FN Thomson Reuters Web of Science™ VR 1.0 PT J AU ROYALL, DR MAHURIN, RK CORNELL, J GRAY, KF AF ROYALL, DR MAHURIN, RK CORNELL, J GRAY, KF TI BEDSIDE ASSESSMENT OF DEMENTIA TYPE USING THE QUALITATIVE EVALUATION OF DEMENTIA SO NEUROPSYCHIATRY NEUROPSYCHOLOGY AND BEHAVIORAL NEUROLOGY LA English DT Article DE QED; CORTICAL AND SUBCORTICAL DEMENTIAS; RATING SCALE ID CLINICAL DIAGNOSTIC-CRITERIA; ADRDA WORK GROUP; ALZHEIMERS-DISEASE; SUBCORTICAL DEMENTIA; DIFFERENTIAL-DIAGNOSIS; COGNITIVE IMPAIRMENT; ILLNESS; SCALE AB Problem: We present a novel dementia assessment instrument, the Qualitative Evaluation of Dementia (QED), designed to discriminate dementia type at the bedside. The QED is a brief, clinically based checklist which operationalizes the approach of a geriatric psychiatrist to the qualitative assessment of dementing illnesses. Scores range from 0 = pure ''subcortical'' illness, to 30 = pure ''cortical'' disease. Internal consistency (Chronbach's alpha = .69) and interrater reliability (r = .93) are acceptable. Blinded raters agree on dementia type in > 90% of cases. When QED scores are mapped against measures of general cognitive function a qualitative picture of dementia typology emerges. Method: The QED's ability to discriminate NINCDS ''Probable'' Alzheimer's disease (AD) from those with ''no dementia'' and ''dementia without cortical features'' was assessed in a cross-sectional sample of 118 consecutive patients presenting to a multidisciplinary geriatric assessment clinic and consultation service. Results: The QED accurately discriminated air three study groups. When combined with the Executive Interview (EXIT), 87.7% of subjects were correctly classified. Misclassification rates ranged from 11.8% for ''Probable'' AD to 13% for ''no dementia.'' Substituting the Mini-Mental State Examination (MMSE) correctly classified 74% of subjects, with misclassification rates ranging from 11.8% for ''Probable'' AD to 40.0% for ''dementia with no cortical features.'' The EXIT was more sensitive than the MMSE to mild cognitive impairment, and subcortical dementia. Conclusions: These results suggest that dementia subtypes can be accurately and reliably assessed using a combination of the QED and either the EXIT or the MMSE. This evaluation can be completed in 20 minutes, and requires no access to brood or laboratory work. The use of the EXIT in this assessment reduces misclassification rates and improves sensitivity in early stages. The implications of this technique for clinical assessment, subject recruitment, and the conceptualization of dementia are discussed. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT PSYCHIAT,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,DEPT MED,SAN ANTONIO,TX. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. RP ROYALL, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 34 TC 26 Z9 26 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0894-878X J9 NEUROPSY NEUROPSY BE JI Neuropsychiatr. Neuropsychol. Behav. Neurol. PD OCT PY 1993 VL 6 IS 4 BP 235 EP 244 PG 10 WC Clinical Neurology; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA MK018 UT WOS:A1993MK01800005 ER PT J AU MANCHOLA, IF DESALLES, AAF FOO, TK ACKERMAN, RH CANDIA, GT KJELLBERG, RN AF MANCHOLA, IF DESALLES, AAF FOO, TK ACKERMAN, RH CANDIA, GT KJELLBERG, RN TI ARTERIOVENOUS MALFORMATION HEMODYNAMICS - A TRANSCRANIAL DOPPLER STUDY SO NEUROSURGERY LA English DT Article DE ARTERIOVENOUS MALFORMATION; BLOOD FLOW; CEREBRAL ANGIOGRAM; DOPPLER ID FLOW VELOCITY; ULTRASOUND; HEMORRHAGE; DIAGNOSIS; EXCISION; AVMS AB CONGENITAL ARTERIOVENOUS MALFORMATION (AVM) of the brain represents a defect in capillary development resulting in a high flow fistula between arterial and venous systems. In this study, AVM hemodynamics were related with clinical findings. Volume flow was calculated based on transcranial Doppler (TCD) and angiographic data. Forty patients admitted to the Massachusetts General Hospital for proton beam therapy (33 +/- 10 yr old; mean +/- SD) were studied. Four symptoms were considered: intracranial bleeding, progressive neurological deficit, seizures, and headache. Fourteen control subjects aged 30 +/- 7 years (mean +/- SD) were normal volunteers. Angiography with calibrated markers permitting magnification correction was available for all patients. Lateral and medial depth limits of the intracranial basal arteries in relation to the TCD temporal window were determined by TCD and angiogram with excellent correlation. Selected depth for data acquisition was determined independently in the angiogram and by TCD. The difference between the two techniques was less than 4 mm. Mean flow velocity, pulsatility index, and vessel diameter were studied. Flow volume was calculated from these data. Mean flow velocity, pulsatility index, vessel diameter, and flow volume were significantly different among AVM feeders, non-feeders, and control arteries. The non-feeding middle cerebral artery, anterior cerebral artery, and posterior cerebral artery flows were 254 +/- 13, 136 +/- 14, and 79 +/- 8 ml/min, respectively. Accordingly, the estimated cerebral flow volume was 938 ml/min. The feeding middle cerebral artery, anterior cerebral artery, and posterior cerebral artery flows were 552 +/- 47, 369 +/- 70, and 484 +/- 67 ml/min, respectively (P < 0.001). The mean flow volume to the AVMs was 913 +/- 227 ml/min, and patients having hemorrhage had significantly lower flow volume (624 +/- 117 ml/min, P < 0.01) than patients having other symptoms. TCD accurately determined the depth limits of the basal cerebral arteries measured against the angiographic determinations. The evaluation of flow volume with vessel diameter measured in the angiogram and flow velocity was close to that reported by authors using other techniques. Analysis of these data disclose important hemodynamic patterns related to AVM symptomatology. These patterns may have therapeutic implications. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT NEUROL, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT NEUROSURG, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT RADIOL, BOSTON, MA 02114 USA. UNIV CALIF LOS ANGELES, SCH MED, DIV NEUROSURG, LOS ANGELES, CA USA. NR 24 TC 38 Z9 40 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD OCT PY 1993 VL 33 IS 4 BP 556 EP 562 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA LZ186 UT WOS:A1993LZ18600002 PM 7901793 ER PT J AU MORI, M BARNARD, GF STANIUNAS, RJ JESSUP, JM STEELE, GD CHEN, LB AF MORI, M BARNARD, GF STANIUNAS, RJ JESSUP, JM STEELE, GD CHEN, LB TI PROTHYMOSIN-ALPHA MESSENGER-RNA EXPRESSION CORRELATES WITH THAT OF C-MYC IN HUMAN COLON-CANCER SO ONCOGENE LA English DT Article ID GENE-EXPRESSION; CELL-PROLIFERATION; LYMPHOCYTES-T; AMEX METHOD; ONCOGENE; PROTEIN; MUCOSA; FAMILY; TRANSCRIPTION; AMPLIFICATION AB Prothymosin alpha (PT-alpha) is a nuclear protein involved in cell proliferation. Transcription of PT-alpha has been reported to be regulated by the c-myc gene in vitro. We identified PT-alpha as being overexpressed in a human colon cancer minus normal mucosa subtraction cDNA library. Northern blot (messenger RNA) analysis showed that both PT-alpha and c-myc genes were overexpressed in human colorectal cancers compared with adjacent normal tissues. Immunohistochemical studies for PT-alpha and c-myc supported these findings. There was no correlation between PT-alpha or c-myc messenger RNA expression and Dukes' stage of colorectal cancer; or between either of these two and actin messenger RNA expression. There was, however, a significant correlation between the PT-alpha expression and c-myc expression (P <0.001). These findings support the hypothesis that PT-alpha gene transcription may be associated with, and possibly under the control of, the c-myc gene in human colorectal cancers. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,44 BINNEY ST,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,DEPT SURG,BOSTON,MA 02215. FU NCI NIH HHS [1F32CA9001, P01CA44704]; NIDDK NIH HHS [T32DK07533] NR 41 TC 108 Z9 108 U1 1 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT PY 1993 VL 8 IS 10 BP 2821 EP 2826 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA LX343 UT WOS:A1993LX34300024 PM 8378090 ER PT J AU GRAGOUDAS, ES EGAN, KM SAORNIL, MA WALSH, SM ALBERT, DM SEDDON, JM AF GRAGOUDAS, ES EGAN, KM SAORNIL, MA WALSH, SM ALBERT, DM SEDDON, JM TI THE TIME-COURSE OF IRRADIATION CHANGES IN PROTON BEAM-TREATED UVEAL MELANOMAS SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1992 ANNUAL MEETING OF THE AMERICAN-ACADEMY-OF-OPHTHALMOLOGY CY NOV, 1992 CL DALLAS, TX SP AMER ACAD OPHTHALMOL ID PLAQUE RADIOTHERAPY; ENUCLEATION; HISTOPATHOLOGY; SURVIVAL; THERAPY AB Background: Although histopathologic changes in uveal melanomas treated by irradiation have been well characterized, the timing of these effects after irradiation has not been previously evaluated. Methods: The series consisted of a total of 92 eyes with uveal melanoma, enucleated at various intervals after proton irradiation (range, 1 month to 8 years) due to complications (n = 66) or tumor growth (n = 22), or at autopsy (n = 4). Study slides were read, using a standard protocol, by two pathologists masked to the timing of the enucleation after irradiation and the reason for the surgery. Results: The prevalence of inflammation decreased whereas fibrosis increased with time from 15% of cases enucleated within 12 months (early cases) to 61% of those enucleated more than 30 months (late cases) after irradiation (P for trend = 0.0005). Tumor necrosis and blood vessel damage occurred early, and the prevalence of these changes was constant over time. Excluding tumors with evidence of growth after irradiation, mitotic figures became progressively less common as the interval between irradiation and enucleation increased (P for trend = 0.015); no mitotic figures were present in 40 high-power fields more than 30 months after irradiation. Conclusion: Histopathologic changes in irradiated melanomas vary according to the time elapsed since irradiation. Inflammation decreases with time whereas fibrosis becomes more prevalent with time after irradiation. Among controlled tumors, mitotic figures appear only in recently irradiated tumors. C1 MASSACHUSETTS EYE & EAR INFIRM,EPIDEMIOL UNIT,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,EYE PATHOL LAB,BOSTON,MA 02114. RP GRAGOUDAS, ES (reprint author), MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 24 TC 24 Z9 24 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 OCT PY 1993 VL 100 IS 10 BP 1555 EP 1559 PG 5 WC Ophthalmology SC Ophthalmology GA MA307 UT WOS:A1993MA30700028 PM 8414415 ER PT J AU HARRIS, WH AF HARRIS, WH TI TOTAL HIP-REPLACEMENT IN THE MIDDLE-AGED PATIENT - CONTEMPORARY CEMENTING FOR FIXATION OF THE FEMORAL COMPONENT SO ORTHOPEDIC CLINICS OF NORTH AMERICA LA English DT Article ID 10-YEAR FOLLOW-UP; BONE CEMENTS; CONTACT; FEMUR C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. RP HARRIS, WH (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114, USA. NR 49 TC 12 Z9 12 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0030-5898 J9 ORTHOP CLIN N AM JI Orthop. Clin. North Am. PD OCT PY 1993 VL 24 IS 4 BP 611 EP 616 PG 6 WC Orthopedics SC Orthopedics GA MC462 UT WOS:A1993MC46200006 PM 8414426 ER PT J AU HARRIS, WH AF HARRIS, WH TI MANAGEMENT OF THE DEFICIENT ACETABULUM USING CEMENTLESS FIXATION WITHOUT BONE-GRAFTING SO ORTHOPEDIC CLINICS OF NORTH AMERICA LA English DT Article ID TOTAL HIP-REPLACEMENT; RECONSTRUCTION C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HARRIS, WH (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114, USA. NR 22 TC 21 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 0030-5898 J9 ORTHOP CLIN N AM JI Orthop. Clin. North Am. PD OCT PY 1993 VL 24 IS 4 BP 663 EP 665 PG 3 WC Orthopedics SC Orthopedics GA MC462 UT WOS:A1993MC46200012 PM 8414432 ER PT J AU KREBS, DE GILLBODY, KM RILEY, PO PARKER, SW AF KREBS, DE GILLBODY, KM RILEY, PO PARKER, SW TI DOUBLE-BLIND, PLACEBO-CONTROLLED TRIAL OF REHABILITATION FOR BILATERAL VESTIBULAR HYPOFUNCTION - PRELIMINARY-REPORT SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID BALANCE; REFLEX; DIZZINESS; THERAPY; GAIT AB Vestibular rehabilitation (VR) is increasingly popular, but few data exist to support enthusiasts' claims of efficacy in improving functional abilities of patients with bilateral vestibular hypofunction (BVH). A double-blind, controlled study of eight subjects (mean, 64 +/- 12 years; seven females, one male) with bilateral vestibular hypofunction was conducted. Subjects in group A received 8 weeks of VR followed by 8 weeks of home VR exercises, whereas those in group B received 8 weeks of control treatment (isometric strengthening exercises) followed by 8 weeks of VR. At the end of 8 weeks, group A walked 8% faster and, during paced gait and stair-climbing, with greater stability, evidenced by a 10% larger maximum moment arm and a 17% decreased double-support duration during gait and stair stance. Group B improved less than 1% during the control treatment. Self-reported Dizziness Handicap Inventory scores did not differ significantly between control and active VR. All subjects improved compared with baseline tests at the 16-week post-test on both functional testing and on the Self-reported Dizziness Handicap Inventory scale. We conclude that in this small sample, VR effectively improved functional, dynamic stability during locomotion, but even strengthening exercises result in self-reported symptomatic improvement. C1 MASSACHUSETTS GEN HOSP,BIOMOT LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT INPATIENT PHYS THERAPY,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT OTONEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MIT,CAMBRIDGE,MA 02139. RP KREBS, DE (reprint author), MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,101 MERRIMAC ST,BOSTON,MA 02114, USA. RI Riley, Patrick/B-3053-2009 NR 24 TC 120 Z9 122 U1 2 U2 7 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD OCT PY 1993 VL 109 IS 4 BP 735 EP 741 PG 7 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA MF897 UT WOS:A1993MF89700017 PM 8233513 ER PT J AU SALMAN, SD AF SALMAN, SD TI A NEW STENT FOR ENDOSCOPIC SINUS SURGERY SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Note ID COMPLICATIONS RP SALMAN, SD (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,243 CHARLES ST,BOSTON,MA 02114, USA. NR 4 TC 7 Z9 7 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD OCT PY 1993 VL 109 IS 4 BP 780 EP 781 PG 2 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA MF897 UT WOS:A1993MF89700027 PM 8233523 ER PT J AU ROBERTS, JD SHAUL, PW AF ROBERTS, JD SHAUL, PW TI ADVANCES IN THE TREATMENT OF PERSISTENT PULMONARY-HYPERTENSION OF THE NEWBORN SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Review ID EXTRACORPOREAL MEMBRANE-OXYGENATION; FREQUENCY JET VENTILATION; INHALED NITRIC-OXIDE; ENDOTHELIUM-DEPENDENT RELAXATION; RESPIRATORY-DISTRESS SYNDROME; ARTERIAL SMOOTH-MUSCLE; RELAXING FACTOR; OSCILLATORY VENTILATION; NECROTIZING TRACHEOBRONCHITIS; FETAL CIRCULATION C1 UNIV TEXAS,SW MED CTR,DEPT PEDIAT,DALLAS,TX 75230. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. RP ROBERTS, JD (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-42397] NR 152 TC 24 Z9 24 U1 1 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0031-3955 J9 PEDIATR CLIN N AM JI Pediatr. Clin. N. Am. PD OCT PY 1993 VL 40 IS 5 BP 983 EP 1004 PG 22 WC Pediatrics SC Pediatrics GA MA095 UT WOS:A1993MA09500006 PM 8414718 ER PT J AU REID, R SANTOSHAM, M CROLL, J THOMPSON, C NEWCOMER, W SIBER, GR AF REID, R SANTOSHAM, M CROLL, J THOMPSON, C NEWCOMER, W SIBER, GR TI ANTIBODY-RESPONSE OF NAVAJO CHILDREN PRIMED WITH PRP-OMP VACCINE TO BOOSTER DOSES OF PRP-OMP VS HBOC VACCINE SO PEDIATRIC INFECTIOUS DISEASE JOURNAL LA English DT Article DE HAEMOPHILUS-INFLUENZAE TYPE-B; HAEMOPHILUS-INFLUENZAE TYPE-B CONJUGATE VACCINE; PRP-OMP; HBOC ID INFLUENZAE TYPE-B; OUTER-MEMBRANE PROTEIN; CONJUGATE VACCINE; INFANTS; IMMUNOGENICITY; POLYSACCHARIDE; POPULATION; EFFICACY; COMPLEX; SAFETY AB We compared in 12- to 15-month-old American Indian infants the safety and immunogenicity of two licensed Haemophilus influenzae type b (Hib) conjugate vaccines, PRP-OMP (PedvaxHib(R)) and HbOC (HibTITER(R)), administered as booster vaccinations. All infants previously received PRP-OMP for their primary Hib vaccinations at 2 and 4 months of age. The geometric mean Hib antibody concentrations (mug/ml) measured by radioactive antigen-binding assay for those receiving PRP-OMP (n = 17) or HbOC (n = 18) were 0.593 and 0.449, respectively, before boosting (P not significant) and 7.46 and 29.5 mug/ml, respectively, after boosting (P < 0.05). PRP-OMP recipients also had lower geometric mean IgG anti-Hib antibody concentrations than HbOC recipients (7.21 vs 28 mug/ml, P = 0.003) and lower bactericidal titers (3.18 vs. 15.4, not significant). We conclude that HbOC vaccine produced a significantly greater booster response than PRP-OMP vaccine when given at 12 to 15 months of age to children primed with two doses of PRP-OMP vaccine at 2 and 4 months of age. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,CTR AMER INDIAN & ALASKAN NAT HLTH,DEPT INT HLTH,BALTIMORE,MD 21205. JOHNS HOPKINS PROJECT,WHITERIVER,AZ. MASSACHUSETTS PUBL HLTH BIOL LABS,BOSTON,MA. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. FU NIAID NIH HHS [AI18125] NR 15 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0891-3668 J9 PEDIATR INFECT DIS J JI Pediatr. Infect. Dis. J. PD OCT PY 1993 VL 12 IS 10 BP 812 EP 815 DI 10.1097/00006454-199310000-00003 PG 4 WC Immunology; Infectious Diseases; Pediatrics SC Immunology; Infectious Diseases; Pediatrics GA MB703 UT WOS:A1993MB70300003 PM 8284116 ER PT J AU BRAMSON, RT MEYER, TL SILBIGER, ML BLICKMAN, JG HALPERN, E AF BRAMSON, RT MEYER, TL SILBIGER, ML BLICKMAN, JG HALPERN, E TI THE FUTILITY OF THE CHEST RADIOGRAPH IN THE FEBRILE INFANT WITHOUT RESPIRATORY SYMPTOMS SO PEDIATRICS LA English DT Article DE CHEST RADIOGRAPHS; SEPSIS WORK-UP; INFANTS; FEVER ID METAANALYSIS; TRIALS; LESS AB Objective. Major pediatric textbooks advocate a chest radiograph as part of the diagnostic evaluation for a sepsis workup for febrile infants less than 3 months old. Very few studies have addressed the value of performing a chest radiograph in this situation. Two studies previously published lack the numbers to statistically justify a conclusion about the need to perform a chest radiograph in the febrile infant. Methods. Evaluated were 197 febrile infants 3 months old or less with a history, physical examination, chest radiograph, and other laboratory studies to determine the cause of their fever. This group of infants was combined with the group of infants from two similar studies published previously in the literature using cumulative meta-analysis. The combined group resulted in 617 infants. Results. The combined group of infants had 361 infants who had no clinical evidence of pulmonary disease on history or physical examination. All 361 infants had normal chest radiograph. These results gave a 95% confidence interval that the chance of a positive chest radiograph in a patient with no pulmonary symptoms would occur less than 1.02% of the time. Conclusions. The generally advocated policy of obtaining a chest radiograph as part of the sepsis workup in febrile infants should be discontinued, and chest radiographs should be obtained only in febrile infants who have clinical indications of pulmonary disease. C1 MASSACHUSETTS GEN HOSP,DIV PEDIAT IMAGING,BOSTON,MA 02114. UNIV S FLORIDA,TAMPA GEN HOSP,COLL MED,DEPT PEDIAT,TAMPA,FL 33620. MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,BOSTON,MA 02114. RP BRAMSON, RT (reprint author), UNIV S FLORIDA,TAMPA GEN HOSP,COLL MED,DEPT RADIOL,TAMPA,FL 33620, USA. NR 14 TC 30 Z9 31 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 OCT PY 1993 VL 92 IS 4 BP 524 EP 526 PG 3 WC Pediatrics SC Pediatrics GA MA223 UT WOS:A1993MA22300003 PM 8414821 ER PT J AU GRANSTEIN, RD MORISON, WL KRIPKE, ML AF GRANSTEIN, RD MORISON, WL KRIPKE, ML TI CARCINOGENICITY OF COMBINED ULTRAVIOLET-B RADIATION AND PSORALEN PLUS ULTRAVIOLET-A IRRADIATION TREATMENT OF MICE SO PHOTODERMATOLOGY PHOTOIMMUNOLOGY & PHOTOMEDICINE LA English DT Article DE UVB, PUVA; SKIN CANCER ID ORAL METHOXSALEN; PSORIASIS; PHOTOCHEMOTHERAPY; RISK AB Psoralen plus ultraviolet A (PUVA) therapy and UVB phototherapy are frequently used in the treatment of psoriasis and other skin diseases. Both treatments are thought to be carcinogenic, but little is known about their interaction in the induction of skin cancer. Tumors induced in mice treated with both PUVA and UVB, either given sequentially or concurrently, seemed to be more antigenic as a group than tumors treated by PUVA alone, as determined by their lower frequency of growth when transplanted into naive mice. In this study, we treated C3H mice with a subcarcinogenic dose of UVB radiation for 4 weeks, followed by PUVA treatment for 41 weeks (sequential experiment) or with both UVB radiation (minimal carcinogenic dose) and PUVA for 41 weeks (concurrent experiment) and monitored the development of skin cancers. Although a few tumors appeared earlier in the groups treated with both UVB and PUVA in both experiments, no significant differences were observed in the rate of tumor development in mice treated with UVB and PUVA versus those treated with PUVA alone. C1 NCI,FREDERICK RES FACIL,FREDERICK,MD 21701. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. MD ANDERSON CANC CTR,HOUSTON,TX. RP GRANSTEIN, RD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 10 TC 1 Z9 1 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0905-4383 J9 PHOTODERMATOL PHOTO JI Photodermatol. Photoimmunol. Photomed. PD OCT PY 1993 VL 9 IS 5 BP 198 EP 202 PG 5 WC Dermatology SC Dermatology GA MA680 UT WOS:A1993MA68000002 ER PT J AU VALON, C SMALLE, J GOODMAN, HM GIRAUDAT, J AF VALON, C SMALLE, J GOODMAN, HM GIRAUDAT, J TI CHARACTERIZATION OF AN ARABIDOPSIS-THALIANA GENE (TMKL1) ENCODING A PUTATIVE TRANSMEMBRANE PROTEIN WITH AN UNUSUAL KINASE-LIKE DOMAIN SO PLANT MOLECULAR BIOLOGY LA English DT Note DE ARABIDOPSIS-THALIANA; KINASE; LEUCINE-RICH MOTIF; MEMBRANE PROTEIN; RECEPTOR ID SERINE THREONINE KINASE; LOCUS RECEPTOR KINASE; LEUCINE-RICH REPEATS; SIGNAL TRANSDUCTION; ADENYLATE-CYCLASE; CATALYTIC SUBUNIT; BRASSICA-OLERACEA; SEQUENCE; FAMILY; MEMBRANE AB We have characterized a novel Arabidopsis gene, designated TMKL1 (for Transmembrane Kinase-Like). The encoded protein is predicted to contain an N-terminal signal peptide, an extracellular domain with seven imperfect leucine-rich repeats, a single hydrophobic transmembrane segment, and a kinase-like intracellular domain which lacks, however, several of the key conserved residues essential for catalytic activity. The TMKL1 protein thus represents a unique and functionally intriguing member of the family of plant proteins related to animal receptor kinases. Northern blot analysis indicates that the TMKL1 gene is transcriptionally active in a variety of organs, and is developmentally regulated during silique maturation. Its possible functions are discussed. C1 CNRS,INST SCI VEGETALES,UPR 40,F-91198 GIF SUR YVETTE,FRANCE. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 30 TC 36 Z9 38 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-4412 J9 PLANT MOL BIOL JI Plant Mol.Biol. PD OCT PY 1993 VL 23 IS 2 BP 415 EP 421 DI 10.1007/BF00029017 PG 7 WC Biochemistry & Molecular Biology; Plant Sciences SC Biochemistry & Molecular Biology; Plant Sciences GA MD517 UT WOS:A1993MD51700018 PM 8219075 ER PT J AU GREVELINK, SA YOUSSEF, DE LOSCALZO, J LERNER, EA AF GREVELINK, SA YOUSSEF, DE LOSCALZO, J LERNER, EA TI SALIVARY-GLAND EXTRACTS FROM THE DEERFLY CONTAIN A POTENT INHIBITOR OF PLATELET-AGGREGATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DISINTEGRIN; FIBRINOGEN RECEPTOR; APYRASE; GLYCOPROTEIN-IIB/IIIA ID PEPTIDE; APYRASE; MAXADILAN; TICK AB Salivary gland extracts of the deerfly contain a potent inhibitor of platelet aggregation, which assists the insect in obtaining a blood meal. The extract prevents platelet aggregation induced by ADP, thrombin, and collagen and inhibits fibrinogen binding to the glycoprotein IIb/IIIa receptor on platelets. The active component in deerfly salivary gland extract appears to be a protein that is comparatively more potent than the disintegrins present in viper venoms. Isolation and characterization of this protein may provide different directions in therapeutics and studies of normal platelet physiology. C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,E BLDG 149,13TH ST,BOSTON,MA 02129. BRIGHAM & WOMENS HOSP,DIV CARDIOVASC,BOSTON,MA 02115. VET ADM MED CTR W ROXBURY,BOSTON,MA 02132. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-40411, HL-43344]; NIAMS NIH HHS [AR07098] NR 18 TC 27 Z9 29 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 OCT 1 PY 1993 VL 90 IS 19 BP 9155 EP 9158 DI 10.1073/pnas.90.19.9155 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MA595 UT WOS:A1993MA59500083 PM 8415671 ER PT J AU TEPPER, RI AF TEPPER, RI TI THE ANTITUMOR AND PROINFLAMMATORY ACTIONS OF IL4 SO RESEARCH IN IMMUNOLOGY LA English DT Article ID NECROSIS-FACTOR; IFN-GAMMA; T-CELLS; INTERLEUKIN-4; EOSINOPHIL; IL-4; EXPRESSION; ADHERENCE; IMMUNITY; POTENT RP TEPPER, RI (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 29 TC 14 Z9 15 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2494 J9 RES IMMUNOL JI Res. Immunol. PD OCT PY 1993 VL 144 IS 8 BP 633 EP 637 DI 10.1016/S0923-2494(05)80017-3 PG 5 WC Immunology SC Immunology GA MN101 UT WOS:A1993MN10100017 PM 8303081 ER PT J AU FREEDMAN, AS AF FREEDMAN, AS TI EXPRESSION AND FUNCTION OF ADHESION RECEPTORS ON NORMAL B-CELLS AND B-CELL NON-HODGKINS-LYMPHOMAS SO SEMINARS IN HEMATOLOGY LA English DT Article ID LYMPHOCYTE HOMING RECEPTOR; FOLLICULAR DENDRITIC CELLS; EPSTEIN-BARR-VIRUS; BONE-MARROW; GERMINAL CENTER; LEUKOCYTE ADHESION; DIFFERENTIAL EXPRESSION; MONOCLONAL-ANTIBODIES; INTEGRIN VLA-4; ENDOTHELIAL LIGAND RP FREEDMAN, AS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU PHS HHS [55207] NR 98 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 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD OCT PY 1993 VL 30 IS 4 BP 318 EP 328 PG 11 WC Hematology SC Hematology GA ME787 UT WOS:A1993ME78700006 PM 7505483 ER PT J AU GROSSBARD, ML NADLER, LM AF GROSSBARD, ML NADLER, LM TI MONOCLONAL-ANTIBODY THERAPY FOR INDOLENT LYMPHOMAS SO SEMINARS IN ONCOLOGY LA English DT Article ID B-CELL LYMPHOMA; NON-HODGKINS-LYMPHOMA; BONE-MARROW TRANSPLANTATION; PHASE-I TRIAL; IDIOTYPE ANTIBODIES; ANTI-CD37 ANTIBODY; ANTITUMOR-ACTIVITY; ALPHA-INTERFERON; CLINICAL-TRIAL; RICIN C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA34183, 1K12CA01730] NR 67 TC 13 Z9 13 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 OCT PY 1993 VL 20 IS 5 SU 5 BP 118 EP 135 PG 18 WC Oncology SC Oncology GA MF182 UT WOS:A1993MF18200010 PM 8211202 ER PT J AU GRIBBEN, JG NADLER, LM AF GRIBBEN, JG NADLER, LM TI MONITORING MINIMAL RESIDUAL DISEASE SO SEMINARS IN ONCOLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; NON-HODGKINS-LYMPHOMA; BONE-MARROW TRANSPLANTATION; CHRONIC MYELOGENOUS LEUKEMIA; CHRONIC MYELOID-LEUKEMIA; B-CELL LYMPHOMA; IMMUNOGLOBULIN-GENE REARRANGEMENTS; LYMPHOBLASTIC-LEUKEMIA; CHROMOSOMAL TRANSLOCATION; MONOCLONAL-ANTIBODIES RP GRIBBEN, JG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 62 TC 10 Z9 10 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 OCT PY 1993 VL 20 IS 5 SU 5 BP 143 EP 155 PG 13 WC Oncology SC Oncology GA MF182 UT WOS:A1993MF18200012 PM 8211204 ER PT J AU BRUGGE, WR ALAVI, A AF BRUGGE, WR ALAVI, A TI CHOLESCINTIGRAPHY IN THE DIAGNOSIS OF THE COMPLICATIONS OF LAPAROSCOPIC CHOLECYSTECTOMY SO SEMINARS IN ULTRASOUND CT AND MRI LA English DT Article RP BRUGGE, WR (reprint author), MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,7 JACKSON BLDG,BOSTON,MA 02114, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0887-2171 J9 SEMIN ULTRASOUND CT JI Semin. Ultrasound CT MRI PD OCT PY 1993 VL 14 IS 5 BP 368 EP 374 DI 10.1016/S0887-2171(05)80056-3 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MC585 UT WOS:A1993MC58500008 PM 8257630 ER PT J AU STOECKLE, JD AF STOECKLE, JD TI THE HIPPOCRATIC PREDICAMENT, AFFORDABILITY, ACCESS, AND ACCOUNTABILITY IN AMERICAN MEDICINE - KAPLAN,RM SO SOCIAL SCIENCE & MEDICINE LA English DT Book Review RP STOECKLE, JD (reprint author), MASSACHUSETTS GEN HOSP,PRIMARY CARE PROGRAM,BOSTON,MA 02114, USA. NR 1 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 0277-9536 J9 SOC SCI MED JI Soc. Sci. Med. PD OCT PY 1993 VL 37 IS 8 BP 1088 EP 1089 DI 10.1016/0277-9536(93)90445-A PG 2 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA LZ549 UT WOS:A1993LZ54900019 ER PT J AU GEORGE, MJ SNYDMAN, DR WERNER, BG DOUGHERTY, NN GRIFFITH, J ROHRER, RH FREEMAN, R JENKINS, R LEWIS, WD AF GEORGE, MJ SNYDMAN, DR WERNER, BG DOUGHERTY, NN GRIFFITH, J ROHRER, RH FREEMAN, R JENKINS, R LEWIS, WD TI USE OF GANCICLOVIR PLUS CYTOMEGALOVIRUS IMMUNE GLOBULIN TO TREAT CMV PNEUMONIA IN ORTHOTOPIC LIVER-TRANSPLANT RECIPIENTS SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT SYMP ON UPDATE ON CYTOMEGALOVIRUS INJECTION IN SOLID-ORGAN TRANSPLANTATION, AT THE 12TH ANNUAL MEETING OF THE AMERICAN-SOC-OF-TRANSPLANT-PHYSICIANS CY MAY 17-19, 1993 CL HOUSTON, TX SP AMER SOC TRANSPLANT PHYSICIANS ID BONE-MARROW TRANSPLANTATION; RENAL-ALLOGRAFT RECIPIENTS; HYPERIMMUNE IMMUNOGLOBULIN; VIRUS PNEUMONIA; INFECTIONS; DISEASE; THERAPY; COMBINATION C1 TUFTS UNIV NEW ENGLAND MED CTR,DEPT MED,BOX 238,750 WASHINGTON ST,BOSTON,MA 02111. TUFTS UNIV,SCH MED,MASSACHUSETTS STATE LAB INST,DEPT MED,BOSTON,MA 02111. HARVARD UNIV,SCH MED,BOSTON,MA 02115. TUFTS UNIV NEW ENGLAND MED CTR,DEPT PATHOL,BOSTON,MA 02111. TUFTS UNIV NEW ENGLAND MED CTR,DEPT SURG,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,TRANSPLANTAT UNIT,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,DEPT SURG,BOSTON,MA 02215. RI Snydman, David/O-3889-2014 OI Snydman, David/0000-0003-0119-3978 FU NIDDK NIH HHS [R10 DK31389] NR 17 TC 32 Z9 32 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD OCT PY 1993 VL 25 IS 5 SU 4 BP 22 EP 24 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA MC564 UT WOS:A1993MC56400005 PM 8212303 ER PT J AU ALPER, JS NATOWICZ, MR AF ALPER, JS NATOWICZ, MR TI ON ESTABLISHING THE GENETIC-BASIS OF MENTAL DISEASE SO TRENDS IN NEUROSCIENCES LA English DT Editorial Material ID LINKAGE; MARKERS; ILLNESS AB Many of the recent studies reporting genetic linkages for mental Illnesses such as schizophrenia and manic depression have been retracted. The authors of this article argue that the fundamental reason for the difficulties in this research field lies in the strongly held preconceived belief that the primary cause of these illnesses is in fact genetic. All scientists hold preconceived ideas. However, such ideas are more likely to result in erroneous conclusions in the study of human behavior than in other more 'objective' research areas. Moreover, it is especially important that researchers studying human behavior be a ware of their biases and learn to compensate for them because of the social consequences of their work. C1 UNIV MASSACHUSETTS,CTR GENET & PUBL POLICY,BOSTON,MA 02125. EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MED GENET,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. RP ALPER, JS (reprint author), UNIV MASSACHUSETTS,DEPT CHEM,BOSTON,MA 02125, USA. NR 16 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD OCT PY 1993 VL 16 IS 10 BP 387 EP 389 DI 10.1016/0166-2236(93)90003-5 PG 3 WC Neurosciences SC Neurosciences & Neurology GA MA593 UT WOS:A1993MA59300003 PM 7504351 ER PT J AU BUTTERTON, JR BOYKO, SA CALDERWOOD, SB AF BUTTERTON, JR BOYKO, SA CALDERWOOD, SB TI USE OF THE VIBRIO-CHOLERAE IRGA GENE AS A LOCUS FOR INSERTION AND EXPRESSION OF HETEROLOGOUS ANTIGENS IN CHOLERA VACCINE STRAINS SO VACCINE LA English DT Article DE VIBRIO-CHOLERAE; VACCINE; CHOLERA TOXIN; SHIGA TOXIN; TRANSCRIPTIONAL REGULATION; IRGA; COMMON MUCOSAL IMMUNE SYSTEM; IN-VIVO MARKER EXCHANGE ID OUTER-MEMBRANE PROTEINS; B-SUBUNIT; ESCHERICHIA-COLI; SHIGELLA TOXIN; ANTIBODY-RESPONSES; FIELD TRIAL; TRANSCRIPTIONAL REGULATION; NUCLEOTIDE-SEQUENCE; SALIVARY-GLANDS; SUICIDE VECTOR AB Vibrio cholerae may be a particularly effective organism for use in delivering heterologous antigens to stimulate a common mucosal immune response. A live attenuated vaccine strain of V. cholerae was constructed from the ctxA deletion mutant 0395-N1, containing the B subunit of Shiga-like toxin I under the transcriptional control of the iron-regulated irgA promoter. The B subunit of Shiga-like toxin I is identical to the B subunit of Shiga toxin (StxB). irgA encodes the major iron-regulated outer membrane protein of V. cholerae, which is a known virulence factor for this organism. Clones of the structural gene irgA from the classical V. cholerae strain 0395, with the gene for the Shiga-like toxin I B subunit inserted under the control of the irgA promoter, were used to introduce an internal deletion of irgA into the chromosome of 0395-N1 by in vivo marker exchange, using the suicide vector plasmid pCVD442. This plasmid contains the sacB gene from Bacillus subtilis, which allowed positive selection for loss of plasmid sequences on exposure to sucrose. The construction of vaccine strains was confirmed by Southern hybridization studies and outer membrane protein analysis. The expression of StxB in the vaccine strain VAC2 following growth in high- or low-iron conditions was shown to be tightly iron-regulated by Western blot analysis and by quantification of StxB using a sandwich enzyme-linked immunosorbent assay. The production of StxB by VAC2 under low-iron conditions was greater than that of the reference strain Shigella dysenteriae 60R. This vaccine strain produced no detectable cytotoxicity in a HeLa cell assay, and showed no increased virulence over the attenuated parent strain, 0395-N1, in a suckling mouse model. We suggest that the V. cholerae irgA gene is a particularly useful locus for the insertion and expression of heterologous antigens in cholera vaccine strains for oral delivery. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NIAID NIH HHS [AI 27329] NR 49 TC 32 Z9 33 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0264-410X J9 VACCINE JI Vaccine PD OCT PY 1993 VL 11 IS 13 BP 1327 EP 1335 DI 10.1016/0264-410X(93)90103-5 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA MC984 UT WOS:A1993MC98400010 PM 8296486 ER PT J AU SCHINKEL, AH ARCECI, RJ SMIT, JJM WAGENAAR, E BAAS, F DOLLE, M TSURUO, T MECHETNER, EB RONINSON, IB BORST, P AF SCHINKEL, AH ARCECI, RJ SMIT, JJM WAGENAAR, E BAAS, F DOLLE, M TSURUO, T MECHETNER, EB RONINSON, IB BORST, P TI BINDING-PROPERTIES OF MONOCLONAL-ANTIBODIES RECOGNIZING EXTERNAL EPITOPES OF THE HUMAN MDR1 P-GLYCOPROTEIN SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article; Proceedings Paper CT CANCER RESEARCH CAMPAIGN CONF ON TARGETED CANCER THERAPY CY DEC 17-19, 1991 CL ROYAL FREE HOSP SCH MED, LONDON, ENGLAND SP UNION INT CONTRE CANC HO ROYAL FREE HOSP SCH MED ID MULTIDRUG-RESISTANCE GENE; DRUG-RESISTANCE; COMPLEMENTARY-DNA; CELLS; EXPRESSION; XENOGRAFT; MELANOMA; REVERSAL; TISSUES AB Monoclonal antibodies (MAbs) recognizing external epitopes of the human MDR1 P-glycoprotein have been used both for the detection of multidrug-resistant cells and as specific inhibitors of P-glycoprotein-mediated multidrug resistance. Using a panel of recently developed transfected or transgenic cell lines containing variants of the human MDR1 and MDR3 P-glycoproteins, we have compared the specificity and binding properties of the previously isolated MAbs MRK16, HYB-241, UIC2 and 4E3, and of the newly isolated MAb 7G4. The removal of 1, 2 or all 3 of the N-glycosylation sites present in the first extracellular loop of MDR1 P-glycoprotein did not significantly affect the binding of these MAbs. In contrast, a 20 amino acid deletion in the first extracellular loop of MDR1 P-glycoprotein completely abolished binding of UIC2, whereas the binding of all other MAbs was hardly affected. None of the MAbs tested bound detectably to cell lines containing a high level of the human MDR3 P-glycoprotein. The differences in the binding specificity between UIC2 and the other tested antibodies parallel the reported functional differences in the ability of these antibodies to inhibit P-glycoprotein-mediated drug efflux. (C) 1993 Wiley-Liss, Inc. C1 NETHERLANDS CANC INST,DIV MOLEC BIOL,PLESMANLAAN 121,1066 CX AMSTERDAM,NETHERLANDS. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. UNIV AMSTERDAM,DEPT NEUROL,AMSTERDAM,NETHERLANDS. UNIV TOKYO,INST APPL MICROBIOL,BUNKYO KU,TOKYO 113,JAPAN. UNIV ILLINOIS,DEPT GENET,CHICAGO,IL 60612. RI Baas, Frank/F-9574-2010 OI Baas, Frank/0000-0003-3912-5428 FU NCI NIH HHS [CA40333] NR 27 TC 83 Z9 87 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD SEP 30 PY 1993 VL 55 IS 3 BP 478 EP 484 DI 10.1002/ijc.2910550326 PG 7 WC Oncology SC Oncology GA MA127 UT WOS:A1993MA12700025 PM 8104165 ER PT J AU ALLAM, A TAGHIAN, A GIOIOSO, D DUFFY, M SUIT, HD AF ALLAM, A TAGHIAN, A GIOIOSO, D DUFFY, M SUIT, HD TI INTRATUMORAL HETEROGENEITY OF MALIGNANT GLIOMAS MEASURED IN-VITRO SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE IN-VITRO SENSITIVITY; SURVIVING FRACTION AT 2 GY; INTRA-TUMORAL HETEROGENEITY; MALIGNANT GLIOMAS ID CELLULAR RADIOSENSITIVITY; RADIATION SENSITIVITY; SURVIVAL CURVES; SUB-POPULATIONS; HUMAN-TUMORS; CELLS; RADIORESPONSIVENESS; RADIOTHERAPY; CARCINOMAS; HEAD AB Purpose: To evaluate the extent of intratumoral heterogeneity of radiation sensitivity in malignant gliomas, by comparing the intrinsic radiation sensitivity of different glioma sublines derived from the same tumor. Methods and Materials: The study was performed on five early established malignant gliomas (passage 3-10). Each specimen was quickly cut into three equal pieces (except for one specimen, where only two pieces were obtained). Each piece was processed independently, disintegrated into single cell suspension using a cocktail of enzymes. Survival curve assays, using colony formation as an end-point, were performed for each subline. Comparison between the intrinsic radiation sensitivity of sublines was calculated using the surviving fraction at 2 Gy and the mean inactivation dose as the measured parameters. The DNA content of the cell lines as well as their cell cycle analysis was determined using flow cytometry. Results: The mean calculated surviving fraction at 2 Gy of all the sublines was 0.37 +/- 0.14, the mean mean inactivation dose was 1.98 +/- 0.63. The intertumoral coefficient of variation for the calculated surviving fraction at 2 Gy of all cell lines was 38%, while that for intratumoral heterogeneity was 25%. Three of the 5 tumors showed a statistically significant difference in the surviving fraction at 2 Gy and mean inactivation dose values of their sublines (p < 0.05). This difference in radiation sensitivity between sublines of the same tumor was not attributed to a difference either in the ploidy status or in the distribution of cells in the cell cycle. Conclusion: There is a significant intratumoral heterogeneity of radiation sensitivity in some malignant gliomas. This heterogeneity may limit the predictive power of surviving fraction at 2 Gy or mean inactivation dose, especially when their values are based upon a single measurement/single biopsy. In the meantime, this heterogeneity may be a factor in the discrepancy between unexpectedly sensitive tumor cell lines in vitro and their high clinical radiation resistance. RP ALLAM, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB RADIAT BIOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA13311] NR 20 TC 22 Z9 22 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 SEP 30 PY 1993 VL 27 IS 2 BP 303 EP 308 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA MC220 UT WOS:A1993MC22000015 PM 8407404 ER PT J AU LO, EH AF LO, EH TI A THEORETICAL-ANALYSIS OF HEMODYNAMIC AND BIOMECHANICAL ALTERATIONS IN INTRACRANIAL AVMS AFTER RADIOSURGERY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE ARTERIOVENOUS MALFORMATION; STEREOTAXIC RADIOSURGERY; CEREBRAL BLOOD FLOW; INTRACRANIAL HEMORRHAGE; BIOMATHEMATICAL MODEL ID CEREBRAL ARTERIOVENOUS-MALFORMATIONS; BLOOD-FLOW; STEREOTAXIC RADIOSURGERY; LINEAR-ACCELERATOR; BRAIN; IRRADIATION; RADIATION; MODEL; MRI AB Purpose: Stereotactic radiosurgery is being increasingly used to treat intracranial arteriovenous malformations (AVMs). However, successful radiosurgery may involve latent periods of 1-2 years prior to AVM obliteration. This latent period include states of altered flow patterns that may or may not influence hemorrhage probabilities. The probability of hemorrhage is likely to be related to the degree of biomechanical stress across the AVM shunt walls. This paper describes a theoretical analysis of the altered hemodynamics and biomechanical stresses within AVM shunts post-radiosurgery. Methods and Materials: The mathematical model is comprised of linked flow compartments that represent the AVM and adjacent normal vasculature. As obliteration of the irradiated shunts occur, changes in flow rates and pressure gradients are calculated based on first order fluid dynamics. Stress on the AVM shunt walls is calculated based on tangential forces due to intramural pressure. Two basic models are presented: a distribution of shunts with fixed thin walls subject to step-function obliteration (Model I), and a distribution of shunts subject to luminal obliteration from slowly thickening walls (Model II). Variations on these models are analyzed, including sequential, selective and random shunt obliteration, and uniform or Poisson distributions of shunt radii. Results: Model I reveals that the range of pressure alterations in the radiosurgically-treated AVM include the possibility of transient increases in the total biomechanical stress within the shunt walls prior to obliteration. Model II demonstrates that uniform luminal narrowing via thickened walls should lead to reduced transmural stresses. The precise temporal pattern of AVM flow decrease and biomechanical stress reduction depends on the selection of shunts that are obliterated. Conclusion: (a) The hemodynamic and biomechanical changes appear to be relatively independent of the shunt distribution but highly dependent on the temporal pattern of the obliterative process, (b) uniformly thickened shunt walls should uniformly decrease biomechanical stresses in the latent period prior to complete obliteration, but if uniform obliteration is not achieved, (c) transient alterations in pressure versus stress relationships may lead to temporarily increased biomechanical stress prior to complete obliteration, and (d) reduction in stress may not reach significant levels until the AVM is almost completely obliterated. RP LO, EH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR IMAGING & PHARMACEUT RES,BOSTON,MA 02129, USA. NR 34 TC 14 Z9 14 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 SEP 30 PY 1993 VL 27 IS 2 BP 353 EP 361 PG 9 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA MC220 UT WOS:A1993MC22000021 PM 8407410 ER PT J AU SHAMOON, H DUFFY, H FLEISCHER, N ENGEL, S SAENGER, P STRELZYN, M LITWAK, M WYLIEROSETT, J FARKASH, A GEIGER, D ENGEL, H FLEISCHMAN, J POMPI, D GINSBERG, N GLOVER, M BRISMAN, M WALKER, E THOMASHUNIS, A GONZALEZ, J GENUTH, S BROWN, E DAHMS, W PUGSLEY, P MAYER, L KERR, D LANDAU, B SINGERMAN, L RICE, T NOVAK, M SMITHBREWER, S MCCONNELL, J DROTAR, D WOODS, D KATIRGI, B LITVENE, M BROWN, C LUSK, M CAMPBELL, R LACKAYE, M RICHARDSON, M LEVY, B CHANG, S HEINHEINEMANN, M BARRON, S ASTOR, L LEBECK, D BRILLON, D DIAMOND, B VASILASDWOSKIN, A LAURENZI, B FOLDI, N RUBIN, M FLYNN, T REPPUCCI, V HEISE, C SANCHEZ, A WHITEHOUSE, F KRUGER, D KAHKONEN, D FACHNIE, J FISK, J CAREY, J COX, M AHMAD, B ANGUS, E CAMPBELL, H FIELDS, D CROSWELL, M BASHA, K CHUNG, P SCHOENHERR, A MOBLEY, M MARCHIORI, K FRANCIS, J KELLY, J ETZWILER, D CALLAHAN, P HOLLANDER, P CASTLE, G BERGENSTAL, R SPENCER, M NELSON, J BEZECNY, L ROETHKE, C ORBAN, M ULRICH, C GILL, L MORGAN, K LAECHELT, J TAYLOR, F FREKING, D TOWEY, A LIEPPMAN, M RAKES, S MANGUM, J COOPER, N UPHAM, P JACOBSON, A CROWELL, S WOLFSDORF, J BEASER, R GANDA, O ROSENZWEIG, J STEWART, C HALFORD, B FRIEDLANDER, E TARSY, D ARRIGG, P SHARUK, G SHAH, S WU, G CAVALLERANO, J POOLE, R SILVER, P CAVICCHI, R FLEMING, D MARCUS, J GRIFFITHS, C CAPPELLA, N NATHAN, D LARKIN, M GODINE, J LYNCH, J NORMAN, D MCKITRICK, C HAGGEN, C DELAHANTY, L ANDERSON, E LOU, P TAYLOR, C CROS, D FOLINO, K BRINK, S ABBOTT, K SICOTTE, K SERVICE, FJ SCHMIDT, A RIZZA, R ZIMMERMAN, B SCHWENK, W MORTENSON, J ZIEGLER, G LUCAS, A HANSON, N SELLNOW, S PACH, J STEIN, D EICKHOFF, B WOODWICK, R TACKMANN, R TRAUTMANN, J ROSTVOLD, J LINK, T DYCK, P DAUBE, J COLLIGAN, R WINDEBANK, A KING, J COLWELL, J WOOD, D MAYFIELD, R PICKET, J CHITWOOD, M BILLINGS, D DABNEY, Y BUSE, J KING, L VALE, S THOMPSON, T BOHM, B LYONS, T HERMAYER, K RICE, A MOLITCH, M SCHAEFER, B JOHNSON, C LYONS, J METZGER, B COHEN, B NISHIDA, T PARQUE, K YUSIM, V MOORE, M JAMPOL, L DINEEN, K STAHL, J RICHINE, L WEINBERG, D LOOSE, I KUSHNER, M MORRISON, A JALBERT, A TILDESLEY, H LEUNG, S BEGG, I JOHNSON, D LALANI, S KENNEDY, T MEADOWS, G KOLTERMAN, O LORENZI, G JONES, K GOLDBAUM, M SWENSON, M LYON, R GIOTTA, M KADLEC, K REED, R KIRSCH, L GOODMAN, J CAHILL, S CLARK, T ABRAM, R SAYNER, L OCHABSKI, R GLORIA, R BIRCHLER, G GRANT, J GRASSE, B CHRISTLE, L ABREU, B GRANT, I HEATON, R ZEITLER, R SIVITZ, W BAYLESS, M SCHROTT, H OLSON, N TINDAL, B SNETSELAAR, L MUELLER, D DUDLER, A SWARTZENDRUBER, J HOFFMAN, R MACINDOE, J KRAMER, J WEINGEIST, T KIMURA, A STONE, E GROUT, T FOUNTAIN, C KARAKAS, S VOGEL, C MONTAGUE, P KEYSER, D MENNEN, S DOGGETT, C ROSE, G DEVET, K MUHLE, P KOWARSKI, A OSTROWSKI, D LEVIN, P CHALEW, S HYLTON, J YOUNGHYMAN, D BARLOW, M MAYER, R ELMAN, M LAKHANPAL, V WEINER, B MILLAR, M BLUM, S BUIE, W MACE, B GREENE, D MARTIN, C FLOYD, J DUNN, F HENRY, D BENNETT, S LASICHAK, A VINE, A ALBERS, J SANDFORD, T LOFTIN, J STEVENS, M ELNER, S MARTONYI, C MCIVER, F STANLEY, S WILLIS, J RYAN, K SPIEGELBERG, T NALEPA, S GLASGOW, B CHAN, E DOTIMAS, P BANTLE, J MECH, M BALLES, M KENNEDY, W KHAN, M KNOBLOCH, W KWONG, C MCKENZIE, L OLSON, J RAMSAY, R ROBINER, W WARHOL, R GENIA, A MCDONOUGH, G MCMICHAEL, B PHILIPH, D PONWITH, L SAHINEN, R STINSON, E VERNESS, J FIMREITE, L STEIN, J GOLDSTEIN, D HALL, M BURNS, T KLACHKO, D GIANGIACOMO, J RAWLINGS, S ASTON, L ENGLAND, J WIEDMEYER, H DAUGHERTY, M LIGHTFOOT, M WILSON, R WILSON, R GRIFFING, G GARDNER, D CONWAY, R BLINDER, K BROWNLEEDUFFECK, M PALMER, N GASH, L SCHADE, D JOHANNES, C REIDY, R BICKNELL, J VOGEL, A DRUMM, D BOYLE, P BURGE, M JONES, N CANADY, J NICKELL, D BAKER, L ILVESCORRESSEL, P SCHWARTZ, S BRAUNSTEIN, S MCBRIDE, J BRUCKER, A RENDLE, L BROWN, M SLADKY, J MASCHAKCAREY, B LAWLEY, D NYBERG, W WEENEY, L SANDBURG, E BYRD, S AGUADO, E MULHOLLAND, N CAHN, D SUSCAVAGE, M EGLER, J VAUGHNNORTON, M COLLINS, C MAMENISKIS, H DRASH, A WESCHE, J BRATKOWSKI, M BECKER, D ARSLANIAN, S DOFT, B LOBES, L RINKOFF, J WARNICKI, J CURTIN, D STEINBERG, D VAGSTAD, G RYAN, C HARRIS, F STERANCHAK, L ARCH, J KELLY, K OSTROSKA, P GUILIANI, M GOOD, M WILLIAMS, T OLSEN, K CAMPBELL, A SHIPE, C CONWIT, R FINEGOLD, D ZAUCHA, M MALONE, J GROVE, N MCMILLAN, D BABIONE, L DECLUE, T PAVAN, P KORTHALS, J SOLC, H MANGIONE, A KITABCHI, A TAYLOR, L JONES, L PITTS, K BERTORINI, T BITTLE, J BURGHEN, G FISHER, J HUGHES, T LINN, J MEYER, D MURPHY, W JUSTICE, M SHERMAN, A WRIGHT, L MURPHY, L RASKIN, P STROWIG, S BASCO, M CERCONE, S RAMIREZ, L ANAND, R WILSON, C GREENLEE, R ANDERSON, W MENDELSON, E VANACEK, P HOWARD, J OUSLEY, C YATES, B CONGER, D MAGUIRE, B BIGGS, M NEWTON, B SHERILL, K ZINMAN, B BARNIE, A EHRLICH, R DANEMAN, D PERLMAN, K LEITER, L GOTTESMAN, I DEVENYI, R MORTIMER, C MOFFAT, K GORDON, A FERGUSON, R CAMELON, K SIMKINS, S LITTLEFIELD, C RODIN, G HARTLEY, K KWAN, J GNANAPANDITHEN, D ROGERS, S HAYE, L ROSE, J MEZEI, S BUNPHY, B MACLEAN, S MACKEEN, L MANDELCORN, M NELLIS, P RUTTAN, L WILSONSMITH, D PALMER, J GINSBERG, J HIRSCH, I KINYOUN, J DOERR, H MAUSETH, R SWEENEY, K VANOTTINGHAM, L THOMSON, L GREENBAUM, C SAMESHIMA, L FARKASHIRSCH, R ROSENBAUM, G RUBNER, N BROWN, T KRAFT, G BROECKEL, J KARLSEN, M KHAKPOUR, D RAMIREZ, M SMIT, B MIX, L DUPRE, J COLBY, P RODGER, W HRAMIAK, I JENNER, M CANNY, C BROWN, W SMITH, T HARTH, J BONDY, S BEATH, S MCCABE, S GOUCHIE, C BLANCHARD, K MCCALLUM, J JUNG, S SUETANG, A LORENZ, R LIPPS, J MCRAE, J MAY, J MAY, M CAMPBELL, P FEMAN, S KILROY, A PULLIAM, C SCHLUNDT, D JANNASCH, K DAVIS, D CULLEN, N ADKINS, T SNELL, M VIRTS, K QUESENBERRY, L SANTIAGO, J LEVANDOSKI, L WHITE, N MCGILL, J BUBB, J SCHMIDT, L STRASBERG, Y CASSO, M NOETZEL, M OLK, R BONIUK, I GRAND, M THOMAS, M WILLIAMS, D NOBEL, G KACIZAK, R ORT, E DAHL, J BREEDING, L HOFFMEYER, G BILYEU, P BLANK, J WALTERS, C BODNAR, J RODRIGUEZ, P ERICKSON, M HEDRICK, S TAMBORLANE, W AHERN, J SHERWIN, R GATCOMB, P STOESSEL, K HELD, N EBERSOLE, J SCANLON, I LOUARD, R WILDSTEIN, C BILODEAU, D FONG, K OTTAVIANO, D LARSON, C CROFFORD, OB LACHIN, J CLEARY, P THOMPSON, D KENNY, D LAN, S LAN, G BRENNEMAN, A OWEN, W ADAMS, K ARNOLD, D CAMPANELL, R LORING, N SCHEIRER, P BECKER, D LAMAS, D DUNEGAN, C VEERAMACHANENI, H WILLIAMS, C ABDULBAAQIY, S KASSOFF, A ADAMS, K GRANT, I HEATON, R DORMAN, J SPIELMAN, R KLEIN, R SIEBERT, C SILVERMAN, R PFEIFER, M SCHUMER, M MORAN, M FARQUHAR, J ENGLAND, J WIEDMEYER, H ROHLFING, C DAVIS, M HUBBARD, L MAGLI, Y THOMAS, S ONOFREY, J JENSEN, K BROTHERS, R ANSAY, S ARMSTRONG, J BADAL, D VANDERHOOFYOUNG, M ESSER, B GEITHMAN, P HURLBURT, D REIMERS, J KEWLEY, K MINER, K STEFFES, M BUCKSA, J RYAN, C CATANZARO, R LUKES, A BAGOVICH, G WOODFILL, T CROW, R HUGHLETT, J SWANSON, C BUZZARD, I STEVENS, M SIELAFF, B PICKERING, B SCHAKEL, S HERMAN, W DASBACH, E SONGER, T JANES, G DEEB, L EWART, R ORCHARD, T CLARK, C CUTTER, G DAVIS, M DEMETS, D FERRIS, F FURBERG, C HORTON, E KEEN, J LOCKWOOD, D PALMBERG, P ROURKE, B TSIATIS, A LEVY, R FRANK, R GRIZZLE, J RUBENSTEIN, A SCHNEIDER, J SKYLER, J NATHAN, DM GENUTH, S LACHIN, J CLEARY, P CROFFORD, O DAVIS, M RAND, L SIEBERT, C AF SHAMOON, H DUFFY, H FLEISCHER, N ENGEL, S SAENGER, P STRELZYN, M LITWAK, M WYLIEROSETT, J FARKASH, A GEIGER, D ENGEL, H FLEISCHMAN, J POMPI, D GINSBERG, N GLOVER, M BRISMAN, M WALKER, E THOMASHUNIS, A GONZALEZ, J GENUTH, S BROWN, E DAHMS, W PUGSLEY, P MAYER, L KERR, D LANDAU, B SINGERMAN, L RICE, T NOVAK, M SMITHBREWER, S MCCONNELL, J DROTAR, D WOODS, D KATIRGI, B LITVENE, M BROWN, C LUSK, M CAMPBELL, R LACKAYE, M RICHARDSON, M LEVY, B CHANG, S HEINHEINEMANN, M BARRON, S ASTOR, L LEBECK, D BRILLON, D DIAMOND, B VASILASDWOSKIN, A LAURENZI, B FOLDI, N RUBIN, M FLYNN, T REPPUCCI, V HEISE, C SANCHEZ, A WHITEHOUSE, F KRUGER, D KAHKONEN, D FACHNIE, J FISK, J CAREY, J COX, M AHMAD, B ANGUS, E CAMPBELL, H FIELDS, D CROSWELL, M BASHA, K CHUNG, P SCHOENHERR, A MOBLEY, M MARCHIORI, K FRANCIS, J KELLY, J ETZWILER, D CALLAHAN, P HOLLANDER, P CASTLE, G BERGENSTAL, R SPENCER, M NELSON, J BEZECNY, L ROETHKE, C ORBAN, M ULRICH, C GILL, L MORGAN, K LAECHELT, J TAYLOR, F FREKING, D TOWEY, A LIEPPMAN, M RAKES, S MANGUM, J COOPER, N UPHAM, P JACOBSON, A CROWELL, S WOLFSDORF, J BEASER, R GANDA, O ROSENZWEIG, J STEWART, C HALFORD, B FRIEDLANDER, E TARSY, D ARRIGG, P SHARUK, G SHAH, S WU, G CAVALLERANO, J POOLE, R SILVER, P CAVICCHI, R FLEMING, D MARCUS, J GRIFFITHS, C CAPPELLA, N NATHAN, D LARKIN, M GODINE, J LYNCH, J NORMAN, D MCKITRICK, C HAGGEN, C DELAHANTY, L ANDERSON, E LOU, P TAYLOR, C CROS, D FOLINO, K BRINK, S ABBOTT, K SICOTTE, K SERVICE, FJ SCHMIDT, A RIZZA, R ZIMMERMAN, B SCHWENK, W MORTENSON, J ZIEGLER, G LUCAS, A HANSON, N SELLNOW, S PACH, J STEIN, D EICKHOFF, B WOODWICK, R TACKMANN, R TRAUTMANN, J ROSTVOLD, J LINK, T DYCK, P DAUBE, J COLLIGAN, R WINDEBANK, A KING, J COLWELL, J WOOD, D MAYFIELD, R PICKET, J CHITWOOD, M BILLINGS, D DABNEY, Y BUSE, J KING, L VALE, S THOMPSON, T BOHM, B LYONS, T HERMAYER, K RICE, A MOLITCH, M SCHAEFER, B JOHNSON, C LYONS, J METZGER, B COHEN, B NISHIDA, T PARQUE, K YUSIM, V MOORE, M JAMPOL, L DINEEN, K STAHL, J RICHINE, L WEINBERG, D LOOSE, I KUSHNER, M MORRISON, A JALBERT, A TILDESLEY, H LEUNG, S BEGG, I JOHNSON, D LALANI, S KENNEDY, T MEADOWS, G KOLTERMAN, O LORENZI, G JONES, K GOLDBAUM, M SWENSON, M LYON, R GIOTTA, M KADLEC, K REED, R KIRSCH, L GOODMAN, J CAHILL, S CLARK, T ABRAM, R SAYNER, L OCHABSKI, R GLORIA, R BIRCHLER, G GRANT, J GRASSE, B CHRISTLE, L ABREU, B GRANT, I HEATON, R ZEITLER, R SIVITZ, W BAYLESS, M SCHROTT, H OLSON, N TINDAL, B SNETSELAAR, L MUELLER, D DUDLER, A SWARTZENDRUBER, J HOFFMAN, R MACINDOE, J KRAMER, J WEINGEIST, T KIMURA, A STONE, E GROUT, T FOUNTAIN, C KARAKAS, S VOGEL, C MONTAGUE, P KEYSER, D MENNEN, S DOGGETT, C ROSE, G DEVET, K MUHLE, P KOWARSKI, A OSTROWSKI, D LEVIN, P CHALEW, S HYLTON, J YOUNGHYMAN, D BARLOW, M MAYER, R ELMAN, M LAKHANPAL, V WEINER, B MILLAR, M BLUM, S BUIE, W MACE, B GREENE, D MARTIN, C FLOYD, J DUNN, F HENRY, D BENNETT, S LASICHAK, A VINE, A ALBERS, J SANDFORD, T LOFTIN, J STEVENS, M ELNER, S MARTONYI, C MCIVER, F STANLEY, S WILLIS, J RYAN, K SPIEGELBERG, T NALEPA, S GLASGOW, B CHAN, E DOTIMAS, P BANTLE, J MECH, M BALLES, M KENNEDY, W KHAN, M KNOBLOCH, W KWONG, C MCKENZIE, L OLSON, J RAMSAY, R ROBINER, W WARHOL, R GENIA, A MCDONOUGH, G MCMICHAEL, B PHILIPH, D PONWITH, L SAHINEN, R STINSON, E VERNESS, J FIMREITE, L STEIN, J GOLDSTEIN, D HALL, M BURNS, T KLACHKO, D GIANGIACOMO, J RAWLINGS, S ASTON, L ENGLAND, J WIEDMEYER, H DAUGHERTY, M LIGHTFOOT, M WILSON, R WILSON, R GRIFFING, G GARDNER, D CONWAY, R BLINDER, K BROWNLEEDUFFECK, M PALMER, N GASH, L SCHADE, D JOHANNES, C REIDY, R BICKNELL, J VOGEL, A DRUMM, D BOYLE, P BURGE, M JONES, N CANADY, J NICKELL, D BAKER, L ILVESCORRESSEL, P SCHWARTZ, S BRAUNSTEIN, S MCBRIDE, J BRUCKER, A RENDLE, L BROWN, M SLADKY, J MASCHAKCAREY, B LAWLEY, D NYBERG, W WEENEY, L SANDBURG, E BYRD, S AGUADO, E MULHOLLAND, N CAHN, D SUSCAVAGE, M EGLER, J VAUGHNNORTON, M COLLINS, C MAMENISKIS, H DRASH, A WESCHE, J BRATKOWSKI, M BECKER, D ARSLANIAN, S DOFT, B LOBES, L RINKOFF, J WARNICKI, J CURTIN, D STEINBERG, D VAGSTAD, G RYAN, C HARRIS, F STERANCHAK, L ARCH, J KELLY, K OSTROSKA, P GUILIANI, M GOOD, M WILLIAMS, T OLSEN, K CAMPBELL, A SHIPE, C CONWIT, R FINEGOLD, D ZAUCHA, M MALONE, J GROVE, N MCMILLAN, D BABIONE, L DECLUE, T PAVAN, P KORTHALS, J SOLC, H MANGIONE, A KITABCHI, A TAYLOR, L JONES, L PITTS, K BERTORINI, T BITTLE, J BURGHEN, G FISHER, J HUGHES, T LINN, J MEYER, D MURPHY, W JUSTICE, M SHERMAN, A WRIGHT, L MURPHY, L RASKIN, P STROWIG, S BASCO, M CERCONE, S RAMIREZ, L ANAND, R WILSON, C GREENLEE, R ANDERSON, W MENDELSON, E VANACEK, P HOWARD, J OUSLEY, C YATES, B CONGER, D MAGUIRE, B BIGGS, M NEWTON, B SHERILL, K ZINMAN, B BARNIE, A EHRLICH, R DANEMAN, D PERLMAN, K LEITER, L GOTTESMAN, I DEVENYI, R MORTIMER, C MOFFAT, K GORDON, A FERGUSON, R CAMELON, K SIMKINS, S LITTLEFIELD, C RODIN, G HARTLEY, K KWAN, J GNANAPANDITHEN, D ROGERS, S HAYE, L ROSE, J MEZEI, S BUNPHY, B MACLEAN, S MACKEEN, L MANDELCORN, M NELLIS, P RUTTAN, L WILSONSMITH, D PALMER, J GINSBERG, J HIRSCH, I KINYOUN, J DOERR, H MAUSETH, R SWEENEY, K VANOTTINGHAM, L THOMSON, L GREENBAUM, C SAMESHIMA, L FARKASHIRSCH, R ROSENBAUM, G RUBNER, N BROWN, T KRAFT, G BROECKEL, J KARLSEN, M KHAKPOUR, D RAMIREZ, M SMIT, B MIX, L DUPRE, J COLBY, P RODGER, W HRAMIAK, I JENNER, M CANNY, C BROWN, W SMITH, T HARTH, J BONDY, S BEATH, S MCCABE, S GOUCHIE, C BLANCHARD, K MCCALLUM, J JUNG, S SUETANG, A LORENZ, R LIPPS, J MCRAE, J MAY, J MAY, M CAMPBELL, P FEMAN, S KILROY, A PULLIAM, C SCHLUNDT, D JANNASCH, K DAVIS, D CULLEN, N ADKINS, T SNELL, M VIRTS, K QUESENBERRY, L SANTIAGO, J LEVANDOSKI, L WHITE, N MCGILL, J BUBB, J SCHMIDT, L STRASBERG, Y CASSO, M NOETZEL, M OLK, R BONIUK, I GRAND, M THOMAS, M WILLIAMS, D NOBEL, G KACIZAK, R ORT, E DAHL, J BREEDING, L HOFFMEYER, G BILYEU, P BLANK, J WALTERS, C BODNAR, J RODRIGUEZ, P ERICKSON, M HEDRICK, S TAMBORLANE, W AHERN, J SHERWIN, R GATCOMB, P STOESSEL, K HELD, N EBERSOLE, J SCANLON, I LOUARD, R WILDSTEIN, C BILODEAU, D FONG, K OTTAVIANO, D LARSON, C CROFFORD, OB LACHIN, J CLEARY, P THOMPSON, D KENNY, D LAN, S LAN, G BRENNEMAN, A OWEN, W ADAMS, K ARNOLD, D CAMPANELL, R LORING, N SCHEIRER, P BECKER, D LAMAS, D DUNEGAN, C VEERAMACHANENI, H WILLIAMS, C ABDULBAAQIY, S KASSOFF, A ADAMS, K GRANT, I HEATON, R DORMAN, J SPIELMAN, R KLEIN, R SIEBERT, C SILVERMAN, R PFEIFER, M SCHUMER, M MORAN, M FARQUHAR, J ENGLAND, J WIEDMEYER, H ROHLFING, C DAVIS, M HUBBARD, L MAGLI, Y THOMAS, S ONOFREY, J JENSEN, K BROTHERS, R ANSAY, S ARMSTRONG, J BADAL, D VANDERHOOFYOUNG, M ESSER, B GEITHMAN, P HURLBURT, D REIMERS, J KEWLEY, K MINER, K STEFFES, M BUCKSA, J RYAN, C CATANZARO, R LUKES, A BAGOVICH, G WOODFILL, T CROW, R HUGHLETT, J SWANSON, C BUZZARD, I STEVENS, M SIELAFF, B PICKERING, B SCHAKEL, S HERMAN, W DASBACH, E SONGER, T JANES, G DEEB, L EWART, R ORCHARD, T CLARK, C CUTTER, G DAVIS, M DEMETS, D FERRIS, F FURBERG, C HORTON, E KEEN, J LOCKWOOD, D PALMBERG, P ROURKE, B TSIATIS, A LEVY, R FRANK, R GRIZZLE, J RUBENSTEIN, A SCHNEIDER, J SKYLER, J NATHAN, DM GENUTH, S LACHIN, J CLEARY, P CROFFORD, O DAVIS, M RAND, L SIEBERT, C TI THE EFFECT OF INTENSIVE TREATMENT OF DIABETES ON THE DEVELOPMENT AND PROGRESSION OF LONG-TERM COMPLICATIONS IN INSULIN-DEPENDENT DIABETES-MELLITUS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID GLUCOSE CONTROL; METABOLIC CONTROL; GLYCEMIC CONTROL; RETINOPATHY; AGE; PREVALENCE; DIAGNOSIS; INFUSION; RISK AB Background. Long-term microvascular and neurologic complications cause major morbidity and mortality in patients with insulin-dependent diabetes mellitus (IDDM). We examined whether intensive treatment with the goal of maintaining blood glucose concentrations close to the normal range could decrease the frequency and severity of these complications. Methods. A total of 1441 patients with IDDM - 726 with no retinopathy at base line (the primary-prevention cohort) and 715 with mild retinopathy (the secondary-intervention cohort) were randomly assigned to intensive therapy administered either with an external insulin pump or by three or more daily insulin injections and guided by frequent blood glucose monitoring or to conventional therapy with one or two daily insulin injections. The patients were followed for a mean of 6.5 years, and the appearance and progression of retinopathy and other complications were assessed regularly. Results. In the primary-prevention cohort, intensive therapy reduced the adjusted mean risk for the development of retinopathy by 76 percent (95 percent confidence interval, 62 to 85 percent), as compared with conventional therapy. In the secondary-intervention cohort, intensive therapy slowed the progression of retinopathy by 54 percent (95 percent confidence interval, 39 to 66 percent) and reduced the development of proliferative or severe nonproliferative retinopathy by 47 percent (95 percent confidence interval, 14 to 67 percent). In the two cohorts combined, intensive therapy reduced the occurrence of microalbuminuria (urinary albumin excretion of greater-than-or-equal-to 40 mg per 24 hours) by 39 percent (95 percent confidence interval, 21 to 52 percent), that of albuminuria (urinary albumin excretion of greater-than-or-equal-to 300 mg per 24 hours) by 54 percent (95 percent confidence interval, 19 to 74 percent), and that of clinical neuropathy by 60 percent (95 percent confidence interval, 38 to 74 percent). The chief adverse event associated with intensive therapy was a two-to-threefold increase in severe hypoglycemia. Conclusions. Intensive therapy effectively delays the onset and slows the progression of diabetic retinopathy, nephropathy, and neuropathy in patients with IDDM. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED, BRONX, NY 10461 USA. CASE WESTERN RESERVE UNIV, CLEVELAND, OH 44106 USA. CORNELL UNIV, MED CTR, NEW YORK, NY 10021 USA. HENRY FORD HOSP, DETROIT, MI 48202 USA. INT DIABET CTR, MINNEAPOLIS, MN USA. JOSLIN DIABET CTR, BOSTON, MA USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. MAYO CLIN & MAYO FDN, ROCHESTER, MN 55905 USA. MED UNIV S CAROLINA, CHARLESTON, SC 29425 USA. NORTHWESTERN UNIV, EVANSTON, IL 60201 USA. UNIV BRITISH COLUMBIA, VANCOUVER V6T 1W5, BC, CANADA. UNIV CALIF SAN DIEGO, LA JOLLA, CA 92093 USA. UNIV IOWA, IOWA CITY, IA 52242 USA. UNIV MARYLAND, SCH MED, BALTIMORE, MD 21201 USA. UNIV MICHIGAN, ANN ARBOR, MI 48109 USA. UNIV MINNESOTA, CENT BIOCHEM LAB, MINNEAPOLIS, MN 55455 USA. UNIV MISSOURI, CENT BACKUP LAB HBAIC, COLUMBIA, MO 65201 USA. UNIV NEW MEXICO, SCH MED, ALBUQUERQUE, NM 87131 USA. UNIV PENN, CHILDRENS HOSP, PHILADELPHIA, PA 19104 USA. UNIV PITTSBURGH, PITTSBURGH, PA 15260 USA. UNIV S FLORIDA, TAMPA, FL 33620 USA. UNIV TENNESSEE, KNOXVILLE, TN 37996 USA. UNIV TEXAS, SW MED CTR, DALLAS, TX 75230 USA. UNIV TORONTO, TORONTO M5S 1A1, ONTARIO, CANADA. UNIV WASHINGTON HOSP, SEATTLE, WA 98105 USA. UNIV WESTERN ONTARIO, LONDON N6A 3K7, ONTARIO, CANADA. VANDERBILT UNIV, NASHVILLE, TN 37240 USA. WASHINGTON UNIV, ST LOUIS, MO 63130 USA. YALE UNIV, SCH MED, NEW HAVEN, CT 06510 USA. NIDDKD, PROGRAM OFF, BETHESDA, MD USA. SO ILLINOIS UNIV, CENT AUTONOM CODING UNIT, CARBONDALE, IL 62901 USA. UNIV WISCONSIN, CENT FUNDUS PHOTOG READING CTR, MADISON, WI 53706 USA. WESTERN PSYCHIAT INST & CLIN, CENT NEUROBEHAV CODING UNIT, PITTSBURGH, PA 15261 USA. UNIV MINNESOTA, CENT ECG READING UNIT, MINNEAPOLIS, MN 55455 USA. UNIV MINNESOTA, CENT NUTR CODING UNIT, MINNEAPOLIS, MN 55455 USA. RP SHAMOON, H (reprint author), DCCT, RES GRP, BOX NDIC DCCT, BETHESDA, MD 20892 USA. RI Rice, Treva/D-1385-2009; Hoffman, Robert/E-3252-2011; Walters, Carl/D-5714-2012; Zinman, Bernard/E-7266-2013 NR 43 TC 11134 Z9 11411 U1 84 U2 613 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD SEP 30 PY 1993 VL 329 IS 14 BP 977 EP 986 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA LY587 UT WOS:A1993LY58700001 ER PT J AU SHIPP, MA HARRINGTON, DP ANDERSON, JR ARMITAGE, JO BONADONNA, G BRITTINGER, G CABANILLAS, F CANELLOS, GP COIFFIER, B CONNORS, JM COWAN, RA CROWTHER, D DAHLBERG, S ENGELHARD, M FISHER, RI GISSELBRECHT, C HORNING, SJ LEPAGE, E LISTER, TA MEERWALDT, JH MONTSERRAT, E NISSEN, NI OKEN, MM PETERSON, BA TONDINI, C VELASQUEZ, WA YEAP, BY AF SHIPP, MA HARRINGTON, DP ANDERSON, JR ARMITAGE, JO BONADONNA, G BRITTINGER, G CABANILLAS, F CANELLOS, GP COIFFIER, B CONNORS, JM COWAN, RA CROWTHER, D DAHLBERG, S ENGELHARD, M FISHER, RI GISSELBRECHT, C HORNING, SJ LEPAGE, E LISTER, TA MEERWALDT, JH MONTSERRAT, E NISSEN, NI OKEN, MM PETERSON, BA TONDINI, C VELASQUEZ, WA YEAP, BY TI A PREDICTIVE MODEL FOR AGGRESSIVE NON-HODGKINS-LYMPHOMA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID LARGE-CELL LYMPHOMA; DIFFUSE HISTIOCYTIC LYMPHOMA; PROGNOSTIC FACTORS; M-BACOD; STAGING CLASSIFICATION; REGRESSION-MODELS; SURVIVAL; ABNORMALITIES; CHEMOTHERAPY; REGIMEN AB Background. Although many patients with intermediate-grade or high-grade (aggressive) non-Hodgkin's lymphoma are cured by combination chemotherapy, the remainder are not cured and ultimately die of their disease. The Ann Arbor classification, used to determine the stage of this disease, does not consistently distinguish between patients with different long-term prognoses. This project was undertaken to develop a model for predicting outcome in patients with aggressive non-Hodgkin's lymphoma on the basis of the patients' clinical characteristics before treatment. Methods. Adults with aggressive non-Hodgkin's lymphoma from 16 institutions and cooperative groups in the United States, Europe, and Canada who were treated between 1982 and 1987 with combination-chemotherapy regimens containing doxorubicin were evaluated for clinical features predictive of overall survival and relapse-free survival. Features that remained independently significant in step-down regression analyses of survival were incorporated into models that identified groups of patients of all ages and groups of patients no more than 60 years old with different risks of death. Results. In 2031 patients of all ages, our model, based on age, tumor stage, serum lactate dehydrogenase concentration, performance status, and number of extranodal disease sites, identified four risk groups with predicted five-year survival rates of 73 percent, 51 percent, 43 percent, and 26 percent. In 1274 patients 60 or younger, an age-adjusted model based on tumor stage, lactate dehydrogenase level, and performance status identified four risk groups with predicted five-year survival rates of 83 percent, 69 percent, 46 percent, and 32 percent. In both models, the increased risk of death was due to both a lower rate of complete responses and a higher rate of relapse from complete response. These two indexes, called the international index and the age-adjusted international index, were significantly more accurate than the Ann Arbor classification in predicting long-term survival. Conclusions. The international index and the age-adjusted international index should be used in the design of future therapeutic trials in patients with aggressive non-Hodgkin's lymphoma and in the selection of appropriate therapeutic approaches for individual patients. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. EASTERN COOPERAT ONCOL GRP,DENVER,CO. NEBRASKA LYMPHOMA STUDY GRP,OMAHA,NE. CANC & LEUKEMIA GRP B,LEBANON,NH. BUNDESMINIST FORSCH & TECHNOL STUDY,ESSEN,GERMANY. MD ANDERSON CANC CTR,HOUSTON,DC. HARVARD UNIV,SCH MED,BOSTON,MA 02115. GRP ETUD LYMPHOMES ADULTE,PARIS,FRANCE. BRITISH COLUMBIA CANC AGCY,VANCOUVER,BC,CANADA. MANCHESTER LYMPHOMA GRP,MANCHESTER,ENGLAND. SW ONCOL GRP,SAN ANTONIO,TX. STANFORD UNIV,STANFORD,CA 94305. ST BARTHOLOMEWS HOSP,LONDON EC1A 7BE,ENGLAND. EUROPEAN ORG RES TREATMENT CANC,LYMPHOMA COOPERAT GRP,BRUSSELS,BELGIUM. HOSP CLIN BARCELONA,BARCELONA 36,SPAIN. FINSEN INST,DK-2100 COPENHAGEN,DENMARK. IST NAZL TUMORI,I-20133 MILAN,ITALY. RP SHIPP, MA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. RI cowan, richard/N-7633-2015 OI cowan, richard/0000-0001-9004-8136 NR 40 TC 2666 Z9 2766 U1 6 U2 44 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 SEP 30 PY 1993 VL 329 IS 14 BP 987 EP 994 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA LY587 UT WOS:A1993LY58700002 ER PT J AU BAKER, DG SCHUMACHER, HR AF BAKER, DG SCHUMACHER, HR TI CURRENT CONCEPTS - ACUTE MONOARTHRITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; SEPTIC ARTHRITIS; SYNOVIAL-FLUID; GONOCOCCAL-INFECTION; BACTERIAL ARTHRITIS; MYCOBACTERIUM-AVIUM; VIRUS-INFECTION; CRYSTALS; DISEASE; OSTEOMYELITIS C1 PHILADELPHIA VET AFFAIRS MED CTR, CTR RHEUMATOL IMMUNOL, UNIV & WOODLAND AVE, PHILADELPHIA, PA 19104 USA. MED COLL PENN, PHILADELPHIA, PA 19129 USA. UNIV PENN, PHILADELPHIA, PA 19104 USA. NR 60 TC 77 Z9 78 U1 0 U2 3 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD SEP 30 PY 1993 VL 329 IS 14 BP 1013 EP 1020 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA LY587 UT WOS:A1993LY58700007 PM 8366902 ER PT J AU GUINEY, TE FALLON, JT KAUFMAN, JA BREWSTER, DC FIENBERG, R AF GUINEY, TE FALLON, JT KAUFMAN, JA BREWSTER, DC FIENBERG, R TI AN 83-YEAR-OLD WOMAN WITH HYPERTENSION, SUDDEN SEVERE BACK PAIN, AND ANURIA - GIANT-CELL AORTITIS, WITH DESCENDING AORTIC DISSECTION AND RUPTURE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID ARTERITIS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GUINEY, TE (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 9 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 SEP 30 PY 1993 VL 329 IS 14 BP 1028 EP 1033 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA LY587 UT WOS:A1993LY58700009 ER PT J AU MARTIN, KA FREEMAN, MW AF MARTIN, KA FREEMAN, MW TI HORMONE REPLACEMENT AND CARDIOVASCULAR RISK-FACTORS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID PROGESTERONE; THERAPY RP MARTIN, KA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 4 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 SEP 30 PY 1993 VL 329 IS 14 BP 1043 EP 1043 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LY587 UT WOS:A1993LY58700020 ER PT J AU QIAN, XQ GOZANI, SN YOON, HS JEON, CJ AGARWAL, K WEISS, MA AF QIAN, XQ GOZANI, SN YOON, HS JEON, CJ AGARWAL, K WEISS, MA TI NOVEL ZINC-FINGER MOTIF IN THE BASAL TRANSCRIPTIONAL MACHINERY - 3-DIMENSIONAL NMR-STUDIES OF THE NUCLEIC-ACID BINDING DOMAIN OF TRANSCRIPTIONAL ELONGATION-FACTOR TFIIS SO BIOCHEMISTRY LA English DT Article ID RNA-POLYMERASE-II; ASCITES TUMOR-CELLS; FACTOR-S-II; OVERHAUSER ENHANCEMENT SPECTROSCOPY; COMPLETE NUCLEOTIDE-SEQUENCE; COLI-UVRA GENE; C-MYC GENE; FACTOR-SII; ESCHERICHIA-COLI; MAGNETIC-RESONANCE AB Transcriptional elongation provides a key control point in the regulation of eukaryotic gene expression. Here we describe homonuclear and N-15-heteronuclear 3D NMR studies of the nucleic acid binding domain of human transcriptional elongation factor TFIIS. This domain contains a Cys4 Zn2+-binding site with no homology to previously characterized Cys4, Cys6, or Cys2-HiS2 Zn fingers. Complete H-1 and N-15 NMR resonance assignment of a 50-residue TFIIS peptide-Zn2+ complex is obtained. Its solution structure, as determined by distance geometry/simulated annealing (DG/SA) calculations, exhibits a novel three-stranded antiparallel, beta-sheet (designated the Zn ribbon). Analogous sequence motifs occur in a wide class of proteins involved in RNA or DNA transactions, including human basal transcriptional initiation factor TFIIE. A three-dimensional model of the TFIIE Cys4 domain is obtained by DG-based homology modeling. The role of the TFIIS Zn ribbon in the control of eukaryotic transcriptional elongation is discussed. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. UNIV CHICAGO,DEPT BIOCHEM,CHICAGO,IL 60637. UNIV CHICAGO,DEPT CHEM,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MOLEC BIOL,CHICAGO,IL 60637. RI Yoon, Ho Sup/A-2193-2011 NR 100 TC 103 Z9 104 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD SEP 28 PY 1993 VL 32 IS 38 BP 9944 EP 9959 DI 10.1021/bi00089a010 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LZ638 UT WOS:A1993LZ63800010 PM 8399164 ER PT J AU EWEN, ME SLUSS, HK WHITEHOUSE, LL LIVINGSTON, DM AF EWEN, ME SLUSS, HK WHITEHOUSE, LL LIVINGSTON, DM TI TGF-BETA INHIBITION OF CDK4 SYNTHESIS IS LINKED TO CELL-CYCLE ARREST SO CELL LA English DT Article ID RETINOBLASTOMA GENE-PRODUCT; SV40 LARGE-T; GROWTH-FACTOR-BETA; SUSCEPTIBILITY GENE; PROTEIN-KINASE; FACTOR-BINDING; G1 PHASE; EXPRESSION; PHOSPHORYLATION; SUPPRESSION AB Transforming growth factor beta1 (TGFbeta1) causes G1 growth arrest and the accumulation of unphosphorylated retinoblastoma protein (Rb) in responsive cells. Cdk4 (cyclin-dependent kinase), a major catalytic subunit of the mammalian D-type G1 cyclins, can phosphorylate Rb in vitro, and at least one D-type cyclin, D2, directs the phosphorylation of Rb in vivo. Here we show that TGFbetga1 induces suppression of cdk4 synthesis in G1 in mink lung epithelial cells. Constitutive cdk4 synthesis in these cells led to TGFbeta1 resistance. It also resulted in growth in low serum medium when these cells were released from contact inhibition. Cdk2 activity was also suppressed by TGFbeta1 action, but its constitutive expression failed to override a TGFbeta1-induced G1 block. Hence, the TGFbeta1 block is primarily mediated by cdk4 modulation. Further evidence suggests that TGFbeta1-induced down-modulation of cdk4 leads to inhibition of cdk2 activation and that both events might contribute to TGFbeta1 growth suppression. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP EWEN, ME (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 56 TC 516 Z9 517 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD SEP 24 PY 1993 VL 74 IS 6 BP 1009 EP 1020 DI 10.1016/0092-8674(93)90723-4 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LY493 UT WOS:A1993LY49300008 PM 8402878 ER PT J AU JAIN, JN MCCAFFREY, PG MINER, Z KERPPOLA, TK LAMBERT, JN VERDINE, GL CURRAN, T RAO, A AF JAIN, JN MCCAFFREY, PG MINER, Z KERPPOLA, TK LAMBERT, JN VERDINE, GL CURRAN, T RAO, A TI THE T-CELL TRANSCRIPTION FACTOR NFAT(P) IS A SUBSTRATE FOR CALCINEURIN AND INTERACTS WITH FOS AND JUN SO NATURE LA English DT Article ID DNA-BINDING ACTIVITY; CYCLOSPORINE-A; SIGNAL TRANSDUCTION; ACTIVATION; IDENTIFICATION; FK-506; PROTEIN; DOMAINS; ASSOCIATION; ENHANCER AB TRANSCRIPTION of lymphokine genes in activated T cells is inhibited by the immunosuppressive agents cyclosporin A and FK506, which act by blocking the phosphatase activity of calcineurin1-3. NFAT, a DNA-binding protein required for interleukin-2 gene transcription, is a potential target for calcineurin, cyclosporin A and FK506(4-11). NFAT contains a subunit (NFAT(p)) which is present in unstimulated T cells and which forms a complex with Fos and Jun proteins in the nucleus of activated T cells9,11. Here we report that NFAT(p) is a DNA-binding phosphoprotein of relative molecular mass approximately 120,000 and is a substrate for calcineurin in vitro. Purified NFAT(p) forms DNA-protein complexes with recombinant Jun homodimers or Jun-Fos heterodimers; the DNA-binding domains of Fos and Jun are essential for the formation of the NFAT(p)-Fos-Jun-DNA complex. The interaction between the lymphoid-specific factor NFAT(p) and the ubiquitous transcription factors Fos and Jun provides a novel mechanism for combinatorial regulation of interleukin-2 gene transcription, which integrates the calcium-dependent and the protein-kinase C-dependent pathways of T-cell activation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. ROCHE INST MOLEC BIOL,ROCHE RES CTR,DEPT MOLEC ONCOL & VIROL,NUTLEY,NJ 07110. HARVARD UNIV,DEPT CHEM,CAMBRIDGE,MA 02138. RI Curran, Tom/C-1164-2008; Curran, Tom/D-7515-2011 OI Curran, Tom/0000-0003-1444-7551; NR 28 TC 625 Z9 629 U1 0 U2 12 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD SEP 23 PY 1993 VL 365 IS 6444 BP 352 EP 355 DI 10.1038/365352a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LY496 UT WOS:A1993LY49600056 PM 8397339 ER PT J AU BURSTEIN, R POTREBIC, S AF BURSTEIN, R POTREBIC, S TI RETROGRADE LABELING OF NEURONS IN THE SPINAL-CORD THAT PROJECT DIRECTLY TO THE AMYGDALA OR THE ORBITAL CORTEX IN THE RAT SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Review DE VISCERAL; NOCICEPTION; FLUOROGOLD; SOMATOSENSORY ID LAMINA-I PROJECTION; LOWER BRAIN-STEM; NUCLEUS SUBMEDIUS; HORSERADISH-PEROXIDASE; PARABRACHIAL NUCLEUS; SOLITARY TRACT; SPINOTHALAMIC TRACT; DORSAL HORN; TRIGEMINAL PROJECTIONS; EFFERENT CONNECTIONS AB The amygdala and orbital cortex are thought to play an important role in the regulation of autonomic functions, hormonal secretion, and behavioral expression in response to sensory stimulation. The responsiveness of neurons in these regions to stimulation of cutaneous and visceral organs indicates that sensory information reaches the amygdala and orbital cortex. In the past, a large number of studies have thoroughly documented multiple neural pathways by which sensory information can reach these regions via relay nuclei in the brainstem and diencephalon. Recent studies reported that the amygdala and orbital cortex also receive direct input from the spinal cord. The aim of this study was to determine the magnitude and the origin of these projections in the rat. Injections of the retrograde tracer Fluoro-Gold (FG), restricted to the amygdala, labeled several hundred neurons bilaterally (60% contralateral) throughout the length of the spinal cord. More than 60% of labeled neurons were found in the lateral reticulated area of the deep dorsal horn and the gray matter surrounding the central canal. Many neurons were also found in the lateral spinal nucleus. Labeled neurons were concentrated in upper lumbar and upper cervical segments. Injections of Fluoro-Gold that were centered in the orbital cortex labeled only a small number of neurons (73% contralateral) within the spinal cord. Most labeled neurons were found in the lateral reticulated area. Neurons located in the intermediate zone and the gray matter surrounding the central canal were found mainly in upper lumbar and upper cervical segments. These findings, together with the anterograde tracing observations, provide evidence for direct projections of spinal cord neurons to the amygdala and orbital cortex. Their laminar distribution in the spinal cord and the involvement of the amygdala and orbital cortex in limbic functions suggest that these pathways may play a role in neuronal circuits that enable somatosensory information, including pain, to affect autonomic, endocrine and behavioral functions. (C) 1993 Wiley-Liss, Inc. C1 HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02115. NR 115 TC 79 Z9 80 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 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD SEP 22 PY 1993 VL 335 IS 4 BP 469 EP 485 DI 10.1002/cne.903350402 PG 17 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA LU971 UT WOS:A1993LU97100001 PM 8227531 ER PT J AU TAUBMAN, MA SMITH, DJ AF TAUBMAN, MA SMITH, DJ TI SIGNIFICANCE OF SALIVARY ANTIBODY IN DENTAL DISEASES SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID BACTERIUM STREPTOCOCCUS-MUTANS; 4 YEARS OLD; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; IMMUNOGLOBULIN-A; IGA ANTIBODIES; SECRETORY IMMUNOGLOBULIN; JUVENILE PERIODONTITIS; NATURAL ANTIBODIES; ORAL IMMUNIZATION; SERUM ANTIBODIES RP TAUBMAN, MA (reprint author), FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE 07009, DE 04733, DE 03420] NR 70 TC 11 Z9 11 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD SEP 20 PY 1993 VL 694 BP 202 EP 215 DI 10.1111/j.1749-6632.1993.tb18354.x PG 14 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MA264 UT WOS:A1993MA26400019 PM 8215056 ER PT J AU KRIEG, M SRICHAI, MB REDMOND, RW AF KRIEG, M SRICHAI, MB REDMOND, RW TI PHOTOPHYSICAL PROPERTIES OF 3,3'-DIALKYLTHIACARBOCYANINE DYES IN ORGANIZED MEDIA - UNILAMELLAR LIPOSOMES AND THIN POLYMER-FILMS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE LIPOSOME; PHOTOPHYSICS; PHOTOSENSITIZER; POLYMER FILM; SINGLET OXYGEN; CYANINE DYE ID SINGLET OXYGEN PRODUCTION; PHOTODYNAMIC-ACTION; LEUKEMIA-CELLS; MEROCYANINE-540; GENERATION; PHOTOSENSITIZATION; PHOTOINACTIVATION; PHOTOCHEMISTRY; LUMINESCENCE; PHOTOLYSIS AB All symmetrical dialkylthiacarbocyanine dyes, with the exception of the diethyl derivatives, are incorporated into liposomes. Absorption and fluorescence data indicate a solubilization site close to the bilayer surface with the alkyl chains penetrating into the lipid bilayer. Incorporation into organized assemblies affects the photophysical parameters of these dyes. Photoisomerization occurring from the first excited state becomes more difficult as the restrictive effect of the solubilization site increases. As a consequence, competing deactivation processes, such as fluorescence and triplet formation, become more efficient with the result that fluorescence quantum yields, triplet yields and singlet oxygen quantum yields are larger in liposomes than in homogeneous solution. Dihexylthiacarbocyanine iodide has a fluorescence quantum yield of 0.27 and 0.10 (25-degrees-C) in dimyristoylphosphatidylcholine liposomes and ethanol, respectively, and the singlet oxygen yield increases by a factor three to 0.006 on going from ethanol to liposomes. The effect of a highly organized environment is even more pronounced in thin polymer films. In these systems, photoisomerization is completely inhibited and only triplet formation is observed in the transient absorption spectrum. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RP KRIEG, M (reprint author), MED COLL WISCONSIN,MACC FUND RES CTR,DEPT PEDIAT,8701 WATERTOWN PLANK RD,MILWAUKEE,WI 53226, USA. FU NCI NIH HHS [CA50733] NR 33 TC 53 Z9 53 U1 0 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD SEP 19 PY 1993 VL 1151 IS 2 BP 168 EP 174 DI 10.1016/0005-2736(93)90101-5 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LZ185 UT WOS:A1993LZ18500009 PM 8373793 ER PT J AU NAKAYAMA, K NAKAYAMA, K NEGISHI, I KUIDA, K SHINKAI, Y LOUIE, MC FIELDS, LE LUCAS, PJ STEWART, V ALT, FW LOH, DY AF NAKAYAMA, K NAKAYAMA, K NEGISHI, I KUIDA, K SHINKAI, Y LOUIE, MC FIELDS, LE LUCAS, PJ STEWART, V ALT, FW LOH, DY TI DISAPPEARANCE OF THE LYMPHOID SYSTEM IN BCL-2 HOMOZYGOUS MUTANT CHIMERIC MICE SO SCIENCE LA English DT Article ID PROGRAMMED CELL-DEATH; FOLLICULAR LYMPHOMA; TRANSGENIC MICE; C-MYC; CHROMOSOMAL BREAKPOINT; B-CELLS; EXPRESSION; SURVIVAL; CLONING; PROTEIN AB The bcl-2 proto-oncogene can prevent the death of many cell types. Mice were generated that were chimeric for the homozygous inactivation of bcl-2. Lymphocytes without Bcl-2 differentiated into phenotypically mature cells. However, in vitro, the mature T cells that lacked Bcl-2 had shorter life-spans and increased sensitivity to glucocorticoids and gamma-irradiation. In contrast, stimulation of CD3 inhibited the death of these cells. T and B cells with no Bcl-2 disappeared from the bone marrow, thymus, and periphery by 4 weeks of age. Thus, Bcl-2 was dispensable for lymphocyte maturation, but was required for a stable immune system after birth. C1 WASHINGTON UNIV, SCH MED, DEPT MED, HOWARD HUGHES MED INST, ST LOUIS, MO 63110 USA. WASHINGTON UNIV, SCH MED, DEPT GENET, ST LOUIS, MO 63110 USA. WASHINGTON UNIV, SCH MED, DEPT MOLEC MICROBIOL, ST LOUIS, MO 63110 USA. HARVARD UNIV, CHILDRENS HOSP,SCH MED,DEPT GENET, HOWARD HUGHES MED INST, BOSTON, MA 02115 USA. CTR BLOOD RES, BOSTON, MA 02115 USA. RI Shinkai, Yoichi/N-3909-2014 OI Shinkai, Yoichi/0000-0002-6051-2484 FU NIAID NIH HHS [AI 15322] NR 36 TC 356 Z9 359 U1 1 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD SEP 17 PY 1993 VL 261 IS 5128 BP 1584 EP 1588 DI 10.1126/science.8372353 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX474 UT WOS:A1993LX47400032 PM 8372353 ER PT J AU WANG, LM MYERS, MG SUN, XJ AARONSON, SA WHITE, M PIERCE, JH AF WANG, LM MYERS, MG SUN, XJ AARONSON, SA WHITE, M PIERCE, JH TI IRS-1 - ESSENTIAL FOR INSULIN-STIMULATED AND IL-4-STIMULATED MITOGENESIS IN HEMATOPOIETIC-CELLS SO SCIENCE LA English DT Article ID TYROSINE KINASE-ACTIVITY; GTPASE-ACTIVATING PROTEIN; SIGNAL-TRANSDUCTION; PHOSPHATIDYLINOSITOL 3'-KINASE; JUXTAMEMBRANE REGION; ATP-BINDING; RECEPTOR; PHOSPHORYLATION; GROWTH; RAS AB Although several interleukin-3 (IL-3)-dependent cell lines proliferate in response to IL-4 or insulin, the 32D line does not. Insulin and IL-4 sensitivity was restored to 32D cells by expression of IRS-1, the principal substrate of the insulin receptor. Although 32D cells possessed receptors for both factors, they lacked the IRS-1-related protein, 4PS, which becomes phosphorylated by tyrosine in insulin- or IL-4-responsive lines after stimulation. These results indicate that factors that bind unrelated receptors can use similar mitogenic signaling pathways in hematopoietic cells and that 4PS and IRS-1 are functionally similar proteins that are essential for insulin- and IL-4-induced proliferation. C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DEPT MED,JOSLIN DIABET CTR,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-43808] NR 31 TC 402 Z9 403 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD SEP 17 PY 1993 VL 261 IS 5128 BP 1591 EP 1594 DI 10.1126/science.8372354 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX474 UT WOS:A1993LX47400034 PM 8372354 ER PT J AU GACZYNSKA, M ROCK, KL GOLDBERG, AL AF GACZYNSKA, M ROCK, KL GOLDBERG, AL TI GAMMA-INTERFERON AND EXPRESSION OF MHC GENES REGULATE PEPTIDE HYDROLYSIS BY PROTEASOMES SO NATURE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-I MOLECULES; ANTIGEN PRESENTATION; LYMPHOCYTE-T; LINKED LMP; PROTEINASE; UBIQUITIN; SUBUNITS AB THE presentation of intracellular proteins to the immune system requires their degradation to small peptides1,2 that then become associated with major histocompatibility complex (MHC) class I molecules3,4. The generation of these peptides may involve the 20S or 26S proteasome particles, which contain multiple proteolytic activities5-14 including distinct sites that preferentially cleave small peptides on the carboxyl side of hydrophobic, basic or acidic residues6,13,14. Degradation of most cell proteins requires their conjugation to ubiquitin before hydrolysis by the 26S proteasome6,13-16. This large complex contains the 20S proteasome as its proteolytic core6,14,16-18. This ubiquitin-dependent proteolytic pathway is implicated in MHC class I presentation11,12. Gamma-interferon (gamma-IFN, a stimulator of antigen presentation1, induces a subclass of proteasomes that contain two MHC-encoded subunits, LMP2 and 7 (refs 5-10). Here we show that gamma-interferon alters the peptidase activities of the 20S and 26S proteasomes without affecting the rates of breakdown of proteins or of ubiquitinated proteins. By enhancing the expression of MHC genes, gamma-IFN increases the proteasomes' capacity to cleave small peptides after hydrophobic and basic residues but reduces cleavage after acidic residues. Moreover, proteasomes of mutants lacking LMP subunits show decreased rates of cleavage after hydrophobic and basic residues. Thus, gamma-IFN and expression of these MHC genes should favour the production by proteasomes of the types of peptides found on MHC class I molecules, which terminate almost exclusively with hydrophobic or basic residues19. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP GACZYNSKA, M (reprint author), HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115, USA. NR 28 TC 467 Z9 469 U1 1 U2 10 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD SEP 16 PY 1993 VL 365 IS 6443 BP 264 EP 267 DI 10.1038/365264a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX471 UT WOS:A1993LX47100058 PM 8396732 ER PT J AU QIAN, XQ JEON, CJ YOON, HS AGARWAL, K WEISS, MA AF QIAN, XQ JEON, CJ YOON, HS AGARWAL, K WEISS, MA TI STRUCTURE OF A NEW NUCLEIC-ACID-BINDING MOTIF IN EUKARYOTIC TRANSCRIPTIONAL ELONGATION-FACTOR TFIIS SO NATURE LA English DT Article ID RNA POLYMERASE-II; ZINC FINGER; CRYSTAL-STRUCTURE; GLUCOCORTICOID RECEPTOR; DNA RECOGNITION; DOMAINS; PROTEIN; COMPLEX; SUBUNIT; BLOCK AB TRANSCRIPTIONAL elongation involves dynamic interactions among RNA polymerase and single-stranded and double-stranded nucleic acids in the ternary complex1-4. In prokaryotes its regulation provides an important mechanism of genetic control1. Analogous eukaryotic mechanisms are not well understood5, but may control expression of proto-oncogenes6,7 and viruses, including the human immunodeficiency virus HIV-1 (ref. 8). The highly conserved eukaryotic transcriptional elongation factor TFIIS9 enables RNA polymerase II (RNAPII) to read though pause or termination sites, nucleosomes and sequence-specific DNA-binding proteins10-14 . Two distinct domains of human TFIIS, which bind RNAPII and nucleic acids, regulate read-through10 and possibly nascent transcript cleavage11-15. Here we describe the three-dimensional NMR16 structure of a Cys4 nucleic-acid-binding domain from human TFIIS9,10. Unlike previously characterized zinc modules17-21, which contain an alpha-helix, this structure consists of a three-stranded beta-sheet. Analogous Cys4, structural motifs may occur in other proteins involved in DNA or RNA transactions22-24, including RNAPII itself25. This new structure, designated the Zn ribbon, extends the repertoire of Zn-mediated peptide architectures26 and highlights the growing recognition of the beta-sheet as a motif of nucleic-acid recognition27,28. C1 UNIV CHICAGO,DEPT BIOCHEM & MOLEC BIOL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT CHEM,CHICAGO,IL 60637. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. RP QIAN, XQ (reprint author), HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. RI Yoon, Ho Sup/A-2193-2011 NR 30 TC 109 Z9 115 U1 1 U2 4 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD SEP 16 PY 1993 VL 365 IS 6443 BP 277 EP 279 DI 10.1038/365277a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX471 UT WOS:A1993LX47100062 PM 7626141 ER PT J AU EMANUEL, EJ BRETT, AS AF EMANUEL, EJ BRETT, AS TI MANAGED COMPETITION AND THE PATIENT-PHYSICIAN RELATIONSHIP SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID UNIVERSAL HEALTH-INSURANCE; HMO DISENROLLMENT; PROMOTE QUALITY; PLAN; ECONOMY; 1990S C1 NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. RP EMANUEL, EJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 23 TC 72 Z9 72 U1 3 U2 4 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD SEP 16 PY 1993 VL 329 IS 12 BP 879 EP 882 DI 10.1056/NEJM199309163291213 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA LW551 UT WOS:A1993LW55100013 PM 8355749 ER PT J AU MEYER, GS AF MEYER, GS TI THE MARKETPLACE IN HEALTH-CARE REFORM SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP MEYER, GS (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 SEP 16 PY 1993 VL 329 IS 12 BP 884 EP 884 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LW551 UT WOS:A1993LW55100017 PM 8355752 ER PT J AU YANNUZZI, LA SORENSON, JA SOBEL, RS DALY, JR DEROSA, JT SEDDON, JM GRAGOUDAS, ES PULIAFITO, CA GELLES, E GONET, R BURTON, TC ROLNICK, C FLOM, T HALLER, J PUSIN, S CASSEL, G APPLEGATE, CA SEIGEL, D SPERDUTO, RD HILLER, R MOWERY, R CHEW, E CULVER, J METZGER, K KALBFLEISCH, N ZARLING, D FARBER, MD BLAIR, N STELMACK, T AXELROD, A WAITR, SE CROSS, A TAMBOLI, A DUNN, M SEDDON, JM SHAMBAN, K LENTO, D AF YANNUZZI, LA SORENSON, JA SOBEL, RS DALY, JR DEROSA, JT SEDDON, JM GRAGOUDAS, ES PULIAFITO, CA GELLES, E GONET, R BURTON, TC ROLNICK, C FLOM, T HALLER, J PUSIN, S CASSEL, G APPLEGATE, CA SEIGEL, D SPERDUTO, RD HILLER, R MOWERY, R CHEW, E CULVER, J METZGER, K KALBFLEISCH, N ZARLING, D FARBER, MD BLAIR, N STELMACK, T AXELROD, A WAITR, SE CROSS, A TAMBOLI, A DUNN, M SEDDON, JM SHAMBAN, K LENTO, D TI RISK-FACTORS FOR BRANCH RETINAL VEIN OCCLUSION SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID ALCOHOL-CONSUMPTION; HEART-DISEASE; PRESSURE; OBESITY AB The objective of our clinic-based case-control study was to identify risk factors for branch retinal vein occlusion. Between 1986 and 1990 data were obtained at five clinical centers from 270 patients with branch retinal vein occlusion and 1,142 controls. Data were collected from interviews, clinical examinations, and laboratory analyses of blood specimens. An increased risk of branch retinal vein occlusion was found in persons with a history of systemic hypertension, a history of cardiovascular disease, an increased body mass index at 20 years of age, a history of glaucoma, and higher serum levels of alpha2-globulin. Risk of branch retinal vein occlusion decreased with higher levels of alcohol consumption and high-density lipoprotein cholesterol. The data suggest a cardiovascular risk profile for patients with branch retinal vein occlusion and indicate that 50% of patients with branch retinal vein occlusion may be attributable to hypertension. Our findings support current public health recommendations to diagnose and treat hypertension, reduce weight, increase physical activity, and maximize serum high-density lipoprotein levels. C1 NEI,BETHESDA,MD 20892. MANHATTAN EYE EAR & THROAT HOSP,NEW YORK,NY 10021. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115. ORKAND CORP,CTR COORDINATING,SILVER SPRING,MD. PHOTOG READING CTR,BOSTON,MA. NR 27 TC 128 Z9 132 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 SEP 15 PY 1993 VL 116 IS 3 BP 286 EP 296 PG 11 WC Ophthalmology SC Ophthalmology GA LW157 UT WOS:A1993LW15700003 ER PT J AU WALLER, S STEINERT, RF AF WALLER, S STEINERT, RF TI SYMPTOMATIC INTRAOCULAR REFLECTIONS FROM OVAL INTRAOCULAR-LENS IMPLANTS SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Letter C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 2 TC 4 Z9 5 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 SEP 15 PY 1993 VL 116 IS 3 BP 374 EP 376 PG 3 WC Ophthalmology SC Ophthalmology GA LW157 UT WOS:A1993LW15700017 PM 8357066 ER PT J AU LI, FP ENG, C AF LI, FP ENG, C TI THE FAMILIAL MUIR-TORRE SYNDROME SO ANNALS OF INTERNAL MEDICINE LA English DT Letter C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RP LI, FP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 3 TC 6 Z9 6 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD SEP 15 PY 1993 VL 119 IS 6 BP 539 EP 539 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LZ275 UT WOS:A1993LZ27500031 PM 8357130 ER PT J AU SONG, CS HER, S SLOMCZYNSKA, M CHOI, SJ JUNG, MH ROY, AK CHATTERJEE, B AF SONG, CS HER, S SLOMCZYNSKA, M CHOI, SJ JUNG, MH ROY, AK CHATTERJEE, B TI A DISTAL ACTIVATION DOMAIN IS CRITICAL IN THE REGULATION OF THE RAT ANDROGEN RECEPTOR GENE PROMOTER SO BIOCHEMICAL JOURNAL LA English DT Article ID HUMAN GLUCOCORTICOID RECEPTOR; TRANSCRIPTION FACTOR; DNA; SUPERFAMILY; BINDING; PROTEIN; RNA; PURIFICATION; CLONING; ELEMENT AB The far upstream region of the rat androgen receptor (AR) gene has been cloned, and the nucleotide sequence up to -2656 bp established. Nested deletion mutants of rat AR 5' flanking sequences were ligated to the luciferase reporter gene, and their promoter activities were examined in transfected COS1 cells. Results show a critical cis-acting domain located between positions -960 and -940. Deletion of this cis element resulted in a greater than 90 % decrease in the promoter activity. A nuclear protein that specifically binds to this 21-nucleotide sequence was identified by gel mobility shift analysis. The -960/-940 cis element has no identity to the binding sequence of any known transcription factor. Furthermore, the cognate binding protein is present in both rat and human (HeLa) cell nuclear extracts. We conclude that a novel trans-activator interacting at the -960/ -940 region plays a critical role in the regulation of AR gene expression. C1 UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NIA NIH HHS [P01-AG06872, R01-AG03527]; NIDDK NIH HHS [R37-DK14744] NR 38 TC 29 Z9 29 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD SEP 15 PY 1993 VL 294 BP 779 EP 784 PN 3 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LY645 UT WOS:A1993LY64500024 PM 8379933 ER PT J AU TRESTMAN, RL COCCARO, EF MITROPOULOU, V GABRIEL, SM HORVATH, T SIEVER, LJ AF TRESTMAN, RL COCCARO, EF MITROPOULOU, V GABRIEL, SM HORVATH, T SIEVER, LJ TI THE CORTISOL RESPONSE TO CLONIDINE IN ACUTE AND REMITTED DEPRESSED MEN SO BIOLOGICAL PSYCHIATRY LA English DT Article DE DEPRESSION; CLONIDINE; CORTISOL ID CORTICOTROPIN-RELEASING FACTOR; GROWTH-HORMONE; PLASMA-CORTISOL; BLOOD-PRESSURE; ENDOGENOUS-DEPRESSION; NORADRENERGIC NEURONS; LOCUS COERULEUS; SECRETION; ACTH; NORADRENALINE AB To assess the relationship between the hypothalamo-pituitary-adrenal (HPA) axis and the noradrenergic system in patients with major depression, 26 normal controls, 32 acutely depressed patients, and 21 patients with remitted depression, all men, were administered intravenous clonidine (2 mug/kg) or placebo. Acute, but not remitted, depressed patients had a greater plasma cortisol baseline than did normal controls (t = 2.0, p < 0.03). Only acutely depressed patients had a greater decrease in plasma cortisol in response to clonidine than to placebo (t = 2.5, p < 0.02). Statistically controlling for both diurnal variation and baseline cortisol, acute, but not remitted, depressed patients had a greater decrease in plasma cortisol in response to clonidine than did the controls (analysis of covariance: F[1,35] = 4.26, p < 0.05). These results support a state-dependent noradrenergic-HPA axis regulatory disturbance in depressed patients, suggesting that clonidine inhibits the elevated plasma cortisol in acute depression but not the normal concentrations observed in remitted depression or healthy controls. C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. MED COLL PENN,PHILADELPHIA,PA 19129. RP TRESTMAN, RL (reprint author), BRONX VET ADM MED CTR,PSYCHIAT SERV,116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NCRR NIH HHS [RR00071]; NIMH NIH HHS [R01-MH41131] NR 43 TC 11 Z9 11 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 SEP 15 PY 1993 VL 34 IS 6 BP 373 EP 379 DI 10.1016/0006-3223(93)90181-C PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MA800 UT WOS:A1993MA80000005 PM 8218604 ER PT J AU KOPANS, DB AF KOPANS, DB TI MAMMOGRAPHY SCREENING FOR BREAST-CANCER SO CANCER LA English DT Editorial Material ID LESIONS RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 14 TC 18 Z9 18 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 SEP 15 PY 1993 VL 72 IS 6 BP 1809 EP 1812 DI 10.1002/1097-0142(19930915)72:6<1809::AID-CNCR2820720603>3.0.CO;2-D PG 4 WC Oncology SC Oncology GA LV847 UT WOS:A1993LV84700002 PM 8364858 ER PT J AU MAYEUX, P DUSANTERFOURT, I MULLER, O MAUDUIT, P SABBAH, M DRUKER, B VAINCHENKER, W FISCHER, S LACOMBE, C GISSELBRECHT, S AF MAYEUX, P DUSANTERFOURT, I MULLER, O MAUDUIT, P SABBAH, M DRUKER, B VAINCHENKER, W FISCHER, S LACOMBE, C GISSELBRECHT, S TI ERYTHROPOIETIN INDUCES THE ASSOCIATION OF PHOSPHATIDYLINOSITOL 3'-KINASE WITH A TYROSINE-PHOSPHORYLATED PROTEIN COMPLEX CONTAINING THE ERYTHROPOIETIN RECEPTOR SO EUROPEAN JOURNAL OF BIOCHEMISTRY LA English DT Article ID COLONY-STIMULATING FACTOR; SIGNAL TRANSDUCTION; CELL-LINE; INTERLEUKIN-2 RECEPTOR; PHOSPHOINOSITIDE 3-KINASE; KINASE-ACTIVITY; GROWTH; ACTIVATION; DOMAINS; UT-7 AB Stimulation of sensitive cells with erythropoietin results in rapid induction of protein tyrosine phosphorylation. Other than tyrosine phosphorylation of one chain of the erythropoietin receptor, the identities of the remaining tyrosine-phosphorylated proteins are undefined. In this report, we demonstrate that the stimulation of the erythropoietin-sensitive human UT7 cells by erythropoietin rapidly resulted in the appearance of phosphatidylinositol 3-kinase activity in anti-phosphotyrosine immunoprecipitates. Erythropoietin action was rapid, detectable after as early as 1 min stimulation, transient, returning to control level after 30 min stimulation and was observed using the erythropoietin concentrations able to stimulate the cell proliferation. Anti-(phosphatidylinositol 3-kinase) antibodies specifically immunoprecipitated I-125-erythropoietin bound to its receptor, strongly suggesting that phosphatidylinositol 3-kinase associated with a protein complex containing the activated erythropoietin receptor. To confirm this result, phosphatidylinositol 3-kinase was immunoprecipitated from erythropoietin-stimulated cells using mild conditions followed by Western analysis using anti-phosphotyrosine antibodies. Five tyrosine phosphorylated proteins were revealed: the cloned chain of the erythropoietin receptor, the regulatory subunit of phosphatidylinositol 3-kinase and three unidentified proteins of 111, 97 and 64 kDa. None of these tyrosine phosphorylated proteins was detected in anti-(phosphatidylinositol 3-kinase) immunoprecipitates from unstimulated cells. Thus, our results show that phosphatidylinositol 3-kinase associates with a tyrosine-phosphorylated protein complex containing the activated erythropoietin receptor. C1 HOP COCHIN, ICAM, INSERM, U332, F-75674 PARIS 14, FRANCE. UNIV PARIS 11, BIOCHIM TRANSPORTS CELLULAIRES LAB, CNRS, URA 1116, F-91405 ORSAY, FRANCE. INST GUSTAVE ROUSSY, INSERM, U362, F-94805 VILLEJUIF, FRANCE. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. RP MAYEUX, P (reprint author), HOP COCHIN, ICAM, INSERM, U363, 27 RUE FAUBOURG ST JACQUES, F-75674 PARIS 14, FRANCE. NR 42 TC 64 Z9 64 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-2956 J9 EUR J BIOCHEM JI Eur. J. Biochem. PD SEP 15 PY 1993 VL 216 IS 3 BP 821 EP 828 DI 10.1111/j.1432-1033.1993.tb18203.x PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LX852 UT WOS:A1993LX85200015 PM 8404901 ER PT J AU ZWEIG, AD VENUGOPALAN, V DEUTSCH, TF AF ZWEIG, AD VENUGOPALAN, V DEUTSCH, TF TI STRESS GENERATED IN POLYIMIDE BY EXCIMER-LASER IRRADIATION SO JOURNAL OF APPLIED PHYSICS LA English DT Article ID POLYMERIC MATERIALS; ORGANIC POLYMERS; SHOCK-WAVES; ABLATION; TISSUE; CORNEA; INJURY; PLASMA; FILMS; SKIN AB Stress transients are generated in polyimide by irradiation with excimer-laser pulses at radiant exposures between 3 X 10(-3) and 10(2) J/cm2 . The duration and peak stress of these transients are measured using piezoelectric film transducers. For all the wavelengths tested (193, 248, 308, 351 nm) we determine three ranges of radiant exposure within which different physical mechanisms govern the stress generation. The scaling of stress with radiant exposure depends on wavelength only in the low fluence regime. In this regime the stresses observed are attributed to subsurface thermal decomposition at 351 and 308 nm and to photodecomposition at 248 and 193 nm. At higher radiant exposure the stress generation is governed either by the thermal expansion of the gaseous ablation products or by the formation and expansion of a dense plasma. The boundary between these two regimes is identified from the variation of the mechanical coupling coefficient with radiant exposure. The results also indicate that heat conduction contributes significantly to the coupling of energy into the target, leading to a reduction in the stresses generated and to an increase in etch depth when ablation is achieved. C1 MASSACHUSETTS GEN HOSP, WELLMAN LABS PHOTOMED, BOSTON, MA 02114 USA. NR 39 TC 58 Z9 58 U1 1 U2 2 PU AMER INST PHYSICS PI MELVILLE PA 1305 WALT WHITMAN RD, STE 300, MELVILLE, NY 11747-4501 USA SN 0021-8979 EI 1089-7550 J9 J APPL PHYS JI J. Appl. Phys. PD SEP 15 PY 1993 VL 74 IS 6 BP 4181 EP 4189 DI 10.1063/1.354422 PG 9 WC Physics, Applied SC Physics GA LY328 UT WOS:A1993LY32800083 ER PT J AU BRADBURY, LE GOLDMACHER, VS TEDDER, TF AF BRADBURY, LE GOLDMACHER, VS TEDDER, TF TI THE CD19 SIGNAL-TRANSDUCTION COMPLEX OF B-LYMPHOCYTES - DELETION OF THE CD19 CYTOPLASMIC DOMAIN ALTERS SIGNAL-TRANSDUCTION BUT NOT COMPLEX-FORMATION WITH TAPA-1 AND LEU-13 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; KINASE-DEPENDENT PATHWAY; T-CELL AGGREGATION; MONOCLONAL-ANTIBODY; ANTIPROLIFERATIVE ANTIBODY; ENDOTHELIAL-CELLS; ANTIGEN RECEPTOR; SURFACE-ANTIGEN; VIRUS RECEPTOR; EXPRESSION AB CD19 expressed on the surface of B lymphocytes is a key member of a cell surface signal transduction complex that includes TAPA-1, Leu 13 and CD21. The human CD19 protein is composed of 540 amino acids with a cytoplasmic domain of 242 amino acids. Although the cytoplasmic domain of CD19 has no sequence homology with other proteins, the cytoplasmic domain of human, mouse, and guinea pig CD19 is highly conserved suggesting that this region of CD19 is at least partially responsible for signaling activity. In this study, the regions of CD19 required for intermolecular associations and signal transduction were determined by comparing a series of carboxyl-terminal cytoplasmic tail deletion mutants and a CD19/L-selectin chimera with native CD19. CD19 expressed in the human Rex T cell line and the K562 erythroleukemia cell line generated transmembrane signals and also associated with endogenous TAPA-1. Deletion of 95% of the CD19 cytoplasmic domain did not affect the ability of CD19 to be expressed or to associate with TAPA-1. However, replacement of the CD19 transmembrane and cytoplasmic domains with those of L-selectin (CD19-LAM) resulted in the loss of CD19 complex formation, suggesting that the membrane spanning domain is critical for this association. Similarly, the induction of homotypic adhesion through CD19 or truncated CD19 was equivalent, whereas homotypic adhesion was not induced via the CD19-LAM chimera. In addition, the cytoplasmic domain was not necessary for CD19 mAb-mediated growth inhibition or internalization. In contrast, the CD19 cytoplasmic domain was required for optimal mAb-induced increases in [Ca2+]i in CD19 cDNA-transfected Rex cells. Thus, the CD19 cytoplasmic domain is responsible for the induction of increased [Ca2+]i, and the transmembrane region is required for cell surface associations with the other members of the CD19 complex and most signaling events. Therefore, mAb binding to CD19 is likely to initiate multiple intracellular signal transduction cascades either through CD19 directly, or through other members of the CD19 complex. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA-34183, CA-54464]; NIAID NIH HHS [AI-26872] NR 49 TC 102 Z9 102 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 SEP 15 PY 1993 VL 151 IS 6 BP 2915 EP 2927 PG 13 WC Immunology SC Immunology GA LY492 UT WOS:A1993LY49200003 PM 7690791 ER PT J AU KASIBHATLA, S NALEFSKI, EA RAO, A AF KASIBHATLA, S NALEFSKI, EA RAO, A TI SIMULTANEOUS INVOLVEMENT OF ALL 6 PREDICTED ANTIGEN-BINDING LOOPS OF THE T-CELL RECEPTOR IN RECOGNITION OF THE MHC ANTIGENIC PEPTIDE COMPLEX SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PARA-AZOPHENYLARSONATE FAB-36-71; SITE-DIRECTED MUTAGENESIS; AMINO-ACID SUBSTITUTIONS; ALPHA-CHAIN; BETA-CHAIN; MONOCLONAL-ANTIBODY; 3-DIMENSIONAL STRUCTURE; HYPERVARIABLE REGIONS; AFFINITY; SPECIFICITY AB The TCR is predicted to resemble the Fab fragment of an Ig molecule and by analogy to possess six Ag binding loops that contact MHC proteins bound with antigenic peptides. We have identified residues in the predicted Ag binding loops (beta1, beta2, and beta3) on a TCR beta-chain that are important in the recognition of the MHC/antigenic peptide complex. Using site-directed mutagenesis, we altered the residues forming the predicted Ag binding site on the beta-chain expressed by the T lymphocyte clone D5, which specifically recognizes p-azobenzenearsonate-conjugated peptides presented by the class II MHC molecule I-A(d). Amino acid substitution of individual residues in each loop affected Ag recognition, demonstrating that all three putative Ag binding loops of the D5 TCR beta-chain are important in interaction with I-A(d)/arsonate-conjugated Ag. Taken together with our previous work on the D5 TCR alpha-chain (Nalefski et al., J. Exp. Med. 175:1553), these results suggest that all six Ag binding loops of the D5 TCR alpha- and beta-chains interact simultaneously with the MHC/peptide complex. Consequently, the area of interaction between the TCR and the MHC/antigenic peptide complex is predicted to be extensive. 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 NIAID NIH HHS [AI22900]; NIGMS NIH HHS [GM46227, 5 T32 GMO7226] NR 66 TC 30 Z9 31 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 SEP 15 PY 1993 VL 151 IS 6 BP 3140 EP 3151 PG 12 WC Immunology SC Immunology GA LY492 UT WOS:A1993LY49200023 PM 8376771 ER PT J AU LERNER, A DADAMIO, L DIENER, AC CLAYTON, LK REINHERZ, EL AF LERNER, A DADAMIO, L DIENER, AC CLAYTON, LK REINHERZ, EL TI CD3-ZETA-ETA-THETA LOCUS IS COLINEAR WITH AND TRANSCRIBED ANTISENSE TO THE GENE ENCODING THE TRANSCRIPTION FACTOR OCT-1 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL ANTIGEN RECEPTOR; BINDING PROTEIN OCT-1; ZETA-CHAIN; MOLECULAR-CLONING; RNA DUPLEX; UNWINDING ACTIVITY; CYCLE EXPRESSION; POINT MUTATIONS; CD3-ZETA; PRODUCTS AB CD3zeta and eta are signal-transducing components of the TCR and are derived from alternative splicing of transcripts from a single genetic locus that also encodes CD3theta. We have isolated two murine cDNA clones that appear to result from antisense transcription through CD3theta-specific exon 10 and CD3eta-specific exon 9. The sequence of these clones shows no open reading frame. Northern analysis with single stranded probes confirms the existence of a ubiquitously expressed >12-kb polyadenylated mRNA antisense to CD3eta. A ''genomic walk,'' which extended 32 kb distal to murine CD3eta exon 9, provided genomic DNA containing a more 5' portion of the antisense transcript. This probe identified two murine thymic cDNA with 91% sequence homology to the human transcription factor Oct-1. Five exons of murine Oct-1 map in an antisense orientation to the CD3zeta/eta/theta locus on the cloned genomic sequences. The murine Oct-1 cDNA and exon 9 of CD3eta hybridize to the same >12-kb mRNA. Similarly, human Oct-1 and previously characterized human genomic sequences homologous to murine CD3eta exon 9 each hybridize to the same >15-kb human mRNA. Thus, the CD3zeta/eta/theta and Oct-1 gene loci are partially overlapping and transcribed in opposite directions. The potential functional implications of these findings are discussed. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP LERNER, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI19807, AI31269] NR 40 TC 31 Z9 32 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 SEP 15 PY 1993 VL 151 IS 6 BP 3152 EP 3162 PG 11 WC Immunology SC Immunology GA LY492 UT WOS:A1993LY49200024 PM 8376772 ER PT J AU HATEBOER, G TIMMERS, HTM RUSTGI, AK BILLAUD, M VANTVEER, LJ BERNARDS, R AF HATEBOER, G TIMMERS, HTM RUSTGI, AK BILLAUD, M VANTVEER, LJ BERNARDS, R TI TATA-BINDING PROTEIN AND THE RETINOBLASTOMA GENE-PRODUCT BIND TO OVERLAPPING EPITOPES ON C-MYC AND ADENOVIRUS E1A PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE RETINOBLASTOMA PROTEIN ID HELIX ZIPPER PROTEIN; TRANSCRIPTION FACTOR; ACTIVATION DOMAIN; COMPLEX; CELLS; IDENTIFICATION; PROMOTERS; MECHANISM; ONCOGENES; INTERACTS AB Using a protein binding assay, we show that the amino-terminal 204 amino adds of the c-Myc protein interact directly with a key component of the basal transcription factor TFIID, the TATA box-binding protein (TBP). Essentially the same region of the c-Myc protein also binds the product of the retinoblastoma gene, the RB protein. c-Myc protein coimmunoprecipitates with TBP in lysates of mammalian cells, demonstrating that the proteins are also complexed in vivo. A short peptide that spans the RB binding site of the E7 protein of human papilloma virus type 16 interferes with the binding of c-Myc to TBP. The same peptide also blocks binding of adenovirus E1A protein to TBP, suggesting that c-Myc and E1A bind to RB and TBP through overlapping epitopes. Furthermore, we show that binding of RB to E1A prevents association of E1A with TBP. Our data suggest that one of the functions of RB and RB-like proteins is to prevent interaction of viral and cellular oncoproteins, such as c-Myc and E1A, with TBP. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. NETHERLANDS CANC INST,DIV MOLEC CARCINOGENESIS,1066 CX AMSTERDAM,NETHERLANDS. UNIV UTRECHT,PHYSIOL CHEM LAB,3521 GG UTRECHT,NETHERLANDS. RP HATEBOER, G (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC GENET,BOSTON,MA 02114, USA. RI Billaud, Marc/M-6954-2013; OI Bernards, Rene/0000-0001-8677-3423 NR 36 TC 129 Z9 130 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 SEP 15 PY 1993 VL 90 IS 18 BP 8489 EP 8493 DI 10.1073/pnas.90.18.8489 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX750 UT WOS:A1993LX75000040 PM 7690963 ER PT J AU BOLDOG, FL GEMMILL, RM WILKE, CM GLOVER, TW NILSSON, AS CHANDRASEKHARAPPA, SC BROWN, RS LI, FP DRABKIN, HA AF BOLDOG, FL GEMMILL, RM WILKE, CM GLOVER, TW NILSSON, AS CHANDRASEKHARAPPA, SC BROWN, RS LI, FP DRABKIN, HA TI POSITIONAL CLONING OF THE HEREDITARY RENAL-CARCINOMA 3-8 CHROMOSOME-TRANSLOCATION BREAKPOINT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SUPPRESSOR GENE; FRAGILE SITE; POLYCYSTIC KIDNEY DISEASE; LUNG CANCER; THYROID CANCER ID POLYCYSTIC KIDNEY-DISEASE; HUMAN-BREAST CARCINOMA; CELL LUNG-CARCINOMA; SHORT ARM; FRAGILE SITES; ALLELIC LOSS; WILMS-TUMOR; DELETION; CANCER; HETEROZYGOSITY AB The chromosome (p14.2;q24.1) translocation t(3;8)has been associated with hereditary renal cancer in one family. Based on cytogenetic analyses and loss-of-heterozygosity experiments, the 3p14 region has been independently implicated as harboring a tumor suppressor gene critical to kidney and lung cancer development. The 3p14.2 region also contains FRA3B, the most sensitive fragile site induced by aphidicolin. A chromosome 3 probe, R7K145, derived from a radiation-reduced hybrid was positioned between the t(3;8) breakpoint and an aphidicolin-induced 3p14 breakpoint. A yeast artificial chromosome (YAC) contig containing R7K145 was developed that crossed the aphidicolin-induced breakpoint on its telomeric side. A subsequent chromosome walk identified a YAC that crossed the 3;8 translocation breakpoint. A lambda sublibrary allowed isolation of clones spanning the rearrangement. Unique and evolutionarily conserved DNA sequences were used to screen a kidney cDNA library. We have identified a gene, referred to as HRCA1 (hereditary renal cancer associated 1), that maps immediately adjacent to the breakpoint. On the basis of its chromosomal position, HRCA1 may be a candidate tumor suppressor gene. C1 ELEANOR ROOSEVELT INST,DENVER,CO 80206. UNIV MICHIGAN,DEPT PEDIAT,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,CTR HUMAN GENET & HUMAN GENOME,ANN ARBOR,MI 48109. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02215. HARVARD UNIV,DANA FARBER CANC INST,BOSTON,MA 02215. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02215. RP BOLDOG, FL (reprint author), UNIV COLORADO,CTR CANC,DIV MED ONCOL,B171,4200 E 9TH AVE,DENVER,CO 80262, USA. FU NCI NIH HHS [CA-43222]; NHGRI NIH HHS [HG00358]; NICHD NIH HHS [HD23826] NR 42 TC 84 Z9 85 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 SEP 15 PY 1993 VL 90 IS 18 BP 8509 EP 8513 DI 10.1073/pnas.90.18.8509 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX750 UT WOS:A1993LX75000044 PM 7690964 ER PT J AU ROIDER, J HILLENKAMP, F FLOTTE, T BIRNGRUBER, R AF ROIDER, J HILLENKAMP, F FLOTTE, T BIRNGRUBER, R TI MICROPHOTOCOAGULATION - SELECTIVE EFFECTS OF REPETITIVE SHORT LASER-PULSES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID THERMAL RETINAL INJURY; RADIATION; BARRIER; DAMAGE AB Repetitive exposure to short laser pulses is shown to cause selective damage to absorbing structures (cells, organelles, or enzymes) with pulse energies below the threshold energy for single-pulse damage. Directly adjacent structures are spared in vivo. Additivity of (presumably nonphotochemical) subthreshold effects is demonstrated. Selective damage to the retinal pigment epithelium with sparing of the neural retina is shown (514 nm, 5 mus, 1-500 pulses at 500 Hz, 2- to 10-muJ pulse energy). A melanin granule model has been developed and applied to the experimental situation. Histological results as well as the basic mechanism for these effects are discussed. C1 UNIV MUNSTER,INST MED PHYS & BIOPHYS,D-48149 MUNSTER,GERMANY. MED LASER CTR GMBH,D-23562 LUBECK,GERMANY. MED UNIV LUBECK,AUGENHEILKUNDE KLIN,D-23538 LUBECK,GERMANY. RP ROIDER, J (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. RI Roider, Johann/E-4513-2010; Birngruber, Reginald/Q-2342-2016 NR 33 TC 118 Z9 124 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 SEP 15 PY 1993 VL 90 IS 18 BP 8643 EP 8647 DI 10.1073/pnas.90.18.8643 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX750 UT WOS:A1993LX75000072 PM 8378341 ER PT J AU WITHKA, JM WYSS, DF WAGNER, G ARULANANDAM, ARN REINHERZ, EL RECNY, MA AF WITHKA, JM WYSS, DF WAGNER, G ARULANANDAM, ARN REINHERZ, EL RECNY, MA TI STRUCTURE OF THE GLYCOSYLATED ADHESION DOMAIN OF HUMAN T-LYMPHOCYTE GLYCOPROTEIN CD2 SO STRUCTURE LA English DT Article DE GLYCOPROTEIN; IMMUNOGLOBULIN; NMR; RECEPTOR ON T CELL ID NUCLEAR-MAGNETIC-RESONANCE; CELL-SURFACE LIGAND; CRYSTAL-STRUCTURE; ALTERNATIVE PATHWAY; SIGNAL TRANSDUCTION; MOLECULAR-CLONING; PROTEIN-STRUCTURE; BINDING-SITES; SOLUBLE FORM; 2ND LIGAND AB Background: CD2, a T-cell specific surface glycoprotein, is critically important for mediating adherence of T cells to antigen-presenting cells or target cells. Domain 1 of human CD2 is responsible for cell adhesion, binding to CD58 (LFA-3) expressed on the cell to which the T cell binds. Human CD2 domain 1 requires N-linked carbohydrate to maintain its native conformation and ability to bind CD58. In contrast, rat CD2 does not require N-linked carbohydrate, and binds to a different ligand, CD48. Results: The three-dimensional structure of the glycosylated form of domain 1 of human CD2 has been determined by NMR spectroscopy. The overall structure resembles the typical beta-barrel of an immunoglobulin variable domain. Nuclear Overhauser enhancement contacts between the protein and the N-linked glycan have been tentatively identified. Conclusion: Based on our results, we propose a model showing how the N-linked glycan might be posi tioned in the human CD2 domain 1 structure. The model provides an explanation for the observed instability of deglycosylated human CD2, and allows residues that are important for CD58 binding to be differentiated from those affecting conformational stability via interactions with the glycan. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. PROCEPT INC,CAMBRIDGE,MA 02139. FU NIAID NIH HHS [AI 21226]; NIGMS NIH HHS [F32GM15646-01] NR 52 TC 55 Z9 56 U1 0 U2 4 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0969-2126 J9 STRUCTURE JI Structure PD SEP 15 PY 1993 VL 1 IS 1 BP 69 EP 81 DI 10.1016/0969-2126(93)90009-6 PG 13 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA NC277 UT WOS:A1993NC27700007 PM 7915183 ER PT J AU CHRISTAKIS, NA ASCH, DA AF CHRISTAKIS, NA ASCH, DA TI BIASES IN HOW PHYSICIANS CHOOSE TO WITHDRAW LIFE-SUPPORT SO LANCET LA English DT Article ID SUSTAINING TREATMENT; ADVANCE DIRECTIVES; DECISION-MAKING; CRITICALLY ILL; CARE; PREFERENCES; EUTHANASIA; ATTITUDES AB We have investigated biases in physicians' decisions regarding the form of life support to withdraw from critically ill patients in whom the decision to withdraw has already been made. Using a specially designed instrument that solicited both self-reported preferences and also responses to experimentally varied clinical vignettes, we surveyed 862 American internists, of whom 481 (56%) responded. Physicians do have preferences about the form of life support withdrawn. From most likely to least likely the order is: blood products, haemodialysis, intravenous vasopressors, total parenteral nutrition, antibiotics, mechanical ventilation, tube feedings, and intravenous fluids. Four biases in decision making were also identified. Physicians prefer to withdraw forms of therapy supporting organs that failed for natural rather than iatrogenic reasons, to withdraw recently instituted rather than longstanding interventions, to withdraw forms of therapy resulting in immediate death rather than delayed death, and to withdraw forms of therapy resulting in delayed death when confronted with diagnostic uncertainty. Because these biases may have clinical, social, and ethical consequences counter to patient goals, and because they may affect the underlying decision whether to withdraw life support at all, they may represent impediments to rational and compassionate decision making in critical care. C1 UNIV PENN, LEONARD DAVIS INST HLTH ECON, PHILADELPHIA, PA 19104 USA. UNIV PENN, SCH MED, DIV FISIOL VEGETAL, PHILADELPHIA, PA 19104 USA. UNIV PENN, DEPT SOCIOL, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA USA. RI Christakis, Nicholas/B-6690-2008; Christakis, Nicholas/C-3205-2009 NR 30 TC 125 Z9 127 U1 2 U2 7 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0140-6736 EI 1474-547X J9 LANCET JI Lancet PD SEP 11 PY 1993 VL 342 IS 8872 BP 642 EP 646 DI 10.1016/0140-6736(93)91759-F PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA LX272 UT WOS:A1993LX27200010 PM 8103146 ER PT J AU FREI, E AF FREI, E TI GENE DELETION - A NEW TARGET FOR CANCER-CHEMOTHERAPY SO LANCET LA English DT Article ID CELL LUNG-CANCER; RETINOBLASTOMA; 5-FLUOROURACIL; INACTIVATION; TOXICITY RP FREI, E (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,44 BINNEY ST,BOSTON,MA 02115, USA. NR 23 TC 12 Z9 12 U1 0 U2 3 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD SEP 11 PY 1993 VL 342 IS 8872 BP 662 EP 664 DI 10.1016/0140-6736(93)91764-D PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA LX272 UT WOS:A1993LX27200015 PM 8103151 ER PT J AU SUSEK, RE AUSUBEL, FM CHORY, J AF SUSEK, RE AUSUBEL, FM CHORY, J TI SIGNAL-TRANSDUCTION MUTANTS OF ARABIDOPSIS UNCOUPLE NUCLEAR CAB AND RBCS GENE-EXPRESSION FROM CHLOROPLAST DEVELOPMENT SO CELL LA English DT Article ID MESSENGER-RNA ACCUMULATION; SACCHAROMYCES-CEREVISIAE; ESCHERICHIA-COLI; PLANT-CELLS; LIGHT; THALIANA; CHLOROPHYLL; PROTEIN; BINDING; MAIZE AB Chloroplast development requires coordinate nuclear and chloroplast gene expression. A putative signal from the chloroplast couples the transcription of certain nuclear genes encoding photosynthesis-related proteins with chloroplast function. We have identified at least three Arabidopsis nuclear genes (GUN1, GUN2, and GUN3) necessary for coupling the expression of some nuclear genes to the functional state of the chloroplast. Homozygous recessive gun mutations allow nuclear gene expression in the absence of chloroplast development and furthermore may interfere with the switch from dark-grown to light-grown development. Other reports suggest this intracellular cross-stalk also involves mitochondrial interactions. The GUN genes thus define steps in one specific branch of a complex interorganellar regulatory network. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT EXTRATERR PHYS,BOSTON,MA 02114. RP SUSEK, RE (reprint author), SALK INST BIOL STUDIES,PLANT BIOL LAB,SAN DIEGO,CA 92186, USA. FU NCRR NIH HHS [RR05595] NR 62 TC 352 Z9 366 U1 4 U2 42 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD SEP 10 PY 1993 VL 74 IS 5 BP 787 EP 799 DI 10.1016/0092-8674(93)90459-4 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LX292 UT WOS:A1993LX29200005 PM 7690685 ER PT J AU BARTEL, DP SZOSTAK, JW AF BARTEL, DP SZOSTAK, JW TI ISOLATION OF NEW RIBOZYMES FROM A LARGE POOL OF RANDOM SEQUENCES SO SCIENCE LA English DT Article ID COMPLEMENTARY-STRAND RNA; CATALYSIS; POLYMERASE; SELECTION; EVOLUTION; DIVERSITY; TEMPLATE; CLEAVAGE; ORIGINS; LIFE AB An iterative in vitro selection procedure was used to isolate a new class of catalytic RNAs (ribozymes) from a large pool of random-sequence RNA molecules. These ribozymes ligate two RNA molecules that are aligned on a template by catalyzing the attack of a 3'-hydroxyl on an adjacent 5'-triphosphate-a reaction similar to that employed by the familiar protein enzymes that synthesize RNA. The corresponding uncatalyzed reaction also yields a 3',5'-phosphodiester bond. In vitro evolution of the population of new ribozymes led to improvement of the average ligation activity and the emergence of ribozymes with reaction rates 7 million times faster than the uncatalyzed reaction rate. RP BARTEL, DP (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 32 TC 564 Z9 578 U1 7 U2 67 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD SEP 10 PY 1993 VL 261 IS 5127 BP 1411 EP 1418 DI 10.1126/science.7690155 PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LW549 UT WOS:A1993LW54900023 PM 7690155 ER PT J AU HELLER, HM BECK, WS DZIECZKOWSKI, JS HARRIS, NL BASGOZ, N UEDA, PL AF HELLER, HM BECK, WS DZIECZKOWSKI, JS HARRIS, NL BASGOZ, N UEDA, PL TI A 28-YEAR-OLD MAN WITH AIDS, PERSISTENT PANCYTOPENIA, AND LYMPHOMA - PARVOVIRUS B19 INFECTION - LARGE-CELL LYMPHOMA - ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID BONE-MARROW FAILURE; EPSTEIN-BARR-VIRUS; PARVOVIRUS-B19-RELATED PANCYTOPENIA; IMMUNOGLOBULIN THERAPY; PROGENITOR CELLS; HIV-INFECTION; APLASIA; ANEMIA; ERYTHROPOIETIN; MANAGEMENT C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HELLER, HM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 33 TC 4 Z9 4 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 SEP 9 PY 1993 VL 329 IS 11 BP 792 EP 799 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA LV642 UT WOS:A1993LV64200009 ER PT J AU MAGUIRE, JH HENSON, JW AF MAGUIRE, JH HENSON, JW TI CASE-8-1993 - CYSTICERCOSIS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID ALBENDAZOLE THERAPY C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP MAGUIRE, JH (reprint author), BRIGHAM & WOMENS HOSP,BOSTON,MA 02115, USA. NR 4 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 SEP 9 PY 1993 VL 329 IS 11 BP 813 EP 813 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LV642 UT WOS:A1993LV64200036 ER PT J AU WILLIAMS, JW SIMEL, DL AF WILLIAMS, JW SIMEL, DL TI DOES THIS PATIENT HAVE SINUSITIS - DIAGNOSING ACUTE SINUSITIS BY HISTORY AND PHYSICAL-EXAMINATION SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID ACUTE MAXILLARY SINUSITIS; CHILDREN; NASAL; RADIOGRAPHY; ULTRASONOGRAPHY; INFECTIONS; ULTRASOUND; ETIOLOGY; SYMPTOMS; SINUSES C1 UNIV TEXAS,HLTH SCI CTR,DIV GEN INTERNAL MED,SAN ANTONIO,TX 78284. VET AFFAIRS MED CTR,AMBULATORY CARE SERV,DURHAM,NC. VET AFFAIRS MED CTR,CTR HLTH SERV RES PRIMARY CARE,DURHAM,NC. DUKE UNIV,MED CTR,DIV GEN INTERNAL MED,DURHAM,NC 27710. RP WILLIAMS, JW (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,AMBULATORY CARE SERV,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 37 TC 112 Z9 113 U1 0 U2 1 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 SEP 8 PY 1993 VL 270 IS 10 BP 1242 EP 1246 DI 10.1001/jama.270.10.1242 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA LV649 UT WOS:A1993LV64900032 PM 8355389 ER PT J AU KHARBANDA, S SALEEM, A RUBIN, E SUKHATME, V BLENIS, J KUFE, D AF KHARBANDA, S SALEEM, A RUBIN, E SUKHATME, V BLENIS, J KUFE, D TI ACTIVATION OF THE EARLY GROWTH RESPONSE-1 GENE AND NUCLEAR PP90(RSK) IN HUMAN MYELOID-LEUKEMIA CELLS BY 1-(BETA-D-ARABINOFURANOSYL)CYTOSINE SO BIOCHEMISTRY LA English DT Article ID PROTEIN-KINASE-C; IMMEDIATE-EARLY GENE; ZINC FINGER PROTEIN; JUN-B GENE; MONOCYTIC DIFFERENTIATION; DNA-SYNTHESIS; 3T3 CELLS; 1-BETA-D-ARABINOFURANOSYLCYTOSINE INCORPORATION; TRANSCRIPTION FACTOR; EGR-1 PROMOTER AB The early growth response 1 (EGR-1) gene is induced by mitogens, differentiating stimuli, and certain genotoxic agents in diverse cell types. The present work has examined the effects of 1-(beta-D-arabinofuranosyl)cytosine (ara-C), an antileukemia agent misincorporates into DNA, on EGR-1 expression. Treatment of HL-525 myeloid leukemia cells with ara-C was associated with transient increases in EGR-1 mRNA levels. Nuclear run-on assays showed that this effect is related at least in part to activation of EGR-1 gene transcription. Sequences responsive to ara-C-induced signals were determined by deletion analysis of the EGR-1 promoter. The results demonstrate that ara-C inducibility of the EGR-1 gene is conferred by a region containing six serum response or CC(A/T)6GG (CArG) motifs. Further analysis demonstrated that the first two distal or 5'-most CArG elements are functional in the ara-C response. An oligomer corresponding to the first CArG element also conferred ara-C inducibility of the minimal thymdine kinase gene promoter, while no inducibility was detectable using a similar oligomer containing a mutated CArG box. Other work has demonstrated that the nuclear serum response factor (SRF) interacts with the CArG box in the EGR-1 promoter and that the serine/threonine pp90rsk protein kinase phosphorylates SRF in vitro at sites phosphorylated in vivo. The present studies demonstrate that ara-C has little if any effect on cytosolic pp90rsk as determined by immunoblotting to assess electrophoretic mobility and by immune-complex kinase assays using S6 peptide as substrate. In contrast, both a decrease in electrophoretic mobility and an increase in S6 peptide phosphorylation confirmed activation of this kinase in the nucleus. Taken together, these findings suggest that ara-C activates a nuclear pp90rsk cascade and that this event may contribute to induction of EGR-1 transcription by a CArG motif-mediated mechanism. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. BETH ISRAEL HOSP,DIV NEPHROL,BOSTON,MA 02215. FU NCI NIH HHS [CA29431] NR 55 TC 18 Z9 18 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 SEP 7 PY 1993 VL 32 IS 35 BP 9137 EP 9142 DI 10.1021/bi00086a019 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LW440 UT WOS:A1993LW44000019 PM 7690249 ER PT J AU WANG, PH LAU, J CHALMERS, TC AF WANG, PH LAU, J CHALMERS, TC TI TIGHT GLUCOSE CONTROL AND DIABETIC COMPLICATIONS - REPLY SO LANCET LA English DT Letter RP WANG, PH (reprint author), HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115, USA. NR 4 TC 0 Z9 0 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 SEP 4 PY 1993 VL 342 IS 8871 BP 618 EP 618 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LV963 UT WOS:A1993LV96300048 ER PT J AU BORGAONKAR, DS SCHMIDT, LC MARTIN, SE KANZER, MD EDELSOHN, L GROWDON, J FARRER, LA AF BORGAONKAR, DS SCHMIDT, LC MARTIN, SE KANZER, MD EDELSOHN, L GROWDON, J FARRER, LA TI LINKAGE OF LATE-ONSET ALZHEIMERS-DISEASE WITH APOLIPOPROTEIN-E TYPE-4 ON CHROMOSOME-19 SO LANCET LA English DT Letter ID GENETIC-LINKAGE; LOCUS C1 MED CTR DELAWARE,DEPT MED NEUROL,NEWARK,DE 19718. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. RP BORGAONKAR, DS (reprint author), CHRISTIANA HOSP,MED CTR DELAWARE,DEPT PATHOL & LAB MED,POB 6001,NEWARK,DE 19718, USA. FU NIA NIH HHS [AG-09029] NR 8 TC 58 Z9 59 U1 0 U2 1 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD SEP 4 PY 1993 VL 342 IS 8871 BP 625 EP 625 DI 10.1016/0140-6736(93)91458-X PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LV963 UT WOS:A1993LV96300066 PM 8102761 ER PT J AU LESTER, J FINK, S ARONIN, N DIFIGLIA, M AF LESTER, J FINK, S ARONIN, N DIFIGLIA, M TI COLOCALIZATION OF D(1) AND D(2) DOPAMINE-RECEPTOR MESSENGER-RNAS IN STRIATAL NEURONS SO BRAIN RESEARCH LA English DT Note DE HYBRIDIZATION; IN-SITU; CAUDATE-PUTAMEN ID CAUDATE-NUCLEUS NEURONS; BASAL GANGLIA; RAT-BRAIN; STRIATOPALLIDAL NEURONS; D-2 RECEPTORS; D2 RECEPTORS; D1; EXPRESSION; LOCALIZATION; AGONISTS AB There is evidence that D1 and D2 dopamine receptor subtypes coexist at the cellular level in the striatum and act synergistically to mediate the effects of dopamine. Other data suggest that these receptor subtypes are largely segregated in different striatal projection pathways. We used in situ hybridization in serial adjacent 4 mum sections to determine the extent of colocalization of D1 and D2 receptor mRNAs in rat striatal neurons. Cellular localization of D1 and D2 receptor mRNA was performed on section pairs that were hybridized with S-35-labeled cDNA or oligonucleotide probes directed against non-homologous regions of D1 and D2 receptor mRNAs. We found that 26-27% of striatal cells containing one receptor subtype also contained the other subtype. Thus, although D1 and D2 receptors are segregated in the majority of striatal neurons, a substantial number of striatal neurons coexpress both dopamine receptor mRNA subtypes. Our findings provide anatomic support for many of the functional interactions that have been described for D1 and D2 receptors. C1 MASSACHUSETTS GEN HOSP,CELLULAR NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV MASSACHUSETTS,MED CTR,DEPT MED,WORCESTER,MA 01655. UNIV MASSACHUSETTS,MED CTR,DEPT CELL BIOL,WORCESTER,MA 01655. FU NIDA NIH HHS [DA07496]; PHS HHS [N516367] NR 29 TC 88 Z9 90 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD SEP 3 PY 1993 VL 621 IS 1 BP 106 EP 110 DI 10.1016/0006-8993(93)90303-5 PG 5 WC Neurosciences SC Neurosciences & Neurology GA LU745 UT WOS:A1993LU74500013 PM 8221060 ER PT J AU NIHEI, K KOWALL, NW AF NIHEI, K KOWALL, NW TI INVOLVEMENT OF NPY-IMMUNOREACTIVE NEURONS IN THE CEREBRAL-CORTEX OF AMYOTROPHIC-LATERAL-SCLEROSIS PATIENTS SO NEUROSCIENCE LETTERS LA English DT Article DE NEUROPEPTIDE-Y (NPY); IMMUNOHISTOCHEMISTRY; CEREBRAL CORTEX; STRIATUM; CORTICAL INTERNEURON; AMYOTROPHIC LATERAL SCLEROSIS (ALS) ID ALZHEIMERS-TYPE DEMENTIA; HUNTINGTONS-DISEASE; NEUROPEPTIDE-Y; ANTISERA AB We performed a quantitative histochemical study of neuropeptide Y (NPY) immunoreactivity in postmortem human brain to further define patterns of neuronal degeneration in amyotrophic lateral sclerosis (ALS). The density of NPY fibers was decreased in ALS motor cortex but not in other cortical regions or striatum. Although, the density of cortical NPY neurons was unchanged in high grade cases, neurons were shrunken and atrophic with pruned dendrites. NPY neurons are less severely affected than parvalbumin neurons which are severely depleted in ALS cortex. This differential involvement of local circuit neurons suggests that a simple excitotoxic model may not adequately explain patterns of neuronal loss in ALS. C1 BEDFORD VET ADM MED CTR,CTR GERIATR RES EDUC CLIN 182B,BEDFORD,MA 01730. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. YAMAGATA UNIV,SCH MED,DEPT INTERNAL MED 3,YAMAGATA 990,JAPAN. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02118. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NIMH NIH HHS [MH31863] NR 14 TC 5 Z9 5 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 SEP 3 PY 1993 VL 159 IS 1-2 BP 67 EP 70 DI 10.1016/0304-3940(93)90800-Z PG 4 WC Neurosciences SC Neurosciences & Neurology GA LY621 UT WOS:A1993LY62100018 PM 8264981 ER PT J AU FUSTER, V AF FUSTER, V TI CORONARY THROMBOLYSIS - A PERSPECTIVE FOR THE PRACTICING PHYSICIAN SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID ACUTE MYOCARDIAL-INFARCTION; HEPARIN RP FUSTER, V (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 19 TC 50 Z9 51 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD SEP 2 PY 1993 VL 329 IS 10 BP 723 EP 725 DI 10.1056/NEJM199309023291009 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA LU583 UT WOS:A1993LU58300009 PM 8345859 ER PT J AU SPILLANE, RM SHEPARD, JAO DELUCA, SA AF SPILLANE, RM SHEPARD, JAO DELUCA, SA TI HIGH-RESOLUTION CT OF THE LUNGS SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB High-resolution computed tomography (CT) of the lung provides detailed visualization of the lung parenchyma. The technique involves the use of thin-section axial tomography. High-resolution CT can facilitate the diagnosis of certain pulmonary processes. It is useful in differentiating similar patterns of abnormalities seen on chest radiographs, such as those seen in lymphangitic carcinomatosis and sarcoidosis, and in delineating the extent of co-morbid lung diseases, such as emphysema and asbestosis. In some chronic processes such as idiopathic pulmonary fibrosis, high-resolution CT can be used for biopsy of areas of active inflammation, thus increasing the diagnostic yield. As clinicians and radiologists become more familiar with high-resolution CT, it is likely that its role in the diagnosis and assessment of lung disease will increase. RP SPILLANE, RM (reprint author), MASSACHUSETTS GEN HOSP,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 SEP 1 PY 1993 VL 48 IS 3 BP 493 EP 498 PG 6 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA LX055 UT WOS:A1993LX05500011 PM 8362698 ER PT J AU LIEBER, CS AF LIEBER, CS TI HERMAN AWARD LECTURE, 1993 - A PERSONAL PERSPECTIVE ON ALCOHOL, NUTRITION, AND THE LIVER SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE 2E1; ACETALDEHYDE; GLUTATHIONE; COLLAGEN; S-ADENOSYL-L-METHIONINE; DILINOLEOYLPHOSPHATIDYLCHOLINE; LIPIDS; FIBROSIS ID CHRONIC ETHANOL-CONSUMPTION; HEPATIC VITAMIN-A; INDUCED LIPID-PEROXIDATION; 1ST PASS METABOLISM; FAT-STORING CELLS; RAT-LIVER; DEHYDROGENASE-ACTIVITY; ACETALDEHYDE ADDUCTS; 1ST-PASS METABOLISM; ACETAMINOPHEN HEPATOTOXICITY AB Alcohol causes primary malnutrition by displacing nutrients in the diet and secondary malnutrition via malabsorption and cellular injury through direct cytotoxicity. Hepatotoxicity results from metabolic disturbances associated with the oxidation of ethanol via liver alcohol dehydrogenase (ADH) and the redox changes produced by the generated NADH (the reduced form of nicotinamide adenine dinucleotide), which in turn affects the metabolism of lipids, carbohydrates, proteins, and purines. Ethanol is also oxidized in liver microsomes by an ethanol-inducible cytochrome P450, which contributes to the alcoholic's tolerance and his increased vulnerability to the toxicity of industrial solvents, anesthetics, commonly prescribed drugs, over-the-counter analgesics, chemical carcinogens, and retinoids. Increased acetaldehyde generation, with formation of protein adducts, results in antibody production, enzyme inactivation, decreased DNA repair, impaired utilization of oxygen, glutathione depletion, free radical-mediated toxicity, lipid peroxidation, and increased collagen synthesis. Therapy may eventually improve with the use of supernutrients such as S-adenosyl-L-methionine, which replenishes glutathione, restores methylation, and attenuates liver injury, as well as dilinolcoyl-phosphatidylcholine, which prevents cirrhosis. C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RP LIEBER, CS (reprint author), BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,LIVER DIS & NUTR SECT,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIAAA NIH HHS [AA 03508, AA 05934]; NIDDK NIH HHS [DK 32810] NR 199 TC 45 Z9 48 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD SEP PY 1993 VL 58 IS 3 BP 430 EP 442 PG 13 WC Nutrition & Dietetics SC Nutrition & Dietetics GA LV751 UT WOS:A1993LV75100019 PM 8237856 ER PT J AU JACQUES, PF SADOWSKI, JA RUSH, D SULSKY, SI PHILLIPS, JCC WILLETT, WC AF JACQUES, PF SADOWSKI, JA RUSH, D SULSKY, SI PHILLIPS, JCC WILLETT, WC TI COMPARISON OF INTAKE AND BLOOD-CONCENTRATIONS OF MICRONUTRIENTS - REPLY SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Letter ID HEALTHY ELDERLY POPULATION; QUESTIONNAIRE C1 EPIDEMIOL RESOURCES INC,NEWTON LOWER FALLS,MA 02162. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CANC EPIDEMIOL & CONTROL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CHANNING LAB,BOSTON,MA 02115. RP JACQUES, PF (reprint author), TUFTS UNIV,USDA,HUMAN NUTR RES CTR AGING,BOSTON,MA 02111, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD SEP PY 1993 VL 58 IS 3 BP 450 EP 451 PG 2 WC Nutrition & Dietetics SC Nutrition & Dietetics GA LV751 UT WOS:A1993LV75100023 ER PT J AU SHANNON, DC AF SHANNON, DC TI ALARMING HEART-RATES SO AMERICAN JOURNAL OF DISEASES OF CHILDREN LA English DT Editorial Material RP SHANNON, DC (reprint author), MASSACHUSETTS GEN HOSP,FRUIT ST,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0002-922X J9 AM J DIS CHILD JI Am. J. Dis. Child. PD SEP PY 1993 VL 147 IS 9 BP 939 EP 940 PG 2 WC Pediatrics SC Pediatrics GA LV721 UT WOS:A1993LV72100009 PM 8362805 ER PT J AU SIMONS, BD MORRISON, AS YOUNG, RH VERHOEKOFTEDAHL, W AF SIMONS, BD MORRISON, AS YOUNG, RH VERHOEKOFTEDAHL, W TI THE RELATION OF SURGERY FOR PROSTATIC HYPERTROPHY TO CARCINOMA OF THE PROSTATE SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE HISTOLOGY; MORTALITY; PROSTATIC HYPERTROPHY; PROSTATIC NEOPLASMS ID CANCER; HYPERPLASIA AB The authors evaluated the risk of death from prostate cancer in Rhode Island men who had had surgery for prostatic hypertrophy during the years 1959-1970. The retrospective follow-up method was used. Among 4,853 men who had had either a transurethral resection or a prostatectomy, age- and time-standardized mortality from prostate cancer was 1.14 (95% confidence interval (Cl) 0.96-1.33) times the rate in the general population of Rhode Island men. The age- and time-standardized mortality ratio was 1.01 (95% Cl 0.77-1.31) for men who had had a suprapubic prostatectomy and 1.18 (95% Cl 0.94-1.47) for men who had had a transurethral resection. The authors used the case-control method to relate the histologic features of prostatic hypertrophy to subsequent prostate cancer. The observed associations were weak and inconsistent. The results of this study suggest that surgically treated prostatic hypertrophy is not an important determinant of prostate cancer. C1 BROWN UNIV,DEPT COMMUNITY HLTH,BOX G-A420,PROVIDENCE,RI 02912. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [R01 CA38707] NR 12 TC 10 Z9 10 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD SEP 1 PY 1993 VL 138 IS 5 BP 294 EP 300 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LW583 UT WOS:A1993LW58300002 PM 7689295 ER PT J AU MACKINNEY, AA CLARK, SS BORCHERDING, W FIZZOTTI, M HONG, R AF MACKINNEY, AA CLARK, SS BORCHERDING, W FIZZOTTI, M HONG, R TI SIMULTANEOUS DEMONSTRATION OF THE PHILADELPHIA-CHROMOSOME IN T-CELLS, B-CELLS, AND MYELOID CELLS SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Note DE T-CELL LYMPHOMA; FLOW CYTOMETRY; CYTOGENETICS; STEM CELL ID CHRONIC MYELOGENOUS LEUKEMIA; CHRONIC MYELOCYTIC-LEUKEMIA; BREAKPOINT CLUSTER REGION; ACUTE LYMPHOBLASTIC-LEUKEMIA; BLAST CRISIS; MALIGNANT-LYMPHOMA; MULTIPLE-MYELOMA; BONE-MARROW; REARRANGEMENT; PATIENT AB A patient presented with lymphoblastic lymphoma in lymph-nodes and chronic myelogenous leukemia (CML) in marrow and peripheral blood. All marrow and unstimulated peripheral blood cells contained the Philadelphia chromosome{t(9:22)}. Lymphoma cells were analyzed by flow cytometry and were identified as T cells (CD2+CD5+CD7+CD34+). All fresh lymphoma cells contained the t(9:22) translocation. Cultures of purified peripheral blood T and B cells and specifically stimulated NK cells revealed that 59% of the B cells, 10% of the NK cells, and none of the normal T cells contained the translocation. The lack of translocation in normal peripheral T cells is attributed to their long lifespan. No rearrangement of immunoglobulin or T cell receptor beta or gamma genes was found in either the leukemia or lymphoma cells. Analysis of the DNA from cryopreserved lymphoma biopsy showed clonal rearrangement within the common breakpoint cluster region of the bcr gene identical to the bcr rearrangement in DNA from leukemia blood cells. The data support the concept that T and B cells originate in the patient's totipotent stem cell from which the CML is also derived. (C) 1993 Wiley-Liss, Inc. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. NR 41 TC 15 Z9 17 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD SEP PY 1993 VL 44 IS 1 BP 48 EP 52 DI 10.1002/ajh.2830440110 PG 5 WC Hematology SC Hematology GA LP906 UT WOS:A1993LP90600009 PM 7688179 ER PT J AU BOLDOG, FL GEMMILL, RM WILKE, CM GLOVER, TW NILSSON, AS CHANDRASEKHARAPPA, SC BROWN, RS LI, FP DRABKIN, HA AF BOLDOG, FL GEMMILL, RM WILKE, CM GLOVER, TW NILSSON, AS CHANDRASEKHARAPPA, SC BROWN, RS LI, FP DRABKIN, HA TI POSITIONAL CLONING OF THE HEREDITARY RENAL-CARCINOMA 3-8 CHROMOSOME-TRANSLOCATION BREAKPOINT SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 ELEANOR ROOSEVELT INST,DENVER,CO 80262. BETH ISRAEL HOSP,BOSTON,MA 02215. UNIV COLORADO,CTR CANC,DENVER,CO 80262. UNIV MICHIGAN,ANN ARBOR,MI 48109. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,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 SEP PY 1993 VL 53 IS 3 SU S BP 26 EP 26 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500027 ER PT J AU PETRUHKIN, K TANZI, RE FISCHER, S PIRASTU, M CHERNOV, I BOUKHGALTER, B CYANIS, E WASCO, W BRZUSTOWICZ, LM MATSEOANE, D DEVOTO, M FIGLIS, AL LOLIDIHNOS, J CAO, A CHUMAKOV, I EVGRAFOV, G STERNLIEB, I WARBURTON, D PENCHASZADEH, G SCHEINBERG, IH GILLIAM, TC AF PETRUHKIN, K TANZI, RE FISCHER, S PIRASTU, M CHERNOV, I BOUKHGALTER, B CYANIS, E WASCO, W BRZUSTOWICZ, LM MATSEOANE, D DEVOTO, M FIGLIS, AL LOLIDIHNOS, J CAO, A CHUMAKOV, I EVGRAFOV, G STERNLIEB, I WARBURTON, D PENCHASZADEH, G SCHEINBERG, IH GILLIAM, TC TI MAPPING THE WILSONS-DISEASE GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 CNR,CAGLIARI,ITALY. COLUMBIA UNIV,NEW YORK,NY 10027. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CEPH,PARIS,FRANCE. CTR MED GENET,MOSCOW,RUSSIA. ST LUKES HOSP,NEW YORK,NY 10025. 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 SEP PY 1993 VL 53 IS 3 SU S BP 55 EP 55 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500055 ER PT J AU WASCO, W GASTON, S ROMANO, D PEPPERCORN, J CROWLEY, A PARADIS, M BUCKLER, A BUSH, A HAINES, J STGEORGEHYSLOP, P GUSELLA, J TANZI, R AF WASCO, W GASTON, S ROMANO, D PEPPERCORN, J CROWLEY, A PARADIS, M BUCKLER, A BUSH, A HAINES, J STGEORGEHYSLOP, P GUSELLA, J TANZI, R TI ISOLATION OF THE FAMILIAL ALZHEIMERS-DISEASE GENE ON CHROMOSOME-14 - PHYSICAL AND TRANSCRIPTIONAL MAPPING SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GENET & AGING LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. UNIV TORONTO,TANZ NEUROSCI INST,TORONTO M5S 1A1,ONTARIO,CANADA. 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 SEP PY 1993 VL 53 IS 3 SU S BP 62 EP 62 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500062 ER PT J AU MACDONALD, M DUYAO, M AMBROSE, C BARNES, G SRINIDHI, J MYERS, R GUSELLA, J AF MACDONALD, M DUYAO, M AMBROSE, C BARNES, G SRINIDHI, J MYERS, R GUSELLA, J TI A CODON DELETION IN THE HUNTINGTONS-DISEASE GENE IS ASSOCIATED WITH THE MAJOR HD CHROMOSOME HAPLOTYPE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. 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 SEP PY 1993 VL 53 IS 3 SU S BP 80 EP 80 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500079 ER PT J AU MYERS, RH MACDONALD, ME KOROSHETZ, WJ DUYAO, MP AMBROSE, CM TAYLOR, SA BARNES, G SRINIDHI, J LIN, CS WHALEY, WL LAZZARINI, AM SCHWARZ, M WOLFF, G BIRD, ED VONSATTEL, JPG GUSELLA, JF AF MYERS, RH MACDONALD, ME KOROSHETZ, WJ DUYAO, MP AMBROSE, CM TAYLOR, SA BARNES, G SRINIDHI, J LIN, CS WHALEY, WL LAZZARINI, AM SCHWARZ, M WOLFF, G BIRD, ED VONSATTEL, JPG GUSELLA, JF TI DE-NOVO EXPANSION OF A CAG REPEAT IN SPORADIC HUNTINGTONS-DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 BU,SCH MED,DEPT NEUROL,BOSTON,MA. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT NEUROL,NEW BRUNSWICK,NJ 08903. RHEIN WESTFAL TH AACHEN,NEUROL KLIN,W-5100 AACHEN,GERMANY. UNIV FREIBURG,INST HUMAN GENET & ANTHROPOL,W-7800 FREIBURG,GERMANY. MCLEAN HOSP,MAILMAN RES CTR,BELMONT,MA 02178. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL NEUROPATH,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 SEP PY 1993 VL 53 IS 3 SU S BP 81 EP 81 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500082 ER PT J AU ANGRIST, M KAUFFMAN, E MATISE, TC SLAUGENHAUPT, SA BOLK, S PUFFENBERGER, EG LIPSON, A CASS, DT REYNA, T WEEKS, DE WEISSENBACH, J CHAKRAVARTI, A AF ANGRIST, M KAUFFMAN, E MATISE, TC SLAUGENHAUPT, SA BOLK, S PUFFENBERGER, EG LIPSON, A CASS, DT REYNA, T WEEKS, DE WEISSENBACH, J CHAKRAVARTI, A TI A GENETIC-LOCUS FOR HIRSCHSPRUNG DISEASE IN THE PERICENTROMERIC REGION OF CHROMOSOME-10 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PITTSBURGH,PITTSBURGH,PA 15260. MASSACHUSETTS GEN HOSP,CHARLESTON,MA. ROYAL ALEXANDRA HOSP CHILDREN,CAMPERDOWN,NSW 2050,AUSTRALIA. WESTMEAD HOSP,WESTMEAD,AUSTRALIA. WILLIAM BEAUMONT ARMY MED CTR,EL PASO,TX 79920. GENETHON,EVRY,FRANCE. RI Weeks, Daniel/B-2995-2012 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 SEP PY 1993 VL 53 IS 3 SU S BP 134 EP 134 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500136 ER PT J AU RAMESH, V JACOBY, LB MACCOLLIN, MM LOUIS, D MOHNEY, TM PULASKI, K KLEY, N SEIZINGER, BR TROFATTER, JA GUSELLA, JF AF RAMESH, V JACOBY, LB MACCOLLIN, MM LOUIS, D MOHNEY, TM PULASKI, K KLEY, N SEIZINGER, BR TROFATTER, JA GUSELLA, JF TI MUTATIONS IN THE NF2 GENE IN NF2 AND NON-NF2 RELATED TUMORS - IMPLICATIONS FOR MERLIN PROTEIN EXPRESSION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,PRINCETON,NJ. NR 0 TC 0 Z9 0 U1 0 U2 3 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 SEP PY 1993 VL 53 IS 3 SU S BP 166 EP 166 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500166 ER PT J AU FOUNTAIN, JW HALUSKA, FG GRAW, SL KAO, WH GITAI, Z BOYER, LA CASTRESANA, JS RUBIO, MP SEIZINGER, B BARNHILL, R WALKER, GJ HAYWARD, NK HOUSMAN, DE AF FOUNTAIN, JW HALUSKA, FG GRAW, SL KAO, WH GITAI, Z BOYER, LA CASTRESANA, JS RUBIO, MP SEIZINGER, B BARNHILL, R WALKER, GJ HAYWARD, NK HOUSMAN, DE TI MORE PRECISE DEFINITION OF THE 9P21 REGION LOST IN MELANOMA AND IDENTIFICATION OF A CANDIDATE GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02139. MIT,CTR CA RES,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. ELEANOR ROOSEVELT INST,DENVER,CO. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BRISTOL MYERS,PRINCETON,NJ. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. QUEENSLAND INST MED RES,BRISBANE,AUSTRALIA. 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 SEP PY 1993 VL 53 IS 3 SU S BP 170 EP 170 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500168 ER PT J AU HUBERT, R MACDONALD, ME GUSELLA, JF ARNHEIM, N AF HUBERT, R MACDONALD, ME GUSELLA, JF ARNHEIM, N TI LINKAGE ANALYSIS OF THE RECOMBINATION HOTSPOT NEAR THE HUNTINGTONS-DISEASE GENE USING SPERM TYPING SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 USC,LOS ANGELES,CA. MASSACHUSETTS GEN HOSP,BOSTON,MA. 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 SEP PY 1993 VL 53 IS 3 SU S BP 178 EP 178 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500180 ER PT J AU BUCKLER, AJ STOTLER, CJ RUTTER, JL MURRELL, J TROFATTER, JA MCCORMICK, MK DEAVEN, L MOYZIS, RK GUSELLA, JF AF BUCKLER, AJ STOTLER, CJ RUTTER, JL MURRELL, J TROFATTER, JA MCCORMICK, MK DEAVEN, L MOYZIS, RK GUSELLA, JF TI CHROMOSOME-SPECIFIC LIBRARIES OF EXONS AND HIGH-RESOLUTION TRANSCRIPTION MAPS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. LOS ALAMOS NATL LAB,LOS ALAMOS,NM 87544. NR 0 TC 0 Z9 0 U1 0 U2 3 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 SEP PY 1993 VL 53 IS 3 SU S BP 192 EP 192 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500190 ER PT J AU MUNROE, DJ BRIC, E LOEBBERT, R WHITTON, T VU, D BUCKLER, A STANTON, V HOUSMAN, DE AF MUNROE, DJ BRIC, E LOEBBERT, R WHITTON, T VU, D BUCKLER, A STANTON, V HOUSMAN, DE TI A YAC CLONE CONTIG AND TRANSCRIPTION MAP OF 11P15 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MIT,CTR CANC RES,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA. 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 SEP PY 1993 VL 53 IS 3 SU S BP 194 EP 194 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500194 ER PT J AU RUTTER, JL CHURCH, DM STOTLER, CJ BANKS, LT MCCORMICK, MK BUCKLER, AJ AF RUTTER, JL CHURCH, DM STOTLER, CJ BANKS, LT MCCORMICK, MK BUCKLER, AJ TI ISOLATION OF GENES ON HUMAN CHROMOSOME-9 USING EXON AMPLIFICATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. UNIV CALIF IRVINE,DEPT BIOCHEM,IRVINE,CA 92717. 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 SEP PY 1993 VL 53 IS 3 SU S BP 195 EP 195 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500197 ER PT J AU TROFATTER, JA GUSELLA, JF BUCKLER, A AF TROFATTER, JA GUSELLA, JF BUCKLER, A TI TRANSCRIPTION MAPPING OF HUMAN CHROMOSOME-22 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. 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 SEP PY 1993 VL 53 IS 3 SU S BP 196 EP 196 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500195 ER PT J AU CORDER, EH SAUNDERS, AM STRITTMATTER, WJ SCHMECHEL, D GASKELL, P SMALL, GW ROSES, AD HAINES, JL PERICAKVANCE, MA AF CORDER, EH SAUNDERS, AM STRITTMATTER, WJ SCHMECHEL, D GASKELL, P SMALL, GW ROSES, AD HAINES, JL PERICAKVANCE, MA TI APOLIPOPROTEIN E4 GENE DOSE AFFECTS THE RISK OF ALZHEIMER-DISEASE IN LATE-ONSET FAMILIES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,JOSEPH & KATHLEEN BRYAN ALZHEIMERS DIS RES CTR,DURHAM,NC 27710. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 2 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 SEP PY 1993 VL 53 IS 3 SU S BP 203 EP 203 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500201 ER PT J AU TANZI, RE PETRUHKIN, K SOARES, B WASCO, W ROMANO, D ROSS, B CHERNOV, I PIRASTU, M HYSLOP, PG GUSELLA, JF SCHEINBERG, IH GILLIAM, TC AF TANZI, RE PETRUHKIN, K SOARES, B WASCO, W ROMANO, D ROSS, B CHERNOV, I PIRASTU, M HYSLOP, PG GUSELLA, JF SCHEINBERG, IH GILLIAM, TC TI ISOLATION AND CHARACTERIZATION OF A CANDIDATE GENE FOR WILSONS-DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY 10032. CNR,IST RIC TALASSEMIE & ANEM MEDITERRANNEE,CAGLIARI,ITALY. UNIV TORONTO,TORONTO M5S 1A1,ONTARIO,CANADA. ST LUKES ROOSEVELT HOSP,NEW YORK,NY. 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 SEP PY 1993 VL 53 IS 3 SU S BP 228 EP 228 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500227 ER PT J AU HAINES, JL SEBOUN, E GOODKIN, DE USUKU, K LINCOLN, R RIMMLER, J GUSELLA, JF ROSES, AD PERICAKVANCE, MA HAUSER, SL AF HAINES, JL SEBOUN, E GOODKIN, DE USUKU, K LINCOLN, R RIMMLER, J GUSELLA, JF ROSES, AD PERICAKVANCE, MA HAUSER, SL TI GENETIC DISSECTION OF THE MULTIPLE-SCLEROSIS GENOTYPE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GENETHON,PARIS,FRANCE. CLEVELAND CLIN,CLEVELAND,OH 44106. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. DUKE UNIV,MED CTR,DURHAM,NC 27710. RI Hauser, Stephen/J-2978-2016 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 SEP PY 1993 VL 53 IS 3 SU S BP 266 EP 266 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500264 ER PT J AU DONEY, MK HOUSEAL, TW SOUKUP, SW RUTTER, JL GUSELLA, JF SCHNEIDER, BF GOLDEN, WL MENON, AG AF DONEY, MK HOUSEAL, TW SOUKUP, SW RUTTER, JL GUSELLA, JF SCHNEIDER, BF GOLDEN, WL MENON, AG TI IDENTIFICATION OF A PUTATIVE TUMOR-SUPPRESSOR LOCUS IN 14Q24-32 THAT IS INVOLVED IN FORMATION AND PROGRESSION OF MENINGIOMAS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV CINCINNATI,CINCINNATI,OH 45267. INTEGRATED GENET VIVIGEN,FRAMINGHAM,MA 01701. UNIV VIRGINIA,CHARLOTTESVILLE,VA 22908. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 7 Z9 7 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 SEP PY 1993 VL 53 IS 3 SU S BP 293 EP 293 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500295 ER PT J AU HALUSKA, FG GITAL, Z KAO, W HOUSMAN, DE FOUNTAIN, JW AF HALUSKA, FG GITAL, Z KAO, W HOUSMAN, DE FOUNTAIN, JW TI CONSTRUCTION OF YAC CONTIGS SPANNING THE 9P21 REGION IMPLICATED IN MALIGNANT-MELANOMA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02139. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. 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 SEP PY 1993 VL 53 IS 3 SU S BP 306 EP 306 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500305 ER PT J AU SACCHI, N NISSON, PE BUCKLER, AJ WATKINS, PC AF SACCHI, N NISSON, PE BUCKLER, AJ WATKINS, PC TI NORMAL AND CHIMERIC AML1 TRANSCRIPTS IN THE T(821) OF ACUTE MYELOGENOUS LEUKEMIA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV MILAN,SCH MED,DEPT BIOL & GENET,I-20122 MILAN,ITALY. LIFE TECHNOL,GAITHERSBURG,MD. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,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 SEP PY 1993 VL 53 IS 3 SU S BP 353 EP 353 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500355 ER PT J AU ALI, G WASCO, W CAI, XG SZABO, P SHEU, KF COOPER, A GASTON, S TANZI, R BLASS, J AF ALI, G WASCO, W CAI, XG SZABO, P SHEU, KF COOPER, A GASTON, S TANZI, R BLASS, J TI ISOLATION AND CHARACTERIZATION OF THE HUMAN E2K GENE - A CANDIDATE FOR THE FAD GENE DEFECT ON CHROMOSOME 14Q24 3 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 CORNELL UNIV,MED CTR,COLL MED,BURKE MED RES INST,NEW YORK,NY 10021. CORNELL UNIV,MED CTR,COLL MED,DIV GERIATR,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,GENET & AGING NEUROL 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 SEP PY 1993 VL 53 IS 3 SU S BP 659 EP 659 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500658 ER PT J AU AMBROSE, CM DUYAO, MP CHURCH, DM DARIGO, KL BARNES, G BUCKLER, AJ GUSELLA, JF MACDONALD, ME AF AMBROSE, CM DUYAO, MP CHURCH, DM DARIGO, KL BARNES, G BUCKLER, AJ GUSELLA, JF MACDONALD, ME TI GENOMIC STRUCTURE OF THE HUNTINGTONS-DISEASE GENE, IT15 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. NR 1 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 SEP PY 1993 VL 53 IS 3 SU S BP 660 EP 660 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500660 ER PT J AU SCHUBACK, DE ADAMS, J CHEN, ZY BATTINELLI, EM CRAIG, I COREY, DP BREAKEFIELD, XO SIMS, KB AF SCHUBACK, DE ADAMS, J CHEN, ZY BATTINELLI, EM CRAIG, I COREY, DP BREAKEFIELD, XO SIMS, KB TI IDENTIFICATION OF MUTATIONS IN THE NORRIE DISEASE GENE AND FURTHER ELUCIDATION OF NORRIN LOCATION AND FUNCTION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV OXFORD,OXFORD,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 3 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 SEP PY 1993 VL 53 IS 3 SU S BP 730 EP 730 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500731 ER PT J AU OZELIUS, L BRESSMAN, S GASSER, T DELEON, D HEWETT, J HEIMAN, G HUNT, A NYGARRD, T MOSKOWITZ, C BRIN, M FAHN, S BREAKEFIELD, XO KRAMER, P AF OZELIUS, L BRESSMAN, S GASSER, T DELEON, D HEWETT, J HEIMAN, G HUNT, A NYGARRD, T MOSKOWITZ, C BRIN, M FAHN, S BREAKEFIELD, XO KRAMER, P TI MOST EARLY-ONSET CASES OF DYSTONIA ARE CAUSED BY THE DYT1 GENE ON CHROMO-9Q34 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. COLUMBIA PRESBYTERIAN MED CTR,NEW YORK,NY 10032. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. 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 SEP PY 1993 VL 53 IS 3 SU S BP 840 EP 840 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500840 ER PT J AU COUGHLIN, EM CHALMERS, RA SLAUGENHAUPT, SA GUSELLA, JF SHIH, VE RAMESH, V AF COUGHLIN, EM CHALMERS, RA SLAUGENHAUPT, SA GUSELLA, JF SHIH, VE RAMESH, V TI IDENTIFICATION OF A MOLECULAR DEFECT IN A FUMARASE DEFICIENT PATIENT AND MAPPING OF THE FUMARASE GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ST GEORGE HOSP,SCH MED,LONDON,ENGLAND. NR 0 TC 0 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 SEP PY 1993 VL 53 IS 3 SU S BP 896 EP 896 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500897 ER PT J AU KAYE, EM SHALISH, C BREAKEFIELD, XO AF KAYE, EM SHALISH, C BREAKEFIELD, XO TI BETA-GALACTOSIDASE GENE MUTATION IN A CHILD WITH SEVERE JUVENILE GM1 GANGLIOSIDOSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,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 SEP PY 1993 VL 53 IS 3 SU S BP 911 EP 911 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33500911 ER PT J AU LERNER, T BOUSTANY, RM SCHULTZ, E DARIGO, K SCHLUMPF, K GUSELLA, J HAINES, J AF LERNER, T BOUSTANY, RM SCHULTZ, E DARIGO, K SCHLUMPF, K GUSELLA, J HAINES, J TI LINKAGE DISEQUILIBRIUM BETWEEN THE JUVENILE NCL GENE (CLN3) AND MARKER LOCI ON CHROMOSOME-16P12.1 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. DUKE UNIV,MED CTR,DIV PEDIAT NEUROL,DURHAM,NC 27710. HARVARD UNIV,SCH MED,DEPT 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 SEP PY 1993 VL 53 IS 3 SU S BP 1032 EP 1032 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33501034 ER PT J AU SCHLUMPF, KS WILSON, PJ GUILLEMETTE, W SYTSMA, M BOVE, CM KWIATKOWSKI, DJ SHORT, MP HAINES, JL AF SCHLUMPF, KS WILSON, PJ GUILLEMETTE, W SYTSMA, M BOVE, CM KWIATKOWSKI, DJ SHORT, MP HAINES, JL TI LINKAGE AND HOMOGENEITY TESTING - LOCALIZATION OF TUBEROUS SCLEROSIS ON CHROMOSOME-9 AND 16 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. 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 SEP PY 1993 VL 53 IS 3 SU S BP 1069 EP 1069 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33501068 ER PT J AU WOODBURY, MA CORDER, EH SAUNDERS, AM STRITTMATTER, WJ SCHMECHEL, D GASKELL, P SMALL, GW ROSES, AD HAINES, JL PERICAKVANCE, MA AF WOODBURY, MA CORDER, EH SAUNDERS, AM STRITTMATTER, WJ SCHMECHEL, D GASKELL, P SMALL, GW ROSES, AD HAINES, JL PERICAKVANCE, MA TI GRADE OF MEMBERSHIP ANALYSIS DISTINGUISHES LINKAGE FROM ALLELIC ASSOCIATION AT THE APOLIPOPROTEIN-E LOCUS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,CTR DEMOG STUDIES,DURHAM,NC 27710. DUKE UNIV,MED CTR,JOSEPH & KATHLEEN BRYAN ALZHEIMERS DIS RES CTR,DURHAM,NC 27710. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. 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 SEP PY 1993 VL 53 IS 3 SU S BP 1105 EP 1105 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33501104 ER PT J AU DUYAO, MP AMBROSE, CM MYERS, RH NOVELLETTO, A PERSICHETTI, E BARNES, G SRINIDHI, J BIRD, E VONSATTEL, JP MACDONALD, ME GUSELLA, JF AF DUYAO, MP AMBROSE, CM MYERS, RH NOVELLETTO, A PERSICHETTI, E BARNES, G SRINIDHI, J BIRD, E VONSATTEL, JP MACDONALD, ME GUSELLA, JF TI TRINUCLEOTIDE REPEAT LENGTH - INSTABILITY AND AGE-OF-ONSET IN HUNTINGTONS-DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. UNIV ROME,DEPT BIOL,I-00100 ROME,ITALY. HARVARD UNIV,SCH MED,DEPT NEUROPATHOL,BOSTON,MA 02115. NR 0 TC 4 Z9 4 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 SEP PY 1993 VL 53 IS 3 SU S BP 1152 EP 1152 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33501151 ER PT J AU HENSKE, EP OZELIUS, L GUSELLA, JF HAINES, JL KWIATKOWSKI, DJ AF HENSKE, EP OZELIUS, L GUSELLA, JF HAINES, JL KWIATKOWSKI, DJ TI DETAILED GENETIC AND PHYSICAL MAPPING OF THE TUBEROUS SCLEROSIS REGION OF 9Q34 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. 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 SEP PY 1993 VL 53 IS 3 SU S BP 1303 EP 1303 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33501304 ER PT J AU MCCORMICK, MK NARANJO, C CHURCH, D CAMPBELL, E MARRONE, B DEAVEN, L MOYZIS, R BUCKLER, A AF MCCORMICK, MK NARANJO, C CHURCH, D CAMPBELL, E MARRONE, B DEAVEN, L MOYZIS, R BUCKLER, A TI IDENTIFICATION OF EXPRESSED SEQUENCES ON HUMAN CHROMOSOME-21 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. LOS ALAMOS NATL LAB,CTR HUMAN GENOME STUDIES,LOS ALAMOS,NM 87544. LOS ALAMOS NATL LAB,DIV LIFE SCI,LOS ALAMOS,NM 87544. UNIV CALIF IRVINE,DEPT BIOCHEM,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 SEP PY 1993 VL 53 IS 3 SU S BP 1327 EP 1327 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33501328 ER PT J AU MURRELL, J BUCKLER, A MCCORMICK, MK AF MURRELL, J BUCKLER, A MCCORMICK, MK TI PHYSICAL MAPPING OF HUMAN-CHROMOSOME REGION-9Q34 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT 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 SEP PY 1993 VL 53 IS 3 SU S BP 1334 EP 1334 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33501332 ER PT J AU SLAUGENHAUPT, SA BLUMENFELD, A LIEBERT, CB MULL, J LUCENTE, DE MONAHAN, M BUCKLER, AJ MCCORMICK, MK BREAKEFIELD, XO GUSELLA, JF AF SLAUGENHAUPT, SA BLUMENFELD, A LIEBERT, CB MULL, J LUCENTE, DE MONAHAN, M BUCKLER, AJ MCCORMICK, MK BREAKEFIELD, XO GUSELLA, JF TI PHYSICAL MAPPING OF THE FAMILIAL DYSAUTONOMIA GENE REGION OF HUMAN CHROMOSOME-9 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NR 1 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 SEP PY 1993 VL 53 IS 3 SU S BP 1360 EP 1360 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33501360 ER PT J AU TIVOL, E SHALISH, C BREAKEFIELD, XO AF TIVOL, E SHALISH, C BREAKEFIELD, XO TI A RAPID PCR-BASED METHOD FOR SCREENING THE HUMAN MAOA GENE FOR EXONIC MUTATIONS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,NEUROSCI UNIT,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 SEP PY 1993 VL 53 IS 3 SU S BP 1632 EP 1632 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA LW335 UT WOS:A1993LW33501632 ER PT J AU SHARKEYMATHIS, PK KAUFFMAN, CA GRAYBILL, JR STEVENS, DA HOSTETLER, JS CLOUD, G DISMUKES, WE BENNETT, J BRADSHER, RW CHAPMAN, SW FISHER, JF KERKERING, TM MEDOFF, G PERFECT, JR PANKEY, GA REX, JH SAAG, MS AF SHARKEYMATHIS, PK KAUFFMAN, CA GRAYBILL, JR STEVENS, DA HOSTETLER, JS CLOUD, G DISMUKES, WE BENNETT, J BRADSHER, RW CHAPMAN, SW FISHER, JF KERKERING, TM MEDOFF, G PERFECT, JR PANKEY, GA REX, JH SAAG, MS TI TREATMENT OF SPOROTRICHOSIS WITH ITRACONAZOLE SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID PRIMARY PULMONARY SPOROTRICHOSIS; HIGH-DOSE KETOCONAZOLE; SPOROTHRIX-SCHENCKII; CUTANEOUS SPOROTRICHOSIS; SYSTEMIC SPOROTRICHOSIS; FUNGAL-INFECTIONS; AMPHOTERICIN-B; THERAPY; ARTHRITIS; EMPHASIS AB PURPOSE: To describe the clinical presentation and outcomes of treatment with itraconazole in patients with sporotrichosis. METHODS: A culture for Sporothrix schenckii or compatible histopathology was required for inclusion in the study. Patients with both cutaneous and systemic sporotrichosis were treated. Patients received from 100 to 600 mg of itraconazole daily for 3 to 18 months. Patients were classified as responders or nonresponders. Responders were further classified as remaining on treatment, relapsed, or free of disease. Nonresponders included patients who failed to respond or progressed during treatment with itraconazole. RESULTS: Twenty-seven patients (mean age: 53 years) were treated with 30 courses of itraconazole. Diabetes mellitus and alcoholism were present in eight and seven patients, respectively. Sites of involvement included lymphocutaneous alone in 9 patients, articular/osseous in 15 (multifocal in 3), and lung in 3. Prior therapy was unsuccessful in 11 patients. Among the 30 courses, there were 25 responders and 5 nonresponders. All 5 nonresponders received at least 200 mg daily of itraconazole for durations that ranged from 6 to 18 months. Of the 25 responders, 7 relapsed 1 to 7 months after treatment durations of 6 to 18 months. Of the 7 who relapsed, 2 are responding to a second course. One responder was lost to follow-up after 10 months of treatment with itraconazole. Of the re 17 responders, 3 remain on treatment, and 14 are free of disease over follow-up durations of 6 to 42 months (mean: 17.6 months). Itraconazole was well tolerated with few side effects noted. CONCLUSIONS: These results document the efficacy of itraconazole in the treatment of cutaneous and systemic sporotrichosis. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. DEPT VET AFFAIRS MED CTR,ANN ARBOR,MI. UNIV MICHIGAN,SCH MED,ANN ARBOR,MI 48104. SANTA CLARA VALLEY MED CTR,SAN JOSE,CA 95128. STANFORD UNIV,SCH MED,SAN JOSE,CA. UNIV ALABAMA,BIRMINGHAM,AL 35294. NIAID,MYCOSES STUDY GRP,BETHESDA,MD 20892. UNIV ARKANSAS MED SCI HOSP,LITTLE ROCK,AR 72205. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. MED COLL GEORGIA,AUGUSTA,GA 30912. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. DUKE UNIV,MED CTR,DURHAM,NC 27710. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA 70121. RP SHARKEYMATHIS, PK (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV INFECT DIS,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIAID NIH HHS [N01-AI-52562] NR 36 TC 87 Z9 88 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 SEP PY 1993 VL 95 IS 3 BP 279 EP 285 DI 10.1016/0002-9343(93)90280-3 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA LX046 UT WOS:A1993LX04600007 PM 8396321 ER PT J AU NUSSBAUM, SR YOUNGER, J VANDEPOL, CJ GAGEL, RF ZUBLER, MA CHAPMAN, R HENDERSON, IC MALLETTE, LE AF NUSSBAUM, SR YOUNGER, J VANDEPOL, CJ GAGEL, RF ZUBLER, MA CHAPMAN, R HENDERSON, IC MALLETTE, LE TI SINGLE-DOSE INTRAVENOUS THERAPY WITH PAMIDRONATE FOR THE TREATMENT OF HYPERCALCEMIA OF MALIGNANCY - COMPARISON OF 30-MG, 60-MG, AND 90-MG DOSAGES SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID CANCER-ASSOCIATED HYPERCALCEMIA; HORMONE-LIKE PEPTIDE; PARATHYROID-HORMONE; HUMORAL HYPERCALCEMIA; AMINOHYDROXYPROPYLIDENE DIPHOSPHONATE; BONE-RESORPTION; APD; BISPHOSPHONATES; MITHRAMYCIN; ETIDRONATE AB PURPOSE: To determine the efficacy, dose-response relationship, and safety of 30, 60, and 90 mg of a single intravenous dose of an aminobisphosphonate, pamidronate (APD), for the treatment of moderate to severe hypercalcemia of PATIENTS AND METHODS: Patients with histologically proven cancer and a corrected serum calcium level of at least 12.0 mg/dL after 48 hours of normal saline hydration were enrolled in a double-blind, multicenter, randomized clinical trial. Pamidronate in 30-, 60-, or 90-mg doses was administered as a single 24-hour infusion. Serum calcium corrected for albumin, urine hydroxyproline, and calcium excretion, and serum parathyroid hormone (PTH) (1-84) were determined before and after pamidronate therapy. RESULTS: Thirty-two men and 18 women entered the study. A dose-response relationship for normalization of corrected serum calcium was seen after pamidronate administration. Corrected serum calcium normalized in 40% of patients who received 30 mg, in 61% of patients who received 60 mg, and in 100% of patients who received 90 mg of pamidronate. The decline in the serum calcium level was associated with decreased osteoclastic skeletal resorption evidenced by a decrease in urine calcium and hydroxyproline excretion. Among those with a normalization corrected serum calcium level the mean (median) duration of normalization of the corrected serum calcium value was 9.2 (4),13.3 (5), and 10.8 (6) days in the 30-, 60-, and 90-mg treatment groups, respectively. The response of hypercalcemia to pamidronate was not significantly influenced by the presence of skeletal metastases. PTH 1-84, suppressed in patients on entry into this study, increased to a greater extent in those patients with osteolytic skeletal metastases compared with those with humoral hypercalcemia of malignancy. Clinical improvement, including improved mental status and decreased anorexia, accompanied the decline in the corrected serum calcium level in all three treatment groups. Side effects included low-grade fever, asymptomatic hypocalcemia, hypomagnesemia, and hypophosphatemia. CONCLUSIONS: A single-dose infusion of 60 to 90 mg of pamidronate was highly effective and well tolerated and normalized corrected serum calcium in nearly all patients (61% to 100%) with hypercalcemia of malignancy. C1 MASSACHUSETTS GEN HOSP,MED RES LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CIBA GEIGY CORP,PHARMACEUT,SUMMIT,NJ 07901. BAYLOR COLL MED,HOUSTON,TX 77030. VET ADM MED CTR,DEPT ENDOCRINE,HOUSTON,TX 77211. HENRY FORD HOSP,DEPT ENDOCRINE,DETROIT,MI 48202. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 35 TC 131 Z9 134 U1 0 U2 5 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 SEP PY 1993 VL 95 IS 3 BP 297 EP 304 DI 10.1016/0002-9343(93)90282-T PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA LX046 UT WOS:A1993LX04600009 PM 8368227 ER PT J AU KAYSEN, GA AF KAYSEN, GA TI THE NEPHROTIC SYNDROME - PATHOGENESIS AND CONSEQUENCES - THE HOMEOSTATIC AND PATHOGENIC CONSEQUENCES OF PROTEINURIA - INTRODUCTION SO AMERICAN JOURNAL OF NEPHROLOGY LA English DT Editorial Material C1 UNIV CALIF DAVIS,SCH MED,DEPT MED,DIV NEPHROL,RENAL BIOCHEM LAB,DAVIS,CA. US DEPT VET AFFAIRS,NO CALIF SYST CLIN,PLEASANT HILL,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0250-8095 J9 AM J NEPHROL JI Am. J. Nephrol. PD SEP-OCT PY 1993 VL 13 IS 5 BP 309 EP 310 DI 10.1159/000168644 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA MR955 UT WOS:A1993MR95500001 PM 8116682 ER PT J AU HUTCHISON, FN AF HUTCHISON, FN TI HORMONAL MODULATION OF PROTEINURIA IN THE NEPHROTIC SYNDROME SO AMERICAN JOURNAL OF NEPHROLOGY LA English DT Article DE PROTEINURIA; NEPHROTIC SYNDROME; RENIN; ANGIOTENSIN; PROSTAGLANDINS; THROMBOXANE; KALLIKREIN; BRADYKININ; DIETARY PROTEIN; CONVERTING ENZYME INHIBITOR ID CONVERTING-ENZYME-INHIBITION; PASSIVE HEYMANN NEPHRITIS; DIETARY-PROTEIN; RENAL HEMODYNAMICS; ALBUMIN SYNTHESIS; ANGIOTENSIN-II; AMINONUCLEOSIDE NEPHROSIS; DIABETIC GLOMERULOPATHY; THROMBOXANE SYNTHESIS; RECEPTOR ANTAGONIST AB Proteinuria is the primary manifestation of a variety of glomerular diseases which are characterized clinically by the nephrotic syndrome. In many cases there is little effective treatment for the primary disease process. However, reduction of proteinuria can frequently improve the hypoalbuminemia, hyperlipidemia and edema which are responsible for the morbidity of the nephrotic syndrome. Proteinuria can be reduced in nephrotic humans and experimental animal models by restriction of dietary protein intake, nonsteroidal anti-inflammatory drug, and by angiotensin-converting enzyme inhibitors. Each of these therapies modifies the activity of locally acting glomerular hormones, autocoids, suggesting that there is a component of proteinuria which is hormonally mediated. The effects of dietary protein, nonsteroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors on nephrotic proteinuria and their potential hormonal mechanisms of action is the subject of this review. C1 MED UNIV S CAROLINA,DEPT INTERNAL MED,DIV NEPHROL,CHARLESTON,SC. RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC. FU NIDDK NIH HHS [DK43186] NR 80 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0250-8095 J9 AM J NEPHROL JI Am. J. Nephrol. PD SEP-OCT PY 1993 VL 13 IS 5 BP 337 EP 346 DI 10.1159/000168648 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA MR955 UT WOS:A1993MR95500005 PM 8116686 ER PT J AU KAYSEN, GA AF KAYSEN, GA TI PLASMA COMPOSITION IN THE NEPHROTIC SYNDROME SO AMERICAN JOURNAL OF NEPHROLOGY LA English DT Review DE ONCOTIC PRESSURE; ALBUMIN; TRANSFERRIN; LIPOPROTEINS; ANALBUMINEMIA; FIBRINOGEN; PROTEIN SYNTHESIS ID LOW-DENSITY LIPOPROTEIN; COLLOID OSMOTIC-PRESSURE; APOLIPOPROTEIN GENE-EXPRESSION; MOLECULAR-WEIGHT PROTEINS; RENAL-VEIN THROMBOSIS; MINIMAL-CHANGE; ANALBUMINEMIC RATS; ALBUMIN SYNTHESIS; DIETARY-PROTEIN; HEYMANN NEPHRITIS AB The nephrotic syndrome is a consequence of urinary loss of intermediate sized plasma proteins and the resulting homeostatic responses to those losses. Plasma protein composition is changed greatly. Intermediate sized proteins, including albumin, transferrin, IgG, hormone binding proteins, and low molecular weight inhibitors of the clotting cascade, are lost in the urine and their concentration in plasma reduced. Synthesis of many proteins secreted by the liver is increased either at the level of transcription or posttranscriptionally. Synthesis of several liver-derived proteins is increased in the absence of their urinary loss, suggesting that hypoalbuminemia or reduced plasma oncotic pressure (pi) stimulates the production or reduces the rate of catabolism of these proteins. Their plasma levels, including those of lipoproteins and elements of the coagulation cascade, are increased. Plasma pi falls and plasma viscosity increases because of the replacement of intermediate sized plasma proteins by larger ones. The plasma concentration of several proteins lost in the urine but not secreted by the liver, such as erythropoietin and IgG, are not defended by increased synthesis, suggesting that increased synthesis of plasma proteins is primarily confined to the liver. Loss of both liver-derived and nonliver-derived proteins may cause reduced immunity, anemia, and deficiency syndromes. Urinary loss of albumin alone is not responsible for decreased plasma pi. The relationship between plasma protein concentration and pi is greatly disturbed in nephrotic rats. In contrast, the relationship between pi and plasma protein concentration is nearly the same in rats with hereditary analbuminemia (NAR) and normal rats, despite the absence of albumin from the plasma of NAR. When proteinuria is induced in NAR the relationship between plasma protein concentration and pi becomes identical to that in nephrotic animals, although no albumin was lost in the urine of NAR. C1 UNIV CALIF DAVIS,SCH MED,DEPT MED,DIV NEPHROL,RENAL BIOCHEM LAB,DAVIS,CA. US DEPT VET AFFAIRS,NO CALIF SYST CLIN,PLEASANT HILL,CA. FU NIDDK NIH HHS [R01 DK 42297] NR 147 TC 35 Z9 37 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0250-8095 J9 AM J NEPHROL JI Am. J. Nephrol. PD SEP-OCT PY 1993 VL 13 IS 5 BP 347 EP 359 DI 10.1159/000168649 PG 13 WC Urology & Nephrology SC Urology & Nephrology GA MR955 UT WOS:A1993MR95500006 PM 8116687 ER PT J AU GONZALEZ, RG GUIMARAES, AR SACHS, GS ROSENBAUM, JF GARWOOD, M RENSHAW, PF AF GONZALEZ, RG GUIMARAES, AR SACHS, GS ROSENBAUM, JF GARWOOD, M RENSHAW, PF TI MEASUREMENT OF HUMAN BRAIN LITHIUM IN-VIVO BY MR SPECTROSCOPY SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE DRUGS, PSYCHOACTIVE; MAGNETIC RESONANCE, SPECTROSCOPY; MAGNETIC RESONANCE, EXPERIMENTAL; BRAIN, MEASUREMENTS; BRAIN, MAGNETIC RESONANCE ID MAGNETIC-RESONANCE SPECTROSCOPY; NMR-SPECTROSCOPY; SURFACE-COIL; METABOLITES; CARBONATE; ILLNESS AB PURPOSE: To quantify lithium in the human brain. METHODS: A Li-7 MR spectroscopy method was developed with special features for high precision including: a) sampling a large cerebral volume to maximize the signal-to-noise ratio; b) adiabatic excitation pulses to ensure uniform spin nutation; c) morphometric analysis of the MR images of the sampled cerebrum; d) a mathematical model derived from empirical data to correct for receiver inhomogeneity effects; and e) a long interpulse delay to eliminate errors arising from uncertain Tl values. RESULTS: A theoretical precision of 5.2% and an accuracy of better than 7.2% in someone with a brain lithium level of 1.0 mEq per liter of cerebral volume and precision and accuracy of 6.8 and 8.6%, respectively, in someone with 0.5 mEq/L brain lithium was calculated. This level of precision was surpassed in phantoms and patients. Brain lithium in 10 patients treated with lithium carbonate varied from 0.52 to 0.87 mEq/L (mean = 0.58 mEq/L; SD = 0.17 mEq/L). Brain-to-serum lithium ratios varied from 0.50 to 0.97 mEq/L (mean = 0.77 mEq/L; SD = 0.14 mEq/L). Substantial variation in brain lithium was observed in patients with similar serum lithium. CONCLUSIONS: A highly reliable method to quantify human brain lithium by Li-7 MR spectroscopy has been implemented. Unexpected variability in brain versus serum levels of lithium was detected in patients with bipolar disease. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,CTR MGH NMR,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. MIT,DEPT NUCL ENGN,RADIOL SCI PROGRAM,CAMBRIDGE,MA 02139. UNIV MINNESOTA,SCH MED,CTR MAGNET RESONANCE RES,MINNEAPOLIS,MN 55455. RP GONZALEZ, RG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,DIV NEURORADIOL,FRUIT ST,BOSTON,MA 02114, USA. FU NIA NIH HHS [AG10679] NR 25 TC 37 Z9 37 U1 2 U2 5 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD SEP-OCT PY 1993 VL 14 IS 5 BP 1027 EP 1037 PG 11 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA LY600 UT WOS:A1993LY60000001 PM 8237676 ER PT J AU SCHOFIELD, DE YUNIS, EJ FLETCHER, JA AF SCHOFIELD, DE YUNIS, EJ FLETCHER, JA TI CHROMOSOME-ABERRATIONS IN MESOBLASTIC NEPHROMA SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID FLOW CYTOMETRIC ANALYSIS; CLEAR CELL-SARCOMA; RENAL TUMORS; CYTOGENETIC ANALYSIS; FIBRO-SARCOMA; SOLID TUMORS; WILMS-TUMOR; DNA CONTENT; INFANCY; KIDNEY AB Mesoblastic nephroma (MN) is the most common renal tumor diagnosed in infancy. Histologically, MNs are designated as classic, cellular, or mixed type based upon variations in cellularity. Recent karyotypic reports have suggested that extra copies of chromosome 11 are a nonrandom occurrence in MNs. We analyzed nuclear suspensions prepared from a group of 17 formalin-fixed, paraffin-embedded tumors to determine the possible role of chromosome 11 copy number in the genesis of MN. Extra copies of D11Z1 (a probe for the centromeric region of chromosome 11) were detected in seven out of 10 MNs with cellular or mixed histology, whereas each of six classic histology MNs were disomic for D11Z1 (P < 0.05). Additional fluorescence in situ hybridization studies utilizing the probes for the a satellite, centromeric regions of chromosomes 7, 8, 9, 12, 17, and 20 were then carried out on all cases with cellular or mixed histology. Five out of 10 cellular or mixed MNs bad extra copies of D8Z1, and four out of 10 bad extra copies of D17Z1, suggesting that gains of chromosomes 8 and 17 may be additional nonrandom cytogenetic events associated with the evolution of MNs. DNA aneuploidy, as determined by image analysis, was detected in three tumors: all bad greater than four chromosomal aberrations documented by fluorescence in situ hybridization. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP PITTSBURGH,DEPT PATHOL,PITTSBURGH,PA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. RP SCHOFIELD, DE (reprint author), CHILDRENS HOSP MED CTR,DEPT PATHOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [1K11CA01498-02] NR 44 TC 54 Z9 54 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 SEP PY 1993 VL 143 IS 3 BP 714 EP 724 PG 11 WC Pathology SC Pathology GA LW898 UT WOS:A1993LW89800008 PM 8395771 ER PT J AU POWELL, PP KLAGSBRUN, M ABRAHAM, JA JONES, RC AF POWELL, PP KLAGSBRUN, M ABRAHAM, JA JONES, RC TI EOSINOPHILS EXPRESSING HEPARIN-BINDING EGF-LIKE GROWTH-FACTOR MESSENGER-RNA LOCALIZE AROUND LUNG MICROVESSELS IN PULMONARY-HYPERTENSION SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID INSITU HYBRIDIZATION; FACTOR-ALPHA; HYPEROXIA; CELLS; LYMPHOCYTES; ASTHMA; PRECURSOR; RECEPTOR; ARTERIES; EXPOSURE AB In pulmonary hypertension, induced in rats breathing high oxygen at normobaric pressure, vascular cell hypertrophy and hyperplasia thicken the walls of lung microvessels (15-100 mum in diameter). Over a 28-day time course, new contractile cells develop from intimal precursor smooth muscle cells, which include intermediate cells and interstitial fibroblasts. Cell labeling studies in vivo have shown that these cells proliferate more than other vascular cells and that most of this activity occurs between 4 and 7 days of hyperoxia. The growth factors responsible for this proliferation are unknown. In the present study, we investigate the expression of mRNA for the epidermal growth factor (EGF)-related protein, heparin-binding EGF-like growth factor (HB-EGF), a newly discovered mitogen for fibroblasts and smooth muscle cells. Northern analysis shows HB-EGF mRNA levels to be low in normal lung but increased 100-fold by day 7 of hyperoxia. In situ hybridization identifies a select group of cells expressing HB-EGF mRNA. In normal lung, hybridizing cells are randomly distributed in the alveolar wall and space. By day 7, they increase in number and cluster around the microvessels. Histochemical techniques identify cells expressing HB-EGF mRNA as eosinophils. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT SURG RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. SCIOS NOVA INC,MT VIEW,CA. FU NHLBI NIH HHS [HL34552] NR 32 TC 70 Z9 71 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 SEP PY 1993 VL 143 IS 3 BP 784 EP 793 PG 10 WC Pathology SC Pathology GA LW898 UT WOS:A1993LW89800014 PM 8362977 ER PT J AU HARRINGER, W FERNANDEZDELCASTILLO, C RATTNER, DW GUERRERO, JL WARSHAW, AL VLAHAKES, GJ AF HARRINGER, W FERNANDEZDELCASTILLO, C RATTNER, DW GUERRERO, JL WARSHAW, AL VLAHAKES, GJ TI EVALUATION AND VALIDATION OF MICROSPHERE TECHNIQUE FOR DETERMINATION OF PANCREATIC BLOOD-FLOW SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE DOGS; ORGAN BLOOD FLOW FULTRASONIC FLOW PROBE; PANCREATIC EMBOLIZATION ID CANINE PANCREAS; LEFT LOBE AB The purpose of this study was to evaluate the radiolabeled microsphere technique for pancreatic blood flow measurements. Using a canine model with an isolated pancreatic circulation, we assessed the shunting of 11- and 15-mum-diam microspheres in the pancreas, correlated pancreatic blood flow measurements obtained with the microsphere technique with those made with an ultrasonic flow probe, and determined the effects of high doses of microspheres on pancreatic blood flow and its measurement. Microspheres of 11 mum demonstrate significant shunting through the pancreatic microcirculation with underestimation of pancreatic blood flow of approximately 10% compared with results obtained with 15-mum microspheres. There is a close linear relationship between flow results obtained with 15-mum microspheres and with an ultrasonic flow probe for both the resting (r = 0.85) and the secretin-stimulated pancreas (r = 0.97). Left atrial injections of very large doses of 15-mum microspheres (50 x 10(6)) caused an acute transient reduction of pancreatic blood flow (to 39% of baseline flow) with a return to baseline values within 2 min. The accuracy of flow results and absence of physiological changes after repeated injections support the use of 15-mum microspheres for pancreatic blood flow measurements. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,DEPT SURG,BOSTON,MA 02114. RI Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 NR 28 TC 7 Z9 7 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 SEP PY 1993 VL 265 IS 3 BP G587 EP G594 PN 1 PG 8 WC Physiology SC Physiology GA MA184 UT WOS:A1993MA18400077 PM 8214079 ER PT J AU MARKOWITZ, AJ WU, GD BIRKENMEIER, EH TRABER, PG AF MARKOWITZ, AJ WU, GD BIRKENMEIER, EH TRABER, PG TI THE HUMAN SUCRASE-ISOMALTASE GENE DIRECTS COMPLEX PATTERNS OF GENE-EXPRESSION IN TRANSGENIC MICE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE TRANSCRIPTION; DIFFERENTIATION; INTESTINE; COLON ID MOUSE SMALL-INTESTINE; EPITHELIAL-CELL TYPES; HORMONE FUSION GENES; CRYPT-VILLUS AXIS; ACID-BINDING-PROTEIN; RAT SMALL-INTESTINE; MESSENGER-RNA; PANETH CELLS; DIFFERENTIATION; ORIGIN AB Sucrase-isomaltase (SI) is an enterocyte-specific gene that is expressed in complex developmental and spatial patterns. In this study, we examine the ability of regulatory elements within the human SI (hSI) gene to direct appropriate cell lineage and spatial patterns of expression in transgenic mice. Transgenic mouse lines were established using a construct containing bases -3424 to +54 of the hSI gene linked to the human growth hormone (hGH) structural gene. In each transgenic line, hGH mRNA and protein were expressed only in the small intestine and colon. In contrast to the endogenous mouse SI (mSI) gene, which was expressed along the entire length of the small intestine, hGH mRNA expression was predominantly found in the distal jejunum and ileum, with very low levels in more proximal portions of the small intestine. However, the pattern of transgene expression along the small intestinal crypt-villus axis was identical to the pattern of the endogenous mSI gene. These results suggest that regulatory elements necessary for intestine-specific transcription and differential expression along the intestinal crypt-villus axis are included in the 5'-flanking region of the hSI gene. Furthermore, these data suggest that different DNA regulatory regions regulate transcription along the horizontal intestinal axis. In the colon, there was aberrant expression of hGH in a subpopulation of enteroendocrine cells that contained peptide tyrosine tyrosine (PYY). This suggests that there are DNA regulatory elements, missing in the transgene construct, which normally suppress expression of the endogenous mSI gene in these cells. Taken together, these findings define the SI gene as a useful model for studies of differentiation, cell lineage determination, and mechanisms of complex spatial gene expression in the intestine. C1 UNIV PENN,SCH MED,DEPT INTERNAL MED,DIV GASTROENTEROL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. JACKSON LAB,BAR HARBOR,ME 04609. FU NIDDK NIH HHS [DK-41393, DK-44621] NR 36 TC 63 Z9 63 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 SEP PY 1993 VL 265 IS 3 BP G526 EP G539 PN 1 PG 14 WC Physiology SC Physiology GA MA184 UT WOS:A1993MA18400070 PM 8214074 ER PT J AU CIGARROA, JE ISSELBACHER, EM DESANCTIS, RW EAGLE, KA AF CIGARROA, JE ISSELBACHER, EM DESANCTIS, RW EAGLE, KA TI MEDICAL PROGRESS - DIAGNOSTIC-IMAGING IN THE EVALUATION OF SUSPECTED AORTIC DISSECTION - OLD STANDARDS AND NEW DIRECTIONS (REPRINTED FROM THE NEW-ENGLAND JOURNAL MED, VOL 328, PG 35, 1993) SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Reprint ID TWO-DIMENSIONAL ECHOCARDIOGRAPHY; TRANSESOPHAGEAL ECHOCARDIOGRAPHY; COMPUTED-TOMOGRAPHY; THORACIC AORTA; ANEURYSM; MANAGEMENT; CT AB Acute aortic dissection is a life-threatening condition, and its prompt diagnosis remains essential for successful management. Although early mortality may be as high as 1 percent per hour [1] among untreated patients, survival can be improved by the rapid institution of appropriate medical or surgical therapy (or both). The Stanford classification system [2] divides aortic dissections anatomically into two types on the basis of location. A dissection in which there is involvement of the ascending aorta, regardless of the site of entry, is defined as type A (this includes De Bakey [3] types I and II and is often described as a proximal dissection). All aortic dissections that do not involve the ascending aorta are defined as type B (these include De Bakey type III and may be referred to as distal dissections). Over the past several decades it has become clear that most patients with type A dissections require urgent surgical repair, whereas those with uncomplicated type B dissections can be treated successfully with medical therapy alone. The optimal care of patients with aortic dissection requires that the diagnosis be made promptly and that its site of origin and extent be identified as rapidly as possible. Furthermore, in the age of thrombolytic therapy for acute myocardial infarction it is crucial to exclude aortic dissection among patients presenting with syndromes involving chest pain, since the administration of such agents to patients with aortic dissection can be catastrophic. RP CIGARROA, JE (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,ACC 469,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 58 TC 9 Z9 9 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 SEP PY 1993 VL 161 IS 3 BP 485 EP 493 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LW474 UT WOS:A1993LW47400003 ER PT J AU BHALLA, M GRILLO, HC MCLOUD, TC SHEPARD, JAO WEBER, AL MARK, EJ AF BHALLA, M GRILLO, HC MCLOUD, TC SHEPARD, JAO WEBER, AL MARK, EJ TI IDIOPATHIC LARYNGOTRACHEAL STENOSIS - RADIOLOGIC FINDINGS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID TRACHEA AB OBJECTIVE. Acquired nonneoplastic laryngotracheal stenosis can be either focal or diffuse. Diffuse tracheal stenosis is caused by sarcoidosis, tuberculosis, histoplasmosis, relapsing polychondritis, tracheopathia osteoplastica, and Wegener's granulomatosis. Focal tracheal stenosis, on the other hand, usually results from placement of an endotracheal or tracheostomy tube or from previous neck trauma. At our institution, since 1971, we have seen 49 cases of focal laryngotracheal stenosis that could not be attributed clinically or histologically to any one of the aforementioned causes. The purpose of this study was to study the radiologic features of these idiopathic laryngotracheal stenoses. MATERIALS AND METHODS. A retrospective review of records showed that radiologic studies were still available in only 15 of the 49 patients with idiopathic laryngotracheal stenoses. All 15 patients had radiographs and plain tomograms, and one patient had a CT scan of the neck. Three radiologists reviewed all the images. RESULTS. The radiologic appearance was variable: the stenoses were from 2 to 4 cm long with a lumen between 3 and 5 mm in diameter at the narrowest portion. The narrowing was concentric and shaped like an hourglass in eight patients (53%) and was eccentric in the other seven (47%). The margins of the stenosis were smooth in nine patients (60%) and irregular and lobulated in six patients (40%). A dominant mass measuring approximately 1 cm in diameter was present in two patients (13%). No evidence of calcification or ossification was seen. CONCLUSION. Idiopathic laryngotracheal stenosis produces focal stenosis of the cervical part of the trachea, 2 to 4 cm long. The lumen is severely compromised, measuring no more than 5 mm in diameter at its narrowest portion. The stenosis can be concentric or eccentric and can have either smooth or lobulated margins. Special attention should be paid to the airways when chest radiographs of patients with a history of prolonged dyspnea and wheezing are reviewed.The prevalence of focal stenosis of the larynx and the upper part of the trachea due to tracheal intubation has declined since the introduction of low-pressure, high-volume retention cuffs. Therefore, idiopathic laryngotracheal stenosis should be considered in the differential diagnosis in patients with focal narrowing of the airway. C1 MASSACHUSETTS GEN HOSP,DEPT THORAC SURG,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP BHALLA, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,ELLISON 234,32 FRUIT ST,BOSTON,MA 02114, USA. NR 9 TC 10 Z9 11 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 SEP PY 1993 VL 161 IS 3 BP 515 EP 517 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LW474 UT WOS:A1993LW47400008 PM 8352095 ER PT J AU GERVAIS, DA WHITMAN, GJ CHEW, FS AF GERVAIS, DA WHITMAN, GJ CHEW, FS TI MULTILOCULAR CYST OF THE KIDNEY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID NEPHROMA C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 4 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 SEP PY 1993 VL 161 IS 3 BP 600 EP 600 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LW474 UT WOS:A1993LW47400030 PM 8352115 ER PT J AU LAZAR, E ROSENTHAL, DI JUPITER, J AF LAZAR, E ROSENTHAL, DI JUPITER, J TI FREE VASCULARIZED FIBULAR GRAFTS - RADIOGRAPHIC EVIDENCE OF REMODELING AND HYPERTROPHY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID BONE-GRAFTS; RECONSTRUCTION; ALLOGRAFTS AB OBJECTIVE. A study was undertaken to determine the growth potential and radiographic appearance of a free vascularized fibular graft as it responds to the mechanical and physiologic features of its new environment. MATERIALS AND METHODS. In a 10-year period, 30 patients underwent reconstruction of a large skeletal defect with a vascularized fibular graft. Radiographic studies were adequate for assessing sequential changes in 21 patients. Hypertrophy was evaluated by serial measurements of the periosteal and endosteal dimensions and was assessed with respect to age, sex, duration and location of the graft, the indication for reconstruction, and fixation apparatus. RESULTS. Hypertrophy of vascularized bone grafts is not rare. Among 21 vascularized fibular grafts, a measurable degree of hypertrophy was found in eight. Hypertrophy was caused by periosteal formation of new bone. The amount of hypertrophy could be considerable; in some cases it reached 2 cm of new cortical bone, resulting in an unusual radiographic appearance of marked cortical thickening. The amount of hypertrophy was greatest in young males, but was independent of diagnosis and site, and could be seen even in grafts bridged by metallic plates. CONCLUSION. Hypertrophy of vascularized bone grafts is a relatively frequent finding and has distinctive radiographic features. It is unclear why hypertrophy occurs to a much greater extent in some grafts than in others. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,BOSTON,MA 02114. NR 12 TC 21 Z9 23 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 SEP PY 1993 VL 161 IS 3 BP 613 EP 615 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LW474 UT WOS:A1993LW47400033 PM 8352118 ER PT J AU LEE, MJ MUELLER, PR VANSONNENBERG, E DAWSON, SL DAGOSTINO, H SAINI, S CATS, AM AF LEE, MJ MUELLER, PR VANSONNENBERG, E DAWSON, SL DAGOSTINO, H SAINI, S CATS, AM TI CT-GUIDED CELIAC GANGLION BLOCK WITH ALCOHOL SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Editorial Material ID PLEXUS AB Celiac ganglion block has been performed without radiologic guidance by surgeons or anesthetists since it was first described by Kappis [1] in 1914. Radiographic guidance for celiac block was first reported in the 1950s [2], and more recently, radiologists have used CT to guide needle placement [3-5]. With CT guidance, more directed positioning of the needle is possible, allowing alcohol to be deposited in the specific ganglion areas. This article reviews our collective experience with CT-guided celiac ganglion block. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. UNIV CALIF SAN DIEGO,DEPT RADIOL,SAN DIEGO,CA 92103. RP LEE, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 7 TC 30 Z9 32 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 SEP PY 1993 VL 161 IS 3 BP 633 EP 636 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LW474 UT WOS:A1993LW47400038 PM 8352122 ER PT J AU WHEATLEY, JR MEZZANOTTE, WS TANGEL, DJ WHITE, DP AF WHEATLEY, JR MEZZANOTTE, WS TANGEL, DJ WHITE, DP TI INFLUENCE OF SLEEP ON GENIOGLOSSUS MUSCLE ACTIVATION BY NEGATIVE-PRESSURE IN NORMAL MEN SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID UPPER AIRWAY PRESSURE; RESPIRATORY ACTIVITY; RESPONSES; REFLEX; APNEA; OCCLUSION; NASAL; WAKEFULNESS; MECHANISM; PATTERN AB An important mechanism controlling genioglossus (GG) muscle activity is the reflex response to negative airway pressure. We hypothesize that this reflex response may be lost during sleep and believe that this loss may be important in the pathogenesis of airway collapse during sleep. Thus, we determined the effect of non-rapid eye movement (NREM) sleep on the GG electromyogram (EMG) response to brief (0.2 to 0.6 s) episodes of negative pressure generation (NPG) in the upper airway of six normal subjects. Up to 100 NPGs (mean 58 +/- 12) were recorded both awake and during stable NREM sleep. During wakefulness, the change in GG moving time average EMG from basal to peak levels (during NPG) was 17.1 +/- 2.5 au (a 154 +/- 22% increase above basal levels). This response was markedly reduced during NREM sleep (2.7 +/- 1.2 au; p < 0.01). The latency of the GG EMG response was 53.8 +/- 11.5 ms during wakefulness (n = 6), but much longer during sleep (132.7 +/- 24.5 ms; n = 3; p < 0.03). We conclude that in normal subjects (1) the GG muscle responds to negative airway pressure by reflex activation during wakefulness, and (2) this reflex activation is reduced or lost during NREM sleep. We speculate that loss of this mechanism during sleep may contribute to pharyngeal collapse in obstructive apnea patients. C1 NATL JEWISH CTR IMMUNOL & RESP MED,DENVER,CO. UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80262. RP WHEATLEY, JR (reprint author), DENVER VA MED CTR,DIV PULM,1055 CLERMONT ST,DENVER,CO 80220, USA. NR 38 TC 139 Z9 140 U1 0 U2 2 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 SEP PY 1993 VL 148 IS 3 BP 597 EP 605 PG 9 WC Respiratory System SC Respiratory System GA LW465 UT WOS:A1993LW46500009 PM 8368629 ER PT J AU CHRISTIANI, DC KERN, DG AF CHRISTIANI, DC KERN, DG TI ASTHMA RISK AND OCCUPATION AS A RESPIRATORY THERAPIST SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID HEALTH-CARE WORKERS; INFECTION; GLUTARALDEHYDE; SUBSENSITIVITY; PRECIPITANTS; RHINOVIRUS; EXPOSURE; LATEX AB In the modern hospital environment, many health care workers are exposed to hazardous substances. Among these hazards are respiratory sensitizers, irritants, and infectious agents. A previous cross-sectional study of Rhode Island respiratory therapists reported an excess risk of asthma after entry into that profession. Before the results of that study were published, we conducted a confirmatory mailed questionnaire survey of 2,086 Massachusetts respiratory therapists and 2,030 physical therapists and physical therapy assistants. Neither the survey questionnaire nor the accompanying cover letter revealed the focus of our investigation. A history of physician-diagnosed asthma was reported by 16% of respiratory therapists and 8% of control subjects. When analysis was restricted to those who developed asthma after entry into their profession, respiratory therapists still had a significant excess, 7.4 versus 2.8%. The odds ratio for respiratory therapy was 2.5 (95% Cl, 1.6 to 3.3) after adjustment for age, family history, atopic history, smoking, and gender. These results confirm the previous report of excess risk of asthma among respiratory therapists. This excess risk develops after entry into the profession and does not appear to be explained by bias or confounding. Efforts should be directed to identifying potential agents responsible for this form of occupational asthma. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114. BROWN UNIV,MEM HOSP RHODE ISL,SCH MED,DEPT MED,PROGRAM OCCUPAT MED,PROVIDENCE,RI 02912. RP CHRISTIANI, DC (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH,OCCUPAT HLTH PROGRAM,665 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NIEHS NIH HHS [ES00002] NR 24 TC 21 Z9 22 U1 0 U2 0 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 SEP PY 1993 VL 148 IS 3 BP 671 EP 674 PG 4 WC Respiratory System SC Respiratory System GA LW465 UT WOS:A1993LW46500021 PM 8368639 ER PT J AU ALLYN, JW KANTOR, HL TEPLICK, R PELTON, M HAHN, C GEFFIN, GA TORCHIANA, DF DAGGETT, WM AF ALLYN, JW KANTOR, HL TEPLICK, R PELTON, M HAHN, C GEFFIN, GA TORCHIANA, DF DAGGETT, WM TI MYOCARDIAL-FUNCTION AND METABOLISM IN ISOLATED CANINE HEART BEFORE, DURING, AND AFTER ONE-HOUR FLOW REDUCTIONS ASSESSED WITH P-31 NMR-SPECTROSCOPY SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT CARDIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A599 EP A599 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800599 ER PT J AU BEHRINGER, EC MURPHY, MT AF BEHRINGER, EC MURPHY, MT TI CERVICAL-SPINE INJURY IN TRAUMA PATIENTS ADMITTED TO THE ICU SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A313 EP A313 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800313 ER PT J AU CULLEN, DJ NEMESKAL, AR ZASLAVSKY, AM AF CULLEN, DJ NEMESKAL, AR ZASLAVSKY, AM TI A NEW THERAPEUTIC INTERVENTION SCORING SYSTEM FOR NON-ICU PATIENTS - INTERMEDIATE TISS SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A284 EP A284 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800284 ER PT J AU DAMBRA, MN LYNCH, KE TORCHIANA, DF HOLMAN, WL AF DAMBRA, MN LYNCH, KE TORCHIANA, DF HOLMAN, WL TI PRE-CABG RECOMBINANT ERYTHROPOIETIN THERAPY REDUCES MEDIASTINAL CHEST TUBE DRAINAGE SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. UNIV ALABAMA,DEPT SURG,BIRMINGHAM,AL 35294. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A95 EP A95 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800095 ER PT J AU DUTTON, RP HURFORD, WE ALFILLE, PH CLEMENT, D AF DUTTON, RP HURFORD, WE ALFILLE, PH CLEMENT, D TI COMPARISON OF THORACIC AND LUMBAR EPIDURAL INFUSIONS OF BUPIVACAINE AND FENTANYL FOR POSTTHORACOTOMY ANALGESIA SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 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 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A273 EP A273 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800273 ER PT J AU FAHMY, NR CARR, DB AF FAHMY, NR CARR, DB TI CHANGES IN PLASMA BETA-ENDORPHIN, CATECHOLAMINES, AND RENIN-ACTIVITY - THEIR CORRELATION TO TOURNIQUET-INDUCED HYPERTENSION IN MAN SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A107 EP A107 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800107 ER PT J AU FAHMY, NR CARR, DB AF FAHMY, NR CARR, DB TI CHANGES IN BETA-ENDORPHIN LEVELS DURING DELIBERATE HYPOTENSION, THEIR CORRELATION WITH HEMODYNAMICS, CATECHOLAMINES, AND RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. NR 3 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A84 EP A84 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800084 ER PT J AU GOTO, T MAROTA, JJA CROSBY, G AF GOTO, T MAROTA, JJA CROSBY, G TI EVIDENCE THAT NITROUS-OXIDE, BUT NOT HALOTHANE, INDUCES PREEMPTIVE ANALGESIA IN THE RAT FORMALIN MODEL SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A858 EP A858 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800857 ER PT J AU HESSELVIK, JF CARLSSON, C LARSSON, J SANDSTEDT, S VONSCHENCK, H AF HESSELVIK, JF CARLSSON, C LARSSON, J SANDSTEDT, S VONSCHENCK, H TI SELENIUM DEFICIENCY IN SERUM AND MUSCLE OF SEPTIC PATIENTS - EFFECT OF ADDING SELENATE OR SELENOMETHIONINE TO TPN SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 LINKOPING UNIV HOSP,DEPT ANESTHESIA,S-58185 LINKOPING,SWEDEN. LINKOPING UNIV HOSP,DEPT SURG,S-58185 LINKOPING,SWEDEN. LINKOPING UNIV HOSP,DEPT CLIN CHEM,S-58185 LINKOPING,SWEDEN. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A262 EP A262 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800262 ER PT J AU HUSAIN, M KAVOSI, M ZAPOL, WM AF HUSAIN, M KAVOSI, M ZAPOL, WM TI EXHALED NITRIC-OXIDE (NO) AND INTRAVENOUS BOLUS INJECTIONS OF NO DONOR COMPOUNDS SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A137 EP A137 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800137 ER PT J AU KEARSE, LA MANBERG, PJ DEBROS, F CHAMOUN, N AF KEARSE, LA MANBERG, PJ DEBROS, F CHAMOUN, N TI EEG BISPECTRAL ANALYSIS PREDICTS MOVEMENT AT INCISION DURING PROPOFOL/N2O ANESTHESIA SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. ASPECT MED SYST INC,FRAMINGHAM,MA. NR 3 TC 1 Z9 1 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 SEP PY 1993 VL 79 IS 3A SU S BP A457 EP A457 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800457 ER PT J AU MAROTA, JJA GOTO, T WILSON, S CROSBY, G AF MAROTA, JJA GOTO, T WILSON, S CROSBY, G TI REGIONAL CHANGES IN BRAIN PREPROENKEPHALIN AND JUN-B, BUT NOT C-FOS, MESSENGER-RNA AFTER BRIEF KETAMINE ANESTHESIA SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 3 TC 1 Z9 1 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 SEP PY 1993 VL 79 IS 3A SU S BP A699 EP A699 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800699 ER PT J AU MAROTA, JJA GOTO, T WILSON, S CROSBY, G AF MAROTA, JJA GOTO, T WILSON, S CROSBY, G TI GENERAL-ANESTHESIA WITH HALOTHANE AND PENTOBARBITAL DIFFERENTIALLY ALTERS REGIONAL PREPROENKEPHALIN GENE-EXPRESSION IN RAT-BRAIN SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A698 EP A698 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800698 ER PT J AU MARTYN, JAJ WANG, C LIU, J AF MARTYN, JAJ WANG, C LIU, J TI BURN TRAUMA ALTERS MYOCARDIAL BETA-ADRENOCEPTOR AND 2ND MESSENGER ACTIVITY SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIOL,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A635 EP A635 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800635 ER PT J AU PETERFREUND, RA FINK, JS AF PETERFREUND, RA FINK, JS TI PROTEIN-KINASE-C ACTIVATION ATTENUATES THE RESPONSE TO ADENOSINE A2A-RECEPTOR STIMULATION - A POTENTIAL MECHANISM FOR REGULATION OF RECEPTOR RESPONSIVENESS SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 4 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A788 EP A788 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800788 ER PT J AU PETERFREUND, RA NIVEN, RW KACMAREK, R AF PETERFREUND, RA NIVEN, RW KACMAREK, R TI SYRINGE ACTUATED METERED-DOSE INHALERS - A QUANTITATIVE LABORATORY EVALUATION OF ALBUTEROL DELIVERY THROUGH NOZZLE EXTENSIONS SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114. AMGEN INC,THOUSAND OAKS,CA 91320. 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 SEP PY 1993 VL 79 IS 3A SU S BP A557 EP A557 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800557 ER PT J AU ROSOW, CE DIBIASE, PM ZASLAVSKY, A BURCH, L AF ROSOW, CE DIBIASE, PM ZASLAVSKY, A BURCH, L TI PROPOFOL VS THIOPENTAL IN INPATIENTS - COMPARISON OF RECOVERY AFTER GENERAL-ANESTHESIA SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A336 EP A336 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800336 ER PT J AU SMALL, SD AF SMALL, SD TI THE 19TH-CENTURY CULTURE OF DEATH AND THE PERSONAL LIBRARY OF WELLS,HORACE - EVIDENCE FOR THE ORIGIN OF ANESTHESIA SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 1993 VL 79 IS 3A SU S BP A1038 EP A1038 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10801034 ER PT J AU SZABO, MD THAL, G LOPEZBRESNAHAN, M CROSBY, G AF SZABO, MD THAL, G LOPEZBRESNAHAN, M CROSBY, G TI EXACERBATION OR UNMASKING OF FOCAL NEUROLOGIC DEFICITS BY SEDATIVE MEDICATION SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. 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 SEP PY 1993 VL 79 IS 3A SU S BP A216 EP A216 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800216 ER PT J AU THAL, G SZABO, MD LOPEZBRESNAHAN, M CROSBY, G AF THAL, G SZABO, MD LOPEZBRESNAHAN, M CROSBY, G TI NEUROLOGIC CHANGES DURING EMERGENCE FROM GENERAL-ANESTHESIA IN NEUROLOGICALLY NORMAL-PATIENTS SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. 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 SEP PY 1993 VL 79 IS 3A SU S BP A192 EP A192 PG 1 WC Anesthesiology SC Anesthesiology GA LY108 UT WOS:A1993LY10800192 ER PT J AU SHEPHERD, KE AF SHEPHERD, KE TI ANESTHESIA NOT RELATED TO FLUDARABINE TOXICITY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP SHEPHERD, KE (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD SEP 1 PY 1993 VL 119 IS 5 BP 437 EP 437 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LZ476 UT WOS:A1993LZ47600023 PM 7687837 ER PT J AU BALCH, CM URIST, MM KARAKOUSIS, CP SMITH, TJ TEMPLE, WJ DRZEWIECKI, K JEWELL, WR BARTOLUCCI, AA MIHM, MC BARNHILL, R WANEBO, HJ AF BALCH, CM URIST, MM KARAKOUSIS, CP SMITH, TJ TEMPLE, WJ DRZEWIECKI, K JEWELL, WR BARTOLUCCI, AA MIHM, MC BARNHILL, R WANEBO, HJ TI EFFICACY OF 2-CM SURGICAL MARGINS FOR INTERMEDIATE-THICKNESS MELANOMAS (1 TO 4 MM) - RESULTS OF A MULTIINSTITUTIONAL RANDOMIZED SURGICAL TRIAL SO ANNALS OF SURGERY LA English DT Article; Proceedings Paper CT 113TH ANNUAL SCIENTIFIC SESSION OF THE AMERICAN-SURGICAL-ASSOC CY APR 01-03, 1993 CL BALTIMORE, MD SP AMER SURG ASSOC ID CUTANEOUS MALIGNANT-MELANOMA; STAGE-I MELANOMA; RESECTION MARGINS; TUMOR THICKNESS; MANAGEMENT; RECURRENCE; EXCISION AB Background A prospective, multi-institutional, randomized surgical trial involving 486 localized melanoma patients was conducted to determine whether excision margins for intermediate-thickness melanomas (1.0 to 4.0 mm) could be safely reduced from the standard 4-cm radius. Methods Patients with 1- to 4-mm-thick melanomas on the trunk or proximal extremities were randomly assigned to receive either a 2- or 4-cm surgical margin. Results The median follow-up time was 6 years. The local recurrence rate was 0.8% for 2-cm margins and 1.7% for 4-cm margins (p value not significant [NS]). The rates of in-transit metastases were 2.1% and 2.5%, respectively (p = NS). Of the six patients with local recurrences, five have died. Recurrence rates did not correlate with surgical margins, even among stratified thickness groups. The overall 5-year survival rate was 79.5% for the 2-cm margin patients and 83.7% for the 4-cm margin patients (p = NS). The need for skin grafting was reduced from 46% with 4-cm surgical margins to 11% with 2-cm surgical margins (p < 0.001). The hospital stay was shortened from 7.0 days for patients receiving 4-cm surgical margins to 5.2 days for those receiving 2-cm margins (p = 0.0001). This reduction was largely due to reduced need for skin grafting, since the hospital stay for those who had a skin graft was 2.5 days longer than that for those who had a primary wound closure (p < 0.01). Conclusion Margins of excision can be safely reduced to 2 cm for patients with intermediate-thickness melanomas. The narrower margins significantly reduced the need for skin grafting and shortened the hospital stay. C1 ROSWELL PK CANC INST,BUFFALO,NY. TOM BAKER CANC CLIN,CALGARY,AB,CANADA. RIGSHOSP,FINSENINST,DK-2100 COPENHAGEN,DENMARK. UNIV ALABAMA,BIRMINGHAM,AL 35294. BROWN UNIV,PROVIDENCE,RI 02912. TUFTS UNIV NEW ENGLAND MED CTR,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV KANSAS,MED CTR,KANSAS CITY,KS 66103. RP BALCH, CM (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,DEPT GEN SURG,BOX 112,1515 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. FU NCI NIH HHS [CA19657, CA2115] NR 15 TC 310 Z9 312 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD SEP PY 1993 VL 218 IS 3 BP 262 EP 269 DI 10.1097/00000658-199309000-00005 PG 8 WC Surgery SC Surgery GA LW602 UT WOS:A1993LW60200005 PM 8373269 ER PT J AU INOUE, Y BODE, BP BECK, DJ LI, AP BLAND, KI SOUBA, WW AF INOUE, Y BODE, BP BECK, DJ LI, AP BLAND, KI SOUBA, WW TI ARGININE TRANSPORT IN HUMAN LIVER - CHARACTERIZATION AND EFFECTS OF NITRIC-OXIDE SYNTHASE INHIBITORS SO ANNALS OF SURGERY LA English DT Article ID AMINO-ACID-TRANSPORT; PLASMA-MEMBRANE VESICLES; SEPTIC SHOCK; RAT-LIVER; ENDOTOXIN; CELLS; HEPATOCYTES AB Objective Arginine transport was characterized and studied in human liver. Summary Background Data Plasma arginine uptake may regulate hepatocyte intracellular availability and the subsequent biosynthesis of nitric oxide (NO), but little is known about arginine transport across the human hepatocyte plasma membrane. Methods The authors characterized plasma membrane transport of 3[H]-L-arginine in hepatic plasma membrane vesicles (HPMVs) and in hepatocytes isolated and cultured from human liver biopsy specimens. They also studied the effects of the NO synthase inhibitors omega-nitro-L-arginine methyl ester (L-NAME) and N-methylarginine (NMA) on arginine transport in HPMVs and in cultured cells. Results Arginine transport was saturable, Na+-independent, temperature and pH sensitive, and was inhibited by the naturally occurring amino acids lysine, homoarginine, and ornithine (System y+ substrates). Arginine transport by both vesicles and cultured hepatocytes was significantly attenuated by NO synthase inhibitors, suggesting that the arginine transporter and the NO synthase enzyme may share a structurally similar arginine binding site. Dixon plot analysis showed the blockade to occur by competitive, rather than noncompetitive, inhibition. In vivo treatment of rats with lipopolysaccharide (LPS) resulted in a twofold stimulation of saturable arginine transport in the liver, This LPS-induced hepatic arginine transport activity was also inhibited by L-NAME. These data indicate that arginine transport by human hepatocytes is mediated primarily by the Na+-independent transport System y+. Conclusions Besides inhibition of the NO synthase enzyme, the ability of arginine derivatives to block NO production may also be due to their ability to competitively inhibit arginine transport across the hepatocyte plasma membrane. The use of selective arginine derivatives that compete with arginine at the plasma membrane level may be a metabolic strategy that can be used to modulate the septic response. C1 UNIV FLORIDA, COLL MED, DEPT SURG, GAINESVILLE, FL 32611 USA. MONSANTO CO, DIV HLTH SCI, ST LOUIS, MO 63166 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG, DIV SURG ONCOL, BOSTON, MA 02114 USA. OI Li, Albert/0000-0001-5772-6265 FU NCI NIH HHS [CA 45327] NR 33 TC 59 Z9 60 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0003-4932 EI 1528-1140 J9 ANN SURG JI Ann. Surg. PD SEP PY 1993 VL 218 IS 3 BP 350 EP 363 DI 10.1097/00000658-199309000-00014 PG 14 WC Surgery SC Surgery GA LW602 UT WOS:A1993LW60200014 PM 7690540 ER PT J AU WAIN, JC AF WAIN, JC TI VIDEO-ASSISTED THORACOSCOPY AND THE STAGING OF LUNG-CANCER SO ANNALS OF THORACIC SURGERY LA English DT Article AB Video-assisted thoracoscopy (VAT) provides an opportunity for evaluation and biopsy within the pleural space and at the pulmonary hilum. The application of a standardized approach for VAT in patients with primary lung cancers was evaluated. Of 49 patients, 6 patients could not be evaluated due to intrapleural adhesions. Of the remaining 43 patients, an unsuspected parietal pleural metastasis was identified in 2, obviating further surgery. The other 41 patients underwent anatomic resection after VAT staging, which was carried out during the same operative procedure. Pathologic staging of the specimens revealed 20 T1 N0, 10 T2 N0, 5 T1 N1, and 6 T2 N1 lesions. Among the T2 lesions, 10 of 16 (63%) involved visceral pleural invasion, all of which were identified at VAT staging. Among the NI lesions, 6 of 11 (55%) were identified at VAT staging; in the remainder, Nl nodes were not accessible to biopsy. No morbidity or mortality was noted. Routine VAT staging in patients with lung cancer is a safe technique, reduces the need for an exploratory thoracotomy, and may identify patients with localized lung cancers who are at high risk for postoperative recurrence. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WAIN, JC (reprint author), MASSACHUSETTS GEN HOSP,DEPT THORAC SURG,GEN THORAC SURG UNIT,WARREN BLDG,SUITE 1109,32 FRUIT ST,BOSTON,MA 02114, USA. NR 5 TC 40 Z9 40 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 SEP PY 1993 VL 56 IS 3 BP 776 EP 778 PG 3 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA LY317 UT WOS:A1993LY31700101 PM 8379793 ER PT J AU HAZELRIGG, SR ROVIARO, G KIRBY, TJ NAUNHEIM, KS MULDER, DS DOWLING, RD LEWIS, RJ LANDRENEAU, RJ WAIN, JC SUGARBAKER, DJ MILLER, JI AF HAZELRIGG, SR ROVIARO, G KIRBY, TJ NAUNHEIM, KS MULDER, DS DOWLING, RD LEWIS, RJ LANDRENEAU, RJ WAIN, JC SUGARBAKER, DJ MILLER, JI TI RESECTIVE THERAPY FOR LUNG-CANCER - PANEL DISCUSSION SO ANNALS OF THORACIC SURGERY LA English DT Discussion C1 UNIV MILAN,OSPED S GIUSEPPE,DIV CHIRURG,CATTEDRA CHIRURG GEN,I-20123 MILAN,ITALY. CLEVELAND CLIN FDN,DEPT THORAC & CARDIOVASC SURG,CLEVELAND,OH 44195. UNIV PITTSBURGH,THORAC SURG SECT,PITTSBURGH,PA 15213. MASSACHUSETTS GEN HOSP,DEPT THORAC SURG,GEN THORAC SURG UNIT,BOSTON,MA 02114. RP HAZELRIGG, SR (reprint author), ST LUKES HOSP,DIV CARDIOTHORAC SURG,MILWAUKEE,WI, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD SEP PY 1993 VL 56 IS 3 BP 787 EP 791 PG 5 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA LY317 UT WOS:A1993LY31700104 ER PT J AU WAIN, JC AF WAIN, JC TI THORACOSCOPY TRAINING IN A RESIDENCY PROGRAM SO ANNALS OF THORACIC SURGERY LA English DT Article AB Video-assisted thoracoscopy (VAT) is rapidly gaining application in a variety of thoracic surgical procedures. As a result, fellowship programs in thoracic surgery need to provide training in VAT techniques. Instruction should include emphasis on aspects of the open procedures, including the anatomic relationships as seen through an open thoracotomy and on cross-sectional imaging techniques. Standardization of the indications for VAT, as well as emphasis on the basic principles of visualization and operative manipulation, will serve to reinforce the advantages and limitations inherent to VAT. An initial exposure to VAT in a nonclinical context, including didactic instruction in the instrumentation and skills, review of videotapes, and animate or inanimate laboratory instruction, provides a controlled setting for learning the fundamentals. Interactive assistance with clinical VAT procedures should be encouraged once the basic principles are learned. Ultimately, guidelines and qualifications for performing VAT procedures should be incorporated into the requirements for thoracic surgical training programs. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WAIN, JC (reprint author), MASSACHUSETTS GEN HOSP,DEPT THORAC SURG,GEN THORAC SURG UNIT,WARREN BLDG,SUITE 1109,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD SEP PY 1993 VL 56 IS 3 BP 799 EP 800 PG 2 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA LY317 UT WOS:A1993LY31700107 PM 8379797 ER PT J AU TEICHER, BA LIU, SD LIU, JT HOLDEN, SA HERMAN, TS AF TEICHER, BA LIU, SD LIU, JT HOLDEN, SA HERMAN, TS TI A CARBONIC-ANHYDRASE INHIBITOR AS A POTENTIAL MODULATOR OF CANCER THERAPIES SO ANTICANCER RESEARCH LA English DT Article DE ACETAZOLAMIDE; TUMOR; PH; HYPERTHERMIA; SR-4233; CABRONIC ANHYDRASE INHIBITORS ID ENVIRONMENTAL-CONDITIONS PH; FSAIIC MURINE FIBROSARCOMA; 4 PLATINUM COMPLEXES; HYPERTHERMIC TEMPERATURES; INTRACELLULAR-PH; TUMOR; CELLS; INVITRO; INVIVO; CYTOTOXICITY AB Since several anticancer drugs are known to become more cytotoxic to cells in an acidic milieu, we have attempted to utilize the carbonic anhydrase inhibitor, Acetazolamide, to acidify the blood and tumor of C3H mice bearing the FSaIIC fibrosarcoma in order to sensitize tumor cells in vivo to CDDP, Melphalan, BCNU, SR4233 or PtCl4 (Fast Black)2 +/- hyperthermia. The direct cytotoxic interactions between the anticancer drugs and Acetazolamide were tested in FSaIIC cells in vitro with the monacidifying diuretic Chlorothrozide as a control. When cells were exposed to CDDP both diuretics protected against cytotoxicity in a dose dependent fashion. In contrast, cells exposed to Melphalan were minimally sensitized and those exposed to BCNU, SR4233, or PtCl4 (Fast Black)2 were essentially unaffected by the presence of the diuretic agents. Both diuretics were essentially non-toxic to cells in vitro, and, interestingly, both drugs markedly protected cells against hyperthermia under low pH conditions. In vitro, however, Acetzolamide produced a tumor growth delay of 2.3 days alone when given at 10 mg/kg i.p. once (the most effective dose) and producted additive growth delays with CDDP and Melphalan, but probably greater than additive delays with SR4233 and PtCl4 (Fast Black)2. When Acetazolamide was given daily for 5 days starting on the day the anticancer drugs were given once (day 7) essentially no further increase in tumor growth delay of nearly 16 days was observed versus only 4,6 days for the drug alone. When hyperthermia (43-degrees-C min.) was delivered locally to the tumor after i.p. injection of the drugs, further growth delays were produced for every drug combination which probably were additive in extent. Blood and urine pH determinations revealed that a pH drop of 1 units occurred in the blood and a pH elevation of 1 to 21 units occurred in the urine 1 hr. after i.p. injection of Acetazolamide. These results indicate that this carbonic anhydrase inhibitor can add to the anticancer activity of the drugs tested. The mechanism may involve its ability to acidify the intratumoral environment, but other mechanisms can not be excluded. 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 [R0I-CA50174, R0ICA 47379] NR 34 TC 96 Z9 98 U1 0 U2 1 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 SEP-OCT PY 1993 VL 13 IS 5A BP 1549 EP 1556 PG 8 WC Oncology SC Oncology GA MG303 UT WOS:A1993MG30300045 PM 8239534 ER PT J AU MACARUSO, P SHANKWEILER, D BYRNE, B CRAIN, S AF MACARUSO, P SHANKWEILER, D BYRNE, B CRAIN, S TI POOR READERS ARE NOT EASY TO FOOL - COMPREHENSION OF ADJECTIVES WITH EXCEPTIONAL CONTROL PROPERTIES SO APPLIED PSYCHOLINGUISTICS LA English DT Article ID SENTENCE COMPREHENSION; TOKEN TEST; PERFORMANCE AB An earlier experiment by Byrne (1981) found that young, poor readers tend to act out sentences containing adjectives with object control, like easy, as though they were adjectives with subject control, like eager. Byrne interpreted this result as evidence that poor readers lag in the acquisition of syntactic knowledge underlying this distinction. However, the possibility that a processing limitation could have contributed to the poor readers' difficulties with object-control adjectives had not been fully explored. In an effort to tease apart these alternatives, we tested comprehension of object-control adjectives in second grade good and poor readers, using both an act-out task and a sentence-picture matching task. Contrary to Byrne's (1981) results, we did not find significant group differences in interpreting object-control adjectives with either task. Reasons for the discrepancy are suggested, and remedies for the pitfalls in designing experiments to assess syntactic knowledge in young children are proposed. C1 UNIV CONNECTICUT,STORRS,CT 06268. HASKINS LABS INC,NEW HAVEN,CT 06511. UNIV NEW ENGLAND,ARMIDALE,NSW 2351,AUSTRALIA. RP MACARUSO, P (reprint author), MASSACHUSETTS GEN HOSP,NEUROLINGUIST LAB,101 MERRIMAC ST,BOSTON,MA 02114, USA. NR 20 TC 4 Z9 4 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0142-7164 J9 APPL PSYCHOLINGUIST JI Appl. Psycholinguist. PD SEP PY 1993 VL 14 IS 3 BP 285 EP 298 DI 10.1017/S0142716400010808 PG 14 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA MJ801 UT WOS:A1993MJ80100002 ER PT J AU WILLIAMS, KP SMITH, JA AF WILLIAMS, KP SMITH, JA TI ISOLATION OF A MEMBRANE-ASSOCIATED CATHEPSIN D-LIKE ENZYME FROM THE MODEL ANTIGEN-PRESENTING CELL, A20, AND ITS ABILITY TO GENERATE ANTIGENIC FRAGMENTS FROM A PROTEIN ANTIGEN IN A CELL-FREE SYSTEM SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; H-2-RESTRICTED T-CELLS; MOUSE CATHEPSIN-D; STAPHYLOCOCCAL NUCLEASE; MACROPHAGE ENDOSOMES; AMINO-ACID; B-CELLS; DETERMINANT SELECTION; PROCESSED ANTIGEN; ACTIVATION C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 63 TC 10 Z9 10 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 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD SEP PY 1993 VL 305 IS 2 BP 298 EP 306 DI 10.1006/abbi.1993.1426 PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LY022 UT WOS:A1993LY02200014 PM 8103981 ER PT J AU KASINATH, BS AF KASINATH, BS TI GLOMERULAR ENDOTHELIAL-CELL PROTEOGLYCANS - REGULATION BY TGF-BETA-1 SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID TRANSFORMING GROWTH-FACTOR; HEPARAN-SULFATE PROTEOGLYCANS; SMOOTH-MUSCLE CELLS; FACTOR-BETA; BASEMENT-MEMBRANE; EPITHELIAL-CELLS; MESANGIAL CELLS; RENAL GLOMERULUS; TISSUE-REPAIR; MATRIX RP KASINATH, BS (reprint author), UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET ADM HOSP,DEPT MED,DIV NEPHROL,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK41517] NR 50 TC 27 Z9 27 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 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD SEP PY 1993 VL 305 IS 2 BP 370 EP 377 DI 10.1006/abbi.1993.1434 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LY022 UT WOS:A1993LY02200022 PM 8373175 ER PT J AU KILLIANY, RJ MOSS, MB ALBERT, MS SANDOR, T TIEMAN, J JOLESZ, F AF KILLIANY, RJ MOSS, MB ALBERT, MS SANDOR, T TIEMAN, J JOLESZ, F TI TEMPORAL-LOBE REGIONS ON MAGNETIC-RESONANCE-IMAGING IDENTIFY PATIENTS WITH EARLY ALZHEIMERS-DISEASE SO ARCHIVES OF NEUROLOGY LA English DT Article ID MEMORY IMPAIRMENT; NUCLEUS BASALIS; NEURONAL LOSS; HIPPOCAMPAL; DEMENTIA; ATROPHY; SCANS AB Objective.-The goal of the study was to examine the volume of selected brain regions in a group of mildly impaired patients with Alzheimer's disease (AD). Five regions were selected for analysis, all of which have been reported to show substantial change in the majority of patients with AD at some time in the course of disease. Design.-Case-control study with the experimenter ''blinded.'' Setting.-Hospital-based magnetic resonance imaging center. Participants.-Fifteen subjects, eight patients with the diagnosis of probable dementia of the Alzheimer type made in concordance with National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association criteria and seven age-matched healthy control subjects. Results.-Three of the volumetric measures were significantly different between patients with AD and controls: the hippocampus, the temporal horn of the lateral ventricles, and the temporal lobe. Two of the measures did not significantly differentiate patients with AD and controls: the amygdala and the basal forebrain. A discriminant function analysis demonstrated that a linear combination of the volumes of the hippocampus and the temporal horn of the lateral ventricles differentiated 100% of the patients and controls from one another. Conclusions.-The results suggest that the hippocampus and the temporal horn of the lateral ventricles may be useful as antemortem markers of AD in mildly impaired patients. C1 BOSTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,80 E CONCORD ST,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. FU NIA NIH HHS [P01-AG04953]; NINDS NIH HHS [T32-NS07152] NR 29 TC 288 Z9 292 U1 0 U2 7 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 SEP PY 1993 VL 50 IS 9 BP 949 EP 954 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA LV723 UT WOS:A1993LV72300010 PM 8363449 ER PT J AU ORTIZBRAVO, E SIECK, MS SCHUMACHER, HR AF ORTIZBRAVO, E SIECK, MS SCHUMACHER, HR TI CHANGES IN THE PROTEINS COATING MONOSODIUM URATE CRYSTALS DURING ACTIVE AND SUBSIDING INFLAMMATION - IMMUNOGOLD STUDIES OF SYNOVIAL-FLUID FROM PATIENTS WITH GOUT AND OF FLUID OBTAINED USING THE RAT SUBCUTANEOUS AIR POUCH MODEL SO ARTHRITIS AND RHEUMATISM LA English DT Article ID CALCIUM PYROPHOSPHATE DIHYDRATE; LOW-DENSITY LIPOPROTEIN; SERUM-PROTEINS; KNEE JOINTS; BINDING; MONOHYDRATE; IMMUNOGLOBULIN; NEUTROPHILS; ADSORPTION; RECEPTOR AB Objective. In this in vivo study, we investigated changes in the proteins that coat monosodium urate (MSU) crystals in human synovial fluid samples and rat air pouch fluid samples obtained sequentially during periods of active and resolving inflammation, in order to evaluate whether in vivo findings are consistent with hypotheses on roles of protein coating based on in vitro findings. Methods. Crystals from patients with gout were isolated from joint fluids with acute inflammation, and subsequently from the same joints at the time inflammation was resolving. Crystals were also obtained using the rat subcutaneous air pouch model. Immunogold was used to label proteins coating MSU crystals, for light microscopy (LM) and transmission electron microscopy (TEM) studies. Results. Dense immunogold-silver labeling for IgG was observed under LM on crystals from fluid with acute inflammation, whereas other proteins (apolipoproteins [Apo], fibronectin, fibrinogen, albumin) were not labeled significantly. Apo B became strongly positive on crystals as the inflammation subsided, whereas other proteins were only weakly positive and IgG became absent or weakly positive. Quantitative TEM evaluation confirmed the LM observations. Conclusion. This study provides the first in vivo evidence supporting the notion derived from previous in vitro studies that proteins coating MSU crystals change as inflammation evolves. Protein coatings may play an important role in the self-limited nature of gouty inflammation. IgG coating MSU crystals may enhance the inflammation. As the inflammation subsides, Apo B could displace the IgG by competitively coating sites on crystals and could contribute in part to the resolution of the acute gouty arthritis. C1 VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL 151-K,WOODLAND & UNIV AVE,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. NR 40 TC 50 Z9 50 U1 0 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 BP 1274 EP 1285 DI 10.1002/art.1780360912 PG 12 WC Rheumatology SC Rheumatology GA MB211 UT WOS:A1993MB21100011 PM 8216421 ER PT J AU BARNETT, ML BLOCH, DB PIKE, MC AF BARNETT, ML BLOCH, DB PIKE, MC TI STABLE FIBROBLAST TRANSFECTANTS EXPRESSING THE INTERLEUKIN-8 RECEPTOR SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S245 EP S245 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81601217 ER PT J AU BAUTISTA, BB SCHUMACHER, HR AF BAUTISTA, BB SCHUMACHER, HR TI INFLAMMATORY MONOARTHRITIS OF LESS-THAN 6 WEEKS DURATION - CAUSES, COURSES AND PREDICTIVE FACTORS SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. 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 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S204 EP S204 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600976 ER PT J AU BLOCH, DB RABKINA, D BLOCH, KD AF BLOCH, DB RABKINA, D BLOCH, KD TI THE IMMUNOREACTIVE REGION IN AUTOANTIGEN GE-1 CONTAINS A NUCLEAR-LOCALIZATION SEQUENCE (NLS) SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. 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 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S106 EP S106 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600398 ER PT J AU BLOCH, DB RABKINA, D BLOCH, KD AF BLOCH, DB RABKINA, D BLOCH, KD TI AUTOANTIGEN GE-3 IS A TARGET OF ANTIBODIES IN THE SERUM OF PATIENTS AND MICE WITH AUTOIMMUNE-DISEASE SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. 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 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S106 EP S106 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600397 ER PT J AU BRIDGES, AJ LORDEN, T AF BRIDGES, AJ LORDEN, T TI SICCA SYNDROME IN WOMEN WITH SILICONE IMPLANTS - ABSENCE OF SERUM AUTOANTIBODIES SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI 53792. MIDDLETON VET ADM HOSP,MADISON,WI 53705. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S70 EP S70 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600190 ER PT J AU GOLDRING, MB BIRKHEAD, JR SUEN, LF YAMIN, R AF GOLDRING, MB BIRKHEAD, JR SUEN, LF YAMIN, R TI USE OF IMMORTALIZED HUMAN CHONDROCYTES IN STUDIES OF IL-1-MEDIATED GENE-EXPRESSION SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S89 EP S89 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600305 ER PT J AU GRAVALLESE, EM DARLING, JM GLIMCHER, LH GLOWACKI, J WANG, JT AF GRAVALLESE, EM DARLING, JM GLIMCHER, LH GLOWACKI, J WANG, JT TI MULTINUCLEATED CELLS IN PIGMENTED VILLONODULAR SYNOVITIS EXPRESS AN OSTEOCLAST PHENOTYPE SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S190 EP S190 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600894 ER PT J AU HASUNUMA, T MORIMOTO, C NISHIOKA, K AF HASUNUMA, T MORIMOTO, C NISHIOKA, K TI CD26 EXPRESSION ON SYNOVIAL-CELLS SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 ST MARIANNA MED UNIV,INST MED SCI,DIV RHEUMATOL,KAWASAKI 216,JAPAN. HARVARD UNIV,SCH MED,DANA FARBER INST,BOSTON,MA 02115. RI Hasunuma, Tomoko/F-3533-2011 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 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S159 EP S159 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600711 ER PT J AU JIAN, YC ZHOU, T WU, JG MOUNTZ, JD AF JIAN, YC ZHOU, T WU, JG MOUNTZ, JD TI THE FAS-LIGAND AND APOPTOSIS IN LPR AND GLD MICE SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35294. BIRMINGHAM VAMC,BIRMINGHAM,AL 35294. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S52 EP S52 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600079 ER PT J AU KATZ, JN GELBERMAN, RH WRIGHT, EA LEW, RA ABRAHAMSSON, SO LIANG, MH AF KATZ, JN GELBERMAN, RH WRIGHT, EA LEW, RA ABRAHAMSSON, SO LIANG, MH TI COMPARATIVE RESPONSIVENESS OF MEASURES OF SYMPTOM SEVERITY, FUNCTIONAL STATUS AND OBJECTIVE NEUROMUSCULAR DEFICITS IN GARPAL TUNNEL-SYNDROME SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,RB BRIGHAM MULTIPURPOSE ARTHRITIS CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S232 EP S232 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81601142 ER PT J AU KATZ, JN GELBERMAN, RH WRIGHT, EA ABRAHAMSSON, SO LEW, RA AF KATZ, JN GELBERMAN, RH WRIGHT, EA ABRAHAMSSON, SO LEW, RA TI DEVELOPMENT OF A GLOBAL INDEX FOR ASSESSING THE OUTCOME OF CARPAL-TUNNEL RELEASE SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,RB BRIGHAM MULTIPURPOSE ARTHRITIS CTR,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S232 EP S232 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81601141 ER PT J AU LAI, WFT YAMIN, R SUEN, LF GOLDRING, MB AF LAI, WFT YAMIN, R SUEN, LF GOLDRING, MB TI REGULATION OF COLLAGEN GENE-EXPRESSION BY PROSTAGLANDINS AND IL-1 IN FIBROBLASTS AND CHONDROCYTES SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S64 EP S64 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600152 ER PT J AU SANZ, I MENESES, G FISCHBACH, M AF SANZ, I MENESES, G FISCHBACH, M TI GENETIC-CHARACTERIZATION OF HUMAN-IMMUNOGLOBULIN HEAVY-CHAIN DIR GENES SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,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 LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S240 EP S240 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81601187 ER PT J AU VEDDER, C HEFENEIDER, SH FREED, AC KHAW, K HAN, SY BAKKE, AC MCCOY, SL BENNETT, RM AF VEDDER, C HEFENEIDER, SH FREED, AC KHAW, K HAN, SY BAKKE, AC MCCOY, SL BENNETT, RM TI PARTIAL CLONING AND EXPRESSION OF A CELL-SURFACE GLYCOPROTEIN HAVING AN IDIOTYPIC CONNECTIVITY WITH ANTI-DNA ANTIBODIES SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97201. 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 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S102 EP S102 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600375 ER PT J AU ZHOU, T JIAN, YC WU, JG MOUNTZ, JD AF ZHOU, T JIAN, YC WU, JG MOUNTZ, JD TI FAS+ COS CELLS AND ANTI-FAS ANTIBODY FOR IN-VIVO LOCALIZATION OF FAS/FAS LIGAND-BINDING AND APOPTOSIS SITES IN AUTOIMMUNE LPR AND GLD MICE SO ARTHRITIS AND RHEUMATISM LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35294. BIRMINGHAM VAMC,BIRMINGHAM,AL 35294. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD SEP PY 1993 VL 36 IS 9 SU S BP S52 EP S52 PG 1 WC Rheumatology SC Rheumatology GA MB816 UT WOS:A1993MB81600080 ER PT J AU NIGAM, SK JIN, YJ JIN, MJ BUSH, KT BIERER, BE BURAKOFF, SJ AF NIGAM, SK JIN, YJ JIN, MJ BUSH, KT BIERER, BE BURAKOFF, SJ TI LOCALIZATION OF THE FK506-BINDING PROTEIN, FKBP-13, TO THE LUMEN OF THE ENDOPLASMIC-RETICULUM SO BIOCHEMICAL JOURNAL LA English DT Article ID CYCLOSPORINE-A; BINDING-PROTEINS; RECEPTOR; CALCINEURIN; ANTIBODIES; RETENTION; MEMBRANE; KINASE; FK506; ALPHA AB The function of the immunophilins, FKBP 12 and FKBP 13, which are binding proteins for the immunosuppressant drug FK506 and rapamycin, remains poorly defined, although it has been suggested that immunophilins and immunophilin-like proteins may play a role in protein sorting/folding and intracellular calcium ion regulation. As a first step towards understanding the function of FKBP 13, we studied its subcellular localization by immunoblotting of well-defined subcellular fractions from a canine pancreatic homogenate and immunocytochemical analysis of an overexpressed cloned cDNA for FKBP 13. Whereas FKBP 12 fractionated entirely into the cytosol, virtually all FKBP 13 was found in the rough microsomal fraction which consisted of highly purified rough endoplasmic reticulum (ER), along with several well-characterized ER markers [the immunoglobulin heavy-chain binding protein (BiP), grp 94 and ribophorin I]. Moreover, FKBP 13 co-banded with the ER markers on isopycnic sucrose gradients. By immunofluorescence, the overexpressed cDNA for FKBP 13 in Hela cells gave an ER-staining pattern highly similar to that of known ER proteins. Addition of the ligand FK506 did not appear to alter the distribution of FKBP 13. Separation of the ER luminal contents and membrane revealed FKBP 13 to be a luminal ER protein. Since the lumen of the ER is where the folding of membrane and secreted proteins occurs, as well as a major site of intracellular calcium storage, it seems possible that FKBP 13 may be involved in one of these functions. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV HAEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. RP NIGAM, SK (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV RENAL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA39542]; NIDDK NIH HHS [DK44503-01A1] NR 24 TC 47 Z9 49 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD SEP 1 PY 1993 VL 294 BP 511 EP 515 PN 2 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LX335 UT WOS:A1993LX33500030 PM 8373365 ER PT J AU WRIGHT, JE ROSOWSKY, A CUCCHI, CA FLATOW, J FREI, E AF WRIGHT, JE ROSOWSKY, A CUCCHI, CA FLATOW, J FREI, E TI METHOTREXATE AND GAMMA-TERT-BUTYL METHOTREXATE TRANSPORT IN CEM AND CEM MTX HUMAN LEUKEMIC LYMPHOBLASTS SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID DIHYDROFOLATE-REDUCTASE; LIPOPHILIC ANTIFOLATE; FOLATE ANTAGONISTS; CELLS; TRIMETREXATE; ANALOGS; RESISTANCE; INVITRO; MONOESTERS; TOXICITY AB In a continuing investigation of determinants of their 200-fold methotrexate resistance and their collateral sensitivity to gamma-tert-butyl methotrexate, the ability of CEM/MTX cells to transport the two drugs was analyzed and compared with that of CEM cells. The K(m) and V(max) values for the influx of methotrexate into CEM cells did not differ significantly from those of CEM/MTX cells, and this was the case for gamma-tert-butyl methotrexate as well. Surface binding and influx rates were proportional to cell surface area, but differences in efflux rates and methotrexate uptake were too large to be explained on this basis. Neither methotrexate nor trimetrexate competed with gamma-tert-butyl methotrexate influx in CEM cells. However, both drugs perturbed the gamma-tert-butyl methotrexate steady state in CEM cells, resulting in slightly less uptake than with gamma-tert-butyl methotrexate alone. However, the major difference between the two cell types was in the methotrexate uptake plateau, which was much greater in the case of the parental cell line. A related observation was the more rapid efflux of methotrexate from CEM/MTX cells than from CEM cells. The poor uptake, the associated meager capacity to polyglutamylate methotrexate and the enhanced methotrexate efflux appear to be responsible for its decreased activity against CEM/MTX cells. Half-lives for gamma-tert-butyl methotrexate efflux were the same in both cell lines, allowing the drug to accumulate to cytotoxic levels despite its inability to form polyglutamates. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP WRIGHT, JE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01-CA25394, P01-CA19589] NR 26 TC 7 Z9 7 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD SEP 1 PY 1993 VL 46 IS 5 BP 871 EP 876 DI 10.1016/0006-2952(93)90496-J PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LX648 UT WOS:A1993LX64800013 PM 8373437 ER PT J AU FINKELSTEIN, DM MOORE, DF SCHOENFELD, DA AF FINKELSTEIN, DM MOORE, DF SCHOENFELD, DA TI A PROPORTIONAL HAZARDS MODEL FOR TRUNCATED AIDS DATA SO BIOMETRICS LA English DT Article DE AIDS; HIV; IDENTIFIABILITY; PROPORTIONAL HAZARDS; TRUNCATED FAILURE TIME DATA ID REGRESSION-MODELS; INCUBATION PERIOD; SURVIVAL-DATA; TRANSFUSION AB An important source of information on the latency period for AIDS is the data from individuals infected by contaminated blood transfusion. However, a difficulty in the analysis and interpretation of these data is that information is available only on individuals who are infected and develop the disease prior to some specific time. In this paper, we propose an approach to the analysis of such data under a proportional hazards model. The proposed approach allows testing for group effects in the presence of multiple explanatory variables. C1 TEMPLE UNIV,PHILADELPHIA,PA 19122. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP FINKELSTEIN, DM (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-47048]; NIAID NIH HHS [AI-24643, AI-30885] NR 11 TC 23 Z9 23 U1 0 U2 1 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD SEP PY 1993 VL 49 IS 3 BP 731 EP 740 DI 10.2307/2532194 PG 10 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA LZ592 UT WOS:A1993LZ59200006 PM 8241369 ER PT J AU RABINOWITZ, D RYAN, L AF RABINOWITZ, D RYAN, L TI LOWER CONFIDENCE-BOUNDS FOR TIME TO CURE SO BIOMETRIKA LA English DT Article DE CLINICAL TRIAL; COUNTING PROCESS; EXCESS RISK; PROPORTIONAL HAZARDS ID SURVIVAL AB Clinicians often wish to know if and when patients with cancer or other life-threatening diseases can be considered cured. Although some parametric approaches are available, no nonparametric methods exist for treating this question. Here, a nonparametric procedure based on the definition that cure occurs when the hazard for death among patients is-no longer greater than the hazard among subjects in the general, population with similar age and demographic characteristics is developed. It is argued that the use of a fully nonparametric approach cannot lead to a nontrivial upper confidence bound for time to cure, and an approach to computing lower confidence bounds for time to cure is developed and applied to data from a clinical trial in colorectal cancer. C1 DANA FARBER CANC INST,BOSTON,MA 02115. RP RABINOWITZ, D (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 NR 9 TC 3 Z9 3 U1 0 U2 0 PU BIOMETRIKA TRUST PI LONDON PA UNIV COLLEGE LONDON GOWER ST-BIOMETRIKA OFFICE, LONDON, ENGLAND WC1E 6BT SN 0006-3444 J9 BIOMETRIKA JI Biometrika PD SEP PY 1993 VL 80 IS 3 BP 681 EP 687 DI 10.1093/biomet/80.3.681 PG 7 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA MM819 UT WOS:A1993MM81900019 ER PT J AU TREVINO, RJ HOROWITZ, PM CHIRGWIN, JM AF TREVINO, RJ HOROWITZ, PM CHIRGWIN, JM TI ELIMINATION OF GLYCEROL ARTIFACTS IN CYCLE SEQUENCING SO BIOTECHNIQUES LA English DT Note ID DNA-POLYMERASE C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV ENDOCRINOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NIGMS NIH HHS [GM 25177] NR 8 TC 3 Z9 3 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 SEP PY 1993 VL 15 IS 3 BP 366 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LW417 UT WOS:A1993LW41700003 PM 8217140 ER PT J AU REDDY, SV TAKAHASHI, S HAIPEK, C CHIRGWIN, JM ROODMAN, GD AF REDDY, SV TAKAHASHI, S HAIPEK, C CHIRGWIN, JM ROODMAN, GD TI TARTRATE-RESISTANT ACID-PHOSPHATASE GENE-EXPRESSION AS A FACILE REPORTER GENE FOR SCREENING TRANSFECTION EFFICIENCY IN MAMMALIAN-CELL CULTURES SO BIOTECHNIQUES LA English DT Note ID TYPE-5 AB The efficiency of DNA transfection into mammalian cell cultures has been monitored using a variety of reporter assays. However the common procedures are expensive, time-consuming and usually cannot identify the transfected cell population directly. In the present communication we describe a simple, inexpensive and efficient method to directly identify DNA transfection in mammalian cells using tartrate-resistant acid phosphatase (TRAP) gene expression. The method involves the transfection of a plasmid (pCT3), which contains TRAP cDNA driven by a CMV promoter into mammalian cells. The cells can then be stained for TRAP activity, and the transfection efficiency can be determined by simply counting the positively transfected cells in a defined area with a microscope. This method permits screening of mammalian cells for transfection efficiency in multi-well plates. After waiting 30-40 minutes to allow the TRAP assay to saturate, wells can be scored in 1-2 minutes with little difficulty in detecting the transfected cells. C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED HEMATOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED ENDOCRINOL,SAN ANTONIO,TX 78284. FU NCI NIH HHS [CA-40035]; NIADDK NIH HHS [AM35188]; NIAMS NIH HHS [AR39539] NR 11 TC 8 Z9 8 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 SEP PY 1993 VL 15 IS 3 BP 444 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LW417 UT WOS:A1993LW41700022 PM 7692895 ER PT J AU MOINGEON, P RODEWALD, HR MCCONKEY, D MILDONIAN, A AWAD, K REINHERZ, EL AF MOINGEON, P RODEWALD, HR MCCONKEY, D MILDONIAN, A AWAD, K REINHERZ, EL TI GENERATION OF NATURAL-KILLER-CELLS FROM BOTH FC-GAMMA-RII/III+ AND FC-GAMMA-RII/III- MURINE FETAL LIVER PROGENITORS SO BLOOD LA English DT Article ID NK CELLS; THYMOCYTE PRECURSORS; LYMPHOCYTES-T; RECEPTOR; ACTIVATION; IL-2; HETEROGENEITY; TRANSDUCTION; FREQUENCIES; EXPRESSION C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP MOINGEON, P (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI21226, AI19807] NR 37 TC 15 Z9 15 U1 1 U2 3 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 SEP 1 PY 1993 VL 82 IS 5 BP 1453 EP 1462 PG 10 WC Hematology SC Hematology GA LX117 UT WOS:A1993LX11700010 PM 8364197 ER PT J AU LEY, K TEDDER, TF KANSAS, GS AF LEY, K TEDDER, TF KANSAS, GS TI L-SELECTIN CAN MEDIATE LEUKOCYTE ROLLING IN UNTREATED MESENTERIC VENULES IN-VIVO INDEPENDENT OF E-SELECTION OR P-SELECTIN SO BLOOD LA English DT Article ID GRANULE MEMBRANE-PROTEIN; ADHESION MOLECULE-1; VASCULAR ENDOTHELIUM; GMP-140; CELLS; GRANULOCYTES; CARBOHYDRATE; NEUTROPHILS; EXPRESSION; INTEGRINS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP LEY, K (reprint author), FREE UNIV BERLIN,DEPT PHYSIOL,ARNIMALLEE 22,D-14195 BERLIN,GERMANY. FU NCI NIH HHS [CA-34183, CA-54464]; NIAID NIH HHS [AI-26872] NR 34 TC 138 Z9 138 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 SEP 1 PY 1993 VL 82 IS 5 BP 1632 EP 1638 PG 7 WC Hematology SC Hematology GA LX117 UT WOS:A1993LX11700032 PM 7689875 ER PT J AU SOIFFER, RJ ROY, DC GONIN, R MURRAY, C ANDERSON, KC FREEDMAN, AS RABINOWE, SN ROBERTSON, MJ SPECTOR, N PESEK, K MAUCH, P NADLER, LM RITZ, J AF SOIFFER, RJ ROY, DC GONIN, R MURRAY, C ANDERSON, KC FREEDMAN, AS RABINOWE, SN ROBERTSON, MJ SPECTOR, N PESEK, K MAUCH, P NADLER, LM RITZ, J TI MONOCLONAL ANTIBODY-PURGED AUTOLOGOUS BONE-MARROW TRANSPLANTATION IN ADULTS WITH ACUTE LYMPHOBLASTIC-LEUKEMIA AT HIGH-RISK OF RELAPSE SO BONE MARROW TRANSPLANTATION LA English DT Article ID VERSUS-HOST DISEASE; 1ST COMPLETE REMISSION; RECOMBINANT INTERLEUKIN-2; HEMATOLOGIC MALIGNANCIES; PROGNOSTIC FACTORS; SURVIVAL; CYCLOPHOSPHAMIDE; IRRADIATION; THERAPY; 2ND AB The prognosis for adults with B lineage ALL who have relapsed after an initial remission is poor. High-dose chemoradiotherapy followed by autologous BMT can induce prolonged clinical remissions in some children with recurrent ALL. In this study, we evaluated the efficacy of autologous BMT in adults. Autologous marrow was treated in vitro with J5 and J2 monoclonal antibodies (CD10/CD9) plus rabbit complement to purge residual ALL cells. Twenty-two adults with B lineage ALL were treated with high-dose chemoradiotherapy followed by infusion of J2/J5 purged autologous BM. The median age was 28 years (range 18-54 years). Twenty-one of 22 patients had experienced at least one relapse prior to BMT. All patients achieved complete hematologic engraftment. Disease-free survival (DFS) in this cohort of patients was 20%, with all survivors alive and free of disease between 2.5 and 7.5 years post-BMT. Age at the time of BMT was an important prognostic factor, with patients < 28 years old faring much better than older individuals (DFS, 45% vs 0%, p = 0.01). Our experience suggests that high-dose chemoradiotherapy followed by infusion of J2/J5 purged autologous marrow is as efficacious in young adults as it is in children and is a reasonable alternative for patients who lack HLA-matched donors. Results in older adults are poor, however, and demonstrate the need for more effective transplant strategies in these individuals. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JOINT CTR RADIAT THERAPY,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP SOIFFER, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JOINT CTR RADIAT THERAPY,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 55207, CA34183] NR 39 TC 45 Z9 45 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD SEP PY 1993 VL 12 IS 3 BP 243 EP 251 PG 9 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA LX825 UT WOS:A1993LX82500012 PM 8241984 ER PT J AU MOLLER, JT SVENNILD, I JOHANNESSEN, NW JENSEN, PF ESPERSEN, K GRAVENSTEIN, JS COOPER, JB DJERNES, M JOHANSEN, SH AF MOLLER, JT SVENNILD, I JOHANNESSEN, NW JENSEN, PF ESPERSEN, K GRAVENSTEIN, JS COOPER, JB DJERNES, M JOHANSEN, SH TI PERIOPERATIVE MONITORING WITH PULSE OXIMETRY AND LATE POSTOPERATIVE COGNITIVE DYSFUNCTION SO BRITISH JOURNAL OF ANAESTHESIA LA English DT Article DE COMPLICATIONS, HYPOXEMIA; MEMORY ID TOTAL HIP-ARTHROPLASTY; GENERAL-ANESTHESIA; MENTAL FUNCTION; ELDERLY PATIENTS; REGIONAL ANESTHESIA; SPINAL-ANESTHESIA; SINGLE-BLIND; HYPOXEMIA; RECOVERY; SURGERY AB In a randomized, blinded clinical study, we have used objective and subjective measures to determine if perioperative monitoring with pulse oximetry-by virtue of its potential to lessen hypoxaemia-would decrease late postoperative cognitive dysfunction. We investigated 736 adult patients undergoing elective procedures (other than cardiac, neurosurgical or for cancer) under-regional or general anaesthesia, allocated randomly to undergo (group I) or not to undergo (group II) pulse oximetry monitoring in the operating theatre and recovery room. Cognitive function was evaluated using the Wechsler memory scale (WMS) and continuous reaction time (RT) test the day before surgery, and on the 7th day after operation or at discharge if that occurred before postoperative day 7. A questionnaire sent 6 weeks after surgery elicited patients' subjective perceptions regarding cognitive abilities. There were no significant differences between the two groups in either the total WMS score, the score for each WMS subtests or RT test The questionnaire revealed that 7% in group I and 11% in group II believed cognitive abilities had decreased (ns). For the 40 patients whose WMS scores were 10 points less after than before operation, a follow-up study was undertaken 3 months after surgery. At that time, the median WMS score had returned to the preoperative value. We conclude that, for these 736 patients, subjective and objective measures did not indicate less postoperative cognitive impairment after perioperative monitoring with pulse oximetry. C1 ESBJERG CENT HOSP,DEPT ANAESTHESIA,ESBJERG,DENMARK. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,BOSTON,MA 02114. UNIV COPENHAGEN,HERLEV HOSP,DEPT ANESTHESIA,DK-2730 HERLEV,DENMARK. UNIV FLORIDA,DEPT ANESTHESIOL,GAINESVILLE,FL 32611. RP MOLLER, JT (reprint author), UNIV COPENHAGEN,RIGSHOSP,DEPT ANAESTHESIA,DK-2100 COPENHAGEN,DENMARK. NR 47 TC 42 Z9 46 U1 2 U2 2 PU PROF SCI PUBL PI LONDON PA TAVISTOCK HOUSE EAST, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-0912 J9 BRIT J ANAESTH JI Br. J. Anaesth. PD SEP PY 1993 VL 71 IS 3 BP 340 EP 347 DI 10.1093/bja/71.3.340 PG 8 WC Anesthesiology SC Anesthesiology GA LX190 UT WOS:A1993LX19000003 PM 8398512 ER PT J AU SALOFFCOSTE, CJ HAMBURG, P HERZOG, DB AF SALOFFCOSTE, CJ HAMBURG, P HERZOG, DB TI NUTRITION AND PSYCHOTHERAPY - COLLABORATIVE TREATMENT OF PATIENTS WITH EATING DISORDERS SO BULLETIN OF THE MENNINGER CLINIC LA English DT Article ID DIETARY-TREATMENT; MANAGEMENT; NERVOSA; BULIMIA AB The nutritionist has a variety of roles in the treatment of patients with eating disorders. The authors describe the psychotherapeutic issues raised in the course of this work. They also discuss how to integrate the nutritionist most effectively into a multidisciplinary team, and in particular bow to build a collaborative relationship with the psychotherapist in creating and implementing a cohesive treatment plan. C1 MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,WACC 805,PARKMAN ST,BOSTON,MA 02114. NR 7 TC 7 Z9 7 U1 0 U2 1 PU MENNINGER FOUNDATION PI TOPEKA PA BOX 829, TOPEKA, KS 66601 SN 0025-9284 J9 B MENNINGER CLIN JI Bull. Menninger Clin. PD FAL PY 1993 VL 57 IS 4 BP 504 EP 516 PG 13 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA MG760 UT WOS:A1993MG76000007 PM 8287018 ER PT J AU BERNSTEIN, ML WHITEHEAD, VM DEVINE, S GRIER, H KUNG, F KRISCHER, J DREYER, Z BELL, B LAND, V BUCHANAN, GR PRATT, C AF BERNSTEIN, ML WHITEHEAD, VM DEVINE, S GRIER, H KUNG, F KRISCHER, J DREYER, Z BELL, B LAND, V BUCHANAN, GR PRATT, C TI IFOSFAMIDE WITH MESNA UROPROTECTION AND ETOPOSIDE IN RECURRENT, REFRACTORY ACUTE-LEUKEMIA IN CHILDHOOD - A PEDIATRIC-ONCOLOGY-GROUP STUDY SO CANCER LA English DT Article DE PEDIATRIC ONCOLOGY; RECURRENT ACUTE LEUKEMIA; CHEMOTHERAPY; IFOSFAMIDE; ETOPOSIDE ID PHASE-II; ENCEPHALOPATHY; TUMORS AB Background. Ifosfamide has previously been shown to be active as a single agent and in combination with doxorubicin, etoposide, and teniposide in pediatric solid tumors and adult acute leukemia. The authors performed a dose-escalation trial of ifosfamide with a fixed dosage of etoposide, with mesna uroprotection, in children with multiply recurrent acute leukemia. Methods. Chemotherapy was administered daily for 5 days. Etoposide 100 mg/m2 was followed by ifosfamide at an initial dosage of 1.6 g/m2. The ifosfamide was escalated in 20% increments to the maximum tolerated dosage in cohorts of three patients. Mesna 400 mg/m2 was given immediately before the ifosfamide and then at 3 and 6 hours after ifosfamide in the initial patients. Subsequent patients were treated with mesna 400 mg/m2 just before ifosfamide, and then every 2 hours to a total dosage equal to the ifosfamide dosage. Results. Forty-four heavily pretreated patients were entered on study. Forty were evaluable for toxicity and 36 for response as well. The maximum tolerated dosage of ifosfamide was 4.0 g/m2/d for 5 days (20 g/m2/course). Overall, 10 patients achieved complete remission, and 3 achieved partial remission. Remissions were brief, although four patients went on to bone marrow transplant while in remission. One patient is still alive. Conclusions. The combination of etoposide and ifosfamide with mesna uroprotection showed promising activity in children with multiply recurrent acute leukemia. C1 WASHINGTON UNIV, SCH MED, DEPT PEDIAT, ST LOUIS, MO 63110 USA. UNIV TEXAS, SW MED CTR, DALLAS, TX 75230 USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA. BAYLOR COLL MED, TEXAS CHILDRENS HOSP, HOUSTON, TX 77030 USA. EMORY UNIV, SCH MED, ATLANTA, GA 30322 USA. PEDIAT ONCOL GRP, STAT OFF, GAINESVILLE, FL USA. UNIV FLORIDA, DEPT PEDIAT, GAINESVILLE, FL 32611 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. BOSTON CHILDRENS HOSP, BOSTON, MA USA. UNIV CALIF SAN DIEGO, DEPT PEDIAT, LA JOLLA, CA 92093 USA. MCGILL UNIV, MONTREAL CHILDRENS HOSP, DEPT PEDIAT, MONTREAL H3H 1P3, QUEBEC, CANADA. FU NCI NIH HHS [CA-41573, CA-20549, CA-03161] NR 17 TC 7 Z9 7 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0008-543X J9 CANCER-AM CANCER SOC JI Cancer PD SEP 1 PY 1993 VL 72 IS 5 BP 1790 EP 1794 DI 10.1002/1097-0142(19930901)72:5<1790::AID-CNCR2820720545>3.0.CO;2-4 PG 5 WC Oncology SC Oncology GA LT807 UT WOS:A1993LT80700044 PM 8348510 ER PT J AU SCHWARTZ, GN TEICHER, BA EDER, JP HOLDEN, SA ARA, G HERMAN, TS KORBUT, T AF SCHWARTZ, GN TEICHER, BA EDER, JP HOLDEN, SA ARA, G HERMAN, TS KORBUT, T TI MODULATION OF ANTITUMOR ALKYLATING-AGENTS BY NOVOBIOCIN, TOPOTECAN, AND LONIDAMINE SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article ID DNA TOPOISOMERASE-II; ASCITES TUMOR-CELLS; HAMSTER OVARY CELLS; CYTO-TOXICITY; LEUKEMIA-CELLS; FIBRO-SARCOMA; NUDE-MICE; PHASE-I; INVITRO; CAMPTOTHECIN AB Topoisomerase I and topoisomerase II allow a metabolically active cell to mobilize its supercoiled chromosomal DNA and undergo replication, transcription, recombination, and repair. Several topoisomerase inhibitors have recently been shown to be active in preclinical systems. Topotecan (SK&F 104864), a water-soluble camptothecin analog, is an inhibitor of topoisomerase I. Novobiocin is an inhibitor of toposiomerase II. Lonidamine depletes cellular adenosine 5'-triphosphate (ATP) and may impede energy-dependent DNA repair, MCF-7 human breast-cancer cells were treated in vitro with topotecan, novobiocin, and lonidamine alone, in paired combinations, and in combination with CDDP and melphalan. The three enzyme inhibitors alone and in combination did not increase tumor cell sensitivity to CDDP. However, the combinations of topotecan/novobiocin and lonidamine/novobiocin did enhance the cytotoxicity of melphalan. Mice bearing the FSaII fibrosarcoma were treated in vivo with topotecan, novobiocin, and lonidamine alone, in paired combinations, and in combination with CDDP, melphalan, BCNU, and cyclophosphamide. The combination of topotecan/novobiocin had the greatest impact on tumor cell sensitivity to each cytotoxic agent tested in both tumor cell-survival and tumor growth-delay assays. This sensitization was greatest at the highest concentrations of the cytotoxic agent tested. Combinations of topoisomerase I and topoisomerase II inhibitors may be useful as modulators of antitumor alkylating agents. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. FU PHS HHS [P01-38493] NR 77 TC 15 Z9 15 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD SEP PY 1993 VL 32 IS 6 BP 455 EP 462 DI 10.1007/BF00685890 PG 8 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA LR870 UT WOS:A1993LR87000008 PM 8258194 ER PT J AU BARNARD, GF STANIUNAS, RJ MORI, M PUDER, M JESSUP, MJ STEELE, GD CHEN, LB AF BARNARD, GF STANIUNAS, RJ MORI, M PUDER, M JESSUP, MJ STEELE, GD CHEN, LB TI GASTRIC AND HEPATOCELLULAR CARCINOMAS DO NOT OVEREXPRESS THE SAME RIBOSOMAL-PROTEIN MESSENGER-RNAS AS COLONIC-CARCINOMA SO CANCER RESEARCH LA English DT Article ID LAMININ-BINDING PROTEIN; INCREASED EXPRESSION; TRANSLATIONAL REGULATION; CELL-PROLIFERATION; COLORECTAL-CANCER; MOLECULAR-CLONING; RIBONUCLEIC-ACID; GENE-EXPRESSION; CDNA CLONES; PROGRESSION AB The levels of a number of ribosomal protein mRNAs are reported to be increased in human colon cancer. We have assessed whether selected ribosomal protein mRNAs are overexpressed in other gastrointestinal malignancies, namely gastric and hepatocellular carcinomas. Subtracted complementary DNA libraries were generated from paired samples of human (a) colorectal carcinoma minus adjacent normal colonic mucosa and (b) hepatocellular carcinoma minus adjacent normal liver. Screening of approximately 3% of these library clones determined that ribosomal protein mRNAs encoding L18 and L37 (not previously reported) and P0 and S6 were overexpressed in one or the other library. Their complementary DNA inserts were then used as probes to evaluate their expression in a larger number of paired tumor/normal surgical samples of human colonic, gastric, and hepatocellular carcinomas, by Northern hybridization. The mRNA signal was greater in the colonic carcinoma than in paired adjacent normal colonic mucosa in 38 of 42 cases for P0 [tumor/normal (T/N) ratio = 3.0 +/- 0.3, mean +/- SE, P < 0.0011 (G. F. Barnard, R. J. Staniunas, S. Bao, K. Mafune, J. L. Gollan, G. D. Steele, Jr., and L. B. Chen, Cancer Res., 52: 3067-3072, 1992), in 25 of 28 cases for L18 (T/N ratio = 3.7 +/- 0.5, P < 0.001), in 27 of 28 cases for L37 (T/N ratio = 5.3 +/- 0.4, P < 0.001), and in 24 of 28 cases for S6 (T/N ratio = 3.1 +/- 0.5, P < 0.01). The level of mRNA overexpression of L18 and S6 did not correlate with the Dukes' stage of disease. In hepatocellular carcinoma samples, using the same four ribosomal protein complementary DNA probes, only P0 mRNA was significantly increased (T/N ratio = 2.8 +/- 0.4, n = 6, P = 0.047). In gastric carcinoma samples, none of these mRNAs was increased (mean T/N ratios = 0.9-1.2, n = 6). Therefore, gastric and hepatocellular carcinomas do not overexpress the same ribosomal protein mRNAs as do colonic carcinoma. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,MAYER 840,44 BINNEY ST,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,DEPT SURG,BOSTON,MA 02215. UNIV MASSACHUSETTS,MED CTR,DIV DIGEST DIS & NUTR,WORCESTER,MA 01605. FU NCI NIH HHS [CA44704, NCI 5F32CA-0900]; NIDDK NIH HHS [DK07533] NR 48 TC 72 Z9 73 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD SEP 1 PY 1993 VL 53 IS 17 BP 4048 EP 4052 PG 5 WC Oncology SC Oncology GA LU579 UT WOS:A1993LU57900036 PM 8395335 ER PT J AU MOSKOWITZ, MA MACFARLANE, R AF MOSKOWITZ, MA MACFARLANE, R TI NEUROVASCULAR AND MOLECULAR MECHANISMS IN MIGRAINE HEADACHES SO CEREBROVASCULAR AND BRAIN METABOLISM REVIEWS LA English DT Review DE TRIGEMINOVASCULAR SYSTEM; MIGRAINE; 5-HT1 RECEPTORS; NEUROPEPTIDES; SUBSTANCE-P; CALCITONIN-GENE-RELATED PEPTIDE; SPREADING DEPRESSION; ERGOT ALKALOIDS; SUMATRIPTAN ID RAT DURA-MATER; NEUROGENIC PLASMA EXTRAVASATION; GENE-RELATED PEPTIDE; TRIGEMINAL GANGLION-CELLS; MIDDLE CEREBRAL-ARTERY; VASCULAR HEAD PAIN; C-FOS; SUBSTANCE-P; BLOOD-VESSELS; BRAIN-STEM AB This chapter reviews the evidence that challenges traditional and unproven notions which perpetuate the singular importance of constriction and dilation to the genesis of migraine pain. New data in experimental laboratory models suggest that migraine headache may develop primarily from metabolic/neurophysiological events (as yet unidentified) within the cortical mantle, or from a disturbance in those regions of brain which closely approximate the distribution of trigeminovascular fibers innervating meningeal blood vessels. Accordingly, this chapter will review the consequences of trigeminovascular activation to pain and meningeal inflammation, and will summarize emerging molecular and pharmacological data suggesting that ergot alkaloids and sumatriptan alleviate pain primarily via activation of prejunctional 5-HT1 heteroreceptors residing on primary afferent trigeminovascular fibers. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,NEUROSURG SERV,BOSTON,MA 02114. ROYAL LONDON HOSP,DEPT NEUROSURG,LONDON,ENGLAND. RP MOSKOWITZ, MA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,NEUROL SERV,STROKE RES LAB,BOSTON,MA 02114, USA. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [NINDS NS 21558] NR 104 TC 199 Z9 200 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1040-8827 J9 CEREBROVAS BRAIN MET JI Cerebrovasc. Brain Metab. Rev. PD FAL PY 1993 VL 5 IS 3 BP 159 EP 177 PG 19 WC Neurosciences SC Neurosciences & Neurology GA LW425 UT WOS:A1993LW42500001 PM 8217498 ER PT J AU BLACK, PM TARBELL, NJ ALEXANDER, E ROCKOFF, M ZHAN, MS LOEFFLER, J AF BLACK, PM TARBELL, NJ ALEXANDER, E ROCKOFF, M ZHAN, MS LOEFFLER, J TI STEREOTAXIC TECHNIQUES IN MANAGING PEDIATRIC BRAIN-TUMORS SO CHILDS NERVOUS SYSTEM LA English DT Article DE PEDIATRICS; STEREOTAXIC; CEREBRAL NEOPLASM; ASTROCYTOMA ID INTRACRANIAL LESIONS; INITIAL MANAGEMENT; MALIGNANT GLIOMAS; BIOPSY; RADIOSURGERY; SURGERY; FRAME; BRACHYTHERAPY; LOCALIZATION; IRRADIATION AB Stereotactic techniques available for managing pediatric brain tumors include not only stereotactic biopsy but also stereotactic craniotomy, brachytherapy, and stereotactic radiosurgery. This paper illustrates the use of these techniques in brain tumors in children over a 2-year period at Children's Hospital, Boston. Stereotactic biopsy was used in six cases of deep-seated tumor, with successful tissue diagnosis in all six. Stereotactic craniotomy, in which excision of a mass was done in the stereotactic frame with computed tomography-guided localization and control, was employed in three children. Interstitial radiation using implanted I-125 seeds was carried out in two children with malignant astrocytomas: in both it provided good local control but there was later distant recurrence. Stereotactic radiosurgery with a modified linear accelerator was used in eight children as adjunctive therapy for local control. These cases illustrate the versatility of stereotactic techniques involved in a comprehensive approach to pediatric brain tumors. C1 CHILDRENS HOSP MED CTR,CTR BRAIN TUMOR,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT ANESTHESIA,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 27 TC 13 Z9 13 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0256-7040 J9 CHILD NERV SYST JI Childs Nerv. Syst. PD SEP PY 1993 VL 9 IS 6 BP 343 EP 347 DI 10.1007/BF00302038 PG 5 WC Clinical Neurology; Pediatrics; Surgery SC Neurosciences & Neurology; Pediatrics; Surgery GA MB239 UT WOS:A1993MB23900010 PM 8269418 ER PT J AU POWELL, AC FUCHS, T FINKELSTEIN, DM GARAN, H CANNOM, DS MCGOVERN, BA KELLY, E VLAHAKES, GJ TORCHIANA, DF RUSKIN, JN AF POWELL, AC FUCHS, T FINKELSTEIN, DM GARAN, H CANNOM, DS MCGOVERN, BA KELLY, E VLAHAKES, GJ TORCHIANA, DF RUSKIN, JN TI INFLUENCE OF IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS ON THE LONG-TERM PROGNOSIS OF SURVIVORS OF OUT-OF-HOSPITAL CARDIAC-ARREST SO CIRCULATION LA English DT Article DE HEART ARREST; ELECTROPHYSIOLOGY; DEFIBRILLATOR; DEATH, SUDDEN; ARRHYTHMIAS ID MALIGNANT VENTRICULAR ARRHYTHMIAS; CORONARY-ARTERY DISEASE; FOLLOW-UP; ANTIARRHYTHMIC THERAPY; FIBRILLATION; INDUCIBILITY; PREDICTION; RECURRENCE; DEATH; TIME AB Background. Survivors of out-of-hospital cardiac arrest not associated with acute myocardial infarction are at high risk for recurrent cardiac arrest and sudden cardiac death. The impact of the implantable cardioverter-defibrillator on long-term prognosis in these patients is uncertain. Methods and Results. Three hundred thirty-one survivors of out-of-hospital cardiac arrest (age, 56+/-13.7 years) underwent electrophysiologically guided therapy. Implantable defibrillators were placed in 150 patients (45.3%), and 181 patients (54.7%) received pharmacological and/or surgical therapy alone. Left ventricular ejection fraction was 35.2+/-16.6% in defibrillator recipients and 45.3+/-18.2% in nondefibrillator patients. Median patient follow-up was 24 months in the defibrillator group and 46 months in the nondefibrillator group. In a proportional hazards model, the independent predictors of total cardiac mortality were left ventricular ejection fraction of less than 0.40 (relative risk, 4.55; 95% confidence interval, 2.44 to 8.33; P=.0001), absence of an implantable defibrillator (relative risk, 2.70; confidence interval, 1.41 to 5.00; P=.017), and persistence of inducible sustained ventricular tachycardia (relative risk, 1.84; 95% confidence interval, 0.97 to 3.49; P=.045). The 1- and 5-year probabilities of survival free of cardiac mortality in patients with left ventricular ejection fraction of less than 0.40 were 94.3% and 69.6% with a defibrillator and 82.1% and 45.3% without a defibrillator, respectively. For patients with left ventricular ejection fraction of 0.40 or more, the 1- and 5-year probabilities of survival free of cardiac mortality were 97.7% and 94.6% with a defibrillator and 95.4% and 86.9% without a defibrillator, respectively. Conclusions. In survivors of out-of-hospital cardiac arrest, the implantable defibrillator is associated with a reduction in cardiac mortality, particularly in patients with impaired left ventricular function. C1 MASSACHUSETTS GEN HOSP,CARDIAC SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. HOSP GOOD SAMARITAN,LOS ANGELES,CA 90017. RP RUSKIN, JN (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC ARRHYTHMIA SERV,BOSTON,MA 02114, USA. NR 36 TC 175 Z9 175 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD SEP PY 1993 VL 88 IS 3 BP 1083 EP 1092 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LV728 UT WOS:A1993LV72800031 PM 8353870 ER PT J AU VANDERVOORT, PM RIVERA, JM MELE, D PALACIOS, IF DINSMORE, RE WEYMAN, AE LEVINE, RA THOMAS, JD AF VANDERVOORT, PM RIVERA, JM MELE, D PALACIOS, IF DINSMORE, RE WEYMAN, AE LEVINE, RA THOMAS, JD TI APPLICATION OF COLOR DOPPLER FLOW MAPPING TO CALCULATE EFFECTIVE REGURGITANT ORIFICE AREA - AN IN-VITRO STUDY AND INITIAL CLINICAL OBSERVATIONS SO CIRCULATION LA English DT Article DE ECHOCARDIOGRAPHY; DOPPLER; VALVULAR REGURGITATION ID MITRAL REGURGITATION; VALVULAR REGURGITATION; QUANTIFICATION; CONVERGENCE; ECHOCARDIOGRAPHY; CONSERVATION; QUANTITATION; MOMENTUM; IMPACT; JET AB Background. Analogous to stenotic valve area in the assessment of valvular stenosis, regurgitant orifice area (ROA) represents a fundamental parameter to assess valvular insufficiency. However, this parameter has not been routinely available up to now. In this study, we introduce the concept and provide the methodology to calculate regurgitant orifice area noninvasively, based on the analysis of the proximal flow convergence zone. Methods and Results. In an in vitro study, we showed the feasibility and the accuracy of calculating effective ROA by the proximal flow convergence method throughout a range of driving pressures. The calculated and true ROA showed an excellent correlation with r=.992, DELTAROA= -1.4+/-2.9 mm2. We then applied this concept clinically in 77 patients with mitral regurgitation and showed a very good correlation between effective ROA calculated by the proximal How convergence method and calculated by the Doppler echocardiographic method: r=.95, DELTAROA=-0.2+/-3.9 mm2. The ROA also correlated very well with Doppler echocardiographic-derived regurgitant stroke volume (r=.93) and regurgitant fraction (r=.82). In a subgroup of 20 patients who underwent invasive evaluation, the calculated effective ROA also correlated well with the angiographic grade of mitral regurgitation (rho=.81). Conclusion. We conclude that effective ROA represents unique information on the severity of a regurgitant lesion and can easily be calculated by the proximal flow convergence method. This new parameter should enhance our understanding and improve the serial assessment of valvular regurgitation. C1 MASSACHUSETTS GEN HOSP,NONINVAS CARDIAC LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CARDIAC CATHETERIZAT LAB,CARDIAC UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP VANDERVOORT, PM (reprint author), CLEVELAND CLIN FDN,DEPT CARDIOL,9500 EUCLID AVE,CLEVELAND,OH 44195, USA. RI rivera, miguel/D-5026-2014 NR 28 TC 156 Z9 157 U1 1 U2 4 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD SEP PY 1993 VL 88 IS 3 BP 1150 EP 1156 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LV728 UT WOS:A1993LV72800039 PM 8353877 ER PT J AU RODRIGUEZ, L THOMAS, JD MONTERROSO, V WEYMAN, AE HARRIGAN, P MUELLER, LN LEVINE, RA AF RODRIGUEZ, L THOMAS, JD MONTERROSO, V WEYMAN, AE HARRIGAN, P MUELLER, LN LEVINE, RA TI VALIDATION OF THE PROXIMAL FLOW CONVERGENCE METHOD - CALCULATION OF ORIFICE AREA IN PATIENTS WITH MITRAL-STENOSIS SO CIRCULATION LA English DT Article DE DOPPLER; ECHOCARDIOGRAPHY; COLOR FLOW MAPPING; MITRAL STENOSIS ID PRESSURE HALF-TIME; VALVE AREA; REGURGITANT FLOW; DOPPLER; ECHOCARDIOGRAPHY; QUANTIFICATION; SURFACE; INVITRO; REGION; EQUATION AB Background. It has been proposed recently that measuring the flow convergence region proximal to an orifice by Doppler flow mapping can provide a means of calculating regurgitant flow rate. Although verified in experimental models, this approach is difficult to validate clinically because there is no ideal gold standard for regurgitant flows in patients. However, this method also can be used to derive cardiac output or flow rate proximal to stenotic orifices and therefore to calculate their areas by the continuity equation (area=flow rate/velocity). Applying this method in mitral stenosis would provide a unique way of validating the underlying concept because the predicted areas could be compared with those measured directly by planimetry. Methods and Results. We studied 40 patients with mitral stenosis using imaging and Doppler echocardiography. Doppler color flow recordings of mitral inflow were obtained from the apex, and the radius of the proximal flow convergence region was measured at its peak diastolic value from the orifice to the first color alias along the axis of flow. Flow rate was calculated assuming uniform radial flow convergence toward the orifice, modified by a factor that accounted for the inflow funnel angle formed by the mitral leaflets. Mitral valve area was then calculated as peak flow rate divided by peak velocity by continuous-wave Doppler. The calculated areas agreed well with those from three comparative techniques over a range of 0.5 to 2.2 cm2: 1) Cross-sectional area by planimetry (y=1.08x-0.13, r=.91, SEE=0.21 cm2); 2) area derived from the Doppler pressure half-time (y=1.02x-0.14, r=.89, SEE=0.24 cm2); and 3) area calculated by the Gorlin equation in the 26 patients who underwent catheterization (y=0.89x+0.08, r=.86, SEE=0.24 cm2). Agreement with planimetry was similar for 22 patients with mitral regurgitation and 18 without it (P>.6), as well as for 6 in atrial fibrillation (P>.2). Conclusions. These results validate the proximal flow convergence concept in the clinical setting and also demonstrate that it can be extended to orifice area calculation using the continuity equation. C1 MASSACHUSETTS GEN HOSP,CARDIAC ULTRASOUND LAB,VINCENT BURNHAM 5,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-38176] NR 44 TC 98 Z9 99 U1 1 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD SEP PY 1993 VL 88 IS 3 BP 1157 EP 1165 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LV728 UT WOS:A1993LV72800040 PM 8353878 ER PT J AU PRENCE, EM NATOWICZ, MR ZALEWSKI, I AF PRENCE, EM NATOWICZ, MR ZALEWSKI, I TI UNUSUAL THERMOLABILITY PROPERTIES OF LEUKOCYTE BETA-HEXOSAMINIDASE - IMPLICATIONS IN SCREENING FOR CARRIERS OF TAY-SACHS-DISEASE SO CLINICAL CHEMISTRY LA English DT Article DE GENETIC DISORDERS; SANDHOFF DISEASE; HETEROZYGOSITY; ANALYTICAL ERROR AB Tay-Sachs disease (TSD), an autosomal recessive neurodegenerative condition, is the result of a deficiency of beta-hexosaminidase A (hex A). Heterozygotic individuals are screened by analysis for hex A and hex B activities; the percent of hex A is the critical determinant of carrier vs noncarrier status. Most laboratories use a heat-inactivation assay that exploits the differential thermolability of the isoenzymes. However, we have found a reciprocal relation between the apparent leukocyte hex A activity and the amount of the sample used in the assay; i.e., a significant increase in the percent of hex A activity with decreasing amounts of sample. Three sets of data indicate that this phenomenon was caused by an effect on the hex B isoenzyme and not on hex A. This variation in hex A activity with sample amount was not observed when a hex A-specific substrate was used. This phenomenon was also not seen in assays of leukocytes from carriers for Sandhoff disease, a condition associated with a reduction in the amount of hex B. Finally, when leukocytes from a TSD homozygote, containing almost no hex A, were analyzed, marked increases in the percent of hex A were observed with decreasing sample concentrations. These data indicate that misdiagnoses could result from variations in sample concentrations used for TSD carrier testing and support the view that the leukocyte concentrations used for these assays should be standardized. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT & PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP PRENCE, EM (reprint author), EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MED GENET,200 TRAPELO RD,WALTHAM,MA 02254, USA. NR 12 TC 14 Z9 14 U1 0 U2 1 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD SEP PY 1993 VL 39 IS 9 BP 1811 EP 1814 PG 4 WC Medical Laboratory Technology SC Medical Laboratory Technology GA LX465 UT WOS:A1993LX46500009 PM 8375052 ER PT J AU WARD, TT THOMAS, RG FYE, CL ARBEIT, R COLTMAN, CA CRAIG, W DANA, BW FINEGOLD, SM LENTINO, J PENN, RL WEINBERG, JB CHOW, B OCHI, S WEBER, JH LAYARD, MW CHANG, P GREENBERG, P RIMLAND, D BALDIWIN, V MIREAULT, K LAWRENCE, W STANKO, S HOBBS, E OLMSTEAD, C INGRAMDRAKE, L NEILL, HB DISNEY, C YU, V HAMILTON, R LYMAN, GH LYMAN, C GALGIANI, J KIZZIER, F AMON, M GRINICH, K SEWELL, D BASSETT, R JACOBSON, I JAMES, KE FETTER, R MONTANO, L HICKS, R SATHER, MR YOUNG, LM WEBER, JH AF WARD, TT THOMAS, RG FYE, CL ARBEIT, R COLTMAN, CA CRAIG, W DANA, BW FINEGOLD, SM LENTINO, J PENN, RL WEINBERG, JB CHOW, B OCHI, S WEBER, JH LAYARD, MW CHANG, P GREENBERG, P RIMLAND, D BALDIWIN, V MIREAULT, K LAWRENCE, W STANKO, S HOBBS, E OLMSTEAD, C INGRAMDRAKE, L NEILL, HB DISNEY, C YU, V HAMILTON, R LYMAN, GH LYMAN, C GALGIANI, J KIZZIER, F AMON, M GRINICH, K SEWELL, D BASSETT, R JACOBSON, I JAMES, KE FETTER, R MONTANO, L HICKS, R SATHER, MR YOUNG, LM WEBER, JH TI TRIMETHOPRIM-SULFAMETHOXAZOLE PROPHYLAXIS IN GRANULOCYTOPENIC PATIENTS WITH ACUTE-LEUKEMIA - EVALUATION OF SERUM ANTIBIOTIC LEVELS IN A RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED DEPARTMENT-OF-VETERANS-AFFAIRS COOPERATIVE STUDY SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID CONTROLLED TRIAL; INFECTION PROPHYLAXIS; CANCER-PATIENTS; CO-TRIMOXAZOLE; SELECTIVE DECONTAMINATION; NEUTROPENIC PATIENTS; BACTERIAL-INFECTION; PREVENTION; CHEMOTHERAPY; CHILDREN AB Despite widespread use of trimethoprim-sulfamethoxazole (TMP-SMZ) for prophylaxis in neutropenic patients, questions remain regarding its efficacy, toxicity, the risk of selection of resistant isolates, and the relation of its activity to selective decolonization vs. the attainment of direct inhibitory levels within blood and tissues. We evaluated the effect of TMP-SMZ (160/800 mg orally every 12 hours) in 42 adult granulocytopenic patients (<100 absolute neutrophils/mm3, mean duration 13.3 days) undergoing chemotherapy for acute leukemia at 11 participating Veterans Administration Medical Centers in a randomized, double-blind, placebo-controlled trial. No significant differences in survival, frequency of bacteremia, overall infections, use of systemic antimicrobial therapy, or adverse effects, including myelosuppression, were observed between patients receiving TMP-SMZ vs. those receiving placebo. All patients acquired trimethoprim-resistant organisms. Concentrations of trimethoprim in serum were significantly lower before febrile episodes than when patients were afebrile. These results suggest that the purported activity of TMP-SMZ may be related to the serum concentration achieved. Moreover, the results highlight the need for additional study of the value of antibiotic prophylaxis in neutropenic patients. C1 DEPT VET AFFAIRS MED CTR,PALO ALTO,CA. DEPT VET AFFAIRS MED CTR,W LOS ANGELES,LA. DEPT VET AFFAIRS MED CTR,ALBUQUERQUE,NM. DEPT VET AFFAIRS MED CTR,BOSTON,MA. DEPT VET AFFAIRS MED CTR,SAN ANTONIO,TX. DEPT VET AFFAIRS MED CTR,MADISON,WI. DEPT VET AFFAIRS MED CTR,HINES,IL. DEPT VET AFFAIRS MED CTR,SHREVEPORT,LA. DEPT VET AFFAIRS MED CTR,DURHAM,NC. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. RP WARD, TT (reprint author), DEPT VET AFFAIRS MED CTR,INFECT DIS SECT 111F,3710 US VET RD,PORTLAND,OR 97207, USA. NR 35 TC 23 Z9 23 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD SEP PY 1993 VL 17 IS 3 BP 323 EP 332 PG 10 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LW237 UT WOS:A1993LW23700002 PM 8218671 ER PT J AU JOHN, JF GRIESHOP, TJ ATKINS, LM PLATT, CG AF JOHN, JF GRIESHOP, TJ ATKINS, LM PLATT, CG TI WIDESPREAD COLONIZATION OF PERSONNEL AT A VETERANS AFFAIRS MEDICAL-CENTER BY METHICILLIN-RESISTANT, COAGULASE-NEGATIVE STAPHYLOCOCCUS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID PROSTHETIC VALVE ENDOCARDITIS; CARDIAC-SURGERY; RIBOSOMAL-RNA; MOLECULAR EPIDEMIOLOGY; GENTAMICIN-RESISTANCE; HOSPITALIZED-PATIENTS; RESTRICTION PATTERNS; GEL-ELECTROPHORESIS; EPIDERMIDIS; BACTEREMIA AB A serial prospective survey of nasal colonization of hospital personnel by methicillin-resistant coagulase-negative staphylococci (MRCNS) was conducted at a Veterans Affairs medical center on three occasions over a 16-month period. The epidemiological typing systems used to assess relatedness included antimicrobial susceptibility profiles; biotyping; phage typing; plasmid profiles; restriction fragment length polymorphism (RFLP) analysis with ribosomal RNA; and plasmid hybridization with a 1.68-MD plasmid as the DNA probe. Forty-three percent of all personnel and 62% of all nurses were colonized with MRCNS. Nurses on the wards (72%) and in the intensive care unit (73%) were significantly more likely to be colonized with MRCNS than nurses who had less contact with patients or those who worked in the operating room. The molecular epidemiological typing systems indicated some degree of relatedness among the strains. Specifically, riboprobe analysis revealed a Dice coefficient of >90%. However, each typing system detected dissimilarity among strains. Further studies are needed to determine the role that such human reservoirs of MRCNS serve in horizontal transmission to and subsequent infection of hospitalized patients. C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC. MED UNIV S CAROLINA,CHARLESTON,SC 29425. NR 59 TC 22 Z9 22 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD SEP PY 1993 VL 17 IS 3 BP 380 EP 388 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LW237 UT WOS:A1993LW23700010 PM 8105982 ER PT J AU RAINVILLE, J AHERN, DK PHALEN, L AF RAINVILLE, J AHERN, DK PHALEN, L TI ALTERING BELIEFS ABOUT PAIN AND IMPAIRMENT IN A FUNCTIONALLY ORIENTED TREATMENT PROGRAM FOR CHRONIC LOW-BACK-PAIN SO CLINICAL JOURNAL OF PAIN LA English DT Article DE BACK PAIN; CHRONIC PAIN; PAIN REHABILITATION ID RESTORATION; DISABILITY AB Objective: This study examined pain and impairment beliefs [measured with the Pain and Impairment Relationship Scale, (PAIRS)] of chronic low back pain patients during rehabilitation and hypothesized that pain beliefs would be stronger in drop-out subjects, decrease during treatment, and after treatment correlate strongly with disability measures. Design: Prospective cohort. Setting: Outpatient, functionally oriented rehabilitation program for chronic low back pain. Patients: 72 consecutive chronic low back pain referral patients disabled from working because of pain. Involvement: Interdisciplinary rehabilitation with a focus on intensive physical reconditioning was employed. Outcome Measures: Program completion versus drop-out groups and pretreatment and posttreatment pain, disability, depression, and PAIRS scores were compared. Results: Thirty patients dropped out and 42 subjects completed treatment. The PAIRS scores at evaluation were similar for both groups. The PAIRS scores improved significantly during treatment (p < 0.001). Posttreatment PAIRS scores correlated highly with disability measures (r = 0.79, p < 0.001). Conclusion: Pain beliefs are of minimal value for predicting treatment compliance, but may be altered during functionally oriented treatment of chronic low back pain. Posttreatment disability closely mirrored attitudes and belief-associated pain and impairment. C1 TUFTS UNIV,SCH MED,DEPT REHABIL MED,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,INST BEHAV MED,BOSTON,MA 02114. PRIDE RES FDN,DALLAS,TX. NR 18 TC 47 Z9 47 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0749-8047 J9 CLIN J PAIN JI Clin. J. Pain PD SEP PY 1993 VL 9 IS 3 BP 196 EP 201 DI 10.1097/00002508-199309000-00007 PG 6 WC Anesthesiology; Clinical Neurology SC Anesthesiology; Neurosciences & Neurology GA LX464 UT WOS:A1993LX46400007 PM 8219520 ER PT J AU HALL, JE AF HALL, JE TI GONADOTROPIN-RELEASING-HORMONE ANTAGONISTS - EFFECTS ON THE OVARIAN FOLLICLE AND CORPUS-LUTEUM SO CLINICAL OBSTETRICS AND GYNECOLOGY LA English DT Article ID HUMAN GRANULOSA-CELLS; LUTEINIZING-HORMONE; STIMULATING-HORMONE; MENSTRUAL-CYCLE; NAL-GLU; SECRETION; SUPPRESSION; INVITRO; WITHDRAWAL; PREVENTION RP HALL, JE (reprint author), MASSACHUSETTS GEN HOSP,REPROD ENDOCRINOL UNIT,BARTLETT HALL EXTENS 5,FRUIT ST,BOSTON,MA 02114, USA. FU NCRR NIH HHS [RR-01066]; NICHD NIH HHS [HD-15080, HD-32837] NR 28 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-9201 J9 CLIN OBSTET GYNECOL JI Clin. Obstet. Gynecol. PD SEP PY 1993 VL 36 IS 3 BP 744 EP 752 DI 10.1097/00003081-199309000-00031 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA LT467 UT WOS:A1993LT46700028 PM 8403621 ER PT J AU GREENE, MF AF GREENE, MF TI PREVENTION AND DIAGNOSIS OF CONGENITAL-ANOMALIES IN DIABETIC PREGNANCIES SO CLINICS IN PERINATOLOGY LA English DT Article ID SERUM ALPHA-FETOPROTEIN; NEURAL-TUBE DEFECTS; FETAL GROWTH DELAY; SPONTANEOUS-ABORTION; MATERNAL HEMOGLOBIN-A1C; VITAMIN SUPPLEMENTATION; MALFORMATION RATES; PRENATAL-DIAGNOSIS; GLYCEMIC CONTROL; INFANTS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. JOSLIN CLIN,BOSTON,MA 02215. RP GREENE, MF (reprint author), BRIGHAM & WOMENS HOSP,DEPT OBSTET & GYNECOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 55 TC 27 Z9 30 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0095-5108 J9 CLIN PERINATOL JI Clin. Perinatol. PD SEP PY 1993 VL 20 IS 3 BP 533 EP 547 PG 15 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA LY564 UT WOS:A1993LY56400004 PM 8222466 ER PT J AU BRUGGE, WR AF BRUGGE, WR TI NONSURGICAL TREATMENT OF GALLSTONES SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Article AB The medical therapy of gallstone disease has undergone many changes in the past decade. Two types of dissolution agents have been developed: oral bile acids and contact-dissolving chemicals. In addition, biliary lithotripsy has been used extensively and has been found to be quite successful when used with oral bile acids. The success of these therapies is largely dependent on the type of gallstone being treated. With the success of laparoscopic cholecystectomy, medical therapy of gallstones has become focused on certain patient populations. The strategy in the coming years will be to develop a comprehensive treatment approach for all types of gallstone patients. Most likely, dissolution therapy will be recommended for the elderly or those who cannot undergo cholecystectomy. Small radiolucent gallstones will be particularly amenable to oral bile salt therapy. Larger radiolucent stones, between 5 to 15 mm, will be candidates for biliary lithotripsy. The challenge for medical therapy in the future will be to develop a noninvasive, rapidly acting, oral dissolution agent that will be capable of dissolving cholesterol and noncholesterol portions of gallstones. RP BRUGGE, WR (reprint author), MASSACHUSETTS GEN HOSP,GI UNIT,7 JACKSON BLDG,FRUIT ST,BOSTON,MA 02114, 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 SEP PY 1993 VL 9 IS 5 BP 835 EP 840 DI 10.1097/00001574-199309000-00017 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LW714 UT WOS:A1993LW71400017 ER PT J AU STAINIER, DYR LEE, RK FISHMAN, MC AF STAINIER, DYR LEE, RK FISHMAN, MC TI CARDIOVASCULAR DEVELOPMENT IN THE ZEBRAFISH .1. MYOCARDIAL FATE MAP AND HEART TUBE FORMATION SO DEVELOPMENT LA English DT Article DE LINEAGE; CARDIAC PROGENITORS; HEART TUBE; MYOCARDIUM; ENDOCARDIUM; HEART BEAT; LOOPING; CARDIAC CHAMBERS ID XENOPUS-LAEVIS; CELL; DIFFERENTIATION; MOVEMENTS; GASTRULA; NEURONS; SYSTEM AB We have analyzed the origin of cardiac progenitors in the zebrafish embryo by injection of single blastomeres with a lineage tracer dye, and examined the formation of the zebrafish heart tube by serial sectioning of immunostained embryos. At the 512-cell stage (early blastula), most cardiac progenitors lie in a marginal zone that extends from 90-degrees longitude (midway between the future dorsal and ventral axis) through 180-degrees longitude (the future ventral axis) to 270-degrees longitude. By focusing on myocardial progenitors located at 90-degrees (and 270-degrees) longitude, we found that a single cell injected in the early blastula can contribute progeny to both the atrium and ventricle. A cell injected in the midblastula contributes progeny to either the atrium or ventricle, but not both. This analysis suggests that, at least for.these myocardial progenitors, the atrial and ventricular lineages separate in the midblastula. Precardiac cells involute early during gastrulation and turn towards the animal pole with other early involuting cells. These cardiogenic cells reach the embryonic axis around the 8-somite stage, and there they coalesce to form a pair of myocardial tubular primordia on either side of the midline. By the 21-somite stage, the tropomyosin-immunoreactive myocardial tubes have moved closer to each other, and a distinct group of cells, the endocardial progenitor cells, sits medially between them. The myocardial tubes then fuse to enclose the endocardial cells and form the definitive heart tube. By 22 hours postfertilization (26-somite stage), the heart tube is clearly beating. The regionalization of cardiac myosin heavy chain expression distinguishes the cardiac chambers at this stage, although they are not morphologically delineated until 36 hours. This work shows that cardiogenic regions can be identified in the early blastula, and that chamber restriction seems to arise in the midblastula. Additionally, it provides the basis for embryological perturbation at the single cell level, as well as for the genetic analysis of heart tube formation in the zebrafish. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP STAINIER, DYR (reprint author), MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,149 13TH ST,BOSTON,MA 02129, USA. FU NHLBI NIH HHS [R01 HL49579] NR 34 TC 217 Z9 221 U1 1 U2 16 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 SEP PY 1993 VL 119 IS 1 BP 31 EP 40 PG 10 WC Developmental Biology SC Developmental Biology GA LZ404 UT WOS:A1993LZ40400003 PM 8275863 ER PT J AU MARYNIUK, MD AF MARYNIUK, MD TI LIPID-LOWERING DIETS - PUTTING GUIDELINES INTO PRACTICE SO DIABETES EDUCATOR LA English DT Article AB The incidence of cardiovascular disease is four to five times greater in people with diabetes than in people without diabetes. Lipid disorders, along with elevated blood pressure, cigarette smoking and abdominal obesity, are major risk factors for people with diabetes. All adults with diabetes should be screened for blood lipid levels including triglycerides, cholesterol, and high-density lipoprotein (HDL) cholesterol. The low-density lipoprotein (LDL) cholesterol should be measured more routinely in people with diabetes than suggested in the National Cholesterol Education Project (NCEP) guidelines. No single diet is best for persons with diabetes. Sometimes a lower fat, higher carbohydrate diet is more acceptable, and other times a lower carbohydrate, higher monounsaturated fatty acid (MUFA) diet is preferred The decision regarding the level of fat in the diet is based both on patient preference as well as serial measurements of metabolic control. Changing eating habits regarding lipids is a gradual process and can best be accomplished when introduced in a staged approach. RP MARYNIUK, MD (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DIABETES EDUCATORS PI CHICAGO PA STE 1240, 444 NORTH MICHIGAN AVE, CHICAGO, IL 60611-3901 SN 0145-7217 J9 DIABETES EDUCATOR JI Diabetes Educ. PD SEP-OCT PY 1993 VL 19 IS 5 BP 431 EP 437 DI 10.1177/014572179301900510 PG 7 WC Endocrinology & Metabolism; Public, Environmental & Occupational Health SC Endocrinology & Metabolism; Public, Environmental & Occupational Health GA MZ610 UT WOS:A1993MZ61000010 PM 8137698 ER PT J AU FENDERSON, BA STAMENKOVIC, I ARUFFO, A AF FENDERSON, BA STAMENKOVIC, I ARUFFO, A TI LOCALIZATION OF HYALURONAN IN MOUSE EMBRYOS DURING IMPLANTATION, GASTRULATION AND ORGANOGENESIS SO DIFFERENTIATION LA English DT Article ID METRIAL GLAND-CELLS; STREPTOMYCES HYALURONIDASE; RAT EMBRYOS; EXTRACELLULAR-MATRIX; NEURAL-TUBE; GLYCOSAMINOGLYCANS; RECEPTOR; SURFACE; REGION; CD44 AB Hyaluronan was localized in postimplantation mouse embryos using CD44, the principal hyaluronan receptor. The specificity of CD44 receptor-globulin labelling was confirmed using Streptomyces hyaluronidase, anti-chondroitin sulfate antibody, and other receptor globulins. Our major findings are summarized as follows: 1. Implantation of the blastocyst into the uterine wall triggers a rapid loss of hyaluronan from the extracellular matrix of decidual cells on the anti-mesometrial side of the uterus. 