FN Thomson Reuters Web of Science™ VR 1.0 PT J AU ZERVOS, AS GYURIS, J BRENT, R AF ZERVOS, AS GYURIS, J BRENT, R TI MXI1, A PROTEIN THAT SPECIFICALLY INTERACTS WITH MAX TO BIND MYC-MAX RECOGNITION SITES SO CELL LA English DT Article ID HUMAN C-MYC; DNA-BINDING; LEUCINE ZIPPER; CELL-DIFFERENTIATION; TRANSFORMATION; EXPRESSION; YEAST; ACTIVATION; TRANSCRIPTION; ONCOGENE AB We used the interaction trap to isolate a novel human protein that specifically interacts with Max. This protein, Mxi1 (for Max interactor 1), contains a bHLH-Zip motif that is similar to that found in Myc family proteins. Mxi1 interacts specifically with Max to form heterodimers that efficiently bind to the Myc-Max consensus recognition site. When bound to DNA by a LexA moiety in yeast, Mxi1 does not stimulate transcription. mxi1 mRNA is expressed in many tissues, and its expression is elevated in U-937 myeloid leukemia cells that have been stimulated to differentiate. These facts are consistent with a model in which Mxi1-Max heterodimers indirectly inhibit Myc function in two ways: first, by sequestering Max, thus preventing the formation of Myc-Max heterodimers, and second, by competing with Myc-Max heterodimers for binding to target sites. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP ZERVOS, AS (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115, USA. RI Tang, Amy/L-3226-2016 OI Tang, Amy/0000-0002-5772-2878 NR 58 TC 694 Z9 697 U1 1 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JAN 29 PY 1993 VL 72 IS 2 BP 223 EP 232 DI 10.1016/0092-8674(93)90662-A PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KK038 UT WOS:A1993KK03800007 PM 8425219 ER PT J AU TREDGET, EE FORSYTH, N UJIFRIEDLAND, A CHAMBERS, M GHAHARY, A SCOTT, PG HOGG, AM BURKE, JF AF TREDGET, EE FORSYTH, N UJIFRIEDLAND, A CHAMBERS, M GHAHARY, A SCOTT, PG HOGG, AM BURKE, JF TI GAS-CHROMATOGRAPHY MASS-SPECTROMETRY DETERMINATION OF O-18(2) IN O-18-LABELED 4-HYDROXYPROLINE FOR MEASUREMENT OF COLLAGEN-SYNTHESIS AND INTRACELLULAR DEGRADATION SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS LA English DT Article ID PROLINE; METABOLISM; KINETICS; INVIVO; TRACER; MODELS; SKIN; LUNG AB The use of gas chromatography-mass spectrometry (GC-MS) and O-18(2), a stable isotope which is incorporated into collagen during the post-translational conversion of proline to hydroxyproline, offers the potential advantages of high levels of sensitivity and specificity as compared to other techniques for measuring rates of collagen synthesis and degradation in vitro and in vivo. Trifluoracetylation and methanol esterification of hydroxyproline yields two derivatives of hydroxyproline: N,O-trifluoroacetyl methyl 4-hydroxy-L-proline (N,O-TFA-Hyp) and N-trifluoroacetyl methyl 4-hydroxy-L-proline (N-TFA-Hyp). In the past, N-TFA-Hyp, which yields the O-16/O-18-containing m/z 182/184 ion pair [M - COOH3]+. when analyzed by electron impact ionization GC-MS, has been proposed for analysis of O-18-enriched collagen. Although N,O-TFA-Hyp can be converted to N-TFA-Hyp by solvolysis, we find that this leads to degradation of the chromatography in GC-MS and demonstrate here that this extra chemical step is unnecessary if the m/z 278/280 ion pair (representing the [M - COOCH3]+. fragment) is measured by selected ion monitoring. By labelling fibroblasts in culture with O-18(2), a sample of isotope-enriched collagen was obtained which was used to calibrate the GC-MS over the range 0.5-49% atom percent enrichment (APE). The greater sensitivity of O-18(2) versus [N-15]proline for labelling newly synthesized collagen was demonstrated by the finding of a ten-fold higher enrichment in the former isotope when administered to cell cultures at the same precursor APE. Thus, the approach described herein permits the determination of total hydroxyproline and A.PE on the same sample avoiding additional processing steps while maintaining the quality of chromatography and the sensitivity of detection. Measurement of absolute rates of both collagen synthesis and intracellular degradation of newly synthesized collagen in cell cultures is thus possible. Preliminary results comparing collagen metabolism in pairs of fibroblasts from hypertrophic scars and normal skin in post-burn patients are presented. C1 UNIV ALBERTA,DEPT ORAL BIOL,EDMONTON T6G 2N8,ALBERTA,CANADA. UNIV ALBERTA,DEPT CHEM,EDMONTON T6G 2B7,AB,CANADA. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. RP TREDGET, EE (reprint author), UNIV ALBERTA,WALTER MCKENZIE CTR,DEPT SURG,2D382,EDMONTON T6G 2B7,AB,CANADA. NR 32 TC 11 Z9 11 U1 1 U2 6 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 29 PY 1993 VL 612 IS 1 BP 7 EP 19 DI 10.1016/0378-4347(93)80361-7 PG 13 WC Chemistry, Analytical SC Chemistry GA KN624 UT WOS:A1993KN62400002 PM 8454705 ER PT J AU HOLZ, GG KUHTREIBER, WM HABENER, JF AF HOLZ, GG KUHTREIBER, WM HABENER, JF TI PANCREATIC BETA-CELLS ARE RENDERED GLUCOSE-COMPETENT BY THE INSULINOTROPIC HORMONE GLUCAGON-LIKE PEPTIDE-1(7-37) SO NATURE LA English DT Article ID ELECTRICAL-ACTIVITY; B-CELLS; GENE-EXPRESSION; CA-2+ CHANNELS; PROTEIN-KINASE; ATP; CURRENTS; RELEASE; ACTIVATION; MODULATION AB NON-INSULIN-DEPENDENT diabetes mellitus (NIDDM, type 2 diabetes) is a disorder of glucose homeostasis characterized by hyperglycaemia, peripheral insulin resistance, impaired hepatic glucose metabolism, and diminished glucose-dependent secretion of insulin from pancreatic beta-cells1. Glucagon-like-peptide-1(7-37) (GLP-1)2 is an intestinally derived hormone that may be useful for the treatment of NIDDM because it acts in vivo to increase the level of circulating insulin, and thus lower the concentration of blood glucose3,4. This therapeutic effect may result from the ability of GLP-1 to compensate for a defect in the glucose signalling pathway that regulates insulin secretion from beta-cells. In support of this concept we report here that GLP-1 confers glucose sensitivity to glucose-resistant beta-cells, a phenomenon we term glucose competence. Induction of glucose competence by GLP-1 results from its synergistic interaction with glucose to inhibit metabolically regulated potassium channels that are also targeted for inhibition by sulphonylurea drugs commonly used in the treatment of NIDDM5. Glucose competence allows membrane depolarization, the generation of action potentials, and Ca2+ influx, events that are known to trigger insulin secretion6,7. RP HOLZ, GG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. RI Holz, George/A-3386-2012 FU NIDDK NIH HHS [R01 DK045817, R01 DK045817-06A2] NR 32 TC 392 Z9 406 U1 0 U2 10 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JAN 28 PY 1993 VL 361 IS 6410 BP 362 EP 365 DI 10.1038/361362a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KJ590 UT WOS:A1993KJ59000061 PM 8381211 ER PT J AU RUBIN, PAD HARRIS, NL WEBER, AL BILYK, JR AF RUBIN, PAD HARRIS, NL WEBER, AL BILYK, JR TI A 73-YEAR-OLD MAN WITH SEVERE FACIAL-PAIN, VISUAL-LOSS, DECREASED OCULAR MOTILITY, AND AN ORBITAL MASS - B-CELL CHRONIC LYMPHOCYTIC-LEUKEMIA SMALL LYMPHOCYTIC LYMPHOMA, WITH INFILTRATION OF ORBITAL MUSCLE, SOFT-TISSUE, AND LACRIMAL GLAND SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID TOLOSA-HUNT SYNDROME; HODGKINS-DISEASE; CAVERNOUS SINUS; APEX SYNDROME; INVOLVEMENT; OPHTHALMOPLEGIA; ASPERGILLOSIS; PARASELLAR; BIOPSY C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RUBIN, PAD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,CTR EYE PLAST & ORBIT,BOSTON,MA 02114, USA. RI wei, chi/H-5730-2011 NR 57 TC 9 Z9 9 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JAN 28 PY 1993 VL 328 IS 4 BP 266 EP 275 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA KJ442 UT WOS:A1993KJ44200009 ER PT J AU LAURIE, A WEISS, M NATHAN, DG SIEFF, CA AF LAURIE, A WEISS, M NATHAN, DG SIEFF, CA TI THE MEMBRANE PROXIMAL SERINE ACIDIC-RICH REGION OF THE HUMAN-BETA COMMON CHAIN IS ESSENTIAL FOR BOTH IL-3 AND GM-CSF INDUCED CELL-PROLIFERATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 115 EP 115 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500418 ER PT J AU SPRINGER, TA AF SPRINGER, TA TI THE DISTINCTIVE FUNCTIONS OF SELECTINS, INTEGRINS, AND IG FAMILY MOLECULES IN REGULATION OF LEUKOCYTE INTERACTION WITH ENDOTHELIUM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 127 EP 127 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500454 ER PT J AU STAMENKOVIC, I SGROI, D BRAESCHANDERSEN, S VARKI, A ARUFFO, A AF STAMENKOVIC, I SGROI, D BRAESCHANDERSEN, S VARKI, A ARUFFO, A TI THE ROLE OF CD22 IN LYMPHOCYTE ADHESION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV CALIF SAN DIEGO,DEPT MOLEC MED,LA JOLLA,CA 92093. BRISTOL MYERS SQUIBB PHARMACEUT INST,SEATTLE,WA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 159 EP 159 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500563 ER PT J AU BRADBURY, LE ZHOU, LJ LEVY, S EVANS, RL TEDDER, TF AF BRADBURY, LE ZHOU, LJ LEVY, S EVANS, RL TEDDER, TF TI MULTIMERIC CD19-CELL SURFACE PROTEIN COMPLEXES REGULATE B-CELL FUNCTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. STANFORD UNIV,MED CTR,SCH MED,STANFORD,CA 94305. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 160 EP 160 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500564 ER PT J AU STAMENKOVIC, I SGROI, D BRAESCHANDERSEN, S VARKI, A ARUFFO, A AF STAMENKOVIC, I SGROI, D BRAESCHANDERSEN, S VARKI, A ARUFFO, A TI THE ROLE OF CD22 IN LYMPHOCYTE ADHESION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV SAN DIEGO,DEPT MOLEC MED,LA JOLLA,CA. BRISTOL MYERS SQUIBB PHARMACEUT INST,SEATTLE,WA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 197 EP 197 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500701 ER PT J AU BRADBURY, LE ZHOU, LJ LEVY, S EVANS, RL TEDDER, TF AF BRADBURY, LE ZHOU, LJ LEVY, S EVANS, RL TEDDER, TF TI MULTIMERIC CD19-CELL SURFACE PROTEIN COMPLEXES REGULATE B-CELL FUNCTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. STANFORD UNIV,MED CTR,SCH MED,STANFORD,CA 94305. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 198 EP 198 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500702 ER PT J AU PILLAI, S CHERAYIL, B CHIODINO, C MACDONALD, K BACHHAWAT, A DESIDERIO, S SMUCKER, C AF PILLAI, S CHERAYIL, B CHIODINO, C MACDONALD, K BACHHAWAT, A DESIDERIO, S SMUCKER, C TI ASSEMBLY AND ORGANIZATION OF PRE-B-CELL AND B-CELL RECEPTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 199 EP 199 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500707 ER PT J AU HIRAYAMA, F KATAYAMA, N NEBEN, S DONALDSON, D NICKBARG, EB CLARK, SC OGAWA, M AF HIRAYAMA, F KATAYAMA, N NEBEN, S DONALDSON, D NICKBARG, EB CLARK, SC OGAWA, M TI SYNERGISTIC INTERACTION BETWEEN INTERLEUKIN-12 (NATURAL-KILLER-CELL STIMULATORY FACTOR, CYTOTOXIC LYMPHOCYTE MATURATION FACTOR) AND STEEL FACTOR IN SUPPORT OF PROLIFERATION OF MURINE LYMPHOHEMATOPOIETIC PROGENITORS IN CULTURE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC 29403. GENET INST,CAMBRIDGE,MA 02140. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 225 EP 225 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500806 ER PT J AU OETTINGER, MA KIRCH, S CUOMO, C AF OETTINGER, MA KIRCH, S CUOMO, C TI GENETIC-ANALYSIS OF RAG-1 AND RAG-2 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 233 EP 233 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500835 ER PT J AU BROWN, D AF BROWN, D TI SPECIALIZED ENDOSOMAL PATHWAYS OF WATER CHANNEL AND PROTON PUMPING ATPASE RECYCLING IN KIDNEY EPITHELIAL-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 263 EP 263 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500942 ER PT J AU EZZELL, RM SAMUELS, M CARDOZO, TJ CRITCHLEY, DR COLL, JL ADAMSON, ED AF EZZELL, RM SAMUELS, M CARDOZO, TJ CRITCHLEY, DR COLL, JL ADAMSON, ED TI EXPRESSION OF CHICKEN VINCULIN COMPLEMENTS THE ADHESION-DEFECTIVE PHENOTYPE OF A MUTANT MOUSE F9 EMBRYONAL CARCINOMA CELL SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,SURG RES LAB,BOSTON,MA 02129. LA JOLLA CANC RES FDN,LA JOLLA,CA 92037. UNIV LEICESTER,DEPT BIOCHEM,LEICESTER LE1 7RH,ENGLAND. RI Coll, Jean-Luc/G-2520-2013 OI Coll, Jean-Luc/0000-0002-2453-3552 NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 270 EP 270 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500962 ER PT J AU MATLIN, KS ZUK, A ZINKL, G KENDALL, DM SCHOENENBERGER, CA AF MATLIN, KS ZUK, A ZINKL, G KENDALL, DM SCHOENENBERGER, CA TI ALTERATIONS OF INTEGRINS IN TRANSFORMED MDCK CELLS LACKING APICAL POLARITY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. MAURICE MULLER INST,BASEL,SWITZERLAND. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 276 EP 276 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500987 ER PT J AU CSERMELY, P KAJTAR, J HOLLOSI, M JALSOVSZKY, G HOLLY, S KAHN, CR GERGELY, P SOTI, C MIHALY, K SOMOGYI, J AF CSERMELY, P KAJTAR, J HOLLOSI, M JALSOVSZKY, G HOLLY, S KAHN, CR GERGELY, P SOTI, C MIHALY, K SOMOGYI, J TI ATP INDUCES A CONFORMATIONAL CHANGE OF THE 90-KDA HEAT-SHOCK PROTEIN (HSP90) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID STEROID-RECEPTOR COMPLEXES; AMINO-ACID SEQUENCE; ROUS-SARCOMA VIRUS; SECONDARY STRUCTURE; DNA-REPLICATION; GLUCOCORTICOID RECEPTOR; AUTOPHOSPHORYLATING ACTIVITY; NUCLEOPROTEIN STRUCTURES; TRANSFORMING PROTEINS; DEPENDENT ACTIVATION AB The 90-kDa heat shock protein (hsp90) is a well conserved, abundant cytosolic protein believed to be a ''chaperone'' of most steroid receptors. We have recently demonstrated that hsp90 has an ATP-binding site and autophosphorylating activity (Csermely, P., and Kahn, C. R. (1991) J. Biol. Chem. 266, 4943-4950). Circular dichroism analysis of highly purified hsp90 from rat liver shows that ATP induces an increase of beta-pleated sheet content of hsp90. Vanadate, molybdate, and heat treatment at 56-degrees-C induce a similar change in the circular dichroism spectrum. Fourier transformed infrared spectroscopy reveals an ATP-induced increase in the interchain interactions of the 90-kDa heat shock protein due to an increase in its beta-pleated sheet content. In further studies we found that ATP: 1) decreases the tryptophan fluorescence of hsp90 by 11.6 +/- 1.9%; 2) increases the hydrophobic character of the protein as determined by its distribution between an aqueous phase and phenyl-Sepharose; and 3) renders hsp90 less susceptible to tryptic digestion. Our results suggest that hsp90 undergoes an ''open --> closed'' conformational change after the addition of ATP, analogous in many respects to the similar changes of the DnaK protein, the immunoglobulin heavy chain binding protein (BiP/GRP78), and hsp70. The ATP-induced conformational change of hsp90 may be important in regulating its association with steroid receptors and other cellular proteins. C1 EOTVOS LORAND UNIV, DEPT ORGAN CHEM, H-1518 BUDAPEST, HUNGARY. HUNGARIAN ACAD SCI, CENT RES INST CHEM, H-1525 BUDAPEST, HUNGARY. BRIGHAM & WOMENS HOSP, DEPT MED, JOSLIN DIABET CTR, DIV RES, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP CSERMELY, P (reprint author), SEMMELWEIS UNIV MED, INST BIOCHEM 1, H-1444 BUDAPEST, HUNGARY. FU NIDDK NIH HHS [DK 36836, DK 33201] NR 67 TC 121 Z9 121 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 25 PY 1993 VL 268 IS 3 BP 1901 EP 1907 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KH620 UT WOS:A1993KH62000062 PM 8420964 ER PT J AU GERARD, NP BAO, L HE, XP GERARD, C AF GERARD, NP BAO, L HE, XP GERARD, C TI MOLECULAR ASPECTS OF THE TACHYKININ RECEPTORS SO REGULATORY PEPTIDES LA English DT Review DE TACHYKININ; SUBSTANCE-P; NEUROPEPTIDE RECEPTOR; NEUROKININ-A; NEUROMEDIN-K; 7 TRANSMEMBRANE SEGMENT RECEPTOR ID SUBSTANCE-P RECEPTOR; CYCLIC-AMP LEVELS; GUINEA-PIG LUNG; K RECEPTOR; GUANINE-NUCLEOTIDES; BINDING-SITES; GASTROINTESTINAL-TRACT; FUNCTIONAL EXPRESSION; DIVALENT-CATIONS; MESSENGER-RNAS C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,INA SUE PERLMUTTER LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,THORNDIKE LAB,BOSTON,MA 02115. RP GERARD, NP (reprint author), HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,300 LONGWOOD AVE,BOSTON,MA 02215, USA. NR 67 TC 91 Z9 92 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD JAN 22 PY 1993 VL 43 IS 1-2 BP 21 EP 35 DI 10.1016/0167-0115(93)90404-V PG 15 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA KG598 UT WOS:A1993KG59800002 PM 8381237 ER PT J AU GUTIERREZRAMOS, JC TORIBIO, ML MARTINEZ, C AF GUTIERREZRAMOS, JC TORIBIO, ML MARTINEZ, C TI EARLY T-CELL DEVELOPMENT SO NATURE LA English DT Letter C1 UNIV AUTONOMA MADRID,CSIC,CTR BIOL MOLEC,E-28049 MADRID,SPAIN. RP GUTIERREZRAMOS, JC (reprint author), CTR BLOOD RES INC,BOSTON,MA 02115, USA. RI Toribio, Maria L/C-2039-2017 OI Toribio, Maria L/0000-0002-8637-0373 NR 5 TC 3 Z9 3 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JAN 21 PY 1993 VL 361 IS 6409 BP 213 EP 213 DI 10.1038/361213a0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH614 UT WOS:A1993KH61400038 PM 8423850 ER PT J AU PASTERNACK, MS MARK, EJ MUSE, VV MAGGARD, M SCHMITT, W BASGOZ, N AISENBERG, AC AF PASTERNACK, MS MARK, EJ MUSE, VV MAGGARD, M SCHMITT, W BASGOZ, N AISENBERG, AC TI A 51-YEAR-OLD ETHIOPIAN WOMAN WITH MYALGIA, WEIGHT-LOSS, AND MEDIASTINAL LYMPHADENOPATHY - TUBERCULOSIS OF MEDIASTINAL LYMPH-NODES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID LYMPHOMATOID GRANULOMATOSIS; PULMONARY TUBERCULOSIS; ESOPHAGEAL-CARCINOMA; COMPUTED-TOMOGRAPHY; HODGKINS-DISEASE; PONCETS DISEASE; SARCOIDOSIS; MANIFESTATIONS; BLASTOMYCOSIS; MANAGEMENT C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP PASTERNACK, MS (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT INFECT DIS UNIT,BOSTON,MA 02114, USA. NR 49 TC 2 Z9 2 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JAN 21 PY 1993 VL 328 IS 3 BP 195 EP 202 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA KG625 UT WOS:A1993KG62500007 ER PT J AU VOLPE, NJ LIEBSCH, NJ MUNZENRIDER, JE LESSELL, S AF VOLPE, NJ LIEBSCH, NJ MUNZENRIDER, JE LESSELL, S TI NEUROOPHTHALMOLOGICAL FINDINGS IN CHORDOMA AND CHONDROSARCOMA OF THE SKULL BASE SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID MESENCHYMAL CHONDROSARCOMA; CRANIAL CHORDOMAS; RADIATION-THERAPY; INTRACRANIAL CHONDROSARCOMA; TUMORS; APPEARANCE; DIAGNOSIS; PALSY; CT AB Review of the clinical features of 48 patients with chordoma and 49 patients with low-grade chondrosarcoma of the skull base disclosed overlapping clinical profiles but distinctive features. Both tumors occurred at all ages but chondrosarcoma tended to occur in the third and fourth decades. Twenty-five (52%) of the patients with chordoma and 24 (49%) of the patients with chondrosarcoma had ocular symptoms (diplopia or visual impairment) as the initial manifestation of the disease. Of the 59 patients (both groups) with diplopia, the diplopia was initially intermittent in 25 (42%). Headache and diplopia from an insidious abducens nerve palsy was most common in both groups. Abducens nerve palsy occurred in 22 (46%) of the patients with chordoma and 23 (47%) of the patients with chondrosarcoma. Normal examination results were more common in patients with chordoma, whereas visual loss, facial numbness, and multiple cranial neuropathies were more common in patients with chondrosarcoma. The similarities in the clinical features of these tumors reflect their common origin at the central skull base and the vulnerability of the abducens nerves at that site. The differences reflect the tendency of chordomas to originate from the clivus and chondrosarcomas to originate from the temporal bone. C1 MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114. HARVARD CYCLOTRON LAB,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. NR 47 TC 48 Z9 48 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD JAN 15 PY 1993 VL 115 IS 1 BP 97 EP 104 PG 8 WC Ophthalmology SC Ophthalmology GA KF915 UT WOS:A1993KF91500014 PM 8420385 ER PT J AU LI, FP DECKER, HJH ZBAR, B STANTON, VP KOVACS, G SEIZINGER, BR ABURATANI, H SANDBERG, AA BERG, S HOSOE, S BROWN, RS AF LI, FP DECKER, HJH ZBAR, B STANTON, VP KOVACS, G SEIZINGER, BR ABURATANI, H SANDBERG, AA BERG, S HOSOE, S BROWN, RS TI CLINICAL AND GENETIC-STUDIES OF RENAL-CELL CARCINOMAS IN A FAMILY WITH A CONSTITUTIONAL CHROMOSOME-3,8 TRANSLOCATION - GENETICS OF FAMILIAL RENAL-CARCINOMA SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE CARCINOMA, RENAL CELL; NEOPLASTIC SYNDROMES, HEREDITARY; KIDNEY NEOPLASMS; CHROMOSOMES, HUMAN, PAIR-3; CHROMOSOMES, HUMAN, PAIR-8 ID VONHIPPEL-LINDAU DISEASE; GRADIENT GEL-ELECTROPHORESIS; TUMOR SUPPRESSOR GENES; SHORT ARM; HEREDITARY; DELETION; 3P; HETEROZYGOSITY; LOCALIZATION; INVOLVEMENT AB Objective: To describe the clinical course and genetic studies of renal carcinoma in members of a family with the constitutional chromosome translocation, t(3;8) (p14;q24). Design: A follow-up study that updates our 1979 report of renal carcinoma in 1 0 of these relatives. Setting: A cancer center and university hospital. Patients: Members of the family, including five carriers of the 3;8 translocation who were in remission of renal cancer. Measurements: Clinical follow-up of the family and genetic analyses of the renal cancer specimens of three patients. Results: Renal carcinoma recurred in all five patients in the family at 1 to 16 years of follow-up. Three patients have died of renal cancer, and two are in a second remission. The renal cancers from three family members consistently reveal loss of the entire derivative chromosome 8, which bears the chromosome 3p segment spanning band p14 to the telomere. In contrast, no genetic change was detected in the derivative chromosome 3 or in normal chromosomes 3 and 8. Conclusions: This family illustrates the importance of clinical follow-up of patients with a hereditary cancer that can develop at multiple foci and recur over time. The inherited 3;8 translocation and loss of the translocated distal chromosome 3p in tumor specimens of family members may help localize the gene or genes involved in the pathogenesis of both familial and sporadic renal carcinoma. C1 NCI,BETHESDA,MD 20892. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. SW BIOMED RES INST,SCOTTSDALE,AZ. RP LI, FP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,MAYER 3A27,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01 CA49455]; NHGRI NIH HHS [HG00299]; NHLBI NIH HHS [HL41484] NR 34 TC 74 Z9 74 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JAN 15 PY 1993 VL 118 IS 2 BP 106 EP 111 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA KF918 UT WOS:A1993KF91800005 PM 8416305 ER PT J AU ABRAHAM, JA DAMM, D BAJARDI, A MILLER, J KLAGSBRUN, M EZEKOWITZ, RAB AF ABRAHAM, JA DAMM, D BAJARDI, A MILLER, J KLAGSBRUN, M EZEKOWITZ, RAB TI HEPARIN-BINDING EGF-LIKE GROWTH-FACTOR - CHARACTERIZATION OF RAT AND MOUSE CDNA CLONES, PROTEIN DOMAIN CONSERVATION ACROSS SPECIES, AND TRANSCRIPT EXPRESSION IN TISSUES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID DIPHTHERIA-TOXIN; FIBROBLAST GROWTH; CELLS; REQUIREMENT; MEMBRANE; RECEPTOR C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT SURG RES,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. RP ABRAHAM, JA (reprint author), SCIOS NOVA INC,MT VIEW,CA 94043, USA. FU NIAID NIH HHS [AI23876-05]; NIGMS NIH HHS [GM47397] NR 20 TC 146 Z9 149 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 15 PY 1993 VL 190 IS 1 BP 125 EP 133 DI 10.1006/bbrc.1993.1020 PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KH402 UT WOS:A1993KH40200020 PM 7678488 ER PT J AU GRANT, AJ KOSKI, G TREISTMAN, SN AF GRANT, AJ KOSKI, G TREISTMAN, SN TI EFFECT OF CHRONIC ETHANOL ON CALCIUM CURRENTS AND CALCIUM-UPTAKE IN UNDIFFERENTIATED PC12 CELLS SO BRAIN RESEARCH LA English DT Article DE PHEOCHROMOCYTOMA; PC12; ETHANOL; CALCIUM FLUX; PATCH CLAMP; TOLERANCE ID NERVE GROWTH-FACTOR; PHEOCHROMOCYTOMA CELLS; VASOPRESSIN RELEASE; K+ CHANNELS; FAST-PHASE; INHIBITION; BRAIN; SYNAPTOSOMES; MECHANISMS; REDUCTION AB Undifferentiated pheochromocytoma (PC12) cells were chronically exposed to 200 mM ethanol for six days. Parallel cultures were maintained without ethanol. Cells chronically exposed to ethanol had significantly larger voltage-gated calcium currents than those grown in the absence of ethanol. Concurrent radioisotopic flux assays confirm that calcium influx is, indeed, increased in the chronically treated cells. However, acute exposure to ethanol at the same concentration as those used for the chronic studies greatly reduced the magnitude of the currents and net calcium influx. C1 UNIV MASSACHUSETTS, MED CTR, DEPT PHARMACOL, 55 LAKE AVE N, WORCESTER, MA 01655 USA. WORCESTER FDN EXPTL BIOL INC, SHREWSBURY, MA 01545 USA. MASSACHUSETTS GEN HOSP, DEPT ANESTHESIA, HENRY K BEECHER MEM RES LABS, BOSTON, MA 02114 USA. FU NIAAA NIH HHS [AA05542, AA0704]; NIDCD NIH HHS [DC00131] NR 31 TC 40 Z9 43 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 EI 1872-6240 J9 BRAIN RES JI Brain Res. PD JAN 15 PY 1993 VL 600 IS 2 BP 280 EP 284 DI 10.1016/0006-8993(93)91384-5 PG 5 WC Neurosciences SC Neurosciences & Neurology GA KG868 UT WOS:A1993KG86800014 PM 8382099 ER PT J AU YOUNG, RH GERSELL, DJ ROTH, LM SCULLY, RE AF YOUNG, RH GERSELL, DJ ROTH, LM SCULLY, RE TI OVARIAN METASTASES FROM CERVICAL CARCINOMAS OTHER THAN PURE ADENOCARCINOMAS - A REPORT OF 12 CASES SO CANCER LA English DT Article DE OVARY; UTERINE CERVIX; SQUAMOUS CELL CARCINOMA; SMALL CELL CARCINOMA; NEUROENDOCRINE CARCINOMA; ADENOSQUAMOUS CARCINOMA; TRANSITIONAL CELL CARCINOMA ID SQUAMOUS-CELL CARCINOMA; STAGE-IB ADENOCARCINOMA; FEMALE GENITAL-TRACT; UTERINE CERVIX; CLINICOPATHOLOGICAL ANALYSIS; ENDOCERVICAL ADENOCARCINOMA; INVASIVE ADENOCARCINOMA; RADICAL HYSTERECTOMY; TUMORS; CANCER AB Twelve cases of ovarian metastases from cervical carcinomas, most with clinical manifestations of ovarian involvement, are reported. The patients were 23-73 years of age (average, 43 years). The ovarian and cervical tumors were synchronous in eight patients; in three, ovarian tumors were discovered 10 months, 2.5, and 3 years after the detection of a cervical neoplasm. In one patient, the cervical tumor was not discovered until autopsy 7 months after presentation. Four patients had abdominal swelling or distention, three had vaginal bleeding, three had an abnormal Papanicolaou smear, and two had masses discovered during pelvic examination. The ovarian tumors, six of which were bilateral, ranged from 5-17 cm (average, 9.5 cm) in maximal dimension in 11 patients; in the 12th patient, the involved ovary was not enlarged. The cervical tumors were grossly evident in 10 patients. They were usually deeply invasive, often with extracervical extension. Four were squamous cell carcinomas; two, small cell carcinomas; one, a mixed small cell carcinoma and adenocarcinoma; one, a mixed poorly differentiated carcinoid and adenocarcinoma; two, adenosquamous carcinomas; one. a transitional cell carcinoma; and one, an undifferentiated carcinoma. Various features, including bilaterality of the ovarian tumors, the finding that the histologic features of the ovarian tumors typically were unusual for a primary ovarian neoplasm, and the presence of extensive extracervical disease, led to the conclusion that the ovarian tumors were metastatic from the cervix. Although ovarian metastases of cervical carcinoma are uncommon, this series illustrates that. occasionally striking examples with clinical manifestations of ovarian involvement occur. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. WASHINGTON UNIV,BARNES HOSP,SCH MED,ST LOUIS,MO 63110. INDIANA UNIV,SCH MED,INDIANAPOLIS,IN 46202. RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 73 TC 30 Z9 30 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 15 PY 1993 VL 71 IS 2 BP 407 EP 418 DI 10.1002/1097-0142(19930115)71:2<407::AID-CNCR2820710223>3.0.CO;2-G PG 12 WC Oncology SC Oncology GA KG998 UT WOS:A1993KG99800022 PM 8380753 ER PT J AU FERRY, JA LINGGOOD, RM CONVERY, KM EFIRD, JT ELISEO, R HARRIS, NL AF FERRY, JA LINGGOOD, RM CONVERY, KM EFIRD, JT ELISEO, R HARRIS, NL TI HODGKIN DISEASE, NODULAR SCLEROSIS TYPE - IMPLICATIONS OF HISTOLOGIC SUBCLASSIFICATION SO CANCER LA English DT Article DE HODGKIN DISEASE; NODULAR SCLEROSIS; SUBCLASSIFICATION; PROGNOSIS; STATISTICAL ANALYSIS; GRADE; SCLEROSIS; NECROSIS ID PROGNOSTIC-SIGNIFICANCE; STAGE-I AB Background. The prognostic significance of the cellular composition of the nodules of Hodgkin disease, nodular sclerosis type (HDNS), is controversial. Methods Tumors from 79 patients with HDNS, who had a median follow-up time of 9.3 years, were studied. Results. Based on British National Lymphoma Investigation criteria, 58 cases were classified as NSI (lowgrade) and 21 as NSII (high-grade). The study included 24 male and 55 female patients, aged 10-57 years (mean, 27 years), who presented with Stage I (13 patients [12A, 1B]), Stage II (45 patients [40A, 5B]), or Stage III (21 patients [16A, 5B]) disease. Fifty-three patients had no relapse, 4 died of other causes, and 49 are in complete clinical remission. Twenty-six patients had progression of disease during therapy or relapsed and 17 were successfully salvaged. Overall length of survival was significantly shorter with NSII (P = 0.0001), extensive necrosis (P = 0.0034), high stage (P = 0.0058), and B symptoms (P = 0.030). Multivariate analysis showed that grade had the strongest effect on overall survival (P = 0.0042; hazard ratio = 10.19). The 5-year survival was 100% for NSI patients and 75% for NSII patients. Only B symptoms were significantly associated with risk of relapse after initial therapy (P = 0.030). For patients who relapsed, only histologic grade predicted subsequent disease-free survival (P = 0.0023; hazard ratio = 26.5). Five-year disease-free survival after first relapse was 94% for NSI patients and 11% for NSII patients. Conclusions. Patients with NSI disease who relapse have a more successful salvage and longer period of survival than do those with NSII disease. Histologic subclassification of HDNS appears clinically relevant, and consideration of histologic subtype may be important when planning therapy. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. MED PRACTICES EVALUAT,BOSTON,MA. RP FERRY, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,FRUIT ST,BOSTON,MA 02114, USA. NR 27 TC 42 Z9 42 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 BP 457 EP 463 DI 10.1002/1097-0142(19930115)71:2<457::AID-CNCR2820710229>3.0.CO;2-U PG 7 WC Oncology SC Oncology GA KG998 UT WOS:A1993KG99800028 PM 8422639 ER PT J AU GORDON, LI ANDERSEN, J GREGORY, S MAZZA, J CHERVENICK, P HAHN, RG OCONNELL, MJ AF GORDON, LI ANDERSEN, J GREGORY, S MAZZA, J CHERVENICK, P HAHN, RG OCONNELL, MJ TI A VM 26-BASED REGIMEN FOR PATIENTS WITH PREVIOUSLY UNTREATED NON-HODGKIN LYMPHOMA - PROLONGED DISEASE-FREE SURVIVAL IN PATIENTS YOUNGER THAN 60 YEARS OF AGE - A PHASE-II TRIAL OF THE EASTERN-COOPERATIVE-ONCOLOGY-GROUP SO CANCER LA English DT Article ID LARGE-CELL LYMPHOMA; MACOP-B; INTERMEDIATE-GRADE; CHEMOTHERAPY; COMBINATION; TENIPOSIDE; BLEOMYCIN AB Background. The epidophyllotoxin VM 26 has been shown to have single-agent activity in patients with diffuse aggressive lymphoma. In an attempt to determine its activity in combination with other agents known to be effective in lymphoma, a Phase II trial of a novel chemotherapy regimen was conducted. Methods. Forty-two patients with Stages II, III, and IV diffuse aggressive lymphoma were treated with teniposide, doxorubicin, prednisone, cyclophosphamide, vincristine, and bleomycin (PATen-CPOB) as part of a Phase II trial of the Eastern Cooperative Oncology Group. Fifty-five percent of patients had Stage IV disease, 21% Stage III, and 24% Stage II. Results. The overall complete response rate was 64%. Of the 27 patients who had complete response, 19 (70% [45% of the entire group]) are still alive without disease (median follow-up, 5.7 years). No patient had a follow-up time of less than 5 years. On examination of factors that were predictive of survival and relapse, it was found that age younger than 60 years was predictive of long-term survival, as 76% of patients younger than 60 years of age were alive without disease. Forty patients were evaluable for toxicity. There were four (10%) early deaths, and six patients (15%) had Grade 4 hematologic toxicity. Conclusions. This alternating combination chemotherapy regimen (PATen-CPOB) results in a complete response rate comparable to what has been reported previously in the literature, but 45% of patients in this series demonstrated long-term disease-free survival. When patients younger than 60 years of age with follow-up times of at least 5 years were considered, disease-free survival was 76%. C1 NORTHWESTERN UNIV,SCH MED,DEPT MED,DIV HEMATOL ONCOL,CHICAGO,IL 60611. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. MARSHFIELD CLIN FDN MED RES & EDUC,DEPT HEMATOL,MARSHFIELD,WI 54449. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA 15261. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. RP GORDON, LI (reprint author), NORTHWESTERN UNIV,SCH MED,ROBERT H LURIE CANC CTR,DIV HEMATOL ONCOL,303 E CHICAGO AVE,CHICAGO,IL 60611, USA. OI Gordon, Leo/0000-0003-1666-7064 FU NCI NIH HHS [CA 17145, CA 2115, CA 23318] NR 17 TC 2 Z9 2 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 BP 464 EP 470 DI 10.1002/1097-0142(19930115)71:2<464::AID-CNCR2820710230>3.0.CO;2-R PG 7 WC Oncology SC Oncology GA KG998 UT WOS:A1993KG99800029 PM 8422640 ER PT J AU ARCECI, RJ STIEGLITZ, K BRAS, J SCHINKEL, A BAAS, F CROOP, J AF ARCECI, RJ STIEGLITZ, K BRAS, J SCHINKEL, A BAAS, F CROOP, J TI MONOCLONAL-ANTIBODY TO AN EXTERNAL EPITOPE OF THE HUMAN MDR1 P-GLYCOPROTEIN SO CANCER RESEARCH LA English DT Article ID MULTIDRUG-RESISTANCE GENE; DOXORUBICIN RESISTANCE; MYELOGENOUS LEUKEMIA; COMPLEMENTARY-DNA; HUMAN-TISSUES; HUMAN-TUMORS; MR 170,000; EXPRESSION; CELLS; CANCER AB A membrane glycoprotein, termed P-glycoprotein, has been shown to be responsible for cross-resistance to a broad range of structurally and functionally distinct cytotoxic agents. P-glycoprotein, encoded in humans by the mdr1 gene, functions as an energy-dependent efflux pump to exclude these cytotoxic agents from the resistant cell. In order to study the phenomenon of multidrug resistance in both normal and neoplastic cells, we have generated a mouse monoclonal antibody directed to an external epitope of the human P-glycoprotein. This monoclonal antibody, 4E3, is an IgG2a class antibody which specifically recognizes the human mdr1 P-glycoprotein but not the mdr3 gene product. The 4E3 monoclonal antibody immunoprecipitates both the glycosylated and nonglycosylated forms of P-glycoprotein under mild denaturation conditions. In addition, 4E3 can detect P-glycoprotein in immunocytochemical analysis of fixed tissue-cultured cells and in analysis of frozen sections of human tissue. Binding of the monoclonal antibody to multidrug-resistant cells does not significantly affect the intracellular accumulation or potentiate the cytotoxicity of daunomycin in multidrug-resistant cells. However, at high concentrations of antibody, 4E3 produces a mild potentiation of vinblastine and actinomycin cytotoxicity in multidrug-resistant cells. This monoclonal antibody will be useful both for analyzing P-glycoprotein expression in normal and neoplastic cells and for isolating live cells expressing the P-glycoprotein without significantly affecting the efflux functions of the transporter. C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. NETHERLANDS CANC INST,1066 CX AMSTERDAM,NETHERLANDS. UNIV AMSTERDAM,ACAD MED CTR,DEPT NEUROL,1105 AZ AMSTERDAM,NETHERLANDS. UNIV AMSTERDAM,ACAD MED CTR,DEPT PATHOL,1105 AZ AMSTERDAM,NETHERLANDS. RP ARCECI, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. RI Baas, Frank/F-9574-2010 OI Baas, Frank/0000-0003-3912-5428 FU NCI NIH HHS [CA48162] NR 46 TC 108 Z9 108 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 1993 VL 53 IS 2 BP 310 EP 317 PG 8 WC Oncology SC Oncology GA KF731 UT WOS:A1993KF73100021 PM 7678072 ER PT J AU NISHIDA, N FUKUDA, Y KOKURYU, H TOGUCHIDA, J YANDELL, DW IKENEGA, M IMURA, H ISHIZAKI, K AF NISHIDA, N FUKUDA, Y KOKURYU, H TOGUCHIDA, J YANDELL, DW IKENEGA, M IMURA, H ISHIZAKI, K TI ROLE AND MUTATIONAL HETEROGENEITY OF THE P53-GENE IN HEPATOCELLULAR-CARCINOMA SO CANCER RESEARCH LA English DT Article ID P53 GENE; CANCER; ALLELOTYPE; LOSSES; OCCUR AB The mutational spectrum of the p53 gene was analyzed in 53 hepatocellular carcinomas. Somatic mutations of the p53 gene were detected in 17 cases (32%). Among these 17 mutations, 9 were missense mutations; the mutations in the other 8 cases were nonsense mutations, deletions, or mutations at the intron-exon junctions. These mutations were found in a wide region stretching from exon 4 to exon 10 without any single mutational hot spot. G:C to T:A transversions were predominant, suggesting the involvement of environmental mutagens in the mutagenesis of the p53 gene in a subset of the hepatocellular carcinoma cases. Mutations of the p53 gene occurred frequently in advanced tumors, although several tumors in the early stages also showed mutations. A deletion map of chromosome 17 was constructed by using 10 polymorphic probes and was compared with the p53 gene mutation in each case. Loss of heterozygosity (LOH) on chromosome 17p was observed in 49% of the cases (24 of 49), and two commonly deleted regions were detected (around the p53 locus and at 17p13.3 to the telomere). Sixteen of the 17 cases with p53 gene mutations showed LOH around the p53 locus, and mutations were rare in hepatocellular carcinomas without LOH. However, no mutations were detected in 8 cases with LOH on 17p, suggesting the possibility that an unidentified tumor suppressor gene(s) located on 17p may have also been involved in hepatocarcinogenesis. C1 KYOTO UNIV,FAC MED,DEPT INTERNAL MED 2,54 KAWAHARA CHO SHOGOIN,SAKYO KU,KYOTO 606,JAPAN. KYOTO UNIV,CTR RADIAT BIOL,SAKYO KU,KYOTO 606,JAPAN. KYOTO UNIV,FAC MED,DEPT ORTHOPAED SURG,KYOTO 606,JAPAN. MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB OPHTHAMOL,BOSTON,MA 02114. NR 31 TC 170 Z9 174 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 15 PY 1993 VL 53 IS 2 BP 368 EP 372 PG 5 WC Oncology SC Oncology GA KF731 UT WOS:A1993KF73100030 PM 8093350 ER PT J AU GALVIN, JM SMITH, AR LALLY, B AF GALVIN, JM SMITH, AR LALLY, B TI CHARACTERIZATION OF A MULTILEAF COLLIMATOR SYSTEM SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE MULTILEAF COLLIMATOR; MLC; PENUMBRA; FIELD SHAPING; CONFORMAL TREATMENT ID CONTROLLED RADIATION-THERAPY; DOSE DISTRIBUTIONS; ROTATION; SIZE AB Commissioning measurements for a multileaf collimator installed on a dual energy accelerator with 6 and 15 MV photons are described. Detailed dosimetric characterization of the multileaf collimator is a requirement for modeling the collimator with treatment planning software. Measurements include a determination of the penumbra width, leaf transmission, between-leaf leakage, and localization of the leaf ends and sides. Standard radiographic film was used for the penumbra measurements, and separate experiments using radiochromic film and thermoluminescent dosimeters were performed to verify that distortions of the dose distribution at an edge due to changing energy sensitivity of silver bromide film are negligible. Films were analyzed with a scanning laser densitometer with a 210 micron spot. Little change in the penumbra edge distribution was noted for different positions of a leaf in the field. Experiments localizing the physical end of the leaves showed less than 1 mm deviation from the 50% decrement line. This small difference is attributed to the shaped end on the leaves. One side of a single leaf corresponded to the 50% decrement line, but the opposite face was aligned with a lower value. This difference is due to the tongue and groove used to decrease between-leaf leakage. For both energies, approximately 2% of photons incident on the multileaf collimator are transmitted and an additional 0.5% leakage occurs between the leaves. Alignment of the leaves to form a straight edge results in a penumbra profile which compares favorably with the standard technique of using alloy blocks. When the edge is stepped, the isodose lines follow the leaf pattern and the boundary is poorly defined compared to divergent blocks. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. UNIV PENN,SCH BIOENGN,PHILADELPHIA,PA 19104. RP GALVIN, JM (reprint author), NYU MED CTR,TISCH HOSP,DIV RADIAT ONCOL,560 1ST AVE,NEW YORK,NY 10016, USA. NR 19 TC 125 Z9 127 U1 1 U2 7 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 15 PY 1993 VL 25 IS 2 BP 181 EP 192 PG 12 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KJ711 UT WOS:A1993KJ71100003 PM 8420867 ER PT J AU TAGHIAN, A RAMSAY, J ALLALUNISTURNER, J BUDACH, W GIOIOSO, D PARDO, F OKUNIEFF, P BLEEHEN, N URTASUN, R SUIT, H AF TAGHIAN, A RAMSAY, J ALLALUNISTURNER, J BUDACH, W GIOIOSO, D PARDO, F OKUNIEFF, P BLEEHEN, N URTASUN, R SUIT, H TI INTRINSIC RADIATION SENSITIVITY MAY NOT BE THE MAJOR DETERMINANT OF THE POOR CLINICAL OUTCOME OF GLIOBLASTOMA-MULTIFORME SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE MALIGNANT GLIOMAS; SF2; INTRINSIC RADIOSENSITIVITY; PREDICTIVE ASSAYS ID GLIOMA CELL-LINES; BRAIN-TUMORS; RADIOSENSITIVITY; SURVIVAL; INVITRO; RADIOTHERAPY; IRRADIATION; THERAPY; INSITU AB Purpose: Many radiobiologic mechanisms may contribute to the clinical radiation resistance of Glioblastoma Multiforme. One of them is considered to be an unusually low intrinsic radiation sensitivity. This is a collaborative study between three laboratories to evaluate the intrinsic radiation sensitivity of 85 cell lines derived from human malignant gliomas as the major cause of the poor clinical results of radiation treatment to these tumors. Methods and Materials: Fifty-one cell lines were early passage. The distribution by histologic type was: 58 glioblastoma, 17 anaplastic astrocytoma, six oligodendroglioma and four astrocytoma grade 2. The intrinsic radiation sensitivity will be expressed by the surviving fraction at 2 Gy (SF2). The SF2 has been determined for single dose irradiation for cell lines on exponential phase, under aerobic conditions, growing on plastic. The patient age, Karnofski Status, histological grade, survival, dose of irradiation for 50 patients are investigated for correlation with SF2 Of the corresponding newly established cell lines. Results: The mean SF2 Of the 85 cell lines was 0.46 (0.12-0.87). The mean SF2 by histologic type was 0.50, 0.34, 0.54 and 0.38 for glioblastoma, anaplastic astrocytoma, oligodendroglioma and astrocytoma grade 2 cell lines, respectively. No correlation was found between SF2 and the patient age or Karnofski status. The difference in SF2 between the 58 glioblastoma and 17 anaplastic astrocytoma cell lines was significant p = 0.002. The difference in actuarial survival between glioblastoma and anaplastic astrocytoma patients was borderline of significance (p = 0.08). The difference in SF2 of cell lines derived from these two groups of patients was of borderline significance (p = 0.08). The difference in radiation sensitivity for anaplastic astrocytoma and glioblastoma cell lines was clearly reflected in the difference in survival for the two groups of patients from where the cell lines were derived. However, no correlation was found between SF2 and survival within each grade. In a multivariate analysis the age, grade and Karnofski status were found to be significant prognostic values for survival with a p values of 0.032, 0.03 and 0.038, respectively, however, the In SF2 was not significant (p = 0.40). The mean SF2 of the 6 oligodendroglioma cell lines (0.54) was comparable to that of glioblastoma multiforme (0.50). The high SF2 for oligodendroglioma does not accord with the much better clinical outcome of these tumors. Conclusions: These data on 85 malignant glioma cell lines show a very broad distribution of SF2 values for irradiation in vitro. SF2 reflected the difference in sensitivity between AA (Grade 3) and GBM (Grade 4). This may suggest that the parameter SF2 is useful to discriminate between the sensitivity of different grades or types of histology in vitro. However, SF2 was not a predictor of the clinical outcome on individual basis for malignant gliomas. The in vitro studies will need to be supplemented by physiologic characterization of the tumors in vivo. Such conclusions would limit the predictive value of current radiation sensitivity assays based on in vitro dose-survival measurement for at least high grade malignant gliomas. C1 UNIV CAMBRIDGE,DEPT CLIN ONCOL,MRC UNIT,CAMBRIDGE,ENGLAND. CROSS CANC INST,DEPT RADIAT ONCOL,RADIOBIOL LAB,EDMONTON T6G 1Z2,ALBERTA,CANADA. RP TAGHIAN, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,EL STEELE LAB RADIAT BIOL,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. RI Ramsay, Jonathan/F-7009-2013 FU NCI NIH HHS [CA13311] NR 34 TC 97 Z9 99 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 15 PY 1993 VL 25 IS 2 BP 243 EP 249 PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KJ711 UT WOS:A1993KJ71100009 PM 8380568 ER PT J AU DOPPKE, KP MORIN, RL CHU, W GERBI, BG GOULD, RG HEFNER, LV MARSDEN, DS PAVLICEK, W RITENOUR, ER SCHOENFELD, AH AF DOPPKE, KP MORIN, RL CHU, W GERBI, BG GOULD, RG HEFNER, LV MARSDEN, DS PAVLICEK, W RITENOUR, ER SCHOENFELD, AH TI A SURVEY OF RADIATION ONCOLOGISTS REGARDING THEIR RADIATION PHYSICS INSTRUCTION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Note DE RADIATION PHYSICS TRAINING; RADIATION ONCOLOGY PROGRAMS; EDUCATION IN RADIATION ONCOLOGY AB The American Association of Physicists in Medicine, Committee on Training of Radiologists conducted a survey of radiation oncologists requesting information regarding their radiation oncology physics training. General questions were asked of the oncologist regarding their radiation oncology practice such as number of oncologists, number of new patients treated, and the size and type of facility in which the practice is located. The oncologist also responded to questions regarding their educational background. The survey requested the radiation oncologists to answer questions regarding the adequacy and importance of their training in specific areas of radiation physics. The responders indicated that the importance of most physics topics in their clinical practice corresponded to the level of their understanding. The survey indicated that for most radiation oncologists their physics instruction was an important and interesting part of their residency program. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MAYO CLIN,JACKSONVILLE,FL. UNIV NEBRASKA,MED CTR,OMAHA,NE 68105. UNIV MINNESOTA HOSP & CLIN,MINNEAPOLIS,MN 55455. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. WILLIAM BEAUMONT HOSP,ROYAL OAK,MI 48072. ST LUKES ROOSEVELT HOSP,NEW YORK,NY. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. UNIV MINNESOTA HOSP & CLIN,MINNEAPOLIS,MN 55455. MONTEFOIORE MED CTR,BRONX,NY. NR 2 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 15 PY 1993 VL 25 IS 2 BP 345 EP 352 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KJ711 UT WOS:A1993KJ71100023 PM 8420885 ER PT J AU MIRALBELL, R URIE, M AF MIRALBELL, R URIE, M TI POTENTIAL IMPROVEMENT OF 3 DIMENSION TREATMENT PLANNING AND PROTON-BEAMS IN FRACTIONATED RADIOTHERAPY OF LARGE CEREBRAL ARTERIOVENOUS-MALFORMATIONS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Note DE ARTERIOVENOUS MALFORMATIONS; COMPARATIVE PLANNING; PROTONS; DOSE VOLUME HISTOGRAM ANALYSIS ID RADIATION-THERAPY; NATURAL-HISTORY; MANAGEMENT; IRRADIATION AB The treatment of large cerebral arteriovenous malformations is a surgical challenge, especially for deep seated brain locations. Furthermore, these lesions are unfit for radiosurgical approaches due to a high risk of complications secondary to high radiation doses to large brain volumes. Fractionated precision radiotherapy can potentially deliver high, uniform, target-contoured dose distributions optimizing the dose reduction to the critical surrounding brain. The results of a study are presented in such a way that dose distributions achievable with proton beams are compared to those with 10 MV x-rays; and the potential improvements with protons evaluated, relying heavily on dose-volume histograms to examine the coverage of the lesion as well as the dose to the normal brain, brain-stem, and optic chiasm. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,HARVARD CYCLOTRON LAB,BOSTON,MA 02114. FU NCI NIH HHS [CA21239-12] NR 19 TC 13 Z9 13 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 15 PY 1993 VL 25 IS 2 BP 353 EP 358 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KJ711 UT WOS:A1993KJ71100024 PM 8380569 ER PT J AU RETSKY, KL FREEMAN, MW FREI, B AF RETSKY, KL FREEMAN, MW FREI, B TI ASCORBIC-ACID OXIDATION PRODUCT(S) PROTECT HUMAN LOW-DENSITY-LIPOPROTEIN AGAINST ATHEROGENIC MODIFICATION - ANTIOXIDANT RATHER THAN PROOXIDANT ACTIVITY OF VITAMIN-C IN THE PRESENCE OF TRANSITION-METAL IONS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RECEPTOR-MEDIATED ENDOCYTOSIS; SMOOTH-MUSCLE CELLS; HUMAN-BLOOD PLASMA; MONOCYTE-MACROPHAGES; LIPID-PEROXIDATION; ATHEROSCLEROSIS; ACCUMULATION; DEGRADATION; EXPRESSION; SUPEROXIDE AB The oxidative modification of low density lipoprotein (LDL) has been proposed as an important causative event in the development of human atherosclerosis. As a corollary of this hypothesis, antioxidants that can prevent LDL oxidation may inhibit atherosclerosis. Oxidative modification of LDL in vitro, either induced by Cu2+ or mediated by cultured arterial wall cells in media containing trace amounts of transition metal ions, is strongly inhibited by vitamin C (L-ascorbic acid (AA)). AA, however, is known to act as a prooxidant rather than an antioxidant in the presence of transition metal ions. We observed that AA is oxidized rapidly when incubated with Cu2+ and LDL, leading to transient formation of dehydro-L-ascorbic acid (DHA). Although AA and DHA can no longer be detected after 3.5 h of incubation, LDL resists oxidative modification for at least 20 h, as assessed by anodic gel electrophoretic mobility. Remarkably, DHA protects LDL more effectively against both Cu2+-induced lipid peroxidation and shifts in electrophoretic mobility than does AA; indeed, AA per se, without oxidation to DHA, offers no protection. By inhibiting oxidative modification of LDL, AA and DHA prevent uptake of LDL by macrophages via the scavenger receptor pathway. When LDL is incubated with DHA followed by gel filtration, LDL remains protected against subsequent Cu2+-induced oxidative modification, suggestive of stable modification of LDL in the presence of DHA. In contrast, DHA is ineffective against a metal ion-independent type of oxidative stress, viz. aqueous peroxyl radicals; under these conditions, only AA is able to inhibit lipid peroxidation in LDL. Our data indicate that vitamin C protects LDL against atherogenic modification by two different mechanisms that may act in concert: (i) free radical scavenging by AA prevents aqueous oxidants from attacking and oxidizing LDL, and (ii) stable modification of LDL by DHA or decomposition product(s) thereof imparts increased resistance to metal ion-dependent oxidation. C1 HARVARD UNIV, SCH PUBL HLTH, DEPT NUTR, 665 HUNTINGTON AVE, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. FU NCRR NIH HHS [SO7RR05446]; NHLBI NIH HHS [HL-45098] NR 48 TC 224 Z9 226 U1 0 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 15 PY 1993 VL 268 IS 2 BP 1304 EP 1309 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KG077 UT WOS:A1993KG07700081 PM 8419332 ER PT J AU ROCK, KL ROTHSTEIN, L GAMBLE, S FLEISCHACKER, C AF ROCK, KL ROTHSTEIN, L GAMBLE, S FLEISCHACKER, C TI CHARACTERIZATION OF ANTIGEN-PRESENTING CELLS THAT PRESENT EXOGENOUS ANTIGENS IN ASSOCIATION WITH CLASS-I MHC MOLECULES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TOXIC LYMPHOCYTES-T; DENDRITIC CELLS; B-CELLS; SOLUBLE-PROTEIN; ACCESSORY CELLS; RECOGNITION; GENERATION; HYBRIDOMAS; INDUCTION; INVITRO AB Exogenous Ag in the extracellular fluids do not gain access to the class I Ag-presenting pathway in most cells. However, there is an APC resident in spleen that can process and present exogenous Ag in association with class I molecules. We characterize the phenotype of this cell. This APC is of low buoyant density, is adherent to Sepharose and glass, and expresses both class II molecules and FcR. This phenotype identifies this APC as a macrophage. Resident, peptone- and thioglycolate-induced peritoneal macrophages also display this Ag-presenting activity. Analysis with CTL clones suggest that this Ag-presenting pathway may be active in only a subset of macrophages. A similar Ag-presenting activity is also present in dendritic cell-enriched populations from spleen although we cannot rule out the possible involvement of contaminating macrophages. In contrast, B and T cells that are resident in spleen and LPS blasts are unable to present exogenous Ag in association with class I molecules. The presentation of exogenous OVA with class I molecules is not inhibited by the inhibitors of thiol proteases, leupeptin, and antipain. The presence of gelonin, a ribosomal inactivating protein, in the extracellular fluids inhibits the ability of these APC to present exogenous OVA. Under identical conditions, gelonin does not inhibit Con A-stimulated T cell proliferation, or LPS-stimulated B cell proliferation and Ag presentation. These results are discussed in relation to the potential pathways through which an Ag in the extracellular fluids is presented with MHC class I molecules. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ROCK, KL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-20248, AI-31337] NR 41 TC 190 Z9 193 U1 1 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1993 VL 150 IS 2 BP 438 EP 446 PG 9 WC Immunology SC Immunology GA KG469 UT WOS:A1993KG46900013 PM 8419476 ER PT J AU CARRERA, AC ALEXANDROV, K ROBERTS, TM AF CARRERA, AC ALEXANDROV, K ROBERTS, TM TI THE CONSERVED LYSINE OF THE CATALYTIC DOMAIN OF PROTEIN-KINASES IS ACTIVELY INVOLVED IN THE PHOSPHOTRANSFER REACTION AND NOT REQUIRED FOR ANCHORING ATP SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ENZYME MECHANISM; PROTEIN-TYROSINE KINASE; PHOSPHORYLATION ID NUCLEOTIDE-BINDING; SUBUNIT; SITE; PURIFICATION; MUTATION; RESIDUES; RECEPTOR AB The study of the various protein kinases reveals that, despite their considerably diversity, they have evolved from a common origin. Eleven conserved subdomains have been described that encompass the catalytic core of these enzymes. One of these conserved regions, subdomain II, contains an invariant lysine residue present in all known protein kinase catalytic domains. Two facts have suggested that this conserved lysine of subdomain II is essential for binding ATP: (i) several investigators have demonstrated that this residue is physically proximal to the ATP molecule, and (ii) conservative substitutions at this site render the kinase inactive. However, these results are also consistent with a functional role of the conserved lysine of subdomain II in orienting or facilitating the transfer of phosphate. To study in more detail the role of subdomain II, we have generated mutants of the protein-tyrosine kinase pp56lck that have single amino acid substitutions within the area surrounding the conserved residue Lys-273 in subdomain II. When compared with wild-type pp56lck, these mutants displayed profound reductions in their phosphotransfer efficiencies and small differences in their affinities for ATP. Further, the substitution of arginine for Lys-273 resulted in a mutant protein unable to transfer the gamma-phosphate of ATP but able to bind 8-azido-ATP with an efficiency similar to that of wild-type pp56lck. These results suggest that the region including Lys-273 of subdomain II is involved in the enzymatic process of phosphate transfer, rather than in anchoring ATP. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CELLULAR & MOLEC BIOL,BOSTON,MA 02115. RI Alexandrov , Kirill /A-5830-2013; OI Alexandrov , Kirill /0000-0002-0957-6511; Carrera, Ana/0000-0002-3999-5434 FU NCI NIH HHS [CA43803] NR 31 TC 122 Z9 127 U1 0 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 15 PY 1993 VL 90 IS 2 BP 442 EP 446 DI 10.1073/pnas.90.2.442 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600018 PM 8421674 ER PT J AU SYMES, AJ RAO, MS LEWIS, SE LANDIS, SC HYMAN, SE FINK, JS AF SYMES, AJ RAO, MS LEWIS, SE LANDIS, SC HYMAN, SE FINK, JS TI CILIARY NEUROTROPHIC FACTOR COORDINATELY ACTIVATES TRANSCRIPTION OF NEUROPEPTIDE GENES IN A NEUROBLASTOMA CELL-LINE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID INTESTINAL POLYPEPTIDE GENE; LEUKEMIA-INHIBITORY FACTOR; CYCLIC-AMP; SYMPATHETIC NEURONS; CHOLINERGIC DIFFERENTIATION; EXPRESSION; INTERLEUKIN-6; PURIFICATION; CULTURE; CLONING AB Differentiation factors have been identified that influence the phenotype of sympathetic neurons by altering expression of classical neurotransmitters and neuropeptides. Investigation of the molecular mechanisms through which such factors act would be facilitated by the availability of a neuronal cell line that responds to these factors in a fashion similar to sympathetic neurons. We have identified a human neuroblastoma cell line, NBFL, that responds to the differentiation factor ciliary neurotrophic factor (CNTF) by coordinately inducing multiple neuropeptide genes as do sympathetic neurons. Treatment of NBFL cells with CNTF increases vasoactive intestinal polypeptide (VIP), somatostatin, and calcitonin gene-related peptide (CGRP) mRNAs but does not change other neurotransmitter properties. The induction of VIP mRNA by CNTF in NBFL cells is dose dependent, rapid, sustained, and independent of new protein synthesis. Genomic 5' flanking sequences located within a 1.59-kilobase region of the human VIP gene and distinct from the previously defined cAMP-responsive element subserve transcriptional activation by CNTF. Further examination of NBFL cells should permit the elucidation of the molecular mechanisms by which CNTF and other differentiation factors coordinately activate neuropeptide gene transcription to influence neuronal differentiation. Similar mechanisms may mediate the effect of CNTF on neuronal survival. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02114. CASE WESTERN RESERVE UNIV,DEPT CIENCIAS,CLEVELAND,OH 44106. RI Symes, Aviva/S-7471-2016 OI Symes, Aviva/0000-0003-2557-9939 FU NIMH NIH HHS [K02MH00892]; NINDS NIH HHS [NS27514] NR 31 TC 67 Z9 67 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 JAN 15 PY 1993 VL 90 IS 2 BP 572 EP 576 DI 10.1073/pnas.90.2.572 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600044 PM 8093644 ER PT J AU HUA, QX SHOELSON, SE INOUYE, K WEISS, MA AF HUA, QX SHOELSON, SE INOUYE, K WEISS, MA TI PARADOXICAL STRUCTURE AND FUNCTION IN A MUTANT HUMAN INSULIN ASSOCIATED WITH DIABETES-MELLITUS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE 2-DIMENSIONAL NMR SPECTROSCOPY; INSULIN ACTIVITY; INSULIN RECEPTOR; PROTEIN DYNAMICS ID NUCLEAR-MAGNETIC-RESONANCE; ABNORMAL INSULIN; RECEPTOR INTERACTIONS; SIDE-CHAIN; MAIN CHAIN; B-CHAIN; PROTEIN; ASSIGNMENT; IDENTIFICATION; CONFORMATION AB The solution structure of a diabetes-associated mutant human insulin (insulin Los Angeles; Phe(B24) --> Ser) was determined by C-13-edited NMR spectroscopy and distance-geometry/simulated annealing calculations. Among vertebrate insulins Phe(B24) is invariant, and in crystal structures the aromatic ring appears to anchor the putative receptor-binding surface through long-range packing interactions in the hydrophobic core. B24 substitutions are of particular interest in relation to the mechanism of receptor binding. In one analogue ([Gly(B24)]insulin), partial unfolding of the B chain has been observed with paradoxical retention of near-native bioactivity. The present study of [Ser(B24)]insulin extends this observation: relative to [Gly(B24)] insulin, near-native structure is restored despite significant loss of function. To our knowledge, our results provide the first structural study of a diabetes-associated mutant insulin and support the hypothesis that insulin undergoes a change in conformation on receptor binding. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JUSLIN DIABET CTR,BOSTON,MA 02115. SHIONOGI & CO LTD,SHIONOGI RES LAB,FUKUSHIMA KU,OSAKA 553,JAPAN. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. NR 31 TC 35 Z9 36 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 JAN 15 PY 1993 VL 90 IS 2 BP 582 EP 586 DI 10.1073/pnas.90.2.582 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600046 PM 8421693 ER PT J AU LOVE, TW QUERTERMOUS, T ZAVODNY, PJ RUNGE, MS CHOU, CC MULLINS, D HUANG, PL SCHNEE, JM KESTIN, AS SAVARD, CE MICHELSON, KD MATSUEDA, GR HABER, E AF LOVE, TW QUERTERMOUS, T ZAVODNY, PJ RUNGE, MS CHOU, CC MULLINS, D HUANG, PL SCHNEE, JM KESTIN, AS SAVARD, CE MICHELSON, KD MATSUEDA, GR HABER, E TI HIGH-LEVEL EXPRESSION OF ANTIBODY-PLASMINOGEN ACTIVATOR FUSION PROTEINS IN HYBRIDOMA CELLS SO THROMBOSIS RESEARCH LA English DT Article DE PROTEIN EXPRESSION; MESSENGER RNA STABILITY; FUSION PROTEINS; HYBRIDOMAS ID IMMUNOGLOBULIN HEAVY-CHAIN; 3' UNTRANSLATED REGION; MESSENGER-RNA; EFFECTOR FUNCTIONS; GENE; STABILITY; SEQUENCE AB We show that the mouse gamma2b heavy chain or human beta-globin 3' untranslated region can greatly enhance protein expression in myeloma cells transfected by genes coding for antibody-plasminogen activator fusion proteins. Expression plasmids were constructed containing a cloned genomic heavy chain variable region from fibrin-specific monoclonal antibody 59D8, a cloned genomic constant region of the mouse gamma2b heavy chain, and DNA sequence coding for either tissue-type plasminogen activator (tPA) or a segment of urokinase (UK) and their respective 3' untranslated sequences. Cell lines transfected with these constructs, pSVtPA(tPA) and pSVUKG(UK), produced extremely low levels of mRNA and protein (0.008-0.06 mug/ml) in comparison with the parental 59D8 myeloma cell line (7.6-10 mug/ml). In vitro nuclear run-off analysis indicated that the low steady-state levels of mRNA encoded by pSVUKG(UK) did not result from a lower rate of transcription of the transfected gene (relative to the rate of transcription of the endogenous heavy chain gene in the 59D8 parent cells). In an attempt to increase protein secretion, we assembled the expression plasmids pSVtPA(Ig), pSVUKG(Ig), and pSVUKG(beta), in which the 3' untranslated region of the mouse gamma2b heavy chain or human beta-globin gene was substituted for the 3' untranslated region of the plasminogen activator gene. Analysis of supernatant media from cell lines transfected with these constructs showed an increase in recombinant protein secretion of 68 to 100 fold in comparison with that from cell lines transfected with pSVtPA(tPA) or pSVUKG(UK). C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. SCHERING PLOUGH CORP,RES,BLOOMFIELD,NJ 07003. EMORY UNIV,DIV CARDIOL,ATLANTA,GA 30322. PRINCETON UNIV,DEPT BIOL,PRINCETON,NJ 08544. MED CTR CENT MASSACHUSETTS,DEPT HEMATOL,WORCESTER,MA 01605. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,PRINCETON,NJ 08543. FU NHLBI NIH HHS [HL-02414, HL-19259] NR 26 TC 3 Z9 3 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0049-3848 J9 THROMB RES JI Thromb. Res. PD JAN 15 PY 1993 VL 69 IS 2 BP 221 EP 229 DI 10.1016/0049-3848(93)90047-R PG 9 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA KP502 UT WOS:A1993KP50200006 PM 8446952 ER PT J AU SZOSTAK, JW AF SZOSTAK, JW TI RIBOZYMES - EVOLUTION EXVIVO SO NATURE LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP SZOSTAK, JW (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 5 TC 10 Z9 10 U1 1 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JAN 14 PY 1993 VL 361 IS 6408 BP 119 EP 120 DI 10.1038/361119a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KG466 UT WOS:A1993KG46600036 PM 7678448 ER PT J AU NARULA, J KHAW, BA DEC, GW PALACIOS, IF SOUTHERN, JF FALLON, JT STRAUSS, HW HABER, E YASUDA, T AF NARULA, J KHAW, BA DEC, GW PALACIOS, IF SOUTHERN, JF FALLON, JT STRAUSS, HW HABER, E YASUDA, T TI RECOGNITION OF ACUTE MYOCARDITIS MASQUERADING AS ACUTE MYOCARDIAL-INFARCTION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note ID ANTIMYOSIN ANTIBODY; DIAGNOSIS; BIOPSY C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,TILTON 2,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV NUCL MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NORTHEASTERN UNIV,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NR 21 TC 88 Z9 92 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 14 PY 1993 VL 328 IS 2 BP 100 EP 104 DI 10.1056/NEJM199301143280205 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA KG467 UT WOS:A1993KG46700005 PM 8416421 ER PT J AU LEWANDROWSKI, KB FLOOD, JG LAPOSATA, M AF LEWANDROWSKI, KB FLOOD, JG LAPOSATA, M TI NORMAL REFERENCE LABORATORY VALUES - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP LEWANDROWSKI, KB (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 14 PY 1993 VL 328 IS 2 BP 142 EP 142 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KG467 UT WOS:A1993KG46700028 ER PT J AU RAAB, M RUDD, CE AF RAAB, M RUDD, CE TI 2-PHASE REGULATION OF THE CD4-P56LCK COMPLEX - ASSEMBLY AND AGGREGATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 52 EP 52 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400170 ER PT J AU LIVINGSTON, DM CHITTENDEN, T DECAPRIO, J ECKNER, R EWEN, ME FARNHAM, P LI, Y FLEMINGTON, E KAELIN, W KREK, W MODJTAHEDI, N SHERR, C SHIRODKAR, S AF LIVINGSTON, DM CHITTENDEN, T DECAPRIO, J ECKNER, R EWEN, ME FARNHAM, P LI, Y FLEMINGTON, E KAELIN, W KREK, W MODJTAHEDI, N SHERR, C SHIRODKAR, S TI BIOCHEMICAL-ANALYSIS OF SIGNALS COMING TO AND EMITTED BY RB AND OTHER CELL-CYCLE REGULATING POCKET PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV WISCONSIN,MCARDLE LAB,MADISON,WI 53706. ST JUDE HOSP & RES INST,MEMPHIS,TN. NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 57 EP 57 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400184 ER PT J AU FISHER, DE SHARP, PA AF FISHER, DE SHARP, PA TI DESIGN OF HIGH-AFFINITY DNA-BINDING MYC ANALOGS - CRITICAL SIDE-CHAIN AND CONFORMATIONAL REQUIREMENTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MIT,CTR CANC RES,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 72 EP 72 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400236 ER PT J AU JAHROUDI, N LYNCH, DC AF JAHROUDI, N LYNCH, DC TI REGULATION OF VONWILLEBRAND-FACTOR GENE-EXPRESSION INVOLVES GATA ELEMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY 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 PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 77 EP 77 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400258 ER PT J AU ABE, M KUFE, DW AF ABE, M KUFE, DW TI CHARACTERIZATION OF CIS-ACTING ELEMENTS REGULATING TRANSCRIPTION OF THE DF3 BREAST CARCINOMA-ASSOCIATED ANTIGEN SO JOURNAL OF CELLULAR BIOCHEMISTRY 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 WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 99 EP 99 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400344 ER PT J AU FRETER, RR IRMINGER, JC PORTER, JA JONES, SD STILES, CD AF FRETER, RR IRMINGER, JC PORTER, JA JONES, SD STILES, CD TI A NOVEL 7-NUCLEOTIDE MOTIF LOCATED IN 3' ULTRANSLATED SEQUENCES OF THE IMMEDIATE-EARLY GENE SET MEDIATES PDGF INDUCTION OF THE JE GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,DIV CLIN ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 107 EP 107 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400378 ER PT J AU JAIN, JN MINER, Z RAO, A AF JAIN, JN MINER, Z RAO, A TI ANALYSIS OF THE PREEXISTING AND NUCLEAR FORMS OF NF-AT (NUCLEAR FACTOR OF ACTIVATED T-CELLS) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 113 EP 113 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400401 ER PT J AU LICHT, J ENGLISH, M RO, M REDDY, J SHAKNOVICH, R GROSSEL, M HANSEN, U AF LICHT, J ENGLISH, M RO, M REDDY, J SHAKNOVICH, R GROSSEL, M HANSEN, U TI FUNCTIONAL AND MUTATIONAL ANALYSIS OF THE DROSOPHILA KRUPPEL TRANSCRIPTIONAL REPRESSOR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 CUNY MT SINAI SCH MED,DIV MOLEC MED,NEW YORK,NY 10029. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 116 EP 116 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400414 ER PT J AU LOW, KG DANIELS, GM MELNER, MH COMB, MJ AF LOW, KG DANIELS, GM MELNER, MH COMB, MJ TI TRANSACTIVATION OF PROENKEPHALIN GENE-EXPRESSION BY HTLV-1 TAX IS DEPENDENT UPON ENKCRE-2/AP-1 BINDING-ELEMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROBIOL LAB,BOSTON,MA 02129. OREGON REG PRIMATE RES CTR,DIV NEUROSCI,BEAVERTON,OR 97006. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 117 EP 117 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400415 ER PT J AU WADE, M HELIN, K HARLOW, E AZIZKHAN, JC AF WADE, M HELIN, K HARLOW, E AZIZKHAN, JC TI STRUCTURAL CHARACTERISTICS OF BINDING TO CELLULAR GENE PROMOTERS BY TRANSCRIPTION FACTOR-E2F SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV N CAROLINA,LINEBERGER COMPREHENS CANC CTR,CHAPEL HILL,NC 27599. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 132 EP 132 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400475 ER PT J AU VOLKER, J RAMEH, L POWELL, C HANSEN, U AF VOLKER, J RAMEH, L POWELL, C HANSEN, U TI CELL-GROWTH AND CELL-CYCLE REGULATION OF THE MAMMALIAN TRANSCRIPTION FACTOR LSF SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 141 EP 141 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400511 ER PT J AU GEORGOPOULOS, K AF GEORGOPOULOS, K TI IKAROS AN EARLY LYMPHOID RESTRICTED REGULATORY PROTEIN-A PUTATIVE MEDIATOR FOR T-CELL SPECIFICATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CBRC,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 158 EP 158 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400580 ER PT J AU LANG, KM HSU, E GRIFFIN, JD AF LANG, KM HSU, E GRIFFIN, JD TI RETINOIC ACID-INDUCED DIFFERENTIATION OF HL-60 CELLS LEADS TO DIFFERENTIAL EXPRESSION AND ALTERNATIVE SPLICING OF HOX 3.5 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 162 EP 162 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400597 ER PT J AU MCCAFFREY, PG PERRINO, BA SODERLING, TR RAO, A AF MCCAFFREY, PG PERRINO, BA SODERLING, TR RAO, A TI NF-ATP - A T-CELL DNA-BINDING PROTEIN THAT IS A TARGET FOR CALCINEURIN AND IMMUNOSUPPRESSIVE DRUGS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV TUMOR VIROL,BOSTON,MA 02115. OREGON HLTH SCI UNIV,VOLLUM INST ADV BIOMED RES,PORTLAND,OR 97201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 184 EP 184 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400682 ER PT J AU SEN, J BURAKOFF, SJ SEN, R AF SEN, J BURAKOFF, SJ SEN, R TI MOLECULAR STRATEGIES IN T-CELL DEVELOPMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT PATHOL,DANA FARBER CANC INST,BOSTON,MA 02115. BRANDEIS UNIV,ROSENSTEIL CTR,WALTHAM,MA 02254. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 208 EP 208 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400778 ER PT J AU LEE, JW MOORE, DD AF LEE, JW MOORE, DD TI ISOLATION OF CDNA CLONES ENCODING PROTEINS THAT SPECIFICALLY INTERACT WITH THYROID-HORMONE RECEPTOR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 218 EP 218 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400815 ER PT J AU LIVINGSTON, DM CHITTENDEN, T DECAPRIO, J ECKNER, R EWEN, ME FARNHAM, P LI, Y FLEMINGTON, E KAELIN, W KREK, W MODJTAHEDI, N SHERR, C SHIRODKAR, S AF LIVINGSTON, DM CHITTENDEN, T DECAPRIO, J ECKNER, R EWEN, ME FARNHAM, P LI, Y FLEMINGTON, E KAELIN, W KREK, W MODJTAHEDI, N SHERR, C SHIRODKAR, S TI BIOCHEMICAL-ANALYSIS OF SIGNALS COMING TO AND EMITTED BY RB AND OTHER CELL-CYCLE REGULATING POCKET PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706. ST JUDE HOSP & RES INST,MEMPHIS,TN. NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 223 EP 223 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400829 ER PT J AU AGARWAL, S WILLIAMS, N WOOD, K HASER, W AUGER, K CARRERA, A KING, F CAMPBELL, K DRUKER, B PALLAS, D ROBERTS, T AF AGARWAL, S WILLIAMS, N WOOD, K HASER, W AUGER, K CARRERA, A KING, F CAMPBELL, K DRUKER, B PALLAS, D ROBERTS, T TI TRACING SIGNALS FROM THE MEMBRANE TO THE NUCLEUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 224 EP 224 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400831 ER PT J AU SNIJDERS, AJ HAASE, VH BERNARDS, A AF SNIJDERS, AJ HAASE, VH BERNARDS, A TI 4 ALTERNATIVELY SPLICED 1TK TYROSINE KINASES DIFFER UPSTREAM OF THEIR TRANSMEMBRANE DOMAIN AND ARE RETAINED IN THE ENDOPLASMIC-RETICULUM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC GENET LAB,CTR CANC,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. RI Haase, Volker Hans/A-6758-2013 OI Haase, Volker Hans/0000-0002-7051-8994 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 241 EP 241 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400892 ER PT J AU ZHOU, SY SHOELSON, SE CHAUDHURI, M GISH, G PAWSON, T SCHAFFHAUSEN, B CANTLEY, LC AF ZHOU, SY SHOELSON, SE CHAUDHURI, M GISH, G PAWSON, T SCHAFFHAUSEN, B CANTLEY, LC TI DEGENERATE PHOSPHOPEPTIDE LIBRARIES MAP MOTIFS FOR SH2 DOMAIN RECOGNITION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MT SINAI HOSP,DIV MOLEC & DEV BIOL,TORONTO,ON M5E 1X5,CANADA. TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. TUFTS UNIV,SCH MED,DEPT BIOCHEM,BOSTON,MA 02111. RI Cantley, Lewis/D-1800-2014; Gish, Gerald/C-7228-2017 OI Cantley, Lewis/0000-0002-1298-7653; NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 241 EP 241 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400894 ER PT J AU BARBER, D DEMARTINO, J SHOWERS, M DANDREA, A AF BARBER, D DEMARTINO, J SHOWERS, M DANDREA, A TI A DOMINANT NEGATIVE ERYTHROPOIETIN RECEPTOR (EPO-R) POLYPEPTIDE ABROGATES EPO-DEPENDENT GROWTH OF A HEMATOPOIETIC-CELL LINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 245 EP 245 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400906 ER PT J AU EDER, M HALLEK, M GRIFFIN, JD ERNST, TJ AF EDER, M HALLEK, M GRIFFIN, JD ERNST, TJ TI THE HUMAN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING-FACTOR RECEPTOR IS CAPABLE OF INITIATING SIGNAL TRANSDUCTION IN NIH 3T3 CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. UNIV MUNICH,KLINIKUM INNENSTADT,MED KLIN,W-8000 MUNICH 2,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 245 EP 245 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400909 ER PT J AU COLLINS, TL BURAKOFF, SJ AF COLLINS, TL BURAKOFF, SJ TI EXPRESSION OF AN LCK DELETION MUTANT CONFERS ENHANCED CD4 SIGNALING CAPABILITY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 251 EP 251 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400933 ER PT J AU RAAB, M RUDD, CE AF RAAB, M RUDD, CE TI 2-PHASE REGULATION OF THE CD4-P56LCK COMPLEX - ASSEMBLY AND AGGREGATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 257 EP 257 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400956 ER PT J AU ROTHSTEIN, DM DASILVA, A SUGITA, K YAMAMOTO, M KANTETI, P MORIMOTO, C SCHLOSSMAN, SF RUDD, CE AF ROTHSTEIN, DM DASILVA, A SUGITA, K YAMAMOTO, M KANTETI, P MORIMOTO, C SCHLOSSMAN, SF RUDD, CE TI HUMAN CD4+ CD45RA+ AND CD45RA-T-CELL SUBSETS EXPRESS CATALYTICALLY ACTIVE CD4-P56LCK AND TCR/CD3-P59FYN COMPLEXES AND POSSESS SIMILAR PATTERNS OF TYROSINE-KINASE SUBSTRATES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 257 EP 257 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400957 ER PT J AU RUDD, CE YAMAMOTO, M BURGESS, K PRASAD, KVS AF RUDD, CE YAMAMOTO, M BURGESS, K PRASAD, KVS TI CD5 ACTS AS A TYROSINE KINASE SUBSTRATE WITHIN A RECEPTOR COMPLEX COMPRISING TCR-ZETA/CD3 P56ICK AND P59FYN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 258 EP 258 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400958 ER PT J AU SAMELSON, LE EGERTON, M ASHE, OR CHEN, D DRUKER, BJ BURGESS, WH AF SAMELSON, LE EGERTON, M ASHE, OR CHEN, D DRUKER, BJ BURGESS, WH TI VCP, THE MAMMALIAN HOMOLOG OF CDC48, IS TYROSINE PHOSPHORYLATED IN RESPONSE TO T-CELL ANTIGEN RECEPTOR ACTIVATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC & CELLULAR BIOL,BOSTON,MA 02115. NICHHD,CELL BIOL METAB BRANCH,BETHESDA,MD 20892. AMER RED CROSS,HOLLAND LAB,ROCKVILLE,MD 20850. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 258 EP 258 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400959 ER PT J AU WINKLER, DG PARK, I PAYNE, NS WALSH, CT STROMINGER, JL SHIN, JY AF WINKLER, DG PARK, I PAYNE, NS WALSH, CT STROMINGER, JL SHIN, JY TI PHOSPHORYLATION BY PKC AND MAP KINASE IN THE UNIQUE N-TERMINAL REGION OF THE TYROSINE KINASE P56LCK SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MOLEC PHARMACOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 260 EP 260 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400968 ER PT J AU LO, SH CHEN, LB AF LO, SH CHEN, LB TI TENSIN, AN ACTIN-BINDING AND SH2-CONTAINING PROTEIN, IS ASSOCIATED WITH A SER THR KINASE-ACTIVITY SO JOURNAL OF CELLULAR BIOCHEMISTRY 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 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 271 EP 271 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401010 ER PT J AU LOH, C RAO, A AF LOH, C RAO, A TI THE RAF KINASE IS ASSOCIATED WITH THE T-CELL RECEPTOR/CD3 COMPLEX SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 271 EP 271 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401012 ER PT J AU KAPELLER, R PRASAD, KVS REPKE, H DUKECOHAN, JS CANTLEY, LC RUDD, CE AF KAPELLER, R PRASAD, KVS REPKE, H DUKECOHAN, JS CANTLEY, LC RUDD, CE TI HIV-1 GP120 AND ANTI-CD4 INDUCED CROSS-LINKING OF CD4-P56LCK MODULATE ASSOCIATED PHOSPHATIDYLINOSITOL 3-KINASE AND PHOSPHATIDYL INOSITOL 4-KINASE ACTIVITIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV RETROVIROL,BOSTON,MA 02115. RI Cantley, Lewis/D-1800-2014 OI Cantley, Lewis/0000-0002-1298-7653 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 287 EP 287 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401072 ER PT J AU ANDO, K AICHENBAUM, F HALLEK, M GRIFFIN, JD AF ANDO, K AICHENBAUM, F HALLEK, M GRIFFIN, JD TI GROWTH-FACTORS INDEPENDENTLY REGULATE EXPRESSION OF CYCLINS-D2 AND CYCLINS-D3 DURING G1-PHASE IN THE HUMAN MYELOID CELL-LINE MO7E SO JOURNAL OF CELLULAR BIOCHEMISTRY 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 WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 291 EP 291 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401090 ER PT J AU LIU, V WEAVER, D AF LIU, V WEAVER, D TI REGULATION OF A DNA DAMAGE RESPONSE IN S-PHASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 295 EP 295 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401104 ER PT J AU AGARWAL, S WILLIAMS, NG PARADIS, H ROBERTS, TM AF AGARWAL, S WILLIAMS, NG PARADIS, H ROBERTS, TM TI DISSECTING SIGNALING PATHWAYS THAT LEAD TO THE PHOSPHORYLATION OF TRANSCRIPTION FACTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 297 EP 297 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401114 ER PT J AU PESTELL, RG TROCCOLI, N ALBANESE, C HOLLENBERG, AN JAMESON, JL AF PESTELL, RG TROCCOLI, N ALBANESE, C HOLLENBERG, AN JAMESON, JL TI THE CHORIONIC-GONADOTROPIN BETA-5 GENE IS STIMULATED BY CAMP AND E1A THROUGH DISTINCT REGIONS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,THYROID UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 302 EP 302 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401134 ER PT J AU TEDDER, TF KANSAS, GS SCHLEIFFENBAUM, B AF TEDDER, TF KANSAS, GS SCHLEIFFENBAUM, B TI ROLE AND REGULATION OF L-SELECTIN IN LEUKOCYTE ATTACHMENT TO ENDOTHELIUM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 325 EP 325 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401214 ER PT J AU SPRINGER, TA AF SPRINGER, TA TI THE DISTINCTIVE FUNCTIONS OF SELECTINS, INTEGRINS, AND IG FAMILY MOLECULES IN REGULATION OF LEUKOCYTE INTERACTION WITH ENDOTHELIUM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 328 EP 328 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401222 ER PT J AU STAMENKOVIC, I AF STAMENKOVIC, I TI THE ROLE OF CD44 IN TUMOR-CELL GROWTH AND MIGRATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 329 EP 329 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401226 ER PT J AU KANSAS, GS LEY, K TEDDER, TF AF KANSAS, GS LEY, K TEDDER, TF TI THE CYTOPLASMIC DOMAIN OF L-SELECTIN IS REQUIRED FOR LYMPHOCYTE ADHESION TO HEV AND LEUKOCYTE ROLLING SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. FREE UNIV BERLIN,DEPT PHYSIOL,W-1000 BERLIN 33,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 338 EP 338 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401258 ER PT J AU LEY, K TEDDER, TF KANSAS, GS AF LEY, K TEDDER, TF KANSAS, GS TI L-SELECTIN TRANSFECTED CELLS ROLL IN RAT MESENTERIC VENULES INVIVO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 FREE UNIV BERLIN,DEPT PHYSIOL,W-1000 BERLIN 33,GERMANY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 343 EP 343 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401276 ER PT J AU NGUYEN, T BROWNELL, GL HOLDEN, SA TEICHER, BA AF NGUYEN, T BROWNELL, GL HOLDEN, SA TEICHER, BA TI INTRACELLULAR-DISTRIBUTION OF VARIOUS BORON-COMPOUNDS FOR USE IN BORON NEUTRON-CAPTURE THERAPY SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID B-10(N,ALPHA)LI-7 REACTION; SPECTROMETRY; PORPHYRIN; CELLS AB The neutron capture reaction in boron (B(n,alpha)Li)-B-10-Li-7 generates two short-range particles with high linear energy transfer. The effect of neutron capture therapy depends on the selective localization of B-10 atoms in target cells. The determination of the distribution of boron compounds in cancer cells at the subcellular level is required for the understanding of the effect of this treatment. The monomeric sulfhydryl borane (BSH) compound has been used clinically in Japan and preclinically in the U.S.A. Recently, new compounds have been developed: a dimeric sulfhydryl borane (BSSB), a boronophenylalanine (BPA), and two porphyrin complexes (BOPP and VCDP). This study demonstrates that the porphyrin complexes (BOPP and VCDP) are more cytotoxic than the other three compounds to the rat 9L gliosarcoma cell line. Using atomic absorption spectrophotometry to determine boron content for cellular uptake studies of these agents, we found that of the five compounds tested BOPP (25 muM) exposure resulted in the greatest boron uptake averaging 305 ng B/10(6) cells. BSSB (500 muM) was second averaging 93 ng B/10(6) cells, BSH (500 muM) third averaging 62 ng B/10(6) cells, VCDP (25 muM) fourth averaging 58 ng B/10(6) cells, and BPA (500 muM) fifth averaging 7.4 ng B/106 cells. Data on the distribution of boron in the nuclei, mitochondria, lysosomes, microsomes, and cytosomes of 9L cells are also presented. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. MIT,DEPT NUCL ENGN,CAMBRIDGE,MA 02139. MIT,WHITAKER COLL,CAMBRIDGE,MA 02139. FU NCI NIH HHS [R01-CA36508, R01-CA47379] NR 21 TC 14 Z9 14 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD JAN 7 PY 1993 VL 45 IS 1 BP 147 EP 155 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KG821 UT WOS:A1993KG82100019 PM 8424808 ER PT J AU DURAND, ML CALDERWOOD, SB WEBER, DJ MILLER, SI SOUTHWICK, FS CAVINESS, VS SWARTZ, MN AF DURAND, ML CALDERWOOD, SB WEBER, DJ MILLER, SI SOUTHWICK, FS CAVINESS, VS SWARTZ, MN TI ACUTE BACTERIAL-MENINGITIS IN ADULTS - A REVIEW OF 493 EPISODES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID SEVERE CHILDHOOD MENINGITIS; LUMBAR PUNCTURE; COMPUTED-TOMOGRAPHY; PURULENT-MENINGITIS; UNITED-STATES; COUNTY; SURVEILLANCE; PROGNOSIS; LISTERIA; CITY AB Background and Methods. To characterize acute bacterial meningitis in adults, we reviewed the charts of all persons 16 years of age or older in whom acute bacterial meningitis was diagnosed at Massachusetts General Hospital from 1962 through 1988. We included patients who were admitted after initial treatment at other hospitals. Results. During the 27-year period, 445 adults were treated for 493 episodes of acute bacterial meningitis, of which 197 (40 percent) were nosocomial. Gram-negative bacilli (other than Haemophilus influenzae) caused 33 percent of the nosocomial episodes but only 3 percent of the community-acquired episodes. In the 296 episodes of community-acquired meningitis, the most common pathogens were Streptococcus pneumoniae (37 percent), Neisseria meningitidis (13 percent), and Listeria monocytogenes (10 percent); these organisms accounted for only 8 percent of the nosocomial episodes. Only 19 of the 493 episodes of meningitis (4 percent) were due to H. influenzae. Nine percent of all patients had recurrent meningitis; many had a cerebrospinal fluid leak. Seizures occurred in 23 percent of patients with community-acquired meningitis, and 28 percent had focal central nervous system findings. Risk factors for death among those with single episodes of community-acquired meningitis included older age (greater-than-or-equal-to 60 years), obtunded mental state on admission, and seizures within the first 24 hours. Among those with single episodes, the in-hospital mortality rate was 25 percent for community-acquired and 35 percent for nosocomial meningitis. The overall case fatality rate was 25 percent and did not vary significantly over the 27 years. Conclusions. In our large urban hospital, a major proportion of cases of acute bacterial meningitis in adults were nosocomial. Recurrent episodes of meningitis were frequent. The overall mortality rate remained high. C1 MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. RP DURAND, ML (reprint author), MASSACHUSETTS GEN HOSP, FAC INFECT DIS, FRUIT ST, BOSTON, MA 02114 USA. NR 54 TC 774 Z9 792 U1 3 U2 27 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JAN 7 PY 1993 VL 328 IS 1 BP 21 EP 28 DI 10.1056/NEJM199301073280104 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA KF507 UT WOS:A1993KF50700004 PM 8416268 ER PT J AU CIGARROA, JE ISSELBACHER, EM DESANCTIS, RW EAGLE, KA AF CIGARROA, JE ISSELBACHER, EM DESANCTIS, RW EAGLE, KA TI DIAGNOSTIC-IMAGING IN THE EVALUATION OF SUSPECTED AORTIC DISSECTION - OLD STANDARDS AND NEW DIRECTIONS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID TWO-DIMENSIONAL ECHOCARDIOGRAPHY; COMPUTED-TOMOGRAPHY; TRANSESOPHAGEAL ECHOCARDIOGRAPHY; THORACIC AORTA; ANEURYSM C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,ACC 469,15 PARKMAN ST,BOSTON,MA 02114. NR 57 TC 247 Z9 260 U1 1 U2 3 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 7 PY 1993 VL 328 IS 1 BP 35 EP 43 DI 10.1056/NEJM199301073280107 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA KF507 UT WOS:A1993KF50700007 PM 8416269 ER PT J AU KRADIN, RL MARK, EJ BLICKMAN, JG BOYCE, JA SHANNON, DC AF KRADIN, RL MARK, EJ BLICKMAN, JG BOYCE, JA SHANNON, DC TI A 7-YEAR-OLD GIRL WITH RECURRENT BOUTS OF SORE THROAT, COUGH, DYSPNEA, AND FEVER - INTERSTITIAL EOSINOPHILIC PNEUMONITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID MAJOR BASIC-PROTEIN; BRONCHOALVEOLAR LAVAGE; HYPERSENSITIVITY PNEUMONITIS; PULMONARY; DISEASE; ASTHMA; LUNG; GRANULOMATOSIS; ASPERGILLOSIS; LYMPHOCYTES C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KRADIN, RL (reprint author), MASSACHUSETTS GEN HOSP,PULM UNIT,BOSTON,MA 02114, USA. NR 53 TC 2 Z9 2 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JAN 7 PY 1993 VL 328 IS 1 BP 48 EP 55 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA KF507 UT WOS:A1993KF50700009 ER PT J AU MASUMOTO, A HEMLER, ME AF MASUMOTO, A HEMLER, ME TI MULTIPLE ACTIVATION STATES OF VLA-4 - MECHANISTIC DIFFERENCES BETWEEN ADHESION TO CS1 FIBRONECTIN AND TO VASCULAR CELL-ADHESION MOLECULE-1 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MONOCLONAL-ANTIBODY; INTEGRIN VLA-4; GPIIB-IIIA; T-CELLS; REGULATED EXPRESSION; LEUKOCYTE ADHESION; INDUCED PHOSPHORYLATION; LYMPHOCYTE ADHERENCE; EXTRACELLULAR-MATRIX; ENDOTHELIAL-CELLS AB We examined the effects of a stimulatory anti-beta1 mAb (TS2/16) and different divalent cations on VLA-4-mediated cell adhesion to vascular cell adhesion molecule-1 (VCAM-1), to the fibronectin-derived CS1 peptide, and to larger fibronectin fragments. Using optimal binding conditions (in the presence of mAb TS2/16 and 1.0 mm Mn2+), the levels of VLA-4-mediated adhesion to VCAM-1 and to CS1 peptide were virtually indistinguishable, and half-maximal inhibition of adhesion to both ligands was achieved using similar levels of an anti-alpha4 antibody. However, using suboptimal adhesion conditions, two critical differences between adhesion to CSI peptide (or larger fibronectin fragments) and VCAM-1 were consistently observed. First, stimulation by added mAb TS2/16 had a substantially greater effect on adhesion to CS1 than to VCAM-1 and second, Ca2+ was much less able to support adhesion to CS1 than to VCAM-1. These two differences between adhesion to CS1 peptide and to VCAM-1 were most obvious among cell lines which synthesized inactive or partly active VLA-4 but were not obvious for fully active VLA-4. Together, these results not only reveal crucial differences in the mechanisms of VLA-4 binding to its two ligands, but also lead to increased understanding of the variable activation states of VLA-4. The differential ability to utilize Ca2+ displayed by VLA-4 in different states of activation and the activation of inactive or partly active VLA-4 by the addition of Mn2+ both point to divalent cation sites playing an essential role in determining VLA-4 regulation and ligand specificity. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NIGMS NIH HHS [GM46526, GM38903] NR 79 TC 250 Z9 251 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 1993 VL 268 IS 1 BP 228 EP 234 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KE603 UT WOS:A1993KE60300036 PM 7677996 ER PT J AU REMOLDODONNELL, E AF REMOLDODONNELL, E TI THE OVALBUMIN FAMILY OF SERPIN PROTEINS SO FEBS LETTERS LA English DT Article DE SERPIN; PROTEASE INHIBITOR; PROTEIN FAMILY ID PLASMINOGEN-ACTIVATOR INHIBITOR-2; ANTI-THROMBIN-III; CHICKEN OVALBUMIN; SIGNAL SEQUENCE; MESSENGER-RNA; GENE; ALPHA-1-ANTITRYPSIN; BIOSYNTHESIS; ORGANIZATION; SUPERFAMILY AB A protein family, the 'Ov-serpins' has been identified by comparing amino acid sequence, protein characteristics and gene organization. The Ov-serpins would not be recognized as a family based on sequence identity alone. This example suggests that combinations of characteristics may need to be examined to identify family groupings within the serpin superfamily. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP REMOLDODONNELL, E (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL41579] NR 27 TC 188 Z9 190 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD JAN 4 PY 1993 VL 315 IS 2 BP 105 EP 108 DI 10.1016/0014-5793(93)81143-N PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA KE975 UT WOS:A1993KE97500001 PM 8417965 ER PT J AU PILKINGTON, GJ DUNAN, JR ROGERS, JP CLARKE, TM KNOTT, JCA AF PILKINGTON, GJ DUNAN, JR ROGERS, JP CLARKE, TM KNOTT, JCA TI GROWTH-FACTOR MODULATION OF SURFACE GANGLIOSIDE EXPRESSION IN CLONED NEOPLASTIC GLIA SO NEUROSCIENCE LETTERS LA English DT Article DE GANGLIOSIDE; GLIA; GROWTH FACTOR; NEOPLASM ID TYPE-2 ASTROCYTE DEVELOPMENT; CILIARY NEUROTROPHIC FACTOR; MONOCLONAL-ANTIBODY A2B5; PROGENITOR-CELL; INVITRO; GLIOMA; DIFFERENTIATION; CULTURE; PASSAGE; BINDING AB Cloned neoplastic astrocytes from a human glioma-derived cell line (IPSB- 1 8) were grown in fetal calf serum (FCS)-supplemented culture medium in the presence of three growth factors. Basic fibroblast growth factor (bFGF), epidermal growth factor (EGF) but not platelet-derived growth factor (PDGF) induced an increase in the number of cells positive for the ganglioside-recognizing monoclonal antibody, A2B5. No such growth factor-mediated induction could be detected in cells maintained in plasma-derived serum (PDS)-supplemented medium. Small molecules, removed from PDS during dialysis, may, therefore, act synergistically with growth factors in the control of ganglioside synthesis. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. RP PILKINGTON, GJ (reprint author), INST PSYCHIAT,DEPT NEUROPATHOL,DE CRESPIGNY PK,DENMARK HILL,LONDON SE5 8AF,ENGLAND. NR 24 TC 15 Z9 15 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 JAN 4 PY 1993 VL 149 IS 1 BP 1 EP 5 DI 10.1016/0304-3940(93)90332-F PG 5 WC Neurosciences SC Neurosciences & Neurology GA KJ847 UT WOS:A1993KJ84700001 PM 8469369 ER PT J AU BOSCIA, RE KORBUT, T HOLDEN, SA ARA, G TEICHER, BA AF BOSCIA, RE KORBUT, T HOLDEN, SA ARA, G TEICHER, BA TI INTERACTION OF TOPOISOMERASE-I INHIBITORS WITH RADIATION IN CIS-DIAMMINEDICHLOROPLATINUM(II)-SENSITIVE AND CIS-DIAMMINEDICHLOROPLATINUM(II)-RESISTANT CELLS-INVITRO AND IN THE FSAIIC FIBROSARCOMA INVIVO SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID DNA TOPOISOMERASES; CYTO-TOXICITY; TUMOR-CELLS; RESISTANT; CAMPTOTHECIN; REPAIR; LINES; HYPERTHERMIA; NOVOBIOCIN; COMPLEXES AB The cytotoxicity of the topoisomerase-I inhibitors, camptothecin and topotecan, toward the SCC-25 human head-and-neck squamous-carcinoma cells and the SCC-25/CDDP sub-line made resistant to cis-diamminedichloroplatinum(II) was assessed alone and in combination with radiation. Topotecan was less cytotoxic than camptothecin in cell culture and the SCC-25/CDDP cell line was more sensitive to either topoisomerase-I inhibitor than was the parental SCC-25 cell line. Both camptothecin and topotecan were effective radiation sensitizers of hypoxic SCC-25 and SCC-25/CDDP cells under normal pH or acidic pH conditions. Sensitizer-enhancement ratios ranged between 1.5 and 1.6 for hypoxic SCC-25 cells and between 1.3 and 1.5 for hypoxic SCC-25/CDDP cells. When the ability of campothecin or topotecan to sensitize the FSaIIC fibrosarcoma to single-dose radiation was assessed using the tumor-cell-survival assay, a sensitizer-enhancement ratio of 1.2 was found with each drug. However, using tumor growth delay of the FSaIIC fibrosarcoma to determine the effect of camptothecin or topotecan to enhance the efficacy of a daily fractionated radiation regimen, topotecan produced a sensitizer-enhancement ratio of 1.4, while that for camptothecin was 1.2. These results indicate that topoisomerase-I inhibitors may retain activity in CDDP-resistant cells and may be effective adjuncts to radiation therapy. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. MED UNIV S CAROLINA,CHARLESTON,SC 29425. FU PHS HHS [P01-19589-15] NR 22 TC 48 Z9 48 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 2 PY 1993 VL 53 IS 1 BP 118 EP 123 DI 10.1002/ijc.2910530122 PG 6 WC Oncology SC Oncology GA KD949 UT WOS:A1993KD94900021 PM 8416195 ER PT B AU MCDERMOTT, TJ TERUYA, J HUANG, FM BLOCH, KJ AF MCDERMOTT, TJ TERUYA, J HUANG, FM BLOCH, KJ BE Hawker, CD TI COMPARISON OF CARCINOEMBRYONIC ANTIGEN (CEA) ASSAYS AND SAMPLE MATRICES SO 19TH NATIONAL MEETING, CLINICAL LIGAND ASSAY SOCIETY, APRIL 19-23, 1993, DETROIT, MICHIGAN: SYLLABUS LA English DT Proceedings Paper CT 19th National Meeting of the Clinical-Ligand-Assay-Society CY APR 19-23, 1993 CL DETROIT, MI SP CLIN LIGAND ASSAY SOC C1 MASSACHUSETTS GEN HOSP,CLIN IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CLINICAL LIGAND ASSAY SOC INC PI WAYNE PA PO BOX 67, WAYNE, MI 48184 PY 1993 BP 156 EP 156 PG 1 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA BA98M UT WOS:A1993BA98M00046 ER PT B AU GUDRAIS, P AF GUDRAIS, P BE Hawker, CD TI COMPARISON OF 2 ULTRASENSITIVE ASSAYS FOR THE DETERMINATION OF PROSTATE-SPECIFIC ANTIGEN (PSA) - TOSOH AIA-1200 AND ABBOTT IMX SO 19TH NATIONAL MEETING, CLINICAL LIGAND ASSAY SOCIETY, APRIL 19-23, 1993, DETROIT, MICHIGAN: SYLLABUS LA English DT Proceedings Paper CT 19th National Meeting of the Clinical-Ligand-Assay-Society CY APR 19-23, 1993 CL DETROIT, MI SP CLIN LIGAND ASSAY SOC C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CLINICAL LIGAND ASSAY SOC INC PI WAYNE PA PO BOX 67, WAYNE, MI 48184 PY 1993 BP 158 EP 158 PG 1 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA BA98M UT WOS:A1993BA98M00048 ER PT B AU GUDRAIS, P AF GUDRAIS, P BE Hawker, CD TI EVALUATION OF A FULLY AUTOMATED ENZYME-IMMUNOASSAY FOR CA-125 ON THE ABBOT IMX SO 19TH NATIONAL MEETING, CLINICAL LIGAND ASSAY SOCIETY, APRIL 19-23, 1993, DETROIT, MICHIGAN: SYLLABUS LA English DT Proceedings Paper CT 19th National Meeting of the Clinical-Ligand-Assay-Society CY APR 19-23, 1993 CL DETROIT, MI SP CLIN LIGAND ASSAY SOC C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CLINICAL LIGAND ASSAY SOC INC PI WAYNE PA PO BOX 67, WAYNE, MI 48184 PY 1993 BP 159 EP 159 PG 1 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA BA98M UT WOS:A1993BA98M00049 ER PT J AU ALEXANDER, E LOEFFLER, JS SCHWARTZ, RB JOHNSON, KA CARVALHO, PA GARADA, BM ZIMMERMAN, RE HOLMAN, BL AF ALEXANDER, E LOEFFLER, JS SCHWARTZ, RB JOHNSON, KA CARVALHO, PA GARADA, BM ZIMMERMAN, RE HOLMAN, BL TI TL-201 TC-99M HMPAO SINGLE-PHOTON EMISSION COMPUTED-TOMOGRAPHY (SPECT) IMAGING FOR GUIDING STEREOTAXIC CRANIOTOMIES IN HEAVILY IRRADIATED MALIGNANT GLIOMA PATIENTS SO ACTA NEUROCHIRURGICA LA English DT Article DE ASTROCYTOMA; RADIATION THERAPY; RADIATION NECROSIS; TL-201 ID BRACHYTHERAPY; TL-201 AB SPECT scanning with TI-201 and Tc-99m offers a unique, inexpensive functional imaging modality to combine with CT stereotactic craniotomy for guiding resection of necrosis and/or tumour in patients treated with escalated doses of radiation (> 6000 cGy) by either brachytherapy or radiosurgery. Thirty-two cases were analyzed, with a detailed description of the imaging and operative techniques. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOINT CTR RADIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ALEXANDER, E (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT SURG NEUROSURG,N-6125,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 8 TC 13 Z9 13 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0001-6268 J9 ACTA NEUROCHIR JI Acta Neurochir. PY 1993 VL 122 IS 3-4 BP 215 EP 217 DI 10.1007/BF01405531 PG 3 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA LM353 UT WOS:A1993LM35300005 PM 8372710 ER PT J AU TESAR, GE ROSENBAUM, JF AF TESAR, GE ROSENBAUM, JF TI RECOGNITION AND MANAGEMENT OF PANIC DISORDER SO ADVANCES IN INTERNAL MEDICINE, VOLUME 38 SE ADVANCES IN INTERNAL MEDICINE LA English DT Review ID CHRONIC FATIGUE SYNDROME; NORMAL CORONARY-ARTERIES; MITRAL-VALVE PROLAPSE; ANXIETY DISORDERS; NORADRENERGIC FUNCTION; HEALTHY-SUBJECTS; PRIMARY-CARE; FOLLOW-UP; DSM-III; BENZODIAZEPINE TREATMENT C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. RP TESAR, GE (reprint author), MASSACHUSETTS GEN HOSP,ACUTE PSYCHIAT SERV,BOSTON,MA 02114, USA. NR 131 TC 6 Z9 6 U1 4 U2 5 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146 SN 0065-2822 J9 ADV INTERNAL MED JI Adv.Intern.Med. PY 1993 VL 38 SI 19 BP 123 EP 149 PG 27 WC Medicine, General & Internal SC General & Internal Medicine GA BZ78L UT WOS:A1993BZ78L00006 PM 8438634 ER PT S AU BURLAND, TG SOLNICAKREZEL, L BAILEY, J CUNNINGHAM, DB DOVE, WF AF BURLAND, TG SOLNICAKREZEL, L BAILEY, J CUNNINGHAM, DB DOVE, WF BE Rose, AH TI PATTERNS OF INHERITANCE, DEVELOPMENT AND THE MITOTIC-CYCLE IN THE PROTIST PHYSARUM-POLYCEPHALUM SO ADVANCES IN MICROBIAL PHYSIOLOGY, VOL 35 SE Advances in Microbial Physiology LA English DT Review ID BETA-TUBULIN GENE; ACETYLATED ALPHA-TUBULIN; AMINO-ACID-SEQUENCE; AMEBAL-PLASMODIAL TRANSITION; PROTEIN HISTIDINE KINASE; MESSENGER-RNA STABILITY; SUBUNIT RIBOSOMAL-RNA; GROUP-I INTRON; CELL-CYCLE; SLIME-MOLD C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, CVRC, BOSTON, MA 02129 USA. UNIV LEICESTER, DEPT GENET, LEICESTER LE1 7RH, ENGLAND. INST PASTEUR, UNITE GENET MOLEC MURINE, F-75015 PARIS, FRANCE. RP UNIV WISCONSIN, MCARDLE LAB, 1400 UNIV AVE, MADISON, WI 53706 USA. FU NCI NIH HHS [CA23076, CA07175] NR 255 TC 52 Z9 53 U1 1 U2 4 PU ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL ROAD, LONDON NW1 7DX, ENGLAND SN 0065-2911 BN 0-12-027735-2 J9 ADV MICROB PHYSIOL JI Adv.Microb.Physiol. PY 1993 VL 35 BP 1 EP 69 DI 10.1016/S0065-2911(08)60096-X PG 69 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ69S UT WOS:A1993BZ69S00001 PM 8310878 ER PT J AU VENET, A WALKER, BD AF VENET, A WALKER, BD TI CYTOTOXIC T-CELL EPITOPES IN HIV SIV INFECTION SO AIDS LA English DT Review DE HIV; SIMIAN IMMUNODEFICIENCY VIRUS (SIV); CYTOTOXIC T-LYMPHOCYTES (CTL); ANTIGEN; MAJOR HISTOCOMPATIBILITY COMPLEX; EPITOPES; VACCINES; ANTIGENIC VARIATION ID HUMAN-IMMUNODEFICIENCY-VIRUS; TOXIC LYMPHOCYTES-T; TUMOR NECROSIS FACTOR; RECOMBINANT VACCINIA VIRUS; SEROPOSITIVE INDIVIDUALS; SYNTHETIC PEPTIDES; FINE SPECIFICITY; EFFECTOR-CELLS; RHESUS-MONKEYS; NEF PROTEIN C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. RP VENET, A (reprint author), INST COCHIN GENET MOLEC,INSERM,U152,IMMUNOL & ONCOL MALAD RETROVIRALES LAB,F-75014 PARIS,FRANCE. NR 106 TC 36 Z9 36 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PY 1993 VL 7 SU 1 BP S117 EP S126 DI 10.1097/00002030-199301001-00016 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LE916 UT WOS:A1993LE91600016 PM 7689848 ER PT J AU CURIEL, TJ WONG, JT GORCZYCA, PF SCHOOLEY, RT WALKER, BD AF CURIEL, TJ WONG, JT GORCZYCA, PF SCHOOLEY, RT WALKER, BD TI CD4+ HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 (HIV-1) ENVELOPE-SPECIFIC CYTOTOXIC LYMPHOCYTES-T DERIVED FROM THE PERIPHERAL-BLOOD CELLS OF AN HIV-1-INFECTED INDIVIDUAL SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID MHC CLASS-II; BISPECIFIC MONOCLONAL-ANTIBODIES; MEDIATED CYTO-TOXICITY; EXOGENOUS ANTIGEN; SEROPOSITIVE INDIVIDUALS; IMMUNODOMINANT EPITOPE; INFECTED INDIVIDUALS; IMMUNOGENIC PEPTIDES; INFLUENZA-VIRUS; B VIRUS AB Virus-specific cytotoxic T lymphocytes (CTL) are frequently of the CD8+ surface phenotype, although CTL of the CD4+ surface phenotype have also been described. Published reports of CTL derived from peripheral blood mononuclear cells (PBMC) of individuals infected with human immunodeficiency virus type 1 (HIV-1) have described primarily cells of the CD8+ surface phenotype. However, CD4+ HIV-1 envelope-specific CTL have been reported after in vitro stimulation with HIV-1 envelope protein of peripheral blood cells obtained from HIV-1-seronegative donors, in peripheral blood cells after vaccination of HIV-1-seronegative persons with HIV-1 envelope proteins, and in cerebrospinal fluid cells of HIV-1-infected individuals. Recently, CD4+ HIV-1 gag-specific CTL were also reported. We now report a patient from whom we derived HIV-1 envelope-specific CTL cell lines of the CD4+ surface phenotype. Our cell culture technique did not employ exogenous viral antigenic stimulation, and may therefore yield cells that more closely reflect those in the underlying populations from which they were derived. These CTL did not appear to have the clear human leukocyte antigen (HLA) class II restriction pattern typically seen in CD4-expressing cells and were not functionally inhibited by anti-CD3 antibody. Further work will be required to define the role of CD4+ CTL in the pathogenesis or HIV-1 disease. C1 MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ALLERGY & IMMUNOL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. RP CURIEL, TJ (reprint author), UNIV COLORADO,HLTH SCI CTR,DEPT MED,DIV INFECT DIS,4200 E 9TH AVE,DENVER,CO 80262, USA. FU NCI NIH HHS [CA 37461-07]; NIAID NIH HHS [R29-AI27050] NR 64 TC 39 Z9 39 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 JAN PY 1993 VL 9 IS 1 BP 61 EP 68 DI 10.1089/aid.1993.9.61 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA KL618 UT WOS:A1993KL61800008 PM 7678973 ER PT J AU MELCHIOR, CL ALLEN, PM AF MELCHIOR, CL ALLEN, PM TI TEMPERATURE IN MICE AFTER ETHANOL - EFFECT OF PROBING AND REGAIN OF RIGHTING REFLEX SO ALCOHOL LA English DT Article DE ALCOHOL; STRESS; THERMOREGULATION; HYPNOSIS ID BODY-TEMPERATURE; STRESS; HYPERTHERMIA; HYPOTHERMIA; MECHANISMS AB The handling involved in rectally probing a mouse in order to measure body temperature is a stress which results in an increase in body temperature. However, after an injection of ethanol the fall in body temperature caused by ethanol is ''acerbated by probing. In mice, decreases in temperature following probing are ethanol-dose dependent and can be generated on both the falling and rising phases of the ethanol induced change in temperature. The effect of probing can be observed when the mice are under the hypnotic influence of ethanol, and regain of righting reflex itself is followed by a fall in temperature. The resumption of motor activity in undisturbed mice following an hypnotic dose of ethanol also is accompanied by a fall in temperature. Therefore, the drop in temperature observed in any of these procedures which involve moving the mice may be attributable to the disruption of heat conservation rather than a stress interaction. C1 W LOS ANGELES VET ADM,BRENTWOOD DIV RES,LOS ANGELES,CA. NR 14 TC 0 Z9 0 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0741-8329 J9 ALCOHOL JI Alcohol PD JAN-FEB PY 1993 VL 10 IS 1 BP 17 EP 20 DI 10.1016/0741-8329(93)90048-S PG 4 WC Substance Abuse; Pharmacology & Pharmacy; Toxicology SC Substance Abuse; Pharmacology & Pharmacy; Toxicology GA KJ126 UT WOS:A1993KJ12600003 PM 8447962 ER PT B AU MILLER, KW AF MILLER, KW BE Alling, C Diamond, I Leslie, SW Sun, GY Wood, WG TI MULTIPLE ACTIONS OF ETHANOL ON ACETYLCHOLINE-RECEPTORS SO ALCOHOL, CELL MEMBRANES, AND SIGNAL TRANSDUCTION IN BRAIN LA English DT Proceedings Paper CT Marcus Wallenberg Symposium on Alcohol, Cell Membranes, and Signal Transduction in Brain CY JUN 28-JUL 01, 1992 CL LUND, SWEDEN SP MARCUS WALLENBERG FDN INT SCI EXCHANGE, NIAAA, SWEDISH MED RES COUNCIL C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44583-2 PY 1993 BP 83 EP 96 PG 14 WC Substance Abuse; Neurosciences; Physiology SC Substance Abuse; Neurosciences & Neurology; Physiology GA BZ52R UT WOS:A1993BZ52R00008 ER PT S AU NITSCH, RM SLACK, BE FARBER, SA BORGHESANI, PR SCHULZ, JG KIM, C FELDER, CC GROWDON, JH WURTMAN, RJ AF NITSCH, RM SLACK, BE FARBER, SA BORGHESANI, PR SCHULZ, JG KIM, C FELDER, CC GROWDON, JH WURTMAN, RJ BE Nitsch, RM Growdon, JH Corkin, S Wurtman, RJ TI RECEPTOR-COUPLED AMYLOID PRECURSOR PROTEIN PROCESSING SO ALZHEIMERS DISEASE: AMYLOID PRECUSOR PROTEINS, SIGNAL TRANSDUCTION, AND NEURONAL TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 7th Meeting of the International-Study-Group-on-the-Pharmacology-of-Memory-Disorders-Associ ated-with-Aging: Alzheimers Disease CY FEB 12-14, 1993 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOC AGING ID ALZHEIMERS-DISEASE; PHOSPHORYLATION; DERIVATIVES; HYDROLYSIS; ACTIVATION; SECRETION; RELEASE; CELLS AB The family of beta-amyloid protein precursors (APP) can be processed via several alternative proteolytic pathways. Some generate potentially amyloidogenic APP derivatives, whereas others preclude the formation of such fragments. The cellular mechanisms regulating the relative activities of these pathways are thus important in determining the factors contributing to the formation of amyloidogenic APP derivatives. In order to investigate whether cell-surface receptor activity can regulate APP processing, HEK 293 cell lines stably expressing human muscarinic acetylcholine receptors (mAChR; subtypes mi, m2, m3, m4) were stimulated with the muscarinic agonist carbachol, and the release of APP derivatives was measured. Carbachol increased the release of large amino-terminal APP-fragments 4- to 6-fold in cell lines expressing the m1 or m3 receptors but not in those expressing m2 or m4 subtypes. This increase was blocked by various protein kinase inhibitors and mimicked by phorbol esters, indicating that it is mediated by protein kinase activation, presumably by protein kinase C (PKC). To determine whether additional cell-surface receptor types linked to this signal transduction pathway could also regulate APP processing, we stimulated differentiated PC-12 cells with bradykinin and found that this neuropeptide also increased the secretion of amino-terminal APP derivatives. We next investigated the possibility that neuronal depolarization might affect APP processing in mammalian brain. Electrically stimulated rat hippocampal slices released two times more amino-terminal APP derivatives than unstimulated control slices. This release increased with increasing stimulation frequencies in the physiological firing range of hippocampal pyramidal cells, and was blocked by tetrodotoxin. These results suggest that, in brain, APP processing is regulated by neuronal activity. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP NITSCH, RM (reprint author), MIT,DEPT BRAIN & COGNIT SCI,E25-604,CAMBRIDGE,MA 02139, USA. RI Schulz, Joachim/H-2430-2011; Farber, Steven/G-5851-2012 OI Farber, Steven/0000-0002-8037-7312 NR 15 TC 26 Z9 26 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-853-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 695 BP 122 EP 127 DI 10.1111/j.1749-6632.1993.tb23039.x PG 6 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BZ92T UT WOS:A1993BZ92T00022 PM 8239269 ER PT S AU SLACK, BE NITSCH, RM LIVNEH, E KUNZ, GM ELDAR, H WURTMAN, RJ AF SLACK, BE NITSCH, RM LIVNEH, E KUNZ, GM ELDAR, H WURTMAN, RJ BE Nitsch, RM Growdon, JH Corkin, S Wurtman, RJ TI REGULATION OF AMYLOID PRECURSOR PROTEIN RELEASE BY PROTEIN-KINASE-C IN SWISS 3T3 FIBROBLASTS SO ALZHEIMERS DISEASE: AMYLOID PRECUSOR PROTEINS, SIGNAL TRANSDUCTION, AND NEURONAL TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 7th Meeting of the International-Study-Group-on-the-Pharmacology-of-Memory-Disorders-Associ ated-with-Aging: Alzheimers Disease CY FEB 12-14, 1993 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOC AGING ID ALZHEIMERS-DISEASE; PHOSPHORYLATION; IDENTIFICATION; ACTIVATION; SECRETION AB Release of the amyloid precursor protein (APP) of Alzheimer's disease from Swiss 3T3 fibroblasts was stimulated in a concentration-dependent manner by phorbol 12-myristate 13-acetate. In fibroblasts overexpressing protein kinase C alpha (PKC alpha), the EC(50) for this response was 7 nM, while in control cells the EC(50) was 63 nM. The effect of PMA. was inhibited by the PKC antagonist H-7 in control cells, but not in cells that overexpressed PKC alpha. Basal release of APP was higher in cells that overexpressed PKC alpha, and was not affected by the phosphatase inhibitor okadaic acid, although this compound doubled APP release from control cells. The results suggest that PKC alpha regulates APP processing in mammalian cells. Alterations in the activity of PKC have been reported to occur in Alzheimer's disease and might potentially contribute to abnormalities of APP metabolism characteristic of this disorder. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. WEIZMANN INST SCI,DEPT CHEM IMMUNOL,IL-76100 REHOVOT,ISRAEL. RP SLACK, BE (reprint author), MIT,DEPT BRAIN & COGNIT SCI,E25-604,CAMBRIDGE,MA 02139, USA. FU NIMH NIH HHS [MH 28783] NR 13 TC 19 Z9 19 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-853-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 695 BP 128 EP 131 DI 10.1111/j.1749-6632.1993.tb23040.x PG 4 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BZ92T UT WOS:A1993BZ92T00023 PM 8239270 ER PT S AU WASCO, W PEPPERCORN, J TANZI, RE AF WASCO, W PEPPERCORN, J TANZI, RE BE Nitsch, RM Growdon, JH Corkin, S Wurtman, RJ TI SEARCH FOR THE GENES RESPONSIBLE FOR FAMILIAL ALZHEIMERS-DISEASE SO ALZHEIMERS DISEASE: AMYLOID PRECUSOR PROTEINS, SIGNAL TRANSDUCTION, AND NEURONAL TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 7th Meeting of the International-Study-Group-on-the-Pharmacology-of-Memory-Disorders-Associ ated-with-Aging: Alzheimers Disease CY FEB 12-14, 1993 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOC AGING ID PRECURSOR PROTEIN GENE; MUTATION; LINKAGE; CHROMOSOME-14; LOCUS AB Inherited or Familial Alzheimer's Disease (PAD) has clearly been shown to be a genetically heterogeneous disorder. Mutations in the gene on chromosome 21 encoding the beta-amyloid protein precursor (APP) have been shown to be linked to 2-3% of FAD kindreds examined around the world. A late onset FAD locus has been mapped to a region of chromosome 19 in which a recently isolated APP-like gene, APLPI has also been localized, making this gene a strong candidate to harbor a late-onset FAD defect. More recently, a major FAD locus has been mapped to the long arm of chromosome 14. The chromosome 14 locus appears to be mainly linked to the gene defect in early onset FAD pedigrees. Besides the FAD loci on chromosome 21, 19, and 14, at least two other loci must exist since the gene defect in some early- and late-onset PAD pedigrees do not appear to segregate with markers from any of these autosomes. As different gene defects responsible for various forms of FAD are discovered, perhaps, a common basis for the etiology of this devastating disorder can be discerned. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL, GENET & AGING LAB, BOSTON, MA 02129 USA. NR 15 TC 9 Z9 10 U1 0 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-853-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 695 BP 203 EP 208 DI 10.1111/j.1749-6632.1993.tb23053.x PG 6 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BZ92T UT WOS:A1993BZ92T00036 PM 8239284 ER PT J AU SHANG, C AF SHANG, C TI BIOELECTROCHEMICAL OSCILLATIONS IN SIGNAL TRANSDUCTION AND ACUPUNCTURE - AN EMERGING PARADIGM SO AMERICAN JOURNAL OF CHINESE MEDICINE LA English DT Article AB Several converging points from recent research results on cellular signal transduction, pattern formation, bioelectromagnetism and acupuncture are reviewed. These converging points indicate the general importance of bioelectrochemical oscillations in morphogenesis and physiology: An organism is not only a system of molecules and cells, but also a system of oscillations. These oscillations precede the morphological changes in development or pathology. Converging discoveries and hypotheses in different fields, and a perspective on their potential application in biomedicine are also discussed in this article. RP SHANG, C (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,149 13TH ST,BOSTON,MA 02129, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU INST ADV RES ASIAN SCI & MED PI CHESTNUT HILL PA PO BOX 67336, CHESTNUT HILL, MA 02167 SN 0192-415X J9 AM J CHINESE MED JI Am. J. Chin. Med. PY 1993 VL 21 IS 1 BP 91 EP 101 DI 10.1142/S0192415X93000121 PG 11 WC Integrative & Complementary Medicine; Medicine, General & Internal SC Integrative & Complementary Medicine; General & Internal Medicine GA LA772 UT WOS:A1993LA77200011 PM 8328428 ER PT J AU CHAKRABORTY, BM MUELLER, WH JOOS, SK HANIS, CL BARTON, SA SCHULL, WJ AF CHAKRABORTY, BM MUELLER, WH JOOS, SK HANIS, CL BARTON, SA SCHULL, WJ TI OBESITY AND UPPER-BODY FAT DISTRIBUTION IN MEXICAN-AMERICAN CHILDREN FROM FAMILIES WITH A DIABETIC PROBAND SO AMERICAN JOURNAL OF HUMAN BIOLOGY LA English DT Article ID FATNESS; LEANNESS; GROWTH; TEXAS; ALERT AB Upper and centralized body fat distribution is associated with non-insulin dependent diabetes mellitus (NIDDM). Few studies have focused on anthropometric characteristics of preadults from families in which there is a diabetic (NIDDM) proband. This study explores the prevalence of upper and centralized body fatness in Mexican American children from the Diabetes Alert study (1981-1983) in Starr County, Texas. Anthropometric data on 165 males and 224 females 9-19 years include measures of adiposity such as skinfold thicknesses and the body mass index (BMI), a measure of overweight. They show rates of obesity two to three times that of White children of comparable age and sex from National Health Surveys. In comparison with U.S. White subjects, Mexican American adults are shorter, have more adiposity and arm muscle mass and have sitting heights and body breadths at the mean of these dimensions for the U.S. population. Children from Diabetes Alert families show only marginal excess of severe obesity (>95th percentile of BMI) when compared to the general population of children surveyed in Starr County schools. Girls from these families, but not boys, have excess fatness in the BMI compared to Mexican American children from the Hispanic Health and Nutrition Examination Survey (HHANES); suprailiac skinfold thicknesses are also greater in children of the Diabetes Alert study than in HHANES children. From 1972 through 1982, Mexican American children in South Texas showed an increase in average stature, weight, and the BMI. These data together suggest that excessive obesity exists and may be increasing in children in populations at risk for NIDDM. The prevention of NIDDM in the Mexican American population may be more effective if educational and promotional interventions include the school aged population. (C) 1993 Wiley-Liss, Inc. C1 UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,POB 20186,HOUSTON,TX 77225. UNIV TEXAS,GRAD SCH BIOMED SCI,CTR DEMOG,HOUSTON,TX 77225. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR 97207. NR 23 TC 3 Z9 3 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1042-0533 J9 AM J HUM BIOL JI Am. J. Hum. Biol. PY 1993 VL 5 IS 5 BP 575 EP 585 DI 10.1002/ajhb.1310050509 PG 11 WC Anthropology; Biology SC Anthropology; Life Sciences & Biomedicine - Other Topics GA MG864 UT WOS:A1993MG86400008 ER PT J AU YAN, WL BOUSTANY, RMN KONRADI, C OZELIUS, L LERNER, T TROFATTER, JA JULIER, C BREAKEFIELD, XO GUSELLA, JF HAINES, JL AF YAN, WL BOUSTANY, RMN KONRADI, C OZELIUS, L LERNER, T TROFATTER, JA JULIER, C BREAKEFIELD, XO GUSELLA, JF HAINES, JL TI LOCALIZATION OF JUVENILE, BUT NOT LATE-INFANTILE, NEURONAL CEROID LIPOFUSCINOSIS ON CHROMOSOME-16 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID DISEASE; LINKAGE; CLN3; MAPS AB The neuronal ceroid lipofuscinoses (NCL) are a group of progressive neurodegenerative disorders characterized by the deposition of autofluorescent proteinaceous fingerprint or curvilinear bodies. We have found that CLN3, the gene underlying the juvenile form of NCL, is very tightly finked to the dinucleotide repeat marker D16S285 on chromosome 16. Integration of D16S285 into the genetic map of chromosome 16 by using the Centre d'Etude du Polymorphisme Humain panel of reference pedigrees yielded a favored marker order in the CLN3 region of qtel-D16S150-.08-D16S285-.04-D16S148-.02-D16S67-ptel. The most likely location of the disease gene, near D16S285 in the D16S150-D16S148 interval, was favored by odds of greater than 104:1 over the adjacent D16S148-D16S67 interval, which was recently reported as the minimum candidate region. Analysis of D16S285 in pedigrees with late-infantile NCL virtually excluded the CLN3 region, suggesting that these two forms of NCL are genetically distinct. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02129. CTR ETUDE POLYMORPHISME HUMAIN,PARIS,FRANCE. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. DUKE UNIV,MED CTR,DEPT PEDIAT NEUROL,DURHAM,NC 27710. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00169, HG00324]; NINDS NIH HHS [NS24279] NR 23 TC 20 Z9 20 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 1993 VL 52 IS 1 BP 89 EP 95 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA KK908 UT WOS:A1993KK90800011 PM 8434611 ER PT J AU ARNAOUT, MA AF ARNAOUT, MA TI CELL-ADHESION MOLECULES IN INFLAMMATION AND THROMBOSIS - STATUS AND PROSPECTS SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article; Proceedings Paper CT WORKSHOP ON THE MORBIDITY AND MORTALITY OF END-STAGE RENAL DISEASE : DKUHD PERSPECTIVES IN END-STAGE RENAL DISEASE CY FEB 27-29, 1992 CL MIAMI, FL SP NIH DE CELL ADHESION MOLECULES; INFLAMMATION; THROMBOSIS; ANTIADHESION THERAPY RP ARNAOUT, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,LEUKOCYTE BIOL & INFLAMMAT PROGRAM,RENAL UNIT,149 & 13TH ST,BOSTON,MA 02129, USA. FU NIAID NIH HHS [AI-21964, AI-28465] NR 10 TC 26 Z9 26 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD JAN PY 1993 VL 21 IS 1 BP 72 EP 76 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA KG849 UT WOS:A1993KG84900015 PM 8418630 ER PT J AU AUSIELLO, DA MASSRY, S AF AUSIELLO, DA MASSRY, S TI BASIC SCIENCE RESEARCH SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Editorial Material RP AUSIELLO, DA (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02129, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD JAN PY 1993 VL 21 IS 1 BP 120 EP 120 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA KG849 UT WOS:A1993KG84900028 PM 8418618 ER PT J AU LAMMER, EJ BADEN, H MARGOLIS, RJ AF LAMMER, EJ BADEN, H MARGOLIS, RJ TI PHENOTYPE OF CRANIOECTODERMAL DYSPLASIA WITH DIFFERENT HAIR AND BONE ABNORMALITIES SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE ECTODERMAL DYSPLASIA; CRANIOECTODERMAL DYSPLASIA; BONE DYSPLASIA; CRANIOSYNOSTOSIS; HAIR FOLLICLE AB We report on a 3-year-old boy with hair abnormalities and a generalized bone dysplasia. He had very short, sparse hair and craniosynostosis. His stature, growth, and limb lengths were normal, as was his neurological development. While this phenotype has some resemblance to cranioectodermal dysplasia, the radiographic and hair abnormalities are different. Histological studies showed abnormalities in the internal root sheath of the hair follicle and the hair shaft. These findings define a new ectodermal dysplasia syndrome of unknown cause. C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,EMBRYOL TERATOL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. NR 14 TC 4 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JAN 1 PY 1993 VL 45 IS 1 BP 9 EP 13 DI 10.1002/ajmg.1320450105 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA KR915 UT WOS:A1993KR91500003 PM 8418667 ER PT J AU FRIEDMAN, JM BIRCH, P GREENE, C BERRY, S KING, R BURKE, W BENNETT, R DECAMPOS, JM FRIEDMAN, JM BIRCH, P HUSON, S KORF, B KRAUSE, W ARMFIELD, K NIIMURA, M INABA, Y NORTH, K ORTENBERG, J DERKALOUSTIAN, V POYHONEN, M RUBENSTEIN, A SHORT, P BOVE, K STINE, S NICHOLSON, L TENCONI, R ZACKAI, E REHBERG, K AF FRIEDMAN, JM BIRCH, P GREENE, C BERRY, S KING, R BURKE, W BENNETT, R DECAMPOS, JM FRIEDMAN, JM BIRCH, P HUSON, S KORF, B KRAUSE, W ARMFIELD, K NIIMURA, M INABA, Y NORTH, K ORTENBERG, J DERKALOUSTIAN, V POYHONEN, M RUBENSTEIN, A SHORT, P BOVE, K STINE, S NICHOLSON, L TENCONI, R ZACKAI, E REHBERG, K TI NATIONAL NEUROFIBROMATOSIS FOUNDATION INTERNATIONAL DATABASE SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE NEUROFIBROMATOSIS; DATABASE; NF1; NF2 ID GENE AB The National Neurofibromatosis Foundation International Database is a system for collecting comprehensive information on the clinical manifestations and natural history of neurofibromatosis. Data are entered into personal computers at participating centres and are pooled at the Central Database and coordinating centre in Vancouver, Canada. The system includes special mechanisms to assure consistency among centres and to maintain patient confidentiality. The database is designed to foster collaborative clinical and molecular genetic research in many aspects of neurofibromatosis. C1 UNIV COLORADO,DEPT PEDIAT,BOULDER,CO 80309. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV WASHINGTON,SEATTLE,WA 98195. FDN IIMENEZ DIAZ,MADRID,SPAIN. UNIV BRITISH COLUMBIA,VANCOUVER V6T 1W5,BC,CANADA. OXFORD REG GENET SERV,OXFORD,ENGLAND. BOSTON CHILDRENS HOSP,BOSTON,MA. SCOTTISH RITE CHILDRENS MED CTR,ATLANTA,GA. IIKEI UNIV,TOKYO,JAPAN. CHILDRENS HOSP,SYDNEY,AUSTRALIA. MONTREAL CHILDRENS HOSP,MONTREAL H3H 1P3,QUEBEC,CANADA. OULU UNIV HOSP,OULU,FINLAND. MT SINAI MED CTR,NEW YORK,NY 10029. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. DUPONT INST,WILMINGTON,DE. UNIV PADUA,PADUA,ITALY. CHILDRENS HOSP,PHILADELPHIA,PA 19104. RP FRIEDMAN, JM (reprint author), UNIV BRITISH COLUMBIA,DEPT MED GENET,226 WESBROOK BLDG,6174 UNIV BLVD,VANCOUVER V6T 1Z3,BC,CANADA. RI North, Kathryn/K-6476-2012 OI North, Kathryn/0000-0003-0841-8009 NR 4 TC 37 Z9 37 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 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JAN 1 PY 1993 VL 45 IS 1 BP 88 EP 91 DI 10.1002/ajmg.1320450121 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA KR915 UT WOS:A1993KR91500019 PM 8418666 ER PT J AU SHUSTER, E AF SHUSTER, E TI A SURGEON WITH ACQUIRED-IMMUNODEFICIENCY-SYNDROME - A THREAT TO PATIENT SAFETY - THE CASE OF BEHRINGER,WILLIAM,H. SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID RIGHTS COMMISSION DECISIONS; AIDS LITIGATION PROJECT; TRANSMISSION; EPIDEMIC; VIRUS; CARE; COURT AB A year ago, the New Jersey case of William H. Behringer, the surgeon with acquired immunodeficiency syndrome (AIDS), caused health experts to focus on health care workers infected with human immunodeficiency virus (HIV) and to call for new policies and guidelines to protect patients against infection. After a year of acrimonious debate over the proper approach to the issues discussed in Behringer, no consensus has emerged. The Centers for Disease Control has quietly abandoned its plan to ease its July 1991 guidelines that call for infected professionals to cease performing invasive procedures or disclose their conditions to their patients. It has now decided to let each state set its own rules and regulations in compliance with its guidelines, or risk financial penalties. The issues discussed in Behringer have remained controversial. This case provides an opportunity to identify reasonable actions that may ensure patient safety without inciting public fears, unduly restricting individual freedom, or violating human rights. RP SHUSTER, E (reprint author), VET AFFAIRS MED CTR,ACC,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 42 TC 1 Z9 1 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 1993 VL 94 IS 1 BP 93 EP 99 DI 10.1016/0002-9343(93)90126-A PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA KG494 UT WOS:A1993KG49400015 PM 8380536 ER PT J AU EMANUEL, EJ AF EMANUEL, EJ TI CRUZAN-II - REPLY SO AMERICAN JOURNAL OF MEDICINE LA English DT Letter RP EMANUEL, EJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 1 TC 0 Z9 0 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 1993 VL 94 IS 1 BP 115 EP 116 DI 10.1016/0002-9343(93)90136-D PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KG494 UT WOS:A1993KG49400025 ER PT J AU ROSSETTI, L FARRACE, S CHOI, SB GIACCARI, A SLOAN, L FRONTONI, S KATZ, MS AF ROSSETTI, L FARRACE, S CHOI, SB GIACCARI, A SLOAN, L FRONTONI, S KATZ, MS TI MULTIPLE METABOLIC EFFECTS OF CGRP IN CONSCIOUS RATS - ROLE OF GLYCOGEN-SYNTHASE AND PHOSPHORYLASE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CALCITONIN GENE-RELATED PEPTIDE; ADENYLATE CYCLASE; INSULIN RESISTANCE ID GENE-RELATED PEPTIDE; DEPENDENT DIABETES-MELLITUS; ISLET AMYLOID POLYPEPTIDE; PERIPHERAL INSULIN RESISTANCE; LIVER PLASMA-MEMBRANES; SKELETAL-MUSCLE CELLS; CALCITONIN GENE; ADENYLATE-CYCLASE; STRIATED-MUSCLE; NONDIABETIC HUMANS AB Calcitonin gene-related peptide (CGRP) is a neuropeptide that is released at the neuromuscular junction in response to nerve excitation. To examine the relationship between plasma CGRP concentration and intracellular glucose metabolism in conscious rats, we performed insulin (22 pmol . kg-1 . min-1) clamp studies combined with the infusion of 0, 20, 50, 100, 200, and 500 pmol . kg-1 . min-1 CGRP (plasma concentrations ranging from 2 x 10(-11) to 5 x 10(-9) M). CGRP antagonized insulin's suppression of hepatic glucose production at plasma concentrations (approximately 10(-10( M) that are only two- to fivefold its basal portal concentration. Insulin-mediated glucose disposal was decreased by 20-32% when CGRP was infused at 50 pmol . kg-1 . min-1 (plasma concentration 3 x 10(-10) M) or more. The impairment in insulin-stimulated glycogen synthesis in skeletal muscle accounted for all of the CGRP-induced decrease in glucose disposal, while whole body glycolysis was increased despite the reduction in total glucose uptake. The muscle glucose 6-phosphate concentration progressively increased during the CGRP infusions. CGRP inhibited insulin-stimulated glycogen synthase in skeletal muscle with a 50% effective dose of 1.9 +/- 0.36 x 10(-10) M. This effect on glycogen synthase was due to a reduction in enzyme affinity for UDP-glucose, with no changes in the maximal velocity. In vitro CGRP stimulated both hepatic and skeletal muscle adenylate cyclase in a dose-dependent manner. These data suggest that 1) CGRP is a potent antagonist of insulin at the level of muscle glycogen synthesis and hepatic glucose production; 2) inhibition of glycogen synthase is its major biochemical action in skeletal muscle; and 3) these effects are present at concentrations of the peptide that may be in the physiological range for portal vein and skeletal muscle. These data underscore the potential role of CGRP in the physiological modulation of intracellular glucose metabolism. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV DIABET,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP ROSSETTI, L (reprint author), YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,DIV ENDOCRINOL F501,1300 MORRIS PK AVE,BRONX,NY 10461, USA. RI Giaccari, Andrea/J-1889-2012; FRONTONI, SIMONA/J-4893-2012 OI Giaccari, Andrea/0000-0002-7462-7792; FU NIDDK NIH HHS [R29 DK-45024] NR 57 TC 29 Z9 30 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 JAN PY 1993 VL 264 IS 1 BP E1 EP E10 PN 1 PG 10 WC Physiology SC Physiology GA KK291 UT WOS:A1993KK29100029 PM 8430777 ER PT J AU FREEMAN, GL PRABHU, SD WIDMAN, LE COLSTON, JT AF FREEMAN, GL PRABHU, SD WIDMAN, LE COLSTON, JT TI AN ANALYSIS OF VARIABILITY OF LEFT-VENTRICULAR PRESSURE DECAY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Note DE DIASTOLE; VENTRICULAR RELAXATION; TAU ID INTACT CANINE HEART; CONSCIOUS DOGS; ISOVOLUMIC RELAXATION; DEPENDENT RELAXATION; DIASTOLIC PROPERTIES; PERFORMANCE; CARDIOLOGY; CHAOS AB This study evaluated whether the time course of left ventricular (LV) pressure decay is consistent from beat to beat in the normal heart under tightly controlled experimental conditions. We determined the variability of LV isovolumic relaxation and compared it with that of other hemodynamic parameters. Pressure decay was evaluated using a monoexponential time constant (T), a half-time (T1/2), and an average rate (R(avg)) in nine chronically instrumented dogs. To eliminate physical factors that could lead to variability, the dogs were studied at paced heart rates after autonomic blockade and during apnea. At a heart rate of 160 beats/min the coefficient of variation (SD/mean, expressed as a percent) was higher for T (4.7%, P < 0.005), T1/2 (5.0%, P < 0.005), and R(avg) (3.2%, P < 0.005) than for dP/dt(max) (1.9%), as well as for end-diastolic volume (1.2%), end-systolic volume (1.2%), or end-systolic pressure (1.8%). Similar differences were present at 200 beats/min. Pressure decay was also assessed during major loading shifts induced by rapid caval occlusion. Surprisingly, comparison of first and last beats did not show significant differences for T or T1/2, but did for all standard hemodynamic parameters and for R(avg), While the best correlation with a relaxation parameter and hemodynamic parameters during changing loading conditions was for R(avg), the correlations were not consistent in every case. We conclude that LV pressure decay shows marked variability, unrelated to the algorithm used to assess it. R(avg), a model independent parameter, may be a useful way to quantify LV pressure fall. C1 AUDIE MURPHY MEM VET HOSP,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MORPHOL,SAN ANTONIO,TX 78284. RI Prabhu, Sumanth/D-5223-2009 NR 23 TC 9 Z9 9 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 JAN PY 1993 VL 264 IS 1 BP H262 EP H268 PN 2 PG 7 WC Physiology SC Physiology GA KK292 UT WOS:A1993KK29200038 PM 8430855 ER PT J AU VATNER, DE KIUCHI, K MANDERS, WT VATNER, SF AF VATNER, DE KIUCHI, K MANDERS, WT VATNER, SF TI EFFECTS OF CORONARY ARTERIAL REPERFUSION ON BETA-ADRENERGIC RECEPTOR-ADENYLYL CYCLASE COUPLING SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ISCHEMIA; MICROSPHERES ID CHRONIC MYOCARDIAL-INFARCTION; ISCHEMIC MYOCARDIUM; CANINE MYOCARDIUM; CONSCIOUS DOGS; BLOOD-FLOW; ONE HOUR; PROTEIN; ASSAY; GS; DECREASES AB The effects of 1 h of coronary arterial occlusion (CAO) followed by 15 min reperfusion (CAR) were examined in nine conscious dogs. Ischemia was verified by decreased regional blood flow (radioactive microspheres) and loss of systolic regional wall motion in the ischemic zone. Beta-Adrenergic receptor density assessed by I-125-labeled cyanopindolol binding in a crude membrane fraction tended to decrease but was not significantly different. However, adenylyl cyclase activity and the guanine nucleotide stimulatory protein (G(s)) were reduced in ischemic subendocardium compared with nonischemic subendocardium. The fraction of beta-adrenergic receptors binding agonist with high affinity increased in ischemic subendocardial and subepicardial layers. Compared with prior data in experiments with 1 h CAO without CAR, the increase in beta-adrenergic receptor density that occurs with myocardial ischemia is rapidly reversed with CAR of 15 min duration, while the decreased fraction of receptors binding agonist with high affinity was reversed to an increase in high-affinity receptors. The global decreases in adenylyl cyclase and G(s), which have been observed with simple CAO, persist but are observed selectively in the previously ischemic subendocardium after CAR. Thus both CAO and CAR affect beta-adrenergic receptors and adenylyl cyclase differently. During CAR, increased numbers of beta-adrenergic receptors binding agonist with high affinity occur potentially as a compensatory mechanism in the face of persistent reductions in adenylyl cyclase activity and G(s). C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. RP VATNER, DE (reprint author), NEW ENGLAND REG PRIMATE RES CTR,1 PINE HILL DR,POB 9102,SOUTHBOROUGH,MA 01772, USA. FU NHLBI NIH HHS [HL-33065, HL-37404, HL-45332] NR 36 TC 20 Z9 20 U1 0 U2 4 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1993 VL 264 IS 1 BP H196 EP H204 PN 2 PG 9 WC Physiology SC Physiology GA KK292 UT WOS:A1993KK29200029 PM 8381610 ER PT J AU GOLDBERG, MA YUCEL, EK SAINI, S HAHN, PF KAUFMAN, JA COHEN, MS AF GOLDBERG, MA YUCEL, EK SAINI, S HAHN, PF KAUFMAN, JA COHEN, MS TI MR ANGIOGRAPHY OF THE PORTAL AND HEPATIC VENOUS SYSTEMS - PRELIMINARY EXPERIENCE WITH ECHOPLANAR IMAGING SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID MAGNETIC-RESONANCE; INSTANT IMAGES; BLOOD-FLOW; MOTION; SONOGRAPHY; APPEARANCE; TISSUE; BODY AB OBJECTIVE. The purpose of this study was to evaluate the ability of echoplanar MR angiography to depict the major hepatic and portal venous structures. SUBJECTS AND METHODS. Echoplanar and conventional MR angiographic examinations were performed in 10 subjects (seven healthy volunteers, three patients with focal hepatic lesions). A gradient-recalled echo (GRE) time-of-flight technique (125/10 [TR/TE], 90-degrees flip angle) was used for echoplanar angiography. Eight complete single-excitation images were acquired at each level in 1.5 sec and then collapsed into a single maximal intensity projection. Conventional time-of-flight MR angiography (34/13, 30-degrees flip angle) also was performed. The vascular anatomy from the right atrium to the splenic vein was imaged (6-mm contiguous levels) in three 10.5-sec breath-holds with echoplanar imaging, as compared with seven 11.5-sec breath-holds with conventional MR angiography. Echoplanar and conventional images were compared quantitatively and qualitatively. RESULTS. Echoplanar imaging was 61% faster than conventional MR angiography. Vessel-to-liver signal-intensity ratios were significantly higher for echoplanar imaging (p < .0001), signal-to-noise ratios were significantly higher for conventional MR angiography (p <.0001), and contrast-to-noise ratios were comparable. Qualitatively, echoplanar imaging and conventional MR angiography provided similar anatomic information about the hepatic and portal veins. CONCLUSION. Angiograms of the hepatic and portal venous systems that are of diagnostic quality can be acquired much more quickly with echoplanar imaging than with conventional MR angiography. RP GOLDBERG, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. RI Cohen, Mark/C-6610-2011 OI Cohen, Mark/0000-0001-6731-4053 NR 28 TC 21 Z9 21 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 1993 VL 160 IS 1 BP 35 EP 40 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KF477 UT WOS:A1993KF47700009 PM 8416642 ER PT J AU LEV, MH CHEW, FS AF LEV, MH CHEW, FS TI TRANSITIONAL CELL-CARCINOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 3 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 1993 VL 160 IS 1 BP 74 EP 74 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KF477 UT WOS:A1993KF47700018 PM 8416652 ER PT J AU MCLOUD, TC FLOWER, CDR AF MCLOUD, TC FLOWER, CDR TI HIGH-RESOLUTION SONOGRAPHY OF THE DIAPHRAGMATIC PLEURA - REPLY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter C1 ADDENBROOKES HOSP,CAMBRIDGE CB2 2QQ,ENGLAND. RP MCLOUD, TC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 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 1993 VL 160 IS 1 BP 204 EP 204 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KF477 UT WOS:A1993KF47700047 ER PT J AU DISLER, DG CHEW, FS AF DISLER, DG CHEW, FS TI ADRENAL PHEOCHROMOCYTOMA - REPLY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter RP DISLER, DG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 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 1993 VL 160 IS 1 BP 210 EP 210 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KF477 UT WOS:A1993KF47700059 ER PT J AU SCHMIDT, J FERNANDEZDELCASTILLO, C RATTNER, DW LEWANDROWSKI, KB MESSMER, K WARSHAW, AL AF SCHMIDT, J FERNANDEZDELCASTILLO, C RATTNER, DW LEWANDROWSKI, KB MESSMER, K WARSHAW, AL TI HYPERONCOTIC ULTRAHIGH MOLECULAR-WEIGHT DEXTRAN SOLUTIONS REDUCE TRYPSINOGEN ACTIVATION, PREVENT ACINAR NECROSIS, AND LOWER MORTALITY IN RODENT PANCREATITIS SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT 33RD ANNUAL MEETING OF THE SOC FOR SURGERY OF THE ALIMENTARY TRACT CY MAY 11-13, 1992 CL SAN FRANCISCO, CA SP SOC SURG ALIMENTARY TRACT ID EXPERIMENTAL HEMORRHAGIC-PANCREATITIS; TRASYLOL THERAPY; RAT; RESUSCITATION; ISCHEMIA; INJURY; SHOCK AB Acinar necrosis in patients with acute pancreatitis can be due to enzymatic injury, ischemia, or both. We hypothesized that novel therapy aimed at an improvement of pancreatic microcirculation early in the course of pancreatitis may reduce the lethality and acinar damage. Forty-six dextran-resistant rats received controlled intraductal infusion of glycodeoxycholic acid (10 mmol/L), followed by intravenous cerulein (5 mug/kg/lh) for 6 hours. Beginning 30 minutes after the induction of pancreatitis, all animals were resuscitated with Ringer's lactate (RL) (8 mL/kg/h intravenously for 9 hours). In addition, they were given intra-aortic bolus infusions (2 mL/kg at 30, 60, 90, and 150 minutes) of either RL, sodium chloride (NaCl) (7.5%) and dextran 60,000 (10%) (HHS-60), NaCl (7.5%) and dextran 500,000 (10%) (HHS-500), or NaCl (0.9%) and dextran 500,000 (10%) (DEX-500). Despite high-volume fluid resuscitation in the groups that received RL and HHS-60, 70% of the animals in each of these groups died within 24 hours. In contrast, the mortality rates in the groups of animals that received HHS-500 and DEX-500 were dramatically reduced to 0% and 10%, respectively (p = 0.005, p = 0.02). Histopathologic scores for acinar necrosis were significantly lower in the group of animals that received DEX-500 (p <0.009) compared with those that received RL and HHS-60. Finally, total amounts of trypsinogen activation peptides in ascites were significantly lower in the animals that received HHS-500 (p <0.004) and DEX-500 (p <0.02) compared with those that received RL and HHS-60. Rapid bolus infusion of hyperoncotic ultrahigh molecular weight dextran solution with or without hypertonic saline but not RL or hypertonic-hyperoncotic saline-dextran significantly reduced pathologic trypsinogen activation, prevented acinar necrosis, and improved survival in acute experimental pancreatitis. We speculate that a sustained improvement of pancreatic microcirculation by ultrahigh molecular weight dextran is the mechanism of action. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,ACC 336,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. UNIV MUNICH,INST SURG RES,W-8000 MUNICH 2,GERMANY. NR 41 TC 43 Z9 43 U1 0 U2 1 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 1993 VL 165 IS 1 BP 40 EP 45 DI 10.1016/S0002-9610(05)80402-7 PG 6 WC Surgery SC Surgery GA KF374 UT WOS:A1993KF37400007 PM 7678189 ER PT J AU SIMON, PM DEMPSEY, JA LANDRY, DM SKATRUD, JB AF SIMON, PM DEMPSEY, JA LANDRY, DM SKATRUD, JB TI EFFECT OF SLEEP ON RESPIRATORY MUSCLE-ACTIVITY DURING MECHANICAL VENTILATION SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID UPPER AIRWAY-RESISTANCE; NREM SLEEP; INDUCED INCREASES; HUMANS; CO2; COMPENSATION; INHIBITION; FREQUENCY AB The purpose of this study was to determine whether consciousness was critical for the expression of neuromechanical inhibition of breathing during mechanical ventilation. This same mechanical ventilation model also was used to evaluate the relative importance of sleep state in causing CO2 retention during sleep. Positive pressure ventilation was used to suppress respiratory muscle activity; CO2 was then added until a reappearance of inspiratory effort, which defined the recruitment threshold (P(CO2)RT). Keeping the mechanics of the respiratory system constant through the use of passive mechanical ventilation allowed us to measure the output of the respiratory controller, independent of these parameters. Eight normal subjects were mechanically hyperventilated with a nasal mask during wakefulness and sleep with matched flow rates, frequencies, and tidal volumes. When inspiratory muscle activity was undetectable and end-tidal P(CO2) (PET(CO2)) fell below 30 mm Hg, inspired CO2 was added in stepped increments until inspiration reoccurred. The sleeping state increased both eupneic PET(CO2) (42 +/- 4 versus 38 +/- 3 mm Hg) and P(CO2)RT (48 +/- 3 versus 46 +/- 2 mm Hg) compared with that during wakefulness. Neuromechanical inhibition of inspiratory muscle activity during mechanical ventilation was present during both wakefulness and sleep, as evidenced by the mean difference between P(CO2)RT and eupneic PET(CO2) of 8 and 6 mm Hg, respectively. Recruitment thresholds during wakefulness and sleep were compared to evaluate the effect of sleep on respiratory motor output independent of changes in load, i.e., respiratory mechanics held constant. P(CO2)RT was higher during sleep than during wakefulness in every subject, indicating a change in set point associated with the loss of the wakefulness stimulus. The difference in mean eupneic PET(CO2) between wakefulness and sleep (4 mm Hg) also was determined to evaluate the effect of sleep on P(CO2) when respiratory mechanics were no longer held constant. The difference in mean eupneic PET(CO2) (4 mm Hg) was greater than the difference in mean P(CO2)RT (2 mm Hg), suggesting that not all the CO2 retention incurred during sleep was due to changes in set point. We conclude that consciousness is not necessary for the expression of neuromechanical inhibition of breathing during mechanical ventilation. Our findings further support the concept that both changes in set point and respiratory load such as an increase in upper airway resistance are important determinants of sleep-induced CO2 retention. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED RES SERV,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,JOHN RANKIN LAB PULM MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT PREVENT MED,JOHN RANKIN LAB PULM MED,MADISON,WI 53706. FU NHLBI NIH HHS [5 PO1 HL-42242-03] NR 24 TC 41 Z9 41 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD JAN PY 1993 VL 147 IS 1 BP 32 EP 37 PG 6 WC Respiratory System SC Respiratory System GA KG846 UT WOS:A1993KG84600006 PM 8420427 ER PT J AU BRYANT, BP LEFTHERIS, K QUINN, JV BRAND, JG AF BRYANT, BP LEFTHERIS, K QUINN, JV BRAND, JG TI MOLECULAR STRUCTURAL REQUIREMENTS FOR BINDING AND ACTIVATION OF L-ALANINE TASTE RECEPTORS SO AMINO ACIDS LA English DT Article DE AMINO ACIDS; STRUCTURE ACTIVITY; L-ALANINE; TASTE RECEPTOR; L-ALANINE ANALOGS; LIGAND BINDING ASSAY ID ICTALURUS-PUNCTATUS; AMINO-ACIDS; CHANNEL CATFISH; SENSATION; SPECIFICITY; STIMULUS; SITES AB L-Alanine binds to and activates specific taste receptors of Ictalurus punctatus, the channel catfish. In order to determine the structural requirements for receptor binding and activation in this model system, a number of analogues of L-alanine were tested using a neurophysiological assay and a competitive ligand binding assay. These assays measured the ability of analogues to activate taste receptors and to displace L-[H-3]alanine from L-alanine binding sites. Of those derivatives with modifications of the sidechain, L-serine, glycine, beta-chloroLalanine and 1-amino-cyclopropane-1-carboxylic acid were the most potent analogues with IC50s similar to and neural responses slightly decremented from that of L-alanine. Derivatives containing branched sidechains or sidechains of otherwise increased volume were considerably less active. All modifications of the alpha-carboxylic acid and the alpha-amine, including amides, esters and various isosteres, led to substantial reduction in the analogues' ability to displace L-[H-3]alanine and, in most cases, very weak stimulatory capability. However, L-lactic acid was a reasonably strong stimulus, but a poor competitor, suggesting that it acts at a different receptor site. Overall, these results indicate the importance of the charged amine and carboxylic acid groups for binding to and activation of the receptor for L-alanine. Moreover, modifications around the chiral center of L-alanine support the hypothesis that receptor binding and activation are separate processes in this model taste system. C1 UNIV PENN,SCH DENT MED,DEPT BIOCHEM,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP BRYANT, BP (reprint author), MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. NR 32 TC 5 Z9 5 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0939-4451 J9 AMINO ACIDS JI Amino Acids PY 1993 VL 4 IS 1-2 BP 73 EP 88 DI 10.1007/BF00805803 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LC116 UT WOS:A1993LC11600008 PM 24190559 ER PT J AU MARTYN, J GRONERT, G WHITE, D AF MARTYN, J GRONERT, G WHITE, D TI REGULATION OF SKELETAL-MUSCLE ACETYLCHOLINE-RECEPTORS - REPLY SO ANESTHESIOLOGY LA English DT Letter ID MOTOR-NEURON LESIONS; RESISTANCE; EXTREMITIES; SENSITIVITY; DISUSE C1 UNIV CALIF DAVIS,SACRAMENTO MED CTR,MED CTR,DEPT ANESTHESIA,SACRAMENTO,CA 95817. RP MARTYN, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 17 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD JAN PY 1993 VL 78 IS 1 BP 217 EP 218 DI 10.1097/00000542-199301000-00042 PG 2 WC Anesthesiology SC Anesthesiology GA KJ616 UT WOS:A1993KJ61600043 ER PT J AU ORCEL, P AF ORCEL, P TI STRESS-FRACTURES OF THE FEMORAL-NECK SO ANNALES DE RADIOLOGIE LA French DT Article DE STRESS FRACTURE; FEMORAL NECK FRACTURE; OSTEOPOROSIS; BONE SCAN; MR IMAGING AB Stress fractures of the femoral neck are often mismanaged, due to their banal or misleading clinical presentation, particularly in the elderly. These fractures could be secondary to an excessive mechanical stress (so-called fatigue fractures), or to a weakened bone resistance (so-called insufficiency fractures), or both. Plain radiographs are mostly useless to an early diagnosis. For this purpose, bone scintiscan and MR Imaging have a much better sensitivity, though their specificity is not absolute. Late diagnosis leads to an increased risk of complete fracture, requiring orthopedic surgery. By contrast, incomplete early-recognized fractures usually heal within few weeks on bedrest. Stress fractures of the femoral neck should be actually considered as a << menace syndrome >> of femoral neck fracture, and therefore need a quick appropriate management. RP ORCEL, P (reprint author), MASSACHUSETTS GEN HOSP,149 NAVY YARD,13TH ST,BOSTON,MA 02129, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU EXPANSION SCI FRANCAISE PI PARIS PA 31 BLVD LATOUR MAUBOURG, 75007 PARIS, FRANCE SN 0003-4185 J9 ANN RADIOL JI Ann. Radiol. PY 1993 VL 36 IS 1 BP 88 EP 93 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KZ936 UT WOS:A1993KZ93600013 PM 8333707 ER PT J AU NETLAND, PA ZIERHUT, M RAIZMAN, MB AF NETLAND, PA ZIERHUT, M RAIZMAN, MB TI POSTTRAUMATIC HERPES-ZOSTER OPHTHALMICUS AS A PRESENTING SIGN OF HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO ANNALS OF OPHTHALMOLOGY LA English DT Article ID IMMUNE-DEFICIENCY SYNDROME AB We present the case of a 38-year-old man who developed herpes zoster ophthalmicus after orbital blunt trauma. Additional evaluation revealed human immunodeficiency virus type 1 (HIV-1) infection. This case shows that varicella-zoster may be activated by local trauma and that herpes zoster ophthalmicus in young patients may indicate underlying HIV-1 infection. C1 NEW ENGLAND EYE CTR,750 WASHINGTON ST,BOSTON,MA 02111. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 5 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC CONTEMPORARY OPHTHALMOLOGY PI SKOKIE PA 4711 GOLF RD, SUITE 408, SKOKIE, IL 60076-1242 SN 0003-4886 J9 ANN OPHTHALMOL JI Ann. Ophthalmol. PD JAN PY 1993 VL 25 IS 1 BP 14 EP 15 PG 2 WC Ophthalmology SC Ophthalmology GA KJ612 UT WOS:A1993KJ61200003 PM 8427484 ER PT J AU SCHUKNECHT, HF GACEK, MR AF SCHUKNECHT, HF GACEK, MR TI COCHLEAR PATHOLOGY IN PRESBYCUSIS SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE COCHLEAR PATHOLOGY; DEAFNESS OF AGING; PRESBYCUSIS ID STRIA VASCULARIS AB A survey of the temporal bone collection at the Massachusetts Eye and Ear Infirmary reveals 21 cases that meet the criterion for the clinical diagnosis of presbycusis. It is evident that the previously advanced concept of four predominant pathologic types of presbycusis is valid, these being sensory, neural, strial, and cochlear conductive. An abrupt high-tone loss signals sensory presbycusis, a flat threshold pattern is indicative of strial presbycusis, and loss of word discrimination is characteristic of neural presbycusis. When the increments of threshold loss present a gradually decreasing linear distribution pattern on the audiometric scale and have no pathologic correlate, it is speculated that the hearing loss is caused by alterations in the physical characteristics of the cochlear duct, and the loss is identified as cochlear conductive presbycusis. It is clear that many individual cases do not separate into a specific type but have mixtures of these pathologic types and are termed mixed presbycusis. About 25% of all cases of presbycusis show none of the above characteristics and are classified as indeterminate presbycusis. C1 HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. RP SCHUKNECHT, HF (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [R01 DC00079] NR 55 TC 332 Z9 348 U1 9 U2 45 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD JAN PY 1993 VL 102 IS 1 SU 158 BP 1 EP 16 PN 2 PG 16 WC Otorhinolaryngology SC Otorhinolaryngology GA KH505 UT WOS:A1993KH50500001 PM 8420477 ER PT J AU GARCIA, CE GIRDHARGOPAL, HV DORFMAN, DM AF GARCIA, CE GIRDHARGOPAL, HV DORFMAN, DM TI KIKUCHI-FUJIMOTO DISEASE OF THE NECK - UPDATE SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE HISTIOCYTOSIS; LYMPHADENITIS; NECROSIS; SYNDROME ID HISTIOCYTIC NECROTIZING LYMPHADENITIS; PLASMACYTOID T-CELLS; GRANULOCYTIC INFILTRATION; MONOCLONAL-ANTIBODY AB Kikuchi-Fujimoto disease (KFD) is a rare entity of uncertain cause that commonly presents with persistently enlarged cervical lymph nodes unresponsive to antibiotic therapy. Although it usually follows a benign course, KFD has been repeatedly misdiagnosed as malignant lymphoma; hence, clinicians and pathologists alike need to be aware of this disease entity. The newest developments regarding the etiology and course of KFD are presented through a review of the literature and a recent illustrative case. