD HUGHES MED INST,BOSTON,MA 02115. DEPT MOLEC & CELL BIOL,DIV BIOCHEM & MOLEC BIOL,BERKELEY,CA 94720. RP ZON, LI (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115, USA. OI Burgess, Shawn/0000-0003-1147-0596 FU NHLBI NIH HHS [HL32259, HL02347]; NIGMS NIH HHS [GM42341] NR 46 TC 168 Z9 174 U1 1 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC PY 1991 VL 88 IS 23 BP 10642 EP 10646 DI 10.1073/pnas.88.23.10642 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GT480 UT WOS:A1991GT48000056 PM 1961730 ER PT J AU PARDO, FS BRISTOW, RG TAGHIAN, A ONG, A BOREK, C AF PARDO, FS BRISTOW, RG TAGHIAN, A ONG, A BOREK, C TI ROLE OF TRANSFECTION AND CLONAL SELECTION IN MEDIATING RADIORESISTANCE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GENE TRANSFER; RADIOSENSITIVITY; NEOMYCIN; ONCOGENES ID HUMAN CELL-LINES; INVITRO RADIOSENSITIVITY; HUMAN-TUMORS; TRANSFORMATION; CULTURE; HETEROGENEITY; RESISTANCE; RADIATION; ONCOGENE; GROWTH AB Transfected oncogenes have been reported to increase the radioresistance of rodent cells. Whether transfected nononcogenic DNA sequences and subsequent clonal selection can result in radioresistant cell populations is unknown. The present set of experiments describe the in vitro radiosensitivity and tumorigenicity of selected clones of primary rat embryo cells and human glioblastoma cells, after transfection with a neomycin-resistance marker (pSV2neo or pCMVneo) and clonal selection. Radiobiological data comparing the surviving fraction at 2 Gy (SF2) and the mean inactivation dose show the induction of radioresistance in two rat embryo cell clones and one glioblastoma clone, as compared to untransfected cells. Wild-type and transfectant clones were injected into three strains of immune-deficient mice (scid, NIH, and nu/nu) to assay for tumorigenicity and metastatic potential. Only the glioblastoma parent line and its transfectant clones were tumorigenic. None of the cells produced spontaneous or experimentally induced metastases. Flow cytometric analyses indicated that the induction of radioresistance could not be attributed to changes in cell kinetics at the time of irradiation. Our results show that transfection of a neomycin-resistance marker and clonal selection can impart radioresistance on both normal and tumor cells. The work also indicates that altered radiation sensitivity does not necessarily correlate with changes in cell-cycle kinetics at the time of irradiation, tumorigenicity, or altered metastatic potential. Our findings have critical implications for transfection studies investigating determinants of cellular radiosensitivity. C1 PRINCESS MARGARET HOSP, TORONTO M4X 1K9, ONTARIO, CANADA. TUFTS UNIV, NEW ENGLAND MED CTR,SCH MED,DEPT RADIAT ONCOL, DIV RADIAT & CANC BIOL, BOSTON, MA 02111 USA. RP PARDO, FS (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT RADIAT ONCOL, COX CANC CTR 3, BOSTON, MA 02114 USA. FU NCI NIH HHS [CA-13311] NR 30 TC 20 Z9 20 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC PY 1991 VL 88 IS 23 BP 10652 EP 10656 DI 10.1073/pnas.88.23.10652 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GT480 UT WOS:A1991GT48000058 PM 1961732 ER PT J AU SHIPP, MA TARR, GE CHEN, CY SWITZER, SN HERSH, LB STEIN, H SUNDAY, ME REINHERZ, EL AF SHIPP, MA TARR, GE CHEN, CY SWITZER, SN HERSH, LB STEIN, H SUNDAY, ME REINHERZ, EL TI CD10/NEUTRAL ENDOPEPTIDASE-24.11 HYDROLYZES BOMBESIN-LIKE PEPTIDES AND REGULATES THE GROWTH OF SMALL-CELL CARCINOMAS OF THE LUNG SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE METALLOENDOPEPTIDASE; AUTOCRINE GROWTH FACTORS; CELL SURFACE ENZYME; COMMON ACUTE LYMPHOBLASTIC LEUKEMIA ANTIGEN ID GASTRIN-RELEASING PEPTIDE; LYMPHOBLASTIC-LEUKEMIA ANTIGEN; BRONCHIAL EPITHELIAL-CELLS; SWISS 3T3 CELLS; NEUTRAL ENDOPEPTIDASE; SUBSTANCE-P; GUINEA-PIG; 24.11 ENKEPHALINASE; CIGARETTE-SMOKE; MESSENGER-RNAS AB Bombesin-like peptides are essential autocrine growth factors for many small cell carcinomas (SCCas) of the lung. Herein, we demonstrate that these malignant pulmonary neuroendocrine cells express low levels of the cell surface metalloendopeptidase CD1O/neutral endopeptidase 24.11 (CD1O/NEP, common acute lymphoblastic leukemia antigen) and that this enzyme hydrolyzes bombesin-like peptides. The growth of bombesin-like peptide-dependent SCCas is inhibited by CD1O/NEP and potentiated by CD1O/NEP inhibition. The results provide evidence that CD1O/NEP is involved in the regulation of tumor cell proliferation. Since SCCa of the lung occurs almost exclusively in cigarette smokers and cigarette smoke inactivates CD1O/NEP, decreased cell surface CD1O/NEP enzymatic activity may be causally related to the development of SCCa of the lung. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235. FREE UNIV BERLIN,INST PATHOL,W-1000 BERLIN 33,GERMANY. RP SHIPP, MA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA49232, CA55095]; NIDA NIH HHS [DA02243] NR 47 TC 191 Z9 191 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC PY 1991 VL 88 IS 23 BP 10662 EP 10666 DI 10.1073/pnas.88.23.10662 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GT480 UT WOS:A1991GT48000060 PM 1660144 ER PT J AU OHNO, T TERADA, M YONEDA, Y SHEA, KW CHAMBERS, RF STROKA, DM NAKAMURA, M KUFE, DW AF OHNO, T TERADA, M YONEDA, Y SHEA, KW CHAMBERS, RF STROKA, DM NAKAMURA, M KUFE, DW TI A BROADLY NEUTRALIZING MONOCLONAL-ANTIBODY THAT RECOGNIZES THE V3 REGION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GLYCOPROTEIN GP120 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HTLV-III/LAV; T4 MOLECULE; ENVELOPE; HIV-1; RETROVIRUS; BINDING; EPITOPE; CELLS; CD4; LYMPHOCYTES AB Previous studies have demonstrated that the principal neutralizing determinant of human immunodeficiency virus type 1 (HIV-1) is located in the V3 loop of glycoprotein gp120. Antibodies prepared against this region using gp120 or peptides as immunogens have been predominantly HIV-1-isolate-specific. In the present studies, murine monoclonal antibodies (mAbs) were prepared against the HIV-1MN strain. One mAb, designated NM-01, was selected for its ability to neutralize both the MN and IIIB strains. Neutralization of H9-cell infectivity as determined by reverse transcriptase assay demonstrated an ID50 of < 1-mu-g/ml for both MN and IIIB. mAb NM-01 also blocked MN and IIIB infectivity in the MT-2 assay and inhibited their reactivity in syncytium formation. The results further demonstrate that mAb NM-01 binds to the V3 loop of gp120 at amino acids 312-326. This mAb reacted equally well with loop peptides from the MN, IIIB, RF, and CDC4 isolates. In contrast, there was less affinity with a similar peptide from the NY5 strain and little if any reactivity with loop peptides from the Z2, Z6, and ELI strains. We also demonstrate that peptides corresponding to the V3 loops of MN and IIIB, but not Z6, block neutralization of IIIB virus by mAb NM-01. These findings indicate that mAb NM-01 reacts with diverse HIV-1 isolates through the Gly-Pro-Gly-Arg sequence of the V3 loop. C1 JIKEI UNIV,DEPT MICROBIOL,FOOD SCI,TOKYO 105,JAPAN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP OHNO, T (reprint author), NISSIN MOLEC BIOL INST INC,20 OVERLAND ST,BOSTON,MA 02215, USA. RI Stroka, Deborah/F-1806-2013 NR 27 TC 74 Z9 74 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC PY 1991 VL 88 IS 23 BP 10726 EP 10729 DI 10.1073/pnas.88.23.10726 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GT480 UT WOS:A1991GT48000073 PM 1961739 ER PT J AU SAKAMOTO, H MICHAELSON, J JONES, WK BHAN, AK ABHYANKAR, S SILVERSTEIN, M GOLAN, DE BURAKOFF, SJ FERRARA, JLM AF SAKAMOTO, H MICHAELSON, J JONES, WK BHAN, AK ABHYANKAR, S SILVERSTEIN, M GOLAN, DE BURAKOFF, SJ FERRARA, JLM TI LYMPHOCYTES WITH A CD4+ CD8- CD3- PHENOTYPE ARE EFFECTORS OF EXPERIMENTAL CUTANEOUS GRAFT-VERSUS-HOST DISEASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE T-CELLS; DIFFERENTIATION; BONE MARROW TRANSPLANTATION ID BONE-MARROW TRANSPLANTATION; MINOR HISTOCOMPATIBILITY BARRIERS; T-CELL RECEPTOR; LETHAL GRAFT; MICE; EXPRESSION; SUBSETS AB Graft-versus-host disease (GVHD) is known to cause profound dysregulation of the immune system, although its effector Mechanisms are Poorly understood. We now describe an effector lymphocyte of unusual phenotype in the skin of mice with GVHD. This cell is of donor origin and expresses several T-cell surface proteins including Thy-1, CD2, and CD4 but does not express CD8, CD3, NK1.1, or macrophage antigens. Mononuclear cells of this phenotype are the predominant lymphocyte in the epidermis of mice with GVHD 3 weeks after transplant but are not detected in transplanted mice without GVHD. Isolation and transfer of these lymphocytes into secondary recipients causes epidermal damage characteristic of GVHD. These data demonstrate that CD4+ CD8- CD3- lymphocytes are an important effector population that can be amplified outside the thymus and that can mediate target organ damage of GVHD. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NR 25 TC 26 Z9 26 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC PY 1991 VL 88 IS 23 BP 10890 EP 10894 DI 10.1073/pnas.88.23.10890 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GT480 UT WOS:A1991GT48000107 PM 1835792 ER PT J AU TERWILLIGER, EF LANGHOFF, E GABUZDA, D ZAZOPOULOS, E HASELTINE, WA AF TERWILLIGER, EF LANGHOFF, E GABUZDA, D ZAZOPOULOS, E HASELTINE, WA TI ALLELIC VARIATION IN THE EFFECTS OF THE NEF GENE ON REPLICATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HTLV-III; NUCLEOTIDE-SEQUENCE; MUTATIONAL ANALYSIS; AIDS VIRUS; PROTEIN; ANTIBODIES; REGION; HIV-1; INDIVIDUALS; INFECTION AB The effects of the viral gene nef on human immunodeficiency virus type 1 (HIV-1) replication in culture were investigated using nef alleles of the HIV-1 IIIB and ELI strains. The results demonstrate significant allelic variation in the effect of nef on virus replication in both an established human CD4+ T-cell line and primary human lymphocytes. In the context of the HXB2 virus, the ELI nef allele but not the IIIB nef allele permits initiation of efficient low-multiplicity infection in primary peripheral blood mononuclear cells, including unfractionated peripheral blood lymphocytes, T cells, and monocyte/macrophages. Within the same genetic context, the IIIB nef allele slightly retards replication of the virus in a T-cell line, whereas the ELI nef allele accelerates replication of the virus. Sequences in the IIIB and ELI genomes outside of nef also moderate the effects of nef on HIV-1 replication. nef did not appear to determine the host-cell preference of the virus. These studies may help to reconcile apparently conflicting reports on the role of nef in HIV-1 replication and suggest that HIV-1 nef may play an important role in viral pathogenesis. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115. FU NIAID NIH HHS [R01-AI28193, UO1-AI24845] NR 30 TC 75 Z9 75 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 DEC PY 1991 VL 88 IS 23 BP 10971 EP 10975 DI 10.1073/pnas.88.23.10971 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GT480 UT WOS:A1991GT48000124 PM 1720558 ER PT J AU SUEMORI, S LYNCHDEVANEY, K PODOLSKY, DK AF SUEMORI, S LYNCHDEVANEY, K PODOLSKY, DK TI IDENTIFICATION AND CHARACTERIZATION OF RAT INTESTINAL TREFOIL FACTOR - TISSUE-SPECIFIC AND CELL-SPECIFIC MEMBER OF THE TREFOIL PROTEIN FAMILY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE INTESTINE; GOBLET CELL; GROWTH FACTOR ID PANCREATIC SPASMOLYTIC POLYPEPTIDE; GROWTH FACTOR-ALPHA; COLON CANCER LINES; FACTOR-BETA; XENOPUS-LAEVIS; BREAST-CANCER; PSP; EXPRESSION; GENE; DIFFERENTIATION AB The trefoil peptide family encompasses a group of small proteins that appear to assume a distinctive secondary structure that leads to intrinsic resistance to protease digestion. Induction of these peptides has been associated with response to injury in the gastrointestinal tract and related organs. Using an oligonucleotide derived from N-terminal amino acid sequencing of a transformed growth-inhibiting protein, a cDNA was cloned from rat intestinal villus epithelial cells that encodes a protein 81 amino acids in length with the characteristic trefoil peptide cysteine residue motif. Northern blot analysis demonstrates specific expression of a single transcript of 0.43 kilobase in small and large intestinal epithelium in rat and man. Indirect immunofluorescent staining with antiserum raised using a synthetic peptide based on the predicted C-terminal sequence of this protein, designated intestinal trefoil factor, demonstrated that it is primarily expressed and secreted onto the intestinal surface by goblet cells, suggesting that it may be an important component of intrinsic mechanisms for defending mucosal integrity. C1 MASSACHUSETTS GEN HOSP,GASTROENTEROL UNIT,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR STUDY INFLAMMATORY BOWEL DIS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP PODOLSKY, DK (reprint author), MASSACHUSETTS GEN HOSP,GASTROENTEROL UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK41557, DK43351, DK34422] NR 34 TC 256 Z9 282 U1 1 U2 7 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 DEC PY 1991 VL 88 IS 24 BP 11017 EP 11021 DI 10.1073/pnas.88.24.11017 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GV877 UT WOS:A1991GV87700008 PM 1763017 ER PT J AU MIGLIACCIO, AR MIGLIACCIO, G DANDREA, A BAIOCCHI, M CROTTA, S NICOLIS, S OTTOLENGHI, S ADAMSON, JW AF MIGLIACCIO, AR MIGLIACCIO, G DANDREA, A BAIOCCHI, M CROTTA, S NICOLIS, S OTTOLENGHI, S ADAMSON, JW TI RESPONSE TO ERYTHROPOIETIN IN ERYTHROID SUBCLONES OF THE FACTOR-DEPENDENT CELL-LINE 32D IS DETERMINED BY TRANSLOCATION OF THE ERYTHROPOIETIN RECEPTOR TO THE CELL-SURFACE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID TRANSCRIPTION FACTOR; EXPRESSION; PROTEIN; CLONING; ANTIGENS; GENE AB Regulation of the expression of the erythropoietin (Epo) receptor (EpoR) gene is under the control of transcriptional regulatory factor GATA-1. GATA-1 is expressed widely among the nonerythroid, factor-dependent subclones of the interleukin 3-dependent mouse cell line 32D. Consequently, to determine whether GATA-1 and EpoR gene expression are linked even in nonerythroid cells, we have studied the correlation of GATA-1 expression with expression and function of EpoR in these cell lines. EpoR mRNA (by RNase protection analysis) and EpoR protein (by specific antibody immunoprecipitation of metabolically labeled EpoR protein) were detectable not only in 32D and 32D Epo (an Epo-dependent subclone) but also in 32D GM, a subclone dependent for growth on granulocyte/macrophage colony-stimulating factor. EpoR mRNA also was detectable by PCR in 32D G, a subclone dependent for growth on granulocyte colony-stimulating factor. However, only 32D Epo cells bound I-125-labeled Epo and expressed EpoR protein on the cell surface, as determined by immunoprecipitation of surface-labeled proteins. These results indicate that, in these factor-dependent cell lines, the major regulatory step determining the erythroid-specific response to Epo is the efficiency of EpoR protein translocation to the cell surface. Mechanisms that could affect lineage-specific translocation are the presence of a chaperone protein, erythroid-specific editing of EpoR mRNA, or altered processing of the EpoR protein to the cell surface. In this model, lineage-restricted responses to growth factors such as Epo are determined not by expression of the genes for growth factor receptors but, rather, by appropriate processing of the receptor protein. C1 IST SUPER SANITA,I-00161 ROME,ITALY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MILAN,DIPARTIMENTO GENET & BIOL MICRORGANISMI,I-20122 MILAN,ITALY. RP MIGLIACCIO, AR (reprint author), NEW YORK BLOOD CTR,HEMATOPOIET GROWTH FACTORS LAB,NEW YORK,NY 10021, USA. NR 28 TC 54 Z9 55 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 DEC PY 1991 VL 88 IS 24 BP 11086 EP 11090 DI 10.1073/pnas.88.24.11086 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GV877 UT WOS:A1991GV87700022 PM 1722318 ER PT J AU TSOMIDES, TJ WALKER, BD EISEN, HN AF TSOMIDES, TJ WALKER, BD EISEN, HN TI AN OPTIMAL VIRAL PEPTIDE RECOGNIZED BY CD8+ T-CELLS BINDS VERY TIGHTLY TO THE RESTRICTING CLASS-I MAJOR HISTOCOMPATIBILITY COMPLEX PROTEIN ON INTACT-CELLS BUT NOT TO THE PURIFIED CLASS-I PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ANTIGEN PRESENTATION; CYTOTOXIC LYMPHOCYTE-T; HUMAN IMMUNODEFICIENCY VIRUS; DISSOCIATION KINETICS; STOICHIOMETRIC IODINATION ID LYMPHOCYTES-T; MOLECULES; ANTIGEN; BETA-2-MICROGLOBULIN; PURIFICATION AB CD8+ cytotoxic T lymphocytes recognize cell surface complexes formed by class I major histocompatibility complex (MHC-I) glycoproteins and antigenic peptides. We have identified a peptide nonamer (termed IV9) derived from the human immunodeficiency virus that is over a millionfold more active (at subpicomolar concentrations) than peptide analogues longer or shorter by one or two amino acid residues. Although IV9 does not detectably bind to isolated MHC-I molecules as measured by equilibrium dialysis, we quantitated its specific binding in unaltered form to MHC-I on intact cells. Less than 1% of cell surface MHC-I forms complexes with IV9, which suffices to trigger maximal cytotoxic T-lymphocyte activity. By contrast, a peptide dodecamer that includes the IV9 sequence and is active at micromolar concentrations does not bind to MHC-I on intact cells, raising the possibility that this longer peptide undergoes processing. Using stoichiometrically iodinated IV9 to obviate the ambiguities associated with trace labeling methods, we measured the dissociation kinetics of purified peptide/MHC-I complexes isolated by affinity chromatography and found these complexes to be exceedingly stable (t1/2 = 200-600 hr). C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. RP TSOMIDES, TJ (reprint author), MIT,DEPT BIOL,CAMBRIDGE,MA 02139, USA. FU NCI NIH HHS [CA14051, R35-CA42504, CA09255] NR 30 TC 192 Z9 193 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD DEC PY 1991 VL 88 IS 24 BP 11276 EP 11280 DI 10.1073/pnas.88.24.11276 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GV877 UT WOS:A1991GV87700061 PM 1722325 ER PT J AU LATRON, F MOOTS, R ROTHBARD, JB GARRETT, TPJ STROMINGER, JL MCMICHAEL, A AF LATRON, F MOOTS, R ROTHBARD, JB GARRETT, TPJ STROMINGER, JL MCMICHAEL, A TI POSITIONING OF A PEPTIDE IN THE CLEFT OF HLA-A2 BY COMPLEMENTING AMINO-ACID CHANGES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID TOXIC LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; MATRIX PEPTIDE; BINDING-SITE; RECOGNITION; ANTIGEN; SPECIFICITY; MUTATIONS; EPITOPES AB Several mutant HLA-A2 molecules have been constructed and expressed in the mutant human B-cell line C1R, which lacks HLA-A and HLA-B antigens, and examined for presentation of a previously defined peptide epitope derived from the influenza matrix protein to appropriate human cytotoxic T-lymphocyte lines. When leucine residue 66 in this matrix peptide containing residues 57-68 (matrix peptide 5768) was replaced by arginine, the resulting matrix peptide 57-68 R66 was not presented to HLA-A2, but the mutation Y116D (tyrosine to aspartic acid at residue 116) in the floor of the peptide binding cleft near its right end dramatically restored peptide presentation. A similar result was obtained by substitution of ornithine for leucine at residue 66. These data provide strong support for a model in which the peptide is orientated with its amino terminus at the left end of the cleft of HLA-A2 and its carboxyl terminus at the right. C1 UNIV OXFORD,INST MOLEC MED,OXFORD,ENGLAND. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,HOWARD HUGHES MED INST,CAMBRIDGE,MA 02138. RP LATRON, F (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA47554] NR 24 TC 44 Z9 44 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 DEC PY 1991 VL 88 IS 24 BP 11325 EP 11329 DI 10.1073/pnas.88.24.11325 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GV877 UT WOS:A1991GV87700071 PM 1763045 ER PT J AU AHMED, AR FOSTER, S ZALTAS, M NOTANI, G AWDEH, Z ALPER, CA YUNIS, EJ AF AHMED, AR FOSTER, S ZALTAS, M NOTANI, G AWDEH, Z ALPER, CA YUNIS, EJ TI ASSOCIATION OF DQW7 (DQB1-STAR-0301) WITH OCULAR CICATRICIAL PEMPHIGOID SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AUTOIMMUNE SUSCEPTIBILITY GENE; HAPLOTYPE ANALYSIS ID MAJOR HISTOCOMPATIBILITY COMPLEX; INHERITED STRUCTURAL POLYMORPHISM; CLASS-II; HAPLOTYPES; ANTIGENS; VULGARIS AB Ocular cicatricial pemphigoid (OCP) is an autoimmune blistering disease that affects the conjunctiva and multiple mucous membranes. Class I and II and complement genetic markers of the major histocompatibility complex were studied in 20 Caucasian OCP patients and members of their families. Frequencies of individual alleles and common fixed or extended haplotypes in the patients were compared with those in normal family control haplotypes and with overall normal Caucasian haplotypes. The most striking increase compared with overall controls was noted in HLA-DQw3 (P = 0.006), unassociated with any extended haplotype. All but 1 of the 20 patients carried DQw3 in linkage with HLA-DR4 (increased significantly with P = 0.042 compared with overall normal genotype controls) or DR5. The DQw3, on analysis by restriction fragment length polymorphism in genomic DNA, was, in every instance, DQw7 (3.1, DQB1*0301). The frequency of DQB1*0301 in patient haplotypes compared with overall normal DR4 and DR5 DQw3-bearing haplotypes was statistically significantly increased (P < 0.003, relative risk = 9.6). The distribution of homozygotes and heterozygotes for DQB1*0301 among the patients was consistent with dominant but not recessive inheritance of DQB1*0301 or a gene, probably a class II allele, in linkage disequilibrium with it as the major histocompatibility complex susceptibility gene for OCP. C1 HARVARD UNIV,SCH DENT MED,DEPT ORAL PATHOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. AMER RED CROSS SERV,NE REG,DEDHAM,MA 02026. MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. RP AHMED, AR (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL 29583]; NICHD NIH HHS [HD 17461]; NIDDK NIH HHS [DK 26844] NR 37 TC 59 Z9 61 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 DEC PY 1991 VL 88 IS 24 BP 11579 EP 11582 DI 10.1073/pnas.88.24.11579 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GV877 UT WOS:A1991GV87700123 PM 1763074 ER PT J AU LEONG, GB ETH, S AF LEONG, GB ETH, S TI LEGAL AND ETHICAL ISSUES IN ELECTROCONVULSIVE-THERAPY SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID SUPREME-COURT HEARING; PSYCHIATRIC MALPRACTICE; BRAIN-DAMAGE; ECT; CALIFORNIA; RESTRAINT; FORM C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90033. RP LEONG, GB (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV B116A12,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 41 TC 4 Z9 4 U1 1 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0193-953X J9 PSYCHIAT CLIN N AM JI Psychiatr. Clin. North Amer. PD DEC PY 1991 VL 14 IS 4 BP 1007 EP 1020 PG 14 WC Psychiatry SC Psychiatry GA HL652 UT WOS:A1991HL65200014 PM 1771147 ER PT J AU SILVERMAN, SG COUGHLIN, BF SELTZER, SE SWENSSON, RG MUELLER, PR AF SILVERMAN, SG COUGHLIN, BF SELTZER, SE SWENSSON, RG MUELLER, PR TI CURRENT USE OF SCREENING LABORATORY TESTS BEFORE ABDOMINAL INTERVENTIONS - A SURVEY OF 603 RADIOLOGISTS SO RADIOLOGY LA English DT Article DE BLOOD, COAGULATION; INTERVENTIONAL PROCEDURES; RADIOLOGY AND RADIOLOGISTS ID PARTIAL THROMBOPLASTIN TIME; HEMOSTATIC EVALUATION; PROTHROMBIN; COAGULATION AB A survey of 2,153 radiologists was conducted to assess both their current practices of evaluating hemostatic function and their use of blood tests before performing image-guided nonvascular abdominal interventions. Among the 603 (28%) who responded, more radiologists routinely perform prothrombin time (81%) or partial thromboplastin time (78%) tests than platelet counts (59%), and relatively few (7%) obtain bleeding times. The most common practice (51%) is to order all of the first three tests. Use of laboratory tests is quite common (> 75%) before biopsy of splenic masses, hemangiomas, or hepatomas and before all catheter insertions. These tests are used less frequently (less-than-or-equal-to 70%) before fine-needle procedures, including biopsy and cyst aspiration. Only one-third of the radiologists alter their evaluation in patients who have taken aspirin. Most respondents (64%) believe that there should be written guidelines on how to evaluate patients before interventional procedures. Virtually all (97%) thought such evaluation should be the radiologist's responsibility. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP SILVERMAN, SG (reprint author), BRIGHAM & WOMENS HOSP,DEPT RADIOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 12 TC 18 Z9 18 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 DEC PY 1991 VL 181 IS 3 BP 669 EP 673 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ752 UT WOS:A1991GQ75200012 PM 1947079 ER PT J AU HYND, GW MARSHALL, RM SEMRUDCLIKEMAN, M AF HYND, GW MARSHALL, RM SEMRUDCLIKEMAN, M TI DEVELOPMENTAL DYSLEXIA, NEUROLINGUISTIC THEORY AND DEVIATIONS IN BRAIN MORPHOLOGY SO READING AND WRITING LA English DT Article; Proceedings Paper CT 16TH INTERNATIONAL RODIN REMEDIATION SCIENTIFIC CONF CY SEP, 1990 CL BOULDER, CO SP RODIN REMEDIAT FDN DE DEVELOPMENTAL DYSLEXIA; NEUROLINGUISTIC; BRAIN MORPHOLOGY; NEUROIMAGING ID CEREBRAL HEMISPHERIC-ASYMMETRY; BIOLOGICAL MECHANISMS; CT SCAN; COMPUTED-TOMOGRAPHY; DISABLED CHILDREN; ATTENTION-DEFICIT; PLANUM-TEMPORALE; LEFT-HANDEDNESS; PATHOLOGY; LATERALIZATION AB Although some form of central nervous system involvement is presumed, evidence establishing a relationship between dyslexia and neurological dysfunction has been correlational. Recently, neuroimaging and postmortem studies have begun to provide direct evidence implicating neuropathological structures in dyslexia. This article reviews computed tomography (CT) and magnetic resonance imaging (MRI) studies examining deviations in brain morphology which appear to be associated with neurolinguistic functioning. Methodological and technical issues are discussed. Based on their own and others research, the authors conclude that dyslexics show variations in specific brain regions, namely, reversed or symmetrical plana temporale (L less-than-or-equal-to R), smaller insular length bilaterally, and symmetrical frontal regions. Moreover, recent studies by the senior author and colleagues suggest that specific reading tasks are associated with specific variations in brain morphology. Symmetrical frontal widths was related to poorer passage comprehension, and reversed frontal area symmetry was related to poor word attack skills. Though many conceptual and technical issues remain unresolved, neuroimaging procedures appear to provide direct evidence supporting the importance of deviations in normal patterns of brain morphology in dyslexia. C1 MED COLL GEORGIA,AUGUSTA,GA 30912. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP HYND, GW (reprint author), UNIV GEORGIA,ATHENS,GA 30602, USA. NR 59 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 0922-4777 J9 READ WRIT JI Read. Writ. PD DEC PY 1991 VL 3 IS 3-4 BP 345 EP 362 DI 10.1007/BF00354967 PG 18 WC Education & Educational Research; Psychology, Educational SC Education & Educational Research; Psychology GA GZ299 UT WOS:A1991GZ29900011 ER PT J AU DAWSON, SL MUELLER, PR AF DAWSON, SL MUELLER, PR TI METALLIC STENTS - VASCULAR AND NONVASCULAR USES - EDITORIAL SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Editorial Material RP DAWSON, SL (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0739-9529 J9 SEMIN INTERVENT RAD JI Semin. Interv. Radiol. PD DEC PY 1991 VL 8 IS 4 BP 228 EP 228 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GU851 UT WOS:A1991GU85100001 ER PT J AU DAWSON, SL LEE, MJ MUELLER, PR AF DAWSON, SL LEE, MJ MUELLER, PR TI METAL ENDOPROSTHESES IN MALIGNANT BILIARY OBSTRUCTION SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114. RP MUELLER, PR (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0739-9529 J9 SEMIN INTERVENT RAD JI Semin. Interv. Radiol. PD DEC PY 1991 VL 8 IS 4 BP 242 EP 251 DI 10.1055/s-2008-1074652 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GU851 UT WOS:A1991GU85100004 ER PT J AU MAZANET, R ANTMAN, KH AF MAZANET, R ANTMAN, KH TI ADJUVANT THERAPY FOR SARCOMAS SO SEMINARS IN ONCOLOGY LA English DT Article ID SOFT-TISSUE SARCOMAS; HIGH-DOSE METHOTREXATE; GYNECOLOGIC ONCOLOGY GROUP; PRIMARY OSTEO-SARCOMA; RADIATION-THERAPY; RANDOMIZED TRIAL; CHEMOTHERAPY; DOXORUBICIN; EXTREMITIES; IFOSFAMIDE RP MAZANET, R (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 64 TC 37 Z9 37 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 1991 VL 18 IS 6 BP 603 EP 612 PG 10 WC Oncology SC Oncology GA GW972 UT WOS:A1991GW97200011 PM 1775977 ER PT J AU WIJDICKS, EFM ROPPER, AH HUNNICUTT, EJ RICHARDSON, GS NATHANSON, JA AF WIJDICKS, EFM ROPPER, AH HUNNICUTT, EJ RICHARDSON, GS NATHANSON, JA TI ATRIAL-NATRIURETIC-FACTOR AND SALT WASTING AFTER ANEURYSMAL SUBARACHNOID HEMORRHAGE SO STROKE LA English DT Article DE HYPONATREMIA; NATRIURETIC PEPTIDES, ATRIAL; SUBARACHNOID HEMORRHAGE ID CEREBROSPINAL-FLUID; HYPONATREMIA; VASOPRESSIN; MANAGEMENT; PEPTIDE; BLOOD; SHEEP; RAT AB Background and Purpose: The causes of volume depletion and hyponatremia after subarachnoid hemorrhage are not fully understood but may be in part due to natriuresis or "cerebral salt wasting." Because previous studies using infrequent hormone sampling have given inconsistent results, we determined if elevations in atrial natriuretic factor concentrations preceeded negative sodium and fluid balances. Methods: We measured diurnal atrial natriuretic factor and vasopressin concentrations and sodium balance for 5 days in 14 consecutive patients after aneurysmal subarachnoid hemorrhage. Results: Plasma concentrations of atrial natriuretic factor on admission were elevated in subarachnoid hemorrhage patients (mean +/- SD 106 +/- 59 pg/ml) compared with acutely ill controls (39 +/- 30 pg/ml). In eight patients, high peak concentrations of atrial natriuretic factor, greater than 300 pg/ml or a twofold increase above baseline, were followed by natriuresis and a negative sodium balance. Three patients, two of whom became hyponatremic, developed cerebral infarcts after natriuresis. Vasopressin concentrations were slightly elevated just after hemorrhage but subsequently declined to normal values. Conclusions: A markedly increased atrial natriuretic factor concentration precedes natriuresis in some patients and, with other abnormalities of water handling possibly including a relatively diminished vasopressin concentration, may cause volume depletion. Patients with natriuresis appear to be at increased risk for delayed cerebral infarction after subarachnoid hemorrhage. C1 ST ELIZABETH HOSP,DIV NEUROL,736 CAMBRIDGE ST,BOSTON,MA 02135. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP ROPPER, AH (reprint author), ST ELIZABETH HOSP,DIV NEUROL,736 CAMBRIDGE ST,BOSTON,MA 02135, USA. FU NEI NIH HHS [EY0577]; NINDS NIH HHS [NS16356] NR 21 TC 77 Z9 79 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 DEC PY 1991 VL 22 IS 12 BP 1519 EP 1524 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA GV161 UT WOS:A1991GV16100007 PM 1835809 ER PT J AU UEMURA, Y MILLER, JM MATSON, WR BEAL, MF AF UEMURA, Y MILLER, JM MATSON, WR BEAL, MF TI NEUROCHEMICAL ANALYSIS OF FOCAL ISCHEMIA IN RATS SO STROKE LA English DT Article DE CEREBRAL ISCHEMIA; FREE RADICALS; RATS ID CEREBRAL-ARTERY OCCLUSION; FREE-RADICALS; XANTHINE-OXIDASE; REPERFUSION INJURY; NEURONAL DAMAGE; BRAIN; ALLOPURINOL; INFARCTION; DEHYDROGENASE; CONVERSION AB Background and Purpose: Increases in uric acid follow experimental stroke, which may be related to free radical formation by xanthine oxidase. The present study examined the time course of changes in xanthine and uric acid and their relationship to changes in the free radical scavengers glutathione, cysteine, and ascorbic acid. Methods: Focal ischemia was induced by occluding the middle cerebral artery, followed by transient occlusion of the common carotid arteries for 60 minutes. At varying time points, animals were sacrificed, and ischemic cortex was dissected. Neurochemical measurements were made by high-performance liquid chromatography with 16-sensor electrochemical detection. Results: Marked increases in uric acid were seen at all time points, with a maximal increase at 1 day and a persistent increase lasting up to 21 days. There were smaller reciprocal decreases in xanthine. Glutathione, cysteine, and ascorbic acid showed significant decreases, consistent with the generation of free radicals. Reductions in levels of cysteine and glutathione were significantly correlated with increases in uric acid levels. Conclusions: These findings confirm marked alterations in purine metabolism following focal ischemia and suggest that xanthine oxidase contributes to the generation of free radicals. C1 MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,STROKE RES LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL & NEUROSURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. ESA INC,BEDFORD,MA. RP BEAL, MF (reprint author), MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS 10828-15A1] NR 34 TC 92 Z9 94 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 DEC PY 1991 VL 22 IS 12 BP 1548 EP 1553 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA GV161 UT WOS:A1991GV16100012 PM 1720576 ER PT J AU DEMETER, JG DEJONG, SA LAWRENCE, AM PALOYAN, E AF DEMETER, JG DEJONG, SA LAWRENCE, AM PALOYAN, E TI ANAPLASTIC THYROID-CARCINOMA - RISK-FACTORS AND OUTCOME SO SURGERY LA English DT Article; Proceedings Paper CT 12TH ANNUAL MEETING OF THE AMERICAN ASSOC OF ENDOCRINE SURGEONS CY APR 14-16, 1991 CL SAN JOSE, CA SP AMER ASSOC ENDOCRINE SURGEONS ID CELL; ANEUPLOIDY; CANCER; GLAND AB Anaplastic thyroid carcinoma, in contrast to well-differentiated thyroid carcinoma, has a dismal prognosis, and little progress has been made in improving survival for this disease. We reviewed our experience during a 23-year period to identify risk factors and possible methods to improve outcome. Between 1966 and 1989, 340 patients with thyroid carcinoma underwent operation. Of these, 17 (5%) were undergoing operative treatment of anaplastic or undifferentiated thyroid carcinoma. The female/male ratio was 3.5:1, and mean age at presentation was 63 years. The most common presenting symptoms included neck mass, voice change, or dysphagia. Unusual presentations included symptomatic bradycardia from compression of the vagus nerve and superior vena cava syndrome. Four patients had a history of well-differentiated thyroid carcinoma. Nine patients had been diagnosed or treated in the past for "goiter" or a neck mass, and four patients had concurrent differentiated thyroid carcinoma associated with the anaplastic tumor. Thus 13 (76%) of 17 patients had a previous thyroid disorder, benign or differentiated malignant, and eight (47%) of 17 patients had previous or concurrent differentiated thyroid carcinoma. At the time of presentation, six patients had unilateral true vocal cord paralysis. At operation, 14 patients had local extension of the tumor and four required tracheostomy. Only five of 12 patients showed response to postoperative radiation therapy. Overall median survival was 12 months, and 13 (76%) of 17 patients died. The two patients alive longer than 12 months had only small foci of anaplastic carcinoma in association with well-differentiated carcinoma. Anaplastic thyroid carcinoma is a locally and systemically aggressive disease, with long-term survival seen only in those with well-localized anaplastic tumor. The major risk factor in this series is a history of previous benign or malignant thyroid disease. Because of this, a more aggressive approach to thyroid masses may be warranted. Long-standing goiters or benign nodules should be followed carefully and considered for resection if they grow or do not respond to medical therapy, and total thyroidectomy for malignant disease may obviate the subsequent development of anaplastic carcinoma. This method of early diagnosis and resection of abnormal thyroid tissue seems to be the only method currently available to improve the nearly uniform fatality of this disease. C1 US DEPT VET AFFAIRS,EDWARD HINES JR HOSP,RES SERV,HINES,IL. LOYOLA UNIV,STRITCH SCH MED,DEPT SURG,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT BIOCHEM,MAYWOOD,IL 60153. NR 20 TC 103 Z9 105 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD DEC PY 1991 VL 110 IS 6 BP 956 EP 963 PG 8 WC Surgery SC Surgery GA GU130 UT WOS:A1991GU13000006 PM 1745983 ER PT J AU DECKER, RA ELSON, P HOGAN, TF CITRIN, DL WESTRING, DW BANERJEE, TK GILCHRIST, KW HORTON, J AF DECKER, RA ELSON, P HOGAN, TF CITRIN, DL WESTRING, DW BANERJEE, TK GILCHRIST, KW HORTON, J TI EASTERN-COOPERATIVE-ONCOLOGY-GROUP STUDY 1879 - MITOTANE AND ADRIAMYCIN IN PATIENTS WITH ADVANCED ADRENOCORTICAL CARCINOMA SO SURGERY LA English DT Article; Proceedings Paper CT 12TH ANNUAL MEETING OF THE AMERICAN ASSOC OF ENDOCRINE SURGEONS CY APR 14-16, 1991 CL SAN JOSE, CA SP AMER ASSOC ENDOCRINE SURGEONS ID ADRENAL-CORTICAL CARCINOMA; THERAPY; TUMORS; ORTHO,PARA'-DDD; FEATURES AB From November 1979 to July 1986, 52 patients (27 women and 25 men; median age 52 years) with advanced adrenocortical carcinoma entered a prospective, nonrandomized study evaluating moderate-dose mitotane and doxorubicin hydrochloride (Adriamycin). Thirty-two tumors (62%) were well differentiated and evidence of hormone production was present in 24 patients (46%). Patients with well-differentiated or functional tumors received mitotane, 6 gm daily; patients for whom mitotane failed or those with poorly differentiated, non-hormone-producing tumors received Adriamycin, 60 mg/m2 every 3 weeks. Initially, 36 patients were treated with mitotane and 16 patients with Adriamycin. Eight patients (22%) responded to mitotane and three (19%) responded to Adriamycin. No response was noted in the 15 patients for whom mitotane failed and who then received Adriamycin. Severe toxicity occurred in 36% of patients who received mitotane and in 26% who received Adriamycin. Overall median survival after onset of treatment was 14 months. We conclude that mitotane or Adriamycin used initially can induce tumor regression in about 22% and 19% of selected patients, respectively. However, Adriamycin is ineffective as second-line chemotherapy for patients with well-differentiated or functioning tumors for whom mitotane is ineffective. C1 MARSHFIELD CLIN FDN MED RES & EDUC,DEPT ONCOL,MARSHFIELD,WI 54449. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. NASSAU CTY MED CTR,DEPT MED,E MEADOW,NY 11554. UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53706. UNION UNIV,DEPT MED,ALBANY,NY 12208. RP DECKER, RA (reprint author), MARSHFIELD CLIN FDN MED RES & EDUC,DEPT SURG,MARSHFIELD,WI 54449, USA. FU NCI NIH HHS [CA-23318] NR 16 TC 58 Z9 59 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD DEC PY 1991 VL 110 IS 6 BP 1006 EP 1013 PG 8 WC Surgery SC Surgery GA GU130 UT WOS:A1991GU13000012 PM 1745969 ER PT J AU DEMETER, JG DEJONG, SA OSLAPAS, R ERNST, K HESSEL, P JAROSZ, H SMITH, M NAYYAR, R LAWRENCE, AM PALOYAN, E AF DEMETER, JG DEJONG, SA OSLAPAS, R ERNST, K HESSEL, P JAROSZ, H SMITH, M NAYYAR, R LAWRENCE, AM PALOYAN, E TI HIGH PHOSPHATE DIET-INDUCED PRIMARY HYPERPARATHYROIDISM - AN ANIMAL-MODEL SO SURGERY LA English DT Article; Proceedings Paper CT 12TH ANNUAL MEETING OF THE AMERICAN ASSOC OF ENDOCRINE SURGEONS CY APR 14-16, 1991 CL SAN JOSE, CA SP AMER ASSOC ENDOCRINE SURGEONS ID PARATHYROID-HORMONE; SECONDARY HYPERPARATHYROIDISM; RATS; METABOLISM; PHOSPHORUS; PREVENTION; CALCIUM; GENESIS; SERUM AB Primary hyperparathyroidism (PHPT) is increasing in incidence and detection, primarily because of the aging of our population and the widespread use of automated serum calcium determination. As a result, a substantial number of "early" cases or "biochemical" PHPT are being detected. The indications for parathyroidectomy in such early cases of PHPT are currently under debate, primarily because of economic issues. These factors underscore the importance of research into the basic mechanisms and natural history of PHPT. We investigated an animal model of diet-induced PHPT that retains two crucial aspects of PHPT: elevation of endogenously produced parathyroid hormone (PTH), accompanied by gross and microscopic changes in the native parathyroid glands. Female Long-Evans rats were divided into six groups of 15 each and fed a control diet (Ca/P of 1:2) or a high-phosphate diet (Ca/P of 1:7) for 1-, 2-, or 3-month intervals. Compared with the control animals, serum PTH levels were elevated at all three time intervals in the experimental group, whereas serum calcium levels were decreased at all time intervals. Serum creatine levels were also elevated at all time intervals, whereas serum phosphorus levels did not change. Parathyroid histopathologic studies demonstrated no change at 1 month, whereas nine of 15 experimental animals showed mild hyperplasia at 2 months and 13 of 14 showed mild to moderate hyperplasia with gland enlargement at 3 months compared with control animals. Histopathologic examination of the kidneys showed no change at 1 month but focal parenchymal inflammation with calcium deposition at 2 and 3 months in the experimental groups. In conclusion, the high-phosphate diet successfully induced the earliest changes of PHPT: elevated PTH levels and parathyroid hyperplasia. However, because renal function was mildly compromised early on, some element of early secondary (renal) hyperparathyroidism may have supervened quickly. Because this model is simple, it may be useful to investigate this complex syndrome further, as well as its natural history and the complications it produces in other organs such as the kidneys. C1 LOYOLA UNIV,STRITCH SCH MED,DEPT SURG,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT MED,MAYWOOD,IL 60153. LOYOLA UNIV,STRITCH SCH MED,DEPT BIOCHEM,MAYWOOD,IL 60153. US DEPT VET AFFAIRS,EDWARD HINES JR HOSP,RES SERV,HINES,IL. NR 24 TC 10 Z9 12 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD DEC PY 1991 VL 110 IS 6 BP 1053 EP 1060 PG 8 WC Surgery SC Surgery GA GU130 UT WOS:A1991GU13000019 PM 1745975 ER PT J AU SWANSON, RS SAWICKA, J WOOD, WC AF SWANSON, RS SAWICKA, J WOOD, WC TI TREATMENT OF CARCINOMA OF THE BREAST IN THE OLDER GERIATRIC-PATIENT SO SURGERY GYNECOLOGY & OBSTETRICS LA English DT Article ID TOTAL MASTECTOMY; CANCER; WOMEN; AGE; RADIATION; TAMOXIFEN AB With recent changes in the management of carcinoma of the breast and a population that is increasingly aging, it behooves us to determine the most appropriate treatment of carcinoma of the breast in the elderly. We reviewed the records of 150 women 80 years of age or greater who were diagnosed between 1970 and 1980 at the Massachusetts General Hospital as having carcinoma of the breast. In these selected patients, treatment with operation or radiotherapy was well tolerated. Of the 103 patients who had mastectomies, only one patient died during the postoperative period. The complication rate from mastectomy was similar to that reported for younger patients. All of the patients who began radiotherapy completed their courses of treatment. Complications from radiotherapy were generally transient and easily tolerated. Five year actuarial survival rates for patients with Stages I and II disease were similar for those receiving primary radiation therapy (67 per cent) or modified radical mastectomy (65 per cent). However, the comparable survival rate for those treated with lumpectomy alone was only 39 per cent. Local and regional failures occurred with lumpectomy, total mastectomy or primary radiation therapy, but not with modified radical mastectomy. We conclude that age alone should not dictate the treatment for carcinoma of the breast. An otherwise healthy elderly woman should be offered the same treatment options for the treatment of carcinoma of the breast as those offered to younger patients. C1 MASSACHUSETTS GEN HOSP,CTR CANC,DEPT RADIAT THERAPY,BOSTON,MA 02114. RP SWANSON, RS (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DEPT SURG,BOSTON,MA 02114, USA. NR 11 TC 23 Z9 23 U1 0 U2 0 PU FRANKLIN H MARTIN FOUNDATION PI CHICAGO PA 55 E ERIE ST, CHICAGO, IL 60611 SN 0039-6087 J9 SURG GYNECOL OBSTET JI Surg. Gynecol. Obstet. PD DEC PY 1991 VL 173 IS 6 BP 465 EP 469 PG 5 WC Obstetrics & Gynecology; Surgery SC Obstetrics & Gynecology; Surgery GA GR782 UT WOS:A1991GR78200007 PM 1948604 ER PT J AU SOIFFER, RJ DEAR, K RABINOWE, SN ANDERSON, KC FREEDMAN, AS MURRAY, C TARBELL, NJ MAUCH, P NADLER, LM RITZ, J AF SOIFFER, RJ DEAR, K RABINOWE, SN ANDERSON, KC FREEDMAN, AS MURRAY, C TARBELL, NJ MAUCH, P NADLER, LM RITZ, J TI HEPATIC-DYSFUNCTION FOLLOWING T-CELL-DEPLETED ALLOGENEIC BONE-MARROW TRANSPLANTATION SO TRANSPLANTATION LA English DT Article ID VENO-OCCLUSIVE DISEASE; NON-HODGKINS-LYMPHOMA; LIVER-DISEASE; VENOCCLUSIVE DISEASE; VENOOCCLUSIVE DISEASE; HOST-DISEASE; GRAFT; CYCLOSPORINE; RADIATION; LEUKEMIA AB We reviewed the medical records of 97 patients undergoing T cell-depleted allogeneic bone marrow transplantation at our institution from 1984 to 1990 to determine the incidence of hepatic dysfunction, including venoocclusive disease of the liver following BMT. All patients received allogeneic marrow that had been purged with monoclonal antibody to the CD6 surface antigen (T12) and rabbit complement as the sole method of graft-versus-host disease prophylaxis. No additional immunosuppressive agents were routinely administered to these patients. Overall, 55% of patients in our series developed two-fold elevations in serum bilirubin, SGOT, or alkaline phosphatase within the first 30 days following BMT. A five-fold elevation in any liver function test was noted in only 19% of patients. Logistic regression analysis revealed that the presence of GVHD, female sex, and administration of amphotericin B all were independently associated with laboratory evidence of hepatic dysfunction. While LFT abnormalities were common in our series, they were generally mild, and the development of VOD was rare. Only three patients (3.1%) fulfilled clinical criteria sufficient to establish a diagnosis of VOD. Among the 86 patients whose ablative regimen consisted of cyclophosphamide (60 mg/kg x 2) and total-body irradiation (1200-1400 cGy in 200 cGy fractions), only 1 patient (1.2%) developed VOD. Our experience suggests that patients undergoing allogeneic BMT are at low risk for VOD and other serious hepatic complications when they receive high-dose cyclophosphamide, fractionated TBI, and T cell-depleted marrow without hepatotoxic medications for GVHD prophylaxis. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,JOINT CTR RADIAT THERAPY,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,JOINT CTR RADIAT THERAPY,SCH MED,DEPT RADIAT THERAPY,BOSTON,MA 02115. RP SOIFFER, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NIAID NIH HHS [AI 29530, N01-AI 62531] NR 34 TC 46 Z9 46 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 DEC PY 1991 VL 52 IS 6 BP 1014 EP 1019 DI 10.1097/00007890-199112000-00015 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA GV969 UT WOS:A1991GV96900015 PM 1750063 ER PT J AU ROSENGARD, BR KORTZ, EO OJIKUTU, CA GUZZETTA, PC SUNDT, TM SMITH, CV NAKAJIMA, K BOORSTEIN, SM HILL, GS SACHS, DH AF ROSENGARD, BR KORTZ, EO OJIKUTU, CA GUZZETTA, PC SUNDT, TM SMITH, CV NAKAJIMA, K BOORSTEIN, SM HILL, GS SACHS, DH TI THE FAILURE OF SKIN-GRAFTING TO BREAK TOLERANCE TO CLASS-I-DISPARATE RENAL-ALLOGRAFTS IN MINIATURE SWINE DESPITE INDUCING MARKED ANTIDONOR CELLULAR-IMMUNITY SO TRANSPLANTATION LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; REJECTION INVIVO; CYCLOSPORINE-A; T-CELLS; TRANSPLANTATION; SURVIVAL; ANTIGEN; INVITRO; RAT; RESPONSES AB Long-term specific tolerance to one haplotype class I plus minor antigen disparate renal allografts develops without exogenous immunosuppression in approximately 35% of miniature swine (n = 128). Previous studies have suggested that this phenomenon is related to limited class I-specific helper T cell activity as evidenced by the failure of antibody class switching in vivo and the ability of exogenous interleukin 2 to elicit antidonor responses in vitro. To determine whether tolerance could be broken by inducing antidonor reactivity with donor antigen and a source of T cell help, multiple skin grafts bearing donor class I plus third-party class II antigens were placed on tolerant animals. Skin grafts were placed at least 3 months after the kidney transplant, at which time all recipients had normal renal function as measured by blood urea nitrogen and serum creatinine. First-set rejection of skin grafts by SLA(ad) and SLA(dd) hosts occurred in 11.8 +/- 1.1 days (mean +/- SEM, n = 6) and in 9.3 +/- 0.9 days (n = 4), respectively. Coincident with skin rejection, most animals developed a transient rise in BUN to 62 +/- 11 mg/dl (n = 10) and a similar rise in Cr to 4.9 +/- 1.2 mg/dl (n = 10), with normal levels returning in all animals within two weeks. Subsequent skin grafts with the same disparity did not undergo second-set rejection and did not induce BUN or Cr elevations. Prior to skin grafting, animals showed no antidonor activity in mixed lymphocyte reaction or cell-mediated lymphocytotoxicity assays. After two skin grafts, all animals developed donor-specific CML and secondary MLR responses, and additional skin grafts amplified this cellular immunity. Development of marked antidonor immunity without a break in tolerance suggested that either graft adaptation or local suppression might be involved in maintaining tolerance to class I MHC antigens. In preliminary studies, an immunized SLA(ad) animal and an immunized SLA(dd) animal were retransplanted with kidneys MHC matched to their first allografts. In both cases, the second graft was accepted permanently without immunosuppression, suggesting that graft adaptation is not necessary for the maintenance of tolerance to renal allografts in miniature swine. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BLDG 149,13TH ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. NR 31 TC 29 Z9 29 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 DEC PY 1991 VL 52 IS 6 BP 1044 EP 1052 DI 10.1097/00007890-199112000-00020 PG 9 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA GV969 UT WOS:A1991GV96900020 PM 1750067 ER PT J AU BIERER, BE JIN, YJ FRUMAN, DA CALVO, V BURAKOFF, SJ AF BIERER, BE JIN, YJ FRUMAN, DA CALVO, V BURAKOFF, SJ TI FK-506 AND RAPAMYCIN - MOLECULAR PROBES OF LYMPHOCYTE-T ACTIVATION SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT INTERNATIONAL CONGRESS ON FK 506 CY AUG 21-24, 1991 CL UNIV PITTSBURGH, PITTSBURGH, PA SP FUJISAWA PHARM HO UNIV PITTSBURGH ID CYTOSOLIC BINDING-PROTEIN; CIS-TRANS ISOMERASE; CELL ACTIVATION; IMMUNOSUPPRESSANT FK506; MACROLIDES FK-506; CYCLOSPORIN-A; CYCLOPHILIN; DISTINCT; IMMUNOPHILIN; EXPRESSION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP BIERER, BE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,ROOM 1610B,44 BINNEY ST,BOSTON,MA 02115, USA. RI Calvo, Victor/L-5024-2014 OI Calvo, Victor/0000-0002-5913-7058 FU NCI NIH HHS [CA39542] NR 32 TC 29 Z9 30 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD DEC PY 1991 VL 23 IS 6 BP 2850 EP 2855 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA GV175 UT WOS:A1991GV17500044 PM 1721296 ER PT J AU OZTURK, M AF OZTURK, M TI P53 MUTATION IN HEPATOCELLULAR-CARCINOMA AFTER AFLATOXIN EXPOSURE SO LANCET LA English DT Article ID HEPATITIS-B VIRUS; EPIDEMIOLOGY; PREVALENCE; CANCER; JAPAN AB Mutations of the p53 gene are found in hepatocellular carcinoma (HCC), the most common form of primary liver cancer. Specific mutations might reflect exposure to specific carcinogens and we have screened HCC samples from patients in 14 different countries to determine the frequency of a hotspot mutation at codon 249 of the tumour suppressor p53 gene. We detected mutations in 17% of tumours (12/72) from four countries in south Africa and the southeast coast of Asia. There was no codon 249 mutation in 95 specimens of HCC from other geographical locations including North America, Europe, Middle East, and Japan. Worldwide, the presence of the codon 249 mutation in HCCs correlated with high risk of exposure to aflatoxins and the hepatitis B virus (HBV). Further studies were completed in two groups of HBV-infected patients at different risks of exposure to aflatoxins. 53% of patients (8/15) from Mozambique at high risk of aflatoxin exposure had a tumour with a codon 249 mutation, in contrast with 8% of patients from Transkei (1/12) who were at low risk. HCC is an endemic disease in Mozambique and accounts for up to two thirds of all tumours in men. A codon 249 mutation of the p53 gene identifies an endemic form of HCC strongly associated with dietary aflatoxin intake. RP OZTURK, M (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02129, USA. RI ozturk, mehmet/G-3330-2014 FU NCI NIH HHS [CA49832, CA35711]; NIAAA NIH HHS [AA00048] NR 22 TC 367 Z9 373 U1 1 U2 12 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD NOV 30 PY 1991 VL 338 IS 8779 BP 1356 EP 1359 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA GR773 UT WOS:A1991GR77300004 PM 1682737 ER PT J AU NASRIN, N BUGGS, C KONG, XF CARNAZZA, J GOEBL, M ALEXANDERBRIDGES, M AF NASRIN, N BUGGS, C KONG, XF CARNAZZA, J GOEBL, M ALEXANDERBRIDGES, M TI DNA-BINDING PROPERTIES OF THE PRODUCT OF THE TESTIS-DETERMINING GENE AND A RELATED PROTEIN SO NATURE LA English DT Article ID SEX-DETERMINING REGION; MOTIF; EXPRESSION; HOMOLOGY; CLONING; CELLS; SRY AB THE upstream region of the human glyceraldehyde-3-phosphate dehydrogenase gene contains an insulin-response element (IRE-A) responsible for insulin-dependent transcription of the gene (ref. 1). The open reading frame of a rat complementary DNA encoding a protein (IRE-ABP) that binds to this sequence contains an HMG box motif 2 that is 67% identical to the mouse candidate gene for the testis-determining factor SRY, and 98% identical to the mouse SRY-like gene, alpha-4(refs 3, 4). Here we report that IRE-ABP and SRY bind to IRE-A DNA with comparable specificity in a DNase-I footprinting assay. Two females with sex reversal were found to have a single amino-acid substitution in the HMG box domain of SRY at position 3 and 7, respectively 5,6. SRY derivatives containing corresponding mutations do not make contact with IRE-A DNA. These results are direct evidence that mouse SRY-like proteins are sequence-specific DNA-binding proteins and identify two amino acids critical to this interaction. Moreover, IRE-A is a candidate SRY-response element. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,DIABET UNIT,50 BLOSSOM ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,BOSTON,MA 02114. NR 17 TC 167 Z9 168 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD NOV 28 PY 1991 VL 354 IS 6351 BP 317 EP 320 DI 10.1038/354317a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GT204 UT WOS:A1991GT20400051 PM 1956382 ER PT J AU GRIBBEN, JG FREEDMAN, AS NEUBERG, D ROY, DC BLAKE, KW WOO, SD GROSSBARD, ML RABINOWE, SN CORAL, F FREEMAN, GJ RITZ, J NADLER, LM AF GRIBBEN, JG FREEDMAN, AS NEUBERG, D ROY, DC BLAKE, KW WOO, SD GROSSBARD, ML RABINOWE, SN CORAL, F FREEMAN, GJ RITZ, J NADLER, LM TI IMMUNOLOGICAL PURGING OF MARROW ASSESSED BY PCR BEFORE AUTOLOGOUS BONE-MARROW TRANSPLANTATION FOR B-CELL LYMPHOMA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID NON-HODGKINS-LYMPHOMA; ACUTE LYMPHOBLASTIC-LEUKEMIA; DOSE COMBINATION CHEMOTHERAPY; BREAKPOINT-CLUSTER REGION; MONOCLONAL-ANTIBODY; FOLLICULAR LYMPHOMAS; CHROMOSOMAL TRANSLOCATION; BREAST-CANCER; T(14-18); ANTIGEN AB Background. The use of autologous bone marrow transplantation is increasing in the management of advanced cancers. Many investigators have attempted to "purge" autologous marrow of residual tumor cells because of concern that reinfused tumor cells might contribute to relapse. The efficacy of purging remains unproved. Methods. We performed clonogenic assays in a tumor cell line in culture to determine the efficiency of immunologic purging. Amplification by the polymerase chain reaction (PCR) was used to detect residual lymphoma cells before and after purging of bone marrow from 114 patients with B-cell non-Hodgkin's lymphoma in whom a translocation (t(l4;18)) that could be amplified by PCR was detected at the time of their initial evaluation. Results. Immunologic purging in vitro resulted in a 3-to-6-log destruction of cells in the tumor cell line. Residual lymphoma cells were detected by PCR in the bone marrow of all patients before purging. No lymphoma cells could be detected in the marrow of 57 patients after purging. Disease-free survival was increased in these 57 patients as compared with those whose marrow contained detectable residual lymphoma (P < 0.00001). The ability to purge residual lymphoma cells was not associated with the degree of bone marrow involvement (P = 0.4494) or the previous response to therapy (P = 0.1298). Conclusions. The inability to purge residual lymphoma cells was the most important prognostic indicator in predicting relapse. These results provide evidence of the clinical usefulness of ex vivo purging of autologous bone marrow in the treatment of patients with lymphoma and suggest that the reinfusion of malignant cells in autologous marrow contributes to relapse. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP GRIBBEN, JG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU FIC NIH HHS [TWO4496]; NCI NIH HHS [CA-34183, CA-40216] NR 49 TC 671 Z9 675 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 NOV 28 PY 1991 VL 325 IS 22 BP 1525 EP 1533 DI 10.1056/NEJM199111283252201 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA GR380 UT WOS:A1991GR38000001 PM 1944436 ER PT J AU ALSTON, TA AF ALSTON, TA TI INHIBITION OF VITAMIN-B12-DEPENDENT METHIONINE BIOSYNTHESIS BY CHLOROFORM AND CARBON-TETRACHLORIDE SO BIOCHEMICAL PHARMACOLOGY LA English DT Note ID NITROUS-OXIDE RP ALSTON, TA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,CARDIAC ANESTHESIA GRP,BOSTON,MA 02114, USA. NR 13 TC 16 Z9 16 U1 0 U2 3 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 NOV 27 PY 1991 VL 42 IS 12 BP R25 EP R28 DI 10.1016/0006-2952(91)90226-U PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GU648 UT WOS:A1991GU64800002 PM 1764111 ER PT J AU POON, M MEGYESI, J GREEN, RS ZHANG, H ROLLINS, BJ SAFIRSTEIN, R TAUBMAN, MB AF POON, M MEGYESI, J GREEN, RS ZHANG, H ROLLINS, BJ SAFIRSTEIN, R TAUBMAN, MB TI INVIVO AND INVITRO INHIBITION OF JE GENE-EXPRESSION BY GLUCOCORTICOIDS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SMOOTH-MUSCLE; GROWTH-FACTOR; RIBONUCLEIC-ACID; MESSENGER-RNA; CELL-LINE; C-JUN; PROTEIN; DEXAMETHASONE; PURIFICATION; RECEPTOR AB Glucocorticoids are potent anti-inflammatory agents which affect cell growth and migration in a wide variety of systems and have profound effects on monocytes, decreasing their circulating number as well as inhibiting their accumulation at sites of inflammation and injury. Although the mechanisms by which glucocorticoids regulate gene induction have been established, the mechanisms by which they inhibit inflammation or cell growth and migration have yet to been determined. JE is one of the most abundant genes induced by platelet-derived growth factor (PDGF) in vitro and is also induced in vivo in response to ischemia or injury. JE encodes a low molecular weight glycoprotein that functions in part as a monocyte chemotactic factor and thus may be important in recruiting monocytes to sites of tissue injury and/or inflammation. We report that glucocorticoids block the induction of JE mRNA by serum or PDGF in cultured vascular smooth muscle cells. The effect of glucocorticoids appears largely due to destabilization of JE mRNA and has specificity for JE, in that other "early" PDGF-inducible genes are not inhibited by glucocorticoids. The effect of glucocorticoids also occurs in vivo: methyl prednisolone blocks the constitutive expression and inhibits the ischemia-induced elevation of JE mRNA levels in rat kidneys. The inhibition of JE mRNA accumulation by glucocorticoids may be related to the anti-inflammatory effects of these agents and defines JE as a member of what may be a group of PDGF-inducible genes that are responsive to corticosteroids. C1 CUNY MT SINAI SCH MED,DEPT MED,BROOKDALE CTR MOLEC BIOL,DIV MOLEC MED,NEW YORK,NY 10029. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CUNY MT SINAI SCH MED,DEPT MED,DIV CARDIOL,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT MED,DIV RENAL,NEW YORK,NY 10029. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CHEM,BOSTON,MA 02115. CUNY MT SINAI SCH MED,DEPT PEDIAT,NEW YORK,NY 10029. FU NCI NIH HHS [CA53901]; NHLBI NIH HHS [HL43302] NR 37 TC 64 Z9 64 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 NOV 25 PY 1991 VL 266 IS 33 BP 22375 EP 22379 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GR564 UT WOS:A1991GR56400052 PM 1939262 ER PT J AU HUANG, D SWANSON, EA LIN, CP SCHUMAN, JS STINSON, WG CHANG, W HEE, MR FLOTTE, T GREGORY, K PULIAFITO, CA FUJIMOTO, JG AF HUANG, D SWANSON, EA LIN, CP SCHUMAN, JS STINSON, WG CHANG, W HEE, MR FLOTTE, T GREGORY, K PULIAFITO, CA FUJIMOTO, JG TI OPTICAL COHERENCE TOMOGRAPHY SO SCIENCE LA English DT Article ID NERVE-FIBER LAYER; MICROSCOPE; REFLECTANCE; THICKNESS; GLAUCOMA; SYSTEM; HEAD AB A technique called optical coherence tomography (OCT) has been developed for noninvasive cross-sectional imaging in biological systems. OCT uses low-coherence interferometry to produce a two-dimensional image of optical scattering from internal tissue microstructure in a way that is analogous to ultrasonic pulse-echo imaging. OCT has longitudinal and lateral spatial resolutions of a few micrometers and can detect reflected signals as small as approximately 10(-10) of the incident optical power. Tomographic imaging is demonstrated in vitro in the peripapillary area of the retina and in the coronary artery, two clinically relevant examples that are representative of transparent and turbid media, respectively. C1 MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. MIT,LINCOLN LAB,LEXINGTON,MA 02173. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR HOSP,LASER RES LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,WELLMAN LABS,BOSTON,MA 02114. RI Schuman, Joel/K-7304-2012; Bakhsh, Turki/C-5625-2011 OI Schuman, Joel/0000-0002-8885-3766; Bakhsh, Turki/0000-0002-5953-4109 FU NIGMS NIH HHS [1-R01-GM35459-06, R01 GM035459] NR 39 TC 7033 Z9 7326 U1 72 U2 617 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD NOV 22 PY 1991 VL 254 IS 5035 BP 1178 EP 1181 DI 10.1126/science.1957169 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GQ834 UT WOS:A1991GQ83400038 PM 1957169 ER PT J AU ROSENSTEIN, Y PARK, JK HAHN, WC ROSEN, FS BIERER, BE BURAKOFF, SJ AF ROSENSTEIN, Y PARK, JK HAHN, WC ROSEN, FS BIERER, BE BURAKOFF, SJ TI CD43, A MOLECULE DEFECTIVE IN WISKOTT-ALDRICH SYNDROME, BINDS ICAM-1 SO NATURE LA English DT Article AB THE protein CD43 (also known as sialophorin, leukosialin, large sialoglycoprotein or gp115) is expressed on the surface of T lymphocytes, monocytes, neutrophils, platelets and some B lymphocytes 1-6. Expression of CD43 is deficient and/or defective in the X-chromosome-linked immunodeficiency disorder Wiscott-Aldrich syndrome 7, suggesting that CD43 might have a role in T-cell activation. We have shown that expression of human CD43 in an HLA-DR-specific murine T-cell hybridoma enhances the antigen-specific response to stimulation by the human lymphoblastoid cell line Daudi, and that Daudi cells bind specifically to purified immobilized CD43 (ref. 8). These data indicate that the specific interaction of CD43 with a ligand on the surface of Daudi cells might contribute to T-cell activation. Here we report evidence that intercellular adhesion molecule-1 (ICAM-1, or CD54), is a ligand for CD43. C1 HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, CTR BLOOD RES, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DIV HEMATOL ONCOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. RP ROSENSTEIN, Y (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV PEDIAT ONCOL, BOSTON, MA 02115 USA. NR 33 TC 251 Z9 253 U1 0 U2 3 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD NOV 21 PY 1991 VL 354 IS 6350 BP 233 EP 235 DI 10.1038/354233a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GQ948 UT WOS:A1991GQ94800050 PM 1683685 ER PT J AU HUA, QX SHOELSON, SE KOCHOYAN, M WEISS, MA AF HUA, QX SHOELSON, SE KOCHOYAN, M WEISS, MA TI RECEPTOR-BINDING REDEFINED BY A STRUCTURAL SWITCH IN A MUTANT HUMAN INSULIN SO NATURE LA English DT Article ID NUCLEAR-MAGNETIC-RESONANCE; SIDE-CHAIN; ASSIGNMENTS AB CRYSTAL Structures of insulin have been determined in various distinct forms 1-5, the relevance of which to receptor recognition has long been the subject of speculation 2,6,7. Recently the crystal structure of an inactive insulin analogue has been determined and, surprisingly, found to have a conformation identical to native insulin 8,9. On this basis Dodson and colleagues have suggested that the known insulin crystal structures reflect an inactive conformation, and that a change in conformation is required for activity-specifically, the carboxy terminal residues of the B-chain are proposed to separate from the amino terminal residues of the A-chain 8. Here we report the solution structure of an active insulin mutant 7,10, determined by two-dimensional NMR, which supports this hypothesis. In the mutant, the carboxy terminal beta-turn and beta-strand of the B-chain are destabilized and do not pack across the rest of the molecule. We suggest that analogous detachment of the carboxy terminal region of the B-chain occurs in native insulin on binding to its receptor. Our finding that partial unfolding of the B-chain exposes an alternative protein surface rationalizes the receptor-binding properties of a series of anomalous insulin analogues 7,11-13, including a mutant insulin associated with diabetes mellitus in man 14,15. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. CHINESE ACAD SCI,INST BIOPHYS,BEIJING,PEOPLES R CHINA. BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. CNRS,UA 32,F-91128 PALAISEAU,FRANCE. NR 30 TC 199 Z9 207 U1 4 U2 14 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD NOV 21 PY 1991 VL 354 IS 6350 BP 238 EP 241 DI 10.1038/354238a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GQ948 UT WOS:A1991GQ94800052 PM 1961250 ER PT J AU HOOVER, HC SAINI, S OCONNELL, JX AF HOOVER, HC SAINI, S OCONNELL, JX TI A 68-YEAR-OLD MAN WITH ALTERED MENTAL STATUS AND AN ABNORMAL TERMINAL ILEUM - MALIGNANT-LYMPHOMA, DIFFUSE, LARGE CLEAVED-CELL AND NON-CLEAVED-CELL TYPE, OF ILEUM, WITH PERFORATION AND INVASION OF ANTERIOR ABDOMINAL-WALL SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID GASTROINTESTINAL-TRACT; CROHNS-DISEASE; ENTERITIS; BOWEL; TUBERCULOSIS; INTESTINE; DISORDERS; PROGNOSIS; SURGERY; TUMOR C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HOOVER, HC (reprint author), MASSACHUSETTS GEN HOSP,SURG ONCOL RES,BOSTON,MA 02114, USA. NR 37 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 NOV 21 PY 1991 VL 325 IS 21 BP 1499 EP 1505 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA GQ406 UT WOS:A1991GQ40600008 ER PT J AU WEINER, A SANDBERG, MA GAUDIO, AR KINI, MM BERSON, EL AF WEINER, A SANDBERG, MA GAUDIO, AR KINI, MM BERSON, EL TI HYDROXYCHLOROQUINE RETINOPATHY SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID CHLOROQUINE RETINOPATHY; RHEUMATOID-ARTHRITIS; RETINITIS PIGMENTOSA; RETINAL TOXICITY; ELECTRORETINOGRAMS; THERAPY AB We analyzed ocular findings from two patients (aged 49 and 60 years) with hydroxychloroquine Plaquenil, Winthrop Pharmaceuticals, Division of Sterling Drug, Inc., New York, New York) retinopathy. Both patients were treated for systemic lupus erythematosus; one patient was treated with 400 to 800 mg of hydroxychloroquine per day (6.1 to 12.2 mg/kg of body weight/day) over a ten-year period, whereas the other received 400 mg/day (6.1 mg/kg of body weight/day) over a 20-year period. Cumulative doses were 1,788 and 2,920 g, respectively. Neither patient had ever been treated with chloroquine. One patient complained of glare and difficulty in adjusting to changes in illumination, whereas the other was asymptomatic. Both had bilateral visual acuities of 20/25, pericentral scotomata, and increased final dark-adapted rod thresholds in the two retinal areas that were tested. Full-field electroretinograms were reduced and delayed, and focal cone electroretinography showed abnormal foveal responses as well. Ophthalmoscopy and fluorescein angiography showed a bull's-eye maculopathy in both eyes of one patient and perifoveal depigmentation in both eyes of the other patient. Retinal function remained stable at follow-up examinations 18 to 24 months after the cessation of hydroxychloroquine treatment. These two cases demonstrate that peripheral retinopathy, as well as maculopathy, can develop in patients who are treated with hydroxychloroquine for systemic lupus erythematosus, and that retinal function may remain stable after discontinuation of hydroxychloroquine treatment. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. FU NEI NIH HHS [EY08398] NR 31 TC 57 Z9 61 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 NOV 15 PY 1991 VL 112 IS 5 BP 528 EP 534 PG 7 WC Ophthalmology SC Ophthalmology GA GN958 UT WOS:A1991GN95800007 PM 1951589 ER PT J AU LOPEZ, MF PATTON, WF UTTERBACK, BL CHUNGWELCH, N BARRY, P SKEA, WM CAMBRIA, RP AF LOPEZ, MF PATTON, WF UTTERBACK, BL CHUNGWELCH, N BARRY, P SKEA, WM CAMBRIA, RP TI EFFECT OF VARIOUS DETERGENTS ON PROTEIN MIGRATION IN THE 2ND-DIMENSION OF 2-DIMENSIONAL GELS SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID SODIUM DODECYL-SULFATE; ENDOTHELIAL-CELLS; ELECTROPHORESIS SYSTEM; IDENTIFICATION; SEPARATION; RESOLUTION C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02129. SLOAN KETTERING MEM CANC CTR,DEPT MOLEC BIOL,NEW YORK,NY 10021. RP LOPEZ, MF (reprint author), MILLIPORE CORP,CORP RES & DEV,BEDFORD,MA 01730, USA. NR 31 TC 32 Z9 32 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD NOV 15 PY 1991 VL 199 IS 1 BP 35 EP 44 DI 10.1016/0003-2697(91)90266-V PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA GQ785 UT WOS:A1991GQ78500007 PM 1807160 ER PT J AU NIEMEYER, CM GELBER, RD TARBELL, NJ DONNELLY, M CLAVELL, LA BLATTNER, SR DONAHUE, K COHEN, HJ SALLAN, SE AF NIEMEYER, CM GELBER, RD TARBELL, NJ DONNELLY, M CLAVELL, LA BLATTNER, SR DONAHUE, K COHEN, HJ SALLAN, SE TI LOW-DOSE VERSUS HIGH-DOSE METHOTREXATE DURING REMISSION INDUCTION IN CHILDHOOD ACUTE LYMPHOBLASTIC-LEUKEMIA (PROTOCOL-81-01 UPDATE) SO BLOOD LA English DT Article ID ACUTE LYMPHOCYTIC-LEUKEMIA; COMBINATION CHEMOTHERAPY; INTENSIVE ASPARAGINASE C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,ROOM 1842,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIAT THERAPY,BOSTON,MA 02115. UNIV PUERTO RICO,DEPT PEDIAT ONCOL,SAN JUAN,PR 00936. UNIV ROCHESTER,MED CTR,DEPT PEDIAT,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,CTR CANC,ROCHESTER,NY 14642. FU NCI NIH HHS [CA 065165, CA 22719, CA 19789] NR 20 TC 67 Z9 67 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 NOV 15 PY 1991 VL 78 IS 10 BP 2514 EP 2519 PG 6 WC Hematology SC Hematology GA GP887 UT WOS:A1991GP88700005 PM 1824248 ER PT J AU DELAGE, R SOIFFER, RJ DEAR, K RITZ, J AF DELAGE, R SOIFFER, RJ DEAR, K RITZ, J TI CLINICAL-SIGNIFICANCE OF BCR-ABL GENE REARRANGEMENT DETECTED BY POLYMERASE CHAIN-REACTION AFTER ALLOGENEIC BONE-MARROW TRANSPLANTATION IN CHRONIC MYELOGENOUS LEUKEMIA SO BLOOD LA English DT Article ID CHRONIC MYELOID-LEUKEMIA; MINIMAL RESIDUAL DISEASE; MESSENGER-RNA; CHRONIC PHASE; CELLS; AMPLIFICATION; RELAPSE; TRANSLOCATION; SEQUENCES; INVITRO C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NIAID NIH HHS [AI29530, N01-AI62531] NR 31 TC 107 Z9 107 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 NOV 15 PY 1991 VL 78 IS 10 BP 2759 EP 2767 PG 9 WC Hematology SC Hematology GA GP887 UT WOS:A1991GP88700039 PM 1824268 ER PT J AU VANDIJKEN, PJ WIMPERIS, J CRAWFORD, JM FERRARA, JLM AF VANDIJKEN, PJ WIMPERIS, J CRAWFORD, JM FERRARA, JLM TI EFFECT OF GRAFT-VERSUS-HOST DISEASE ON HEMATOPOIESIS AFTER BONE-MARROW TRANSPLANTATION IN MICE SO BLOOD LA English DT Article ID MINOR HISTOCOMPATIBILITY BARRIERS; T-CELL; STEM-CELLS; PROLIFERATIVE CAPACITY; PRECURSOR FREQUENCY; LETHAL GRAFT; THROMBOCYTOPENIA; RECONSTITUTION; PROGENITORS; CULTURE C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,ROOM 1610,44 BINNEY ST,BOSTON,MA 02115. UNIV HOSP CHILDREN & YOUTH HET WILHELMINA KINDERZIEKENHUIS,UTRECHT,NETHERLANDS. CHILDRENS HOSP MED CTR,DIV PEDIAT ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. NR 38 TC 19 Z9 19 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1991 VL 78 IS 10 BP 2773 EP 2779 PG 7 WC Hematology SC Hematology GA GP887 UT WOS:A1991GP88700041 PM 1824270 ER PT J AU LEVISOHN, LF ISACSON, O AF LEVISOHN, LF ISACSON, O TI EXCITOTOXIC LESIONS OF THE RAT ENTORHINAL CORTEX - EFFECTS OF SELECTIVE NEURONAL DAMAGE ON ACQUISITION AND RETENTION OF A NONSPATIAL REFERENCE MEMORY TASK SO BRAIN RESEARCH LA English DT Article DE ENTORHINAL CORTEX; N-METHYL-D-ASPARTATE; NEURONAL LOSS; REFERENCE MEMORY; RAT; ALZHEIMERS DISEASE ID ALZHEIMERS-DISEASE; DENTATE GYRUS; ALTERNATION PERFORMANCE; HIPPOCAMPAL-FORMATION; UNIT-ACTIVITY; STIMULATION; RECOVERY; DISSOCIATION; DEMENTIA; PATHWAY AB The neurotoxin N-methyl-D-aspartate was used to induce selective bilateral neuronal loss in the entorhinal cortex, in order to model one aspect of the neurodegeneration observed in Alzheimer's disease, Down's syndrome and aging. Lesioned, sham-lesioned and intact control rats learned a reference memory task involving a brightness discrimination for water reward. Rats were trained over 1 week until reaching criteria and tested for retention after a 10-day interval. Lesioned rats showed impaired retention compared to shams and controls, but were able to reacquire the task. Anatomical analysis confirmed excitotoxic lesions of the entorhinal cortex, and showed collateral sprouting of acetylcholinesterase-stained fibers into the outer molecular layer of the dentate gyrus, indicating denervation plasticity in the hippocampus. This functional anatomical study of the entorhinal cortex demonstrates the importance of the entorhinal cortex in memory retention, and raises the possibility that functional deficits in certain neurodegenerative diseases may be modeled by partial neuronal loss in the entorhinal cortex. C1 HARVARD UNIV, MCLEAN HOSP,SCH MED,PROGRAM NEUROSCI, NEUROREGENERAT LAB,MRC 119, BELMONT, MA 02178 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. FU NINDS NIH HHS [NS29178-01A1] NR 52 TC 43 Z9 44 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD NOV 15 PY 1991 VL 564 IS 2 BP 230 EP 244 DI 10.1016/0006-8993(91)91458-D PG 15 WC Neurosciences SC Neurosciences & Neurology GA GR677 UT WOS:A1991GR67700005 PM 1810624 ER PT J AU SUZUSHIMA, H HATTORI, T ASOU, N WANG, JX NISHIKAWA, K OKUBO, T ANDERSON, P TAKATSUKI, K AF SUZUSHIMA, H HATTORI, T ASOU, N WANG, JX NISHIKAWA, K OKUBO, T ANDERSON, P TAKATSUKI, K TI DISCORDANT GENE AND SURFACE EXPRESSION OF THE T-CELL RECEPTOR CD3 COMPLEX IN ADULT T-CELL LEUKEMIA-CELLS SO CANCER RESEARCH LA English DT Article ID VIRUS TYPE-I; HUMAN LYMPHOCYTES-T; ANTIGEN RECEPTOR; MONOCLONAL-ANTIBODIES; T3-MOLECULAR COMPLEX; PERIPHERAL-BLOOD; MESSENGER-RNA; CHAIN; INTERLEUKIN-2; ACTIVATION AB Cell surface expression of the T-cell receptor (TCR)/CD3 complex on the cells from 11 acute type adult T-cell leukemia (ATL) and 4 lymphoma type ATL patients was examined by flow cytometry. Cells from 10 of 11 acute ATL patients were TCR-alpha-beta+ and CD3+, and their mean fluorescence intensities were low (TCR-alpha-beta, 25.3-84.6; CD3, 22.8-87.8). Cells from two of four lymphoma type ATL did not express this complex, and the other two were CD3+, TCR-alpha-beta-. In contrast, the mean fluorescence intensity of the TCR/CD3 complex in cells from a patient with T4 chronic lymphocytic leukemia was not low (TCR-alpha-beta, 129.9; CD3,117.1). mRNA expressions of the TCR-alpha, beta, and CD3-gamma, delta, epsilon, and xi-chains were examined by Northern blots. ATL cells from two acute and two lymphoma types expressed amounts of this complex equal to or greater than those expressed by T4 chronic lymphocytic leukemia. CD3-delta and TCR-beta mRNA in ATL and T4 chronic lymphocytic leukemia cells were equally stable to actinomycin D treatment. The synthesis of CD3 xi-protein by ATL cells was detected by Western blotting assay. On the basis of these findings, we discuss the possible involvement of the TCR/CD3 complex in activation of ATL cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP SUZUSHIMA, H (reprint author), KUMAMOTO UNIV,SCH MED,DEPT INTERNAL MED 2,1-1-1 HONJO,KUMAMOTO 860,JAPAN. NR 38 TC 19 Z9 21 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 NOV 15 PY 1991 VL 51 IS 22 BP 6084 EP 6088 PG 5 WC Oncology SC Oncology GA GP271 UT WOS:A1991GP27100011 PM 1834326 ER PT J AU GARBER, JE GOLDSTEIN, AM KANTOR, AF DREYFUS, MG FRAUMENI, JF LI, FP AF GARBER, JE GOLDSTEIN, AM KANTOR, AF DREYFUS, MG FRAUMENI, JF LI, FP TI FOLLOW-UP-STUDY OF 24 FAMILIES WITH LI-FRAUMENI SYNDROME SO CANCER RESEARCH LA English DT Article ID BREAST-CANCER RISK; CARCINOMA; SARCOMA; CHILDREN; MOTHERS; TUMORS AB The Li-Fraumeni cancer family syndrome is manifested by susceptibility to breast cancer, sarcomas, and other neoplasms in children and young adults. The present study utilized clinical follow-up data on 545 members of 24 Li-Fraumeni kindreds living and cancer-free at family ascertainment. Two hypotheses were tested based on a model of autosomal dominant genetic predisposition: (a) that syndrome cancers would continue to occur excessively during follow-up compared to the general population, and (b) that the tumors would occur primarily among those family members likely to carry the gene. Population cancer rates were compared with cancer rates in follow-up of the cohort from ascertainment to 1988. Risk of carrying the gene for the syndrome at the time of ascertainment was calculated for each family member under two models with somewhat different definitions of affection with the syndrome. Cancer occurrence after ascertainment was then analyzed according to the risks. Cancer did continue to occur excessively among the entire cohort during follow-up [relative risk (RR 2.1)]. The excess was greatest below age 20 (RR 21.1), declined with increasing age, and was most pronounced for neoplasms featured in the syndrome (RR 18.2). Among persons less than age 45, at least 87% of cancers occurred in those at higher risk of carrying the gene under both genetic models (RR 22.9 and 21.3). The clinical data, therefore, reliably identify individuals likely to carry a dominantly inherited gene conferring susceptibility to a specific constellation of neoplasms. Recent identification of a germ line mutation in the tumor suppressor gene p53 in persons with the syndrome may, if confirmed, have implications for ultimately defining the component tumors of the syndrome and for the causes and prevention of those tumors arising outside these families. C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. RP GARBER, JE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 23 TC 207 Z9 211 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 NOV 15 PY 1991 VL 51 IS 22 BP 6094 EP 6097 PG 4 WC Oncology SC Oncology GA GP271 UT WOS:A1991GP27100013 PM 1933872 ER PT J AU AISENBERG, AC WILKES, BM JACOBSON, JO AF AISENBERG, AC WILKES, BM JACOBSON, JO TI DIFFERENT T-CELL RECEPTOR GENE CONFIGURATIONS IN T-CELL NEOPLASMS AND ACUTE LYMPHOBLASTIC-LEUKEMIA SO CANCER RESEARCH LA English DT Article ID CHRONIC LYMPHOCYTIC-LEUKEMIA; ACUTE MYELOGENOUS LEUKEMIA; GAMMA-CHAIN GENE; B-CELL; BETA-CHAIN; DELTA GENE; REGION GENES; REARRANGEMENT; IMMUNOGLOBULIN; LINEAGE AB Southern blotting and multiple restriction enzymes were used to analyze T-cell receptor (TCR) and immunoglobulin heavy chain genes in 20 postthymic T-cell neoplasms, ten prethymic and thymic T-cell tumors, and 45 cases of precursor-B acute lymphoblastic leukemia (ALL). Immunoglobulin heavy chain, never rearranged in a postthymic specimen and only once in a prethymic/thymic sample, was rearranged in all but two cases of precursor-B ALL. In contrast, biallelic rearrangement of TCR-beta with deletion of the first constant region germline fragment was regularly seen in T-cell neoplasms, but only twice in the 45 precursor-B ALL cases. TCR-gamma was rearranged in all but one postthymic sample, in all prethymic/thymic samples, and in approximately half of precursor-B ALL specimens as well. Preferential use of V-gamma regions was evident among the various disorders: V8 and V10 in postthymic neoplasms; and V3, V5, V7, and, particularly, V9 in precursor-B ALL. In all the studied conditions, TCR-delta was rarely in germline configuration. Extensive biallelic deletion of J-delta-1, J-delta-2, and C-delta, almost always (19 of 20 specimens) present in postthymic neoplasms, was observed in only a minority (14 of 45) of precursor-B ALL samples. In precursor-B ALL, rearranged antigen receptor genes were more frequently found in common acute lymphoblastic leukemia antigen-positive and terminal deoxynucleotidyl transferase-positive specimens. Furthermore, TCR gene rearrangement in that disorder was characterized by a hierarchical pattern: TCR-beta was not rearranged without TCR-gamma nor TCR-gamma without TCR-delta. Despite uncertainty of the mechanism, the various disorders can be distinguished on the basis of characteristic antigen receptor gene patterns. RP AISENBERG, AC (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,HEMATOL ONCOL UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 30020] NR 48 TC 13 Z9 13 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 NOV 15 PY 1991 VL 51 IS 22 BP 6103 EP 6109 PG 7 WC Oncology SC Oncology GA GP271 UT WOS:A1991GP27100015 PM 1834327 ER PT J AU PUISIEUX, A LIM, S GROOPMAN, J OZTURK, M AF PUISIEUX, A LIM, S GROOPMAN, J OZTURK, M TI SELECTIVE TARGETING OF P53 GENE MUTATIONAL HOTSPOTS IN HUMAN CANCERS BY ETIOLOGICALLY DEFINED CARCINOGENS SO CANCER RESEARCH LA English DT Note ID ANTI-DIOL EPOXIDE; LUNG-CANCER; DNA DAMAGE; BENZOPYRENE; STRAND; REPAIR; AFLATOXIN-B1; FREQUENT; BACTERIA; INVITRO AB In lung and liver cancers, p53 mutations are mostly G:C to T:A transversions. This type of mutation is known to be induced by benzo(a)pyrene and aflatoxin B1 which are associated with the etiology of lung and liver cancers, respectively. Using a novel assay based on DNA polymerase fingerprint analysis, we identified p53 nucleotides targeted by these carcinogens. Thirteen of 14 nucleotide residues of the p53 gene which underwent G:C to T:A mutations in lung cancers were targeted by benzo(a)pyrene. Similarly, aflatoxin B, formed adducts at a mutational hotspot specific for liver cancer. The same nucleotide (third base of codon 249), which mutates rarely in lung cancers, was not a target for benzo(a)pyrene. These in vitro observations indicate that p53 mutational hotspots identified in different tumors are selected targets specifically for the etiologically defined environmental carcinogens. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,149 13TH ST,BOSTON,MA 02129. JOHNS HOPKINS UNIV,DEPT ENVIRONM HLTH SCI,BALTIMORE,MD 21205. RI ozturk, mehmet/G-3330-2014 FU NCI NIH HHS [CA 49832] NR 31 TC 259 Z9 266 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 15 PY 1991 VL 51 IS 22 BP 6185 EP 6189 PG 5 WC Oncology SC Oncology GA GP271 UT WOS:A1991GP27100028 PM 1933877 ER PT J AU SHASTRY, BS GREENSTEIN, D AF SHASTRY, BS GREENSTEIN, D TI THE ASSEMBLY OF FUNCTIONAL PREINITIATION COMPLEXES AND TRANSCRIPTION OF 5S-RNA-ENCODING GENES CONTAINING POINT MUTATIONS SO GENE LA English DT Article DE HAMSTER; RECOMBINANT DNA; RNA POLYMERASE III; FOOTPRINTING; MUTATIONS; STABLE COMPLEX ID RNA-POLYMERASE-III; DIRECTS SPECIFIC INITIATION; INTERNAL CONTROL REGION; RIBOSOMAL-RNA; XENOPUS-LAEVIS; EUKARYOTIC GENES; MULTIPLE FACTORS; FACTOR-A; BINDING; DNA AB The transcription of several Syrian hamster 5S RNA-encoding genes (5S genes) containing single and multiple point mutations in and around the intragenic control region has been analyzed in a HeLa cell-free system. Although most genes with point mutations displayed normal levels of transcription, several exhibited a three- to fivefold reduction in transcription. These mutations interfere with the interaction between the 5S genes and the soluble factors. The above studies help to establish the importance of specific nucleotides within the 5S gene for productive interactions of individual transcription factors in vitro. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP SHASTRY, BS (reprint author), OAKLAND UNIV,EYE RES INST,ROCHESTER,MI 48309, USA. NR 46 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD NOV 15 PY 1991 VL 107 IS 2 BP 269 EP 278 DI 10.1016/0378-1119(91)90327-8 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA GW140 UT WOS:A1991GW14000012 PM 1748297 ER PT J AU HAJJAR, RJ BONVENTRE, JV AF HAJJAR, RJ BONVENTRE, JV TI OSCILLATIONS OF INTRACELLULAR CALCIUM INDUCED BY VASOPRESSIN IN INDIVIDUAL FURA-2-LOADED MESANGIAL CELLS - FREQUENCY-DEPENDENCE ON BASAL CALCIUM-CONCENTRATION, AGONIST CONCENTRATION, AND TEMPERATURE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CYTOSOLIC FREE CALCIUM; RENAL EPITHELIAL-CELLS; CA-2+ OSCILLATIONS; FURA-2; HEPATOCYTES; MUSCLE; FLUORESCENCE; CHANNELS; MODEL AB Intracellular free calcium concentration ([Ca2+]i) was measured in fura-2-loaded single rat mesangial cells by dual wavelength spectrofluorometry. Stimulation with arginine vasopressin (AVP) caused an initial sharp rise of [Ca2+]i followed by repetitive spikes. The frequency of the oscillations was dependent on the concentration of AVP. At 0.1, 1.0, 10.0, and 100.0 nM AVP, the frequencies of oscillations were 0.17 +/- 0.05 (n = 6), 0.32 +/- 0.05 (n = 6), 0.49 +/- 0.05 (n = 6), and 0.48 +/- 0.05 min-1 (n = 5), respectively. Reduction in extracellular [Ca2+] reduced the frequency of AVP-induced oscillations but did not abolish the oscillations. The frequency of calcium oscillations, upon stimulation with 1.0 nM AVP, was directly correlated with the basal [Ca2+]i prior to stimulation. Oscillation frequency increased with increasing temperature. An Arrhenius plot between 24 and 37-degrees-C indicated a strong temperature dependency of the oscillations with a Q(10) of 3.0. Protein kinase C stimulation by active phorbol esters inhibited AVP-induced calcium oscillations but not the initial [Ca2+] response to AVP. These observations are consistent with a model incorporating a feedback loop linking [Ca2+]i to the mechanism of [Ca2+]i increase. Ca2+-induced Ca2+ release may be involved, whereby inositol 1,4,5-trisphosphate (inositol 1,4,5-P3) formation releases Ca2+ from an inositol 1,4,5-P3-sensitive pool, with subsequent Ca2+ uptake and release from an inositol 1,4,5-P3-insensitive pool. C1 MASSACHUSETTS GEN HOSP,MED SERV,RENAL UNIT,JACKSON 8,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. FU NIDDK NIH HHS [DK39249, DK38452, DK39773] NR 34 TC 29 Z9 29 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 NOV 15 PY 1991 VL 266 IS 32 BP 21589 EP 21594 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GP804 UT WOS:A1991GP80400044 PM 1939188 ER PT J AU OKAZAKI, T ZAJAC, JD IGARASHI, T OGATA, E KRONENBERG, HM AF OKAZAKI, T ZAJAC, JD IGARASHI, T OGATA, E KRONENBERG, HM TI NEGATIVE REGULATORY ELEMENTS IN THE HUMAN PARATHYROID-HORMONE GENE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSCRIPTIONAL REGULATION; EUKARYOTIC PROMOTERS; 5'-FLANKING REGION; GLOBIN GENE; EXPRESSION; SILENCER; RAT; BINDING; CELLS; SEQUENCE AB We have identified and characterized a pair of negative regulatory elements far upstream of the transcription start site of the human parathyroid hormone (hPTH) gene. Transfection of various types of cultured cells with a fusion plasmid containing 4.7 kilobase pairs of the 5'-flanking portion of the hPTH gene linked to the chloramphenicol acetyltransferase (CAT)-coding sequence generated only 10% of the CAT activity of a plasmid containing 684 base pairs of the 5'-flanking region of the hPTH gene. Deletion analyses reveal that there are at least two separate upstream DNA elements in the hPTH gene responsible for the negative regulation. We find that these cultured cells possess nuclear factors which specifically bind to several short DNA sequences within these elements and that these sequences can suppress transcription of the hPTH gene. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP OKAZAKI, T (reprint author), UNIV TOKYO,SCH MED,DEPT INTERNAL MED 4,3-28-6 MEJIRODAI,BUNKYO KU,TOKYO 112,JAPAN. FU NIDDK NIH HHS [DK11794] NR 31 TC 47 Z9 47 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 NOV 15 PY 1991 VL 266 IS 32 BP 21903 EP 21910 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GP804 UT WOS:A1991GP80400087 PM 1939213 ER PT J AU PANCHAMOORTHY, G MCLEAN, J MODLIN, RL MORITA, CT ISHIKAWA, S BRENNER, MB BAND, H AF PANCHAMOORTHY, G MCLEAN, J MODLIN, RL MORITA, CT ISHIKAWA, S BRENNER, MB BAND, H TI A PREDOMINANCE OF THE T-CELL RECEPTOR V-GAMMA-2/V-DELTA-2 SUBSET IN HUMAN MYCOBACTERIA-RESPONSIVE T-CELLS SUGGESTS GERMLINE GENE ENCODED RECOGNITION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CYTO-TOXIC ACTIVITY; HEAT-SHOCK PROTEIN; TCR-GAMMA-DELTA+; ANTIGEN RECEPTOR; LYMPHOCYTES-T; MONOCLONAL-ANTIBODIES; PERIPHERAL-BLOOD; DNA-POLYMERASE; BETA-CHAIN; CLONES AB Little is known about the nature of Ag recognition by the TCR-gamma-delta. The recent observation that gamma-delta-T cells preferentially recognize mycobacterial Ag provides a model to examine the molecular basis of gamma-delta-TCR recognition. Here, examination of the Mycobacteria-stimulated peripheral blood T cells with TCR-specific mAb revealed a predominance of T cells bearing V-gamma-2/V-delta-2 gene products. PCR cloning and sequence analysis of the TCR chains demonstrated extensive junctional diversity indicating that the response was polyclonal. The marked in vitro gamma-delta-T cell response to Mycobacteria was also detected in newborns before encounters with foreign Ag and exclusively involved the same V-gene usage observed in adults. Together, these results suggest that a major mechanism of gamma-delta-T cell reactivity involves recognition mediated by germline-encoded segments of the TCR. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOCHEM LAB,M640,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. UNIV CALIF LOS ANGELES,SCH MED,DIV DERMATOL,LOS ANGELES,CA 90033. UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90033. ST ELIZABETH HOSP,PULM MED UNIT,BRIGHTON,MA 02135. TUFTS UNIV,SCH MED,DEPT MED,BOSTON,MA 02111. RI Morita, Craig/C-1365-2011; OI Modlin, Robert/0000-0003-4720-031X NR 62 TC 125 Z9 125 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 NOV 15 PY 1991 VL 147 IS 10 BP 3360 EP 3369 PG 10 WC Immunology SC Immunology GA GQ171 UT WOS:A1991GQ17100017 PM 1658147 ER PT J AU FLACHSKAMPF, FA OSHEA, JP GRIFFIN, BP GUERRERO, L WEYMAN, AE THOMAS, JD AF FLACHSKAMPF, FA OSHEA, JP GRIFFIN, BP GUERRERO, L WEYMAN, AE THOMAS, JD TI PATTERNS OF NORMAL TRANSVALVULAR REGURGITATION IN MECHANICAL VALVE PROSTHESES SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID DOPPLER ECHOCARDIOGRAPHY; HEART-VALVES; FLOW; INVITRO AB The magnitude and spatial distribution of normal leakage through mechanical prosthetic valves were studied in an in vitro model of mitral regurgitation. The effective regurgitant orifice was calculated from regurgitant rate at different transvalvular pressure differences and flow velocities. This effective orifice area was 0.6 to 2 mm2 for three tilting disc prostheses (Medtronic-Hall sizes 21, 25 and 29) and 0.2 to 1.1 mm2 for three bileaflet valves (St. Jude Medical sizes 21, 25 and 33). In the single disc valves, Doppler color flow examination disclosed a prominent central regurgitant jet around the central hole for the strut, accompanied by minor leakage along the rim of the disc (central to peripheral jet area ratio 3.3 +/- 1.2). The bileaflet prostheses showed a peculiar complex pattern: in planes parallel to the two disc axes, convergent peripherally arising jets were visualized, whereas in orthogonal planes several diverging jets were seen. Mounting the disc and bileaflet valves on a water-filled tube allowed reproduction and interpretation of this pattern: for the bileaflet valve, the jets originated predominantly from valve ring protrusions that contained the axis hinge points and created a converging V pattern in planes parallel to the leaflets and a diverging V pattern in orthogonal planes. Similar patterns were observed during transesophageal echocardiography in 20 patients with a normally functioning St. Jude prosthesis. In 10 patients with a Medtronic-Hall valve, a dominant central jet was observed with one or more smaller peripheral jets. The median central to peripheral jet area ratio was 5 to 1. In summary, in two types of mechanical valve prostheses, effective leakage orifice areas are reported and criteria proposed for the differentiation of "physiologic" and pathologic regurgitation based on the spatial configuration of the jets. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NONINVAS CARDIAC LAB,BOSTON,MA 02114. NR 13 TC 34 Z9 34 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 NOV 15 PY 1991 VL 18 IS 6 BP 1493 EP 1498 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GP894 UT WOS:A1991GP89400011 PM 1939951 ER PT J AU LIN, HY HARRIS, TL FLANNERY, MS ARUFFO, A KAJI, EH GORN, A KOLAKOWSKI, LF LODISH, HF GOLDRING, SR AF LIN, HY HARRIS, TL FLANNERY, MS ARUFFO, A KAJI, EH GORN, A KOLAKOWSKI, LF LODISH, HF GOLDRING, SR TI EXPRESSION CLONING OF AN ADENYLATE-CYCLASE COUPLED CALCITONIN RECEPTOR SO SCIENCE LA English DT Article ID G-PROTEINS AB A calcitonin receptor complementary DNA (cDNA) was cloned by expression of a cDNA library from a porcine kidney epithelial cell line in COS cells. The 482-amino acid receptor has high affinity for salmon calcitonin (dissociation constant K(d) almost-equal-to 6 nM) and is functionally coupled to increases in intracellular cyclic adenosine monophosphate (cAMP). The receptor shows no sequence similarity to other reported G protein-coupled receptors but is homologous to the parathyroid hormone-parathyroid hormone-related peptide (PTH-PTHrP) receptor, indicating that the receptors for these hormones, which regulate calcium homeostasis, represent a new family of G protein-coupled receptors. C1 WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MED SERV,ARTHRIT UNIT,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. FU NHLBI NIH HHS [HL-41484]; NIADDK NIH HHS [AM 03564] NR 19 TC 408 Z9 416 U1 0 U2 4 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD NOV 15 PY 1991 VL 254 IS 5034 BP 1022 EP 1024 DI 10.1126/science.1658940 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GP883 UT WOS:A1991GP88300050 PM 1658940 ER PT J AU JUPPNER, H ABOUSAMRA, AB FREEMAN, M KONG, XF SCHIPANI, E RICHARDS, J KOLAKOWSKI, LF HOCK, J POTTS, JT KRONENBERG, HM SEGRE, GV AF JUPPNER, H ABOUSAMRA, AB FREEMAN, M KONG, XF SCHIPANI, E RICHARDS, J KOLAKOWSKI, LF HOCK, J POTTS, JT KRONENBERG, HM SEGRE, GV TI A G-PROTEIN LINKED RECEPTOR FOR PARATHYROID-HORMONE AND PARATHYROID-HORMONE RELATED PEPTIDE SO SCIENCE LA English DT Article ID CANINE RENAL CORTEX; OSTEO-SARCOMA CELLS; HUMORAL HYPERCALCEMIA; PLASMA-MEMBRANE; OK CELLS; CLONING; STIMULATION; EXPRESSION; MALIGNANCY; SEQUENCE AB The complementary DNA encoding a 585-amino acid parathyroid hormone-parathyroid hormone-related peptide (PTH-PTHrP) receptor with seven potential membrane-spanning domains was cloned by COS-7 expression using an opossum kidney cell complementary DNA (cDNA) library. The expressed receptor binds PTH and PTHrP with equal affinity, and both ligands equivalently stimulate adenylate cyclase. Striking homology with the calcitonin receptor and lack of homology with other G protein-linked receptors indicate that receptors for these calcium-regulating hormones are related and represent a new family. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. VET ADM OUTPATIENT CLIN,BOSTON,MA 02108. TUFTS UNIV,SCH DENT MED,BOSTON,MA 02111. OI Hock, Janet/0000-0001-8873-2545; Abou-Samra, Abdul/0000-0001-8735-1142 FU NIDDK NIH HHS [DK 11794] NR 32 TC 995 Z9 1006 U1 3 U2 18 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD NOV 15 PY 1991 VL 254 IS 5034 BP 1024 EP 1026 DI 10.1126/science.1658941 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GP883 UT WOS:A1991GP88300051 PM 1658941 ER PT J AU MISICKA, A LIPKOWSKI, AW FANG, L KNAPP, RJ DAVIS, P KRAMER, T BURKS, TF YAMAMURA, HI CARR, DB HRUBY, VJ AF MISICKA, A LIPKOWSKI, AW FANG, L KNAPP, RJ DAVIS, P KRAMER, T BURKS, TF YAMAMURA, HI CARR, DB HRUBY, VJ TI TOPOGRAPHICAL REQUIREMENTS FOR DELTA-OPIOID LIGANDS - PRESENCE OF A CARBOXYL GROUP IN POSITION-4 IS NOT CRITICAL FOR DELTORPHIN HIGH DELTA-RECEPTOR AFFINITY AND ANALGESIC ACTIVITY SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID CONFORMATIONAL PROPERTIES; PEPTIDE; SELECTIVITY; ANALOGS C1 UNIV ARIZONA,DEPT CHEM,TUCSON,AZ 85721. UNIV ARIZONA,DEPT PHARMACOL,TUCSON,AZ 85721. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. NR 23 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 14 PY 1991 VL 180 IS 3 BP 1290 EP 1297 DI 10.1016/S0006-291X(05)81335-X PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA GP332 UT WOS:A1991GP33200018 PM 1659410 ER PT J AU NATOWICZ, MR PRENCE, EM CAJOLET, A AF NATOWICZ, MR PRENCE, EM CAJOLET, A TI MARKED VARIATION IN BLOOD BETA-HEXOSAMINIDASE IN GAUCHER DISEASE SO CLINICA CHIMICA ACTA LA English DT Article DE BETA-HEXOSAMINIDASE; GAUCHER DISEASE AB Gaucher disease is due to a primary deficiency of acid beta-glucosidase activity and is associated with secondary elevations of several plasma/serum lysosomal enzyme activities, including beta-hexosaminidase. We analyzed plasma and serum beta-hexosaminidase A & B activities in 55 patients with enzyme-documented Gaucher disease. The mean beta-hexosaminidase activity was increased and the percent of the A isozyme decreased, consistent with earlier studies. Gaucher disease patients had 2,067 +/- 1,491 nmol ml-1 h-1 units of beta-hexosaminidase activity with 51.9 +/- 15.5% beta-hexosaminidase A compared to 1,086 +/- 260 nmol ml-1 h-1 and 67.8 +/- 4.0% beta-hexosaminidase A in normal controls and 965 +/- 261 nmol ml-1 h-1 and 43.6 +/- 5.5% beta-hexosaminidase A in Tay-Sachs disease heterozygotes. Contrary to previous reports, marked heterogeneity of both total plasma/serum enzyme activity and isozyme pattern was noted, as some patients had normal enzyme levels and others had severe reductions in the percent of hexosaminidase A. These data argue against the suggestions of recent studies that routine serum beta-hexosaminidase testing done in Tay-Sachs disease heterozygote detection programs can be effectively used to screen for patients with Gaucher disease. C1 SHRIVER CTR MENTAL RETARDAT,DIV BIOCHEM,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP NATOWICZ, MR (reprint author), SHRIVER CTR MENTAL RETARDAT,DIV MED GENET,200 TRAPELO RD,WALTHAM,MA 02254, USA. NR 9 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0009-8981 J9 CLIN CHIM ACTA JI Clin. Chim. Acta PD NOV 9 PY 1991 VL 203 IS 1 BP 17 EP 22 DI 10.1016/0009-8981(91)90152-3 PG 6 WC Medical Laboratory Technology SC Medical Laboratory Technology GA GU040 UT WOS:A1991GU04000002 PM 1837502 ER PT J AU POLISSON, RF ROSENBERG, AE HEYL, JT SCULLY, RE ALEXANDER, AS SPRINGFIELD, D AF POLISSON, RF ROSENBERG, AE HEYL, JT SCULLY, RE ALEXANDER, AS SPRINGFIELD, D TI AN 84-YEAR-OLD MAN WITH A SLOWLY ENLARGING MASS IN THE LEFT POPLITEAL SPACE - EXTRASKELETAL MYXOID CHONDROSARCOMA OF SYNOVIUM OF KNEE-JOINT SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID ROUGH ENDOPLASMIC-RETICULUM; CHORDOID SARCOMA; TISSUE; ULTRASTRUCTURE; CHROMOSOME-22; TUMORS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP POLISSON, RF (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 36 TC 2 Z9 2 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 7 PY 1991 VL 325 IS 19 BP 1361 EP 1367 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA GN470 UT WOS:A1991GN47000007 ER PT J AU SIDDIQUE, T BROWN, RH AF SIDDIQUE, T BROWN, RH TI GENETIC-BASIS OF FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SIDDIQUE, T (reprint author), NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611, 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 NOV 7 PY 1991 VL 325 IS 19 BP 1383 EP 1383 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA GN470 UT WOS:A1991GN47000020 ER PT J AU TANZI, RE GEORGEHYSLOP, PS GUSELLA, JF AF TANZI, RE GEORGEHYSLOP, PS GUSELLA, JF TI MOLECULAR-GENETICS OF ALZHEIMER-DISEASE AMYLOID SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID BETA-PROTEIN GENE; HEREDITARY CEREBRAL-HEMORRHAGE; PRECURSOR PROTEIN; 1ST-DEGREE RELATIVES; NEXIN-II; LINKAGE; CHROMOSOME-21; RISK; DOMAIN; CDNA RP TANZI, RE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT GENET,MOLEC NEUROGENET LAB,BOSTON,MA 02129, USA. FU NHGRI NIH HHS [HG00317] NR 50 TC 53 Z9 54 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 NOV 5 PY 1991 VL 266 IS 31 BP 20579 EP 20582 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GN001 UT WOS:A1991GN00100001 PM 1939107 ER PT J AU SOSA, MAG DEGASPERI, R KIM, YS FAZELY, F SHARMA, P RUPRECHT, RM AF SOSA, MAG DEGASPERI, R KIM, YS FAZELY, F SHARMA, P RUPRECHT, RM TI SERINE PHOSPHORYLATION-INDEPENDENT DOWN-REGULATION OF CELL-SURFACE CD4 BY NEF SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Letter ID HIV RP SOSA, MAG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. NR 6 TC 17 Z9 17 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD NOV PY 1991 VL 7 IS 11 BP 859 EP 860 DI 10.1089/aid.1991.7.859 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA GR010 UT WOS:A1991GR01000001 ER PT J AU DISLER, D DELUCA, SA AF DISLER, D DELUCA, SA TI NECROTIZING ASPIRATION PNEUMONIA SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Infectious disease is the most common etiology of a cavitary lung process, which can occur with necrotizing pneumonia, lung abscess and septic pulmonary embolism. Other infectious causes of pulmonary cavitation include cavitating fungal or mycobacterial granulomas and superinfection of preexisting spaces. Noninfectious causes of cavitation that should be considered in the differential diagnosis are infarction from thromboembolic disease or vasculitis, necrotic primary or metastatic tumor, rheumatoid nodules and air-filled congenital cysts. The clinical history combined with radiographic features can be helpful in diagnosing the underlying cause of cavitation. RP DISLER, D (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD NOV PY 1991 VL 44 IS 5 BP 1719 EP 1721 PG 3 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA GQ618 UT WOS:A1991GQ61800019 PM 1950968 ER PT J AU FERRY, JA PETTIT, CK ROSENBERG, AE HARRIS, NL AF FERRY, JA PETTIT, CK ROSENBERG, AE HARRIS, NL TI FUNGI IN MEGAKARYOCYTES - AN UNUSUAL MANIFESTATION OF FUNGAL INFECTION OF THE BONE-MARROW SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE FUNGUS; MEGAKARYOCYTES; EMPERIPOLESIS; ACQUIRED IMMUNE DEFICIENCY SYNDROME; CRYPTOCOCCUS; HISTOPLASMA ID ACQUIRED IMMUNODEFICIENCY SYNDROME; EMPERIPOLESIS; MYELODYSPLASIA; LEUKEMIA; AIDS AB When fungi infect the bone marrow, typically they are associated with granuloma formation and/or necrosis, and the fungi are found within histiocytes or admixed with necrotic debris. Recently two bone marrow biopsy specimens were encountered in which fungi were confined to the cytoplasm of megakaryocytes, a finding not previously reported in the literature. The first case was that of a 46-year-old man with pulmonary histoplasmosis and no known immunodeficiency. The second was that of a 38-year-old man with the acquired immune deficiency syndrome and cryptococcal meningitis. In the first case, many megakaryocytes contained fungal forms consistent with Histoplasma. In the second, one small cluster of megakaryocytes contained several budding yeast consistent with Cryptococcus. Neither marrow biopsy specimen had necrosis, granulomas, or histiocytic infiltration. In both cases, because of the unusual localization of the fungi, they were initially overlooked. The bone marrow may contain fungi even in the absence of abnormalities suggesting fungal infection on routinely stained sections. A silver stain or a periodic acid-Schiff stain should be performed on all marrow biopsy specimens in cases of known or suspected fungal infection outside the marrow. The phenomenon of megakaryocyte emperipolesis is well known, and this process may be responsible for the apparent ability of megakaryocytes to internalize fungi. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FERRY, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 28 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD NOV PY 1991 VL 96 IS 5 BP 577 EP 581 PG 5 WC Pathology SC Pathology GA GN547 UT WOS:A1991GN54700005 PM 1719795 ER PT J AU YOUNG, RH ZUKERBERG, LR AF YOUNG, RH ZUKERBERG, LR TI MICROCYSTIC TRANSITIONAL CELL CARCINOMAS OF THE URINARY-BLADDER - A REPORT OF 4 CASES SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE BLADDER CANCER; CYSTS ID ADENOCARCINOMA AB Four transitional cell carcinomas of the urinary bladder that on microscopic examination were found to have cysts are described. The tumors occurred in patients from 35 to 69 years of age and were all deeply invasive; two were grade 2 and two grade 3 (of three grades). Cysts were prominent in all of the cases and predominated in one of them. In the latter case, the cysts caused major problems in interpretation. The cysts, which usually were round to oval and were as large as 1.2 mm, were of varying sizes. They usually were lined by transitional cells or low columnar cells showing mucinous differentiation; occasionally they were lined by a single layer of flattened cells or the lining epithelium was denuded. Elongated, irregular branching spaces also were present. Recognition of these tumors is facilitated by their association with typical transitional cell carcinoma, but when the cysts predominate, awareness of this change may be essential in establishing the diagnosis, particularly in a biopsy specimen. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 8 TC 47 Z9 49 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD NOV PY 1991 VL 96 IS 5 BP 635 EP 639 PG 5 WC Pathology SC Pathology GA GN547 UT WOS:A1991GN54700014 PM 1951186 ER PT J AU YOUNG, GP TAYLOR, AS AF YOUNG, GP TAYLOR, AS TI CONVERSION OF PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA IN A CHILD WITH A SLOW VERAPAMIL INFUSION - CASE-REPORT AND LITERATURE-REVIEW SO AMERICAN JOURNAL OF EMERGENCY MEDICINE LA English DT Article DE PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA; PEDIATRIC CARDIAC ARRHYTHMIAS; VERAPAMIL; ADENOSINE RP YOUNG, GP (reprint author), PORTLAND VET AFFAIRS MED CTR,EMERGENCY MED SERV,POB 1034 11C4,PORTLAND,OR 97207, USA. 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 0735-6757 J9 AM J EMERG MED JI Am. J. Emerg. Med. PD NOV PY 1991 VL 9 IS 6 BP 603 EP 608 DI 10.1016/0735-6757(91)90123-2 PG 6 WC Emergency Medicine SC Emergency Medicine GA GM672 UT WOS:A1991GM67200019 PM 1834070 ER PT J AU HOLLENBERG, AN ARNOLD, A AF HOLLENBERG, AN ARNOLD, A TI HYPERCALCEMIA WITH LOW-NORMAL SERUM INTACT PTH - A NOVEL PRESENTATION OF PRIMARY HYPERPARATHYROIDISM SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID PARATHYROID-HORMONE AB The diagnosis of primary hyperparathyroidism has rested on the finding of hypercalcemia coupled with an elevated serum parathyroid hormone (PTH) level. Over 300 consecutive patients with primary hyperparathyroidism have had elevated or high-normal serum PTH levels using a specific immunoradiometric assay. Here we present a patient who proved to have surgically documented primary hyperparathyroidism in whom PTH levels were completely normal in all assays used. In the immunoradiometric assay, his normal result was unprecedentedly low (17 to 28 pg/mL; normal, 10 to 60 pg/mL) for this condition, and in a range consistent with non-PTH-dependent hypercalcemia or familial hypocalciuric hypercalcemia. This rare biochemical presentation of primary hyperparathyroidism should be considered in the differential diagnosis of hypercalcemia. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. FU NIDDK NIH HHS [DK11794] NR 6 TC 28 Z9 28 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD NOV PY 1991 VL 91 IS 5 BP 547 EP 548 DI 10.1016/0002-9343(91)90193-2 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA GR537 UT WOS:A1991GR53700017 PM 1951417 ER PT J AU SALMAN, SD AF SALMAN, SD TI COMPLICATIONS OF ENDOSCOPIC SINUS SURGERY SO AMERICAN JOURNAL OF OTOLARYNGOLOGY LA English DT Article RP SALMAN, SD (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 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 0196-0709 J9 AM J OTOLARYNG JI Am. J. Otolaryngol. PD NOV-DEC PY 1991 VL 12 IS 6 BP 326 EP 328 DI 10.1016/0196-0709(91)90028-E PG 3 WC Otorhinolaryngology SC Otorhinolaryngology GA HL725 UT WOS:A1991HL72500004 PM 1812775 ER PT J AU ADAMIS, AP MEKLIR, B JOYCE, NC AF ADAMIS, AP MEKLIR, B JOYCE, NC TI INSITU INJURY-INDUCED RELEASE OF BASIC-FIBROBLAST GROWTH-FACTOR FROM CORNEAL EPITHELIAL-CELLS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Note ID SUBENDOTHELIAL EXTRACELLULAR-MATRIX; ANGIOGENIC PROTEIN; ENDOTHELIUM; KERATECTOMY; BINDING; EYE AB Basic-fibroblast growth factor (b-FGF) binds to heparan sulfate proteoglycan in Bowman's layer of the cornea. The mechanism by which the molecule is deposited in Bowman's layer is the subject of controversy since b-FGF lacks a signal peptide sequence for extracellular secretion. Using immunofluorescence, the authors studied the presence and distribution of b-FGF in the bovine cornea and the conditions under which it could be released and bound to Bowman's layer. The results indicate that corneal epithelium contains b-FGF but that uninjured corneas do not contain detectable levels of b-FGF in Bowman's layer. Injury to the corneal epithelium results in the binding of b-FGF to Bowman's layer. Removal of the intact corneal epithelium without cell injury does not result in the binding of b-FGF to Bowman's layer. These findings suggest that one mechanism for the release of b-FGF from corneal epithelial cells is passive leakage after cell injury with secondary binding to Bowman's layer. C1 EYE RES INST,PHARMACOL UNIT,20 STANIFORD ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. FU NEI NIH HHS [R01-EY 05767] NR 14 TC 46 Z9 47 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 NOV PY 1991 VL 139 IS 5 BP 961 EP 967 PG 7 WC Pathology SC Pathology GA GN548 UT WOS:A1991GN54800001 PM 1951634 ER PT J AU CANTIELLO, HF STOW, JL PRAT, AG AUSIELLO, DA AF CANTIELLO, HF STOW, JL PRAT, AG AUSIELLO, DA TI ACTIN-FILAMENTS REGULATE EPITHELIAL NA+ CHANNEL ACTIVITY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ION TRANSPORT; CYTOSKELETON; EPITHELIA ID SKELETAL-MUSCLE; BINDING-PROTEIN; SODIUM-CHANNEL; RAT-KIDNEY; CELL LINE; MEMBRANE; CYTOSKELETON; POLYMERIZATION; ASSOCIATION; MACROPHAGES AB The functional role of the cytoskeleton in the control of ion channel activity is unknown. In the present study, immunocolocalization of Na+ channels with specific antibodies and fluorescein isothiocyanate-phalloidin to stain the cortical cytoskeleton indicates that actin is always present in close proximity to apical Na+ channels in A6 cells. The patch-clamp technique was used to assess the effect of cortical actin networks on apical Na+ channels in these A6 epithelial cells. The actin filament disrupter, cytochalasin D (5-mu-g/ml), induced Na+ channel activity in cell-attached patches within 5 min of addition. Cytochalasin D also induced and/or increased Na+ channel activity in 90% of excised patches tested within 2 min. Addition of short actin filaments (> 5-mu-M) to excised patches also induced channel activity. This effect was enhanced by addition of ATP and/or cytochalasin D. The effect of actin on Na+ channel activity was reversed by addition of the G actin-binding protein DNase I or completely prevented by treatment of the excised patches with this enzyme. Addition of the actin-binding protein, filamin, reversibly inhibited both spontaneous and actin-induced Na+ channels. Thus actin filament networks, achieved by either depolymerizing endogenous actin filaments by treatment with cytochalasin D, the addition of exogenous short actin filaments plus ATP, or actin plus cytochalasin D, regulate apical Na+ channel activity. This conclusion was supported by the observation that the addition of short actin filaments in the form of actin-gelsolin complexes in molar ratios < 8:1 was also effective in activating Na+ channels. We have thus demonstrated a functional role for the cortical actin network in the regulation of epithelial Na+ channels that may complement a structural role for membrane protein targetting and assembly. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP CANTIELLO, HF (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,JACKSON 8,FRUIT ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK-19406] NR 31 TC 185 Z9 191 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 NOV PY 1991 VL 261 IS 5 BP C882 EP C888 PN 1 PG 7 WC Physiology SC Physiology GA GQ780 UT WOS:A1991GQ78000020 PM 1659214 ER PT J AU GOODYEAR, LJ HIRSHMAN, MF SMITH, RJ HORTON, ES AF GOODYEAR, LJ HIRSHMAN, MF SMITH, RJ HORTON, ES TI GLUCOSE TRANSPORTER NUMBER, ACTIVITY, AND ISOFORM CONTENT IN PLASMA-MEMBRANES OF RED AND WHITE SKELETAL-MUSCLE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GLUCOSE TRANSPORT; CYTOCHALASIN-B BINDING; INTRINSIC ACTIVITY; GLUT-1; GLUT-4; INSULIN; EXERCISE ID INSULIN ACTION; EXERCISE; PROTEIN; RATS; METABOLISM; MECHANISM; BINDING AB The fiber type composition of a skeletal muscle is an important determinant of its ability to take up glucose. Although numerous factors may account for this phenomenon, we have hypothesized that fiber type differences in glucose transporter number, isoform content, and/or intrinsic activity play an important role. Skeletal muscle plasma membranes were prepared from red and white gastrocnemius muscle from male Sprague-Dawley rats that were either exercised on a treadmill (1 h, 20 m/min, 10% grade), injected with 20 U insulin, or remained sedentary. In sedentary rats, plasma membrane glucose transporter number (cytochalasin B binding) was 2.4-fold greater in red compared with white muscle. Exercise and insulin both increased glucose transporter number by 40% in red muscle and twofold in white muscle. Maximal velocity of glucose transport (V(max)) was 2-fold greater in red compared with white muscle, whereas exercise and insulin increased V(max) by 2.3-fold in red muscle and 3.6-fold in white muscle. Glucose transporter turnover number, a measure of the average intrinsic activity of transporters in the plasma membrane, was not different between red and white muscle and increased 80-90% with exercise and insulin in both red and white muscle. Both GLUT-1 and GLUT-4 isoform content were greater in red than white muscle. These results suggest that fiber type differences in rates of glucose uptake in resting, insulin-stimulated, and contraction-stimulated skeletal muscle may be due to differences in the number but not the intrinsic activity of glucose transporter proteins. C1 UNIV VERMONT,DEPT MED,METAB UNIT,BURLINGTON,VT 05405. HARVARD UNIV,SCH MED,JOSLIN RES LAB,METAB SECT,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-26317, T32-DK-07523] NR 31 TC 126 Z9 126 U1 0 U2 4 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 NOV PY 1991 VL 261 IS 5 BP E556 EP E561 PN 1 PG 6 WC Physiology SC Physiology GA GQ780 UT WOS:A1991GQ78000029 PM 1951679 ER PT J AU MARATHIAS, KP PREFFER, FI PINTO, C KRADIN, RL AF MARATHIAS, KP PREFFER, FI PINTO, C KRADIN, RL TI MOST HUMAN PULMONARY INFILTRATING LYMPHOCYTES DISPLAY THE SURFACE IMMUNE PHENOTYPE AND FUNCTIONAL-RESPONSES OF SENSITIZED T-CELLS SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID LIMITING-DILUTION ANALYSIS; LEUKOCYTE-COMMON ANTIGEN; HUMAN PERIPHERAL-BLOOD; HUMAN-LUNG; MONOCLONAL-ANTIBODIES; CIGARETTE SMOKERS; HELPER-INDUCER; PROLIFERATIVE RESPONSES; INTERFERON-GAMMA; GENE-EXPRESSION AB Pulmonary infiltrating lymphocytes (PIL) isolated directly from human lung were examined for their surface immune phenotype by monoclonal antibody staining and cytofluorimetry. In order to purify PIL, resected lungs were enzymatically digested with collagenase and DNase and subjected to density centrifugation and nylon-wool column separation. In some cases, CD4+ lymphocytes were further purified with alpha-CD8 and complement. The majority of pulmonary lymphocytes were CD2+ (87 +/- 1%) and CD3+ (73 +/- 4%). Virtually all of the CD3+ PIL were Ti-alpha-beta+. Greater than 90% of both CD4+ or CD8+ PIL were CD45RO+ and CD45RA-, consistent with prior antigen sensitization in vivo. A subset of CD4+ PIL (34 +/- 4%) expressed Leu8, the human congener of the murine MEL-14 lymphocyte homing receptor, whereas most homologous CD4+ peripheral blood lymphocytes were Leu8+ (75 +/- 8; P < 0.01). HLA-DR surface antigens were expressed by 45 +/- 5% of CD4+ PIL versus 9 +/- 1% of CD4+ peripheral blood lymphocytes (P < 0.001). There was no significant difference in the percentage of low-affinity interleukin-2 (IL-2) receptor-positive CD4+ lymphocytes in lung and blood (9 +/- 3% versus 13 +/- 2%). Analysis of the DNA synthetic cell cycle showed that approximately 5% of blood CD4+ lymphocytes and approximately 25% of CD4+ PIL were in S/G2/M. Compared to homologous blood T cells, purified PIL displayed enhanced proliferative responses to IL-2 and diminished responses to the lectin phytohemagglutinin. Lectin-stimulated PIL showed greater secretion of interferon-gamma and IL-2 than did blood lymphocytes. We conclude that T lymphocytes isolated from human lung parenchyma display the surface immune phenotype and functional activities of sensitized T "memory" cells. We hypothesize that compartmentalization of sensitized T cells in the lung parenchyma may provide a mechanism by which circulating immune T cells may be sampled for restimulation by inhaled antigens. C1 MASSACHUSETTS GEN HOSP,PULM IMMUNOL & MOLEC BIOL,COX BLDG,5TH FLOOR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-43827] NR 53 TC 35 Z9 35 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD NOV PY 1991 VL 5 IS 5 BP 470 EP 476 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA GP728 UT WOS:A1991GP72800010 PM 1931075 ER PT J AU KATTAPURAM, SV ROSENTHAL, DI AF KATTAPURAM, SV ROSENTHAL, DI TI PERCUTANEOUS BIOPSY OF SKELETAL LESIONS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID PRIMARY BONE-TUMORS; NEEDLE-BIOPSY; COMPUTED-TOMOGRAPHY; ASPIRATION-BIOPSY; TREPHINE BIOPSY; THORACIC SPINE; CERVICAL-SPINE; HAND DRILL; RADIOLOGISTS AB Percutaneous needle biopsy of lesions affecting the musculoskeletal system should be considered a routine radiologic procedure. Although relatively safe, the procedure requires expertise. An experienced radiologist and the cooperation of a skilled pathologist are essential. Consultation with the orthopedic surgeon is also important, especially when resection of the lesion is contemplated. Recent advances in imaging techniques and the availability of various cutting and trephine needles have made it easier to perform biopsies safely and accurately, even in difficult locations. The procedure obviates surgery in many instances and facilitates appropriate surgical planning in others. This review offers a pragmatic approach to percutaneous needle biopsy of skeletal lesions. It is hoped that more radiologists will be encouraged to undertake these valuable procedures. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,15 PARKMAN ST,ACC-515,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 56 TC 50 Z9 52 U1 0 U2 2 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 NOV PY 1991 VL 157 IS 5 BP 935 EP 942 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GL406 UT WOS:A1991GL40600006 PM 1927811 ER PT J AU PALMER, WE RIVITZ, SM CHEW, FS AF PALMER, WE RIVITZ, SM CHEW, FS TI BILATERAL BRONCHOGENIC CYSTS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 3 TC 5 Z9 5 U1 0 U2 1 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 NOV PY 1991 VL 157 IS 5 BP 950 EP 950 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GL406 UT WOS:A1991GL40600009 PM 1927814 ER PT J AU HANSEN, ME GELLER, SC YUCEL, EK EGGLIN, TK WALTMAN, AC AF HANSEN, ME GELLER, SC YUCEL, EK EGGLIN, TK WALTMAN, AC TI TRANSFEMORAL VENOUS CATHETERIZATION THROUGH INFERIOR VENA-CAVAL FILTERS - RESULTS IN 7 CASES SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID PULMONARY-EMBOLISM; GREENFIELD; PLACEMENT; PROGRESS AB Use of the transfemoral route for venous catheterization has been considered contraindicated in patients with inferior vena caval (IVC) filters. The transjugular route has been used instead in such patients when subsequent diagnostic or therapeutic procedures are required. Many radiologists, however, are more accustomed to the transfemoral approach, and may not find the transjugular route a desirable alternative. We describe seven patients with previously placed IVC filters in whom the transfemoral route was used to perform pulmonary arteriography (five patients) or to place additional IVC filters (two patients). After venographic confirmation of caval patency, filters were catheterized under fluoroscopic control and the procedures were performed. All procedures were technically successful; no complications occurred. We believe the transfemoral route to be a safe and feasible approach for performing venous procedures in selected patients with IVC filters, obviating the less familiar and potentially more hazardous transjugular approach. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,VASC RADIOL SECT,BOSTON,MA 02114. NR 12 TC 5 Z9 5 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 NOV PY 1991 VL 157 IS 5 BP 967 EP 970 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GL406 UT WOS:A1991GL40600014 PM 1927819 ER PT J AU FILLMORE, DJ YUCEL, EK BRIGGS, SE STEINBERG, FL WALTMAN, AC AF FILLMORE, DJ YUCEL, EK BRIGGS, SE STEINBERG, FL WALTMAN, AC TI MR ANGIOGRAPHY OF VASCULAR GRAFTS IN CHILDREN SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note ID FEMORAL-ARTERY; CATHETERIZATION; COMPLICATIONS; INFANTS C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. CEDARS SINAI MED CTR,DEPT RADIOL,LOS ANGELES,CA 90048. NR 8 TC 8 Z9 8 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 NOV PY 1991 VL 157 IS 5 BP 1069 EP 1071 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GL406 UT WOS:A1991GL40600032 PM 1927794 ER PT J AU FERRY, JA MALT, RA YOUNG, RH AF FERRY, JA MALT, RA YOUNG, RH TI RENAL ANGIOMYOLIPOMA WITH SARCOMATOUS TRANSFORMATION AND PULMONARY METASTASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE ANGIOMYOLIPOMA; SARCOMA; KIDNEY; LIVER; FOCAL NODULAR HYPERPLASIA ID LYMPH-NODE INVOLVEMENT AB We report the case of a 49-year-old woman with a large renal angiomyolipoma that invaded the liver. In some areas, the tumor had the appearance of a typical angiomyolipoma; however, it also had foci where the spindle cells of the lesion showed marked cytologic atypia and mitotic activity, giving it the appearance of a high-grade sarcoma. Immunohistochemical studies demonstrated expression of vimentin, desmin, and muscle-specific actin by the sarcoma cells; these findings were consistent with leiomyosarcoma. A second, small typical angiomyolipoma was also present in the kidney. In addition, the liver exhibited focal nodular hyperplasia. Three weeks after resection of the primary renal tumor, pulmonary metastases were diagnosed by fine-needle aspiration biopsy. This is the first report of a case of angiomyolipoma with sarcomatous transformation and biopsy-proven metastatic disease. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP FERRY, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LAB,BOSTON,MA 02114, USA. NR 24 TC 94 Z9 99 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 NOV PY 1991 VL 15 IS 11 BP 1083 EP 1088 DI 10.1097/00000478-199111000-00008 PG 6 WC Pathology; Surgery SC Pathology; Surgery GA GL411 UT WOS:A1991GL41100008 PM 1928559 ER PT J AU SIMON, PM SKATRUD, JB BADR, MS GRIFFIN, DM IBER, C DEMPSEY, JA GARBER, E LANDRY, D AF SIMON, PM SKATRUD, JB BADR, MS GRIFFIN, DM IBER, C DEMPSEY, JA GARBER, E LANDRY, D TI ROLE OF AIRWAY MECHANORECEPTORS IN THE INHIBITION OF INSPIRATION DURING MECHANICAL VENTILATION IN HUMANS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID CHRONIC RESPIRATORY-FAILURE; BREATHING PATTERN; HYPERCAPNIC VENTILATION; MUSCLE-ACTIVITY; LUNG-VOLUME; ANESTHESIA; SLEEP; PRESSURE; AEROSOL; BREATHLESSNESS AB The purpose of this study was to demonstrate a neuromechanical inhibitory effect on respiratory muscle activity during mechanical ventilation and to determine whether upper and lower airway receptors provide this inhibitory feedback. Several protocols were completed during mechanical ventilation: (1) positive and negative pressure changes in the upper airway, (2) airway anesthesia to examine the consequences of receptor blockade on respiratory muscle activity, (3) increasing FRC with positive end-expiratory pressure to study the effect of hyperinflation or stretch on respiratory muscle activity, and (4) use of heart-lung transplant patients to determine the effects of vagal denervation on respiratory muscle activity. All subjects were mechanically hyperventilated with positive pressure until inspiratory muscle activity was undetectable and the end-tidal PCO2 decreased to less than 30 mm Hg. End-tidal PCO2 (PET(CO2)) was increased by either adding CO2 to the inspired gas or decreasing tidal volume (50 ml/min). The PET(CO2) where a change in inspiratory muscle activity occurred was taken as the recruitment threshold (PCO2RT). Neuromechanical feedback caused significant inspiratory muscle inhibition during mechanical ventilation, as evidenced by the difference between PCO2RT and PET(CO2) during spontaneous eupnea (45 +/- 4 versus 39 +/- 4 mm Hg) and a lower PCO2RT when tidal volume was reduced with a constant frequency and fraction of inspired CO2. Recruitment threshold was unchanged during positive and negative pressure ventilation, during upper and lower airway anesthesia, and in vagally denervated lung transplant patients. These findings demonstrate that neuromechanical feedback causes highly significant inhibition of inspiratory muscle activity during mechanical ventilation; upper and lower airway receptors do not appear to mediate this effect. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,MADISON,WI 53705. UNIV WISCONSIN,JOHN RANKIN LAB PULM MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT PREVENT MED,MADISON,WI 53706. HENNEPIN CTY MED CTR,DEPT MED,MINNEAPOLIS,MN 55415. FU NHLBI NIH HHS [P01 HL-42242] NR 37 TC 60 Z9 60 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD NOV PY 1991 VL 144 IS 5 BP 1033 EP 1041 PG 9 WC Respiratory System SC Respiratory System GA GP082 UT WOS:A1991GP08200006 PM 1952428 ER PT J AU VONSATTEL, JPG MYERS, RH HEDLEYWHYTE, ET ROPPER, AH BIRD, ED RICHARDSON, EP AF VONSATTEL, JPG MYERS, RH HEDLEYWHYTE, ET ROPPER, AH BIRD, ED RICHARDSON, EP TI CEREBRAL AMYLOID ANGIOPATHY WITHOUT AND WITH CEREBRAL HEMORRHAGES - A COMPARATIVE HISTOLOGICAL STUDY SO ANNALS OF NEUROLOGY LA English DT Article ID CENTRAL NERVOUS-SYSTEM; HYPERTENSIVE INTRACEREBRAL HEMORRHAGE; GIANT-CELL ARTERITIS; CONGOPHILIC ANGIOPATHY; GRANULOMATOUS-ANGIITIS; ALZHEIMERS DISEASE; BRAIN HEMORRHAGE; VASCULAR CHANGES; AGING BRAIN; COMPLICATIONS AB To identify those factors associated with cerebral hemorrhage among brains with cerebral amyloid angiopathy (CAA), we undertook a comparative postmortem histopathological study of amyloid-containing vessels in the brains of patients with and without hemorrhage. Those without hemorrhage were represented by the following two groups: (1) elderly patients from a large general hospital (n = 66; age range, 75-107 years) and (2) patients with various neuropsychiatric disorders (n = 70; age range, 27-96 years). CAA was found in 45% of the first group and in 54% of the second group. The findings in these patients were compared with those in 17 brains in which both CAA and cerebral hemorrhage were present. We found that CAA was more severe in the brains with cerebral hemorrhage than in those without, and that fibrinoid necrosis was seen only in the brains with cerebral hemorrhage (12 of the 17 brains). Microaneurysms occurred only in the presence of severe, rather than moderate or mild, CAA. Serial sections in 2 brains of patients with cerebral hemorrhage showed fibrinoid necrosis, microaneurysms, and vascular rupture in close association with the hemorrhage. In 2 patients, hemorrhage was precipitated by trauma, and in 1, it was secondary to metastatic carcinoma. The features of brains from patients with CAA that are most consistently related to cerebral hemorrhage are (1) a severe degree of CAA and (2) the presence of fibrinoid necrosis, with or without microaneurysms. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. MCLEAN HOSP,CTR BRAIN TISSUE RESOURCE,BELMONT,MA 02178. HARVARD UNIV,SCH MED,BELMONT,MA 02178. FU NIA NIH HHS [AG 06865, AG P50]; NIMH NIH HHS [MH/NS 31862] NR 82 TC 331 Z9 338 U1 2 U2 8 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD NOV PY 1991 VL 30 IS 5 BP 637 EP 649 DI 10.1002/ana.410300503 PG 13 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA GM890 UT WOS:A1991GM89000002 PM 1763890 ER PT J AU GARCIAMERINO, A AF GARCIAMERINO, A TI CONTINUOUS MUSCLE-FIBER ACTIVITY ASSOCIATED WITH THYMOMA - REPLY SO ANNALS OF NEUROLOGY LA English DT Letter ID ACETYLCHOLINE RP GARCIAMERINO, A (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 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 NOV PY 1991 VL 30 IS 5 BP 736 EP 736 DI 10.1002/ana.410300520 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA GM890 UT WOS:A1991GM89000019 ER PT J AU WILLIAMS, IM STEPHENS, JF RICHARDSON, EP STIRLING, G ROBINSON, P AF WILLIAMS, IM STEPHENS, JF RICHARDSON, EP STIRLING, G ROBINSON, P TI BRAIN AND RETINAL MICROEMBOLI DURING CARDIAC-SURGERY SO ANNALS OF NEUROLOGY LA English DT Letter ID OPEN-HEART-SURGERY C1 CSIRO,DIV COAL & ENERGY TECHNOL,N RYDE,NSW 2113,AUSTRALIA. MASSACHUSETTS GEN HOSP,CHARLES S KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. ALFRED HOSP,DEPT CARDIOTHORAC SURG,MELBOURNE,AUSTRALIA. UNIV MELBOURNE,DEPT ANAT,PARKVILLE,VIC 3052,AUSTRALIA. RP WILLIAMS, IM (reprint author), MONASH UNIV,ALFRED HOSP,DEPT MED,NEUROOPHTHALMOL LAB,MELBOURNE,VIC 3181,AUSTRALIA. NR 8 TC 6 Z9 6 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 NOV PY 1991 VL 30 IS 5 BP 736 EP 737 DI 10.1002/ana.410300521 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA GM890 UT WOS:A1991GM89000020 PM 1763902 ER PT J AU MACDONALD, RS STEELGOODWIN, L SMITH, RJ AF MACDONALD, RS STEELGOODWIN, L SMITH, RJ TI INFLUENCE OF DIETARY FIBER ON INSULIN-RECEPTORS IN RAT INTESTINAL-MUCOSA SO ANNALS OF NUTRITION AND METABOLISM LA English DT Article DE INSULIN RECEPTORS; DIETARY FIBER; INTESTINE; BRAN; TYROSINE KINASE; DIET ID DEPENDENT DIABETES-MELLITUS; EPITHELIAL-CELLS; GLUCOSE-TRANSPORT; BLOOD-GLUCOSE; PROLIFERATION; COLON; METABOLISM; BRAN; IDENTIFICATION; JEJUNUM AB This study was designed to determine the effect of dietary carbohydrate and fiber on mucosal insulin receptors, in order to correlate changes in cellular proliferation with hormonal responsiveness. In two protocols insulin binding was significantly affected by the consumption of dietary fiber. Compared to fiber-free, feeding corn bran increased binding in the duodenum 30% and ileum 50% but decreased binding in the jejunum 44%, and feeding guar gum increased binding in the colon 73% but decreased binding in the jejunum 40%. Feeding wheat bran or oat bran increased binding 50% in the small intestine compared to cellulose or fiber-free. Receptor autophosphorylation was 30% higher with fiber-free or wheat bran feeding than cellulose or oat bran. These changes in receptor binding and activity may correlate with altered rates of cell proliferation induced by dietary fiber. C1 HARVARD UNIV,ELLIOT P JOSLIN RES LABS,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MACDONALD, RS (reprint author), UNIV MISSOURI,DEPT FOOD SCI & NUTR,122 ECKLES HALL,COLUMBIA,MO 65211, USA. NR 36 TC 8 Z9 8 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0250-6807 J9 ANN NUTR METAB JI Ann. Nutr. Metab. PD NOV-DEC PY 1991 VL 35 IS 6 BP 328 EP 338 DI 10.1159/000177665 PG 11 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA GW296 UT WOS:A1991GW29600003 PM 1664197 ER PT J AU NIEMEYER, CM REITER, A RIEHM, H DONNELLY, M GELBER, RD SALLAN, SE AF NIEMEYER, CM REITER, A RIEHM, H DONNELLY, M GELBER, RD SALLAN, SE TI COMPARATIVE RESULTS OF 2 INTENSIVE TREATMENT PROGRAMS FOR CHILDHOOD ACUTE LYMPHOBLASTIC-LEUKEMIA - THE BERLIN-FRANKFURT-MUNSTER AND DANA-FARBER-CANCER-INSTITUTE PROTOCOLS SO ANNALS OF ONCOLOGY LA English DT Article DE ACUTE LEUKEMIA; LYMPHOBLASTIC; CHILDHOOD; TREATMENT; COMPARATIVE ANALYSIS AB We analyzed two of the most successful trials for childhood acute lymphoblastic leukemia, from the Berlin-Frankfurt-Munster group (BFM) and the Dana-Farber Cancer Institute (DFCI), to determine their similarities and differences and suggest ways to improve future treatments. Protocol ALL-BFM 81 (n = 611) was conducted between 1981-1983 in 37 centers in West Germany and Austria; Protocol DFCI 81-01 (n = 286) was conducted between 1981-1985 in seven centers within the United States. The BFM study used a risk score, based on peripheral lymphoblast count, liver size, and spleen size at the time of diagnosis to assign patients into one of the three treatment arms. The DFCI study classified patients into two groups: standard risk patients (age 2-9 years, with white blood count < 20,000/mm3, and with no T-cell markers, mediastinal mass, nor central nervous system disease), and high risk patients (all others). Both studies involved intensive chemotherapy, although treatment strategies, cumulative drug doses and cranial radiation protocols differed. Study populations in the two trials were comparable with respect to age, sex, white blood count and proportion of patients with T-cell markers at the time of diagnosis. Using DFCI risk group criteria, 37% of BFM and 38% of DFCI patients were classified as standard risk. Median follow-up times were 6.8 years and 6.1 years, respectively. Six-year event-free survival percentages (+/- standard error) were nearly identical: BFM 69% (+/- 2%) and DFCI 70% (+/- 3%) overall; BFM 79% (+/- 3%) and DFCI 80% (+/- 5%) for standard risk patients; and BFM 63% (+/- 2%) and DFCI 63% (+/- 4%) for high risk patients. In both studies, outcomes for boys and girls were similar. The BFM study had a higher incidence of testicular relapse (p = 0.004) and CNS relapse (p = 0.004; especially among the 177 non-irradiated patients), than the DFCI study, but a lower incidence of death in remission (p = 0.20). While none of the five infants less than one year old in the DFCI protocol were successfully treated, seven of 10 infants in the BFM trial remained disease-free (p = 0.0004). Because the patterns of relapse differed, we recommend the integration of major components of each program into a single, new protocol in order to improve outcome. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HANOVER MED SCH,KINDERKLIN,W-3000 HANNOVER 61,GERMANY. FU NCI NIH HHS [CA 34183, CA 06516] NR 7 TC 40 Z9 40 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 NOV-DEC PY 1991 VL 2 IS 10 BP 745 EP 749 PG 5 WC Oncology SC Oncology GA GY157 UT WOS:A1991GY15700013 PM 1801880 ER PT J AU DOUGHERTY, MJ COMPTON, C TALBERT, M WOOD, WC AF DOUGHERTY, MJ COMPTON, C TALBERT, M WOOD, WC TI SARCOMAS OF THE GASTROINTESTINAL-TRACT - SEPARATION INTO FAVORABLE AND UNFAVORABLE PROGNOSTIC GROUPS BY MITOTIC COUNT SO ANNALS OF SURGERY LA English DT Article ID SMOOTH-MUSCLE TUMORS; SOFT-TISSUE SARCOMAS; RADIATION-THERAPY; CHEMOTHERAPY; LEIOMYOSARCOMA; STOMACH; BOWEL AB The authors reviewed the Massachusetts General Hospital experience with primary malignant stromal tumors of the gastrointestinal tract since 1962. Fifty-one of fifty-five lesions "ere leiomyosarcomas, and the most common anatomic location was the stomach (47%), followed by small intestine (24%), rectum (11%), colon (7%), duodenum (5%), and esophagus (5%), Most patients presented with gastrointestinal bleeding. There were peaks in age incidence in the fourth and sixth decades. All patients underwent surgery initially, and 40 of 55 had resections with "curative intent." Radiation therapy and chemotherapy were employed to a lesser extent, mainly in a palliative setting. The authors found that using number of mitoses per high-power field as the sole determinant of tumor grade yielded two very distinct clinical populations. Patients curatively resected with low-grade lesions had a better than 80% disease-free survival at 8 years, compared with a mean disease-free interval of only 18 months for high-grade lesions. In resectable disease, tumor grade appears to be the single most important prognostic factor. For gastric lesions there was no apparent advantage in extended resections compared with lesser resections encompassing all gross disease. Because of limited numbers of patients, no benefit could be demonstrated for adjuvant radiotherapy. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,SURG ONCOL UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,DEPT PATHOL,,BOSTON,MA 02114. NR 36 TC 87 Z9 90 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD NOV PY 1991 VL 214 IS 5 BP 569 EP 574 DI 10.1097/00000658-199111000-00006 PG 6 WC Surgery SC Surgery GA GN257 UT WOS:A1991GN25700006 PM 1953109 ER PT J AU TSAO, SW MOK, CH OIKE, K MUTO, M GOODMAN, HM SHEETS, EE BERKOWITZ, RS KNAPP, RC LAU, CC AF TSAO, SW MOK, CH OIKE, K MUTO, M GOODMAN, HM SHEETS, EE BERKOWITZ, RS KNAPP, RC LAU, CC TI INVOLVEMENT OF P53 GENE IN THE ALLELIC DELETION OF CHROMOSOME 17P IN HUMAN OVARIAN-TUMORS SO ANTICANCER RESEARCH LA English DT Article DE ALLELIC LOSS; 17P; P53; OVARIAN TUMORS ID BREAST-CANCER; PROTO-ONCOGENE; CARCINOMAS; MUTATIONS; ACTIVATION; HETEROZYGOSITY; OCCUR AB Previous reports have shown that one copy of the chromosome 17 was frequently lost in human ovarian cancers (1). The position of the allelic deletion has not been mapped and involvement of p53 gene has not been determined. In this study, we have shown that in human ovarian carcinoma, the commonest region of allelic loss in chromosome 17p is 17p 13.3 (65%) and 17p13.1 (63.7%) and p53 gene was usually involved in the deletion (66.7%; 6 out of 9 informative cases). Allelic loss was also observed at region 17p12 - 11.1 but at a lower frequency (38.6% to 37.5%). The pattern of allelic loss of p53 gene was consistent in both primary and secondary metastatic tumors of the same patient. No gross rearrangement of p53 was however observed at the remaining allele using Southern blot analysis. Allelic loss of p53 gene was closely associated with 17p 13.3, the terminal portion of chromosome 17p. The high frequency of allelic loss of p53 gene in ovarian carcinomas conformed with recent findings in cancers of colon, breast, lung and brain suggesting inactivation of p53 gene play a rate limiting step in pathogenesis of human malignancies. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP TSAO, SW (reprint author), BRIGHAM & WOMENS HOSP,DEPT OBSTET & GYNECOL,DIV GYNECOL ONCOL,SEELEY MUDD BLDG,RM 210,BOSTON,MA 02115, USA. NR 28 TC 49 Z9 50 U1 0 U2 0 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDNTIOU-KALAMOU RD KAPANDRITI, POB 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD NOV-DEC PY 1991 VL 11 IS 6 BP 1975 EP 1982 PG 8 WC Oncology SC Oncology GA HB244 UT WOS:A1991HB24400005 PM 1776830 ER PT J AU GRAYSON, ML ELIOPOULOS, GM WENNERSTEN, CB RUOFF, KL DEGIROLAMI, PC FERRARO, MJ MOELLERING, RC AF GRAYSON, ML ELIOPOULOS, GM WENNERSTEN, CB RUOFF, KL DEGIROLAMI, PC FERRARO, MJ MOELLERING, RC TI INCREASING RESISTANCE TO BETA-LACTAM ANTIBIOTICS AMONG CLINICAL ISOLATES OF ENTEROCOCCUS-FAECIUM - A 22-YEAR REVIEW AT ONE INSTITUTION SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID PENICILLIN-BINDING PROTEINS; IDENTIFICATION; AMPICILLIN; SUSCEPTIBILITY; INFECTIONS AB To identify any change in the antibiotic resistance of Enterococcus faecium, we examined the antibiotic susceptibilities of clinical strains (n = 84) isolated at one institution during the 22 years since 1968. A significant increase in resistance to penicillin was observed during the study period: the MICs of penicillin for 50 and 90% of isolates tested were 16 and 64-mu-g/ml, respectively, from 1969 to 1988 (n = 48; geometric mean MIC, 14-mu-g/ml), whereas they were 256 and 512-mu-g/ml, respectively, from 1989 to 1990 (n = 36; geometric mean MIC, 123-mu-g/ml) (P < 0.001). A comparable increase in resistance to ampicillin was also noted (P < 0.001). No strains produced detectable beta-lactamase. In contrast, susceptibilities to vancomycin, teicoplanin, and ciprofloxacin remained stable. High-level resistance to gentamicin was observed in none of 48 isolates from 1969 to 1988, but was present in 22 of 36 strains (61%) from 1989 to 1990 (P < 0.001) and was significantly associated with resistance (MIC, greater-than-or-equal-to 128-mu-g/ml) to penicillin (P < 0.001). To assess the potential evolution of antibiotic resistance in this species, clinical isolates (n = 24) were compared with strains isolated in 1968 from a human population in the Solomon Islands that was never exposed to antibiotics. Solomon Island isolates were significantly more susceptible than all clinical strains to penicillin, ampicillin, and vancomycin (P < 0.001 for each), but they exhibited no differences in susceptibility to teicoplanin or ciprofloxacin. The penicillin-binding affinity of penicillin-binding protein 5 (PBP 5) in penicillin-resistant clinical strains (MIC, 512-mu-g/ml) was notably lower than that in strains with more typical susceptibilities, suggesting an alteration in this PBP as a possible mechanism for increased penicillin resistance. Solomon Island strains most susceptible to penicillin demonstrated a prominent PBP 5* and the absence of PBP 5. These changes in the antibiotic resistance of E. faecium emphasize the importance of identifying this species in patients with serious enterococcal infections and the necessity of assessing its susceptibility to both beta-lactams and aminoglycosides if effective therapy is to be identified. C1 NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. NEW ENGLAND DEACONESS HOSP,MICROBIOL LAB,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 15 TC 141 Z9 143 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD NOV PY 1991 VL 35 IS 11 BP 2180 EP 2184 PG 5 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA GM872 UT WOS:A1991GM87200003 PM 1803989 ER PT J AU HUOVINEN, P JACOBY, GA AF HUOVINEN, P JACOBY, GA TI SEQUENCE OF THE PSE-1 BETA-LACTAMASE GENE SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; CRYSTAL-STRUCTURE; PSEUDOMONAS; TRANSPOSONS; RESISTANCE; ENZYMES; FAMILY; PC1 AB The nucleotide sequence of the PSE-1 beta-lactamase gene from Tn1403 indicates that it is contained in an integron and encodes a class A enzyme differing from PSE-4 and CARB-3 by single amino acid substitutions. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NATL PUBL HLTH INST,ANTIMICROBIAL RES UNIT,SF-20520 TURKU,FINLAND. RI Huovinen, Pentti/C-1917-2009 FU NIAID NIH HHS [AI20415] NR 22 TC 34 Z9 36 U1 2 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD NOV PY 1991 VL 35 IS 11 BP 2428 EP 2430 PG 3 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA GM872 UT WOS:A1991GM87200045 PM 1804019 ER PT J AU OFFENSPERGER, WB OFFENSPERGER, S WALTER, E BLUM, HE GEROK, W AF OFFENSPERGER, WB OFFENSPERGER, S WALTER, E BLUM, HE GEROK, W TI SULFATED POLYANIONS DO NOT INHIBIT DUCK HEPATITIS-B VIRUS-INFECTION SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID HUMAN-IMMUNODEFICIENCY-VIRUS; DEXTRAN SULFATE; ANTIVIRAL STRATEGIES; INVITRO; REPLICATION; HEPARIN; HIV; POLYSACCHARIDES; MOLECULES; BINDING AB On the basis of the antiviral action of sulfated polyanions in human immunodeficiency virus and other viral infections, we studied the effect of dextran sulfate and heparin on duck hepatitis B virus infection. These agents do not affect viral uptake and replication in liver cells in vitro or in vivo. Sulfated polyanions, therefore, appear to have no potential for the treatment of hepadnavirus infections. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,GASTROINTESTINAL UNIT,BOSTON,MA 02129. RP OFFENSPERGER, WB (reprint author), UNIV FREIBURG,DEPT MED,W-7800 FREIBURG,GERMANY. NR 27 TC 13 Z9 13 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD NOV PY 1991 VL 35 IS 11 BP 2431 EP 2433 PG 3 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA GM872 UT WOS:A1991GM87200046 PM 1804020 ER PT J AU SALEM, M KASINSKI, N ANDREI, AM BRUSSEL, T GOLD, MR CONN, A CHERNOW, B AF SALEM, M KASINSKI, N ANDREI, AM BRUSSEL, T GOLD, MR CONN, A CHERNOW, B TI HYPOMAGNESEMIA IS A FREQUENT FINDING IN THE EMERGENCY DEPARTMENT IN PATIENTS WITH CHEST PAIN SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; SERUM MAGNESIUM; ARRHYTHMIAS; CALCIUM; HEART; HYPERMAGNESEMIA; HYPOKALEMIA; DEPLETION AB Study Objective. - To evaluate the frequency of low blood levels of total and ultrafilterable magnesium (total and ultrafilterable hypomagnesemia) in patients with chest pain in the emergency department, and to determine if hypomagnesemia is associated with other clinically important diagnostic and outcome variables in cardiac care. Setting. - An emergency department of a university teaching hospital. Design. - Prospective study of extracellular magnesium homeostasis in patients with chest pain in the emergency department and a cohort of patients without chest pain with a clinical indication for blood sampling. Patients. - During a 4-month period, 147 patients presenting to the emergency department were studied: 67 patients (mean +/- SD age, 61.4 +/- 13 years) with a chief complaint of chest pain (study group) and 80 patients (55.6 +/- 19 years) with other diagnoses (control group). Results. - Total and ultrafilterable hypomagnesemia occurred more frequently in patients with chest pain (20/67 [30%] and 9/67 [13%]) than in the control group (12/80 [15%] and 3/80 [4%]). Patients with a chief complaint of chest pain who were receiving diuretic medications were hypomagnesemic more frequently (9/16 [56%]) than patients not receiving diuretics (12/51 [23%]). In patients with chest pain admitted to the hospital with a diagnosis of "rule out" myocardial infarction, the frequency of hypokalemia was greater among hypomagnesemic patients (6/14 [43%]) than normomagnesemic patients (3/31 [10%]). A similar frequency of hypomagnesemia was noted in patients with a final diagnosis of myocardial infarction (4/15 [27%]) when compared with other patients admitted with chest pain (10/31 [32%]) in whom myocardial infarction was excluded. No association was noted among hypomagnesemia and length of hospital stay or the occurrence of hypotension or dysrhythmias. Conclusions. - Total and ultrafilterable hypomagnesemia are frequent occurrences in patients with and without chest pain in the emergency department. Diuretic use is associated with hypomagnesemia in patients presenting with chest pain in the emergency department. These results support the concept that hypomagnesemia is common in patients with chest pain in the emergency department and is associated with hypokalemia but is not predictive of whether the patient with chest pain has had an acute myocardial infarction. C1 SINAI HOSP,DEPT MED,BELVEDERE AVE GREENSPRING,BALTIMORE,MD 21215. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT ANESTHESIOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT CRIT CARE MED,BALTIMORE,MD 21205. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT EMERGENCY SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIOL CRIT CARE,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA 02114. NR 35 TC 24 Z9 24 U1 1 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV PY 1991 VL 151 IS 11 BP 2185 EP 2190 DI 10.1001/archinte.151.11.2185 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA GP585 UT WOS:A1991GP58500010 PM 1953221 ER PT J AU ROPPER, AH COLE, D LOUIS, DN AF ROPPER, AH COLE, D LOUIS, DN TI CLINICOPATHOLOGICAL CORRELATION IN A CASE OF PUPILLARY DILATION FROM CEREBRAL-HEMORRHAGE SO ARCHIVES OF NEUROLOGY LA English DT Article ID HERNIATION AB A patient who developed pupillary dilation on the side of a large cerebral hemorrhage underwent serial examinations, computed tomography, and magnetic resonance imaging. Autopsy dissection was performed to allow in situ examination of the structures near the third nerves and tentorial edge. The origin of the oculomotor nerve was displaced medially, causing the distal nerve to "kink" over the clivus just posterior to the clinoid. Transtentorial herniation of the medial temporal lobe did not appear to play a role in third-nerve compression. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. RP ROPPER, AH (reprint author), TUFTS UNIV,ST ELIZABETHS HOSP,SCH MED,DIV NEUROL,736 CAMBRIDGE ST,BOSTON,MA 02135, USA. NR 14 TC 13 Z9 13 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD NOV PY 1991 VL 48 IS 11 BP 1166 EP 1169 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA GP074 UT WOS:A1991GP07400015 PM 1953403 ER PT J AU SCHMAHMANN, JD AF SCHMAHMANN, JD TI AN EMERGING CONCEPT - THE CEREBELLAR CONTRIBUTION TO HIGHER FUNCTION SO ARCHIVES OF NEUROLOGY LA English DT Review ID SUPERIOR TEMPORAL SULCUS; NICTITATING-MEMBRANE RESPONSE; INFERIOR PARIETAL LOBULE; FRONTAL EYE FIELD; RHESUS-MONKEY; CORTICOPONTINE PROJECTION; HORSERADISH-PEROXIDASE; ASSOCIATION CORTEX; CINGULATE CORTEX; PONTINE NUCLEI AB Recent clinical and research reports suggest that the cerebellum may contribute to the modulation of higher order behavior. This article presents a critical review of both earlier and more current clinical observations that raise this possibility, as well as a review of the salient laboratory data that appear to support this contention. It also summarizes the relevant anatomic work concerning the contributions to the corticopontocerebellar pathways from the higher order cerebral association areas, which have been implicated as partial anatomic substrates for this putative cerebellar role in higher function. Finally, it provides a framework for the understanding of this correlation, concludes with suggestions for future areas of investigation, and recommends that patients with cerebellar lesions be studied from a neurobehavioral point of view. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SCHMAHMANN, JD (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,FRUIT ST,BOSTON,MA 02114, USA. NR 263 TC 563 Z9 566 U1 3 U2 23 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD NOV PY 1991 VL 48 IS 11 BP 1178 EP 1187 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA GP074 UT WOS:A1991GP07400018 PM 1953406 ER PT J AU SCHUMAN, JS NOECKER, RJ PULIAFITO, CA JACOBSON, JJ SHEPPS, GJ NAN, W AF SCHUMAN, JS NOECKER, RJ PULIAFITO, CA JACOBSON, JJ SHEPPS, GJ NAN, W TI ENERGY-LEVELS AND PROBE PLACEMENT IN CONTACT TRANSSCLERAL SEMICONDUCTOR DIODE-LASER CYCLOPHOTOCOAGULATION IN HUMAN CADAVER EYES SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID NEODYMIUM-YAG CYCLOPHOTOCOAGULATION; PHOTOCOAGULATION; RETINA AB We investigated the effects of semiconductor diode laser contact transscleral cyclophotocoagulation in human cadaver eyes by gross examination, light microscopy, and scanning electron microscopy to determine optimum clinical treatment parameters. Irradiation was performed using a continuous-wave semiconductor diode laser with a fiberoptic probe. At 1.0 to 1.25 mm posterior to the limbus, spots were centered on the pars plicata by gross examination. Exposures of less than 2 J produced no visible damage. A 2- to 3-J exposure produced mild whitening of the ciliary processes, while 4- to 5-J exposures created more intense whitening of the pars plicata. Energies higher than 5 J frequently produced explosive tissue damage. Light microscopy of tissue treated with 1.8 to 6 J at 1.0 to 1.25 mm posterior to the limbus revealed coagulation necrosis of the nonpigmented and pigmented epithelium, with evidence of thermal coagulation of the ciliary stroma and stromal vasculature. Coagulation necrosis was more intense with longer exposure times. We found the optimum parameters for contact transscleral diode laser cyclophotocoagulation in cadaver eyes to be 3 to 4.5 J of energy delivered with the anterior edge of the probe 1.0 to 1.25 mm posterior to the limbus. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,HOWE LAB OPHTHALMOL,MORSE LASER CTR,BOSTON,MA 02114. RP SCHUMAN, JS (reprint author), TUFTS UNIV,SCH MED,NEW ENGLAND MED CTR HOSP,NEW ENGLAND EYE CTR,750 WASHINGTON ST,BOSTON,MA 02111, USA. RI Schuman, Joel/K-7304-2012 OI Schuman, Joel/0000-0002-8885-3766 FU NEI NIH HHS [5 T32 EY07097-02] NR 17 TC 42 Z9 43 U1 1 U2 1 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 NOV PY 1991 VL 109 IS 11 BP 1534 EP 1538 PG 5 WC Ophthalmology SC Ophthalmology GA GP106 UT WOS:A1991GP10600032 PM 1755733 ER PT J AU WEISS, J ADAMS, E WHITCOMB, RW CROWLEY, WF JAMESON, JL AF WEISS, J ADAMS, E WHITCOMB, RW CROWLEY, WF JAMESON, JL TI NORMAL SEQUENCE OF THE GONADOTROPIN-RELEASING-HORMONE GENE IN PATIENTS WITH IDIOPATHIC HYPOGONADOTROPIC HYPOGONADISM SO BIOLOGY OF REPRODUCTION LA English DT Article ID KALLMANN SYNDROME; DNA; DEFICIENCY; FAMILIES; DELETION; ANOSMIA AB Idiopathic hypogonadotropic hypogonadism (IHH) results from absent or greatly diminished secretion of GnRH. Defects in the GnRH gene have been identified in an animal model of IHH and have been hypothesized as a possible basis for GnRH deficiency in humans. In this study, we used the polymerase chain reaction to clone and sequence the coding regions, promoter, and 3' untranslated tract of the GnRH genes from both alleles of four unrelated patients with IHH. One of the patients studied is a member of a kindred in which X-linked inheritance has been excluded by father-to-son transmission of the disease. No DNA sequence mutations were found. We conclude that most cases of IHH in humans do not involve mutations in the GnRH gene and are presumably caused by mutations at one or more other genetic loci that are required for normal function of GnRH-producing neurons. C1 MASSACHUSETTS GEN HOSP,DEPT MED,THYROID UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WEISS, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,REPROD ENDOCRINE UNIT,BHX-5,BOSTON,MA 02114, USA. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [P30 HD028138, HD-23519, HD-15788, R01 HD015788, U54 HD029164] NR 17 TC 46 Z9 47 U1 0 U2 1 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD NOV PY 1991 VL 45 IS 5 BP 743 EP 747 DI 10.1095/biolreprod45.5.743 PG 5 WC Reproductive Biology SC Reproductive Biology GA GM582 UT WOS:A1991GM58200013 PM 1756212 ER PT J AU FRIDOVICHKEIL, JL GUDAS, JM BRYAN, IB PARDEE, AB AF FRIDOVICHKEIL, JL GUDAS, JM BRYAN, IB PARDEE, AB TI IMPROVED EXPRESSION VECTORS FOR EUKARYOTIC PROMOTER ENHANCER STUDIES SO BIOTECHNIQUES LA English DT Note ID MAMMALIAN-CELLS; GENE; TRANSCRIPTION; SEQUENCE; PLASMID; RNA AB We describe two transfectable vectors designed to facilitate the functional analysis of eukaryotic promoter/enhancer sequences. The first, pJFCAT1, is an improved chloramphenicol acetyltransferase (CAT) reporter gene expression vector with two features that distinguish it from the majority of other CAT vectors currently in use: 1) it carries a trimer cassette of the simian virus 40 major late polyadenylation site to block plasmid-initiated read-through expression of CAT, and 2) it includes the phage f1 origin of replication, permitting generation of single-stranded copies to serve as templates for oligonucleotide-directed mutagenesis or single-strand DNA sequencing. The promoterless pJFCAT1 directs little if any CAT activity in transfected mouse L cells and, therefore, may be particularly useful for the analysis of weak promoters whose activity is otherwise masked by background CAT expression. The second vector, pTAG-1, uses human-beta-globin as a reporter gene and was designed to facilitate the analysis of reporter gene expression at the RNA level. Like pJFCAT1, pTAG-1 also includes the simian virus 40 polyadenylation site trimer cassette located just upstream of the promoter insertion site. We have used each of these vectors to study functional elements in the human and mouse thymidine kinase promoters. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115. FU NCI NIH HHS [CA22427, T32CA09361, CA08317-03] NR 20 TC 51 Z9 51 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD NOV PY 1991 VL 11 IS 5 BP 572 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GN890 UT WOS:A1991GN89000001 PM 1725108 ER PT J AU HUBEL, A TONER, M CRAVALHO, EG YARMUSH, ML TOMPKINS, RG AF HUBEL, A TONER, M CRAVALHO, EG YARMUSH, ML TOMPKINS, RG TI INTRACELLULAR ICE FORMATION DURING THE FREEZING OF HEPATOCYTES CULTURED IN A DOUBLE COLLAGEN GEL SO BIOTECHNOLOGY PROGRESS LA English DT Article ID ISOLATED RAT HEPATOCYTES; CRYOPRESERVATION; RECOVERY; DIMETHYLSULFOXIDE; CRYOMICROSCOPY; CONFIGURATION; ERYTHROCYTES; MEMBRANE; INJURY; OVA AB During freezing, intracellular ice formation (IIF) has been correlated with loss in viability for a wide variety of biological systems. Hence, determination of IIF characteristics is essential in the development of an efficient methodology for cryopreservation. In this study, IIF characteristics of hepatocytes cultured in a collagen matrix were determined using cryomicroscopy. Four factors influenced the IIF behavior of the hepatocytes in the matrix: cooling rate, final cooling temperature, concentration of Me2SO, and time in culture prior to freezing. The maximum cumulative fraction of cells with IIF increased with increasing cooling rate. For cultured cells frozen in Dulbecco's modified Eagle's medium (DMEM), the cooling rate for which 50% of the cells formed ice (B50) was 70-degrees-C/min for cells frozen after 1 day in culture and decreased to 15-degrees-C/min for cells frozen after 7 days in culture. When cells were frozen in a 0.5 M Me2SO + DMEM solution, the value of B50 decreased from 70 to 50-degrees-C/min for cells in culture for 1 day and from 15 to 10-degrees-C/min for cells in culture for 7 days. The value of the average temperature for IIF (T(IIF)) for cultured cells was only slightly depressed by the addition of Me2SO when compared to the IIF behavior of other cell types. The results of this study indicate that the presence of the collagen matrix alters significantly the IIF characteristics of hepatocytes. Thus freezing studies using hepatocytes in suspension are not useful in predicting the freezing behavior of hepatocytes cultured in a collagen matrix. Furthermore, the weak effect of Me2SO on IIF characteristics implies that lower concentrations of Me2SO (O.5 M) may be just as effective in preserving viability. Finally, the value of B50 measured in this study indicates that cooling rates nearly an order of magnitude faster than those previously investigated could be used for cryopreservation of the hepatocytes in a collagen gel. C1 MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08855. RP YARMUSH, ML (reprint author), MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139, USA. NR 28 TC 39 Z9 39 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 8756-7938 J9 BIOTECHNOL PROGR JI Biotechnol. Prog. PD NOV-DEC PY 1991 VL 7 IS 6 BP 554 EP 559 DI 10.1021/bp00012a011 PG 6 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA GU896 UT WOS:A1991GU89600011 PM 1367755 ER PT J AU MCCLOSKEY, M ALIMINOSA, D SOKOL, SM AF MCCLOSKEY, M ALIMINOSA, D SOKOL, SM TI FACTS, RULES, AND PROCEDURES IN NORMAL CALCULATION - EVIDENCE FROM MULTIPLE SINGLE-PATIENT STUDIES OF IMPAIRED ARITHMETIC FACT RETRIEVAL SO BRAIN AND COGNITION LA English DT Article ID MENTAL MULTIPLICATION SKILL; TEMPORAL ASPECTS; ACQUISITION; KNOWLEDGE C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MCCLOSKEY, M (reprint author), JOHNS HOPKINS UNIV,DEPT COGNIT SCI,BALTIMORE,MD 21218, USA. FU NINDS NIH HHS [NS21047] NR 42 TC 116 Z9 120 U1 1 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0278-2626 J9 BRAIN COGNITION JI Brain Cogn. PD NOV PY 1991 VL 17 IS 2 BP 154 EP 203 DI 10.1016/0278-2626(91)90074-I PG 50 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA GZ987 UT WOS:A1991GZ98700005 PM 1799451 ER PT J AU ROUSH, GC BARNHILL, RL AF ROUSH, GC BARNHILL, RL TI CORRELATION OF CLINICAL PIGMENTARY CHARACTERISTICS WITH HISTOPATHOLOGICALLY-CONFIRMED DYSPLASTIC NEVI IN NONFAMILIAL MELANOMA PATIENTS - STUDIES OF MELANOCYTIC NEVI-IX SO BRITISH JOURNAL OF CANCER LA English DT Article ID CUTANEOUS MALIGNANT-MELANOMA; SUN EXPOSURE; RISK-FACTOR; NEVOCYTIC NEVI; LESIONS; ORIGIN; NAEVI AB The dysplastic melanocytic nevus (DMN) is the key clinical marker for the familial dysplastic nevus syndrome and has also been associated with high risk for non-familial melanoma. Characterisations of DMN itself have been qualitative and on a case-by-case basis. In this study, we provided clinical and histological characterisations for each of 150 pigmented lesions from 150 patients with prior malignant melanoma. The steps involved in the study were as follows: (1) The two to four clinicians characterised pigmented lesions on each of 150 patients, and the lesion closest in characteristics to an atypical nevus was quantitatively described based on size, border characteristics and colour characteristics; (2) The lesion was then removed and independently quantified by a single dermatopathologist without knowledge of the clinical features; (3) We computed the correlation between each of the clinical variables and each of the histologic features for each of the 150 patients. Histologic diagnosis of dysplastic nevus was strongly associated with total number of palpable arm nevi, total number of any arm nevi, total number of nevi on the body of any type, and total number of clinically atypical nevi on the body (correlation coefficients 23.2% to 30.4% with P < 0.01 in each instance). There were also strong correlations between the counts of numbers of nevi and certain types of architectural histologic features, including fusion (bridging of junctional nests), lymphocyte response and fibroplasia of the papillary dermis. Histologic evaluation of solar elastosis was negatively correlated with total numbers of nevi and total number of clinically atypical nevi (P < 0.01). Freckling on forearm and on shoulders showed no significant positive or negative correlations with any of the histologic features nor with overall diagnosis of dysplastic nevus. We conclude that observations regarding total numbers of nevi (either normal or clinically atypical nevi) are correlated with nuclear and architectural histologic dysplasia on biopsy of the most atypical pigmented lesions. C1 MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,WARREN 827,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DERMATOL SERV,BOSTON,MA 02114. CANC PREVENT RES INST,NEW YORK,NY. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 25 TC 8 Z9 8 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD NOV PY 1991 VL 64 IS 5 BP 943 EP 947 DI 10.1038/bjc.1991.431 PG 5 WC Oncology SC Oncology GA GN192 UT WOS:A1991GN19200028 PM 1931621 ER PT J AU MCCORMICK, S GOFF, DC AF MCCORMICK, S GOFF, DC TI APPARENT DECREASE IN SCHIZOPHRENIA SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Letter RP MCCORMICK, S (reprint author), MASSACHUSETTS GEN HOSP,ERICH LINDEMANN MENTAL HLTH CTR,BOSTON,MA 02114, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD NOV PY 1991 VL 159 BP 725 EP 725 PG 1 WC Psychiatry SC Psychiatry GA GQ106 UT WOS:A1991GQ10600027 PM 1756356 ER PT J AU HODGSON, J AF HODGSON, J TI MECHANISMS OF VISUAL WORD RECOGNITION IN FLUENT DYSLEXIC READERS SO BULLETIN OF THE PSYCHONOMIC SOCIETY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PSYCHONOMIC SOC INC PI AUSTIN PA 1710 FORTVIEW RD, AUSTIN, TX 78704 SN 0090-5054 J9 B PSYCHONOMIC SOC PD NOV PY 1991 VL 29 IS 6 BP 492 EP 492 PG 1 WC Psychology, Mathematical SC Psychology GA GL115 UT WOS:A1991GL11500224 ER PT J AU ZIETMAN, AL LINGGOOD, RM BROOKES, AR CONVERY, K PIRO, A AF ZIETMAN, AL LINGGOOD, RM BROOKES, AR CONVERY, K PIRO, A TI RADIATION-THERAPY IN THE MANAGEMENT OF EARLY STAGE HODGKINS-DISEASE PRESENTING IN LATER LIFE SO CANCER LA English DT Article ID PROGNOSTIC FACTORS; AGE AB This study examined the contention that although elderly patients with Hodgkin's disease have a worse prognosis overall than younger patients, a subgroup of older patients fit enough to be managed like younger patients can fare just as well. A retrospective analysis was made on 29 patients older than 60 years of age with Stage I and II Hodgkin's disease treated by radiation therapy alone. Fourteen of these patients were managed optimally, i.e., were adequately staged (defined by one or more of the following: laparotomy, computed tomography [CT] scan, and/or lymphangiogram), followed by radical radiation therapy (mantle or inverted-Y). The remaining 15 patients, because of their general medical condition, were managed suboptimally with limited staging and/or involved-field irradiation. None of the 14 patients managed optimally relapsed over a median of 4.75 years of follow-up compared with 10 of 15 patients in the suboptimal group. For the optimally managed versus suboptimally managed groups, the actuarial 5-year disease-free survival rates were 61% and 6%, respectively; the actuarial overall survival rates (death from all causes) were 61% and 19%, respectively; and the disease-specific survival rates were 100% and 39%, respectively. Only three of the patients irradiated radically had acute complications severe enough to warrant a break in treatment. In the opinion of the authors, those elderly patients able to tolerate adequate staging and radical radiation therapy can anticipate a high likelihood of cure. C1 SALEM HOSP,DEPT RADIAT MED,SALEM,MA. RP ZIETMAN, AL (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114, USA. NR 12 TC 14 Z9 14 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD NOV 1 PY 1991 VL 68 IS 9 BP 1869 EP 1873 DI 10.1002/1097-0142(19911101)68:9<1869::AID-CNCR2820680903>3.0.CO;2-H PG 5 WC Oncology SC Oncology GA GK168 UT WOS:A1991GK16800002 PM 1913538 ER PT J AU MUNTZ, HG FERRY, JA FLYNN, D FULLER, AF TARRAZA, HM AF MUNTZ, HG FERRY, JA FLYNN, D FULLER, AF TARRAZA, HM TI STAGE IE PRIMARY MALIGNANT-LYMPHOMAS OF THE UTERINE CERVIX SO CANCER LA English DT Article ID NATIONAL-CANCER-INSTITUTE; NON-HODGKINS LYMPHOMAS; LARGE-CELL LYMPHOMA; RADIATION-THERAPY; COMBINATION CHEMOTHERAPY; HISTIOCYTIC LYMPHOMA; SURVIVAL; HISTOLOGY; SARCOMA; VAGINA AB The experience of the authors with primary non-Hodgkin's lymphoma of the uterine cervix from 1980 to 1986 included five Ann Arbor Stage IE cases successfully managed by meticulous staging and radiation therapy. The clincopathologic features of the patients are described and compared with 38 previously reported Stage IE cases. When all 43 patients were evaluated, the median age was 40 years of age (range, 20 to 80 years of age) and 77% were premenopausal. Most patients (74%) reported abnormal vaginal bleeding, although approximately 20% were asymptomatic. The primary cervical tumors were typically of large size, with half exceeding 4 cm in diameter. Using the International Federation of Gynecology and Obstetrics (FIGO) system for staging cervical cancer, stage distribution was 44% Stage I, 42% Stage II, 12% Stage III, and 2% Stage IV. Histologically, approximately 70% were of the diffuse, large cell type (Working Formulation). External beam radiation therapy supplemented by brachytherapy or hysterectomy was used for 76% of the patients reviewed. There was only one treatment failure among the 28 patients whose treatment included radiation and whose cases were followed for at least 2 years. This experience and a review of the literature indicate that most cases of primary lymphoma of the uterine cervix are Ann Arbor Stage IE, and can be cured with traditional combinations of surgery and radiation therapy after careful evaluation. C1 MASSACHUSETTS GEN HOSP,VINCENT MEM GYNECOL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT INNERE MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 42 TC 51 Z9 53 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD NOV 1 PY 1991 VL 68 IS 9 BP 2023 EP 2032 DI 10.1002/1097-0142(19911101)68:9<2023::AID-CNCR2820680930>3.0.CO;2-V PG 10 WC Oncology SC Oncology GA GK168 UT WOS:A1991GK16800028 PM 1913551 ER PT J AU LIN, CW AF LIN, CW TI PHOTODYNAMIC THERAPY OF MALIGNANT TUMORS-RECENT DEVELOPMENTS SO CANCER CELLS-A MONTHLY REVIEW LA English DT Review ID TRANSPLANTABLE BLADDER-TUMORS; CHINESE-HAMSTER CELLS; CARCINOMA-CELLS; SUBCELLULAR-LOCALIZATION; ALUMINUM PHTHALOCYANINE; BIOLOGICAL-ACTIVITIES; MAMMARY-TUMOR; PHOTOFRIN-II; LUNG-CANCER; HEMATOPORPHYRIN AB Photodynamic therapy (PDT) is a promising new cancer treatment modality in which tumor cells are killed as a result of photoactivation of a tumor-localizing photosensitizing agent. Since activating light can be targeted specifically to tumors, and tumor-selective photosensitizing agents are being developed, this treatment has the potential to induce highly selective destruction of malignant cells. To date, PDT has been applied to a large variety of human carcinomas, resulting in successful eradication of single tumor nodules and several types of superficial tumors. Current research is aimed at improving the efficacy and tumor-selectivity of photosensitizing agents and at elucidating the photodynamic mechanisms that result in cell death and tumor destruction. The most immediate benefits of PDT are likely to be seen in patients treated with a combination of this and other forms of therapy. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP LIN, CW (reprint author), MASSACHUSETTS GEN HOSP,UROL RES LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 32259] NR 67 TC 27 Z9 27 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 1042-2196 J9 CANCER CELL-MON REV PD NOV PY 1991 VL 3 IS 11 BP 437 EP 444 PG 8 WC Oncology; Medicine, Research & Experimental SC Oncology; Research & Experimental Medicine GA GR445 UT WOS:A1991GR44500004 PM 1760245 ER PT J AU BARTEL, DP ZAPP, ML GREEN, MR SZOSTAK, JW AF BARTEL, DP ZAPP, ML GREEN, MR SZOSTAK, JW TI HIV-1 REV REGULATION INVOLVES RECOGNITION OF NON-WATSON-CRICK BASE-PAIRS IN VIRAL-RNA SO CELL LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; BACTERIOPHAGE-T4 DNA-POLYMERASE; MESSENGER-RNA; TARGET SEQUENCE; RIBOSOMAL-RNA; TRANS-ACTIVATOR; SECONDARY STRUCTURE; RIBONUCLEIC-ACID; XENOPUS OOCYTES; BINDING-SITES AB We have used an iterative in vitro genetic selection to identify the important structural features of the viral RNA element bound by the Rev protein of human immunodeficiency virus type 1 (HIV-1). Functional Rev-binding RNAs were selected from a pool of 10(13) variants of the wild-type Rev-binding domain. Bases conserved among the binding species define a 20 nucleotide core binding element. Covariation of some of these conserved bases indicates that the Rev-binding element is a stem-bulge-stem with a G:G base pair in the bulge. Mutational studies show that this non-Watson-Crick base pair is required for Rev binding in vitro and Rev responsiveness in vivo. We propose that the G:G base pair distorts the sugar-phosphate backbone of viral RNA and that this distortion is a critical determinant of recognition by Rev. C1 UNIV MASSACHUSETTS,MED CTR,PROGRAM MOLEC MED,WORCESTER,MA 01605. RP BARTEL, DP (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 49 TC 351 Z9 354 U1 2 U2 11 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD NOV 1 PY 1991 VL 67 IS 3 BP 529 EP 536 DI 10.1016/0092-8674(91)90527-6 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GN664 UT WOS:A1991GN66400009 PM 1934059 ER PT J AU TIAN, QS STREULI, M SAITO, H SCHLOSSMAN, SF ANDERSON, P AF TIAN, QS STREULI, M SAITO, H SCHLOSSMAN, SF ANDERSON, P TI A POLYADENYLATE BINDING-PROTEIN LOCALIZED TO THE GRANULES OF CYTOLYTIC LYMPHOCYTES INDUCES DNA FRAGMENTATION IN TARGET-CELLS SO CELL LA English DT Article ID BACTERIOPHAGE-T7 RNA-POLYMERASE; MEMBRANE-GLYCOPROTEINS; CD8+ LYMPHOCYTES; LYSIS; EXPRESSION; APOPTOSIS; PERFORIN; ENDONUCLEASE; INHIBITION; MECHANISM AB Cytolytic lymphocytes (CTLs) are characterized by their inclusion of cytoplasmic granules containing effector molecules such as perforin and the serine proteases. Here we describe the cDNA cloning and functional characterization of two related isoforms of a cytolytic granule protein designated TIA-1. Sequence analysis reveals that the 40 kd TIA-1 isoform (rp40-TIA-1) is structurally related to the poly(A)-binding proteins, possessing three RNA-binding domains and a carboxy-terminal, glutamine-rich auxiliary domain. The 15 kd TIA-1 isoform, the major species present in cytolytic granules, appears to be derived from the carboxy-terminal auxiliary domain of rp40-TIA-1 by proteolytic processing. Both natural and recombinant TIA-1 were found to induce DNA fragmentation in digitonin permeabilized thymocytes, suggesting that these molecules may be the granule components responsible for inducing apoptosis in CTL targets. C1 HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DEPT RHEUMATOL & IMMUNOL, BOSTON, MA 02115 USA. RP HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV TUMOR IMMUNOL, BOSTON, MA 02115 USA. FU NCI NIH HHS [R01CA53595-01]; NIAID NIH HHS [AI12069-17] NR 48 TC 333 Z9 339 U1 0 U2 3 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0092-8674 EI 1097-4172 J9 CELL JI Cell PD NOV 1 PY 1991 VL 67 IS 3 BP 629 EP 639 DI 10.1016/0092-8674(91)90536-8 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GN664 UT WOS:A1991GN66400018 PM 1934064 ER PT J AU HASS, R PFANNKUCHE, HJ KHARBANDA, S GUNJI, H MEYER, G HARTMANN, A HIDAKA, H RESCH, K KUFE, D GOPPELTSTRUBE, M AF HASS, R PFANNKUCHE, HJ KHARBANDA, S GUNJI, H MEYER, G HARTMANN, A HIDAKA, H RESCH, K KUFE, D GOPPELTSTRUBE, M TI PROTEIN-KINASE-C ACTIVATION AND PROTOONCOGENE EXPRESSION IN DIFFERENTIATION RETRODIFFERENTIATION OF HUMAN U-937 LEUKEMIA-CELLS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID HUMAN MONOCYTIC DIFFERENTIATION; ARACHIDONIC-ACID METABOLISM; PHORBOL ESTER; GENE-EXPRESSION; U937 CELLS; TUMOR PROMOTION; INDUCTION; MOUSE; ONCOGENE; FOS AB Human U-937 leukemia cells differentiate along the monocytic lineage following 3-day exposures to 12-O-tetradecanoylphorbol-13-acetate (TPA). This induction of differentiation is accompanied by adherence and loss of proliferation, as well as expression/repression of differentiation-associated genes. Long term culture of TPA-differentiated U-937 cells in the absence of phorbol ester for 32-36 days resulted in a process of retrodifferentiation. The retrodifferentiated cells detached from the substrate and reinitiated proliferation. Other cellular parameters, such as glycosidase activities, cytokine release, and filament expression, returned to levels similar to that observed in uninduced cells. Treatment of U-937 cells with TPA resulted in a rapid translocation of protein kinase C (PKC) from the cytosol to cell membrane fractions within 2-8 min. Increased levels of membrane-associated PKC activity persisted until 17-29 days. However, longer periods of incubation were associated with a return to the distribution of PKC in control cells. Activation of PKC has been implicated in the regulation of certain immediate early response genes, and in the present studies, TPA rapidly induced c-fos and c-jun gene expression. Levels of c-fos and c-jun transcripts remained elevated during periods of PKC activation and also returned to levels observed in control cells by 30-36 days, when the cells entered retrodifferentiation. Staurosporine, a nonspecific inhibitor of PKC, partially blocked TPA-induced adherence and growth inhibition and concomitantly prevented TPA-induced c-fos and c-jun gene expression. These findings thus suggest that PKC activation is involved in both regulation of early response gene expression and controlling the state of development during differentiation/retrodifferentiation of U-937 cells. C1 MED SCH HANNOVER,DEPT MOLEC PHARMACOL,W-3000 HANNOVER,GERMANY. GERMAN CANC RES CTR,DEPT VIROL,W-6900 HEIDELBERG,GERMANY. NAGOYA UNIV,SCH MED,DEPT PHARMACOL,NAGOYA,AICHI 466,JAPAN. RP HASS, R (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 NR 41 TC 56 Z9 56 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD NOV PY 1991 VL 2 IS 11 BP 541 EP 548 PG 8 WC Cell Biology SC Cell Biology GA GP056 UT WOS:A1991GP05600002 PM 1814434 ER PT J AU FUKAYAMA, S KEARNS, AK SKURAT, RM TASHJIAN, AH BRINGHURST, FR AF FUKAYAMA, S KEARNS, AK SKURAT, RM TASHJIAN, AH BRINGHURST, FR TI PROTEIN KINASE-A-DEPENDENT INHIBITION OF ALKALINE-PHOSPHATASE RELEASE BY SAOS-2 HUMAN OSTEOBLASTIC CELLS - STUDIES IN NEW MUTANT-CELL LINES THAT EXPRESS A CYCLIC AMP-RESISTANT PHENOTYPE SO CELL REGULATION LA English DT Article ID OSTEO-SARCOMA CELLS; CHICKEN EPIPHYSEAL CARTILAGE; PARATHYROID-HORMONE RECEPTORS; VESICLE-ENRICHED FRACTIONS; I REGULATORY SUBUNIT; PTH-RELATED PROTEIN; SOMATOSTATIN GENE; DIRECT MODULATION; PHOSPHOLIPASE-C; FREE CALCIUM AB We have established mutant SaOS-2 cell lines that express a cyclic AMP (cAMP)-resistant phenotype to investigate the regulation and functional importance of orthophosphoric-monoester phosphohydrolase alkaline optimum (ALPase) in the action of parathyroid hormone (PTH). Cells were stably transfected with a plasmid that directs the synthesis of a mutant form of the type I regulatory subunit of protein kinase A (PKA) under the control of the metallothionein promotor. There was no significant difference between parental SaOS-2 cells and the mutant lines in the affinity or number of receptors for 125-I-Nle8,18Tyr34bPTH1-34NH2, either in the absence or presence of Zn2+. When cAMP-dependent gene transcription was examined using transient transfection with a somatostatin promoter-chloramphenicol acetyl transferase (CAT) reporter plasmid, CAT activity stimulated by human PTH and dibutyryl cAMP (DBcAMP) was inhibited by > 90% in the presence of Zn2+ in the mutant cell lines. In contrast, activation by a phorbol ester of a pentameric collagenase promoter/CAT construct containing five tandem copies of the AP-1 response element (5x-TRE-CAT) was unaffected in Zn2+-treated mutant cells. The inhibitory actions of PTH and DBcAMP on ALPase release were blunted by up to 80-90% in the mutant cell lines in the presence of Zn2+; there were no significant differences in the magnitude of inhibitory effects between these agonists. We conclude that the inhibitory action of PTH on ALPase release in SaOS-2 cells is mediated via activation of PKA. These cAMP-resistant cell lines will be especially useful in elucidating signal transduction mechanism(s) for PTH in human osteoblastic cells. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,TOXICOL LAB,BOSTON,MA 02115. RP FUKAYAMA, S (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114, USA. FU NIADDK NIH HHS [AM-11794]; NIDDK NIH HHS [DK-10206] NR 46 TC 10 Z9 10 U1 0 U2 1 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1044-2030 J9 CELL REGUL PD NOV PY 1991 VL 2 IS 11 BP 889 EP 896 PG 8 WC Cell Biology SC Cell Biology GA GQ269 UT WOS:A1991GQ26900003 PM 1667091 ER PT J AU FISHER, CM AF FISHER, CM TI LACUNAR INFARCTS - A REVIEW SO CEREBROVASCULAR DISEASES LA English DT Review DE LACUNAR INFARCTS; STROKE; CEREBROVASCULAR DISEASE ID BASILAR ARTERY; COMMUNICATING ARTERY; HUMAN THALAMUS; BASAL GANGLIA; OCCLUSION; TERRITORY; HEMIPARESIS; LESIONS; STROKE RP FISHER, CM (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114, USA. NR 46 TC 180 Z9 183 U1 1 U2 7 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-9770 J9 CEREBROVASC DIS JI Cerebrovasc. Dis. PD NOV-DEC PY 1991 VL 1 IS 6 BP 311 EP 320 PG 10 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA GW240 UT WOS:A1991GW24000003 ER PT J AU GOLD, MR DEC, GW COCCASPOFFORD, D THOMPSON, BT AF GOLD, MR DEC, GW COCCASPOFFORD, D THOMPSON, BT TI ESMOLOL AND VENTILATORY FUNCTION IN CARDIAC PATIENTS WITH COPD SO CHEST LA English DT Article ID BETA-BLOCKERS; ASTHMATICS; BLOCKADE; ATENOLOL; DRUGS AB To assess the effects of acute cardioselective beta blockade on ventilatory function in patients with COPD and active cardiac disorders, 50 patients were studied during intravenous infusion of esmolol. All patients had an obstructive ventilatory component on baseline pulmonary function testing, and 58 percent had a significant bronchodilator response to inhaled albuterol. Esmolol infusion (8 to 24 mg/ min) produced large decreases in heart rate (84 +/- 2 to 69 +/- 2 beats/min, p < 0.01) and SBP (124 +/- 3 to 106 +/- 3 mm Hg, p < 0.01). Despite this marked hemodynamic response, there was no significant group effect of beta blockade on pulmonary function. No patient experienced dyspnea or wheezing with acute esmolol infusion; however, three patients (6 percent) developed asymptomatic decreases of FEV1. It is concluded that acute beta blockade with esmolol can be achieved in patients with COPD and cardiac disorders with little risk of bronchospasm. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. NR 23 TC 24 Z9 24 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 NOV PY 1991 VL 100 IS 5 BP 1215 EP 1218 DI 10.1378/chest.100.5.1215 PG 4 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA GN722 UT WOS:A1991GN72200010 PM 1682112 ER PT J AU GWATHMEY, JK HAJJAR, RJ SOLARO, RJ AF GWATHMEY, JK HAJJAR, RJ SOLARO, RJ TI CONTRACTILE DEACTIVATION AND UNCOUPLING OF CROSSBRIDGES - EFFECTS OF 2,3-BUTANEDIONE MONOXIME ON MAMMALIAN MYOCARDIUM SO CIRCULATION RESEARCH LA English DT Article DE 2,3-BUTANEDIONE MONOXIME; DIACETYL MONOXIME; CALCIUM; TROPONIN-C; CROSSBRIDGE KINETICS; ACTION POTENTIALS ID INTRACELLULAR CALCIUM TRANSIENTS; ADRENOCEPTOR BLOCKING-AGENTS; FERRET PAPILLARY-MUSCLES; RAT VENTRICULAR MYOCYTES; AEQUORIN LIGHT OUTPUT; ISOLATED HEART-MUSCLE; SKELETAL-MUSCLE; SARCOPLASMIC-RETICULUM; BUTANEDIONE MONOXIME; DIACETYL MONOXIME AB We investigated the effects of 1 and 3 mM 2,3-butanedione monoxime (BDM, diacetyl monoxime) on excitation and contraction of cardiac muscle in several types of preparations at various levels of organization. We selected a concentration of BDM that was not expected to affect sarcolemmal calcium flux and action potential duration in cardiac tissue. Two indicators were used to record intracellular calcium. Aequorin, a bioluminescent calcium indicator, was used in studies with ferret papillary muscle preparations, and fura-2, a fluorescent calcium indicator, was used in studies with guinea pig cardiac myocytes. In both cases, addition of BDM resulted in a reduction of peak intracellular calcium released from the sarcoplasmic reticulum and a reduction of peak twitch force. The duration of the action potential of isolated myocytes was slightly abbreviated in the presence of BDM. In studies on the calcium current in the myocytes, addition of BDM was associated with reduced calcium current at any potential. Peak calcium current was reduced by 7.9 +/- 1% in the presence of BDM. In tetanized ferret papillary muscles, BDM reduced maximal calcium-activated force by 30 +/- 5% and increased the calcium ion concentration required for half-maximal force by 0.1 +/- 0.01-mu-M. The Hill coefficient was reduced from 5.00 +/- 0.11 to 3.40 +/- 0.20. Maximal shortening velocity of ferret papillary muscles was increased in the presence of BDM from 1.55 +/- 0.24 to 2.04 +/- 0.33 mm/sec. Ca2+ binding to troponin C in skinned fiber preparations from guinea pig, bovine, and canine hearts was unaffected by addition of up to 10 mM BDM. Our results indicate that BDM affects both calcium availability and responsiveness of the myofilaments to Ca2+. Uncoupling of contractile activation from excitation may also result from altered crossbridge kinetics. C1 UNIV MARYLAND,DEPT PHYSIOL,BALTIMORE,MD 21201. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. UNIV ILLINOIS,DEPT PHYSIOL & BIOPHYS,CHICAGO,IL 60680. HARVARD UNIV,CHARLES A DANA RES INST,SCH MED,CAMBRIDGE,MA 02138. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,HARVARD THORNDIKE LAB,DIV CARDIOVASC,BOSTON,MA 02215. FU NHLBI NIH HHS [HL-22231, HL-36797, HL-39091] NR 44 TC 171 Z9 173 U1 0 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 NOV PY 1991 VL 69 IS 5 BP 1280 EP 1292 PG 13 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA GN521 UT WOS:A1991GN52100012 PM 1934358 ER PT J AU LEE, MJ SAINI, S BRINK, JA MORRISON, MC HAHN, PF MUELLER, PR AF LEE, MJ SAINI, S BRINK, JA MORRISON, MC HAHN, PF MUELLER, PR TI MALIGNANT SMALL-BOWEL OBSTRUCTION AND ASCITES - NOT A CONTRAINDICATION TO PERCUTANEOUS GASTROSTOMY SO CLINICAL RADIOLOGY LA English DT Article ID EXPERIENCE AB Percutaneous gastrostomy (PG) with gastropexy was performed for relief of malignant small bowel obstruction in 12 patients with extensive ascites. Abdominal paracentesis was performed before PG in nine patients and after PG in one patient. Gastrostomy catheters were inserted without complication in all patients. Clinical follow up revealed that pericatheter leakage of ascitic fluid and skin excoriation occurred only in the three patients who did not have paracentesis performed before PG. No dislodgement of gastrostomy catheters occurred but mild peritonitis was noted in one patient. Our experience suggests that although in the past extensive ascites was a relative contraindication for PG, these patients can now be successfully treated with a combination of ultrasound-guided paracentesis to reduce pericatheter leakage of ascitic fluid, and gastropexy to prevent catheter dislodgement. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 10 TC 28 Z9 28 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9260 J9 CLIN RADIOL JI Clin. Radiol. PD NOV PY 1991 VL 44 IS 5 BP 332 EP 334 DI 10.1016/S0009-9260(05)81270-X PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GN980 UT WOS:A1991GN98000010 PM 1836988 ER PT J AU HARTWELL, TD PARKER, CB POOLE, WK DAVIS, VG MULLER, JE BRAUNWALD, E RUTHERFORD, J STRAUSS, HW ROBERTS, R SOBEL, BE JAFFE, AS WILLERSON, JT THOMAS, LJ AF HARTWELL, TD PARKER, CB POOLE, WK DAVIS, VG MULLER, JE BRAUNWALD, E RUTHERFORD, J STRAUSS, HW ROBERTS, R SOBEL, BE JAFFE, AS WILLERSON, JT THOMAS, LJ TI REPRODUCTIBILITY OF CENTRALIZED LABORATORY INTERPRETATIONS OF MEASURES OF MYOCARDIAL INFARCT SIZE, VENTRICULAR-FUNCTION, AND VENTRICULAR ELECTRICAL INSTABILITY SCINTIGRAPHY SO CORONARY ARTERY DISEASE LA English DT Article DE REPRODUCTIBILITY OF RESULTS; MYOCARDIAL INFARCTION; LABORATORIES; VENTRICULAR FUNCTION; QUALITY CONTROL; MEASUREMENT VARIABILITY ID TISSUE PLASMINOGEN-ACTIVATOR; INTRA-CORONARY THROMBOLYSIS; INTRAVENOUS STREPTOKINASE; RADIONUCLIDE ANGIOGRAPHY; CREATINE-PHOSPHOKINASE; EJECTION FRACTION; RANDOMIZED TRIAL; INTERVENTIONS; REPERFUSION; MULTICENTER AB In many clinical studies of acute myocardial infarction, measurements such as infarct occurrence and size and ventricular function have proven useful in the assessment of the effects of new therapies. The importance of these measures is increasing as mortality from acute infarction continues to decrease. In the Multicenter Investigation of the Limitation of Infarct Size study of 985 patients with suspected or confirmed acute myocardial infarction, several such measures were obtained in centralized core laboratories to reduce interlaboratory variations. In particular, core laboratories were responsible for measurement of serial changes in plasma creatine kinase activity, pyrophosphate scintigrams, ambulatory ECGs, radionuclide ventriculograms, and ECGs. To quantitate the variability in measurements made by these core laboratories, duplicate, blinded data were submitted to the laboratories on 88 patients. In general, the five core laboratories had reliability coefficients of about 90%. The analysis of these quality control data supports the feasibility of monitoring core laboratories with duplicate samples. They also provided quantitative information on the variability of the duplicate measurements and on the relative magnitude of patient-to-patient variability versus measurement error. Because measurement errors between duplicate readings generally were small, these data provide additional verification of the data from the multiple publications of the Multicenter Investigation of the Limitation of Infarct Size study. C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BAYLOR COLL MED,HOUSTON,TX 77030. WASHINGTON UNIV,MED CTR,BIOMED COMP LAB,ST LOUIS,MO 63130. UNIV TEXAS,SW MED CTR,AUSTIN,TX 78712. RP HARTWELL, TD (reprint author), RES TRIANGLE INST,POB 12194,RES TRIANGLE PK,NC 27709, USA. NR 34 TC 0 Z9 0 U1 1 U2 1 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 0954-6928 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD NOV PY 1991 VL 2 IS 9 BP 977 EP 984 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GV223 UT WOS:A1991GV22300002 ER PT J AU LU, HR GOLD, HK WU, ZM DECOCK, F JANG, IK PAUWELS, P COLLEN, D AF LU, HR GOLD, HK WU, ZM DECOCK, F JANG, IK PAUWELS, P COLLEN, D TI ACCELERATION AND PERSISTENCE OF RECOMBINANT TISSUE PLASMINOGEN-ACTIVATOR INDUCED ARTERIAL EVERSION GRAFT RECANALIZATION WITH A SINGLE BOLUS INJECTION OF F(AB')2 FRAGMENTS OF THE ANTIPLATELET GLYCOPROTEIN IIB/IIIA ANTIBODY 7E3 SO CORONARY ARTERY DISEASE LA English DT Article DE THROMBOLYTIC THERAPY, CORONARY THROMBOSIS; GRAFT OCCLUSION, VASCULAR ID MONOCLONAL-ANTIBODY; THROMBOLYTIC THERAPY; GPIIB/IIIA ANTIBODY; RECEPTOR; MODEL; REPERFUSION; THROMBOSIS; DOGS; PA AB The effects of F(ab')2 fragments of the monoclonal antiplatelet glycoprotein llb/llla antibody 7E3, 7E3-F(ab')2, were studied in a combined arterial and venous thrombosis preparation in heparinized dogs (100 U/kg/h intravenously [IV]). The arterial thrombus preparation consisted of a 3-cm everted (inside-out) carotid arterial segment, inserted into the femoral artery; the venous thrombus was a I-125-fibrin-labeled whole blood clot produced in the contralateral femoral vein. Spontaneous occlusion of the everted arterial segment occurred in all 24 dogs and persisted for 60 minutes. In five control dogs (group l) given an IV bolus of 5 mg/kg of aspirin, arterial occlusion persisted throughout a 2-hour observation period and was still present at 24 hours; the extent of venous clot lysis after 120 minutes was 23% +/- 6% (mean +/- SEM). In five dogs given an IV bolus injection of 0.8 mg/kg 7E3-F(ab')2, the arterial occlusion persisted throughout the observation period and was still present after 24 hours; venous clot lysis was 41% +/- 3% (P = 0.028 vs aspirin group). In eight dogs given a 5-mg/kg aspirin bolus and a 0.5-mg/kg recombinant tissue plasminogen activator (rt-PA) infusion over 60 minutes, recanalization occurred in three dogs but the grafts were occluded at 24 hours; the extent of venous clot lysis in this group was 76% +/- 8% (P < 0.001 vs aspirin group). In six dogs given a bolus injection of 0.8 mg/kg of 7E3-F(ab')2 and an infusion of 0.5 mg/kg of rt-PA over 60 minutes, arterial graft recanalization occurred in all dogs (P = 0.006 vs aspirin and rt-PA group), and was still present at 24 hours (P < 0.001 vs aspirin and rt-PA); venous clot lysis in this group was 90% +/- 3% (P = 0.2 vs aspirin and rt-PA). ADP-induced ex vivo platelet aggregation was completely abolished after 7E3-F(ab')2 injection and had only partially recovered after 24 hours. Template bleeding times were prolonged from approximately 2 minutes before to greater than 30 minutes after 7E3-F (ab')2 injection but had partially returned to normal within 24 hours. This study confirms that the monoclonal antibody 7E3, relative to aspirin, enhances and accelerates arterial platelet-rich clot lysis induced with rt-PA and shows that it prevents both early (within 2 hours) and late (24 hours) reocclusion. C1 CATHOLIC UNIV LEUVEN,CTR THROMBOSIS & VASC RES,CAMPUS GASTHUISBERG,HERESTR 49,B-3000 LOUVAIN,BELGIUM. CATHOLIC UNIV LEUVEN,EXPTL CARDIOL LAB,B-3000 LOUVAIN,BELGIUM. CATHOLIC UNIV LEUVEN,DEPT HISTOPATHOL,B-3000 LOUVAIN,BELGIUM. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA 02114. RP COLLEN, D (reprint author), CATHOLIC UNIV LEUVEN,CTR THROMBOSIS & VASC RES,CAMPUS GASTHUISBERG,HERESTR 49,B-3000 LOUVAIN,BELGIUM. NR 19 TC 13 Z9 13 U1 0 U2 0 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 0954-6928 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD NOV PY 1991 VL 2 IS 9 BP 1039 EP 1046 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GV223 UT WOS:A1991GV22300009 ER PT J AU TOMPKINS, RG AF TOMPKINS, RG TI SPOTLIGHT ON AN EDITORIAL-BOARD MEMBER - COMPTON,CAROLYN SO CRITICAL CARE MEDICINE LA English DT Editorial Material RP TOMPKINS, RG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD NOV PY 1991 VL 19 IS 11 BP 1338 EP 1338 DI 10.1097/00003246-199111000-00005 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA GN718 UT WOS:A1991GN71800005 ER PT J AU KHILNANI, P GOLDSTEIN, B TODRES, ID AF KHILNANI, P GOLDSTEIN, B TODRES, ID TI DOUBLE LUMEN UMBILICAL VENOUS CATHETERS IN CRITICALLY ILL NEONATES - A RANDOMIZED PROSPECTIVE-STUDY SO CRITICAL CARE MEDICINE LA English DT Article DE COMPLICATIONS; CATHETERIZATION, CENTRAL VENOUS; INFANTS, NEWBORN; CRITICAL CARE; VENOUS PRESSURE, CENTRAL; RADIOGRAPHY; UMBILICAL VEINS; INTENSIVE CARE UNIT, NEONATAL; MONITORING, PHYSIOLOGICAL; RESPIRATORY DISTRESS SYNDROME, INFANT ID COMPLICATIONS AB Objectives: To compare relative efficacies and complications associated with the use of double lumen vs. single lumen umbilical venous catheters in critically ill neonates. Design: Prospective randomized control trial. Setting. Neonatal ICU. Patients: Forty-three critically ill neonates. Interventions: Group 1 patients (n = 20) received single lumen umbilical venous catheters and group 2 patients (n = 23) received double lumen catheters. A record of the following information was kept: demographic data including diagnosis and indication for umbilical venous catheter insertion, catheter tip location, length of catheterization (days), number of additional iv catheters and complications (sepsis, hepatic necrosis, thrombosis, or mechanical complications). Measurements and Main Results: Double lumen umbilical venous catheters were well tolerated and were associated with no significant increased risk of mechanical complications when compared with single lumen umbilical venous catheters. The number of additional iv catheters required (0.8 +/- 0.1 [SD]) was significantly (p < .05) less in the double lumen umbilical venous catheter group as compared with additional iv catheters required (2.3 +/- 0.8) in the single lumen umbilical venous catheter group. Conclusion: Double lumen umbilical venous catheters are well tolerated for short-term use, decrease the need for additional venous catheters in critically ill neonates, and may not significantly increase the risk of mechanical complications when compared with single lumen umbilical venous catheters. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEONATAL & PEDIAT INTENS CARE UNIT,BOSTON,MA 02114. UNIV ROCHESTER,STRONG CHILDRENS CRIT CARE CTR,ROCHESTER,NY 14627. RP KHILNANI, P (reprint author), HENRICO DOCTORS HOSP,PEDIAT INTENS CARE UNIT,1602 SKIPWITH RD,RICHMOND,VA 23229, USA. NR 6 TC 20 Z9 21 U1 1 U2 4 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 NOV PY 1991 VL 19 IS 11 BP 1348 EP 1351 DI 10.1097/00003246-199111000-00007 PG 4 WC Critical Care Medicine SC General & Internal Medicine GA GN718 UT WOS:A1991GN71800007 PM 1935151 ER PT J AU ROGERS, MB HOSLER, BA GUDAS, LJ AF ROGERS, MB HOSLER, BA GUDAS, LJ TI SPECIFIC EXPRESSION OF A RETINOIC ACID-REGULATED, ZINC-FINGER GENE, REX-1, IN PREIMPLANTATION EMBRYOS, TROPHOBLAST AND SPERMATOCYTES SO DEVELOPMENT LA English DT Article DE RETINOIC ACID; EMBRYONAL CARCINOMA CELLS; EMBRYONIC STEM CELLS; ZINC-FINGER PROTEINS; EMBRYOGENESIS; PLACENTA; SPERMATOGENESIS ID CARCINOMA CELL-DIFFERENTIATION; LEUKEMIA INHIBITORY FACTOR; TRANSCRIPTION FACTOR-IIIA; MOUSE EMBRYO; STEM-CELLS; BLASTOCYST INJECTION; SPERMATOGENIC CELLS; VISCERAL ENDODERM; TESTIS CELLS; VITAMIN-A AB We have previously isolated a cDNA clone for a gene whose expression is reduced by retinoic acid (RA) treatment of F9 embryonal carcinoma cells. The nucleotide sequence indicated that this gene, Rex-1, encodes a zinc-finger protein and thus may be a transcriptional regulator. The Rex-1 message level is high in two lines of embryonic stem cells (CCE and D3) and is reduced when D3 cells are induced to differentiate using four different growth conditions. As expected for a stem-cell-specific message, Rex-1 mRNA is present in the inner cell mass (ICM) of the day 4.5 mouse blastocyst. It is also present in the polar trophoblast of the blastocyst. One and two days later, Rex-1 message is found in the ectoplacental cone and extraembryonic ectoderm of the egg cylinder (trophoblast-derived tissues), but its abundance is much reduced in the embryonic ectoderm which is directly descended from the ICM. Rex-1 is expressed in the day 18 placenta (murine gestation is 18 days), a tissue which is largely derived from trophoblast. The only tested adult tissue that contains detectable amounts of Rex-1 mRNA is the testis. In situ hybridization and northern analyses of RNA from germ-cell-deficient mouse testis and stage-specific germ cell preparations suggest that Rex-1 expression is limited to spermatocytes (germ cells undergoing meiosis). These results suggest that Rex-1 is involved in trophoblast development and spermatogenesis, and is a useful marker for studies of early cell fate determination in the ICM. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [R01 CA39036] NR 54 TC 213 Z9 218 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD NOV PY 1991 VL 113 IS 3 BP 815 EP 824 PG 10 WC Developmental Biology SC Developmental Biology GA GT172 UT WOS:A1991GT17200010 PM 1821852 ER PT J AU WOLFSDORF, JI LAFFEL, LMB PASQUARELLO, C VERNON, A HERSKOWITZ, RD AF WOLFSDORF, JI LAFFEL, LMB PASQUARELLO, C VERNON, A HERSKOWITZ, RD TI SPLIT-MIXED INSULIN REGIMEN WITH HUMAN ULTRALENTE BEFORE SUPPER AND NPH (ISOPHANE) BEFORE BREAKFAST IN CHILDREN AND ADOLESCENTS WITH IDDM SO DIABETES CARE LA English DT Note ID DEPENDENT DIABETIC-PATIENTS; NOCTURNAL HYPOGLYCEMIA; DAWN PHENOMENON; INFUSION; PORCINE; BOVINE; INJECTIONS; MELLITUS; LOOP AB Objective: Fasting hyperglycemia is common in patients with insulin-dependent diabetes mellitus (IDDM) treated with twice-daily subcutaneous insulin regimens. We Postulated that substituting human ultralente insulin for the presupper dose of intermediate-acting insulin would improve overnight glycemic control in children and adolescents with IDDM. Research Design and Methods: This 6-mo double-blind crossover study compared a conventional insulin regimen, a mixture of human NPH and regular given before both breakfast and supper (NPH), with a novel twice-daily regimen in which human ultralente replaced NPH before the evening meal (ultralente). This study was comprised of 20 children and adolescents (mean age and duration of IDDM 11.3 +/- 2.9 and 2.4 +/- 1.3 yr, respectively) from the Youth Clinic of the Joslin Diabetes Center, all of whom regularly performed self-monitoring of blood glucose (SMBG) and had been treated exclusively with human insulin (mean daily dose 0.75 +/- 0.22 U/kg). Subjects performed SMBG on a prescribed schedule with a glucose meter with an electronic memory, and recorded results of blood glucose measurements, insulin dosages, and episodes of hypoglycemia. Monthly measurements were obtained for height, weight, and mean daily insulin dosages and average blood glucose level before breakfast, lunch, supper, bedtime snack, and between 0200 and 0300 were calculated. Nonfasting serum lipids were measured at entry, crossover, and the end of the study. Results: After 3 mo, mean HbA, did not differ significantly (9.1 +/- 1.7 vs. 9.5 +/- 1.4%, NPH and ultralente, respectively). Mean fasting blood glucose was significantly lower on ultralente (9.6 +/- 1.9 vs. 10.3 +/- 2.2 mM, P < 0.05, and blood glucose showed a similar trend (0.05 < P < 0.1) before lunch (8.9 +/- 1.7 vs. 9.8 2.6 mM. Mean blood glucose before bedtime snack was significantly lower (P < 0.01) on NPH (8.4 +/- 1.9 vs. 10.0 +/- 2.1 mM) but did not differ significantly before supper or between 0200 and 0300. On the two regimens, growth and serum lipids were normal and similar, and no differences were observed in the incidence or severity of hypoglycemia. Conclusions: Compared with a mixed dose of regular and NPH, a similar dose of a mixture of regular and human ultralente insulin before supper caused a modest reduction in fasting blood glucose levels but was associated with higher blood glucose levels before the bedtime snack. Overall glycemic control, reflected in HbA, values, was not significantly improved. C1 JOSLIN DIABET CTR,DEPT PEDIAT,BOSTON,MA. CHILDRENS HOSP MED CTR,DIV ENDOCRINOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. NR 37 TC 4 Z9 4 U1 1 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD NOV PY 1991 VL 14 IS 11 BP 1100 EP 1106 DI 10.2337/diacare.14.11.1100 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GM852 UT WOS:A1991GM85200030 PM 1797498 ER PT J AU ABOUSAMRA, AB ZAJAC, JD SCHIFFERALBERTS, D SKURAT, R KEARNS, A SEGRE, GV BRINGHURST, FR AF ABOUSAMRA, AB ZAJAC, JD SCHIFFERALBERTS, D SKURAT, R KEARNS, A SEGRE, GV BRINGHURST, FR TI CYCLIC ADENOSINE-3',5'-MONOPHOSPHATE (CAMP)-DEPENDENT AND CAMP-INDEPENDENT REGULATION OF PARATHYROID-HORMONE RECEPTORS ON UMR-106-01 OSTEOBLASTIC OSTEOSARCOMA CELLS SO ENDOCRINOLOGY LA English DT Article ID ADENYLATE-CYCLASE ACTIVITY; DEPENDENT PROTEIN-KINASE; OSTEO-SARCOMA CELLS; ROS 17/2.8 CELLS; CYTOSOLIC CALCIUM; PLASMA-MEMBRANES; RAT OSTEOSARCOMA; DOWN-REGULATION; CANINE KIDNEY; BINDING AB The osteoblast-like cells, UMR 106-01, express PTH receptors that are coupled to adenylate cyclase. Recently, we reported the isolation of a UMR 106-01 subclone, UMR 4-7, that is stably transfected with a Zn++-inducible mutant of the regulatory subunit of protein kinase A. Incubation of UMR 4-7 cells with Zn++ renders the cells unresponsive to cAMP agonists. This subclone, therefore, seemed particularly suitable for studies of PTH receptor regulation. In UMR 106-01 cells, PTH receptors are strikingly down-regulated by pretreatment with 8-Br-cAMP or 3-isobutyl-1-methylxanthine for 2 days. In UMR 4-7 cells, this effect is totally prevented by prior and concurrent treatment with Zn++. Zn++ addition to UMR 106 cells does not modify these responses. Treatment with the PTH agonist [Nle8,18,Tyr34]bovine PTH(1-34)NH2 [(NlePTH(1-34)] also markedly down-regulates PTH receptors in UMR 106 cells, but this effect is only partially inhibited in Zn++-induced UMR 4-7 cells. At high doses, the PTH antagonist, [Nle8,18,Tyr34]bovine PTH(3-34)NH2 [NlePTH(3-34)] also (partially) reduces PTH receptor availability. Receptor regulation by NlePTH(3-34) is not blocked in the cAMP-resistant cells, however. Coincubation of submaximal doses of NlePTH(1-34) (1 nM) with NlePTH(3-34) (1-mu-M) reduces receptor availability more than when the cells are exposed to either ligand alone. This decrease is only partially inhibited in Zn++-induced UMR 4-7 cells. In contrast to its additive effect on receptor regulation, NlePTH(3-34) efficiently competes for binding to the PTH receptor in UMR 106-01 cells and antagonizes the stimulatory effects of NlePTH(1-34) on both intracellular cAMP accumulation and gene expression driven by a transiently transfected synthetic cAMP-responsive enhancer. In conclusion, homologous down-regulation of PTH receptors is mediated by activation of both cAMP-dependent (via protein kinase A) and cAMP-independent pathways. PTH activates both pathways, whereas the effect of NlePTH(3-34) appears to be exclusively cAMP-independent. These results give new insights into mechanisms of PTH receptor regulation. RP ABOUSAMRA, AB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114, USA. OI Abou-Samra, Abdul/0000-0001-8735-1142 NR 32 TC 30 Z9 30 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1991 VL 129 IS 5 BP 2547 EP 2554 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GM349 UT WOS:A1991GM34900041 PM 1718728 ER PT J AU GLASS, DJ AF GLASS, DJ TI WASTE MANAGEMENT - BIOLOGICAL TREATMENT OF HAZARDOUS WASTES SO ENVIRONMENT LA English DT Editorial Material ID BIODEGRADATION; DEGRADATION; BACTERIA; TRICHLOROETHYLENE; INOCULATION; SEDIMENTS RP GLASS, DJ (reprint author), MASSACHUSETTS GEN HOSP,OFF TECHNOL AFFAIRS,BOSTON,MA 02114, USA. NR 40 TC 1 Z9 1 U1 0 U2 0 PU HELDREF PUBLICATIONS PI WASHINGTON PA 1319 EIGHTEENTH ST NW, WASHINGTON, DC 20036-1802 SN 0013-9157 J9 ENVIRONMENT JI Environment PD NOV PY 1991 VL 33 IS 9 BP 5 EP & PG 0 WC Environmental Sciences; Environmental Studies SC Environmental Sciences & Ecology GA GQ009 UT WOS:A1991GQ00900003 ER PT J AU PERKINS, DL BERRIZ, G WANG, YS SMITH, JA GEFTER, ML AF PERKINS, DL BERRIZ, G WANG, YS SMITH, JA GEFTER, ML TI COMPARISON OF CLASS I-RESTRICTED AND II-RESTRICTED T-CELL RECOGNITION OF THE IDENTICAL PEPTIDE SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID TOXIC LYMPHOCYTES-T; ANTIGEN-BINDING SITE; MHC CLASS-II; INFLUENZA NUCLEOPROTEIN; FOREIGN ANTIGEN; SYNTHETIC PEPTIDES; PROTEIN ANTIGEN; MOLECULES; EPITOPES; REPERTOIRE AB There is structural and functional evidence that both class I- and II-restricted T cells recognize short processed peptides bound to MHC molecules. Although the structural conformation of bound peptides remains unknown, no evidence of distinct structural motifs of class I- or class II-restricted peptides has been described. Conversely, two algorithms proposed to predict T cell epitopes, and based on primary amino acid sequence or tertiary structure, are both compatible with many observed class I- and class II-restricted peptides. We previously identified eight class I-restricted peptides which were also recognized by class II-restricted T cells. Based on functional and direct binding studies, additional examples of peptides with both class I and II restrictions have been identified. In this study, we have directly compared the fine specificity of T cell recognition of a single epitope in a single mouse strain in the context of both class I- and class II-restricted responses. Based on a panel of analogue peptides with amino acid substitutions and peptides of various lengths, we observed several striking similarities in the recognition patterns of both class I- and class II-restricted T cells. In addition, some characteristics of recognition were different in the two systems indicating that the recognition processes were similar but not identical. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP PERKINS, DL (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,IMMUNOGENET & TRANSPLANTAT LAB,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK 01693] NR 36 TC 8 Z9 8 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD NOV PY 1991 VL 21 IS 11 BP 2781 EP 2789 DI 10.1002/eji.1830211120 PG 9 WC Immunology SC Immunology GA GQ080 UT WOS:A1991GQ08000019 PM 1718759 ER PT J AU COTRAN, PR BRUNS, GAP BERSON, EL DRYJA, TP AF COTRAN, PR BRUNS, GAP BERSON, EL DRYJA, TP TI GENETIC-ANALYSIS OF PATIENTS WITH RETINITIS-PIGMENTOSA USING A CLONED CDNA PROBE FOR THE HUMAN GAMMA SUBUNIT OF CYCLIC-GMP PHOSPHODIESTERASE SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE CYCLIC GMP PHOSPHODIESTERASE; PHOTOTRANSDUCTION; RETINITIS-PIGMENTOSA; USHERS SYNDROME; LINKAGE DISEQUILIBRIUM; RESTRICTION FRAGMENT LENGTH POLYMORPHISM; RETINAL DEGENERATION; GENETIC EYE DISEASES; CHROMOSOME-17 ID RETINAL DEGENERATION; PHOTORECEPTOR CELLS; GUANOSINE MONOPHOSPHATE; CGMP-PHOSPHODIESTERASE; BINDING-PROTEIN; MOUSE RETINA; DNA; ACCUMULATION; TRANSDUCIN; DEFECT C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. CHILDRENS HOSP,DIV GENET,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. FU NEI NIH HHS [EY 06051-01, P50 EY 02014] NR 25 TC 18 Z9 18 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 NOV PY 1991 VL 53 IS 5 BP 557 EP 564 DI 10.1016/0014-4835(91)90213-X PG 8 WC Ophthalmology SC Ophthalmology GA GP172 UT WOS:A1991GP17200001 PM 1683837 ER PT J AU SANDERS, KM STERN, TA OGARA, PT FIELD, TS RAUCH, SL LIPSON, RE EAGLE, KA AF SANDERS, KM STERN, TA OGARA, PT FIELD, TS RAUCH, SL LIPSON, RE EAGLE, KA TI DELIRIUM DURING IABP THERAPY - INCIDENCE AND MANAGEMENT SO GENERAL HOSPITAL PSYCHIATRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD NOV PY 1991 VL 13 IS 6 BP 379 EP 379 DI 10.1016/0163-8343(91)90095-E PG 1 WC Psychiatry SC Psychiatry GA GQ996 UT WOS:A1991GQ99600043 ER PT J AU YELICK, PC KOZAK, C KWON, YK SELDIN, MF HECHT, NB AF YELICK, PC KOZAK, C KWON, YK SELDIN, MF HECHT, NB TI THE MOUSE TRANSITION PROTEIN-1 GENE CONTAINS A B1 REPETITIVE ELEMENT AND IS LOCATED ON CHROMOSOME-1 SO GENOMICS LA English DT Article ID CONSERVED LINKAGE GROUP; NUCLEOTIDE-SEQUENCE; CDNA CLONE; MAMMALIAN SPERMATIDS; MESSENGER-RNA; DNA; LOCALIZATION; TP1; SPERMATOGENESIS; IDENTIFICATION C1 TUFTS UNIV,DEPT BIOL,MEDFORD,MA 02115. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CELLULAR & MOLEC BIOL,BOSTON,MA 02115. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. FU NHGRI NIH HHS [HG 00101]; NIGMS NIH HHS [GM 29224] NR 36 TC 17 Z9 18 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD NOV PY 1991 VL 11 IS 3 BP 687 EP 694 DI 10.1016/0888-7543(91)90076-Q PG 8 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA GK046 UT WOS:A1991GK04600021 PM 1685480 ER PT J AU GOODMAN, A SULLINGER, JC RICE, LW FULLER, AF AF GOODMAN, A SULLINGER, JC RICE, LW FULLER, AF TI CLEAR CELL ADENOCARCINOMA OF THE VAGINA - A 2ND PRIMARY IN A DIETHYLSTILBESTROL-EXPOSED WOMAN SO GYNECOLOGIC ONCOLOGY LA English DT Article ID PRIMARY-CARCINOMA; CERVICAL ECTROPION; ARTIFICIAL VAGINA; ADENOSIS; RECURRENCE; EPITHELIUM; NEOVAGINA; SURVIVAL; ORIGIN C1 MASSACHUSETTS GEN HOSP,DEPT GYNECOL,DIV GYNECOL ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. RP GOODMAN, A (reprint author), TUFTS UNIV,NEW ENGLAND MED CTR,BOX 289,750 WASHINGTON ST,BOSTON,MA 02111, USA. NR 38 TC 6 Z9 6 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 NOV PY 1991 VL 43 IS 2 BP 173 EP 177 DI 10.1016/0090-8258(91)90067-F PG 5 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA GU864 UT WOS:A1991GU86400017 PM 1743561 ER PT J AU WARD, W RICHARDSON, A AF WARD, W RICHARDSON, A TI EFFECT OF AGE ON LIVER PROTEIN-SYNTHESIS AND DEGRADATION SO HEPATOLOGY LA English DT Review ID SENESCENT HUMAN-FIBROBLASTS; TRANSFER-RNA-SYNTHETASES; LABILE ENZYME MOLECULES; AGING HUMAN-FIBROBLASTS; PERFUSED RAT-LIVER; MOUSE-LIVER; DIETARY RESTRICTION; PARENCHYMAL-CELLS; TRANSLATIONAL ACTIVITY; ALTERED DEGRADATION C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG01188, AG01548, AG06819] NR 130 TC 57 Z9 57 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 NOV PY 1991 VL 14 IS 5 BP 935 EP 948 DI 10.1002/hep.1840140529 PG 14 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GN098 UT WOS:A1991GN09800028 PM 1937398 ER PT J AU ROSAI, J BONFIGLIO, TA CORSON, JM FECHNER, RE HARRIS, NL LIVOLSI, VA SILVERBERG, SG AF ROSAI, J BONFIGLIO, TA CORSON, JM FECHNER, RE HARRIS, NL LIVOLSI, VA SILVERBERG, SG TI RECOMMENDATIONS ON QUALITY-CONTROL AND QUALITY ASSURANCE IN ANATOMIC PATHOLOGY (REPRINTED FROM AM J SURG PATHOL, VOL 15, PG 1007-1009, 1991) SO HUMAN PATHOLOGY LA English DT Reprint C1 UNIV ROCHESTER,MED CTR,ROCHESTER,NY 14642. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. UNIV VIRGINIA,CHARLOTTESVILLE,VA 22903. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV PENN,MED CTR,PHILADELPHIA,PA 19104. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NR 0 TC 4 Z9 4 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD NOV PY 1991 VL 22 IS 11 BP 1099 EP 1101 PG 3 WC Pathology SC Pathology GA GT371 UT WOS:A1991GT37100005 ER PT J AU LIOU, HC EDDY, R SHOWS, T LISOWSKAGROSPIERRE, B GRISCELLI, C DOYLE, C MANNHALTER, J EIBL, M GLIMCHER, LH AF LIOU, HC EDDY, R SHOWS, T LISOWSKAGROSPIERRE, B GRISCELLI, C DOYLE, C MANNHALTER, J EIBL, M GLIMCHER, LH TI AN HLA-DR-ALPHA-PROMOTER DNA-BINDING PROTEIN IS EXPRESSED UBIQUITOUSLY AND MAPS TO HUMAN CHROMOSOME-22 AND CHROMOSOME-5 SO IMMUNOGENETICS LA English DT Article ID II GENE-EXPRESSION; HISTOCOMPATIBILITY COMPLEX GENES; CYCLIC-AMP; B-CELL; MULTIGENE FAMILY; RESPONSE ELEMENT; LEUCINE ZIPPER; HUMAN GENOME; SEQUENCES; TRANSCRIPTION AB The class II major histocompatibility complex antigens are a family of integral membrane proteins whose expression is tissue-specific and developmentally regulated. Three consensus sequences, X1, X2, and Y, separated by an interspace element, is found upstream from all class II genes. Deletion of each of these sequences eliminates expression of class II genes in vitro or in transgenic mice. Here we further characterize the expression of a cDNA encoding a DNA binding protein (human X-box binding protein, hXBP-1) which, like the proteins in whole nuclear extract, recognizes both the X2 promoter element of the human DR-alpha and DP-beta and mouse A-alpha genes. The hXBP-1 cDNA hybridizes to human RNA species of approximately 2.2 kilobases (kb) and 1.6 kb, which are expressed in class II negative as well as class II positive cells. hXBP-1 transcripts are present in several class II deficient mutant B cell lines, although in one such line, 6.1.6, levels were somewhat reduced. Chromosome mapping studies demonstrate that hXBP-1 arises from a small gene family, two of whose members map to human chromosomes 5 and 22. Taken together, these data suggest a high degree of complexity in the transcriptional control of the class II gene family. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,665 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC CTR,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. HOP NECKER ENFANTS MALAD,F-75730 PARIS 15,FRANCE. VIENNA MED SCH,VIENNA,AUSTRIA. FU NIGMS NIH HHS [GM 36864] NR 39 TC 11 Z9 11 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD NOV PY 1991 VL 34 IS 5 BP 286 EP 292 DI 10.1007/BF00211992 PG 7 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA GM524 UT WOS:A1991GM52400002 PM 1718857 ER PT J AU GHASSEMI, M HEYDARI, AR RICHARDSON, A AF GHASSEMI, M HEYDARI, AR RICHARDSON, A TI INDUCTION OF HEAT-SHOCK PROTEINS IN LYMPHOCYTES INCREASES WITH MITOGEN STIMULATION SO IMMUNOLOGY LETTERS LA English DT Article DE HEAT SHOCK; LYMPHOCYTE; HEAT SHOCK PROTEIN; HYPERTHERMIA ID T STRESS RESPONSE; HUMAN HSP70 GENE; HYPERTHERMIC STRESS; EXPRESSION; FAMILY AB The effect of the growth state of a cell on the ability of hyperthermia to induce the synthesis of heat shock proteins (HSPs) was studied in resting and concanavalin A (ConA)-stimulated lymphocytes. Hyperthermia induced the synthesis of hsp 110, hsp 90, hsc 70, and hsp 70 in both resting and ConA-stimulated lymphocytes, and ConA-treatment induced the synthesis of the hsp 90 and hsc 70 at normal temperature. The induction of the synthesis of hsp 110 and hsp 70 by hyperthermia was 3- to 6-fold higher for lymphocytes cultured with ConA for 12 and 24 h than in non-stimulated lymphocytes. Thus, lymphocytes induced to undergo proliferation showed a greater response to hyperthermia than resting lymphocytes. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG 01548] NR 30 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-2478 J9 IMMUNOL LETT JI Immunol. Lett. PD NOV PY 1991 VL 30 IS 3 BP 333 EP 337 DI 10.1016/0165-2478(91)90047-E PG 5 WC Immunology SC Immunology GA GP587 UT WOS:A1991GP58700010 PM 1800319 ER PT J AU DUNCAN, MJ HILLMAN, JD AF DUNCAN, MJ HILLMAN, JD TI DNA-SEQUENCE AND INVITRO MUTAGENESIS OF THE GENE ENCODING THE FRUCTOSE-1,6-DIPHOSPHATE-DEPENDENT L-(+)-LACTATE DEHYDROGENASE OF STREPTOCOCCUS-MUTANS SO INFECTION AND IMMUNITY LA English DT Article ID HUMAN ORAL CAVITY; COLONIZATION; BACTERIOCIN; EXPRESSION; CLONING; STRAIN AB Previously, the fructose-1,6-diphosphate-dependent L-(+)-lactate dehydrogenase gene of Streptococcus mutans JH1000 was cloned into Escherichia coli (J. D. Hillman, M. J. Duncan, and K. P. Stashenko, Infect. Immun. 58:1290-1295, 1990). In the present study, the nucleotide sequence of 1.29 kb of S. mutans DNA which contained the promoter and protein-coding region of the gene was determined. In vitro disruption of the gene was achieved by deletion of the promoter and a major portion of the protein-coding sequence. Subsequently, a tetracycline resistance gene from S. mutans was inserted at the deletion site as a marker for selection. In addition, evidence from Southern hybridization showed that S. mutans JH1000 contained a single copy of the lactate dehydrogenase gene. RP DUNCAN, MJ (reprint author), FORSYTH DENT CTR,DEPT MOLEC GENET,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE04529] NR 15 TC 19 Z9 20 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 NOV PY 1991 VL 59 IS 11 BP 3930 EP 3934 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GM530 UT WOS:A1991GM53000013 PM 1937751 ER PT J AU TEICHER, BA VARSHNEY, A KHANDEKAR, V HERMAN, TS AF TEICHER, BA VARSHNEY, A KHANDEKAR, V HERMAN, TS TI EFFECT OF HYPOXIA AND ACIDOSIS ON THE CYTOTOXICITY OF 6 METAL(LIGAND)4(RHODAMINE-123)2 COMPLEXES AT NORMAL AND HYPERTHERMIC TEMPERATURES SO INTERNATIONAL JOURNAL OF HYPERTHERMIA LA English DT Article DE TETRACHLOROPLATINATE; PH; HYPOXIA ID 4 PLATINUM COMPLEXES; MOUSE MAMMARY-TUMOR; RHODAMINE 123; CELLS; CIS-DIAMMINEDICHLOROPLATINUM(II); INVITRO; LETHALITY; ANTITUMOR; RESISTANT; INVIVO AB Several analogues of PtCl4(Rh-123)2 in which the metal may be Pt or Pd and the coordinated ligand may be -Cl, -CN or -NO2 were prepared and tested in cell culture with EMT-6 cells at normal (37-degrees-C) and hyperthermic (42-degrees-C and 43-degrees-C) temperatures and various environmental conditions (normally oxygenated vs. hypoxic and pH 7.40 vs. pH 6.45). Pd is a much more reactive metal than Pt, while -CN and -NO2 are more tightly bound ligands than is -Cl. The goal of these studies was to define the complex with the least cytotoxicity at 37-degrees-C and the greatest enhancement in cytotoxicity under hyperthermic conditions. The Pt complexes Pt(CN)4(Rh-123)2 and Pt(NO2)4(Rh-123)2 were much less cytotoxic than PtCl4(Rh-123)2 under both normothermic and hyperthermic conditions. The Pd complexes were, in general, more cytotoxic than the corresponding Pt complexes. The level of metal (Pt or Pd) in the cells did not appear to be a major factor in the level of cytotoxicity obtained. Complexes which were not cytotoxic at 37-degrees-C regardless of oxygenation level or pH did not become cytotoxic at hyperthermic temperatures. In conclusion, the optimal members of this series were the complexes with chloro ligands, indicating that aquation is probably a necessary step in the cytotoxic mechanism and cytotoxicity at 37-degrees-C was necessary to obtain cytotoxicity at higher temperatures. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01-CA47379, R01-CA36508] NR 26 TC 4 Z9 4 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0265-6736 J9 INT J HYPERTHER JI Int. J. Hyperthermia PD NOV-DEC PY 1991 VL 7 IS 6 BP 857 EP 868 DI 10.3109/02656739109056454 PG 12 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GQ184 UT WOS:A1991GQ18400005 PM 1806641 ER PT J AU HERMAN, TS TEICHER, BA HOLDEN, SA AF HERMAN, TS TEICHER, BA HOLDEN, SA TI ADDITION OF MITOMYCIN-C TO CIS-DIAMMINEDICHLOROPLATINUM(II)/HYPERTHERMIA RADIATION-THERAPY IN THE FSAIIC FIBROSARCOMA SO INTERNATIONAL JOURNAL OF HYPERTHERMIA LA English DT Article DE MITOMYCIN-C; CISPLATIN; CHEMOTHERAPY; RODENT TUMORS ID HYPOXIC TUMOR-CELLS; HAMSTER OVARY CELLS; CYTO-TOXICITY; CIS-DIAMMINEDICHLOROPLATINUM; MAMMALIAN-CELLS; FIBRO-SARCOMA; HYPERTHERMIA; INVITRO; INVIVO; CANCER AB Hyperthermia (temperatures greater-than-or-equal-to 42-degrees-C) is used clinically to improve the effectiveness of radiation therapy and, although therapeutic gains have been reported, efficacy is limited when tumours are large and/or radiation tolerance is reduced. In order to improve the utility of the hyperthermia/radiation combination we have tested the addition of cisplatin (CDDP) in the laboratory and in the clinic. Our clinical studies have shown that the CDDP/hyperthermia/radiation combination is tolerable and effective, but laboratory investigations demonstrated a relative lack of cytotoxicity in the hypoxic tumour subpopulation. In order to improve the effectiveness of the CDDP/hyperthermia/radiation combination against hypoxic cells we have evaluated the addition of mitomycin C, a hypoxic cell cytotoxic agent to this combination. Mitomycin C (5 mg/kg) i.p. produced a tumour growth delay (TGD) of about 5.3 days in the FSaIIC murine fibrosarcoma; hyperthermia (43-degrees-C x 30 min) caused only about 1.4 day TGD and the combination of mitomycin C followed immediately by hyperthermia caused a TGD of about 8.6 days. CDDP (5 mg/kg) i.p. followed by hyperthermia and then 3 Gy on day 1 only of a 5 day x 3 Gy radiation protocol produced a TGD of about 25 days. With the addition of mitomycin C just before CDDP a TGD of about 44 days resulted. Whole tumour excision experiments demonstrated that mitomycin C was highly interactive with CDDP at 37-degrees-C and was dose-modifying. When used with CDDP and hyperthermia, however, mitomycin C added little additional cytotoxicity. Hoechst 33342 dye diffusion-determined tumour subpopulation studies indicated a marked effect of the addition of mitomycin C in the dim (enriched in hypoxic cells) subpopulation and nearly equal cytotoxicity in both bright (enriched in euoxic cells) and dim cells resulted. These investigations suggest considerable potential therapeutic efficacy to the addition of mitomycin C to the CDDP/hyperthermia/radiation combination. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP HERMAN, TS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01-CA36508, R01-CA47379] NR 55 TC 6 Z9 6 U1 0 U2 4 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0265-6736 J9 INT J HYPERTHER JI Int. J. Hyperthermia PD NOV-DEC PY 1991 VL 7 IS 6 BP 893 EP 903 DI 10.3109/02656739109056457 PG 11 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GQ184 UT WOS:A1991GQ18400008 PM 1806643 ER PT J AU TEICHER, BA HOLDEN, SA RUDOLPH, MB SOTOMAYOR, EA HERMAN, TS AF TEICHER, BA HOLDEN, SA RUDOLPH, MB SOTOMAYOR, EA HERMAN, TS TI EFFECT OF ENVIRONMENTAL-CONDITIONS (PH, OXYGENATION AND TEMPERATURE) ON THE CYTOTOXICITY OF FLAVONE ACETIC-ACID AND ITS DIMETHYLAMINOETHYL ESTER SO INTERNATIONAL JOURNAL OF HYPERTHERMIA LA English DT Article DE FLAVONE ACETIC ACID; DIMETHYLAMINOETHYL-FLAVONE-8-ACETATE; HYPOXIA; HYPERTHERMIA; PH ID CYTO-TOXICITY; TUMOR-CELLS; COLON-38 TUMORS; FIBRO-SARCOMA; SOLID TUMORS; RADIATION; HYPERTHERMIA; THERAPY; ENHANCEMENT; NSC-347512 AB Bioflavonoids are known to inhibit enzymes in the glycolytic pathway and have been reported to decrease tumour blood flow. The antineoplastic capabilities of flavone acetic acid (FAA), dimethylaminoethyl-flavone-8-acetate (FAA ester) and quercitin (Q) as a function of pH, level of oxygenation and in conjunction with hyperthermia or SR-4233. In vitro, exposure of FSaIIC murine fibrosarcoma cells to various concentrations of FAA or FAA ester for 1 h demonstrated that both drugs were slightly more toxic toward hypoxic cells at 37-degrees-C and pH 7.40 (but were somewhat less cytotoxic at pH 6.45 and 37-degrees-C) than towards normally oxygenated cells. The cytotoxicity of FAA and FAA ester increased only minimally by concomitant treatment of cells at 42-degrees-C or 43-degrees-C. When temperatures of tumour-bearing mice anaesthetized with chloral hydrate and pentobarbital were measured both FAA (200 mg/kg) and Q (200 mg/kg) caused a more rapid drop in tumour versus core temperature, indicating a relative shutdown of tumour blood flow had been produced by these flavonoids. In Hoechst 33342 dye-defined subpopulations, both FAA and Q were only minimally cytotoxic in the subpopulation enriched in euoxic (bright) cells, producing surviving fractions of 0.70 and 0.29, respectively but were approximately 2-fold and 3-fold respectively more toxic towards the subpopulation enriched in hypoxic (dim) cells. When FAA preceded hyperthermia approximately a 3-4-fold increase in cell kill resulted from the combination in both subpopulations. Finally, when SR-4233, a selective hypoxic cell cytotoxic agent, was administered prior to FAA or Q and followed by hyperthermia the level of tumour cell killing increased so that the surviving fractions were 0.009 and 0.0055, respectively, in the dim cell subpopulation. These results indicate that FAA, FAA ester and Q may be most effectively used in a setting involving a combined modality regimen with a focus on the hypoxic tumour cell subpopulation. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01-CA47379] NR 43 TC 1 Z9 1 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0265-6736 J9 INT J HYPERTHER JI Int. J. Hyperthermia PD NOV-DEC PY 1991 VL 7 IS 6 BP 905 EP 915 DI 10.3109/02656739109056458 PG 11 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GQ184 UT WOS:A1991GQ18400009 PM 1806644 ER PT J AU SUIT, HD HALL, EJ AF SUIT, HD HALL, EJ TI DEDICATION TO ELLIS,FRANK SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Item About an Individual C1 COLUMBIA UNIV,CTR RADIOL RES,NEW YORK,NY 10032. RP SUIT, HD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD NOV PY 1991 VL 21 IS 6 BP 1399 EP 1401 PG 3 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GR727 UT WOS:A1991GR72700001 PM 1938547 ER PT J AU SUIT, H DUBOIS, W AF SUIT, H DUBOIS, W TI THE IMPORTANCE OF OPTIMAL TREATMENT PLANNING IN RADIATION-THERAPY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE IMPROVED DOSE DISTRIBUTION; TUMOR CONTROL PROBABILITY; RADIATION DOSE; GAMMA-50; RADIATION COMPLICATIONS ID BREAST-CARCINOMA; CERVICAL-CANCER; UTERINE CERVIX; TUMOR-CONTROL; SOFT-TISSUE; IRRADIATION; SARCOMA; COMPLICATIONS; PROSTATE; SURVIVAL AB There are two classes of failure in radiation therapy: local control not achieved and radiation-induced morbidity. Technical developments which permit the employment of treatment volumes which achieve a closer approximation to the target volume can confidently be asserted to yield clinical gains in terms of higher tumor control rates and/or reduced severity/frequency of radiation induced morbidity. The magnitude of the gains and the cost and effort to realize those gains may need to be assessed by the technique of the "clinical trial." Such gains will be the consequence of a higher dose to the target and/or the irradiation of smaller volumes of non-target tissues. An important fact is that unirradiated tissues do not develop radiation-related injury. Selected categories of radiation injuries that appear in non-target tissues are here reviewed. Valuable advances in the technology of radiation therapy are virtually certain for the near term. This bodes well, indeed, for our future patients. RP SUIT, H (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 51 TC 28 Z9 28 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD NOV PY 1991 VL 21 IS 6 BP 1471 EP 1478 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GR727 UT WOS:A1991GR72700009 PM 1938555 ER PT J AU ABE, Y URANO, M KENTON, LA KAHN, J WILLET, CG AF ABE, Y URANO, M KENTON, LA KAHN, J WILLET, CG TI THE ACCELERATED REPOPULATION OF A MURINE FIBROSARCOMA, FSA-II, DURING THE FRACTIONATED-IRRADIATION AND THE LINEAR-QUADRATIC MODEL SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE REPOPULATION; ACCELERATED REPOPULATION; FRACTIONATION; L-Q MODEL; ALPHA/BETA-RATIO; FSA-II TUMOR ID REPAIR CAPACITY; DOSE FRACTIONS; FIBRO-SARCOMA; X-RAYS; SURVIVAL; RADIATION; HYPERFRACTIONATION; RESPONSES; RECOVERY; NUMBER AB Radiation response of a spontaneous mouse fibrosarcoma, FSa-II, to various fractionated doses was studied in vivo together with single dose cell survival curves. Early generation isotransplants were used. Animals were C3Hf/Sed mice derived from our defined flora mouse colony. Lung colony and TD50 assays were used to determine cell survival. Surviving fractions were determined following fractionated irradiations of 1.0 to 5.0 Gy each per fraction with interfractional time intervals of 4 hr. The alpha/beta ratio based on fractionated irradiations was 8.8 Gy for aerobic FSa-II tumor cells and flexure dose was less than 1.3 Gy. Multiple fractions of 5.0 Gy each given with 4, 12, and 24 hr intervals showed an increase in survival with increasing interfractional time interval, suggesting a rapid repopulation of tumor cells between fractions; namely, cell doubling time was shortened between fractions after the first 5.0 Gy doses. These results indicated that tumor cell repopulation is a critical factor in the fractionated radiotherapy. Linear-quadratic model was fitted to single dose survival data. Single dose survival curve of aerobic FSa-II tumor cells following lung colony assays which allowed determination of minimal survival of approximately 3.0 x 10(-3) showed that alpha, beta, and alpha/beta ratios were 0.25 Gy-1, 0.048 Gy-2, and 8.47 Gy, respectively. Single dose survival curve of the same aerobic cells determined by both lung colony and TD50 assays to a survival level of approximately 3.0 x 10(-6) demonstrated that alpha, beta, and alpha/beta ratios were 0.375, 0.0127, and 29.5, respectively. Similar determination for hypoxic FSa-II tumor cells showed that alpha, beta values were smaller whereas the alpha/beta ratio was much larger than for aerobic cells. The oxygen enhancement ratio calculated by the alpha/beta ratios was greater than 3.0. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,EDWIN L STEELE LAB,BOSTON,MA 02114. FU NCI NIH HHS [CA 26350] NR 24 TC 13 Z9 13 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD NOV PY 1991 VL 21 IS 6 BP 1529 EP 1534 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GR727 UT WOS:A1991GR72700017 PM 1938563 ER PT J AU SOUGAWA, M URANO, M AF SOUGAWA, M URANO, M TI SIGNIFICANCE OF ADDITIVE HEAT EFFECT IN THE THERAPEUTIC GAIN FACTOR IN COMBINED HYPERTHERMIA AND RADIOTHERAPY - MURINE TUMOR RESPONSE AND FOOT REACTION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE THERMAL ENHANCEMENT RATIO; THERAPEUTIC GAIN FACTOR; MOUSE TUMOR; COMBINED RADIATION AND HYPERTHERMIA; HYPERTHERMIA; NORMAL TISSUE ID HYPOXIC CELL FRACTION; X-RAYS; RADIATION; MOUSE; PH; INVIVO; ENHANCEMENT; TISSUE; HYPERGLYCEMIA; ACIDITY AB The thermal enhancement ratio (TER) and therapeutic gain factor (TGF) were evaluated for combined hyperthermia and radiation treatments of a murine fibrosarcoma, FSa-II. The TER is the ratio of the radiation dose that induces a given reaction without hyperthermia to that with hyperthermia. The TGF is defined as the ratio of TER for tumor response to TER for normal tissue response. Tumors in the subcutaneous tissue of the right foot were irradiated with graded radiation doses when they reached an average diameter of 6 mm (110 mm3). Hyperthermia was given by immersing animal feet in a constant temperature water bath 10 min before or after irradiation. The tumor growth time to reach 500 mm3 was obtained for each tumor and the median tumor growth time was calculated for each treatment group. For the normal tissue study, the non-tumor bearing murine foot was treated, as was the tumor, and the foot reaction was scored after treatment, according to our numerical score system for radiation damage, until the 35th post-treatment day and averaged. Using the fraction of animals showing a given average foot reaction score in a treatment group, the RD50, or the radiation dose to induce the given foot reaction or greater, was calculated. A single heating at 45.5-degrees-C for 10 min and a step-down heating (first heat 45.5-degrees-C for 10 min immediately followed by the second heat at 41.5-degrees-C for 60 min) prolonged the tumor growth time, indicating that hyperthermia per se resulted in some cell killing. The prolongation was greater following step-down heating than following single heating. These heat treatments alone induced no noticeable heat damage on the foot, but decreased the threshold dose observed on the radiation dose response curves for the foot reaction. Accordingly, TER and TGF were evaluated with or without normalizing this thermal effect. TER's for both tumor and foot responses without normalization were greater than the TER's after normalization and decreased with increasing radiation dose (between 1.9 and 7.1 or greater for tumor and between 1.3 and 4.3 or greater for foot reaction), whereas the normalized TER's were relatively constant (between 1.6 and 1.7 for tumor and between 0.7 and 1.5 for foot reaction). TGF's without normalization were greater than those obtained after normalization. The former was large at small doses and decreased with increasing radiation dose (between 1.5 and 4.0 or greater), whereas the latter was within 0.8 and 1.3 and relatively independent of radiation dose. TGF's following step-down heating were greater than the TGF following single heating (> 3.0 and between 1.5 and 2.0 for SDH and single heating given before radiation). This greater non-normalized TGF is likely due to the additive effect of hyperthermia, that is, due to the greater thermal effect on the tumor than the normal foot. Similarly, greater TGF's following step-down heating may be due to greater damage, induced by this heating, to the tumor. TGF following hyperthermia given before or after radiation appeared to depend on the heat dose applied. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,EDWIN L STEELE LAB,BOSTON,MA 02114. FU NCI NIH HHS [CA26350] NR 37 TC 2 Z9 2 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD NOV PY 1991 VL 21 IS 6 BP 1561 EP 1568 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GR727 UT WOS:A1991GR72700021 PM 1938566 ER PT J AU HALLAHAN, DE VIRUDACHALAM, S BECKETT, M SHERMAN, ML KUFE, D WEICHSELBAUM, RR AF HALLAHAN, DE VIRUDACHALAM, S BECKETT, M SHERMAN, ML KUFE, D WEICHSELBAUM, RR TI MECHANISMS OF X-RAY-MEDIATED PROTOONCOGENE C-JUN EXPRESSION IN RADIATION-INDUCED HUMAN SARCOMA CELL-LINES SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Note DE X-RAY-MEDIATED GENE EXPRESSION; C-JUN PROTOONCOGENE; RADIATION-INDUCED HUMAN SARCOMAS ID PROTEIN KINASE-C; ONCOGENE; INHIBITORS; AP-1; ACTIVATION; ENCODES; INVITRO; RNA AB c-jun is a protooncogene associated with neoplastic transformation and is transcriptionally induced by ionizing radiation. To examine the possible mechanisms of radiation-induced c-jun transcription, we analyzed RNA from human tumor cell lines RIT-3 and STSAR-5 following x-irradiation in the presence of protein kinase inhibitors, or the absence of serum and calcium. Protoonocogene c-jun expression increased several fold following irradiation of these radiation-induced human sarcoma cell lines. The expression of c-jun was not altered following irradiation in conditioned medium containing serum as compared to that of cells in serum free medium. Depletion of PKC by prolonged TPA treatment resulted in inhibition of c-jun expression. In addition, nonspecific protein kinase inhibitors, staurosporin and H7 attenuated c-jun expression, whereas the analogue of ATP (sangivamycin) did not. Furthermore, the selective inhibitor of cAMP dependent protein kinase HA 1004 did not alter radiation-mediated c-jun induction. These data indicate that ionizing radiation exposure results in c-jun induction which is dependent upon the activation of PKC. Protein kinase C activation and the subsequent expression of the protooncogene c-jun by ionizing radiation may further define the molecular mechanisms of radiation-induced neoplastic transformation. C1 UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. PRITZKER SCH MED,CHICAGO,IL. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA 41068] NR 27 TC 37 Z9 37 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD NOV PY 1991 VL 21 IS 6 BP 1677 EP 1681 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GR727 UT WOS:A1991GR72700040 PM 1801783 ER PT J AU BRASCH, RC CAVAGNA RUMMENY, E BERNARDINO, ME LASSER, EC HIGGINS, CB PAVONE ROCKLAGE, S KORMANO, M VEXLER, VS PATRIZIO DEHAEN, C LAUFFER WHITE, DH TWEEDLE, MF BARNHART, TL STARK, DD MATTREY, RF AF BRASCH, RC CAVAGNA RUMMENY, E BERNARDINO, ME LASSER, EC HIGGINS, CB PAVONE ROCKLAGE, S KORMANO, M VEXLER, VS PATRIZIO DEHAEN, C LAUFFER WHITE, DH TWEEDLE, MF BARNHART, TL STARK, DD MATTREY, RF TI MAGNETIC-RESONANCE FOR LIVER IMAGING - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 UNIV CALIF SAN FRANCISCO, DEPT RADIOL, CONTRAST MEDIA LAB, SAN FRANCISCO, CA 94143 USA. UNIV MUNSTER, DEPT RADIOL, W-4400 MUNSTER, GERMANY. EMORY UNIV, SCH MED, ATLANTA, GA 30322 USA. UNIV CALIF SAN DIEGO, SCH MED, DEPT RADIOL, LA JOLLA, CA 92093 USA. UNIV CALIF SAN FRANCISCO, DEPT RADIOL, SAN FRANCISCO, CA 94143 USA. SALUTAR INC, SUNNYVALE, CA USA. UNIV TURKU, DEPT DIAGNOST RADIOL, SF-20520 TURKU 52, FINLAND. ACAD SCI USSR, INST CHEM PHYS, MOSCOW V-71, USSR. BRACCO IND CHIM SPA, DIV RES & DEV, MILAN, ITALY. UNIV CALIF SAN FRANCISCO, DEPT RADIOL, SAN FRANCISCO, CA 94143 USA. BRISTOL MYERS SQUIBB PHARMACEUT RES INST, DEPT CONTRAST MEDIA, NEW BRUNSWICK, NJ USA. MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. MOLEC BIOSYST INC, SAN DIEGO, CA USA. UNIV CALIF SAN DIEGO, LA JOLLA, CA 92093 USA. NR 0 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 NOV PY 1991 VL 26 SU 1 BP S150 EP S155 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600052 ER PT J AU DAWSON, P JANOFF, AS SCHLIEF, R DEHAEN, C GRABOWSKI WOLF, GL MORRIS, TW MATTREY, RF LIPTON, MJ WIDDER HOLTZ LASSER, EC FLAIM, SF SCHNEIDER SCHLIEF, R VIOLANTE, MR HARNISH PARVEZ BARNHART, JL FRITZZIEROTH, B AF DAWSON, P JANOFF, AS SCHLIEF, R DEHAEN, C GRABOWSKI WOLF, GL MORRIS, TW MATTREY, RF LIPTON, MJ WIDDER HOLTZ LASSER, EC FLAIM, SF SCHNEIDER SCHLIEF, R VIOLANTE, MR HARNISH PARVEZ BARNHART, JL FRITZZIEROTH, B TI ULTRASOUND CONTRAST AGENTS - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 SINTET SA,GENEVA,SWITZERLAND. LIPOSOME CO INC,PRINCETON,NJ. BRACCO IND CHIM SPA,DIV RES & DEV,MILAN,ITALY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. UNIV ROCHESTER,MED CTR,DEPT RADIOL,ROCHESTER,NY 14642. UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. UNIV CHICAGO,DEPT RADIOL,CHICAGO,IL 60637. SCHERING AG,CLIN DEV DIAGNOST,BERLIN,GERMANY. UNIV ROCHESTER,DEPT RADIOL,ROCHESTER,NY 14627. UNIV ROCHESTER,CTR BIOMED ULTRASOUND,ROCHESTER,NY 14627. MOLEC BIOSYST INC,SAN DIEGO,CA. NIHON SCHERING KK,RES DEPT,OSAKA,JAPAN. UNIV CALIF SAN DIEGO,SCH MED,DEPT RADIOL,LA JOLLA,CA 92093. ALLIANCE PHARMACEUT CORP,DIV PHARMACOL TOXICOL,SAN DIEGO,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S198 EP S200 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600069 ER PT J AU FISCHER KORMANO, T KRAUSE, W WOLF, GL WIDDER SELTZER, SE GRABOWSKI, EF JANOFF, AS KATZBERG, RW BRASCH, RC SPECK, U SCHNEIDER, M MATTREY, RF HOPKINS AF FISCHER KORMANO, T KRAUSE, W WOLF, GL WIDDER SELTZER, SE GRABOWSKI, EF JANOFF, AS KATZBERG, RW BRASCH, RC SPECK, U SCHNEIDER, M MATTREY, RF HOPKINS TI IODINATED LIPOSOMAL AGENTS - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 UNIV TURKU,DEPT DIAGNOST RADIOL,SF-20520 TURKU 52,FINLAND. SCHERING AG,SBU DIAGNOST,BERLIN,GERMANY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. CORNELL UNIV,MED CTR,NEW YORK,NY 10021. LIPOSOME CO INC,PRINCETON,NJ. UNIV ROCHESTER,MED CTR,DEPT RADIOL,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT MED,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT UROL,ROCHESTER,NY 14642. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,CONTRAST MEDIA LAB,SAN FRANCISCO,CA 94143. SINTET SA,GENEVA,SWITZERLAND. UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. RI Krause, Werner/A-7350-2009 OI Krause, Werner/0000-0002-5397-9430 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 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S175 EP S176 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600060 ER PT J AU GOLDSTEIN ROCKLAGE, S KOENIG, SH HIGGINS, CB FRITZZIEROTH, B WOLF, GL DAWSON, P NIEMI, P AF GOLDSTEIN ROCKLAGE, S KOENIG, SH HIGGINS, CB FRITZZIEROTH, B WOLF, GL DAWSON, P NIEMI, P TI MAGNETIC-RESONANCE AGENTS FOR THE BRAIN - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 SALUTAR INC,SUNNYVALE,CA. IBM CORP,THOMAS J WATSON RES CTR,YORKTOWN HTS,NY 10598. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,SAN FRANCISCO,CA 94143. NIHON SCHERING KK,RES DEPT,OSAKA,JAPAN. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. UNIV TURKU,DEPT DIAGNOST RADIOL,SF-20520 TURKU 52,FINLAND. 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 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S253 EP S254 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600087 ER PT J AU GOLMAN CAVAGNA LIPTON, MJ HIGGINS, CB WOLF, GL BRASCH, RC KOENIG, SH JANOFF, AS JOSEPHSON, L AF GOLMAN CAVAGNA LIPTON, MJ HIGGINS, CB WOLF, GL BRASCH, RC KOENIG, SH JANOFF, AS JOSEPHSON, L TI NEWER MAGNETIC-RESONANCE-IMAGING AGENTS AND TECHNIQUES - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 UNIV CHICAGO,DEPT RADIOL,CHICAGO,IL 60637. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,SAN FRANCISCO,CA 94143. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,CONTRAST MEDIA LAB,SAN FRANCISCO,CA 94143. IBM CORP,THOMAS J WATSON RES CTR,YORKTOWN HTS,NY 10598. LIPOSOME CO INC,PRINCETON,NJ. ADV MAGNET INC,CAMBRIDGE,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 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S263 EP S265 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600091 ER PT J AU SOVAK, M NORMAN, A WOLF, GC DEHAEN, C SPECK, U NIENDORF, HP KATZBERG, RW AF SOVAK, M NORMAN, A WOLF, GC DEHAEN, C SPECK, U NIENDORF, HP KATZBERG, RW TI STATE-OF-THE-ART PRESENTATIONS - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 UNIV CALIF SAN DIEGO,SCH MED,DEPT RADIOL,LA JOLLA,CA 92093. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. BRACCO IND CHIM SPA,DIV RES & DEV,MILAN,ITALY. SCHERING AG,SBU DIAGNOST,BERLIN,GERMANY. SCHERING AG,CLIN DEV DIAGN,BERLIN,GERMANY. UNIV ROCHESTER,MED CTR,DEPT RADIOL,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT MED,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT UROL,ROCHESTER,NY 14642. 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 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S15 EP S15 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600005 ER PT J AU TANIMOTO, A STARK, DD AF TANIMOTO, A STARK, DD TI CELL-SPECIFIC CONTRAST AGENTS FAIL TO DETECT HEPATITIS SO INVESTIGATIVE RADIOLOGY LA English DT Article; Proceedings Paper CT SYMP ON CONTRAST MEDIA RESEARCH ( CMR 91 ) CY JUL 08-12, 1991 CL CAMBRIDGE, ENGLAND SP BRACCO IND CHIM, BRISTOL MYERS SQUIBB PHARM, LAB GUERBET, MALLINCKRODT MED, NYCOMED, SCHERING, STERLING WINTHROP PHARM, ADV MAGNET, ALLIANCE PHARM, BERLEX LABS ID SUPERPARAMAGNETIC IRON-OXIDE; RESONANCE C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. NR 10 TC 3 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S139 EP S141 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600048 PM 1667002 ER PT J AU TWEEDLE, M ADZAMLI, IK LIPTON, MJ HIGGINS, CB WOLF, GL CARVLIN, M ADAMS, DF BRASCH, RC AF TWEEDLE, M ADZAMLI, IK LIPTON, MJ HIGGINS, CB WOLF, GL CARVLIN, M ADAMS, DF BRASCH, RC TI CARDIAC MAGNETIC-RESONANCE-IMAGING AGENTS - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 BRISTOL MYERS SQUIBB PHARMACEUT RES INST,NEW BRUNSWICK,NJ. UNIV MASSACHUSETTS,MED CTR,DEPT RADIOL,WORCESTER,MA 01605. UNIV MASSACHUSETTS,MED CTR,DEPT NUCL MED,WORCESTER,MA 01605. UNIV CHICAGO,DEPT RADIOL,CHICAGO,IL 60637. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,SAN FRANCISCO,CA 94143. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. SQUIBB DIAGNOST,PRINCETON,NJ. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,CONTRAST MEDIA LAB,SAN FRANCISCO,CA 94143. 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 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S245 EP S247 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600084 ER PT J AU WATSON, A NIENDORF, HP TWEEDLE, M WOLF, GL PARVEZ BRASCH, RC CARVLIN, M ANDREW, E GRABOWSKI, EF MEYER, D ADAMS, DF RANGANATHAN, RS WATSON FRITZZIEROTH, B SPECK, U DEHAEN, C WHITE, D KOENIG, SH HIGGINS, CB ADJAMLI LAUFFER MORRIS, TW NORMAN, A AF WATSON, A NIENDORF, HP TWEEDLE, M WOLF, GL PARVEZ BRASCH, RC CARVLIN, M ANDREW, E GRABOWSKI, EF MEYER, D ADAMS, DF RANGANATHAN, RS WATSON FRITZZIEROTH, B SPECK, U DEHAEN, C WHITE, D KOENIG, SH HIGGINS, CB ADJAMLI LAUFFER MORRIS, TW NORMAN, A TI LANTHANIDE CHELATES - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 SALUTAR INC,SUNNYVALE,CA. SCHERING AG,CLIN RES DIAGNOST,BERLIN,GERMANY. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,DEPT CONTRAST MEDIA,NEW BRUNSWICK,NJ. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,CONTRAST MEDIA LAB,SAN FRANCISCO,CA 94143. SQUIBB DIAGNOST,PRINCETON,NJ. NYCOMED AS,CLIN RES & DEV,OSLO,NORWAY. CORNELL UNIV,MED CTR,NEW YORK,NY 10021. LAB GUERBET,AULNAY SOUS BOIS,FRANCE. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. NIHON SCHERING KK,RES DEPT,OSAKA,JAPAN. SCHERING AG,SBU DIAGNOST,BERLIN,GERMANY. BRACCO IND CHIM SPA,DIV RES & DEV,MILAN,ITALY. MALLINCKRODT MED INC,DIV SCI & TECHNOL,ST LOUIS,MO. IBM CORP,THOMAS J WATSON RES CTR,YORKTOWN HTS,NY 10598. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,SAN FRANCISCO,CA 94143. UNIV ROCHESTER,MED CTR,DEPT RADIOL,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT MED,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT UROL,ROCHESTER,NY 14642. UNIV CALIF LOS ANGELES,JONSSON COMPREHENS CANC CTR,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT RADIOL SCI,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT RADIAT ONCOL,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S232 EP S235 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600080 ER PT J AU WOLF, GL HALPERN, E AF WOLF, GL HALPERN, E TI NEW METHODS FOR COST-PERFORMANCE ASSESSMENT IN DIAGNOSTIC-IMAGING SO INVESTIGATIVE RADIOLOGY LA English DT Article; Proceedings Paper CT SYMP ON CONTRAST MEDIA RESEARCH ( CMR 91 ) CY JUL 08-12, 1991 CL CAMBRIDGE, ENGLAND SP BRACCO IND CHIM, BRISTOL MYERS SQUIBB PHARM, LAB GUERBET, MALLINCKRODT MED, NYCOMED, SCHERING, STERLING WINTHROP PHARM, ADV MAGNET, ALLIANCE PHARM, BERLEX LABS C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 1 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S12 EP S14 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600004 PM 1808105 ER PT J AU WOLF, GL BROWN, DC LASSER, EC MATTREY, RF BRASCH, RC DEHAEN, C ANDREW, E HOPKINS AF WOLF, GL BROWN, DC LASSER, EC MATTREY, RF BRASCH, RC DEHAEN, C ANDREW, E HOPKINS TI CLINICAL-TRIALS OF NEWER IODINATED AGENTS - DISCUSSION SO INVESTIGATIVE RADIOLOGY LA English DT Discussion C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. WINTHROP PHARMACEUT,DEPT MED,NEW YORK,NY. UNIV CALIF SAN DIEGO,SCH MED,DEPT RADIOL,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,CONTRAST MEDIA LAB,SAN FRANCISCO,CA 94143. BRACCO IND CHIM SPA,DIV RES & DEV,MILAN,ITALY. NYCOMED AS,CLIN RES & DEV,OSLO,NORWAY. 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 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD NOV PY 1991 VL 26 SU 1 BP S208 EP S208 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ306 UT WOS:A1991GQ30600072 ER PT J AU DAVIES, JP HARRIS, WH AF DAVIES, JP HARRIS, WH TI EFFECT OF HAND MIXING TOBRAMYCIN ON THE FATIGUE-STRENGTH OF SIMPLEX-P SO JOURNAL OF BIOMEDICAL MATERIALS RESEARCH LA English DT Article ID ACRYLIC BONE CEMENTS; MECHANICAL-PROPERTIES AB In a recent study, we showed that the presence of gentamicin in Palacos R or erythromycin plus colistin in Simplex P bone cement did not significantly decrease the fatigue strength of the cement. [J.P. Davies, D.0. O'Connor, D.W. Burke, and W.H. Harris, "Influence of antibiotic impregnation on the fatigue life of Simplex P and Palacos R acrylic bone cements, with and without centrifugation," J. Biomed. Mater. Res., 23, 379-397 (1989)] However, the commercially prepared Palacos R with Gentamicin and AKZ (Simplex P with colistin and erythromycin) which were tested are not approved by the FDA for use in the United States. Because of this, many surgeons in the United States hand mix tobramycin with the cement in the operating room if a case calls for the use of antibiotic-impregnated cement. In this study, we determined the effect of adding 1.2 g of tobramycin to one pack (40 g) of Simplex P powder on the fatigue strength of the cement. The effect of centrifugation on the fatigue strength of Simplex P with the tobramycin added was also assessed. Simplex P was prepared according to the manufacturer's instructions with and without the addition of 1.2 g tobramycin per 40-g pack and with and without centrifugation. Fifteen specimens of each of the four cement preparations were tested in fully reversed tension-compression fatigue at +/-15 MPa, 2 Hz. The fatigue strength of the uncentrifuged and centrifuged Simplex P was not significantly reduced by the tobramycin. Centrifugation significantly increased the fatigue life of Simplex P both with and without the addition of tobramycin. The fatigue life of the Simplex P with tobramycin was increased by a factor of 8 by centrifugation. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 12 TC 34 Z9 34 U1 0 U2 2 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9304 J9 J BIOMED MATER RES JI J. Biomed. Mater. Res. PD NOV PY 1991 VL 25 IS 11 BP 1409 EP 1414 DI 10.1002/jbm.820251108 PG 6 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA GK545 UT WOS:A1991GK54500007 PM 1797811 ER PT J AU BACHHAWAT, AK PILLAI, S AF BACHHAWAT, AK PILLAI, S TI DISTINCT INTRACELLULAR FATES OF MEMBRANE AND SECRETORY IMMUNOGLOBULIN HEAVY-CHAINS IN A PRE-B CELL-LINE SO JOURNAL OF CELL BIOLOGY LA English DT Article ID ANTIGEN RECEPTOR CHAINS; SURFACE MU-CHAIN; ENDOPLASMIC-RETICULUM; BINDING-PROTEIN; BREFELDIN-A; LIGHT CHAIN; GOLGI DEGRADATION; EXPRESSION; TRANSPORT; GENE AB The intracellular fates of membrane and secretory immunoglobulin heavy chains were examined in a pre-B cell line that has switched to the gamma-isotype. The membrane form of the heavy chain (gamma-m) was rapidly degraded while the secretory form (gamma-s) was retained intracellularly in association with BiP. The degradation of gamma-m could not be inhibited by ammonium chloride, chloroquine, or monensin suggesting that it occurred in a nonlysosomal compartment. The inability to detect any Endo H-resistant form of gamma-m before its degradation suggested that degradation occurs before entry into the Golgi compartment. Degradation of gamma-m could be inhibited by incubation at 24-degrees-C. In a derivative of this cell line expressing a transfected kappa gene, gamma-s formed disulfide linked tetramers with kappa and was secreted, while gamma-m, although associated with kappa, continued to be rapidly degraded. These observations suggest that membrane and secretory heavy chain proteins are retained by distinct intracellular mechanisms. Although masking of the CH1 domain abrogates gamma-s retention, this domain does not influence the intracellular fate of gamma-m. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP BACHHAWAT, AK (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC IMMUNOL LAB,MOLEC GENET GRP,BOSTON,MA 02129, USA. FU NIAID NIH HHS [AI-27385] NR 51 TC 14 Z9 14 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD NOV PY 1991 VL 115 IS 3 BP 619 EP 624 DI 10.1083/jcb.115.3.619 PG 6 WC Cell Biology SC Cell Biology GA GM780 UT WOS:A1991GM78000005 PM 1918156 ER PT J AU CARPEN, O DUSTIN, ML SPRINGER, TA SWAFFORD, JA BECKETT, LA CAULFIELD, JP AF CARPEN, O DUSTIN, ML SPRINGER, TA SWAFFORD, JA BECKETT, LA CAULFIELD, JP TI MOTILITY AND ULTRASTRUCTURE OF LARGE GRANULAR LYMPHOCYTES ON LIPID BILAYERS RECONSTITUTED WITH ADHESION RECEPTORS LFA-1, ICAM-1, AND 2 ISOFORMS OF LFA-3 SO JOURNAL OF CELL BIOLOGY LA English DT Article ID NATURAL-KILLER CELLS; FUNCTION-ASSOCIATED ANTIGEN-3; SHEEP ERYTHROCYTE RECEPTOR; IMMUNE-SYSTEM; ENDOTHELIAL-CELLS; MOLECULE-1 ICAM-1; CD2; ACTIVATION; SURFACE; PROTEIN AB Large granular lymphocytes, mediators of NK activity, bind to other cells using both the LFA (lymphocyte function-associated)-1-ICAM and the CD2-LFA-3 adhesion pathways. Here we have studied the motility and ultrastructure of large granule lymphocyte (LGL) on lipid bilayers containing purified LFA-1, ICAM-1, and the transmembrane and glycophosphatidylinositol isoforms of LFA-3. LGLs moved at 8-mu-m/min on ICAM-1 but poorly (< 1 mu-m/min) on its receptor pair LFA-1. TM-LFA-3 promoted locomotion at a rate close to ICAM-1, whereas the cells were less motile on GPI-LFA-3. The difference in the rates of locomotion on the two isoforms of LFA-3 is presumably attributable to their difference in anchoring and lateral mobility in the bilayer. In spite of the variation in motility the ultra-structure of the adhering cells was similar on all four ligands. LGLs contacted the membrane variably, i.e., cells adhering only in a few small areas or in larger areas were detected on each ligand. The relative percentage of the plasma membrane facing the lipid bilayer was greatest on ICAM-1 and least on the transmembrane isoform of LFA-3, demonstrating no correlation with motility. The ratio of adjacent plasma membrane to lipid bilayer was virtually constant for all four ligands. Activation of the LGLs with a combination of CD2 mAb T11(2) and T11(3) (T11(2/3) mAb) reduced the movement on ICAM-1 and virtually immobilized the cells on the other bilayers. In the presence of T11(2/3) mAb, the area of cell membrane attaching to bilayers containing ICAM-1 and GPI-LFA-3 was decreased and the percentage of plasma membrane facing other cells was increased. No preferential orientation of the Golgi apparatus or degranulation was detected in the absence or presence of T11(2/3) mAb, but a significantly lower percentage of LGLs on ICAM-1 contained a profile of the Golgi apparatus after exposure to T11(2/3) mAb. The results demonstrate that the motility of LGLs depends on the type of receptor in the opposing bilayer, the receptor mobility in the bilayer, and the activation of the cells. The ultrastructure of LGLs binding to any of the adhesion molecules does not have the characteristics of LGLs in cytolytic contact with target cells, suggesting that the mediation of an attack on a target requires more complex stimulus than any one of the single adhesion proteins tested here. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CHANNING LABS,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. RP CARPEN, O (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA31798]; NIADDK NIH HHS [AM36308]; NIAID NIH HHS [AI23083] NR 46 TC 31 Z9 31 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD NOV PY 1991 VL 115 IS 3 BP 861 EP 871 DI 10.1083/jcb.115.3.861 PG 11 WC Cell Biology SC Cell Biology GA GM780 UT WOS:A1991GM78000025 PM 1717493 ER PT J AU NEUHAUS, H HU, MCT HEMLER, ME TAKADA, Y HOLZMANN, B WEISSMAN, IL AF NEUHAUS, H HU, MCT HEMLER, ME TAKADA, Y HOLZMANN, B WEISSMAN, IL TI CLONING AND EXPRESSION OF CDNAS FOR THE ALPHA-SUBUNIT OF THE MURINE LYMPHOCYTE-PEYERS PATCH ADHESION MOLECULE SO JOURNAL OF CELL BIOLOGY LA English DT Article ID AMINO-ACID SEQUENCE; PRE-MESSENGER RNA; NODE HOMING RECEPTOR; VONWILLEBRAND-FACTOR; INTERACTION DOMAINS; INTEGRIN VLA-4; CELL-CELL; FIBRONECTIN; GLYCOPROTEIN; HOMOLOGY AB cDNA clones encoding the ce chain of the murine lymphocyte-Peyer's patch adhesion molecule (LPAM), which is associated with lymphocyte homing, have been isolated by screening with the human VLA-4 (alpha-4h) probe. Several alpha-4 antigenic determinants were identified on COS-7 cells after transfection. From overlapping clones, approximately 5 kb of contiguous nucleotide sequence have been determined, encoding a protein sequence of 1039 amino acids for the LPAM alpha-chain (alpha-4m). LPAM is a member of the integrin family of cell-surface heterodimers, and alpha-4m is the murine homologue of the human alpha-4h chain. The two proteins have a total sequence similarity of 84%, with an almost perfect conservation (31/32 amino acids) in the cytoplasmic domain. Like alpha-4h, alpha-4m is distinct from other integrin alpha-chains because it has neither an I-domain nor a COOH-terminal cleavage site. The positions of the characteristic Cysteine residues are conserved, and a putative protease cleavage site is located near the middle of the protein sequence. The NH2-terminal part of the protein contains seven homologous repeats, and three of them include putative divalent cation-binding sites. These sites are among the most conserved between the alpha-4m sequence and other ce chains, and may therefore be involved in the binding of integrin alpha and beta-chains, An additional cDNA clone was isolated which shares a sequence of perfect homology with the alpha-4m encoding CDNAS, but has a unique 3' poly-A end. This observation correlates with the fact that three discrete murine RNA bands are observed in Northern blot experiments using alpha-4m as a probe, whereas only two human RNA species are described for alpha-4h, indicating a higher complexity for murine than for human sequences. C1 STANFORD UNIV,MED CTR,SCH MED,DEPT PATHOL,EXPTL ONCOL LAB,STANFORD,CA 94305. STANFORD UNIV,MED CTR,SCH MED,HOWARD HUGHES MED INST,STANFORD,CA 94305. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. OI takada, yoshikazu/0000-0001-5481-9589 FU NCI NIH HHS [CA 42551]; NIAID NIH HHS [AI 19512]; NIGMS NIH HHS [GM 38903] NR 44 TC 53 Z9 55 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD NOV PY 1991 VL 115 IS 4 BP 1149 EP 1158 DI 10.1083/jcb.115.4.1149 PG 10 WC Cell Biology SC Cell Biology GA GP802 UT WOS:A1991GP80200024 PM 1840602 ER PT J AU KROLL, MH HARRIS, TS MOAKE, JL HANDIN, RI SCHAFER, AI AF KROLL, MH HARRIS, TS MOAKE, JL HANDIN, RI SCHAFER, AI TI VONWILLEBRAND-FACTOR BINDING TO PLATELET GPIB INITIATES SIGNALS FOR PLATELET ACTIVATION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE THROMBOSIS; ADHESION; PHOSPHOLIPASES; PROTEIN KINASE-C; CALCIUM ID MURINE MONOCLONAL-ANTIBODY; GLYCOPROTEIN-IIB/IIIA COMPLEX; VWF MULTIMERS; FACTOR-VIII; AGGREGATION; CELLS; FIBRINOGEN; INHIBITORS; METABOLISM; PROTEINS AB The hypothesis that von Willebrand factor (vWF) binding to platelet membrane glycoprotein Ib (GpIb) initiates intracellular pathways of platelet activation was studied. We measured the biochemical responses of intact human platelets treated with ristocetin plus vWF multimers purified from human cryo-precipitate. vWF plus ristocetin causes the breakdown of phosphatidylinositol 4,5-bisphosphate, the production of phosphatidic acid (PA), the activation of protein kinase C (PKC), increase of ionized cytoplasmic calcium ([Ca2+]i), and the synthesis of thromboxane A2. PA production, PKC activation, and the rise of [Ca2+]i stimulated by the ristocetin-induced binding of vWF multimers to platelets are inhibited by an anti-GpIb monoclonal antibody, but are unaffected by anti-GpIIb-IIIa monoclonal antibodies. Indomethacin also inhibits these responses without impairing platelet aggregation induced by vWF plus ristocetin. These results indicate that vWF binding to platelets initiates specific intraplatelet signaling pathways. The mechanism by which this occurs involves an arachidonic acid metabolite-dependent activation of phospholipase C after vWF binding to platelet membrane GpIb. This signal then causes PKC activation and increases of [Ca2+]i, which promote platelet secretion and potentiate aggregation. C1 BAYLOR COLL MED,HOUSTON VET AFFAIRS MED CTR,HOUSTON,TX 77030. RICE UNIV,HOUSTON,TX 77251. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL02311, HL36045, HL35387] NR 27 TC 228 Z9 231 U1 0 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD NOV PY 1991 VL 88 IS 5 BP 1568 EP 1573 DI 10.1172/JCI115468 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GN727 UT WOS:A1991GN72700018 PM 1939645 ER PT J AU PARKOS, CA DELP, C ARNAOUT, MA MADARA, JL AF PARKOS, CA DELP, C ARNAOUT, MA MADARA, JL TI NEUTROPHIL MIGRATION ACROSS A CULTURED INTESTINAL EPITHELIUM - DEPENDENCE ON A CD11B CD18-MEDIATED EVENT AND ENHANCED EFFICIENCY IN PHYSIOLOGICAL DIRECTION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PARACELLULAR; INTEGRIN; INFLAMMATION ID LFA-1 MEMBRANE MOLECULE; LEUKOCYTE TRANSMIGRATION; ELECTROLYTE TRANSPORT; MONOCLONAL-ANTIBODIES; VASCULAR ENDOTHELIUM; CELL LINE; ADHERENCE; ADHESION; MONOCYTES; DEFICIENCY AB Neutrophils (PMN) migrate across intestinal epithelia in many disease states. Although such migration serves as a histological index of disease activity, little is known concerning the molecular events underlying PMN-intestinal epithelial interactions. We have studied chemotactic peptide-driven movement of PMN across cultured monolayers of the human intestinal epithelial cell line T84. Using a transmigration microassay, we show that both the decreased transepithelial resistance (76 +/- 3%) and transmigration (4 +/- 0.6 X 10(5) PMN.cm-2, when PMN applied at 6 X 10(6) . cm-2) are largely prevented by MAbs which recognize either subunit of the PMN surface heterodimeric adhesion glycoprotein, CD11b/CD18. In contrast, such PMN-epithelial interactions are unaffected by MAbs recognizing either of the remaining two alpha-subunits CD11a or CD11c. PMN from a leukocyte adherence deficiency patient also failed to migrate across epithelial monolayers thus confirming a requirement for CD11/18 integrins. By modifying our microassay, we were able to assess PMN transmigration across T84 monolayers in the physiological direction (which, for technical reasons, has not been studied in epithelia): transmigration was again largely attenuated by MAb to CD18 or CD11b (86 +/- 2% and 73 +/- 3% inhibition, respectively) but was unaffected by MAb to CD11a, CD11c. For standard conditions of PMN density, PMN transmigration in the physiological direction was 5-20 times more efficient than in the routinely studied opposite direction. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,CTR DIGEST DIS,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP PARKOS, CA (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,20 SHATTUCK ST,ROOM 1424A,BOSTON,MA 02115, USA. RI Parkos, Charles/B-3896-2009 FU NIAID NIH HHS [AI21964]; NIDDK NIH HHS [DK 33506, DK35932] NR 42 TC 289 Z9 290 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD NOV PY 1991 VL 88 IS 5 BP 1605 EP 1612 DI 10.1172/JCI115473 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GN727 UT WOS:A1991GN72700023 PM 1682344 ER PT J AU HAFFAJEE, AD SOCRANSKY, SS SMITH, C DIBART, S AF HAFFAJEE, AD SOCRANSKY, SS SMITH, C DIBART, S TI RELATION OF BASE-LINE MICROBIAL PARAMETERS TO FUTURE PERIODONTAL ATTACHMENT LOSS SO JOURNAL OF CLINICAL PERIODONTOLOGY LA English DT Article DE ATTACHMENT LOSS; RISK FACTORS; PERIODONTAL DISEASES; SUBGINGIVAL MICROBIOTA ID BACTEROIDES-GINGIVALIS; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; PROGRESSIVE PERIODONTITIS; IMMUNOLOGICAL FEATURES; SUBGINGIVAL PLAQUE; LESIONS; INTERMEDIUS; DISEASES; LEVEL AB The relationship between the level of subgingival species at baseline and subsequent attachment loss in a subject was examined. 38 subjects (14-71 years) with prior evidence of periodontal destruction were monitored 2 x for pocket depth and attachment level at 6 sites per tooth at baseline and 2 months. A subject was considered to exhibit new attachment loss if 1 or more sites increased 3 mm or more in attachment level in 2 months. Subgingival plaque samples were taken at the baseline visit from the mesial aspect of each tooth (28 sites) using Gracey curettes. Samples were dispersed, diluted and plated on Trypticase soy agar supplemented with 5% sheep blood. After 7 days of anaerobic incubation, the colonies were lifted onto nylon filters, lysed and the DNA fixed to the filters. Digoxygenin-labeled DNA probes were used to enumerate 14 subgingival species. 17 of 38 subjects (44.7%) exhibited new attachment loss in 2 months. The % of the total viable count of each species was averaged for each subject. The species enumerated and the mean % of the total cultivable microbiota averaged across the active and inactive subjects were as follows; B gingivalis 2.3, 1.2; W. recta 1.3, 0.6; B. intermedius I 2.5, 2.0; B. forsythus 1.5, 1.2; A. actinomycetemcomitans serotype a 1.1, 0.8; F. nucleatum ss vincentii 1.1, 1.0; S. intermedius 2.0, 1.9; P micros 1.5, 1.5, B. intermedius II 1.6, 1.7; A. actinomycetemcomitans serotype b 0.4, 0.6; S. sanguis I 1.8, 2.1; S. sanguis II 2.7, 3.0; V parvula 3.9, 4.2; C. ochracea 0.9, 1.8. Significantly higher levels of B. gingivalis and W recta and significantly lower levels of C ochracea were found in active subjects prior to breakdown. Odds ratios were computed at different threshold levels for each species. Significant ratios for new disease were B. gingivalis 5.6. W recta 3.8, V parvula 0.16 and C ochracea 0.08. When subjects were subset into those with localized (less-than-or-equal-to 30% affected sites) and widespread disease groups, B. gingivalis and B. intermedius I were elevated in active localized disease subjects and C ochracea in inactive subjects. P micros and W recta were elevated in active widespread disease subjects. Discriminant analysis using the significantly related species was useful in predicting subjects at risk for new attachment loss overall and in both groups. Such data suggest that levels of microorganisms may be useful indicators of future attachment loss. RP HAFFAJEE, AD (reprint author), FORSYTH DENT CTR,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-02847, DE-04881] NR 30 TC 100 Z9 102 U1 0 U2 4 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6979 J9 J CLIN PERIODONTOL JI J. Clin. Periodontol. PD NOV PY 1991 VL 18 IS 10 BP 744 EP 750 DI 10.1111/j.1600-051X.1991.tb00066.x PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA GQ077 UT WOS:A1991GQ07700004 PM 1661304 ER PT J AU SOCRANSKY, SS HAFFAJEE, AD SMITH, C DIBART, S AF SOCRANSKY, SS HAFFAJEE, AD SMITH, C DIBART, S TI RELATION OF COUNTS OF MICROBIAL SPECIES TO CLINICAL STATUS AT THE SAMPLED SITE SO JOURNAL OF CLINICAL PERIODONTOLOGY LA English DT Article DE PERIODONTAL DISEASES; SUBGINGIVAL MICROBIOTA; DNA PROBES; PERIODONTAL POCKETS ID PLAQUE AB The purpose of the present investigation was to relate clinical characteristics at a site to the frequency of detection, absolute counts and proportions of 14 subgingival species. Subgingival plaque samples were removed by curette from the mesial surface of 2299 teeth in 3 healthy and 87 subjects with periodontal attachment loss. Samples were dispersed,diluted and plated on Trypticase soy agar supplemented with 5% sheep blood. After 7 days of anaerobic incubation, colonies were lifted onto nylon filters, lysed and the DNA fixed to the filters. Digoxygenin-labeled DNA probes were used to identify colonies of each test species. Measurements of pocket depth, attachment level, recession, redness, bleeding on probing and suppuration were made at each sampled site. Total viable counts at sites ranged from 10(3) to > 10(8) and were strongly related to pocket depth. Mean total counts at sites < 3 mm averaged 4.6 x 10(6), while mean counts at sites > 7 mm averaged 2.0 x 10(7). Species enumerated and % of sites colonized were as follows; V. parvula 44; S. sanguis II 36; B. intermedius I 33; C. ochracea 31; B. intermedius II 30; S. sanguis I 29; B. gingivalis 27; S. intermedius 25; P. micros 24; W. recta 23; F. nucleatum ss vincentii 18; B. forsythus 15; A. actinomycetemcomitans serotype a 10; A. actinomycetemcomitans serotype b 8. Counts of B. intermedius II were higher at sites which exhibited gingival redness while B. intermedius I was higher at sites which bled on probing. A. actinomycetemcomitans serotype b was more frequent and at higher mean % at sites without recession. The opposite was true for S. sanguis II. B. gingivalis was somewhat more prevalent and at higher levels at suppurating sites. B. gingivalis, B. intermedius I and II and B. forsythus were found more frequently and at higher levels at sites with deeper pockets, while, V. parvula was less prevalent at sites with pocket depths < 4 mm. B. gingivalis, B. intermedius I and A. actinomycetemcomitans serotype b increased with increasing pocket depth in both localized and widespread disease subjects, but mean counts were higher in the localized disease subjects at any pocket depth. Only W. recta was found at higher levels at deep sites in widespread disease subjects when compared with similar sites in localized disease subjects. No suspected pathogens were detected in 38% of shallow sites, 31% of intermediate sites and 22% of deep sites. 2/3 of deep pockets, but less than 1/2 of shallow pockets harbored at least 2 of the suspected pathogens. RP SOCRANSKY, SS (reprint author), FORSYTH DENT CTR,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-02487, DE-04881] NR 10 TC 199 Z9 206 U1 0 U2 8 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6979 J9 J CLIN PERIODONTOL JI J. Clin. Periodontol. PD NOV PY 1991 VL 18 IS 10 BP 766 EP 775 DI 10.1111/j.1600-051X.1991.tb00070.x PG 10 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA GQ077 UT WOS:A1991GQ07700008 PM 1661305 ER PT J AU ROSENBAUM, JF BIEDERMAN, J HIRSHFELD, DR BOLDUC, EA CHALOFF, J AF ROSENBAUM, JF BIEDERMAN, J HIRSHFELD, DR BOLDUC, EA CHALOFF, J TI BEHAVIORAL-INHIBITION IN CHILDREN - A POSSIBLE PRECURSOR TO PANIC DISORDER OR SOCIAL PHOBIA SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT SYMP AT THE 11TH NATIONAL CONF ON ANXIETY DISORDERS - SOCIAL PHOBIA : ADVANCES IN UNDERSTANDING AND TREATMENT CY APR 00-07, 1991 CL CHICAGO, IL ID UNFAMILIAR; PARENTS C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP ROSENBAUM, JF (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 22 TC 76 Z9 79 U1 0 U2 5 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD NOV PY 1991 VL 52 SU S BP 5 EP 9 PG 5 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA GR306 UT WOS:A1991GR30600002 PM 1757458 ER PT J AU HIBBS, ML JAKES, S STACKER, SA WALLACE, RW SPRINGER, TA AF HIBBS, ML JAKES, S STACKER, SA WALLACE, RW SPRINGER, TA TI THE CYTOPLASMIC DOMAIN OF THE INTEGRIN LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1 BETA-SUBUNIT - SITES REQUIRED FOR BINDING TO INTERCELLULAR-ADHESION MOLECULE-1 AND THE PHORBOL ESTER STIMULATED PHOSPHORYLATION SITE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID AMINO-ACID-SEQUENCE; PROTEIN KINASE-C; CELL-ADHESION; FIBRONECTIN RECEPTOR; TRANSMEMBRANE LINKAGE; EPITHELIAL-CELLS; LFA-1; CLONING; EXPRESSION; DEFICIENCY AB We have defined the regions of the cytoplasmic domain of the leukocyte integrin lymphocyte function-associated antigen 1 (LFA-1) that are required for active binding of its extracellular domain to intercellular adhesion molecule 1 (ICAM-1). The NH2-terminal 28 amino acids in the cytoplasmic domain are dispensable, but a segment of 5 amino acids including three contiguous threonines (758-760) and Phe 766 in the COOH-terminal third of the cytoplasmic domain are required for binding to ICAM-1. Mutation and phosphoamino acid analysis show that Ser 756 is the major residue phosphorylated in response to phorbol ester. Furthermore, multiple mutations demonstrate that serine phosphorylation can be dissociated from phorbol ester-stimulated binding of LFA-1 to ICAM-1. The sites we have defined are previously unremarked, are well conserved in the beta-1, beta-3, and beta-7 integrin subunits, and may be of broad importance in regulating adhesiveness of integrins. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. BOEHRINGER INGLEHEIM PHARMACEUT,RIDGEFIELD,CT 06877. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RI Hibbs, Margaret/D-7013-2011 FU PHS HHS [37198] NR 49 TC 242 Z9 242 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 1 PY 1991 VL 174 IS 5 BP 1227 EP 1238 DI 10.1084/jem.174.5.1227 PG 12 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA GM803 UT WOS:A1991GM80300028 PM 1682411 ER PT J AU DANG, NH TORIMOTO, Y SHIMAMURA, K TANAKA, T DALEY, JF SCHLOSSMAN, SF MORIMOTO, C AF DANG, NH TORIMOTO, Y SHIMAMURA, K TANAKA, T DALEY, JF SCHLOSSMAN, SF MORIMOTO, C TI 1F7 (CD26) - A MARKER OF THYMIC MATURATION INVOLVED IN THE DIFFERENTIAL REGULATION OF THE CD3 AND CD2 PATHWAYS OF HUMAN THYMOCYTE ACTIVATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL ACTIVATION; T3-ANTIGEN RECEPTOR COMPLEX; DIPEPTIDYL PEPTIDASE-IV; HUMAN LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; ANTIGEN-RECEPTOR; T3-MOLECULAR COMPLEX; ALTERNATIVE PATHWAY; SURFACE MOLECULE; DISCRETE STAGES AB We have recently shown that solid-phase immobilization of anti-1F7 recognizing the 110-kDa CD26 Ag is comitogenic for human peripheral blood T cell activation via both the CD3 and CD2 pathways. We have also demonstrated that binding of anti-1F7 leads to the disappearance of CD26 surface expression, and this anti-1F7-induced modulation results in an increase in anti-CD3 or anti-CD2-mediated peripheral blood T cell activation. In this report, we extended these findings by examining the expression and functional relationship of 1F7 on the CD3 and CD2 pathways of activation of human thymocytes. We now demonstrated that most of the anti-1F7 reactivity is found on medullary thymocytes, the population of thymocytes expressing high level of CD3 (CD3H). We have also shown that binding of anti-1F7 can induce a decrease in CD26 surface expression, with no detectable effect on the surface expression of CD3 or CD2. Most importantly, we showed that solid-phase immobilization of anti-1F7 has a comitogenic effect on thymocyte activation induced by anti-CD3 but not anti-CD2. In addition, anti-1F7-induced modulation of CD26 results in an enhancement in CD3-mediated but not CD2-mediated human thymocyte activation. The observed functional effect of CD26 on the CD3/TCR pathway of activation is mainly restricted to mature thymocytes as distinguished by high surface expression of CD5, although CD26 is also functionally associated with the CD3/TCR pathway on cells expressing low level of CD5. Demonstrating that CD26 involvement in the regulation of human thymocyte activation is restricted mainly to the CD3 pathway, unlike its involvement with both the CD3 and CD2 pathways of mature peripheral blood T lymphocyte activation, our data hence suggested that CD26 may play a role in thymic differentiation and maturation via the differential engagement of the CD3 pathway. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. TOKAI UNIV,SCH MED,DEPT PATHOL,ISEHARA,KANAGAWA 25911,JAPAN. FU NIAID NIH HHS [AI-12069]; NIAMS NIH HHS [AR-33713] NR 45 TC 79 Z9 79 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 NOV 1 PY 1991 VL 147 IS 9 BP 2825 EP 2832 PG 8 WC Immunology SC Immunology GA GL580 UT WOS:A1991GL58000001 PM 1717577 ER PT J AU LAMPE, MA PATARCA, R IREGUI, MV CANTOR, H AF LAMPE, MA PATARCA, R IREGUI, MV CANTOR, H TI POLYCLONAL B-CELL ACTIVATION BY THE ETA-1 CYTOKINE AND THE DEVELOPMENT OF SYSTEMIC AUTOIMMUNE-DISEASE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LPR-LPR MICE; LUPUS-ERYTHEMATOSUS; T-CELLS; LYMPHOCYTES-B; IMMUNOGLOBULIN; EXPRESSION; DEFINITION; GENOTYPE; SLE AB Studies of systemic autoimmune disease have led to the view that initiation and progression of the disease process reflects chronic and sustained B cell activation by unidentified polyclonal activating agents. In earlier studies, we found that T cells from MRL/1 mice, which develop murine lupus, express very high levels of a newly defined T cell cytokine, Eta-1. Inasmuch as chronic and sustained B cell stimulation by T cells is a cardinal feature of MRL/1 disease, we determined the effects of this cytokine on Ig production by B cells. We show that both recombinant and biochemically purified natural Eta-1 stimulate IgM and IgG production by mixtures of B cells and macrophages from the autoimmune MRL/1 strain. Additional studies suggest that optimal Ig production by Eta-1 may require macrophages and reflect enhanced Ig production by large B cells. These findings support the view that elevated levels of endogenous Eta-1 may cause chronic and sustained polyclonal B cell activation that leads to autoimmune disease in this murine model. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOPATHOL LAB,BOSTON,MA 02115. FU NIAID NIH HHS [AI-12184, AI-13600] NR 20 TC 97 Z9 100 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 NOV 1 PY 1991 VL 147 IS 9 BP 2902 EP 2906 PG 5 WC Immunology SC Immunology GA GL580 UT WOS:A1991GL58000012 PM 1918998 ER PT J AU BURSTEIN, HJ TEPPER, RI LEDER, P ABBAS, AK AF BURSTEIN, HJ TEPPER, RI LEDER, P ABBAS, AK TI HUMORAL IMMUNE FUNCTIONS IN IL-4 TRANSGENIC MICE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID STIMULATORY FACTOR-I; IMMUNOGLOBULIN HEAVY-CHAIN; INDUCER LYMPHOCYTES-T; HUMAN IGE SYNTHESIS; RESTING B-CELLS; MONOCLONAL-ANTIBODIES; EPSILON-TRANSCRIPTS; GROWTH-FACTOR; INTERLEUKIN-4; EXPRESSION AB We have analyzed mice expressing IL-4 as a transgene, and found that expression of this lymphokine has profound effects on B cell function. B cells from transgenic mice exhibit phenotypic changes, including an increase in size and elevated expression of class II MHC. IL-4 increases the quantity of IgE produced by transgenic-derived B cells in response to LPS stimulation. In vivo, IL-4 markedly affects the serum Ig isotype repertoire. Serum levels of IgG1 and IgE are elevated, and levels of IgG2a, IgG2b, and IgG3 are depressed in IL-4 transgenic mice. Ag-specific antibody responses to immunization with hapten-carrier conjugates are also affected by IL-4. Transgenic mice show increased anti-hapten IgE and IgG1 and reduced anti-hapten IgG2a, IgG2b, and IgG3, compared with wild-type mice. Ag-specific IgE is substantially induced by T cell-dependent Ag, but not T cell-independent Ag, suggesting that cognate T-B interactions in addition to IL-4 are required for generating IgE responses in vivo. In vivo treatment with the anti-IL-4 mAb 11B11 reverses many of the isotype alterations in the transgenic mice, indicating that these changes arise as a direct consequence of IL-4 secretion. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,HEMATOL ONCOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP BURSTEIN, HJ (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,LMRC ROOM 519,221 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [R01AI25022]; NIGMS NIH HHS [T32 GM007753, 2T32GM07753-11] NR 34 TC 78 Z9 78 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1991 VL 147 IS 9 BP 2950 EP 2956 PG 7 WC Immunology SC Immunology GA GL580 UT WOS:A1991GL58000019 PM 1919000 ER PT J AU LYNN, WA RAETZ, CRH QURESHI, N GOLENBOCK, DT AF LYNN, WA RAETZ, CRH QURESHI, N GOLENBOCK, DT TI LIPOPOLYSACCHARIDE-INDUCED STIMULATION OF CD11B CD18 EXPRESSION ON NEUTROPHILS - EVIDENCE OF SPECIFIC RECEPTOR-BASED RESPONSE AND INHIBITION BY LIPID A-BASED ANTAGONISTS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; ESCHERICHIA-COLI; MURINE SPLENOCYTES; BINDING PROTEINS; HUMAN-MONOCYTES; LPS BINDING; ENDOTOXIN; INDUCTION; CACHECTIN; RELEASE AB Gram-negative bacterial septicemia is a common clinical syndrome resulting, in part, from the activation of phagocytic leukocytes by LPS. By using flow cytometry, we have characterized LPS-induced expression of the beta-2 integrin CD11b/CD18. After exposure to Salmonella minnesota R595 LPS, expression of neutrophil CD11b/CD18 is rapidly upregulated, beginning within 5 min and achieving a peak fluorescence (typically two- to threefold over base line) by 30 min. The increase in CD11b/CD18 expression was similar in kinetics and magnitude to that produced by FMLP, PMA, and human rTNF-alpha. Concentrations of LPS necessary to stimulate a response were as low as 1 ng/ml of R595 LPS; a maximal response was observed between 30 and 100 ng/ml. The upregulation of CD11b/CD18 due to LPS was not interrupted by protein synthesis inhibitors. A group of glucosamine disaccharide lipid A-like molecules: Rhodobacter sphaeroides lipid A, lipid IV(A), KDO2IV(A), and deacylated LPS were able to block the stimulatory effect of LPS. This inhibition was specific for the actions of LPS as stimulation of polymorphonuclear leukocytes (PMN) by FMLP, human rTNF-alpha, PMA, and rewarming were not altered by the disaccharide inhibitors. PMN which were exposed to the specific disaccharide LPS antagonists and then washed, were refractory to stimulation by LPS. The monosaccharide lipid A precursor lipid X also blocked stimulation of neutrophils by LPS, although with a 100-fold reduction in potency. Unlike the disaccharide inhibitors, PMN exposed to lipid X were still responsive to LPS stimulation after washing. The PMN response to LPS was less sensitive in the absence of serum, although upregulation of CD11b/CD18 could still be seen using higher concentrations of LPS. Monoclonal antibody directed against CD14 (clone 3C10), also specifically inhibited LPS induced PMN CD11b/CD18 expression both in the presence and absence of serum. These findings support the hypothesis that LPS stimulates neutrophils by interacting with specific cellular receptors. C1 BOSTON UNIV,BOSTON CITY HOSP,SCH MED,DEPT MED,MAXWELL FINLAND LAB INFECT DIS,ROOM 315,BOSTON,MA 02118. MERCK SHARP & DOHME LTD,DEPT BIOCHEM,RAHWAY,NJ 07065. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. FU PHS HHS [K11-000840] NR 49 TC 143 Z9 144 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 NOV 1 PY 1991 VL 147 IS 9 BP 3072 EP 3079 PG 8 WC Immunology SC Immunology GA GL580 UT WOS:A1991GL58000037 PM 1717586 ER PT J AU CAMERINI, D WALZ, G LOENEN, WAM BORST, J SEED, B AF CAMERINI, D WALZ, G LOENEN, WAM BORST, J SEED, B TI THE T-CELL ACTIVATION ANTIGEN CD27 IS A MEMBER OF THE NERVE GROWTH-FACTOR TUMOR-NECROSIS-FACTOR RECEPTOR GENE FAMILY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MOLECULAR-CLONING; NEUROTROPHIC FACTOR; MONONUCLEAR-CELLS; LYMPHOCYTES-B; EXPRESSION; DIFFERENTIATION; CARCINOMAS; SEQUENCES; FORM; CDNA AB CD27 is a dimeric membrane glycoprotein found on the surface of most human T lymphocytes. Activation of T cells by engagement of the Ag receptor increases CD27 surface expression, and anti-CD27 antibodies augment Ag receptor-mediated T cell proliferation. In this study a cDNA-encoding CD27 was isolated by expression and immunoselection in COS cells. The predicted polypeptide was found to belong to a recently characterized family of cysteine-rich receptors whose known ligands include nerve growth factor and TNF-alpha and -beta. Structural similarities suggest that CD27 belongs to a lymphocyte-specific subgroup of the family, comprised of the B cell Ag CD40, the rat T cell subset Ag OX40, and the mouse T cell activation Ag 4-1BB. Recent studies suggest some of these molecules may play a role in the survival of activated cells. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NETHERLANDS CANC INST,DIV IMMUNOL,1066 CX AMSTERDAM,NETHERLANDS. NR 53 TC 236 Z9 241 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1991 VL 147 IS 9 BP 3165 EP 3169 PG 5 WC Immunology SC Immunology GA GL580 UT WOS:A1991GL58000051 PM 1655907 ER PT J AU MYERS, RH VONSATTEL, JP PASKEVICH, PA KIELY, DK STEVENS, TJ CUPPLES, LA RICHARDSON, EP BIRD, ED AF MYERS, RH VONSATTEL, JP PASKEVICH, PA KIELY, DK STEVENS, TJ CUPPLES, LA RICHARDSON, EP BIRD, ED TI DECREASED NEURONAL AND INCREASED OLIGODENDROGLIAL DENSITIES IN HUNTINGTONS-DISEASE CAUDATE-NUCLEUS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE ASTROCYTE; CAUDATE NUCLEUS; HUNTINGTONS DISEASE; NEURON; OLIGODENDROCYTE ID NEOSTRIATUM; NEUROGENESIS; CHOREA; ORIGIN; ONSET; TIME; RAT AB Decreased density of neurons was found throughout the head of the caudate nucleus in Huntington's disease (HD), with the most severe neuronal loss early in the disease in the medial region. The density of reactive astrocytes is inversely proportional to the neuronal loss. In cases of mild Huntington's disease which had no identifiable abnormality on conventional neuropathologic evaluation (grade 0), there is a reduction in neuron density without an accompanying reactive astrocytosis. The pattern for decrease in neurons and accompanying astrocytosis suggests that the earliest changes occur in the most medial portion of the head of the caudate nucleus and subsequently sweep laterally across the caudate nucleus to the internal capsule. An increased density of oligodendrocytes is observed in the head of the caudate nucleus for the lower grades (0, 1 and 2). The decreased neuronal and increased oligodendroglial densities may be of significance in understanding the pathogenesis of HD. These altered densities, observed in the absence of reactive astrocytosis, suggest that these changes may not represent recent effects of disease, but rather that HD gene expression may influence brain cell densities from early in the life of the gene carrier. C1 HARVARD UNIV,SCH MED,DEPT NEUROL NEUROPATHOL,BOSTON,MA 02115. MCLEAN HOSP,MAILMAN RES CTR,PSYCHIAT RES LABS,BELMONT,MA 02178. BOSTON UNIV,SCH PUBL HLTH,BOSTON,MA 02215. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. MCLEAN HOSP,MAILMAN RES CTR,RALPH LOWELL LABS,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. RP MYERS, RH (reprint author), BOSTON UNIV,SCH MED,DEPT NEUROL,80 E CONCORD ST,BOSTON,MA 02118, USA. FU PHS HHS [16367, 31862] NR 24 TC 129 Z9 132 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD NOV PY 1991 VL 50 IS 6 BP 729 EP 742 DI 10.1097/00005072-199111000-00005 PG 14 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA GM854 UT WOS:A1991GM85400005 PM 1836225 ER PT J AU SUCHER, NJ LIPTON, SA AF SUCHER, NJ LIPTON, SA TI REDOX MODULATORY SITE OF THE NMDA RECEPTOR-CHANNEL COMPLEX - REGULATION BY OXIDIZED GLUTATHIONE SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Note DE EXCITATORY AMINO ACID RECEPTORS; N-METHYL-D-ASPARTATE RECEPTOR; REDOX MODULATION; NMDA-ACTIVATED CURRENT; INTRACELLULAR CA2+ LEVELS ID CEREBELLAR GRANULE CELLS; RETINAL GANGLION-CELLS; CENTRAL NEURONS; NERVOUS-SYSTEM; GLUTAMATE; ACID; RAT; NEUROTOXICITY; RESPONSES; REDUCTION AB We monitored increases in both intracellular calcium concentration ([Ca2+]i) and whole-cell current responses induced by N-methyl-D-aspartate (NMDA), applied with coagonist glycine, using fura-2 digital imaging and patch-clamp recording techniques. Extracellular application of oxidized glutathione (GSSG), but not reduced glutathione (GSH), inhibited responses mediated by activation of the NMDA subtype of glutamate receptor in cultures of rat cortical and retinal ganglion cell neurons. The NMDA responses were persistently inhibited by GSSG (500-mu-M to 10 mM) until introduction of a selective sulfhydryl reducing agent, dithiothreitol, which resulted in complete recovery of the responses. Exposure of the neurons to 5,5-dithio-bis-2-nitrobenzoic acid (DTNB), an efficacious oxidizing agent, also resulted in persistently smaller responses to NMDA. The addition of GSSG following exposure to DTNB, however, did not result in a further decrement in NMDA responses in our experimental paradigm. These findings suggest that a predominant action of GSSG is oxidation of vicinal thiol groups to form a peptide disulfide bond(s) comprising the redox modulatory site of the NMDA receptor-channel complex. Evidence for such regulatory sulfhydryl centers associated with the NMDA receptor has been presented previously. Moreover, the fact that DTNB produced little if any additional attenuation of the NMDA [Ca2+]i response when administered after GSSG implies that GSSG is also an efficacious oxidant at this site. GSSG displayed little or no effect on [Ca2+]i responses elicited by high extracellular K+ or by kainate, suggesting that, at least under the conditions of the present experiments, GSSG was somewhat selective for the NMDA redox modulatory site. Based on these observations, we suggest that GSSG exerts its NMDA-specific redox effects in a novel extracellular manner. C1 CHILDRENS HOSP MED CTR,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,ENDERS BLDG,SUITE 361,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. OI Sucher, Nikolaus/0000-0001-6233-1612 FU NEI NIH HHS [EY05477, EY09024]; NINDS NIH HHS [NS07264] NR 38 TC 102 Z9 104 U1 0 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD NOV PY 1991 VL 30 IS 3 BP 582 EP 591 DI 10.1002/jnr.490300316 PG 10 WC Neurosciences SC Neurosciences & Neurology GA GQ849 UT WOS:A1991GQ84900015 PM 1666131 ER PT J AU PIKE, MC AF PIKE, MC TI IMAGING OF INFLAMMATORY SITES IN THE 1990S - NEW HORIZONS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID HMPAO-LABELED LEUKOCYTES; GA-67 CITRATE; LOCALIZATION; INFECTION; SCINTIGRAPHY; ABSCESSES; GA-67-CITRATE; GRANULOCYTES; LESIONS; SCAN RP PIKE, MC (reprint author), MASSACHUSETTS GEN HOSP,ARTHRIT UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 27 TC 5 Z9 6 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD NOV PY 1991 VL 32 IS 11 BP 2034 EP 2036 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GP127 UT WOS:A1991GP12700006 PM 1941135 ER PT J AU WALTMAN, A AF WALTMAN, A TI A DECISION-ANALYSIS APPROACH TO THE TREATMENT OF THE PATIENT WITH SUSPECTED PULMONARY EMBOLI AND AN INTERMEDIATE PROBABILITY LUNG-SCAN SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material RP WALTMAN, A (reprint author), MASSACHUSETTS GEN HOSP,ANGIOG GRAY 2,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD NOV PY 1991 VL 32 IS 11 BP 2056 EP 2056 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GP127 UT WOS:A1991GP12700010 ER PT J AU GREENE, R AF GREENE, R TI IMMUNOSCINTIGRAPHY FOR LUNG-CANCER DETECTION - REALITY TESTING SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP GREENE, R (reprint author), HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD NOV PY 1991 VL 32 IS 11 BP 2069 EP 2070 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GP127 UT WOS:A1991GP12700014 PM 1941140 ER PT J AU ROSS, DS AF ROSS, DS TI EVALUATION OF THE THYROID-NODULE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Review ID FINE-NEEDLE ASPIRATION; AUTONOMOUSLY FUNCTIONING NODULE; SUBCLINICAL HYPERTHYROIDISM; PATHOLOGICAL FINDINGS; MULTINODULAR GOITER; SUPPRESSIVE THERAPY; CLONAL ORIGIN; FOLLOW-UP; CARCINOMA; BIOPSY AB The evaluation and management of thyroid nodules remains an area of controversy. The past decade has witnessed two important advances. The increased availability and acceptance of fine-needle aspiration biopsy of thyroid nodules has dramatically altered the clinician's approach to this disease, and provides for the single most precise method for selecting appropriate patients for surgery. The introduction of high-resolution thyroid ultrasonography provides for anatomic definition that is clearly superior to thyroid scintigraphy. However, radionuclide imaging of the thyroid remains critical for determining the functional status of abnormal thyroid tissue. While aspiration, ultrasound, and scintigraphy all have appropriate indications, utility, and limitations, no single test or group of tests substitutes for careful clinical assessment and followup. This review attempts to provide a practical approach to the evaluation and management of the thyroid nodule. C1 HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP ROSS, DS (reprint author), MASSACHUSETTS GEN HOSP, THYROID ASSOCIATES, THYROID UNIT ACC730 S, BOSTON, MA 02114 USA. NR 104 TC 66 Z9 67 U1 1 U2 1 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 EI 1535-5667 J9 J NUCL MED JI J. Nucl. Med. PD NOV PY 1991 VL 32 IS 11 BP 2181 EP 2192 PG 12 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GP127 UT WOS:A1991GP12700037 PM 1658255 ER PT J AU OKAMOTO, Y HEELEY, JD DOGON, IL SHINTANI, H AF OKAMOTO, Y HEELEY, JD DOGON, IL SHINTANI, H TI EFFECTS OF PHOSPHORIC-ACID AND TANNIC-ACID ON DENTIN COLLAGEN SO JOURNAL OF ORAL REHABILITATION LA English DT Article ID PEPTIDES AB We examined the effects of phosphoric acid, the most common enamel etchant in composite resin therapy, on dentine collagen. Dentine collagen pretreated with 7 M phosphoric acid was shown to be more susceptible to trypsin digestion than untreated collagen. This susceptibility increased with increasing duration of exposure to the acid. The results indicate that phosphoric acid induces a conformational change in dentine collagen (denaturation or perturbation) similar to that observed with 0.39 M HCl, which has a similar pH value (0.65). However, phosphoric acid-pretreated dentine collagen, when treated with tannic acid for 2h, became as resistant to tryptic digestion as intact dentine collagen. The present results suggest that tannic acid may work as a dentine conditioner in composite resin therapy, in view of the fact that phosphoric acid etchant is applied, either deliberately or inadvertently, to dentine, and would thus induce denaturation or perturbation of collagen. C1 FORSYTH DENT CTR,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,CAMBRIDGE,MA 02138. RP OKAMOTO, Y (reprint author), HIROSHIMA UNIV,SCH DENT,1-2-3 KASUMI,MINAMI KU,HIROSHIMA 734,JAPAN. FU NCRR NIH HHS [RR-05483] NR 13 TC 35 Z9 37 U1 2 U2 4 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0305-182X J9 J ORAL REHABIL JI J. Oral Rehabil. PD NOV PY 1991 VL 18 IS 6 BP 507 EP 512 DI 10.1111/j.1365-2842.1991.tb00073.x PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA GQ025 UT WOS:A1991GQ02500005 PM 1762024 ER PT J AU FISHMAN, JA SAMIA, JA FUGLESTAD, J ROSE, RM AF FISHMAN, JA SAMIA, JA FUGLESTAD, J ROSE, RM TI THE EFFECTS OF EXTRACELLULAR-MATRIX (ECM) PROTEINS ON THE ATTACHMENT OF PNEUMOCYSTIS-CARINII TO LUNG-CELL LINES INVITRO SO JOURNAL OF PROTOZOOLOGY LA English DT Note DE FIBRONECTIN; FLUORESCEIN; LAMININ ID RAT LUNG; FIBRONECTIN AB Pneumocystis carinii cells labeled with fluorescein isothiocyanate were co-cultured with tissue culture cells. Measurements of attachment was determined by the tissue culture cell fluorescence after washing out the P. carinii organisms. The effects of the extracellular matrix proteins, laminin and fibronectin, on the binding of P. carinii onto the monolayer of cultured cells were investigated for better understanding of organism-cell interactions. The intermalization of P. carinii by MRC5 cells was observed. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,DIV PULM & CRIT CARE MED,BOSTON,MA 02114. RP FISHMAN, JA (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [P01-HL43510]; PHS HHS [K08-H101916] NR 10 TC 9 Z9 9 U1 0 U2 0 PU SOC PROTOZOOLOGISTS PI LAWRENCE PA 810 E 10TH ST, LAWRENCE, KS 66044 SN 0022-3921 J9 J PROTOZOOL PD NOV-DEC PY 1991 VL 38 IS 6 BP S34 EP S37 PG 4 WC Zoology SC Zoology GA HA630 UT WOS:A1991HA63000039 PM 1818190 ER PT J AU KOZIEL, H WILLIAMS, DJ ARMSTRONG, MYK RICHARDS, FF FISHMAN, JA EZEKOWITZ, RA WARNER, A FUGLESTAD, J ROSE, RM AF KOZIEL, H WILLIAMS, DJ ARMSTRONG, MYK RICHARDS, FF FISHMAN, JA EZEKOWITZ, RA WARNER, A FUGLESTAD, J ROSE, RM TI NEW RAPID METHOD FOR THE STUDY OF PNEUMOCYSTIS-CARINII INTERACTION WITH ALVEOLAR MACROPHAGES SO JOURNAL OF PROTOZOOLOGY LA English DT Note DE ADHESION; FLUOROMETRY; NOMARSKI OPTICS ID ATTACHMENT; INVITRO AB Understanding the pathophysiology of Pneumocystis carinii infection has been limited by the availability of methods for precisely measuring the interaction of P. carinii with host cells. Here we describe a new method which allows for the rapid assessment of P. carinii binding to, and internalization by, adherent alveolar macrophages. The method is based on the detection of fluorescein-labelled P. carinii by an automated fluorescence measurement system. C1 NEW ENGLAND DEACONESS HOSP,DIV PULM & CRIT CARE MED,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,MED CTR,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RP KOZIEL, H (reprint author), YALE UNIV,MACARTHUR CTR MOLEC PARASITOL,NEW HAVEN,CT 06520, USA. FU AHRQ HHS [HS 43510] NR 11 TC 6 Z9 6 U1 0 U2 0 PU SOC PROTOZOOLOGISTS PI LAWRENCE PA 810 E 10TH ST, LAWRENCE, KS 66044 SN 0022-3921 J9 J PROTOZOOL PD NOV-DEC PY 1991 VL 38 IS 6 BP S173 EP S174 PG 2 WC Zoology SC Zoology GA HA630 UT WOS:A1991HA63000098 PM 1818154 ER PT J AU SOHEN, S ROMAIN, PL ROTHSTEIN, DM YAMANE, T TANAKA, S ANDERSON, P SCHLOSSMAN, SF MORIMOTO, C AF SOHEN, S ROMAIN, PL ROTHSTEIN, DM YAMANE, T TANAKA, S ANDERSON, P SCHLOSSMAN, SF MORIMOTO, C TI PHENOTYPIC ABNORMALITIES IN CD8+ LYMPHOCYTE-T SUBSETS IN PATIENTS WITH RHEUMATOID-ARTHRITIS SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE CD8; CD45RA; CD29; S6F1; RA ID PERIPHERAL-BLOOD LYMPHOCYTES; SYNOVIAL-FLUID LYMPHOCYTES; SYNDROME VIRUS-REPLICATION; SUPPRESSOR CELL-ACTIVITY; DEFINES 2 TYPES; MONOCLONAL-ANTIBODIES; T8+ POPULATION; INDUCER CELLS; HELPER-CELLS; DIFFERENTIATION AB We analyzed the cell surface phenotype of CD8+ cells in both peripheral blood and synovial fluid (SF) of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Utilizing the monoclonal antibodies anti-CD45RA, anti-CD29 and anti-S6F1-, one can define both suppressor effector (CD45RA+CD29-S6F1-) and killer effector (CD45RA-CD29+S6F1+) cells within the CD8 population. In patients with OA, normal proportions of CD8+CD45RA+, CD8+CD29+ and CD8+S6F1+ cells were found in both peripheral blood and SF. The peripheral blood of patients with RA, in contrast, showed a decreased percentage of CD8+CD45RA+ cells (13.4 +/- 2.6) (p < 0.05), but a normal percentage of CD8+CD29+ and CD8+S6F1+ cells. In the SF of patients with RA, we observed a more dramatic decrease in CD8+CD45RA+ suppressor effector cells (6.4 +/- 5.0) (p < 0.001), a significant increase in killer effector cells as measured by both CD8+CD29+ (35.5 +/- 9.9) (p < 0.001) and CD8+S6F1+ cells (28.2 +/- 11.4) (p < 0.01). These changes may contribute to the immunologic abnormalities previously noted in this disease and may provide some insight into the pathophysiologic mechanisms of RA. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. UNIV MASSACHUSETTS,MED CTR,DEPT MED,DIV RHEUMATOL & IMMUNOL,BOSTON,MA 02125. KINKI UNIV,SCH MED,DEPT ORTHOPED,HIGASHIOSAKA,OSAKA 577,JAPAN. FU NIAID NIH HHS [AI-12069, AI-29417]; NIAMS NIH HHS [AR-33713] NR 41 TC 13 Z9 13 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 NOV PY 1991 VL 18 IS 11 BP 1649 EP 1654 PG 6 WC Rheumatology SC Rheumatology GA GT516 UT WOS:A1991GT51600004 PM 1724013 ER PT J AU SUGAR, JA BELFER, M ISRAEL, E HERZOG, DB AF SUGAR, JA BELFER, M ISRAEL, E HERZOG, DB TI A 3-YEAR-OLD BOYS CHRONIC DIARRHEA AND UNEXPLAINED DEATH SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Note DE CHRONIC DIARRHEA; MUNCHAUSEN BY PROXY ID MUNCHAUSEN SYNDROME; CHILD-ABUSE; PROXY; IPECAC AB The fatal case of a three year-old boy hospitalized for chronic diarrhea is described. The diagnosis of Munchausen's by Proxy is discussed, and the approach to such cases is explored. C1 UNIV MICHIGAN,SCH MED,ANN ARBOR,MI 48104. HARVARD UNIV,SCH MED,DEPT SOCIAL MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PEDIAT CONSULTAT LIAISON SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,BOSTON,MA 02114. NR 17 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD NOV PY 1991 VL 30 IS 6 BP 1015 EP 1021 DI 10.1097/00004583-199111000-00023 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA GQ606 UT WOS:A1991GQ60600023 PM 1757428 ER PT J AU BLOOMBERG, J JELLINEK, M AF BLOOMBERG, J JELLINEK, M TI CONCISE GUIDE TO CHILD AND ADOLESCENT-PSYCHIATRY - DULCAN,MK, POPPER,CW SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BLOOMBERG, J (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD NOV PY 1991 VL 30 IS 6 BP 1027 EP 1027 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA GQ606 UT WOS:A1991GQ60600032 ER PT J AU LOWITT, MH DOVER, JS AF LOWITT, MH DOVER, JS TI NECROBIOSIS LIPOIDICA SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID WIDESPREAD GRANULOMA-ANNULARE; LIMITED JOINT MOBILITY; DIABETES-MELLITUS; NODULAR NECROBIOSIS; FIBRINOLYTIC AGENTS; DIABETICORUM; ASPIRIN; XANTHOGRANULOMA; DIPYRIDAMOLE; SARCOIDOSIS AB Necrobiosis lipoidica has distinctive clinical and histopathologic features. Although theories abound, its cause and pathogenesis remain unknown. Despite many reports of effective treatments, a critical review of the literature suggests that none is uniformly effective. C1 NEW ENGLAND DEACONESS HOSP,DEPT MED,110 FRANCIS ST,SUITE 7H,BOSTON,MA 02215. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. NR 112 TC 99 Z9 100 U1 1 U2 9 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD NOV PY 1991 VL 25 IS 5 BP 735 EP 748 DI 10.1016/S0190-9622(08)80961-9 PN 1 PG 14 WC Dermatology SC Dermatology GA GN037 UT WOS:A1991GN03700001 PM 1802895 ER PT J AU SANFILIPPO, AJ PICARD, MH NEWELL, JB ROSAS, E DAVIDOFF, R THOMAS, JD WEYMAN, AE AF SANFILIPPO, AJ PICARD, MH NEWELL, JB ROSAS, E DAVIDOFF, R THOMAS, JD WEYMAN, AE TI ECHOCARDIOGRAPHIC ASSESSMENT OF PATIENTS WITH INFECTIOUS ENDOCARDITIS - PREDICTION OF RISK FOR COMPLICATIONS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID DIMENSIONAL ECHOCARDIOGRAPHY; BACTERIAL-ENDOCARDITIS; CLINICAL IMPLICATIONS; VALVE ENDOCARDITIS; VEGETATION SIZE; M-MODE AB To enhance the echocardiographic identification of high risk lesions in patients with infectious endocarditis, the medical records and two-dimensional echocardiograms of 204 patients with this condition were analyzed. The occurrence of specific clinical complications was recorded and vegetations were assessed with respect to predetermined morphologic characteristics. The overall complication rates were roughly equivalent for patients with mitral (53%), aortic (62%), tricuspid (77%) and prosthetic valve (61%) vegetations, as well as for those with nonspecific valvular changes but no discrete vegetations (57%), although the distribution of specific complications varied considerably among these groups. There were significantly fewer complications in patients without discernible valvular abnormalities (27%). In native left-sided valve endocarditis, vegetation size, extent, mobility and consistency were all found to be significant univariate predictors of complications. In multivariate analysis, vegetation size, extent and mobility emerged as optimal predictors and an echocardiographic score based on these factors predicted the occurrence of complications with 70% sensitivity and 92% specificity in mitral valve endocarditis and with 76% sensitivity and 62% specificity in aortic valve endocarditis. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. OI Picard, Michael/0000-0002-9264-3243 FU NHLBI NIH HHS [HL-07535] NR 25 TC 177 Z9 184 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 NOV 1 PY 1991 VL 18 IS 5 BP 1191 EP 1199 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GM591 UT WOS:A1991GM59100003 PM 1918695 ER PT J AU KEITH, DA GLYMAN, ML AF KEITH, DA GLYMAN, ML TI INFRATEMPORAL SPACE PATHOSIS MIMICKING TMJ DISORDERS SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article ID FACIAL TRISMUS; ACTINOMYCOSIS; HEAD; NECK AB Symptoms of temporomandibular joint disorders-facial pain or jaw movement limitation-can be caused by other problems in the infratemporal space. C1 MASSACHUSETTS GEN HOSP,ORAL & MAXILLOFACIAL SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD COMMUNITY PLAN,WANG AMBULATORY CARE CTR 230,BOSTON,MA 02114. RP KEITH, DA (reprint author), HARVARD UNIV,SCH DENT MED,BOSTON,MA 02114, USA. NR 12 TC 4 Z9 5 U1 0 U2 0 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD NOV PY 1991 VL 122 IS 12 BP 59 EP 61 PG 3 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA GP562 UT WOS:A1991GP56200015 PM 1800544 ER PT J AU KYOMEN, HH NOBEL, KW WEI, JY AF KYOMEN, HH NOBEL, KW WEI, JY TI THE USE OF ESTROGEN TO DECREASE AGGRESSIVE PHYSICAL BEHAVIOR IN ELDERLY MEN WITH DEMENTIA SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID PLASMA TESTOSTERONE; ALZHEIMERS-DISEASE; SYMPTOMS; EFFICACY; MAMMALS; FAMILY; BRAIN C1 HARVARD UNIV,SCH MED,DIV AGING,643 HUNTINGTON AVE,BOSTON,MA 02115. HEBREW REHABIL CTR AGED,DEPT MED,BOSTON,MA. BROCKTON W ROXBURY DEPT VET AFFAIRS MED CTR,BOSTON,MA. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. MCLEAN HOSP,DEPT GEROPSYCHIAT,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT & SOCIAL SERV,BOSTON,MA 02114. HARVARD UNIV,CTR GERIATR RES EDUC & CLIN,CAMBRIDGE,MA 02138. NR 33 TC 58 Z9 59 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD NOV PY 1991 VL 39 IS 11 BP 1110 EP 1112 PG 3 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA GN729 UT WOS:A1991GN72900010 PM 1753051 ER PT J AU FROHMAN, EM FROHMAN, TC GUPTA, S DEFOUGEROLLES, A VANDENNOORT, S AF FROHMAN, EM FROHMAN, TC GUPTA, S DEFOUGEROLLES, A VANDENNOORT, S TI EXPRESSION OF INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) IN ALZHEIMERS-DISEASE SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article DE ALZHEIMERS DISEASE; INTERCELLULAR ADHESION MOLECULE-1; NEURITIC PLAQUE; ENDOTHELIUM; LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1 ID TUMOR NECROSIS FACTOR; HLA-DR; ANTIGEN PRESENTATION; LFA-1; CELLS; ASTROCYTES; INTERFERON; MICROGLIA; INDUCTION; GAMMA AB In this study, 13 clinically and pathologically diagnosed cases of Alzheimer's disease were analyzed for the presence of intercellular adhesion molecule 1 (ICAM-I), ICAM-2, lymphocyte function associated antigen-1 (LFA-1), HLA-DR, LN-1, and LN-2. ICAM-1 was observed primarily on neuritic plaques and cerebrovascular endothelium. ICAM-1 was also shown to be present in brain tissue derived from 14 normal cases; however, the degree of immunoreactivity was quantitatively less compared to Alzheimer cases and was largely restricted to cerebrovascular endothelium. LFA-1 was shown to be present on microglial cells and leukocytes. Consistent with the findings of previous reports, HLA-DR was found to be expressed on microglial cells. In this study we failed to demonstrate dual immunolocalization for ICAM-1 and LFA-1, ICAM-1 and HLA-DR, or ICAM-1 and LN-2. As microglial cells express both HLA-DR and LFA-1, they may serve to mediate antigen presentation functions by interacting with lymphocyte ICAM-1. Alternately, the expression of these immune-associated glycoproteins on glial cells may be epiphenomenal occurring secondary to some aspect of the disease process. Finally, the presence of ICAM-1 within neuritic plaques raises the question as to whether adhesion may play some role in the process of neurite outgrowth and neurodegeneration. C1 UNIV CALIF IRVINE, CALIF COLL MED, DEPT NEUROL, IRVINE, CA 92717 USA. UNIV CALIF IRVINE, CALIF COLL MED, DEPT MED, IRVINE, CA 92717 USA. CTR BLOOD RES, BOSTON, MA 02115 USA. FU NIA NIH HHS [AG00538] NR 19 TC 69 Z9 69 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 NOV PY 1991 VL 106 IS 1 BP 105 EP 111 DI 10.1016/0022-510X(91)90202-I PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA GU086 UT WOS:A1991GU08600017 PM 1685745 ER PT J AU DRETLER, SP BHATTA, KM AF DRETLER, SP BHATTA, KM TI CLINICAL-EXPERIENCE WITH HIGH-POWER (140 MJ), LARGE FIBER (320 MICRON) PULSED DYE-LASER LITHOTRIPSY SO JOURNAL OF UROLOGY LA English DT Article DE URETERAL CALCULI; LASER SURGERY; LITHOTRIPSY AB The pulsed dye laser, at 504 nm. wavelength with a pulse duration of 1-mu-sec., was used at 140 mj. per pulse via a 320-mu. (core) fiber for fragmentation of 72 ureteral calculi. The fragmentation efficiency and clinical results using the 140 mj./320-mu. fiber were compared to previous experience using the 60 mj./200-mu. (core) fiber. Fragmentation efficiency was significantly improved requiring many fewer laser pulses to fragment calculi of similar size and composition, and decreasing the need for auxiliary methods to complete stone fragmentation. The higher energy and larger fiber allowed for more efficient ureteroscopic ureteral stone fragmentation without compromising tissue safety. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DRETLER, SP (reprint author), MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114, USA. NR 7 TC 18 Z9 18 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 NOV PY 1991 VL 146 IS 5 BP 1228 EP 1231 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA GM831 UT WOS:A1991GM83100007 PM 1682511 ER PT J AU DUGAN, TC SHIPLEY, WU YOUNG, RH VERHEY, LJ ALTHAUSEN, AF HENEY, NM MCMANUS, PL ABRAHAM, EH AF DUGAN, TC SHIPLEY, WU YOUNG, RH VERHEY, LJ ALTHAUSEN, AF HENEY, NM MCMANUS, PL ABRAHAM, EH TI BIOPSY AFTER EXTERNAL BEAM RADIATION-THERAPY FOR ADENOCARCINOMA OF THE PROSTATE - CORRELATION WITH ORIGINAL HISTOLOGICAL GRADE AND CURRENT PROSTATE SPECIFIC ANTIGEN LEVELS SO JOURNAL OF UROLOGY LA English DT Article DE PROSTATIC NEOPLASMS; ADENOCARCINOMA; ANTIGENS, NEOPLASM; RADIOTHERAPY; BIOPSY ID POST-IRRADIATION BIOPSY; STAGE-C ADENOCARCINOMA; RADICAL PROSTATECTOMY; BOOST THERAPY; CARCINOMA; CANCER; RECURRENCE; ULTRASOUND; PREVALENCE AB We obtained post-irradiation biopsies in 37 men with initially stage T3 prostatic adenocarcinoma treated by external beam radiotherapy. Eligibility for post-irradiation biopsy included no clinical local failure, interval since treatment of 24 months or more and no endocrine therapy. Of the 37 patients 23 (62%) had negative biopsies while 14 (38%) had positive biopsies. Of 23 patients whose original cancer was well or moderately differentiated 18 (78%) had negative biopsies, compared to only 5 of 14 (36%) of those with poorly differentiated cancer (p < 0.03). Among 19 patients whose current serum prostate specific antigen (PSA) value is less than 2.5 ng./ml. 15 (79%) had negative biopsies, compared to only 4 of 14 (29%) with a PSA level of greater than 2.5 ng./ml. (p < 0.02). These results strongly suggest that there is a low probability of positive post-irradiation biopsy regardless of its significance in men with a normal prostate by palpation and a normal serum PSA value. However, short followup since biopsy precludes analysis of the predictive value of post-irradiation biopsy on long-term local and distant disease status. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CTR CANC,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,CTR CANC,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,CTR CANC,SCH MED,DEPT UROL,BOSTON,MA 02114. FU NCI NIH HHS [CA 21239] NR 24 TC 77 Z9 77 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 NOV PY 1991 VL 146 IS 5 BP 1313 EP 1316 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA GM831 UT WOS:A1991GM83100027 PM 1719244 ER PT J AU THALI, M OLSHEVSKY, U FURMAN, C GABUZDA, D POSNER, M SODROSKI, J AF THALI, M OLSHEVSKY, U FURMAN, C GABUZDA, D POSNER, M SODROSKI, J TI CHARACTERIZATION OF A DISCONTINUOUS HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GP120 EPITOPE RECOGNIZED BY A BROADLY REACTIVE NEUTRALIZING HUMAN MONOCLONAL-ANTIBODY SO JOURNAL OF VIROLOGY LA English DT Article ID CD4 RECEPTOR-BINDING; ENVELOPE GLYCOPROTEIN; HTLV-III/LAV; T4 MOLECULE; RETROVIRUS; HIV-1; AIDS; CHIMPANZEES; IDENTIFICATION; INFECTIVITY AB While one hypervariable, linear neutralizing determinant on the human immunodeficiency virus type 1 (HIV-1) gp120 envelope glycoprotein has been well characterized, little is known about the conserved, discontinuous gp120 epitopes recognized by neutralizing antibodies in infected individuals. Here, the epitope recognized by a broadly reactive neutralizing monoclonal antibody (F105) derived from an HIV-1-infected patient was characterized by examining the effects of changes in conserved gp120 amino acids on antibody reactivity. The F105 epitope was disrupted by changes in gp120 amino acids 256 and 257, 368 to 370, 421, and 470 to 484, which is consistent with the discontinous nature of the epitope. Three of these regions are proximal to those previously shown to be important for CD4 binding, which is consistent with the ability of the F105 antibody to block gp120-CD4 interaction. Since F105 recognition was more sensitive to amino acid changes in each of the four identified gp120 regions than was envelope glycoprotein function, replication-competent mutant viruses that escaped neutralization by the F105 antibody were identified. These studies identify a conserved, functional HIV-1 gp120 epitope that is immunogenic in man and may serve as a target for therapeutic or prophylactic intervention. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115. BROWN UNIV,PROVIDENCE,RI 02912. FU NIAID NIH HHS [AI24755, AI26926, AI31783] NR 34 TC 228 Z9 228 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1991 VL 65 IS 11 BP 6188 EP 6193 PG 6 WC Virology SC Virology GA GL296 UT WOS:A1991GL29600063 PM 1717717 ER PT J AU KWONG, KK HOPKINS, AL BELLIVEAU, JW CHESLER, DA PORKKA, LM MCKINSTRY, RC FINELLI, DA HUNTER, GJ MOORE, JB BARR, RG ROSEN, BR AF KWONG, KK HOPKINS, AL BELLIVEAU, JW CHESLER, DA PORKKA, LM MCKINSTRY, RC FINELLI, DA HUNTER, GJ MOORE, JB BARR, RG ROSEN, BR TI PROTON NMR IMAGING OF CEREBRAL BLOOD-FLOW USING (H2O)-O-17 SO MAGNETIC RESONANCE IN MEDICINE LA English DT Note ID MAGNETIC-RESONANCE SPECTROSCOPY; MEAN TRANSIT TIME; BRAIN; TRACER; VOLUME; O-17; MR C1 CASE WESTERN RESERVE UNIV,DEPT ANAT,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,DEPT RADIOL,CLEVELAND,OH 44106. SAN FRANCISCO GEN HOSP,DEPT RADIOL,SAN FRANCISCO,CA 94110. RP KWONG, KK (reprint author), MASSACHUSETTS GEN HOSP,MGH NMR CTR,DEPT RADIOL,BLDG 149,BOSTON,MA 02129, USA. FU NCI NIH HHS [5P01CA48729-02, R01-CA40303]; NHLBI NIH HHS [R01-HL39810] NR 24 TC 45 Z9 46 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD NOV PY 1991 VL 22 IS 1 BP 154 EP 158 DI 10.1002/mrm.1910220116 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GN341 UT WOS:A1991GN34100015 PM 1798389 ER PT J AU BALDWIN, RD AF BALDWIN, RD TI PUTATIVE RADIONUCLIDE FEATURES OF LEFT-VENTRICULAR HYPERTROPHY SO MEDICAL HYPOTHESES LA English DT Article AB Distinctive changes in the left ventricular cavity seen with nuclear ventriculographic studies are described. These changes are postulated to be uniquely associated with left ventricular hypertrophy. RP BALDWIN, RD (reprint author), US DEPT VET AFFAIRS,NUCL MED SERV 115,MED & REG OFF CTR,TOGUS,ME 04330, USA. NR 0 TC 0 Z9 0 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 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD NOV PY 1991 VL 36 IS 3 BP 221 EP 222 DI 10.1016/0306-9877(91)90136-M PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW727 UT WOS:A1991GW72700013 PM 1838575 ER PT J AU CATLIN, EA UITVLUGT, ND DONAHOE, PK POWELL, DM HAYASHI, M MACLAUGHLIN, DT AF CATLIN, EA UITVLUGT, ND DONAHOE, PK POWELL, DM HAYASHI, M MACLAUGHLIN, DT TI MULLERIAN INHIBITING SUBSTANCE BLOCKS EPIDERMAL GROWTH-FACTOR RECEPTOR PHOSPHORYLATION IN FETAL-RAT LUNG MEMBRANES SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID FIBROBLAST-PNEUMONOCYTE FACTOR; FACTOR-BETA; TYROSINE KINASE; DUCT REGRESSION; INVITRO; PROTEIN; MATURATION; RABBIT; CELLS; PHOSPHATIDYLCHOLINE C1 MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT PATHOL,PISCATAWAY,NJ 08854. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP CATLIN, EA (reprint author), MASSACHUSETTS GEN HOSP,NEONATAL INTENS CARE UNIT,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA17393] NR 44 TC 18 Z9 18 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD NOV PY 1991 VL 40 IS 11 BP 1178 EP 1184 DI 10.1016/0026-0495(91)90213-G PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GN830 UT WOS:A1991GN83000011 PM 1943746 ER PT J AU BRADLEY, TB AF BRADLEY, TB TI LITERARY RULES AND WRITING SO MILITARY MEDICINE LA English DT Letter RP BRADLEY, TB (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASSN MILITARY SURG US PI BETHESDA PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0026-4075 J9 MIL MED JI Milit. Med. PD NOV PY 1991 VL 156 IS 11 BP A6 EP A6 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA GP395 UT WOS:A1991GP39500001 ER PT J AU GROVE, JR BANERJEE, P BALASUBRAMANYAM, A COFFER, PJ PRICE, DJ AVRUCH, J WOODGETT, JR AF GROVE, JR BANERJEE, P BALASUBRAMANYAM, A COFFER, PJ PRICE, DJ AVRUCH, J WOODGETT, JR TI CLONING AND EXPRESSION OF 2 HUMAN P70 S6 KINASE POLYPEPTIDES DIFFERING ONLY AT THEIR AMINO TERMINI SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID RIBOSOMAL-PROTEIN S6; MESSENGER-RNAS; PHOSPHORYLATION; IDENTIFICATION; ACTIVATION; CELLS; LIVER; CDNA; PURIFICATION; SEQUENCE AB Two classes of human cDNA encoding the insulin/mitogen-activated p70 S6 kinase have been isolated; the two classes differ only in the 5' region, such that the longer polypeptide (p70 S6 kinase alpha-I; calculated M(r) 58,946) consists of 525 amino acids, of which the last 502 residues are identical in sequence to the entire polypeptide encoded by the second cDNA (p70 S6 kinase alpha-II; calculated M(r) 56,153). Both p70 S6 kinase polypeptides predicted by these cDNAs are present in p70 S6 kinase purified from rat liver, and each is thus expressed in vivo. Moreover, both polypeptides are expressed from a single mRNA transcribed from the (longer) p70 S6 kinase alpha-I cDNA through the utilization of different translational start sites. Although the two p70 S6 kinase polypeptides differ by only 23 amino acid residues, the slightly longer alpha-I polypeptide exhibits anomalously slow mobility on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), migrating at an apparent M(r) of 90,000 probably because of the presence of six consecutive Arg residues immediately following the initiator methionine. Transient expression of p70 alpha-I and alpha-II S6 kinase cDNA in COS cells results in a 2.5- to 4-fold increase in overall S6 kinase activity. Upon immunoblotting, the recombinant p70 polypeptides appear as a closely spaced ladder of four to five bands between 65 and 70 kDa (alpha-II) and 85 and 90 kDa (alpha-I). Transfection with the alpha-II cDNA yields only the smaller set of bands, while transfection with the alpha-I cDNA generates both sets of bands. Mutation of Met-24 in the alpha-I cDNA to Leu or Thr suppresses synthesis of the alpha-II polypeptides. Only the p70 alpha-I and alpha-II polypeptides of slowest mobility on SDS-PAGE comigrate with the 70-and 90-kDa proteins observed in purified rat liver S6 kinase. Moreover, it is the recombinant p70 polypeptides of slowest mobility that coelute with S6 kinase activity on anion-exchange chromatography. The slower mobility and higher enzymatic activity of these p70 proteins is due to Ser/Thr phosphorylation, inasmuch as treatment with phosphatase 2A inactivates kinase activity and increases the mobility of the bands on SDS-PAGE in an okadaic acid-sensitive manner. Thus, the recombinant p70 S6 kinase undergoes multiple phosphorylation and partial activation in COS cells. Acquisition of S6 protein kinase catalytic function, however, is apparently restricted to the most extensively phosphorylated recombinant polypeptides. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIABET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. LUDWIG INST CANC RES,LONDON WIP 8BT,ENGLAND. RI Coffer, Paul/A-5769-2009; Woodgett, Jim/F-1087-2010 OI Woodgett, Jim/0000-0003-3731-5797 FU NIDDK NIH HHS [DK01410, DK41513] NR 35 TC 142 Z9 150 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD NOV PY 1991 VL 11 IS 11 BP 5541 EP 5550 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GL382 UT WOS:A1991GL38200018 PM 1922062 ER PT J AU HU, QJ BAUTISTA, C EDWARDS, GM DEFEOJONES, D JONES, RE HARLOW, E AF HU, QJ BAUTISTA, C EDWARDS, GM DEFEOJONES, D JONES, RE HARLOW, E TI ANTIBODIES SPECIFIC FOR THE HUMAN RETINOBLASTOMA PROTEIN IDENTIFY A FAMILY OF RELATED POLYPEPTIDES SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID LARGE T-ANTIGEN; HUMAN PROSTATE CARCINOMA; ADENOVIRUS E1A PROTEINS; REGION 1A PROTEINS; GENE-PRODUCT; RB GENE; SUSCEPTIBILITY GENE; EXPRESSION; SV40; TRANSFORMATION AB Even though the retinoblastoma gene is one of the best-studied tumor suppressor genes, little is known about its functional role. Like all tumor suppressor gene products, the retinoblastoma protein (pRB) is thought to inhibit some aspect of cell proliferation. It also appears to be a cellular target of several DNA tumor virus-transforming proteins, such as adenovirus E1A, human papillomavirus E7, or simian virus 40 large T antigen. To help in the analysis of pRB, we have prepared a new set of anti-human pRB monoclonal antibodies. In addition to being useful reagents for the study of human pRB, these antibodies display several unexpected properties. They can be used to distinguish different subsets of the pRBs on the basis of their phosphorylation states. Some are able to recognize pRB homologs in other species, including mice, chickens, and members of the genus Xenopus. In addition, some of these antibodies can bind directly to other cellular proteins that, like pRB, were originally identified through their association with adenovirus E1A. These immunologically cross-reactive proteins include the p107 and p300 proteins, and their recognition by antibodies raised against pRB suggests that several members of the E1A-targeted cellular proteins form a structurally and functionally related family. C1 COLD SPRING HARBOR LAB, POB 100, COLD SPRING HARBOR, NY 11724 USA. MASSACHUSETTS GEN HOSP, CTR CANC, BOSTON, MA 02129 USA. MERCK SHARP & DOHME LTD, DEPT CANC RES, W POINT, PA 19486 USA. FU NCI NIH HHS [CA13106] NR 46 TC 147 Z9 147 U1 0 U2 2 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 NOV PY 1991 VL 11 IS 11 BP 5792 EP 5799 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GL382 UT WOS:A1991GL38200044 PM 1717832 ER PT J AU ZAJCHOWSKI, DA SAGER, R AF ZAJCHOWSKI, DA SAGER, R TI INDUCTION OF ESTROGEN-REGULATED GENES DIFFERS IN IMMORTAL AND TUMORIGENIC HUMAN MAMMARY EPITHELIAL-CELLS EXPRESSING A RECOMBINANT ESTROGEN-RECEPTOR SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID HUMAN-BREAST-CANCER; CATHEPSIN-D; PROGESTERONE RECEPTORS; TUMOR PROGRESSION; MAMMALIAN-CELLS; GROWTH-FACTORS; LINES; PROTEIN; TISSUE; MCF-7 AB Studies on estrogen receptor (ER)-positive human breast cancer cell lines have shown that estrogen treatment positively modulates the expression of the genes encoding transforming growth factor-alpha (TGF-alpha), 52-kDa cathepsin-D, and pS2. To determine whether these genes would be similarly regulated by estrogens in normal human mammary epithelial cells, we stably transfected immortal nontumorigenic human mammary epithelial cells with an ER-encoding expression vector. ER-negative tumor cells were also transfected for comparison. Levels of TGF-alpha and 52-kDa cathepsin-D mRNA were enhanced by estrogen treatment of both ER-transfected immortal and tumorigenic cells, demonstrating that the ER by itself is sufficient to elicit estrogenic regulation of the expression of these genes. In contrast, expression of the pS2 gene was detected only in the ER-transfected tumor cells. The ER in both cell lines is capable of recognizing the pS2 promoter, however, since estrogen enhanced the activity of an introduced pS2-CAT reporter plasmid in transient expression analyses. These and other experiments with somatic cell hybrids between the immortal cells and ER+/pS2+MCF-7 tumor cells, where pS2 gene expression is extinguished, support the conclusion that the immortal nontumorigenic cells encode gene products that block endogenous pS2 expression. These results also imply that such repressors are not active in the tumor cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. FU NCI NIH HHS [CA-39814] NR 50 TC 42 Z9 43 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD NOV PY 1991 VL 5 IS 11 BP 1613 EP 1623 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GQ909 UT WOS:A1991GQ90900006 PM 1664044 ER PT J AU PETERMAN, TK GOODMAN, HM AF PETERMAN, TK GOODMAN, HM TI THE GLUTAMINE-SYNTHETASE GENE FAMILY OF ARABIDOPSIS-THALIANA - LIGHT REGULATION AND DIFFERENTIAL EXPRESSION IN LEAVES, ROOTS AND SEEDS SO MOLECULAR & GENERAL GENETICS LA English DT Article DE GLUTAMINE SYNTHETASE; ARABIDOPSIS-THALIANA; GENE EXPRESSION; LIGHT-REGULATION; GENE FAMILY ID PHASEOLUS-VULGARIS L; NUCLEOTIDE-SEQUENCE; START SITE; CHLOROPLAST; CDNA; PLANTS; POLYPEPTIDES; NITROGEN; PROTEINS; ISOENZYMES AB Glutamine synthetase (GS) plays an important role in the assimilation of nitrogen by higher plants. We present here a molecular analysis of the GS polypeptides, mRNAs, and genes of Arabidopsis thaliana. Western blot analysis of leaf and root protein extracts revealed at least two distinct GS polypeptides; 43 kDa and 39 kDa GS polypeptides were present in leaves, while only a 39 kDa GS was detected in roots. The 43 kDa GS polypeptide is light-inducible. In etiolated seedlings only the 39 kDa GS was detected. However, upon greening the 43 kDa GS increased to levels comparable to those observed in light-grown plants. Four distinct GS cDNA clones, lambda-Atgsl1, lambda-Atgsr1, lambda-Atgsr2 and lambda-Atkb6 were isolated and characterized. Their complete nucleotide and deduced amino acid sequences are presented. The coding sequences of the four clones are 70-88% similar while their 5' and 3' untranslated regions exhibit less than 50% similarity. Northern blots of leaf, root and germinated seed RNA revealed that the four cDNAs hybridize to mRNAs which are differentially expressed in the organs of Arabidopsis thaliana. Lambda-Atgsl1 is leaf-specific and hybridizes to a 1.6 kb mRNA. Both lambda-Atgsr1 and lambda-Atgskb6 hybridize to 1.4 kb mRNAs which are expressed in both roots and germinated seeds. Lambda-Atgsr2 hybridizes to a 1.4 kb mRNA, which is primarily expressed in roots with low levels of expression in seeds and leaves. Lambda-Atgsl1, which represents the leaf-specific mRNA, is induced by light. Lambda-Atgsl1 mRNA levels increase during the greening of etiolated seedlings while lambda-Atgsr1 levels remain constant. Southern blot analysis indicated that the Arabidopsis genome contains at least four and possibly five distinct GS genes. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 56 TC 119 Z9 130 U1 1 U2 11 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD NOV PY 1991 VL 230 IS 1-2 BP 145 EP 154 DI 10.1007/BF00290662 PG 10 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA GR246 UT WOS:A1991GR24600022 PM 1684022 ER PT J AU PRUITT, AA AF PRUITT, AA TI CENTRAL-NERVOUS-SYSTEM INFECTIONS IN CANCER-PATIENTS SO NEUROLOGIC CLINICS LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; NEUROLOGIC MANIFESTATIONS; MARROW TRANSPLANTATION; BACTERIAL-MENINGITIS; ENCEPHALITIS; FEATURES; THERAPY; TRIALS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 38 TC 25 Z9 25 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8619 J9 NEUROL CLIN JI Neurol. Clin. PD NOV PY 1991 VL 9 IS 4 BP 867 EP 888 PG 22 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA GN655 UT WOS:A1991GN65500006 PM 1758429 ER PT J AU LEVINE, DN CALVANIO, R RINN, WE AF LEVINE, DN CALVANIO, R RINN, WE TI THE PATHOGENESIS OF ANOSOGNOSIA FOR HEMIPLEGIA SO NEUROLOGY LA English DT Article ID RIGHT CEREBRAL INFARCTION; LEFT SPATIAL NEGLECT; RIGHT-HEMISPHERE; UNAWARENESS; LESIONS AB We compared patients with unawareness of hemiplegia lasting more than 1 month after right hemisphere stroke with other patients with right hemisphere stroke who became aware of hemiplegia within a few days after onset. Patients with persistent unawareness invariably had severe left hemisensory loss and usually had severe left spatial neglect. They were almost always apathetic; their thought lacked direction, clarity, and flexibility, and they had at least moderate impairment of intellect and memory. Their right hemisphere strokes were large and always affected the central gyri or their thalamic connections and capsular pathways. In addition, there was evidence of at least mild left hemisphere damage, most commonly caused by age-associated atrophy. The pathogenesis of anosognosia for hemiplegia may involve failure to discover paralysis because proprioceptive mechanisms that ordinarily inform an individual about the position and movement of limbs are damaged, and the patient, because of additional cognitive defects, lacks the capacity to make the necessary observations and inferences to diagnose the paralysis. We discuss the implications of this "discovery" theory and contrast it with other explanations of anosognosia. C1 SPAULDING REHABIL HOSP,NEUROL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NR 48 TC 112 Z9 114 U1 3 U2 8 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV PY 1991 VL 41 IS 11 BP 1770 EP 1781 PG 12 WC Clinical Neurology SC Neurosciences & Neurology GA GQ467 UT WOS:A1991GQ46700013 PM 1944907 ER PT J AU BUZZI, MG CARTER, WB SHIMIZU, T HEATH, H MOSKOWITZ, MA AF BUZZI, MG CARTER, WB SHIMIZU, T HEATH, H MOSKOWITZ, MA TI DIHYDROERGOTAMINE AND SUMATRIPTAN ATTENUATE LEVELS OF CGRP IN PLASMA IN RAT SUPERIOR SAGITTAL SINUS DURING ELECTRICAL-STIMULATION OF THE TRIGEMINAL GANGLION SO NEUROPHARMACOLOGY LA English DT Article DE CALCITONIN GENE-RELATED PEPTIDE; NEUROGENIC INFLAMMATION; MIGRAINE; PREJUNCTIONAL RECEPTORS; 5-HT1D ID GENE-RELATED PEPTIDE; SUBSTANCE-P; DURA MATER; BLOOD-VESSELS; VASCULAR HEADACHES; GUINEA-PIG; EXTRAVASATION; GR43175; RELEASE; TACHYKININS AB Vasoactive neuropeptides, present in unmyelinated C-fibers, can be released from perivascular sensory axons by antidromic stimulation, to mediate vasodilation and extravasation of plasma protein (neurogenic inflammation). In this report, the effects of antidromic trigeminal stimulation on levels of calcitonin gene-related peptide (CGRP) in plasma were examined in the superior sagittal sinus and the effects of drugs that have been shown previously to block extravasation of neurogenic plasma determined. The levels of immunoreactive CGRP in plasma were measured both before and during electrical stimulation of the trigeminal ganglion (0.1-1.0 mA, 5 msec, 5 Hz, 3-5 min), using a highly specific and sensitive immunochemiluminometric assay. Levels of CGRP increased and became maximal within the first minute of stimulation. The increases were detectable at intensities of current as small as 0.1 mA. Peak levels related to the intensity of the stimulus. Samples from femoral arterial blood did not show concomitant increases at 1 min. Pretreatment with dihydroergotamine (DHE) (50-mu-g/kg i.v.) did not change the baseline levels but decreased levels of CGRP during stimulation (0.3 mA), by 55% at 1 min and 50% at 3 min. Sumatriptan (GR43175) (300-mu-g/kg) attenuated the increase by 57% at 3 min (0.1 mA, 5 msec, 5 Hz) but not after 1 min of stimulation, although decreases were observed at the latter time during an individual experiment. Drug-induced attentuation of levels of CGRP in plasma may reflect inhibition of release, to thereby provide evidence to explain blockade of neurogenic extravasation of plasma. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114. MAYO CLIN & MAYO FDN,DEPT MED,ENDOCRINE RES UNIT,ROCHESTER,MN 55905. RI Moskowitz, Michael/D-9916-2011 FU NIDDK NIH HHS [DK-07352, DK-32526]; NINDS NIH HHS [NS-21558] NR 36 TC 213 Z9 217 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0028-3908 J9 NEUROPHARMACOLOGY JI Neuropharmacology PD NOV PY 1991 VL 30 IS 11 BP 1193 EP 1200 DI 10.1016/0028-3908(91)90165-8 PG 8 WC Neurosciences; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA GN931 UT WOS:A1991GN93100008 PM 1663596 ER PT J AU DELAMAZA, MS FOSTER, CS AF DELAMAZA, MS FOSTER, CS TI NECROTIZING SCLERITIS AFTER OCULAR SURGERY - A CLINICOPATHOLOGICAL STUDY SO OPHTHALMOLOGY LA English DT Article ID PERIPHERAL ULCERATIVE KERATITIS; WEGENERS GRANULOMATOSIS; RHEUMATOID-ARTHRITIS; IMMUNE-COMPLEXES; CATARACT-SURGERY; ANTICYTOPLASMIC AUTOANTIBODIES; INTRAOCULAR LENSES; VASCULITIS; DISEASE; HYPOCOMPLEMENTEMIA AB Necrotizing scleritis may appear after trauma to the sclera. The authors studied 1 0 patients in whom necrotizing scleritis developed after ocular surgery, The interval between surgery and onset of scleritis varied from 2 weeks to 6 months. Nine patients (90%) were found to have an underlying autoimmune vasculitic systemic disease, which was subsequently treated with immunosuppression. One patient was found to have a local infectious process, which was treated with antibiotics. Appropriate studies led to the discovery and subsequent treatment of a systemic disease or an infectious process in 6 of the 10 patients; the other 4 patients had been previously diagnosed. Results of immunohistochemical studies on resected conjunctival and/or sclera suggest local immune complex deposition, increased HLA-DR expression, and increased helper T-cell participation in conjunctiva and/or scleral tissues after trauma in patients with underlying systemic autoimmune vasculitic disease. The results emphasize the need for meticulous diagnostic pursuit of potentially lethal systemic autoimmune vasculitic disease in patients with necrotizing scleritis after intraocular surgery. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,OCULAR IMMUNOL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 47 TC 53 Z9 54 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD NOV PY 1991 VL 98 IS 11 BP 1720 EP 1726 PG 7 WC Ophthalmology SC Ophthalmology GA GN663 UT WOS:A1991GN66300027 ER PT J AU DUBINETT, SM CALLAHAN, RJ XIA, WJ AHMAD, M STRAUSS, HW KRADIN, RL AF DUBINETT, SM CALLAHAN, RJ XIA, WJ AHMAD, M STRAUSS, HW KRADIN, RL TI CYTOKINE ADMINISTRATION ALTERS THE DISTRIBUTION OF ACTIVATED LYMPHOCYTES TO THE LUNG SO PATHOBIOLOGY LA English DT Article DE CYTOKINES; LYMPHOCYTE TRAFFICKING; CANCER IMMUNOTHERAPY; INTERFERON-GAMMA; INTERLEUKIN-1-ALPHA; INTERLEUKIN-2; TUMOR NECROSIS FACTOR-ALPHA ID TUMOR-INFILTRATING LYMPHOCYTES; ADOPTIVE IMMUNOTHERAPY; ADVANCED CANCER; LYMPHOID-CELLS; AUTOLOGOUS LYMPHOCYTES; MONOCLONAL-ANTIBODIES; INVIVO DISTRIBUTION; RECOMBINANT IL-2; NECROSIS FACTOR; INTERLEUKIN-2 AB The effects of intraperitoneal injections of recombinant interleukin-1-alpha (IL-1; 250,000 U/day), interleukin-2 (IL-2; 50,000 units/day), interferon-gamma (IFN-gamma; 50,000 U/day) and tumor necrosis factor-alpha (TNF; 100,000 U/day), on the biodistribution of concanavalin A (Con A)-activated, indium-111-labeled lympohocytes were evaluated in BALB/c mice. Syngeneic spleen cells were activated for 48 h in medium with Con A (5-mu-g/ml) and maintained in culture for 72 h in IL-2 (1,000 U/ml). Groups of 12 mice were treated for 4 days with either one of the cytokines or saline. On day 4, mice received 10(7) lymphocytes (3-5-mu-Ci) intravenously. Mice were sacrificed at 4 and 24 h following injection and the percent of administered dose per organ was determined. TNF and IL-1 produced a significant increase in lung uptake of radiolabeled lymphocytes at 4 and 24 h, whereas IL-2 and IFN-gamma decreased uptake at both time points. IL-1 increased uptake by liver at 4 and 24 h while IL-2 increased uptake only at 4 h. We conclude that the distribution of activated lymphocytes following adoptive transfer is altered by cytokines. This finding may have important implications for cell delivery during adoptive immunotherapy. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,IMMUNOPATHOL UNIT,BOX 5,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,PULM UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,NUCL MED UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT PULM & CRIT CARE MED,LOS ANGELES,CA 90024. VET ADM WADSWORTH MED CTR,LOS ANGELES,CA 90073. FU NCI NIH HHS [CA43244]; NHLBI NIH HHS [HL07354] NR 31 TC 6 Z9 6 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-2008 J9 PATHOBIOLOGY JI Pathobiology PD NOV-DEC PY 1991 VL 59 IS 6 BP 372 EP 377 DI 10.1159/000163680 PG 6 WC Cell Biology; Pathology SC Cell Biology; Pathology GA GB517 UT WOS:A1991GB51700002 PM 1930689 ER PT J AU ROSENBERGER, PB AF ROSENBERGER, PB TI ATTENTION-DEFICIT SO PEDIATRIC NEUROLOGY LA English DT Review ID MINIMAL BRAIN-DYSFUNCTION; HYPERACTIVE-CHILDREN; NEGLECT SYNDROME; FOLLOW-UP; METHYLPHENIDATE; DISORDER; BEHAVIOR; MEMORY; ADULTS; FAMILIES AB Attention deficit, among the most commonly diagnosed functional deficits in pediatric neurology, is, like epilepsy, most often idiopathic. It can also be a symptom of many neuropathologic states. Although a lifelong problem, attention deficit is most troublesome during school years, because, like asthma, it is highly sensitive to environmental influence. The neurologist can consider attention deficit in its own right, apart from hyperkinesis and other associated behavior disorders, as a cognitive limitation and handicap to academic progress. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DIV CHILD NEUROL,BOSTON,MA 02114. RP ROSENBERGER, PB (reprint author), MASSACHUSETTS GEN HOSP,LEARNING DISORDERS UNIT,ACC 705,BOSTON,MA 02114, USA. NR 107 TC 13 Z9 13 U1 2 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0887-8994 J9 PEDIATR NEUROL JI Pediatr. Neurol. PD NOV-DEC PY 1991 VL 7 IS 6 BP 397 EP 405 DI 10.1016/0887-8994(91)90021-C PG 9 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA GY744 UT WOS:A1991GY74400001 PM 1797006 ER PT J AU PERRIN, JM STEIN, REK AF PERRIN, JM STEIN, REK TI REINTERPRETING DISABILITY - CHANGES IN SUPPLEMENTAL SECURITY INCOME FOR CHILDREN SO PEDIATRICS LA English DT Article C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX MUNICIPAL HOSP CTR,BRONX,NY 10461. RP PERRIN, JM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WACC 715,BOSTON,MA 02114, USA. NR 6 TC 25 Z9 25 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 NOV PY 1991 VL 88 IS 5 BP 1047 EP 1051 PG 5 WC Pediatrics SC Pediatrics GA GM934 UT WOS:A1991GM93400025 PM 1844354 ER PT J AU SIMON, HK AF SIMON, HK TI RESIDENT RELATED LIABILITY IN THE EMERGENCY DEPARTMENT SO PEDIATRICS LA English DT Letter RP SIMON, HK (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,135 COMMONWEALTH AVE,UNIT 3,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 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 NOV PY 1991 VL 88 IS 5 BP 1076 EP 1076 PG 1 WC Pediatrics SC Pediatrics GA GM934 UT WOS:A1991GM93400041 PM 1945621 ER PT J AU HWANG, I KOHCHI, T HAUGE, BM GOODMAN, HM SCHMIDT, R CNOPS, G DEAN, C GIBSON, S IBA, K LEMIEUX, B ARONDEL, V DANHOFF, L SOMERVILLE, C AF HWANG, I KOHCHI, T HAUGE, BM GOODMAN, HM SCHMIDT, R CNOPS, G DEAN, C GIBSON, S IBA, K LEMIEUX, B ARONDEL, V DANHOFF, L SOMERVILLE, C TI IDENTIFICATION AND MAP POSITION OF YAC CLONES COMPRISING ONE-THIRD OF THE ARABIDOPSIS GENOME SO PLANT JOURNAL LA English DT Article ID POLYMORPHISM LINKAGE MAP; THALIANA; YEAST; DNA AB YAC clones corresponding to 125 Arabidopsis thaliana RFLP markers have been identified. At least one YAC clone has been isolated for each of the RFLP markers tested. Based on CHEF gel analysis of 196 clones, the mean insert size of the available Arabidopsis YAC libraries is approximately 160 kb. The YACs of known genetic map location encompass about 30% of the Arabidopsis genome. The results presented here represent a first step towards assembly of an overlapping YAC library of the A. thaliana genome. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. JOHN INNES CTR,AFRC,INST PLANT SCI RES,CAMBRIDGE LAB,NORWICH NR4 7UJ,ENGLAND. MICHIGAN STATE UNIV,US DOE,PLANT RES LAB,E LANSING,MI 48824. RI Somerville, Christopher/A-4048-2009 OI Somerville, Christopher/0000-0003-4647-0094 NR 11 TC 56 Z9 56 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0960-7412 J9 PLANT J JI Plant J. PD NOV PY 1991 VL 1 IS 3 BP 367 EP 374 DI 10.1046/j.1365-313X.1991.t01-5-00999.x PG 8 WC Plant Sciences SC Plant Sciences GA GW290 UT WOS:A1991GW29000011 PM 1844889 ER PT J AU VACANTI, CA LANGER, R SCHLOO, B VACANTI, JP AF VACANTI, CA LANGER, R SCHLOO, B VACANTI, JP TI SYNTHETIC-POLYMERS SEEDED WITH CHONDROCYTES PROVIDE A TEMPLATE FOR NEW CARTILAGE FORMATION SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID ARTICULAR-CARTILAGE AB A new approach for tissue creation using synthetic biocompatible and biodegradable polymers as templates onto which cells are seeded is presented. This report concerns the generation of homogeneous plates of stable mature cartilage in vivo. The delivery of chondrocytes on synthetic polymers configured to provide a large surface area for cell attachment and thus to allow cell function and survival by diffusion of nutrients has resulted in the creation of macroscopic plates of up to 100 mg of new cartilage subcutaneously in 19 of 21 animals. The approximate dimensions and configuration of the original templates were maintained as new cartilage was formed and the polymers resorbed. C1 MIT,DEPT CHEM ENGN,CAMBRIDGE,MA 02139. DEBORAH HEART & LUNG CTR,DEPT PATHOL,BROWNS MILLS,NJ 08015. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. RP VACANTI, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIOL,WHITE 5,BOSTON,MA 02114, USA. NR 18 TC 413 Z9 439 U1 4 U2 25 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 NOV PY 1991 VL 88 IS 5 BP 753 EP 759 DI 10.1097/00006534-199111000-00001 PG 7 WC Surgery SC Surgery GA GM634 UT WOS:A1991GM63400001 PM 1924560 ER PT J AU GORNET, MF RANDOLPH, MA SCHOFIELD, BH YAREMCHUK, MJ WEILAND, AJ AF GORNET, MF RANDOLPH, MA SCHOFIELD, BH YAREMCHUK, MJ WEILAND, AJ TI IMMUNOLOGICAL AND ULTRASTRUCTURAL-CHANGES DURING EARLY REJECTION OF VASCULARIZED BONE ALLOGRAFTS SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID HUMORAL IMMUNE-RESPONSE; ORGAN ALLOGRAFTS; TRANSPLANTATION; RATS; MECHANISMS; SURVIVAL; GRAFTS; MODEL; DOGS; MICE AB This investigation evaluated ultrastructural changes during the earliest phase of immunologic rejection of vascularized bone allografts in a genetically defined rat model. These results were correlated with the cell-mediated and humoral immunologic responses during this time period. Employing a model for heterotopic allograft transplantation, 33 rats divided into four categories were evaluated. Group I consisted of ungrafted (naive) Lewis and Brown Norway rats; group II consisted of Lewis-to-Lewis vascularized bone isografts; group III consisted of Lewis-to-Brown Norway vascularized bone allografts; and group IV consisted of Lewis-to-Brown Norway vascularized bone allografts in rats receiving cyclosporine (10 mg/kg/day). Experimental animals were sacrificed at 3, 5, and 7 days. Immunologic analysis was performed using a cell-mediated lymphocytotoxicity assay and a complement-dependent cytotoxic antibody assay. The results of this study show that rejection of vascularized bone allografts appears as early as 3 days postoperatively, with osteocytes and vascular endothelium being the first elements affected. This early rejection is probably a manifestation of the humoral response. All changes secondary to rejection were arrested by cyclosporine. C1 CORNELL UNIV,HOSP SPECIAL SURG,DEPT ORTHOPAED SURG,535 & 70TH ST,NEW YORK,NY 10021. NATL ACAD SCI,INST MED,DIV HLTH SCI POLICY,WASHINGTON,DC 20418. MASSACHUSETTS GEN HOSP,DIV PLAST SURG,BOSTON,MA 02114. JOHNS HOPKINS UNIV,SCH MED,DEPT ORTHOPAED SURG,BALTIMORE,MD 21205. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIADDK NIH HHS [AM25791] NR 35 TC 17 Z9 18 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 NOV PY 1991 VL 88 IS 5 BP 860 EP 868 DI 10.1097/00006534-199111000-00019 PG 9 WC Surgery SC Surgery GA GM634 UT WOS:A1991GM63400019 PM 1924573 ER PT J AU MAY, JW AF MAY, JW TI THE HONOR AND RESPONSIBILITY OF TEACHING IN PLASTIC-SURGERY SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Editorial Material RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,NO 353,BOSTON,MA 02114, USA. NR 8 TC 6 Z9 6 U1 0 U2 1 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 NOV PY 1991 VL 88 IS 5 BP 869 EP 873 PG 5 WC Surgery SC Surgery GA GM634 UT WOS:A1991GM63400020 PM 1924574 ER PT J AU HABER, DA SOHN, RL BUCKLER, AJ PELLETIER, J CALL, KM HOUSMAN, DE AF HABER, DA SOHN, RL BUCKLER, AJ PELLETIER, J CALL, KM HOUSMAN, DE TI ALTERNATIVE SPLICING AND GENOMIC STRUCTURE OF THE WILMS-TUMOR GENE-WT1 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ALTERNATIVE SPLICING; GENOMIC STRUCTURE ID DNA-BINDING PROTEINS; FINGER; SEQUENCE; DELETION; GROWTH; LOCUS AB The chromosome 11p13 Wilms tumor susceptibility gene WT1 appears to play a crucial role in regulating the proliferation and differentiation of nephroblasts and gonadal tissue. The WT1 gene consists of 10 exons, encoding a complex pattern of mRNA species: four distinct transcripts are expressed, the presence or absence of two alternative splices. Splice I consists of a separate exon, encoding 17 amino acids, which is inserted between the proline-rich amino terminus and the zinc finger domains. Splice II arises from the use of an alternative 5' splice junction and results in the insertion of 3 amino acids between zinc fingers 3 and 4. RNase protection analysis demonstrates that the most prevalent splice variant in both human and mouse is that which contains both alternative splices, whereas the least common is the transcript missing both splices. The relative distribution of splice variants is highly conserved between normal fetal kidney tissue and Wilms tumors that have intact WT1 transcripts. The ratio of these different WT1 mRNA species is also maintained as a function of development in the mouse kidney and in various mouse tissues expressing WT1. The conservation in structure and relative levels of each of the four WT1 mRNA species suggests that each encoded polypeptide makes a significant contribution to normal gene function. The control Of cellular proliferation and differentiation exerted by the WT1 gene products may involve interactions between four polypeptides with distinct targets and functions. C1 MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. RP HABER, DA (reprint author), MIT,CTR CANC RES,CAMBRIDGE,MA 02139, USA. FU NCI NIH HHS [CA 08605]; NHGRI NIH HHS [HG00299] NR 21 TC 541 Z9 555 U1 3 U2 17 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 NOV PY 1991 VL 88 IS 21 BP 9618 EP 9622 DI 10.1073/pnas.88.21.9618 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GM781 UT WOS:A1991GM78100050 PM 1658787 ER PT J AU ROSENBERG, CL WONG, E PETTY, EM BALE, AE TSUJIMOTO, Y HARRIS, NL ARNOLD, A AF ROSENBERG, CL WONG, E PETTY, EM BALE, AE TSUJIMOTO, Y HARRIS, NL ARNOLD, A TI PRAD1, A CANDIDATE BCL1 ONCOGENE - MAPPING AND EXPRESSION IN CENTROCYTIC LYMPHOMA SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE D11S287E; CHROMOSOME-11Q13; CYCLIN; PARATHYROID; BREAST CANCER ID B-CELL LYMPHOMA; INTERMEDIATE LYMPHOCYTIC LYMPHOMA; CHROMOSOME-TRANSLOCATION; GENE REARRANGEMENTS; MALIGNANT-LYMPHOMA; MOLECULAR ANALYSIS; MULTIPLE-MYELOMA; PROTO-ONCOGENE; MYC ONCOGENE; LOCUS AB Rearrangement of the BCL1 (B-cell lymphoma 1) region on chromosome 11q13 appears to be highly characteristic of centrocytic lymphoma and also is found infrequently in other B-cell neoplasms. Rearrangement is thought to deregulate a nearby protooncogene, but transcribed sequences in the immediate vicinity of BCL1 breakpoints had not been identified. PRAD1, previously designated D11S287E, was identified on 11q13 as a chromosomal breakpoint region rearranged with the parathyroid hormone gene in a subset of parathyroid adenomas; this highly conserved putative oncogene, which encodes a novel cyclin, has been linked to BCL1 and implicated also in subsets of breast and squamous cell neoplasms with 11q13 amplification. We report pulsed-field gel electrophoresis data showing BCL1 and PRAD1 to be no more than 130 kilobases apart. PRAD1 mRNA is abundantly expressed in seven of seven centrocytic lymphomas (Kiel classification), in contrast to 13 closely related but noncentrocytic lymphomas. Three of the seven centrocytic lymphomas had detectable BCL1 DNA rearrangement. Also, two unusual cases of CLL with BCL1 rearrangement overexpressed PRAD1, in contrast to five CLL controls. Thus, PRAD1 is an excellent candidate "BCL1 oncogene." Its overexpression may be a key consequence of rearrangement of the BCL1 vicinity in B-cell neoplasms and a unifying pathogenetic feature in centrocytic lymphoma. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. WISTAR INST,PHILADELPHIA,PA 19104. YALE UNIV,SCH MED,DEPT HUMAN GENET,NEW HAVEN,CT 06510. FU NIDDK NIH HHS [DK11794] NR 51 TC 439 Z9 442 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV PY 1991 VL 88 IS 21 BP 9638 EP 9642 DI 10.1073/pnas.88.21.9638 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GM781 UT WOS:A1991GM78100054 PM 1682919 ER PT J AU SHAFER, GE EMERY, DW GUSTAFSSON, K GERMANA, S ANDERSON, WF SACHS, DH LEGUERN, C AF SHAFER, GE EMERY, DW GUSTAFSSON, K GERMANA, S ANDERSON, WF SACHS, DH LEGUERN, C TI EXPRESSION OF A SWINE CLASS-II GENE IN MURINE BONE-MARROW HEMATOPOIETIC-CELLS BY RETROVIRAL-MEDIATED GENE-TRANSFER SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MAJOR HISTOCOMPATIBILITY COMPLEX; DR BETA-GENE; RETROVIRAL VECTOR ID LONG-TERM EXPRESSION; STEM-CELLS; MINIATURE SWINE; HLA-DR; ADENOSINE-DEAMINASE; NUCLEOTIDE-SEQUENCE; CHAIN GENE; VECTORS; CDNA; ANTIGEN AB As a first step in assessing the efficacy of a gene transfer approach to the induction of transplantation tolerance in our miniature swine model, double-copy retroviral vectors engineered to express a drug-resistance marker (neomycin) and a swine class II DRB cDNA were constructed. Infectious particles containing these vectors were produced at a titer of > 1 x 10(6) G418-resistant colony-forming units/ml using both ecotropic and amphotropic packaging cell lines. Flow cytometric analysis of DRA-transfected murine fibroblasts subsequently transduced with virus-containing supernatants demonstrated that the transferred sequences were sufficient to produce DR surface expression. Cocultivation of murine bone marrow with high-titer producer lines leads to the transduction of 40% of granulocyte/macrophage colony-forming units (CFU-GM) as determined by the frequency of colony formation under G418 selection. After nearly 5 weeks in long-term bone marrow culture, virus-exposed marrow still contained G418-resistant CFU-GM at a frequency of 25%. In addition, virtually all of the transduced and selected colonies contained DRB-specific transcripts. These results suggest that a significant proportion of very primitive myelopoietic precursor cells can be transduced with the DRB recombinant vector and that vector sequences are expressed in the differentiated progeny of these cells. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,DIV CANC BIOL DIAG & CTR,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. NR 30 TC 24 Z9 24 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 NOV PY 1991 VL 88 IS 21 BP 9760 EP 9764 DI 10.1073/pnas.88.21.9760 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GM781 UT WOS:A1991GM78100081 PM 1946400 ER PT J AU BAHRAM, S ARNOLD, D BRESNAHAN, M STROMINGER, JL SPIES, T AF BAHRAM, S ARNOLD, D BRESNAHAN, M STROMINGER, JL SPIES, T TI 2 PUTATIVE SUBUNITS OF A PEPTIDE PUMP ENCODED IN THE HUMAN MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II REGION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID NUCLEOTIDE-BINDING FOLD; RESISTANT HUMAN-CELLS; P-GLYCOPROTEIN GENE; HLA-B ANTIGENS; MULTIDRUG-RESISTANCE; CYSTIC-FIBROSIS; BACTERIAL TRANSPORT; ENDOGENOUS ANTIGEN; PROTEIN; MUTATIONS AB The class II region of the human major histocompatibility complex (MHC) may encode several genes controlling the processing of endogenous antigen and the presentation of peptide epitopes by MHC class I molecules to cytotoxic T lymphocytes. A previously described peptide supply factor (PSF1) is a member of the multidrug-resistance family of transporters and may pump cytosolic peptides into the membrane-bound compartment where class I molecules assemble. A second transporter gene, PSF2, was identified 10 kilobases (kb) from PSF1, near the class II DOB gene. The complete sequences of PSF1 and PSF2 were determined from cDNA clones. The translation products are closely related in sequence and predicted secondary structure. Both contain a highly conserved ATP-binding fold and share 25% homology in a hydrophobic domain with a tentative number of eight membrane-spanning segments. Based on the principle dimeric organization of these two domains in other transporters, PSF1 and PSF2 may function as complementary subunits, independently as homodimers, or both. Taken together with previous genetic evidence, the coregulation of PSF1 and PSF2 by gamma-interferon and the to-some-degree coordinate transcription of these genes suggest a common role in peptide-loading of class I molecules, although a distinct function of PSF2 cannot be ruled out. RP BAHRAM, S (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-30581]; NIDDK NIH HHS [DK-30241] NR 52 TC 172 Z9 175 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 NOV PY 1991 VL 88 IS 22 BP 10094 EP 10098 DI 10.1073/pnas.88.22.10094 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GP895 UT WOS:A1991GP89500039 PM 1946428 ER PT J AU BRASH, DE RUDOLPH, JA SIMON, JA LIN, A MCKENNA, GJ BADEN, HP HALPERIN, AJ PONTEN, J AF BRASH, DE RUDOLPH, JA SIMON, JA LIN, A MCKENNA, GJ BADEN, HP HALPERIN, AJ PONTEN, J TI A ROLE FOR SUNLIGHT IN SKIN-CANCER - UV-INDUCED P53 MUTATIONS IN SQUAMOUS-CELL CARCINOMA SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE UV LIGHT; TUMOR SUPPRESSOR GENES ID ULTRAVIOLET-RADIATION; MAMMALIAN-CELLS; STRAND SPECIFICITY; ESCHERICHIA-COLI; SHUTTLE VECTOR; DNA-SEQUENCE; GENE; MUTAGENESIS; PHOTOPRODUCT; MELANOMA AB Sunlight is a carcinogen to which everyone is exposed. Its UV component is the major epidemiologic risk factor for squamous cell carcinoma of the skin. Of the multiple steps in tumor progression. those that are sunlight-related would be revealed if they contained mutations specific to UV. In a series of New England and Swedish patients, we find that 14/24 (58%) of invasive squamous cell carcinomas of the skin contain mutations in the p53 tumor suppressor gene, each altering the amino acid sequence. Involvement of UV light in these p53 mutations is indicated by the presence in three of the tumors of a CC --> TT double-base change, which is only known to be induced by UV. UV is also implicated by a UV-like occurrence of mutations exclusively at dipyrimidine sites, including a high frequency of C --> T substitutions. p53 mutations in internal malignancies do not show these UV-specific mutations. The dipyrimidine specificity also implicates dipyrimidine photoproducts containing cytosine as oncogenic photoproducts. We believe these results identify a carcinogen-related step in a gene involved in the subsequent human cancer. C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. DERMATOPATHOL ASSOCIATES NEW YORK,NEW ROCHELLE,NY 10805. UNIV HOSP UPPSALA,DEPT PATHOL,S-75185 UPPSALA,SWEDEN. RP BRASH, DE (reprint author), YALE UNIV,SCH MED,DEPT THERAPEUT RADIOL,NEW HAVEN,CT 06510, USA. FU NCI NIH HHS [CA39238] NR 52 TC 1408 Z9 1420 U1 12 U2 89 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 NOV PY 1991 VL 88 IS 22 BP 10124 EP 10128 DI 10.1073/pnas.88.22.10124 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GP895 UT WOS:A1991GP89500045 PM 1946433 ER PT J AU KOBIERSKI, LA CHU, HM TAN, Y COMB, MJ AF KOBIERSKI, LA CHU, HM TAN, Y COMB, MJ TI CAMP-DEPENDENT REGULATION OF PROENKEPHALIN BY JUND AND JUNB - POSITIVE AND NEGATIVE EFFECTS OF AP-1 PROTEINS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE OPIOID; PROTEIN KINASE-A; TRANSCRIPTIONAL REGULATION; 2ND-MESSENGER-INDUCIBLE ENHANCER ID IMMEDIATE EARLY GENES; MESSENGER-RNA CONTENT; CYCLIC-AMP; SOMATOSTATIN GENE; ADRENAL-MEDULLA; C-FOS; EXPRESSION; TRANSCRIPTION; CELLS; NEUROPEPTIDE AB We demonstrate that JunD, a component of the AP-1 transcription factor complex, activates transcription of the human proenkephalin gene in a fashion that is completely dependent upon the cAMP-dependent protein kinase, protein kinase A. Activation of proenkephalin transcription by JunD is dependent upon a previously characterized cAMP-, phorbol ester-, and Ca2+-inducible enhancer, and JunD is shown to bind the enhancer as a homodimer. Another component of the AP-1 transcription complex, JunB, is shown to inhibit activation mediated by JunD. As a homodimer JunB is unable to bind the enhancer; however in the presence of c-Fos, high-affinity binding is observed. Furthermore, JunB is shown to activate transcription of genes linked to both cAMP and phorbol ester response elements in a protein kinase A-dependent fashion, further blurring the distinction between these response elements. These results demonstrate that the transcriptional activity of an AP-1-related protein is regulated by the cAMP-dependent second-messenger pathway and suggest that JunD and other AP-1-related proteins may play an important role in the regulation of gene expression by cAMP-dependent intracellular signaling pathways. C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOLEC NEUROBIOL LAB,BOSTON,MA 02129. FU NIDA NIH HHS [DA05706-01, DAK02 0151] NR 36 TC 150 Z9 150 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 NOV PY 1991 VL 88 IS 22 BP 10222 EP 10226 DI 10.1073/pnas.88.22.10222 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GP895 UT WOS:A1991GP89500065 PM 1719551 ER PT J AU ZHANG, ZJ DAVIDSON, L EISENBARTH, G WEINER, HL AF ZHANG, ZJ DAVIDSON, L EISENBARTH, G WEINER, HL TI SUPPRESSION OF DIABETES IN NONOBESE DIABETIC MICE BY ORAL-ADMINISTRATION OF PORCINE INSULIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DIABETES; TOLERANCE; AUTOIMMUNITY; IMMUNOTHERAPY; INSULIN ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; COLLAGEN-INDUCED ARTHRITIS; NOD MICE; II COLLAGEN; IMMUNE-RESPONSES; MELLITUS; MOUSE; RATS; LYMPHOCYTES AB Nonobese diabetic (NOD) mice spontaneously develop an autoimmune form of diabetes associated with insulitis. A number of immunomodulatory therapies have been investigated as a treatment for the disease process. Oral administration of the autoantigens myelin basic protein and collagen type II suppresses experimental models of encephalomyelitis and arthritis. We have now found that oral administration of insulin delays the onset and reduces the incidence of diabetes in NOD mice over a 1-year period in animals administered 1 mg of porcine insulin orally twice a week for 5 weeks and then weekly until 1 year of age. As expected, orally administered insulin had no metabolic effect on blood glucose levels. The severity of lymphocytic infiltration of pancreatic islets was also reduced by oral administration of insulin. Furthermore, splenic T cells from animals orally treated with insulin adoptively transfer protection against diabetes, demonstrating that oral insulin administration generates active cellular mechanisms that suppress disease. These results show that oral insulin affects diabetes and the pancreatic cellular inflammatory process in the NOD mouse and raise the possibility that oral administration of insulin or other pancreatic autoantigens may provide a new approach for the treatment of autoimmune diabetes. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. RP ZHANG, ZJ (reprint author), BRIGHAM & WOMENS HOSP,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [2P30DE36836]; NIDDK NIH HHS [DK32083] NR 37 TC 494 Z9 504 U1 4 U2 9 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 NOV PY 1991 VL 88 IS 22 BP 10252 EP 10256 DI 10.1073/pnas.88.22.10252 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GP895 UT WOS:A1991GP89500071 PM 1946445 ER PT J AU RUNGE, MS QUERTERMOUS, T ZAVODNY, PJ LOVE, TW BODE, C FREITAG, M SHAW, SY HUANG, PL CHOU, CC MULLINS, D SCHNEE, JM SAVARD, CE ROTHENBERG, ME NEWELL, JB MATSUEDA, GR HABER, E AF RUNGE, MS QUERTERMOUS, T ZAVODNY, PJ LOVE, TW BODE, C FREITAG, M SHAW, SY HUANG, PL CHOU, CC MULLINS, D SCHNEE, JM SAVARD, CE ROTHENBERG, ME NEWELL, JB MATSUEDA, GR HABER, E TI A RECOMBINANT CHIMERIC PLASMINOGEN-ACTIVATOR WITH HIGH-AFFINITY FOR FIBRIN HAS INCREASED THROMBOLYTIC POTENCY INVITRO AND INVIVO SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE UROKINASE; TISSUE PLASMINOGEN ACTIVATOR; FIBRINOLYSIS; ANTIBODY TARGETING ID ACUTE MYOCARDIAL-INFARCTION; UROKINASE; THERAPY; CHAIN; CONJUGATION; ANTIBODIES; BINDING; PLASMA; FORM AB A recombinant plasminogen activator with high fibrin affinity and specificity was expressed by transfecting hybridoma cells with a plasmid that combines sequence coding for low molecular mass (32 kDa) single-chain urokinase-type plasminogen activator [scuPA(32kDa)] and anti-fibrin monoclonal antibody 59D8. The expression of the recombinant molecule [r-scuPA(32kDa)-59D8] was optimized by replacing the 3' untranslated region (initially that of high molecular mass scuPA) in the plasmid with the 3' untranslated region of either beta-globin or mouse immunoglobulin. This modification resulted in a > 100-fold improvement in the level of protein expression. The 103-kDa r-scuPA(32kDa)-59D8 protein displayed catalytic activity indistinguishable from that of high molecular mass scuPA and fibrin binding comparable to that of native antibody 59D8. r-scuPA(32kDa)-59D8 was 6 times more potent than high molecular mass scuPA in lysing a human plasma clot in vitro and was 20 times more potent than high molecular mass scuPA in the rabbit jugular vein model of thrombolysis. Molecules of this type may serve as prototypes for highly specific, antibody-targeted enzymes suitable for human use. C1 MASSACHUSETTS GEN HOSP,GEN MED SERV,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. SCHERING PLOUGH CORP,BLOOMFIELD,NJ 07003. UNIV HEIDELBERG,MED CARDIOL KLIN 3,W-6900 HEIDELBERG,GERMANY. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,PRINCETON,NJ 08543. PRINCETON UNIV,PRINCETON,NJ 08544. RP RUNGE, MS (reprint author), EMORY UNIV,DIV CARDIOL,ATLANTA,GA 30322, USA. FU NHLBI NIH HHS [HL-28015, HL-19259, HL-41808] NR 27 TC 56 Z9 56 U1 0 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV PY 1991 VL 88 IS 22 BP 10337 EP 10341 DI 10.1073/pnas.88.22.10337 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GP895 UT WOS:A1991GP89500088 PM 1946453 ER PT J AU ABRAHAM, SA COLES, NA COLEY, CM STRAUSS, HW BOUCHER, CA EAGLE, KA AF ABRAHAM, SA COLES, NA COLEY, CM STRAUSS, HW BOUCHER, CA EAGLE, KA TI CORONARY RISK OF NONCARDIAC SURGERY SO PROGRESS IN CARDIOVASCULAR DISEASES LA English DT Review ID PERIPHERAL VASCULAR-DISEASE; ABDOMINAL AORTIC-ANEURYSM; SILENT MYOCARDIAL ISCHEMIA; DIPYRIDAMOLE-THALLIUM SCINTIGRAPHY; CARDIAC SURGICAL PROCEDURES; ARTERY BYPASS-SURGERY; EXTRA-ANATOMIC BYPASS; CAROTID ENDARTERECTOMY; PREOPERATIVE ASSESSMENT; GENERAL-ANESTHESIA C1 MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,GEN MED UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. NR 141 TC 27 Z9 27 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0033-0620 J9 PROG CARDIOVASC DIS JI Prog. Cardiovasc. Dis. PD NOV-DEC PY 1991 VL 34 IS 3 BP 205 EP 234 DI 10.1016/0033-0620(91)90014-D PG 30 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GP899 UT WOS:A1991GP89900004 PM 1947125 ER PT J AU VANKAMMEN, DP AF VANKAMMEN, DP TI THE BIOCHEMICAL BASIS OF RELAPSE AND DRUG RESPONSE IN SCHIZOPHRENIA - REVIEW AND HYPOTHESIS SO PSYCHOLOGICAL MEDICINE LA English DT Review ID PLASMA HOMOVANILLIC-ACID; DOPAMINE-BETA-HYDROXYLASE; THYROTROPIN-RELEASING-HORMONE; EARLY NEUROLEPTIC RESPONSE; PSYCHIATRIC-PATIENTS; CEREBROSPINAL-FLUID; GROWTH-HORMONE; MONOAMINE METABOLITES; ADENYLATE-CYCLASE; LONG-TERM AB This review of the literature suggests that antipsychotic drug response is determined by dopamine (DA) turnover and norepinephrine (NE) activity prior to treatment. The data suggest that NE modulates the DA system. Drug-free psychotic patients with relatively increased DA and NE activity, including release, are more likely to be treatment responsive, while patients who show evidence of enhanced DA and NE activity during treatment with antipsychotic drugs are likely to relapse soon after neuroleptic withdrawal. Basal release of DA and NE is decreased and associated with residual positive and negative symptoms. Improvement during neuroleptic treatment is associated with decreases in DA and NE phasic or stimulus induced release. The variable response to antipsychotic drugs is most likely to be a result of dysregulated DA and NE release, i.e. under state-dependent control, rather than evidence of a heterogeneous aetiology. Because catecholamines regulate gain, signal-to-noise ratio and gating in the brain, this model allows for environmental factors to interact with biochemical state and drug treatment. The author proposes that impaired homeostasis of NE and DA in schizophrenia causes instability in NE and DA neuronal firing and release, presumably related to mechanisms down-stream from the receptors, such as G proteins. This instability of catecholamine release may explain the observed variability in clinical states and drug response in schizophrenia. C1 UNIV PITTSBURGH,WESTERN PSYCHIAT INST & CLIN,SCH MED,PITTSBURGH,PA 15213. RP VANKAMMEN, DP (reprint author), US DEP VET AFFAIRS,HIGHLAND DR VET ADM MED CTR,PITTSBURGH,PA 15206, USA. FU NIMH NIH HHS [R01-MH44841-01] NR 189 TC 18 Z9 19 U1 4 U2 5 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD NOV PY 1991 VL 21 IS 4 BP 881 EP 895 PG 15 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA GV147 UT WOS:A1991GV14700006 PM 1685791 ER PT J AU YUCEL, EK WALTMAN, AC AF YUCEL, EK WALTMAN, AC TI COMPRESSION US IN ISOLATED CALF VENOUS THROMBOSIS - REPLY SO RADIOLOGY LA English DT Editorial Material ID LOWER-EXTREMITY; DEEP; THROMBOPHLEBITIS RP YUCEL, EK (reprint author), MASSACHUSETTS GEN HOSP, DEPT RADIOL, 32 FRUIT ST, BOSTON, MA 02114 USA. NR 9 TC 2 Z9 2 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMERICA PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA SN 0033-8419 J9 RADIOLOGY JI Radiology PD NOV PY 1991 VL 181 IS 2 BP 352 EP 353 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GL841 UT WOS:A1991GL84100006 ER PT J AU MOORE, EH LEBLANC, J MONTESI, SA RICHARDSON, ML SHEPARD, JAO MCLOUD, TC AF MOORE, EH LEBLANC, J MONTESI, SA RICHARDSON, ML SHEPARD, JAO MCLOUD, TC TI EFFECT OF PATIENT POSITIONING AFTER NEEDLE ASPIRATION LUNG-BIOPSY SO RADIOLOGY LA English DT Article DE BIOPSIES, COMPLICATIONS; LUNG, BIOPSY; LUNG NEOPLASMS; PNEUMOTHORAX ID PULMONARY-LESIONS; PNEUMOTHORAX; DIAGNOSIS AB Fifty-five patients who underwent fluoroscopically guided needle aspiration lung biopsy were randomly assigned to one of two postbiopsy treatment groups: Patients were placed recumbent with puncture site either down (n = 36) or up (n = 19) for at least 1 hour. No significant difference in pneumothorax rate was seen between the two groups. Chest tube placement, however, was required in 21% (four of 19) of the puncture-site-up group versus 3% (one of 36) of the puncture-site-down group, which was a significant difference (P = .04). Puncture-site-down postbiopsy positioning reduces the proportion of patients requiring chest tube placement after lung biopsy. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. UNIV WASHINGTON,MED CTR,DEPT RADIOL,SEATTLE,WA 98195. NR 11 TC 52 Z9 53 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 NOV PY 1991 VL 181 IS 2 BP 385 EP 387 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GL841 UT WOS:A1991GL84100012 PM 1924776 ER PT J AU SAINI, S LI, W WALLNER, B HAHN, PF EDELMAN, RR AF SAINI, S LI, W WALLNER, B HAHN, PF EDELMAN, RR TI MR IMAGING OF LIVER METASTASES AT 1.5 T - SIMILAR CONTRAST DISCRIMINATION WITH T1-AND T2-WEIGHTED PULSE SEQUENCES SO RADIOLOGY LA English DT Article DE LIVER NEOPLASMS, MR STUDIES; LIVER NEOPLASMS, SECONDARY; MAGNETIC RESONANCE (MR), PULSE SEQUENCES ID HEPATIC HEMANGIOMAS; DIFFERENTIATION; LESIONS; TUMORS AB The authors evaluated soft-tissue contrast on spin-echo (SE) proton density-weighted, SE T2-weighted, SE short-echo-time (TE) T1-weighted, and gradient-echo (GRE) images of 34 patients with known hepatic tumors who underwent high-field-strength (1.5-T) magnetic resonance imaging. For solid liver tumors, the difference in the mean lesion-liver contrast-to-noise ratios (C/Ns) with T1- (GRE and SE) and T2-weighted pulse sequences was not statistically significant (P > .05). For nonsolid liver tumors, the T2-weighted images provided significantly greater (P < .05) mean lesion-liver C/N than T1-weighted GRE images. Mean liver signal-to-noise ratio was significantly greater on T1-weighted GRE (P < .0001) and T1-weighted SE (P < .05) images than on T2- and proton density-weighted images. Qualitative analysis of T1-weighted (SE and GRE) images and proton density- plus T2-weighted images showed that lesion conspicuity was similar in 25 of 32 patients (78%). The results suggest that liver tumor imaging at high field strength can be performed with short-TE T1-weighted (SE or GRE) or conventional T2-weighted pulse sequences. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. BETH ISRAEL HOSP,BOSTON,MA 02215. UNIV ULM,W-7900 ULM,GERMANY. CAPITAL INST MED,BEIJING FRIENDSHIP HOSP,BEIJING,PEOPLES R CHINA. RP SAINI, S (reprint author), HARVARD UNIV,SCH MED,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02115, USA. NR 17 TC 22 Z9 22 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 NOV PY 1991 VL 181 IS 2 BP 449 EP 453 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GL841 UT WOS:A1991GL84100025 PM 1924787 ER PT J AU BELLIVEAU, JW KENNEDY, DN MCKINSTRY, RC BUCHBINDER, BR WEISSKOFF, RM COHEN, MS VEVEA, JM BRADY, TJ ROSEN, BR AF BELLIVEAU, JW KENNEDY, DN MCKINSTRY, RC BUCHBINDER, BR WEISSKOFF, RM COHEN, MS VEVEA, JM BRADY, TJ ROSEN, BR TI FUNCTIONAL MAPPING OF THE HUMAN VISUAL-CORTEX BY MAGNETIC-RESONANCE-IMAGING SO SCIENCE LA English DT Article ID POSITRON-EMISSION TOMOGRAPHY; CEREBRAL BLOOD-VOLUME; HUMAN-BRAIN; COMPUTED-TOMOGRAPHY; COGNITIVE NEUROSCIENCE; STRIATE CORTEX; INSTANT IMAGES; FLOW; CONTRAST; NMR AB Knowledge of regional cerebral hemodynamics has widespread application for both physiological research and clinical assessment because of the well-established interrelation between physiological function, energy metabolism, and localized blood supply. A magnetic resonance technique was developed for quantitative imaging of cerebral hemodynamics, allowing for measurement of regional cerebral blood volume during resting and activated cognitive states. This technique was used to generate the first functional magnetic resonance maps of human task activation, by using a visual stimulus paradigm. During photic stimulation, localized increases in blood volume (32 +/- 10 percent, n = 7 subjects) were detected in the primary visual cortex. Center-of-mass coordinates and linear extents of brain activation within the plane of the calcarine fissure are reported. C1 MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CTR NMR,DEPT NEUROL,BOSTON,MA 02114. RI Kennedy, David/H-3627-2012; Cohen, Mark/C-6610-2011 OI Cohen, Mark/0000-0001-6731-4053 FU NCI NIH HHS [R01-CA40303, P01-CA48729]; NHLBI NIH HHS [R01-HL39810] NR 42 TC 1152 Z9 1200 U1 2 U2 75 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD NOV 1 PY 1991 VL 254 IS 5032 BP 716 EP 719 DI 10.1126/science.1948051 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GN474 UT WOS:A1991GN47400043 PM 1948051 ER PT J AU YOUNG, RH CLEMENT, PB AF YOUNG, RH CLEMENT, PB TI PATHOLOGY OF THE FEMALE GENITAL-TRACT AND PERITONEUM - SELECTED TOPICS - INTRODUCTION SO SEMINARS IN DIAGNOSTIC PATHOLOGY LA English DT Editorial Material RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. 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 0740-2570 J9 SEMIN DIAGN PATHOL JI Semin. Diagn. Pathol. PD NOV PY 1991 VL 8 IS 4 BP 203 EP 203 PG 1 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA GP727 UT WOS:A1991GP72700001 ER PT J AU YOUNG, RH CLEMENT, PB AF YOUNG, RH CLEMENT, PB TI PSEUDONEOPLASTIC GLANDULAR LESIONS OF THE UTERINE CERVIX SO SEMINARS IN DIAGNOSTIC PATHOLOGY LA English DT Article DE CERVIX; PSEUDONEOPLASTIC LESIONS; GLANDULAR LESIONS RP YOUNG, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 0 TC 63 Z9 64 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0740-2570 J9 SEMIN DIAGN PATHOL JI Semin. Diagn. Pathol. PD NOV PY 1991 VL 8 IS 4 BP 234 EP 249 PG 16 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA GP727 UT WOS:A1991GP72700003 PM 1759058 ER PT J AU YOUNG, RH SCULLY, RE AF YOUNG, RH SCULLY, RE TI METASTATIC TUMORS IN THE OVARY - A PROBLEM-ORIENTED APPROACH AND REVIEW OF THE RECENT LITERATURE SO SEMINARS IN DIAGNOSTIC PATHOLOGY LA English DT Review DE OVARY; METASTATIC TUMORS; ENDOMETRIOID TUMORS; MUCINOUS TUMORS; SMALL CELL TUMORS RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 0 TC 82 Z9 87 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0740-2570 J9 SEMIN DIAGN PATHOL JI Semin. Diagn. Pathol. PD NOV PY 1991 VL 8 IS 4 BP 250 EP 276 PG 27 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA GP727 UT WOS:A1991GP72700004 PM 1759059 ER PT J AU BRUMMELSMITH, K AF BRUMMELSMITH, K TI HOME HEALTH-CARE - HOW LONG WILL IT REMAIN LOW TECH SO SOUTHERN CALIFORNIA LAW REVIEW LA English DT Article ID PROGRAM C1 OREGON HLTH SCI UNIV,MED & FAMILY MED,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. NR 26 TC 0 Z9 0 U1 0 U2 0 PU UNIV SOUTHERN CALIF PI LOS ANGELES PA LAW CENTER UNIV PARK, LOS ANGELES, CA 90089-0071 SN 0038-3910 J9 SOUTHERN CALIF LAW R JI South. Calif. Law Rev. PD NOV PY 1991 VL 65 IS 1 BP 491 EP 502 PG 12 WC Law SC Government & Law GA HF351 UT WOS:A1991HF35100021 PM 11645843 ER PT J AU TERAYAMA, Y MEYER, JS KAWAMURA, J AF TERAYAMA, Y MEYER, JS KAWAMURA, J TI COGNITIVE RECOVERY CORRELATES WITH LONG-TERM INCREASES OF CEREBRAL PERFUSION AFTER HEAD-INJURY SO SURGICAL NEUROLOGY LA English DT Article DE CHRONIC HEAD INJURY; COGNITIVE PROGNOSIS; CEREBRAL BLOOD FLOW ID MULTI-INFARCT DEMENTIA; GLASGOW OUTCOME SCALE; BLOOD-FLOW FLUCTUATE; AUTOREGULATION; INHALATION; PRESSURE AB Prospective measurements of cerebral blood flow (CBF) and Cognitive Capacity Screening Examinations (CCSE) were obtained following head injury among 42 patients for a mean total follow-up interval of 10 years. Clinical data obtained at the time of injury and detailed neurological examinations at each follow-up visit were correlated with serial CBF and CCSE scores. Comparisons of the group of patients who cognitively improved (n = 32) were made with the group that did not (n = 10). Of the total group, 76% showed cognitive improvements for as long as 10 years after injury, with CBF increases toward normal. Predictors for long-term cognitive improvements include: higher initial Glasgow Coma Scales, earlier recovery from coma, absence of signs of brain stem injury, and improvements of cerebral perfusion and autoregulation. Failure to improve correlated with low initial Glasgow Coma Scales, signs of brain stem injury, and persistent impairments of cerebral perfusion. C1 BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,2002 HOLCOMBE BLVD,HOUSTON,TX 77211. BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77211. NR 35 TC 7 Z9 7 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0090-3019 J9 SURG NEUROL JI Surg. Neurol. PD NOV PY 1991 VL 36 IS 5 BP 335 EP 342 DI 10.1016/0090-3019(91)90021-Z PG 8 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA GK804 UT WOS:A1991GK80400001 PM 1745957 ER PT J AU CHRISTMAS, NJ MEAD, MD RICHARDSON, EP ALBERT, DM AF CHRISTMAS, NJ MEAD, MD RICHARDSON, EP ALBERT, DM TI SECONDARY OPTIC-NERVE TUMORS SO SURVEY OF OPHTHALMOLOGY LA English DT Review DE BRAIN TUMORS; LEUKEMIA; LYMPHOMA; METASTASIS; OCULAR MELANOMA; OPTIC NERVE; ORBITAL TUMORS; RETINOBLASTOMA; SECONDARY TUMORS ID CANCER INSTITUTE EXPERIENCE; RETICULUM-CELL SARCOMA; MENINGEAL CARCINOMATOSIS; MULTIPLE-MYELOMA; MONOCLONAL GAMMOPATHY; OCULAR MANIFESTATIONS; ISOLATED METASTASIS; UVEAL MELANOMA; LUNG-CANCER; EXTENSION AB Secondary tumors of the optic nerve are more common than primary optic nerve tumors. The involvement of the optic nerve may arise from direct invasion from intraocular malignancies, from hematopoietic malignancy, from meningeal carcinomatosis, or from distant primary tumors. Orbital tumors rarely invade the optic nerve, and brain tumors involve it only in their late stages. C1 MASSACHUSETTS EYE & EAR HOSP,DEPT OPHTHALMOL,DAVID G COGAN EYE PATHOL LAB,243 CHARLES ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROPATHOL LAB,BOSTON,MA 02114. FU NEI NIH HHS [EY01917] NR 97 TC 23 Z9 24 U1 0 U2 1 PU SURVEY OPHTHALMOLOGY INC PI BROOKLINE PA 7 KENT ST SUITE 4, BROOKLINE, MA 02146 SN 0039-6257 J9 SURV OPHTHALMOL JI Surv. Ophthalmol. PD NOV-DEC PY 1991 VL 36 IS 3 BP 196 EP 206 DI 10.1016/0039-6257(91)90002-W PG 11 WC Ophthalmology SC Ophthalmology GA GT721 UT WOS:A1991GT72100002 PM 1776123 ER PT J AU HALL, MC KOCH, MO MCDOUGAL, WS AF HALL, MC KOCH, MO MCDOUGAL, WS TI METABOLIC CONSEQUENCES OF URINARY-DIVERSION THROUGH INTESTINAL SEGMENTS SO UROLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID TOTAL BLADDER REPLACEMENT; ILEAL CONDUIT; KOCK POUCH; FOLLOW-UP; CONTINENT UROSTOMY; RENAL-FUNCTION; COLON CONDUIT; YOUNG-ADULTS; COMPLICATIONS; URETEROSIGMOIDOSTOMY C1 VANDERBILT UNIV,MED CTR,DEPT UROL,NASHVILLE,TN 37240. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114. NR 101 TC 36 Z9 37 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0094-0143 J9 UROL CLIN N AM JI Urol. Clin. N. Am. PD NOV PY 1991 VL 18 IS 4 BP 725 EP 735 PG 11 WC Urology & Nephrology SC Urology & Nephrology GA LA253 UT WOS:A1991LA25300014 PM 1949404 ER PT J AU HASEGAWA, K HUANG, JK WANDS, JR OBATA, H LIANG, TJ AF HASEGAWA, K HUANG, JK WANDS, JR OBATA, H LIANG, TJ TI ASSOCIATION OF HEPATITIS-B VIRAL PRECORE MUTATIONS WITH FULMINANT HEPATITIS-B IN JAPAN SO VIROLOGY LA English DT Note ID E-ANTIGEN; NON-A; VIRUS-INFECTION; CYTO-TOXICITY; CORE ANTIGEN; ANTIBODY; GENOME; IDENTIFICATION; HEPATOCYTES C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT MED,CTR CANC,MOLEC HEPATOL LAB,149 13TH ST,7TH FLOOR,BOSTON,MA 02114. TOKYO WOMENS MED COLL,INST GASTROENTEROL,TOKYO 162,JAPAN. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. FU NCI NIH HHS [R01CA54524]; NIDDK NIH HHS [DK01952] NR 26 TC 64 Z9 67 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD NOV PY 1991 VL 185 IS 1 BP 460 EP 463 DI 10.1016/0042-6822(91)90799-H PG 4 WC Virology SC Virology GA GJ980 UT WOS:A1991GJ98000054 PM 1926786 ER PT J AU MORELAND, RB GARCEA, RL AF MORELAND, RB GARCEA, RL TI CHARACTERIZATION OF A NUCLEAR-LOCALIZATION SEQUENCE IN THE POLYOMAVIRUS CAPSID PROTEIN VP1 SO VIROLOGY LA English DT Note ID SIMIAN VIRUS-40 INFECTION; LOCATION SIGNAL; SACCHAROMYCES-CEREVISIAE; SPECIFIES MIGRATION; POLYPEPTIDE; EXPRESSION; TRANSPORT; PROMOTER; DOMAIN; SITE C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,D1620,44 BINNEY ST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA 37667, R01 CA037667] NR 31 TC 46 Z9 47 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD NOV PY 1991 VL 185 IS 1 BP 513 EP 518 DI 10.1016/0042-6822(91)90811-O PG 6 WC Virology SC Virology GA GJ980 UT WOS:A1991GJ98000066 PM 1656604 ER PT J AU MILLS, JA AF MILLS, JA TI ASPIRIN, THE AGELESS REMEDY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID PROSTAGLANDIN RP MILLS, JA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 7 TC 9 Z9 9 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 OCT 31 PY 1991 VL 325 IS 18 BP 1303 EP 1304 DI 10.1056/NEJM199110313251808 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA GM041 UT WOS:A1991GM04100008 PM 1922226 ER PT J AU CHUDLER, EH FOOTE, WE POLETTI, CE AF CHUDLER, EH FOOTE, WE POLETTI, CE TI TOPOGRAPHY OF C1 NERVE-EVOKED AND TRIGEMINAL-EVOKED POTENTIALS IN THE VENTROBASAL COMPLEX OF THE CAT THALAMUS SO NEUROSCIENCE LETTERS LA English DT Article DE EVOKED POTENTIAL; C1 NERVE; VIBRISSAE; TRIGEMINAL; THALAMUS ID NUCLEUS VENTRALIS POSTEROMEDIALIS; HORSERADISH-PEROXIDASE; REPRESENTATION; PROJECTIONS; NEURONS; ORIGINS; MONKEY; CELLS; TRANSPORT; NECK AB In order to provide information pertaining to the C1 nerve representation in the thalamus, C1 nerve- and trigeminal-evoked potentials were recorded throughout the ventrobasal complex of the cat thalamus. Contralateral electrical stimulation of the C1 nerve and maxillary division of the trigeminal nerve elicited multiphasic positive-to-negative responses with mean maximum positive peak latencies of 2.2 ms and 2.7 ms, respectively. Ipsilateral stimulation failed to elicit a thalamic response. Construction of isopotential contour maps revealed that the foci of activity elicited by contralateral C1 nerve and trigeminal stimulation were located in the dorsolateral and ventromedial sections of ventroposterior medial nucleus (VPM), respectively. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PAIN RES LAB,BOSTON,MA 02114. FU NINDS NIH HHS [NS 23357] NR 20 TC 1 Z9 1 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 OCT 28 PY 1991 VL 132 IS 1 BP 33 EP 36 DI 10.1016/0304-3940(91)90426-T PG 4 WC Neurosciences SC Neurosciences & Neurology GA GN665 UT WOS:A1991GN66500010 PM 1787915 ER PT J AU GRUNDY, P TELZEROW, P PATERSON, MC HABER, D BERMAN, B LI, F GARBER, J AF GRUNDY, P TELZEROW, P PATERSON, MC HABER, D BERMAN, B LI, F GARBER, J TI CHROMOSOME-11 UNIPARENTAL ISODISOMY PREDISPOSING TO EMBRYONAL NEOPLASMS SO LANCET LA English DT Letter ID ADRENOCORTICAL CARCINOMA; WILMS TUMOR; 11P15.5 C1 CROSS CANC INST,DEPT PEDIAT,EDMONTON T6G 1Z2,ALBERTA,CANADA. UNIV ALBERTA,FAC MED,EDMONTON T6G 2E1,ALBERTA,CANADA. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. CASE WESTERN RESERVE UNIV,SCH MED,DEPT PEDIAT,CLEVELAND,OH 44106. NCI,CLIN EPIDEMIOL BRANCH,CLIN STUDIES SECT,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. RP GRUNDY, P (reprint author), CROSS CANC INST,DEPT MED,EDMONTON T6G 1Z2,ALBERTA,CANADA. NR 10 TC 71 Z9 72 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD OCT 26 PY 1991 VL 338 IS 8774 BP 1079 EP 1080 DI 10.1016/0140-6736(91)91937-P PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA GM253 UT WOS:A1991GM25300041 PM 1681381 ER PT J AU FINN, SF HYMAN, BT STOREY, E MILLER, JM BEAL, MF AF FINN, SF HYMAN, BT STOREY, E MILLER, JM BEAL, MF TI EFFECTS OF AGING ON QUINOLINIC ACID LESIONS IN RAT STRIATUM SO BRAIN RESEARCH LA English DT Article DE AGING; URIC ACID; N-METHYL-D-ASPARTATE; KYNURENIC ACID ID METHYL-D-ASPARTATE; PERFORMANCE LIQUID-CHROMATOGRAPHY; CEREBROSPINAL-FLUID; ALZHEIMERS-DISEASE; NEUROPEPTIDE-Y; NERVOUS-SYSTEM; KYNURENIC ACID; AGED RATS; BRAIN; GLUTAMATE AB Several neurologic illnesses in which excitotoxic mechanisms may play a role increase in prevalence with age. In the present study we examined the susceptibility of rats to quinolinic acid striatal lesions at 1, 4 and 20 months of age, and susceptibility to N-methyl-D-aspartate (NMDA) at 1 and 4 months of age. The extent of the lesions was quantitated with measurements of substance P-like immunoreactivity (SPLI) and gamma-aminobutyric acid (GABA). The lesions in the 4- and 20-month-old age groups showed significantly smaller depletions of SPLI and GABA than those in 1-month-old animals. Neuropeptide Y-like immunoreactivity (NPYLI) and somatostatin-like immunoreactivity (SLI) were unchanged in the lesioned striata. NMDA lesions were also attenuated in 4-month- and 12-month-old animals as compared with 1-month-old animals. Uric acid concentrations showed marked dose-dependent increases in the lesioned striatum, and to a lesser extent in the overlying cerebral cortex, in all 3 age groups. There were no changes of SLI, NPYLI or SPLI with aging in the cerebral cortex or hippocampus. Kynurenine and kynurenic acid concentrations showed significant increases with aging in frontal cortex. The present results show a reduced susceptibility of animals to striatal quinolinic acid and NMDA lesions with normal aging. The delayed onset of several neurodegenerative illnesses is therefore unlikely to be due to an increasing susceptibility to excitotoxin lesions with aging. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Storey, Elsdon/A-9889-2013 FU DS NIH HHS [NINCDS 16367]; NIA NIH HHS [IP05AG05134] NR 37 TC 16 Z9 16 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD OCT 25 PY 1991 VL 562 IS 2 BP 276 EP 280 DI 10.1016/0006-8993(91)90631-5 PG 5 WC Neurosciences SC Neurosciences & Neurology GA GP151 UT WOS:A1991GP15100012 PM 1837750 ER PT J AU SPRINGER, TA AF SPRINGER, TA TI CELL-ADHESION - A BIRTH CERTIFICATE FOR CD2 SO NATURE LA English DT Editorial Material ID RECEPTOR CD2; BINDING; LFA-3; FRAGMENT; DOMAINS RP SPRINGER, TA (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 16 TC 22 Z9 22 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 24 PY 1991 VL 353 IS 6346 BP 704 EP 705 DI 10.1038/353704a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GL696 UT WOS:A1991GL69600039 PM 1719420 ER PT J AU MATSUI, Y TOKSOZ, D NISHIKAWA, S NISHIKAWA, SI WILLIAMS, D ZSEBO, K HOGAN, BLM AF MATSUI, Y TOKSOZ, D NISHIKAWA, S NISHIKAWA, SI WILLIAMS, D ZSEBO, K HOGAN, BLM TI EFFECT OF STEEL FACTOR AND LEUKEMIA INHIBITORY FACTOR ON MURINE PRIMORDIAL GERM-CELLS IN CULTURE SO NATURE LA English DT Article ID TYROSINE KINASE RECEPTOR; C-KIT; GROWTH-FACTOR; W-LOCUS; SI-LOCUS; PROTO-ONCOGENE; MOUSE; LIGAND; EXPRESSION; IDENTIFICATION AB DESPITE the importance of germ cells to the survival of species, surprisingly little is known about their embryological origin, proliferation, migration and entry into mitotic arrest or meiosis 1-5. Mutations in the murine Dominant White Spotting (W) and Steel genes, which respectively encode the c-kit tyrosine kinase receptor and the c-kit ligand (or Steel factor), impair the development of primordial germ cells (PGCs) in vivo, as well as haematopoietic stem cells and neural crest-derived melanoblast 3,6-16. Here we use a monoclonal antibody against c-kit tyrosine kinase receptor and recombinant Steel factor to study the c-kit receptor-ligand system in cultured PGCs. In addition, we show that leukaemia inhibitory factor (also known as differentiation inhibitory activity) 17,18, a factor secreted by STO fibroblasts, can stimulate proliferation of primordial germ cells in vitro. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT CELL BIOL,NASHVILLE,TN 37232. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,BOSTON,MA 02115. KUMAMOTO UNIV,INST MED IMMUNOL,DEPT PATHOL,KUMAMOTO 860,JAPAN. AMGEN INC,AMGEN CTR,THOUSAND OAKS,CA 91320. NR 28 TC 360 Z9 374 U1 2 U2 5 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 24 PY 1991 VL 353 IS 6346 BP 750 EP 752 DI 10.1038/353750a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GL696 UT WOS:A1991GL69600067 PM 1719421 ER PT J AU SACHS, DH AF SACHS, DH TI SPECIFIC TRANSPLANTATION TOLERANCE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID TOTAL LYMPHOID IRRADIATION; BONE-MARROW; ADULT MICE; ALLOGRAFTS; ACCEPTANCE; INDUCTION; CHIMERISM; DISEASE RP SACHS, DH (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 12 TC 21 Z9 21 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 OCT 24 PY 1991 VL 325 IS 17 BP 1240 EP 1242 DI 10.1056/NEJM199110243251708 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA GL282 UT WOS:A1991GL28200008 PM 1922212 ER PT J AU EAGLE, KA AF EAGLE, KA TI RULING OUT ACUTE MYOCARDIAL-INFARCTION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP EAGLE, KA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 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 OCT 24 PY 1991 VL 325 IS 17 BP 1250 EP 1250 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA GL282 UT WOS:A1991GL28200015 ER PT J AU EMANUEL, LL BARRY, MJ STOECKLE, JD ETTELSON, LM EMANUEL, EJ AF EMANUEL, LL BARRY, MJ STOECKLE, JD ETTELSON, LM EMANUEL, EJ TI ADVANCE DIRECTIVES FOR MEDICAL-CARE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP EMANUEL, LL (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 5 TC 3 Z9 3 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 OCT 24 PY 1991 VL 325 IS 17 BP 1256 EP 1256 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA GL282 UT WOS:A1991GL28200028 ER PT J AU ABRUTYN, E BERLIN, JA AF ABRUTYN, E BERLIN, JA TI INTRATHECAL THERAPY IN TETANUS - A METAANALYSIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID MUHIMBILI-MEDICAL-CENTRE; DAR-ES-SALAAM; NEONATAL TETANUS; SERUM HORSE; IMMUNOGLOBULIN; SEROTHERAPY; EXPERIENCE; TRIAL AB Objective. - To assess the efficacy of intrathecal therapy with tetanus antibody (antitetanus equine serum or human tetanus immune globulin) in neonatal and adult tetanus using meta-analytical techniques. Data Sources. - Clinical trials identified by searching MEDLINE and by reviewing bibliographies of published articles. Study Selection. - Studies in English with concurrent controls treated without intrathecal therapy Data Extraction. - Data were extracted by one author and verified by the second; conflicts were resolved by discussion. Data Synthesis. - No major treatment effect was found in neonatal tetanus when all studies were considered. A benefit was suggested for antitetanus equine serum in adult disease, but this finding should be accepted with caution. Subgroup analyses were limited in power. Methodological difficulties in neonatal and adult trials were common and safety has not been established. Conclusions. - Intrathecal therapy for tetanus with either antitetanus equine serum or human tetanus immune globulin is not of proven benefit and should only be given in the context of well-designed, controlled trials. C1 UNIV PENN,SCH MED,GEN INTERNAL MED SECT,CLIN EPIDEMIOL UNIT,PHILADELPHIA,PA 19104. RP ABRUTYN, E (reprint author), MED COLL PENN,VET AFFAIRS MED CTR,INFECT DIS SECT,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19129, USA. NR 33 TC 32 Z9 32 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 23 PY 1991 VL 266 IS 16 BP 2262 EP 2267 DI 10.1001/jama.266.16.2262 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA GK661 UT WOS:A1991GK66100036 PM 1833565 ER PT J AU LUKACOVA, D MATSUEDA, GR HABER, E REED, GL AF LUKACOVA, D MATSUEDA, GR HABER, E REED, GL TI INHIBITION OF FACTOR-XIII ACTIVATION BY AN ANTIPEPTIDE MONOCLONAL-ANTIBODY SO BIOCHEMISTRY LA English DT Article ID FIBRIN-STABILIZING FACTOR; CATALYZED CROSS-LINKING; COAGULATION FACTOR-XIII; ALPHA-2-PLASMIN INHIBITOR; HEMORRHAGIC DISORDER; FIBRINOLIGASE; CROSSLINKING; PLATELETS; PROTEINS; BINDING AB As the final enzyme in the coagulation cascade, activated fibrin stabilizing factor or factor XIII catalyzes the intermolecular cross-linking of fibrin chains. To study this enzyme in plasma, we derived a monoclonal antibody (MAb 309) against a peptide sequence (NH2-G-V-N-L-Q-E-F-C-COOH) in the thrombin activation site of factor XIII. Radioimmunoassays indicate that MAb 309 binds specifically to both platelet and plasma factor XIII. Peptide inhibition studies demonstrate that the MAb binds equally well to the factor XIII (FXIII) zymogen and the active form of FXIII (FXIIIa). In immunoblots of whole platelet lysates, MAb 309 binds only to FXIII and does not cross-react with other proteins. In saturation binding studies, the antibody shows a binding avidity of (1.75 +/- 0.35) x 10(9) M-1. MAb 309 also inhibited 99% of apparent FXIIIa activity in a standard transglutaminase assay. SDS-PAGE analysis of fibrin clots showed that MAb 309 inhibited fibrin gamma-gamma cross-linking. Moreover, MAb 309 accelerated the lysis of plasma clots, consistent with inhibition of fibrin-fibrin and fibrin-alpha-2-antiplasmin cross-linking. Immunoblotting experiments revealed that MAb 309 affected apparent FXIIIa activity by inhibiting the thrombin activation of the FXIII zymogen. In addition to its utility as a specific probe for the FXIII a-subunit, the strategy used to obtain MAb 309 may be used to generate-MAbs that inhibit the activation of other coagulation factor zymogens. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,JACKSON 14,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. PRINCETON UNIV,PRINCETON,NJ 08544. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,PRINCETON,NJ 08543. FU NHLBI NIH HHS [HL02348, HL28015] NR 44 TC 20 Z9 20 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 22 PY 1991 VL 30 IS 42 BP 10164 EP 10170 DI 10.1021/bi00106a013 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GL468 UT WOS:A1991GL46800013 PM 1681898 ER PT J AU SHOELSON, SE CHATTERJEE, S CHAUDHURI, M BURKE, TR AF SHOELSON, SE CHATTERJEE, S CHAUDHURI, M BURKE, TR TI SOLID-PHASE SYNTHESIS OF NONHYDROLYZABLE PHOSPHOTYROSYL PEPTIDE ANALOGS WITH N-ALPHA-FMOC-(O,O-DI-TERT-BUTYL)PHOSPHONO-PARA-METHYLPHENYLALANINE SO TETRAHEDRON LETTERS LA English DT Article DE PHOSPHOTYROSINE; TYROSINE KINASE; PROTEIN TYROSINE PHOSPHATASE; ENZYME INHIBITOR; PEPTIDE SYNTHESIS ID INSULIN-RECEPTOR; PHOSPHATASES AB A new, protected derivative of phosphonomethylphenylalanine is used to synthesize nonhydrolyzable analogs of phosphotyrosyl peptides for use as inhibitors and affinity ligands of proteins that recognize phosphotyrosyl sequences. C1 BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NCI,MED CHEM LAB,BETHESDA,MD 20892. RP SHOELSON, SE (reprint author), BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115, USA. RI Burke, Terrence/N-2601-2014 NR 19 TC 37 Z9 37 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4039 J9 TETRAHEDRON LETT JI Tetrahedron Lett. PD OCT 21 PY 1991 VL 32 IS 43 BP 6061 EP 6064 DI 10.1016/0040-4039(91)80753-S PG 4 WC Chemistry, Organic SC Chemistry GA GL927 UT WOS:A1991GL92700003 ER PT J AU BEVILACQUA, M BUTCHER, E FURIE, B FURIE, B GALLATIN, M GIMBRONE, M HARLAN, J KISHIMOTO, K LASKY, L MCEVER, R PAULSON, J ROSEN, S SEED, B SIEGELMAN, M SPRINGER, T STOOLMAN, L TEDDER, T VARKI, A WAGNER, D WEISSMAN, I ZIMMERMAN, G AF BEVILACQUA, M BUTCHER, E FURIE, B FURIE, B GALLATIN, M GIMBRONE, M HARLAN, J KISHIMOTO, K LASKY, L MCEVER, R PAULSON, J ROSEN, S SEED, B SIEGELMAN, M SPRINGER, T STOOLMAN, L TEDDER, T VARKI, A WAGNER, D WEISSMAN, I ZIMMERMAN, G TI SELECTINS - A FAMILY OF ADHESION RECEPTORS SO CELL LA English DT Letter ID MOLECULES C1 ICOS,SE BOTHELL,WA 98021. BOEHRINGER INGELHEIM,RIDGEFIELD,CT 06877. GENENTECH INC,S SAN FRANCISCO,CA 94080. CYTEL,LA JOLLA,CA 92037. CTR BLOOD RES,BOSTON,MA 02115. UNIV TEXAS,SW MED CTR,DALLAS,TX 75230. STANFORD UNIV,MED CTR,SCH MED,STANFORD,CA 94305. TUFTS UNIV,BOSTON,MA 02111. UNIV WASHINGTON,SEATTLE,WA 98104. UNIV UTAH,MED CTR,SALT LAKE CITY,UT 84112. UNIV OKLAHOMA,OKLAHOMA CITY,OK 73104. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV MICHIGAN,ANN ARBOR,MI 48109. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. RP BEVILACQUA, M (reprint author), BRIGHAM & WOMENS HOSP,BOSTON,MA 02115, USA. NR 2 TC 287 Z9 295 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 OCT 18 PY 1991 VL 67 IS 2 BP 233 EP 233 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GL470 UT WOS:A1991GL47000003 PM 1717161 ER PT J AU SCHIRO, JA CHAN, BMC ROSWIT, WT KASSNER, PD PENTLAND, AP HEMLER, ME EISEN, AZ KUPPER, TS AF SCHIRO, JA CHAN, BMC ROSWIT, WT KASSNER, PD PENTLAND, AP HEMLER, ME EISEN, AZ KUPPER, TS TI INTEGRIN-ALPHA-2-BETA-1 (VLA-2) MEDIATES REORGANIZATION AND CONTRACTION OF COLLAGEN MATRICES BY HUMAN-CELLS SO CELL LA English DT Article ID FIBRONECTIN RECEPTOR EXPRESSION; FIBROBLAST TRACTION; SURFACE RECEPTORS; INTEGRIN; ADHESION; BINDING; MORPHOGENESIS; GLYCOPROTEIN; LATTICES; HOMOLOGY AB The capacity of cells to organize and contract collagen fibrils is fundamental to processes as diverse as embryogenesis and wound healing. We analyzed different beta-1 integrins on diploid fibroblasts for their role in modifying the tertiary structure of collagen matrices. Using monoclonal antibodies that block the interaction of integrins with their ligands, evidence was obtained that alpha-2-beta-1 integrin is required for the contraction of a type I collagen matrix. Further supporting the role of alpha-2-beta-1, cell lines expressing minimal levels of this integrin uniformly failed to contract collagen matrices. In addition, transfection of a full-length alpha-2 cDNA into one such cell line led to enhanced cell surface expression of alpha-2-beta-1 and conferred the de novo capacity to contract collagen matrices. C1 WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP SCHIRO, JA (reprint author), WASHINGTON UNIV,SCH MED,DEPT MED,DIV DERMATOL,ST LOUIS,MO 63110, USA. FU NIAID NIH HHS [AI 25082]; NIAMS NIH HHS [AR 12129, AR 40124] NR 30 TC 335 Z9 337 U1 0 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD OCT 18 PY 1991 VL 67 IS 2 BP 403 EP 410 DI 10.1016/0092-8674(91)90191-Z PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GL470 UT WOS:A1991GL47000019 PM 1913826 ER PT J AU PELLETIER, J BRUENING, W KASHTAN, CE MAUER, SM MANIVEL, JC STRIEGEL, JE HOUGHTON, DC JUNIEN, C HABIB, R FOUSER, L FINE, RN SILVERMAN, BL HABER, DA HOUSMAN, D AF PELLETIER, J BRUENING, W KASHTAN, CE MAUER, SM MANIVEL, JC STRIEGEL, JE HOUGHTON, DC JUNIEN, C HABIB, R FOUSER, L FINE, RN SILVERMAN, BL HABER, DA HOUSMAN, D TI GERMLINE MUTATIONS IN THE WILMS-TUMOR SUPPRESSOR GENE ARE ASSOCIATED WITH ABNORMAL UROGENITAL DEVELOPMENT IN DENYS-DRASH SYNDROME SO CELL LA English DT Article ID ZINC FINGER PROTEIN; P53 GENE; CHROMOSOME-11; DELETION; CANCER; LOCUS; DNA; PSEUDOHERMAPHRODITISM; BINDING; SRY AB Denys-Drash syndrome is a rare human condition in which severe urogenital aberrations result in renal failure, pseudohermaphroditism, and Wilms' tumor (nephroblastoma). To investigate its possible role, we have analyzed the coding exons of the Wilms' tumor suppressor gene (WT1) for germline mutations. In ten independent cases of Denys-Drash syndrome, point mutations in the zinc finger domains of one WT1 gene copy were found. Nine of these mutations are found within exon 9 (zinc finger III); the remaining mutation is in exon 8 (zinc finger II). These mutations directly affect DNA sequence recognition. In two families analyzed, the mutations were shown to arise de novo. Wilms' tumors from three individuals and one juvenile granulosa cell tumor demonstrate reduction to homozygosity for the mutated WT1 allele. Our results provide evidence of a direct role for WT1 in Denys-Drash syndrome and thus urogenital system development. C1 MCGILL UNIV,MCGILL CANC CTR,MONTREAL H3G 1Y6,QUEBEC,CANADA. UNIV MINNESOTA,SCH MED,DEPT PEDIAT NEPHROL,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. OREGON HLTH SCI UNIV,DEPT PEDIAT,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT PATHOL,PORTLAND,OR 97201. HOP NECKER ENFANTS MALAD,INSERM,U73,F-75730 PARIS 15,FRANCE. HOP NECKER ENFANTS MALAD,INSERM,U192,F-75730 PARIS 15,FRANCE. UNIV WASHINGTON,SCH MED,DEPT PEDIAT,SEATTLE,WA 98195. SUNY STONY BROOK,DEPT PEDIAT,STONY BROOK,NY 11794. CHILDRENS MEM HOSP,DIV PEDIAT ENDOCRINOL,CHICAGO,IL 60614. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114. RP PELLETIER, J (reprint author), MIT,CTR CANC RES,CAMBRIDGE,MA 02139, USA. FU NCI NIH HHS [1K08CA 01356]; NHGRI NIH HHS [HG00299] NR 50 TC 694 Z9 707 U1 0 U2 12 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD OCT 18 PY 1991 VL 67 IS 2 BP 437 EP 447 DI 10.1016/0092-8674(91)90194-4 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GL470 UT WOS:A1991GL47000022 PM 1655284 ER PT J AU TELFER, JC RUDD, CE AF TELFER, JC RUDD, CE TI A 32-KD GTP-BINDING PROTEIN ASSOCIATED WITH THE CD4-P56LCK AND CD8-P56LCK T-CELL RECEPTOR COMPLEXES SO SCIENCE LA English DT Article ID TYROSINE KINASE P56LCK; HUMAN LYMPHOCYTES-T; PHOSPHOLIPASE-C; CROSS-LINKING; ACTIVATION; CD4; RAS; POLYPEPTIDES; PRODUCT AB The guanosine triphosphate (GTP)-binding proteins include signal-transducing heterotrimeric G proteins (for example, G(s), G(i)), smaller GTP-binding proteins that function in protein sorting, and the oncogenic protein p21(ras). The T cell receptor complexes CD4-p56lck and CD8-p56lck were found to include a 32- to 33-kilodalton phosphoprotein (p32) that was recognized by an antiserum to a consensus GTP-binding region in G proteins. Immununoprecipitated CD4 and CD8 complexes bound GTP and hydrolyzed it to guanosine diphosphate (GDP). The p32 protein was covalently linked to [alpha-P-32]GTP by ultraviolet photoaffinity labeling. These results demonstrate an interaction between T cell receptor complexes and an intracellular GTP-binding protein. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 30 TC 68 Z9 68 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 18 PY 1991 VL 254 IS 5030 BP 439 EP 441 DI 10.1126/science.1925604 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GK729 UT WOS:A1991GK72900052 PM 1925604 ER PT J AU PULVERER, BJ KYRIAKIS, JM AVRUCH, J NIKOLAKAKI, E WOODGETT, JR AF PULVERER, BJ KYRIAKIS, JM AVRUCH, J NIKOLAKAKI, E WOODGETT, JR TI PHOSPHORYLATION OF C-JUN MEDIATED BY MAP KINASES SO NATURE LA English DT Article ID V-JUN; PROTEIN; AP-1; TRANSCRIPTION; ACTIVATION; ENCODES AB THE proto-oncogene c-jun is a component of the AP-1 transcription factor family involved in the mediation of nuclear events elicited by extracellular stimuli 1-3. The c-jun protein is negatively regulated by phosphorylation of residues near the carboxy terminus which are dephosphorylated in response to phorbol esters 4. Here we identify two serine residues in the amino terminal A1 transactivation domain which are phosphorylated in response to a variety of mitogens, phorbol esters and activated ras (ref. 5). We present evidence that mitogen-activated protein-serine (MAP) kinases (pp54 and pp42/44) specifically phosphorylate these sites and that their phosphorylation positively regulates the transacting activity of c-jun. The MAP kinase enzymes pp54 and pp42/44 are regulated by tyrosine as well as serine/threonine phosphorylation 6,7. MAP kinase activation of c-jun may underlie the common stimulation of this transcription factor by mitogens, growth factors and oncogenes. C1 LUDWIG INST CANC RES,91 RIDING HOUSE ST,LONDON W1P 8BT,ENGLAND. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. RI Woodgett, Jim/F-1087-2010 OI Woodgett, Jim/0000-0003-3731-5797 NR 20 TC 1323 Z9 1334 U1 0 U2 14 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 17 PY 1991 VL 353 IS 6345 BP 670 EP 674 DI 10.1038/353670a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GK672 UT WOS:A1991GK67200075 PM 1922387 ER PT J AU SYSTROM, DM MARK, EJ SHEPARD, JAO DOWLING, WJ HOOPER, DC AF SYSTROM, DM MARK, EJ SHEPARD, JAO DOWLING, WJ HOOPER, DC TI A 63-YEAR-OLD OBESE DIABETIC WOMAN WITH A PLEURA-BASED MASS IN THE RIGHT UPPER LOBE - PULMONARY NOCARDIOSIS, WITH LOCALIZED CHRONIC ORGANIZING PNEUMONIA (INFLAMMATORY PSEUDOTUMOR) - CHRONIC OSTEOMYELITIS OF CONTIGUOUS RIBS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID ACQUIRED IMMUNODEFICIENCY SYNDROME; FINE-NEEDLE ASPIRATION; PLASMA-CELL GRANULOMA; CHEST WALL; COMPUTED-TOMOGRAPHY; BREAST-CANCER; UNITED-STATES; LUNG; DISEASE; ACTINOMYCOSIS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SYSTROM, DM (reprint author), MASSACHUSETTS GEN HOSP,MED,BOSTON,MA 02114, USA. NR 97 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 OCT 17 PY 1991 VL 325 IS 16 BP 1155 EP 1165 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA GK538 UT WOS:A1991GK53800008 ER PT J AU LAVIE, CJ MILANI, RV AF LAVIE, CJ MILANI, RV TI NATIONAL CHOLESTEROL EDUCATION-PROGRAMS RECOMMENDATIONS, AND IMPLICATIONS OF MISSING HIGH-DENSITY-LIPOPROTEIN CHOLESTEROL IN CARDIAC REHABILITATION PROGRAMS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Note ID CORONARY-ARTERY DISEASE; LIPID-LOWERING THERAPY C1 MASSACHUSETTS GEN HOSP,CARDIOVASC HLTH CTR,DEPT PREVENT MED,BOSTON,MA 02114. RP LAVIE, CJ (reprint author), OCHSNER HEART & VASC INST,DEPT INTERNAL MED,CARDIOL SECT,1514 JEFFERSON HIGHWAY,NEW ORLEANS,LA 70121, USA. RI Lavie, Carl/A-6014-2011; Milani, Richard/A-6045-2011 NR 9 TC 38 Z9 38 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD OCT 15 PY 1991 VL 68 IS 10 BP 1087 EP 1088 DI 10.1016/0002-9149(91)90500-K PG 2 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GL862 UT WOS:A1991GL86200018 PM 1927923 ER PT J AU LEVIN, LA SEDDON, JM TOPPING, T AF LEVIN, LA SEDDON, JM TOPPING, T TI RETINAL-PIGMENT EPITHELIAL TEARS ASSOCIATED WITH TRAUMA SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID BRUCH MEMBRANE AB Two previously healthy patients, a 66-year-old man with blunt trauma to the right eye, and a 28-year-old man with head trauma from a motorcycle accident, were observed to have parafoveal retinal pigment epithelial tears after injury. In both patients, fluorescin angiography demonstrated mottled window defects in the areas of the tears, and blocked fluorescence in the areas of the rolled-up pigment epithelium. Neither eye had evidence of pigment epithelial detachments. We hypothesize that this unusual phenomenon is caused by an acute tractional force oriented tangentially to the macular plane, the result of a rapid spherically expansile deformation of the globe during trauma. C1 OPHTHALM CONSULTANTS,BOSTON,MA. RP LEVIN, LA (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 13 TC 12 Z9 12 U1 0 U2 1 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 OCT 15 PY 1991 VL 112 IS 4 BP 396 EP 400 PG 5 WC Ophthalmology SC Ophthalmology GA GJ131 UT WOS:A1991GJ13100005 PM 1928241 ER PT J AU CHOW, JW FINE, MJ SHLAES, DM QUINN, JP HOOPER, DC JOHNSON, MP RAMPHAL, R WAGENER, MM MIYASHIRO, DK YU, VL AF CHOW, JW FINE, MJ SHLAES, DM QUINN, JP HOOPER, DC JOHNSON, MP RAMPHAL, R WAGENER, MM MIYASHIRO, DK YU, VL TI ENTEROBACTER BACTEREMIA - CLINICAL-FEATURES AND EMERGENCE OF ANTIBIOTIC-RESISTANCE DURING THERAPY SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE CEPHALOSPORINS; DRUG RESISTANCE, MICROBIAL; ENTEROBACTER; SEPTICEMIA; AMINOGLYCOSIDES ID SERIOUS BACTERIAL-INFECTIONS; GRAM-NEGATIVE BACTERIA; INDUCIBLE BETA-LACTAMASES; CEFTRIAXONE THERAPY; CEPHALOSPORINS; CEFTAZIDIME; CLOACAE; CEFAMANDOLE; PSEUDOMONAS; GENTAMICIN AB Objectives: To study the effect of previously administered antibiotics on the antibiotic susceptibility profile of Enterobacter, the factors affecting mortality, and the emergence of antibiotic resistance during therapy for Enterobacter bacteremia. Design: Prospective, observational study of consecutive patients with Enterobacter bacteremia. Setting: Three university tertiary care centers, one major university-affiliated hospital, and two university-affiliated Veterans Affairs medical centers. Patients: A total of 129 adult patients were studied. Measurements: The two main end points were emergence of resistance during antibiotic therapy and death. Main Results: Previous administration of third-generation cephalosporins was more likely to be associated with multiresistant Enterobacter isolates in an initial, positive blood culture (22 of 32, 69%) than was administration of antibiotics that did not include a third-generation cephalosporin (14 of 71, 20%; P < 0.001). Isolation of multiresistant Enterobacter sp. in the initial blood culture was associated with a higher mortality rate (12 of 37, 32%) than was isolation of a more sensitive Enterobacter sp. (14 of 92, 15%; P = 0.03). Emergence of resistance to third-generation cephalosporin therapy (6 of 31, 19%) occurred more often than did emergence of resistance to aminoglycoside (1 of 89, 0.01%; P = 0.001) or other beta-lactam (0 of 50; P = 0.002) therapy. Conclusions: More judicious use of third-generation cephalosporins may decrease the incidence of nosocomial multiresistant Enterobacter spp., which in turn may result in a lower mortality for Enterobacter bacteremia. When Enterobacter organisms are isolated from blood, it may be prudent to avoid third-generation cephalosporin therapy regardless of in-vitro susceptibility. C1 UNIV PITTSBURGH,SCH MED,968 SCAIFE,PITTSBURGH,PA 15261. PITTSBURGH DEPT VET AFFAIRS MED CTR,PITTSBURGH,PA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CLEVELAND DEPT VET AFFAIRS MED CTR,CLEVELAND,OH. MICHAEL REESE HOSP & MED CTR,CHICAGO,IL 60616. UNIV FLORIDA,GAINESVILLE,FL 32611. FU PHS HHS [5T32A107333] NR 44 TC 606 Z9 620 U1 7 U2 30 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 OCT 15 PY 1991 VL 115 IS 8 BP 585 EP 590 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA GJ902 UT WOS:A1991GJ90200001 PM 1892329 ER PT J AU MCCARTHY, PL ABHYANKAR, S NEBEN, S NEWMAN, G SIEFF, C THOMPSON, RC BURAKOFF, SJ FERRARA, JLM AF MCCARTHY, PL ABHYANKAR, S NEBEN, S NEWMAN, G SIEFF, C THOMPSON, RC BURAKOFF, SJ FERRARA, JLM TI INHIBITION OF INTERLEUKIN-1 BY AN INTERLEUKIN-1 RECEPTOR ANTAGONIST PREVENTS GRAFT-VERSUS-HOST DISEASE SO BLOOD LA English DT Note ID TUMOR-NECROSIS-FACTOR; BONE-MARROW TRANSPLANTATION; FACTOR-ALPHA; CELLS; EXPRESSION; MOUSE C1 DFCI,DEPT PEDIAT ONCOL,BOSTON,MA. SYNERGEN INC,BOULDER,CO. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV HEMATOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT IMMUNOL,BOSTON,MA 02115. FU NCI NIH HHS [5-PO1-CA39542]; NIAID NIH HHS [1-K08AI00926] NR 29 TC 174 Z9 174 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 OCT 15 PY 1991 VL 78 IS 8 BP 1915 EP 1918 PG 4 WC Hematology SC Hematology GA GK542 UT WOS:A1991GK54200002 PM 1832996 ER PT J AU OKUDA, K DRUKER, B KANAKURA, Y KOENIGSMANN, M GRIFFIN, JD AF OKUDA, K DRUKER, B KANAKURA, Y KOENIGSMANN, M GRIFFIN, JD TI INTERNALIZATION OF THE GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR RECEPTOR IS NOT REQUIRED FOR INDUCTION OF PROTEIN TYROSINE PHOSPHORYLATION IN HUMAN MYELOID CELLS SO BLOOD LA English DT Article ID GM-CSF RECEPTOR; GROWTH-FACTOR RECEPTORS; FACTOR-I; SIGNAL TRANSDUCTION; INTERLEUKIN-3 RECEPTORS; HEMATOPOIETIC-CELLS; HUMAN-NEUTROPHILS; DOWN-MODULATION; KINASE-ACTIVITY; FMS ONCOGENE C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA34183, CA36167] NR 49 TC 34 Z9 34 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 OCT 15 PY 1991 VL 78 IS 8 BP 1928 EP 1935 PG 8 WC Hematology SC Hematology GA GK542 UT WOS:A1991GK54200005 PM 1832997 ER PT J AU YAMADA, H IWASE, S MOHRI, M KUFE, D AF YAMADA, H IWASE, S MOHRI, M KUFE, D TI INVOLVEMENT OF A NUCLEAR FACTOR-KAPPA-B-LIKE PROTEIN IN INDUCTION OF THE MACROPHAGE COLONY-STIMULATING FACTOR GENE BY TUMOR-NECROSIS-FACTOR SO BLOOD LA English DT Article ID HUMAN MONOCYTIC DIFFERENTIATION; RNA POLYMERASE-II; GROWTH-FACTOR; FACTOR-ALPHA; TRANSCRIPTION FACTOR; CELL-LINES; POSTTRANSCRIPTIONAL REGULATION; HEMATOPOIETIC-CELLS; INTERLEUKIN-6 GENE; FACTOR CSF-1 C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,ROOM 1610,BOSTON,MA 02115. FU NCI NIH HHS [CA42802, CA34183] NR 51 TC 43 Z9 43 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 1991 VL 78 IS 8 BP 1988 EP 1995 PG 8 WC Hematology SC Hematology GA GK542 UT WOS:A1991GK54200014 PM 1912581 ER PT J AU ANTIN, JH BIERER, BE SMITH, BR FERRARA, J GUINAN, EC SIEFF, C GOLAN, DE MACKLIS, RM TARBELL, NJ LYNCH, E REICHERT, TA BLYTHMAN, H BOULOUX, C RAPPEPORT, JM BURAKOFF, SJ WEINSTEIN, HJ AF ANTIN, JH BIERER, BE SMITH, BR FERRARA, J GUINAN, EC SIEFF, C GOLAN, DE MACKLIS, RM TARBELL, NJ LYNCH, E REICHERT, TA BLYTHMAN, H BOULOUX, C RAPPEPORT, JM BURAKOFF, SJ WEINSTEIN, HJ TI SELECTIVE DEPLETION OF BONE-MARROW LYMPHOCYTES-T WITH ANTI-CD5 MONOCLONAL-ANTIBODIES - EFFECTIVE PROPHYLAXIS FOR GRAFT-VERSUS-HOST DISEASE IN PATIENTS WITH HEMATOLOGIC MALIGNANCIES SO BLOOD LA English DT Article ID COUNTERFLOW CENTRIFUGAL ELUTRIATION; CHRONIC MYELOGENOUS LEUKEMIA; CELL DEPLETION; SEQUENCE POLYMORPHISMS; TRANSPLANT RECIPIENTS; CHAIN IMMUNOTOXIN; CLINICAL-TRIAL; INCREASED RISK; CHRONIC PHASE; PREVENTION C1 SANOFI RES,NEW YORK,NY. BECTON DICKINSON INC,FRANKLIN,NJ. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,DIV BIOSTAT,BOSTON,MA 02115. RP ANTIN, JH (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA16516, CA39542]; NCRR NIH HHS [RR263504] NR 48 TC 111 Z9 112 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 OCT 15 PY 1991 VL 78 IS 8 BP 2139 EP 2149 PG 11 WC Hematology SC Hematology GA GK542 UT WOS:A1991GK54200033 PM 1717080 ER PT J AU BAST, RC KNAUF, S EPENETOS, A DHOKIA, B DALY, L TANNER, M SOPER, J CREASMAN, W GALL, S KNAPP, RC ZURAWSKI, VR SCHLOM, J KUFE, DW RITTS, RE AF BAST, RC KNAUF, S EPENETOS, A DHOKIA, B DALY, L TANNER, M SOPER, J CREASMAN, W GALL, S KNAPP, RC ZURAWSKI, VR SCHLOM, J KUFE, DW RITTS, RE TI COORDINATE ELEVATION OF SERUM MARKERS IN OVARIAN-CANCER BUT NOT IN BENIGN DISEASE SO CANCER LA English DT Article ID TUMOR-ASSOCIATED ANTIGEN; PLACENTAL ALKALINE-PHOSPHATASE; ANTIBODY IMMUNORADIOMETRIC ASSAY; MONOCLONAL-ANTIBODY; CA-125 LEVELS; PREOPERATIVE EVALUATION; MALIGNANT DISEASES; BREAST-CANCER; PELVIC MASSES; CARCINOMA AB Effective screening for occult ovarian cancer will require a strategy that is both sensitive and specific. Preliminary data suggest that CA 125 is elevated at diagnosis in a majority of patients with ovarian cancer. Although CA 125 is sufficiently specific to prompt its evaluation as one component of a strategy to detect ovarian cancer in postmenopausal women, a further improvement in specificity would facilitate cost-effective screening. In an attempt to develop a more specific screening strategy, multiple markers were assayed in a panel of sera from 47 patients with ovarian cancer and in a separate panel of sera from 50 individuals with benign disease whose serum CA 125 levels exceeded 35 U/ml. Among the patients with ovarian cancer, elevations of CA 125 (> 35 U/ml) were observed in 91%, CA 15-3 (> 30 U/ml) in 57%, TAG 72 (> 10 U/ml) in 49%, placental alkaline phosphatase (PLAP) in 25%, human milk fat globule protein (HMFG) 1 in 77%, HMFG2 in 62%, and NB/70K in 57%. Among the 50 sera selected from patients with benign disease, CA 125 was more than 35 U/ml in 100% and more than 65 U/ml in 42%. Among those patients with benign disease and elevated CA 125, NB/70K was elevated in 62%, HMFG1 in 26%, and HMFG2 in 12%, whereas TAG 72 and CA 15-3 were elevated in only 6% and 2%, respectively. In addition PLAP appeared promising; elevated enzyme levels were not found in the benign disease group. Among patients with ovarian cancer with CA 125 levels more than 35 U/ml, either TAG 72 or CA 15-3 was elevated in 77%. In the false-positive group, only 6% had elevations of one or the other marker. The CA 125 levels in cancer patients were, however, substantially greater than in patients with benign disease. If sera from patients with ovarian cancer were diluted to a range comparable to that found in benign disease, at least one of the two confirmatory tests was elevated in 63% of the samples from the malignant cases. Consequently, use of CA 15-3 and TAG 72 in combination with CA 125 can increase the apparent specificity of the CA 125 assay for distinguishing malignant from benign disease. Prospective studies will be required to test critically whether the use of additional serum markers in combination with the CA 125 assay would contribute to the specificity of a cost-effective screening strategy for ovarian cancer. C1 CENTOCOR INC,MALVERN,PA. UNIV ROCHESTER,SCH MED,ROCHESTER,NY 14627. HAMMERSMITH HOSP,IMPERIAL CANC RES FUND ONCOL GRP,LONDON W12 0HS,ENGLAND. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NCI,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. DUKE UNIV,MED CTR,DEPT MICROBIOL IMMUNOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DUKE COMPREHENS CANC CTR,DURHAM,NC 27710. RP BAST, RC (reprint author), DUKE UNIV,MED CTR,DEPT MED,POB 3843,DURHAM,NC 27710, USA. RI Bast, Robert/E-6585-2011 OI Bast, Robert/0000-0003-4621-8462 FU NCI NIH HHS [1-R44-CA40945, 5-R01-CA39930] NR 48 TC 47 Z9 47 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD OCT 15 PY 1991 VL 68 IS 8 BP 1758 EP 1763 DI 10.1002/1097-0142(19911015)68:8<1758::AID-CNCR2820680819>3.0.CO;2-# PG 6 WC Oncology SC Oncology GA GH289 UT WOS:A1991GH28900018 PM 1913520 ER PT J AU MEDEIROS, LJ HARRIS, NL AF MEDEIROS, LJ HARRIS, NL TI 4F2 EXPRESSION BY NON-HODGKINS-LYMPHOMA - REPLY SO CANCER LA English DT Letter ID DIFFERENTIATION ANTIGEN EXPRESSION; ACTIVATION C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP MEDEIROS, LJ (reprint author), NCI,PATHOL LAB,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD OCT 15 PY 1991 VL 68 IS 8 BP 1860 EP 1860 PG 1 WC Oncology SC Oncology GA GH289 UT WOS:A1991GH28900040 ER PT J AU BOOTHMAN, DA WANG, MZ LEE, SW AF BOOTHMAN, DA WANG, MZ LEE, SW TI INDUCTION OF TISSUE-TYPE PLASMINOGEN-ACTIVATOR BY IONIZING-RADIATION IN HUMAN-MALIGNANT MELANOMA-CELLS SO CANCER RESEARCH LA English DT Article ID DNA-DAMAGING AGENTS; PROTEIN KINASE-C; MESSENGER-RNA; UV-IRRADIATION; ESCHERICHIA-COLI; MAMMALIAN-CELLS; GENE-EXPRESSION; X-IRRADIATION; IDENTIFICATION; TRANSFORMATION AB Two differently timed extracellular and intracellular enzymatic and mRNA peaks of tissue-type plasminogen activator (t-PA) were induced following ionizing radiation. The first peak appeared within 10 min following X-irradiation but rapidly declined. The appearance of early t-PA mRNA transcripts and enzymatic activity were not prevented by actinomycin D treatment. In contrast, cycloheximide prevented the early, minor enzymatic induction peak of t-PA. Stabilization of t-PA mRNA transcripts appears to be an early initial response of human cells to ionizing radiation, since the synthesis of new mRNA transcripts within the first 30 min was not observed via nuclear run-on analyses. Nearly 12 h following X-irradiation, a second major enzymatic peak of t-PA was observed. Cycloheximide or actinomycin D treatments blocked the later t-PA response. t-PA mRNA levels were induced > 100-fold in 4 h by ionizing radiation as assayed via Northern or nuclear run-on analyses. During the major induction period, t-PA mRNA transcripts reached their maximum levels at 4-8 h, and intracellular enzyme levels accumulated 6-8 h after X-irradiation. Unirradiated U1-Mel cells demonstrated only low basal levels of t-PA mRNA and enzymatic activity. Similar induction responses were found following UV-irradiation or 12-O-tetradecanoyl-phorbol-13-acetate (PMA) treatments. Normal human fibroblast (ie., GM 2936B, GM2907A, and IMR-90) cells also demonstrated the induction of t-PA, although only one later enzymatic peak was detected. The induction of t-PA mRNA levels and intracellular and extracellular enzymatic activities for these cells were 50-fold lower than with U1-Mel cells given equitoxic doses of X-rays. Differential expression of t-PA in some tumor as compared to normal tissues may be utilized in future chemotherapeutic regimens. C1 HARVARD UNIV,DANA FARBER CANC INST,DIV CANC GENET,BOSTON,MA 02215. RP BOOTHMAN, DA (reprint author), UNIV MICHIGAN,DIV CANC BIOL,DEPT RADIAT ONCOL,1331 E ANN ST,RM 4131,ANN ARBOR,MI 48109, USA. NR 48 TC 55 Z9 55 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 OCT 15 PY 1991 VL 51 IS 20 BP 5587 EP 5595 PG 9 WC Oncology SC Oncology GA GJ908 UT WOS:A1991GJ90800025 PM 1913677 ER PT J AU ISHIKAWA, J XU, HJ HU, SX YANDELL, DW MAEDA, S KAMIDONO, S BENEDICT, WF TAKAHASHI, R AF ISHIKAWA, J XU, HJ HU, SX YANDELL, DW MAEDA, S KAMIDONO, S BENEDICT, WF TAKAHASHI, R TI INACTIVATION OF THE RETINOBLASTOMA GENE IN HUMAN BLADDER AND RENAL-CELL CARCINOMAS SO CANCER RESEARCH LA English DT Article ID HUMAN PROSTATE CARCINOMA; SUSCEPTIBILITY GENE; ALTERED EXPRESSION; HUMAN SARCOMAS; RB GENE; OSTEO-SARCOMA; DNA-SEQUENCE; TUMOR-CELLS; ESTABLISHMENT; LINE AB The retinoblastoma (RB) gene was the first tumor suppressor gene isolated and its inactivation is associated with the pathogenesis of several types of human cancer. In this study, we investigated the involvement of the RB gene in bladder and renal cell carcinomas by determining the loss of heterozygosity (LOH) at the RB locus and by DNA, RNA, and protein analysis of the RB gene. Whenever possible, the latter included Western blotting and immunohistochemical staining of the RB protein. In bladder carcinoma, 2 of the 8 cell lines we studied had an inactivated RB gene; one cell line lacked RB expression Without a gross RB deletion, whereas the other cell line expressed only the underphosphorylated form of the RB protein. None of 16 low-grade noninvasive bladder carcinomas showed an alteration in RB protein by direct Western blot analysis, whereas 2 of 14 high-grade, invasive tumors had no RB protein as measured by both Western blotting and immunohistochemical staining. This suggests that the loss of RB function may be more important in the progression of bladder cancer than in its initiation, although more extensive studies are required. LOH within the RB locus was observed in 5 of 27 informative cases of primary bladder, ureter, or renal pelvis carcinoma. However, none of the 5 cases with LOH at the RB locus had a functional loss of RB protein expression. In renal cell carcinoma, one of the 12 cell lines had a gross homozygous deletion of the RB gene, and 2 of 32 primary tumors were negative for RB protein expression. LOH at the RB locus also was found in only 2 of 30 informative cases, one of which lacked RB expression. These results are the first to demonstrate the involvement of RB inactivation in the development of advanced primary bladder carcinoma and suggest that RB loss could have a role in certain renal cell carcinomas. Our data, however, show no correlation between LOH at the RB locus in bladder cancer and actual inactivation of the RB gene al the protein level. This may suggest that there is a second tumor suppressor or recessive cancer gene on chromosome 13 in bladder cancer and/or that the mechanism of RB inactivation in bladder cancer frequently involves independent mutations of each RB allele. C1 BAYLOR COLL MED,CTR BIOTECHNOL,400 RES FOREST DR,THE WOODLANDS,TX 77381. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. KOBE UNIV,SCH MED,DEPT PATHOL,CHUO KU,KOBE 650,JAPAN. KOBE UNIV,SCH MED,DEPT UROL,CHUO KU,KOBE 650,JAPAN. FU NEI NIH HHS [EY06195, EY02715] NR 55 TC 187 Z9 190 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 OCT 15 PY 1991 VL 51 IS 20 BP 5736 EP 5743 PG 8 WC Oncology SC Oncology GA GJ908 UT WOS:A1991GJ90800048 PM 1913692 ER PT J AU MATSUYAMA, T YAMADA, A ROTHSTEIN, DM ANDERSON, KC SCHLOSSMAN, SF MORIMOTO, C AF MATSUYAMA, T YAMADA, A ROTHSTEIN, DM ANDERSON, KC SCHLOSSMAN, SF MORIMOTO, C TI CD45 ISOFORMS ASSOCIATED WITH DISTINCT FUNCTIONS OF CD4 CELLS DERIVED FROM UNUSUAL HEALTHY DONORS LACKING CD45RA - LYMPHOCYTES-T SO CELLULAR IMMUNOLOGY LA English DT Article ID LEUKOCYTE-COMMON ANTIGEN; PROTEIN TYROSINE PHOSPHATASES; MONOCLONAL-ANTIBODY; SURFACE RECEPTORS; INDUCER CELLS; ACTIVATION; EXPRESSION; PATHWAY; FAMILY; SUBSET C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TRANSPLANTAT,44 BINNEY ST,BOSTON,MA 02115. FU NCI NIH HHS [CA-50947]; NIAID NIH HHS [AI-12069]; NIAMS NIH HHS [AR-33713] NR 48 TC 11 Z9 11 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 OCT 15 PY 1991 VL 137 IS 2 BP 406 EP 419 DI 10.1016/0008-8749(91)90089-T PG 14 WC Cell Biology; Immunology SC Cell Biology; Immunology GA GH270 UT WOS:A1991GH27000012 PM 1716520 ER PT J AU FREEDMAN, AS FREEMAN, GJ RHYNHART, K NADLER, LM AF FREEDMAN, AS FREEMAN, GJ RHYNHART, K NADLER, LM TI SELECTIVE INDUCTION OF B7/BB-1 ON INTERFERON-GAMMA STIMULATED MONOCYTES - A POTENTIAL MECHANISM FOR AMPLIFICATION OF T-CELL ACTIVATION THROUGH THE CD28 PATHWAY SO CELLULAR IMMUNOLOGY LA English DT Article ID IA-ANTIGEN EXPRESSION; MONOCLONAL-ANTIBODIES; HUMAN-LYMPHOCYTES; ACCESSORY CELLS; B-CELLS; RECEPTOR; SIGNAL; INTERLEUKIN-2; PROLIFERATION; MOLECULES C1 HARVARD UNIV,SCH MED,DEPT MED,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DEPT PATHOL,CAMBRIDGE,MA 02138. RP FREEDMAN, AS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [5K08 CA01105, CA40216] NR 52 TC 347 Z9 348 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD OCT 15 PY 1991 VL 137 IS 2 BP 429 EP 437 DI 10.1016/0008-8749(91)90091-O PG 9 WC Cell Biology; Immunology SC Cell Biology; Immunology GA GH270 UT WOS:A1991GH27000014 PM 1716521 ER PT J AU GOLENBOCK, DT HAMPTON, RY QURESHI, N TAKAYAMA, K RAETZ, CRH AF GOLENBOCK, DT HAMPTON, RY QURESHI, N TAKAYAMA, K RAETZ, CRH TI LIPID-A-LIKE MOLECULES THAT ANTAGONIZE THE EFFECTS OF ENDOTOXINS ON HUMAN MONOCYTES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LIPOPOLYSACCHARIDE-BINDING PROTEINS; MACROPHAGE TUMOR-CELLS; MURINE SPLENOCYTES; INDUCTION; PRECURSORS; CACHECTIN; INVITRO; SITES AB Lipopolysaccharide (LPS) endotoxin is implicated as the bacterial product responsible for the clinical syndrome of Gram-negative septicemia. Although the lipid A domain of LPS appears to be responsible for the toxicity of endotoxin, lipid A from the photosynthetic bacterium Rhodobacter sphaeroides (RSLA) and a disaccharide precursor of lipid A from enteric bacteria, termed lipid IV(A), have little activity on human cells. Using the human promonomyelocytic cell line THP-1 and human monocytic cells, we now show that both lipid IV(A) and RSLA are antagonists of LPS. Complete, apparently competitive, inhibition of LPS activity is possible at a 10-100-fold excess of antagonist, as judged by measuring the release of cytokines and prostaglandin E2. Both antagonists prevent monocyte stimulation by endotoxin extracted from a variety of Gram-negative bacteria. Cells pretreated with either inhibitor and subsequently washed still show attenuated responses to LPS. Stimulation of monocytes by whole Gram-negative bacteria is also antagonized in a dose-dependent manner. Lipid X has no inhibitory effect in the same dose range as lipid IV(A) and RSLA. These findings rule out LPS sequestration as the explanation for the observed antagonism. Neither inhibitor alters monocyte stimulation by phorbol 12-myristate 13-acetate, Staphylococcus aureus, or purified protein derivative, demonstrating specificity for LPS. Although RSLA appears to inhibit LPS when tested with macrophages from both humans and mice, lipid IV(A) had the unique ability to act as an LPS antagonist with human-derived cells but to exhibit LPS-like effects with murine-derived cells. Like LPS, lipid IV(A) Stimulated the release of both tumor necrosis factor-alpha and arachidonic acid from murine-derived RAW 264.7 macrophage tumor cells. The range of concentrations necessary for lipid IV(A) to induce LPS-like effects in murine cells was similar to that necessary to antagonize the actions of LPS in human monocytes. The agonist activities of lipid IV(A) were completely inhibitable by RSLA. This unique species-dependent pharmacology observed with lipid IV(A) may reflect differences between human and murine LPS receptors. RSLA and lipid IV(A) may be useful in defining the role of LPS in Gram-negative bacterial infections and may prove to be prototypical therapeutic agents for the treatment of Gram-negative septicemia. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BIOCHEM,MADISON,WI 53706. MERCK SHARP & DOHME LTD,DEPT BIOCHEM,W POINT,PA 19486. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. RP GOLENBOCK, DT (reprint author), UNIV WISCONSIN HOSP & CLIN,DEPT MED,MADISON,WI 53729, USA. FU NIAID NIH HHS [AI00840]; NIGMS NIH HHS [GM-36054] NR 33 TC 341 Z9 347 U1 2 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 15 PY 1991 VL 266 IS 29 BP 19490 EP 19498 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GK667 UT WOS:A1991GK66700057 PM 1918061 ER PT J AU TORIMOTO, Y DANG, NH VIVIER, E TANAKA, T SCHLOSSMAN, SF MORIMOTO, C AF TORIMOTO, Y DANG, NH VIVIER, E TANAKA, T SCHLOSSMAN, SF MORIMOTO, C TI COASSOCIATION OF CD26 (DIPEPTIDYL PEPTIDASE-IV) WITH CD45 ON THE SURFACE OF HUMAN LYMPHOCYTES-T SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LEUKOCYTE-COMMON ANTIGEN; CELL ACTIVATION ANTIGEN; TYROSINE-PROTEIN-KINASE; MONOCLONAL-ANTIBODY; PERIPHERAL-BLOOD; SIGNAL TRANSDUCTION; RECEPTOR; ASSOCIATION; PHOSPHATASE; RAT AB In the present report, we demonstrated that modulation of CD26 from T cell surface induced by anti-CD26 (1F7) led to enhanced phosphorylation of CD3 zeta-tyrosine residues and increased CD4 associated p56lck tyrosine kinase activity. We further showed that CD26 was comodulated on the T cell surface with CD45, a known membrane-linked protein tyrosine phosphatase and that anti-CD26 was capable of precipitating CD45 from T cell lysates. These findings strongly suggest that CD26 may be closely associated with the CD45 protein tyrosine phosphatase on T cell surface and further support the notion that the interaction of CD26 with CD45 results in enhanced tyrosine kinase activity, zeta-chain phosphorylation, and T cell activation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIAID NIH HHS [AI-12069, AI-29530]; NIAMS NIH HHS [AR-33713] NR 42 TC 215 Z9 216 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 OCT 15 PY 1991 VL 147 IS 8 BP 2514 EP 2517 PG 4 WC Immunology SC Immunology GA GK972 UT WOS:A1991GK97200012 PM 1680916 ER PT J AU BLUMBERG, RS TERHORST, C BLEICHER, P MCDERMOTT, FV ALLAN, CH LANDAU, SB TRIER, JS BALK, SP AF BLUMBERG, RS TERHORST, C BLEICHER, P MCDERMOTT, FV ALLAN, CH LANDAU, SB TRIER, JS BALK, SP TI EXPRESSION OF A NONPOLYMORPHIC MHC CLASS-I-LIKE MOLECULE, CD1D, BY HUMAN INTESTINAL EPITHELIAL-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID DENDRITIC EPIDERMAL-CELLS; DELTA-ANTIGEN RECEPTOR; NORMAL HUMAN-SKIN; GAMMA-DELTA; INTRAEPITHELIAL LYMPHOCYTES; T-CELLS; THYMIC DIFFERENTIATION; MONOCLONAL-ANTIBODY; ALPHA-CHAINS; BETA-CHAINS AB The human CD1 locus encodes three nonpolymorphic MHC class I-like cell surface glycoproteins, CD1a-c, which are expressed primarily by immature thymocytes. A mAb and antipeptide antiserum were utilized to determine the tissue distribution of a fourth CD1 molecule, CD1d. Within the lymphoid lineage, CD1d was expressed on B cells but not on thymocytes. Immunoperoxidase staining of fresh frozen intestinal tissues demonstrated that the majority of intestinal epithelial cells, with the exception of cells at the base of some crypts, expressed CD1d. The CD1d staining was observed in the cytoplasm and along the basolateral membranes of the epithelial cells. The intestinal epithelial cell expression of CD1d was confirmed by immunoblotting with a CD1d antipeptide antiserum. Further immunoperoxidase studies indicated that CD1d, unlike murine CD1, was also expressed by nonlymphoid tissues outside of the gastrointestinal tract. The expression of CD1d outside the lymphoid and myeloid lineages clearly distinguishes this molecule from CD1a-c and suggests that it may serve a distinct function. The prominent expression of CD1d by intestinal epithelial cells suggests that this molecule may be an important ligand for T lymphocytes within the gut-associated lymphoid tissue. C1 BRIGHAM & WOMENS HOSP,DIV GASTROENTEROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,WELLMAN LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BETH ISRAEL HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02215. FU NCI NIH HHS [CA-01310]; NIDDK NIH HHS [DK36835, 1 KO8 DK01886-01] NR 56 TC 220 Z9 220 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 OCT 15 PY 1991 VL 147 IS 8 BP 2518 EP 2524 PG 7 WC Immunology SC Immunology GA GK972 UT WOS:A1991GK97200013 PM 1717564 ER PT J AU SPERTINI, O LUSCINSKAS, FW KANSAS, GS MUNRO, JM GRIFFIN, JD GIMBRONE, MA TEDDER, TF AF SPERTINI, O LUSCINSKAS, FW KANSAS, GS MUNRO, JM GRIFFIN, JD GIMBRONE, MA TEDDER, TF TI LEUKOCYTE ADHESION MOLECULE-1 (LAM-1, L-SELECTIN) INTERACTS WITH AN INDUCIBLE ENDOTHELIAL-CELL LIGAND TO SUPPORT LEUKOCYTE ADHESION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NODE HOMING RECEPTOR; T-CELLS; LYMPHOCYTE RECIRCULATION; MONOCLONAL-ANTIBODIES; VASCULAR ENDOTHELIUM; NEUTROPHIL ADHERENCE; INTERACTION DOMAINS; SURFACE MOLECULE; MEL-14 ANTIGEN; HUMAN HOMOLOG AB The human lymphocyte homing receptor, LAM-1, mediates the adhesion of lymphocytes to specialized high endothelial venules (HEV) of peripheral lymph nodes. We now report that LAM-1 is also a major mediator of leukocyte attachment to activated human endothelium. In a novel adhesion assay, LAM-1 was shown to mediate approximately 50% of the adhesion of both lymphocytes and neutrophils to TNF-activated human umbilical vein endothelial cells at 4-degrees-C. The contribution of LAM-1 to leukocyte adhesion was only detectable when the assays were carried out under rotating (nonstatic) conditions, suggesting that LAM-1 is involved in the initial attachment of leukocytes to endothelium. In this assay at 37-degrees-C, essentially all lymphocyte attachment to endothelium was mediated by LAM-1, VLA-4/VCAM-1, and the CD11/CD18 complex, whereas neutrophil attachment was mediated by LAM-1, endothelial-leukocyte adhesion molecule-1, and CD11/CD18. Thus, multiple receptors are necessary to promote optimal leukocyte adhesion to endothelium. LAM-1 also appeared to be involved in optimal neutrophil transendothelial migration using a videomicroscopic in vitro transmigration model system. LAM-1-dependent leukocyte adhesion required the induction and surface expression of a neuraminidase-sensitive molecule that was expressed for at least 24 h on activated endothelium. Expression of the LAM-1 ligand by endothelium was optimally induced by LPS and the proinflammatory cytokines TNF-alpha and IL-1-beta, whereas IFN-gamma and IL-4 induced lower levels of expression. The LAM-1 ligand on HEV and cytokine treated endothelium may be similar carbohydrate-containing molecules, because phosphomannan monoester core complex from yeast Hansenula hostii cell wall blocked binding of lymphocytes to both cell types, and identical epitopes on LAM-1-mediated lymphocyte attachment to HEV and activated endothelium. Thus, LAM-1 and its inducible endothelial ligand constitute a new pair of adhesion molecules that may regulate initial leukocyte/endothelial interactions at sites of inflammation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV VASC RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA-36167, CA-34183]; NIAID NIH HHS [AI-26872] NR 72 TC 387 Z9 391 U1 0 U2 5 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD OCT 15 PY 1991 VL 147 IS 8 BP 2565 EP 2573 PG 9 WC Immunology SC Immunology GA GK972 UT WOS:A1991GK97200021 PM 1717567 ER PT J AU BROWNING, MJ HUNEYCUTT, BS HUANG, AS REISS, CS AF BROWNING, MJ HUNEYCUTT, BS HUANG, AS REISS, CS TI REPLICATION-DEFECTIVE VIRUSES MODULATE IMMUNE-RESPONSES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID VESICULAR STOMATITIS-VIRUS; CYTOLYTIC LYMPHOCYTES-T; INTERFERING PARTICLES; CLASS-I; ANTIGEN PRESENTATION; CELLS; PATHWAYS; GLYCOPROTEIN; MICE AB By immunizing inbred mice with purified replication-competent, defective virus particles, or an admixture of the two, differential effects on the cellular immune system have been uncovered. Defective virus, exemplified by the vesicular stomatitis virus (VSV) defective interfering particle (DI 0.33), induced in BALB/c mice low levels of proliferating, IL-2 secreting, and cytolytic Ag-specific T lymphocytes. This was not caused by a dominant suppressor cell response, or by a failure to stimulate lymphokine-secreting cells, but appeared to reflect a reduced efficiency of priming as compared with standard virus. Mice primed with a mixture of wt and DI virus showed reduced proliferation compared with mice primed with wt virus. When histocompatible target cells were sensitized by pure DI particles, they were neither recognized nor lysed by CD8+ CTL. Cells co-infected with wt and DI particles were not as readily lysed by CD8+ CTL as cells infected by VSV alone. The extent of this reduction was dependent on the concentration of DI particles. This suggests that DI particles may have prevented the proper presentation of endogenously synthesized Ag for recognition by CD8+ CTL. Metabolic labeling studies indicated that the presence of DI particles suppressed the synthesis of viral proteins in dually infected cells. However, CD4+ T lymphocyte clones recognized and efficiently lysed histocompatible Ia+ cells infected with DI particles alone or co-infected with replication-competent and defective virus. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. OI Reiss, Carol/0000-0003-4353-8882 FU NCRR NIH HHS [SO7 RR05526]; NIAID NIH HHS [R01 AI18083, R37 AI20896] NR 32 TC 11 Z9 13 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 OCT 15 PY 1991 VL 147 IS 8 BP 2685 EP 2691 PG 7 WC Immunology SC Immunology GA GK972 UT WOS:A1991GK97200038 PM 1655896 ER PT J AU CUNNINGHAM, LA HANSEN, JT SHORT, MP BOHN, MC AF CUNNINGHAM, LA HANSEN, JT SHORT, MP BOHN, MC TI THE USE OF GENETICALLY ALTERED ASTROCYTES TO PROVIDE NERVE GROWTH-FACTOR TO ADRENAL CHROMAFFIN CELLS GRAFTED INTO THE STRIATUM SO BRAIN RESEARCH LA English DT Article DE RETROVIRAL VECTOR; TRANSPLANTATION; PARKINSONS DISEASE; 6-HYDROXYDOPAMINE; STRIATUM ID N-METHYLTRANSFERASE PNMT; VASOACTIVE INTESTINAL PEPTIDE; ADVANCED PARKINSONS-DISEASE; MEDULLA GRAFTS; MESSENGER-RNA; RAT-BRAIN; NEURITE OUTGROWTH; ASTROGLIAL CELLS; CAUDATE-NUCLEUS; NEURAL CREST AB Transplantation of adrenal chromaffin cells into the striatum of Parkinson's disease patients is unlikely to become a reliable therapy unless techniques are devised to improve cell survival. To address this issue, we investigated the use of genetically altered astrocytes that constitutively secrete beta-nerve growth factor (NGF) to provide trophic support for adrenal chromaffin cells grafted into the dopamine-denervated striatum of the rat. Primary rat astrocytes were altered genetically in vitro by infection with a retroviral vector harboring a mouse beta-NGF transgene under constitutive long terminal repeat transcriptional control. Confluent cultures of these genetically altered astrocytes secrete NGF into their culture medium at a rate of approximately 9 pg/10(5) cells/h. This rate of NGF secretion is at least 10-fold higher than that of confluent sister cultures of uninfected astrocytes. The effects of the NGF-secreting astrocytes on the survival and neuronal transformation of dissociated adrenal chromaffin cells were assessed in vitro and following transplantation into the dopamine-denervated striatum of the adult rat. In vitro experiments demonstrated that neuritic outgrowth is stimulated when postnatal day 12 chromaffin cells are grown on a monolayer of the genetically altered astrocytes. When co-grafted with genetically altered astrocytes, young postnatal chromaffin cells displayed extensive neuritic outgrowth within the host brain 2 weeks postimplantation, whereas chromaffin cells grafted alone or with normal astrocytes retain an endocrine-like morphology. Survival of the chromaffin cells is also enhanced 3-6-fold when co-grafted with the genetically altered astrocytes. In addition, the neuronally transformed chromaffin cells appear to lose adrenergic properties as assessed by diminished immunoreactivity to the adrenergic marker, phenylethanolamine-N-methyltransferase. Although their survival is also enhanced approximately 4-fold relative to controls, adult chromaffin cells do not convert to a neuronal morphology when co-grafted with the genetically altered astrocytes. These studies demonstrate that rat astrocytes carrying a mouse NGF transgene provide trophic support for intrastriatal chromaffin cell grafts. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. RP CUNNINGHAM, LA (reprint author), UNIV ROCHESTER,SCH MED & DENT,DEPT NEUROBIOL & ANAT,BOX 603,ROCHESTER,NY 14642, USA. FU NIA NIH HHS [T32AG00107]; NINDS NIH HHS [NS08906, NS25778] NR 79 TC 69 Z9 69 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD OCT 11 PY 1991 VL 561 IS 2 BP 192 EP 202 DI 10.1016/0006-8993(91)91595-R PG 11 WC Neurosciences SC Neurosciences & Neurology GA GN050 UT WOS:A1991GN05000002 PM 1686984 ER PT J AU LAZAROU, LP SNELL, RG MACDONALD, ME GUSELLA, JF WASMUTH, JJ SHAW, DJ AF LAZAROU, LP SNELL, RG MACDONALD, ME GUSELLA, JF WASMUTH, JJ SHAW, DJ TI MBOI RFLP AT THE D4S43 (C4H) LOCUS SO NUCLEIC ACIDS RESEARCH LA English DT Note ID HUNTINGTONS-DISEASE C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. RP LAZAROU, LP (reprint author), UNIV WALES COLL MED,INST MED GENET,HEATH PK,CARDIFF CF4 4XW,S GLAM,WALES. NR 2 TC 1 Z9 1 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD OCT 11 PY 1991 VL 19 IS 19 BP 5445 EP 5445 DI 10.1093/nar/19.19.5445-a PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GK752 UT WOS:A1991GK75200059 PM 1681512 ER PT J AU RUSTGI, AK COMPTON, CC YUCEL, EK SCULLY, RE PODOLSKY, DK KELSEY, PB FIENBERG, R AF RUSTGI, AK COMPTON, CC YUCEL, EK SCULLY, RE PODOLSKY, DK KELSEY, PB FIENBERG, R TI A 76-YEAR-OLD MAN WITH RECURRENT GASTROINTESTINAL-BLEEDING - DIEULAFOYS VASCULAR MALFORMATION - GASTRITIS WITH HELICOBACTER-PYLORI INFECTION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID CALIBER-PERSISTENT ARTERY; ARTERIOVENOUS MALFORMATION; EXULCERATIO SIMPLEX; CARCINOID-TUMORS; TRACT; ANGIODYSPLASIA; DISEASE; STOMACH; HEMORRHAGE; COLON C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RUSTGI, AK (reprint author), MASSACHUSETTS GEN HOSP,MED,BOSTON,MA 02114, USA. NR 74 TC 11 Z9 11 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 OCT 10 PY 1991 VL 325 IS 15 BP 1086 EP 1096 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA GJ108 UT WOS:A1991GJ10800008 ER PT J AU BLOCH, KJ AF BLOCH, KJ TI SJOGREN CONNECTIONS - A CITATION-CLASSIC COMMENTARY ON SJOGRENS-SYNDROME - A CLINICAL, PATHOLOGICAL, AND SEROLOGICAL STUDY OF 62 CASES BY BLOCH,K.J., BUCHANAN,W.W., WOHL,M.J., AND BUNIM,J.J. SO CURRENT CONTENTS/CLINICAL MEDICINE LA English DT Article RP BLOCH, KJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU INST SCI INFORM INC PI PHILADELPHIA PA 3501 MARKET ST, PHILADELPHIA, PA 19104 SN 0891-3358 J9 CC/CLIN MED PD OCT 7 PY 1991 IS 40 BP 8 EP 8 PG 1 WC Multidisciplinary Sciences; Social Sciences, Interdisciplinary SC Science & Technology - Other Topics; Social Sciences - Other Topics GA GF430 UT WOS:A1991GF43000001 ER PT J AU ROSENBERG, I CHERAYIL, BJ ISSELBACHER, KJ PILLAI, S AF ROSENBERG, I CHERAYIL, BJ ISSELBACHER, KJ PILLAI, S TI MAC-2-BINDING GLYCOPROTEINS - PUTATIVE LIGANDS FOR A CYTOSOLIC BETA-GALACTOSIDE LECTIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IGE-BINDING PROTEIN; MONOCLONAL-ANTIBODIES; SEQUENCE; MAC-2; RECOGNITION; HOMOLOGY; ANTIGEN; SHEETS; CELL AB Mac-2, a galactose-binding lectin secretion by activated macrophages, is the major non-integrin laminin-binding protein in these cells. Mac-2 is also expressed by epithelial cells in the intestine and kidney. We wished to identify intestinal glycoproteins other than laminin that have a high affinity for Mac-2 and that could be considered as candidate ligands or partners for this lectin in intestinal epithelium. Certain lines of human colon adenocarcinoma cells produce two Mac-2-binding glycoproteins (M2BP-1 and M2BP-2) that were identified by their avid association with Mac-2 following detergent lysis and immunoprecipitation. These glycoproteins do not share a common epitope with Mac-2, and the interaction between Mac-2 and these proteins is mediated through the carbohydrate-binding domain of Mac-2 and sugar moieties on M2BP-1 and M2BP-2. M2BP-1 (98 kDa) and M2BP-2 (70 kDa) were purified by immunoaffinity chromatography and were specifically eluted with either galactose or lactose. Peptide maps revealed that M2BP-1 and M2BP-2 are structurally related. M2BP-1 is secreted and could conceivably associate with Mac-2 extracellularly. N-terminal sequence analysis of M2BP-2 suggests that these glycoproteins represent a unique subset of candidate ligands for this mammalian beta-galactoside lectin. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC GENET GRP,MOLEC IMMUNOL LAB,BLDG 149,13TH ST,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NIAID NIH HHS [AI-27835]; NIDDK NIH HHS [DK07191] NR 19 TC 99 Z9 101 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 5 PY 1991 VL 266 IS 28 BP 18731 EP 18736 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GJ472 UT WOS:A1991GJ47200052 PM 1917996 ER PT J AU LEE, ME DHADLY, MS TEMIZER, DH CLIFFORD, JA YOSHIZUMI, M QUERTERMOUS, T AF LEE, ME DHADLY, MS TEMIZER, DH CLIFFORD, JA YOSHIZUMI, M QUERTERMOUS, T TI REGULATION OF ENDOTHELIN-1 GENE-EXPRESSION BY FOS AND JUN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR AP-1; INDUCIBLE ENHANCER; LEUCINE ZIPPER; C-FOS; PROTEIN COMPLEXES; CELLS; BINDING; PROMOTER; DNA; SEQUENCE AB The endothelin peptides constitute a family of potent vasoconstrictor molecules. Endothelin-1 (ET1) is secreted by vascular endothelial cells and may have a role in the regulation of vascular tone. To better understand the function of ET1, we have investigated the transcriptional regulation of the ET1 gene. Utilizing reporter gene transfection experiments, we have previously identified two promoter regions, located at base pairs -148 to -117 (Region A) and -117 to -98 (Region B) of the ET1 gene. Both regions are necessary for high level ET1 transcription in endothelial cells. A nuclear protein binding to the GATA motif in Region A has been identified and proven to be necessary for expression of the ET1 gene. However, the cis-acting sequences and their cognate binding proteins for Region B have not been investigated. To identify protein binding motifs in Region B we performed DNase I footprinting and gel mobility shift assays using a DNA fragment encoding base pairs -204 to -94 of the ET1 gene. Results from these studies indicated that the AP1 consensus sequence (GTGACTAA) in Region B as the only protein-binding motif. Site-directed mutagenesis of the ET1 AP1 site resulted in a 30-fold reduction in promoter activity, establishing the functional significance of this sequence. Additional experiments investigated the role of Jun and Fos in ET1 transcription. By employing antisera to Jun and Fos in gel mobility shift assays, both of these proteins were identified as endothelial cell nuclear proteins binding to the ET1 AP1 sequence. In trans-activation experiments, we showed that cotransfection of c-fos and c-jun expression plasmids markedly increased the transcription rate of chloramphenicol acetyltransferase reporter plasmids containing three synthetic ET1 AP1 sites. Taken together, these data indicate the importance of the AP1 recognition sequence, and the role of Fos and Jun proteins in the regulation of ET1 gene transcription. C1 MASSACHUSETTS GEN HOSP,GEN MED SERV,CARDIAC UNIT,BOSTON,MA 02114. UNIV TOKYO,MED UNIT,DEPT INTERNAL MED 3,BUNKYO KU,TOKYO 113,JAPAN. RP LEE, ME (reprint author), HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115, USA. NR 44 TC 131 Z9 133 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 5 PY 1991 VL 266 IS 28 BP 19034 EP 19039 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GJ472 UT WOS:A1991GJ47200096 PM 1918021 ER PT J AU ARUFFO, A KOLANUS, W WALZ, G FREDMAN, P SEED, B AF ARUFFO, A KOLANUS, W WALZ, G FREDMAN, P SEED, B TI CD62/P-SELECTIN RECOGNITION OF MYELOID AND TUMOR-CELL SULFATIDES SO CELL LA English DT Article ID GRANULE MEMBRANE-PROTEIN; ENDOTHELIAL VONWILLEBRAND-FACTOR; WEIBEL-PALADE BODIES; ACTIVATED PLATELETS; ADHESIVE INTERACTION; MONOCLONAL-ANTIBODY; NEUTROPHIL ADHESION; SEQUENCE HOMOLOGY; HOMING RECEPTOR; SIALYL-LEX AB CD62, also called PADGEM protein, GMP-140, or P-selectin, is a granule membrane protein of endothelial cells and platelets that is mobilized to the plasma membrane following exposure to mediators such as thrombin, histamine, complement components, or peroxides. Data presented to date suggest that one ligand of CD62 includes CD15 (Lewis x determinant) and sialic acid. We show here that sulfatides, heterogeneous 3-sulfated galactosyl ceramides, are an apparently unrelated ligand of CD62. Sulfatides are expressed on the plasma membrane of, and are excreted by, granulocytes, and constitute the principal ligand for CD62 on the plasma membrane of some tumor cells. CD62 binds to sulfatides adsorbed to plastic as avidly as it binds to myeloid or tumor cells. We find that granulocytes excrete sulfatides at a rate predicted to allow them to be rapidly released from CD62 once they have exited the bloodstream. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. GOTHENBURG UNIV,DEPT MED BIOCHEM,S-40033 GOTHENBURG,SWEDEN. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA 98121. RP ARUFFO, A (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI27849]; NIDDK NIH HHS [DK43031] NR 44 TC 285 Z9 285 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 OCT 4 PY 1991 VL 67 IS 1 BP 35 EP 44 DI 10.1016/0092-8674(91)90570-O PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GJ320 UT WOS:A1991GJ32000005 PM 1717159 ER PT J AU PELLETIER, J BRUENING, W LI, FP HABER, DA GLASER, T HOUSMAN, DE AF PELLETIER, J BRUENING, W LI, FP HABER, DA GLASER, T HOUSMAN, DE TI WT1 MUTATIONS CONTRIBUTE TO ABNORMAL GENITAL SYSTEM-DEVELOPMENT AND HEREDITARY WILMS-TUMOR SO NATURE LA English DT Article ID SEX-DETERMINING REGION; GENE; DNA; CHROMOSOME-11; DELETION AB WILMS' tumour (WT), aniridia, genitourinary abnormalities and mental retardation form a symptom group (WAGR syndrome) associated with hemizygous deletions of DNA in chromosome band 11p13 (refs 1, 2). However, it has not been clear whether hemizygosity at a single locus contributes to more than one phenotype. The tumour suppressor gene for Wilms' tumour, WT1, has been characterized 3,4: it is expressed at high levels in the glomeruli of the kidney 5, as well as the gonadal ridge of the developing gonad 5, the Sertoli cells of the testis 6 and the epithelial and granulosa cells of the ovary 6, suggesting a developmental role in the genital system in addition to the kidney. We now report constitutional mutations within the WT1 genes of two individuals with a combination of WT and genital abnormalities as evidence of a role for a recessive oncogene in mammalian development. C1 MCGILL UNIV,CTR CANC,MONTREAL H3G 1Y6,QUEBEC,CANADA. NCI,DIV CANC ETIOL,CLIN EPIDEMIOL BRANCH,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. RP PELLETIER, J (reprint author), MIT,CTR CANC RES,CAMBRIDGE,MA 02139, USA. NR 16 TC 368 Z9 371 U1 1 U2 3 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 3 PY 1991 VL 353 IS 6343 BP 431 EP 434 DI 10.1038/353431a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GH606 UT WOS:A1991GH60600057 PM 1654525 ER PT J AU PODOLSKY, DK AF PODOLSKY, DK TI INFLAMMATORY BOWEL-DISEASE .2. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID DISTAL ULCERATIVE-COLITIS; 5-AMINOSALICYLIC ACID ENEMAS; COOPERATIVE CROHN DISEASE; TOTAL PARENTERAL-NUTRITION; POUCH-ANAL ANASTOMOSIS; LONG-TERM; DOUBLE-BLIND; COLORECTAL-CANCER; CONTROLLED TRIAL; ELEMENTAL DIET C1 MASSACHUSETTS GEN HOSP,CTR STUDY INFLAMMATORY BOWEL DIS,BOSTON,MA 02114. RP PODOLSKY, DK (reprint author), MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK34422, P30 DK43351] NR 139 TC 246 Z9 246 U1 2 U2 6 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 OCT 3 PY 1991 VL 325 IS 14 BP 1008 EP 1016 DI 10.1056/NEJM199110033251406 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA GH447 UT WOS:A1991GH44700006 PM 1886623 ER PT J AU BLOCH, KJ AF BLOCH, KJ TI EXCEPTIONALLY HIGH SERUM IGM LEVELS - (CASE 18-1991) - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP BLOCH, KJ (reprint author), MASSACHUSETTS GEN HOSP,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 OCT 3 PY 1991 VL 325 IS 14 BP 1047 EP 1047 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA GH447 UT WOS:A1991GH44700030 ER PT J AU HELLER, HM FUHRER, J AF HELLER, HM FUHRER, J TI DISSEMINATED SPOROTRICHOSIS IN PATIENTS WITH AIDS - CASE-REPORT AND REVIEW OF THE LITERATURE SO AIDS LA English DT Review DE SPOROTRICHOSIS; FUNGEMIA; HIV-1 ID ACQUIRED IMMUNODEFICIENCY SYNDROME; CUTANEOUS SPOROTRICHOSIS; SPOROTHRIX-SCHENCKII; ITRACONAZOLE; FUNGEMIA AB Sporotrichosis is the disease caused by the dimorphic fungus Sporothrix schenkii. Disseminated sporotrichosis is an uncommon infection which usually occurs in alcoholics or patients receiving immunosuppressive medication. We report a case of a patient with AIDS who had disseminated sporotrichosis which was progressive and fatal despite antifungal therapy. Four previously reported cases of disseminated sporotrichosis in patients with AIDS are reviewed. Disseminated sporotrichosis occurs in patients with HIV-1 infection and severe CD4 lymphocyte depletion. It usually presents with diffuse cutaneous lesions and is associated with polyarticular arthritis. Response to treatment is variable and chronic suppressive therapy is probably needed to prevent relapse. C1 SUNY STONY BROOK,DEPT MED,DIV INFECT DIS,STONY BROOK,NY 11794. RP HELLER, HM (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 13 TC 58 Z9 60 U1 0 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD OCT PY 1991 VL 5 IS 10 BP 1243 EP 1246 DI 10.1097/00002030-199110000-00014 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA GM224 UT WOS:A1991GM22400014 PM 1664732 ER PT J AU YAN, X LASKER, JM ROSMAN, AS LIEBER, CS AF YAN, X LASKER, JM ROSMAN, AS LIEBER, CS TI ISOELECTRIC-FOCUSING WESTERN BLOTTING - A NOVEL AND PRACTICAL METHOD FOR QUANTITATION OF CARBOHYDRATE-DEFICIENT TRANSFERRIN IN ALCOHOLICS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Note DE CARBOHYDRATE-DEFICIENT TRANSFERRIN (CDT); ISOELECTRIC FOCUSING; WESTERN BLOTTING; ALCOHOLISM; MARKERS ID SERUM TRANSFERRIN; LIVER; ABUSE; CONSUMPTION; MARKERS; DISEASE; VARIANT; FORMS AB Carbohydrate-deficient transferrin (CDT) has been described as the single, most accurate marker of chronic alcohol consumption. Rapid, sensitive, and specific measurement of serum CDT levels can thus provide important clinical information concerning patient diagnosis and treatment. To date, however, methods used for assessing CDT concentrations [e.g., analytical isoelectric focusing combined with immunofixation and micro anion-exchange chromatography followed by radioimmunoassay (RIA)] have not been practical enough for widespread laboratory application. In the present study, we examined the use of a different technique, namely isoelectric focusing (IEF) combined with Western blotting (IEF/WB). Serum proteins (20-40-mu-g) were first focused according to isoelectric points (pI) on high-resolution agarose IEF gels (ampholyte pH range of 5-8) containing nonionic detergent. The focused proteins were transferred electrophoretically to nitrocellulose filters, and then stained immunochemically with antihuman transferrin IgG. IEF/WB completely resolved CDT (focusing at pI 5.7 and 5.9) from other serum transferring isoforms, as assessed with neuraminidase-generated CDT standards. Computerized densitometric scanning of the immunoblots allowed CDT levels to be quantitated directly rather than as a quotient. Serum CDT content determined by IEF/WB was highly correlated (r2 = 0.962; n = 17) with values determined previously by RIA. In a larger subject group, CDT levels (mg/liter) measured by IEF/WB were 139 +/- 54 in recently-drinking alcoholics (n = 58), 81 +/- 8 in abstaining alcoholics (n = 7), and 68 +/- 16 in healthy control subjects (n = 16). These IEF/WB values for serum CDT are highly similar to those reported using other quantitation methods. Importantly, CDT levels as measured by IEF/WB were not influenced by the severity of liver disease among the recently-drinking alcoholics nor did nondrinkers with liver disease exhibit elevated IEF/WB CDT values. Serum CDT/total transferrin ratios (the latter measured by ELISA) offered no advantage over serum CDT alone to distinguish active and heavy drinking. In conclusion, we have developed a sensitive, accurate, and most importantly, practical method for quantitation of serum CDT, a highly-reliable marker of chronic alcohol consumption. Routine implementation of this technique by clinical laboratories can rapidly provide the physician with a powerful diagnostic tool. C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,130 W KINGSBRIDGE RD,BRONX,NY 10468. MT SINAI MED SCH,NEW YORK,NY 10468. NR 28 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD OCT PY 1991 VL 15 IS 5 BP 814 EP 821 PG 8 WC Substance Abuse SC Substance Abuse GA GL409 UT WOS:A1991GL40900014 ER PT J AU KINNEY, TB DELUCA, SA AF KINNEY, TB DELUCA, SA TI PARATHYROID HYPERPLASIA AS A CAUSE OF RECURRENT HYPERPARATHYROIDISM SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Parathyroid hyperplasia is second only to adenoma as the most common cause of hyperparathyroidism. Symptoms are most likely to result from elevated serum calcium levels. Symptoms include nephrocalcinosis and nephrolithiasis. Studies that may help confirm a suspected diagnosis include ultrasonography, computed tomography, radionuclide scanning with thallium and/or technetium, and magnetic resonance imaging. Surgical treatment consists of excision of all but part of one parathyroid gland if all of the glands are enlarged. RP KINNEY, TB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD OCT PY 1991 VL 44 IS 4 BP 1253 EP 1259 PG 7 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA GJ517 UT WOS:A1991GJ51700017 PM 1927840 ER PT J AU GRIFFIN, BP FLACHSKAMPF, FA SIU, S WEYMAN, AE THOMAS, JD AF GRIFFIN, BP FLACHSKAMPF, FA SIU, S WEYMAN, AE THOMAS, JD TI THE EFFECTS OF REGURGITANT ORIFICE SIZE, CHAMBER COMPLIANCE, AND SYSTEMIC VASCULAR-RESISTANCE ON AORTIC REGURGITANT VELOCITY SLOPE AND PRESSURE HALF-TIME SO AMERICAN HEART JOURNAL LA English DT Article ID WAVE DOPPLER ECHOCARDIOGRAPHY; IMPROVED CARDIAC-PERFORMANCE; HEMODYNAMIC CONSEQUENCES; AFTERLOAD REDUCTION; INSUFFICIENCY; THERAPY AB The determinants of the aortic regurgitant velocity profile have been investigated using computer and in vitro simulations in which regurgitant orifice area, ventricular and aortic compliance, and systemic vascular resistance could be independently varied. In the study, regurgitant fraction was altered, either by changing the size of the regurgitant orifice or by holding the regurgitant orifice constant and changing chamber compliance or systemic vascular resistance. Upon increasing regurgitant fraction by increasing the size of the regurgitant orifice, the slope got steeper and the pressure half-time shortened, the response anticipated in current clinical practice. However, when the regurgitant orifice was kept constant and regurgitation fraction was increased by increasing the systemic vascular resistance or by increasing the compliance of the left ventricle, slope became less steep and pressure half-time lengthened. Multivariate analysis was used to quantity the relationship of regurgitant fraction to slope and pressure half-time. When orifice area was allowed to vary, slope was related directly (multiple r = 0.78, p < 0.001) and half-time was related inversely (multiple r = 0.66, p < 0.001) to regurgitant fraction. With the orifice area fixed, however, directionally opposite responses were seen; slope varied inversely (multiple r = 0.87, p < 0.001), whereas half-time varied directly (multiple r = 0.88, p < 0.001) with regurgitant fraction. This study suggests that the utility of the slope and pressure half-time of the regurgitant velocity tracing in clinical practice relates to their ability to discriminate regurgitant orifices of differing sizes. However, these findings also suggest caution in the conventional interpretation of these indices in individual patients in whom changes in regurgitant fraction are produced by pharmacologic manipulation of the systemic vascular resistance. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NONINVAS CARDIAC LAB,ZERO EMERSON PL,SUITE 2F,BOSTON,MA 02114. NR 19 TC 22 Z9 22 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD OCT PY 1991 VL 122 IS 4 BP 1049 EP 1056 DI 10.1016/0002-8703(91)90471-S PN 1 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GJ122 UT WOS:A1991GJ12200017 PM 1927856 ER PT J AU WOLOSCHUK, DMM WERMELING, JR PRUEMER, JM AF WOLOSCHUK, DMM WERMELING, JR PRUEMER, JM TI STABILITY AND COMPATIBILITY OF FLUOROURACIL AND MANNITOL DURING SIMULATED Y-SITE ADMINISTRATION SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article DE ADDITIVES; ANTINEOPLASTIC AGENTS; CONCENTRATION; DEXTROSE; DIURETICS; FLUOROURACIL; INCOMPATIBILITIES; INJECTIONS; MANNITOL; SODIUM CHLORIDE; STABILITY; VEHICLES ID CISPLATIN; CHEMOTHERAPY; ADMIXTURES; RECURRENT; INFUSION; CANCER; HEAD; NECK AB The stability and compatibility of fluorouracil admixtures with mannitol during simulated Y-site administration was studied. Fluorouracil injection 50 mg/mL was diluted with 5% dextrose injection, 0.9% sodium chloride injection, and 5% dextrose and 0.45% sodium chloride injection to final concentrations of 1 and 2 mg/mL. Combinations of fluorouracil admixtures with 20% mannitol injection were made using equal volumes in glass test tubes; immediately after mixing and at one, two, and four hours, the samples were examined for visual incompatibilities. Duplicate combinations of fluorouracil admixtures with 20% mannitol injection were made using equal volumes in plastic syringes; immediately after mixing with internal standard in glass test tubes and at 2, 4, 8, and 24 hours, samples were removed for chemical analysis. A high-performance liquid chromatographic assay was used to determine fluorouracil concentrations. No evidence of precipitation, color change, or haze was observed. During the 24-hour study, fluorouracil concentrations remained within 6% of initial concentrations for all combinations with mannitol. Fluorouracil 1 and 2 mg/mL in 5% dextrose injection, 0.9% sodium chloride injection, and 5% dextrose and 0.45% sodium chloride injection was chemically stable and visually compatible when combined with 20% mannitol injection during simulated Y-site administration. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL RES LAB,MADISON,WI 53705. UNIV CINCINNATI HOSP,CINCINNATI,OH. RP WOLOSCHUK, DMM (reprint author), HLTH SCI CTR,DEPT PHARMACEUT SERV,ROOM MS-189,820 SHERBROOK ST,WINNIPEG R3A 1RD,MANITOBA,CANADA. NR 8 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD OCT PY 1991 VL 48 IS 10 BP 2158 EP 2160 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GH077 UT WOS:A1991GH07700021 PM 1781472 ER PT J AU BERSON, EL ROSNER, B SANDBERG, MA WEIGEL, C DIFRANCO DRYIA, TP AF BERSON, EL ROSNER, B SANDBERG, MA WEIGEL, C DIFRANCO DRYIA, TP TI CLINICAL FINDINGS IN PATIENTS WITH DOMINANT RETINITIS-PIGMENTOSA AND MUTATIONS OF THE RHODOPSIN GENE SO AMERICAN JOURNAL OF HUMAN GENETICS 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 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 2 EP 2 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900008 ER PT J AU DRYJA, TP HAHN, LB MCGEE, TL COWLEY, GS BERSON, EL AF DRYJA, TP HAHN, LB MCGEE, TL COWLEY, GS BERSON, EL TI MUTATION SPECTRUM OF THE RHODOPSIN GENE AMONG PATIENTS WITH AUTOSOMAL DOMINANT RETINITIS-PIGMENTOSA SO AMERICAN JOURNAL OF HUMAN GENETICS 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 UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 2 EP 2 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900009 ER PT J AU TAGLE, DA BLACK, T VALDES, J RICHARDS, J MACDONALD, M BARNES, G GUSELLA, J COLLINS, FS AF TAGLE, DA BLACK, T VALDES, J RICHARDS, J MACDONALD, M BARNES, G GUSELLA, J COLLINS, FS TI IDENTIFICATION AND ANALYSIS OF POLYMORPHIC (CA)N DINUCLEOTIDE REPEATS IN THE HUNTINGTONS-DISEASE REGION (4P16.3) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV MICHIGAN,MED CTR,ANN ARBOR,MI 48109. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 17 EP 17 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900079 ER PT J AU BATES, GP MACDONALD, ME MONACO, AP BAXENDALE, S VALDES, J TAGLE, D LIN, C WHALEY, WL YOUNGMAN, S WASMUTH, JJ COLLINS, F GUSELLA, JF LEHRACH, H AF BATES, GP MACDONALD, ME MONACO, AP BAXENDALE, S VALDES, J TAGLE, D LIN, C WHALEY, WL YOUNGMAN, S WASMUTH, JJ COLLINS, F GUSELLA, JF LEHRACH, H TI DEFINITION OF THE PHYSICAL AND GENETIC LIMITS OF THE HUNTINGTONS-DISEASE GENE CANDIDATE REGION AND PROGRESS TOWARDS ITS ISOLATION AS A YAC CONTIG SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 IMPERIAL CANC RES FUND,GENOME ANAL LAB,LONDON WC2A 3PX,ENGLAND. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 21 EP 21 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900099 ER PT J AU BORRESEN, AL HOVIG, E ANDERSEN, TI SMITHSORENSEN, B MALKIN, D LYSTAD, S NESLAND, J FRIEND, S AF BORRESEN, AL HOVIG, E ANDERSEN, TI SMITHSORENSEN, B MALKIN, D LYSTAD, S NESLAND, J FRIEND, S TI ANALYSIS OF P53 TUMOR AND GERM LINE MUTATIONS IN HUMAN BREAST CARCINOMAS USING CONSTANT DENATURANT GEL-ELECTROPHORESIS, CDGE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NORWEGIAN RADIUM HOSP,NORSK HYDROS INST CANC RES,DEPT GENET,OSLO 3,NORWAY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114. RI Hovig, Eivind/H-2474-2011 OI Hovig, Eivind/0000-0002-9103-1077 NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 44 EP 44 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900217 ER PT J AU YANDELL, DW HERRERA, GE DAYTON, SH DRYJA, TP LUDEKE, BI AF YANDELL, DW HERRERA, GE DAYTON, SH DRYJA, TP LUDEKE, BI TI PENETRANCE OF RB GENE-MUTATIONS - 2 FAMILIES WITH A LOW-PENETRANCE FORM OF HEREDITARY RETINOBLASTOMA CARRY THE SAME MISSENSE MUTATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 45 EP 45 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900221 ER PT J AU LI, FP AF LI, FP TI LI-FRAUMENI SYNDROME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 55 EP 55 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900271 ER PT J AU SEIZINGER, BR AF SEIZINGER, BR TI TUMOR SUPPRESSOR GENES AND HEREDITARY TUMOR SYNDROMES IN THE HUMAN NERVOUS-SYSTEM - ISOLATING THE GENES FOR VONHIPPEL LINDAU DISEASE AND NF-2 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 62 EP 62 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900304 ER PT J AU BARTON, NW DOPPELT, SI MANKIN, HJ BRADY, RO AF BARTON, NW DOPPELT, SI MANKIN, HJ BRADY, RO TI REVERSAL OF THE CLINICAL MANIFESTATIONS OF GAUCHER DISEASE BY ENZYME REPLACEMENT THERAPY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 112 EP 112 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900551 ER PT J AU SHIH, VE MANDELL, R KRISHNAMOORTHY, KS AF SHIH, VE MANDELL, R KRISHNAMOORTHY, KS TI A TRIAL OF DIETOTHERAPY IN FUMARASE DEFICIENCY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 1 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 114 EP 114 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900559 ER PT J AU TOONE, J APPLEGARTH, D LEVY, H AF TOONE, J APPLEGARTH, D LEVY, H TI PRENATAL-DIAGNOSIS OF NONKETOTIC HYPERGLYCINEMIA (NKH) BY ASSAY OF CHORIONIC VILLUS (CVS) GLYCINE CLEAVAGE ENZYME (GCE) AND AMNIOTIC-FLUID GLYCINE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 BRITISH COLUMBIA CHILDRENS HOSP,VANCOUVER,BC,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 114 EP 114 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900562 ER PT J AU DEUTSCH, CK HRECZKO, T HOLMES, LB AF DEUTSCH, CK HRECZKO, T HOLMES, LB TI OBJECTIVE DIAGNOSIS OF DYSMORPHOLOGY - A CASE-STUDY OF JOHANSON-BLIZZARD SYNDROME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 ALBERTA CHILDRENS PROV GEN HOSP,CALGARY,ALBERTA,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,WALTHAM,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 141 EP 141 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900722 ER PT J AU STOLER, JM HOLMES, LB AF STOLER, JM HOLMES, LB TI CLINODACTYLY - AN OBJECTIVE ASSESSMENT SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,EMBRYOL TERATOL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 166 EP 166 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900871 ER PT J AU ALTHERR, MR JOHNSON, V MACDONALD, M PLUMMER, S GUSELLA, J WASMUTH, J AF ALTHERR, MR JOHNSON, V MACDONALD, M PLUMMER, S GUSELLA, J WASMUTH, J TI MOLECULAR-DETECTION OF 4P DELETIONS USING PCR-BASED POLYMORPHISMS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV CALIF IRVINE,IRVINE,CA 92717. UNIV S DAKOTA,SCH MED,VERMILLION,SD 57069. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 181 EP 181 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30900960 ER PT J AU GANDELMAN, K MEYN, S MACDONALD, M WHALEY, LW GUSELLA, J FENG, TY AF GANDELMAN, K MEYN, S MACDONALD, M WHALEY, LW GUSELLA, J FENG, TY TI CRITICAL REGION RESPONSIBLE FOR THE WOLF-HIRSCHHORN SYNDROME - 2MB DISTAL TO D4S43 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 YALE UNIV,NEW HAVEN,CT 06520. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 310 EP 310 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30901725 ER PT J AU BLUMENFELD, A TROFATTER, JA LUCENTE, DE AXELROD, FB MAAYAN, C HAINES, JL BREAKEFIELD, XO GUSELLA, JF AF BLUMENFELD, A TROFATTER, JA LUCENTE, DE AXELROD, FB MAAYAN, C HAINES, JL BREAKEFIELD, XO GUSELLA, JF TI ADVANCES IN LINKAGE ANALYSIS IN FAMILIAL DYSAUTONOMIA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NYU MED CTR,NEW YORK,NY 10016. HEBREW UNIV JERUSALEM,HADASSAH MED SCH,IL-91010 JERUSALEM,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 336 EP 336 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30901876 ER PT J AU GOTO, J FIGLEWICZ, DA LUTCHMAN, M BROWN, RH KRIZUS, A ROULEAU, GA AF GOTO, J FIGLEWICZ, DA LUTCHMAN, M BROWN, RH KRIZUS, A ROULEAU, GA TI LINKAGE MAPPING OF FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MCGILL UNIV,CTR RES NEUROSCI,MONTREAL H3A 2T5,QUEBEC,CANADA. MASSACHUSETTS GEN HOSP,DAY NEUROMUSCULAR LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 341 EP 341 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30901906 ER PT J AU HAINES, JL SHORT, MP KWIATKOWSKI, DJ ANDERMANN, E MICKLE, J GUSELLA, JF AMOS, JA AF HAINES, JL SHORT, MP KWIATKOWSKI, DJ ANDERMANN, E MICKLE, J GUSELLA, JF AMOS, JA TI HETEROGENEITY IN TUBEROUS SCLEROSIS - LOCALIZATION OF TSC1 WITHIN 9Q34, AND TESTS OF LINKAGE TO 11Q AND 14Q MARKERS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. MONTREAL NEUROL HOSP & INST,DEPT NEUROGENET,MONTREAL H3A 2B4,QUEBEC,CANADA. BOSTON UNIV,MED CTR,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 341 EP 341 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30901910 ER PT J AU PERICAKVANCE, MA HAINES, JL STGEORGEHYSLOP, PH BEBOUT, J HAYNES, C TANZI, R YAMAOKA, L GUSELLA, JF ROSES, AD AF PERICAKVANCE, MA HAINES, JL STGEORGEHYSLOP, PH BEBOUT, J HAYNES, C TANZI, R YAMAOKA, L GUSELLA, JF ROSES, AD TI JOINT LINKAGE ANALYSIS OF CHROMOSOME-19 AND CHROMOSOME-21 LOCI IN FAMILIAL ALZHEIMER-DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC 27710. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. UNIV TORONTO,TANZ NEUROSCI INST,TORONTO M5S 1A1,ONTARIO,CANADA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 355 EP 355 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30901989 ER PT J AU ROULEAU, GA NAROD, SA FAUCHER, MC HAINES, JA GUSELLA, JF AF ROULEAU, GA NAROD, SA FAUCHER, MC HAINES, JA GUSELLA, JF TI THERE IS NO NON-ALLELIC GENETIC-HETEROGENEITY IN NEUROFIBROMATOSIS TYPE-2 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MCGILL UNIV,CTR RES NEUROSCI,MONTREAL H3A 2T5,QUEBEC,CANADA. MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 357 EP 357 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902006 ER PT J AU TROFATTER, JA ROULEAU, G GUSELLA, JF HAINES, JL AF TROFATTER, JA ROULEAU, G GUSELLA, JF HAINES, JL TI GENETIC-MAPPING OF A DINUCLEOTIDE REPEAT AT THE CYTOCHROME-P-450 DEBRISOQUINE LOCUS (CYP2DP8) ON CHROMOSOME-22 WITH FURTHER APPLICATION TO RAPID POLYMORPHISM IDENTIFICATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. MONTREAL GEN HOSP,DEPT NEUROL,MONTREAL H3G 1A4,QUEBEC,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 362 EP 362 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902034 ER PT J AU HENSKE, EP OZELIUS, L KWIATKOWSKI, DJ AF HENSKE, EP OZELIUS, L KWIATKOWSKI, DJ TI CONSTRUCTION OF A RADIATION HYBRID CONTAINING 20 CM OF HUMAN DNA SURROUNDING THE ASS LOCUS ON 9Q 32-34 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASS GEN HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 379 EP 379 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902136 ER PT J AU LERNER, TJ ROMANO, D MCCOLLIN, M MENON, A ROULEAU, G TANZI, RE DENNY, CT GUSELLA, J AF LERNER, TJ ROMANO, D MCCOLLIN, M MENON, A ROULEAU, G TANZI, RE DENNY, CT GUSELLA, J TI PHYSICAL MAPPING OF HUMAN CHROMOSOME-22 USING YEAST ARTIFICIAL CHROMOSOMES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. MCGILL UNIV,CTR RES NEUROSCI,MONTREAL H3A 2T5,QUEBEC,CANADA. UNIV CALIF LOS ANGELES,MED CTR,DEPT PEDIAT,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 383 EP 383 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902159 ER PT J AU MENON, AG SNYDER, HL MURDOCK, C TROFATTER, JA MACCOLLIN, M LERNER, T HAINES, J EMANUEL, B ROULEAU, G GUSELLA, JF AF MENON, AG SNYDER, HL MURDOCK, C TROFATTER, JA MACCOLLIN, M LERNER, T HAINES, J EMANUEL, B ROULEAU, G GUSELLA, JF TI PHYSICAL MAPPING OF THE NEUROFIBROMATOSIS TYPE-2 (NF-2) LOCUS ON CHROMOSOME-22 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MONTREAL GEN HOSP,MONTREAL H3G 1A4,QUEBEC,CANADA. NR 0 TC 1 Z9 1 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 384 EP 384 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902163 ER PT J AU REICHEL, E NAVIA, B BERSON, EL BRUNS, G AF REICHEL, E NAVIA, B BERSON, EL BRUNS, G TI PROXIMAL XP LOCI - LONG-RANGE RESTRICTION MAPS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BERMAN GUND LAB,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DIV GENET,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 385 EP 385 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902168 ER PT J AU TANZI, RE ROMANO, D PATTERSON, D GUSELLA, JF AF TANZI, RE ROMANO, D PATTERSON, D GUSELLA, JF TI GENERATION OF CHROMOSOME-21-SPECIFIC STSS FOR PHYSICAL MAPPING USING YEAST ARTIFICIAL CHROMOSOMES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 ELEANOR ROOSEVELT INST CANC RES,DENVER,CO. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 388 EP 388 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902185 ER PT J AU SIMS, K BENSON, G HOTAMISLIGIL, G GIRMEN, S LEBO, R GOLBUS, M SAHA, BK ANTONARAKIS, S DELACHAPELLE, A ROPERS, HH BREAKEFIELD, XO AF SIMS, K BENSON, G HOTAMISLIGIL, G GIRMEN, S LEBO, R GOLBUS, M SAHA, BK ANTONARAKIS, S DELACHAPELLE, A ROPERS, HH BREAKEFIELD, XO TI FURTHER GENETIC AND PHYSICAL MAPPING OF THE NORRIE DISEASE LOCUS ON XP11.3 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. UNIV HELSINKI,SF-00100 HELSINKI 10,FINLAND. CATHOLIC UNIV NIJMEGEN,NIJMEGEN,NETHERLANDS. NR 0 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 389 EP 389 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902194 ER PT J AU VALDES, J TAGLE, D BATES, G ALTHERR, M MACDONNALD, M BROWNSTEIN, B GUSELLA, J WASMUTH, J LEHRACH, H COLLINS, F AF VALDES, J TAGLE, D BATES, G ALTHERR, M MACDONNALD, M BROWNSTEIN, B GUSELLA, J WASMUTH, J LEHRACH, H COLLINS, F TI CONTINUING CHARACTERIZATION OF THE HUNTINGTON DISEASE REGION WITH YEAST ARTIFICIAL CHROMOSOMES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. IMPERIAL CANC RES FUND,GENOME ANAL LAB,LONDON WC2A 3PX,ENGLAND. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. MASSACHUSSETTS GEN HOSP,CHARLESTON,MA. WASHINGTON UNIV,ST LOUIS,MO 63130. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 390 EP 390 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902201 ER PT J AU WASMUTH, JJ GUSELLA, JF ALTHERR, MR PLUMMER, S TAYLOR, S MACDONALD, M COLLINS, FS TAGLE, D AF WASMUTH, JJ GUSELLA, JF ALTHERR, MR PLUMMER, S TAYLOR, S MACDONALD, M COLLINS, FS TAGLE, D TI DNA MARKER STUDIES OF POSSIBLE GENE CONVERSION EVENTS INVOLVING THE HUNTINGTON DISEASE REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV CALIF IRVINE,IRVINE,CA 92717. MASSACHUSSETTS GEN HOSP,CTR NEUROSCI,BOSTON,MA. HOWARD HUGHES INST,ANN ARBOR,MI. UNIV MICHIGAN,SCH MED,ANN ARBOR,MI 48104. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 391 EP 391 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902207 ER PT J AU GU, Z RAMESH, V KOZICH, V KORSON, MS KRAUS, JP SHIH, VE AF GU, Z RAMESH, V KOZICH, V KORSON, MS KRAUS, JP SHIH, VE TI IDENTIFICATION OF A MOLECULAR GENETIC-DEFECT IN HOMOCYSTINURIA DUE TO CYSTATHIONINE BETA-SYNTHASE DEFICIENCY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,AMINO ACID DISORDER LAB,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 406 EP 406 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902296 ER PT J AU HOTAMISLIGIL, GS GIRMEN, AS KONRADI, C FINK, S BAENZIGER, J SULLIVAN, J GROWDON, J BREAKEFIELD, XO AF HOTAMISLIGIL, GS GIRMEN, AS KONRADI, C FINK, S BAENZIGER, J SULLIVAN, J GROWDON, J BREAKEFIELD, XO TI ALLELIC VARIATIONS IN MAO GENES MARK ACTIVITY STATES AND MAY PREDICT VULNERABILITY TO PARKINSON DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. INDIANA UNIV,MED CTR,DEPT PSYCHIAT,ALCOHOL RES CTR,INDIANAPOLIS,IN 46204. INDIANA UNIV,MED CTR,DEPT PATHOL,ALCOHOL RES CTR,INDIANAPOLIS,IN 46204. NR 0 TC 0 Z9 0 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 407 EP 407 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902298 ER PT J AU MACDONALD, ME LIN, C BATES, GP ALTHERR, M WASMUTH, J LEHRACH, H GUSELLA, JF AF MACDONALD, ME LIN, C BATES, GP ALTHERR, M WASMUTH, J LEHRACH, H GUSELLA, JF TI COMPLEX PATTERNS OF LINKAGE DISEQUILIBRIUM IN THE HUNTINGTON DISEASE REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92719. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 412 EP 412 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902332 ER PT J AU MYERS, RH TAYLOR, SAM BATES, GP MACDONALD, ME GASTON, SM WHALEY, WL WASMUTH, J LEHRACH, H GUSELLA, JF AF MYERS, RH TAYLOR, SAM BATES, GP MACDONALD, ME GASTON, SM WHALEY, WL WASMUTH, J LEHRACH, H GUSELLA, JF TI ABSENCE OF LARGE DELETIONS OR INSERTIONS IN THE HUNTINGTON DISEASE GENE CANDIDATE REGION AMONG NEW MUTANTS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. HARVARD UNIV,MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 414 EP 414 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902344 ER PT J AU OZELIUS, L KRAMER, P DELEON, D BRESSMAN, S RISCH, N SCHUBACK, D BRIN, M KWIATKOWSKI, D BURKE, R GUSELLA, JF FAHN, S BREAKEFIELD, XO AF OZELIUS, L KRAMER, P DELEON, D BRESSMAN, S RISCH, N SCHUBACK, D BRIN, M KWIATKOWSKI, D BURKE, R GUSELLA, JF FAHN, S BREAKEFIELD, XO TI STRONG ALLELE ASSOCIATION BETWEEN THE TORSION DYSTONIA GENE AND LOCI ON CHROMOSOME 9Q34 IN ASHKENAZIC JEWS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. COLUMBIA PRESBYTERIAN MED CTR,NEW YORK,NY 10032. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. NR 0 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 415 EP 415 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902347 ER PT J AU TANZI, RE ROMANO, D MCCLATCHEY, A HAINES, JL GUSELLA, JF STGEORGEHYSLOP, PH AF TANZI, RE ROMANO, D MCCLATCHEY, A HAINES, JL GUSELLA, JF STGEORGEHYSLOP, PH TI ANALYSIS OF THE APP GENE IN FAMILIAL ALZHEIMERS-DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. UNIV TORONTO,TANZ NEUROSCI INST,TORONTO M5S 1A1,ONTARIO,CANADA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 420 EP 420 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902376 ER PT J AU TAYLOR, SAM BUCKLER, A MACDONALD, ME BATES, G LEHRACH, H LIN, C HOUSMAN, D GUSELLA, JF AF TAYLOR, SAM BUCKLER, A MACDONALD, ME BATES, G LEHRACH, H LIN, C HOUSMAN, D GUSELLA, JF TI THE ISOLATION OF A CDNA FROM THE HUNTINGTONS-DISEASE CANDIDATE REGION BY EXON AMPLIFICATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 420 EP 420 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902377 ER PT J AU WANG, JZ ROJAS, CV BROWN, R HOFFMAN, EP AF WANG, JZ ROJAS, CV BROWN, R HOFFMAN, EP TI MOLECULAR ANALYSIS OF DOMINANT PERIODIC PARALYSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PITTSBURGH,SCH MED,DEPT MOLEC GENET & BIOCHEM,PITTSBURGH,PA 15261. MASSACHUSETTS GEN HOSP,CTR DAY NEUROMUSCULAR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 422 EP 422 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902391 ER PT J AU LUDEKE, BI BEAUCHAMP, RL YANDELL, DW AF LUDEKE, BI BEAUCHAMP, RL YANDELL, DW TI POINT MUTATION SPECTRUM IN 2 SIMILAR TUMOR SUPPRESSOR GENES - CHARACTERIZATION OF 122 NATURALLY-OCCURRING SOMATIC AND GERMINAL MUTATIONS IN THE RB AND P53 GENES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 449 EP 449 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902548 ER PT J AU DAYTON, SH BRACHMAN, D ZHANG, DS SHIPLEY, WU WEICHSELBAUM, RR YANDELL, DW AF DAYTON, SH BRACHMAN, D ZHANG, DS SHIPLEY, WU WEICHSELBAUM, RR YANDELL, DW TI POINT MUTATIONS OF THE P53 GENE IN HUMAN TRANSITIONAL CELL-CARCINOMA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV CHICAGO,CHICAGO,IL 60637. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 453 EP 453 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902574 ER PT J AU TOGUCHIDA, J YAMAGUCHI, T HERRERA, G BEAUCHAMP, R YANDELL, DW AF TOGUCHIDA, J YAMAGUCHI, T HERRERA, G BEAUCHAMP, R YANDELL, DW TI A SURVEY OF GERM-LINE AND SOMATIC P53 GENE-MUTATIONS IN PATIENTS WITH BONE AND SOFT-TISSUE SARCOMAS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. KYOTO UNIV,KYOTO 606,JAPAN. NR 0 TC 4 Z9 4 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 458 EP 458 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902603 ER PT J AU HERRON, BJ ODONNELL, JJ SHIH, VE GUSELLA, JF RAMESH, V AF HERRON, BJ ODONNELL, JJ SHIH, VE GUSELLA, JF RAMESH, V TI AG TO GG TRANSITION AT A SPLICE ACCEPTOR OF ORNITHINE AMINOTRANSFERASE GENE RESULTS IN AN EXON DELETION IN GYRATE ATROPHY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,DEPT OPHTHALMOL,SAN FRANCISCO,CA 94143. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 SU S BP 491 EP 491 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA GR309 UT WOS:A1991GR30902797 ER PT J AU MACDONALD, ME LIN, C SRINIDHI, L BATES, G ALTHERR, M WHALEY, WL LEHRACH, H WASMUTH, J GUSELLA, JF AF MACDONALD, ME LIN, C SRINIDHI, L BATES, G ALTHERR, M WHALEY, WL LEHRACH, H WASMUTH, J GUSELLA, JF TI COMPLEX PATTERNS OF LINKAGE DISEQUILIBRIUM IN THE HUNTINGTON DISEASE REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID NON-RANDOM ASSOCIATION; DNA MARKERS; GENE; LOCALIZATION; CHROMOSOME-4; TELOMERE; LOCUS; MUTATION; SEGMENT; D4S95 AB The genetic defect causing Huntington disease (HD) has been mapped to 4p16.3 by linkage analysis using DNA markers. Two apparently contradictory classes of recombination events in HD kindreds preclude precise targeting of efforts to clone the disease gene. Here, we report a new recombination event that increases support for an internal candidate region of 2.5 Mb between D4S10 and D4S168. Analysis of 23 DNA polymorphisms in 4p16.3 revealed a complex pattern of association with the disease gene that failed to narrow the size of the candidate region. The degree of linkage disequilibrium did not show a continuous increase across the physical map, nor was a region of extreme disequilibrium identified. Markers displaying no association with the disorder were interspersed with and, in many cases, close to markers displaying significant disequilibrium. Comparison of closely spaced marker pairs on normal and HD chromosomes, as well as analysis of haplotypes across the HD region, suggest that simple recombination subsequent to a single original HD mutation cannot easily explain the pool of HD chromosomes seen today. A number of different mechanisms could contribute to the diversity of haplotypes observed on HD chromosomes, but it is likely that there has been more than one and possibly several independent origins of the HD mutation. C1 MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. RI Bates, Gillian/E-1146-2012 OI Bates, Gillian/0000-0002-4041-6305 FU NHGRI NIH HHS [HG00169]; NINDS NIH HHS [NS22031, NS16367] NR 33 TC 78 Z9 79 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 BP 723 EP 734 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA GG665 UT WOS:A1991GG66500004 PM 1680285 ER PT J AU HAINES, JL SHORT, MP KWIATKOWSKI, DJ JEWELL, A ANDERMANN, E BEJJANI, B YANG, CH GUSELLA, JF AMOS, JA AF HAINES, JL SHORT, MP KWIATKOWSKI, DJ JEWELL, A ANDERMANN, E BEJJANI, B YANG, CH GUSELLA, JF AMOS, JA TI LOCALIZATION OF ONE GENE FOR TUBEROUS SCLEROSIS WITHIN 9Q32-9Q34, AND FURTHER EVIDENCE FOR HETEROGENEITY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID LINKAGE; LOCUS AB Tuberous sclerosis (TSC) is an autosomal dominant disorder with both neurological and cutaneous manifestations often resulting in significant disability. Although it has been studied clinically and biochemically for many years, the underlying pathophysiology remains unknown. Genetic linkage analysis provides an alternative strategy for understanding the genetic etiology of this disease. Genetic linkage of a gene for TSC to loci in 9q32-9q34 has been reported but has not been a universal finding, since absence of linkage to 9q loci, as well as linkage to loci on 11q, have also been reported. We present here data on 22 families (21 previously unreported) segregating TSC. Our results strongly support a TSC locus in the 9q32-34 region for approximately one-third of families and provide significant evidence for genetic heterogeneity. Application of newly described highly polymorphic dinucleotide repeat marker loci in TSC greatly enhanced the informativeness of our pedigrees and was vital for detecting the heterogeneity. No clear evidence of linkage to chromosome 11q22 markers was found, suggesting that a still unidentified TSC locus elsewhere in the genome may account for the majority of TSC families. C1 MASSACHUSETTS GEN HOSP, HEMATOL ONCOL UNIT, BOSTON, MA 02114 USA. BOSTON UNIV, MED CTR, CTR HUMAN GENET, BOSTON, MA 02215 USA. MONTREAL NEUROL HOSP & INST, DEPT NEUROGENET, MONTREAL H3A 2B4, QUEBEC, CANADA. RP HAINES, JL (reprint author), MASSACHUSETTS GEN HOSP, MOLEC NEUROGENET LAB, BLDG 149, 6TH FLOOR, 13TH ST, BOSTON, MA 02129 USA. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00324]; NINDS NIH HHS [NS24279] NR 28 TC 70 Z9 70 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 EI 1537-6605 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1991 VL 49 IS 4 BP 764 EP 772 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA GG665 UT WOS:A1991GG66500008 PM 1897523 ER PT J AU DEGROOTKOSOLCHAROEN, J AF DEGROOTKOSOLCHAROEN, J TI PANDEMONIUM OVER GLOVES - USE AND ABUSE SO AMERICAN JOURNAL OF INFECTION CONTROL LA English DT Article RP DEGROOTKOSOLCHAROEN, J (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0196-6553 J9 AM J INFECT CONTROL JI Am. J. Infect. Control PD OCT PY 1991 VL 19 IS 5 BP 225 EP 227 DI 10.1016/S0196-6553(05)80252-4 PG 3 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA GK193 UT WOS:A1991GK19300002 PM 1755546 ER PT J AU KLIBANOV, AL KHAW, BA NOSSIFF, N ODONNELL, SM HUANG, L SLINKIN, MA TORCHILIN, VP AF KLIBANOV, AL KHAW, BA NOSSIFF, N ODONNELL, SM HUANG, L SLINKIN, MA TORCHILIN, VP TI TARGETING OF MACROMOLECULAR CARRIERS AND LIPOSOMES BY ANTIBODIES TO MYOSIN HEAVY-CHAIN SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article; Proceedings Paper CT US-USSR JOINT SYMP ON CARDIOVASCULAR AND PULMONARY BIOLOGY AND MEDICINE CY SEP 18-20, 1990 CL SUZDAL, USSR DE ANTIMYOSIN; CHELATING POLYMER; LIPOSOME; MONOCLONAL ANTIBODY; MYOCARDIAL INFARCTION; RADIOIMMUNOIMAGING ID CIRCULATION TIME; IMMUNOLIPOSOMES; TUMORS AB Macromolecular carriers and liposomes were covalently coupled to monoclonal antibodies against cardiac myosin heavy chain. Deferoxamine-modified polymers bound tightly with Ga-67 and Ga-68 radioisotopes. Ternary deferoxamine-polylysine antibody conjugates specifically targeted the radioisotopes to a myosin-coated microplate. Scatchard analysis revealed a high affinity of the conjugate for the target with a K(as) of approximately 10(8) M-1. Liposomes that contained immobilized antimyosin antibodies were targeted specifically to the myosin-coated plate. Additional coating of these liposomes with polyethylene glycol reduced specific binding to the target in vitro. However, because of the presence of polyethylene glycol on the surface of liposomes, these liposomes had a long half-life and slowly cleared from the blood-stream after intravenous injection. These immunoliposomes showed up to 16- to 18-fold specific localization to the necrotic areas of the myocardium in rabbits with experimental infarction. C1 UNIV TENNESSEE,DEPT BIOCHEM,KNOXVILLE,TN 37996. MASSACHUSETTS GEN HOSP,DIV NUCL MED,BOSTON,MA 02114. RP KLIBANOV, AL (reprint author), MOSCOW EXPTL CARDIOL INST,MOSCOW 121552,USSR. NR 17 TC 11 Z9 11 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 OCT PY 1991 VL 261 IS 4 SU S BP 60 EP 65 PG 6 WC Physiology SC Physiology GA GL126 UT WOS:A1991GL12600012 PM 1928455 ER PT J AU TEDDER, TF AF TEDDER, TF TI CELL-SURFACE RECEPTOR SHEDDING - A MEANS OF REGULATING FUNCTION SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP TEDDER, TF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 9 TC 48 Z9 48 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD OCT PY 1991 VL 5 IS 4 BP 305 EP 306 PG 2 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA GJ514 UT WOS:A1991GJ51400001 PM 1654954 ER PT J AU YODER, IC HALL, DA AF YODER, IC HALL, DA TI HYSTEROSALPINGOGRAPHY IN THE 1990S SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Review ID FALLOPIAN-TUBE OBSTRUCTION; MULLERIAN DUCT ANOMALIES; SOLUBLE CONTRAST-MEDIA; UTERINE LEIOMYOMAS; DIFFERENTIAL-DIAGNOSIS; BALLOON TUBOPLASTY; MR; SONOGRAPHY; UTERUS; ABNORMALITIES AB All physicians involved in the evaluation and treatment of infertility rely heavily on the information provided by hysterosalpingography. For many years this study has provided images of the lumina of the fallopian tubes that are not available by other diagnostic means, and it also gives the most accurate outline of the uterine cavity. Hysterosalpingography will therefore continue to be a valuable study in the upcoming decade, and it is important now to take account of the many advances in technology that impinge on the execution and interpretation of this study. In this article we first update the continuing debate about elements of the study itself, involving techniques and the choice of contrast material. We also consider surgical advances. such as the widespread use of microsurgical reconstruction of the fallopian tube, that increase the demand for hysterosalpingography. Since radiologists are asked to evaluate the results of surgery. it is essential for them to be familiar with the postoperative appearances of the fallopian tube. Finally. we consider what must be by far the most important development of the 1990s, the continuing integration of hysterosalpingography with new interventional and imaging techniques. Fallopian tube catheterization expands the examination of the fallopian tube and offers new therapeutic applications. Transvaginal sonography and MR imaging have allowed noninvasive exploration of the female pelvis. Correlation of hysterosalpingography and MR imaging is particularly useful in the diagnosis of uterine myomas and congenital uterine duplication anomalies when surgery to preserve or enhance the reproductive capacity of the uterus is indicated. Sonography and MR imaging should be correlated with hysterosalpingography to provide a more efficient diagnostic and therapeutic approach to the common mechanical causes of infertility. RP YODER, IC (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 70 TC 29 Z9 31 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 OCT PY 1991 VL 157 IS 4 BP 675 EP 683 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GF743 UT WOS:A1991GF74300001 PM 1892018 ER PT J AU GOLDBERG, MA SAINI, S HAHN, PF EGGLIN, TK MUELLER, PR AF GOLDBERG, MA SAINI, S HAHN, PF EGGLIN, TK MUELLER, PR TI DIFFERENTIATION BETWEEN HEMANGIOMAS AND METASTASES OF THE LIVER WITH ULTRAFAST MR IMAGING - PRELIMINARY-RESULTS WITH T2 CALCULATIONS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID CAVERNOUS HEMANGIOMA; MAGNETIC-RESONANCE; HEPATIC HEMANGIOMAS; HEPATOCELLULAR-CARCINOMA; INSTANT IMAGES; TUMORS; RELAXATION; VALUES; BODY; ABDOMEN AB We studied the efficacy of T2 measurements at high field strength in distinguishing between liver hemangiomas and hepatic metastases when an ultrafast (single-excitation) MR imaging technique is used. Fourteen patients with known liver tumors were imaged in a 2.0-T prototype ultrafast MR scanner with a spin-echo (infinite TR and TE of 30-340 msec) pulse sequence. Each image was obtained with a total data acquisition time of 20 msec. T2 calculations for hepatic metastases (n = 6) showed a mean of 79.3 +/- 13.5 msec, whereas hemangiomas (n = 8) showed a T2 of 139.8 +/- 18.8 msec (p < .0001). T2 values of lesions had a smaller relative standard deviation than previously reported, and the range of T2 values of hemangiomas (1 19-181 msec) and metastases (68-103 msec) did not overlap. Our preliminary results suggest that T2 calculations with ultrafast MR imaging may be useful for differentiating hemangiomas from metastases. We hypothesize that T2 values obtained from ultrafast MR images are more reliable than those obtained from conventional MR images, primarily because of the elimination of T1 information and effects of motion on image signal intensity. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. NR 25 TC 31 Z9 31 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 OCT PY 1991 VL 157 IS 4 BP 727 EP 730 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GF743 UT WOS:A1991GF74300011 PM 1892026 ER PT J AU CHEW, FS WEISSLEDER, R AF CHEW, FS WEISSLEDER, R TI RADIATION-INDUCED OSTEOCHONDROMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP CHEW, FS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 3 TC 8 Z9 8 U1 0 U2 1 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 OCT PY 1991 VL 157 IS 4 BP 792 EP 792 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GF743 UT WOS:A1991GF74300025 PM 1892038 ER PT J AU ZUKERBERG, LR FERRY, JA HARRIS, NL AF ZUKERBERG, LR FERRY, JA HARRIS, NL TI LYMPHOCYTIC GASTRITIS - REPLY SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Letter ID T-CELL LYMPHOMA RP ZUKERBERG, LR (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 8 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD OCT PY 1991 VL 15 IS 10 BP 1014 EP 1016 DI 10.1097/00000478-199110000-00017 PG 3 WC Pathology; Surgery SC Pathology; Surgery GA GG486 UT WOS:A1991GG48600016 ER PT J AU SILBERT, BS LIPKOWSKI, AW CEPEDA, MS SZYFELBEIN, SK OSGOOD, PF CARR, DB AF SILBERT, BS LIPKOWSKI, AW CEPEDA, MS SZYFELBEIN, SK OSGOOD, PF CARR, DB TI ENHANCED POTENCY OF RECEPTOR-SELECTIVE OPIOIDS AFTER ACUTE BURN INJURY SO ANESTHESIA AND ANALGESIA LA English DT Article ID RAT SPINAL-CORD; BETA-ENDORPHIN; ANALGESIA; MORPHINE; STRESS; KAPPA; ANTINOCICEPTION; INFLAMMATION; INCREASES; SITES AB Dose-response curves of three receptor-selective opioids were established in a group of nonburned and a group of burned rats. Morphine (mu-agonist), biphalin (mu- and delta-agonist), and U50488H (kappa-agonist) were administered to each group, and analgesia was measured by tail flick latency testing. Each opioid had a significant increase in potency (i.e., a decrease in ED50 values) in the burned (15% body surface area) compared with the nonburned groups. Moderate doses of each drug (i.e., ED50 doses estimated from nonburned group data) in each case augmented stress-induced analgesia in the burned group. Analgesic doses failed to prevent a significant increase in plasma beta-endorphin and corticosterone after larger surface area (25%) burns. Regardless of receptor specificity, opioid analgesic potency is increased acutely after burn injuries. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,ANALGES PEPTIDE RES UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED ENDOCRINOL,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA. ST VINCENTS HOSP,DEPT ANESTHESIA,MELBOURNE,VIC,AUSTRALIA. UNIV WARSAW,DEPT CHEM,PL-00325 WARSAW,POLAND. HOSP ST IGNATIUS,DEPT ANESTHESIA,BOGOTA,COLOMBIA. FU NINDS NIH HHS [NS 23357] NR 24 TC 15 Z9 15 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 OCT PY 1991 VL 73 IS 4 BP 427 EP 433 PG 7 WC Anesthesiology SC Anesthesiology GA GG685 UT WOS:A1991GG68500011 PM 1897768 ER PT J AU DERSHWITZ, M ROSOW, CE DIBIASE, PM ZASLAVSKY, A AF DERSHWITZ, M ROSOW, CE DIBIASE, PM ZASLAVSKY, A TI EFFECTS OF MIDAZOLAM AND OR BUTORPHANOL .1.2. REPLY SO ANESTHESIOLOGY LA English DT Letter C1 MASSACHUSETTS GEN HOSP,ANESTHESIA SERV,BOSTON,MA 02114. RP DERSHWITZ, M (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. 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 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD OCT PY 1991 VL 75 IS 4 BP 707 EP 707 DI 10.1097/00000542-199110000-00031 PG 1 WC Anesthesiology SC Anesthesiology GA GH568 UT WOS:A1991GH56800030 ER PT J AU ALBERS, GW SHERMAN, DG GRESS, DR PAULSETH, JE PETERSEN, P AF ALBERS, GW SHERMAN, DG GRESS, DR PAULSETH, JE PETERSEN, P TI STROKE PREVENTION IN NONVALVULAR ATRIAL-FIBRILLATION - A REVIEW OF PROSPECTIVE RANDOMIZED TRIALS SO ANNALS OF NEUROLOGY LA English DT Review ID ORAL ANTICOAGULANT-THERAPY; THROMBOEMBOLIC COMPLICATIONS; RISK-FACTORS; INTRACEREBRAL HEMORRHAGE; ANTITHROMBOTIC THERAPY; FRAMINGHAM; POPULATION AB Patients with atrial fibrillation are at risk for cerebral embolism; however, the roles of chronic anticoagulation or antiplatelet therapy for stroke prevention in patients with nonvalvular atrial fibrillation have been controversial. Recently, the results of three large prospective randomized trials that examined the risks and benefits of warfarin or aspirin for stroke prophylaxis in patients with nonvalular atrial fibrillation were reported. All three studies revealed a reduction in the stroke rate for patients treated with warfarin and a small incidence of major bleeding. One of the studies also reported a reduced stroke rate in aspirin-treated patients. The reduction of thromboembolic events associated with chronic warfarin therapy appears to outweigh the risks of significant bleeding for most patients with nonvalvular atrial fibrillation. Aspirin may offer an alternative for subgroups of patients who are at low risk for stroke or those who are not good candidates for anticoagulation. C1 HAMILTON CIVIC HOSP,DEPT NEUROL,HAMILTON,ONTARIO,CANADA. UNIV TEXAS,HLTH SCI CTR,DIV NEUROL,SAN ANTONIO,TX 78284. UNIV COPENHAGEN HOSP,RIGSHOSP,DK-2100 COPENHAGEN,DENMARK. VET ADM MED CTR,PALO ALTO,CA 94304. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP ALBERS, GW (reprint author), STANFORD UNIV,MED CTR,DEPT NEUROL & NEUROL SCI,STANFORD,CA 94305, USA. NR 38 TC 91 Z9 94 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD OCT PY 1991 VL 30 IS 4 BP 511 EP 518 DI 10.1002/ana.410300402 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA GJ815 UT WOS:A1991GJ81500001 PM 1789680 ER PT J AU FLEXON, PB NADOL, JB SCHUKNECHT, HF MONTGOMERY, WW MARTUZA, RL AF FLEXON, PB NADOL, JB SCHUKNECHT, HF MONTGOMERY, WW MARTUZA, RL TI BILATERAL ACOUSTIC NEUROFIBROMATOSIS (NEUROFIBROMATOSIS-2) - A DISORDER DISTINCT FROM VONRECKLINGHAUSENS NEUROFIBROMATOSIS (NEUROFIBROMATOSIS-1) SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE BILATERAL ACOUSTIC NEUROFIBROMATOSIS; TEMPORAL BONE; VONRECKLINGHAUSENS DISEASE ID GENETIC-LINKAGE AB A case report of bilateral acoustic neurofibromatosis (NF-2) is presented with temporal bone histopathology. The distinct clinical and genetic features of NF-2 are reviewed in the context of recent data that show it to be a disorder distinct from classic von Recklinghausen's disease (NF-1). C1 MASSACHUSETTS EYE & EAR HOSP,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROSURG,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 14 TC 4 Z9 4 U1 0 U2 0 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD OCT PY 1991 VL 100 IS 10 BP 830 EP 834 PG 5 WC Otorhinolaryngology SC Otorhinolaryngology GA GJ128 UT WOS:A1991GJ12800008 PM 1952650 ER PT J AU MATHISEN, DJ GRILLO, HC WAIN, JC HILGENBERG, AD AF MATHISEN, DJ GRILLO, HC WAIN, JC HILGENBERG, AD TI MANAGEMENT OF ACQUIRED NONMALIGNANT TRACHEOESOPHAGEAL FISTULA SO ANNALS OF THORACIC SURGERY LA English DT Article ID CUFFED TRACHEAL TUBES; VENTILATION AB Acquired, nonmalignant tracheoesophageal fistula is an uncommon and difficult problem to manage. The most common cause is a complication of endotracheal or tracheostomy tubes. Most are diagnosed while patients still require mechanical ventilation. We use a conservative approach until patients are weaned from ventilation. A tracheostomy tube is placed so that the balloon rests below the fistula, if possible, to prevent contamination of the tracheobronchial tree. A gastrostomy tube is placed for drainage and a separate jejunostomy tube for nutrition. Single-stage repair is done after the patient is weaned from mechanical ventilation. Esophageal diversion is rarely required. We have performed 41 operations on 38 patients. Simple division and closure of the fistula was done in 9 patients and tracheal resection and reconstruction in the remainder. The esophageal defect was closed in two layers and a viable strap muscle interposed between the two suture lines. There were four deaths (10.9%). There were three recurrent fistulas and one delayed tracheal stenosis. All were successfully managed. Of the 34 surviving patients, 33 aliment themselves orally and 32 breathe without the need for a tracheal appliance. RP MATHISEN, DJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,WARREN 1109,BOSTON,MA 02114, USA. NR 13 TC 78 Z9 82 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD OCT PY 1991 VL 52 IS 4 BP 759 EP 765 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA GM201 UT WOS:A1991GM20100007 PM 1929626 ER PT J AU GEFFIN, GA REYNOLDS, TR TITUS, JS OKEEFE, DD DAGGETT, WM AF GEFFIN, GA REYNOLDS, TR TITUS, JS OKEEFE, DD DAGGETT, WM TI RELATION OF MYOCARDIAL PROTECTION TO CARDIOPLEGIC SOLUTION PH - MODULATION BY CALCIUM AND MAGNESIUM SO ANNALS OF THORACIC SURGERY LA English DT Article ID SARCOPLASMIC-RETICULUM; ISCHEMIC ARREST; PRESERVATION; OXYGENATION; CONTRACTION; CELLS; CA-2+; TEMPERATURE; PERFORMANCE; REPERFUSION AB The relationship between myocardial preservation and cardioplegic solution pH was assessed in isolated, perfused rat hearts. A base solution without calcium or magnesium and the same solution containing 0.2 mmol/L ionized calcium or 16 mmol/L magnesium or both ions were studied at several values of pH between 6.8 and 8.7. Hearts were arrested at 8-degrees-C by multidose infusions of these bicarbonate-buffered solutions bubbled with oxygen and a varying percentage of carbon dioxide to control pH. Diastolic tone (left ventricular balloon) and adenosine triphosphate (ATP) depletion during arrest both increased as the cardioplegic solution became more alkaline. Calcium increased these effects of pH. Magnesium weakened the effect of pH on diastolic tone, maintained ATP at all pH levels, and inhibited the effects of calcium on the relationships of pH to diastolic tone and ATP. When data from all solutions were considered together, ATP depletion was shown to be linearly related to diastolic tone. Calcium depressed functional recovery (left ventricular developed pressure during reperfusion expressed as a percentage of its prearrest value) at all pH levels. With the other solutions, recovery was similar and best within a broad and relatively alkaline pH range. With the solution containing calcium and magnesium, at pH levels of 8.28 +/- 0.02, 7.87 +/- 0.03, 7.58 +/- 0.02, 7.41 +/- 0.01, 7.06 +/- 0.02, and 6.80 +/- 0.01, recovery at 5 minutes of reperfusion was 101.4% +/- 3.7%, 102.9% +/- 2.8%, 107.3% +/- 3.7%, 102.8% +/- 2.9%, 91.8% +/- 3.6%, and 94.3% +/- 3.5%, respectively. This effect of alkalinity was short-lived. Extreme alkalinity of the base, acalcemic solution produced the calcium paradox, as reported previously. Good preservation of ATP by the most acid solutions did not predict good functional recovery. Magnesium increased the persistence of frequent extrasystoles during early reperfusion, but the effect was attenuated by calcium. The data support the inclusion of magnesium in cardioplegic solutions, particularly when they contain calcium, show that cardioplegic solution pH can have major effects on the arrested heart, and suggest that a relatively alkaline pH may modestly benefit functional recovery. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GEFFIN, GA (reprint author), MASSACHUSETTS GEN HOSP,SURG CARDIOVASC UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL 12777] NR 31 TC 7 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD OCT PY 1991 VL 52 IS 4 BP 955 EP 964 PG 10 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA GM201 UT WOS:A1991GM20100056 PM 1929661 ER PT J AU KONG, XB ZHU, QY RUPRECHT, RM WATANABE, KA ZEIDLER, JM GOLD, JWM POLSKY, B ARMSTRONG, D CHOU, TC AF KONG, XB ZHU, QY RUPRECHT, RM WATANABE, KA ZEIDLER, JM GOLD, JWM POLSKY, B ARMSTRONG, D CHOU, TC TI SYNERGISTIC INHIBITION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 REPLICATION INVITRO BY 2-DRUG AND 3-DRUG COMBINATIONS OF 3'-AZIDO-3'-DEOXYTHYMIDINE, PHOSPHONOFORMATE, AND 2',3'-DIDEOXYTHYMIDINE SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID IMMUNE-DEFICIENCY SYNDROME; ALPHA-A-INTERFERON; REVERSE-TRANSCRIPTASE; FOSCARNET; AZIDOTHYMIDINE; INFECTIVITY; HIV AB The effects of 3'-azido-3'-deoxythymidine (AZT), phosphonoformate (PFA), and 2',3'-dideoxythymidine (ddT) and their combinations on human immunodeficiency type 1 (HIV-1) replication were studied by measuring the HIV-1 p24 antigen expression and reverse transcriptase (RT) release in HIV-1-infected MT4 cells in vitro. RT activity was also measured in a cell-free system by using poly(rA)-oligo(dT) as the primer-template, and cell growth inhibition was measured in noninfected MT4 cells. The interactions of these two- and three-drug combinations were evaluated by the combination index (CI) method and isobologram techniques. The 50% effective concentrations (EC50s) of AZT, PFA, and ddT were 0.014 to 0.005, 9.4 to 8.8, and 8.4 to 2.5-mu-M, respectively, for p24 enzyme-linked immunosorbent assays (ELISAs) and 0.0055 to 0.0034, 1.43 to 1.37, and 2.87 to 2.83-mu-M, respectively, for RT activity in vitro; for RT activity in the cell-free system, the EC50s were 0.00019 to 0.00024, 0.012 to 0.02, and 0.00074 to 0.0005-mu-M, for AZT-5'-triphosphate, PFA, and ddT-5'-triphosphate, respectively. AZT in combination with PFA (1:200) or ddT (1:5) as well as the combination of these three drugs (1:200:5) synergistically inhibited HIV-1 replication and RT activity in the cell-free system over a wide range of drug concentrations, with the CIs ranging from 0.5 to 0.9, in which CIs of < 1, 1, and > 1 indicate synergism, additive effect, and antagonism, respectively. Three- and two-drug combinations of AZT, PFA, and ddT showed similar degrees of synergism against HIV-1 replication in p24 assays and RT release assays, whereas the combination of AZT and ddT was found to be the most selective in terms of its anti-HIV-1 effect versus cytotoxicity. Dose reduction indices calculated from both HIV-1 replication inhibition, as measured by p24 ELISA and by RT activity in the cell-free system, indicated that two- and three-drug combinations at high effect levels and the selected combination ratios allow 2- to 240-fold dose reduction over the single drug alone in terms of their anti-HIV-1 effects. The three-drug combination showed the highest dose reduction index. These findings suggest that increased efficacy and reduced toxicity may be achieved in AIDS therapy by using AZT, PFA, and ddT in two- or three-drug combinations. C1 MEM SLOAN KETTERING CANC CTR,BIOCHEM PHARMACOL LAB,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,ORGAN CHEM LAB,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,INFECT DIS SERV,NEW YORK,NY 10021. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. RI Chou, Ting-Chao/B-4111-2009 OI Chou, Ting-Chao/0000-0002-3340-1594 FU NCI NIH HHS [CA 18856]; NIAID NIH HHS [UO1-AI 26056] NR 27 TC 42 Z9 42 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD OCT PY 1991 VL 35 IS 10 BP 2003 EP 2011 PG 9 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA GJ408 UT WOS:A1991GJ40800010 PM 1722077 ER PT J AU DOUKAS, AG ZWEIG, AD FRISOLI, JK BIRNGRUBER, R DEUTSCH, TF AF DOUKAS, AG ZWEIG, AD FRISOLI, JK BIRNGRUBER, R DEUTSCH, TF TI NONINVASIVE DETERMINATION OF SHOCK-WAVE PRESSURE GENERATED BY OPTICAL-BREAKDOWN SO APPLIED PHYSICS B-PHOTOPHYSICS AND LASER CHEMISTRY LA English DT Article ID LASER-INDUCED BREAKDOWN; SPATIAL DYNAMICS; WATER; CAVITATION; LIQUIDS; PULSES AB Shock waves generated by a laser-induced plasma were investigated using a pump-and-probe technique. Both 7-ns and 40-ps laser pulses at 1.06-mu-m were employed to initiate breakdown in water. Two He Ne laser beams were used as a velocity probe, allowing the accurate measurement of the shock velocity around the plasma. The maximum shock pressure was determined from the measured shock velocities, the jump condition and the equation of state for water. The conservation of the total momentum of the shock front was used to derive expressions for the shock velocity, particle velocity and shock pressure vs. the distance (r) from the center of the plasma. For a shock wave of spherical symmetry, the shock pressure is proportional to 1/r2. Our work shows that the expanding plasma initially induces a shock wave; the shock wave dissipates rapidly becoming an acoustic wave within 300-500-mu-m. RP DOUKAS, AG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LAB PHOTOMED,BOSTON,MA 02114, USA. RI Birngruber, Reginald/Q-2342-2016 NR 31 TC 72 Z9 78 U1 1 U2 6 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0721-7269 J9 APPL PHYS B-PHOTO PD OCT PY 1991 VL 53 IS 4 BP 237 EP 245 DI 10.1007/BF00357143 PG 9 WC Physics, Applied SC Physics GA GP064 UT WOS:A1991GP06400008 ER PT J AU WAXMAN, DJ LAPENSON, DP AOYAMA, T GELBOIN, HV GONZALEZ, FJ KORZEKWA, K AF WAXMAN, DJ LAPENSON, DP AOYAMA, T GELBOIN, HV GONZALEZ, FJ KORZEKWA, K TI STEROID-HORMONE HYDROXYLASE SPECIFICITIES OF 11 CDNA-EXPRESSED HUMAN CYTOCHROME-P450S SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID RAT HEPATIC CYTOCHROME-P-450; HUMAN-LIVER; DIRECTED EXPRESSION; TESTOSTERONE OXIDATION; DEPENDENT EXPRESSION; IDENTIFICATION; METABOLISM; ISOZYMES; SEQUENCE; 16-ALPHA-HYDROXYLASE C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP WAXMAN, DJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JF-525,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK33765, R01 DK033765] NR 38 TC 280 Z9 284 U1 2 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD OCT PY 1991 VL 290 IS 1 BP 160 EP 166 DI 10.1016/0003-9861(91)90602-F PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA GE531 UT WOS:A1991GE53100020 PM 1898086 ER PT J AU MERKLE, RK HELLAND, DE WELLES, JL SHILATIFARD, A HASELTINE, WA CUMMINGS, RD AF MERKLE, RK HELLAND, DE WELLES, JL SHILATIFARD, A HASELTINE, WA CUMMINGS, RD TI GP160 OF HIV-I SYNTHESIZED BY PERSISTENTLY INFECTED MOLT-3 CELLS IS TERMINALLY GLYCOSYLATED - EVIDENCE THAT CLEAVAGE OF GP160 OCCURS SUBSEQUENT TO OLIGOSACCHARIDE PROCESSING SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; O-LINKED OLIGOSACCHARIDES; CONCANAVALIN-A-SEPHAROSE; HAMSTER OVARY CELLS; ROUS-SARCOMA VIRUS; ENVELOPE GLYCOPROTEIN; ENDOPROTEOLYTIC CLEAVAGE; STRUCTURAL DETERMINANTS; SYNCYTIUM FORMATION; AIDS PATIENTS C1 UNIV GEORGIA,DEPT BIOCHEM,ATHENS,GA 30602. UNIV GEORGIA,COMPLEX CARBOHYDRATE RES CTR,ATHENS,GA 30602. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115. FU NIAID NIH HHS [AI 27135] NR 40 TC 20 Z9 20 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD OCT PY 1991 VL 290 IS 1 BP 248 EP 257 DI 10.1016/0003-9861(91)90616-Q PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA GE531 UT WOS:A1991GE53100034 PM 1898096 ER PT J AU WIESELTHIER, JS TRELOAR, V KOH, HK RAO, BK AHMED, AR AF WIESELTHIER, JS TRELOAR, V KOH, HK RAO, BK AHMED, AR TI MULTIPLE CRUSTED PLAQUES IN A WOMAN WITH SYSTEMIC LUPUS-ERYTHEMATOSUS - PEMPHIGUS ERYTHEMATOSUS (PE) SO ARCHIVES OF DERMATOLOGY LA English DT Note C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RP WIESELTHIER, JS (reprint author), BOSTON UNIV,SCH MED,BOSTON,MA 02118, USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD OCT PY 1991 VL 127 IS 10 BP 1571 EP & PG 0 WC Dermatology SC Dermatology GA GK624 UT WOS:A1991GK62400020 ER PT J AU BARSKY, AJ WYSHAK, G KLERMAN, GL AF BARSKY, AJ WYSHAK, G KLERMAN, GL TI TRANSIENT HYPOCHONDRIASIS - A NEW SOMATOFORM DIAGNOSIS - REPLY SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter C1 HARVARD UNIV,SCH PUBL HLTH,CTR POPULAT STUDIES,CAMBRIDGE,MA 02138. CORNELL UNIV,MED CTR,COLL MED,DEPT PSYCHIAT,NEW YORK,NY 10021. RP BARSKY, AJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,PSYCHIAT SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 2 TC 1 Z9 1 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD OCT PY 1991 VL 48 IS 10 BP 955 EP 956 PG 2 WC Psychiatry SC Psychiatry GA GJ812 UT WOS:A1991GJ81200011 ER PT J AU LANCASTER, TR SINGER, DE SHEEHAN, MA OERTEL, LB MARAVENTANO, SW HUGHES, RA KISTLER, JP AF LANCASTER, TR SINGER, DE SHEEHAN, MA OERTEL, LB MARAVENTANO, SW HUGHES, RA KISTLER, JP TI THE IMPACT OF LONG-TERM WARFARIN THERAPY ON QUALITY-OF-LIFE - EVIDENCE FROM A RANDOMIZED TRIAL SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID ATRIAL-FIBRILLATION; FUNCTIONAL STATUS; HYPERTENSION AB To determine the effect of long-term warfarin sodium therapy on quality of life, we surveyed 333 patients participating in a randomized, controlled trial of warfarin for the prevention of stroke in nonrheumatic atrial fibrillation. No significant differences between warfarin-treated and control patients were found on well-validated measures of functional status, well-being, and health perceptions. For example, the summary score for health perceptions was 68.8 in the warfarin-treated vs 66.6 in the control group (scale of 0 to 100; 95% confidence intervals for the difference, -1.6 to 6.0). In contrast, patients taking warfarin who had a bleeding episode had a significant decrease in health perceptions (-11.9; 95% confidence interval, -4.1 to -91.6). Warfarin therapy is not usually associated with a significant decrease in perceived health, unless a bleeding episode has occurred. Negative effects of warfarin treatment on health perceptions may be balanced by confidence in its protective effects. C1 MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BULFINCH 1,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,WANG AMBULATORY CARE CTR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. FU NHLBI NIH HHS [HL 33233-05] NR 17 TC 132 Z9 134 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD OCT PY 1991 VL 151 IS 10 BP 1944 EP 1949 DI 10.1001/archinte.151.10.1944 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA GK641 UT WOS:A1991GK64100005 PM 1929681 ER PT J AU FISHER, CM AF FISHER, CM TI VISUAL HALLUCINATIONS AND RACING THOUGHTS ON EYE CLOSURE AFTER MINOR SURGERY SO ARCHIVES OF NEUROLOGY LA English DT Article AB Two hours after minor surgery under local anesthesia, a 67-year-old man developed vivid visual hallucinations that were present only when he closed his eyes. After lasting 4 hours, the hallucinations were succeeded by racing thoughts, lasting 2 hours, and then by illusionary movements of his body. The reaction was attributed to the effect of lidocaine. The case resembles one previously reported. RP FISHER, CM (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114, USA. NR 4 TC 8 Z9 8 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD OCT PY 1991 VL 48 IS 10 BP 1091 EP 1092 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA GJ526 UT WOS:A1991GJ52600023 PM 1929906 ER PT J AU CHENG, SS PINSON, W LOPEZ, RR CRASS, RA JOHNSON, RS AF CHENG, SS PINSON, W LOPEZ, RR CRASS, RA JOHNSON, RS TI EFFECT OF DONOR-DISSEMINATED INTRAVASCULAR COAGULATION IN LIVER-TRANSPLANTATION SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 62ND ANNUAL SCIENTIFIC SESSION OF THE PACIFIC COAST SURGICAL ASSOC CY FEB 18, 1991 CL PEBBLE BEACH, CA SP PACIFIC COAST SURG ASSOC ID PRESERVATION; GENDER AB It is not known whether disseminated intravascular coagulation, present in a large percentage of organ donors, affects patient outcome after liver transplantation. We reviewed our first 55 liver transplantations and identified 10 donors with disseminated intravascular coagulation. We compared the perioperative courses of the 10 recipients of these transplanted livers with those of 10 matched controls whose donors did not have disseminated intravascular coagulation. Disseminated intravascular coagulation recipients did not require more blood products during or after surgery; their hepatic enzyme levels and prothrombin times after surgery were not statistically significantly higher than those of the controls. There was no difference in hospital stay, number of episodes of rejection, retransplantations, or deaths. The presence of disseminated intravascular coagulation in donors did not adversely affect graft function or patient outcome and should not be a sole criterion for rejecting a liver for transplantation. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT SURG,NASHVILLE,TN 37232. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. OREGON HLTH SCI UNIV,DEPT SURG,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT CLIN PATHOL,PORTLAND,OR 97201. NR 24 TC 3 Z9 3 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 OCT PY 1991 VL 126 IS 10 BP 1292 EP 1296 PG 5 WC Surgery SC Surgery GA GJ524 UT WOS:A1991GJ52400020 PM 1929832 ER PT J AU KOCHOYAN, M KEUTMANN, HT WEISS, MA AF KOCHOYAN, M KEUTMANN, HT WEISS, MA TI ALTERNATING ZINC FINGERS IN THE HUMAN MALE-ASSOCIATED PROTEIN ZFY - HX3H AND HX4H MOTIFS ENCODE A LOCAL STRUCTURAL SWITCH SO BIOCHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR-IIIA; ENHANCER BINDING-PROTEIN; SEX-DETERMINING REGION; XENOPUS; DOMAIN; GENE; DYNAMICS; MODEL AB The two-finger repeat in the human male-associated protein ZFY provides a model for comparative 2D-NMR studies of classical and variant Zn fingers. This repeat is defined in part by an alternation in spacing between consensus (HX3H) and variant (HX4H) histidine spacings. To investigate the effects of a "switch" between alternative histidine spacings, we have designed an HX3H analogue of a representative HX4H domain of known structure [ZFY-6; Kochoyan, M., Havel, T., Nguyen, D. T., Dahl, C. E., Keutmann, H. T., & Weiss, M. A. (1991) Biochemistry 30, 3371-3386]. The HX3H analogue (designated ZFY-switch) forms a tetrahedral Co2+ complex whose thermodynamic stability is similar to that of the parent peptide. 2D-NMR studies demonstrate that ZFY-switch and ZFY-6, although similar in overall structure, exhibit significant local changes near the site of deletion. Whereas the HX4H site in the native finger forms a nonstandard loop, the HX3H site in ZFY-switch folds as a 3(10) extension of the C-terminal alpha-helix, as observed in the NMR solution structure of a consensus HX3H domain [Lee, M. S., Gippert, G. P., Soman, K. V., Case, D. A., & Wright, P. E. (1989) Science 245, 635-637] and in the crystal structure of a representative Zn finger-DNA complex [Pavletich, N. P., & Pabo, C. O. (1991) Science 252, 809-817]. We propose that variant histidine spacings (HX3H and HX4H) encode a local switch between alternative surface architectures with implications for models of protein-DNA recognition. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. BIOP POLYTECH,CNRS,URA 32,F-91128 PALAISEAU,FRANCE. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 32 TC 25 Z9 25 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 1 PY 1991 VL 30 IS 39 BP 9396 EP 9402 DI 10.1021/bi00103a002 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GH408 UT WOS:A1991GH40800002 PM 1892840 ER PT J AU PAMPFER, S ARCECI, RJ POLLARD, JW AF PAMPFER, S ARCECI, RJ POLLARD, JW TI ROLE OF COLONY STIMULATING FACTOR-I (CSF-1) AND OTHER LYMPHO-HEMATOPOIETIC GROWTH-FACTORS IN MOUSE PREIMPLANTATION DEVELOPMENT SO BIOESSAYS LA English DT Review ID LEUKEMIA INHIBITORY FACTOR; EMBRYO DEVELOPMENT INVITRO; REPRODUCTIVE-TRACT; PROTEIN-KINASE; CO-CULTURE; FACTOR-I; EXPRESSION; IMPLANTATION; CELLS; MACROPHAGES AB Mouse pre-implantation development appears to be under the control of paracrine and autocrine growth factors. The epithelium of the oviduct and the uterus together, with the population of macrophages and lymphocytes present in the reproductive tract from the onset of pregnancy, are thought to be the major sources of paracrine growth factors targeted to the developing embryos. Some of the growth factors are synthesized by both uterine epithelial cells and activated lympho-hematopoietic cells, suggesting a partial overlap of the regulatory signals used by the reproductive and lympho-hematopoietic systems. Such growth factors may be the long sought-after mediators of the synchrony between the pre-implantation embryo and the sex-steroid hormone-induced changes in the uterus. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. RP PAMPFER, S (reprint author), ALBERT EINSTEIN COLL MED,DEPT DEV BIOL & CANC,NEW YORK,NY 10461, USA. FU NICHD NIH HHS [HD25074]; NIGMS NIH HHS [IGM38156] NR 49 TC 92 Z9 92 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0265-9247 J9 BIOESSAYS JI Bioessays PD OCT PY 1991 VL 13 IS 10 BP 535 EP 540 DI 10.1002/bies.950131007 PG 6 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA GL843 UT WOS:A1991GL84300006 PM 1836724 ER PT J AU OTTO, MW FAVA, M ROSENBAUM, JF MURPHY, CF AF OTTO, MW FAVA, M ROSENBAUM, JF MURPHY, CF TI PERCEPTUAL ASYMMETRY, PLASMA-CORTISOL, AND RESPONSE TO TREATMENT IN DEPRESSED OUTPATIENTS SO BIOLOGICAL PSYCHIATRY LA English DT Article ID DEXAMETHASONE SUPPRESSION TEST; ADENOSYL-L-METHIONINE; CEREBRAL LATERALITY; SUBTYPES; TIME AB Perceptual asymmetries as indicated by dichotic listening tasks have been associated with both subtype of depression and response to antidepressant treatment. To examine the association between this relatively new measure and more traditional measures of hypothalamic-pituitary-adrenal axis (HPA) activation in depression, we assessed perceptual asymmetry and basal plasma cortisol in a sample of depressed outpatients undergoing a double-blind, placebo-controlled medication trial. Each measure was examined for its ability to predict response to treatment. Perceptual asymmetry was significantly associated with plasma cortisol levels, and was also a significant predictor of treatment response. The association between plasma cortisol and treatment response did not reach significance. Our findings are limited by relatively small sample sizes but encourage further examination of perceptual asymmetry measures as predictors of treatment response and in relation to HPA activation in depression. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC-815,BOSTON,MA 02114, USA. NR 33 TC 14 Z9 15 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 OCT 1 PY 1991 VL 30 IS 7 BP 703 EP 710 DI 10.1016/0006-3223(91)90015-E PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA GH689 UT WOS:A1991GH68900006 PM 1958767 ER PT J AU MEYERSWALLEN, VN MANGANARO, TF KURODA, T CONCANNON, PW MACLAUGHLIN, DT DONAHOE, PK AF MEYERSWALLEN, VN MANGANARO, TF KURODA, T CONCANNON, PW MACLAUGHLIN, DT DONAHOE, PK TI THE CRITICAL PERIOD FOR MULLERIAN DUCT REGRESSION IN THE DOG EMBRYO SO BIOLOGY OF REPRODUCTION LA English DT Article ID INHIBITING SUBSTANCE; BOVINE; IMMUNOASSAY; TESTES; CELLS; FETAL; ONTOGENY; HORMONE; CULTURE; BIRTH AB The embryonic period during which Mullerian duct regression and Mullerian Inhibiting Substance (MIS) secretion occur was determined in canine embryos removed from timed pregnancies (32, 36, 37, 39, 42, and 46 days gestation). Sex chromosomes of each embryo were identified in metaphase spreads prepared from fibroblast cultures. Testicular differentiation, defined by seminiferous tubule formation and the presence of Sertoli cells and Leydig cells, and the degree of Mullerian duct regression were determined by careful morphologic analysis of histologic sections of canine embryonic gonads (n = 20) and Mullerian ducts (n = 20). MIS was detected immunohistochemically in embryonic testes using avidin-biotin complex enhancement of a specific rabbit polyclonal anti-MIS antibody. Testicular differentiation was observed at 36 days gestation. The earliest evidence of Mullerian duct regression in male embryos was observed at 36 days gestation, and regression was completed by 46 days gestation. Positive staining for MIS was present in testes from 36 to 46 days (n = 9). Staining was absent in the undifferentiated testis (n = 1) at 32 days gestation and in ovaries at all ages tested (n = 10). Thus, MIS is normally present throughout the critical period for Mullerian duct regression in the embryonic male dog. C1 CORNELL UNIV,NEW YORK STATE COLL VET MED,DEPT PHYSIOL,ITHACA,NY 14853. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LABS,BOSTON,MA 02114. RP MEYERSWALLEN, VN (reprint author), CORNELL UNIV,NEW YORK STATE COLL VET MED,DEPT CLIN SCI,429 VRT,ITHACA,NY 14853, USA. FU NCI NIH HHS [CA 17393]; NCRR NIH HHS [RR 03622]; NICHD NIH HHS [HD 19393] NR 34 TC 22 Z9 23 U1 0 U2 1 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD OCT PY 1991 VL 45 IS 4 BP 626 EP 633 DI 10.1095/biolreprod45.4.626 PG 8 WC Reproductive Biology SC Reproductive Biology GA GG148 UT WOS:A1991GG14800017 PM 1751638 ER PT J AU WARE, JA KANG, JH DECENZO, MT SMITH, M WATKINS, SC SLAYTER, HS SAITOH, M AF WARE, JA KANG, JH DECENZO, MT SMITH, M WATKINS, SC SLAYTER, HS SAITOH, M TI PLATELET ACTIVATION BY A SYNTHETIC HYDROPHOBIC POLYMER, POLYMETHYLMETHACRYLATE SO BLOOD LA English DT Article ID MURINE MONOCLONAL-ANTIBODY; IONIZED CALCIUM-CONCENTRATION; GLYCOPROTEIN-IIB-IIIA; PROTEIN KINASE-C; VONWILLEBRAND-FACTOR; THROMBASTHENIC PLATELETS; FIBRINOGEN RECEPTORS; ARTIFICIAL SURFACES; BINDING-SITE; AEQUORIN C1 BETH ISRAEL HOSP,DEPT SURG,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. BETH ISRAEL HOSP,CHARLES A DANA RES INST,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WARE, JA (reprint author), BETH ISRAEL HOSP,DEPT MED,DIV CARDIOVASC,HARVARD THORNDIKE LAB,GZ-409,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NHLBI NIH HHS [HL33014, HL38820]; PHS HHS [02271] NR 43 TC 24 Z9 24 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 1 PY 1991 VL 78 IS 7 BP 1713 EP 1721 PG 9 WC Hematology SC Hematology GA GH251 UT WOS:A1991GH25100011 PM 1912561 ER PT J AU TOOTHAKER, LE GONZALEZ, DA TUNG, N LEMONS, RS LEBEAU, MM ARNAOUT, MA CLAYTON, LK TENEN, DG AF TOOTHAKER, LE GONZALEZ, DA TUNG, N LEMONS, RS LEBEAU, MM ARNAOUT, MA CLAYTON, LK TENEN, DG TI CELLULAR MYOSIN HEAVY-CHAIN IN HUMAN-LEUKOCYTES - ISOLATION OF 5' CDNA CLONES, CHARACTERIZATION OF THE PROTEIN, CHROMOSOMAL LOCALIZATION, AND UP-REGULATION DURING MYELOID DIFFERENTIATION SO BLOOD LA English DT Article ID ACTIN-BINDING PROTEIN; COMPLETE SEQUENCE; MESSENGER-RNA; DNA-SEQUENCE; PHAGOCYTOSIS; MACROPHAGES; CELLS; GENE; EXPRESSION; FILAMENTS C1 BETH ISRAEL HOSP,DIV HEMATOL ONCOL,RES E ROOM 219,330 BROOKLINE AVE,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,PROGRAM CELL & DEV BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. UNIV UTAH,MED CTR,DEPT PEDIAT,SALT LAKE CITY,UT 84112. UNIV CHICAGO,HEMATOL ONCOL SECT,CHICAGO,IL 60637. FU NCI NIH HHS [CA42557, CA41456] NR 39 TC 65 Z9 66 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 OCT 1 PY 1991 VL 78 IS 7 BP 1826 EP 1833 PG 8 WC Hematology SC Hematology GA GH251 UT WOS:A1991GH25100025 PM 1912569 ER PT J AU SHIPP, MA STEFANO, GB SWITZER, SN GRIFFIN, JD REINHERZ, EL AF SHIPP, MA STEFANO, GB SWITZER, SN GRIFFIN, JD REINHERZ, EL TI CD10 (CALLA) NEUTRAL ENDOPEPTIDASE 24.11 MODULATES INFLAMMATORY PEPTIDE-INDUCED CHANGES IN NEUTROPHIL MORPHOLOGY, MIGRATION, AND ADHESION PROTEINS AND IS ITSELF REGULATED BY NEUTROPHIL ACTIVATION SO BLOOD LA English DT Article ID LYMPHOBLASTIC-LEUKEMIA ANTIGEN; COLONY-STIMULATING FACTOR; MONOCLONAL-ANTIBODY; OPIOID NEUROPEPTIDES; SURFACE EXPRESSION; HOMING RECEPTOR; SUB-POPULATIONS; DOWN-REGULATION; MYELOID CELLS; KINASE-C C1 SUNY COLL OLD WESTBURY,MULTIDISCIPLINARY CTR STUDY AGING,OLD WESTBURY,NY 11568. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP SHIPP, MA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA49232]; NIMH NIH HHS [MH-08078] NR 44 TC 143 Z9 144 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 1 PY 1991 VL 78 IS 7 BP 1834 EP 1841 PG 8 WC Hematology SC Hematology GA GH251 UT WOS:A1991GH25100026 PM 1717072 ER PT J AU SEIDMAN, CE SCHMIDT, EV SEIDMAN, JG AF SEIDMAN, CE SCHMIDT, EV SEIDMAN, JG TI CIS-DOMINANCE OF RAT ATRIAL-NATRIURETIC-FACTOR GENE REGULATORY SEQUENCES IN TRANSGENIC MICE SO CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY LA English DT Article; Proceedings Paper CT SATELLITE SYMP OF THE 13TH SCIENTIFIC MEETING OF THE INTERNATIONAL SOC OF HYPERTENSION : A DECADE OF ATRIAL NATRIURETIC FACTOR RESEARCH CY JUN 21-23, 1990 CL OTTAWA, CANADA SP INT SOC HYPERTENS DE ANF; TRANSGENIC MICE; TISSUE-SPECIFIC EXPRESSION ID EXPRESSION; HEART AB We have produced transgenic mice that express the prokaryotic marker protein chloramphenicol acetyltransferase under the control of regulatory sequences derived from the rat atrial natriuretic factor gene. The transgene, which contains 2.4 kilobases of the rat atrial natriuretic factor gene regulatory region, was found to direct 4000-fold more chloramphenicol acetyltransferase expression in adult atria than in ventricles. Low-level activity was also detected in the hypothalamus, demonstrating that these sequences contain the signals necessary for cardiac and central nervous system expression of the hormone atrial natriuretic factor. Developmental analyses showed early, high-level transgene expression in fetal atrial and ventricular tissues but marked reduction of ventricular transgene expression following birth. Further, the developmental expression patterns of the endogenous murine atrial natriuretic factor gene and rat transgene were found to be quite distinct. Although both the rat and mouse atrial natriuretic factor genes are activated early in embryogenesis, perinatal ventricular expression appears to differ in these two rodent species. The transgene is expressed in a pattern analagous to the neonatal rat rather than the endogenous murine gene. These studies demonstrate that the cis-acting signals required for correct tissue specificity and developmental regulation of the rat atrial natriuretic factor gene are encoded in this 2.4-kilobase fragment and that these sequences act in a dominant fashion. C1 MASSACHUSETTS GEN HOSP,CTR CANC,CHILDRENS SERV,BOSTON,MA 02129. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT GENET,BOSTON,MA 02115. RP SEIDMAN, CE (reprint author), BRIGHAM & WOMENS HOSP,DIV CARDIOL,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL41474, HL19259, HL35642] NR 22 TC 30 Z9 30 U1 0 U2 0 PU NATL RESEARCH COUNCIL CANADA PI OTTAWA PA RESEARCH JOURNALS, MONTREAL RD, OTTAWA ON K1A 0R6, CANADA SN 0008-4212 J9 CAN J PHYSIOL PHARM JI Can. J. Physiol. Pharmacol. PD OCT PY 1991 VL 69 IS 10 BP 1486 EP 1492 PG 7 WC Pharmacology & Pharmacy; Physiology SC Pharmacology & Pharmacy; Physiology GA GZ125 UT WOS:A1991GZ12500015 PM 1723347 ER PT J AU EHARA, S KATTAPURAM, SV EGGLIN, TK AF EHARA, S KATTAPURAM, SV EGGLIN, TK TI EWINGS-SARCOMA - RADIOGRAPHIC PATTERN OF HEALING AND BONY COMPLICATIONS IN PATIENTS WITH LONG-TERM SURVIVAL SO CANCER LA English DT Article ID PROGNOSTIC FACTORS; LOCAL-CONTROL; RADIOTHERAPY; CHEMOTHERAPY AB The radiographic appearance of Ewing's sarcoma was studied retrospectively in 22 patients who survived 5 years or longer after diagnosis and treatment. Expected changes from treatment, including regression of the extraosseous soft tissue mass, periostitis, and reconstitution of the cortex, occurred in all patients. Local recurrence occurred in one patient 10 years after complete remission whereas secondary osteosarcoma occurred more than 5 years after complete remission in two other cases. Both recurrent and secondary tumors presented as new lytic foci at the site of the original primary lesion. Lytic changes from radiation (radiation osteitis) may develop more than 2 years after treatment and in this sample; such findings were widely distributed in the radiation port. The authors conclude that bone remodeling and postradiation changes occur slowly over 2 years after treatment, and that any localized lysis at the primary site is suspicious for recurrence or secondary neoplasm. Knowledge of the expected changes and patterns of local recurrence and secondary neoplasms helps one to detect any significant change in its early phase. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 11 TC 7 Z9 7 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 OCT 1 PY 1991 VL 68 IS 7 BP 1531 EP 1535 DI 10.1002/1097-0142(19911001)68:7<1531::AID-CNCR2820680712>3.0.CO;2-T PG 5 WC Oncology SC Oncology GA GF966 UT WOS:A1991GF96600011 PM 1893352 ER PT J AU GOODMAN, A ZUKERBERG, LR NIKRUI, N SCULLY, RE AF GOODMAN, A ZUKERBERG, LR NIKRUI, N SCULLY, RE TI VAGINAL ADENOSIS AND CLEAR CELL-CARCINOMA AFTER 5-FLUOROURACIL TREATMENT FOR CONDYLOMAS SO CANCER LA English DT Article ID INTRA-EPITHELIAL NEOPLASIA; STEVENS-JOHNSON SYNDROME; HUMAN PAPILLOMAVIRUS DNA; TOPICAL 5-FLUOROURACIL; ADENOSQUAMOUS CARCINOMA; CERVICAL ECTROPION; UTERINE CERVIX; GENITAL-TRACT; ADENOCARCINOMA; WOMEN AB Vaginal adenosis and clear cell adenocarcinoma of the vagina occurred in a 44-year-old woman after treatment for condylomata acuminata. She had no known exposure to diethylstilbestrol (DES) in utero. Biopsy-proven vaginal adenosis appeared 8 months after intravaginal 5-fluorouracil application for recurrent urogenital condylomata acuminata. Forty months later, biopsies showed residual adenosis with foci of clear cell adenocarcinoma. Although clear cell adenocarcinoma is associated with vaginal adenosis and cervical ectropion in DES-exposed women, its occurrence in adenosis after 5-fluorouracil therapy has not been reported to the authors' knowledge. In this report, this rare but serious complication of treatment of condylomata acuminata is highlighted, and the literature regarding the development of non-DES-associated vaginal adenosis is discussed. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT GYNECOL,BOSTON,MA 02114. NR 53 TC 28 Z9 28 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD OCT 1 PY 1991 VL 68 IS 7 BP 1628 EP 1632 DI 10.1002/1097-0142(19911001)68:7<1628::AID-CNCR2820680727>3.0.CO;2-R PG 5 WC Oncology SC Oncology GA GF966 UT WOS:A1991GF96600026 PM 1893363 ER PT J AU KNUDSON, A VANDEWOUDE, GF FRIEND, SH CAVENEE, WK BRODEUR, GM AF KNUDSON, A VANDEWOUDE, GF FRIEND, SH CAVENEE, WK BRODEUR, GM TI DEVELOPMENTAL GENETICS AND CHILDHOOD-CANCER - AACR SPECIAL CONFERENCE IN CANCER-RESEARCH SO CANCER RESEARCH LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. LUDWIG INST CANC RES,MONTREAL H3A 1A1,QUEBEC,CANADA. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. RP KNUDSON, A (reprint author), FOX CHASE CANC INST,7701 BURHOLME AVE,PHILADELPHIA,PA 19111, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 1 PY 1991 VL 51 IS 19 BP 5435 EP 5439 PG 5 WC Oncology SC Oncology GA GH250 UT WOS:A1991GH25000057 PM 1655251 ER PT J AU MCGREW, JT ROCK, KL AF MCGREW, JT ROCK, KL TI STIMULATION OF HUMAN JURKAT CELLS BY MONOCLONAL-ANTIBODY CROSS-LINKING OF TRANSFECTED-LY-6A.2 (TAP) MOLECULES SO CELLULAR IMMUNOLOGY LA English DT Article ID LYMPHOCYTES-T; ACCESSORY CELL; LY-6 LOCUS; ACTIVATION; EXPRESSION; RECEPTOR; PROLIFERATION; COMPLEX; INHIBITION; HYBRIDOMA C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NIGMS NIH HHS [R01-GM38515 732CA09130-15] NR 27 TC 5 Z9 5 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 OCT 1 PY 1991 VL 137 IS 1 BP 118 EP 126 DI 10.1016/0008-8749(91)90062-G PG 9 WC Cell Biology; Immunology SC Cell Biology; Immunology GA GE773 UT WOS:A1991GE77300012 PM 1653114 ER PT J AU SAVAGE, COS HUGHES, CCW PEPINSKY, RB WALLNER, BP FREEDMAN, AS POBER, JS AF SAVAGE, COS HUGHES, CCW PEPINSKY, RB WALLNER, BP FREEDMAN, AS POBER, JS TI ENDOTHELIAL-CELL LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-3 AND AN UNIDENTIFIED LIGAND ACT IN CONCERT TO PROVIDE COSTIMULATION TO HUMAN PERIPHERAL-BLOOD CD4+T-CELLS SO CELLULAR IMMUNOLOGY LA English DT Article ID ACTIVATED T-CELLS; INTERLEUKIN-2 PRODUCTION; PROLIFERATIVE RESPONSES; RECEPTOR COMPLEX; INTERFERON; INVOLVEMENT; ANTIBODIES; INDUCTION; MOLECULES; AUGMENT C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. 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. RI Hughes, Christopher/F-7510-2010 FU NCI NIH HHS [5KO8CA01105]; NHLBI NIH HHS [HL36028] NR 31 TC 73 Z9 73 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD OCT 1 PY 1991 VL 137 IS 1 BP 150 EP 163 DI 10.1016/0008-8749(91)90065-J PG 14 WC Cell Biology; Immunology SC Cell Biology; Immunology GA GE773 UT WOS:A1991GE77300015 PM 1679377 ER PT J AU KALIN, NH SHELTON, SE TAKAHASHI, LK AF KALIN, NH SHELTON, SE TAKAHASHI, LK TI DEFENSIVE BEHAVIORS IN INFANT RHESUS-MONKEYS - ONTOGENY AND CONTEXT-DEPENDENT SELECTIVE EXPRESSION SO CHILD DEVELOPMENT LA English DT Article ID DORSOLATERAL PREFRONTAL CORTEX; INHIBITION; SEPARATION; VARIABLES; SHYNESS; LIFE; CUES; AGE C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP KALIN, NH (reprint author), UNIV WISCONSIN,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIMH NIH HHS [R01 MH046729, 1 RO1 MH-46729] NR 40 TC 70 Z9 70 U1 1 U2 4 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0009-3920 J9 CHILD DEV JI Child Dev. PD OCT PY 1991 VL 62 IS 5 BP 1175 EP 1183 DI 10.1111/j.1467-8624.1991.tb01598.x PG 9 WC Psychology, Educational; Psychology, Developmental SC Psychology GA GR257 UT WOS:A1991GR25700022 PM 1756661 ER PT J AU PADWA, BL EVANS, CA PILLEMER, FC AF PADWA, BL EVANS, CA PILLEMER, FC TI PSYCHOSOCIAL ADJUSTMENT IN CHILDREN WITH HEMIFACIAL MICROSOMIA AND OTHER CRANIOFACIAL DEFORMITIES SO CLEFT PALATE-CRANIOFACIAL JOURNAL LA English DT Article DE CRANIOFACIAL; PSYCHOSOCIAL; SYMMETRY; HEMIFACIAL MICROSOMIA ID MALFORMATIONS; CHILDHOOD AB Psychosocial adjustment was evaluated in different groups of children with craniofacial deformities in order to examine the relationships between symmetry, functional impairments, and social adaptation. Thirty patients, ages 6 through 16 years, were assessed using a battery of standard psychologic measures including Human Figure Drawing, Tasks of Emotional Adjustment, and Children's Depression inventory. Parents and teachers also provided ratings of the children' s functioning using the Child Behavior Checklist (parent and teacher forms). Scores on the outcome measures were summarized with descriptive statistics and then multivariate analyses of variance were conducted to determine the differences in psychosocial development between children with symmetric versus asymmetric craniofacial deformities and between the presence or absence of a functional impairment in children with craniofacial deformities. The results indicate that children with symmetric craniofacial deformities score poorer on measures of psychosocial adjustment than children with asymmetric deformities (F = 3.20, p < 0.015); however, differences among the groups with or without functional impairments were not significant. C1 CHILDRENS HOSP MED CTR,DEPT DENT,300 LONGWOOD AVE,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,ORAL & MAXILLOFACIAL SURG,BOSTON,MA 02114. HARVARD UNIV,SCH DENT MED,CAMBRIDGE,MA 02138. NR 20 TC 17 Z9 17 U1 0 U2 0 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 1055-6656 J9 CLEFT PALATE-CRAN J JI Cleft Palate-Craniofac. J. PD OCT PY 1991 VL 28 IS 4 BP 354 EP 359 DI 10.1597/1545-1569(1991)028<0354:PAICWH>2.3.CO;2 PG 6 WC Dentistry, Oral Surgery & Medicine; Surgery SC Dentistry, Oral Surgery & Medicine; Surgery GA GL604 UT WOS:A1991GL60400007 PM 1742303 ER PT J AU GROWDON, JH NADER, TM SCHOENFELD, J WURTMAN, RJ AF GROWDON, JH NADER, TM SCHOENFELD, J WURTMAN, RJ TI L-THREONINE IN THE TREATMENT OF SPASTICITY SO CLINICAL NEUROPHARMACOLOGY LA English DT Article DE L-THREONINE; GLYCINE; AMINO ACID; SPASTICITY ID PARAPLEGIA AB Preclinical data indicate that the administration of the amino acid L-threonine increases glycine levels in rat spinal cord. In order to investigate glycinergic mechanisms in spasticity, and other signs of the upper motor syndrome, we gave 4.5 and 6.0 g/day of L-threonine to 18 patients with familial spastic paraparesis (FSP) according to a double-blind, crossover protocol. The response to treatment at the end of each 2-week period was based upon three measures: the physician's global impressions; the patients' global impressions; and semiquantitative ratings of strength, muscle tone, DTRs, walking, hopping, and running. Blood and CSF were collected during each treatment period for amino acid analyses. Based upon the severity rating scales, there was a statistically significant (p < 0.02) decrease in motor impairment and spasticity during L-threonine administration compared to placebo treatment; significant treatment effects were not found on the physician's and patients' global impressions. Plasma and CSF levels of threonine increased significantly during L-threonine treatment but glycine levels did not change. These data indicate that L-threonine significantly suppressed the signs of spasticity even though the benefits were not clinically valuable. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. RP GROWDON, JH (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,ACC 830,BOSTON,MA 02114, USA. FU NCRR NIH HHS [5-M01-RR-01066] NR 25 TC 14 Z9 14 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-5664 J9 CLIN NEUROPHARMACOL JI Clin. Neuropharmacol. PD OCT PY 1991 VL 14 IS 5 BP 403 EP 412 DI 10.1097/00002826-199110000-00003 PG 10 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA GG341 UT WOS:A1991GG34100003 PM 1742749 ER PT J AU HODGE, WA AF HODGE, WA TI PREVENTION OF DEEP-VEIN THROMBOSIS AFTER TOTAL KNEE ARTHROPLASTY - COUMADIN VERSUS PNEUMATIC CALF COMPRESSION SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID VENOUS THROMBOEMBOLISM; REPLACEMENT AB The rate of deep vein thrombosis (DVT) after total knee arthroplasty (TKA) without prophylaxis has been reported as high as 84%. Coumadin anticoagulation and pneumatic calf compression (PCC) boots are two current therapies that have been thought to be effective in reducing this high rate of DVT. To investigate these two methods, a nonrandomized prospective study was designed. The first group involved treating 48 consecutive knee arthroplasties with a regimen of coumadin anticoagulation. The second group involved 81 consecutive knee arthroplasties treated with sequential PCC boots. Bilateral lower extremity venography was performed between the eighth and tenth hospital postoperative days. The overall incidence of DVT in the coumadin group was 33%, with 29% having calf thrombi and 6% having thigh thrombi. The overall incidence of DVT in the boot group was 31%, with 27% having calf thrombi and 6% having thigh thrombi. In both groups, there were no treatment-related complications. Cost analysis of the administration of each type of therapy showed coumadin to be approximately 50% more expensive than PCC boots. Although coumadin and PCC boot therapy are safe and effective in reducing the incidence of DVT after TKA, there are economic factors that make the latter a more favorable option. RP HODGE, WA (reprint author), MASSACHUSETTS GEN HOSP,5 LONGFELLOW PL 201,BOSTON,MA 02114, USA. NR 13 TC 14 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 OCT PY 1991 IS 271 BP 101 EP 105 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA GJ573 UT WOS:A1991GJ57300014 PM 1914282 ER PT J AU CHARLAND, SL DICKERSON, RN RAJTER, JJ SETTLE, RG AF CHARLAND, SL DICKERSON, RN RAJTER, JJ SETTLE, RG TI THE EFFECT OF SEPSIS ON HEPATIC CYTOCHROME-P-450 ACTIVITY IN PARENTERALLY FED RATS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 PHILADELPHIA COLL PHARM & SCI,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. RI Dickerson, Roland/C-5185-2008 NR 0 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD OCT PY 1991 VL 39 IS 3 BP A682 EP A682 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GF369 UT WOS:A1991GF36900125 ER PT J AU HAMMOND, TG ONORATO, JJ MORRE, DJ BRAZY, PC AF HAMMOND, TG ONORATO, JJ MORRE, DJ BRAZY, PC TI INCREASED SODIUM-DEPENDENT COTRANSPORT IN RENAL BRUSH-BORDER MEMBRANE-VESICLES (BBMVS) PURIFIED BY AQUEOUS 2 PHASE PARTITIONING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. PURDUE UNIV,W LAFAYETTE,IN 47907. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD OCT PY 1991 VL 39 IS 3 BP A771 EP A771 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GF369 UT WOS:A1991GF36900609 ER PT J AU ROUSH, GC BARNHILL, RL AF ROUSH, GC BARNHILL, RL TI THE CLINICAL DESIGNATION, DYSPLASTIC NEVUS, FROM INDIVIDUAL PIGMENTED LESION CHARACTERISTICS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CANC PREVENT RES INST,NEW YORK,NY. MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DERMATOL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD OCT PY 1991 VL 39 IS 3 BP A676 EP A676 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GF369 UT WOS:A1991GF36900097 ER PT J AU BECK, GJ BERG, RL COGGINS, CH GASSMAN, JJ HUNSICKER, LG SCHLUCHTER, MD WILLIAMS, GW AF BECK, GJ BERG, RL COGGINS, CH GASSMAN, JJ HUNSICKER, LG SCHLUCHTER, MD WILLIAMS, GW TI DESIGN AND STATISTICAL ISSUES OF THE MODIFICATION OF DIET IN RENAL-DISEASE TRIAL SO CONTROLLED CLINICAL TRIALS LA English DT Article DE RANDOMIZED; CLINICAL TRIAL; DIET; BLOOD PRESSURE; DESIGN; SLOPE; RENAL ID GLOMERULAR-FILTRATION-RATE; CLINICAL-TRIALS; PROTEIN RESTRICTION; LONGITUDINAL DATA; BLOOD-PRESSURE; PROGRESSION; FAILURE; INSUFFICIENCY; NEPHROPATHY; DIABETICS AB The Modification of Diet in Renal Disease Trial is a multicenter randomized clinical trial for men and women aged 18-70 years with chronic renal disease who are not on dialysis and who have not had a kidney transplant. Study participants are randomized in a 2 x 2 factorial design to diets containing different amounts of protein and phosphorus and to two levels of blood pressure control. The prescribed modifications differ depending on the level of a patient's kidney function. The primary outcome variable to compare diet or blood pressure groups is each patient's slope (or the change) in glomerular filtration rate with time. This paper describes the study design with particular emphasis on sample size determination. Special statistical analysis issues that arise with slope as the outcome are also discussed. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV IOWA,IOWA CITY,IA 52242. RP BECK, GJ (reprint author), CLEVELAND CLIN FDN,DEPT BIOSTAT & EPIDEMIOL,DESK P88,9500 EUCLID AVE,CLEVELAND,OH 44195, USA. NR 42 TC 66 Z9 66 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD OCT PY 1991 VL 12 IS 5 BP 566 EP 586 DI 10.1016/0197-2456(91)90069-X PG 21 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA GY822 UT WOS:A1991GY82200003 PM 1664792 ER PT J AU HARRIS, CL TONER, M HUBEL, A CRAVALHO, EG YARMUSH, ML TOMPKINS, RG AF HARRIS, CL TONER, M HUBEL, A CRAVALHO, EG YARMUSH, ML TOMPKINS, RG TI CRYOPRESERVATION OF ISOLATED HEPATOCYTES - INTRACELLULAR ICE FORMATION UNDER VARIOUS CHEMICAL AND PHYSICAL CONDITIONS SO CRYOBIOLOGY LA English DT Article ID GAS BUBBLE FORMATION; ISOLATED PROTOPLASTS; COOLING RATE; GRANULOCYTES; NUCLEATION; VIABILITY; SURVIVAL; EMBRYOS; CELLS; OVA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02139. MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. NR 32 TC 31 Z9 35 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0011-2240 J9 CRYOBIOLOGY JI Cryobiology PD OCT PY 1991 VL 28 IS 5 BP 436 EP 444 DI 10.1016/0011-2240(91)90052-P PG 9 WC Biology; Physiology SC Life Sciences & Biomedicine - Other Topics; Physiology GA GJ432 UT WOS:A1991GJ43200005 PM 1752131 ER PT J AU GORELICK, FS AF GORELICK, FS TI PANCREAS - EDITORIAL OVERVIEW SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Editorial Material RP GORELICK, FS (reprint author), US DEP VET AFFAIRS,ADM OFF RES SERV,950 CAMPBELL AVE,W HAVEN,CT 06516, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD OCT PY 1991 VL 7 IS 5 BP 687 EP 690 DI 10.1097/00001574-199110000-00001 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GH010 UT WOS:A1991GH01000001 ER PT J AU SHAHANI, B CROS, D AF SHAHANI, B CROS, D TI MOTOR UNIT VOLUNTARY RECRUITMENT SO CURRENT OPINION IN NEUROLOGY AND NEUROSURGERY LA English DT Article ID MOTONEURON FIRING RATES; MAGNETIC STIMULATION; HUMAN-BRAIN; CONTRACTIONS; FATIGUE; ACTIVATION; RESPONSES; PATTERNS; MUSCLES; CORTEX AB The combined roles of spatial and temporal recruitment of motor units in the adjustment of force output are well known. In this review, recent information concerning the regulatory factors of motor unit recruitment and firing patterns are reviewed. These new data include futher studies on motor innervation of antagonistic muscles, clinical quantification of recruitment, changes in motor unit firing rate during fatiguing contractions, and the possible neural factor underlying these changes. Abnormalities of motor unit firing pattern in relation to lesions of the central nervous system are also reviewed. Finally, the effects of transcortical magnetic stimulation on single motor unit firing patterns are discussed. RP SHAHANI, B (reprint author), MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LAB,BOSTON,MA 02114, USA. NR 27 TC 0 Z9 0 U1 0 U2 0 PU CURRENT SCIENCE LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0951-7383 J9 CURR OPIN NEUROL NEU PD OCT PY 1991 VL 4 IS 5 BP 756 EP 759 PG 4 WC Neurosciences SC Neurosciences & Neurology GA GH009 UT WOS:A1991GH00900019 ER PT J AU SHORE, JW BILYK, JR AF SHORE, JW BILYK, JR TI CLINICAL PRESENTATION, DIAGNOSIS, AND TREATMENT OF EYELID TUMORS SO CURRENT OPINION IN OPHTHALMOLOGY LA English DT Review AB Eyelid tumors continue to be relatively common periocular lesions. Because of the many types of neoplasms that can potentially occur on the eyelids, as well as the varied clinical presentation of each individual type, the need for biopsy and careful histopathologic examination cannot be overemphasized. A review of adenocystic carcinoma of the lacrimal gland, sebaceous gland carcinoma, and Merkel cell carcinoma of the eyelids is presented, along with reviews of other rare lesions. Clinical presentation and diagnostic modalities, including computed tomography, histopathology, immunohistochemistry, and electron microscopy are discussed. Management options including surgery, cryotherapy, and radiotherapy are also discussed. RP SHORE, JW (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,50 STANIFORD ST,3RD FLOOR,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 1040-8738 J9 CURR OPIN OPHTHALMOL PD OCT PY 1991 VL 2 IS 5 BP 579 EP 589 DI 10.1097/00055735-199110000-00010 PG 11 WC Ophthalmology SC Ophthalmology GA GJ707 UT WOS:A1991GJ70700010 ER PT J AU SOBER, AJ LEW, RA KOH, HK BARNHILL, RL AF SOBER, AJ LEW, RA KOH, HK BARNHILL, RL TI EPIDEMIOLOGY OF CUTANEOUS MELANOMA - AN UPDATE SO DERMATOLOGIC CLINICS LA English DT Article RP SOBER, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT DERMATOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 51 Z9 51 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8635 J9 DERMATOL CLIN JI Dermatol. Clin. PD OCT PY 1991 VL 9 IS 4 BP 617 EP 629 PG 13 WC Dermatology SC Dermatology GA GL856 UT WOS:A1991GL85600002 PM 1934636 ER PT J AU AXELROD, L AF AXELROD, L TI PERSPECTIVES IN DIABETES - INSULIN, PROSTAGLANDINS, AND THE PATHOGENESIS OF HYPERTENSION SO DIABETES LA English DT Article ID TISSUE BLOOD-FLOW; FATTY-ACID REESTERIFICATION; SYMPATHETIC NERVOUS-SYSTEM; ISOLATED RAT ADIPOCYTES; ADIPOSE-TISSUE; PROSTACYCLIN PRODUCTION; ENDOTHELIAL-CELLS; CULTURED HUMAN; INTRAVENOUS-INFUSION; STIMULATION AB Hypertension is associated with hyperinsulinemia in the presence or absence of obesity or glucose intolerance. Physiological concentrations of insulin decrease the catecholamine-induced production of prostaglandin I2 (PGI2; prostacyclin) and PGE2, two potent vasodilators, in adipose tissue, one of the largest organs in the body. This finding suggests that hyperinsulinemia increases peripheral vascular resistance and blood pressure by inhibiting the stimulatory effect of adrenergic agonists (and perhaps other agonists) on the production of PGI2 and PGE2 in adipose tissue (and perhaps other tissues). This concept is supported by evidence that PGI2 and PGE2 modulate vascular reactivity in states of health and disease. For example, during insulin deficiency, i.e., in diabetic ketoacidosis, PGI2 and PGE2 production by adipose tissue are increased, and peripheral vascular resistance and blood pressure are decreased. This hypothesis is also supported by evidence that blood flow through rat and human adipose tissue is decreased in obesity and that insulin decreases the blood flow through adipose tissue in nonobese rats. Thus, insulin may regulate PGI2 and PGE2 production by adipose tissue (and possibly other tissues) through a wide range of concentrations with important physiological and clinical consequences. C1 HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, MED SERV, BOSTON, MA 02114 USA. RP AXELROD, L (reprint author), MASSACHUSETTS GEN HOSP, DIABET UNIT, BOSTON, MA 02114 USA. NR 65 TC 42 Z9 44 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD OCT PY 1991 VL 40 IS 10 BP 1223 EP 1227 DI 10.2337/diabetes.40.10.1223 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GG608 UT WOS:A1991GG60800001 PM 1936584 ER PT J AU SCHNEYER, AL SLUSS, PM WHITCOMB, RW MARTIN, KA SPRENGEL, R CROWLEY, WF AF SCHNEYER, AL SLUSS, PM WHITCOMB, RW MARTIN, KA SPRENGEL, R CROWLEY, WF TI PRECURSORS OF ALPHA-INHIBIN MODULATE FOLLICLE-STIMULATING-HORMONE RECEPTOR-BINDING AND BIOLOGICAL-ACTIVITY SO ENDOCRINOLOGY LA English DT Article ID RAT GRANULOSA-CELLS; GROWTH FACTOR-BETA; FACTOR-I; LUTEINIZING-HORMONE; PARATHYROID-HORMONE; AROMATASE-ACTIVITY; FLUID CONTAINS; HUMAN SERUM; SUBUNIT; INSULIN AB Although several forms of monomeric alpha-inhibin have been isolated from follicular fluid, no biological function has yet been ascribed to these posttranslationally processed forms of the alpha-subunit precursor protein. Moreover, previous studies of a FSH receptor binding competitor (FRBC) isolated and characterized from porcine follicular fluid (pFF) suggested certain biochemical similarities between this protein and alpha-inhibin precursors. We, therefore, investigated the hypothesis that alpha-inhibin and/or its precursors might represent autocrine and/or paracrine modulators of FSH action in the ovary, accounting for some of this FRBC activity and thereby exerting some degree of regulation over follicular maturation. Three separate sources of alpha-inhibin proteins were investigated for FRBC activity, including pFF, human FF (hFF), and a 293 cell line into which the full-length human alpha-inhibin cDNA had been stably transfected. Conditioned medium from these transfected cells contained several forms of alpha-inhibin precursors as well as mature alpha-inhibin, but no beta-subunit or intact inhibin. Alpha-Inhibin proteins from all three sources, purified by a variety of methods, including immunoaffinity chromatography on an anti-alpha-inhibin column, inhibited FSH binding to both natural tissue FSH receptors as well as recombinant rat FSH receptors expressed in 293 cells. Furthermore, dimeric inhibin and activin, medium from untransfected 293 cells, and non-alpha-inhibin-containing purification fractions were inactive in either assay. In addition, purified recombinant alpha-inhibin proteins were partial in vitro FSH antagonists in a bioassay in which cAMP generation from 293 cells expressing the recombinant FSH receptor is used as an index of FSH biological activity. These same fractions of hFF containing FRBC activity did not bind to LH receptors, thereby demonstrating receptor specificity for this activity. Using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting with alpha-inhibin or FRBC antisera, a 57,000 mol wt protein was identified in FRBC-active fractions from all three sources, suggesting that the active moiety was the full-length alpha-inhibin precursor protein or a large mol wt fragment, but not mature alpha-inhibin. Lastly, all FRBC activity from all three sources was extracted by an alpha-inhibin immunoaffinity column and was recoverable upon elution. These results demonstrate that proteins derived from the alpha-inhibin precursor modulate FSH binding to its receptor as well as its biological activity. Since alpha-inhibin precursors have been reported in FF at concentrations exceeding 2.5-mu-g/ml, the potency of the FSH antagonism determined for alpha-inhibin is consistent with a potential physiological role for alpha-inhibin as an autocrine or paracrine FSH modulator. C1 UNIV ROCHESTER, MED CTR, DEPT UROL, ROCHESTER, NY 14642 USA. UNIV HEIDELBERG, CTR MOLEC BIOL, MOLEC NEUROENDOCRINOL LAB, W-6900 HEIDELBERG, GERMANY. RP HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED, REPROD ENDOCRINOL UNIT, BHX-5, BOSTON, MA 02114 USA. FU NICHD NIH HHS [U01 HD044417, HD-25941, HD-15080, HD-19302] NR 56 TC 129 Z9 130 U1 2 U2 2 PU ENDOCRINE SOC PI WASHINGTON PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD OCT PY 1991 VL 129 IS 4 BP 1987 EP 1999 PG 13 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GH336 UT WOS:A1991GH33600042 PM 1915079 ER PT J AU YAMAGUCHI, Y FLIER, JS YOKOTA, A BENECKE, H BACKER, JM MOLLER, DE AF YAMAGUCHI, Y FLIER, JS YOKOTA, A BENECKE, H BACKER, JM MOLLER, DE TI FUNCTIONAL-PROPERTIES OF 2 NATURALLY-OCCURRING ISOFORMS OF THE HUMAN INSULIN-RECEPTOR IN CHINESE-HAMSTER OVARY CELLS SO ENDOCRINOLOGY LA English DT Article ID TYROSINE KINASE-ACTIVITY; STRUCTURAL DIFFERENCES; ENDOCYTIC SYSTEM; MESSENGER-RNA; GROWTH-FACTOR; BINDING; HORMONE; INTERNALIZATION; MUTATION; REPLACEMENT AB We and others have previously demonstrated that the human insulin receptor messenger RNA (mRNA) is alternatively spliced such that the 36-nucleotide sequence encoded by exon 11 of the receptor gene is included (Ex11+) or excluded (Ex11-). Although both Ex11- and Ex11+ insulin receptors which differ in the presence or absence of 12 amino acids in the carboxy-terminal alpha-subunit have been demonstrated to function as insulin receptors when independently overexpressed and studied, the possibility that subtle functional differences between the two isoforms exists has received limited attention. Given that the relative abundance of the two mRNA transcripts is highly regulated in a tissue-specific manner, differences in the functional properties of the two receptor variants might contribute to tissue-specific differences in insulin receptor function and insulin action that are known to exist. To address this hypothesis, we transfected cDNAs encoding the two receptor isoforms into Chinese hamster ovary (CHO) cells and prepared several stable CHO cell lines expressing high numbers of Ex11- or Ex11+ receptors. Several functional properties of the expressed insulin receptors were compared in parallel with the following results: 1) steady state binding of insulin to cells expressing the Ex11- isoform exhibited higher (almost-equal-to 2-fold) affinity; 2) using two different methods, a significant difference in receptor-mediated insulin internalization was noted such that the Ex11- isoform displayed a higher (almost-equal-to 25% increase in the rate constant, K(e)) rate of internalization; 3) partially purified Ex11- and Ex11+ receptors displayed similar maximal and insulin dose-response characteristics for receptor autophosphorylation and kinase activity toward an exogenous substrate (poly Glu-Tyr, 4:1); 4) the ability of expressed Ex11- and Ex11+ receptors to couple to a metabolic (glucose incorporation into glycogen) and mitogenic (thymidine incorporation into DNA) action of insulin was not discernibly different. Thus, when expressed in CHO cells, the two alternatively spliced isoforms of the insulin receptor have subtle differences in insulin binding affinity and the kinetics of ligand-stimulated internalization that would be expected to influence the pattern of insulin receptor expression and signaling in vivo in a tissue-specific manner. C1 BETH ISRAEL HOSP,SL 436,330 BROOKLINE AVE,BOSTON,MA 02215. BETH ISRAEL HOSP,CHARLES A DANA RES INST,DEPT MED,BOSTON,MA 02215. BETH ISRAEL HOSP,THORNDIKE LAB,DEPT MED,BOSTON,MA 02215. JOSLIN DIABET CTR,DEPT MED,DIV RES,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02215. FU NIDDK NIH HHS [NIDDK 28082-10] NR 42 TC 125 Z9 128 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD OCT PY 1991 VL 129 IS 4 BP 2058 EP 2066 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GH336 UT WOS:A1991GH33600051 PM 1655392 ER PT J AU SIEFF, CA AF SIEFF, CA TI NEW HATS FOR HEMATOPOIETIC HORMONES SO EXPERIMENTAL HEMATOLOGY LA English DT Editorial Material ID COLONY-STIMULATING FACTOR; GROWTH-FACTOR; MOLECULAR-CLONING; CSF RECEPTOR; GM-CSF; INTERLEUKIN-3-DEPENDENT PROLIFERATION; PROGENITOR CELLS; EXPRESSION; DIFFERENTIATION; SUPERFAMILY C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. RP SIEFF, CA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL & HEMATOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 28 TC 3 Z9 3 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 OCT PY 1991 VL 19 IS 9 BP 857 EP 860 PG 4 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA GH135 UT WOS:A1991GH13500001 PM 1893960 ER PT J AU WIGHTMAN, B BURGLIN, TR GATTO, J ARASU, P RUVKUN, G AF WIGHTMAN, B BURGLIN, TR GATTO, J ARASU, P RUVKUN, G TI NEGATIVE REGULATORY SEQUENCES IN THE LIN-14 3'-UNTRANSLATED REGION ARE NECESSARY TO GENERATE A TEMPORAL SWITCH DURING CAENORHABDITIS-ELEGANS DEVELOPMENT SO GENES & DEVELOPMENT LA English DT Article DE C-ELEGANS; LIN-14; HETEROCHRONIC GENE; GAIN-OF-FUNCTION MUTATION; 3' UTR ID ECDYSONE-INDUCIBLE GENE; C-ELEGANS; PATTERN-FORMATION; MESSENGER-RNA; MOLECULAR-GENETICS; EARLY PUFF; ENCODES 2; DROSOPHILA; PROTEINS; BINDING AB The heterochronic gene lin-14 controls the temporal sequence of developmental events in the Caenorhabditis elegans postembryonic cell lineage. It encodes a nuclear protein that normally is present in most somatic cells of late embryos and L1 larvae but is absent at later stages. Two lin-14 gain-of-function mutations delete 3'-untranslated sequences causing an inappropriately high level of the lin-14 nuclear protein late in development. These mutations identify a negative regulatory element that controls the formation of the lin-14 protein temporal gradient. The 21-kb lin-14 gene is differentially spliced to generate three lin-14 transcripts that encode protein products with variable amino-terminal regions and a constant carboxy-terminal region. The sequence of the gene revealed no protein sequence similarity to any proteins in various data bases. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP WIGHTMAN, B (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. OI arasu, prema/0000-0003-1962-8773 NR 35 TC 120 Z9 129 U1 1 U2 7 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 OCT PY 1991 VL 5 IS 10 BP 1813 EP 1824 DI 10.1101/gad.5.10.1813 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA GJ654 UT WOS:A1991GJ65400009 PM 1916264 ER PT J AU ARASU, P WIGHTMAN, B RUVKUN, G AF ARASU, P WIGHTMAN, B RUVKUN, G TI TEMPORAL REGULATION OF LIN-14 BY THE ANTAGONISTIC ACTION OF 2 OTHER HETEROCHRONIC GENES, LIN-4 AND LIN-28 SO GENES & DEVELOPMENT LA English DT Article DE LIN-14; LIN-4; LIN-28; LIN-29; HETEROCHRONIC GENES; C-ELEGANS; DEVELOPMENTAL SWITCH ID CAENORHABDITIS-ELEGANS; DEVELOPMENTAL SWITCH; C-ELEGANS; EXPRESSION; GENETICS AB Heterochronic genes form a regulatory pathway that controls the temporal sequence of the Caenorhabditis elegans postembryonic cell lineage. One of these genes, lin-14, encodes a nuclear protein that constitutes a temporal developmental switch. During wild-type development, lin-14 protein is abundant during early larval stage 1 (L1) to specify L1-specific cell lineages but is nearly undetectable at L2 and later stages to specify L2-specific and later cell lineages. To determine the roles played by other genes in executing this temporal switch, we have analyzed how lin-14 expression is regulated by other heterochronic genes. lin-4 is required to down-regulate lin-14 protein levels during the L1 stage, whereas lin-28 positively regulates lin-14 protein levels. The lin-4 gene product is a candidate for interacting with the negative regulatory element in the 3'-untranslated region of lin-14. lin-29 mutations do not affect lin-14 protein levels, consistent with lin-29 acting downstream of lin-14. Switching off lin-14 expression during the L1 stage is not triggered by the passage of time per se but, rather, is normally dependent on feeding or the feeding-dependent initiation of postembryonic cell division. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP ARASU, P (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. OI arasu, prema/0000-0003-1962-8773 NR 12 TC 80 Z9 85 U1 2 U2 3 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 OCT PY 1991 VL 5 IS 10 BP 1825 EP 1833 DI 10.1101/gad.5.10.1825 PG 9 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA GJ654 UT WOS:A1991GJ65400010 PM 1916265 ER PT J AU BIGGS, PJ AF BIGGS, PJ TI CALCULATION OF SHIELDING DOOR THICKNESSES FOR RADIATION-THERAPY FACILITIES USING THE ITS MONTE-CARLO PROGRAM SO HEALTH PHYSICS LA English DT Article AB Shielding calculations for door thicknesses for megavoltage radiotherapy facilities with mazes are generally straightforward. To simplify the calculations, the standard formalism adopts several approximations relating to the average beam path, scattering coefficients, and the mean energy of the spectrum of scattered radiation. To test the accuracy of these calculations, the Monte Carlo program, ITS, was applied to this problem by determining the dose and energy spectrum of the radiation at the door for 4- and 10-MV bremsstrahlung beams incident on a phantom at isocenter. This was performed for mazes, one termed "standard" and the other a shorter maze where the primary beam is incident on the wall adjacent to the door. The peak of the photon-energy spectrum at the door was found to be the same for both types of maze, independent of primary beam energy, and also, in the case of the conventional maze, of the primary beam orientation. The spectrum was harder for the short maze and for 10 MV vs. 4 MV. The thickness of the lead door for a short maze configuration was 1.5 cm for 10 MV and 1.2 cm for 4 MV vs. approximately < 1 mm for a conventional maze. For the conventional maze, the Monte Carlo calculation predicts the dose at the door to be lower than given by NCRP 49 and NCRP 51 by about a factor of 2 at 4 MV but to be the same at 10 MV. For the short maze, the Monte Carlo predicts the dose to be a factor of 3 lower for 4 MV and about a factor of 1.5 lower for 10 MV. Experimental results support the Monte Carlo findings for the short maze. RP BIGGS, PJ (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, DEPT RADIAT ONCOL, BOSTON, MA 02114 USA. NR 11 TC 8 Z9 8 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PD OCT PY 1991 VL 61 IS 4 BP 465 EP 472 DI 10.1097/00004032-199110000-00001 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA GH834 UT WOS:A1991GH83400001 PM 1917483 ER PT J AU FREEDMAN, AS NADLER, LM AF FREEDMAN, AS NADLER, LM TI IMMUNOLOGICAL MARKERS IN NON-HODGKINS-LYMPHOMA SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; T-CELL LEUKEMIA; HUMAN LYMPHOCYTES-B; TRANSFERRIN RECEPTOR EXPRESSION; MALIGNANT GERMINAL-CENTER; MONOCLONAL-ANTIBODY; ANTIGEN CALLA; IMMUNOBLASTIC LYMPHOMA; NEUTRAL ENDOPEPTIDASE; CLINICAL-FEATURES C1 HARVARD UNIV,SCH MED,MED,BOSTON,MA 02115. RP FREEDMAN, AS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 154 TC 49 Z9 51 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD OCT PY 1991 VL 5 IS 5 BP 871 EP 889 PG 19 WC Oncology; Hematology SC Oncology; Hematology GA GF402 UT WOS:A1991GF40200004 PM 1938759 ER PT J AU WANDS, JR BLUM, HE AF WANDS, JR BLUM, HE TI HEPATITIS-B AND C-VIRUS AND ALCOHOL-INDUCED LIVER-INJURY SO HEPATOLOGY LA English DT Editorial Material ID POLYMERASE CHAIN-REACTION; NON-A-HEPATITIS; HEPATOCELLULAR-CARCINOMA; ANTIBODIES; GENOME; SERUM; DNA; IDENTIFICATION; PREVALENCE; ASSAY RP WANDS, JR (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,149 13TH ST,BOSTON,MA 02129, USA. NR 35 TC 15 Z9 15 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 OCT PY 1991 VL 14 IS 4 BP 730 EP 733 DI 10.1016/0270-9139(91)90065-4 PN 1 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GH580 UT WOS:A1991GH58000024 PM 1655608 ER PT J AU BLUM, HE ZHANG, ZS GALUN, E VONWEIZSACKER, F LIANG, TJ WANDS, JR AF BLUM, HE ZHANG, ZS GALUN, E VONWEIZSACKER, F LIANG, TJ WANDS, JR TI HEPATITIS-B VIRUS X-GENE FUNCTION - X-ANTIGEN IS NOT REQUIRED FOR VIRAL REPLICATION AND GENE-EXPRESSION SO HEPATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02129. 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A91 EP A91 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100172 ER PT J AU CHUNG, RT MCHUTCHISON, JG PERSON, JL REDEKER, AG DIENSTAG, JL KAPLAN, LM AF CHUNG, RT MCHUTCHISON, JG PERSON, JL REDEKER, AG DIENSTAG, JL KAPLAN, LM TI A NONREACTIVE RECOMBINANT IMMUNOBLOT ASSAY (RIBA) DOES NOT EXCLUDE HEPATITIS-C VIRUS (HCV) INFECTION IN PATIENTS WITH SPORADIC NON-A, NON-B HEPATITIS SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. UNIV SO CALIF, DIV GASTROINTESTINAL & LIVER DIS, LOS ANGELES, CA 90089 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A65 EP A65 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100071 ER PT J AU CHUNG, RT DIENSTAG, JL KAPLAN, LM AF CHUNG, RT DIENSTAG, JL KAPLAN, LM TI PRECISE QUANTITATION OF HEPATITIS-C RNA USING A COMPETITIVE POLYMERASE CHAIN-REACTION - CORRELATION OF CLINICAL COURSE WITH LEVELS OF CIRCULATING RNA SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A65 EP A65 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100069 ER PT J AU HASEGAWA, K HUANG, JK BLUM, HE WANDS, JR BENPORATH, E LIANG, TJ AF HASEGAWA, K HUANG, JK BLUM, HE WANDS, JR BENPORATH, E LIANG, TJ TI INVITRO CHARACTERIZATION OF HBV MUTANTS ASSOCIATED WITH FULMINANT-HEPATITIS SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC HEPATOL & GI UNIT,BOSTON,MA 02114. RAMBAM MED CTR,VIROL LAB,HAIFA,ISRAEL. 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A206 EP A206 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100634 ER PT J AU HASEGAWA, K SHAPIRO, CN ALTER, MJ LIANG, TJ AF HASEGAWA, K SHAPIRO, CN ALTER, MJ LIANG, TJ TI LACK OF AN ASSOCIATION OF HEPATITIS-B VIRUS PRECORE MUTATIONS WITH FULMINANT HEPATITIS-B IN USA SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC HEPATOL & GASTROINTESTINAL UNIT,BOSTON,MA 02114. CTR DIS CONTROL,HEPATITIS BRANCH,ATLANTA,GA 30333. 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A78 EP A78 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100120 ER PT J AU JEFFERS, L LALOS, A FINDOR, A REDDY, R SILVA, M GEORGE, G LARUE, S DEMEDINA, M REINDOLLAR, R SCHIFF, E LIANG, J AF JEFFERS, L LALOS, A FINDOR, A REDDY, R SILVA, M GEORGE, G LARUE, S DEMEDINA, M REINDOLLAR, R SCHIFF, E LIANG, J TI HEPATITIS-C VIRAL-RNA IN RIBA-2 INDETERMINATE AND RIBA-2 NEGATIVE PATIENTS WITH CHRONIC LIVER-DISEASE SO HEPATOLOGY LA English DT Meeting Abstract C1 UNIV MIAMI, SCH MED, DIV HEPATOL, MIAMI, FL 33152 USA. VET ADM MED CTR, MIAMI, FL 33125 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A207 EP A207 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100638 ER PT J AU KATKOV, WN DIENSTAG, JL RUBIN, RH DELMONICO, F AUCHINCLOSS, H COSIMI, AB AF KATKOV, WN DIENSTAG, JL RUBIN, RH DELMONICO, F AUCHINCLOSS, H COSIMI, AB TI CONSERVATIVE MANAGEMENT OF BILE LEAKS FOLLOWING T-TUBE REMOVAL IN LIVER-TRANSPLANT PATIENTS SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,TRANSPLANTAT UNIT,BOSTON,MA 02114. NR 0 TC 6 Z9 6 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 OCT PY 1991 VL 14 IS 4 BP A51 EP A51 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100014 ER PT J AU LEFKOWITCH, JH SCHIFF, ER DAVIS, GL PERRILLO, RP LINDSAY, K BODENHEIMER, HC BALART, LA ORTEGA, TJ PAYNE, J DIENSTAG, JL GIBAS, A JACOBSON, IM TAMBURRO, C CAREY, W SAMPLINER, R VANTHIEL, DH FEIT, D ALBRECHT, J MESCHIEVITZ, C SANGHVI, B AF LEFKOWITCH, JH SCHIFF, ER DAVIS, GL PERRILLO, RP LINDSAY, K BODENHEIMER, HC BALART, LA ORTEGA, TJ PAYNE, J DIENSTAG, JL GIBAS, A JACOBSON, IM TAMBURRO, C CAREY, W SAMPLINER, R VANTHIEL, DH FEIT, D ALBRECHT, J MESCHIEVITZ, C SANGHVI, B TI HISTOLOGIC FEATURES OF HEPATITIS-C (HC) - COMPARISON WITH HEPATITIS-B (HB) IN 2 MULTICENTER TRIALS OF RECOMBINANT ALPHA-INTERFERON (RIFN) THERAPY (RX) SO HEPATOLOGY LA English DT Meeting Abstract C1 COLUMBIA UNIV,NEW YORK,NY 10027. UNIV MIAMI,CORAL GABLES,FL 33124. UNIV FLORIDA,GAINESVILLE,FL 32611. WASHINGTON UNIV,ST LOUIS,MO 63130. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. BROWN UNIV,PROVIDENCE,RI 02912. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA 70121. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CORNELL UNIV,MED CTR,NEW YORK HOSP,NEW YORK,NY 10021. UNIV LOUISVILLE,LOUISVILLE,KY 40292. CLEVELAND CLIN,CLEVELAND,OH 44106. VET ADM MED CTR,TUCSON,AZ 85723. UNIV PITTSBURGH,PITTSBURGH,PA 15260. SCHERING PLOUGH CORP,BLOOMFIELD,NJ 07003. CONNAUGHT LABS LTD,N YORK M2N 5T8,ONTARIO,CANADA. RUSH PRESBYTERIAN HOSP,CHICAGO,IL. NR 2 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A129 EP A129 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100326 ER PT J AU LEVEILLE, C WEISSLEDER, R GATMAITAN, Z ARIAS, IM AF LEVEILLE, C WEISSLEDER, R GATMAITAN, Z ARIAS, IM TI SERIAL QUANTITATION BY SEROLOGY AND ASIALOGLYCOPROTEIN RECEPTOR-SPECIFIC NMR IMAGING OF WILD-TYPE AND MULTIDRUG RESISTANT HUMAN HEPATOCELLULAR-CARCINOMA IN SCID MICE SO HEPATOLOGY LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,CTR NUCL MAGNET RESONANCE,BOSTON,MA 02114. NR 0 TC 2 Z9 2 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 OCT PY 1991 VL 14 IS 4 BP A109 EP A109 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100245 ER PT J AU LIANG, TJ RUSTGI, V AF LIANG, TJ RUSTGI, V TI PERSISTENCE OF HCV GENOMES IN PATIENTS TREATED WITH ALPHA-INTERFERON SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC HEPATOL & GASTROINTESTINAL UNIT,BOSTON,MA 02114. FAIRFAX HOSP,DEPT MED,FALLS CHURCH,VA 22046. 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A211 EP A211 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100654 ER PT J AU LIANG, TJ JEFFERS, L FINDOR, A REDDY, R SILVA, M DEMEDINA, M SCHIFF, E AF LIANG, TJ JEFFERS, L FINDOR, A REDDY, R SILVA, M DEMEDINA, M SCHIFF, E TI LACK OF EVIDENCE FOR HEPATITIS-C VIRUS-INFECTION IN NON-A, NON-B FULMINANT AND LATE-ONSET HEPATIC-FAILURE SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC HEPATOL & GASTROINTESTINAL UNIT,BOSTON,MA 02114. UNIV MIAMI,SCH MED,MIAMI,FL 33152. VET ADM MED CTR,MIAMI,FL 33125. NR 0 TC 6 Z9 6 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 OCT PY 1991 VL 14 IS 4 BP A129 EP A129 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100324 ER PT J AU MCHUTCHISON, JG CHUNG, RT REDEKER, AG DIENSTAG, JL KAPLAN, LM AF MCHUTCHISON, JG CHUNG, RT REDEKER, AG DIENSTAG, JL KAPLAN, LM TI LOSS OF SEROLOGIC MARKERS AND VIRAL-RNA DOES NOT RELIABLY PREDICT ERADICATION OF CHRONIC HEPATITIS-C VIRUS-INFECTION SO HEPATOLOGY LA English DT Meeting Abstract C1 UNIV SO CALIF,DIV GASTROINTESTINAL & LIVER DIS,LOS ANGELES,CA 90089. 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A79 EP A79 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100125 ER PT J AU OZTURK, M BRESSAC, B PUISIEUX, A KEW, M VOLKMANN, M BOZCALI, S MURA, JB DELAMONTE, S CARLSON, R BLUM, H WANDS, J TAKAHASHI, H VONWEIZSACKER, F GALUN, E KAR, S CARR, B SCHRODER, C ERKEN, E VARINLI, S RUSTGI, V PRAT, J TODA, G KOCH, H LIANG, X TANG, Z SHOUVAL, D LEE, H VYAS, G SAROSI, I AF OZTURK, M BRESSAC, B PUISIEUX, A KEW, M VOLKMANN, M BOZCALI, S MURA, JB DELAMONTE, S CARLSON, R BLUM, H WANDS, J TAKAHASHI, H VONWEIZSACKER, F GALUN, E KAR, S CARR, B SCHRODER, C ERKEN, E VARINLI, S RUSTGI, V PRAT, J TODA, G KOCH, H LIANG, X TANG, Z SHOUVAL, D LEE, H VYAS, G SAROSI, I TI P53 HOTSPOT MUTATION IN HEPATOCELLULAR-CARCINOMA IS LINKED TO AFLATOXIN EXPOSURE SO HEPATOLOGY LA English DT Meeting Abstract C1 SHANGHAI MED UNIV,SHANGHAI,PEOPLES R CHINA. HADASSAH UNIV HOSP,JERUSALEM,ISRAEL. INST PATHOL,HEMER,GERMANY. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA. UNIV WITWATERSRAND,JOHANNESBURG 2001,SOUTH AFRICA. GERMAN CANC RES CTR,W-6900 HEIDELBERG 1,GERMANY. HOSP SANTA CRUZ & SAN PABLO,BARCELONA,SPAIN. UNIV PITTSBURGH,PITTSBURGH,PA 15260. CUKUROVA UNIV,ADANA,TURKEY. JIKEI UNIV,TOKYO,JAPAN. SEOUL NATL UNIV,SEOUL 151,SOUTH KOREA. FAIRFAX HOSP,FALLS CHURCH,VA 22046. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. RI ozturk, mehmet/G-3330-2014 NR 0 TC 0 Z9 0 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 OCT PY 1991 VL 14 IS 4 BP A94 EP A94 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100185 ER PT J AU PACE, R OSULLIVAN, B SCOTT, J WANDS, J COOKSLEY, WGE AF PACE, R OSULLIVAN, B SCOTT, J WANDS, J COOKSLEY, WGE TI A HEPATITIS-B VIRUS (HBV) VARIANT IN AUSTRALIAN ABORIGINES SO HEPATOLOGY LA English DT Meeting Abstract C1 ROYAL BRISBANE HOSP FDN,BRISBANE,AUSTRALIA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI cooksley, william/G-7742-2011 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A215 EP A215 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100669 ER PT J AU PUISIEUX, A PONCHEL, F OZTURK, M AF PUISIEUX, A PONCHEL, F OZTURK, M TI EXPRESSION OF WILD-TYPE P53 IS NOT COMPATIBLE WITH THE GROWTH OF HEPATOCELLULAR-CARCINOMA CELLS SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA. RI ozturk, mehmet/G-3330-2014 NR 0 TC 0 Z9 0 U1 0 U2 2 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 OCT PY 1991 VL 14 IS 4 BP A108 EP A108 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100243 ER PT J AU ROSELLE, G MENDENHALL, C MORITZ, T WEESNER, R AF ROSELLE, G MENDENHALL, C MORITZ, T WEESNER, R TI IMMUNOLOGICAL PREDICTOR VARIABLES FOR SURVIVAL IN PATIENTS WITH MODERATE AND SEVERE ALCOHOLIC HEPATITIS (AH) SO HEPATOLOGY LA English DT Meeting Abstract C1 US DEPT VET AFFAIRS,WASHINGTON,DC. 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A235 EP A235 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100747 ER PT J AU SHIOTA, G RHOADS, DB NAKAMURA, T SCHMIDT, EV AF SHIOTA, G RHOADS, DB NAKAMURA, T SCHMIDT, EV TI HEPATOCYTE GROWTH-FACTOR INHIBITS GROWTH OF HEPATOCELLULAR-CARCINOMA CELLS SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA. KYUSHU UNIV,FAC SCI,DEPT BIOL,FUKUOKA 812,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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A111 EP A111 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100255 ER PT J AU SPEEG, KV MALDONADO, AL MUIRHEAD, D AF SPEEG, KV MALDONADO, AL MUIRHEAD, D TI THE INVIVO EFFECT OF CYCLOSPORINE (CSA) ON COLCHICINE SECRETION BY THE LIVER CANALICULAR MULTIDRUG TRANSPORTER SO HEPATOLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A163 EP A163 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100463 ER PT J AU TAKAHASHI, H NAKADA, T PUISIEUX, I CARLSON, R WANDS, JR AF TAKAHASHI, H NAKADA, T PUISIEUX, I CARLSON, R WANDS, JR TI TARGETING LAK CELLS TO INTRAHEPATIC TUMORS REQUIRES SPECIFIC ANTIBODY THAT BINDS TUMOR-CELL SURFACE-ANTIGEN SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A126 EP A126 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100314 ER PT J AU WEESNER, R MENDENHALL, C MORITZ, T ROSELLE, G AF WEESNER, R MENDENHALL, C MORITZ, T ROSELLE, G TI THE CLINICAL-SIGNIFICANCE OF LIVER-SPLEEN SCANS IN PATIENTS WITH MODERATE TO SEVERE ALCOHOLIC HEPATITIS SO HEPATOLOGY LA English DT Meeting Abstract C1 US DEPT VET AFFAIRS,WASHINGTON,DC. 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1991 VL 14 IS 4 BP A236 EP A236 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GK111 UT WOS:A1991GK11100753 ER PT J AU KASZNIAK, AW KEYL, PM ALBERT, MS AF KASZNIAK, AW KEYL, PM ALBERT, MS TI DEMENTIA AND THE OLDER DRIVER SO HUMAN FACTORS LA English DT Article ID ALZHEIMERS-DISEASE; BRAIN-DAMAGE AB The association between dementia and driving errors in older adults has been anecdotally noted by clinicians and caregivers. However, until recently, little empirical documentation of this association existed. This paper provides a critical review of available research on dementia and driving and discusses issues that must be considered in attempting to apply this developing body of research to practical problems, such as the relicensing process for selected drivers. This is followed by a discussion of recent research relevant to the development of potential procedures for screening patients with dementing illness-particularly Alzheimer's disease-for probable driving risk. C1 JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP KASZNIAK, AW (reprint author), UNIV ARIZONA,DEPT PSYCHOL,TUCSON,AZ 85721, USA. NR 44 TC 27 Z9 28 U1 2 U2 5 PU HUMAN FACTORS SOC PI SANTA MONICA PA BOX 1369, SANTA MONICA, CA 90406 SN 0018-7208 J9 HUM FACTORS JI Hum. Factors PD OCT PY 1991 VL 33 IS 5 BP 527 EP 537 PG 11 WC Behavioral Sciences; Engineering, Industrial; Ergonomics; Psychology, Applied; Psychology SC Behavioral Sciences; Engineering; Psychology GA GQ075 UT WOS:A1991GQ07500005 PM 1769673 ER PT J AU YOUNG, RH EBLE, JN AF YOUNG, RH EBLE, JN TI UNUSUAL FORMS OF CARCINOMA OF THE URINARY-BLADDER SO HUMAN PATHOLOGY LA English DT Article DE BLADDER; CARCINOMA; TRANSITIONAL CELL CARCINOMA; SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; SARCOMATOID CARCINOMA; MICROCYSTIC CARCINOMA ID TRANSITIONAL-CELL-CARCINOMA; HUMAN CHORIONIC-GONADOTROPIN; PRIMARY CHORIOCARCINOMA; UNDIFFERENTIATED CARCINOMA; VERRUCOUS CARCINOMA; PRIMARY ADENOCARCINOMA; INTESTINAL METAPLASIA; UROTHELIAL CARCINOMA; MUSCULARIS MUCOSAE; ECTOPIC PRODUCTION C1 INDIANA UNIV,SCH MED,DEPT PATHOL,INDIANAPOLIS,IN 46202. INDIANA UNIV,SCH MED,DEPT EXPTL ONCOL,INDIANAPOLIS,IN 46202. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RICHARD L ROUDEBUSH VET ADM MED CTR,INDIANAPOLIS,IN 46202. RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 158 TC 99 Z9 103 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD OCT PY 1991 VL 22 IS 10 BP 948 EP 965 DI 10.1016/0046-8177(91)90003-8 PG 18 WC Pathology SC Pathology GA GP864 UT WOS:A1991GP86400003 PM 1842384 ER PT J AU SUNDAY, ME CHOI, N SPINDEL, ER CHIN, WW MARK, EJ AF SUNDAY, ME CHOI, N SPINDEL, ER CHIN, WW MARK, EJ TI GASTRIN-RELEASING PEPTIDE GENE-EXPRESSION IN SMALL-CELL AND LARGE CELL UNDIFFERENTIATED LUNG CARCINOMAS SO HUMAN PATHOLOGY LA English DT Article DE BOMBESIN; IMMUNOHISTOCHEMISTRY; INSITU HYBRIDIZATION; LUNG TUMORS; PROGNOSIS ID HUMAN-FETAL LUNG; NEURO-ENDOCRINE DIFFERENTIATION; MESSENGER-RNA; CLINICAL-SIGNIFICANCE; CHROMOGRANIN-A; BOMBESIN GENE; TUMORS; CANCER; MARKERS; ABNORMALITIES C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. RP SUNDAY, ME (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU PHS HHS [R29-38401-01] NR 47 TC 32 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 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD OCT PY 1991 VL 22 IS 10 BP 1030 EP 1039 DI 10.1016/0046-8177(91)90011-D PG 10 WC Pathology SC Pathology GA GP864 UT WOS:A1991GP86400011 PM 1668786 ER PT J AU VENUGOPALAN, V NISHIOKA, NS MIKIC, BB AF VENUGOPALAN, V NISHIOKA, NS MIKIC, BB TI THE EFFECT OF CO2-LASER PULSE REPETITION RATE ON TISSUE ABLATION RATE AND THERMAL-DAMAGE SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING LA English DT Note ID CONTINUOUS-WAVE CO2-LASER; BIOLOGICAL TISSUE; ER-YAG; OSTEOTOMIES; PARAMETERS; DURATION; DEPTH; MODEL AB The ablation rate and thermal damage in skin produced by a superpulsed CO2 laser operating at pulse repetition rates between 1 and 900 Hz was measured. When delivering a fixed number of pulses (20 or 30) of equal energy, a 55-60% increase in the amount of tissue ablated was observed when the pulse repetition rate rose from 10 to 200 Hz. At pulse repetition rates greater than 200 Hz no further increase was seen. Under identical conditions, an 80% increase in the zone of thermal damage was observed when the pulse repetition rate was increased from 1 to 60 Hz. The large increases in tissue ablation and tissue damage may indicate the existence of a layer of mixed-phase (i.e., liquid and vapor) or metastable liquid which can store significant amounts of thermal energy between pulses. The data suggest that CO2 lasers should be operated at relatively low repetition rates for optimal performance. C1 MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139. RP VENUGOPALAN, V (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 21 TC 20 Z9 20 U1 0 U2 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 0018-9294 J9 IEEE T BIO-MED ENG JI IEEE Trans. Biomed. Eng. PD OCT PY 1991 VL 38 IS 10 BP 1049 EP 1052 DI 10.1109/10.88452 PG 4 WC Engineering, Biomedical SC Engineering GA GG471 UT WOS:A1991GG47100014 PM 1761294 ER PT J AU DENNING, SM JONES, DM WARE, RE WEINHOLD, KJ BRENNER, MB HAYNES, BF AF DENNING, SM JONES, DM WARE, RE WEINHOLD, KJ BRENNER, MB HAYNES, BF TI ANALYSIS OF CLONES DERIVED FROM HUMAN CD7+CD4-CD8-CD3- THYMOCYTES SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE T-CELL PRECURSOR; T-CELL DIFFERENTIATION; T-CELL RECEPTOR; THYMUS ID T-CELL-RECEPTOR; NATURAL-KILLER-CELLS; EXPRESS FUNCTIONAL TRANSCRIPTS; MONOCLONAL-ANTIBODY; ANTIGEN RECEPTOR; ALPHA-BETA; INVITRO DIFFERENTIATION; CD3+WT31 LYMPHOCYTES; CD4+8+ THYMOCYTES; PERIPHERAL-BLOOD AB The differentiation of human thymocyte precursors was studied by analysis of clonal progeny of CD4-CD8-CD3- (triple negative or TN) thymocytes. Using a culture system of phytohemagglutinin, IL-2, and irradiated allogeneic lymphoid feeder cells, we found that 48% of clones (104 total) derived from TN thymocyte suspensions were TCR-gamma-delta-cells, 12% of clones were TCR-alpha-beta-cells, and 34% were CD16+CD3- cells. Importantly, 6% of clones were novel subsets of CD4+CD8-CD3- or CD4-CD8+CD3- thymocytes. The majority of TCR-alpha,beta, TCR-gamma-delta, and CD16+CD3- clones expressed low levels of CD4. Molecular analysis of freshly isolated TN- thymocytes prior to in vitro culture demonstrated that up to 40% of cells had TCR-gamma, delta, and beta-gene rearrangements, but were negative in indirect immunofluorescence assays for cytoplasmic TCR-delta and beta. These data provide evidence at the clonal level for the presence of precursors of the TCR-alpha-beta and TCR-gamma-delta-lineages in the human TN thymocyte pool. Moreover, a substantial proportion of freshly isolated human TN thymocytes had already undergone TCR gene rearrangement prior to in vitro culture. Whether these precursors of the TCR-alpha-beta and TCR-gamma-delta-lineages mature from cells already containing TCR gene rearrangements into sTCR+ cells or differentiate in vitro from cells with TCR genes in germline configuration remains to be determined. Nonetheless, these data demonstrate that the predominant clone types that grow out of human TN thymocytes in vitro are TCR-gamma-delta and NK cells. C1 DUKE UNIV,SCH MED,DIV CARDIOL,DURHAM,NC 27710. DUKE UNIV,SCH MED,DIV RHEUMATOL & IMMUNOL,DURHAM,NC 27710. DUKE UNIV,SCH MED,DEPT MED,DURHAM,NC 27710. DUKE UNIV,SCH MED,DIV HEMATOL & ONCOL,DURHAM,NC 27710. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT RHEUMATOL & IMMUNOL,IMMUNOCHEM LAB,BOSTON,MA 02115. FU NCI NIH HHS [CA28936, CA47724]; NIAID NIH HHS [AI19368] NR 73 TC 26 Z9 26 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 OCT PY 1991 VL 3 IS 10 BP 1015 EP 1024 DI 10.1093/intimm/3.10.1015 PG 10 WC Immunology SC Immunology GA GK703 UT WOS:A1991GK70300010 PM 1721831 ER PT J AU CHUMAS, JC SCULLY, RE AF CHUMAS, JC SCULLY, RE TI SEBACEOUS TUMORS ARISING IN OVARIAN DERMOID CYSTS SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article AB The clinicopathologic features of five cases of sebaceous tumors arising in ovarian dermoid cysts and of three previously reported cases are reviewed. They occurred in women with an average age of 58 years and were classified as sebaceous adenoma (five cases), basal cell carcinoma with sebaceous differentiation (two cases), and sebaceous carcinoma (one case). Follow-up information was available for all cases. One patient with basal cell carcinoma with sebaceous differentiation had a pelvic recurrence 2 1/2 years after diagnosis. In no other case did the sebaceous tumor recur or metastasize during follow-up periods of 1 to 6 years. One patient died of a squamous cell carcinoma that arose in the same dermoid cyst as the sebaceous tumor. These tumors represent a rare form of monodermal neoplasia in dermoid cysts. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP CHUMAS, JC (reprint author), SUNY STONY BROOK,DEPT PATHOL,STONY BROOK,NY 11794, USA. NR 16 TC 22 Z9 22 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 OCT PY 1991 VL 10 IS 4 BP 356 EP 363 DI 10.1097/00004347-199110000-00008 PG 8 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA GH079 UT WOS:A1991GH07900007 PM 1774106 ER PT J AU YOUNG, RH SILVA, EG SCULLY, RE AF YOUNG, RH SILVA, EG SCULLY, RE TI OVARIAN AND JUXTAOVARIAN ADENOMATOID TUMORS - A REPORT OF 6 CASES SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article ID UTERUS; MESOTHELIOMA AB Five ovarian adenomatoid tumors and one juxtaovarian tumor of this type in women 23 to 79 (average 54) years of age are described. Four were less-than-or-equal-to 7 mm in diameter; the other two were 1.4 cm and 5 cm. The five ovarian tumors were located predominantly in the hilus, with focal extension into the medulla. Microscopic examination showed the lesions to be characterized by round, oval, or elongated tubules, some of which were cystically dilated, and vacuoles occasionally containing basophilic secretion. Hyaline bodies were present in one case. Follow-up in these cases and the 10 previously reported similar cases that include follow-up information has been benign. The microscopic features of the ovarian adenomatoid tumor are typically diagnostic, but, as illustrated by one of our cases and another in the literature, some features that simulate those of yolk sac tumor may cause diagnostic difficulty when the tumor occurs in a young patient. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT PATHOL,HOUSTON,TX 77025. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. NR 22 TC 24 Z9 24 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 OCT PY 1991 VL 10 IS 4 BP 364 EP 371 DI 10.1097/00004347-199110000-00009 PG 8 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA GH079 UT WOS:A1991GH07900008 PM 1774107 ER PT J AU MACKLIS, RM OLTIKAR, A SALLAN, SE AF MACKLIS, RM OLTIKAR, A SALLAN, SE TI WILMS-TUMOR PATIENTS WITH PULMONARY METASTASES SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT 32ND ANNUAL MEETING OF THE AMERICAN SOC FOR THERAPEUTIC RADIOLOGY AND ONCOLOGY CY OCT 15-19, 1990 CL MIAMI BEACH, FL SP AMER SOC THERAPEUT RADIOL & ONCOL DE WILMS TUMOR; PULMONARY METASTASES; WHOLE LUNG RADIOTHERAPY; LATE EFFECTS; 2ND MALIGNANT NEOPLASMS ID THERAPY; PROGNOSIS; DIAGNOSIS; 2ND; IRRADIATION; CHILDHOOD; CHILDREN; CANCER AB We have evaluated the clinicopathologic characteristics, survival probabilities, patterns of treatment failure, and late toxicities in a group of 51 Wilms' tumor patients with pulmonary metastases evaluated at our center between 1968 and 1988 and treated intensively with surgery, multiagent chemotherapy, and radiotherapy. Twenty-one patients had pulmonary metasases at diagnosis (Stage IV-p) and 30 had pulmonary relapse after initial treatment for nonmetastatic disease. With a median follow-up time of 83 months, actuarial 5- and 10-year survival probability for the group as a whole is 59%. For the subset of patients with favorable histology Stage IV-p disease, 10-year survival probability is 77%, whereas for the subset with relapsed anaplastic or sarcomatous disease, 10-year survival probability is 22%. The lung was the predominant site of failure even in patients who had received relatively high doses of pulmonary radiotherapy. Late effects seen in patients with over 10 years of follow-up included musculoskeletal and soft tissue growth abnormalities (93% incidence) as well as breast hypoplasia and endocrinologic abnormalities. Second malignant neoplasms of the breast, thyroid, and pancreas were observed at post-treatment intervals of 17, 3.5 and 12 years, respectively. C1 CHILDRENS HOSP MED CTR,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP MACKLIS, RM (reprint author), CHILDRENS HOSP MED CTR,JOINT CTR RADIAT THERAPY,50 BINNEY ST,BOSTON,MA 02115, USA. NR 29 TC 12 Z9 12 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT PY 1991 VL 21 IS 5 BP 1187 EP 1193 PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GL715 UT WOS:A1991GL71500011 PM 1657840 ER PT J AU NEWMAN, LA CLEVELAND, RH BLICKMAN, JG HILLMAN, RE JARAMILLO, D AF NEWMAN, LA CLEVELAND, RH BLICKMAN, JG HILLMAN, RE JARAMILLO, D TI VIDEOFLUOROSCOPIC ANALYSIS OF THE INFANT SWALLOW SO INVESTIGATIVE RADIOLOGY LA English DT Article DE INFANTS; SWALLOWING; VIDEOFLUOROSCOPY ID RELIABILITY AB A better understanding of the abnormal infant swallowing mechanism requires better knowledge of the normal infant swallow. Twenty-one full-term infants under six months of age were examined using videofluoroscopy of the swallowing portion of upper gastrointestinal examinations. Components of the oral and pharyngeal stages of swallowing were evaluated. Results showed high reliability between two raters in obtaining measurement data. There was variability in suck and oral transit time, which was correlated to the number of sucks per swallow. All infants appeared to move their tongue in a "stripping" motion, and collected the material in various sites in the oral cavity or oropharynx before initiation of the swallow. The incidence of nasopharyngeal reflux was low (9.5%). The majority of infants demonstrated a slight residue in their valleculae and hesitation in the cervical esophagus. These findings indicate that videofluoroscopy provides an objective and systematic method for analyzing the infant swallowing mechanism. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DIV PEDIAT RADIOL,BOSTON,MA 02115. BOSTON UNIV,DEPT COMMUN DISORDERS,BOSTON,MA 02215. NR 10 TC 31 Z9 33 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD OCT PY 1991 VL 26 IS 10 BP 870 EP 873 DI 10.1097/00004424-199110000-00005 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GK705 UT WOS:A1991GK70500005 PM 1960027 ER PT J AU VENEGAS, JG YAMADA, Y HALES, CA AF VENEGAS, JG YAMADA, Y HALES, CA TI CONTRIBUTIONS OF DIFFUSION JET FLOW AND CARDIAC ACTIVITY TO REGIONAL VENTILATION IN CFV SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE GAS TRANSPORT MECHANISMS; CARDIOGENIC OSCILLATIONS; POSITRON EMISSION TOMOGRAPHY ID CARDIOGENIC OSCILLATIONS; GAS-TRANSPORT; BLOOD-GASES; EXCHANGE; DOGS; INEQUALITY; FREQUENCY; LUNG AB The magnitude and regional distribution of local gas transport during constant-flow ventilation (CFV) were quantified by imaging the washout of nitrogen 13 ((NN)-N-13) from anesthetized and paralyzed mongrel dogs with positron emission tomography. Equal jet flows, through two 2-mm-ID bronchial catheters 1 cm distal to the carina, were adjusted to provide eucapnic CFV (total flow = 57.6 ml. s-1.kg-1). Basal, midheart, and apical transverse sections were studied in supine and prone anesthetized dogs. The ventilation per unit volume (sV) of selected areas was computed from local (NN)-N-13 concentration vs. time curves during washout. To separate the regional contributions of CFV and cardiogenic oscillation to enhanced molecular diffusion, additional supine dogs were also studied during unilateral CFV. In this protocol the CFV jet flow was delivered to a single lung while the contralateral lung was left apneic. For each lung, washout data were obtained under CFV and apnea both living and postmortem animals. The local contributions of diffusion, CFV jet effects, and cardiac activity to gas transport were evaluated and tested for additive and multiplicative synergistic interactions. The regional distribution of gas transport during CFV was found to be highly nonuniform and characterized by higher ventilation to regions located close to the main bronchi and those located in the direction in which the CFV jet pointed. No major differences were observed between supine and prone positions. This regional pattern of ventilation distribution was found to be the result of complementary and nearly multiplicative interaction between the regional effects of the CFV jet, concentrated in the central airways, and the preferential cardiogenic gas transport enhancement in ventral regions close to the heart. The data were also analyzed with a model that divides the regional diffusive gas transport resistance into a central component, affected by the CFV jet, and a peripheral component, affected only by cardiac activity. This analysis showed substantial regional heterogeneities in the effects of the different gas transport mechanisms, which are consistent with the geometry of the bronchial tree and the location of the heart in the dog. The results indicate that regional nonuniformities must be considered when modeling gas transport in CFV. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,PULM UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP VENEGAS, JG (reprint author), MASSACHUSETTS GEN HOSP,DEPT BIOMED ENGN,CLN-2,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-38267] NR 23 TC 6 Z9 6 U1 1 U2 1 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 OCT PY 1991 VL 71 IS 4 BP 1540 EP 1553 PG 14 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA GJ961 UT WOS:A1991GJ96100049 PM 1757380 ER PT J AU PASTER, BJ DEWHIRST, FE WEISBURG, WG TORDOFF, LA FRASER, GJ HESPELL, RB STANTON, TB ZABLEN, L MANDELCO, L WOESE, CR AF PASTER, BJ DEWHIRST, FE WEISBURG, WG TORDOFF, LA FRASER, GJ HESPELL, RB STANTON, TB ZABLEN, L MANDELCO, L WOESE, CR TI PHYLOGENETIC ANALYSIS OF THE SPIROCHETES SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI; RNA-POLYMERASE; LYME-DISEASE; SP-N; LEPTOSPIRA; BORRELIA; ACID; TREPONEMA; FERMENTATION; BACTEROIDES AB The 16S rRNA sequences were determined for species of Spirochaeta, Treponema, Borrelia, Leptospira, Leptonema, and Serpula, using a modified Sanger method of direct RNA sequencing. Analysis of aligned 16S rRNA sequences indicated that the spirochetes form a coherent taxon composed of six major clusters or groups. The first group, termed the treponemes, was divided into two subgroups. The first treponeme subgroup consisted of Treponema pallidum, Treponema phagedenis, Treponema denticola, a thermophilic spirochete strain, and two species of Spirochaeta, Spirochaeta zuelzerae and Spirochaeta stenostrepta, with an average interspecies similarity of 89.9%. The second treponeme subgroup contained Treponema bryantii, Treponema pectinovorum, Treponema saccharophilum, Treponema succinifaciens, and rumen strain CA, with an average interspecies similarity of 89.9%. The average interspecies similarity between the two treponeme subgroups was 84.2%. The division of the treponemes into two subgroups was verified by single-base signature analysis. The second spirochete group contained Spirochaeta aurantia, Spirochaeta halophila, Spirochaeta bajacaliforniensis, Spirochaeta litoralis, and Spirochaeta isovalerica, with an average similarity of 87.4%. The Spirochaeta group was related to the treponeme group, with an average similarity of 81.9%. The third spirochete group contained borrelias, including Borrelia burgdorferi, Borrelia anserina, Borrelia hermsii, and a rabbit tick strain. The borrelias formed a tight phylogenetic cluster, with average similarity of 97%. The borrelia group shared a common branch with the Spirochaeta group and was closer to this group than to the treponemes. A single spirochete strain isolated from the shrew constituted the fourth group. The fifth group was composed of strains of Serpula (Treponema) hyodysenteriae and Serpula (Treponema) innocens. The two species of this group were closely related, with a similarity of greater than 99%. Leptonema illini, Leptospira biflexa, and Leptospira interrogans formed the sixth and most deeply branching group. The average similarity within this group was 83.2%. This study represents the first demonstration that pathogenic and saprophytic Leptospira species are phylogenetically related. The division of the spirochetes into six major phylogenetic clusters was defined also by sequence signature elements. These signature analyses supported the conclusion that the spirochetes represent a monophylectic bacterial phylum. C1 GENE TRAK SYST,FRAMINGHAM,MA 01701. ABBOTT LABS,ABBOTT PK,IL 60064. USDA,NATL ANIM DIS CTR,AMES,IA 50010. UNIV ILLINOIS,DEPT MICROBIOL,URBANA,IL 61801. USDA ARS,NO REG RES CTR,PEORIA,IL 61604. RP PASTER, BJ (reprint author), FORSYTH DENT CTR,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-04881, DE-08303] NR 60 TC 212 Z9 215 U1 0 U2 10 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD OCT PY 1991 VL 173 IS 19 BP 6101 EP 6109 PG 9 WC Microbiology SC Microbiology GA GH455 UT WOS:A1991GH45500021 PM 1917844 ER PT J AU JASTY, M BRAGDON, CR MALONEY, WJ HAIRE, T HARRIS, WH AF JASTY, M BRAGDON, CR MALONEY, WJ HAIRE, T HARRIS, WH TI INGROWTH OF BONE IN FAILED FIXATION OF POROUS-COATED FEMORAL COMPONENTS SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID REPLACEMENT AB In five straight-stemmed, proximally porous-coated femoral components that were retrieved at revision arthroplasty from patients who had radiographic and clinical evidence of loosening, there was growth of bone into the porous coating. The components had been inserted during a primary arthroplasty in one woman and four men. The patients ranged in age from thirty-seven to sixty-seven years. Three patients were heavy, and all five were active. All patients had had an excellent early result from the initial arthroplasty; at the one-year follow-up, the mean Harris hip score had been 91 points. Pain in the hip developed in all of the patients, between one and three years after the index procedure. Initial radiographs had revealed excellent position and fixation of the prosthetic components, but the components then subsided between one and three and one-half years after the index procedure. All of the femoral components were found to be grossly loose at the revision operation. Nevertheless, all of the prosthetic components demonstrated growth of bone into 4 to 44 per cent (mean, 24 per cent) of the pore spaces available for ingrowth. Woven bone and fracture callus were found in the curettings from the proximal part of the femur. The findings in these five patients suggest that late failure of uncemented porous-surfaced femoral components can occur despite the presence of extensive ingrowth of bone. These failures may be the result of fatigue fractures of the trabeculae of the osseous ingrowth into the porous surfaces. Caution is warranted in the liberal use of these prosthetic components in heavy, active patients. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JASTY, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,ORTHOPAED BIOMECH LABS,BOSTON,MA 02114, USA. NR 17 TC 38 Z9 38 U1 0 U2 0 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 OCT PY 1991 VL 73A IS 9 BP 1331 EP 1337 PG 7 WC Orthopedics; Surgery SC Orthopedics; Surgery GA GM833 UT WOS:A1991GM83300007 PM 1918115 ER PT J AU CHAN, PY LAWRENCE, MB DUSTIN, ML FERGUSON, LM GOLAN, DE SPRINGER, TA AF CHAN, PY LAWRENCE, MB DUSTIN, ML FERGUSON, LM GOLAN, DE SPRINGER, TA TI INFLUENCE OF RECEPTOR LATERAL MOBILITY ON ADHESION STRENGTHENING BETWEEN MEMBRANES CONTAINING LFA-3 AND CD2 SO JOURNAL OF CELL BIOLOGY LA English DT Article ID FUNCTION-ASSOCIATED ANTIGEN-3; SUPPORTED PLANAR MEMBRANES; CELL-ADHESION; MOLECULAR-CLONING; T-CELL; TRANSLATIONAL DIFFUSION; PHOSPHOLIPID-BILAYERS; PLASMA-MEMBRANE; IMMUNE-SYSTEM; GLYCOPROTEIN AB We have used an in vitro model system of glass-supported planar membranes to study the effects of lateral mobility of membrane-bound receptors on cell adhesion. Egg phosphatidylcholine (PC) bilayers were reconstituted with two anchorage isoforms of the adhesion molecule lymphocyte function-associated antigen 3 (LFA-3). The diffusion coefficient of glycosyl phosphatidylinositol (GPI)-anchored LFA-3 approached that of phospholipids in the bilayers, whereas the transmembrane (TM)-anchored isoform of LFA-3 was immobile. Both static and laminar flow assays were used to quantify the strength of adherence to the lipid bilayers of the T lymphoma cell line Jurkat that expresses the counter-receptor CD2. Cell adhesion was dependent on LFA-3 density and was more efficient on membranes containing the GPI isoform than the TM isoform. Kinetic measurements demonstrated an influence of contact time on the strength of adhesion to the GPI isoform at lower site densities (25-50 sites/mu-m2), showing that the mobility of LFA-3 is important in adhesion strengthening. At higher site densities (1,500 sites/mu-m2) and longer contact times (20 min), Jurkat cell binding to the TM and GPI isoforms of LFA-3 showed equivalent adhesion strengths, although adhesion strength of the GPI isoform developed twofold more rapidly than the TM isoform. Reduction of CD2 mobility on Jurkat cells at 5-degrees-C greatly decreased the rate of adhesion strengthening with the TM isoform of LFA-3, resulting in a 30-fold difference between the two LFA-3 isoforms. Our results demonstrate that the ability of a membrane receptor and its membrane-bound counter-receptor to diffuse laterally enhances cell adhesion both by allowing accumulation of ligands in the cell contact area and by increasing the rate of receptor-ligand bond formation. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DIV HEMATOL,BOSTON,MA 02115. RP CHAN, PY (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA31798, CA39542]; NHLBI NIH HHS [HL15157] NR 50 TC 172 Z9 173 U1 0 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD OCT PY 1991 VL 115 IS 1 BP 245 EP 255 DI 10.1083/jcb.115.1.245 PG 11 WC Cell Biology SC Cell Biology GA GH249 UT WOS:A1991GH24900022 PM 1717480 ER PT J AU TAKADA, Y MURPHY, E PIL, P CHEN, C GINSBERG, MH HEMLER, ME AF TAKADA, Y MURPHY, E PIL, P CHEN, C GINSBERG, MH HEMLER, ME TI MOLECULAR-CLONING AND EXPRESSION OF THE CDNA FOR ALPHA-3 SUBUNIT OF HUMAN ALPHA-3-BETA-1 (VLA-3), AN INTEGRIN RECEPTOR FOR FIBRONECTIN, LAMININ, AND COLLAGEN SO JOURNAL OF CELL BIOLOGY LA English DT Article ID AMINO-ACID SEQUENCE; CELL-ADHESION RECEPTORS; GROWTH FACTOR-BETA; VONWILLEBRAND-FACTOR; SUBSTRATE ADHESION; SURFACE RECEPTORS; PROTEIN SEQUENCES; GLYCOPROTEIN-IIB; MAMMALIAN-CELLS; SARCOMA CELLS AB alpha-3-beta-1 (VLA-3), a member of the integrin family of cell adhesion receptors, may function as a receptor for fibronectin, laminin, and collagen. A partial cDNA clone (2.4 kb) for the human alpha-3 subunit was selected from an endothelial cell lambda-gt11 cDNA library by specific antibody screening. Several overlapping cDNA clones were subsequently obtained, of a total length of 4.6 kb from various cDNA libraries. The reconstructed alpha-3 cDNA was expressed on the surface of chinese hamster ovary cells as detected by an alpha-3-specific mAb after transfection, suggesting that the cDNA is authentic. Within this sequence was an open reading frame, encoding for 1,051 amino acids, including a signal peptide of 32 residues, a long extracellular domain (959 residues), a transmembrane domain (28 residues), and a short cytoplasmic segment (32 residues). Overall, the alpha-3 amino acid sequence was 25-37% similar to the other integrin alpha-subunits that are cleaved, with most similarity to the alpha-6 sequence (37%), and less similarity to those alpha-subunits that have I domains (15-20%, excluding the I domain sequence itself). Features most like those in other alpha subunits are (a) the positions of 18/19 cysteine residues, (b) three potential metal binding domains of the general structure DX(D/N)X(D/N)GXXD, and (c) the predicted transmembrane domain. The mass of alpha-3 calculated from its amino acid sequence is 113,505. The human-alpha-3 sequence was 89% identical to hamster galactoprotein b3, and 70% similar to the chicken CSAT antigen band 2 protein partial sequence, suggesting that these two polypeptides are homologues of human alpha-3. C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV TUMOR VIROL, BOSTON, MA 02115 USA. RP TAKADA, Y (reprint author), Scripps Res Inst, RES INST, COMM VASC BIOL, LA JOLLA, CA 92037 USA. OI takada, yoshikazu/0000-0001-5481-9589 FU NHLBI NIH HHS [HL-28235]; NIGMS NIH HHS [GM38903, GM47157] NR 54 TC 131 Z9 132 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD OCT PY 1991 VL 115 IS 1 BP 257 EP 266 DI 10.1083/jcb.115.1.257 PG 10 WC Cell Biology SC Cell Biology GA GH249 UT WOS:A1991GH24900023 PM 1655803 ER PT J AU BYERS, TJ KUNKEL, LM WATKINS, SC AF BYERS, TJ KUNKEL, LM WATKINS, SC TI THE SUBCELLULAR-DISTRIBUTION OF DYSTROPHIN IN MOUSE SKELETAL, CARDIAC, AND SMOOTH-MUSCLE SO JOURNAL OF CELL BIOLOGY LA English DT Article ID DUCHENNE MUSCULAR-DYSTROPHY; ULTRASTRUCTURAL-LOCALIZATION; NEUROMUSCULAR-JUNCTIONS; PLASMA-MEMBRANE; ALPHA-ACTININ; PROTEIN; CELL; SURFACE; MDX; ANTIBODY AB We use a highly specific and sensitive antibody to further characterize the distribution of dystrophin in skeletal, cardiac, and smooth muscle. No evidence for localization other than at the cell surface is apparent in skeletal muscle and no 427-kD dystrophin labeling was detected in sciatic nerve. An elevated concentration of dystrophin appears at the myotendinous junction and the neuromuscular junction, labeling in the latter being more intense specifically in the troughs of the synaptic folds. In cardiac muscle the distribution of dystrophin is limited to the surface plasma membrane but is notably absent from the membrane that overlays adherens junctions of the intercalated disks. In smooth muscle, the plasma membrane labeling is considerably less abundant than in cardiac or skeletal muscle and is found in areas of membrane underlain by membranous vesicles. As in cardiac muscle, smooth muscle dystrophin seems to be excluded from membrane above densities that mark adherens junctions. Dystrophin appears as a doublet on Western blots of skeletal and cardiac muscle, and as a single band of lower abundance in smooth muscle that corresponds most closely in molecular weight to the upper band of the striated muscle doublet. The lower band of the doublet in striated muscle appears to lack a portion of the carboxyl terminus and may represent a dystrophin isoform. Isoform differences and the presence of dystrophin on different specialized membrane surfaces imply multiple functional roles for the dystrophin protein. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,ELECTRON MICROSCOPY LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BYERS, TJ (reprint author), CHILDRENS HOSP MED CTR,MED CTR,HOWARD HUGHES MED INST,BOSTON,MA 02115, USA. FU NINDS NIH HHS [NS23740] NR 52 TC 217 Z9 218 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD OCT PY 1991 VL 115 IS 2 BP 411 EP 421 DI 10.1083/jcb.115.2.411 PG 11 WC Cell Biology SC Cell Biology GA GL281 UT WOS:A1991GL28100011 PM 1918148 ER PT J AU YAEGER, PC STILES, CD ROLLINS, BJ AF YAEGER, PC STILES, CD ROLLINS, BJ TI HUMAN KERATINOCYTE GROWTH-PROMOTING ACTIVITY ON THE SURFACE OF FIBROBLASTS SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID HUMAN EPIDERMAL-KERATINOCYTES; CELL-GROWTH; NUCLEOTIDE-SEQUENCE; SIGNAL TRANSDUCTION; FACTOR-ALPHA; FACTOR-BETA; 3T3 CELLS; DIFFERENTIATION; PROLIFERATION; LOCALIZATION AB To proliferate in serum-containing medium, normal human keratinocytes must be co-cultured with fibroblast feeder cells. Conditioned medium from feeder cell cultures cannot substitute for the cells themselves. We tested the hypothesis that fibroblasts display a keratinocyte growth-promoting activity on their outer cell surface. The results of our investigation showed that (1) glutaraldehyde-fixed fibroblast feeder cells promote keratinocyte growth, (2) the growth-promoting effect requires contact between fixed fibroblasts and keratinocytes, and (3) feeder activity is highly enriched within the plasma membrane fraction of fibroblasts. We conclude that at least part of the fibroblast "feeder" activity involves a keratinocyte growth-promoting factor which is bound to the outer surface of fibroblast plasma membranes. C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT CELLULAR & MOLEC BIOL, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA53091]; NICHD NIH HHS [HD24926] NR 31 TC 33 Z9 33 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0021-9541 EI 1097-4652 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD OCT PY 1991 VL 149 IS 1 BP 110 EP 116 DI 10.1002/jcp.1041490114 PG 7 WC Cell Biology; Physiology SC Cell Biology; Physiology GA GK158 UT WOS:A1991GK15800013 PM 1939339 ER PT J AU HASS, R BRACH, M KHARBANDA, S GIESE, G TRAUB, P KUFE, D AF HASS, R BRACH, M KHARBANDA, S GIESE, G TRAUB, P KUFE, D TI INHIBITION OF PHORBOL ESTER-INDUCED MONOCYTIC DIFFERENTIATION BY DEXAMETHASONE IS ASSOCIATED WITH DOWN-REGULATION OF C-FOS AND C-JUN (AP-1) SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID TRANSCRIPTION FACTOR AP-1; PROTEIN KINASE-C; GENE-EXPRESSION; U937 CELLS; GLUCOCORTICOID RECEPTOR; DNA-BINDING; PROSTANOID SYNTHESIS; SEQUENCE ELEMENTS; MAMMALIAN-CELLS; VIMENTIN GENE AB Previous studies have shown that treatment of human myeloid leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with induction of monocytic differentiation and expression of the c-jun and c-fos early response genes. The present work demonstrates that the glucocorticoid dexamethasone inhibits TPA-induced increases in c-jun and c-fos mRNA levels in U-937 leukemia cells. These findings were associated with a block in appearance of the monocytic phenotype, including inhibition of TPA-induced increases in lamin A, lamin C, and vimetin transcripts. Other studies have demonstrated that TPA-induced monocytic differentiation and expression of the c-jun and c-fos genes in myeloid leukemia cells are regulated by protein kinase C (PKC). The finding that dexamethasone has no effect on TPA-induced activation of PKC suggests that this glucocorticoid inhibits signals downstream or parallel to this enzyme. Nuclear run-on assays demonstrate that: (1) induction of c-jun and c-fos expression by TPA is regulated by transcriptional mechanisms, (2) TPA-induced expression of c-jun and c-fos does not require protein synthesis, and (3) TPA-induced expression of both genes is inhibited at the transcriptional level by dexamethasone. To further define the effects of dexamethasone at the molecular level, we prepared a series of deleted c-jun promoter fragments linked to the chloramphenicol acetyltransferase (CAT) gene. Increases in CAT activity during transient expression of these constructs in TPA-treated U-937 cells could be assigned to the region (-97 to -20) of the promoter that contains the AP-1 binding site. This induction of CAT activity was sensitive to dexamethasone. These findings suggest that dexamethasone down-regulates TPA-induced transcription of the c-jun gene during monocytic differentiation by inhibiting activation of the AP-1 site. C1 MAX PLANCK INST CELL BIOL,LADENBURG,GERMANY. RP HASS, R (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115, USA. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 FU NCI NIH HHS [CA42802] NR 56 TC 36 Z9 38 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD OCT PY 1991 VL 149 IS 1 BP 125 EP 131 DI 10.1002/jcp.1041490116 PG 7 WC Cell Biology; Physiology SC Cell Biology; Physiology GA GK158 UT WOS:A1991GK15800015 PM 1939341 ER PT J AU WALDHAUSER, F BOEPPLE, PA SCHEMPER, M MANSFIELD, MJ CROWLEY, WF AF WALDHAUSER, F BOEPPLE, PA SCHEMPER, M MANSFIELD, MJ CROWLEY, WF TI SERUM MELATONIN IN CENTRAL PRECOCIOUS PUBERTY IS LOWER THAN IN AGE-MATCHED PREPUBERTAL CHILDREN SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID MONKEYS MACACA-MULATTA; RHESUS-MONKEYS; PHOTOPERIODISM; REPRODUCTION; GROWTH AB In children a progressive decrease in nocturnal serum melatonin (MT) has been shown with advancing age, suggesting a reduction in the amplitude of the circadian MT curve with maturation. Whether this alteration of MT levels is related to human sexual maturation or occurs independently remains to be elucidated. Also, the impact of gonadal steroids on the MT rhythm remains an open question. We examined 56 patients (51 females and 5 males) with central precocious puberty (52 idiopathic and 4 neurogenic). Patients were studied before and 3, 6, and 12 months after initiation of GnRH analog treatment. Three hundred and thirty-seven endocrinologically normal subjects (190 males and 147 females) served as controls. In all subjects nocturnal serum MT (blood collection between 2300 and 0100 h) was measured with a highly specific RIA. In young patients, aged 1-5 yr, we found significantly lower MT levels than in age-matched controls. Pubertal patients, aged 5-9 yr, displayed nocturnal MT levels in the same range as control subjects approaching normal pubertal age. In contrast to endocrinologically normal children, there was no age-dependent decrease in nocturnal MT in untreated precocious puberty; rather, it appeared that serum MT had already declined in association with the onset of sexual maturation. Although there was a significant difference in weight between patients and age-matched controls, the low MT values in patients 1-5 yr old were only partly explained by the weight difference (P < 0.0009); their pubertal status also contributed significantly (P < 0.006). Pituitary-gonadal suppression induced by long term GnRH analog treatment did not result in a return to prepubertal MT levels; rather, nocturnal MT decreased during therapy. The collected data indicate that nocturnal serum MT levels are related to sexual maturation, since serum MT is similar in precocious puberty and normal pubertal children. Since suppression of the pituitary-gonadal axis did not result in increases in nocturnal MT levels in young patients with precocity (i.e. return to age-appropriate levels), the reduction of nocturnal MT with normal puberty is not likely to be dependent on pubertal gonadotropin or sex steroid milieu. C1 MASSACHUSETTS GEN HOSP, REPROD ENDOCRINE UNIT, BOSTON, MA 02114 USA. UNIV VIENNA, DEPT SURG 2, A-1090 VIENNA, AUSTRIA. CHILDRENS HOSP MED CTR, DIV ENDOCRINOL, BOSTON, MA 02115 USA. RP WALDHAUSER, F (reprint author), UNIV VIENNA, DEPT PEDIAT, WAEHRINGER GUERTEL 18-20, A-1090 VIENNA, AUSTRIA. FU NCRR NIH HHS [RR-02172, RR-01066]; NICHD NIH HHS [HD-18169] NR 26 TC 96 Z9 101 U1 0 U2 3 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 OCT PY 1991 VL 73 IS 4 BP 793 EP 796 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GF684 UT WOS:A1991GF68400017 PM 1909703 ER PT J AU KARGA, H LEE, JK VICKERY, AL THOR, A GAZ, RD JAMESON, JL AF KARGA, H LEE, JK VICKERY, AL THOR, A GAZ, RD JAMESON, JL TI RAS ONCOGENE MUTATIONS IN BENIGN AND MALIGNANT THYROID NEOPLASMS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID PAPILLARY CARCINOMAS; TUMORIGENESIS; TUMORS; DNA AB Current models for tumorigenesis propose that a series of genetic alterations occur during the progression from the normal cell to the malignant phenotype. Mutations in each of the three ras genes (K-ras, H-ras, and N-ras) have been identified in many human neoplasms, including thyroid cancer. In this study we examined genomic DNA from benign and malignant thyroid neoplasms for mutations that are known to activate the ras oncogenes (codons 12, 13, and 61). DNA from frozen surgically excised tissue (n = 8) and from formalin-fixed paraffin-embedded tissue (n = 30) was amplified by the polymerase chain reaction and screened for mutations using oligonucleotide-specific hybridization. No mutations were identified in follicular adenomas (n = 9). In follicular carcinomas, 2 of 14 tumors contained mutations (N-ras 61, Gln to Arg), and both of these patients had bone metastases. One of 15 papillary carcinomas had a ras mutation (H-ras 12, Gly to Ser). In contrast to other studies, we found that ras mutations are relatively uncommon in both benign and malignant thyroid neoplasms. Studies of larger numbers of tumors and comparisons of different patient populations will be required to assess a possible association of mutations in N-ras 61 with clinically aggressive follicular cancer. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL, THYROID UNIT,JACKSON 1021,FRUIT ST, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT SURG, BOSTON, MA 02114 USA. RI Ain, Kenneth/A-5179-2012; OI Ain, Kenneth/0000-0002-2668-934X; Jameson, James/0000-0001-9538-4059 NR 20 TC 138 Z9 138 U1 0 U2 5 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 OCT PY 1991 VL 73 IS 4 BP 832 EP 836 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GF684 UT WOS:A1991GF68400023 PM 1890154 ER PT J AU REIMANN, KA SNYDER, GB CHALIFOUX, LV WAITE, BCD MILLER, MD YAMAMOTO, H SPERTINI, O LETVIN, NL AF REIMANN, KA SNYDER, GB CHALIFOUX, LV WAITE, BCD MILLER, MD YAMAMOTO, H SPERTINI, O LETVIN, NL TI AN ACTIVATED CD8+ LYMPHOCYTE APPEARS IN LYMPH-NODES OF RHESUS-MONKEYS EARLY AFTER INFECTION WITH SIMIAN IMMUNODEFICIENCY VIRUS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ACQUIRED IMMUNE DEFICIENCY SYNDROME; CYTOTOXIC LYMPHOCYTE-T; MHC CLASS-II; REGULATORY LYMPHOCYTE-T; LYMPHOCYTE-T SUBSET ID MEMORY T-CELLS; HELPER-INDUCER; HOMOSEXUAL MEN; AIDS; SUBSETS; SUPPRESSOR; MACAQUES; LYMPHADENOPATHY; POPULATIONS; REPLICATION AB Although alterations in T lymphocyte subset distribution and function in the peripheral blood of HIV-infected humans are well defined, the extent to which these reflect changes in other lymphoid compartments is unclear. We have characterized the coincident changes in PBL and lymph nodes (LN)1 after simian immunodeficiency virus of macaques (SIV(mac)) infection of rhesus monkeys. Whereas no consistent change in CD8+ PBL was noted during the first 60 d after infection, CD8+ lymphocytes increased significantly in number in LN. These CD8+ LN lymphocytes exhibited an increased expression of MHC class II and a decreased expression of leukocyte adhesion molecule-1, suggesting that they were activated, but interestingly did not express CD25 (IL-2 receptor). Moreover, there was no evidence that these CD8+ LN cells were proliferating, suggesting that they had migrated to the LN. These changes in the LN CD8+ lymphocyte population preceded any detectable change in the light microscopic appearance of the LN. When SIV(mac)- specific effector T cell responses were assessed, the magnitude of virus-specific effector activity was nearly identical in the PBL and LN of each monkey studied. However, the presence of SIV(mac)-specific effector cells in the LN did not correlate with the presence of CD8+, MHC class II+ cells. These findings suggest that this numerically important CD8+ lymphocyte subpopulation may serve a regulatory function. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP REIMANN, KA (reprint author), HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,ONE PINE HILL DR,SOUTHBOROUGH,MA 01772, USA. FU NCRR NIH HHS [RR00168, RR00055]; NIAID NIH HHS [AI20729] NR 31 TC 31 Z9 31 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT PY 1991 VL 88 IS 4 BP 1113 EP 1120 DI 10.1172/JCI115410 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GJ508 UT WOS:A1991GJ50800007 PM 1717508 ER PT J AU KUSARI, J VERMA, US BUSE, JB HENRY, RR OLEFSKY, JM AF KUSARI, J VERMA, US BUSE, JB HENRY, RR OLEFSKY, JM TI ANALYSIS OF THE GENE-SEQUENCES OF THE INSULIN-RECEPTOR AND THE INSULIN-SENSITIVE GLUCOSE TRANSPORTER (GLUT-4) IN PATIENTS WITH COMMON-TYPE NON-INSULIN-DEPENDENT DIABETES-MELLITUS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE INSULIN RECEPTOR GENE; INSULIN RESISTANCE; INSULIN-SENSITIVE GLUCOSE TRANSPORTER (GLUT-4) GENE; NON-INSULIN-DEPENDENT DIABETES-MELLITUS; POLYMORPHISM; SEQUENCING ID POLYMERASE CHAIN-REACTION; HUMAN SKELETAL-MUSCLE; KINASE-ACTIVITY; ENZYMATIC AMPLIFICATION; MORBIDLY OBESE; PIMA-INDIANS; GENOMIC DNA; NIDDM; RESISTANCE; BINDING AB Insulin resistance is a common feature of non-insulin-dependent diabetes mellitus (NIDDM) and "diabetes susceptibility genes" may be involved in this abnormality. Two potential candidate genes are the insulin receptor (IR) and the insulin-sensitive glucose transporter (GLUT-4). To elucidate whether structural defects in the IR and/or GLUT-4 could be a primary cause of insulin resistance in NIDDM, we have sequenced the entire coding region of the GLUT-4 gene from DNA of six NIDDM patients. Since binding properties of the IRs from NIDDM subjects are normal, we also analyzed the sequence of exons 16-22 (encoding the entire cytoplasmic domain of the IR) of the IR gene from the same six patients. When compared with the normal IR sequence, no difference was found in the predicted amino acid sequence of the IR cytoplasmic domain derived from the NIDDM patients. Sequence analysis of the GLUT-4 gene revealed that one patient was heterozygous for a mutation in which isoleucine (ATC) was substituted for valine (GTC) at position 383. Consequently, the GLUT-4 sequence at position 383 was determined in 24 additional NIDDM patients and 30 nondiabetic controls and all showed only the normal sequence. From these studies, we conclude that the insulin resistance seen in the great majority of subjects with the common form of NIDDM is not due to genetic variation in the coding sequence of the IR-beta-subunit, nor to any single mutation in the GLUT-4 gene. Possibly, a subpopulation of NIDDM patients exists displaying variation in the GLUT-4 gene. C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. RP KUSARI, J (reprint author), US DEPT VET AFFAIRS,VET ADM MED CTR,V-111G,3350 LA JOLLA VILLAGE DR,SAN DIEGO,CA 92161, USA. FU NIDDK NIH HHS [DK-33649] NR 44 TC 84 Z9 87 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT PY 1991 VL 88 IS 4 BP 1323 EP 1330 DI 10.1172/JCI115437 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GJ508 UT WOS:A1991GJ50800034 PM 1918382 ER PT J AU ANDERSON, K AF ANDERSON, K TI TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID BLOOD PRODUCTS; BONE-MARROW; MALIGNANCIES; CHEMOTHERAPY; IRRADIATION; PREVENTION; SURGERY RP ANDERSON, K (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 21 TC 9 Z9 9 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 OCT PY 1991 VL 9 IS 10 BP 1727 EP 1730 PG 4 WC Oncology SC Oncology GA GH456 UT WOS:A1991GH45600003 PM 1919623 ER PT J AU GREM, J ODWYER, P ELSON, P SIMON, N TRUMP, D FRONTIERA, M FALKSON, G VOGL, S AF GREM, J ODWYER, P ELSON, P SIMON, N TRUMP, D FRONTIERA, M FALKSON, G VOGL, S TI CISPLATIN, CARBOPLATIN, AND CYCLOPHOSPHAMIDE COMBINATION CHEMOTHERAPY IN ADVANCED-STAGE OVARIAN-CARCINOMA - AN EASTERN-COOPERATIVE-ONCOLOGY-GROUP PILOT-STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID HIGH-DOSE CARBOPLATIN; RANDOMIZED TRIAL; CANCER PATIENTS; RESIDUAL DISEASE; PLATINUM ANALOG; PHASE-II; DOXORUBICIN; REGIMENS C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53706. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV PRETORIA,PRETORIA,SOUTH AFRICA. FU NCI NIH HHS [CA 18281, CA 21076, CA 21115] NR 37 TC 19 Z9 19 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD OCT PY 1991 VL 9 IS 10 BP 1793 EP 1800 PG 8 WC Oncology SC Oncology GA GH456 UT WOS:A1991GH45600012 PM 1919629 ER PT J AU WHIPPEN, DA CANELLOS, GP AF WHIPPEN, DA CANELLOS, GP TI BURNOUT SYNDROME IN THE PRACTICE OF ONCOLOGY - RESULTS OF A RANDOM SURVEY OF 1,000 ONCOLOGISTS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID PHYSICIANS; STRESS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 7 TC 198 Z9 206 U1 2 U2 5 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 OCT PY 1991 VL 9 IS 10 BP 1916 EP 1920 PG 5 WC Oncology SC Oncology GA GH456 UT WOS:A1991GH45600025 PM 1919641 ER PT J AU HERZOG, DB AF HERZOG, DB TI RECENT ADVANCES IN BULIMIA-NERVOSA - INTRODUCTION SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,BOSTON,MA 02114. RP HERZOG, DB (reprint author), HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1991 VL 52 SU S BP 3 EP 3 PG 1 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA GM191 UT WOS:A1991GM19100001 ER PT J AU HERZOG, DB KELLER, MB LAVORI, PW SACKS, NR AF HERZOG, DB KELLER, MB LAVORI, PW SACKS, NR TI THE COURSE AND OUTCOME OF BULIMIA-NERVOSA SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT SYMP ON RECENT ADVANCES IN BULIMIA NERVOSA / 1991 ANNUAL MEETING OF THE AMERICAN PSYCHIATRIC ASSOC CY MAY 12, 1991 CL NEW ORLEANS, LA SP AMER PSYCHIAT ASSOC ID FOLLOW-UP; EATING DISORDERS; ANOREXIA-NERVOSA; 2-YEAR; WOMEN AB Although knowledge of the long-term course and outcome of bulimia nervosa is critical to the effective management of the bulimic patient, research in this area is still in its infancy. Comparisons between existing outcome studies are complicated by differences in research design and methods, a lingering confusion over the definition of terms such as recovery and relapse, and the possibility of multiple forms of bulimia nervosa with varying outcomes. Nonetheless, these studies agree that bulimia nervosa is a chronic disorder, characterized by high rates of relapse and persistent subclinical symptomatology. Future investigations into the course and outcome of bulimia nervosa should focus on the derivation of a universally acceptable terminology and the identification of clinical and psychosocial variables predicting recovery. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. RP HERZOG, DB (reprint author), MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,ACC 725,15 PARKMAN ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [R01 MH 38333-01A3] NR 21 TC 37 Z9 37 U1 1 U2 2 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1991 VL 52 SU S BP 4 EP 8 PG 5 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA GM191 UT WOS:A1991GM19100002 PM 1938989 ER PT J AU GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ AF GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ TI DEPRESSION OVERVIEW - SYMPTOMS AND TREATMENT STRATEGIES SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. UNIV PITTSBURGH,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA 15261. SUNY ALBANY,ALBANY,NY 12222. RP GERSHON, S (reprint author), UNIV PITTSBURGH,MED CTR,PITTSBURGH,PA 15260, USA. NR 0 TC 4 Z9 4 U1 1 U2 1 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1991 VL 52 IS 10 BP 437 EP 438 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA GL634 UT WOS:A1991GL63400017 ER PT J AU GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ AF GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ TI THE ELDERLY PATIENT AND DEPRESSION - SPECIAL CONSIDERATIONS SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material C1 UNIV PITTSBURGH,MED CTR,PITTSBURGH,PA 15260. SUNY ALBANY,ALBANY,NY 12222. MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. UNIV PITTSBURGH,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA 15261. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1991 VL 52 IS 10 BP 438 EP 439 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA GL634 UT WOS:A1991GL63400018 ER PT J AU GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ AF GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ TI DRUG LEVEL MONITORING - UNIQUE ADVANTAGES SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. UNIV PITTSBURGH,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA 15261. SUNY ALBANY,ALBANY,NY 12222. RP GERSHON, S (reprint author), UNIV PITTSBURGH,MED CTR,PITTSBURGH,PA 15260, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1991 VL 52 IS 10 BP 440 EP 441 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA GL634 UT WOS:A1991GL63400019 ER PT J AU GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ AF GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ TI MIXED ANXIETY DEPRESSION - A NEW DIAGNOSTIC CATEGORY FOR DSM-IV - TREATMENT IMPLICATIONS SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. UNIV PITTSBURGH,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA 15261. SUNY ALBANY,ALBANY,NY 12222. RP GERSHON, S (reprint author), UNIV PITTSBURGH,MED CTR,PITTSBURGH,PA 15260, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1991 VL 52 IS 10 BP 441 EP 442 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA GL634 UT WOS:A1991GL63400020 ER PT J AU GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ AF GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ TI DEPRESSION AND ASSOCIATED INSOMNIA - THERAPEUTIC OPTIONS SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. SUNY ALBANY,ALBANY,NY 12222. UNIV PITTSBURGH,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA 15261. RP GERSHON, S (reprint author), UNIV PITTSBURGH,MED CTR,PITTSBURGH,PA 15260, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1991 VL 52 IS 10 BP 442 EP 443 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA GL634 UT WOS:A1991GL63400021 ER PT J AU GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ AF GERSHON, S ROSENBAUM, JF REYNOLDS, CF PEREL, JM BARLOW, DH KUPFER, DJ MANN, JJ TI SUICIDALITY AND TREATMENT INTERVENTION - INSIGHTS AND PERSPECTIVES SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. UNIV PITTSBURGH,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA 15261. SUNY ALBANY,ALBANY,NY 12222. RP GERSHON, S (reprint author), UNIV PITTSBURGH,MED CTR,PITTSBURGH,PA 15260, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD OCT PY 1991 VL 52 IS 10 BP 443 EP 444 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA GL634 UT WOS:A1991GL63400022 ER PT J AU KASHKET, S VANHOUTE, J LOPEZ, LR STOCKS, S AF KASHKET, S VANHOUTE, J LOPEZ, LR STOCKS, S TI LACK OF CORRELATION BETWEEN FOOD RETENTION ON THE HUMAN DENTITION AND CONSUMER PERCEPTION OF FOOD STICKINESS SO JOURNAL OF DENTAL RESEARCH LA English DT Article ID CLEARANCE; SALIVA AB When dental health professionals advise that sticky foods be avoided, it is left to the consumer to choose correctly among different foods. In this study, comparisons were made among consumer ratings of stickiness of 21 commercially available foods and objective measurements of tooth retention of each of the foods. No correlation was found between the two, and neither the rates of clearance of food particles from the teeth nor the rates of clearance of food-derived sugars from the saliva correlated with ratings of food stickiness. Cookies, crackers, and potato chips were most retentive, whereas caramels, jelly beans, raisins, and milk chocolate bars were among those poorly retained. Clearance rates appeared to vary inversely with initial retention. However, chocolate-caramel bars exhibited high initial retention and a very rapid rate of clearance from the teeth. The findings show that consumers cannot accurately assess the retentiveness of foods and, thus, the advice simply to avoid sticky ones is inadequate. C1 FORSYTH DENT CTR,DEPT MICROBIOL,BOSTON,MA 02115. FORSYTH DENT CTR,CTR RES ORAL & BIOL EFFECTS FOODS,BOSTON,MA 02115. RP KASHKET, S (reprint author), FORSYTH DENT CTR,DEPT BIOCHEM,140 FENWAY,BOSTON,MA 02115, USA. NR 17 TC 35 Z9 37 U1 0 U2 5 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD OCT PY 1991 VL 70 IS 10 BP 1314 EP 1319 DI 10.1177/00220345910700100101 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA GP327 UT WOS:A1991GP32700001 PM 1939824 ER PT J AU WANG, CY STASHENKO, P AF WANG, CY STASHENKO, P TI KINETICS OF BONE-RESORBING ACTIVITY IN DEVELOPING PERIAPICAL LESIONS SO JOURNAL OF DENTAL RESEARCH LA English DT Article ID TISSUE-CULTURE; RESORPTION; INVITRO; STIMULATION AB The presence and kinetics of bone-resorbing activity in periapical lesions were studied with a rat model system. Lesions were found to expand most rapidly between induction on day 0 and day 15 ("active phase"), with enlargement occurring at a slower rate thereafter (days 20 and 30, "chronic phase"), as assessed by measurement of magnified radiographs and automated image analysis. Pooled extracts of periapical tissues obtained on day 15 contained significant levels of bone-resorbing activity, as determined by Ca-45 release from pre-labeled fetal rat long bones. Normal rat dental pulp and periodontal ligament contained no activity. In two kinetic experiments, highest levels of bone-resorbing activity were detected in tissues on days 10 (10.4% and 11.6% specific Ca-45 release/mg/mL) and 15 (8.9%). Activity declined thereafter on day 20 (4.4% and 6.1%) to near baseline levels by day 30 (1.4% and 3.3%). Identical levels of resorbing activity were found in the presence or absence of polymyxin-B, an inhibitor of bacterial lipopolysaccharide. These findings demonstrate that bone-resorbing activity is temporally related to periapical bone destruction and suggest that this model may be useful for studies of mediators that are involved in the pathogenesis of inflammatory bone resorption. RP WANG, CY (reprint author), FORSYTH DENT CTR,DEPT IMMUNOL,140 THE FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-09018] NR 24 TC 41 Z9 41 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD OCT PY 1991 VL 70 IS 10 BP 1362 EP 1366 DI 10.1177/00220345910700100901 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA GP327 UT WOS:A1991GP32700009 PM 1939830 ER PT J AU ROSS, DS GRAICHEN, R AF ROSS, DS GRAICHEN, R TI INCREASED RAT FEMUR OSTEOCALCIN MESSENGER-RNA CONCENTRATIONS FOLLOWING INVIVO ADMINISTRATION OF THYROID-HORMONE SO JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION LA English DT Article DE THYROID HORMONE; OSTEOCALCIN ID BONE GLA PROTEIN; SERUM OSTEOCALCIN; L-THYROXINE; HYPERTHYROIDISM; DENSITY; CELLS; GENE; 1,25-DIHYDROXYVITAMIN-D3; SUPPRESSION; METABOLISM AB Thyroid hormone has a direct resorptive effect on bone. Thyroid hormone therapy in doses that suppress pituitary TSH production result in a reduction in bone density. Osteocalcin is a bone matrix protein. Serum levels are a sensitive marker for bone turnover and are increased in hyperthyroid patients. In order to establish an animal model to study the effects of thyroid hormone on bone turnover, we measured rat femur osteocalcin mRNA following in vivo administration of thyroid hormone. Young CD rats weighing 60-90 g were given daily ip injections of T3, T4, or saline (control) for 12 days. Blood was obtained for radioimmunoassays, and RNA was extracted from femurs and analyzed by Northern blot using a 60-mer synthetic oligonucleotide probe corresponding to bases 360-420 of rat osteocalcin mRNA, labeled with [32P] ATP by 5'-end-labeling. Serum TSH concentrations were suppressed to subnormal levels by the lowest doses of T3 and T4, and to undetectable levels by the higher doses. Increases in serum T3 and T4 concentrations were proportional to the dose of each administered hormone. T3, 5 and 10-mu-g/l g body weight, resulted in a 43% and 62% increase in osteocalcin mRNA, respectively. T4, 5, 10, and 20-mu-g/100 g body weight. resulted in a 35%, 47%, and 135% increase in osteocalcin mRNA, respectively. These data demonstrate that in vivo administration of either T4, or T3 to young rats results in a significant dose-dependent increase in femur osteocalcin mRNA concentrations. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ROSS, DS (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,THYROID UNIT,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK-01415] NR 34 TC 7 Z9 7 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0391-4097 J9 J ENDOCRINOL INVEST JI J. Endocrinol. Invest. PD OCT PY 1991 VL 14 IS 9 BP 763 EP 766 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GQ753 UT WOS:A1991GQ75300008 PM 1761812 ER PT J AU SY, MS GUO, YJ STAMENKOVIC, I AF SY, MS GUO, YJ STAMENKOVIC, I TI DISTINCT EFFECTS OF 2 CD44 ISOFORMS ON TUMOR-GROWTH INVIVO SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID HYALURONATE RECEPTOR; CELL-ADHESION; MOLECULE; LYMPHOMA; GLYCOPROTEIN; ACTIVATION; ANTIBODIES; EXPRESSION; PROTEIN; SURFACE AB Tumor growth is dependent in part on interactions between tumor cells and the extracellular matrix of host tissues. Expression of the cell surface glycoprotein CD44/Pgp-1, which mediates cell-substrate interactions is increased in many types of malignancies, but the role of CD44 in tumor growth is largely undefined. Recently, two isoforms of CD44 have been identified: an 80-90 kD form, which has high affinity for cell bound hyaluronate and a 150 kD form which does not mediate attachment to hyaluronate-coated surfaces. In this work, human B cell lymphoma cells stably transfected with cDNA clones encoding either of the two CD44 isoforms were compared for tumorigenicity and metastatic potential in nude mice. Expression of the 80-90 kD form but not the 150 kD form of CD44 greatly enhanced both local tumor formation and metastatic proclivity of the lymphoma cells. Our results suggest that CD44 polypeptides may play an important role in regulating primary and metastatic tumor development in vivo. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,PATHOL RES LAB,BLDG 149,7TH FLOOR,13TH ST,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NIAID NIH HHS [AI-27740]; NIGMS NIH HHS [GM-43257] NR 29 TC 327 Z9 331 U1 1 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD OCT 1 PY 1991 VL 174 IS 4 BP 859 EP 866 DI 10.1084/jem.174.4.859 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA GJ109 UT WOS:A1991GJ10900014 PM 1919439 ER PT J AU ARUFFO, A MELNICK, MB LINSLEY, PS SEED, B AF ARUFFO, A MELNICK, MB LINSLEY, PS SEED, B TI THE LYMPHOCYTE GLYCOPROTEIN-CD6 CONTAINS A REPEATED DOMAIN-STRUCTURE CHARACTERISTIC OF A NEW FAMILY OF CELL-SURFACE AND SECRETED PROTEINS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID T DIFFERENTIATION ANTIGEN; MONOCLONAL-ANTIBODY; MOLECULAR-CLONING; SEQUENCE; RECOGNITION; SUPERFAMILY; EXPRESSION; ANTI-T12; RECEPTOR; SERUM AB The isolation, characterization, and expression of a full-length cDNA encoding the human T cell glycoprotein CD6 is described. COS cells transfected with the CD6 clone express a 90-kD protein that reacts with all available anti-CD6 monoclonal antibodies. RNA blot hybridization analysis indicates that CD6 transcripts are predominantly restricted to cells in the T lineage. The predicted CD6 sequence is 468 amino acids long, with the typical features of a type I integral membrane protein. The cytoplasmic domain of CD6 contains two serine residues, one or both of which are substrates for phosphorylation during T cell activation. The extracellular domain of CD6 is significantly related to the extracellular domain of the human mouse T cell antigen CD5, the cysteine-rich domain of the bovine and mouse type I macrophage scavenger receptor, the extracellular domain of the sea urchin spermatozoa protein that crosslinks the egg peptide speract, the mammalian complement factor 1, and the human lung tumor antigen L3. These molecules, therefore, constitute a new gene superfamily that is well conserved across species boundaries. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP ARUFFO, A (reprint author), BRISTOL MYERS SQUIBB INC,PHARMACEUT RES INST,3005 1ST AVE,SEATTLE,WA 98121, USA. FU NIAID NIH HHS [AI-27849]; NIDDK NIH HHS [DK-43031] NR 32 TC 137 Z9 138 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD OCT 1 PY 1991 VL 174 IS 4 BP 949 EP 952 DI 10.1084/jem.174.4.949 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA GJ109 UT WOS:A1991GJ10900025 PM 1919444 ER PT J AU PIKE, MC COSTELLO, K SOUTHWICK, FS AF PIKE, MC COSTELLO, K SOUTHWICK, FS TI STIMULATION OF HUMAN POLYMORPHONUCLEAR LEUKOCYTE PHOSPHATIDYLINOSITOL-4-PHOSPHATE KINASE BY CONCANAVALIN-A AND FORMYL-METHIONYL-LEUCYL-PHENYLALANINE IS CALCIUM-INDEPENDENT - CORRELATION WITH MAINTENANCE OF ACTIN ASSEMBLY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN-NEUTROPHILS; PHOSPHOINOSITIDE TURNOVER; INTRACELLULAR CALCIUM; CHEMOTACTIC PEPTIDES; RABBIT NEUTROPHILS; RESPIRATORY BURST; POLYPHOSPHOINOSITIDES; GELSOLIN; PROTEIN; CELLS AB Chemoattractants directly stimulate the enzyme activity that synthesizes phosphatidylinositol-4,5-bisphosphate (PIP2), phosphoinositol-4-monophosphate (PIP) kinase. The present study determined whether stimulation of this enzyme correlates with actin assembly by assessing the calcium dependence of this reaction. Incubation of neutrophils with 5 to 100-mu-g/ml Con A caused a concentration-dependent increase in PIP kinase activity ranging from 1.38- to 3.4-fold. The effective concentration which stimulated PIP kinase by 50% (17-mu-g/ml, EC50) corresponded with the EC50 for Con A-induced superoxide production (32-mu-g/ml). Like chemoattractants, the increase in PIP kinase by Con A was characterized by a 2.6-fold increase in the maximum velocity (V(max)) of the enzyme, and no change in the K(m) for ATP. The kinetics of FMLP- and Con A-induced filamentous actin formation preceded stimulation of PIP kinase and was sustained over the same time period that this increased enzyme activity was noted. Although transmembrane signaling by FMLP and Con A requires an increase in intracellular calcium for some polymorphonuclear leukocyte (PMN) functional responses, calcium depletion of PMN by incubation with 100-mu-M Quin 2 A/M and 5 mM EGTA did nto prevent the stimulation of PIP kinase by FMLP or Con A. In addition, calcium depletion did not prevent the increase in filamentous actin formation by FMLP and Con A in PMN. These findings demonstrate that Con A increases PIP kinase activity in human PMN and that PIP kinase stimulation and maintenance of actin assembly are independent of calcium fluxes in these cells. Because PIP2 controls the function of the actin-regulatory proteins, profilin and gelsolin, changes in the synthetic rate of PIP2 through regulation of PIP kinase may provide a molecular basis for the prolonged stimulation of actin assembly in human PMN by agonists such as Con A and FMLP. C1 UNIV FLORIDA,DIV INFECT DIS,GAINESVILLE,FL 32610. RP PIKE, MC (reprint author), MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,BULFINCH 1,BOSTON,MA 02114, USA. FU NIAID NIH HHS [P01 AI28465, R01 AI023262, R01 AI28386] NR 35 TC 10 Z9 10 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD OCT 1 PY 1991 VL 147 IS 7 BP 2270 EP 2275 PG 6 WC Immunology SC Immunology GA GH524 UT WOS:A1991GH52400031 PM 1655888 ER PT J AU SCHILLER, JH LINDSTROM, M WITT, PL HANK, JA MAHVI, D WAGNER, RJ SONDEL, P BORDEN, EC AF SCHILLER, JH LINDSTROM, M WITT, PL HANK, JA MAHVI, D WAGNER, RJ SONDEL, P BORDEN, EC TI IMMUNOLOGICAL EFFECTS OF LEVAMISOLE INVITRO SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE LEVAMISOLE; DUKES C-COLORECTAL CARCINOMA; 5-FLUOROURACIL ID ADJUVANT THERAPY; HUMAN-MONOCYTES; 2',5'-OLIGOADENYLATE SYNTHETASE; INDOLEAMINE 2,3-DIOXYGENASE; THORACIC IRRADIATION; HUMAN-LYMPHOCYTES; RANDOMIZED TRIAL; HODGKINS-DISEASE; GENERATED INVIVO; COLON-CARCINOMA AB Levamisole, an antihelminthic drug with immunological properties, has recently been reported to have antitumor activity when administered with 5-fluorouracil in patients with Duke's C colorectal carcinoma. The mechanism of this antitumor effect is unknown, but has been postulated to be related to levamisole's immunomodulatory properties. To define further the immunomodulatory activities of levamisole, we studied the in vitro effects of levamisole on monocyte and lymphocyte cytotoxicity, activation, and proliferation; induction of cytokine-induced proteins; and expression of tumor-associated antigens. Experiments utilized peripheral blood mononuclear cells from normal donors incubated in the presence of increasing concentrations of levamisole (0.1 to 100-mu-g/ml). Levamisole had no consistent effect on induction of 2',5'-oligoadenylate synthetase activity or indoleamine-2,3-dioxygenase activity, or production of tumor necrosis factor. Levamisole had no effect on monocyte cytotoxicity or expression of HLA-DR, HLA-DQ, HLA-DP, and the Fc receptor. Similarly, levamisole had no significant effect on NK or LAK cytotoxicity or the immunological activation of T-lymphocytes, assessed by expression of CD3, CD4, CD8, CD16, CD25, and CD56. Proliferation of lymphocytes from normal donors, patients with benign polyps, and patients with malignancies, with or without IL-2 or irradiated LS174T cells, was not significantly increased overall. No significant enhancement in the expression of three tumor-associated antigens (880364, NRCO-4, and ING-1) and the intercellular adhesion molecule-1 (ICAM-1) antigen on four human cancer cell lines was observed following in vitro exposure to levamisole. We conclude that levamisole is not a potent modulator of the immune parameters we examined, and that the mechanism behind the unique clinical interaction between levamisole and 5-fluorouracil in colorectal carcinoma remains to be identified. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT BIOSTAT,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT SURG,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT HUMAN ONCOL,MADISON,WI 53705. UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53706. FU NCI NIH HHS [NCI-CM-87215-18] NR 43 TC 19 Z9 19 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD OCT PY 1991 VL 10 IS 5 BP 297 EP 306 DI 10.1097/00002371-199110000-00001 PG 10 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA GH358 UT WOS:A1991GH35800001 PM 1790137 ER PT J AU JOHNSON, VA MERRILL, DP VIDELER, JA CHOU, TC BYINGTON, RE ERON, JJ DAQUILA, RT HIRSCH, MS AF JOHNSON, VA MERRILL, DP VIDELER, JA CHOU, TC BYINGTON, RE ERON, JJ DAQUILA, RT HIRSCH, MS TI 2-DRUG COMBINATIONS OF ZIDOVUDINE, DIDANOSINE, AND RECOMBINANT INTERFERON-ALPHA A INHIBIT REPLICATION OF ZIDOVUDINE-RESISTANT HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SYNERGISTICALLY INVITRO SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; PHASE-I TRIAL; DOUBLE-BLIND; 2',3'-DIDEOXYINOSINE DDI; REVERSE-TRANSCRIPTASE; AZIDOTHYMIDINE AZT; KAPOSIS SARCOMA; HIV INFECTION; THERAPY AB Optimal management of human immunodeficiency virus type 1 (HIV-1) infections may require combinations of anti-HIV-1 agents. Zidovudine(AZT, 3'-azido-3'-deoxythymidine), didanosine (ddI, 2',3'-dideoxyinosine), and recombinant interferon-alpha A (rIFN-alpha-A) were evaluated in two-drug regimens against replication of AZT-resistant HIV-1 in vitro. AZT-sensitive and AZT-resistant isolate pairs derived from two individuals before and after extended AZT monotherapy were studied. Drug interactions using peripheral blood mononuclear cells infected with HIV-1 were evaluated mathematically. Synergistic interactions were seen among AZT, ddI, and rIFN-alpha-A in two-drug regimens against AZT-resistant HIV-1 in vitro, even when AZT was included in the treatment regimen. Mixtures of wild-type and mutant reverse transcriptase genes were found in one of the late-AZT therapy, isolates, suggesting that the mechanism of synergy of AZT-containing regimens may involve inhibition of AZT-sensitive viruses in the viral pool. These studies suggest that AZT may be useful in drug combination regimens, even when AZT-resistant viruses are isolated in vitro. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MEM SLOAN KETTERING CANC CTR,BIOCHEM PHARMACOL LAB,NEW YORK,NY 10021. RP JOHNSON, VA (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114, USA. RI Chou, Ting-Chao/B-4111-2009 OI Chou, Ting-Chao/0000-0002-3340-1594 FU NCI NIH HHS [CA-12464, CA-35020]; NIAID NIH HHS [AI-26056] NR 65 TC 129 Z9 129 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD OCT PY 1991 VL 164 IS 4 BP 646 EP 655 PG 10 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA GF805 UT WOS:A1991GF80500003 PM 1716649 ER PT J AU VANDERHORST, C JONCAS, J AHRONHEIM, G GUSTAFSON, N STEIN, G GURWITH, M FLEISHER, G SULLIVAN, J SIXBEY, J ROLAND, S FRYER, J CHAMPNEY, K SCHOOLEY, R SUMAYA, C PAGANO, JS AF VANDERHORST, C JONCAS, J AHRONHEIM, G GUSTAFSON, N STEIN, G GURWITH, M FLEISHER, G SULLIVAN, J SIXBEY, J ROLAND, S FRYER, J CHAMPNEY, K SCHOOLEY, R SUMAYA, C PAGANO, JS TI LACK OF EFFECT OF PERORAL ACYCLOVIR FOR THE TREATMENT OF ACUTE INFECTIOUS-MONONUCLEOSIS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID EPSTEIN-BARR VIRUS; NUCLEAR ANTIGEN; REPLICATION; ANTIBODIES; CELLS; DNA AB Perorally administered acyclovir was evaluated in the therapy of acute infectious mononucleosis in a multicentered, randomized, double-blind, placebo-controlled trial. A total of 120 patients received 600 mg of acyclovir or placebo five times daily for 10 days. All patients were entered into the study within 7 days of symptom onset and had a positive Monospot test. Analysis of mean values and time to resolution of fever, lymphadenopathy, weight change, hepatomegaly, splenomegaly, liver function tests, atypical lymphocytes, hours of bed rest, sense of well-being, and return to normal activities revealed no significant differences. There was a trend toward suppression of Epstein-Barr virus excretion in the oropharynx in acyclovir recipients. No toxicity was detected in patients treated with acyclovir. Under the conditions of the study, there was no evidence that treatment with perorally administered acyclovir affected the course of infectious mononucleosis. C1 UNIV N CAROLINA, SCH MED, LINEBERGER COMPREHENS CANC CTR, CHAPEL HILL, NC 27514 USA. UNIV N CAROLINA, SCH PUBL HLTH, DEPT BIOSTAT, CHAPEL HILL, NC 27514 USA. RES TRIANGLE INST, RES TRIANGLE PK, NC 27709 USA. BURROUGHS WELLCOME CO, RES TRIANGLE PK, NC 27709 USA. UNIV MASSACHUSETTS, SCH MED, DEPT PEDIAT, WORCESTER, MA 01605 USA. MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. MICHIGAN STATE UNIV, SCH MED, DEPT MED, E LANSING, MI 48824 USA. CHILDRENS HOSP, PHILADELPHIA, PA 19104 USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA. UNIV TEXAS, SCH MED, DEPT PEDIAT, SAN ANTONIO, TX 78285 USA. HOP ST JUSTINE, DEPT MICROBIOL & IMMUNOL, MONTREAL H3T 1C5, QUEBEC, CANADA. UNIV MONTREAL, MONTREAL H3C 3J7, QUEBEC, CANADA. RP VANDERHORST, C (reprint author), UNIV N CAROLINA, DEPT MED, DIV INFECT DIS, CB 7030, CHAPEL HILL, NC 27599 USA. FU NIAID NIH HHS [AI-07151] NR 15 TC 53 Z9 54 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD OCT PY 1991 VL 164 IS 4 BP 788 EP 792 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA GF805 UT WOS:A1991GF80500027 PM 1654364 ER PT J AU KOUL, O PRADAMALUF, M MCCLUER, RH ULLMAN, MD AF KOUL, O PRADAMALUF, M MCCLUER, RH ULLMAN, MD TI RAPID ISOLATION OF MONOSIALOGANGLIOSIDES FROM BOVINE BRAIN GANGLIOSIDES BY SELECTIVE-OVERLOAD CHROMATOGRAPHY SO JOURNAL OF LIPID RESEARCH LA English DT Note DE GM1; Q-SEPHAROSE ID LIQUID-CHROMATOGRAPHY; SEPARATION AB A procedure for rapid isolation of monosialogangliosides from purified bovine brain gangliosides has been developed. It utilizes the selective difference in association between monosialogangliosides and polysialogangliosides for the ion-exchange resin Q-Sepharose. When the ion-exchange column is overloaded with a bovine brain ganglioside mixture in the proper ganglioside to column bed-volume ratio, the polysialogangliosides are selectively retained by the column while the monosialogangliosides emerge with the void volume without the use of salt for elution. With the critical ganglioside to bed-volume ratio (1 g:8.32 ml), and an appropriate column bed-height to column radius ratio of 6.9, monosialogangliosides are reproducibly obtained in high purity with greater than 90% yield. The method has been used at both the analytical and preparative scale. We call this separation technique selective-overload chromatography. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. VET ADM MED CTR,RES GRECC,BEDFORD,MA 01730. RP KOUL, O (reprint author), EK SHRIVER CTR,DIV BIOCHEM,200 TRAPELO RD,WALTHAM,MA 02254, USA. NR 11 TC 5 Z9 5 U1 0 U2 1 PU LIPID RESEARCH INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD OCT PY 1991 VL 32 IS 10 BP 1712 EP 1715 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GL740 UT WOS:A1991GL74000016 PM 1797951 ER PT J AU ANSON, JA KOSHY, M FERGUSON, L CROWELL, RM AF ANSON, JA KOSHY, M FERGUSON, L CROWELL, RM TI SUBARACHNOID HEMORRHAGE IN SICKLE-CELL DISEASE SO JOURNAL OF NEUROSURGERY LA English DT Article DE ANEMIA; ANEURYSM; BLOOD TRANSFUSION; SICKLE-CELL DISEASE; SUBARACHNOID HEMORRHAGE ID INTRACRANIAL ANEURYSMS; TRANSFUSION THERAPY; ANEMIA; HEMOGLOBINOPATHIES; COMPLICATIONS; MANAGEMENT; ANESTHESIA; ADHERENCE; OCCLUSION; PATIENT AB The neurological complications of sickle-cell disease include cerebral infarction and intracerebral hemorrhage; subarachnoid hemorrhage (SAH) has been infrequently reported. Among 325 patients with sickle-cell disease followed at the University of Illinois between 1975 and 1989, 11 cases of SAH were identified. Aneurysms were found in 10 of these patients, three of whom had multiple aneurysms. All of the patients had some degree of anemia and nine underwent craniotomy without hematological or neurological complications. From this review it appears that SAH is not uncommon in sickle-cell disease patients and tends to occur at a younger age and with smaller aneurysm size than in the general population. With proper perioperative management, including exchange transfusions to reduce the proportion of hemoglobin S to less than 30%, these patients can undergo angiography and craniotomy without an increased incidence of complications. The techniques used in managing sickle-cell disease patients with SAH are discussed. C1 UNIV ILLINOIS HOSP,DEPT NEUROSURG,CHICAGO,IL 60612. UNIV ILLINOIS HOSP,DEPT HEMATOL,CHICAGO,IL 60612. MICHAEL REESE HOSP & MED CTR,DEPT NEUROSURG,CHICAGO,IL 60616. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. NR 41 TC 43 Z9 44 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 OCT PY 1991 VL 75 IS 4 BP 552 EP 558 DI 10.3171/jns.1991.75.4.0552 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA GG765 UT WOS:A1991GG76500007 PM 1885973 ER PT J AU MACFARLANE, R TERAMURA, A OWEN, CJ CHASE, S DELATORRE, R GREGORY, KW PETERSON, JW BIRNGRUBER, R PARRISH, JA ZERVAS, NT AF MACFARLANE, R TERAMURA, A OWEN, CJ CHASE, S DELATORRE, R GREGORY, KW PETERSON, JW BIRNGRUBER, R PARRISH, JA ZERVAS, NT TI TREATMENT OF VASOSPASM WITH A 480-NM PULSED-DYE LASER SO JOURNAL OF NEUROSURGERY LA English DT Article DE PULSED-DYE LASER; VASOSPASM; COMMON CAROTID ARTERY; BASILAR ARTERY; SUBARACHNOID HEMORRHAGE; RABBIT; DOG ID REGENERATED ENDOTHELIUM; ANGIOPLASTY; ABSORPTION; DURATION; ARTERIES; INJURY AB Laser energy at a wavelength of 480 nm was applied in 1-mu-sec pulses of 3 to 10 mJ to two models of vasospasm. Rabbit common carotid arteries (CCA's) were constricted chronically by the application of human blood within a silicone sheath. Peak vasospasm developed 24 to 48 hours later, and persisted for up to 6 days. Endovascular laser treatment was delivered to 40 CCA's via a 200-mu-m diameter silica quartz fiber introduced through the femoral artery. The CCA caliber increased from 60% of the pre-vasospasm control diameter to a minimum post-laser diameter of 83% of control. No instances of laser-induced perforation or of arterial thrombosis were observed for up to 60 days after treatment. Prophylactic laser application to nine normal vessels was able to attenuate the development of vasospasm if blood was applied immediately thereafter (88% vs. 59% of control diameter, p < 0.02), but not if blood was applied 7 days later. Studies in 16 normal CCA's established that there was a considerable margin between the laser energy required to induce dilatation and that which caused perforation, providing that the fiber remained relatively central within the artery. Morphological examination demonstrated focal loss of endothelial cells immediately after laser application, followed approximately 7 days later by the development of areas of intimal hyperplasia. Only minimal changes were observed in the medial or adventitial layers. In a second study, the basilar artery of seven dogs was constricted chronically by two intracisternal injections of autologous blood 3 days apart. Five dogs received endovascular laser treatment 7 or 10 days after the first injection, when basilar artery diameter was reduced to a mean of 61% and 77% of control, respectively. Immediately following treatment, basilar artery diameter increased to 104% and 102% of resting diameter, respectively. Both untreated and laser-treated arteries were smaller than the control diameter at 30 days (80% and 82%, respectively), but in each group the vasodilatory response to hypercapnia was preserved. These findings indicate that 1-mu-sec laser pulses are well tolerated by systemic and cerebral arteries in two different animal models, and suggest that the 480-nm pulsed-dye laser may have an application for the treatment or prophylaxis of cerebral vasospasm. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. ADDENBROOKES HOSP,DEPT NEUROL SURG,CAMBRIDGE CB2 2QQ,ENGLAND. RI Birngruber, Reginald/Q-2342-2016 FU NHLBI NIH HHS [HL22573] NR 20 TC 15 Z9 15 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 OCT PY 1991 VL 75 IS 4 BP 613 EP 622 DI 10.3171/jns.1991.75.4.0613 PG 10 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA GG765 UT WOS:A1991GG76500015 PM 1885979 ER PT J AU ALPERT, N AF ALPERT, N TI OPTIMIZATION OF REGIONAL CEREBRAL BLOOD-FLOW MEASUREMENTS WITH PET SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID POSITRON EMISSION TOMOGRAPHY; (H2O)-O-15; DISPERSION RP ALPERT, N (reprint author), MASSACHUSETTS GEN HOSP,DIV NUCL MED,FRUIT ST,BOSTON,MA 02114, USA. NR 10 TC 3 Z9 3 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD OCT PY 1991 VL 32 IS 10 BP 1934 EP 1936 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GH706 UT WOS:A1991GH70600024 PM 1919736 ER PT J AU STRACK, S AF STRACK, S TI FACTOR-ANALYSIS OF MCMI-II AND PACL BASIC PERSONALITY-SCALES IN A COLLEGE SAMPLE SO JOURNAL OF PERSONALITY ASSESSMENT LA English DT Article ID CLINICAL MULTIAXIAL INVENTORY; ADJECTIVE CHECK LIST; MILLON RP STRACK, S (reprint author), US DEPT VET AFFAIRS,OUTPATIENT CLIN,PSYCHOL SERV 116B,425 S HILL ST,LOS ANGELES,CA 90013, USA. NR 23 TC 12 Z9 12 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0022-3891 J9 J PERS ASSESS JI J. Pers. Assess. PD OCT PY 1991 VL 57 IS 2 BP 345 EP 355 DI 10.1207/s15327752jpa5702_12 PG 11 WC Psychology, Clinical; Psychology, Social SC Psychology GA GG107 UT WOS:A1991GG10700012 PM 16370885 ER PT J AU CLARK, HW AF CLARK, HW TI POLICY AND MEDICAL-LEGAL ISSUES IN THE PRESCRIBING OF CONTROLLED SUBSTANCES SO JOURNAL OF PSYCHOACTIVE DRUGS LA English DT Article DE PRESCRIBING; CHRONIC PAIN; MEDICAL-LEGAL; NATIONAL PRACTITIONER DATA BANK; ELECTRONIC DATA TRANSFER; STATE LAWS; FEDERAL LAWS; OPIOIDS; BENZODIAZEPINES AB The physician who prescribes controlled substances is faced with an array of laws, regulatory policies, and professional attitudes about their use. Prescriptions for these scheduled drugs are furthermore monitored by the pharmacists who dispense them. Certain drugs, such as the opioids and the benzodiazepines, are considered so potentially abusive that special programs have been recommended to track the behavior of physician prescribers. Multiple copy programs have been implemented in some states. More recent proposals recommend electronic data transfer (EDT) of pharmacy information to centralized processing points so that misprescribing physicians and doctor-shopping patients can be identified. Regulators concerned about physician behavior and confronted by demands of nonphysicians to prescribe controlled substances may find EDT a good solution. Physicians should be concerned about being censured for misprescribing, because such actions may lead to inclusion in the National Practitioner Data Bank. With all of the regulatory concerns about controlled substances, those physicians who would employ longterm opioid therapy for their chronic pain patients must follow certain basic guidelines to be able to defend themselves against allegations of deviant professional behavior. Such procedures as conducting a history and physical examination, maintaining a written treatment plan, consulting with knowledgeable colleagues, and assessing for addictive behavior can provide the practitioner with safeguards. C1 SAN FRANCISCO VET AFFAIRS MED CTR,DEPT PSYCHIAT,SUBST ABUSE SERV,SUBST ABUSE PROGRAM,SAN FRANCISCO,CA 94121. SAN FRANCISCO VET AFFAIRS MED CTR,DEPT PSYCHIAT,SUBST ABUSE SERV,HIV PROGRAM,SAN FRANCISCO,CA 94121. RP CLARK, HW (reprint author), UNIV CALIF SAN FRANCISCO,PSYCHIAT,SAN FRANCISCO,CA 94143, USA. FU NIDA NIH HHS [R18-DA06097] NR 13 TC 7 Z9 7 U1 0 U2 1 PU HAIGHT-ASHBURY PUBL PI SAN FRANCISCO PA 409 CLAYTON ST, SAN FRANCISCO, CA 94117 SN 0279-1072 J9 J PSYCHOACTIVE DRUGS JI J. Psychoact. Drugs PD OCT-DEC PY 1991 VL 23 IS 4 BP 321 EP 328 PG 8 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA HJ339 UT WOS:A1991HJ33900002 PM 1813603 ER PT J AU SONG, JD LEE, C LIN, CHS CHEN, LB AF SONG, JD LEE, C LIN, CHS CHEN, LB TI ELECTRON-MICROSCOPIC STUDIES OF THE ENDOPLASMIC-RETICULUM IN WHOLE-MOUNT CULTURED-CELLS FIXED WITH POTASSIUM-PERMANGANATE SO JOURNAL OF STRUCTURAL BIOLOGY LA English DT Article ID LIVING CELLS; LOCALIZATION; ANTIBODIES; RAT C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NICHD NIH HHS [HD24926]; NIGMS NIH HHS [GM38318] NR 24 TC 8 Z9 17 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1047-8477 J9 J STRUCT BIOL JI J. Struct. Biol. PD OCT PY 1991 VL 107 IS 2 BP 106 EP 115 DI 10.1016/1047-8477(91)90014-N PG 10 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA GM774 UT WOS:A1991GM77400002 PM 1807347 ER PT J AU FIFER, MA AF FIFER, MA TI WHAT DOES POSITRON EMISSION TOMOGRAPHY TEACH US ABOUT CORONARY ANGIOPLASTY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Editorial Material ID MYOCARDIAL PERFUSION; ABNORMALITIES; DYSFUNCTION; METABOLISM; ANGINA; HEART C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FIFER, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,WACC 478,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 19 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 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD OCT PY 1991 VL 18 IS 4 BP 979 EP 981 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GH897 UT WOS:A1991GH89700013 PM 1894872 ER PT J AU VIRGIN, HW TYLER, KL AF VIRGIN, HW TYLER, KL TI ROLE OF IMMUNE CELLS IN PROTECTION AGAINST AND CONTROL OF REOVIRUS INFECTION IN NEONATAL MICE SO JOURNAL OF VIROLOGY LA English DT Article ID CENTRAL NERVOUS-SYSTEM; LYMPHOCYTE-T CLONES; VIRUS-INFECTION; MONOCLONAL-ANTIBODY; VIRAL HEMAGGLUTININ; MOLECULAR-BASIS; GENE; CLEARANCE; VIRULENCE; INVIVO AB We studied the role of T cells in resistance to reovirus intestinal and central nervous system infection. Transfer of reovirus-immune adult spleen cells protected neonatal mice from (i) lethal infection with reovirus serotype 3 Dearing (T3D, footpad inoculation) and serotype 3 clone 9 (T3C9, oral inoculation) and (ii) hydrocephalus caused by serotype 1 Lang (T1L, intracranial [i.c.] inoculation). Cell-mediated protection was not serotype specific. While immune cells protected against T1L i.c., they failed to protect against 1/5,000 of the dose of T3D i.c. Two types of experiments showed that both CD4 and CD8 T cells are involved in reovirus resistance. First, immune cell-mediated protection against T3D was abrogated by in vivo treatment with anti-CD4 monoclonal antibody (MAb) and significantly inhibited by in vivo treatment with anti-CD8 MAb. Second, T3C9-infected neonatal mice treated with anti-CD4 and/or anti-CD8 developed a novel disease phenotype, an oily hair syndrome, associated with severe hepatobiliary pathology and increased viral titer in heart and liver. Immune cells and an MAb to the cell attachment protein sigma-1 (MAb G5) protected by different mechanisms. Immune cells were more effective than sigma-1 MAb G5 at controlling primary replication, while sigma-1 MAb G5 was more effective than immune cells at inhibiting neural spread of virus. We conclude that both CD4 and CD8 T cells are important for reovirus resistance, that cells and antibody act preferentially at different stages in pathogenesis in vivo, and that adoptively transferred immune cells can protect both the central nervous system and intestine. C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. OI Tyler, Kenneth/0000-0003-3294-5888 FU NIAID NIH HHS [K11 AI00610]; NINDS NIH HHS [2 P50 NS16998] NR 51 TC 25 Z9 25 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 OCT PY 1991 VL 65 IS 10 BP 5157 EP 5164 PG 8 WC Virology SC Virology GA GF097 UT WOS:A1991GF09700004 PM 1654436 ER PT J AU RAPTIS, L MARCELLUS, R CORBLEY, MJ KROOK, A WHITFIELD, J ANDERSON, SK HALIOTIS, T AF RAPTIS, L MARCELLUS, R CORBLEY, MJ KROOK, A WHITFIELD, J ANDERSON, SK HALIOTIS, T TI CELLULAR RAS GENE ACTIVITY IS REQUIRED FOR FULL NEOPLASTIC TRANSFORMATION BY POLYOMAVIRUS SO JOURNAL OF VIROLOGY LA English DT Article ID MIDDLE-T-ANTIGEN; PROTEIN KINASE-C; GTPASE ACTIVATING PROTEIN; TYROSINE PHOSPHORYLATION; CELLS; VIRUS; PP60C-SRC; PRODUCT; ASSOCIATION; EXPRESSION AB To investigate the role of ras gene activity in cellular transformation by polyomavirus, murine C3H10T1/2 cells were rendered ras deficient by transfection with an antisense ras gene construct. Ras deficiency resulted in a partial suppression of the polyomavirus-induced transformed phenotype. The production of viral middle T antigen and its association with pp60c-src, increased membrane-associated protein kinase C activity, and morphological transformation were unaffected by the downregulation of c-ras gene expression. On the other hand, stimulated proliferation, focus formation on confluent monolayers of normal cells, and colony formation in soft agar were all greatly reduced in cells containing reduced p21ras levels. It is concluded that ras gene activity is needed for full cell transformation by polyomavirus. C1 QUEENS UNIV,DEPT PATHOL,KINGSTON K7L 3N6,ONTARIO,CANADA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NATL RES COUNCIL CANADA,INST BIOL SCI,CELL SYST SECT,OTTAWA K1A 0R6,ONTARIO,CANADA. BIOTECHNOL RES INST,MONTREAL H4P 2R2,QUEBEC,CANADA. RP RAPTIS, L (reprint author), QUEENS UNIV,DEPT MICROBIOL & IMMUNOL,KINGSTON K7L 3N6,ONTARIO,CANADA. RI Anderson, Stephen/B-1727-2012; Krook, Anna/K-1192-2015 OI Anderson, Stephen/0000-0002-7856-4266; Krook, Anna/0000-0002-0891-0258 NR 54 TC 41 Z9 41 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 OCT PY 1991 VL 65 IS 10 BP 5203 EP 5210 PG 8 WC Virology SC Virology GA GF097 UT WOS:A1991GF09700010 PM 1654439 ER PT J AU MARSILIO, E CHENG, SH SCHAFFHAUSEN, B PAUCHA, E LIVINGSTON, DM AF MARSILIO, E CHENG, SH SCHAFFHAUSEN, B PAUCHA, E LIVINGSTON, DM TI THE T/T COMMON REGION OF SIMIAN VIRUS-40 LARGE T-ANTIGEN CONTAINS A DISTINCT TRANSFORMATION-GOVERNING SEQUENCE SO JOURNAL OF VIROLOGY LA English DT Note ID LARGE TUMOR-ANTIGEN; ADENOVIRUS E1A GENE; SV40 LARGE-T; RAT EMBRYO FIBROBLASTS; DNA-BINDING DOMAIN; MUTATIONAL ANALYSIS; FUNCTIONAL DOMAINS; NUCLEAR LOCATION; MUTANTS; CELLS AB Simian virus 40 large T antigen (T) can transform cultured cells, but the mechanisms by which it functions are not entirely understood. Several lines of evidence have suggested that the amino-terminal approximately 130 residues of T may be sufficient to confer the transforming capability. Oligonucleotide-directed mutagenesis was used to generate a series of deletion and substitution mutants within the amino-terminal 82 residues of T, the segment which is shared with simian virus 40 small t antigen (t). Results of stability and transformation assays of these mutants strongly suggest that the 1-to-82 region of T contains sequences which govern T transforming activity and affect in vivo stability. Instability and a defect in transforming activity could be separated from one another genetically. Thus, the 1-to-82 region appears to contain a specific region that contributes to the transforming function of the protein. This segment operates by means other than the simple binding of pRb and/or p107. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. GENZYME CORP,CELLULAR REGULAT LAB,FRAMINGHAM,MA 01701. TUFTS UNIV,DEPT BIOCHEM,BOSTON,MA 02111. NR 51 TC 48 Z9 48 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 OCT PY 1991 VL 65 IS 10 BP 5647 EP 5652 PG 6 WC Virology SC Virology GA GF097 UT WOS:A1991GF09700073 PM 1654462 ER PT J AU HEYMAN, SN BREZIS, M EPSTEIN, FH SPOKES, K SILVA, P ROSEN, S AF HEYMAN, SN BREZIS, M EPSTEIN, FH SPOKES, K SILVA, P ROSEN, S TI EARLY RENAL MEDULLARY HYPOXIC INJURY FROM RADIOCONTRAST AND INDOMETHACIN SO KIDNEY INTERNATIONAL LA English DT Article ID PERFUSED RAT-KIDNEY; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; THICK ASCENDING LIMB; TUBULAR-NECROSIS; PROXIMAL TUBULE; CONTRAST-MEDIA; RISK-FACTORS; BLOOD-FLOW; FAILURE; ISCHEMIA AB We evaluated the acute changes in cortical and outer medullary oxygen tension and the alterations in renal function and morphology within the first 90 minutes after the administration of indomethacin and iothalamate to anesthetized Sprague-Dawley rats. Both agents were found to produce marked and protracted outer medullary hypoxia averaging 12 +/- 4 and 9 +/- 2 mm Hg, respectively (mean +/- SE). Given together to salt depleted uninephrectomized rats they produced an early hypoxic injury localized selectively in the outer medulla. This lesion progressed from 3 +/- 1% of medullary thick ascending limbs (mTALs) at 15 minutes to 22 +/- 7% at 24 hours. Condensed "dark" cells were observed at 15 minutes, probably representing a type of early injury. Residual red cell mass, quantified in the outer medullary vasculature of perfusion-fixed kidneys and presumably reflecting stasis, was substantially increased in iothalamate treated rats. Red cells mass in the interbundle zone correlated with mTAL necrosis. Taken together, these results show an early period of medullary hypoxia, accompanied by a selective injury to mTALs in the central interbundle zone with apparent stasis. These findings contrast sharply with the ischemia-reflow pattern of renal damage and emphasize the important role of medullary hypoxia in the genesis of acute renal failure in this model. C1 BETH ISRAEL HOSP,DEPT PATHOL,330 BROOKLINE AVE,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. HEBREW UNIV JERUSALEM,HADASSAH UNIV HOSP,SCH MED,HARVARD CTR STUDY KIDNEY DIS,JERUSALEM,ISRAEL. HEBREW UNIV JERUSALEM,HADASSAH UNIV HOSP,SCH MED,DEPT MED,JERUSALEM,ISRAEL. RI Brezis, Mayer/A-1041-2010 FU NIDDK NIH HHS [DK 18078, DK 39249] NR 43 TC 205 Z9 208 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD OCT PY 1991 VL 40 IS 4 BP 632 EP 642 DI 10.1038/ki.1991.255 PG 11 WC Urology & Nephrology SC Urology & Nephrology GA GT736 UT WOS:A1991GT73600007 PM 1745012 ER PT J AU HDOUBLER, PB PETERSEN, M SHEK, W AUCHINCLOSS, H ABBOTT, WM ORKIN, RW AF HDOUBLER, PB PETERSEN, M SHEK, W AUCHINCLOSS, H ABBOTT, WM ORKIN, RW TI SPONTANEOUSLY HYPERTENSIVE AND WISTAR KYOTO RATS ARE GENETICALLY DISPARATE SO LABORATORY ANIMAL SCIENCE LA English DT Article AB Spontaneously hypertensive rats (SHR) are one of the most common animal models use to study essential hypertension in humans. Because SHR and normotensive Wistar Kyoto (WKY) rats were both established from the same parental, normotensive Wistar stock, WKY animals have been used almost exclusively as control animals in studies of SHR. Recently, the suitability of WKY rats as normotensive controls for SHR has been challenged. To establish whether or not SHR and WKY rats share the same immunologic backgrounds, we initially performed a series of skin grafting experiments on these animals. In all cases, grafts of SHR donor skin to WKY recipients and of WKY donor skin to SHR recipients resulted in complete rejection within 7 to 10 days. In addition, grafts of WKY donor skin to other WKY recipients resulted in graft rejection. By contrast, skin grafts between SHRs were always accepted. To further characterize the genetic distinctions between SHR and WKY rats, allelic profiles based on a series of immunologic and biochemical markers were established for each strain. These findings clearly establish that SHR and WKY rats differ at the major histocompatibility complex, in specific blood group antigens, and in a panel of isozymic markers. Moreover, whereas SHRs have the same genetic profiles irrespective of source, some colonies of WKY rats are outbred, as judged by their variant allelic profiles. C1 CHARLES RIVER LABS, WILMINGTON, MA 01887 USA. HARVARD UNIV, SCH MED, DEPT SURG, BOSTON, MA 02114 USA. RP HDOUBLER, PB (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, DIV VASC, SURG SERV, BOSTON, MA 02114 USA. FU NHLBI NIH HHS [HL34780]; NIAMS NIH HHS [AR25527] NR 12 TC 8 Z9 8 U1 1 U2 1 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI MEMPHIS PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA SN 0023-6764 J9 LAB ANIM SCI JI Lab. Anim. Sci. PD OCT PY 1991 VL 41 IS 5 BP 471 EP 473 PG 3 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA HB766 UT WOS:A1991HB76600017 PM 1666150 ER PT J AU SAMSON, MJ METSON, R WANG, CC MONTGOMERY, WW AF SAMSON, MJ METSON, R WANG, CC MONTGOMERY, WW TI PRESERVATION OF THE FACIAL-NERVE IN THE MANAGEMENT OF RECURRENT PLEOMORPHIC ADENOMA SO LARYNGOSCOPE LA English DT Article ID PAROTID-GLAND; RADIATION-THERAPY; TUMORS; RADIOTHERAPY AB Whether to preserve or sacrifice a facial nerve involved with benign neoplasm is one of the most difficult intraoperative decisions confronting the head and neck surgeon. We reviewed 21 cases of recurrent pleomorphic adenoma treated with subtotal excision and facial nerve preservation, followed by postoperative radiation therapy. Of the 17 patients with microscopic residual tumor at completion of surgery, 16 (94%) remain free of recurrence with an average follow-up of 5.9 years. Only one of four patients (25%) with a large postoperative tumor load remains free of disease. Facial nerve function is normal in 20 of 21 patients. Preservation of the facial nerve with postoperative irradiation should be considered as an alternative to nerve sacrifice in selected cases of recurrent pleomorphic adenoma. C1 MASSACHUSETTS EYE & EAR HOSP,DEPT OTOLARYNGOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA 02114. RP METSON, R (reprint author), ZERO EMERSON PL,BOSTON,MA 02114, USA. NR 16 TC 33 Z9 33 U1 0 U2 0 PU LARYNGOSCOPE CO PI ST LOUIS PA 10 S BROADWAY 14TH FLOOR, ST LOUIS, MO 63102-1741 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD OCT PY 1991 VL 101 IS 10 BP 1060 EP 1062 PG 3 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA GU814 UT WOS:A1991GU81400006 PM 1656154 ER PT J AU HAREGEWOIN, A HOM, RC SOMAN, G FINBERG, RW AF HAREGEWOIN, A HOM, RC SOMAN, G FINBERG, RW TI MURINE T-CELL HYBRIDOMA-DERIVED PRODUCTS REGULATE THE GROWTH OF SKELETAL-MUSCLE MYOBLASTS SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID FIBROBLAST GROWTH; LYMPHOCYTES-T; MUSCULAR-DYSTROPHY; FACTOR-BETA; DIFFERENTIATION; INVITRO; INTERLEUKIN-2; LYMPHOKINE; EXPRESSION; ANTIGEN AB We have analyzed the effects of T cell products on the growth of murine myoblasts. Supernatants from some T cell hybridomas were shown to have either growth factor activity or growth inhibitory activity on two myoblast lines raised in our laboratory from two different strains of mice and also on the C2C12 myoblast line. The hybridoma-derived growth factor activity was shown not to require cofactors contained in serum as its effects could be demonstrated in assays done in serum-free media. Further studies on the effects of purified lymphokines on myoblasts using recombinant IL-2, IL-3, IL-4, IL-6, and GM-CSF showed these lymphokines not to have any growth stimulatory activity indicating that factor(s) other than the ones tested may be operative. Characterization by dialysis and column chromatography of hybridoma supernatants revealed the presence of a low-molecular-weight inhibitor and a higher-molecular-weight growth factor that was found in several hybridoma supernatants. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP HAREGEWOIN, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU PHS HHS [2 PO1 DR33506, A12038] NR 35 TC 1 Z9 1 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 OCT PY 1991 VL 10 IS 5 BP 391 EP 396 PG 6 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA GR699 UT WOS:A1991GR69900009 PM 1768742 ER PT J AU MIURA, O DANDREA, A KABAT, D IHLE, JN AF MIURA, O DANDREA, A KABAT, D IHLE, JN TI INDUCTION OF TYROSINE PHOSPHORYLATION BY THE ERYTHROPOIETIN RECEPTOR CORRELATES WITH MITOGENESIS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID FREE CALCIUM-CONCENTRATION; AMINO-TERMINAL DOMAIN; MYELOID CELL-LINES; SENSITIVE V-ABL; SIGNAL TRANSDUCTION; CYTOPLASMIC DOMAINS; PROTEIN-KINASE; BETA-CHAIN; GROWTH; INTERLEUKIN-3 AB A role for tyrosine phosphorylation in the signal-transducing mechanisms of several hematopoietic growth factors has been hypothesized. To extend these observations, we have examined the effects of erythropoietin (Epo) on tyrosine phosphorylation in an Epo-responsive cell that was obtained by transfecting the murine erythropoietin receptor (EpoR) into an interleukin-3 (IL-3)-dependent cell line. By two-dimensional analysis of phosphotyrosine-containing proteins isolated with a monoclonal antibody (1G2) against phosphotyrosine, Epo and IL-3 were found to rapidly induce tyrosine phosphorylation of comparable substrates of 92, 70, and 56 kDa. In addition, Epo uniquely induced phosphorylation of a 72-kDa substrate while IL-3 uniquely induced phosphorylation of a 140-kDa substrate. Immunoprecipitation and mixing experiments indicated that the 72-kDa substrate may represent a small fraction of the EpoR. To explore the significance of tyrosine phosphorylation, we generated two mutants of the EpoR that lacked 108 or 146 amino acids at their carboxyl termini. In addition we constructed an internally deleted mutant that lacked 20 amino acids in a region of sequence homology with the IL-2 receptor-beta-chain. Although all mutants were expressed at comparable levels and had comparable binding affinities for Epo, only the mutant lacking 108 amino acids at the carboxyl terminus retained significant mitogenic activity or the ability to induce tyrosine phosphorylation. C1 ST JUDE CHILDRENS RES HOSP, DEPT BIOCHEM, MEMPHIS, TN 38105 USA. UNIV TENNESSEE, CTR HLTH SCI, DEPT BIOCHEM, MEMPHIS, TN 38163 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. OREGON HLTH SCI UNIV, DEPT BIOCHEM & MOLEC BIOL, PORTLAND, OR 97201 USA. FU NCI NIH HHS [CA25810, P30 CA21765]; NIDDK NIH HHS [R01 DK42932] NR 41 TC 234 Z9 236 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD OCT PY 1991 VL 11 IS 10 BP 4895 EP 4902 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GJ401 UT WOS:A1991GJ40100010 PM 1656216 ER PT J AU PAL, SK ZINKEL, SS KIESSLING, AA COOPER, GM AF PAL, SK ZINKEL, SS KIESSLING, AA COOPER, GM TI C-MOS EXPRESSION IN MOUSE OOCYTES IS CONTROLLED BY INITIATOR-RELATED SEQUENCES IMMEDIATELY DOWNSTREAM OF THE TRANSCRIPTION INITIATION SITE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ACTIVE RIBONUCLEIC-ACID; PROTO-ONCOGENE PRODUCT; DEVELOPMENTAL REGULATION; GENE-EXPRESSION; CHLORAMPHENICOL ACETYLTRANSFERASE; EARLY EMBRYOGENESIS; MEIOTIC MATURATION; ZONA-PELLUCIDA; GERM-CELLS; PROMOTER AB We have employed transient expression assays to analyze the sequences that direct c-mos transcription in mouse oocytes. Plasmids containing the chloramphenicol acetyltransferase (CAT) gene fused to either a 2.4-kb or a 731-bp fragment from the 5'-flanking region of c-mos produced similar levels of CAT activity when injected into nuclei of growing oocytes. BAL 31 deletions revealed that sequences up to 20 bp upstream of the major transcription start site could be removed without any significant loss of CAT activity. Promoter activity only decreased when these deletions closely approached the transcription start site, which was mapped at 53 nucleotides upstream of the first ATG in the c-mos open reading frame. On the other hand, deletion of sequences within 20 nucleotides downstream of the transcription initiation site resulted in a 10-fold reduction in CAT expression. A similar decrease in promoter activity was observed as a result of point mutations in these 5' untranslated sequences. Thus, sequences immediately downstream of the transcription start site, including a consensus sequence (PyPyCAPyPyPyPyPy) present in the initiator elements of several genes, appear to regulate c-mos expression in mouse oocytes. Reverse transcription-polymerase chain reaction analysis of RNA from injected oocytes showed that this regulation is manifest at the transcriptional level. Expression of c-mos in mouse oocytes thus appears to be directed by a simple promoter consisting only of sequences immediately surrounding the transcription start site, including an initiator element in the untranslated leader. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. FAULKNER HOSP,FAULKNER CTR REPROD MED,BOSTON,MA 02130. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. FU NCI NIH HHS [CA08667]; NICHD NIH HHS [HD26594] NR 40 TC 30 Z9 30 U1 1 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 OCT PY 1991 VL 11 IS 10 BP 5190 EP 5196 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GJ401 UT WOS:A1991GJ40100041 PM 1833632 ER PT J AU WAEBER, G MEYER, TE LESIEUR, M HERMANN, HL GERARD, N HABENER, JF AF WAEBER, G MEYER, TE LESIEUR, M HERMANN, HL GERARD, N HABENER, JF TI DEVELOPMENTAL STAGE-SPECIFIC EXPRESSION OF CYCLIC ADENOSINE-3',5'-MONOPHOSPHATE RESPONSE ELEMENT-BINDING PROTEIN CREB DURING SPERMATOGENESIS INVOLVES ALTERNATIVE EXON SPLICING SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID GLUTAMIC-ACID DECARBOXYLASE; TRANSCRIPTION FACTOR CREB; GENE-TRANSCRIPTION; SERTOLI CELLS; MESSENGER-RNA; SECRETED FORM; GERM-CELLS; AMP; DNA; PHOSPHORYLATION AB Spermatogenesis is a temporally regulated developmental process by which the gonadotropin-responsive somatic Sertoli and Leydig cells act interdependently to direct the maturation of the germinal cells. The metabolism of Sertoli and Leydig cells is regulated by the pituitary gonadotropins FSH and LH, which, in turn, activate adenylate cyclase. Because the cAMP-second messenger pathway is activated by FSH and LH, we postulated that the cAMP-responsive element-binding protein (CREB) plays a physiological role in Sertoli and Leydig cells, respectively. Immunocytochemical analyses of rat testicular sections show a remarkably high expression of CREB in the haploid round spermatids and, to some extent, in pachytene spermatocytes and Sertoli cells. Although most of the CREB antigen is detected in the nuclei, some CREB antigen is also present in the cytoplasm. Remarkably, the cytoplasmic CREB results from the translation of a unique alternatively spliced transcript of the CREB gene that incorporates an exon containing multiple stop codons inserted immediately up-stream of the exons encoding the DNA-binding domain of CREB. Thus, the RNA containing the alternatively spliced exon encodes a truncated transcriptional transactivator protein lacking both the DNA-binding domain and nuclear translocation signal of CREB. Most of the CREB transcripts detected in the germinal cells contain the alternatively spliced exon, suggesting a function of the exon to modulate the synthesis of CREB. In the Sertoli cells we observe a striking cyclical (12-day periodicity) increase in the levels of CREB mRNA that coincides with the splicing out of the restrictive exon containing the stop codons. Because earlier studies established that FSH-stimulated cAMP levels in Sertoli cells are also cyclical, and the CREB gene promoter contains cAMP-responsive enhancers, we suggest that the alternative RNA splicing controls a positive autoregulation of CREB gene expression mediated by cAMP. RP WAEBER, G (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK-30457, DK-25532] NR 52 TC 151 Z9 152 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD OCT PY 1991 VL 5 IS 10 BP 1418 EP 1430 PG 13 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GL389 UT WOS:A1991GL38900008 PM 1723142 ER PT J AU WAEBER, G HABENER, JF AF WAEBER, G HABENER, JF TI NUCLEAR TRANSLOCATION AND DNA RECOGNITION SIGNALS COLOCALIZED WITHIN THE BZIP DOMAIN OF CYCLIC ADENOSINE-3',5'-MONOPHOSPHATE RESPONSE ELEMENT-BINDING PROTEIN CREB SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID TRANSCRIPTIONAL ACTIVATION; PROGESTERONE-RECEPTOR; AMP; GENE; IDENTIFICATION; LOCALIZATION; SEQUENCE; ADENOSINE-3',5'-MONOPHOSPHATE; MIGRATION; TRANSPORT AB CREB is a cAMP-responsive nuclear DNA-binding protein that binds to cAMP response elements and stimulates gene transcription upon activation of the cAMP signalling pathway. The protein consists of an amino-terminal transcriptional transactivation domain and a carboxyl-terminal DNA-binding domain (bZIP domain) comprised of a basic region and a leucine zipper involved in DNA recognition and dimerization, respectively. Recently, we discovered a testis-specific transcript of CREB that contains an alternatively spliced exon encoding multiple stop codons. CREB encoded by this transcript is a truncated protein lacking the bZIP domain. We postulated that the antigen detected by CREB antiserum in the cytoplasm of germinal cells is the truncated CREB that must also lack its nuclear translocation signal (NTS). To test this hypothesis we prepared multiple expression plasmids encoding carboxyl-terminal deletions of CREB and transiently expressed them in COS-1 cells. By Western immunoblot analysis as well as immunocytochemistry of transfected cells, we show that CREB proteins truncated to amino acid 286 or shorter are sequestered in the cytoplasm, whereas a CREB of 295 amino acids is translocated into the nucleus. Chimeric CREBs containing a heterologous NTS fused to the first 248 or 261 amino acids of CREB are able to drive the translocation of the protein into the nucleus. Thus, the nine amino acids in the basic region involved in DNA recognition between positions 287 and 295 (RRKKKEYVK) of CREB contain the NTS. Further, mutation of the lysine at position 290 in CREB to an asparagine diminishes nuclear translocation of the protein. We conclude that 1) the NTS and DNA-binding bZIP domains of CREB are colocalized; 2) dimerization of CREB is not necessary for nuclear translocation; and 3) any proposed biological functions for the truncated CREB consisting of the transcriptional transactivation domain would probably take place in the cytoplasm. RP WAEBER, G (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK-25532, DK-30457] NR 40 TC 67 Z9 67 U1 0 U2 3 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD OCT PY 1991 VL 5 IS 10 BP 1431 EP 1438 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GL389 UT WOS:A1991GL38900009 PM 1837841 ER PT J AU KNEPEL, W VALLEJO, M CHAFITZ, JA HABENER, JF AF KNEPEL, W VALLEJO, M CHAFITZ, JA HABENER, JF TI THE PANCREATIC ISLET-SPECIFIC GLUCAGON G3 TRANSCRIPTION FACTORS RECOGNIZE CONTROL ELEMENTS IN THE RAT SOMATOSTATIN AND INSULIN-I GENES SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID CELL-SPECIFIC EXPRESSION; DNA-BINDING PROTEINS; AMP-RESPONSIVE ELEMENT; CYCLIC-AMP; PROMOTER ELEMENT; CONTROL REGION; BETA-CELLS; ENHANCER; SEQUENCES; REGULATOR AB The rat glucagon gene 5'-flanking region contains a pancreatic islet-specific enhancer-like element, G3. It has been shown previously that G3-binding and transactivating proteins are present in islet cell lines expressing the glucagon, somatostatin, and insulin genes, but not in several nonislet cell lines. The present study now shows that the glucagon G3 transcription factor binds to DNA sequences within cis-acting elements of the rat somatostatin and rat insulin-I genes that have been defined by others as pancreatic islet-specific transcriptional enhancers. In addition, when fused to glucagon or somatostatin minimal promoters in reporter plasmids, these enhancer elements of the three islet hormone-producing genes functionally activate transcription when transfected into islet cell lines producing glucagon, insulin, or somatostatin. The enhancer elements of the three different islet polypeptide hormone genes define a potential consensus motif that binds islet cell type-specific transcription factors. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114. FU NIDDK NIH HHS [DK-30834, DK-30457] NR 33 TC 44 Z9 45 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD OCT PY 1991 VL 5 IS 10 BP 1457 EP 1466 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GL389 UT WOS:A1991GL38900012 PM 1685554 ER PT J AU DRUST, DS TROCCOLI, NM JAMESON, JL AF DRUST, DS TROCCOLI, NM JAMESON, JL TI BINDING-SPECIFICITY OF CYCLIC ADENOSINE 3',5'-MONOPHOSPHATE-RESPONSIVE ELEMENT (CRE)-BINDING PROTEINS AND ACTIVATING TRANSCRIPTION FACTORS TO NATURALLY-OCCURRING CRE SEQUENCE VARIANTS SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID AMP RESPONSE ELEMENT; ALPHA-SUBUNIT GENE; LEUCINE ZIPPER DOMAIN; DNA-BINDING; NUCLEAR FACTOR; EXPRESSION; ENHANCER; DISTINCT; CDNA; FOS AB The human glycoprotein hormone alpha-gene contains a palindromic cAMP-responsive element (CRE), TGACGTCA, which is critical for both basal and cAMP-stimulated expression. Members of the CRE-binding protein (CREB)/activating transcription factor transcription family as well as members of the Jun/Fos family have been shown to bind to this sequence. In nonprimate species, the alpha-gene contains a variant of the CRE sequence TGAtGTCA, which differs by a single base substitution. The functional properties of promoters containing variant CREs were examined in transient expression assays in JEG-3 cells (human placental cells) and GH3 cells (rat pituitary cells). Relative to the palindromic CRE, the basal level of expression was reduced with the variant CRE constructions. However, 8-bromo-cAMP stimulated the expression of constructions containing either the palindromic or the variant CREs. Protein interactions with the palindromic and variant CREs were also examined. By Southwestern blot analyses in which proteins were initally separated on a denaturing sodium dodecyl sulfate-gel, transferred to a membrane, and then probed with radio-labeled DNA, several different proteins were bound by either the palindromic or the variant CRE sequences. However, the binding of the variant CRE to CREB was markedly reduced. In nondenaturing gel shift assays, multiple protein-DNA complexes were also formed with both types of CREs, but the variant CRE lacked a major complex that may correspond to homodimers of CREB. To determine the protein composition of these complexes, the gel shift bands were eluted and subjected to Southwestern blot analysis. CREB was identified as one of the protein components in several of the gel shift complexes formed with the variant CRE. We conclude that although the variant CRE binds CREB homodimers poorly, CREB can still interact with this element when associated with other proteins. Thus, variants of the palindromic CRE sequence may provide a mechanism for specifying interactions with different combinations of CREBs. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,THYROID UNIT,JACKSON 1021,BOSTON,MA 02114. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD-23519, HD-23262] NR 42 TC 46 Z9 46 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD OCT PY 1991 VL 5 IS 10 BP 1541 EP 1551 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GL389 UT WOS:A1991GL38900022 PM 1837842 ER PT J AU ZUNIGA, G ROPPER, AH FRANK, J AF ZUNIGA, G ROPPER, AH FRANK, J TI SARCOID PERIPHERAL NEUROPATHY SO NEUROLOGY LA English DT Article ID MANIFESTATIONS; POLYNEUROPATHY; NERVE AB We studied 10 patients with sarcoidosis and peripheral neuropathy. Six had a subacute or chronic axonal sensorimotor neuropathy without cranial neuropathy, beginning months to years after established systemic sarcoidosis. One patient had severe enough diaphragmatic weakness to require mechanical ventilation. Four patients had atypical neuropathies: acute Guillain-Barre syndrome, mononeuritis multiplex, unilateral lumbosacral plexopathy, and a purely sensory neuropathy, all before systemic sarcoidosis became evident, and all except one had cranial nerve abnormalities. Autopsy in one patient with sensorimotor neuropathy showed only scattered foci of lymphocytes in spinal roots and ganglia with nerve fiber loss. C1 ST ELIZABETH HOSP,DEPT NEUROL,DIV NEUROL,736 CAMBRIDGE ST,BOSTON,MA 02135. MASSACHUSETTS GEN HOSP,NEURO ICU,BOSTON,MA 02114. NR 24 TC 50 Z9 51 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD OCT PY 1991 VL 41 IS 10 BP 1558 EP 1561 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA GK878 UT WOS:A1991GK87800006 PM 1656324 ER PT J AU KAMENS, J BRENT, R AF KAMENS, J BRENT, R TI A YEAST TRANSCRIPTION ASSAY DEFINES DISTINCT REL AND DORSAL DNA RECOGNITION SEQUENCES SO NEW BIOLOGIST LA English DT Article DE REL PROTEINS; DORSAL; SACCHAROMYCES-CEREVISIAE; DNA BINDING; COOPERATIVITY; TRANSCRIPTION ACTIVATION; DIMERIZATION ID NF-KAPPA-B; VIRUS STRAIN-T; V-REL; C-REL; RETICULOENDOTHELIOSIS VIRUS; SACCHAROMYCES-CEREVISIAE; PROTOONCOGENE PRODUCT; ONCOGENE ENCODES; ESCHERICHIA-COLI; BINDING-PROTEIN C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP KAMENS, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,500 BLOSSOM ST,BOSTON,MA 02114, USA. NR 53 TC 30 Z9 30 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4674 J9 NEW BIOL PD OCT PY 1991 VL 3 IS 10 BP 1005 EP 1013 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA GL955 UT WOS:A1991GL95500014 PM 1768648 ER PT J AU KHAW, BA MOUSA, SA AF KHAW, BA MOUSA, SA TI COMPARATIVE-ASSESSMENT OF EXPERIMENTAL MYOCARDIAL-INFARCTION WITH TC-99(M)-HEXAKIS-T-BUTYL-ISONITRILE (SESTAMIBI), IN-111 ANTIMYOSIN AND TL-201 SO NUCLEAR MEDICINE COMMUNICATIONS LA English DT Article AB The monocationic Tc-99m-hexakis-2-methoxy-2-methyl propyl isonitrile (Tc-99m-sestamibi) is a myocardial perfusion marker with potential clinical value in the diagnosis of ischaemic heart disease. The kinetics of this compound in experimental myocardial infarction in rabbits was compared to the distributions of In-111-antimyosin Fab and Tl-201 at 24 h of persistent left anterior descending (LAD) coronary artery occlusion. The maximum uptake of In-111-antimyosin in the infarct was as high as 0.34% injected dose per gram (i.d. g-1), whereas normal myocardial activity was only 0.045% i.d. g-1. Maximal Tl-201 and Tc-99m-sestamibi uptakes in normal myocardium were 0.16 and 0.14% i.d. g-1, respectively. Because of their faster blood clearances Tc-99m-sestamibi and Tl-201 were able to delineate regions of radiotracer distribution defects early. In-111-antimyosin required a longer circulation time for in vivo infarct visualization because of slower blood clearance. The data also demonstrated that in persistent LAD occlusion infarction in rabbits, the inverse distribution of sestamibi and Tl-201 relative to antimyosin localization (indicator of myocyte necrosis) is not significantly different (I/N(sestamibi) = 0.213 I/N(AM) + 115.7, r = 0.91, and I/N(Tl-201) = 0.181 I/N(AM) + 114.4, r = 0.89). RP KHAW, BA (reprint author), MASSACHUSETTS GEN HOSP,DIV NUCL MED,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0143-3636 J9 NUCL MED COMMUN JI Nucl. Med. Commun. PD OCT PY 1991 VL 12 IS 10 BP 853 EP 863 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GH999 UT WOS:A1991GH99900004 PM 1838801 ER EF