FN Thomson Reuters Web of Science™ VR 1.0 PT J AU NUSRAT, AR CHAPMAN, HA AF NUSRAT, AR CHAPMAN, HA TI AN AUTOCRINE ROLE FOR UROKINASE IN PHORBOL ESTER-MEDIATED DIFFERENTIATION OF MYELOID CELL-LINES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CATHEPSIN-B; CELL ADHESION; HL60 CELLS; PHORBOL MYRISTATE ACETATE; UROKINASE RECEPTOR ID PLASMINOGEN-ACTIVATOR INHIBITOR-2; HUMAN ALVEOLAR MACROPHAGES; RECEPTOR-BOUND UROKINASE; CATHEPSIN-B; HUMAN-MONOCYTES; GENE-EXPRESSION; LEUKEMIA-CELLS; ADHERENCE; BINDING; INVITRO AB The human myeloid cell line HL60 secretes urokinase-type plasminogen activator (uPA) and expresses its receptor. When stimulated with phorbol myristate acetate (PMA), both secretion of uPA and the expression of its receptor are up-regulated, and these cells differentiate to an adherent phenotype. This adhesive response is markedly reduced in the presence of uPA antibodies. The PMA response is restored by the addition of native uPA, an amino-terminal fragment of uPA (residues 1-143) devoid of proteolytic activity, or a synthetic peptide (residues 12-32) from the uPA growth factor domain known to mediate receptor binding. In contrast, the addition of catalytically active low molecular weight uPA, which is missing the growth factor domain, or a peptide from the catalytic domain (residues 247-266) is ineffective. The influence of uPA antibodies on a second marker of macrophage differentiation, cysteine proteinase activity, was also examined. Cysteine proteinase activity of HL60 cells is increased in PMA-treated cells after 24 h but it fails to increase in the presence of anti-uPA. This increase in cathepsin B-like activity is also restored by exogenous uPA. These experiments indicate that an autocrine interaction of the growth factor domain of uPA with its receptor mediates an essential step in PMA-mediated myeloid cell differentiation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP NUSRAT, AR (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,DIV RESP,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-35505, HL8002]; NIEHS NIH HHS [ES 0002] NR 54 TC 136 Z9 136 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAR PY 1991 VL 87 IS 3 BP 1091 EP 1097 DI 10.1172/JCI115070 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FB171 UT WOS:A1991FB17100044 PM 1847936 ER PT J AU SONG, HS WRAY, SH AF SONG, HS WRAY, SH TI BEE STING OPTIC NEURITIS - A CASE-REPORT WITH VISUAL EVOKED-POTENTIALS SO JOURNAL OF CLINICAL NEURO-OPHTHALMOLOGY LA English DT Article DE BEE STING OPTIC NEURITIS; PATTERN VISUAL EVOKED POTENTIAL; PATTERN ELECTRORETINOGRAM ID PATTERN ELECTRORETINOGRAM; WASP AB Simultaneous recordings of the pattern visual evoked potential and the pattern electroretinogram were recorded in a case of unilateral optic neuritis following a bee sting on the eye. The patient presented with severe eye pain, apoplectic visual loss, acute optic disc swelling and minimal signs of ocular inflammation and eyelid edema. The vision failed to recover. The electrophysiological recordings initially showed a delay in the P100 wave of the pattern visual evoked potential. On followup, a normal latency and amplitude of the P50 wave of the pattern electroretinogram was recorded with the flaterning of the N95 component, but the pattern visual evoked potential was absent. The data suggests that the optic nerve was demyelinated acutely, and that subsequently axonal loss and degeneration of retinal ganglion cells occurred. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROVISUAL DISORDERS UNIT,BOSTON,MA 02114. NR 26 TC 27 Z9 27 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0272-846X J9 J CLIN NEURO-OPHTHAL PD MAR PY 1991 VL 11 IS 1 BP 45 EP 49 PG 5 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA FA527 UT WOS:A1991FA52700010 PM 1827460 ER PT J AU GOTTLIEB, D CALVANIO, R LEVINE, DN AF GOTTLIEB, D CALVANIO, R LEVINE, DN TI REAPPEARANCE OF THE VISUAL PERCEPT AFTER INTENTIONAL BLINKING IN A PATIENT WITH BALINT SYNDROME SO JOURNAL OF CLINICAL NEURO-OPHTHALMOLOGY LA English DT Article DE BALINT SYNDROME; FADING; BLINK ID EYE-MOVEMENTS AB We present a patient with Balint's syndrome who complained of fading of the scenes under visual fixation. When he intentionally blinked, the faded visual percept reappeared. The disappearance of the visual percept may be explained as the result of either unstable visual fixation or of saturation of the visual pathways. The role of blinking in reviving the visual percept may be explained accordingly as causing a refixation of the target under visual fixation or as resetting the visual pathways for visual processing. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. SPAULDING REHABIL HOSP,NEUROL SERV,BOSTON,MA 02114. NR 31 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0272-846X J9 J CLIN NEURO-OPHTHAL PD MAR PY 1991 VL 11 IS 1 BP 62 EP 65 PG 4 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA FA527 UT WOS:A1991FA52700016 PM 1827464 ER PT J AU CANNISTRA, SA AF CANNISTRA, SA TI WHY SHOULD THE CLONOGENIC CELL ASSAY BE PROGNOSTICALLY IMPORTANT IN OVARIAN-CANCER SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID ADVANCED OVARIAN-CANCER; CISPLATIN; CARCINOMA; SURVIVAL RP CANNISTRA, SA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 11 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAR PY 1991 VL 9 IS 3 BP 368 EP 370 PG 3 WC Oncology SC Oncology GA EZ656 UT WOS:A1991EZ65600002 PM 1999705 ER PT J AU GELBER, RD GOLDHIRSCH, A AF GELBER, RD GOLDHIRSCH, A TI QUALITY-ADJUSTED SURVIVAL ANALYSIS - REPLY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter ID ADJUVANT THERAPY; BREAST-CANCER; ENDPOINT C1 INT BREAST CANC STUDY GRP,BERN,SWITZERLAND. INST BREAST CANC STUDY GRP,LUGANO,SWITZERLAND. RP GELBER, RD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAR PY 1991 VL 9 IS 3 BP 526 EP 526 PG 1 WC Oncology SC Oncology GA EZ656 UT WOS:A1991EZ65600024 ER PT J AU HENDERSON, IC AF HENDERSON, IC TI CHEMOTHERAPY, TAMOXIFEN, AND BREAST-CANCER - RECONCILING DIFFERENCES - REPLY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter RP HENDERSON, IC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAR PY 1991 VL 9 IS 3 BP 527 EP 528 PG 2 WC Oncology SC Oncology GA EZ656 UT WOS:A1991EZ65600026 ER PT J AU FAVA, M ROSENBAUM, JF AF FAVA, M ROSENBAUM, JF TI SUICIDALITY AND FLUOXETINE - IS THERE A RELATIONSHIP SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID BORDERLINE AB A recent report of six depressed patients who developed intense, violent suicidal preoccupation after 2 to 7 weeks of fluoxetine treatment prompted the authors to survey 27 psychiatrists who treated 1017 depressed outpatients with antidepressants during 1989: 3.5% (8/231) of those treated with fluoxetine alone, 6.5% (4/62) of those treated with fluoxetine and tricyclics, 1.3% (5/385) of those treated with tricyclics alone or with lithium, and 3.0% (3/101) of those treated with other antidepressants became suicidal only after treatment with these antidepressants was initiated. None of these patients, however, reported intense suicidal thoughts of the degree described in the previously reported six cases. The difference in incidence of suicidal ideation occurring only after initiation of treatment was not significant between patients treated with fluoxetine alone and those receiving the other antidepressant treatments. RP FAVA, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CLIN PSYCHOPHARMACOL UNIT,ACC 815,BOSTON,MA 02114, USA. NR 13 TC 103 Z9 103 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD MAR PY 1991 VL 52 IS 3 BP 108 EP 111 PG 4 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA FE630 UT WOS:A1991FE63000004 PM 2005073 ER PT J AU SMITH, DJ TAUBMAN, MA ALISALAAM, P AF SMITH, DJ TAUBMAN, MA ALISALAAM, P TI IMMUNOGLOBULIN ISOTYPES IN HUMAN MINOR GLAND SALIVA SO JOURNAL OF DENTAL RESEARCH LA English DT Article ID CELLS AB Lower labial, upper labial, palatine (minor), and parotid (major) gland saliva samples from 18 young adult males were quantitatively assayed for the presence of IgA1, IgA2, IgM, and IgG. The mean (+/- standard deviation) concentrations of IgA (sum of IgA1 + IgA2) were 79 +/- 42-mu-g/mL (parotid), 111 +/- 42-mu-g/mL (lower labial), 69 +/- 72-mu-g/mL (upper labial), and 88 +/- 68-mu-g/mL (palatine). Total IgA concentrations were positively correlated among different minor-gland samples from the same subject, although these correlations did not reach significance. Upper-labial-gland saliva samples contained significantly (at least p < 0.05) lower concentrations of IgA1 than those found in parotid or lower-labial minor-gland secretions. All three minor-gland sources of saliva contained significantly (p < 0.002) higher levels of IgG than did parotid saliva. Upper-labial fluids had significantly (p < 0.02) higher IgG concentrations than lower-labial saliva. IgM could be detected in 89% of parotid saliva samples and 75% of the palatine saliva samples. Palatine IgM concentrations (8.2 +/- 17.8-mu-g/mL) were significantly (p < 0.05) higher than parotid IgM concentrations (0.6 +/- 0.4-mu-g/mL). IgM was detected much less frequently and at lower concentrations in lower- and upper-labial-gland saliva. These data reveal that minor-gland saliva from different oral sites may contain distinctive immunoglobulin isotype patterns, and expressions of host defense may vary within each micro-environment. RP SMITH, DJ (reprint author), FORSYTH DENT CTR,DEPT IMMUNOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-04733, DE-06153] NR 17 TC 19 Z9 19 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD MAR PY 1991 VL 70 IS 3 BP 167 EP 170 DI 10.1177/00220345910700030201 PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FD585 UT WOS:A1991FD58500002 PM 1999553 ER PT J AU EGEA, E IGLESIAS, A SALAZAR, M MORIMOTO, C KRUSKALL, MS AWDEH, Z SCHLOSSMAN, SF ALPER, CA YUNIS, EJ AF EGEA, E IGLESIAS, A SALAZAR, M MORIMOTO, C KRUSKALL, MS AWDEH, Z SCHLOSSMAN, SF ALPER, CA YUNIS, EJ TI THE CELLULAR BASIS FOR LACK OF ANTIBODY-RESPONSE TO HEPATITIS-B VACCINE IN HUMANS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID SURFACE-ANTIGEN HBSAG; MAJOR HISTOCOMPATIBILITY COMPLEX; CONTROLLED CLINICAL-TRIAL; HUMORAL IMMUNE-RESPONSE; LYMPHOCYTE-T CLONES; GENETIC-REGULATION; IR GENES; HLA-DR; CELLS; EFFICACY AB We had previously obtained evidence that among normal subjects the humoral antibody response to hepatitis B surface antigen (HBsAg) was bimodally distributed with about 14% of subjects producing < 1,000 estimated radioimmunoassay RIA units. From the study of major histocompatibility complex (MHC) markers in the very poor responders who produced < 36 estimated RIA units of antibody, it appeared that there was an excess of homozygotes for two extended haplotypes [HLA-B8, SC01, DR3] and [HLA-B44, FC31, DR7]. This finding suggested that a poor response was inherited as a recessive trait requiring nonresponse genes for HBsAg on both MHC haplotypes and was strengthened by finding a much lower antibody response among prospectively immunized homozygotes for [HLA-B8, SC01, DR3] compared with heterozygotes. In the present study, we have analyzed the cellular basis for nonresponse to this antigen by examining antigen-specific proliferation of T cells from responders and nonresponders in the presence and absence of autologous CD8+ (suppressor) cells. Peripheral blood cells from nonresponders to HBsAg failed to undergo a proliferative response to recombinant HBsAg in vitro, whereas cells from responders proliferated vigorously. This failure of cells from nonresponders to proliferate was not reversed in cell mixtures containing CD4+ and antigen-presenting cells devoid of CD8+ cells. There was no difference between responders and nonresponders with respect to the number of circulating T cells or their subsets, or the proliferative response to mitogens such as pokeweed or phytohemagglutinin or another antigen, tetanus toxoid. Our results indicate that our HBsAg nonresponding subjects have a very specific failure in antigen presentation or the stimulation of T helper cells, or both. Our evidence is against specific immune suppression as the basis for their nonresponsiveness. The failure of antigen presentation or T cell help is consistent with recessive inheritance of nonresponsiveness and suggests that response is dominantly inherited. C1 CTR BLOOD RES INC,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-29583]; NIAID NIH HHS [AI-14157]; NICHD NIH HHS [HD-17461] NR 54 TC 106 Z9 109 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD MAR 1 PY 1991 VL 173 IS 3 BP 531 EP 538 DI 10.1084/jem.173.3.531 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EZ663 UT WOS:A1991EZ66300002 PM 1825504 ER PT J AU HYND, GW SEMRUDCLIKEMAN, M LORYS, AR NOVEY, ES ELIOPULOS, D LYYTINEN, H AF HYND, GW SEMRUDCLIKEMAN, M LORYS, AR NOVEY, ES ELIOPULOS, D LYYTINEN, H TI CORPUS-CALLOSUM MORPHOLOGY IN ATTENTION DEFICIT-HYPERACTIVITY DISORDER - MORPHOMETRIC ANALYSIS OF MRI SO JOURNAL OF LEARNING DISABILITIES LA English DT Article ID INFANTILE-AUTISM; CHILDREN; DYSFUNCTION; DOMINANCE; SEX; CT C1 ATHENS MAGNET IMAGING,MED,ATHENS,GA. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. N SHORE UNIV HOSP,CHILD NEUROPSYCHOL,MANHASSET,NY 11030. UNIV JYVASKYLA,FINNISH ACAD SCI,DEPT PSYCHOL,SF-40100 JYVASKYLA 10,FINLAND. RP HYND, GW (reprint author), UNIV GEORGIA,CTR CLIN & DEV NEUROPSYCHOL,DEPT SPECIAL EDUC,EXC ADERHOLD HALL,ATHENS,GA 30602, USA. NR 46 TC 252 Z9 257 U1 1 U2 6 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 SN 0022-2194 J9 J LEARN DISABIL JI J. Learn. Disabil. PD MAR PY 1991 VL 24 IS 3 BP 141 EP 146 PG 6 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA EY753 UT WOS:A1991EY75300002 PM 2026955 ER PT J AU LEVINE, RL DOBKIN, JA ROZENTAL, JM SATTER, MR NICKLES, RJ AF LEVINE, RL DOBKIN, JA ROZENTAL, JM SATTER, MR NICKLES, RJ TI BLOOD-FLOW REACTIVITY TO HYPERCAPNIA IN STRICTLY UNILATERAL CAROTID DISEASE - PRELIMINARY-RESULTS SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID CEREBRAL-CIRCULATION; STENOSIS; ARTERY; PERFUSION; OCCLUSION; ISCHEMIA; STROKE; BYPASS; RCBF AB To show a relationship between degree of carotid arterial stenosis and cerebral blood flow reactivity (RES%) to induced hypercapnia, fluorine-18-fluoromethane and positron emission tomography (PET) was used to study 18 patients with carotid distribution transient ischaemic attacks (TIA), all free of stroke, who had angiographic-proven unilateral arterial disease. Non-involved carotid arteries were either normal or had non-stenotic plaque. Either normal arteries or non-stenotic ulcerations in the symptomatic carotid arteries were present in five of 18 (28%), ipsilateral carotid stenosis from 50-99% was present in eight of 18 (44%), and ipsilateral internal carotid occlusion was present in five of 18 (28%) patients. In comparison with 14 normal controls, all patients with symptomatic middle cerebral artery (MCA) flow territories had significantly lower mean (SEM) RES% [5.0 (0.2) vs 4.0 (0.9), p < 0.04]. Symptomatic anterior borderzone (ABZ) RES% was also significantly lower [4.6 (0.4) vs 3.3 (0.9), p < 0.04], than controls. In patient subgroup comparisons, the 50-99% stenosis subgroup clearly had the lowest MCA RES% [3.4 (0.2)] as well as the lowest ABZ RES% [2.8 (0.4)] on their symptomatic sides. Age, expired pCO2, mean arterial blood pressure, serum glucose, serum haematocrit and number, type and estimated duration of TIAs were not significantly different between subgroups. Linear regression showed a significant relationship between RES% and both measured percentage-stenosis (p = 0.04) and residual luminal diameter (p = 0.05) in symptomatic MCA territories. This approached significance in symptomatic ABZ regions. This preliminary data set suggests that unilateral carotid stenosis can and does result in impaired CO2 reactivity following hypercapnia. The relative normality of CO2 reactivity in those with carotid occlusion is discussed. C1 UNIV WISCONSIN HOSP & CLIN,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED PHYS,MADISON,WI 53705. NR 25 TC 28 Z9 28 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD MAR PY 1991 VL 54 IS 3 BP 204 EP 209 DI 10.1136/jnnp.54.3.204 PG 6 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA FB085 UT WOS:A1991FB08500004 PM 1903147 ER PT J AU WIERZBICKA, MM WIEGNER, AW LOGIGIAN, EL YOUNG, RR AF WIERZBICKA, MM WIEGNER, AW LOGIGIAN, EL YOUNG, RR TI ABNORMAL MOST-RAPID ISOMETRIC CONTRACTIONS IN PATIENTS WITH PARKINSONS-DISEASE SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID SINGLE MOTOR UNITS; TARGETED FORCE IMPULSES; VOLUNTARY CONTRACTIONS; BALLISTIC CONTRACTIONS; ANTAGONIST MUSCLES; TRAJECTORY CONTROL; MOVEMENTS; TREMOR; BRADYKINESIA; RECRUITMENT AB Fast isometric elbow flexor muscle contractions of specified amplitude in six normal subjects were compared with those of 11 patients with Parkinson's disease. Despite treatment, all patients exhibited deficits in this motor task. Three patients were able to produce rapid force pulses with normal contraction times, but the variability of their force responses was increased in comparison with the highly stereotyped responses produced by normal subjects. The other eight patients had prolonged contraction times and segmentation of the force profiles. The integrated area of the first agonist EMG burst and the rate of development of force (dF/dt) were less at any target level than what was needed to produce a fast response. The area of the EMG burst, however, did increase with target amplitude, and the relative increase of dF/dt, with target amplitude, was normal. It is concluded that the motor program subserving fast muscle contraction is preserved in Parkinson's disease, but its execution is characterised by improper scaling of motor output. C1 MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NR 27 TC 64 Z9 64 U1 1 U2 3 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD MAR PY 1991 VL 54 IS 3 BP 210 EP 216 DI 10.1136/jnnp.54.3.210 PG 7 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA FB085 UT WOS:A1991FB08500005 PM 2030347 ER PT J AU YAPOR, WY CROWELL, RM AF YAPOR, WY CROWELL, RM TI SUPERIOR HYPOPHYSEAL ARTERY ANEURYSM - REPORT OF 2 CASES SO JOURNAL OF NEUROSURGERY LA English DT Article DE ANEURYSM; SUPERIOR HYPOPHYSEAL ARTERY; INTERNAL CAROTID ARTERY; CLIP ID INTERNAL CAROTID-ARTERY; FENESTRATED CLIPS AB Two cases of saccular intracranial aneurysms arising from the superior hypophyseal artery take-off from the internal carotid artery are presented. The angiographic findings and technical details of the operative approach are discussed. Particular attention is focused on the use of fenestrated angled clips. C1 RESURRECT MED CTR,CHICAGO,IL. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 10 TC 4 Z9 4 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 MAR PY 1991 VL 74 IS 3 BP 501 EP 503 DI 10.3171/jns.1991.74.3.0501 PG 3 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA EZ166 UT WOS:A1991EZ16600021 PM 1993916 ER PT J AU FISCHMAN, AJ PIKE, MC KROON, D FUCELLO, AJ REXINGER, D TENKATE, C WILKINSON, R RUBIN, RH STRAUSS, HW AF FISCHMAN, AJ PIKE, MC KROON, D FUCELLO, AJ REXINGER, D TENKATE, C WILKINSON, R RUBIN, RH STRAUSS, HW TI IMAGING FOCAL SITES OF BACTERIAL-INFECTION IN RATS WITH INDIUM-111-LABELED CHEMOTACTIC PEPTIDE ANALOGS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; CHEMOATTRACTANT RECEPTORS; NEUTROPHILS; PROTEIN; CELLS AB Four DTPA-derivatized chemotactic peptide analogs: ForNleLFNleYK-DTPA (P1), ForMLFNH(CH2)6NH-DTPA (P2), ForNleLFK(NH2)-DTPA (P3), and ForNleLFK-DTPA (P4), were synthesized and evaluated for in vitro bioactivity and receptor binding. The peptides were radiolabeled with 111In by transchelation and their biodistribution determined in rats at 5, 30, 60 and 120 min after injection. Localization at sites of infection was determined by scintillation camera imaging in animals with deep-thigh infection due to Escherichia coli. Images were recorded from 5 min to 2 hr after injection. All peptides maintained biologic activity (EC50 for O2-production by human PMN's: 3-150 nM) and the ability to bind to the oligopeptide chemoattractant receptor on human PMN's (EC50 for binding: 7.5-50 nM); biologic activity and receptor binding were highly correlated (r = 0.99). For all the peptides, blood clearance was rapid (half-lives: 21.5, 33.1, 31.6, and 28.7 min for P1, P2, P3, and P4, respectively). Biodistributions of the individual peptides were similar with low levels of accumulation in the heart, lung, liver, spleen, and gastrointestinal tract. In the kidney, P1 had much greater accumulation than other organs. All peptides yielded high quality images of the infection sites within 1 hr of injection. This study demonstrates that 111Inlabeled chemotactic peptide analogs were effective agents for the external imaging of focal sites of infection. C1 MASSACHUSETTS GEN HOSP,MED SERV,INFECT DIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,ARTHRITIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RW JOHNSON PHARMACEUT RES INST,RARITAN,NJ. RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,FRUIT ST,BOSTON,MA 02114, USA. NR 33 TC 106 Z9 107 U1 1 U2 3 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAR PY 1991 VL 32 IS 3 BP 483 EP 491 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC460 UT WOS:A1991FC46000026 PM 2005457 ER PT J AU WOLOHAN, MJ ZALESKE, DJ AF WOLOHAN, MJ ZALESKE, DJ TI HEMIEPIPHYSEAL RECONSTRUCTION USING TISSUE DONATED FROM FETAL LIMBS IN A MURINE MODEL SO JOURNAL OF ORTHOPAEDIC RESEARCH LA English DT Article DE EPIPHYSIS; RECONSTRUCTION; TRANSPLANTATION; FETAL TISSUE ID GROWTH AB Epiphyseal reconstruction in the immature skeleton could have great clinical significance. Hemiepiphyseal reconstruction was performed in a murine model by transplanting fetal tissue to surgically created defects in postnatal mice. Reconstruction is facilitated by the existence of inbred strains. While the reconstruction as performed here did not completely restore the growth characteristics of the epiphysis, the model represents a potentially fruitful interface between basic and clinical biology. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,ACC 507,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIAMS NIH HHS [AR39380] NR 17 TC 7 Z9 7 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0736-0266 J9 J ORTHOPAED RES JI J. Orthop. Res. PD MAR PY 1991 VL 9 IS 2 BP 180 EP 185 DI 10.1002/jor.1100090205 PG 6 WC Orthopedics SC Orthopedics GA EW656 UT WOS:A1991EW65600004 PM 1992067 ER PT J AU HESSEBIBER, S MARINO, M AF HESSEBIBER, S MARINO, M TI FROM HIGH-SCHOOL TO COLLEGE - CHANGES IN WOMENS SELF-CONCEPT AND ITS RELATIONSHIP TO EATING PROBLEMS SO JOURNAL OF PSYCHOLOGY LA English DT Article ID ANOREXIA-NERVOSA; PHYSICAL ATTRACTIVENESS; ATTITUDES TEST; SOCIAL-CLASS; BULIMIA; STUDENTS; PREVALENCE; SYMPTOMS; POPULATION; DISORDER C1 MASSACHUSETTS GEN HOSP,CTR FAMILY DEV,BOSTON,MA 02114. RP HESSEBIBER, S (reprint author), BOSTON COLL,DEPT SOCIOL,CHESTNUT HILL,MA 02167, USA. NR 71 TC 17 Z9 17 U1 3 U2 6 PU HELDREF PUBLICATIONS PI WASHINGTON PA 1319 EIGHTEENTH ST NW, WASHINGTON, DC 20036-1802 SN 0022-3980 J9 J PSYCHOL JI J. Psychol. PD MAR PY 1991 VL 125 IS 2 BP 199 EP 216 PG 18 WC Psychology, Multidisciplinary SC Psychology GA FJ747 UT WOS:A1991FJ74700007 PM 2061863 ER PT J AU NICKMAN, SL AF NICKMAN, SL TI THE ADOPTION DEBATE CONTINUED - REPLY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter RP NICKMAN, SL (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD MAR PY 1991 VL 30 IS 2 BP 334 EP 334 DI 10.1097/00004583-199103000-00032 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA FB921 UT WOS:A1991FB92100033 ER PT J AU KISHIMOTO, C HUNG, GL ISHIBASHI, M KHAW, BA KOLODNY, GM ABELMANN, WH YASUDA, T AF KISHIMOTO, C HUNG, GL ISHIBASHI, M KHAW, BA KOLODNY, GM ABELMANN, WH YASUDA, T TI NATURAL EVOLUTION OF CARDIAC-FUNCTION, CARDIAC PATHOLOGY AND ANTIMYOSIN SCAN IN A MURINE MYOCARDITIS MODEL SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID MYOSIN-SPECIFIC ANTIBODY; VIRAL MYOCARDITIS; IMMUNOLOGICAL IDENTIFICATION; LYMPHOCYTE SUBSETS; DIFFERENT KINETICS; PERIPHERAL-BLOOD; INFARCTION; LOCALIZATION; FRAGMENTS; HEART AB Serial technetium-99m radionuclide ventriculograms, indium-111 antimyosin antibody scans and tissue biodistribution studies were performed in C3H/He mice with experimentally induced viral encephalomyocarditis and the results were compared with pathologic assessments of myocardial necrosis. Postinfection ejection fraction decreased on days 10 (20.7 +/- 5.5%, n = 6), 20 (18.6 +/- 15.2%, n =5), 30 (18.5 +/- 7.7%, n = 5) and 150 (30.0 +/- 18.7, n = 6) (p < 0.001) in comparison with that in uninfected control mice (63.3 +/- 3.1%, n = 6). In the same group of animals, indium-111 antimyosin antibody scans showed intense positive myocardial accumulation on day 10 (in six of six mice) and only slight accumulation on day 20 (in one of five mice). In the chronic stage, two of five mice on day 30 and two of six mice on day 150 still showed positive untake. The antimyosin scan myocardium to lung uptake ratio (expressed as mean count density [mean counts/pixel of the region] ratio) increased greatly on day 10 (p < 0.001 versus values in uninfected control mice) but not subsequently. Biodistribution studies of the indium-111 antimyosin antibody showed that the heart to blood count ratio was significantly higher on day 10 (p < 0.001 versus values in control mice) but not on days 20, 30 and 150. Pathologic examination showed active and ongoing severe myocardial necrosis with dilated ventricles on day 10. On day 20, there was less active necrosis and healing had appeared to begin. On days 30 and 150, myocardial fibrosis increased. This study reveals a depression in cardiac function in the acute stage of myocarditis that correlates with severe myocardial necrosis and intense uptake of radiolabeled antimyosin. Severe left ventricular dysfunction appeared within 10 days of infection with the encephalomyocarditis virus and continued until day 30. After 5 months, left ventricular function improved in mice that had survived. C1 MASSACHUSETTS GEN HOSP,DIV NUCL MED,TILTON 2,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. CHARLES A DANA RES INST,BOSTON,MA. HARVARD UNIV,BETH ISRAEL HOSP,THORNDIKE LAB,BOSTON,MA 02215. BETH ISRAEL HOSP,DIV CARDIOVASC,BOSTON,MA 02215. BETH ISRAEL HOSP,DIV NUCL MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-26205] NR 21 TC 20 Z9 22 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1991 VL 17 IS 3 BP 821 EP 827 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA EY741 UT WOS:A1991EY74100035 PM 1847155 ER PT J AU YOSHIKAWA, TT AF YOSHIKAWA, TT TI ELIMINATION OF TUBERCULOSIS FROM THE UNITED-STATES SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Editorial Material RP YOSHIKAWA, TT (reprint author), US DEPT VET AFFAIRS,OFF GERIATR & EXTENDED CARE,WASHINGTON,DC, USA. NR 13 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD MAR PY 1991 VL 39 IS 3 BP 312 EP 314 PG 3 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA FC070 UT WOS:A1991FC07000015 PM 2005348 ER PT J AU DEFOSSEZ, SM YODER, IC PAPANICOLAOU, N ROSEN, BR MCGOVERN, F AF DEFOSSEZ, SM YODER, IC PAPANICOLAOU, N ROSEN, BR MCGOVERN, F TI NONSPECIFIC MAGNETIC-RESONANCE APPEARANCE OF RENAL ONCOCYTOMAS - REPORT OF 3 CASES AND REVIEW OF THE LITERATURE SO JOURNAL OF UROLOGY LA English DT Review DE KIDNEY NEOPLASMS; MAGNETIC RESONANCE IMAGING AB We report the magnetic resonance appearance of 3 cases of solitary renal oncocytomas. All lesions were of low to moderate signal intensity on T1-weighted images and became considerably brighter on the more heavily T2-weighted images. One lesion contained a large central area of cystic degeneration, while the other 2 were solid. A central stellate scar was present in the smaller of the 2 solid lesions. Our observations lend further support to earlier reports on the nonspecific magnetic resonance features of oncocytomas. C1 MASSACHUSETTS GEN HOSP,DIV URORADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV MAGNET RESONANCE IMAGING,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,UROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP DEFOSSEZ, SM (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 14 TC 16 Z9 16 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD MAR PY 1991 VL 145 IS 3 BP 552 EP 554 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA FA699 UT WOS:A1991FA69900024 PM 1997708 ER PT J AU GERTLER, JP WEIBE, DA OCASIO, VH ABBOTT, WM AF GERTLER, JP WEIBE, DA OCASIO, VH ABBOTT, WM TI HYPOXIA INDUCES PROCOAGULANT ACTIVITY IN CULTURED HUMAN VENOUS ENDOTHELIUM SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID PLASMINOGEN-ACTIVATOR-INHIBITOR; FACTOR-V; HEMOSTATIC PROPERTIES; CELLS; COAGULATION; ISCHEMIA; MANAGEMENT; EXPRESSION; INDUCTION; PATHWAY AB Although it normally presents a nonthrombogenic surface, endothelium is capable of procoagulant activity and suppression of native anticoagulant properties. We theorized that hypoxia could shift normal endothelium into a procoagulant state and tested this hypothesis in cultured human umbilical venous endothelial cells. Human umbilical venous endothelial cells were obtained from fresh umbilical cords. Passage two cells were placed in control (PO2 > 120 mm Hg) or hypoxic (PO2 < 60 mm Hg) media and incubated in control or hypoxic environments for 24 hours. In additional experiments, cells were reoxygenated for 4 or 48 hours after the initial hypoxic period. Cells were then assayed for procoagulant activity expressed as thromboplastin unit equivalents per 100,000 cells based on a thromboplastin standard curve. Results are expressed as percent increase in thromboplastin unit equivalents/100,000 cells +/- standard error versus control. Statistical significance was assessed by paired t test with p < 0.05 considered significant. More than 95% of cells in all experimental and control preparations were viable after completion of the protocols. No morphologic variation was noted among the control and hypoxic groups. For cells rendered hypoxic without reoxygenation, the mean increase in procoagulant activity for the group (n = 4) versus control was 77% +/- 13% (p = 0.01). In the hypoxia and 4-hour reoxygenation group (n = 4), the mean increase in procoagulant activity was 141% +/- 43% (p < 0.05). In cells reoxygenated for 48 hours after hypoxia (n = 8), the mean increase in procoagulant activity was 198% +/- 34% (p < 0.001). Twenty four hours of hypoxia produces a statistically significant rise in procoagulant activity, which appears to augment after 48 hours of reoxygenation. This observed procoagulant activity is not associated with loss of cell viability and is present on intact human umbilical venous endothelial cells monolayers. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV VASC SURG,BOSTON,MA 02114. RP GERTLER, JP (reprint author), SUNY HLTH SCI CTR,DEPT SURG,DIV VASC SURG,BOX 40,450 CLARKSON AVE,BROOKLYN,NY 11203, USA. FU NHLBI NIH HHS [HL 34780-06] NR 27 TC 45 Z9 48 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD MAR PY 1991 VL 13 IS 3 BP 428 EP 433 PG 6 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA FA966 UT WOS:A1991FA96600012 PM 1999864 ER PT J AU MORELAND, RB MONTROSS, L GARCEA, RL AF MORELAND, RB MONTROSS, L GARCEA, RL TI CHARACTERIZATION OF THE DNA-BINDING PROPERTIES OF THE POLYOMAVIRUS CAPSID PROTEIN-VP1 SO JOURNAL OF VIROLOGY LA English DT Article ID VIRUS-40 NUCLEOPROTEIN COMPLEXES; HIGH-LEVEL EXPRESSION; SIMIAN VIRUS-40; ESCHERICHIA-COLI; INTRACELLULAR FORMS; CLONED GENES; CHROMATIN; INVITRO; VIRION; VP1 AB The major capsid protein of polyomavirus, VP1, has been expression cloned in Escherichia coli, and the recombinant VP1 protein has been purified to near homogeneity (A. D. Leavitt, T. M. Roberts, and R. L. Garcer, J. Biol. Chem. 260:12803-12809, 1985). With this recombinant protein, a nitrocellulose filter transfer assay was developed for detecting DNA binding to VP1 (Southwestern assay). In optimizing conditions for this assay, dithiothreitol was found to inhibit DNA binding significantly. With recombinant VP1 proteins deleted at the carboxy and amino termini, a region of the protein affecting DNA binding was identified within the first 7 amino acids (MAPKRKS) of the VP1 amino terminus. Southwestern analysis of virion proteins separated by two-dimensional gel electrophoresis demonstrated equivalent DNA binding among the different VP1 isoelectric focusing subspecies, suggesting thbat VP1 phosphorylation does not modulate this function. By means of partial proteolysis of purified recombinant VP1 capsomeres for assessing structural features of the protein domain affecting DNA binding, a trypsin-sensitive site at lysine 28 was found to eliminate VP1 binding to DNA. The binding constant of recombinant VP1 to polyomavirus DNA was determined by an immunoprecipitation assay (R. D. G. McKay, J. Mol. Biol. 145:471-488, 1981) to be 1 x 10(-11) to 2 x 10(-11) M, which was not significantly different from its affinity for plasmid DNA. McKay analysis of deleted VPI proteins and VP1-beta-galactosidase fusion proteins indicated that the amino terminus was both necessary and sufficient for DNA binding. As shown by electron microscopy, DNA inhibited in vitro capsomere self-assembly into capsidlike structures (D. M. Salunke, D. L. D. Caspar, and R. L. Garcea, Cell 46:895-904, 1986). Thus, VP1 is a high-affinity, non-sequence-specific DNA-binding protein with the binding function localized near its trypsin-accessible amino terminus. The inhibitory effects of disulfide reagents on DNA binding and of DNA on capsid assembly suggest possible intermediate steps in virion assembly. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. FU NCI NIH HHS [CA37887, R01 CA037667] NR 51 TC 78 Z9 78 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1991 VL 65 IS 3 BP 1168 EP 1176 PG 9 WC Virology SC Virology GA EY750 UT WOS:A1991EY75000014 PM 1847446 ER PT J AU BONVENTRE, JV NEMENOFF, R AF BONVENTRE, JV NEMENOFF, R TI RENAL TUBULAR ARACHIDONIC-ACID METABOLISM SO KIDNEY INTERNATIONAL LA English DT Article ID TUMOR NECROSIS FACTOR; GLOMERULAR MESANGIAL CELLS; SPONTANEOUSLY HYPERTENSIVE RATS; CORTICAL COLLECTING TUBULE; EPIDERMAL GROWTH-FACTOR; THICK ASCENDING LIMB; PROTEIN KINASE-C; FACTOR RECEPTOR-KINASE; FACTOR GENE-EXPRESSION; BETA-GAMMA-SUBUNITS C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,MED SERV,DIABET UNIT,BOSTON,MA 02144. RP BONVENTRE, JV (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,MED SERV,RENAL UNIT,FRUIT ST,BOSTON,MA 02144, USA. FU NIDDK NIH HHS [DK38165, DK38452, DK39773] NR 165 TC 61 Z9 61 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD MAR PY 1991 VL 39 IS 3 BP 438 EP 449 DI 10.1038/ki.1991.55 PG 12 WC Urology & Nephrology SC Urology & Nephrology GA EY193 UT WOS:A1991EY19300008 PM 1905765 ER PT J AU CANNISTRA, SA DICARLO, J GROSHEK, P KANAKURA, Y BERG, D MAYER, RJ GRIFFIN, JD AF CANNISTRA, SA DICARLO, J GROSHEK, P KANAKURA, Y BERG, D MAYER, RJ GRIFFIN, JD TI SIMULTANEOUS ADMINISTRATION OF GRANULOCYTE MACROPHAGE COLONY-STIMULATING FACTOR AND CYTOSINE-ARABINOSIDE FOR THE TREATMENT OF RELAPSED ACUTE MYELOID-LEUKEMIA SO LEUKEMIA LA English DT Article ID ACUTE MYELOBLASTIC-LEUKEMIA; FACTOR RECEPTOR; CELLS; EXPRESSION; PHASE; TRIAL AB The treatment of patients with relapsed or refractory acute myeloid leukemia (AML) with high dose cytosine arabinoside (ara-C) results in short-lived complete response rates of 30-50%. We have previously shown that entry of myeloid leukemic cells into S phase can be accelerated in vitro through the use of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF), resulting in enhancement of ara-C-mediated cytotoxicity. In order to evaluate the in vivo biological and clinical effects of this strategy in patients with high risk AML, we treated three patients with either refractory or relapsed disease with a continuous infusion of rhGM-CSF (0.45-mu-g/kg/h aglycoprotein) for 18 h, followed by the institution of high dose ara-C and continuation of rhGM-CSF throughout the 4 day duration of ara-C treatment. Prior to therapy, no patient had detectable levels of circulating rhGM-CSF, and there was no evidence of GM-CSF receptor occupancy in leukemic myeloblasts. After 18 h of rhGM-CSF therapy, all patients had biologically active levels of circulating rhGM-CSF (7.9-12.0 ng/ml), and two patients showed a significant degree of leukemic GM-CSF receptor occupancy without evidence of GM-CSF receptor down-regulation. A significant rise in the S phase fraction of leukemic myeloblasts was observed at 18 h of rhGM-CSF treatment in all three patients (29-56% increment). The toxicity of combined rhGM-CSF/ara-C therapy included pericarditis and cerebellar degeneration in one patient, fever and mild renal dysfunction in two patients, and mild hepatic dysfunction in all three patients. Each patient showed a transient rise in the absolute neutrophil and blast count during rhGM-CSF/ara-C administration, followed by profound, but clinically tolerable, myelosuppression. No patient developed clinical evidence of leukostasis. There was one death related to pericardial tamponade, one death related to refractory disease, and one clinical and cytogenetic remission. These results suggest that exogenously administered rhGM-CSF is capable of rapidly mobilizing leukemic cells into S phase in vivo and theoretically should be useful in overcoming kinetic resistance to ara-C. Clinical trials of this regimen in patients with high risk AML who are not already pharmacologically resistant to ara-C are warranted. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. RP CANNISTRA, SA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 36167, CA 34183, CA 42802] NR 23 TC 85 Z9 86 U1 1 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD MAR PY 1991 VL 5 IS 3 BP 230 EP 238 PG 9 WC Oncology; Hematology SC Oncology; Hematology GA FL312 UT WOS:A1991FL31200010 PM 1826536 ER PT J AU PATTON, JP NASH, DB ABRUTYN, E AF PATTON, JP NASH, DB ABRUTYN, E TI URINARY-TRACT INFECTION - ECONOMIC-CONSIDERATIONS SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID SINGLE-DOSE THERAPY; COST-BENEFIT-ANALYSIS; TRIMETHOPRIM-SULFAMETHOXAZOLE; NOSOCOMIAL INFECTIONS; ACUTE DYSURIA; SIGNIFICANT BACTERIURIA; PERIODIC INSTILLATIONS; EXCRETORY UROGRAPHY; ANTIBIOTIC-THERAPY; RANDOMIZED TRIAL C1 UNIV PENN,LEONARD DAVIS INST HLTH ECON,GEN INTERNAL MED SECT,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19129. VET AFFAIRS MED CTR,PHILADELPHIA,PA. NR 94 TC 102 Z9 107 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAR PY 1991 VL 75 IS 2 BP 495 EP 513 PG 19 WC Medicine, General & Internal SC General & Internal Medicine GA EZ546 UT WOS:A1991EZ54600017 PM 1996046 ER PT J AU JACOBSON, JO WILKES, BM HARRIS, NL AF JACOBSON, JO WILKES, BM HARRIS, NL TI POLYCLONAL REARRANGEMENT OF THE T-CELL ANTIGEN RECEPTOR GENES IN HODGKINS-DISEASE - IMPLICATIONS FOR DIAGNOSIS SO MODERN PATHOLOGY LA English DT Article DE HODGKINS DISEASE; T-CELL ANTIGEN RECEPTOR GENES; T-CELL LYMPHOMA ID BETA-CHAIN GENE; CHRONIC LYMPHOCYTIC-LEUKEMIA; REED-STERNBERG CELLS; LYMPHOPROLIFERATIVE DISORDERS; GAMMA-CHAIN; IMMUNOGLOBULIN GENES; MONOCLONAL-ANTIBODY; LYMPHOID NEOPLASMS; MARKERS; EXPRESSION AB Distinction between Hodgkin's disease and peripheral T-cell lymphoma can be difficult, based on routine morphologic and immunohistologic stains. To assess the utility of Southern blot analysis, we investigated the genes for the beta (T(beta)) and gamma (T(gamma)) chains of the T-cell antigen receptor and immunoglobin heavy and light chains in 15 unselected cases of Hodgkin's disease. Following digestion with the restriction enzyme EcoRI, the intensity of the germline band corresponding to the first constant region of T(beta) was reduced when compared with the intensity of the second constant region germline band, a pattern consistent with polyclonal rearrangement of this gene. Hybridization of EcoRI-digested DNA with a probe recognizing the joining regions of T(gamma) revealed multiple rearranged bands corresponding to the known limited recombinatorial possibilities of this gene. Clonal rearrangement of T(beta) and T(gamma) was never demonstrated, although the banding pattern seen with T(gamma) could easily be misinterpreted as such. The findings in Hodgkin's disease were identical to those obtained in hyperplastic lymph nodes, normal thymuses, and normal peripheral blood enriched for T-cells. We then examined the status of T-cell receptor and immunoglobulin genes in six cases that could not be definitely classified as either Hodgkin's disease or T-cell lymphoma by either morphology or immunohistology. Clonal T-cell receptor gene rearrangement was found in three cases, supporting the diagnosis of T-cell lymphoma. Our study confirms the polyclonal lineage of the major fraction of T-cells and B-cells in Hodgkin's disease, a finding that may have diagnostic importance. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP JACOBSON, JO (reprint author), MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114, USA. NR 42 TC 15 Z9 15 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD MAR PY 1991 VL 4 IS 2 BP 172 EP 177 PG 6 WC Pathology SC Pathology GA FD775 UT WOS:A1991FD77500008 PM 1646454 ER PT J AU BUCKLER, AJ PELLETIER, J HABER, DA GLASER, T HOUSMAN, DE AF BUCKLER, AJ PELLETIER, J HABER, DA GLASER, T HOUSMAN, DE TI ISOLATION, CHARACTERIZATION, AND EXPRESSION OF THE MURINE WILMS-TUMOR GENE (WT1) DURING KIDNEY DEVELOPMENT SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID RETINOBLASTOMA GENE; ENCODED PROTEIN; DNA; ASSOCIATION; DELETION; PRODUCT; CHROMOSOME-11; MUTATION; ONCOGENE; 11P15.5 AB The human Wilms' tumor predisposition gene, WT1, is a Cys-His zinc finger polypeptide which appears to be a transcription factor controlling gene expression during embryonic kidney development. In order to analyze the role of the WT1 gene in nephroblast differentiation, we have isolated the murine homolog of human WT1. An extremely high level of amino acid sequence conservation (> 95%) extends throughout all regions of the predicted mouse and human WT1 polypeptides. Two alternative splices within the WT1 transcript have been conserved between mice and humans, suggesting that these have functional significance. Expression of the mouse WT1 mRNA in fetal kidney increases during late gestation, peaks just prior to or shortly after birth, and declines dramatically by 15 days postpartum. Developmental regulation of WT1 expression appears to be selective for the kidney. The restriction of WT1 expression to a limited number of tissues is in contrast to previously described tumor suppressor genes. In addition, the narrow window of time during which WT1 is expressed at high levels in the kidney is consistent with the origin of Wilms' tumor from primitive nephroblasts and the postulated role of this gene as a negative regulator of growth. C1 MIT,CTR CANC RES,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [1K08CA01356, CA08605]; NHGRI NIH HHS [HG00299] NR 36 TC 231 Z9 233 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1991 VL 11 IS 3 BP 1707 EP 1712 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EZ331 UT WOS:A1991EZ33100057 PM 1671709 ER PT J AU MEINKOTH, JL MONTMINY, MR FINK, JS FERAMISCO, JR AF MEINKOTH, JL MONTMINY, MR FINK, JS FERAMISCO, JR TI INDUCTION OF A CYCLIC AMP-RESPONSIVE GENE IN LIVING CELLS REQUIRES THE NUCLEAR FACTOR CREB SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DEPENDENT PROTEIN-KINASE; ALPHA-SUBUNIT GENE; SOMATOSTATIN GENE; TRANSCRIPTION FACTOR; CAMP; ELEMENT; PHOSPHORYLATION; IDENTIFICATION; ENHANCER; BINDING AB We constructed cell lines containing various enhancer elements cloned upstream from a marker gene. By microinjection of specific antibodies directed against transcriptional activator proteins into these cell lines, we have developed a functional assay for factors which regulate the activity of target promoters. Here we show that microinjection of a highly specific antibody to the cyclic AMP enhancer element-binding (CREB) protein diminishes gene expression in response to cyclic AMP in living fibroblasts. C1 UNIV CALIF SAN DIEGO,CTR CANC,LA JOLLA,CA 92093. SALK INST BIOL STUDIES,CLAYTON FDN LABS PEPTIDE BIOL,LA JOLLA,CA 92037. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02114. NR 28 TC 48 Z9 48 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAR PY 1991 VL 11 IS 3 BP 1759 EP 1764 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EZ331 UT WOS:A1991EZ33100067 PM 1847503 ER PT J AU FERBER, S GROSS, DJ VILLAKOMAROFF, L DANEHY, F VOLLENWEIDER, F MEYER, K LOEKEN, MR KAHN, CR HALBAN, PA AF FERBER, S GROSS, DJ VILLAKOMAROFF, L DANEHY, F VOLLENWEIDER, F MEYER, K LOEKEN, MR KAHN, CR HALBAN, PA TI HETEROGENEITY OF EXPRESSION AND SECRETION OF NATIVE AND MUTANT [ASPB10]INSULIN IN ATT20 CELLS SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID TRANSFECTED GENE; HUMAN PROINSULIN; ATT-20 CELLS; INSULIN; DNA; PATHWAY; ACID; FIBROBLASTS; STABILITY; FRAGMENTS AB AtT20 (pituitary corticotroph) cells were transfected with either the native or a mutant [Asp(B10)]rat insulin II gene, using a plasmid containing the insulin gene and a neomycin resistance gene under the control of independent constitutive promoters. The cellular immunoreactive insulin (IRI) content ranged from 0.8-440 ng/10(6) cells, with the highest value similar to that found for a rat insulinoma cell line (RIN) and corresponding to approximately 1% that of native pancreatic B-cells. There was a direct correlation between insulin mRNA levels and IRI content and no correlation between mRNA levels and rat insulin II gene copy number. Furthermore, in some lines the insulin II transgene was lost even though the gene encoding neomycin resistance was retained. IRI release was stimulated up to 4-fold by isobutylmethylxanthine in all lines transfected with the native rat insulin II gene, and HPLC analysis showed most IRI as fully processed insulin, with less than 5% as proinsulin. These cells, thus, directed most proinsulin to secretory granules for conversion and regulated release regardless of the absolute amount of IRI expressed. One of the lines transfected with the Asp(B10) mutant gene (line AA9) released nearly 50% of IRI as proinsulin under basal conditions, with stimulation of insulin, but not proinsulin, release by isobutylmethylxanthine. This confirmed our previous finding of partial diversion of this mutant proinsulin from the regulated to the constitutive pathway. A second line (IC6) expressing the same mutant gene at much higher levels appeared to direct all mutant proinsulin to the regulated pathway, suggesting that for this particular mutant proinsulin, the secretory pathway employed by the transfected cells can be affected by the amount of proinsulin synthesized. C1 CHILDRENS HOSP MED CTR,DEPT NEUROL,ENDERS 250,300 LONGWOOD AVE,BOSTON,MA 02115. JOSLIN DIABET CTR,ELLIOTT P JOSLIN RES LAB,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HADASSAH UNIV HOSP,DEPT ENDOCRINOL & METAB,IL-91120 JERUSALEM,ISRAEL. UNIV GENEVA,SCH MED,LABS RECH LOUIS JEANTET,CH-1211 GENEVA 4,SWITZERLAND. OI Ferber, Sarah/0000-0003-2764-2786 FU NICHD NIH HHS [HD-18655]; NIDDK NIH HHS [DK-35292, DK-3320] NR 34 TC 17 Z9 17 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD MAR PY 1991 VL 5 IS 3 BP 319 EP 326 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FE674 UT WOS:A1991FE67400002 PM 1890988 ER PT J AU NOEL, G KEUTMANN, HT MAINS, RE AF NOEL, G KEUTMANN, HT MAINS, RE TI INVESTIGATION OF THE STRUCTURAL REQUIREMENTS FOR PEPTIDE PRECURSOR PROCESSING IN ATT-20 CELLS USING SITE-DIRECTED MUTAGENESIS OF PROADRENOCORTICOTROPIN ENDORPHIN SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID PRO-ADRENOCORTICOTROPIN-ENDORPHIN; OPIOMELANOCORTIN MESSENGER-RNA; BETA-LIPOTROPIN PRECURSOR; AMINO-TERMINAL FRAGMENT; NUCLEOTIDE-SEQUENCE; COMMON PRECURSOR; MOUSE PITUITARY; ENDOPLASMIC-RETICULUM; SECRETORY GRANULES; JOINING PEPTIDE AB Mouse pro-ACTH/endorphin (or POMC) contains in its sequence each of the four possible pairs of basic amino acids recognized as potential cleavage sites in the production of bioactive peptides from higher mol wt precursors: KR (lysine-arginine), RR, RK, and KK. To examine the structural requirements for processing and routing in one region of pro-ACTH/endorphin, a reporter mutation was introduced into the mouse pro-ACTH/endorphin cDNA; a methionine residue was mutated to an isoleucine residue to allow biosynthetic double labeling with [H-3]Ile and [S-35]Met. Analysis of stable cell lines expressing the reporter cDNA indicated that this mutation did not affect processing or secretion. Therefore, additional mutations were introduced on the reporter background to investigate important structural features of the precursor. First, the tripeptide signal for N-linked glycosylation in the N-terminal glycopeptide (Asn65, Ser66, Ser67) was disrupted by the conservative substitution of asparagine65 with a glutamine residue. Secondly, O-glycosylation was prevented by substitution of threonine45 with an alanine residue. Finally, lysine50 was mutated to an arginine residue, transforming the RK doublet preceding the gamma-3MSH sequence into an RR doublet. The results show that the enzymatic machinery of AtT-20 cells fails to cleave efficiently at the Arg-Lys (RK) site even after elimination of any possible structural hindrance by carbohydrate side-chains. Elimination of O-linked oligosaccharides to the N-terminal side of gamma-3MSH did not allow cleavage at the RK site, and elimination of N-linked oligosaccharides did not alter the processing and routing of pro-ACTH/endorphin in AtT-20 cells. However, mutation of the RK sequence to RR allowed extensive cleavage regardless of the occurrence of O- or N-glycosylation. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,725 N WOLFE ST,BALTIMORE,MD 21205. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. FU NIDA NIH HHS [DA-00097]; NIDDK NIH HHS [DK-32948] NR 55 TC 24 Z9 24 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD MAR PY 1991 VL 5 IS 3 BP 404 EP 413 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FE674 UT WOS:A1991FE67400011 PM 1653894 ER PT J AU WOOD, SC FORMAN, SA MILLER, KW AF WOOD, SC FORMAN, SA MILLER, KW TI SHORT CHAIN AND LONG-CHAIN ALKANOLS HAVE DIFFERENT SITES OF ACTION ON NICOTINIC ACETYLCHOLINE-RECEPTOR CHANNELS FROM TORPEDO SO MOLECULAR PHARMACOLOGY LA English DT Article ID CULTURED MUSCLE-CELLS; AFFINITY BINDING-SITE; H-3 CHLORPROMAZINE; LOCAL-ANESTHETICS; NONCOMPETITIVE BLOCKERS; DELTA-SUBUNIT; ALPHA-SUBUNIT; CURRENTS; MEMBRANES; ALCOHOLS AB At nicotinic acetylcholine receptors, short chain n-alcohols (alkanols) have excitatory actions, whereas long chain alkanols inhibit channel activity. This study tests a previously proposed unitary hypothesis that suggests that these contrasting actions can be accounted for by interaction at just one hydrophobic site within the ion channel lumen. All alkanols bind to this site, but only long chain alkanols are large enough to completely block the channel. Short chain alkanols are too small to cause any channel occlusion, and in binding to the site they stabilize the open state of the receptor and enhance ion flux. In this study, we assay integrated agonist-stimulated ion efflux over 15 msec, as a measure of receptor activity. In nicotinic acetylcholine receptor-rich membrane vesicles from Torpedo, we show that, in contradiction to this elegant model, long chain and short chain alkanols appear to act at different sites. Firstly, ethanol and octanol do not complete for a single site on the receptor. Secondly, alkanol chain length dependencies for inhibition and for flux enhancement are significantly different. Thirdly, intermediate length alkanols do not partially inhibit channels, as required by the model; high concentrations of these alkanols completely inhibit the response. Fourthly, careful measurements, including determination of the free alkanol concentration, of inhibitory potencies of alkanols from propanol to decanol show no evidence for a steric contribution to the ability of an alkanol to inhibit the ion channel. Furthermore, our results suggest that the inhibitory effect of long chain alkanols may be mediated by a discrete site on nicotinic acetylcholine receptors, whereas there is no evidence that a protein site is involved in the excitatory mechanism of short chain alkanols. Indeed, it seems more likely that short chain alkanols may have a nonspecific site of action. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. UNIV OXFORD,DEPT BIOCHEM,OXFORD,ENGLAND. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIAAA NIH HHS [AA-07040]; NIGMS NIH HHS [GM15904] NR 30 TC 76 Z9 77 U1 0 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD MAR PY 1991 VL 39 IS 3 BP 332 EP 338 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FD156 UT WOS:A1991FD15600010 PM 1706469 ER PT J AU KOSKI, G LAWRENCE, K RIGHI, D AF KOSKI, G LAWRENCE, K RIGHI, D TI ETHANOL-INDUCED INHIBITION OF CARBACHOL-STIMULATED UPTAKE OF CALCIUM IN PC12 PHEOCHROMOCYTOMA CELLS SO NEUROPHARMACOLOGY LA English DT Article DE ALCOHOL; CALCIUM FLUX; NICOTINIC RECEPTOR; DESENSITIZATION; ION CHANNELS ID NICOTINIC ACETYLCHOLINE-RECEPTOR; PROTEIN KINASE-C; NEUROTRANSMITTER RELEASE; CHANNELS; LINE; SODIUM; DEPOLARIZATION; NEURONS AB Using a rapid-quench technique the effects of ethanol on the uptake of Ca-45(2+) into PC12 pheochromocytoma cells were studied in suspension. At concentrations achieved during acute intoxication in man (25-100 mM), ethanol inhibited both the carbachol-stimulated and K+-induced uptake of calcium. Inhibition of carbachol-stimulated uptake of Ca2+ occurred rapidly, within seconds at 27-degrees-C, whereas inhibition of K+-induced uptake of Ca2+ developed more slowly. This disparity between the kinetics of these ethanol-induced inhibitions was unexpected, because the uptake of Ca2+, evoked by either stimulus, is thought to occur predominantly through a common pathway, namely voltage-sensitive Ca2+ channels. This difference may reflect differential effects of ethanol on multiple carbachol-activated pathways for entry of Ca2+. Alternatively, carbachol may facilitate the inhibitory action of ethanol on voltage-dependent channels. This apparent facilitation was manifested principally by a more rapid onset of inhibition, although the extent of inhibition by ethanol, in the presence of carbachol, was also increased. In preincubation experiments, ethanol did not enhance the apparent agonist-induced desensitization of carbachol-evoked uptake of Ca2+. Nevertheless, an acute interaction between cholinergic agonists and ethanol, affecting homeostasis of Ca2+ may play a role in the pathophysiology of alcohol intoxication. RP KOSKI, G (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BIOCHEM PHARMACOL LAB,BOSTON,MA 02114, USA. FU NCRR NIH HHS [SO7RR05486-23]; NIAAA NIH HHS [AA07040-03] NR 26 TC 6 Z9 6 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0028-3908 J9 NEUROPHARMACOLOGY JI Neuropharmacology PD MAR PY 1991 VL 30 IS 3 BP 267 EP 274 DI 10.1016/0028-3908(91)90154-4 PG 8 WC Neurosciences; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA FC480 UT WOS:A1991FC48000008 PM 1852262 ER PT J AU NORTON, S KIMLER, BF MULLENIX, PJ AF NORTON, S KIMLER, BF MULLENIX, PJ TI PROGRESSIVE BEHAVIORAL-CHANGES IN RATS AFTER EXPOSURE TO LOW-LEVELS OF IONIZING-RADIATION INUTERO SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Article DE RADIATION; FETAL; INUTERO; RAT; BEHAVIOR; BRAIN; MORPHOMETRIC ANALYSIS; CORRELATION ID HYPERACTIVITY; MATURATION; CORTEX; ACTS AB The deleterious effects of ionizing radiation on the developing brain may be not only prolonged but progressive. Fetuses were exposed to 0.75 Gy of ionizing radiation on gestational day 15 through whole body exposure of the pregnant rat. Three behavioral tests (gait analysis, continuous corridor activity and photographic analysis of sequences of behavioral acts) were performed at 1 and 3 months, postnatally. Body weight and thickness of the cerebral cortex of irradiated rats were 10-15 percent below controls throughout the period of study. Behavior in all tests was more affected at 3 months than at 1 month of age. Gait of control rats, as measured by the angle of advance of hind feet, widened about 20 percent for males and 40 percent for females from 1 to 3 months, as expected, while, in irradiated rats, the angle widened only about 10 percent. Continuous corridor activity increased less than 10 percent in controls and about 35 percent in irradiated rats over the same period. In photographic analysis of behavior, controls increased their time spent standing by about 50 percent in males and 20 percent in females from 1 to 3 months of age. Irradiated males increased time standing only about 10 percent and irradiated females decreased about 30 percent over the same period. The data obtained in these experiments support other evidence that some behavioral alterations from perinatal exposure to radiation become more marked with maturation. C1 UNIV KANSAS,MED CTR,DEPT RADIAT ONCOL,RAINBOW BLVD & 39TH ST,KANSAS CITY,KS 66103. FORSYTH RES INST,BOSTON,MA 02115. FU NICHD NIH HHS [HD 21666]; NINDS NIH HHS [NS 16694] NR 27 TC 16 Z9 16 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0892-0362 J9 NEUROTOXICOL TERATOL JI Neurotoxicol. Teratol. PD MAR-APR PY 1991 VL 13 IS 2 BP 181 EP 188 DI 10.1016/0892-0362(91)90009-L PG 8 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA FD442 UT WOS:A1991FD44200009 PM 2046638 ER PT J AU BREAKEFIELD, XO DELUCA, NA AF BREAKEFIELD, XO DELUCA, NA TI HERPES-SIMPLEX VIRUS FOR GENE DELIVERY TO NEURONS SO NEW BIOLOGIST LA English DT Review ID CENTRAL-NERVOUS-SYSTEM; LATENCY-ASSOCIATED TRANSCRIPT; POLYMERASE CHAIN-REACTION; COLI BETA-GALACTOSIDASE; IMMEDIATE-EARLY GENES; RAT SENSORY NEURONS; LONG UNIQUE REGION; OVARY-APRT GENE; PSEUDORABIES VIRUS; DELETION MUTANTS C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MED GENET,NEUROSCI PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,TUMOR VIRUS GENET LAB,BOSTON,MA 02115. RP BREAKEFIELD, XO (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROGENET UNIT,BOSTON,MA 02129, USA. FU NIAID NIH HHS [AI24306]; NINDS NIH HHS [NS24279] NR 130 TC 134 Z9 134 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4674 J9 NEW BIOL PD MAR PY 1991 VL 3 IS 3 BP 203 EP 218 PG 16 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA GK718 UT WOS:A1991GK71800002 PM 1652278 ER PT J AU FISHMAN, JA STRAUSS, HW FISCHMAN, AJ NEDELMAN, M CALLAHAN, R KHAW, BA RUBIN, RH AF FISHMAN, JA STRAUSS, HW FISCHMAN, AJ NEDELMAN, M CALLAHAN, R KHAW, BA RUBIN, RH TI IMAGING OF PNEUMOCYSTIS-CARINII PNEUMONIA WITH IN-111 LABELED NONSPECIFIC POLYCLONAL IGG - AN EXPERIMENTAL-STUDY IN RATS SO NUCLEAR MEDICINE COMMUNICATIONS LA English DT Article AB The relative sensitivity of imaging with Ga-67-citrate (Ga-67) and non-specific human polyclonal IgG radiolabelled with In-111 (In-111-IgG) for the detection of Pneumocystis carinii pneumonia (PCP) was determined in rats. Pneumocystis carinii pneumonia was induced by low protein diet and dexamethasone. The course of the disease was monitored by serial imaging with In-111-IgG and Ga-67. Diffuse accumulation of both radiopharmaceuticals was observed in the lungs of infected animals (infection was verified by histological examination of the lungs), however, accumulation of In-111-IgG was consistently higher. In rats with early PCP, In-111-IgG imaging revealed pulmonary accumulation in animals with normal chest radiographs and Ga-67 scans. In animals successfully treated for PCP, decreased pulmonary accumulation of In-111-IgG coincided with histological improvements. Several animals developed superinfection with bacteria or fungi. These animals had striking focal accumulation of In-111-IgG, in addition to the pattern of generalized uptake. Gallium concentration in these animals did not show this focal accumulation. These observations suggest that In-111-IgG may be useful for detecting PCP and pulmonary abscesses in the immunocompromised host. RP FISHMAN, JA (reprint author), MASSACHUSETTS GEN HOSP,CHEM SERV,INFECT DIS UNIT,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [K08HL01916, R01-HL43510] NR 0 TC 12 Z9 12 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0143-3636 J9 NUCL MED COMMUN JI Nucl. Med. Commun. PD MAR PY 1991 VL 12 IS 3 BP 175 EP 187 DI 10.1097/00006231-199103000-00002 PG 13 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FB060 UT WOS:A1991FB06000002 PM 1857579 ER PT J AU LINDENBERG, OS ALEXANDER, EM GENDROP, SC NENCIOLI, M WILLIAMS, DG AF LINDENBERG, OS ALEXANDER, EM GENDROP, SC NENCIOLI, M WILLIAMS, DG TI A REVIEW OF THE LITERATURE ON COCAINE ABUSE IN PREGNANCY SO NURSING RESEARCH LA English DT Review ID MOTHERS; EXPOSURE; INFANTS; GROWTH; PREVALENCE; OUTCOMES; NEWBORN; HEALTH; RISK; CARE AB The primary research literature on cocaine abuse in pregnancy from 1982 to 1989 was reviewed. This article is a synthesis of current knowledge regarding the effects of maternal cocaine use during pregnancy on obstetrical, neonatal, and infant health and developmental outcomes. Consistencies and inconsistencies in the findings, a critique of key methodological issues, and suggestions for future research are provided. C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CHELSEA MEM HLTH CTR,PRENATAL PROGRAM,BOSTON,MA 02114. BOSTON CITY HOSP,HIGH RISK PRENATAL CLIN,BOSTON,MA 02118. BOSTON DEPT HLTH & HOSP,BOSTON,MA. RP LINDENBERG, OS (reprint author), UNIV MASSACHUSETTS,COLL NURSING,BOSTON,MA 02125, USA. NR 39 TC 28 Z9 29 U1 1 U2 1 PU AMER J NURSING CO PI NEW YORK PA 555 W 57TH ST, NEW YORK, NY 10019-2961 SN 0029-6562 J9 NURS RES JI Nurs. Res. PD MAR-APR PY 1991 VL 40 IS 2 BP 69 EP 75 PG 7 WC Nursing SC Nursing GA FD680 UT WOS:A1991FD68000002 ER PT J AU LAMMIE, GA FANTL, V SMITH, R SCHUURING, E BROOKES, S MICHALIDES, R DICKSON, C ARNOLD, A PETERS, G AF LAMMIE, GA FANTL, V SMITH, R SCHUURING, E BROOKES, S MICHALIDES, R DICKSON, C ARNOLD, A PETERS, G TI D11S287, A PUTATIVE ONCOGENE ON CHROMOSOME-11Q13, IS AMPLIFIED AND EXPRESSED IN SQUAMOUS-CELL AND MAMMARY CARCINOMAS AND LINKED TO BCL-1 SO ONCOGENE LA English DT Article ID HUMAN-BREAST-TUMORS; ENDOCRINE NEOPLASIA TYPE-1; FIBROBLAST GROWTH-FACTORS; PROTO-ONCOGENE; INT-2 GENE; PARATHYROID ADENOMA; MOLECULAR-CLONING; CO-AMPLIFICATION; MESSENGER-RNA; SARCOMA DNA AB Approximately 15 to 20% of primary breast cancers and an even higher proportion of squamous cell carcinomas of the head and neck show amplification of DNA markers on band q13 of human chromosome 11. However, known genes within the amplified region, such as the FGF-related oncogenes INT-2 and HST-1, are very rarely expressed in these tumors. Here we show that another candidate oncogene, designated D11S287, implicated in the pathogenesis of parathyroid adenomas, is also amplified in breast cancers. Significantly, it is consistently co-amplified with INT-2 and HST-1 in 36 out of 202 primary tumors, including one case in which the amplified unit did not encompass the translocation breakpoint marker BCL-1. This implies that D11S287 is on the same side of the breakpoint as INT-2, and pulsed-field gel electrophoresis indicates that D11S287 is less than 250 kb from the BCL-1 marker. Since D11S287 RNA was present at elevated levels in a group of tumors and cell lines in which the 11q13 region is amplified, it may be the key oncogene on this amplified unit, and could also be activated by BCL-1 translocations. C1 ST BARTHOLOMEWS HOSP,IMPERIAL CANC RES FUND LABS,DOMINION HOUSE,59 BARTHOLOMEW CLOSE,LONDON EC1A 7BE,ENGLAND. NETHERLANDS CANC INST,1066 CX AMSTERDAM,NETHERLANDS. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 52 TC 462 Z9 463 U1 1 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR PY 1991 VL 6 IS 3 BP 439 EP 444 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA FT344 UT WOS:A1991FT34400013 PM 2011398 ER PT J AU ROSENBERG, CL KIM, HG SHOWS, TB KRONENBERG, HM ARNOLD, A AF ROSENBERG, CL KIM, HG SHOWS, TB KRONENBERG, HM ARNOLD, A TI REARRANGEMENT AND OVEREXPRESSION OF D11S287E, A CANDIDATE ONCOGENE ON CHROMOSOME 11Q13 IN BENIGN PARATHYROID TUMORS SO ONCOGENE LA English DT Article ID ENDOCRINE NEOPLASIA TYPE-1; B-CELL LYMPHOMAS; HORMONE GENE; MOLECULAR-CLONING; DNA POLYMORPHISMS; PROTO-ONCOGENE; BREAST-CANCER; AMPLIFICATION; INT-2; ABNORMALITIES AB We report the detailed molecular characterization of a human parathyroid adenoma with a clonal parathyroid hormone gene rearrangement. This rearrangement is similar to one we characterized recently in an independent adenoma. In these two, plus a third partially characterized adenoma, one allele of the PTH gene, on 11p15, is rearranged with DNA from the D11S287 region on 11q13. This region contains a transcribed sequence, D11S287E, distinct from known 11q13 oncogenes, that is expressed in all parathyroid tissues examined, but is overexpressed dramatically in all three tumors with PTH gene-D11S287 rearrangements. These findings suggest that overexpression of D11S287E, perhaps driven by the misplaced PTH gene's regulatory elements, contributed to the development of these benign tumors. D11S287E is a new candidate oncogene with potential importance in parathyroid adenomas and perhaps other tumors with 11q13 abnormalities. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT HUMAN GENET,BUFFALO,NY 14263. FU NIDDK NIH HHS [DK07028, DK11794]; NIGMS NIH HHS [GM20454] NR 41 TC 231 Z9 231 U1 0 U2 3 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR PY 1991 VL 6 IS 3 BP 449 EP 453 PG 5 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA FT344 UT WOS:A1991FT34400015 PM 2011400 ER PT J AU BORODIC, GE COZZOLINO, D FERRANTE, R WIEGNER, AW YOUNG, RR AF BORODIC, GE COZZOLINO, D FERRANTE, R WIEGNER, AW YOUNG, RR TI INNERVATION ZONE OF ORBICULARIS OCULI MUSCLE AND IMPLICATIONS FOR BOTULINUM A TOXIN THERAPY SO OPHTHALMIC PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article DE BOTULINUM TOXIN; BLEPHAROSPASM; FACIAL NERVE; ORBICULARIS OCULI; INNERVATION ZONE AB Motor points (areas of maximal sensitivity to electrical stimulation) were found in constant locations over orbicularis oculi when measured in both eyes of six normal subjects. All subjects had a motor point at the lateral terminus of the upper lid crease and the medial extent of the lower lid crease. A study of the innervation zone [distribution of neuromuscular junctions (NMJ)] was conducted on strips of pretarsal and preseptal portions of the upper eyelid orbicularis that had been removed routinely during involutional ptosis surgery. There was no significant difference in NMJ concentration between the medial and lateral sections, as determined by cholinesterase staining. Therefore, we concluded that the innervation zone is diffuse for the orbicularis muscle within this portion of the upper eyelid. Single-point injections of botulinum toxin were then compared to the conventional multiple injections sites on separate eyes in 10 patients with benign essential blepharospasm. Eight of the 10 patients reported greater relief on the side given injections into multiple points; the other two patients experienced no difference between the two methods. Both histologic data and clinical observation of response to botulinum toxin injection suggest the innervation zone for the upper orbicularis is diffuse. Thus, we conclude that multiple injections are superior to the injection of a single motor point. RP BORODIC, GE (reprint author), MASSACHUSETTS GEN HOSP,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL & NEUROL,BOSTON,MA 02114, USA. NR 0 TC 37 Z9 37 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 MAR PY 1991 VL 7 IS 1 BP 54 EP 60 DI 10.1097/00002341-199103000-00007 PG 7 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA EY705 UT WOS:A1991EY70500007 PM 1708272 ER PT J AU GREINER, JV CHANES, LA GLONEK, T AF GREINER, JV CHANES, LA GLONEK, T TI COMPARISON OF PHOSPHATE METABOLITES OF THE OCULAR HUMORS SO OPHTHALMIC RESEARCH LA English DT Article DE AQUEOUS HUMOR; VITREOUS BODY; PHOSPHATIC METABOLITES; P-31; NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY ID NUCLEAR MAGNETIC-RESONANCE; CRYSTALLINE LENS; CORNEA AB Ocular humors (aqueous humor and vitreous body) were obtained from porcine eyes. Perchloric acid extracts were prepared from aqueous and vitreous aspirates, and phosphorus-31 nuclear magnetic resonance spectroscopy P-31-NMR performed. Resonance signals from four high-energy phosphate groups (phosphocreatine, adenosine tri- and diphosphate and the dinucleotides) and nine low-energy phosphate groups [dihydroxyacetone phosphate, hexose-6-phosphate, alpha-glycerophosphate, fructose-1,6-diphosphate, ethanolamine phosphate, choline phosphate, inorganic orthophosphate (Pi), glycerol-3-phosphorylethanolamine and glycerol-3-phosphorylcholine] were present in the aqueous humor and/or vitreous body. Vitreous body phosphates significantly elevated relative to that of the aqueous humor were: DHAP, Hex 6-P, alpha-GP, Fru 1,6-diP, CP, GPE, PCr, ATP, ADP, and the dinucleotides; only Pi was significantly lower. Six metabolic indices (monoesters, diesters, monoesters/diesters, monoesters/Pi, ATP/Pi, energy modulus) were determined; all vitreous body indices were significantly higher than those of the aqueous humor. In particular, the energy modulus, a measure of overall metabolic energy status, was higher in the vitreous body (0.121 +/- 0.047) than in the aqueous humor (0.05 +/- 0.021). C1 EYE RES INST,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,CORNEA SERV,BOSTON,MA 02114. CHICAGO COLL OSTEOPATH MED,MAGNET RESONANCE LAB,CHICAGO,IL 60615. RP GREINER, JV (reprint author), BETH ISRAEL HOSP,DIV OPHTHALMOL,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NEI NIH HHS [EY07063] NR 29 TC 12 Z9 12 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0030-3747 J9 OPHTHALMIC RES JI Ophthalmic Res. PD MAR-APR PY 1991 VL 23 IS 2 BP 92 EP 97 PG 6 WC Ophthalmology SC Ophthalmology GA FQ533 UT WOS:A1991FQ53300005 PM 1870846 ER PT J AU SEDDON, J GRAGOUDAS, E EGAN, K POLIVOGIANIS, L FINN, S ALBERT, D AF SEDDON, J GRAGOUDAS, E EGAN, K POLIVOGIANIS, L FINN, S ALBERT, D TI STANDARDIZED DATA-COLLECTION AND CODING IN EYE DISEASE EPIDEMIOLOGY - THE UVEAL MELANOMA DATA SYSTEM SO OPHTHALMIC SURGERY AND LASERS LA English DT Article ID PROTON-BEAM IRRADIATION; SURVIVAL FOLLOWING ENUCLEATION; PROGNOSTIC FACTOR; THERAPY AB The Uveal Melanoma Data System of the Massachusetts Eye and Ear Infirmary is a computerized database designed for data management and analysis with a broad range of clinical research applications. The system was created in 1980 and has evolved to include standardized data collection forms for all aspects of uveal melanoma patient care such as initial examination, treatment, and follow-up, as well as precoded forms for computer entry, which facilitate quality control measures and data analysis. Excerpts from current versions of these forms are presented. The Uveal Melanoma Data System has been used for a variety of clinical epidemiologic investigations. Examples of its application, including descriptive studies, prognostic factor studies, and treatment evaluations, are discussed. The model has potential broad application for clinical ophthalmic research in other specialty areas. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,OPHTHALM PATHOL LAB,BOSTON,MA 02114. RP SEDDON, J (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EPIDEMIOL UNIT,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 21 TC 8 Z9 8 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0022-023X J9 OPHTHALMIC SURG LAS JI Ophthalmic Surg. Lasers PD MAR PY 1991 VL 22 IS 3 BP 127 EP 136 PG 10 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA FC958 UT WOS:A1991FC95800001 PM 2030892 ER PT J AU GRAGOUDAS, ES EGAN, KM SEDDON, JM GLYNN, RJ WALSH, SM FINN, SM MUNZENRIDER, JE SPAR, MD AF GRAGOUDAS, ES EGAN, KM SEDDON, JM GLYNN, RJ WALSH, SM FINN, SM MUNZENRIDER, JE SPAR, MD TI SURVIVAL OF PATIENTS WITH METASTASES FROM UVEAL MELANOMA SO OPHTHALMOLOGY LA English DT Article ID CUTANEOUS MALIGNANT-MELANOMA; PROTON-BEAM IRRADIATION; LONG-TERM SURVIVALS; CHOROIDAL MELANOMA; SYSTEMIC CHEMOTHERAPY; COMPLETE RESPONSES; ADJUVANT THERAPY; OCULAR MELANOMA; LIVER; REGRESSION AB The authors evaluated a series of 145 consecutive patients with metastases from uveal melanoma, after proton beam irradiation, to assess the effect of early diagnosis and treatment for metastases on survival. Metastases were diagnosed between 7 weeks and 8.3 years (median, 2.4 years) after proton beam irradiation. Most patients (n = 94) were symptomatic before diagnosis; the remainder were first detected during screening examination. Liver involvement was documented in nearly all patients (n = 136). The majority of patients had died from metastases by the close of the study (n = 137). Significantly longer survival occurred among patients diagnosed during screening examination (P = 0.004) and among younger patients (P = 0.03). The majority of patients received some form of treatment for metastases (69%). Median survival was 2.0 months for patients receiving no treatment compared with 5.2 months for those receiving treatment for metastases (P = .0001). However, the overall 1-year survival rate was poor (13%). Prophylactic adjuvant therapy could be explored as a means to increase disease-free survival in patients with uveal melanoma. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA 02114. RP GRAGOUDAS, ES (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 36 TC 208 Z9 212 U1 2 U2 8 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD MAR PY 1991 VL 98 IS 3 BP 383 EP 390 PG 8 WC Ophthalmology SC Ophthalmology GA FA654 UT WOS:A1991FA65400025 PM 2023760 ER PT J AU KANE, MA KELLEY, K ROSS, SE PORTANOVA, LB AF KANE, MA KELLEY, K ROSS, SE PORTANOVA, LB TI ISOLATION OF A GASTRIN RELEASING PEPTIDE RECEPTOR FROM NORMAL RAT PANCREAS SO PEPTIDES LA English DT Article DE GASTRIN RELEASING PEPTIDE; BOMBESIN; RECEPTOR ID BOMBESIN-LIKE PEPTIDES; SWISS 3T3 CELLS; GASTROINTESTINAL-TRACT; CROSS-LINKING; IMMUNOREACTIVITY; BINDING; IDENTIFICATION; LOCALIZATION; MEMBRANES; GROWTH AB The presence of a putative GRP receptor on rat pancreatic particulate membranes was demonstrated by covalent cross-linking to I-125-gastrin releasing peptide (GRP), which revealed a radioactive band with M(r) = 80-90 kDa on reduced SDS-PAGE. Fresh rat pancreatic membranes contained a GRP receptor which was solubilized with Triton X-100 as assessed by its failure to sediment at 100,000 x g for one hour and its ability to pass through a 0.22-mu filter. When I-125-GRP binding was studied using Sephadex G50 gel filtration chromatography to separate bound from unbound ligand, substantial amounts of I-125-GRP binding were observed in rat crude solubilized pancreatic membranes, but essentially no specific binding was observed until the crude solubilized membranes were fractionated by ammonium sulfate precipitation. Specific I-125-GRP binding was 500, 700 and 1400 fmol/mg protein, respectively, in the 0-25%, 25-50% and 50-80% saturated ammonium sulfate fractions (I-125-I-GRP concentration = 1 nM). Specific binding was temperature dependent, saturable and of high affinity (K(D) = 2.3 nM). A unique 70 kDa band was visualized by silver staining of the SDS-PAGE of eluates of GRP(14-27) affinity gels compared with eluates of control affinity gels incubated with the 25-50% (NH4)2 SO4 fraction. The lower M(r) than that observed with covalent cross-linking may represent the binding subunit of a larger receptor protein. This ligand-affinity isolated protein is thus a good candidate for the GRP receptor, or the binding subunit of it, from normal rat pancreas. C1 UNIV COLORADO,CTR CANC,DENVER,CO 80220. RP KANE, MA (reprint author), UNIV COLORADO,HLTH SCI CTR,DENVER VET AFFAIRS MED CTR,MED ONCOL SECT,111F,1055 CLERMONT ST,DENVER,CO 80220, USA. FU PHS HHS [R29-44763] NR 35 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0196-9781 J9 PEPTIDES JI Peptides PD MAR-APR PY 1991 VL 12 IS 2 BP 207 EP 213 DI 10.1016/0196-9781(91)90001-6 PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA FE045 UT WOS:A1991FE04500001 PM 1648710 ER PT J AU WOLFF, MS MICHEL, TH KREBS, DE WATTS, NT AF WOLFF, MS MICHEL, TH KREBS, DE WATTS, NT TI CHRONIC PAIN - ASSESSMENT OF ORTHOPEDIC PHYSICAL-THERAPISTS KNOWLEDGE AND ATTITUDES SO PHYSICAL THERAPY LA English DT Article DE ATTITUDE OF HEALTH PERSONNEL; PAIN; TESTS AND MEASUREMENTS; GENERAL ID TERMINALLY ILL; MANAGEMENT; PATIENT AB Orthopedic physical therapists' knowledge of pain mechanisms and methods of pain management and their attitudes toward working with patients with benign chronic pain were studied. A random sample of 500 members' of the American Physical Therapy Association's Section on Orthopaedics received by mail a 36-item questionnaire. Statistical analysis of scores, using frequencies, means, and correlations, was performed on the 119 (23.8%) usable returns. All but 4% of the respondents preferred to work with patients who are not likely to have chronic pain. Seventy-two percent believed their entry-level education in pain management and theory was very inadequate or less than adequate to deal with an orthopedic patient population. Pain knowledge scores were low (35.8 out of 46 points), and the scores on positive attitudes toward treating patients with benign chronic pain were lower (20.5 out of 36 points). The study suggests specific deficiencies in orthopedic physical therapists' knowledge of clinical pain mechanisms and management and potentially undesirable attitudes toward treating patients with chronic pain. C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,ADV MATTER SCI PROGRAM PHYS THERAPY,BOSTON,MA 02108. NR 32 TC 10 Z9 10 U1 0 U2 2 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 MAR PY 1991 VL 71 IS 3 BP 207 EP 214 PG 8 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA FG200 UT WOS:A1991FG20000007 PM 2000436 ER PT J AU SHEEN, J AF SHEEN, J TI MOLECULAR MECHANISMS UNDERLYING THE DIFFERENTIAL EXPRESSION OF MAIZE PYRUVATE, ORTHOPHOSPHATE DIKINASE GENES SO PLANT CELL LA English DT Article ID ORTHO-PHOSPHATE DIKINASE; RIBULOSE-BISPHOSPHATE CARBOXYLASE; MESSENGER-RNAS; HIGHER-PLANTS; PHOSPHOENOLPYRUVATE CARBOXYLASE; TRANSIENT EXPRESSION; DNA-SEQUENCES; SMALL SUBUNIT; LEAVES; PROMOTER AB I describe here the organization of maize C4 chloroplast and non-C4 cytosolic pyruvate, orthophosphate dikinase (PPDK) genes and the molecular mechanisms underlying their differential expression. The maize C4 chloroplast PPDK gene (C4ppdkZm1) appears to have been created by the addition of an exon encoding the chloroplast transit peptide at a site upstream of a cytosolic PPDK gene (cyppdkZm1). A splice acceptor sequence located in the first exon of cyppdkZm1 allows the fusion of the transit peptide to the cyppdkZm1 sequences. A second cyPPDK gene (cyppdkZm2) shares extensive homology with cyppdkZm1 in the coding region and in the 5' flanking region up to the TATA box. By a novel protoplast transient expression method, I show that the light-inducible expression of C4ppdkZm1 is controlled by two expression programs mediated through separate upstream regulatory elements that are active in leaf, but inactive in root and stem. Light-mediated C4ppdkZm1 expression in maize is apparently uncoupled from leaf development and partially associated with chloroplast development. For cyppdkZm1 expression, distinct upstream elements and a specific TATA promoter element, located in the first intron of C4ppdkZm1, are required. The low expression of cyppdkZm2 can be attributed to an absence of upstream positive elements and weak activity of the TATA promoter element. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP SHEEN, J (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115, USA. NR 78 TC 143 Z9 153 U1 0 U2 13 PU AMER SOC PLANT PHYSIOLOGISTS PI ROCKVILLE PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 SN 1040-4651 J9 PLANT CELL JI Plant Cell PD MAR PY 1991 VL 3 IS 3 BP 225 EP 245 DI 10.1105/tpc.3.3.225 PG 21 WC Biochemistry & Molecular Biology; Plant Sciences; Cell Biology SC Biochemistry & Molecular Biology; Plant Sciences; Cell Biology GA FE131 UT WOS:A1991FE13100003 PM 1668653 ER PT J AU CANNON, B AF CANNON, B TI AN HISTORICAL NOTE ON ENDOTRACHEAL INTUBATION SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Letter RP CANNON, B (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,DIV PLAST SURG,BOSTON,MA 02114, USA. NR 2 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 MAR PY 1991 VL 87 IS 3 BP 583 EP 583 DI 10.1097/00006534-199103000-00048 PG 1 WC Surgery SC Surgery GA FA388 UT WOS:A1991FA38800036 PM 1998035 ER PT J AU MAY, JW AF MAY, JW TI SAUCERIZATION AND SKIN COVER FOR OSTEOMYELITIS - BACK TO SQUARE ONE - REPLY SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Letter ID LOWER-EXTREMITY RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,LEVEL 4,SUITE 453,BOSTON,MA 02114, USA. NR 2 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 MAR PY 1991 VL 87 IS 3 BP 590 EP 590 DI 10.1097/00006534-199103000-00063 PG 1 WC Surgery SC Surgery GA FA388 UT WOS:A1991FA38800051 ER PT J AU GIURINI, JM CHRZAN, JS GIBBONS, GW HABERSHAW, GM AF GIURINI, JM CHRZAN, JS GIBBONS, GW HABERSHAW, GM TI CHARCOTS DISEASE IN DIABETIC-PATIENTS - CORRECT DIAGNOSIS CAN PREVENT PROGRESSIVE DEFORMITY SO POSTGRADUATE MEDICINE LA English DT Article ID NEUROPATHIC FOOT; ARTHROPATHY; MELLITUS AB Patients are usually quick to report an orthopedic problem because of the pain and disability it causes. That is what is so misleading about Charcot's disease. Pain is often absent, and the earliest signs of bone and joint destruction are unexplained swelling, warmth, and redness. In diabetic patients, Charcot's joint disease must be promptly ruled out or treated. Continued use of the affected foot can be very destructive. The authors summarize the approach that they find most useful at their diabetic referral clinic. C1 NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. JOSLIN DIABETES CTR,BOSTON,MA. RP GIURINI, JM (reprint author), HARVARD UNIV,SCH MED,DEPT SURG,DIV PODIATRY,185 PILGRIM RD,BOSTON,MA 02115, USA. NR 14 TC 23 Z9 24 U1 0 U2 0 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 0032-5481 J9 POSTGRAD MED JI Postgrad. Med. PD MAR PY 1991 VL 89 IS 4 BP 163 EP 169 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA FB285 UT WOS:A1991FB28500020 PM 2000350 ER PT J AU HALLAHAN, DE SUKHATME, VP SHERMAN, ML VIRUDACHALAM, S KUFE, D WEICHSELBAUM, RR AF HALLAHAN, DE SUKHATME, VP SHERMAN, ML VIRUDACHALAM, S KUFE, D WEICHSELBAUM, RR TI PROTEIN-KINASE-C MEDIATES X-RAY INDUCIBILITY OF NUCLEAR SIGNAL TRANSDUCERS EGR1 AND JUN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE PROTEIN KINASE INHIBITORS; IMMEDIATE EARLY GENES; RADIATION INJURY ID SERUM GROWTH-FACTORS; G0/G1 TRANSITION; CULTURED-CELLS; DNA DAMAGE; GENE; FOS; ENCODES; PROTOONCOGENE; RADIOTHERAPY; ACTIVATION AB The cellular response to ionizing radiation includes growth arrest and DNA repair followed by proliferation. Induction of immediate early response genes may participate in signal transduction preceding these phenotypic responses. We analyzed mRNA expression for different classes of immediate early genes (JUN, EGR1, and FOS) after cellular x-irradiation. Increased expression of the EGR1 and JUN genes was observed within 0.5-3 hr following x-ray exposure. Preincubation with cycloheximide was associated with superinduction of JUN and EGR1 in x-irradiated cells. Inhibition of protein kinase C activity by prolonged stimulation with phorbol 12-myristate 13-acetate or the protein kinase inhibitor H7 prior to irradiation attenuated the increase in EGR1 and JUN transcripts. FOS expression was not coregulated with that of EGR1 following x-irradiation, suggesting a distinct regulatory pathway of this gene as compared with its regulation following serum and phorbol ester. These data implicate the EGR1 and JUN proteins as signal transducers during the cellular response to radiation injury and suggest that this effect is mediated in part by a protein kinase C-dependent pathway. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. UNIV CHICAGO,PRITZKER SCH MED,HOWARD HUGHES MED INST,DEPT MOLEC & CELLULAR BIOL,CHICAGO,IL 60637. UNIV CHICAGO,PRITZKER SCH MED,HOWARD HUGHES MED INST,DEPT MED,CHICAGO,IL 60637. RP HALLAHAN, DE (reprint author), UNIV CHICAGO,PRITZKER SCH MED,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637, USA. FU NCI NIH HHS [CA41068-04] NR 46 TC 274 Z9 276 U1 1 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 MAR PY 1991 VL 88 IS 6 BP 2156 EP 2160 DI 10.1073/pnas.88.6.2156 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FC216 UT WOS:A1991FC21600026 PM 1900938 ER PT J AU PANTAZIS, P KHARBANDA, S GOUSTIN, AS GALANOPOULOS, T KUFE, D AF PANTAZIS, P KHARBANDA, S GOUSTIN, AS GALANOPOULOS, T KUFE, D TI COEXPRESSION OF THE GENES FOR PLATELET-DERIVED GROWTH FACTOR-B-CHAIN RECEPTOR AND MACROPHAGE COLONY-STIMULATING FACTOR-I RECEPTOR DURING MONOCYTIC DIFFERENTIATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE RNA BLOT HYBRIDIZATION; IMMUNOPRECIPITATION; GEL ELECTROPHORESIS; IMMUNOFLUORESCENCE ID PROMYELOCYTIC LEUKEMIA-CELLS; SIS-TRANSFORMED-CELLS; FMS PROTO-ONCOGENE; C-FMS; PHORBOL DIESTER; FACTOR-I; EXPRESSION; CSF-1; PURIFICATION; HOMODIMER AB Receptors for platelet-derived growth factor (PDGF) have not been identified previously to our knowledge in human myeloid cells that also produce PDGF. Here we report that phorbol ester-treated myeloid cells differentiated along the monocytic lineage express both a full-length 5.5-kilobase (kb) mRNA and a predominant, truncated 4.6-kb mRNA coding for the PDGF B-chain receptor (PDGF-BR). PDGF-BR was identified in phorbol ester-differentiated myeloid cells by indirect immunofluorescence with an antibody specific to PDGF-BR. This anti-PDGF-BR was also used in immunoprecipitation studies to demonstrate that lysates of phorbol ester-differentiated myeloid cells contain PDGF-BR molecules of 37 kDa to 130 kDa. The results also show that the tandemly linked genes for PDGF-BR and the macrophage colony-stimulating factor 1 receptor are coexpressed in the phorbol ester-differentiated myeloid cells. Expression of these two receptor genes has not been shown previously in any cell type to our knowledge. C1 CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. WAYNE STATE UNIV,CTR MOLEC BIOL,DETROIT,MI 48201. RP PANTAZIS, P (reprint author), ST JOSEPH HOSP,CANC RES LAB,STEHLIN FDN CANC RES,1918 CHENEVERT,HOUSTON,TX 77003, USA. FU NCI NIH HHS [CA34183] NR 36 TC 19 Z9 19 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR PY 1991 VL 88 IS 6 BP 2481 EP 2485 DI 10.1073/pnas.88.6.2481 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FC216 UT WOS:A1991FC21600094 PM 1848705 ER PT J AU BLOCH, KJ NG, BP BISHARA, SM BLOCH, M AF BLOCH, KJ NG, BP BISHARA, SM BLOCH, M TI INHIBITION OF IMMUNE COMPLEX-INDUCED ENTEROPATHY BY 3 DIFFERENT PLATELET-ACTIVATING-FACTOR RECEPTOR ANTAGONISTS SO PROSTAGLANDINS LA English DT Article ID PAF-ACETHER; EFFECTOR SUBSTANCE; BOWEL NECROSIS; GUINEA-PIG; SRI 63-675; RAT; RELEASE; NEUTROPHILS; RESPONSES; ENDOTOXIN AB We previously showed that intravenous injection of rat anti-BSA-BSA complexes (IC) prepared in 5x antigen excess rapidly induced a striate pattern of serosal (to mucosal) hemorrhage and vascular congestion throughout the small intestine of the Sprague-Dawley rat. In this study, we tested the effect of three different platelet-activating factor (PAF) receptor antagonists on the development of lesions. L-652, 731, a synthetic derivative of kadsurenone (at doses of 1.3-2.7 mg/kg), SRI 63-675, a substituted quinolinium compound (6.7-15 mg/kg), and WEB 2086, a thienotriazolodiazepine (5-25 mg/kg) were each capable of completely or partially inhibiting IC-induced enteropathy in the majority of animals tested. Pretreatment with WEB 2086 prevented IC-induced hemoconcentration but not neutropenia. The antagonists did not lower the level of blood complement nor interfere with the fall in complement induced by administration of IC. The ability of PAF receptor antagonists to completely or partially inhibit IC-induced small intestinal lesions suggests that endogenous PAF is a major mediator of IC-induced enteropathy. C1 MASSACHUSETTS GEN HOSP,GEN MED SERV,CLIN IMMUNOL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN MED SERV,ALLERGY UNIT,BOSTON,MA 02114. RP BLOCH, KJ (reprint author), HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115, USA. FU NIADDK NIH HHS [AM 33506] NR 29 TC 3 Z9 3 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0090-6980 J9 PROSTAGLANDINS JI Prostaglandins PD MAR PY 1991 VL 41 IS 3 BP 237 EP 249 DI 10.1016/0090-6980(91)90044-G PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FA970 UT WOS:A1991FA97000005 PM 1649481 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R AF SILVA, JA LEONG, GB WEINSTOCK, R TI MISIDENTIFICATION SYNDROME AND MALE PSEUDOCYESIS SO PSYCHOSOMATICS LA English DT Article ID PERSPECTIVE; SELF C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. RP SILVA, JA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,PSYCHIAT SERV,B116A WARD 206A,LOS ANGELES,CA 90073, USA. NR 23 TC 12 Z9 12 U1 1 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD SPR PY 1991 VL 32 IS 2 BP 228 EP 230 PG 3 WC Psychiatry; Psychology SC Psychiatry; Psychology GA FE052 UT WOS:A1991FE05200016 PM 2027947 ER PT J AU KLESMER, J AF KLESMER, J TI CONCISE GUIDE TO GERIATRIC PSYCHIATRY - SPAR,JE, LARUE,A SO PSYCHOSOMATICS LA English DT Book Review RP KLESMER, J (reprint author), MASSACHUSETTS GEN HOSP,CONSULTAT PSYCHOSOMAT PSYCHIAT,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 SPR PY 1991 VL 32 IS 2 BP 234 EP 235 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA FE052 UT WOS:A1991FE05200018 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI SEROTONIN IN MAJOR PSYCHIATRIC-DISORDERS - COCCARO,EF, MURPHY,DL SO PSYCHOSOMATICS LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP GREENBERG, DB (reprint author), HARVARD UNIV,SCH MED,PSYCHIAT,BOSTON,MA 02115, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD SPR PY 1991 VL 32 IS 2 BP 235 EP 235 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA FE052 UT WOS:A1991FE05200019 ER PT J AU GERWECK, LE FELLENZ, MP AF GERWECK, LE FELLENZ, MP TI THE SIMULTANEOUS DETERMINATION OF INTRACELLULAR PH AND CELL ENERGY STATUS SO RADIATION RESEARCH LA English DT Article ID CREATINE-PHOSPHOKINASE EQUILIBRIUM; EXTRACELLULAR PH; HYPERTHERMIC SENSITIVITY; FREE MG2+; MISONIDAZOLE; ANALOGS; SINGLE; MUSCLE; BRAIN RP GERWECK, LE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,EDWIN L STEELE LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-22860] NR 26 TC 7 Z9 7 U1 0 U2 1 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD MAR PY 1991 VL 125 IS 3 BP 257 EP 261 DI 10.2307/3578107 PG 5 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA FB507 UT WOS:A1991FB50700004 PM 2000448 ER PT J AU GREENE, R AF GREENE, R TI WILLIAMS,FRANCIS,H. - FATHER OF CHEST RADIOLOGY IN NORTH-AMERICA SO RADIOGRAPHICS LA English DT Article DE RADIOLOGY AND RADIOLOGISTS; HISTORY RP GREENE, R (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 9 TC 0 Z9 0 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 MAR PY 1991 VL 11 IS 2 BP 325 EP 332 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC036 UT WOS:A1991FC03600011 PM 2028067 ER PT J AU BRINK, JA FERRUCCI, JT AF BRINK, JA FERRUCCI, JT TI USE OF CT FOR PREDICTING GALLSTONE COMPOSITION - A DISSENTING VIEW SO RADIOLOGY LA English DT Article DE COMPUTED TOMOGRAPHY (CT), TISSUE CHARACTERIZATION; GALLBLADDER, CALCULI; OPINION ID INVITRO; CHOLESTEROL C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. NR 9 TC 8 Z9 8 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 MAR PY 1991 VL 178 IS 3 BP 633 EP 634 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EY097 UT WOS:A1991EY09700008 PM 1994392 ER PT J AU SCHAEFER, CM GREENE, R LLEWELLYN, HJ MROSE, HE PILESPELLMAN, EA RUBENS, JR LINDEMANN, SR AF SCHAEFER, CM GREENE, R LLEWELLYN, HJ MROSE, HE PILESPELLMAN, EA RUBENS, JR LINDEMANN, SR TI INTERSTITIAL LUNG-DISEASE - IMPACT OF POSTPROCESSING IN DIGITAL STORAGE PHOSPHOR IMAGING SO RADIOLOGY LA English DT Article DE DIAGNOSTIC RADIOLOGY, OBSERVER PERFORMANCE; LUNG, DISEASES; LUNG, RADIOGRAPHY; RADIOGRAPHY, DIGITAL; RECEIVER OPERATING CHARACTERISTIC CURVE (ROC) ID SPATIAL-RESOLUTION REQUIREMENTS; OBSERVER PERFORMANCE; CHEST RADIOGRAPHY; ROC ANALYSIS; DETECTABILITY; IMAGES AB The ability to resolve the fine linear structures of interstitial lung disease is one measure of the limiting performance characteristics of an imaging system. Conventional screen-film radiography was compared with six algorithms of isodose storage phosphor digital radiography (0.2-mm x 10-bit pixel matrix) in the detection of interstitial lung abnormality documented by means of computed tomography in 40 patients with abnormalities and 25 healthy control subjects. Performance was evaluated with an analysis of variance (the Fisher paired comparison test; P < .05) of the average receiver operating characteristic area of 2,730 observations by six readers. The moderately and the more markedly high-frequency edge-enhanced algorithms of storage phosphor digital radiographs were equivalent in performance to screen-film radiography. The default mode, low- and medium-frequency edge-enhanced algorithms, and gray scale reversed mode of storage phosphor digital radiography were inferior to screen-film radiography. The authors conclude that high-frequency edge-enhanced algorithms can perform as well as screen-film radiography in the detection of interstitial disease. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 24 TC 48 Z9 48 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 MAR PY 1991 VL 178 IS 3 BP 733 EP 738 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EY097 UT WOS:A1991EY09700027 PM 1994410 ER PT J AU REIMER, P WEISSLEDER, R LEE, AS BUETTNER, S WITTENBERG, J BRADY, TJ AF REIMER, P WEISSLEDER, R LEE, AS BUETTNER, S WITTENBERG, J BRADY, TJ TI ASIALOGLYCOPROTEIN RECEPTOR FUNCTION IN BENIGN LIVER-DISEASE - EVALUATION WITH MR IMAGING SO RADIOLOGY LA English DT Article DE HEPATITIS; IRON; LIVER, CIRRHOSIS; LIVER, DISEASES; LIVER, FATTY; LIVER, MR STUDIES; MAGNETIC RESONANCE (MR), CONTRAST ENHANCEMENT; SPLEEN, MR STUDIES ID SUPERPARAMAGNETIC IRON-OXIDE; HEPATIC BINDING-PROTEIN; DESIALYLATED GLYCOPROTEINS; CLEARANCE; FIBROSIS AB An arabinogalactan-coated ultra-small superparamagnetic iron oxide (AG-USPIO) preparation specific for asialoglycoprotein (ASG) receptors on hepatocytes was used as a magnetic resonance (MR) imaging contrast agent in the evaluation of a spectrum of benign liver diseases in animal models. The activity of hepatocyte ASG receptors, which directly reflects liver function, was directly assessed by measuring liver relaxation times in vitro and MR signal intensity in vivo. The following measurements allowed three-dimensional assessment of liver function: (a) liver relaxation time, (b) native MR signal intensities of liver, (c) response of liver to the AG-USPIO probe (percentage decrease of liver signal intensity after intravenous administration of 10-mu-mol/kg of AG-USPIO: normal liver 55%, fatty liver 57%, acute hepatitis 36%, chronic hepatitis 29%, and cirrhosis 46%), and (d) redistribution of hepatocyte-specific AG-USPIO to the spleen (present in hepatitis and cirrhosis but not in normal liver and fatty liver). The results of this study indicate that cellular hepatic abnormalities can be detected and quantitated with MR receptor imaging. C1 MASSACHUSETTS GEN HOSP,MGH NMR CTR,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [P01, CA 48279] NR 40 TC 58 Z9 59 U1 2 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 MAR PY 1991 VL 178 IS 3 BP 769 EP 774 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EY097 UT WOS:A1991EY09700034 PM 1994416 ER PT J AU FISHER, DM LITT, L COTE, CJ AF FISHER, DM LITT, L COTE, CJ TI USE OF OXIMETRY DURING MR IMAGING OF PEDIATRIC-PATIENTS SO RADIOLOGY LA English DT Letter C1 UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT RADIOL,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. RP FISHER, DM (reprint author), UNIV CALIF SAN FRANCISCO,DEPT ANESTHESIA,SAN FRANCISCO,CA 94143, USA. NR 2 TC 2 Z9 2 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 MAR PY 1991 VL 178 IS 3 BP 891 EP 892 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EY097 UT WOS:A1991EY09700068 PM 1994444 ER PT J AU GREENE, R ANDERSON, DJ GEFTER, WB LEVITT, RG MCLOUD, T OESTMANN, J SCHAEFER, C SPIRN, PW STARK, P AF GREENE, R ANDERSON, DJ GEFTER, WB LEVITT, RG MCLOUD, T OESTMANN, J SCHAEFER, C SPIRN, PW STARK, P TI THORACIC RADIOLOGY SO RADIOLOGY LA English DT Editorial Material DE COMPUTED TOMOGRAPHY (CT), HIGH-RESOLUTION; RADIOGRAPHY, DIGITAL; RADIOGRAPHY, TECHNOLOGY; RADIOLOGICAL-SOCIETY-OF-NORTH-AMERICA, 76TH SCIENTIFIC ASSEMBLY AND ANNUAL MEET; THORAX, CT; THORAX, MR STUDIES C1 WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. HOSP UNIV PENN,PHILADELPHIA,PA 19104. LOMA LINDA UNIV,MED CTR,LOMA LINDA,CA 92350. THOMAS JEFFERSON UNIV,PHILADELPHIA,PA 19107. HANOVER MED SCH,W-3000 HANNOVER 61,GERMANY. ALTON MEM HOSP,ALTON,IL. RP GREENE, R (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 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 MAR PY 1991 VL 178 IS 3 BP 916 EP 918 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EY097 UT WOS:A1991EY09700078 PM 1994453 ER PT J AU HUNTER, DW CASTANEDA, F CRAGG, AH DARCY, MD HU, XP LONGLEY, DG MARTIN, LG MATALON, T STEINBERG, F STILLMAN, A THORPE, P VOGELZANG, RL YUCEL, EK AF HUNTER, DW CASTANEDA, F CRAGG, AH DARCY, MD HU, XP LONGLEY, DG MARTIN, LG MATALON, T STEINBERG, F STILLMAN, A THORPE, P VOGELZANG, RL YUCEL, EK TI CARDIOVASCULAR INTERVENTIONAL RADIOLOGY SO RADIOLOGY LA English DT Editorial Material DE ARTERIES, GRAFTS AND PROSTHESES; ARTERIES, LASER ANGIOPLASTY; ARTERIES, US STUDIES; FILTERS; RADIOLOGICAL-SOCIETY-OF-NORTH-AMERICA, 76TH SCIENTIFIC ASSEMBLY AND ANNUAL MEET C1 UNIV IOWA HOSP & CLIN,IOWA CITY,IA 52242. EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. EMORY UNIV,ATLANTA,GA 30322. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. CREIGHTON UNIV,MED CTR,OMAHA,NE 68178. NW MEM HOSP,CHICAGO,IL 60611. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP HUNTER, DW (reprint author), UNIV MINNESOTA HOSP & CLIN,MINNEAPOLIS,MN 55455, USA. NR 0 TC 0 Z9 0 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 MAR PY 1991 VL 178 IS 3 BP 918 EP 920 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EY097 UT WOS:A1991EY09700079 PM 1994454 ER PT J AU NIEMIERKO, A GOITEIN, M AF NIEMIERKO, A GOITEIN, M TI CALCULATION OF NORMAL TISSUE COMPLICATION PROBABILITY AND DOSE-VOLUME HISTOGRAM REDUCTION SCHEMES FOR TISSUES WITH A CRITICAL ELEMENT ARCHITECTURE SO RADIOTHERAPY AND ONCOLOGY LA English DT Article DE NORMAL TISSUE COMPLICATION PROBABILITY; COMPLICATION PROBABILITY; BIOPHYSICAL MODELS; DOSE-VOLUME HISTOGRAM; TISSUE ARCHITECTURE; CRITICAL ELEMENT ID RADIATION-THERAPY; OPTIMIZATION; MODEL AB We investigate a model of normal tissue complication probability for tissues that may be represented by a critical element architecture. We derive formulas for complication probability that apply to both a partial volume irradiation and to an arbitrary inhomogeneous dose distribution. The dose-volume isoeffect relationship which is a consequence of a critical element architecture is discussed and compared to the empirical power law relationship. A dose-volume histogram reduction scheme for a "pure" critical element model is derived. In addition, a point-based algorithm which does not require precomputation of a dose-volume histogram is derived. The existing published dose-volume histogram reduction algorithms are analyzed. We show that the existing algorithms, developed empirically without an explicit biophysical model, have a close relationship to the critical element model at low levels of complication probability. However, we also show that they have aspects which are not compatible with a critical element model and we propose a modification to one of them to circumvent its restriction to low complication probabilities. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP NIEMIERKO, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,DIV RADIAT BIOPHYS,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 21239, CA 50628] NR 26 TC 164 Z9 165 U1 2 U2 4 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0167-8140 J9 RADIOTHER ONCOL JI Radiother. Oncol. PD MAR PY 1991 VL 20 IS 3 BP 166 EP 176 DI 10.1016/0167-8140(91)90093-V PG 11 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FG741 UT WOS:A1991FG74100004 PM 1852908 ER PT J AU FREEDMAN, AS NADLER, LM AF FREEDMAN, AS NADLER, LM TI CELLULAR INTERACTIONS WITHIN THE GERMINAL CENTER SO RESEARCH IN IMMUNOLOGY LA English DT Editorial Material ID FOLLICULAR DENDRITIC CELLS; CENTER B-CELLS; LYMPH-NODES; T-CELLS; RETICULUM CELLS; ACTIVATION PATHWAY; ANTIGENIC PROFILE; LYMPHOCYTES-T; ADHESION; FIBRONECTIN C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP FREEDMAN, AS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [5K08 CA01105, CA40216] NR 58 TC 7 Z9 7 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 MAR-APR PY 1991 VL 142 IS 3 BP 232 EP 236 DI 10.1016/0923-2494(91)90065-Q PG 5 WC Immunology SC Immunology GA FU745 UT WOS:A1991FU74500008 PM 1896611 ER PT J AU KVEDAR, JC BADEN, HP AF KVEDAR, JC BADEN, HP TI NAIL CHANGES IN CUTANEOUS DISEASE SO SEMINARS IN DERMATOLOGY LA English DT Article RP KVEDAR, JC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WARREN 5,32 FRUIT ST,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [K08 AR01804-02, AR06838] NR 0 TC 7 Z9 7 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0278-145X J9 SEMIN DERMATOL JI Semin. Dermatol. PD MAR PY 1991 VL 10 IS 1 BP 65 EP 70 PG 6 WC Dermatology SC Dermatology GA FA722 UT WOS:A1991FA72200012 PM 2018721 ER PT J AU LEE, MJ SAINI, S BRINK, JA GIRARD, M MUELLER, PR AF LEE, MJ SAINI, S BRINK, JA GIRARD, M MUELLER, PR TI INTERVENTIONAL RADIOLOGY OF THE PLEURAL SPACE - DIAGNOSTIC THORACENTESIS, THERAPEUTIC THORACENTESIS, PLEURAL BIOPSY, AND PLEURAL SCLEROSIS SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Article C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 0 TC 7 Z9 7 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 MAR PY 1991 VL 8 IS 1 BP 23 EP 28 DI 10.1055/s-2008-1074623 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC456 UT WOS:A1991FC45600004 ER PT J AU LEE, MJ SAINI, S BRINK, JA MORRISON, MC GOLDBERG, M MUELLER, PR AF LEE, MJ SAINI, S BRINK, JA MORRISON, MC GOLDBERG, M MUELLER, PR TI INTERVENTIONAL RADIOLOGY OF THE PLEURAL SPACE - MANAGEMENT OF THORACIC EMPYEMA WITH IMAGE-GUIDED CATHETER DRAINAGE SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Article C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 0 TC 7 Z9 7 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 MAR PY 1991 VL 8 IS 1 BP 29 EP 35 DI 10.1055/s-2008-1074624 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC456 UT WOS:A1991FC45600005 ER PT J AU MATHISEN, DJ AF MATHISEN, DJ TI A SURGEONS VIEW OF INTERVENTIONAL RADIOLOGY IN GENERAL THORACIC-SURGERY PATIENTS SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Article C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 0 TC 7 Z9 7 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 MAR PY 1991 VL 8 IS 1 BP 85 EP 87 DI 10.1055/s-2008-1074631 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC456 UT WOS:A1991FC45600012 ER PT J AU DUKER, JS BLUMENKRANZ, MS AF DUKER, JS BLUMENKRANZ, MS TI DIAGNOSIS AND MANAGEMENT OF THE ACUTE RETINAL NECROSIS (ARN) SYNDROME SO SURVEY OF OPHTHALMOLOGY LA English DT Review DE ACUTE RETINAL NECROSIS; ARN; BARN; BILATERAL ACUTE RETINAL NECROSIS; CYTOMEGALOVIRUS RETINITIS; HERPES SIMPLEX VIRUS; RETINAL DETACHMENT; VARICELLA ZOSTER VIRUS; UVEITIS; VITRITIS ID HERPES-ZOSTER OPHTHALMICUS; CYTOMEGALO-VIRUS RETINITIS; MULTIFOCAL CHOROIDITIS; INTRAVENOUS ACYCLOVIR; SIMPLEX RETINITIS; UVEITIS; DETACHMENT; ENCEPHALITIS; ADULT; NEOVASCULARIZATION AB The acute retinal necrosis (ARN) syndrome represents a specific pattern of clinical presentation for certain herpes virus infections in the posterior segment of the eye. The classically described triad of the ARN syndrome consists of (1) an arteritis and phlebitis of the retinal and choroidal vasculature, (2) a confluent, necrotizing retinitis that preferentially affects the peripheral retina, and (3) a moderate to severe vitritis. Anterior segment inflammation, optic neuritis, and late retinal detachment are also common features of this disorder. Definitive evidence now implicates at least two members of the herpes virus family; varicella zoster virus and herpes simplex virus as causative agents. This paper summarizes the clinical presentation, as well as the currently recommended treatment regimen for the ARN syndrome, highlighting recent advances that have resulted in a significant improvement in the visual prognosis for affected patients. C1 WILLIAM BEAUMONT HOSP,ROYAL OAK,MI 48072. RP DUKER, JS (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,EYE RES INST,BOSTON,MA 02115, USA. NR 86 TC 124 Z9 133 U1 0 U2 0 PU SURVEY OPHTHALMOLOGY INC PI BROOKLINE PA 7 KENT ST SUITE 4, BROOKLINE, MA 02146 SN 0039-6257 J9 SURV OPHTHALMOL JI Surv. Ophthalmol. PD MAR-APR PY 1991 VL 35 IS 5 BP 327 EP 343 DI 10.1016/0039-6257(91)90183-G PG 17 WC Ophthalmology SC Ophthalmology GA FE198 UT WOS:A1991FE19800001 PM 2038718 ER PT J AU LEW, MA KEHOE, K RITZ, J ANTMAN, KH NADLER, L TAKVORIAN, T MAYER, R KALISH, L FINBERG, R AF LEW, MA KEHOE, K RITZ, J ANTMAN, KH NADLER, L TAKVORIAN, T MAYER, R KALISH, L FINBERG, R TI PROPHYLAXIS OF BACTERIAL-INFECTIONS WITH CIPROFLOXACIN IN PATIENTS UNDERGOING BONE-MARROW TRANSPLANTATION SO TRANSPLANTATION LA English DT Article ID ACUTE NONLYMPHOCYTIC LEUKEMIA; PLACEBO-CONTROLLED TRIAL; GRAM-NEGATIVE SEPSIS; TRIMETHOPRIM-SULFAMETHOXAZOLE; GRANULOCYTOPENIC PATIENTS; CO-TRIMOXAZOLE; DOUBLE-BLIND; ANTIBIOTIC-PROPHYLAXIS; LYMPHOBLASTIC-LEUKEMIA; NEUTROPENIC PATIENTS AB Twenty-six oncology patients, 25 of whom received bone marrow transplants, were enrolled in a prospective, randomized, double-blinded, placebo-controlled trial assessing the efficacy of ciprofloxacin, 750 mg p.o. b.i.d., for preventing bacterial infections during prolonged neutropenia. Treatment was begun within 48 hr of initiation of chemotherapy and continued until the absolute granulocyte count recovered to greater-than-or-equal-to 500/mu-l, or until the onset of fever (greater-than-or-equal-to 38.3-degrees-C). Seven evaluable subjects received ciprofloxacin, and 11 received placebo. Risk factors for infection were comparable in both groups. Fever occurred in all study subjects, but onset was delayed in ciprofloxacin recipients (median = 6 days after the fall of the absolute granulocyte count to less-than-or-equal-to 500/mu-l vs. 3 days for placebo recipients, P = 0.01). No clinically or microbiologically documented infections occurred in ciprofloxacin recipients vs. 10 infections in placebo recipients (5 bacteremias, 4 skin/soft tissue infections, 1 urinary tract infection, P = 0.0003). Ciprofloxacin recipients required fewer days of therapeutic antimicrobials (median: 28 antibiotic-days vs. 49, P0.02). The bioavailability of ciprofloxacin appeared comparable to that found in previously published studies of normal volunteers and patients not receiving chemotherapy. Adverse effects and colonization by ciprofloxacin-resistant microorganisms were monitored, but the sample sizes were too small to permit meaningful conclusions about these safety parameters. Ciprofloxacin appears to be effective for preventing bacterial infections in neutropenic patients. Additional trials are needed to establish the optimal dose of ciprofloxacin and to compare its safety and efficacy with those of currently used prophylactic regimens. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. RI Finberg, Robert/E-3323-2010; Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA-34183]; NIAID NIH HHS [N01-AI-62531] NR 52 TC 66 Z9 68 U1 0 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR PY 1991 VL 51 IS 3 BP 630 EP 636 DI 10.1097/00007890-199103000-00017 PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA FC649 UT WOS:A1991FC64900017 PM 2006519 ER PT J AU AAGAARD, J MADSEN, PO AF AAGAARD, J MADSEN, PO TI BACTERIAL PROSTATITIS - NEW METHODS OF TREATMENT SO UROLOGY LA English DT Article ID FLUID; PH AB Four different clinical categories of prostatitis are recognized at present: acute bacterial prostatitis, chronic bacterial prostatitis, nonbacterial prostatitis, and prostatodynia. Treatment results of chronic bacterial prostatitis have, in the past, been rather poor. In addition to local factors (e.g., prostatic calculi), the poor results may well be due, in part, to lack of penetration of the various drugs used into the prostatic tissue and fluid, mostly because of unfavorable lipid solubility, degree of ionization, protein binding, and unfavorable pH gradients from the plasma to prostatic fluid. All of these factors determine the diffusion of a drug into prostatic tissue and fluid. The minimum inhibitory concentrations (MIC) of the various drugs used and the concentration of the drugs actually obtained in the prostate, combined with the influence of pH, inoculum size, and effect of prostatic fluid and prostatic extract on MIC, are important factors in determining at least the theoretical efficacy of various drugs in the treatment of chronic bacterial prostatitis. The new fluoroquinolones have excellent penetration into both animal and human prostates and very low MIC for the infecting organisms and should, from a theoretical standpoint, be ideal in the treatment of chronic bacterial prostatitis. Few clinical studies have been done, and only prospective, randomized clinical trials will determine the relative efficacy of the various quinolones in the treatment of chronic bacterial prostatitis. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT SURG,MADISON,WI 53706. NR 12 TC 8 Z9 8 U1 0 U2 1 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD MAR PY 1991 VL 37 IS 3 SU S BP 4 EP 8 DI 10.1016/0090-4295(91)80088-O PG 5 WC Urology & Nephrology SC Urology & Nephrology GA FC424 UT WOS:A1991FC42400002 PM 2003343 ER PT J AU SHOCKLEY, TR LIN, KE NAGY, JA TOMPKINS, RG DVORAK, HF YARMUSH, ML AF SHOCKLEY, TR LIN, KE NAGY, JA TOMPKINS, RG DVORAK, HF YARMUSH, ML TI PENETRATION OF TUMOR-TISSUE BY ANTIBODIES AND OTHER IMMUNOPROTEINS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID MONOCLONAL-ANTIBODY; COLON-CARCINOMA; CELLS; LOCALIZATION; CANCER; PROTEINS; GROWTH C1 RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,POB 909,PISCATAWAY,NJ 08854. RUTGERS STATE UNIV,CTR ADV BIOTECHNOL & MED,PISCATAWAY,NJ 08854. MIT,DEPT CHEM ENGN,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT PATHOL,BOSTON,MA 02215. NR 35 TC 40 Z9 41 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 FEB 28 PY 1991 VL 618 BP 367 EP 382 DI 10.1111/j.1749-6632.1991.tb27257.x PG 16 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FQ403 UT WOS:A1991FQ40300026 PM 2006796 ER PT J AU FRIEDBERG, JS TOMPKINS, RG RAKESTRAW, SL WARREN, SW FISCHMAN, AJ YARMUSH, ML AF FRIEDBERG, JS TOMPKINS, RG RAKESTRAW, SL WARREN, SW FISCHMAN, AJ YARMUSH, ML TI ANTIBODY-TARGETED PHOTOLYSIS - BACTERIOCIDAL EFFECTS OF SN (IV) CHLORIN E6- DEXTRAN-MONOCLONAL ANTIBODY CONJUGATES SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID CYTO-TOXIC AGENTS; HEMATOPORPHYRIN; CELLS; PHTHALOCYANINE; INFECTION; INVITRO; PHOTOSENSITIZATION; DETERMINANTS; THERAPY C1 RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,POB 909,PISCATAWAY,NJ 08854. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. SHRINERS BURN INST,BOSTON,MA 02114. RUTGERS STATE UNIV,CTR ADV BIOTECHNOL & MED,PISCATAWAY,NJ 08854. NR 32 TC 30 Z9 30 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 FEB 28 PY 1991 VL 618 BP 383 EP 393 DI 10.1111/j.1749-6632.1991.tb27258.x PG 11 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FQ403 UT WOS:A1991FQ40300027 PM 1706578 ER PT J AU LYNCH, DC AF LYNCH, DC TI THE FINE-STRUCTURE OF VONWILLEBRAND-FACTOR MULTIMERS AND TYPE-IIA VONWILLEBRAND DISEASE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID HUMAN-ENDOTHELIAL CELLS; FACTOR VWF CDNA; ANTIHEMOPHILIC FACTOR; SUBUNIT COMPOSITION; BIOSYNTHESIS; ANTIGEN; PROTEIN; POLYPEPTIDE; EXPRESSION; SECRETION RP LYNCH, DC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL31311] NR 22 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 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD FEB 28 PY 1991 VL 614 BP 138 EP 152 DI 10.1111/j.1749-6632.1991.tb43699.x PG 15 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FW076 UT WOS:A1991FW07600013 PM 2024881 ER PT J AU COLLER, BS SCUDDER, LE BEER, J GOLD, HK FOLTS, JD CAVAGNARO, J JORDAN, R WAGNER, C IULIUCCI, J KNIGHT, D GHRAYEB, J SMITH, C WEISMAN, HF BERGER, H AF COLLER, BS SCUDDER, LE BEER, J GOLD, HK FOLTS, JD CAVAGNARO, J JORDAN, R WAGNER, C IULIUCCI, J KNIGHT, D GHRAYEB, J SMITH, C WEISMAN, HF BERGER, H TI MONOCLONAL-ANTIBODIES TO PLATELET GLYCOPROTEIN IIB/IIIA AS ANTITHROMBOTIC AGENTS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; UNSTABLE ANGINA-PECTORIS; CANINE CORONARY-ARTERIES; IIB-IIIA COMPLEX; THROMBASTHENIC PLATELETS; PLASMINOGEN-ACTIVATOR; VITRONECTIN RECEPTOR; THROMBUS FORMATION; GLANZMANNS THROMBASTHENIA; FIBRINOGEN INTERACTION C1 MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02111. UNIV WISCONSIN,DEPT MED,DIV CARDIOL,MADISON,WI 53742. HAZELTON LABS AMER INC,DEPT TOXICOL,VIENNA,VA 22180. CENTOCOR INC,MALVERN,PA 19355. RP COLLER, BS (reprint author), SUNY STONY BROOK,DEPT MED,DIV HEMATOL,STONY BROOK,NY 11794, USA. FU PHS HHS [29586, 19278, 26215] NR 74 TC 141 Z9 143 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD FEB 28 PY 1991 VL 614 BP 193 EP 213 DI 10.1111/j.1749-6632.1991.tb43703.x PG 21 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FW076 UT WOS:A1991FW07600017 PM 2024884 ER PT J AU PUTLITZ, JZ DATTA, S MADISON, LD MACCHIA, E JAMESON, JL AF PUTLITZ, JZ DATTA, S MADISON, LD MACCHIA, E JAMESON, JL TI HUMAN THYROID HORMONE-BETA-1 RECEPTOR PRODUCED BY RECOMBINANT BACULOVIRUS-INFECTED INSECT CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID EXPRESSION C1 MASSACHUSETTS GEN HOSP,THYROID UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. INST ENDOCRINOL,PISA,ITALY. OI Jameson, James/0000-0001-9538-4059 NR 12 TC 5 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD FEB 28 PY 1991 VL 175 IS 1 BP 285 EP 290 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EZ636 UT WOS:A1991EZ63600042 ER PT J AU MILLER, JB AF MILLER, JB TI ORDER, ORDER SO NATURE LA English DT Letter RP MILLER, JB (reprint author), MASSACHUSETTS GEN HOSP,CTR NEUROSCI,BOSTON,MA 02129, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 28 PY 1991 VL 349 IS 6312 BP 734 EP 734 DI 10.1038/349734c0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EZ666 UT WOS:A1991EZ66600020 ER PT J AU JACOBY, GA ARCHER, GL AF JACOBY, GA ARCHER, GL TI MECHANISMS OF DISEASE - NEW MECHANISMS OF BACTERIAL-RESISTANCE TO ANTIMICROBIAL AGENTS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID PENICILLIN-BINDING PROTEIN; GRAM-NEGATIVE BACILLI; PLASMID-DETERMINED RESISTANCE; SPECTRUM BETA-LACTAMASES; OUTER-MEMBRANE PROTEINS; STAPHYLOCOCCUS-AUREUS; ESCHERICHIA-COLI; PSEUDOMONAS-AERUGINOSA; AMINOGLYCOSIDE RESISTANCE; METHICILLIN RESISTANCE C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DIV INFECT DIS,RICHMOND,VA 23298. RP JACOBY, GA (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114, USA. FU NIAID NIH HHS [AI-20415, AI-21772] NR 182 TC 218 Z9 239 U1 9 U2 12 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 FEB 28 PY 1991 VL 324 IS 9 BP 601 EP 612 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA EY886 UT WOS:A1991EY88600006 PM 1992321 ER PT J AU KAPLAN, LM GRAEMECOOK, F FERRUCCI, JT SCULLY, RE PACK, MA MADSEN, JC AF KAPLAN, LM GRAEMECOOK, F FERRUCCI, JT SCULLY, RE PACK, MA MADSEN, JC TI A 61-YEAR-OLD CAMBODIAN WOMAN WITH RECURRENT BOUTS OF ABDOMINAL-PAIN AND FEVER - MESENTERIC VENOUS THROMBOSIS - INFARCTION OF ILEUM - FATTY CHANGE OF LIVER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID SOUTHEAST ASIAN REFUGEES; ANTITHROMBIN-III DEFICIENCY; INFLAMMATORY BOWEL-DISEASE; VEIN-THROMBOSIS; INTESTINAL TUBERCULOSIS; CLINICAL-FEATURES; PROTEIN-C; ISCHEMIA; DIAGNOSIS; INFECTION C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KAPLAN, LM (reprint author), MASSACHUSETTS GEN HOSP,MED,BOSTON,MA 02114, USA. NR 87 TC 3 Z9 3 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 28 PY 1991 VL 324 IS 9 BP 613 EP 623 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA EY886 UT WOS:A1991EY88600007 ER PT J AU FEHMANN, HC HABENER, JF AF FEHMANN, HC HABENER, JF TI FUNCTIONAL RECEPTORS FOR THE INSULINOTROPIC HORMONE GLUCAGONLIKE PEPTIDE-I(7-37) ON A SOMATOSTATIN SECRETING CELL-LINE SO FEBS LETTERS LA English DT Article DE GLUCAGONLIKE PEPTIDE-I(7-37); RECEPTOR; SOMATOSTATIN-SECRETING CELL; PANCREATIC ISLET ID PERFUSED RAT PANCREAS; GENE-EXPRESSION; RELEASE; PEPTIDE; GLUCOSE; AMIDE; SEQUENCE; ISLETS AB Glucagon-like peptide-I (7-37) [(GLP-I(7-37)] is an intestinal peptide hormone that has potent insulinotropic activities in vivo in response to oral nutrients, in the isolated perfused pancreas, and in vitro in cultured B cells. GLP-I(7-37) receptor binding and GLP-I(7-37)-induced cAMP generation and hormone secretion was studied using cell lines producing insulin/B cell (beta-TC-1), glucagon/A cell (INR1G9) and somatostatin/D cell (RIN 1027-B2). [I-125]GLP-I(7-37) bound specifically to both B and D cells but not to A cells. GLP-I(7-37) induced cAMP-formation in B and D cells with a maximum response at 10 nmol/l (B cells) or at 100 nmol/l (D cells). Insulin secretion from perifused B cells was stimulated by GLP-I(7-37) (maximum at 10 nmol/l) and 10 nmol/l GLP-I(7-37) released somatostatin from perifused D cells. GLP-I(7-37) did not influence cAMP or glucagon secretion from A cells. These data indicate that pancreatic B and D cells, but not the A cells are influenced directly by GLP-I(7-37) via binding to specific receptors. Our findings support a model of physiologic regulation of insulin secretion whereby GLP-I(7-37) released from the intestine in response to oral nutrients potently stimulates insulin secretion via an endocrine mechanism that in turn may be dampened by a feed-back suppression by the release of somatostatin. In addition, suppression of the secretion of glucagon, a hormone whose actions are counter-regulatory to those of insulin, may occur by paracrine mechanisms involving GLP-I(7-37)-mediated stimulation of both insulin and somatostatin secretion. C1 HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. RP FEHMANN, HC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC ENDOCRINOL LAB,50 BLOSSOM ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK 30457, DK 30834] NR 30 TC 82 Z9 85 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD FEB 25 PY 1991 VL 279 IS 2 BP 335 EP 340 DI 10.1016/0014-5793(91)80182-3 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FA591 UT WOS:A1991FA59100042 PM 1672112 ER PT J AU SELLAR, GC DEBEER, MC LELIAS, JM SNYDER, PW GLICKMAN, LT FELSBURG, PJ WHITEHEAD, AS AF SELLAR, GC DEBEER, MC LELIAS, JM SNYDER, PW GLICKMAN, LT FELSBURG, PJ WHITEHEAD, AS TI DOG SERUM AMYLOID-A PROTEIN - IDENTIFICATION OF MULTIPLE ISOFORMS DEFINED BY CDNA AND PROTEIN ANALYSES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HIGH-DENSITY LIPOPROTEIN; MESSENGER-RNA; GENE-EXPRESSION; SAA; SEQUENCE; MOUSE; INDUCTION; DNA; HYBRIDIZATION; POLYARTERITIS AB Five distinct serum amyloid A (SAA) cDNA clones have been isolated from a library constructed using hepatic mRNA isolated from an individual beagle dog with canine pain syndrome. This implies the existence of at least three SAA genes in the dog genome. One clone predicts a truncated "amyloid A-like" SAA molecule and offers a possible alternative mechanism for the pathogenesis of secondary amyloidosis. Relative to the human and mouse SAA proteins, an additional peptide of eight amino acids is specified by each of the dog cDNA clones. The existence of this peptide in all acute phase dog SAA proteins was confirmed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate of acute phase high density lipoprotein and provides supporting evidence for gene conversion as a mechanism for maintaining the homogeneity of the SAA gene family within a species. Analysis of hepatic RNA following induction of an acute phase response shows a dramatic increase in SAA mRNA concentration; the SAA transcripts show a transient increase in size early in inflammation due to an increase in polyadenylation. C1 CHILDRENS HOSP MED CTR,CTR BLOOD RES,DIV IMMUNOL,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. UNIV KENTUCKY,MED CTR,DIV RHEUMATOL,LEXINGTON,KY 40536. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT HEMATOL & ONCOL,BOSTON,MA 02215. PURDUE UNIV,SCH VET MED,DEPT PATHOBIOL,W LAFAYETTE,IN 47907. NR 46 TC 31 Z9 32 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 FEB 25 PY 1991 VL 266 IS 6 BP 3505 EP 3510 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200028 PM 1995613 ER PT J AU LIM, SK GARDELLA, T THOMPSON, A ROSENBERG, J KEUTMANN, H POTTS, J KRONENBERG, H NUSSBAUM, S AF LIM, SK GARDELLA, T THOMPSON, A ROSENBERG, J KEUTMANN, H POTTS, J KRONENBERG, H NUSSBAUM, S TI FULL-LENGTH CHICKEN PARATHYROID-HORMONE - BIOSYNTHESIS IN ESCHERICHIA-COLI AND ANALYSIS OF BIOLOGIC ACTIVITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TERMINAL 1-34 FRAGMENT; ADRENOCORTICAL-CELLS; STIMULATION; PEPTIDE AB Chicken parathyroid hormone (cPTH) has been reported to stimulate adrenal steroidogenesis and to have unusual potency on traditional PTH target tissues. To evaluate these properties, chicken PTH-(1-88) has been expressed in Escherichia coli using a plasmid encoding a fusion protein which links together growth hormone, a factor Xa recognition site, and chicken PTH-(1-88). The growth hormone-cPTH fusion protein required the presence of 0.02% sodium dodecyl sulfate to remain in solution and be cleaved by factor Xa. The high performance liquid chromatography-purified recombinant cPTH-(1-88) and chemically synthesized cPTH-(1-34) had similar potency in rat osteosarcoma (ROS 17/2.8) cells, opossum kidney (OK) cells, and dispersed primary chicken kidney cells. The biologic potencies of cPTH-(1-34) and cPTH-(1-88) in radioreceptor binding and cAMP generation in both bone- and kidney-derived cell lines were less than those of human (h)PTH-(1-34). In dispersed chicken kidney cells, cAMP production by cPTH-(1-34) and cPTH-(1-88) was similar to that stimulated by human PTH-(1-34). No stimulation of steroidogenesis could be detected when recombinant chicken PTH-(1-88) was added to dispersed chicken adrenal cells. The biologic activity of recombinant chicken PTH-(1-88) purified from E. coli was comparable with that of chicken PTH-(1-88) expressed by mammalian COS cells. Thus, the full-length chicken PTH did not exhibit enhanced potency, when compared with human PTH in ROS 17/2.8, OK cell lines, and dispersed chicken kidney cells and did not demonstrate the novel steroidogenic action previously reported in adrenal cells. The successful production of chicken PTH-(1-88) will enhance our understanding of the structure-activity relationships for PTH, particularly the sequence-dependent metabolism of the hormone. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LIM, SK (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114, USA. NR 19 TC 8 Z9 8 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 FEB 25 PY 1991 VL 266 IS 6 BP 3709 EP 3714 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200056 PM 1847386 ER PT J AU SELLMAYER, A UEDELHOVEN, WM WEBER, PC BONVENTRE, JV AF SELLMAYER, A UEDELHOVEN, WM WEBER, PC BONVENTRE, JV TI ENDOGENOUS NONCYCLOOXYGENASE METABOLITES OF ARACHIDONIC-ACID MODULATE GROWTH AND MESSENGER-RNA LEVELS OF IMMEDIATE-EARLY RESPONSE GENES IN RAT MESANGIAL CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID C-FOS EXPRESSION; PROTEIN KINASE-C; LIPOXYGENASE METABOLITES; NA+/H+ EXCHANGE; PHORBOL ESTER; DNA-SYNTHESIS; INHIBITION; PROLIFERATION; LEUKOTRIENES; STIMULATION AB The role of endogenous arachidonic acid and its metabolites as mediators of cell growth was studied in rat mesangial cells. Inhibitors of the cytochrome P450 monooxygenase and lipoxygenase systems (nordihydroguaiaretic acid (NDGA), SK&F 525A, and ketoconazole) significantly reduced serum-stimulated cell growth as determined by cell counts and incorporation of [H-3] thymidine. Inhibition of cyclooxygenase or lipoxygenases alone had no effect on cell growth. Stimulation with arginine vasopressin, epidermal growth factor, or phorbol myristate acetate increased [H-3]thymidine incorporation and mRNA levels of the immediate-early response genes c-fas and Egr-1. These increases in [H-3]thymidine incorporation and mRNA levels were reduced by NDGA and ketoconazole. NDGA, SK&F 525A, and ketoconazole had no effect on cellular ATP levels. Indomethacin had no effect upon cell growth. 14,15-Epoxyeicosatrienoic acid potentiated the effect of arginine vasopressin to enhance [H-3]thymidine incorporation. Reverse-phase high pressure liquid chromatography analysis of lipid extracts from cells prelabeled with [H-3]arachidonic acid resulted in the detection of a radioactive peak which eluted with lipoxygenase and monooxygenase products, with the same retention time as vicinal dihydroxyeicosatrienoic acids. This peak increased after stimulation with arginine vasopressin or epidermal growth factor and was reduced by preincubation with NDGA. Furthermore, analysis of unlabeled cell extracts by gas chromatography-mass spectrometry revealed the presence of a compound with epoxyeicosatrienoic acid-like characteristics. These results indicate that mesangial cells in culture likely produce products of the cytochrome P450 monooxygenase system that are important endogenous mediators of the growth response to mitogenic agents. C1 MASSACHUSETTS GEN HOSP,MED SERV,ARTHRITIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. UNIV MUNICH,KREISLAUFKRANKHEITEN,INST PROPHYLAXE & EPIDEMIOL,W-8000 MUNICH,GERMANY. FU NIDDK NIH HHS [DK 38165, DK 38452, DK 39773] NR 51 TC 143 Z9 144 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 FEB 25 PY 1991 VL 266 IS 6 BP 3800 EP 3807 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200069 PM 1899867 ER PT J AU FINK, JS VERHAVE, M WALTON, K MANDEL, G GOODMAN, RH AF FINK, JS VERHAVE, M WALTON, K MANDEL, G GOODMAN, RH TI CYCLIC AMP-INDUCED AND PHORBOL ESTER-INDUCED TRANSCRIPTIONAL ACTIVATION ARE MEDIATED BY THE SAME ENHANCER ELEMENT IN THE HUMAN VASOACTIVE-INTESTINAL-PEPTIDE GENE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-KINASE-C; SIGNAL-TRANSDUCTION PATHWAYS; DNA-BINDING PROTEIN; TRANS-ACTING FACTOR; NUCLEAR FACTOR CREB; FACTOR AP-1; METALLOTHIONEIN GENE; SOMATOSTATIN GENE; ADENYLATE-CYCLASE; CATALYTIC SUBUNIT AB Transcription of the human vasoactive intestinal peptide (VIP) gene is regulated by both cyclic AMP and phorbol esters. A 17-nucleotide enhancer element within the human VIP gene mediates transcriptional activation by both phorbol esters and forskolin. Mutations of this element decrease responses to both agents, suggesting that the trans-acting proteins that mediate both modes of transcriptional regulation have similar DNA-binding characteristics. The response of the VIP enhancer element to forskolin, but not to 12-O-tetradecanoylphorbol-13-acetate, was attenuated by treatment with a recombinant inhibitor of the cAMP-dependent protein kinase, suggesting that the cAMP-dependent protein kinase and protein kinase C second messenger pathways that converge on this single enhancer element are distinct. The transcriptional activator cAMP-responsive element-binding (CREB) proteins and the c-fos.c-Jun complex interact with the VIP enhancer. The dual second messenger responses of the VIP gene may result from the interaction of this second messenger enhancer with different transcriptional activator proteins. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. OREGON HLTH SCI UNIV,VOLLUM INST ADV BIOMED RES,PORTLAND,OR 97201. NEW ENGLAND MED CTR HOSP,DIV PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02111. SUNY STONY BROOK,DEPT NEUROBIOL & BEHAV,STONY BROOK,NY 11794. RP FINK, JS (reprint author), HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA37370]; NINDS NIH HHS [KO7 NS00885, R01 NS27514] NR 49 TC 70 Z9 70 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 FEB 25 PY 1991 VL 266 IS 6 BP 3882 EP 3887 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200080 PM 1847391 ER PT J AU KLEYMAN, TR KRAEHENBUHL, JP ERNST, SA AF KLEYMAN, TR KRAEHENBUHL, JP ERNST, SA TI CHARACTERIZATION AND CELLULAR-LOCALIZATION OF THE EPITHELIAL NA+ CHANNEL - STUDIES USING AN ANTI-NA+ CHANNEL ANTIBODY RAISED BY AN ANTIIDIOTYPIC ROUTE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MEDULLARY COLLECTING DUCT; TOAD URINARY-BLADDER; SODIUM-CHANNEL; MONOCLONAL-ANTIBODIES; BASOLATERAL MEMBRANE; AMILORIDE ANTIBODIES; APICAL MEMBRANE; KIDNEY-CELLS; RECEPTOR; TRANSPORT AB Amiloride-sensitive Na+ channels are expressed at the apical membrane of high resistance, Na+-transporting epithelial. The specific interaction of amiloride with this transport protein suggested the feasibility of raising anti-Na+ channel antibodies by an antiidiotypic approach designed to generate antibodies directed against the amiloride-binding domain on the channel. Antiidiotypic monoclonal antibody RA6.3 mimicked the effect of amiloride by inhibiting Na+ transport across A6 cell monolayers when applied to the apical cell surface. Inhibition of transport required pretreatment of the apical cell surface with trypsin in the presence of amiloride in order to enhance accessibility of the antibody to the amiloride-binding site. This antibody specifically immunoprecipitated a large 750,000-700,000 Da protein from [S-35]methionine-labeled A6 cell cultures, which was resolved further under reducing conditions as a set of polypeptides with apparent molecular masses of 260,000-230,000, 180,000, 140,000-110,000, and 70,000 Da. The antibody recognized the 140,000-Da subunit, known to contain the amiloride-binding domain, on immunoblots of purified A6 cell Na+ channel. Immunoprecipitation of apical or basolateral plasma membrane proteins selectively labeled with I-125 demonstrated that expression of the oligomeric Na+ channel was restricted to the apical plasma membrane. Immunocytochemical localization in A6 cultures revealed apical membrane as well as cytosolic immunoreactive sites. Immunostaining was also observed at or near the basolateral plasma membrane. C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. SWISS INST EXPTL CANC RES,CH-1066 EPALINGES,SWITZERLAND. UNIV MICHIGAN,DEPT ANAT & CELL BIOL,ANN ARBOR,MI 48109. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. UNIV LAUSANNE,DEPT BIOCHEM,CH-1000 LAUSANNE 17,SWITZERLAND. RP KLEYMAN, TR (reprint author), UNIV PENN,DEPT MED,RENAL SECT,700 CLIN RES BLDG,PHILADELPHIA,PA 19104, USA. FU NCRR NIH HHS [RR05385]; NIDDK NIH HHS [DK27559] NR 43 TC 57 Z9 57 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 25 PY 1991 VL 266 IS 6 BP 3907 EP 3915 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY682 UT WOS:A1991EY68200084 PM 1847393 ER PT J AU TSUCHIYA, T NAKAYAMA, Y OZAWA, T AF TSUCHIYA, T NAKAYAMA, Y OZAWA, T TI RESPONSE OF ADRENAL SYMPATHETIC EFFERENT NERVE ACTIVITY TO MECHANICAL AND THERMAL STIMULATIONS OF THE FACIAL SKIN AREA IN ANESTHETIZED RATS SO NEUROSCIENCE LETTERS LA English DT Article DE ADRENAL MEDULLA; AUTONOMIC NERVOUS SYSTEM; SYMPATHETIC EFFERENT NERVE ACTIVITY; REFLEX; MECHANICAL STIMULATION OF FACIAL SKIN; THERMAL STIMULATION OF FACIAL SKIN; TRIGEMINAL NERVE; RAT ID MEDULLARY FUNCTIONS; REFLEX CHANGES AB The effect of mechanical and thermal stimulations to the forehead or cheek innervated by the trigeminal nerve on adrenal sympathetic efferent nerve activity was studied in alpha-chloralose-urethane anesthetized rats. Innoxious mechanical stimulations to the forehead or cheek caused a reflex decrease of nerve activity, while noxious mechanical stimulations to the forehead or cheek caused a reflex increase in activity. Thermal stimulation of the forehead and bilateral cheeks at below 15-degrees-C or above 45-degrees-C increased activity though it failed to do so between 20 and 40-degrees-C. These excitatory responses lasted only as long as the period of the stimulations. These results suggest that excitatory reflex responses mediated by supraspinal circuit to adrenal nerve activity are not, characteristically, of an enduring nature. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. RP TSUCHIYA, T (reprint author), TOKYO METROPOLITAN GERIATR HOSP & INST GERONTOL,DEPT AUTONOM NERVOUS SYST,35-2 SAKAECHO,TOKYO 173,JAPAN. NR 8 TC 6 Z9 6 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 FEB 25 PY 1991 VL 123 IS 2 BP 240 EP 243 DI 10.1016/0304-3940(91)90940-U PG 4 WC Neurosciences SC Neurosciences & Neurology GA FC479 UT WOS:A1991FC47900026 PM 2027537 ER PT J AU KWIATKOWSKI, DJ AF KWIATKOWSKI, DJ TI DINUCLEOTIDE REPEAT POLYMORPHISM AT THE ABL LOCUS (9Q34) SO NUCLEIC ACIDS RESEARCH LA English DT Note RP KWIATKOWSKI, DJ (reprint author), MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BLDG 149,13TH ST,8 W,BOSTON,MA 02129, USA. NR 2 TC 28 Z9 28 U1 0 U2 4 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD FEB 25 PY 1991 VL 19 IS 4 BP 967 EP 967 DI 10.1093/nar/19.4.967 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900060 PM 2017388 ER PT J AU KWIATKOWSKI, DJ PERMAN, S AF KWIATKOWSKI, DJ PERMAN, S TI DINUCLEOTIDE REPEAT POLYMORPHISM AT THE GSN LOCUS (9Q32-34) SO NUCLEIC ACIDS RESEARCH LA English DT Note RP KWIATKOWSKI, DJ (reprint author), MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BLDG 149,13TH ST,8 W,BOSTON,MA 02129, USA. NR 2 TC 28 Z9 28 U1 0 U2 4 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD FEB 25 PY 1991 VL 19 IS 4 BP 967 EP 967 DI 10.1093/nar/19.4.967 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA089 UT WOS:A1991FA08900059 PM 2017388 ER PT J AU KROLEWSKI, AS WARRAM, JH VALSANIA, P MARTIN, BC LAFFEL, LMB CHRISTLIEB, AR AF KROLEWSKI, AS WARRAM, JH VALSANIA, P MARTIN, BC LAFFEL, LMB CHRISTLIEB, AR TI EVOLVING NATURAL-HISTORY OF CORONARY-ARTERY DISEASE IN DIABETES-MELLITUS SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID HEART-DISEASE; MYOCARDIAL-INFARCTION; BLOOD-PRESSURE; CARDIOVASCULAR-DISEASE; INSULIN RESISTANCE; PARENTAL HISTORY; RISK-FACTORS; HYPERTENSION; GLUCOSE; POPULATION AB White diabetic patients are at high risk of developing coronary artery disease (CAD). The natural history of CAD in insulin-dependent (ID) and noninsulin-dependent (NID) diabetes mellitus (DM) is reviewed to gain insight into the mechanisms responsible for the development of premature or accelerated atherosclerosis in diabetic patients. In both IDDM and NIDDM, the risk of CAD increases with lengthening duration of diabetes; the risk, however, does not grow as a constant multiple of the nondiabetic risk of CAD, suggesting that the cumulative exposure to diabetes plays a significant role as a risk factor for CAD only in a subset of patients. This is consistent with the hypothesis that the diabetic milieu has an impact on the progression of atherosclerotic lesions but not on their initiation. This hypothesis is corroborated further by the observation that CAD does not occur in diabetic patients in populations with a low risk of CAD among nondiabetic patients. The component of the diabetic milieu responsible for promotion of atherosclerotic lesions is unknown. There is evidence, however, of a direct or indirect role of hyperinsulinemia in this process. C1 NEW ENGLAND DEACONESS HOSP,JOSLIN DIABET CTR,DIV CLIN,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KROLEWSKI, AS (reprint author), NEW ENGLAND DEACONESS HOSP,JOSLIN DIABET CTR,DIV RES,EPIDEMIOL & GENET SECT,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK41526] NR 40 TC 47 Z9 49 U1 0 U2 0 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 FEB 21 PY 1991 VL 90 SU 2A BP S56 EP S61 DI 10.1016/0002-9343(91)90040-5 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA EZ476 UT WOS:A1991EZ47600015 PM 1994719 ER PT J AU RAND, LI AF RAND, LI TI DIABETIC-RETINOPATHY - CAN WE MODIFY ITS COURSE SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID RISK; PROGRESSION; DIAGNOSIS; GLUCOSE; CELLS; LESS; AGE AB With the exception of panretinal laser photocoagulation, no therapy has been shown to modify the course of diabetic retinopathy. Success in developing new therapies for diabetic retinopathy will depend on how well the disease process is understood and on whether interventions can be identified that ameliorate or circumvent critical stages in the development of the disease. A model of the disease process is presented to serve as a frame-work on which pieces of the puzzle can be placed and new areas of potential interventional therapy can be conceptualized. RP RAND, LI (reprint author), JOSLIN DIABETES CTR, BEETHAM EYE INST, DIABET EYE CARE, 164 BIGELOW RD, W NEWTON, MA 02165 USA. NR 22 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9343 EI 1555-7162 J9 AM J MED JI Am. J. Med. PD FEB 21 PY 1991 VL 90 SU 2A BP S66 EP S69 DI 10.1016/0002-9343(91)90042-V PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA EZ476 UT WOS:A1991EZ47600017 PM 1994721 ER PT J AU SIMONSON, DC DZAU, VJ AF SIMONSON, DC DZAU, VJ TI WORKSHOP-IX - LIPIDS, INSULIN, DIABETES SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material ID MELLITUS; DISEASE RP SIMONSON, DC (reprint author), JOSLIN DIABET CTR,CLIN RES,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 9 TC 4 Z9 4 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 FEB 21 PY 1991 VL 90 SU 2A BP S85 EP S86 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA EZ476 UT WOS:A1991EZ47600021 PM 1994726 ER PT J AU SPERTINI, O KANSAS, GS MUNRO, JM GRIFFIN, JD TEDDER, TF AF SPERTINI, O KANSAS, GS MUNRO, JM GRIFFIN, JD TEDDER, TF TI REGULATION OF LEUKOCYTE MIGRATION BY ACTIVATION OF THE LEUKOCYTE ADHESION MOLECULE-1 (LAM-1) SELECTIN SO NATURE LA English DT Article ID NODE HOMING RECEPTOR; HIGH ENDOTHELIAL VENULES; PROTEIN KINASE-C; INTERACTION DOMAINS; HUMAN HOMOLOG; LYMPHOCYTES; LFA-1; PHOSPHORYLATION; MECHANISM; MAC-1 AB A CENTRAL feature of host defence is the ability of leukocytes to enter tissues in response to immune or inflammatory stimuli. The leukocyte adhesion molecule-1 (LAM-1) regulates the migration of human leukocytes by mediating the binding both of lymphocytes to high endothelial venules of peripheral lymph nodes and of neutrophils to endothelium at inflammatory sites 1-10. As lymphocytes and neutrophils express the same LAM-1 protein 11,12, it is not clear how lineage-specific differences in leukocyte migration are controlled. We now report that the affinity of LAM-1 for a carbohydrate-based ligand, PPME 13-16, is dramatically increased following lymphocyte and neutrophil activation by lineage-specific stimuli. In addition, activation of lymphocytes by physiological stimuli enhanced LAM-1-dependent binding to high endothelial venules. Thus, transient changes in LAM-1 affinity after leukocyte stimulation probably directly influence leukocyte migration. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP SPERTINI, O (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. NR 30 TC 278 Z9 280 U1 0 U2 4 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 21 PY 1991 VL 349 IS 6311 BP 691 EP 694 DI 10.1038/349691a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EY627 UT WOS:A1991EY62700046 PM 1705015 ER PT J AU MONCURE, AC GRIFFIN, BP BREWSTER, DC FALLON, JT FERRUCCI, JT YUCEL, EK HUTTER, AM BLAND, EF MARK, EJ HUANG, PL AF MONCURE, AC GRIFFIN, BP BREWSTER, DC FALLON, JT FERRUCCI, JT YUCEL, EK HUTTER, AM BLAND, EF MARK, EJ HUANG, PL TI A 69-YEAR-OLD MAN WITH ABDOMINAL-PAIN 6 WEEKS AFTER A CORONARY REVASCULARIZATION PROCEDURE - DISSECTING ANEURYSM OF AORTA, WITH RUPTURE INTO PERICARDIAL CAVITY AND CARDIAC-TAMPONADE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MONCURE, AC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 3 Z9 3 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 21 PY 1991 VL 324 IS 8 BP 547 EP 555 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA EX918 UT WOS:A1991EX91800008 ER PT J AU BALDWIN, SW TSE, A GOSSETT, LS TAYLOR, EC ROSOWSKY, A SHIH, C MORAN, RG AF BALDWIN, SW TSE, A GOSSETT, LS TAYLOR, EC ROSOWSKY, A SHIH, C MORAN, RG TI STRUCTURAL FEATURES OF 5,10-DIDEAZA-5,6,7,8-TETRAHYDROFOLATE THAT DETERMINE INHIBITION OF MAMMALIAN GLYCINAMIDE RIBONUCLEOTIDE FORMYLTRANSFERASE SO BIOCHEMISTRY LA English DT Article ID DENOVO PURINE SYNTHESIS; DIHYDROFOLATE-REDUCTASE; CHICKEN LIVER; L1210 CELLS; FOLATE METABOLISM; METHOTREXATE; TRANSFORMYLASE; ANALOGS; DERIVATIVES; ENZYME AB We have investigated the structural features of 5,10-dideaza-5,6,7,8-tetrahydrofolate (DDATHF) that determine the activity of this compound as an inhibitor of glycinamide ribonucleotide formyltransferase (GARFT) purified from mouse L 1210 cells. 5-Deazatetrahydrofolate was as good an inhibitor of GARFT as DDATHF, indicating that isosteric replacement of nitrogen by carbon at the 5-position of tetrahydrofolate is sufficient for inhibition of GARFT. 5,10-Dideazafolic acid, 5,8,10-trideazatetrahydrofolate, and 2-desamino-5,10-dideazatetrahydrofolate were poor inhibitors of GARFT, indicating that a reduced pyridopyrimidine ring, N-8, and the 2-amino group of DDATHF, respectively, play an important role in the binding of tetrahydrofolate analogues to this enzyme. DDATHF analogues in which the phenyl ring was replaced either by a cyclohexyl ring or by methylene groups retained activity as inhibitors. 5,10-Dideazatetrahydrohomofolate was about 6 times more potent as an inhibitor of GARFT than DDATHF, but 5,10-dideazatetrahydronorfolate had about one-fifth of the activity of DDATHF. An analogue of DDATHF in which the glutamic acid side chain was replaced by aspartic acid (which was not a substrate for polyglutamation and was only weakly cytotoxic) was equiactive with DDATHF as an inhibitor of purified GARFT. Surprisingly, 5,10-dideazatetrahydropteroic acid was about as active as DDATHF as an inhibitor of GARFT, an indication that the glutamic acid in the side chain of DDATHF does not play a role in this ligand-enzyme interaction. The polyglutamate derivatives of DDATHF bound up to 100 times tighter to GARFT than DDATHF itself; longer chain polyglutamates conformed to Goldstein's zone B behavior under experimental conditions and were projected to be in zone C, i.e., stoichiometric inhibition, in vivo. We conclude that the presence of carbon at the 5-position of tetrahydrofolate analogues is sufficient for inhibition of GARFT, that N-8 and the 2-amino group are involved in binding of DDATHF to GARFT, probably through hydrogen bonds, and that the structures of the phenyl ring and amino acid side chain of DDATHF analogues are not primary determinants of GARFT inhibition by monoglutamate forms of these compounds. We also conclude that polyglutamation plays a major role in the potent cytotoxicity of DDATHF. C1 UNIV SO CALIF,DEPT BIOCHEM,LOS ANGELES,CA 90033. UNIV SO CALIF,DEPT PEDIAT,LOS ANGELES,CA 90033. UNIV SO CALIF,DEPT PHARM,LOS ANGELES,CA 90033. HARVARD UNIV,SCH MED,DEPT MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. PRINCETON UNIV,DEPT CHEM,PRINCETON,NJ 08544. UNIV SO CALIF,NORRIS COMPREHENS CANC CTR,LOS ANGELES,CA 90033. ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [CA-42367, CA-27605] NR 47 TC 126 Z9 126 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 FEB 19 PY 1991 VL 30 IS 7 BP 1997 EP 2006 DI 10.1021/bi00221a037 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EY207 UT WOS:A1991EY20700037 PM 1993209 ER PT J AU HELFGOTT, SM MOSCISCKI, RA MARTIN, JS LORENZO, C KIEVAL, R MCKENNA, M NADOL, J TRENTHAM, DE AF HELFGOTT, SM MOSCISCKI, RA MARTIN, JS LORENZO, C KIEVAL, R MCKENNA, M NADOL, J TRENTHAM, DE TI CORRELATION BETWEEN ANTIBODIES TO TYPE-II COLLAGEN AND TREATMENT OUTCOME IN BILATERAL PROGRESSIVE SENSORINEURAL HEARING-LOSS SO LANCET LA English DT Article ID INNER-EAR DISEASE; RELAPSING POLYCHONDRITIS; RHEUMATOID-ARTHRITIS; SERUM ANTIBODIES; AUTOIMMUNITY AB Our aim was to assess whether "idiopathic" bilateral progressive sensorineural hearing loss (BPSHL) has an immunological cause in some patients; antibodies to native type II collagen were sought by an ELISA in eighteen patients with BPSHL, before and after corticosteroid treatment, and in twelve patients with Meniere's disease, fifteen with otosclerosis, eighteen with rheumatoid arthritis, nine with fibrositis, and nine healthy controls. A positive result was defined as a mean dilution titre of 2 or more. Eight of eighteen BPSHL patients had positive titres - significantly (p < 0.005) more than in any other group (one Meniere's disease, two otosclerosis, and no others). The mean antibody titre was higher in the BPSHL group than in any other group (2.02[SEM 0.62] vs 0.17 [0.17]) Meniere's disease, 0.44 [0.32] otosclerosis, 0 all others; p < 0.005). The nine BPSHL patients who showed a clinical response to corticosteroids (improvement in at least one tone by audiogram or 25 db in speech discrimination score) had the highest mean antibody titre (3.46 [0.88] vs 0.59 [0.59] for the nine non-responsive patients; p < 0.04). We suggest that in some patients with BPSHL, immunity to type II collagen, a major constituent of the inner ear, may be important in the pathogenesis of the disorder. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR HOSP,DIV OTORHINOLARYNGOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HELFGOTT, SM (reprint author), BETH ISRAEL HOSP,DEPT MED,RES E,ROOM 319,330 BROOKLINE AVE,BOSTON,MA 02215, USA. NR 23 TC 43 Z9 43 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 FEB 16 PY 1991 VL 337 IS 8738 BP 387 EP 389 DI 10.1016/0140-6736(91)91165-Q PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA EX605 UT WOS:A1991EX60500003 PM 1671423 ER PT J AU ANDERSON, KC BARUT, BA RITZ, J FREEDMAN, AS TAKVORIAN, T RABINOWE, SN SOIFFER, R HEFLIN, L CORAL, F DEAR, K MAUCH, P NADLER, LM AF ANDERSON, KC BARUT, BA RITZ, J FREEDMAN, AS TAKVORIAN, T RABINOWE, SN SOIFFER, R HEFLIN, L CORAL, F DEAR, K MAUCH, P NADLER, LM TI MONOCLONAL ANTIBODY-PURGED AUTOLOGOUS BONE-MARROW TRANSPLANTATION THERAPY FOR MULTIPLE-MYELOMA SO BLOOD LA English DT Article ID HIGH-DOSE CHEMORADIOTHERAPY; B-CELL DIFFERENTIATION; HUMAN-PLASMA CELLS; ELIMINATION; MELPHALAN; ANTIGEN; RECONSTITUTION; EXPRESSION; COMPLEMENT; SURVIVAL C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIAT THERAPY,BOSTON,MA 02115. RP ANDERSON, KC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA 50947, 5K08 CA01105, CA 34183] NR 60 TC 86 Z9 86 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 FEB 15 PY 1991 VL 77 IS 4 BP 712 EP 720 PG 9 WC Hematology SC Hematology GA EX922 UT WOS:A1991EX92200005 PM 1993214 ER PT J AU SCHRIEVER, F FREEMAN, G NADLER, LM AF SCHRIEVER, F FREEMAN, G NADLER, LM TI FOLLICULAR DENDRITIC CELLS CONTAIN A UNIQUE GENE REPERTOIRE DEMONSTRATED BY SINGLE-CELL POLYMERASE CHAIN-REACTION SO BLOOD LA English DT Article ID TUMOR NECROSIS FACTOR; HUMAN B-CELLS; RETICULUM CELLS; ANTIGENIC PROFILE; LYMPH-NODES; CDNA; EXPRESSION; RECEPTOR; FOLLICLES; CLONING C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP SCHRIEVER, F (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA40216] NR 31 TC 42 Z9 42 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 FEB 15 PY 1991 VL 77 IS 4 BP 787 EP 791 PG 5 WC Hematology SC Hematology GA EX922 UT WOS:A1991EX92200015 PM 1825182 ER PT J AU FERRUCCI, JT AF FERRUCCI, JT TI LIVER-TUMOR IMAGING SO CANCER LA English DT Article; Proceedings Paper CT NATIONAL CONF ON ADVANCES IN CANCER IMAGING CY JAN 24-26, 1990 CL NEW YORK, NY SP AMER CANC SOC ID HEPATIC METASTASES; DELAYED CT; ARTERIAL PORTOGRAPHY; CONTRAST ENHANCEMENT; NEOPLASMS; BENIGN AB Liver tumor imaging is the paradigm of the dilemma of diagnostic decision-making in the current era of abundant high technology. In part, this is a reflection of the multiplicity of imaging techniques now in wide use worldwide. These include ultrasound (US), radionuclide scintigraphy (RNS), computed tomography (CT), magnetic resonance imaging (MRI), and techniques especially designed for staging the extent of known liver cancer, such as computed tomography during arterial portography (CTAP) and intraoperative ultrasound (IOUS). Most authorities concede that CT scanning is the single test most closely fitting the designation "gold standard" for liver tumor imaging, although MRI, a less mature technique, is already preferred by some. Local factors profoundly influence the selection and sequence of imaging studies, including available equipment, radiologic skills, institutional interests, and especially the specific clinical circumstances of the patient. Thus, diagnostic algorithms or decision trees for sequential imaging workup of liver tumor suspects tend to be somewhat institution specific. RP FERRUCCI, JT (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 25 TC 24 Z9 24 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 FEB 15 PY 1991 VL 67 IS 4 SU S BP 1189 EP 1195 DI 10.1002/1097-0142(19910215)67:4+<1189::AID-CNCR2820671514>3.0.CO;2-# PG 7 WC Oncology SC Oncology GA EW818 UT WOS:A1991EW81800013 PM 1846773 ER PT J AU TEICHER, BA HERMAN, TS TANAKA, J EDER, JP HOLDEN, SA BUBLEY, G COLEMAN, CN FREI, E AF TEICHER, BA HERMAN, TS TANAKA, J EDER, JP HOLDEN, SA BUBLEY, G COLEMAN, CN FREI, E TI MODULATION OF ALKYLATING-AGENTS BY ETANIDAZOLE AND FLUOSOL-DA CARBOGEN IN THE FSAIIC FIBROSARCOMA AND EMT6 MAMMARY-CARCINOMA SO CANCER RESEARCH LA English DT Article ID MELPHALAN ANTITUMOR-ACTIVITY; MURINE TUMOR; PERFLUOROCHEMICAL EMULSION; CYTO-TOXICITY; FIBRO-SARCOMA; HOECHST 33342; RADIATION; CELL; ENHANCEMENT; RADIOSENSITIVITY AB Tumor cell survival assay in the FSaIIC murine fibrosarcoma demonstrated that when the modulator Fluosol-DA (0.3 ml; 12 ml/kg i.v.) was administered just prior to an alkylating agent plus carbogen breathing for 6 h or the modulator etanidazole (1 g/kg i.p.) was administered just prior to an alkylating agent, the combination treatment produced significantly more tumor cell killing across the dosage range of each alkylating agent tested compared with the alkylating agent alone. Each alkylating agent produced a dose-dependent log-linear tumor cell survival curve. There was an increase in tumor cell killing of 5-10-fold when either Fluosol-DA/carbogen or etanidazole was added to treatment with the alkylating agent. For cis-diamminedichloroplatinum(II) (CDDP) and N,N',N"-triethylenethiophosphoramide, the modulators used in combination increased tumor cell killing by only 2-3-fold over that obtained with a single modulator, but for the other alkylating agents, tumor cell killing was increased by 10-50-fold when the combination of modulators was used. Bone marrow granulocyte-macrophage colony-forming unit survival assays showed that the combination of modulators with the alkylating agents resulted in only small increases in bone marrow toxicity of the alkylating agents except for N,N',N"-triethylenethiophosphoramide and L-phenylalanine mustard (L-PAM), for which the toxicity to the bone marrow granulocyte-macrophage colony-forming unit was increased by 5-10-fold compared with the alkylating agents alone. The Hoechst 33342 dye diffusion defined tumor cell subpopulation assay, also in the FSaIIC tumor, demonstrated that the combination of modulators increased the toxicity of CDDP, cyclophosphamide, L-PAM, and 1,3-bis(2-chloroethyl)-1-nitrosourea by 9-55-fold compared with the alkylating agent alone in both the bright (euxoic-enriched) and dim (hypoxic-enriched) cells. For each alkylating agent except 1,3-bis(2-chloroethyl)-1-nitrosourea, the increase in tumor cell killing was greater in the dim cells than in the bright cells. Finally, tumor growth delay studies in both the FSaIIC tumor and the EMT-6 murine mammary adenocarcinoma confirmed that the combination of modulators significantly increased the tumor growth delay caused by CDDP, carboplatin, cyclophosphamide, N,N',N"-triethylenethiophosphoramide, L-PAM, and 1,3-bis(2-chloroethyl)-1-nitrosourea. The greatest increases (4-5-fold) were observed for carboplatin and L-PAM in the FSaIIC tumor and CDDP and cyclophosphamide in the EMT-6 tumor. These results suggest that Fluosol-DA/carbogen together with etanidazole may be an effective modulator combination of alkylating agents in the clinic. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. BETH ISRAEL HOSP,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 [P01-CA38493, P01-CA19589] NR 49 TC 23 Z9 23 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 FEB 15 PY 1991 VL 51 IS 4 BP 1086 EP 1091 PG 6 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700005 PM 1825474 ER PT J AU BAILEY, H MULCAHY, RT TUTSCH, KD ROZENTAL, JM ALBERTI, D ARZOOMANIAN, RZ TOMBES, MB TRUMP, DL WILDING, G AF BAILEY, H MULCAHY, RT TUTSCH, KD ROZENTAL, JM ALBERTI, D ARZOOMANIAN, RZ TOMBES, MB TRUMP, DL WILDING, G TI A PHASE-I STUDY OF SR-2508 AND CYCLOPHOSPHAMIDE ADMINISTERED BY INTRAVENOUS-INJECTION SO CANCER RESEARCH LA English DT Article ID HYPOXIC CELL RADIOSENSITIZER; SENSITIZER MISONIDAZOLE; TRIAL; CHEMOTHERAPY; PHARMACOKINETICS; NITROIMIDAZOLES; ENHANCEMENT; MELPHALAN; CANCER; PLUS AB SR-2508, a less lipophilic and neurotoxic analogue of the nitroimidazole, misonidazole, has exhibited significant chemosensitization properties in preclinical studies with alkylating agents. A phase I trial was carried out to assess toxicity and possible pharmacological interactions of the combination of short infusions of SR-2508 and cyclophosphamide (CP). Patients were randomly assigned to receive either CP alone followed in 3 wk by CP + SR-2508, or CP + SR-2508 followed by CP alone. All additional courses were CP + SR-2508. The maximum tolerated dose of the combination was determined by dose escalation of SR-2508 while the dose of CP remained fixed, initially 1.0 g/m2, and then a second maximum tolerated dose was determined with CP at 1.6 g/m2. One hundred seventeen evaluable courses were administered to 39 patients, the majority of whom had received prior treatment. Somewhat unexpectedly, reversible grade 4 granulocytopenia was the dose-limiting toxicity occurring in four of five evaluable first combination courses at level 6 (SR-2508, 11.3 g/m2; CP, 1.0 g/m2), the initial maximum tolerated dose. SR-2508 enhanced CP-induced myelosuppression as exhibited by the significant difference (p < 0.001) between the 27 paired courses (CP versus CP + SR-2508) for WBC nadirs over levels 1 to 6. The neurotoxicity encountered was similar to that seen in past clinical trials, being reversible, mild, and usually peripheral in nature. There was one treatment-related death (neutropenic sepsis) on study. No other significant toxicity was seen. SR-2508 exhibited linear pharmacokinetics over the dose range studied. The SR-2508 area under the concentration-time curve increased linearly with dose (r = 0.858; p < 0.001). No other parameters were dose related. Neither drug appeared to affect the pharmacokinetics of the other, and CP pharmacokinetic values were consistent with those from prior studies. Due to the interaction noted between the two agents and the preclinical data suggesting preferential enhancement of antitumor efficacy under this combination, phase II study appears warranted. C1 UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53792. UNIV WISCONSIN,DEPT NEUROL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NCI NIH HHS [CA42325, N01-CM57735] NR 30 TC 11 Z9 11 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 FEB 15 PY 1991 VL 51 IS 4 BP 1099 EP 1104 PG 6 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700007 PM 1825475 ER PT J AU BAILEY, H TUTSCH, KD ARZOOMANIAN, RZ TOMBES, MB ALBERTI, D BRUGGINK, J WILDING, G AF BAILEY, H TUTSCH, KD ARZOOMANIAN, RZ TOMBES, MB ALBERTI, D BRUGGINK, J WILDING, G TI PHASE-I CLINICAL-TRIAL OF FAZARABINE AS A 24-HOUR CONTINUOUS INFUSION SO CANCER RESEARCH LA English DT Article ID LYMPHOBLASTIC CELLS MOLT-4; NSC 281272; ARABINOSYL-5-AZACYTOSINE; 1-BETA-D-ARABINOFURANOSYL-5-AZACYTOSINE; 5-AZACYTIDINE; DNA; METABOLISM; XENOGRAFTS; KINETICS; LEUKEMIA AB A phase I trial of fazarabine (ara-AC, 1-beta-D-arabinofuranosyl-5-azacytosine, NSC 281272) administered as a 24-h continuous infusion was performed in 24 adults with solid tumor malignancies. The majority of patients had received prior marrow-suppressive therapy. Level 7 (54.5 mg/m2/h for 24 h) was the maximum tolerated dose since during 6 evaluable first courses, 2 episodes of grade 4 granulocytopenia and 3 episodes of grade 3 occurred. Moderate thrombocytopenia also occurred at level 7 with 3 episodes of grade 1 and 1 episode of grade 4 thrombocytopenia during 6 first course treatments. Minimal myelosuppression, principally leukpenia, was seen prior to level 7. The nadir WBC through 47 courses had a linear relationship with plasma steady-state concentrations of ara-AC. The only other toxicity noted was moderate nausea/vomiting, which did not appear to be dose related. Plasma steady-state concentrations of ara-AC were reached in all patients within 4-6 h and ranged from 1.1-mu-M (11 mg/m2/h for 24 h) to 7.5-mu-M (54.5 mg/m2/h for 24 h). The mean total body clearance of ara-AC for 47 courses, levels 1-7, was 592 +/- 147 (SD) ml/min/m2 which is similar to prior pharmacokinetic data from the 24-h and 72-h infusion trials of the Pediatric and Medicine Branches, respectively. There were no objective disease responses during the trial. The recommended adult phase II dose for a 24-h infusion of ara-AC is 45-50 mg/m2/h. C1 UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NCI NIH HHS [N01-CM57735] NR 15 TC 11 Z9 12 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 FEB 15 PY 1991 VL 51 IS 4 BP 1105 EP 1108 PG 4 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700008 PM 1705165 ER PT J AU LIN, CW SHULOK, JR WONG, YK SCHANBACHER, CF CINCOTTA, L FOLEY, JW AF LIN, CW SHULOK, JR WONG, YK SCHANBACHER, CF CINCOTTA, L FOLEY, JW TI PHOTOSENSITIZATION, UPTAKE, AND RETENTION OF PHENOXAZINE NILE BLUE DERIVATIVES IN HUMAN BLADDER-CARCINOMA CELLS SO CANCER RESEARCH LA English DT Article ID MALIGNANT-TUMORS; HEMATOPORPHYRIN; THERAPY; INVITRO; PHOTOINACTIVATION; RHODAMINE-123; INACTIVATION; LOCALIZATION; TEMPERATURE; DEPENDENCE AB The overall goal of our research is to develop effective new photosensitizers for tumor-selective photodynamic therapy. Phenoxazine dyes, including several Nile blue analogues, are known to localize selectively in animal tumors. Structural modifications yielded several series of analogues with substantially higher 1O2 yields and different photochemical and physicochemical properties. This study examined the photosensitization potency, cellular uptake, and retention of these derivatives in human bladder carcinoma cells (MGH-U1) in culture. Nile blue derivatives containing halogens and/or sulfur substitutes were selected to exhibit different 1O2 yields, pKa values, and hydrophobicities. The effectiveness of these derivatives in mediating photokilling of tumor cells in vitro corresponded well with the 1O2 yields of these compounds, indicating that structural modifications which resulted in increased 1O2 yields enhanced potency in mediating photocytotoxicity in vitro. Using derivatives (sat-NBS and sat-NBS-6I) with the highest 1O2 quantum yield (0.35 and 0.821), over 90% cell kill was achieved at a sensitizer concentration of 5 x 10(-8) M, about 3 orders of magnitude more effective than hematoporphyrin derivative, the only sensitizer currently available clinically. This result suggests that some of the oxazine derivatives could potentially be effective photosensitizers. The correspondence between 1O2 yield and photosensitizing potency, together with results showing enhanced photocytotoxicity in the presence of D2O and reduced photocytotoxicity under hypoxic conditions, strongly suggests that the generation of 1O2 is a major mechanism mediating the photocytotoxic effect. The uptake of Nile blue derivatives by cells in culture exhibited a pattern of rapid initial uptake followed by a gradual increase in cellular dye contents. The uptake does not correlate directly with the individual pKa values or hydrophobicities of the derivatives, indicating that the structural modifications that increased 1O2 yields did not significantly alter the uptake and retention of Nile blue derivatives. The highly concentrative uptake by and slow efflux from dye-loaded cells were consistent with an active mechanism for the cellular accumulation of these dyes. On the other hand, the retention of the compounds was directly proportional to dye concentration in the medium over a 1000-fold range of concentrations, and the uptake could proceed at temperatures below 2-degrees-C; these observations excluded endocytosis or a carrier-mediated mechanism for the uptake. The uptake was also unaffected by the presence of serum in the medium. Based on these results, we hypothesize that Nile blue derivatives transport across the cell membrane possibly as deprotonated forms and, upon entering the cell, either partition into lipophilic areas of the cell membranes and/or become sequestered in certain intracellular organelles. C1 ROWLAND INST SCI INC,CAMBRIDGE,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LIN, CW (reprint author), MASSACHUSETTS GEN HOSP,UROL RES LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 32259] NR 34 TC 59 Z9 59 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD FEB 15 PY 1991 VL 51 IS 4 BP 1109 EP 1116 PG 8 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700009 PM 1847656 ER PT J AU MAXWELL, M NABER, SP WOLFE, HJ HEDLEYWHYTE, ET GALANOPOULOS, T NEVILLEGOLDEN, J ANTONIADES, HN AF MAXWELL, M NABER, SP WOLFE, HJ HEDLEYWHYTE, ET GALANOPOULOS, T NEVILLEGOLDEN, J ANTONIADES, HN TI EXPRESSION OF ANGIOGENIC GROWTH-FACTOR GENES IN PRIMARY HUMAN ASTROCYTOMAS MAY CONTRIBUTE TO THEIR GROWTH AND PROGRESSION SO CANCER RESEARCH LA English DT Article ID ENDOTHELIAL-CELL MITOGEN; HUMAN-TUMOR CELLS; FACTOR RECEPTOR; MESSENGER-RNAS; BOVINE BRAIN; EGF RECEPTOR; FACTOR-ALPHA; NUCLEOTIDE-SEQUENCE; PROTEIN; HEPARIN AB Astrocytomas are highly malignant brain tumors and are among the most neovascularized solid tumors. We have investigated the expression of the angiogenic growth factors acidic fibroblast growth factor and transforming growth factor-alpha, together with its receptor epidermal growth factor receptor, in 30 primary astrocytomas. Both acidic fibroblast growth factor and transforming growth factor-alpha, together with epidermal growth factor receptor, are found to be greatly overexpressed in these tumors when compared with normal brain. This overexpression of angiogenic growth factors may underlie the intense neovascularization characteristic of astrocytomas. C1 HARVARD UNIV,SCH PUBL HLTH,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV OXFORD,DEPT CLIN NEUROL,OXFORD,ENGLAND. TUFTS UNIV,NEW ENGLAND MED CTR,DEPT PATHOL,BOSTON,MA 02111. FU NCI NIH HHS [CA30101]; NHLBI NIH HHS [HL29583] NR 41 TC 111 Z9 112 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 FEB 15 PY 1991 VL 51 IS 4 BP 1345 EP 1351 PG 7 WC Oncology SC Oncology GA EX827 UT WOS:A1991EX82700044 PM 1705174 ER PT J AU RIMM, IJ GHAYUR, T GASSER, DL ROSENKRANTZ, K BURAKOFF, SJ SEIDMAN, JG FERRARA, JLM AF RIMM, IJ GHAYUR, T GASSER, DL ROSENKRANTZ, K BURAKOFF, SJ SEIDMAN, JG FERRARA, JLM TI ALLOREACTIVE LYMPHOCYTES FROM T-CELL RECEPTOR (BETA-CHAIN) TRANSGENIC MICE DO NOT MEDIATE A GRAFT-VERSUS-HOST REACTION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HISTOCOMPATIBILITY COMPLEX ANTIGENS; II H-2 DIFFERENCES; MARROW TRANSPLANTATION; MUTUAL RECOGNITION; DONOR ORIGIN; DISEASE; EXPRESSION; MOUSE; GENE; TOLERANCE AB The injection of mature T cells into a tolerant or immunocompromised allogeneic host animal produces a graft versus host response (GVHR) that can result in splenomegaly, immunosuppression and death of the host animal. We demonstrate here that lymphocytes from T cell receptor beta-chain (TCR-beta) transgenic mice, in which the expression of the transgene inhibits endogenous beta- and gamma-gene rearrangements and thus causes abnormal T cell development, are unable to mediate a GVHR. The GVHR was measured after the injection of lymphocytes from transgenic mice into normal F1 mice and also after transplantation of bone marrow and lymphocytes from transgenic mice into lethally irradiated F1 recipients. In both systems, cells from transgenic mice failed to produce a significant GVHR. Cells from the transgenic mice were able to recognize the foreign histocompatibility Ag of the host in vitro and in vivo although the transgenic mice rejected skin grafts more slowly than controls. Thus, lymphocytes from transgenic mice were unable to produce a GVHR despite the presence of alloreactive T cells. These results suggest that lymphocytes from TCR-beta transgenic mice fail to mediate a GVHR either because lymphocytes with a single transgenic TCR-beta chain have a limited ability to recognize allogenic cells in vivo or because the transgenic mice lack lymphocyte subsets that are important for the mediation of a GVHR. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. UNIV PENN,DEPT HUMAN GENET,PHILADELPHIA,PA 19104. RP RIMM, IJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 30 TC 15 Z9 15 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 FEB 15 PY 1991 VL 146 IS 4 BP 1130 EP 1133 PG 4 WC Immunology SC Immunology GA EW681 UT WOS:A1991EW68100008 PM 1825104 ER PT J AU VIVIER, E MORIN, P TIAN, QS DALEY, J BLUE, ML SCHLOSSMAN, SF ANDERSON, P AF VIVIER, E MORIN, P TIAN, QS DALEY, J BLUE, ML SCHLOSSMAN, SF ANDERSON, P TI EXPRESSION AND TYROSINE PHOSPHORYLATION OF THE T-CELL RECEPTOR ZETA-SUBUNIT IN HUMAN THYMOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN LYMPHOCYTES-T; ANTIGEN RECEPTOR; CD4+8+ THYMOCYTES; TRANSGENIC MICE; DISCRETE STAGES; ACTIVATION; TOLERANCE; COMPLEX; THYMUS; SELECTION AB Recent evidence suggests that the zeta-subunit of the TCR complex plays a critical role in transducing signals initiated by the Ag receptor heterodimer. Because thymic maturation involves specific interactions between the TCR complex and thymic stromal cells, the zeta-subunit has been postulated to also play a role in this process. To assess the potential for zeta to contribute to thymocyte maturation, we have used an anti-zeta mAb (TIA-2) to quantitate its expression in mature (CD3(bright)) and immature (CD3(dim) and CD3-) populations of human thymocytes. Using both flow cytometric and immunoblotting analysis, we found that the relative expression of TCR-zeta varied directly with the surface expression of CD3. Importantly, TCR-zeta was detected in the majority of CD3- thymocytes, indicating that its expression precedes the surface appearance of CD3:TCR. In thymocytes, TCR-zeta was found to be constitutively phosphorylated on tyrosine residues. The relative expression of phospho-zeta varied directly with the maturational stage of the thymocyte, with the mature (CD3(bright)), single positive cells accounting for most of the phospho-zeta found in the human thymus. The expression of phospho-zeta could be significantly increased by activating thymocytes with mAb reactive with either CD3 or CD2. These results suggest that TCR-zeta is functionally linked to the major thymocyte activation receptors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. NR 44 TC 17 Z9 17 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 FEB 15 PY 1991 VL 146 IS 4 BP 1142 EP 1148 PG 7 WC Immunology SC Immunology GA EW681 UT WOS:A1991EW68100010 PM 1704030 ER PT J AU ROTHSTEIN, DM YAMADA, A SCHLOSSMAN, SF MORIMOTO, C AF ROTHSTEIN, DM YAMADA, A SCHLOSSMAN, SF MORIMOTO, C TI CYCLIC REGULATION OF CD45 ISOFORM EXPRESSION IN A LONG-TERM HUMAN CD4+CD45RA+ T-CELL LINE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LEUKOCYTE-COMMON ANTIGEN; RECEPTOR BETA-CHAIN; HUMAN LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; HELPER-INDUCER; DIFFERENTIAL EXPRESSION; ACTIVATION; SUBSET; UCHL1; SUBPOPULATIONS AB The CD45 Ag family is comprised of at least five isoforms generated by the alternative splicing of three exons encoded by a single leukocyte common Ag gene. These isoforms, differentially expressed on subsets of T cells, are widely believed to delineate maturational status. Thus, cells expressing the high molecular mass CD45RA+ isoforms (220 and 205 kDa) are believed to represent naive cells, whereas those lacking CD45RA and expressing high density CD45RO (180 kDa) represent memory cells. This is based on findings that after activation, CD45RA+ cells "convert" to the CD45RA- phenotype, losing CD45RA and gaining CD45RO. This conversion is believed to be both unidirectional and irreversible. We now report a strategy for the development of polyclonal CD45RA+ cell lines derived from peripheral blood CD4+CD45RA+ cells. However, in such cell lines, CD45RA expression was not constant, but varied cyclically with restimulation. After restimulation, CD45RA expression decreased significantly, nadiring on days 5 to 7. However, CD45RA was fully re-expressed by days 14 to 16. These cells coexpressed high density CD45RO, which did not vary through the stimulatory cycle. Cells sorted CD45RA- on day 7 of the cycle rapidly reexpress CD45RA. Metabolic labeling revealed that the 220 kDa CD45RA isoform is no longer synthesized. Synthesis of the 205 kDa (CD45RA) isoform decreased significantly early after stimulation, but then increased back to baseline after day 12. The 180-kDa (CD45RO) isoform followed an opposite pattern. Our results document that alternative splicing of the different CD45 isoforms is highly regulated after activation and that conversion from CD45RA+ to CD45RA- is neither unidirectional, nor irreversible. RP ROTHSTEIN, DM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,M-755,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-12069]; NIAMS NIH HHS [AR-33713] NR 54 TC 209 Z9 209 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 FEB 15 PY 1991 VL 146 IS 4 BP 1175 EP 1183 PG 9 WC Immunology SC Immunology GA EW681 UT WOS:A1991EW68100015 PM 1671403 ER PT J AU LETVIN, NL LORD, CI KING, NW WYAND, MS MYRICK, KV HASELTINE, WA AF LETVIN, NL LORD, CI KING, NW WYAND, MS MYRICK, KV HASELTINE, WA TI RISKS OF HANDLING HIV SO NATURE LA English DT Letter C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP LETVIN, NL (reprint author), HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772, USA. NR 3 TC 27 Z9 27 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 14 PY 1991 VL 349 IS 6310 BP 573 EP 573 DI 10.1038/349573a0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EX570 UT WOS:A1991EX57000039 PM 2000134 ER PT J AU FLETCHER, JA KOZAKEWICH, HP HOFFER, FA LAGE, JM WEIDNER, N TEPPER, R PINKUS, GS MORTON, CC CORSON, JM AF FLETCHER, JA KOZAKEWICH, HP HOFFER, FA LAGE, JM WEIDNER, N TEPPER, R PINKUS, GS MORTON, CC CORSON, JM TI DIAGNOSTIC RELEVANCE OF CLONAL CYTOGENETIC ABERRATIONS IN MALIGNANT SOFT-TISSUE TUMORS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CHROMOSOME-ABNORMALITIES; EWINGS-SARCOMA; SOLID TUMORS; RHABDOMYOSARCOMA; TRANSLOCATION; EXPERIENCE; CHILDHOOD; LEUKEMIA AB Background. Malignant soft-tissue tumors often present substantial diagnostic challenges. Chromosome aberrations that might be diagnostic have been identified in some types of soft-tissue tumors, but the overall frequency and diagnostic relevance of these aberrations have not been established. Methods. We attempted to determine the karyotypes of a series of 62 consecutive, unselected malignant spindle-cell or small round-cell soft-tissue tumors (from 46 adults and 16 children) after direct harvesting of cells or short-term culture. All tumors were examined independently by immunohistochemical staining in addition to routine light-microscopical evaluation, and all but two tumors were examined by electron microscopy. Results. Metaphases were obtained from 61 of the 62 tumors, and clonal chromosome aberrations were identified in 55 (89 percent). In the six tumors that yielded metaphases but lacked apparent clonal aberrations, the normal metaphases were found to originate from non-neoplastic stromal elements within the tumor specimens. Thus, all tumors in which karyotyping was successful contained clonal chromosome aberrations. Forty of 62 tumors (65 percent) contained clonal chromosome aberrations that either suggested or confirmed a specific diagnosis; in 15 of these tumors (24 percent of all tumors), the aberrations were important in establishing the final diagnosis. Cytogenetic analyses were particularly informative about small round-cell tumors from children: 8 of 14 round-cell tumors contained diagnostically important chromosome aberrations. Using the combined approaches of light and electron microscopy, immunohistochemistry, and cytogenetics, we established an unambiguous diagnosis for 60 of 62 tumors. Conclusions. Cytogenetic analyses reveal clonal chromosome aberrations in virtually all malignant soft-tissue tumors. These clonal chromosome aberrations, particularly in small round-cell tumors in children, often have diagnostic relevance. C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP FLETCHER, JA (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [1-K11-CA-01498-01]; NIA NIH HHS [AG-00294] NR 34 TC 264 Z9 264 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 FEB 14 PY 1991 VL 324 IS 7 BP 436 EP 442 DI 10.1056/NEJM199102143240702 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA EX363 UT WOS:A1991EX36300002 PM 1988828 ER PT J AU LEHMANN, LS RODRIGUEZ, L AF LEHMANN, LS RODRIGUEZ, L TI CLOZAPINE AND THE MANDATORY MONITORING-SYSTEM SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP LEHMANN, LS (reprint author), US DEPT VET AFFAIRS,WASHINGTON,DC 20420, USA. NR 2 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 FEB 14 PY 1991 VL 324 IS 7 BP 490 EP 490 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EX363 UT WOS:A1991EX36300011 ER PT J AU SOUTHERN, J AF SOUTHERN, J TI CASE-23-1990 - GIANT-CELL ARTERITIS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID POLYMYALGIA RHEUMATICA; MONOCLONAL GAMMOPATHY; MALIGNANCY RP SOUTHERN, J (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 FEB 14 PY 1991 VL 324 IS 7 BP 496 EP 497 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA EX363 UT WOS:A1991EX36300025 ER PT J AU BROOKS, R MCGOVERN, BA GARAN, H RUSKIN, JN AF BROOKS, R MCGOVERN, BA GARAN, H RUSKIN, JN TI CURRENT TREATMENT OF PATIENTS SURVIVING OUT-OF-HOSPITAL CARDIAC-ARREST SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID CORONARY-ARTERY DISEASE; IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR; MALIGNANT VENTRICULAR ARRHYTHMIAS; ACUTE MYOCARDIAL-INFARCTION; SIGNAL-AVERAGED ELECTROCARDIOGRAM; ANTIARRHYTHMIC DRUG EFFICACY; LONG-TERM SURVIVAL; SUDDEN-DEATH; FOLLOW-UP; CLINICAL CHARACTERISTICS AB Most out-of-hospital cardiac arrests result from the sudden onset of a sustained ventricular arrhythmia in the absence of a new myocardial infarction. Individuals who survive cardiac arrest are at high risk for recurrent arrhythmias and sudden unexpected death. To prevent recurrent cardiac arrest, effective treatment must be provided during hospitalization after the initial episode. Caring for the survivor of cardiac arrest requires a detailed clinical investigation to define the underlying cardiac anatomy and left ventricular function and to elucidate the mechanism and characteristics of the patient's arrhythmia. Appropriate antiarrhythmic therapy, such as drugs or a nonpharmacological intervention (eg, implantable cardioverter-defibrillator), is then selected based on these considerations. In addition, ischemia is treated aggressively with beta-adrenergic blocking agents and, when appropriate, with surgical coronary artery revascularization. RP BROOKS, R (reprint author), MASSACHUSETTS GEN HOSP, CARDIAC UNIT, BOSTON, MA 02114 USA. NR 115 TC 21 Z9 21 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA SN 0098-7484 EI 1538-3598 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD FEB 13 PY 1991 VL 265 IS 6 BP 762 EP 768 DI 10.1001/jama.265.6.762 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA EW479 UT WOS:A1991EW47900031 PM 1899276 ER PT J AU FRETZ, H ALBERS, MW GALAT, A STANDAERT, RF LANE, WS BURAKOFF, SJ BIERER, BE SCHREIBER, SL AF FRETZ, H ALBERS, MW GALAT, A STANDAERT, RF LANE, WS BURAKOFF, SJ BIERER, BE SCHREIBER, SL TI RAPAMYCIN AND FK506 BINDING-PROTEINS (IMMUNOPHILINS) SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Note ID PEPTIDYL-PROLYL ISOMERASE; IMMUNOSUPPRESSANT FK506; POLYACRYLAMIDE GELS; CYCLOPHILIN; DEPROTECTION; DISTINCT; ESTERS C1 HARVARD UNIV,DEPT CHEM,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. RI Standaert, Robert/D-9467-2013 OI Standaert, Robert/0000-0002-5684-1322 NR 18 TC 144 Z9 144 U1 1 U2 7 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD FEB 13 PY 1991 VL 113 IS 4 BP 1409 EP 1411 DI 10.1021/ja00004a051 PG 3 WC Chemistry, Multidisciplinary SC Chemistry GA EX603 UT WOS:A1991EX60300051 ER PT J AU BERSOHN, MM VEMURI, R SCHUIL, DW WEISS, RS PHILIPSON, KD AF BERSOHN, MM VEMURI, R SCHUIL, DW WEISS, RS PHILIPSON, KD TI EFFECT OF TEMPERATURE ON SODIUM-CALCIUM EXCHANGE IN SARCOLEMMA FROM MAMMALIAN AND AMPHIBIAN HEARTS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE RECONSTITUTION; SARCOLEMMAL VESICLE; SODIUM-CALCIUM ION EXCHANGE; (DOG HEART); (FROG HEART); (RABBIT HEART) ID RAT-BRAIN; MEMBRANES; VESICLES; TRANSPORT AB We have investigated temperature dependence of Ca2+ uptake by the cardiac sarcolemmal Na+ -Ca2+ exchanger from dog, rabbit and bullfrog. In native rabbit sarcolemmal vesicles, Ca2+ affinity of the Na+ -Ca2+ exchanger is unchanged from 7 to 37-degrees-C; however, the initial velocity of Ca2+ uptake declines much more steeply below 22-degrees-C than above 22-degrees-C. In native dog sarcolemma, the temperature dependence of Na+-Ca2+ exchange velocity is similar to that of native rabbit. However, in frog heart the velocity of Na+-Ca2+ exchange declines much more slowly with decreasing temperature at both temperature ranges. Reconstitution of the Na+-Ca2+ exchanger into artificial lipid vesicles consisting of either asolectin or phosphatidylserine, phosphatidylcholine, and cholesterol has little effect on temperature dependence of Na+-Ca2+ exchange velocity in any of the three species. We conclude that the lesser temperature sensitivity of the cardiac sarcolemmal Na+-Ca2+ exchanger of a poikilothermic species is at least partly an intrinsic property of the transport protein. C1 SEPULVEDA VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PHYSIOL,LOS ANGELES,CA 90024. RP BERSOHN, MM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,CARDIOL SECT W111E,LOS ANGELES,CA 90073, USA. FU NHLBI NIH HHS [HL27821] NR 17 TC 39 Z9 39 U1 1 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD FEB 11 PY 1991 VL 1062 IS 1 BP 19 EP 23 DI 10.1016/0005-2736(91)90329-7 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EZ980 UT WOS:A1991EZ98000004 PM 1998706 ER PT J AU RUVKUN, G FINNEY, M AF RUVKUN, G FINNEY, M TI REGULATION OF TRANSCRIPTION AND CELL IDENTITY BY POU DOMAIN PROTEINS SO CELL LA English DT Review ID DNA-SEQUENCE; BINDING; COMPLEX; OCT-1 C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. RP RUVKUN, G (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 29 TC 224 Z9 225 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 FEB 8 PY 1991 VL 64 IS 3 BP 475 EP 478 DI 10.1016/0092-8674(91)90227-P PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EX361 UT WOS:A1991EX36100002 PM 1991317 ER PT J AU LI, P WOOD, K MAMON, H HASER, W ROBERTS, T AF LI, P WOOD, K MAMON, H HASER, W ROBERTS, T TI RAF-1 - A KINASE CURRENTLY WITHOUT A CAUSE BUT NOT LACKING IN EFFECTS SO CELL LA English DT Review ID PROTEIN-KINASE; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION; REQUIREMENT; EXPRESSION; RECEPTOR; FAMILY C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP LI, P (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115, USA. NR 24 TC 154 Z9 155 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD FEB 8 PY 1991 VL 64 IS 3 BP 479 EP 482 DI 10.1016/0092-8674(91)90228-Q PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EX361 UT WOS:A1991EX36100003 PM 1846778 ER PT J AU KAELIN, WG PALLAS, DC DECAPRIO, JA KAYE, FJ LIVINGSTON, DM AF KAELIN, WG PALLAS, DC DECAPRIO, JA KAYE, FJ LIVINGSTON, DM TI IDENTIFICATION OF CELLULAR PROTEINS THAT CAN INTERACT SPECIFICALLY WITH THE T/E1A-BINDING REGION OF THE RETINOBLASTOMA GENE-PRODUCT SO CELL LA English DT Article ID SV40 LARGE-T; SUSCEPTIBILITY GENE; DNA-BINDING; ADENOVIRUS E1A; RB GENE; SV40-TRANSFORMED CELLS; ENCODED PROTEIN; OSTEO-SARCOMA; 1A PROTEINS; EXPRESSION AB The SV40 T antigen (T)/adenovirus E1A-binding domain of the retinoblastoma gene product (pRB) has been fused to S. japonicum glutathione S-transferase, and the chimera, bound to insoluble glutathione, was used to search for cellular proteins that can interact specifically with pRB. At least seven such proteins were detected in extracts of multiple human tumor cell lines. These proteins failed to bind to a family of pRB fusion proteins that harbor inactivating mutations in the T/E1A-binding domain and to the wild-type fusion protein in the presence of a peptide replica of the pRB-binding domain of T. Therefore, the binding of one or more of these proteins may contribute to the growth-suppressing function of pRB. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. NCI,USN,MED ONCOL BRANCH,BETHESDA,MD 20814. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. RP KAELIN, WG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. RI Wang, Nianshuang/C-1463-2010; kaye, frederic/E-2437-2011 FU NCI NIH HHS [R01 CA057327] NR 66 TC 535 Z9 537 U1 1 U2 13 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD FEB 8 PY 1991 VL 64 IS 3 BP 521 EP 532 DI 10.1016/0092-8674(91)90236-R PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EX361 UT WOS:A1991EX36100008 PM 1825028 ER PT J AU WORKMAN, JL TAYLOR, ICA KINGSTON, RE AF WORKMAN, JL TAYLOR, ICA KINGSTON, RE TI ACTIVATION DOMAINS OF STABLY BOUND GAL4 DERIVATIVES ALLEVIATE REPRESSION OF PROMOTERS BY NUCLEOSOMES SO CELL LA English DT Article ID RNA POLYMERASE-II; TRANSCRIPTIONALLY ACTIVE CHROMATIN; IMMEDIATE EARLY PROTEIN; DNA-BINDING; GLUCOCORTICOID RECEPTOR; HYPERSENSITIVE SITES; REGULATORY PROTEIN; MAJOR LATE; TATA-BOX; YEAST AB GAL4 derivatives containing an activation domain alleviated repression of a promoter during nucleosome assembly. A GAL4 derivative lacking an activation domain stably bound the promoter during nucleosome assembly but was not sufficient to preserve promoter function. The activation domain of GAL4 derivatives was essential for preserving promoter function, and thus the transcriptional stimulatory activity attributable to these activation domains increased dramatically during nucleosome assembly. Furthermore, promoter-bound activation domains allowed the formation of preinitiation complexes after nucleosome assembly. Finally, GAL4 derivatives containing activation domains significantly stimulated transcription through bacterially produced yeast TFIID only from nucleosome-assembled templates. These data indicate that acidic activation domains stimulate transcription by enhancing the ability of basal transcription factors to compete with nucleosomes for occupancy of the promoter. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP WORKMAN, JL (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 66 TC 209 Z9 209 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD FEB 8 PY 1991 VL 64 IS 3 BP 533 EP 544 DI 10.1016/0092-8674(91)90237-S PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EX361 UT WOS:A1991EX36100009 PM 1991320 ER PT J AU HOOPER, DC WOLFSON, JS AF HOOPER, DC WOLFSON, JS TI FLUOROQUINOLONE ANTIMICROBIAL AGENTS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID URINARY-TRACT INFECTIONS; INTRAVENOUS ORAL CIPROFLOXACIN; FEBRILE NEUTROPENIC PATIENTS; PELVIC INFLAMMATORY DISEASE; SINGLE-DOSE CIPROFLOXACIN; SOFT-TISSUE INFECTIONS; TRAVELERS DIARRHEA; CLINICAL EFFICACY; TRIMETHOPRIM-SULFAMETHOXAZOLE; RANDOMIZED TRIAL C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HOOPER, DC (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,INFECT DIS UNIT,32 FRUIT ST,BOSTON,MA 02114, USA. NR 125 TC 448 Z9 456 U1 7 U2 22 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 FEB 7 PY 1991 VL 324 IS 6 BP 384 EP 394 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA EW296 UT WOS:A1991EW29600006 PM 1987461 ER PT J AU THOR, A BENZ, C MOORE, D GOLDMAN, E EDGERTON, S LANDRY, J SCHWARTZ, L MAYALL, B HICKEY, E WEBER, LA AF THOR, A BENZ, C MOORE, D GOLDMAN, E EDGERTON, S LANDRY, J SCHWARTZ, L MAYALL, B HICKEY, E WEBER, LA TI STRESS RESPONSE PROTEIN (SRP-27) DETERMINATION IN PRIMARY HUMAN BREAST CARCINOMAS - CLINICAL, HISTOLOGIC, AND PROGNOSTIC CORRELATIONS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID HEAT-SHOCK PROTEIN; REGULATED 24K PROTEIN; PROGESTERONE RECEPTORS; GENE-TRANSCRIPTION; MOLECULAR-WEIGHT; PS2 GENE; EXPRESSION; CELLS; ESTROGEN; CANCER AB Expression of an estrogen-regulated protein known as the 27000-d heat-shock or stress-response protein (srp-27) was evaluated in human breast carcinomas and established breast cancer cell lines. Results obtained by Northern and Western blot analyses and immunohistochemical methods were concordant. Immunohistochemical assessment of srp-27 expression in 300 breast carcinomas (with median patient follow-up of 8 years) was performed. Twenty-six percent of lymph node-negative and 45% of lymph node-positive tumors were overexpressors. Univariate analysis demonstrated significant correlations between srp-27 overexpression and estrogen receptor (ER) content, pS2 protein expression, nodal metastases, advanced T stage, lymphatic/vascular invasion, and a shorter disease-free survival period (but not a shorter overall survival) for the study population as a whole. Regression tree analysis showed that srp-27 expression was an independent prognostic indicator for disease-free survival only in patients with one to three positive lymph nodes. The Cox proportional hazards model confirmed the independent prognostic significance of nodal involvement, T stage, and ER content but failed to recognize srp-27 overexpression as a significant independent parameter predictive of patient outcome in the patient population as a whole. The observed associations between srp-27 overexpression and more aggressive tumors suggest a biologic role for srp-27 in human breast carcinomas. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. UNIV CALIF LAWRENCE LIVERMORE NATL LAB,DIV BIOMED SCI,LIVERMORE,CA 94550. UNIV LAVAL,CANC RES CTR,QUEBEC CITY G1K 7P4,QUEBEC,CANADA. UNIV S FLORIDA,DEPT BIOL,TAMPA,FL 33620. RP THOR, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-46966, CA-44768]; NIGMS NIH HHS [GM-32381] NR 35 TC 159 Z9 160 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD FEB 6 PY 1991 VL 83 IS 3 BP 170 EP 178 DI 10.1093/jnci/83.3.170 PG 9 WC Oncology SC Oncology GA EW649 UT WOS:A1991EW64900007 PM 1988702 ER PT J AU DATTA, S MURPHY, MT CARR, DB BADER, AM JOHNSON, MD AF DATTA, S MURPHY, MT CARR, DB BADER, AM JOHNSON, MD TI MATERNAL AND FETAL PLASMA ATRIAL-NATRIURETIC-PEPTIDE CONCENTRATIONS DURING ELECTIVE CESAREAN-SECTION SO ACTA ANAESTHESIOLOGICA SCANDINAVICA LA English DT Article DE ANESTHESIA, SPINAL; ATRIAL NATRIURETIC PEPTIDE; CESAREAN SECTION; PREGNANCY ID NORMAL-PREGNANCY; HUMAN-FETUS; BLOOD; HORMONE AB Atrial natriuretic peptide (ANP) is stored in the atrial cardiocyte and is capable of exerting potent, selective, and transient effects on fluid and electrolyte balance and on blood pressure. Because fluid shifts and hemodynamic adjustments occur during parturition, ANP might play a homeostatic role in the parturient and fetoplacental unit. We measured maternal and fetal plasma ANP concentrations in 19 parturients during elective caesarean section. Plasma ANP levels were also measured in seven nonpregnant women of the same age group. The baseline ANP concentration in parturients was significantly higher (29.77 +/- 6.06 pg/ml vs 7.37 +/- 2.1 pg/ml; mean +/- s.e.mean) than in their nonpregnant counterparts. The umbilical artery (UA) ANP concentration was significantly higher than the umbilical vein concentration (91.91 +/- 14.91 pg/ml vs. 40.04 +/- 9.71 pg/ml). Factors under the anaesthesiologist's control may influence maternal and fetal plasma ANP levels. There was a significant correlation between the volume of maternal Ringer's lactate infusion received and maternal ANP concentration. A significant correlation was seen between the total dose of ephedrine administered acutely prior to delivery and the UA ANP concentration. These data suggest that: 1) increased blood volume during pregnancy is associated with increased maternal plasma ANP levels, and 2) the fetus can produce its own ANP, and is thereby capable of responding to ANP stimulating factors. C1 MASSACHUSETTS GEN HOSP,ANALGES PEPTIDE RES UNIT,BOSTON,MA 02114. RP DATTA, S (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT ANAESTHESIA,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 16 TC 12 Z9 12 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-5172 J9 ACTA ANAESTH SCAND JI Acta Anaesthesiol. Scand. PD FEB PY 1991 VL 35 IS 2 BP 93 EP 96 PG 4 WC Anesthesiology SC Anesthesiology GA EY354 UT WOS:A1991EY35400001 PM 1827231 ER PT J AU POZNANSKY, MC LEVER, A RICHARDSON, J HASELTINE, WA SODROSKI, J AF POZNANSKY, MC LEVER, A RICHARDSON, J HASELTINE, WA SODROSKI, J TI HIV-1 AS A VECTOR FOR GENE TRANSDUCTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115. ST GEORGE HOSP,SCH MED,LONDON,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 129 EP 130 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000013 ER PT J AU LANGHOFF, E TERWILLIGER, E BOS, HJ POZNANSKY, M SODROSKI, J HASELTINE, WA AF LANGHOFF, E TERWILLIGER, E BOS, HJ POZNANSKY, M SODROSKI, J HASELTINE, WA TI HIV-1 GROWTH IN PRIMARY-CELL ISOLATES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,DEPT CANC BIOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 175 EP 175 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000095 ER PT J AU TERWILLIGER, EF LANGHOFF, E HASELTINE, WA AF TERWILLIGER, EF LANGHOFF, E HASELTINE, WA TI A NEW ROLE FOR THE NEF GENE OF HIV SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,DEPT CANC BIOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 180 EP 180 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000104 ER PT J AU RUPRECHT, RM SOSA, G DEGASPERI, R BERNARD, LD HALL, J FAZELY, F AF RUPRECHT, RM SOSA, G DEGASPERI, R BERNARD, LD HALL, J FAZELY, F TI DOWN REGULATION OF HIV-1 PRODUCTION AND GENE-EXPRESSION MEDIATED BY THE HIV-1 LTR IN NEF-EXPRESSING CELL-LINES SO AIDS RESEARCH AND HUMAN RETROVIRUSES 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 MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 181 EP 181 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000106 ER PT J AU REINHERZ, EL AF REINHERZ, EL TI LYMPHOCYTES-T - A 1990 PERSPECTIVE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 183 EP 183 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000110 ER PT J AU REPKE, H KAUFMANN, R ULBRICHT, S BUCHNER, K HUCHO, F KALYANARAMAN, VS PYLE, S HASELTINE, W SCHOLZ, D SCHMIDT, HE AF REPKE, H KAUFMANN, R ULBRICHT, S BUCHNER, K HUCHO, F KALYANARAMAN, VS PYLE, S HASELTINE, W SCHOLZ, D SCHMIDT, HE TI COMPARATIVE BINDING-STUDIES REVEAL A VERY HIGH-AFFINITY CD4 BINDING OF GP120 RELEASED FROM HIV-1 INFECTED-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HUMBOLDT UNIV,BEREICH MED CHARITE,INST PHARMACOL & TOXICOL,O-1040 BERLIN,GERMANY. HUMBOLDT UNIV,BEREICH MED CHARITE,INST VIROL,O-1040 BERLIN,GERMANY. FREE UNIV BERLIN,INST BIOCHEM,W-1000 BERLIN 33,GERMANY. ADV BIOSCI LABS INC,KENSINGTON,MD 20895. PROGRAM RESOURCES INC,AIDS VACCINE PROGRAM,FREDERICK,MD 21701. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. ACAD SCI GDR,INST ISOTOPE RES,O-1115 BERLIN,GERMANY. NR 0 TC 4 Z9 4 U1 0 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 200 EP 200 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000138 ER PT J AU PAUL, JR JOHNSON, VA TROCHA, A WALKER, BD AF PAUL, JR JOHNSON, VA TROCHA, A WALKER, BD TI INHIBITION OF HIV-1 REPLICATION INVITRO BY HIV-1-SPECIFIC CYTOTOXIC LYMPHOCYTE-T CLONES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD FEB PY 1991 VL 7 IS 2 BP 205 EP 205 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA EY300 UT WOS:A1991EY30000146 ER PT J AU PROVENZALE, J DELUCA, SA AF PROVENZALE, J DELUCA, SA TI TUBEROUS SCLEROSIS SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Tuberous sclerosis is an inherited disorder characterized by a triad of signs-mental retardation, seizures and adenoma sebaceum. The hamartomas that commonly affect multiple organ systems can be seen on plain film radiography. Computed tomography and ultrasonography are useful for assessing whether lesions are present in the abdomen, kidneys and brain. The hamartomas tend to bleed, causing symptoms and prompting the need for evaluation. RP PROVENZALE, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD FEB PY 1991 VL 43 IS 2 BP 470 EP 472 PG 3 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA EV963 UT WOS:A1991EV96300010 PM 1990733 ER PT J AU HUANG, PL BROOKS, R CARPENTER, C GARAN, H AF HUANG, PL BROOKS, R CARPENTER, C GARAN, H TI ANTIARRHYTHMIC THERAPY GUIDED BY PROGRAMMED ELECTRICAL-STIMULATION IN CARDIAC SARCOIDOSIS WITH VENTRICULAR-TACHYCARDIA SO AMERICAN HEART JOURNAL LA English DT Note C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA 02114. NR 6 TC 13 Z9 13 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD FEB PY 1991 VL 121 IS 2 BP 599 EP 601 DI 10.1016/0002-8703(91)90734-Y PN 1 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA EW634 UT WOS:A1991EW63400029 PM 1990769 ER PT J AU WANG, CC AF WANG, CC TI IMPROVED LOCAL-CONTROL OF NASOPHARYNGEAL CARCINOMA AFTER INTRACAVITARY BRACHYTHERAPY BOOST SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS LA English DT Article DE CARCINOMA OF NASOPHARYNX; NASOPHARYNGEAL BRACHYTHERAPY BOOST ID RADIATION-THERAPY; IRRADIATION AB In 1976 we began using intracavitary cesium boost technique as a portion of comprehensive treatment of primary T2 and T3 nasopharyngeal carcinoma. At first, we offered this procedure sporadically to patients with T1 lesions. For the past 10 years, intracavitary boost has been offered to all patients except those with T4 lesions. The radiation therapy program consists of external beam dose of 60-64 Gy, either once daily (q.d.) or twice daily (b.i.d.) schedule, followed by 10-15 Gy boost to mucosal surface by intracavitary implant, making a total of approximately 75 Gy. This article presents the experience at the Massachusetts General Hospital with 146 patients with T1-3 carcinoma of the nasopharynx irradiated from 1970 through 1988. Seventy-six patients were treated with intracavitary boost and 70 patients were treated up to 65-70 Gy by external beam alone. The overall 5-year actuarial local control rate for the T1 lesions was 93% after radiation therapy and intracavitary boost as compared with 54% without brachytherapy boost (p value = 0.057). For the T1-2 lesions, the corresponding local rates after external radiation therapy and brachytherapy boost and after external beam irradiation without boost were 90 and 59%, respectively, with p = 0.001. For the T3 lesions, the rates were 100 and 64%, respectively, with p = 0.090. The reason for improved local control is unclear and may be due to a somewhat higher mucosal dose to the nasopharynx. Hopefully, the improved beneficial local control effects may be reflected in improved patient survival. However, such data required a controlled randomized clinical trial for confirmation. C1 HARVARD UNIV,SCH MED,DEPT RADIAT THERAPY,BOSTON,MA 02115. RP WANG, CC (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DEPT RADIAT MED,BOSTON,MA 02114, USA. NR 12 TC 71 Z9 81 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 FEB PY 1991 VL 14 IS 1 BP 5 EP 8 PG 4 WC Oncology SC Oncology GA EV479 UT WOS:A1991EV47900002 PM 1987739 ER PT J AU ENGSTROM, PF RYAN, LM FALKSON, G HALLER, DG AF ENGSTROM, PF RYAN, LM FALKSON, G HALLER, DG TI PHASE-II STUDY OF AMINOTHIADIAZOLE IN ADVANCED SQUAMOUS-CELL CARCINOMA OF THE ESOPHAGUS SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS LA English DT Article DE ESOPHAGEAL SQUAMOUS CELL CARCINOMA; AMINOTHIADIAZOLE; ALLOPURINOL; PHASE-II TRIAL ID 2-AMINO-1,3,4-THIADIAZOLE AB Twenty-three patients with advanced inoperable squamous cell carcinoma of the esophagus were treated with aminothiadiazole (A-TD) 125 mg/m2 weekly plus allopurinol daily in a phase II cooperative group trial. No patients responded to treatment; 17 patients progressed, three showed stable disease, and three were unevaluable. There were no life-threatening hematologic or metabolic toxicities. The median survival from study entry was 5 months. A-TD is not active in advanced squamous cell carcinoma of the esophagus. C1 FOX CHASE CANC INST,PHILADELPHIA,PA 19111. HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV PRETORIA,PRETORIA,SOUTH AFRICA. HOSP UNIV PENN,PHILADELPHIA,PA 19104. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 FU NCI NIH HHS [CA 18281, CA 21115, CA 23318] NR 8 TC 12 Z9 12 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 FEB PY 1991 VL 14 IS 1 BP 33 EP 35 DI 10.1097/00000421-199102000-00007 PG 3 WC Oncology SC Oncology GA EV479 UT WOS:A1991EV47900007 PM 1987735 ER PT J AU RANSOM, DT NEUBERG, D LOPRINZI, CL TORMEY, DC BLUM, RH HARRIS, JE ASBURY, RF FALKSON, G AF RANSOM, DT NEUBERG, D LOPRINZI, CL TORMEY, DC BLUM, RH HARRIS, JE ASBURY, RF FALKSON, G TI A PILOT-STUDY OF 3 SEQUENTIAL CHEMOTHERAPEUTIC REGIMENS IN METASTATIC BREAST-CANCER SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS LA English DT Article DE BREAST CANCER; CHEMOTHERAPY; CYCLOPHOSPHAMIDE; DOXORUBICIN; 5-FLUOROURICIL; DIBROMODULCITOL; MITOXANTRONE; VINBLASTINE; THIOTEPA; VINCRISTINE ID PHASE II; ADRIAMYCIN; DIBROMODULCITOL; THERAPY; METHOTREXATE; VINBLASTINE; THIOTEPA; VATH AB The aim of this pilot study was to estimate the toxicity and response rate of an alternating chemotherapeutic program in chemotherapy-naive metastatic breast cancer patients. Treatment consisted of regimen A (given days 1-28): cyclophosphamide 100 mg/m2 PO days 1-14, doxorubicin 30 mg/m2 i.v. days 1 and 8, and 5-fluorouracil 500 mg/m2 i.v. days 1 and 8 (CAF regimen); regimen B (given days 29-56): dibromodulcitol 135 mg/m2 p.o. days 30-39, mitoxantrone 9 mg/m2 i.v. day 29, and vincristine 1.2 mg/m2 i.v. (maximum 2.0 mg) day 29 (DMV regimen); and regimen C (given days 57-84): thiotepa 12 mg/m2, doxorubicin 45 mg/m2 and vinblastine 4.5 mg/m2 all i.v. on day 57. There were 27 eligible patients with a median age of 51 years (range 34-78). On 14 episodes the leukocyte count fell to < 1 x 10(9)/L during the first six cycles of treatment (14% of 99 cycles). There were no treatment-related deaths. Common non-life-threatening toxicities included thrombocytopenia, anemia, vomiting, and alopecia. Despite having no drugs in common, the leukocyte and platelet nadirs after CAF correlated with the nadir counts after DMV (r values of 0.6829 and 0.5892, respectively; p = 0.01). Among the 23 patients with measurable and/or evaluable disease there were five complete responses (22%) and nine partial responses (39%), with a median time to treatment failure of 29 weeks. The overall median survival was 19 months. C1 HARVARD UNIV, SCH PUBL HLTH, DANA FARBER CANC INST, BOSTON, MA 02115 USA. UNIV WISCONSIN, CTR CLIN CANC, MADISON, WI 53706 USA. NYU MED CTR, NEW YORK, NY 10016 USA. RUSH PRESBYTERIAN ST LUKES MED CTR, CHICAGO, IL 60612 USA. GENESEE HOSP, ROCHESTER, NY 14607 USA. UNIV PRETORIA, PRETORIA 0002, SOUTH AFRICA. RP MAYO CLIN & MAYO FDN, DEPT ONCOL, ROCHESTER, MN 55905 USA. FU NCI NIH HHS [CA-21115, CA-23318, CA-13650] NR 11 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0277-3732 EI 1537-453X J9 AM J CLIN ONCOL-CANC JI Am. J. Clin. Oncol.-Cancer Clin. Trials PD FEB PY 1991 VL 14 IS 1 BP 45 EP 48 DI 10.1097/00000421-199102000-00010 PG 4 WC Oncology SC Oncology GA EV479 UT WOS:A1991EV47900010 PM 1898999 ER PT J AU LINDGRENFURMAGA, EM SCHUNA, AA WOLFF, NL GOODFRIEND, TL AF LINDGRENFURMAGA, EM SCHUNA, AA WOLFF, NL GOODFRIEND, TL TI COST OF SWITCHING HYPERTENSIVE PATIENTS FROM ENALAPRIL MALEATE TO LISINOPRIL SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article DE COSTS; DOSAGE; ECONOMICS; ENALAPRIL MALEATE; EQUIVALENCY, THERAPEUTIC; HYPERTENSION; HYPOTENSIVE AGENTS; LISINOPRIL ID MK421; MK521 AB The costs and potential savings associated with switching patients in a hypertension clinic from enalapril maleate to lisinopril were analyzed. Patients taking enalapril were randomized to receive lisinopril or to continue taking enalapril. For the 47 patients randomized, data were collected for 25 patients switched to an equal milligram dosage of lisinopril and for 21 patients who continued to receive a constant dosage of enalapril. To maintain blood pressure control, it was necessary to double the dosage of lisinopril in five patients (20%) and halve it in one patient (4%), while the enalapril dosage was doubled in two patients (9.5%). The total direct cost of switching patients to lisinopril was $66.33 per patient. The annual drug cost savings per patient for switching to lisinopril would be $52.08, $46.80, and $120.24 for therapy with one 5-, 10-, and 20-mg tablet per day, respectively. A patient would have to receive 15, 17, or 7 months of therapy with 5-, 10-, or 20-mg tablets of lisinopril, respectively, before a net cost savings would be realized. In the evaluation of a less expensive therapeutic alternative, the total cost of switching must be considered. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PHARM SERV,MADISON,WI 53705. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,HLTH SERV RES,MADISON,WI 53705. UNIV WISCONSIN,DEPT PREVENT MED,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. RP LINDGRENFURMAGA, EM (reprint author), UNIV ILLINOIS,COLL PHARM,DEPT PHARM PRACTICE,MC 886,ROOM 244,833 S WOOD ST,CHICAGO,IL 60680, USA. NR 8 TC 19 Z9 19 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD FEB PY 1991 VL 48 IS 2 BP 276 EP 279 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EV467 UT WOS:A1991EV46700023 PM 1848392 ER PT J AU KINTZEL, PE KENNEDY, PE AF KINTZEL, PE KENNEDY, PE TI STABILITY OF AMPHOTERICIN-B IN 5-PERCENT DEXTROSE INJECTION AT CONCENTRATIONS USED FOR ADMINISTRATION THROUGH A CENTRAL VENOUS LINE SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article DE ADDITIVES; AMPHOTERICIN-B; ANTIFUNGALS; CONCENTRATION; DEXTROSE; INCOMPATIBILITIES; INJECTIONS; STABILITY; STORAGE; TEMPERATURE; VEHICLES AB The stability of amphotericin B in 5% dextrose injection was studied at concentrations used for administration through a central venous line. Amphotericin B 60, 80, and 100 mg was diluted in 50 mL of 5% dextrose injection; final mean +/- S.D. concentrations after adjustment for total volume were 0.92 +/- 0.01, 1.20 +/- 0.03, and 1.40 +/- 0.03 mg/mL, respectively. For each concentration, six admixtures were prepared; of these, three were stored at 25-degrees-C and three at 6-degrees-C. Amphotericin B concentration was tested at 0, 4, 12, 24, and 36 hours by stability-indicating high-performance liquid chromatography. The admixtures were inspected visually at each time point for precipitation, turbidity, gas formation, and color change, and the pH was measured. Concentrations of amphotericin B remained within 3% of initial concentrations at each time point at both storage temperatures. No precipitation, turbidity, gas formation, or color change was observed, and no changes in pH were measured. Amphotericin B in 5% dextrose injection was stable at concentrations of 0.92, 1.20, and 1.40 mg/mL when stored at 6 and 25-degrees-C for up to 36 hours. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NIH,WARREN G MAGNUSON CLIN CTR,PHARMACEUT DEV SERV,ANALYT LAB,BETHESDA,MD 20892. RP KINTZEL, PE (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284, USA. NR 7 TC 14 Z9 14 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD FEB PY 1991 VL 48 IS 2 BP 283 EP 285 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EV467 UT WOS:A1991EV46700025 PM 2003501 ER PT J AU KLEYMAN, TR ZEBROWITZ, JR AF KLEYMAN, TR ZEBROWITZ, JR TI DISTINCT EPITOPES ON AMILORIDE .2. VARIABLY RESTRICTED EPITOPES DEFINED BY MONOCLONAL ANTI-AMILORIDE ANTIBODIES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE EPITHELIAL SODIUM CHANNEL; SODIUM-HYDROGEN EXCHANGER; AMILORIDE ANTIBODIES ID SODIUM-TRANSPORT; RECEPTOR; ANALOGS; INHIBITION; EXCHANGE; HORMONE; PROBE AB Specific regions of amiloride appear to participate in binding to receptors on amiloride-sensitive transport proteins. Previous studies characterizing epitopes on amiloride recognized by anti-amiloride antibodies have demonstrated that antibodies recognize specific domains on amiloride and that these epitopes are determined, in part, by the site on amiloride used to couple to carrier protein. The 3,5-diaminopyrazinyl and guanidinocarbonyl moieties were identified as distinct epitopes. Since Na+-selective transport proteins are sensitive to changes of the halide on the amiloride molecule, additional monoclonal anti-amiloride antibodies were raised to determine whether the C-6 halo group of amiloride could be identified as an important site for drug-antibody binding. The epitopes recognized by a series of three monoclonal antibodies raised against amiloride coupled to rabbit serum albumin through its C-5 NH2-group were defined. Two antibodies recognize extensive regions on the amiloride molecule, including both the acylguanidino and pyrazinyl groups. In addition, both antibodies are sensitive to changes in the C-6 halo group on amiloride. A third antibody was relatively insensitive to changes in the halide in the C-6 position of the pyrazine ring of amiloride and recognized a more restricted epitope on amiloride. C1 UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP KLEYMAN, TR (reprint author), UNIV PENN,DEPT MED,RENAL & ELECTROLYTE SECT,700 CRB,PHILADELPHIA,PA 19104, USA. NR 20 TC 4 Z9 4 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 FEB PY 1991 VL 260 IS 2 BP C271 EP C276 PN 1 PG 6 WC Physiology SC Physiology GA EY855 UT WOS:A1991EY85500013 PM 1705099 ER PT J AU ODA, A DALEY, JF KANG, JG SMITH, M WARE, JA SALZMAN, EW AF ODA, A DALEY, JF KANG, JG SMITH, M WARE, JA SALZMAN, EW TI QUASI-SIMULTANEOUS MEASUREMENT OF IONIZED CALCIUM AND ALPHA-GRANULE RELEASE IN INDIVIDUAL PLATELETS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE FLOW CYTOMETRY; INDO-1; CALCIUM CHANNEL ID FURA-2-LOADED HUMAN-PLATELETS; FLOW-CYTOMETRY; PLASMA-MEMBRANE; ACTIVATION; THROMBIN; SECRETION; RECEPTOR; ADP; HETEROGENEITY; MOBILIZATION AB The effect of alpha-thrombin and ADP on calcium mobilization and alpha-granule release in individual platelets was investigated by flow cytometry. alpha-Thrombin (4.5 nM) caused a uniform rise of free cytosolic calcium ([Ca2+]i) among indo-1-loaded human platelets. Despite the uniformity of this effect, approximately 20% of the cells failed to secrete alpha-granule content, as shown by binding of fluorescein isothiocyanate (FITC)-conjugated S12 monoclonal antibody. ADP (10-mu-M) caused a similar brisk and uniform rise of calcium but did not increase S12 binding to any platelets. On the other hand, with alpha-thrombin (0.5 nM), calcium mobilization was heterogeneous and paralleled granule release. [Ca2+]i increase rapidly in some platelets, while only slowly in others. When an electronic gate was set according to FITC-S12 fluorescence, cells with a greater secretory response proved to be those with a higher calcium level. With both alpha-thrombin and ADP, chelation of external calcium by EGTA (2 mM) reduced calcium response of individual cells. NiCl2 (1 mM) also inhibited calcium rise of individual platelets to the same extent as EGTA (2 mM) in spite of the presence of 1 mM CaCl2 in the extracellular media. The effects of EGTA and NiCl2 were not limited to a particular subpopulation of cells. These data suggest that the putative Ni2+ -inhibitable divalent cation channel(s) may be responsible for the increased influx of calcium that occurs during platelet activation by alpha-thrombin and ADP. It appears that these calcium channels contribute to the elevation of [Ca2+]i among virtually all the platelets. C1 BETH ISRAEL HOSP,DEPT SURG,330 BROOKLINE AVE,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-38820, HL-33014] NR 24 TC 16 Z9 16 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 FEB PY 1991 VL 260 IS 2 BP C242 EP C248 PN 1 PG 7 WC Physiology SC Physiology GA EY855 UT WOS:A1991EY85500009 PM 1847585 ER PT J AU BIEDERMAN, J FARAONE, SV KEENAN, K STEINGARD, R TSUANG, MT AF BIEDERMAN, J FARAONE, SV KEENAN, K STEINGARD, R TSUANG, MT TI FAMILIAL ASSOCIATION BETWEEN ATTENTION-DEFICIT DISORDER AND ANXIETY DISORDERS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DIAGNOSTIC INTERVIEW; PSYCHIATRIC-ILLNESS; CHILDREN; CHILDHOOD; PREVALENCE; MOTHERS AB Background and Method: This study tested hypotheses about patterns of familial association between attention deficit disorder (ADD) and anxiety disorders among 356 first-degree relatives of 73 clinically referred children with ADD and 26 normal comparison children. Through structured diagnostic interviews with trained raters, relatives were assessed for adult and childhood psychopathology. After stratifying the sample of ADD probands into those with anxiety disorders and those without, the authors examined patterns of aggregation of ADD and anxiety disorders in the relatives of these probands as well as in the relatives of the normal comparison subjects. Results: Familial risk analyses revealed that 1) familial risk for anxiety disorders was higher among all ADD probands than among the normal subjects; 2) familial risk for ADD was similar in the relatives of the ADD probands and of the probands with ADD and anxiety disorder; 3) the relatives of the ADD probands with and without anxiety disorders were at greater risk for ADD than the relatives of the normal subjects; 4) the risk for anxiety disorders was two times higher in the relatives of the probands who had ADD with anxiety disorder than in those of the ADD probands without anxiety disorders; and 5) there was a tendency for ADD probands' relatives who themselves had ADD to have a higher risk for anxiety disorders than ADD probands' relatives who did not have ADD (cosegregation). Conclusions: The results were most consistent with the hypotheses indicating that ADD and anxiety disorders segregate independently in families. C1 HARVARD UNIV,MASSACHUSETTS MENTAL HLTH CTR,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. BROCKTON W ROXBURY VET ADM MED CTR,PSYCHIAT SERV,BOSTON,MA. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH-41314] NR 29 TC 124 Z9 126 U1 4 U2 6 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 FEB PY 1991 VL 148 IS 2 BP 251 EP 256 PG 6 WC Psychiatry SC Psychiatry GA EV209 UT WOS:A1991EV20900020 PM 1987825 ER PT J AU SAINI, S MODIC, MT HAMM, B HAHN, PF AF SAINI, S MODIC, MT HAMM, B HAHN, PF TI ADVANCES IN CONTRAST-ENHANCED MR-IMAGING SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Review ID SUPERPARAMAGNETIC IRON-OXIDE; PULSE SEQUENCE OPTIMIZATION; ACUTE MYOCARDIAL-INFARCTION; BENIGN EXTRAAXIAL TUMORS; LYMPH-NODE METASTASES; FOCAL SPLENIC TUMORS; GD-DTPA ENHANCEMENT; SOFT-TISSUE TUMORS; GADOLINIUM-DTPA; FERRITE PARTICLES C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. FREE UNIV BERLIN,SCH MED,W-1000 BERLIN 45,GERMANY. CLEVELAND CLIN EDUC FDN,DIV RADIOL,CLEVELAND,OH 44106. FREE UNIV BERLIN,KLINIKUM STEGLITZ,DEPT RADIOL,W-1000 BERLIN 45,GERMANY. RP SAINI, S (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 142 TC 39 Z9 39 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 FEB PY 1991 VL 156 IS 2 BP 235 EP 254 PG 20 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EU535 UT WOS:A1991EU53500002 ER PT J AU LEE, MJ SAINI, S HAMM, B TAUPITZ, M HAHN, PF SENETERRE, E FERRUCCI, JT AF LEE, MJ SAINI, S HAMM, B TAUPITZ, M HAHN, PF SENETERRE, E FERRUCCI, JT TI FOCAL NODULAR HYPERPLASIA OF THE LIVER - MR FINDINGS IN 35 PROVED CASES SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID HEPATOCELLULAR-CARCINOMA; HEPATIC-TUMORS; GD-DTPA AB MR images of 28 patients with 35 lesions of hepatic focal nodular hyperplasia were reviewed to determine the frequency of findings considered typical of this condition (isointensity on T1- and T2-weighted pulse sequences, a central hyperintense scar on T2-weighted images, and homogeneous signal intensity). Fifteen lesions were imaged at 0.6 T with T1- and T2-weighted spin-echo (SE) pulse sequences; 20 lesions were imaged at 1.5 T with T1-weighted SE and gradient-echo pulse sequences and T2-weighted SE pulse sequences. Diagnosis of focal nodular hyperplasia was made pathologically in 25 patients, with nuclear scintigraphy in four, and with follow-up imaging in six. Only seven lesions (20%) were isointense relative to normal liver on both T1- and T2-weighted SE images. On T1-weighted SE images, 21 lesions (60%) were isointense relative to normal liver, 12 (34%) were hypointense, and two (6%) were hyperintense. On T2-weighted SE images, 12 lesions (34%) were isointense and 23 (66%) were hyperintense relative to normal liver. A central scar was present in 17 lesions (49%) and was hypointense relative to the lesion on T1-weighted images and hyperintense on T2-weighted images. Twenty lesions (57%) were of homogeneous signal intensity throughout the lesion, except for the presence of a central scar. All three MR imaging characteristics were present in three cases (9%). We conclude that hepatic focal nodular hyperplasia has a wide range of signal intensity on MR imaging. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. FREE UNIV BERLIN,KLINIKUM STEGLITZ,DEPT RADIOL,W-1000 BERLIN 45,GERMANY. NR 11 TC 77 Z9 77 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 FEB PY 1991 VL 156 IS 2 BP 317 EP 320 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EU535 UT WOS:A1991EU53500013 PM 1898806 ER PT J AU ZUKERBERG, LR ROSENBERG, AE RANDOLPH, G PILCH, BZ GOODMAN, ML AF ZUKERBERG, LR ROSENBERG, AE RANDOLPH, G PILCH, BZ GOODMAN, ML TI SOLITARY FIBROUS TUMOR OF THE NASAL CAVITY AND PARANASAL SINUSES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE SOLITARY FIBROUS TUMOR; FIBROUS MESOTHELIOMA; NASAL CAVITY; PARANASAL SINUSES ID NON-EPITHELIAL TUMORS; NONEPITHELIAL TUMORS; NASOPHARYNX; MESOTHELIOMA; PLEURA AB We report two solitary fibrous tumors of the nasal cavity and paranasal sinuses that were histologically and immunohistochemically virtually identical to solitary fibrous tumors (fibrous mesotheliomas) of the pleura. One tumor arose in a 48-year-old woman and the other in a 45-year-old woman. Both patients presented with nasal symptoms, and both patients are alive without evidence of disease 6 months and 1 year after excision. The tumors had a disorganized or "patternless" arrangement of spindle cells in a collagenous background and prominent vascular channels of varying size. Immunoperoxidase stains on paraffin sections showed staining of the cells for vimentin only; there was no staining for keratin, S-100 protein, desmin, and actin. Both cases presented some degree of diagnostic difficulty and had to be distinguished from other spindle cell tumors of the nasal cavity and paranasal sinuses, such as hemangiopericytoma, angiofibroma, and fibrous histiocytoma. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR HOSP,DEPT EAR NOSE & THROAT PATHOL,BOSTON,MA 02114. RP ZUKERBERG, LR (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,WARREN 2,BOSTON,MA 02114, USA. NR 22 TC 125 Z9 127 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 FEB PY 1991 VL 15 IS 2 BP 126 EP 130 DI 10.1097/00000478-199102000-00004 PG 5 WC Pathology; Surgery SC Pathology; Surgery GA EU738 UT WOS:A1991EU73800004 PM 1989459 ER PT J AU MALUF, HM KING, ME DELUCA, FR NAVARRO, J TALERMAN, A YOUNG, RH AF MALUF, HM KING, ME DELUCA, FR NAVARRO, J TALERMAN, A YOUNG, RH TI GIANT MULTILOCULAR PROSTATIC CYSTADENOMA - A DISTINCTIVE LESION OF THE RETROPERITONEUM IN MEN - A REPORT OF 2 CASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE PROSTATE; RETROPERITONEUM; MULTILOCULAR CYSTADENOMA AB Two examples of large, multiloculated, cystic tumors that arose within the pelvis in men of 28 and 37 years of age are described. The tumors were composed of glands and cysts lined by prostatic-type epithelium lying in a hypocellular fibrous stroma. The prostatic nature of the lesions was confirmed by immunohistochemical staining of the epithelium for prostate-specific antigen and prostatic acid phosphatase. Two apparently similar lesions were found in the literature; one tumor was attached to the prostate by a pedicle, and the other arose in the retrovesical space. These tumors, for which we propose the designation "giant multilocular prostatic cystadenoma," appear to be benign, although they may recur if incompletely excised. They may pose considerable diagnostic difficulty if the prostatic nature of the epithelium is not appreciated, an error that is likely if a relationship to the prostate is not recognized. This lesion should be included in the differential diagnosis of retroperitoneal cystic tumors in men. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HOSP CORDOBA,CORDOBA,ARGENTINA. UNIV ILLINOIS,COLL MED,DEPT PATHOL,CHICAGO,IL 60680. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10461. THOMAS JEFFERSON UNIV,DEPT PATHOL & CELL BIOL,PHILADELPHIA,PA 19107. NR 13 TC 26 Z9 29 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 FEB PY 1991 VL 15 IS 2 BP 131 EP 135 DI 10.1097/00000478-199102000-00005 PG 5 WC Pathology; Surgery SC Pathology; Surgery GA EU738 UT WOS:A1991EU73800005 PM 1989460 ER PT J AU BANNON, MG AF BANNON, MG TI TERMINATION OF HICCUPS OCCURRING UNDER ANESTHESIA SO ANESTHESIOLOGY LA English DT Letter RP BANNON, MG (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 6 TC 3 Z9 3 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 FEB PY 1991 VL 74 IS 2 BP 385 EP 385 DI 10.1097/00000542-199102000-00038 PG 1 WC Anesthesiology SC Anesthesiology GA EV645 UT WOS:A1991EV64500038 PM 1990922 ER PT J AU PHILBIN, DM ROSOW, CE SCHNEIDER, RC KOSKI, G DAMBRA, MN AF PHILBIN, DM ROSOW, CE SCHNEIDER, RC KOSKI, G DAMBRA, MN TI FENTANYL AND SUFENTANIL ANESTHESIA REVISITED - ESTABLISH AN EFFECTIVE PLASMA-CONCENTRATION AND ACHIEVE IT AT THE RIGHT TIME - REPLY SO ANESTHESIOLOGY LA English DT Letter RP PHILBIN, DM (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. 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 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD FEB PY 1991 VL 74 IS 2 BP 389 EP 390 DI 10.1097/00000542-199102000-00044 PG 2 WC Anesthesiology SC Anesthesiology GA EV645 UT WOS:A1991EV64500044 ER PT J AU KOWALL, NW BEAL, MF AF KOWALL, NW BEAL, MF TI GLUTAMATE-IMMUNOREACTIVE, GLUTAMINASE-IMMUNOREACTIVE, AND TAURINE-IMMUNOREACTIVE NEURONS DEVELOP NEUROFIBRILLARY TANGLES IN ALZHEIMERS-DISEASE SO ANNALS OF NEUROLOGY LA English DT Article ID CEREBRAL-CORTEX; SENILE DEMENTIA; ACID DECARBOXYLASE; RAT-BRAIN; PLAQUES; ANTIBODY; LOCALIZATION; POSTMORTEM; NEOCORTEX; PRESENILE AB Although formation of neurofibrillary tangles is a major pathological feature of Alzheimer's disease (AD), the neurotransmitter content of neurofibrillary tangle-bearing neurons has not been well characterized. We studied the hippocampus of 6 patients with pathologically verified AD and 6 control subjects using a monoclonal antibody to glutamyl-glutamate and polyclonal antisera against glutaminase and taurine. In normal hippocampus, glutamate and glutaminase stained pyramidal neurons in the cornu ammonis (CA) fields and the subiculum, as well as the dentate granule cells. Fiber staining was better seen with glutamate antisera, which in AD specimens showed reduced numbers of glutamate-immunoreactive fibers in the molecular layer of the dentate gyrus. In AD specimens, glutamate- and glutaminase-immunoreactive pyramidal neurons in the hippocampal CA fields were decreased in number and remaining neurons showed irregular shortened and disorganized dendritic fields. Taurine immunoreactivity was localized to a subset of hippocampal pyramidal neurons, which showed similar degenerative changes in AD specimens. Glutamate-, glutaminase-, and taurine-stained neurons were found to contain neurofibrillary tangles using either double immunofluorescence with tau antisera, double immunoperoxidase stains, or silver and thioflavine S counterstains. These studies show that two distinct neurochemically defined populations of pyramidal neurons in allocortex frequently show degenerative changes and develop neurofibrillary tangles in AD. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KOWALL, NW (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114, USA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NIA NIH HHS [IP50 AG 05134] NR 37 TC 57 Z9 58 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD FEB PY 1991 VL 29 IS 2 BP 162 EP 167 DI 10.1002/ana.410290208 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA EW939 UT WOS:A1991EW93900007 PM 1672808 ER PT J AU FONTAINE, B HANSON, MP VONSATTEL, JP MARTUZA, RL GUSELLA, JF AF FONTAINE, B HANSON, MP VONSATTEL, JP MARTUZA, RL GUSELLA, JF TI LOSS OF CHROMOSOME-22 ALLELES IN HUMAN SPORADIC SPINAL SCHWANNOMAS SO ANNALS OF NEUROLOGY LA English DT Article ID BILATERAL ACOUSTIC NEUROFIBROMATOSIS; GENETIC-LINKAGE; TUMORS; CANCER AB Acoustic neuromas occur either as sporadic solitary tumors in the general population or as inherited bilateral tumors typically in patients with neurofibromatosis type 2. Loss of heterozygosity for markers on the long arm of chromosome 22 has been reported in both instances, and neurofibromatosis type 2 has been genetically linked to a marker on the long arm of this autosome, suggesting that a unique locus on chromosome 22 is implicated in tumorigenesis of both sporadic and inherited acoustic neuromas. To determine whether the locus for neurofibromatosis type 2 might also be responsible for tumorigenesis of those schwannomas distinct from acoustic neuromas in people without neurofibromatosis type 2, we studied the DNA content of three sporadic spinal schwannomas. In all three, we found loss of heterozygosity for at least three markers on the long arm of chromosome 22, indicating a partial or total monosomy 22 in the tumor. Our results suggest that a locus on chromosome 22 is responsible for tumorigenesis in schwann cells regardless of their location in the central nervous system, and that some other mechanism (genetic or nongenetic) might account for the relative high proportion of schwannomas developing from the eighth cranial nerve. C1 MASSACHUSETTS GEN HOSP,CTR NEUROSCI,MOLEC NEUROGENET LAB,13TH ST,BLDG 149,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA. FU NINDS NIH HHS [NS22224, NS20012, NS24279] NR 19 TC 26 Z9 26 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD FEB PY 1991 VL 29 IS 2 BP 183 EP 186 DI 10.1002/ana.410290211 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA EW939 UT WOS:A1991EW93900010 PM 2012386 ER PT J AU COIFFIER, B SHIPP, MA CABANILLAS, F CROWTHER, D ARMITAGE, JO CANELLOS, GP AF COIFFIER, B SHIPP, MA CABANILLAS, F CROWTHER, D ARMITAGE, JO CANELLOS, GP TI REPORT OF THE 1ST WORKSHOP ON PROGNOSTIC FACTORS IN LARGE-CELL LYMPHOMAS SO ANNALS OF ONCOLOGY LA English DT Editorial Material ID NON-HODGKINS LYMPHOMA; DIFFUSE HISTIOCYTIC LYMPHOMA; UNDIFFERENTIATED LYMPHOMA; AGGRESSIVE LYMPHOMAS; MALIGNANT-LYMPHOMAS; DNA CONTENT; M-BACOD; T-CELL; CHEMOTHERAPY; SURVIVAL C1 CHRISTIE HOSP & HOLT RADIUM INST,CANC RES CAMPAIGN,DEPT MED ONCOL,MANCHESTER M20 9BX,LANCS,ENGLAND. UNIV NEBRASKA,MED CTR,DEPT INTERNAL MED,OMAHA,NE 68105. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV TEXAS,MD ANDERSON HOSP & TUMOR INST,DEPT LYMPHOMA,HOUSTON,TX 77030. DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA. RP COIFFIER, B (reprint author), CTR HOSP LYON SUD,SERV HEMATOL,F-69310 PIERRE BENITE,FRANCE. NR 44 TC 23 Z9 23 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 FEB PY 1991 VL 2 SU 2 BP 213 EP 217 PG 5 WC Oncology SC Oncology GA FB412 UT WOS:A1991FB41200034 PM 1675583 ER PT J AU RICE, LB ELIOPOULOS, GM WENNERSTEN, C GOLDMANN, D JACOBY, GA MOELLERING, RC AF RICE, LB ELIOPOULOS, GM WENNERSTEN, C GOLDMANN, D JACOBY, GA MOELLERING, RC TI CHROMOSOMALLY MEDIATED BETA-LACTAMASE PRODUCTION AND GENTAMICIN RESISTANCE IN ENTEROCOCCUS-FAECALIS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID GROUP-D STREPTOCOCCI; STAPHYLOCOCCUS-AUREUS; PLASMID; TRANSPOSON; GENE; PENICILLINASE; ERYTHROMYCIN; SEQUENCE; STRAINS; INVITRO AB We have analyzed four distinct strains of multiply resistant, beta-lactamase-producing enterococci isolated during an outbreak of colonization with these strains on an infant-toddler surgical ward at The Children's Hospital in Boston, Mass. All four strains were resistant to erythromycin, penicillin, and tetracycline and to high levels of gentamicin and streptomycin. One strain was also resistant to chloramphenicol. Plasmid profiles revealed four different plasmid patterns, with the number of identified plasmids ranging from zero to three. The gene coding for beta-lactamase production could be transferred at low frequency (< 10(-8)) to an enterococcal recipient from one strain in conjunction with all of the other resistance determinants. Probes derived from the staphylococcal beta-lactamase gene and gentamicin resistance gene failed to hybridize with any of the detectable plasmids, but both genes were present on restriction fragments of genomic DNA in all strains. Our results indicate that the beta-lactamase genes and gentamicin resistance genes in these strains are integrated into the bacterial chromosome. The cotransmissibility of the resistance determinants raises the possibility of their incorporation into a multiresistance transposable genetic element. C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT MED,INFECT DIS SECT,BOSTON,MA 02215. CHILDRENS HOSP MED CTR,INFECT DIS SECT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT MICROBIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. FU NIAID NIH HHS [AI20415] NR 28 TC 59 Z9 61 U1 2 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD FEB PY 1991 VL 35 IS 2 BP 272 EP 276 PG 5 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA EV742 UT WOS:A1991EV74200013 PM 1902647 ER PT J AU BADEN, HP AF BADEN, HP TI EPILYT FOR SCALP PSORIASIS SO ARCHIVES OF DERMATOLOGY LA English DT Letter RP BADEN, HP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114, USA. NR 1 TC 1 Z9 1 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 FEB PY 1991 VL 127 IS 2 BP 274 EP 274 PG 1 WC Dermatology SC Dermatology GA EX080 UT WOS:A1991EX08000031 PM 1991005 ER PT J AU GLYNN, RJ SEDDON, JM KRUG, JH SAHAGIAN, CR CHIAVELLI, ME CAMPION, EW AF GLYNN, RJ SEDDON, JM KRUG, JH SAHAGIAN, CR CHIAVELLI, ME CAMPION, EW TI FALLS IN ELDERLY PATIENTS WITH GLAUCOMA SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID VISUAL-FIELD LOSS; HIP FRACTURE; RISK-FACTORS; COMMUNITY AB We analyzed the determinants of serious falls among 489 ambulatory elders aged 65 years and older who received a comprehensive examination at a glaucoma consultation service. For the previous year, at least one fall requiring medical attention or restricted activity was reported by 9.6% (95% confidence interval [Cl], 7.0% to 12.2%) of participants. Using logistic regression to adjust for potential confounding variables, the greatest single risk factor for falls was the use of nonmiotic topical eye medications (odds ratio [OR], 5.4; 95% Cl, 1.8 to 16.4). Additional risk factors for falls were female sex (OR, 2.3; 95% Cl, 1.1 to 4.7) and use of cardiac medications (OR, 2.5; 95% Cl, 1.1 to 5.6). Three other characteristics were also associated with the risk of falls: use of miotic eye medications (OR, 3.2; 95% Cl, 1.0 to 10.1); visual field impairment of 40% or greater (OR, 3.0; 95% Cl, 0.94 to 9.8); and use of sedatives (OR, 2.4; 95% Cl, 0.89 to 6.7). These findings suggest that ocular and systemic medications are the major predictors of falls even in this elderly population seeking ophthalmologic care for glaucoma. Medications appear to pose a greater risk for falls than even major visual impairment. C1 MASSACHUSETTS EYE & EAR HOSP,EPIDEMIOL UNIT,243 CHARLES ST,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR HOSP,GLAUCOMA CONSULTAT SERV,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR HOSP,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GEN INTERNAL MED UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV AGING,BOSTON,MA 02114. NR 27 TC 90 Z9 91 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD FEB PY 1991 VL 109 IS 2 BP 205 EP 210 PG 6 WC Ophthalmology SC Ophthalmology GA EX564 UT WOS:A1991EX56400019 PM 1993029 ER PT J AU HEYER, WD JOHNSON, AW NORRIS, DN TISHKOFF, D KOLODNER, RD AF HEYER, WD JOHNSON, AW NORRIS, DN TISHKOFF, D KOLODNER, RD TI SACCHAROMYCES-CEREVISIAE PROTEINS INVOLVED IN HYBRID DNA FORMATION INVITRO SO BIOCHIMIE LA English DT Article; Proceedings Paper CT MEETING ON REC A AND RELATED PROTEINS : FROM RECOMBINATION TO SOS FUNCTIONS CY SEP 17-21, 1990 CL SACLAY, FRANCE SP CNRS, DEPT BIOL, DUPONT, EUROPEAN DNA REPAIR NETWORK, LIGUE CONTRE CANC, MINIST RECH & TECHNOL FRANCE, TOXICOL GENET, NATL SCI FDN, TRANSGENE, US BIOCHEM DE SACCHAROMYCES-CEREVISIAE; RECOMBINATION; STRAND EXCHANGE; HYBRID DNA ID SINGLE-STRANDED-DNA; EXCHANGE STIMULATORY FACTOR; SIMIAN VIRUS-40 DNA; RECA PROTEIN; HUMAN-CELLS; GENETIC-RECOMBINATION; HOMOLOGOUS RECOMBINATION; PARTIAL-PURIFICATION; ESCHERICHIA-COLI; MEIOTIC CELLS AB RecA-like activities that can form hybrid DNA in vitro have been identified in a wide variety of organisms. We have previously described the strand exchange protein 1 (SEP1) from the yeast Saccharomyces cerevisiae that can form hybrid DNA in vitro. Purified as an M(r) 132 000 polypeptide, recent molecular and immunological studies have now shown that the native form is an M(r) 175 000 polypeptide containing strand exchange activity. The gene encoding SEP1 has been cloned and sequenced. The primary sequence failed to reveal any significant sequence homology to other sequences in data base searches. In vivo SEP1 was found to be essential for normal meiosis as cells containing a homozygous insertion mutation in the SEP1 gene failed to sporulate. In order to identify additional factors that are involved in hybrid DNA formation in S cerevisiae, we used an in vitro stimulation assay to identify proteins that reconstitute strand exchange activity in reactions containing limiting amounts of SEP1. We have identified two proteins that functionally interact with SEP1. First, an M(r) 34 000 single-stranded DNA binding protein stimulated the reaction by lowering the requirement for SEP1 about 3-4 fold. This protein is a fragment of the large subunit of a hetero-trimeric complex called yRP-A (yRF-A) which is thought to be the functional eukaryotic equivalent of single-stranded DNA binding proteins in prokaryotes. The gene encoding this protein (RPAl) is essential for growth. Second, an M(r) 33 000 polypeptide, termed Stimulatory Factor 1 (SF1), dramatically stimulated the SEP1 catalyzed reaction by lowering the requirement for SEP1 about 300 fold. This protein specifically stimulated SEP1 in a way that is quantitatively and qualitatively different from previously found stimulation of strand exchange proteins. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL & MOLEC BIOL,BOSTON,MA 02115. FU NIGMS NIH HHS [1F32GM13594-01, GM29383] NR 45 TC 3 Z9 3 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0300-9084 J9 BIOCHIMIE JI Biochimie PD FEB-MAR PY 1991 VL 73 IS 2-3 BP 269 EP 276 DI 10.1016/0300-9084(91)90212-J PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP161 UT WOS:A1991FP16100018 PM 1883885 ER PT J AU FLETCHER, JA LYNCH, EA KIMBALL, VM DONNELLY, M TANTRAVAHI, R SALLAN, SE AF FLETCHER, JA LYNCH, EA KIMBALL, VM DONNELLY, M TANTRAVAHI, R SALLAN, SE TI TRANSLOCATION (9-22) IS ASSOCIATED WITH EXTREMELY POOR PROGNOSIS IN INTENSIVELY TREATED CHILDREN WITH ACUTE LYMPHOBLASTIC-LEUKEMIA SO BLOOD LA English DT Article ID BONE-MARROW TRANSPLANTATION; PHILADELPHIA-CHROMOSOME; BCR GENE; CHILDHOOD; ABNORMALITIES; HETEROGENEITY C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CYTOGENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP FLETCHER, JA (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 22719, CA 19589]; PHS HHS [NIA-A600294] NR 33 TC 123 Z9 125 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 FEB 1 PY 1991 VL 77 IS 3 BP 435 EP 439 PG 5 WC Hematology SC Hematology GA EV332 UT WOS:A1991EV33200002 PM 1991160 ER PT J AU CAPLAN, D AF CAPLAN, D TI AGGRAMMATISM IS A THEORETICALLY COHERENT APHASIC CATEGORY SO BRAIN AND LANGUAGE LA English DT Note ID GRAMMATICAL MORPHEMES; AGRAMMATISM; DEFICIT RP CAPLAN, D (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROPSYCHOL LAB,VINCENT BURNHAM 725,FRUIT ST,BOSTON,MA 02114, USA. NR 23 TC 16 Z9 16 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 0093-934X J9 BRAIN LANG JI Brain Lang. PD FEB PY 1991 VL 40 IS 2 BP 274 EP 281 DI 10.1016/0093-934X(91)90128-N PG 8 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA FC530 UT WOS:A1991FC53000007 PM 1709816 ER PT J AU FISHER, CM AF FISHER, CM TI VISUAL HALLUCINATIONS ON EYE CLOSURE ASSOCIATED WITH ATROPINE TOXICITY - A NEUROLOGICAL ANALYSIS AND COMPARISON WITH OTHER VISUAL HALLUCINATIONS SO CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES LA English DT Article ID PEDUNCULAR HALLUCINOSIS; BRAIN; HYPOTHESIS; INFARCTION; FIELD AB Visual hallucinations of remarkable intensity began shortly after intravenous atropine and persisted for 11 days. They were present only when the eyes were closed and were associated with heightened dreaming and disturbed sleep. The patient remained lucid and described his experiences to his attendants. Our patient's hallucinations bore some resemblance to hypnagogic hallucinations and this became the basis for the hypothesis that the hallucinations originated in the sleep-dream system of the brain stem. It is speculated that a similar site - a metabolic locus minoris resistentiae may play a part in other types of visual hallucinations and in delirium. RP FISHER, CM (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114, USA. NR 47 TC 27 Z9 28 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 FEB PY 1991 VL 18 IS 1 BP 18 EP 27 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA EZ416 UT WOS:A1991EZ41600004 PM 2036612 ER PT J AU SILVA, JA LEONG, GB LONGHITANO, M BOTELLO, TE AF SILVA, JA LEONG, GB LONGHITANO, M BOTELLO, TE TI DELUSION OF FETAL DUPLICATION IN A CAPGRAS PATIENT SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Note AB A case of Capgras syndrome in a pregnant patient is described. In addition to perceiving living family members as impostors, she believed that there was a double or twin of her fetus. She conceptualized her "twins" differently than the way she viewed doubles of family members. Her fetus may represent the youngest "person" to have been duplicated. The relationship of Capgras syndrome to misidentification phenomena is discussed. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90089. UNIV SO CALIF,INST PSYCHIAT LAW & BEHAV SCI,LOS ANGELES,CA 90089. NR 19 TC 2 Z9 2 U1 1 U2 1 PU CANADIAN PSYCHIATRIC ASSOC PI OTTAWA PA SUITE 200, 237 ARGYLE AVE, OTTAWA ON K2P 1B8, CANADA SN 0706-7437 J9 CAN J PSYCHIAT JI Can. J. Psychiat.-Rev. Can. Psychiat. PD FEB PY 1991 VL 36 IS 1 BP 46 EP 47 PG 2 WC Psychiatry SC Psychiatry GA FA896 UT WOS:A1991FA89600008 PM 2029683 ER PT J AU KOZAKEWICH, H PEREZATAYDE, AR GOORIN, AM WILKINSON, RH GEBHARDT, MC VAWTER, GF AF KOZAKEWICH, H PEREZATAYDE, AR GOORIN, AM WILKINSON, RH GEBHARDT, MC VAWTER, GF TI OSTEOSARCOMA IN YOUNG-CHILDREN SO CANCER LA English DT Article ID OSTEO-SARCOMA; CANCER; FAMILY AB The clinicopathologic features of osteosarcoma in 12 children younger than 6 years of age treated at The Children's Hospital and Dana-Farber Cancer Institute, Boston, during a 70-year time period are presented. Only one of six children treated before 1972 is a long-term survivor. Four of six children (67%) treated after 1972 are disease-free with an average follow-up of 8.8 years. The year 1972 marked the onset of use of effective chemotherapy in osteosarcoma, namely, high-dose methotrexate and leucovorin rescue. It would appear that the pathologic features and behavior of osteosarcoma in young children is similar to that of osteosarcoma in older children and adolescents. A combination of complete (wide) surgical resection or amputation and aggressive chemotherapy offers the best chance of long-term survival. C1 CHILDRENS HOSP MED CTR,DEPT HEMATOL & ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT ORTHOPED SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KOZAKEWICH, H (reprint author), CHILDRENS HOSP MED CTR,DEPT PATHOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 15 TC 13 Z9 13 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 FEB 1 PY 1991 VL 67 IS 3 BP 638 EP 642 DI 10.1002/1097-0142(19910201)67:3<638::AID-CNCR2820670319>3.0.CO;2-T PG 5 WC Oncology SC Oncology GA EU100 UT WOS:A1991EU10000018 PM 1985758 ER PT J AU AARONSON, NK MEYEROWITZ, BE BARD, M BLOOM, JR FAWZY, FI FELDSTEIN, M FINK, D HOLLAND, JC JOHNSON, JE LOWMAN, JT PATTERSON, WB WARE, JE AF AARONSON, NK MEYEROWITZ, BE BARD, M BLOOM, JR FAWZY, FI FELDSTEIN, M FINK, D HOLLAND, JC JOHNSON, JE LOWMAN, JT PATTERSON, WB WARE, JE TI QUALITY-OF-LIFE RESEARCH IN ONCOLOGY - PAST ACHIEVEMENTS AND FUTURE PRIORITIES SO CANCER LA English DT Article; Proceedings Paper CT 2ND WORKSHOP ON METHODOLOGY IN BEHAVIORAL AND PSYCHOSOCIAL CANCER RESEARCH CY DEC 05-08, 1989 CL SANTA MONICA, CA SP AMER CANC SOC, DEPT RES, AMER CANC SOC, DEPT SERV & REHAB ID BREAST-CANCER; VALIDITY AB The status of quality of life research in oncology is assessed, and priorities for future research with regard to conceptual and theoretical developments, focus and content of research, research designs and practical strategies for research implementation, and transferring information to clinical practice and medical policy decision-making are identified. There is general agreement that quality of life is a subjective and multidimensional construct, yet comprehensive theoretical models have not been developed and applied fully. We recommend that future research be based on conceptual models that explicate the interrelationships among quality of life domains throughout the stages of cancer care. These models, and the longitudinal research that follows from them, should attend specifically to cross-class and cross-cultural issues to avoid overgeneralization from theory and research that are based largely on the views of the majority culture. We encourage the inclusion of this theory-based quality of life assessment as a standard component of clinical trials. Success in this endeavor will require additional standardization of quality of life measures for use across a range of cancer patient populations, including the development of age-specific norms and instruments designed to assess the entire family system. C1 UNIV SO CALIF,DEPT PSYCHOL,SGM 501,LOS ANGELES,CA 90089. NETHERLANDS CANC INST,1066 CX AMSTERDAM,NETHERLANDS. AMER CANC SOC,ATLANTA,GA. UNIV CALIF BERKELEY,BERKELEY,CA 94720. UNIV CALIF LOS ANGELES,INST NEUROPSYCHIAT,LOS ANGELES,CA 90024. FRONTIER SCI & TECHNOL RES FDN INC,BROOKLINE,MA. AMER CANC SOC,CALIF DIV,OAKLAND,CA. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. AMER CANC SOC,ATLANTA,GA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NEW ENGLAND MED CTR HOSP,BOSTON,MA 02111. NR 10 TC 126 Z9 143 U1 1 U2 4 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 FEB 1 PY 1991 VL 67 IS 3 SU S BP 839 EP 843 DI 10.1002/1097-0142(19910201)67:3+<839::AID-CNCR2820671415>3.0.CO;2-0 PG 5 WC Oncology SC Oncology GA FL822 UT WOS:A1991FL82200014 PM 1986855 ER PT J AU TEICHER, BA HERMAN, TS HOLDEN, SA EPELBAUM, R LIU, SD FREI, E AF TEICHER, BA HERMAN, TS HOLDEN, SA EPELBAUM, R LIU, SD FREI, E TI LONIDAMINE AS A MODULATOR OF ALKYLATING AGENT ACTIVITY INVITRO AND INVIVO SO CANCER RESEARCH LA English DT Article ID ASCITES TUMOR-CELLS; MOUSE MAMMARY-TUMOR; CARCINOMA-CELLS; FIBRO-SARCOMA; PHASE-II; MURINE; RADIOSENSITIVITY; CULTURE; RHODAMINE-123; MITOCHONDRIA AB We are searching for relatively nontoxic compounds that can positively modulate the efficacy of antitumor alkylating agents. Lonidamine inhibits cellular energy metabolism and could potentially increase damage by alkylating agents if cellular defenses are energy requiring. Exposure of cells to lonidamine (500-mu-M) for 2 h under hypoxic conditions followed by 1-h exposures to lonidamine plus alkylating agents under normally oxygenated conditions in vitro significantly increased the cell kill achieved by cis-diamminedichloroplatinum(II) (CDDP) approximately 5-fold and by D-tetraplatin approximately 10-fold at 90% inhibitory concentration in MCF-7/CDDP (CDDP-resistant) cells. Carboplatin cytotoxicity, however, was little changed. In the MCF-7 parent cell line, treatment with lonidamine increased CDDP cytotoxicity by approximately 10-fold, D-tetraplatin by approximately 10-fold, and carboplatin by approximately 8-fold at the 90% inhibitory concentration. for L-phenylalanine mustard (melphalan), N,N',N'-triethylenethiophosphoramide (thiotepa), and N,N'-bis(2-chloroethyl)-N-nitrosourea, little resistance was evident in the MCF-7/CDDP lines compared with the parent line. Treatment with lonidamine increased the cytotoxicity of each drug by 1.5- to 3-fold in both cell lines. When exposure to lonidamine was extended to 24 h before and 12 h after drug exposure in MCF-7 normally oxgenated cultures, CDDP (250-mu-M) cytotoxicity was increased by approximately 100-fold, but melphalan cytotoxicity was increased only 2- to 3-fold over the concentration range tested. In the FSaIIC murine fibrosarcoma tumor system, five i.p. injections of 50 mg/kg of lonidamine over 36 h increased the tumor cell kill by CDDP and carboplatine approximately 2- to 3-fold over the dose range tested when the platinum complexes were given i.p. immediately after the third lonidamine injection. When cyclophosphamide and thiotepa were given in the same schedule, 10-fold increases in tumor cell killing were evident on tumor excision assay over the dosage ranges. The increase in bone marrow toxicity caused by lonidamine in addition to the alkylating agents was less than for tumor cells. Finally, in the EMT6 murine mammary carcinoma, use of lonidamine at 500 mg/kg twice daily along with CDDP, carboplatin, thiotepa, and cyclophosphamide significantly increased tumor growth delays by approximately 1.6- to 3.0-fold. The results suggest that lonidamine can positively modulate antitumor alkylating agent cytotoxicity and may be a clinically useful adjunctive therapy with these drugs. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [1P01-CA38493] NR 31 TC 57 Z9 57 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 FEB 1 PY 1991 VL 51 IS 3 BP 780 EP 784 PG 5 WC Oncology SC Oncology GA EV569 UT WOS:A1991EV56900006 PM 1988117 ER PT J AU FRIDOVICHKEIL, JL GUDAS, JM DOU, QP BOUVARD, I PARDEE, AB AF FRIDOVICHKEIL, JL GUDAS, JM DOU, QP BOUVARD, I PARDEE, AB TI GROWTH-RESPONSIVE EXPRESSION FROM THE MURINE THYMIDINE KINASE PROMOTER - GENETIC-ANALYSIS OF DNA-SEQUENCES SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID CIS-ACTING ELEMENT; CELL-CYCLE; MESSENGER-RNA; C-MYC; TRANSCRIPTIONAL CONTROL; MUSCLE-CELLS; PROTEIN; INDUCTION; BINDING; INVITRO AB As a first step toward elucidating the biochemical basis of gene regulation at the G1-S boundary of the cell cycle, we have identified regions of the murine thymidine kinase (TK) promoter sufficient to confer appropriately growth-responsive expression to a heterologous gene. Using a series of TK promoter-chloramphenicol acetyltransferase (CAT) gene fusion constructs, we have identified sequences located between -174 base pairs upstream and +159 base pairs downstream of the TK translation initiation site that are sufficient to drive efficient S phase-specific expression of the CAT reporter gene in transfected murine fibroblasts. Both deletion analysis and site-specific mutagenesis experiments indicated that an Sp 1 consensus binding site is critical to the activity of this promoter. Synchronized populations of BALB/c 3T3 cells stably transfected with either TK promoter-CAT fusion constructs or TK promoter-beta-globin fusion constructs expressed their respective reporter genes in an S phase-specific manner following serum stimulation. In each case, reporter gene expression was reduced during quiescence and G1 and rose upon entry of cells into S phase. The TK sequences included in these constructs therefore contained information sufficient to confer S phase-specific regulation to these two reporter genes. These results set the stage for a more detailed analysis of the sequences and transacting factors responsible for regulating murine TK gene expression and may lead to insights into the control of proliferation in normal and transformed cells. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP FRIDOVICHKEIL, JL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA08317-03, CA22427] NR 68 TC 36 Z9 36 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 FEB PY 1991 VL 2 IS 2 BP 67 EP 76 PG 10 WC Cell Biology SC Cell Biology GA EY544 UT WOS:A1991EY54400001 PM 2069870 ER PT J AU RAGOZZINO, MW GREENE, R AF RAGOZZINO, MW GREENE, R TI BILATERAL REEXPANSION PULMONARY-EDEMA FOLLOWING UNILATERAL PLEUROCENTESIS SO CHEST LA English DT Note ID RE-EXPANSION; PNEUMOTHORAX; PERMEABILITY; RABBITS AB Acute ipsilateral pulmonary edema following reexpansion of the lung after pleurocentesis or pneumothorax is a well described entity. We report the unusual occurrence of bilateral pulmonary edema following unilateral pleurocentesis in a young male without heart disease. Various hypotheses regarding the mechanism of reexpansion pulmonary edema include increased capillary permeability due to hypoxic injury, decreased surfactant production, altered pulmonary perfusion and mechanical stretching of membranes. This case suggests that forces leading to ipsilateral reexpansion pulmonary edema also affect the contralateral lung. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP RAGOZZINO, MW (reprint author), DELANEY RADIOLOGISTS,WILMINGTON,NC, USA. NR 22 TC 22 Z9 24 U1 0 U2 1 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD FEB PY 1991 VL 99 IS 2 BP 506 EP 508 DI 10.1378/chest.99.2.506 PG 3 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA EW488 UT WOS:A1991EW48800054 PM 1989821 ER PT J AU BREWSTER, DC AF BREWSTER, DC TI CLINICAL AND ANATOMICAL CONSIDERATIONS FOR SURGERY IN AORTOILIAC DISEASE AND RESULTS OF SURGICAL-TREATMENT SO CIRCULATION LA English DT Article; Proceedings Paper CT CONF ON THE TRANSCATHETER THERAPIES IN PERIPHERAL AND NONCORONARY VASCULAR DISEASE CY JAN 22-23, 1990 CL DALLAS, TX SP ABBOTT LAB, BARD, CARDIOSURG DIV, BOSTON SCI, DEVICES VASC INTERVENT, G V MED, MALLINCKRODT MED, MEDASONICS, SCHNEIDER DE AORTOILIAC SURGERY; AORTA; ILIAC ARTERIES; TRANSLUMINAL PERCUTANEOUS ANGIOPLASTY; STENOSES ID CORONARY-ARTERY DISEASE; OCCLUSIVE DISEASE; AORTOBIFEMORAL BYPASS; VASCULAR-SURGERY; AORTOFEMORAL BYPASS; LOWER-EXTREMITIES; CARDIAC RISK; RECONSTRUCTION; GRAFTS; MANAGEMENT AB A variety of surgical procedures are available for the treatment of occlusive disease involving the aorta and iliac arteries. Use of the most appropriate operation in each patient, determined principally by disease location and patient risk, can provide highly effective relief of disabling claudication or limb-threatening ischemia with low morbidity and mortality rates. The excellent, durable results of current surgical practice should serve as the standard with which newer treatment modalities must be compared. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 55 TC 32 Z9 33 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB PY 1991 VL 83 IS 2 SU S BP 42 EP 52 PG 11 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EY594 UT WOS:A1991EY59400006 ER PT J AU SHANNON, RP GELPI, RJ HITTINGER, L VATNER, DE HOMCY, CJ GRAHAM, RM VATNER, SF AF SHANNON, RP GELPI, RJ HITTINGER, L VATNER, DE HOMCY, CJ GRAHAM, RM VATNER, SF TI INOTROPIC RESPONSE TO NOREPINEPHRINE IS AUGMENTED EARLY AND MAINTAINED LATE IN CONSCIOUS DOGS WITH PERINEPHRITIC HYPERTENSION SO CIRCULATION RESEARCH LA English DT Article DE SYSTEMIC HYPERTENSION; LEFT VENTRICULAR HYPERTROPHY; CONTRACTILITY; BETA-ADRENERGIC RECEPTORS; ADENYLATE CYCLASE ID LEFT-VENTRICULAR HYPERTROPHY; CARDIAC-HYPERTROPHY; RENOVASCULAR HYPERTENSION; SYMPATHOMIMETIC AMINES; RENAL-HYPERTENSION; BETA-RECEPTOR; RATS; VOLUME; HEART; RESPONSIVENESS AB We studied the inotropic responses to intravenous infusions of norepinephrine in nine conscious chronically instrumented dogs before and early (2-4 weeks) in the development of perinephritic hypertension; seven conscious dogs were studied later (approximately 14 weeks), during a more stable phase of hypertension. Perinephritic hypertension was associated with a 24% increase in left ventricular (LV) mass during developing hypertension; no further increase was seen during the stable hypertension phase. LV end-systolic stress was increased early (p < 0.01) but was normalized later. The LV end-systolic stress-volume relation demonstrated an enhanced contractile response to norepinephrine during developing hypertension, which returned toward control later in the course of stable hypertension. The LV dP/dt responses to norepinephrine (0.4-mu-g/kg/min) were significantly greater during developing hypertension (7,509 +/- 337 mm Hg/sec, p < 0.05) compared with the control period (4,737 +/- 286 mm Hg/sec) and returned toward the control value during stable hypertension (5,168 +/- 465 mm Hg/sec). The enhanced inotropic responses to norepinephrine in developing hypertension were preserved in the presence of ganglionic blockade, suggesting that the augmentation was not mediated via reflex mechanisms. These physiological responses were associated with an increase in beta-adrenergic receptor density, but no significant change in basal or maximal adenylate cyclase stimulation occurred during developing hypertension. Thus, in contrast to prior studies in anesthetized animals, the inotropic response to beta-adrenergic stimulation is not depressed in conscious dogs but is enhanced selectively during the development of hypertension and maintained during stable hypertension. C1 NEW ENGLAND REG PRIMATE RES CTR,DEPT MED,1 PINE HILL DR,SOUTHBOROUGH,MA 01772. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-38070, HL-37404, HL-33107] NR 45 TC 11 Z9 11 U1 0 U2 5 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD FEB PY 1991 VL 68 IS 2 BP 543 EP 554 PG 12 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA EW637 UT WOS:A1991EW63700021 PM 1671344 ER PT J AU NUSSBAUM, S AF NUSSBAUM, S TI IMMUNOMETRIC ASSAYS OF PARATHYRIN IN THE DIAGNOSIS OF HYPERCALCEMIC INDIVIDUALS SO CLINICAL CHEMISTRY LA English DT Editorial Material ID 2-SITE IMMUNORADIOMETRIC ASSAY; PRIMARY HYPERPARATHYROIDISM; DIFFERENTIAL-DIAGNOSIS; HORMONE; MALIGNANCY RP NUSSBAUM, S (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114, USA. NR 11 TC 12 Z9 12 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 FEB PY 1991 VL 37 IS 2 BP 142 EP 143 PG 2 WC Medical Laboratory Technology SC Medical Laboratory Technology GA EY835 UT WOS:A1991EY83500003 PM 1993316 ER PT J AU WONG, JT COLVIN, RB AF WONG, JT COLVIN, RB TI SELECTIVE REDUCTION AND PROLIFERATION OF THE CD4+ AND CD8+ T-CELL SUBSETS WITH BISPECIFIC MONOCLONAL-ANTIBODIES - EVIDENCE FOR INTER-T-CELL-MEDIATED CYTOLYSIS SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID TOXIC LYMPHOCYTES-T; TARGET-CELLS; ALLOGRAFT-REJECTION; MULTIPLE-SCLEROSIS; DIABETES-MELLITUS; HYBRID HYBRIDOMAS; PERIPHERAL-BLOOD; RECEPTOR COMPLEX; NEGATIVE SIGNAL; LYSIS C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WONG, JT (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,ALLERGY IMMUNOL UNIT,BOSTON,MA 02114, USA. FU NCI NIH HHS [T32-CA09216]; NIAID NIH HHS [AI27050] NR 35 TC 26 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 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD FEB PY 1991 VL 58 IS 2 BP 236 EP 250 DI 10.1016/0090-1229(91)90139-2 PG 15 WC Immunology; Pathology SC Immunology; Pathology GA EU251 UT WOS:A1991EU25100006 PM 1824687 ER PT J AU DERSHWITZ, M ROSOW, CE DIBIASE, PM JOSLYN, AF SANDERSON, PE AF DERSHWITZ, M ROSOW, CE DIBIASE, PM JOSLYN, AF SANDERSON, PE TI PROPHYLAXIS OF POSTOPERATIVE VOMITING BY ONDANSETRON SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract C1 GLAXO INC,DEPT GASTROENTEROL,RES TRIANGLE PK,NC. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD FEB PY 1991 VL 49 IS 2 BP 184 EP 184 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EZ620 UT WOS:A1991EZ62000244 ER PT J AU Janmey, PA AF Janmey, Paul A. TI Mechanical properties of cytoskeletal polymers SO CURRENT OPINION IN CELL BIOLOGY LA English DT Article AB The mechanical properties of cytoplasm are dominated by microfilaments, microtubules, and intermediate filaments, collectively termed the cytoskeleton. This review discusses how the physical properties of these biopolymer systems are related to their molecular structures and interactions, and how remodelling of these biopolymers in vivo affects cell shape and motility. C1 [Janmey, Paul A.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Hematol Unit, Boston, MA 02114 USA. [Janmey, Paul A.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02114 USA. [Janmey, Paul A.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02114 USA. [Janmey, Paul A.] Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Janmey, PA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Hematol Unit, Boston, MA 02114 USA. FU Whitaker Foundation FX I am most grateful to Thomas P Stossel and Soren Hvidt for a critical reading of the manuscript and to the Whitaker Foundation for support of this work. NR 51 TC 75 Z9 75 U1 1 U2 7 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0955-0674 EI 1879-0410 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD FEB PY 1991 VL 3 IS 1 BP 4 EP 11 DI 10.1016/0955-0674(91)90159-V PG 8 WC Cell Biology SC Cell Biology GA V39FV UT WOS:000209397800002 PM 1854482 ER PT J AU Hartwig, JH Kwiatkowski, DJ AF Hartwig, John H. Kwiatkowski, David J. TI Actin-binding proteins SO CURRENT OPINION IN CELL BIOLOGY LA English DT Article AB Much new information on the sequence, structure, and function of filament crosslinking, capping, and severing proteins is now known. Other significant findings include identification of a new abundant monomer-sequestering protein in platelets, and evidence that many actin-binding proteins interact with phosphoinositides and that this interaction may have metabolic consequences. C1 [Hartwig, John H.] Massachusetts Gen Hosp, Hematoloncol Unit, Charlestown, MA 02129 USA. [Hartwig, John H.] Harvard Univ, Sch Med, Anat & Cellular Biol Dept, Boston, MA 02114 USA. [Kwiatkowski, David J.] Harvard Univ, Sch Med, Dept Cellular & Dev Biol, Boston, MA 02114 USA. RP Hartwig, JH (reprint author), Massachusetts Gen Hosp, Hematoloncol Unit, Bldg 149,13th St,8 West, Charlestown, MA 02129 USA. FU USPHS [GM36507, PO1AI 28465]; Council for Tobacco Research, USA; Edwin S Webster Foundation FX This work was supported by USPHS grants GM36507, PO1AI 28465 and grants from the Council for Tobacco Research, USA and the Edwin S Webster Foundation. D Kwiatkowski is an Established Investigator of the American Heart Association. NR 82 TC 255 Z9 256 U1 2 U2 5 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0955-0674 EI 1879-0410 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD FEB PY 1991 VL 3 IS 1 BP 87 EP 97 DI 10.1016/0955-0674(91)90170-4 PG 11 WC Cell Biology SC Cell Biology GA V39FV UT WOS:000209397800013 PM 1854489 ER PT J AU KOYASU, S DADAMIO, L CLAYTON, LK REINHERZ, EL AF KOYASU, S DADAMIO, L CLAYTON, LK REINHERZ, EL TI T-CELL RECEPTOR ISOFORMS AND SIGNAL TRANSDUCTION SO CURRENT OPINION IN IMMUNOLOGY LA English DT Article ID NATURAL-KILLER CELLS; ZETA-CHAIN; ANTIGEN RECEPTOR; TYROSINE PHOSPHORYLATION; MOLECULAR-CLONING; ACTIVATION; COMPLEX; EXPRESSION; LOCALIZATION; GENE AB Recent cDNA and genomic cloning have identified CD3-eta as an alternatively spliced product of the same gene locus that encodes CD3-zeta. Three distinct T-cell receptor isoforms have now been identified. A current view of the signal transduction function of these isoforms in thymocytes and T cells is discussed. RP KOYASU, S (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Koyasu, Shigeo/J-5583-2015 OI Koyasu, Shigeo/0000-0001-9585-3038 NR 36 TC 12 Z9 12 U1 0 U2 3 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD FEB PY 1991 VL 3 IS 1 BP 32 EP 39 DI 10.1016/0952-7915(91)90073-A PG 8 WC Immunology SC Immunology GA FA867 UT WOS:A1991FA86700007 PM 1828948 ER PT J AU DINAUER, MC EZEKOWITZ, RAB AF DINAUER, MC EZEKOWITZ, RAB TI INTERFERON-GAMMA AND CHRONIC GRANULOMATOUS-DISEASE SO CURRENT OPINION IN IMMUNOLOGY LA English DT Article ID NEUTROPHIL CYTOCHROME-B; RESPIRATORY BURST OXIDASE; CYTOSOLIC COMPONENTS; NADPH OXIDASE; EXPRESSION; CHAIN; GENE; DEFICIENCY; CLONING; FORMS AB The molecular and biochemical characterization of many components of the phagocyte oxidase complex that generates superoxide have greatly advanced our understanding of this important pathway. Genetic defects in one or more of the components of this host defense system result in the chronic granulomatous disease phenotype. Biochemical advances and the results of a clinical trial that established the efficacy of recombinant human interferon-gamma for prophylaxis of infections in chronic granulomatous disease are the highlights of recent achievements in this area of phagocyte biology. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DINAUER, MC (reprint author), CHILDRENS HOSP MED CTR,DIV HEMATOL & ONCOL,ENDERS 7,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 33 TC 9 Z9 9 U1 0 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD FEB PY 1991 VL 3 IS 1 BP 61 EP 64 DI 10.1016/0952-7915(91)90078-F PG 4 WC Immunology SC Immunology GA FA867 UT WOS:A1991FA86700012 PM 1905138 ER PT J AU LEVITON, A PAGANO, M KUBAN, KCK KRISHNAMOORTHY, KS SULLIVAN, KF ALLRED, EN AF LEVITON, A PAGANO, M KUBAN, KCK KRISHNAMOORTHY, KS SULLIVAN, KF ALLRED, EN TI THE EPIDEMIOLOGY OF GERMINAL MATRIX HEMORRHAGE DURING THE 1ST HALF-DAY OF LIFE SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID RESPIRATORY-DISTRESS SYNDROME; BLOOD-BRAIN-BARRIER; INTRAVENTRICULAR HEMORRHAGE; INTRACRANIAL HEMORRHAGE; PREMATURE-INFANTS; CEREBROVENTRICULAR HEMORRHAGE; SONOGRAPHIC DIAGNOSIS; OBSTETRIC FACTORS; PREVENTION; BETAMETHASONE AB The personal and maternal characteristics of 27 babies with early-onset germinal matrix hemorrhage (EGMH) were compared with those of 280 babies with normal cranial ultrasonograms, studied in a separate clinical trial. None of the mothers of the babies with EGMH had high blood pressure or pre-eclampsia during pregnancy. Gestational age < 30 weeks and initial pH < 7.2 indicated increased risks of EGMH, and maternal receipt of steroids indicated reduced risk of EGMH. Thus prenatal and immediately perinatal factors appear to convey much of the information about the risk of EGMH. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP LEVITON, A (reprint author), CHILDRENS HOSP MED CTR,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NICHD NIH HHS [HD 18655]; NINDS NIH HHS [NS 20658, NS 20807] NR 46 TC 33 Z9 33 U1 1 U2 2 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 FEB PY 1991 VL 33 IS 2 BP 138 EP 145 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA EU670 UT WOS:A1991EU67000006 PM 2015981 ER PT J AU VARDI, P CRISA, L JACKSON, RA EISENBARTH, GS AF VARDI, P CRISA, L JACKSON, RA EISENBARTH, GS TI PREDICTIVE VALUE OF INTRAVENOUS GLUCOSE-TOLERANCE TEST INSULIN-SECRETION LESS THAN OR GREATER THAN THE 1ST PERCENTILE IN ISLET CELL ANTIBODY POSITIVE RELATIVES OF TYPE-1 (INSULIN-DEPENDENT) DIABETIC-PATIENTS SO DIABETOLOGIA LA English DT Article DE INTRAVENOUS GLUCOSE TOLERANCE TEST; ISLET CELL ANTIBODIES; PREDICTION ID MELLITUS AB We have followed-up 35 islet cell antibody-positive first degree relatives of patients with Type 1 (insulin-dependent) diabetes mellitus for an average of 1,300 days with sequential intravenous glucose tolerance tests. At the time of analysis and manuscript submission approximately half (18 of 35) had developed diabetes during follow-up. At initial intravenous glucose tolerance test, 11 had a 1 + 3 min insulin secretion below the first percentile of insulin secretion compared to 225 similarly studied normal control subjects. Six islet cell antibody positive relatives on follow-up developed an intravenous glucose tolerance test less than the first percentile. Fifteen out of 17 (88%) of these islet cell antibody positive relatives with secretion ever found to be below the first percentile are now overtly diabetic (positive predictive value = 88%) and insulin-treated, while only 3 of 18 (17%) without an intravenous glucose tolerance test demonstrating loss of first phase insulin secretion have progressed to diabetes (with approximately 1,300 days of follow-up for both groups relative risk or odds ratio with intravenous glucose tolerance test ever below vs never below the first percentile = 38, p < 0.001). Intravenous glucose tolerance test response below the first percentile preceded diabetes by an average of 656 days. Even when first phase insulin secretion is below the first percentile, the absolute value of 1 + 3 min insulin above basal insulin correlates with the time to development of diabetes (r = 0.586, p < 0.001). With our current duration of follow-up, the negative predictive value (intravenous glucose tolerance test never below the first percentile) is 83%, and overall accuracy 86%. Incidence rates of diabetes development amongst our islet cell antibody positive relatives with follow-up while intravenous glucose tolerance test is below the first percentile is 0.48 per year (15 conversions to diabetes amongst 17 relatives in 30.8 patient years of follow-up) vs 0.05 per year (three diabetic patients in 55.5 patient years) with intravenous glucose tolerance test greater than the first percentile. C1 JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. UNIV CALIF DAVIS,SACRAMENTO MED CTR,SACRAMENTO,CA 95817. DIABET & ENDOCRINE ASSOCIATES,SAN DIEGO,CA. HUMANA HOSP,DIABET CTR EXCELLENCE,MESA,AZ. NEW ENGLAND DIABET & ENDOCRINE CTR,CHESTNUT HILL,MA. PEDIAT ADOLESCENT DIABET CTR,MORRISTOWN,NJ. FU NIDDK NIH HHS [DK33790, DK39233, R01-DK32083] NR 16 TC 106 Z9 108 U1 1 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD FEB PY 1991 VL 34 IS 2 BP 93 EP 102 DI 10.1007/BF00500379 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FA035 UT WOS:A1991FA03500006 PM 2065854 ER PT J AU CARNES, M GOODMAN, BM LENT, SJ AF CARNES, M GOODMAN, BM LENT, SJ TI HIGH-RESOLUTION SPECTRAL-ANALYSIS OF PLASMA ADRENOCORTICOTROPIN REVEALS A MULTIFACTORIAL FREQUENCY STRUCTURE SO ENDOCRINOLOGY LA English DT Article ID HUMAN PITUITARY INVITRO; INTRINSIC PULSATILITY; EPISODIC SECRETION; HORMONE-SECRETION; ACTH; CORTICOTROPIN; RELEASE; DECONVOLUTION; OSCILLATIONS; ALGORITHMS AB Time series of plasma ACTH concentrations were analyzed with a high resolution spectral analysis program based on digital Fourier transforms. Both coherent signal and stochastic aspects of the time series were analyzed. Samples were collected at 2- and 15-min intervals in control rats and rats immunoneutralized against CRH. The individual and composite spectral distributions revealed significant structure at both the higher and lower ranges of frequencies studied, with multiple periodicities between 4-220 min in both groups. CRH immunoneutralization consistently reduced the amplitude by 82% and compressed the frequency distribution for waveforms with periods longer than 15 min by 23%. A systematic break in the slopes of the background continua occurred between 10 and 15 min in the 2-min time series. This break was unaffected by CRH immunoneutralization. Digital Fourier transform analysis of our ACTH time series suggests a system with a more complex high frequency structure than has previously been appreciated. Our analyses suggest a biological system with the following characteristics: 1) both a fast and a slow response to a fairly constant unspecified fast forcing; 2) the slow response is initiated by the fast response and represents an imperfect integration due to feedback processes; 3) CRH alters the ability of the fast forcing to elicit a slow response without altering the fast response or ACTH clearance; and 4) this alteration consists of both amplitude and frequency modulation in the signal output. This view of ACTH secretion suggest an adaptive and energy-efficient system. C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,CTR SPACE SCI & ENGN,MADISON,WI 53706. RP CARNES, M (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED SERV,GERIATR SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NIDDK NIH HHS [DK-40759] NR 46 TC 13 Z9 13 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD FEB PY 1991 VL 128 IS 2 BP 902 EP 910 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300038 PM 1846594 ER PT J AU WEAVER, DR PROVENCIO, I CARLSON, LL REPPERT, SM AF WEAVER, DR PROVENCIO, I CARLSON, LL REPPERT, SM TI MELATONIN RECEPTORS AND SIGNAL TRANSDUCTION IN PHOTOREFRACTORY SIBERIAN HAMSTERS (PHODOPUS-SUNGORUS) SO ENDOCRINOLOGY LA English DT Article ID GOLDEN-HAMSTERS; PINEAL MELATONIN; REFRACTORINESS; PHOTOPERIODS; BRAIN; LOCALIZATION; TERMINATION; PITUITARY; BINDING; EXPOSURE AB In seasonally breeding mammals, seasonal alterations in day length are perceived via the pineal hormone melatonin. When exposed to short day lengths, hamsters and other long-day breeders undergo gonadal regression. With chronic exposure ( > 20 weeks) to short days, however, the animals become photorefractory, or insensitive to the inhibitory influence of short-day melatonin patterns, and gonadal recrudescence occurs. In this report, we examined photorefractory Siberian hamsters and long-day housed control hamsters to examine whether this apparent insensitivity to melatonin is due to alterations in melatonin receptors or signal transduction. In vitro autoradiographic assessment of melatonin receptors using I-125-labeled 2-iodomelatonin (I-MEL) revealed that melatonin receptor distribution, affinity, density, and G protein coupling are unaltered in photorefractory animals. In each animal, high-affinity (dissociation constant approximately 40 pM) 2-iodomelatonin binding sites were observed in the hypophysial pars tuberalis, in the suprachiasmatic nucleus of the hypothalamus, and in the thalamus (paraventricular nucleus, reuniens nucleus, and nucleus of the stria medullaris). The nonhydrolyzable GTP analog, GTP-gamma-S (100-mu-M) caused a 10-fold reduction in melatonin receptor affinity in the pars tuberalis in both photorefractory and control hamsters, demonstrating receptor-G protein coupling in both groups. Furthermore, melatonin 910 nM) inhibited forskolin-stimulated cAMP accumulation in median eminence/pars tuberalis explants in photorefractory animals, just as previously observed in explants from long-day hamsters. These results suggest that melatonin receptors, receptor-G protein coupling, and inhibition of adenylyl cyclase by melatonin are not altered in photorefractory hamsters. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP WEAVER, DR (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DEV CHRONOBIOL LAB,JACKSON 1226,BOSTON,MA 02114, USA. OI Weaver, David/0000-0001-7941-6719 FU NIDDK NIH HHS [DK-42125] NR 31 TC 53 Z9 53 U1 0 U2 2 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD FEB PY 1991 VL 128 IS 2 BP 1086 EP 1092 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300062 PM 1846576 ER PT J AU MAITER, D UNDERWOOD, LE MARTIN, JB KOENIG, JI AF MAITER, D UNDERWOOD, LE MARTIN, JB KOENIG, JI TI NEONATAL TREATMENT WITH MONOSODIUM GLUTAMATE - EFFECTS OF PROLONGED GROWTH-HORMONE (GH)-RELEASING HORMONE DEFICIENCY ON PULSATILE GH SECRETION AND GROWTH IN FEMALE RATS SO ENDOCRINOLOGY LA English DT Article ID SEXUAL DIMORPHISM; MEDIAN-EMINENCE; TREATED MICE; SOMATOSTATIN; PITUITARY; SOMATOMEDIN; INSULIN; OBESITY; CRANIOPHARYNGIOMA; HYPOTHALAMUS AB Administrations of monosodium glutamate (MSG) to neonatal rodents produces permanent lesions of hypothalamic arcuate neurons that secrete GH-releasing hormone (GHRH). The present study was intended to determine the consequences of GHRH deficiency on the pulsatile GH secretory pattern and growth in MSG-treated female rats and to compare these effects with those observed in male littermates. Male and female rats were injected with MSG [4 mg/g body wt (BW), sc] or saline (controls) on days 2, 4, 6, 8, and 10 after birth. Immunoreactive GHRH concentrations were decreased in the hypothalamus (by 60%) and in the median eminence (by 95%) of adult male and female MSG-treated rats. In contrast, somatostatin concentrations were unaffected. BW and linear growth were severely impaired in male MSG-treated rats, but in MSG-lesioned females BW was not different from controls, and the attenuation of longitudinal growth was less severe and the obesity more pronounced than in males. These sex differences occurred despite similar reductions (by 55%) in serum insulin-like growth factor I concentrations in male and female MSG-treated rats. MSG treatment also produced decreases in pituitary wt and GH content (by 60%), independent of sex. Pulsatile GH secretion was studied by serial blood sampling of chronically cannulated, freely moving rats. Plasma GH patterns were analyzed by the PULSAR program. Compared to controls, treatment with MSG led to a marked inhibition (by 90%) of GH secretion in both sexes. Significant reductions in GH pulse amplitude (-95%) and pulse duration (-62%) were observed in males, whereas pulse amplitude (-85%), pulse frequency (-67%), and baseline GH concentrations (-80%) were markedly reduced in females. The GH responses to an iv bolus injection of rat GHRH (1-mu-g/rat) was severely blunted in both male and female MSG-treated rats. This study demonstrates that GHRH deficiency in female rats results in a marked inhibition of GH pulses, as in males, but also causes severe and sex-specific reductions in GH basal secretion and pulse frequency. These observations suggest that hypothalamic GHRH secretion in female rats is more continuous than in males and is aa determinant of the elevated interpulse secretion affected by arcuate lesions in female animals, compared to males. These sex-related differences in growth rates may result in part from the tendency of female MSG-lesioned rats to become more obese than males, and the development of obesity, in turn, may antagonize the factors that tend to slow linear growth. Additionally, the more deleterious consequences of GHRH deficiency in male animals may be due to loss of GH pulses, which appear to promote growth more effectively and which are normally more prominent in males than females. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV N CAROLINA,DEPT PEDIAT,DIV PEDIAT ENDOCRINOL,CHAPEL HILL,NC 27599. FU NICHD NIH HHS [HD-08299]; NIDDK NIH HHS [DK-26252, DK-39251] NR 43 TC 63 Z9 63 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD FEB PY 1991 VL 128 IS 2 BP 1100 EP 1106 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300064 PM 1989848 ER PT J AU HOERMANN, R KEUTMANN, HT AMIR, SM AF HOERMANN, R KEUTMANN, HT AMIR, SM TI CARBOHYDRATE MODIFICATIONS TRANSFORM HUMAN CHORIONIC-GONADOTROPIN INTO A POTENT STIMULATOR OF ADENOSINE-3',5'-MONOPHOSPHATE AND GROWTH-RESPONSES IN FRTL-5 THYROID-CELLS SO ENDOCRINOLOGY LA English DT Article ID HUMAN LUTEINIZING-HORMONE; THYROTROPIC ACTIVITY; ALPHA-SUBUNIT; SIALIC-ACID; RECEPTOR; TRANSDUCTION; MEMBRANES; INVITRO; MOIETY; SIGNAL AB To delineate the role of carbohydrate moiety in the expression of in vitro thyrotropic activity of hCG, its variants that lacked sialic acid residues or the entire carbohydrate moiety on one or both subunits were prepared. They along with intact hCG were then tested for their abilities to bind to TSH receptor and stimulate cAMP production and growth responses in FRTL-5 cells. The removal of sialic acid from either one or both subunits sharply increased the [I-125] bovine TSH binding-inhibiting activity of hCG in the receptor assay. among the variants tested, desialylated hCG (as-hCG) was the most potent inhibitor, followed by alpha-as-beta, as-alpha-beta, and hCG in that order. With respect to their abilities to stimulate cAMP generation in the cells, the activities of all desialylated hCG variants were markedly higher than that of hCG itself, and as in the receptor assay, as-hCG was the most potent stimulator tested. At the same concentration 9100-mu-g/ml), as-alpha-beta, alpha-as-beta, and hCG were approximately only 57%, 46%, and 27% as active as as-hCG in activating cAMP production. The findings in the growth assay were entirely consistent with those noted in the cAMP response assay. Among the deglycosylated hybrids examined, alpha-dg-beta was the most effective in activating cAMP release. An equivalent dose (200-mu-g/ml) was about 1.7, 2.7, and 3.8 times as active as dg-hCG, dg-alpha-beta, and hCG, respectively. The deglycosylated variants of hCG showed a similar pattern of activity in growth response and cAMP accumulation assays. In both cases, alpha-dg-beta was the most potent stimulator, while hCG was the least active. No significant difference between the potencies of dg-alpha-beta and alpha-dg-beta was discerned in the receptor assay; however, deglycosylated hCG (dg-hCG) was sharply more active. Results of these studies strongly suggest that the optimal expression of in vitro thyrotropic activity of hCG variants in FRTL-5 cells may require an alpha-subunit, with intact carbohydrate, in combination with the deglycosylated beta-subunit. Further, they demonstrate that modification of the hCG carbohydrate moiety alone can transform it from a weak agonist to a potent stimulator of in vitro thyrotropic bioactivity. These results also provide further evidence to support the notion that the degree of expression f thyrotropic activity is strongly affected by the species in which the studies are performed. C1 HARVARD UNIV,BETH ISRAEL HOSP,CHARLES A DANA RES INST,DEPT MED,THORNDIKE LAB,BOSTON,MA 02215. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ENDOCRINE UNIT,BOSTON,MA 02114. FU NCI NIH HHS [CA-31218] NR 21 TC 32 Z9 32 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD FEB PY 1991 VL 128 IS 2 BP 1129 EP 1135 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EV503 UT WOS:A1991EV50300068 PM 1846577 ER PT J AU YAMADA, A NOJIMA, Y SUGITA, K DANG, NH SCHLOSSMAN, SF MORIMOTO, C AF YAMADA, A NOJIMA, Y SUGITA, K DANG, NH SCHLOSSMAN, SF MORIMOTO, C TI CROSS-LINKING OF VLA/CD29 MOLECULE HAS A CO-MITOGENIC EFFECT WITH ANTI-CD3 ON CD4 CELL ACTIVATION IN SERUM-FREE CULTURE SYSTEM SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID FIBRONECTIN RECEPTOR COMPLEX; T-CELLS; LYMPHOCYTES-T; MONOCLONAL-ANTIBODIES; SURFACE RECEPTORS; INDUCER CELLS; EXPRESSION; SUBSET; PROLIFERATION; ADHESION AB In this study, we demonstrated that antibodies reactive with a common beta-1 subunit (CD29) of the VLA family of antigens could synergize with CD3 but not CD2 in inducing CD4 cell proliferation in a serum-free culture system. The extent of activation was similar to that obtained when CD4 cells were cultured with anti-CD3 plus fibronectin. The proliferative response induced via the CD3-CD29 pathway was associated with the interleukin (IL) 2 autocrine pathway, including IL 2 production and IL 2 receptor expression. Specifically, cross-linking of VLA-5, but not other members of the VLA family of antigens with the CD3 molecule induced strong CD4 cell activation. However, cross-linking of CD3 with other cell surface antigens such as CD4 did not induce CD4 cell activation in this serum-free culture system. The above results strongly suggest that the VLA/CD29 family of antigens may play an important role in regulating CD4 T cell activation via the CD3-T cell receptor pathway. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIAID NIH HHS [AI 12069]; NIAMS NIH HHS [AR 33713] NR 36 TC 44 Z9 44 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD FEB PY 1991 VL 21 IS 2 BP 319 EP 325 DI 10.1002/eji.1830210212 PG 7 WC Immunology SC Immunology GA FA425 UT WOS:A1991FA42500011 PM 1705510 ER PT J AU BIERER, BE SCHREIBER, SL BURAKOFF, SJ AF BIERER, BE SCHREIBER, SL BURAKOFF, SJ TI THE EFFECT OF THE IMMUNOSUPPRESSANT FK-506 ON ALTERNATE PATHWAYS OF T-CELL ACTIVATION SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID CYTOSOLIC BINDING-PROTEIN; PEPTIDYL-PROLYL ISOMERASE; ANTIGEN-RECEPTOR COMPLEX; CYCLOSPORIN-A; MONOCLONAL-ANTIBODIES; RAPAMYCIN AY-22,989; SIGNAL TRANSDUCTION; GENE-EXPRESSION; GROWTH-FACTOR; CYCLE BLOCK AB Structurally unrelated, FK-506 and cyclosporin (CsA) bind to and inhibit the action of distinct cytoplasmic receptors. FK-506-binding protein (FKBP) and cyclophilin (CyP), respectively. These receptors, termed immunophilins, share no sequence similarity, and yet both have been demonstrated to be capable of catalyzing the cis-trans isomerization of peptidyl-prolyl bonds (rotamase activity). Because FK-506 and CsA bind to different intracellular target structures, we investigated the spectrum of action of FK-506, in comparison to CsA, on T cell activation. We have shown that FK-506, like CsA, is able to inhibit T cell activation mediated not only by the T cell receptor-CD3 complex, but also via another surface molecule, CD2. T cell proliferation, stimulation of interleukin 2 production, and induction of apoptosis were all sensitive to inhibition by both FK-506 and CsA. With each parameter of activation, FK-506 is approximately 10-100-fold more effective than CsA. In contrast, FK-506 did not affect T cell proliferation induced by anti-CD28 monoclonal antibody in the presence of phorbol 12-myristate 13-acetate. This CD28 pathway, however, was inhibitable by a structural homolog of FK-506, rapamycin, demonstrating that the mechanism of action of FK-506 has specificity. These data suggest that immunophilins or the complex of drug coupled to immunophilin (i.e. FK-506/FKBP, CsA/CyP) are involved in and regulate selective pathways of T cell stimulation. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,DEPT CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP BIERER, BE (reprint author), HARVARD UNIV,DANA FARBER CANC INST,DIV PEDIAT ONCOL,ROOM 1610B,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 39542]; NIAID NIH HHS [AI 28554]; NIGMS NIH HHS [GM 38627] NR 62 TC 94 Z9 97 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 FEB PY 1991 VL 21 IS 2 BP 439 EP 445 DI 10.1002/eji.1830210228 PG 7 WC Immunology SC Immunology GA FA425 UT WOS:A1991FA42500027 PM 1705513 ER PT J AU BLUMBERG, RS SANCHO, J LEY, SC MCDERMOTT, FV TAN, KN BREITMEYER, J TERHORST, C AF BLUMBERG, RS SANCHO, J LEY, SC MCDERMOTT, FV TAN, KN BREITMEYER, J TERHORST, C TI GENETIC RECONSTITUTION OF THE T-CELL RECEPTOR (TCR) ALPHA/BETA-HETERODIMER RESTORES THE ASSOCIATION OF CD3-ZETA WITH THE TCR/CD3 COMPLEX SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTIGEN RECEPTOR; ZETA-CHAIN; CD3 COMPLEX; MOLECULAR-CLONING; BETA-CHAINS; ENDOPLASMIC-RETICULUM; EPSILON-SUBUNIT; ETA-CHAIN; EXPRESSION; CDNA AB The cell surface expression of the T cell receptor (TcR)/CD3 complex and, consequently, the functional competence of the cell is partly dependent on CD3 zeta. In its absence, a pentameric complex (TcR alpha/beta/CD3 gamma-delta-epsilon) is formed which is inefficiently transported to the cell surface. Reconstitution of CD3 zeta by transfection, in turn, restores the cell surface expression and function of the complex. Through the use of transfection experiments, we here provide direct evidence that the association of CD3 zeta-2 with the TcR/CD3 complex is dependent on the presence of both the TcR alpha and beta polypeptide chains. Despite wild-type levels of the CD3 zeta protein in a TcR alpha-negative mutant human T cell line, a complex was formed intracellularly which lacked CD3 zeta-2 and consisted of beta-gamma-delta-epsilon and beta-2-gamma-delta-epsilon. Upon transfection of the mutant a TcR alpha cDNA, a TcR/CD3 complex which contained CD3 zeta-2 was observed intracellularly. In contrast to the partial subcomplex on the cell surface of the untransfected cell line, the TcR/CD3 complex on the transfectant was functional as demonstrated by its ability to mobilize intracellular calcium after stimulation with a mitogenic CD3 epsilon-specific monoclonal antibody. Transient transfection studies performed in COS cell fibroblasts indicated that CD3 zeta-2 was not interacting with the TcR alpha protein alone, implying that a conformation provided by either the TcR alpha/beta heterodimer or the TcR alpha/beta/CD3 gamma-delta-epsilon complex was necessary for the association of CD3 zeta-2. Transfection studies performed in a TcR alpha/beta-negative murine T-T hybridoma confirmed the requirement of both the TcR alpha and beta proteins in CD3 zeta-2 binding. We conclude that the TcR alpha and beta chains harbor polypeptide sequences essential for the association of CD3 zeta-2 with the TcR/CD3 complex. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC IMMUNOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,TUMOR IMMUNOL LAB,BOSTON,MA 02115. RP BLUMBERG, RS (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV GASTROENTEROL,75 FRANCIS ST,BOSTON,MA 02115, USA. RI Sancho, Jaime/O-3228-2013 OI Sancho, Jaime/0000-0003-3852-7951 FU NIAID NIH HHS [AI 27893, AI 15066]; NIDDK NIH HHS [1KO8 DK01886-01] NR 53 TC 15 Z9 15 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD FEB PY 1991 VL 21 IS 2 BP 473 EP 481 DI 10.1002/eji.1830210233 PG 9 WC Immunology SC Immunology GA FA425 UT WOS:A1991FA42500032 PM 1825637 ER PT J AU ROCKWELL, WB EHRLICH, HP AF ROCKWELL, WB EHRLICH, HP TI AN IBUPROFEN-ANTAGONIZED PLASMIN INHIBITOR RELEASED BY HUMAN ENDOTHELIAL-CELLS SO EXPERIMENTAL AND MOLECULAR PATHOLOGY LA English DT Article ID DERMAL MICROCIRCULATION; BURN INJURY; PROSTAGLANDINS; RAT; PURIFICATION; FIBRINOLYSIS; THROMBOXANE; ISCHEMIA; FLUID C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,WOUND HEALING LAB,51 BLOSSOM ST,BOSTON,MA 02114. FU NIGMS NIH HHS [GM 32705] NR 28 TC 0 Z9 0 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 0014-4800 J9 EXP MOL PATHOL JI Exp. Mol. Pathol. PD FEB PY 1991 VL 54 IS 1 BP 1 EP 9 PG 9 WC Pathology SC Pathology GA EY951 UT WOS:A1991EY95100001 PM 1995315 ER PT J AU TYSK, C RIEDESEL, H LINDBERG, E PANZINI, B PODOLSKY, D JARNEROT, G AF TYSK, C RIEDESEL, H LINDBERG, E PANZINI, B PODOLSKY, D JARNEROT, G TI COLONIC GLYCOPROTEINS IN MONOZYGOTIC TWINS WITH INFLAMMATORY BOWEL-DISEASE SO GASTROENTEROLOGY LA English DT Article ID ULCERATIVE-COLITIS; CROHNS-DISEASE; INTESTINAL PERMEABILITY; MUCUS; MUCIN; RELATIVES; SMOKING C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. OREBRO MED CTR HOSP,DEPT MED,DIV GASTROENTEROL,OREBRO,SWEDEN. FU NIDDK NIH HHS [DK34422] NR 22 TC 74 Z9 74 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD FEB PY 1991 VL 100 IS 2 BP 419 EP 423 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ER722 UT WOS:A1991ER72200017 PM 1985038 ER PT J AU WILLIAMS, JH DRINKA, TJK GREENBERG, JR FARRELLHOLTAN, J EUHARDY, R SCHRAM, M AF WILLIAMS, JH DRINKA, TJK GREENBERG, JR FARRELLHOLTAN, J EUHARDY, R SCHRAM, M TI DEVELOPMENT AND TESTING OF THE ASSESSMENT OF LIVING SKILLS AND RESOURCES (ALSAR) IN ELDERLY COMMUNITY-DWELLING VETERANS SO GERONTOLOGIST LA English DT Article DE FUNCTIONAL; INSTRUMENTAL ACTIVITIES OF DAILY LIVING; EVALUATION ID GERIATRICS; BURDEN; INDEX C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,GERIATR SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705. DIVINE SAVIOR HOSP,PORTAGE,WI. UNIV WISCONSIN,SCH SOCIAL WORK,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. NR 25 TC 33 Z9 33 U1 4 U2 5 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD FEB PY 1991 VL 31 IS 1 BP 84 EP 91 PG 8 WC Gerontology SC Geriatrics & Gerontology GA FJ237 UT WOS:A1991FJ23700012 PM 2007479 ER PT J AU GRAEMECOOK, F MARK, EJ AF GRAEMECOOK, F MARK, EJ TI PULMONARY MUCINOUS CYSTIC TUMORS OF BORDERLINE MALIGNANCY SO HUMAN PATHOLOGY LA English DT Article DE LUNG; MUCINOUS CYST; BORDERLINE MALIGNANT TUMOR ID BRONCHIOLOALVEOLAR CARCINOMA; BRONCHIOLAR CARCINOMA; CYSTADENOMAS; LUNG C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 23 TC 39 Z9 40 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 FEB PY 1991 VL 22 IS 2 BP 185 EP 190 DI 10.1016/0046-8177(91)90041-M PG 6 WC Pathology SC Pathology GA EW699 UT WOS:A1991EW69900014 PM 2001880 ER PT J AU GOODFRIEND, TL AF GOODFRIEND, TL TI ANGIOTENSINS - A FAMILY THAT GROWS FROM WITHIN SO HYPERTENSION LA English DT Editorial Material DE ANGIOTENSINS; ANGIOTENSIN CONVERTING ENZYME INHIBITORS; RENIN-ANGIOTENSIN SYSTEM ID II RECEPTOR SUBTYPES C1 UNIV WISCONSIN,DEPT PHARMACOL & INTERNAL MED,MADISON,WI 53706. RP GOODFRIEND, TL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705, USA. NR 10 TC 14 Z9 14 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 FEB PY 1991 VL 17 IS 2 BP 139 EP 140 PG 2 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA EW658 UT WOS:A1991EW65800003 PM 1991646 ER PT J AU MARCUS, DM CARPENTER, JL OBRIEN, JM KIVELA, T BRAUNER, E TARKKANEN, A VIRTANEN, I ALBERT, DM AF MARCUS, DM CARPENTER, JL OBRIEN, JM KIVELA, T BRAUNER, E TARKKANEN, A VIRTANEN, I ALBERT, DM TI PRIMITIVE NEUROECTODERMAL TUMOR OF THE MIDBRAIN IN A MURINE MODEL OF RETINOBLASTOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE RETINOBLASTOMA; TRANSGENIC MICE; PRIMITIVE NEUROECTODERMAL TUMOR; TRILATERAL RETINOBLASTOMA; BRAIN TUMOR ID TRILATERAL RETINOBLASTOMA; GENE; EXPRESSION; COMPLEX AB The first heritable model of retinoblastoma was established by retina-specific expression of simian virus 40 T-antigen (SV40 T-ag) in transgenic mice. Bilateral, multifocal ocular tumors were observed in 100% of transgene-bearing mice. Central nervous system neoplasms occurred at a lower rate (27%) and represented the murine counterpart of human trilateral retinoblastoma. The authors characterized the transgenic brain tumors and found them to be primitive neuroectodermal tumors (PNET) of the midbrain. Murine brain tumors do not involve the pineal gland and most closely resemble undifferentiated suprasellar or parasellar tumors occasionally observed in human trilateral retinoblastoma. The murine malignancies arose from the subependymal cells of the cerebral aqueduct. Immunohistochemical and ultrastructural examination revealed that the transgenic brain tumors were undifferentiated and lacked all antigens associated with normal murine neuronal, glial, and ependymal cells. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. ANGELL MEM ANIM HOSP,DEPT PATHOL & MED,BOSTON,MA. UNIV HELSINKI,DEPT OPHTHALMOL,SF-00100 HELSINKI 10,FINLAND. UNIV HELSINKI,DEPT ANAT,SF-00100 HELSINKI 10,FINLAND. RI Kivela, Tero/C-9241-2009 OI Kivela, Tero/0000-0003-1198-4394 FU NEI NIH HHS [EY01917] NR 29 TC 23 Z9 24 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB PY 1991 VL 32 IS 2 BP 293 EP 301 PG 9 WC Ophthalmology SC Ophthalmology GA EX766 UT WOS:A1991EX76600007 PM 1993580 ER PT J AU OCONNOR, PJ MORGAN, WP KOLTYN, KF RAGLIN, JS TURNER, JG KALIN, NH AF OCONNOR, PJ MORGAN, WP KOLTYN, KF RAGLIN, JS TURNER, JG KALIN, NH TI AIR-TRAVEL ACROSS 4 TIME ZONES IN COLLEGE SWIMMERS SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE BLOOD PRESSURE; HEART RATE; MOOD; MUSCLE SORENESS; PERCEIVED EXERTION; SALIVARY CORTISOL ID SALIVARY CORTISOL-LEVELS; CIRCADIAN-RHYTHMS; HUMAN-PERFORMANCE; JET-LAG; EXERCISE; SLEEP AB Eighteen female and 22 male college swimmers were flown across four time zones in east-to-west (E-W) and west-to-east (W-E) directions. A pre- and postflight paced swim of 182.9 m at an intensity equal to 90% of the swimmers' maximal velocity was completed, and salivary cortisol, heart rate (HR), and rated perceived exertion were measured. Blood pressure, HR, muscle soreness, and mood were also assessed at rest on the day before and on the day after travel. Because training volumes for both females and males were greater (P < 0.001) in the week before W-E than E-W travel, the W-E and E-W data were analyzed separately. Two-way repeated-measures analyses of variance revealed that pre- and postexercise cortisol decreased after E-W travel and increased after W-E travel in comparison to preflight values. Resting and exercise HR responses to air travel were small in magnitude, and their significance depended on the direction of travel. Effort sense was not altered by air travel, but significant (P < 0.001) improvements in mood and reductions in muscle soreness were observed after E-W and W-E travel for both genders. It was concluded that 1) female and male college swimmers have similar responses to air travel and 2) air travel across four time zones during heavy swim training does not have negative physiological, perceptual, or affective consequences. C1 UNIV WISCONSIN,SPORT PSYCHOL LAB,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,MADISON,WI 53706. INDIANA UNIV,DEPT KINESIOL,BLOOMINGTON,IN 47405. RP OCONNOR, PJ (reprint author), ARIZONA STATE UNIV,EXERCISE & SPORT RES INST,PEBE 210,TEMPE,AZ 85287, USA. NR 29 TC 30 Z9 30 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD FEB PY 1991 VL 70 IS 2 BP 756 EP 763 PG 8 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA EX526 UT WOS:A1991EX52600037 PM 2022567 ER PT J AU WHITE, MF AF WHITE, MF TI STRUCTURE AND FUNCTION OF TYROSINE KINASE RECEPTORS SO JOURNAL OF BIOENERGETICS AND BIOMEMBRANES LA English DT Review DE INSULIN RECEPTOR; EGF RECEPTOR; PDGF RECEPTOR; TYROSINE KINASE; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION ID EPIDERMAL GROWTH-FACTOR; HUMAN INSULIN-RECEPTOR; ALTERED AUTOPHOSPHORYLATION SITES; TRANSFORMING GENE-PRODUCT; ATP-BINDING SITE; PROTEIN-KINASE; EGF-RECEPTOR; BETA-SUBUNIT; SIGNAL TRANSDUCTION; PHOSPHATIDYLINOSITOL KINASE AB Over the past ten years, several growth factor receptors have been shown to be ligand-regulated tyrosine kinases. Tyrosine kinase activity is essential for signal transmission, suggesting that phosphorylation cascades may play an important role. Considerable effort has gone into understanding the structure and function of tyrosine kinase receptors in order to define their mechanisms of signal transmission. However, the protein substrates of the receptor kinases have proven to be difficult to isolate and clone. This review focuses on the receptors for insulin, epidermal growth factor, and platelet-derived growth factor. They are all tyrosine kinases, but emerging evidence suggests that they utilize multiple separate signal transduction pathways. Work carried out during the next several years should yield considerable insight into the complexity of the components which interact with these tyrosine kinase receptors to regulate cellular growth and metabolism. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02215. RP WHITE, MF (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK38712] NR 83 TC 35 Z9 35 U1 3 U2 7 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0145-479X J9 J BIOENERG BIOMEMBR JI J. Bioenerg. Biomembr. PD FEB PY 1991 VL 23 IS 1 BP 63 EP 82 PG 20 WC Biophysics; Cell Biology SC Biophysics; Cell Biology GA EW523 UT WOS:A1991EW52300005 PM 1849136 ER PT J AU MALONEY, WJ KRUSHELL, RJ JASTY, M HARRIS, WH AF MALONEY, WJ KRUSHELL, RJ JASTY, M HARRIS, WH TI INCIDENCE OF HETEROTOPIC OSSIFICATION AFTER TOTAL HIP-REPLACEMENT - EFFECT OF THE TYPE OF FIXATION OF THE FEMORAL COMPONENT SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article AB The incidence and severity of heterotopic ossification after sixty-five consecutive primary uncemented total hip replacements were compared with those after seventy consecutive primary hybrid total hip replacements (consisting of an uncemented acetabular component and a cemented femoral component). All patients had had the arthroplasty because of osteoarthrosis. The sex distribution, prevalence of bilateral disease of the hip, and frequency of previous operations were similar in both groups. All of the operations were performed by one surgeon who used the same operative approach. Preoperative, immediate postoperative, and six-month follow-up radiographs were reviewed for all patients. For 90 per cent of the hips, radiographs that were made after a minimum follow-up of one year were also reviewed. In the group of patients who had an uncemented femoral component, there was a statistically significant increase in the frequency of heterotopic bone and in its severity. Either none or only class-I ectopic bone developed in 74 per cent of the hips in the hybrid group, compared with 40 per cent of the hips in the uncemented group (p < 0.005). In contrast, class-III or IV heterotopic ossification was evident in 13 per cent of the hips in the hybrid group, compared with 38 per cent of the hips in the uncemented group (p < 0.005). None of the patients in the hybrid group needed reoperation for excision of ectopic bone, but four (6 per cent) of the patients in the uncemented group needed such a reoperation because of severe limitation of motion. Because most of the major factors associated with the development of heterotopic ossification (incision, surgeon, diagnosis, sex distribution, and history of heterotopic ossification) were the same in each group and the acetabular components that were used were identical in all hips, the data suggest that, in this series, use of the uncemented femoral component was associated in some way with an increased risk of heterotopic ossification. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 20 TC 51 Z9 53 U1 0 U2 1 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 FEB PY 1991 VL 73A IS 2 BP 191 EP 193 PG 3 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FA234 UT WOS:A1991FA23400006 PM 1899666 ER PT J AU WITT, J PESS, G GELBERMAN, RH AF WITT, J PESS, G GELBERMAN, RH TI TREATMENT OF DE QUERVAIN TENOSYNOVITIS - A PROSPECTIVE-STUDY OF THE RESULTS OF INJECTION OF STEROIDS AND IMMOBILIZATION IN A SPLINT SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article AB In a prospective study of non-operative treatment of de Quervain tenosynovitis, ninety-nine wrists of ninety-five consecutively seen patients who had this diagnosis had an injection of one milliliter of a 1 per cent lidocaine solution and one milliliter of a suspension containing forty milligrams of methylprednisolone acetate. Twelve patients (twelve wrists) were lost to follow-up. Of the remaining eighty-seven writst, fifty-four (62 per cent) had a satisfactory outcome at a mean of eighteen months (minimum follow-up, twelve months). The duration of symptoms before treatment did not affect the outcome. The result in thirty-three wrists (38 per cent) was considered unsatisfactory. Thirty of these wrists were subsequently treated with operative release of the first dorsal compartment, and twenty-two (73 per cent) of the thirty were found to have a separate compartment for the extensor pollicis brevis. The prevalence of a separate compartment is significantly higher than that in the general population, as shown in anatomical studies of cadavera. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. NR 19 TC 68 Z9 68 U1 2 U2 2 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD FEB PY 1991 VL 73A IS 2 BP 219 EP 222 PG 4 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FA234 UT WOS:A1991FA23400010 PM 1993717 ER PT J AU PRINCE, MR FRISOLI, JK GOETSCHKES, MM STRINGHAM, JM LAMURAGLIA, GM AF PRINCE, MR FRISOLI, JK GOETSCHKES, MM STRINGHAM, JM LAMURAGLIA, GM TI RAPID SERUM CAROTENE LOADING WITH HIGH-DOSE BETA-CAROTENE - CLINICAL IMPLICATIONS SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Note ID ERYTHROPOIETIC PROTOPORPHYRIA; ATHEROSCLEROTIC PLAQUE; LASER ANGIOPLASTY; DYE-LASER; PLASMA; ABSORPTION; THERAPY AB The kinetics of serum beta-carotene loading were evaluated to help determine the minimum time required to load fatty tissues, including atherosclerotic plaque and skin, with beta-carotene. Loading atherosclerotic plaque with yellow beta-carotene pigment increases absorption of blue laser radiation, potentially enhancing the selectivity and quality of laser angioplasty. Five healthy volunteers received 300 mg beta-carotene daily (the maximum FDA recommended dose) for 21 days in three divided doses with meals. Serum total carotenoid levels increased exponentially with a 10-day time constant from an average of 1.7-6.5-mu-g/ml (p < 10-4). The skin began to yellow visibly at 10 days and became increasingly yellow for several weeks thereafter, suggesting that augmenting the yellow color of fatty tissues and atherosclerotic plaque with oral beta-carotene may require a minimum of several weeks to attain the maximum effect. RP PRINCE, MR (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL07377, HL44274] NR 19 TC 24 Z9 25 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 FEB PY 1991 VL 17 IS 2 BP 343 EP 347 DI 10.1097/00005344-199102000-00023 PG 5 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA EU561 UT WOS:A1991EU56100023 PM 1709242 ER PT J AU SU, B WANECK, GL FLAVELL, RA BOTHWELL, ALM AF SU, B WANECK, GL FLAVELL, RA BOTHWELL, ALM TI THE GLYCOSYL PHOSPHATIDYLINOSITOL ANCHOR IS CRITICAL FOR LY-6A/E-MEDIATED T-CELL ACTIVATION SO JOURNAL OF CELL BIOLOGY LA English DT Article ID MULTIGENE FAMILY; LY-6 LOCUS; TRANSMEMBRANE PROTEIN; MEMBRANE-PROTEINS; SECRETORY PROTEIN; TAP MOLECULE; RECEPTOR; SURFACE; ANTIGEN; LYMPHOMA AB Ly-6E, a glycosyl phosphatidylinositol (GPI)-anchored murine alloantigen that can activate T cells upon antibody cross-linking, has been converted into an integral membrane protein by gene fusion. This fusion product, designated Ly-6ED(b), was characterized in transiently transfected COS cells and demonstrated to be an integral cell surface membrane protein. Furthermore, the fusion antigen can be expressed on the surface of the BW5147 class "E" mutant cell line, which only expresses integral membrane proteins but not GPI-anchored proteins. The capability of this fusion antigen to activate T cells was examined by gene transfer studies in D10G4.1, a type 2 T cell helper clone. When transfected into D10 cells, the GPI-anchored Ly-6E antigen, as well as the endogenous GPI-anchored Ly-6A antigen, can initiate T cell activation upon antibody cross-linking. In contrast, the transmembrane anchored Ly-6ED(b) antigen was unable to mediate T cell activation. Our results demonstrate that the GPI-anchor is critical to Ly-6A/E-mediated T cell activation. C1 YALE UNIV,SCH MED,DEPT BIOL,IMMUNOBIOL SECT,NEW HAVEN,CT 06510. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. YALE UNIV,SCH MED,HOWARD HUGHES MED INST,NEW HAVEN,CT 06510. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. RP SU, B (reprint author), YALE UNIV,SCH MED,DEPT PATHOL,NEW HAVEN,CT 06510, USA. FU NIGMS NIH HHS [GM-40924] NR 30 TC 97 Z9 98 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD FEB PY 1991 VL 112 IS 3 BP 377 EP 384 DI 10.1083/jcb.112.3.377 PG 8 WC Cell Biology SC Cell Biology GA EV177 UT WOS:A1991EV17700002 PM 1825084 ER PT J AU HARTWIG, JH DESISTO, M AF HARTWIG, JH DESISTO, M TI THE CYTOSKELETON OF THE RESTING HUMAN BLOOD-PLATELET - STRUCTURE OF THE MEMBRANE SKELETON AND ITS ATTACHMENT TO ACTIN-FILAMENTS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID BINDING PROTEIN; ERYTHROCYTE-MEMBRANE; GLYCOPROTEIN-IB; ALPHA-ACTININ; ACTIVATION; IDENTIFICATION; REORGANIZATION; LOCALIZATION; ASSOCIATION; SPECTRIN AB We used high-resolution EM and immunocytochemistry in combination with different specimen preparation techniques to resolve the ultrastructure of the resting platelet cytoskeleton. The periphery of the cytoskeleton, an electron-dense subplasmalemmal region in thin section electron micrographs, is a tightly woven planar sheet composed of a spectrin-rich network whose interstices contain GPIb/IX-actin-binding protein (ABP) complexes. This membrane skeleton connects to a system of curved actin filaments (F-actin) that emanate from a central oval core of F-actin cross-linked by ABP. The predominant interaction of the radial actin filaments with the membrane skeleton is along their sides, and the strongest connection between the membrane skeleton and F-actin is via ABP-GPIb ligands, although there is evidence for spectrin attaching to the ends of the radial actin filaments as well. Since a mechanical separation of the F-actin cores and radial F-actin-GPIb-ABP complexes from the underlying spectrin-rich skeleton leads to the latter's expansion, it follows that the spectrin-based skeleton of the resting cell may be held in a compressed form by interdigitating GPIb/IX complexes which are immobilized by radial F-actin-ABP anchors. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02114. RP HARTWIG, JH (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,HEMATOL ONCOL UNIT,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-19429]; NIGMS NIH HHS [GM-36507] NR 41 TC 190 Z9 193 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD FEB PY 1991 VL 112 IS 3 BP 407 EP 425 DI 10.1083/jcb.112.3.407 PG 19 WC Cell Biology SC Cell Biology GA EV177 UT WOS:A1991EV17700005 PM 1991790 ER PT J AU MITLAK, BH ALPERT, M LO, C DELMONICO, F NEER, RM AF MITLAK, BH ALPERT, M LO, C DELMONICO, F NEER, RM TI PARATHYROID FUNCTION IN NORMOCALCEMIC RENAL-TRANSPLANT RECIPIENTS - EVALUATION BY CALCIUM INFUSION SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HYPERCALCEMIC HYPERPARATHYROIDISM; IONIZED CALCIUM; HORMONE LEVELS; SERUM; INVIVO; ASSAY; MANAGEMENT; INVITRO AB The extent to which secondary hyperparathyroidism may involute remains poorly defined. Renal transplantation offers a clinical situation in which metabolic stimuli for hyperparathyroidism are removed. To examine whether hyperparathyroidism resolves after transplantation, we evaluated 11 renal transplant recipients who had been normocalcemic 6 or more months after transplantation using a sensitive 2-site immunoradiometric assay for intact serum PTH. Nine of the 11 had PTH concentrations within the normal range. Of these 9, 6 were found to have abnormal parathyroid function when challenged with an iv calcium infusion. The other 2 patients demonstrated significantly elevated basal PTH concentrations and elevated ionized calcium despite normal total serum calcium and albumin concentrations. In both, the PTH response to infused calcium was markedly abnormal, confirming hyperparathyroidism. The estimated renal threshold phosphate concentration was low in 4 of 9 patients with normal basal PTH concentrations and in both with elevated basal PTH. Bone mineral density, measured at the radius by single photon absorptiometry and at the spine by dual energy x-ray absorptiometry, was normal in 8 of the 9 transplant recipients who had normal basal PTH concentrations. C1 MASSACHUSETTS GEN HOSP, TRANSPLANTAT SERV, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. RP MITLAK, BH (reprint author), MASSACHUSETTS GEN HOSP, ENDOCRINE UNIT, BULFINCH 3, BOSTON, MA 02114 USA. FU NCRR NIH HHS [RR-1066] NR 30 TC 25 Z9 25 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD FEB PY 1991 VL 72 IS 2 BP 350 EP 355 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EX403 UT WOS:A1991EX40300018 PM 1991804 ER PT J AU ROSS, DS ARDISSON, LJ NUSSBAUM, SR MESKELL, MJ AF ROSS, DS ARDISSON, LJ NUSSBAUM, SR MESKELL, MJ TI SERUM OSTEOCALCIN IN PATIENTS TAKING L-THYROXINE WHO HAVE SUBCLINICAL HYPERTHYROIDISM SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Note ID BONE GLA PROTEIN; HYPOTHYROIDISM; METABOLISM; TURNOVER; DISEASE; DENSITY; THERAPY AB Serum osteocalcin, an index of osteoblastic activity, is increased in hyperthyroidism. Serum osteocalcin levels are negatively correlated with bone density in patients with overt hyperthyroidism. Osteocalcin levels are also elevated in patients with multinodular goiter and subclinical hyperthyroidism. We therefore measured serum osteocalcin levels in patients taking T4 to determine if they correlated with the degree of TSH suppression. Despite an upward trend in serum osteocalcin measurements with decreasing TSH concentrations, there was no significant difference in serum osteocalcin among groups of patients with normal (0.5-5.0 mu/L), mildly reduced (0.1-0.5 mU/L), or undetectable serum TSH (< 0.01 mU/L). However, a weak negative correlation was seen between serum TSH and osteocalcin concentrations (r = 0.29, slope = -0.28, P < 0.05). Osteocalcin did not correlate with either serum free T4 or free T3 concentrations. Serum PTH concentrations were not different among the three patient groups. Our data suggest that osteocalcin is not a useful clinical marker for increased bone turnover in patients with subclinical hyperthyroidism due to T4 therapy. However, the trend towards higher osteocalcin levels in patients with suppressed serum TSH values, and the weak negative correlation between serum TSH and osteocalcin are consistent with findings of reduced bone density in these patients. C1 MASSACHUSETTS GEN HOSP, DEPT MED, ENDOCRINE UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP ROSS, DS (reprint author), MASSACHUSETTS GEN HOSP, DEPT MED, THYROID UNIT, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK-01415] NR 19 TC 29 Z9 29 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD FEB PY 1991 VL 72 IS 2 BP 507 EP 509 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EX403 UT WOS:A1991EX40300044 PM 1991818 ER PT J AU FERNANDEZCHECA, JC GARCIARUIZ, C OOKHTENS, M KAPLOWITZ, N AF FERNANDEZCHECA, JC GARCIARUIZ, C OOKHTENS, M KAPLOWITZ, N TI IMPAIRED UPTAKE OF GLUTATHIONE BY HEPATIC MITOCHONDRIA FROM CHRONIC ETHANOL-FED RATS - TRACER KINETIC-STUDIES INVITRO AND INVIVO AND SUSCEPTIBILITY TO OXIDANT STRESS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE COMPARTMENTALIZATION; TRANSPORT; OXIDANT STRESS; GLUTATHIONE ESTER; CELL DEATH; TERT-BUTYLHYDROPEROXIDE ID HEPATOCYTIC GLUTATHIONE; EFFLUX; LIVER; INHIBITION; METABOLISM; DEPLETION; CELLS AB Isolated hepatocytes incubated with [S-35]-methionine were examined for the time-dependent accumulation of [S-35]-glutathione (GSH) in cytosol and mitochondria, the latter confirmed by density gradient purification. In GSH-depleted and -repleted hepatocytes, the increase of specific activity of mitochondrial GSH lagged behind cytosol, reaching nearly the same specific activity by 1-2 h. However, in hepatocytes from ethanol-fed rats, the rate of increase of total GSH specific radioactivity in mitochondria was markedly suppressed. In in vivo steady-state experiments, the mass transport of GSH from cytosol to mitochondria and vice versa was 18 nmol/min per g liver, indicating that the half-life of mitochondrial GSH was approximately 18 min in controls. The fractional transport rate of GSH from cytosol to mitochondria, but not mitochondria to cytosol, was significantly reduced in the livers of ethanol-fed rats. Thus, ethanol-fed rats exhibit a decreased mitochondrial GSH pool size due to an impaired entry of cytosol GSH into mitochondria. Hepatocytes from ethanol-fed rats exhibited a greater susceptibility to the oxidant stress-induced cell death from tert-butylhydroperoxide. Incubation with glutathione monoethyl ester normalized the mitochondrial GSH and protected against the increased susceptibility to t-butylhydroperoxide, which was directly related to the lowered mitochondrial GSH pool size in ethanol-fed cells. C1 US DEP VET AFFAIRS,OUTPATIENT CLIN,LOS ANGELES,CA 90033. RP FERNANDEZCHECA, JC (reprint author), UNIV SO CALIF,SCH MED,DIV GASTROINTESTINAL & LIVER DIS,2025 ZONAL AVE,LAC 11221,LOS ANGELES,CA 90033, USA. RI Garcia-Ruiz, Carmen/L-8211-2014; Fernandez-Checa, Jose Carlos/L-8342-2014 OI Garcia-Ruiz, Carmen/0000-0002-2652-6102; Fernandez-Checa, Jose Carlos/0000-0003-3422-2990 FU NIDDK NIH HHS [DK30312] NR 38 TC 196 Z9 197 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB PY 1991 VL 87 IS 2 BP 397 EP 405 DI 10.1172/JCI115010 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EW295 UT WOS:A1991EW29500004 PM 1991826 ER PT J AU GELMAN, R NEUBERG, D AF GELMAN, R NEUBERG, D TI MAKING COCKTAILS VERSUS MAKING SOUP SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID LARGE-CELL LYMPHOMA; DIFFUSE HISTIOCYTIC LYMPHOMA; NON-HODGKINS LYMPHOMAS; CHEMOTHERAPY; CYCLOPHOSPHAMIDE; VINCRISTINE; PREDNISONE; CHOP; ADRIAMYCIN; TRIAL C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GELMAN, R (reprint author), HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 19 TC 11 Z9 11 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 FEB PY 1991 VL 9 IS 2 BP 200 EP 203 PG 4 WC Oncology SC Oncology GA EV470 UT WOS:A1991EV47000002 PM 1988568 ER PT J AU CASSILETH, PA CHEUVART, B SPIERS, ASD HARRINGTON, DP CUMMINGS, FJ NEIMAN, RS BENNETT, JM OCONNELL, MJ AF CASSILETH, PA CHEUVART, B SPIERS, ASD HARRINGTON, DP CUMMINGS, FJ NEIMAN, RS BENNETT, JM OCONNELL, MJ TI PENTOSTATIN INDUCES DURABLE REMISSIONS IN HAIRY-CELL LEUKEMIA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID INTERFERON; ALPHA C1 HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. UNION UNIV,ALBANY,NY 12208. BROWN UNIV,PROVIDENCE,RI 02912. ROGER WILLIAMS GEN HOSP,PROVIDENCE,RI 02908. INDIANA UNIV,MED CTR,INDIANAPOLIS,IN 46204. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. RP CASSILETH, PA (reprint author), HOSP UNIV PENN,6 PENN TOWERS,3400 SPRUCE ST,PHILADELPHIA,PA 19104, USA. FU NCI NIH HHS [CA15488, CA06594, CA23318] NR 10 TC 99 Z9 101 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD FEB PY 1991 VL 9 IS 2 BP 243 EP 246 PG 4 WC Oncology SC Oncology GA EV470 UT WOS:A1991EV47000008 PM 1988572 ER PT J AU SAPHNER, T TORMEY, DC GRAY, R AF SAPHNER, T TORMEY, DC GRAY, R TI VENOUS AND ARTERIAL THROMBOSIS IN PATIENTS WHO RECEIVED ADJUVANT THERAPY FOR BREAST-CANCER SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID TAMOXIFEN TREATMENT; ANTITHROMBIN-III; PROTEIN-C; CHEMOTHERAPY; THROMBOEMBOLISM; CARCINOMA; REGIMEN; TRIAL; RISK C1 UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53792. HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [CA21076, CA21115, CA23318] NR 28 TC 291 Z9 297 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 FEB PY 1991 VL 9 IS 2 BP 286 EP 294 PG 9 WC Oncology SC Oncology GA EV470 UT WOS:A1991EV47000014 PM 1988575 ER PT J AU ELIAS, AD AYASH, LJ EDER, JP WHEELER, C DEARY, J WEISSMAN, L SCHRYBER, S HUNT, M CRITCHLOW, J SCHNIPPER, L FREI, E ANTMAN, KH AF ELIAS, AD AYASH, LJ EDER, JP WHEELER, C DEARY, J WEISSMAN, L SCHRYBER, S HUNT, M CRITCHLOW, J SCHNIPPER, L FREI, E ANTMAN, KH TI A PHASE-I STUDY OF HIGH-DOSE IFOSFAMIDE AND ESCALATING DOSES OF CARBOPLATIN WITH AUTOLOGOUS BONE-MARROW SUPPORT SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CELL LUNG-CANCER; TUBULAR NEPHROTOXICITY; UNRESECTABLE SARCOMA; CISPLATIN; MESNA; ETOPOSIDE; TRIAL; CYCLOPHOSPHAMIDE; NEUROTOXICITY; CHEMOTHERAPY C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,DIV HEMATOL ONCOL & SURG,BOSTON,MA 02215. RP ELIAS, AD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 13849] NR 32 TC 55 Z9 55 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 FEB PY 1991 VL 9 IS 2 BP 320 EP 327 PG 8 WC Oncology SC Oncology GA EV470 UT WOS:A1991EV47000018 PM 1846407 ER PT J AU HEIJL, L DAHLEN, G SUNDIN, Y WENANDER, A GOODSON, JM AF HEIJL, L DAHLEN, G SUNDIN, Y WENANDER, A GOODSON, JM TI A 4-QUADRANT COMPARATIVE-STUDY OF PERIODONTAL TREATMENT USING TETRACYCLINE-CONTAINING DRUG DELIVERY FIBERS AND SCALING SO JOURNAL OF CLINICAL PERIODONTOLOGY LA English DT Article DE LOCAL DRUG DELIVERY; TETRACYCLINE; PERIODONTAL TREATMENT; MICROBIOLOGY; PROBING DEPTH; GINGIVITIS ID DISEASE; THERAPY; PLAQUE AB The present study describes results on selected clinical and microbiological parameters obtained by periodontal treatment with ethylene vinyl acetate fibers containing 25% by weight tetracycline hydrochloride placed into the periodontal pocket alone or in combination with scaling. Supragingival plaque control was maintained throughout the study by weekly professional cleaning and 0.2% chlorhexidine mouthrinses. Controls included untreated sites and sites treated by conventional scaling alone in a 4-quadrant split-mouth design. The experiment was conducted on 95 teeth from 10 subjects with periodontal pockets greater-than-or-equal-to 6 mm which initially bled on probing. All treatments resulted in changes indicative of effective therapy. Pocket depth was reduced, bleeding on probing decreased and gingival index scores decreased. Parallel to the clinical changes, all treatments reduced total bacterial numbers, % black-pigmented Bacteroides, motile bacteria, non-motile rods, and produced a proportionate increase in cocci. Fiber therapy with or without scaling reduced bacterial counts by approximately 2 orders of magnitude when evaluated at 62 days post-therapy. The combination of fiber therapy with scaling was particularly effective, suggesting a possible synergy between these forms of therapy. The combined therapy eliminated bleeding on probing, and black-pigmented Bacteroides, and produced the greatest mean reduction in pocket depth. C1 GOTHENBURG UNIV,S-41124 GOTHENBURG,SWEDEN. PUBL DENTAL HLTH SERV,GOTHENBURG,SWEDEN. FORSYTH DENT CTR,BOSTON,MA 02115. FU NIDCR NIH HHS [DE-05334] NR 20 TC 73 Z9 75 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6979 J9 J CLIN PERIODONTOL JI J. Clin. Periodontol. PD FEB PY 1991 VL 18 IS 2 BP 111 EP 116 DI 10.1111/j.1600-051X.1991.tb01699.x PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA EY022 UT WOS:A1991EY02200007 PM 2005224 ER PT J AU HAFFAJEE, AD SOCRANSKY, SS LINDHE, J KENT, RL OKAMOTO, H YONEYAMA, T AF HAFFAJEE, AD SOCRANSKY, SS LINDHE, J KENT, RL OKAMOTO, H YONEYAMA, T TI CLINICAL RISK INDICATORS FOR PERIODONTAL ATTACHMENT LOSS SO JOURNAL OF CLINICAL PERIODONTOLOGY LA English DT Article DE EPIDEMIOLOGY; ATTACHMENT LOSS; PREDICTION ID ADULT SUBJECTS; ORAL HYGIENE; DISEASE; PROGRESSION AB The purpose of the present investigation was to evaluate the association of baseline clinical parameters of periodontal disease with disease progression in the following year. 271 randomly selected subjects from Ushiku Japan were monitored for overt gingivitis and plaque accumulation at 4 sites per tooth and probing pocket depth, probing attachment level and bleeding on probing at 6 sites per tooth for all teeth at baseline and 1 year. A subject was considered to exhibit additional attachment loss if one or more sites increased 3 mm or more in a probing attachment level measurement in one year. The clinical variables included age, sex, number of missing teeth, mean pocket depth and attachment level. In addition, the % of sites which exhibited overt gingivitis, visible plaque, pocket depths, attachment levels or gingival recession over certain mm thresholds or bled on probing were determined. chi-2 analysis was used to seek significant associations between the baseline clinical variables and subsequent attachment loss in a subject. Only 74 of the 271 subjects (27.3%) exhibited additional attachment loss of 3 mm or more at 1 or more sites after 1 year. Older subjects had a greater risk of disease progression than younger subjects. There were no significant differences in % of individuals exhibiting additional attachment loss when divided on the basis of sex, number of missing teeth or % of sites with overt gingivitis. However, the greater the % of sites with visible plaque or which bled on probing, the greater was the likelihood of subsequent attachment loss. Increasing mean levels of pocket depth or attachment level or increasing %s of sites exhibiting prior attachment loss were strongly related to the proportion of individuals with subsequent attachment loss. Gingival recession exhibited similar but weaker relationships. Log-linear analysis suggested that the association between bleeding on probing, age, or plaque levels with additional attachment loss may be explained by the association of these variables with baseline attachment loss. The analyses were repeated with a positive subject defined as having only 1 active site or 2 or more active sites. 37 subjects fit the 1st criterion and the remaining 37 the 2nd criterion. The associations observed were almost identical to those found when subjects were considered positive on the basis of 1 or more changing sites. Discriminant analysis was used to classify subjects as active or inactive using up to 11 predictor variables. 217 of 271 subjects (80%) were correctly classified by discriminant analysis using all 11 predictor variables with a sensitivity of 65% and specificity of 86%. Logistic regression analysis employing 4 predictor variables produced an overall agreement, sensitivity and specificity of 78%, 38% and 93%, respectively. C1 GOTHENBURG UNIV,S-41124 GOTHENBURG,SWEDEN. NIPPON DENT UNIV TOKYO,TOKYO,JAPAN. RP HAFFAJEE, AD (reprint author), FORSYTH DENT CTR,DEPT PERIODONTOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-04881] NR 15 TC 154 Z9 160 U1 0 U2 14 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6979 J9 J CLIN PERIODONTOL JI J. Clin. Periodontol. PD FEB PY 1991 VL 18 IS 2 BP 117 EP 125 DI 10.1111/j.1600-051X.1991.tb01700.x PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA EY022 UT WOS:A1991EY02200008 PM 2005225 ER PT J AU TESAR, GE ROSENBAUM, JF POLLACK, MH OTTO, MW SACHS, GS HERMAN, JB COHEN, LS SPIER, SA AF TESAR, GE ROSENBAUM, JF POLLACK, MH OTTO, MW SACHS, GS HERMAN, JB COHEN, LS SPIER, SA TI DOUBLE-BLIND, PLACEBO-CONTROLLED COMPARISON OF CLONAZEPAM AND ALPRAZOLAM FOR PANIC DISORDER SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID AGORAPHOBIA; ANXIETY; BENZODIAZEPINES; IMIPRAMINE; DEPRESSION; EFFICACY; ATTACKS; THERAPY; TRIAL AB To test the reported antipanic efficacy of clonazepam, the authors randomized 72 subjects with panic disorder to 6 weeks of treatment with either alprazolam, clonazepam, or placebo. Endpoint analysis demonstrated a significant beneficial effect of both active treatments, but not placebo treatment, on the frequency of panic attacks, overall phobia ratings, and the extent of disability. Comparison of the two active treatments revealed no significant differences and no consistent tendency for one agent to be favored over another, although power to detect small differences was limited. Sedation and ataxia were the most common side effects reported, but these effects were mild and transient and did not interfere with treatment outcome. The results of this double-blind, placebo-controlled trial are consistent with previous reports of clonazepam's antipanic efficacy. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP TESAR, GE (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,WACC-815,BOSTON,MA 02114, USA. NR 36 TC 126 Z9 127 U1 0 U2 7 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD FEB PY 1991 VL 52 IS 2 BP 69 EP 76 PG 8 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA FA526 UT WOS:A1991FA52600004 PM 1993639 ER PT J AU SEKALY, RP CROTEAU, G BOWMAN, M SCHOLL, P BURAKOFF, S GEHA, RS AF SEKALY, RP CROTEAU, G BOWMAN, M SCHOLL, P BURAKOFF, S GEHA, RS TI THE CD4 MOLECULE IS NOT ALWAYS REQUIRED FOR THE T-CELL RESPONSE TO BACTERIAL ENTEROTOXINS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID CLASS-II MOLECULES; HLA-DR; STAPHYLOCOCCAL ENTEROTOXINS; MHC MOLECULES; TARGET-CELLS; COMPLEX; ANTIGEN; RECEPTOR; RECOGNITION; L3T4 AB T cells respond in a V-beta-restricted fashion to bacterial enterotoxins bound to major histocompatibility complex (MHC) class II molecules. The requirement for CD4 in MHC class II-restricted T cell responses is very well established. We have assessed the role of CD4 in the T cell response to the bacterial enterotoxins Staphylococcal enterotoxin A (SEA), SEB, and toxic shock syndrome toxin 1. Three CD4- murine T cell hybridomas were transfected with the human CD4 molecule and assayed for interleukin 2 production in the presence of accessory cells bearing human MHC class II molecules and of the appropriate enterotoxin. The results clearly indicate that CD4- cells responded even to suboptimal concentrations of enterotoxin(s) equally well as CD4+ cells. Furthermore, expression of CD4 did not result in the acquisition of previously undetectable reactivity to enterotoxins. These results suggest that unlike the case with antigen-specific responses, formation of a T cell receptor-CD3/CD4 supramolecular complex is not always essential for T cell activation by bacterial enterotoxins. C1 CHILDRENS HOSP MED CTR, DIV IMMUNOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT PEDIAT, BOSTON, MA 02115 USA. RP SEKALY, RP (reprint author), INST RECH CLIN MONTREAL, IMMUNOL LAB, 110 PINE AVE W, MONTREAL H2W 1R7, QUEBEC, CANADA. FU NIAID NIH HHS [AI-28046, AI-21163, AI-20373] NR 27 TC 32 Z9 32 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 EI 1540-9538 J9 J EXP MED JI J. Exp. Med. PD FEB 1 PY 1991 VL 173 IS 2 BP 367 EP 371 DI 10.1084/jem.173.2.367 PG 5 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EV175 UT WOS:A1991EV17500011 PM 1988539 ER PT J AU TONETTI, M CAVALLERO, A BOTTA, GA NIEDERMAN, R EFTIMIADI, C AF TONETTI, M CAVALLERO, A BOTTA, GA NIEDERMAN, R EFTIMIADI, C TI INTRACELLULAR PH REGULATES THE PRODUCTION OF DIFFERENT OXYGEN METABOLITES IN NEUTROPHILS - EFFECTS OF ORGANIC-ACIDS PRODUCED BY ANAEROBIC-BACTERIA SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE HYDROGEN ION CONCENTRATION; BUTYRATES; METABOLISM; CALORIMETRY; OXYGEN RADICALS; PHAGOCYTES ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; HYDROGEN-PEROXIDE FORMATION; FATTY-ACIDS; BY-PRODUCT; GENERATING SYSTEM; RESPIRATORY BURST; SUPEROXIDE ANION; NADPH OXIDASE; SUCCINIC ACID; GRANULOCYTES AB The effects of short chain carboxylic acids (SCCA), namely succinic, butyric, and iso-butyric, on neutrophil metabolic activation were assessed. SCCA induced a significant decrease in O2.-recovery and chemiluminescent response in neutrophils activated with the diacylglycerol analog tetradecanoyl-phorbol-acetate (TPA). SCCA did not alter O2 consumption, H2O2 production, or the calorimetrically determined energy expenditure occurring during the metabolic burst. SCCA also induced a significant acidification of intracellular pH (pH(i)). These results are consistent with an increased divalent versus univalent O2 reduction performed by the NADPH oxidase at a more acidic intracellular pH. C1 FORSYTH RES INST,DEPT PHARMACOL & CELL BIOL,BOSTON,MA. UNIV GENOA,FAC MED,INST MICROBIOL,I-16126 GENOA,ITALY. UNIV UDINE,FAC MED,INST BIOL,I-33100 UDINE,ITALY. RI Eftimiadi, Costantino/F-3491-2015 OI Eftimiadi, Costantino/0000-0003-1510-4614 FU NIDCR NIH HHS [DE-08415, DE-04881] NR 39 TC 28 Z9 30 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD FEB PY 1991 VL 49 IS 2 BP 180 EP 188 PG 9 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ET889 UT WOS:A1991ET88900009 PM 1846905 ER PT J AU ROSOWSKY, A BADER, H FREISHEIM, JH AF ROSOWSKY, A BADER, H FREISHEIM, JH TI SYNTHESIS AND BIOLOGICAL-ACTIVITY OF METHOTREXATE ANALOGS WITH 2 ACID GROUPS AND A HYDROPHOBIC AROMATIC RING IN THE SIDE-CHAIN .43. SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID HUMAN DIHYDROFOLATE-REDUCTASE; SITE-DIRECTED MUTAGENESIS; ALPHA-LYTIC PROTEASE; PEPTIDE BORONIC ACID; ANTITUMOR-ACTIVITY; GLUTAMATE MOIETY; SERINE PROTEASE; AMINOPTERIN; DERIVATIVES; INHIBITION AB The heretofore unknown gamma-(m-carboxyanilide) and gamma-(m-boronoanilide) derivatives of methotrexate (MTX) and the gamma-(m-carboxyanilide) derivatives of aminopterin (AMT) were prepared and tested as inhibitors of dihydrofolate reductase (DHFR) and as inhibitors of cell growth in culture with the aim of comparing their activity with that of N-alpha-(4-amino-4-deoxypteroyl)-N-delta-hemiphthaloyl-L-ornithine, a potent antifolate whose side chain likewise contains a hydrophobic aromatic ring with an acid group on the ring. All three anilides were potent DHFR inhibitors, with activity comparable to MTX and AMT. The gamma-(m-boronoanilide) displayed growth inhibitory potency similar to that of the hemiphthaloylornithine analogue, with an IC50 of only 0.7 nM. This compound, which is the most potent of the gamma-amides of MTX tested to date, is also the first reported example of an antifolate with a B(OH)2 group in the side chain and is especially novel because of its potential to form a stable tetrahedral boronate complex by reaction with electron rich OH or NH2 groups in the active site of DHFR or other folate enzymes. In antitumor assays against L1210 leukemia in mice, N-alpha-(4-amino-4-deoxypteroyl)-N-delta-hemiphthaloyl-L-ornithine gave a T/C of > 263% at 20 mg/kg (qdx9) and 300% at 16 mg/kg (bidx10), whereas maximally tolerated doses of MTX of 8 mg/kg (qdx9) and 1 mg/kg (bidx10) gave T/C values of 213 and 188%, respectively. MTX gamma-(m-boronoanilide) was also active, with a T/C of 175% at 32 mg/kg (qdx9), the highest dose tested. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MED COLL OHIO,DEPT BIOCHEM,TOLEDO,OH 43699. RP ROSOWSKY, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA25394, CA41461] NR 29 TC 10 Z9 10 U1 1 U2 3 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 FEB PY 1991 VL 34 IS 2 BP 574 EP 579 DI 10.1021/jm00106a016 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA EX563 UT WOS:A1991EX56300016 PM 1995880 ER PT J AU ROZENTAL, JM LEVINE, RL NICKLES, RJ AF ROZENTAL, JM LEVINE, RL NICKLES, RJ TI CHANGES IN GLUCOSE-UPTAKE BY MALIGNANT GLIOMAS - PRELIMINARY-STUDY OF PROGNOSTIC-SIGNIFICANCE SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE MALIGNANT GLIOMA; PET SCAN; TUMOR BIOENERGETICS; PATIENT PROGNOSIS ID MAGNETIC-RESONANCE SPECTROSCOPY; POSITRON EMISSION TOMOGRAPHY; CEREBRAL GLIOMAS; 8-DRUGS-IN-ONE-DAY CHEMOTHERAPY; ADULT PATIENTS; BRAIN-TUMOR; DEXAMETHASONE; RADIOTHERAPY; METABOLISM; PET AB Sequential positron emission tomographic scans with [F-18]-2-fluorodeoxyglucose (PET-FDG) were performed on 14 patients with malignant gliomas. All patients had prior brain irradiation. Five patients received adjuvant eight-drugs-in-one-day chemotherapy (experimental subjects) and 9 did not (control subjects). Ratios between the maximal tumor regional cerebral metabolic rate for glucose (rCMRGlu) and the contralateral white matter rCMRGlu, the glucose uptake ratio, were determined. Percent changes in the ratio 1 day after chemotherapy in experimental subjects, and 30 days after the baseline scan in controls, were of prognostic significance. In both groups, patients with the largest percent changes in rCMRGlu had the shortest survival. In contrast, the baseline glucose uptake ratio did not predict length of survival. C1 UNIV WISCONSIN,SCH MED,DEPT NEUROL,MADISON,WI 53792. UNIV WISCONSIN,SCH MED,DEPT RADIOL,MADISON,WI 53792. UNIV WISCONSIN,SCH MED,DEPT MED PHYS,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT NEUROL SURG,MADISON,WI 53792. UNIV WISCONSIN,SCH MED,DEPT RADIOL,MADISON,WI 53706. RP ROZENTAL, JM (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL & RES SERV,NEUROL SERV 127,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA14520]; NCRR NIH HHS [RR03186] NR 30 TC 33 Z9 34 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD FEB PY 1991 VL 10 IS 1 BP 75 EP 83 DI 10.1007/BF00151248 PG 9 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA ER691 UT WOS:A1991ER69100007 PM 2022974 ER PT J AU OLDENDORF, WH STOLLER, BE AF OLDENDORF, WH STOLLER, BE TI RAT-BRAIN FREE GLUCOSE AND LACTATE MEASUREMENT BY A NOVEL METHOD USING BISECTING DECAPITATION-EXTRUSION AND ENZYME DENATURATION AT 5 SECONDS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE BRAIN FREE GLUCOSE; BRAIN LACTATE; ASPIRATION-EXTRUSION SYRINGE; BISECTING DECAPITATION; HEAT DENATURATION; UREA DENATURATION AB This study investigates a novel method as a means for animal decapitation with rapid brain removal and enzyme denaturation. Briefly, the rat head is simultaneously decapitated and bisected. Either half of the in situ brain is aspirated under -250 mm Hg pressure into a modified small plastic syringe and then extruded through a needle as a fine strand into a relatively large volume of 2 M urea at 95-degrees-C. After cooling, sonication, and centrifugation of the brain homogenate, the supernatant is measured enzymatically for brain free glucose and lactate concentration. Enzyme denaturation is effected within 4-6 s. The results are in good agreement with published values for glucose and lactate using other rapid enzyme inactivation techniques. C1 UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. RP OLDENDORF, WH (reprint author), W LOS ANGELES VET ADM,RES SERV,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 9 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD FEB PY 1991 VL 56 IS 2 BP 611 EP 614 DI 10.1111/j.1471-4159.1991.tb08193.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA ET732 UT WOS:A1991ET73200034 PM 1988559 ER PT J AU STEFANO, GB SHIPP, MA SCHARRER, B AF STEFANO, GB SHIPP, MA SCHARRER, B TI A POSSIBLE IMMUNOREGULATORY FUNCTION FOR [MET]-ENKEPHALIN-ARG6-PHE7 INVOLVING HUMAN AND INVERTEBRATE GRANULOCYTES SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE [MET]-ENKEPHALIN-ARG6-PHE7; MYTILUS EDULIS; GRANULOCYTES; HUMAN; IMMUNOCYTE ID OPIOID NEUROPEPTIDES; BETA-ENDORPHIN; ENKEPHALIN; HEMOCYTES AB Opioid peptides and their analogs have been shown to stimulate adherence, conformational changes and locomotory activity in human as well as invertebrate granulocytes. The present study demonstrates that [Met]-enkephalin-Arg6-Phe7, and opioid substance thus far not included in these immunological tests, exhibits stimulatory effects comparable to those of [Met]-enkephalin in this regard. Furthermore, since neutral endopeptidase 24.11 (enkephalinase; CD10/NEP) exists in invertebrate immunocyte membranes, we demonstrate that its specific inhibitor, phosphoramidon, potentiates the effects of the heptapeptide in inducing conformational change in both human and invertebrate granulocytes. Additionally, the major metabolic products of NEP activity, Phe-Met-Arg-Phe and Tyr-Gly-Gly, appear to be potent antagonists of this enzyme activity, especially the tetrapeptide. The effects of heptapeptide stimulation showed a major difference between vertebrate and invertebrate immunocytes with respect to their time course, namely, the speed of their onset. [Met]-enkephalin-Arg6-Phe7 markedly stimulated the locomotory activity of these cells which becomes most noticeable within 15-45 min for Mytilus cells and ina 5-15 min period for human cells. It also enhanced the mobility and velocity of the responsive human (5-mu-m/min) and invertebrate cells (2.1-mu-m/min). C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT ANAT & STRUCT BIOL,BRONX,NY 10461. RP STEFANO, GB (reprint author), SUNY COLL OLD WESTBURY,MULTIDISCIPLINARY CTR STUDY AGING,OLD WESTBURY,NY 11568, USA. FU BHP HRSA HHS [MBRS 08180]; NCI NIH HHS [CA 49232]; NIAMS NIH HHS [MARC 17138] NR 17 TC 46 Z9 47 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD FEB PY 1991 VL 31 IS 2 BP 97 EP 103 DI 10.1016/0165-5728(91)90015-Y PG 7 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA EZ710 UT WOS:A1991EZ71000002 PM 1991823 ER PT J AU MCGRAIL, KM PHILLIPS, JM SWEADNER, KJ AF MCGRAIL, KM PHILLIPS, JM SWEADNER, KJ TI IMMUNOFLUORESCENT LOCALIZATION OF 3 NA,K-ATPASE ISOZYMES IN THE RAT CENTRAL-NERVOUS-SYSTEM - BOTH NEURONS AND GLIA CAN EXPRESS MORE THAN ONE NA,K-ATPASE SO JOURNAL OF NEUROSCIENCE LA English DT Article ID 2 DIFFERENT NA,K-ATPASES; (NA+ + K+)-ATPASE; IMMUNOCYTOCHEMICAL LOCALIZATION; ADHESION MOLECULE; ALPHA-SUBUNIT; OPTIC-NERVE; CYTOCHEMICAL-LOCALIZATION; ADENOSINE-TRIPHOSPHATASE; CATALYTIC SUBUNIT; MESSENGER-RNA AB In the CNS, there are multiple isozymes of the sodium and potassium ion-stimulated adenosine triphosphatase (Na,K-ATPase) that have differences in affinity for Na+, ATP, and cardiac glycosides. Three forms of the catalytic subunit (designated alpha-1, alpha-2, and alpha-3) are known to be derived from different genes, but little is known of the cellular distributions of the proteins or their physiological roles. Isozyme-specific monoclonal antibodies permitted the immunofluorescent localization of the 3 Na,K-ATPase in the rat CNS, and markedly different patterns of staining were seen. All 3 isozymes were detected, singly or in combination, in 1 or more neuronal structures, while both alpha-1 and alpha-2 were detected in glia. Many different neuroanatomic structures or cell types stained for more than 1 isozyme. Even when a structure or region stained for more than 1 isozyme, the pattern of staining was frequently dissimilar, suggesting complex differences in gene expression and cellular localization. C1 MASSACHUSETTS GEN HOSP,WELLMAN 4,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. FU NHLBI NIH HHS [HL 36271]; NINDS NIH HHS [NS 07009, NS 27653] NR 38 TC 280 Z9 280 U1 0 U2 3 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD FEB PY 1991 VL 11 IS 2 BP 381 EP 391 PG 11 WC Neurosciences SC Neurosciences & Neurology GA EW680 UT WOS:A1991EW68000008 PM 1846906 ER PT J AU ROCCO, TP AF ROCCO, TP TI THALLIUM-201-CHLORIDE FOR THE DETECTION OF VIABLE MYOCARDIUM SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID THALLIUM REDISTRIBUTION; TL-201 DEFECTS; TIME COURSE; REVERSIBILITY; MECHANISMS; KINETICS; SPECT C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BROCKTON W ROXBURY VET ADM MED CTR,BOSTON,MA. NR 30 TC 2 Z9 2 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD FEB PY 1991 VL 32 IS 2 BP 200 EP 203 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EX291 UT WOS:A1991EX29100005 PM 1772473 ER PT J AU TAKAHASHI, H WANDS, JR AF TAKAHASHI, H WANDS, JR TI PROGNOSIS OF HEPATOCELLULAR-CARCINOMA - KNOWN TO BE POOR - YET DIFFICULT TO PREDICT SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID HEPATOBILIARY AGENT; FEATURES; TUMOR C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. NR 19 TC 3 Z9 3 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD FEB PY 1991 VL 32 IS 2 BP 235 EP 236 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EX291 UT WOS:A1991EX29100012 PM 1846911 ER PT J AU YAOITA, H UEHARA, T BROWNELL, AL RABITO, CA AHMAD, M KHAW, BA FISCHMAN, AJ STRAUSS, HW AF YAOITA, H UEHARA, T BROWNELL, AL RABITO, CA AHMAD, M KHAW, BA FISCHMAN, AJ STRAUSS, HW TI LOCALIZATION OF TECHNETIUM-99M-GLUCARATE IN ZONES OF ACUTE CEREBRAL INJURY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID EPITHELIAL-CELL LINE; BLOOD-FLOW; COMPUTED-TOMOGRAPHY; GLUCOSE-UTILIZATION; FOCAL ISCHEMIA; RAT-BRAIN; INFARCTION; KIDNEY; CT; QUANTIFICATION AB The potential structural similarity of technetium-99m-labeled glucaric acid (99mTc-glucarate) to that of fructose suggests that this agent may enter cells by a sugar transport system. Studies with LLC-PK1 cells demonstrated inhibition of 99mTc-glucarate uptake by fructose, confirming this potential relationship. Since anaerobic metabolism can use either glucose or fructose, we hypothesized that 99mTc-glucarate may concentrate in areas of acute ischemic injury. To test this hypothesis, 63 adult rats with middle cerebral artery (MCA) occlusion followed by reperfusion were injected with 99mTc-glucarate and in vivo and ex vivo images were acquired. Seven animals were also studied with 18FDG and high resolution PET imaging. The radionuclide images were compared to the results of triphenyl tetrazolium chloride (TTC) staining and conventional histopathology. Thirty-five rats had significant accumulation of 99mTc-glucarate and no TTC staining (indicating infarction) in the involved hemisphere. Of the remaining 28 rats with TTC staining (suggesting viability) of the involved hemisphere, 16 (57%) had 99mTc-glucarate accumulation. In the seven rats that were studied with both 99mTc-glucarate and 18FDG, 99mTc-glucarate accumulated at the center of the occluded MCA territory while 18FDG activity was decreased in this region. These results suggest that 99mTc-glucarate is a sensitive marker of acute severe cerebral injury, but its mechanism of localization is probably different from that of 18FDG. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 37 TC 22 Z9 22 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD FEB PY 1991 VL 32 IS 2 BP 272 EP 278 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EX291 UT WOS:A1991EX29100021 PM 1704054 ER PT J AU NARULA, J SOUTHERN, JF ABRAHAM, S PIERI, P KHAW, BA YASUDA, T AF NARULA, J SOUTHERN, JF ABRAHAM, S PIERI, P KHAW, BA YASUDA, T TI MYOCARDITIS SIMULATING MYOCARDIAL-INFARCTION - CASE PRESENTATION AND DISCUSSION SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID MYOSIN-SPECIFIC ANTIBODY; VENTRICULAR ENDOMYOCARDIAL BIOPSY; MONOCLONAL ANTIMYOSIN ANTIBODY; 100 CONSECUTIVE PATIENTS; NORMAL CORONARY-ARTERIES; CARDIAC MYOSIN; DILATED CARDIOMYOPATHIES; HEART-FAILURE; LIGHT-CHAINS; CONGESTIVE CARDIOMYOPATHY C1 MASSACHUSETTS GEN HOSP,DIV NUCL MED,TILTON 2,32 FRUIT ST,BOSTON,MA 02114. NR 65 TC 3 Z9 3 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD FEB PY 1991 VL 32 IS 2 BP 312 EP 318 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EX291 UT WOS:A1991EX29100028 PM 1992036 ER PT J AU SHAMBERGER, RC HOLZMAN, RS GRISCOM, NT TARBELL, NJ WEINSTEIN, HJ AF SHAMBERGER, RC HOLZMAN, RS GRISCOM, NT TARBELL, NJ WEINSTEIN, HJ TI CT QUANTITATION OF TRACHEAL CROSS-SECTIONAL AREA AS A GUIDE TO THE SURGICAL AND ANESTHETIC MANAGEMENT OF CHILDREN WITH ANTERIOR MEDIASTINAL MASSES SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article DE HODGKINS DISEASE; LYMPHOMA; TERATOMA; MEDIASTINAL MASS; TRACHEA; COMPRESSION ID HODGKINS-DISEASE; GENERAL-ANESTHESIA; AIRWAY-OBSTRUCTION; PATIENT; DIMENSIONS; INDUCTION C1 CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT ANESTHESIA,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT RADIOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT RADIAT THERAPY,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. RP SHAMBERGER, RC (reprint author), CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT SURG,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 15 TC 41 Z9 44 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0022-3468 J9 J PEDIATR SURG JI J. Pediatr. Surg. PD FEB PY 1991 VL 26 IS 2 BP 138 EP 142 DI 10.1016/0022-3468(91)90894-Y PG 5 WC Pediatrics; Surgery SC Pediatrics; Surgery GA EV975 UT WOS:A1991EV97500005 PM 2023069 ER PT J AU ARNOW, D HARRISON, RH AF ARNOW, D HARRISON, RH TI AFFECT IN EARLY MEMORIES OF BORDERLINE PATIENTS SO JOURNAL OF PERSONALITY ASSESSMENT LA English DT Article C1 MASSACHUSETTS GEN HOSP,BUNKER,HILL HLTH CTR,BOSTON,MA 02114. BOSTON UNIV,BOSTON,MA 02215. NR 27 TC 7 Z9 7 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0022-3891 J9 J PERS ASSESS JI J. Pers. Assess. PD FEB PY 1991 VL 56 IS 1 BP 75 EP 83 DI 10.1207/s15327752jpa5601_7 PG 9 WC Psychology, Clinical; Psychology, Social SC Psychology GA EV771 UT WOS:A1991EV77100008 PM 16370903 ER PT J AU HENSLER, JG ORDWAY, GA GAMBARANA, C ARESO, P FRAZER, A AF HENSLER, JG ORDWAY, GA GAMBARANA, C ARESO, P FRAZER, A TI SEROTONERGIC NEURONS DO NOT INFLUENCE THE REGULATION OF BETA-ADRENOCEPTORS INDUCED BY EITHER DESIPRAMINE OR ISOPROTERENOL SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID RAT CEREBRAL-CORTEX; ADRENERGIC-RECEPTOR-BINDING; QUANTITATIVE AUTORADIOGRAPHY; DOWN-REGULATION; BRAIN CORTEX; ANTIDEPRESSANTS; CLENBUTEROL; AGONIST; SLICES; SITES AB It has been suggested that 5-hydroxytryptamine (serotonin)-containing neurons influence the regulation of central beta adrenoceptors caused by antidepressants. [H-3]Dihydroalprenolol ([H-3]DHA) was the radioligand used in these previous studies to measure beta adrenoceptors. In this study, we compared the binding characteristics of [H-3]DHA with those of [I-125]iodopindolol ([I-125]IPIN) and used [I-125]IPIN to study effects of lesioning serotonergic nerves on the regulation of beta adrenoceptors. A comparison was made in homogenates prepared from rat frontal cortex of the specific binding of [H-3]DHA with that of [I-125-IPIN to beta adrenoceptors. Nonlinear regression analysis of saturation experiments of [H-3]DHA binding to cortical homogenates indicated that a two-component binding model fit the data significantly better than a one-component model. A dissociation constant value of 0.47 +/- 0.16 nM and a B(max) value of 62 +/- 7 fmol/mg protein were obtained for the high-affinity site. The low-affinity site was poorly defined. Rosenthal transformations of the saturation isotherms for [H-3]DHA binding were clearly curvilinear. By contrast, nonlinear regression analysis of saturation experiments of the binding of [I-125]IPIN indicated that the binding of this radioligand was described adequately by a one-component model and yielded a dissociation constant value of 147 +/- 10 pM with a B(max) of 80 +/- 5 fmol/mg protein. Rosenthal transformations of the [I-125]IPIN data were linear. From such data, it was inferred that [H-3]DHA binds to some site in addition to beta adrenoceptors, whereas [I-125]IPIN does not. In frontal cortical homogenates of rats treated with 5,7-dihydroxytryptamine (5,7-DHT), the density of specific binding sites for [H-3]DHA was significantly increased, whereas no increase in the specific binding of [I-125]IPIN was observed. Moreover, when [I-125]IPIN was used as the ligand to measure beta adrenoceptors, lesioning serotonergic neurons with 5,7-DHT did not prevent the down-regulation of beta adrenoceptors induced by chronic administration of desipramine. Furthermore, as assessed by quantitative autoradiography using [I-125]IPIN, the down-regulation of subtypes of beta adrenoceptors in different regions of brain, produced by chronic intraventricular infusion of the direct acting agonist isoproterenol, was not altered in rats pretreated with 5,7-DHT. We conclude that 5,7-DHT-induced lesioning of serotonergic neurons does not influence the down-regulation of beta adrenoceptors as a result of repeated administration of the tricyclic antidepressant desipramine or chronic infusion of the agonist isoproterenol when [I-125]IPIN is used as the radioligand to measure these receptors. Interestingly, treatment of rats with 5,7-DHT resulted in a significant reduction in the binding of [I-125]IPIN to beta1 adrenoceptors in nine of 13 areas of the brain examined and a significant reduction in beta-2 adrenoceptors in five of the areas, suggesting the presence of beta adrenoceptors on serotonergic neurons in many areas of the brain. C1 UNIV PENN,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. RP HENSLER, JG (reprint author), DEPT VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT,151E,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIMH NIH HHS [MH 29094, MH 14654, MH 09834] NR 44 TC 14 Z9 14 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD FEB PY 1991 VL 256 IS 2 BP 656 EP 664 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EY611 UT WOS:A1991EY61100037 PM 1847207 ER PT J AU MANKIN, HJ JENNINGS, LC TREADWELL, BV TRIPPEL, SB AF MANKIN, HJ JENNINGS, LC TREADWELL, BV TRIPPEL, SB TI GROWTH-FACTORS AND ARTICULAR-CARTILAGE SO JOURNAL OF RHEUMATOLOGY LA English DT Article; Proceedings Paper CT 2ND SYMP ON OSTEOARTHRITIS : UPDATE ON DIAGNOSIS AND THERAPY CY OCT 02-05, 1990 CL VAL DAVID, CANADA SP ROUSSEL CANADA DE GROWTH FACTORS; ARTICULAR CARTILAGE; BASIC FIBROBLAST GROWTH FACTOR; TRANSFORMING GROWTH FACTOR-BETA ID FACTOR-BETA; PROTEOGLYCANS; METABOLISM; CULTURES; SERUM AB Studies of articular cartilage over the decades have demonstrated a surprisingly brisk rate of synthesis of the matrix proteins which appears to vary considerably with metabolic, physicochemical and pathological state of the tissue. It has become evident that much of this activity is directed by low molecular weight protein mediators which act at specific receptor sites. Platelet derived growth factor (PDGF) is of limited action in normal cartilage, but insulin and its analogues, insulin growth factor-I and II are powerful stimulants of DNA synthesis. Basic fibroblast growth factor stimulates both DNA and protein synthesis and works synergistically with other factors. Transforming growth factor beta potentiates the action of the mitogens and enhances and regulates proteoglycan synthesis. These actions may be of special importance in osteoarthritis and lacerative injury to cartilage. RP MANKIN, HJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,ORTHOPED RES LABS,BOSTON,MA 02114, USA. NR 13 TC 8 Z9 8 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD FEB PY 1991 VL 18 SU 27 BP 66 EP 67 PG 2 WC Rheumatology SC Rheumatology GA FA474 UT WOS:A1991FA47400024 ER PT J AU ODELL, K MCNEIL, MR ROSENBEK, JC HUNTER, L AF ODELL, K MCNEIL, MR ROSENBEK, JC HUNTER, L TI PERCEPTUAL CHARACTERISTICS OF VOWEL AND PROSODY PRODUCTION IN APRAXIC, APHASIC, AND DYSARTHRIC SPEAKERS SO JOURNAL OF SPEECH AND HEARING RESEARCH LA English DT Article DE CONSONANT ARTICULATION; PERCEPTUAL ANALYSIS; APRAXIA OF SPEECH; ATAXIC DYSARTHRIA; CONDUCTION APHASIA ID SPEECH; COARTICULATION; PATTERNS C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,SPEECH PATHOL & AUDIOL SERV,MADISON,WI. UNIV WISCONSIN,DEPT AFRICAN LANGUAGES & LINGUIST,MADISON,WI 53706. RP ODELL, K (reprint author), UNIV WISCONSIN,DEPT COMMUNICAT DISORDERS,MADISON,WI 53706, USA. FU NICHD NIH HHS [5030 HD03352]; PHS HHS [N518797] NR 70 TC 51 Z9 52 U1 1 U2 4 PU AMER SPEECH-LANG-HEARING ASSN PI ROCKVILLE PA 10801 ROCKVILLE PIKE RD, ROCKVILLE, MD 20852-3279 SN 0022-4685 J9 J SPEECH HEAR RES JI J. Speech Hear. Res. PD FEB PY 1991 VL 34 IS 1 BP 67 EP 80 PG 14 WC Language & Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA FA503 UT WOS:A1991FA50300010 PM 2008083 ER PT J AU CUNNINGHAM, JJ LYDON, MK BRIGGS, SE DECHEKE, M AF CUNNINGHAM, JJ LYDON, MK BRIGGS, SE DECHEKE, M TI ZINC AND COPPER STATUS OF SEVERELY BURNED CHILDREN DURING TPN SO JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION LA English DT Article DE ZINC; COPPER; PARENTERAL NUTRITION; BURNS ID TOTAL PARENTERAL-NUTRITION; ENDOGENOUS MEDIATOR LEM; THERMAL-INJURY; SERUM COPPER; DISEASE; INFANTS AB Alterations in zinc (Zn) and copper (Cu) homeostasis have been reported during the acute recovery period following thermal injury in both children and adults. Increased urinary losses of Zn and Cu and decreased plasma concentrations of Zn, Cu, and ceruloplasmin (CP), the major copper transport protein, occur despite adequate provision of these elements in enteral feedings. We now report data for moderately to severely burned children receiving total parenteral nutrition (TPN) supplemented to provide Zn and Cu. Hyperzincuria occurred consistently when 50-mu-g/kg Zn was delivered daily to older children. Similarly, when younger children received 100-mu-g/kg Zn daily, profound hyperzincuria ensued despite a reduction in total plasma Zn. Hypozincemia was accompanied by low levels of Zn in the plasma subfraction normally associated with albumin-bound Zn. The delivery of Cu via TPN was 4-12-mu-g/kg daily, and urinary Cu losses were not elevated. Plasma total Cu and plasma CP were invariably reduced. These findings are discussed in relation to guidelines published for pediatric trace element supplementation during TPN. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV MASSACHUSETTS,GRAD SCH,MICROANAL LAB,AMHERST,MA 01003. RP CUNNINGHAM, JJ (reprint author), SHINERS BURNS INST,NUTR SUPPORT UNIT,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 25 TC 17 Z9 17 U1 0 U2 1 PU AMER COLL NUTRITION PI NEW YORK PA C/O HOSP. JOINT DIS. 301 E. 17TH ST., NEW YORK, NY 10003 SN 0731-5724 J9 J AM COLL NUTR JI J. Am. Coll. Nutr. PD FEB PY 1991 VL 10 IS 1 BP 57 EP 62 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA EU868 UT WOS:A1991EU86800010 PM 1901324 ER PT J AU LI, JJ BRAMLET, SG CARTER, EA BURKE, JF AF LI, JJ BRAMLET, SG CARTER, EA BURKE, JF TI THE RAT LUNG ORGANOTYPIC CULTURE - AN INVITRO MODEL FOR STUDYING SURFACTANT METABOLISM ABNORMALITIES SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Article ID RESPIRATORY-DISTRESS SYNDROME; C-REACTIVE PROTEIN; DIPALMITOYL PHOSPHATIDYLCHOLINE; GRANULAR PNEUMOCYTES; LAMELLAR BODIES; II CELLS; APOLIPOPROTEIN; CLEARANCE; LIPOSOMES; BINDING AB The amount of surfactant present in the intra-alveolar space is mainly regulated by the synthesis and recycling of surfactant by type II pneumocytes. Biochemical analyses have shown that the surfactant level is frequently diminished and that protein-rich exudate can further interfere with surfactant function in the lungs of adult respiratory distress syndrome (ARDS) patients. The microenvironmental changes that occur in the alveoli of burned patients, who are prone to developing ARDS, are unclear. Therefore, using an in vitro rat lung organotypic culture, we showed that the sera of rats with a 3-day old, third-degree thermal injury (25-30% total body surface area) inhibited surfactant synthesis in organotypically cultured rat lung cells. Surfactant precursor, H-3-choline, incorporation into the surfactant was 58% of control. Using liposomes made of dipalmitoyl phosphatidylcholine and phosphatidylglycerol (8:1, v/v) or surfactant we showed that surfactant endocytosis by purified type II alveolar cells is an active, temperature-dependent process, and correlates with the quantity of surfactant present in the milieu. We also found that plasma protein-rich fluid interfered with surfactant endocytosis by the purified type II pneumocytes. These two processes of inhibition of surfactant synthesis and its reutilization by these cells may contribute to the pathogenesis of ARDS. C1 MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,DEPT PEDIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 41 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1079-6061 J9 J TRAUMA JI J. Trauma-Injury Infect. Crit. Care PD FEB PY 1991 VL 31 IS 2 BP 174 EP 181 PG 8 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA EY743 UT WOS:A1991EY74300003 PM 1994076 ER PT J AU BREWSTER, DC CAMBRIA, RP MONCURE, AC DARLING, RC LAMURAGLIA, GM GELLER, SC ABBOTT, WM AF BREWSTER, DC CAMBRIA, RP MONCURE, AC DARLING, RC LAMURAGLIA, GM GELLER, SC ABBOTT, WM TI AORTOCAVAL AND ILIAC ARTERIOVENOUS-FISTULAS - RECOGNITION AND TREATMENT SO JOURNAL OF VASCULAR SURGERY LA English DT Article; Proceedings Paper CT 38TH SCIENTIFIC MEETING OF THE NORTH AMERICAN CHAPTER OF THE INTERNATIONAL SOC FOR CARDIOVASCULAR SURGERY CY JUN 04-06, 1990 CL LOS ANGELES, CA SP INT SOC CARDIOVASC SURG, N AMER CHAPTER ID ABDOMINAL AORTIC-ANEURYSM; CAVAL FISTULA; AUTO-TRANSFUSION; COMPLICATION; SECONDARY; DISEASE; RUPTURE; MANAGEMENT; HEMATURIA; DIAGNOSIS AB Despite the well characterized physiologic effects of aortocaval or iliac arteriovenous fistulas, patients with such uncommon lesions may manifest a diverse array of symptoms, and diagnosis is often delayed or overlooked. To examine clinical features that facilitate recognition and allow successful repair, a 30-year experience with 20 such fistulas was reviewed. Fourteen fistulas were caused by aneurysm erosion, four followed iatrogenic injury during lumbar disk surgery, and two developed from abdominal gunshot wounds. The interval from presumed occurrence to diagnosis ranged from 3 hours to 8 years. The diagnosis was not recognized before surgery in five (25%) patients. Back pain (70%) was the most common symptom. The presence of a typical abdominal bruit (80%) was the most reliable physical finding, but its significance was occasionally overlooked or misinterpreted. Congestive heart failure was prominent in only seven (35%) patients. Severe lower extremity edema and mottling was the primary manifestation in eight cases, often causing initial confusion with venous thrombosis. Hematuria (5 patients) and oliguric renal failure (4 patients), both fully reversible after fistula repair, also caused diagnostic uncertainty. The mean preoperative cardiac output was 12.2 L/min, falling to 5.4 L/min with fistula repair. Mean blood loss was 5960 ml, supporting use of intraoperative autotransfusion. Two operative deaths (10%) occurred, both in patients not correctly diagnosed before surgery. Despite varied modes of presentation, prompt recognition and use of appropriate operative techniques should achieve successful repair. C1 MASSACHUSETTS GEN HOSP,DIV VASC SURG,GEN SURG SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,VASC RADIOL SECT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. NR 46 TC 75 Z9 80 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD FEB PY 1991 VL 13 IS 2 BP 253 EP 265 PG 13 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA EX035 UT WOS:A1991EX03500010 PM 1990167 ER PT J AU GELLER, AI AF GELLER, AI TI INFLUENCE OF THE HELPER VIRUS ON EXPRESSION OF BETA-GALACTOSIDASE FROM A DEFECTIVE HSV-1 VECTOR, PHSVLAC SO JOURNAL OF VIROLOGICAL METHODS LA English DT Article DE HSV-1 VECTOR; GENE TRANSFER; GENE THERAPY; HSV-1 LATENCY ID GENE; RETROVIRUS; TYPE-1; MUTANTS; LINEAGE; CELLS AB Defective herpes simplex virus type 1 (HSV-1) vectors can deliver genes into both mitotic and postmitotic cells, including neurons and these vectors, therefore, have great potential use. pHSVlac, the prototype HSV-1 vector, expresses the E. coli Lac Z gene from the HSV-1 immediate early 4/5 promoter. pHSVlac can stably express beta-galactosidase in a range of mammalian cell lines and in neurons from throughout the nervous system, both in culture and in the adult rat brain. Thus, HSV-1 vectors may be useful for studying HSV-1 latency, neuronal physiology, and performing gene therapy for neurological conditions. A virus stock of pHSVlac consists of identical HSV-1 particles containing either pHSV1ac DNA or the HSV-1 helper virus DNA. Thus, a cell can be infected with the pHSVlac virus, the helper virus, or both; consequently, it is important to determine if the helper virus influences the behavior of pHSVlac. The effect of the helper virus on expression of beta-galactosidase from pHSVlac was investigated: it was demonstrated first, that pHSVlac can be efficiently packaged into HSV-1 virus particles using each of five HSV-1 temperature sensitive (ts) mutants as helper virus. Second, pHSVlac grown with each of the five HSV-1 ts mutants expressed high levels of beta-galactosidase. Third, pHSVlac grown with HSV-1 strain 17 ts K as helper virus expresses the same amount of beta-galactosidase in the absence or presence of ts K. Thus, pHSVlac can efficiently express a gene independent of the HSV-1 helper virus. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROGENET LAB,BOSTON,MA 02114. EUNICE KENNEDY SCHRIVER CTR,DIV MOLEC NEUROGENET,WALTHAM,MA. RI Geller, Alfred/C-6469-2012 NR 20 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-0934 J9 J VIROL METHODS JI J. Virol. Methods PD FEB-MAR PY 1991 VL 31 IS 2-3 BP 229 EP 238 DI 10.1016/0166-0934(91)90161-R PG 10 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Virology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Virology GA FE975 UT WOS:A1991FE97500010 PM 1650784 ER PT J AU IMBALZANO, AN COEN, DM DELUCA, NA AF IMBALZANO, AN COEN, DM DELUCA, NA TI HERPES-SIMPLEX VIRUS TRANSACTIVATOR ICP4 OPERATIONALLY SUBSTITUTES FOR THE CELLULAR TRANSCRIPTION FACTOR SP1 FOR EFFICIENT EXPRESSION OF THE VIRAL THYMIDINE KINASE GENE SO JOURNAL OF VIROLOGY LA English DT Article ID RNA POLYMERASE-II; TEMPERATURE-SENSITIVE MUTANTS; MAJOR REGULATORY PROTEIN; DNA-BINDING PROPERTIES; IMMEDIATE-EARLY GENE; TYPE-1 LATE GENE; MACROMOLECULAR-SYNTHESIS; INVITRO TRANSCRIPTION; NUCLEOTIDE-SEQUENCE; TRANS INDUCTION AB The herpes simplex virus type 1 (HSV-1) ICP4 protein is a transcriptional activator of many eucaryotic RNA polymerase II promoters. The HSV-1 thymidine kinase gene (tk) promoter is induced by ICP4 and contains binding sites for the cellular transcription factors TFIID, Sp1, and CCAAT-binding proteins, each of which affects expression of the tk gene. In this study, the effects of mutations in these sites on the transcription of tk in the presence and absence of ICP4 were determined during viral infection. Only the TATA box was necessary for efficient expression in the presence of ICP4; however, ICP4 apparently can still induce tk transcription even when the TATA box is disrupted. Alteration of the Sp1 sites had a minor effect on ICP4-induced expression in comparison to a large effect in the absence of ICP4, indicating that ICP4 can operationally substitute for the function of the transcription factor Sp1. In addition, tk was still expressed with the kinetics of an early gene in the absence of binding sites for Sp1 and CCAAT-binding proteins. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NIAID NIH HHS [AI26126, AI27431] NR 62 TC 47 Z9 47 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD FEB PY 1991 VL 65 IS 2 BP 565 EP 574 PG 10 WC Virology SC Virology GA ET445 UT WOS:A1991ET44500002 PM 1846184 ER PT J AU SHEPARD, AA DELUCA, NA AF SHEPARD, AA DELUCA, NA TI A 2ND-SITE REVERTANT OF A DEFECTIVE HERPES-SIMPLEX VIRUS ICP4 PROTEIN WITH RESTORED REGULATORY ACTIVITIES AND IMPAIRED DNA-BINDING PROPERTIES SO JOURNAL OF VIROLOGY LA English DT Article ID IMMEDIATE-EARLY GENE; TEMPERATURE-SENSITIVE MUTANTS; THYMIDINE KINASE GENE; MACROMOLECULAR-SYNTHESIS; NEGATIVE REGULATION; VIRAL POLYPEPTIDES; TRANS INDUCTION; RNA SYNTHESIS; ALPHA-GENES; TYPE-1 AB A mutant of herpes simplex virus type 1, vi12, encodes a DNA-binding- and transactivation-deficient ICP4 polypeptide. Because of the mutation, the vi12 virus does not grow on Vero cells but must be propagated on cells that express complementing levels of wild-type ICP4 (E5 cells). A pseudorevertant of vi12, designated pril2, was isolated on the basis of the restored ability to replicate on Vero cells. In addition to the original i12 insertion mutation at amino acid 320, the ICP4 molecule expressed from pri12 possesses an alanine to valine substitution at amino acid 342 within the ICP4 gene. The infectivity of pri12 on Vero cells as measured by burst size is elevated by 5 orders of magnitude relative to that observed for vi12, reflecting the restored ability of the mutant ICP4 molecule possessing the alanine to valine substitution to activate transcription and thus support viral replication. Despite the restored regulatory activities, of the pri12 ICP4 molecule, the ability of the pseudorevertant ICP4 molecule to form a high-affinity, specific interaction with the consensus binding site was still impaired relative to that of wild-type ICP4. This observation suggests that the in vitro-measured DNA-binding properties of ICP4 may not reflect the functional interactions occurring in vivo that mediate transcriptional activation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,COMM VIROL,BOSTON,MA 02115. FU NIAID NIH HHS [AI27431] NR 56 TC 34 Z9 34 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD FEB PY 1991 VL 65 IS 2 BP 787 EP 795 PG 9 WC Virology SC Virology GA ET445 UT WOS:A1991ET44500027 PM 1846199 ER PT J AU POMERANTZ, RJ FEINBERG, MB ANDINO, R BALTIMORE, D AF POMERANTZ, RJ FEINBERG, MB ANDINO, R BALTIMORE, D TI THE LONG TERMINAL REPEAT IS NOT A MAJOR DETERMINANT OF THE CELLULAR TROPISM OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO JOURNAL OF VIROLOGY LA English DT Note ID HTLV-III; PERIPHERAL-BLOOD; AIDS VIRUS; T-CELL; INFECTION; HIV-1; ESTABLISHMENT; RETROVIRUSES; SEQUENCES; PROTEIN AB The long terminal repeats (LTRs) of human immunodeficiency virus type 1 (HIV-1) strains from the central nervous systems of four patients with AIDS and of an HIV-1 isolate which is highly macrophage-tropic were isolated by using the polymerase chain reaction. In transient transfection assays, these LTRs demonstrated no significant difference in basal or stimulated levels of transcription in any of a variety of cell lines tested, compared with expression directed from the LTR of a T-lymphocyte-tropic strain of HIV-1. Chimeric viruses were created with the LTRs of the macrophage-tropic and brain-derived viruses ligated to the viral backbone from a T-lymphocyte-tropic strain. No change in cellular tropism was demonstrated with these chimeric viruses. Thus, unlike the LTRs of some murine retroviruses, the LTR of HIV-1 does not appear to play a major role in determining cellular tropism. C1 WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV INFECT DIS,BOSTON,MA 02114. FU NHLBI NIH HHS [HL43510]; NIAID NIH HHS [AI99030, AI226463] NR 36 TC 36 Z9 37 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD FEB PY 1991 VL 65 IS 2 BP 1041 EP 1045 PG 5 WC Virology SC Virology GA ET445 UT WOS:A1991ET44500064 PM 1987367 ER PT J AU NADOL, JB KROUSE, JH AF NADOL, JB KROUSE, JH TI THE HYPOTYMPANUM AND INFRALABYRINTHINE CELLS IN CHRONIC OTITIS-MEDIA SO LARYNGOSCOPE LA English DT Article ID CHOLESTEATOMA AB Despite the localization implied by the term "chronic otitis media," little attention has been paid to the role of the hypotympanum in chronic active otitis media. Most authors have emphasized the role of recurrent cholesteatoma or unexenterated cells in the mastoid cell system as causes of recurrent disease. Seven cases are reported in which clinical evidence indicated that recurrent chronic otitis media was limited to the hypotympanum and infralabyrinthine cell system. In the five cases in which revision surgery was done, exenteration of this area resulted in an asymptomatic ear. The anatomy, radiographic evaluation, and surgical approach to the hypotympanum are reviewed. Careful inspection of the hypotympanum in primary surgery for chronic ear disease and exenteration of the hypotympanic and proximal infralabrinthine cell tract are advocated when these regions contain cholesteatoma or extensive granulomatous disease. RP NADOL, JB (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOL & LARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 15 TC 8 Z9 8 U1 0 U2 0 PU LARYNGOSCOPE CO PI ST LOUIS PA 10 S BROADWAY 14TH FLOOR, ST LOUIS, MO 63102-1741 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD FEB PY 1991 VL 101 IS 2 BP 137 EP 141 PG 5 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA EX029 UT WOS:A1991EX02900007 PM 1992263 ER PT J AU ANDREEFF, M STONE, R YOUNG, C TONG, W ERVIN, T TAFURI, A KOLITZ, J RIFKIND, R KUFE, D MARKS, P AF ANDREEFF, M STONE, R YOUNG, C TONG, W ERVIN, T TAFURI, A KOLITZ, J RIFKIND, R KUFE, D MARKS, P TI HEXAMETHYLENE BISACETAMIDE (HMBA) IN MYELODYSPLASTIC SYNDROMES (MDS) AND ACUTE MYELOID-LEUKEMIA (AML) SO LEUKEMIA LA English DT Meeting Abstract C1 MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD FEB PY 1991 VL 5 IS 2 BP 174 EP 174 PG 1 WC Oncology; Hematology SC Oncology; Hematology GA FH647 UT WOS:A1991FH64700018 ER PT J AU FISEL, CR ACKERMAN, JL BUXTON, RB GARRIDO, L BELLIVEAU, JW ROSEN, BR BRADY, TJ AF FISEL, CR ACKERMAN, JL BUXTON, RB GARRIDO, L BELLIVEAU, JW ROSEN, BR BRADY, TJ TI MR CONTRAST DUE TO MICROSCOPICALLY HETEROGENEOUS MAGNETIC-SUSCEPTIBILITY - NUMERICAL SIMULATIONS AND APPLICATIONS TO CEREBRAL PHYSIOLOGY SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article ID TRANSVERSE RELAXATION; SPIN RELAXATION; BRAIN IRON; BLOOD-FLOW; DIFFUSION; RESONANCE; PARTICLES; SYSTEMS; FIELDS; TISSUE C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. UNIV CALIF SAN DIEGO,DEPT RADIOL,SAN DIEGO,CA 92103. RP FISEL, CR (reprint author), MASSACHUSETTS GEN HOSP,CTR NMR,BOSTON,MA 02129, USA. RI Garrido, Leoncio/K-3092-2014; Ackerman, Jerome/E-2646-2015 OI Garrido, Leoncio/0000-0002-7587-1260; Ackerman, Jerome/0000-0001-5176-7496 FU NCI NIH HHS [2T32CA09362-06A1, P01-CA48729, R01-CA-40303] NR 38 TC 288 Z9 289 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD FEB PY 1991 VL 17 IS 2 BP 336 EP 347 DI 10.1002/mrm.1910170206 PG 12 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EW712 UT WOS:A1991EW71200005 PM 2062208 ER PT J AU CLINE, HE HARDY, CJ PEARLMAN, JD AF CLINE, HE HARDY, CJ PEARLMAN, JD TI FAST MR CARDIAC PROFILING WITH 2-DIMENSIONAL SELECTIVE PULSES SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article ID MAGNETIC-RESONANCE; SPATIAL LOCALIZATION; IMAGE-FORMATION; NMR; EXCITATION; OPTIMIZATION; DIMENSIONS; HEART C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP CLINE, HE (reprint author), GE,CORP RES & DEV,POB 8,SCHENECTADY,NY 12301, USA. NR 24 TC 13 Z9 13 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD FEB PY 1991 VL 17 IS 2 BP 390 EP 401 DI 10.1002/mrm.1910170211 PG 12 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EW712 UT WOS:A1991EW71200010 PM 2062212 ER PT J AU BERWICK, DM MURPHY, JM GOLDMAN, PA WARE, JE BARSKY, AJ WEINSTEIN, MC AF BERWICK, DM MURPHY, JM GOLDMAN, PA WARE, JE BARSKY, AJ WEINSTEIN, MC TI PERFORMANCE OF A 5-ITEM MENTAL-HEALTH SCREENING-TEST SO MEDICAL CARE LA English DT Article DE SCREENING; MENTAL HEALTH; ROC ANALYSIS; FUNCTIONAL STATUS QUESTIONNAIRE ID DIAGNOSTIC INTERVIEW SCHEDULE; CHARACTERISTIC ROC ANALYSIS; PRIMARY CARE; QUESTIONNAIRE; DEPRESSION; DISORDER; VALIDITY; POPULATION; SERVICES; DISTRESS AB We compared the screening accuracy of a short, five-item version of the Mental Health Inventory (MHI-5) with that of the 18-item MHI, the 30-item version of the General Health Questionnaire (GHQ-30), and a 28-item Somatic Symptom Inventory (SSI-28). Subjects were newly enrolled members of a health maintenance organization (HMO), and the criterion diagnoses were those found through use of the Diagnostic Interview Schedule (DIS) in a stratified sample of respondents to an initial, mailed GHQ. To compare questionnaires, we used receiver operating characteristic analysis, comparing areas under curves through the method of Hanley and McNeil. The MHI-5 was as good as the MHI-18 and the GHQ-30, and better than the SSI-28, for detecting most significant DIS disorders, including major depression, affective disorders generally, and anxiety disorders. Areas under curve for the MHI-5 ranged from 0.739 (for anxiety disorders) to 0.892 (for major depression). Single items from the MHI also performed well. In this population, short screening questionnaires, and even single items, may detect the majority of people with DIS disorders while incurring acceptably low false-positive rates. Perhaps such extremely short questionnaires could more commonly reach use in actual practice than the longer versions have so far, permitting earlier assessment and more appropriate treatment of psychiatrically troubled patients in primary care settings. C1 HARVARD COMMUNITY HLTH PLAN,BOSTON,MA. NEW ENGLAND MED CTR HOSP,INST IMPROVEMENT MED CARE & HLTH,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. NR 31 TC 752 Z9 758 U1 5 U2 40 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD FEB PY 1991 VL 29 IS 2 BP 169 EP 176 DI 10.1097/00005650-199102000-00008 PG 8 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA EX225 UT WOS:A1991EX22500008 PM 1994148 ER PT J AU LAIHO, M RONNSTRAND, L HEINO, J DECAPRIO, JA LUDLOW, JW LIVINGSTON, DM MASSAGUE, J AF LAIHO, M RONNSTRAND, L HEINO, J DECAPRIO, JA LUDLOW, JW LIVINGSTON, DM MASSAGUE, J TI CONTROL OF JUNB AND EXTRACELLULAR-MATRIX PROTEIN EXPRESSION BY TRANSFORMING GROWTH FACTOR-BETA-1 IS INDEPENDENT OF SIMIAN VIRUS-40 T-ANTIGEN-SENSITIVE GROWTH-INHIBITORY EVENTS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID RETINOBLASTOMA SUSCEPTIBILITY GENE; SV40 LARGE-T; PLASMINOGEN-ACTIVATOR INHIBITOR; FACTOR-BETA INDUCTION; CELL-CYCLE; PERICELLULAR DEPOSITION; EXOGENOUS UROKINASE; MAMMALIAN-CELLS; OSTEO-SARCOMA; MESSENGER-RNA AB Treatment of Mv1Lu mink lung epithelial cells with transforming growth factor-beta-1 (TGF-beta-1) prevents phosphorylation of the retinoblastoma susceptibility gene product, RB, in late G1 phase of the cell cycle, which is thought to retain RB in a growth-suppressive state. This effect is paralleled by cell cycle arrest in late G1 (M. Laiho, J. A. DeCaprio, J. W. Ludlow, D. M. Livingston, and J. Massague, Cell 62:175-185, 1990). Arrest can be prevented by expression of simian virus 40 T antigen, which binds to underphosphorylated RB, presumably blocking its growth-suppressive activity. The response of cells to TGF-beta-1, however, is complex and includes changes in the levels of expression of genes encoding nuclear transcription factors and extracellular matrix components. To define the relationships among various components of the TGF-beta-1 response, we have investigated the effect of TGF-beta-1 on cells whose growth-inhibitory response to this factor is prevented by T antigen. TGF-beta-1 addition to exponentially growing Mv1Lu cells increased the levels of junB mRNA and of three extracellular matrix proteins: plasminogen activator inhibitor-1, fibronectin, and thrombospondin. Kinetically, the effects on junB and plasminogen activator inhibitor-1 expression occurred faster (half-maximal at 1 to 2 h) than the effects on fibronectin and thrombospondin expression (half-maximal at 6 to 10 h). These effects either preceded or overlapped, respectively, the withdrawal of Mv1Lu cells from the cell cycle. Expression of a transfected T-antigen gene in Mv1Lu cells, however, did not prevent any of these responses to TGF-beta-1. The results indicate that TGF-beta-1-stimulated expression of junB and extracellular matrix proteins in Mv1Lu cells can occur independently of the T-antigen-sensitive events that lead to growth arrest. C1 MEM SLOAN KETTERING CANC CTR,HOWARD HUGHES MED INST,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,CELL BIOL & GENET PROGRAM,NEW YORK,NY 10021. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV NEOPLAST DIS MECHANISMS,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Ronnstrand, Lars/A-2429-2011 FU NCI NIH HHS [CA 39240, CA 34610, CA 50661] NR 60 TC 106 Z9 107 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1991 VL 11 IS 2 BP 972 EP 978 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EV176 UT WOS:A1991EV17600042 PM 1990295 ER PT J AU RAMESH, V GUSELLA, JF SHIH, VE AF RAMESH, V GUSELLA, JF SHIH, VE TI MOLECULAR PATHOLOGY OF GYRATE ATROPHY OF THE CHOROID AND RETINA DUE TO ORNITHINE AMINOTRANSFERASE DEFICIENCY SO MOLECULAR BIOLOGY & MEDICINE LA English DT Article ID KETOACID-TRANSAMINASE DEFICIENCY; DELTA-AMINOTRANSFERASE; L-ORNITHINE-2-OXOACID AMINOTRANSFERASE; BIOCHEMICAL HETEROGENEITY; SACCHAROMYCES-CEREVISIAE; NUCLEOTIDE-SEQUENCE; HUMAN CHROMOSOME-10; MOUSE CHROMOSOME-7; STRUCTURAL GENE; MESSENGER-RNA C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP RAMESH, V (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,BOSTON,MA 02114, USA. FU NEI NIH HHS [EYO5633]; NINDS NIH HHS [NS05096, NS20012] NR 66 TC 16 Z9 17 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0735-1313 J9 MOL BIOL MED PD FEB PY 1991 VL 8 IS 1 BP 81 EP 93 PG 13 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA GC512 UT WOS:A1991GC51200008 PM 1682785 ER PT J AU TAYLOR, RG LEVY, HL MCINNES, RR AF TAYLOR, RG LEVY, HL MCINNES, RR TI HISTIDASE AND HISTIDINEMIA - CLINICAL AND MOLECULAR CONSIDERATIONS SO MOLECULAR BIOLOGY & MEDICINE LA English DT Article ID PHENYLALANINE AMMONIA-LYASE; DELAYED-TYPE HYPERSENSITIVITY; HERPES-SIMPLEX VIRUS; UROCANIC ACID ISOMERS; SYSTEMIC IMMUNE SUPPRESSION; THYROID-HORMONE SYNTHESIS; UV-INDUCED SUPPRESSION; HUMAN STRATUM-CORNEUM; DISTINCT T-CELLS; CONTACT HYPERSENSITIVITY C1 UNIV TORONTO,DEPT MOLEC & MED GENET,TORONTO M5S 1A1,ONTARIO,CANADA. HOSP SICK CHILDREN,RES INST,DEPT PEDIAT,TORONTO M5G 1X8,ONTARIO,CANADA. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HOSP SICK CHILDREN,RES INST,DEPT GENET,TORONTO M5G 1X8,ONTARIO,CANADA. NR 147 TC 44 Z9 44 U1 0 U2 2 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0735-1313 J9 MOL BIOL MED PD FEB PY 1991 VL 8 IS 1 BP 101 EP 116 PG 16 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA GC512 UT WOS:A1991GC51200010 PM 1943682 ER PT J AU MOSKOWITZ, MA AF MOSKOWITZ, MA TI THE VISCERAL ORGAN BRAIN - IMPLICATIONS FOR THE PATHOPHYSIOLOGY OF VASCULAR HEAD PAIN SO NEUROLOGY LA English DT Review ID DIVERGENT AXON COLLATERALS; TRIGEMINAL GANGLION-CELLS; PRIMARY AFFERENT NEURONS; GENE-RELATED PEPTIDE; SUBSTANCE-P; CEREBRAL-ARTERIES; BLOOD-VESSELS; PIAL-ARTERIES; SPINAL-CORD; DURA MATER RP MOSKOWITZ, MA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114, USA. NR 59 TC 128 Z9 129 U1 0 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD FEB PY 1991 VL 41 IS 2 BP 182 EP 186 PN 1 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA EX218 UT WOS:A1991EX21800004 PM 1992359 ER PT J AU HENSLER, JG KOVACHICH, GB FRAZER, A AF HENSLER, JG KOVACHICH, GB FRAZER, A TI A QUANTITATIVE AUTORADIOGRAPHIC STUDY OF SEROTONIN-1A RECEPTOR REGULATION - EFFECT OF 5,7-DIHYDROXYTRYPTAMINE AND ANTIDEPRESSANT TREATMENTS SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE SEROTONIN-1A RECEPTOR; 5,7-DIHYDROXYTRYPTAMINE; MONOAMINE OXIDASE INHIBITORS; SEROTONIN UPTAKE INHIBITORS; HYPOTHERMIA; ANTIDEPRESSANTS ID MONOAMINE-OXIDASE INHIBITORS; CENTRAL NERVOUS-SYSTEM; STIMULATED ADENYLATE-CYCLASE; PUTATIVE 5-HT1A AGONISTS; DORSAL RAPHE NEURONS; RAT-BRAIN; ELECTROCONVULSIVE SHOCK; BINDING-SITES; FILM AUTORADIOGRAPHY; H-3 CYANOIMIPRAMINE AB There have been few studies investigating the effect of treatments that alter serotonergic neurotransmission on the density of serotonin1A (5-hydroxytryptamine1A [5-HT-1A]) receptors, even though lesioning serotonergic neurons has been reported to enhance certain responses thought to be due to activation of 5-HT1A receptors and repeated treatment of rats with different types of antidepressants can diminish 5-HT1A-mediated responses. Consequently, the binding of H-3-8-hydroxy-2-(di-n-propylamino)-tetralin (DPAT) to 5-HT1A receptors in serotonergic cell body and terminal field areas of rat brain was measured by quantitative autoradiography following either the lesioning of serotonergic neurons with 5,7-dihydroxytryptamine (5,7-DHT), or after chronic administration of monoamine oxidase inhibitors (MAOIs) (clorgyline, phenelzine, or tranylcypromine) or inhibitors of 5-HT uptake (citalopram or sertraline). Treatment of rats with 5,7-DHT did not cause any significant increase in binding of H-3-DPAT to 5-HT1A receptors in any area of the brain examined. There was no significant reduction in the binding of H-3-DPAT in terminal field areas of serotonergic innervation in rats treated with 5,7-DHT except in the CA2/CA3 region of the hippocampus (33% to 35% reduction). In the dorsal and median raphe nuclei, the specific binding of H-3-DPAT was reduced by treatment of rats with 5,7-DHT. In lesioned rats, the binding of H-3-cyanoimipramine (H-3-CN-IMI) to uptake sites for serotonin was essentially eliminated in all terminal field areas examined, as well as in the dorsal and median raphe nuclei. Repeated administration of clorgyline, phenelzine, tranylcypromine, citalopram, or sertraline produced an attenuation of the hypothermic response of rats to acute subcutaneous injection of the 5-HT1A-receptor-agonist DPAT. In spite of this change in 5-HT1A responsivity, these treatments caused in the same animals no consistent change in the binding of H-3-DPAT in either serotonergic cell body or terminal field areas. Of the five drugs studied that diminished DPAT-induced hypothermia, only phenelzine and clorgyline significantly reduced the binding of H-3-DPAT, and even then in only a few of the 12 areas of brain measured. As a result of treatment of rats with tranylcypromine there was a significant increase in the binding of H-3-DPAT in the CA2/CA3 region of the hippocampus. We find, therefore, little evidence that the changes in the sensitivity of 5-HT1A-mediated behavioral and electrophysiologic responses following treatment with 5,7-DHT or chronic administration of antidepressant drugs are a result of changes in the density of 5-HT1A receptors as measured by the binding of H-3-DPAT in discrete areas of the brain of the rat. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PHARMACOL,PHILADELPHIA,PA 19104. RP HENSLER, JG (reprint author), VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT 151E,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIMH NIH HHS [MH 14654, MH 09834, MH 29024] NR 73 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 FEB PY 1991 VL 4 IS 2 BP 131 EP 144 PG 14 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA EZ503 UT WOS:A1991EZ50300008 PM 2025379 ER PT J AU ZAGER, EL AF ZAGER, EL TI ISOLATED TRIGEMINAL SENSORY LOSS SECONDARY TO A DISTAL ANTERIOR INFERIOR CEREBELLAR ARTERY ANEURYSM - CASE-REPORT SO NEUROSURGERY LA English DT Article DE ANTERIOR INFERIOR CEREBELLAR ARTERY; CEREBRAL ANEURYSM; POSTERIOR FOSSA; TRIGEMINAL NERVE ID INTERNAL AUDITORY ARTERY; CEREBELLOPONTINE ANGLE; FACIAL NEURALGIA; HEMIFACIAL SPASM; GIANT ANEURYSM; NEUROPATHY; MEATUS AB A previously healthy 25-year-old woman suddenly developed right-sided facial numbness and a headache. The neurological examination was within normal limits with the exception of meningismus and right-sided facial sensory loss. A computed tomographic scan and a magnetic resonance imaging study demonstrated an acute hematoma in the right cerebellopontine angle. A 4-vessel cerebral angiogram revealed no abnormalities. Posterior fossa exploration disclosed a large, partially thrombosed, fusiform anterior inferior cerebellar artery aneurysm, which indented the pons at the trigeminal root entry zone. The aneurysm was excised, and the patient made an excellent recovery. She was left with a persistent trigeminal sensory deficit. Anterior inferior cerebellar artery aneurysms are rare lesions that generally present with a cerebellopontine angle syndrome; occasionally, facial sensory loss is also a feature. Isolated trigeminal sensory findings, as illustrated in this case, are extremely unusual in posterior fossa vascular lesions. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. NR 48 TC 15 Z9 15 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD FEB PY 1991 VL 28 IS 2 BP 288 EP 291 PG 4 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA EU430 UT WOS:A1991EU43000018 PM 1997900 ER PT J AU DEMILIA, JC MATHEYPREVOT, B JAROS, K WOLF, B STEELE, G SUMMERHAYES, IC AF DEMILIA, JC MATHEYPREVOT, B JAROS, K WOLF, B STEELE, G SUMMERHAYES, IC TI PRENEOPLASTIC LESIONS INDUCED BY MYC AND SRC ONCOGENES IN A HETEROTOPIC RAT COLON SO ONCOGENE LA English DT Article ID PROTEIN-KINASE ACTIVITY; TRANSGENIC MICE; CELL-LINES; COLORECTAL CANCERS; GENE-MUTATIONS; HA-RAS; TRANSFORMATION; CARCINOMA; DEREGULATION; VIRUS AB With the use of viral vectors harboring myc and src oncogenes, we have assessed the potential contribution of these different elements to colonic neoplasia using a transplantation technique resulting in the formation of a heterotopic colon in Wistar Furth rats. While myc alone induced atypia and some dysplasia, src induced focal dysplastic lesions throughout the colon mucosa with evidence of metaplasia. In contrast, lesions induced by myc and src acting cooperatively, were highly dysplastic with evidence of tumor formation after protracted periods. These results indicated the formation of histologically distinct preneoplastic lesions elicited by the action of a single oncogene in colon implants with the production of adenocarcinomas when such oncogenic elements act cooperatively. This model provides an opportunity for studies of the action of different oncogenes, acting singly or in combination, in the multi-step progression to colon tumor formation. C1 NEW ENGLAND DEACONESS HOSP,CANC BIOL LAB,50 BINNEY ST,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [CA44704] NR 23 TC 17 Z9 17 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB PY 1991 VL 6 IS 2 BP 303 EP 309 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA FZ134 UT WOS:A1991FZ13400017 PM 2000223 ER PT J AU ORMEROD, LD RUOFF, KL MEISLER, DM WASSON, PJ KINTNER, JC DUNN, SP LASS, JH VANDERIJN, I AF ORMEROD, LD RUOFF, KL MEISLER, DM WASSON, PJ KINTNER, JC DUNN, SP LASS, JH VANDERIJN, I TI INFECTIOUS CRYSTALLINE KERATOPATHY - ROLE OF NUTRITIONALLY VARIANT STREPTOCOCCI AND OTHER BACTERIAL FACTORS SO OPHTHALMOLOGY LA English DT Article ID EXPERIMENTAL ENDOCARDITIS; PSEUDOMONAS-AERUGINOSA; VIRIDANS STREPTOCOCCI; EXOPOLYSACCHARIDE PRODUCTION; ACANTHAMOEBA KERATITIS; DEFICIENT STREPTOCOCCI; ANTIBIOTIC-RESISTANCE; PENICILLIN THERAPY; CYSTIC-FIBROSIS; CORNEAL GRAFT AB Infectious crystalline keratopathy (ICK) is a chronic corneal infection characterized by interlamellar plaques of gram-positive coccal bacteria in the absence of inflammatory cells. It generally occurs within a corneal graft. Viridans streptococci are usually isolated, but the clinical response to antibiotics is poor and disparate with the in vitro antimicrobial sensitivities. These features suggest the possibility of unusual bacterial factors in pathogenesis. Four cases caused by nutritionally variant viridans streptococci are described. The organisms were fully characterized. They have a rare nutritional requirement for pyridoxal and require defined culture conditions and specific identification. Nutritional variant streptococci (NVS) are principally described as causing endocarditis, another infection involving an avascular collagenous tissue, and exhibiting similar biologic behavior. Electronmicrographic evidence is also adduced that suggests the possible importance of intracorneal glycocalyx deposition. Such factors might explain the anomalous clinical characteristics of this condition. C1 MICHIGAN CORNEAL CONSULTANTS,SOUTHFIELD,MI. CASE WESTERN RESERVE UNIV,DIV OPHTHALMOL,CLEVELAND,OH 44106. UNIV HOSP CLEVELAND,CLEVELAND,OH 44106. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. WILLIAM BEAUMONT HOSP,ROYAL OAK,MI 48072. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,FRANCIS BLAKE BACTERIOL LABS,BOSTON,MA 02114. CLEVELAND CLIN EDUC FDN,DEPT OPHTHALMOL,CLEVELAND,OH 44106. WAKE FOREST UNIV,MED CTR,WINSTON SALEM,NC 27109. RP ORMEROD, LD (reprint author), EYE RES INST,20 STANIFORD ST,BOSTON,MA 02114, USA. NR 59 TC 45 Z9 49 U1 2 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD FEB PY 1991 VL 98 IS 2 BP 159 EP 169 PG 11 WC Ophthalmology SC Ophthalmology GA EW405 UT WOS:A1991EW40500014 PM 2008273 ER PT J AU LATINA, MA RANKIN, GA AF LATINA, MA RANKIN, GA TI INTERNAL AND TRANSCONJUNCTIVAL NEODYMIUM - YAG LASER REVISION OF LATE FAILING FILTERS SO OPHTHALMOLOGY LA English DT Article ID REOPENING FILTRATION FISTULAS; ARGON-LASER; PHOTOCOAGULATION; BLEBS AB Seven cases of hypofunctioning trabeculectomies or full-thickness filters were treated using the Q-switched neodymium: YAG (Nd:YAG) laser delivered either transconjunctivally, gonioscopically, or by a combination approach. In four eyes, internal laser revision was attempted initially. Internal revision was successful in one case, where the sclerostomy had become occluded by a fibrous membrane. The Nd:YAG laser was then focused transconjunctivally onto the episcleral fibrous tissue within the bleb in the three eyes treated unsuccessfully by the internal approach and used as a primary treatment in three additional cases. Transconjunctival laser treatment was successful in producing an immediate and substantial decrease in intraocular pressure (IOP) (mean IOP reduction of 12 mmHg at 2 hours posttreatment) in all cases. In six of seven cases, there was a persistent reduction of intraocular pressure with an average of 5.7 months of follow-up. Transconjunctival Nd:YAG laser revision of hypofunctioning filters may be effective in restoring filtration in selected cases. C1 MASSACHUSETTS GEN HOSP,JOSLIN CLIN,BEECHAM EYE INST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,GLAUCOMA CONSULTAT SERV,BOSTON,MA 02114. RP LATINA, MA (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 12 TC 7 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 FEB PY 1991 VL 98 IS 2 BP 215 EP 221 PG 7 WC Ophthalmology SC Ophthalmology GA EW405 UT WOS:A1991EW40500022 PM 2008280 ER PT J AU LIU, T GIBBONS, RJ HAY, DI SKOBE, Z AF LIU, T GIBBONS, RJ HAY, DI SKOBE, Z TI BINDING OF ACTINOMYCES-VISCOSUS TO COLLAGEN - ASSOCIATION WITH THE TYPE-1 FIMBRIAL ADHESIN SO ORAL MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE ACTINOMYCES-VISCOSUS; COLLAGEN AB Treatment of hydroxyapatite (HA) with human type I or type III collagen strongly promoted adhesion of Actinomyces viscosus LY7 cells. Treatment with human type V collagen was somewhat less effective while treatment with human type IV or rat type I collagen was significantly less effective. Electron microscopic observations revealed that A. viscosus cells also attached to fibrils prepared from human type I collagen. The alpha 1 (1) polypeptide chain derived from type I collagen was ineffective in promoting binding and the alpha 2 (1) polypeptide chain exhibited moderate activity. Heat- or urea-denatured type I collagens were also ineffective in promoting binding. Mutants of A. viscosus that possess type 1 fimbriae, but not type 2 fimbriae or no fimbriae, also bound to collagen-treated HA; this suggests that the adhesin responsible was associated with type 1 fimbriae. Strains of Actinomyces israelii and Actinomyces odontolyticus also exhibited strong binding to collagen-treated HA, while Actinomyces naeslundii ATCC 12104 did not. The avidity of Actinomyces species for collagen would seem to be least partially responsible for the high proportions of these organisms found on cemental and root tooth surfaces. C1 FORSYTH DENT CTR,DEPT ELECTRON MICROSCOPY,140 FENWAY,BOSTON,MA 02115. FORSYTH DENT CTR,DEPT MICROBIOL,BOSTON,MA 02115. FU NIDCR NIH HHS [DE 02847, DE 07009, DE 08601] NR 0 TC 32 Z9 34 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0055 J9 ORAL MICROBIOL IMMUN JI Oral Microbiol. Immunol. PD FEB PY 1991 VL 6 IS 1 BP 1 EP 5 DI 10.1111/j.1399-302X.1991.tb00443.x PG 5 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology GA EW404 UT WOS:A1991EW40400001 PM 1682868 ER PT J AU EFTIMIADI, C STASHENKO, P TONETTI, M MANGIANTE, PE MASSARA, R ZUPO, S FERRARINI, M AF EFTIMIADI, C STASHENKO, P TONETTI, M MANGIANTE, PE MASSARA, R ZUPO, S FERRARINI, M TI DIVERGENT EFFECT OF THE ANAEROBIC-BACTERIA BY-PRODUCT BUTYRIC-ACID ON THE IMMUNE-RESPONSE - SUPPRESSION OF LYMPHOCYTE-T PROLIFERATION AND STIMULATION OF INTERLEUKIN-1 BETA-PRODUCTION SO ORAL MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE BUTYRATE; T-CELL; MACROPHAGE; INTERLEUKIN-1; CYTOKINE; PERIODONTAL DISEASE AB The effects of short-chain fatty acids (SCFA) produced by anaerobic bacteria, namely propionic, butyric and iso-butyric on T-cell proliferation was investigated. A dose-dependent inhibition of both phytohemagglutinin-induced blastogenesis and mixed lymphocyte culture was observed in the millimolar range of SCFA concentrations. The tested SCFA displayed different levels of suppression. The degree of activity was in the following order: butyrate > propionate > isobutyrate. T-cell inhibition was partially reversed, at least for propionic and isobutyric acids, by increasing the concentration of macrophages in the assay system. Furthermore, butyric acid displayed an interesting biphasic stimulation of monocyte interleukin-1 beta production, a cytokine with a powerful bone-resorbing activity. Since millimolar concentrations of SCFA are present in gingival fluid from periodontal pockets, the observed results support the role of these byproducts of anaerobic metabolism in the pathogenesis of periodontal diseases. RP EFTIMIADI, C (reprint author), FORSYTH DENT CTR,DEPT IMMUNOL,140 FENWAY,BOSTON,MA 02115, USA. RI Eftimiadi, Costantino/F-3491-2015 OI Ferrarini, Manlio/0000-0002-6154-2570; Eftimiadi, Costantino/0000-0003-1510-4614 FU NIDCR NIH HHS [DE 04815, DE 07378] NR 0 TC 22 Z9 23 U1 1 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0055 J9 ORAL MICROBIOL IMMUN JI Oral Microbiol. Immunol. PD FEB PY 1991 VL 6 IS 1 BP 17 EP 23 DI 10.1111/j.1399-302X.1991.tb00446.x PG 7 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology GA EW404 UT WOS:A1991EW40400004 PM 1945479 ER PT J AU DOHERTY, LB ROHR, FJ LEVY, HL AF DOHERTY, LB ROHR, FJ LEVY, HL TI DETECTION OF PHENYLKETONURIA IN THE VERY EARLY NEWBORN BLOOD SPECIMEN SO PEDIATRICS LA English DT Article DE PHENYLKETONURIA; NEWBORN SCREENING; EARLY DISCHARGE; BREAST-FEEDING; COLOSTRUM ID HUMAN-MILK; TERM; HYPERPHENYLALANINEMIA; INFANTS; MOTHERS; AGE AB Early hospital discharge of newborns is leading to collection of newborn screening blood specimen during the first day of life in increasing numbers of newborns. There is concern that neonates with phenylketonuria who are tested this early may be missed. To examine this question, the authors screened specimens collected during the first 24 hours of life from 23 neonates at risk for hyperphenylalaninemia. The blood phenylalanine level in each of the 6 neonates with phenylketonuria and a seventh with mild hyperphenylalaninemia was greater than 2 mg/dL as early as 4 hours of age and 6 mg/dL or greater by 24 hours of age. A newborn screening phenylalanine cutoff level of 2 mg/dL would have identified all of these neonates within the first 24 hours of life, but a cutoff level of 4 mg/dL would have missed 2 of the 6 with phenylketonuria before 24 hours of life. Newborn screening programs should adopt a blood phenylalanine level of 2 mg/dL as the cutoff for suspicion of phenylketonuria and request for a second specimen. Breast-fed affected neonates had higher early blood phenylalanine elevations that formula-fed neonates, perhaps reflecting the higher protein (phenylalanine) content of colostrum. C1 CHILDRENS HOSP MED CTR,BIOCHEM GENET UNIT,GARDNER 648,300 LONGWOOD AVE,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NEUROL SERV,JOSEPH P KENNEDY JR LABS,BOSTON,MA 02114. MASSACHUSETTS DEPT PUBL HLTH,STATE LAB INST,NEWBORN SCREENING PROGRAM,BOSTON,MA 02130. FU NHLBI NIH HHS [N01-HO-42809]; NINDS NIH HHS [NS-05096] NR 22 TC 22 Z9 23 U1 1 U2 3 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 FEB PY 1991 VL 87 IS 2 BP 240 EP 244 PG 5 WC Pediatrics SC Pediatrics GA EW342 UT WOS:A1991EW34200021 PM 1987536 ER PT J AU MUSASHI, M YANG, YC PAUL, SR CLARK, SC SUDO, T OGAWA, M AF MUSASHI, M YANG, YC PAUL, SR CLARK, SC SUDO, T OGAWA, M TI DIRECT AND SYNERGISTIC EFFECTS OF INTERLEUKIN-11 ON MURINE HEMATOPOIESIS IN CULTURE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HEMATOPOIETIC STEM CELL; GROWTH FACTOR; INTERLEUKIN ID MULTIPOTENTIAL HEMATOPOIETIC PROGENITORS; COLONY-STIMULATING FACTOR; STEM-CELLS; INTERLEUKIN-3-DEPENDENT PROLIFERATION; DIFFERENTIATION AB We have examined the effects of a stromal cell-derived cytokine designated interleukin 11 (IL-11) on the proliferation of murine hemopoietic progenitors in methylcellulose culture. COS cell-conditioned medium containing IL-11 supported formation of granulocyte/macrophage colonies and a small number of multilineage colonies including blast cell colonies in cultures of marrow cells from normal mice. When tested with marrow cells harvested 2 days after injection of 5-fluorouracil at 150 mg/kg, IL-11 enhanced interleukin 3-dependent colony formation, whereas IL-11 alone supported only scant colony formation. Serial observations (mapping studies) of cultures of post-5-fluorouracil spleen cells indicated that the mechanism of the synergistic effect of IL-11 is to shorten the dormant period of stem cells, an effect very similar to that of interleukin 6. When pooled blast cells were plated into medium containing IL-11 and erythropoietin, only macrophage colonies were observed. Thus, IL-11 can directly support the proliferation of committed macrophage progenitors and, like interleukin 6 and granulocyte colony-stimulating factor, act synergistically with interleukin 3 to shorten the G0 period of early progenitors. C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. VET AFFAIRS MED CTR,CHARLESTON,SC 29403. GENET INST,CAMBRIDGE,MA 02140. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BIOMAT RES INST CO LTD,YOKOHAMA,JAPAN. RI Musashi, Manabu/D-9935-2012 FU NIDDK NIH HHS [DK32294] NR 18 TC 221 Z9 224 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 FEB PY 1991 VL 88 IS 3 BP 765 EP 769 DI 10.1073/pnas.88.3.765 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EW400 UT WOS:A1991EW40000018 PM 1825140 ER PT J AU GOLDBERG, MB BOYKO, SA CALDERWOOD, SB AF GOLDBERG, MB BOYKO, SA CALDERWOOD, SB TI POSITIVE TRANSCRIPTIONAL REGULATION OF AN IRON-REGULATED VIRULENCE GENE IN VIBRIO-CHOLERAE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE TRANSCRIPTIONAL ACTIVATION; LYSR FAMILY; FUR; IRGA; IRGB ID ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; PROTEINS; TOXIN; IDENTIFICATION; COLONIZATION; ANGUILLARUM; EXPRESSION; INSERTION; CULTURES AB We have previously described a virulence gene in Vibrio cholerae (irgA) that is more than 850-fold regulated in response to iron. Negative regulation of irgA by iron occurred at the transcriptional level, and there was a dyad symmetric nucleotide sequence in the vicinity of the irgA promoter homologous to the Fur binding site in Escherichia coli. When irgA was cloned into E. coli, we showed that transcription of irgA required 900 base pairs of DNA upstream of the irgA promoter that contained an open reading frame in inverse orientation to irgA. In the present study, we show that this upstream region of DNA encodes a gene in inverse orientation to irgA (named irgB) that is also negatively regulated by iron. Insertional inactivation of irgB on the V. cholerae chromosome leads to loss of expression of a chromosomal irgA'-'phoA fusion (in which the primes indicate truncated genes), which is restored to normal by provision of irgB on a plasmic in trans. DNA sequencing of irgB shows that the protein product (IrgB) is homologous to the LysR family of positive transcriptional activators, and secondary structure analysis of irgB predicts a helix-turn-helix DNA binding motif. The promoters of irgB and irgA are divergent but overlap each other and the previously defined Fur-binding site. We propose a model for iron regulation of irgA expression in V. cholerae. In the presence of sufficient iron, transcription of both irgA and irgB is negatively regulated by a Fur-like protein. In low iron conditions, negative regulation of transcription is removed, and production of IrgB leads to positive transcriptional activation of irgA. It seems likely that the high induction ratio of irgA expression under low- and high-iron conditions (850-fold) relates to the fact that its cognate positive transcriptional activator (irgB) is itself negatively regulated by iron. 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 [AI27329] NR 27 TC 86 Z9 87 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB PY 1991 VL 88 IS 4 BP 1125 EP 1129 DI 10.1073/pnas.88.4.1125 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EY617 UT WOS:A1991EY61700009 PM 1705025 ER PT J AU DOU, QP FRIDOVICHKEIL, JL PARDEE, AB AF DOU, QP FRIDOVICHKEIL, JL PARDEE, AB TI INDUCIBLE PROTEINS BINDING TO THE MURINE THYMIDINE KINASE PROMOTER IN LATE G1/S PHASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CELL-CYCLE REGULATION; DNA BINDING PROTEINS; SP1 ID RNA POLYMERASE-II; CELL-CYCLE; DNA-SYNTHESIS; GENE; TRANSCRIPTION; SEQUENCE; GROWTH; SP1 AB By performing DNase I footprint and bandshift analyses of a 170-base-pair region of the murine thymidine kinase promoter, we identified an inducible DNA binding activity that we named Yi. Yi binding activity was not detected in G0 and G1 extracts, but it was observed as cells crossed the G1/S boundary. Yi proteins bind specifically to a consensus sequence (CCCNCNNNCT) found at three distinct sites in this promoter region. We also observed a murine Sp1 binding activity that was constitutive throughout the cell cycle. We propose that the G1/S-specific Yi binding is important for murine thymidine kinase gene regulation and perhaps also for initiation of DNA synthesis. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115. FU NCI NIH HHS [CA22427]; NIGMS NIH HHS [GM24571] NR 28 TC 77 Z9 77 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB PY 1991 VL 88 IS 4 BP 1157 EP 1161 DI 10.1073/pnas.88.4.1157 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EY617 UT WOS:A1991EY61700016 PM 1996317 ER PT J AU BACHOR, R SHEA, CR GILLIES, R HASAN, T AF BACHOR, R SHEA, CR GILLIES, R HASAN, T TI PHOTOSENSITIZED DESTRUCTION OF HUMAN BLADDER-CARCINOMA CELLS TREATED WITH CHLORIN E6-CONJUGATED MICROSPHERES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE LASER; PHOTODYNAMIC; DRUG-DELIVERY SYSTEM ID TUMOR-BEARING MICE; CELLULAR-UPTAKE; LEUKEMIA-CELLS; INVITRO; PHOTOTOXICITY; MECHANISMS; REMISSION; THERAPY; CANCER; LINES AB A photosensitizer conjugate, chlorin e6 (Ce6) covalently bound to 1-mu-m-diameter polystyrene microspheres, has been investigated in the photodynamic destruction of MGH-U1 human bladder carcinoma cells in vitro. The microspheres were taken up avidly by the carcinoma cells; confocal laser scanning fluorescence microscopy showed them to be localized in the cytoplasm, apparently within lysosomes, visualized by labeling with acridine orange. In contrast, fluorescence of unconjugated Ce6 was present within most cellular membranes. Use of Ce6-microsphere conjugates led to a 20-fold-higher mean intracellular concentration, compared with unconjugated Ce6. Cells incubated in the presence of Ce6-microsphere conjugates (0.43-mu-M equivalent) and subsequently irradiated at 659 nm with a dye laser pumped by an argon-ion laser showed dose-dependent phototoxicity, leading to total inhibition of colony formation at a radiant exposure of 5 J/cm2; in contrast, cells incubated with either unconjugated Ce6 (0.43-mu-M) or unconjugated microspheres before laser irradiation were unaffected. Cells pretreated with Ce6-microsphere conjugates and irradiated in the presence of 90% (H2O)-H-2 showed significantly increased phototoxicity, an effect consistent with an important role for excited-state singlet oxygen in the mechanism of injury. In solution, however, photosensitized generation of singlet oxygen with Ce6-microsphere conjugates was 9 times less efficient than with unconjugated Ce6. The markedly greater phototoxicity of Ce6-microsphere conjugates compared to unconjugated Ce6 was therefore a consequence of the high intracellular Ce6 concentration attained by phagocytosis of the conjugates and their particular sites of intracellular localization. Thus, these conjugates are an efficient system for the delivery of photosensitizing drugs to carcinoma cells. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT UROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. RI Winstein, Carolee/A-8375-2008 FU NIAMS NIH HHS [GMA-1 2R01-AR23595] NR 51 TC 98 Z9 99 U1 1 U2 9 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB PY 1991 VL 88 IS 4 BP 1580 EP 1584 DI 10.1073/pnas.88.4.1580 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EY617 UT WOS:A1991EY61700103 PM 1996360 ER PT J AU FARAONE, SV BIEDERMAN, J KEENAN, K TSUANG, MT AF FARAONE, SV BIEDERMAN, J KEENAN, K TSUANG, MT TI SEPARATION OF DSM-III ATTENTION-DEFICIT DISORDER AND CONDUCT DISORDER - EVIDENCE FROM A FAMILY-GENETIC STUDY OF AMERICAN CHILD PSYCHIATRIC-PATIENTS SO PSYCHOLOGICAL MEDICINE LA English DT Article ID DIAGNOSTIC INTERVIEW SCHEDULE; MINIMAL BRAIN-DYSFUNCTION; LA-TOURETTES SYNDROME; HYPERACTIVE-CHILDREN; ANTISOCIAL-BEHAVIOR; FOLLOW-UP; PARENTS; PREVALENCE; BOYS; HETEROGENEITY AB Using family study methodology and assessments by blind raters, this study tested hypotheses about patterns of familial association between DSM-III attention deficit disorder (ADD) and antisocial disorders (childhood conduct (CD) and oppositional disorder (OPD) and adult antisocial personality disorder) among 457 first-degree relatives of clinically referred children and adolescents with ADD (73 probands, 264 relatives), psychiatric (26 probands, 101 relatives) and normal controls (26 probands, 92 relatives). Among the 73 ADD probands, 33 (45%) met criteria for OPD, 24 (33%) met criteria for CD, and 16 (22%) had no antisocial diagnosis. After stratifying the ADD sample into those with CD (ADD + CD), those with OPD (ADD + OPD) and those with neither (ADD) familial risk analysis revealed the following: (1) relatives of each ADD proband subgroup were at significantly greater risk for ADD than relatives of both psychiatric and normal controls; (2) the morbidity risk for ADD was highest among relatives of ADD + CD probands (38%), moderate among relatives of ADD + OPD (17%) and ADD probands (24%) and lowest among relatives of psychiatric and normal controls (5% for both); (3) the risk for any antisocial disorder was highest among relatives of ADD + CD (34%) and ADD + OPD (24%) which were significantly greater than the risk to relatives of ADD probands (11%), psychiatric (7%) and normal controls (4%); and (4) both ADD and antisocial disorders occurred in the same relatives more often than expected by chance alone. Although these findings suggest that ADD with and without antisocial disorders may be aetiologically distinct disorders, they are also consistent with a multifactorial hypothesis in which ADD, ADD + OPD and ADD + CD fall along a continuum of increasing levels of familial aetiological factors and, correspondingly, severity of illness. C1 MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS MENTAL HLTH CTR,SCH MED,DEPT PSYCHIAT,CAMBRIDGE,MA 02138. BROCKTON W ROXBURY VET ADM MED CTR,PSYCHIAT SERV,BROCKTON,MA. FU NIMH NIH HHS [R01 MH-41314-01A2] NR 74 TC 160 Z9 164 U1 5 U2 7 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD FEB PY 1991 VL 21 IS 1 BP 109 EP 121 PG 13 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA FE054 UT WOS:A1991FE05400013 PM 2047486 ER PT J AU LEE, AS WEISSLEDER, R BRADY, TJ WITTENBERG, J AF LEE, AS WEISSLEDER, R BRADY, TJ WITTENBERG, J TI LYMPH-NODES - MICROSTRUCTURAL ANATOMY AT MR IMAGING SO RADIOLOGY LA English DT Article DE LYMPHATIC SYSTEM, MR STUDIES; MAGNETIC RESONANCE (MR), CONTRAST ENHANCEMENT ID MAGNETIC-RESONANCE; RELAXATION-TIMES; LYMPHADENOPATHY AB High-resolution microscopic magnetic resonance (MR) images of rodent lymph nodes were directly correlated with sections obtained for histologic study to determine the microstructural anatomy of lymph modes seen at MR imaging and to evaluate signal intensity changes induced by a novel intravenous lymphotropic MR contrast agent (ultrasmall superparamagnetic iron oxide [USPIO]). High-resolution T2-weighted images of unenhanced lymph nodes demonstrated medullary sinus as regions of low signal intensity structures. After a single intravenous administration of USPIO (160-mu-mol/kg), both T1-weighted and T2-weighted images showed areas of focal signal intensity loss in medullary sinuses corresponding to the distribution of uptake by macrophages. Lymph follicles appeared unchanged in signal intensity, as they are largely devoid of macrophages. This model of microscopic MR imaging should provide the basis for (a) understanding differences between patterns of contrast-enhanced normal lymph nodes and those of diseased ones and (b) guiding the development of targeting strategies for novel pharmaceuticals at the cellular level. C1 MASSACHUSETTS GEN HOSP,CTR MGH NMR,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 14 TC 62 Z9 64 U1 0 U2 1 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD FEB PY 1991 VL 178 IS 2 BP 519 EP 522 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EU035 UT WOS:A1991EU03500044 PM 1987619 ER PT J AU LITTRUP, PJ KANE, RA WILLIAMS, CR EGGLIN, TK LEE, F TORPPEDERSEN, S CHURCH, PA AF LITTRUP, PJ KANE, RA WILLIAMS, CR EGGLIN, TK LEE, F TORPPEDERSEN, S CHURCH, PA TI DETERMINATION OF PROSTATE VOLUME WITH TRANSRECTAL US FOR CANCER SCREENING .1. COMPARISON WITH PROSTATE-SPECIFIC ANTIGEN ASSAYS SO RADIOLOGY LA English DT Article DE CANCER SCREENING; PROSTATE, BIOPSY; PROSTATE, HYPERPLASIA; PROSTATE, NEOPLASMS; PROSTATE, US STUDIES ID DIGITAL RECTAL EXAMINATION; RADICAL PROSTATECTOMY; TREATED PATIENTS; ADENOCARCINOMA; DIAGNOSIS; MARKER AB To investigate whether radiologists can objectively define a high-risk group for prostate cancer, the researchers measured gland volume and compared it with results of a screening blood test, prostate-specific antigen (PSA) assay. A total of 768 men, aged 55-71 years, were self-referred to two prostate cancer screening programs using transrectal ultrasound (US) and digital rectal examination. In patients with no evidence of cancer, statistically significant increases in mean PSA values were noted with increasing gland volume ranges (P < .05). PSA values in patients with cancer were more likely to exceed the volume-adjusted 95th percentile (mean + [1.65.standard deviation]) than those in patients with negative biopsy results (P < .005). Patients with PSA values above the volume-adjusted 95th percentile have an estimated risk for prostate cancer up to nine times that of the general screening population. The researchers conclude that knowledge of transrectal US gland volume and prostate-specific antigen assay type are important objective variables for future prostate cancer screening programs. The volume-adjusted 95th percentiles presented may help guide cost-effective management of current early detection efforts. C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT UROL,BOSTON,MA 02215. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. ST JOSEPH MERCY HOSP,DEPT RADIOL,ANN ARBOR,MI 48104. RP LITTRUP, PJ (reprint author), HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT RADIOL,185 PILGRIM RD,BOSTON,MA 02215, USA. NR 20 TC 37 Z9 37 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 FEB PY 1991 VL 178 IS 2 BP 537 EP 542 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EU035 UT WOS:A1991EU03500047 PM 1702894 ER PT J AU CLARK, JR DREYFUSS, AI AF CLARK, JR DREYFUSS, AI TI THE ROLE OF CISPLATIN IN TREATMENT REGIMENS FOR SQUAMOUS-CELL CARCINOMA OF THE HEAD AND NECK SO SEMINARS IN ONCOLOGY LA English DT Review ID LOCALLY ADVANCED HEAD; CALIFORNIA-ONCOLOGY-GROUP; CONTINUOUS-INFUSION CISPLATIN; PREVIOUSLY UNTREATED PATIENTS; 5-DAY CONTINUOUS INFUSION; ADVANCED RESECTABLE HEAD; SPLIT COURSE RADIATION; COMBINATION CHEMOTHERAPY; ADJUVANT CHEMOTHERAPY; CIS-PLATINUM RP CLARK, JR (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 120 TC 20 Z9 20 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 FEB PY 1991 VL 18 IS 1 SU 3 BP 34 EP 48 PG 15 WC Oncology SC Oncology GA FC768 UT WOS:A1991FC76800005 PM 2003226 ER PT J AU ARONIN, N CHASE, K FOLSOM, R CHRISTAKOS, S DIFIGLIA, M AF ARONIN, N CHASE, K FOLSOM, R CHRISTAKOS, S DIFIGLIA, M TI IMMUNOREACTIVE CALCIUM-BINDING PROTEIN (CALBINDIN-D28K) IN INTERNEURONS AND TRIGEMINOTHALAMIC NEURONS OF THE RAT NUCLEUS CAUDALIS LOCALIZED WITH PEROXIDASE AND IMMUNOGOLD METHODS SO SYNAPSE LA English DT Article DE SPINAL TRIGEMINAL NUCLEUS; ULTRASTRUCTURE; DOUBLE-LABELING ID SPINAL TRIGEMINAL COMPLEX; CENTRAL NERVOUS-SYSTEM; HORSERADISH-PEROXIDASE; SUBSTANTIA GELATINOSA; BASAL GANGLIA; DORSAL HORN; BRAIN-STEM; CELLS; CEREBELLUM; CORD AB Calbindin-D28k is a highly abundant protein found in neurons in selected brain regions, including cells in sensory systems of the brainstem. Because of its capacity to bind cytosolic Ca++, calbindin-D28k is thought to contribute to the regulation of compartmental Ca++ concentrations in neurons. In this study of the rat spinal trigeminal nucleus, calbindin-D28k was localized with immunoperoxidase and immunogold methods. Results showed that immunoreactive calbindin-D28k neurons were widely distributed to all regions of the nucleus, but were particularly numerous in the substantia gelatinosa. Some trigeminothalamic neurons that were identified by retrograde labeling of a conjugated wheat-germ agglutinin with horseradish peroxidase also contained calbindin-D28k immunoreactivity. Most of the calbindin-D28k labeling was found in cell bodies and dendrites. Axon terminals were rarely stained. More discrete labeling with a gold-conjugated second antibody showed that the predominant site of calbindin-D28k was the matrix of cytoplasm. Gold label was also heavily associated with euchromatin within nuclei. These findings show that immunoreactive calbindin-D28k is localized to both interneurons and projecting neurons of the spinal trigeminal nucleus. Many of these cells are likely to receive glutamatergic afferent inputs, which may act in part by increasing Ca++ flux into the neurons. Calbindin-D28k has a high capacity for buffering Ca++ and under some conditions may protect neurons against glutamate-induced excitotoxicity. We speculate that calbindin-D28k may function to regulate calcium concentrations in spinal trigeminal neurons. C1 UNIV MASSACHUSETTS,SCH MED,DEPT MED,WORCESTER,MA 01655. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT BIOCHEM & MOLEC BIOL,NEWARK,NJ 07103. FU NIDDK NIH HHS [DK-38961]; NINDS NIH HHS [NS-23357, NS-20270] NR 31 TC 16 Z9 17 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 0887-4476 J9 SYNAPSE JI Synapse PD FEB PY 1991 VL 7 IS 2 BP 106 EP 113 DI 10.1002/syn.890070204 PG 8 WC Neurosciences SC Neurosciences & Neurology GA EU633 UT WOS:A1991EU63300003 PM 1707189 ER PT J AU ROSENGARD, BR OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K BOORSTEIN, SM HILL, GS SACHS, DH AF ROSENGARD, BR OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K BOORSTEIN, SM HILL, GS SACHS, DH TI RENAL-TRANSPLANTATION IN MINIATURE SWINE - PRELIMINARY EVIDENCE THAT GRAFT INFILTRATING LEUKOCYTES SUPPRESS DONOR-SPECIFIC CELL-MEDIATED LYMPHOCYTOTOXICITY IN COCULTURE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 13TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 19-24, 1990 CL SAN FRANCISCO, CA SP TRANSPLANTAT SOC ID MAJOR HISTOCOMPATIBILITY COMPLEX; HOST DISEASE; T-CELLS; ALLOGRAFTS; ANTIGEN; SURVIVAL; RATS C1 NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 4B13,BETHESDA,MD 20892. FRANCIS SCOTT KEY MED CTR,DEPT PATHOL,BALTIMORE,MD. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HOWARD HUGHES MED INST,BALTIMORE,MD. NR 17 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1991 VL 23 IS 1 BP 189 EP 191 PN 1 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA EV390 UT WOS:A1991EV39000072 PM 1990511 ER PT J AU WEE, SL COSIMI, AB PREFFER, FI ROTHLEIN, R FAANES, R CONTI, D COLVIN, RB AF WEE, SL COSIMI, AB PREFFER, FI ROTHLEIN, R FAANES, R CONTI, D COLVIN, RB TI FUNCTIONAL CONSEQUENCES OF ANTI-ICAM-1 (CD54) IN CYNOMOLGUS MONKEYS WITH RENAL-ALLOGRAFTS SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 13TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 19-24, 1990 CL SAN FRANCISCO, CA SP TRANSPLANTAT SOC C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,IMMUNOPATHOL UNIT,BOSTON,MA 02114. BOEHRINGER INGELHEIM PHARMACEUT INC,RIDGEFIELD,CT. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [P01-HL18646] NR 3 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1991 VL 23 IS 1 BP 279 EP 280 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA EV390 UT WOS:A1991EV39000109 PM 1671301 ER PT J AU SUNDT, TM LEGUERN, C SMITH, CV SACHS, DH AF SUNDT, TM LEGUERN, C SMITH, CV SACHS, DH TI IDENTIFICATION OF A CD4 POLYMORPHISM IN SWINE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 13TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 19-24, 1990 CL SAN FRANCISCO, CA SP TRANSPLANTAT SOC ID MONOCLONAL-ANTIBODIES; T4 C1 NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. RP SUNDT, TM (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114, USA. NR 5 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1991 VL 23 IS 1 BP 419 EP 420 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA EV390 UT WOS:A1991EV39000164 PM 1990575 ER PT J AU COSIMI, AB DELMONICO, FL WRIGHT, JK WEE, SL PREFFER, FI BEDLE, M COLVIN, RB AF COSIMI, AB DELMONICO, FL WRIGHT, JK WEE, SL PREFFER, FI BEDLE, M COLVIN, RB TI OKT4A MONOCLONAL-ANTIBODY IMMUNOSUPPRESSION OF CYNOMOLGUS RENAL-ALLOGRAFT RECIPIENTS SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 13TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 19-24, 1990 CL SAN FRANCISCO, CA SP TRANSPLANTAT SOC ID THERAPY C1 MASSACHUSETTS GEN HOSP,IMMUNOPATHOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. ORTHO PHARMACEUT CORP,RARITAN,NJ 08869. RP COSIMI, AB (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,TRANSPLANTAT UNIT,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-18648] NR 5 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1991 VL 23 IS 1 BP 501 EP 503 PN 1 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA EV390 UT WOS:A1991EV39000199 PM 1990600 ER PT J AU WEE, SL COLVIN, RB STROKA, DM JOLLIFFE, LK COSIMI, AB AF WEE, SL COLVIN, RB STROKA, DM JOLLIFFE, LK COSIMI, AB TI ANALYSIS OF CELLULAR EVENTS WITHIN STABLE AND REJECTING ALLOGRAFTS IN CYNOMOLGUS MONKEYS SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 13TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 19-24, 1990 CL SAN FRANCISCO, CA SP TRANSPLANTAT SOC ID MONOCLONAL-ANTIBODY; LYMPHOCYTES; CELLS C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,IMMUNOPATHOL UNIT,BOSTON,MA 02114. ORTHO PHARMACEUT CORP,RARITAN,NJ 08869. RP WEE, SL (reprint author), MASSACHUSETTS GEN HOSP,TRANSPLANTAT UNIT,WHITE 546,BOSTON,MA 02114, USA. RI Stroka, Deborah/F-1806-2013 FU NHLBI NIH HHS [HL-18646] NR 15 TC 2 Z9 2 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1991 VL 23 IS 1 BP 821 EP 823 PN 1 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA EV390 UT WOS:A1991EV39000329 PM 1990702 ER PT J AU MOSES, RD AUCHINCLOSS, H AF MOSES, RD AUCHINCLOSS, H TI DEFECTS IN ACCESSORY MOLECULE AND OTHER CELL-SURFACE MOLECULE INTERACTIONS ARE RESPONSIBLE FOR WEAK MOUSE HELPER T-CELL RESPONSES TO XENOANTIGENS SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 13TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 19-24, 1990 CL SAN FRANCISCO, CA SP TRANSPLANTAT SOC ID EXPRESSION; MHC; CD4 RP MOSES, RD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,TRANSPLANTAT UNIT,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL36372, HL18646] NR 11 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1991 VL 23 IS 1 BP 883 EP 884 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA EV390 UT WOS:A1991EV39000354 PM 1671311 ER PT J AU FLYNN, DF SHIPLEY, WU AF FLYNN, DF SHIPLEY, WU TI MANAGEMENT OF SPINAL-CORD COMPRESSION SECONDARY TO METASTATIC PROSTATIC-CARCINOMA SO UROLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID DECOMPRESSION; ANTERIOR; STABILIZATION; DIAGNOSIS; NEOPLASMS; DISEASE; TUMOR C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FLYNN, DF (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DEPT RADIAT MED,BOSTON,MA 02114, USA. NR 20 TC 25 Z9 25 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0094-0143 J9 UROL CLIN N AM JI Urol. Clin. N. Am. PD FEB PY 1991 VL 18 IS 1 BP 145 EP 152 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA EW377 UT WOS:A1991EW37700016 PM 1992568 ER PT J AU SOSA, MAG FAZELY, F KOCH, JA VERCELLOTTI, SV RUPRECHT, RM AF SOSA, MAG FAZELY, F KOCH, JA VERCELLOTTI, SV RUPRECHT, RM TI N-CARBOXYMETHYLCHITOSAN-N,O-SULFATE AS AN ANTI-HIV-1 AGENT SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; DEXTRAN SULFATE; REVERSE-TRANSCRIPTASE; SELECTIVE INHIBITORS; ENVELOPED VIRUSES; HTLV-III; HIV; INVITRO; POTENT; REPLICATION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. V LABS INC,COVINGTON,LA. FU NIAID NIH HHS [UO1-AI24845] NR 41 TC 46 Z9 50 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JAN 31 PY 1991 VL 174 IS 2 BP 489 EP 496 DI 10.1016/0006-291X(91)91443-G PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EV749 UT WOS:A1991EV74900013 PM 1704225 ER PT J AU GOITEIN, M AF GOITEIN, M TI WAITING PATIENTLY - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP GOITEIN, M (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 JAN 31 PY 1991 VL 324 IS 5 BP 337 EP 337 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EU922 UT WOS:A1991EU92200017 ER PT J AU HEYES, MP SWARTZ, KJ MARKEY, SP BEAL, MF AF HEYES, MP SWARTZ, KJ MARKEY, SP BEAL, MF TI REGIONAL BRAIN AND CEREBROSPINAL-FLUID QUINOLINIC ACID CONCENTRATIONS IN HUNTINGTONS-DISEASE SO NEUROSCIENCE LETTERS LA English DT Article DE QUINOLINIC ACID; HUNTINGTONS DISEASE; EXCITOTOXIN; NEURODEGENERATION; BRAIN; CEREBROSPINAL FLUID ID RAT-BRAIN; NEUROPEPTIDE-Y; NEURONS; QUANTIFICATION; LESIONS AB Many of the characteristic neuroanatomical and neurochemical features of Huntington's disease (HD) are produced in experimental animals by an intrastriatal injection of the endogenous N-methyl-D-aspartate receptor agonist quinoline acid (QUIN). Conceivably, a chronic over-production of QUIN in brain could be involved in the pathogenesis of HD. To investigate this hypothesis, concentrations of QUIN were measured both in cerebrospinal fluid (CSF) and postmortem tissue from patients with HD and neurologically normal age-matched controls. CSF QUIN concentrations were slightly lower in patients with HD, however the changes were not significant. Mean concentrations of QUIN tended to be lower in HD putamen, dentate nucleus and several cortical regions, although significant reductions were found only in Brodmann areas 17, 20 and 28. The mechanisms responsible for these small reductions in brain QUIN concentrations remain to be determined. These results do not support the hypothesis that a chronic increase of QUIN production is responsible for neurodegeneration in HD. C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. HARVARD UNIV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL RES LABS,NEUROCHEM LAB,BOSTON,MA 02114. RP HEYES, MP (reprint author), NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BLDG 10,ROOM 3D40,BETHESDA,MD 20892, USA. FU NIMH NIH HHS [MHNS 31862]; PHS HHS [16367] NR 31 TC 56 Z9 57 U1 1 U2 1 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 JAN 28 PY 1991 VL 122 IS 2 BP 265 EP 269 DI 10.1016/0304-3940(91)90874-S PG 5 WC Neurosciences SC Neurosciences & Neurology GA EY494 UT WOS:A1991EY49400033 PM 1827518 ER PT J AU HOLTZMAN, EJ SOPER, BW STOW, JL AUSIELLO, DA ERCOLANI, L AF HOLTZMAN, EJ SOPER, BW STOW, JL AUSIELLO, DA ERCOLANI, L TI REGULATION OF THE G-PROTEIN ALPHA-I-2-SUBUNIT GENE IN LLC-PK1 RENAL-CELLS AND ISOLATION OF PORCINE GENOMIC CLONES ENCODING THE GENE PROMOTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SIGNAL TRANSDUCTION; ALPHA-SUBUNIT; ADENYLATE-CYCLASE; BINDING-PROTEINS; MAMMALIAN-CELLS; MESSENGER-RNA; CEREBRAL-CORTEX; PERTUSSIS TOXIN; DNA; EXPRESSION AB Heterotrimeric G-proteins function as signal transducers for a variety of hormone-coupled enzyme and ion transport systems in eukaryotic cells. We have studied G-protein-coupled processes that appear to be developmentally regulated in polarized pig kidney cells (LLC-PK1). Following trypsinization, LLC-PK1 cells differentiate from a rounded cell type to a fully polarized epithelium by 7 days of culture. During this differentiation, the expression of G-protein alpha-i-2 subunit mRNA was not detected until day 4 of culture, it peaked at day 6, and declined thereafter. In contrast, G-protein alpha-(s) subunit mRNA which peaked on day 4 was easily detected on all culture days. The presence of the alpha-i-2 protein on epithelial cell basolateral membranes followed the same pattern of mRNA expression during culture. To understand the developmental expression of the alpha-i-2 subunit in non-polarized cells and its potential regulation by hormones and second messengers in polarized cells at the transcriptional level, genomic DNA segments encoding the alpha-i-2 gene promoter were isolated from an EMBL-3 porcine genomic library. S1 nuclease analysis of LLC-PK1 mRNA with cRNA probes derived from these DNA segments revealed major and a minor transcriptional start sites 131 and 171 base pairs upstream of the translation initiation site. The porcine and human alpha-i-2 subunit genes shared a 78% sequence identity in their 5' flanks which suggested an evolutionary conversation of cis elements required to influence their transcription. The porcine alpha-i-2 gene promoter was identified by fusing DNA segments encoding putative 5'-flanking areas of the gene to a plasmid that contained a firefly luciferase reporter gene but lacked a promoter. The minimal promoter was found between -130 and -60 base pairs from the major transcription start site. No typical "TATA-like" sequences were found. However, a "GC" box and a "TGTGG" sequence were two potential cis elements required for basal transcription of the porcine gene promoter which shared a 76% sequence identity to the promoter of another GTP-binding protein, the human c-Ha-ras proto-oncogene. Transcription of the gene was inhibited following treatment of renal cells with 10(-8) M dexamethasone. These studies suggest that alpha-i-2 gene expression is regulated in LLC-PK1 cells. Identification of the gene's promoter and 5'-flanking sequences provide a basis for elucidating "cis-acting" DNA sequences and "trans-acting" protein factors that act in concert to control the transcriptional regulation of the alpha-i-2 gene which may modulate G-protein coupled effector responses in vasopressin-sensitive renal epithelia. C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 19406] NR 58 TC 39 Z9 39 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 JAN 25 PY 1991 VL 266 IS 3 BP 1763 EP 1771 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EU497 UT WOS:A1991EU49700064 PM 1899094 ER PT J AU HANES, SD BRENT, R AF HANES, SD BRENT, R TI A GENETIC MODEL FOR INTERACTION OF THE HOMEODOMAIN RECOGNITION HELIX WITH DNA SO SCIENCE LA English DT Article ID DROSOPHILA EMBRYO; TRANSCRIPTIONAL ACTIVATOR; ANTENNAPEDIA HOMEODOMAIN; BINDING-SPECIFICITY; ANTERIOR PATTERN; LAMBDA-REPRESSOR; BICOID PROTEIN; AMINO-ACID; SEQUENCE; OPERATOR AB The Bicoid homeodomain protein controls anterior development in the Drosophila embryo by binding to DNA and regulating gene expression. With the use of genetic assays in yeast, the interaction between the Bicoid homeodomain and a series of mutated DNA sites was studied. These experiments defined important features of homeodomain binding sites, identified specific amino acid-base pair contacts, and suggested a model for interaction of the recognition alpha-helices of Bicoid and Antennapedia-class homeodomain proteins with DNA. The model is in general agreement with results of crystallographic and magnetic resonance studies, but differs in important details. It is likely that genetic studies of protein-DNA interaction will continue to complement conventional structural approaches. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP HANES, SD (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 41 TC 193 Z9 194 U1 0 U2 3 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD JAN 25 PY 1991 VL 251 IS 4992 BP 426 EP 430 DI 10.1126/science.1671176 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA EU504 UT WOS:A1991EU50400040 PM 1671176 ER PT J AU LEAF, A AF LEAF, A TI CARDIOLOGY AND THE QUALITY OF MEDICAL-PRACTICE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article RP LEAF, A (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 17 TC 7 Z9 7 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JAN 23 PY 1991 VL 265 IS 4 BP 482 EP 485 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA ET377 UT WOS:A1991ET37700027 ER PT J AU FARNETT, L MULROW, CD LINN, WD LUCEY, CR TULEY, MR AF FARNETT, L MULROW, CD LINN, WD LUCEY, CR TULEY, MR TI THE J-CURVE PHENOMENON AND THE TREATMENT OF HYPERTENSION - IS THERE A POINT BEYOND WHICH PRESSURE REDUCTION IS DANGEROUS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID CORONARY HEART-DISEASE; DIASTOLIC BLOOD-PRESSURE; MYOCARDIAL-INFARCTION; ELDERLY PATIENTS; FOLLOW-UP; MORTALITY; RISK; TRIAL; FRAMINGHAM; CARE AB We critically appraised the medical literature to evaluate whether there is a point beyond which blood pressure reduction in hypertensive subjects is no longer beneficial and possibly even deleterious. Thirteen studies that stratified cardiovascular outcomes by level of achieved blood pressure in treated hypertensive subjects who had been followed up for at least 1 year were critiqued by four independent reviewers. Data addressing population, protocol, and methodological characteristics were evaluated. Studies did not show a consistent J-shaped relationship between treated blood pressure and stroke, but they did demonstrate a consistent J-shaped relationship for cardiac events and diastolic blood pressure. The beneficial therapeutic threshold point was 85 mm Hg. We conclude that low treated diastolic blood pressure levels, ie, below 85 mm Hg, are associated with increased risk of cardiac events. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78248. UNIV TEXAS,COLL PHARM,AUSTIN,TX 78712. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN INTERNAL MED,SAN ANTONIO,TX 78284. NR 41 TC 295 Z9 300 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 JAN 23 PY 1991 VL 265 IS 4 BP 489 EP 495 DI 10.1001/jama.265.4.489 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA ET377 UT WOS:A1991ET37700029 PM 1824642 ER PT J AU TEICHER, BA HOLDEN, SA HERMAN, TS SOTOMAYOR, EA KHANDEKAR, V ROSBE, KW BRANN, TW KORBUT, TT FREI, E AF TEICHER, BA HOLDEN, SA HERMAN, TS SOTOMAYOR, EA KHANDEKAR, V ROSBE, KW BRANN, TW KORBUT, TT FREI, E TI CHARACTERISTICS OF 5 HUMAN TUMOR-CELL LINES AND SUBLINES RESISTANT TO CIS-DIAMMINEDICHLOROPLATINUM(II) SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID OVARIAN-CARCINOMA CELLS; PLATINUM ANALOGS TETRAPLATIN; ALKYLATING AGENT RESISTANCE; MURINE LEUKEMIA-CELLS; AMINO-ACID-TRANSPORT; ENHANCED DNA-REPAIR; CYTO-TOXICITY; CROSS-RESISTANCE; CIS-DICHLORODIAMMINEPLATINUM; GLUTATHIONE DEPLETION AB In order to study the mechanisms responsible for resistance to CDDP, 5 human tumor cell lines were made resistant to CDDP by repeated in vitro exposures. After cloning it was found that the cell lines developed were between 3.3-fold and 17-fold more resistant to CDDP than the parental cell lines at the IC90. These lines were also resistant to carboplatin and tetraplatin; however, resistance to tetraplatin was lower than to the other platinum complexes. Sensitivity was also assessed to Adria, MTX, 5-FU, chlorambucil, 4-HC, 4-HIF, BCNU, Thiotepa, HN2, Mito C and L-PAM, and no consistent cross-resistance was observed. As compared with the parental lines, non-protein sulfhydryl content was elevated in 3 resistant lines, and protein sulfhydryl was elevated in all 5 lines, as was glutathione-S-transferase activity. Measurements of platinum in whole cells and nuclei after exposure of the cultures to 25-mu-M CDDP for either 1 or 6 hr showed that nuclear levels reflected those in whole cells and that, per mg protein, platinum levels were lower in resistant cells at both time points. Formation of DNA cross-links, determined by alkaline elution, was lower in resistant cell lines than in parental cell lines, but did not correlate with the absolute cell kill observed. These results indicate that cellular resistance to CDDP often involves decreases in drug accumulation and increases in protein sulfhydryl content. Possible strategies for overcoming these mechanisms are discussed. 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 [P01 CA38493, R01 CA36508] NR 72 TC 98 Z9 99 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD JAN 21 PY 1991 VL 47 IS 2 BP 252 EP 260 DI 10.1002/ijc.2910470214 PG 9 WC Oncology SC Oncology GA EV221 UT WOS:A1991EV22100013 PM 1846350 ER PT J AU SPRINGER, TA AF SPRINGER, TA TI CELL-ADHESION - STICKY SUGARS FOR SELECTINS SO NATURE LA English DT Editorial Material ID CARBOHYDRATE; ANTIGEN C1 GENENTECH INC,DEPT IMMUNOBIOL,S SAN FRANCISCO,CA 94080. RP SPRINGER, TA (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 25 TC 479 Z9 481 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD JAN 17 PY 1991 VL 349 IS 6306 BP 196 EP 197 DI 10.1038/349196a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ET519 UT WOS:A1991ET51900030 PM 1987472 ER PT J AU VONWEIZSACKER, F LABEIT, S KOCH, HK OEHLERT, W GEROK, W BLUM, HE AF VONWEIZSACKER, F LABEIT, S KOCH, HK OEHLERT, W GEROK, W BLUM, HE TI A SIMPLE AND RAPID METHOD FOR THE DETECTION OF RNA IN FORMALIN-FIXED, PARAFFIN-EMBEDDED TISSUES BY PCR AMPLIFICATION SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID POLYMERASE; VIRUS C1 INST PATHOL,W-7800 FREIBURG,GERMANY. UNIV FREIBURG,DEPT MED,W-7800 FREIBURG,GERMANY. EUROPEAN MOLEC BIOL LAB,W-6900 HEIDELBERG,GERMANY. RP VONWEIZSACKER, F (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02129, USA. NR 6 TC 36 Z9 37 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JAN 15 PY 1991 VL 174 IS 1 BP 176 EP 180 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA ET207 UT WOS:A1991ET20700028 PM 1703409 ER PT J AU FITZGERALD, GB BAUMAN, C HUSSOIN, S WICK, MM AF FITZGERALD, GB BAUMAN, C HUSSOIN, S WICK, MM TI 2,4-DIHYDROXYBENZYLAMINE - A SPECIFIC INHIBITOR OF GLUTATHIONE-REDUCTASE SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID DOPAMINE; LEVODOPA; ENZYME; AGENTS; CELLS; METABOLISM; ANALOGS AB The high intracellular level of glutathione is maintained, in part, by the important redox enzyme glutathione reductase. This report describes the properties of a new inhibitor of glutathione reductase, 2,4-dihydroxybenzylamine (2,4-DHBA). The inhibition of glutathione reductase by both 2,4-DHBA and 1,3-bischloroethyl-nitrosourea (BCNU) requires the presence of the co-factor NADPH. However, the inhibition caused by 2,4-DHBA was found to occur much more rapidly. Inhibition of glutathione reductase was time dependent, involved a stoichiometric titration of the enzyme, and was not reversed by gel-filtration indicating an irreversible inhibitory mechanism. The drug interacted at two inhibitory sites as determined by a Hill-type plot analysis. 2,4-DHBA was shown to compete with the substrate oxidized glutathione, and the reducing agents, glutathione and dithioerythritol, were found to protect the enzyme from its inhibitory effect. These results suggest that the inhibition may entail a free radical effect at or near the active site. A structure-activity analysis with other meta-dihydroxybenzene derivatives revealed that the inhibition of glutathione reductase was unique to 2,4-dihydroxybenzylamine. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC DERMATOL ONCOL LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. FU NCI NIH HHS [CA24988] NR 20 TC 21 Z9 21 U1 0 U2 1 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 JAN 15 PY 1991 VL 41 IS 2 BP 185 EP 190 DI 10.1016/0006-2952(91)90475-K PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EV522 UT WOS:A1991EV52200006 PM 1989629 ER PT J AU KANAKURA, Y DRUKER, B WOOD, KW MAMON, HJ OKUDA, K ROBERTS, TM GRIFFIN, JD AF KANAKURA, Y DRUKER, B WOOD, KW MAMON, HJ OKUDA, K ROBERTS, TM GRIFFIN, JD TI GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR AND INTERLEUKIN-3 INDUCE RAPID PHOSPHORYLATION AND ACTIVATION OF THE PROTOONCOGENE RAF-1 IN A HUMAN FACTOR-DEPENDENT MYELOID CELL-LINE SO BLOOD LA English DT Note ID KINASE-ACTIVITY; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION; GROWTH-FACTORS; PROTEINS; REQUIREMENT; MEMBRANE; RECEPTOR C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA34183, CA36167, CA47843] NR 30 TC 119 Z9 119 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 JAN 15 PY 1991 VL 77 IS 2 BP 243 EP 248 PG 6 WC Hematology SC Hematology GA ER719 UT WOS:A1991ER71900004 PM 1845931 ER PT J AU EDER, JP WHEELER, CA TEICHER, BA SCHNIPPER, LE AF EDER, JP WHEELER, CA TEICHER, BA SCHNIPPER, LE TI A PHASE-I CLINICAL-TRIAL OF NOVOBIOCIN, A MODULATOR OF ALKYLATING AGENT CYTOTOXICITY SO CANCER RESEARCH LA English DT Article ID RESISTANT; CELLS AB Antineoplastic drug resistance is a major obstacle to improved treatment of most adult cancers in humans. Novobiocin, an antibacterial agent which inhibits the eukaryotic topoisomerase II enzyme, increases the cytotoxicity of several alkylating agents in vitro by the formation of lethal DNA-DNA interstrand cross-links, perhaps by decreasing the repair of drug monoadducts. In murine tumors treated in vivo novobiocin markedly potentiates alkylating agent cytotoxicity without concomitant increases in host toxicity. With this background, a Phase I trial of novobiocin and cyclophosphamide was performed in refractory cancer patients. Novobiocin was given p.o. for 96 h; 750 mg/m2 of i.v. cyclophosphamide was administered at 48 h. Thirty-four patients received 65 courses. The dose-limiting toxicity of novobiocin in this trial was vomiting. The maximum tolerated dose was 6 g/day. Six of 34 patients had Grade III or IV mylosuppression but no dose escalation effect was noted. Three patients developed allergic reactions which resolved completely. No other significant toxicity occurred. While no dose-dependent effect on serum novobiocin levels occurred, 18 of 19 patients treated at greater-than-or-equal-to-4 g daily had serum levels greater-than-or-equal-to-100-mu-g/ml at steady state, a level which corresponds to levels used in vitro and seen in vivo where the murine novobiocin half-life of 82 min is far less than that seen in humans (6.0 h). Two of 30 evaluable patients had partial responses. Four other patients had stable disease. Four of six had prior disease progression on cyclophosphamide combination therapy. Novobiocin is well tolerated in patients receiving cyclophosphamide and blood levels are in the drug-potentiating range. Phase II trials in cyclophosphamide refractory patients are anticipated. C1 BETH ISRAEL HOSP,CHARLES A DANA RES INST,THORNDIKE LABS,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP EDER, JP (reprint author), BETH ISRAEL HOSP,CHARLES A DANA RES INST,DEPT MED,BOSTON,MA 02215, USA. NR 16 TC 50 Z9 51 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 JAN 15 PY 1991 VL 51 IS 2 BP 510 EP 513 PG 4 WC Oncology SC Oncology GA ET789 UT WOS:A1991ET78900009 PM 1985770 ER PT J AU SCHWARTZ, LH KOERNER, FC EDGERTON, SM SAWICKA, JM RIO, MC BELLOCQ, JP CHAMBON, P THOR, AD AF SCHWARTZ, LH KOERNER, FC EDGERTON, SM SAWICKA, JM RIO, MC BELLOCQ, JP CHAMBON, P THOR, AD TI PS2 EXPRESSION AND RESPONSE TO HORMONAL-THERAPY IN PATIENTS WITH ADVANCED BREAST-CANCER SO CANCER RESEARCH LA English DT Article ID 5' FLANKING REGION; CELL-LINE MCF-7; PROGESTERONE RECEPTORS; ENDOCRINE THERAPY; ESTROGEN; GENE; PROTEIN; ACTIVATION; TAMOXIFEN AB Seventy-two patients with advanced breast carcinoma (42% bone, 25% visceral, 5.5% soft tissue, and 27.5% multiple site metastases) were evaluated to determine the relationship between tumor expression of the estrogen-regulated protein pS2, estrogen receptor (ER) or progesterone receptor (PgR) content, and response to hormonal therapy. Twenty-nine % of tumors were pS2 positive, 64% were ER positive, and 29% were PgR positive. Of the ER-positive patients (n = 43), 15 (35%) had > 10% of the invasive carcinoma which immunostained for pS2 (these were considered pS2 positive). Only 3 of 24 ER-negative tumors were pS2 positive. A weak association between pS2 expression and ER content (P = 0.08) but not PgR content was observed. Of pS2-positive patients, 52% had a partial or complete response to hormonal therapy. In 24% of pS2-positive patients the disease stabilized with treatment. In contrast, 27% of pS2-negative patients had a partial or complete response. In 10% of these patients the disease stabilized. Similar associations between therapeutic response and ER or PgR were not observed. The odds of having a clinical response to hormonal therapy was greater for pS2-positive than for ER- or PgR-positive tumors. pS2 expression may define a subset of ER-positive tumors that are more likely to respond to hormonal treatment. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT THERAPY,BOSTON,MA 02114. FAC MED STRASBOURG,INST CHIM BIOL,MOLEC BIOL LAB,F-67085 STRASBOURG,FRANCE. FU NCI NIH HHS [P01 CA44768] NR 30 TC 134 Z9 142 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 JAN 15 PY 1991 VL 51 IS 2 BP 624 EP 628 PG 5 WC Oncology SC Oncology GA ET789 UT WOS:A1991ET78900026 PM 1985778 ER PT J AU GUNJI, H KHARBANDA, S KUFE, D AF GUNJI, H KHARBANDA, S KUFE, D TI INDUCTION OF INTERNUCLEOSOMAL DNA FRAGMENTATION IN HUMAN MYELOID-LEUKEMIA CELLS BY 1-BETA-D-ARABINOFURANOSYLCYTOSINE SO CANCER RESEARCH LA English DT Note ID 1-BETA-D-ARABINOFURANOSYLCYTOSINE INCORPORATION; GENES; FOS; TRANSCRIPTION; ELONGATION; INHIBITORS; INTERACTS; TEMPLATE; ELEMENTS; BETA AB The present results demonstrate that treatment of human U-937 myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with DNA fragmentation at multiples of approximately 200 base pairs. The extent of ara-C-induced DNA fragmentation was dependent on drug concentration and time of exposure. This pattern of internucleosomal DNA cleavage has been observed during programmed cell death and was associated in the present studies with loss of clonogenic survival. The results also demonstrate that the c-jun protooncogene is induced by ara-C during periods of DNA cleavage. These findings suggest that ara-C activates a program involving both oligonucleosomal DNA fragmentation and changes in early response gene expression. RP GUNJI, H (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA29431] NR 21 TC 232 Z9 234 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 JAN 15 PY 1991 VL 51 IS 2 BP 741 EP 743 PG 3 WC Oncology SC Oncology GA ET789 UT WOS:A1991ET78900045 PM 1985792 ER PT J AU LIU, Z WILLIAMS, KP CHANG, YH SMITH, JA AF LIU, Z WILLIAMS, KP CHANG, YH SMITH, JA TI SINGLE AMINO-ACID SUBSTITUTION ALTERS T-CELL DETERMINANT SELECTION DURING ANTIGEN PROCESSING OF STAPHYLOCOCCUS-AUREUS NUCLEASE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; IMMUNOGENIC PEPTIDES; PROTEIN ANTIGENS; MHC RESTRICTION; IA MOLECULES; RECOGNITION; CLONES; BINDING; REGION; SITE AB The effect of amino acid residues outside of T cell determinant regions of Staphylococcus aureus nuclease (Nase) on the activation of T cell hybridomas has been investigated. T cell hybridomas derived from BALB/c mice immunized with Nase were screened against a nested set of overlapping synthetic peptides spanning the entire Nase molecule. Five regions of Nase, encompassing residues 1 to 20, 21, to 40, 61 to 80, 101 to 120, and 112 to 130, were found to be the T cell determinants. Region 61 to 80 is the immunodominant site. Mutants of Nase with a single amino acid substitution outside the defined T cell determinants were tested for their ability to stimulate the T cell hybridomas. The substitution of arginine for glutamic acid at residue 43 markedly reduces the antigenic potency of the protein for I-E(d) restricted T cell hybridomas, which recognize Nase peptides comprised of residues 21 to 40 (p21-40) or 112 to 130 (p112-130). In contrast, the stimulatory capacity of this mutant for I-A(d) restricted T cell hybridomas remains unchanged. Our results suggest that selective regulation of an immune response may be achieved by appropriately mutagenizing protein Ag. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. NR 30 TC 34 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 JAN 15 PY 1991 VL 146 IS 2 BP 438 EP 443 PG 6 WC Immunology SC Immunology GA EU505 UT WOS:A1991EU50500006 PM 1702801 ER PT J AU MICHALEK, MT BENACERRAF, B ROCK, KL AF MICHALEK, MT BENACERRAF, B ROCK, KL TI WEAK BASE AMINES CAN INHIBIT CLASS-I MHC-RESTRICTED ANTIGEN PRESENTATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TOXIC LYMPHOCYTES-T; INFLUENZA NUCLEOPROTEIN; SOLUBLE-PROTEIN; CELLS; RECOGNITION; ACTIVATION; PEPTIDES; IDENTIFICATION; MOLECULES; HYBRIDOMA AB This report describes the effects of NH4Cl, CH3NH2, and chloroquine on class I and II MHC-restricted Ag presentation. OVA-specific T-T hybridomas were used to detect processed OVA in association with class I, H-2K(b), and class II, I-A(d/b), molecules on a B lymphoblastoid APC. OVA, internalized by APC under hypertonic conditions, was presented in association with class I and II MHC molecules. Treating the APC with NH4Cl or CH3NH2 inhibited class I- and II-restricted Ag presentation. In contrast, chloroquine markedly inhibited class II, but not class I-restricted Ag presentation. Controls indicated that drug-treated APC were fully competent to interact with T cells and present processing-independent antigenic peptides in association with both class I and II MHC molecules. NH4Cl and CH3NH2 did not inhibit the uptake of radiolabeled Ag by the APC. After the proteolytic removal of H-2K(b) from the surface of APC, NH4Cl and CH3NH2-treated and control APC regenerated identical amounts of surface H-2K(b) and this regeneration required de novo protein synthesis. These latter results indicate that NH4Cl and CH3NH2 can inhibit Ag presentation without affecting the synthesis, transport, or surface expression of H-2K(b). Also, NH4Cl did not affect the transport of H-2D(b) to the surface of mutant RMA-S cells that were cultured with exogenous peptides. Taken together these results strongly suggest that NH4Cl and CH3NH2 but not chloroquine can inhibit a critical and early intracellular step in class I-restricted Ag presentation while simultaneously inhibiting class II-restricted Ag presentation. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP MICHALEK, MT (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [T32CA09130, CA46967]; NIAID NIH HHS [AI20248] NR 34 TC 22 Z9 22 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1991 VL 146 IS 2 BP 449 EP 456 PG 8 WC Immunology SC Immunology GA EU505 UT WOS:A1991EU50500008 PM 1987272 ER PT J AU SOBEL, RA TUOHY, VK LEES, MB AF SOBEL, RA TUOHY, VK LEES, MB TI PARENTAL MHC MOLECULE HAPLOTYPE EXPRESSION IN (SJL/J X SWR)F1 MICE WITH ACUTE EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS INDUCED WITH 2 DIFFERENT SYNTHETIC PEPTIDES OF MYELIN PROTEOLIPID PROTEIN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HISTOCOMPATIBILITY COMPLEX ANTIGENS; 13)F1 GUINEA-PIGS; T-CELL HYBRIDOMAS; MONOCLONAL-ANTIBODIES; BASIC-PROTEIN; CLASS-I; ENCEPHALITOGENIC DETERMINANT; NERVOUS-SYSTEM; MOUSE; IMMUNOPATHOLOGY AB To determine if the Ag that induces an autoimmune disease influences parental MHC haplotype molecule expression in situ in MHC heterozygotes, acute experimental allergic encephalomyelitis (EAE) was induced with different encephalitogenic peptides in (SJL/J x SWR)F1 mice. The mice were sensitized with either a synthetic peptide corresponding to mouse myelin proteolipid protein (PLP) residues 103-116 YKTTICGKGLSATV which induces EAE in SWR (H-2q), but not SJL/J (H-2s) mice or a synthetic peptide corresponding to PLP residues 139-151 HCLGKWLGHPDKF which is encephalitogenic in SJL/J but not SWR mice. Mice were killed when they were moribund or at 30 days after sensitization. Twelve of 18 F1 mice given PLP peptide 103-116 and 12 of 17 mice given PLP peptide 139-151 developed EAE within 2 to 3 wk after sensitization. Cryostat sections of brain samples from F1 and parental mice were immunostained with a panel of mAb identifying H-2s and H-2q class I and II MHC molecules. In brains of controls, class I MHC molecules were expressed on choroid plexus, endothelial cells, and microglia whereas class II MHC molecules were absent. In EAE lesions, class I and II MHC molecules were present on inflammatory and parenchymal cells, but the degree of parental haplotype molecule expression did not vary with the different peptide Ag tested. Thus, in (SJL/J x SWR)F1 mice, myelin PLP peptides 103-116 and 139-151 are co-dominant Ag with respect to clinical and histologic disease and parental haplotype MHC molecule expression. We propose a unifying hypothesis consistent with these results and previous observations of differential Ia expression in (responder x non-responder)F1 guinea pigs. We suggest that MHC molecules may bind locally derived peptide Ag in inflammatory sites and that these interactions influence levels of MHC haplotype molecules on APC. C1 EK SHRIVER CTR,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. RP SOBEL, RA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT,COX 5,BOSTON,MA 02114, USA. FU NICHD NIH HHS [HD 04147]; NINDS NIH HHS [NS 16945, NS 26773] NR 50 TC 18 Z9 18 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1991 VL 146 IS 2 BP 543 EP 549 PG 7 WC Immunology SC Immunology GA EU505 UT WOS:A1991EU50500021 PM 1702806 ER PT J AU AMBROSINO, DM KANCHANA, MV DELANEY, NR FINBERG, RW AF AMBROSINO, DM KANCHANA, MV DELANEY, NR FINBERG, RW TI HUMAN B-CELLS SECRETE PREDOMINANTLY LAMBDA L-CHAINS IN THE ABSENCE OF H-CHAIN EXPRESSION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LIGHT CHAIN; ANTIBODIES AB Ig H and L chains are independently assembled in B cells and then secreted together as a functional protein. H chains cannot be secreted without assembly to L chains; however, L chains can be secreted in the absence of H chains by both mice and human cells. To examine the influence of H chain expression on human L chain isotype selection (kappa or lambda), we compared the kappa/lambda ratio of L chains unassociated with H chains (free L chains) to the kappa/lambda ratio of L chains associated with H chains. Culture supernatants of human splenocytes were assayed for kappa and lambda L chains. Free L chains were the predominant form of L chains detected in unstimulated cultures, accounting for 68 to 70% of the total. This was in contrast to the minor proportion that free L chains represented ( < 20%) in cultures stimulated with PWM or LPS (p < 0.01). Furthermore, the kappa/lambda ratio of light chains detected in unstimulated cultures was 0.5 as compared to 1.3 for PWM stimulated cultures (p = 0.0001). To demonstrate that the decreased kappa/lambda ratio of L chains in the supernatants of cultures of unstimulated B cells was due to free L chains, we measured the kappa/lambda ratio of IgG and IgM-associated L chains. In both the stimulated and unstimulated cultures, the kappa/lambda ratio of L chains associated with H chains was greater than the ratio determined for free L chains. Free L chains were shown to be predominantly lambda as compared to the predominantly kappa phenotype of L chains associated with H chains. Thus absence of H chain expression affects selection of L chain isotypes secreted by human B cells. RP AMBROSINO, DM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU NIAID NIH HHS [AI24659] NR 15 TC 8 Z9 9 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1991 VL 146 IS 2 BP 599 EP 602 PG 4 WC Immunology SC Immunology GA EU505 UT WOS:A1991EU50500029 PM 1898958 ER PT J AU NEAR, RI BRUCCOLERI, R NOVOTNY, J HUDSON, NW WHITE, A MUDGETTHUNTER, M AF NEAR, RI BRUCCOLERI, R NOVOTNY, J HUDSON, NW WHITE, A MUDGETTHUNTER, M TI THE SPECIFICITY PROPERTIES THAT DISTINGUISH MEMBERS OF A SET OF HOMOLOGOUS ANTIDIGOXIN ANTIBODIES ARE CONTROLLED BY H-CHAIN MUTATIONS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID VARIABLE REGION; MONOCLONAL-ANTIBODIES; IMMUNE-RESPONSE; BINDING SPECIFICITY; SOMATIC MUTATION; EXPRESSION; SEQUENCES; AFFINITY; HEAVY; MOUSE AB Five murine A/J strain and anti-digoxin mAb (35-20, 40-40, 40-120, 40-140, and 40-160) have highly homologous H and L chain V regions, only differing by somatic mutation, yet differ in affinity and specificity. The availability of the VH and VL genomic clones from one hybridoma, 40-140, has now allowed studied involving in vitro mutagenesis and chain recombination among these five hybridomas. To determine the relative contributions of the mutations found in either VH or VL to the overall binding properties of these antibodies, we recombined the 40-140VH with the VL of each hybridoma. The 40-140VH gene was transfected into hybridoma variants that produce only VL. The recombinant antibodies show that the mutations present in VH, rather than in VL, affect the fine specificity properties of these antibodies, whereas, the mutations among both VH and VL chains are important in determining antigen affinity. From mutations present in VH that affect fine specificity properties, the comparison of the antibody sequences, and from the previously measured binding properties, we predicted and tested selected VH mutations for their ability to alter specificity or affinity by doing site-directed in vitro mutagenesis. The results for the somatic mutations found in this group of antibodies show: 1) VH mutations control the fine specificity properties that distinguish different members of this group; 2) in particular, VH residues 54 and 55 in CDR2 control the distinguishing characteristics of specificities between these antibodies; and 3) by mutagenesis, we had the unusual result of being able to alter Ag specificity without affecting affinity. A computer model of the 40-140 antibody binding site was generated which indicates that VH residues 54 and 55 are highly accessible. C1 SQUIBB INST MED RES,PRINCETON,NJ 08543. HARVARD UNIV,SCH MED,BOSTON,MA 02114. INDIANA UNIV,SCH MED,DEPT MED,INDIANAPOLIS,IN 46223. RP NEAR, RI (reprint author), MASSACHUSETTS GEN HOSP,CELLULAR & MOLEC RES LAB,JACKSON 14,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-19259] NR 43 TC 22 Z9 22 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1991 VL 146 IS 2 BP 627 EP 633 PG 7 WC Immunology SC Immunology GA EU505 UT WOS:A1991EU50500033 PM 1898959 ER PT J AU STACKER, SA SPRINGER, TA AF STACKER, SA SPRINGER, TA TI LEUKOCYTE INTEGRIN P150,95 (CD11C/CD18) FUNCTIONS AS AN ADHESION MOLECULE-BINDING TO A COUNTER-RECEPTOR ON STIMULATED ENDOTHELIUM SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MONOCLONAL-ANTIBODIES; COMPLEMENT RECEPTOR; GLYCOPROTEIN FAMILY; HUMAN-MONOCYTES; ALPHA-SUBUNIT; HUMAN-NEUTROPHILS; LFA-1; MAC-1; CELLS; DIFFERENTIATION AB p150,95 is a member of the beta-2 family of integrins, which includes both LFA-1 and Mac-1. These molecules are known to play a role in the adhesion of lymphocytes, granulocytes, and monocytes to various cell types including vascular endothelium. p150,95 is presumed to have an adhesive function because of its structural relationship to the other beta-2 integrins and the ability of anti-p150,95 mAb to inhibit some myeloid cell interactions with tumor cells, endothelial cells, and other substrates. In an endeavor to demonstrate directly that p150,95 can act as an adhesion molecule, we raised an mAb (CBRp150/4G1) to the alpha subunit of p150,95, which allows for the purification of functional intact p150,95 heterodimers. The antibody was selected by using a high pH elution ELISA. The assay was designed to select for antibodies directed to the alpha-chain of p150,95, which could be readily dissociated from p150,95 under conditions of high pH and 2 mM MgCl2. p150,95 purified under these conditions with CBRp150/4G1-Sepharose could be immunoprecipitated by using antibodies to the alpha- and beta-chains of p150,95 indicating that the structural integrity of the heterodimer was preserved during purification and elution. Elution in the absence of divalent cations yielded primarily dissociated alpha and beta subunits. Other antibodies previously made to p150,95 alpha-chain such as SHCL3 were greatly reduced in their efficiency of yielding intact heterodimer under these conditions. Mapping of the epitopes by using chimeric molecules of p150,95/Mac-1 revealed that antibodies that react with the divalent cation sites of p150,95 are inferior for the purification of intact p150,95. The adhesive capacity of p150,95 was demonstrated by the specific binding of 18-h rIL-1-beta or LPS-stimulated endothelial cells to purified p150,95 absorbed to plastic microtiter plates. These results indicate that p150,95 can function independently as an adhesion molecule and that it can interact with a counter-receptor on stimulated endothelium. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. FU NCI NIH HHS [CA31799] NR 40 TC 134 Z9 135 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1991 VL 146 IS 2 BP 648 EP 655 PG 8 WC Immunology SC Immunology GA EU505 UT WOS:A1991EU50500036 PM 1702811 ER PT J AU BALK, SP BLEICHER, PA TERHORST, C AF BALK, SP BLEICHER, PA TERHORST, C TI ISOLATION AND EXPRESSION OF CDNA-ENCODING THE MURINE HOMOLOGS OF CD1 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL RECEPTOR; NORMAL HUMAN-SKIN; CLASS-I ANTIGENS; GAMMA-DELTA; MONOCLONAL-ANTIBODY; INTRAEPITHELIAL LYMPHOCYTES; THYMIC DIFFERENTIATION; SURFACE-ANTIGENS; HUMAN THYMOCYTES; DENDRITIC CELLS AB The cDNA encoding the murine CD1.1 and CD1.2 gene products were isolated and their complete nucleotide sequence was determined. The nucleotide sequence and genomic organization of these molecules were similar to human CD1. The sequences in the alpha-1-alpha-3 domains were almost identical to previously reported genomic clones from a different strain, indicating limited polymorphism amoung these molecules. The predicted amino acid sequence in the transmembrane region and in the cytoplasmic tail was identical for CD1.1 and CD1.2. The two cDNA were also homologous in the 5' untranslated region but diverged in the 3' untranslated region. In contrast to human CD1, which is expressed at high levels in thymus, the expression of CD1 message in murine thymus was not detected in either thymus leukemia Ag positive or negative strains. Cells expressing murine CD1.1 were generated after transfer of the CD1.1 cDNA into murine cell lines. Immunoprecipitation with a rat anti-mouse CD1.1 mAb showed that the transfected CD1 was expressed on the cell surface as a beta-2-microglobulin-linked heterodimer. These results demonstrate that the murine and human CD1 genes, although encoding homologous transmembrane glycoproteins, are expressed in distinct tissues and may serve different functions. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC IMMUNOL LAB,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. RP BALK, SP (reprint author), BETH ISRAEL HOSP,DEPT HEMATOL ONCOL,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NCI NIH HHS [CA-01310]; NIAMS NIH HHS [AR07098] NR 47 TC 85 Z9 88 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1991 VL 146 IS 2 BP 768 EP 774 PG 7 WC Immunology SC Immunology GA EU505 UT WOS:A1991EU50500053 PM 1702817 ER PT J AU HABER, DA HOUSMAN, DE AF HABER, DA HOUSMAN, DE TI RATE-LIMITING STEPS - THE GENETICS OF PEDIATRIC CANCERS SO CELL LA English DT Review ID WILMS TUMOR; RETINOBLASTOMA GENE; MUTATIONS; ONCOGENE; ALLELES C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP HABER, DA (reprint author), MIT,CTR CANC RES,CAMBRIDGE,MA 02139, USA. NR 20 TC 46 Z9 46 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JAN 11 PY 1991 VL 64 IS 1 BP 5 EP 8 DI 10.1016/0092-8674(91)90200-I PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ET175 UT WOS:A1991ET17500002 PM 1846091 ER PT J AU CONN, PM CROWLEY, WF AF CONN, PM CROWLEY, WF TI GONADOTROPIN-RELEASING-HORMONE AND ITS ANALOGS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID CENTRAL PRECOCIOUS PUBERTY; FOLLICLE-STIMULATING-HORMONE; POLYCYSTIC OVARIAN DISEASE; IDIOPATHIC HYPOGONADOTROPIC HYPOGONADISM; HUMAN MENSTRUAL-CYCLE; HUMAN-BREAST CANCER; PROTEIN KINASE-C; SEX STEROID-SECRETION; BONE-MINERAL DENSITY; ACTING GNRH AGONIST C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. RP CONN, PM (reprint author), UNIV IOWA,COLL MED,DEPT PHARMACOL,IOWA CITY,IA 52242, USA. FU NICHD NIH HHS [HD15080, HD19899, HD24697, R01 HD015788, U54 HD028138, U54 HD029164] NR 158 TC 347 Z9 354 U1 1 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 JAN 10 PY 1991 VL 324 IS 2 BP 93 EP 103 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA EQ977 UT WOS:A1991EQ97700005 PM 1984190 ER PT J AU GRESS, DR EICHHORN, JH YOUNG, T HEDLEYWHYTE, ET HOCHBERG, FH BAZARI, H HUANG, PL KISTLER, JP AF GRESS, DR EICHHORN, JH YOUNG, T HEDLEYWHYTE, ET HOCHBERG, FH BAZARI, H HUANG, PL KISTLER, JP TI A 60-YEAR-OLD WOMAN WITH HYPERTENSION, SEIZURES, AND MILD RENAL-FAILURE - RENAL CHOLESTEROL EMBOLISM (AFTER CORONARY ANGIOGRAPHIC PROCEDURES) - RENAL TUBULAR ATROPHY AND INTERSTITIAL FIBROSIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID ATHEROEMBOLISM; EMBOLIZATION; INFARCTION; SPECTRUM C1 MASSACHUSETTS GEN HOSP,EMERGENCY SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GRESS, DR (reprint author), MASSACHUSETTS GEN HOSP,CLIN STROKE SERV,BOSTON,MA 02114, USA. NR 20 TC 3 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 JAN 10 PY 1991 VL 324 IS 2 BP 113 EP 120 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA EQ977 UT WOS:A1991EQ97700008 ER PT J AU RAGHAVAN, D SHIPLEY, WU RUSSELL, PJ GARNICK, MB RICHIE, JP AF RAGHAVAN, D SHIPLEY, WU RUSSELL, PJ GARNICK, MB RICHIE, JP TI BIOLOGY AND MANAGEMENT OF BLADDER-CANCER - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID PLOIDY C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. RP RAGHAVAN, D (reprint author), ROYAL PRINCE ALFRED HOSP,CAMPERDOWN,NSW 2050,AUSTRALIA. NR 7 TC 0 Z9 0 U1 0 U2 2 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JAN 10 PY 1991 VL 324 IS 2 BP 126 EP 126 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EQ977 UT WOS:A1991EQ97700013 ER PT J AU ANDERSON, KC WEINSTEIN, HJ AF ANDERSON, KC WEINSTEIN, HJ TI TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID SURGERY RP ANDERSON, KC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 6 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 JAN 10 PY 1991 VL 324 IS 2 BP 128 EP 129 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA EQ977 UT WOS:A1991EQ97700020 ER PT J AU BARSKY, AJ COLES, NA ODONNELL, C EAGLE, KA AF BARSKY, AJ COLES, NA ODONNELL, C EAGLE, KA TI DENIAL AND SILENT ISCHEMIA - WHICH COMES 1ST - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP BARSKY, AJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JAN 9 PY 1991 VL 265 IS 2 BP 213 EP 213 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EQ602 UT WOS:A1991EQ60200022 ER PT J AU KANAKURA, Y DRUKER, B DICARLO, J CANNISTRA, SA GRIFFIN, JD AF KANAKURA, Y DRUKER, B DICARLO, J CANNISTRA, SA GRIFFIN, JD TI PHORBOL 12-MYRISTATE 13-ACETATE INHIBITS GRANULOCYTE-MACROPHAGE COLONY STIMULATING FACTOR-INDUCED PROTEIN TYROSINE PHOSPHORYLATION IN A HUMAN FACTOR-DEPENDENT HEMATOPOIETIC-CELL LINE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID KINASE-C; INSULIN-RECEPTOR; PHOSPHOTYROSINE PHOSPHATASE; INDEPENDENT MECHANISMS; GROWTH-FACTORS; BETA-SUBUNIT; INTERLEUKIN-3; DIFFERENTIATION; EXPRESSION; CD45 AB The human myeloid cell line MO7 requires either granulocyte-macrophage colony stimulating factor (GM-CSF) or interleukin 3 (IL-3) for proliferation. We have previously shown that both GM-CSF and IL-3 transiently induce tyrosine phosphorylation of a number of proteins, including two cytosolic proteins, p93 and p70, which are maximally phosphorylated 5-15 min after addition of growth factor to factor-deprived cells. GM-CSF-induced proliferation of MO7 cells was found to be inhibited by two activators of protein kinase C, phorbol 12-myristate 13-acetate (PMA) and bryostatin-1. PMA did not affect surface expression or affinity of the GM-CSF receptor put significantly inhibited GM-CSF-induced tyrosine phosphorylation of another protein, p42. Pretreatment of cells with sodium orthovanadate to inhibit protein tyrosine phosphatases (PTPase) partially reversed the inhibitory effects of PMA. These results suggest that one aspect of GM-CSF and IL-3 signal transduction, protein tyrosine phosphorylation, can be inhibited by a mechanism which does not involve receptor down-regulation, and may involve either inhibition of a receptor-activated tyrosine kinase, activation of a protein tyrosine phosphatase, or both. This mechanism could be important in exerting control of proliferation of some types of hematopoietic cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA34183, CA36167, CA47843] NR 53 TC 77 Z9 77 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 JAN 5 PY 1991 VL 266 IS 1 BP 490 EP 495 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EQ339 UT WOS:A1991EQ33900072 PM 1845978 ER PT J AU LETVIN, NL HARRIS, NL VONSATTEL, JP TABAS, JH SCULLY, RE HUANG, PL HARMON, DC MARTUZA, RL AF LETVIN, NL HARRIS, NL VONSATTEL, JP TABAS, JH SCULLY, RE HUANG, PL HARMON, DC MARTUZA, RL TI A 45-YEAR-OLD MAN WITH HIV-INFECTION, AN EPIDURAL MASS, AND A HISTORY OF TREATED PULMONARY TUBERCULOSIS AND A SEMINOMA - SEMINOMA OF TESTIS METASTATIC TO C4 REGION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID ACQUIRED IMMUNODEFICIENCY SYNDROME; IMMUNE-DEFICIENCY SYNDROME; BENIGN LYMPHOEPITHELIAL LESION; SYNDROME-RELATED COMPLEX; CAT-SCRATCH DISEASE; GERM-CELL TUMORS; TESTICULAR SEMINOMA; AIDS; ABSCESS; MALIGNANCIES C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LETVIN, NL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 40 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 JAN 3 PY 1991 VL 324 IS 1 BP 42 EP 51 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA EQ503 UT WOS:A1991EQ50300008 ER PT J AU WARNER, CD BRANCH, SK BURKE, JF CHAMBERS, LM YOUNG, VR AF WARNER, CD BRANCH, SK BURKE, JF CHAMBERS, LM YOUNG, VR TI MICRODERIVATIZATION OF 4-[O-18]HYDROXYPROLINE AND QUANTITATION WITH A BENCHTOP MASS-SPECTROMETER SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS LA English DT Article ID COLLAGEN; DEGRADATION; INVIVO; SKIN; RATS AB Accurate estimation of in vivo turnover rates of collagen is complicated by amino acid reutilization. It was previously shown that the ideal, non-recycling tracer was [O-18]hydroxyproline synthesized in vivo. The analytical method for measuring turnover rates with [O-18]hydroxyproline must include analyte quantitation for pool size determination and isotope ratio measurement for determining levels of label incorporation. For ease of use and widest availability, a benchtop gas chromatograph-mass spectrometer in the electron-impact ionization mode was chosen. Here we present a versatile procedure for hydroxyproline derivatization that is well suited for routine, large-scale determination of analyte concentrations and relative levels of O-18 incorporation. C1 MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP WARNER, CD (reprint author), SHRINERS BURN INST,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 11 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR-BIOMED JI J. Chromatogr.-Biomed. Appl. PD JAN 2 PY 1991 VL 562 IS 1-2 BP 625 EP 637 DI 10.1016/0378-4347(91)80613-H PG 13 WC Chemistry, Analytical SC Chemistry GA EV983 UT WOS:A1991EV98300056 PM 2026725 ER PT B AU SCHRIEVER, F NADLER, LM AF SCHRIEVER, F NADLER, LM BE RACZ, P DIJKSTRA, CD GLUCKMAN, JC TI ANTIGENIC PHENOTYPE OF ISOLATED HUMAN FOLLICULAR DENDRITIC CELLS SO ACCESSORY CELLS IN HIV AND OTHER RETROVIRAL INFECTIONS: MORPHOLOGICAL AND FUNCTIONAL ASPECTS LA English DT Proceedings Paper CT 2ND WORKSHOP ON MORPHOLOGICAL AND FUNCTIONAL ASPECTS OF ACCESSORY CELLS IN RETROVIRAL INFECTIONS CY NOV 23-24, 1990 CL INST TROP MED, HAMBURG, FED REP GER SP EUROPEAN COMMUNITY PROJECT IMMUNOPATHOL & IMMUNOL HIV RELATED DIS HO INST TROP MED RP SCHRIEVER, F (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5323-4 PY 1991 BP 9 EP 17 PG 9 WC Immunology; Pathology; Virology SC Immunology; Pathology; Virology GA BU09M UT WOS:A1991BU09M00002 ER PT J AU AOBA, T MORENO, EC AF AOBA, T MORENO, EC TI STRUCTURAL RELATIONSHIP OF AMELOGENIN PROTEINS TO THEIR REGULATORY FUNCTION OF ENAMEL MINERALIZATION SO ACS SYMPOSIUM SERIES LA English DT Article ID DEVELOPING BOVINE ENAMEL; APATITE CRYSTAL-GROWTH; AMINO-TERMINAL SEGMENT; PROLINE-RICH PROTEINS; DENTAL ENAMEL; MATRIX PROTEINS; BIOLOGICAL INTEREST; PROTEOLYTIC-ENZYME; CALCIUM APATITES; ACID-SEQUENCE AB Observations in situ and in vitro suggest that the regulatory mechanism of enamel mineralization in porcine amelogenesis involves the parent amelogenin (major matrix proteins secreted by the ameloblast) which is selectively adsorbed onto originally precipitating apatite crystals, thereby inhibiting apatite crystal growth. This phenomenon has been observed in supersaturated solutions having ionic composition similar to that of the liquid phase surrounding the enamel crystals in vivo. The adsorption affinity of amelogenin (and its inhibitory activity) is lost with cleavages of specific segments, suggesting that known enzymatic degradation of the secreted proteins plays a role in controlling the kinetics of enamel mineralization. Studies using fragments of the amelogenin (and a synthetic peptide) indicate that both the hydrophobic and hydrophilic sequences, at the N- and C- termini respectively, are essential for the proposed function of the amelogenin as a crystal growth regulator. RP AOBA, T (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. NR 66 TC 14 Z9 15 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0097-6156 J9 ACS SYM SER PY 1991 VL 444 BP 85 EP 106 PG 22 WC Chemistry, Multidisciplinary SC Chemistry GA EV849 UT WOS:A1991EV84900007 ER PT J AU GOUDSOUZIAN, NG AF GOUDSOUZIAN, NG TI DOSE-RESPONSE TO PANCURONIUM IN IDENTICAL-TWINS - REPLY SO ACTA ANAESTHESIOLOGICA SCANDINAVICA LA English DT Letter RP GOUDSOUZIAN, NG (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-5172 J9 ACTA ANAESTH SCAND JI Acta Anaesthesiol. Scand. PD JAN PY 1991 VL 35 IS 1 BP 91 EP 91 PG 1 WC Anesthesiology SC Anesthesiology GA EU348 UT WOS:A1991EU34800018 ER PT J AU GROOP, LC RATHEISER, K LUZI, L MELANDER, A SIMONSON, DC PETRIDES, A BONADONNA, RC WIDEN, E DEFRONZO, RA AF GROOP, LC RATHEISER, K LUZI, L MELANDER, A SIMONSON, DC PETRIDES, A BONADONNA, RC WIDEN, E DEFRONZO, RA TI EFFECT OF SULFONYLUREA ON GLUCOSE-STIMULATED INSULIN-SECRETION IN HEALTHY AND NON-INSULIN-DEPENDENT DIABETIC SUBJECTS - A DOSE-RESPONSE STUDY SO ACTA DIABETOLOGICA LA English DT Article DE INSULIN; C-PEPTIDE; GLUCOSE; GLIPIZIDE; NON-INSULIN-DEPENDENT DIABETES-MELLITUS ID SULFONYLUREA THERAPY; NORMAL HUMANS; C-PEPTIDE; BETA-CELL; HYPERGLYCEMIA; GLYBURIDE; GLIPIZIDE; MELLITUS; DRUGS; SERUM AB The effect of a rapid-acting sulphonylurea, glipizide, on the dose-response relationship between the beta-cell response (insulin and C-peptide secretion) and the ambient plasma glucose concentration was examined in 12 healthy and 6 non-insulin-dependent diabetic subjects. The subjects participated in two sets of experiments which were performed in random order: (A) four hyperglycaemic clamp studies, during which the plasma glucose concentration was raised for 120 min by 1 (only in healthy subjects), 3, 7, and 17 mmol/l; and (B) the same four hyperglycaemic clamp studies preceded by ingestion of 5 mg glipizide. All subjects participated in a further study, in which glipizide was ingested and the plasma glucose concentration was maintained at the basal level. In control subjects in the absence of glipizide, the first-phase plasma insulin response (0-10 min) increased progressively with increasing plasma glucose concentration up to 10 mmol/l, above which it tended to plateau. Glipizide augmented the first-phase insulin response without changing the slope of the regression line relating plasma insulin to glucose concentrations. The second-phase plasma insulin response (20-120 min) increased linearly with increasing hyperglycaemia (r = 0.997). Glipizide alone increased the plasma insulin response by 180 pmol/l. A similar increase in plasma insulin response following glipizide was observed at each hyperglycaemic step, indicating that glipizide did not affect the sensitivity of the beta-cell to glucose. First-phase insulin secretion was reduced in the type 2 (non-insulin-dependent) diabetic patients, and was not influenced by glipizide. The dose-response curve relating second-phase insulin secretion to the ambient plasma glucose concentration was significantly (P < 0.001) flatter in the diabetic patients than in the control subjects. Glipizide alone increased the plasma insulin response by 60 pmol/l without changing the slope of the dose-response curve. It is concluded that, in both type 2 diabetic patients and healthy subjects: (A) sulphonylurea augments glucose-stimulated second-phase insulin secretion without changing the sensitivity of the beta-cell to glucose; (B) first-phase insulin secretion is reduced in non-insulin-dependent diabetic patients with fasting hyperglycaemia and is not influenced by sulphonylurea. C1 YALE UNIV,SCH MED,NEW HAVEN,CT 06510. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV LUND,DEPT PHARMACOL & TOXICOL,S-21401 MALMO,SWEDEN. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV DIABET,SAN ANTONIO,TX 78284. RP GROOP, LC (reprint author), UNIV HELSINKI,DEPT MED 4,UNIONKATU 38,SF-00170 HELSINKI 17,FINLAND. RI Luzi, Livio/M-2696-2016 OI Luzi, Livio/0000-0003-3183-0552 FU FIC NIH HHS [F05-TWO-3451]; NCRR NIH HHS [RR 125]; NIADDK NIH HHS [AM-24092] NR 30 TC 26 Z9 26 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0940-5429 J9 ACTA DIABETOL JI Acta Diabetol. PY 1991 VL 28 IS 2 BP 162 EP 168 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GQ144 UT WOS:A1991GQ14400006 PM 1777653 ER PT J AU LOUIS, DN EDGERTON, S THOR, AD HEDLEYWHYTE, ET AF LOUIS, DN EDGERTON, S THOR, AD HEDLEYWHYTE, ET TI PROLIFERATING CELL NUCLEAR ANTIGEN AND KI-67 IMMUNOHISTOCHEMISTRY IN BRAIN-TUMORS - A COMPARATIVE-STUDY SO ACTA NEUROPATHOLOGICA LA English DT Article DE PROLIFERATING CELL NUCLEAR ANTIGEN (PCNA); KI-67; IMMUNOHISTOCHEMISTRY; NERVOUS SYSTEM TUMORS ID MONOCLONAL-ANTIBODY KI-67; S-PHASE CELLS; CYCLIN PCNA; DNA-REPLICATION; PROTEIN; ASTROCYTOMAS; MALIGNANCIES; TISSUES AB Proliferating cell nuclear antigen (PCNA) is a 36-kDa DNA polymerase-partial derivative auxiliary protein which accumulates in the nucleus during S phase of the cell cycle. Immunohistochemical labeling indices (LI) of PCNA and Ki-67 were compared using an avidin-biotin complex method on frozen sections of 27 nervous system tumors, 3 normal cerebral cortices, and 3 peripheral nerves. In glial tumors, PCNA and Ki-67 LI increased with increasing tumor grade (Daumas-Duport system). In 5 low-grade glial tumors, PCNA and Ki-67 LI were less-than-or-equal-to 1%, except for one optic nerve glioma (Ki-67 LI = 6%). In 7 grade 3 astrocytomas and 1 mixed glioma, PCNA LI were less-than-or-equal-to 1-1.5%, while Ki-67 LI were 2%-10%. In 7 grade 4 astrocytomas and 1 metastatic carcinoma, PCNA LI ranged from 6%-15% while Ki-67 LI ranged from 17%-30%. In 5 of 6 schwannomas, focally high PCNA LI (4%-65%) were noted, despite low LI with Ki-67 (less-than-or-equal-to 1.6%). Scattered normal schwann cell nuclei also stained with PCNA, but normal cerebral cortex did not. These data suggest that: (1) in higher-grade gliomas, PCNA may be more specific S-phase marker, although a less sensitive proliferation marker, than Ki-67; (2) PCNA LI do not distinguish low-grade gliomas from grade 3 astrocytomas; (3) in schwannomas, PCNA may not reflect proliferative activity since it seems to react with an epitope present in normal schwann cells; and (4) the variable PCNA staining pattern introduces greater difficulties in cell counting than with Ki-67. These factors may limit the use of this anti-PCNA antibody in evaluating nervous system tumors. RP LOUIS, DN (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02114, USA. NR 21 TC 154 Z9 156 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0001-6322 J9 ACTA NEUROPATHOL JI Acta Neuropathol. PY 1991 VL 81 IS 6 BP 675 EP 679 PG 5 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA FN853 UT WOS:A1991FN85300013 PM 1679278 ER PT J AU BESS, FH LICHTENSTEIN, MJ LOGAN, SA AF BESS, FH LICHTENSTEIN, MJ LOGAN, SA TI MAKING HEARING IMPAIRMENT FUNCTIONALLY RELEVANT - LINKAGES WITH HEARING DISABILITY AND HANDICAP SO ACTA OTO-LARYNGOLOGICA LA English DT Article; Proceedings Paper CT INTERNATIONAL WORKSHOP ON HEARING IN THE AGED CY NOV 26-29, 1989 CL HELSINGOR, DENMARK SP COMMISS EUROPEAN COMMUNITIES C1 BILL WILKERSON HEARING & SPEECH CTR,NASHVILLE,TN. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP BESS, FH (reprint author), VANDERBILT UNIV,SCH MED,DIV HEARING & SPEECH SCI,1114 19TH AVE S,NASHVILLE,TN 37212, USA. NR 20 TC 3 Z9 3 U1 1 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6489 J9 ACTA OTO-LARYNGOL JI Acta Oto-Laryngol. PY 1991 SU 476 BP 226 EP 231 PG 6 WC Otorhinolaryngology SC Otorhinolaryngology GA FA468 UT WOS:A1991FA46800035 ER PT J AU BOEPPLE, PA CROWLEY, WF AF BOEPPLE, PA CROWLEY, WF TI GONADOTROPIN-RELEASING-HORMONE ANALOGS AS THERAPEUTIC PROBES IN HUMAN GROWTH AND DEVELOPMENT - EVIDENCE FROM CHILDREN WITH CENTRAL PRECOCIOUS PUBERTY SO ACTA PAEDIATRICA SCANDINAVICA LA English DT Article DE GROWTH; GONADOTROPIN-RELEASING HORMONE ANALOGS; CENTRAL PRECOCIOUS PUBERTY ID LONG-TERM TREATMENT; CYPROTERONE-ACETATE; SKELETAL MATURATION; SOMATIC GROWTH; AGONIST; HEIGHT; GIRLS AB Statural growth and skeletal development were assessed in 87 girls with idiopathic central precocious puberty (CPP) during gonadotrophin-releasing hormone analogue (GnRHa)-induced suppression of gonadarche. Before the start of therapy, mean chronological age (CA) was 6.3 years and mean bone age (BA) was 10.6 years. During up to 6 consecutive years of complete suppression of gonadal sex steroid secretion, the mean height velocity decreased from 10.8 cm/year to prepubertal rates. At each interval height velocity was found to be inversely and negatively correlated with BA such that girls with advanced BAs grew at rates well below prepubertal norms but appropriately for their degree of skeletal maturation. Skeletal maturation similarly slowed during prolonged GnRHa administration (DELTA-BA/DELTA-CA = 0.6 +/- 0.1 over 3 years, mean +/- SD, n = 66) and was also negatively correlated with the BA before the start of therapy. Predicted adult height increased progressively during therapy; however, when analysed as changes in height SDS(BA), the impact of treatment was variable and correlated positively with the initial degree of skeletal maturation. The effect of GnRHa therapy on growth in children with CPP requires long-term study and is best analysed by employing a developmental perspective. C1 MASSACHUSETTS GEN HOSP, DEPT MED, PEDIAT ENDOCRINE UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CHILDRENS SERV, BOSTON, MA 02114 USA. RP CROWLEY, WF (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT MED, REPROD UNIT, BOSTON, MA 02114 USA. NR 19 TC 1 Z9 1 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-656X J9 ACTA PAEDIATR SCAND PY 1991 SU 372 BP 33 EP 38 PG 6 WC Pediatrics SC Pediatrics GA FP053 UT WOS:A1991FP05300007 ER PT J AU MINTZ, J PHIPPS, CC ARRUDA, MJ GLYNN, SM SCHNEIDER, NG JARVIK, ME AF MINTZ, J PHIPPS, CC ARRUDA, MJ GLYNN, SM SCHNEIDER, NG JARVIK, ME TI COMBINED USE OF ALCOHOL AND NICOTINE GUM SO ADDICTIVE BEHAVIORS LA English DT Article ID CHEWING-GUM; SMOKING CESSATION; TRIAL C1 UNIV CALIF LOS ANGELES,BRENTWOOD DIV,W LOS ANGELES VET ADM MED CTR,LOS ANGELES,CA 90024. RP MINTZ, J (reprint author), UNIV CALIF LOS ANGELES,BRENTWOOD VET ADM HOSP 691 B117,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90073, USA. NR 14 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4603 J9 ADDICT BEHAV JI Addict. Behav. PY 1991 VL 16 IS 1-2 BP 1 EP 10 DI 10.1016/0306-4603(91)90034-F PG 10 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA EZ512 UT WOS:A1991EZ51200001 PM 2048453 ER PT J AU BIERER, BE BURAKOFF, SJ AF BIERER, BE BURAKOFF, SJ TI T-CELL RECEPTORS - ADHESION AND SIGNALING SO ADVANCES IN CANCER RESEARCH LA English DT Review ID FUNCTION-ASSOCIATED ANTIGEN-3; LYMPHOCYTE HOMING RECEPTORS; LFA-1 MEMBRANE MOLECULE; PROTEIN KINASE P56LCK; CLASS-II MHC; MONOCLONAL-ANTIBODIES; ERYTHROCYTE RECEPTOR; CYTOPLASMIC DOMAIN; CROSS-LINKING; BETA-SUBUNIT C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP BIERER, BE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 34129]; NIAID NIH HHS [AI 17258, AI 28554] NR 137 TC 44 Z9 44 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0065-230X J9 ADV CANCER RES JI Adv.Cancer Res. PY 1991 VL 56 BP 49 EP 76 DI 10.1016/S0065-230X(08)60477-7 PG 28 WC Oncology SC Oncology GA FN839 UT WOS:A1991FN83900002 PM 2028842 ER PT J AU GARG, HG LYON, NB AF GARG, HG LYON, NB TI STRUCTURE OF COLLAGEN FIBRIL-ASSOCIATED, SMALL PROTEOGLYCANS OF MAMMALIAN ORIGIN SO ADVANCES IN CARBOHYDRATE CHEMISTRY AND BIOCHEMISTRY LA English DT Review ID DERMATAN SULFATE PROTEOGLYCAN; HUMAN ARTICULAR-CARTILAGE; HUMAN-SKIN FIBROBLASTS; AMINO-ACID-SEQUENCE; CULTURED HUMAN-FIBROBLASTS; MEMBRANE GLYCOPROTEIN-IB; RABBIT CORNEAL STROMA; FACTOR-BINDING DOMAIN; PROTEODERMATAN SULFATE; CALF SKIN C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. SHRINERS BURNS INST,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. NR 129 TC 21 Z9 21 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 0065-2318 J9 ADV CARBOHYD CHEM BI JI Adv. Carbohydr. Chem. Biochem. PY 1991 VL 49 BP 239 EP 261 DI 10.1016/S0065-2318(08)60184-5 PG 23 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA MC410 UT WOS:A1991MC41000007 PM 1814173 ER PT B AU AUSUBEL, FM DAVIS, KR SCHOTT, EJ DONG, X MINDRINOS, M AF AUSUBEL, FM DAVIS, KR SCHOTT, EJ DONG, X MINDRINOS, M BE HENNECKE, H VERMA, DPS TI IDENTIFICATION OF SIGNAL TRANSDUCTION PATHWAYS LEADING TO THE EXPRESSION OF ARABIDOPSIS-THALIANA DEFENSE GENES SO ADVANCES IN MOLECULAR GENETICS OF PLANT-MICROBE INTERACTIONS, VOL 1 SE CURRENT PLANT SCIENCE AND BIOTECHNOLOGY IN AGRICULTURE LA English DT Proceedings Paper CT 5TH INTERNATIONAL SYMP ON THE MOLECULAR GENETICS OF PLANT-MICROBE INTERACTIONS CY SEP 09-14, 1990 CL INTERLAKEN, SWITZERLAND SP SWISS FED INST TECHNOL, CIBA GEIGY, HOFFMANN LA ROCHE, SANDOZ, SWEIZER AKAD NATURWISSENSCH, SWEIZER NATIONALFONDS, NESTLE, SCHERING, SCHWEIZER GESELL MIKROBIOL, INT SOC PLANT MOLEC BIOL RP AUSUBEL, FM (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA DORDRECHT BN 0-7923-1082-9 J9 CURR PLANT SCI BIOT PY 1991 VL 10 BP 357 EP 364 PG 8 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Plant Sciences; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Plant Sciences; Genetics & Heredity GA BV46F UT WOS:A1991BV46F00055 ER PT J AU SWEET, WH AF SWEET, WH TI DEAFFERENTATION SYNDROMES IN HUMANS - A GENERAL DISCUSSION SO ADVANCES IN PAIN RESEARCH AND THERAPY LA English DT Article ID PAIN; ROOTS RP SWEET, WH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROSURG,BOSTON,MA 02114, USA. NR 34 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0722 J9 ADV PAIN RES THER JI Adv. Pain Res. Ther. PY 1991 VL 19 BP 259 EP 274 PG 16 WC Neurosciences SC Neurosciences & Neurology GA GP961 UT WOS:A1991GP96100018 ER PT J AU CARR, DB AF CARR, DB TI CAVEATS IN THE EVALUATION OF STRESS HORMONE RESPONSES IN ANALGESIC TRIALS SO ADVANCES IN PAIN RESEARCH AND THERAPY LA English DT Editorial Material ID BETA-ENDORPHIN IMMUNOREACTIVITY; CORTICOTROPIN-RELEASING FACTOR; DOSE FENTANYL ANESTHESIA; CORONARY-ARTERY SURGERY; MULTIPLE OPIATE RECEPTORS; CEREBROSPINAL-FLUID; CARDIAC-SURGERY; MORPHINE ANESTHESIA; METABOLIC RESPONSE; OXYGEN ANESTHESIA C1 SHRINERS BURN INST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED ENDOCRINOL,BOSTON,MA 02114. RP CARR, DB (reprint author), MASSACHUSETTS GEN HOSP,ANALGES PEPTIDE RES UNIT,BOSTON,MA 02114, USA. NR 59 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0722 J9 ADV PAIN RES THER JI Adv. Pain Res. Ther. PY 1991 VL 18 BP 599 EP 605 PG 7 WC Neurosciences SC Neurosciences & Neurology GA FD808 UT WOS:A1991FD80800042 ER PT J AU PARKER, J LANE, J AXELROD, L AF PARKER, J LANE, J AXELROD, L TI COOPERATION OF ADIPOCYTES AND ENDOTHELIAL-CELLS IS NECESSARY FOR CATECHOLAMINE-STIMULATED PGI2 PRODUCTION BY RAT ADIPOSE-TISSUE SO ADVANCES IN PROSTAGLANDIN THROMBOXANE AND LEUKOTRIENE RESEARCH LA English DT Review C1 MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. RP PARKER, J (reprint author), MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02114, USA. 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 0361-5952 J9 ADV PROSTAG THROMB L JI Adv. Prostag. Thrombox. Leukot. Res. PY 1991 VL 21 BP 659 EP 662 PN A-B PG 4 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA EL206 UT WOS:A1991EL20600144 PM 1825394 ER PT B AU GRILLO, HC PEZZUOLI, G ZANNINI, P AF GRILLO, HC PEZZUOLI, G ZANNINI, P BE MOODY, FG MONTORSI, W MONTORSI, M ZENNARO, F TI TRACHEOBRONCHIAL SURGERY SO ADVANCES IN SURGERY SE SERONO SYMPOSIA PUBLICATIONS FROM RAVEN PRESS LA English DT Proceedings Paper CT 2ND WORLD WEEK OF PROFESSIONAL UPDATING IN SURGERY IN SURGICAL AND ONCOLOGICAL DISCIPLINES OF THE UNIVERSITY OF MILAN CY JUL 15-20, 1990 CL MILAN, ITALY RP GRILLO, HC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-873-2 J9 SERONO SYM PY 1991 VL 84 BP 91 EP 94 PG 4 WC Surgery SC Surgery GA BV79P UT WOS:A1991BV79P00021 ER PT B AU MATHISEN, D GRILLO, HC AF MATHISEN, D GRILLO, HC BE MOODY, FG MONTORSI, W MONTORSI, M ZENNARO, F TI SPECIAL PROBLEMS IN GENERAL THORACIC-SURGERY - HOW WE DO IT AT THE MASSACHUSETTS-GENERAL-HOSPITAL SO ADVANCES IN SURGERY SE SERONO SYMPOSIA PUBLICATIONS FROM RAVEN PRESS LA English DT Proceedings Paper CT 2ND WORLD WEEK OF PROFESSIONAL UPDATING IN SURGERY IN SURGICAL AND ONCOLOGICAL DISCIPLINES OF THE UNIVERSITY OF MILAN CY JUL 15-20, 1990 CL MILAN, ITALY RP MATHISEN, D (reprint author), MASSACHUSETTS GEN HOSP,WARREN 1109,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-873-2 J9 SERONO SYM PY 1991 VL 84 BP 103 EP 109 PG 7 WC Surgery SC Surgery GA BV79P UT WOS:A1991BV79P00025 ER PT B AU HYMAN, BT ARRIAGADA, PV VANHOESEN, GW AF HYMAN, BT ARRIAGADA, PV VANHOESEN, GW BE GROWDON, JH CORKIN, S RITTERWALKER, E WURTMAN, RJ TI PATHOLOGICAL-CHANGES IN THE OLFACTORY SYSTEM IN AGING AND ALZHEIMERS-DISEASE SO AGING AND ALZHEIMERS DISEASE: SENSORY SYSTEMS, NEURONAL GROWTH, AND NEURONAL METABOLISM SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT 6TH MEETING OF THE INTERNATIONAL STUDY GROUP ON THE PHARMACOLOGY OF MEMORY DISORDERS ASSOCIATED WITH AGING : AGING AND ALZHEIMERS DISEASE CY FEB 15-17, 1991 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOCIATED WITH AGING, CTR BRAIN SCI METAB CHARITABLE TRUST, AMER CYANAMID, AMER LECITHIN, ASTRA RES CTR, BAYER, BRISTOL MYERS SQUIBB, COCA COLA, CYANAMID ITALIA, FERRER INT RP HYMAN, BT (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. NR 0 TC 18 Z9 18 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-726-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 640 BP 14 EP 19 PG 6 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA BW43U UT WOS:A1991BW43U00003 ER PT B AU NITSCH, R PITTAS, A BLUSZTAJN, JK SLACK, BE GROWDON, JH WURTMAN, RJ AF NITSCH, R PITTAS, A BLUSZTAJN, JK SLACK, BE GROWDON, JH WURTMAN, RJ BE GROWDON, JH CORKIN, S RITTERWALKER, E WURTMAN, RJ TI ALTERATIONS OF PHOSPHOLIPID METABOLITES IN POSTMORTEM BRAIN FROM PATIENTS WITH ALZHEIMERS-DISEASE SO AGING AND ALZHEIMERS DISEASE: SENSORY SYSTEMS, NEURONAL GROWTH, AND NEURONAL METABOLISM SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT 6TH MEETING OF THE INTERNATIONAL STUDY GROUP ON THE PHARMACOLOGY OF MEMORY DISORDERS ASSOCIATED WITH AGING : AGING AND ALZHEIMERS DISEASE CY FEB 15-17, 1991 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOCIATED WITH AGING, CTR BRAIN SCI METAB CHARITABLE TRUST, AMER CYANAMID, AMER LECITHIN, ASTRA RES CTR, BAYER, BRISTOL MYERS SQUIBB, COCA COLA, CYANAMID ITALIA, FERRER INT RP NITSCH, R (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114, USA. NR 0 TC 16 Z9 16 U1 0 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-726-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 640 BP 110 EP 113 PG 4 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA BW43U UT WOS:A1991BW43U00019 ER PT B AU TANZI, RE HYMAN, BT AF TANZI, RE HYMAN, BT BE GROWDON, JH CORKIN, S RITTERWALKER, E WURTMAN, RJ TI STUDIES OF AMYLOID BETA-PROTEIN PRECURSOR EXPRESSION IN ALZHEIMERS-DISEASE SO AGING AND ALZHEIMERS DISEASE: SENSORY SYSTEMS, NEURONAL GROWTH, AND NEURONAL METABOLISM SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT 6TH MEETING OF THE INTERNATIONAL STUDY GROUP ON THE PHARMACOLOGY OF MEMORY DISORDERS ASSOCIATED WITH AGING : AGING AND ALZHEIMERS DISEASE CY FEB 15-17, 1991 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOCIATED WITH AGING, CTR BRAIN SCI METAB CHARITABLE TRUST, AMER CYANAMID, AMER LECITHIN, ASTRA RES CTR, BAYER, BRISTOL MYERS SQUIBB, COCA COLA, CYANAMID ITALIA, FERRER INT RP TANZI, RE (reprint author), MASSACHUSETTS GEN HOSP,EXPTL NEUROPATHOL LAB,BOSTON,MA 02114, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-726-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 640 BP 149 EP 154 PG 6 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA BW43U UT WOS:A1991BW43U00026 ER PT J AU LLOVERAS, B EDGERTON, S THOR, AD AF LLOVERAS, B EDGERTON, S THOR, AD TI EVALUATION OF INVITRO BROMODEOXYURIDINE LABELING OF BREAST CARCINOMAS WITH THE USE OF A COMMERCIAL KIT SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE BROMODEOXYURIDINE; S-PHASE; BREAST CARCINOMA ID DNA FLOW-CYTOMETRY; S-PHASE FRACTION; MONOCLONAL-ANTIBODY; CELL-KINETICS; PROLIFERATIVE ACTIVITY; PROPOSED CLASSIFICATION; PROGNOSTIC FACTORS; HUMAN-TUMORS; CANCER; INDEX AB The prognostic significance of S-phase fraction analyses of breast carcinomas has been reported by several investigators. The Cell Proliferation Kit (Amersham Corporation, Arlington Heights, IL), which uses in vitro bromodeoxyuridine (BRDU) labeling to evaluate cell cycle kinetics without a flow cytometer or radio-isotopes, simplifies this assay for the clinical-based laboratory by providing standardized reagents and recommended methods. This study was performed to determine whether data derived from its use were comparable to published S-phase data from the use of thymidine labeling, BRDU, or other methods on breast carcinomas. Primary infiltrating ductal carcinomas (n = 142) and primary lobular carcinomas (n = 6) showed mean and median BRDU labeling of 4.63% and 3%, 1.3% and 1%, respectively, with a range of 0-28%. Benign lesions always had less than 3% BRDU uptake (n = 21). Estrogen receptor (ER) and progesterone receptor (PR) status correlated with BRDU labeling (P < 0.05), with the highest S-phase fractions in ER- and PR-negative tumors. Correlations between BRDU uptake and histologic tumor type or size were observed. Significant correlations between BRDU uptake and lymph node status, patient age, or histologic tumor grade were not observed. S-phase studies of breast carcinomas using other techniques have shown similar data, therefore, the Cell Proliferation Kit appears to be a practical and useful method for in vitro S-phase analysis that allows concomitant histologic examination of the same tumor tissue sample. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. NR 38 TC 37 Z9 37 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD JAN PY 1991 VL 95 IS 1 BP 41 EP 47 PG 7 WC Pathology SC Pathology GA EQ528 UT WOS:A1991EQ52800007 PM 1987751 ER PT J AU KWIATKOWSKI, DJ NYGAARD, TG SCHUBACK, DE PERMAN, S TRUGMAN, JM BRESSMAN, SB BURKE, RE BRIN, MF OZELIUS, L BREAKEFIELD, XO FAHN, S KRAMER, PL AF KWIATKOWSKI, DJ NYGAARD, TG SCHUBACK, DE PERMAN, S TRUGMAN, JM BRESSMAN, SB BURKE, RE BRIN, MF OZELIUS, L BREAKEFIELD, XO FAHN, S KRAMER, PL TI IDENTIFICATION OF A HIGHLY POLYMORPHIC MICROSATELLITE VNTR WITHIN THE ARGININOSUCCINATE SYNTHETASE LOCUS - EXCLUSION OF THE DYSTONIA GENE ON 9Q32-34 AS THE CAUSE OF DOPA-RESPONSIVE DYSTONIA IN A LARGE KINDRED SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID MULTILOCUS LINKAGE ANALYSIS; BETA-HYDROXYLASE ACTIVITY; TORSION DYSTONIA; HUMAN CHROMOSOME-9; LOCALIZATION; REGION AB Dopa-responsive dystonia is a clinical variant of idiopathic torsion dystonia that is distinguished from other forms of dystonia by the frequent cooccurrence of parkinsonism, diurnal fluctuation of symptoms, and its dramatic therapeutic response to L-dopa. Linkage of a gene causing classic dystonia in a large non-Jewish kindred (DYT1) and in a group of Ashkenazi Jewish families, to the gelsolin (GSN) and arginino-succinate synthetase (ASS) loci on chromosome 9q32-34, respectively, was recently determined. Here we report the discovery of a highly informative (GT)n repeat VNTR polymorphism within the ASS locus. Analysis of a large kindred with dopa-responsive dystonia, using this new polymorphism and conventional RFLPs for the 9q32-34 region, excludes loci in this region as a cause of this form of dystonia. This provides proof of genetic heterogeneity between classic idiopathic torsion dystonia and dopa-responsive dystonia. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. COLUMBIA UNIV COLL PHYS & SURG,DEPT NEUROL,NEW YORK,NY 10032. OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. UNIV VIRGINIA,HLTH SCI CTR,DEPT NEUROL,CHARLOTTESVILLE,VA 22903. RI Burke, Robert/B-7226-2011 OI Burke, Robert/0000-0002-4760-8553 FU NHLBI NIH HHS [HL01582]; NINDS NIH HHS [NS01174, NS26836] NR 45 TC 45 Z9 44 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 JAN PY 1991 VL 48 IS 1 BP 121 EP 128 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA ET188 UT WOS:A1991ET18800017 PM 1985454 ER PT J AU HARRIS, PE KENDALLTAYLOR, P AF HARRIS, PE KENDALLTAYLOR, P TI ISOLATED ALDOSTERONE DEFICIENCY IN A PATIENT WITH AUTOIMMUNE ADRENALITIS SO AMERICAN JOURNAL OF MEDICINE LA English DT Note C1 UNIV NEWCASTLE UPON TYNE,SCH MED,NEWCASTLE TYNE NE1 7RU,TYNE & WEAR,ENGLAND. RP HARRIS, PE (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 TC 3 Z9 3 U1 0 U2 0 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 JAN PY 1991 VL 90 IS 1 BP 124 EP 124 DI 10.1016/0002-9343(91)90515-Y PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA ET987 UT WOS:A1991ET98700018 PM 1986578 ER PT J AU DOMINGUES, RC MIKULIS, D SWEARINGEN, B TOMPKINS, R ROSEN, BR AF DOMINGUES, RC MIKULIS, D SWEARINGEN, B TOMPKINS, R ROSEN, BR TI SUBCUTANEOUS SACROCOCCYGEAL MYXOPAPILLARY EPENDYMOMA - CT AND MR FINDINGS SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article RP DOMINGUES, RC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 8 TC 11 Z9 11 U1 0 U2 0 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 JAN-FEB PY 1991 VL 12 IS 1 BP 171 EP 172 PG 2 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA EN938 UT WOS:A1991EN93800035 PM 1899505 ER PT J AU HOERR, RA MATTHEWS, DE BIER, DM YOUNG, VR AF HOERR, RA MATTHEWS, DE BIER, DM YOUNG, VR TI LEUCINE KINETICS FROM [H-2(3)]- AND [C-13]LEUCINE INFUSED SIMULTANEOUSLY BY GUT AND VEIN SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE STABLE ISOTOPES; AMINO ACID KINETICS; SPLANCHNIC BED; HUMAN; FIRST-PASS EFFECT ID CHAIN AMINO-ACIDS; YOUNG MEN; PROTEIN-SYNTHESIS; ALPHA-KETOISOCAPROATE; DIETARY LEUCINE; METABOLISM; TISSUES; TRACER; ABSORPTION; HUMANS AB In amino acid tracer kinetic studies of the fed state, ingested amino acid may be taken up during its initial transit through splanchnic tissues and thus not enter the plasma compartment where tracer is infused. To investigate this possibility, adult human subjects received simultaneous intravenous (iv) and intragastric (ig) leucine tracer infusions, first during a postabsorptive (PA) 4-h primed continuous ig infusion of L-[1-C-13]-leucine and L-[5,5,5-H-2(3)]leucine iv, followed on a separate day by a fed infusion, in which an ig infusion of a liquid formula was started 2 h before the tracer infusion and continued throughout the tracer study. Subjects were accustomed to a constant experimental diet supplying 1.5 g protein.kg-1.day-1 and 41-45 kcal.kg-1.day-1 for 7 and 12 days before the PA and fed studies, respectively. For the PA study, plasma enrichment for the ig tracer was 3.34 +/- 0.27 (SE) mol %excess and for the iv tracer it was 4.18 +/- 0.10 (P < 0.02). Enrichments of alpha-ketoisocaproic acid (KIC) were 3.24 +/- 0.16 (ig) and 3.02 +/- 0.14 (iv), respectively [not significant (NS)]. For the fed study, plasma leucine enrichment for the ig tracer was 2.15 +/- 0.14 and for the iv tracer was 2.84 +/- 0.09 (P < 0.02). KIC enrichments were 2.02 +/- 0.08 (ig) and 2.24 +/- 0.08 (iv), respectively (NS). In the PA study, the ratio of the plasma leucine enrichments for the ig and iv tracers was 0.80 +/- 0.06 and in the fed experiment, 0.76 +/- 0.05, respectively. In contrast, the ratio of the plasma KIC enrichments formed from the ig and iv tracers was 0.99 +/- 0.09 for the PA experiment and 0.90 +/- 0.10 for the fed experiment. This dual-tracer infusion approach demonstrates that ig-administered leucine tracer is removed in a first pass through splanchnic tissues (PA experiment 19 +/- 7%, fed experiment 24 +/- 5%) but may be transminated and released as KIC. C1 MIT,SCH SCI,HUMAN NUTR LAB,50 AMES ST,CAMBRIDGE,MA 02139. MIT,CTR CLIN RES,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. CORNELL UNIV,MED CTR,COLL MED,DEPT MED,NEW YORK,NY 10021. CORNELL UNIV,MED CTR,COLL MED,DEPT SURG,NEW YORK,NY 10021. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT PEDIAT,ST LOUIS,MO 63110. FU NCRR NIH HHS [RR-88]; NIDDK NIH HHS [DK-38429, DK-15856] NR 35 TC 121 Z9 122 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1991 VL 260 IS 1 BP E111 EP E117 PN 1 PG 7 WC Physiology SC Physiology GA EU065 UT WOS:A1991EU06500038 PM 1987785 ER PT J AU FARAONE, SV BIEDERMAN, J KEENAN, K TSUANG, MT AF FARAONE, SV BIEDERMAN, J KEENAN, K TSUANG, MT TI A FAMILY-GENETIC STUDY OF GIRLS WITH DSM-III ATTENTION-DEFICIT DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DIAGNOSTIC INTERVIEW SCHEDULE; HYPERACTIVE-CHILDREN; PSYCHIATRIC-DISORDER; BOYS; PSYCHOPATHOLOGY; PREVALENCE; PARENTS AB Objective: The authors evaluated family-genetic risk factors in girls with attention deficit disorder and compared these results to findings in the authors' previous study of boys with attention deficit disorder. Method: Twenty-one girls with attention deficit disorder and 20 normal comparison girls were consecutively ascertained from a pool of existing and new referrals from a pediatric psychopharmacology unit and a medical pediatric unit of the same urban hospital. First-degree relatives of the attention deficit disordered girls (N = 69) and of the normal girls (N = 71) were also assessed. Both groups of girls and their relatives were evaluated on the basis of structured diagnostic interviews conducted by raters who were blind to the clinical status of the probands. Results: The relatives of the girls with attention deficit disorder had higher risks for attention deficit disorder, antisocial disorders, major depression, and anxiety disorders. The higher risk for attention deficit disorder could not be accounted for by gender or generation of relative, age of proband, social class, or family intactness. These findings are highly consistent with the findings in the authors' previous study of boys with attention deficit disorder, which was conducted with identical methods. Conclusion: This study provides further support for the validity of the diagnosis of attention deficit disorder in girls and suggests that the genders share a common biological substrate. C1 MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT UNIT,PEDIAT PSYCHOPHARMACOL UNIT ACC 725,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PSYCHIAT EPIDEMIOL & GENET,BOSTON,MA 02115. FU NIMH NIH HHS [MH-41314] NR 29 TC 118 Z9 120 U1 1 U2 5 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 JAN PY 1991 VL 148 IS 1 BP 112 EP 117 PG 6 WC Psychiatry SC Psychiatry GA EQ124 UT WOS:A1991EQ12400019 PM 1984694 ER PT J AU LEE, MJ SAINI, S GELLER, SC WARSHAW, AL MUELLER, PR AF LEE, MJ SAINI, S GELLER, SC WARSHAW, AL MUELLER, PR TI PANCREATITIS WITH PSEUDOANEURYSM FORMATION - A PITFALL FOR THE INTERVENTIONAL RADIOLOGIST SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID REAL-TIME; SECONDARY C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 10 TC 33 Z9 35 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 JAN PY 1991 VL 156 IS 1 BP 97 EP 98 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EP262 UT WOS:A1991EP26200018 PM 1898577 ER PT J AU CHEW, FS AF CHEW, FS TI BUCKLED MENISCUS REVISITED - REPLY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter RP CHEW, FS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 2 TC 1 Z9 1 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 JAN PY 1991 VL 156 IS 1 BP 200 EP 200 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EP262 UT WOS:A1991EP26200047 ER PT J AU WARSHAW, AL AF WARSHAW, AL TI IMPLICATIONS OF PERITONEAL CYTOLOGY FOR STAGING OF EARLY PANCREATIC-CANCER SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT 31ST ANNUAL MEETING OF THE SOC FOR SURGERY OF THE ALIMENTARY TRACT CY MAY 15-16, 1990 CL SAN ANTONIO, TX SP SOC SURG ALIMENTARY TRACT ID CARCINOMA; LAPAROSCOPY; THERAPY; ADENOCARCINOMA; IRRADIATION; DIAGNOSIS; ASCITES; BIOPSY; CELLS AB Cytologic examination of peritoneal washings was performed in 40 patients with pancreatic ductal adenocarcinoma (35 head, 5 body) whose tumors had been selected as potentially resectable by computed tomographic (CT) findings. Saline (100 mL) was instilled and aspirated at laparoscopy in 27 patients and at laparotomy in 13. Malignant cells were found in the peritoneal washings in 12 of 40 patients (30%): 29% in cancers of the pancreatic head versus 40% in the body; 33% at laparoscopy versus 23% at laparotomy; and in 4 of 8 patients with ascites versus 8 of 32 without ascites. The cytology was positive in 6 of 8 patients (75%) who had a prior percutaneous needle biopsy versus 6 of 32 (19%) of those who did not (p < 0.01). Liver metastases were found in six patients, all with negative cytology. One of 10 pancreatic head cancers with positive cytology was resectable versus 13 of 25 with negative cytology (p < 0.05). Survival was significantly longer in patients with negative cytology. We conclude that (1) pancreatic cancer sheds malignant cells into the peritoneum early and commonly; (2) laparoscopic lavage is an effective means of cytologic study; (3) ascites is not a precondition for cytologic study, nor does its presence necessarily imply carcinomatosis; (4) intraperitoneal spread of cancer cells may be promoted by tumor biopsy; (5) cytologic findings provide an additional index of resectability; and (6) cytologic findings appear to correlate with duration of survival. This study shows that even "localized" pancreatic cancer is often not contained and suggests caution with biopsy of potentially curable lesions. C1 HARVARD UNIV,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02115. RP WARSHAW, AL (reprint author), MASSACHUSETTS GEN HOSP,SURG SERV,ACC 336,BOSTON,MA 02114, USA. NR 24 TC 230 Z9 231 U1 0 U2 3 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD JAN PY 1991 VL 161 IS 1 BP 26 EP 30 DI 10.1016/0002-9610(91)90356-I PG 5 WC Surgery SC Surgery GA ET756 UT WOS:A1991ET75600004 PM 1824810 ER PT J AU LACK, EE SCHLOO, BL AZUMI, N TRAVIS, WD GRIER, HE KOZAKEWICH, HPW AF LACK, EE SCHLOO, BL AZUMI, N TRAVIS, WD GRIER, HE KOZAKEWICH, HPW TI UNDIFFERENTIATED (EMBRYONAL) SARCOMA OF THE LIVER - CLINICAL AND PATHOLOGICAL-STUDY OF 16 CASES WITH EMPHASIS ON IMMUNOHISTOCHEMICAL FEATURES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE UNDIFFERENTIATED SARCOMA; EMBRYONAL SARCOMA; LIVER ID MALIGNANT FIBROUS HISTIOCYTOMA; HEPATOCELLULAR-CARCINOMA; CYTOKERATIN EXPRESSION; SMOOTH-MUSCLE; TUMORS; CHILDHOOD; RHABDOMYOSARCOMA; MESENCHYMOMA; KERATIN; CHILDREN AB Undifferentiated (embryonal) sarcoma of the liver is a primitive mesenchymal neoplasm with predilection for individuals in the first 2 decades of life. In this study (10 boys, 6 girls), children in the age range of 6-10 years were most commonly affected (63%). Clinical features most frequently noted on presentation were abdominal pain or a palpable mass. In two cases there was cardiac involvement caused by invasion of the inferior vena cava with extension into the right atrium and ventricle; both children died of progressive dyspnea from tumor embolization to the lungs. One patient was a member of a kindred with the cancer family syndrome (Li-Fraumeni syndrome). There were 13 tumor-related deaths (86% mortality); one child was alive with recurrent tumor in the upper abdomen. Complete surgical resection was attempted in 10 of 15 children who underwent exploratory laparotomy; 2 were alive and well 1 and 5 years later, whereas 1 patient had a recurrence in the upper abdomen 3 years after diagnosis. Ultrastructural study (five cases) and immunohistochemistry (11 cases) supported a mesenchymal origin for the tumor, but failed to identify any diagnostic immunophenotype or specific line of differentiation. Coexpression of vimentin and cytokeratin was seen in three cases. Prompt detection of this aggressive tumor with complete surgical resection is the key to a successful outcome, but this is very difficult to achieve. Recent experience suggests that aggressive adjuvant chemotherapy may improve survival in some cases. C1 CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. NIH,DEPT PATHOL,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. RP LACK, EE (reprint author), GEORGETOWN UNIV,SCH MED,DEPT PATHOL,BASIC SCI BLDG,ROOM 161,3900 RESERVOIR RD NW,WASHINGTON,DC 20007, USA. NR 50 TC 66 Z9 73 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 JAN PY 1991 VL 15 IS 1 BP 1 EP 16 DI 10.1097/00000478-199101000-00001 PG 16 WC Pathology; Surgery SC Pathology; Surgery GA ER243 UT WOS:A1991ER24300001 PM 1702267 ER PT J AU HARRIS, N DEMIRJIAN, Z AF HARRIS, N DEMIRJIAN, Z TI PLASMACYTOID T-ZONE CELL-PROLIFERATION IN A PATIENT WITH CHRONIC MYELOMONOCYTIC LEUKEMIA - HISTOLOGIC AND IMMUNOHISTOLOGIC CHARACTERIZATION SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE PLASMACYTOID T-CELL; PLASMACYTOID MONOCYTE; CHRONIC MYELOMONOCYTIC LEUKEMIA; LYMPH NODES ID LYMPHADENITIS; MONOCYTES; LYMPHOMA; PHENOTYPE AB The term "plasmacytoid T-zone cells" has been used to describe distinctive cells that occur in clusters in the paracortex of some reactive lymph nodes. Recently, tumorous proliferations of these cells have been described in several patients with myelomonocytic leukemias. Neither the nature of these cells nor their relationship to myeloid leukemia has been conclusively established. We report the case of a 64-year-old woman with chronic myelomonocytic leukemia who developed lymphadenopathy that proved to be due to tumorous accumulation of plasmacytoid T-zone cells in the interfollicular regions of the lymph nodes. She underwent splenectomy because of symptomatic splenomegaly; the resected spleen also contained aggregates of plasmacytoid T-zone cells, in addition to extramedullary hematopoiesis. On treatment with busulphan and prednisone, the lymphadenopathy resolved and did not recur. The patient died 7 years later with blast transformation of her myelomonocytic leukemia and no recurrence of lymphadenopathy. The aggregates of plasmacytoid T-zone cells were architecturally and cytologically distinct from the leukemic infiltrates of myeloid cells in the spleen, and there was no evidence of differentiation of these cells into myeloid or monocytic cells. A panel of monoclonal antibodies on paraffin sections revealed no lineage-specific T- or B-cell markers (UCHL1-, L26-), and the plasmacytoid cells were positive for CD68 (KP1) and L60 (CD43), as well as faintly positive for 4KB5 (CD45RA) and MB1 (CD45R). They did not stain with antibodies to myeloid lineage antigens CD15, lysozyme, or myeloperoxidase. The combination of clinical, morphologic, and immunologic features of plasmacytoid T-zone cells in this case suggests that these cells may be of monocytic lineage but are not direct precursors of mature monocytic or granulocytic cells, and may not be part of the neoplastic clone in patients with myelomonocytic leukemia. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HARRIS, N (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,WARREN 2,FRUIT ST,BOSTON,MA 02114, USA. NR 19 TC 29 Z9 30 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 JAN PY 1991 VL 15 IS 1 BP 87 EP 95 DI 10.1097/00000478-199101000-00011 PG 9 WC Pathology; Surgery SC Pathology; Surgery GA ER243 UT WOS:A1991ER24300011 PM 1845925 ER PT J AU VACANTI, CA LODHIA, KL AF VACANTI, CA LODHIA, KL TI FATAL MASSIVE AIR-EMBOLISM DURING TRANSURETHRAL RESECTION OF THE PROSTATE SO ANESTHESIOLOGY LA English DT Article DE ANESTHETIC TECHNIQUES, SPINAL; COMPLICATIONS; EMBOLISM, AIR; PROSTATECTOMY RP VACANTI, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 4 TC 18 Z9 18 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 JAN PY 1991 VL 74 IS 1 BP 186 EP 187 DI 10.1097/00000542-199101000-00028 PG 2 WC Anesthesiology SC Anesthesiology GA ET504 UT WOS:A1991ET50400028 PM 1986645 ER PT J AU SCHWARDT, JD GOBRAN, SR NEUFELD, GR AUKBURG, SJ SCHERER, PW AF SCHWARDT, JD GOBRAN, SR NEUFELD, GR AUKBURG, SJ SCHERER, PW TI SENSITIVITY OF CO2 WASHOUT TO CHANGES IN ACINAR STRUCTURE IN A SINGLE-PATH MODEL OF LUNG AIRWAYS SO ANNALS OF BIOMEDICAL ENGINEERING LA English DT Article DE CONVECTION; DIFFUSION; PULMONARY GAS EXCHANGE; NUMERICAL MODEL; PHASE-III SLOPE ID GAS; DIFFUSION; PLATEAU AB A numerical solution of the convection-diffusion equation with an alveolar source term in a single-path model (SPM) of the lung airways simulates steady state CO2 washout. The SPM is used to examine the effects of independent changes in physiologic and acinar structure parameters on the slope and height of Phase III of the single-breath CO2 washout curve. The parameters investigated include tidal volume, breathing frequency, total cardiac output, pulmonary arterial CO2 tension, functional residual capacity, pulmonary bloodflow distribution, alveolar volume, total acinar airway cross sectional area, and gas-phase molecular diffusivity. Reduced tidal volume causes significant steepening of Phase III, which agrees well with experimental data. Simulations with a fixed frequency and tidal volume show that changes in bloodflow distribution, model airway cross section, and gas diffusivity strongly affect the slope of Phase III while changes in cardiac output and in pulmonary arterial CO2 tension strongly affect the height of Phase III. The paper also discusses differing explanations for the slope of Phase III, including sequential emptying, stratified inhomogeneity, and the issue of asymmetry, in the context of the SPM. C1 UNIV PENN,SCH ENGN & APPL SCI,DEPT BIOENGN,220 S 33RD ST,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT ANESTHESIA,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. FU NHLBI NIH HHS [HL-33891] NR 29 TC 38 Z9 38 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0090-6964 J9 ANN BIOMED ENG JI Ann. Biomed. Eng. PY 1991 VL 19 IS 6 BP 679 EP 697 DI 10.1007/BF02368076 PG 19 WC Engineering, Biomedical SC Engineering GA GY714 UT WOS:A1991GY71400003 PM 1781569 ER PT J AU CRONINGOLOMB, A CORKIN, S RIZZO, JF COHEN, J GROWDON, JH BANKS, KS AF CRONINGOLOMB, A CORKIN, S RIZZO, JF COHEN, J GROWDON, JH BANKS, KS TI VISUAL DYSFUNCTION IN ALZHEIMERS-DISEASE - RELATION TO NORMAL AGING SO ANNALS OF NEUROLOGY LA English DT Article ID SPATIAL CONTRAST SENSITIVITY; CEREBRAL-LESIONS; OPTIC-NERVE; VISION; PATTERN; DEGENERATION; INFORMATION; DEMENTIA; IMPAIRMENT; PERCEPTION AB In patients with Alzheimer's disease (AD), compared with age-matched and young healthy control subjects, visual deficits in the following functions were observed: color, steroacuity, contrast sensitivity, and backward masking (homogeneous and pattern). Critical flicker fusion thresholds were normal, relative to age-matched healthy subjects. For color, the majority of the errors were tritanomalous (blue axis). Color and stereoacuity deficits were unrelated to severity of dementia, in accordance with models of vision that describe these functions as modular rather than diffuse for cortical localization. Although contrast sensitivity was depressed throughout the frequency range in AD, more patients were impaired at low than at high spatial frequencies, contrasting with the observed normal aging pattern of high-frequency loss. Healthy elderly subjects showed depressed critical flicker fusion thresholds and reduced contrast sensitivity at high frequencies, relative to the young group; differences between these groups were not found for the other vision tests. A subset of the AD group received detailed neuro-ophthalmological examination, and no abnormalities were found. This finding, taken together with normal thresholds for critical flicker fusion, suggest that the widespread visual dysfunction reported here is more likely to be related to known pathological changes in primary visual and association cortex in AD than to changes in the retina or optic nerve. C1 MIT,CLIN RES CTR,CAMBRIDGE,MA 02139. MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. FU NCRR NIH HHS [RR00088]; NIA NIH HHS [AG08117, 1 P50 AG05134] NR 52 TC 192 Z9 196 U1 3 U2 20 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JAN PY 1991 VL 29 IS 1 BP 41 EP 52 DI 10.1002/ana.410290110 PG 12 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA ER080 UT WOS:A1991ER08000008 PM 1996878 ER PT J AU CANELLOS, GP AF CANELLOS, GP TI IS THERE AN EFFECTIVE SALVAGE THERAPY FOR ADVANCED HODGKINS-DISEASE SO ANNALS OF ONCOLOGY LA English DT Article DE SALVAGE THERAPY; HODGKINS DISEASE ID BONE-MARROW TRANSPLANTATION; COMBINATION CHEMOTHERAPY; PROGNOSTIC FACTORS; MOPP CHEMOTHERAPY; ETOPOSIDE; SURVIVAL; VINCRISTINE; MANAGEMENT; LOMUSTINE; BLEOMYCIN AB The availability of increasing numbers of active agents has led to the development of a succession of regimens for use as alternative and second-line therapy following relapse from or refractoriness to MOPP (mechlorethamine/vincristine/procarbazine/prednisone) or its variants. ABVD (doxorubicin/bleomycin/vinblastine/dacarbazine) has been the most widely used and has been considered non-cross-resistant. Other programs containing the nitrosourea lomustine have been used with results similar to those with ABVD. A relatively small fraction of relapsed patients remain failure free at 5 years (about 20% to 30%) despite a 30% to 60% second-line complete response (CR) rate. The few randomized trials (Cancer and Leukemia Group B [CALGB], European Organization for Research and Treatment of Cancer) evaluable to assess the efficacy of alternating MOPP/ABVD compared with MOPP alone have shown a small but significant advantage in freedom from progression and/or survival favoring the complex regimens over MOPP. The CALGB trial (8251) included a third arm of ABVD alone. The ABVD and MOPP/ABVD arms had a higher CR rate and superior failure-free survival (FFS) than did MOPP, but have thus far shown no difference between ABVD and alternating MOPP/ABVD, suggesting that full doses of a single regimen are equivalent to the more complex multidrug regimen. The next step in the CALGB program was to attempt to improve ABVD. The substitution of etoposide, an active single agent, for dacarbazine and bleomycin in ABVD resulted in a new regimen, EVA (etoposide/vinblastine/doxorubicin). This program has already demonstrated a 66% response rate in MOPP-resistant/relapsed patients (CALGB 8751). The median FFS is about 10 months and closely resembles the FFS curve of ABVD used as a crossover treatment for relapse/resistance in the MOPP alone arm of the CALGB trial mentioned above. The EVA program is without pulmonary toxicity and offers the potential for etoposide dose escalation. Future trials could compare ABVD with EVA as primary therapy, especially if ABVD is equivalent to the hybrid in the current Intergroup trial (CALGB 8952). High-dose therapy with autologous bone marrow transplantation (ABMT) or stem cell support represents intensive salvage treatment for those who fail at least two regimens. In 1989, 240 patients were reported with a CR rate of 46%, whereas 35% were continuously free of disease at 3 years. The criteria that predict a good response are as follows: 0 performance status; sensitive relapse; and failure of up to two regimens. Longer follow-up is still required to determine the final effect of ABMT. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP CANELLOS, GP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 45 TC 33 Z9 33 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 JAN PY 1991 VL 2 SU 1 BP 1 EP 7 PG 7 WC Oncology SC Oncology GA EV300 UT WOS:A1991EV30000002 PM 1710484 ER PT J AU ANBAZHAGAN, R GELBER, RD BETTELHEIM, R GOLDHIRSCH, A GUSTERSON, BA AF ANBAZHAGAN, R GELBER, RD BETTELHEIM, R GOLDHIRSCH, A GUSTERSON, BA TI ASSOCIATION OF C-ERBB-2 EXPRESSION AND S-PHASE FRACTION IN THE PROGNOSIS OF NODE POSITIVE BREAST-CANCER SO ANNALS OF ONCOLOGY LA English DT Article DE C-ERBB-2; S-PHASE; BREAST CANCER ID SHORT-TERM PROGNOSIS; MYC-PROTO-ONCOGENE; HER-2 NEU ONCOGENE; C-MYC; CARCINOMAS CORRELATE; AMPLIFICATION; RECEPTOR; GENE; OVEREXPRESSION; LOCALIZATION AB An immunohistochemical study was performed on 211 primary breast carcinomas for c-erbB-2 expression. All patients had involvement of axillary lymph nodes and all were randomised onto one of the Ludwig Breast Cancer Trials I-IV between July 1978 and August 1981. c-erbB-2 overexpression significantly correlated with high S-phase fraction, four or more positive axillary nodes involved, estrogen receptor negative primaries, progesterone receptor negative primaries, high grade tumours and DNA aneuploidy. With a nine year median follow-up c-erbB-2 positive tumours had worse disease-free survival (p = 0.0002) and overall survival (p < 0.0001). Multivariate analyses using proportional hazard regression models demonstrated that c-erbB-2 positivity continued to predict a poor outcome even when accounting for the effects of other prognostic factors. C1 INT BREAST CANC STUDY GRP,INST CANC RES,HADDOW LABS,CENT PATHOL REVIEW,COTSWOLD RD,SUTTON SM2 5NG,SURREY,ENGLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. INT BREAST CANC STUDY GRP,BERN,SWITZERLAND. RI gusterson, barry/D-3752-2009 NR 42 TC 50 Z9 50 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 JAN PY 1991 VL 2 IS 1 BP 47 EP 53 PG 7 WC Oncology SC Oncology GA EU743 UT WOS:A1991EU74300013 PM 1672597 ER PT J AU ROSENZWEIG, A SEIDMAN, CE AF ROSENZWEIG, A SEIDMAN, CE TI ATRIAL-NATRIURETIC-FACTOR AND RELATED PEPTIDE-HORMONES SO ANNUAL REVIEW OF BIOCHEMISTRY LA English DT Review DE ANF; BNP; CNP; CARDIAC HORMONES ID MYOCARDIAL-CELL HYPERTROPHY; AFFINITY CROSS-LINKING; VASCULAR SMOOTH-MUSCLE; FACTOR GENE-EXPRESSION; AMINO-ACID-SEQUENCE; FRAGMENT CONFERS INDUCIBILITY; PARTICULATE GUANYLATE-CYCLASE; CENTRAL NERVOUS-SYSTEM; MESSENGER-RNA; RAT-HEART C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV CARDIOL,BOSTON,MA 02115. RP ROSENZWEIG, A (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL02228, HL19259, HL41474] NR 174 TC 316 Z9 320 U1 2 U2 3 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4154 J9 ANNU REV BIOCHEM JI Annu. Rev. Biochem. PY 1991 VL 60 BP 229 EP 255 DI 10.1146/annurev.bi.60.070191.001305 PG 27 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FV909 UT WOS:A1991FV90900008 PM 1652921 ER PT J AU BENACERRAF, B AF BENACERRAF, B TI WHEN ALL IS SAID AND DONE SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Editorial Material DE TRAINING; IR GENES; MHC RESTRICTION; ANTIGEN PROCESSING; RETICULOENDOTHELIAL SYSTEM ID L-GLUTAMIC ACID60-L-ALANINE30-L-TYROSINE10; SUPPRESSOR T-CELLS; IMMUNE-RESPONSES INVITRO; GENETIC-CONTROL; B-LYMPHOCYTES; IR GENES; ANTIGEN PRESENTATION; HISTOINCOMPATIBLE-T; NONRESPONDER MICE; SYNGENEIC CELLS AB Dr. Benacerraf describes his experience in training immunologists for a period of over 30 years. He then analyzes the circumstances in which selected discoveries were made in his laboratory and the events and reasoning that led to these findings. The following topics are discussed: The phagocytic activity of the reticulo-endothelial system. The pathogenesis of immune complex diseases. The impact of activated macrophages on tumor rejection. The evidence that T-cell immunity is specific for internal protein determinants generated by antigen processing. The maturation of the antibody response in terms of antibody affinity. The discovery of Ir gene control of specific immune responses and the role of MHC molecules as presenters of peptide antigens to T cells. The generation of alloreactivity. Lastly, he addresses the administration of science and, particularly, the problems related to the transfer of technology to industrial partners. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP BENACERRAF, B (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 78 TC 5 Z9 5 U1 0 U2 0 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1991 VL 9 BP 1 EP 26 PG 26 WC Immunology SC Immunology GA FF998 UT WOS:A1991FF99800001 PM 1910673 ER PT J AU DUSTIN, ML SPRINGER, TA AF DUSTIN, ML SPRINGER, TA TI ROLE OF LYMPHOCYTE ADHESION RECEPTORS IN TRANSIENT INTERACTIONS AND CELL LOCOMOTION SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE CELL ADHESION; LYMPHOCYTES-T; CELL MIGRATION; REGULATION; LATERAL MOBILITY ID FUNCTION-ASSOCIATED ANTIGEN-3; TUMOR NECROSIS FACTOR; NATURAL-KILLER CELLS; HUMAN T-CELLS; EXTRACELLULAR-MATRIX RECEPTOR; GRANULE MEMBRANE-PROTEIN; HIGH ENDOTHELIAL VENULES; THYMIC EPITHELIAL-CELLS; INTEGRIN BETA-CHAINS; NODE HOMING RECEPTOR AB Lymphocytes adhere to other cells and extracellular matrix in the process of immunological recognition and lymphocyte recirculation. This review focuses on regulation of lymphocyte adhesion and the use of adhesion mechanisms by lymphocytes to obtain information about their immediate environment. The CD2 and LFA-1 adhesion receptors appear to have distinct roles in the regulation of adhesion and modulation of T lymphocyte activation. Adhesion mediated by interaction of CD2 with LFA-3 is dramatically altered by surface charge and adhesion receptor density in such a way that this pathway is latent in resting T lymphocytes but becomes active over a period of hours following T-cell activation. CD2 ligation can mediate or enhance T-cell activation, suggesting that signals from CD2/LFA-3 adhesive interactions are integrated with signals from the T-cell antigen receptor during immunological recognition. A model for the role of LFA-3 lateral diffusion in adhesion is presented, based on the lateral diffusion of different LFA-3 forms in glass supported planar membranes. Interaction of LFA-1 with ICAMs is also regulated by cell activation but in a different way than in interaction of CD2 with LFA-3. LFA-1 avidity for ICAMs is transiently increased by T-cell activation over a period of minutes. Cycles of avidity change are also observed for other T lymphocyte integrins which bind to extracellular matrix components. We propose that integrin avidity cycles may have an important role in the interconnected phenomena of locomotion, initial cell-cell adhesion, and cell-cell de-adhesion. Recent observations on recirculation of T lymphocyte subpopulations are discussed in the context of general lessons learned from study of the CD2/LFA-3 and LFA-1/ICAM adhesion mechanisms. C1 CTR BLOOD RES,BOSTON,MA. HARVARD UNIV,SCH MED,COMM CELL & DEV BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. OI Dustin, Michael/0000-0003-4983-6389 FU NCI NIH HHS [CA31798, CA31799] NR 217 TC 538 Z9 540 U1 0 U2 5 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1991 VL 9 BP 27 EP 66 PG 40 WC Immunology SC Immunology GA FF998 UT WOS:A1991FF99800002 PM 1716919 ER PT J AU LEVINSON, JR GUINEY, TE BOUCHER, CA AF LEVINSON, JR GUINEY, TE BOUCHER, CA TI FUNCTIONAL TESTS FOR MYOCARDIAL-ISCHEMIA SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE EXERCISE STRESS TESTING; THALLIUM SCINTIGRAPHY; NUCLEAR CARDIOLOGY; ECHOCARDIOGRAPHY ID CORONARY-ARTERY DISEASE; TL-201; TOMOGRAPHY; INFARCTION; PERFUSION; TRIAL AB Functional tests for myocardial ischemia are numerous. Most depend upon a combination of either exercise or pharmacologic intervention with analysis of the electrocardiogram, of regional perfusion with radionuclide imaging, or of regional wall motion with radionuclide imaging or echocardiography. While each test has unique features, especially at the research level, they are generally quite similar in clinical practice, so the clinician is advised to concentrate on one or two in which local expertise is high. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LEVINSON, JR (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114, USA. NR 21 TC 0 Z9 0 U1 0 U2 0 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4219 J9 ANNU REV MED JI Annu. Rev. Med. PY 1991 VL 42 BP 119 EP 126 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FE086 UT WOS:A1991FE08600012 PM 2035957 ER PT J AU BECK, WS AF BECK, WS TI DIAGNOSIS OF MEGALOBLASTIC-ANEMIA SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE COBALAMIN; FOLATE; HOMOCYSTEINE; METHYLMALONATE ID CHROMATOGRAPHY MASS-SPECTROMETRY; DEOXYURIDINE SUPPRESSION TEST; SERUM COBALAMIN LEVELS; METHYLMALONIC ACID; VITAMIN-B12 LEVELS; TOTAL HOMOCYSTEINE; DEFICIENCY; MALABSORPTION; QUANTITATION; DNA AB Megaloblastic anemia can be due to cobalamin deficiency, folate deficiency, or refractory forms of bone marrow disease. This essay reviews current thinking on the diagnostic procedures available to a physician considering these disorders. The questions to be answered are as follows: Is a megaloblastic anemia present? Is there a deficieny of cobalamin or folate? If a deficiency is present, what is its cause? Various diagnostic tests are discussed with regard to the differences in their sensitivity and metabolic implications. In particular, we consider the newest diagnostic tests for cobalamin deficiency, serum homocysteine, and methylmalonate, which appear to be highly sensitive predictors of clinical morbidity. Application of these tests suggests that many more patients are cobalamin-deficient than had been supposed. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP BECK, WS (reprint author), HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115, USA. NR 58 TC 32 Z9 32 U1 2 U2 4 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4219 J9 ANNU REV MED JI Annu. Rev. Med. PY 1991 VL 42 BP 311 EP 322 DI 10.1146/annurev.med.42.1.311 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA FE086 UT WOS:A1991FE08600031 PM 2035976 ER PT J AU HOMCY, CJ VATNER, SF VATNER, DE AF HOMCY, CJ VATNER, SF VATNER, DE TI BETA-ADRENERGIC-RECEPTOR REGULATION IN THE HEART IN PATHOPHYSIOLOGIC STATES - ABNORMAL ADRENERGIC RESPONSIVENESS IN CARDIAC DISEASE SO ANNUAL REVIEW OF PHYSIOLOGY LA English DT Review DE DESENSITIZATION; GTP-REGULATORY PROTEINS; ADENYLYL CYCLASE; CATECHOLAMINES; HEART FAILURE ID ADENYLATE-CYCLASE SYSTEM; FAILING HUMAN-HEART; CATECHOLAMINE-INDUCED DESENSITIZATION; AGONIST-INDUCED DESENSITIZATION; SITE-DIRECTED MUTAGENESIS; TERNARY COMPLEX MODEL; MYOCARDIAL BLOOD-FLOW; ALTERED MEMBRANE FORM; MESSENGER-RNA LEVELS; BETA-2-ADRENERGIC RECEPTOR C1 HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02115 USA. NEW ENGLAND REG PRIMATE RES CTR, SOUTHBOROUGH, MA 01772 USA. MASSACHUSETTS GEN HOSP, CARDIAC UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CHILDRENS SERV, BOSTON, MA 02114 USA. BRIGHAM & WOMENS HOSP, BOSTON, MA 02115 USA. RP HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. FU NHLBI NIH HHS [HL-19259, HL-37404, HL-38070] NR 130 TC 83 Z9 85 U1 0 U2 4 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4278 EI 1545-1585 J9 ANNU REV PHYSIOL JI Annu. Rev. Physiol. PY 1991 VL 53 BP 137 EP 159 DI 10.1146/annurev.physiol.53.1.137 PG 23 WC Physiology SC Physiology GA FA889 UT WOS:A1991FA88900008 PM 1645945 ER PT J AU JACOBY, GA SUTTON, L AF JACOBY, GA SUTTON, L TI PROPERTIES OF PLASMIDS RESPONSIBLE FOR PRODUCTION OF EXTENDED-SPECTRUM BETA-LACTAMASES SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID GRAM-NEGATIVE BACTERIA; BROAD-SPECTRUM; ESCHERICHIA-COLI; KLEBSIELLA-PNEUMONIAE; PSEUDOMONAS-AERUGINOSA; CONFERRING RESISTANCE; AMPICILLIN RESISTANCE; CLINICAL ISOLATE; R-FACTORS; CEPHALOSPORINS AB The extended-spectrum beta-lactamases are believed to arise by mutations which alter the configuration around the active site of TEM- and SHV-type enzymes so as to increase their efficiency with otherwise nonhydrolyzable cephalosporins and monobactams. This hypothesis predicts that the genes for these new enzymes should be found on the same wide variety of plasmids that encode TEM-1, TEM-2 and SHV-1 beta-lactamases and that at least some of them should be mediated by transposons. Fifteen plasmids, each encoding an extended-spectrum beta-lactamase, were examined. Unlike the average TEM plasmid, all were large, ranging in size from 80 to 300 kb. All determined resistance to multiple antimicrobial agents, ranging from 5 to 11, and some conferred resistance to heavy metals and UV radiation as well. The plasmids belonged to a limited number of incompatibility (Inc) groups, including IncC, IncFI, IncHI2, and IncM. Because most of the mutations giving rise to extended-spectrum activity are G . C --> A . T transitions and some of the mutant genes have as many as four base substitutions, a plasmid-determined mutator gene was searched for, but no such property was found. Several techniques were used to detect transposition of the extended-spectrum beta-lactamase genes, but a mobile genetic element could not be demonstrated even though eight of the plasmids hybridized with a DNA probe derived from the tnpR gene of Tn3. The genesis of extended-spectrum beta-lactamases may not be as simple as has been supposed. RP JACOBY, GA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. FU NIAID NIH HHS [AI20415] NR 54 TC 127 Z9 134 U1 0 U2 5 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JAN PY 1991 VL 35 IS 1 BP 164 EP 169 PG 6 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA EQ538 UT WOS:A1991EQ53800029 PM 1849707 ER PT J AU DAVIDSON, M KAHN, RS POWCHIK, P WARNE, P LOSONCZY, MF KAMINSKY, R APTER, S JAFF, S DAVIS, KL AF DAVIDSON, M KAHN, RS POWCHIK, P WARNE, P LOSONCZY, MF KAMINSKY, R APTER, S JAFF, S DAVIS, KL TI CHANGES IN PLASMA HOMOVANILLIC-ACID CONCENTRATIONS IN SCHIZOPHRENIC-PATIENTS FOLLOWING NEUROLEPTIC DISCONTINUATION SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID CATECHOLAMINE METABOLITES; DOPAMINE METABOLISM; DEBRISOQUIN; RAT; HALOPERIDOL; HVA AB Changes in plasma levels of the dopamine metabolite homovanillic acid have been reported to correlate with changes in the severity of schizophrenic symptoms during neuroleptic administration and after neuroleptic discontinuation. This study examined the effects of discontinuation of neuroleptic treatment on plasma homovanillic acid levels in 23 patients with chronic schizophrenia. It was hypothesized that clinical decompensation would be associated with increased plasma homovanillic acid levels. Plasma homovanillic acid was measured during administration of neuroleptic medication and during a subsequent 6-week drug-free period. Nine patients decompensated during the drug-free period and 14 patients did not. Following drug discontinuation, plasma homovanillic acid concentrations were higher in schizophrenic patients who decompensated than in those who did not. Furthermore, peak plasma homovanillic acid elevation after discontinuation of neuroleptic medication was significantly correlated with peak of Brief Psychiatric Rating Scale increases. The data suggest that, in some schizophrenic patients, symptomatic decompensation after discontinuation of neuroleptic treatment is associated with increases in dopamine turnover. RP DAVIDSON, M (reprint author), MT SINAI HOSP,SCH MED,BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,PSYCHIAT SERV 116A,BRONX,NY 10468, USA. NR 24 TC 56 Z9 56 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 1991 VL 48 IS 1 BP 73 EP 76 PG 4 WC Psychiatry SC Psychiatry GA ET378 UT WOS:A1991ET37800009 PM 1670618 ER PT J AU BARSKY, AJ WYSHAK, G LATHAM, KS KLERMAN, GL AF BARSKY, AJ WYSHAK, G LATHAM, KS KLERMAN, GL TI THE RELATIONSHIP BETWEEN HYPOCHONDRIASIS AND MEDICAL ILLNESS SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article AB Forty-one Diagnostic and Statistical Manual of Mental Disorders-lll-Revised hypochondriacs were accrued from a primary care practice. Seventy-five control subjects were selected at random from among the remainder of the patients in the same clinic. All subjects completed a structured diagnostic interview and standardized self-report questionnaires. Medical morbidity was assessed with a medical record audit and with primary physicians' ratings. The hypochondriacal and comparison samples did not differ in aggregate medical morbidity, although the hypochondriacal sample had more undiagnosed complaints and nonspecific findings in their medical records. Within the comparison sample, higher levels of medical morbidity were associated with higher levels of hypochondriacal symptoms. This occurred primarily because the most serious medical disorders were associated with more bodily preoccupation, disease conviction, and somatization. Within the hypochondriacal sample, no correlation was found between the degree of hypochondriasis and the extent of medical morbidity. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,CTR POPULAT STUDIES,BOSTON,MA 02115. CORNELL UNIV,MED CTR,COLL MED,DEPT PSYCHIAT,NEW YORK,NY 10021. RP BARSKY, AJ (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,WARREN 631,FRUIT ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH 40487] NR 21 TC 30 Z9 30 U1 0 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD JAN PY 1991 VL 151 IS 1 BP 84 EP 88 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA ET488 UT WOS:A1991ET48800013 PM 1985612 ER PT J AU BERSON, EL ROSNER, B SANDBERG, MA DRYJA, TP AF BERSON, EL ROSNER, B SANDBERG, MA DRYJA, TP TI OCULAR FINDINGS IN PATIENTS WITH AUTOSOMAL DOMINANT RETINITIS-PIGMENTOSA AND A RHODOPSIN GENE DEFECT (PRO-23-HIS) SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID BOVINE RHODOPSIN; LIGHT DEPRIVATION; ELECTRORETINOGRAM; CHROMOSOME-3; EXPRESSION; MEMBRANE; MICE AB Ocular findings are presented from 17 unrelated patients with a form of autosomal dominant retinitis pigmentosa and the same cytosine-to-adenine transversion in codon 23 of the rhodopsin gene corresponding to a substitution of histidine for proline in the 23rd amino acid of rhodopsin (designated rhodopsin, Pro-23-His). On average, these patients (mean age, 37 years) had significantly better visual acuity and larger electroretinographic amplitudes than 131 unrelated patients (mean age, 32 years) with autosomal dominant retinitis pigmentosa without this mutation. However, these 17 patients from separate families, as well as 12 relatives with the mutation from four of these families, showed interfamilial and intrafamilial variability with respect to severity of their ocular disease, suggesting that some factor(s) other than this gene defect itself is involved in the expression of their condition. This form of retinitis pigmentosa can now be detected by testing leukocyte DNA from peripheral blood. Some mechanisms by which this mutation in the rhodopsin gene could lead to rod photoreceptor cell death are suggested. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. RP BERSON, EL (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY02014, EY00169] NR 43 TC 140 Z9 141 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD JAN PY 1991 VL 109 IS 1 BP 92 EP 101 PG 10 WC Ophthalmology SC Ophthalmology GA EU519 UT WOS:A1991EU51900033 PM 1987956 ER PT J AU GLYNN, RJ SCHEIN, OD SEDDON, JM POGGIO, EC GOODFELLOW, JR SCARDINO, VA SHANNON, MJ KENYON, KR AF GLYNN, RJ SCHEIN, OD SEDDON, JM POGGIO, EC GOODFELLOW, JR SCARDINO, VA SHANNON, MJ KENYON, KR TI THE INCIDENCE OF ULCERATIVE KERATITIS AMONG APHAKIC CONTACT-LENS WEARERS IN NEW-ENGLAND SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID USERS AB We conducted a population-based incidence study in five New England states to quantify the risk of ulcerative keratitis associated with contact lens use among aphakic persons. All practicing ophthalmologists in the five-state area were surveyed to identify prospectively all new cases of ulcerative keratitis during a 4-month period. The number of aphakic persons using specific types of contact lenses was estimated through a telephone survey of 4178 households identified by random digit dialing. The annualized incidence of ulcerative keratitis among aphakic persons using contact lenses was estimated to be 52 cases per 10 000 aphakic contact lens wearers (95% confidence interval (CI), 31.1 to 86.9). The risk of ulcerative keratitis varied substantially by lens use, with extended wear having an estimated seven-fold greater risk relative to daily wear (95% CI, 1.6 to 30.2). Rates of ulcerative keratitis in aphakic persons using contact lenses were much greater than rates among cosmetic wearers of the same lens type: for daily-wear lenses, aphakic persons were estimated to have 6.3 times the risk of cosmetic wearers (95% CI, 1.9 to 21.0), and for extended-wear lenses, aphakic persons were estimated to have 8.7 times the risk of cosmetic wearers (95% CI, 3.5 to 21.9). These risks are useful in assessing the benefits and risks of contact lens wear as an alternative to other methods of aphakic correction. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,EPIDEMIOL UNIT,BOSTON,MA 02114. ABT ASSOCIATES INC,CAMBRIDGE,MA. NR 19 TC 12 Z9 12 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD JAN PY 1991 VL 109 IS 1 BP 104 EP 107 PG 4 WC Ophthalmology SC Ophthalmology GA EU519 UT WOS:A1991EU51900035 PM 1987926 ER PT J AU SPIELMAN, AI BERNSTEIN, A HAY, DI BLUM, M BENNICK, A AF SPIELMAN, AI BERNSTEIN, A HAY, DI BLUM, M BENNICK, A TI PURIFICATION AND CHARACTERIZATION OF A RABBIT SALIVARY PROTEIN, A POTENT INHIBITOR OF CRYSTAL-GROWTH OF CALCIUM-PHOSPHATE SALTS SO ARCHIVES OF ORAL BIOLOGY LA English DT Article DE SALIVA; CALCIFICATION; CRYSTAL GROWTH INHIBITOR; PROLINE-RICH PROTEIN; PRECIPITATION ID PROLINE-RICH PROTEINS; COMPLETE COVALENT STRUCTURE; HUMAN-PAROTID SALIVA; PRIMATE MACACA-FASCICULARIS; BINDING; PHOSPHOPROTEIN; SEQUENCE; PEPTIDE; PHOSPHOGLYCOPROTEIN; PRECIPITATION AB Human saliva is supersaturated with respect to basic calcium phosphate salts but is stabilized by specific macromolecules that inhibit calcium phosphate precipitation. One of the families of inhibitory proteins in human and monkey saliva is the acidic proline-rich proteins. The purpose of this study was to isolate and characterize inhibitors of calcium phosphate precipitation from rabbit parotid saliva. Saliva was fractionated by immunoaffinity chromatogaphy and anion exchange chromatography. Individual fractions were assayed for their ability to inhibit calcium phosphate crystal growth and the fraction associated with the inhibition was purified by repeated anion exchange chromatography, preparative gel electrohoresis and electroelution. A major (APRP) and two minor proteins (AM1, AM2) that were inhibitory were purified. APRP is an acidic proline-rich phospho-glycoprotein and a very potent inhibitor of secondary crystal growth of calcium phosphate as it was active at a concentration of 2 x 10(-8) M in a standard assay. The N-terminal sequence of one APRP was E Y E N L D G S L A A T Q N D D D ? Q and a clostripain fragment of APRP had the following N-terminal sequence P Q H R P P R P G G H - ? ? ? ? S P P P ? G N ? ? ? P P P. Although the N-terminal segment of APRP does not resembles that of proline-rich proteins, alignment of the clostripian fragment with the repeat region of such proteins from rat, mouse, monkey and man revealed a high degree of similarity, indicating a structural relationship with the proline-rich protein family. C1 UNIV TORONTO,DEPT BIOCHEM,TORONTO M5S 1A8,ONTARIO,CANADA. FORSYTH DENT CTR,BOSTON,MA 02115. FU NIDCR NIH HHS [DE 7009, DE 3915, DE 8601] NR 26 TC 10 Z9 10 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0003-9969 J9 ARCH ORAL BIOL JI Arch. Oral Biol. PY 1991 VL 36 IS 1 BP 55 EP 63 DI 10.1016/0003-9969(91)90054-X PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA EY992 UT WOS:A1991EY99200008 PM 2012527 ER PT J AU CHAN, KH SWARTS, JD DOYLE, WJ WOLF, GL AF CHAN, KH SWARTS, JD DOYLE, WJ WOLF, GL TI ASSESSMENT OF MIDDLE-EAR STATUS DURING EXPERIMENTAL OTITIS-MEDIA USING MAGNETIC-RESONANCE-IMAGING SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Article ID CHILDREN AB Magnetic resonance imaging has proved to be a useful tool for in vivo imaging of a variety of tissues. In this study, magnetic resonance imaging was applied to the middle ear of experimental animals with otitis media. Results showed that the presence and distribution of effusion within the middle-ear space could be readily determined. Moreover, following injection of gadolinium-diethylenetria-minepentaacetic acid, a contrast agent, the inflamed middle-ear mucosa could be resolved. A comparison between magnetic resonance imaging and tympanometry with respect to the diagnosis of effusion showed that negative pressure tympanograms were equivocal (50% effusion) and that flat or normal tympanograms were in error in approximately 20% of the observations. These data document a role for magnetic resonance imaging in in vivo studies of the pathogenesis of otitis media with effusion. C1 UNIV PITTSBURGH,SCH MED,DEPT OTOLARYNGOL,PITTSBURGH,PA 15261. CHILDRENS HOSP PITTSBURGH,DEPT RADIOL,PITTSBURGH,PA 15213. MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,BOSTON,MA 02114. FU NINDS NIH HHS [NS16337] NR 10 TC 18 Z9 18 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 JAN PY 1991 VL 117 IS 1 BP 91 EP 95 PG 5 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA EU060 UT WOS:A1991EU06000022 PM 1986769 ER PT J AU WILLIAMS, DA AF WILLIAMS, DA TI IN SEARCH OF THE SELF-RENEWING HEMATOPOIETIC STEM-CELL SO BLOOD CELLS LA English DT Note ID GROWTH-FACTOR; SI-LOCUS; MARROW; LIGAND; MOUSE; IDENTIFICATION; PROLIFERATION; PURIFICATION; EXPRESSION; GENERATION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP WILLIAMS, DA (reprint author), CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 23 TC 4 Z9 4 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1991 VL 17 IS 2 BP 296 EP 300 PG 5 WC Hematology SC Hematology GA FN569 UT WOS:A1991FN56900006 PM 1717082 ER PT J AU ROODMAN, GD KUEHL, TJ VANDEBERG, JL MUIRHEAD, DY AF ROODMAN, GD KUEHL, TJ VANDEBERG, JL MUIRHEAD, DY TI INUTERO BONE-MARROW TRANSPLANTATION OF FETAL BABOONS WITH MISMATCHED ADULT BABOON MARROW SO BLOOD CELLS LA English DT Article; Proceedings Paper CT 6TH ANNUAL SYMP ON MOLECULAR BIOLOGY OF HEMOPOIESIS - FRONTIERS IN BONE MARROW TRANSPLANTATION : FETAL HEMATOPOIESIS CY JUN, 1990 CL FARMINGTON, CT DE INUTERO; FETAL; BABOONS; BONE MARROW TRANSPLANTATION ID HEMATOPOIETIC STEM-CELLS; MOUSE FETUSES AB In utero bone marrow transplantation to fetuses offers the potential advantage of ameliorating the effects of genetic disorders by transplanting allogeneic hematopoietic stem cells into recipients who are immunoincompetent and require no preparative regimen. Therefore, we undertook studies to examine the feasibility of in utero bone marrow transplantation of unrelated allogeneic adult bone marrow into fetal baboons. Thirty-one baboon fetuses were transplanted between the ages of 60 and 160 days gestation (normal gestation, 182 days) with unrelated allogeneic adult bone marrow containing a different isozyme of glucose-phosphate isomerase (GPI). Approximately one third of the 80-day fetuses demonstrated engraftment 1 month after transplantation. Three of three of the initial chimeras died in utero 45 to 80 days after transplantation and the remaining chimeras lost their graft. Furthermore, 80-day fetal baboons were able to recognize donor cells, maternal cells, and other adult baboon peripheral blood cells in a mixed lymphocyte culture (MLC) reaction but still could engraft with allogeneic bone marrow. In contrast all nonchimeric animals survived to term. These data suggest that fetal transplantation of primates is feasible using techniques employed in these studies and that transplantation of younger fetuses who are immunocompetent should be attempted. C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. SW FDN BIOMED RES,SAN ANTONIO,TX 78284. RP ROODMAN, GD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 8 TC 21 Z9 21 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1991 VL 17 IS 2 BP 367 EP 375 PG 9 WC Hematology SC Hematology GA FN569 UT WOS:A1991FN56900016 PM 1833000 ER PT J AU MACFARLANE, R MOSKOWITZ, MA TASDEMIROGLU, E WEI, EP KONTOS, HA AF MACFARLANE, R MOSKOWITZ, MA TASDEMIROGLU, E WEI, EP KONTOS, HA TI POSTISCHEMIC CEREBRAL BLOOD-FLOW AND NEUROEFFECTOR MECHANISMS SO BLOOD VESSELS LA English DT Article; Proceedings Paper CT 7TH INTERNATIONAL SATELLITE SYMP OF THE 11TH INTERNATIONAL CONGRESS OF PHARMACOLOGY : VASCULAR NEUROEFFECTOR MECHANISMS CY JUL 08-11, 1990 CL BONN, FED REP GER DE CEREBRAL ISCHEMIA; CORTICAL HYPEREMIA; TRIGEMINAL NERVE; ACETYLCHOLINE; ENDOTHELIUM-DEPENDENT RELAXING FACTOR ID SUBSTANCE-P; HYPERTENSION; ACETYLCHOLINE; RELEASE AB The influence of neuroeffector mechanisms in the regulation of postischemic cerebral blood flow was investigated by microsphere determination in 8 cats after chronic unilateral vascular deafferentation by trigeminal ganglionectomy. The animals were subjected to 90 min of reperfusion following 10 min of global ischemia induced by 4-vessel occlusion and systemic hypotension. Cortical hyperemia 30 min after reperfusion was attenuated by up to 48% in cortical gray matter ipsilateral to the side of trigeminal ganglionectomy (p < 0.01). Axon reflex mechanisms involving the release of neuropeptides from peripheral sensory nerve fibers, such as substance P (SP), calcitonin gene-related peptide (CGRP) and neurokinin A (NKA), mediate this response. SP and NKA cause vasodilation by endothelium-dependent mechanisms (endothelium-dependent relaxing factor), whereas CGRP relaxes vascular smooth muscle by direct receptor interactions. Studies were therefore undertaken to determine the extent to which endothelium-dependent mechanisms mediate the hyperemia following global cerebral ischemia. In 7 intact cats, the postischemic response of pial arterioles to the topical application of acetylcholine (ACh; 10(-7) M), an endothelial-dependent vasodilator, was measured using a closed cranial window technique. Although ACh increased pial arteriolar caliber by 17% under resting conditions, the same dose elicited a vasoconstrictor response (87% of pre-ACh diameter 30 min after reperfusion) for the first 60 min of reperfusion after 10 min of ischemia. ACh-induced vasodilation was restored by 75 min (105%), but was less than control even at 120 min (109 vs. 117%; p < 0.05). The ability of sensory denervation to attenuate cortical hyperemia, combined with the demonstrated loss of endothelium-dependent vasodilation during the early postischemic period, indicates that CGRP, a nonendothelium-dependent vasodilator, is a likely mediator of postischemic hyperperfusion. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,STROKE RES LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV,BOSTON,MA 02114. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED,DIV CARDIOL,RICHMOND,VA 23298. FU NINDS NIH HHS [NS26361] NR 18 TC 21 Z9 21 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0303-6847 J9 BLOOD VESSELS PD JAN-JUN PY 1991 VL 28 IS 1-3 BP 46 EP 51 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FB336 UT WOS:A1991FB33600007 PM 2001479 ER PT J AU SOIFFER, RJ MAUCH, P TARBELL, NJ ANDERSON, KC FREEDMAN, AS RABINOWE, SN TAKVORIAN, T MURREY, CI CORAL, F BOSSERMAN, L DEAR, K NADLER, LM RITZ, J AF SOIFFER, RJ MAUCH, P TARBELL, NJ ANDERSON, KC FREEDMAN, AS RABINOWE, SN TAKVORIAN, T MURREY, CI CORAL, F BOSSERMAN, L DEAR, K NADLER, LM RITZ, J TI TOTAL LYMPHOID IRRADIATION TO PREVENT GRAFT-REJECTION IN RECIPIENTS OF HLA NONIDENTICAL T-CELL-DEPLETED ALLOGENEIC MARROW SO BONE MARROW TRANSPLANTATION LA English DT Article ID SEVERE APLASTIC-ANEMIA; TOTAL-BODY IRRADIATION; TRANSPLANT RECIPIENTS; LYMPHOCYTES-T; ANTITHYMOCYTE GLOBULIN; RHEUMATOID-ARTHRITIS; HODGKINS-DISEASE; IMMUNE-RESPONSES; DONOR ANTIGENS; FAILURE AB Patients who undergo transplantation with genotypically non-identical T cell-depleted bone marrow are at high risk of graft failure. We have previously shown that graft failure in this setting is an active immunologic process in which CD3 + CD8 + host T cells specifically cytotoxic for donor hematopoietic cells mediate rejection of the graft. In order to reduce the incidence of graft rejection in these patients, we conducted a pilot trial of total lymphoid irradiation (TLI) as an adjunct to total body irradiation (TBI) in an attempt to suppress the activity of residual host derived alloreactive lymphocytes capable of mediating rejection. Ten adults (ages 17-42 years) with hematologic malignancies were treated with TLI prior to hospitalization for allogeneic bone marrow transplantation (BMT). The BMT preparative regimen consisted of cyclophosphamide (60 mg/kg x 2) followed by TBI. The majority of patients received 750 cGy TLI delivered to two complementary radiation ports in five equal 150 cGy fractions. Nine of 10 recipients of genotypically non-identical CD6-depleted marrow who were pre-treated with TLI experienced full hematologic engraftment compared with none of four similar patients previously transplanted without TLI (p = 0.001). TLI induced significant lymphopenia in patients prior to marrow infusion, but had no suppressive effects on the reconstitution of donor lymphocytes. TLI, in combination with T cell depletion of donor marrow, may decrease the rate of graft rejection in individuals who lack perfectly matched HLA-identical sibling donors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT RADIAT THERAPY,BOSTON,MA 02115. RP SOIFFER, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [N01-AI62531, AI29530] NR 58 TC 44 Z9 45 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD JAN PY 1991 VL 7 IS 1 BP 23 EP 33 PG 11 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA FB258 UT WOS:A1991FB25800005 PM 2043874 ER PT J AU AMBROSINO, DM AF AMBROSINO, DM TI IMPAIRED POLYSACCHARIDE RESPONSES IN IMMUNODEFICIENT PATIENTS - RELEVANCE TO BONE-MARROW TRANSPLANT PATIENTS SO BONE MARROW TRANSPLANTATION LA English DT Article; Proceedings Paper CT INTERNATIONAL COURSE ON BONE MARROW TRANSPLANTATION IN CHILDREN CY NOV 28-DEC 01, 1990 CL ERICE, ITALY ID INFLUENZAE TYPE-B; CAPSULAR POLYSACCHARIDE; HEMOPHILUS-INFLUENZAE; ANTIBODY-RESPONSE; IGG-SUBCLASS; CONJUGATE VACCINE; LYMPHOCYTE-T; CHILDREN; CELLS; DEFICIENCY AB Bone marrow transplant patients are at increased risk for pneumococcal and H. influenzae type b (HIB) infections. These polysaccharide encapsulated bacteria are also pathogens for young healthy children. In healthy children age related susceptibility has been associated with poor response to polysaccharides and low serum IgG2 subclass antibody concentrations. Of note, immune reconstitution following bone morrow transplantation has been characterized by slow return of both the response to polysaccharides and IgG2 serum concentrations. Thus immune reconstitution following bone marrow transplantation is similar to the maturation that occurs in healthy children. RP AMBROSINO, DM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 35 TC 5 Z9 6 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. PY 1991 VL 7 SU 3 BP 48 EP 51 PG 4 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA FR137 UT WOS:A1991FR13700013 PM 1855089 ER PT B AU COBURN, JW SALUSKY, IB NORRIS, KC GOODMAN, WG AF COBURN, JW SALUSKY, IB NORRIS, KC GOODMAN, WG BE MORII, H TI ORAL AND PARENTERAL CALCITRIOL FOR THE MANAGEMENT OF END-STAGE RENAL-DISEASE SO CALCIUM-REGULATING HORMONES I : ROLE IN DISEASE AND AGING SE CONTRIBUTIONS TO NEPHROLOGY LA English DT Proceedings Paper CT INTERNATIONAL SYMP ON CALCIUM-REGULATING HORMONES, BODY FUNCTIONS AND KIDNEY CY JUL 11-13, 1990 CL NARA, JAPAN RP COBURN, JW (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,NEPHROL SECT W111L,WILSHIRE & SAWTELLE BLVD,LOS ANGELES,CA 90073, USA. NR 0 TC 21 Z9 21 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5371-4 J9 CONTRIB NEPHROL JI Contrib.Nephrol. PY 1991 VL 90 BP 166 EP 182 PG 17 WC Endocrinology & Metabolism; Pathology; Pharmacology & Pharmacy; Physiology; Urology & Nephrology SC Endocrinology & Metabolism; Pathology; Pharmacology & Pharmacy; Physiology; Urology & Nephrology GA BU27H UT WOS:A1991BU27H00025 PM 1959343 ER PT J AU AHN, GH SCULLY, RE AF AHN, GH SCULLY, RE TI CLEAR CELL-CARCINOMA OF THE INGUINAL REGION ARISING FROM ENDOMETRIOSIS SO CANCER LA English DT Article ID ADENOCARCINOMA; MALIGNANCY; THERAPY; HERNIA AB The second and third examples of clear cell carcinoma of the inguinal region arising from endometriosis are reported. In one patient a right inguinal mass was excised along with an inguinal lymph node dissection. The tumor recurred in the retroperitoneum and was removed, and postoperative radiation therapy was administered. The patient died of recurrent tumor after 11 years. The other patient was treated by excision of a left inguinal mass and an inguinal lymph node dissection and was alive without recurrence 4 years and 8 months later. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP AHN, GH (reprint author), NEW ENGLAND DEACONESS HOSP,MEISSNER LAB,196 PILGRIM RD,BOSTON,MA 02215, USA. NR 27 TC 22 Z9 22 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 1991 VL 67 IS 1 BP 116 EP 120 DI 10.1002/1097-0142(19910101)67:1<116::AID-CNCR2820670121>3.0.CO;2-E PG 5 WC Oncology SC Oncology GA EQ089 UT WOS:A1991EQ08900020 PM 1985706 ER PT J AU RAY, RA MORTON, CC LIPINSKI, KK CORSON, JM FLETCHER, JA AF RAY, RA MORTON, CC LIPINSKI, KK CORSON, JM FLETCHER, JA TI CYTOGENETIC EVIDENCE OF CLONALITY IN A CASE OF PIGMENTED VILLONODULAR SYNOVITIS SO CANCER LA English DT Article ID TRANSITIONAL CELL-CARCINOMA; PRIMARY LUNG-TUMOR; CHROMOSOME CHANGE; RECEPTOR; TISSUE; INVOLVEMENT; EXPRESSION; GENE AB Pigmented villonodular synovitis is an uncommon benign lesion that is characterized by diffuse synovial proliferation. Based on animal models, this lesion has been conjectured previously to be reactive in nature. In this report, the authors present the histologic and cytogenetic findings for a pigmented villonodular synovitis that was excised from the right knee of a 47-year-old man. Trisomy 7 was observed in 24 of 75 (35%) metaphases obtained from short-term culture of cells from this tumor. These findings suggest that some cases of pigmented villonodular synovitis represent clonal, neoplastic proliferations. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115. NEW ENGLAND MED CTR HOSP,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. FU NIA NIH HHS [AG00294] NR 34 TC 81 Z9 83 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 JAN 1 PY 1991 VL 67 IS 1 BP 121 EP 125 DI 10.1002/1097-0142(19910101)67:1<121::AID-CNCR2820670122>3.0.CO;2-P PG 5 WC Oncology SC Oncology GA EQ089 UT WOS:A1991EQ08900021 PM 1985707 ER PT J AU EDER, JP ELIAS, AD AYASH, L WHEELER, CA SHEA, TC SCHNIPPER, LE FREI, E ANTMAN, KH AF EDER, JP ELIAS, AD AYASH, L WHEELER, CA SHEA, TC SCHNIPPER, LE FREI, E ANTMAN, KH TI A PHASE-I TRIAL OF CONTINUOUS-INFUSION CYCLOPHOSPHAMIDE IN REFRACTORY CANCER-PATIENTS SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article ID HIGH-DOSE CYCLOPHOSPHAMIDE; BONE-MARROW TRANSPLANTATION; THERAPY; CHEMOTHERAPY; TOXICITY AB Cyclophosphamide demonstrates enhanced tumoricidal activity with decreased bone marrow toxicity when given on a divided-dose schedule in certain animal models. A total of 22 patients presenting with refractory metastatic cancer were treated in a phase I trial of continuous infusion of cyclophosphamide over 96 h. Granulocytopenia of < 500/mu-l that lasted for > 14 days or thrombocytopenia of < 25,000/mu-l that lasted for > 14 days was the target dose-limiting toxicity in the absence of nonhematologic grade 4 toxicity. The maximal tolerated dose was 7 g/m2. Three patients died. Of 21 evaluable patients, 9 responded, including 8/9 who had experienced disease progression during prior oxazaphosphorine-containing combination chemotherapy. Clinically meaningful responses were observed in patients who had demonstrated clinical resistance to an oxazaphosphorine drug given at lower doses. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. BETH ISRAEL HOSP,CHARLES A DANA RES INST,THORNDIKE LABS,BOSTON,MA 02215. RP EDER, JP (reprint author), BETH ISRAEL HOSP,DEPT MED,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NCI NIH HHS [P01CA-38493] NR 24 TC 6 Z9 6 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. PY 1991 VL 29 IS 1 BP 61 EP 65 DI 10.1007/BF00686337 PG 5 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA GQ470 UT WOS:A1991GQ47000011 PM 1742850 ER PT J AU TEICHER, BA HERMAN, TS TANAKA, J DEZUBE, B PARDEE, A FREI, E AF TEICHER, BA HERMAN, TS TANAKA, J DEZUBE, B PARDEE, A FREI, E TI FLUOSOL-DA CARBOGEN WITH LONIDAMINE OR PENTOXIFYLLINE AS MODULATORS OF ALKYLATING-AGENTS IN THE FSAIIC FIBROSARCOMA SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article ID MELPHALAN ANTITUMOR-ACTIVITY; IRRADIATED HELA-CELLS; ASCITES TUMOR-CELLS; CYTO-TOXICITY; PERFLUOROCHEMICAL EMULSION; ARTERIAL-DISEASE; OXYGENATION CONDITIONS; HUMAN-LYMPHOCYTES; FIBRO-SARCOMA; ENHANCEMENT AB In an effort to increase the efficacy of several antineoplastic alkylating agents (CDDP, L-PAM, CTX, or BCNU), we examined the effect of the modulator Fluosol-DA/carbogen in combination with a second modulator, either lonidamine or pentoxifylline, on the survival of FSaIIC tumor cells and of bone marrow CFU-GM from tumor-bearing C3H mice. Fluosol-DA/carbogen increased the tumor-cell killing activity of each alkylating agent by about 10 times. In contrast, lonidamine alone did not significantly increase the cytocidal activity of any of the alkylating agents tested. However, in combination with Fluosol-DA/carbogen, the use of lonidamine produced about a 100-fold increase in the tumor cell kill achieved with CDDP as compared with CDDP alone. No increase in tumor cell kill over that produced with the single modulator Fluosol-DA/carbogen was seen following the addition of lonidamine to the combination treatment with L-PAM, CTX, or BCNU. Unfortunately, although neither lonidamine nor Fluosol-DA/carbogen alone significantly increased alkylator toxicity to bone marrow CFU-GM, the combination of modulators increased the toxicity of each alkylating agent to bone marrow by about 10 times. Pentoxifylline caused an increase in alkylator activity against the FSaIIC fibrosarcoma only when used with BCNU; this effect was further augmented by the addition of Fluosol-DA/carbogen. The combination of modulators pentoxifylline plus Fluosol-DA/carbogen was more effective than Fluosol-DA/carbogen alone only when the former was used with BCNU, whereas only minimal increases in tumor-cell killing activity were obtained with this modulator combination and CDDP, L-PAM, or CTX. Pentoxifylline increased the bone marrow CFU-GM toxicity of L-PAM by about 10 times. The bone marrow CFU-GM toxicity was further increased by Fluosol-DA/carbogen, as was the toxicity of each of the other alkylating agents. Lonidamine plus Fluosol-DA/carbogen may be useful in increasing the therapeutic efficacy of CDDP, and the combination of pentoxifylline plus Fluosol-DA/carbogen might improve the antitumor activity of BCNU. 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 [1PO1-CA38493] NR 57 TC 9 Z9 9 U1 0 U2 1 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. PY 1991 VL 28 IS 1 BP 45 EP 50 DI 10.1007/BF00684955 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA FL749 UT WOS:A1991FL74900008 PM 1904012 ER PT J AU TEICHER, BA HERMAN, TS SHULMAN, L BUBLEY, G COLEMAN, CN FREI, E AF TEICHER, BA HERMAN, TS SHULMAN, L BUBLEY, G COLEMAN, CN FREI, E TI COMBINATION OF ETANIDAZOLE WITH CYCLOPHOSPHAMIDE AND PLATINUM COMPLEXES SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE PLATINUM COMPLEXES; CYCLOPHOSPHAMIDE; ETANIDAZOLE ID CARBOPLATIN; INVIVO; RADIOSENSITIZERS; MISONIDAZOLE; FIBROSARCOMA; CHEMOTHERAPY; ENHANCEMENT; CARCINOMA; TOXICITY; INVITRO AB In an effort to improve the therapeutic efficacy and selectivity of cyclophosphamide (CTX), cis-diamminedichloroplatinum(II) (CDDP), and carboplatin (Carbo), these antitumor alkylating agents were combined with the 2-nitroimidazole drug etanidazole (ETA). As revealed by tumor-cell survival assay in the FSaIIC murine fibrosarcoma, the addition of ETA (1 g/kg, i.p.) just prior to the i.p. injection of various doses of the alkylating agents resulted in increases in the tumor-cell kill produced by each drug (CTX, 10-fold; CDDP, 20-fold; and Carbo, 5- to 15-fold), whereas toxicity to bone marrow granulocyte-macrophage colony-forming units (CFU-GM) increased only about 0- to 3-fold. When CTX was combined with either CDDP or Carbo, striking increases in tumor-cell killing were observed (20- to 100-fold across the CDDP dose range and 5- to 20-fold across the dose range of Carbo), which were supra-additive for CDDP and additive for Carbo as, revealed by isobologram analysis. The addition of ETA to these alkylating-agent combinations produced a further approx. 20-fold increase in tumor-cell kill for both CTX/CDDP and CTX/Carbo. This effect was greatest at the lowest dose of the platinum drug tested and was supra-additive in the case of CDDP and additive for Carbo. Following treatment with ETA/CTX/CDDP, bone marrow CFU-GM toxicity increased only about 5-fold over that of CTX/CDDP alone, but the injection of ETA/CTX/Carbo resulted in a 10- to 20-fold increase in bone marrow toxicity as compared with that obtained using CTX/Carbo alone. Tumor growth-delay studies revealed significant increases in the antitumor effect of the alkylating agents when these were given in combination with ETA. Both the ETA/CTX/CDDP and the ETA/CTX/Carbo combinations produced tumor growth delays of 23 days, which represented approx. 1.6-fold increases over those obtained using the alkylating-agent combinations alone. These results suggest that ETA could significantly improve the therapeutic efficacy of these alkylating agents, whether they are given individually or in combination. C1 BETH ISRAEL HOSP,BOSTON,MA 02215. JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU PHS HHS [P01-37859] NR 34 TC 12 Z9 12 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. PY 1991 VL 28 IS 3 BP 153 EP 158 DI 10.1007/BF00685502 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA FW191 UT WOS:A1991FW19100001 PM 1830248 ER PT J AU LEE, MM RATLIFF, J FITZGERALD, GB WICK, MM AF LEE, MM RATLIFF, J FITZGERALD, GB WICK, MM TI THE MECHANISM OF DIFFERENTIAL SENSITIVITY TO METHOTREXATE OF NORMAL AND MALIGNANT HUMAN EPIDERMAL-CELLS SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE METHOTREXATE; SENSITIVITY; SQUAMOUS-CELL CARCINOMA; EPIDERMAL CELLS ID HUMAN KERATINOCYTES; CARCINOMA AB Squamous carcinoma cells are much more sensitive (> 10(4) times) to the cytotoxic effects of methotrexate (MTX) and 5-fluorodeoxyuridine (FUDR) than are normal human keratinocytes as measured by cell growth. Among the drugs tested, this phenomenon was found to be specific for MTX and FUDR, since arabinosylcytidine (ARA-C), 13-bis-chloroethylnitrosourea (BCNU), and daunomycin failed to show differences in inhibition between the normal and malignant cell lines. Drug uptake studies did not reveal a significant difference in MTX intracellular levels between malignant and normal epidermal cell lines at 60 min. Thymidine (TdR) salvage was assessed by examining the effects of the presence of 3-mu-M TdR on MTX-induced cytotoxicity. On the withdrawal of TdR, normal cells demonstrated an increased level of inhibition amounting to 4 orders of magnitude, whereas the squamous-cell carcinoma cells showed no change in sensitivity. Interestingly, the immortal nontumorigenic keratinocyte line (NM-110) was similarly not rescued by the addition of TdR. The high degree of sensitivity to MTX shown by squamous-cell carcinoma (SCC) and NM-110 cells is attributable to a significant diminution of their ability to use exogenous TdR as compared with that of normal keratinocytes and might be indicative of a biochemical change associated with cellular immortality. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC DERMATOL ONCOL LAB,44 BINNEY ST,ROOM 1720,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. FU NCI NIH HHS [CA 24988] NR 14 TC 3 Z9 3 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. PY 1991 VL 28 IS 3 BP 181 EP 184 DI 10.1007/BF00685506 PG 4 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA FW191 UT WOS:A1991FW19100005 PM 1855274 ER PT J AU LICHT, JD GONIN, R ANTMAN, KH AF LICHT, JD GONIN, R ANTMAN, KH TI PHASE-II TRIAL OF TRIMETREXATE IN PATIENTS WITH ADVANCED SOFT-TISSUE SARCOMA SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Note DE TRIMETREXATE; SOFT-TISSUE SARCOMA; PHASE-II ID DIHYDROFOLATE-REDUCTASE; FOLATE ANTAGONIST; METHOTREXATE; PHARMACOKINETICS; CELLS AB Trimetrexate, a lipophilic, 2,4-diaminoquinazoline derivative of methotrexate, enters cells by passive diffusion rather than via a transport system. Trimetrexate has shown promising activity in animal model systems. A total of 16 patients with metastatic soft-tissue sarcoma who had received only one prior chemotherapy regimen were treated with trimetrexate (8 mg/m2 given intravenously daily for 5 days) every 3 weeks. Treatment-related toxicity included greater-than-or-equal-to grade 2 neutropenia (8/16), thrombocytopenia (3/16), mucositis (4/16) and skin rash (3/16). No partial or complete responses were observed in 15 evaluable patients (95% confidence interval for true response rate, 0-22%) Six subjects showed stabilization of disease for periods ranging from 2 to 9 months. At this dose and on this schedule, trimetrexate appears to have little activity against refractory soft-tissue sarcomas. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. RP LICHT, JD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,44 BINNEY ST,BOSTON,MA 02115, USA. NR 11 TC 8 Z9 8 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. PY 1991 VL 28 IS 3 BP 223 EP 225 DI 10.1007/BF00685515 PG 3 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA FW191 UT WOS:A1991FW19100014 PM 1830249 ER PT J AU FREEDMAN, AS PEDRAZZINI, A NADLER, LM AF FREEDMAN, AS PEDRAZZINI, A NADLER, LM TI B-CELL MONOCLONAL-ANTIBODIES AND THEIR USE IN CLINICAL ONCOLOGY SO CANCER INVESTIGATION LA English DT Review ID ACUTE LYMPHOBLASTIC-LEUKEMIA; HUMAN LYMPHOCYTES-B; AUTOLOGOUS BONE-MARROW; EPSTEIN-BARR VIRUS; NON-HODGKINS LYMPHOMA; COMPLEMENT RECEPTOR SUBTYPES; MALIGNANT GERMINAL-CENTER; T-CELL; HAIRY-CELL; DIFFERENTIATION ANTIGEN AB The use of MAbs directed against B-cell markers has identified considerably more heterogeneity within B-cell neoplasms than was evident by standard morphologic and histochemical techniques. Using markers specific for lineage and state of differentiation, it is possible to correlate malignant B cells to their normal cellular counterparts. Considering the complexity of normal B-cell ontogeny, differentiation, and function, it is not surprising that these malignancies reflect this diversity. Hopefully, with increasing characterization of the normal function of cell surface molecules, as well as the subpopulations of normal cells to which these malignancies correspond, we will have a better understanding of the biologic and clinical behavior of these malignancies. 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 NCI NIH HHS [CA34183, CA25369, CA40216] NR 145 TC 4 Z9 4 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1991 VL 9 IS 1 BP 69 EP 84 DI 10.3109/07357909109032802 PG 16 WC Oncology SC Oncology GA FH957 UT WOS:A1991FH95700009 PM 2012999 ER PT J AU CHUNG, RY SEIZINGER, AB SEIZINGER, BR AF CHUNG, RY SEIZINGER, AB SEIZINGER, BR TI TUMOR SUPPRESSOR GENES AND CANCER OF THE HUMAN NERVOUS-SYSTEM SO CANCER INVESTIGATION LA English DT Review ID RETINOBLASTOMA SUSCEPTIBILITY GENE; LARGE T-ANTIGEN; RENAL-CELL CARCINOMA; SHORT ARM; P53 GENE; ANCHORAGE INDEPENDENCE; COLORECTAL CARCINOMAS; ENDOCRINE NEOPLASIA; TRANSFORMED-CELLS; BREAST-CANCER C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP CHUNG, RY (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114, USA. NR 108 TC 15 Z9 15 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1991 VL 9 IS 4 BP 429 EP 438 DI 10.3109/07357909109084641 PG 10 WC Oncology SC Oncology GA GE789 UT WOS:A1991GE78900005 PM 1884250 ER PT J AU LEONE, LA MEITNER, PA MYERS, TJ GRACE, WR GAJEWSKI, WH FINGERT, HJ ROTMAN, B AF LEONE, LA MEITNER, PA MYERS, TJ GRACE, WR GAJEWSKI, WH FINGERT, HJ ROTMAN, B TI PREDICTIVE VALUE OF THE FLUORESCENT CYTOPRINT ASSAY (FCA) - A RETROSPECTIVE CORRELATION STUDY OF INVITRO CHEMOSENSITIVITY AND INDIVIDUAL-RESPONSES TO CHEMOTHERAPY SO CANCER INVESTIGATION LA English DT Article ID HUMAN-PLASMA; PHARMACOKINETICS; CHROMATOGRAPHY; KINETICS; INFUSION; CANCER AB The potential clinical usefulness of the fluorescent cytoprint assay (FCA) was assessed retrospectively in 73 cancer patients by correlating individual tumor chemosensitivity in vitro with responses to chemotherapy. The data show that the FCA has a sensitivity of 98%, specificity of 81%, and predictive accuracies of 85% and 97% for positive and negative clinical responses, respectively. C1 BROWN UNIV,DIV BIOL & MED,PROVIDENCE,RI 02912. RHODE ISL HOSP,DEPT MED ONCOL,PROVIDENCE,RI 02902. ANALYT BIOSYST CORP,DIV RES,WARWICK,RI. MEM HOSP,PAWTUCKET,RI 02860. ST VINCENTS HOSP & MED CTR,NEW YORK,NY 10011. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ST ELIZABETH HOSP,BRIGHTON,MA 02135. NR 32 TC 18 Z9 18 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1991 VL 9 IS 5 BP 491 EP 503 DI 10.3109/07357909109018947 PG 13 WC Oncology SC Oncology GA GN592 UT WOS:A1991GN59200002 PM 1933482 ER PT J AU KOCHEVAR, IE WALSH, AA GREEN, HA SHERWOOD, M SHIH, AG SUTHERLAND, BM AF KOCHEVAR, IE WALSH, AA GREEN, HA SHERWOOD, M SHIH, AG SUTHERLAND, BM TI DNA DAMAGE INDUCED BY 193-NM RADIATION IN MAMMALIAN-CELLS SO CANCER RESEARCH LA English DT Article ID EXCIMER LASER ABLATION; XERODERMA PIGMENTOSUM CELLS; ULTRAVIOLET-RADIATION; UV-RADIATION; CORNEA; REPAIR; NM; QUANTITATION; SENSITIVITY; CEREVISIAE AB The contribution of DNA damage to the effects of 193-nm excimer laser radiation on mammalian cells in culture was studied in order to evaluate the mutagenic potential of this UV wavelength in vivo. Two approaches were taken: measurement of pyrimidine dimer-specific endonuclease-sensitive sites/megabase and comparison of the 193-nm radiation-induced cytotoxicity in normal versus DNA repair-deficient cells. The formation of pyrimidine dimer-specific endonuclease-sensitive sites/megabase was inversely related to the thickness of the cytoplasm overlying the nuclei of normal human fibroblasts (NHF) and Chinese hamster ovary cells. The results of these measurements and a calculation of the absorption coefficient of cytoplasm indicate that each 1-mu-m of cytoplasm attenuates the incident radiation by >90% and, therefore, the nuclear DNA in tissue will be highly protected from 193-nm radiation by overlying cytoplasm. The reduction in colony-forming ability induced by 254-nm, 193-nm, and X-ray radiation was measured in NHF, xeroderma pigmentosum (group A) cells, and ataxia telangiectasia cells. Xeroderma pigmentosum (group A) cells were 16.5 times more sensitive to 254-nm radiation but only 3.5 times more sensitive to 193-nm radiation than NHF cells, indicating that cyclobutylpyrimidine dimers were not the major lethal lesion formed at 193 nm. AT cells were 3.4 times more sensitive to X-rays than NHF cells, but these cell types were almost equally sensitive to 193-nm radiation, indicating that 193 nm did not induce the same type of lethal lesions as X-rays. C1 BROOKHAVEN NATL LAB,DEPT BIOL,UPTON,NY 11973. RP KOCHEVAR, IE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,DEPT DERMATOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA23096]; NIGMS NIH HHS [GM30755] NR 26 TC 21 Z9 21 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 JAN 1 PY 1991 VL 51 IS 1 BP 288 EP 293 PG 6 WC Oncology SC Oncology GA EQ683 UT WOS:A1991EQ68300048 PM 1988091 ER PT J AU CASLAVSKA, V GRON, P KENT, RL JOSHIPURA, K DEPAOLA, PF AF CASLAVSKA, V GRON, P KENT, RL JOSHIPURA, K DEPAOLA, PF TI CAF2 IN ENAMEL BIOPSIES 6 WEEKS AND 18 MONTHS AFTER FLUORIDE TREATMENT SO CARIES RESEARCH LA English DT Article DE AMMONIUM FLUORIDE; CALCIUM FLUORIDE; TOPICAL FLUORIDE TREATMENT ID CALCIUM-FLUORIDE; CARIES PREVENTION; DENTAL-CARIES; DISSOLUTION; INVIVO; PHOSPHATE; RETENTION; KINETICS AB Fluoride concentrations were studied in enamel biopsies from maxillary central incisors 6 weeks and 18 months after fluoride treatment. In the short-term study biopsies were obtained prior to and after treatment with acidic sodium or ammonium fluoride. The findings showed that large amounts of fluoride were deposited in enamel from NH4F treatment (mean concentration 84,723 ppm), indicating substantial CaF2 formation. NaF treatment resulted in mean fluoride concentrations of 7,818 ppm. In the 18-month study, biopsies from 58 placebo-treated teeth were analyzed for total fluoride (mean 1,733 ppm). Twenty-five additional biopsies from placebo-treated and 58 from NH4F-treated teeth were analyzed for KOH-soluble (CaF2) and KOH-nonsoluble (apatitic) fluoride. The mean values for total fluoride were 1,669 and 2,085 ppm in the placebo-treated and in the NH4F-treated groups, respectively. The corresponding mean values KOH-nonsoluble fluoride were 1,467 and 1,731 ppm and for KOH-soluble fluoride 202 and 354 ppm, respectively. The increase in enamel fluoride after fluoride treatment was only marginally significant. Biopsies from the ammonium fluoride treated group were significantly more likely to have high (30 vs. 8%) and moderate (28 vs. 16%) CaF2 levels and less likely to have low levels than biopsies of placebo-treated teeth (chi-square = 8.0 with 2 d.f.; p = 0.018). It is concluded that very substantial amounts of CaF2 are present in enamel 6 weeks after treatment, and small amounts may persist in the surface enamel for as long as 18 months. RP CASLAVSKA, V (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-5067] NR 20 TC 6 Z9 6 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0008-6568 J9 CARIES RES JI Caries Res. PD JAN-FEB PY 1991 VL 25 IS 1 BP 21 EP 26 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FC171 UT WOS:A1991FC17100003 PM 2070378 ER PT J AU CASLAVSKA, V DUSCHNER, H AF CASLAVSKA, V DUSCHNER, H TI EFFECT OF A SURFACE-ACTIVE CATION ON FLUORIDE ENAMEL INTERACTIONS INVITRO SO CARIES RESEARCH LA English DT Article DE SURFACE-ACTIVE CATION; ZONYL FSC; AMMONIUM FLUORIDE; SODIUM FLUORIDE; ENAMEL; ELECTRON SPECTROSCOPY ID SODIUM-FLUORIDE; TOPICAL APPLICATIONS; AMINE HYDROFLUORIDE; AMMONIUM FLUORIDE; BOVINE ENAMEL AB After in vitro treatments of bovine enamel with NaF/Zonyl FSC and NH4F in-depth profiles of the chemical composition of the outermost zone of surface enamel were obtained with electron spectroscopy. The most important finding of the study was that after the treatments with nearly neutral as well as slightly acidic solutions of NH4F the ammonium cation was found on the enamel surfaces. Similarly a Zonyl FSC layer was detected on the enamel surfaces after the NaF/Zonyl FSC treatment, while sodium ion was never detected on the enamel surfaces. The implication is that the sorption of these cations plays a role in fluoride-enamel interactions. C1 UNIV MARBURG,FACHBEREICH PHYS CHEM KERNCHEM,HANS MEERWEIN STR,W-3550 MARBURG,GERMANY. FORSYTH DENT CTR,BOSTON,MA 02115. NR 21 TC 3 Z9 3 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0008-6568 J9 CARIES RES JI Caries Res. PD JAN-FEB PY 1991 VL 25 IS 1 BP 27 EP 33 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FC171 UT WOS:A1991FC17100004 PM 2070379 ER PT J AU PETROSSIAN, GA TUZCU, EM ZISKIND, AA BLOCK, PC PALACIOS, I AF PETROSSIAN, GA TUZCU, EM ZISKIND, AA BLOCK, PC PALACIOS, I TI ATRIAL SEPTAL OCCLUSION IMPROVES THE ACCURACY OF MITRAL-VALVE AREA DETERMINATION FOLLOWING PERCUTANEOUS MITRAL BALLOON VALVOTOMY SO CATHETERIZATION AND CARDIOVASCULAR DIAGNOSIS LA English DT Article DE ASD; MITRAL STENOSIS; PERCUTANEOUS MITRAL BALLOON VALVOTOMY ID STENOSIS; ECHOCARDIOGRAPHY; VALVULOPLASTY AB We investigated the impact of the atrial communication on the mitral valve area calculation after percutaneous mitral balloon valvotomy in 17 patients (15 women, 2 men; mean age 56 +/- 4 years). The hemodynamic measurements and mitral valve area calculations were performed with and without balloon occlusion of the atrial septal puncture site. The mitral valve area determined with balloon occlusion was significantly smaller than the mitral valve area determined without occlusion (1.6 +/- 0.1 vs. 1.9 +/- 0.1 cm2, P < 0.01), and was similar to the echocardiographically determined valve area (1.6 +/- 0.1 cm2). This decrease in the calculated mitral valve area with occlusion was associated with a decrease in the measured cardiac output, without a change in the mitral valve gradient or the diastolic filling period. Occlusion of the atrial septal puncture site may permit more accurate determination of the mitral valve area and thus provide a better reference point for future comparison should the question of restenosis arise. C1 MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. NR 11 TC 22 Z9 22 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0098-6569 J9 CATHETER CARDIO DIAG JI Catheter. Cardiovasc. Diagn. PD JAN PY 1991 VL 22 IS 1 BP 21 EP 24 DI 10.1002/ccd.1810220105 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA ER658 UT WOS:A1991ER65800004 PM 1995169 ER PT J AU DATTA, R SHERMAN, ML STONE, RM KUFE, D AF DATTA, R SHERMAN, ML STONE, RM KUFE, D TI EXPRESSION OF THE JUN-B GENE DURING INDUCTION OF MONOCYTIC DIFFERENTIATION SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID PROTEIN KINASE-C; NECROSIS FACTOR-ALPHA; DNA-BINDING DOMAIN; GROWTH-FACTOR; HL-60 CELLS; LEUCINE ZIPPERS; PROMOTER REGION; LEUKEMIA-CELLS; ONCOGENE JUN; FACTOR-II AB The AP-1 protein complex binds to specific DNA sequences that regulate transcription of genes responsive to certain growth factors and phorbol esters. This complex is composed of products of the jun and fos gene families. The present studies have examined the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the regulation of jun-B gene expression during induction of monocytic differentiation. Low levels of jun-B transcripts were present in uninduced HL-60 promyelocytic leukemia cells. In contrast, treatment with TPA was associated with rapid increases in jun-B mRNA levels that were maximal at 3 h and remained elevated at 48 h. The induction of jun-B expression by TPA in these cells preceded that of the c-jun and c-fos genes. Similar increases in jun-B transcripts were detectable in TPA-treated THP-1 and U-937 myeloid leukemia cells, although expression of this gene was transient in the more differentiated THP-1 cells. Run-on assays demonstrated low levels of jun-B gene activation in untreated HL-60 cells, whereas TPA treatment was associated with a 6-fold increase in the transcription rate of this gene. This induction of jun-B expression occurred in the absence of de novo protein synthesis. In contrast, inhibition of protein synthesis was associated with superinduction of TPA-induced jun-B mRNA levels and an increase in stability of this transcript. These findings suggest that jun-B gene expression is regulated at both the transcriptional and posttranscriptional levels during induction of monocytic differentiation. The results also demonstrate that other inducers of monocytic differentiation, 1,25-dihydroxyvitamin D3 and bryostatin 1, similarly induce jun-B gene expression in myeloid leukemia cells. Moreover, treatment of normal human monocytes with TPA was associated with transient expression of jun-B transcripts. Taken together, these findings suggest that activation of the jun-B gene may contribute to the transcriptional regulation of certain target genes expressed during induction of monocytic differentiation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. FU NCI NIH HHS [CA42802, CA01902] NR 53 TC 44 Z9 44 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 JAN PY 1991 VL 2 IS 1 BP 43 EP 49 PG 7 WC Cell Biology SC Cell Biology GA ET575 UT WOS:A1991ET57500006 PM 2007095 ER PT J AU SAITO, H STREULI, M AF SAITO, H STREULI, M TI MOLECULAR CHARACTERIZATION OF PROTEIN TYROSINE PHOSPHATASES SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID LEUKOCYTE-COMMON ANTIGEN; TRANSFORMING-GENE-PRODUCT; ROUS-SARCOMA VIRUS; PRE-MESSENGER RNA; T-CELL RECEPTOR; HUMAN-PLACENTA; KINASE P56LCK; CD4 RECEPTOR; SIGNAL TRANSDUCTION; LYMPHOCYTES-T C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP SAITO, H (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-57732]; NIAID NIH HHS [AI-26598] NR 78 TC 86 Z9 86 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD JAN PY 1991 VL 2 IS 1 BP 59 EP 65 PG 7 WC Cell Biology SC Cell Biology GA ET575 UT WOS:A1991ET57500008 PM 1848775 ER PT J AU ROPPER, AH GRESS, DR AF ROPPER, AH GRESS, DR TI COMPUTERIZED-TOMOGRAPHY AND CLINICAL-FEATURES OF LARGE CEREBRAL HEMORRHAGES SO CEREBROVASCULAR DISEASES LA English DT Article DE CEREBRAL HEMORRHAGE; HERNIATION; COMA; HYDROCEPHALUS ID INTRACEREBRAL HEMORRHAGE; PROGNOSTIC VALUE; CT SCAN; CONSCIOUSNESS; DISPLACEMENT; HEMATOMAS; BRAIN; LEVEL; MRI AB We studied 17 consecutive patients with nonaneurysmal cerebral hemorrhages larger than 55 cm3 to determine the computerized tomographic correlates of stupor and coma. Coma was associated with 8 mm or greater pineal displacement in 8 of 14 comatose patients. An extension of the clot that occupied or displaced the lower diencephalic region explained coma in the remaining 6 patients with less than 8 mm horizontal pineal displacement. All patients with diencephalic clot were comatose. Three initially drowsy or stuporous patients had 3 mm mean pineal displacement. Massive hydrocephalus occurred in 5 patients, always associated with diencephalic clot, and therefore never independently accounting for coma. Clot volume could be estimated from: volume (cm3) = [largest clot diameter (cm) x 14] - 14. We incidentally found that at least 6 of the 17 massive hemorrhages had progressed from smaller clots. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,STROKE SERV,BOSTON,MA 02114. RP ROPPER, AH (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROL NEUROSURG INTENS CARE UNIT,BOSTON,MA 02114, USA. NR 12 TC 10 Z9 10 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-9770 J9 CEREBROVASC DIS JI Cerebrovasc. Dis. PD JAN-FEB PY 1991 VL 1 IS 1 BP 38 EP 42 DI 10.1159/000108814 PG 5 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA FM813 UT WOS:A1991FM81300006 ER PT J AU SCHECTER, A FURST, P FURST, C PAPKE, O BALL, M DAI, LC QUYNH, HT PHOUNG, NTN BEIM, A VLASOV, B CHONGCHET, V CONSTABLE, JD CHARLES, K AF SCHECTER, A FURST, P FURST, C PAPKE, O BALL, M DAI, LC QUYNH, HT PHOUNG, NTN BEIM, A VLASOV, B CHONGCHET, V CONSTABLE, JD CHARLES, K TI DIOXINS, DIBENZOFURANS AND SELECTED CHLORINATED ORGANIC-COMPOUNDS IN HUMAN-MILK AND BLOOD FROM CAMBODIA, GERMANY, THAILAND, THE USA, THE USSR, AND VIETNAM SO CHEMOSPHERE LA English DT Article ID HUMAN ADIPOSE-TISSUE; HUMAN-BREAST MILK; UNITED-STATES; DIBENZODIOXINS; 2,3,7,8-TCDD; VETERANS; EXPOSURE; NORTH; PCBS; DDE AB This paper reports general population blood polychlorinated dioxin and dibenzofuran (PCDD/F) levels for various geographical regions in the north and south of Vietnam in pooled samples from 112 persons, the results of 85 individual analyses of blood from Germany, and levels from a pool of whole blood from 100 U.S. residents. This paper also presents selected population data for PCDD/Fs and certain other chlorinated chemicals such as PCBs and other chlorinated xenobiotics in human milk from locations in Vietnam, Cambodia, and Thailand. These represent new samples from seventy persons from the general population from three less industrialized Asian countries; these are compared with our previous findings from several hundred persons from Germany, the Soviet Union, and the United States. C1 NORTH RHINE WESTPHALIA, FED STATE CONTROL LAB FOOD & ENVIRONM CHEM, W-4400 MUNSTER, GERMANY. ERGO FORSCHUNGSGESELL MBH, W-2000 HAMBURG 50, GERMANY. HANDI UNIV, COLL MED, HANOI, VIETNAM. MINIST HLTH, HANOI, VIETNAM. COLL MED, HO CHI MINH CITY, VIETNAM. OBSTET & GYNECOL HOSP, HO CHI MINH CITY, VIETNAM. INST ECOL TOXICOL, BAIKALSK, USSR. INST ORTHOPED SURG, IRKUTSK, USSR. VAJIRA METROPOLIS HOSP, BANGKOK, THAILAND. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT SURG, BOSTON, MA 02114 USA. RP SCHECTER, A (reprint author), SUNY HLTH SCI CTR, COLL MED, DEPT PREVENT MED, CLIN CAMPUS, 88 ALDRICH AVE, BINGHAMTON, NY 13903 USA. NR 25 TC 32 Z9 35 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0045-6535 EI 1879-1298 J9 CHEMOSPHERE JI Chemosphere PY 1991 VL 23 IS 11-12 BP 1903 EP 1912 DI 10.1016/0045-6535(91)90037-E PG 10 WC Environmental Sciences SC Environmental Sciences & Ecology GA HB255 UT WOS:A1991HB25500036 ER PT J AU MURPHY, JM JELLINEK, M QUINN, D SMITH, G POITRAST, FG GOSHKO, M AF MURPHY, JM JELLINEK, M QUINN, D SMITH, G POITRAST, FG GOSHKO, M TI SUBSTANCE-ABUSE AND SERIOUS CHILD MISTREATMENT - PREVALENCE, RISK, AND OUTCOME IN A COURT SAMPLE SO CHILD ABUSE & NEGLECT LA English DT Article DE SUBSTANCE ABUSE; CHILD ABUSE AND NEGLECT; RISK FACTORS ID NEGLECTED CHILDREN; PARENTS; ALCOHOLISM C1 BOSTON JUVENILE COURT,BOSTON,MA. RP MURPHY, JM (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,ACC 725,BOSTON,MA 02114, USA. NR 25 TC 165 Z9 166 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PY 1991 VL 15 IS 3 BP 197 EP 211 DI 10.1016/0145-2134(91)90065-L PG 15 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA FE424 UT WOS:A1991FE42400006 PM 2043972 ER PT J AU TAYLOR, CG NORMAN, DK MURPHY, JM JELLINEK, M QUINN, D POITRAST, FG GOSHKO, M AF TAYLOR, CG NORMAN, DK MURPHY, JM JELLINEK, M QUINN, D POITRAST, FG GOSHKO, M TI DIAGNOSED INTELLECTUAL AND EMOTIONAL IMPAIRMENT AMONG PARENTS WHO SERIOUSLY MISTREAT THEIR CHILDREN - PREVALENCE, TYPE, AND OUTCOME IN A COURT SAMPLE SO CHILD ABUSE & NEGLECT LA English DT Article DE CHILD ABUSE AND NEGLECT; PARENTAL PSYCHOPATHOLOGY; PARENTAL IQ ID BATTERED CHILDREN C1 BOSTON JUVENILE COURT,BOSTON,MA. RP TAYLOR, CG (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,ACC 725,BOSTON,MA 02114, USA. NR 37 TC 67 Z9 67 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PY 1991 VL 15 IS 4 BP 389 EP 401 DI 10.1016/0145-2134(91)90023-7 PG 13 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA GD909 UT WOS:A1991GD90900008 PM 1959072 ER PT J AU MARCELLIN, P CALMUS, Y TAKAHASHI, H ZIGNEGO, AL CHATENOUD, L GALANAUD, LP LEIBOWITCH, M BACH, JF BENHAMOU, JP TIOLLAIS, P WANDS, J GUILLEVIN, L BRECHOT, C AF MARCELLIN, P CALMUS, Y TAKAHASHI, H ZIGNEGO, AL CHATENOUD, L GALANAUD, LP LEIBOWITCH, M BACH, JF BENHAMOU, JP TIOLLAIS, P WANDS, J GUILLEVIN, L BRECHOT, C TI LATENT HEPATITIS-B VIRUS (HBV) INFECTION IN SYSTEMIC NECROTIZING VASCULITIS SO CLINICAL AND EXPERIMENTAL RHEUMATOLOGY LA English DT Article DE POLYARTERITIS NODOSA; HEPATITIS-B VIRUS ID MONONUCLEAR BLOOD-CELLS; CHRONIC LIVER-DISEASE; SURFACE-ANTIGEN; POLYARTERITIS NODOSA; IMMUNE-COMPLEXES; VIRAL-DNA; SEQUENCES; SERUM; RADIOIMMUNOASSAY; TRANSMISSION AB We have investigated hepatitis B virus (HBV) infection in systemic necrotizing vasculitis (SNV). Our approach included the detection of the viral surface antigen (HBsAg) with a radioimmunoassay employing monoclonal anti-HBs (m-RIA); in addition, HBV DNA was looked for in serum and peripheral mononuclear blood cells. Among 28 subjects with SNV, 12 were found to be positive for HBsAg with the conventional test (p-RIA) and 7 additional subjects had anti-HBc and/or anti-HBs. From the 16 HBsAg negative individuals, 9 had HBsAg epitopes identified in serum with the m-RIA test and 1 had a low amount of circulating viral DNA. In contrast, only 1 among 6 subjects with other systemic vasculitis showed a positive test for m-RIA and HBV DNA assays; this individual had acquired HIV infection through transfusions which were also probably the source of his HBV infection. HBV DNA sequences were identified in peripheral mononuclear blood cells of 9 from the 37 tested, including 2 individuals who were HBsAg positive only with m-RIA. Therefore, our study indicates a much higher rate of HBV infection in patients with polyarteritis nodosa than previously suspected. C1 UNIV PARIS 13,HOP AVICENNE,SERV MED INTERNE,125 RUE STALINGRAD,F-93009 BOBIGNY,FRANCE. INST PASTEUR,INSERM,U163,UNITE RECOMBINAISON & EXPRESS GENET,F-75724 PARIS 15,FRANCE. HOP BEAUJON,SERV HEPATOL,CLICHY,FRANCE. HOP BEAUJON,INSERM,U24,CLICHY,FRANCE. HOP ST ANTOINE,SERV HEPATOGASTROENTEROL,F-75571 PARIS 12,FRANCE. MASSACHUSETTS GEN HOSP,MOLEC HEPATOL LAB,E CHARLESTON,MA 02129. HOP NECKER ENFANTS MALAD,INSERM,U25,F-75730 PARIS 15,FRANCE. HOP ANTOINE BECLERE,SERV MED INTERNE,CLAMART,FRANCE. HOP TARNIER,SERV DERMATOL,PARIS,FRANCE. CHU LAENNEC NECKER,UNITE HEPATOL,LAENNEC NECKER,FRANCE. CHU LAENNEC NECKER,INSERM,U75,LAENNEC NECKER,FRANCE. NR 32 TC 25 Z9 25 U1 0 U2 0 PU CLINICAL & EXPER RHEUMATOLOGY PI PISA PA VIA SANTA MARIA 31, 56126 PISA, ITALY SN 0392-856X J9 CLIN EXP RHEUMATOL JI Clin. Exp. Rheumatol. PD JAN-FEB PY 1991 VL 9 IS 1 BP 23 EP 28 PG 6 WC Rheumatology SC Rheumatology GA FA296 UT WOS:A1991FA29600005 PM 1675938 ER PT J AU ARNOLD, A MOTOKURA, T BLOOM, T KRONENBERG, H RUDERMAN, J JUPPNER, H KIM, HG AF ARNOLD, A MOTOKURA, T BLOOM, T KRONENBERG, H RUDERMAN, J JUPPNER, H KIM, HG TI THE PUTATIVE ONCOGENE PRAD1 ENCODES A NOVEL CYCLIN SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID CHROMOSOMAL BREAKPOINT; PARATHYROID ADENOMAS; CANDIDATE ONCOGENE; MOLECULAR-CLONING; BCL-1 LOCUS; CELL; LYMPHOMAS; TRANSLOCATION; REARRANGEMENT; T(11-14) C1 HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. OI Bloom, Theodora/0000-0002-0222-4177 NR 22 TC 21 Z9 21 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1991 VL 56 BP 93 EP 97 PG 5 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800012 PM 1840271 ER PT J AU RUSTGI, AK DYSON, N HILL, D BERNARDS, R AF RUSTGI, AK DYSON, N HILL, D BERNARDS, R TI THE C-MYC ONCOPROTEIN FORMS A SPECIFIC COMPLEX WITH THE PRODUCT OF THE RETINOBLASTOMA GENE SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID DNA-BINDING; ACTIVATES TRANSCRIPTION; PROTEIN; TRANSFORMATION; MUTATIONS; REGIONS; MEMBER; FAMILY C1 MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC GENET,BOSTON,MA 02129. APPL BIOTECHNOL INC,CAMBRIDGE,MA 02142. HARVARD UNIV,SCH MED,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC ONCOL,BOSTON,MA 02129. OI Bernards, Rene/0000-0001-8677-3423 NR 20 TC 8 Z9 8 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1991 VL 56 BP 163 EP 167 PG 5 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800020 PM 1840250 ER PT J AU MEYERSON, M FAHA, B SU, LK HARLOW, E TSAI, LH AF MEYERSON, M FAHA, B SU, LK HARLOW, E TSAI, LH TI THE CYCLIN-DEPENDENT KINASE FAMILY SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID MATURATION-PROMOTING FACTOR; ADENOVIRUS E1A PROTEINS; SEA-URCHIN EGGS; CELL-CYCLE; SACCHAROMYCES-CEREVISIAE; FISSION YEAST; CDC2 PROTEIN; M-PHASE; DNA-REPLICATION; MESSENGER-RNA C1 MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. RI Meyerson, Matthew/E-7123-2012 FU NCI NIH HHS [CA-55339] NR 63 TC 24 Z9 25 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1991 VL 56 BP 177 EP 186 PG 10 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800022 PM 1840251 ER PT J AU CHITTENDEN, T LIVINGSTON, DM KAELIN, WG AF CHITTENDEN, T LIVINGSTON, DM KAELIN, WG TI RB ASSOCIATES WITH AN E2F-LIKE, SEQUENCE-SPECIFIC DNA-BINDING PROTEIN SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID RETINOBLASTOMA-SUSCEPTIBILITY GENE; E2F TRANSCRIPTION FACTOR; ADENOVIRUS E1A PROTEINS; LARGE T-ANTIGEN; TRANS-ACTIVATION; CELL-CYCLE; PRODUCT; EXPRESSION; IDENTIFICATION; PROMOTER C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 33 TC 18 Z9 18 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1991 VL 56 BP 187 EP 195 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800023 PM 1819485 ER PT J AU MAMON, H WILLIAMS, N WOOD, K FRAZIER, AL LI, P ZMUIDZINAS, A KREMER, N DACANGELO, G QI, H SMITH, K FEIG, L PIWNICAWORMS, H HALEGOUA, S ROBERTS, T AF MAMON, H WILLIAMS, N WOOD, K FRAZIER, AL LI, P ZMUIDZINAS, A KREMER, N DACANGELO, G QI, H SMITH, K FEIG, L PIWNICAWORMS, H HALEGOUA, S ROBERTS, T TI NEW PERSPECTIVES ON RAF-1 - THE INVOLVEMENT OF P21RAS IN THE ACTIVATION OF RAF-1 AND A POTENTIAL ROLE FOR RAF-1 IN EVENTS OCCURRING LATER IN THE CELL-CYCLE SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; NERVE GROWTH-FACTOR; PROTEIN-KINASE-C; HA-RAS MUTATION; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION; DEPENDENT PHOSPHORYLATION; RAPID PHOSPHORYLATION; M-PHASE; SERINE C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BASF BIORES CORP,CAMBRIDGE,MA 02139. SUNY,DEPT NEUROBIOL,NEW YORK,NY 11784. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT MED,HANOVER,NH 03756. TUFTS UNIV,SCH MED,DEPT BIOCHEM,BOSTON,MA 02111. TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 55 TC 8 Z9 8 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1991 VL 56 BP 251 EP 263 PG 13 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800030 PM 1819489 ER PT J AU WILLIAMS, ME AF WILLIAMS, ME TI HYPERKALEMIA SO CRITICAL CARE CLINICS LA English DT Article RP WILLIAMS, ME (reprint author), JOSLIN DIABET CTR,RENAL UNIT,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 0 TC 14 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 0749-0704 J9 CRIT CARE CLIN JI Crit. Care Clin. PD JAN PY 1991 VL 7 IS 1 BP 155 EP 174 PG 20 WC Critical Care Medicine SC General & Internal Medicine GA EX013 UT WOS:A1991EX01300011 PM 2007212 ER PT J AU RAO, A AF RAO, A TI SIGNALING MECHANISMS IN T-CELLS SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Review ID PROTEIN-KINASE-C; HUMAN LYMPHOCYTES-T; NF-KAPPA-B; ANTIGEN RECEPTOR COMPLEX; CYTOPLASMIC FREE CALCIUM; INDUCED LYMPHOKINE PRODUCTION; PEPTIDYL-PROLYL ISOMERASE; DNA-BINDING PROTEINS; PHOSPHOLIPASE-C; TYROSINE PHOSPHORYLATION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR BIOL,BOSTON,MA 02115. RP RAO, A (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,RM 628,MAYER BLDG,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA42471]; NIAID NIH HHS [AI2900] NR 233 TC 77 Z9 77 U1 0 U2 0 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 SN 1040-8401 J9 CRIT REV IMMUNOL JI Crit. Rev. Immunol. PY 1991 VL 10 IS 6 BP 495 EP 519 PG 25 WC Immunology SC Immunology GA FE915 UT WOS:A1991FE91500003 PM 1650561 ER PT J AU CANTIELLO, HF AUSIELLO, DA AF CANTIELLO, HF AUSIELLO, DA TI DEVELOPMENT OF EPITHELIAL NA+ CHANNELS AND REGULATION BY GUANINE-NUCLEOTIDE REGULATORY (G) PROTEINS AND PHOSPHOLIPIDS SO CURRENT TOPICS IN MEMBRANES LA English DT Review ID MEDULLARY COLLECTING DUCT; GTP-BINDING-PROTEINS; TOAD URINARY-BLADDER; ARACHIDONIC-ACID METABOLITES; ISLET-ACTIVATING PROTEIN; KIDNEY PROXIMAL TUBULES; MUSCARINIC K+ CHANNELS; ADENYL CYCLASE SYSTEM; SENSITIVE G-PROTEIN; CELL LINE LLC-PK1 C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RENAL UNIT,BOSTON,MA 02114. NR 209 TC 4 Z9 4 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 J9 CURR TOP MEMBR JI Curr. Top. Membr. PY 1991 VL 39 BP 395 EP 436 PG 42 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MG418 UT WOS:A1991MG41800012 ER PT J AU SPITS, H YSSEL, H BROCKELHURST, C KRANGEL, M AF SPITS, H YSSEL, H BROCKELHURST, C KRANGEL, M TI EVIDENCE FOR CONTROLLED GENE REARRANGEMENTS AND CYTOKINE PRODUCTION DURING DEVELOPMENT OF HUMAN TCR-GAMMA-DELTA+ LYMPHOCYTES SO CURRENT TOPICS IN MICROBIOLOGY AND IMMUNOLOGY LA English DT Article ID CELL RECEPTOR-GAMMA; DENDRITIC EPIDERMAL-CELLS; PERIPHERAL-BLOOD; FETAL THYMOCYTES; TRANSGENIC MICE; CLONES; EXPRESSION; THYMUS; DIVERSITY; INDUCTION C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. RP SPITS, H (reprint author), DNAX RES INST MOLEC & CELLULAR BIOL INC, MOLEC & CELLULAR BIOL RES INST, 901 CALIF AVE, PALO ALTO, CA 94304 USA. RI Yssel, Hans/C-6406-2009 OI Yssel, Hans/0000-0001-7454-1836 NR 24 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0070-217X J9 CURR TOP MICROBIOL JI Curr.Top.Microbiol.Immunol. PY 1991 VL 173 BP 47 EP 55 PG 9 WC Immunology; Microbiology SC Immunology; Microbiology GA GA068 UT WOS:A1991GA06800008 ER PT J AU UYEMURA, K BAND, H OHMEN, J BRENNER, MB REA, TH MODLIN, RL AF UYEMURA, K BAND, H OHMEN, J BRENNER, MB REA, TH MODLIN, RL TI GAMMA-DELTA T-CELLS IN LEPROSY LESIONS SO CURRENT TOPICS IN MICROBIOLOGY AND IMMUNOLOGY LA English DT Article ID INTESTINAL INTRAEPITHELIAL LYMPHOCYTES; DENDRITIC EPIDERMAL-CELLS; HEAT-SHOCK PROTEIN; MYCOBACTERIUM-TUBERCULOSIS; SKIN-LESIONS; RECEPTOR; ANTIGEN; EXPRESSION; DIVERSITY; CLONES C1 UNIV SO CALIF, SCH MED, DERMATOL SECT, LOS ANGELES, CA 90033 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, IMMUNOCHEM LAB, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT RHEUMATOL & IMMUNOL, BOSTON, MA 02115 USA. RP UYEMURA, K (reprint author), UNIV CALIF LOS ANGELES, SCH MED, DEPT MICROBIOL & IMMUNOL, DIV DERMATOL, LOS ANGELES, CA 90024 USA. NR 17 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0070-217X J9 CURR TOP MICROBIOL JI Curr.Top.Microbiol.Immunol. PY 1991 VL 173 BP 203 EP 207 PG 5 WC Immunology; Microbiology SC Immunology; Microbiology GA GA068 UT WOS:A1991GA06800028 ER PT J AU BAND, H PORCELLI, SA PANCHAMOORTHY, G MCLEAN, J MORITA, CT ISHIKAWA, S MODLIN, RL BRENNER, MB AF BAND, H PORCELLI, SA PANCHAMOORTHY, G MCLEAN, J MORITA, CT ISHIKAWA, S MODLIN, RL BRENNER, MB TI ANTIGENS AND ANTIGEN-PRESENTING MOLECULES FOR GAMMA-DELTA T-CELLS SO CURRENT TOPICS IN MICROBIOLOGY AND IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; DENDRITIC EPIDERMAL-CELLS; HUMAN LYMPHOCYTES-T; HEAT-SHOCK PROTEIN; MYCOBACTERIUM-TUBERCULOSIS; RECEPTOR GENES; RECOGNITION; CLONES; SPECIFICITY; IDENTIFICATION C1 HARVARD UNIV, SCH MED, DEPT RHEUMATOL & IMMUNOL, BOSTON, MA 02115 USA. TUFTS UNIV, SCH MED, DEPT MED, BOSTON, MA 02111 USA. ST ELIZABETH HOSP, PULM MED UNIT, BOSTON, MA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MICROBIOL & IMMUNOL, DIV DERMATOL, LOS ANGELES, CA 90024 USA. RP BAND, H (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, IMMUNOCHEM LAB, BOSTON, MA 02115 USA. RI Morita, Craig/C-1365-2011 NR 41 TC 0 Z9 0 U1 0 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0070-217X J9 CURR TOP MICROBIOL JI Curr.Top.Microbiol.Immunol. PY 1991 VL 173 BP 229 EP 234 PG 6 WC Immunology; Microbiology SC Immunology; Microbiology GA GA068 UT WOS:A1991GA06800032 ER PT J AU WAGNER, JA AF WAGNER, JA TI THE FIBROBLAST GROWTH-FACTORS - AN EMERGING FAMILY OF NEURAL GROWTH-FACTORS SO CURRENT TOPICS IN MICROBIOLOGY AND IMMUNOLOGY LA English DT Review ID PROTEIN KINASE-C; RIBONUCLEIC-ACID TRANSCRIPTS; CAPILLARY ENDOTHELIAL-CELLS; INDUCED NEURITE OUTGROWTH; SMOOTH-MUSCLE CELLS; SWISS 3T3 CELLS; PC12 CELLS; FACTOR RECEPTOR; BOVINE BRAIN; FACTOR FGF C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. RP WAGNER, JA (reprint author), HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. NR 138 TC 89 Z9 89 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0070-217X J9 CURR TOP MICROBIOL JI Curr. Top. Microbiol. Immunol. PY 1991 VL 165 BP 95 EP 118 PG 24 WC Immunology; Microbiology SC Immunology; Microbiology GA FC404 UT WOS:A1991FC40400006 PM 2032466 ER PT J AU SEIZINGER, BR KLINGER, HP JUNIEN, C NAKAMURA, Y LEBEAU, M CAVENEE, W EMANUEL, B PONDER, B NAYLOR, S MITELMAN, F LOUIS, D MENON, A NEWSHAM, I DECKER, J KAELBLING, M HENRY, I VONDEIMLING, A AF SEIZINGER, BR KLINGER, HP JUNIEN, C NAKAMURA, Y LEBEAU, M CAVENEE, W EMANUEL, B PONDER, B NAYLOR, S MITELMAN, F LOUIS, D MENON, A NEWSHAM, I DECKER, J KAELBLING, M HENRY, I VONDEIMLING, A TI REPORT OF THE COMMITTEE ON CHROMOSOME AND GENE LOSS IN HUMAN NEOPLASIA SO CYTOGENETICS AND CELL GENETICS LA English DT Article C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MOLEC GENET,BRONX,NY 10461. UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE CB2 1QP,ENGLAND. INSERM,U73,UNITE RECH BIOL PRENATALE,F-75016 PARIS,FRANCE. JAPANESE FDN CANC RES,INST CANC,DIV BIOCHEM,TOKYO 170,JAPAN. UNIV CHICAGO,CHICAGO,IL 60637. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA 19104. RP SEIZINGER, BR (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114, USA. RI von Deimling, Andreas/F-7774-2013 OI von Deimling, Andreas/0000-0002-5863-540X NR 0 TC 213 Z9 215 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1080 EP 1096 DI 10.1159/000133722 PG 17 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900003 ER PT J AU LIU, AW WEISSBECKER, KA DELGADOESCUETA, A SERRATOSA, JM TREIMAN, L SPARKES, R PARK, MS AF LIU, AW WEISSBECKER, KA DELGADOESCUETA, A SERRATOSA, JM TREIMAN, L SPARKES, R PARK, MS TI LINKAGE STUDIES OF JUVENILE MYOCLONIC EPILEPSY SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,DEPT NEUROL,LOS ANGELES,CA 90024. LOUISIANA STATE UNIV,MED CTR,DEPT BIOCHEM & GENET,NEW ORLEANS,LA 70112. UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,NEUROL & RES SERV,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED GENET,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT SURG,TISSUE TYPING LAB,LOS ANGELES,CA 90024. NR 2 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1913 EP 1914 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900175 ER PT J AU BURLEY, MW ATTWOOD, J MALAS, S GILLETT, G ISLAM, I LOVEGROVE, J POVEY, S HAMPSON, RM DESAI, S AFFARA, NA YATES, JR WEBB, D OSBORNE, J FRYER, AE MUELLER, R SUPER, M CRAIG, S BECHHANSEN, T BENHAM, F HUNT, D KWIATKOWSKI, DJ AF BURLEY, MW ATTWOOD, J MALAS, S GILLETT, G ISLAM, I LOVEGROVE, J POVEY, S HAMPSON, RM DESAI, S AFFARA, NA YATES, JR WEBB, D OSBORNE, J FRYER, AE MUELLER, R SUPER, M CRAIG, S BECHHANSEN, T BENHAM, F HUNT, D KWIATKOWSKI, DJ TI LINKAGE STUDIES IN TUBEROUS SCLEROSIS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV LONDON UNIV COLL,GALTON LAB,MRC,HUMAN BIOCHEM GENET UNIT,LONDON NW1 2HE,ENGLAND. UNIV CAMBRIDGE,DEPT PATHOL,DIV CELLULAR & GENET PATHOL,CAMBRIDGE,ENGLAND. ROYAL UNITED HOSP,BATH UNIT RES PAEDIAT,BATH,AVON,ENGLAND. ROYAL LIVERPOOL HOSP,DEPT CYTOGENET,REG GEN SERV,LIVERPOOL L7 8XP,MERSEYSIDE,ENGLAND. GEN INFIRM,DEPT CLIN GENET,LEEDS LS1 3EX,W YORKSHIRE,ENGLAND. ROYAL MANCHESTER CHILDRENS HOSP,PAEDIAT GENET UNIT,MANCHESTER M27 1HA,LANCS,ENGLAND. UNIV OXFORD,GENET LAB,OXFORD OX1 3QU,ENGLAND. ALBERTA CHILDRENS PROV GEN HOSP,ALBERTA HEREDITARY DIS PROGRAM,CALGARY T2T 5C7,ALBERTA,CANADA. UNIV LONDON UNIV COLL,DEPT GENET & BIOMETRY,LONDON NW1 2HE,ENGLAND. MASSACHUSETTS GEN HOSP,CHARLESTON,MA 02129. NR 2 TC 0 Z9 0 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1935 EP 1936 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900234 ER PT J AU FRANKLIN, D ATTWOOD, J BURLEY, MW MALAS, S JEREMIAH, S PHILLIPS, J RETIEF, A YATES, JR CRAIG, S ARMOUR, J AFFARA, N KWIATKOWSKI, DJ POVEY, S AF FRANKLIN, D ATTWOOD, J BURLEY, MW MALAS, S JEREMIAH, S PHILLIPS, J RETIEF, A YATES, JR CRAIG, S ARMOUR, J AFFARA, N KWIATKOWSKI, DJ POVEY, S TI A GENETIC-MAP OF 9Q34 BY MULTIPLE 2 POINT ANALYSIS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV LONDON UNIV COLL,MRC,HUMAN BIOCHEM GENET UNIT,GALTON LAB,LONDON NW1 2HE,ENGLAND. VANDERBILT UNIV,DEPT PEDIAT,NASHVILLE,TN 37232. UNIV STELLENBOSCH,FAC MED,SCH MED,MRC,CYTOGENET RES UNIT,TYGERBERG 7505,SOUTH AFRICA. UNIV CAMBRIDGE,DEPT PATHOL,DIV CELLULAR & GENET PATHOL,CAMBRIDGE CB2 1QP,ENGLAND. UNIV OXFORD,GENET LAB,OXFORD OX1 3QU,ENGLAND. UNIV LEICESTER,DEPT GENET,LEICESTER LE1 7RH,ENGLAND. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. NR 7 TC 1 Z9 1 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1938 EP 1938 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900239 ER PT J AU HAINES, JL SHORT, MP KWIATKOWSKI, DJ ANDERMANN, E MICKLE, J GUSELLA, JF AMOS, JA AF HAINES, JL SHORT, MP KWIATKOWSKI, DJ ANDERMANN, E MICKLE, J GUSELLA, JF AMOS, JA TI HETEROGENEITY IN TUBEROUS SCLEROSIS LOCALIZATION OF TSC1 TO 9Q34, AND LINKAGE ANALYSIS WITH 11Q AND 14Q MARKERS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02129. MONTREAL NEUROL HOSP & INST,DEPT NEUROGENET,MONTREAL H3A 2B4,QUEBEC,CANADA. BOSTON UNIV,MED CTR,CTR HUMAN GENET,BOSTON,MA 02215. NR 0 TC 1 Z9 1 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1939 EP 1940 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900242 ER PT J AU JANSSEN, B SAMPSON, J SANDKUYL, L FLEURY, P LINDHOUT, D CONNOR, M SMITH, M HAINES, J AMOS, J KWIATKOWSKI, D SHORT, P NORTHRUP, H BLANTON, S POVEY, S BURLEY, M NELLIST, M BROOKCARTER, P MICKLE, J FAHSOLD, R ROTT, HD HALLEY, D AF JANSSEN, B SAMPSON, J SANDKUYL, L FLEURY, P LINDHOUT, D CONNOR, M SMITH, M HAINES, J AMOS, J KWIATKOWSKI, D SHORT, P NORTHRUP, H BLANTON, S POVEY, S BURLEY, M NELLIST, M BROOKCARTER, P MICKLE, J FAHSOLD, R ROTT, HD HALLEY, D TI MAPPING STUDIES IN TUBEROUS SCLEROSIS A COLLABORATIVE EFFORT SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract ID GENE C1 ACAD HOSP ROTTERDAM DIJKZIGT,DEPT CLIN GENET,ROTTERDAM,NETHERLANDS. UNIV HOSP WALES,INST MED GENET,CARDIFF,WALES. UNIV AMSTERDAM,ACAD MED CTR,DEPT NEUROL,1105 AZ AMSTERDAM,NETHERLANDS. UNIV GLASGOW,DUNCAN GUTHRIE INST,DEPT MED GENET,GLASGOW G12 8QQ,SCOTLAND. UNIV CALIF IRVINE,IRVINE,CA 92717. MASSACHUSETTS GEN HOSP,DIV NEUROGENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. BOSTON UNIV,SCH MED,CTR HUMAN GENET,BOSTON,MA 02118. UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. UNIV LONDON UNIV COLL,MRC,HUMAN BIOCHEM GENET UNIT,LONDON WC1E 6BT,ENGLAND. UNIV WALES COLL CARDIFF,INST MED GENET,CARDIFF CF1 3NS,S GLAM,WALES. UNIV ERLANGEN NURNBERG,INST MED GENET,W-8520 ERLANGEN,GERMANY. NR 8 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1940 EP 1940 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900244 ER PT J AU KWIATKOWSKI, DJ WEIMER, K OZELIUS, L GUSELLA, JF HAINES, JL AF KWIATKOWSKI, DJ WEIMER, K OZELIUS, L GUSELLA, JF HAINES, JL TI A GT POLYMORPHISM MAP OF 9Q SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROGENET,BOSTON,MA 02129. NR 0 TC 1 Z9 1 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1941 EP 1941 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900246 ER PT J AU GAILANI, MR PETTY, EM HORSTHEMKE, B ARNOLD, A MARX, SJ BALE, AE AF GAILANI, MR PETTY, EM HORSTHEMKE, B ARNOLD, A MARX, SJ BALE, AE TI PHYSICAL MAPPING OF CHROMOSOME-11Q12-13 BY PULSED FIELD GEL-ELECTROPHORESIS (PFGE) SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT HUMAN GENET,NEW HAVEN,CT 06510. INST HUMAN GENET & ANTHROPOL,ESSEN,GERMANY. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1959 EP 1959 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900287 ER PT J AU PERICAKVANCE, MA HAINES, JL STGEORGEHYSLOP, P BEBOUT, JL HAYNES, CA TANZI, R YAMAOKA, LH GUSELLA, JF ROSES, AD AF PERICAKVANCE, MA HAINES, JL STGEORGEHYSLOP, P BEBOUT, JL HAYNES, CA TANZI, R YAMAOKA, LH GUSELLA, JF ROSES, AD TI COLLABORATIVE LINKAGE ANALYSIS OF CHROMOSOME-19 AND CHROMOSOME-21 LOCI IN FAMILIAL ALZHEIMER-DISEASE (FAD) SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC 27710. MASSACHUSETTS GEN HOSP,DEPT MOLEC NEUROGENET,BOSTON,MA 02114. UNIV TORONTO,CTR RES NEURODEGENERAT DIS,TORONTO M5S 1A8,ONTARIO,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 2024 EP 2024 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900445 ER PT J AU GASTON, SM TANZI, RE STEWART, GD ROMANO, DM GARDINER, K DANG, T BOWLIN, R RIDER, S MCCORMICK, MK KURNIT, DM GUSELLA, JF PATTERSON, D AF GASTON, SM TANZI, RE STEWART, GD ROMANO, DM GARDINER, K DANG, T BOWLIN, R RIDER, S MCCORMICK, MK KURNIT, DM GUSELLA, JF PATTERSON, D TI CLONING OF HUMAN CHROMOSOME-21 INTO YEAST ARTIFICIAL CHROMOSOMES - PROGRESS OF THE CHROMOSOME-21 JOINT YAC EFFORT SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. UNIV MICHIGAN,MED CTR,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. UNIV COLORADO,HLTH SCI CTR,ELEANOR ROOSEVELT INST CANC RES,DENVER,CO 80262. UNIV CALIF SAN FRANCISCO,CTR HUMAN GENOME MAPPING,SAN FRANCISCO,CA 94143. UNIV CALIF LOS ALAMOS SCI LAB,LOS ALAMOS,NM 87544. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 2036 EP 2036 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900469 ER PT J AU CHEN, ZY HSU, PYP POWELL, JF HENDRIKS, RW BREAKEFIELD, XO CRAIG, IW AF CHEN, ZY HSU, PYP POWELL, JF HENDRIKS, RW BREAKEFIELD, XO CRAIG, IW TI LONG-RANGE PHYSICAL MAPPING AND ORGANIZATION OF THE REGION INCLUDING THE GENES FOR MONOAMINE OXIDASE-A AND OXIDASE-B, (MAOA AND MAOB) SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV OXFORD,DEPT BIOCHEM,GENET LAB,OXFORD OX1 3QU,ENGLAND. UA MED CTR,RES SERV,BOSTON,MA 02132. INST PSYCHIAT,DEPT NEUROSCI,LONDON SE5 8AF,ENGLAND. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,BOSTON,MA 02129. RI Powell, John/G-4412-2011 OI Powell, John/0000-0001-6124-439X NR 0 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 2059 EP 2059 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900534 ER PT J AU IONASESCU, VV HAINES, JL TROFATTER, J SUMMERS, AM IONASESCU, R SEARBY, CC AF IONASESCU, VV HAINES, JL TROFATTER, J SUMMERS, AM IONASESCU, R SEARBY, CC TI MAPPING OF 2 LOCI FOR X-LINKED RECESSIVE CHARCOT-MARIE-TOOTH NEUROPATHY SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract ID LINKAGE C1 UNIV IOWA,DEPT PEDIAT,IOWA CITY,IA 52242. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02129. N YORK GEN HOSP,CTR CLIN GENET DIAGNOST,N YORK M2K 1E1,ONTARIO,CANADA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 2068 EP 2068 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900556 ER PT J AU GUIGO, R KNUDSEN, S DRAKE, N SMITH, TF AF GUIGO, R KNUDSEN, S DRAKE, N SMITH, TF TI A RULE-BASED APPROACH FOR GENE STRUCTURE RECOGNITION SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RI sebastianovitsch, stepan/G-8507-2013; Guigo, Roderic/D-1303-2010 OI Guigo, Roderic/0000-0002-5738-4477 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 2146 EP 2146 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900691 ER PT J AU SCHUFFENECKER, I NAROD, SA EZEKOWITZ, RAB SOBOL, H FEUNTEUN, J LENOIR, GM AF SCHUFFENECKER, I NAROD, SA EZEKOWITZ, RAB SOBOL, H FEUNTEUN, J LENOIR, GM TI THE GENE FOR MANNOSE-BINDING PROTEIN MAPS TO CHROMOSOME-10 AND IS A MARKER FOR MULTIPLE ENDOCRINE NEOPLASIA TYPE-2 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID MEDULLARY-THYROID CARCINOMA; LINKAGE ANALYSIS; POLYMORPHISM; COMPLEMENT; LECTINS; PATHWAY AB Human mannose-binding lectin (MBL) is a serum protein which appears to function as an opsonin in first line host defense. In situ hybridization studies assign the human MBL gene to chromosome 10q11.2 --> q21. A restriction fragment length polymorphism (RFLP) was found using TaqI with a 0.8-kb cDNA probe for MBL (probe 48-11), yielding heterozysity in 34% of individuals tested. Using this biallelic RFLP, linkage analysis of 30 families confirms the assignment of MBL to the region of multiple endocrine neoplasia, type 2a (MEN2A) with a maximum lod score of 7.54 at a recombination fraction of 0.00 (males) and 0.097 females). The presence of two crossovers between MEN2A and MBL in these families indicates that a defect of MBL itself is not the cause of the hereditary thyroid cancer syndrome. The addition of MBL to the genetic map of the pericentromeric region of chromosome 10 should prove useful for improved localization of the MEN2A mutation. C1 INT AGCY RES CANC,150 COURS ALBERT THOMAS,F-69372 LYONS,FRANCE. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. INST GUSTAVE ROUSSY,F-94805 VILLEJUIF,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. CTR LEON BERARD,GENET ONCOL UNIT,F-69373 LYONS,FRANCE. CTR HOSP LYON SUD,F-69310 PIERRE BENITE,FRANCE. NR 27 TC 16 Z9 16 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 56 IS 2 BP 99 EP 102 DI 10.1159/000133058 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA FF587 UT WOS:A1991FF58700008 PM 1672848 ER PT J AU RUVKUN, G WIGHTMAN, B BURGLIN, T ARASU, P AF RUVKUN, G WIGHTMAN, B BURGLIN, T ARASU, P TI DOMINANT GAIN-OF-FUNCTION MUTATIONS THAT LEAD TO MISREGULATION OF THE C-ELEGANS HETEROCHRONIC GENE LIN-14, AND THE EVOLUTIONARY IMPLICATIONS OF DOMINANT MUTATIONS IN PATTERN-FORMATION GENES SO DEVELOPMENT LA English DT Article; Proceedings Paper CT JOINT MEETING OF THE 9TH JOHN INNES SYMP / BRITISH SOC FOR DEVELOPMENT BIOLOGY : MOLECULAR AND CELLULAR BASIS OF PATTERN FORMATION CY SEP, 1990 CL UNIV E ANGLIA, NORWICH, ENGLAND SP BRIT SOC DEV BIOL HO UNIV E ANGLIA DE HETEROCHRONIC GENES; C-ELEGANS; LIN-14 GENE; CELL LINEAGE; DOMINANT MUTATION; EVOLUTION ID NEMATODE CAENORHABDITIS-ELEGANS; EPIDERMAL GROWTH-FACTOR; DEVELOPMENTAL SWITCH; MOLECULAR-GENETICS; HOMEOTIC GENE; CELL LINEAGE; RNA-BINDING; DROSOPHILA; PROTEINS; SEQUENCES AB The heterochronic gene lin-14 controls the temporal sequence of developmental events in the C. elegans postembryonic cell lineage. It encodes a nuclear protein that is normally present in most somatic cells of late embryos and L1 larvae but not in later larval stages or adults. Two lin-14 gain-of-function mutations cause an inappropriately high level of the lin-14 nuclear protein late in development. These mutations delete 3' untranslated sequences from the lin-14 mRNAs and identify a negative regulatory element that controls the formation of the lin-14 protein temporal gradient. The 21 kb lin-14 gene contains 13 exons that are differentially spliced to generate two lin-14 protein products with variable N-terminal regions and a constant C-terminal region. No protein sequence similarity to any proteins in various databases was found. The temporal and cellular expression patterns of lin-14 protein accumulation is altered by mutations in the heterochronic genes lin-4 and lin-28. The lin-4 gene is required to down-regulate lin-14 protein levels during the mid-L1 stage. The lin-4 gene product could be the trans-acting factor that binds to the negative regulatory element in the lin-14 3' untranslated region. In contrast, the lin-28 gene activity positively regulates lin-14 protein levels during early L1. Thus, these genes act antagonistically to regulate the lin-14 temporal switch. The normal down-regulation of lin-14 within 10 h of hatching is not determined by the passage of time per se, but rather is triggered when feeding induces post-embryonic development. Loss of lin-28 gene activity causes precocious down-regulation of lin-14 protein levels before feeding, whereas loss of lin-4 gene activity does not affect the level of lin-14 protein before feeding. These data suggest that to trigger the lin-14 temporal switch, the lin-4 gene is up-regulated after feeding which in turn down-regulates lin-14 via its 3' untranslated region. We speculate on the evolutionary implications of dominant mutations in pattern-formation genes. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP RUVKUN, G (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. OI arasu, prema/0000-0003-1962-8773 NR 46 TC 2 Z9 2 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PY 1991 SU 1 BP 47 EP 54 PG 8 WC Developmental Biology SC Developmental Biology GA GA050 UT WOS:A1991GA05000007 ER PT J AU KOLODNY, EH RAGHAVAN, S KRIVIT, W AF KOLODNY, EH RAGHAVAN, S KRIVIT, W TI LATE-ONSET KRABBE DISEASE (GLOBOID-CELL LEUKODYSTROPHY) - CLINICAL AND BIOCHEMICAL FEATURES OF 15 CASES SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE KRABBE DISEASE; GLOBOID CELL LEUKODYSTROPHY; GALACTOCEREBROSIDASE; SPASTIC TETRAPARESIS; BONE MARROW TRANSPLANTATION ID LEUCODYSTROPHY; INFANTILE AB The diagnosis of late-onset variants of Krabbe disease (globoid cell leukodystrophy) has been facilitated by the recognition of galactocerebrosidase deficiency as its biochemical hallmark. Fifteen patients, ages 4-73, are presented. Signs included pes cavus, optic disc pallor, progressive spastic tetraparesis, a sensorimotor demyelinating neuropathy and hypodense lesions in the parieto-occipital periventricular white matter. Although intellect was preserved in more than half the cases, significant intrafamilial variability in mental functioning was encountered in 3 families. Bone marrow transplantation was successful in 1 13-year-old girl, but caused the death of 2 teenage twin sisters. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. UNIV MINNESOTA,SCH MED,DEPT PEDIAT,MINNEAPOLIS,MN 55455. RP KOLODNY, EH (reprint author), EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,200 TRAPELO RD,WALTHAM,MA 02254, USA. NR 22 TC 68 Z9 70 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PY 1991 VL 13 IS 4-5 BP 232 EP 239 DI 10.1159/000112166 PG 8 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA GW321 UT WOS:A1991GW32100010 PM 1817026 ER PT J AU OKAMOTO, M KARASIK, A WHITE, MF KAHN, CR AF OKAMOTO, M KARASIK, A WHITE, MF KAHN, CR TI COORDINATE PHOSPHORYLATION OF INSULIN-RECEPTOR KINASE AND ITS 175,000-MR ENDOGENOUS SUBSTRATE IN RAT HEPATOCYTES SO DIABETES LA English DT Article ID GROWTH FACTOR-I; STIMULATES TYROSINE PHOSPHORYLATION; INTACT-CELLS; PROTEIN; ADIPOCYTES; GLYCOPROTEIN; ANTIBODY C1 JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-31036, DK-36836, DK-33201] NR 30 TC 9 Z9 9 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD JAN PY 1991 VL 40 IS 1 BP 66 EP 72 DI 10.2337/diabetes.40.1.66 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EN929 UT WOS:A1991EN92900010 PM 1849850 ER PT J AU NATHAN, DM FOGEL, HA GODINE, JE LOU, PL DAMICO, DJ REGAN, CDJ TOPPING, TM AF NATHAN, DM FOGEL, HA GODINE, JE LOU, PL DAMICO, DJ REGAN, CDJ TOPPING, TM TI ROLE OF DIABETOLOGIST IN EVALUATING DIABETIC-RETINOPATHY SO DIABETES CARE LA English DT Article ID PREVALENCE; DIAGNOSIS; AGE; OPHTHALMOSCOPY; PHOTOGRAPHY; DURATION; RISK AB Objective: To evaluate the ability of diabetologists to screen diabetic patients for diabetic retinopathy. Research Design and Methods: Comparison of eye examination performed by diabetologists with direct ophthalmoscopy through an undilated pupil and by opthalmologists through a dilated pupil with seven-field stereoscopic fundus photography (gold standard). The study consisted of 67 insulin-dependent and non-insulin-dependent diabetic outpatients attending a diabetes clinic. Results: On the basis of fundus photography, patients were classified as having no or insignificant (30%), minimal (31%), moderate (24%), or severe (15%) retinopathy. The diabetologists and opthalmologists performed similarly in their ability to classify severity of diabetic retinopathy accurately. When no or insignificant retinopathy (isolated microaneurysms only) was detected by examination, clinically significant retinopathy detected by fundus photography was highly unlikely (< 5%). On the other hand, if more than isolated microaneurysms were seen on examination, all examiners missed more severe lesions detected by fundus photography. Patients with corrected visual acuity worse than 20/30 had a high likelihood (100%) of moderate or severe retinopathy. Conclusions: Motivated well-trained diabetologists can screen for diabetic retinopathy. The absence of detectable lesions by direct ophthalmoscopy indicates that automatic referral to an opthalmologist is not necessary. However, if any level of retinopathy is detected or corrected acuity is worse than 20/30, referral to an ophthalmologist is required. In this setting, fundus photography is advised because it is th most sensitive means of detecting clinically significant retinopathy. If other nonophthalmologists can be trained to achieve similar results, current recommendations for ophthalmologic referral that require annual ophthalmologic examinations for most diabetic patients may need to be reconsidered. C1 MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. MASSACHUSETTS EYE & EAR HOSP, DIABET RETINA CLIN, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT OPHTHALMOL, BOSTON, MA 02115 USA. RP NATHAN, DM (reprint author), MASSACHUSETTS GEN HOSP, DIABET UNIT, 32 FRUIT ST, BOSTON, MA 02114 USA. NR 20 TC 39 Z9 39 U1 0 U2 2 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 JAN PY 1991 VL 14 IS 1 BP 26 EP 33 DI 10.2337/diacare.14.1.26 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EP576 UT WOS:A1991EP57600005 PM 1991432 ER PT J AU BONADONNA, RC DEFRONZO, RA AF BONADONNA, RC DEFRONZO, RA TI GLUCOSE-METABOLISM IN OBESITY AND TYPE-2 DIABETES SO DIABETES & METABOLISM LA English DT Article; Proceedings Paper CT INTERNATIONAL WORKSHOP ON NON-INSULIN DEPENDENT DIABETES TODAY CY SEP 07-08, 1990 CL HELSINGOR, DENMARK DE NIDDM; OBESITY; INSULIN-RESISTANCE; INSULIN SECRETION; GLUCOSE METABOLISM ID BODY-FAT DISTRIBUTION; HUMAN SKELETAL-MUSCLE; HEPATIC GLYCOGEN FORMATION; AMINO-ACID METABOLISM; INVIVO INSULIN ACTION; RAT ADIPOSE-CELLS; MAGNETIC-RESONANCE SPECTROSCOPY; SYNTHASE PHOSPHATASE-ACTIVITY; TRANSPORTER MESSENGER-RNA; PANCREATIC BETA-CELLS AB The aim of this review is to provide a comprehensive summary of the subject of glucose metabolism in normal and obese subjects, and in those with type 2 diabetes. The following topics are discussed: - Glucose and insulin metabolism, including characterization of the role of various organs in maintaining glucose homeostasis in the basal state and after food. - The action of insulin and the concept of insulin resistance, its main characteristics as revealed by studies of glucose metabolism in liver and skeletal muscle, the two organs primarily involved. Changes in insulin secretion in obese subjects and in diabetics are reviewed. - Finally, the development of diabetes as a consequence of increasing insulin resistance in the obese diabetic subject is discussed. The principal features - insulin resistance, elevated free fatty acid levels and glucotoxicity - are emphasized. A possible explanation of how obesity leads to diabetes, emphasizing the role played by upper body fat distribution, is provided. C1 UNIV TEXAS,HLTH SCI CTR,DIV DIABET,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP BONADONNA, RC (reprint author), UNIV PISA,CNR,INST CLIN PHYSIOL,I-56100 PISA,ITALY. FU NCRR NIH HHS [MOI-RR-01346]; NIDDK NIH HHS [DK24092] NR 240 TC 39 Z9 40 U1 0 U2 1 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0338-1684 J9 DIABETES METAB JI Diabetes Metab. PY 1991 VL 17 IS 1BIS BP 112 EP 135 PG 24 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FP437 UT WOS:A1991FP43700008 PM 1936466 ER PT J AU KRALL, LP AF KRALL, LP TI THE TREATMENT OF NIDDM IN THE DECADE OF THE 90S SO DIABETES RESEARCH AND CLINICAL PRACTICE LA English DT Article; Proceedings Paper CT INTERNATIONAL DIAMICRON SYMP CY SEP 24, 1991 CL MONTREAL, CANADA SP SERVIER INT RES INST FRANCE, SERVIER CANADA ID TOLBUTAMIDE; GLICLAZIDE AB On the occasion of the introduction of gliclazide (Diamicron(R)) in Canada, it seems useful to assess the use of oral hypoglycemics in the treatment of NIDDM. Various types of diabetes occur when insufficient insulin is produced or when various factors reduce the receptor efficacy. Most of the factors involved are favorably affected by the action of sulfonylureas. Many NIDDM patients exhibit poor compliance with regard to exercise and diet, and require oral hypoglycemics. Combinations of oral hypoglycemics and insulin are very useful in patients responding poorly to either type of treatment since this gives effective insulin levels with improved receptor activity. Diamicron(R) offers advantages since it reduces blood glucose effectively, has few side effects and no evidence of long-term problems or toxicity. Studies have shown that there is a significant antiplatelet aggregation effect and a beneficial effect on the fibrinolytic system with gliclazide (but not necessarily with other oral hypoglycemics), which may be useful in preventing or attenuating some long-term complications of diabetes, e.g. diabetic retinopathy. In a study at the Joslin Clinic, three groups of patients with NIDDM were examined: dietary failures, secondary failures with first generation oral hypoglycemics, and poorly regulated patients treated with insulin. After three months of treatment with Diamicron(R), all 10 dietary failure patients improved, as did three of the 10 secondary failure cases and five of the insulin-treated patients. Receptor studies indicated increased sensitivity in some cases, without a consistent change in numbers. Some patients with the poorest response to insulin alone had the best results with combined therapy, although it took almost eight weeks to achieve this. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KRALL, LP (reprint author), JOSLIN DIABETES CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 10 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 0168-8227 J9 DIABETES RES CLIN PR JI Diabetes Res. Clin. Pract. PY 1991 VL 14 SU 2 BP S15 EP S20 DI 10.1016/0168-8227(91)90004-W PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GZ563 UT WOS:A1991GZ56300004 PM 1794261 ER PT J AU GANDA, OP AF GANDA, OP TI MICROALBUMINURIA - MEASUREMENTS, DETERMINANTS AND ACCOMPANIMENTS SO DIABETES RESEARCH AND CLINICAL PRACTICE LA English DT Editorial Material ID DIABETIC SUBJECTS RP GANDA, OP (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 18 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0168-8227 J9 DIABETES RES CLIN PR JI Diabetes Res. Clin. Pract. PY 1991 VL 11 IS 3 BP 137 EP 140 DI 10.1016/S0168-8227(05)80025-7 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FC571 UT WOS:A1991FC57100001 PM 2036935 ER PT J AU NEBERT, DW NELSON, DR COON, MJ ESTABROOK, RW FEYEREISEN, R FUJIIKURIYAMA, Y GONZALEZ, FJ GUENGERICH, FP GUNSALUS, IC JOHNSON, EF LOPER, JC SATO, R WATERMAN, MR WAXMAN, DJ AF NEBERT, DW NELSON, DR COON, MJ ESTABROOK, RW FEYEREISEN, R FUJIIKURIYAMA, Y GONZALEZ, FJ GUENGERICH, FP GUNSALUS, IC JOHNSON, EF LOPER, JC SATO, R WATERMAN, MR WAXMAN, DJ TI THE P450 SUPERFAMILY - UPDATE ON NEW SEQUENCES, GENE-MAPPING, AND RECOMMENDED NOMENCLATURE SO DNA AND CELL BIOLOGY LA English DT Article ID AMINO-ACID SEQUENCE; CDNA-DIRECTED EXPRESSION; YEAST CANDIDA-TROPICALIS; NUCLEOTIDE-SEQUENCE; MOLECULAR-CLONING; MESSENGER-RNAS; HUMAN-LIVER; CHROMOSOMAL LOCALIZATION; CYTOCHROME-P450 CDNA; RAT AB We provide here a list of 154 P450 genes and seven putative pseudogenes that have been characterized as of October 20, 1990. These genes have been described in a total of 23 eukaryotes (including nine mammalian and one plant species) and six prokaryotes. Of 27 gene families so far described, 10 exist in all mammals. These 10 families comprise 18 subfamilies, of which 16 and 14 have been mapped in the human and mouse genomes, respectively; to date, each subfamily appears to represent a cluster of tightly linked genes. We propose here a modest revision of the initially proposed (Nebert et al., DNA 6, 1-11, 1987) and updated (Nebert et al., DNA 8, 1-13, 1989) nomenclature system based on evolution of the superfamily. For the gene we recommend that the italicized root symbol CYP for human (Cyp for mouse), representing cytochrome P450, be followed by an Arabic number denoting the family, a letter designating the subfamily (when two or more exist), and an Arabic numeral representing the individual gene within the subfamily. A hyphen should precede the final number in mouse genes. We suggest that the human nomenclature system be used for other species. This system is consistent with our earlier proposed nomenclature for P450 of all eukaryotes and prokaryotes, except that we are discouraging the future use of cumbersome Roman numerals. C1 UNIV N CAROLINA,DEPT BIOCHEM & BIOPHYS,CHAPEL HILL,NC 27599. UNIV MICHIGAN,DEPT BIOL CHEM,ANN ARBOR,MI 48109. UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235. OREGON STATE UNIV,DEPT ENTOMOL,CORVALLIS,OR 97331. TOHOKU UNIV,FAC SCI,DEPT CHEM,SENDAI,MIYAGI 980,JAPAN. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. VANDERBILT UNIV,MED CTR,SCH MED,DEPT BIOCHEM,NASHVILLE,TN 37232. VANDERBILT UNIV,MED CTR,SCH MED,CTR MOLEC TOXICOL,NASHVILLE,TN 37232. UNIV ILLINOIS,DEPT BIOCHEM,URBANA,IL 61801. SCRIPPS CLIN & RES FDN,DEPT BASIC & CLIN RES,LA JOLLA,CA 92037. UNIV CINCINNATI,MED CTR,DEPT MOLEC GENET BIOCHEM & MICROBIOL,CINCINNATI,OH 45267. OSAKA UNIV,INST PROT RES,OSAKA 565,JAPAN. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP NEBERT, DW (reprint author), UNIV CINCINNATI,MED CTR,DEPT ENVIRONM HLTH,CINCINNATI,OH 45267, USA. RI Feyereisen, Rene/I-3140-2012; OI Feyereisen, Rene/0000-0002-9560-571X; Nelson, David/0000-0003-0583-5421 NR 115 TC 1111 Z9 1126 U1 3 U2 40 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1044-5498 J9 DNA CELL BIOL JI DNA Cell Biol. PD JAN-FEB PY 1991 VL 10 IS 1 BP 1 EP 14 DI 10.1089/dna.1991.10.1 PG 14 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA EU671 UT WOS:A1991EU67100001 PM 1991046 ER PT J AU WONG, M BRUCE, S JOSEPH, D LIVELY, H AF WONG, M BRUCE, S JOSEPH, D LIVELY, H TI ESTIMATING LEFT-VENTRICULAR EJECTION FRACTION FROM 2-DIMENSIONAL ECHOCARDIOGRAMS - VISUAL AND COMPUTER-PROCESSED INTERPRETATIONS SO ECHOCARDIOGRAPHY-A JOURNAL OF CARDIOVASCULAR ULTRASOUND AND ALLIED TECHNIQUES LA English DT Article DE DIGITAL ECHOCARDIOGRAPHY; EJECTION FRACTION; INTRAOBSERVER ERRORS AB Digital echocardiography makes computer-processed estimates of ejection fraction feasible for clinical use but increases physician reading time. The practicabilities were examined by three novice fellows and four experienced attendings. Ejection fraction was visually estimated from playback of videotape or cine-loop displays. Ejection fraction was also estimated from single tracings of endocardium, digitized and applied to biplane Simpson's rule, and expressed in whole units. Differences between fellows' and attendings' visual estimates were close to 0 +/- 6.4 median standard deviation. The 95% confidence intervals for reproducing visual and computer-processed ejection fractions ranged from 15% to 46% of mean ejection fraction; for comparing the two methods, from 7% to 36%. Intraobserver reading errors varied widely and with one observer, systematically, and were independent of experience, but dependent on the quality of signals. Computer-processed readings of ejection fraction should be reserved for images of reasonable quality and for confirming visually estimated ejection fractions between the lower limits of normal (45%-50%) to moderately severely depressed (25%-30%), when accuracy is clinically relevant or when a serial change is at the confidence limits of the reader and needs verification. RP WONG, M (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,CARDIOL SECT W111E,LOS ANGELES,CA 90073, USA. NR 0 TC 16 Z9 16 U1 0 U2 0 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 0742-2822 J9 ECHOCARDIOGR-J CARD JI Echocardiography-J. Cardiovasc. Ultrasound Allied Tech. PD JAN PY 1991 VL 8 IS 1 BP 1 EP 7 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA EX710 UT WOS:A1991EX71000001 PM 10149242 ER PT J AU CALLAWAY, E AF CALLAWAY, E TI TOWARDS A PHARMACOLOGY OF INFORMATION-PROCESSING - DISCUSSION SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Discussion C1 SAN FRANCISCO VET ADM MED CTR,TIBURON,CA 94920. NR 4 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 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PY 1991 SU 42 BP 173 EP 176 PG 4 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA HB514 UT WOS:A1991HB51400019 ER PT J AU CHIAPPA, KH CROS, D DAY, B FANG, JJ MACDONELL, R MAVROUDAKIS, N AF CHIAPPA, KH CROS, D DAY, B FANG, JJ MACDONELL, R MAVROUDAKIS, N TI MAGNETIC STIMULATION OF THE HUMAN MOTOR CORTEX - IPSILATERAL AND CONTRALATERAL FACILITATION EFFECTS SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article; Proceedings Paper CT SYMP ON TRANSCRANIAL MAGNETIC STIMULATION AND THE MOTOR EVOKED POTENTIAL CY AUG, 1989 CL CHICAGO, IL SP E PARALYZED VET ASSOC, NATL PARALYSIS ASSOC, CHICAGO NEUROSURG CTR, FDN INVESTIGAT NEUROL DISORDERS, AMER PARALYSIS ASSOC DE MOTOR EVOKED POTENTIAL; FACILITATION ID BRAIN-STIMULATION; INTACT MAN; ELECTRICAL-STIMULATION; NERVOUS PROPAGATION; RESPONSES; MUSCLES; PATHWAYS; EXCITABILITY; NEURONS; SCALP AB Voluntary contraction of a muscle greatly increases the amplitude and decreases the latency of the motor potentials evoked by electromagnetic coil brain stimulation (facilitation). Facilitation has also been observed with contraction of a nearby ipsilateral and a contralateral homologous muscle. We studied these facilitatory relationships in 5 normal subjects in small hand, forearm and upper arm muscles using surface-recorded compound motor action potentials, single motor unit recordings, and post stimulus time histograms. There was no evidence for spread of facilitation between any pair of muscles if the muscle from which motor evoked potentials (MEPs) were recorded was completely at rest during brain stimulation, although this sometimes required training to accomplish or could not be achieved. Thus, although spread of facilitation has been observed by others under these conditions, we did not find this effect. There may be significant interindividual variations in the degree of facilitatory spread. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,CLIN NEUROPHYSIOL LAB,BOSTON,MA 02114. NR 39 TC 3 Z9 3 U1 1 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PY 1991 SU 43 BP 186 EP 201 PG 16 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA HB515 UT WOS:A1991HB51500016 ER PT B AU DANDREA, AD KOO, JW AF DANDREA, AD KOO, JW BE GURLAND, HJ MORAN, J SAMTLEBEN, W SCIGALLA, P WIECZOREK, L TI STRUCTURE AND FUNCTION OF THE ERYTHROPOIETIN RECEPTOR IN STABLE ERYTHROPOIETIN-DEPENDENT TRANSFECTANTS SO ERYTHROPOIETIN IN RENAL AND NON-RENAL ANEMIAS: UPDATE ON BASIC RESEARCH AND CLINICAL APPLICATIONS SE CONTRIBUTIONS TO NEPHROLOGY LA English DT Proceedings Paper CT 3RD INTERNATIONAL WORKSHOP ON TREATMENT OF ANEMIA WITH RECOMBINANT HUMAN ERTHROPOIETIN CY JUN 07-10, 1990 CL TELFS BUCHEN, AUSTRIA SP BOEHRINGER MANNHEIM RP DANDREA, AD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5272-6 J9 CONTRIB NEPHROL JI Contrib.Nephrol. PY 1991 VL 88 BP 48 EP 56 PG 9 WC Genetics & Heredity; Pharmacology & Pharmacy; Urology & Nephrology SC Genetics & Heredity; Pharmacology & Pharmacy; Urology & Nephrology GA BS94D UT WOS:A1991BS94D00005 PM 1645637 ER PT B AU GUSELLA, JF AF GUSELLA, JF BE LINDSTEN, J PETTERSSON, U TI DNA MARKERS IN NEUROGENETIC DISORDERS SO ETIOLOGY OF HUMAN DISEASE AT THE DNA LEVEL SE NOBEL SYMPOSIUM LA English DT Proceedings Paper CT NOBEL SYMP ON THE ETIOLOGY OF HUMAN DISEASE AT THE DNA LEVEL CY JUN 11-14, 1990 CL KARLSKOGA, SWEDEN SP NOBEL FDN, ALFRED NOBELS BJORKBORN FDN RP GUSELLA, JF (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-761-2 J9 NOBEL SYMP PY 1991 VL 80 BP 71 EP 80 PG 10 WC Genetics & Heredity; Pathology SC Genetics & Heredity; Pathology GA BT27H UT WOS:A1991BT27H00007 ER PT J AU BULLER, R MAIER, W GOLDENBERG, IM LAVORI, PW BENKERT, O AF BULLER, R MAIER, W GOLDENBERG, IM LAVORI, PW BENKERT, O TI CHRONOLOGY OF PANIC AND AVOIDANCE, AGE OF ONSET IN PANIC DISORDER, AND PREDICTION OF TREATMENT RESPONSE - A REPORT FROM THE CROSS-NATIONAL COLLABORATIVE PANIC STUDY SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE LA English DT Article DE PANIC DISORDER; AGE OF ONSET; AVOIDANCE BEHAVIOR; AGORAPHOBIA; TREATMENT RESPONSE; IMIPRAMINE; ALPRAZOLAM ID PSYCHIATRIC-DISORDERS; LIFETIME PREVALENCE; ANXIETY DISORDERS; MAJOR DEPRESSION; AGORAPHOBIA; ATTACKS AB The relevance of the chronology between panic disorder and avoidance behavior and of an early, medium or late onset of panic disorder was tested. Groups from the sample of the cross-national collaborative panic study (CNCPS) were compared for differences in basic characteristics and for the ability to predict treatment response. Patients who developed avoidance behavior before the full syndrome of panic disorder had less often a full agoraphobia but were not different in their response to treatment. Patients with an early onset of panic disorder suffered more often from agoraphobia. The treatment response was similar in the groups with early, medium or late onset of panic disorder. Neither the chronology between panic disorder and avoidance behavior nor the age of onset of panic disorder predicted outcome in short-term treatment with alprazolam or imipramine. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BIOSTAT UNIT,BOSTON,MA 02114. RP BULLER, R (reprint author), UNIV MAINZ,DEPT PSYCHIAT,UNTERE ZAHLBACHER STR 8,W-6500 MAINZ,GERMANY. NR 32 TC 10 Z9 10 U1 4 U2 7 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0940-1334 J9 EUR ARCH PSY CLIN N JI Eur. Arch. Psych. Clin. Neurosci. PY 1991 VL 240 IS 3 BP 163 EP 168 DI 10.1007/BF02190758 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA EY956 UT WOS:A1991EY95600006 PM 1827602 ER PT J AU ZIETMAN, AL SUIT, HD OKUNIEFF, PG DONNELLY, SM DIEMAN, S WEBSTER, S AF ZIETMAN, AL SUIT, HD OKUNIEFF, PG DONNELLY, SM DIEMAN, S WEBSTER, S TI THE LIFE SHORTENING EFFECTS OF TREATMENT WITH DOXORUBICIN AND OR LOCAL IRRADIATION ON A COHORT OF YOUNG C3HF/SED MICE SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID RADIATION; TUMORS; ADRIAMYCIN; DIHYDROXYANTHRAQUINONE; SURVIVAL; THERAPY; CANCER; RATS AB The long-term consequences of treating a cohort of C3Hf/Sed mice in early life with either local-field single dose radiation, systemic doxorubicin, or both, are reported in this study. Significant life shortening was observed in all treatment groups. Median survival times (days) from time of treatment were: control, 690; 35 Gy, 560; 70 Gy, 460; 5 mg/kg doxorubicin, 580; 10 mg/kg doxorubicin, 350; 35 Gy + 5 mg/kg doxorubicin, 510; 70 Gy + 10 mg/kg doxorubicin, 310. Mice receiving hind limb irradiation died principally from induced sarcomas in a dose dependent fashion (80% after 70 Gy and 55% after 35 Gy). Those treated with doxorubicin alone showed an increase in the actuarial incidence of spontaneous malignancies but died mainly from non-malignant causes. Histological examination did not reveal any characteristic cardiac, renal or pulmonary lesions. Doxorubicin did not increase the rate of development of radiation induced sarcomas in mice treated with combined modality. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT RADIAT BIOL,EDWIN STEELE LAB,BOSTON,MA 02114. FU NCI NIH HHS [CA13311] NR 21 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1991 VL 27 IS 6 BP 778 EP 781 DI 10.1016/0277-5379(91)90188-J PG 4 WC Oncology SC Oncology GA FW011 UT WOS:A1991FW01100027 PM 1829923 ER PT J AU PIERI, P YASUDA, T FISCHMAN, AJ AHMAD, M MOORE, R YAOITA, H STRAUSS, HW AF PIERI, P YASUDA, T FISCHMAN, AJ AHMAD, M MOORE, R YAOITA, H STRAUSS, HW TI MYOCARDIAL ACCUMULATION AND CLEARANCE OF TC-99M TEBOROXIME AT 100-PERCENT, 75-PERCENT, 50-PERCENT AND ZERO CORONARY BLOOD-FLOW IN DOGS SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE TEBOROXIME; MYOCARDIAL PERFUSION; TECHNETICUM; RADIONUCLIDE IMAGING ID PLASMINOGEN-ACTIVATOR; IMAGING AGENT; PERFUSION; SQ30217; STREPTOKINASE; THROMBOLYSIS; SQ-30217; KINETICS; TL-201 AB Sequential changes in the regional distribution of technetium-99m-Teboroxime (SQ30217) were evaluated in nine dogs with graded coronary artery stenosis, occlusion and reperfusion of either the left anterior descending or left circumflex arteries. Tc-99m-Teboroxime accumulation recorded by planar imaging was compared with directly measured coronary blood flow (Doppler) and regional myocardial perfusion (microspheres). Serial images were recorded beginning at the time of injection and continuing for the next 18 min. The data were summed from minutes 2-3, 3-6, 4-8 and 9-18 after injection for comparison with the other parameters. Myocardial clearance of Teboroxime was analysed at each level of blood flow. There was a linear relationship between the Teboroxime activity ratio (abnormal/normal) and coronary blood flow (r = 0.96) and regional myocardial perfusion (r = 0.99). Zones of diminished perfusion were least apparent in the summed images recorded during minutes 2-3. In later images, the lesions were well visualized. The myocardial clearance half-times at 100%, 75% and 50% flow were not significantly different, while clearance half-time at total occlusion was significantly (P < 0.01) faster. In the 3-6, 4-8 and 9-18 minutes summed images, the Teboroxime activity ratio increased significantly (P < 0.01) after reperfusion compared with total occlusion. C1 HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. RP STRAUSS, HW (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 15 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6997 J9 EUR J NUCL MED JI Eur. J. Nucl. Med. PY 1991 VL 18 IS 9 BP 725 EP 731 DI 10.1007/BF00956713 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GE584 UT WOS:A1991GE58400004 PM 1936048 ER PT J AU NIKAIDO, T BRADLEY, DW PARDEE, AB AF NIKAIDO, T BRADLEY, DW PARDEE, AB TI MOLECULAR-CLONING OF TRANSCRIPTS THAT ACCUMULATE DURING THE LATE G1 PHASE IN CULTURED MOUSE CELLS SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID RESTRICTION POINT CONTROL; KINASE MESSENGER-RNA; GROWTH FACTOR-I; C-FOS GENE; NUCLEOTIDE-SEQUENCE; TRANSFORMED-CELLS; DNA-SYNTHESIS; G0/G1 TRANSITION; PROTO-ONCOGENE; 3T3 CELLS C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DIV MED SCI,PROGRAM CELL & DEV BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULATION,BOSTON,MA 02115. FU NIGMS NIH HHS [GM 24571] NR 49 TC 34 Z9 34 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD JAN PY 1991 VL 192 IS 1 BP 102 EP 109 DI 10.1016/0014-4827(91)90163-O PG 8 WC Oncology; Cell Biology SC Oncology; Cell Biology GA EP869 UT WOS:A1991EP86900015 PM 1984406 ER PT J AU OBERLEY, TD ALLEN, RG SCHULTZ, JL LAUCHNER, LJ AF OBERLEY, TD ALLEN, RG SCHULTZ, JL LAUCHNER, LJ TI ANTIOXIDANT ENZYMES AND STEROID-INDUCED PROLIFERATION OF KIDNEY TUBULAR CELLS SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Note DE ANTIOXIDANT ENZYMES; LIPOSOMES; PROLIFERATION; CELL CULTURE; FREE RADICALS AB Diethylstilbestrol induces proliferation of Syrian hamster renal proximal tubular cells. By counting the number of cells in culture, we showed that liposomes containing superoxide dismutase or catalase suppressed diethylstibestrol-induced proliferation, whereas empty liposomes or liposomes containing inactivated superoxide dismutase did not. Liposomes containing antioxidant enzymes did not suppress proliferation of cells in control media or of cells treated with ethinyl estradiol. In the absence of liposomes, exogenous superoxide dismutase did not suppress diethylstilbestrol-induced proliferation. The decrease in cell number when diethylstilbestrol-treated cells were treated with antioxidant enzyme-containing liposomes was not due to decreased cell viability. Results were confirmed by measuring a correlate of cell proliferation immunohistochemically, using an antibody to proliferation cell nuclear antigen. A larger proportion of diethylstilbestrol-treated cells than of control cells showed nuclear immunostaining with this antibody. The number of cells immunostained in diethylstilbestrol-treated cultures was sharply decreased by the addition of superoxide dismutase- or catalase-containing liposomes. Our studies suggest a role for active oxygen species in diethylstilbestrol-induced proliferation of cultured proximal tubular cells. RP OBERLEY, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SECT,LAB SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA 22008] NR 0 TC 19 Z9 19 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1991 VL 10 IS 1 BP 79 EP 83 DI 10.1016/0891-5849(91)90024-W PG 5 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA EY737 UT WOS:A1991EY73700012 PM 2050299 ER PT B AU BAND, H PORCELLI, SA PANCHAMOORTHY, G MCLEAN, J MORITA, CT ISHIKAWA, S MODLIN, RL BRENNER, MB AF BAND, H PORCELLI, SA PANCHAMOORTHY, G MCLEAN, J MORITA, CT ISHIKAWA, S MODLIN, RL BRENNER, MB BE PFEFFER, K HEEG, K WAGNER, H RIETHMULLER, G TI ANTIGENS AND ANTIGEN-PRESENTING MOLECULES FOR GAMMA-DELTA T-CELLS SO FUNCTION AND SPECIFICITY OF GAMMA/DELTA T CELLS SE CURRENT TOPICS IN MICROBIOLOGY AND IMMUNOLOGY LA English DT Proceedings Paper CT INTERNATIONAL WORKSHOP ON FUNCTION AND SPECIFICITY OF GAMMA/DELTA T CELLS CY OCT 14-16, 1990 CL SCHLOSS ELMAU, FED REP GER SP DEUT FORTSCHUNGSGEMEINSCH ID MAJOR HISTOCOMPATIBILITY COMPLEX; DENDRITIC EPIDERMAL-CELLS; HUMAN LYMPHOCYTES-T; HEAT-SHOCK PROTEIN; MYCOBACTERIUM-TUBERCULOSIS; RECEPTOR GENES; RECOGNITION; CLONES; SPECIFICITY; IDENTIFICATION RP BAND, H (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOCHEM LAB,BOSTON,MA 02115, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN PA BERLIN BN 3-540-53781-3 J9 CURR TOP MICROBIOL JI Curr.Top.Microbiol.Immunol. PY 1991 VL 173 BP 229 EP 234 PG 6 WC Biochemistry & Molecular Biology; Immunology; Microbiology SC Biochemistry & Molecular Biology; Immunology; Microbiology GA BT82B UT WOS:A1991BT82B00032 ER PT J AU WINTER, HS HENDREN, RB FOX, CH RUSSELL, GJ PEREZATAYDE, A BHAN, AK FOLKMAN, J AF WINTER, HS HENDREN, RB FOX, CH RUSSELL, GJ PEREZATAYDE, A BHAN, AK FOLKMAN, J TI HUMAN INTESTINE MATURES AS NUDE-MOUSE XENOGRAFT SO GASTROENTEROLOGY LA English DT Article ID NORMAL COLONIC MUCOSA; ATHYMIC MICE; ADENOMATOUS POLYPS; TRANSPLANTATION; DIFFERENTIATION; ADENOCARCINOMA; ANTIBODIES; RATS C1 CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP WINTER, HS (reprint author), CHILDRENS HOSP MED CTR,DEPT PEDIAT,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI27747]; NIDDK NIH HHS [DK33506] NR 19 TC 36 Z9 37 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JAN PY 1991 VL 100 IS 1 BP 89 EP 98 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA EM765 UT WOS:A1991EM76500013 PM 1983853 ER PT J AU RUSSELL, GJ HARMATZ, PR AF RUSSELL, GJ HARMATZ, PR TI MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II EXPRESSION ON ENTEROCYTES - TO PRESENT OR NOT TO PRESENT SO GASTROENTEROLOGY LA English DT Editorial Material ID RAT SMALL-INTESTINE; EPITHELIAL-CELLS; ANTIGEN PRESENTATION; LYMPHOCYTES; INDUCTION; DISEASE; SYSTEM RP RUSSELL, GJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 27 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JAN PY 1991 VL 100 IS 1 BP 274 EP 276 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA EM765 UT WOS:A1991EM76500040 PM 1983833 ER PT J AU LEE, EY WANG, TC CLOUSE, RE DESCHRYVERKECSKEMETI, K AF LEE, EY WANG, TC CLOUSE, RE DESCHRYVERKECSKEMETI, K TI GASTRIC-CARCINOMA, EPIDERMAL GROWTH-FACTOR, AND EPIDERMAL GROWTH-FACTOR RECEPTOR SO GASTROENTEROLOGY LA English DT Letter C1 MASSACHUSETTS GEN HOSP,DIV GASTROENTEROL,BOSTON,MA 02114. WASHINGTON UNIV,MED CTR,DIV GASTROENTEROL,ST LOUIS,MO 63110. CASE WESTERN RESERVE UNIV,INST PATHOL,CLEVELAND,OH 44106. RP LEE, EY (reprint author), UNIV KENTUCKY,MARKEY CANC CTR,DEPT PATHOL,LEXINGTON,KY 40536, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JAN PY 1991 VL 100 IS 1 BP 289 EP 289 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA EM765 UT WOS:A1991EM76500043 PM 2006930 ER PT J AU FLETCHER, JA KOZAKEWICH, HP PAVELKA, K GRIER, HE SHAMBERGER, RC KORF, B MORTON, CC AF FLETCHER, JA KOZAKEWICH, HP PAVELKA, K GRIER, HE SHAMBERGER, RC KORF, B MORTON, CC TI CONSISTENT CYTOGENETIC ABERRATIONS IN HEPATOBLASTOMA - A COMMON PATHWAY OF GENETIC ALTERATIONS IN EMBRYONAL LIVER AND SKELETAL-MUSCLE MALIGNANCIES SO GENES CHROMOSOMES & CANCER LA English DT Article ID BECKWITH-WIEDEMANN SYNDROME; NEURO-BLASTOMA; DOUBLE-MINUTES; SOLID TUMORS; N-MYC; RHABDOMYOSARCOMA; PROGNOSIS; CHILDHOOD; CARCINOMA; ONCOGENE AB Cytogenetic analyses of four consecutive hepatoblastomas revealed near-diploid stemline karyotypes with relatively simple chromosome aberrations. Cytogenetic abnormalities shared by each tumor included trisomy for all of part of chromosome 2 and trisomy for chromosome 20. In two cases, partial trisomy for chromosome 2 resulted from direct duplication of long arm material with the shortest region of overlap being 2q23-2q35. In one tumor, each metaphase also contained a variable number of double minute chromosomes found not to derive from NMYC amplification. Interestingly, trisomy for 2q and trisomy 20 are also characteristic events in pediatric embryonal rhabdomyosarcomas. Furthermore, others have reported loss of heterozygosity for the short arm of chromosome 11 in both hepatoblastoma and childhood embryonal rhabdomyosarcoma, and both these malignant diseases are associated with Beckwith-Wiedemann syndrome. These cytogenetic and molecular findings suggest a parallel pathway of genetic steps in the initiation and/or progression of tumors of embryonal liver and skeletal muscle. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP FLETCHER, JA (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NIA NIH HHS [AGG00294] NR 24 TC 56 Z9 56 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 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD JAN PY 1991 VL 3 IS 1 BP 37 EP 43 DI 10.1002/gcc.2870030107 PG 7 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA EY238 UT WOS:A1991EY23800006 PM 1648956 ER PT B AU HASELTINE, WA AF HASELTINE, WA BE HASELTINE, WA WONGSTAAL, F TI REGULATION OF HIV-1 REPLICATION BY TAT AND REV SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP HASELTINE, WA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 11 Z9 11 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 1 EP 42 PG 42 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00001 ER PT B AU HELLAND, DE REPKE, H CAPUTO, A HASELTINE, WA AF HELLAND, DE REPKE, H CAPUTO, A HASELTINE, WA BE HASELTINE, WA WONGSTAAL, F TI THE EXOGENOUS TRANSACTIVATION ACTIVITY OF HIV-1 TAT SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP HELLAND, DE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 301 EP 310 PG 10 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00017 ER PT B AU KALLAND, KH LANGHOFF, E BOS, HJ GOTTLINGER, H HASELTINE, WA AF KALLAND, KH LANGHOFF, E BOS, HJ GOTTLINGER, H HASELTINE, WA BE HASELTINE, WA WONGSTAAL, F TI RETROVIRAL REGULATORY PROTEINS AND THE NUCLEOLUS SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP KALLAND, KH (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 377 EP 390 PG 14 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00023 ER PT B AU LU, YC HEY, A TOUZJIAN, N STENZEL, M HASELTINE, W AF LU, YC HEY, A TOUZJIAN, N STENZEL, M HASELTINE, W BE HASELTINE, WA WONGSTAAL, F TI CELLULAR TRANSCRIPTION FACTORS WHICH REGULATE HIV-1 REPLICATION SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP LU, YC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 415 EP 435 PG 21 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00026 ER PT B AU TERWILLIGER, EF LANGHOFF, E HASELTINE, WA AF TERWILLIGER, EF LANGHOFF, E HASELTINE, WA BE HASELTINE, WA WONGSTAAL, F TI THE NEF GENE OF HIV-1 - A REVIEW OF RECENT RESULTS SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP TERWILLIGER, EF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 457 EP 471 PG 15 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00029 ER PT B AU LANGHOFF, E TERWILLIGER, EF KALLAND, KH POZNANSKY, MC BOS, H BACON, OML SODROSKI, JS HASELTINE, WA AF LANGHOFF, E TERWILLIGER, EF KALLAND, KH POZNANSKY, MC BOS, H BACON, OML SODROSKI, JS HASELTINE, WA BE HASELTINE, WA WONGSTAAL, F TI HIV-1 INFECTION OF HUMAN DENDRITIC CELLS SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP LANGHOFF, E (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 511 EP 525 PG 15 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00033 ER PT B AU RAUCH, SD NEUMANN, PE AF RAUCH, SD NEUMANN, PE BE RUBEN, RJ VANDEWATER, TR STEEL, KP TI MALFORMATION AND DEGENERATION IN THE INNER-EAR OF MOS TRANSGENIC MICE SO GENETICS OF HEARING IMPAIRMENT SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON GENETICS OF HEARING IMPAIRMENT CY SEP 24-26, 1990 CL NEW YORK, NY SP NEW YORK ACAD SCI, DEAFNESS RES FDN, NIH NIDCD RP RAUCH, SD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [K08 DC00012] NR 0 TC 0 Z9 0 U1 1 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-682-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 630 BP 268 EP 269 DI 10.1111/j.1749-6632.1991.tb19601.x PG 2 WC Genetics & Heredity; Neurosciences; Otorhinolaryngology SC Genetics & Heredity; Neurosciences & Neurology; Otorhinolaryngology GA BW41A UT WOS:A1991BW41A00033 PM 1952602 ER PT J AU ALLITTO, BA MACDONALD, ME BUCAN, M RICHARDS, J ROMANO, D WHALEY, WL FALCONE, B IANAZZI, J WEXLER, NS WASMUTH, JJ COLLINS, FS LEHRACH, H HAINES, JL GUSELLA, JF AF ALLITTO, BA MACDONALD, ME BUCAN, M RICHARDS, J ROMANO, D WHALEY, WL FALCONE, B IANAZZI, J WEXLER, NS WASMUTH, JJ COLLINS, FS LEHRACH, H HAINES, JL GUSELLA, JF TI INCREASED RECOMBINATION ADJACENT TO THE HUNTINGTON DISEASE-LINKED D4S10 MARKER SO GENOMICS LA English DT Article ID SOMATIC MAMMALIAN-CELLS; G8 D4S10; INSITU HYBRIDIZATION; DNA MARKERS; GENE; LOCUS; CHROMOSOME-4; LOCALIZATION; D4S90; FRAGMENTS C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. COLUMBIA UNIV,DEPT NEUROL,NEW YORK,NY 10032. HEREDITARY DIS FDN,SANTA MONICA,CA 90401. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. RP ALLITTO, BA (reprint author), MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114, USA. RI Haines, Jonathan/C-3374-2012 FU NINDS NIH HHS [NS22031, NS16367, NS20012] NR 40 TC 52 Z9 53 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 JAN PY 1991 VL 9 IS 1 BP 104 EP 112 DI 10.1016/0888-7543(91)90226-5 PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA EP972 UT WOS:A1991EP97200013 PM 1672283 ER PT J AU MISSON, JP TAKAHASHI, T CAVINESS, VS AF MISSON, JP TAKAHASHI, T CAVINESS, VS TI ONTOGENY OF RADIAL AND OTHER ASTROGLIAL CELLS IN MURINE CEREBRAL-CORTEX SO GLIA LA English DT Article DE ASTROCYTES; RADIAL GLIA; NEOCORTEX; HISTOGENESIS ID FIBRILLARY ACIDIC PROTEIN; CENTRAL NERVOUS-SYSTEM; GLIAL-CELLS; REELER MOUSE; FETAL MONKEY; ASTROCYTES; RAT; WALL; TRANSFORMATION; NEOCORTEX AB Three cell forms of astroglial lineage populate the prenatal and early postnatal murine cerebral wall. In the present review we consider the ontogeny of these cell forms with respect to histogenetic events of the perinatal period. Classic bipolar radial glial cells predominate prior to E17. The bipolar coexist with monopolar radial forms in the perinatal period. Both bipolar and monopolar radial forms coexist with multipolar astrocytes in the course of the first postnatal week and are ultimately succeeded by the multipolar cells. The shift from bipolar cells from the ventricular zone to the upper intermediate zone and cortical strata. Arborization appears to occur both at the growing tips and along the shaft of the processes of both bipolar and monopolar radial cell types. As arborization continues, the processes of the monopolar radial cells come to resemble those of the multipolar astrocytes. Eventually the radial cells are fully transformed into the multipolar astrocytic forms. During this period of transition, radial processes in the cortex appear to be degenerating, suggesting that regressive processes contribute to the cytologic transformation. This sequence of transformations begins late in the period of neuronal migration and continues through the early stages of growth and differentiation in the murine cerebral cortex. The signals that induce these changes may arise from differentiating neurons within the cortex. These transformations occur at a time when radial glial fibers are no longer required as guides for neuronal migration, and the glial population assumes new roles related to the development and operation of cortical neuronal circuits. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT NEUROL DEV NEUROBIOL,BOSTON,MA 02114. STATE UNIV LIEGE,SCH MED,PHYSIOL & DEV NEUROBIOL LAB,B-4000 LIEGE,BELGIUM. FU NINDS NIH HHS [NS 12005] NR 50 TC 190 Z9 191 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 0894-1491 J9 GLIA JI Glia PY 1991 VL 4 IS 2 BP 138 EP 148 DI 10.1002/glia.440040205 PG 11 WC Neurosciences SC Neurosciences & Neurology GA FC745 UT WOS:A1991FC74500004 PM 1709615 ER PT J AU PRAGER, JM ROSENBLUM, J MIKULIS, DJ DIAMOND, S FREITAG, FG AF PRAGER, JM ROSENBLUM, J MIKULIS, DJ DIAMOND, S FREITAG, FG TI EVALUATION OF HEADACHE PATIENTS BY MRI SO HEADACHE QUARTERLY-CURRENT TREATMENT AND RESEARCH LA English DT Article ID WHITE-MATTER LESIONS; MIGRAINE; DEMENTIA AB One hundred patients with severe headache were examined by magnetic resonance. The most common abnormalities seen are focal white matter abnormalities (WMA) on the long TR images. Forty-seven percent of 58 patients with common migraine had WMA. Forty-four percent of 19 patients with classic migraine showed WMA. The frequency increased with patient age. The relationship between WMA, the duration of symptoms, and a history of vasoactive medication is examined. The remainder of the patients had cluster, tension-type (muscle contraction), or post-traumatic headaches, Our results suggest that WMA are seen with increased frequency in patients with migraine. These abnormalities may reflect a low grade vascular insufficiency with resulting perivascular gliosis. C1 UNIV CHICAGO,DEPT RADIOL,DIV NEURORADIOL,CHICAGO,IL 60637. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. LOUIS A WEISS MEM HOSP,DIAMOND HEADACHE CLIN,CHICAGO,IL. LOUIS A WEISS MEM HOSP,IMPATIENT HEADACHE UNIT,CHICAGO,IL. CHICAGO MED SCH,PHARMACOL & MOLEC BIOL,N CHICAGO,IL. NR 11 TC 10 Z9 10 U1 0 U2 0 PU INT UNIV PRESS INC PI MADISON PA 59 BOSTON POST RD PO BOX 1524, MADISON, CT 06443-1524 J9 HEADACHE Q-CURR TREA JI Headache Q.-Curr. Treat. Res. PY 1991 VL 2 IS 3 BP 192 EP 196 PG 5 WC Neurosciences SC Neurosciences & Neurology GA GL567 UT WOS:A1991GL56700005 ER PT B AU LEAF, A AF LEAF, A BE SIMOPOULOS, AP KIFER, RR MARTIN, RE BARLOW, SM TI CARDIOVASCULAR .1. CELL-VESSEL WALL INTERACTIONS SO HEALTH EFFECTS OF OMEGA3 POLYUNSATURATED FATTY ACIDS IN SEAFOODS SE WORLD REVIEW OF NUTRITION AND DIETETICS LA English DT Proceedings Paper CT 2ND INTERNATIONAL CONF ON THE HEALTH EFFECTS OF OMEGA3 POLYUNSATURATED FATTY ACIDS IN SEAFOOD CY MAR 20-23, 1990 CL WASHINGTON, DC SP US DEPT COMMERCE, NATL OCEAN & ATMOSPER ADM, NATL MARINE FISHERIES SERV, AMER ASSOC WORLD HLTH, CTR GENET NUTRIT & HLTH, INT ASSOC FISH MEAL MANUFACTURERS, NATL FISHERIES INST, US FDA, NCI, NIAAA, NIH, NIAMSD, NICHHD RP LEAF, A (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5244-0 J9 WORLD REV NUTR DIET JI World Rev.Nutr.Diet. PY 1991 VL 66 BP 31 EP 33 PG 3 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA BS88U UT WOS:A1991BS88U00007 PM 2053346 ER PT B AU HALLAQ, H LEAF, A AF HALLAQ, H LEAF, A BE SIMOPOULOS, AP KIFER, RR MARTIN, RE BARLOW, SM TI EFFECTS OF OMEGA-3 AND OMEGA-6 POLYUNSATURATED FATTY-ACIDS ON THE ACTION OF CARDIAC-GLYCOSIDES ON CULTURED RAT MYOCARDIAL-CELLS SO HEALTH EFFECTS OF OMEGA3 POLYUNSATURATED FATTY ACIDS IN SEAFOODS SE WORLD REVIEW OF NUTRITION AND DIETETICS LA English DT Proceedings Paper CT 2ND INTERNATIONAL CONF ON THE HEALTH EFFECTS OF OMEGA3 POLYUNSATURATED FATTY ACIDS IN SEAFOOD CY MAR 20-23, 1990 CL WASHINGTON, DC SP US DEPT COMMERCE, NATL OCEAN & ATMOSPER ADM, NATL MARINE FISHERIES SERV, AMER ASSOC WORLD HLTH, CTR GENET NUTRIT & HLTH, INT ASSOC FISH MEAL MANUFACTURERS, NATL FISHERIES INST, US FDA, NCI, NIAAA, NIH, NIAMSD, NICHHD RP HALLAQ, H (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PREVENT MED,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK 38165] NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5244-0 J9 WORLD REV NUTR DIET JI World Rev.Nutr.Diet. PY 1991 VL 66 BP 250 EP 254 PG 5 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA BS88U UT WOS:A1991BS88U00027 PM 1905086 ER PT J AU STRONG, A WOLFF, H KINDER, S LUBISCHER, A AF STRONG, A WOLFF, H KINDER, S LUBISCHER, A TI DRUG ADMINISTRATION IN RELATION TO MEALS IN THE INSTITUTIONAL SETTING SO HEART & LUNG LA English DT Article AB To investigate adherence to literature recommendations for administration of five cardiovascular drugs in relation to mealtimes, data from records of 183 adult patients in two short-term and two long-term care settings were tabulated. Ninety-three percent of patients taking quinidine sulfate and 85% of patients taking the other four study drugs received one or more doses incorrectly. Findings show that timing recommendations for dosing in relation to meals are not considered in these institutions when drug administration schedules are established. The practice of arbitrary schedule selection could have serious consequences, including adverse physiologic and financial impact on the patient from loss of therapeutic effectiveness or development of drug toxicosis. Medication schedules need to be designed to achieve the greatest drug bioavailability. RP STRONG, A (reprint author), PORTLAND VET AFFAIRS MED CTR,ANP 111B,POB 1034,PORTLAND,OR 97207, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0147-9563 J9 HEART LUNG JI Heart Lung PD JAN PY 1991 VL 20 IS 1 BP 39 EP 44 PG 6 WC Cardiac & Cardiovascular Systems; Nursing; Respiratory System SC Cardiovascular System & Cardiology; Nursing; Respiratory System GA EW501 UT WOS:A1991EW50100009 PM 1988391 ER PT J AU BARNHILL, RL BARNHILL, MA BERWICK, M MIHM, MC AF BARNHILL, RL BARNHILL, MA BERWICK, M MIHM, MC TI THE HISTOLOGIC SPECTRUM OF PIGMENTED SPINDLE CELL NEVUS - A REVIEW OF 120 CASES WITH EMPHASIS ON ATYPICAL VARIANTS SO HUMAN PATHOLOGY LA English DT Review DE MELANOCYTIC NEVUS; MELANOMA; SKIN C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. YALE UNIV,SCH MED,DEPT EPIDEMIOL & PUBL HLTH,NEW HAVEN,CT 06510. RP BARNHILL, RL (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,DIV DERMATOPATHOL,WARREN 827,BOSTON,MA 02114, USA. RI Berwick, Marianne/E-9608-2010; OI Berwick, Marianne/0000-0001-5062-2180 NR 10 TC 62 Z9 62 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 JAN PY 1991 VL 22 IS 1 BP 52 EP 58 DI 10.1016/0046-8177(91)90061-S PG 7 WC Pathology SC Pathology GA ET395 UT WOS:A1991ET39500009 PM 1985078 ER PT J AU EGEA, GE YUNIS, I SPIES, T STROMINGER, J AWDEH, ZL ALPER, CA YUNIS, EJ AF EGEA, GE YUNIS, I SPIES, T STROMINGER, J AWDEH, ZL ALPER, CA YUNIS, EJ TI ASSOCIATION OF POLYMORPHISMS IN THE HLA-B REGION WITH EXTENDED HAPLOTYPES SO IMMUNOGENETICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; GENES; IDENTIFICATION; VARIANTS; CLUSTER; DNA AB Genomic probes from the HLA-B region of the major histocompatibility complex (MHC) were used to study the association of restriction fragment length polymorphisms (RFLPs) with various MHC alleles, complotypes, and extended haplotypes. The two DNA probes, M20A and R5A, were derived from previously cloned cosmids and are located 38 and 110 kilobases (kb) centromeric to HLA-B, respectively. Five different RFLP variants occurring in five different haplotypic combinations were detected within a panel of 40 homozygous-typing cells and cells from 21 families using Bst EII. In two informative families with HLA-B/DR recombinations the inheritance of the RFLP variants was consistent with their mapping between HLA-B and complotypes. The R5A/M20A haplotypic pattern 6.5 kb/3.0 kb (A) had a normal Caucasian frequency of approximately 0.43 and was found in all independent examples of the extended haplotypes [HLA-B8,SCO1,DR3], [HLA-B18,F1C30, DR3], [HLA-Bw62,SC33,DR4], [HLA-B44,SC30,DR4], and [HLA-Bw47,FC91,0,DR7]. The patterns 6.9 kb/3.0 kb (B), 6.5 kb/4.7 kb (C), 1.45 kb/3.0 kb (D), and 6.9 kb/4.7 kb (E) had normal Caucasian frequencies of approximately 0.23, 0.15, 0.15, and 0.04 and were found on all independent examples of [HLA-B38,SC21, DR4], [HLA-Bw57,SC61,DR7], [HLA-B7,SC31,DR2], and [HLA-B44,FC31,DR7], respectively. Individual complotypes or HLA-B alleles which were markers of extended haplotypes showed variable associations. For example, HLA-B7 and the complotype SC31 were associated with all R5A/M20A RFLP haplotypes except haplotype E, although [HLA-B7,SC31,DR7] was associated exclusively with haplotype D. HLA-B27, not known to be part of an extended haplotype, was surprisingly exclusively associated with the 6.5 kb/4.7 kb or C haplotypic pattern in all five instances tested. These findings support the concept of regional conservation of DNA on independent examples of extended haplotypes. The results also further characterize these haplotypes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. AMER RED CROSS,BLOOD SERV,NE REG,DEDHAM,MA 02026. CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. FU NCI NIH HHS [CA 20531]; NHLBI NIH HHS [HL 29583]; NIAID NIH HHS [AI 14157] NR 21 TC 29 Z9 29 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JAN PY 1991 VL 33 IS 1 BP 4 EP 11 PG 8 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA EV728 UT WOS:A1991EV72800002 PM 1671666 ER PT J AU CEBRA, JJ CUFF, CF RUBIN, DH AF CEBRA, JJ CUFF, CF RUBIN, DH TI RELATIONSHIP BETWEEN ALPHA/BETA T-CELL RECEPTOR/CD8+ PRECURSORS FOR CYTOTOXIC LYMPHOCYTES-T IN THE PEYER,MURINE PATCHES AND THE INTRAEPITHELIAL COMPARTMENT PROBED BY ORAL INFECTION WITH REOVIRUS SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID PEYERS PATCHES C1 VET AFFAIRS MED CTR,DEPT MED,PHILADELPHIA,PA. RP CEBRA, JJ (reprint author), UNIV PENN,DEPT BIOL,415 S UNIV AVE,PHILADELPHIA,PA 19104, USA. NR 4 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 321 EP 323 DI 10.1007/BF02919715 PG 3 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600028 PM 1659604 ER PT J AU AAGAARD, J GASSER, T RHODES, P MADSEN, PO AF AAGAARD, J GASSER, T RHODES, P MADSEN, PO TI MICS OF CIPROFLOXACIN AND TRIMETHOPRIM FOR ESCHERICHIA-COLI - INFLUENCE OF PH, INOCULUM SIZE AND VARIOUS BODY-FLUIDS SO INFECTION LA English DT Article; Proceedings Paper CT 7TH SILS MARIA SYMP : PROSTATITIS CY 1990 CL SILS MARIA, SWITZERLAND SP BAYER ID INVITRO ACTIVITY; PROSTATIC FLUID AB The influence of pH, inoculum size, human urine and prostatic extract on the MICs of ciprofloxacin and trimethoprim for Escherichia coli was investigated. There was no influence by the bacterial inoculum size within wide ranges on either drug. An increase in pH had a variable influence on the MICs of trimethoprim for E. coli but lowered those of ciprofloxacin considerably. Human prostatic extract increased the trimethoprim MIC for E. coli but lowered those of ciprofloxacin as compared to Mueller Hinton broth. Human urine increased the MICs of both drugs for E. coli. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,TECH LAB,MADISON,WI 53705. KANTONSSPITAL,UROL ABT,CH-4004 BASEL,SWITZERLAND. RP AAGAARD, J (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 5 TC 8 Z9 8 U1 0 U2 2 PU MMW MEDIZIN VERLAG GMBH PI MUNICH 80 PA NEUMARKTER STRASSE 18, W-8000 MUNICH 80, GERMANY SN 0300-8126 J9 INFECTION JI Infection PY 1991 VL 19 SU 3 BP S167 EP S169 DI 10.1007/BF01643691 PG 3 WC Infectious Diseases SC Infectious Diseases GA FJ043 UT WOS:A1991FJ04300015 PM 2055655 ER PT J AU FRICK, J MADSEN, PO RUTISHAUSER NEAL FOWLER, JE WEIDNER, W SCHAEFFER, AJ BERGMAN GASSER, T PFAU, A NICKEL, JC ECHOLS BLENK, H RIEDASCH, G NABER, KG MARGET, W SVENSON KALLENIUS PHILPOTT, AC MADSEN, PO BAERT, L RUSKIN BUSCH AF FRICK, J MADSEN, PO RUTISHAUSER NEAL FOWLER, JE WEIDNER, W SCHAEFFER, AJ BERGMAN GASSER, T PFAU, A NICKEL, JC ECHOLS BLENK, H RIEDASCH, G NABER, KG MARGET, W SVENSON KALLENIUS PHILPOTT, AC MADSEN, PO BAERT, L RUSKIN BUSCH TI PROSTATITIS - (VII-SILS-MARIA SYMPOSIUM 1990) - DISCUSSIONS SO INFECTION LA English DT Discussion C1 UNIV ILLINOIS,COLL MED,DIV UROL,CHICAGO,IL 60680. UNIV GOTTINGEN,UROL KLIN,W-3400 GOTTINGEN,GERMANY. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. KANTONSSPITAL,UROL ABT,CH-4004 BASEL,SWITZERLAND. HADASSAH MED CTR,IL-91120 JERUSALEM,ISRAEL. QUEENS UNIV,KINGSTON GEN HOSP,DEPT UROL,KINGSTON K7L 2V7,ONTARIO,CANADA. LAB MED MIKROBIOL & IMMUNOL,W-8500 NURNBERG 90,GERMANY. UNIV HEIDELBERG,ZENTRUM CHIRURG,UROL ABT,W-6900 HEIDELBERG,GERMANY. ELISABETH HOSP,UROL KLIN,W-8440 STRAUBING,GERMANY. UNIV COLORADO,HLTH SCI CTR,DIV UROL,DENVER,CO 80262. WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SERV,MADISON,WI 53705. UNIV ZIEKENHUIS ST PETER,DEPT UROL,B-3000 LOUVAIN,BELGIUM. RP FRICK, J (reprint author), LANDESKRANKENANSTALTEN SALZBURG,UROL ABT,MULLNER HAUPTSTR 48,A-5020 SALZBURG,AUSTRIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MMW MEDIZIN VERLAG GMBH PI MUNICH 80 PA NEUMARKTER STRASSE 18, W-8000 MUNICH 80, GERMANY SN 0300-8126 J9 INFECTION JI Infection PY 1991 VL 19 SU 3 BP S178 EP S188 PG 11 WC Infectious Diseases SC Infectious Diseases GA FJ043 UT WOS:A1991FJ04300017 ER PT J AU MADSEN, PO AAGAARD, J AF MADSEN, PO AAGAARD, J TI PHARMACOKINETICS OF QUINOLONE DERIVATIVES IN THE PROSTATE SO INFECTION LA English DT Article; Proceedings Paper CT 7TH SILS MARIA SYMP : PROSTATITIS CY 1990 CL SILS MARIA, SWITZERLAND SP BAYER ID CHRONIC BACTERIAL PROSTATITIS; FLUID AB The pharmacokinetics of six quinolone derivatives were investigated in the human and dog prostate. The possible therapeutic applications of these findings are discussed. RP MADSEN, PO (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,UROL SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 7 TC 2 Z9 2 U1 0 U2 0 PU MMW MEDIZIN VERLAG GMBH PI MUNICH 80 PA NEUMARKTER STRASSE 18, W-8000 MUNICH 80, GERMANY SN 0300-8126 J9 INFECTION JI Infection PY 1991 VL 19 SU 3 BP S154 EP S156 DI 10.1007/BF01643687 PG 3 WC Infectious Diseases SC Infectious Diseases GA FJ043 UT WOS:A1991FJ04300011 PM 1647370 ER PT J AU KIRKLAND, TN QURESHI, N TAKAYAMA, K AF KIRKLAND, TN QURESHI, N TAKAYAMA, K TI DIPHOSPHORYL LIPID-A DERIVED FROM LIPOPOLYSACCHARIDE (LPS) OF RHODOPSEUDOMONAS-SPHAEROIDES INHIBITS ACTIVATION OF 70Z/3 CELLS BY LPS SO INFECTION AND IMMUNITY LA English DT Article ID NF-KAPPA-B; STRUCTURAL DETERMINATION; SALMONELLA-TYPHIMURIUM; TRANSCRIPTION; INDUCTION; PURIFICATION; ATCC-17023; PRECURSORS; LOCATION; MUTANT AB Diphosphoryl lipid A derived from nontoxic lipopolysaccharide (LPS) of Rhodopseudomonas sphaeroides ATCC 17023 did not stimulate the murine pre-B cell line 70Z/3 to synthesize surface immunoglobulin or kappa mRNA. However, it effectively blocked Escherichia coli LPS-induced activation of 70Z/3 cells in a concentration-dependent manner. This inhibition was specific only to cells activated by LPS, since it did not inhibit activation of 70Z/3 cells by gamma interferon. Maximal inhibitory effect occurred when the antagonist was added within 2 h before adding the LPS. These results strongly suggested that R. sphaeroides diphosphoryl lipid A is competing with E. coli LPS for physiological lipid A receptors on the 70Z/3 cells. C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. VET ADM MED CTR,SAN DIEGO,CA 92161. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL LAB,MADISON,WI 53705. RP KIRKLAND, TN (reprint author), UNIV CALIF SAN DIEGO,DEPT PATHOL,LA JOLLA,CA 92093, USA. FU NIGMS NIH HHS [GM-36054] NR 26 TC 56 Z9 56 U1 1 U2 1 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 JAN PY 1991 VL 59 IS 1 BP 131 EP 136 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP751 UT WOS:A1991EP75100020 PM 1898897 ER PT J AU QURESHI, N TAKAYAMA, K KURTZ, R AF QURESHI, N TAKAYAMA, K KURTZ, R TI DIPHOSPHORYL-LIPID-A OBTAINED FROM THE NONTOXIC LIPOPOLYSACCHARIDE OF RHODOPSEUDOMONAS-SPHAEROIDES IS AN ENDOTOXIN ANTAGONIST IN MICE SO INFECTION AND IMMUNITY LA English DT Note ID TUMOR NECROSIS FACTOR; PERFORMANCE LIQUID-CHROMATOGRAPHY; COMPLETE STRUCTURAL DETERMINATION; SALMONELLA-TYPHIMURIUM; ESCHERICHIA-COLI; PURIFICATION; ATCC-17023; INDUCTION; INTERLEUKIN-1; MECHANISMS AB Diphosphoryl lipid A (DPLA) obtained from the nontoxic lipopolysaccharide (LPS) of Rhodopseudomonas sphaeroides ATCC 17023 did not induce interleukin-1 release by murine peritoneal macrophages. However, it blocked this induction by toxic deep-rough chemotype LPS (ReLPS) from Escherichia coli D31m4. Previously, we obtained similar results on the induction of tumor necrosis factor (TNF) by macrophages. These results showed that DPLA is able to block in vitro the induction of two important mediators of gram-negative bacterial sepsis. We then wanted to determine whether DPLA could also block the induction of TNF by LPS in animals. Mice were treated with 100-mu-g of R. sphaeroides DPLA and challenged 60 min later with 1.0-mu-g of ReLPs from E. coli. The serum TNF level was measured after 60 min. Treatment of mice with this DPLA blocked the rapid and transient rise of TNF caused by ReLPS. This result suggested that R. sphaeroides DPLA might be able to protect animals against endotoxin shock caused by gram-negative bacterial infection. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. FU NIAID NIH HHS [AI-25856]; NIGMS NIH HHS [GM-36054] NR 31 TC 106 Z9 107 U1 0 U2 1 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 JAN PY 1991 VL 59 IS 1 BP 441 EP 444 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP751 UT WOS:A1991EP75100065 PM 1987057 ER PT J AU HARTSTEIN, AI WARD, TT AF HARTSTEIN, AI WARD, TT TI METHICILLIN-RESISTANT STAPHYLOCOCCUS-AUREUS SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Editorial Material C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP HARTSTEIN, AI (reprint author), OREGON HLTH SCI UNIV,DEPT MED,DIV INFECT DIS,L457,3181 SAM JACKSON PK RD,PORTLAND,OR 97201, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD JAN PY 1991 VL 12 IS 1 BP 9 EP 10 PG 2 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA FM812 UT WOS:A1991FM81200004 PM 1999646 ER PT J AU ZAPOL, WM AF ZAPOL, WM TI A NORDIC ECMO SAGA OR WHITHER ECMO SO INTENSIVE CARE MEDICINE LA English DT Editorial Material ID AIRWAY PRESSURE RP ZAPOL, WM (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114, USA. NR 3 TC 9 Z9 9 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0342-4642 J9 INTENS CARE MED JI Intensive Care Med. PY 1991 VL 17 IS 2 BP 69 EP 70 DI 10.1007/BF01691424 PG 2 WC Critical Care Medicine SC General & Internal Medicine GA FE509 UT WOS:A1991FE50900001 PM 1865038 ER PT J AU ALBERT, M SMITH, LA SCHERR, PA TAYLOR, JO EVANS, DA FUNKENSTEIN, HH AF ALBERT, M SMITH, LA SCHERR, PA TAYLOR, JO EVANS, DA FUNKENSTEIN, HH TI USE OF BRIEF COGNITIVE TESTS TO IDENTIFY INDIVIDUALS IN THE COMMUNITY WITH CLINICALLY DIAGNOSED ALZHEIMERS-DISEASE SO INTERNATIONAL JOURNAL OF NEUROSCIENCE LA English DT Article DE EPIDEMIOLOGY; ALZHEIMERS DISEASE; SCREENING TESTS; COGNITION, ELDERLY ID MINI-MENTAL STATE; POPULATION; DEMENTIA; CAPACITY; HEALTH C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV NEUROL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,CHANNING LAB,BOSTON,MA 02115. RP ALBERT, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,MGH E,BOSTON,MA 02114, USA. FU NIA NIH HHS [N01-AG-12106, AG06789, N0I-AG-O-2107] NR 21 TC 344 Z9 344 U1 2 U2 5 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0020-7454 J9 INT J NEUROSCI JI Int. J. Neurosci. PY 1991 VL 57 IS 3-4 BP 167 EP 178 DI 10.3109/00207459109150691 PG 12 WC Neurosciences SC Neurosciences & Neurology GA FD170 UT WOS:A1991FD17000001 PM 1938160 ER PT J AU FAVA, M BOROFSKY, GF AF FAVA, M BOROFSKY, GF TI SEXUAL DISINHIBITION DURING TREATMENT WITH A BENZODIAZEPINE - A CASE-REPORT SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Article DE BENZODIAZEPINE; DISINHIBITION; SEXUAL BEHAVIOR; PANIC ATTACKS; ANTI-ANXIETY; SEXUAL PROMISCUITY ID PANIC DISORDER; LORAZEPAM WITHDRAWAL; ALPRAZOLAM; CLONAZEPAM; MANIA; SWITCH; DRUGS AB We are reporting a case of a woman with a history of drug abuse, alcohol abuse, and sexual promiscuity as a teenager who later on in life had become very religious, sober and sexually abstinent. A few years later, she began having anxiety and panic attacks, typically when in physical proximity to men and sought treatment. The patient became clearly sexually disinhibited while treated with clonazepam, a high potency anti-anxiety benzodiazepine, and her "inappropriate" sexual behavior ceased when the medication was discontinued. Given her history, it is likely that the medication weakened the already fragile defenses by the removal of the "warning signals" represented by her panic attacks. The result was a more direct expression of her sexual drive in the form of strip tease dancing and sexual promiscuity. This case suggests the importance of carefully examining the history of a patient's capacity for regulating sexual drive before prescribing an anti-anxiety drug. RP FAVA, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CLIN PSYCHOPHARMACOL UNIT,ACC-815,BOSTON,MA 02114, USA. NR 22 TC 9 Z9 9 U1 0 U2 0 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 1991 VL 21 IS 1 BP 99 EP 104 DI 10.2190/P43X-NQVX-UX70-46AT PG 6 WC Psychiatry SC Psychiatry GA FJ060 UT WOS:A1991FJ06000010 PM 2066261 ER PT J AU RAUCH, SL STERN, TA ZUSMAN, RM AF RAUCH, SL STERN, TA ZUSMAN, RM TI NEUROPSYCHIATRIC CONSIDERATIONS IN THE TREATMENT OF HYPERTENSION SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Article DE HYPERTENSION; NEUROPSYCHIATRY; SIDE EFFECTS; DEPRESSION; BETA-BLOCKERS; GANGLIONIC BLOCKERS; DIURETICS; CALCIUM CHANNEL BLOCKERS; ANGIOTENSIN CONVERTING ENZYME INHIBITORS; VASODILATORS ID ANTIHYPERTENSIVE THERAPY; MYOCARDIAL-INFARCTION; CALCIUM-ANTAGONISTS; BETA-BLOCKERS; PROPRANOLOL; VERAPAMIL; CLONIDINE; WITHDRAWAL; CAPTOPRIL; MANIA AB Algorithms have been developed to guide the treatment of simple hypertension. The basic algorithms are modified in the face of concurrent medical conditions, taking into account the various pharmacological effects of antihypertensive agents. This article reviews the neuropsychiatric effects of the major classes of antihypertensive agents (ganglionic blockers, centrally acting agents, diuretics, vasodilators, beta-blockers, calcium channel blockers and angiotensin converting enzyme inhibitors). The purported efficacy of some antihypertensive agents in the treatment of psychiatric conditions is also discussed. Beneficial as well as adverse neuropsychiatric effects are reviewed. In this way, guidelines for the treatment of hypertension are suggested which take into account a broad spectrum of neuropsychiatric considerations. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,WARREN 605 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 82 TC 2 Z9 2 U1 1 U2 1 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 1991 VL 21 IS 3 BP 291 EP 308 PG 18 WC Psychiatry SC Psychiatry GA GH608 UT WOS:A1991GH60800007 PM 1955279 ER PT J AU HAMBURG, P AF HAMBURG, P TI INTERPRETATION AND EMPATHY - READING LACAN WITH KOHUT SO INTERNATIONAL JOURNAL OF PSYCHO-ANALYSIS LA English DT Article RP HAMBURG, P (reprint author), MASSACHUSETTS GEN HOSP,GEN PSYCHIAT PRACTICE & EATING DISORDERS UNIT,ACC 805,BOSTON,MA 02114, USA. NR 13 TC 7 Z9 7 U1 0 U2 1 PU INST PSYCHO-ANALYSIS PI LONDON PA 63 NEW CAVENDISH STREET, LONDON, ENGLAND W1M 7RD SN 0020-7578 J9 INT J PSYCHOANAL JI Int. J. Psycho-Anal. PY 1991 VL 72 BP 347 EP 361 PN 2 PG 15 WC Psychology, Psychoanalysis SC Psychology GA FR603 UT WOS:A1991FR60300014 PM 1874595 ER PT J AU URANO, M KAHN, J REYNOLDS, R AF URANO, M KAHN, J REYNOLDS, R TI THE EFFECT OF 5-FLUOROURACIL AT ELEVATED-TEMPERATURES ON A SPONTANEOUS MOUSE-TUMOR - ARRHENIUS ANALYSIS AND TUMOR RESPONSE SO INTERNATIONAL JOURNAL OF RADIATION BIOLOGY LA English DT Article ID MURINE FIBRO-SARCOMA; HYPERTHERMIA; THERMOCHEMOTHERAPY; INVIVO; PH; PHARMACOKINETICS; FLUOROURACIL; COMBINATION; CARCINOMA; BLEOMYCIN AB In a series of studies to investigate activation energies and thermal enhancements of various chemotherapeutic agents the effect of 5-fluorouracil (5FU), an antimetabolite, on murine tumour cells was studied at elevated temperatures. Animal tumours were early generation isotransplants of a spontaneous fibrosarcoma, FSa-II tumours, and C3Hf/Sed mice were used throughout. Cell survival curves for 5FU were obtained as a function of treatment time by in vitro treatment-in vivo lung colony assay at temperatures between 37.0 and 43.5-degrees-C. The D0, or the treatment time to reduce surviving fraction from S to S/e in the exponential portion of the survival curve, decreased slightly from 37-degrees-C treatment to 41.5-degrees-C treatment. The D0 decreased substantially from 41.5-degrees-C to 43.5-degrees-C. Arrhenius-plot analysis indicated that the activation energies were 92.9 and 731 kJ/M at temperatures between 37 and 41.5-degrees-C, and between 41.5 and 43.5-degrees-C, respectively. The activation energy of 92.9 kJ/M for the temperature range from 37 to 41.5-degrees-C was the lowest of the other agents, bleomycin, cis-diamminedichloroplatinum and 1,3-bis(2-chloroethyl)-N-nitrosourea, which have been investigated in our laboratory. This indicated that the thermal enhancement was smallest among these agents. In vivo experiments failed to demonstrate thermal enhancement of the anti-tumour effect of 5FU. Namely, combined 5FU and heat treatments at 41.5 and 43.5-degrees-C did not prolong the tumour growth time compared with 5FU given at room temperature. No pH effect was found in an in vitro experiment and glucose administration did not enhance the anti-tumour effect of 5FU. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. RP URANO, M (reprint author), UNIV KENTUCKY,MED CTR,DEPT RADIAT MED,800 ROSE ST,LEXINGTON,KY 40536, USA. FU NCI NIH HHS [CA26350] NR 29 TC 9 Z9 9 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 JAN PY 1991 VL 59 IS 1 BP 239 EP 249 DI 10.1080/09553009114550211 PG 11 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 EV615 UT WOS:A1991EV61500021 PM 1671070 ER PT J AU PASTER, BJ LEE, A FOX, JG DEWHIRST, FE TORDOFF, LA FRASER, GJ OROURKE, JL TAYLOR, NS FERRERO, R AF PASTER, BJ LEE, A FOX, JG DEWHIRST, FE TORDOFF, LA FRASER, GJ OROURKE, JL TAYLOR, NS FERRERO, R TI PHYLOGENY OF HELICOBACTER-FELIS SP-NOV, HELICOBACTER-MUSTELAE, AND RELATED BACTERIA SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID PYLORI SUBSP MUSTELAE; CAMPYLOBACTER-PYLORI; SPIRAL ORGANISMS; GASTRIC ANTRUM; GENUS CAMPYLOBACTER; STOMACH; INFECTION; ABORTION; ANIMALS; DISEASE AB Strain CS1T (T = type strain) is a gram-negative, microaerophilic, urease-positive, spiral-shaped bacterium that was isolated from the gastric mucosa of a cat. Additional strains which possessed biochemical and ultrastructural characteristics similar to those of strain CS1T were isolated from the gastric mucosa of cats and dogs. The guanine-plus-cytosine content of the DNA of strain CS1T was 42.5 mol%. The 16S rRNA sequences of strain CS1T, strain DS3 (a spiral-shaped isolate from a dog), and Helicobacter mustelae were determined by direct RNA sequencing, using a modified Sanger method. These sequences were compared with the 16S rRNA sequences of Helicobacter pylori, "Flexispira rappini," Wolinella succinogenes, and 11 species of campylobacters. A dendrogram was constructed based upon sequence similarities. Strains CS1T and DS3 were very closely related (level of similarity, 99.3%). Two major phylogenetic groups were formed; one group consisted of strains CS1T and DS3, H. mustelae, H. pylori, "F. rappini," and W. succinogenes, and the other group contained the true campylobacters. The average level of similarity between members of these two groups was 84.9%. Within the first group, strains CS1T and DS3, H. pylori, and H. mustelae formed a cluster of organisms with an interspecies similarity level of 94.5%. The phylogenetic positions of W. succinogenes and "F. rappini" were just outside this cluster. On the basis of the results of this study, we believe that strains CS1T ( = ATCC 49179T) and DS3 represent a new species of the genus Helicobacter, for which we propose the name Helicobacter felis. C1 UNIV NEW S WALES,SYDNEY,NSW 2033,AUSTRALIA. MIT,DIV COMPARAT MED,CAMBRIDGE,MA 02139. RP PASTER, BJ (reprint author), FORSYTH DENT CTR,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-26731]; NIAID NIH HHS [AI-25590, AI-25631] NR 42 TC 190 Z9 191 U1 1 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1991 VL 41 IS 1 BP 31 EP 38 PG 8 WC Microbiology SC Microbiology GA ER651 UT WOS:A1991ER65100007 PM 1704791 ER PT J AU STANTON, TB JENSEN, NS CASEY, TA TORDOFF, LA DEWHIRST, FE PASTER, BJ AF STANTON, TB JENSEN, NS CASEY, TA TORDOFF, LA DEWHIRST, FE PASTER, BJ TI RECLASSIFICATION OF TREPONEMA-HYODYSENTERIAE AND TREPONEMA-INNOCENS IN A NEW GENUS, SERPULA GEN-NOV, AS SERPULA-HYODYSENTERIAE COMB-NOV AND SERPULA-INNOCENS COMB-NOV SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID SWINE-DYSENTERY; BACTEROIDES-UREOLYTICUS; ESCHERICHIA-COLI; SELECTIVE MEDIUM; LIQUID-MEDIUM; LYME-DISEASE; SPIROCHETE; PHYLOGENY; PROTEINS; GROWTH AB The intestinal anaerobic spirochetes Treponema hyodysenteriae B78T (T = type strain), B204, B169, and A-1, Treponema innocens B256T and 4/71, Treponema succinifaciens 6091T, and Treponema bryantii RUS-1T were compared by performing DNA-DNA reassociation experiments, sodium dodecyl sulfate-polyacrylamide gel electrophoresis of cell proteins, restriction endonuclease analysis of DNA, and 16S rRNA sequence analysis. DNA-DNA relative reassociation experiments in which the S1 nuclease method was used showed that T. hyodysenteriae B78T and B204 had 93% sequence homology with each other and approximately 40% sequence homology with T. innocens B256T and 4/71. Both T. hyodysenteriae B78T and T. innocens B256T exhibited neglible levels of DNA homology (less-than-or-equal-to-5%) with T. succinifaciens 6091T. The results of comparisons of protein electrophoretic profiles corroborated the DNA-DNA reassociation results. We found high levels of similarity (greater-than-or-equal-to-96%) in electrophoretic profiles among T. hyodysenteriae strains, moderate levels of similarity (43 to 49%) between T. hyodysenteriae and T. innocens, and no detectable similarity between the profiles of either T. hyodysenteriae or T. innocens and those of T. succinifaciens, T. bryantii, and Escherichia coli. Restriction endonuclease analysis of DNA was not useful in assessing genetic relationships since there was heterogeneity even between strains of T. hyodysenteriae. Partial 16S rRNA sequences of the intestinal spirochetes were determined by using a modified Sanger method and were compared in order to evaluate the phylogenetic relationships among these and other spirochetes. The 16S rRNA sequences of T. hyodysenteriae B78T, B204, and A-1 were nearly identical (99.8 to 99.9% base sequence similarity). T. innocens B256T and 4/71 were closely related to the T. hyodysenteriae strains (99.4 and 99.0% similarity). Strains of T. hyodysenteriae and T. innocens exhibited low levels of 16S rRNA similarity (average, 76.5%) with T. pallidum, Borrelia burgdorferi, and various other spirochetes. The results of our investigations indicate that T. hyodysenteriae and T. innocens are distinct but related species of spirochetes. T. hyodysenteriae and T. innocens are only distantly related to T. pallidum, the type species of the genus Treponema, and to other spirochetes. Consequently, we propose that the species T. hyodysenteriae and T. innocens be transferred to a new genus, Serpula, gen. nov. C1 FORSYTH DENT CTR,BOSTON,MA 02115. RP STANTON, TB (reprint author), USDA ARS,NATL ANIM DIS CTR,PHYSIOPATHOL RES UNIT,AMES,IA 50010, USA. NR 54 TC 92 Z9 92 U1 1 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1991 VL 41 IS 1 BP 50 EP 58 PG 9 WC Microbiology SC Microbiology GA ER651 UT WOS:A1991ER65100010 PM 1704792 ER PT J AU PILLAI, S AF PILLAI, S TI IMMUNOGLOBULIN TRANSPORT IN B-CELL DEVELOPMENT SO INTERNATIONAL REVIEW OF CYTOLOGY-A SURVEY OF CELL BIOLOGY LA English DT Review ID CHAIN BINDING-PROTEIN; ANTIGEN RECEPTOR COMPLEX; GLUCOSE-REGULATED PROTEIN; AMINO-ACID SUBSTITUTION; LYMPHOCYTES-PRE-B; IGM HEAVY-CHAINS; SURFACE MU-CHAIN; LIGHT-CHAIN; VARIABLE-REGION; BONE-MARROW C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NIAID NIH HHS [AI 27835] NR 88 TC 11 Z9 11 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0074-7696 J9 INT REV CYTOL JI Int.Rev.Cytol. PY 1991 VL 130 BP 1 EP 36 DI 10.1016/S0074-7696(08)61500-4 PG 36 WC Cell Biology SC Cell Biology GA MC394 UT WOS:A1991MC39400001 PM 1778727 ER PT J AU OGILVY, CS SILVERBERG, KR BORGES, LF AF OGILVY, CS SILVERBERG, KR BORGES, LF TI SPROUTING OF CORNEAL SENSORY FIBERS IN RATS TREATED AT BIRTH WITH CAPSAICIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE CORNEAL INNERVATION; CAPSAICIN; NEURONAL SPROUTING; SENSORY FIBERS; KERATITIS ID NEONATAL CAPSAICIN; AXONAL-TRANSPORT; NEURONS; NERVES; DEGENERATION; DENERVATION; LESIONS; SYSTEM; MICE AB Normal structure and function of corneal epithelium is known to be related to proper innervation. To investigate possible trophic actions of sensory neurons on corneal epithelium, corneal innervation and various physical parameters were studied in normal rats and in rats treated as neonates with intraperitoneal injections of capsaicin. Corneal lesions were noted in treated rats which varied from multiple punctate areas of corneal opacity to deep stromal opacity with ulceration and neovascularization. These lesions waxed and waned throughout the animal's life. In addition, mechanical threshold of the corneal reflex was higher in capsaicin-treated rats. The tear rate in response to a provocative test was diminished in treated rats, presumably due to reduced afferent trigeminal input to the brain stem; blinking rates were more frequent in these animals. Using fluorescent retrograde tracing techniques, the number of cells innervating the cornea in capsaicin-treated rats was found to be significantly less compared with control animals. Innervation in the cornea (examined using a gold chloride technique) demonstrated a decrease in the number of corneal large axons in treated rats with neurite sprouting of these axons yielding a higher density of nerve fibers compared with controls. Thus, sprouting of residual sensory neurons occurs in response to the partial corneal denervation produced by capsaicin, and this sprouting does not functionally compensate to prevent the development of chronic keratitis. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,FRUIT ST,BOSTON,MA 02114. FU NINDS NIH HHS [K08-NS 00990] NR 25 TC 31 Z9 33 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 1991 VL 32 IS 1 BP 112 EP 121 PG 10 WC Ophthalmology SC Ophthalmology GA EU054 UT WOS:A1991EU05400015 PM 1987092 ER PT J AU EPSTEIN, DL ROHEN, JW AF EPSTEIN, DL ROHEN, JW TI MORPHOLOGY OF THE TRABECULAR MESHWORK AND INNER-WALL ENDOTHELIUM AFTER CATIONIZED FERRITIN PERFUSION IN THE MONKEY EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE TRABECULAR MESHWORK; SCHLEMMS CANAL; CATIONIZED FERRITIN; RHESUS MONKEY; AQUEOUS HUMOR OUTFLOW; ENDOTHELIAL CELLS OF SCHLEMMS CANAL ID AQUEOUS-HUMOR OUTFLOW; PRESSURE-DEPENDENT CHANGES; PHYSIOLOGICAL RANGE 0; INTRAOCULAR-PRESSURE; FINE-STRUCTURE; GRADED LEVELS; MACACA-IRUS; 50 MMHG; ACID AB Nine eyes of five cynomolgus monkeys were perfused through the anterior chamber with cationized ferritin (CF) at normal and increased intraocular pressure. After perfusion with glutaraldehyde, the morphologic appearance of the endothelial lining of Schlemm's canal (SC) and of the adjacent regions was analyzed using tangential and sagittal srerial sections. The CF, which binds to negatively charged surfaces, was observed to be adherent to the free surfaces of trabecular cell membranes and to accumulate in the cribriform layer underlining the endothelial lining of SC. Tangential sections of the inner-wall endothelium demonstrated that separations of the adjacent cell membranes occur between the tight junctions forming openings or lacunae and bent, tunnel-like channels that represent continuous paracellular pathways. Complete staining of these inner-wall paracellular pathways with CF were observed indicating that the adjoining membranes are negatively charged and that the perfused fluid had passed through these intercellular channels. These paracellular pathways appeared enlarged and were more easily identified at elevated perfusion pressure. In general, intracytoplasmic vacuoles demonstrated heavy staining with CF on their luminal surface but only faint staining on the adluminal (cribriform-facing) surface. Apparent giant vacuoles were observed to be often not real intracellular vacuoles but rather dilatations of the paracellular spaces. This study demonstrates that there are paracellular routes through the inner-wall endothelium by which high molecular-weight substances such as ferritin and macrophages can leave the anterior chamber. Probably there are both transcytoplasmic and paracellular mechanisms of aqueous outflow that may vary under different conditions of pressure or flow. C1 DEPT ANAT,ERLANGEN,GERMANY. RP EPSTEIN, DL (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY-01894] NR 28 TC 85 Z9 88 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 1991 VL 32 IS 1 BP 160 EP 171 PG 12 WC Ophthalmology SC Ophthalmology GA EU054 UT WOS:A1991EU05400022 PM 1987099 ER PT J AU KLEIN, A CARSON, GC NOVELLINE, RA MUELLER, CF HARRIS, JH AF KLEIN, A CARSON, GC NOVELLINE, RA MUELLER, CF HARRIS, JH TI THE CURRENT STATUS OF FACULTY STAFFING AND RESIDENT TRAINING IN EMERGENCY RADIOLOGY - RESULTS OF A SURVEY SO INVESTIGATIVE RADIOLOGY LA English DT Article DE EMERGENCY RADIOLOGY STAFFING; RADIOLOGY RESIDENCY CURRICULUM; RADIOLOGY RESIDENT TRAINING; EMERGENCY RADIOLOGY AB The results of a survey of United States and Canadian radiology residency programs in hospitals maintaining major emergency departments indicate that (1) radiologic faculty assignment to emergency medicine may include "all faculty," "specific faculty," "specific and other faculty," "general," and "musculoskeletal" faculty; (2) a chief of emergency radiology section is designated in less than 35% of radiology departments providing emergency room services; (3) radiology resident rotation in emergency radiology occurs in less than 2/3 of the surveyed programs; and (4) radiology resident experience in emergency radiology ranges from two to 16 weeks in 40% of these programs, the remainder being "unspecified." The effect of this circumstance upon the emergency department patient care and resident teaching in emergency radiology is discussed and remedial suggestions presented. C1 UNIV TEXAS,SCH MED,DEPT RADIOL,6431 FANNIN,SUITE 2132 MSB,HOUSTON,TX 77030. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT RADIOL,WINSTON SALEM,NC 27103. HERMANN HOSP,HOUSTON,TX 77030. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. OHIO STATE UNIV,DEPT RADIOL,COLUMBUS,OH 43210. NR 4 TC 9 Z9 9 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 JAN PY 1991 VL 26 IS 1 BP 86 EP 89 DI 10.1097/00004424-199101000-00018 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA ER525 UT WOS:A1991ER52500015 PM 2022459 ER PT J AU GABUZDA, D OLSHEVSKY, U BERTANI, P HASELTINE, WA SODROSKI, J AF GABUZDA, D OLSHEVSKY, U BERTANI, P HASELTINE, WA SODROSKI, J TI IDENTIFICATION OF MEMBRANE ANCHORAGE DOMAINS OF THE HIV-1 GP160 ENVELOPE GLYCOPROTEIN PRECURSOR SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE ENVELOPE GLYCOPROTEINS; TRANSMEMBRANE PROTEIN; GP41; GP160; MEMBRANE ANCHORAGE; STOP TRANSFER ID HUMAN IMMUNODEFICIENCY VIRUS; STOP-TRANSFER; HTLV-III/LAV; CELL-LINE; T-CELLS; PROTEIN; TYPE-1; EXPRESSION; SEQUENCE; FUSION AB The gp41 transmembrane protein of human immunodeficiency virus type 1 (HIV-1) contains a hydrophobic membrane-spanning domain that serves to anchor the gp120-gp41 complex on the surface of infected cells and virions. To study the requirements for membrane anchorage, conservative amino acid substitutions in three residues at a time were made within this hydrophobic gp41 region. The complete gp160 precursor as well as the gp120 exterior envelope glycoprotein were exported into the supernatant of expressing cells for two mutants with amino acid substitutions in residues 687-689 and 697-699. The soluble gp160 molecules exhibited a binding ability for CD4 on the surface of SupT1 cells that was 33-36% that of the soluble gp120 glycoproteins. These results implicate residues 687-689 and 697-699 as important components of the stop-transfer signal that anchors the gp160 envelope glycoprotein precursor in the membrane. The data also suggest that characteristics in addition to hydrophobicity are required for stop-transfer signals. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,HUMAN RETROVIROL,JFB 621,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DIV CANC BIOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI 24755] NR 38 TC 26 Z9 26 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 1 BP 34 EP 40 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP176 UT WOS:A1991EP17600005 PM 1984054 ER PT J AU GOLDFELD, AE BIRCHLIMBERGER, K SCHOOLEY, RT WALKER, BD AF GOLDFELD, AE BIRCHLIMBERGER, K SCHOOLEY, RT WALKER, BD TI HIV-1 INFECTION DOES NOT INDUCE TUMOR-NECROSIS-FACTOR-ALPHA OR INTERFERON-BETA GENE-TRANSCRIPTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV-1; TNF-ALPHA-IFN-BETA; GENE TRANSCRIPTION; H9-CELLS, BT4-CELLS, AND U937-CELLS; SENDAI VIRUS ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; TOXIC LYMPHOCYTES-T; FACTOR-ALPHA; BETA; REPLICATION; INVITRO; INDIVIDUALS; INHIBITION; DISORDERS AB An early host defense against infection by RNA or DNA viruses is the induction, within infected cells, of tumor necrosis factor-alpha (TNF-alpha) gene transcription. The protein product of the TNF-alpha gene alone, or together with different types of interferons, inhibits viral propagation in diverse cell types. In this study, the effect of acute and chronic human immunodeficiency virus type 1 (HIV-1) infection on the transcription of the TNF-alpha and interferon-beta (IFN-beta). genes was examined in susceptible monocyte and T-cell lines as well as in primary human mononuclear phagocytes. Although Sendai virus, a prototypic inducer of TNF-alpha and IFN-beta mRNA, induced the transcription of both genes in the monocyte cell lines and TNF-alpha in the T-cell line and in primary mononuclear phagocytes, transcription of these genes was not inducible by HIV-1. Therefore, HIV-1 was able to infect these cells without triggering the transcription of genes encoding proteins important in immediate antiviral cellular defenses. These results may explain in part how HIV-1 is able to establish persistent intracellular infections and escape acute host responses that have evolved to combat viral infection. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,55 FRUIT ST,GRAY BLDG,4TH FLOOR,BOSTON,MA 02114. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA37461]; NIAID NIH HHS [AI28568] NR 25 TC 44 Z9 44 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 1 BP 41 EP 47 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP176 UT WOS:A1991EP17600006 PM 1845771 ER PT J AU RUPRECHT, RM BERNARD, LD BRONSON, R SOSA, MAG MULLANEY, S AF RUPRECHT, RM BERNARD, LD BRONSON, R SOSA, MAG MULLANEY, S TI CASTANOSPERMINE VS ITS 6-O-BUTANOYL ANALOG - A COMPARISON OF TOXICITY AND ANTIVIRAL ACTIVITY INVITRO AND INVIVO SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE CASTANOSPERMINE; 6-O-BUTANOYLCASTANOSPERMINE; INHIBITION OF GLYCOSYLATION; INHIBITION OF HIV-1 ENV-INDUCED SYNCYTIUM FORMATION; ANALYSIS IN CULTURED CELLS AND IN MICE; RAUSCHER MURINE LEUKEMIA VIRUS; TOXICITY; ANTIVIRAL ACTIVITY ID SYNCYTIUM FORMATION; GLUCOSIDASE; INHIBITORS; HIV; 3'-AZIDO-3'-DEOXYTHYMIDINE; REPLICATION; SUPPRESSION; VIRUSES; DISEASE; AIDS AB Inhibitors of glycoprotein processing, such as castanospermine (1,6,7,8-tetrahydroxyoctahydroindolizine), have been shown previously to inhibit human immunodeficiency virus type 1 (HIV-1) with acceptable toxicity in cultured human cells. In prior experiments, we have tested the toxicity and antiviral efficacy of castanospermine in mice infected with the Rauscher murine leukemia virus (RLV). When compared with 3'-azido-3'-deoxythymidine (AZT, zidovudine), castanospermine was less effective and more toxic. Since the 6-O-butanoyl analog of castanospermine was previously found to have a more favorable activity profile than the parent compound against HIV-1 in cultured cells, we compared the antiviral efficacy of both compounds in parallel in vitro and in vivo in the RLV system. Plaque formation in the XC assay was inhibited with a 50% inhibitory concentration (IC50) of 2.4 mu-M for the 6-O-butanoyl analog of castanospermine, as compared to 9 mu-M for castanospermine. For both compounds, concentrations resulting in significant cytotoxicity were about ten times higher. Both compounds significantly decreased HIV-1 env-induced syncytium formation in a novel in vitro assay. In RLV-exposed mice, the 6-O-butanoyl analog showed no advantage over the parent compound: both curves for toxicity as well as antiviral efficacy were super-imposable. We conclude that the 6-O-butanoyl analog of castanospermine as well as castanospermine itself are active antiviral agents in mice and that prolonged oral administration is tolerable. However, in comparison to AZT, their antiviral activity profiles are less favorable. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. TUFTS UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02111. TUFTS UNIV,SCH VET MED,DEPT PATHOL,MEDFORD,MA 02155. RP RUPRECHT, RM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,44 BINNEY ST,BOSTON,MA 02115, USA. FU PHS HHS [UO1 A124845-02, N01-A1-72664] NR 25 TC 25 Z9 25 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 1 BP 48 EP 55 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP176 UT WOS:A1991EP17600007 PM 1984055 ER PT J AU LU, YC TOUZJIAN, N STENZEL, M DORFMAN, T SODROSKI, JG HASELTINE, WA AF LU, YC TOUZJIAN, N STENZEL, M DORFMAN, T SODROSKI, JG HASELTINE, WA TI THE NF-KAPPA-B INDEPENDENT CIS-ACTING SEQUENCES IN HIV-1 LTR RESPONSIVE TO T-CELL ACTIVATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV-1-LONG TERMINAL REPEAT; TRANSCRIPTION INITIATION; T-CELL ACTIVATION ID HUMAN IMMUNODEFICIENCY VIRUS; TRANSCRIPTION FACTOR; EXPRESSION AB The rate of transcription initiation directed by the long terminal repeat (LTR) of HIV-1 increases in response to mitogenic stimuli of T cells. Here we show that the response of the HIV-1 LTR may be governed by two independent sequences located 5' to the site of transcription initiation sequences that bind either NFAT-1 or NFkB. The rate of LTR-directed gene expression increased in response to treatment with either a phorbol ester or tumor necrosis factor alpha if either the NFAT-1 or NFkB binding sites were deleted, but failed to respond to these mitogenic stimuli if both sequences were absent. The HIV-1 mutant virus containing both NFkB and NFAT-1 deletion was able to replicate although at a much decreased growth rate, while the deletion of NFAT-1 alone increased the viral growth rate in Jurkat cells. Neither deletion of NFkB nor deletion of NFAT-1 decreased activation of viral replication by phorbol ester. RP LU, YC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [2R01-AI28785]; PHS HHS [5U01-A124845, U01-A124845] NR 9 TC 26 Z9 26 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 2 BP 173 EP 177 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EU101 UT WOS:A1991EU10100011 PM 1987353 ER PT J AU HEAGY, W GROOPMAN, J SCHINDLER, J FINBERG, R AF HEAGY, W GROOPMAN, J SCHINDLER, J FINBERG, R TI IFN-GAMMA TO TREAT PATIENTS WITH AIDS - REPLY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Letter ID ACQUIRED IMMUNODEFICIENCY SYNDROME; INTERFERON-GAMMA; KAPOSIS SARCOMA; RECOMBINANT; ACTIVATION; INVITRO; INVIVO; ALPHA C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. BIOGEN INC,CAMBRIDGE,MA. RP HEAGY, W (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 NR 21 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 298 EP 300 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900014 ER PT J AU HASELTINE, WA AF HASELTINE, WA TI NEW INSIGHTS ON HIV-1 REPLICATION AND PATHOGENESIS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV RETROVIROL,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 306 EP 307 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900022 ER PT J AU RUPRECHT, RM LEE, JS ARMANY, RS FAZELY, F AF RUPRECHT, RM LEE, JS ARMANY, RS FAZELY, F TI ACUTE RETROVIRAL EXPOSURE AND HOST IMMUNITY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 311 EP 312 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900032 ER PT J AU HIRSCH, MS AF HIRSCH, MS TI COMBINATION CHEMOTHERAPY FOR SENSITIVE AND RESISTANT HIV-1 ISOLATES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY 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 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 316 EP 316 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900042 ER PT J AU DAQUILA, RT VIDELER, JA BECHTEL, LB JOHNSON, VA MERRILL, DP ERON, J KAPLAN, JC HIRSCH, MS AF DAQUILA, RT VIDELER, JA BECHTEL, LB JOHNSON, VA MERRILL, DP ERON, J KAPLAN, JC HIRSCH, MS TI SPECIFIC PCR DETECTION AND DNA-SEQUENCE ANALYSIS OF THE AZT-RESISTANT RT GENOTYPE OF HIV-1 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY 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 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 346 EP 347 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900112 ER PT J AU JOHNSON, VA MERRILL, DP VIDELER, JA CHOU, TC BYINGTON, RE KAPLAN, JC DAGUILA, RT HIRSCH, MS AF JOHNSON, VA MERRILL, DP VIDELER, JA CHOU, TC BYINGTON, RE KAPLAN, JC DAGUILA, RT HIRSCH, MS TI INHIBITION OF ZIDOVUDINE-RESISTANT HIV-1 ISOLATES INVITRO BY 2-DRUG COMBINATION REGIMENS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. 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 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 354 EP 354 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900129 ER PT J AU POZNANSKY, MC WALKER, B HASELTINE, WA SODROSKI, J LANGHOFF, E AF POZNANSKY, MC WALKER, B HASELTINE, WA SODROSKI, J LANGHOFF, E TI A RAPID METHOD FOR QUANTITATING THE FREQUENCY OF PERIPHERAL-BLOOD CELLS CONTAINING HIV-1 DNA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS TYPE-1; PERIPHERAL BLOOD MONONUCLEAR CELLS; CD4+ T-CELLS; HIV-1 DNA; POLYMERASE CHAIN REACTION ID HUMAN IMMUNODEFICIENCY VIRUS; T-CELL; EXPRESSION; POLYMERASE; INFECTION; TYPE-1 AB This article describes a novel approach to quantitative polymerase chain reactions (PCR). The technique is simple to execute, can be performed in a single tube, and is suitable for automation. In addition, the counting and lysis of low numbers of cells (1-100) can be confirmed by phase contrast microscopy. In this study, the technique was used to determine the frequency of occurrence of DNA from the human immunodeficiency virus (type 1) in leukocyte subsets of peripheral blood mononuclear cells (PBMC) from sero-positive individuals. It was confirmed that the frequency of infected CD4+ T cells varied from 0.01 to 0.0001. In addition, HIV-1 DNA was detected in the B cell/dendritic cell-enriched subpopulation in four of nine HIV-1-positive individuals in the study. C1 MASSACHUSETTS GEN HOSP,DEPT INFECT DIS,BOSTON,MA 02114. RP POZNANSKY, MC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115, USA. NR 19 TC 38 Z9 38 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 4 BP 368 EP 373 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FC522 UT WOS:A1991FC52200002 PM 1672549 ER PT J AU AMERONGEN, HM WELTZIN, R FARNET, CM MICHETTI, P HASELTINE, WA NEUTRA, MR AF AMERONGEN, HM WELTZIN, R FARNET, CM MICHETTI, P HASELTINE, WA NEUTRA, MR TI TRANSEPITHELIAL TRANSPORT OF HIV-1 BY INTESTINAL M-CELLS - A MECHANISM FOR TRANSMISSION OF AIDS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS TYPE-1; TRANSEPITHELIAL TRANSPORT; M-CELLS ID HUMAN IMMUNODEFICIENCY VIRUS; FOLLICLE-ASSOCIATED EPITHELIUM; PEYERS PATCHES; CYTOCHEMICAL ANALYSIS; HOST; PHOSPHATASE; RESPONSES; DEFENSE; BINDING; RAT AB This study was designed to determine whether human immunodeficiency virus type 1 (HIV-1) might enter the host by penetrating epithelial barriers through antigen-transporting M cells in lymphoid follicle-associated epithelia. Interaction of HIV-1 with epithelial cells was examined using mucosal explants from Peyer's patches of mice and rabbits. HIV-1 adhered to the luminal membranes of M cells of both species, and was endocytosed and delivered to intraepithelial spaces containing lymphocytes and macrophages. These observations suggest that M cells, which are numerous in the human rectal mucosa, may efficiently deliver HIV-1 to target cells in mucosal lymphoid tissue, and that such transport may contribute to sexual transmission of AIDS. C1 CHILDRENS HOSP MED CTR,DEPT MED,GASTROINTESTINAL CELL BIOL LAB,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV RETROVIROL,BOSTON,MA 02115. OI Farnet, Chris/0000-0003-4927-198X FU NIAID NIH HHS [AI24845]; NICHD NIH HHS [HD17557]; NIDDK NIH HHS [DK34854] NR 31 TC 179 Z9 184 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 8 BP 760 EP 765 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FX686 UT WOS:A1991FX68600003 PM 1856788 ER PT J AU LEE, JS MULLANEY, S BRONSON, R SHARPE, AH JAENISCH, R BALZARINI, J DECLERCQ, E RUPRECHT, RM AF LEE, JS MULLANEY, S BRONSON, R SHARPE, AH JAENISCH, R BALZARINI, J DECLERCQ, E RUPRECHT, RM TI TRANSPLACENTAL ANTIRETROVIRAL THERAPY WITH 9-(2-PHOSPHONYLMETHOXYETHYL)ADENINE IS EMBRYOTOXIC IN TRANSGENIC MICE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE 9-(2-PHOSPHONYLMETHOXYETHYL)ADENINE (PMEA); MOLONEY MURINE LEUKEMIA VIRUS; TRANSPLACENTAL ANTIRETROVIRAL THERAPY; TRANSGENIC MICE ID HUMAN IMMUNODEFICIENCY VIRUS; MOLONEY LEUKEMIA-VIRUS; GERM LINE; TRANSMISSION; WOMEN; AIDS; HIV; RETROVIRUSES; INTEGRATION; SECRETIONS AB Transgenic Mov-14 mice, which carry the provirus of Moloney murine leukemia virus (Mo-MuLV) in the germ line and begin to produce infectious virus on embryonic day 14, were used to evaluate the ability of 9-(2-phosphonylmethoxyethyl)adenine (PMEA) to cross the placenta and protect embryos from viremia. We have used the Mov-14 model previously to demonstrate the antiviral efficacy and lack of teratogenicity of transplacental therapy with 3'-azido-3'-deoxythymidine (zidovudine, ZDV). PMEA was administered to pregnant females by daily intraperitoneal injection or by osmotic pump. In contrast to ZDV, PMEA was either noneffective in preventing viremia in the offspring or embryotoxic, depending on the dose. The specific toxic effects seen were resorption of pregnancy, low birth weight, and neonatal death. Histopathological analysis of neonatal mice exposed to PMEA showed severe lymphoid depletion of the thymus. We conclude that PMEA therapy is contraindicated for use during pregnancy. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,BOSTON,MA 02115. CATHOLIC UNIV LEUVEN,REGA INST MED RES,EXPTL CHEMOTHERAPY LAB,B-3000 LOUVAIN,BELGIUM. TUFTS UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02111. TUFTS UNIV,SCH VET MED,BOSTON,MA 02111. MIT,WHITEHEAD INST BIOMED RES,DEPT BIOL,CAMBRIDGE,MA 02139. FU PHS HHS [N01-A1-72664] NR 31 TC 11 Z9 11 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 9 BP 833 EP 838 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GD597 UT WOS:A1991GD59700001 PM 1895203 ER PT J AU BENNETT, CL GRAF, L HUNTERYOUNG, N DALEY, J MAKADON, HJ AF BENNETT, CL GRAF, L HUNTERYOUNG, N DALEY, J MAKADON, HJ TI INTENSITY OF IN-HOSPITAL CARE FOR PERSONS WITH AIDS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE INTENSITY OF RESOURCE USE; TERMINAL CARE ID COSTS AB We evaluated the intensity of medical care for 30 consecutive AIDS patients at one hospital, using methodology based on the Delay Tool of Selker et al. Of 25 AIDS patients who survived hospitalization, 15 had at least one delay day in the hospital. Major factors associated with care that could have been provided at an alternative site included difficulty with skilled nursing facility placement in 20% of the patients, difficulty coordinating out-of-hospital care in 28%, and scheduling of outpatient surgical procedures in 12%. For the 15 patients who could have received some of their care at a lower intensity setting, a median of 7 hospital days could have been potentially saved with better coordination of outpatient care and increased availability of skilled nursing facilities. The five patients who died in hospital also used large amounts of resources and had long lengths of stay. Prior studies of non-AIDS patients revealed similar results, suggesting that, for reasons of quality of care, quality of life, and economics, policy-makers must develop managed care programs, skilled nursing facilities that accept AIDS patients, inpatient psychiatry facilities, and increased hospice availability. C1 UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET AFFAIRS MED CTR,DEPT GEN MED,LOS ANGELES,CA 90024. DEPT VET AFFAIRS,WESTERN REG SPECIAL STUDIES GRP,LOS ANGELES,CA. CLIN PARTNERS INC,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT MED,DIV GEN MED & PRIMARY CARE,BOSTON,MA 02115. RP BENNETT, CL (reprint author), RAND CORP,1700 MAIN ST,SANTA MONICA,CA 90407, USA. RI Bennett, Charles/C-2050-2008 NR 8 TC 11 Z9 11 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 9 BP 856 EP 860 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GD597 UT WOS:A1991GD59700005 PM 1895205 ER PT J AU FAZELY, F HASELTINE, WA RODGER, RF RUPRECHT, RM AF FAZELY, F HASELTINE, WA RODGER, RF RUPRECHT, RM TI POSTEXPOSURE CHEMOPROPHYLAXIS WITH ZDV OR ZDV COMBINED WITH INTERFERON-ALPHA - FAILURE AFTER INOCULATING RHESUS-MONKEYS WITH A HIGH-DOSE OF SIV SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE ZDV; INTERFERON-ALPHA; COMBINATION THERAPY; POSTEXPOSURE CHEMOPROPHYLAXIS; SIMIAN IMMUNODEFICIENCY VIRUS ID HUMAN IMMUNODEFICIENCY VIRUS; PROPHYLACTIC ZIDOVUDINE; STLV-III; 3'-AZIDO-3'-DEOXYTHYMIDINE; RETROVIRUS; EXPOSURE; VIREMIA; DISEASE; MACAQUE; MODEL AB Presently, no information is available regarding the efficacy of chemoprophylaxis in controlled human trials following accidental exposure to the human immunodeficiency virus (HIV). Using the closely related simian immunodeficiency virus (SIV) in rhesus monkeys, which develop a disease closely resembling human AIDS, we tested the efficacy of either single-agent 3'-azido-3'-deoxythymidine (ZDV) or the combination of ZDV plus recombinant human interferon-alpha (IFN-alpha). Treatment was started 3 h following inoculation of a high dose of SIV and continued for 21 days. SIV-inoculated control animals remained untreated. Virus was recovered from all monkeys on day 8, and by week 7 all had seroconverted. In contrast to monkeys treated with ZDV alone, animals given combination therapy had lower levels of p27 gag antigen compared to untreated controls on day 8 (p = 0.043). We conclude that neither treatment regimen could prevent infection after high-dose virus exposure; however, combination therapy may have depressed the level of virus replication more effectively than ZDV alone. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. TSI MASON RES INST,WORCESTER,MA. NR 22 TC 52 Z9 52 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 11 BP 1093 EP 1097 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GN380 UT WOS:A1991GN38000003 PM 1753337 ER PT J AU KAZEMI, H HOOP, B AF KAZEMI, H HOOP, B TI GLUTAMIC-ACID AND GAMMA-AMINOBUTYRIC-ACID NEUROTRANSMITTERS IN CENTRAL CONTROL OF BREATHING SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Review DE AMINO ACID NEUROTRANSMITTERS; CENTRAL CONTROL OF VENTILATION; CHEMORECEPTION ID METHYL-D-ASPARTATE; HYDROGEN-ION REGULATION; VENTRAL SURFACE; AMINO-ACIDS; KAINIC ACID; CARDIOVASCULAR FUNCTION; VENTROLATERAL MEDULLA; RESPIRATORY CONTROL; GABA RECEPTORS; BRAIN AB We review recent cross-disciplinary experimental and theoretical investigations on metabolism of the amino acid neurotransmitter glutamic acid and gamma-aminobutyric acid (GABA) in the brain during hypoxia and hypercapnia and their possible role in central control of breathing. The roles of classical modifiers of central chemical drive to breathing (H+ and cholinergic mechanisms) are summarized. A brief perspective on the current widespread interest in GABA and glutamate in central control is given. The basic biochemistry of these amino acids and their roles in ammonia and bicarbonate metabolism are discussed. This review further addresses recent work on central respiratory effects of inhibitory GABA and excitatory glutamate. Current understanding of the sites and mechanisms of action of these amino acids on or near the ventral surface of the medulla is reviewed. We focus particularly on tracer kinetic investigations of glutamatergic and GABAergic mechanisms in hypoxia and hypercapnia and their possible role in the ventilatory response to hypoxia. We conclude with some speculative remarks on the critical importance of these investigations and suggest specific directions of research in central mechanisms of respiratory control. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP KAZEMI, H (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-29493, HL-29620] NR 55 TC 88 Z9 92 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JAN PY 1991 VL 70 IS 1 BP 1 EP 7 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA ER676 UT WOS:A1991ER67600001 PM 1672687 ER PT J AU PULKKINEN, WS MILLER, SI AF PULKKINEN, WS MILLER, SI TI A SALMONELLA-TYPHIMURIUM VIRULENCE PROTEIN IS SIMILAR TO A YERSINIA-ENTEROCOLITICA INVASION PROTEIN AND A BACTERIOPHAGE-LAMBDA OUTER-MEMBRANE PROTEIN SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI; SIGNAL SEQUENCES; VIBRIO-CHOLERAE; DNA; CLONING; FRAGMENTS; MUTANTS; GENES; RNA; ELECTROPHORESIS AB The PhoP-PhoQ-regulated pagC locus is essential for full virulence and survival within macrophages of Salmonella typhimurium. The protein product, DNA sequence, and transcript of pagC were determined. The pagC locus encodes a single 188-amino-acid membrane protein that is similar to the ail-encoded eucaryotic cell invasion protein of Yersinia enterocolitica and the lom-encoded protein of bacteriophage lambda. The similarity of PagC and Ail to Lom leads us to hypothesize that Lom is a virulence protein and that bacteriophage gene transfer and lysogeny could have led to the development of proteins essential to survival within macrophages and eucaryotic cell invasion. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,INFECT DIS UNIT,BOSTON,MA 02114. FU NIAID NIH HHS [AI00917-01] NR 45 TC 114 Z9 117 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1991 VL 173 IS 1 BP 86 EP 93 PG 8 WC Microbiology SC Microbiology GA EP951 UT WOS:A1991EP95100013 PM 1846140 ER PT J AU LOVETT, ST KOLODNER, RD AF LOVETT, ST KOLODNER, RD TI NUCLEOTIDE-SEQUENCE OF THE ESCHERICHIA-COLI RECJ CHROMOSOMAL REGION AND CONSTRUCTION OF RECJ-OVEREXPRESSION PLASMIDS SO JOURNAL OF BACTERIOLOGY LA English DT Article ID SITE-SPECIFIC RECOMBINASES; RELEASE FACTOR-II; GENETIC-RECOMBINATION; PHASE VARIATION; MOLECULAR ANALYSIS; TYPE-1 FIMBRIAE; DNA; RNA; IDENTIFICATION; K-12 AB The nucleotide sequence of the recJ gene of Escherichia coli K-12 and two upstream coding regions was determined. Three regions were identified within these two upstream genes that exhibited weak to moderate promoter activity in fusions to the galK gene and are candidates for the recJ promoter. recJ appeared to be poorly translated: the recJ nucleotide sequence revealed a suboptimal initiation codon GUG, no discernible ribosome-binding consensus sequence, and relatively nonbiased synonymous codon usage. Comparison of the sequence of this region of the chromosome with DNA data bases identified the gene immediately downstream of recJ as prfB, which encodes translational release factor 2 and has been mapped near recJ at 62 min. No significant homology between recJ and other previously sequenced regions of DNA was detected. However, protein sequence comparisons with a gene upstream of recJ, denoted xprb, revealed significant homology with several site-specific recombination proteins. Its genetic function is presently unknown. Knowledge of the nucleotide sequence of recJ allowed the construction of a plasmid from which overexpression of RecJ protein could be induced. Supporting the notion that translation of recJ is limiting, a strong T7 bacteriophage promoter upstream of recJ did not, by itself, allow high-level expression of RecJ protein. The addition of a ribosome-binding sequence fused to the initiator GTG of recJ in this construction was necessary to promote expression of high levels of RecJ protein. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. OI Lovett, Susan/0000-0003-2792-1857 FU NIGMS NIH HHS [GM26017] NR 60 TC 46 Z9 49 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1991 VL 173 IS 1 BP 353 EP 364 PG 12 WC Microbiology SC Microbiology GA EP951 UT WOS:A1991EP95100047 PM 1987126 ER PT J AU HUALA, E MOON, AL AUSUBEL, FM AF HUALA, E MOON, AL AUSUBEL, FM TI AEROBIC INACTIVATION OF RHIZOBIUM-MELILOTI NIFA IN ESCHERICHIA-COLI IS MEDIATED BY LON AND 2 NEWLY IDENTIFIED GENES, SNOB AND SNOC SO JOURNAL OF BACTERIOLOGY LA English DT Article ID CYSTEINE RESIDUES; PROTEIN; MUTANTS; DNA; MUTAGENESIS; EXPRESSION; CLONING AB The Rhizobium meliloti NifA protein is an oxygen-sensitive transcriptional regulator of nitrogen fixation genes. Regulation of NifA activity by oxygen occurs at the transcriptional level through fixLJ and at the posttranslational level through the sensitivity of NifA to oxygen. We have previously reported that the NifA protein is sensitive to oxygen in Escherichia coli as well as in R. meliloti. To investigate whether the posttranslational regulation of NifA is dependent on host factors conserved between R. meliloti and E. coli, we carried out a Tn5 mutagenesis of E. coli and isolated mutants with increased NifA activity under aerobic conditions. Fifteen insertion mutations occurred at three unlinked loci. One locus is the previously characterized lon gene; the other two loci, which we have named snoB and snoC, define previously uncharacterized E. coli genes. The products of snoC and lon affect the rate of NifA degradation, whereas the product of snoB may affect both NifA degradation and inactivation. A snoB lon double mutant showed a higher level of NifA accumulation than did a lon mutant, suggesting that the snoB product affects the ability of NifA to be degraded by a lon-independent pathway. The effects of a snoC mutation and a lon mutation were not additive, suggesting that the snoC and lon products function in the same degradative pathway. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RI Huala, Eva/B-1377-2009 NR 30 TC 9 Z9 9 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1991 VL 173 IS 1 BP 382 EP 390 PG 9 WC Microbiology SC Microbiology GA EP951 UT WOS:A1991EP95100050 PM 1846139 ER PT J AU JANMEY, PA AF JANMEY, PA TI A TORSION PENDULUM FOR MEASUREMENT OF THE VISCOELASTICITY OF BIOPOLYMERS AND ITS APPLICATION TO ACTIN NETWORKS SO JOURNAL OF BIOCHEMICAL AND BIOPHYSICAL METHODS LA English DT Article DE TORSION PENDULUM; ACTIN; SHEAR MODULUS; NETWORK; VISCOELASTICITY; RHEOLOGY; GEL; BIOPOLYMER ID F-ACTIN; MECHANICAL-PROPERTIES; FIBRIN CLOTS; RHEOLOGY; GELSOLIN; MUSCLE AB This report describes the design, construction, and method of operation of a torsion pendulum which is specifically designed for the measurement of soft and fragile biopolymer gels. The pendulum can be assembled and employed in a standard biological laboratory and provides data that currently require access to specialized equipment usually limited to physics or material science laboratories. This instrument measures the shear moduli of viscoelastic materials by applying or oscillating shear forces to a disc-shaped sample and measuring the resulting angular displacement of a pendulum attached to one face of the sample. The device is easily constructed using commercially available materials and no specialized machinery. Shear stresses as low as 0.03 Pa and shear rates as low as 0.00003 s-1 can be measured in steady shear experiments, and dynamic shear moduli from 1 to 2500 Pa measured by oscillatory measurements with sample volumes as low as 0.5 ml. The use of the torsion pendulum is illustrated by measuring the effects of two different actin binding proteins on the viscoelasticity of actin filament networks. RP JANMEY, PA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,HEMATOL UNIT,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [AR38910] NR 22 TC 51 Z9 51 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-022X J9 J BIOCHEM BIOPH METH JI J. Biochem. Biophys. Methods PD JAN PY 1991 VL 22 IS 1 BP 41 EP 53 DI 10.1016/0165-022X(91)90080-G PG 13 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EP505 UT WOS:A1991EP50500005 PM 2005359 ER PT J AU RILEY, PO SCHENKMAN, ML MANN, RW HODGE, WA AF RILEY, PO SCHENKMAN, ML MANN, RW HODGE, WA TI MECHANICS OF A CONSTRAINED CHAIR-RISE SO JOURNAL OF BIOMECHANICS LA English DT Article ID HIP AB A sit-to-stand task is analyzed by a method which estimates the segmental and whole body center of mass (CoM) kinematics and kinetics using bilateral whole body kinematic data from nine healthy young female subjects. The sit-to-stand, or chair-rise, task is constrained with regard to chair height, pace, initial lower limb position and arm use. The chair-rise maneuver is divided into four phases: (1) the flexion momentum phase; (2) the momentum transfer phase; (3) the vertical extension phase; and (4) the stabilization phase; the first three are examined in detail here. The momentum transfer phase, which immediately follows lift-off from the seat of the chair, is the most dynamic portion of the event, demanding a high degree of coordination. This maneuver is analyzed in order to determine if trunk movement is used only to position the body center of gravity or if the trunk motion generates momentum which is important during the brief but critical period of dynamic equilibrium immediately following lift-off from the chair. Our evidence points to the latter case and indicates that inter-segmental momentum transfer is possible during this period. C1 MIT,CAMBRIDGE,MA 02139. RP RILEY, PO (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. RI Riley, Patrick/B-3053-2009 FU PHS HHS [H133E80024-89] NR 15 TC 125 Z9 127 U1 0 U2 12 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0021-9290 J9 J BIOMECH JI J. Biomech. PY 1991 VL 24 IS 1 BP 77 EP 85 DI 10.1016/0021-9290(91)90328-K PG 9 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA FC285 UT WOS:A1991FC28500008 PM 2026635 ER PT J AU HARRIGAN, TP HARRIS, WH AF HARRIGAN, TP HARRIS, WH TI A FINITE-ELEMENT STUDY OF THE EFFECT OF DIAMETRAL INTERFACE GAPS ON THE CONTACT AREAS AND PRESSURES IN UNCEMENTED CYLINDRICAL FEMORAL TOTAL HIP COMPONENTS SO JOURNAL OF BIOMECHANICS LA English DT Note AB Uncemented femoral total hip components rely entirely on contact with the prepared femur for their initial fixation. The contact areas and stresses between a straight tubular bone and a metal cylindrical prosthesis 12.5 cm long and 13 mm in diameter were calculated in a finite element model which includes uniform diametral gaps varying from 20 to 500-mu-m, using transverse loads from 100 to 2000 N. Frictionless three-dimensional contact elements were used between the bone and the prosthesis. Contact stresses were high and irregular in all cases, and the contact areas were small. Two regions of contact were apparent for lower loads and larger gaps. A third region of contact occurred near the distal tip of the implant at higher loads. This region of contact markedly increased the contact stresses at the distal tip of the prosthesis. A 20-mu-m overlap between bone and implant was modelled to assess a slight interference fit. The contact stress distribution in this case was markedly different from the stress distribution with a 20-mu-m diametral gap. The data collectively indicates that gaps of less than 20-mu-m between bone and implant can substantially change contact stress distributions. C1 MASSACHUSETTS GEN HOSP,HIP & IMPLANT UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HARRIGAN, TP (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114, USA. NR 6 TC 17 Z9 18 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0021-9290 J9 J BIOMECH JI J. Biomech. PY 1991 VL 24 IS 1 BP 87 EP 91 DI 10.1016/0021-9290(91)90329-L PG 5 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA FC285 UT WOS:A1991FC28500009 PM 2026636 ER PT J AU CAPE, EG LEVINE, RA YOGANATHAN, AP AF CAPE, EG LEVINE, RA YOGANATHAN, AP TI A NEW THEORETICAL-MODEL FOR NONINVASIVE QUANTIFICATION OF MITRAL REGURGITATION - REPLY SO JOURNAL OF BIOMECHANICS LA English DT Letter C1 MASSACHUSETTS GEN HOSP,CARDIAC ULTRASOUND LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP CAPE, EG (reprint author), GEORGIA INST TECHNOL,SCH CHEM ENGN,CARDIOVASC FLUID MECHAN LAB,ATLANTA,GA 30332, USA. NR 4 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 0021-9290 J9 J BIOMECH JI J. Biomech. PY 1991 VL 24 IS 6 BP 494 EP 494 DI 10.1016/0021-9290(91)90161-F PG 1 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA FN433 UT WOS:A1991FN43300011 ER PT J AU HARRIGAN, TP HARRIS, WH AF HARRIGAN, TP HARRIS, WH TI A 3-DIMENSIONAL NONLINEAR FINITE-ELEMENT STUDY OF THE EFFECT OF CEMENT-PROSTHESIS DEBONDING IN CEMENTED FEMORAL TOTAL HIP COMPONENTS SO JOURNAL OF BIOMECHANICS LA English DT Article ID STEM DESIGN AB A three-dimensional non-linear finite element analysis of a cemented femoral component in which the component was partially debonded from the cement mantle was used to assess the effects of debonding on stresses in the cement. Three cases of partial cement-metal debonding were modelled with debonding of the proximal portion of the implant down to a horizontal plane which was 35, 62.5, or 82.5 mm below the prosthesis collar. Each situation was studied under loads simulating both gait and stair climbing. Also, complete debonding between the implant and the surrounding cement mantle was modeled for loads simulating pit. Under stair climbing loads with partial cement-metal debonding, hoop stresses of 13-18 MPa were observed in the cement at the cement-metal interface at the proximal postero-medial corner of the implant. Similarly, in stair climbing, the maximum principal stresses in the cement were also adjacent to the proximal postero-medial region of the implant. These stresses were compressive and increased from 15 MPa with fully bonded interfaces to 48 MPa with debonding down to 82.5 mm below the prosthesis collar. Under gait loads, complete debonding caused high compressive stresses up to 34.9 MPa in the cement distal to the prosthesis tip. Thus, cement failure subsequent to prosthesis debonding is likely in the proximal region in a partially debonded implant due to stair climbing loads and is likely below the prosthesis tip in a fully debonded implant due to gait loading, C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HIP & IMPLANT UNIT,BOSTON,MA 02114. RP HARRIGAN, TP (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114, USA. NR 17 TC 99 Z9 101 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0021-9290 J9 J BIOMECH JI J. Biomech. PY 1991 VL 24 IS 11 BP 1047 EP 1058 DI 10.1016/0021-9290(91)90021-E PG 12 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA GT790 UT WOS:A1991GT79000006 PM 1761581 ER PT J AU GELBERMAN, RH SIEGEL, DB WOO, SLY AMIEL, D TAKAI, S LEE, D AF GELBERMAN, RH SIEGEL, DB WOO, SLY AMIEL, D TAKAI, S LEE, D TI HEALING OF DIGITAL FLEXOR TENDONS - IMPORTANCE OF THE INTERVAL FROM INJURY TO REPAIR - A BIOMECHANICAL, BIOCHEMICAL, AND MORPHOLOGICAL-STUDY IN DOGS SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID PASSIVE MOBILIZATION AB The effect of an elapsed interval of time between injury and operative repair of the flexor tendons was investigated in a canine model. Transected intrasynovial flexor tendons were repaired either immediately or after a delay of seven or twenty-one days. The biomechanical, biochemical, and morphological characteristics were compared at three and six weeks. The values for angular rotation, linear excursion, ultimate load, and linear slope were determined; concentrations of collagen and reducible collagen cross-links, an index of newly synthesized collagen, were measured; and the ultrastructural morphology of the tendons was examined by high-voltage electron microscopy. For the tendons that were repaired immediately, the values for angular rotation were 9.4 +/- 3.2 and 13.0 +/- 3.7 degrees at three and six weeks; for those that were repaired at seven days, 4.1 +/- 1.3 and 2.5 +/- 1.4 degrees; and for those that were repaired at twenty-one days, 2.7 +/- 0.8 and 4.7 +/- 0.7 degrees. There was a significant effect of the delay until repair on the angular rotation and linear excursion in all three groups (p < 0.005 for both). Tensile testing of the bone-tendon complex revealed no significant effect of the delay on the values for ultimate load (p > 0.05). There were no significant differences in total concentration of collagen at the sites of repair or in the levels of reducible Schiff-base cross-links (indicators of newly synthesized cross-links) in tendons from the three groups. CLINICAL RELEVANCE: The time from injury to repair of the intrasynovial flexor tendons, considered as an isolated variable, has a significant effect on the function of the tendons in dogs. To provide optimum conditions for restoration of the gliding surface, repair of transected tendons within the first few days after injury appears warranted. RP GELBERMAN, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WACC 427,BOSTON,MA 02114, USA. FU NIADDK NIH HHS [AM34078]; NIAMS NIH HHS [5R01-AR33097-11] NR 34 TC 18 Z9 18 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD JAN PY 1991 VL 73A IS 1 BP 66 EP 75 PG 10 WC Orthopedics; Surgery SC Orthopedics; Surgery GA EV418 UT WOS:A1991EV41800009 PM 1985996 ER PT J AU BURKE, DW OCONNOR, DO ZALENSKI, EB JASTY, M HARRIS, WH AF BURKE, DW OCONNOR, DO ZALENSKI, EB JASTY, M HARRIS, WH TI MICROMOTION OF CEMENTED AND UNCEMENTED FEMORAL COMPONENTS SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Article ID TOTAL HIP-REPLACEMENT; CONTACT; STEM AB We evaluated the initial stability of cemented and uncemented femoral components within the femoral canals of cadaver femurs during simulated single limb stance and stair climbing. Both types were very stable in simulated single limb stance (maximum micromotion of 42-mu-m for cemented and 30-mu-m for uncemented components). However, in simulated stair climbing, the cemented components were much more stable than the uncemented components (76-mu-m as against 280-mu-m). There was also greater variation in the stability of uncemented components in simulated stair climbing, with two of the seven components moving 200-mu-m or more. Future implant designs should aim to improve the initial stability of cementless femoral components under torsional loads; this should improve the chances of bony ingrowth. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LABS,HIP & IMPLANT SURG UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 20 TC 153 Z9 156 U1 0 U2 5 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 JAN PY 1991 VL 73 IS 1 BP 33 EP 37 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA EV325 UT WOS:A1991EV32500010 PM 1991771 ER PT J AU ELIAS, AD AYASH, LJ EDER, JP WHEELER, C DEARY, J WEISSMAN, L HUNT, M CRITCHLOW, J SCHNIPPER, L FREI, E ANTMAN, KH AF ELIAS, AD AYASH, LJ EDER, JP WHEELER, C DEARY, J WEISSMAN, L HUNT, M CRITCHLOW, J SCHNIPPER, L FREI, E ANTMAN, KH TI ESCALATING DOSES OF CARBOPLATIN WITH HIGH-DOSE IFOSFAMIDE USING AUTOLOGOUS BONE-MARROW AS SUPPORT - A PHASE-I STUDY SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY LA English DT Article; Proceedings Paper CT SATELLITE SYMPOSIUM TO THE 15TH INTERNATIONAL CANCER CONGRESS - IFOSFAMIDE IN TUMOR THERAPY : QUESTIONS FOR THE NINETIES CY 1990 CL HAMBURG, GERMANY DE HIGH-DOSE IFOSFAMIDE; CARBOPLATIN; BONE MARROW ID PREVIOUSLY TREATED PATIENTS; CELL LUNG-CANCER; TUBULAR NEPHROTOXICITY; UNRESECTABLE SARCOMA; MESNA; TRIAL; CISPLATIN; NEUROTOXICITY; TUMORS AB In this phase I study, 16 adult cancer patients were treated with concurrent 4-day continuous infusions of ifosfamide at 12 g/m2 and escalating doses of carboplatin (400-1600 mg/m2) to determine the major non-haematological dose-limiting toxicity of the combination. Mesna was given by continuous infusion over 5 days for uroprotection (total dose per course = 15 g/m2). Autologous bone marrow support, which was mandated for subsequent dose levels once granulocytes remained below 500/mu-l for more than 14 days in at least 2 patients entered at a given dose level, was used at dose levels above 400 mg/m2 carboplatin. Renal toxicity became dose-limiting at the maximum tolerated dose level of 1600 mg/m2 carboplatin. Temporary creatinine elevations above 2 mg/dl (median peak 2.6 mg/dl) were observed in 3 and irreversible renal toxicity occurred in 1 (peak creatinine 6.9 mg/dl, chronic creatinine 5-6 mg/dl) of the 5 patients entered at this dose level. Severe confusion and lethargy associated with rising creatinine developed in 2 patients. Two complete and four partial responses were documented in 14 heavily pretreated evaluable patients. The complete responses continue at 14+ and 20+ months in a patient with germ cell carcinoma and Ewing's sarcoma, respectively. Carboplatin appears to contribute to the renal toxicity of ifosfamide. Nevertheless, the combination of carboplatin and ifosfamide at 80% and 75% of the single-agent maximal tolerated doses respectively produced acceptable non-haematological toxicity. Further studies in the treatment of sarcoma, germ cell, ovarian and lung carcinomas with this combination are warranted. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV HEMATOL ONCOL & SURG,BOSTON,MA 02215. RP ELIAS, AD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 13849] NR 32 TC 0 Z9 0 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. PY 1991 VL 117 SU 4 BP S208 EP S213 DI 10.1007/BF01613229 PG 6 WC Oncology SC Oncology GA HG409 UT WOS:A1991HG40900014 PM 1795009 ER PT J AU SEEBER, S RADFORD, JA LOEFFLER, TM CERNY, T BRADE, WP WAGNER, T LUTZ, M BUDACH WOLF, M MERTELSMANN, R HARSTRICK, A WINKELMANN HAVEMANN, K RITTER GOSS EPHRONIDIS ELIAS, AD GASSMANN, W STEWARD AF SEEBER, S RADFORD, JA LOEFFLER, TM CERNY, T BRADE, WP WAGNER, T LUTZ, M BUDACH WOLF, M MERTELSMANN, R HARSTRICK, A WINKELMANN HAVEMANN, K RITTER GOSS EPHRONIDIS ELIAS, AD GASSMANN, W STEWARD TI IFOSFAMIDE IN TUMOR-THERAPY - QUESTIONS FOR THE NINETIES - DISCUSSION SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY LA English DT Discussion C1 CHRISTIE HOSP & HOLT RADIUM INST,CANC RES CAMPAIGN,DEPT MED ONCOL,WILMSLOW RD,MANCHESTER M20 9BX,LANCS,ENGLAND. MED CTR DORTMUND,DEPT INTERNAL MED,W-4600 DORTMUND,GERMANY. UNIV BERN,INSELSPITAL,INST MED ONKOL,CH-3010 BERN,SWITZERLAND. ASTA MED AG,W-6000 FRANKFURT 1,GERMANY. MED UNIV LUBECK,INNERE MED KLIN,W-2400 LUBECK,GERMANY. UNIV TUBINGEN,DEPT HAEMATOL & MED ONCOL,W-7400 TUBINGEN 1,GERMANY. UNIV MARBURG,DEPT INTERNAL MED,DIV HAEMATOL ONCOL,W-3550 MARBURG,GERMANY. UNIV HANNOVER,SCH MED,DEPT HAEMATOL & ONCOL,W-3000 HANNOVER 61,GERMANY. PHILIPPS UNIV HOSP,DEPT INTERNAL MED,DIV HAEMATOL ONCOL,W-3550 MARBURG,GERMANY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115. UNIV KIEL,DEPT INTERNAL MED 2,W-2300 KIEL 1,GERMANY. RI Radford, John/N-1331-2015 OI Radford, John/0000-0001-7898-2786 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 0171-5216 J9 J CANCER RES CLIN JI J. Cancer Res. Clin. Oncol. PY 1991 VL 117 SU 4 BP S228 EP S231 PG 4 WC Oncology SC Oncology GA HG409 UT WOS:A1991HG40900018 ER PT J AU ELICES, MJ URRY, LA HEMLER, ME AF ELICES, MJ URRY, LA HEMLER, ME TI RECEPTOR FUNCTIONS FOR THE INTEGRIN VLA-3 - FIBRONECTIN, COLLAGEN, AND LAMININ BINDING ARE DIFFERENTIALLY INFLUENCED BY ARG-GLY-ASP PEPTIDE AND BY DIVALENT-CATIONS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID EXTRACELLULAR-MATRIX RECEPTORS; CELL-SURFACE RECEPTORS; MONOCLONAL-ANTIBODY; VITRONECTIN RECEPTOR; ADHESION RECEPTORS; SARCOMA CELLS; BETA-SUBUNIT; ALPHA-V; FAMILY; PROTEIN AB The capability of the integrin VLA-3 to function as a receptor for collagen (Coll), laminin (Lm), and fibronectin (Fn) was addressed using both whole cell adhesion assays and ligand affinity columns. Analysis of VLA-3-mediated cell adhesion was facilitated by the use of a small cell lung carcinoma line (NCI-H69), which expresses VLA-3 but few other integrins. While VLA-3 interaction with Fn was often low or undetectable in cells having both VLA-3 and VLA-5, NCI-H69 cells readily attached to Fn in a VLA-3-dependent manner. Both Arg-Gly-Asp (RGD) peptide inhibition studies, and Fn fragment affinity columns suggested that VLA-3, like VLA-5, may bind to the RGD site in human Fn. However, unlike Fn, both Coll and Lm supported VLA-3-mediated adhesion that was not inhibited by RGD peptide, and was totally unaffected by the presence of VLA-5. In addition, VLA-3-mediated binding to Fn was low in the presence of Ca++, but was increased 6.6-fold with Mg++, and 30-fold in the presence of Mn++. In contrast, binding to Coll was increased only 1.2-fold with Mg++, and 1.7-fold in Mn++, as compared to the level seen with Ca++. Together, these experiments indicate that VLA-3 can bind Coll, Lm, and Fn, and also show that (a) VLA-3 can recognize both RGD-dependent and RGD-independent ligands, and (b) different VLA-3 ligands have distinctly dissimilar divalent cation sensitivities. RP ELICES, MJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 17007]; NIGMS NIH HHS [GM 38903] NR 60 TC 421 Z9 423 U1 2 U2 6 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD JAN PY 1991 VL 112 IS 1 BP 169 EP 181 DI 10.1083/jcb.112.1.169 PG 13 WC Cell Biology SC Cell Biology GA EQ997 UT WOS:A1991EQ99700015 PM 1986004 ER PT J AU STRITTMATTER, SM VALENZUELA, D VARTANIAN, T SUDO, Y ZUBER, MX FISHMAN, MC AF STRITTMATTER, SM VALENZUELA, D VARTANIAN, T SUDO, Y ZUBER, MX FISHMAN, MC TI GROWTH CONE TRANSDUCTION - G0 AND GAP-43 SO JOURNAL OF CELL SCIENCE LA English DT Article; Proceedings Paper CT JOINT 1991 ANNUAL MEETING OF THE BRITISH SOC FOR CELL BIOLOGY / BRITISH SOC FOR DEVELOPMENTAL BIOLOGY : NERVE CELL BIOLOGY CY APR, 1991 CL LEEDS, ENGLAND SP BRIT SOC CELL BIOL, BRIT SOC DEV BIOL DE GAP-43; GROWTH CONE; GTP-BINDING PROTEINS; SIGNAL TRANSDUCTION; G0 ID PROTEIN-KINASE-C; EXTRACELLULAR-MATRIX PROTEIN; CALMODULIN-BINDING PROTEIN; NERVE GROWTH; NEURITE OUTGROWTH; BETA-2-ADRENERGIC RECEPTOR; SUBSTRATUM ADHESION; CALCIUM CHANNELS; AXON GROWTH; PC12 CELLS AB The neuronal growth cone plays a crucial role in forming the complex brain architecture achieved during development, and similar nerve terminal mechanisms may operate to modify synaptic structure during adulthood. The growth cone leads the elongating axon towards appropriate synaptic targets by altering motility in response to a variety of extracellular signals. Independently of extrinsic clues, neurons mainfest intrinsic control of their growth and form (Banker and Cowan, 1979). Hence, there must be intracellular proteins which control nerve cell shape, so-called 'plasticity' or 'growth' genes. GAP-43 may be such a molecule (Skene and Willard, 1981; Benowitz and Lewis, 1983). For example, GAP-43 is localized to the growth cone membrane (Meiri et al. 1986; Skene et al. 1986) and can enhance filopodial formation even in non-neuronal cells (Zuber et al. 1989a). It includes a small region at the amino terminus for membrane association and perhaps growth cone targeting (Zuber et al. 1989b, Liu et al. 1991). We have found that G(o), a member of the G protein family that links receptors and second messengers, is the major non-cytoskeletal protein in the growth cone membrane (Strittmatter et al. 1990). Double staining immunohistochemistry for GAP-43 and G(o) shows that the distributions of the two proteins are quite similar. Purified GAP-43 regulates the activity of purified G(o) (Strittmatter et al. 1990), a surprising observation since GAP-43 is an intracellular protein. We have compared the mechanism of GAP-43 activation of G(o) with that of G protein-linked receptors. GAP-43 resembles receptor activation in that both serve primarily to increase the rate of dissociation of bound GDP, with consequent increase in GTP-gamma-S binding and GTPase activity. Neither affects the intrinsic rate of hydrolysis of bound GTP by G(o). They differ, however, in that pertussis toxin blocks interaction of the receptor with G(o), but not that of GAP-43. Furthermore, whereas GAP-43 activates both isolated alpha(o) subunits and alpha-beta-gamma-trimers, receptors require the presence of the beta-gamma-subunits. Thus like receptors, GAP-43 is a guanine nucleotide release protein, but of a novel class. The interactions between G(o) and GAP-43 suggest that G(o) plays a pivotal role in growth cone function, coordinating the effects of both extracellular signals and intracellular growth proteins. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,CARDIOVASC RES CTR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP STRITTMATTER, SM (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,DEV BIOL LAB,BOSTON,MA 02114, USA. RI Strittmatter, Stephen/F-5739-2011 OI Strittmatter, Stephen/0000-0001-8188-3092 NR 64 TC 13 Z9 13 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PY 1991 SU 15 BP 27 EP 33 PG 7 WC Cell Biology SC Cell Biology GA HP989 UT WOS:A1991HP98900006 ER PT J AU EHRLICH, HP ROCKWELL, WB CORNWELL, TL RAJARATNAM, JBM AF EHRLICH, HP ROCKWELL, WB CORNWELL, TL RAJARATNAM, JBM TI DEMONSTRATION OF A DIRECT ROLE FOR MYOSIN LIGHT CHAIN KINASE IN FIBROBLAST-POPULATED COLLAGEN LATTICE CONTRACTION SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID DYSTROPHICA RECESSIVE FIBROBLASTS; INDUCED CELL CONTRACTION; SMOOTH-MUSCLE; DERMAL FIBROBLASTS; CATALYTIC SUBUNIT; PROTEIN-KINASE; CAMP; PHOSPHORYLATION; PURIFICATION; CALMODULIN AB Mixing feed fibroblasts with soluble collagen and serum-supplemented culture medium at 37-degrees-C results in the entrapment of cells within the polymerizing collagen matrix. This cellular-collagen complex is referred to as a fibroblast-populated collagen lattice (FPCL). In time, this FPCL undergoes a reduction in size called lattice contraction. The proposed mechanism for lattice contraction is cellular force produced by cytoplasmic microfilaments which organize collagen fibrils compacting the matrix. When the regulatory subunits of myosin, myosin light chains, are phosphorylated by myosin light chain kinase (MLCK), myosin ATPase activity is increased and actin-myosin dynamic filament sliding occurs. Elevated levels of myosin ATPase are required for maximal lattice contraction. Cholera toxin inhibits lattice contraction by increasing intracellular levels of cAMP. It is proposed that increased cytoplasmic concentrations of cAMP promote phosphorylation of MLCK, the enzyme important for maximizing myosin ATPase activity. Phosphorylating MLCK in vitro inhibits activity by decreasing its sensitivity to calcium-calmodulin complex. A decrease in MLCK activity would result in lower levels of myosin ATPase activity. MLCK, purified from turkey gizzard, was subjected to limited proteolytic digestion to produce calmodulin-independent-MLCK. The partially digested kinase does not require calcium-calmodulin for activation. Independent-MLCK is not subject to inhibition by phosphorylation. The electroporetic inoculation of independent-MLCK into fibroblasts before FPCL manufacture produced enhanced lattice contraction. Lattice contraction, in the presence of cholera toxin, was restored to normal levels by the prior electroporetic introduction of independent-MLCK. These findings support the hypothesis that increases in cAMP hinder lattice contraction by a mechanism involving inhibition of MLCK and myosin ATPase. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. NHLBI,BETHESDA,MD 20892. RP EHRLICH, HP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,SHRINERS BURNS INST,WOUND HEALING LAB,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [GM-32705] NR 21 TC 54 Z9 54 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD JAN PY 1991 VL 146 IS 1 BP 1 EP 7 DI 10.1002/jcp.1041460102 PG 7 WC Cell Biology; Physiology SC Cell Biology; Physiology GA EU576 UT WOS:A1991EU57600001 PM 1846633 ER PT J AU OUELLETTE, EM AF OUELLETTE, EM TI LEGAL ISSUES IN THE TREATMENT OF CHILDREN WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER SO JOURNAL OF CHILD NEUROLOGY LA English DT Article AB The treatment of children with attention deficit hyperactivity disorder (ADHD) has raised a number of legal issues. Tort issues include medical malpractice and battery claims. Suits have charged physicians with negligent misdiagnosis of ADHD, and failure to obtain adequate informed consent for the use of stimulant medications, primarily by inadequate provision of information about side effects. Coercive use of medications by school systems, in the absence of parental consent, has raised issues about battery. Constitutional questions are present concerning limitations on parental rights to decline medical care for their children balanced against the State's interest in safeguarding the health and welfare of children. Children's own equal protection, due process, and privacy rights are also at issue, as well as their constitutional and statutory right to an education. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP OUELLETTE, EM (reprint author), MASSACHUSETTS GEN HOSP,DEPT PEDIAT NEUROL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 9 TC 4 Z9 4 U1 1 U2 5 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PY 1991 VL 6 SU S BP S68 EP S75 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA EV301 UT WOS:A1991EV30100008 PM 2002217 ER PT J AU LAFLECHE, G ALBERT, MS AF LAFLECHE, G ALBERT, MS TI DEFICITS ON FRONTAL TASKS IN EARLY ALZHEIMERS-DISEASE SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 50 EP 50 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600155 ER PT J AU GROOP, LC SALORANTA, C SHANK, M BONADONNA, RC FERRANNINI, E DEFRONZO, RA AF GROOP, LC SALORANTA, C SHANK, M BONADONNA, RC FERRANNINI, E DEFRONZO, RA TI THE ROLE OF FREE FATTY-ACID METABOLISM IN THE PATHOGENESIS OF INSULIN RESISTANCE IN OBESITY AND NONINSULIN-DEPENDENT DIABETES-MELLITUS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID GLUCOSE-TOLERANCE; PLASMA-GLUCOSE; POSTRECEPTOR DEFECTS; LIPID OXIDATION; RECEPTOR; BINDING; INVIVO; MUSCLE; HYPERGLYCEMIA; CARBOHYDRATE AB To investigate the mechanisms of insulin resistance in obesity and noninsulin-dependent diabetes mellitus (NIDDM), we examined oxidative and nonoxidative pathways of free fatty acid (FFA) and glucose metabolism in 14 lean and 17 obese (with normal oral glucose tolerance) nondiabetic subjects and in 8 lean and 8 obese subjects with NIDDM. FFA and glucose metabolism were measured using the sequential insulin clamp technique in combination with indirect calorimetry and infusion of [3-H-3]glucose and [1-C-14]palmitate. Obesity was characterized by enlarged fat mass, which correlated positively with the plasma FFA concentration (r = 0.62; P < 0.01). FFA metabolism was less sensitive to insulin in obese than in lean nondiabetic subjects, but this defect could be overcome by increasing the plasma insulin concentration. NIDDM patients showed normal sensitivity to the inhibitory action of insulin FFA metabolism; however, maximal suppression by insulin was impaired. The combination of obesity and NIDDM was associated with a further enhancement of reesterification of FFA than observed in either condition alone. In both obesity and NIDDM, the dose-response curve for suppression of hepatic glucose production by insulin was impaired. While obesity was primarily characterized by reduced sensitivity to the stimulatory action of insulin on oxidative and nonoxidative pathways of glucose metabolism, resistance to the effect of insulin on glucose metabolism in NIDDM was characterized by a reduced maximal response. The combination of obesity and NIDDM further impaired the sensitivity of liver glucose output and glucose oxidation to insulin. The hypothesis is advanced that in uncomplicated obesity, increased availability and oxidation of FFA leads, by the FFA/glucose cycle, to the impairment in glucose utilization. In NIDDM, on the other hand, the defect in glucose utilization is primary, and the enhanced rate of FFA oxidation may represent a compensatory phenomenon. C1 UNIV PISA, CNR, INST CLIN PHYSIOL, I-56100 PISA, ITALY. UNIV PISA, MED CLIN 2, I-56100 PISA, ITALY. UNIV TEXAS, HLTH SCI CTR, DEPT MED, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. RP GROOP, LC (reprint author), HELSINKI UNIV HOSP, DEPT MED, UNIONINKATU 38, SF-00170 HELSINKI, FINLAND. FU FIC NIH HHS [F05-TWO-3451]; NCRR NIH HHS [RR-125]; NIADDK NIH HHS [AM-24092] NR 53 TC 262 Z9 268 U1 0 U2 10 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1991 VL 72 IS 1 BP 96 EP 107 PG 12 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ518 UT WOS:A1991EQ51800017 PM 1986032 ER PT J AU SKATES, SJ SINGER, DE AF SKATES, SJ SINGER, DE TI QUANTIFYING THE POTENTIAL BENEFIT OF CA-125 SCREENING FOR OVARIAN-CANCER SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE SCREENING; STOCHASTIC MODEL; OVARIAN NEOPLASMS; RADIOIMMUNOASSAY; SIMULATION ID MONOCLONAL-ANTIBODY; COST-EFFECTIVENESS; BREAST-CANCER; LEAD TIME; MODELS; RELEVANCE; CARCINOMA; DISEASE AB We develop a stochastic model of screening for ovarian cancer with serum levels of the CA 125 radioimmunoassay, a tumor-specific marker. The natural history of the disease is constructed using a four stage model characterized by a multivariate distribution for duration in each stage. Preserving its important features, we simplify the model to a function of two parameters; the average duration in stage I and the coefficient of variation of duration in each stage. A yearly screening program is superimposed using exponential CA 125 growth curves which result in stage-specific sensitivities corresponding to values reported in the literature. By implementing a computer simulation of the stochastic model, we estimate the benefit due to screening. This benefit is expressed as expected years of life saved per case of ovarian cancer. The model incorporates the stochastic nature of the disease process, allows easy analysis of repeated screens, and automatically accounts for correlation between subsequent tests. It provides the basis for planning optimal screening strategies with CA 125 testing. RP SKATES, SJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,GEN INTERNAL MED UNIT,BOSTON,MA 02114, USA. NR 40 TC 45 Z9 45 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 IS 4-5 BP 365 EP 380 DI 10.1016/0895-4356(91)90075-K PG 16 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA FD427 UT WOS:A1991FD42700005 PM 2010780 ER PT J AU TULEY, MR MULROW, CD MCMAHAN, CA AF TULEY, MR MULROW, CD MCMAHAN, CA TI ESTIMATING AND TESTING AN INDEX OF RESPONSIVENESS AND THE RELATIONSHIP OF THE INDEX TO POWER SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE RESPONSIVENESS; POWER; RELIABILITY; VALIDITY; SENSITIVITY TO CHANGE; EVALUATIVE INSTRUMENT ID HEALTH-STATUS AB Responsiveness has been proposed as a criterion, in addition to reliability and validity, to evaluate instruments that measure quality of life or functional status. The responsiveness index measures the change in a quality of life score due to a treatment relative to the variability of changes in that score within a stable control group. We derive the expected value, variance and distribution of the responsiveness index and give a large sample distribution for comparing the responsiveness of two different instruments. We also give the relationship between the responsiveness index and the power of a test of treatment effect. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GERIATR RES EDUC & CLIN CTR,SAN ANTONIO,TX 78284. RP TULEY, MR (reprint author), JOHN L MCCLELLAN MEM VET ADM MED CTR,LITTLE ROCK HLTH SERV RES & DEV FIELD PROGRAM,LITTLE ROCK,AR 72205, USA. NR 11 TC 55 Z9 56 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 IS 4-5 BP 417 EP 421 DI 10.1016/0895-4356(91)90080-S PG 5 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA FD427 UT WOS:A1991FD42700010 PM 2010785 ER PT J AU GROOP, LC BONADONNA, RC SHANK, M PETRIDES, AS DEFRONZO, RA AF GROOP, LC BONADONNA, RC SHANK, M PETRIDES, AS DEFRONZO, RA TI ROLE OF FREE FATTY-ACIDS AND INSULIN IN DETERMINING FREE FATTY-ACID AND LIPID OXIDATION IN MAN SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE FREE FATTY ACID; INSULIN; LIPID OXIDATION; GLUCOSE DISPOSAL ID GLUCOSE; RESISTANCE; VALIDATION; MUSCLE AB Plasma FFA oxidation (measured by infusion of C-14-palmitate) and net lipid oxidation (indirect calorimetry) are both inhibited by insulin. The present study was designed to examine whether these insulin-mediated effects on lipid metabolism resulted from a decline in circulating FFA levels or from a direct action of the hormone on FFA/lipid oxidation. Nine subjects participated in two euglycemic insulin clamps, performed with and without heparin. During each insulin clamp study insulin was infused at two rates, 4 and 20 mU/m2 . min for 120 min. The studies were performed with indirect calorimetry and 3-H-3-glucose and C-14-palmitate infusion. During the control study plasma FFA fell from 610 +/- 46 to 232 +/- 42 to 154 +/- 27 mu-mol/liter, respectively. When heparin was infused basal plasma FFA concentration remained constant. During the control study, FFA/lipid oxidation rates decreased in parallel with the fall in the plasma FFA concentration. During the insulin/heparin study, plasma C-14-FFA oxidation remained unchanged while net lipid oxidation decreased. In conclusion, when the plasma FFA concentration is maintained unchanged by heparin infusion, insulin has no direct effect on FFA turnover and disposal. These results thus suggest that plasma FFA oxidation is primarily determined by the plasma FFA concentrations, while net lipid oxidation is regulated by both the plasma FFA and the insulin level. C1 YALE UNIV,SCH MED,DEPT MED,DIV ENDOCRINOL DIABET,NEW HAVEN,CT 06504. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV DIABET,SAN ANTONIO,TX 78284. VET ADM MED CTR,SAN ANTONIO,TX 78284. RP GROOP, LC (reprint author), HELSINKI UNIV HOSP,DEPT MED 4,UNIONINKATU 38,SF-00170 HELSINKI,FINLAND. FU FIC NIH HHS [FO5 TWO 3451]; NCRR NIH HHS [RR125]; NIADDK NIH HHS [AM 24092] NR 29 TC 154 Z9 154 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1991 VL 87 IS 1 BP 83 EP 89 DI 10.1172/JCI115005 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EQ976 UT WOS:A1991EQ97600013 PM 1985114 ER PT J AU CHEN, LA VATNER, DE VATNER, SF HITTINGER, L HOMCY, CJ AF CHEN, LA VATNER, DE VATNER, SF HITTINGER, L HOMCY, CJ TI DECREASED-GS-ALPHA MESSENGER-RNA LEVELS ACCOMPANY THE FALL IN GS AND ADENYLYL CYCLASE ACTIVITIES IN COMPENSATED LEFT-VENTRICULAR HYPERTROPHY - IN HEART-FAILURE, ONLY THE IMPAIRMENT IN ADENYLYL CYCLASE ACTIVATION PROGRESSES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CATECHOLAMINES; GI-ALPHA-2 MESSENGER RNA; PRESSURE OVERLOAD; BETA-ADRENERGIC RECEPTOR ID MYOCARDIAL BLOOD-FLOW; FAILING HUMAN-HEART; BETA-ADRENERGIC RECEPTORS; CONSCIOUS DOGS; PRESSURE-OVERLOAD; DOWN-REGULATION; G-PROTEINS; DESENSITIZATION; SUBSENSITIVITY; NOREPINEPHRINE AB We have previously reported that there is a global reduction in adenylyl cyclase associated with a decrement in G(s) functional activity in cardiac sarcolemma from animals with pressure overload-induced hypertrophy and heart failure. This study was performed to determine whether hypertrophy alone in the absence of heart failure is sufficient to promote these changes and whether the superimposition of heart failure intensified these changes. Basal and stimulated adenylyl cyclase and G(s) activity, as determined in the S49 cyc- reconstitution assay, were measured in sarcolemma from normal (NL), left ventricular hypertrophy (LVH) and heart failure (HF) animals. Simultaneously, we measured the mRNA level encoding for the G(s-alpha) subunit. These studies indicate that G(s) activity and G(s-alpha) mRNA are decreased by approximately 30% both in the failing heart and even in the heart with compensated hypertrophy before heart failure develops (G(s) activity, pmol cyclic AMP/10 min per mu-G, NL 4.2 +/- 0.4, LVH 3.0 +/- 0.2, HF 3.2 +/- 0.3; G(s-alpha) mRNA, pg/10 mu-G RNA, NL 131 +/- 9.0, LVH 104 +/- 7.4, Hf 97.4 +/- 9.1; P < 0.05 as compared with NL for LVh and HF). Accompanying this decrement in G(S) activity is a fall in adenylyl cyclase, both basal and stimulated. However, we also identified a further decrease in adenylyl cyclase without any additional change in G(s) or in its alpha subunit mRNA level. This is seen only in the sarcolemma from animals with heart failure as compared with those with compensated LV hypertrophy (e.g., NaF-stimulated activity, pmol cycle AMP/min per mg, NL 420.2 +/- 17.5, LVH 347.1 +/- 29.6, Hf 244.2 +/- 27.3; P < 0.05 compared with NL for LVH and HF, P < 0.05 compared with LVH for HF). In summary, these studies indicate that both G(s) and adenylyl cyclase activities fall in parallel with the development of LV hypertrophy followed by a further decrement in adenylyl cyclase, independent of G(s), in the setting of heart failure. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC UNIT,JACKSON 14,BOSTON,MA 02114. NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. FU NCRR NIH HHS [RR-00168]; NHLBI NIH HHS [HL-19259, HL-38070] NR 45 TC 69 Z9 70 U1 0 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1991 VL 87 IS 1 BP 293 EP 298 DI 10.1172/JCI114985 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EQ976 UT WOS:A1991EQ97600039 PM 1824633 ER PT J AU BURGESS, RC ROTH, BJ PASCUALLEONE, A SHIELDS, RW CHOKROVERTY, S CADWELL, JA MURRAY, NMF SMITH, IS MILLS, KA NEWMAN, RW RANDOLPH, K CHIAPPA, K ROTHWELL, J EVANS, AL CLAUS, D JALINOUS, R AF BURGESS, RC ROTH, BJ PASCUALLEONE, A SHIELDS, RW CHOKROVERTY, S CADWELL, JA MURRAY, NMF SMITH, IS MILLS, KA NEWMAN, RW RANDOLPH, K CHIAPPA, K ROTHWELL, J EVANS, AL CLAUS, D JALINOUS, R TI MAGNETIC STIMULATORS SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY LA English DT Discussion C1 CLEVELAND CLIN EDUC FDN,EMG LAB,CLEVELAND,OH 44106. VET ADM MED CTR,CADWELL LABS,LYONS,NJ 07939. GEN INFIRM,DEPT NEUROPHYSIOL,LEEDS LS1 3EX,W YORKSHIRE,ENGLAND. UNIV OXFORD,OXFORD,ENGLAND. MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LAB,BOSTON,MA 02114. MRC,INST NEUROL,HUMAN MOVEMENT & BALANCE UNIT,LONDON WC1E 6AS,ENGLAND. ROYAL FREE HOSP,DEPT CHILD HLTH,LONDON,ENGLAND. UNIV ERLANGEN NURNBERG,DEPT NEUROL,W-8520 ERLANGEN,GERMANY. NINCDS,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. NINCDS,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RI Roth, Bradley/A-4920-2008 NR 3 TC 2 Z9 2 U1 0 U2 5 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0736-0258 J9 J CLIN NEUROPHYSIOL JI J. Clin. Neurophysiol. PD JAN PY 1991 VL 8 IS 1 BP 121 EP 128 DI 10.1097/00004691-199101000-00015 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA EY613 UT WOS:A1991EY61300014 ER PT J AU HAYES, DF AF HAYES, DF TI WHAT WOULD YOU DO IF THIS WERE YOUR ... WIFE, SISTER, MOTHER, SELF SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID NEGATIVE BREAST-CANCER; ADJUVANT THERAPY; TUMORS RP HAYES, DF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 13 TC 14 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 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1991 VL 9 IS 1 BP 1 EP 3 PG 3 WC Oncology SC Oncology GA EP763 UT WOS:A1991EP76300001 PM 1985157 ER PT J AU SCHWENN, MR BLATTNER, SR LYNCH, E WEINSTEIN, HJ AF SCHWENN, MR BLATTNER, SR LYNCH, E WEINSTEIN, HJ TI HIC-COM - A 2-MONTH INTENSIVE CHEMOTHERAPY REGIMEN FOR CHILDREN WITH STAGE-III AND STAGE-IV BURKITT-LYMPHOMA AND B-CELL ACUTE LYMPHOBLASTIC-LEUKEMIA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID HIGH-DOSE METHOTREXATE; NON-HODGKINS LYMPHOMA; INTRATHECAL CYTOSINE-ARABINOSIDE; EFFECTIVE THERAPY; CYCLOPHOSPHAMIDE C1 BOSTON FLOATING HOSP INFANTS & CHILDREN,DIV PEDIATR HEMATOL,BOSTON,MA. MAINE CHILDRENS CANC PROGRAM,PORTLAND,ME. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. NR 24 TC 82 Z9 84 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1991 VL 9 IS 1 BP 133 EP 138 PG 6 WC Oncology SC Oncology GA EP763 UT WOS:A1991EP76300018 PM 1985162 ER PT J AU JENIKE, MA BAER, L BUTTOLPH, L AF JENIKE, MA BAER, L BUTTOLPH, L TI BUSPIRONE AUGMENTATION OF FLUOXETINE IN PATIENTS WITH OBSESSIVE-COMPULSIVE DISORDER SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID LITHIUM C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JENIKE, MA (reprint author), MASSACHUSETTS GEN HOSP,OCD CLIN & RES UNIT,BULFINCH 3,FRUIT ST,BOSTON,MA 02114, USA. NR 11 TC 70 Z9 71 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JAN PY 1991 VL 52 IS 1 BP 13 EP 14 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA EV493 UT WOS:A1991EV49300005 PM 1988411 ER PT J AU POLLACK, MH ROSENBAUM, JF AF POLLACK, MH ROSENBAUM, JF TI FLUOXETINE TREATMENT OF COCAINE ABUSE IN HEROIN-ADDICTS SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID DESIPRAMINE AB The authors administered fluoxetine to 11 cocaine-abusing heroin addicts entered in a methadone maintenance program to determine whether it would decrease cocaine craving and use. Three patients discontinued treatment within a few days of initiation because of lack of any acute therapeutic effect. The remaining 8 received fluoxetine for at least 1 week and were followed up over 1 to 6 months. Of these 8, 5 (63%) were successfully treated for cocaine abuse. Three case examples are presented. Fluoxetine may prove a useful addition to the therapeutic armamentarium in the treatment of cocaine abuse. C1 HABIT MANAGEMENT INST,BOSTON,MA. RP POLLACK, MH (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,ACC 815-15,PARKMAN ST,BOSTON,MA 02114, USA. NR 11 TC 72 Z9 72 U1 1 U2 2 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JAN PY 1991 VL 52 IS 1 BP 31 EP 33 PG 3 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA EV493 UT WOS:A1991EV49300011 PM 1988415 ER PT J AU LEE, MJ YODER, IC PAPANICOLAOU, N TUNG, GA AF LEE, MJ YODER, IC PAPANICOLAOU, N TUNG, GA TI LARGE GARTNER DUCT CYST ASSOCIATED WITH A SOLITARY CROSSED ECTOPIC KIDNEY - IMAGING FEATURES SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE GENITOURINARY TRACT, ABNORMALITIES; ANOMALIES, CONGENITAL; PELVIS, CYSTS; MAGNETIC RESONANCE IMAGING ID VAGINA; URETER AB A large Gartner duct cyst associated with solitary crossed renal ectopia was diagnosed in a young woman presenting with dyspareunia and pelvic pain. Among the radiologic imaging modalities used, magnetic resonance imaging and sonography were the most helpful in determining the cystic nature of the mass, its separation from other pelvic organs, as well as its contiguity with the lateral wall of the vagina. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 9 TC 11 Z9 11 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD JAN-FEB PY 1991 VL 15 IS 1 BP 149 EP 151 DI 10.1097/00004728-199101000-00025 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA ET718 UT WOS:A1991ET71800025 PM 1987186 ER PT J AU MATSUMOTO, AK KOPICKYBURD, J CARTER, RH TUVESON, DA TEDDER, TF FEARON, DT AF MATSUMOTO, AK KOPICKYBURD, J CARTER, RH TUVESON, DA TEDDER, TF FEARON, DT TI INTERSECTION OF THE COMPLEMENT AND IMMUNE-SYSTEMS - A SIGNAL TRANSDUCTION COMPLEX OF THE LYMPHOCYTE-B CONTAINING COMPLEMENT RECEPTOR TYPE-2 AND CD19 SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID EPSTEIN-BARR VIRUS; COBRA VENOM FACTOR; MONOCLONAL-ANTIBODY; C3B/C4B RECEPTOR; CELL ACTIVATION; LIGAND-BINDING; MEMBRANE IGM; C3D RECEPTOR; T-CELLS; EXPRESSION AB The complement system augments the humoral immune response, possibly by a mechanism that involves the B lymphocyte membrane receptor, CR2, which binds the C3dg fragment of C3 and triggers several B cell responses in vitro. The present study demonstrates that CR2 associates with a complex of membrane proteins that may mediate signal transduction by ligand CR2. Monoclonal antibodies to CR2 immunoprecipitated from digitonin lysates of Raji B lymphoblastoid cells a membrane complex containing CR2, approximately equimolar amounts of CD19, which is a member of the immunoglobulin superfamily, and three unidentified components: p130, p50 and p20. The complex, which was immunoprecipitated also with anti-CD19, could be dissociated by Nonidet P-40, accounting for its absence in previous studies of CR2. Expression of recombinant CR2 and CD19 in K562 erythroleukemia cells led to formation of a complex that contained not only these two proteins but also p130, p50, and p20, and another component, p14. These unidentified components of the CR2/CD19 complex coimmunoprecipitated with CD19 and not with CR2 from singly transfected cells, indicating primary association with the former. CD19 replicated the capacity of CR2 to interact synergistically with MIgM for increasing free intracellular Ca2+, suggesting that the complex mediates this function of CR2. Therefore, CR2 associates directly with CD19 to become a ligand-binding subunit of a pre-existing signal transduction complex of the B cell that may be representative of a family of membrane protein complexes. This interaction between the complement and immune systems differs from the between immunoglobulin and Clq by involving membrane rather than plasma proteins, and by having complement involved in the afferent phase of the immune response. C1 JOHNS HOPKINS UNIV,SCH MED,DIV MOLEC & CLIN RHEUMATOL,725 N WOLFE ST,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI-22833, AI-28191]; NIGMS NIH HHS [T32 GM-07309] NR 52 TC 272 Z9 276 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1991 VL 173 IS 1 BP 55 EP 64 DI 10.1084/jem.173.1.55 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EP659 UT WOS:A1991EP65900007 PM 1702139 ER PT J AU CHERAYIL, BJ PILLAI, S AF CHERAYIL, BJ PILLAI, S TI THE OMEGA/DELTA-5-SURROGATE IMMUNOGLOBULIN LIGHT CHAIN IS EXPRESSED ON THE SURFACE OF TRANSITIONAL LYMPHOCYTES-B IN MURINE BONE-MARROW SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MU-HEAVY-CHAINS; GENE REARRANGEMENT; ALLELIC EXCLUSION; TRANSGENIC MICE; CELL LINE; OMEGA; PROTEIN AB The membrane immunoglobulin heavy chain (mu-m) plays a feedback role during the pre-B stage of B lymphocyte differentiation. In pre-B cell lines, mu-m associates with two surrogate light chain proteins. The omega-chain is disulfide linked to mu and was predicted to be the product of the lambda-5 gene. The iota-chain is noncovalently associated with mu-m. We demonstrate that the omega-protein is indeed the product of the lambda-5 gene and the mu, omega, and iota are coassociated in the same complex. Antibodies against the omega/lambda-5 protein demonstrate the existence of a subpopulation of "transitional" bone marrow B cells that express mu-m and omega on the cell surface. The majority of these cells also express surface kappa-light chains, indicating that in B lymphoid ontogeny the lambda-5 gene is inactivated after the onset of kappa-light chain expression. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC IMMUNOL LAB,MOLEC GENET GRP,BLDG 149,13TH ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIAID NIH HHS [AI-27835] NR 32 TC 85 Z9 85 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1991 VL 173 IS 1 BP 111 EP 116 DI 10.1084/jem.173.1.111 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EP659 UT WOS:A1991EP65900012 PM 1898658 ER PT J AU SIEGEL, DB GELBERMAN, RH AF SIEGEL, DB GELBERMAN, RH TI RADIAL STYLOIDECTOMY - AN ANATOMICAL STUDY WITH SPECIAL REFERENCE TO RADIOCARPAL INTRACAPSULAR LIGAMENTOUS MORPHOLOGY SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Article AB This study determines the anatomical relationship of the radiocarpal ligaments to the radial styloid process, and the effect of three specific styloidectomies on the integrity of the these ligaments. Thirty fresh cadaveric wrists were dissected. The origins, insertions, and dimensions of each ligament was determined. The thirty wrists were divided randomly into three equal groups and the ten wrists in each group had three types of styloidectomy: short oblique, vertical oblique, and horizontal. The styloid fragments and wrists were then reexamined to determine the integrity of the ligaments. All styloidectomies removed the radial collateral ligament origin. Vertical oblique styloidectomy removed additionally 92% of the radioscaphocapitate and 21% of the radiolunatotriquetral ligament. Horizontal styloidectomy removed 95% of the radioscaphocapitate, and 46% of the radiolunatotriquetral ligament. These findings indicate that the degree of radiocarpal ligament disruption that occurs after styloidectomy may be predicted accurately by correlating the amount of styloid removed, with the consistent ligamentous anatomy of this area. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,WACC 527,BOSTON,MA 02114. NR 0 TC 18 Z9 20 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD JAN PY 1991 VL 16A IS 1 BP 40 EP 44 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA EU716 UT WOS:A1991EU71600008 PM 1995691 ER PT J AU YAMADA, A NIKAIDO, T NOJIMA, Y SCHLOSSMAN, SF MORIMOTO, C AF YAMADA, A NIKAIDO, T NOJIMA, Y SCHLOSSMAN, SF MORIMOTO, C TI ACTIVATION OF HUMAN CD4 LYMPHOCYTES-T - INTERACTION OF FIBRONECTIN WITH VLA-5 RECEPTOR ON CD4 CELLS INDUCES THE AP-1 TRANSCRIPTION FACTOR SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INTERLEUKIN-2 GENE; SURFACE RECEPTORS; ANTIGEN RECEPTOR; EXPRESSION; PROMOTER; ENHANCER; ELEMENTS AB Fibronectin synergized with anti-CD3 antibody to promote CD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when CD4 cells were cultured with anti-CD3 alone or fibronectin alone. In addition, anti-CD29 (integrin-beta-1) as well as anti-VLA-5 (human fibronectin receptor) antibodies blocked this CD4 cell activation in this system. Although anti-CD3 alone or fibronectin alone cannot induce IL-2 message by CD4 cells, the combination of anti-CD3 plus fibronectin induced IL-2 message by CD4 cells. In an analysis of the molecular mechanism by which IL-2 message was generated, we showed that a fibronectin-VLA-5 fibronectin receptor interaction may contribute an independent signal distinct from the CD3 pathway of activation by the induction of an AP-1 transcriptional factor. Thus the VLA-5 fibronectin receptor on CDd4 cells can play a complementary role in CD3-TCR-mediated signal transduction through its interaction with fibronectin. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. WISTAR INST,PHILADELPHIA,PA 19104. FU NIAID NIH HHS [AI-12069]; NIAMS NIH HHS [AR-33713] NR 28 TC 161 Z9 161 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1991 VL 146 IS 1 BP 53 EP 56 PG 4 WC Immunology SC Immunology GA EQ340 UT WOS:A1991EQ34000009 PM 1670606 ER PT J AU VIVIER, E MORIN, P OBRIEN, C DRUKER, B SCHLOSSMAN, SF ANDERSON, P AF VIVIER, E MORIN, P OBRIEN, C DRUKER, B SCHLOSSMAN, SF ANDERSON, P TI TYROSINE PHOSPHORYLATION OF THE FC-GAMMA-RIII(CD16) - ZETA COMPLEX IN HUMAN NATURAL-KILLER-CELLS - INDUCTION BY ANTIBODY-DEPENDENT CYTOTOXICITY BUT NOT BY NATURAL KILLING SO JOURNAL OF IMMUNOLOGY LA English DT Article ID FC-GAMMA-RECEPTOR; MONOCLONAL-ANTIBODIES; HUMAN-LYMPHOCYTES; LYMPHOKINE GENES; CYTO-TOXICITY; EXPRESSION; ACTIVATION; CD16; IGG; TRANSCRIPTION AB NK cells are large granular lymphocytes capable of killing certain tumor cells and virally infected cells in a non-MHC-restricted manner. NK cells can also effect an antibody dependent cytotoxicity that is triggered by CD16, an FcR for IgG. In NK cells, CD16 is expressed in association with zeta, a signal transducing subunit of the TCR complex. Here we show that, just as T cell activation via the TCR complex results in tyrosine phosphorylation of zeta-TCR, NK cell activation via CD16 results in tyrosine phosphorylation of zeta-NK. Whereas antibody-dependent cytotoxicity also results in tyrosine phosphorylation of zeta, natural cytotoxicity does not. Our results indicate that zeta-functions as a transducing element for antibody dependent, but not antibody independent killing by NK cells. Consequently, NK cells are likely to express at least two distinct receptor complexes capable of triggering cytolytic effector function. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,NEOPLAST DIS MECHANISMS LAB,BOSTON,MA 02115. NR 28 TC 152 Z9 153 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1991 VL 146 IS 1 BP 206 EP 210 PG 5 WC Immunology SC Immunology GA EQ340 UT WOS:A1991EQ34000034 PM 1701792 ER PT J AU HAREGEWOIN, A SINGH, B GUPTA, RS FINBERG, RW AF HAREGEWOIN, A SINGH, B GUPTA, RS FINBERG, RW TI A MYCOBACTERIAL HEAT-SHOCK PROTEIN-RESPONSIVE GAMMA-DELTA T-CELL CLONE ALSO RESPONDS TO THE HOMOLOGOUS HUMAN HEAT-SHOCK PROTEIN - A POSSIBLE LINK BETWEEN INFECTION AND AUTOIMMUNITY SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID LYMPHOCYTES-T; STRESS PROTEINS; ANTIGEN; TUBERCULOSIS; ARTHRITIS; BACTERIAL; RECEPTOR; DELTA; PLANT AB Prokaryotic and eukaryotic cells respond to a variety of stress conditions by increasing the synthesis of a family of proteins collectively known as heat-shock proteins (HSP). One of these, a 65-kDa HSP that is highly conserved in many bacteria, is a major target of the immune response to mycobacteria. A gamma-delta-T cell clone from a healthy donor that recognizes not only the 65-kDa mycobacterial HSP but also the recombinant human homologue of this HSP protein was raised. Like alpha-beta-T cell clones, which recognize mycobacterial HSP, the clone requires antigen-presenting cells for antigen-induced proliferation and can also be directly activated via receptor cross-linking through CD3 or the delta-chain of the gamma-delta-T cell receptor. These data suggest that the induction of a gamma-delta-T cell response by bacterial antigens could lead to the expansion of cells that respond to autologous proteins and, therefore, may result in the development of autoimmunity. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MCMASTER UNIV,DEPT BIOCHEM,HAMILTON L8S 4L8,ONTARIO,CANADA. RP HAREGEWOIN, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU NIAID NIH HHS [AI-20382, AI-27740] NR 33 TC 57 Z9 58 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1991 VL 163 IS 1 BP 156 EP 160 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA EP678 UT WOS:A1991EP67800026 PM 1984462 ER PT J AU WARFEL, AH CARDOZO, C YOO, OH ZUCKERFRANKLIN, D AF WARFEL, AH CARDOZO, C YOO, OH ZUCKERFRANKLIN, D TI CYSTATIN-C AND CATHEPSIN-B PRODUCTION BY ALVEOLAR MACROPHAGES FROM SMOKERS AND NONSMOKERS SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE ANTIPROTEINASE; PROTEINASE; CYSTEINE PROTEINASES; INFLAMMATION; EMPHYSEMA; LUNGS ID BRONCHOALVEOLAR LAVAGE FLUID; ALPHA-1-PROTEINASE INHIBITOR; PERITONEAL-MACROPHAGES; PROTEINASE-INHIBITORS; CIGARETTE-SMOKING; DOWN-REGULATION; GAMMA-TRACE; NEUTROPHIL; ELASTASE; STIMULATION AB The capacity of alveolar macrophages (AM) obtained from smokers and nonsmokers to secrete cathespin B and its inhibitor cystatin C was examined because of the concept that an imbalance in the production of proteolytic enzymes and/or their inhibitors could be responsible for the lung damage seen in smokers. Quantitation of immunoprecipitates on Western blots showed that the amount of total cystatin C secreted into the culture medium by AM of smokers was significantly greater than the amount secreted by cells obtained from nonsmokers, whereas the difference between the amount of cathespin B secreted by the AM of smokers and that from nonsmokers did not appear significant. The cystatin C found in the medium conditioned by AM of nonsmokers appeared to be more heterogeneous in molecular size, presenting either as a single band of about 14 Kd or as a high-molecular-weight triplet of about 69 Kd, 63 Kd, and 57.3 Kd. Furthermore, in some cases there were single or doublet bands at 14 Kd as well as the high-molecular-weight triplets. In contrast, smokers AM-conditioned medium uniformly possessed both the low-and the high-molecular-weight cystatin C. Cathepsin B was not detected in Western blots at its reported molecular weights but was identified at the exact area occupied by the higher molecular weight cystatin C, i.e., at bands corresponding to 69 Kd, 63 Kd, and 57.3 Kd. Therefore, it is clear that in culture media of AM, cystatin C and cathepsin B are present as proteinase-antiproteinase complexes. The observation also suggests that in smokers an excess of cystatin C may be elaborated, which, if further substantiated, would show for the first time a likely role for this proteinase inhibitor in vivo. C1 NYU MED CTR, DEPT MED, 550 1ST AVE, NEW YORK, NY 10016 USA. BRONX VET ADM MED CTR, DIV PULM & CRIT CARE MED, NEW YORK, NY USA. CUNY MT SINAI SCH MED, NEW YORK, NY 10029 USA. FU NCI NIH HHS [CA16247]; NIADDK NIH HHS [AM-01431, AM-12274] NR 30 TC 29 Z9 29 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD JAN PY 1991 VL 49 IS 1 BP 41 EP 47 PG 7 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA EP033 UT WOS:A1991EP03300006 PM 1984484 ER PT J AU GROSS, SK DANIEL, PF EVANS, JE MCCLUER, RH AF GROSS, SK DANIEL, PF EVANS, JE MCCLUER, RH TI LIPID-COMPOSITION OF LYSOSOMAL MULTILAMELLAR BODIES OF MALE-MOUSE URINE SO JOURNAL OF LIPID RESEARCH LA English DT Article DE KIDNEY; GALABIOSYLCERAMIDE; GLOBOTRIAOSYLCERAMIDE; DOLICHOL; UBIQUINONE; PHOSPHATIDYLCHOLINE; ETHER LIPID; N-3 FATTY ACID ID PERFORMANCE LIQUID-CHROMATOGRAPHY; RAT-LIVER; KIDNEY GLYCOSPHINGOLIPIDS; PHOSPHOLIPIDS; LOCALIZATION; DOLICHOL; BIS(MONOACYLGLYCERO)PHOSPHATE; LACTOSYLCERAMIDE; DYSFUNCTIONS; UBIQUINONE AB Previous studies from our laboratory have shown that male C57BL/6J mice excrete into the urine multilamellar lysosomal bodies that contain specific neutral glycosphingolipids. These mice excrete approximately 20-30% of their kidney glycolipids each day. The significance and function of this secretion of multilamellar lysosomal organelles is unknown. To characterize these excreted bodies further, we report here their neutral lipid and phospholipid composition. The bodies were collected by differential centrifugation, extracted with chloroform-methanol, and lipids were fractionated into neutral lipids, glycolipids, and phospholipids. The neutral lipids consisted primarily of cholesterol, dolichol, and ubiquinone. The phospholipid fraction consisted primarily of a single molecular species of phosphatidylcholine. This lipid which comprises more than 90% of the total phospholipids was found to contain 16:0 ether and C22:6 n-3 fatty acid as determined by gas-liquid chromatography-mass spectrometry. The glycosphingolipids as reported previously consisted primarily of galabiosylceramides and globotriaosylceramides. This membrane lipid composition is different from any previously reported cellular organelle. C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DEPT BIOCHEM,200 TRAPELO RD,WALTHAM,MA 02254. BOSTON UNIV,SCH MED,DEPT BIOCHEM,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. FU NINDS NIH HHS [NS-15037] NR 33 TC 8 Z9 8 U1 0 U2 1 PU LIPID RESEARCH INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD JAN PY 1991 VL 32 IS 1 BP 157 EP 164 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EW565 UT WOS:A1991EW56500017 PM 2010687 ER PT J AU NEUMEYER, JL GAO, YG KULA, NS BALDESSARINI, RJ AF NEUMEYER, JL GAO, YG KULA, NS BALDESSARINI, RJ TI R-ENANTIOMERS AND S-ENANTIOMERS OF 11-HYDROXY-N-ALLYLNORAPORPHINE AND 10,11-DIHYDROXY-N-ALLYLNORAPORPHINE - SYNTHESIS AND AFFINITY FOR DOPAMINE-RECEPTORS IN RAT-BRAIN TISSUE SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID GUANINE-NUCLEOTIDE; AGONIST; AUTORECEPTORS; BINDING; STIMULATION; APORPHINES; STRIATUM; CODEINE; POTENT; D1 AB The R-(-)- and S-(+)-enantiomers of 11-hydroxy-N-allyl (4), and 10,11-dihydroxy-N-allyl (3) congeners of 11-hydroxy-N-n-propylnoraporphine (11-OH-NPa, 2) or N-n-propylnorapomorphine (NPA, 1) were synthesized. Binding affinity of these compounds at dopamine (DA) receptor sites was evaluated with a membrane preparation of corpus striatum from rat brain. The R/S enantiomeric receptor affinity ratio was enhanced by allylic substitution of 3 and 4 and their R isomers had high DA receptor affinity similar to that of the N-n-propyl congeners. These N-allylaporphines are proposed as useful precursors to the preparation of their tritiated N-n-propyl enantiomers. C1 MASSACHUSETTS GEN HOSP,MAILMAN RES CTR,MCLEAN DIV,DEPT PSYCHIAT,BELMONT,MA 02178. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. RP NEUMEYER, JL (reprint author), NORTHEASTERN UNIV,COLL PHARM & ALLIED HLTH PROFESS,MED CHEM SECT,BOSTON,MA 02115, USA. FU NIMH NIH HHS [MH-47370, MH-34006] NR 41 TC 8 Z9 8 U1 0 U2 0 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 JAN PY 1991 VL 34 IS 1 BP 24 EP 28 DI 10.1021/jm00105a005 PG 5 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA ET545 UT WOS:A1991ET54500005 PM 1671415 ER PT J AU ROSOWSKY, A BADER, H FREISHEIM, JH AF ROSOWSKY, A BADER, H FREISHEIM, JH TI ANALOGS OF METHOTREXATE AND AMINOPTERIN WITH GAMMA-METHYLENE AND GAMMA-CYANO SUBSTITUTION OF THE GLUTAMATE SIDE-CHAIN .40. SYNTHESIS AND INVITRO BIOLOGICAL-ACTIVITY SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID LIPID-SOLUBLE DIESTERS; DIHYDROFOLATE-REDUCTASE; ANTITUMOR-ACTIVITY; ACID-DERIVATIVES; 3',5'-DICHLOROMETHOTREXATE; REPLACEMENT; FLUOROMETHOTREXATE; ENHANCEMENT; MONOESTERS; INHIBITION AB Analogues of methotrexate (MTX) and aminopterin (AMT) modified at the gamma-position of the glutamate side chain were synthesized and evaluated as dihydrofolate reductase (DHFR) inhibitors and tumor cell growth inhibitors. Condensations of 4-amino-4-deoxy-N-10-methylpteroic acid (mAPA) with dimethyl DL-4-methyleneglutamate in the presence of diethyl phosphorocyanidate (DEPC) followed by alkaline hydrolysis yielded N-(4-amino-4-deoxy-N-10-methylpteroyl)-DL-4-methyleneglutamic acid (gamma-methyleneMTX). Condensation of 4-amino-4-deoxy-N-10-formylpteroic acid (fAPA) with dimethyl-DL-4-methyleneglutamate by the mixed carboxylic-carbonic anhydride method yielded N-(4-amino-4-deoxypteroyl)-DL-4-methyleneglutamic acid (gamma-methyleneAMT). Also prepared via DEPC coupling was a mixture of the four possible diastereomers of N-(4-amino-4-deoxy-N-10-methylpteroyl)-4-cyanoglutamic acid (gamma-cyanoMTX). The requisite intermediate-gamma-tert-butyl-alpha-methyl 4-cyanoglutamate, as a DL-threo/DL-erythro mixture, was prepared from methyl N-alpha-Boc-O-tosyl-L-serinate by reaction with sodium tert-butyl cyanoacetate followed by mild trifluoroacetic treatment to selectively remove the Boc group. The gamma-methylene derivatives of MTX and AMT are attractive because of their potential to act as Michael acceptors within the DHFR active site. gamma-CyanoMTX may be viewed as a cogener of the nonpolyglutamated MTX analogue-gamma-fluoroMTX. n vitro bioassay data for the gamma-methylene and gamma-cyano compounds support the idea that the active site of DHFR, already known for its ability to tolerate modification of the gamma-carboxyl group of MTX and AMT, can likewise accommodate substitution on the gamma-carbon itself. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MED COLL OHIO,DEPT BIOCHEM,TOLEDO,OH 43699. RP ROSOWSKY, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA25394, CA41461] NR 23 TC 12 Z9 12 U1 0 U2 1 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 JAN PY 1991 VL 34 IS 1 BP 203 EP 208 DI 10.1021/jm00105a031 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA ET545 UT WOS:A1991ET54500031 PM 1992118 ER PT J AU ROSOWSKY, A FORSCH, RA MORAN, RG FREISHEIM, JH AF ROSOWSKY, A FORSCH, RA MORAN, RG FREISHEIM, JH TI SYNTHESIS AND BIOLOGICAL-ACTIVITY OF THE 2-DESAMINO AND 2-DESAMINO-2-METHYL ANALOGS OF AMINOPTERIN AND METHOTREXATE .42. SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID X-RAY STRUCTURE; DIHYDROFOLATE-REDUCTASE; FOLYLPOLYGLUTAMATE SYNTHETASE; THYMIDYLATE SYNTHASE; ANTITUMOR-ACTIVITY; SIDE-CHAIN; FOLIC-ACID; FOLATE ANALOGS; CELL-GROWTH; INHIBITION AB The previously undescribed 2-desamino and 2-desamino-2-methyl analogues of aminopterin (AMT) and methotrexate (MTX) were synthesized from 2-amino-5-(chloromethyl)pyrazine-3-carbonitrile. The AMT analogues were obtained via a three-step sequence consisting of condensation with di-tert-butyl N-(4-aminobenzoyl)-L-glutamate, heating with formamidine or acetamidine acetate, and mild acidolysis with trifluoroacetic acid. The MTX analogues were prepared similarly, except that 2-amino-5-(chloromethyl)pyrazine-3-carbonitrile was condensed with 4-(N-methylamino)benzoic acid and the resulting product was annulated with formamidine or or acetamidine acetate to obtain the 2-desamino and 2-desamino-2-methyl analogues, respectively, of 4-amino-4-deoxy-N-10-methylpteroic acid. Condenstion with di-tert-butyl L-glutamate in the presence of diethyl phosphorocyanidate followed by ester cleavage with trifluoroacetic acid was then carried out. Retention of the L configuration in the glutamate moiety during this synthesis was demonstrated by rapid and essentially complete hydrolysis with carboxypeptidase G1 under conditions that likewise cleaved the L enantiomer of MTX but left the D enantiomer unaffected. The 2-desamino and 2-desamino-2-methyl analogues of AMT and MTX inhibited the growth of tumor cells, but were very poor inhibitors of dihydrofolate reductase (DHFR). These unexpected results suggested that activity in intact cells was due to metabolism of the 2-desamino compounds to polyglutamates. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. UNIV SO CALIF,CTR COMPREHENS CANC,CANC RES LAB,LOS ANGELES,CA 90033. MED COLL OHIO,DEPT BIOCHEM,TOLEDO,OH 43699. RP ROSOWSKY, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA25394, CA39867, CA41461] NR 48 TC 7 Z9 7 U1 1 U2 4 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 JAN PY 1991 VL 34 IS 1 BP 227 EP 234 DI 10.1021/jm00105a036 PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA ET545 UT WOS:A1991ET54500036 PM 1992122 ER EF