2. Hyaluronan appears early in development in the yolk cavity, and the basement membranes of primitive ectoderm and primitive endoderm. 3. During gastrulation, mesodermal cells enter a hyaluronan-rich environment, but lack a pericellular hyaluronan coat themselves. 4. In limb bud embryos, hyaluronan is present throughout the cranial mesenchyme, but is generally not present in the branchial bars, somites, or limb buds. 5. At mid-gestation, hyaluronan is present in the axial skeleton, craniofacial mesenchyme, endocardial cushions of the heart, smooth muscle of the gastrointestinal tract, and connective tissue throughout the body. The pattern of hyaluronan expression in the day 13 fetus is nearly identical to the published distribution of transforming growth factor beta (TGF beta), suggesting a close functional relationship between these molecules. Together, the results suggest that hyaluronan is involved in the formation of early mesoderm, differentiation of craniofacial mesenchyme, and morphogenesis of the axial skeleton. C1 BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA 98121. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP FENDERSON, BA (reprint author), THOMAS JEFFERSON UNIV,DEPT PATHOL & CELL BIOL,1020 LOCUST ST,ROOM 233 JEFFERSON HALL,PHILADELPHIA,PA 19107, USA. FU NCI NIH HHS [CA 55735] NR 65 TC 61 Z9 61 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD SEP PY 1993 VL 54 IS 2 BP 85 EP 98 PG 14 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA LY040 UT WOS:A1993LY04000003 PM 7694885 ER PT J AU BLEDAY, R BRAIDT, J RUOFF, K SHELLITO, PC ACKROYD, FW AF BLEDAY, R BRAIDT, J RUOFF, K SHELLITO, PC ACKROYD, FW TI QUANTITATIVE CULTURES OF THE MUCOSAL-ASSOCIATED BACTERIA IN THE MECHANICALLY PREPARED COLON AND RECTUM SO DISEASES OF THE COLON & RECTUM LA English DT Article DE QUANTITATIVE CULTURES; COLON MUCOSA ID BOWEL AB Little is known about the mucosal microflora of the colon and rectum at the time of elective surgery. Our objective was to determine the concentrations of anaerobic and aerobic bacteria associated with the mucosa of the mechanically prepared large bowel. Ten patients were studied after a standard polyethylene glycol-electrolyte lavage preparation. No patient had taken antibiotics in the preceding four weeks. Sterile wire brushes passed through the colonoscope during advancement were used to culture the rectal, transverse colon, and cecal mucosa. Total anaerobic, aerobic, Gram-positive, and enteric bacterial counts were determined along with specific cultures for Bacteroides fragilis, Clostridium difficile, Escherichia coli, Pseudomonas aeruginosa, enterococcus, and staphylococcus species. The results showed that there was a significant increase (P < 0.01) in aerobes, anaerobes, enterics, Gram positives, B. fragilis, and E. coli mucosal counts with proximal progression. Aerobes showed a steady gradient, while anaerobes demonstrated an increase from the rectum to the transverse colon but no change between the transverse colon and cecum. We conclude that, in the prepared bowel, there is an increase in the mucosal bacterial counts in the more proximal portions of the bowel. The results may serve as a baseline for future studies on the mucosal-associated bacteria of the large intestine. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MIKROBIOL,BOSTON,MA 02114. RP BLEDAY, R (reprint author), HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT SURG,110 FRANCIS ST,SUITE 3A,BOSTON,MA 02215, USA. NR 7 TC 11 Z9 11 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0012-3706 J9 DIS COLON RECTUM JI Dis. Colon Rectum PD SEP PY 1993 VL 36 IS 9 BP 844 EP 849 DI 10.1007/BF02047381 PG 6 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA LW414 UT WOS:A1993LW41400009 PM 8375226 ER PT J AU HOESS, A WATSON, S SIBER, GR LIDDINGTON, R AF HOESS, A WATSON, S SIBER, GR LIDDINGTON, R TI CRYSTAL-STRUCTURE OF AN ENDOTOXIN-NEUTRALIZING PROTEIN FROM THE HORSESHOE-CRAB, LIMULUS ANTI-LPS FACTOR, AT 1.5 ANGSTROM RESOLUTION SO EMBO JOURNAL LA English DT Article DE ENDOTOXIN-NEUTRALIZING PROTEIN; HORSESHOE CRAB; MEMBRANE INSERTION; SEPTIC SHOCK; X-RAY STRUCTURE ID PERMEABILITY-INCREASING PROTEIN; GRAM-NEGATIVE BACTEREMIA; SEPTIC SHOCK; ANTILIPOPOLYSACCHARIDE FACTOR; LIPOPOLYSACCHARIDE FACTOR; 3-DIMENSIONAL STRUCTURE; PSEUDOMONAS-AERUGINOSA; TRITON X-114; POLYMYXIN-B; EXOTOXIN-A AB Lipopolysaccharide (LPS), or endotoxin, is the major mediator of septic shock, a serious complication of Gram-negative bacterial infections in humans. Molecules that bind LPS and neutralize its biological effects or enhance its clearance could have important clinical applications. Limulus anti-LPS factor (LALF) binds LPS tightly, and, in animal models, reduces mortality when administered before or after LPS challenge or bacterial infection. Here we present the high resolution structure of a recombinant LALF. It has a single domain consisting of three alpha-helices packed against a four-stranded beta-sheet. The wedge-shaped molecule has a striking charge distribution and amphipathicity that suggest how it can insert into membranes. The binding site for LPS probably involves an extended amphipathic loop, and we propose that two mammalian LPS-binding proteins will have a similar loop. The amphipathic loop structure may be used in the design of molecules with therapeutic properties against septic shock. C1 HARVARD UNIV, SCH MED,DANA FARBER CANC INST,XRAY CRYSTALLOG LAB, 44 BINNEY ST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV INFECT DIS, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. CAPE COD INC, FALMOUTH, MA 02540 USA. NR 43 TC 201 Z9 203 U1 1 U2 5 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0261-4189 J9 EMBO J JI Embo J. PD SEP PY 1993 VL 12 IS 9 BP 3351 EP 3356 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LU513 UT WOS:A1993LU51300001 PM 8253062 ER PT J AU SHEEN, J AF SHEEN, J TI PROTEIN PHOSPHATASE-ACTIVITY IS REQUIRED FOR LIGHT-INDUCIBLE GENE-EXPRESSION IN MAIZE SO EMBO JOURNAL LA English DT Article DE CHLOROPHYLL; LIGHT-INDUCIBLE GENES; MAIZE GREENING; OKADAIC ACID; PROTEIN PHOSPHATASE ID SERINE THREONINE PHOSPHATASES; PROMOTER OKADAIC ACID; DNA-BINDING PROTEINS; DIFFERENTIAL EXPRESSION; HIGHER-PLANTS; PHOSPHOENOLPYRUVATE CARBOXYLASE; CHLOROPLAST DEVELOPMENT; PHYTOCHROME REGULATION; TRANSCRIPTION FACTORS; TRANSDUCTION PATHWAY AB Chlorophyll accumulation and photosynthetic gene activation are two hallmarks of greening process in etiolated maize leaves in response to light signals. However, very little is known about the relevant signal transduction pathways mediating these essential processes that lead to photosynthetic competence. It is shown here that a potent and specific protein phosphatase 1 (PP1) and PP2A inhibitor, okadaic acid, efficiently blocks chlorophyll accumulation induced by light in etiolated maize leaves. In addition, the light-inducible expression of two photosynthetic fusion genes can be specifically suppressed by the structurally unrelated PPI and PP2A inhibitors, okadaic acid and calyculin A, using a sensitive and physiological maize protoplast transient assay. The specificity and effective concentration of the inhibitors in vivo and in vitro strongly suggest that PP1 is required for transmitting tight signals. Intriguingly, several partial cDNAs encoding novel as well as conserved PP1 can be identified in maize leaves using the polymerase chain reaction. Studies of chimeric promoters indicate that PP1 activity is essential for the interaction of multiple regulatory elements. Although PP1 and PP2A have been implicated in the suppression of gene activity in yeast and animals, the present data indicate that PP1 appears to be essential for light-dependent gene activation in plants. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP SHEEN, J (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114, USA. NR 90 TC 152 Z9 153 U1 0 U2 5 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD SEP PY 1993 VL 12 IS 9 BP 3497 EP 3505 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LU513 UT WOS:A1993LU51300017 PM 8253076 ER PT J AU ZHANG, J BOTTARO, A LI, S STEWART, V ALT, FW AF ZHANG, J BOTTARO, A LI, S STEWART, V ALT, FW TI A SELECTIVE DEFECT IN IGG2B SWITCHING AS A RESULT OF TARGETED MUTATION OF THE I-GAMMA-2B PROMOTER AND EXON SO EMBO JOURNAL LA English DT Article DE CLASS SWITCHING; GENE TARGETING; GERMLINE TRANSCRIPTION; I-GAMMA-2B; RAG-2-DEFICIENT BLASTOCYST COMPLEMENTATION ID HEAVY-CHAIN SWITCH; MURINE B-CELLS; EPSILON-TRANSCRIPTS; INTERFERON-GAMMA; CIRCULAR DNA; STEM-CELLS; C-EPSILON; IMMUNOGLOBULIN; EXPRESSION; INTERLEUKIN-4 AB LPS stimulation of B lymphocytes induces germline transcription of and subsequent switching to the gamma2b gene. Mature germline transcripts contain an I exon (non-coding) spliced to the Cgamma2b exons. To investigate the role of germline transcription and/or transcripts in heavy chain class switching, we have replaced the germline Igamma2b promoter and I exon in ES cells with an expressed neomycin resistance gene. The mutated chromosome retains the downstream target sequence for switch recombination (S regions) and all sequences necessary for expression of a switched gamma2b gene. Wild-type or mutant ES cells were injected into RAG-2 deficient blastocysts to generate somatic chimeras in which all lymphocytes were ES-cell derived. Chimeras derived from injection of heterozygous mutant ES cells had normal levels of serum IgG2b, but their splenic B cells showed a partial decrease in ability to switch to gamma2b. Strikingly, B lymphocytes from chimeras derived by injection of homozygous mutant ES cells were deficient in IgG2b production both in vivo and in vitro, but normal with respect to production of other Ig heavy chain isotypes. Additional studies demonstrated that lack of ability to produce IgG2b by the mutant B cells correlated with lack of germline transcription and resulted from a specific defect in class-switch recombination to Sgamma2b. Together, these studies demonstrate that the I region is an important regulatory element for control of class-switch recombination. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP ZHANG, J (reprint author), HARVARD UNIV,CHILDRENS HOSP,HOWARD HUGHES MED INST,CTR BLOOD RES,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-20047, AI31541] NR 47 TC 188 Z9 189 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD SEP PY 1993 VL 12 IS 9 BP 3529 EP 3537 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LU513 UT WOS:A1993LU51300020 PM 8253079 ER PT J AU ROTHER, KI LEVITSKY, LL AF ROTHER, KI LEVITSKY, LL TI DIABETES-MELLITUS DURING ADOLESCENCE SO ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA LA English DT Review ID BLOOD-GLUCOSE CONTROL; GROWTH FACTOR-I; SUBCUTANEOUS INSULIN INFUSION; IMPROVED METABOLIC CONTROL; IMPROVED GLYCEMIC CONTROL; HORMONE-BINDING-PROTEIN; LIMITED JOINT MOBILITY; DAWN PHENOMENON; MICROVASCULAR COMPLICATIONS; SOMATOSTATIN ANALOG C1 MASSACHUSETTS GEN HOSP, WANG AMBULATORY CARE CTR 709, PEDIAT ENDOCRINE UNIT, 15 PARKMAN ST, BOSTON, MA 02114 USA. MAYO CLIN & MAYO FDN, DEPT PEDIAT, ROCHESTER, MN 55905 USA. HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02115 USA. NR 145 TC 3 Z9 3 U1 1 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0889-8529 J9 ENDOCRIN METAB CLIN JI Endocrinol. Metabol. Clin. North Amer. PD SEP PY 1993 VL 22 IS 3 BP 553 EP 572 PG 20 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LY546 UT WOS:A1993LY54600007 PM 8243447 ER PT J AU BRAMSON, RT BLICKMAN, JG AF BRAMSON, RT BLICKMAN, JG TI PEDIATRIC BRONCHOGRAPHY PERFORMED THROUGH THE FLEXIBLE BRONCHOSCOPE - REPLY SO EUROPEAN JOURNAL OF RADIOLOGY LA English DT Letter RP BRAMSON, RT (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV PEDIAT IMAGING,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0720-048X J9 EUR J RADIOL JI Eur. J. Radiol. PD SEP PY 1993 VL 17 IS 2 BP 135 EP 136 DI 10.1016/0720-048X(93)90055-R PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MA099 UT WOS:A1993MA09900019 ER PT J AU GAA, J LEE, MJ GEORGI, M AF GAA, J LEE, MJ GEORGI, M TI CT IN PSEUDOMEMBRANOUS COLITIS SO FORTSCHRITTE AUF DEM GEBIETE DER RONTGENSTRAHLEN UND DER NEUEN BILDGEBENDEN VERFAHREN LA German DT Article DE COMPUTED TOMOGRAPHY; PSEUDOMEMBRANOUS COLITIS; CLOSTRIDIUM-DIFFICILE; ANTIBIOTICS ID PSEUDO-MEMBRANOUS COLITIS; COMPUTED-TOMOGRAPHY; APPEARANCE; DIAGNOSIS AB Pseudomembranous colitis (PMC) is an infectious colitis usually occurring as a complication of antibiotic therapy. The computed tomography (CT) findings of 10 patients with PMC are reviewed. All patients demonstrated an abnormal large bowel wall with an average thickness of 13 mm (range 7 - 31 mm). Additional, but less frequent findings included mesenteric inflammation, ascites, pleural effusions, and dilatation of the large or small bowel. Pancolonic involvement was seen in 7 cases, while three patients had focal colitis. Although the CT appearance of PMC is not specific, the diagnosis may be suggested in the proper clinical setting. C1 UNIV HEIDELBERG, KLINIKUM MANNHEIM, INST KLIN RADIOL, W-6800 MANNHEIM 1, GERMANY. MASSACHUSETTS GEN HOSP, DEPT GASTROINTESTINAL RADIOL, BOSTON, MA 02114 USA. NR 20 TC 2 Z9 2 U1 0 U2 0 PU GEORG THIEME VERLAG KG PI STUTTGART PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY SN 0936-6652 J9 ROFO FORTSCHR RONTG JI Fortschritte Geb. Rontgenstr. Neuen Bildgebenden Verfahren PD SEP PY 1993 VL 159 IS 3 BP 218 EP 221 DI 10.1055/s-2008-1032753 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LZ078 UT WOS:A1993LZ07800003 PM 8374107 ER PT J AU MORI, M STANIUNAS, RJ BARNARD, GF JESSUP, JM STEELE, GD CHEN, LB AF MORI, M STANIUNAS, RJ BARNARD, GF JESSUP, JM STEELE, GD CHEN, LB TI THE SIGNIFICANCE OF CARBONIC-ANHYDRASE EXPRESSION IN HUMAN COLORECTAL-CANCER SO GASTROENTEROLOGY LA English DT Article ID IMMUNOHISTOCHEMICAL LOCALIZATION; LAMININ RECEPTOR; MESSENGER-RNA; HUMAN COLON; EVOLUTION; CARCINOMA; ISOZYMES; PROTEINS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL M840,44 BINNEY ST,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,DEPT SURG,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT GASTROENTEROL,BOSTON,MA 02115. UNIV MASSACHUSETTS,MED CTR,DIV DIGEST DIS & NUTR,WORCESTER,MA 01605. FU NCI NIH HHS [T32CA09580, P0ICA44704, P0ICA19589] NR 22 TC 81 Z9 81 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD SEP PY 1993 VL 105 IS 3 BP 820 EP 826 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LV382 UT WOS:A1993LV38200022 PM 8359652 ER PT J AU WU, GD BEER, DG MOORE, JH ORRINGER, MB APPELMAN, HD TRABER, PG AF WU, GD BEER, DG MOORE, JH ORRINGER, MB APPELMAN, HD TRABER, PG TI SUCRASE-ISOMALTASE GENE-EXPRESSION IN BARRETT-ESOPHAGUS AND ADENOCARCINOMA SO GASTROENTEROLOGY LA English DT Article ID INTESTINAL METAPLASIA; EPITHELIUM; CANCER; CRYPT; CELLS; TRANSCRIPTION; CHEMOTHERAPY; CARCINOMAS; ENTEROCYTE; DYSPLASIA C1 UNIV PENN, SCH MED, DEPT INTERNAL MED, DIV GASTROENTEROL, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA USA. UNIV MICHIGAN, SCH MED, DEPT SURG, ANN ARBOR, MI 48104 USA. UNIV MICHIGAN, SCH MED, DEPT PATHOL, ANN ARBOR, MI 48104 USA. FU NCI NIH HHS [CA 46592]; NIDDK NIH HHS [DK41393, DK44621] NR 51 TC 40 Z9 40 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 EI 1528-0012 J9 GASTROENTEROLOGY JI Gastroenterology PD SEP PY 1993 VL 105 IS 3 BP 837 EP 844 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LV382 UT WOS:A1993LV38200024 PM 8359653 ER PT J AU MILNE, GT WEAVER, DT AF MILNE, GT WEAVER, DT TI DOMINANT-NEGATIVE ALLELES OF RAD52 REVEAL A DNA-REPAIR RECOMBINATION COMPLEX INCLUDING RAD51 AND RAD52 SO GENES & DEVELOPMENT LA English DT Article DE RAD52; RAD51; DOUBLE-STRAND BREAK REPAIR; NEGATIVE DOMINANCE ID TRUNCATED RECA GENES; SACCHAROMYCES-CEREVISIAE; ESCHERICHIA-COLI; PROTEIN; YEAST; COMPLEMENTATION; MUTATIONS AB Saccharomyes cerevisiae rad52 mutants are characterized by severe defects in double-strand break (DSB) repair and recombination. In this study we have identified several regions of RAD52 that are required for these biological functions. We cloned and characterized a RAD52 homolog from Kluyveromyces lactis that partially complemented S. cerevisiae rad52 mutants while exhibiting negative dominance in wild-type (RAD52) strains. The dominant negative effect was suppressed by overexpression of RAD51, an additional gene known to be required for DSB repair and recombination, indicating a genetic interaction between these loci. Furthermore, GAL4 two-hybrid analysis revealed a physical interaction between Rad51 and the carboxy-terminal one-third of Rad52. Deletion alleles of rad52 (with or without the Rad51 association domain) also produced dominant negative defects, suggesting the disruption of repair through nonfunctional interactions with other DSB repair and recombination proteins. RAD51 relieved the negative dominance of each of these alleles either by competitive titration or functional activation of mutant or heterologous Rad52 proteins. These results demonstrate the importance of Rad52-Rad51 interactions and point to the formation of a higher order repair/recombination complex potentially containing other yet unidentified components. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. RP MILNE, GT (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. NR 31 TC 210 Z9 213 U1 0 U2 2 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 SEP PY 1993 VL 7 IS 9 BP 1755 EP 1765 DI 10.1101/gad.7.9.1755 PG 11 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA LW555 UT WOS:A1993LW55500010 PM 8370524 ER PT J AU TOGUCHIDA, J MCGEE, TL PATERSON, JC EAGLE, JR TUCKER, S YANDELL, DW DRYJA, TP AF TOGUCHIDA, J MCGEE, TL PATERSON, JC EAGLE, JR TUCKER, S YANDELL, DW DRYJA, TP TI COMPLETE GENOMIC SEQUENCE OF THE HUMAN RETINOBLASTOMA SUSCEPTIBILITY GENE SO GENOMICS LA English DT Article ID DNA-SEQUENCES; HEREDITARY RETINOBLASTOMA; ESTERASE-D; LOCUS; PCR; ORGANIZATION; DELETIONS; AMPLIFICATION; POLYMORPHISMS; EVOLUTION C1 MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. FU NEI NIH HHS [EY08088, EY05321] NR 37 TC 136 Z9 142 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 0888-7543 J9 GENOMICS JI Genomics PD SEP PY 1993 VL 17 IS 3 BP 535 EP 543 DI 10.1006/geno.1993.1368 PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA LX233 UT WOS:A1993LX23300001 PM 7902321 ER PT J AU HENSKE, EP OZELIUS, L GUSELLA, JF HAINES, JL KWIATKOWSKI, DJ AF HENSKE, EP OZELIUS, L GUSELLA, JF HAINES, JL KWIATKOWSKI, DJ TI A HIGH-RESOLUTION LINKAGE MAP OF HUMAN 9Q34.1 SO GENOMICS LA English DT Article ID TUBEROUS SCLEROSIS; GENE; CHROMOSOME-9Q; POLYMORPHISM; PROGRAM; MARKER; LOCUS C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV EXPTL MED & HEMATOL ONCOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. RI Haines, Jonathan/C-3374-2012 FU AHRQ HHS [HS22031]; NHGRI NIH HHS [HG00169, HG00598] NR 18 TC 26 Z9 26 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 0888-7543 J9 GENOMICS JI Genomics PD SEP PY 1993 VL 17 IS 3 BP 587 EP 591 DI 10.1006/geno.1993.1376 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA LX233 UT WOS:A1993LX23300009 PM 8244374 ER PT J AU XIA, YR BACHINSKY, DR SMITH, JA MCCLUSKEY, RT WARDEN, CH LUSIS, AJ AF XIA, YR BACHINSKY, DR SMITH, JA MCCLUSKEY, RT WARDEN, CH LUSIS, AJ TI MAPPING OF THE GLYCOPROTEIN-330 (GP330) GENE TO MOUSE CHROMOSOME-2 SO GENOMICS LA English DT Note ID LDL-RECEPTOR; ALPHA-2-MACROGLOBULIN RECEPTOR; LIPOPROTEIN RECEPTOR; HEYMANN NEPHRITIS; PROTEIN; LOCALIZATION; ANTIBODIES; SEQUENCE C1 UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT MOLEC GENET,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT MICROBIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,INST MOLEC BIOL,LOS ANGELES,CA 90024. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MOLEC BIOL,BOSTON,MA 02114. FU NCI NIH HHS [CAO9216]; NHLBI NIH HHS [HL42488, HL30568] NR 18 TC 10 Z9 11 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 0888-7543 J9 GENOMICS JI Genomics PD SEP PY 1993 VL 17 IS 3 BP 780 EP 781 DI 10.1006/geno.1993.1408 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA LX233 UT WOS:A1993LX23300041 PM 8244399 ER PT J AU CASEY, AC BELL, DA LAGE, JM FULLER, AF NIKRUI, N RICE, LW AF CASEY, AC BELL, DA LAGE, JM FULLER, AF NIKRUI, N RICE, LW TI EPITHELIAL OVARIAN-TUMORS OF BORDERLINE MALIGNANCY - LONG-TERM FOLLOW-UP SO GYNECOLOGIC ONCOLOGY LA English DT Article ID PATHOLOGICAL ASSESSMENT; HISTOLOGIC FEATURES; SEROUS TUMORS; CARCINOMA; NEOPLASMS; PROGNOSIS; BEHAVIOR; IMPLANTS C1 HARVARD UNIV,SCH MED,VINCENT GYNECOL SERV,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT GYNECOL,DIV GYNECOL ONCOL,BOSTON,MA 02114. NR 32 TC 60 Z9 60 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 SEP PY 1993 VL 50 IS 3 BP 316 EP 322 DI 10.1006/gyno.1993.1218 PG 7 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA MC190 UT WOS:A1993MC19000010 PM 8406194 ER PT J AU SUPPES, T BALDESSARINI, RJ FAEDDA, GL TONDO, L TOHEN, M AF SUPPES, T BALDESSARINI, RJ FAEDDA, GL TONDO, L TOHEN, M TI DISCONTINUATION OF MAINTENANCE TREATMENT IN BIPOLAR DISORDER - RISKS AND IMPLICATIONS SO HARVARD REVIEW OF PSYCHIATRY LA English DT Review ID RECURRENT AFFECTIVE DISORDERS; MANIC-DEPRESSIVE PATIENTS; TERM LITHIUM TREATMENT; AFFECTIVE-ILLNESS; DOUBLE-BLIND; PROPHYLACTIC LITHIUM; MIXED MANIA; FOLLOW-UP; MEDICATION COMPLIANCE; ANTI-DEPRESSANTS AB There is abundant evidence for substantial long-term prophylactic efficacy of lithium in bipolar manic-depressive disorders. Interruption of such treatment carries an extraordinarily high risk of recurrence within several months, even after several years of stability. Even a sharp reduction in dose may carry some risk. Gradual discontinuation of lithium was accompanied by markedly reduced risk of early recurrence. There is suggestive evidence that the phenomenon of high risk of recurrence after abrupt interruption of maintenance treatment may occur with other disorder and treatments, including neuroleptics in schizophrenia and possibly antidepressants in recurrent depression. The phenomenon of discontinuation-associated iatrogenic risk of early recurrence of major psychiatric illness has clear clinical implications. These include the need to evaluate safer methods of interrupting long-term maintenance treatment, particularly when clinical indications tor rapid cessation are compelling and gradual discontinuation is not feasible. Questions also arise concerning interpretation of existing experimental studies of maintenance treatments that require interruption of treatment, reduction of dose, or crossover to a placebo, as well as the ethical and scientifically unambiguous design of future studies of this kind. C1 HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MCLEAN DIV,PSYCHIAT LABS,BELMONT,MA. MASSACHUSETTS GEN HOSP,MCLEAN DIV,PSYCHOT DISORDERS PROGRAM,BELMONT,MA. RI Faedda, Gianni/E-6379-2012 OI Faedda, Gianni/0000-0001-6197-0543 FU NIMH NIH HHS [MH-47370, MH-48444, MH-31154] NR 157 TC 55 Z9 55 U1 4 U2 5 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD SEP-OCT PY 1993 VL 1 IS 3 BP 131 EP 144 DI 10.3109/10673229309017072 PG 14 WC Psychiatry SC Psychiatry GA MU381 UT WOS:A1993MU38100001 PM 9384841 ER PT J AU MELLO, NK MENDELSON, JH LUKAS, SE GASTFRIEND, DR TEOH, SK HOLMAN, BL AF MELLO, NK MENDELSON, JH LUKAS, SE GASTFRIEND, DR TEOH, SK HOLMAN, BL TI BUPRENORPHINE TREATMENT OF OPIATE AND COCAINE ABUSE - CLINICAL AND PRECLINICAL STUDIES SO HARVARD REVIEW OF PSYCHIATRY LA English DT Article ID DRUG-SEEKING BEHAVIOR; FEMALE RHESUS-MONKEY; LUTEINIZING-HORMONE; INTRAVENOUS COCAINE; ANTERIOR-PITUITARY; ABRUPT WITHDRAWAL; OPIOID DEPENDENCE; OPERANT ANALYSIS; BRAIN PERFUSION; ACUTE TOLERANCE AB Buprenorphine, an opioid mixed agonist-antagonist, is a potent analgesic that appears to be effective for the treatment of opiate abuse. Recent preclinical studies have shown that buprenorphine also significantly reduces cocaine self-administration by rhesus monkeys for periods up to 120 days. This unexpected finding has led to clinical trials to evaluate buprenorphine's effectiveness for the treatment of dependence on both cocaine and opiates, as defined by DSM-III-R criteria. Buprenorphine's safety in combination with cocaine and opiates and its effects on electroencephalographic sleep patterns and regional cerebral blood flow were evaluated during inpatient studies. Buprenorphine (4 or 8 mg/day given sublingually) did not accentuate the cardiovascular and respiratory changes induced by an acute challenge dose of cocaine (30 mg given intravenously) or morphine (10 mg given intravenously) alone. In an outpatient open trial, buprenorphine significantly reduced both opiate and cocaine abuse by patients who had abused these drugs for more than 10 years. Most of these patients had failed in other drug abuse treatment programs. Reports of needle sharing also decreased significantly, and no patient tested positive for human immunodeficiency virus (HIV). The apparent safety and effectiveness of buprenorphine, combined with a high level of patient acceptance, led the Food and Drug Administration to grant a compassionate extension of the approved period for outpatient buprenorphine treatment from 26 to 52 weeks. Clinical trials of buprenorphine are ongoing. Possible mechanisms underlying buprenorphine-cocaine interactions are now under investigation. C1 MASSACHUSETTS GEN HOSP,ADDICT SERV,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115. RP MELLO, NK (reprint author), HARVARD UNIV,MCLEAN HOSP,SCH MED,ALCOHOL DRUG ABUSE RES CTR,115 MILL ST,BELMONT,MA 02178, USA. FU NIDA NIH HHS [DA 00101, DA 00064, DA 00115] NR 109 TC 40 Z9 40 U1 5 U2 7 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD SEP-OCT PY 1993 VL 1 IS 3 BP 168 EP 183 DI 10.3109/10673229309017075 PG 16 WC Psychiatry SC Psychiatry GA MU381 UT WOS:A1993MU38100004 PM 9384844 ER PT J AU SCHOUTEN, R AF SCHOUTEN, R TI LEGAL LIABILITY AND MANAGED CARE SO HARVARD REVIEW OF PSYCHIATRY LA English DT Article RP SCHOUTEN, R (reprint author), MASSACHUSETTS GEN HOSP,LAW & PSYCHIAT SERV,WARREN 605,FRUIT ST,BOSTON,MA 02114, USA. NR 3 TC 1 Z9 1 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD SEP-OCT PY 1993 VL 1 IS 3 BP 189 EP 190 DI 10.3109/10673229309017077 PG 2 WC Psychiatry SC Psychiatry GA MU381 UT WOS:A1993MU38100006 PM 9384846 ER PT J AU BUSSE, PM CLARK, JR BEARD, CJ DREYFUSS, AI LUCARINI, JW ROSSI, R CASEY, D NORRIS, CM AF BUSSE, PM CLARK, JR BEARD, CJ DREYFUSS, AI LUCARINI, JW ROSSI, R CASEY, D NORRIS, CM TI PRIMARY SITE MANAGEMENT FOLLOWING INDUCTION CHEMOTHERAPY WITH CISPLATINUM, 5-FLUOROURACIL, AND LEUCOVORIN SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK LA English DT Article ID NECK-CANCER; HEAD; CARCINOMA; CISPLATIN; INFUSION AB A phase II clinical trial was initiated in 1987 to evaluate a new induction regimen of cis-platinum, 5-fluorouracil, and leucovorin (PFL) for patients with stages III-IV squamous cell carcinoma of the head and neck. Ninety patients were treated and followed for a median duration of 18 months. The median age was 55 and 87% of the patients had stage IV disease. The rates of complete and overall clinical response following three cycles of PFL were 57% and 80%, respectively; the rate of complete response at the primary site was 72%. Eighty-four percent of patients were treated to the primary site with radiation alone (median dose 68 Gy in daily 1.8-Gy fractions) irrespective of the location of the primary site or initial T-stage. The acute tolerance to full-course radiation following PFL was acceptable. The actuarial rate of primary site control for patients treated with radiation was 67% at 36 months. An important prognostic indicator for primary site control was a complete clinical response to induction PFL. For patients who achieved a complete response, radiation or surgery followed by radiation controlled primary site disease equally well at 70%. Patients with a partial response did less well. For these patients, surgery and radiation appeared slightly better than radiation alone. (C) 1993 John Wiley & Sons. Inc. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,HEAD & NECK TUMOR SERV,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,DEPT OTOLARYNGOL HEAD & NECK SURG,JOINT CTR RADIAT THERAPY,BOSTON,MA 02215. RP BUSSE, PM (reprint author), HARVARD UNIV,JOINT CTR RADIAT THERAPY,50 BINNEY ST,CAMBRIDGE,MA 02138, USA. NR 10 TC 7 Z9 7 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1043-3074 J9 HEAD NECK-J SCI SPEC JI Head Neck-J. Sci. Spec. Head Neck PD SEP-OCT PY 1993 VL 15 IS 5 BP 413 EP 418 DI 10.1002/hed.2880150508 PG 6 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA LR992 UT WOS:A1993LR99200007 PM 8407313 ER PT J AU DEVI, BG HENDERSON, GI FROSTO, TA SCHENKER, S AF DEVI, BG HENDERSON, GI FROSTO, TA SCHENKER, S TI EFFECT OF ETHANOL ON RAT FETAL HEPATOCYTES - STUDIES ON CELL REPLICATION, LIPID-PEROXIDATION AND GLUTATHIONE SO HEPATOLOGY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; ALCOHOLIC LIVER-DISEASE; VITAMIN-E; REDUCED GLUTATHIONE; OXYGEN RADICALS; ENZYMES; METABOLISM; GROWTH; INJURY; DEPLETION AB Studies have shown that ethanol at moderate concentrations inhibits epidermal growth factor-dependent replication of fetal rat hepatocytes in culture. This may account for the growth/development impairment associated with fetal alcohol syndrome and decreased liver regeneration in alcoholic liver disease. In this study, we further define the mechanism(s) of the negative impact of ethanol on fetal rat hepatocytes and provide evidence that ethanol-induced injury to these cells is associated with membrane damage caused by lipid peroxidation, altered cell glutathione homeostasis and deranged mitochondrial structure and function. Exposure of fetal rat hepatocyte replication to ethanol (2 mg/ml) promptly resulted in blockade of replication, as indicated by a 40% reduction in DNA synthesis (p < 0.05). Assessment of cell injury on the basis of lactate dehydrogenase and ALT leakage indicated a statistically significant but not appreciable effect, whereas Cr-51 leakage was more substantially increased (p < 0.05). Within 6 hr of ethanol exposure, superoxide radical levels increased more than twofold (P < 0.05). We noted a 56% increase in levels of diene conjugates, a 131% increase in malonaldehyde concentration and a 66% increase in fluorescent products of lipid peroxidation (all p < 0.05). Glutathione levels were decreased to 47% below control values (p < 0.05). Electron microscopic studies illustrated a slight disruption of mitochondrial structure (enlargement of mitochondria and dilation of cristae). This disruption was accompanied by mitochondrial swelling (increased permeability), altered mitochondrial membrane potential (a 16% decrease in rhodamine uptake), a 28% decrease in succinate dehydrogenase activity and a 30% decrease in cellular ATP level (p < 0.05). Pretreatment of fetal rat hepatocytes with 0.1 mmol/L N-acetylcysteine or S-adenosylmethionine for 24 hr Prevented the ethanol-induced reduction of ATP and glutathione levels, essentially restored cell replication, ameliorated Cr-51 leakage and decreased malonaldehyde and diene conjugate levels to 41% to 65% and 25% above control values, respectively. Pretreatment with 0.1 mmol/L vitamin E fully normalized malonaldehyde and diene conjugate levels and Cr-51 leakage but failed to improve ATP levels or to increase significantly cell replication and glutathione levels. Concomitant administration of glutathione precursors with ethanol, rather than pretreatment, did not alter the impaired cell replication. Thus our data underscore the importance of cellular glutathione and ATP in preventing ethanol-induced decreases in fetal cell replication and suggest that alleviation of cellular lipid peroxidation alone is not sufficient to prevent this abnormality in fetal rat hepatocyte function. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL & NUTR,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NIAAA NIH HHS [R01 AA07514, KO2 AA00121] NR 77 TC 79 Z9 82 U1 0 U2 4 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 SEP PY 1993 VL 18 IS 3 BP 648 EP 659 DI 10.1016/0270-9139(93)90367-V PG 12 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LV018 UT WOS:A1993LV01800024 PM 8359806 ER PT J AU GOLDRING, SR GORN, AH YAMIN, M KRANE, SM WANG, JT AF GOLDRING, SR GORN, AH YAMIN, M KRANE, SM WANG, JT TI CHARACTERIZATION OF THE STRUCTURAL AND FUNCTIONAL-PROPERTIES OF CLONED CALCITONIN RECEPTOR CDNAS SO HORMONE AND METABOLIC RESEARCH LA English DT Article; Proceedings Paper CT WORKSHOP ON CALCITONIN, AT THE 23RD EUROPEAN SYMPOSIUM ON CALCIFIED TISSUE CY APR, 1993 CL HEIDELBERG, GERMANY DE CALCITONIN; RECEPTOR; HORMONE; BONE; RENAL ID HORMONE-RELATED PEPTIDE; PARATHYROID-HORMONE; EXPRESSION CLONING; MOLECULAR-CLONING; CROSS-LINKING; CELL-LINES; CYCLASE; RAT AB We have recently cloned CTRs from cDNA libraries prepared from porcine renal and human ovarian cell lines. In situ hybridization and Northern analysis confirm the widespread distribution of CTR mRNA in numerous tissues. Hydropathy plots of the predicted amino acid sequence of the receptors demonstrate multiple hydrophobic regions that could generate 7 transmembrane spanning domains, similar to other G protein-coupled receptors. Searches of databanks for proteins with related amino acid sequences reveals that the CTRs are closely related to the receptors for parathyroid hormone/parathyroid hormone related peptide, secretin, vasoactive intestinal peptide, growth hormone releasing hormone, glucagon-like peptide-1 and glucagon. These receptors have no significant sequence homology to other G protein-coupled receptors, and therefore, appear to comprise a distinct receptor family. Expression of the hCTR or pCTR in COS cells results in expression of high affinity CTRs which are coupled to adenylate cyclase (AC). The hCTR, however, demonstrates higher affinity for human and salmon CT compared to the pCTR. Both CTRs demonstrate low affinity binding and AC activation in response to calcitonin gene related peptide, amylin or secretin, providing a possible explanation for the cross-reactivity among these peptides in vivo. Stable transfectants expressing the pCTR increase cAMP levels and increases in cytosolic free Ca2+ concentration consistent with dual coupling to AC and phospholipase C. Additional studies will help to establish the structural basis for this functional property as well as the evolutionary relationship of the members of this newly identified family of receptors. C1 HARVARD UNIV,SCH MED,DEPT MED & MED SERV,ARTHRITIS UNIT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,SCH DENT MED,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. FU NIAMS NIH HHS [AR-03564] NR 21 TC 27 Z9 28 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0018-5043 J9 HORM METAB RES JI Horm. Metab. Res. PD SEP PY 1993 VL 25 IS 9 BP 477 EP 480 DI 10.1055/s-2007-1002153 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LW634 UT WOS:A1993LW63400006 PM 8225201 ER PT J AU YOSHIKAWA, TT NORMAN, DC AF YOSHIKAWA, TT NORMAN, DC TI ANTIBIOTIC-THERAPY - WHAT TO CONSIDER WHEN TREATING GERIATRIC-PATIENTS SO HOSPITAL FORMULARY LA English DT Review AB The epidemiology, etiology, clinical manifestations, diagnostic approach, and therapeutic choices may be quite different for infections that occur in elderly patients compared with those that occur in younger adults. Given these variables, it is essential for clinicians who care for older patients to understand how to prescribe antibiotics appropriately for this population. This article examines the unique characteristics of infections in the elderly as well as provides recommendations on the use of specific antibiotic agents commonly used to treat infections in geriatric patients. RP YOSHIKAWA, TT (reprint author), US DEPT VET AFFAIRS,OFF GERIATR & EXTENDED CARE 114,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ADVANSTAR COMMUNICATIONS PI DULUTH PA 131 W FIRST ST, DULUTH, MN 55802 SN 0098-6909 J9 HOSP FORMUL PD SEP PY 1993 VL 28 IS 9 BP 754 EP & PG 0 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LZ519 UT WOS:A1993LZ51900003 PM 10128820 ER PT J AU QUINTANILLAMARTINEZ, L WILKINS, EW FERRY, JA HARRIS, NL AF QUINTANILLAMARTINEZ, L WILKINS, EW FERRY, JA HARRIS, NL TI THYMOMA - MORPHOLOGIC SUBCLASSIFICATION CORRELATES WITH INVASIVENESS AND IMMUNOHISTOLOGIC FEATURES - A STUDY OF 122 CASES SO HUMAN PATHOLOGY LA English DT Article DE THYMOMA CLASSIFICATION; HISTOLOGY; CARCINOMA; IMMUNOPHENOTYPE ID THYMIC EPITHELIAL TUMORS; MYASTHENIA-GRAVIS; CLINICAL STAGES; PROGNOSIS; CARCINOMA; COMPONENT C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,WARREN 2,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,THORAC SURG UNIT,BOSTON,MA 02114. NR 33 TC 79 Z9 81 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 SEP PY 1993 VL 24 IS 9 BP 958 EP 969 DI 10.1016/0046-8177(93)90109-T PG 12 WC Pathology SC Pathology GA LX830 UT WOS:A1993LX83000005 PM 8253462 ER PT J AU HAUPERT, GT NORMAN, JA LO, LC TYMIAK, AA AF HAUPERT, GT NORMAN, JA LO, LC TYMIAK, AA TI PHYSICOCHEMICAL CHARACTERIZATION OF A NA,K-ATPASE INHIBITOR ISOLATED FROM BOVINE HYPOTHALAMUS SO HYPERTENSION LA English DT Meeting Abstract C1 BRISTOL MYERS SQUIBB PHARMACEUT RES INST,PRINCETON,NJ. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. COLUMBIA UNIV,NEW YORK,NY 10027. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD SEP PY 1993 VL 22 IS 3 BP 433 EP 433 PG 1 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LW313 UT WOS:A1993LW31300144 ER PT J AU TANG, SS DIAMANT, D JUNG, FF INGELFINGER, JR AF TANG, SS DIAMANT, D JUNG, FF INGELFINGER, JR TI IMMORTALIZATION OF RAT RENAL PROXIMAL TUBULAR CELL (RPTC) LINES EXPRESSING COMPONENTS OF THE RENIN-ANGIOTENSIN SYSTEM (RAS) SO HYPERTENSION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD SEP PY 1993 VL 22 IS 3 BP 444 EP 444 PG 1 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LW313 UT WOS:A1993LW31300199 ER PT J AU DRIEVER, W RANGINI, Z AF DRIEVER, W RANGINI, Z TI CHARACTERIZATION OF A CELL-LINE DERIVED FROM ZEBRAFISH (BRACHYDANIO-RERIO) EMBRYOS SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL LA English DT Article DE ZEBRAFISH; CELL LINE; CHROMOSOMES; TRANSFECTION; PROMOTER STRENGTH ID TRANSGENIC FISH; GENE-TRANSFER; STEM-CELLS; EXPRESSION; SEQUENCES; MUTATION; ELECTROPORATION; TRANSMISSION; SELECTION; PROMOTERS AB During the last decade, zebrafish (Brachydanio rerio) have emerged as a novel and attractive system to study embryogenesis and organogenesis in vertebrates. The main reason is that both extensive genetic studies and detailed embryologic analysis are possible using this small tropical fresh water teleost. However, in vitro analysis using cell culture or molecular genetics are still far less advanced than in other vertebrate systems. Here we report the generation and characterization of a fibroblast like cell line, ZF4, derived from 1-day-old zebrafish embryos. The hyperploid cell line has been stable in multiple passages for more than 2 yr now and is the first zebrafish cell line that can be maintained in conventional medium containing mammalian serum. Using a series of plasmids for expression of a marker gene, we evaluate in ZF4 cells the relative strength of expression from several different viral, fish, and mammalian promoters. Stable integration can be obtained by using G418 selection. We hope that our cell line will be a useful tool for the analysis of gene regulation in zebrafish. RP DRIEVER, W (reprint author), MASSACHUSETTS GEN HOSP E 4216,CARDIOVASC RES CTR,149 13TH ST,BOSTON,MA 02129, USA. NR 47 TC 74 Z9 75 U1 0 U2 14 PU SOC IN VITRO BIOLOGY PI UPPER MARLBORO PA 9315 LARGO DR W #255, UPPER MARLBORO, MD 20774-4755 SN 1071-2690 J9 IN VITRO CELL DEV-AN JI In Vitro Cell. Dev. Biol.-Anim. PD SEP PY 1993 VL 29 IS 9 BP 749 EP 754 PG 6 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA MD189 UT WOS:A1993MD18900013 PM 8407719 ER PT J AU AWWAD, JT TOTH, TL SCHIFF, I AF AWWAD, JT TOTH, TL SCHIFF, I TI ABNORMAL UTERINE BLEEDING IN THE PERIMENOPAUSE SO INTERNATIONAL JOURNAL OF FERTILITY LA English DT Article DE MENOPAUSE; PERIMENOPAUSE; UTERINE BLEEDING (ABNORMAL); HYSTERECTOMY; MEDICAL (STEROIDAL) TREATMENT ID MENSTRUAL BLOOD-LOSS; HORMONE REPLACEMENT THERAPY; ORAL-CONTRACEPTIVE USE; ESTROGEN THRESHOLD HYPOTHESIS; LEUPROLIDE ACETATE DEPOT; ENDOMETRIAL ABLATION; MEFENAMIC-ACID; LEIOMYOMATA UTERI; DOUBLE-BLIND; MENOPAUSAL TRANSITION AB Abnormal uterine bleeding is probably one of the most common gynecologic complaints in the perimenopause. It is a significant cause of hysterectomy, which is the second most common surgical procedure performed on women in the United States, and thus is a major health issue. Management consists of a stepwise evaluation of all possible organic causes of uterine bleeding. Advancements in technology have allowed considerable improvements in the resolution of many diagnostic tools. Direct visualization of the uterine cavity is now an invaluable adjunct to blind endometrial sampling. Consequently, therapy can be tailored more appropriately and efficiently, either by newly developed medical strategies or through selective, minimally invasive surgery. In light of these perspectives, some of the recent diagnostic and therapeutic trends in the management of abnormal uterine bleeding in perimenopausal women are presented. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,VINCENT MEM GYNECOL SERV,BOSTON,MA 02114. NR 92 TC 17 Z9 17 U1 0 U2 1 PU MEDICAL SCIENCE PUBLISHING INT INC PI PORT WASHINGTON PA 405 MAIN ST, PORT WASHINGTON, NY 11050 SN 0020-725X J9 INT J FERTIL PD SEP-OCT PY 1993 VL 38 IS 5 BP 261 EP 269 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA ME794 UT WOS:A1993ME79400001 PM 8298664 ER PT J AU ZIETMAN, AL SHIPLEY, WU KAUFMAN, DS AF ZIETMAN, AL SHIPLEY, WU KAUFMAN, DS TI THE COMBINATION OF CISPLATIN-BASED CHEMOTHERAPY AND RADIATION IN THE TREATMENT OF MUSCLE-INVADING TRANSITIONAL-CELL CANCER OF THE BLADDER SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE CARCINOMA OF BLADDER; RADIATION; TRANSURETHRAL RESECTION; CHEMOTHERAPY ID NEO-ADJUVANT CHEMOTHERAPY; M-VAC METHOTREXATE; RADICAL RADIOTHERAPY; CISPLATIN CHEMOTHERAPY; TRANSURETHRAL RESECTION; SALVAGE CYSTECTOMY; PROSPECTIVE TRIAL; THERAPEUTIC GAIN; URINARY-BLADDER; CARCINOMA AB Radical cystectomy is the standard of care for patients with muscle-invading transitional cell carcinoma of the bladder. More limited surgery is only useful in highly selected patients and radiation therapy alone gives overall local-control rates under 40%. Phase II studies have shown that when radiation and trans-urethral surgery are combined with cis-platin based chemotherapy local-control rates increase such that the majority of patients preserve a tumor-free functional bladder. Up to 85% of patients selected for bladder sparing therapy on the basis of their initial response to chemo-radiation may keep their bladders. This figure could increase further when other powerful prognostic factors such as the presence of hydronephrosis, the presence of carcinoma in situ, and DNA ploidy are also taken into account in initial patient selection. The activity of cisplatin combinations in metastatic disease is not in doubt with up to 50% response rates generally reported. The hope that this will translate into the eradication of micrometastatic disease (known to be present in up to 40% of patients at diagnosis) has yet to be borne out. Those randomized trials so far reported have not shown any survival advantage when combined-modality therapy is compared to radiation alone. The addition of combination chemotherapy to radiation does not increase bladder morbidity but carries a considerable systemic penalty. Thus, despite promising Phase II studies, until local control and survival benefit is proven in a randomized trial it should continue to be regarded as experimental. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV MED ONCOL,BOSTON,MA 02114. RP ZIETMAN, AL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,GENITOURINARY ONCOL UNIT,BOSTON,MA 02114, USA. NR 66 TC 34 Z9 35 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 SEP 1 PY 1993 VL 27 IS 1 BP 161 EP 170 PG 10 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LX662 UT WOS:A1993LX66200021 PM 8365937 ER PT J AU COHEN, MS FORDHAM, J AF COHEN, MS FORDHAM, J TI DEVELOPMENTS IN MAGNETIC-RESONANCE-IMAGING SO INVESTIGATIVE RADIOLOGY LA English DT Article ID CONTRAST AGENTS; PERFUSION; HEART; MRI RP COHEN, MS (reprint author), MASSACHUSETTS GEN HOSP,NMR CTR,BOSTON,MA, USA. NR 33 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 SEP PY 1993 VL 28 SU 4 BP S32 EP S37 DI 10.1097/00004424-199309001-00007 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LZ448 UT WOS:A1993LZ44800007 PM 8225900 ER PT J AU WOLF, GL GAZELLE, S AF WOLF, GL GAZELLE, S TI CURRENT STATUS OF RADIOGRAPHIC CONTRAST-MEDIA SO INVESTIGATIVE RADIOLOGY LA English DT Article ID RANDOMIZED CONTROLLED TRIALS; HIGH-OSMOLALITY; AGENTS; QUALITY; SAFETY C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP WOLF, GL (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 17 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 SEP PY 1993 VL 28 SU 4 BP S2 EP S4 DI 10.1097/00004424-199309001-00002 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LZ448 UT WOS:A1993LZ44800002 PM 8225898 ER PT J AU WOLF, GL SKORTON, DJ AF WOLF, GL SKORTON, DJ TI ADVANCES IN IMAGING - CONTEMPORARY-ISSUES FOR THE CARDIOLOGIST AND THE RADIOLOGIST SO INVESTIGATIVE RADIOLOGY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV IOWA,COLL MED,IOWA CITY,IA 52242. UNIV IOWA,COLL ENGN,IOWA CITY,IA 52242. RP WOLF, GL (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, 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 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD SEP PY 1993 VL 28 SU 4 BP S1 EP S1 DI 10.1097/00004424-199309001-00001 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LZ448 UT WOS:A1993LZ44800001 ER PT J AU JASTY, M AF JASTY, M TI PARTICULATE DEBRIS AND FAILURE OF TOTAL HIP REPLACEMENTS SO JOURNAL OF APPLIED BIOMATERIALS LA English DT Article ID CEMENTED FEMORAL COMPONENTS; SYNOVIAL-LIKE MEMBRANE; BONE-RESORPTION; ARTHROPLASTIES; LYSIS; INTERFACE C1 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 42 TC 59 Z9 61 U1 0 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1045-4861 J9 J APPL BIOMATER JI J. Appl. Biomater. PD FAL PY 1993 VL 4 IS 3 BP 273 EP 276 DI 10.1002/jab.770040310 PG 4 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA LT931 UT WOS:A1993LT93100009 PM 10146311 ER PT J AU BROWN, RA GELBERMAN, RH SEILER, JG ABRAHAMSSON, SO WEILAND, AJ URBANIAK, JR SCHOENFELD, DA FURCOLO, D AF BROWN, RA GELBERMAN, RH SEILER, JG ABRAHAMSSON, SO WEILAND, AJ URBANIAK, JR SCHOENFELD, DA FURCOLO, D TI CARPAL-TUNNEL RELEASE - A PROSPECTIVE, RANDOMIZED ASSESSMENT OF OPEN AND ENDOSCOPIC METHODS SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article AB To define the role of two-portal endoscopic carpal-tunnel release as a method for the treatment of compression of the median nerve at the wrist, a prospective, randomized, multicenter study was performed on 169 hands in 145 patients. Either open or endoscopic carpal-tunnel release was performed in all of the patients who had clinical signs and symptoms consistent with carpal tunnel syndrome, had not responded to or had refused non-operative management, and had had electrodiagnostic studies consistent with carpal tunnel syndrome. Follow-up evaluations were performed at twenty-one, forty-two, and eighty-four days. At the end of the follow-up period, both the open and endoscopic methods had resulted in high levels of achievement of the primary outcomes (relief of pain and paresthesias). The numbness and paresthesias were relieved in eighty (98 per cent) of eighty-two hands in the open-release group compared with seventy-seven (99 per cent) of seventy-eight hands in the endoscopic-release group. This parameter was not recorded for three hands in the open-release group or six hands in the endoscopic-release group. The satisfaction of the patients with the procedure, graded on a scale of 0 to 100 per cent, averaged 84 per cent in the open-release group compared with 89 per cent in the group that had had endoscopic release. We found no significant differences between the two groups with regard to the secondary quantitative-outcome measurements, including two-point discrimination, postoperative interstitial-pressure data for the carpal canal, Semmes-Weinstein monofilament testing, and motor strength. The open technique resulted in more tenderness of the scar than did the endoscopic method. Thirty-two (39 per cent) of eighty-two hands in the open-release group and fifty (64 per cent) of seventy-eight hands in the endoscopic-release group were not tender at eighty-four days. This parameter was not recorded for three hands in the open-release group and six hands in the endoscopic-release group. The open method also resulted in a longer interval until the patient could return to work (median, twenty-eight days, compared with fourteen days for the open-release and endoscopic-release groups). Four complications occurred- in the endoscopic carpal-tunnel release group: one partial transection of the superficial palmar arch, one digital-nerve contusion, one ulnar-nerve neurapraxia, and one wound hematoma. An additional complication - transection of the common digital nerve of the ring and small fingers and the medial 20 per cent of the median nerve - occurred during the pre-study trial period, in a hand that had had endoscopic carpal-tunnel release. Preliminary analysis suggests that functional outcomes are achieved more quickly when the endoscopic method is used. However, the greater rate of complications indicates that intraoperative safety must be improved before endoscopic carpal-tunnel release is performed on a widespread basis. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,WACC-527,BOSTON,MA 02114. LUND UNIV,DEPT HAND SURG,S-21401 MALMO,SWEDEN. HOSP SPECIAL SURG,NEW YORK,NY 10021. DUKE UNIV,MED CTR,DEPT SURG,DIV ORTHOPAED SURG,DURHAM,NC 27710. NR 36 TC 243 Z9 253 U1 1 U2 6 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 SEP PY 1993 VL 75A IS 9 BP 1265 EP 1275 PG 11 WC Orthopedics; Surgery SC Orthopedics; Surgery GA MA592 UT WOS:A1993MA59200002 PM 8408148 ER PT J AU BARRACK, RL BURKE, DW COOK, SD SKINNER, HB HARRIS, WH AF BARRACK, RL BURKE, DW COOK, SD SKINNER, HB HARRIS, WH TI COMPLICATIONS RELATED TO MODULARITY OF TOTAL HIP COMPONENTS SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Article AB We report complications from the use of modular components in 20 hip replacements in 18 patients. Fifteen complications (in 13 patients) were related to failure of a modular interface after operation. Femoral head detachment from its trunnion was seen in 6 hips from trauma (3), reduction of a dislocation (2), and normal activity (1). In one case the base of the trunnion fractured below an extra-long modular head. In seven other hips the modular polyethylene liner dislodged from its shell, causing severe damage to the shell in four cases with extensive metallosis. In one other hip an asymmetrical polyethylene liner rotated, resulting in impingement of the femoral component and recurrent dislocation. Operative errors were seen in five cases: implantation of a trial acetabular component in one; and mismatching between the size of the femoral head and the acetabular component in the others. Surgeons who use hip replacements with modular components should be aware of the potential for operative error and of the importance of early treatment for postoperative mechanical failure. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,DEPT ORTHOPAED SURG,SAN FRANCISCO,CA 94143. NR 12 TC 61 Z9 62 U1 0 U2 1 PU BRITISH EDITORIAL SOC BONE JOINT SURGERY PI LONDON PA 22 BUCKINGHAM STREET, LONDON, ENGLAND WC2N 6ET SN 0301-620X J9 J BONE JOINT SURG BR JI J. Bone Joint Surg.-Br. Vol. PD SEP PY 1993 VL 75 IS 5 BP 688 EP 692 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA LW756 UT WOS:A1993LW75600005 PM 8376421 ER PT J AU BELL, NH YERGEY, AL VIEIRA, NE OEXMANN, MJ SHARY, JR AF BELL, NH YERGEY, AL VIEIRA, NE OEXMANN, MJ SHARY, JR TI DEMONSTRATION OF A DIFFERENCE IN URINARY CALCIUM, NOT CALCIUM-ABSORPTION, IN BLACK-AND-WHITE ADOLESCENTS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID D-ENDOCRINE SYSTEM; VITAMIN-D; DIETARY CALCIUM; 1,25-DIHYDROXYVITAMIN-D; CHROMATOGRAPHY; CHILDREN; ASSAY; AGE AB Bone mineral density (BMD) of the forearm, lumbar spine, and femoral neck is greater in black than in white children. Studies were performed to determine whether differences in intestinal absorption of calcium or urinary calcium or both account for an assumed more positive calcium balance and greater bone mass in black children. Normal black and white boys and girls were admitted to a metabolic ward and given a constant daily diet containing 1000 mg calcium, 60% as calcium carbonate, for 2 1/2 days (study 1) or 3 1/2 days (study II). Fasting blood and 24 h urine collections were obtained, and in study II, unidirectional fractional absorption of calcium (alpha) was determined with stable isotopes of calcium. It was found that (1) serum 25-hydroxyvitamin D (25-OHD) and urinary calcium were lower and serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] was higher in black than in white children, and (2) alpha was higher in boys than in girls with no racial difference, and (3) there were significant positive correlations between alpha and urinary calcium in the blacks and in the black and white children together. It is concluded that (1) alpha is higher in boys than in girls and (2) a lower urinary calcium, not increased intestinal absorption of calcium, is the means for a more positive calcium balance in blacks that accounts for the racial difference in BMD. C1 MED UNIV SO CAROLINA,DEPT MED,CHARLESTON,SC 29401. MED UNIV SO CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29401. NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. RP BELL, NH (reprint author), MED UNIV SO CAROLINA,RALPH H JOHNSON VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29401, USA. FU NCRR NIH HHS [MO1 RR0170]; NIAMS NIH HHS [R01 AR36066] NR 20 TC 71 Z9 71 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD SEP PY 1993 VL 8 IS 9 BP 1111 EP 1115 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LU336 UT WOS:A1993LU33600011 PM 8237481 ER PT J AU TEICHER, BA HOLDEN, SA KHANDAKAR, V HERMAN, TS AF TEICHER, BA HOLDEN, SA KHANDAKAR, V HERMAN, TS TI ADDITION OF A TOPOISOMERASE-I INHIBITOR TO TRIMODALITY THERAPY [CIS-DIAMMINEDICHLOROPLATINUM(II) HEAT RADIATION] IN A MURINE TUMOR SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY LA English DT Article DE TOPOISOMERASE-I; TRIMODALITY THERAPY; CISPLATIN; HEAT; RADIATION; MOUSE TUMOR ID MELPHALAN ANTITUMOR-ACTIVITY; AGENT ACTIVITY INVITRO; MOUSE MAMMARY-TUMOR; FLUOSOL-DA CARBOGEN; ALKYLATING-AGENTS; CYTO-TOXICITY; FSAIIC FIBROSARCOMA; PLATINUM COMPLEXES; DNA TOPOISOMERASES; CANCER XENOGRAFTS AB The cytotoxicity of the topoisomerase I inhibitors, camptothecin and topotecan, toward exponentially growing EMT-6 murine mammary carcinoma cells under various conditions of oxygenation, pH and temperature was assessed. Under normal pH (pH 7.40) conditions both camptothecin and topotecan were more cytotoxic toward normally oxygenated cells. Both agents were more cytotoxic under acidic pH (pH 6.45) and the differential in cytotoxicity due to the cellular oxygenation level disappeared. Neither camptothecin nor topotecan was enhanced in cytotoxicity by hyperthermia (42-degrees-C or 43-degrees-C, 60 min) during drug exposure. Both camptothecin and topotecan killed increasing numbers of FSaIIC tumor cells with increasing dose of the drugs in vivo in a log/linear manner. Local hyperthermia (43-degrees-C, 30 min) increased the tumor cell killing of the drugs but decreased the toxicity of these agents to the bone marrow granulocyte/macrophage-colony-forming units. Topotecan was a more effective modulator of cisplatin than was camptothecin, as determined by FSaIIC tumor cell survival assay and by FSaIIC tumor growth delay. Although both camptothecin and topotecan were effective additions to a treatment regimen including cisplatin and daily fractionated radiation (5x3Gy), neither of these topoisomerase I inhibitors increased the tumor growth delay produced by the trimodality regimen of cisplatin/hyperthermia/radiation. C1 JOINT CANC 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 NCPDCID CDC HHS [NCI RO1-47379, NCI RO1-50174] NR 54 TC 14 Z9 14 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-5216 J9 J CANCER RES CLIN JI J. Cancer Res. Clin. Oncol. PD SEP PY 1993 VL 119 IS 11 BP 645 EP 651 DI 10.1007/BF01215982 PG 7 WC Oncology SC Oncology GA LT471 UT WOS:A1993LT47100003 PM 8394365 ER PT J AU ZUSMAN, RM HIGGINS, J CHRISTENSEN, D BOUCHER, CA AF ZUSMAN, RM HIGGINS, J CHRISTENSEN, D BOUCHER, CA TI BEPRIDIL IMPROVES LEFT-VENTRICULAR PERFORMANCE IN PATIENTS WITH ANGINA-PECTORIS SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article DE CALCIUM CHANNEL BLOCKADE; EXERCISE; DIASTOLIC FUNCTION; LUSITROPY ID CORONARY-ARTERY DISEASE; FAMILIAL HYPERTROPHIC CARDIOMYOPATHY; STABLE ANGINA; DIASTOLIC FUNCTION; ANTIHYPERTENSIVE THERAPY; MOLECULAR-BASIS; BETA-BLOCKERS; DOUBLE-BLIND; EXERCISE; VERAPAMIL AB Patients with coronary artery disease and angina pectoris have abnormalities of left ventricular (LV) diastolic performance. These abnormalities, which exist when the patients are at rest and not experiencing angina, are presumably secondary to abnormalities of intracellular calcium metabolism. Twenty-three patients with chronic exertional angina pectoris participated in a placebo-controlled, randomized, cross-over trial of bepridil hydrochloride. Angina frequency, nitroglycerin (NTG) consumption, and treadmill exercise capacity were assessed, and each patient underwent first-pass radionuclide cineangiography while receiving placebo or bepridil to assess LV performance. Bepridil decreased angina frequency from 8.5 +/- 0.6 to 4.4 +/- 1.5 episodes per week (p < 0.01) and NTG consumption from 7.2 +/- 2.4 to 3.6 +/- 1.5 tablets per week (p < 0.01). Total treadmill exercise time, time to onset of angina, and time to 1-mm ST segment depression increased significantly during bepridil therapy. Cardiac output (CO), stroke volume (SV), and ejection fraction (EF) increased at rest and during peak upright bicycle exercise. Peak ejection rate and peak filling rate increased, and time to peak ejection rate and time to peak filling rate decreased at rest and at peak exercise during bepridil therapy. In addition, early diastolic filling fraction increased and atrial filling volume decreased during bepridil treatment. Bepridil is effective as monotherapy for treatment of patients with exertional angina; its use is associated with increased exercise capacity and decreased angina frequency and NTG consumption as well as improved LV systolic and diastolic performance at rest and during peak exercise. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ZUSMAN, RM (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,DIV HYPERTENS & VASC MED,CARDIAC UNIT,15 PARKMAN ST,ACC 482,BOSTON,MA 02114, USA. NR 45 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0160-2446 J9 J CARDIOVASC PHARM JI J. Cardiovasc. Pharmacol. PD SEP PY 1993 VL 22 IS 3 BP 474 EP 480 DI 10.1097/00005344-199309000-00020 PG 7 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA LU081 UT WOS:A1993LU08100020 PM 7504141 ER PT J AU CARPENTIER, JL PACCAUD, JP BAECKER, J GILBERT, A ORCI, L KAHN, CR AF CARPENTIER, JL PACCAUD, JP BAECKER, J GILBERT, A ORCI, L KAHN, CR TI 2 STEPS OF INSULIN-RECEPTOR INTERNALIZATION DEPEND ON DIFFERENT DOMAINS OF THE BETA-SUBUNIT SO JOURNAL OF CELL BIOLOGY LA English DT Article ID CULTURED HUMAN-LYMPHOCYTES; TYROSINE KINASE-ACTIVITY; LOW-DENSITY LIPOPROTEIN; FACTOR-II RECEPTOR; COATED PITS; GROWTH-FACTOR; CYTOPLASMIC DOMAIN; PLASMA-MEMBRANE; SURFACE REDISTRIBUTION; RAPID INTERNALIZATION AB The internalization of signaling receptors such as the insulin receptor is a complex, multi-step process. The aim of the present work was to determine the various steps in internalization of the insulin receptor and to establish which receptor domains are implicated in each of these by the use of receptors possessing in vitro mutations. We find that kinase activation and autophosphorylation of all three regulatory tyrosines 1146, 1150, and 1151, but not tyrosines 1316 and 1322 in the COOH-terminal domain, are required for the ligand-specific stage of the internalization process; i.e., the surface redistribution of the receptor from microvilli where initial binding occurs to the nonvillous domain of the cell. Early intracellular steps in insulin signal transduction involving the activation of phosphatidylinositol 3'-kinase are not required for this redistribution. The second step of internalization consists in the anchoring of the receptors in clathrin-coated pits. In contrast to the first ligand specific step, this step is common to many receptors including those for transport proteins and occurs in the absence of kinase activation and receptor autophosphorylation, but requires a juxtamembrane cytoplasmic segment of the beta-subunit of the receptor including a NPXY sequence. Thus, there are two independent mechanisms controlling insulin receptor internalization which depend on different domains of the beta-subunit. C1 UNIV GENEVA,DEPT MORPHOL,CH-1211 GENEVA 4,SWITZERLAND. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,DEPT MED,DIV RES,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-31036, DK-44541] NR 66 TC 51 Z9 52 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD SEP PY 1993 VL 122 IS 6 BP 1243 EP 1252 DI 10.1083/jcb.122.6.1243 PG 10 WC Cell Biology SC Cell Biology GA LY150 UT WOS:A1993LY15000008 PM 8376461 ER PT J AU SPECTOR, NL RYAN, C SAMSON, W LEVINE, H NADLER, LM ARRIGO, AP AF SPECTOR, NL RYAN, C SAMSON, W LEVINE, H NADLER, LM ARRIGO, AP TI HEAT-SHOCK PROTEIN IS A UNIQUE MARKER OF GROWTH ARREST DURING MACROPHAGE DIFFERENTIATION OF HL-60 CELLS SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID PROMYELOCYTIC LEUKEMIA-CELLS; HUMAN LYMPHOCYTES-B; DROSOPHILA DEVELOPMENT; EXPRESSION; PHOSPHORYLATION; GENES; HSP27; INDUCTION; TRANSCRIPTION; LOCALIZATION AB Prior to morphologic and functional maturation, terminally differentiating hematopoietic cells first exit the cell cycle and undergo growth arrest. Relatively little is known about which molecules regulate differentiation-induced growth arrest. In the present report, we sought to determine whether the mammalian low molecular weight heat shock protein (hsp28) was a candidate growth-regulatory molecule during human hematopoiesis. To this end, hsp28 protein expression was examined during phorbol ester (PMA)-induced macrophage differentiation of the human HL-60 promyelocytic leukemic cell line. Whereas hsp28 was constitutively expressed at relatively low levels in an unphosphorylated state, hsp28 was rapidly phosphorylated within 4 hr following PMA-induced differentiation, preceding increased hsp28 protein levels at 24-48 h. In contrast to other differentiative agents, hsp28 steady state mRNA and protein were regulated concordantly in response to macrophage differentiation. More importantly, these changes were transient, and occurred concomitant with the down-regulation of cellular proliferation and the onset of G1 phase cell cycle arrest. In total, these observations implicate hsp28 as an intermediary in the myelomonocytic differentiative pathway of promyelocytic leukemic cells, and will shed light on the events regulating this process. (C) 1993 Wiley-Liss, Inc. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. UNIV CLAUDE BERNARD LYON 1,STRESS CELLULAIRE LAB,CNRS,UMR 106,VILLEURBANNE,FRANCE. RP SPECTOR, NL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-40216-06, 1F32CA08954-01] NR 34 TC 63 Z9 63 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 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD SEP PY 1993 VL 156 IS 3 BP 619 EP 625 DI 10.1002/jcp.1041560322 PG 7 WC Cell Biology; Physiology SC Cell Biology; Physiology GA LU994 UT WOS:A1993LU99400021 PM 8360264 ER PT J AU TSAI, G SLUSHER, BS SIM, L COYLE, JT AF TSAI, G SLUSHER, BS SIM, L COYLE, JT TI IMMUNOCYTOCHEMICAL DISTRIBUTION OF N-ACETYLASPARTYLGLUTAMATE IN THE RAT FOREBRAIN AND GLUTAMATERGIC PATHWAYS SO JOURNAL OF CHEMICAL NEUROANATOMY LA English DT Article DE GLUTAMATE; IMMUNOCYTOCHEMISTRY ID ACIDIC DIPEPTIDASE ACTIVITY; ACETYL-ASPARTYL-GLUTAMATE; OLFACTORY-BULB; VISUAL-SYSTEM; MITRAL CELLS; SPINAL-CORD; BRAIN; IMMUNOREACTIVITY; LOCALIZATION; PROJECTIONS AB N-acetylaspartylglutamate (NAAG) is an acidic dipeptide found in high concentration throughout the rat central nervous system. NAAG has been proposed as a neurotransmitter/modulator in some excitatory glutamatergic pathways where it is released by a Ca2+-dependent process with neuronal activity. Previous immunocytochemical studies have revealed few neurons exhibiting NAAG-like immunoreactivity (LI) in the forebrain, especially in putative glutamatergic neurons. In this study, we present a detailed map of NAAG-LI in rat forebrain utilizing a modified fixation technique that markedly enhances sensitivity. NAAG-LI is located in most of the putative glutamatergic pathways in the forebrain including pyramidal neurons in motor and sensory cortices and the hippocampal formation. Co-localization of NAAG-LI to cholinergic systems of the forebrain was quite extensive with the exception of the striatal local circuit neurons. A noteworthy feature of NAAG-LI-positive neuronal groups is that they were often configured in hierarchical relationships. For example, the pyramidal neurons of the motor cortex and the motor neurons of the brainstem and and spinal cord expressed NAAG-LI; also, several inter-related components of the limbic system stained for NAAG-LI. Taken together, these findings indicate that NAAG is a neuropeptide localized to subpopulations of neurons throughout forebrain as well as in brainstem and spinal cord C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,115 MILL ST,BELMONT,MA 02178. HARVARD UNIV,SCH MED,DEPT NEUROSCI,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 30 TC 25 Z9 25 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0891-0618 J9 J CHEM NEUROANAT JI J. Chem. Neuroanat. PD SEP-OCT PY 1993 VL 6 IS 5 BP 277 EP 292 DI 10.1016/0891-0618(93)90033-Z PG 16 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA MB941 UT WOS:A1993MB94100001 PM 7903856 ER PT J AU KEARSE, LA LOPEZBRESNAHAN, M MCPECK, K TAMBE, V AF KEARSE, LA LOPEZBRESNAHAN, M MCPECK, K TAMBE, V TI LOSS OF INTRAOPERATIVE SOMATOSENSORY-EVOKED POTENTIALS DURING INTRAMEDULLARY SPINAL-CORD INJURY PREDICTS POSTOPERATIVE NEUROLOGIC DEFICITS IN MOTOR FUNCTION SO JOURNAL OF CLINICAL ANESTHESIA LA English DT Article DE NEUROLOGIC DEFICITS; SOMATOSENSORY EVOKED POTENTIALS; SPINAL CORD TUMOR; INTRAMEDULLARY AB Study Objectives: To estimate the sensitivity and specificity of somatosensory evoked potentials (SSEPs) for predicting new postoperative motor neurologic deficits during intramedullary spinal cord surgery; to establish whether SSEPs more accurately predicted postoperative deficits in position and vibration sense than in strength. Design: Prospective open and retrospective study. Setting: University-affiliated hospital. Patients: 20 patients with intramedullary spinal cord tumors scheduled for surgery with intraoperative SSEPs. Interventions: Median, ulnar, and tibial nerve cortical and subcortical SSEPs were recorded continuously. Measurements and Main Results: Conventional intraoperative SSEP criteria considered indicative of neurologic injury were modified and defined as either the complete and permanent loss of the SSEP or the simultaneous amplitude reduction of 50% or greater in the nearest recording electrode rostral to the surgical site and 0.5 millisecond increase in the central latency. Our definition required confirmation of both amplitude and latency changes on a repeated average. All patients had 1 or more SSEPs, which were reproducible and sufficiently stable for analysis throughout the operation. Six patients developed new postoperative neurologic deficits. One had new motor deficits in an extremity from which no baseline SSEPs could be elicited. In each of the other 5 patients, significant SSEP changes preceded the postoperative motor deficits in the extremity or extremities monitored. In no patient without a new postoperative motor deficit was there a significant change in the SSEP. In only 2 of these 5 patients was there a documented postoperative loss or diminution in vibration or position sense. Conclusions: Intraoperative SSEP changes during intramedullary spinal cord surgery are a sensitive predictor of new postoperative motor deficits, but such changes may not correlate reliably with postoperative deficits in position or vibration sense. In this setting SSEP monitoring serves primarily to reassure the operating team that, when the SSEPs remain constant, the surgery has not caused additional injury. RP KEARSE, LA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 24 Z9 24 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0952-8180 J9 J CLIN ANESTH JI J. Clin. Anesth. PD SEP-OCT PY 1993 VL 5 IS 5 BP 392 EP 398 DI 10.1016/0952-8180(93)90103-L PG 7 WC Anesthesiology SC Anesthesiology GA LZ131 UT WOS:A1993LZ13100008 PM 8217175 ER PT J AU CRYNS, VL ALEXANDER, JM KLIBANSKI, A ARNOLD, A AF CRYNS, VL ALEXANDER, JM KLIBANSKI, A ARNOLD, A TI THE RETINOBLASTOMA GENE IN HUMAN PITUITARY-TUMORS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID CUSHINGS-DISEASE; CANDIDATE ONCOGENE; CHROMOSOME 11Q13; CLONAL ORIGIN; ADENOMAS; DNA; REARRANGEMENT; CANCER AB Functional inactivation of the retinoblastoma (RB) tumor suppressor gene is important in the pathogenesis of many human tumors. Recently, the frequent occurrence of pituitary tumors was reported in mice genetically engineered to have one defective RB allele, a genetic background analogous to that of patients with familial retinoblastoma. The molecular pathogenesis of human pituitary tumors is largely unknown, and the potential role of RB gene inactivation in these neoplasma has not been examined. Consequently, we studied 20 human pituitary tumors (12 clinically nonfunctioning tumors, 4 somatotroph adenomas, 2 prolactinomas, and 2 corticotroph adenomas) for tumor-specific allelic loss of the RB gene using a highly informative polymorphic locus within the gene. Control leukocyte DNA samples from 18 of these 20 patients were heterozygous at this locus, permitting genetic evaluation of their paired tumor specimens. In contrast to the pituitary tumors in the mouse model, none of these 18 human tumors exhibited RB allelic loss. These findings indicate that RB gene inactivation probably does not play an important role in the pathogenesis of common types of human pituitary tumors. C1 MASSACHUSETTS GEN HOSP, CTR CANC, WELLMAN 503, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, ENDOCRINE UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, NEUROENDOCRINE UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. FU NCI NIH HHS [1F32-CA-0938101]; NIDDK NIH HHS [5T32-DK-0702817, DK-11794] NR 24 TC 126 Z9 129 U1 0 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD SEP PY 1993 VL 77 IS 3 BP 644 EP 646 DI 10.1210/jc.77.3.644 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LX033 UT WOS:A1993LX03300014 PM 7690360 ER PT J AU WAGNER, CR MORRIS, TE SHIPLEY, GD HOSENPUD, JD AF WAGNER, CR MORRIS, TE SHIPLEY, GD HOSENPUD, JD TI REGULATION OF HUMAN AORTIC ENDOTHELIAL CELL-DERIVED MESENCHYMAL GROWTH-FACTORS BY ALLOGENEIC LYMPHOCYTES IN-VITRO - A POTENTIAL MECHANISM FOR CARDIAC ALLOGRAFT VASCULOPATHY SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE TRANSPLANTATION IMMUNOLOGY; VASCULAR SMOOTH MUSCLE; CORONARY DISEASE; LYMPHOCYTES; CHRONIC REJECTION ID SMOOTH-MUSCLE CELLS; CORONARY-ARTERY DISEASE; MONOCLONAL-ANTIBODY; TRANSPLANTATION; ATHEROSCLEROSIS; PROTEIN; ARTERIOSCLEROSIS; REJECTION; INFECTION; ACTIN AB Cardiac allograft vasculopathy is thought to be triggered by an alloreactive response to the donor coronary vasculature, resulting in smooth muscle cell proliferation and ultimate occlusion of the donor coronary arteries. To determine whether allogeneic lymphocytes are capable of regulating endothelial-derived smooth muscle cell (SMC) growth factors, human aortic endothelial cells (HAECs) were exposed to allogeneic lymphocytes. The HAEC-lymphocyte co-cultures were assessed for (a) lymphocyte proliferation in response to the allogeneic HAECs; (b) release of soluble factors that stimulate human aortic SMC proliferation; and (c) alteration of HAEC mRNA levels for a panel of known SMC growth factors. Co-culture conditioned medium increased SMC proliferation, compared to medium conditioned by HAECs alone. HAECs exposed to allogeneic lymphocytes increased their expression of mRNA for basic fibroblast growth factor, transforming growth factors alpha and beta, and platelet derived growth factor A and B chains. These results demonstrate that allogeneic lymphocytes are capable of inducing HAECs to increase mRNA levels for several mesenchymal growth factors and to release bioactive products capable of stimulating SMC cell proliferation in vitro. Additionally, the data support the hypothesis that alloreactive lymphocytes can stimulate allogeneic donor endothelial cells to produce growth factors that may contribute to the intimal thickening seen in cardiac allograft vasculopathy. C1 PORTLAND VET AFFAIRS MED CTR,IMMUNOL RES LAB,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MED,OREGON CARDIAC TRANSPLANT PROGRAM,IMMUNOBIOL RES LAB,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT CELL BIOL,OREGON CARDIAC TRANSPLANT PROGRAM,IMMUNOBIOL LAB,PORTLAND,OR 97201. FU NHLBI NIH HHS [HL-43369] NR 32 TC 27 Z9 27 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD SEP PY 1993 VL 92 IS 3 BP 1269 EP 1277 DI 10.1172/JCI116699 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LX770 UT WOS:A1993LX77000023 PM 8376585 ER PT J AU WANG, TC BONNERWEIR, S OATES, PS CHULAK, M SIMON, B MERLINO, GT SCHMIDT, EV BRAND, SJ AF WANG, TC BONNERWEIR, S OATES, PS CHULAK, M SIMON, B MERLINO, GT SCHMIDT, EV BRAND, SJ TI PANCREATIC GASTRIN STIMULATES ISLET DIFFERENTIATION OF TRANSFORMING GROWTH-FACTOR ALPHA-INDUCED DUCTULAR PRECURSOR CELLS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PANCREATIC DUCTS; ISLETS; GASTRIN; TRANSFORMING GROWTH FACTOR-ALPHA ID TRANSGENIC MICE; GASTROINTESTINAL-TRACT; GENE-EXPRESSION; RAT PANCREAS; TGF-ALPHA; FACTOR-I; INSULIN; OVEREXPRESSION; NESIDIOBLASTOSIS; HYPOGLYCEMIA AB Gastrin is transiently expressed in fetal islets during a critical period of their development from protodifferentiated islet precursors in fetal pancreatic ducts. To examine the possible role of gastrin as an islet cell growth factor, postnatal islet growth was studied in transgenic mice which overexpress gastrin and TGFalpha in their pancreas. Overexpression of a TGFalpha transgene causes metaplastic ductules containing numerous insulin expressing cells that resemble protodifferentiated precursors of the fetal pancreas. However, islet mass of the TGFalpha transgenic mice was not increased. Pancreatic overexpression of gastrin from a chimeric insulin/gastrin transgene transcribed from the insulin promoter markedly decreased the TGFalpha-stimulated increase in pancreatic duct mass. Furthermore, pancreatic coexpression of both gastrin and TGFalpha significantly increased islet mass in mice expressing both transgenes. These findings indicate that TGFalpha and gastrin can act synergistically to stimulate islet growth, although neither peptide alone is sufficient. Islet growth may possibly be stimulated through gastrin promoting the differentiation of insulin-positive cells in the TGFalpha-induced metaplastic ducts. This transgenic study suggests that islet neogenesis can be reactivated in the ductular epithelium of the adult pancreas by local expression of two growth factors, gastrin and TGFalpha. C1 MASSACHUSETTS GEN HOSP,DEPT MED,GASTROINTESTINAL UNIT,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. JOSLIN DIABET CTR,JOSLIN RES CTR,BOSTON,MA 02215. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. FU NIDDK NIH HHS [DK 44523, DK01937, DK 42147] NR 38 TC 208 Z9 214 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD SEP PY 1993 VL 92 IS 3 BP 1349 EP 1356 DI 10.1172/JCI116708 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LX770 UT WOS:A1993LX77000032 PM 8376589 ER PT J AU SENGELOV, H KJELDSEN, L DIAMOND, MS SPRINGER, TA BORREGAARD, N AF SENGELOV, H KJELDSEN, L DIAMOND, MS SPRINGER, TA BORREGAARD, N TI SUBCELLULAR-LOCALIZATION AND DYNAMICS OF MAC-1 (ALPHA(M)BETA(2)) IN HUMAN NEUTROPHILS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE SECRETORY VESICLES; GELATINASE GRANULES; SPECIFIC GRANULES; CD11B; FREE-FLOW ELECTROPHORESIS ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; P150,95 GLYCOPROTEIN FAMILY; LINKED-IMMUNOSORBENT-ASSAY; RADICAL-GENERATING SYSTEM; ALKALINE-PHOSPHATASE; PLASMA-MEMBRANE; INTRACELLULAR VESICLES; COMPLEMENT RECEPTOR; NADPH OXIDASE; GRANULES AB The subcellular localization of Mac-1 was determined in resting and stimulated human neutrophils after disruption by nitrogen cavitation and fractionation on two-layer Percoll density gradients. Light membranes were further separated by high voltage free flow electrophoresis. Mac-1 was determined by an ELISA with monoclonal antibodies that were specific for the alpha-chain (CD11b). In unstimulated neutrophils, 75% of Mac-1 colocalized with specific granules including gelatinase granules, 20% with secretory vesicles and the rest with plasma membranes. Stimulation with nanomolar concentrations of FMLP resulted in the translocation of Mac-1 from secretory vesicles to the plasma membrane, and only minimal translocation from specific granules and gelatinase granules. Stimulation with PMA or Ionomycin resulted in full translocation of Mac-1 from secretory vesicles and gelatinase granules to the plasma membrane, and partial translocation of Mac-1 from specific granules. These findings were corroborated by flow cytometry, which demonstrated a 6-10-fold increase in the surface membrane content of Mac-1 in response to stimulation with FMLP, granulocyte-macrophage colony stimulating factor, IL-8, leukotriene B4, platelet-activating factor, TNF-alpha, and zymosan-activated serum, and a 25-fold increase in response to Ionomycin. Thus, secretory vesicles constitute the most important reservoir of Mac-1 that is incorporated into the plasma membrane during stimulation with inflammatory mediators. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RP SENGELOV, H (reprint author), UNIV COPENHAGEN,RIGSHOSP,DEPT HEMATOL L-4041,GRAULOCYTE RES LAB,9 BLEGDAMSVEJ,DK-2100 COPENHAGEN,DENMARK. FU NCI NIH HHS [CA 31799] NR 42 TC 220 Z9 221 U1 0 U2 6 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD SEP PY 1993 VL 92 IS 3 BP 1467 EP 1476 DI 10.1172/JCI116724 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LX770 UT WOS:A1993LX77000048 PM 8376598 ER PT J AU HESS, D TABOR, T AF HESS, D TABOR, T TI COMPARISON OF 6 METHODS TO CALCULATE AIRWAY-RESISTANCE DURING MECHANICAL VENTILATION IN ADULTS SO JOURNAL OF CLINICAL MONITORING LA English DT Article DE AIRWAY-RESISTANCE; VENTILATION-MECHANICAL ID ENDOTRACHEAL-TUBE; FLOW RESISTANCE; PRESSURE; WORK AB Objective. A variety of methods are used to calculate indices of lung mechanics. We conducted this study to compare 6 methods of calculating airway resistance. Methods. Data were recorded from 20 adult mechanically ventilated patients. All were relaxed and breathing in synchrony with the ventilator, and an end-inspiratory pause sufficient to produce a pressure plateau (0.5-1.5 s) was used. Pressure and flow rate were measured at the proximal airway using a calibrated lung mechanics analyzer (VenTrak, Med Science, St Louis, MO). Flow rate, pressure, and volume were printed simultaneously. Airway resistance was calculated using 6 methods: Suter, Krieger, Neergard, Bergman, Comroe, and Jonson. Results. Mean calculated resistances (+/- SD) (cm H2O/L/s) were 11.7 +/- 4.8 (Suter method), 13.3 +/- 5.0 (Krieger method), 14.9 +/- 5.3 (Neergard method), 25.0 +/- 6.6 (Bergman method), 24.7 +/- 6.4 (Comroe method), and 26.9 +/- 4.8 (Jonson method). By repeated measures analysis of variance, these differences were significant (p < 0.001). Using Scheffe analysis, no difference was found between the calculations using the Bergman, Comroe, and Jonson methods; these were significantly greater than the other 3 methods (p < 0.05). Conclusions. Methods that evaluate expiratory resistance (Comroe, Bergman, and Jonson) produce higher values than methods that evaluate inspiratory resistance (Suter and Neergard) or a combination of inspiratory and expiratory resistance (Krieger). Because of these differences, investigators should clearly describe their calculations when reporting airway resistance values. C1 YORK HOSP,DEPT RES,YORK,PA. RP HESS, D (reprint author), MASSACHUSETTS GEN HOSP,DEPT RESP CARE,ELLISON 4,BOSTON,MA 02114, USA. NR 14 TC 8 Z9 8 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0748-1977 J9 J CLIN MONITOR JI J. Clin. Monit. PD SEP PY 1993 VL 9 IS 4 BP 275 EP 282 DI 10.1007/BF02886698 PG 8 WC Anesthesiology SC Anesthesiology GA LX482 UT WOS:A1993LX48200006 PM 8301335 ER PT J AU ELGHAZZAWI, ZF WELCH, JP LADIN, Z FORDCARLETON, P COOPER, JB AF ELGHAZZAWI, ZF WELCH, JP LADIN, Z FORDCARLETON, P COOPER, JB TI ALGORITHM TO IDENTIFY COMPONENTS OF ARTERIAL BLOOD-PRESSURE SIGNALS DURING USE OF AN INTRAAORTIC BALLOON PUMP SO JOURNAL OF CLINICAL MONITORING LA English DT Article DE MEASUREMENT-TECHNIQUES ALGORITHMS; EQUIPMENT BLOOD-PRESSURE; MONITORING BLOOD-PRESSURE AB Existing bedside cardiovascular monitors often inaccurately measure arterial blood pressure during intra-aortic balloon pump (IABP) assist. We have developed an algorithm that correctly identifies features of arterial pressure waveforms in the presence of IABP. The algorithm is adaptive, functions in real-time, and uses information from the electrocardiographic (ECG) and arterial blood pressure signals to extract features and numeric values from the arterial blood pressure waveform. In its current form, it requires reliable ECG beat detection and was not intended to operate under conditions of extremely poor balloon timing. The algorithm was evaluated by an expert (P.F-C.) on a limited data set, which consisted of 12 1-minute epochs of data recorded from 6 intensive care unit patients. A criterion for selection of patients was that the ECG beat detector could detect ECG beats correctly from the waveforms. The overall sensitivity and positive predictivity for beat detection were 94.04% and 100%, respectively. For feature identification, the overall sensitivity was greater than 89%, positive predictivity was 100%, and the false-positive rate was 0%. The performance measures may be biased by the criteria for patient selection. This approach to identifying waveform features during IABP improves the accuracy of measurements. The utility of using 2 sources of information to improve measurement accuracy has been demonstrated and should be applicable to other physiologic signal-processing applications. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. SIEMENS MED ELECTR,PHYSIOL SIGNAL PROC GRP,DANVERS,MA. PROTOCOL SYST INC,BEAVERTON,OR. BOSTON UNIV,DEPT ENGN,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 17 TC 3 Z9 3 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0748-1977 J9 J CLIN MONITOR JI J. Clin. Monit. PD SEP PY 1993 VL 9 IS 4 BP 297 EP 308 DI 10.1007/BF02886704 PG 12 WC Anesthesiology SC Anesthesiology GA LX482 UT WOS:A1993LX48200011 PM 8301340 ER PT J AU FREI, E FREIREICH, EJ AF FREI, E FREIREICH, EJ TI THE CLINICAL CANCER RESEARCHER - STILL AN EMBATTLED SPECIES SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID COMBINATION CHEMOTHERAPY; DOSE METHOTREXATE; SCIENCE; SARCOMA; THERAPY; TUMOR C1 UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX 77025. RP FREI, E (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 49 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 SEP PY 1993 VL 11 IS 9 BP 1639 EP 1651 PG 13 WC Oncology SC Oncology GA LW369 UT WOS:A1993LW36900003 PM 8355033 ER PT J AU ASSELIN, BL WHITIN, JC COPPOLA, DJ RUPP, IP SALLAN, SE COHEN, HJ AF ASSELIN, BL WHITIN, JC COPPOLA, DJ RUPP, IP SALLAN, SE COHEN, HJ TI COMPARATIVE PHARMACOKINETIC STUDIES OF 3 ASPARAGINASE PREPARATIONS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE LYMPHOCYTIC-LEUKEMIA; ESCHERICHIA-COLI; INTENSIVE ASPARAGINASE; PHARMACOLOGY; INDUCTION; CHILDREN C1 UNIV ROCHESTER,STRONG CHILDRENS RES CTR,ROCHESTER,NY 14627. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [5P01CA34183-06, P30 CA11199]; PHS HHS [00199-03] NR 25 TC 215 Z9 224 U1 1 U2 3 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 SEP PY 1993 VL 11 IS 9 BP 1780 EP 1786 PG 7 WC Oncology SC Oncology GA LW369 UT WOS:A1993LW36900021 PM 8355045 ER PT J AU WEST, DC GRIER, HE AF WEST, DC GRIER, HE TI RETHINKING MANAGEMENT OF LOCALIZED NEUROBLASTOMA - REPLY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter ID N-MYC ONCOGENE; NEURO-BLASTOMA; AMPLIFICATION; EXPERIENCE; THERAPY RP WEST, DC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD SEP PY 1993 VL 11 IS 9 BP 1834 EP 1834 PG 1 WC Oncology SC Oncology GA LW369 UT WOS:A1993LW36900031 ER PT J AU BHALLA, M NOBLE, ER SHEPARD, JAO MCLOUD, TC AF BHALLA, M NOBLE, ER SHEPARD, JAO MCLOUD, TC TI NORMAL POSITION OF TRACHEA AND ANTERIOR JUNCTION LINE ON CT SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE MEDIASTINUM; MEDIASTINUM, ANATOMY; THORAX, ANATOMY; COMPUTED TOMOGRAPHY ID EMPYEMA; LUNG AB Objective and Methods: In unilateral diseases of the chest accompanied by either volume loss or expansion there is mediastinal shift and mediastinal ''herniation'' of one lung into the opposite hemithorax. This may also be accompanied by changes in the size of the hemithoraces. Although early detection of these changes may be difficult on chest radiography, one can detect all these changes on CT with greater ease. Since the normal range of position of the mediastinal structures on CT and the symmetry of the hemithoraces have not been studied before, we conducted a prospective study of normal chest CT to define the range of position of the trachea and the anterior junction line, as well as the normal range of differences in the parasagittal diameters of the two hemithoraces. Results: The trachea was less-than-or-equal-to 1.6 cm to the right and 0.7 cm to the left of midline; the anterior junction line was less-than-or-equal-to 1 cm to the right and 2 cm to the left. The hemithoraces were asymmetric in 84%, with the difference in the parasagittal diameters of the two hemithoraces less-than-or-equal-to 1.5 cm. Conclusion: These data may help radiologists detect subtle mediastinal shifts and asymmetry in patients with unilateral pleural or pulmonary disease. C1 MED UNIV S CAROLINA,DEPT RADIOL,CHARLESTON,SC 29425. RP BHALLA, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 14 TC 3 Z9 5 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD SEP-OCT PY 1993 VL 17 IS 5 BP 714 EP 718 DI 10.1097/00004728-199309000-00009 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LX477 UT WOS:A1993LX47700009 PM 8370826 ER PT J AU CLEVELAND, M AF CLEVELAND, M TI EXERCISE GUIDELINES SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Letter RP CLEVELAND, M (reprint author), PORTLAND VET AFFAIRS MED CTR,INTERNAL MED & SPORTS,PORTLAND,OR 97207, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD SEP PY 1993 VL 8 IS 9 BP 522 EP 522 DI 10.1007/BF02600119 PG 1 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA LZ337 UT WOS:A1993LZ33700012 PM 8410428 ER PT J AU BURGESON, RE AF BURGESON, RE TI TYPE-VII COLLAGEN, ANCHORING FIBRILS, AND EPIDERMOLYSIS-BULLOSA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Review ID ACQUISITA ANTIGEN; GENETIC-LINKAGE; HUMAN-SKIN; EPIDERMAL-KERATINOCYTES; BASEMENT-MEMBRANE; TISSUE FORM; EXPRESSION; AUTOIMMUNITY; PROCOLLAGEN; DIAGNOSIS AB The anchoring fibrils at the dermal-epidermal junction have been well characterized as ultrastructural entities. From their appearance, it was proposed that they fortified the attachment of the epidermis to the dermis. This hypothesized function was strengthened by observations indicating that the anchoring fibrils were abnormal, diminished, or absent from individuals with dystrophic epidermolysis bullosa. Therefore, characterization of the molecular constituents of the anchoring fibrils and their interactions with other basement membrane and dermal components might lead to identification of the gene defects underlying at least some forms of epidermolysis bullosa. Type VII collagen was identified as the protein component of anchoring fibrils in 1986. Since then, the major characteristics of the molecule have been described. These are consistent with a model wherein secreted type VII collagen molecules form disulfide-bond stabilized antiparallel dimers. The dimers then condense laterally into unstaggered arrays that are the anchoring fibrils. This arrangement allows for the protrusion of large globular domains (NC-1) from both ends of the fibrils. The aggregated triple-helical domains extend into the papillary dermis and entrap fibrous dermal components. The NC-1 domains are believed to interact with components of the basement membrane and thus to mediate the attachment of the basement membrane to the dermis. This model predicts that mutations in the type VII collagen gene that prevent the secretion of the molecule will be the most devastating, whereas mutations in the regions encoding the globular domains may show more variable phenotype. Ultimately, understanding the function of type VII collagen at the molecular level will be the key to devising strategies to moderate the pathophysiology of dystrophic epidermolysis bullosa. RP BURGESON, RE (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 47 TC 194 Z9 201 U1 2 U2 12 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD SEP PY 1993 VL 101 IS 3 BP 252 EP 255 DI 10.1111/1523-1747.ep12365129 PG 4 WC Dermatology SC Dermatology GA LX786 UT WOS:A1993LX78600003 PM 8370960 ER PT J AU SHEA, CR OLACK, GA MORRISON, H CHEN, N HASAN, T AF SHEA, CR OLACK, GA MORRISON, H CHEN, N HASAN, T TI PHOTOTOXICITY OF LUMIDOXYCYCLINE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE TETRACYCLINE; PHOTOPRODUCT; PHOTOSENSITIZATION ID CELL-MEMBRANE DISRUPTION; HUMAN CARCINOMA-CELLS; ORGANIC-PHOTOCHEMISTRY; SINGLET OXYGEN; DOXYCYCLINE PHOTOSENSITIZATION; TETRACYCLINE; PHOTOPRODUCTS; LUMITETRACYCLINE; RHODAMINE-123; LOCALIZATION AB Doxycycline (DOTC) is a photosensitizing drug whose mechanism of phototoxicity is complicated by the large variety of stable photoproducts formed. To assess the role of a DOTC photoproduct, lumidoxycycline (LuDOTC), in the photosensitization mechanism of DOTC, MGH-U1 human bladder carcinoma cells were treated in vitro with either DOTC or LuDOTC, and irradiated with the 351-nm emission of an argon-ion laser. Both DOTC and LuDOTC were phototoxic and caused radiant-exposure-dependent inhibition of cellular incorporation of tritiated thymidine. On an absorbed-photon basis, DOTC was about five times as phototoxic as LuDOTC. Cellular uptake of DOTC was about five times as great as that of LuDOTC. Epifluorescence microscopy showed localization of LuDOTC predominantly within cellular membranes, particularly of mitochondria, as well as a low level of LuDOTC fluorescence diffusely within the cytoplasm. Epifluorescence microscopy of cells labeled with the mitochondrial probe, rhodamine 123, showed mitochondrial fragmentation and altered mitochondrial membrane integrity after LuDOTC photosensitization; these effects depended on radiant exposure and were partially reversible by 24 h after irradiation. For both DOTC and LuDOTC phototoxicity was increased by irradiation in the presence of deuterium oxide and decreased in the presence of sodium azide, effects consistent with an important mechanistic role for singlet oxygen, O2(1DELTAg), in the injury. In solution, LuDOTC and DOTC had similar quantum yields for generation of O2(1DELTAg) as measured by time-resolved spectroscopy and by O2(1DELTAg) trapping. LuDOTC was photostable in solution, but DOTC underwent significant photodegradation. These data demonstrate that DOTC photoproducts such as LuDOTC have significant photobiologic activity and may play an important role in the phototoxicity mechanism of DOTC. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,FRUIT ST,BOSTON,MA 02114. CORNELL UNIV,MED CTR,NEW YORK HOSP,COLL MED,DIV DERMATOPATHOL,NEW YORK,NY 10021. PURDUE UNIV,DEPT CHEM,W LAFAYETTE,IN 47907. FU NIAMS NIH HHS [5R01-AR39286, R29-AR38918] NR 40 TC 17 Z9 17 U1 0 U2 1 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD SEP PY 1993 VL 101 IS 3 BP 329 EP 333 DI 10.1111/1523-1747.ep12365484 PG 5 WC Dermatology SC Dermatology GA LX786 UT WOS:A1993LX78600017 PM 8370969 ER PT J AU COUPAYEGERARD, B KLEYMAN, TR AF COUPAYEGERARD, B KLEYMAN, TR TI DIFFERENTIAL ARRIVAL OF NEWLY SYNTHESIZED APICAL AND BASOLATERAL PLASMA-MEMBRANE PROTEINS IN THE EPITHELIAL-CELL LINE A6 SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE EPITHELIAL POLARITY; A6-CELLS; BIOTIN; PROTEIN TRAFFICKING; PROTEIN SYNTHESIS ID ENDOPLASMIC-RETICULUM; BIOGENETIC PATHWAYS; MDCK CELLS; BULK FLOW; SURFACE; CACO-2; GLYCOPROTEINS; TRANSPORT; RATES; NA+ AB The labeling of specific cell surface proteins with biotin was used to examine both protein distribution and delivery of newly synthesized proteins to the apical and basolateral cell surface in A6 cells. Steady-state metabolic labeling with [S-35]methionine followed by specific cell surface biotinylation demonstrated polarization of membrane proteins. The delivery of newly synthesized proteins to the apical or basolateral cell surface was examined by metabolic labeling with [S-35]methionine using a pulse-chase protocol in combination with specific cell surface biotinylation. Newly synthesized biotinylated proteins at the apical cell surface reached a maximum after a 5 min chase, and then fell over the remainder of a 2 hr chase. The bulk flow of newly synthesized proteins to the basolateral membrane slowly rose to a maximum after 90 min. The detergent Triton X-114 was used to examine delivery of hydrophilic and hydrophobic proteins to the cell surface. Delivery of both hydrophilic and hydrophobic proteins to the apical cell surface reached a maximum 5 to 10 min into the chase period. The arrival of hydrophilic proteins at the basolateral surface showed early delivery and a maximum peak delivery at 120 min into the chase period. In contrast, only an early peak of delivery of newly synthesized hydrophobic proteins to the basolateral membrane was observed. C1 VET AFFAIRS MED CTR,DEPT MED & PHYSIOL,PHILADELPHIA,PA 19104. RP COUPAYEGERARD, B (reprint author), UNIV PENN,DEPT MED & PHYSIOL,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 25 TC 4 Z9 4 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD SEP PY 1993 VL 135 IS 3 BP 225 EP 235 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA LZ363 UT WOS:A1993LZ36300004 PM 8271262 ER PT J AU ALTERMAN, AI MCLELLAN, AT SHIFMAN, RB AF ALTERMAN, AI MCLELLAN, AT SHIFMAN, RB TI DO SUBSTANCE-ABUSE PATIENTS WITH MORE PSYCHOPATHOLOGY RECEIVE MORE TREATMENT SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID ADDICTION SEVERITY INDEX; ANTISOCIAL PERSONALITY-DISORDER; ALCOHOLICS; DIAGNOSIS; VALIDITY AB The association between psychopathology at treatment entry and the amount of treatment services received was evaluated in 104 alcohol-dependent and 100 cocaine-dependent male veterans treated for 1 month in either a day hospital or inpatient program Measures of psychopathology included the Addiction Severity Index psychiatric composite score, the presence or absence of an antisocial personality disorder diagnosis, and the total number of additional lifetime or current psychiatric diagnoses. Patients with higher admission Addiction Severity Index psychiatric composite scores received more medical, alcohol, family/social, and psychiatric services. There was also preliminary evidence that patients who received more treatment showed greater improvement 7 months after admission. The relationships between the other measures of psychopathology and treatment services failed to achieve overall statistical significance, although significant relationships were found in several individual areas. C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA. TEMPLE UNIV,DEPT PSYCHOL,PHILADELPHIA,PA 19122. RP ALTERMAN, AI (reprint author), UNIV PENN,SCH MED,TREATMENT RES CTR,PHILADELPHIA,PA 19104, USA. NR 28 TC 48 Z9 48 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD SEP PY 1993 VL 181 IS 9 BP 576 EP 582 DI 10.1097/00005053-199309000-00009 PG 7 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LX800 UT WOS:A1993LX80000009 PM 8245927 ER PT J AU BEAL, MF BROUILLET, E JENKINS, B HENSHAW, R ROSEN, B HYMAN, BT AF BEAL, MF BROUILLET, E JENKINS, B HENSHAW, R ROSEN, B HYMAN, BT TI AGE-DEPENDENT STRIATAL EXCITOTOXIC LESIONS PRODUCED BY THE ENDOGENOUS MITOCHONDRIAL INHIBITOR MALONATE SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE MALONATE; EXCITOTOXICITY; MITOCHONDRIA; HUNTINGTONS DISEASE; AGING; NEURODEGENERATIVE DISEASES; STRIATUM ID GLUTAMATE; RECEPTOR; RATS AB Intrastriatal injection of malonate, a reversible inhibitor of succinate dehydrogenase (SDH), produced age-dependent striatal lesions, which were significantly greater in 4- and 12-month-old animals than in 1-month-old animals. Both histologic and neurochemical studies showed that the lesions were significantly attenuated by administration of the noncompetitive NMDA receptor antagonist MK-801. Water-suppressed chemical shift magnetic resonance imaging showed that malonate produces increased striatal lactate concentrations and striatal lesions on T2-weighted scans that were attenuated by MK-801. Neurochemical characterization of the lesions showed significant decreases in markers of medium-sized spiny neurons (GABA and substance P), whereas a marker of medium-sized aspiny neurons (somatostatin) was not different from control values, consistent with an NMDA receptor-mediated mechanism. The effects of intrastriatal injections of malonate on ATP concentrations were compared with those of the irreversible SDH inhibitor 3-nitropropionic acid (3-NP). The ATP depletions following an equimolar injection of malonate were less marked and more transient than those of 3-NP. These results show that the competitive SDH inhibitor malonate produces more transient and milder bioenergetic defects than 3-NP, which are associated with selective activation of NMDA receptors. The results strengthen the possibility that a subtle impairment of energy metabolism may play a role in the pathogenesis of Huntington's disease. C1 MASSACHUSETTS GEN HOSP,MGH NMR CTR,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BEAL, MF (reprint author), MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,NEUROL SERV,WARREN 4,BOSTON,MA 02114, USA. RI Brouillet, Emmanuel/B-4784-2014 OI Brouillet, Emmanuel/0000-0001-6322-7403 FU DS NIH HHS [NINDS 16367]; NINDS NIH HHS [NINDS NS10828] NR 15 TC 247 Z9 252 U1 1 U2 17 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD SEP PY 1993 VL 61 IS 3 BP 1147 EP 1150 DI 10.1111/j.1471-4159.1993.tb03633.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LT335 UT WOS:A1993LT33500045 PM 7689641 ER PT J AU LOUIS, DN RUBIO, MP CORREA, KM GUSELLA, JF VONDEIMLING, A AF LOUIS, DN RUBIO, MP CORREA, KM GUSELLA, JF VONDEIMLING, A TI MOLECULAR-GENETICS OF PEDIATRIC BRAIN-STEM GLIOMAS - APPLICATION OF PCR TECHNIQUES TO SMALL AND ARCHIVAL BRAIN-TUMOR SPECIMENS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE ASTROCYTOMA; BRAIN STEM; CHROMOSOME-17; EPIDERMAL GROWTH FACTOR RECEPTOR GENE; GLIOMA; P53 GENE; POLYMERASE CHAIN REACTION ID POLYMERASE CHAIN-REACTION; P53 MUTATIONS; HUMAN ASTROCYTOMAS; SUPPRESSOR GENE; TISSUE; DNA; HETEROZYGOSITY; AMPLIFICATION; CHROMOSOME-10; ASSOCIATION AB Brain stem gliomas are pediatric astrocytomas that histologically resemble adult supratentorial astrocytomas such as glioblastomas multiforme (GBM). Our molecular genetic studies have suggested that adult GBM can be divided into two genetic subsets: tumors with p53 tumor suppressor gene mutations and chromosome 17p loss that occur more commonly in younger patients; and tumors with epidermal growth factor receptor (EGFR) gene amplification that occur more commonly in older patients. Brain stem gliomas have not been studied since biopsies of these tumors are rare and extremely small. We investigated the molecular genetic composition of seven brain stem glioblastomas (two small biopsies, five autopsies) using polymerase chain reaction (PCR) assays for chromosomal loss, gene mutation and gene amplification. Four cases lost portions of chromosome 17p that included the p53 gene. These four cases and one additional case had mutations in the p53 gene. None of the cases showed amplification of the EGFR gene. Allelic losses of the long arm of chromosome 10 were noted in four cases. These results suggest similarities between pediatric brain stem glioblastomas and those GBM that occur in younger adult patients, and confirm the utility of PCR-based means of studying small and archival brain tumor specimens. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,MOLEC NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV BONN,INST NEUROPATHOL,W-5300 BONN,GERMANY. RP LOUIS, DN (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,NEUROSURG SERV,WARREN 3,BOSTON,MA 02114, USA. RI Rubio, Mari-Paz/K-4364-2014; von Deimling, Andreas/F-7774-2013 OI Rubio, Mari-Paz/0000-0003-3963-5903; von Deimling, Andreas/0000-0002-5863-540X FU NCI NIH HHS [CA 09144, CA 57683] NR 47 TC 102 Z9 102 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 SEP PY 1993 VL 52 IS 5 BP 507 EP 515 DI 10.1097/00005072-199309000-00009 PG 9 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA LW557 UT WOS:A1993LW55700009 PM 8103086 ER PT J AU HALMAN, MH WORTH, JL SANDERS, KM RENSHAW, PF MURRAY, GB AF HALMAN, MH WORTH, JL SANDERS, KM RENSHAW, PF MURRAY, GB TI ANTICONVULSANT USE IN THE TREATMENT OF MANIC SYNDROMES IN PATIENTS WITH HIV-1 INFECTION SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID AIDS DEMENTIA COMPLEX; LITHIUM AB A retrospective chart review identified 11 patients with type 1 human immunodeficiency virus (HIV) who presented to an HIV/AIDS psychiatric service with an acute manic episode. Demographic data, neurodiagnostic studies, and treatment results are discussed. Abnormal brain magnetic resonance imaging significantly predicted poor tolerance of lithium and neuroleptics. Anticonvulsants were an effective alternative. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,ROBERT B ANDREWS UNIT,FRUIT ST,WANG 812,BOSTON,MA 02114. MCLEAN HOSP,CTR BRAIN IMAGING,BELMONT,MA 02178. HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA 02115. NR 15 TC 26 Z9 29 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD FAL PY 1993 VL 5 IS 4 BP 430 EP 434 PG 5 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MD593 UT WOS:A1993MD59300012 PM 8286943 ER PT J AU LOPEZBRESNAHAN, MV KEARSE, LA YANEZ, P YOUNG, TI AF LOPEZBRESNAHAN, MV KEARSE, LA YANEZ, P YOUNG, TI TI ANTERIOR COMMUNICATING ARTERY COLLATERAL FLOW PROTECTION AGAINST ISCHEMIC CHANGE DURING CAROTID ENDARTERECTOMY SO JOURNAL OF NEUROSURGERY LA English DT Article DE CAROTID ENDARTERECTOMY; CEREBRAL ANGIOGRAPHY; CEREBRAL ISCHEMIA; COLLATERAL FLOW; ELECTROENCEPHALOGRAPHY ID CEREBRAL-ISCHEMIA; SURGERY; EEG AB The purpose of this study was to determine whether preoperative angiographic patterns of collateral cerebral blood flow correlate with protection against intraoperative electroencephalographic (EEG) evidence of cerebral ischemia caused by carotid artery cross-clamping during carotid endarterectomy. Previous studies have shown that contralateral carotid artery occlusion and intracranial stenoses are associated with cerebral ischemia during carotid endarterectomy; however, the angiographic collateral flow patterns associated with cerebral ischemia have not been identified. This paper reports a retrospective study of 67 patients who underwent two- to four-vessel cerebral angiography followed by carotid endarterectomy with 16-channel EEG monitoring. The angiograms were reviewed for extracranial occlusive disease and collateral flow patterns, and the EEG recordings were analyzed for ischemic changes during carotid artery cross-clamping. Statistical analysis was by Fisher's exact test. Cross-filling of the anterior and middle cerebral arteries from the contralateral carotid artery through the anterior communicating artery correlated with a decreased incidence of EEG ischemic changes. Only 21% of patients with this collateral flow pattern showed ischemic changes compared to 50% of patients without this pattern (p < 0.03). Three angiographic findings occurring in combination on the side contralateral to surgery correlated with EEG ischemia: 1) occlusion of the contralateral internal carotid artery (five of seven or 71%, p < 0.03); 2) collateral flow from the external carotid circulation to the internal carotid circulation via the ophthalmic artery; and 3) collateral flow from the posterior circulation to the contralateral anterior circulation via the posterior communicating artery. The data presented here corroborate the correlation between contralateral carotid artery occlusion and cerebral ischemia during carotid endarterectomy. They also demonstrate that cross-filling of the anterior and middle cerebral arteries by the contralateral carotid artery protects against such ischemia. This collateral flow may serve as an indicator of tolerance to carotid artery cross-clamping. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LOPEZBRESNAHAN, MV (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. NR 12 TC 36 Z9 37 U1 0 U2 1 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 SEP PY 1993 VL 79 IS 3 BP 379 EP 382 DI 10.3171/jns.1993.79.3.0379 PG 4 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA LU690 UT WOS:A1993LU69000010 PM 8360734 ER PT J AU COSGROVE, GR VILLEMURE, JG AF COSGROVE, GR VILLEMURE, JG TI CEREBRAL HEMICORTICECTOMY FOR EPILEPSY SO JOURNAL OF NEUROSURGERY LA English DT Letter ID HEMISPHERECTOMY C1 MONTREAL NEUROL HOSP & INST,MONTREAL H3A 2B4,QUEBEC,CANADA. RP COSGROVE, GR (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 9 TC 11 Z9 11 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 SEP PY 1993 VL 79 IS 3 BP 473 EP 473 PG 1 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA LU690 UT WOS:A1993LU69000028 PM 8360751 ER PT J AU WAKASUGI, S FISCHMAN, AJ BABICH, JW CALLAHAN, RJ ELMALEH, DR WILKINSON, R STRAUSS, HW AF WAKASUGI, S FISCHMAN, AJ BABICH, JW CALLAHAN, RJ ELMALEH, DR WILKINSON, R STRAUSS, HW TI MYOCARDIAL SUBSTRATE UTILIZATION AND LEFT-VENTRICULAR FUNCTION IN ADRIAMYCIN CARDIOMYOPATHY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID BRANCHED FATTY-ACID; HYPERTROPHIC CARDIOMYOPATHY; RAT-HEART; METABOLISM; VIABILITY; HAMSTERS; SCINTIGRAPHY; DOXORUBICIN; ISONITRILE; TECHNETIUM-99M-SESTAMIBI AB We evaluated alterations of substrate utilization in a rat model adriamycin cardiomyopathy with deteriorating left ventricular function. Rats were treated with adriamycin (2 mg/kg), once week for 6, 8, 9 and 10 wk. Fluorine-18-F-deoxyglucose (F-18-FDG) and I-125-beta-methyl-branched fatty acid (I-125-BMIPP) were used as tracers of glucose and fatty acid metabolism and Tc-99m-hexakis (2-methoxyisobutyl-isonitrile) (Tc-99m-MIBI) was used as a myocardial blood flow tracer. Left ventricular ejection fraction (LVEF) calculated from gated blood pool images was used as an indicator of cardiac function. LVEF was normal in the 6-wk group (78.0% +/- 4.8%), abruptly decreased in the 8-wk group (43.1% +/- 10.1%) and further deteriorated in the 9-wk group (27.6% +/- 13.4%). Accumulation of F-18-FDG (%kgID/g) in the hearts of adriamycin treated animals progressively decreased compared to controls (2.19% +/- 0.38%); 1.47% +/- 0.42% (p < 0.01) at 6 wk, 1.22% +/- 0.27% (p < 0.001) at 8 wk, 0.69% +/- 0.56% (p < 0.001) at 9 wk and 0.50% +/- 0.08% (p < 0.001) at 10 wk. This decrease occurred earlier than the deterioration in LVEF. Myocardial accumulation of I-125-BMIPP decreased in the advanced stages of adriamycin cardiomyopathy and was well correlated with the decrease in F-18-FDG accumulation. However, the decrease was less profound than for F-18-FDG; 53.7% +/- 9.8% versus 31.6% +/- 25.4% of control at 9 wk (p = NS), 49.5% +/- 15.3% versus 22.6% +/- 3.5% of control at 10 wk (p < 0.05). Accumulation of Tc-99m-MIBI did not differ between controls and the adriamycin treated groups. There were no differences in blood glucose levels between controls and adriamycin treatment groups. Both glucose and fatty acid utilization are decreased in adriamycin-induced cardiomyopathy and these critical impairments in energy metabolism are associated with heart failure. Impaired myocardial glucose utilization measured with F-18-FDG may be a particularly sensitive marker of adriamycin cardiomyopathy. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. NR 34 TC 35 Z9 38 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD SEP PY 1993 VL 34 IS 9 BP 1529 EP 1535 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LU701 UT WOS:A1993LU70100029 PM 8355075 ER PT J AU HUNTER, GJ CHOI, NC MCLOUD, TC FISCHMAN, AJ AF HUNTER, GJ CHOI, NC MCLOUD, TC FISCHMAN, AJ TI LUNG-TUMOR METASTASIS TO BREAST DETECTED BY FLUORINE-18-FLUORODEOXYGLUCOSE PET SO JOURNAL OF NUCLEAR MEDICINE LA English DT Note ID POSITRON EMISSION TOMOGRAPHY; GLUCOSE; CANCER; NEOPLASMS; FLOW AB We report a case of breast metastasis from a large-cell bronchogenic adenocarcinoma. Serial F-18-fluorodeoxyglucose (FDG) positron emission tomography (PET) was used to monitor the response of the primary lesion to radiation therapy. In the 7-wk interval between studies, an area of markedly increased FDG uptake appeared in the right breast. On subsequent biopsy this proved to be a metastatic deposit from the primary lesion. breast metastasis is uncommon. The ability of FDG-PET to detect metastatic lesions from primary lung tumor is variable. In this case, the finding of the new breast lesion resulted in introduction of chemotherapy to the treatment program. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. RP HUNTER, GJ (reprint author), MASSACHUSETTS GEN HOSP,CTR PET,MGH NMR CTR,DEPT RADIOL,BLDG 149,13TH ST,CHARLESTOWN NAVY YARD,BOSTON,MA 02129, USA. NR 12 TC 9 Z9 9 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD SEP PY 1993 VL 34 IS 9 BP 1571 EP 1573 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LU701 UT WOS:A1993LU70100034 PM 8394885 ER PT J AU RABITO, CA MOORE, RH BOUGAS, C DRAGOTAKES, SC AF RABITO, CA MOORE, RH BOUGAS, C DRAGOTAKES, SC TI NONINVASIVE REAL-TIME MONITORING OF RENAL-FUNCTION - REPLY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Letter RP RABITO, CA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD SEP PY 1993 VL 34 IS 9 BP 1616 EP 1617 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LU701 UT WOS:A1993LU70100045 ER PT J AU HUNT, MK HEBERT, JR SORENSEN, G HARRIS, DR HSIEH, J MORRIS, DH STODDARD, AM AF HUNT, MK HEBERT, JR SORENSEN, G HARRIS, DR HSIEH, J MORRIS, DH STODDARD, AM TI IMPACT OF A WORKSITE CANCER PREVENTION PROGRAM ON EATING PATTERNS OF WORKERS SO JOURNAL OF NUTRITION EDUCATION LA English DT Article AB Changes in the consumption of foods targeted by a cancer prevention intervention based on seven food-focused messages were measured in Treatwell, a randomized, controlled worksite nutrition intervention study aimed at reducing dietary fat and increasing dietary fiber. Changes in food intake of employees in five sites fully implementing the intervention were compared with those in eight control sites in order to assess the impact of the intervention on eating behavior. Food intake was measured using a semi-quantitative food frequency questionnaire (FFQ). Some messages addressed consumption of one food, and others three or four foods in a category. Fourteen foods representing the seven messages from the FFQ and summary questions were analyzed. The intervention messages were delivered to workers through activities such as classes on nutrition and weight management, taste tests, food demonstrations, and point-of-purchase nutrition education programs. A total of 1762 workers responded both to the baseline and the follow-up surveys. The reported change values represent the average of the mean worksite values, thereby assigning equal weight to each worksite, which served as the unit of analysis. Workers in companies where the full intervention was implemented decreased their use of margarine and butter as spreads (p<0.01) and increased their intake of vegetables (p<0.02) significantly more than did workers in control companies. There also was a suggestion of trends in the hypothesized direction for consumption of foods targeted by other eating pattern messages in intervention compared with control companies. RP HUNT, MK (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 16 Z9 16 U1 1 U2 1 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0022-3182 J9 J NUTR EDUC JI J. Nutr. Educ. PD SEP-OCT PY 1993 VL 25 IS 5 BP 236 EP 244 PG 9 WC Education, Scientific Disciplines; Nutrition & Dietetics SC Education & Educational Research; Nutrition & Dietetics GA NJ465 UT WOS:A1993NJ46500004 ER PT J AU COLIN, W AF COLIN, W TI CONDUCTION-VELOCITY OF THE HUMAN INFERIOR ALVEOLAR NERVE - A PRELIMINARY-REPORT SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY LA English DT Article ID SOMATOSENSORY EVOKED-POTENTIALS; ELECTRICAL-STIMULATION; MAXILLOFACIAL SURGERY; TRIGEMINAL NERVE; MANDIBULAR NERVE; RECOVERY; REGENERATION; DYSESTHESIA; ANESTHESIA; NEUROPATHY C1 MASSACHUSETTS GEN HOSP,DEPT ORAL & MAXILLOFACIAL SURG,BOSTON,MA 02114. RP COLIN, W (reprint author), HARVARD UNIV,SCH DENT MED,DEPT ORAL & MAXILLOFACIAL SURG,188 LONGWOOD AVE,CAMBRIDGE,MA 02138, USA. NR 53 TC 13 Z9 14 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0278-2391 J9 J ORAL MAXIL SURG JI J. Oral Maxillofac. Surg. PD SEP PY 1993 VL 51 IS 9 BP 1018 EP 1023 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA LW366 UT WOS:A1993LW36600015 PM 8355091 ER PT J AU SOUBA, WW AF SOUBA, WW TI TOTAL PARENTERAL-NUTRITION WITH GLUTAMINE IN BONE-MARROW TRANSPLANTATION AND OTHER CLINICAL-APPLICATIONS SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SOUBA, WW (reprint author), MASSACHUSETTS GEN HOSP,DIV SURG ONCOL,BOSTON,MA 02114, USA. NR 4 TC 7 Z9 7 U1 0 U2 0 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD SEP-OCT PY 1993 VL 17 IS 5 BP 403 EP 403 DI 10.1177/0148607193017005403 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA LY893 UT WOS:A1993LY89300002 PM 8289402 ER PT J AU HERSKOWITZDUMONT, R WOLFSDORF, JI JACKSON, RA EISENBARTH, GS AF HERSKOWITZDUMONT, R WOLFSDORF, JI JACKSON, RA EISENBARTH, GS TI DISTINCTION BETWEEN TRANSIENT HYPERGLYCEMIA AND EARLY INSULIN-DEPENDENT DIABETES-MELLITUS IN CHILDHOOD - A PROSPECTIVE-STUDY OF INCIDENCE AND PROGNOSTIC FACTORS SO JOURNAL OF PEDIATRICS LA English DT Article ID ISLET CELL ANTIBODIES; NATURAL-HISTORY; HIGH-RISK; GLUCOSE AB We prospectively studied 63 children with transient hyperglycemia to determine their risk of acquiring insulin-dependent diabetes mellitus (IDDM) and to evaluate the predictive value of immunologic markers of prediabetes and of the intravenous glucose tolerance test. Children with transient hyperglycemia were identified by a prospective systematic review of the laboratory reports of a large children's hospital and an office-based pediatric practice and by referral from pediatricians. Transient hyperglycemia occurred in 0.46% of children seen in the children's hospital and in 0.013% of children attending a pediatric office practice. Insulin-dependent diabetes mellitus developed within 18 months of identification in 32% of children in whom transient hyperglycemia was discovered in the absence of a serious illness, compared with 2.3% of children identified during a serious illness (relative risk, 13.9; 95% confidence interval, 1.56 to 123.5). Islet cell antibodies and competitive insulin autoantibodies each had a 100% positive predictive value for IDDM; the negative predictive value of islet cell antibodies and competitive insulin autoantibodies was 96% and 98%, respectively. The stimulated insulin release during an intravenous glucose tolerance test, adjusted for age, had the highest overall accuracy of prediction. All children less than 6 years of age with stimulated insulin release levels <85 pmol/L (12 muU/ml) subsequently had IDDM, as did an 11-year-old child whose stimulated insulin release level was below the lst percentile of 170 pmol/L (24 muU/ml). To date, no child whose stimulated insulin release level was above the 5th percentile has had IDDM. We conclude that when transient hyperglycemia occurs during a serious intercurrent illness, the risk of progression to IDDM is low. In contrast, one third of children in whom transient hyperglycemia is identified without a serious illness can be expected to have IDDM within 1 year. A combination of islet cell antibodies, competitive insulin autoantibodies, and stimulated insulin release levels during an intravenous glucose tolerance test can accurately distinguish children with prediabetes from those with presumed benign transient increases in plasma glucose concentrations. C1 CHILDRENS HOSP MED CTR, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP HERSKOWITZDUMONT, R (reprint author), NEW ENGLAND DEACONESS HOSP, JOSLIN DIABETES CTR, PEDIAT SECT, 1 JOSLIN PL, BOSTON, MA 02215 USA. FU NIDDK NIH HHS [P30 DK36836] NR 21 TC 31 Z9 33 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 SEP PY 1993 VL 123 IS 3 BP 347 EP 354 DI 10.1016/S0022-3476(05)81731-7 PG 8 WC Pediatrics SC Pediatrics GA LW160 UT WOS:A1993LW16000002 PM 8355109 ER PT J AU SWENSEN, CH FULLER, S CLEMENTS, R AF SWENSEN, CH FULLER, S CLEMENTS, R TI STAGE OF RELIGIOUS FAITH AND REACTIONS TO TERMINAL CANCER SO JOURNAL OF PSYCHOLOGY AND THEOLOGY LA English DT Article ID COUPLES; SPOUSE; DEATH AB This study focused on the impact of terminal cancer on the lives of patients and their spouses as a function of the stage of religious faith of the subjects. Patients at more complex stages of faith reported higher overall quality of life; higher quality of socioeconomic life, family life, and psychological and spiritual life; and greater marital intimacy than patients at simpler stages of faith. Patients, regardless of stage of faith, reported the most important factor in their quality of life was their personal relationships, and this importance increased after the diagnosis of cancer. The spouses' quality of life seemed mostly related to the state of the patients' health. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SWENSEN, CH (reprint author), PURDUE UNIV,W LAFAYETTE,IN 47907, USA. NR 21 TC 20 Z9 20 U1 0 U2 2 PU ROSEMEAD SCHOOL PSYCHOLOGY PI LA MIRADA PA 13800 BIOLA AVENUE, BIOLA UNIVERSITY, LA MIRADA, CA 90639-0001 SN 0091-6471 J9 J PSYCHOL THEOL JI J. Psychol. Theol. PD FAL PY 1993 VL 21 IS 3 BP 238 EP 245 PG 8 WC Psychology, Multidisciplinary; Religion SC Psychology; Religion GA MF821 UT WOS:A1993MF82100007 ER PT J AU ERBACH, GT SEMPLE, JP MILFORD, E GOGUEN, J OSATHANONDH, R KURNICK, JT AF ERBACH, GT SEMPLE, JP MILFORD, E GOGUEN, J OSATHANONDH, R KURNICK, JT TI PHENOTYPIC CHARACTERISTICS OF LYMPHOCYTE POPULATIONS ISOLATED FROM MIDDLE GESTATION HUMAN PLACENTA SO JOURNAL OF REPRODUCTIVE IMMUNOLOGY LA English DT Article DE PLACENTA; LYMPHOCYTES; CD3; CD56; GAMMA DELTA-T-CELLS; HLA ID LARGE GRANULAR LYMPHOCYTES; EARLY-PREGNANCY DECIDUA; T-CELL SUBSETS; GAMMA-DELTA; CHORIOCARCINOMA CELLS; TROPHOBLAST; BIOPSIES; ANTIGENS; CLONES; IMPLANTATION AB In order to characterize the phenotypic composition of populations of lymphoid cells in maternal and fetal tissues during the period of middle gestation, mononuclear cells were isolated from maternal peripheral blood, fetal spleen, fetal thymus and placenta of 18-24 week pregnancies. Peripheral blood and placental isolates were stained for a number of lymphoid cell markers by indirect immunofluorescence and analyzed by flow cytometry. Studies were performed on both freshly isolated mononuclear cell preparations and in vitro cultured cells after selective expansion in interleukin 2 (IL2). Fresh placental mononuclear cell isolates were an average 20% CD3+; their CD4/CD8 ratios varied among individuals. An average of 68% of the lymphocytes isolated from maternal peripheral blood were CD3+ Placental and maternal peripheral blood isolates had comparable percentages of CD16+ and CD20+ cells, while CD56+ cells were present at significantly greater numbers in the lymphocyte compartment of placenta (17%) than in peripheral blood (3%); P < 0.01). Lymphocyte isolates were expanded by culture with IL2 and PHA and stained to determine if propagated lymphocyte populations are representative of initial isolates. Expansion of all lymphocyte isolates favored CD3 phenotypes and CD8 phenotypes. Compared to expanded placenta-derived populations, expanded peripheral blood lymphocytes were similar with regard to percentages of all phenotypes except gamma/deltaT cells which represented more of placental lymphocytes (10%) than peripheral lymphocytes (5%; P < 0.01). Surface HLA typing determined propagated placenta-derived lymphocytes to be of maternal and not fetal origin. In vitro propagation of placental mononuclear cell isolates may therefore provide populations of maternal CD3+ lymphocytes for assessment of function and specificity. C1 BRIGHAM & WOMENS HOSP,DIV WOMENS & PERINATAL PATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV WOMENS & PERINATAL PATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,TISSUE TYPING LAB,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. RP ERBACH, GT (reprint author), MASSACHUSSETTS GEN HOSP E,PATHOL RES LAB,BOSTON,MA, USA. FU NCI NIH HHS [5-T-32-CA 09216] NR 29 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-0378 J9 J REPROD IMMUNOL JI J. Reprod. Immunol. PD SEP PY 1993 VL 25 IS 1 BP 1 EP 13 DI 10.1016/0165-0378(93)90038-J PG 13 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA MB991 UT WOS:A1993MB99100001 PM 8271236 ER PT J AU HERZOG, DB STALEY, JE CARMODY, S ROBBINS, WM VANDERKOLK, BA AF HERZOG, DB STALEY, JE CARMODY, S ROBBINS, WM VANDERKOLK, BA TI CHILDHOOD SEXUAL ABUSE IN ANOREXIA-NERVOSA AND BULIMIA-NERVOSA - A PILOT-STUDY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE ANOREXIA NERVOSA; BULIMIA NERVOSA; CHILDHOOD SEXUAL ABUSE ID BORDERLINE PERSONALITY-DISORDER; EATING DISORDERS; STRUCTURED INTERVIEW; EXPERIENCES; WOMEN; DISSOCIATION; SYMPTOMATOLOGY; VICTIMIZATION; BEHAVIOR; INCEST AB Objectives: The aims of this pilot study were to determine the feasibility and scientific merit of coordinating a large-scale investigation of childhood sexual abuse (CSA) in outpatient-eating disordered women and to evaluate the usefulness and potential adverse effects of a semistructured trauma interview. Method: The sample was randomly selected from subjects participating in a naturalistic longitudinal study of anorexia nervosa (AN) and bulimia nervosa (BN). The refusal rate was 26%. Twenty women with DSM-III-R AN/BN were assessed with the traumatic antecedents interview (TAI); a brief semistructured follow-up interview was administered over the telephone 3 to 8 weeks after the first interview. Subjects also completed the Dissociative Experiences Scale (DES). Results: Thirteen subjects (65%) reported CSA, and those with more comorbidity reported CSA more frequently. Subjects with a history of CSA had significantly higher scores on the DES. Minimal adverse consequences to the TAI were noted. Conclusions: The high compliance rate, high prevalence of CSA, and high DES scores among our pilot sample support the merit of studying CSA in a larger sample. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,TRAUMA CLIN,BOSTON,MA 02114. 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 MH38333] NR 35 TC 34 Z9 35 U1 1 U2 3 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 SEP PY 1993 VL 32 IS 5 BP 962 EP 966 DI 10.1097/00004583-199309000-00011 PG 5 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA LV190 UT WOS:A1993LV19000012 PM 8407770 ER PT J AU SPRICHBUCKMINSTER, S BIEDERMAN, J MILBERGER, S FARAONE, SV LEHMAN, BK AF SPRICHBUCKMINSTER, S BIEDERMAN, J MILBERGER, S FARAONE, SV LEHMAN, BK TI ARE PERINATAL COMPLICATIONS RELEVANT TO THE MANIFESTATION OF ADD - ISSUES OF COMORBIDITY AND FAMILIALITY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE ATTENTION DEFICIT DISORDER; PERINATAL COMPLICATIONS; RISK ID ATTENTION-DEFICIT DISORDER; HYPERACTIVE-CHILDREN; CONDUCT DISORDER; FAMILY; INTERVIEW; ASSOCIATION; PREVALENCE; PARENTS; SAMPLE; BOYS AB Objective: We evaluated the role of pregnancy, delivery, and infancy complications (PDICs) in the etiology of attention deficit disorder (ADD) addressing issues of comorbidity and familiality by formulating and testing multiple hypotheses. Method: Subjects were six to 17-year-old boys with DSM-III attention deficit disorder (ADD, N = 73), psychiatric (N = 26), and normal (N = 26) controls and their relatives. Information on PDICs was obtained from the mothers in a standardized manner blind to the proband's clinical status. Results: Using odds ratio analyses, an association was found between ADD and PDICs that was strongest for the comorbid and nonfamilial subtypes. In contrast, noncomorbid and familial ADD subgroups differed less from normal controls in the risk for PDICs. Conclusions: The increased risk for PDICs in nonfamilial ADD children and the lack of evidence for increased risk among familial ADD patients suggests that PDICs may be part of nongenetic etiologic mechanisms in this disorder, especially for children who have comorbid disorders. C1 MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,ACC-725,15 PARKMAN ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [NIMH R01 MH-41314-01A2] NR 31 TC 63 Z9 64 U1 1 U2 3 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 SEP PY 1993 VL 32 IS 5 BP 1032 EP 1037 DI 10.1097/00004583-199309000-00023 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA LV190 UT WOS:A1993LV19000024 PM 8407748 ER PT J AU BIEDERMAN, J FARAONE, SV CHEN, WJ AF BIEDERMAN, J FARAONE, SV CHEN, WJ TI SOCIAL-ADJUSTMENT INVENTORY FOR CHILDREN AND ADOLESCENTS - CONCURRENT VALIDITY IN ADHD CHILDREN SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE ADAPTIVE FUNCTIONING; ATTENTION-DEFICIT HYPERACTIVITY DISORDER; COMORBIDITY ID INTERVIEW; DISORDER AB Objective: The assessment of children's adaptive functioning has broad-range implications for clinical practice, research, and public health, and relatively few well-developed assessment instruments are available. The validity of the Social Adjustment Inventory for Children and Adolescents (SAICA). a semistructured interview schedule that assesses adaptive functioning in children and adolescents, was examined. Method: Two groups of index children were examined: 140 attention-deficit hyperactivity disorder (ADHD) children (both psychiatric and pediatric referrals) and 120 normal comparisons. Results: Concurrent validity was found for the SAICA in its significant association with the social competence scales of the Child Behavior Checklist and DSM-III-R's Global Assessment of Functioning. It was also found that among ADHD children, psychiatric comorbidity conferred an increased risk for worse adaptive functioning. Conclusions: These findings suggest the SAICA is an effective way to assess adaptive functioning. Moreover, its ability to discriminate ADHD from control children and its association with psychiatric comorbidity indicate the SAICA measures adaptive functioning within a range relevant for studies of psychopathology. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,ACC-725,15 PARKMAN ST,BOSTON,MA 02114, USA. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [NIMH R01 MH-41314-01A2] NR 13 TC 60 Z9 60 U1 2 U2 6 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 SEP PY 1993 VL 32 IS 5 BP 1059 EP 1064 DI 10.1097/00004583-199309000-00027 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA LV190 UT WOS:A1993LV19000028 PM 8407752 ER PT J AU LAVIE, CJ MILANI, RV LITTMAN, AB AF LAVIE, CJ MILANI, RV LITTMAN, AB TI BENEFITS OF CARDIAC REHABILITATION AND EXERCISE TRAINING IN SECONDARY CORONARY PREVENTION IN THE ELDERLY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; QUALITY-OF-LIFE; HEART-DISEASE; ENDOCARDITIS PROPHYLAXIS; RISK-FACTORS; MEN; PATTERNS; OLDER; AGE; CHOLESTEROL AB Objectives. The aim of this study was to determine the effects of cardiac rehabilitation and exercise training on plasma lipids, indexes of obesity and exercise capacity in the elderly and to compare the benefits in elderly patients with coronary heart disease with benefits in a younger cohort. Background. Despite the well proved benefits of cardiac rehabilitation and exercise training, elderly patients with coronary heart disease are frequently not referred or vigorously encouraged to pursue this therapy. In addition, only limited data are available for these elderly patients on the benefits of cardiac rehabilitation on plasma lipids, indexes of obesity and exercise capacity. Methods. At two large multispecialty teaching institutions, baseline and post-rehabilitation data including plasma lipids, indexes of obesity and exercise capacity were compared in 92 elderly patients (greater-than-or-equal-to 65 years, mean age 70.1 +/- 4.1 years) and 182 younger patients (<65 years, mean 53.9 +/- 7.4 years) enrolled in phase II cardiac rehabilitation and exercise programs after a major cardiac event. Results. At baseline, body mass index (26.0 +/- 3.9 vs. 27.8 +/- 4.2 kg/M2, p < 0.001), triglycerides (141 +/- 55 vs. 178 +/- 105 mg/dl, p < 0.01) and estimated metabolic equivalents (METs) (5.6 +/- 1.6 vs. 7.7 +/- 3.0, p < 0.0001) were lower and high density lipoprotein cholesterol was greater (40.4 +/- 12.1 vs. 37.5 +/- 10.4 mg/dl, p < 0.05) in the elderly than in younger patients. After rehabilitation, the elderly demonstrated significant improvements in METs (5.6 +/- 1.6 vs. 7.5 +/- 2.3, p < 0.0001), body mass index (26.0 +/- 3.9 vs. 25.6 +/- 3.8 kg/m2, p < 0.01), percent body fat (24.4 +/- 7.0 vs. 22.9 +/- 7.2%, p < 0.0001), high density lipoprotein cholesterol (40.4 +/- 12.1 vs. 43.0 +/- 11.4 mg/dl, p < 0.001) and the ratio of low density to high density lipoprotein, cholesterol (3.6 +/- 1.3 vs. 3.3 +/- 1.0, p < 0.01) and a decrease in triglycerides that approached statistical significance (141 +/- 55 vs. 130 +/- 76 mg/dl, p = 0.14) but not in total cholesterol or low density lipoprotein cholesterol. Improvements in functional capacity, percent body fat and body mass index, as well as lipids, were statistically similar in the older and younger patients. Conclusions. Despite baseline differences, improvements in exercise capacity, obesity indexes and lipids were very similar in older and younger patients enrolled in cardiac rehabilitation and exercise training. These data emphasize that elderly patients should not be categorically denied the psychosocial, physical and risk factor benefits of secondary coronary prevention including formal cardiac rehabilitation and supervised exercise training. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,CTR CARDIOVASC HLTH,BEHAV MED UNIT,BOSTON,MA 02114. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA 70121. 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 48 TC 173 Z9 174 U1 1 U2 5 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 SEP PY 1993 VL 22 IS 3 BP 678 EP 683 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MQ361 UT WOS:A1993MQ36100008 PM 8354798 ER PT J AU ANDERSON, RC CARNES, M CLARK, A DEPROSSE, CA HORBACH, N MORLEY, J OUSLANDER, J RAPPAPORT, S SAND, P STONE, AR VENABLE, DD ZIRKER, W AF ANDERSON, RC CARNES, M CLARK, A DEPROSSE, CA HORBACH, N MORLEY, J OUSLANDER, J RAPPAPORT, S SAND, P STONE, AR VENABLE, DD ZIRKER, W TI EFFECTS OF TERODILINE ON URINARY-INCONTINENCE AMONG OLDER NONINSTITUTIONALIZED WOMEN SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID MOTOR URGE INCONTINENCE; NURSING-HOME PATIENTS; DOUBLE-BLIND; DETRUSOR INSTABILITY; GERIATRIC-PATIENTS; ELDERLY WOMEN; CROSSOVER; DYSFUNCTION; MANAGEMENT; OXYBUTYNIN AB Objective: To determine the effectiveness of terodiline, a drug with calcium antagonist and anticholinergic properties, on the frequency of incontinence in older non-institutionalized women. Design: Randomized, placebo-controlled, parallel-group, double-blind trial. Setting: Twelve outpatient clinics across the United States affiliated with programs in either geriatrics, gynecology, or urology. Participants: Ninety-eight women, age 60 or older, with symptoms of urge incontinence and self-reported frequency of incontinence four or more times per week and involuntary bladder contractions on dual-channel water cystometry. Main Outcome Measures: Self-reported urinary frequency urgency number of incontinence episodes, and number of heavily soaked pads. Results: Eighty-one women, average age 71, completed the trial, 40 in the active drug group, 41 in the placebo group. Incontinence frequency and the number of heavily soaked pads were reduced in the active drug group by 64% and 55%, respectively, and by 21% (P = 0.002) and 9% (P = 0.04) in the placebo group. No patients dropped out due to adverse effects. An intention-to-treat analysis of all 98 patients yielded the same conclusion. Conclusion: Terodiline is highly effective in reducing incontinence in older, noninstitutionalized women with urge incontinence. Because of its potential association with polymorphic ventricular tachycardia (torsades de pointes), terodiline must undergo further testing to define its safety before it can be recommended for clinical use in the incontinent geriatric population. C1 WOMENS UROL CTR, SEATTLE, WA USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI USA. OREGON HLTH SCI UNIV, PORTLAND, OR 97201 USA. UNIV IOWA HOSP & CLIN, IOWA CITY, IA 52242 USA. GEORGE WASHINGTON UNIV, MED CTR, WASHINGTON, DC 20037 USA. ST LOUIS UNIV, MED CTR, ST LOUIS, MO 63103 USA. METHODIST HOSP INDIANA, INDIANAPOLIS, IN 46202 USA. EVANSTON HOSP CORP, EVANSTON, IL 60201 USA. UNIV CALIF DAVIS, SACRAMENTO MED CTR, MED CTR, SACRAMENTO, CA 95817 USA. LOUISIANA STATE UNIV, MED CTR, SHREVEPORT, LA 71105 USA. VET ADM MED CTR, NORTHPORT, NY 11768 USA. NR 36 TC 2 Z9 2 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0002-8614 EI 1532-5415 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD SEP PY 1993 VL 41 IS 9 BP 915 EP 922 PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA LW378 UT WOS:A1993LW37800003 ER PT J AU GERETY, MB CHIODO, LK KANTEN, DN TULEY, MR CORNELL, JE AF GERETY, MB CHIODO, LK KANTEN, DN TULEY, MR CORNELL, JE TI MEDICAL-TREATMENT PREFERENCES OF NURSING-HOME RESIDENTS - RELATIONSHIP TO FUNCTION AND CONCORDANCE WITH SURROGATE DECISION-MAKERS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID LONG-TERM CARE; LIFE-SUSTAINING TREATMENTS; CARDIOPULMONARY RESUSCITATION; HEALTH-STATUS; DEPRESSION; PATIENT; PREDICTIONS; PHYSICIANS; ATTITUDES; CAPACITY AB Objective: To describe treatment preferences of nursing home residents, concordance with decisions by self-selected proxies and to establish the relationship of sociodemographic and functional measures to decisions. Setting and Subjects: 52 patient-proxy pairs at a Veterans Affairs nursing home. Methods: Treatment preferences were elicited from residents and proxies regarding cardiopulmonary resuscitation, mechanical ventilation, and intensive care unit care. Hospitalization, intravenous antibiotics, intravenous fluid administration, and tube feeding were presented in three separate health scenarios. Concordance was determined for the entire interview and separately for each scenario. Treatment-seeking intensity and decision-making consistency were scored and used to explore associations with sociodemographic variables and function. Results: Subjects were predominantly male (97%) and non-Hispanic white (74%); average age was 70 +/- 12 years, with 4 +/- 2.9 diagnoses. Residents accepted 70% of all treatments. The proportion of subjects accepting interventions declined parallel to health status in each scenario. Only 7/52 (13%) subjects made inconsistent decisions. Resident treatment acceptance was inversely associated with GDS scores but not associated with any other sociodemographic or functional measure. Concordance with proxies was no greater than chance. Proxies' decisions were not systematically biased against resident preferences or influenced by patient characteristics. Conclusions: Veterans desired most treatments, but adjusted preferences according to health status and were not inconsistent. Depressive symptoms should be addressed prior to advance directive selection. The patient remains the best source of information, but proxies' decisions exhibit no bias and are not affected by patient status. C1 UNIV TEXAS,HLTH SCI CTR,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GEN MED,SAN ANTONIO,TX 78284. RP GERETY, MB (reprint author), AUDIE L MURPHY VET MEM HOSP,GRECC 182,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 38 TC 68 Z9 68 U1 3 U2 6 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 SEP PY 1993 VL 41 IS 9 BP 953 EP 960 PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA LW378 UT WOS:A1993LW37800009 PM 8204138 ER PT J AU GRANDALIANO, G BISWAS, P CHOUDHURY, GG ABBOUD, HE AF GRANDALIANO, G BISWAS, P CHOUDHURY, GG ABBOUD, HE TI SIMVASTATIN INHIBITS PDGF-INDUCED DNA-SYNTHESIS IN HUMAN GLOMERULAR MESANGIAL CELLS SO KIDNEY INTERNATIONAL LA English DT Article ID GROWTH-FACTOR PDGF; PROTEIN-KINASE-C; MEVALONATE; EXPRESSION; INJURY; RAT; GLOMERULOSCLEROSIS; MICROINJECTION; PROLIFERATION; NIH-3T3-CELLS AB Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase ameliorate glomerular pathology and renal dysfunction in different models of glomerular disease. This effect has generally been attributed to a decrease in the circulating levels of cholesterol. Focal or diffuse mesangial cell proliferation is a common feature of glomerular pathology. There is now evidence from studies in vitro and in vivo that platelet-derived growth factor (PDGF) is an important mediator of glomerular hypercellularity. The activity of HMGCoA reductase has previously been shown to be a requirement for cell growth. In the present study, we examined the effect of simvastatin, an HMGCoA reductase inhibitor, on PDGF-induced DNA synthesis and PDGF B chain gene expression in human glomerular mesangial cells. In addition, we investigated the effect of simvastatin on phospholipase C (PLC) and protein kinase C (PKC) activation stimulated by PDGF. We demonstrate that treatment of the cells with simvastatin completely inhibits PDGF-induced DNA synthesis. This inhibition is reversed by mevalonate but not by cholesterol or farnesol, two major metabolites of the mevalonate pathway. On the other hand inhibition of HMGCoA reductase does not influence PDGF-induced activation of PLC and PKC, or PDGF B chain gene expression. These data suggest that simvastatin acts at a late step in the PDGF mitogenic pathway without interfering with other early cellular responses elicited by this growth factor. These studies also raise the possibility that the ameliorative effect of HMGCoA reductase inhibitors on glomerular pathology may be mediated, at least in part, by a direct cellular effect. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RI Grandaliano, Giuseppe/G-2963-2012 FU NIDDK NIH HHS [DK 43988, DK 33665] NR 34 TC 102 Z9 103 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 SEP PY 1993 VL 44 IS 3 BP 503 EP 508 DI 10.1038/ki.1993.274 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA LT428 UT WOS:A1993LT42800004 PM 8231022 ER PT J AU WEBER, GF CANTOR, H AF WEBER, GF CANTOR, H TI HIV GLYCOPROTEIN AS A SUPERANTIGEN - A MECHANISM OF AUTOIMMUNITY AND IMPLICATIONS FOR A VACCINATION STRATEGY SO MEDICAL HYPOTHESES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; CD4+ T-CELLS; MONOCLONAL-ANTIBODIES; ENVELOPE GLYCOPROTEIN; INFECTED INDIVIDUALS; PATHOGENESIS; DOMAIN; MICE; IDENTIFICATION; DEPLETION AB The pathogenic effects of HIV may reflect mimicry of several key immunological molecules. The surface glycoprotein of HIV has superantigenic properties responsible for the sequential deletion of T-cell clones. In addition, the glycoprotein has several regions sharing homology with class II MHC products. It can elicit cross-reactive antibodies which block replenishment of these T-cells in the thymus. The usefulness of conventional vaccination strategies in the fight against AIDS has been subject to debate. Based on these considerations, we argue that effective vaccines should avoid viral sequences homologous to class II MHC proteins which might exacerbate this process. RP WEBER, GF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,IMMUNOPATHOL LAB,BOSTON,MA 02115, USA. NR 36 TC 9 Z9 9 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 SEP PY 1993 VL 41 IS 3 BP 247 EP 250 DI 10.1016/0306-9877(93)90241-H PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LX720 UT WOS:A1993LX72000013 PM 8259084 ER PT J AU NIEMIERKO, A GOITEIN, M AF NIEMIERKO, A GOITEIN, M TI SAMPLING TECHNIQUES FOR THE EVALUATION OF TREATMENT PLANS - COMMENT SO MEDICAL PHYSICS LA English DT Letter C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP NIEMIERKO, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 5 TC 9 Z9 9 U1 0 U2 0 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0094-2405 J9 MED PHYS JI Med. Phys. PD SEP-OCT PY 1993 VL 20 IS 5 BP 1377 EP 1380 DI 10.1118/1.597103 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MC661 UT WOS:A1993MC66100010 PM 8289720 ER PT J AU TOMERA, JF LILFORD, K AF TOMERA, JF LILFORD, K TI CALCIUM AND SKELETAL-MUSCLE - A MULTIPLE-REGRESSION ON SIGNAL-TRANSDUCTION MECHANISMS IN BURN TRAUMA SO METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY LA English DT Article DE BURN TRAUMA; CALCIUM; MULTIPLE REGRESSION; POLYINOSITOL PHOSPHATES; PYTHAGOREAN THEOREM; SIGNAL TRANSDUCTION SYSTEMS; SKELETAL MUSCLE; VECTORIAL ANALYSIS AB The novelty of applying three-dimensional graphic capabilities involving area and vector changes was used to understand variations in inositol derivatives and their comodulating influence on calcium (Ca2+) in skeletal muscle under the duress of burn trauma. Burn injury was achieved by scalding of predefined areas (0, 20% and 50%) on the dorsal and ventral surfaces of mice. At day 21, Ca-45(2+) influx and efflux procedures were performed. Through multiple regression, the dependency of intracellular Ca2+ was determined with respect to three polyinositol forms each representing independence simultaneously. The contribution of each of these parameters was assigned to a three-dimensional axis. Vector analysis determined the relationship of intracellular Ca2+ to each of the independent parameters in control, 20% and 50% burn groups. Such vector analysis allows for a clear visualization of the interrelationships that exist between secondary (viz, IP3) and tertiary (viz, Ca2+) messenger systems. This clear visualization may allow for a greater understanding of messenger systems that may lead to more effective treatment of the systemic effects of severe burn trauma. C1 SHRINERS BURNS INST,ANESTHESIA SERV,CLIN PHARMACOL LAB,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIOL,BOSTON,MA 02115. NR 13 TC 12 Z9 12 U1 0 U2 0 PU J R PROUS SA PI BARCELONA PA APARTADO DE CORREOS 540, PROVENZA 388, 08025 BARCELONA, SPAIN SN 0379-0355 J9 METHOD FIND EXP CLIN JI Methods Find. Exp. Clin. Pharmacol. PD SEP PY 1993 VL 15 IS 7 BP 471 EP 482 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MB590 UT WOS:A1993MB59000008 PM 8255127 ER PT J AU MARTIN, GR JAIN, RK AF MARTIN, GR JAIN, RK TI FLUORESCENCE RATIO IMAGING MEASUREMENT OF PH GRADIENTS - CALIBRATION AND APPLICATION IN NORMAL AND TUMOR-TISSUES SO MICROVASCULAR RESEARCH LA English DT Article ID INTRACELLULAR PH; SPATIAL MEASUREMENTS; CYTOPLASMIC PH; CELLS; MICROSCOPY; INVIVO C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114. RP MARTIN, GR (reprint author), CARNEGIE MELLON UNIV,DEPT CHEM ENGN,PITTSBURGH,PA 15213, USA. FU NCI NIH HHS [CA-56591] NR 25 TC 39 Z9 39 U1 0 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0026-2862 J9 MICROVASC RES JI Microvasc. Res. PD SEP PY 1993 VL 46 IS 2 BP 216 EP 230 DI 10.1006/mvre.1993.1048 PG 15 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA LX330 UT WOS:A1993LX33000010 PM 8246820 ER PT J AU MAEDA, T TSAI, AYM SAITO, H AF MAEDA, T TSAI, AYM SAITO, H TI MUTATIONS IN A PROTEIN-TYROSINE-PHOSPHATASE GENE (PTP2) AND A PROTEIN-SERINE THREONINE PHOSPHATASE GENE (PTC1) CAUSE A SYNTHETIC GROWTH DEFECT IN SACCHAROMYCES-CEREVISIAE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID INTACT YEAST-CELLS; HIGH-EFFICIENCY TRANSFORMATION; FISSION-YEAST; MOLECULAR CHARACTERIZATION; PHOSPHORYLATION SITES; P34CDC2 KINASE; CLONING; DNA; MORPHOGENESIS; HOMOLOGY AB Two protein tyrosine phosphatase genes, PTP1 and PTP2, are known in Saccharomyces cerevisiae. However, the functions of these tyrosine phosphatases are unknown, because mutations in either or both phosphatase genes have no clear phenotypic effects. In this report, we demonstrate that although ptp2 has no obvious phenotype by itself, it has a profound effect on cell growth when combined with mutations in a novel protein phosphatase gene. Using a colony color sectoring assay, we isolated 25 mutants in which the expression of PTP1 or PTP2 is required for growth. Complementation tests of the mutants showed that they have a mutation in one of three genes. Cloning and sequence determination of one of these gene, PTC1, indicated that it encodes a homolog of the mammalian protein serine/threonine phosphatase 2C (PP2C). The amino acid sequence of the PTC1 product is approximately 35% identical to PP2C. Disruption of PTC1 indicated that the PTC1 function is nonessential. In contrast, ptc1 ptp2 double mutants showed a marked growth defect. To examine whether PTC1 encodes an active protein phosphatase, a glutathione S-transferase (GST)-PTC1 fusion gene was constructed and expressed in Escherichia coli. Purified GST-PTC1 fusion protein hydrolyzed a serine phosphorylated substrate in the presence of the divalent cation Mg2+ or Mn2+. GST-PTC1 also had weak (approximately 0.5% of its serine phosphatase activity) protein tyrosine phosphatase activity. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA-51132] NR 65 TC 139 Z9 141 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD SEP PY 1993 VL 13 IS 9 BP 5408 EP 5417 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LU493 UT WOS:A1993LU49300028 PM 8395005 ER PT J AU NEY, PA ANDREWS, NC JANE, SM SAFER, B PURUCKER, ME WEREMOWICZ, S MORTON, CC GOFF, SC ORKIN, SH NIENHUIS, AW AF NEY, PA ANDREWS, NC JANE, SM SAFER, B PURUCKER, ME WEREMOWICZ, S MORTON, CC GOFF, SC ORKIN, SH NIENHUIS, AW TI PURIFICATION OF THE HUMAN NF-E2 COMPLEX - CDNA CLONING OF THE HEMATOPOIETIC CELL-SPECIFIC SUBUNIT AND EVIDENCE FOR AN ASSOCIATED PARTNER SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID BETA-GLOBIN LOCUS; DOMINANT CONTROL REGION; PORPHOBILINOGEN DEAMINASE GENE; SULFATE-POLYACRYLAMIDE GELS; SODIUM DODECYL-SULFATE; TRANSGENIC MICE; TRANSCRIPTION FACTORS; CHROMATIN STRUCTURE; ERYTHROID PROMOTER; RNA-POLYMERASE AB The human globin locus control region-binding protein, NF-E2, was purified by DNA affinity chromatography. Its tissue-specific component, p45 NF-E2, was cloned by use of a low-stringency library screen with murine p45 NF-E2 cDNA (N. C. Andrews, H. Erdjument-Bromage, M. B. Davidson, P. Tempst, and S. H. Orkin, Nature (London] 362:722-728, 1993). The human p45 NF-E2 gene was localized to chromosome 12q13 by fluorescent in situ hybridization. Human p45 NF-E2 and murine p45 NF-E2 are highly homologous basic region-leucine zipper (bZIP) proteins with identical DNA-binding domains. Immunoprecipitation experiments demonstrated that p45 NF-E2 is associated in vivo with an 18-kDa protein (p18). Because bZIP proteins bind DNA as dimers, we infer that native NF-E2 must be a heterodimer of 45- and 18-kDa subunits. Although AP-1 and CREB copurified with NF-E2, no evidence was found for heterodimer formation between p45 NF-E2 and proteins other than p18. Thus, p18 appears to be the sole specific partner of p45 NF-E2 in erythroid cells. Cloning of human p45 NF-E2 should permit studies of the role of NF-E2 in globin gene regulation and erythroid differentiation. C1 NHLBI, MOLEC HEMATOL LAB, BETHESDA, MD 20892 USA. HARVARD UNIV, CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST, DEPT PEDIAT,DIV HEMATOL ONCOL, BOSTON, MA 02115 USA. HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HOWARD HUGHES MED INST, BOSTON, MA 02115 USA. RP NHLBI, CLIN HEMATOL BRANCH, BETHESDA, MD 20892 USA. RI Jane, Stephen/D-6659-2011; OI Andrews, Nancy/0000-0003-0243-4462 NR 51 TC 166 Z9 168 U1 0 U2 1 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 SEP PY 1993 VL 13 IS 9 BP 5604 EP 5612 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LU493 UT WOS:A1993LU49300046 PM 8355703 ER PT J AU WAYS, DK QIN, WX COOK, P PARKER, PJ MENKE, JB HAO, EH SMITH, AM JONES, C HERSHMAN, JM GEFFNER, ME SU, F SAMUELS, HH USALA, SJ AF WAYS, DK QIN, WX COOK, P PARKER, PJ MENKE, JB HAO, EH SMITH, AM JONES, C HERSHMAN, JM GEFFNER, ME SU, F SAMUELS, HH USALA, SJ TI DOMINANT AND NONDOMINANT NEGATIVE C-ERBA-BETA-1 RECEPTORS ASSOCIATED WITH THYROID-HORMONE RESISTANCE SYNDROMES AUGMENT 12-O-TETRADECANOYL-PHORBOL-13-ACETATE INDUCTION OF THE COLLAGENASE PROMOTER AND EXHIBIT DEFECTIVE 3,5,3'-TRIIODOTHYRONINE-MEDIATED REPRESSION SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID PROTEIN-KINASE-C; TRANSCRIPTION FACTOR AP-1; LIGAND-BINDING DOMAIN; RETINOIC ACID RECEPTORS; GENERALIZED RESISTANCE; DNA-BINDING; MOLECULAR HETEROGENEITY; FUNCTIONAL-PROPERTIES; RESPONSE ELEMENTS; PHORBOL ESTERS AB C-erbA receptors and v-erbA have been shown to functionally interact with 12-0-tetradecanoyl-phorbol-13-acetate (TPA)-inducible gene expression. These proteins enhance trans-activation by c-jun, and the c-erbA receptors in the presence of thyroid hormone repress TPA and c-jun induction of transcription. Also, v-erbA can abrogate T3-mediated repression. We have examined how dominant negative (S and CL) and nondominant negative (G-H) receptors cloned from various patients with thyroid hormone resistance syndromes affect expression of the collagenase promoter induced with TPA. The CL receptor (ARG315HIS mutation) has a 2-fold reduction in T3-binding affinity compared with human c-erbAbeta1 wild-type (WT) receptor, whereas the G-H receptor (ARG311HIS) and S receptor (deletion, THR codon 332) have T3-binding affinities reduced by 100-fold and greater than 100-fold, respectively. These mutant receptors were cotransfected with a collagenase promoter (-1200 to +63 base pairs) chloramphenicol acetyltransferase reporter gene (Col-CAT) into COS-7 cells. Levels of CAT reporter gene expression after transient transfection were determined in the presence or absence of 3-10 nM T3 and the presence or absence of 100 nM TPA. Unoccupied CL receptor and G-H and S receptors stimulated TPA-induced Col-CAT expression 1.5- to 9-fold. The CL receptor with thyroid hormone totally repressed TPA induction of the collagenase receptor. In the presence of thyroid hormone, the enhancing effects by S and G-H receptors on TPA-induced Col-CAT expression were unaffected and minimally diminished, respectively. However, when WT receptor was cotransfected with G-H or S receptors at 1:1 molar ratios in the presence of T3, the transcriptional enhancement was completely abrogated. Similar results with WT and mutant receptors on Col-CAT activity were seen in cells transiently transfected with a constitutively active protein kinase C construct corresponding to the catalytic domain of protein kinase C-alpha and grown in the absence of TPA. We conclude that human mutant c-erbAbeta1 receptors, dominant and nondominant negative, have functional properties similar to v-erbA in terms of effects on a TPA-inducible promoter. The transcriptional enhancement of a TPA-inducible gene by the human mutants can be overcome by T3-activated WT receptor. This effect of WT on mutant receptor function may diminish a potential neoplastic effect of the human mutant receptors. C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. IMPERIAL CANC RES FUND, PROT PHOSPHORYLAT LAB, LONDON WC2A 3PX, ENGLAND. E CAROLINA UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, GREENVILLE, NC 27858 USA. NYU MED CTR, DEPT MED, DIV MOLEC ENDOCRINOL, NEW YORK, NY 10016 USA. UNIV CALIF LOS ANGELES, LOS ANGELES MED CTR, DEPT PEDIAT, LOS ANGELES, CA 90024 USA. NYU MED CTR, DEPT PHARMACOL, NEW YORK, NY 10016 USA. RP WAYS, DK (reprint author), E CAROLINA UNIV, SCH MED, DEPT MED, ENDOCRINOL SECT, GREENVILLE, NC 27858 USA. RI Parker, Peter/D-5192-2013 FU NCI NIH HHS [CA-43823]; NIDDK NIH HHS [DK-16636, DK-42807] NR 59 TC 12 Z9 12 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD SEP PY 1993 VL 7 IS 9 BP 1112 EP 1120 DI 10.1210/me.7.9.1112 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LZ180 UT WOS:A1993LZ18000002 PM 8247013 ER PT J AU LINDEN, J TAYLOR, HE ROBEVA, AS TUCKER, AL STEHLE, JH RIVKEES, SA FINK, JS REPPERT, SM AF LINDEN, J TAYLOR, HE ROBEVA, AS TUCKER, AL STEHLE, JH RIVKEES, SA FINK, JS REPPERT, SM TI MOLECULAR-CLONING AND FUNCTIONAL EXPRESSION OF A SHEEP-A3 ADENOSINE RECEPTOR WITH WIDESPREAD TISSUE DISTRIBUTION SO MOLECULAR PHARMACOLOGY LA English DT Article ID NUCLEOTIDE-BINDING PROTEINS; A1-ADENOSINE RECEPTORS; BOVINE BRAIN; GENES AB Using the polymerase chain reaction, an A3 adenosine receptor has been cloned from the hypophysial par tuberalis of sheep. The clone encodes a 317-amino acid protein that is 72% identical to the rat A3 adenosine receptor. In contrast to rat, where abundant A3 mRNA transcript is found primarily in testis, the sheep transcript is most abundant in lung, spleen, and pineal gland and is present in moderate levels in brain, kidney, and testis. The agonist N6-amino[I-125]iodobenzyladenosine binds with high affinity (K(d) congruent-to 6 nm) and specificity to recombinant A3 adenosine receptors expressed transiently in COS-1 cells or stably in CHO K1 cells. The potency order of agonists is N6-aminoiodobenzyladenosine > N-ethylcarboxamidoadenosine greater-than-or-equal-to (R)-phenylisopropyladenosine much greater than cyclopentyladenosine. Little or no binding of purine nucleotides was detected. The potency order of antagonists is 3-(3-iodo-4-aminobenzyl)-8-(4-oxyace-tate)phenyl-1-propylxanthine (I-ABOPX) (K(i) = 3 nm) > 1,3-dipropyl-8-(4-acrylate)phenylxanthine (BW-A1433) > 1,3-dipropyl-8-sulfophenylxanthine = xanthine amine cogener much greater than 8-cyclopentyl-1,3-dipropylxanthine. Enprofylline does not bind. These data indicate that, in contrast to A1 adenosine receptors, A3 adenosine receptors preferentially bind ligands with aryl rings in the N6-position of adenine and in the C-8-position of xanthine. Among antagonists, the A3 adenosine receptor preferentially binds 8-phenylxanthines with acidic versus basic para-substituents (I-ABOPX > BW-A1433 > 1,3-dipropyl-8-sulfophenylxanthine = xanthine amine cogener). Agonists reduce forskolin-stimulated cAMP accumulation in Chinese hamster ovary cells stably transfected with recombinant sheep A3 adenosine receptors; the reduction is blocked by BW-A1433 but not by 8-cyclopentyl-1,3-dipropylxanthine. These data suggest that (i) A3 adenosine receptors display unusual structural diversity for species homologs, (ii) in contrast to rat, sheep A3 adenosine receptors have a broad tissue distribution, and (iii) some xanthines with acidic side chains bind with high affinity to A3 adenosine receptors. C1 MASSACHUSETTS GEN HOSP,DEV CHRONOBIOL LAB,JACKSON 1226,BOSTON,MA 02114. UNIV VIRGINIA,HLTH SCI CTR,DEPT INTERNAL MED,CHARLOTTESVILLE,VA 22908. MASSACHUSETTS GEN HOSP,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV VIRGINIA,HLTH SCI CTR,DEPT MOLEC PHYSIOL & BIOL PHYS,CHARLOTTESVILLE,VA 22908. FU NHLBI NIH HHS [HL37942]; NIDDK NIH HHS [DK42125, P30-DK38942] NR 21 TC 207 Z9 209 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD SEP PY 1993 VL 44 IS 3 BP 524 EP 532 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LY915 UT WOS:A1993LY91500006 PM 8396714 ER PT J AU WASCO, W GURUBHAGAVATULA, S DPARADIS, M ROMANO, DM SISODIA, SS HYMAN, BT NEVE, RL TANZI, RE AF WASCO, W GURUBHAGAVATULA, S DPARADIS, M ROMANO, DM SISODIA, SS HYMAN, BT NEVE, RL TANZI, RE TI ISOLATION AND CHARACTERIZATION OF APLP2 ENCODING A HOMOLOG OF THE ALZHEIMERS ASSOCIATED AMYLOID BETA-PROTEIN PRECURSOR SO NATURE GENETICS LA English DT Article ID MESSENGER-RNA; GENETIC-LINKAGE; DISEASE LOCUS; CDNA; LOCALIZATION; PEPTIDE; CHROMOSOME-14; RECEPTOR; MUTATION; MAPS AB Familial Alzheimer's disease (FAD) is a genetically heterogeneous disorder that includes a rare early-onset form linked to mutations in the amyloid b protein precursor (APP) gene. Clues to the function of APP derive from the recent finding that it is a member of a highly conserved protein family that includes the mammalian amyloid precursor-like protein (APLP1) gene which maps to the same general region of human chromosome 19 linked to late-onset FAD. Here we report the isolation of the human APLP2 gene. We show that APLP2 is a close relative of APP and exhibits a very similar pattern of expression in the brain and throughout the body. Like APP, APLP2 contains a cytoplasmic domain predicted to couple with the GTP-binding protein G(o) indicating that it may be an additional cell surface activator of this G protein. C1 MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02115 USA. MCLEAN HOSP, MAILMAN RES CTR, BELMONT, MA 02178 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT PATHOL, BALTIMORE, MD 21205 USA. JOHNS HOPKINS UNIV, SCH MED, NEUROPATHOL LAB, BALTIMORE, MD 21205 USA. RP WASCO, W (reprint author), MASSACHUSETTS GEN HOSP, CTR NEUROSCI, GENET & AGING LAB, BOSTON, MA 02129 USA. FU NIA NIH HHS [AG08487]; NINDS NIH HHS [NS30428] NR 51 TC 303 Z9 308 U1 1 U2 2 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD SEP PY 1993 VL 5 IS 1 BP 95 EP 100 DI 10.1038/ng0993-95 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA LV565 UT WOS:A1993LV56500025 PM 8220435 ER PT J AU CRONINGOLOMB, A SUGIURA, R CORKIN, S GROWDON, JH AF CRONINGOLOMB, A SUGIURA, R CORKIN, S GROWDON, JH TI INCOMPLETE ACHROMATOPSIA IN ALZHEIMERS-DISEASE SO NEUROBIOLOGY OF AGING LA English DT Article DE ALZHEIMER; COLOR; DEMENTIA; ACHROMATOPSIA; VISION; TRITANOMALOUS ID GANGLION-CELL DEGENERATION; AGE-RELATED-CHANGES; VISUAL-CORTEX; SENILE DEMENTIA; AREA V4; DYSFUNCTION; SENSITIVITY; PATHWAYS; DEFICITS; PLAQUES AB We report that patients with Alzheimer's disease (AD) have a selective deficit in blue hue discrimination, as assessed with three clinical measures of color vision. The Farnsworth D-15 Test, the Lanthony New Color Test, and the City University Color Vision Test were administered to 32 patients with AD (ranging in dementia severity from mild to severe) and 32 age-matched normal control subjects (NCS). Of the AD patients, 11 who were representative of the larger group for age, education level, and dementia severity received a complete neuro-ophthalmological examination that ruled out obvious disorders of the anterior visual structures. AD patients made significantly more tritan (blue) errors than NCS on all three color vision tests but did not make more protan (red) or deutan (green) errors on two of the three tests. The results support the conclusion that there is a deficit in color discrimination in AD that is specific to blue hues, and oppose the hypothesis that AD does not deleteriously affect the color-opponent visual channel. In the absence of obvious damage to anterior visual structures, the likely substrates for the observed deficit are peristriate and inferotemporal visual cortices, which are subject to significant neuropathology in AD. C1 MIT, DEPT BRAIN & COGNIT SCI, CAMBRIDGE, MA 02139 USA. MIT, CLIN RES CTR, CAMBRIDGE, MA 02139 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. RP CRONINGOLOMB, A (reprint author), BOSTON UNIV, DEPT PSYCHOL, 64 CUMMINGTON ST, BOSTON, MA 02215 USA. FU NCRR NIH HHS [RR00088]; NIA NIH HHS [AG08117] NR 55 TC 55 Z9 55 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0197-4580 EI 1558-1497 J9 NEUROBIOL AGING JI Neurobiol. Aging PD SEP-OCT PY 1993 VL 14 IS 5 BP 471 EP 477 DI 10.1016/0197-4580(93)90105-K PG 7 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA LW589 UT WOS:A1993LW58900008 PM 8247229 ER PT J AU FISHER, CM AF FISHER, CM TI BASILAR ARTERY EMBOLISM AFTER SURGERY UNDER GENERAL-ANESTHESIA - A CASE-REPORT SO NEUROLOGY LA English DT Note RP FISHER, CM (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114, USA. NR 2 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD SEP PY 1993 VL 43 IS 9 BP 1856 EP 1857 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA LY058 UT WOS:A1993LY05800050 PM 8414051 ER PT J AU BALDESSARINI, RJ CENTORRINO, F FLOOD, JG VOLPICELLI, SA HUSTONLYONS, D COHEN, BM AF BALDESSARINI, RJ CENTORRINO, F FLOOD, JG VOLPICELLI, SA HUSTONLYONS, D COHEN, BM TI TISSUE CONCENTRATIONS OF CLOZAPINE AND ITS METABOLITES IN THE RAT SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE CLOZAPINE; CLOZAPINE-N-OXIDE; DRUG ASSAY; FLUOXETINE; LIQUID CHROMATOGRAPHY; NORCLOZAPINE; PHOTODIODE-ARRAY; SPECTROPHOTOMETRY; VALPROIC ACID ID PLASMA-LEVELS; BRAIN; FLUOXETINE AB Clozapine (CLZ) and its metabolites norclozapine (NOR) and clozapine-N-oxide (NOX) were assayed in rat serum and brain tissue after intraperitoneal injection of CLZ. Clozapine levels rose with dose, averaging 28 ng/ml (87 nmol/L) serum per milligram/kilogram dose. Brain- and serum-CLZ levels correlated closely, averaging 24-fold higher in brain. Norclozapine and NOX averaged approximately 58% and 13% of CLZ in serum, respectively, whereas in brain, NOR was detected only at doses greater than or equal to 10 mg/kg (approximately 5.6% of CLZ) and NOX was undetectable. Levels peaked within 30 minutes, and elimination of CLZ from brain and CLZ or NOR from blood was very rapid (half-life = 1.5 to 1.6 hours). A week of daily dosing with CLZ led to no accumulation of drug.in brain; a week of fluoxetine pretreatment increased analyte concentrations (serum, 86%; brain, 61%), but valproate had little effect. C1 HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CLIN CHEM LAB,BOSTON,MA 02114. RP BALDESSARINI, RJ (reprint author), MCLEAN HOSP,MAILMAN RES CTR,115 MILL ST,BELMONT,MA 02178, USA. FU NIMH NIH HHS [NIMH MH-14275, NIMH MH-31154, NIMH MH-34006] NR 25 TC 174 Z9 174 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD SEP PY 1993 VL 9 IS 2 BP 117 EP 124 PG 8 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LU681 UT WOS:A1993LU68100004 PM 8216694 ER PT J AU AMES, D WIRSHING, WC MARDER, SR YUWILER, A BRAMMER, GL MIDHA, KK VANPUTTEN, T AF AMES, D WIRSHING, WC MARDER, SR YUWILER, A BRAMMER, GL MIDHA, KK VANPUTTEN, T TI ADJUNCTIVE FLUOXETINE IN HALOPERIDOL-STABILIZED SCHIZOPHRENICS SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD SEP PY 1993 VL 9 IS 2 SU S BP S116 EP S116 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV408 UT WOS:A1993LV40800252 ER PT J AU COYLE, JT PUTTFARKEN, P BERGER, U MEYERHOFF, J PASSANI, L AF COYLE, JT PUTTFARKEN, P BERGER, U MEYERHOFF, J PASSANI, L TI N-ACETYL GLUTAMATE - DUAL ROLE AS SYNAPTIC GLUTAMATE PRECURSOR AND NMDA ANTAGONIST SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC & DEV NEUROSCI LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD SEP PY 1993 VL 9 IS 2 SU S BP S37 EP S38 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV408 UT WOS:A1993LV40800080 ER PT J AU GROER, M HILL, J WILHITE, A WILKINSON, E AF GROER, M HILL, J WILHITE, A WILKINSON, E TI IMMUNOLOGICAL CONSEQUENCES OF PERIODS OF SEPARATION IN INFANT MICE AND MOTHERS AND IMMUNOLOGICAL RESPONSES OF SEPARATED MICE TO STROKING SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,BOSTON,MA 02114. UNIV TENNESSEE,CTR HLTH SCI,COLL MED,MEMPHIS,TN 38163. 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 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD SEP PY 1993 VL 9 IS 2 SU S BP S169 EP S169 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV408 UT WOS:A1993LV40800375 ER PT J AU WIRSHING, WC WEST, LJ AF WIRSHING, WC WEST, LJ TI IMPACT OF PUBLIC-OPINION AND NEWS MEDIA ON PSYCHOPHARMACOLOGY IN THE 1990S SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD SEP PY 1993 VL 9 IS 2 SU S BP S57 EP S58 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV408 UT WOS:A1993LV40800120 ER PT J AU TOWNSEND, DJ AF TOWNSEND, DJ TI EYELID REANIMATION - REPLY SO OPHTHALMIC PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Letter RP TOWNSEND, DJ (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115, 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 0740-9303 J9 OPHTHALMIC PLAST REC JI Ophthalmic Plast. Reconstr. Surg. PD SEP PY 1993 VL 9 IS 3 BP 229 EP 229 DI 10.1097/00002341-199309000-00064 PG 1 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA LV015 UT WOS:A1993LV01500011 ER PT J AU HEILIGENHAUS, A SHORE, JW RUBIN, PAD FOSTER, CS AF HEILIGENHAUS, A SHORE, JW RUBIN, PAD FOSTER, CS TI LONG-TERM RESULTS OF MUCOUS-MEMBRANE GRAFTING IN OCULAR CICATRICIAL PEMPHIGOID - IMPLICATIONS FOR PATIENT SELECTION AND SURGICAL CONSIDERATIONS SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1992 ANNUAL MEETING OF THE AMERICAN-ACADEMY-OF-OPHTHALMOLOGY CY NOV, 1992 CL DALLAS, TX SP AMER ACAD OPHTHALMOL ID IMMUNOSUPPRESSIVE THERAPY; ANTIBODIES; COMPLEMENT; ENTROPION; CELLS AB Background: Buccal mucous membrane grafting was performed in 26 eyes of 20 patients with advanced ocular cicatricial pemphigoid. The disease causes abnormalities of the eyelid margin and conjunctiva, which results in mechanical damage to the cornea. The authors' short-term results showed that mucous membrane grafting was effective in reversing these abnormalities if the disease was first medically controlled by chemotherapy or was in remission. Methods: At the end of 2 years of follow-up, the authors reviewed all records and photographs of these patients. Results: Serious postoperative corneal complications developed in 16 eyes (61.5%), causing worsened visual acuity in 8. The postoperative complications were associated with severe keratoconjunctivitis sicca in 14 eyes (87.5%), progression of subepithelial conjunctival fibrosis and postoperative exacerbation of ocular cicatricial pemphigoid inflammatory activity in 8 eyes, and advanced ankyloblepharon in 7 eyes. The condition of one eye was unchanged. The beneficial effect of grafting was maintained in nine eyes. Conclusions: The authors' observations indicate that mucous membrane grafting should not be performed when patients have severe keratoconjunctivitis sicca, very advanced ocular cicatricial pemphigoid, or active conjunctival inflammation uncontrolled by immunosuppression. The authors suggest complete control of inflammation before surgery and perioperative treatment with systemic prednisone while maintaining any ongoing immunosuppressive chemotherapy. The selection of alternative surgical approaches is discussed. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. UNIV ESSEN GESAMTHSCH,DEPT OPHTHALMOL,W-4300 ESSEN 1,GERMANY. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,EYE PLAST & ORBIT SERV,BOSTON,MA 02114. NR 28 TC 35 Z9 35 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD SEP PY 1993 VL 100 IS 9 BP 1283 EP 1288 PG 6 WC Ophthalmology SC Ophthalmology GA LX192 UT WOS:A1993LX19200008 PM 8371912 ER PT J AU AKOVA, YA JABBUR, NS NEUMANN, R FOSTER, CS AF AKOVA, YA JABBUR, NS NEUMANN, R FOSTER, CS TI ATYPICAL OCULAR ATOPY SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1992 ANNUAL MEETING OF THE AMERICAN-ACADEMY-OF-OPHTHALMOLOGY CY NOV, 1992 CL DALLAS, TX SP AMER ACAD OPHTHALMOL ID KERATOCONJUNCTIVITIS AB Background: Atopic keratoconjunctivitis (AKC) is defined as a chronic keratoconjunctivitis associated with atopic dermatitis, but severe progressive keratoconjunctivitis as a sole manifestation of atopy also may occur. The authors report three patients with a longstanding history of chronic conjunctivitis with bilateral pannus formation. These patients denied any history of major atopy at the time of presentation. Methods: All patients were evaluated for collagen vascular disease and for evidence of atopy. Conjunctival biopsy was obtained in each case and was analyzed by light microscopy and by immunohistochemical techniques. Results: Systemic evaluation for collagen vascular disease was negative. Serum IgE levels were elevated in one patient. Conjunctival biopsy suggested atopy in all patients with characteristic histopathologic findings. Referral to an allergist showed wheal and flare reactions to multiple ubiquitous environmental allergens. Two patients then disclosed a history of atopic dermatitis and another confessed a history of asthma. Each patient responded well to environmental control of allergens, topical cromolyn sodium 4%, and systemic antihistamine therapy with subsequent resolution of the chronic conjunctivitis. The corneal complications were managed with pannus resection and postoperative mitomycin C drops in two patients. Conclusion: These patients suffered from the progressive blinding consequences of a chronic keratoconjunctivitis, which we believe is an atypical form of AKC. In this report, it is suggested that atopy should be considered in some cases of external ocular inflammation, even in the absence of the characteristic findings of systemic atopy. Conjunctival biopsy is a valuable diagnostic tool in such cases. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,IMMUNOL SERV,243 CHARLES ST,BOSTON,MA 02114. ANKARA HOSP,DEPT OPHTHALMOL,ANKARA,TURKEY. NR 10 TC 6 Z9 7 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 SEP PY 1993 VL 100 IS 9 BP 1367 EP 1371 PG 5 WC Ophthalmology SC Ophthalmology GA LX192 UT WOS:A1993LX19200024 PM 8371925 ER PT J AU DELAMAZA, MS JABBUR, NS FOSTER, CS AF DELAMAZA, MS JABBUR, NS FOSTER, CS TI AN ANALYSIS OF THERAPEUTIC DECISION FOR SCLERITIS SO OPHTHALMOLOGY LA English DT Article ID IMMUNOSUPPRESSIVE THERAPY; NONNECROTIZING SCLERITIS; SCLERAL DISEASE; MANAGEMENT; CYCLOSPORINE AB Purpose: To compare the long-term efficacy of different systemic therapeutic regimens for patients with noninfectious anterior scleritis to establish guidelines for institution of therapy. Methods: Therapeutic failure of systemic nonsteroidal anti-inflammatory drugs (NSAIDs), systemic steroidal anti-inflammatory drugs, and systemic nonsteroidal immunosuppressive drugs was evaluated in 132 patients with noninfectious anterior scleritis (diffuse, nodular, or necrotizing types). Results: In patients with diffuse scleritis, therapeutic failure for initial regimens occurred in 7% of patients treated with NSAIDs, in 16% of patients treated with steroids, and in 27% of patients treated with immunosuppressive drugs. In patients with nodular scleritis, therapeutic failure for initial regimens occurred in 9% of patients treated with NSAIDs, in 28% of patients treated with steroids, and in 25% of patients treated with immunosuppressive drugs. Addition or substitution of steroids or immunosuppressive drugs as second- or third-line therapies helped control the scleritis. In patients with necrotizing scleritis, therapeutic failure for initial regimens occurred in 1 00% of patients treated with NSAIDs, in 91% of patients treated with steroids, and in 26% of patients treated with immunosuppressive drugs. Conclusions: In patients with diffuse and nodular scleritis, NSAIDs should be the initial choice; in case of therapeutic failure, steroids should be added or substituted as second-line therapy, tapering and discontinuing them as soon as possible while maintaining remission with continued NSAIDs; in case of therapeutic failure, immunosuppressive drugs should be added or substituted as third-line therapy. In patients with necrotizing scleritis, immunosuppressive drugs should be the initial choice. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,OCULAR ONCOL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 19 TC 44 Z9 44 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 SEP PY 1993 VL 100 IS 9 BP 1372 EP 1376 PG 5 WC Ophthalmology SC Ophthalmology GA LX192 UT WOS:A1993LX19200025 PM 8371926 ER PT J AU RIZZO, JF AF RIZZO, JF TI OCCULT RETINAL AND CHOROIDAL VASCULAR-DISEASE - THE VALUE OF TIMED AND DIRECTED FLUORESCEIN ANGIOGRAPHY SO OPHTHALMOLOGY LA English DT Article ID BRANCH VEIN OCCLUSION; MIGRAINE; COCAINE; ABUSE AB Background. Acute vascular disease of the choroid or large vessels of the retina is usually accompanied by funduscopic signs. In instances of monocular visual loss, such objective signs are important diagnostic clues that the pathology is in the eye and not in the optic nerve. Methods: Fluorescein angiography was timed in a consistent manner, and photographs were taken at two frames per second. Orientation of the camera was customized for each patient based on the location of the visual field defect. Results: Eight patients with monocular visual loss were referred because the cause of the visual loss was not evident. In each patient, fluorescein angiography showed vascular disease of either the choroid or retina, despite normal-appearing fundi. Conclusions: Fluorescein angiography can detect otherwise occult vascular disease of the retina or choroid. In eyes with monocular scotomas, the angiogram should be performed with the camera oriented with respect to the location of the visual field defect. Accurately timed, rapid sequence photography provides additional information about rate and symmetry of flow. Focal areas of hypoperfusion often are incidental but deserve added consideration when they correspond to the location of a scotoma. C1 HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 31 TC 6 Z9 6 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 SEP PY 1993 VL 100 IS 9 BP 1407 EP 1416 PG 10 WC Ophthalmology SC Ophthalmology GA LX192 UT WOS:A1993LX19200030 PM 8371931 ER PT J AU EISENBERG, E VOS, BP STRASSMAN, AM AF EISENBERG, E VOS, BP STRASSMAN, AM TI THE NMDA ANTAGONIST MEMANTINE BLOCKS PAIN BEHAVIOR IN A RAT MODEL OF FORMALIN-INDUCED FACIAL-PAIN SO PAIN LA English DT Article DE TONIC PAIN; FORMALIN TEST; NMDA RECEPTOR ANTAGONIST; MEMANTINE ID METHYL-D-ASPARTATE; AMINO-ACID ANTAGONISTS; HORN NOCICEPTIVE NEURONS; DORSAL HORN; CENTRAL SENSITIZATION; RECEPTOR ANTAGONISTS; HYPERALGESIA; GLUTAMATE; MK-801; INVOLVEMENT AB Recent studies have provided evidence that excitatory amino acid antagonists can exert analgesic effects in animals. These studies, however, have focused primarily on phasic pain or hyperalgesia rather than tonic pain. The present study evaluates the effects of systemic administration of Memantine (1-amino-3,5-dimethyl-adamantane), a clinically used N-methyl-D-aspartate (NMDA) receptor antagonist, on formalin-induced phasic and tonic pain behavior in the rat. Memantine (2.5, 5.0, 10.0 and 20.0 mg/kg) or normal saline was injected i.p. 1 h prior to a s.c. injection of formalin (5%, 50 mul) into the vibrissal pad of adult rats (n = 5/group). Pain behavior was measured by the number of seconds of formalin-induced face grooming during a 42-min post-injection observation period. Saline-injected animals displayed a biphasic face-grooming response, consisting of an early, phasic phase (0-6 min) and a delayed, prolonged tonic phase (12-42 min). Memantine at doses of 2.5-10 mg/kg produced a significant dose-related inhibition of the second phase (65-93%) and a much smaller inhibition of the first phase (up to 52%). A higher dose (20 mg/kg) further inhibited both phases but also produced other motor effects (increased exploratory and decreased freezing behavior, hind-paw weakness and gait ataxia) which were not observed at the lower doses. These results suggest that the NMDA receptor antagonist Memantine can block formalin-induced tonic and, to a lesser extent, phasic pain, at doses that do not alter other observed motor behaviors. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,PAIN PHYSIOL LAB,BOSTON,MA 02114. FU NINDS NIH HHS [NS-24594] NR 33 TC 89 Z9 91 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD SEP PY 1993 VL 54 IS 3 BP 301 EP 307 DI 10.1016/0304-3959(93)90029-O PG 7 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA LW915 UT WOS:A1993LW91500004 PM 8233544 ER PT J AU CHAPMAN, PH DAVIS, KR AF CHAPMAN, PH DAVIS, KR TI SURGICAL-TREATMENT OF SPINAL LIPOMAS IN CHILDHOOD (REPRINTED FROM CONCEPTS IN PEDIATRIC NEUROSURGERY, VOL 3, PG 178, 1983) SO PEDIATRIC NEUROSURGERY LA English DT Reprint RP CHAPMAN, PH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV NEUROSURG,BOSTON,MA 02114, USA. NR 9 TC 20 Z9 20 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1016-2291 J9 PEDIATR NEUROSURG JI Pediatr. Neurosurg. PD SEP-OCT PY 1993 VL 19 IS 5 BP 267 EP 275 DI 10.1159/000120743 PG 9 WC Clinical Neurology; Pediatrics; Surgery SC Neurosciences & Neurology; Pediatrics; Surgery GA LU190 UT WOS:A1993LU19000008 PM 8398852 ER PT J AU BRISCOE, DM HOFFER, FA TU, N HARMON, WE AF BRISCOE, DM HOFFER, FA TU, N HARMON, WE TI DUPLEX-DOPPLER EXAMINATION OF RENAL-ALLOGRAFTS IN CHILDREN - CORRELATION BETWEEN RENAL BLOOD-FLOW AND CLINICAL FINDINGS SO PEDIATRIC RADIOLOGY LA English DT Article ID RESISTIVE INDEX; SONOGRAPHY; TRANSPLANTS; REJECTION; DYSFUNCTION; ULTRASOUND; DIAGNOSIS AB We reviewed the diastolic blood flow (DBF), pulsatility index (PI), and resistive index (RI) in 211 duplex Doppler ultrasound examinations of 63 pediatric renal transplant recipients. We correlated our findings with the clinical diagnosis, independently determined at the time of ultrasound examination. DBE evaluated in 202 examinations, was found to be decreased, absent, or reversed in acute rejection (kappa = 0.4, p < 0.01) and acute tubular necrosis (ATN) (kappa = 0.3, p < 0.01). The PI and RI were evaluated in 87 and 78 ultrasound examinations respectively. The range of normal PI and RI values in recipients between six and 18 years of age were similar to those reported in adults. However, normal PI and RI values were somewhat higher in recipients less than six years of age who had received adult donor allografts. Overall, the PI was greater than 1.5 in acute rejection (kappa = 0.3, p < 0.05) and ATN (kappa = 0.3, p < 0.01), but not in chronic rejection (kappa < 0, p = NS). The RI was greater than 0.7 in chronic rejection (kappa = 0.3, p < 0.05) and ATN (kappa = 0.3, p < 0.05), but not in acute rejection (kappa = 0.03, p = NS). We conclude that the PI and RI vary in pediatric recipients of renal allografts and are not associated with a specific clinical diagnosis. C1 CHILDRENS HOSP MED CTR,DEPT RADIOL,300 LONGWOOD AVE,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT MED,DIV NEPHROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. NR 18 TC 13 Z9 15 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-0449 J9 PEDIATR RADIOL JI Pediatr. Radiol. PD SEP PY 1993 VL 23 IS 5 BP 365 EP 368 DI 10.1007/BF02011960 PG 4 WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging GA LX436 UT WOS:A1993LX43600010 PM 8233689 ER PT J AU MCGINNIS, HD BLICKMAN, JG AF MCGINNIS, HD BLICKMAN, JG TI BUBBLY INTRAPLEURAL MUCOUS SIMULATING CONGENITAL LOBAR EMPHYSEMA SO PEDIATRIC RADIOLOGY LA English DT Article AB A neonate presented for an esophageal atresia repair and developed respiratory distress in the immediate post-operative period. The initial conventional chest radiographs suggested that there was a right sided pneumothorax, however, this did not resolve, even after the placement of two chest tubes. A CT examination suggested that the findings were due to hyperinflation of the right upper lobe. Thoracoscopy was performed and revealed a complex pneumothorax composed of bubbly mucous from a post-operative pleuro-esophageal fistula. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,14 FRUIT ST,BOSTON,MA 02114. NR 6 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-0449 J9 PEDIATR RADIOL JI Pediatr. Radiol. PD SEP PY 1993 VL 23 IS 5 BP 386 EP 387 DI 10.1007/BF02011967 PG 2 WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging GA LX436 UT WOS:A1993LX43600017 PM 8233696 ER PT J AU HO, PTC ESTROFF, JA KOZAKEWICH, H SHAMBERGER, RC LILLEHEI, CW GRIER, HE DILLER, L AF HO, PTC ESTROFF, JA KOZAKEWICH, H SHAMBERGER, RC LILLEHEI, CW GRIER, HE DILLER, L TI PRENATAL DETECTION OF NEUROBLASTOMA - A 10-YEAR EXPERIENCE FROM THE DANA-FARBER-CANCER-INSTITUTE-AND-CHILDRENS-HOSPITAL SO PEDIATRICS LA English DT Article DE NEUROBLASTOMA; PRENATAL DIAGNOSIS; ULTRASONOGRAPHY; INFANT; MALIGNANCY ID ADRENAL NEURO-BLASTOMA; DIAGNOSIS; INFANTS; MORTALITY; PROGNOSIS; TUMOR; GLAND AB Objectives. To assess the relative frequency of, the clinical and pathological correlates in, and the prognosis of the subset of infants with neuroblastoma who were identified initially by prenatal ultrasonography. Design. Retrospective review of all patients with neuroblastoma evaluated between 1982 and 1992. Setting. Large, urban, tertiary care children's hospital in Boston, Massachusetts. Patients. Eleven infants with neuroblastoma initially detected with prenatal sonograms were identified. Results. Nine patients had adrenal tumors; two had thoracic paraspinal tumors. Typical diagnostic evidence for neuroblastoma including a palpable abdominal mass and elevations in urinary catecholamines were not commonly seen postnatally. These patients had multiple favorable prognostic indicators including low stage of disease (10/11), favorable biological markers including cellular DNA content (5/5) and N-myc oncogene copy number (5/5), and histopathology suggestive for neuroblastoma in situ (7/11). All patients were treated by surgical resection. One patient exhibited progression of disease postoperatively, but demonstrated a complete clinical response to multiagent chemotherapy. Overall survival in our population was excellent with no deaths seen at a mean follow-up of 37 months (range 3 to 120 months). Conclusions. Patients with neuroblastoma identified by prenatal ultrasonography generally, although not exclusively, follow a clinically favorable course in which surgical resection is curative. Chemotherapy is not indicated unless substantial progression of disease occurs. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. NR 38 TC 56 Z9 56 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 SEP PY 1993 VL 92 IS 3 BP 358 EP 364 PG 7 WC Pediatrics SC Pediatrics GA LV815 UT WOS:A1993LV81500003 PM 8361790 ER PT J AU GUT, IG FARMER, R HUANG, RC KOCHEVAR, IE AF GUT, IG FARMER, R HUANG, RC KOCHEVAR, IE TI UPPER EXCITED-STATE PHOTOCHEMISTRY OF DNA SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID SINGLE-STRAND BREAKS; AQUEOUS-SOLUTION; HUMAN-CELLS; PHOTOPRODUCTS; DIMERS; NM; CYCLOBUTANE; IRRADIATION; PHOTOLYSIS; RADIATION AB The quantum yields for cyclobutylpyrimidine dimers, alkali-labile sites, and frank strand breaks in double-stranded DNA have been measured using low-intensity radiation at 199.8, 217.8, and 239.5 nm from a Raman-shifted frequency quadrupled Nd:YAG laser. The quantum yield for cyclobutylpyrimidine dimers was also measured using 254 nm radiation from a low-pressure mercury lamp. The quantum yield for cyclobutylpyrimidine dimers is constant within a factor of two between 254 and 199.8 nm except for 239.5 nm, indicating that upper excited singlet states of bases convert efficiently to the lowest singlet state. The quantum yields for alkali-labile sites and frank strand breaks both increase as the wavelength decreases but follow different patterns. These results indicate that alkali-labile sites form from a higher excited state of the base, whereas frank strand breaks form by excitation of the sugar-phosphate backbone. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WOLLMAN LABS PHOTOMED,BOSTON,MA 02114. FU NIAMS NIH HHS [AR25395] NR 26 TC 19 Z9 19 U1 0 U2 1 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD SEP PY 1993 VL 58 IS 3 BP 313 EP 317 DI 10.1111/j.1751-1097.1993.tb09567.x PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LZ209 UT WOS:A1993LZ20900001 PM 8234462 ER PT J AU GUCCIONE, AA AF GUCCIONE, AA TI DIAGNOSIS AND TREATMENT IN PHYSICAL THERAPY - AN INVESTIGATION OF THEIR RELATIONSHIP - COMMENTARY SO PHYSICAL THERAPY LA English DT Editorial Material RP GUCCIONE, AA (reprint author), MASSACHUSETTS GEN HOSP,PHYS THERAPY SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 SEP PY 1993 VL 73 IS 9 BP 577 EP 578 PG 2 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA LV726 UT WOS:A1993LV72600003 ER PT J AU KIGIN, CM AF KIGIN, CM TI PERCEPTIONS OF ACUTE-CARE PHYSICAL THERAPY PRACTICE - ISSUES FOR PHYSICAL THERAPIST PREPARATION - COMMENTARY SO PHYSICAL THERAPY LA English DT Editorial Material RP KIGIN, CM (reprint author), MASSACHUSETTS GEN HOSP,PHYS THERAPY SERV,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 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 SEP PY 1993 VL 73 IS 9 BP 595 EP 596 PG 2 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA LV726 UT WOS:A1993LV72600008 ER PT J AU ROTHKOPF, DM CHU, B BERN, S MAY, JW AF ROTHKOPF, DM CHU, B BERN, S MAY, JW TI THE EFFECT OF DEXTRAN ON MICROVASCULAR THROMBOSIS IN AN EXPERIMENTAL RABBIT MODEL SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID MOLECULAR WEIGHT DEXTRAN; EFFICACY; HEPARIN; SURGERY AB Although low molecular weight dextran is commonly utilized in clinical microsurgery, few experimental data are available documenting its efficacy. Bilateral 2-mm arterial inversion grafts were constructed in the femoral arteries of New Zealand White rabbits. The experimental group (n = 40 grafts) received a 5-day constant infusion of intravenous dextran 40 at 2.1 ml/hour, and the control group (n = 50 grafts) received no infusion. Whereas 85 percent (34/40) of the dextran grafts were patent at 1 week, only 48 percent (24/50) of the control grafts were patent (p = 0.0003). Scanning electron micrographs revealed a decrease in both platelet and fibrin deposition in the patent dextran arterial inversion grafts versus the patent control specimens. As a marked diminution in microvascular thrombosis was demonstrated at a clinically relevant dose, the continued use of intravenous dextran 40 in clinical microsurgery is supported by this study. C1 UNIV MASSACHUSETTS, MED CTR, DEPT SURG, DIV PLAST & RECONSTRUCT SURG, WORCESTER, MA 01605 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT GEN SURG, DIV PLAST & RECONSTRUCT SURG, BOSTON, MA 02114 USA. NR 27 TC 35 Z9 37 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD SEP PY 1993 VL 92 IS 3 BP 511 EP 515 DI 10.1097/00006534-199309000-00021 PG 5 WC Surgery SC Surgery GA LR608 UT WOS:A1993LR60800021 PM 7688131 ER PT J AU JUPITER, JB AF JUPITER, JB TI APPLICATION OF MAXILLOFACIAL MINIPLATING AND MICROPLATING SYSTEMS TO THE HAND - DISCUSSION SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Discussion RP JUPITER, JB (reprint author), MASSACHUSETTS GEN HOSP,AMBULATORY CARE CTR 529A,ORTHOPED TRAUMA SERV,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 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 SEP PY 1993 VL 92 IS 4 BP 708 EP 709 PG 2 WC Surgery SC Surgery GA LU793 UT WOS:A1993LU79300021 ER PT J AU BURNS, JC FRIEDMANN, T DRIEVER, W BURRASCANO, M YEE, JK AF BURNS, JC FRIEDMANN, T DRIEVER, W BURRASCANO, M YEE, JK TI VESICULAR STOMATITIS-VIRUS G GLYCOPROTEIN PSEUDOTYPED RETROVIRAL VECTORS - CONCENTRATION TO VERY HIGH-TITER AND EFFICIENT GENE-TRANSFER INTO MAMMALIAN AND NONMAMMALIAN CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GENE THERAPY; ZEBRAFISH ID MURINE LEUKEMIA-VIRUS; GERM-LINE TRANSMISSION; BRACHYDANIO-RERIO; EXPRESSION; FISH; DNA; SURFACE AB The restricted host-cell range and low titer of retroviral vectors limit their use for stable gene transfer in eukaryotic cells. To overcome these limitations, we have produced murine leukemia virus-derived vectors in which the retroviral envelope glycoprotein has been completely replaced by the G glycoprotein of vesicular stomatitis virus. Such vectors can be concentrated by ultracentrifugation to titers >10(9) colony-forming units/ml and can infect cells, such as hamster and fish cell lines, that are ordinarily resistant to infection with vectors containing the retroviral envelope protein. The ability to concentrate vesicular stomatitis virus G glycoprotein pseudotyped vectors will facilitate gene therapy model studies and other gene transfer experiments that require direct delivery of vectors in vivo. The availability of these pseudotyped vectors will also facilitate genetic studies in nonmammalian species, including the important zebrafish developmental system, through the efficient introduction and expression of foreign genes. C1 MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. VIAGENE INC,SAN DIEGO,CA 92121. UNIV CALIF SAN DIEGO,SCH MED,CTR MOLEC GENET,LA JOLLA,CA 92093. RP BURNS, JC (reprint author), UNIV CALIF SAN DIEGO,SCH MED,DEPT PEDIAT 0609D,LA JOLLA,CA 92093, USA. RI Burns, Jane/J-6167-2015 FU NCI NIH HHS [CA-58317]; NHLBI NIH HHS [HL-01855]; NICHD NIH HHS [HD-20034] NR 28 TC 997 Z9 1030 U1 3 U2 18 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 SEP 1 PY 1993 VL 90 IS 17 BP 8033 EP 8037 DI 10.1073/pnas.90.17.8033 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LV644 UT WOS:A1993LV64400027 PM 8396259 ER PT J AU TYMIAK, AA NORMAN, JA BOLGAR, M DIDONATO, GC LEE, H PARKER, WL LO, LC BEROVA, N NAKANISHI, K HABER, E HAUPERT, GT AF TYMIAK, AA NORMAN, JA BOLGAR, M DIDONATO, GC LEE, H PARKER, WL LO, LC BEROVA, N NAKANISHI, K HABER, E HAUPERT, GT TI PHYSICOCHEMICAL CHARACTERIZATION OF A OUABAIN ISOMER ISOLATED FROM BOVINE HYPOTHALAMUS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ENDOGENOUS DIGITALIS; ACTIVE SODIUM TRANSPORT; SODIUM PUMP; CIRCULAR DICHROISM SPECTROSCOPY; MASS SPECTROMETRY ID K+-ATPASE INHIBITOR; SODIUM-TRANSPORT INHIBITOR; NA+; IDENTIFICATION; HYPERTENSION; COMPOUND AB Recent reports have shown the presence of a ouabain-like inhibitor of Na+/K+-ATPase in humans. We have purified a bovine hypothalamic Na+/K+-ATPase inhibitory factor (HIF) by using affinity chromatography combined with HPLC. This inhibitor has a molecular weight of 584 as determined by ion-spray mass spectrometry, making it isobaric with ouabain. Glycosidase treatment or acid hydrolysis of HIF released Only L-rhamnose, the hexose isomer found in ouabain, as detected by chiral GC/MS. Additionally, enzymatically generated desrhamnosyl HIF was found to have a molecular weight of 438, as does ouabagenin, the aglycone of ouabain. HIF and its aglycone were indistinguishable from ouabain and ouabagenin, respectively, by reversed-phase HPLC retention times. However, derivatization with naphthoylimidazole followed by HPLC revealed different retention times for naphthoylation products of HIF and ouabain. Subsequent CD spectroscopy on isolated naphthoylation products of HIF and ouabain confirmed that they were different. This study provides chromatographic and spectroscopic evidence that ouabain and HIF are isomeric cardenolides. The structural difference is presumed to account for the significant differences in biological properties observed for HIF and ouabain. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SERV MED,RENAL UNIT,BOSTON,MA 02114. COLUMBIA UNIV,DEPT CHEM,NEW YORK,NY 10027. RI Lo, Lee-Chiang/G-9165-2015 OI Lo, Lee-Chiang/0000-0002-5821-1690 FU PHS HHS [34509] NR 25 TC 199 Z9 200 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD SEP 1 PY 1993 VL 90 IS 17 BP 8189 EP 8193 DI 10.1073/pnas.90.17.8189 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LV644 UT WOS:A1993LV64400059 PM 8396262 ER PT J AU MOEBIUS, U PALLAI, P HARRISON, SC REINHERZ, EL AF MOEBIUS, U PALLAI, P HARRISON, SC REINHERZ, EL TI DELINEATION OF AN EXTENDED SURFACE-CONTACT AREA ON HUMAN CD4 INVOLVED IN CLASS-II MAJOR HISTOCOMPATIBILITY COMPLEX BINDING SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CD4 MUTAGENESIS; T-CELL FUNCTION; AIDS ID TOXIC LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; STRUCTURAL-ANALYSIS; FUNCTIONAL SUBSETS; ATOMIC-STRUCTURE; CELLS RECOGNIZE; GP120 BINDING; RECEPTOR; ANTIGEN; MHC AB We describe a detailed mapping of the class II major histocompatibility complex (MHC) binding site using site-directed mutagenesis in conjunction with high-resolution CD4 structural data. Residues on all lateral surfaces of domain 1 and the neighboring portions of domain 2 participate in contacting class II MHC. Thus, in addition to the C'C'' ridge that forms the human immunodericiency virus type 1 gp120 binding site, apparent MHC contacts extend over the BED face of domain 1 and across the interdomain groove onto the FG loop of domain 2. Several models of the CD4/class II MHC interaction accounting for the extent of the CD4 surface involved are discussed, including the possibility that CD4 may contact more than one class II MHC molecule using different surfaces. C1 HOWARD HUGHES MED INST,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. RP MOEBIUS, U (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT IMMUNOBIOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI27336, AI30361, P30AI28691] NR 35 TC 73 Z9 75 U1 2 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 SEP 1 PY 1993 VL 90 IS 17 BP 8259 EP 8263 DI 10.1073/pnas.90.17.8259 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LV644 UT WOS:A1993LV64400073 PM 8367491 ER PT J AU TYAN, ML AF TYAN, ML TI MURINE FETAL DEVELOPMENT ENHANCED BY DIETARY VITAMIN-A, CORN-OIL, AND INOSITOL SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID PLACENTAL-LACTOGEN RELEASE; HUMAN TROPHOBLASTIC CELLS; CONGENIC MICE; RETINOIC ACID; REPRODUCTIVE-PERFORMANCE; PHOSPHATE PRODUCTION; GROWTH-FACTORS; H-2; RATS; SUPPLEMENTATION AB Previous work on the effects of dietary vitamin A on craniofacial anomalies in mice revealed that 18-day-old fetuses from dams given 200 IU of vitamin A in corn oil daily in their diet weighed approximately 10% more than fetuses from mothers fed the unsupplemented standard mouse diet, Purina 5001. In the experiments reported here, it has been found that water-soluble vitamin A (200 IU/day) and myo-inositol (5 mg/day) added separately to the diets of pregnant mice increased the weight of 11-day gestations by approximately 25% and enhanced development of the eyes by the equivalent of 0.5-1.0 day without significantly affecting development of the liver or hind limbs. Corn oil alone (0.2 ml/day) had a similar effect on weight and eye development of 11-day fetuses and, in addition, growth of the hind limbs was enhanced modestly. The addition to the diet of vitamin A (200 IU/day) dissolved in corn oil (0.2 ml/day) resulted in a 25% increase in the weight of the 11-day fetuses and enhanced development of the eyes and hind limbs by the equivalent of about 1 day of gestation, suggesting that corn oil contains a factor(s) that interacts with vitamin A to accelerate limb development. Corn oil contains very small quantities of beta-carotene or retinol (<1.0 IU vitamin A/ml); however, it is a rich source of the essential growth factors linoleic and linolenic acids and of inositol esters. The data suggest that the growth-promoting actions of dietary corn oil are due in part to the inositol esters. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90073. RP TYAN, ML (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 42 TC 3 Z9 3 U1 1 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD SEP PY 1993 VL 203 IS 4 BP 485 EP 489 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA PC069 UT WOS:A1993PC06900013 PM 8351289 ER PT J AU LANSKY, MR AF LANSKY, MR TI FAMILY GENESIS OF AGGRESSION SO PSYCHIATRIC ANNALS LA English DT Article C1 W LOS ANGELES VA MED CTR, BRENTWOOD DIV, FAMILY TREATMENT PROGRAM, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, MED SCH FAC, LOS ANGELES PSYCHOANALYT INST, LOS ANGELES, CA USA. NR 13 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0048-5713 J9 PSYCHIAT ANN JI Psychiatr. Ann. PD SEP PY 1993 VL 23 IS 9 BP 494 EP 499 PG 6 WC Psychiatry SC Psychiatry GA LX368 UT WOS:A1993LX36800003 ER PT J AU CALLAHAN, AM FAVA, M ROSENBAUM, JF AF CALLAHAN, AM FAVA, M ROSENBAUM, JF TI DRUG-INTERACTIONS IN PSYCHOPHARMACOLOGY SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Review ID MONOAMINE-OXIDASE INHIBITORS; STATE PLASMA-CONCENTRATIONS; TRICYCLIC ANTI-DEPRESSANTS; LITHIUM-CARBONATE; VALPROIC ACID; SERUM LITHIUM; DIAZEPAM INTERACTION; ORAL-CONTRACEPTIVES; REDUCED HALOPERIDOL; COMBINED FLUOXETINE C1 MASSACHUSETTS GEN HOSP,COORDINATED SCI UNIT,WACC 815,15 PARKMAN ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. NR 178 TC 21 Z9 21 U1 2 U2 2 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 SEP PY 1993 VL 16 IS 3 BP 647 EP 671 PG 25 WC Psychiatry SC Psychiatry GA LV810 UT WOS:A1993LV81000012 PM 8415238 ER PT J AU WILLINGHAM, DB KOROSHETZ, WJ AF WILLINGHAM, DB KOROSHETZ, WJ TI EVIDENCE FOR DISSOCIABLE MOTOR-SKILLS IN HUNTINGTONS-DISEASE PATIENTS SO PSYCHOBIOLOGY LA English DT Article ID PARKINSONS-DISEASE; PREMOTOR CORTEX; MEMORY; PERFORMANCE; MOVEMENT; AMNESIA; ALZHEIMERS; IMPLICIT; LESIONS; TASK AB It has been proposed that the striatum is critical for acquiring new motor skills. Previous experiments have shown that patients with striatal dysfunction are impaired in acquiring new motor skills, but the tasks have always used stimuli that move in a repeating, predictable pattern. Four experiments showed that Huntington's disease (HD) patients are impaired in learning such skills, but can learn at a normal rate skills that require the learning of a new perceptual-motor mapping. HD patients were impaired in learning a repeating motor sequence in a keypressing task. When the repeating sequence was removed and the stimulus-response mapping was made spatially incompatible, HD patients showed normal learning. HD patients learned a maze task when responding with a computer mouse but were impaired on a variation that required keypress responses. Control subjects showed no sensitivity to the repetitive sequence of movements in the mouse version, but part of their knowledge was sequence based in the keypress version. The neural basis of motor skill components is discussed. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP WILLINGHAM, DB (reprint author), UNIV VIRGINIA,DEPT PSYCHOL,GILMER HALL,CHARLOTTESVILLE,VA 22903, USA. NR 64 TC 122 Z9 122 U1 0 U2 3 PU PSYCHONOMIC SOC INC PI AUSTIN PA 1710 FORTVIEW RD, AUSTIN, TX 78704 SN 0889-6313 J9 PSYCHOBIOLOGY JI Psychobiology PD SEP PY 1993 VL 21 IS 3 BP 173 EP 182 PG 10 WC Psychology; Psychology, Multidisciplinary SC Psychology GA LX433 UT WOS:A1993LX43300001 ER PT J AU GREENBERG, DB YOUNGER, J KAUFMAN, SD AF GREENBERG, DB YOUNGER, J KAUFMAN, SD TI MANAGEMENT OF LITHIUM IN PATIENTS WITH CANCER SO PSYCHOSOMATICS LA English DT Review ID CARBONATE; CHEMOTHERAPY; THERAPY; CARBAMAZEPINE; NEUTROPENIA; TOXICITY; SYSTEM AB This article reviews the management of lithium in patients who require optimum management of cancer and simultaneous prevention of mania or depression in lithium-sensitive affective illness. Two cases are described. Discussion focuses on whether lithium should be continued during chemotherapy and radiation treatment, the complications that would lead to lithium toxicity in an otherwise stable patient, the likely settings for hypothyroidism, and the role of lithium to stabilize steroid-induced affective changes. The authors conclude that lithium may be withheld 1 or 2 days before cytotoxic chemotherapy and restarted when the patient is able to drink. It may be given as usual through routine radiation treatment, but it should be discontinued during cranial radiation. Calcium, renal, cardiac, and thyroid functions should be monitored. C1 MASSACHUSETTS GEN HOSP,DEPT MED,HEPATOGASTROENTEROL SECT,BOSTON,MA 02114. NR 43 TC 8 Z9 8 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD SEP-OCT PY 1993 VL 34 IS 5 BP 388 EP 394 PG 7 WC Psychiatry; Psychology SC Psychiatry; Psychology GA LU809 UT WOS:A1993LU80900002 PM 8140187 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI CHRONIC FATIGUE SYNDROME - DAWSON,DM, SABIN,TD SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GREENBERG, DB (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD SEP-OCT PY 1993 VL 34 IS 5 BP 456 EP 457 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA LU809 UT WOS:A1993LU80900014 ER PT J AU GOLDBERG, MA LEE, MJ FISCHMAN, AJ MUELLER, PR ALPERT, NM THRALL, JH AF GOLDBERG, MA LEE, MJ FISCHMAN, AJ MUELLER, PR ALPERT, NM THRALL, JH TI FLUORODEOXYGLUCOSE PET OF ABDOMINAL AND PELVIC NEOPLASMS - POTENTIAL ROLE IN ONCOLOGIC IMAGING SO RADIOGRAPHICS LA English DT Article DE ABDOMEN, NEOPLASMS; EMISSION CT (ECT); NEOPLASMS, EMISSION CT (ECT); NEOPLASMS, RADIONUCLIDE STUDIES; PELVIC ORGANS, NEOPLASMS ID POSITRON EMISSION TOMOGRAPHY; F-18 FLUORODEOXYGLUCOSE; RADIATION NECROSIS; MALIGNANT-LYMPHOMA; COLORECTAL TUMORS; GLUCOSE ANALOG; BRAIN-TUMORS; FLUORINE-18-FLUORODEOXYGLUCOSE; DIFFERENTIATION; RADIOTHERAPY AB Fluorine-18-fluoro-2-deoxyglucose (FDG) positron emission tomography (PET) was used to image 38 patients with known or suspected malignant processes involving the abdomen or pelvis (including primary [n = 2] and secondary [n = 19] fiver tumors, recurrent colon carcinoma [n = 1], lymphoma [n = 15], and cavernous hemangioma [n = 1]). PET results were compared with those from concurrent computed tomographic (CI) studies. Conspicuity of metastatic liver lesions on PET images often exceeded that of lesions on CT scans. Two well-differentiated primary liver tumors failed to show increased FDG uptake. Thirteen of the 15 patients with lymphoma had active disease, as determined with CT or clinical findings; 12 of 13 had increased FDG uptake on PET images. The false-negative result occurred a patient with a low-grade lymphoma. The recurrent colorectal lesion was well demonstrated by PET, but further study is needed to determine whether it can be used to distinguish recurrent disease from radiation-induced changes. PET may be useful in determining the response to oncologic therapy, but PET does not reliably allow exclusion of low-grade lymphoma or well-differentiated hepatic lesions. Clinical correlation is always required in evaluating the significance of PET findings, as inflammatory conditions can also result in increased FDG uptake. RP GOLDBERG, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 50 TC 58 Z9 59 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0271-5333 J9 RADIOGRAPHICS JI Radiographics PD SEP PY 1993 VL 13 IS 5 BP 1047 EP 1062 PG 16 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LX216 UT WOS:A1993LX21600008 PM 8210589 ER PT J AU ATHANASOULIS, CA AF ATHANASOULIS, CA TI COMPLICATIONS OF VENA-CAVA FILTERS SO RADIOLOGY LA English DT Editorial Material DE EDITORIALS; INTERVENTIONAL PROCEDURES, COMPLICATIONS; VENAE-CAVAE, FILTERS ID GREENFIELD FILTER; MIGRATION RP ATHANASOULIS, CA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 17 TC 56 Z9 56 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 SEP PY 1993 VL 188 IS 3 BP 614 EP 615 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LT863 UT WOS:A1993LT86300004 PM 8351319 ER PT J AU GAZELLE, GS MUELLER, PR RAAFAT, N HALPERN, EF CARDENOSA, G WARSHAW, AL AF GAZELLE, GS MUELLER, PR RAAFAT, N HALPERN, EF CARDENOSA, G WARSHAW, AL TI CYSTIC NEOPLASMS OF THE PANCREAS - EVALUATION WITH ENDOSCOPIC RETROGRADE PANCREATOGRAPHY SO RADIOLOGY LA English DT Article DE ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERP); PANCREAS, CYSTS; PANCREAS, NEOPLASMS ID DIFFERENTIAL-DIAGNOSIS; LATENT MALIGNANCY; DUCTAL ECTASIA; CYSTADENOMA; TUMORS AB Images from endoscopic retrograde pancreatography performed in 38 patients with cystic pancreatic neoplasms were reviewed to determine whether they might allow differentiation of malignant from benign lesions. Twenty-three patients had histologically proved benign lesions; 15 had frankly malignant lesions. Images were classified into four groups on the basis of the appearance of the pancreatic duct: (a) normal, (b) showing narrowing or draping; (c) showing communication with a cystic space, and (d) showing obstruction. Of the 23 patients with benign lesions, eight had normal studies, 11 had studies showing narrowing or draping, three had studies showing communication, and one had a study showing obstruction. Of the 15 patients with malignant lesions, one had a normal study, three had studies showing narrowing or draping, two had studies showing communication, and nine had studies showing obstruction. Overall, there was a significant difference in the rates of pancreatographic findings for benign and malignant tumors (P = .001). Although no finding proved to be an absolute indicator of benign or malignant disease, obstruction occurred with 60% of malignant tumors and was seen with only one benign lesion (4%). C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GAZELLE, GS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 14 TC 31 Z9 32 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 SEP PY 1993 VL 188 IS 3 BP 633 EP 636 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LT863 UT WOS:A1993LT86300010 PM 8394590 ER PT J AU PALMER, WE BROWN, JH ROSENTHAL, DI AF PALMER, WE BROWN, JH ROSENTHAL, DI TI ROTATOR CUFF - EVALUATION WITH FAT-SUPPRESSED MR ARTHROGRAPHY SO RADIOLOGY LA English DT Article; Proceedings Paper CT 79TH SCIENTIFIC ASSEMBLY AND 1992 ANNUAL MEETING OF THE RADIOLOGICAL SOC OF NORTH AMERICA CY NOV 28-DEC 03, 1992 CL CHICAGO, IL SP RADIOL SOC N AMER DE MAGNETIC RESONANCE (MR), COMPARATIVE STUDIES; SHOULDER, ARTHROGRAPHY; SHOULDER, INJURIES; SHOULDER, MR ID GADOLINIUM-DTPA; SHOULDER; TEARS; DIAGNOSIS AB Thirty-seven shoulders with rotator cuff diagnoses proved at arthrography, arthroscopy, or open surgery were examined prospectively with magnetic resonance (MR) arthrography. T1-weighted MR images were obtained with and without fat suppression after intraarticular injection of gadopentetate dimeglumine. Without fat suppression, overall accuracy was 84%. False-positive fall-thickness tears were diagnosed in three patients who were proved to have partial tears. False-negative normal tendons were diagnosed in two patients who had partial tears. The corresponding sensitivity and specificity were 90% and 75%, respectively. With the aid of fat-suppressed imaging, full-thickness and partial cuff tears were identified with 100% sensitivity and specificity. Fat-suppressed images also showed intratendinous contrast material imbibition in three tom cuffs with frayed, friable tendon margins. Fat suppression in MR arthrography is valuable in the differentiation of partial from full-thickness cuff tears and in the detection of small partial tears of the inferior tendon surface. RP PALMER, WE (reprint author), MASSACHUSETTS GEN HOSP,DEPT BONE & JOINT RADIOL,15 PARKMAN ST,WACC STE 515,BOSTON,MA 02114, USA. NR 21 TC 124 Z9 126 U1 0 U2 3 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD SEP PY 1993 VL 188 IS 3 BP 683 EP 687 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LT863 UT WOS:A1993LT86300019 PM 8351333 ER PT J AU LEE, MJ PAPANICOLAOU, N NOCKS, BN VALDEZ, JA YODER, IC AF LEE, MJ PAPANICOLAOU, N NOCKS, BN VALDEZ, JA YODER, IC TI FLUOROSCOPICALLY GUIDED PERCUTANEOUS SUPRAPUBIC CYSTOSTOMY FOR LONG-TERM BLADDER DRAINAGE - AN ALTERNATIVE TO SURGICAL CYSTOSTOMY SO RADIOLOGY LA English DT Article DE BLADDER, INTERVENTIONAL PROCEDURE; CATHETERS AND CATHETERIZATION; INTERVENTIONAL PROCEDURES ID PLACEMENT; TUBE AB Percutaneous large-bore suprapubic cystostomy catheters were placed under fluoroscopic guidance in 60 patients as an alternative to surgical cystostomy. Foley catheters (16-20 F) were placed in 57 of the patients in a one-stage procedure. Ten-French catheters were initially placed in three patients because of difficulty in dilating percutaneous tracks because of obesity (one patient) or dense scar tissue (two patients). Three weeks later, 18-F Foley catheters were placed in these three patients when mature tracks had developed, making dilation easier. Minor complications occurred in three patients, including superficial track bleeding in two and urosepsis in one. Fifteen patients were lost to follow-up. Suprapubic catheters provided excellent long-term drainage (range, 0.5-36 months; mean, 16 months; median, 18 months) in the remaining 45 patients. The authors conclude that percutaneous suprapubic catheter placement is a safe and effective procedure that provides excellent long-term bladder drainage. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,UROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LEE, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 11 TC 22 Z9 22 U1 0 U2 2 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD SEP PY 1993 VL 188 IS 3 BP 787 EP 789 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LT863 UT WOS:A1993LT86300036 PM 8351348 ER PT J AU WOLFSON, M AF WOLFSON, M TI VALUE OF INTRADIALYTIC PARENTERAL-NUTRITION - COMMENT SO SEMINARS IN DIALYSIS LA English DT Letter RP WOLFSON, M (reprint author), PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97224, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0894-0959 J9 SEMIN DIALYSIS JI Semin. Dial. PD SEP-OCT PY 1993 VL 6 IS 5 BP 324 EP 324 DI 10.1111/j.1525-139X.1993.tb00505.x PG 1 WC Urology & Nephrology SC Urology & Nephrology GA LY139 UT WOS:A1993LY13900012 ER PT J AU MUELLER, PR AF MUELLER, PR TI UPDATE IN INTERVENTIONAL NEURORADIOLOGY .1. FOREWORD SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Editorial Material RP MUELLER, PR (reprint author), MASSACHUSETTS GEN HOSP,DIV HEAD ABDOMINAL IMAGING & INTERVENT 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 SEP PY 1993 VL 10 IS 3 BP U188 EP U188 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LY237 UT WOS:A1993LY23700001 ER PT J AU AUSIELLO, DA AF AUSIELLO, DA TI RENAL TUBULAR TRANSPORT MECHANISMS SO SEMINARS IN NEPHROLOGY LA English DT Article ID NEPHROGENIC DIABETES-INSIPIDUS; ANTIDIURETIC-HORMONE; G-PROTEIN; MOLECULAR-CLONING; NA+ CHANNEL; EXPRESSION CLONING; WATER PERMEABILITY; EPITHELIAL-CELLS; COLLECTING DUCT; COATED PITS C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP AUSIELLO, DA (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,149 13TH ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK 19406, DK38452] NR 48 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 0270-9295 J9 SEMIN NEPHROL JI Semin. Nephrol. PD SEP PY 1993 VL 13 IS 5 BP 472 EP 478 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA LX616 UT WOS:A1993LX61600007 PM 7692578 ER PT J AU DRINKA, PJ SIEBERS, M VOEKS, SK AF DRINKA, PJ SIEBERS, M VOEKS, SK TI POOR POSITIVE PREDICTIVE VALUE OF LOW SENSITIVE THYROTROPIN ASSAY LEVELS FOR HYPERTHYROIDISM IN NURSING-HOME RESIDENTS SO SOUTHERN MEDICAL JOURNAL LA English DT Article ID THYROID-STIMULATING HORMONE; SERUM THYROTROPIN; MULTINODULAR GOITER AB We assessed the positive predictive value of a low thyrotropin (TSH) level on sensitive TSH (STSH) assay as an indicator of hyperthyroidism. In 742 determinations on nursing home residents who were not taking thyroid hormone, we identified 15 with low TSH levels. None of the residents had a completely suppressed (undetectable) TSH level upon initial testing or an elevated total triiodothyronine (T3) or thyroxine (T4) level. Half the patients in whom total T3 was measured had low levels. Of 11 surviving residents, four subsequently had a normal TSH level and six others had a normal free T4 level. Only one patient had a slight elevation of the free T4 level. None of the residents were diagnosed as having hyperthyroidism. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. UNIV WISCONSIN,DEPT INTERNAL MED,MADISON,WI 53706. RP DRINKA, PJ (reprint author), WISCONSIN VET HOME,KING,WI 54946, USA. NR 8 TC 4 Z9 5 U1 0 U2 0 PU SOUTHERN MEDICAL ASSN PI BIRMINGHAM PA 35 LAKESHORE DR PO BOX 190088, BIRMINGHAM, AL 35219 SN 0038-4348 J9 SOUTHERN MED J JI South.Med.J. PD SEP PY 1993 VL 86 IS 9 BP 1004 EP 1007 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA LX611 UT WOS:A1993LX61100006 PM 8367743 ER PT J AU KISTLER, JP SINGER, DE MILLENSON, MM BAUER, KA GRESS, DR BARZEGAR, S HUGHES, RA SHEEHAN, MA MARAVENTANO, SW OERTEL, LB ROSNER, B ROSENBERG, RD AF KISTLER, JP SINGER, DE MILLENSON, MM BAUER, KA GRESS, DR BARZEGAR, S HUGHES, RA SHEEHAN, MA MARAVENTANO, SW OERTEL, LB ROSNER, B ROSENBERG, RD TI EFFECT OF LOW-INTENSITY WARFARIN ANTICOAGULATION ON LEVEL OF ACTIVITY OF THE HEMOSTATIC SYSTEM IN PATIENTS WITH ATRIAL-FIBRILLATION SO STROKE LA English DT Article DE ANTICOAGULANTS; ATRIAL FIBRILLATION; CLINICAL TRIALS; WARFARIN ID RISK FACTOR; STROKE; ACTIVATION; FRAGMENT; F1+2; ASPIRIN; BLOOD AB Background and Purpose: The Boston Area Anticoagulation Trial for Atrial Fibrillation (BAATAF) demonstrated that low-intensity warfarin anticoagulation can, with safety, sharply reduce the rate of stroke in patients with nonvalvular atrial fibrillation. The beneficial effect of warfarin was presumably related to a decrease in clot formation in the cardiac atria and subsequent embolization. Methods: To assess the effect of warfarin therapy on in vivo clotting in patients in the BAATAF, we measured the plasma level of prothrombin activation fragment F1+2. One sample was obtained from 125 patients from the BAATAF; 62 were taking warfarin and 63 were not taking warfarin (control group). Results: The warfarin group had a 71% lower mean F1+2 level than the control group (mean F1+2 of 1.57 nmol/L in the control group compared with a mean of 0.46 nmol/L in the warfarin group; P<.001). F1+2 levels were higher in older subjects but were consistently lower in the warfarin group at all ages. Fifty-two percent of patients in the control group were taking chronic aspirin therapy at the time their F1+2 level was measured. Control patients taking aspirin had F1+2 levels very similar to control patients not taking aspirin (mean of 1.52 nmol/L for control patients on aspirin compared with 1.64 nmol/L for control patients off aspirin; P>.1). Conclusions: We conclude that prothrombin activation was significantly suppressed in vivo by warfarin but not aspirin among patients in the BAATAF. These findings correlate with the marked reduction in ischemic stroke noted among patients in the warfarin treatment group observed in the BAATAF. C1 MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. BETH ISRAEL HOSP,MED SERV,BOSTON,MA 02215. BROCKTON W ROXBURY DEPT VET AFFAIRS MED CTR,BOSTON,MA. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-33233, HL-07516, HL-33014] NR 21 TC 43 Z9 44 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 SEP PY 1993 VL 24 IS 9 BP 1360 EP 1365 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA LW042 UT WOS:A1993LW04200014 PM 8362431 ER PT J AU KAPLAN, SS OGILVY, CS GONZALEZ, R GRESS, D PILESPELLMAN, J AF KAPLAN, SS OGILVY, CS GONZALEZ, R GRESS, D PILESPELLMAN, J TI EXTRACRANIAL VERTEBRAL ARTERY PSEUDOANEURYSM PRESENTING AS SUBARACHNOID HEMORRHAGE SO STROKE LA English DT Note DE EMBOLIZATION, THERAPEUTIC; SUBARACHNOID HEMORRHAGE; VERTEBRAL ARTERY ID ANEURYSM; TRAUMA; INJURY AB Background and Purpose: True aneurysms of the extracranial vertebral artery are rare. The usual pathogenesis of aneurysms in this location is either penetrating or blunt trauma with resultant pseudoaneurysm formation. We report a postpartum patient with a presumed traumatic pseudoaneurysm of the extracranial vertebral artery presenting with subarachnoid hemorrhage. Case Description: A 41-year-old woman had three episodes of neck stiffness 1 month after an uncomplicated vaginal delivery. The last episode, 3 days before admission, was accompanied by intense neck and head pain and paresthesias that extended into the left arm, thumb, and forefinger. Results: Lumbar puncture showed subarachnoid hemorrhage. Angiography revealed a left vertebral artery dissection from C6-7 to C3 with pseudoaneurysm at C5-6. Computed tomography demonstrated impingement of the C6 root at the foramen by this lesion. The lesion was successfully treated by balloon occlusion of the vertebral artery. Conclusions: We present a patient with an extracranial vertebral pseudoaneurysm with subarachnoid hemorrhage and cervical root impingement. To our knowledge, this is the first case of such a lesion presenting as subarachnoid hemorrhage. The lesion was successfully treated using endovascular techniques. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,FRUIT ST,BOSTON,MA 02114. NR 35 TC 14 Z9 14 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 SEP PY 1993 VL 24 IS 9 BP 1397 EP 1399 PG 3 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA LW042 UT WOS:A1993LW04200021 PM 8362438 ER PT J AU EZZELL, RM CARTER, EA YARMUSH, ML TOMPKINS, RG AF EZZELL, RM CARTER, EA YARMUSH, ML TOMPKINS, RG TI THERMAL-INJURY INDUCED CHANGES IN THE RAT INTESTINE BRUSH-BORDER CYTOSKELETON SO SURGERY LA English DT Article ID MACROMOLECULAR PERMEABILITY; BURN PATIENTS; ACTIN; TRANSLOCATION; VILLIN; MYOSIN; PHOSPHORYLATION; LOCALIZATION; EPITHELIUM; FIMBRIN AB Background. The brush border cytoskeleton maintains the selective absorptive surface of the intestine epithelium. Increased intestinal permeability caused by cutaneous thermal injury may be the result of changes in the organization of the brush border cytoskeleton. Methods. In this study we used electron and laser confocal microscopy to examine the temporal and spatial organization of the rat brush border cytoskeleton after thermal injury. Results. Vesiculation of microvilli and disruption of core actin filament bundles were observed in rats with burns covering 20% total body surface area (TBSA). In rats with 40% TBSA burns changes in the brush border cytoskeleton were more pronounced, resulting in increased vesiculation of microvilli and disruption of terminal web actin filaments. Confocal microscopy of corresponding areas of the gut epithelium after staining with rhodamine-phalloidin showed rearrangement of brush border actin filaments. Although tight junctions were intact, the apical region of the gut epithelium in rats with 40% TBSA burns was constricted, possibly because of contraction of brush border actin filaments. Changes in brush border structure and cytoskeletal organization were most pronounced in the ileum of rats 18 hours after injury. Conclusions. These findings suggest that disruption of the brush border cytoskeleton may, in part, be responsible for the loss of intestinal barrier function after thermal injury in animal models. C1 RUTGERS UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. SHRINERS BURNS INST,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG RES LABS,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,SURG RES LABS,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,PEDIAT GASTROINTESTINAL & NUTR LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,PEDIAT GASTROINTESTINAL & NUTR LAB,BOSTON,MA 02114. FU NIGMS NIH HHS [GM21700] NR 31 TC 13 Z9 14 U1 1 U2 2 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 SEP PY 1993 VL 114 IS 3 BP 591 EP 597 PG 7 WC Surgery SC Surgery GA LW043 UT WOS:A1993LW04300019 PM 8367816 ER PT J AU WARSHAW, AL AF WARSHAW, AL TI REFLECTIONS ON LAPAROSCOPIC SURGERY SO SURGERY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. NR 0 TC 9 Z9 9 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 SEP PY 1993 VL 114 IS 3 BP 629 EP 630 PG 2 WC Surgery SC Surgery GA LW043 UT WOS:A1993LW04300026 PM 8367823 ER PT J AU ADAMIS, AP FILATOV, V TRIPATHI, BJ TRIPATHI, RC AF ADAMIS, AP FILATOV, V TRIPATHI, BJ TRIPATHI, RC TI FUCHS ENDOTHELIAL DYSTROPHY OF THE CORNEA SO SURVEY OF OPHTHALMOLOGY LA English DT Review DE CORNEAL EDEMA; CORNEAL ENDOTHELIUM; CORNEAL TRANSPLANTATION; DESCEMET MEMBRANE; FUCHS DYSTROPHY; GROWTH FACTORS; GUTTAE ID POSTERIOR COLLAGENOUS LAYER; FIBROBLAST GROWTH-FACTOR; AQUEOUS-HUMOR; DESCEMETS-MEMBRANE; PENETRATING KERATOPLASTY; FREEZE-FRACTURE; DISORDERS; CELLS; KERATOCONUS; GLAUCOMA AB Fuchs' endothelial dystrophy of the cornea is a significant cause of corneal blindness in the United States. The disease is characterized by a slow, continuous loss of morphologically and physiologically altered endothelial cells, eventually leading to corneal edema. The endothelial cells synthesize a thickened Descemet's membrane with focal excrescences of altered basement membrane material (guttae). This review details the epidemiological, clinical, and laboratory data that have accumulated on Fuchs' dystrophy. Several hypotheses regarding the pathogenesis of Fuchs' dystrophy are discussed, including the possible influences of aberrent embryogenesis, hormones, and injury on the development of the disease. The current state of medical and surgical management is summarized, along with the future prospects for treatment. C1 YALE UNIV,SCH MED,DEPT OPHTHALMOL & VISUAL SCI,NEW HAVEN,CT 06510. UNIV CHICAGO,PRITZKER SCH MED,DEPT OPHTHALMOL & VISUAL SCI,CHICAGO,IL 60637. RP ADAMIS, AP (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 132 TC 118 Z9 121 U1 0 U2 7 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0039-6257 J9 SURV OPHTHALMOL JI Surv. Ophthalmol. PD SEP-OCT PY 1993 VL 38 IS 2 BP 149 EP 168 DI 10.1016/0039-6257(93)90099-S PG 20 WC Ophthalmology SC Ophthalmology GA MA693 UT WOS:A1993MA69300001 PM 8235998 ER PT J AU SAMUELS, MH HENRY, P LUTHER, M RIDGWAY, EC AF SAMUELS, MH HENRY, P LUTHER, M RIDGWAY, EC TI PULSATILE TSH SECRETION DURING 48-HOUR CONTINUOUS TRH INFUSIONS SO THYROID LA English DT Article ID THYROTROPIN-RELEASING-HORMONE; HYPOTHYROID RATS; GROWTH-HORMONE; PROLACTIN SECRETION; SERUM THYROTROPIN; PITUITARY-TUMORS; LONG-TERM; RESPONSES; MEN; SOMATOSTATIN AB Thyroid-stimulating hormone (TSH), like other anterior pituitary hormones, is normally secreted in a series of pulses over 24 h. However, the factors that control TSH pulse generation are unknown. We investigated the potential role of thyrotropin-releasing hormone (TRH) in TSH pulse generation by measuring TSH pulses during constant TRH infusions. Two groups of subjects were studied: five healthy subjects and five subjects with treated primary hypothyroidism and normal TSH levels. Each subject underwent four separate studies: (1) TSH levels were measured every 15 min over 24 h (baseline study). (2) TSH levels were measured every 15 min over 48 h during TRH infusions at 0.1 mug/min (low dose TRH study). (3) TSH levels were measured every 15 min over 48 h during TRH infusions at 0.5 mug/min (medium dose TRH study). (4) TSH levels were measured every 15 min over 48 h during TRH infusions at 1.0 mug/min (high dose TRH study). TSH pulses were located by cluster analysis. We found that constant TRH infusions at any of the doses utilized did not alter TSH pulse frequency in normal or treated hypothyroid subjects, although pulse amplitude increased. Normal subjects had lower TSH pulse amplitude than treated hypothyroid subjects at all TRH doses, perhaps due to slightly higher serum T3 levels. This suggests that, at least acutely, pulsatile input of TRH to the pituitary gland does not determine pulsatile TSH release. However, TRH may modulate TSH pulse amplitude. C1 UNIV COLORADO,HLTH SCI CTR,DIV ENDOCRINOL,DENVER,CO 80262. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP SAMUELS, MH (reprint author), OREGON HLTH SCI UNIV,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. FU NCRR NIH HHS [M01-RR-00051, M01-RR-01-346] NR 29 TC 16 Z9 17 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD FAL PY 1993 VL 3 IS 3 BP 201 EP 206 DI 10.1089/thy.1993.3.201 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MA711 UT WOS:A1993MA71100005 PM 8257859 ER PT J AU SHIVDASANI, RA ANDERSON, KC AF SHIVDASANI, RA ANDERSON, KC TI TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE - SCRATCHING THE SURFACE SO TRANSFUSION LA English DT Editorial Material ID RELATIVES; RISK RP SHIVDASANI, RA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 7 TC 8 Z9 8 U1 0 U2 1 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD SEP PY 1993 VL 33 IS 9 BP 696 EP 697 DI 10.1046/j.1537-2995.1993.33994025014.x PG 2 WC Hematology SC Hematology GA LZ237 UT WOS:A1993LZ23700001 PM 8212111 ER PT J AU SUGRUE, MW LEWIS, EA ANDERSEN, J ANDERSON, KC AF SUGRUE, MW LEWIS, EA ANDERSEN, J ANDERSON, KC TI REDUCTION OF ISOHEMAGGLUTININ (IH) IN MAJOR ABO-INCOMPATIBLE BONE-MARROW (BM) TRANSPLANTS BY IN-VIVO NEUTRALIZATION USING FRESH-FROZEN PLASMA SO TRANSFUSION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD SEP PY 1993 VL 33 IS 9 SU S BP S62 EP S62 PG 1 WC Hematology SC Hematology GA LZ447 UT WOS:A1993LZ44700237 ER PT J AU SMITH, CV SUZUKI, T GUZZETTA, PC NAKAJIMA, K SUNDT, TM MIXON, A SPITZER, TR ECKHAUS, MA SACHS, DH AF SMITH, CV SUZUKI, T GUZZETTA, PC NAKAJIMA, K SUNDT, TM MIXON, A SPITZER, TR ECKHAUS, MA SACHS, DH TI BONE-MARROW TRANSPLANTATION IN MINIATURE SWINE .4. DEVELOPMENT OF MYELOABLATIVE REGIMENS THAT ALLOW ENGRAFTMENT ACROSS MAJOR HISTOCOMPATIBILITY BARRIERS SO TRANSPLANTATION LA English DT Article ID VERSUS-HOST DISEASE; T-CELL DEPLETION; RENAL-ALLOGRAFT SURVIVAL; TOTAL-BODY IRRADIATION; MHC RECOMBINANT SWINE; CLASS-I; IMMUNOLOGICAL CHARACTERIZATION; COMPLEX; TOLERANCE; ANTIGENS AB Studies of the myeloablative regimens capable of permitting successful BMT across MHC barriers in miniature swine have been performed. To minimize graft-versus-host disease (GVHD), engraftment was studied in the Fl-->P combination (i.e., MHC homozygous [''parental''] swine receiving bone marrow from one-haplotype matched MHC heterozygous [''F1''] donors). Animals given total body irradiation (TBI) up to 1100 cGy, 10 cGy/min, in a single dose failed to engraft. Increasing the dose rate led to unacceptable extramedullary toxicity without improving engraftment. Eleven different fractionated TBI regimens were tested in this F1-->parent model. At all of the dose rates tested, a total dose of less than 1000 cGy was insufficient for engraftment, and a total dose of 1400 cGy led to unacceptable toxicity. Between these extremes, a window was defined in which engraftment could be obtained without unacceptable extramedullary toxicity utilizing 2 equally divided fractions of TBI delivered 24 hr apart. The addition of 50 mg/kg cyclophosphamide i.v. to fractionated TBI (1150 cGy total dose [500 + 650]) also permitted engraftment, with decreased incidence of interstitial pneumonitis as compared to fractionated TBI (1300 cGy total dose [650x2]). Both of these regimens were also confirmed to permit engraftment between heterozygous donors and recipients sharing a single common haplotype (''F1-->F1''). The regimen of 1300 cGy (650x2) also permitted engraftment in completely MHC mismatched BMT, but with subsequent death from GVHD. These studies of the myeloablative regimens permitting engraftment across defined MHC barriers in miniature swine provide a basis for further studies of allogeneic BMT and GVHD in this large animal preclinical model. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH EAST,BLDG 149,13TH ST,BOSTON,MA 02129. FU NCI NIH HHS [NCI R01 CA55553-01]; NHLBI NIH HHS [NHLBI 5R01 HL46532-02]; NIAID NIH HHS [NRSA F32 AI08577-01] NR 42 TC 20 Z9 20 U1 0 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD SEP PY 1993 VL 56 IS 3 BP 541 EP 549 DI 10.1097/00007890-199309000-00010 PG 9 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA LZ870 UT WOS:A1993LZ87000010 PM 8212147 ER PT J AU ZIETMAN, AL COEN, JJ SHIPLEY, WU ALTHAUSEN, AF AF ZIETMAN, AL COEN, JJ SHIPLEY, WU ALTHAUSEN, AF TI ADJUVANT IRRADIATION AFTER RADICAL PROSTATECTOMY FOR ADENOCARCINOMA OF PROSTATE - ANALYSIS OF FREEDOM FROM PSA FAILURE SO UROLOGY LA English DT Article ID POSTOPERATIVE RADIATION-THERAPY; SEMINAL-VESICLE INVOLVEMENT; METASTATIC DISSEMINATION; LOCAL-CONTROL; RADIOTHERAPY; CARCINOMA; ANTIGEN; TUMOR; PENETRATION; MARGINS AB A total of 84 consecutive men with extracapsular disease after radical prostatectomy who received postoperative irradiation and no adjuvant endocrine therapy were analyzed. Failure was defined as the development of clinical disease recurrence either locally or at a distant site, the development of detectable prostate-specific antigen (PSA) when postoperatively it had been undetectable, or any rise in PSA when postoperatively it still had been detectable. Sixteen of the 84 men had nodal disease. Overall, five-year actuarial freedom from relapse was 60 percent. For node-negative men, it was 64 percent and for node-positive men 43 percent. For the 68 men with pathologic Stage T3N0 disease, five-year freedom from relapse was 73 percent when seminal vesicles were negative and 43 percent when involved. Tumor grade also predicted the likelihood of recurrence. In a multivariate analysis the time interval from surgery to radiation and the level of postoperative PSA (detectable versus undetectable) did not influence the likelihood of relapse nor the median time to relapse. Fourteen separate patients treated with radiation alone for palpable tumor recurrence were also analyzed. Fewer than 40 percent were disease-free only two years after irradiation. We conclude that when treatment failure is defined in biochemical as well as clinical terms postoperative irradiation reduces the rate of relapse at five years relative to recently reported series in which adjuvant irradiation was not given. The additional morbidity is low. Whether or not this will translate into an overall cause-specific survival gain is currently unclear. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT UROL,BOSTON,MA 02114. RP ZIETMAN, AL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 33 TC 62 Z9 62 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD SEP PY 1993 VL 42 IS 3 BP 292 EP 299 DI 10.1016/0090-4295(93)90618-K PG 8 WC Urology & Nephrology SC Urology & Nephrology GA LX672 UT WOS:A1993LX67200010 PM 7691014 ER PT J AU KOPANS, DB AF KOPANS, DB TI SCREENING MAMMOGRAPHY SO LANCET LA English DT Letter ID CARCINOMA; FOLLOW RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 6 TC 0 Z9 0 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 AUG 28 PY 1993 VL 342 IS 8870 BP 550 EP 550 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LU582 UT WOS:A1993LU58200036 PM 8102680 ER PT J AU KOMORI, T OKADA, A STEWART, V ALT, FW AF KOMORI, T OKADA, A STEWART, V ALT, FW TI LACK OF N-REGIONS IN ANTIGEN RECEPTOR VARIABLE REGION GENES OF TDT-DEFICIENT LYMPHOCYTES SO SCIENCE LA English DT Article ID T-CELL RECEPTOR; GAMMA-DELTA; JUNCTIONAL DIVERSITY; B-CELL; V(D)J RECOMBINATION; CHAIN DIVERSITY; STEM-CELLS; EXPRESSION; INSERTION; SEGMENTS AB During the assembly of immunoglobulin and T cell receptor variable region genes from variable (V), diversity (D), and joining (J) segments, the germline-encoded repertoire is further diversified by processes that include the template-independent addition of nucleotides (N regions) at gene segment junctions. Terminal deoxynucleotidyl transferase (TdT)-deficient lymphocytes had no N regions in their variable region genes, which shows that TdT is responsible for N region addition. In addition, certain variable region genes appeared at increased frequency in TdT-deficient thymocytes, which indicates that N region addition also influences repertoire development by alleviating sequence-specific constraints imposed on the joining of particular V, D, and J segments. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RP KOMORI, T (reprint author), CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI20047] NR 50 TC 330 Z9 330 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD AUG 27 PY 1993 VL 261 IS 5125 BP 1171 EP 1175 DI 10.1126/science.8356451 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LU586 UT WOS:A1993LU58600033 PM 8356451 ER PT J AU MURPHY, JG GERSH, BJ MAIR, DD FUSTER, V MCGOON, MD ILSTRUP, DM MCGOON, DC KIRKLIN, JW DANIELSON, GK AF MURPHY, JG GERSH, BJ MAIR, DD FUSTER, V MCGOON, MD ILSTRUP, DM MCGOON, DC KIRKLIN, JW DANIELSON, GK TI LONG-TERM OUTCOME IN PATIENTS UNDERGOING SURGICAL REPAIR OF TETRALOGY OF FALLOT SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID SUDDEN-DEATH; FOLLOW-UP; VENTRICULAR ARRHYTHMIAS; SURVIVAL; AGE AB Background. Although corrective surgery for tetralogy of Fallot has been available for more than 30 years, the occurrence of late sudden death in patients in whom surgery was apparently successful remains worrisome. Methods. We studied long-term survival among 163 patients who survived 30 days after complete repair of tetralogy of Fallot, examining follow-up hospital records and death certificates when relevant. Results. The overall 32-year actuarial survival rate among all patients who survived surgery was 86 percent, as compared with an expected rate of 96 percent in a control population matched for age and sex (P<0.01). Thirty-year actuarial survival rates were calculated for the patient subgroups. The survival rates among patients less than 5 years old, 5 to 7 years old, and 8 to 11 years old were 90, 93, and 91 percent, respectively - slightly less than the expected rates (P<0.001, P = 0.06, and P = 0.02). Among patients 12 years old or older at the time of surgery, the survival rate was 76 percent, as compared with an expected rate of 93 percent (P<0.001). The performance of a palliative Blalock-Taussig shunt procedure before repair, unlike the performance of a Waterston or Potts shunt procedure, was not associated with reduced long-term survival, nor was the need for a trans-annular patch at the time of surgery. Independent predictors of long-term survival were older age at operation (P = 0.02) and a higher ratio of right ventricular to left ventricular systolic pressure after surgery (P = 0.008). Late sudden death from cardiac causes occurred in 10 patients during the 32-year period. Conclusions. Among patients with surgically repaired tetralogy of Fallot, the rate of long-term survival after the postoperative period is excellent but remains lower than that in the general population. The risk of late sudden death is small. C1 MAYO CLIN & MAYO FDN,PEDIAT CARDIOL SECT,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,DEPT BIOSTAT,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,DIV THORAC & CARDIOVASC SURG,ROCHESTER,MN 55905. MASSACHUSETTS GEN HOSP,DIV CARDIOL,BOSTON,MA 02114. UNIV ALABAMA,MED CTR,DEPT SURG,BIRMINGHAM,AL 35233. RP MURPHY, JG (reprint author), MAYO CLIN & MAYO FDN,DIV CARDIOVASC DIS & INTERNAL MED,200 1ST ST SW,ROCHESTER,MN 55905, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 26 TC 487 Z9 508 U1 3 U2 14 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 AUG 26 PY 1993 VL 329 IS 9 BP 593 EP 599 DI 10.1056/NEJM199308263290901 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA LU217 UT WOS:A1993LU21700001 PM 7688102 ER PT J AU ANDERSON, KC SHIVDASANI, RA AF ANDERSON, KC SHIVDASANI, RA TI GRAFT-VERSUS-HOST DISEASE - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID TRANSFUSION RP ANDERSON, KC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 4 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 AUG 26 PY 1993 VL 329 IS 9 BP 665 EP 665 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LU217 UT WOS:A1993LU21700029 ER PT J AU MARGOLESE, L WANECK, GL SUZUKI, CK DEGEN, E FLAVELL, RA WILLIAMS, DB AF MARGOLESE, L WANECK, GL SUZUKI, CK DEGEN, E FLAVELL, RA WILLIAMS, DB TI IDENTIFICATION OF THE REGION ON THE CLASS-I HISTOCOMPATIBILITY MOLECULE THAT INTERACTS WITH THE MOLECULAR CHAPERONE, P88 (CALNEXIN, IP90) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHAIN BINDING-PROTEIN; ENDOPLASMIC-RETICULUM MEMBRANE; VIRUS-G-PROTEIN; HEAVY-CHAIN; T-CELL; INTRACELLULAR-TRANSPORT; SURFACE EXPRESSION; PEPTIDE-BINDING; QA-2 ANTIGEN; BETA-2-MICROGLOBULIN AB During early stages in their biogenesis, murine class I histocompatibility molecules interact transiently with a molecular chaperone of the endoplasmic reticulum designated p88. Using a series of mutant class I heavy chains we mapped the region of the heavy chain that interacts with p88. Domain deletion mutants of the H-2D(b) and H-2K(b) molecules revealed that most of the extracellular portion of the heavy chain and the bulk of the cytoplasmic domain were not required for the association. However, replacement of the transmembrane segment and cytoplasmic domain with a glycosyl phosphatidylinositol anchor from Q7b resulted in a heavy chain that was incapable of interaction with p88. These results suggested that the primary site of interaction with p88 is within a region containing the transmembrane segment and several flanking amino acids of the class I heavy chain. This finding was supported by replacing the glycosyl phosphatidylinositol anchor of the noninteracting Q7b protein with segments of the D(b) heavy chain containing the putative interaction site and showing that the hybrids were capable of associating with p88. The apparent lack of interaction between segments of p88 and the class I heavy chain that are present within the lumen of the endoplasmic reticulum was also observed when the association between p88 and the a chain of the T cell receptor was examined. The full-length transmembrane a chain formed a complex with p88, whereas a soluble variant consisting of most of the luminal portion of the alpha chain exhibited only minimal interaction. Thus, p88 is capable of associating with nascent integral membrane proteins through transmembrane interactions that are unavailable to the major soluble chaperone of the endoplasmic reticulum, BiP (GRP78). C1 UNIV TORONTO,DEPT BIOCHEM,MED SCI BLDG,TORONTO M5S 1A8,ONTARIO,CANADA. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02129. NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. YALE UNIV,SCH MED,IMMUNOBIOL SECT,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,HOWARD HUGHES MED INST,NEW HAVEN,CT 06510. FU NIGMS NIH HHS [GM46467] NR 56 TC 78 Z9 78 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 AUG 25 PY 1993 VL 268 IS 24 BP 17959 EP 17966 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LT743 UT WOS:A1993LT74300050 PM 8349678 ER PT J AU TANASIJEVIC, MJ MYERS, MG THOMA, RS CRIMMINS, DL WHITE, MF SACKS, DB AF TANASIJEVIC, MJ MYERS, MG THOMA, RS CRIMMINS, DL WHITE, MF SACKS, DB TI PHOSPHORYLATION OF THE INSULIN-RECEPTOR SUBSTRATE IRS-1 BY CASEIN KINASE-II SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID STIMULATES TYROSINE PHOSPHORYLATION; EPIDERMAL GROWTH-FACTOR; SERINE PHOSPHORYLATION; SKELETAL-MUSCLE; ALPHA-SUBUNIT; BETA-SUBUNIT; RAT-LIVER; PROTEIN; CALMODULIN; ACTIVATION AB IRS-1, a principal substrate of the insulin receptor, is phosphorylated on serine, threonine, and tyrosine residues in a variety of tissues during insulin stimulation. Casein kinase II, an insulin-sensitive serine/threonine kinase, catalyzed the in vitro incorporation of 1 to 2 mol of phosphate/mol of recombinant rat IRS-1. Two-dimensional phosphopeptide mapping of IRS-1 phosphorylated by casein kinase II in vitro and IRS-1 immunoprecipitated from intact Chinese hamster ovary cells demonstrated multiple common phosphopeptides, suggesting that overexpressed IRS-1 is a substrate for casein kinase II in these cells. Moreover, the common phosphopeptides that appeared to be insulin-sensitive in intact cells comprised 22% of casein kinase II-catalyzed P-32 incorporation into IRS-1 in vitro. These data suggest that casein kinase II mediates a portion of the insulin-stimulated serine/threonine phosphorylation of overexpressed IRS-1 in vivo. By using phosphoamino acid analysis, strong cation exchange analysis, manual Edman degradation, and automated amino acid sequencing, Thr-502 was identified as the major casein kinase II-catalyzed phosphorylation site in rat IRS-1. Furthermore, Ser-99, an additional site labeled at low yield, appeared to be contained in an insulin-sensitive phosphopeptide. Thus, casein kinase II-catalyzed phosphorylation of IRS-1 may be a component of the intracellular insulin signalling cascade. C1 BRIGHAM & WOMENS HOSP, DEPT PATHOL, MRB 615, 75 FRANCIS ST, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, JOSLIN DIABET CTR, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. WASHINGTON UNIV, SCH MED, HOWARD HUGHES MED INST, ST LOUIS, MO 63110 USA. OI Sacks, David/0000-0003-3100-0735 FU NIDDK NIH HHS [DK 43682, DK 43808] NR 53 TC 69 Z9 71 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD AUG 25 PY 1993 VL 268 IS 24 BP 18157 EP 18166 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LT743 UT WOS:A1993LT74300076 PM 8349691 ER PT J AU PAUL, RV WACKYM, PS BUDISAVLJEVIC, M EVERETT, E NORRIS, JS AF PAUL, RV WACKYM, PS BUDISAVLJEVIC, M EVERETT, E NORRIS, JS TI REGULATION OF ATRIAL-NATRIURETIC-PEPTIDE CLEARANCE RECEPTORS IN MESANGIAL CELLS BY GROWTH-FACTORS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SMOOTH-MUSCLE CELLS; ANGIOTENSIN-II; ENDOTHELIAL-CELLS; PROLIFERATIVE NEPHRITIS; GUANYLATE-CYCLASE; C-RECEPTORS; CYCLIC-GMP; RAT; PDGF; EXPRESSION AB Rat mesangial cells can express both 130-kDa guanylyl cyclase-coupled and 66-kDa non-coupled atrial natriuretic peptide (ANP) receptors (ANPR-A and ANPR-C, respectively). Exposure of mesangial cells, grown in 20% fetal calf serum, to 0.1% serum for 24 h increased total ANP receptor density more than 2-fold (B(max) = 87 versus 37 fmol/mg of cell protein) without changing binding affinity (K(d) = 94 versus 88 pM). Radioligand binding and cross-linking studies demonstrated that up-regulation of ANP binding after serum deprivation was entirely due to an increase in ANPR-C, with little or no change in ANPR-A. Inhibition of protein synthesis with cycloheximide blocked up-regulation after serum deprivation. Steady-state ANPR-C mRNA level was increased 15-fold by serum deprivation, as judged by Northern blotting. There was no change in ANPR-A mRNA. Platelet-derived growth factor and phorbol myristate acetate, when added to low serum medium, blocked or reversed the effect of serum deprivation on ANPR-C. We conclude that synthesis and expression of ANPR-C but not ANPR-A is suppressed by serum, platelet-derived growth factor, and phorbol myristate acetate. Suppression of ANPR-C in vivo could contribute to mesangial cell proliferative responses to growth factors. C1 MED UNIV S CAROLINA,DEPT BIOCHEM & MOLEC BIOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. VET AFFAIRS MED CTR,RALPH H JOHNSON DEPT,DIV NEPHROL,CHARLESTON,SC. FU NCI NIH HHS [R01-CA-49949] NR 47 TC 25 Z9 25 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 AUG 25 PY 1993 VL 268 IS 24 BP 18205 EP 18212 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LT743 UT WOS:A1993LT74300083 PM 8349696 ER PT J AU MUSZBEK, L LAPOSATA, M AF MUSZBEK, L LAPOSATA, M TI COVALENT MODIFICATION OF PROTEINS BY ARACHIDONATE AND EICOSAPENTAENOATE IN PLATELETS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FATTY-ACID ACYLATION; N-MYRISTOYLTRANSFERASE; MYRISTOYL-COA; PROSTAGLANDIN BIOSYNTHESIS; EUKARYOTIC PROTEINS; CELLULAR PROTEINS; BINDING; INTERMEDIATE(S); IDENTIFICATION; SPECIFICITY AB The posttranslational modification of proteins by fatty acids has been shown to involve long chain-saturated fatty acids, predominantly palmitate. In the present study, we demonstrated by metabolic labeling of human platelets with [H-3]arachidonate and [H-3]eicosapentaenoate that these polyunsaturated fatty acids can also become covalently linked to proteins. The extent of binding of arachidonate to proteins was somewhat less than that of palmitate. Arachidonate binding to platelet proteins was not significantly influenced by the inhibition of cyclooxygenase and lipoxygenase. This finding and the high performance liquid chromatography analysis of radiolabeled products removed from proteins by selective cleavage techniques established that arachidonate, and not its metabolic products, was the protein-linked radiolabeled moiety in [H-3] arachidonate-labeled platelets. A 7.5-fold higher concentration of unlabeled palmitate competed to a small extent with [H-3]arachidonate for protein labeling. Both arachidonate and eicosapentaenoate were bound to proteins almost exclusively through ester linkages. It was further demonstrated that 61 and 66% of total protein-linked arachidonate and eicosapentaenoate, respectively, were bound via thioester bonds. In contrast, 91% of the binding of palmitate to proteins occurred via thioester linkages. As demonstrated by SDS-polyacrylamide gel electrophoresis and fluorography, the patterns of palmitoylated and arachidonoylated proteins were similar but not identical, with selected proteins only palmitoylated or only arachidonoylated. [H-3]Eicosapentaenate labeled the same set of proteins as [H-3]arachidonate. The fluorographic pattern of H-3-arachidonoylated proteins was not changed by cyclooxygenase and lipoxygenase inhibitors. The binding of a polyunsaturated fatty acid to a protein in place of a saturated fatty acid could significantly influence the hydrophobic interactions of the protein and, thereby, have important functional implications. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,CLIN LABS,RM 249,GRAY BLDG,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 43159] NR 31 TC 30 Z9 30 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 AUG 25 PY 1993 VL 268 IS 24 BP 18243 EP 18248 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LT743 UT WOS:A1993LT74300088 PM 8349700 ER PT J AU WOOD, KW ROBERTS, TM AF WOOD, KW ROBERTS, TM TI ONCOGENES AND PROTEIN-KINASES IN NEURONAL GROWTH-FACTOR ACTION SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Review ID PC12 PHEOCHROMOCYTOMA CELLS; GTPASE-ACTIVATING PROTEIN; MICROTUBULE-ASSOCIATED PROTEIN-2; COLONY-STIMULATING FACTOR; FACTOR-INDUCED DIFFERENTIATION; CHICKEN-EMBRYO FIBROBLASTS; ADRENAL CHROMAFFIN CELLS; COMPLETE CODING SEQUENCE; SERINE THREONINE KINASE; MITOGENIC SIGNAL TRANSDUCTION C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP WOOD, KW (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,B450,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA3803, CA5066] NR 279 TC 21 Z9 21 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD AUG 23 PY 1993 VL 1155 IS 2 BP 133 EP 150 DI 10.1016/0304-419X(93)90002-T PG 18 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LV637 UT WOS:A1993LV63700002 PM 8357824 ER PT J AU RUDD, CE JANSSEN, O PRASAD, KVS RAAB, M DASILVA, A TELFER, JC YAMAMOTO, M AF RUDD, CE JANSSEN, O PRASAD, KVS RAAB, M DASILVA, A TELFER, JC YAMAMOTO, M TI SRC-RELATED PROTEIN-TYROSINE KINASES AND THEIR SURFACE-RECEPTORS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Review ID T-CELL RECEPTOR; EPIDERMAL GROWTH-FACTOR; ROUS-SARCOMA VIRUS; GTPASE-ACTIVATING PROTEIN; AMINO-TERMINAL DOMAIN; CD45 PHOSPHOTYROSINE PHOSPHATASE; NATURAL-KILLER-CELLS; PDGF BETA-RECEPTOR; DIFFERENT SIGNALING PATHWAYS; GAP-ASSOCIATED PROTEINS C1 HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. RP RUDD, CE (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV TUMOR IMMUNOL, BOSTON, MA 02115 USA. RI Janssen, Ottmar/E-9735-2010 FU PHS HHS [R01 12069] NR 339 TC 86 Z9 86 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD AUG 23 PY 1993 VL 1155 IS 2 BP 239 EP 266 DI 10.1016/0304-419X(93)90007-Y PG 28 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LV637 UT WOS:A1993LV63700007 PM 8357828 ER PT J AU HOSPELHORN, AC MILBURY, CM ABBOTT, WM ORKIN, RW AF HOSPELHORN, AC MILBURY, CM ABBOTT, WM ORKIN, RW TI SUBSTRATE INFLUENCES EXTRACELLULAR-MATRIX ORGANIZATION BY HUMAN VASCULAR ENDOTHELIAL-CELLS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG RES UNIT,VASC CELL BIOL LAB,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 22 PY 1993 VL 206 BP 15 EP COLL PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA LP321 UT WOS:A1993LP32101043 ER PT J AU MOERLEIN, SM SWANSON, DP CALLAHAN, RJ AF MOERLEIN, SM SWANSON, DP CALLAHAN, RJ TI PHARMACY PRACTICE AND PET SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 WASHINGTON UNIV,MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. UNIV PITTSBURGH,SCH PHARM,PITTSBURGH,PA 15261. MASSACHUSETTS GEN HOSP,DIV NUCL MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 22 PY 1993 VL 206 BP 24 EP NUCL PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA LP322 UT WOS:A1993LP32200024 ER PT J AU BURKE, TR SMYTH, MS OTAKA, A NOMIZU, M CASE, RD SHOELSON, SE ROLLER, PP AF BURKE, TR SMYTH, MS OTAKA, A NOMIZU, M CASE, RD SHOELSON, SE ROLLER, PP TI SYNTHESIS OF PHOSPHONO(DIFLUOROMETHYL) PHENYLALANINE (F2PMP) ANALOGS SUITABLY PROTECTED FOR SOLID-PHASE SYNTHESIS OF SH2 INHIBITORY PEPTIDES CONTAINING PHOSPHOTYROSYL MIMETICS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,DCT,DTP,MED CHEM LAB,BETHESDA,MD 20892. HARVARD UNIV,JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 22 PY 1993 VL 206 BP 106 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA LP321 UT WOS:A1993LP32102496 ER PT J AU FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL AF FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL TI ACUTE-PANCREATITIS SO LANCET LA English DT Article ID COMPUTED-TOMOGRAPHY; GALLSTONE PANCREATITIS; PERITONEAL-LAVAGE; CONTROLLED TRIAL; NECROSIS; MULTICENTER; INFECTION; SEVERITY; SPHINCTEROTOMY; SOMATOSTATIN C1 MASSACHUSETTS GEN HOSP,DEPT SURG,15 PARKMAN ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 37 TC 34 Z9 34 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 AUG 21 PY 1993 VL 342 IS 8869 BP 475 EP 479 DI 10.1016/0140-6736(93)91598-G PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA LU075 UT WOS:A1993LU07500015 PM 8102434 ER PT J AU FOY, BD LEE, J MORGAN, J TONER, M TOMPKINS, RG YARMUSH, ML AF FOY, BD LEE, J MORGAN, J TONER, M TOMPKINS, RG YARMUSH, ML TI OPTIMIZATION OF HEPATOCYTE ATTACHMENT TO MICROCARRIERS - IMPORTANCE OF OXYGEN SO BIOTECHNOLOGY AND BIOENGINEERING LA English DT Article DE HEPATOCYTES; MICROCARRIERS; OXYGEN; ARTIFICIAL LIVER ID MATRIX PERFUSION SYSTEM; CELL-CULTURE SYSTEM; MAMMALIAN-CELLS; RAT-LIVER; TRANSPLANTATION; REQUIREMENTS; CULTIVATION; DEPENDENCE; INTERFERON; TERM AB Many potential applications of primary hepatocytes cultured on microcarriers, such as an artificial liver or hepatocyte transplantation, would benefit from having a large number of hepatocytes attached to each microcarrier. In addition, the supply of primary hepatocytes is usually limited, so the efficient utilization of hepatocytes during attachment to microcarriers is necessary. Several physical parameters involved in the attachment process have been investigated, and the number of cells attached per microcarrier and the fraction of hepatocytes which attach have been quantitatively monitored. Variation of the partial pressure of gas phase oxygen in the incubation flask produced significant effects on the attachment of hepatocytes to microcarriers, with higher partial pressures of oxygen found to be necessary for attachment. In addition, variation of fluid depth and cell number, both of which influence the partial pressure of oxygen at the cell surface, affected hepatocyte attachment. The partial pressure of oxygen at the cell surface as a function of the physical parameters was analyzed using a simple one-dimensional theoretical model. Variations in the cell-to-microcarrier ratio used for incubation indicate that a compromise must be made in terms of maximizing the number of cells per microcarrier and the fraction of total hepatocytes which attach. The maximum number of hepatocytes per microcarrier obtained in this work was approximately 100. The best attachment fraction, defined as the ratio of the number of hepatocytes attached to the total number added to the incubation, was approximately 90%. (C) 1993 John Wiley & Sons, Inc. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BIGELOW 1302,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA 02114. CHUNG ANG UNIV,DEPT BIOTECHNOL,SEOUL,SOUTH KOREA. RUTGERS UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. OI Morgan, Jeffrey/0000-0002-7546-3443 NR 29 TC 31 Z9 31 U1 0 U2 3 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3592 J9 BIOTECHNOL BIOENG JI Biotechnol. Bioeng. PD AUG 20 PY 1993 VL 42 IS 5 BP 579 EP 588 DI 10.1002/bit.260420505 PG 10 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA LN598 UT WOS:A1993LN59800004 PM 18613079 ER PT J AU WYRICK, SD BOOTH, RG MYERS, AM OWENS, CE KULA, NS BALDESSARINI, RJ MCPHAIL, AT MAILMAN, RB AF WYRICK, SD BOOTH, RG MYERS, AM OWENS, CE KULA, NS BALDESSARINI, RJ MCPHAIL, AT MAILMAN, RB TI SYNTHESIS AND PHARMACOLOGICAL EVALUATION OF 1-PHENYL-3-AMINO-1,2,3,4-TETRAHYDRONAPHTHALENES AS LIGANDS FOR A NOVEL RECEPTOR WITH SIGMA-LIKE NEUROMODULATORY ACTIVITY SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID RAT STRIATAL TISSUE; BINDING-SITES; DOPAMINE SYNTHESIS; CORPUS STRIATUM; BW234U; BRAIN AB Certain novel 1-phenyl-3-amino-1,2,3,4-tetrahydronaphthalenes (1-phenyl-3-aminotetralins, PATs) produced stimulation (ca. 30% above basal levels) of tyrosine hydroxylase (TH) activity at 0.1 muM concentrations in rodent brain tissue. This effect on TH was blocked by the putative sigma-receptor antagonist BMY-14802, suggesting involvement of a novel neuromodulatory sigma-like receptor. Within the new phenylaminotetralin series, a correlation was found between the ability to stimulate TH and the potency to compete for binding sites labeled by (+/-)-[H-3]1-phenyl-3-(NN-dimethylamino)-6-chloro-7-hydroxy-1,2,3,4-tetrahydronaphthalene {[H-3](+/-)-4}. trans-Catechol analogs had low affinity for [H-3]4 sites, and although they inhibited TH activity, this effect was not blocked by known sigma or dopamine antagonists. Analogs with dihydroxy substituents (catechols), as well as nitrogen substituents larger than methyl, had little affinity for [H-3]4 binding sites and did not significantly affect TH activity. The pharmacology of the [H-3]4 binding site is unique from that of any known sigma or dopamine receptor, thus the effects appear to be mediated by a previously uncharacterized binding site/receptor. The site has stereoselectivity for the (1R,3S)-(-)-isomer of 1-phenyl-3-(N,N-dimethylamino)-1,2,3,4-tetrahydronaphthalene; this isomer is also more active at stimulating TH. Thus, certain 1-phenyl-3-amino-1,2,3,4-tetrahydronaphthalenes appear to be selective probes of a novel receptor type that mediates cr-like neuromodulatory activity and may have pharmacotherapeutic utility in conditions in which modulation of dopamine function is important. C1 UNIV N CAROLINA,BRAIN & DEV RES CTR,CHAPEL HILL,NC 27599. DUKE UNIV,DEPT CHEM,DURHAM,NC 27708. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BELMONT,MA 02178. RP WYRICK, SD (reprint author), UNIV N CAROLINA,SCH PHARM,DIV MED CHEM & NAT PROD,CB 7360,CHAPEL HILL,NC 27599, USA. FU NIMH NIH HHS [MH-40537, MH-34006, MH-47370] NR 41 TC 46 Z9 46 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD AUG 20 PY 1993 VL 36 IS 17 BP 2542 EP 2551 DI 10.1021/jm00069a013 PG 10 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA LU544 UT WOS:A1993LU54400013 PM 8102651 ER PT J AU CHOW, YK HIRSCH, MS KAPLAN, JC DAQUILA, RT AF CHOW, YK HIRSCH, MS KAPLAN, JC DAQUILA, RT TI HIV-1 ERROR REVEALED SO NATURE LA English DT Letter RP CHOW, YK (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114, USA. NR 5 TC 38 Z9 38 U1 0 U2 2 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD AUG 19 PY 1993 VL 364 IS 6439 BP 679 EP 679 DI 10.1038/364679a0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LT677 UT WOS:A1993LT67700034 PM 7689174 ER PT J AU CHATURVEDI, N HEDLEYWHYTE, ET DREYER, EB AF CHATURVEDI, N HEDLEYWHYTE, ET DREYER, EB TI LATERAL GENICULATE-NUCLEUS IN GLAUCOMA SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID RETINAL GANGLION-CELLS; OPEN-ANGLE GLAUCOMA; OPTIC-NERVE DAMAGE; OCULAR HYPERTENSION; LAMINA CRIBROSA; X-LIKE; MONKEY; SEGREGATION; PERCEPTION; SENSITIVITY AB To assess glaucomatous damage to the lateral geniculate nucleus of the thalamus, as well as to its magnocellular and parvocellular layers, we examined the autopsy sections of the lateral geniculate nucleus of individuals with and without glaucoma. Five patients with a documented history of glaucoma and five controls with no ophthalmic or chronic central nervous system disease were included in this study. Neurons were counted in autopsy sections of the lateral geniculate nucleus. Cells were counted in 40 random microscopic fields of the magnocellular and parvocellular layers respectively. The mean magnocellular cell density for the glaucoma group of 2.72 +/- 0.13 cells per square millimeter (mean +/- SEM) was significantly less than that for the control group of 3.76 +/- 0.13 cells per square millimeter (P < .001). There was no statistical difference in the parvocellular layer. These data suggest that glaucoma leads to greater loss of magnocellular tissue at the level of the lateral geniculate. C1 MASSACHUSETTS EYE & EAR INFIRM,GLAUCOMA CONSULTAT SERV,243 CHARLES ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NINDS NIH HHS [K08-NS01395] NR 33 TC 113 Z9 117 U1 3 U2 3 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 AUG 15 PY 1993 VL 116 IS 2 BP 182 EP 188 PG 7 WC Ophthalmology SC Ophthalmology GA LR277 UT WOS:A1993LR27700008 PM 8352303 ER PT J AU SRIVASTAVA, PK WAXMAN, DJ AF SRIVASTAVA, PK WAXMAN, DJ TI SEX-DEPENDENT EXPRESSION AND GROWTH-HORMONE REGULATION OF CLASS-ALPHA AND CLASS-MU GLUTATHIONE-S-TRANSFERASE MESSENGER-RNAS IN ADULT-RAT LIVER SO BIOCHEMICAL JOURNAL LA English DT Article ID PLATINUM ANTICANCER DRUGS; THYROID-HORMONE; CDNA SEQUENCES; CIS-PLATINUM; FEMALE RATS; P-450 FORMS; TESTOSTERONE; RESISTANCE; MODULATION; CYTOCHROME-P450 AB The sex-dependent expression and growth hormone (GH) regulation of rat liver glutathione S-transferase (GST) was examined using oligonucleotide probes that distinguish between closely related class Alpha (Ya1, Ya2, Yc) and class Mu (Yb1, Yb2, Yb3) GST mRNAs [Waxman, Sundseth, Srivastava and Lapenson (1992) Cancer Res. 52, 5797-5802]. Northern-blot analysis revealed that the steady-state levels of GST Ya1, Yb1 and Yb2 mRNAs are 2.5-3-fold higher in male as compared with female rat liver. In contrast, GST Yc and Ya2 mRNAs were expressed at a 2-3-fold higher level in female rat liver. Microsomal GST mRNA did not exhibit significant sex-dependent differences in rat liver. Treatment of male rats with GH by continuous infusion suppressed expression of the male-dominant GST Ya1, Yb1 and Yb2 mRNAs to levels at or below those found in female rat liver. This suppressive effect of GH was liver-specific, insofar as GH treatment did not alter kidney GST Ya1 mRNA levels. Hypophysectomy increased expression of the male-dominant GSTs, particularly in female rats (e.g. 8-fold elevation of GST Ya1 mRNA). GST Yc mRNA was increased approx. 2-fold in hypophysectomized males, indicating that this mRNA is subject to negative regulation by one or more pituitary-dependent factors. Continuous GH treatment of the hypophysectomized rats suppressed the expression of mRNA of GSTs Ya1, Yb1 and Yb2 when given as a continuous infusion, but not when given by an intermittent (twice daily) GH-injection schedule. Combination of continuous exposure to GH with thyroxine treatment resulted in a more complete suppression of GSTs Ya1, Yb1 and Yb2. In contrast, thyroxine increased the expression of GST Yc in hypophysectomized rats. These studies establish that several Alpha and Mu class GSTs are expressed in a sex-dependent fashion in adult rat liver, where they are regulated by multiple pituitary-dependent hormones through pretranslational mechanisms. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NR 54 TC 47 Z9 47 U1 0 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD AUG 15 PY 1993 VL 294 BP 159 EP 165 PN 1 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU522 UT WOS:A1993LU52200023 PM 8363567 ER PT J AU KIM, DK BONVENTRE, JV AF KIM, DK BONVENTRE, JV TI PURIFICATION OF A 100-KDA PHOSPHOLIPASE-A(2) FROM SPLEEN, LUNG AND KIDNEY - ANTISERUM RAISED TO PIG SPLEEN PHOSPHOLIPASE-A(2) RECOGNIZES A SIMILAR FORM IN BOVINE LUNG, KIDNEY AND PLATELETS, AND IMMUNOPRECIPITATES PHOSPHOLIPASE-A(2) ACTIVITY SO BIOCHEMICAL JOURNAL LA English DT Article ID CA2+-SENSITIVE CYTOSOLIC PHOSPHOLIPASE-A2; ARACHIDONOYL-HYDROLYZING PHOSPHOLIPASE-A2; SOLUBLE PHOSPHOLIPASE-A2; MESANGIAL CELLS; RAT SPLEEN; ACID; CONTAINS; MEMBRANE; PROTEIN; U937 AB Phospholipase A2 (PLA2) plays a key role in the production of intracellular and extracellular chemical mediators such as arachidonic acid, eicosanoids and platelet-activating factor, which modulate membrane channel activity, signal transduction, are vasoactive and chemotactic, and are implicated in many pathophysiological mechanisms of inflammation and tissue injury. We previously identified, purified and characterized an arachidonic acid-selective cytosolic 1 00-110 kDa PLA2 from bovine platelets and rat kidney that is activated during cell stimulation. The purification schemes previously published resulted in low yields of enzyme, insufficient for extensive biochemical characterization. We report the purification of a large-molecular-mass (100 kDa) PLA2 from pig spleen, bovine kidney and bovine lung, using a novel large-scale purification scheme. The enzyme was purified to near homogeneity from an acidified extract obtained from 4.8 kg of pig spleen by sequential use of DEAE-cellulose anionic exchange, Butyl-Toyopearl hydrophobic chromatography and DEAE-5PW h.p.l.c., and further purified by non-denaturing PAGE. This purification scheme will permit the preparation of quantities of purified native enzyme sufficient to study its properties and regulation. To generate antiserum against the PLA2 enzyme, the 100 kDa protein was excised and electroeluted from SDS/PAGE gels of the active fractions after DEAE-5PW h.p.l.c., and this was used as antigen. This polyclonal antibody against pig spleen 100 kDa PLA2 protein reacted with 100 kDa bands in preparations partially purified from bovine platelets, kidney and lung as well as pig spleen, and immunoprecipitated PLA2 activity from these sources. The antibody also immunoprecipitated a 100 kDa protein from cytosolic fractions of cultured renal mesangial cells, human erythroleukaemia cells and human monocytic U937 cells. Considerable PLA2 activity was present in the immunoprecipitates. To our knowledge this antibody is unique in its ability to permit measurement of PLA2 activity in the immunoprecipitate itself, and will be a useful tool for the study of the regulation and the activation mechanisms of the native PLA2 enzyme. C1 POHANG INST SCI & TECHNOL,DEPT LIFE SCI,POHANG 790330,SOUTH KOREA. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. FU NIDDK NIH HHS [DK 39773, DK 38452]; NINDS NIH HHS [NS 10828] NR 34 TC 55 Z9 55 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD AUG 15 PY 1993 VL 294 BP 261 EP 270 PN 1 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU522 UT WOS:A1993LU52200037 PM 8363579 ER PT J AU SHIPP, MA LOOK, AT AF SHIPP, MA LOOK, AT TI HEMATOPOIETIC DIFFERENTIATION ANTIGENS THAT ARE MEMBRANE-ASSOCIATED ENZYMES - CUTTING IS THE KEY SO BLOOD LA English DT Review ID ACUTE LYMPHOBLASTIC-LEUKEMIA; DIPEPTIDYL PEPTIDASE-IV; NEUTRAL ENDOPEPTIDASE 24.11; T-CELL ACTIVATION; AMINO-ACID SEQUENCE; HUMAN LYMPHOCYTE-T; HUMAN AMINOPEPTIDASE-N; ACUTE MYELOBLASTIC-LEUKEMIA; BRUSH-BORDER MEMBRANE; HUMAN-BONE-MARROW C1 ST JUDE CHILDRENS RES HOSP, DEPT EXPTL ONCOL, MEMPHIS, TN 38101 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT PEDIAT, MEMPHIS, TN 38163 USA. RP SHIPP, MA (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT MED, 44 BINNEY ST, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA-21765, CA-42804, CA-55095] NR 233 TC 337 Z9 340 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD AUG 15 PY 1993 VL 82 IS 4 BP 1052 EP 1070 PG 19 WC Hematology SC Hematology GA LT742 UT WOS:A1993LT74200002 PM 8102558 ER PT J AU RABINOWE, SN SOIFFER, RJ GRIBBEN, JG DALEY, H FREEDMAN, AS DALEY, J PESEK, K NEUBERG, D PINKUS, G LEAVITT, PR SPECTOR, NA GROSSBARD, ML ANDERSON, K ROBERTSON, MJ MAUCH, P CHAYTMARCUS, K RITZ, J NADLER, LM AF RABINOWE, SN SOIFFER, RJ GRIBBEN, JG DALEY, H FREEDMAN, AS DALEY, J PESEK, K NEUBERG, D PINKUS, G LEAVITT, PR SPECTOR, NA GROSSBARD, ML ANDERSON, K ROBERTSON, MJ MAUCH, P CHAYTMARCUS, K RITZ, J NADLER, LM TI AUTOLOGOUS AND ALLOGENEIC BONE-MARROW TRANSPLANTATION FOR POOR-PROGNOSIS PATIENTS WITH B-CELL CHRONIC LYMPHOCYTIC-LEUKEMIA SO BLOOD LA English DT Article ID MULTIVARIATE SURVIVAL ANALYSIS; PROLYMPHOCYTIC LEUKEMIA; DOUBLING TIME; FLUDARABINE; AGENT; FEATURES; PATTERN; DISEASE C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL & BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL & MED,BOSTON,MA 02115. FU NCI NIH HHS [CA34183] NR 29 TC 161 Z9 163 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 AUG 15 PY 1993 VL 82 IS 4 BP 1366 EP 1376 PG 11 WC Hematology SC Hematology GA LT742 UT WOS:A1993LT74200041 PM 7688995 ER PT J AU KOPANS, DB AF KOPANS, DB TI BREAST-CANCER DETECTION IN AN INSTITUTION - IS MAMMOGRAPHY DETRIMENTAL SO CANCER LA English DT Article; Proceedings Paper CT WORKSHOP ON BREAST CANCER DETECTION IN YOUNGER WOMEN : A CURRENT ASSESSMENT CY FEB 01-02, 1993 CL NEW YORK, NY SP AMER CANC SOC ID SCREENING TRIAL; TUMOR SIZE; AGE; SURVIVAL; WOMEN; MORTALITY; INTERVAL; RATES AB The poor results of the National Breast Screening Study of Canada regarding the screening of women aged 40-49 have been interpreted to suggest that mammography might be detrimental. Our comparison of women who had mammography and had their cancers detected by mammography with women who did not have mammography and had palpable cancers suggest that this is not the case. There is no detrimental effect; rather, the use of mammography results in an improvement in survival. The poor results of the National Breast Screening Study likely are due to the unbalanced allocation of women with advanced cancers to the screened group, the poor quality of the mammography in the trial, and an insufficient sample size. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,15 PARKMAN ST,LEVEL 2,SUITE 219,BOSTON,MA 02114, USA. NR 21 TC 5 Z9 5 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD AUG 15 PY 1993 VL 72 IS 4 SU S BP 1457 EP 1460 DI 10.1002/1097-0142(19930815)72:4+<1457::AID-CNCR2820721407>3.0.CO;2-E PG 4 WC Oncology SC Oncology GA LR752 UT WOS:A1993LR75200006 PM 8339238 ER PT J AU XU, YY WANDS, JR DELAMONTE, SM AF XU, YY WANDS, JR DELAMONTE, SM TI CHARACTERIZATION OF THREAD PROTEINS EXPRESSED IN NEUROECTODERMAL TUMORS SO CANCER RESEARCH LA English DT Article ID ALZHEIMERS-DISEASE; SECRETORY PROTEIN; GROWTH; BRAIN; GENE; NERVE AB Neuronal thread protein is a novel 21-kDa protein that accumulates in brains with Alzheimer's disease and exhibits developmentally associated changes in the level of expression. Recently, we discovered that primary human primitive neuroectodermal tumor (PNETs), malignant astrocytomas, and several human PNET and glioblastoma cell lines also express thread protein immunoreactivity. However, in addition to the 21-kDa species, there are approximately 17- and approximately 14-kDa thread protein-immunoreactive molecules expressed in both PNET and glioblastoma cell lines and a fourth -8-kDa thread protein detected in glioblastoma cell lines. Metabolic labeling studies demonstrated that the 21-kDa thread proteins are phosphorylated, whereas the approximately 17-, approximately 14-, and approximately 8-kDa thread proteins are not. Glycosylated residues were not detected in either the PNET- or glioblastoma-derived thread proteins. Using a panel of monoclonal antibodies, we observed differences between PNET and glioblastoma cells suggesting that the thread proteins expressed in neuronal and glial cells are distinct. The levels of thread protein immunoreactivity in both PNET and glial cells were highest during the log phase of cell growth and lowest in serum-starved, nonproliferating cultures. The findings suggest that there are several distinct neuronal and glial derived thread proteins expressed in the central nervous system and that their levels of expression may be modulated with cell growth. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ALZHEIMERS DIS RES CTR,MED SERV,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV NEUROPATHOL,BOSTON,MA 02129. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [R01-AA02666]; NINDS NIH HHS [R01-NS29793] NR 22 TC 17 Z9 18 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 AUG 15 PY 1993 VL 53 IS 16 BP 3823 EP 3829 PG 7 WC Oncology SC Oncology GA LR765 UT WOS:A1993LR76500033 PM 7687927 ER PT J AU LIU, ZR WILLIAMS, KP CHANG, YH SMITH, JA AF LIU, ZR WILLIAMS, KP CHANG, YH SMITH, JA TI IMMUNODOMINANCE - A SINGLE AMINO-ACID SUBSTITUTION WITHIN AN ANTIGENIC SITE ALTERS INTRAMOLECULAR SELECTION OF T-CELL DETERMINANTS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; STAPHYLOCOCCAL NUCLEASE; PROTEIN ANTIGEN; REPERTOIRE; SELF; RECOGNITION; TOLERANCE; PRODUCTS; DISTANT; CLONES AB The mechanism of immunodominance was studied by mutating a single amino acid residue within an immunodominant determinant of Staphylococcus aureus nuclease (Nase). Residues 81 to 100, which can be further reduced to 86 to 100, were determined to be the immunodominant determinant of Nase in H-2k mice. By introducing selected single amino acid substitutions into the peptide encompassing residues 86 to 100 (p86-100), residue 90 was shown to be one of the critical amino acids for T cell recognition, inasmuch as most of the T cells recognizing p86-100 do not respond to a p86-100 analog with a substitution of leucine for ala nine at the residue 90. A mutant of Nase with a replacement of alanine by leucine at residue 90 (A90L) was constructed, and for A90L region 112 to 130, which is a subdominant determinant in Nase, becomes immunodominant. Although unable to respond to Nase, T cells primed in vivo with the peptides covering various cryptic determinants proliferate when challenged with A90L in vitro. Our results suggest that at the protein level there is competition among potential T cell determinants of protein Ag for binding to MHC molecules, and that this competition plays a role in determining which determinant may become immunodominant. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 23 TC 33 Z9 34 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 AUG 15 PY 1993 VL 151 IS 4 BP 1852 EP 1858 PG 7 WC Immunology SC Immunology GA LR904 UT WOS:A1993LR90400011 PM 7688387 ER PT J AU SALLES, G RODEWALD, HR CHIN, BS REINHERZ, EL SHIPP, MA AF SALLES, G RODEWALD, HR CHIN, BS REINHERZ, EL SHIPP, MA TI INHIBITION OF CD10 NEUTRAL ENDOPEPTIDASE 24.11 PROMOTES B-CELL RECONSTITUTION AND MATURATION IN-VIVO SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE COMMON ACUTE LYMPHOBLASTIC LEUKEMIA ANTIGEN; LYMPHOID PROGENITORS; DIFFERENTIATION; CELL SURFACE ENZYME ID LYMPHOBLASTIC-LEUKEMIA ANTIGEN; SUBSTANCE-P; BONE-MARROW; CALLA; ENKEPHALINASE; LYMPHOPOIESIS; LUNG; TACHYKININS; PROGENITORS; POPULATION AB The common acute lymphoblastic leukemia antigen [(CALLA) CD10, neutral endopeptidase 24.11 (NEP)] is a cell-surface zinc metalloprotease expressed by a subpopulation of early murine B-lymphoid progenitors and by bone marrow stromal cells that support the earliest stages of B lymphopoiesis. In previous in vitro studies in which uncommitted murine hematopoietic progenitors plated on a stromal cell layer differentiate into immature B cells, the inhibition of CD10/NEP increased early lymphoid colony numbers. To further characterize CD10/NEP function during lymphoid ontogeny in vivo, we utilized a Ly5 congenic mouse model in which the lymphoid differentiation of uncommitted hematopoietic progenitors from Ly5.1 donors was followed in sublethally irradiated Ly5.2 recipients treated with a specific long-acting CD10/NEP inhibitor {N-[L-(1-carboxy-2-phenyl)ethyl]-L-phenylalanyl-beta-alanine (SCH32615)}. The expression of Ly5.1, B220, and surface IgM (sIgM) was utilized to characterize donor-derived hematopoietic cells (Ly5.1+), B lymphocytes (B220+), and mature B cells (B220+ sIgM+) from the lymphoid organs of recipient animals treated with SCH32615 or vehicle alone. SCH32615-treated animals had higher percentages of Ly5.1+ donor splenocytes than animals treated with vehicle alone (16.9% vs. 10.4%, 63% increase, P = 0.013). Animals treated with the CD10/NEP inhibitor also had relatively more Ly5.1+ splenic B (B220+) cells than vehicle-treated animals (14.4% vs. 8.2%, 75% increase, P = 0.018). To more specifically characterize the effects of CD10/NEP inhibition on B-cell differentiation, Ly5.1+ splenocytes from animals treated with SCH32615 or vehicle alone were analyzed for coexpression of B220 and sIgM. Animals treated with the CD10/NFP inhibitor had a significantly higher percentage of mature donor B cells (Ly5.1+ B220+ sIgM+, 10.2% vs. 5.2%, 90% increase, P = 0.006) and a more modest relative increase in immature donor B cells (Ly5.1+ B220+ sIgM-, 4.7% vs. 3.4%, 38% increase, P = not significant). Taken together, these results suggest that CD10/NEP inhibition promotes the reconstitution and maturation of splenic B cells. Therefore, CD10/NEP may function to regulate B-cell ontogeny in vivo by hydrolyzing a peptide substrate that stimulates B-cell proliferation and/or differentiation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,44 BINNEY ST,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. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA49232] NR 37 TC 37 Z9 37 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 AUG 15 PY 1993 VL 90 IS 16 BP 7618 EP 7622 DI 10.1073/pnas.90.16.7618 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LT437 UT WOS:A1993LT43700042 PM 8356064 ER PT J AU CASTILLO, L CHAPMAN, TE SANCHEZ, M YU, YM BURKE, JF AJAMI, AM VOGT, J YOUNG, VR AF CASTILLO, L CHAPMAN, TE SANCHEZ, M YU, YM BURKE, JF AJAMI, AM VOGT, J YOUNG, VR TI PLASMA ARGININE AND CITRULLINE KINETICS IN ADULTS GIVEN ADEQUATE AND ARGININE-FREE DIETS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ORNITHINE-ALPHA-KETOGLUTARATE; AMINO-ACID; GAS-CHROMATOGRAPHY; HEALTHY-SUBJECTS; METABOLISM; RAT; REQUIREMENTS; LOCALIZATION; GLUTAMINE; INFUSION AB The fluxes of arginine and citrulline through plasma and the rate of conversion of labeled citrulline to arginine were estimated in two pilot studies (with a total of six adult subjects) and in a dietary study with five healthy young men. These latter subjects received an L-amino acid-based diet that was arginine-rich or arginine-free each for 6 days prior to conduct, on day 7, of an 8-hr (first 3 hr, fast; final 5 hr, fed) primed continuous intravenous infusion protocol using L-[guanidino-C-13]arginine, L-[5,5-H-2(2)]citrulline, and L-[5,5,5-H-2(3)]leucine, as tracers. A pilot study indicated that citrulline flux was about 20% higher (P < 0.05) when determined with [ureido-C-13]citrulline compared with [H-2(2)]citrulline, indicating recycling of the latter tracer. Mean citrulline fluxes were about 8-11 mumol.kg-1.hr-1 for the various metabolic/diet groups and did not differ significantly between fast and fed states or arginine-rich and arginine-free periods. Arginine fluxes (mean +/- SD) were 60.2 +/- 5.4 and 73.3 +/- 13.9 mumol.kg-1.hr-1 for fast and fed states during the arginine-rich period, respectively, and were significantly lowered (P < 0.05), by 20-40%, during the arginine-free period, especially for the fed state, where this was due largely to reduced entry of dietary arginine into plasma. The conversion of plasma citrulline to arginine approximated 5.5 mumol.kg-1.hr-1 for the various groups and also was unaffected by arginine intake. Thus, endogenous arginine synthesis is not markedly responsive to acute alterations in arginine intake in healthy adults. We propose that arginine homeostasis is achieved largely via modulating arginine intake and/or the net rate of arginine degradation. C1 SHRINERS BURNS INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. TRACER TECHNOL INC,SOMERVILLE,MA 02145. RP CASTILLO, L (reprint author), MIT,SCH SCI,HUMAN NUTR LAB,CAMBRIDGE,MA 02139, USA. FU NCRR NIH HHS [RR88]; NIDDK NIH HHS [DK15856]; NIGMS NIH HHS [GM02700] NR 46 TC 155 Z9 155 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 15 PY 1993 VL 90 IS 16 BP 7749 EP 7753 DI 10.1073/pnas.90.16.7749 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LT437 UT WOS:A1993LT43700069 PM 8356080 ER PT J AU JIN, YJ BURAKOFF, SJ AF JIN, YJ BURAKOFF, SJ TI THE 25-KDA FK506-BINDING PROTEIN IS LOCALIZED IN THE NUCLEUS AND ASSOCIATES WITH CASEIN KINASE-II AND NUCLEOLIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE IMMUNOSUPPRESSANT-BINDING PROTEIN ID STEROID-RECEPTOR COMPLEXES; RAPAMYCIN-BINDING-PROTEIN; HEAT-SHOCK PROTEIN; P70 S6 KINASE; CYCLOSPORINE-A; MOLECULAR-CLONING; PROLYL ISOMERASE; ACTIVATION; CALCINEURIN; FK506 AB FK506-binding proteins (FKBPs) have been identified as the cellular receptors of the immunosuppressive drugs FK506 and rapamycin. Recently, we cloned a 25-kDa FKBP family member (FKBP25) and found that FKBP25 contains a nuclear localization sequence and several potential casein kinase II phosphorylation sites. It has been previously shown that phosphorylation of proteins by casein kinase II can enhance their nuclear localization. Here we demonstrate that FKBP25 is localized to the nucleus and that a glutathione S-transferase fusion protein of FKBP25 (GST-FKBP25) can be phosphorylated by casein kinase II. Also a stable FKBP25/casein kinase II complex was formed when the GST-FKBP25 fusion protein was incubated either with purified casein kinase II or with cell lysates. Furthermore, when GST-FKBP25 was incubated with nuclear lysates, nucleolin, a major nuclear substrate of casein kinase II, was found associated with the GST-FKBP25/casein kinase II complex. Casein kinase II phosphorylation of several cytosolic and nuclear substrates, including nucleolin, appears to be important for the regulation of cell growth. The interaction of FKBP25 with casein kinase II may regulate these functions. 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 PEDIAT,BOSTON,MA 02115. NR 46 TC 110 Z9 112 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 AUG 15 PY 1993 VL 90 IS 16 BP 7769 EP 7773 DI 10.1073/pnas.90.16.7769 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LT437 UT WOS:A1993LT43700073 PM 7689229 ER PT J AU MARASCO, WA HASELTINE, WA CHEN, SY AF MARASCO, WA HASELTINE, WA CHEN, SY TI DESIGN, INTRACELLULAR EXPRESSION, AND ACTIVITY OF A HUMAN ANTI-HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GP120 SINGLE-CHAIN ANTIBODY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS TYPE-1 ENVELOPE PROTEIN; INTRACELLULAR ANTIBODY; AIDS; CD4+ T-CELLS; GENE THERAPY ID HUMAN MONOCLONAL-ANTIBODY; AMINO-ACID SUBSTITUTION; HTLV-III/LAV ENVELOPE; ENDOPLASMIC-RETICULUM; VARIABLE REGION; AIDS PATIENTS; GLYCOPROTEIN; PROTEIN; BINDING; CD4 AB A single-chain antibody, derived from a human monoclonal antibody that recognizes the CD4 binding region of the human immunodeficiency virus type 1 (HIV-1) envelope protein, has been designed for intracellular expression in eukaryotic cells. The single-chain antibody is composed of an immunoglobulin heavy-chain leader sequence and heavy- and light-chain variable regions that are joined by an inter-chain linker. The antibody is stably expressed and retained in the endoplasmic reticulum and is not toxic to the cells. The antibody binds to the envelope protein within the cell and inhibits processing of the envelope precursor and syncytia formation. The infectivity of the HIV-1 particles produced by cells that express the single-chain antibody is substantially reduced. These studies illustrate the feasibility of designing antibodies that bind and inactivate molecules intracellularly. Antibodies that act on target molecules within cells should provide a useful tool for research as well as for control of infectious and other diseases. C1 HARVARD UNIV,SCH MED,SCH PUBL HLTH,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115. RP MARASCO, WA (reprint author), HARVARD UNIV,SCH MED,SCH PUBL HLTH,DANA FARBER CANC INST,DEPT MED,DIV HUMAN RETROVIROL,BOSTON,MA 02115, USA. FU NCI NIH HHS [KO8-CA01507, P30-CA06516]; NIAID NIH HHS [P30AI28691] NR 36 TC 218 Z9 224 U1 0 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 15 PY 1993 VL 90 IS 16 BP 7889 EP 7893 DI 10.1073/pnas.90.16.7889 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LT437 UT WOS:A1993LT43700097 PM 8356098 ER PT J AU SWERDLOW, DL RIES, AA AF SWERDLOW, DL RIES, AA TI VIBRIO-CHOLERAE NON-01 - THE 8TH PANDEMIC SO LANCET LA English DT Editorial Material C1 CTR DIS CONTROL & PREVENT,ATLANTA,GA. RP SWERDLOW, DL (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114, USA. NR 12 TC 57 Z9 58 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 AUG 14 PY 1993 VL 342 IS 8868 BP 382 EP 383 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA LR900 UT WOS:A1993LR90000002 PM 8101894 ER PT J AU CORDER, EH SAUNDERS, AM STRITTMATTER, WJ SCHMECHEL, DE GASKELL, PC SMALL, GW ROSES, AD HAINES, JL PERICAKVANCE, MA AF CORDER, EH SAUNDERS, AM STRITTMATTER, WJ SCHMECHEL, DE GASKELL, PC SMALL, GW ROSES, AD HAINES, JL PERICAKVANCE, MA TI GENE DOSE OF APOLIPOPROTEIN-E TYPE-4 ALLELE AND THE RISK OF ALZHEIMERS-DISEASE IN LATE-ONSET FAMILIES SO SCIENCE LA English DT Article ID LINKAGE; LOCUS; CHROMOSOME-14; PROTEIN AB The apolipoprotein E type 4 allele (APOE-epsilon4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE-epsilon4 alleles in 42 families with late onset AD. Thus APOE-epsilon4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE-epsilon4 was virtually sufficient to cause AD by age 80. C1 DUKE UNIV,MED CTR,JOSEPH & KATHLEEN BRYAN ALZHEIMERS DIS RES CTR,DEPT MED,DURHAM,NC 27710. DUKE UNIV,MED CTR,JOSEPH & KATHLEEN BRYAN ALZEHEIMERS DIS RES CTR,DEPT NEUROL,DURHAM,NC 27710. DUKE UNIV,MED CTR,JOSEPH & KATHLEEN BRYAN ALZEHEIMERS DIS RES CTR,DEPT NEUROBIOL,DURHAM,NC 27710. VET ADM MED CTR,DURHAM,NC 27705. UNIV CALIF LOS ANGELES,CTR HLTH SCI,NEUROPSYCHIAT INST & HOSP,LOS ANGELES,CA 90024. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. RI Haines, Jonathan/C-3374-2012 NR 23 TC 5128 Z9 5214 U1 44 U2 339 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD AUG 13 PY 1993 VL 261 IS 5123 BP 921 EP 923 DI 10.1126/science.8346443 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LR897 UT WOS:A1993LR89700041 PM 8346443 ER PT J AU TALAL, N AF TALAL, N TI LESSONS FROM AUTOIMMUNITY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID INTERSPECIES IDIOTYPE; INDUCTION; NETWORK; MICE C1 UNIV TEXAS, HLTH SCI CTR, DEPT MED, SAN ANTONIO, TX 78284 USA. RP TALAL, N (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR, CLIN IMMUNOL SECT, SAN ANTONIO, TX 78284 USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD AUG 12 PY 1993 VL 690 BP 19 EP 23 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX021 UT WOS:A1993LX02100004 ER PT J AU HANNA, MG RANSOM, JH POMATO, N PETERS, L BLOEMENA, E VERMORKEN, JB HOOVER, HC AF HANNA, MG RANSOM, JH POMATO, N PETERS, L BLOEMENA, E VERMORKEN, JB HOOVER, HC TI ACTIVE SPECIFIC IMMUNOTHERAPY OF HUMAN COLORECTAL-CARCINOMA WITH AN AUTOLOGOUS TUMOR-CELL BACILLUS-CALMETTE-GUERIN VACCINE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID ADJUVANT THERAPY; MELANOMA; CANCER C1 FREE UNIV AMSTERDAM HOSP, AMSTERDAM, NETHERLANDS. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. RP HANNA, MG (reprint author), ORGANON TEKNIKA BIOTECHNOL RES INST, 1330-A PICCARD DR, ROCKVILLE, MD 20850 USA. NR 15 TC 0 Z9 0 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD AUG 12 PY 1993 VL 690 BP 135 EP 146 PG 12 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LX021 UT WOS:A1993LX02100016 ER PT J AU LIPTON, SA CHOI, YB PAN, ZH LEI, SZZ CHEN, HSV SUCHER, NJ LOSCALZO, J SINGEL, DJ STAMLER, JS AF LIPTON, SA CHOI, YB PAN, ZH LEI, SZZ CHEN, HSV SUCHER, NJ LOSCALZO, J SINGEL, DJ STAMLER, JS TI A REDOX-BASED MECHANISM FOR THE NEUROPROTECTIVE AND NEURODESTRUCTIVE EFFECTS OF NITRIC-OXIDE AND RELATED NITROSO-COMPOUNDS SO NATURE LA English DT Article ID RECEPTOR-CHANNEL COMPLEX; NMDA RECEPTOR; GLUTAMATE NEUROTOXICITY; SUPEROXIDE-DISMUTASE; MODULATORY SITE; NEURONAL INJURY; NERVOUS-SYSTEM; PEROXYNITRITE; INHIBITION; OXIDATION AB CONGENERS of nitrogen monoxide (NO) are neuroprotective and neurodestructive1-7. To address this apparent paradox, we considered the effects on neurons of compounds characterized by alternative redox states of NO: nitric oxide (NO.) and nitrosonium ion (NO+)8. Nitric oxide, generated from NO. donors or synthesized endogenously after NMDA (N-methyl-D-aspartate) receptor activation, can lead to neurotoxicity3,4. Here, we report that NO.-mediated neurotoxicity is engendered, at least in part, by reaction with superoxide anion (O2.-), apparently leading to formation of peroxynitrite (ONOO-), and not by NO. alone. In contrast, the neuroprotective effects of NO result from downregulation of NMDA-receptor activity by reaction with thiol group(s) of the receptor's redox modulatory site1. This reaction is not mediated by NO. itself, but occurs under conditions supporting S-nitrosylation of NMDA receptor thiol (reaction or transfer of NO+). Moreover, the redox versatility of NO allows for its interconversion from neuroprotective to neurotoxic species by a change in the ambient redox milieu. The details of this complex redox chemistry of NO may provide a mechanism for harnessing neuroprotective effects and avoiding neurotoxicity in the central nervous system. C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT NEUROL,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV NEUROL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV CARDIOVASC,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV RESP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BROCKTON W ROXBURY VET ADM MED CTR,CARDIOL SECT,BOSTON,MA 02115. HARVARD UNIV,DEPT CHEM,CAMBRIDGE,MA 02138. RP LIPTON, SA (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,CELLULAR & MOLEC NEUROSCI LAB,300 LONGWOOD AVE,ENDERS BLDG,BOSTON,MA 02115, USA. OI Sucher, Nikolaus/0000-0001-6233-1612 NR 34 TC 2089 Z9 2159 U1 5 U2 53 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD AUG 12 PY 1993 VL 364 IS 6438 BP 626 EP 632 DI 10.1038/364626a0 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LR771 UT WOS:A1993LR77100053 PM 8394509 ER PT J AU SIMON, HB AF SIMON, HB TI HYPERTHERMIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID NEUROLEPTIC MALIGNANT SYNDROME; RECURRENT FEBRILE SEIZURES; WHOLE-BODY HYPERTHERMIA; EXERTIONAL HEATSTROKE; FEVER; HEAT; TEMPERATURE C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SIMON, HB (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,INFECT DIS UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 48 TC 146 Z9 157 U1 1 U2 8 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 AUG 12 PY 1993 VL 329 IS 7 BP 483 EP 487 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA LR443 UT WOS:A1993LR44300008 PM 8332154 ER PT J AU DATTA, AK TAKAYAMA, K AF DATTA, AK TAKAYAMA, K TI BIOSYNTHESIS OF A NOVEL 3-OXO-2-TETRADECYLOCTADECANOATE-CONTAINING PHOSPHOLIPID BY A CELL-FREE-EXTRACT OF CORYNEBACTERIUM-DIPHTHERIAE SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE CORYNOMYCOLIC ACID; PHOSPHOLIPID; (CORYNEBACTERIUM) ID BACTERIONEMA-MATRUCHOTII; MYCOLIC ACIDS; FREE SYSTEM; TREHALOSE AB We have isolated, purified, and identified by chemical analyses and mass spectrometry, a novel 3-oxo-2-tetradecyloctadecanoate (dehydrocorynomycolate)-containing phospholipid (PL-1) from the chloroform-methanol extract of Corynebacterium diphtheriae. This phospholipid was separated from all of the other known dehydrocorynomycolate and 3-hydroxy-2-tetradecyloctadecanoate (corynomycolate)-containing lipids and found to be unstable even at -20-degrees-C. It was present in trace amounts as a homologous series (molecular weights of 1400 and 1404 as the methyl esters) and composed of a dehydrocorynomycolate, a phosphate group, a diacylglycerol, and an unidentified amine-containing component. Because of the complexity of these phospholipids, their complete structural determination is yet to be completed. A cell-free extract of C diphtheriae catalyzed the incorporation of radiolabel from [C-14]palmitic acid into PL-1. This incorporation was ATP-dependent, and the rate was linear with respect to both time and protein concentration. The radiolabel was incorporated primarily into the dehydrocorynomycoloyl moiety of PL-1. While avidin did not show any significant effect, cerulenin showed a marked inhibition of this reaction. Based on these results, we suggest that this dehydrocorynomycolate-containing PL-1 may be the long-sought acyl carrier-containing product of a Claisen-type condensation. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,2500 OVERLOOK TERR,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. FU NIGMS NIH HHS [GM-36054] NR 27 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD AUG 11 PY 1993 VL 1169 IS 2 BP 135 EP 145 DI 10.1016/0005-2760(93)90198-I PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA LT360 UT WOS:A1993LT36000003 PM 8343537 ER PT J AU FEN, Z DHADLY, MS YOSHIZUMI, M HILKERT, RJ QUERTERMOUS, T EDDY, RL SHOWS, TB LEE, ME AF FEN, Z DHADLY, MS YOSHIZUMI, M HILKERT, RJ QUERTERMOUS, T EDDY, RL SHOWS, TB LEE, ME TI STRUCTURAL ORGANIZATION AND CHROMOSOMAL ASSIGNMENT OF THE GENE ENCODING THE HUMAN HEPARIN-BINDING EPIDERMAL GROWTH FACTOR-LIKE GROWTH-FACTOR DIPHTHERIA-TOXIN RECEPTOR SO BIOCHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR SP1; FACTOR-ALPHA-PROMOTER; FACTOR PRECURSOR; MESSENGER-RNA; HUMAN GENOME; EXPRESSION; PROTEIN; SEQUENCE; CELLS; FOS AB Heparin-binding epidermal growth factor-like growth factor(HB-EGF) is a recently identified, potent smooth muscle cell mitogen of macrophage origin. It is expressed in a highly regulated fashion in vascular endothelial and smooth muscle cells, indicating a potentially important role for this gene in atherosclerosis. In addition, the HB-EGF precursor has recently been found to function as a receptor for diphtheria toxin. Using an HB-EGF cDNA probe, we cloned the human gene encoding HB-EGF. The HB-EGF gene contains six exons and five intervening sequences spanning 14 kb of DNA. By primer extension and S1 nuclease analysis, we located a major transcription start site (corresponding to an A residue) 14 bp beyond the 5' end of the HB-EGF cDNA. There were no TATAAA or CCAAT consensus sequences upstream of the transcription start site. The density of primer extension bands generated by RNA from endothelial cells treated with tumor necrosis factor-alpha (TNF-alpha) was 10 times higher than that of bands generated by the control, indicating that TNF-alpha increased the level of HB-EGF mRNA. Using transient reporter gene transfection experiments, we show that 2.0 kb of HB-EGF 5'-flanking sequence has promoter activity in bovine aortic endothelial cells. By analysis of DNA isolated from human-mouse somatic hybrid cell lines, we assign the HB-EGF gene to chromosome 5. By functional study, chromosome 5 has been associated with diphtheria toxin susceptibility. C1 HARVARD UNIV,SCH PUBL HLTH,CARDIOVASC BIOL LAB,665 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV CARDIOVASC,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. VANDERBILT UNIV,MED CTR,SCH MED,DIV CARDIOL,NASHVILLE,TN 37232. ROSWELL PK MEM INST,DEPT HUMAN GENET,BUFFALO,NY 14163. NR 44 TC 50 Z9 50 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD AUG 10 PY 1993 VL 32 IS 31 BP 7932 EP 7938 DI 10.1021/bi00082a014 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LV436 UT WOS:A1993LV43600014 PM 8347598 ER PT J AU KAWAGUCHI, S HEMLER, ME AF KAWAGUCHI, S HEMLER, ME TI ROLE OF THE ALPHA-SUBUNIT CYTOPLASMIC DOMAIN IN REGULATION OF ADHESIVE ACTIVITY MEDIATED BY THE INTEGRIN VLA-2 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GLYCOPROTEIN-IIB-IIIA; MONOCLONAL-ANTIBODY; CELL-ADHESION; GPIIB-IIIA; T-CELLS; EXTRACELLULAR-MATRIX; BETA-SUBUNIT; COMPLEMENT RECEPTORS; FIBRONECTIN RECEPTOR; PLATELET ACTIVATION AB To investigate the role of the alpha subunit cytoplasmic domain in the regulation of VLA-2 functional activity, we expressed several chimeric and deleted forms of the alpha2 subunit in two different human cell lines, K562 and RD. Each mutant construct formed surface VLA-2 heterodimers as efficiently as wild type alpha2 subunit, except for a construct (X2CO1127) truncated just before the consensus GFFKR cytoplasmic domain motif, that was not expressed at the cell surface. Truncation of the alpha2 cytoplasmic domain just after the GFFKR motif resulted in a complete loss of constitutive activity of VLA-2 in RD cells. If the integrin was already constitutively inactive, as in K562 cells, the cytoplasmic domain deletion had no effect. In both K562 and RD cells, cytoplasmic tail deletion eliminated up-regulation of adhesion in response to the phorbol ester, phorbol 12-myristate 13-acetate (PMA). In comparison, exchange of the alpha2 cytoplasmic domain with the alpha4 or alpha5 cytoplasmic domains had no effect on constitutive activity (in RD cells), or on constitutive inactivity (in K562 cells) and did not eliminate PMA-stimulated activity (in K562 or RD cells). These results clearly demonstrate that the cytoplasmic domain of an alpha chain (not necessarily from alpha2 itself) is required to maintain VLA-2 constitutive activity and to allow a responsiveness to PMA stimulation. In cases where VLA-2 was either constitutively inactive (as in K562 cells) or inactive due to cytoplasmic domain deletion (e.g. in RD cells), agents such as Mn2+ or the anti-beta1 monoclonal antibody TS2/16 caused a marked increase in adhesive function, thus proving that the integrins were not irreversibly inactive, and that cellular regulatory constraints could be bypassed by extracellular stimuli. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,RM M613,44 BINNEY ST,BOSTON,MA 02115. FU NIGMS NIH HHS [GM46526] NR 62 TC 85 Z9 85 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 AUG 5 PY 1993 VL 268 IS 22 BP 16279 EP 16285 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LQ336 UT WOS:A1993LQ33600031 PM 8344915 ER PT J AU DASILVA, AJ RUDD, CE AF DASILVA, AJ RUDD, CE TI A 72-KILODALTON FYN-RELATED POLYPEPTIDE (P72FYN-R) BINDS TO THE ANTIGEN-RECEPTOR/CD3 (TCR/CD3) COMPLEX SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-TYROSINE KINASE; CELL ANTIGEN RECEPTOR; AMINO-TERMINAL DOMAIN; MIDDLE-T ANTIGEN; SIGNAL TRANSDUCTION; CROSS-LINKING; CD4 RECEPTOR; LYMPHOCYTE-T; ZETA-CHAIN; P56LCK AB Protein-tyrosine kinases play crucial roles in the activation and transformation of T lymphocytes. In this study, we have identified a variant of the fyn kinase at 70-72 kDa (termed p72fyn-R) that can preferentially associate with the TcR/CD3 complex in certain T cells. Phosphoamine acid analysis revealed that the CD3-associated p72fyn-R is labeled on both tyrosine and serine/threonine residues. TcR/CD3-associated p72fyn-R could be specifically reprecipitated using anti-fyn antisera to both the N and C terminus of p59fyn. In addition, two-dimensional phosphotryptic peptide map patterns of TcR/CD3-associated p72fyn and anti-fyn-precipitable p72 were identical. By contrast, a comparison of p72fyn-R and p62fyn showed similarities and differences. p72fyn-R possesses a peptide corresponding to the autophosphorylation site that migrates in the same position as found for p59/62fyn. However, p72fyn-R possessed at least four novel phosphorylated sites labeled on serine and threonine residues that are absent in the p62fyn pattern. Phosphatase digestion experiments indicated that p72fyn-R is more resistant to dephosphorylation than p59/62fyn. Two-dimensional phosphotryptic analysis indicated that the novel serine/threonine phosphorylation sites were responsible for the resistance to phosphatase digestion. Although the exact nature of the relationship between p72fyn-R and p59/62fyn remains undetermined, these data indicate that TcR/CD3 may utilize novel variants of src-related kinases in the generation of signals which regulate T-cell growth. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP DASILVA, AJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. FU PHS HHS [R01 12069] NR 39 TC 18 Z9 18 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 AUG 5 PY 1993 VL 268 IS 22 BP 16537 EP 16543 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LQ336 UT WOS:A1993LQ33600066 PM 8344934 ER PT J AU SASSANFAR, M SZOSTAK, JW AF SASSANFAR, M SZOSTAK, JW TI AN RNA MOTIF THAT BINDS ATP SO NATURE LA English DT Article ID MOLECULAR RECOGNITION; RECEPTOR AB RNAs that contain specific high-affinity binding sites for small molecule ligands immobilized on a solid support are present at a frequency of roughly one in 10(10)-10(11) in pools of random sequence RNA molecules1,2. Here we describe a new in vitro selection procedure designed to ensure the isolation of RNAs that bind the ligand of interest in solution as well as on a solid support. We have used this method to isolate a remarkably small RNA motif that binds ATP, a substrate in numerous biological reactions and the universal biological high-energy intermediate. The selected ATP-binding RNAs contain a consensus sequence, embedded in a common secondary structure. The binding properties of ATP analogues and modified RNAs show that the binding interaction is characterized by a large number of close contacts between the ATP and RNA, and by a change in the conformation of the RNA. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP SASSANFAR, M (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115, USA. NR 17 TC 421 Z9 427 U1 3 U2 34 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD AUG 5 PY 1993 VL 364 IS 6437 BP 550 EP 553 DI 10.1038/364550a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA LQ667 UT WOS:A1993LQ66700062 PM 7687750 ER PT J AU SPITZER, TR HARRIS, NL KATTAPURAM, SV BECK, WS SCULLY, RE DOW, EC AF SPITZER, TR HARRIS, NL KATTAPURAM, SV BECK, WS SCULLY, RE DOW, EC TI A 49-YEAR-OLD MAN WITH MYELOFIBROSIS, MYELOID METAPLASIA, AND OSTEOLYTIC LESIONS OF THE LEFT FEMUR - GRANULOCYTIC SARCOMA INVOLVING BONE, SOFT-TISSUE, AND LYMPH-NODES, COMPLICATING MYELOFIBROSIS, WITH MYELOID METAPLASIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID VERA STUDY-GROUP; POLYCYTHEMIA-VERA; ESSENTIAL THROMBOCYTHEMIA; ACUTE-LEUKEMIA; MYELOPROLIFERATIVE DISORDERS; TRANSFORMATION; CELLS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SPITZER, TR (reprint author), MASSACHUSETTS GEN HOSP,BONE MARROW TRANSPLANT PROGRAM,BOSTON,MA 02114, USA. NR 32 TC 1 Z9 1 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 5 PY 1993 VL 329 IS 6 BP 417 EP 423 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA LQ339 UT WOS:A1993LQ33900009 ER PT J AU BLUMENTHAL, D AF BLUMENTHAL, D TI ADMINISTRATIVE ISSUES IN HEALTH-CARE REFORM SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID COSTS RP BLUMENTHAL, D (reprint author), MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 11 TC 7 Z9 7 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 5 PY 1993 VL 329 IS 6 BP 428 EP 429 DI 10.1056/NEJM199308053290612 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA LQ339 UT WOS:A1993LQ33900012 PM 8326980 ER PT J AU GROVE, JR PRICE, DJ BANERJEE, P BALASUBRAMANYAM, A AHMAD, MF AVRUCH, J AF GROVE, JR PRICE, DJ BANERJEE, P BALASUBRAMANYAM, A AHMAD, MF AVRUCH, J TI REGULATION OF AN EPITOPE-TAGGED RECOMBINANT RSK-1 S6 KINASE BY PHORBOL ESTER AND ERK/MAP KINASE SO BIOCHEMISTRY LA English DT Article ID RIBOSOMAL PROTEIN-S6 KINASE; MYELIN BASIC-PROTEIN; XENOPUS EGGS; PHOSPHORYLATION; PURIFICATION; SERINE; ACTIVATION; EXPRESSION; THREONINE; ANTIBODIES AB Phorbol ester tumor promoters (TPA) activate the endogenous erk/MAP kinases and Rsk S6 kinases but not the p70 S6 kinase in COS cells. DNA sequences encoding the rat Rsk-1 S6 kinase (homologous to Xenopus rskalpha), modified by insertion of a peptide epitope at the polypeptide aminoterminus, were expressed transiently in COS cells. TPA stimulates the 40S and peptide kinase activity of the recombinant epitope-tagged Rsk-1, as well as the extent of Rsk-1 autophosphorylation in vitro (P-32-Ser >> P-32-Thr). Indications that the conformation of the recombinant Rsk-1 polypeptide is substantially changed after activation by TPA in situ include a retarded mobility of the Rsk-1 polypeptide on SDS-PAGE and the appearance of new P-32-peptides during autophosphorylation in vitro. All these features of the TPA-activated Rsk-1 S6 kinase are abolished by dephosphorylation of the kinase in vitro with Ser/Thr phosphatase-2A. TPA increases P-32 incorporation into recombinant Rsk-1 by 2-3-fold (P-32-Ser >> P-32-Thr). Peptide mapping exhibits a single major P-32-peptide in Rsk-1 isolated from unstimulated cells and 10-12 additional P-32 peptides after TPA treatment in situ. Phosphorylation of basal or phosphatase-2A-treated recombinant Rsk-1 in vitro with erk2/MAP kinase increases Rsk-1 40S kinase, peptide kinase, and autophosphorylating activity, retards migration of Rsk-1 polypeptides on SDS-PAGE, and generates new sites of Rsk-1 autophosphorylation in vitro. By contrast, TPA-activated Rsk-1 is not altered in these properties by phosphorylation in vitro with erk2/MAP kinase. Activation of Rsk-1 in situ with TPA diminishes by over 90% the extent of Rsk-1 phosphorylation achieved in vitro by erk2/MAP kinase, as compared to the parallel phosphorylation of a phosphatase-2A-treated Rsk-1; basal Rsk-1 is intermediate. Peptide maps of phosphatase-2A-treated Rsk-1 after phosphorylation in vitro with erk2/MAP kinase exhibit P-32-peptides that comigrate with nearly all of the P-32-peptides present in TPA-activated-P-32 Rsk-1 labeled in situ, plus several P-32-peptides characteristic of Rsk-1 autophosphorylation in vitro. If Rsk-1 is heat inactivated to prevent autophosphorylation during treatment with erk2/MAP kinase in vitro, a greatly simplified Rsk-1 peptide map (P-32-Thr > P-32-Ser) is obtained that lacks not only the characteristic sites of Rsk-1 in vitro autophosphorylation but many of the P-32-peptides that comigrate with P-32-Rsk-1 peptides labeled in situ during TPA activation. Thus, erk/MAP kinase or enzymes with very similar specificity are likely the sole upstream activator mediating TPA stimulation of Rsk-1 kinase in COS cells and act together with Rsk-1 autophosphorylation to achieve the final Rsk-1 phosphorylation state observed in situ. C1 MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [K12 DK01410, DK17776] NR 33 TC 64 Z9 66 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 AUG 3 PY 1993 VL 32 IS 30 BP 7727 EP 7738 DI 10.1021/bi00081a018 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LV435 UT WOS:A1993LV43500018 PM 7688567 ER PT J AU BALDESSARINI, RJ KULA, NS MCGRATH, CR BAKTHAVACHALAM, V KEBABIAN, JW NEUMEYER, JL AF BALDESSARINI, RJ KULA, NS MCGRATH, CR BAKTHAVACHALAM, V KEBABIAN, JW NEUMEYER, JL TI ISOMERIC SELECTIVITY AT DOPAMINE-D(3) RECEPTORS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note DE AMINOTETRALINS; DOPAMINE-D(3) RECEPTORS; 7-OH-DPAT (7-HYDROXY-2-(N,N-DI-N-PROPYLAMINO)TETRALIN) ID RAT-BRAIN AB Racemic 7-hydroxy-N,N-dipropylaminotetralin (7-OH-DPAT) shows greater affinity for limbic-selective dopamine D3 receptors than for more ubiquitous dopamine D2 receptors. R(+)-7-OH-DPAT was prepared and evaluated in radioreceptor assays using membranes of fibroblasts expressing the human dopamine D3 receptor as well as rat striatal membranes containing dopamine D2. receptors. This enantiomer had 2-fold greater D3 affinity than the racemate and similarly greater D3 vs. D2 selectivity (64-fold). The results may facilitate development of D3 selective agents and evaluation of functions of these receptors. C1 MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,NATICK,MA. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,NATICK,MA. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,NATICK,MA. RBI,NATICK,MA. FU NIMH NIH HHS [NIMH MH-34006, NIMH MH-47370] NR 5 TC 40 Z9 40 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD AUG 3 PY 1993 VL 239 IS 1-3 BP 269 EP 270 DI 10.1016/0014-2999(93)91011-B PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LR547 UT WOS:A1993LR54700044 PM 8223909 ER PT J AU SCHEININ, A SODERLING, E SCHEININ, U GLASS, RL KALLIO, ML AF SCHEININ, A SODERLING, E SCHEININ, U GLASS, RL KALLIO, ML TI XYLITOL-INDUCED CHANGES OF ENAMEL MICROHARDNESS PARALLELED BY MICRORADIOGRAPHIC OBSERVATIONS SO ACTA ODONTOLOGICA SCANDINAVICA LA English DT Article DE CARIOGENICITY TEST; DENTAL CARIES; DENTAL ENAMEL; REMINERALIZATION; XYLITOL AB The study, aimed to analyze the feasibility of a prospective field study, was carried out in Polynesian children with rampant untreated caries. Slabs of bovine enamel were inserted for 8-12 days in cavities and subsequently replaced by permanent fillings. Before use, the surface of the slab was polished, and one half predemineralized and tested for microhardness. The follow-up in 30 subjects involved 54 slabs, 30 from negative controls with no added sweets and 24 from subjects receiving 20 g/day of xylitol in candy. The microhardness of the slabs was reassessed, and the difference between measurements calculated and tested for significance. The differences between the groups were highly significant, the predemineralized halves showing pronounced rehardening at exposure to xylitol. Parallel microradiographic observations conformed with the above findings. The results indicate that the use of a noncariogenic sweetener might be of value in high caries risk subjects. C1 UNIV TURKU,INST DENT,DEPT ORAL BIOL,SF-20520 TURKU 52,FINLAND. FORSYTH SCH RES & ADV STUDY DENT,BOSTON,MA. RP SCHEININ, A (reprint author), UNIV TURKU,INST DENT,DEPT CARIOL,LEMMINKAISENKATU 2,SF-20520 TURKU 52,FINLAND. NR 5 TC 6 Z9 6 U1 0 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6357 J9 ACTA ODONTOL SCAND JI Acta Odontol. Scand. PD AUG PY 1993 VL 51 IS 4 BP 241 EP 246 DI 10.3109/00016359309040573 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA LW199 UT WOS:A1993LW19900008 PM 8237308 ER PT J AU RIEUMONT, MJ DELUCA, SA AF RIEUMONT, MJ DELUCA, SA TI NEUROIMAGING EVALUATION IN MULTIPLE-SCLEROSIS SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Although clinical evaluation remains the cornerstone in the diagnosis of multiple sclerosis, magnetic resonance imaging (MRI) has emerged as the ancillary study of choice. An important diagnostic tool, MRI can also be used to assess disease load, activity and progression, and distinguish between acute and chronic lesions. As technology advances, it will play an essential role in monitoring disease progression and assessing the results of therapy. RP RIEUMONT, MJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 6 Z9 6 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 AUG PY 1993 VL 48 IS 2 BP 273 EP 276 PG 4 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA LR026 UT WOS:A1993LR02600011 PM 8342480 ER PT J AU BONOMI, PD FINKELSTEIN, D AISNER, S ETTINGER, D AF BONOMI, PD FINKELSTEIN, D AISNER, S ETTINGER, D TI EST-2582 PHASE-II TRIAL OF CISPLATIN IN METASTATIC OR RECURRENT THYMOMA SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS LA English DT Article DE THYMOMA; CISPLATIN-INDUCED REMISSION; PHASE-II TRIAL; ECOG ID MALIGNANT THYMOMA; INVASIVE THYMOMA; CIS-PLATINUM; CHEMOTHERAPY; CARCINOMA AB In 1982 there were four reports of cisplatin-induced remissions of invasive thymoma. These observations led the Eastern Cooperative Oncology Group (ECOG) to conduct a Phase II trial of cisplatin (50 Mg/M2 intravenously every 3 weeks). During a 4-year period 24 patients were entered on this trial; 3 were excluded because review of histologic material failed to confirm the presence of thymoma. The characteristics of the remaining 21 patients were as follows: median age, 5 1; males/females, 11/10; ECOG performance status, 0-1/2-3, 16/5; previous treatment with chemotherapy, 3; previous surgery, 20; previous radiation, 15; weight loss, <5%/greater-than-or-equal-to 5%: 17/4. One patient was eliminated from response analysis because of failure to return for follow-up tumor measurements. The following responses were observed in the remaining 20 patients. Partial remission, 2 (10%); stable disease, 8 (40%); and progression, 10 (50%). The median survival was 76 weeks, and the 2-year survival rate was 39%. Four patients experienced severe nausea and vomiting, but life-threatening and lethal toxicities were not observed. Cisplatin given at this dose was relatively ineffective in producing tumor regression in recurrent or metastatic thymoma. C1 RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MARYLAND,BALTIMORE,MD 21201. JOHNS HOPKINS UNIV HOSP,CTR ONCOL,BALTIMORE,MD 21205. FU NCI NIH HHS [CA 16116, CA 23318, CA 25988] NR 12 TC 43 Z9 46 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3732 J9 AM J CLIN ONCOL-CANC JI Am. J. Clin. Oncol.-Cancer Clin. Trials PD AUG PY 1993 VL 16 IS 4 BP 342 EP 345 DI 10.1097/00000421-199308000-00014 PG 4 WC Oncology SC Oncology GA LN787 UT WOS:A1993LN78700014 PM 8328413 ER PT J AU RADDISH, M GOLDMANN, DA KAPLAN, LC PERRIN, JM AF RADDISH, M GOLDMANN, DA KAPLAN, LC PERRIN, JM TI THE IMMUNIZATION STATUS OF CHILDREN WITH SPINA-BIFIDA SO AMERICAN JOURNAL OF DISEASES OF CHILDREN LA English DT Article ID PERTUSSIS IMMUNIZATION; HEALTH-CARE; DIPHTHERIA; VACCINE; TETANUS; RISK AB Objective.-To estimate immunization levels among children with spina bifida and describe factors that may influence immunization completeness. Research Design.-Cross-sectional survey. Setting.-Tertiary care referral center. Patients.-One hundred twenty children, from 4 months to 18 years of age, seen in the myelodysplasia clinic of Children's Hospital, Boston, Mass, from February through August 1990. Results.-Fifty-eight percent of the children 2 years of age or older and 55% of the children 7 years of age or older had completed the immunization series recommended by the American Academy of Pediatrics. All but one child had an identified primary care provider. Lower immunization levels at 24 months of age occurred in older and in poorer children. Most children (80%) received the first diphtheria and tetanus toxoids and pertussis and oral poliovirus vaccines on time. Immunization delay increased from 20% to 50% through the 18-month diphtheria and tetanus toxoids and pertussis and oral poliovirus vaccines and declined to 24% at school entry. Conclusions.-Many children with spina bifida are underimmunized despite having an identified source of primary care. C1 CHILDRENS HOSP MED CTR,HOSP EPIDEMIOL PROGRAM,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV CONNECTICUT,CHILDRENS HOSP,CTR CHILDREN SPECIAL HLTH CARE NEEDS,NEWINGTON,CT. RP RADDISH, M (reprint author), UNIV UTAH,DEPT PEDIAT,SALT LAKE CITY,UT 84112, USA. NR 25 TC 21 Z9 21 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0002-922X J9 AM J DIS CHILD JI Am. J. Dis. Child. PD AUG PY 1993 VL 147 IS 8 BP 849 EP 853 PG 5 WC Pediatrics SC Pediatrics GA LR711 UT WOS:A1993LR71100017 PM 8352219 ER PT J AU NATOWICZ, MR ALPER, JK ALPER, JS AF NATOWICZ, MR ALPER, JK ALPER, JS TI GENETIC CONDITIONS AND THE SCOPE OF THE AMERICANS-WITH-DISABILITIES-ACT SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Letter ID DISCRIMINATION C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. UNIV MASSACHUSETTS,CTR DISABIL LAW,BOSTON,MA 02125. UNIV MASSACHUSETTS,DEPT CHEM,BOSTON,MA 02125. RP NATOWICZ, MR (reprint author), EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MED GENET,WALTHAM,MA, USA. NR 7 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 AUG PY 1993 VL 53 IS 2 BP 534 EP 535 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA LN820 UT WOS:A1993LN82000032 PM 8328467 ER PT J AU HEYMANN, SJ BREWER, TF AF HEYMANN, SJ BREWER, TF TI THE INFECTIOUS RISKS OF TRANSFUSIONS IN THE UNITED-STATES - A DECISION-ANALYTIC APPROACH SO AMERICAN JOURNAL OF INFECTION CONTROL LA English DT Article AB Introduction: The development of AIDS as a result of HIV transmission and of cirrhosis as a result of chronic non-A, non-B hepatitis are the greatest infectious risks associated with transfusion in the United States. The goal of this study is to provide explicit quantitative guidelines to determine when the risk of death from all causes associated with transfusion exceeds the risk associated with anemia. Methods: This study uses a decision-analytic model. Results: On the basis of reported transfusion complication rates and an independent worst-case calculation of the risk of AIDS and non-A, non-B hepatitis, transfusion with red blood cells should be recommended as long as each unit received reduces the patient's risk of dying from anemia by at least 1/1100. Discussion: Because of the relative safety of the blood supply as a result of universal screening and donor deferral, the overestimation in practice of fatal infectious complications, and the possible underestimation of the risk of anemia, undertransfusion has the potential to be as serious a problem in the United States as is overtransfusion. Although caution should be exercised not to undertransfuse when a patient has an appreciable risk of anemia-associated death, we must be wary not to overtransfuse for temporary relief of morbidity. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,FRUIT ST,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0196-6553 J9 AM J INFECT CONTROL JI Am. J. Infect. Control PD AUG PY 1993 VL 21 IS 4 BP 174 EP 182 DI 10.1016/0196-6553(93)90028-3 PG 9 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA LT602 UT WOS:A1993LT60200002 PM 8239047 ER PT J AU RUSSELL, GJ NAGLERANDERSON, C ANDERSON, P BHAN, AK AF RUSSELL, GJ NAGLERANDERSON, C ANDERSON, P BHAN, AK TI CYTOTOXIC POTENTIAL OF INTRAEPITHELIAL LYMPHOCYTES (IELS) - PRESENCE OF TIA-1, THE CYTOLYTIC GRANULE-ASSOCIATED PROTEIN, IN HUMAN IELS IN NORMAL AND DISEASED INTESTINE SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Note ID T-CELL RECEPTOR; MONOCLONAL-ANTIBODY; PERFORIN; EXPRESSION; GUT AB Human intestinal intraepithelial lymphocytes (IELs) have phenotypic characteristics of cytotoxic T cells, yet a cytotoxic function has not been demonstrated in redirected lysis assays. A monoclonal antibody that reacts with a cytotoxic granule-associated protein, TIA-1, was used in this study to identify this protein in many, but not all, IELs of normal human proximal small intestine. Furthermore, in active celiac disease, in which the number of IELs is significantly increased, a corresponding increase in the number of TIA-1 cells was found. These results indicate that whereas cytotoxicity of human IELs has been difficult to demonstrate, they contain at least one of the proteins associated with cytotoxicity, and a failure to demonstrate this function may be related to the in vitro assay system used. C1 CHILDRENS HOSP MED CTR,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP RUSSELL, GJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT COX 5,100 BLOSSOM ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK33506, DK43351] NR 18 TC 33 Z9 33 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 AUG PY 1993 VL 143 IS 2 BP 350 EP 354 PG 5 WC Pathology SC Pathology GA LQ675 UT WOS:A1993LQ67500005 PM 8342592 ER PT J AU BACHINSKY, DR GANG, Z NILES, JL MCLAUGHLIN, M ABBATE, M ANDRES, G BROWN, D MCCLUSKEY, RT AF BACHINSKY, DR GANG, Z NILES, JL MCLAUGHLIN, M ABBATE, M ANDRES, G BROWN, D MCCLUSKEY, RT TI DETECTION OF 2 FORMS OF GP330 - THEIR ROLE IN HEYMANN NEPHRITIS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID BRUSH-BORDER ANTIGENS; RECEPTOR-ASSOCIATED PROTEIN; LIPOPROTEIN RECEPTOR; ALPHA-2-MACROGLOBULIN RECEPTOR; MONOCLONAL-ANTIBODIES; LDL-RECEPTOR; ULTRASTRUCTURAL-LOCALIZATION; IMMUNOELECTRON MICROSCOPY; INDUCED REDISTRIBUTION; MEMBRANE GLYCOPROTEIN AB Heymann nephritis is characterized by glomerular immune deposits that contain a glycoprotein called gp330. The deposits are believed to result from shedding of immune complexes formed on podocytes. Complexes are also shed from proximal tubule cells, when antibodies combine with gp330 on the cell surface. We performed the present study to investigate what portion of the gp330 molecule is shed, using a rabbit antiserum against a peptide deduced to be in the cytoplasmic domain of gp330, as well as a rabbit antiserum and two monoclonal antibodies that recognize extracellular epitopes of gp330. The anti-cytoplasmic peptide antiserum precipitated from Fx1A (a crude renal cortical membrane preparation), a protein with a mass of about 440 kd that was reactive with two monoclonal anti-gp330 antibodies. (In our experiments, the protein called gp330 generally has a mass estimated to be about 440 kd.) The anti-cytoplasmic peptide antiserum also reacted with a truncated gp330 protein produced in transfected COS cells. Immunohistochemical studies showed that all the antibodies recognized the same group of epithelial cells. However, as seen in immunoultrastructural studies of proximal tubules, the anti-cytoplasmic peptide antiserum reacted only with components at the base of microvilli, whereas the anti-gp330 ectodomain antibodies identified material not only at the base, but over the surface of microvilli as well. In rats with Heymann nephritis, glomerular deposits and material shed into tubule lumens reacted with antibodies against extracellular epitopes of gp330, but not with the anticytoplasmic peptide antiserum. We propose that there are two forms of gp330 on the cell surface of proximal renal tubules. One form is restricted to coated pit regions at the base of microvilli and has a cytoplasmic domain containing a sequence deduced from a partial complementary DNA encoding gp330. The other form is present over microvilli (and possibly at the base of microvilli as well) and lacks the cytoplasmic domain deduced from the complementary DNA. The complexes that are shed in Heymann nephritis contain either a portion of gp330 cleaved from the full-length molecule or a form of gp330 that lacks the cytoplasmic domain. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,149 13TH ST,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED SERV,RENAL UNIT,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT GENET,BOSTON,MA 02129. FU NCI NIH HHS [5-T32-CA 09216-12]; NIDDK NIH HHS [DK 38452, DK-36807] NR 41 TC 55 Z9 56 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 AUG PY 1993 VL 143 IS 2 BP 598 EP 611 PG 14 WC Pathology SC Pathology GA LQ675 UT WOS:A1993LQ67500030 PM 8342605 ER PT J AU BAGBY, SP KIRK, EA MITCHELL, LH OREILLY, MM HOLDEN, WE STENBERG, PE BAKKE, AC AF BAGBY, SP KIRK, EA MITCHELL, LH OREILLY, MM HOLDEN, WE STENBERG, PE BAKKE, AC TI PROLIFERATIVE SYNERGY OF ANG-II AND EGF IN PORCINE AORTIC VASCULAR SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE HYPERTROPHY; HYPERPLASIA; FLOW CYTOMETRY; CELL CYCLE ANALYSIS; PROTEIN SYNTHESIS; DEOXYRIBONUCLEIC ACID SYNTHESIS; CELL SIZE; HYDROGEN-3-LABELED THYMIDINE INCORPORATION; SULFUR-35-LABELED METHIONINE INCORPORATION; VASCULAR GROWTH; INDOMETHACIN; LOSARTAN ID EPIDERMAL GROWTH-FACTOR; ANGIOTENSIN-II; DNA-SYNTHESIS; FLOW-CYTOMETRY; C-MYC; RAT; HYPERTROPHY; HYPERTENSION; STIMULATION; RECEPTORS AB To test growth effects of angiotensin II (ANG II) in porcine vascular smooth muscle cells (VSMC) and potential ANG II synergy with epidermal growth factor (EGF), we exposed subconfluent, near-quiescent porcine aortic VSMC to ANG II, EGF, or ANG II + EGF (each 10(-9) M) in Dulbecco's modified Eagle's-Ham's F-12 medium with insulin + 0.4% fetal calf serum (FCS) selected for minimal ANG II-degrading capacity. Cell number and DNA and protein synthesis (by [H-3]thymidine and [S-35]methionine incorporation, respectively) were determined serially over 1-6 days. ANG II alone induced an early 20% increase and then a plateau in cell number over the 0.4% FCS control (P < 0.01; n = 8), thus without sustained increase in proliferation rate. Yet ANG II alone did not increase fractional DNA or protein synthesis (each as cpm/10(3) cells) and, by flow cytometry, reduced S phase fraction without increase in cell size. EGF alone induced brisk DNA synthesis yet minimal cell division over days 0-4, thus late-cycle arrest. ANG II + EGF, despite no increase in fractional DNA or protein synthesis rates over EGF alone, induced significant indomethacin-resistant dose-dependent (P < 0.001) increase in cell proliferation rate over EGF alone with a median effective dose of 5 x 10(-10) M ANG II, thus proliferative synergy. We propose that 1) ANG II induces a subpopulation of cells arrested in or beyond S phase to proceed through mitosis but does not influence G1 traversal or S phase entry and 2) ANG II + EGF achieve proliferative synergy by complementary actions at sequential cell cycle loci, with EGF supporting progression from G0/G1 to S phase and ANG II inducing completion of mitosis by cells already in or beyond S phase (''late-cycle completion''). C1 PORTLAND VET AFFAIRS MED CTR,DEPT MED,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,DEPT PATHOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NR 30 TC 25 Z9 26 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 AUG PY 1993 VL 265 IS 2 BP F239 EP F249 PN 2 PG 11 WC Physiology SC Physiology GA LW032 UT WOS:A1993LW03200087 PM 8368333 ER PT J AU IVESTER, CT KENT, RL TAGAWA, H TSUTSUI, H IMAMURA, T COOPER, G MCDERMOTT, PJ AF IVESTER, CT KENT, RL TAGAWA, H TSUTSUI, H IMAMURA, T COOPER, G MCDERMOTT, PJ TI ELECTRICALLY STIMULATED CONTRACTION ACCELERATES PROTEIN-SYNTHESIS RATES IN ADULT FELINE CARDIOCYTES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MYOSIN HEAVY CHAIN; 2,3-BUTANEDIONE MONOXIME; TRANSLATION; HYPERTROPHY ID HEART-CELLS; 2,3-BUTANEDIONE MONOXIME; CARDIAC MYOCYTES; VENTRICULAR MYOCYTES; MAMMALIAN MYOCARDIUM; THYROID-HORMONE; GENE-EXPRESSION; LOAD REGULATION; BREAST MUSCLE; HYPERTROPHY AB Cardiocytes were induced to contract via electrical field stimulation with an 8 V/cm electrical square-wave pulse of 5 ms at 0.125-2.0 Hz for up to 6 h. Protein synthesis rates were measured as rate of incorporation of [H-3]-phenylalanine into total cell protein. Rates of protein synthesis were accelerated 43 +/- 4%, P < 0.001, by 4 h. The acceleration of total protein synthesis showed a frequency dependence between 0.125 and 0.5 Hz. In addition to accelerating rates of total protein synthesis, electrical stimulation of contraction accelerated fractional rates of synthesis of myosin heavy chain by 42 +/-8%, P < 0.05. Protein synthesis rates were not accelerated upon electrical stimulation using subthreshold voltages. Addition of 100 ng/ml of actinomycin D had no effect on the ability of electrical stimulation of contraction to accelerate protein synthesis. To uncouple excitation-contraction coupling, 2,3-butanedione monoxime (BDM) was used to block actin-myosin cross-bridge interactions. BDM significantly decreased the ability of electrical stimulation to accelerate protein synthesis rates. C1 MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT MED,CHARLESTON,SC 29401. MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT CELL BIOL & ANAT,CHARLESTON,SC 29401. MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT PHARMACOL,CHARLESTON,SC 29401. MED UNIV S CAROLINA,GAZES CARDIAC RES INST,DEPT PHYSIOL,CHARLESTON,SC 29401. MED UNIV S CAROLINA,RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. RI Tsutsui, Hiroyuki/A-4070-2012 NR 44 TC 49 Z9 49 U1 2 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD AUG PY 1993 VL 265 IS 2 BP H666 EP H674 PN 2 PG 9 WC Physiology SC Physiology GA LW032 UT WOS:A1993LW03200033 PM 8368369 ER PT J AU SILVA, P EPSTEIN, FH KARNAKY, KJ REICHLIN, S FORREST, JN AF SILVA, P EPSTEIN, FH KARNAKY, KJ REICHLIN, S FORREST, JN TI NEUROPEPTIDE-Y INHIBITS CHLORIDE SECRETION IN THE SHARK RECTAL GLAND SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE SQUALUS-ACANTHIAS; NEUROTRANSMITTERS; VASOACTIVE INTESTINAL PEPTIDE; ADENOSINE 3',5'-CYCLIC MONOPHOSPHATE; THEOPHYLLINE; FORSKOLIN; ADENYLATE CYCLASE; PROCAINE; CALCIUM CHANNEL BLOCKERS ID VASOACTIVE INTESTINAL POLYPEPTIDE; ION-TRANSPORT; PEPTIDE-YY; RAT; SOMATOSTATIN; VIP; DOGFISH; CELLS; IMMUNOREACTIVITY; LOCALIZATION AB We studied the effects of the 36-amino acid peptide, neuropeptide Y (NPY), on salt secretion by the rectal gland of Squalus acanthias. We used three preparations: whole isolated perfused glands, freshly prepared separated rectal gland tubules, and confluent monolayers of cultured rectal gland cells. In perfused glands NPY inhibited secretion stimulated by vasoactive intestinal peptide (VIP), forskolin, or adenosine 3',5'-cyclic monophosphate (cAMP) and theophylline. Maximal inhibition of 63 +/- 3.4% was seen at 3 x 10(-8) M NPY, with half-maximal effect at 3 x 10(-9) M. NPY did not inhibit the basal activity of rectal gland adenylate cyclase or that stimulated by VIP. The inhibitory action of NPY was not prevented by procaine, nifedipine, or diltiazem, suggesting that it was not secondary to the release of somatostatin or other unknown neurotransmitters from rectal gland nerves. In confirmation, somatostatin was not detected in the venous effluent after administration of NPY. NPY also inhibited transport-related oxygen consumption in separated rectal gland tubules and inhibited short-circuit current generated by confluent monolayers of primary cultures of rectal gland cells. The results indicate that NPY inhibits chloride secretion by a direct action on cells of the shark rectal gland at a site distal to the generation of cAMP. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,CTR STUDY KIDNEY DIS,JOSLIN DIABETES CTR,BOSTON,MA 02215. TUFTS UNIV,SCH MED,DEPT MED,BOSTON,MA 02111. MED UNIV S CAROLINA,DEPT ANAT & CELL BIOL,CHARLESTON,SC 29401. MED UNIV S CAROLINA,MARINE BIOMED & ENVIRONM SCI PROGRAM,CHARLESTON,SC 29401. YALE UNIV,SCH MED,DEPT MED,NEW HAVEN,CT 06520. MT DESERT ISL BIOL LAB,SALSBURY COVE,ME 04672. RP SILVA, P (reprint author), NEW ENGLAND DEACONESS HOSP,DEPT MED,110 FRANCIS ST,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK-39429, DK-18078, DK-16684] NR 39 TC 20 Z9 20 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD AUG PY 1993 VL 265 IS 2 BP R439 EP R446 PN 2 PG 8 WC Physiology SC Physiology GA LW032 UT WOS:A1993LW03200073 PM 8103643 ER PT J AU FAVA, M ROSENBAUM, JF PAVA, JA MCCARTHY, MK STEINGARD, RJ BOUFFIDES, E AF FAVA, M ROSENBAUM, JF PAVA, JA MCCARTHY, MK STEINGARD, RJ BOUFFIDES, E TI ANGER ATTACKS IN UNIPOLAR DEPRESSION .1. CLINICAL CORRELATES AND RESPONSE TO FLUOXETINE TREATMENT SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DISORDERS; HOSTILITY; SYMPTOM AB Objective: Anger attacks are sudden, intense spells of anger associated with a surge of autonomic arousal including such symptoms as tachycardia, sweating, flushing, and a feeling of being out of control. The purpose of this study was to determine whether depressed patients with and without anger attacks exhibit distinct psychological characteristics and whether these attacks respond to treatment with fluoxetine. Method: The Anger Attacks Questionnaire, the Hamilton Rating Scale for Depression, the Symptom Questionnaire, and the Cook-Medley Hostility, Scale were among the scales administered at the Depression Research Program of the Clinical Psychopharmacology Unit at the Massachusetts General Hospital to 127 medication-free outpatients with major depression and to 85 of these patients after 8 weeks of open treatment with a fixed dose (20 mg/day) of fluoxetine. Results: At baseline, 44% of the depressed outpatients reported having anger attacks; these patients had significantly higher scores on measures of anxiety, somatization, and state and trait hostility than did the subjects who did not exhibit such attacks. After treatment, there were significant reductions in these measures, and the anger attacks disappeared in the majority (71%) of the patients who bad previously reported them. There was a trend toward greater overall clinical improvement for patients with anger attacks than for patients without them. Conclusions: This study identified a subgroup of highly irritable and hostile depressed patients who report the presence of anger attacks and have a psychological profile distinct from that of depressed patients without anger attacks. Furthermore, fluoxetine treatment appears to be beneficial in reducing anger and hostility in these patients. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FAVA, M (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 20 TC 191 Z9 192 U1 1 U2 4 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD AUG PY 1993 VL 150 IS 8 BP 1158 EP 1163 PG 6 WC Psychiatry SC Psychiatry GA LP806 UT WOS:A1993LP80600004 PM 7848377 ER PT J AU ROSENBAUM, JF FAVA, M PAVA, JA MCCARTHY, MK STEINGARD, RJ BOUFFIDES, E AF ROSENBAUM, JF FAVA, M PAVA, JA MCCARTHY, MK STEINGARD, RJ BOUFFIDES, E TI ANGER ATTACKS IN UNIPOLAR DEPRESSION .2. NEUROENDOCRINE CORRELATES AND CHANGES FOLLOWING FLUOXETINE TREATMENT SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID THYROTROPIN-RELEASING-HORMONE; ENDOGENOUS-DEPRESSION; PROLACTIN RESPONSE; PSYCHIATRIC-PATIENTS; HEALTHY-SUBJECTS; TRH; SECRETION; AGGRESSION; DISORDERS; AGE AB Objective: Neuroendocrine derangements have been reported in both depression and aggressive behavior. The purpose of this study was to evaluate whether the subset of depressed patients with anger attacks have a distinctive neuroendocrine abnormality. Method: The thyrotropin-releasing hormone (TRH) test was administered to 25 patients with major depression, 12 of whom reported having anger attacks, at the Depression Research Program of the Clinical Psychopharmacology Unit at the Massachusetts General Hospital. Twenty-two subjects underwent the TRH test again after 8 weeks of treatment with fluoxetine, a relatively selective serotonin uptake inhibitor. Results: The depressed patients with anger attacks bad a blunted prolactin response to TRH stimulation compared to the depressed patients without anger attacks. Treatment with fluoxetine was followed by an overall increase in the prolactin response to TRH among the depressed patients with anger attacks. The prolactin response to TRH also tended to predict the degree of response to treatment. Conclusions: These results suggest that the subset of depressed patients with anger attacks may have a greater central serotonergic dysregulation than depressed patients without such attacks. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ROSENBAUM, JF (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 40 TC 45 Z9 46 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD AUG PY 1993 VL 150 IS 8 BP 1164 EP 1168 PG 5 WC Psychiatry SC Psychiatry GA LP806 UT WOS:A1993LP80600005 PM 8328558 ER PT J AU BERNSTEIN, DP COHEN, P VELEZ, CN SCHWABSTONE, M SIEVER, LJ SHINSATO, L AF BERNSTEIN, DP COHEN, P VELEZ, CN SCHWABSTONE, M SIEVER, LJ SHINSATO, L TI PREVALENCE AND STABILITY OF THE DSM-III-R PERSONALITY-DISORDERS IN A COMMUNITY-BASED SURVEY OF ADOLESCENTS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DISTURBANCE; DYSFUNCTION AB Objective: The purpose of this study was to estimate the prevalence, concurrent validity, and stability of DSM-III-R personality disorders in a large community-based sample of adolescents. Method: A randomly selected community sample of 733 youths ranging in age from 9 to 19 years was followed over a 2-year period. The protocol consisted of structured interviews with the adolescents and their mothers and self-report questionnaires. Algorithms for 1 0 DSM-III-R axis II disorders were developed to produce diagnoses at two levels of severity; these were validated against multiple indicators of distress and functional impairment. Results: The overall prevalence of personality disorders peaked at age 12 in boys and at age 13 in girls and declined thereafter. Obsessive-compulsive personality disorder was the most prevalent moderate axis II disorder, narcissistic personality disorder the most prevalent severe disorder, and schizotypal personality disorder the least prevalent axis II disorder, based on both moderate and severe diagnostic thresholds. All moderate axis II disorders were associated with significantly greater odds for at least five of 12 diagnostic validators. Longitudinal follow-up revealed that although most axis II disorders did not persist over a 2-year period, subjects with disorders identified earlier remained at elevated risk for receiving a diagnosis again at follow-up. Conclusions: These findings suggest that a substantial minority of adolescents who are not in treatment qualify for DSM-III-R personality disorder diagnoses and that these diagnoses are associated with increased risk of psychological distress and functional impairment. C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. NEW YORK STATE PSYCHIAT INST & HOSP,DEPT PSYCHIAT,NEW YORK,NY 10032. NEW YORK STATE PSYCHIAT INST & HOSP,DEPT EPIDEMIOL,NEW YORK,NY 10032. RP BERNSTEIN, DP (reprint author), BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,PSYCHIAT SERV 116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. FU NIDA NIH HHS [DA-03188]; NIMH NIH HHS [NIMH MH-36971] NR 20 TC 244 Z9 249 U1 2 U2 12 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD AUG PY 1993 VL 150 IS 8 BP 1237 EP 1243 PG 7 WC Psychiatry SC Psychiatry GA LP806 UT WOS:A1993LP80600018 PM 8328570 ER PT J AU BHALLA, M SILVER, RM SHEPARD, JAO MCLOUD, TC AF BHALLA, M SILVER, RM SHEPARD, JAO MCLOUD, TC TI CHEST CT IN PATIENTS WITH SCLERODERMA - PREVALENCE OF ASYMPTOMATIC ESOPHAGEAL DILATATION AND MEDIASTINAL LYMPHADENOPATHY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID INTERSTITIAL LUNG-DISEASE; HIGH-RESOLUTION CT; PROGRESSIVE SYSTEMIC-SCLEROSIS; FIBROSING ALVEOLITIS; COMPUTED-TOMOGRAPHY; RADIOGRAPHY; PNEUMONIA AB OBJECTIVE. The high-resolution CT findings of chronic diff use interstitial lung disease associated with scleroderma have been reported previously. This study determined the prevalence of esophageal dilatation and mediastinal adenopathy on high-resolution CT scans in patients with this disease. MATERIALS AND METHODS. We retrospectively reviewed the high-resolution CT scans of 25 patients with scleroderma who had diffuse interstitial lung disease. Esophageal dilatation was diagnosed if the esophagus below the aortic arch had a single, large, nonloculated collection of intraluminal air on four or more consecutive axial images and if the luminal diameter of such an air-filled esophagus exceeded 10 mm in the coronal plane. The presence of fluid or an air-fluid level was also considered abnormal. For mediastinal adenopathy, we used the American Thoracic Society lymph node mapping scheme and the size criteria described previously. RESULTS. Asymptomatic esophageal dilatation was detected in 20 patients (80%) and mediastinal adenopathy was present in 15 (60%). CONCLUSION. Our results suggest that CT is useful in the detection of mediastinal adenopathy and asymptomatic esophageal involvement in patients with scleroderma. These findings can be used to narrow the differential diagnosis in patients in whom CT shows diffuse interstitial lung disease. Furthermore, the early detection of esophageal involvement in these patients shows the need for treatment to forestall the complications of esophageal dysmotility and accompanying chronic gastroesophageal reflux. C1 MED UNIV S CAROLINA,DEPT MED,DIV RHEUMATOL & IMMUNOL,CHARLESTON,SC 29425. RP BHALLA, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 25 TC 41 Z9 45 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 AUG PY 1993 VL 161 IS 2 BP 269 EP 272 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LW472 UT WOS:A1993LW47200007 PM 8333359 ER PT J AU STALLMEYER, MJB CHEW, FS AF STALLMEYER, MJB CHEW, FS TI EOSINOPHILIC GASTROENTERITIS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP STALLMEYER, MJB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 3 TC 5 Z9 6 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD AUG PY 1993 VL 161 IS 2 BP 296 EP 296 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LW472 UT WOS:A1993LW47200013 PM 8333365 ER PT J AU THRALL, JH AF THRALL, JH TI RADIOLOGY PERFORMED BY NONRADIOLOGISTS IN THE UNITED-STATES - WHO DOES WHAT SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note ID PHYSICIANS RP THRALL, JH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,FOUNDERS HOUSE 2,55 FRUIT ST,BOSTON,MA 02114, USA. NR 8 TC 4 Z9 4 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 AUG PY 1993 VL 161 IS 2 BP 430 EP 431 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LW472 UT WOS:A1993LW47200042 ER PT J AU WITTENBERG, J AF WITTENBERG, J TI THE DIAGNOSIS OF COLONIC OBSTRUCTION ON PLAIN ABDOMINAL RADIOGRAPHS - START WITH THE CECUM, LEAVE THE RECTUM TO LAST SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article RP WITTENBERG, J (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114, USA. NR 5 TC 2 Z9 2 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 AUG PY 1993 VL 161 IS 2 BP 443 EP 444 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LW472 UT WOS:A1993LW47200045 PM 8333391 ER PT J AU KLEINMAN, GM YOUNG, RH SCULLY, RE AF KLEINMAN, GM YOUNG, RH SCULLY, RE TI PRIMARY NEUROECTODERMAL TUMORS OF THE OVARY - A REPORT OF 25 CASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE OVARY; NEUROECTODERMAL TUMOR; MONODERMAL TERATOMA; GLIOMA; NEUROBLASTOMA; EPENDYMOMA ID LEYDIG-CELL TUMORS; MATURE CYSTIC TERATOMA; MIXED MULLERIAN TUMOR; NEURO-BLASTOMA; CLINICOPATHOLOGICAL ANALYSIS; DIFFERENTIAL-DIAGNOSIS; ROUND-CELL; EPENDYMOMA; CARTILAGE; CARCINOMA AB Twenty-five primary ovarian neuroectodermal tumors occurred in females from 6 to 69 (average, 23) years of age; they had the usual presenting symptoms of abdominal swelling or pain. The tumors, which varied from cystic to solid, ranged from 4 to 20 cm (average, 14 cm) in diameter. Microscopic examination revealed three histologic categories-differentiated, primitive, and anaplastic- with the tumors in the first group having a better prognosis than those in the other two groups. Five of the six differentiated gliomas were pure ependymomas, and one was an ependymoma with an astrocytoma component; none contained teratomatous elements. Two patients with stage I tumors were alive 4 and 5 years postoperatively. The one patient with stage IIA tumor was free of disease at 3 years; one of the two patients with a stage III tumor died of tumor after 5 years, and one had two recurrences but was alive and well at 5 years. Twelve tumors were primitive, resembling medulloepithelioma, ependymoblastoma, neuroblastoma or medulloblastoma. Seven tumors had teratomatous foci of other types, including three dermoid cysts. Three patients with stage I tumors were alive at 7 months, 3 years, and 9 years postoperatively; six of seven patients with stage Ill tumors died of tumor 2 to 20 months postoperatively, and one was alive with disease at 1 year. Seven tumors were anaplastic, resembling glioblastoma. All contained foci of squamous epithelium. One patient with stage IA tumor died of tumor at 2 years, but two were free of tumor after 3 and 4 years. One patient with a stage IIA tumor died of disease after 5 years; another was alive with tumor at 1 year. One patient with a stage III tumor died after 4 months. The differential diagnosis of neuroectodermal tumors of the ovary includes many primary and metastatic ovarian neoplasms of diverse types, and distinction among them is important. Neuroectodermal tumors should be considered when examining unusual ovarian tumors, particularly if the patient is young. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 61 TC 119 Z9 125 U1 1 U2 2 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 AUG PY 1993 VL 17 IS 8 BP 764 EP 778 DI 10.1097/00000478-199308000-00002 PG 15 WC Pathology; Surgery SC Pathology; Surgery GA LN339 UT WOS:A1993LN33900002 PM 8393302 ER PT J AU KAPLAN, MA JACOBSON, JO FERRY, JA HARRIS, NL AF KAPLAN, MA JACOBSON, JO FERRY, JA HARRIS, NL TI T-CELL LYMPHOMA OF THE VULVA IN A RENAL-ALLOGRAFT RECIPIENT WITH ASSOCIATED HEMOPHAGOCYTOSIS SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE T-CELL LYMPHOMA, VULVAR LYMPHOMA; POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDER; IMMUNOSUPPRESSION; EPSTEIN-BARR VIRUS; HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I ID EPSTEIN-BARR-VIRUS; ANGIOCENTRIC IMMUNOPROLIFERATIVE LESIONS; TRANSPLANT RECIPIENT; MOLECULAR ANALYSIS; VIRAL-DNA; IMMUNODEFICIENCY; PATIENT; INFECTION; GENES; REARRANGEMENT AB The risk of B-cell lymphoma is greatly increased in transplant patients, whereas T-cell lymphomas have only rarely been reported in these patients. Although T-cell lymphomas in nonimmunosuppressed patients may be associated with either human T-cell lymphotropic virus type I (HTLV-I) or Epstein-Barr virus (EBV), these viruses have not been reported in association with post-transplant T-cell lymphoma. We report a case of T-cell lymphoma of the vulva arising in a renal allograft recipient receiving azathioprine and prednisone. The unusual clinical presentation led to difficulty in diagnosis because of a resemblance to either an infectious process or squamous cell carcinoma. The large cell lymphoma involved the dermis and subcutaneous fat of the vulva and was associated with hemophagocytosis in lymph nodes and bone marrow. The tumor had a mature, aberrant T-cell immunophenotype (CD3+ CD4+ CD7+ CD2- CD5- CD30+). Rearrangement of the T-cell receptor beta and gamma chain genes was found, but there was no evidence of either EBV or HTLV-I genomes. This case adds to the clinical and morphologic spectrum of T-cell lymphomas reported in allograft recipients and suggests that known lymphotropic viruses do not commonly have a role in post-transplant T-cell lymphoma. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,WARREN 2,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,HEMATOL ONCOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 46 TC 55 Z9 56 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 AUG PY 1993 VL 17 IS 8 BP 842 EP 849 DI 10.1097/00000478-199308000-00010 PG 8 WC Pathology; Surgery SC Pathology; Surgery GA LN339 UT WOS:A1993LN33900010 PM 8393304 ER PT J AU SILVERSTEIN, JH SILVA, DA IBERTI, TJ AF SILVERSTEIN, JH SILVA, DA IBERTI, TJ TI OPIOID ADDICTION IN ANESTHESIOLOGY SO ANESTHESIOLOGY LA English DT Review DE NARCOTIC DEPENDENCE; PHYSICIAN IMPAIRMENT; SUBSTANCE ABUSE ID SUBSTANCE-ABUSE; IMPAIRED PHYSICIANS; TRAINING-PROGRAMS; DRUG-ABUSE; LEGAL ISSUES; ALCOHOLISM; URINE; NALTREXONE; ADULTERANTS; EXCRETION C1 CUNY MT SINAI SCH MED,DEPT ANESTHESIOL,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT SURG,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. RP SILVERSTEIN, JH (reprint author), BRONX VET AFFAIRS MED CTR,ANESTHESIA SECT,BOX 112A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 94 TC 17 Z9 21 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD AUG PY 1993 VL 79 IS 2 BP 354 EP 375 DI 10.1097/00000542-199308000-00022 PG 22 WC Anesthesiology SC Anesthesiology GA LP761 UT WOS:A1993LP76100021 PM 8267716 ER PT J AU STEINER, LA DROP, LJ CASTELLI, I ALFILLE, PH SCHOUTEN, R WELCH, CA AF STEINER, LA DROP, LJ CASTELLI, I ALFILLE, PH SCHOUTEN, R WELCH, CA TI DIAGNOSIS OF MYOCARDIAL INJURY BY REAL-TIME RECORDING OF ST SEGMENTS OF THE ELECTROCARDIOGRAM IN A PATIENT RECEIVING GENERAL-ANESTHESIA FOR ELECTROCONVULSIVE-THERAPY SO ANESTHESIOLOGY LA English DT Note DE HEART, ELECTROCARDIOGRAM; MYOCARDIAL ISCHEMIA; MONITOR SYSTEMS; ELECTROCONVULSIVE THERAPY, CARDIOVASCULAR COMPLICATIONS ID RESPONSES; ISCHEMIA AB ELECTROCONVULSIVE therapy (ECT) is associated with short-lasting but important changes in autonomic nervous system activity.1-3 The autonomic response to ECT is characterized by initial parasympathetic stimulation immediately followed by subsequent sympathetic stimulation. Typically, transient bradycardia is first seen immediately after the seizure, after which sinus tachycardia and arterial hypertension are observed, frequently associated with cardiac arrhythmias.2-4 Though these changes usually are self-limited, a hyperdynamic state in most elderly patients represents an important risk factor.5 Hypotension after ECT warrants an immediate search for a cause. In this case report, we present arterial hypotension immediately after ECT with subsequent refractory myocardial failure and subendocardial infarction. We made the initial diagnosis of myocardial injury because a tabulated record of real-time ST-segment data was available at the bedside, allowing immediate decisions about appropriate pharmacologic support measures. To validate the observations in this patient, we also present data on ST segments of the electrocardiogram (ECG) and hemodynamic variables recorded during the first treatment in a comparison group of ten patients with the admission diagnosis of depression who presented for ECT. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,ANESTHESIA SERV,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RI Steiner, Luzius/C-9836-2011 NR 15 TC 9 Z9 9 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 AUG PY 1993 VL 79 IS 2 BP 383 EP 388 DI 10.1097/00000542-199308000-00026 PG 6 WC Anesthesiology SC Anesthesiology GA LP761 UT WOS:A1993LP76100025 PM 8342848 ER PT J AU SWERDLOW, DL GRIFFIN, PM AF SWERDLOW, DL GRIFFIN, PM TI THE HEMOLYTIC-UREMIC SYNDROME AND ESCHERICHIA-COLI O157-H7 INFECTION - RESPONSE SO ANNALS OF INTERNAL MEDICINE LA English DT Letter ID O157-H7; OUTBREAK C1 CTR DIS CONTROL & PREVENT, ATLANTA, GA 30333 USA. RP SWERDLOW, DL (reprint author), MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD AUG 1 PY 1993 VL 119 IS 3 BP 250 EP 250 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA LU903 UT WOS:A1993LU90300024 ER PT J AU MIHICH, E HEMLER, ME AF MIHICH, E HEMLER, ME TI ADHESION MOLECULES - CELLULAR RECOGNITION MECHANISMS - THE PEZCOLLER-FOUNDATION SYMPOSIA, ROVERETO, JUNE 24-26, 1992 SO ANNALS OF ONCOLOGY LA English DT Note C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP MIHICH, E (reprint author), ROSWELL PK CANC INST,ELM & CARLTON ST,BUFFALO,NY 14263, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD AUG PY 1993 VL 4 IS 7 BP 545 EP 547 PG 3 WC Oncology SC Oncology GA LQ680 UT WOS:A1993LQ68000008 PM 8363986 ER PT J AU MONTGOMERY, WW BLAUGRUND, SM VARVARES, MA AF MONTGOMERY, WW BLAUGRUND, SM VARVARES, MA TI THYROPLASTY - A NEW APPROACH SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE LARYNGEAL FRAMEWORK SURGERY; PHONOSURGERY; THYROPLASTY; VOCAL CORD PARALYSIS ID COMPRESSION AB A new type of thyroplasty implant (prosthesis) has been designed to be used as part of a surgical operation that accomplishes medial displacement of a paralyzed vocal cord. The implant is inserted through a rectangular window fashioned in the thyroid lamina on the side of the vocal cord paralysis. Instruments for measuring the location and outline of the window in the thyroid lamina are presented. A thyroplasty saw blade is introduced. By using this blade, a window of precise measurement can be constructed without injury to the underlying perichondrium. The implant is constructed from a biocompatible, medical-grade polymer. Four sizes each are available for the male and female larynges. The proper-size implant can be selected with a measuring device. It is not necessary to alter the implant at the time of surgery; it snaps into place and suturing is not necessary. Once the implant is inserted, its medial or lateral displacement is not possible; on the other hand, the implant can be easily removed if vocal cord function returns, or if a change to a different-size implant is indicated. The design of the implant will close the posterior commissure. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. LENOX HILL HOSP,DEPT OTOLARYNGOL,NEW YORK,NY 10021. RP MONTGOMERY, WW (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114, USA. NR 9 TC 64 Z9 69 U1 0 U2 1 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 AUG PY 1993 VL 102 IS 8 BP 571 EP 579 PG 9 WC Otorhinolaryngology SC Otorhinolaryngology GA LT025 UT WOS:A1993LT02500001 PM 8352479 ER PT J AU HARA, M KIMURA, RS AF HARA, M KIMURA, RS TI MORPHOLOGY OF THE MEMBRANA-LIMITANS SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE COCHLEA; GUINEA PIG; MEMBRANA-LIMITANS; PERILYMPH; RECONSTRUCTION; VESTIBULE ID INNER AB The morphology of the membrana limitans (ML) was studied by light and electron microscopy to further understand its functional significance. The ML is a porous shield composed of a few to several layers of tightly packed fibrocytes that separate the perilymphatic space of the cochlea and saccule from that of the utricle and canal system. These fibrocytes are thinner on the side of the vestibule. They show many desmosomes and gap junctions and are interspersed with fibrils. The 3-dimensional reconstruction from celloidin sections shows that the ML, as it is viewed from the anterior side, is rectangular in shape, with various surface curvatures and an invagination toward the internal aperture of the vestibular aqueduct. Horseradish peroxidase, a tracer substance, placed on either side of the ML fails to pass to the opposite side. The ML and trabecular meshwork may be a factor contributing to differential sensitivity of cochlear and vestibular sensory cells in the presence of noxious substances. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,ELECTRON MICROSCOPY LAB,243 CHARLES ST,BOSTON,MA 02114. UNIV TOKYO,DEPT OTOLARYNGOL,TOKYO 113,JAPAN. FU NIDCD NIH HHS [HAR8 R01 DC 00073-28] NR 10 TC 14 Z9 14 U1 0 U2 1 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 AUG PY 1993 VL 102 IS 8 BP 625 EP 630 PG 6 WC Otorhinolaryngology SC Otorhinolaryngology GA LT025 UT WOS:A1993LT02500011 PM 8352488 ER PT J AU PUSKAS, JD ALLEN, MS MONCURE, AC WAIN, JC HILGENBERG, AD WRIGHT, C GRILLO, HC MATHISEN, DJ COOLEY, DA MCLAUGHLIN, JS AF PUSKAS, JD ALLEN, MS MONCURE, AC WAIN, JC HILGENBERG, AD WRIGHT, C GRILLO, HC MATHISEN, DJ COOLEY, DA MCLAUGHLIN, JS TI PULMONARY ARTERIOVENOUS-MALFORMATIONS - THERAPEUTIC OPTIONS SO ANNALS OF THORACIC SURGERY LA English DT Article; Proceedings Paper CT 29TH ANNUAL MEETING OF THE SOC OF THORACIC SURGEONS CY JAN 25-27, 1993 CL SAN ANTONIO, TX SP SOC THORAC SURGEONS ID HEREDITARY HEMORRHAGIC TELANGIECTASIA; FISTULAS; EMBOLIZATION AB We have treated 21 patients (13 female, 8 male) with pulmonary arteriovenous malformations (PAVMs). Mean age at diagnosis was 37.5 years (range, 15 to 72 years). Presenting symptoms included dyspnea on exertion (67%), hereditary hemorrhagic telangiectasia (57%), and major neurologic events (33%). In our early experience, 8 patients had no specific treatment; their case histories illustrate the major neurologic complications of untreated PAVMs. Nine patients (8 primarily, 1 after recurrence) underwent conservative surgical excision; 4 had lobectomy, and 5 had segmentectomy or subsegmental excision. One patient underwent staged bilateral thoracotomies for multiple bilateral lesions. The arterial oxygen tension was found to increase after excision of large or solitary PAVMs. All surgically treated patients were relieved of dyspnea, and none had postoperative recurrence of PAVMs or neurologic complications related to PAVMs. Five patients underwent balloon occlusion of PAVMs. Two patients chose to have solitary PAVMs occluded rather than undergo thoracotomy. One underwent surgical excision 5 years later, and the other required repeat balloon embolization 4 years later when recanalization of the PAVMs was documented. Three patients with numerous PAVMs received palliation with multiple balloon embolizations. The high incidence of associated ma or neurologic complications mandates aggressive treatment of PAVMs whenever feasible. Conservative surgical resection remains the treatment of choice. Balloon embolization offers an alternative therapy for patients who are poor surgical risks or those whose lesions are too numerous to resect. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GEN THORAC SURG UNIT,BOSTON,MA 02114. NR 20 TC 83 Z9 87 U1 1 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 AUG PY 1993 VL 56 IS 2 BP 253 EP 258 PG 6 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA LR781 UT WOS:A1993LR78100010 PM 8347006 ER PT J AU GUYTON, RA SCHONBERGER, JPAM EVERTS, PAM JETT, GK GRAY, LA GIELCHINSKY, I RAESS, DH VLAHAKES, GJ WOOLLEY, SR GANGAHAR, DM SOLTANZADEH, H PICCIONE, WJ VAUGHN, CC BOONSTRA, PW BUCKLEY, MJ AF GUYTON, RA SCHONBERGER, JPAM EVERTS, PAM JETT, GK GRAY, LA GIELCHINSKY, I RAESS, DH VLAHAKES, GJ WOOLLEY, SR GANGAHAR, DM SOLTANZADEH, H PICCIONE, WJ VAUGHN, CC BOONSTRA, PW BUCKLEY, MJ TI POSTCARDIOTOMY SHOCK - CLINICAL-EVALUATION OF THE BVS-5000 BIVENTRICULAR SUPPORT SYSTEM SO ANNALS OF THORACIC SURGERY LA English DT Article ID VENTRICULAR ASSIST DEVICE; STUNNED MYOCARDIUM; CARDIOGENIC-SHOCK; BYPASS AB This prospective trial evaluated the safety and efficacy of a new pulsatile, temporary ventricular assist device, the BVS 5000. Patients were eligible for treatment if they were hemodynamically unstable despite maximal pharmacologic and intraaortic balloon pump therapy, were free of concomitant complications, and were less than 6 hours from the first attempt to separate from cardiopulmonary bypass. Fifty-five postcardiotomy patients were enrolled; 31 met all selection criteria and the remainder failed to meet criteria (n = 15) or were not successfully supported (n = 9). The BVS 5000 effectively restored hemodynamics: Mean arterial pressure increased (77.1 +/- 0.8 mm Hg on-support versus 50.1 +/- 15.3 mm Hg presupport; p = 0.0001). Cardiac index increased (2.3 +/- 0.3 L . min-1 . m-2 on-support versus 1.6 +/- 0.6 L . min-1 . m-2 presupport; p = 0.0013). Left ventricular filling pressure decreased (11.9 +/- 4.5 mm Hg on-support versus 23.8 +/- 8.7 mm Hg presupport; p = 0.0030). The most frequent complication was bleeding in 42 patients (76%). Of the patients meeting all criteria, 17 (55%) were weaned from support and 9 (29%) were discharged. Survival was significantly influenced by presupport cardiac arrest events. Survival among patients not experiencing arrest was 47%. Eight patients are long-term survivors and were asymptomatic in New York Heart Association class I or II at 1-year follow-up. The BVS 5000 restored hemodynamics, permitted myocardial recovery, and improved survival in a group of patients who would have otherwise died. C1 IOWA METHODIST MED CTR,DES MOINES,IA. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. PHOENIX BAPTIST HOSP,PHOENIX,AZ. UNIV HOSP GRONINGEN,GRONINGEN,NETHERLANDS. EMORY UNIV,ATLANTA,GA 30322. CATHARINA HOSP,EINDHOVEN,NETHERLANDS. BAYLOR UNIV,MED CTR,DALLAS,TX. JEWISH HOSP,LOUISVILLE,KY. NEWARK BETH ISRAEL MED CTR,NEWARK,NJ 07112. ST FRANCIS HOSP,BEECH GROVE,IN. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV UTRECHT HOSP,3511 GV UTRECHT,NETHERLANDS. BRYAN MEM HOSP,LINCOLN,NE. NR 13 TC 55 Z9 55 U1 0 U2 1 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 AUG PY 1993 VL 56 IS 2 BP 346 EP 356 PG 11 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA LR781 UT WOS:A1993LR78100025 PM 8347020 ER PT J AU KILMER, SL LEE, MS GREVELINK, JM FLOTTE, TJ ANDERSON, RR AF KILMER, SL LEE, MS GREVELINK, JM FLOTTE, TJ ANDERSON, RR TI THE Q-SWITCHED ND-YAG LASER EFFECTIVELY TREATS TATTOOS - A CONTROLLED, DOSE-RESPONSE STUDY SO ARCHIVES OF DERMATOLOGY LA English DT Article ID CARBON-DIOXIDE LASER; RUBY-LASER; SELECTIVE PHOTOTHERMOLYSIS; DECORATIVE TATTOOS; HUMAN-SKIN; REMOVAL; CO2-LASER; PULSES AB Background and Design: The Q-switched ruby laser was recently shown to remove tattoos without scarring. The Q-switched neodymium: yttrium aluminum garnet (Nd:YAG) laser, which targets black ink with a longer wavelength that has less absorption by melanin, should effectively treat tattoos with fewer pigmentary alterations. A prospective, blinded, controlled study was conducted to assess the ability of the Q-switched Nd:YAG laser (1064 nm, 10 ns, 5 Hz) to remove tattoos. Twenty-five patients with 39 blue-black or multicolored tattoos (14 previously untreated, 25 Q-switched ruby laser-resistant) were exposed in randomly derived quadrants with 6, 8, 10, or 12 J/cm2 at 3 to 4 week intervals for a total of four treatment sessions. Results: An excellent response (> 75% ink removal) was seen in 77% of the black tattoos and more than 95% of the black ink cleared in 11 (28%) of 39 tattoos at 10 to 12 J/cm2 after four treatment sessions. Colored inks were not as effectively removed. Response was related to fluence with greatest improvement noted in the quadrants treated with 10 and 12 J/cm2. No significant side effects, including pigmentary changes or scarring, were noted. Histopathologic examination demonstrated persistence of tattoo ink in clinically clear areas and confirmed the absence of fibrosis and granulomatous changes. Conclusion: The Q-switched Nd:YAG laser (1064 nm) effectively treats black tattoos with an excellent cosmetic outcome. Bright colors were minimally responsive to treatment. Higher doses were more effective and equally well tolerated. C1 HARVARD UNIV, SCH MED, DEPT DERMATOL, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, DEPT DERMATOL, BOSTON, MA 02114 USA. NR 30 TC 148 Z9 156 U1 0 U2 5 PU AMER MEDICAL ASSOC PI CHICAGO PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA SN 0003-987X EI 1538-3652 J9 ARCH DERMATOL JI Arch. Dermatol. PD AUG PY 1993 VL 129 IS 8 BP 971 EP 978 DI 10.1001/archderm.129.8.971 PG 8 WC Dermatology SC Dermatology GA LR787 UT WOS:A1993LR78700005 PM 8352621 ER PT J AU GREEN, HA BURD, EE NISHIOKA, NS COMPTON, CC AF GREEN, HA BURD, EE NISHIOKA, NS COMPTON, CC TI SKIN-GRAFT TAKE AND HEALING FOLLOWING 193-NM EXCIMER, CONTINUOUS-WAVE CARBON-DIOXIDE (CO2), PULSED CO2, OR PULSED HOLMIUM-YAG LASER-ABLATION OF THE GRAFT BED SO ARCHIVES OF DERMATOLOGY LA English DT Article ID TISSUE ABLATION; THERMAL-DAMAGE; CO2-LASER; INCISIONS; SCALPEL; EXCISION; ELECTROSURGERY; REGENERATION; WOUNDS; KNIFE AB Background: Ablative lasers have been used for cutaneous surgery for greater than two decades since they can remove skin and skin lesions bloodlessly and efficiently. Because full-thickness skin wounds created after thermal laser ablation may require skin grafting in order to heal, we have examined the effect of the residual laser-induced thermal damage in the wound bed on subsequent skin graft take and healing. In a pig model, four different pulsed and continuous-wave lasers with varying wavelengths and radiant energy exposures were used to create uniform fascial graft bed thermal damage of approximately 25, 160, 470, and 1100 mum. Meshed split-thickness skin graft take and healing on the thermally damaged fascial graft beds were examined on a gross and microscopic level on days 3 and 7, and then weekly up to 42 days. Results: Laser-induced thermal damage on the graft bed measuring greater than 160+/-60 mum in depth significantly decreased skin graft take. Other deleterious effects included delayed graft revascularization, increased inflammatory cell infiltrate at the graft-wound bed interface, and accelerated formation of hypertrophied fibrous tissue within the graft bed and underlying muscle. Conclusions: Ablative lasers developed for cutaneous surgery should create less than 160+/-60 mum of residual thermal damage to permit optimal skin graft take and healing. Pulsed carbon dioxide and 193-nm excimer lasers may be valuable instruments for the removal of full-thickness skin, skin lesions, and necrotic tissue, since they create wound beds with minimal thermal damage permitting graft take comparable to that achieved with standard surgical techniques. C1 BOSTON UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02118. UNIV BRISTOL,BRISTOL ROYAL INFIRM,DEPT PATHOL & MICROBIOL,BRISTOL BS2 8HW,AVON,ENGLAND. MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS INST,DEPT PATHOL,BOSTON,MA 02114. FU NIGMS NIH HHS [R01 GM35242] NR 54 TC 30 Z9 30 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 AUG PY 1993 VL 129 IS 8 BP 979 EP 988 DI 10.1001/archderm.129.8.979 PG 10 WC Dermatology SC Dermatology GA LR787 UT WOS:A1993LR78700006 PM 8352622 ER PT J AU ANDERSON, RR GERONEMUS, R KILMER, SL FARINELLI, W FITZPATRICK, RE AF ANDERSON, RR GERONEMUS, R KILMER, SL FARINELLI, W FITZPATRICK, RE TI COSMETIC TATTOO INK DARKENING - A COMPLICATION OF Q-SWITCHED AND PULSED-LASER TREATMENT SO ARCHIVES OF DERMATOLOGY LA English DT Article ID RUBY-LASER; SELECTIVE PHOTOTHERMOLYSIS AB Background: High-energy, short-pulse lasers, eg, Q-switched lasers, emitting visible and near-infrared light have recently been developed for removing tattoos, with little risk of scarring. The mechanisms of action, and possible adverse effects other than scarring and hypopigmentation, are not fully understood. Observations: We describe five cases of pulsed-laser-induced, immediate, irreversible darkening of cosmetic, white, flesh (skin-color), and pink-red colored tattoos. Irreversible ink darkening can be an insidious complication, because immediate whitening of the skin temporarily obscures the subsequently impressive color change. Among these cases, irreversible ink darkening occurred with Q-switched ruby (694 nm), Q-switched neodymium (Nd):YAG (1064 nm/532 nm), and pulsed green dye (510 nm) lasers. Attempts to remove the darkened ink with further laser treatment failed in two cases, and surgical excision was necessary. In the other three cases, subsequent laser treatments successfully removed the darkened ink. The red cosmetic-tattoo ink used in one of the cases was placed in agar in vitro and was converted to a black compound immediately on Q-switched ruby laser exposure. Ferric oxide, a brown-red ingredient commonly used in cosmetic tattoos, was similarly tested and blackened in vitro by Q-switched ruby laser exposures. Conclusions: Although most tattoos are not darkened by laser treatment, short-pulsed lasers over a wide spectrum can cause immediate darkening of some tattoo inks. Patients should be warned of the potential for irreversible cosmetic tattoo darkening, and test-site exposures should be performed prior to treatment. In some cases, subsequent laser treatments may remove the blackened ink. The mechanism probably involves, at least for some tattoos, reduction of ferric oxide (Fe2O3, ''rust'') to ferrous oxide (FeO, jet black), but the chemical reaction that is involved remains unknown. C1 DERMATOL ASSOCIATES SAN DIEGO, ENCINITAS, CA USA. NYU, NEW YORK, NY 10003 USA. RP MASSACHUSETTS GEN HOSP, WELLMAN LABS PHOTOMED, DEPT DERMATOL, BOSTON, MA 02114 USA. NR 9 TC 110 Z9 110 U1 2 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA SN 0003-987X EI 1538-3652 J9 ARCH DERMATOL JI Arch. Dermatol. PD AUG PY 1993 VL 129 IS 8 BP 1010 EP 1014 DI 10.1001/archderm.129.8.1010 PG 5 WC Dermatology SC Dermatology GA LR787 UT WOS:A1993LR78700010 PM 8352605 ER PT J AU CUMMINGS, JL AF CUMMINGS, JL TI FRONTAL-SUBCORTICAL CIRCUITS AND HUMAN-BEHAVIOR SO ARCHIVES OF NEUROLOGY LA English DT Review ID PARAMEDIAN THALAMIC INFARCTION; OBSESSIVE-COMPULSIVE DISORDER; BASAL GANGLIA; HUNTINGTONS-DISEASE; PARKINSONS-DISEASE; MOOD DISORDERS; BLOOD-FLOW; LESIONS; LOBE; DEMENTIA AB objective.-This synthetic review was performed to demonstrate the utility of frontal-subcortical circuits in the explanation of a wide range of human behavioral disorders. Data Sources.-Reports of patients with degenerative disorders or focal lesions involving frontal lobe or linked subcortical structures were chosen from the English literature. Individual case reports and group investigations from peer-reviewed journals were evaluated. Study Selection.-Studies were included if they described patient behavior in detail or reported pertinent neuropsychological findings and had compelling evidence of a disorder affecting frontal-subcortical circuits. Data Extraction.-Information was used if the report from which it was taken met study selection criteria. Data Synthesis.-Five parallel segregated circuits link the frontal lobe and subcortical structures. Clinical syndromes observed with frontal lobe injury are recapitulated with lesions of subcortical member structures of the circuits. Each prefrontal circuit has a signature behavioral syndrome: executive function deficits occur with lesions of the dorsolateral prefrontal circuit, disinhibition with lesions of the orbito-frontal circuit, and apathy with injury to the anterior cingulate circuit. Depression, mania, and obsessive-compulsive disorder may also be mediated by frontal-subcortical circuits. Movement disorders identify involvement of the basal ganglia component of frontal-subcortical circuits. Conclusions.-Frontal-subcortical circuits mediate many aspects of human behavior. C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. RP CUMMINGS, JL (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, NEUROBEHAV UNIT, BEHAV NEUROSCI SECT, BLDG 256B 691B116AF, LOS ANGELES, CA 90073 USA. RI Frank, David/E-8213-2012 NR 71 TC 1466 Z9 1491 U1 7 U2 47 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD AUG PY 1993 VL 50 IS 8 BP 873 EP 880 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA LR028 UT WOS:A1993LR02800018 PM 8352676 ER PT J AU MERCHANT, SN SCHUKNECHT, HF RAUCH, SD MCKENNA, MJ ADAMS, JC WUDARSKY, R NADOL, JB AF MERCHANT, SN SCHUKNECHT, HF RAUCH, SD MCKENNA, MJ ADAMS, JC WUDARSKY, R NADOL, JB TI THE NATIONAL TEMPORAL BONE, HEARING, AND BALANCE PATHOLOGY RESOURCE REGISTRY SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Article AB The National Temporal Bone, Hearing, and Balance Pathology Resource Registry has been established with funding provided by the National Institute on Deafness and Other Communication Disorders of the National Institutes of Health. The registry is meant to serve as a national resource for researchers and the public to stimulate and facilitate human otopathologic research. It will maintain a computerized database of currently active and inactive temporal bone and auditory brain-stem collections throughout the United States. In addition, it will encourage human temporal bone research by disseminating pertinent information, developing and fostering temporal bone professional educational activities, implementing a national temporal bone acquisition network, and encouraging investigative collaborations in the study of the human temporal bone and brain structures. It will also identify otopathologic collections at risk of being discarded or lost and will develop mechanisms and strategies to conserve them. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. DEAFNESS RES FDN,NEW YORK,NY. NR 2 TC 10 Z9 10 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0886-4470 J9 ARCH OTOLARYNGOL JI Arch. Otolaryngol. Head Neck Surg. PD AUG PY 1993 VL 119 IS 8 BP 846 EP 853 PG 8 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA LR030 UT WOS:A1993LR03000006 PM 8343246 ER PT J AU HARRIS, NL AF HARRIS, NL TI LOW-GRADE B-CELL LYMPHOMA OF MUCOSA-ASSOCIATED LYMPHOID-TISSUE AND MONOCYTOID B-CELL LYMPHOMA - RELATED ENTITIES THAT ARE DISTINCT FROM OTHER LOW-GRADE B-CELL LYMPHOMAS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Editorial Material ID PERIPHERAL-BLOOD INVOLVEMENT; MARGINAL ZONE LYMPHOCYTES; MALIGNANT-LYMPHOMA; MONOCLONAL-ANTIBODIES; GASTRIC LYMPHOMA; BONE-MARROW; EXPRESSION; DIAGNOSIS; FEATURES; MALT RP HARRIS, NL (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,WARREN 2,BOSTON,MA 02114, USA. NR 47 TC 65 Z9 65 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD AUG PY 1993 VL 117 IS 8 BP 771 EP 775 PG 5 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA LR011 UT WOS:A1993LR01100001 PM 8343039 ER PT J AU MILLER, AL MAAS, JW CONTRERAS, S SELESHI, E TRUE, JE BOWDEN, C CASTIGLIONI, J AF MILLER, AL MAAS, JW CONTRERAS, S SELESHI, E TRUE, JE BOWDEN, C CASTIGLIONI, J TI ACUTE EFFECTS OF NEUROLEPTICS ON UNMEDICATED SCHIZOPHRENIC-PATIENTS AND CONTROLS SO BIOLOGICAL PSYCHIATRY LA English DT Article DE METHOXYHYDROXYPHENYLGLYCOL; HOMOVANILLIC ACID; SCHIZOPHRENIA; HALOPERIDOL CHALLENGE; NEUROLEPTIC; DEBRISOQUIN ID PLASMA HOMOVANILLIC-ACID; BRAIN DOPAMINE METABOLISM; CHRONIC HALOPERIDOL TREATMENT; CEREBROSPINAL-FLUID; ENDOGENOUS DOPAMINE; CLONIDINE TREATMENT; DEBRISOQUIN; NEURONS; NOREPINEPHRINE; APOMORPHINE AB Acute administration of haloperidol (0.2 mg/kg) produced many more side effects in normal controls than in unmedicated schizophrenic patients. Prior to the neuroleptic challenge, both groups were on the peripheral monoamine oxidase inhibitor, debrisoquin, for at least 1 week, in order to enhance the relative contribution of CNS catecholamine metabolites to those measured in both plasma and urine. The patient group had higher plasma levels of methoxyhydroxyphenylglycol (MHPG) and homovanillic acid (HVA) and higher urinary MHPG output than controls, but there were no effects of haloperidol challenge, compared to placebo challenge. In both groups there were significant declines in plasma HVA levels from 8:30 AM to 12 NOON. These declines were unaffected by the haloperidol challenge. Explanations for the marked differences in behavioral effects of haloperidol on patients and controls include the possibility that dopamine receptor numbers were increased in the brains of the schizophrenic patients. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP MILLER, AL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NCRR NIH HHS [MO1-RR01346]; NIMH NIH HHS [MH40935] NR 81 TC 23 Z9 23 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD AUG 1 PY 1993 VL 34 IS 3 BP 178 EP 187 DI 10.1016/0006-3223(93)90389-U PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LT691 UT WOS:A1993LT69100010 PM 8104509 ER PT J AU LI, FP AF LI, FP TI MOLECULAR EPIDEMIOLOGY STUDIES OF CANCER IN FAMILIES SO BRITISH JOURNAL OF CANCER LA English DT Review ID RETINOBLASTOMA SUSCEPTIBILITY GENE; LI-FRAUMENI SYNDROME; COLORECTAL CANCERS; PROSTATE-CANCER; BREAST-CANCER; WILMS-TUMOR; IDENTIFICATION; MUTATIONS; NEOPLASMS; SARCOMA C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RP LI, FP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 33 TC 13 Z9 13 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 AUG PY 1993 VL 68 IS 2 BP 217 EP 219 DI 10.1038/bjc.1993.318 PG 3 WC Oncology SC Oncology GA LP945 UT WOS:A1993LP94500001 PM 8347474 ER PT J AU LIVINGSTON, DM KAELIN, W CHITTENDEN, T QIN, X AF LIVINGSTON, DM KAELIN, W CHITTENDEN, T QIN, X TI STRUCTURAL AND FUNCTIONAL CONTRIBUTIONS TO THE G1 BLOCKING ACTION OF THE RETINOBLASTOMA PROTEIN - (THE 1992 GORDON HAMILTON FAIRLEY MEMORIAL LECTURE) SO BRITISH JOURNAL OF CANCER LA English DT Review ID SUSCEPTIBILITY GENE-PRODUCT; ADENOVIRUS E1A PROTEINS; LARGE T-ANTIGENS; SV40 LARGE-T; CELL-CYCLE; CARCINOMA-CELLS; MYC PROMOTER; RB GENE; C-MYC; TRANSCRIPTION AB The retinoblastoma gene product (RB) contributes to normal cell growth control. One of its functions is manifest as a block to exit from G1, which is carried out by an RB subspecies which is un- or underphosphorylated. After RB phosphorylation, a process which occurs towards the end of G1 in cycling cells, the block is lifted allowing a cell to enter S. Here, we review a series of results which speak to the elements of RB structure which contribute to this activity. Included is its internal colinear protein receptor domain (i.e. the 'pocket'). C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LIVINGSTON, DM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 33 TC 14 Z9 16 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 AUG PY 1993 VL 68 IS 2 BP 264 EP 268 DI 10.1038/bjc.1993.325 PG 5 WC Oncology SC Oncology GA LP945 UT WOS:A1993LP94500008 PM 8347480 ER PT J AU WEBSTER, R PULFORD, K JONES, M MICKLEM, K DEWAELE, M MAYNE, K TSE, A MASON, DY AF WEBSTER, R PULFORD, K JONES, M MICKLEM, K DEWAELE, M MAYNE, K TSE, A MASON, DY TI ZB51 - A MONOCLONAL-ANTIBODY REACTIVE WITH HUMAN PLASMA-CELLS SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article ID MULTIPLE-MYELOMA; BONE-MARROW; INTRACELLULAR ANTIGENS; EXPRESSION; LEUKEMIA; HETEROGENEITY; LYMPHOCYTES; ADHESION; SMEARS; BLOOD AB Several monoclonal antibodies have been raised in the past which react with human plasma cells but they have all shown additional reactions with other cell types. In this paper we describe a new monoclonal antibody, ZB51, which recognizes an intracellular antigen in normal plasma cells in cryostat tissue sections and cell smears, and which also reacts with neoplastic cells in most cases of myeloma and with plasma cell lines. The antibody shows minimal reactivity with a few eosinophils and myelocytes in bone marrow and stains a myeloid cell line. Whilst normal epithelium is not labelled, antibody ZB51 stains two carcinoma cell lines. Although it was not possible to characterize the target antigen in terms of molecular weight, the reactivity of antibody ZB51 with normal and neoplastic plasma cells makes it a useful new immunocytochemical reagent. C1 JOHN RADCLIFFE HOSP,LRF IMMUNODIAGNOST UNIT,OXFORD OX3 9DU,ENGLAND. JOHN RADCLIFFE HOSP,DEPT HAEMATOL,OXFORD OX3 9DU,ENGLAND. VUB,ACAD ZIEKENHUIS,HEMATOL IMMUNOL LAB,BRUSSELS,BELGIUM. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. RI Pulford, Karen/B-3609-2009; Jones, Margaret/B-4083-2009 OI Pulford, Karen/0000-0002-2989-789X; NR 33 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD AUG PY 1993 VL 84 IS 4 BP 602 EP 607 DI 10.1111/j.1365-2141.1993.tb03134.x PG 6 WC Hematology SC Hematology GA LR730 UT WOS:A1993LR73000009 PM 8217816 ER PT J AU LOSTY, P KIERCE, B AF LOSTY, P KIERCE, B TI BOTRYOID WILMS-TUMOR - AN UNUSUAL VARIANT SO BRITISH JOURNAL OF UROLOGY LA English DT Note C1 OUR LADYS HOSP SICK CHILDREN,DEPT PAEDIAT SURG PATHOL,DUBLIN 12,IRELAND. OUR LADYS HOSP SICK CHILDREN,CHILDRENS RES CTR,DUBLIN 12,IRELAND. RP LOSTY, P (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,WARREN 11,BOSTON,MA 02114, USA. NR 2 TC 7 Z9 8 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0007-1331 J9 BRIT J UROL JI Br. J. Urol. PD AUG PY 1993 VL 72 IS 2 BP 251 EP 252 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA LT103 UT WOS:A1993LT10300028 PM 8402036 ER PT J AU SIMON, L AF SIMON, L TI PATHOGENESIS OF OSTEOPOROSIS SO BULLETIN ON THE RHEUMATIC DISEASES LA English DT Article ID BONE-MINERAL DENSITY; INVOLUTIONAL OSTEOPOROSIS; TRABECULAR BONE; WOMEN C1 MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SIMON, L (reprint author), NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215, USA. NR 16 TC 1 Z9 1 U1 0 U2 0 PU ARTHRITIS FOUNDATION PI ATLANTA PA 1314 SPRING STREET NW, ATLANTA, GA 30309 SN 0007-5248 J9 B RHEUM DIS JI Bull. Rheum. Dis. PD AUG PY 1993 VL 42 IS 5 BP 1 EP 3 PG 3 WC Rheumatology SC Rheumatology GA LW438 UT WOS:A1993LW43800001 PM 8242160 ER PT J AU FISHER, CM AF FISHER, CM TI CONCERNING MIND SO CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES LA English DT Article AB The nature of the human mind is addressed from a neurological viewpoint. First from reported observations on subjects born blind with congenital cataract. who acquired vision after surgery. the concept of the primacy of somatosensation is developed. Therefrom some principles of the organization of higher sensory functions in the dominant parietal. occipital and temporal lobes are deduced. Sentience is traced to somatosensation. Some characteristics of the mind and of thinking are described. The non-existence ot' the unconscious is inferred. The question of free will is approached. Using neurological experience it is demonstrated that a good case for operation of a free will is difficult to establish. Positing the absence of a free will may be beneficial in the analysis and management of behavior. Finally the opportunity to study the nature and mechanism of the emotions in clinical neurology is outlined. RP FISHER, CM (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 23 TC 2 Z9 2 U1 0 U2 2 PU CANADIAN J NEUROL SCI INC PI CALGARY PA PO BOX 4220, STATION C EDITORIAL & SUBSCRIPTION SERV, CALGARY AB T2T 5N1, CANADA SN 0317-1671 J9 CAN J NEUROL SCI JI Can. J. Neurol. Sci. PD AUG PY 1993 VL 20 IS 3 BP 247 EP 253 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA LV339 UT WOS:A1993LV33900014 PM 8221393 ER PT J AU HUNCHAREK, M AF HUNCHAREK, M TI INCIDENCE OF HYPERCALCEMIA IN PATIENTS WITH MALIGNANCY REFERRED TO A COMPREHENSIVE CANCER CENTER SO CANCER LA English DT Letter RP HUNCHAREK, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 4 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 AUG 1 PY 1993 VL 72 IS 3 BP 956 EP 956 DI 10.1002/1097-0142(19930801)72:3<956::AID-CNCR2820720348>3.0.CO;2-7 PG 1 WC Oncology SC Oncology GA LP720 UT WOS:A1993LP72000046 PM 8334649 ER PT J AU RUBIO, MP VONDEIMLING, A YANDELL, DW WIESTLER, OD GUSELLA, JF LOUIS, DN AF RUBIO, MP VONDEIMLING, A YANDELL, DW WIESTLER, OD GUSELLA, JF LOUIS, DN TI ACCUMULATION OF WILD-TYPE P53 PROTEIN IN HUMAN ASTROCYTOMAS SO CANCER RESEARCH LA English DT Note ID ACTIVATING MUTATIONS; GENE-MUTATIONS; BREAST-CANCER; BRAIN-TUMORS; LUNG-CANCER; CELL-LINES; EXPRESSION; FORMS; HETEROZYGOSITY; CHROMOSOME-17 AB We have previously described 10 astrocytomas with accumulation of p53 protein but no mutations in p53 exons 5-8, and we have suggested that they might represent overexpression of wild type protein or mutations in less conserved regions of the gene. To investigate these possibilities further, we studied the tumors with immunohistochemistry for wild type and mutant p53 protein and showed that all cases stained with the wild type PAb 1801 antibody but only one case stained with the mutant-specific PAb 240 antibody. To support the hypothesis that the accumulated p53 protein is wild type in most cases, we used single-strand conformation polymorphism analysis and DNA sequencing to evaluate p53 exons 4, 9, and 10 and did not detect mutations at these loci. Although the product of the MDM2 oncogene binds wild type p53 and may account for p53 accumulation, slot-blot analysis of these astrocytOmas did not detect MDM2 gene amplification. Thus, evidence suggests that some astrocytomas may accumulate wild type p53 protein but not as a result of MDM2 gene amplification. Furthermore, PAb 1801 immunohistochemistry may not be an adequate method of screening astrocytomas for p53 mutations. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL SERV,MOLEC NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV BONN,INST NEUROPATHOL,W-5300 BONN,GERMANY. RI Rubio, Mari-Paz/K-4364-2014; von Deimling, Andreas/F-7774-2013 OI Rubio, Mari-Paz/0000-0003-3963-5903; von Deimling, Andreas/0000-0002-5863-540X FU NCI NIH HHS [CA 57683] NR 31 TC 141 Z9 141 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 AUG 1 PY 1993 VL 53 IS 15 BP 3465 EP 3467 PG 3 WC Oncology SC Oncology GA LP641 UT WOS:A1993LP64100005 PM 8339248 ER PT J AU WEISS, JN VENKATESH, N AF WEISS, JN VENKATESH, N TI METABOLIC-REGULATION OF CARDIAC ATP-SENSITIVE K+ CHANNELS SO CARDIOVASCULAR DRUGS AND THERAPY LA English DT Article DE ATP-SENSITIVE POTASSIUM CHANNELS; MYOCARDIAL ISCHEMIA; HYPOXIA; METABOLIC INHIBITION; GLYCOLYSIS; ACTION POTENTIAL DURATION; POTASSIUM ACCUMULATION; POTASSIUM LOSS ID RAT VENTRICULAR MYOCYTES; EXTRACELLULAR POTASSIUM; MYOCARDIAL ISCHEMIA; ARRHYTHMIAS; HEART; ACCUMULATION; GLYCOLYSIS; INFARCTION; MODULATION; MUSCLE AB Activation of ATP-sensitive K+ (K(ATP)) channels has been implicated as a cause of increased cellular K+ efflux and action potential duration (APD) shortening during myocardial ischemia, hypoxia, and selective glycolytic inhibition, since selective K(ATP) channel antagonists partially or completely block increased cellular K+ efflux and APD shortening under these conditions. During substrate-free hypoxia or myocardial ischemia in intact rabbit ventricle, unidirectional K+ efflux rate during systole approximately doubled and APD decreased by almost-equal-to 40% after 10 minutes. In patch-clamped guinea pig ventricular myocytes, similar changes could be produced by activation of <0.5% of the maximal K(ATP) channel conductance. Furthermore, from studying the desensitizing effects of ADP(i) on the ATP sensitivity of K(ATP) channels in excised inside-out patches, it was estimated that the rapid changes in the cytosolic ATP/ADP ratio during ischemia and hypoxia were of sufficient magnitude to activate K(ATP) channels to this degree. During selective glycolytic inhibition, however, the global cytosolic ATP/ADP ratio in intact heart remained normal despite an increase in cellular K+ efflux comparable to ischemia and hypoxia. In patch-clamped saponin-permeabilized ventricular myocytes. K(ATP) channels were preferentially suppressed by glycolytic ATP production compared to ATP generated by mitochondria or by the creatinine kinase reaction, and functional glycolytic enzymes were found to be associated with K(ATP) channels in excised membrane patches. We hypothesize that sarcolemma-associated glycolytic enzymes may be important in maintaining a high local cytosolic ATP/ADP ratio in the vicinity of K(ATP) channels, where sarcolemmal ATPases are tending to depress the local ATP/ADP ratio. C1 UNIV CALIF LOS ANGELES, DEPT MED CARDIOL, CARDIOVASC RES LAB, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, W LOS ANGELES VA MED CTR, LOS ANGELES, CA USA. FU NHLBI NIH HHS [1R01 HL36729, 1K04 HL01890, 1R29 HL38366] NR 19 TC 71 Z9 71 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0920-3206 J9 CARDIOVASC DRUG THER JI Cardiovasc. Drugs Ther. PD AUG PY 1993 VL 7 SU 3 BP 499 EP 505 DI 10.1007/BF00877614 PG 7 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA MB806 UT WOS:A1993MB80600004 PM 8251419 ER PT J AU HASS, R HIRANO, M KHARBANDA, S RUBIN, E MEINHARDT, G KUFE, D AF HASS, R HIRANO, M KHARBANDA, S RUBIN, E MEINHARDT, G KUFE, D TI RESISTANCE TO PHORBOL ESTER-INDUCED DIFFERENTIATION OF A U-937 MYELOID-LEUKEMIA CELL VARIANT WITH A SIGNALING DEFECT UPSTREAM TO RAF-1 KINASE SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID C-JUN EXPRESSION; TUMOR NECROSIS FACTOR; PROTEIN-KINASE; MONOCYTIC DIFFERENTIATION; OKADAIC ACID; LINE U-937; MOLECULAR-CLONING; GENE-EXPRESSION; GROWTH-FACTORS; RETINOIC ACID AB Previous studies have demonstrated that treatment of human U-937 myeloid leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with growth arrest and induction of monocytic differentiation. The present work describes the isolation of a U-937 cell variant, designated TUR, which is unresponsive to the growth-inhibitory effects of this agent. The results demonstrate that, in contrast to U-937 cells, the TUR line fails to respond to TPA with induction of the c-jun, junB, c-fos, and EGR-1 early response genes. The finding that these cells also fail to exhibit adherence or induction of the tumor necrosis factor and c-fms genes further supports their resistance to TPA-induced differentiation. In contrast, TUR cells responded to 1,25-dihydroxyvitamin D3, another inducer of monocytic differentiation, with growth arrest and induction of early response gene and c-fms transcripts. TUR cells also responded to okadaic acid, an inhibitor of type 1 and 2A protein phosphatases, with similar changes in gene expression. Further characterization of TUR cells has demonstrated decreased expression of protein kinase C as compared to wild-type U-937 cells. We also demonstrate that although treatment of U-937 cells with TPA is associated with activation of the Raf-1 serine/threonine kinase, there was no detectable decrease in electrophoretic mobility of this protein in TPA-treated TUR cells. Taken together, these findings indicate that the TUR variant is defective in TPA-induced signaling events upstream to activation of Raf-1 kinase. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 FU NCI NIH HHS [CA42802, CA34183] NR 52 TC 35 Z9 35 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD AUG PY 1993 VL 4 IS 8 BP 657 EP 663 PG 7 WC Cell Biology SC Cell Biology GA LR308 UT WOS:A1993LR30800005 PM 8398907 ER PT J AU FRIDOVICHKEIL, JL MARKELL, PJ GUDAS, JM PARDEE, AB AF FRIDOVICHKEIL, JL MARKELL, PJ GUDAS, JM PARDEE, AB TI DNA-SEQUENCES REQUIRED FOR SERUM-RESPONSIVE REGULATION OF EXPRESSION FROM THE MOUSE THYMIDINE KINASE PROMOTER SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID RETINOBLASTOMA GENE-PRODUCT; CELL-CYCLE; MESSENGER-RNA; STIMULATED CELLS; PROTEIN-BINDING; MUSCLE-CELLS; G1/S PHASE; S-PHASE; TRANSCRIPTION; GROWTH AB We have used site-specific mutagenesis and thymidine kinase (TK) promoter/reporter gene transfection experiments to investigate DNA sequences required for serum-responsive regulation of expression from the mouse thymidine kinase promoter. Mutations were targeted to each of three previously described protein binding domains (MT1, MT2, and MT3) upstream of the TK translation initiation site, as well as to sequences within the TK first exon in order to address each of the following three questions: (a) Do these sequences play any role in regulation? (b) Do all of these sites play the same role? and (c) If any controls are observed, do they act positively or negatively on gene expression? The results of these experiments indicated that, in the wild-type TK promoter, at least some of these sequences do play a role in regulation, that not all of these sites appear to play the same role, and that some of the targeted elements act positively on gene expression, whereas others appear to act negatively. In particular, mutagenesis of the Spl site within MT1 virtually eliminated promoter function, whereas mutations in either the MT2 site or the TK first exon rendered reporter gene expression nearly constitutive with respect to serum. Thus, both MT2 and sequences within the TK first exon appear to contain negatively acting elements. In contrast, mutation or deletion of the MT3 site produced a much less pronounced effect on reporter gene regulation. These results support recent observations from our laboratory (Q-P. Dou et al., manuscript in preparation) indicating that although the protein complexes that bind to these various sites are similar, they are not identical. Although the exact roles and interplay of these elements and the factors that bind them remain unclear, the functional significance of these sequences is established. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115. FU NCI NIH HHS [CA22427, CA08317-03] NR 51 TC 17 Z9 17 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD AUG PY 1993 VL 4 IS 8 BP 679 EP 687 PG 9 WC Cell Biology SC Cell Biology GA LR308 UT WOS:A1993LR30800008 PM 8398909 ER PT J AU TSOUNIS, S MILONAS, J GILLIAM, F AF TSOUNIS, S MILONAS, J GILLIAM, F TI HEMI-FIELD PATTERN-REVERSAL VISUAL-EVOKED POTENTIALS IN MIGRAINE SO CEPHALALGIA LA English DT Article ID PATHWAYS; PAIN AB A study of hemi-field pattern reversal visual evoked potentials recorded in the interictal phase was carried out in 44 patients (22 with migraine with aura, 22 without aura) in order to determine whether migraine patients with or without aura and with headaches with strong unilateral predominance, either left or right, exhibit abnormalities after hemi-field stimulation. No differences of P100 latency were found between them and a group of 20 normal individuals, between patients suffering from migraine with aura and migraine without aura and between the affected and the non-affected side of the head. Only in a subgroup of 14 patients with headaches constantly lateralized to a single side, either left or right, was the P100 latency significantly shorter on the affected side (p < 0.001, t-test) compared with the contralateral non-affected side. The results indicate that in both types of migraine there is a common underlying pathogenetic mechanism and the affected retrochiasmatic optic radiation has an increased response to sensory input modulation. C1 AXEPA HOSP,DEPT NEUROL,SALONIKA,GREECE. MASSACHUSETTS GEN HOSP,DEPT CLIN NEUROPHYSIOL,BOSTON,MA 02114. RP TSOUNIS, S (reprint author), MENTAL HOSP THESSALONIKI,DEPT CLIN NEUROPHYSIOL,36 KONSTANTINOUPOLEOS STR,GR-56429 SALONIKA,GREECE. NR 20 TC 20 Z9 20 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0333-1024 J9 CEPHALALGIA JI Cephalalgia PD AUG PY 1993 VL 13 IS 4 BP 267 EP 271 DI 10.1046/j.1468-2982.1993.1304267.x PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA LT231 UT WOS:A1993LT23100013 PM 8374942 ER PT J AU HUNTER, JH STANFORD, W SMITH, JM GRILLO, HC WEILER, JM AF HUNTER, JH STANFORD, W SMITH, JM GRILLO, HC WEILER, JM TI EXPIRATORY COLLAPSE OF THE TRACHEA PRESENTING AS WORSENING ASTHMA SO CHEST LA English DT Note ID ACQUIRED TRACHEOMALACIA AB A 50-year-old woman with lifelong asthma had nearly total expiratory collapse of her distal trachea. The signs and symptoms were similar to those of asthma except for a pronounced upper airway component to her wheezing and the immediate onset of dyspnea on exertion. Surgical repair led to significant improvement in symptoms and resolution of tracheal collapse on expiration. Ultrafast computed tomography was a valuable adjunct to bronchoscopy in diagnosis and management. Expiratory collapse of the trachea should be considered in the differential diagnosis of wheezing and intractable reactive airway disease. C1 UNIV IOWA,COLL MED,DEPT RADIOL,IOWA CITY,IA 52242. MASSACHUSETTS GEN HOSP,GEN THORAC SURG UNIT,BOSTON,MA 02114. RP HUNTER, JH (reprint author), UNIV IOWA,COLL MED,DEPT INTERNAL MED,IOWA CITY,IA 52242, USA. NR 20 TC 7 Z9 7 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 AUG PY 1993 VL 104 IS 2 BP 633 EP 635 DI 10.1378/chest.104.2.633 PG 3 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA LT002 UT WOS:A1993LT00200068 PM 8339666 ER PT J AU CINCOTTA, AH SCHILLER, BC LANDRY, RJ HERBERT, SJ MIERS, WR MEIER, AH AF CINCOTTA, AH SCHILLER, BC LANDRY, RJ HERBERT, SJ MIERS, WR MEIER, AH TI CIRCADIAN NEUROENDOCRINE ROLE IN AGE-RELATED-CHANGES IN BODY-FAT STORES AND INSULIN SENSITIVITY OF THE MALE SPRAGUE-DAWLEY RAT SO CHRONOBIOLOGY INTERNATIONAL LA English DT Article DE CIRCADIAN RHYTHMS; INSULIN RESISTANCE; METABOLISM; PROLACTIN; CORTICOSTERONE; OBESITY; AGING ID HAMSTER MESOCRICETUS-AURATUS; IMPAIRED GLUCOSE-TOLERANCE; TEMPORAL SYNERGISM; SYRIAN-HAMSTER; LIPOGENIC RESPONSIVENESS; PROLACTIN PERMITS; RESISTANCE; OBESITY; RHYTHMS; HYPERINSULINEMIA AB A role for circadian neuroendocrine rhythms in the age-related development of obesity and insulin resistance was investigated in the male Sprague-Dawley rat. The phases and amplitudes of the plasma rhythms of several metabolic hormones (i.e., corticosterone, prolactin, insulin, and triiodothyronine) differed in lean, insulin-sensitive (3-week-old rats), insulin-resistant (8-week-old rats) and obese, insulin-resistant (44-week-old rats) animals. Simulation of the daily rhythms of endogenous corticosterone and prolactin by daily injections of the hormones at times corresponding to the peak levels found in 3-week-old rats reversed age-related increases in insulin resistance and body fat in older (5-6-month-old) rats. Ten such daily injections of corticosterone and prolactin in 12-14-week-old rats produced long-term reductions in body fat stores (30%), plasma insulin concentration (40%), and insulin resistance (60%) (determined by a glucose tolerance test) measured 11-14 weeks after the treatment. Alterations in circadian neuroendocrine rhythms may account for age-related changes in carbohydrate and lipid metabolism in the male Sprague-Dawley rat, and resetting of these rhythms by appropriately timed daily injections of corticosterone and prolactin may help maintain metabolism characteristic of younger animals. C1 HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. LOUISIANA STATE UNIV,DEPT ZOOL & PHYSIOL,BATON ROUGE,LA 70803. RP CINCOTTA, AH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 60 TC 21 Z9 22 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0742-0528 J9 CHRONOBIOL INT JI Chronobiol. Int. PD AUG PY 1993 VL 10 IS 4 BP 244 EP 258 DI 10.3109/07420529309059707 PG 15 WC Biology; Physiology SC Life Sciences & Biomedicine - Other Topics; Physiology GA LQ047 UT WOS:A1993LQ04700003 PM 8403068 ER PT J AU VOLPICELLI, SA CENTORRINO, F PUOPOLO, PR KANDO, J FRANKENBURG, FR BALDESSARINI, RJ FLOOD, JG AF VOLPICELLI, SA CENTORRINO, F PUOPOLO, PR KANDO, J FRANKENBURG, FR BALDESSARINI, RJ FLOOD, JG TI DETERMINATION OF CLOZAPINE, NORCLOZAPINE, AND CLOZAPINE-N-OXIDE IN SERUM BY LIQUID-CHROMATOGRAPHY SO CLINICAL CHEMISTRY LA English DT Note DE NEUROACTIVE DRUGS; TRIPOLIDINE INTERNAL STANDARD; CHROMATOGRAPHY; REVERSED-PHASE ID GAS-CHROMATOGRAPHY; PLASMA AB We report a new assay to measure the serum concentration of the atypical antipsychotic drug clozapine and two major metabolites, norclozapine and clozapine-N-oxide. The analytes and an internal standard (triprolidine) were extracted from alkalinized samples into ethyl acetate and back-extracted into 0.1 mol/L HCl. The acid extracts were chromatographed on a reversed-phase liquid chromatographic column with photodiode array detection (210-340 nm). With the 254-nm signal, between-run imprecision (CV) was <2% for clozapine and norclozapine at 400 mug/L, and 4.1% for clozapine-N-oxide at 100 mug/L. Absolute recovery exceeded 65%, and the detection limit was approximately 3-4 mug/L. In 25 patients at steady state at a mean daily clozapine dosage of 269 mg (3.09 mg/kg), clozapine averaged 231 +/- 144 mug/L (mean +/- SD); norclozapine and clozapine-N-oxide concentrations averaged 84% and 23% that of clozapine. Analyte concentrations were significantly correlated with daily dose. The method's ability to quantify clozapine and two major metabolites simultaneously with precision and sensitivity makes it useful in pharmacokinetic studies and therapeutic monitoring. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,CHEM LAB,GRAY 5,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,BELMONT,MA 02178. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. FU NIMH NIH HHS [NIMH MH-31154, NIMH MH-47370] NR 14 TC 72 Z9 74 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD AUG PY 1993 VL 39 IS 8 BP 1656 EP 1659 PG 4 WC Medical Laboratory Technology SC Medical Laboratory Technology GA LT228 UT WOS:A1993LT22800016 PM 8353952 ER PT J AU SHERIDAN, RL RYAN, CM PASTERNACK, MS WEBER, JM TOMPKINS, RG AF SHERIDAN, RL RYAN, CM PASTERNACK, MS WEBER, JM TOMPKINS, RG TI FLAVOBACTERIAL SEPSIS IN MASSIVELY BURNED PEDIATRIC-PATIENTS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID MENINGOSEPTICUM INFECTION; TRIMETHOPRIM-SULFAMETHOXAZOLE; WOUND BIOPSY; SUSCEPTIBILITY; PNEUMONIA AB An experience with wound sepsis due to Flavobacterium meningosepticum in two pediatric burn patients is described. This organism, which is typically found in water and soil, generally has low pathogenicity but may become clinically important in immunocompromised hosts. It is typically resistant to antibiotics prescribed for infections caused by aerobic, gram-negative bacteria. When flavobacteria are suspected as pathogens, initial therapy should begin with ciprofloxacin, trimethoprim-sulfamethoxazole, or clindamycin. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT INFECT DIS SERV,BOSTON,MA 02114. RP SHERIDAN, RL (reprint author), BOSTON UNIV,SHRINERS BURNS INST,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 31 TC 25 Z9 25 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD AUG PY 1993 VL 17 IS 2 BP 185 EP 187 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA LP455 UT WOS:A1993LP45500005 PM 8399864 ER PT J AU FISHER, CM AF FISHER, CM TI COMPLEX HALLUCINATORY STATE OCCURRING POSTSURGERY - A CASE-REPORT SO CLINICAL NEUROPHARMACOLOGY LA English DT Note DE HALLUCINATIONS; POSTSURGERY; ABNORMAL MENTAL STATE ID VISUAL HALLUCINATIONS; EYE CLOSURE AB A patient had unpleasant complex hallucinatory activity beginning 36 h postsurgery that lasted 48 h. Closing the eyes precipitated a flood of visual imagery that immediately roused the patient and prevented sleep. The imagery was predominantly visual, but there were auditory and narrative components suggesting a relationship to dreaming. An electroencephalogram showed that the hallucinatory activity was related to a recurring sequence of drowsiness, a few vertex slow waves, a myoclonic jerk, and arousal. Morphine was a prime suspect as the causative agent. The basic disturbance probably lay in the sleep-dream system. The syndrome has not been fully defined in the past. RP FISHER, CM (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 3 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-5664 J9 CLIN NEUROPHARMACOL JI Clin. Neuropharmacol. PD AUG PY 1993 VL 16 IS 4 BP 366 EP 371 DI 10.1097/00002826-199308000-00010 PG 6 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA LM717 UT WOS:A1993LM71700010 PM 8374917 ER PT J AU SHERMAN, JC LUST, B AF SHERMAN, JC LUST, B TI A NOTE ON CONTINUITY OF UNIVERSAL GRAMMAR - REPLY TO CAIRNS, MCDANIEL AND HSU SO COGNITION LA English DT Discussion C1 CORNELL UNIV,DEPT HUMAN DEV & FAMILY STUDIES,ITHACA,NY 14853. CORNELL UNIV,DEPT MODERN LANGUAGES & LINGUIST,ITHACA,NY 14853. RP SHERMAN, JC (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROPSYCHOL LAB,VINCENT BURNHAM 725,BOSTON,MA 02114, USA. NR 11 TC 1 Z9 1 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0010-0277 J9 COGNITION JI Cognition PD AUG PY 1993 VL 48 IS 2 BP 195 EP 197 DI 10.1016/0010-0277(93)90031-P PG 3 WC Psychology, Experimental SC Psychology GA LZ708 UT WOS:A1993LZ70800006 ER PT J AU BAGLIVO, J OLIVIER, D PAGANO, M AF BAGLIVO, J OLIVIER, D PAGANO, M TI ANALYSIS OF DISCRETE-DATA - RERANDOMIZATION METHODS AND COMPLEXITY SO COMPUTATIONAL STATISTICS & DATA ANALYSIS LA English DT Article DE GOODNESS-OF-FIT TESTS; LOG-LINEAR MODELS; MAX TEST; MULTINOMIAL MODELS; CONTINGENCY TABLES; CHI-SQUARED TEST; LIKELIHOOD RATIO TEST; POWER DIVERGENCE STATISTIC ID OF-FIT TESTS; CONTINGENCY-TABLES; DISTRIBUTIONS AB Analysis of discrete data, and especially contingency table data, plays a central role in biostatistics. Traditional methods rely on approximations based on asymptotic results which are very powerful but not always appropriate. In this article we show that efficient rerandomization methods may be developed for many commonly used models and tests: multinomial testing, specifically goodness-of-fit and max tests; and goodness-of-fit of log-linear models for contingency tables. The feasibility (complexity) of these algorithms is a function of the sufficient statistics for the models. By contrast, algorithms which require the explicit enumeration of all outcomes in the sample space are exponential in the degrees of freedom, and are usually not feasible except when sample sizes are unrealistically small. The algorithms we present are different from recently proposed methods since we show how to calculate permutation distributions of commonly used statistics rather than calculating p-values for exact tests, and we emphasize underlying probability formulas rather than implementation details. C1 BOSTON COLL,DEPT MATH,CHESTNUT HILL,MA 02167. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 19 TC 7 Z9 7 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-9473 J9 COMPUT STAT DATA AN JI Comput. Stat. Data Anal. PD AUG PY 1993 VL 16 IS 2 BP 175 EP 184 DI 10.1016/0167-9473(93)90112-7 PG 10 WC Computer Science, Interdisciplinary Applications; Statistics & Probability SC Computer Science; Mathematics GA LR057 UT WOS:A1993LR05700003 ER PT J AU MOHIMEN, A NEUMANN, R FOSTER, CS AHMED, AR AF MOHIMEN, A NEUMANN, R FOSTER, CS AHMED, AR TI DETECTION AND PARTIAL CHARACTERIZATION OF OCULAR CICATRICIAL PEMPHIGOID ANTIGENS ON COLO AND SCABER TUMOR-CELL LINES SO CURRENT EYE RESEARCH LA English DT Article ID MEMBRANE ZONE ANTIBODIES; INDIRECT IMMUNOFLUORESCENCE; CIRCULATING AUTOANTIBODIES; RHEUMATOID-ARTHRITIS; PROTEIN; RADIOIMMUNOASSAY; PLAKOGLOBIN; AUTOIMMUNE; SUBSTANCE; CARCINOMA AB Ocular cicatricial pemphigoid (OCP) is a chronic autoimmune inflammatory disease which affects the conjunctiva and other squamous epithelial mucous membranes resulting in a scarring process. It is characterized by the deposition of an antibasement membrane zone (BMZ) antibody in vivo, Sera from 11 patients with active OCP were studied. Using monkey esophagus and normal skin as substrate, weak staining of the BMZ was observed in conventional indirect immunofluorescence (IIF) assay. Using salt split human skin as substrate, the OCP sera demonstrated binding to the epidermal side of the split. in low titers with weak staining. Ten of the 11 sera were positive on an immunoblot assay using COLO and SCaBER tumor cell lysates demonstrating 230, 205, 160. and 85 kD proteins. Sera from six bullous pemphigoid (BP) patients. with only cutaneous involvement and high titer of anti-BMZ antibody, as detected by IIF, also bound to 230, 160, and 85 kD proteins on both lysates in comigration experiments. Serum from five normal individuals and two patients each with severe atopic conjunctival disease. erythema multiforme with chronic conjunctivitis and systemic lupus erythematosus (SLE). did not demonstrate those bands. When the two lysates were first absorbed with BP sera and then the same lysates were immunoblotted with OCP sera, in all ten OCP sera the 230, 160. and 85 kD bands were eliminated and only a single 205 kD band was uniformly present. These results indicate that OCP sera recognize peptide(s) present in 230. 205 and 160 kD proteins in lysates from COLO and SCaBER tumor cells. These proteins contain the immunodominant region of the BMZ molecule(s) in which the OCP antigen(s) reside. The OCP antigen(s) appears to be distinct from the BP antigen(s). C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. RP MOHIMEN, A (reprint author), HARVARD UNIV,SCH DENT MED,DEPT ORAL PATHOL,CTR BLOOD RES,BOSTON,MA 02115, USA. FU NEI NIH HHS [EY08378]; NIDCR NIH HHS [DE09978] NR 41 TC 22 Z9 22 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD AUG PY 1993 VL 12 IS 8 BP 741 EP 752 DI 10.3109/02713689308995770 PG 12 WC Ophthalmology SC Ophthalmology GA LW715 UT WOS:A1993LW71500008 PM 8222735 ER PT J AU LIPTON, SA AF LIPTON, SA TI MOLECULAR MECHANISMS OF TRAUMA-INDUCED NEURONAL DEGENERATION SO CURRENT OPINION IN NEUROLOGY AND NEUROSURGERY LA English DT Review ID METHYL-D-ASPARTATE; EXCITATORY AMINO-ACIDS; SPINAL-CORD INJURY; PROTEIN-KINASE-C; CONCUSSIVE BRAIN INJURY; HIPPOCAMPAL PYRAMIDAL NEURONS; FIBROBLAST GROWTH-FACTOR; FOCAL CEREBRAL-ISCHEMIA; CENTRAL-NERVOUS-SYSTEM; NITRIC-OXIDE AB Recent studies suggest that various neuron-specific responses, including activation of glutamate receptors, muscarinic receptors, and oxidative stress, contribute to the events leading to brain and spinal cord neuronal degeneration after trauma. These specific mechanisms and possible future treatments are highlighted in this review. C1 BETH ISRAEL HOSP,BOSTON,MA 02215. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 109 TC 51 Z9 52 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 AUG PY 1993 VL 6 IS 4 BP 588 EP 596 PG 9 WC Neurosciences SC Neurosciences & Neurology GA LN915 UT WOS:A1993LN91500016 PM 8400474 ER PT J AU HYMAN, SE AF HYMAN, SE TI MOLECULAR AND CELL BIOLOGY OF ADDICTION SO CURRENT OPINION IN NEUROLOGY AND NEUROSURGERY LA English DT Article ID RAT NUCLEUS-ACCUMBENS; VENTRAL TEGMENTAL AREA; DELTA-OPIOID RECEPTOR; DOPAMINE TRANSPORTER; PHARMACOLOGICAL CHARACTERIZATION; OPIATE WITHDRAWAL; CHRONIC COCAINE; LOCUS-CERULEUS; C-FOS; SEROTONIN TRANSPORTER AB Progress was made during the past year in several important areas relevant to cellular and molecular research on addiction. This includes a better understanding of the functioning of neural circuitry involved in the reinforcing properties of drugs of abuse, the cloning of complementary DNA's encoding important molecular targets of addictive drugs, including the first opiate receptors to be cloned, and progress in understanding the molecular basis of adaptive processes underlying dependence and withdrawal. RP HYMAN, SE (reprint author), MASSACHUSETTS GEN HOSP,E BLDG 149 13TH ST CNY,BOSTON,MA 02129, USA. NR 34 TC 13 Z9 13 U1 0 U2 2 PU CURRENT SCIENCE LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0951-7383 J9 CURR OPIN NEUROL NEU PD AUG PY 1993 VL 6 IS 4 BP 609 EP 613 PG 5 WC Neurosciences SC Neurosciences & Neurology GA LN915 UT WOS:A1993LN91500019 PM 8400475 ER PT J AU NICHOLS, DH GENADRY, RR AF NICHOLS, DH GENADRY, RR TI PELVIC RELAXATION OF THE POSTERIOR COMPARTMENT SO CURRENT OPINION IN OBSTETRICS & GYNECOLOGY LA English DT Article AB Relaxation of the posterior compartment may involve the upper, middle, and/or lower portion of the posterior vaginal wall and result in a variety of disorders including enterocele, rectocele, and perineal defects. When symptomatic, singly, or in combination with other abnormalities, they deserve full evaluation and surgical correction. Their management and technical considerations for repair and prevention of recurrence are outlined including fecal incontinence. RP NICHOLS, DH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02114, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 1040-872X J9 CURR OPIN OBSTET GYN JI Curr. Opin. Obstet. Gynecol. PD AUG PY 1993 VL 5 IS 4 BP 458 EP 464 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA LR686 UT WOS:A1993LR68600005 PM 8400041 ER PT J AU RAYMOND, G HOLMES, LB AF RAYMOND, G HOLMES, LB TI CARDIO-FACIO-CUTANEOUS (CFC) SYNDROME - NEUROLOGICAL FEATURES IN 2 CHILDREN SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Note ID NOONAN SYNDROME; ANOMALIES; PATIENT; GROWTH AB Cardio-facio-cutaneous (CFC) syndrome consists of heart defects, a characteristic facial appearance, ectodermal abnormalities, growth retardation and developmental delay. The authors report two children with this condition, drawing particular attention to the neurological manifestations. The neurological features are neuro-opthalmological findings such as strabismus, ptosis and nystagmus, cortical atrophy, ventriculomegaly, mental retardation, seizures and hypotonia. These manifestations may allow differentiation of CFC from Noonan syndrome, which shares many of the physical features, but not these neurological features. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RAYMOND, G (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114, USA. NR 20 TC 18 Z9 20 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD AUG PY 1993 VL 35 IS 8 BP 727 EP 732 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA LP227 UT WOS:A1993LP22700009 PM 7687572 ER PT J AU LI, XP GOLDEN, J FAUSTMAN, DL AF LI, XP GOLDEN, J FAUSTMAN, DL TI FAULTY MAJOR HISTOCOMPATABILITY COMPLEX CLASS-II I-E EXPRESSION IS ASSOCIATED WITH AUTOIMMUNITY IN DIVERSE STRAINS OF MICE - AUTOANTIBODIES, INSULITIS, AND SIALADENITIS SO DIABETES LA English DT Article ID NONOBESE DIABETIC MICE; NOD MICE; DIABETOGENIC GENE; PREVENTION; MOUSE; MELLITUS; CELLS; SUSCEPTIBILITY; CHROMOSOME-1; DESTRUCTION AB Many regions and loci of the murine genome contribute to the pancreatic and salivary gland autoimmunity observed in the diabetic NOD mouse. Examination of the major histocompatibility complex region of the NOD mouse has revealed a defect in the expression of the major histocompatibility complex class II gene, I-E. To determine the isolated role of faulty I-E expression in abnormal self-recognition, we examined six commonly used inbred strains of mice on diverse genetic backgrounds that also do not express I-E, i.e., C57BL/10, SJL, ACA, DBA/1, NOD, and 129. Autoimmunity was assessed by the presence of inflammatory cell infiltrates (0, +/-, +, + +, + + +, + + + +) within and among the pancreatic islets and salivary glands, and autoantibodies to self determinants. At 6 mo of age, inflammatory infiltrates in the pancreas (0, 3 mice; +/-, 3 mice; +, 7 mice; ++, 6 mice; +++, 1 mouse; ++++, 5 mice) and/or salivary glands (0, 0 mice; +/-, 3 mice; +, 1 mouse; ++, 4 mice; +++, 6 mice; + + + +, 10 mice) were detected as well as autoantibodies in all 24 mice of all I-E- mouse strains on diverse genetic backgrounds. This indicates that defective expression of this single locus, in isolation, is sufficient for the spontaneous development of autoreactivity. In contrast, the simultaneous examination of 19 I-E+ mice on five commonly used inbred strains of mice (BALB/c, C67/KsJ, B10.BR, B10.A [2R], and B10.A [5R]) demonstrated no signs of humoral or cellular autoimmunity with target gland destruction or lymphocytic invasion. Our data suggest that many commonly used inbred strains of mice represent models of autoimmunity attributable to this single defective gene. The penetrance of pathology secondary to a defect in this gene appears to occur independently of a given major histocompatibility complex haplotype or background murine strain and for these murine models, does not lead to diabetic hyperglycemia. C1 MASSACHUSETTS GEN HOSP E,DIABET UNIT,IMMUNOBIOL LABS,BLDG 149,13TH ST,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NR 27 TC 11 Z9 12 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 AUG PY 1993 VL 42 IS 8 BP 1166 EP 1172 DI 10.2337/diabetes.42.8.1166 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LN587 UT WOS:A1993LN58700012 PM 8325448 ER PT J AU CASTANO, L ZIEGLER, AG ZIEGLER, R SHOELSON, S EISENBARTH, GS AF CASTANO, L ZIEGLER, AG ZIEGLER, R SHOELSON, S EISENBARTH, GS TI CHARACTERIZATION OF INSULIN AUTOANTIBODIES IN RELATIVES OF PATIENTS WITH TYPE-I DIABETES SO DIABETES LA English DT Article ID ISLET-CELL ANTIBODIES; SPONTANEOUS HYPOGLYCEMIA; CIRCULATING INSULIN; BINDING ANTIBODIES; MELLITUS; AUTOIMMUNITY; CHILDREN; PROTEINS; ASSAY AB We studied in detail the anti-insulin autoantibodies in 29 nondiabetic relatives of patients with type I diabetes. The affinity of the autoantibodies for [I-125]human insulin was high (1.34 x 10(9)-20.71 x 10(9) L/mol), and the capacity was low (0.84 x 10(-12)-37.80 x 10(-12) M). The product of affinity x capacity of each relative's antibodies directly correlated (r = 0.99) with the level of antibodies determined in our standard radioassay. The autoantibodies from each of the subjects studied had the same rank order of affinities for insulin from different species. Guinea pig, fish insulin, and insulin containing Trp rather than Leu in position 13 of the A-chain inhibited minimally the human insulin binding. Human proinsulin, insulin containing Gln rather than Glu in position 17 of the A-chain, and desoctapeptide insulin (des B23-30) all inhibited binding effectively. Insulin autoantibodies in relatives of patients with type I diabetes share common epitope(s), which suggests a common pathogenic mechanism for production of such antibodies. The epitopes from this initial analysis appear to include amino acids B1-B3 and A8-A13. The region recognized can be distinguished from the insulin receptor binding domain. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,BOSTON,MA 02115. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,BOSTON,MA 02215. RI Castano, Luis/C-3084-2009; Ziegler, Anette-Gabriele/M-4614-2014 OI Ziegler, Anette-Gabriele/0000-0002-6290-5548 FU NIDDK NIH HHS [DK-32083, DK-36836] NR 36 TC 56 Z9 56 U1 0 U2 4 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD AUG PY 1993 VL 42 IS 8 BP 1202 EP 1209 DI 10.2337/diabetes.42.8.1202 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LN587 UT WOS:A1993LN58700017 PM 8325453 ER PT J AU WULSIN, LR JACOBSON, AM RAND, LI AF WULSIN, LR JACOBSON, AM RAND, LI TI PSYCHOSOCIAL ADJUSTMENT TO ADVANCED PROLIFERATIVE DIABETIC-RETINOPATHY SO DIABETES CARE LA English DT Article ID PERSONALITY; PREVALENCE; DIAGNOSIS; MELLITUS; ILLNESS; RISK; AGE AB OBJECTIVE - To identify the major problems with adjustment to the advanced stages of proliferative diabetic retinopathy and to examine the relationship between adjustment and visual acuity. RESEARCH DESIGN AND METHODS - A cross-sectional descriptive cohort study was conducted at the referral-based eye unit at Joslin Diabetes Center in Boston, Massachusetts. We studied 47 adults with IDDM and advanced proliferative diabetic retinopathy. Thirty reported recent visual loss, and 17 had more stable vision. RESULTS - Psychosocial Adjustment to Illness Scale scores were significantly elevated relative to a normative diabetic sample (t = 2.94, P < 0.01). Our proliferative diabetic retinopathy sample reported the most difficulties in the domain of health-care orientation. No significant differences were observed in adjustment scores between those with recent partial visual loss and those with more stable vision. However, visual acuity in the best eye correlated significantly with the proliferative diabetic retinopathy sample's total adjustment score (r = -0.34, P = 0.02) and with 4 of 7 adjustment subscales. CONCLUSIONS- These results suggest that advanced proliferative diabetic retinopathy may be associated with particular difficulties in adjustment that are more related to best visual acuity than to recent visual loss. Relatively mild visual impairment may have significant psychosocial impact. C1 JOSLIN DIABET CTR, WP BEETHAM EYE UNIT, BOSTON, MA USA. JOSLIN DIABET CTR, MENTAL HLTH UNIT, BOSTON, MA USA. RP WULSIN, LR (reprint author), UNIV CINCINNATI, DEPT PSYCHIAT, 231 BETHESDA AVE, ML 559, CINCINNATI, OH 45267 USA. FU NIDDK NIH HHS [DK-27845]; NIMH NIH HHS [T32 MH-16259] NR 22 TC 13 Z9 13 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 EI 1935-5548 J9 DIABETES CARE JI Diabetes Care PD AUG PY 1993 VL 16 IS 8 BP 1061 EP 1066 DI 10.2337/diacare.16.8.1061 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LN778 UT WOS:A1993LN77800001 PM 8375233 ER PT J AU DIMARIO, U ANASTASI, E CRISA, L PERFETTI, R VARDI, P ZIEGLER, AG SOELDNER, JS AF DIMARIO, U ANASTASI, E CRISA, L PERFETTI, R VARDI, P ZIEGLER, AG SOELDNER, JS TI CIRCULATING ANTIIMMUNOGLOBULIN ANTIBODIES BEFORE THE ONSET OF TYPE-I DIABETES-MELLITUS - INVERSE CORRELATION WITH INSULIN AUTOANTIBODIES AND RATE OF PROGRESSION TO DIABETES IN ICA POSITIVE INDIVIDUALS SO DIABETES NUTRITION & METABOLISM LA English DT Article DE ANTIIMMUNOGLOBULIN ANTIBODIES; INSULIN AUTOANTIBODIES; TYPE-I DIABETES-MELLITUS; PREDIABETES ID ISLET-CELL ANTIBODIES; INTRAVENOUS GLUCOSE; FOLLOW-UP; AUTOIMMUNITY; RELATIVES; IDIOTYPES; PERIOD AB The presence of anti-immunoglobulin antibodies (alphaIgAb) compared with that of insulin autoantibodies (IAAb) and islet cell antibodies (ICA), has been investigated in subjects (n=18) at a high risk of developing Type I diabetes, half of whom have subsequently developed the disease. Correlations with clinical parameters or with the rate of progression to diabetes have been evaluated. alphaIgAb were present in 7 of the 9 patients who developed Type I diabetes (Group A) and in 3 of those without clinical symptoms of the disease (Group B). IAAb were positive in 6 of the 9 subjects in Group A and in 5 of Group B (ICA were present in all the subjects but one ). AlphaIgAb were inversely correlated with IAAb. AlphaIgAb levels showed a direct correlation with the number of days to overt diabetes; IAAb levels showed an inverse correlation in a similar evaluation. AlphaIgAb and IAAb, in addition to ICA, are of value in monitoring some of the early pre-clinical pathogenetic events. C1 JOSLIN RES CLIN,BOSTON,MA. UNIV ROME,DEPT ENDOCRINOL,I-00100 ROME,ITALY. RI Ziegler, Anette-Gabriele/M-4614-2014 OI Ziegler, Anette-Gabriele/0000-0002-6290-5548 NR 25 TC 0 Z9 0 U1 0 U2 1 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-3402 J9 DIABETES NUTR METAB JI Diabetes Nutr. Metab. PD AUG PY 1993 VL 6 IS 4 BP 195 EP 201 PG 7 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA MD295 UT WOS:A1993MD29500003 ER PT J AU LUND, T SHAIKH, S KENDALL, E CAMPBELL, RD HATTORI, M MAKINO, S COOKE, A AF LUND, T SHAIKH, S KENDALL, E CAMPBELL, RD HATTORI, M MAKINO, S COOKE, A TI RFLP ANALYSIS OF THE MHC CLASS-III REGION DEFINES UNIQUE HAPLOTYPES FOR THE NONOBESE DIABETIC, CATARACT SHIONOGI AND THE NONOBESE NONDIABETIC MOUSE STRAINS SO DIABETOLOGIA LA English DT Article DE MHC CLASS-III REGION; NONOBESE DIABETIC MOUSE; NONOBESE NONDIABETIC MOUSE; CATARACT SHIONOGI MOUSE; TYPE-1 (INSULIN-DEPENDENT) DIABETES-MELLITUS; RESTRICTION FRAGMENT LENGTH POLYMORPHISMS ID MAJOR HISTOCOMPATIBILITY COMPLEX; A BETA-CHAIN; SISTER STRAINS; MAP POSITION; GENES; MICE; H-2-COMPLEX; PREVENTION; ALPHA; LOCUS AB The non-obese diabetic (NOD) mouse strain which spontaneously develops diabetes is a model for human Type 1 (insulin-dependent) diabetes mellitus. At least one of several genes controlling diabetes in the NOD mouse has been mapped to the MHC. Although previous experiments have implicated the MHC class II genes in the development of the disease, the existence of other MHC linked susceptibility genes has not been ruled out. In order to identify these susceptibility genes we have further characterized the MHC haplotype of the NOD mouse and two non-diabetic sister strains, the non-obese non-diabetic (NON) and cataract Shionogi (CTS). We have examined the mouse MHC class III region for the presence of homologous genes to 17 newly isolated human MHC class III region genes (G1, G2, G4, G6, G7a/valyl-tRNA synthetase, HSP70, G8, G9, G10, G12, G13, G14, G15, G16, G17 and G18). We detect unique hybridizing DNA fragments for 16 of the 17 genes in six inbred mouse strains (NOD, NON, CTS, B10, BALB/c and CBA/J) indicating that this part of the H-2 region is similar to the human MHC class III region. Using a panel of restriction enzymes we have defined RFLPs for 6 (G2, G6, HSP70, G12, G16, G18) of the 16 cross-hybridizing probes. The RFLPs demonstrate that NOD, NON and CTS mouse strains each have a distinct MHC haplotype in the MHC class III region. C1 UNIV LONDON UNIV COLL, SCH MED, MED MOLEC BIOL UNIT, LONDON WC1E 6BT, ENGLAND. UNIV OXFORD, DEPT BIOCHEM, MRC, IMMUNOCHEM UNIT, OXFORD, ENGLAND. HARVARD UNIV, SCH MED, JOSLIN DIABET CTR, BOSTON, MA 02115 USA. SHIONOGI ABUHARI LABS, SHIGA, JAPAN. UNIV CAMBRIDGE, DEPT PATHOL, DIV IMMUNOL, CAMBRIDGE, ENGLAND. RP LUND, T (reprint author), UCL, SCH MED, DEPT IMMUNOL, 40-50 TOTTENHAM ST, LONDON W1P 9PG, ENGLAND. RI Cooke, Anne/E-8709-2012 FU Wellcome Trust NR 35 TC 10 Z9 10 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD AUG PY 1993 VL 36 IS 8 BP 727 EP 733 DI 10.1007/BF00401143 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LP033 UT WOS:A1993LP03300006 PM 8104833 ER PT J AU ALARCON, C RHODES, CJ AF ALARCON, C RHODES, CJ TI TRANSLATIONAL CONTROL OF PROINSULIN SYNTHESIS IN ISOLATED ISLETS - GLUCOSE-INDUCED PHOSPHORYLATION OF AN INITIATION-FACTOR SO DIABETOLOGIA LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD AUG PY 1993 VL 36 SU 1 BP A65 EP A65 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LZ274 UT WOS:A1993LZ27400243 ER PT J AU CHARLES, MA DUNN, F NATHAN, D SCAVINI, M AF CHARLES, MA DUNN, F NATHAN, D SCAVINI, M TI INSULIN ANTIBODY-LEVELS AFTER 2-3 YEARS OF INTRAPERITONEAL OR INTRAVENOUS INSULIN USING IMPLANTABLE INSULIN DELIVERY SO DIABETOLOGIA LA English DT Meeting Abstract C1 SAN RAFFAELLE HOSP,MILAN,ITALY. UNIV CALIF IRVINE,IRVINE,CA 92717. DUKE UNIV,DURHAM,NC 27706. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD AUG PY 1993 VL 36 SU 1 BP A161 EP A161 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LZ274 UT WOS:A1993LZ27400610 ER PT J AU MCGLADE, J BRUNKHORST, B ANDERSON, D MBAMALU, G SETTLEMAN, J DEDHAR, S ROZAKISADCOCK, M CHEN, LB PAWSON, T AF MCGLADE, J BRUNKHORST, B ANDERSON, D MBAMALU, G SETTLEMAN, J DEDHAR, S ROZAKISADCOCK, M CHEN, LB PAWSON, T TI THE N-TERMINAL REGION OF GAP REGULATES CYTOSKELETAL STRUCTURE AND CELL-ADHESION SO EMBO JOURNAL LA English DT Article DE CELL ADHESION; CYTOSKELETON; GAP ID GTPASE-ACTIVATING PROTEIN; EPIDERMAL GROWTH-FACTOR; RAS P21 GTPASE; MOLECULAR-CLONING; TYROSINE KINASES; FOCAL ADHESIONS; GENE-PRODUCT; SH2 DOMAINS; BINDING; PHOSPHORYLATION AB Ras GTPase activating protein (GAP) possesses a C-terminal domain that interacts with GTP-bound Ras, and an N-terminal region containing two SH2 domains and an SH3 domain. In addition to its association with Ras, GAP binds stably to autophosphorylated betaPDGF receptors, and to two cytoplasmic phosphoproteins: p62, an RNA binding protein, and p190, which possesses GAP activity towards small guanine nucleotide binding proteins in the Rho/Rac family. To define the region of GAP that mediates these interactions with cellular phosphoproteins, and to investigate the biological significance of these complexes, a truncated GAP polypeptide (GAP-N) containing residues 1-445 was stably expressed in Rat-2 fibroblasts. GAP-N contains the SH2 and SH3 domains, but lacks the Ras GTPase activating domain. Stimulation of cells expressing GAP-N with PDGF induced association of GAP-N with the betaPDGF receptor, and phosphorylation of GAP-N on tyrosine, consistent with the notion that GAP SH2 domains direct binding to the autophosphorylated betaPDGF receptor in vivo. GAP-N bound constitutively to p190 in both serum-deprived and growth factor-stimulated cells. This GAP-N-p190 complex had Rho GAP activity in vitro. The expression of GAP-N in Rat-2 cells correlated with changes in the cytoskeleton and in cell adhesion, typified by the disruption of action stress fibres, a reduction in focal contacts, and an impaired ability to adhere to fibronectin. These results suggest that the N-terminal domain of GAP can direct interactions with cellular phosphoproteins in vivo, and thereby exert an effector function which modulates the cytoskeleton and cell adhesion. This effect of GAP-N on the cytoskeleton correlates with its association with p190, and may therefore result from regulation of Rho/Rac GTPases by the GAP-p190 complex. GAP may therefore couple growth factors to control of cell shape and attachment. C1 UNIV SASKATCHEWAN,SASKATOON CANC CTR,SASKATOON S7N 4H4,SK,CANADA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MGH,CTR CANC,BOSTON,MA 02129. SUNNYBROOK HLTH SCI CTR,TORONTO M4N 3M5,ON,CANADA. RP MCGLADE, J (reprint author), MT SINAI HOSP,SAMUEL LUNENFELD RES INST,600 UNIV AVE,TORONTO M5G 1X5,ONTARIO,CANADA. RI Pawson, Tony/E-4578-2013 FU NIGMS NIH HHS [5RO1 GM38318-8195206] NR 32 TC 193 Z9 193 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD AUG PY 1993 VL 12 IS 8 BP 3073 EP 3081 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LP429 UT WOS:A1993LP42900010 PM 8344248 ER PT J AU CARNES, M GOODMAN, BM LENT, SJ VO, H AF CARNES, M GOODMAN, BM LENT, SJ VO, H TI HIGH-INTENSITY VENOUS SAMPLING REVEALS SUBTLE ALTERATIONS IN PLASMA ADRENOCORTICOTROPIN PATTERNS IN OLD RATS SO ENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; DIMINISHED DIURNAL SECRETION; ULTRADIAN RHYTHMS; SPECTRAL-ANALYSIS; PULSE FREQUENCY; ACTH; CORTICOSTERONE; PULSATILE; PITUITARY; CORTISOL AB Dysregulation of the hypothalamic-pituitary-adrenocortical axis has been theoretically linked to the processes of aging for decades. To investigate the effect of age on high frequency rhythms of plasma ACTH at the time of circadian activation, integrated 2-min blood samples were collected over 4 h in 10 young and 14 old rats with simultaneous plasma volume replacement. Plasma ACTH time series were analyzed in the time and frequency domains. Relative to young rats, old rats had a significantly later onset of the diurnal surge, more spectral power (R2) at lower frequencies, a lack of correlation between the slope of the spectral background continuum and the R2 at periods less than approximately 11 min, a stretching of the time scale in the composite spectra by 18.5%, and an amplitude reduction of the major composite spectral peak by 31%. These findings support the existence of subtle, but significant, alterations in the pattern of plasma ACTH with age and a delayed response of the hypothalamic-pituitary-adrenocortical axis to circadian activation. The differences in spectra suggest a weaker coupling with age between the high frequency signal input (that may reflect depolarization of groups of corticotrophs) and the system response, which could account for the delay in onset of the diurnal surge seen in the time domain. C1 UNIV WISCONSIN, DEPT MED, MADISON, WI 53705 USA. UNIV WISCONSIN, DEPT BIOSTAT, MADISON, WI 53705 USA. UNIV WISCONSIN, DEPT SPACE SCI, MADISON, WI 53705 USA. UNIV WISCONSIN, CTR ENGN, MADISON, WI 53705 USA. RP CARNES, M (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR, CTR GERIATR RES EDUC & CLIN, 2500 OVERLOOK TERRACE, MADISON, WI 53705 USA. FU NIDDK NIH HHS [DK-40759] NR 52 TC 11 Z9 11 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD AUG PY 1993 VL 133 IS 2 BP 608 EP 616 DI 10.1210/en.133.2.608 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LQ846 UT WOS:A1993LQ84600027 PM 8393770 ER PT J AU URENA, P KONG, XF ABOUSAMRA, AB JUPPNER, H KRONENBERG, HM POTTS, JT SEGRE, GV AF URENA, P KONG, XF ABOUSAMRA, AB JUPPNER, H KRONENBERG, HM POTTS, JT SEGRE, GV TI PARATHYROID-HORMONE (PTH) PTH-RELATED PEPTIDE RECEPTOR MESSENGER RIBONUCLEIC-ACIDS ARE WIDELY DISTRIBUTED IN RAT-TISSUES SO ENDOCRINOLOGY LA English DT Article ID CENTRAL NERVOUS-SYSTEM; HUMORAL HYPERCALCEMIA; SMOOTH-MUSCLE; MOLECULAR-CLONING; EXPRESSION; PROTEIN; CALCIUM; CELLS; GENE; RNA AB PTH/PTH-related peptide (PTHrP) receptor mRNAs are widely distributed in rat tissues. PTH and PTHrP, a peptide responsible for hypercalcemia associated with cancers, bind equivalently to common receptors that initially were cloned from rat bone and opossum renal cell cDNA libraries. In this study we used rat PTH/PTHrP receptor cDNA to probe for receptor expression in different rat tissues by Northern blot analysis. PTH/PTHrP receptor transcripts are highly expressed in PTH target tissues, kidney and bone. Receptor transcripts, however, also are expressed in many other tissues, including aorta, adrenal gland, bladder, brain, cerebellum, breast, heart, ileum, liver, lung, skeletal muscle, ovary, placenta, skin, spleen, stomach, uterus, and testes. The major transcript in most tissues is 2.3-2.5 kilobases in size. At least two larger mRNAs are observed in kidney and liver, and smaller transcripts are found in kidney, skin, and testes. The most abundant testicular transcript is 1.4-1.5 kilobases in size, and it hybridizes with two different cDNA probes that encode portions of the receptor sequence from the putative fourth transmembrane domain to its C-terminal end. It does not hybridize, however, with a probe encoding the first 107 residues of the receptor sequence. Although, PTH/PTHrP receptor mRNAs are highly expressed in kidney and bone, classic PTH targets that are associated with calcium homeostasis, their wide tissue distribution suggests that PTH and/or PTHrP have other physiological roles, particularly in these other tissues. The mechanisms leading to tissue-specific expression of PTH/PTHrP receptor transcripts of different sizes and the functions of these mRNAs remain to be determined. C1 MASSACHUSETTS GEN HOSP, ENDOCRINE UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02114 USA. OI Abou-Samra, Abdul/0000-0001-8735-1142 FU NIDDK NIH HHS [DK-11794] NR 52 TC 260 Z9 267 U1 0 U2 3 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD AUG PY 1993 VL 133 IS 2 BP 617 EP 623 DI 10.1210/en.133.2.617 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LQ846 UT WOS:A1993LQ84600028 PM 8393771 ER PT J AU MARKESICH, DC ELZAATARI, FAK GRAHAM, DY AF MARKESICH, DC ELZAATARI, FAK GRAHAM, DY TI ACTIVITY OF CLARITHROMYCIN AGAINST INTRACELLULAR MYCOBACTERIUM-PARATUBERCULOSIS - PUTATIVE AGENT OF CROHNS-DISEASE SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY LA English DT Article DE MYCOBACTERIUM-PARATUBERCULOSIS; CROHNS DISEASE; SUSCEPTIBILITY; CLARITHROMYCIN; MYCOBACTERIA AB Objective: To test whether Mycobacterium paratuberculosis, the putative etiologic agent of Crohn's disease, was senisitive to clarithromycin. Design: To test the susceptibility of two mycobactin-dependent mycobacteria, M. paratuberculosis and M. avium subsp. silvaticum, to clarithromycin grown in mouse monocyte/macrophage cell line J774A.1. Results: Clarithromycin, 2 and 4 mug/ml, inhibited M. paratuberculosis (80 and 25% of control, respectively) but was less effective against M. avium subsp. silvaticum (80 and 82% of control, respectively) growing intracellularly in the murine macrophage cell line J-774A.1. Conclusions: Clarithromycin shows promise for use in double-blind controlled trials for testing the hypothesis that M. paratuberculosis is etiologically related to Crohn's disease. C1 VET AFFAIRS MED CTR 111D,INFLAMMATORY BOWEL DIS LAB,2002 HOLCOMBE BLVD,HOUSTON,TX 77030. NR 0 TC 7 Z9 7 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-691X J9 EUR J GASTROEN HEPAT JI Eur. J. Gastroenterol. Hepatol. PD AUG PY 1993 VL 5 IS 8 BP 613 EP 615 DI 10.1097/00042737-199308000-00010 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LV086 UT WOS:A1993LV08600010 ER PT J AU VIVIER, E DASILVA, AJ ACKERLY, M LEVINE, H RUDD, CE ANDERSON, P AF VIVIER, E DASILVA, AJ ACKERLY, M LEVINE, H RUDD, CE ANDERSON, P TI ASSOCIATION OF A 70-KDA TYROSINE PHOSPHOPROTEIN WITH THE CD16-ZETA-GAMMA COMPLEX EXPRESSED IN HUMAN NATURAL-KILLER-CELLS SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE NATURAL KILLER; TYROSINE PHOSPHORYLATION; CD16; ZETA-ASSOCIATED PROTEIN ID FC-EPSILON-RI; RECEPTOR ZETA-CHAIN; T-CELL; ANTIGEN RECEPTOR; SIGNAL TRANSDUCTION; GAMMA-RIII; IGG FC; PROTEIN; KINASE; PHOSPHORYLATION AB The CD16:zeta:gamma receptor complex allows natural killer (NK) cells to recognize and eliminate antibody-coated target cells. Whereas the ectodomain of CD16 is the receptor for Fcgamma domains of immunoglobulins, disulfide-linked homo- and heterodimers composed of zeta and gamma are required for the cell surface expression, and signal transduction properties of the complex. Engagement of CD16 activates the tyrosine kinase pathway, which induces the tyrosine phosphorylation of several substrates, including the zeta subunit and the phospholipase C gamma-1 and gamma-2 isoforms. Here we show that CD16 stimulation of either peripheral blood NK cells, leukemic NK cells, or Jurkat transformants expressing a CD16:zeta:gamma receptor complex, results in the tyrosine phosphorylation of a 70 kDa zeta-associated protein (pp70). Similarly, a 70-kDa zeta-associated phosphoprotein in T cells has been shown to be a tyrosine kinase (ZAP-70). Peptide mapping analysis indicates that the 70-kDa zeta-associated phosphoproteins from T cells and NK cells are structurally indistinguishable. We conclude that the CD 16:zeta:gamma complex may use a ZAP-70-related non-receptor tyrosine kinase, in the CD16 signaling cascade leading to NK 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 PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. FU NCI NIH HHS [CA53595] NR 34 TC 59 Z9 59 U1 0 U2 2 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 AUG PY 1993 VL 23 IS 8 BP 1872 EP 1876 DI 10.1002/eji.1830230821 PG 5 WC Immunology SC Immunology GA LT241 UT WOS:A1993LT24100020 PM 8344348 ER PT J AU GRIFFIN, JD CARLESSO, N MATULONIS, U ERNST, T OKUDA, K MATSUGUCHI, T DRUKER, B AF GRIFFIN, JD CARLESSO, N MATULONIS, U ERNST, T OKUDA, K MATSUGUCHI, T DRUKER, B TI THE P21OBCR/ABL ONCOGENE ACTIVATES IL-3/GM-CSF RECEPTOR SIGNAL-TRANSDUCTION PATHWAYS IN MYELOID CELL-LINES SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA. NR 0 TC 2 Z9 2 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 AUG PY 1993 VL 21 IS 8 BP 1010 EP 1010 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA MW613 UT WOS:A1993MW61300006 ER PT J AU ARCICI, RJ VISSER, M DUNISSIECONOMOU, K MOGUL, M DAHL, G AF ARCICI, RJ VISSER, M DUNISSIECONOMOU, K MOGUL, M DAHL, G TI MDR1 P-GLYCOPROTEIN EXPRESSION AND FUNCTION DURING HUMAN HEMATOLYMPHOPOIETIC DIFFERENTIATION AND MYELOGENOUS LEUKEMIA SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA. CHILDRENS HOSP,BOSTON,MA. UNIV AMSTERDAM,AMSTERDAM,NETHERLANDS. STANFORD UNIV,PALO ALTO,CA 94304. NR 0 TC 0 Z9 0 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 AUG PY 1993 VL 21 IS 8 BP 1078 EP 1078 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA MW613 UT WOS:A1993MW61300248 ER PT J AU GORDON, MS COSTA, J SLEDGE, GW HAYES, D GALLI, S HOFFMAN, R MERICA, E RICH, W HARKINS, B MCGUIRE, B DEMETRI, G AF GORDON, MS COSTA, J SLEDGE, GW HAYES, D GALLI, S HOFFMAN, R MERICA, E RICH, W HARKINS, B MCGUIRE, B DEMETRI, G TI PHASE-I TRIAL OF RECOMBINANT METHIONYL HUMAN STEM-CELL FACTOR (SCF) IN WOMEN WITH LOCALLY ADVANCED (IIIB) OR METASTATIC (IV) BREAST-CANCER TREATED WITH CYCLOPHOSPHAMIDE (C) AND DOXORUBICIN (A) SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 INDIANA UNIV,INDIANAPOLIS,IN 46204. DANA FARBER CANC INST,BOSTON,MA. AMGEN INC,THOUSAND OAKS,CA. NR 0 TC 0 Z9 0 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 AUG PY 1993 VL 21 IS 8 BP 1151 EP 1151 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA MW613 UT WOS:A1993MW61300518 ER PT J AU ZHOU, D DIFIGLIA, M AF ZHOU, D DIFIGLIA, M TI BASIC FIBROBLAST GROWTH-FACTOR ENHANCES THE GROWTH OF POSTNATAL NEOSTRIATAL GABAERGIC NEURONS IN-VITRO SO EXPERIMENTAL NEUROLOGY LA English DT Article ID CEREBELLAR GRANULE CELLS; CENTRAL NERVOUS-SYSTEM; D-ASPARTATE RECEPTOR; RAT-BRAIN; HIPPOCAMPAL-NEURONS; STRIATAL CULTURES; NEURITE EXTENSION; CORTICAL-NEURONS; FACTOR FGF; C-FOS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP ZHOU, D (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,CELLULAR NEUROBIOL LAB,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS 16367] NR 50 TC 22 Z9 22 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD AUG PY 1993 VL 122 IS 2 BP 171 EP 188 DI 10.1006/exnr.1993.1118 PG 18 WC Neurosciences SC Neurosciences & Neurology GA LY556 UT WOS:A1993LY55600001 PM 8405257 ER PT J AU SHELDON, LA KINGSTON, RE AF SHELDON, LA KINGSTON, RE TI HYDROPHOBIC COILED-COIL DOMAINS REGULATE THE SUBCELLULAR-LOCALIZATION OF HUMAN HEAT-SHOCK FACTOR-II SO GENES & DEVELOPMENT LA English DT Article DE HEAT SHOCK FACTOR-II; COILED-COIL STRUCTURES; LEUCINE ZIPPER; SUBCELLULAR LOCALIZATION ID NF-KAPPA-B; DNA-BINDING SPECIFICITY; TRANSCRIPTION FACTOR; LEUCINE ZIPPER; SACCHAROMYCES-CEREVISIAE; GLUCOCORTICOID RECEPTOR; MOLECULAR-CLONING; NUCLEAR LOCATION; PROTEIN; ACTIVATION AB HSF2, one of the heat shock transcription factors in mammalian cells, is localized to the cytoplasm during normal growth and moves to the nucleus upon activation. Heat shock transcription factors in metazoans contain four hydrophobic heptad repeat sequences, three in the amino terminus and one in the carboxyl terminus, which are predicted to form alpha-helical coiled-coil structures analogous to the leucine zipper. Here, we show that point mutations in either of two amino-terminal zippers or in the carboxy-terminal zipper disrupt normal localization of HSF2 and cause it to be constitutively nuclear. We demonstrate further that two sequences immediately surrounding the amino-terminal zipper domain are required for nuclear localization. These sequences fit the consensus for a bipartite nuclear localization signal (NLS). We suggest that interactions between the amino- and carboxy-terminal zippers normally mask the NLS sequences of HSF2 and that these interactions are disrupted upon activation to expose the NLS sequences and allow transport of HSF2 to the nucleus. We conclude that zipper domains can regulate subcellular localization. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. FU NIGMS NIH HHS [GM43901] NR 50 TC 83 Z9 87 U1 0 U2 1 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 AUG PY 1993 VL 7 IS 8 BP 1549 EP 1558 DI 10.1101/gad.7.8.1549 PG 10 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA LR776 UT WOS:A1993LR77600007 PM 8339932 ER PT J AU BUCKWALTER, MS TESTA, CM NOEBELS, JL CAMPER, SA AF BUCKWALTER, MS TESTA, CM NOEBELS, JL CAMPER, SA TI GENETIC-MAPPING AND EVALUATION OF CANDIDATE GENES FOR SPASMODIC, A NEUROLOGICAL MOUSE MUTATION WITH ABNORMAL STARTLE RESPONSE SO GENOMICS LA English DT Article ID FEAR-POTENTIATED STARTLE; CALCIUM-BINDING PROTEIN; GLUTAMATE RECEPTORS; MOLECULAR-CLONING; ACOUSTIC STARTLE; MAMMALIAN BRAIN; ANNEXIN-VI; CHROMOSOME-11; FAMILY; P68 C1 UNIV MICHIGAN,SCH MED,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,NEUROSCI PROGRAM,ANN ARBOR,MI 48109. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. BAYLOR COLL MED,DEV NEUROGENET LAB,HOUSTON,TX 77030. OI Camper, Sally/0000-0001-8556-3379; Noebels, Jeffrey /0000-0002-2887-0839 FU NINDS NIH HHS [NS19613, R01NS29709] NR 38 TC 22 Z9 22 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 AUG PY 1993 VL 17 IS 2 BP 279 EP 286 DI 10.1006/geno.1993.1322 PG 8 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA LP815 UT WOS:A1993LP81500002 PM 8406478 ER PT J AU GORLIN, JB HENSKE, E WARREN, ST KUNST, CB DURSO, M PALMIERI, G HARTWIG, JH BRUNS, G KWIATKOWSKI, DJ AF GORLIN, JB HENSKE, E WARREN, ST KUNST, CB DURSO, M PALMIERI, G HARTWIG, JH BRUNS, G KWIATKOWSKI, DJ TI ACTIN-BINDING PROTEIN (ABP-280) FILAMIN GENE (FLN) MAPS TELOMERIC TO THE COLOR-VISION LOCUS (R/GCP) AND CENTROMERIC TO G6PD IN XQ28 SO GENOMICS LA English DT Note ID YEAST ARTIFICIAL CHROMOSOMES; DREIFUSS MUSCULAR-DYSTROPHY; INCONTINENTIA PIGMENTI; HUMAN XQ24-XQ28; X-CHROMOSOME; FACTOR-VIII; DNA PROBES; IDENTIFICATION; LOCALIZATION; LINKAGE C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV EXPTL MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. EMORY UNIV,SCH MED,DEPT PEDIAT,ATLANTA,GA 30322. EMORY UNIV,SCH MED,DEPT BIOCHEM,ATLANTA,GA 30322. INT INST GENET & BIOPHYS,NAPLES,ITALY. EMORY UNIV,SCH MED,HOWARD HUGHES MED INST,ATLANTA,GA 30322. RP GORLIN, JB (reprint author), CHILDRENS HOSP MED CTR,DIV HEMATOL,BLOOD BANK,FARLEY 4,300 LONGWOOD AVE,BOSTON,MA 02115, USA. RI Warren, Stephen/A-2498-2012; OI Palmieri, Giuseppe/0000-0002-4350-2276 FU NHLBI NIH HHS [HL18658, HL02158, HL01582]; Telethon [109] NR 23 TC 36 Z9 36 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 0888-7543 J9 GENOMICS JI Genomics PD AUG PY 1993 VL 17 IS 2 BP 496 EP 498 DI 10.1006/geno.1993.1354 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA LP815 UT WOS:A1993LP81500034 PM 8406501 ER PT J AU GARG, HG THOMPSON, BT DAHLBERG, CGW JOSEPH, PM SPENCE, CR HALES, CA AF GARG, HG THOMPSON, BT DAHLBERG, CGW JOSEPH, PM SPENCE, CR HALES, CA TI CHEMICAL-COMPOSITION OF 2 COMMERCIAL HEPARINS WITH DIFFERING ANTIPROLIFERATIVE EFFECT ON SMOOTH-MUSCLE CELLS SO GLYCOCONJUGATE JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 2 TC 0 Z9 0 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0282-0080 J9 GLYCOCONJUGATE J JI Glycoconjugate J. PD AUG PY 1993 VL 10 IS 4 BP 252 EP 252 DI 10.1007/BF01209904 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LY104 UT WOS:A1993LY10400103 ER PT J AU BACKER, AE HOLGERSSON, J BINNS, RM SAMUELSSON, BE AF BACKER, AE HOLGERSSON, J BINNS, RM SAMUELSSON, BE TI STRUCTURAL-ANALYSIS BY GC/MS OF RELEASED OLIGOSACCHARIDES FROM GLYCOSPHINGOLIPIDS FROM DIFFERENT ORGANS OF A SEMI-INBRED PIG STRAIN SO GLYCOCONJUGATE JOURNAL LA English DT Meeting Abstract C1 GOTHENBURG UNIV,SAHLGRENS HOSP,DEPT MED BIOCHEM,S-41345 GOTHENBURG,SWEDEN. GOTHENBURG UNIV,SAHLGRENS HOSP,DEPT CLIN CHEM & TRANSFUS MED,S-41345 GOTHENBURG,SWEDEN. AFRC,BABRAHAM,ENGLAND. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 1 TC 1 Z9 1 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0282-0080 J9 GLYCOCONJUGATE J JI Glycoconjugate J. PD AUG PY 1993 VL 10 IS 4 BP 298 EP 298 DI 10.1007/BF01210044 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LY104 UT WOS:A1993LY10400243 ER PT J AU HARTNETT, ME GILBERT, MM HIROSE, T RICHARDSON, TM KATSUMI, O AF HARTNETT, ME GILBERT, MM HIROSE, T RICHARDSON, TM KATSUMI, O TI GLAUCOMA AS A CAUSE OF POOR VISION IN SEVERE RETINOPATHY OF PREMATURITY SO GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY LA English DT Article ID OPTIC-NERVE FIBERS; PREFERENTIAL LOOKING; YOUNG-CHILDREN; VISUAL-ACUITY; INFANTS AB Despite surgical reattachment of the retina in infants with severe retinopathy of prematurity (ROP), visual acuity may decline. We performed gonioscopy and applanation tonometry on 26 eyes of 17 infants with severe ROP who were randomly selected and followed prospectively for 2 years. Of these 26 eyes, one eye of one patient had only peripheral retinocryopexy for threshold stage III disease and had an attached retina before enrollment into the study. Sixteen infants subsequently underwent vitrectomy, scleral buckle, or both. Retinal reattachment of the posterior pole was present in at least one eye each of 10 of the 17 infants. Glaucoma was diagnosed in 5 of the 10 patients; all 5 showed a decrease in visual acuity of greater than 1 octave. Of the 5 infants without glaucoma, 3 showed visual improvement, and 2 remained the same. Although we studied a small number of cases, our results suggest that glaucoma may be a cause of visual decline in infants with severe ROP. A decline in visual acuity in infants with severe ROP and surgical retinal reattachment may warn us of glaucoma, as this diagnosis is difficult to make in these small infants. C1 HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. SCHEPENS EYE RES INST,BOSTON,MA. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RP HARTNETT, ME (reprint author), RETINA ASSOCIATES,100 CHARLES RIVER PLAZA,BOSTON,MA 02114, USA. NR 26 TC 9 Z9 9 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0721-832X J9 GRAEF ARCH CLIN EXP JI Graefes Arch. Clin. Exp. Ophthalmol. PD AUG PY 1993 VL 231 IS 8 BP 433 EP 438 DI 10.1007/BF02044227 PG 6 WC Ophthalmology SC Ophthalmology GA LP810 UT WOS:A1993LP81000001 PM 8224940 ER PT J AU RUBIN, RH FERRARO, MJ AF RUBIN, RH FERRARO, MJ TI UNDERSTANDING AND DIAGNOSING INFECTIOUS COMPLICATIONS IN THE IMMUNOCOMPROMISED HOST - CURRENT ISSUES AND TRENDS SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; HERPES-SIMPLEX VIRUS; RENAL-TRANSPLANT RECIPIENT; SYNDROME AIDS; LEGIONNAIRES-DISEASE; PNEUMOCYSTIS-CARINII; CYTOMEGALO-VIRUS; IDENTIFICATION; FOSCARNET; PATIENT C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP RUBIN, RH (reprint author), MASSACHUSETTS GEN HOSP,CLIN INVEST PROGRAM,32 FRUIT ST,BOSTON,MA 02114, USA. NR 41 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 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD AUG PY 1993 VL 7 IS 4 BP 795 EP 812 PG 18 WC Oncology; Hematology SC Oncology; Hematology GA LN536 UT WOS:A1993LN53600004 PM 8354657 ER PT J AU STRUYK, L KURNICK, JT HAWES, GE VANLAAR, JM SCHIPPER, R OKSENBERG, JR STEINMAN, L DEVRIES, RRP BREEDVELD, FC VANDENELSEN, P AF STRUYK, L KURNICK, JT HAWES, GE VANLAAR, JM SCHIPPER, R OKSENBERG, JR STEINMAN, L DEVRIES, RRP BREEDVELD, FC VANDENELSEN, P TI T-CELL RECEPTOR V-GENE USAGE IN SYNOVIAL-FLUID LYMPHOCYTES OF PATIENTS WITH CHRONIC ARTHRITIS SO HUMAN IMMUNOLOGY LA English DT Article ID VARIABLE REGION GENES; RHEUMATOID-ARTHRITIS; BETA-CHAIN; MONOCLONAL-ANTIBODIES; MULTIPLE-SCLEROSIS; EXPRESSION; HETEROGENEITY; TISSUE; ENCEPHALOMYELITIS; REARRANGEMENTS AB In this study we analyzed the usage frequencies of the TCR V-gene segments by alphabeta+ T cells present in synovial fluid of 17 patients with chronic arthritis, including rheumatoid arthritis. The results of this study, obtained from semiquantitative PCR analyses, showed that in all patients most of the TCR Valpha- and Vbeta-gene segments could be detected both in fresh PBMCs and in fresh SFMCs. The relative frequencies of use of these V-region genes were variable between the different patients. Although there was some skewing of increased usage frequencies of particular TCR Valpha and Vbeta genes among SFMC-derived TCPs when compared with PBMCs, we could not correlate such increased TCR V-gene usage with the inflammation in the joints as a disease-specific marker. C1 LEIDEN UNIV HOSP,DEPT IMMUNOHEMATOL,POB 9600,2300 RD LEIDEN,NETHERLANDS. LEIDEN UNIV HOSP,BLOOD BANK,2333 AA LEIDEN,NETHERLANDS. LEIDEN UNIV HOSP,DEPT RHEUMATOL,2333 AA LEIDEN,NETHERLANDS. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. STANFORD UNIV,DEPT NEUROL & NEUROL SCI,STANFORD,CA 94305. FU NIAMS NIH HHS [AR 39993] NR 38 TC 54 Z9 54 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD AUG PY 1993 VL 37 IS 4 BP 237 EP 251 DI 10.1016/0198-8859(93)90507-W PG 15 WC Immunology SC Immunology GA MJ081 UT WOS:A1993MJ08100006 PM 8300409 ER PT J AU HOLTZMAN, EJ KOLAKOWSKI, LF OBRIEN, D CRAWFORD, JD AUSIELLO, DA AF HOLTZMAN, EJ KOLAKOWSKI, LF OBRIEN, D CRAWFORD, JD AUSIELLO, DA TI A NULL MUTATION IN THE VASOPRESSIN-V2 RECEPTOR GENE (AVPR2) ASSOCIATED WITH NEPHROGENIC DIABETES-INSIPIDUS IN THE HOPEWELL KINDRED SO HUMAN MOLECULAR GENETICS LA English DT Article AB Congenital nephrogenic diabetes insipidus (DIR) is a rare X-linked hereditary disorder in which the renal collecting duct is unresponsive to arginine vasopressin; thus, the urine is consistently hypotonic to plasma. Recently, the association between the V2 receptor gene (AVPR2) and DIR has been proven. We have determined the gene sequence of four family members, from three generations, of a large North American family with CNDI who were originally part of the study used to formulate the Hopewell hypothesis. It had been proposed that a single DIR gene defect was introduced to North America by a member of an Ulster Scot kindred arriving on the ship Hopewell in 1761. DNA sequencing of the AVPR2 has identified a single base transversion from G-->A which changes tryptophan 71 to a stop codon in affected patients. This point mutation causes a truncation of the receptor leading to an essentially null allele. These data and other recently described mutations in the AVPR2 in North American pedigrees, descended from Ulster Scot ancestors and other origins, make the assertion of a founder effect proposed in the Hopewell hypothesis invalid. C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,PEDIAT ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP HOLTZMAN, EJ (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,RENAL UNIT,149 13TH ST,BOSTON,MA 02129, USA. FU NIDDK NIH HHS [DK19406] NR 17 TC 24 Z9 24 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD AUG PY 1993 VL 2 IS 8 BP 1201 EP 1204 DI 10.1093/hmg/2.8.1201 PG 4 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA LV836 UT WOS:A1993LV83600016 PM 8401502 ER PT J AU HUSTMYER, FG SCHIPANI, E PEACOCK, M AF HUSTMYER, FG SCHIPANI, E PEACOCK, M TI BSMI POLYMORPHISM AT THE PARATHYROID-HORMONE RECEPTOR LOCUS (PTHR) IN 3 POPULATIONS SO HUMAN MOLECULAR GENETICS LA English DT Note C1 INDIANA UNIV,DEPT MED,INDIANAPOLIS,IN 46202. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ENDOCRINE UNIT,BOSTON,MA 02114. FU NCRR NIH HHS [M01RR750-21]; NIADDK NIH HHS [AM 11794] NR 1 TC 6 Z9 6 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD AUG PY 1993 VL 2 IS 8 BP 1330 EP 1330 DI 10.1093/hmg/2.8.1330 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA LV836 UT WOS:A1993LV83600049 PM 8104630 ER PT J AU BOSTWICK, DG SRIGLEY, J GRIGNON, D MAKSEM, J HUMPHREY, P VANDERKWAST, TH BOSE, D HARRISON, J YOUNG, RH AF BOSTWICK, DG SRIGLEY, J GRIGNON, D MAKSEM, J HUMPHREY, P VANDERKWAST, TH BOSE, D HARRISON, J YOUNG, RH TI ATYPICAL ADENOMATOUS HYPERPLASIA OF THE PROSTATE - MORPHOLOGIC CRITERIA FOR ITS DISTINCTION FROM WELL-DIFFERENTIATED CARCINOMA SO HUMAN PATHOLOGY LA English DT Article DE PROSTATE; ATYPICAL ADENOMATOUS HYPERPLASIA; ADENOSIS; ATYPIA; CARCINOMA; INTRAEPITHELIAL NEOPLASIA; NEOPLASMS ID NUCLEOLAR ORGANIZER REGIONS; BASAL-CELL HYPERPLASIA; SCLEROSING ADENOSIS; MORPHOMETRIC ANALYSIS; BASEMENT-MEMBRANE; GLAND; CANCER; DIAGNOSIS; LESION; TUMOR C1 MAYO CLIN & MAYO FDN,BIOSTAT SECT,ROCHESTER,MN 55905. UNIV TORONTO,SUNNYBROOK HLTH SCI CTR,DEPT PATHOL,TORONTO M5S 1A1,ONTARIO,CANADA. HARPER GRACE HOSP,DEPT PATHOL,DETROIT,MI 48201. WAYNE STATE UNIV,DETROIT,MI 48202. MERCY HOSP,MED CTR,DEPT PATHOL,DES MOINES,IA. WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. ERASMUS UNIV ROTTERDAM,DEPT PATHOL,3000 DR ROTTERDAM,NETHERLANDS. UNIV MARYLAND,DEPT PATHOL,BALTIMORE,MD 21201. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP BOSTWICK, DG (reprint author), MAYO CLIN & MAYO FDN,DIV PATHOL,SURG PATHOL SECT,200 1ST ST SW,ROCHESTER,MN 55905, USA. NR 48 TC 157 Z9 160 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 AUG PY 1993 VL 24 IS 8 BP 819 EP 832 DI 10.1016/0046-8177(93)90131-Y PG 14 WC Pathology SC Pathology GA LT274 UT WOS:A1993LT27400002 PM 8375853 ER PT J AU SHIN, DH MARK, EJ SUEN, HC GRILLO, HC AF SHIN, DH MARK, EJ SUEN, HC GRILLO, HC TI PATHOLOGICAL STAGING OF PAPILLARY CARCINOMA OF THE THYROID WITH AIRWAY INVASION BASED ON THE ANATOMIC MANNER OF EXTENSION TO THE TRACHEA - A CLINICOPATHOLOGICAL STUDY BASED ON 22 PATIENTS WHO UNDERWENT THYROIDECTOMY AND AIRWAY RESECTION SO HUMAN PATHOLOGY LA English DT Article DE THYROID CARCINOMA; TRACHEA; LYMPHATICS ID MANAGEMENT C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN THORAC SURG UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 14 TC 50 Z9 50 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 AUG PY 1993 VL 24 IS 8 BP 866 EP 870 DI 10.1016/0046-8177(93)90136-5 PG 5 WC Pathology SC Pathology GA LT274 UT WOS:A1993LT27400007 PM 8375857 ER PT J AU BELDA, F LESTER, SC PINKUS, JL PINKUS, GS FLETCHER, JA AF BELDA, F LESTER, SC PINKUS, JL PINKUS, GS FLETCHER, JA TI LINEAGE-RESTRICTED CHROMOSOME-TRANSLOCATION IN A BENIGN FIBROUS TUMOR OF THE BREAST SO HUMAN PATHOLOGY LA English DT Note DE CHROMOSOME ABERRATIONS; BREAST TUMOR; CLONALITY ID GROWTH-FACTOR-BETA C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. NR 21 TC 10 Z9 10 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 AUG PY 1993 VL 24 IS 8 BP 923 EP 927 DI 10.1016/0046-8177(93)90145-7 PG 5 WC Pathology SC Pathology GA LT274 UT WOS:A1993LT27400016 PM 8375863 ER PT J AU ENTINE, G REDUS, RH FEYDER, A BIGGS, PJ AF ENTINE, G REDUS, RH FEYDER, A BIGGS, PJ TI RECENT RESULTS WITH A CDTE IMAGING PORTAL SCANNER FOR RADIATION-THERAPY SO IEEE TRANSACTIONS ON NUCLEAR SCIENCE LA English DT Article; Proceedings Paper CT 1992 IEEE NUCLEAR SCIENCE SYMP / MEDICAL IMAGING CONF ( NSS/MIC ) CY OCT 25-31, 1992 CL ORLANDO, FL SP IEEE ID TO-NOISE ANALYSIS; RADIOTHERAPY; SYSTEM; LOCALIZATION; VERIFICATION; DETECTORS AB One of the most promising means for improving the quality of radiation therapy is the use of real-time imaging systems for routine portal position verification. We have constructed a prototype portal imager using a linear array of 256 CdTe photovoltaic detectors, each 2 x 2 x 2 mm. The array is attached to a compact linear wanner which is to be mounted in a cassette shaped package located below the patient table. The array of detectors is moved under the patient during image acquisition. The high stopping power of the CdTe allows a high contrast image to be made using a single linac pulse for each array position. In tests conducted with a 4 MV linac, this system produced 50 cm x 35 cm images with an open field signal-to-noise ratio of 143 and 2 mm spatial resolution in less than 3 seconds. This corresponds to a signal-to-noise ratio of 1 for 1% contrast objects. Ultimately, a signal-to-noise ratio greater than 5 at 1% contrast should be achievable with no loss of spatial resolution or increase in acquisition time. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP ENTINE, G (reprint author), RADIAT MONITORING DEVICES INC,WATERTOWN,MA, USA. RI Chang, Yong/B-3541-2009 NR 15 TC 15 Z9 15 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 0018-9499 J9 IEEE T NUCL SCI JI IEEE Trans. Nucl. Sci. PD AUG PY 1993 VL 40 IS 4 BP 1012 EP 1016 DI 10.1109/23.256703 PN 1 PG 5 WC Engineering, Electrical & Electronic; Nuclear Science & Technology SC Engineering; Nuclear Science & Technology GA LV991 UT WOS:A1993LV99100132 ER PT J AU AIURA, K GELFAND, JA BURKE, JF THOMPSON, RC DINARELLO, CA AF AIURA, K GELFAND, JA BURKE, JF THOMPSON, RC DINARELLO, CA TI INTERLEUKIN-1 (IL-1) RECEPTOR ANTAGONIST PREVENTS STAPHYLOCOCCUS-EPIDERMIDIS-INDUCED HYPOTENSION AND REDUCES CIRCULATING LEVELS OF TUMOR-NECROSIS-FACTOR AND IL-1-BETA IN RABBITS SO INFECTION AND IMMUNITY LA English DT Article ID HUMAN MONONUCLEAR-CELLS; SHOCK-LIKE STATE; ESCHERICHIA-COLI; ACTIVATED PLATELETS; CYTOKINE SYNTHESIS; IMPROVES SURVIVAL; HUMAN MONOCYTES; SEPTIC SHOCK; ENDOTOXEMIA; BLOCKADE AB Similar to shock in gram-negative sepsis, shock from gram-positive organisms is mediated, in part, by tumor necrosis factor (TNF) and interleukin-I (IL-1). In the present study, rabbits were infused with IL-1 receptor antagonist (IL-1ra) prior to and during Staphylococcus epidermidis-induced hypotension. After injection of bacteria, a maximal fall in mean arterial pressure to -42% below baseline occurred at 200 min in vehicle-treated animals compared with a nonsignificant decrease of only 7% in the IL-1ra-treated group (P < 0.01, vehicle versus IL-1ra). A similar attenuation was observed in the fall in systemic vascular resistance (P < 0.05). After the injection of S. epidermidis, TNF levels rose to a peak elevation of 475 +/- 160 U/ml in vehicle-treated rabbits, but in rabbits receiving IL-1ra, maximal TNF levels rose only to 85 +/- 23 U/ml (P < 0.01). Plasma IL-1beta reached maximal concentrations at 180 min of 364 +/- 71 pg/ml in vehicle-treated animals but only 145 +/- 12 pg/ml in rabbits given IL-1ra (P < 0.05). The reductions in TNF and IL-1 were not due to interference by IL-1ra in the respective assays. In vitro, IL-1ra inhibited S. epidermidis-induced TNF from mononuclear cells by 31% +/- 11%, from spleen cells by 17% +/- 4% (P < 0.05), and from whole blood by 42% +/- 17%. Despite the near reversal of the fall in mean arterial pressure and systemic vascular resistance in IL-1ra-treated rabbits, leukopenia and thrombocytopenia were unaffected. These results demonstrate that IL-1ra blocks shock-like hemodynamic parameters and reduces circulating IL-1 and TNF levels in a model of gram-positive sepsis. C1 TUFTS UNIV,DEPT MED,DIV GEOG MED,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. TUFTS UNIV NEW ENGLAND MED CTR,BOSTON,MA 02111. SYNERGEN INC,BOULDER,CO 80301. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FU NIAID NIH HHS [AI15614]; NIGMS NIH HHS [GM21700] NR 44 TC 69 Z9 72 U1 0 U2 4 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 AUG PY 1993 VL 61 IS 8 BP 3342 EP 3350 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LP357 UT WOS:A1993LP35700034 PM 8335365 ER PT J AU MANTHEY, CL PERERA, PY QURESHI, N STUTZ, PL HAMILTON, TA VOGEL, SN AF MANTHEY, CL PERERA, PY QURESHI, N STUTZ, PL HAMILTON, TA VOGEL, SN TI MODULATION OF LIPOPOLYSACCHARIDE-INDUCED MACROPHAGE GENE-EXPRESSION BY RHODOBACTER-SPHAEROIDES LIPID-A AND SDZ-880.431 SO INFECTION AND IMMUNITY LA English DT Article ID TUMOR-NECROSIS-FACTOR; MURINE PERITONEAL-MACROPHAGES; RHODOPSEUDOMONAS-SPHAEROIDES; MESSENGER-RNA; HUMAN-NEUTROPHILS; INDUCIBLE GENES; BINDING-PROTEIN; HUMAN MONOCYTES; LPS BINDING; IFN-GAMMA AB Rhodobacter sphaeroides lipid A (RsDPLA) and SDZ 880.431 (3-aza-lipid X4-phosphate) are prototypic lipopolysaccharide (LPS) antagonists. Herein, we examined the ability of these structures to regulate murine macrophage tumor necrosis factor (TNF) secretion and LPS-inducible gene expression (tumor necrosis factor alpha [TNF-alpha], interleukin-1beta [IL-1beta], IP-10, type 2 TNF receptor [TNFR-2], D3, and D8 genes). We report that RsDPLA alone (> 1 mug/ml) induced low levels of TNF-alpha secretion and a selective pattern of gene expression in peritoneal exudate macrophages; SDZ 880.431 alone was completely inactive. When LPS was present at a low concentration (1 ng/ml), RxDPLA and SDZ 880.431 blocked TNF secretion and gene induction in a concentration-dependent fashion. In general, gene induction was measurably reduced by 10 to 30 ng of RsDPLA per ml or 300 ng of SDZ 880.431 per ml, but inhibition could be uniformly overridden by increasing the concentration of LPS. Although induction of all six genes by LPS was suppressed by either inhibitor, effective inhibitor concentrations depended on the gene of interest. Induction of TNFR-2 by LPS was relatively resistant to inhibition by RxDPLA, and induction of TNFR-2 and D3 was relatively resistant to inhibition by SDZ 880.431. When LPS was present at greater-than-or-equal-to 100 ng/ml, correspondingly high concentrations (greater-than-or-equal-to 20 mug/ml) of either inhibitor influenced gene expression in a bidirectional manner. Under these conditions, LPS-induced expression of IP-10, D3, and D8 was suppressed regardless of the LPS concentration used (concentrations tested up to 50 mug/ml), while expression of TNF-alpha mRNA was enhanced about fourfold. In toto, RsDPIA and SDZ 880.431, when present at low concentrations, act in a manner consistent with competitive inhibition of LPS, while at higher concentrations, these structures inhibit certain LPS responses noncompetitively and synergize with LPS for other responses. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT MICROBIOL,4301 JONES BRIDGE RD,BETHESDA,MD 20814. 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. SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. CLEVELAND CLIN EDUC FDN,RES INST,DEPT IMMUNOL,CLEVELAND,OH 44106. FU NIAID NIH HHS [AI 08451] NR 46 TC 22 Z9 22 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 AUG PY 1993 VL 61 IS 8 BP 3518 EP 3526 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LP357 UT WOS:A1993LP35700056 PM 8335383 ER PT J AU WILLIAMS, DM GRUBBS, BG SCHACHTER, J MAGEE, DM AF WILLIAMS, DM GRUBBS, BG SCHACHTER, J MAGEE, DM TI GAMMA-INTERFERON LEVELS DURING CHLAMYDIA-TRACHOMATIS PNEUMONIA IN MICE SO INFECTION AND IMMUNITY LA English DT Note ID TUMOR NECROSIS FACTOR; DELTA-T-CELLS; ROLE INVIVO; IFN-GAMMA; MOUSE; INFECTION; IMMUNITY; ACTIVATION; ALPHA; AGENT AB Host defense against murine Chlamydia trachomatis (mouse pneumonitis agent [MoPn]) in a murine model was investigated. Gamma interferon (IFN-gamma) was produced in the lungs by both MoPn-susceptible nude athymic (nu/nu) and MoPn-resistant heterozygous (nu/+) mice. In vivo depletion of IFN-gamma in nu/nu mice led to exacerbation of infection. Fluorescence-activated cell sorter analysis disclosed induction of GL3 antibody-positive cells (putatively gamma/delta+ T cells) in nu/nu mouse lung during infection with MoPn. Treatment of nu/nu mice in vivo with antibody to NK cells (anti-asialo GM1 antibody) or to gamma/delta cells (UC7-13D5) did not significantly decrease IFN-gamma production in the lung. However, treatment of severe combined immunodeficiency mice (which lack gamma/delta cells) with antibody to NK cells significantly reduced lung IFN-gamma levels. C1 STATE CHEST HOSP,DEPT IMMUNOL,SAN ANTONIO,TX 78223. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV CALIF SAN FRANCISCO,DEPT CARDIOL,SAN FRANCISCO,CA 94143. RP WILLIAMS, DM (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DIV INFECT DIS,SAN ANTONIO,TX 78284, USA. FU NIAID NIH HHS [AI 22380] NR 25 TC 24 Z9 25 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 AUG PY 1993 VL 61 IS 8 BP 3556 EP 3558 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LP357 UT WOS:A1993LP35700065 PM 8335389 ER PT J AU RATHBUN, G OLTZ, EM ALT, FW AF RATHBUN, G OLTZ, EM ALT, FW TI COMPARISON OF RAG GENE-EXPRESSION IN NORMAL AND TRANSFORMED PRECURSOR LYMPHOCYTES SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE CELL-BASED MODEL SYSTEMS; LYMPHOID PROGENITORS; V(D)J RECOMBINASE ACTIVITY ID B-CELL LINES; PRE-B; RECOMBINASE ACTIVITY; V(D)J RECOMBINATION; REARRANGEMENT; SEGMENTS; TRANSCRIPTION; GENOME AB Analyses of mechanisms that regulate V(D)J recombination have relied heavily on the use of transformed precursor lymphocyte cell lines. We now show that such lines have highly variable and frequently Low levels of recombination activating genes (RAG)-l and -2 gene expression. We also show that expression levels of the RAG genes can vary > 100-fold between different subcloned cells of an individual pre-B line. We discuss these findings in the context of normal regulation of RAG gene expression and the implication for the use of transformed pre-B cell lines as models for studying control of V(D)J recombination activity. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,HOWARD HUGHES MED INST,DEPT MED,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. FU NIAID NIH HHS [AI20047]; PHS HHS [UO1 A131541] NR 20 TC 17 Z9 17 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 AUG PY 1993 VL 5 IS 8 BP 997 EP 1000 DI 10.1093/intimm/5.8.997 PG 4 WC Immunology SC Immunology GA LR659 UT WOS:A1993LR65900022 PM 8398992 ER PT J AU TEICHER, BA DUPUIS, NP KUSUMOTO, T LIU, M LIU, F MENON, K SCHWARTZ, GN FREI, E AF TEICHER, BA DUPUIS, NP KUSUMOTO, T LIU, M LIU, F MENON, K SCHWARTZ, GN FREI, E TI DECREASED TUMOR OXYGENATION AFTER CYCLOPHOSPHAMIDE, REOXYGENATION AND THERAPEUTIC ENHANCEMENT WITH A PERFLUBRON EMULSION CARBOGEN BREATHING SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE TUMOR OXYGENATION; CYCLOPHOSPHAMIDE; PERFLUBRON EMULSION; CARBOGEN BREATHING ID LEWIS LUNG-CARCINOMA; MELPHALAN ANTITUMOR-ACTIVITY; FLUOSOL-DA; CYTO-TOXICITY; BLOOD-FLOW; MAMMARY-CARCINOMA; RADIATION-THERAPY; SOLID TUMORS; RIF-1 TUMOR; X-RAYS AB Oxygen profiles of the rat mammary 13672 carcinoma were determined using a pO2 histograph prior to treatment and 24 h and 48 h after i.p. administration of a single dose of cyclophosphamide (300 mg/kg). The tumors were severely hypoxic at 24 h post the administration of cyclophosphamide. There was little increase in oxygenation of the tumors at 48 h post therapy compared with 24 h post therapy indicating that reoxygenation after cyclophosphamide was occurring very slowly in this tumor. Carbogen breathing improved the oxygenation of the tumors under each of the conditions studied. Administration of the perflubron emulsion (8 ml/kg) produced little or no change in the oxygenation of the tumors under normal air breathing conditions. However, the addition of carbogen breathing to administration of the perflubron emulsion increased the oxygenation of the tumors to levels equal to or greater than carbogen breathing at the mean/median pO2's. Perhaps most significantly, administration of the perflubron emulsion with carbogen breathing increased the oxygenation of the most hypoxic regions of the tumors but carbogen breathing alone did not. The growth delay of the Lewis lung carcinoma increased with increasing dose.of the perflubron emulsion along with cyclophosphamide (3 x 150 mg/kg) and carbogen breathing (6 h). This combination treatment was most effective when the cyclophosphamide was prepared in the perflubron emulsion. The number of lung metastases decreased in a manner parallel with increased efficacy of the treatment toward the primary tumor. 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. NR 48 TC 7 Z9 7 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD AUG PY 1993 VL 3 IS 2 BP 197 EP 203 PG 7 WC Oncology SC Oncology GA LP940 UT WOS:A1993LP94000011 PM 21573348 ER PT J AU KUSUMOTO, T TEICHER, BA HOLDEN, SA COLEMAN, CN LIU, SD SOTOMAYOR, EA AF KUSUMOTO, T TEICHER, BA HOLDEN, SA COLEMAN, CN LIU, SD SOTOMAYOR, EA TI REVERSAL OF DRUG-RESISTANCE BY EXPOSURE OF MCF-7 OR MCF-7 CDDP HUMAN BREAST-CARCINOMA CELLS TO SR-4233 OR ETANIDAZOLE UNDER HYPOXIC CONDITIONS SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE DRUG RESISTANCE; BREAST CARCINOMA CELLS; SR-4233; ETANIDAZOLE ID FSAIIC MURINE FIBROSARCOMA; SENSITIZER MISONIDAZOLE; SOLID TUMORS; ENHANCEMENT; MELPHALAN; RADIATION; INVITRO; INVIVO; AGENT; RADIOSENSITIZATION AB Drug resistance is a major problem in cancer therapy. The MCF-7/CDDP cell line, a subline of the MCF-7 human breast carcinoma cell line which is resistant to cis-diamminedichloroplatinum(II), is also resistant to carboplatin, D-tetraplatin and to a lesser degree to melphalan, thiotepa and BCNU compared with the MCF-7 parental cell line. This resistance persists both under normally oxygenated conditions and after 2 h of exposure to hypoxic conditions prior to exposure to the antitumor alkylating agents under normally oxygenated conditions. When the MCF-7 parental cells and MCF-7/CDDP cells were treated with SR-4233 (20 muM) or etanidazole (5 mM) for 2 h prior to and during exposure to the antitumor alkylating agents there was no change in the sensitivity and resistance patterns of the cell lines. However, if the MCF-7 parental cells and the MCF-7/CDDP cells were exposed to SR-4233 (20 muM) or etanidazole (5 mM) for 2 h under hypoxic conditions followed by release of the hypoxia and exposure to the antitumor alkylating agents for 1 h under normally oxygenated conditions the resistance of the MCF-7/CDDP was reversed so that both the MCF-7 parental and MCF-7/CDDP cell lines were essentially equally sensitive to the six antitumor alkylating agents. These results indicate that non-cytotoxic concentrations of modulators such as SR-4233 or etanidazole may be useful in reversing resistance to the C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP KUSUMOTO, T (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 42 TC 3 Z9 3 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD AUG PY 1993 VL 3 IS 2 BP 205 EP 211 PG 7 WC Oncology SC Oncology GA LP940 UT WOS:A1993LP94000012 PM 21573349 ER PT J AU LEE, I LEVITT, SH SONG, CW AF LEE, I LEVITT, SH SONG, CW TI IMPROVED TUMOR OXYGENATION AND RADIOSENSITIZATION BY COMBINATION WITH NICOTINAMIDE AND PENTOXIFYLLINE SO INTERNATIONAL JOURNAL OF RADIATION BIOLOGY LA English DT Article ID FLUOSOL-DA 20-PERCENT; MURINE TUMOR; NORMAL-TISSUES; HYPOXIC CELLS; MOUSE-TUMORS; BLOOD-FLOW; INVIVO; PERFUSION; HETEROGENEITY; HYPERTHERMIA AB We hypothesized that the combination of pentoxifylline (PTX) and nicotinamide (NA) can reduce the radioresistance of FSaII murine fibrosarcoma by improving oxygenation of the hypoxic tumour cells. The purpose of this study was to test the hypothesis; first, tumour blood flow after treatment with NA, PTX, and the combination (PTX+NA) was measured using laser Doppler flowmetry. Second, intratumour PO2 after various treatments was measured polarographically using 02 microelectrodes. Third, the radiation response was also measured, i.e. after an exposure to 20 Gy, the time required to reach a four-fold increase in initial tumour volume was 18 days in the saline-treated control group, 21 days in the NA-treated group, 26 days in the PTX-treated group, but was 36 days in PTX+NA treated group. Interestingly, tumour blood flow significantly increased at 10 min after injection of PTX+NA. The mean PO2 in untreated control tumours was 7.5 mmHg, increasing to 13-1 mmHg after 500 mg/kg of NA alone. Repeated injections of PTX with 100 mg/kg/day for 3 days significantly increased intratumour PO2 to 17.2 mmHg. Compared with PTX alone, PTX+NA slightly increased intratumour PO2 from 17.2 to 18.5 mmHg. However, the percentage of regions having values < 2.5 mmHg significantly decreased from 5 % with PTX alone to 1 % with PTX+NA. In conclusion, single or multiple injections of PTX may increase available 02 in the tumour and thus ameliorate hypoxia in tumour microregions. As previously reported, the subsequent injection of NA may efficiently oxygenate acutely hypoxic cells. Consequently, PTX+NA may increase the radioresponse of tumours by oxygenating chronic as well as acutely hypoxic cells. PTX alone or in combination with NA is potentially useful to radiosensitize tumours. C1 UNIV MINNESOTA,SCH MED,DEPT THERAPEUT RADIOL,MINNEAPOLIS,MN 55455. RP LEE, I (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [NCI CA-13353] NR 43 TC 24 Z9 24 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0955-3002 J9 INT J RADIAT BIOL JI Int. J. Radiat. Biol. PD AUG PY 1993 VL 64 IS 2 BP 237 EP 244 DI 10.1080/09553009314551351 PG 8 WC Biology; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA LW734 UT WOS:A1993LW73400014 PM 8103549 ER PT J AU WANG, CC MCINTYRE, J AF WANG, CC MCINTYRE, J TI REIRRADIATION OF LARYNGEAL CARCINOMA - TECHNIQUES AND RESULTS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT 34TH ANNUAL MEETING OF THE AMERICAN SOC FOR THERAPEUTIC RADIOLOGY AND ONCOLOGY CY NOV 08-13, 1992 CL SAN DIEGO, CA SP AMER SOC THERAPEUT RADIOL & ONCOL DE LARYNX; CARCINOMA; REIRRADIATION AB Purpose: Occasionally in the long-term survivors of early carcinoma of the larynx, following radiation therapy a second carcinoma may arise from the previously irradiated larynx. Traditionally, management of such lesions is by non-radiation means in the belief that a further full course of radiation therapy is not possible and may exceed the tolerance of the normal laryngeal structures. Unfortunately, surgical treatment of the second carcinoma is often either total or partial laryngectomy which may not be acceptable to the patients and therefore radiation therapy is used as an alternative. Methods and Materials: This paper presents our experience in re-irradiation of laryngeal carcinomas arising from the previously irradiated larynx. As of October 1992 a total of 20 patients were available for evaluation. Most patients had Stage I and II laryngeal carcinoma and received high doses of re-irradiation ranging from 60 to 70 Gy either by conventional or accelerated hyperfractionation schemes. Results: The 5-year actuarial local control and survival rates were 60 to 93%, respectively. The majority of the survivors had relatively normal and functional larynges. Those who failed locally had total laryngectomy without significant postoperative complications. Conclusion: With this information the radiation tolerance of laryngeal structures is found to be much higher than commonly believed and re-irradiation for early carcinoma of the larynx is possible and proved to be a useful alternative to surgery and laryngectomy is therefore reserved for failure. The techniques of re-irradiation will be discussed. RP WANG, CC (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 2 TC 40 Z9 43 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 AUG 1 PY 1993 VL 26 IS 5 BP 783 EP 785 PG 3 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LR644 UT WOS:A1993LR64400007 PM 8344846 ER PT J AU WANG, CC AF WANG, CC TI DECISION-MAKING FOR REIRRADIATION OF NASOPHARYNGEAL CARCINOMA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Editorial Material RP WANG, CC (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 4 TC 5 Z9 5 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 AUG 1 PY 1993 VL 26 IS 5 BP 903 EP 903 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LR644 UT WOS:A1993LR64400023 PM 8344861 ER PT J AU HARRER, T JASSOY, C HARRER, E JOHNSON, RP WALKER, BD AF HARRER, T JASSOY, C HARRER, E JOHNSON, RP WALKER, BD TI INDUCTION OF HIV-1 REPLICATION IN A CHRONICALLY INFECTED T-CELL LINE BY CYTOTOXIC T-LYMPHOCYTES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE ACH-2; CYTOTOXIC T-CELLS; HIV-1; HIV-1 REPLICATION; TNF-ALPHA ID HUMAN-IMMUNODEFICIENCY-VIRUS; TUMOR-NECROSIS-FACTOR; FACTOR-ALPHA; CEREBROSPINAL-FLUID; FINE SPECIFICITY; KAPPA-B; TYPE-1; INTERLEUKIN-1; PEPTIDES; PROTEIN AB CD8-positive cytotoxic T cells (CTLs) are activated by recognition of peptide bound to MHC class I molecules on target cells. This human leukocyte antigen-restricted process induces not only lysis of target cells but also secretion of lymphokines by the CTLs, including TNF-alpha, TNF-beta, and IFN-gamma. In this study we show that activation of HIV-1-specific CTL clones by their cognate peptide epitopes induces HIV-1 replication in the chronically HIV-1-infected T-cell line ACH-2. The HIV-1-inducing activity correlates with increased levels of TNF-alpha produced by these CTLs, and can be inhibited by anti-TNF-alpha antibodies, indicating that the effect is mediated by this cytokine. These studies suggest that activation of CTL in vivo could lead to enhanced viral replication. Although HIV-1-specific CTLs may serve as a host defense to inhibit virus replication, the induction of TNF-alpha production by these cells may facilitate viral replication in infected bystander cells, contributing to viral persistence and disease pathogenesis. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HARRER, T (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114, USA. FU NIAID NIH HHS [AI26463, AI28568, AI30914] NR 40 TC 20 Z9 20 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD AUG PY 1993 VL 6 IS 8 BP 865 EP 871 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LM633 UT WOS:A1993LM63300002 PM 8315573 ER PT J AU WHEATLEY, JR TANGEL, DJ MEZZANOTTE, WS WHITE, DP AF WHEATLEY, JR TANGEL, DJ MEZZANOTTE, WS WHITE, DP TI INFLUENCE OF SLEEP ON ALAE-NASI EMG AND NASAL RESISTANCE IN NORMAL MEN SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE UPPER AIRWAY PHYSIOLOGY; NON-RAPID-EYE-MOVEMENT SLEEP; AIR-WAY PATENCY ID UPPER AIRWAY; MUSCLE RESPONSES; NORMAL HUMANS; FLOW; PRESSURE; WAKEFULNESS; ACTIVATION AB The influence of sleep on the upper airway musculature varies considerably, with some muscles maintaining their activity at waking levels and others falling substantially. The influence of sleep on the alae nasi (AN), a dilator muscle of the nasal airway, has been minimally studied to date. Thus we determined the effect of non-rapid-eye-movement (NREM) sleep on the AN electromyogram and its relationship to nasal resistance (Rn) in nine normal supine males. Phasic inspiratory AN activity decreased from 20 +/- 6 arbitrary units during wakefulness to 5 +/- 1 arbitrary units (P < 0.001) at the onset of stage 2 NREM sleep and remained unchanged for two subsequent hours of NREM sleep. However, the Rn at the onset of NREM sleep remained similar to awake values (5.7 +/- 0.9 cmH2O . l-1 . s) and increased only after 1 h of NREM sleep (8.6 +/- 1.7 cmH2O . l-1 . s, P < 0.05), thus demonstrating little relationship to AN activity. We conclude that Rn increases slightly after 1 h of sleep, whereas AN activity decreases at stage 2 sleep onset. Thus AN activity has little influence on Rn during sleep. C1 DENVER VET AFFAIRS MED CTR,NATL JEWISH CTR IMMUNOL & RESP MED,DIV PULM,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80220. NR 29 TC 12 Z9 12 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD AUG PY 1993 VL 75 IS 2 BP 626 EP 632 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA LT582 UT WOS:A1993LT58200021 PM 8226461 ER PT J AU CONHAIM, RL HARMS, BA AF CONHAIM, RL HARMS, BA TI PERFUSION OF ALVEOLAR SEPTA IN ISOLATED RAT LUNGS IN ZONE-1 SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE ZONE-1 LUNGS; FLUORESCENCE MICROSCOPY; RAPID FREEZING; PULMONARY MICROCIRCULATION; ALVEOLAR VESSELS; EXTRA-ALVEOLAR VESSELS; PULMONARY MICROVASCULAR FILTRATION; PULMONARY INTERSTITIUM ID INSITU DOG LUNGS; INTERSTITIAL COMPLIANCE; FILTRATION COEFFICIENT; PULMONARY-EDEMA; RABBIT LUNGS; PERMEABILITY; PRESSURE; VESSELS; VOLUME; FLUID AB The combination of high inflation and low vascular pressures in zone 1 lungs is assumed to collapse alveolar vessels, making them inaccessible to vascular liquid. To test this assumption, we perfused isolated rat lungs in zone 1 (n = 5) with fluorescent albumin solution (inflation pressure = 25 cmH2O, pulmonary arterial pressure = 10 cmH2O, left atrial pressure = 0 cmH2O; flow = 0.11 +/- 0.06 ml . 100 g body wt-1 . min-1) and rapidly froze them. Histologically, 33 +/- 19% (SD) of alveolar septa fluoresced, demonstrating that the perfusate had not been excluded. However, we could not resolve whether the fluorescence originated in the septal microvascular lumen or in the adjacent perimicrovascular interstitial space. To address this issue, we perfused an additional lung with horseradish peroxidase (HRP) and examined it by transmission electron microscopy. HRP filled interstitial spaces around septal vessels and extraseptal alveolar comer vessels, but because the septal vascular lumina were too compressed, we were unable to determine whether they also contained HRP. Therefore we perfused two additional lungs with particles of colloidal gold (0.05 mum diam). Using transmission electron microscopy, we found gold particles in 15-25% of septal vascular lumina, demonstrating that septal vessels were at least partially accessible in zone 1. Our interpretation is that filtration in zone 1 may occur from septal vessels and extraseptal alveolar vessels. Furthermore, results of the HRP study suggest that the perimicrovascular interstitial space is less compressible than the septal vascular lumen. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,DEPT SURG,MADISON,WI 53706. NR 31 TC 11 Z9 11 U1 0 U2 5 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 AUG PY 1993 VL 75 IS 2 BP 704 EP 711 PG 8 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA LT582 UT WOS:A1993LT58200032 PM 8226472 ER PT J AU MONTALESCOT, G FISCHMAN, AJ STRAUSS, HW WILKINSON, RA AHMAD, M FITZGIBBON, C ROBINSON, DW ZAPOL, WM AF MONTALESCOT, G FISCHMAN, AJ STRAUSS, HW WILKINSON, RA AHMAD, M FITZGIBBON, C ROBINSON, DW ZAPOL, WM TI IMAGING THE OVINE HEPARIN-PROTAMINE INTERACTION WITH IN-111 PROTAMINE SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE PULMONARY HYPERTENSION; THROMBOXANE; INDIUM-111-PROTAMINE; HEPARIN; MACROPHAGE ID PULMONARY INTRAVASCULAR MACROPHAGES; AWAKE SHEEP; COMPLEMENT ACTIVATION; THROMBOXANE RELEASE; LUNG; VASOCONSTRICTION; HYPERTENSION; REVERSAL; ANTICOAGULATION; RESPONSES AB Protamine reversal of heparin anticoagulation occasionally induces the release of thromboxane into plasma with catastrophic pulmonary hypertension. To examine the site of neutralization, we labeled protamine sulfate with In-111 and compared activity scans after administration of labeled protamine in unheparinized and heparin-anticoagulated sheep. Protamine administration in sheep without prior heparinization did not cause thromboxane release, pulmonary hypertension, or significant leukopenia, and In-111-protamine was rapidly cleared from the lungs (half time 0.48 +/- 0.08 min). Neutralization of heparin anticoagulation by labeled protamine produced elevated plasma thromboxane, pulmonary vasoconstriction, leukopenia, and prolonged pulmonary clearance of In-111-protamine (half time 3.32 +/- 0.43 min). In rats, protamine reversal of heparin anticoagulation did not induce either thromboxane synthesis or pulmonary hypertension, and In-111-protamine cleared rapidly from the lungs. Thus the ovine heparin-protamine reaction produces concomitant pulmonary sequestration of heparin-protamine complexes, thromboxane release, and pulmonary vasoconstriction; this did not occur in the rat. The lung specificity of the reaction and interspecies differences suggest that ovine pulmonary intravascular macrophages may be activated by heparin-protamine complexes to release thromboxane and provoke acute pulmonary vasoconstriction. C1 MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,ARTHRITIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-42397] NR 29 TC 13 Z9 15 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD AUG PY 1993 VL 75 IS 2 BP 963 EP 971 PG 9 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA LT582 UT WOS:A1993LT58200064 PM 8226502 ER PT J AU BERGMAN, RJ TRUONG, TC HAHN, TJ AF BERGMAN, RJ TRUONG, TC HAHN, TJ TI OSTEOPROGENITOR CELL DEFECTS IN AGE-RELATED OSTEOPOROSIS IN THE MOUSE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 W LOS ANGELES VAMC, CTR GERIATR RES EDUC & CLIN, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S364 EP S364 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500990 ER PT J AU BOGADO, CE KIERNAN, MS DEMAY, MB AF BOGADO, CE KIERNAN, MS DEMAY, MB TI IDENTIFICATION OF SEQUENCES THAT ENHANCE THE EFFECTS OF 1,25(OH)2D(3) ON OSTEOCALCIN GENE-TRANSCRIPTION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S213 EP S213 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500384 ER PT J AU BOYCE, BE WINDLE, JJ REDDY, SV WRIGHT, K LEACH, RJ ROODMAN, GD AF BOYCE, BE WINDLE, JJ REDDY, SV WRIGHT, K LEACH, RJ ROODMAN, GD TI TARGETING SV40 T-ANTIGEN TO THE OSTEOCLAST IN TRANSGENIC MICE CAUSES OSTEOPETROSIS, TRANSFORMATION AND APOPTOSIS OF OSTEOCLASTS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 CANC THERAPY RES CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S118 EP S118 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500005 ER PT J AU BRUNS, DE FERGUSON, JE PEARSON, WR JUPPNER, H SEGRE, GV SEANER, R BRUNS, ME AF BRUNS, DE FERGUSON, JE PEARSON, WR JUPPNER, H SEGRE, GV SEANER, R BRUNS, ME TI EXPRESSION OF PARATHYROID-HORMONE PARATHYROID HORMONE-RELATED PROTEIN-RECEPTOR IN THE HUMAN UTEROPLACENTAL UNIT, UMBILICAL-CORD AND PLACENTAL VESSELS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV VIRGINIA,DEPT OBSTET & GYNECOL,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,DEPT BIOCHEM,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,DEPT PATHOL,CHARLOTTESVILLE,VA 22908. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S188 EP S188 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500285 ER PT J AU CHIBA, S LEE, K SAITO, H DEEDS, J NEER, R SEGRE, G AF CHIBA, S LEE, K SAITO, H DEEDS, J NEER, R SEGRE, G TI MOLECULAR ANALYSIS OF FRACTURE-HEALING SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S240 EP S240 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500494 ER PT J AU CRYNS, V THOR, A LOUIS, D BENEDICT, W ARNOLD, A AF CRYNS, V THOR, A LOUIS, D BENEDICT, W ARNOLD, A TI TUMOR-SUPPRESSOR GENE ABNORMALITIES IN HUMAN PARATHYROID CARCINOMA SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BAYLOR COLL MED,THE WOODLANDS,TX. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S148 EP S148 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500126 ER PT J AU DEEDS, JD LEE, K SEGRE, GV AF DEEDS, JD LEE, K SEGRE, GV TI LOCALIZATION OF PARATHYROID-HORMONE PARATHYROID-HORMONE RELATED PEPTIDE RECEPTOR MESSENGER-RNA TO PLACENTA PARIETAL ENDODERM AND CYTOTROPHOBLAST CELLS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S189 EP S189 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500288 ER PT J AU DRAKE, M GARDELLA, T ABOUSAMRA, AB SEGRE, GV AF DRAKE, M GARDELLA, T ABOUSAMRA, AB SEGRE, GV TI MUTATIONAL ANALYSIS OF THE RAT PTH/PTHRP RECEPTOR - STRUCTURAL DETERMINANTS FOR ACTIVATION OF THE STIMULATORY G-PROTEIN SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S128 EP S128 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500048 ER PT J AU FERMOR, B MASON, DJ LEE, K SEGRE, GV GOWEN, M SKERRY, TM AF FERMOR, B MASON, DJ LEE, K SEGRE, GV GOWEN, M SKERRY, TM TI DIFFERENCES IN PERIOSTEAL AND TRABECULAR GENE-EXPRESSION IN GROWING BONE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV BRISTOL SCH VET SCI,BRISTOL,ENGLAND. SMITHKLINE BEECHAM PHARMACEUT,KING OF PRUSSIA,PA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S198 EP S198 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500326 ER PT J AU FUKAYAMA, S LANSKE, B KRONENBERG, HM BRINGHURST, FR AF FUKAYAMA, S LANSKE, B KRONENBERG, HM BRINGHURST, FR TI REGULATION OF HEAT-SHOCK PROTEIN-70 (HSP-70) MESSENGER-RNA BY PARATHYROID-HORMONE (PTH) IN PORCINE KIDNEY LLC-PK1 CELLS - A MODEL OF CAMP-INDEPENDENT GENE-REGULATION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S184 EP S184 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500268 ER PT J AU FULEIHAN, GE HALL, JE PORRINO, N GLEASON, R CROWLEY, WF AF FULEIHAN, GE HALL, JE PORRINO, N GLEASON, R CROWLEY, WF TI INTACT PARATHYROID-HORMONE LEVELS ACROSS THE MENSTRUAL-CYCLE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NR 0 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S188 EP S188 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500284 ER PT J AU GARDELLA, TJ WILSON, AK KEUTMANN, HT BRINGHURST, R POTTS, JT KRONENBERG, HM NUSSBAUM, SR AF GARDELLA, TJ WILSON, AK KEUTMANN, HT BRINGHURST, R POTTS, JT KRONENBERG, HM NUSSBAUM, SR TI STRUCTURE-FUNCTION-RELATIONSHIPS IN PTH AND PTHRP - STUDIES WITH HYBRID PEPTIDES AND AMINO-TERMINAL FRAGMENTS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S188 EP S188 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500287 ER PT J AU GORN, AH RUDOLF, SM YAMIN, M KRANE, SM GOLDRING, SR AF GORN, AH RUDOLF, SM YAMIN, M KRANE, SM GOLDRING, SR TI THE CLONING OF A HUMAN OSTEOCLAST CALCITONIN RECEPTOR FROM A GIANT-CELL TUMOR OF BONE (OSTEOCLASTOMA) SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ARTHRITIS UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S384 EP S384 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20501069 ER PT J AU GOTO, K ROSEN, V WOZNEY, JM KRONENBERG, HM DEMAY, MB AF GOTO, K ROSEN, V WOZNEY, JM KRONENBERG, HM DEMAY, MB TI TRANSCRIPTIONAL INDUCTION OF OSTEOCALCIN-CAT FUSION GENE-EXPRESSION BY RHBMP-2 SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. GENET INST INC,CAMBRIDGE,MA 02140. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S324 EP S324 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500827 ER PT J AU GUO, J ABOUSAMRA, AB BRINGHURST, FR AF GUO, J ABOUSAMRA, AB BRINGHURST, FR TI REGULATION OF PHOSPHATE-UPTAKE AND PHOSPHOLIPASE-C BY PARATHYROID-HORMONE IS SELECTIVELY MODULATED BY THE LEVEL OF PTH PTHRP RECEPTOR EXPRESSION IN STABLY TRANSFECTED LLC-PK1 CELLS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1993 VL 8 SU 1 BP S176 EP S176 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LR205 UT WOS:A1993LR20500237 ER EF