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,JOINT CTR OTOLARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,JOINT CTR OTOLARYNGOL,BOSTON,MA 02115. NR 19 TC 42 Z9 43 U1 0 U2 0 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD JAN PY 1993 VL 102 IS 1 BP 11 EP 15 PN 1 PG 5 WC Otorhinolaryngology SC Otorhinolaryngology GA KG980 UT WOS:A1993KG98000003 PM 8420463 ER PT J AU REINKE, KR AF REINKE, KR TI DAVINCI,LEONARDO RIGHT-TO-LEFT MIRRORED WRITING REVISITED SO ANNALS OF PLASTIC SURGERY LA English DT Note AB Leonardo Da Vinci's anatomical drawings continue to attract the attention of the medical community. One of the intriguing aspects of these drawings is Da Vinci's use of right-to-left mirrored writing. Many hypotheses have been proposed to explain his mirrored writing. This article presents a new explanation that takes into consideration the drawing material used and Da Vinci's known innovative ability. A collection of his anatomical drawings is currently on display in Boston at the Museum of Fine Arts. RP REINKE, KR (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,DIV PLAST & RECONSTRUCT SURG,32 FRUIT ST,BOSTON,MA 02114, USA. NR 20 TC 3 Z9 3 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0148-7043 J9 ANN PLAS SURG JI Ann. Plast. Surg. PD JAN PY 1993 VL 30 IS 1 BP 89 EP 92 DI 10.1097/00000637-199301000-00014 PG 4 WC Surgery SC Surgery GA KH223 UT WOS:A1993KH22300014 PM 8333692 ER PT J AU LEWANDROWSKI, KB SOUTHERN, JF PINS, MR COMPTON, CC WARSHAW, AL AF LEWANDROWSKI, KB SOUTHERN, JF PINS, MR COMPTON, CC WARSHAW, AL TI CYST FLUID ANALYSIS IN THE DIFFERENTIAL-DIAGNOSIS OF PANCREATIC CYSTS - A COMPARISON OF PSEUDOCYSTS, SEROUS CYSTADENOMAS, MUCINOUS CYSTIC NEOPLASMS, AND MUCINOUS CYSTADENOCARCINOMA SO ANNALS OF SURGERY LA English DT Article ID CARCINOEMBRYONIC ANTIGEN; MICROCYSTIC-ADENOMAS; LESIONS; AMYLASE; TUMORS; ASSAYS AB Pancreatic cystic lesions include inflammatory pseudocysts, benign serous tumors, and mucinous neoplasms, some of which are malignant. Clinical and radiologic indices are often inadequate to discriminate reliably among these possibilities. In an attempt to develop new preoperative diagnostic criteria to assist in decisions regarding therapy, the authors have performed cyst fluid analysis for tumor markers (carcinoembryonic antigen: CEA, CA 125, and CA 19.9), amylase content, amylase isoenzymes, relative viscosity, and cytology on 26 pancreatic cysts. The cases included nine pseudocysts, five serous cystadenomas, 4 mucinous cystic neoplasms, 7 mucinous cystadenocarcinomas, and one mucinous ductal adenocarcinoma with cystic degeneration. Carcinoembryonic antigen levels were high (> 367) in all benign and malignant mucinous cysts, but were low (< 23) in the pseudocysts and benign serous cystadenomas, an indication that CEA discriminates between mucinous and nonmucinous cysts (p < 0.0001). Values for CA 125 were high in all malignant cysts, low in pseudocysts, and variable in mucinous cystic neoplasms and serous cystadenomas. Levels of Ca 19.9 were nondiscriminatory. Cyst fluid amylase and lipase content were variable but were generally high in pseudocysts and low in cystic tumors. Amylase isoenzyme analysis was useful to differentiate pseudocysts from cystic tumors. Measurement of the relative viscosity in cyst fluid showed high (> serum viscosity) values in 89% of mucinous tumors and low values (< serum) in all pseudocysts and serous cystadenomas (p < 0.01). Cytologic analysis of cyst fluids was of limited value in differentiating pseudocysts from serous cystadenoma, but in seven of eight mucinous tumors provided useful diagnostic information and correctly classified three of five malignant tumors. The authors conclude that cyst fluid analysis can provide a preoperative classification of these diagnostically difficult lesions. The combination of viscosity, CEA, CA 125, and cytology can reliably distinguish malignant cystic tumors and potentially premalignant mucinous cystic neoplasms from pseudocysts and serous cystadenomas. Amylase content with isoenzyme analysis is useful to identify pseudocysts. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LEWANDROWSKI, KB (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,GRAY 5,BOSTON,MA 02114, USA. NR 17 TC 226 Z9 232 U1 0 U2 8 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD JAN PY 1993 VL 217 IS 1 BP 41 EP 47 DI 10.1097/00000658-199301000-00008 PG 7 WC Surgery SC Surgery GA KH580 UT WOS:A1993KH58000008 PM 8424699 ER PT J AU LEHRER, RI LICHTENSTEIN, AK GANZ, T AF LEHRER, RI LICHTENSTEIN, AK GANZ, T TI DEFENSINS - ANTIMICROBIAL AND CYTOTOXIC PEPTIDES OF MAMMALIAN-CELLS SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE CYTOTOXIC; ANTIMICROBIAL; NEUTROPHIL; MACROPHAGE; PANETH CELL ID RABBIT ALVEOLAR MACROPHAGES; CHRONIC GRANULOMATOUS-DISEASE; HUMAN NEUTROPHIL DEFENSINS; MICROBICIDAL CATIONIC PROTEINS; CANDIDA-ALBICANS; CYTO-TOXICITY; OUTER-MEMBRANE; POLYMORPHONUCLEAR LEUKOCYTES; NONOXIDATIVE MECHANISMS; SALMONELLA-TYPHIMURIUM AB Defensins are antimicrobial and cytotoxic peptides that contain 29-35 amino acid residues, including six invariant cysteines whose intromolecular disulfide bonds cyclize and stabilize them in a complexly folded, triple-stranded beta-sheet configuration. Generated by the proteolytic processing of 93-95 amino acid precursor peptides, they constitute > 5% of the total cellular protein in human and rabbit neutrophils (polymorphonucleated neutrophils-PMN) and are also produced by rabbit lung macrophages and by mouse and rabbit small intestinal Paneth cells. Despite their prominence in rat PMN, defensins are not found in murine PMN. The antimicrobial spectrum of defensins includes gram positive and gram negative bacteria, mycobacteria, T. pallidum, many fungi, and some enveloped viruses. Defensins exert nonspecific cytotoxic activity against a wide range of normal and malignant targets, including cells resistant to TNF-alpha and NK-cytolytic factor. They appear to kill mammalian target cells and micro-organisms by a common mechanism, which involves initial electrostatic interactions with negatively charged target cell surface molecules (likely the head groups of polar membrane lipids), followed by insertion into the cell membranes which they permeabilize, forming voltage-regulated channels. In addition to their antimicrobial and cytotoxic properties, some defensins act as opsonins, while others inhibit protein kinase C, bind specifically to the ACTH receptor and block steroidogenesis or act as selective chemoattractants for monocytes. Defensins are a newly delineated family of effector molecules whose contribution to host defense, inflammation, and cytotoxicity may be considerable for humans, even though it is unlikely to be revealed by experimentation with mice. C1 W LOS ANGELES VET ADM HOSP,DEPT MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,CTR HLTH SCI,WILL ROGERS INST PULMONARY RES,LOS ANGELES,CA 90024. RP LEHRER, RI (reprint author), UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT MED,LOS ANGELES,CA 90024, USA. FU NHLBI NIH HHS [HL 35640]; NIAID NIH HHS [AI 22839, AI 29595] NR 101 TC 785 Z9 828 U1 3 U2 33 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 1993 VL 11 BP 105 EP 128 PG 24 WC Immunology SC Immunology GA KX306 UT WOS:A1993KX30600005 PM 8476558 ER PT J AU AISENBERG, AC AF AISENBERG, AC TI UTILITY OF GENE REARRANGEMENTS IN LYMPHOID MALIGNANCIES SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE IMMUNOGLOBULIN GENE REARRANGEMENTS; T-CELL RECEPTOR GENE REARRANGEMENTS; LYMPHOMA; LYMPHOCYTIC LEUKEMIA ID T-CELL RECEPTOR; ACUTE LYMPHOBLASTIC-LEUKEMIA; CHRONIC LYMPHOCYTIC-LEUKEMIA; NON-HODGKINS-LYMPHOMA; PRE-B-CELLS; BURKITT-LYMPHOMA; BETA-CHAIN; IMMUNOGLOBULIN; NEOPLASMS; ANTIGEN AB Molecular genetic study of lymphoid neoplasms by Southern blotting or polymerase chain reaction permits the ready detection of gene rearrangements. Clonal rearrangements of immunoglobulin and T-cell receptor genes identify neoplasms of B- and T-cell lineage, respectively. Additionally, lymphoma-specific chromosome translocations involving oncogenes are detected with the same molecular techniques. Probes are currently available to study the c-myc translocations of Burkitt's lymphoma, the bcl-2 translocations of follicular lymphomas, and the bcl-1 translocations of centrocytic lymphoma. RP AISENBERG, AC (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,HEMATOL ONCOL UNIT,BOSTON,MA 02114, USA. NR 36 TC 19 Z9 19 U1 0 U2 1 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 1993 VL 44 BP 75 EP 84 DI 10.1146/annurev.med.44.1.75 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA KW478 UT WOS:A1993KW47800008 PM 8476269 ER PT J AU MOSKOWITZ, MA CUTRER, FM AF MOSKOWITZ, MA CUTRER, FM TI SUMATRIPTAN - A RECEPTOR-TARGETED TREATMENT FOR MIGRAINE SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE MIGRAINE; SEROTONIN RECEPTOR SUBTYPES; NEUROGENIC INFLAMMATION ID NEUROGENIC PLASMA EXTRAVASATION; RAT DURA-MATER; SUBCUTANEOUS SUMATRIPTAN; ORAL SUMATRIPTAN; GR43175; STIMULATION; NEURONS; BRAIN; CONTRACTION; ACTIVATION AB Sumatriptan, recently introduced for the treatment of migraine, heralds the beginning of a molecular era in the pharmacological treatment of migraine headache. An indole (non-ergot alkaloid) derivative with agonist properties at a receptor resembling the 5-HT1D Subtype (so-called 5-HT1-like receptor),1 sumatriptan is the first antimigraine medication to exhibit receptor-selective properties. Clinical data indicate that sumatriptan relieves headache, nausea, and photophobia in a majority of acute migraine patients, and it possesses favorable side effect and safety profiles. Of great importance, sumatriptan acts through a novel mechanism that we now know is shared by dihydroergotamine and other useful compounds for the treatment of acute migraine headaches. In this summary, we briefly review the drug's mechanism of action and the emerging clinical experience with its use. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MOSKOWITZ, MA (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,STROKE RES LAB,BOSTON,MA 02114, USA. RI Moskowitz, Michael/D-9916-2011 NR 43 TC 117 Z9 118 U1 0 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 1993 VL 44 BP 145 EP 154 DI 10.1146/annurev.med.44.1.145 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA KW478 UT WOS:A1993KW47800013 PM 8386498 ER PT J AU MITLAK, BH NUSSBAUM, SR AF MITLAK, BH NUSSBAUM, SR TI DIAGNOSIS AND TREATMENT OF OSTEOPOROSIS SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE BONE DENSITOMETRY; FRACTURE ID POSTMENOPAUSAL BONE LOSS; PERFORMANCE LIQUID-CHROMATOGRAPHY; ESTROGEN REPLACEMENT THERAPY; CALCIUM SUPPLEMENTATION; SALMON-CALCITONIN; CONTROLLED TRIAL; FRACTURE RATE; HIP FRACTURE; DOUBLE-BLIND; WHITE WOMEN AB Osteoporotic bone fractures are a significant public health problem resulting in substantial morbidity and for those who suffer a hip fracture, a significant one-year mortality. Bone densitometry provides an important measure of fracture risk and the newer techniques are useful in the management of individuals with osteoporosis. Estrogen administration will preserve bone mass in postmenopausal women, and the optimal intake of calcium and vitamin D is being evaluated. Newer agents such as calcitonin and bisphosphonates may provide potent therapies for preventing bone loss. This review focuses on bone densitometry as a diagnostic tool and on the use of therapeutic agents for osteoporosis. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MITLAK, BH (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114, USA. NR 44 TC 12 Z9 13 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 1993 VL 44 BP 265 EP 277 DI 10.1146/annurev.med.44.1.265 PG 13 WC Medicine, General & Internal SC General & Internal Medicine GA KW478 UT WOS:A1993KW47800024 PM 8476248 ER PT B AU MAZZULLI, T HIRSCH, MS AF MAZZULLI, T HIRSCH, MS BE Mills, J Corey, L TI COMBINATION THERAPY FOR HIV-1 INFECTION SO ANTIVIRAL CHEMOTHERAPY: NEW DIRECTIONS FOR CLINICAL APPLICATIONS AND RESEARCH, VOLUME 3 LA English DT Proceedings Paper CT 3rd Triennial Conference on Antiviral Chemotherapy CY NOV, 1991 CL SAN FRANCISCO, CA RP MAZZULLI, T (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PRENTICE HALL PI ENGLEWOOD CLIFFS PA ENGLEWOOD CLIFFS, NJ 07632 BN 0-13-050717-2 PY 1993 BP 385 EP 416 PG 32 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA BB87Z UT WOS:A1993BB87Z00035 ER PT J AU ALIMINOSA, D MCCLOSKEY, M GOODMANSCHULMAN, R SOKOL, SM AF ALIMINOSA, D MCCLOSKEY, M GOODMANSCHULMAN, R SOKOL, SM TI REMEDIATION OF ACQUIRED DYSGRAPHIA AS A TECHNIQUE FOR TESTING INTERPRETATIONS OF DEFICITS SO APHASIOLOGY LA English DT Article ID GRAPHEMIC BUFFER; AGRAPHIA AB This article describes a brain-damaged patient, J.E.S., whose pattern of impaired spelling suggested deficits affecting the graphemic output lexicon, the graphemic buffer, and the phoneme-grapheme conversion process. A remediation study was undertaken to test the assumptions of graphemic output lexicon and graphemic buffer impairment. The results supported the conclusion of an output lexicon deficit, but raised questions about the hypothesized buffer deficit. The study accordingly illustrates a way in which remediation procedures may be used to test interpretations of deficits, and the models upon which these interpretations are based. C1 BALTIMORE CITY PUBL SCH SYST,BALTIMORE,MD. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP ALIMINOSA, D (reprint author), JOHNS HOPKINS UNIV,DEPT COGNIT SCI,BALTIMORE,MD 21218, USA. NR 15 TC 40 Z9 40 U1 0 U2 1 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0268-7038 J9 APHASIOLOGY JI Aphasiology PD JAN-FEB PY 1993 VL 7 IS 1 BP 55 EP 69 DI 10.1080/02687039308249499 PG 15 WC Clinical Neurology SC Neurosciences & Neurology GA KG795 UT WOS:A1993KG79500004 ER PT B AU SPRINGER, TA AF SPRINGER, TA BE Thomas, ED TI ADHESION RECEPTORS IN INFLAMMATION - A PRECIS SO APPLICATION OF BASIC SCIENCE TO HEMATOPOIESIS AND TREATMENT OF DISEASE SE BRISTOL-MYERS SQUIBB CANCER SYMPOSIA LA English DT Proceedings Paper CT 15TH BRISTOL-MYERS SQUIBB SYMP ON CANCER RESEARCH : APPLICATION OF BASIC SCIENCE TO HEMATOPOIESIS AND TREATMENT OF DISEASE CY NOV 04-05, 1991 CL SEATTLE, WA SP BRISTOL MYERS SQUIBB RP SPRINGER, TA (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,DEPT PATHOL,200 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-999-2 J9 BRIS MYER C PY 1993 VL 15 BP 231 EP 239 PG 9 WC Hematology; Pathology; Physiology SC Hematology; Pathology; Physiology GA BY70B UT WOS:A1993BY70B00015 ER PT J AU LINDSEY, JC RYAN, LM AF LINDSEY, JC RYAN, LM TI A 3-STATE MULTIPLICATIVE MODEL FOR RODENT TUMORIGENICITY EXPERIMENTS SO APPLIED STATISTICS-JOURNAL OF THE ROYAL STATISTICAL SOCIETY SERIES C LA English DT Article DE EM ALGORITHM; PIECEWISE EXPONENTIAL; PROPORTIONAL HAZARDS; TUMORIGENICITY EXPERIMENTS; TUMOR LETHALITY ID SURVIVAL-SACRIFICE EXPERIMENTS; ANIMAL CARCINOGENESIS EXPERIMENTS; ILLNESS-DEATH MODEL; NONPARAMETRIC-ESTIMATION; PREVALENCE DATA; EM ALGORITHM; ONSET; TESTS; RATES AB A three-state illness-death model provides a useful way to represent data from rodent tumorigenicity experiments. Some of the earliest proposals use fully parametric models based on, for example, Weibull distributional assumptions. Recently, nonparametric versions of this model have been proposed, but these generally require large data sets with frequent interim sacrifices to yield stable estimates. As a compromise between these extremes, others have considered semiparametric models. In this paper, we develop a model that assumes a multiplicative relationship between death rates with and without tumour and a piecewise exponential model for the base-line transition rates. The model can be fitted with information from a single sacrifice. An EM algorithm provides a useful way to fit the model, since the likelihood corresponds to that from a standard piecewise exponential survival model when time to tumour onset is known. We discuss the relationship between the piecewise exponential model and other recent proposals and illustrate the method with data from two carcinogenicity studies. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 NR 40 TC 30 Z9 32 U1 0 U2 1 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0035-9254 J9 APPL STAT-J ROY ST C JI Appl. Stat.-J. R. Stat. Soc. PY 1993 VL 42 IS 2 BP 283 EP 300 DI 10.2307/2986233 PG 18 WC Statistics & Probability SC Mathematics GA KT568 UT WOS:A1993KT56800002 ER PT J AU MUGA, A ARRONDO, JLR BELLON, T SANCHO, J BERNABEU, C AF MUGA, A ARRONDO, JLR BELLON, T SANCHO, J BERNABEU, C TI STRUCTURAL AND FUNCTIONAL-STUDIES ON THE INTERACTION OF SODIUM DODECYL-SULFATE WITH BETA-GALACTOSIDASE SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID TRANSFORM INFRARED-SPECTROSCOPY; SARCOPLASMIC-RETICULUM; PROTEIN COMPLEXES; SECONDARY STRUCTURE; ESCHERICHIA-COLI; MODEL MEMBRANES; APOCYTOCHROME-C; SPECTRA; CHROMATOGRAPHY; SIZE C1 UNIV BASQUE COUNTRY,FAC SCI,DEPT BIOCHEM,POB 644,E-48080 BILBAO,SPAIN. CSIC,CTR INVEST BIOL,E-28006 MADRID,SPAIN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RI Bernabeu, Carmelo/L-3226-2014; Muga, Arturo/N-1174-2014 OI Bernabeu, Carmelo/0000-0002-1563-6162; Muga, Arturo/0000-0003-0345-6882 NR 40 TC 79 Z9 79 U1 0 U2 9 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN PY 1993 VL 300 IS 1 BP 451 EP 457 DI 10.1006/abbi.1993.1061 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KG984 UT WOS:A1993KG98400061 PM 8424679 ER PT J AU FAEDDA, GL TONDO, L TEICHER, MH BALDESSARINI, RJ GELBARD, HA FLORIS, GF AF FAEDDA, GL TONDO, L TEICHER, MH BALDESSARINI, RJ GELBARD, HA FLORIS, GF TI SEASONAL MOOD DISORDERS - PATTERNS OF SEASONAL RECURRENCE IN MANIA AND DEPRESSION SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID AFFECTIVE-ILLNESS; HOSPITAL ADMISSION; SUICIDE; THERAPY AB DSM-III-R criteria, applied retrospectively in a research-oriented psychiatric clinic, identified patients (N=146) with a mood disorder and a seasonal pattern of recurrence (seasonal mood disorder). The seasonal mood disorder syndrome was not rare (10% of all mood disorders); diagnostic distribution was as follows: recurrent depression, 51%, and bipolar disorder, 49%, with 30% of the latter having mania (bipolar disorder type I) and 19% having hypomania (bipolar disorder type II). Most patients were women (71%); onset age averaged 29 years, with a mean of eight cycles in 12 years of illness; mean episode duration was 5.0 months. Mood disorder was found in a high proportion (68%) of the families. All but one patient followed one of two seasonal patterns in equal frequency: type A, fall-winter depression with or without spring-summer mania or hypomania; and type B, spring-summer depression with or without fall-winter mania or hypomania. Both types showed consistent times of onset and remission. These results emphasize that DSM-III-R seasonal mood disorder includes severe cases of recurrent depression and bipolar disorder and support a distinction between two seasonal subtypes. C1 HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,PSYCHOT DISORDERS PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MCLEAN HOSP,MAILMAN RES CTR,DEV BIOPSYCHIAT PROGRAM,BELMONT,MA 02178. MCLEAN HOSP,MAILMAN RES CTR,BIPOLAR DISORDERS RES PROGRAM,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CTR LUCID BINI,CAGLIARI,ITALY. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT PSYCHIAT,BRONX,NY 10461. RP FAEDDA, GL (reprint author), HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,PSYCHIAT RES LAB,BOSTON,MA 02115, USA. RI Lawson, David/A-7422-2012; OI Faedda, Gianni/0000-0001-6197-0543 FU NIMH NIH HHS [MH-31154, MH-36224, MH-47370] NR 51 TC 117 Z9 118 U1 0 U2 4 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 1993 VL 50 IS 1 BP 17 EP 23 PG 7 WC Psychiatry SC Psychiatry GA KG777 UT WOS:A1993KG77700003 PM 8422217 ER PT J AU GRAYBILL, JR AF GRAYBILL, JR BE Bribiesca, LB TI TREATMENT OF SYSTEMIC MYCOSES IN PATIENTS WITH AIDS SO ARCHIVES OF MEDICAL RESEARCH, VOL 24 NO 4 LA English DT Proceedings Paper CT International Iberoamerican Symposium: Advances in Host-Parasite Interactions in Fungal Research CY OCT 06-09, 1992 CL MEXICO CITY, MEXICO SP UNIVESIDAD NACL AUTONOMA MEXICO, FAC MED, DEPT MICROBIOL & PARASITOL, SOCIEDAD MEXICANA MICOLOGIA, JANSSEN RES FDN, CONSEJO NACL CIEN & TECNOLOGIA, ORG ESTADOS AMERICANOS, ORG PANAMERICANA SALUD, UNIVESIDAD NACL AUTONOMA MEXICO, DIRECC GEN INTERCAMBIO ACADEMICO DE SYSTEMIC MYCOSES; AIDS; TREATMENTS C1 AUDIE L MURPHY MEM VET ADM MED CTR,INFECT DIS SECT,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INST MEXICANO SEGURO SOCIAL PI MEXICO CITY PA PO BOX 73-032, MEXICO CITY CP 06720, MEXICO PY 1993 BP 403 EP 412 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA BZ84T UT WOS:A1993BZ84T00006 ER PT J AU FUNKENSTEIN, HH ALBERT, MS COOK, NR WEST, CG SCHERR, PA CHOWN, MJ PILGRIM, D EVANS, DA AF FUNKENSTEIN, HH ALBERT, MS COOK, NR WEST, CG SCHERR, PA CHOWN, MJ PILGRIM, D EVANS, DA TI EXTRAPYRAMIDAL SIGNS AND OTHER NEUROLOGIC FINDINGS IN CLINICALLY DIAGNOSED ALZHEIMERS-DISEASE - A COMMUNITY-BASED STUDY SO ARCHIVES OF NEUROLOGY LA English DT Article ID PARKINSONS-DISEASE; DEMENTIA; POPULATION; PREVALENCE AB The association between findings on the neurologic examination and the clinical diagnosis of Alzheimer's disease was investigated among 467 individuals from a geographically defined community population. Participants were selected by stratified random sampling based on their memory performance in a population survey of community residents 65 years of age and older. Each participant underwent a structured medical, psychiatric, neurologic, and neuropsychologic examination. Of the 467 persons examined there were 134 cases of probable Alzheimer's disease and 167 control subjects. Multiple logistic regression analysis was used to estimate the degree to which the presence of each of several neurologic examination findings affected the age- and sex-adjusted relative odds of having clinically diagnosed Alzheimer's disease. The most striking associations with the diagnosis of Alzheimer's disease were seen with various measures of extrapyramidal dysfunction. These increased relative odds were not markedly affected by excluding from the analysis cases with severe cognitive impairment. The results suggest that involvement of the extrapyramidal system is a common finding in Alzheimer's disease. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,CNY-9,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,CHANNING LAB,BOSTON,MA 02115. FU NIA NIH HHS [AG06789, N01-AG12106, R01-AG05362] NR 34 TC 55 Z9 55 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD JAN PY 1993 VL 50 IS 1 BP 51 EP 56 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA KG092 UT WOS:A1993KG09200011 PM 8418800 ER PT J AU KHETARPAL, U AF KHETARPAL, U TI AUTOSOMAL DOMINANT SENSORINEURAL HEARING-LOSS - FURTHER TEMPORAL BONE FINDINGS SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Note C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL & MAXILLOFACIAL SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KHETARPAL, U (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC 00079] NR 2 TC 37 Z9 40 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 1993 VL 119 IS 1 BP 106 EP 108 PG 3 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA KF914 UT WOS:A1993KF91400015 PM 8417734 ER PT J AU KUNKEL, CF SCREMIN, AME EISENBERG, B GARCIA, JF ROBERTS, S MARTINEZ, S AF KUNKEL, CF SCREMIN, AME EISENBERG, B GARCIA, JF ROBERTS, S MARTINEZ, S TI EFFECT OF STANDING ON SPASTICITY, CONTRACTURE, AND OSTEOPOROSIS IN PARALYZED MALES SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article DE CONTRACTURE; DUAL PHOTON ABSORPTIOMETRY; H-REFLEX; OSTEOPOROSIS; PARALYSIS; SPASTICITY ID BONE-MINERAL DENSITY; SPINAL-CORD INJURY; STIMULATION C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV NEW MEXICO,SCH MED,DEPT REHABIL,ALBUQUERQUE,NM 87131. UNIV NEW MEXICO,SCH MED,DEPT ORTHOPED,ALBUQUERQUE,NM 87131. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,REHABIL MED SERV,LOS ANGELES,CA 90024. RP KUNKEL, CF (reprint author), VET AFFAIRS MED CTR,REHABIL MED SERV 117,2100 RIDGECREST DR SE,ALBUQUERQUE,NM 87108, USA. NR 21 TC 90 Z9 100 U1 0 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD JAN PY 1993 VL 74 IS 1 BP 73 EP 78 PG 6 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA KF917 UT WOS:A1993KF91700015 PM 8420525 ER PT J AU LANGNER, KD NIEDRIG, M FULTZ, P ANDERSON, D REINER, G REPKE, H GELDERBLOM, H SEED, B HILFENHAUS, J ZETTLMEISSL, G AF LANGNER, KD NIEDRIG, M FULTZ, P ANDERSON, D REINER, G REPKE, H GELDERBLOM, H SEED, B HILFENHAUS, J ZETTLMEISSL, G TI ANTIVIRAL EFFECTS OF DIFFERENT CD4-IMMUNOGLOBULIN CONSTRUCTS AGAINST HIV-1 AND SIV - IMMUNOLOGICAL CHARACTERIZATION, PHARMACOKINETIC DATA AND INVIVO EXPERIMENTS SO ARCHIVES OF VIROLOGY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; RECOMBINANT SOLUBLE CD4; ENVELOPE GLYCOPROTEIN; SYNCYTIUM FORMATION; INFECTED-CELLS; HIGH-AFFINITY; T4 ANTIGEN; BINDING; RECEPTOR; AIDS AB The CD4 cell surface antigen belongs to the immunoglobulin superfamily and is the primary receptor for the human immunodeficiency virus 1 (HIV-1). The high affinity interaction between HIV-1 and CD4 is mediated by the viral envelope glycoprotein gp120. Recombinant soluble CD4 (rsCD4) has been shown in vitro to be an effective inhibitor of HIV-1 and HIV-2 propagation in lymphoid cells. A variety of antibody-like molecules were constructed, consisting of different parts of the extracellular domain of CD4 fused to immunoglobulin constant regions. The fusion proteins were expressed in mammalian cell lines and purified via affinity chromatography. The specificity and anti-viral effects of the different CD4-immunoglobulin constructs against HIV were analysed by different immunological tests, i.e., immunofluorescence, neutralisation and in vitro assays. In pharmacokinetic studies, differences were found in serum half-life between the four- and two-domain CD4 constructs in cynomolgus monkeys and between glycosylated and deglycosylated CD4-Fc constructs in rabbits. In two in vivo experiments using the four-domain CD4-Fc in SIV-infected macaques, no beneficial effects were observed. C1 BEHRINGWERKE AG,FORSCHUNGSLAB,W-3550 MARBURG,GERMANY. EMORY UNIV,YERKES REG PRIMATE RES CTR,ATLANTA,GA 30322. HUMBOLDT UNIV BERLIN,BEREICH MED CHARITE,INST PHARMACOL & TOXICOL,O-1040 BERLIN,GERMANY. ROBERT KOCH INST,W-1000 BERLIN 65,GERMANY. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. FU NCRR NIH HHS [RR-00165] NR 49 TC 8 Z9 8 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1993 VL 130 IS 1-2 BP 157 EP 170 DI 10.1007/BF01319004 PG 14 WC Virology SC Virology GA LC650 UT WOS:A1993LC65000013 PM 8503781 ER PT J AU WU, XC NG, SC NEAR, RI WONG, SL AF WU, XC NG, SC NEAR, RI WONG, SL TI EFFICIENT PRODUCTION OF A FUNCTIONAL SINGLE-CHAIN ANTIDIGOXIN ANTIBODY VIA AN ENGINEERED BACILLUS-SUBTILIS EXPRESSION-SECRETION SYSTEM SO BIO-TECHNOLOGY LA English DT Article ID ANTIGEN-BINDING PROTEIN; ESCHERICHIA-COLI; DIGITALIS INTOXICATION; MONOCLONAL-ANTIBODIES; FAB FRAGMENTS; FV; GENES; SEQUENCE; RECOMBINANT; POLYMERASE AB We have applied a Bacillus subtilis expression-secretion system to produce a functional antidigoxin SCA (single-chain antibody consisting of V(L)-linker-V(H)) and the individual variable domains of light (V(L)) and heavy (V(H)) chains. The secreted antidigoxin SCA can be affinity purified in one step by applying the culture supernatant directly to a ouabain-Sepharose column. N-terminal sequence determination indicated that the protein has the expected N-terminus with the signal peptide properly processed. Affinity and ligand specificity studies demonstrated that the engineered antidigoxin SCA has almost identical properties as those of the parental monoclonal antibody. The use of B. subtilis WB600, an engineered, six-extracellular protease-deficient strain, is vital for the production of antidigoxin SCA in high quality and quantity (5 mg/liter in a shake flask culture). All the secreted SCAs are biologically active. The ability to produce secreted SCAs by the B. subtilis expression system provides a simple and efficient means to analyze the binding properties of engineered antibodies generated through rational design or site-directed mutagenesis. C1 UNIV CALGARY, DEPT BIOL SCI, DIV BIOCHEM, CALGARY T2N 1N4, ALBERTA, CANADA. BRISTOL MYERS SQUIBB PHARMACEUT RES INST, DEPT MOLEC BIOL MACROMOLEC, PRINCETON, NJ 08543 USA. MASSACHUSETTS GEN HOSP, CELLULAR & MOLEC BIOL RES LAB, BOSTON, MA 02114 USA. NR 53 TC 57 Z9 60 U1 0 U2 4 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0733-222X J9 BIO-TECHNOL JI Bio-Technology PD JAN PY 1993 VL 11 IS 1 BP 71 EP 76 DI 10.1038/nbt0193-71 PG 6 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA LM371 UT WOS:A1993LM37100025 PM 7763487 ER PT J AU LU, Y RAPTIS, L ANDERSON, S CORBLEY, MJ ZHOU, YC PROSS, H HALIOTIS, T AF LU, Y RAPTIS, L ANDERSON, S CORBLEY, MJ ZHOU, YC PROSS, H HALIOTIS, T TI RAS MODULATES COMMITMENT AND MATURATION OF 10T1/2 FIBROBLASTS TO ADIPOCYTES (VOL 70, PG 1249, 1992) SO BIOCHEMISTRY AND CELL BIOLOGY-BIOCHIMIE ET BIOLOGIE CELLULAIRE LA English DT Correction, Addition C1 QUEENS UNIV,DEPT MICROBIOL & IMMUNOL,KINGSTON K7L 3N6,ONTARIO,CANADA. BIOTECHNOL RES INST,DEPT MOLEC IMMUNOL,MONTREAL H4P 2R2,PQ,CANADA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP LU, Y (reprint author), QUEENS UNIV,DEPT PATHOL,CANC RES LABS,KINGSTON K7L 3N6,ONTARIO,CANADA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU NATL RESEARCH COUNCIL CANADA PI OTTAWA PA RESEARCH JOURNALS, MONTREAL RD, OTTAWA ON K1A 0R6, CANADA SN 0829-8211 J9 BIOCHEM CELL BIOL JI Biochem. Cell Biol. PD JAN-FEB PY 1993 VL 71 IS 1-2 BP 102 EP 102 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA LR139 UT WOS:A1993LR13900017 ER PT B AU WANG, JT GOLDRING, SR AF WANG, JT GOLDRING, SR BE Morrey, BF TI THE ROLE OF PARTICULATE ORTHOPEDIC IMPLANT MATERIALS IN PERI-IMPLANT OSTEOLYSIS - MECHANISMS OF GRANULOMA-FORMATION AND PARTICLE-INDUCED OSTEOLYSIS SO BIOLOGICAL, MATERIAL, AND MECHANICAL CONSIDERATIONS OF JOINT REPLACEMENT SE BRISTOL-MYERS SQUIBB / ZIMMER ORTHOPAEDIC SYMPOSIUM SERIES LA English DT Proceedings Paper CT 7TH ANNUAL BRISTOL-MYERS SQUIBB / ZIMMER ORTHOPAEDIC RESEARCH SYMP : BIOLOGICAL, MATERIAL, AND MECHANICAL CONSIDERATIONS OF JOINT REPLACEMENT CY OCT 29-31, 1992 CL SAN ANTONIO, TX SP BRISTOL MYERS, SQUIBB, ZIMMER RP WANG, JT (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,MED SERV,ARTHRIT UNIT,BOSTON,MA 02114, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0008-6 J9 BRIS MYER Z PY 1993 BP 119 EP 126 PG 8 WC Engineering, Biomedical; Materials Science, Multidisciplinary; Orthopedics SC Engineering; Materials Science; Orthopedics GA BY98W UT WOS:A1993BY98W00011 ER PT J AU BIERER, BE AF BIERER, BE TI EFFECTS OF RAPAMYCIN ON P70 S6-PROTEIN KINASE SO BIOMEDICINE & PHARMACOTHERAPY LA English DT Note RP BIERER, BE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0753-3322 J9 BIOMED PHARMACOTHER JI Biomed. Pharmacother. PY 1993 VL 47 IS 4 BP 175 EP 175 DI 10.1016/0753-3322(93)90016-E PG 1 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LN132 UT WOS:A1993LN13200016 ER PT J AU KISTER, A MAGARSHAK, Y MALINSKY, J AF KISTER, A MAGARSHAK, Y MALINSKY, J TI THE THEORETICAL-ANALYSIS OF THE PROCESS OF RNA MOLECULE SELF-ASSEMBLY SO BIOSYSTEMS LA English DT Article ID SINGLE-STRANDED RNA; SECONDARY STRUCTURE; SEQUENCES; ALGORITHM; PREDICTION; PRINCIPLE AB The Kinetic approach to the problem of the RNA structure prediction based on the analysis of the molecule self-formation is proposed. Re-structurization that occurs during processing is described in terms of Markov processes. A new formalism designating nucleotides by complex numbers is proposed, leading to the complex unitary space of nucleic vectors. Properties of structure and transition matrices are discussed in relation to the analysis of RNA structural formation processes. The non-linear dynamic behavior of secondary structure transitions is analyzed. Soliton-like oscillations of RNA and DNA tertiary structures are predicted. The Monte-Carlo simulation of the RNA structure self-formation is used to calculate the ensemble of the secondary structures of the tRNA(Ala) precursor from Bombix mori formed during processing. C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RP KISTER, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 33 TC 8 Z9 8 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0303-2647 J9 BIOSYSTEMS JI Biosystems PY 1993 VL 30 IS 1-3 BP 31 EP 48 DI 10.1016/0303-2647(93)90060-P PG 18 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA LN564 UT WOS:A1993LN56400004 PM 7690610 ER PT J AU KISTER, A MUCHNIK, I BOUZIDA, D REINHERZ, EL SMITH, T AF KISTER, A MUCHNIK, I BOUZIDA, D REINHERZ, EL SMITH, T TI EFFICIENT PATTERN COMPARATIVE METHOD FOR SELECTING FUNCTIONALLY IMPORTANT MOTIFS IN PROTEIN SEQUENCES - APPLICATION TO ZINC ENZYMES SO BIOSYSTEMS LA English DT Article ID THERMOLYSIN; ENDOPEPTIDASE-24.11; IDENTIFICATION; RESOLUTION; SITE AB We have developed a pattern comparative method for identifying functionally important motifs in protein sequences. The essence of most standard pattern comparative methods is a comparison of patterns occurring in different sequences using an optimized weight matrix. In contrast, our approach is based on a measure of similarity among all the candidate motifs within the same sequence. This method may prove to be particularly efficient for proteins encoding the same biochemical function, but with different primary sequences, and when tertiary structure information from one or more sequences is available. We have applied this method to a special class of zinc-binding enzymes known as endopeptidases, C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. BOSTON UNIV,BIOMOLEC ENGN RES CTR,BOSTON,MA 02215. RI sebastianovitsch, stepan/G-8507-2013 FU NCI NIH HHS [CA 49232]; NLM NIH HHS [LM05205] NR 12 TC 1 Z9 1 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0303-2647 J9 BIOSYSTEMS JI Biosystems PY 1993 VL 30 IS 1-3 BP 233 EP 240 DI 10.1016/0303-2647(93)90073-L PG 8 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA LN564 UT WOS:A1993LN56400017 PM 8374078 ER PT J AU POWELSON, JA COSIMI, AB WEE, SL AF POWELSON, JA COSIMI, AB WEE, SL TI MONOCLONAL-ANTIBODIES IN ORGAN-TRANSPLANTATION SO BIOTECHNOLOGY ADVANCES LA English DT Review DE MONOCLONAL ANTIBODY; TRANSPLANTATION; IMMUNOSUPPRESSION; REJECTION; TOLERANCE; OKT3; CD3; CD4; INTERLEUKIN-2; ICAM-1 ID RENAL-ALLOGRAFT RECIPIENTS; KIDNEY-TRANSPLANTATION; CARDIAC ALLOGRAFT; ACUTE REJECTION; THERAPY; OKT3; INDUCTION; ICAM-1; ADHESION; INVIVO AB Monoclonal antibody (mAb) technology has made possible the production of designer proteins, specifically reactive with almost any conceivable biological molecule. Using these reagents, the surface molecules on cells crucial for allograft rejection have been identified and described in detail. These structures can now be selectively targeted by mAb-based therapy in order to prevent rejection. For instance, the CD3 molecule, expressed on all mature T lymphocytes, triggers T cell activation, a key event in rejection. OKT3, an anti-CD3 mAb, disrupts T cell function and is now the agent of choice for the treatment of severe rejection episodes. MAbs targeting other T cell molecules are currently being investigated. Some of the most promising, the anti-CD4, anti-ICAM-1, and anti-interleukin 2 receptor mAbs, have already induced donor-specific tolerance in rodent models. These hosts accept permanently a genetically incompatible graft after only a limited period of mAb therapy. Interestingly, anti-ICAM-1 also diminishes the ischemic injury of preservation. The development of these new molecular agents, effectively directed to specific cellular targets, will likely play an increasingly important role in future clinical protocols, and perhaps finally provide a means to achieve long-term tolerance in human allograft recipients. RP POWELSON, JA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 56 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 0734-9750 J9 BIOTECHNOL ADV JI Biotechnol. Adv. PY 1993 VL 11 IS 4 BP 725 EP 740 DI 10.1016/0734-9750(93)90001-4 PG 16 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA MA498 UT WOS:A1993MA49800001 PM 14538055 ER PT J AU WUCHERPFENNIG, AL DEWHIRST, FE STASHENKO, P AF WUCHERPFENNIG, AL DEWHIRST, FE STASHENKO, P TI PLATELET-ACTIVATING-FACTOR INCREASES INTRACELLULAR CALCIUM IN ISOLATED OSTEOCLASTS BUT DOES NOT MODIFY BONE-RESORPTION SO BONE LA English DT Article DE OSTEOCLASTS; PLATELET-ACTIVATING FACTOR; INTRACELLULAR CALCIUM; BONE RESORPTION ID ISOLATED RAT OSTEOCLASTS; EXTRACELLULAR CALCIUM; OSTEOBLASTIC CELLS; CYTOSOLIC CALCIUM; CALCITONIN; ELEVATION; FURA-2; PH AB Platelet activating factor (PAF) is an inflammatory mediator secreted by activated macrophages and granulocytes. Since PAF has been previously demonstrated to increase intracellular calcium in isolated osteoclasts, the effect of PAF on bone resorption was examined. This was compared to effects seen after addition of calcium ionophores and calcitonin, an inhibitor of bone resorption, in order to determine if an increase in [Ca++]i inhibits osteoclast-mediated resorption. The results demonstrate that PAF has no effect on either unstimulated or PTH-induced bone resorption. Calcium ionophores, ionomycin, and A23187, at concentrations that increased [Ca++]i, failed to modulate resorption in the fetal long bone assay. In addition, salmon calcitonin did not change [Ca++]i in spite of its strong inhibition of bone resorption. Taken together, these results demonstrate that the second messenger pathways involved in osteoclast downregulation can be independent of [Ca++]i, and may involve other messenger systems. RP WUCHERPFENNIG, AL (reprint author), FORSYTH RES INST,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE 05590-02, DE 07378] NR 34 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 8756-3282 J9 BONE JI Bone PD JAN-FEB PY 1993 VL 14 IS 1 BP 13 EP 18 DI 10.1016/8756-3282(93)90250-E PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KJ836 UT WOS:A1993KJ83600003 PM 8442997 ER PT J AU SOIFFER, RJ RITZ, J AF SOIFFER, RJ RITZ, J TI SELECTIVE T-CELL DEPLETION OF DONOR ALLOGENEIC MARROW WITH ANTI-CD6 MONOCLONAL-ANTIBODY - RATIONALE AND RESULTS SO BONE MARROW TRANSPLANTATION LA English DT Article; Proceedings Paper CT Symposium on Immunology of Bone Marrow Transplantation: Current Controversies CY JUN 03-05, 1993 CL KIEL, GERMANY SP AMGEN, ROCHE, BAXTER, ASTA MEDICA, TROPON, FARMITALIA, SANDOZ, VESTAR, WELLCOME, LEDERLE, GLAXO, KNOLL, GRUNENTHAL, LILLY ID VERSUS-HOST DISEASE; BONE-MARROW; GRAFT; TRANSPLANTATION; PREVENTION; LEUKEMIA; COMPLEMENT; PHASE; TRIAL AB Acute and chronic graft-versus-host disease (GVHD) are responsible for a significant fraction of the morbidity and mortality of allogeneic bone marrow transplantation. Attempts to reduce the incidence of GVHD by exhaustive T cell depletion of donor marrow have frequently been associated with an increase in graft failure and disease relapse. For the past 10 years, we have evaluated the use of a monoclonal antibody (T12) that selectively targets the CD6 determinant on mature T cells. 171 patients with hematologic malignancies have received donor marrow depleted of mature T cells with anti-CD6 and rabbit complement. Initial engraftment in recipients of HLA-matched marrow has been >98% with 96% of patients showing stable hematologic reconstitution. The incidence of acute GVHD in this population was only 15%. Chronic GVHD has developed in 5% of patients. Overall, transplant-related mortality was 17%. Examination of peripheral blood lymphocyte reconstitution in the early post-BMT period has been helpful in predicting which patients will ultimately go on to develop GVHD. Treatment of recipients of CD6 depleted marrow with low doses of interleukin-2 post-BMT can expand the number of circulating NK cells and may be associated with a decrease in disease relapse rate RP SOIFFER, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU PHS HHS [A129530] NR 15 TC 13 Z9 13 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 1993 VL 12 SU 3 BP S7 EP S10 PG 4 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA MQ071 UT WOS:A1993MQ07100002 PM 8124262 ER PT J AU VONDEIMLING, A VONAMMON, K SCHOENFELD, D WIESTLER, OD SEIZINGER, BR LOUIS, DN AF VONDEIMLING, A VONAMMON, K SCHOENFELD, D WIESTLER, OD SEIZINGER, BR LOUIS, DN TI SUBSETS OF GLIOBLASTOMA-MULTIFORME DEFINED BY MOLECULAR GENETIC-ANALYSIS SO BRAIN PATHOLOGY LA English DT Article ID HUMAN-MALIGNANT ASTROCYTOMA; HUMAN GLIOMAS; HETEROZYGOSITY; AMPLIFICATION; EXPRESSION; CHROMOSOME-17; TUMORIGENESIS; SURVIVAL AB Glioblastoma multiforme is a clinically and histologically heterogeneous lesion; however, to date, it has not been possible to subdivide glioblastomas on a clinical, histopathological or biological basis. Previous studies have demonstrated that loss of portions of chromosomes 10 and 17 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequent genetic alterations in glioblastoma. We therefore examined 74 glioblastomas from 67 patients for loss of heterozygosity on chromosomes 10 and 17, and for amplification of the epidermal growth factor receptor gene, to determine whether glioblastomas can be subtyped on a genetic basis. Using Southern blot analysis we were able to detect different patterns of genomic alterations. Eighteen of 67 informative patients were characterized by a loss of heterozygosity on the short arm of chromosome 17 in the tumor tissue. Forty-five of 64 informative patients showed a loss of heterozygosity on chromosome 10. Amplification of the epidermal growth factor receptor gene was noted in 25 of 67 patients and was restricted to those glioblastomas that had lost portions of chromosome 10. Epidermal growth factor receptor gene amplification occurred significantly more often in patients without chromosome 17p loss than in patients with chromosome 17p loss (p = 0.01). In addition, those glioblastomas with a loss of chromosome 17p occurred in patients significantly younger than those with glioblastomas characterized by EGFR gene amplification (p = 0.001). These data emphasize the genetic heterogeneity of glioblastoma and suggest the division of glioblastoma into genetic subsets. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02129. UNIV BONN,MED CTR,INST NEUROPATHOL,W-5300 BONN,GERMANY. UNIV ZURICH,DEPT NEUROSURG,CH-8091 ZURICH,SWITZERLAND. MASSACHUSETTS GEN HOSP,CTR BIOSTAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02129. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,ONCOL DRUG DISCOVERY,PRINCETON,NJ 08543. RI von Deimling, Andreas/F-7774-2013 OI von Deimling, Andreas/0000-0002-5863-540X FU NCI NIH HHS [CA 09144] NR 36 TC 310 Z9 313 U1 1 U2 6 PU INT SOC NEUROPATHOLOGY PI ZURICH PA ISN JOURNAL PO BOX, CH-8033 ZURICH, SWITZERLAND SN 1015-6305 J9 BRAIN PATHOL JI Brain Pathol. PD JAN PY 1993 VL 3 IS 1 BP 19 EP 26 PG 8 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA KK704 UT WOS:A1993KK70400003 PM 8269081 ER PT S AU TAYLORPAPADIMITRIOU, J DSOUZA, B BURCHELL, J KYPRIANOU, N BERDICHEVSKY, F AF TAYLORPAPADIMITRIOU, J DSOUZA, B BURCHELL, J KYPRIANOU, N BERDICHEVSKY, F BE Squartini, F Bevilacqua, G Conte, PF Surbone, A TI THE ROLE OF TUMOR-ASSOCIATED ANTIGENS IN THE BIOLOGY AND IMMUNOTHERAPY OF BREAST-CANCER SO BREAST CANCER: FROM BIOLOGY TO THERAPY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Pisa Symposia in Oncology, to Celebrate the 650th Anniversary of the Founding of the University of Pisa CY OCT 19-21, 1992 CL PISA, ITALY SP UNIV PISA, NATL INST CANC RES, SANTA CHIARA HOSP, ASSOC ITALIANA ONCOL MEDICA ID POLYMORPHIC EPITHELIAL MUCIN; MOLECULAR-CLONING; GROWTH-FACTOR; CELL-LINES; MYOEPITHELIAL CELLS; NEU ONCOGENE; CORE PROTEIN; EXPRESSION; CARCINOMAS; RECEPTOR C1 UNIV MARYLAND HOSP,DEPT SURG,DIV UROL,BALTIMORE,MD 21205. DANA FARBER CANC INST,BOSTON,MA 02115. RP TAYLORPAPADIMITRIOU, J (reprint author), IMPERIAL CANC RES FUND,44 LINCOLNS INN FIELDS,LONDON WC2A 3PX,ENGLAND. RI Burchell, Joy/G-4560-2012 NR 54 TC 10 Z9 10 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-803-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 698 BP 31 EP 47 DI 10.1111/j.1749-6632.1993.tb17189.x PG 17 WC Oncology; Medicine, Research & Experimental; Multidisciplinary Sciences; Pathology; Pharmacology & Pharmacy SC Oncology; Research & Experimental Medicine; Science & Technology - Other Topics; Pathology; Pharmacology & Pharmacy GA BZ51X UT WOS:A1993BZ51X00003 PM 8279769 ER PT J AU GILCHRIST, KW GRAY, R VANDRIELKULKER, AMJ MESKER, WE PLOEMZAAIJER, JJ PLOEM, JS TAYLOR, SG TORMEY, DC AF GILCHRIST, KW GRAY, R VANDRIELKULKER, AMJ MESKER, WE PLOEMZAAIJER, JJ PLOEM, JS TAYLOR, SG TORMEY, DC TI HIGH DNA CONTENT AND PROGNOSIS IN LYMPH-NODE POSITIVE BREAST-CANCER - A CASE-CONTROL STUDY BY THE UNIVERSITY OF LEIDEN AND ECOG SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE BREAST CANCER; DNA ANEUPLOIDY; LEYTAS; IMAGE CYTOMETRY; PROGNOSIS ID ONCOLOGY-GROUP TRIAL; IMAGE CYTOMETRY; FLOW-CYTOMETRY; SOLID TUMORS; CARCINOMA; PLOIDY; CMFP AB To investigate whether breast cancer cells with unusually high nuclear DNA content are associated with an adverse outcome, Eastern Cooperative Oncology Group investigators selected breast cancer trial patients who suffered an early death (ED) within two years after diagnosis to compare with other trial patients who had a survival of at least 7.5 years. Paraffin blocks of primary breast cancers were obtained from 93 evaluable patients who had been enrolled in two surgical adjuvant trials for lymph node positive (LN +) disease (T1-3N1M0). Single cell monolayer preparations from these blocks were stained with acriflavine-Feulgen and analyzed by image analysis for DNA content with the automated Leiden Television Analysis System (LEYTAS). Standard prognostic variables (estrogen receptor(ER) status, number of lymph nodes with metastases, and size of the cancer) were compared with three DNA content characteristics: DNA ploidy status, number of nuclei with > 5 C DNA content, and percent of nuclei with > 5 C. Estimates of the odds ratio in multivariate comparisons showed that ER negativity was associated with ED (p = 0.0005) and an odds ratio estimate using negative/positive of 4.87. The number of positive lymph,nodes associated with ED had a p-value of 0.0005 and an odds ratio estimate of 4.63 when comparing the > 3 nodes group to the 1-3 nodes group. In contrast, the strongest association for any of the DNA content characteristics with ED had a p-value of 0.017 and an odds ratio estimate of 2.76. This power of association disappeared when stratified on ER status. Therefore, the presence of breast cancer cells with highly aneuploid (i.e. > 5 C) DNA content does not possess independent prognostic information in LN + breast cancer. An association remains to be tested in lymph node negative breast cancer. C1 DANA FABER CANC INST,BOSTON,MA. LEIDEN UNIV,DEPT CYTOCHEM & CYTOMETRY,SYLVIUS LAB,LEIDEN,NETHERLANDS. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. RP GILCHRIST, KW (reprint author), UNIV WISCONSIN,WISCONSIN COMPREHENSIVE CANC CTR,CLIN SCI CTR K4550,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NCI NIH HHS [CA 21115] NR 21 TC 8 Z9 8 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 1993 VL 28 IS 1 BP 1 EP 8 DI 10.1007/BF00666350 PG 8 WC Oncology SC Oncology GA MM820 UT WOS:A1993MM82000001 PM 8123866 ER PT J AU LAURIE, A WEISS, M NATHAN, DG SIEFF, CA AF LAURIE, A WEISS, M NATHAN, DG SIEFF, CA TI HUMAN IL-3 RECEPTOR FUNCTION IN TRANSFECTED BA/F3 CELLS REQUIRES THE BETA-SUBUNIT PROXIMAL CYTOPLASMIC DOMAIN BUT NOT THE CYTOPLASMIC DOMAIN OF THE ALPHA-SUBUNIT SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PY 1993 VL 84 SU 1 BP 21 EP 21 PG 1 WC Hematology SC Hematology GA LC683 UT WOS:A1993LC68300081 ER PT J AU CHYLACK, LT PADHYE, N KHU, PM WEHNER, C WOLFE, J MCCARTHY, D ROSNER, B FRIEND, J AF CHYLACK, LT PADHYE, N KHU, PM WEHNER, C WOLFE, J MCCARTHY, D ROSNER, B FRIEND, J TI LOSS OF CONTRAST SENSITIVITY IN DIABETIC-PATIENTS WITH LOCS-II CLASSIFIED CATARACTS SO BRITISH JOURNAL OF OPHTHALMOLOGY LA English DT Article ID GRADING SYSTEM; GLARE; VISION; CHART AB Contrast sensitivity function (CSF) was assessed in a population of diabetics with moderate cataracts to determine if CSF testing provides more information about visual dysfunction than Snellen or Lotmar interferometric visual acuity. With the Lens Opacities Classification Systems Version II (LOCS II) of cataract classification it was possible to grade accurately the type and severity of cataract and nuclear brunescence. The presence of statistically significant relationships between increasing LOCS II classification (worsening cataract) and diminished function, even when the regression model was controlled for Snellen visual acuity, supports the thesis that CSF measurements do provide more information about cataract related visual loss than Snellen acuity alone. Statistically significant (p less-than-or-equal-to 0.05) relationships existed between different morphological types of cataract, nuclear colour, and CSF at specific frequencies. The frequencies affected differed with cataract type or nuclear colour, and with distance and near CSF. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. CHANNING LABS,BOSTON,MA. RP CHYLACK, LT (reprint author), BRIGHAM & WOMENS HOSP,CTR CLIN CATARACT RES,221 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 20 TC 22 Z9 22 U1 0 U2 1 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-1161 J9 BRIT J OPHTHALMOL JI Br. J. Ophthalmol. PD JAN PY 1993 VL 77 IS 1 BP 7 EP 11 DI 10.1136/bjo.77.1.7 PG 5 WC Ophthalmology SC Ophthalmology GA KH119 UT WOS:A1993KH11900003 PM 8435406 ER PT J AU BASTILLE, JD AF BASTILLE, JD TI SALARIES AND PROFESSIONAL AUTHORITY - NEW JURISDICTIONS SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Editorial Material RP BASTILLE, JD (reprint author), MASSACHUSETTS GEN HOSP,TREADWELL LIB,BOSTON,MA 02114, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD JAN PY 1993 VL 81 IS 1 BP 80 EP 81 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA KH515 UT WOS:A1993KH51500017 PM 8428198 ER PT J AU DRINKA, PJ OLSON, J BAUWENS, S VOEKS, SK CARLSON, I WILSON, M AF DRINKA, PJ OLSON, J BAUWENS, S VOEKS, SK CARLSON, I WILSON, M TI LACK OF ASSOCIATION BETWEEN FREE TESTOSTERONE AND BONE-DENSITY SEPARATE FROM AGE IN ELDERLY MALES SO CALCIFIED TISSUE INTERNATIONAL LA English DT Editorial Material DE MALE; OSTEOPOROSIS; FREE TESTOSTERONE ID HYPOGONADAL MEN; OSTEOPOROSIS AB It is unclear what proportion of the variance in bone density in elderly males is accounted for by testosterone status. We studied 112 ambulatory, elderly volunteers (mean age 71.7 years) and determined free testosterone (FT), as well as bone density measurements by photon absorptiometry at multiple sites. Our studies of 35 of these subjects 4 years later included morning FT and dual energy X-ray absorptiometry. There were no significant correlations between FT and bone density at multiple scanning sites with the effects of age partialed out. We suspect that our inability to detect a significant effect of FT on bone density was related to the relative strength of other determinants of bone density, as well as to the fact that FT values are far more dynamic than bone density. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. WISCONSIN VET HOME,KING,WI 54946. MENDOTA MENTAL HLTH INST,MADISON,WI 53704. MANAGED CARE RESOURCES INC,CHESAPEAKE,VA. UNIV WISCONSIN HOSP,DEPT PATHOL & LAB MED,MADISON,WI 53792. RP DRINKA, PJ (reprint author), UNIV WISCONSIN,DEPT INTERNAL MED & GERIATR,MADISON,WI 53706, USA. NR 12 TC 69 Z9 70 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD JAN PY 1993 VL 52 IS 1 BP 67 EP 69 DI 10.1007/BF00675629 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KE710 UT WOS:A1993KE71000012 PM 8453508 ER PT J AU WANG, X KLEYMAN, TR TOHDA, H MARUNAKA, Y OBRODOVICH, H AF WANG, X KLEYMAN, TR TOHDA, H MARUNAKA, Y OBRODOVICH, H TI 5-(N-ETHYL-N-ISOPROPYL)AMILORIDE SENSITIVE NA+ CURRENTS IN INTACT FETAL DISTAL LUNG EPITHELIAL-CELLS SO CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY LA English DT Note DE NA+ CHANNELS; 5-(N-ETHYL-N-ISOPROPYL)AMILORIDE; ALVEOLAR EPITHELIUM; WHOLE-CELL PATCH CLAMP; K+ CHANNELS ID ION-TRANSPORT; CHANNEL; ALVEOLAR; AMILORIDE; CULTURE AB To determine whether primary cultures of rat fetal distal lung epithelium (FDLE) possessed L-type Na+ channels on their plasma membrane we performed experiments with 5-(N-ethyl-N-isopropyl)amiloride (EIPA) and other amiloride analogs. Short-circuit current (I(sc)) was decreased by the apical application of amiloride and benzamil, but was unaffected by 10 muM dimethylamiloride (DMA). EIPA decreased I(sc) when added to either the apical or basal sides. Greatest effects were seen with bilateral EIPA, where half-maximal effects occurred in the micromolar range. Measurements of intracellular pH with the fluorescent dye BCECF demonstrated that DMA impaired (IC50 = 71 nM) the ability of FDLE to recover from intracellular acidification. Nystatin perforated patch clamp techniques showed that FDLE had nonrectifying Na+ currents but no detectable Cl- currents. The whole-cell currents were reversibly decreased by 20 muM concentrations of EIPA, benzamil. and amiloride but were unaffected by 20 muM DMA. These studies indicate that there are EIPA-sensitive Na+ conductances in intact FDLE and suggest the presence of L-type Na+ conductances on their apical membrane and EIPA-sensitive K+ channels on the basolateral membrane. C1 UNIV TORONTO,HOSP SICK CHILDREN,DIV RESP RES,555 UNIV AVE,TORONTO M5G 1X8,ONTARIO,CANADA. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NR 17 TC 31 Z9 31 U1 0 U2 0 PU NATL RESEARCH COUNCIL CANADA PI OTTAWA PA RESEARCH JOURNALS, MONTREAL RD, OTTAWA ON K1A 0R6, CANADA SN 0008-4212 J9 CAN J PHYSIOL PHARM JI Can. J. Physiol. Pharmacol. PD JAN PY 1993 VL 71 IS 1 BP 58 EP 62 PG 5 WC Pharmacology & Pharmacy; Physiology SC Pharmacology & Pharmacy; Physiology GA LA790 UT WOS:A1993LA79000009 PM 8390327 ER PT J AU EICHHORN, JH YOUNG, RH SCULLY, RE AF EICHHORN, JH YOUNG, RH SCULLY, RE TI NONPULMONARY SMALL-CELL CARCINOMAS OF EXTRAGENITAL ORIGIN METASTATIC TO THE OVARY SO CANCER LA English DT Article DE OVARY; METASTASIS; SMALL CELL CARCINOMA; MERKEL CELL CARCINOMA; INTESTINAL TRACT; THYMUS ID UNDIFFERENTIATED CARCINOMA; DNA CONTENT; TUMOR; COLON; NEUROENDOCRINE; LUNG; SKIN; HYPERCALCEMIA AB Seven small cell carcinomas of extragenital and extrapulmonary origin that metastasized to the ovary are described. The tumors occurred in women who were 21-77 years of age (mean, 49 years) and were discovered at, or close to, the time of presentation. The primary sites were the intestine (three cases), thymus (two cases), and inguinal skin (one case), and in one case it was undetermined. The ovarian tumors, four of which were bilateral, ranged from 1.2 to 25 cm in diameter (mean, 11 cm). Microscopic examination showed typical features of small (oat) cell carcinoma in six cases; one neoplasm resembled a small cell carcinoma of intermediate cell type and contained rare glands. On immunohistochemical examination, six of six tumors stained for cytokeratin, five of five for neuron-specific enolase, two of six for chromogranin, and none of four for vimentin. The primary cutaneous tumor was a Merkel cell carcinoma. The patient with that case died at 8 months. Two patients with intestinal tumors died at 1 and 2 months, and one is free of disease at 4 years after receiving chemotherapy. Both patients with mediastinal tumors received chemotherapy; one died at 11 months and one had brain metastases at 5 months and was lost to follow-up. The final case is recent. The differential diagnoses in these cases include primary ovarian small cell carcinomas of hypercalcemic and pulmonary types and various other small cell malignant tumors metastatic to the ovary. Consideration of a variety of clinical and pathologic features should enable these important distinctions to be made. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. RP EICHHORN, JH (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115, USA. NR 43 TC 16 Z9 16 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 1993 VL 71 IS 1 BP 177 EP 186 DI 10.1002/1097-0142(19930101)71:1<177::AID-CNCR2820710128>3.0.CO;2-G PG 10 WC Oncology SC Oncology GA KF763 UT WOS:A1993KF76300027 PM 8380114 ER PT J AU DEZUBE, BJ SHERMAN, ML FRIDOVICHKEIL, JL ALLENRYAN, J PARDEE, AB AF DEZUBE, BJ SHERMAN, ML FRIDOVICHKEIL, JL ALLENRYAN, J PARDEE, AB TI DOWN-REGULATION OF TUMOR-NECROSIS-FACTOR EXPRESSION BY PENTOXIFYLLINE IN CANCER-PATIENTS - A PILOT-STUDY SO CANCER IMMUNOLOGY IMMUNOTHERAPY LA English DT Note DE CACHEXIA; TUMOR NECROSIS FACTOR; PENTOXIFYLLINE ID IMMUNODEFICIENCY-VIRUS TYPE-1; CACHECTIN; INDUCTION; DECREASES AB The wasting syndrome (cachexia) characterized by anorexia, malaise, and weight loss is observed in many patients with cancer or chronic infection. The excessive levels of tumor necrosis factor-alpha (TNF)/cachectin reported in 50% of cancer patients exhibiting clinically active disease may therefore mediate, at least in part, the cachexia associated with malignancy. Pentoxifylline, a substituted methylxanthine approved for treatment of intermittent claudication, has been shown in preclinical studies to down-regulate TNF RNA expression as well as TNF activity. We report that pentoxifylline suppressed TNF RNA levels on all three occasions in patients with initially elevated levels of TNF RNA. Pentoxifylline did not suppress TNF RNA to subnormal levels in all five patients with initially normal TNF RNA levels. Four patients reported an increased sense of well-being, improved appetite and ability to perform die activities of daily living. Two of these five patients with normal TNF levels each had a weight gain of more than 5% after 3 weeks of pentoxifylline therapy suggesting that, although TNF may be important in die pathogenesis of cancer cachexia, other anorexia-producing cytokines that are potentially affected by pentoxifylline may also be involved. No severe adverse effects were observed. Taken together these findings suggest that pentoxifylline can down-regulate TNF expression and improve the sense of well-being in cancer patients. A larger study with a randomized, double-blind, placebo-controlled design and more sophisticated estimates of quality of life will be needed to confirm these observations. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,DEPT MED,DIV MED ONCOL,BOSTON,MA 02215. RP DEZUBE, BJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. NR 27 TC 53 Z9 54 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-7004 J9 CANCER IMMUNOL IMMUN JI Cancer Immunol. Immunother. PD JAN PY 1993 VL 36 IS 1 BP 57 EP 60 DI 10.1007/BF01789132 PG 4 WC Oncology; Immunology SC Oncology; Immunology GA JY735 UT WOS:A1993JY73500009 PM 7678547 ER PT J AU HAYES, DF AF HAYES, DF TI WE MAY BE LOST, BUT WERE SURE MAKIN GOOD TIME SO CANCER INVESTIGATION LA English DT Editorial Material ID BREAST-CANCER; CARCINOMA; SURVIVAL RP HAYES, DF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BREAST EVALUAT,44 BINNEY ST,BOSTON,MA 02115, USA. NR 12 TC 2 Z9 2 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 1993 VL 11 IS 1 BP 88 EP 90 DI 10.3109/07357909309020266 PG 3 WC Oncology SC Oncology GA KJ376 UT WOS:A1993KJ37600014 PM 8155093 ER PT J AU CAREY, RW HILGENBERG, AD WILKINS, EW CHOI, NC MATHISEN, DJ GRILLO, HC WAIN, JC LOGAN, DL BROMBERG, C AF CAREY, RW HILGENBERG, AD WILKINS, EW CHOI, NC MATHISEN, DJ GRILLO, HC WAIN, JC LOGAN, DL BROMBERG, C TI LONG-TERM FOLLOW-UP OF NEOADJUVANT CHEMOTHERAPY WITH 5-FLUOROURACIL AND CISPLATIN WITH SURGICAL RESECTION AND POSSIBLE POSTOPERATIVE RADIOTHERAPY AND OR CHEMOTHERAPY IN SQUAMOUS-CELL CARCINOMA OF THE ESOPHAGUS SO CANCER INVESTIGATION LA English DT Article ID RADIATION-THERAPY; CANCER AB Seventy patients with local squamous cell carcinoma of the esophagus were treated between 1981 and 1990 with preoperative chemotherapy, surgical resection, and possible postoperative radiation therapy and/or chemotherapy. Chemotherapy included two cycles of 5-fluorouracil (1000 mg/M2) by continuous intravenous infusion on days 1-4 and cisplatin (100 mg/m2) on day 4. Complete clinical response (CCR) was achieved in 28 (41%) patients, partial clinical response (PCR) in 17 (25%), and no response in 23 (34%). Fifty-five (81%) patients were resected, 6 (9%) were explored, and 7 (10%) were unable to have surgery. Microscopic analysis of 55 resected patients showed 50 (91%) with active tumor, 1 (2%) with necrotic tumor, and 4 (7%) with a pathological complete response to chemotherapy. Twenty-six of the 55 resected patients (47%) had no gross evidence of disease at the time of surgical inspection. Median overall survival was 21.86 months (range 2-107 months) for all patients and 26.71 months (range 2-107 months) for resected patients. Actuarial 5-year survival rate was 31% for all patients and 39% for resected patients. Prolonged survival correlates with complete clinical response to chemotherapy, low pathological stage of disease, and successful resection of the lesion. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED SERV,BOSTON,MA 02114. ALBANY MED COLL,ALBANY,NY 12208. RP CAREY, RW (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,MED ONCOL UNIT,COX 2,100 BLOSSOM ST,BOSTON,MA 02114, USA. NR 11 TC 35 Z9 35 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 1993 VL 11 IS 2 BP 99 EP 105 DI 10.3109/07357909309024826 PG 7 WC Oncology SC Oncology GA KV593 UT WOS:A1993KV59300001 PM 8462027 ER PT J AU BRUCE, JL PRICE, BD COLEMAN, CN CALDERWOOD, SK AF BRUCE, JL PRICE, BD COLEMAN, CN CALDERWOOD, SK TI OXIDATIVE INJURY RAPIDLY ACTIVATES THE HEAT-SHOCK TRANSCRIPTION FACTOR BUT FAILS TO INCREASE LEVELS OF HEAT-SHOCK PROTEINS SO CANCER RESEARCH LA English DT Note ID DNA-BINDING; CELLS AB When cells are exposed to heat shock, heavy metals, amino acid analogues, and other stresses, the heat shock transcription factor (HSF) is activated. The HSF then binds to the promoter of the heat shock genes, stimulating transcription of the heat shock proteins. Here, we demonstrate that exposure of NIH-3T3 cells to oxidants (H2O2 or menadione) also causes activation of the HSF. This activation is not blocked by inhibitors of protein synthesis (cycloheximide) or by inhibitors of protein kinases (2-aminopurine or genistein). In addition, the oxidant activated HSF is located in the nucleus of the cells. However, oxidant activation of the HSF does not result in the accumulation of hsp70 mRNA or of heat shock proteins. This is in contrast to the accumulation of heat shock proteins seen after heat shock activation of the HSF. This suggests that oxidant induced activation of HSF binding may have a function different from that of heat induced activation of HSF binding. RP BRUCE, JL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JOINT CTR RADIAT THERAPY,STRESS PROT GRP,RM JF205,BOSTON,MA 02115, USA. FU NCI NIH HHS [R29CA-44940]; PHS HHS [R01 47407] NR 19 TC 115 Z9 118 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 1 PY 1993 VL 53 IS 1 BP 12 EP 15 PG 4 WC Oncology SC Oncology GA KD719 UT WOS:A1993KD71900004 PM 8416735 ER PT J AU GELBER, RD GOLDHIRSCH, A COLE, BF AF GELBER, RD GOLDHIRSCH, A COLE, BF TI EVALUATION OF EFFECTIVENESS - Q-TWIST SO CANCER TREATMENT REVIEWS LA English DT Article ID ADJUSTED SURVIVAL ANALYSIS; CANCER-PATIENTS; BREAST-CANCER; QUALITY; LIFE; THERAPIES C1 OSPED CIVICO, SERV ONCOL, CH-6900 LUGANO, SWITZERLAND. RP HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV BIOSTAT & EPIDEMIOL, 44 BINNEY ST, BOSTON, MA 02115 USA. RI Cole, Bernard/I-3775-2012 FU NCI NIH HHS [CA-06516] NR 15 TC 45 Z9 45 U1 0 U2 3 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0305-7372 EI 1532-1967 J9 CANCER TREAT REV JI Cancer Treat. Rev. PD JAN PY 1993 VL 19 SU A BP 73 EP 84 DI 10.1016/0305-7372(93)90060-5 PG 12 WC Oncology SC Oncology GA KM111 UT WOS:A1993KM11100010 PM 7679323 ER PT B AU HARTHORNE, JW AF HARTHORNE, JW GP ORGANIZING COMM VTH ASIAN/PACIFIC SYMP CARDIAC PACING & ELECTROPHYSIOL TI FUTURE DIRECTIONS IN CARDIAC PACING - TRAINING AND CERTIFICATION SO CARDIAC PACING AND ELECTROPHYSIOLOGY TODAY LA English DT Proceedings Paper CT Vth Asian/Pacific Symposium on Cardiac Pacing and Electrophysiology: Cardiac Pacing and Electrophysiology Today - A New Era of Therapeutic Arrhythmology CY AUG 01-04, 1993 CL MAKUHARI, JAPAN C1 MASSACHUSETTS GEN HOSP,PACEMAKER LAB,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SIMUL INTERNATIONAL INC PI TOKYO PA C/O 9TH-KOWA BLDG 8-10 AKASAKA 1 CHOME MINATO-KU, TOKYO 107, JAPAN BN 4-88329-001-8 PY 1993 BP 5 EP 6 PG 2 WC Cardiac & Cardiovascular Systems; Surgery SC Cardiovascular System & Cardiology; Surgery GA BD17D UT WOS:A1993BD17D00002 ER PT J AU HANSEN, ME YUCEL, EK WALTMAN, AC AF HANSEN, ME YUCEL, EK WALTMAN, AC TI STIR IMAGING OF SYNTHETIC VASCULAR GRAFT INFECTION SO CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Article DE GRAFT INFECTION; MAGNETIC RESONANCE IMAGING AB Nine patients with suspected prosthetic vascular graft infection were studied with axial spin echo (SE) and short TI inversion recovery (STIR) magnetic resonance imaging. Images were assessed for presence and extent of abnormality. All patients had either surgical (8/9) or bacteriologic (6/9) confirmation of infection. STIR images better defined the extent of infection and had greater fat-fluid contrast than SE images in 6/9 studies. In 3 cases with peri-graft fluid alone, T2-weighted images had slightly greater contrast, although the STIR images were still diagnostic. STIR imaging can offer improved accuracy in evaluation of suspected prosthetic graft infection when used in conjunction with SE techniques. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. NR 0 TC 9 Z9 9 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0174-1551 J9 CARDIOVASC INTER RAD JI Cardiovasc. Interv. Radiol. PD JAN-FEB PY 1993 VL 16 IS 1 BP 30 EP 36 DI 10.1007/BF02603034 PG 7 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA KH412 UT WOS:A1993KH41200010 PM 8435833 ER PT J AU GRABOWSKI, EF RODRIGUEZ, M MCDONNELL, SL AF GRABOWSKI, EF RODRIGUEZ, M MCDONNELL, SL TI PLATELET-ADHESION AGGREGATION IN AN INVITRO MODEL OF CORONARY-ARTERY STENOSIS SO CATHETERIZATION AND CARDIOVASCULAR DIAGNOSIS LA English DT Article DE CONTRAST MEDIA; FLOWING BLOOD; ENDOTHELIAL CELLS; VIDEOMICROSCOPY ID CONTRAST-MEDIA; FLOWING BLOOD; SHEAR RATE; DIFFUSION; WALL AB Platelet adhesion/aggregation (PAA)at a site of coronary artery stenosis is believed to be a Process strongly modulated by local shear rates and the functional state of neighboring endothelium. One purpose of the present work, therefore, is to describe an in vitro model for the direct imaging of such PAA. Another is to apply the model to the question as to whether the use of nonionic vs. ionic contrast media (CM) in the presence of vascular endothelium contributes to PAA at the stenosis site. Toward these ends, we utilized a special flow chamber which incorporates a monolayer of endothelial cells (ECs), a step 66% flowpath constriction at a site preadsorbed with microfibrillar collagen, and arterial shear rates. By epifluorescence microscopy and digital image analysis of video recordings, PAA was found to be greater with dysfunctional ECs (pretreated with lysine acetylsalicylate) than with normal ECs, thereby confirming a modulatory role in PAA of functionally intact ECs. When nonionic (iohexol) or ionic (ioxaglate, diatrizoate) CM was added to the flowing blood at a concentration of 20% by non-red cell volume, PAA was inhibited in the order diatrizoate ioxaglate > iohexol > saline control. No inhibition by any CM was seen, however, when chamber prefill culture medium containing 20% by volume CM was displaced by CM-free blood, in simulation of bolus administration of CM. In terms of inhibition of PAA during percutaneous transluminal coronary angioplasty (PTCA), therefore, our model provides a conceptual basis by which one may anticipate in flowing blood no clear benefit of ionic over nonionic CM. This is because the greater antiplatelet effects of the ionic CM are lost with hemodilution by CM-free blood, while a greater anti-EC effect is likely to persist. C1 CORNELL UNIV,MED CTR,NEW YORK HOSP,DEPT PEDIAT,DIV CARDIAC,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL 33095] NR 17 TC 20 Z9 20 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 0098-6569 J9 CATHETER CARDIO DIAG JI Catheter. Cardiovasc. Diagn. PD JAN PY 1993 VL 28 IS 1 BP 65 EP 71 DI 10.1002/ccd.1810280113 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KE009 UT WOS:A1993KE00900012 PM 8416335 ER PT J AU KHARBANDA, S RUBIN, E DATTA, R HASS, R SUKHATME, V KUFE, D AF KHARBANDA, S RUBIN, E DATTA, R HASS, R SUKHATME, V KUFE, D TI TRANSCRIPTIONAL REGULATION OF THE EARLY GROWTH RESPONSE-1 GENE IN HUMAN MYELOID-LEUKEMIA CELLS BY OKADAIC ACID SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID COLONY-STIMULATING FACTOR; HUMAN MONOCYTIC DIFFERENTIATION; FINGER-ENCODING GENE; C-FOS ENHANCER; PROTEIN-PHOSPHORYLATION; MOLECULAR-CLONING; TUMOR PROMOTERS; CULTURED-CELLS; PHORBOL ESTERS; ACTIN GENE AB The early growth response 1 (EGR-1) gene is induced after mitogenic stimulation of diverse cell types. The present work has examined the effects of okadaic acid, an inhibitor of protein phosphatases 1 and 2A, on EGR-1 expression during monocytic differentiation of U-937 myeloid leukemia cells. Treatment of U-937 cells with okadaic acid was associated with transient increases in EGR-1 mRNA levels. These increases were maximal at 6 h and occurred in the absence of de novo protein synthesis. Nuclear run-on assays demonstrated that although EGR-1 transcription is detectable in untreated U-937 cells, this rate is increased 6-fold by okadaic acid. Sequences responsive to okadaic acid-induced signals were determined by deletion analysis of the EGR-1 promoter. The results demonstrate that okadaic acid-induced EGR-1 transcription is dependent on the presence of CC (A/T)6 GG (CArG) motifs. The EGR-1 promoter contains six CArG boxes. However, only the 5'-most distal (first) CArG sequence conferred okadaic acid inducibility. A 40-base pair oligomer corresponding to the first CArG element also conferred okadaic acid inducibility of the minimal thymidine kinase gene promoter. In contrast, there was no inducibility using a similar oligomer containing a mutated CArG box. Finally, binding of nuclear proteins to the first CArG sequence was similar for control and okadaic acid-treated cells. Taken together, these results suggest that okadaic acid activates EGR-1 transcription and that this event is mediated at least in part by a single CArG element. C1 UNIV CHICAGO,HOWARD HUGHES MED INST,DEPT MED,CHICAGO,IL 60637. UNIV CHICAGO,HOWARD HUGHES MED INST,DEPT MOLEC GENET & CELL BIOL,CHICAGO,IL 60637. RP KHARBANDA, S (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115, USA. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 FU NCI NIH HHS [CA42802, CA34183] NR 49 TC 35 Z9 35 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD JAN PY 1993 VL 4 IS 1 BP 17 EP 23 PG 7 WC Cell Biology SC Cell Biology GA KF716 UT WOS:A1993KF71600003 PM 8381016 ER PT B AU CARTER, EA AF CARTER, EA BE Knook, DL Wisse, E TI EFFECT OF THERMAL-INJURY ON KUPFFER CELL CYTOKINE PRODUCTION SO CELLS OF THE HEPATIC SINUSOID, VOL 4 LA English DT Proceedings Paper CT 6th International Symposium on Cells of the Hepatic Sinusoid CY AUG 23-27, 1992 CL KUPFFER CELL FDN, ANTWERP, BELGIUM SP KUPFFER CELL FDN, NATL FONDS WETENSCHAPPELIJK ONDERZOEK HO KUPFFER CELL FDN RP CARTER, EA (reprint author), MASSACHUSETTS GEN HOSP,COMBINED PROGRAM GASTROENTEROL & NUTR,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KUPFFER CELL FOUNDATION PI LEIDEN PA PO BOX 2215, 2301 CE LEIDEN, NETHERLANDS BN 90-800079-5-1 PY 1993 BP 51 EP 52 PG 2 WC Gastroenterology & Hepatology; Immunology SC Gastroenterology & Hepatology; Immunology GA BZ42Z UT WOS:A1993BZ42Z00014 ER PT J AU CAO, BN HUNEYCUTT, BS GAPUD, CP ARCECI, RJ REISS, CS AF CAO, BN HUNEYCUTT, BS GAPUD, CP ARCECI, RJ REISS, CS TI LYMPHOKINE EXPRESSION PROFILE OF RESTING AND STIMULATED CD4+ CTL CLONES SPECIFIC FOR THE GLYCOPROTEIN OF VESICULAR STOMATITIS-VIRUS SO CELLULAR IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; T-CELL; LYMPHOCYTES-T; FACTOR-I; CDNA; INTERLEUKIN-2; CLONING; ENCEPHALOMYELITIS; LYMPHOTOXIN; CYTOLYSIS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL & ONCOL,BOSTON,MA 02115. OI Reiss, Carol/0000-0003-4353-8882 FU NIAID NIH HHS [AI 18083, R37AI 20896]; NIGMS NIH HHS [GM 38156] NR 27 TC 4 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD JAN PY 1993 VL 146 IS 1 BP 147 EP 156 DI 10.1006/cimm.1993.1013 PG 10 WC Cell Biology; Immunology SC Cell Biology; Immunology GA KK789 UT WOS:A1993KK78900013 PM 8381052 ER PT B AU YAMAKAWA, K PETERSON, JW SIBILIA, R KAOUTZANIS, M ZERVAS, NT AF YAMAKAWA, K PETERSON, JW SIBILIA, R KAOUTZANIS, M ZERVAS, NT BE Findlay, JM TI INACTIVITY OF PDGF-RECEPTORS IN CANINE BASILAR ARTERY SO CEREBRAL VASOSPASM SE DEVELOPMENTS IN NEUROLOGY LA English DT Proceedings Paper CT Vth International Conference on Cerebral Vasospasm CY MAY 17-21, 1993 CL EDMONTON, CANADA C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-444-81535-X J9 DEVEL NEUR PY 1993 VL 8 BP 145 EP 147 PG 3 WC Cardiac & Cardiovascular Systems; Neurosciences; Physiology SC Cardiovascular System & Cardiology; Neurosciences & Neurology; Physiology GA BZ51N UT WOS:A1993BZ51N00036 ER PT B AU PETERSON, JW AF PETERSON, JW BE Findlay, JM TI ERYTHROCYTES, HEMOGLOBIN, AND VASOSPASM - A BRIEF REVIEW SO CEREBRAL VASOSPASM SE DEVELOPMENTS IN NEUROLOGY LA English DT Proceedings Paper CT Vth International Conference on Cerebral Vasospasm CY MAY 17-21, 1993 CL EDMONTON, CANADA C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 1 U2 1 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-444-81535-X J9 DEVEL NEUR PY 1993 VL 8 BP 187 EP 190 PG 4 WC Cardiac & Cardiovascular Systems; Neurosciences; Physiology SC Cardiovascular System & Cardiology; Neurosciences & Neurology; Physiology GA BZ51N UT WOS:A1993BZ51N00046 ER PT B AU KAOUTZANIS, M PETERSON, JW ANDERSON, R MCAULIFFE, DJ SIBILIA, R YOKOTA, M ZERVAS, NT AF KAOUTZANIS, M PETERSON, JW ANDERSON, R MCAULIFFE, DJ SIBILIA, R YOKOTA, M ZERVAS, NT BE Findlay, JM TI VASODILATION MECHANISM AFTER THE IN-VITRO APPLICATION OF PULSED-DYE LASER SO CEREBRAL VASOSPASM SE DEVELOPMENTS IN NEUROLOGY LA English DT Proceedings Paper CT Vth International Conference on Cerebral Vasospasm CY MAY 17-21, 1993 CL EDMONTON, CANADA C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-444-81535-X J9 DEVEL NEUR PY 1993 VL 8 BP 405 EP 408 PG 4 WC Cardiac & Cardiovascular Systems; Neurosciences; Physiology SC Cardiovascular System & Cardiology; Neurosciences & Neurology; Physiology GA BZ51N UT WOS:A1993BZ51N00098 ER PT B AU PETERSON, JW SIBILIA, R YAMAKAWA, K KAOUTZANIS, M ZERVAS, NT AF PETERSON, JW SIBILIA, R YAMAKAWA, K KAOUTZANIS, M ZERVAS, NT BE Findlay, JM TI COMPLEMENT-INDUCED HEMOLYSIS OF SUBARACHNOID ERYTHROCYTES SO CEREBRAL VASOSPASM SE DEVELOPMENTS IN NEUROLOGY LA English DT Proceedings Paper CT Vth International Conference on Cerebral Vasospasm CY MAY 17-21, 1993 CL EDMONTON, CANADA C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-444-81535-X J9 DEVEL NEUR PY 1993 VL 8 BP 443 EP 447 PG 5 WC Cardiac & Cardiovascular Systems; Neurosciences; Physiology SC Cardiovascular System & Cardiology; Neurosciences & Neurology; Physiology GA BZ51N UT WOS:A1993BZ51N00106 ER PT J AU Hoop, B Kazemi, H Liebovitch, L AF Hoop, Bernard Kazemi, Homayoun Liebovitch, Larry TI Rescaled range analysis of resting respiration SO CHAOS LA English DT Article AB Fluctuations in resting depth of breathing (tidal volume) at constant breathing rate in the anesthetized adult rat exhibit fractal properties when analyzed by a rescaled range method characterized by a mean (+/- SD) exponent H=0.83 +/- 0.02 and 0.92 +/- 0.03 with and without sighs, respectively, for up to 400 breaths. Values of H determined from shuffled tidal volumes and simulated tidal volumes taken randomly from a Gaussian distribution of mean and variance approximating that of the actual data are consistent with the expected value of H=0.5 for an independent random process with finite variances. An empirical description is proposed to predict the change in H with length of time record. C1 [Hoop, Bernard; Kazemi, Homayoun] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Med Serv Pulm & Crit Care Unit, Boston, MA 02114 USA. [Liebovitch, Larry] Columbia Univ, Dept Ophthalmol, Coll Phys & Surg, New York, NY 10032 USA. RP Hoop, B (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Med Serv Pulm & Crit Care Unit, Boston, MA 02114 USA. FU American Heart Association; Whitaker Foundation; U.S. National Institutes of Health FX This work was supported in part by The American Heart Association, the Whitaker Foundation, and the U.S. National Institutes of Health. The authors thank P. Pappagianopoulos, T.J. MacVeigh, and J.D. Murray for technical advice and assistance. NR 9 TC 16 Z9 17 U1 0 U2 1 PU AMER INST PHYSICS PI MELVILLE PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1, MELVILLE, NY 11747-4501 USA SN 1054-1500 J9 CHAOS JI Chaos PD JAN PY 1993 VL 3 IS 1 BP 27 EP 29 DI 10.1063/1.165976 PG 3 WC Mathematics, Applied; Physics, Mathematical SC Mathematics; Physics GA V22XR UT WOS:000208308400005 ER PT S AU SCREMIN, OU JENDEN, DJ AF SCREMIN, OU JENDEN, DJ BE Cuello, AC TI ACETYLCHOLINE TURNOVER AND RELEASE - THE INFLUENCE OF ENERGY-METABOLISM AND SYSTEMIC CHOLINE AVAILABILITY SO CHOLINERGIC FUNCTION AND DYSFUNCTION SE PROGRESS IN BRAIN RESEARCH LA English DT Proceedings Paper CT 8TH INTERNATIONAL CHOLINERGIC SYMP CY JUL, 1992 CL STE ADELE, CANADA SP ASTRA ARCUS, BAYER, BRISTOL MYERS SQUIBB, DAIICHI PHARM, DUPONT PHARMA, FOND RECH SANTE QUEBEC, INST REC JOUVEINAL, INT SOC NEUOCHEM, KABI PHARMA, MCGILL UNIV, FAC MED RP SCREMIN, OU (reprint author), UCLA,W LOS ANGELES VET ADM MED CTR,SCH MED,LOS ANGELES,CA 90024, USA. RI Cuello, A. Claudio/N-8211-2015 NR 0 TC 7 Z9 7 U1 0 U2 1 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA AMSTERDAM SN 0079-6123 BN 0-444-89717-8 J9 PROG BRAIN RES PY 1993 VL 98 BP 191 EP 195 PG 5 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy; Physiology SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy; Physiology GA BZ03G UT WOS:A1993BZ03G00024 ER PT J AU RAKUGI, H JACOB, HJ KRIEGER, JE INGELFINGER, JR PRATT, RE AF RAKUGI, H JACOB, HJ KRIEGER, JE INGELFINGER, JR PRATT, RE TI VASCULAR INJURY INDUCES ANGIOTENSINOGEN GENE-EXPRESSION IN THE MEDIA AND NEOINTIMA SO CIRCULATION LA English DT Article DE ANGIOTENSIN; RNA, MESSENGER; BALLOONS; SMOOTH MUSCLE CELLS; HYBRIDIZATION; DUP 753 ID SMOOTH-MUSCLE CELLS; FACTOR-A-CHAIN; MESSENGER-RNA; RAT AORTA; LOCALIZATION; PROLIFERATION; HYPERTROPHY; MIGRATION; SYSTEM; HYPERTENSION AB Background. Angiotensin II promotes growth of vascular smooth muscle cells in vitro via the autocrine production of growth factors such as platelet-derived growth factor, basic fibroblast growth factor, and transforming growth factor-beta. Furthermore, experimental studies have demonstrated that angiotensin infusion can enhance smooth muscle proliferation after balloon injury in vivo. Consistent with this, angiotensin converting enzyme inhibitors have been shown to prevent myointimal proliferation. The origin of vascular angiotensin that participate in this process is of interest. We have demonstrated the presence of angiotensinogen messenger RNA (mRNA) in the adventitial and medial layers of the rat aorta and have speculated that local angiotensinogen production may play an important role during myointimal proliferation. To provide further evidence toward this hypothesis, we compared the localization and expression of angiotensinogen mRNA in control and balloon injured vessels using in situ hybridization. Methods and Results. Abdominal aorta of Sprague-Dawley rats were studied before or after injury with a balloon catheter. Neointimal hyperplasia developed as documented morphologically by a progressive increase in the ratio of neointimal to medial thickness from 0.17 at 1 week to 1.17 at 6 weeks after injury. Angiotensinogen mRNA was detected clearly in the adventitia and media of control and injured aorta. However, at 1 week after injury, the medial-to-adventitial angiotensinogen mRNA ratio was higher in the injured aorta, suggesting increased gene expression in the media compared with control. Of potential importance, angiotensinogen mRNA was also detected in the neointima of the injured aorta, and this was also highest at 1 week after injury. Conclusions. These data are consistent with the hypothesis thal balloon injury leads to activation of the vascular renin-angiotensin system, which may participate in the myointimal proliferation. C1 STANFORD UNIV,MED CTR,SCH MED,FALK CARDIOVASC RES CTR,DIV CARDIOVASC MED,300 PASTEUR DR,STANFORD,CA 94305. MASSACHUSETTS GEN HOSP,DIV PEDIAT NEPHROL,BOSTON,MA 02114. RI Krieger, Jose/C-3117-2011; OI Krieger, Jose/0000-0001-5464-1792 FU NHLBI NIH HHS [HL-35252, HL-35610, HL-42663] NR 28 TC 124 Z9 126 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JAN PY 1993 VL 87 IS 1 BP 283 EP 290 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA KG434 UT WOS:A1993KG43400031 PM 8419017 ER PT J AU WALDOR, MK WILSON, B SWARTZ, M AF WALDOR, MK WILSON, B SWARTZ, M TI CELLULITIS CAUSED BY LEGIONELLA-PNEUMOPHILA SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID LEGIONNAIRES-DISEASE; PATIENT; INFECTIONS; BLOOD AB A patient with lymphoma presented with pneumonia. While receiving antibiotics, he developed a rapidly spreading cellulitis. The soft tissues were debrided in the operating room, and pathological examination showed fat necrosis and a fibrinopurulent exudate in the fibroadipose tissue; direct immunofluorescence of the debrided tissue revealed the presence of Legionella pneumophila. Culture of the specimen obtained during the operation yielded L. pneumophila. To our knowledge, this represents the first case report of cellulitis due to L. pneumophila. C1 MASSACHUSETTS GEN HOSP,DEPT MED,INFECT DIS UNIT,BOSTON,MA 02114. NR 22 TC 14 Z9 14 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1993 VL 16 IS 1 BP 51 EP 53 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KG117 UT WOS:A1993KG11700008 PM 8448318 ER PT J AU AHMED, AR HAMEED, A AF AHMED, AR HAMEED, A TI BULLOUS PEMPHIGOID AND DERMATITIS-HERPETIFORMIS SO CLINICS IN DERMATOLOGY LA English DT Article AB In this article, the association of malignancy with bullous pemphigoid and dermatitis herpetiformis is discussed. RP AHMED, AR (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0738-081X J9 CLIN DERMATOL JI Clin. Dermatol. PD JAN-MAR PY 1993 VL 11 IS 1 BP 47 EP 52 PG 6 WC Dermatology SC Dermatology GA LJ708 UT WOS:A1993LJ70800008 PM 8339200 ER PT J AU SHERMAN, JC LUST, B AF SHERMAN, JC LUST, B TI CHILDREN ARE IN CONTROL SO COGNITION LA English DT Article; Proceedings Paper CT 13TH ANNUAL BOSTON UNIV CONF ON LANGUAGE DEVELOPMENT CY OCT, 1988 CL BOSTON, MA ID LANGUAGE; SUBJECT; ENGLISH AB We argue on the basis of recent experimental results that modular principles of universal grammar (UG) play a continuous role in the first language acquisition of control. Our results involve both comprehension and production data from 108 3- to 8-year old children who are acquiring English. The results provide evidence against the hypothesis that there is a ''stage '' at which children do not know fundamental grammatical principles of control, or fail to apply the basic structural analysis relevant to control. We suggest that previous proposals for this hypothesis have been misled by (1) attention to only one aspect of the knowledge of control, namely choice of antecedent in comprehension of the embedded null subject in these structures and (2) misinterpretation of the nature of the principle by which children overgeneralize the choice of object as antecedent in control structures. Although the new results do replicate delay in acquisition with the unique subject-control verb ''promise ''. they suggest that this delay is caused by a need to integrate modular principles of UG with language-specific principles by which the lexicon and syntax (constituent structure and case) are related. The overgeneralization of choice of object as antecedent is shown to reflect a continuous principle of syntactic minimality. C1 CORNELL UNIV,DEPT HUMAN DEV & FAMILY STUDIES,ITHACA,NY 14853. CORNELL UNIV,DEPT MODERN LANGUAGES & LINGUIST,ITHACA,NY 14853. RP SHERMAN, JC (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROPSYCHOL LAB,VINCENT BURNHAM 725,BOSTON,MA 02114, USA. FU PHS HHS [00942] NR 81 TC 13 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0010-0277 J9 COGNITION JI Cognition PD JAN PY 1993 VL 46 IS 1 BP 1 EP 51 DI 10.1016/0010-0277(93)90021-M PG 51 WC Psychology, Experimental SC Psychology GA KF862 UT WOS:A1993KF86200001 PM 8432089 ER PT J AU JUAN, LJ WALTER, PP TAYLOR, ICA KINGSTON, RE WORKMAN, JL AF JUAN, LJ WALTER, PP TAYLOR, ICA KINGSTON, RE WORKMAN, JL TI NUCLEOSOME CORES AND HISTONE H1 IN THE BINDING OF GAL4 DERIVATIVES AND THE REACTIVATION OF TRANSCRIPTION FROM NUCLEOSOME TEMPLATES IN-VITRO SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 58th Annual Cold Spring Harbor Symposia on Quantitative Biology: DNA and Chromosomes CY JUN 02-09, 1993 CL COLD SPRING HARBOR, NY SP COLD SPRING HARBOR LAB ID RNA-POLYMERASE-II; IMMEDIATE EARLY PROTEIN; PSEUDORABIES VIRUS; MAJOR LATE; INVITRO; DNA; CHROMATIN; INITIATION; MECHANISM; PROMOTER C1 PENN STATE UNIV,CTR GENE REGULAT,UNIV PK,PA 16802. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP JUAN, LJ (reprint author), PENN STATE UNIV,DEPT MOLEC & CELL BIOL,UNIV PK,PA 16802, USA. RI Juan, Li-Jung/H-6631-2015 FU NIGMS NIH HHS [GM-47867] NR 35 TC 9 Z9 9 U1 0 U2 4 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 1993 VL 58 BP 213 EP 223 PG 11 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA NR751 UT WOS:A1993NR75100025 PM 7956032 ER PT J AU TAUBER, J STEINERT, RF AF TAUBER, J STEINERT, RF TI PSEUDO-KAYSER-FLEISCHER RING OF THE CORNEA ASSOCIATED WITH NONWILSONIAN LIVER-DISEASE - A CASE-REPORT AND LITERATURE-REVIEW SO CORNEA LA English DT Review DE KAYSER-FLEISCHER RING; NONWILSONIAN LIVER DISEASE AB The Kayser-Fleischer ring of the cornea is usually considered a pathognomonic finding of Wilson's disease. A case of a Kayser-Fleischer ring associated with non-Wilsonian liver disease is presented. The pathophysiology of copper deposition in the cornea and the differential diagnosis of this rare finding are discussed. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CORNEA SERV,BOSTON,MA 02114. NR 0 TC 17 Z9 22 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3740 J9 CORNEA JI Cornea PD JAN PY 1993 VL 12 IS 1 BP 74 EP 77 DI 10.1097/00003226-199301000-00013 PG 4 WC Ophthalmology SC Ophthalmology GA KE951 UT WOS:A1993KE95100013 PM 8458236 ER PT J AU ZAPOL, WM AF ZAPOL, WM TI IATROGENIC COMPLICATIONS IN THE INTENSIVE-CARE UNIT SO CRITICAL CARE MEDICINE LA English DT Editorial Material DE IATROGENIC DISEASE; ACCIDENT PREVENTION; COMPLICATIONS; INTENSIVE CARE UNIT; NURSING STAFF, HOSPITAL; CRITICAL CARE RP ZAPOL, WM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 3 TC 5 Z9 5 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1993 VL 21 IS 1 BP 8 EP 9 DI 10.1097/00003246-199301000-00005 PG 2 WC Critical Care Medicine SC General & Internal Medicine GA KG575 UT WOS:A1993KG57500005 PM 8420735 ER PT J AU BARRETT, SA MOURANI, S VILLAREAL, CA GONZALES, JM ZIMMERMAN, JL AF BARRETT, SA MOURANI, S VILLAREAL, CA GONZALES, JM ZIMMERMAN, JL TI RHABDOMYOLYSIS ASSOCIATED WITH STATUS-ASTHMATICUS SO CRITICAL CARE MEDICINE LA English DT Article DE ASTHMA; LACTIC ACIDOSIS; RHABDOMYOLYSIS; STATUS ASTHMATICUS; BRONCHOSPASM; MYOGLOBINURIA; BETA-AGONISTS; RESPIRATORY FAILURE; CORTICOSTEROIDS; CREATINE PHOSPHOKINASE; PULMONARY EMERGENCIES; RENAL EMERGENCIES ID ACUTE HYDROCORTISONE MYOPATHY; ACUTE RENAL-FAILURE C1 UNIV TEXAS,HLTH SCI CTR,AUDIE MURPHY VET ADM HOSP,SAN ANTONIO,TX 78284. RP BARRETT, SA (reprint author), BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030, USA. NR 13 TC 20 Z9 20 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1993 VL 21 IS 1 BP 151 EP 153 DI 10.1097/00003246-199301000-00026 PG 3 WC Critical Care Medicine SC General & Internal Medicine GA KG575 UT WOS:A1993KG57500026 PM 8420722 ER PT J AU PATARCA, R SAAVEDRA, RA CANTOR, H AF PATARCA, R SAAVEDRA, RA CANTOR, H TI MOLECULAR AND CELLULAR BASIS OF GENETIC-RESISTANCE TO BACTERIAL-INFECTION - THE ROLE OF THE EARLY T-LYMPHOCYTE ACTIVATION-1/OSTEOPONTIN GENE SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Review DE AUTOIMMUNITY; BLOOD COAGULATION; BONE; CELL ADHESION; CYTOKINES; FLAVIVIRUSES; GENE EXPRESSION REGULATION; LYMPHOID CELL ACTIVATION; NEOPLASIA; RICKETTSIA ID EXPERIMENTAL SCRUB TYPHUS; BONE PHOSPHOPROTEIN OSTEOPONTIN; ACID (GLA)-CONTAINING PROTEIN; SYSTEMIC LUPUS-ERYTHEMATOSUS; CSF MESSENGER-RNA; LPR-LPR MICE; SECRETED PHOSPHOPROTEIN; AUTOIMMUNE-DISEASE; AMINO-ACID; NEOPLASTIC TRANSFORMATION AB The realization that soluble mediators of immune function, termed cytokines, can interact with nonimmunological cells has led to new insights into the role of the immune system in regulating cell growth and differentiation of other organ systems. The additional finding that dysregulation of these interactions can lead to a variety of clinical disorders has opened the possibility of new forms of therapy. A recent example of this aspect of cytokine biology comes from studies of a protein designated early T-lymphocyte activation-1/osteopontin (Eta-1/Op), which may play an essential role in immune resistance to certain bacterial and viral pathogens. Analysis of the structure of this protein has revealed that it is almost identical to several proteins associated with neoplasia and bone structure/function. The purpose of this review is to provide a summary of our current knowledge regarding the structure and function of Eta-1/Op and the potential relationship of this gene to several clinical disorders. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT ORTHOPED SURG,SKELETAL DISORDERS & REHABIL L,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. RP PATARCA, R (reprint author), UNIV MIAMI,SCH MED,E M PAPPER LAB CLIN IMMUNOL,POB 016960,MIAMI,FL 33101, USA. FU NIAID NIH HHS [AI12184, AI13600]; NIAMS NIH HHS [IR29AR41046-01] NR 107 TC 183 Z9 184 U1 0 U2 1 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 1993 VL 13 IS 3-4 BP 225 EP 246 PG 22 WC Immunology SC Immunology GA MP579 UT WOS:A1993MP57900003 PM 8110377 ER PT J AU SMITH, DJ TAUBMAN, MA AF SMITH, DJ TAUBMAN, MA TI EMERGENCE OF IMMUNE COMPETENCE IN SALIVA SO CRITICAL REVIEWS IN ORAL BIOLOGY & MEDICINE LA English DT Article; Proceedings Paper CT SYMP ON CONTEMPORARY DEVELOPMENTS IN SALIVARY RESEARCH CY NOV 06-10, 1991 CL BUFFALO, NY SP UNIV BUFFALO, SCH DENT MED, UNILEVER RES, COLGATE PALMOLIVE, NIDR DE SALIVARY IGA; SIGA1; SIGA2; STREPTOCOCCUS-MITIS; STREPTOCOCCUS-SALIVARIUS AB Saliva contains essentially no IgA at birth. However, secretory immune responses to oral and non-oral microbial antigens emerge early in life. We have investigated the characteristics of these responses in salivas of infants less than 1 month through 4 years of age, using cross-sectional and longitudinal approaches. Antibody specificities (IgA, IgA1, and IgA2) were measured in ELISA and Western blot analysis to antigens of Streptococcus mitis and S. salivarius that colonize during the neonatal period. Antibodies reactive with S. sanguis and mutans streptococci, which colonize later in the infant's life, were also determined. Concurrent investigation of the oral flora of each infant was performed and related to the observed antibody specificities. The secretory nature of the immunoglobulins in these salivas was analyzed immunologically and chromatographically. The primary molecular form of salivary IgA was dimeric in all salivas tested. Both IgA subclasses were found, although a subset of infant salivas initially contained >90% IgA1. IgM (>1 mug/ml) was detected in 58% of 3- to 17-week-old infants. By 2 months of age, salivas from most infants contained IgA antibody reactive with at least two S. mitis components. Many salivas also contained antibody reactive with S. salivarius components. By the end of the first year, most salivas contained IgA1 and IgA2 antibody to S. mitis antigens. Maturation of secretory responses in the second and third year was evidenced by the appearance of increased concentrations and additional specificities of salivary IgA antibodies to S. mitis antigens. Antibody to S. mitis, S. salivarius, and S. sanguis extracellular components was detected only after infection with the respective species. However, salivary IgA antibody to mutans streptococci occasionally was detected before colonization was demonstrated. RP SMITH, DJ (reprint author), FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-06153] NR 0 TC 17 Z9 17 U1 0 U2 1 PU INT AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314-3406 SN 1045-4411 J9 CRIT REV ORAL BIOL M JI Crit. Rev. Oral Biol. Med. PY 1993 VL 4 IS 3-4 BP 335 EP 341 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA LL908 UT WOS:A1993LL90800011 PM 8373988 ER PT J AU YARMUSH, ML THORPE, WP STRONG, L RAKESTRAW, SL TONER, M TOMPKINS, RG AF YARMUSH, ML THORPE, WP STRONG, L RAKESTRAW, SL TONER, M TOMPKINS, RG TI ANTIBODY-TARGETED PHOTOLYSIS SO CRITICAL REVIEWS IN THERAPEUTIC DRUG CARRIER SYSTEMS LA English DT Review DE IMMUNOCONJUGATE; PHOTODYNAMIC THERAPY; ANTIBODY LASER; PHOTOLYSIS ID PHOTODYNAMIC THERAPY DOSIMETRY; MONOCLONAL-ANTIBODY; SINGLET OXYGEN; PORPHYRIN PHOTOSENSITIZATION; BENZOPORPHYRIN DERIVATIVES; SILICON NAPHTHALOCYANINE; ALUMINUM PHTHALOCYANINE; PHOTORADIATION THERAPY; PHYSIOLOGICAL BARRIERS; MALIGNANT-TUMORS AB The technique of Antibody Targeted Photolysis (ATPL) is reviewed from an historical perspective with a summary of the literature since the first experiments were performed in 1983. Attention is given to both the biological and photophysical properties of the various immunoconjugates that have been developed. References to critical discoveries and competing technologies in the photodynamic literature are given. Topics include: synthesis of immunoconjugates, in vitro vs. in vivo toxicity, in vivo biodistribution, immunoconjugate delivery, photosensitizer selection based on photophysical properties, light delivery for specific applications, oxygen requirements, and other physicochemical phenomena. A mathematical model of the dynamics for cell killing based upon the transport of phototoxins to the cell surface is developed. A generalized set of coupled differential equations is given, which conveniently summarizes the manifold requirements stressed earlier for successful cell killing. Solutions are then presented for an idealized set of conditions appropriate for an isolated tumor cell. Suggestions for further improvements and follow-up experiments are made that could help in the evolution of ATPL into a useful clinical therapy and/or probe for cell biological studies. C1 MASSACHUSETTS GEN HOSP, SURG SERV, BOSTON, MA 02114 USA. SHRINERS BURNS INST, SURG SERV, BOSTON, MA 02114 USA. RP YARMUSH, ML (reprint author), RUTGERS UNIV, DEPT CHEM & BIOCHEM ENGN, POB 909, PISCATAWAY, NJ 08855 USA. NR 139 TC 42 Z9 43 U1 1 U2 3 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 SN 0743-4863 J9 CRIT REV THER DRUG JI Crit. Rev. Ther. Drug Carr. Syst. PY 1993 VL 10 IS 3 BP 197 EP 252 PG 56 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MA843 UT WOS:A1993MA84300001 PM 8258158 ER PT J AU TONER, M RINKES, IHMB CRAVALHO, EG TOMPKINS, RG YARMUSH, ML AF TONER, M RINKES, IHMB CRAVALHO, EG TOMPKINS, RG YARMUSH, ML TI A CONTROLLED RATE FREEZING DEVICE FOR CRYOPRESERVATION OF BIOLOGICAL TISSUE SO CRYO-LETTERS LA English DT Article DE FREEZING APPARATUS; TEMPERATURE CONTROLLER; CRYOPRESERVATION; BIOLOGICAL TISSUE AB A controlled rate freezing device was designed and characterized for the cryopreservation of biological tissue. Thermal control of the specimen was achieved by balancing the convective cooling power of a cold gaseous nitrogen stream with electrical power dissipation on the heater layer. The device was designed to: (1) control the cooling and warming rates over several orders-of-magnitude up to 100-degrees-C/min; (2) achieve a uniform temperature on the surface of the heater layer between 0-degrees and -80-degrees-C; (3) contain sufficient surface area (4.7 x 7.5 cm2) for tissue specimens or cultured cells; and (4) have multi-step capability which included the capability to maintain constant temperature for long periods. A specific example involving the cryopreservation of cultured hepatocytes is illustrated and demonstrates that the controlled rate freezing device could be used for any tissue type provided it fits on the heater layer surface area. For larger size tissues, cooling channels and heater layers with appropriate sizes could easily be built. C1 MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. RP TONER, M (reprint author), MASSACHUSETTS GEN HOSP,SURG RES LAB,5 WEST,BOSTON,MA 02129, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU CRYO LETTERS PI CAMBRIDGE PA 7 WOOTTON WAY, CAMBRIDGE, CAMBS, ENGLAND CB3 9LX SN 0143-2044 J9 CRYO-LETT JI Cryo-Lett. PD JAN-FEB PY 1993 VL 14 IS 1 BP 43 EP 56 PG 14 WC Biology; Physiology SC Life Sciences & Biomedicine - Other Topics; Physiology GA KL083 UT WOS:A1993KL08300007 ER PT B AU GOITEIN, M AF GOITEIN, M BE Jani, SK TI CT SIMULATION - AN OVERVIEW SO CT SIMULATION FOR RADIOTHERAPY LA English DT Proceedings Paper CT Conference on CT Simulation for Radiotherapy Treatment Planning CY SEP 16-17, 1991 CL UNIV IOWA, IOWA CITY, IA SP UNIV IOWA COLL, DEPT RADIOL, AMER ASSOC PHYSICISTS MED, AMER COLL MED PHYS, AMER SOC THERAPEUT RADIOL & ONCOL, THERATRONICS INT LTD HO UNIV IOWA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,DIV RADIAT BIOPHYS,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MEDICAL PHYSICS PUBLISHING PI MADISON PA 4513 VERNON BLVD, MADISON, WI 53705 BN 0-944838-32-4 PY 1993 BP 161 EP 171 PG 11 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA BA26Y UT WOS:A1993BA26Y00013 ER PT J AU SUZUKI, R ANDERSON, PJ AF SUZUKI, R ANDERSON, PJ TI A TEMPERATURE-DEPENDENT ACTION OF FLUORIDE ON AQUEOUS OUTFLOW FACILITY OF THE CALF EYE SO CURRENT EYE RESEARCH LA English DT Article ID GUANINE-NUCLEOTIDE; VERVET MONKEY; AGENTS AB A number of investigators have studied the effect of metabolic inhibitors on the facility of aqueous outflow from the enucleated eye perfused eye at ''room temperature''. Some inhibitors such as iodoacetate and iodoacetamide increased the facility, others such as p-chloromercuri-benzoate decreased it. Most however, including sodium fluoride, were reported to have had no effect. We have found that 10 mM sodium fluoride had a very small effect on facility of aqueous outflow at room temperature (22-degrees-C), but reduced the facility as much as 50% (average 30%) at 35-degrees-C. The magnitude of the sodium fluoride effect did not appear to be dependent on calcium levels in the medium, but the presence of Ca2+ significantly prolonged its duration. Iodoacetamide and iodoacetate both increased facility at 35-degrees-C in a manner similar to previous findings at room temperature except that at 8-10 mM, iodoacetate caused a 55% decrease; under these conditions, there was considerable release of tissue debris into the anterior chamber which probably blocked the TM. A number of other agents, such as 2,4-dinitrophenol, KCN, and 2-deoxyglucose were studied, but none produced any marked effect on facility. These results emphasize that temperature may profoundly modify the effect of metabolically active agents. The mechanism of the fluoride effect has not been determined but it is consistent with the action of F on the G protein associated with phospholipase C. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. YAMAGUCHI UNIV,SCH MED,DEPT OPHTHALMOL,UBE,YAMAGUCHI 755,JAPAN. FU PHS HHS [R01 3921] NR 19 TC 6 Z9 6 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD JAN PY 1993 VL 12 IS 1 BP 1 EP 7 DI 10.3109/02713689308999489 PG 7 WC Ophthalmology SC Ophthalmology GA KL084 UT WOS:A1993KL08400001 PM 8436006 ER PT S AU ANGELICO, MC LAFFEL, L KROLEWSKI, AS AF ANGELICO, MC LAFFEL, L KROLEWSKI, AS BE Belfiore, F Bergman, RN Molinatti, GM TI APPLICATION OF DENATURING GRADIENT GEL-ELECTROPHORESIS TO DETECT DNA POLYMORPHISMS IN THE RENIN GENE IN IDDM PATIENTS WITH AND WITHOUT DIABETIC NEPHROPATHY SO CURRENT TOPICS IN DIABETES RESEARCH SE FRONTIERS IN DIABETES LA English DT Proceedings Paper CT 4TH INTERNATIONAL DIABETES CONF CY MAR 18-20, 1992 CL FLORENCE, ITALY RP ANGELICO, MC (reprint author), JOSLIN DIABET CTR,DIV RES,EPIDEMIOL & GENET SECT,BOSTON,MA 02215, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA BASEL SN 0251-5342 BN 3-8055-5779-5 J9 FRONT DIABETES JI Front.Diabetes PY 1993 VL 12 BP 227 EP 230 PG 4 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA BZ35Q UT WOS:A1993BZ35Q00019 ER PT J AU HENTATI, A BEJAOUI, K PERICAKVANCE, MA HENTAT, F YENHUNG, W FIGLEWICZ, DA BENHAMIDA, C BENHAMIDA, M BROWN, RH SIDDIQUE, T AF HENTATI, A BEJAOUI, K PERICAKVANCE, MA HENTAT, F YENHUNG, W FIGLEWICZ, DA BENHAMIDA, C BENHAMIDA, M BROWN, RH SIDDIQUE, T TI THE GENE LOCUS FOR ONE FORM OF JUVENILE AMYOTROPHIC-LATERAL-SCLEROSIS MAPS TO CHROMOSOME 2Q33-Q35 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. DUKE UNIV,MED CTR,DURHAM,NC 27710. INST NATL NEUROL,TUNIS,TUNISIA. MONTREAL GEN HOSP,MONTREAL H3G 1A4,QUEBEC,CANADA. NR 0 TC 1 Z9 1 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 1993 VL 64 IS 2 BP 89 EP 89 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LR187 UT WOS:A1993LR18700017 ER PT J AU KWIATKOWSKI, DJ ARMOUR, J BALE, AE FOUNTAIN, JW GOUDIE, D HAINES, JL KNOWLES, MA PILZ, A SLAUGENHAUPT, S POVEY, S AF KWIATKOWSKI, DJ ARMOUR, J BALE, AE FOUNTAIN, JW GOUDIE, D HAINES, JL KNOWLES, MA PILZ, A SLAUGENHAUPT, S POVEY, S TI REPORT ON THE 2ND INTERNATIONAL WORKSHOP ON HUMAN CHROMOSOME-9 SO CYTOGENETICS AND CELL GENETICS LA English DT Editorial Material ID GENE; LOCALIZATION; DELETIONS C1 UNIV LEICESTER,DEPT GENET,LEICESTER LE1 7RH,ENGLAND. YALE UNIV,DEPT GENET,NEW HAVEN,CT 06520. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE,ENGLAND. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. MARIE CURIE RES INST,OXTED,SURREY,ENGLAND. UNIV LONDON UNIV COLL,DEPT GENET & BIOMETRY,LONDON WC1E 6BT,ENGLAND. UNIV LONDON UNIV COLL,MRC,HUMAN BIOCHEM GENET LAB,GALTON LAB,LONDON WC1E 6BT,ENGLAND. RP KWIATKOWSKI, DJ (reprint author), BRIGHAM & WOMENS HOSP,DIV EXPTL MED,221 LONGWOOD AVE,BOSTON,MA 02115, USA. RI Haines, Jonathan/C-3374-2012 NR 20 TC 54 Z9 54 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 1993 VL 64 IS 2 BP 94 EP 103 PG 10 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LR187 UT WOS:A1993LR18700028 ER PT J AU BLUMENFELD, A SLAUGENHAUPT, SA LUCENTE, DE LIEBERT, CB AXELROD, FB MAAYAN, C MONAHAN, M OZELIUS, LJ TROFATTERL, JA HAINES, JL BREAKEFIELD, XO GUSELLA, JF AF BLUMENFELD, A SLAUGENHAUPT, SA LUCENTE, DE LIEBERT, CB AXELROD, FB MAAYAN, C MONAHAN, M OZELIUS, LJ TROFATTERL, JA HAINES, JL BREAKEFIELD, XO GUSELLA, JF TI THE GENE FOR FAMILIAL DYSAUTONOMIA IS LINKED TO CHROMOSOME-9 AND SHOWS STRONG LINKAGE DISEQUILIBRIUM WITH D9S58 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. NYU,SCH MED,DEPT PEDIAT,NEW YORK,NY 10003. HADASSAH UNIV HOSP,DEPT PEDIAT,IL-91120 JERUSALEM,ISRAEL. NR 0 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 1993 VL 64 IS 2 BP 108 EP 108 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LR187 UT WOS:A1993LR18700034 ER PT J AU HAINES, JL SHORT, MP SCHLUMPF, K GUILLEMETTE, W MURRELL, J WILSON, P SYTSMA, M BOVE, C PERICAKVANCE, M KWIATKOWSKI, DJ AF HAINES, JL SHORT, MP SCHLUMPF, K GUILLEMETTE, W MURRELL, J WILSON, P SYTSMA, M BOVE, C PERICAKVANCE, M KWIATKOWSKI, DJ TI REFINED LOCALIZATION OF TUBEROUS SCLEROSIS (TSC) GENES ON CHROMOSOME-9 AND CHROMOSOME-16 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DIV EXPTL MED,BOSTON,MA 02115. NR 0 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 1993 VL 64 IS 2 BP 114 EP 114 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LR187 UT WOS:A1993LR18700055 ER PT J AU LIEBERT, CB SLAUGENHAUPT, SA BLUMENFELD, A LUCENTE, DE GUSELLA, JF AF LIEBERT, CB SLAUGENHAUPT, SA BLUMENFELD, A LUCENTE, DE GUSELLA, JF TI IDENTIFICATION OF SIMPLE SEQUENCE REPEAT (SSR) POLYMORPHISMS ON HUMAN CHROMOSOME-9 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NR 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 1993 VL 64 IS 2 BP 116 EP 116 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LR187 UT WOS:A1993LR18700059 ER PT J AU LUCENTE, DE BLUMENFELD, A SLAUGENHAUPT, SA LIEBERT, CB MONAHAN, M TROFATTER, JA HAINES, JL GUSELLA, JF AF LUCENTE, DE BLUMENFELD, A SLAUGENHAUPT, SA LIEBERT, CB MONAHAN, M TROFATTER, JA HAINES, JL GUSELLA, JF TI A HIGH-RESOLUTION MAP OF 9Q22.3-Q33 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NR 0 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 1993 VL 64 IS 2 BP 116 EP 116 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LR187 UT WOS:A1993LR18700060 ER PT J AU OZELIUS, L KRAMER, P BRESSMAN, S HEWETT, J DELEON, D RISCH, N FAHN, S BREAKEFIELD, X AF OZELIUS, L KRAMER, P BRESSMAN, S HEWETT, J DELEON, D RISCH, N FAHN, S BREAKEFIELD, X TI DYSTONIA GENE (DYT1) ON CHROMOSOME-9Q34 APPEARS TO BE RESPONSIBLE FOR MOST EARLY-ONSET CASES SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. COLUMBIA UNIV,NEW YORK,NY 10027. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. 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 1993 VL 64 IS 2 BP 117 EP 117 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LR187 UT WOS:A1993LR18700065 ER PT J AU RUTTER, JL BANKS, LT STOTLER, CJ MCCORMICK, MK BUCKLER, AJ AF RUTTER, JL BANKS, LT STOTLER, CJ MCCORMICK, MK BUCKLER, AJ TI ISOLATION OF GENES ON HUMAN CHROMOSOME-9 USING EXON AMPLIFICATION SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. LOS ALAMOS NATL LAB,LOS ALAMOS,NM 87544. 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 1993 VL 64 IS 2 BP 119 EP 119 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LR187 UT WOS:A1993LR18700074 ER PT J AU SLAUGENHAUPT, SA BLUMENFELD, A ARNOLD, J LIEBERT, CB MULL, J LUCENTE, DE MONAHAN, M MCCORMICK, MK GUSELLA, JF AF SLAUGENHAUPT, SA BLUMENFELD, A ARNOLD, J LIEBERT, CB MULL, J LUCENTE, DE MONAHAN, M MCCORMICK, MK GUSELLA, JF TI PHYSICAL MAPPING OF THE FAMILIAL DYSAUTONOMIA GENE REGION OF HUMAN CHROMOSOME-9 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. LOS ALAMOS NATL LAB,LOS ALAMOS,NM 87544. UNIV GEORGIA,DEPT GENET,ATHENS,GA 30602. 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 1993 VL 64 IS 2 BP 120 EP 120 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LR187 UT WOS:A1993LR18700075 ER PT J AU SYLLA, BS LAMARTINE, J WANG, Q PAULY, S LENOIR, GM HABER, D SKARE, J NELSON, DL ROMEO, G TSUJI, S AF SYLLA, BS LAMARTINE, J WANG, Q PAULY, S LENOIR, GM HABER, D SKARE, J NELSON, DL ROMEO, G TSUJI, S TI CHARACTERIZATION OF AN XLP PATIENT CARRYING AN INTERSTITIAL DELETION AT XQ25 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract ID LINKED LYMPHOPROLIFERATIVE SYNDROME; FAMILY C1 IST GIANNIAN GASLINI,GENOA,ITALY. BRAIN RES INST,NIIGATA,JAPAN. INT AGCY RES CANC,F-69372 LYON,FRANCE. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BOSTON UNIV,CTR HUMAN GENET,BOSTON,MA 02215. BAYLOR COLL MED,HOUSTON,TX 77030. NR 4 TC 3 Z9 3 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 1993 VL 64 IS 3-4 BP 189 EP 189 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA LZ100 UT WOS:A1993LZ10000097 ER PT J AU CHAPLIN, D BRONSON, S DEMMER, L KOZONO, H TAILLONMILLER, P SPIES, T GERAGHTY, D AF CHAPLIN, D BRONSON, S DEMMER, L KOZONO, H TAILLONMILLER, P SPIES, T GERAGHTY, D TI DEVELOPMENT OF AN STS MAP OF THE HLA COMPLEX USING YEAST ARTIFICIAL CHROMOSOME CLONES SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. 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 1993 VL 62 IS 2-3 BP 76 EP 76 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA KP384 UT WOS:A1993KP38400003 ER PT J AU TAGLE, DA VALDES, J HINTON, L MORGAN, J BATES, G MACDONALD, M GUSELLA, J LEHRACH, H LOVETT, M COLLINS, FS AF TAGLE, DA VALDES, J HINTON, L MORGAN, J BATES, G MACDONALD, M GUSELLA, J LEHRACH, H LOVETT, M COLLINS, FS TI MAGNETIC CAPTURE OF CDNAS USING A POOL OF 6 YACS THAT SPAN THE HD CANDIDATE REGION SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 ICRF,GENOME ANAL LAB,LONDON,ENGLAND. UNIV MICHIGAN,HEREDITARY DIS FDN,COLLABORAT RES GRP,ANN ARBOR,MI 48109. UNIV MICHIGAN,MICHIGAN HUMAN GENOME CTR,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. GENELABS INC,DEPT HUMAN GENET,REDWOOD CITY,CA. MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. 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 1993 VL 62 IS 2-3 BP 86 EP 86 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA KP384 UT WOS:A1993KP38400043 ER PT J AU HAMMOND, TG MAJEWSKI, RR MORRE, DJ SCHELL, K MORRISSEY, LW AF HAMMOND, TG MAJEWSKI, RR MORRE, DJ SCHELL, K MORRISSEY, LW TI FORWARD SCATTER PULSE WIDTH SIGNALS RESOLVE MULTIPLE POPULATIONS OF ENDOSOMES SO CYTOMETRY LA English DT Article DE ENDOCYTOSIS; FLOW CYTOMETRY; KIDNEY; TOAD BLADDER; PULSE PROCESSING; VACUOLAR ATPASE; OFFSET ID FLOW-CYTOMETRY; MEMBRANE-VESICLES; DISCRIMINATION; BLADDER; CELLS; DNA AB The technique of pulse width analysis, developed to optimize cell size resolution in cell cycle kinetics, has not previously been applied to small particles such as endosomes. Offset is used to subtract a portion of the beam diameter from forward scatter pulse width signals to optimize visualization and discrimination of small particles. We identify multiple endosomal populations by offset pulse width of light scatter parameters. Specifically, linear forward scatter pulse width measurements reveal at least two populations of endosomes in the rat renal cortex, the rat renal papilla, and the luminal endothelium of the toad urinary bladder. Logarithmically amplified forward scatter pulse width measurements display the full dynamic range of these signals, resolving additional populations not manifest with linear amplification. To confirm that the endosomes observed were resolved from optical and electronic noise, we examined physiological function. The endosomes acidified after supplying ATP to the intrinsic membrane H+-ATPase present. Further, electron microscopy of sorted endosomal populations from the toad urinary bladder confirmed identity and homogeneity of the fraction. Flow cytometric analysis of endosomal populations by multiparametric techniques including pulse width analysis of structural parameters and pulse height analysis of fluorescence from entrapped fluorophores allows identification, isolation, and quantification of multiple endosomal populations. C1 UNIV WISCONSIN,CTR COMPREHENS CANC,FLOW CYTOMETRY LAB,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,NEPHROL SECT,MADISON,WI 53705. PURDUE UNIV,DEPT MED CHEM & PHARMACOGNOSY,W LAFAYETTE,IN 47907. RP HAMMOND, TG (reprint author), UNIV WISCONSIN,CTR CLIN SCI H4510,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NCI NIH HHS [P30-CA14520] NR 26 TC 21 Z9 21 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 0196-4763 J9 CYTOMETRY JI Cytometry PY 1993 VL 14 IS 4 BP 411 EP 420 DI 10.1002/cyto.990140410 PG 10 WC Biochemical Research Methods; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KZ452 UT WOS:A1993KZ45200009 PM 8513696 ER PT J AU CROOP, JM AF CROOP, JM TI P-GLYCOPROTEIN STRUCTURE AND EVOLUTIONARY HOMOLOGIES SO CYTOTECHNOLOGY LA English DT Review DE DRUG RESISTANCE; MDR; MULTIDRUG RESISTANCE; P-GLYCOPROTEIN ID MULTIDRUG-RESISTANCE GENE; CANCER CELL-LINE; BACTERIAL TRANSPORT PROTEINS; CHINESE-HAMSTER CELLS; EHRLICH ASCITES TUMOR; PLASMODIUM-FALCIPARUM; MDR-GENE; CHLOROQUINE RESISTANCE; DNA-SEQUENCES; COMPLEMENTARY-DNA AB Analysis of multidrug resistant cell lines has led to the identification of the P-glycoprotein multigene family. Two of the three classes of mammalian P-glycoproteins have the ability to confer cellular resistance to a broad range of structurally and functionally diverse cytotoxic agents. P-glycoproteins are integral membrane glycoproteins comprised of two similar halves, each consisting of six membrane spanning domains followed by a cytoplasmic domain which includes a nucleotide binding fold. The P-glycoprotein is a member of a large superfamily of transport proteins which utilize ATP to translocate a wide range of substrates across biological membranes. This superfamily includes transport complexes comprised of multicomponent systems, half P-glycoproteins and P-glycoprotein-like homologs which appear to require 12 alpha-helical transmembrane domains and two nucleotide binding folds for substrate transport. P-glycoprotein homologs have been isolated and characterized from a wide range of species. Amino acid sequences, the similarities between the halves and intron/exon boundaries have been compared to understand the evolutionary origins of the P-glycoprotein. C1 HARVARD UNIV, CHILDRENS HOSP, BOSTON, MA 02115 USA. RP HARVARD UNIV, DANA FARBER CANC INST, DIV PEDIAT ONCOL, BOSTON, MA USA. FU NCI NIH HHS [CA48162] NR 143 TC 30 Z9 30 U1 1 U2 3 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0920-9069 EI 1573-0778 J9 CYTOTECHNOLOGY JI Cytotechnology PY 1993 VL 12 IS 1-3 BP 1 EP 32 DI 10.1007/BF00744656 PG 32 WC Biotechnology & Applied Microbiology; Cell Biology SC Biotechnology & Applied Microbiology; Cell Biology GA MU790 UT WOS:A1993MU79000002 PM 7765321 ER PT J AU POWELL, SN ABRAHAM, EH AF POWELL, SN ABRAHAM, EH TI THE BIOLOGY OF RADIORESISTANCE - SIMILARITIES, DIFFERENCES AND INTERACTIONS WITH DRUG-RESISTANCE SO CYTOTECHNOLOGY LA English DT Review DE CELL CYCLE ARREST; CELL MEMBRANE; DNA REPAIR; ONCOGENE; RADIATION RESISTANCE; SIGNAL TRANSDUCTION ID DOUBLE-STRAND BREAKS; FIBROBLAST GROWTH-FACTOR; CHINESE-HAMSTER CELLS; HUMAN-TUMOR-CELLS; PROTEIN-KINASE-C; IONIZING-RADIATION SENSITIVITY; SISTER CHROMATID EXCHANGE; AORTIC ENDOTHELIAL-CELLS; RAT EMBRYO CELLS; DNA-REPAIR AB Cells and tissues have developed a variety of ways of responding to a hostile environment, be it from drugs (toxins) or radiation (summarized in Fig. 1). Three categories of radiation damage limitation are: (i) DNA repair (ii) changes in cellular metabolism (iii) changes in cell interaction (cell contact or tissue-based resistance; whole organism based resistance). DNA repair has been evaluated predominantly by the study of repair-deficient mutants. The function of the repair genes they lack is not fully understood, but some of their important interactions are now characterized. For example, the interaction of transcription factors with nucleotide excision repair is made clear by the genetic syndromes of xeroderma-pigmentosum groups B, D and G. These diseases demonstrate ultraviolet light sensitivity and general impairment of transcription: they are linked by impaired unwinding of the DNA required for both transcription and repair. The transfer of DNA into cells is sometimes accompanied by a change in sensitivity to radiation, and this is of special interest when this is the same genetic change seen in tumors. DNA repair has a close relationship with the cell cycle and cell cycle arrest in response to damage may determine sensitivity to that damage. DNA repair mechanisms in response to a variety of drugs and types of radiation can be difficult to study because of the inability to target the damage to defined sequences in vivo and the lack of a satisfactory substrate for in vitro studies. Changes in cellular metabolism as a result of ionizing radiation can impart radiation resistance, which is usually transient in vitro, but may be more significant in vivo for tissues or tumors. The mechanisms by which damage is sensed by cells is unknown. The detection of free radicals is thought likely, but distortion to DNA structure or strand breakage and a direct effect on membranes are other possibilities for which there is evidence. Changes in extracellular ATP occur in response to damage, and this could be a direct membrane effect. External purinergic receptors can then be involved in signal transduction pathways resulting in altered levels of thiol protection or triggering apoptosis. Changes in the functional level of proteins as a consequence of ionizing radiation include transcription factors, for example c-jun and c-fos; cell cycle arrest proteins such as GADD (growth arrest and DNA damage inducible proteins) and p53; growth factors such as FGF, PDGF; and other proteins leading to radioresistance. Mechanisms for intercellular resistance could be mediated by cell contact, such as gap junctions, which may help resistance to radiation in non-cycling cells. Paracrine response mechanisms, such as the release of angiogenic factors via membrane transport channels may account for tissue and tumor radiation resistance. Endocrine response mechanisms may also contribute to tissue or tumor resistance. RP POWELL, SN (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 117 TC 19 Z9 19 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0920-9069 J9 CYTOTECHNOLOGY JI Cytotechnology PY 1993 VL 12 IS 1-3 BP 325 EP 345 DI 10.1007/BF00744671 PG 21 WC Biotechnology & Applied Microbiology; Cell Biology SC Biotechnology & Applied Microbiology; Cell Biology GA MU790 UT WOS:A1993MU79000017 PM 7764455 ER PT J AU LU, XY PERKINS, LA PERRIMON, N AF LU, XY PERKINS, LA PERRIMON, N TI THE TORSO PATHWAY IN DROSOPHILA - A MODEL SYSTEM TO STUDY RECEPTOR TYROSINE KINASE SIGNAL-TRANSDUCTION SO DEVELOPMENT LA English DT Article; Proceedings Paper CT Meeting of the British-Society-for-Developmental-Biology: Signals, Polarity and Adhesion in Development CY APR, 1993 CL NORWICH, ENGLAND SP BRIT SOC DEV BIOL DE DROSOPHILA; SIGNAL TRANSDUCTION; EMBRYOGENESIS; PATTERN FORMATION ID TERMINAL REGIONS; PROTEIN-KINASE; BODY PATTERN; PHOSPHOTYROSINE PHOSPHATASE; EMBRYONIC TERMINI; BICOID PROTEIN; DORSAL PROTEIN; GENE TAILLESS; RAF; MELANOGASTER AB In the Drosophila embryo, specification of terminal cell fates that result in the formation of both the head (acron) and tail (telson) regions is under the control of the torso (tor) receptor tyrosine kinase. The current knowledge suggests that activation of tor at the egg pole initiates a signal transduction pathway that is mediated sequentially by the guanine nucleotide releasing factor son of sevenless (Sos), the p21(Ras1) GTPase, the serine/threonine kinase D-raf and the tyrosine/threonine kinase MAPKK (Dsor1). Subsequently, it is postulated that activation, possibly by phosphorylation, of a transcription factor at the egg poles activates the transcription of the terminal gap genes tailless and huckebein. These gap genes, which encode putative transcription factors, then control the expression of more downstream factors that ultimately result in head and tail differentiation. Also involved in tor signaling is the non-receptor protein tyrosine phosphatase corkscrew (csw). Here, we review the current model and discuss future research directions in this field. C1 MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,BOSTON,MA 02114. RP LU, XY (reprint author), HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT GENET,200 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 70 TC 28 Z9 28 U1 0 U2 2 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 1993 SU S BP 47 EP 56 PG 10 WC Developmental Biology SC Developmental Biology GA NP855 UT WOS:A1993NP85500007 PM 8049487 ER PT J AU JONES, SD HO, L SMITH, JC YORDAN, C STILES, CD MERCOLA, M AF JONES, SD HO, L SMITH, JC YORDAN, C STILES, CD MERCOLA, M TI THE XENOPUS PLATELET-DERIVED GROWTH-FACTOR ALPHA-RECEPTOR - CDNA CLONING AND DEMONSTRATION THAT MESODERM INDUCTION ESTABLISHES THE LINEAGE-SPECIFIC PATTERN OF LIGAND AND RECEPTOR GENE-EXPRESSION SO DEVELOPMENTAL GENETICS LA English DT Article DE PDGF; PDGF RECEPTOR; TYROSINE KINASE; GROWTH FACTOR ID CENTRAL-NERVOUS-SYSTEM; PDGF RECEPTOR; DEVELOPMENTAL EXPRESSION; KINASE FAMILY; ACTIN GENES; FACTOR-A; CELLS; PURIFICATION; MUTATION; LAEVIS AB We have cloned the Xenopus PDGF alpha receptor cDNA and have used this clone, along with cDNA encoding PDGF A, to examine their expression pattern in Xenopus embryos and to determine the factors responsible for lineage specificity. Recombinant Xenopus alpha receptor expressed in COS cells exhibits PDGF-A-dependent tyrosine kinase activity. We find that receptor mRNA is present in cultured marginal zone tissue explants and in animal cap tissue induced to form mesoderm either by grafting to vegetal tissue or by treatment with recombinant activin A. In contrast, PDGF A mRNA is expressed in cultured, untreated animal cap tissue and is suppressed by mesoderm induction. These results suggest that ectodermally produced PDGF A may act on the mesoderm during gastrulation and that mesoderm induction establishes the tissue pattern of ligand and receptor expression. C1 HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,25 SHATTUCK ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NATL INST MED RES,DEV BIOL LAB,LONDON NW7 1AA,ENGLAND. FU NICHD NIH HHS [HD28460, HD24926] NR 43 TC 27 Z9 30 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 0192-253X J9 DEV GENET JI Dev. Genet. PY 1993 VL 14 IS 3 BP 185 EP 193 DI 10.1002/dvg.1020140305 PG 9 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA LM476 UT WOS:A1993LM47600004 PM 8358864 ER PT J AU COLWELL, JA AF COLWELL, JA TI VASCULAR THROMBOSIS IN TYPE-II DIABETES-MELLITUS SO DIABETES LA English DT Editorial Material ID PLASMINOGEN-ACTIVATOR INHIBITOR-1; CARDIOVASCULAR RISK-FACTORS; HUMAN-ENDOTHELIAL-CELLS; DENSITY-LIPOPROTEIN; INSULIN RESISTANCE; ATHEROSCLEROSIS; PROINSULIN; SECRETION; INVIVO C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR, CHARLESTON, SC USA. RP COLWELL, JA (reprint author), MED UNIV S CAROLINA, DIV ENDOCRINOL DIABET & METAB, 171 ASHLEY AVE, CHARLESTON, SC 29425 USA. NR 30 TC 100 Z9 102 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0012-1797 J9 DIABETES JI Diabetes PD JAN PY 1993 VL 42 IS 1 BP 8 EP 11 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KE025 UT WOS:A1993KE02500002 PM 8420821 ER PT J AU LEAHY, JL AF LEAHY, JL TI INCREASED PROINSULIN INSULIN RATIO IN PANCREAS EXTRACTS OF HYPERGLYCEMIC RATS SO DIABETES LA English DT Article ID DEPENDENT DIABETES-MELLITUS; BETA-CELL; INTRACELLULAR DEGRADATION; CIRCULATING PROINSULIN; ELEVATED PROINSULIN; SERUM-INSULIN; GLUCOSE; ISLETS; NIDDM; DYSFUNCTION AB The plasma ratio of proinsulin/insulin is raised in people with NIDDM. A relative hypersecretion of proinsulin is thought to be the cause, because pancreas extracts from diabetic rats have a raised proinsulin/insulin ratio. We tested the hypothesis that the pancreatic proinsulin/insulin mismatch results from hyperglycemia-induced beta-cell degranulation. Normal rats made hyperglycemic with 48-h glucose infusions had a raised pancreatic percentage of proinsulin. In contrast, rats infused with enough glucose to induce compensatory hyperinsulinemia without changing the plasma glucose level had a normal percentage of proinsulin. The raised percentage of proinsulin in the hyperglycemic rats reflected a reduction in pancreatic insulin content. Administering an inhibitor of insulin release, diazoxide, to hyperglycemic rats blocked the fall in pancreatic insulin content and prevented the rise in the percentage of proinsulin. Normal rats infused with tolbutamide for 3 days and enough glucose to maintain euglycemia had a 50% reduction in pancreatic insulin content. The beta-cell degranulation from this nonhyperglycemic mechanism resulted in a raised pancreatic percentage of proinsulin. In summary, chronic hyperglycemia causes beta-cell degranulation primarily because of hyperstimulated insulin release. The net result is a rise in the ratio of immature (proinsulin-rich) to mature (insulin-rich) granules, which is reflected as an increased relative proportion of proinsulin. Mobilization of these proinsulin-enriched granules may explain the relative hypersecretion of proinsulin that occurs with diabetes. C1 NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. JOSLIN DIABET CTR,DIV RES,BOSTON,MA. HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-36836, DK-38543] NR 32 TC 37 Z9 39 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD JAN PY 1993 VL 42 IS 1 BP 22 EP 27 DI 10.2337/diabetes.42.1.22 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KE025 UT WOS:A1993KE02500004 PM 8420818 ER PT J AU KAISER, N SASSON, S FEENER, EP BOUKOBZAVARDI, N HIGASHI, S MOLLER, DE DAVIDHEISER, S PRZYBYLSKI, RJ KING, GL AF KAISER, N SASSON, S FEENER, EP BOUKOBZAVARDI, N HIGASHI, S MOLLER, DE DAVIDHEISER, S PRZYBYLSKI, RJ KING, GL TI DIFFERENTIAL REGULATION OF GLUCOSE-TRANSPORT AND TRANSPORTERS BY GLUCOSE IN VASCULAR ENDOTHELIAL AND SMOOTH-MUSCLE CELLS SO DIABETES LA English DT Article ID INSULIN-RESPONSIVE TISSUES; DEPENDENT HEXOSE-TRANSPORT; HUMAN SKELETAL-MUSCLE; DIABETIC COMPLICATIONS; PRIMARY CULTURE; NEURONAL CELLS; SOLEUS MUSCLE; RAT-BRAIN; PROTEIN; EXPRESSION AB Hyperglycemia has been implicated in the pathogenesis of both micro- and macrovascular complications in diabetes. Little is known, however, about glucose transporters and their regulation in the vascular system. In this study, the regulation of glucose transporters by glucose was examined in cultured BAECs and BSMCs, and in human arterial smooth muscle cells. Both BAECs and BSMCs transported glucose via the facilitated diffusion transport system. Glucose-transport activity in vascular smooth muscle cells was inversely and reversibly regulated by glucose. Exposure of BSMCs and HSMCs to high glucose decreased V(max) for 2DG and 3-O-MG uptake, whereas K(m) remained unchanged. The hexose-transport system of BAECs exhibited lower 2DG and 3-O-MG uptake compared with BSMCs and showed little or no adaptation to changes in ambient glucose. Northern blot analysis demonstrated that GLUT1 mRNA levels in BAECs and BSMCs were unaffected by the concentration of glucose in the medium. GLUT2-5 mRNA could not be detected by Northern blot analysis. GLUT1 protein, quantified by Western blot analysis, was more abundant in BSMCs than in BAECs and was decreased by approximately 50% when medium glucose was elevated from 1.2 to 22 mM for 24 h. The alterations in the level of GLUT1 protein correlated with the changes observed in transport activity. These observations suggest differential regulation of glucose transporter in response to glucose between smooth muscle and endothelial cells. The sites of autoregulation may involve translational control and/or the stability of the protein in the smooth muscle cells. The ability of vascular smooth muscle cells to down-regulate glucose transport in response to chronic hyperglycemia may serve as a protective mechanism against possible adverse effects of increased intracellular glucose. C1 JOSLIN DIABET CTR, DIV RES, 1 JOSLIN PL, BOSTON, MA 02215 USA. HEBREW UNIV JERUSALEM, HADASSAH MED SCH, DEPT ENDOCRINOL & METAB, IL-91010 JERUSALEM, ISRAEL. HEBREW UNIV JERUSALEM, HADASSAH MED SCH, DEPT PHARMACOL, IL-91010 JERUSALEM, ISRAEL. HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DEPT MED, BOSTON, MA 02115 USA. BETH ISRAEL HOSP, DEPT MED, BOSTON, MA 02215 USA. CASE WESTERN RESERVE UNIV, DEPT ANAT, CLEVELAND, OH 44106 USA. FU NEI NIH HHS [EY-05110]; NIDDK NIH HHS [DK-36836, P30 DK036836] NR 50 TC 189 Z9 193 U1 2 U2 13 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0012-1797 J9 DIABETES JI Diabetes PD JAN PY 1993 VL 42 IS 1 BP 80 EP 89 DI 10.2337/diabetes.42.1.80 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KE025 UT WOS:A1993KE02500011 PM 7678404 ER PT J AU DANNE, T SPIRO, MJ SPIRO, RG AF DANNE, T SPIRO, MJ SPIRO, RG TI EFFECT OF HIGH GLUCOSE ON TYPE-IV COLLAGEN PRODUCTION BY CULTURED GLOMERULAR EPITHELIAL, ENDOTHELIAL, AND MESANGIAL CELLS SO DIABETES LA English DT Article ID BASEMENT-MEMBRANE; DIABETIC CONTROL; COMPONENTS; PROTEINS; RAT; COMPLICATIONS; LAMININ AB Immunochemical and metabolic radiolabeling procedures revealed that homogeneous cultures of calf glomerular epithelial, endothelial, and mesangial cells actively synthesize type IV collagen (primarily as alpha1(IV)3) which is secreted into the medium and incorporated into the extracellular matrix. Exposure of confluent cultures of the three cell types to a high glucose concentration (30 mM) for 60 h resulted in a pronounced increase (two- to threefold) in type IV collagen production over that observed at a physiological level (5 mM) of this sugar, as determined by either immunoblotting or fluorography of electrophoretically separated media or cell-matrix components. The elevated glucose did not bring about a change in the rate of cell proliferation or fibronectin production. Moreover, studies with mannitol indicated that the stimulation of type IV collagen synthesis was not a function of hyperosmolarity. In contrast to the glomerular cells, glucose-induced enhancement of formation of this collagen was not observed in 3T3 cells despite a substantial acceleration in the consumption of this sugar. Time studies indicated that the response of the glomerular cells to high glucose occurs over an extended period (maximal at approximately 78 h) and, furthermore, that the stimulatory effect on type IV collagen production is only slowly reversed after restoration of the glucose to a normal level. We believe that these findings are relevant to an understanding of the sequence of events that lead to the development of diabetic glomerular lesions. C1 JOSLIN DIABETES CTR,ELLIOTT P JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-31315]; NIDDK NIH HHS [DK-17477] NR 31 TC 132 Z9 133 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 1993 VL 42 IS 1 BP 170 EP 177 DI 10.2337/diabetes.42.1.170 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KE025 UT WOS:A1993KE02500023 PM 8420814 ER PT J AU BONADONNA, RC SACCOMANI, MP SEELY, L ZYCH, KS FERRANNINI, E COBELLI, C DEFRONZO, RA AF BONADONNA, RC SACCOMANI, MP SEELY, L ZYCH, KS FERRANNINI, E COBELLI, C DEFRONZO, RA TI GLUCOSE-TRANSPORT IN HUMAN SKELETAL-MUSCLE - THE INVIVO RESPONSE TO INSULIN SO DIABETES LA English DT Article ID DIABETES-MELLITUS; SOMATOSTATIN; METABOLISM; DISPOSAL; KINETICS; HYPERGLYCEMIA; RESISTANCE; FOREARM; INVITRO; OBESE AB Transmembrane glucose transport plays a key role in determining insulin sensitivity. We have measured in vivo WBGU, FGU, and K(in) and K(out) of 3-0-methyl-D-glucose in forearm skeletal muscle by combining the euglycemic clamp technique, the forearm-balance technique, and a novel dual-tracer (1-[H-3]-L-glucose and 3-0-[C-14]-methyl-D-glucose) technique for measuring in vivo transmembrane transport. Twenty-seven healthy, lean subjects were studied. During saline infusion, insulin concentration, FGU (n = 6), K(in), and K(out) (n = 4) were similar to baseline. During SRIF-induced hypoinsulinemia (insulin <15 pM, n = 4) WBGU was close to 0, and FGU, K(in), and K(out) were unchanged from basal (insulin = 48 pM) values. During insulin clamps at plasma insulin levels of approximately 180 (n = 4), approximately 420 (n = 5), approximately 3000 (n = 4), and approximately 9500 pM (n = 4), WBGU was 14.2 +/- 1.3, 34.2 +/- 4.1 (P < 0.05 vs. previous step), 55.8 +/- 1.8 (P < 0.05 vs. previous step), and 56.1 +/- 6.3 mumol . min-1 . kg-1 of body weight (NS vs. previous step), respectively. Graded hyperinsulinemia concomitantly increased FGU from a basal value of 4.7 +/- 0.5 mumol . min-1 . kg-1 up to 10.9 +/- 2.3 (P < 0.05 vs. basal value), 26.6 +/- 4.5 (P < 0.05 vs. previous step), 54.8 +/- 4.3 (P < 0.05 vs. previous step), and 61.1 +/- 10.8 mumol - min-1 - kg-1 Of forearm tissues (NS vs. previous step), respectively. K(in) Of 3-O-methyl-D-glucose in forearm skeletal muscle was increased by hyperinsulinemia from a basal value of 6.6 . 10(-2) +/- 0.38 . 10(-2) to 10.0 . 10(-2) +/- 1.4 . 10(-2) (p < 0.05 vs. baseline), 17.2 . 10(-2) +/- 2.2 . 10(-2) (P < 0.05 vs. previous step), 26.3 . 10(-2) +/- 1.8 . 10(-2) (P < 0.05 vs. previous step), and 29.8 . 10(-2) +/- 5.3 . 10(-2) . min-1 (NS vs. previous step), respectively. FGU and K(in) were positively correlated (r = 0.88, P < 0.01). K(out) of 3-0-methyl-D-glucose did not change from the basal value at the lowest insulin dose (3.9 . 10(-2) +/- 1.1 . 10(-2) vs. 3.8 . 10(-2) +/- 0.33 . 10(-2) . 10(-2) . min-1, NS), but rose significantly at the following insulin steps to 6.1 . 10(-2) +/- 0.8. 10(-2), 6.9 . 10(-2) +/- 0.5 . 10(-2), and 11.9 . 10(-2) +/- 0.3 . 10(-2) . min-1 (P < 0.05 for all three vs baseline). Thus, in human skeletal muscle, in vivo, insulin stimulates K(in) and uptake of glucose in a parallel fashion, whereas SRIF-induced acute hypoinsulinemia does not seem to affect transmembrane transport or uptake of glucose. C1 UNIV PADUA,DEPT ELECTR & INFORMAT,I-35100 PADUA,ITALY. 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,METAB UNIT,VIA SAVI 8,I-56100 PISA,ITALY. FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK 24092] NR 38 TC 71 Z9 71 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD JAN PY 1993 VL 42 IS 1 BP 191 EP 198 DI 10.2337/diabetes.42.1.191 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KE025 UT WOS:A1993KE02500026 PM 8093605 ER PT J AU FOSS, MC AOKI, TT AF FOSS, MC AOKI, TT TI RESTORATION OF FUEL HOMEOSTASIS IN IDDM PATIENTS DURING PREGNANCY BY AN OPEN-LOOP INSULIN INFUSION SYSTEM SO DIABETES CARE LA English DT Article ID DIABETES-MELLITUS; GLUCOSE; MOTHERS; MALFORMATIONS; CARBOHYDRATE; METABOLISM; INFANTS; ACID; RATS AB OBJECTIVE - To characterize the effects of subcutaneous insulin pump therapy on the metabolic response (CHO and lipid oxidation, and nonoxidative glucose metabolism) to a glucose challenge of diabetic women at early pregnancy. RESEARCH DESIGN AND METHODS- Seven nondiabetic and seven IDDM pregnant patients on insulin pump therapy were studied at the first trimester. Fuel oxidation rates were determined by indirect calorimetry, and blood levels of substrates and hormones were measured before and for 2 h after ingestion of a 50 g oral glucose load. RESULTS- The increments in npRQ and CHO oxidation rates after the glucose meals m the diabetic women on insulin pump therapy were similar to those in the normal subjects. The glucose disposal data during the 2 h of the studies revealed that die amounts of oxidative and nonoxidative glucose utilization in the control subjects and in the IDDM patients on insulin pump therapy did not show significant differences. CONCLUSIONS - This investigation demonstrated that the treatment of IDDM patients during early pregnancy by an open-loop insulin infusion system is sufficient to normalize their glucose-processing capability with respect to cellular oxidative and nonoxidative glucose metabolism in response to an oral glucose challenge, but some abnormalities in their blood profiles of glucose, lactate, and pyruvate persisted. C1 UNIV CALIF DAVIS,DEPT INTERNAL MED,DAVIS,CA 95616. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. RP FOSS, MC (reprint author), USP,SCH MED RIBEIRAO PRETO,DEPT MED,BR-14049 RIBEIRAO PRE,SP,BRAZIL. FU NIADDK NIH HHS [AM-20530, AM-15191] NR 36 TC 0 Z9 0 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JAN PY 1993 VL 16 IS 1 BP 103 EP 109 DI 10.2337/diacare.16.1.103 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KE571 UT WOS:A1993KE57100017 PM 8422762 ER PT J AU MATHEWS, CHE DETMER, K LAWRENCE, HJ LARGMAN, C AF MATHEWS, CHE DETMER, K LAWRENCE, HJ LARGMAN, C TI EXPRESSION OF THE HOX-2.2 HOMEOBOX GENE IN MURINE EMBRYONIC EPIDERMIS SO DIFFERENTIATION LA English DT Article ID RESTRICTED EXPRESSION; MOUSE CHROMOSOME-11; PATTERN-FORMATION; RETINOIC ACID; BOX GENE; COMPLEX; DROSOPHILA; HOMEODOMAIN; SEQUENCE; PROTEIN AB The expression of the Hox 2.2 gene was studied in mouse fetal skin by in situ hybridization with an anti-sense RNA probe derived from the homeobox region of this gene. In contrast to the expression of Hox 2.2 in spinal cord, which is strongest in 11-day embryos, and is greatly diminished by day 14 and day 17, the signal for Hox 2.2 in skin could be not be detected in 11-day epidermis, was barely detectable on day 14, became strong on day 17, and decreased in new-born animals (day 19). RNase protection assays using Hox 2.2 homeobox-containing and 3' flanking region probes confirmed that the signals detected in 17-day fetal skin by in situ hybridization represent Hox 2.2 transcripts, and that the message is expressed throughout the day 15 to day 18 period during which the epidermis is undergoing terminal differentiation. RNase protection analysis also revealed two alternatively spliced forms of the Hox 2.2 mRNA are present throughout fetal skin development. Northern gel analysis of 17-day fetal skin using a Hox 2.2 homeobox-containing probe at high stringency showed two bands of 1.6 and 1.9 kb, respectively. The 1.9 kb band was greatly enhanced by hybridization at reduced stringency, suggesting the expression of additional homeobox genes with homology to Hox 2.2. These results suggest that the Hox 2.2 homeobox gene plays a role in epidermal development. C1 SAN FRANCISCO VA MED CTR,4150 CLEMENT ST,SAN FRANCISCO,CA 94121. UC DAVIS,SCH MED,DEPT INTERNAL MED,DAVIS,CA. NR 45 TC 19 Z9 19 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD JAN PY 1993 VL 52 IS 2 BP 177 EP 184 DI 10.1111/j.1432-0436.1993.tb00628.x PG 8 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA KN788 UT WOS:A1993KN78800006 PM 8097172 ER PT J AU NELSON, DR KAMATAKI, T WAXMAN, DJ GUENGERICH, FP ESTABROOK, RW FEYEREISEN, R GONZALEZ, FJ COON, MJ GUNSALUS, IC GOTOH, O OKUDA, K NEBERT, DW AF NELSON, DR KAMATAKI, T WAXMAN, DJ GUENGERICH, FP ESTABROOK, RW FEYEREISEN, R GONZALEZ, FJ COON, MJ GUNSALUS, IC GOTOH, O OKUDA, K NEBERT, DW TI THE P450 SUPERFAMILY - UPDATE ON NEW SEQUENCES, GENE-MAPPING, ACCESSION NUMBERS, EARLY TRIVIAL NAMES OF ENZYMES, AND NOMENCLATURE SO DNA AND CELL BIOLOGY LA English DT Review ID LIVER MICROSOMAL CYTOCHROME-P-450; AMINO-ACID-SEQUENCE; PHENOBARBITAL-INDUCIBLE CYTOCHROME-P-450; CHAIN CLEAVAGE ENZYME; CONGENITAL ADRENAL-HYPERPLASIA; STEROID 21-HYDROXYLASE GENES; RAT HEPATIC CYTOCHROME-P-450; CDNA-DIRECTED EXPRESSION; ENCODING HUMAN AROMATASE; OMEGA-HYDROXYLASE CYTOCHROME-P-450 AB We provide here a list of 221 P450 genes and 12 putative pseudogenes that have been characterized as of December 14, 1992. These genes have been described in 31 eukaryotes (including 11 mammalian and 3 plant species) and 11 prokaryotes. Of 36 gene families so far described, 12 families exist in all mammals examined to date. These 12 families comprise 22 mammalian subfamilies, of which 17 and 15 have been mapped in the human and mouse genome, respectively. To date, each subfamily appears to represent a cluster of tightly linked genes. This revision supersedes the previous updates [Nebert et al., DNA 6, 1-11, 1987; Nebert et al., DNA 8, 1-13, 1989; Nebert et al., DNA Cell Biol. 10, 1-14 (1991)] in which a nomenclature system, based on divergent evolution of the superfamily, has been described. For the gene and cDNA, 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. ''P'' (''p'' in mouse) after the gene number denotes a pseudogene. If a gene is the sole member of a family, the subfamily letter and gene number need not be included. We suggest that the human nomenclature system be used for all species other than mouse. The mRNA and enzyme in all species (including mouse) should include all capital letters, without italics or hyphens. This nomenclature system is identical to that proposed in our 1991 update. Also included in this update is a listing of available data base accession numbers for P450 DNA and protein sequences. We also discuss the likelihood that this ancient gene superfamily has existed for more than 3.5 billion years, and that the rate of P450 gene evolution appears to be quite nonlinear. Finally, we describe P450 genes that have been detected by expressed sequence tags (ESTs), as well as the relationship between the P450 and the nitric oxide synthase gene superfamilies, as a likely example of convergent evolution. C1 UNIV CINCINNATI,MED CTR,DEPT ENVIRONM HLTH,CINCINNATI,OH 45267. UNIV CINCINNATI,MED CTR,CTR ENVIRONM GENET,CINCINNATI,OH 45267. UNIV N CAROLINA,DEPT BIOCHEM & BIOPHYS,CHAPEL HILL,NC 27599. HOKKAIDO UNIV,FAC PHARMACEUT SCI,SAPPORO,HOKKAIDO 060,JAPAN. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. VANDERBILT UNIV,MED CTR,SCH MED,DEPT BIOCHEM,NASHVILLE,TN 37232. VANDERBILT UNIV,MED CTR,SCH MED,CTR MOLEC TOXICOL,NASHVILLE,TN 37232. UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235. UNIV ARIZONA,DEPT ENTOMOL,TUCSON,AZ 85721. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. UNIV MICHIGAN,DEPT BIOL CHEM,ANN ARBOR,MI 48109. UNIV ILLINOIS,DEPT BIOCHEM,URBANA,IL 61801. SAITAMA CANC CTR,INA,SAITAMA 362,JAPAN. HIROSHIMA UNIV,SCH DENT,DEPT BIOCHEM,HIROSHIMA 734,JAPAN. RI Feyereisen, Rene/I-3140-2012; OI Feyereisen, Rene/0000-0002-9560-571X; Nelson, David/0000-0003-0583-5421 FU NIEHS NIH HHS [P30 ES06096] NR 614 TC 1557 Z9 1602 U1 10 U2 110 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 1993 VL 12 IS 1 BP 1 EP 51 DI 10.1089/dna.1993.12.1 PG 51 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA KL191 UT WOS:A1993KL19100001 PM 7678494 ER PT J AU DELAMAZA, MS HEMADY, RK FOSTER, CS AF DELAMAZA, MS HEMADY, RK FOSTER, CS TI INFECTIOUS SCLERITIS - REPORT OF 4 CASES SO DOCUMENTA OPHTHALMOLOGICA LA English DT Article DE ANTIMICROBIAL THERAPY; CORNEOSCLERITIS; INFECTION; SCLERAL BIOPSY; SCLERITIS ID ACANTHAMOEBA KERATITIS; LYME-DISEASE; NECROTIZING SCLERITIS; PSEUDOMONAS KERATITIS; LENS WEARERS; EPISCLERITIS; MANIFESTATIONS; SCLEROKERATITIS; CORNEOSCLERITIS; ARTHRITIS AB While systemic autoimmune diseases are the main possibilities in the differential diagnosis of scleritis, other less common etiologies such as infections must also be considered. The authors report four cases of infectious scleritis to review predisposing factors, clinical characteristics, methods of diagnostic approach, and response to therapy. Two patients had primary scleritis and two patients had secondary scleritis following extension of primary corneal infection (corneoscleritis). Diagnoses included three local infections (one each with Staphylococcus. Acanthamoeba, and herpes simplex) and one systemic infection (Lyme disease). Stains, cultures, or immunologic studies from scleral, conjunctival, and/or corneal tissues, and serologic tests were used to make the diagnosis. Medical therapy, including antimicrobial agents, was instituted in all patients, and surgical procedures were additionally required in two patients (scleral grafting in one and two penetrating keratoplasties in another); the patient who required two penetrating keratoplasties had corneoscleritis and underwent eventual enucleation. Infectious agents should be considered in the differential diagnosis of scleritis. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,OCULAR IMMUNOL SERV,BOSTON,MA 02114. NR 47 TC 25 Z9 26 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0012-4486 J9 DOC OPHTHALMOL JI Doc. Ophthalmol. PY 1993 VL 83 IS 1 BP 33 EP 41 PG 9 WC Ophthalmology SC Ophthalmology GA LF650 UT WOS:A1993LF65000003 ER PT J AU FOSTER, CS WU, HK MERCHANT, A AF FOSTER, CS WU, HK MERCHANT, A TI SYSTEMIC (SERUM) SOLUBLE INTERLEUKIN-2 RECEPTOR LEVELS IN CORNEAL TRANSPLANT RECIPIENTS SO DOCUMENTA OPHTHALMOLOGICA LA English DT Article DE CORNEAL TRANSPLANT; REJECTION; SOLUBLE INTERLEUKIN-2 RECEPTOR ID ALLOGRAFT-REJECTION AB Elevated soluble interleukin-2 receptor levels (sIL-2R), a measure of T cell activation, have been used as a serum marker for early rejection in solid organ transplant patients. In this preliminary study, we measured sequential sIL-2R levels of 53 otherwise immunologically normal corneal transplant recipients. Eleven of these transplants rejected; sIL-2R was significantly elevated during the acute rejection episode, compared to pre-rejection and post-rejection levels (p = 0.01). Five patients' sIL-2R rose one to nine months prior to rejection. These data indicate that sIL-2R levels may correlate with corneal graft rejection and may be predictive of impending rejection. A larger prospective study with many immunologically normal patients and careful monitoring of sIL-2R levels prior to and during the acute rejection episode will be necessary to determine the value of sIL-2R monitoring as a predictive tool for corneal graft rejection. RP FOSTER, CS (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,MOLEC MED SERV,HILLS IMMUNOL LAB,BOSTON,MA 02114, USA. NR 23 TC 8 Z9 8 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0012-4486 J9 DOC OPHTHALMOL JI Doc. Ophthalmol. PY 1993 VL 83 IS 1 BP 83 EP 90 DI 10.1007/BF01203574 PG 8 WC Ophthalmology SC Ophthalmology GA LF650 UT WOS:A1993LF65000009 PM 8334924 ER PT S AU WENNBERG, JE BARRY, MJ FOWLER, FJ MULLEY, A AF WENNBERG, JE BARRY, MJ FOWLER, FJ MULLEY, A BE Warren, KS Mosteller, F TI OUTCOMES RESEARCH, PORTS, AND HEALTH-CARE REFORM SO DOING MORE GOOD THAN HARM: THE EVALUATION OF HEALTH CARE INTERVENTIONS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Doing More Good Than Harm: The Evaluation of Health Care Interventions CY MAR 22-25, 1993 CL NEW YORK, NY SP NEW YORK ACAD SCI, L W FROHLICH CHARITABLE TRUST ID BENIGN PROSTATIC HYPERPLASIA; TRANS-URETHRAL RESECTION; MORTALITY; PROSTATECTOMY; REOPERATION C1 MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,BOSTON,MA 02119. UNIV MASSACHUSETTS,SURVEY RES CTR,BOSTON,MA 02125. RP WENNBERG, JE (reprint author), DARTMOUTH COLL SCH MED,CTR EVALUAT CLIN SCI,HANOVER,NH 03755, USA. NR 14 TC 48 Z9 49 U1 0 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-833-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 703 BP 52 EP 62 DI 10.1111/j.1749-6632.1993.tb26335.x PG 11 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA BA22S UT WOS:A1993BA22S00009 PM 8192318 ER PT J AU LIPTON, SA AF LIPTON, SA TI HIV-RELATED NEURONAL INJURY - PREVENTION BY CA2+ CHANNEL AND NMDA ANTAGONISTS SO DRUGS IN DEVELOPMENT LA English DT Proceedings Paper CT Investigators Meeting on CA2-Plus Antagonists in the Central Nervous System CY APR 01-04, 1992 CL SANTA FE, NM SP MILES INST PRECLIN PHARM DE AIDS; DEMENTIA; HIV-1; N-METHYL-D-ASPARTATE RECEPTOR; VOLTAGE-DEPENDENT CALCIUM CHANNELS ID RECEPTOR-MEDIATED NEUROTOXICITY; AMINO-ACID NEUROTOXICITY; COAT PROTEIN; CEREBROSPINAL-FLUID; QUINOLINIC ACID; NERVOUS-SYSTEM; FRONTAL-CORTEX; INFECTION; AIDS; BRAINS C1 CHILDRENS HOSP MED CTR,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. NR 21 TC 0 Z9 0 U1 0 U2 0 PU NEVA PRESS PI BRANFORD PA P O BOX 347, BRANFORD, CT 06405 SN 1066-7008 J9 DRUG DEV JI Drug. Dev. PY 1993 VL 2 BP 127 EP 134 PG 8 GA MV625 UT WOS:A1993MV62500014 ER PT J AU FAUX, SF MCCARLEY, RW NESTOR, PG SHENTON, ME POLLAK, SD PENHUNE, V MONDROW, E MARCY, B PETERSON, A HORVATH, T DAVIS, KL AF FAUX, SF MCCARLEY, RW NESTOR, PG SHENTON, ME POLLAK, SD PENHUNE, V MONDROW, E MARCY, B PETERSON, A HORVATH, T DAVIS, KL TI P300 TOPOGRAPHIC ASYMMETRIES ARE PRESENT IN UNMEDICATED SCHIZOPHRENICS SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE AUDITORY EVENT-RELATED POTENTIALS; P300; SCALP TOPOGRAPHY; NEUROLEPTICS; SCHIZOPHRENIA ID EVENT-RELATED POTENTIALS; BRAIN ELECTRICAL-ACTIVITY; CEREBRAL BLOOD-FLOW; EVOKED-POTENTIALS; NEGATIVE SYMPTOMS; ABNORMALITIES; AUDITORY-P3; VOLUME; STATE; DRUG AB Our laboratory has repeatedly found a left < right auditory P300 temporal lobe topographic asymmetry in right-handed, medicated schizophrenics. To determine whether this asymmetry was attributable to the effects of antipsychotic medications, we collected auditory ''odd-ball'' P300 event-related potentials from 14 right-handed, unmedicated schizophrenics (withdrawn from medication for an average of 21 days) and 14 right-handed, normal controls. Analysis of normalized P300 amplitudes showed a statistically significant difference in the voltage distributions between groups (a group by temporal electrode site interaction) that was consistent with a left < right temporal voltage asymmetry in schizophrenics but not in the normal controls. We conclude that P300 topographic asymmetries are present in unmedicated schizophrenics. These data are compatible with the growing body of data suggesting left temporal lobe structural abnormalities in schizophrenia. C1 BRONX VET ADM MED CTR,DEPT PSYCHIAT,BRONX,NY. MT SINAI MED SCH,BRONX,NY. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BROCKTON,MA. BROCKTON VA MED CTR,BROCKTON,MA. MASSACHUSETTS MENTAL HLTH CTR,BROCKTON,MA. RI Pollak, Seth/G-2345-2011; McCarley, Robert/N-5562-2014 OI McCarley, Robert/0000-0001-5705-7495 FU NIMH NIH HHS [MHK-K01-MH00746-02, NIMH 40799, T32MH16259] NR 42 TC 76 Z9 76 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD JAN-FEB PY 1993 VL 88 IS 1 BP 32 EP 41 DI 10.1016/0168-5597(93)90026-L PG 10 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA KK845 UT WOS:A1993KK84500005 PM 7681389 ER PT J AU ABDI, K LI, XP MENTZER, SJ AF ABDI, K LI, XP MENTZER, SJ TI SEMIDRY PHASTTRANSFER DETECTION OF BIOTINYLATED CELL-SURFACE MOLECULES SO ELECTROPHORESIS LA English DT Article ID POLYACRYLAMIDE GEL-ELECTROPHORESIS; PROTEINS; PHASTSYSTEM; ANTIGENS; LFA-1 AB The PhastTransfer system is a semi-dry electrophoretic unit designed to optimize the transfer of small amounts of protein. Because of its efficiency, we adapted the PhastTransfer system for the detection of labeled membrane molecules. Biotin was used as the membrane molecule label because it permitted the long-term storage of labeled lysates as well as the flexibility of derivatizing several different functional groups. After immunoaffinity separation using magnetic microspheres, the protein was electrophoretically separated with the PhastSystem and transferred with the PhastTransfer unit. Using an avidin-linked enzyme amplification system, less than 10 ng of loaded protein could be detected on the transfer membrane. Based on these findings, the PhastTransfer system is a fast, reproducible, and convenient method for the transfer of small quantities of labeled cell surface protein. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,75 FRANCIS ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NHLBI NIH HHS [HL47078] NR 19 TC 7 Z9 7 U1 0 U2 2 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD JAN-FEB PY 1993 VL 14 IS 1-2 BP 73 EP 77 DI 10.1002/elps.1150140113 PG 5 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA KT849 UT WOS:A1993KT84900012 PM 8462519 ER PT J AU VANTVEER, LJ BEIJERSBERGEN, RL BERNARDS, R AF VANTVEER, LJ BEIJERSBERGEN, RL BERNARDS, R TI N-MYC SUPPRESSES MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I GENE-EXPRESSION THROUGH DOWN-REGULATION OF THE P50 SUBUNIT OF NF-KAPPA-B SO EMBO JOURNAL LA English DT Article DE MHC CLASS-I; NEUROBLASTOMA; NF-ALEPH-B/N-MYC ID DNA-BINDING SUBUNIT; TRANSCRIPTION FACTORS; NUCLEAR FACTOR; P65 SUBUNIT; ENHANCER; PROTEIN; SEQUENCE; REL; INHIBITION; PROMOTER AB In neuroblastoma, N-myc suppresses the expression of major histocompatibility complex (MHC) Class I antigens by reducing the binding of a nuclear factor to the enhancer-A element in the MHC Class I gene promoter. We show here that the p50 subunit of NF-kappaB is part of this complex and that expression of p50 mRNA is suppressed by N-myc. Transfection of a p50 expression vector in neuroblastoma cells that express N-myc at a high level leads to restoration of factor binding to the MHC Class I gene enhancer, restores enhancer activity and leads to re-expression of MHC Class I antigens at the cell surface. These data indicate that the p50 subunit of NF-kappaB is involved in the regulation of MHC Class I antigen expression and that N-myc down-regulates MHC Class I gene expression primarily through suppression of p50 expression. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP VANTVEER, LJ (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC GENET,149 13TH ST,BOSTON,MA 02129, USA. OI Bernards, Rene/0000-0001-8677-3423 NR 35 TC 58 Z9 58 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD JAN PY 1993 VL 12 IS 1 BP 195 EP 200 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KG621 UT WOS:A1993KG62100021 PM 8428579 ER PT J AU GACZYNSKA, M ROCK, KL GOLDBERG, AL AF GACZYNSKA, M ROCK, KL GOLDBERG, AL TI ROLE OF PROTEASOMES IN ANTIGEN PRESENTATION SO ENZYME & PROTEIN LA English DT Article DE PROTEOLYSIS; ANTIGEN PRESENTATION; MAJOR HISTOCOMPATIBILITY COMPLEX ID TOXIC LYMPHOCYTES-T; CLASS-I; CELL BIOLOGY; PROTEIN; ATP; DEGRADATION; PROTEOLYSIS; UBIQUITIN; IDENTIFICATION; MOLECULE AB Recent studies have demonstrated that the proteasome, in addition to functioning in the complete degradation of cell proteins, is the source of most antigenic peptides presented to the immune system on major histocompatibility complex (MHC)-class I molecules. In this process, intracellular and viral proteins are degraded in the cytosol to 8- to 9-amino acid fragments, which are then transported into the endoplasmic reticulum, where they become associated with MHC-class I molecules and are thus delivered to the cell surface. A variety of evidence has shown that the proteasome and ATP-ubiquitin-dependent pathway are critical in this process: (1) In cells, selective inhibitors of proteasome function inhibit the bulk of protein degradation and thus prevent the generation of peptides necessary for class I presentation and the appearance of MHC on the cell surface. (2) Mutations that block ubiquitin conjugation prevent the generation of an antigenic peptide. (3) Modifications that lead to rapid degradation of a protein by the ubiquitin pathway enhance antigen presentation. (4) gamma-Interferon (gamma-IFN) induces new proteasome subunits, LMP2 and LMP7, encoded in the MHC region that are incorporated in place of constitutive proteasome subunits. Their incorporation does not affect rates of protein breakdown but causes changes in peptidase activities, i.e. they increase rates of cleavage after basic and hydrophobic residues and decrease cleavage after acidic residues. Transfections of cells with LMP2 or LMP7 cause similar changes in these peptidase activities as are caused by gamma-IFN. These modifications in peptidase activities should enhance the production of those types of peptides which are preferentially transported into endoplasmic reticulum and selectively bound to MHC-class I molecules. C1 HARVARD UNIV,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA. RP GACZYNSKA, M (reprint author), HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115, USA. NR 38 TC 51 Z9 51 U1 3 U2 6 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1019-6773 J9 ENZYME PROTEIN JI Enzyme Protein PY 1993 VL 47 IS 4-6 BP 354 EP 369 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PY959 UT WOS:A1993PY95900017 PM 7697133 ER PT J AU ANTMAN, KH AF ANTMAN, KH TI GM-CSF IN MARROW TRANSPLANTATION SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID COLONY-STIMULATING FACTOR; CIRCULATING HEMATOPOIETIC PROGENITORS; HIGH-DOSE CYCLOPHOSPHAMIDE; STEM-CELL TRANSPLANTATION; TOTAL-BODY IRRADIATION; LARGE-SCALE COLLECTION; BONE-MARROW; CANCER-PATIENTS; AUTOLOGOUS TRANSPLANTATION; BREAST-CANCER AB Bone marrow transplantation (BMT) is being increasingly used in a wide variety of diseases. During the period of re-engraftment the patient is particularly susceptible to a number of opportunistic infections which can radically affect acute morbidity and mortality. Recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) has been shown to mobilise haemopoietic progenitor cells for use after high-dose therapy, to enhance myeloid engraftment and stimulate mature monocytes/macrophages and neutrophils. Evidence is emerging that GM-CSF may be useful in BMT. A review of clinical trials in patients receiving BMT has revealed that the administration of rhGM-CSF significantly reduces the duration to re-engraftment, number of antibiotic treatment days, and the period of hospitalisation. Thus, rhGM-CSF appears to be a useful adjunct to BMT. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ANTMAN, KH (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED ONCOL,BOSTON,MA 02115, USA. NR 53 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 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1993 VL 29A SU 3 BP S2 EP S6 DI 10.1016/0959-8049(93)90623-N PG 5 WC Oncology SC Oncology GA LP531 UT WOS:A1993LP53100002 PM 8398365 ER PT J AU CRAIG, W AF CRAIG, W TI PHARMACODYNAMICS OF ANTIMICROBIAL AGENTS AS A BASIS FOR DETERMINING DOSAGE REGIMENS SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT SYMP ON DEVELOPMENTS IN THE TREATMENT OF INFECTIOUS DISEASES, IN HONOR OF MARC F MICHEL CY OCT 30-31, 1991 CL ROTTERDAM, NETHERLANDS ID THIGH-INFECTION AB Pharmacodynamic parameters, such as the rate of bactericidal activity with increasing drug concentrations, post-antibiotic effect, sub-MIC effects, post-antibiotic leukocyte enhancement and first-exposure effect, more accurately describe the time course of antimicrobial activity than the MIC and MBC. Aminoglycosides and quinolones exhibit concentration-dependent killing and induce prolonged post-antibiotic effects. The amount of drug rather than the dosing frequency determines the efficacy of these drugs. However, high peak levels can reduce the emergence of resistance, and once-daily dosing of aminoglycosides can also reduce nephrotoxicity and ototoxicity. On the other hand, beta-lactam antibiotics show time-dependent killing and produce prolonged post-antibiotic effects only with staphylococci. The frequency of drug administration is an important determinant of outcome for these drugs, as the duration of time serum levels exceed the MIC is the major determinant of efficacy. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP CRAIG, W (reprint author), UNIV WISCONSIN,DEPT MED,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 10 TC 42 Z9 42 U1 1 U2 2 PU FRIEDR VIEWEG SOHN VERLAG GMBH PI WIESBADEN 1 PA PO BOX 5829, W-6200 WIESBADEN 1, GERMANY SN 0934-9723 J9 EUR J CLIN MICROBIOL JI Eur. J. Clin. Microbiol. Infect. Dis. PY 1993 VL 12 SU 1 BP 6 EP 8 PG 3 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA KX959 UT WOS:A1993KX95900003 ER PT J AU RUBIN, RH AF RUBIN, RH TI FUNGAL AND BACTERIAL-INFECTIONS IN THE IMMUNOCOMPROMISED HOST SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT SYMP ON DEVELOPMENTS IN THE TREATMENT OF INFECTIOUS DISEASES, IN HONOR OF MARC F MICHEL CY OCT 30-31, 1991 CL ROTTERDAM, NETHERLANDS ID IMMUNODEFICIENCY AB As the number of immunocompromised patients increases due to the spread of the AIDS epidemic and the successes being achieved with transplantation, cancer chemotherapy and immunosuppressive therapy, increased attention is being turned to the prevention and treatment of the infections that afflict these individuals. The risk of infection in these patients is determined by the interaction between the epidemiologic exposures that the patient experiences and the net state of immunosuppression (the greater the exposure, the greater the chances of infection even in an immunologically competent individual; the greater the net state of immunosuppression, the greater the chances of infection even with minimal exposures). The bacterial and fungal infections that affect these patients are reviewed and strategies of antimicrobial management defined, recognizing that there are three modes of use of antimicrobial agents in these patients: therapeutic administration to treat dinical infection, and prophylactic and pre-emptive administration to prevent or abort clinical infection. These last two are of particular importance in this patient population because the prime aim of the infectious disease clinician in dealing with these problems is the prevention of clinical disease. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP RUBIN, RH (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 11 TC 16 Z9 16 U1 0 U2 0 PU FRIEDR VIEWEG SOHN VERLAG GMBH PI WIESBADEN 1 PA PO BOX 5829, W-6200 WIESBADEN 1, GERMANY SN 0934-9723 J9 EUR J CLIN MICROBIOL JI Eur. J. Clin. Microbiol. Infect. Dis. PY 1993 VL 12 SU 1 BP 42 EP 48 DI 10.1007/BF02389877 PG 7 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA KX959 UT WOS:A1993KX95900010 ER PT J AU CRAIG, W AF CRAIG, W TI RELEVANCE OF ANIMAL-MODELS FOR CLINICAL TREATMENT SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT SYMP ON DEVELOPMENTS IN THE TREATMENT OF INFECTIOUS DISEASES, IN HONOR OF MARC F MICHEL CY OCT 30-31, 1991 CL ROTTERDAM, NETHERLANDS ID PSEUDOMONAS-AERUGINOSA; ANTIBIOTIC-THERAPY; INFECTIONS; THIGH; MICE AB The use of animal models has become an integral part of the evaluation of drugs for antimicrobial chemotherapy. Animal models can be used to define the penetration of antimicrobial agents at foci of infections, the time course of in vivo antimicrobial therapy, dose-response relationships, and the influence of therapy on the pathophysiologic consequences of infection. Animal models have been useful in the delineation of many of the basic principles currently used in clinical practice and in the selection of new agents and new therapeutic approaches for clinical trials in humans. In spite of the many positive aspects of animal models, several problems, such as altered pharmacokinetics in animals, can preclude direct application of results to clinical practice. Studies in animal models cannot replace the need for human dinical trials. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP CRAIG, W (reprint author), UNIV WISCONSIN,DEPT MED,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 15 TC 13 Z9 13 U1 0 U2 0 PU FRIEDR VIEWEG SOHN VERLAG GMBH PI WIESBADEN 1 PA PO BOX 5829, W-6200 WIESBADEN 1, GERMANY SN 0934-9723 J9 EUR J CLIN MICROBIOL JI Eur. J. Clin. Microbiol. Infect. Dis. PY 1993 VL 12 SU 1 BP 55 EP 57 PG 3 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA KX959 UT WOS:A1993KX95900012 ER PT J AU GALVIN, F FREEMAN, GJ RAZIWOLF, Z BENACERRAF, B NADLER, L REISER, H AF GALVIN, F FREEMAN, GJ RAZIWOLF, Z BENACERRAF, B NADLER, L REISER, H TI EFFECTS OF CYCLOSPORINE-A, FK-506, AND MYCALAMIDE-A ON THE ACTIVATION OF MURINE-CD4+ T-CELLS BY THE MURINE B7-ANTIGEN SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Note DE B7; COSTIMULATORY SIGNALS; CYCLOSPORINE-A; FK-506; MYCALAMIDE-A ID COSTIMULATORY SIGNAL; INTERLEUKIN-2; PROLIFERATION; STREPTOMYCES; CYCLOPHILIN; ANTIGEN-B7; RECEPTOR; PATHWAY AB The murine B7 (mB7) protein is a potent co-stimulatory molecule for the activation of murine CD4+ T cells. We have previously shown that stable mB7-transfected Chinese hamster ovary (CHO) cells synergize with either anti-CD3 monoclonal antibodies (mAb) or concanavalin A to stimulate T cell activation. In addition, mB7 can synergize with phorbol 12-myristate 13-acetate (PMA) to induce T cell activation in an alternative pathway. In the present report we describe the effects of three immunosuppressive drugs, cyclosporin A (CsA), FK 506, and mycalamide A on mB7-mediated T cell activation. The immunophilin ligands CsA and FK 506 block activation of murine CD4+ T cells by the combination of anti-CD3 mAb and CHO-mB7 cells but do not affect activation by CHO-mB7 cells and PMA. These results support the relevance of pharmacological studies of immunosuppressive compounds in the murine model prior to their application in man. In contrast to the effects of CsA and FK 506, mycalamide A blocks activation of murine CD4+ T cells by anti-CD3 mAb and mB7 as well as activation by mB7 and PMA. On a molar basis, mycalamide A appears to be at least 10-fold more potent than FK 506 which is 100-fold more potent than CsA. Because of its effects on multiple activation pathways and because of its potency. mycalamide A could have considerable therapeutic potential. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GYNAKOL ENDOKRINOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA-40216, CA-46967]; NIAID NIH HHS [AI-30169] NR 23 TC 44 Z9 45 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 JAN PY 1993 VL 23 IS 1 BP 283 EP 286 DI 10.1002/eji.1830230145 PG 4 WC Immunology SC Immunology GA KJ132 UT WOS:A1993KJ13200044 PM 7678228 ER PT B AU JONES, RC AF JONES, RC BE Bishop, JE Evans, TW Laurent, GJ TI ROLE OF INTERSTITIAL FIBROBLASTS AND INTERMEDIATE CELLS IN MICROVASCULAR WALL REMODELING IN PULMONARY-HYPERTENSION SO EUROPEAN RESPIRATORY REVIEW, VOL 3, REVIEW NO 16, OCTOBER 1993: PROCEEDINGS OF AN INTERNATIONAL CONFERENCE ON THE PULMONARY VASCULATURE IN HEALTH AND DISEASE LA English DT Proceedings Paper CT International Conference on the Pulmonary Vasculature in Health and Disease CY SEP 07-09, 1992 CL NATL HEART & LUNG INST, LONDON, ENGLAND SP BRIT HEART FDN, CORDA, COSTAR, FLEXCELL CORP, GARFIELD WESTON TRUST, GLASO, ICI AMERICAS INC, LILLY RES LABS, PHARMACIA BIOSYST LTD, PORTLAND PRESS, WELLCOME FDN, WELLCOME TRUST HO NATL HEART & LUNG INST DE HYPEROXIA; LUNG MICROVESSELS; NEOMUSCULARIZATION; VASCULAR CELL PHENOTYPE C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,MOLEC & CELL BIOL UNIT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MUNKSGAARD PI COPENHAGEN K PA 35 NORRE SOGADE POSTBOX 2148, DK-1016 COPENHAGEN K, DENMARK PY 1993 BP 569 EP 575 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System SC Cardiovascular System & Cardiology; Respiratory System GA BA06Y UT WOS:A1993BA06Y00008 ER PT J AU NEBEN, S HEMMAN, S MONTGOMERY, M FERRARA, J MAUCH, P AF NEBEN, S HEMMAN, S MONTGOMERY, M FERRARA, J MAUCH, P TI HEMATOPOIETIC STEM-CELL DEFICIT OF TRANSPLANTED BONE-MARROW PREVIOUSLY EXPOSED TO CYTOTOXIC AGENTS SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE DONOR MARROW; CYTOTOXIC AGENTS; HEMATOPOIETIC STEM CELL TRANSPLANTATION; LONG-TERM HEMATOPOIESIS; PRIMITIVE STEM CELLS ID SELF-RENEWAL CAPACITY; COLONY-FORMING-UNITS; CFU; REPOPULATION; MICE AB High-dose chemotherapy and/or total body irradiation followed by autologous bone marrow rescue has improved the survival of patients with a variety of malignancies. Candidates for autologous bone marrow transplantation (ABMT) often have received prior exposure to cytotoxic agents, some of which may damage primitive stem cells. We have developed an in vivo murine model to evaluate the effects of a number of individual cytotoxic agents on the ability of syngeneic donor marrow to provide long-term hematopoiesis in recipients following high-dose total body irradiation. Marrow was experimentally obtained by giving donor mice 6 weekly injections of saline, cytosine arabinoside, cyclophosphamide, cisplatin, 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), or busulfan, drugs known to have differing effects on primitive hematopoietic stem cells. After time to allow recovery of marrow and peripheral blood counts, 1x10(7) marrow cells from these mice were transplanted into lethally irradiated syngeneic recipients. Five to 6 months after marrow transplantation, the quality of long-term hematopoietic recovery was measured by WBC counts, marrow cellularity, CFU-S content, and determinations of stem cell self-renewal. Abnormalities were noted with the use of donor marrow exposed to all cytotoxic agents. Recipients of marrow previously exposed to cytosine arabinoside, an agent that spares the most primitive stem cells, were the least affected. Recipients of marrow previously exposed to busulfan, an agent known to damage primitive stem cells, were most affected with a decrease in peripheral blood counts, marrow cellularity, stem cell content, self-renewal capacity, and long-term survival. A decrease in hematopoietic stem cell self-renewal was seen in recipients of marrow previously exposed to cyclophosphamide, cisplatin, and BCNU even when marrow cellularity and CFU-S content were normal. These data suggest that the capacity of syngeneic donor marrow to provide long-term hematopoiesis in lethally irradiated recipients is dependent on its donor marrow primitive stem cell content. Long-term hematopoiesis may be severely compromised in recipients of donor stem cells previously exposed to cytotoxic agents which damage primitive stem cells. C1 HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT RADIAT ONCOL,50 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [R0 1 CA 10941-21] NR 33 TC 83 Z9 85 U1 0 U2 2 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JAN PY 1993 VL 21 IS 1 BP 156 EP 162 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA KZ185 UT WOS:A1993KZ18500029 PM 8435103 ER PT J AU FERRANTE, RJ KOWALL, NW CIPOLLONI, PB STOREY, E BEAL, MF AF FERRANTE, RJ KOWALL, NW CIPOLLONI, PB STOREY, E BEAL, MF TI EXCITOTOXIN LESIONS IN PRIMATES AS A MODEL FOR HUNTINGTONS-DISEASE - HISTOPATHOLOGIC AND NEUROCHEMICAL CHARACTERIZATION SO EXPERIMENTAL NEUROLOGY LA English DT Article ID QUINOLINIC ACID LESIONS; PERFORMANCE LIQUID-CHROMATOGRAPHY; SOMATOSTATIN-NEUROPEPTIDE-Y; CONTAINING STRIATAL NEURONS; D-ASPARTATE RECEPTOR; BASAL GANGLIA; CEREBROSPINAL-FLUID; RAT STRIATUM; CHOLINERGIC NEURONS; KYNURENIC ACID C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,NEUROL SERV,EXPTL NEUROPATHOL LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,NEUROL SERV,EXPTL NEUROCHEM LAB,BOSTON,MA 02114. EDITH NOURSE ROGERS MEM VA MED CTR,BEDFORD,MA. BOSTON UNIV,SCH MED,DEPT ANAT,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. RP FERRANTE, RJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. RI Kowall, Neil/G-6364-2012; Storey, Elsdon/A-9889-2013 OI Kowall, Neil/0000-0002-6624-0213; FU NINDS NIH HHS [NS25588, NS16367, NS20967] NR 94 TC 179 Z9 182 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 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD JAN PY 1993 VL 119 IS 1 BP 46 EP 71 DI 10.1006/exnr.1993.1006 PG 26 WC Neurosciences SC Neurosciences & Neurology GA KL763 UT WOS:A1993KL76300006 PM 8432351 ER PT J AU WEBER, GF BRUCH, HP AF WEBER, GF BRUCH, HP TI HYDROXYETHYL STARCH AND DISEASES MEDIATED BY FREE-RADICALS SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Letter C1 UNIV LUEBECK,CHIRURG KLIN,W-2400 LUBECK,GERMANY. RP WEBER, GF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. RI Bruch, Hans-Peter/E-7731-2010 NR 6 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 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD JAN PY 1993 VL 14 IS 1 BP 96 EP 97 DI 10.1016/0891-5849(93)90515-V PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA KF442 UT WOS:A1993KF44200013 PM 7681025 ER PT B AU FREI, E GOORIN, A AF FREI, E GOORIN, A BE Novak, JF McMaster, JH TI OSTEOGENIC-SARCOMA - THE DEVELOPMENT OF CURATIVE TREATMENT SO FRONTIERS OF OSTEOSARCOMA RESEARCH: INTERDISCIPLINARY SURVEY OF CLINICAL AND RESEARCH ADVANCES LA English DT Proceedings Paper CT 1st International Meeting on Interdisciplinary Research in Osteosarcoma CY OCT 16-18, 1991 CL PITTSBURGH, PA SP ALLEGHENY GEN HOSP, ALLEGHENY SINGER RES INST, DEPUY, H J HEINZ CO FDN, KRISTIN LEE MCMASTER MEM FUND, ORTHO BIOTECH, PPG IND FDN, SANDOZ PHARM CORP, SMITH & NEPHEW RICHARDS INC, SMITHKLINE BEECHAM, STUART MED INC, ROBERT & MARY WEISBROD FDN C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 3 Z9 3 U1 0 U2 0 PU HOGREFE & HUBER PUBLISHERS PI TORONTO PA 12 BRUCE PARK AVE, TORONTO ON M4P 2S3, CANADA BN 0-88937-113-X PY 1993 BP 5 EP 13 PG 9 WC Anatomy & Morphology; Biochemistry & Molecular Biology; Oncology; Endocrinology & Metabolism; Pathology SC Anatomy & Morphology; Biochemistry & Molecular Biology; Oncology; Endocrinology & Metabolism; Pathology GA BZ52E UT WOS:A1993BZ52E00002 ER PT B AU PITCHER, JD GEBHARDT, MC SPRINGFIELD, DS ROSENBERG, AE MANKIN, HJ AF PITCHER, JD GEBHARDT, MC SPRINGFIELD, DS ROSENBERG, AE MANKIN, HJ BE Novak, JF McMaster, JH TI OSTEOSARCOMA - THE MASSACHUSETTS-GENERAL-HOSPITAL BOSTON-CHILDRENS-HOSPITAL 20-YEAR EXPERIENCE SO FRONTIERS OF OSTEOSARCOMA RESEARCH: INTERDISCIPLINARY SURVEY OF CLINICAL AND RESEARCH ADVANCES LA English DT Proceedings Paper CT 1st International Meeting on Interdisciplinary Research in Osteosarcoma CY OCT 16-18, 1991 CL PITTSBURGH, PA SP ALLEGHENY GEN HOSP, ALLEGHENY SINGER RES INST, DEPUY, H J HEINZ CO FDN, KRISTIN LEE MCMASTER MEM FUND, ORTHO BIOTECH, PPG IND FDN, SANDOZ PHARM CORP, SMITH & NEPHEW RICHARDS INC, SMITHKLINE BEECHAM, STUART MED INC, ROBERT & MARY WEISBROD FDN C1 MASSACHUSETTS GEN HOSP,ORTHOPAED ONCOL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HOGREFE & HUBER PUBLISHERS PI TORONTO PA 12 BRUCE PARK AVE, TORONTO ON M4P 2S3, CANADA BN 0-88937-113-X PY 1993 BP 17 EP 23 PG 7 WC Anatomy & Morphology; Biochemistry & Molecular Biology; Oncology; Endocrinology & Metabolism; Pathology SC Anatomy & Morphology; Biochemistry & Molecular Biology; Oncology; Endocrinology & Metabolism; Pathology GA BZ52E UT WOS:A1993BZ52E00003 ER PT B AU GEBHARDT, MC SPRINGFIELD, DS TAKESHITA, H KUSUZAKI, K LEW, R MANKIN, HJ AF GEBHARDT, MC SPRINGFIELD, DS TAKESHITA, H KUSUZAKI, K LEW, R MANKIN, HJ BE Novak, JF McMaster, JH TI DNA-PLOIDY AS A PREDICTOR OF OUTCOME IN OSTEOSARCOMA AND PRELIMINARY-RESULTS OF ADRIAMYCIN BINDING AND P-GLYCOPROTEIN IMMUNODETECTION IN OSTEOSARCOMA BIOPSY SPECIMENS SO FRONTIERS OF OSTEOSARCOMA RESEARCH: INTERDISCIPLINARY SURVEY OF CLINICAL AND RESEARCH ADVANCES LA English DT Proceedings Paper CT 1st International Meeting on Interdisciplinary Research in Osteosarcoma CY OCT 16-18, 1991 CL PITTSBURGH, PA SP ALLEGHENY GEN HOSP, ALLEGHENY SINGER RES INST, DEPUY, H J HEINZ CO FDN, KRISTIN LEE MCMASTER MEM FUND, ORTHO BIOTECH, PPG IND FDN, SANDOZ PHARM CORP, SMITH & NEPHEW RICHARDS INC, SMITHKLINE BEECHAM, STUART MED INC, ROBERT & MARY WEISBROD FDN C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ORTHOPAED ONCOL UNIT,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU HOGREFE & HUBER PUBLISHERS PI TORONTO PA 12 BRUCE PARK AVE, TORONTO ON M4P 2S3, CANADA BN 0-88937-113-X PY 1993 BP 65 EP 69 PG 5 WC Anatomy & Morphology; Biochemistry & Molecular Biology; Oncology; Endocrinology & Metabolism; Pathology SC Anatomy & Morphology; Biochemistry & Molecular Biology; Oncology; Endocrinology & Metabolism; Pathology GA BZ52E UT WOS:A1993BZ52E00007 ER PT B AU KLOEN, P JENNINGS, CL TAKESHITA, H GEBHARDT, MC SPRINGFIELD, DS MANKIN, HJ AF KLOEN, P JENNINGS, CL TAKESHITA, H GEBHARDT, MC SPRINGFIELD, DS MANKIN, HJ BE Novak, JF McMaster, JH TI TRANSFORMING GROWTH-FACTOR-BETA RECEPTOR PROFILE AND GROWTH-PATTERN DIFFER AMONG 8 HUMAN OSTEOSARCOMA CELL-LINES SO FRONTIERS OF OSTEOSARCOMA RESEARCH: INTERDISCIPLINARY SURVEY OF CLINICAL AND RESEARCH ADVANCES LA English DT Proceedings Paper CT 1st International Meeting on Interdisciplinary Research in Osteosarcoma CY OCT 16-18, 1991 CL PITTSBURGH, PA SP ALLEGHENY GEN HOSP, ALLEGHENY SINGER RES INST, DEPUY, H J HEINZ CO FDN, KRISTIN LEE MCMASTER MEM FUND, ORTHO BIOTECH, PPG IND FDN, SANDOZ PHARM CORP, SMITH & NEPHEW RICHARDS INC, SMITHKLINE BEECHAM, STUART MED INC, ROBERT & MARY WEISBROD FDN C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ORTHOPAED ONCOL SERV,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU HOGREFE & HUBER PUBLISHERS PI TORONTO PA 12 BRUCE PARK AVE, TORONTO ON M4P 2S3, CANADA BN 0-88937-113-X PY 1993 BP 519 EP 523 PG 5 WC Anatomy & Morphology; Biochemistry & Molecular Biology; Oncology; Endocrinology & Metabolism; Pathology SC Anatomy & Morphology; Biochemistry & Molecular Biology; Oncology; Endocrinology & Metabolism; Pathology GA BZ52E UT WOS:A1993BZ52E00069 ER PT B AU BRAND, SJ BABYATSKY, M BACHWICH, D DEMEDIUK, B TILLOTSON, L WANG, TC AF BRAND, SJ BABYATSKY, M BACHWICH, D DEMEDIUK, B TILLOTSON, L WANG, TC BE Walsh, JH TI REGULATION OF GASTRIN GENE-TRANSCRIPTION SO GASTRIN LA English DT Proceedings Paper CT MEETING ON GASTRIN CY FEB 09-12, 1992 CL DANA POINT, CA SP ASTRA HASSLE, GLAXO, SANDOZ PHARM US, MERCK SHARP & DOHME RES LABS, MARION MERRELL DOW, BYK GULDEN, CASCAN, SANDOZ GERMANY, ASTRA CHEM, DAIICHI PHARM RP BRAND, SJ (reprint author), MASSACHUSETTS GEN HOSP,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0060-4 PY 1993 BP 73 EP 89 PG 17 WC Biochemistry & Molecular Biology; Gastroenterology & Hepatology; Physiology SC Biochemistry & Molecular Biology; Gastroenterology & Hepatology; Physiology GA BY42H UT WOS:A1993BY42H00007 ER PT J AU FOX, JG BLANCO, MC YAN, L SHAMES, B POLIDORO, D DEWHIRST, FE PASTER, BJ AF FOX, JG BLANCO, MC YAN, L SHAMES, B POLIDORO, D DEWHIRST, FE PASTER, BJ TI ROLE OF GASTRIC PH IN ISOLATION OF HELICOBACTER-MUSTELAE FROM THE FECES OF FERRETS SO GASTROENTEROLOGY LA English DT Article ID CAMPYLOBACTER-PYLORI INFECTION; TO-PERSON TRANSMISSION; ANIMAL-MODEL; C-PYLORI; IMMUNE-RESPONSE; SUBSP-MUSTELAE; COLONIZATION; POPULATION; CARCINOMA; ANTIBODY C1 FORSYTH DENT CTR,BOSTON,MA 02115. RP FOX, JG (reprint author), MIT,DIV COMPARAT MED,37 VASSAR ST 45-104,CAMBRIDGE,MA 02139, USA. FU NCI NIH HHS [P01-CA26731]; NCRR NIH HHS [RR01046, RR07036] NR 33 TC 52 Z9 56 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 JAN PY 1993 VL 104 IS 1 BP 86 EP 92 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KJ901 UT WOS:A1993KJ90100011 PM 8380398 ER PT J AU FLETCHER, JA KOZAKEWICH, HP SCHOENBERG, ML MORTON, CC AF FLETCHER, JA KOZAKEWICH, HP SCHOENBERG, ML MORTON, CC TI CYTOGENETIC FINDINGS IN PEDIATRIC ADIPOSE TUMORS - CONSISTENT REARRANGEMENT OF CHROMOSOME-8 IN LIPOBLASTOMA SO GENES CHROMOSOMES & CANCER LA English DT Article ID DIAGNOSTIC RELEVANCE; LIPOSARCOMA; EXPRESSION; CHILDHOOD; ABNORMALITIES; ABERRATIONS AB Characteristic cytogenetic aberrations have been reported in adult lipomas and liposarcomas, but few karyotypes have been reported for pediatric adipose neoplasms. In this report we describe a consistent rearrangement, der(8)(pter-->q13::q24.1-->qter), in 2 of 3 lipoblastomas. A similar der(8) was present in the only other published lipoblastoma karyotype, but this der(8) has not been reported in lipomas, liposarcomas, or nonadipose solid tumors. We investigated the potential specificity of der(8)(pter-->q13::q24.1-->qter) by karyotyping an unselected series of nonlipoblastoma adipose tumors in children and young adults. The series included 14 lipomas, 2 atypical lipomas (''well-differentiated liposarcomas''), and 2 angiomyolipomas; der(8) was not found in any tumor from this series. Three lipomas, however, contained rearrangements in the region of chromosome band 12q14, as has been described frequently in adult lipomas. Because clinical features in lipoblastoma can mimic those in liposarcoma, recognition of der(8)(pter-->q13::q24.1-->qter) is of potential diagnostic relevance. C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,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 [1K11CA01498-02] NR 24 TC 61 Z9 61 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 1993 VL 6 IS 1 BP 24 EP 29 DI 10.1002/gcc.2870060106 PG 6 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA KJ351 UT WOS:A1993KJ35100004 PM 7680218 ER PT J AU PERICAKVANCE, MA STGEORGEHYSLOP, PH GASKELL, PC GROWDON, J CRAIN, BJ HULETTE, C GUSELLA, JF YAMAOKA, L TANZI, RE ROSES, AD HAINES, JL AF PERICAKVANCE, MA STGEORGEHYSLOP, PH GASKELL, PC GROWDON, J CRAIN, BJ HULETTE, C GUSELLA, JF YAMAOKA, L TANZI, RE ROSES, AD HAINES, JL TI LINKAGE ANALYSIS IN FAMILIAL ALZHEIMER-DISEASE - DESCRIPTION OF THE DUKE AND BOSTON DATA SETS SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT Genetic Analysis Workshop 8: Issues in the Analysis of Complex Diseases and Their Risk Factors ( GAW8 ) CY NOV 08-10, 1992 CL WATSONVILLE, CA SP NIH, SANDOZ PHARM DE FAMILIAL ALZHEIMER DISEASE; LINKAGE; FAMILIES; FAD ID 1ST-DEGREE RELATIVES; GENETIC-LINKAGE; DEMENTIA; RISK; CHROMOSOME-21; DISORDER; MARKERS AB Familial Alzheimer disease is a neurological disorder of adult onset. Three research centers have each contributed their families and genetic linkage data for combined analyses. The data from the Duke and Boston centers, comprising 73 pedigrees for whom numerous markers on chromosomes 19 and 21 were typed, are described. (C) 1993 Wiley-Liss, Inc. C1 DUKE UNIV,MED CTR,J&K BRYAN ALZHEIMER DIS RES CTR,DURHAM,NC 27710. UNIV TORONTO,TANZI NEUROSCI INST,TORONTO M5S 1A1,ONTARIO,CANADA. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. RP PERICAKVANCE, MA (reprint author), DUKE UNIV,MED CTR,DIV NEUROL,POB 2900,DURHAM,NC 27710, USA. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00324]; NIA NIH HHS [AG05134]; NINDS NIH HHS [NS30428] NR 17 TC 6 Z9 6 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1993 VL 10 IS 6 BP 361 EP 364 DI 10.1002/gepi.1370100605 PG 4 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA MM366 UT WOS:A1993MM36600003 PM 8314027 ER PT J AU ELSTON, RC SPENCE, MA HAINES, JL MARAZITA, ML PERICAKVANCE, MA SIERVOGEL, RM MACCLUER, JW AF ELSTON, RC SPENCE, MA HAINES, JL MARAZITA, ML PERICAKVANCE, MA SIERVOGEL, RM MACCLUER, JW TI GENETIC-ANALYSIS WORKSHOP-8 - ISSUES IN THE ANALYSIS OF COMPLEX DISEASES AND THEIR RISK-FACTORS - PREFACE SO GENETIC EPIDEMIOLOGY LA English DT Editorial Material C1 UNIV CALIF LOS ANGELES,NPI,MENTAL RETARDAT UNIT,LOS ANGELES,CA 90024. MASSACHUSETTS GEN HOSP,DEPT NEUROGENET,BOSTON,MA 02129. UNIV PITTSBURGH,CLEFT PALATE CRANIOFACIAL CTR,PITTSBURGH,PA 15261. DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC 27710. WRIGHT STATE UNIV,SCH MED,DEPT COMMUNITY HLTH,YELLOW SPRINGS,OH 45387. SW FDN BIOMED RES,DEPT GENET,SAN ANTONIO,TX 78228. RP ELSTON, RC (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,1901 PERDIDO ST,NEW ORLEANS,LA 70112, USA. NR 0 TC 1 Z9 1 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1993 VL 10 IS 6 BP R19 EP R20 DI 10.1002/gepi.1370100602 PG 2 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA MM366 UT WOS:A1993MM36600001 ER PT J AU YUNIS, EJ SALAZAR, M AF YUNIS, EJ SALAZAR, M TI GENETICS OF LIFE-SPAN IN MICE SO GENETICA LA English DT Article DE MHC (MAJOR HISTOCOMPATIBILITY COMPLEX); TCR (T CELL RECEPTORS); THYMUS; VIRAL INFECTION ID T-CELLS; HISTOCOMPATIBILITY COMPLEX; MEDIATED CYTOTOXICITY; INFLUENCE LONGEVITY; IMMUNE-RESPONSE; DISEASE; IMMUNODEFICIENCY; ASSOCIATION; GENERATION; TRAITS AB Thymic involution that occurs earlier in some individuals than others may be the; result of complex interactions between genetic factors and the environment. Such interactions may produce defects of thymus-dependent immune regulation associated with susceptibility to developing autoimmune diseases, malignancy, and an increased number of infections associated with aging. The major histocompatibility complex may be important in determining profiles of cause of death and length of life in mice. Genetic influences on life span involve interactions between loci and allelic interactions during life which may change following viral infections or exposure to other environmental factors. We have used different experimental protocols to study the influence of H-2 on life span and found that interactions between genetic regions, are inconsistent, particularly when comparing mice infected or not infected with Sendai virus. Genes important for life span need to be studied against many genetic backgrounds and under differing environmental conditions because of the complexity of the genetics of life span. Several genetic models were used to demonstrate that the MHC is a marker of life span in backcross and intercross male mice of the H-2(d) and H-2(b) genotypes in B10 congenic mice. Females lived longer than males in backcross and intercross mice, while males lived longer than females in B10 congenics. H-2(d) was at a disadvantage for life span in backcross mice of the dilute brown and brown males exposed to Sendai infection, but intercross mice not exposed to Sendai virus of the same genotype were not at a disadvantage. H-2(d) mice were not disadvantaged when compared to H-2(b) in B10 congenics that had not been exposed to Sendai virus infection but the reverse was true when they were exposed. Overall, all our studies suggest that genetic influences in life span may involve interactions between loci and many allelic interactions in growing animals or humans. These genetic influences on life span may vary after they are exposed to infections or other environmental conditions. This paper emphasizes the need to use several genetic models, especially animals that have been monitored for infections, to study the genetics of life span. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP YUNIS, EJ (reprint author), DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-06516]; NIA NIH HHS [R01-AG-02329] NR 65 TC 14 Z9 14 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0016-6707 J9 GENETICA JI Genetica PY 1993 VL 91 IS 1-3 BP 211 EP 223 DI 10.1007/BF01435999 PG 13 WC Genetics & Heredity SC Genetics & Heredity GA MT350 UT WOS:A1993MT35000018 PM 8125271 ER PT J AU MOBBS, CV AF MOBBS, CV TI GENETIC INFLUENCES ON GLUCOSE NEUROTOXICITY, AGING, AND DIABETES - A POSSIBLE ROLE FOR GLUCOSE HYSTERESIS SO GENETICA LA English DT Article ID FEMALE C57BL/6J MICE; HYPOTHALAMIC-LESIONED RATS; BETA-CELL FUNCTION; INSULIN RESISTANCE; REPRODUCTIVE SENESCENCE; ESTRADIOL ACCUMULATION; GOLD THIOGLUCOSE; AGE; HYPERINSULINEMIA; INTOLERANCE AB Glucose may drive some age-correlated impairments and may mediate some effects of dietary restriction on senescence. The hypothesis that cumulative deleterious effects of glucose may impair hypothalamic neurons during aging, leading to hyperinsulinemia and other age-correlated pathologies, is examined in the context of genetic influences. Susceptibility to toxic effects of gold-thio-glucose (GTG) is correlated with longevity across several mouse strains. GTG and chronic hyperglycemia induce specific impairments in the ventromedial hypothalamus similar to impairments which occur during aging. GTG and a high-calorie diet both induce chronic hyperinsulinemia, leading initially to hypoglycemia, followed by the development of insulin resistance and hyperglycemia. Aging in humans and rodents appears to entail a similar pattern of hyperinsulinemia followed by insulin resistance. In humans, genetic susceptibility to high-calorie diet-induced impairments in glucose metabolism is extremely common in many indigenous populations, possibly due to the selection of the 'thrifty genotype'. It is suggested that the 'thrifty genotype' may entail enhanced sensitivity to the neurotoxic effects of glucose, and may represent an example of antagonistic pleiotropy in human evolution. These data are consistent with the hypothesis that genetic susceptibility of hypothalamic neurons to the cumulative toxic effects of glucose (glucose neurohumoral hysteresis) may correlate with genetic influences on longevity. C1 BRONX VET AFFAIRS MED CTR,MOLEC MED & DIAGNOST LAB,NEW YORK,NY 10129. RP MOBBS, CV (reprint author), MT SINAI SCH MED,FISHBERG CTR NEUROBIOL,NEW YORK,NY 10129, USA. NR 95 TC 7 Z9 8 U1 1 U2 3 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0016-6707 J9 GENETICA JI Genetica PY 1993 VL 91 IS 1-3 BP 239 EP 253 DI 10.1007/BF01436001 PG 15 WC Genetics & Heredity SC Genetics & Heredity GA MT350 UT WOS:A1993MT35000020 PM 8125273 ER PT J AU TANZI, R GASTON, S BUSH, A ROMANO, D PETTINGELL, W PEPPERCORN, J PARADIS, M GURUBHAGAVATULA, S JENKINS, B WASCO, W AF TANZI, R GASTON, S BUSH, A ROMANO, D PETTINGELL, W PEPPERCORN, J PARADIS, M GURUBHAGAVATULA, S JENKINS, B WASCO, W TI GENETIC-HETEROGENEITY OF GENE DEFECTS RESPONSIBLE FOR FAMILIAL ALZHEIMER-DISEASE SO GENETICA LA English DT Article ID AMYLOID PRECURSOR PROTEIN; BETA-PROTEIN; MESSENGER-RNA; CEREBRAL-HEMORRHAGE; HUMAN-BRAIN; APP GENE; MUTATION; LINKAGE; CDNA; LOCALIZATION AB Inherited Alzheimer's disease is a genetically heterogeneous disorder that involves gene defects on at least five chromosomal loci. Three of these loci have been found by genetic linkage studies to reside on chromosomes 21, 19, and 14. On chromosomes 21, the gene encoding the precursor protein of Alzheimer-associated amyloid (APP) has been shown to contain several mutations in exons 16 and 17 which account for roughly 2-3 % of familial Alzheimer's disease (FAD). The other loci include what appears to be a susceptibility gene on chromosome 19 associated with late-onset (> 65 years) FAD, and a major early-onset FAD gene defect on the long arm of chromosome 14. In other early- and late-onset FAD kindreds, the gene defects involved do not appear to be linked to any of these three loci, indicating the existence of additional and as of yet unlocalized FAD genes. This review provides a historical perspective of the search for FAD gene defects and summarizes the progress made in world-wide attempts to isolate and characterize the genes responsible for this disorder. RP TANZI, R (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP,CTR NEUROSCI,SCH MED, DEPT NEUROL, GENET & AGING LAB, BOSTON, MA 02129 USA. FU NINDS NIH HHS [NS30428] NR 57 TC 30 Z9 30 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0016-6707 J9 GENETICA JI Genetica PY 1993 VL 91 IS 1-3 BP 255 EP 263 DI 10.1007/BF01436002 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA MT350 UT WOS:A1993MT35000021 PM 8125274 ER PT S AU MACDONALD, ME AMBROSE, CM DUYAO, MP GUSELLA, JF AF MACDONALD, ME AMBROSE, CM DUYAO, MP GUSELLA, JF BE Davies, KE Warren, ST TI CAPTURING A CAGEY KILLER SO GENOME REARRANGEMENT AND STABILITY SE GENOME ANALYSIS LA English DT Proceedings Paper CT Banbury Conference on DNA Repeats and Human Gene Mutations CY 1992 CL COLD SPRING HARBOR LAB, COLD SPRING HARBOR, NY SP COLD SPRING HARBOR LAB HO COLD SPRING HARBOR LAB C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. NR 0 TC 1 Z9 1 U1 1 U2 1 PU COLD SPRING HARBOR LABORATORY PRESS PI PLAINVIEW PA 10 SKYLINE DRIVE, PLAINVIEW, NY 11803-2500 SN 1050-8430 BN 0-87969-388-6 J9 GENOME ANAL PY 1993 VL 7 BP 25 EP 41 PG 17 WC Genetics & Heredity SC Genetics & Heredity GA BZ95T UT WOS:A1993BZ95T00002 ER PT J AU WASCO, W BROOK, JD TANZI, RE AF WASCO, W BROOK, JD TANZI, RE TI THE AMYLOID PRECURSOR-LIKE PROTEIN (APLP) GENE MAPS TO THE LONG ARM OF HUMAN CHROMOSOME-19 SO GENOMICS LA English DT Note ID FAMILIAL ALZHEIMERS-DISEASE; CDNA; LINKAGE; RECEPTOR; MUTATION C1 CITY HOSP, CTR MED GENET, NOTTINGHAM NG5 1PB, ENGLAND. RP WASCO, W (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT NEUROL, BOSTON, MA 02114 USA. OI Brook, John David/0000-0002-5946-6740 FU NINDS NIH HHS [NS30428] NR 17 TC 42 Z9 43 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN PY 1993 VL 15 IS 1 BP 237 EP 239 DI 10.1006/geno.1993.1047 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA KK685 UT WOS:A1993KK68500047 PM 8432545 ER PT J AU LEGRAND, EK BURKE, JF COSTA, DE KIORPES, TC AF LEGRAND, EK BURKE, JF COSTA, DE KIORPES, TC TI DOSE RESPONSIVE EFFECTS OF PDGF-BB, PDGF-AA, EGF, AND BFGF ON GRANULATION-TISSUE IN A GUINEA-PIG PARTIAL THICKNESS SKIN EXCISION MODEL SO GROWTH FACTORS LA English DT Article DE WOUND HEALING; GUINEA PIG; GROWTH FACTOR; PDGF; EGF; FGF ID GROWTH-FACTORS; WOUNDS AB A guinea pig partial thickness skin excision model was used to evaluate the effects of recombinant human PDGF-BB, PDGF-AA, EGF, and bFGF on granulation tissue (neodermis) formation. These growth factors tended to increase the thickness of the granulation tissue bed when assessed histologically at day 7. Using only four animals per group, PDGF-BB at 30 and 100 mug/ml consistently and significantly increased the thickness of the granulation bed 2-3 times that of control. Except for the increased thickness, the granulation tissue appeared normal. PDGF-AA and EGF also significantly increased the granulation tissue thickness, and bFGF gave indications of an effect. There was no evidence of synergistic effects between PDGF-BB, EGF, and/or bFGF. C1 ETHICON INC,PHARMACEUT RES & DEV,SOMERVILLE,NJ 08876. MASSACHUSETTS GEN HOSP,TRAUMA SERV,BOSTON,MA 02114. OI LeGrand, Edmund/0000-0001-7083-7509 NR 18 TC 25 Z9 25 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 1993 VL 8 IS 4 BP 307 EP & PG 0 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA LL968 UT WOS:A1993LL96800006 PM 8347346 ER PT B AU SCHOTT, RJ MORROW, LA AF SCHOTT, RJ MORROW, LA BE Cummins, P TI THE ROLE OF GROWTH-FACTORS IN ANGIOGENESIS SO GROWTH FACTORS AND THE CARDIOVASCULAR SYSTEM SE DEVELOPMENTS IN CARDIOVASCULAR MEDICINE LA English DT Proceedings Paper CT Symposium on the Growth Factors in the Heart, at the XIIIth Congress of the European-Society-of-Cardiology CY 1991 CL AMSTERDAM, NETHERLANDS SP EUROPEAN SOC CARDIOL, WORKING GRP PATHOPHYSIOL CARDIAC MYOCYTE C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-2401-3 J9 DEV CARDIOVASC MED PY 1993 VL 147 BP 149 EP 168 PG 20 WC Cardiac & Cardiovascular Systems; Physiology SC Cardiovascular System & Cardiology; Physiology GA BZ48L UT WOS:A1993BZ48L00009 ER PT J AU RUBIN, SC KAIREMO, KJA BROWNELL, AL DAGHIGHIAN, F FEDERICI, MG PENTLOW, KS FINN, RD LAMBRECHT, RM HOSKINS, WJ LEWIS, JL LARSON, SM AF RUBIN, SC KAIREMO, KJA BROWNELL, AL DAGHIGHIAN, F FEDERICI, MG PENTLOW, KS FINN, RD LAMBRECHT, RM HOSKINS, WJ LEWIS, JL LARSON, SM TI HIGH-RESOLUTION POSITRON EMISSION TOMOGRAPHY OF HUMAN OVARIAN-CANCER IN NUDE RATS USING I-124 LABELED MONOCLONAL-ANTIBODIES SO GYNECOLOGIC ONCOLOGY LA English DT Article ID CELL-SURFACE ANTIGENS; EXPRESSION C1 MEM SLOAN KETTERING CANC CTR,DEPT SURG,GYNECOL SERV,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,DEPT MED IMAGING,NUCL MED SERV,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,DEPT MED PHYS,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,PHYS RES LAB,BOSTON,MA 02114. KING FAISAL SPECIALIST HOSP & RES CTR,DEPT RADIONUCLIDE & CYCLOTRON OPERAT,RIYADH 11211,SAUDI ARABIA. FU NCI NIH HHS [CA 52477] NR 20 TC 25 Z9 25 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD JAN PY 1993 VL 48 IS 1 BP 61 EP 67 DI 10.1006/gyno.1993.1010 PG 7 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA KK690 UT WOS:A1993KK69000010 PM 8423023 ER PT J AU FRANCIS, HW NADOL, JB AF FRANCIS, HW NADOL, JB TI PATTERNS OF INNERVATION OF OUTER HAIR-CELLS IN A CHIMPANZEE .1. AFFERENT AND RECIPROCAL SYNAPSES SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELL; ORGAN OF CORTI; AFFERENT INNERVATION ID HUMAN ORGAN; CORTI; COCHLEA; CAT AB Three varieties of synaptic specialization, afferent, efferent, and reciprocal, have been demonstrated at the base of outer hair cells of one chimpanzee. The purpose of the present study was to investigate the innervation density of afferent and reciprocal synapses in the three rows and three turns of the organ of Corti. The data presented is based on light and electron microscopy from one aged chimpanzee using serial section electron microscopy. Afferent fibers make contact with outer hair cells as either terminal swellings or en passant contacts. In addition to membrane specialization, presynaptic bodies were present at the majority of afferent synapses. The mean innervation density of afferent endings was highest in the middle turn. Reciprocal endings were found on 74% of all outer hair cells. The average number of reciprocal endings increased from the base to apex and, except in the apical turn, from the first to third row of outer hair cells. On the basis of morphological criteria, endings with a reciprocal synapses were more similar to afferent than to efferent endings. C1 MASSACHUSETTS EYE & EAR INFIRM,OTOPATHOL LAB,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. FU NIDCD NIH HHS [R01 DC00152-12] NR 26 TC 15 Z9 15 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1993 VL 64 IS 2 BP 184 EP 190 DI 10.1016/0378-5955(93)90004-K PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700004 PM 8432689 ER PT J AU FRANCIS, HW NADOL, JB AF FRANCIS, HW NADOL, JB TI PATTERNS OF INNERVATION OF OUTER HAIR-CELLS IN A CHIMPANZEE .2. EFFERENT ENDINGS SO HEARING RESEARCH LA English DT Article DE EFFERENT INNERVATION; OUTER HAIR CELL; ORGAN OF CORTI ID GUINEA-PIG ORGAN; ENKEPHALIN-LIKE IMMUNOREACTIVITY; CORTI; LOCALIZATION; COCHLEA; MICROSCOPY AB A morphometric analysis of the efferent innervation of the outer hair cells in the organ of Corti of one chimpanzee was performed. There was a wide variability in the size of efferent endings which ranged from approximately 0.1 to 4.5 mum3 in volume. Based on the size distribution of endings, a volume of 1.0 mum3 was chosen to divide efferent endings into two groups, 'large' and 'small'. The incidence of large efferent fibers decreased from base to apex and from the first to third row of each turn, whereas the incidence of small efferents increased from base to apex and from the first to third row in each turn. This data was interpreted to suggest that at least two types of efferent endings may exist at the base of outer hair cells of the organ of Corti in the chimpanzee. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,OTOPATHOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. FU NIDCD NIH HHS [R01 DC00152-12] NR 21 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1993 VL 64 IS 2 BP 217 EP 221 DI 10.1016/0378-5955(93)90009-P PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700009 PM 8432693 ER PT J AU KAHN, CR FOLLI, F AF KAHN, CR FOLLI, F TI MOLECULAR DETERMINANTS OF INSULIN ACTION SO HORMONE RESEARCH LA English DT Article DE INSULIN; PHOSPHORYLATION; INSULIN RECEPTORS; INSULIN RECEPTOR SUBSTRATE-1; PHOSPHOINOSITOL 3-KINASE ID TYROSINE KINASE-ACTIVITY; DIABETES-MELLITUS PATIENTS; RECEPTOR KINASE; ALTERED EXPRESSION; 3T3-L1 ADIPOCYTES; SKELETAL-MUSCLE; BETA-SUBUNIT; PROTEIN; BINDING; PHOSPHORYLATION AB Insulin rapidly stimulates tyrosine phosphorylation of a 185-kDa protein in most cell types. This protein, insulin receptor substrate 1 (IRS-1), has been implicated as the first postreceptor step in insulin signal transmission based on studies with insulin receptor mutants. In cell culture and in vitro, phosphorylated IRS-1 associates with the lipid-metabolizing enzyme phosphatidylinositol 3-kinase (PI 3-kinase), resulting in activation of this enzyme. Thus, the insulin receptor, IRS-1 and PI-3 kinase represent three of the earliest steps in insulin action at the cellular level. We have recently demonstrated that insulin is capable of stimulating PI 3-kinase activity in liver and muscle in vivo in animals and that IRS-1 phosphorylation may play a significant role in the association/activation with PI 3-kinase in vivo. RP KAHN, CR (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. OI folli, franco/0000-0001-9824-5222 NR 63 TC 18 Z9 21 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 1993 VL 39 SU 3 BP 93 EP 101 DI 10.1159/000182793 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ME187 UT WOS:A1993ME18700017 PM 7505252 ER PT J AU BUTENANDT CAPRIO, S KAHN, CR FERRANINI, E TAMBORLANE, WV BONADONNA, RC ROMER MARIN WIT ANTANASIO AF BUTENANDT CAPRIO, S KAHN, CR FERRANINI, E TAMBORLANE, WV BONADONNA, RC ROMER MARIN WIT ANTANASIO TI INSULIN INSENSITIVITY IN CHILDHOOD AND ADULTHOOD - DISCUSSION SO HORMONE RESEARCH LA English DT Discussion C1 JOSHN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215. UNIV PISA,CNR,INST CLIN PHYSIOL,METAB UNIT,I-56100 PISA,ITALY. YALE UNIV,DEPT PEDIAT ENDOCRINOL,NEW HAVEN,CT 06510. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 1993 VL 39 SU 3 BP 115 EP 115 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ME187 UT WOS:A1993ME18700021 ER PT J AU YUNIS, JJ DEULOFEUT, R YUNIS, EJ YUNIS, E AF YUNIS, JJ DEULOFEUT, R YUNIS, EJ YUNIS, E TI 2 NEW MHC CLASS-II HAPLOTYPES FOUND IN A BLACK-POPULATION OF COLOMBIA SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED,DANA FARBER CANC INST,DEPT PATHOL, DIV IMMUNOGENET, BOSTON, MA 02115 USA. UNIV NACL COLOMBIA, BOGOTA, COLOMBIA. CTR BLOOD RES, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0198-8859 EI 1879-1166 J9 HUM IMMUNOL JI Hum. Immunol. PY 1993 VL 37 SU 1 BP 21 EP 21 PG 1 WC Immunology SC Immunology GA LW989 UT WOS:A1993LW98900035 ER PT J AU DEULOFEUT, R SALAZAR, M DEULOFEUT, H YUNIS, DE MARCUSBAGLEY, D AWDEH, Z ALPER, CA YUNIS, EJ AF DEULOFEUT, R SALAZAR, M DEULOFEUT, H YUNIS, DE MARCUSBAGLEY, D AWDEH, Z ALPER, CA YUNIS, EJ TI T-CELL PRECURSOR FREQUENCIES TO HBSAG BY LIMITING DILUTION STRONGLY SUGGEST A DEFECT IN T-CELLS RATHER THAN IN ANTIGEN-PRESENTING CELLS SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PY 1993 VL 37 SU 1 BP 32 EP 32 PG 1 WC Immunology SC Immunology GA LW989 UT WOS:A1993LW98900058 ER PT J AU DEULOFEUT, H YUNIS, EJ DEULOFEUT, R SALAZAR, M KRUSKALL, MS YUNIS, DE MARCUSBAGLEY, D AWDEH, Z ALPER, CA AF DEULOFEUT, H YUNIS, EJ DEULOFEUT, R SALAZAR, M KRUSKALL, MS YUNIS, DE MARCUSBAGLEY, D AWDEH, Z ALPER, CA TI LACK OF RESPONSE TO HBSAG IS DUE TO A DEFECT IN T-CELLS SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PY 1993 VL 37 SU 1 BP 35 EP 35 PG 1 WC Immunology SC Immunology GA LW989 UT WOS:A1993LW98900062 ER PT J AU YUNIS, JJ SALAZAR, M DEULOFEUT, R IGLESIAS, A NATES, J YUNIS, E YUNIS, EJ AF YUNIS, JJ SALAZAR, M DEULOFEUT, R IGLESIAS, A NATES, J YUNIS, E YUNIS, EJ TI DRB1-ASTERISK-0404 ALLELE AND RHEUMATOID-ARTHRITIS IN THE GUAMBIANO AMERINDIAN TRIBE OF COLOMBIA SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED,DEPT PATHOL,DANA FARBER CANC INST, DIV IMMUNOGENET, BOSTON, MA 02115 USA. CTR BLOOD RES, BOSTON, MA USA. UNIV NACL COLOMBIA, FAC MED, SECC GENET, BOGOTA, COLOMBIA. INST NACL SALUD, BOGOTA, COLOMBIA. UNIV CAUCA, POPAYAN, COLOMBIA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0198-8859 EI 1879-1166 J9 HUM IMMUNOL JI Hum. Immunol. PY 1993 VL 37 SU 1 BP 52 EP 52 PG 1 WC Immunology SC Immunology GA LW989 UT WOS:A1993LW98900094 ER PT J AU YUNIS, JJ MOHIMEN, A NEUMAN, R FOSTER, CS ALPER, CA YUNIS, EJ AHMED, AR AF YUNIS, JJ MOHIMEN, A NEUMAN, R FOSTER, CS ALPER, CA YUNIS, EJ AHMED, AR TI IMMUNOGENETICS OF DRUG-RELATED OR PSEUDO-OCULAR CICATRICIAL PEMPHIGOID SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,IMMUNOL & UVEITIS SERV,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ORAL PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PY 1993 VL 37 SU 1 BP 53 EP 53 PG 1 WC Immunology SC Immunology GA LW989 UT WOS:A1993LW98900095 ER PT J AU AWDEH, ZL FICI, DA ALPER, CA RONCO, P YUNIS, EJ AF AWDEH, ZL FICI, DA ALPER, CA RONCO, P YUNIS, EJ TI THE ROLE OF HLA-DPB1 IN PRIMARY MLR SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 CTR BLOOD RES, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PY 1993 VL 37 SU 1 BP 155 EP 155 PG 1 WC Immunology SC Immunology GA LW989 UT WOS:A1993LW98900297 ER PT J AU AWDEH, ZL FICI, DA ALPER, CA RONCO, P YUNIS, EJ AF AWDEH, ZL FICI, DA ALPER, CA RONCO, P YUNIS, EJ TI MIXED LYMPHOCYTE-REACTIVITY IN 3 FAMILIES MISMATCHED FOR HLA-DPB1 SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 CTR BLOOD RES, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PY 1993 VL 37 SU 1 BP 155 EP 155 PG 1 WC Immunology SC Immunology GA LW989 UT WOS:A1993LW98900296 ER PT J AU YUNIS, JJ DELGADO, MB WILLIAMSON, JM YUNIS, EJ BING, DH AF YUNIS, JJ DELGADO, MB WILLIAMSON, JM YUNIS, EJ BING, DH TI GENERIC DRB ALLELE TYPING BY PCR-SSOP - AN APPROACH TO RESOLVE IDENTITY IN FORENSIC SAMPLES WITH UNINFORMATIVE DQA1 ALLELE TYPING SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV IMMUNOGENET,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PY 1993 VL 37 SU 1 BP 156 EP 156 PG 1 WC Immunology SC Immunology GA LW989 UT WOS:A1993LW98900298 ER PT J AU COLONNA, M BROOKS, EG FALCO, M FERRARA, GB STROMINGER, JL AF COLONNA, M BROOKS, EG FALCO, M FERRARA, GB STROMINGER, JL TI ALLOSPECIFIC NATURAL-KILLER-CELLS ARE GENERATED BY RECIPROCAL STIMULATION ACROSS A DIALLELIC POLYMORPHISM OF HLA-C SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. IST NAZL RIC CANC,IMMUNOGENET LAB,I-16132 GENOA,ITALY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. RI Falco, Michela/K-1574-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD JAN PY 1993 VL 36 IS 1 BP 66 EP 66 DI 10.1016/0198-8859(93)90102-7 PG 1 WC Immunology SC Immunology GA KQ949 UT WOS:A1993KQ94900100 ER PT J AU HAYASHI, K YANDELL, DW AF HAYASHI, K YANDELL, DW TI HOW SENSITIVE IS PCR-SSCP SO HUMAN MUTATION LA English DT Review DE MUTATIONAL ANALYSIS; POLYMERASE CHAIN REACTION (PCR); SINGLE-STRAND CONFORMATION POLYMORPHISM (SSCP); DNA TESTING ID POLYMERASE CHAIN-REACTION; CONFORMATION POLYMORPHISM ANALYSIS; GRADIENT GEL-ELECTROPHORESIS; SINGLE BASE SUBSTITUTIONS; POINT MUTATIONS; RAPID DETECTION; GENOMIC DNA; GENE; SEQUENCE; RNA AB Single-strand conformation polymorphism analysis (SSCP) is a rapid method for detection of minor sequence changes in polymerase chain reaction-amplified DNA. Since the first reported use of SSCP in 1989 (Orita et al., 1989), this tehnique has been used widely to detect mutations in oncogenes, tumor suppressor genes, and genes responsible for genetic diseases. Published mutations that have been detected using this technique include base substitutions, small insertions and deletions, and rearrangements. This technique has also been applied for the detection of DNA polymorphisms at various loci of the human genome (reviewed by Hayashi, 1991; Hayashi, 1993). However, many factors can influence the sensitivity of SSCP, and its optimization is highly empirical. In this review, we estimate the percentage of mutations that can be detected by this technique under various controlled conditions, and describe some critical elements affecting sensitivity. (C) 1993 Wiley-Liss, Inc. C1 KYUSHU UNIV,INST GENET INFORMAT,DIV GENOME ANAL,FUKUOKA 812,JAPAN. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. FU NEI NIH HHS [EY07573, EY08690] NR 42 TC 412 Z9 427 U1 4 U2 25 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1993 VL 2 IS 5 BP 338 EP 346 DI 10.1002/humu.1380020503 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA LZ776 UT WOS:A1993LZ77600002 PM 8257985 ER PT J AU CARRINGTON, M COLONNA, M SPIES, T STEPHENS, JC MANN, DL AF CARRINGTON, M COLONNA, M SPIES, T STEPHENS, JC MANN, DL TI HAPLOTYPIC VARIATION OF THE TRANSPORTER ASSOCIATED WITH ANTIGEN PROCESSING (TAP) GENES AND THEIR EXTENSION OF HLA CLASS-II REGION HAPLOTYPES SO IMMUNOGENETICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; MHC; MOLECULES; PROTEIN; PATHWAY; FAMILY; CELLS; SB AB Stable cell surface presentation of HLA class I molecules requires active transport of antigenic peptides across the endoplasmic reticulum by products of two genes, TAP1 and TAP2, which map in the major histocompatibility complex class II region. Alleles of each gene are derived from a combination of variable sites at each locus. In this study, TAP1 and TAP2 alleles were identified in homozygous typing cell (HTC) lines, allowing resolution of specific haplotypes in conjunction with the highly polymorphic HLA class II region haplotypes. Three alleles at each TAP locus were found from which eight haplotypes could be assigned. Determination of TAP1 and TAP2 alleles in cell lines homozygous at DR, DQ, and DP created eight additional haplotypes beyond the number observed with these class II genes alone. Complete analysis of DR, DQ, TAP, and DP genotypes in 66 HTCs resulted in the following groups: 1) 46 homozygotes; 2) nine homozygous at DR, DQ, and TAP, but heterozygous at DP; 3) four homozygous at DR, DQ, and DP, but heterozygous at one or both TAP genes; 4) four homozygous at DR and DQ, but heterozygous at TAP and DP; and 5) three complex genotypes heterozygous at DP, TAP, and at least one of DQA1, DQB1, or DRB1 loci. TAP1 and TAP2 genes map in an area of frequent recombination. TAP alleles were determined in five DQB1, DPB1 recombinant individuals, three of which were informative. Recombination was found between DQB1 and the TAP loci in two individuals and between TAP and DPB1 in the other individual. C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. RP CARRINGTON, M (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. OI Colonna, Marco/0000-0001-5222-4987 FU NCI NIH HHS [N01-CO-74102] NR 33 TC 100 Z9 100 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JAN PY 1993 VL 37 IS 4 BP 266 EP 273 PG 8 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA KD737 UT WOS:A1993KD73700004 PM 8267790 ER PT J AU CARINI, C PINI, C DIFELICE, G FATTOROSSI, A FRATAZZI, C AF CARINI, C PINI, C DIFELICE, G FATTOROSSI, A FRATAZZI, C TI CD23/FC-EPSILON-RII EXPRESSION ON PHYTOHEMAGGLUTININ-A-ACTIVATED OR PHORBOL-(12)MYRISTATE-(13)ACETATE-CA2+-ACTIVATED HUMAN TONSIL T-CELLS SO INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY LA English DT Article DE CD23; T-CELLS; IGE; LOW-AFFINITY RECEPTOR; FC-EPSILON-RII ID IGE-BINDING-FACTORS; FC-EPSILON-RECEPTORS; LOW-AFFINITY RECEPTOR; EPSTEIN-BARR VIRUS; HUMAN B-CELL; MONOCLONAL-ANTIBODY; HUMAN-LYMPHOCYTES; MONONUCLEAR-CELLS; RAT LYMPHOCYTES; DIFFERENTIATION AB The low-affinity Fc receptor for IgE, CD23/FcepsilonRII, has been expressed in T cell lines and pathologic T cells, but its presence on normal human T cells is still debated. We studied the expression of CD23/FcepsilonRII on purified T cells from normal peripheral blood mononuclear cells (PBMC) or tonsil T cells stimulated with 10 mug/ml phytohemagglutinin A (PHA) or phorbol-12myristate-13-acetate PMA) Ca2+. Using two-dimensional flow cytometry, the tonsil T-cell-enriched population showed > 10% of CD23/FcepsilonRII expression when coexpressed with the CD3 antigen. CD4+ T cells appear to be principally involved in the expression of CD23/FcepsilonRII, although we were unable to detect a clear expression of CD23/FcepsilonRII in PBMC that were activated with either PHA or PMA Ca2+. PHA stimulation resulted in the release of IgE binding factor (fgEBF). The induction of CD23/FcepsilonRII expression in PHA- and PMA-Ca2+-activated T cells was enhanced by IL-4, but not by IgE or IL-6. IL-4 also augmented the PHA- and PMA-Ca2+-induced release of IgEBF. The addition of supernatant from the Epstein-Barr virus (EBV)-infected cell line to PHA-or PMA-Ca2+-stimulated tonsil T cells did not increase CD23/FcepsilonRII expression. The expression of CD23/FcepsilonRII mRNA was detected in RNA prepared from a tonsil T-cell-enriched population by Northern blot analysis. C1 UNIV ROME,DEPT ALLERGY & CLIN IMMUNOL,I-00100 ROME,ITALY. IST SUPER SANITA,DEPT IMMUNOL,I-00161 ROME,ITALY. ARMY MED CTR,DEPT MED,PRATICA DI MARE,ITALY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV VIRAL PATHOGENESIS,BOSTON,MA 02115. RP CARINI, C (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,665 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 47 TC 8 Z9 8 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-2438 J9 INT ARCH ALLERGY IMM JI Int. Arch. Allergy Immunol. PY 1993 VL 101 IS 1 BP 31 EP 38 PG 8 WC Allergy; Immunology SC Allergy; Immunology GA LF602 UT WOS:A1993LF60200005 PM 8499771 ER PT J AU YOUNG, RH KOZAKEWICH, HPW SCULLY, RE AF YOUNG, RH KOZAKEWICH, HPW SCULLY, RE TI METASTATIC OVARIAN-TUMORS IN CHILDREN - A REPORT OF 14 CASES AND REVIEW OF THE LITERATURE SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Review DE OVARY; METASTASIS; CHILDREN; NEUROBLASTOMA; RHABDOMYOSARCOMA; EWINGS SARCOMA; RHABDOID TUMOR; CARCINOID TUMOR ID CELL-CARCINOMA; TERATOMA AB Fourteen cases of neoplasms metastatic to the ovaries in children 10 weeks to 15 years of age are reported. Eight tumors were neuroblastomas, 7 primary in the adrenal gland, and 1 primary in the posterior mediastinum. Three tumors were rhabdomyosarcomas primary in the ethmoid sinus, right occipital region, and left thigh, respectively. The final three tumors were a Ewing's sarcoma, a rhabdoid tumor, and a carcinoid tumor primary in the fibula, kidney, and lung, respectively. The ovarian involvement was an autopsy finding in nine of the patients. Three of the remaining five patients presented clinically with manifestations suggesting a primary ovarian tumor, and the final two patients, who had known extraovarian primary tumors, had symptomatic ovarian masses discovered during life. In one case of neuroblastoma and the case of rhabdoid tumor, the ovarian metastases were initially misinterpreted pathologically as primary ovarian cancers; the primary renal tumor was not discovered until autopsy in the latter case. The ovarian tumors were bilateral in 8 of the 14 cases. Ovarian enlargement was present in 10 cases. Our experience and that in the literature indicates that the childhood tumor that spreads to the ovary most frequently is the neuroblastoma and that rhabdomyosarcoma is the most common sarcoma of childhood that spreads to the ovary. The clinical features and the frequent bilaterality of ovarian metastatic tumors are helpful diagnostic features in many cases, but when the ovarian tumor is the presenting manifestation of the disease, is unilateral, or both, differentiation from various primary ovarian tumors may be difficult. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 37 TC 38 Z9 38 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD JAN PY 1993 VL 12 IS 1 BP 8 EP 19 DI 10.1097/00004347-199301000-00002 PG 12 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA KD246 UT WOS:A1993KD24600002 PM 8418081 ER PT J AU CLEMENT, PB YOUNG, RH AF CLEMENT, PB YOUNG, RH TI FLORID MESOTHELIAL HYPERPLASIA ASSOCIATED WITH OVARIAN-TUMORS - A POTENTIAL SOURCE OF ERROR IN TUMOR-DIAGNOSIS AND STAGING SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE OVARIAN TUMOR; MESOTHELIAL HYPERPLASIA; ENDOMETRIOSIS ID SEROUS BORDERLINE TUMORS; PROLIFERATION; ENDOMETRIOSIS; MICROINVASION; MALIGNANCY; PATHOLOGY AB Five ovarian tumors were associated with florid mesothelial hyperplasia that in four cases created initial problems in histologic classification and staging of the tumors. In two cases, small nests, cords, and gland-like arrangements of atypical mesothelial cells within the cyst wall of a serous or mullerian mucinous tumor of borderline malignancy were initially considered to possibly represent, or were misdiagnosed as, foci of stromal invasion, lymphatic invasion, or both. In the three other cases-an endometrioid adenocarcinoma, a struma ovarii, and a yolk sac tumor-papillary and sheet-like proliferations of mesothelial cells involved the extraovarian pelvic peritoneum; in one of the cases, necrosis of the mesothelial cells was prominent. These foci of extraovarian mesothelial hyperplasia were interpreted as metastatic tumor intraoperatively (three cases) and on initial microscopic examination (two cases). Factors that may have predisposed to the mesothelial hyperplasia included large size of the primary tumor (two cases), the presence of metastatic tumor elsewhere in the pelvis (three cases), ascites (two cases), and coexistent endometriosis (two cases). Distinction of mesothelial proliferations from invasive or metastatic ovarian tumor is obviously important in correct classification, staging, and management of the tumor. Awareness of the occasional occurrence of florid mesothelial hyperplasia in patients with ovarian neoplasms and attention to the histologic, histochemical, and immunohistochemical features of the mesothelial proliferation should facilitate the correct diagnosis. C1 UNIV BRITISH COLUMBIA,DEPT PATHOL,VANCOUVER V6T 1W5,BC,CANADA. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP CLEMENT, PB (reprint author), VANCOUVER GEN HOSP,DEPT PATHOL,VANCOUVER V5Z 1M9,BC,CANADA. NR 17 TC 28 Z9 28 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD JAN PY 1993 VL 12 IS 1 BP 51 EP 58 DI 10.1097/00004347-199301000-00007 PG 8 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA KD246 UT WOS:A1993KD24600007 PM 8418078 ER PT J AU SERAFETINIDES, EA AF SERAFETINIDES, EA TI CEREBRAL-DOMINANCE, SLEEP AND DREAM PHENOMENA SO INTERNATIONAL JOURNAL OF NEUROSCIENCE LA English DT Article DE CEREBRAL DOMINANCE AND SLEEP ID COGNITIVE ASYMMETRIES; EEG ASYMMETRY; REM-SLEEP; LATERALITY; MENTATION; WAKINGS; NREM AB Evidence from human and animal studies is discussed in relation to the role played by the cerebral hemispheres in the genesis of sleep and particularly dream phenomena. The inconclusiveness of such research is commented upon and suggestions for further research are outlined. C1 UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90024. RP SERAFETINIDES, EA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,DEPT PSYCHIAT,BLDG 258,ROOM 403,LOS ANGELES,CA 90073, USA. NR 34 TC 4 Z9 4 U1 0 U2 0 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 1993 VL 71 IS 1-4 BP 63 EP 70 DI 10.3109/00207459309000593 PG 8 WC Neurosciences SC Neurosciences & Neurology GA PM316 UT WOS:A1993PM31600008 PM 8407156 ER PT J AU TEICHER, BA SOTOMAYOR, EA ROBINSON, MF DUPUIS, NP SCHWARTZ, GN FREI, E AF TEICHER, BA SOTOMAYOR, EA ROBINSON, MF DUPUIS, NP SCHWARTZ, GN FREI, E TI TUMOR OXYGENATION AND RADIOSENSITIZATION BY PENTOXIFYLLINE AND A PERFLUBRON EMULSION CARBOGEN BREATHING SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE TUMOR OXYGENATION; PENTOXIFYLLINE; RADIOSENSITIZATION; PERFLUOROCHEMICAL EMULSION ID FLUOSOL-DA 20-PERCENT; SQUAMOUS-CELL CARCINOMA; LEWIS LUNG-CARCINOMA; RADIATION-THERAPY; PERFLUOROCHEMICAL EMULSION; ARTERIAL-DISEASE; PHASE-I/II; ADJUVANT; MICE; DISORDERS AB Oxygen tension measurements were made in three tumors: (i) the murine FSaII fibrosarcoma, (ii) the rat 9L gliosarcoma and (iii) the rat 13672 mammary adenocarcinoma using a pO2 histograph. Tumor oxygenation measurements were made while the animals breathed air or breathed carbogen (95% oxygen/5% carbon dioxide). Pentoxifylline or a perflubron emulsion was administered to the animals and tumor oxygen measurements were repeated under both breathing conditions. Both pentoxifylline and the perflubron emulsion improved the oxygenation of the FSaII fibrosarcoma under air breathing conditions but did not alter the oxygen profiles of either rat tumor compared with air breathing alone. Carbogen breathing increased the oxygenation of all tumors. Pentoxifylline administration did not change the oxygen profiles of the tumors under carbogen breathing conditions but administration of the perflubron emulsion increased the oxygenation of all three tumors under carbogen breathing conditions compared with carbogen breathing alone. Co-administration of pentoxifylline and the perflubron emulsion enhanced the radiation response of the Lewis lung tumor to daily fractionated radiation under air breathing conditions with a dose modifying factor of 1.65 and under carbogen breathing conditions with a dose modifying factor of 2.25. Over a range of perflubron emulsion doses, pentoxifylline increased the growth delay of the Lewis lung tumor in a constant manner. These results indicate that pentoxifylline and the perflubron emulsion have the largest impact on the oxygenation of more hypoxic tumors and that administration of the perflubron emulsion/carbogen breathing is the most effective means of increasing tumor oxygenation and radiation response. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 53 TC 17 Z9 17 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1993 VL 2 IS 1 BP 13 EP 21 PG 9 WC Oncology SC Oncology GA KC894 UT WOS:A1993KC89400002 PM 21573510 ER PT J AU SUIT, HD SPIRO, IJ AF SUIT, HD SPIRO, IJ TI DOES INCREASE IN LOCAL-CONTROL PROBABILITY MEAN A GREATER CURABILITY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 98 EP 99 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400005 ER PT J AU WANG, CC AF WANG, CC TI HEAD AND NECK - TREATMENT OF PRIMARY AND RELAPSED NASOPHARYNGEAL CARCINOMA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 99 EP 99 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400006 ER PT J AU SHIPLEY, WU ZEITMAN, AL AF SHIPLEY, WU ZEITMAN, AL TI BLADDER-CANCER - THE COMBINATION OF CHEMOTHERAPY AND IRRADIATION IN THE TREATMENT OF PATIENTS WITH MUSCLE-INVADING TUMORS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,GENITOURINARY ONCOL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 106 EP 106 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400020 ER PT J AU MACKLIS, RM WEST, DC SHAMBERGER, RC KOZAKEWICH, HP KREISSMAN, SG GRIER, HE AF MACKLIS, RM WEST, DC SHAMBERGER, RC KOZAKEWICH, HP KREISSMAN, SG GRIER, HE TI LOCAL-CONTROL IN STAGE-III NEUROBLASTOMA PATIENTS OVER ONE-YEAR OF AGE - THE JOINT CENTER CHILDRENS-HOSPITAL DANA-FARBER-CANCER-INSTITUTE EXPERIENCE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 131 EP 132 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400068 ER PT J AU HUG, EB FITZEK, MM MUNZENRIDER, JE LIEBSCH, NJ AF HUG, EB FITZEK, MM MUNZENRIDER, JE LIEBSCH, NJ TI LOCALLY CHALLENGING TUMORS OF THE AXIAL SKELETON - RESULTS OF COMBINED PROTON AND PHOTON RADIATION-THERAPY USING 3-D TREATMENT PLANNING SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,HARVARD CYCLOTRON LAB,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 156 EP 156 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400109 ER PT J AU GALL, KP THORNTON, AF MUNZENRIDER, J ROSENTHAL, S AF GALL, KP THORNTON, AF MUNZENRIDER, J ROSENTHAL, S TI EXPERIENCE USING RADIOPAQUE FIDUCIAL POINTS FOR PATIENT ALIGNMENT DURING RADIOTHERAPY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT THERAPY,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 161 EP 161 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400116 ER PT J AU TAGHIAN, A BUDACH, W RUKA, W FREEMAN, J GIOIOSO, D SUIT, H AF TAGHIAN, A BUDACH, W RUKA, W FREEMAN, J GIOIOSO, D SUIT, H TI TCD50 OF HUMAN GLIOBLASTOMA-MULTIFORME XENOGRAFTS INTO NUDE-MICE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 165 EP 166 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400123 ER PT J AU ALLAM, A TAGHIAN, A GIOIOSO, D DUFFY, M SUIT, HD AF ALLAM, A TAGHIAN, A GIOIOSO, D DUFFY, M SUIT, HD TI INTRATUMORAL HETEROGENEITY OF MALIGNANT GLIOMAS MEASURED IN-VITRO SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 167 EP 167 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400125 ER PT J AU GERWECK, L ZIETMAN, A ZAIDI, T AF GERWECK, L ZIETMAN, A ZAIDI, T TI SIMULTANEOUS EVALUATION OF DETERMINANTS OF RADIOCURABILITY - INTRINSIC CELL RADIOSENSITIVITY, CLONOGENIC FRACTION, AND HYPOXIC FRACTION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 169 EP 170 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400129 ER PT J AU WILLETT, CG CHEEK, R WARLAND, G SHELLITO, PC COMPTON, CC AF WILLETT, CG CHEEK, R WARLAND, G SHELLITO, PC COMPTON, CC TI PROLIFERATING CELL NUCLEAR ANTIGEN (PCNA) - PREDICTOR OF PATHOLOGICAL RESPONSE OF ADVANCED RECTAL-CANCER TO PREOPERATIVE IRRADIATION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 170 EP 171 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400131 ER PT J AU TAMLER, B WANG, CC EFIRD, J CHEN, YC LEWIS, A ZLOTECKI, R AF TAMLER, B WANG, CC EFIRD, J CHEN, YC LEWIS, A ZLOTECKI, R TI IS PHOTON IRRADIATION EFFECTIVE IN MANAGING ADENOID CYSTIC CARCINOMA OF THE HEAD AND NECK SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS 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 PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 174 EP 174 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400138 ER PT J AU ARA, G TEICHER, BA AF ARA, G TEICHER, BA TI THE HYPOXIC CELL SENSITIZER SR-4233 ACTS AS AN UNCOUPLER OF OXIDATIVE-PHOSPHORYLATION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS 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 PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 196 EP 197 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400173 ER PT J AU LING, C SMITH, A BRICKNER, T KUTCHER, G GERBER, R HUGHES, B KLINE, R OWEN, J HANLON, A WALLACE, M HANKS, G AF LING, C SMITH, A BRICKNER, T KUTCHER, G GERBER, R HUGHES, B KLINE, R OWEN, J HANLON, A WALLACE, M HANKS, G TI TREATMENT PLANNING - CERVIX - A PATTERNS OF CARE STUDY REPORT SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ST FRANCIS HOSP,TULSA,OK. WASHINGTON UNIV,ST LOUIS,MO 63130. ST VINCENT HOSP,PORTLAND,OR. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. AMER COLL RADIOL,PHILADELPHIA,PA. FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 199 EP 199 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400178 ER PT J AU NIXON, AJ RECHT, A NEUBERG, D GELMAN, R CONNOLLY, JL SCHNITT, S HARRIS, JR AF NIXON, AJ RECHT, A NEUBERG, D GELMAN, R CONNOLLY, JL SCHNITT, S HARRIS, JR TI THE RELATIONSHIP BETWEEN TIME FROM SURGERY TO THE START OF RADIATION-THERAPY (RT) AND RECURRENCE IN PATIENTS TREATED WITH BREAST-CONSERVING SURGERY AND RT WITHOUT SYSTEMIC THERAPY (ST) SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 BETH ISRAEL MED CTR,JOINT CTR RADIAT THERAPY,NEW YORK,NY 10003. BETH ISRAEL MED CTR,DEPT PATHOL,NEW YORK,NY 10003. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 201 EP 201 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400181 ER PT J AU PARDO, FS HSU, DW SCHMIDT, EV EFIRD, J LINGGOOD, RM AF PARDO, FS HSU, DW SCHMIDT, EV EFIRD, J LINGGOOD, RM TI ELEVATED PCNA EXPRESSION IN PITUITARY-ADENOMAS FAILING DEFINITIVE RADIATION-THERAPY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROPATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 205 EP 205 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400187 ER PT J AU ACHESON, JM PARDO, FS BOREK, C SCHMIDT, EV AF ACHESON, JM PARDO, FS BOREK, C SCHMIDT, EV TI TRANSDOMINANT NEGATIVE MUTATIONS IN P53 DO NOT ALWAYS RESULT IN ALTERED RADIATION SENSITIVITY AND METASTATIC POTENTIAL SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. TUFTS UNIV,DEPT PHYSIOL,BOSTON,MA 02111. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 212 EP 212 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400197 ER PT J AU SOBCZAK, ML CENTENO, BA SHIPLEY, WU PREFFER, FI BOYLE, BJ ZIETMAN, AL COLVIN, RB AF SOBCZAK, ML CENTENO, BA SHIPLEY, WU PREFFER, FI BOYLE, BJ ZIETMAN, AL COLVIN, RB TI CELL KINETIC FACTORS PREDICTING LOCAL-CONTROL FOLLOWING RADIATION-THERAPY FOR PROSTATE-CANCER - AN ASSESSMENT OF PERCENT-S-PHASE, TOTAL PROLIFERATIVE FRACTION AND DNA-PLOIDY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 226 EP 227 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400221 ER PT J AU ZIETMAN, AL COEN, JJ SHIPLEY, WU ALTHAUSEN, AF AF ZIETMAN, AL COEN, JJ SHIPLEY, WU ALTHAUSEN, AF TI ADJUVANT RADIATION-THERAPY FOR PATHOLOGICAL T3 PROSTATE-CANCER SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114. NR 0 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 229 EP 230 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400226 ER PT J AU WANG, CC EFIRD, JT AF WANG, CC EFIRD, JT TI DOES PROLONGED TREATMENT COURSE ADVERSELY AFFECT LOCAL-CONTROL OF CARCINOMA OF THE LARYNX SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 236 EP 237 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400237 ER PT J AU NIEMIERKO, A GOITEIN, M AF NIEMIERKO, A GOITEIN, M TI IMPLEMENTATION OF A MODEL FOR ESTIMATING NORMAL TISSUE COMPLICATION PROBABILITY - DERIVATION OF MODEL PARAMETERS FROM CLINICAL-DATA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 240 EP 241 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400244 ER PT J AU PILEPICH, MV CAPLAN, R ALSARRAF, M JOHN, M DOGGETT, RLS SAUSE, WT LAWTON, CA ABRAMS, RA ROTMAN, M RUBIN, P SHIPLEY, WU COX, JD AF PILEPICH, MV CAPLAN, R ALSARRAF, M JOHN, M DOGGETT, RLS SAUSE, WT LAWTON, CA ABRAMS, RA ROTMAN, M RUBIN, P SHIPLEY, WU COX, JD TI PHASE-III TRIAL OF HORMONAL CYTOREDUCTION IN CONJUNCTION WITH DEFINITIVE RADIOTHERAPY IN LOCALLY ADVANCED PROSTATE CARCINOMA - THE EMERGING ROLE OF PSA IN THE ASSESSMENT OF OUTCOME SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 C MCAULEY HLTH SYST,ANN ARBOR,MI. AMER COLL RADIOL,PHILADELPHIA,PA. WAYNE STATE UNIV,DETROIT,MI 48202. JOHNS HOPKINS UNIV HOSP,CTR ONCOL,BALTIMORE,MD 21205. KAWEAH DELTA CANC CARE CTR,VISALIA,CA. RADIAT ONCOL CTR,SACRAMENTO,CA. LATTER DAY ST HOSP,SALT LAKE CITY,UT 84143. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MED COLL WISCONSIN,MILWAUKEE,WI 53226. MD ANDERSON CANC CTR,HOUSTON,TX. SUNY HLTH SCI CTR,BROOKLYN,NY. UNIV ROCHESTER,MED CTR,ROCHESTER,NY 14642. NR 0 TC 13 Z9 13 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 246 EP 246 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400253 ER PT J AU LEWIS, A WANG, CC MIKETIC, L DAVIS, K PARDO, FS AF LEWIS, A WANG, CC MIKETIC, L DAVIS, K PARDO, FS TI MULTIMODAL MANAGEMENT OF PARAGANGLIOMAS OF THE HEAD AND NECK SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. UNIV PITTSBURGH,CTR CANC,DEPT RADIOL,PITTSBURGH,PA 15260. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 251 EP 251 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400260 ER PT J AU FUNG, CY WILLETT, CG EFIRD, J KAUFMAN, DS SHELLITO, PC AF FUNG, CY WILLETT, CG EFIRD, J KAUFMAN, DS SHELLITO, PC TI IMPROVED OUTCOME WITH ESCALATED RADIATION DOSING FOR ANAL CARCINOMA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 278 EP 278 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400305 ER PT J AU HAHN, CA EFIRD, JT SUIT, HD AF HAHN, CA EFIRD, JT SUIT, HD TI RATES OF DISTANT METASTASES IN LOCALLY RECURRENT SOFT-TISSUE SARCOMAS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 294 EP 294 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400332 ER PT J AU ANNE, PR EFIRD, JT SPIRO, IJ GEBHARDT, M SUIT, HD AF ANNE, PR EFIRD, JT SPIRO, IJ GEBHARDT, M SUIT, HD TI EWINGS-SARCOMA - COMPARISON OF LOCAL TREATMENT WITH RADIATION OR RADIATION PLUS SURGERY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPED SURG,BOSTON,MA 02114. NR 0 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 295 EP 296 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400335 ER PT J AU LEE, I GERWECK, LE BOUCHER, Y DEMHARTNER, TJ MENDELLO, C JAIN, RK AF LEE, I GERWECK, LE BOUCHER, Y DEMHARTNER, TJ MENDELLO, C JAIN, RK TI IMPROVED PHYSIOLOGICAL-PARAMETERS IN MURINE AND HUMAN TUMORS BY NICOTINAMIDE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 305 EP 305 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400352 ER PT J AU HAREGEWOIN, A ALEXANDER, E BLACK, PM LOEFFLER, JS AF HAREGEWOIN, A ALEXANDER, E BLACK, PM LOEFFLER, JS TI NITRIC-OXIDE (NO) PRODUCTION BY A GLIOBLASTOMA (GBM) CELL-LINE - POSSIBLE IMPLICATIONS FOR PATHOGENESIS AND RADIATION-THERAPY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CTR BRAIN TUMOR,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1993 VL 27 SU 1 BP 307 EP 307 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA LV404 UT WOS:A1993LV40400355 ER PT J AU BORNSTEIN, BA ZOURANJIAN, PS HANSEN, JL FRASER, SM GELWAN, LA TEICHER, BA SVENSSON, GK AF BORNSTEIN, BA ZOURANJIAN, PS HANSEN, JL FRASER, SM GELWAN, LA TEICHER, BA SVENSSON, GK TI LOCAL HYPERTHERMIA, RADIATION-THERAPY, AND CHEMOTHERAPY IN PATIENTS WITH LOCAL-REGIONAL RECURRENCE OF BREAST-CARCINOMA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE HYPERTHERMIA; RADIOTHERAPY; CHEMOTHERAPY; CISPLATIN; RECURRENT BREAST CANCER; TUMOR CONTROL; COMPLICATIONS; REIRRADIATION ID PROGNOSTIC FACTORS; MALIGNANCIES; CISPLATIN; CANCER; TUMORS; DRUGS AB We retrospectively reviewed the response rate and the acute and long-term toxicity of combined treatment using radiation therapy, hyperthermia, and chemotherapy in 29 patients with locally or regionally recurrent or advanced adenocarcinoma of the breast who completed at least 4 of the 6 prescribed hyperthermia treatments as part of a Phase I-II trial. Thirty-nine separate hyperthermia treatment fields were evaluated. Cisplatin alone or cisplatin with etanidazole or bleomycin was delivered just prior to hyperthermia once weekly. Hyperthermia was delivered to a target minimum tumor temperature of 43-degrees-C +/- 0.5 for 60 min. Following hyperthermia, a 400 cGy fraction of radiation was given. The radiation fraction size on other days was 200 cGy. Twenty-two fields had previously been irradiated and 17 fields had not. Prior chemotherapy had been given in 24 of 29 patients (83%) and hormonal therapy given in 21 (72%). The median follow-up time is 10 months; 16/29 patients (55%) have died of disease. The overall complete response rate for all fields was 53%. Response rate was not related to any clinical factor, radiation dose, microwave or ultrasound technique, type of chemotherapy, or tumor temperatures, but the number of patients in the study population was small. A statistically significant association between the likelihood of complications and the total radiation therapy dose (previous radiation and present radiation) was found. Persistent ulceration lasting greater than 1 month after completing treatment was seen in 67% of previously irradiated fields compared to 21% of fields that had not been previously treated (p = 0.015). Surgical wound repair was needed for 38% of fields with a history of prior irradiation versus 6% of those without prior treatment (p = 0.050). A statistically significant radiation therapy dose response was found for the likelihood of these complications. None of the hyperthermia temperature parameters studied correlated with an increased risk of complication. We conclude that the combination of radiation therapy, hyperthermia, and chemotherapy results in a high rate of complete response. However, in patients who have been treated with prior radiation therapy, this combination may be more locally toxic than treatment with hyperthermia and radiation therapy alone. The precise impact of chemotherapy on the therapeutic index of hyperthermia and radiation therapy remains to be determined in randomized clinical trials. C1 HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP BORNSTEIN, BA (reprint author), HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,50 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-31303] NR 20 TC 35 Z9 36 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 1 PY 1993 VL 25 IS 1 BP 79 EP 85 PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KF812 UT WOS:A1993KF81200012 PM 7677990 ER PT J AU NIEMIERKO, A GOITEIN, M AF NIEMIERKO, A GOITEIN, M TI MODELING OF NORMAL TISSUE-RESPONSE TO RADIATION - THE CRITICAL VOLUME MODEL SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE MODELING; NORMAL TISSUE; COMPLICATION PROBABILITY; NORMAL TISSUE COMPLICATION PROBABILITY; DOSE-RESPONSE; TREATMENT PLANNING ID COMPLICATION PROBABILITY; TOLERANCE; KIDNEY; OPTIMIZATION; IRRADIATION; HISTOGRAMS; THERAPY; CURVES AB Purpose: A model for calculating normal tissue complication probability in response to therapeutic doses of radiation is presented. Methods and Materials: The model which we call the ''critical volume model'' is based on a concept of functional subunits defined either structurally (e.g., nephrons) or functionally, and an assumption that normal tissue complication probability is fully determined by the number or fraction of surviving functional subunits composing an organ or tissue. The essential features of the model are that it takes into account variations in tissue radiosensitivity and architecture of an organ for a single patient and for a patient population, and predicts the normal tissue complication probability under conditions of 3-dimensional inhomogeneity of the dose distribution. The model can be used for Integral Response, or ''parallel,'' organs (where all functional subunits are performing the same function in parallel and the output of the organ is the sum of the outputs of the functional subunits and for Critical Element, or ''serial,'' organs (where damage to one functional subunit results in an expression of damage for the whole organ). The model combines into one compact scheme new concepts and several ideas and models which have been previously developed by other investigators. Results: The behavior of the model is presented and discussed for the example of the kidney, with clinical nephritis as the functional endpoint. Conclusions: The model has the potential to be a useful tool for evaluation and optimization of 3-dimensional treatment plans for a variety of types of normal tissues. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP NIEMIERKO, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,DIV RADIAT BIOPHYS,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 50628, CA 21239] NR 32 TC 161 Z9 170 U1 2 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 1 PY 1993 VL 25 IS 1 BP 135 EP 145 PG 11 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KF812 UT WOS:A1993KF81200020 PM 8416870 ER PT J AU SHIPLEY, WU AF SHIPLEY, WU TI RADIATION AS ADJUNCTIVE THERAPY TO CYSTECTOMY FOR BLADDER-CANCER SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Letter RP SHIPLEY, WU (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,GENITOURINARY ONCOL UNIT,BOSTON,MA 02114, USA. NR 4 TC 1 Z9 1 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 1 PY 1993 VL 25 IS 1 BP 153 EP 154 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KF812 UT WOS:A1993KF81200025 PM 8416874 ER PT J AU EATON, KA DEWHIRST, FE RADIN, MJ FOX, JG PASTER, BJ KRAKOWKA, S MORGAN, DR AF EATON, KA DEWHIRST, FE RADIN, MJ FOX, JG PASTER, BJ KRAKOWKA, S MORGAN, DR TI HELICOBACTER-ACINONYX SP-NOV, ISOLATED FROM CHEETAHS WITH GASTRITIS SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID PYLORI SUBSP-MUSTELAE; CAMPYLOBACTER-PYLORI; ANIMAL-MODEL; HOMOSEXUAL MEN; GEN-NOV; BACTERIUM; STOMACH; RNA; INFECTION; PHYLOGENY AB Four strains of a novel Helicobacter species were isolated from the stomachs of cheetahs (Acinonyx jubilatus) with gastritis. These isolates were phenotypically similar to Helicobacter pylori. The isolates were gram-negative, spiral bacteria which grew under microaerophilic conditions at 37-degrees-C, but not at 25 or 42-degrees-C, and produced urease, catalase, oxidase, alkaline phosphatase, and gamma-glutamyl transpeptidase. The isolates did not ferment glucose, mannitol, inositol, sorbitol, rhamnose, sucrose, melibiose, amygdalin, or arabinose; hydrolyze hippurate or indoxyl acetate; or reduce nitrate. They did not produce H2S from triple sugar iron agar, and they did not grow in the presence of 1.0% glycine or 1.5% NaCl. They were resistant to nalidixic acid and sensitive to cephalothin and metronidazole. Cells were typically 0.3 by 2.0 mum and possessed tufts of two to five sheathed, monopolar flagella. The G+C content of strain 90-119 was 30 mol%. Cluster analysis of densitometry scans of polyacrylamide protein gels revealed more than 70% similarity of the cheetah isolates to H. pylori, less than 60% similarity to Helicobacter felis, and less than 50% similarity to Helicobacter mustelae. Complete 16S rRNA sequences were determined for two of the cheetah isolates. Phylogenetic analysis was performed by comparing the cheetah sequences to those of 19 reference strains, including H. pylori, H. felis (two strains), H. mustelae, Helicobacter muridarum, ''Flexispira rappini,'' Wolinella succinogenes, Campylobacter coli, Campylobacter concisus, Campylobacter curvus, Campylobacter fetus, Campylobacter hyointestinalis, Campylobacter jejuni, Campylobacter lari, Campylobacter rectus, Campylobacter sputorum subsp. bubulus, a Campylobacter sp. (Pig isolate), [Bacteroides] gracilis, and [Bacteroides] ureolyticus. The 16S rRNA sequences for 13 of the 19 reference species have not previously been reported. Phylogenetic analysis demonstrated that the cheetah isolates were most closely related to H. pylori (97.4% similarity), H. felis (96.1% similarity), and H. mustelae (93.4% similarity). On the basis of these findings, we propose that these isolates represents a novel species of Helicobacter, which we designate Helicobacter acinonyx. The type strain is 90-119 (CCUG 29263, ATCC 51101). C1 FORSYTH DENT CTR,BOSTON,MA 02115. MIT,DIV COMPARAT MED,CAMBRIDGE,MA 02139. PROCTER & GAMBLE CO,CINCINNATI,OH 45339. RP EATON, KA (reprint author), OHIO STATE UNIV,DEPT VET PATHOBIOL,1925 COFFEY RD,COLUMBUS,OH 43210, USA. FU NIDCR NIH HHS [DE-08303, DE-04881]; NIDDK NIH HHS [DK-39570] NR 37 TC 127 Z9 127 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1993 VL 43 IS 1 BP 99 EP 106 PG 8 WC Microbiology SC Microbiology GA KG457 UT WOS:A1993KG45700015 PM 8379970 ER PT J AU PASTER, BJ RUSSELL, JB YANG, CMJ CHOW, JM WOESE, CR TANNER, R AF PASTER, BJ RUSSELL, JB YANG, CMJ CHOW, JM WOESE, CR TANNER, R TI PHYLOGENY OF THE AMMONIA-PRODUCING RUMINAL BACTERIA PEPTOSTREPTOCOCCUS-ANAEROBIUS, CLOSTRIDIUM-STICKLANDII, AND CLOSTRIDIUM-AMINOPHILUM SP-NOV SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID AMINO-ACIDS; MONENSIN; RUMEN; RNA; DEAMINATION; TRANSPORT; ECOSYSTEM; SODIUM AB In Previous studies, gram-positive bacteria which grew rapidly with peptides or an amino acid as the sole energy source were isolated from bovine rumina. Three isolates, strains C, F(T) (T = type strain), and SR, were considered to be ecologically important since they produced up to 20-fold more ammonia than other ammonia-producing ruminal bacteria. On the basis of phenotypic criteria, the taxonomic position of these new isolates was uncertain. In this study, the 16S rRNA sequences of these isolates and related bacteria were determined to establish the phylogenetic positions of the organisms. The sequences of strains C, F(T), and SR and reference strains of Peptostreptococcus anaerobius, Clostridium sticklandii, Clostridium coccoides, Clostridium aminovalericum, Acetomaculum ruminis, Clostridium leptum, Clostridium lituseburense, Clostridium acidiurici, and Clostridium barkeri were determined by using a modified Sanger dideoxy chain termination method. Strain C, a large coccus purported to belong to the genus Peptostreptococcus, was closely related to P. anaerobius, with a level of sequence similarity of 99.6%. Strain SR, a heat-resistant, short, rod-shaped organism, was closely related to C. sticklandii, with a level of sequence similarity of 99.9%. However, strain F(T), a heat-resistant, pleomorphic, rod-shaped organism, was only distantly related to some clostridial species and P. anaerobius. On the basis of the sequence data, it was clear that strain F(T) warranted designation as a separate species. The closest known relative of strain F(T) was C. coccoides (level of similarity, only 90.6%). Additional strains that are phenotypically similar to strain F(T) were isolated in this study. On the basis of phenotypic and phylogenetic differences, we believe that strain F(T) represents a new species of the genus Clostridium, for which we propose the name Clostridium aminophilum. C1 USDA ARS,ITHACA,NY 14853. FORSYTH DENT CTR,BOSTON,MA 02115. CORNELL UNIV,MICROBIOL SECT,ITHACA,NY 14853. UNIV OKLAHOMA,DEPT BOT & MICROBIOL,NORMAN,OK 73019. UNIV ILLINOIS,DEPT MOLEC BIOL,CHAMPAIGN,IL 61820. FU NIDCR NIH HHS [DE-04881, DE-08303] NR 35 TC 81 Z9 82 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1993 VL 43 IS 1 BP 107 EP 110 PG 4 WC Microbiology SC Microbiology GA KG457 UT WOS:A1993KG45700016 PM 8427801 ER PT S AU HALL, JE TAYLOR, AE MARTIN, KA CROWLEY, WF AF HALL, JE TAYLOR, AE MARTIN, KA CROWLEY, WF BE Tolis, G Bringer, J Chrousos, GP TI NEW APPROACHES TO THE STUDY OF THE NEUROENDOCRINE ABNORMALITIES OF WOMEN WITH THE POLYCYSTIC OVARIAN SYNDROME SO INTRAOVARIAN REGULATORS AND POLYCYSTIC OVARIAN SYNDROME: RECENT PROGRESS ON CLINICAL AND THERAPEUTIC ASPECTS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT SYMP ON INTRAOVARIAN REGULATORS AND POLYCYSTIC OVARIAN SYNDROME: RECENT PROGRESS ON CLINICAL AND THERAPEUTIC ASPECTS, AT THE 9TH INTERNATIONAL CONGRESS OF ENDOCRINOLOGY CY AUG 24-26, 1992 CL ATHENS, GREECE SP NICHHD, HELLENIC MINIST HLTH & WELFARE, ABBOTT LABS, BIOANAL, BIOATRIKA, BIOMEDICA, ICI, FARAN LABS, LAKATSA DIAGNOST CTR, IPSEN INT RP HALL, JE (reprint author), MASSACHUSETTS GEN HOSP,NATL CTR INFERTIL RES,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-779-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 687 BP 182 EP 192 PG 11 WC Endocrinology & Metabolism; Pathology; Physiology; Reproductive Biology SC Endocrinology & Metabolism; Pathology; Physiology; Reproductive Biology GA BY50K UT WOS:A1993BY50K00021 ER PT S AU CROWLEY, WF HALL, JE MARTIN, KA ADAMS, J TAYLOR, AE AF CROWLEY, WF HALL, JE MARTIN, KA ADAMS, J TAYLOR, AE BE Tolis, G Bringer, J Chrousos, GP TI AN OVERVIEW OF THE DIAGNOSTIC CONSIDERATIONS IN POLYCYSTIC OVARIAN SYNDROME SO INTRAOVARIAN REGULATORS AND POLYCYSTIC OVARIAN SYNDROME: RECENT PROGRESS ON CLINICAL AND THERAPEUTIC ASPECTS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT SYMP ON INTRAOVARIAN REGULATORS AND POLYCYSTIC OVARIAN SYNDROME: RECENT PROGRESS ON CLINICAL AND THERAPEUTIC ASPECTS, AT THE 9TH INTERNATIONAL CONGRESS OF ENDOCRINOLOGY CY AUG 24-26, 1992 CL ATHENS, GREECE SP NICHHD, HELLENIC MINIST HLTH & WELFARE, ABBOTT LABS, BIOANAL, BIOATRIKA, BIOMEDICA, ICI, FARAN LABS, LAKATSA DIAGNOST CTR, IPSEN INT RP CROWLEY, WF (reprint author), MASSACHUSETTS GEN HOSP,NATL CTR INFERTIL RES,BOSTON,MA 02114, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-779-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 687 BP 235 EP 241 PG 7 WC Endocrinology & Metabolism; Pathology; Physiology; Reproductive Biology SC Endocrinology & Metabolism; Pathology; Physiology; Reproductive Biology GA BY50K UT WOS:A1993BY50K00027 ER PT J AU ROTH, BJ ELSON, P SLEDGE, GW EINHORN, LH TRUMP, DL AF ROTH, BJ ELSON, P SLEDGE, GW EINHORN, LH TRUMP, DL TI 5-AZACYTIDINE (NSC-102816) IN REFRACTORY GERM-CELL TUMORS - A PHASE-II TRIAL OF THE EASTERN-COOPERATIVE-ONCOLOGY-GROUP SO INVESTIGATIONAL NEW DRUGS LA English DT Note DE TESTICULAR CANCER; 5-AZACYTIDINE; CISPLATIN-REFRACTORY; GERM CELL TUMORS ID DNA METHYLATION; DIFFERENTIATION C1 INDIANA UNIV,MED CTR,INDIANAPOLIS,IN 46204. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. DUKE UNIV,MED CTR,DURHAM,NC 27710. FU NCI NIH HHS [2R35CA 39844-07, CA21115, CA49883] NR 6 TC 11 Z9 12 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1993 VL 11 IS 2-3 BP 201 EP 202 DI 10.1007/BF00874155 PG 2 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA LZ110 UT WOS:A1993LZ11000010 PM 7505269 ER PT J AU BERNSTEIN, ML WHITEHEAD, VM GRIER, H DUBOWY, R LAND, V DEVINE, S MURPHY, S KUNG, F AF BERNSTEIN, ML WHITEHEAD, VM GRIER, H DUBOWY, R LAND, V DEVINE, S MURPHY, S KUNG, F TI A PHASE-I TRIAL OF FAZARABINE IN REFRACTORY PEDIATRIC SOLID TUMORS - A PEDIATRIC-ONCOLOGY-GROUP STUDY SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE FAZARABINE; PEDIATRIC SOLID TUMOR; PHASE I TRIAL ID ARABINOFURANOSYL-5-AZACYTOSINE; ARABINOSYL-5-AZACYTOSINE; CANCER AB Fazarabine is a synthetic analog of cytosine arabinoside and 5-azacytidine that incorporates structural features of both compounds. Xenograft studies showed good activity against a variety of transplanted tumors. Initial studies in adults employed both a continuous infusion schedule and a daily bolus x 5 schedule. Myelotoxicity, especially neutropenia, was dose-limiting, with excessive myelotoxicity seen on the daily bolus x 5 at 72 mg/M(2)/day. Since short infusions may be administered in Ringer's lactate rather than either dimethylsulfoxide or dimethylacetamide required for continuous infusion, this study examined a daily x 5 schedule in children with refractory solid tumors. The initial dosage was 30 mg/M(2)/day, 80% of the maximum tolerated dosage in adults, with subsequent 30% dosage escalations. A total of 18 patients were enrolled, with a wide spectrum of pediatric solid tumors. Myelosuppression was the only significant toxicity, and was excessive at 78 mg/M(2)/day. Therefore, on this bolus regimen, 65 mg/M(2)/day for 5 days was the maximum tolerated dosage. One patient with medulloblastoma had stable disease for 65 days. No other responses were seen. C1 DANA FARBER CANC INST,BOSTON,MA. BOSTON CHILDRENS HOSP,BOSTON,MA. SYRACUSE UNIV,SYRACUSE,NY. WASHINGTON UNIV,ST LOUIS,MO. CHILDRENS MEM HOSP,CHICAGO,IL. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. PEDIAT ONCOL GRP,OPERAT OFF,ST LOUIS,MO 63108. RP BERNSTEIN, ML (reprint author), MCGILL UNIV,MONTREAL CHILDRENS HOSP,SERV HEMATOL,2300 TUPPER ST,MONTREAL,PQ,CANADA. FU NCI NIH HHS [CA-07431, CA-33587, CA-41573] NR 12 TC 7 Z9 7 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1993 VL 11 IS 4 BP 309 EP 312 DI 10.1007/BF00874429 PG 4 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA MR907 UT WOS:A1993MR90700007 PM 7512539 ER PT J AU WEISSLEDER, R WANG, YM PAPISOV, M BOGDANOV, A SCHAFFER, B BRADY, TJ WITTENBERG, J AF WEISSLEDER, R WANG, YM PAPISOV, M BOGDANOV, A SCHAFFER, B BRADY, TJ WITTENBERG, J TI POLYMERIC CONTRAST AGENTS FOR MR IMAGING OF ADRENAL-GLANDS SO JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE ADRENAL GLAND, MR; CONTRAST ENHANCEMENT; CONTRAST MEDIA; GADOLINIUM; INDIUM, RADIOACTIVE AB A variety of adrenal imaging agents have been used in nuclear medicine, but no agent has been developed for magnetic resonance (MR) imaging. The authors have previously observed accumulation of aminated macromolecules in adrenal glands. They now report the synthesis of a model polymeric aminated contrast agent for enhanced MR imaging of the adrenal glands. The model agent consisted of a poly-L-lysine conjugate (molecular weight, 245 kd) that had 70% free epsilon amino groups and 30% diethylenetriaminepentaacetic acid (DTPA)-derivatized amino groups to bind indium-111 or gadolinium. One hour after intravenous administration of this compound, adrenal uptake was 10.1% +/- 0.7 of injected dose per gram of tissue. When all free epsilon amino groups of the polylysine were completely substituted with DTPA, adrenal uptake was 3.4 times lower, indicating the importance of free amino groups for adrenal uptake. MR imaging in rats showed that a dose of 0.08 mmol of gadolinium per kilogram of the agent was sufficient to enhance the signal intensity of adrenal glands. Three hours after intravenous administration of the agent, signal intensity of the adrenal glands was 186% of precontrast values (liver, 165%; kidney, 91%). Fluorescence microscopy showed that the agent accumulated primarily in the cortical zona glomerulosa and in the adrenal medulla. These initial studies demonstrate the feasibility of designing contrast agents for MR imaging of the adrenal glands. RP WEISSLEDER, R (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,CTR MGH NMR,MR PHARMACEUT PROGRAM,32 FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [1 ROI CA54886-01] NR 0 TC 6 Z9 6 U1 0 U2 3 PU SOC MAGNETIC RESONANCE IMAGING PI EASTON PA 1991 NORTHAMPTON ST, EASTON, PA 18042-3189 SN 1053-1807 J9 JMRI-J MAGN RESON IM JI JMRI-J. Magn. Reson. Imaging PD JAN-FEB PY 1993 VL 3 IS 1 BP 93 EP 97 DI 10.1002/jmri.1880030116 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KJ725 UT WOS:A1993KJ72500013 PM 8428107 ER PT J AU ANZUETO, A ANDRADE, FH MAXWELL, LC LEVINE, SM LAWRENCE, RA JENKINSON, SG AF ANZUETO, A ANDRADE, FH MAXWELL, LC LEVINE, SM LAWRENCE, RA JENKINSON, SG TI DIAPHRAGMATIC FUNCTION AFTER RESISTIVE BREATHING IN VITAMIN-E-DEFICIENT RATS SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE RESPIRATORY MUSCLE; DIAPHRAGM; FREE RADICALS; VITAMIN-E DEFICIENCY; LIPID PEROXIDATION; GLUTATHIONE; FATIGUE; CONTRACTILE PROPERTIES ID LIPID-PEROXIDATION; LIQUID-CHROMATOGRAPHY; OXIDATIVE STRESS; EXERCISE; GLUTATHIONE; MECHANISMS; SELENIUM; TOXICITY; PERFORMANCE; PROTECTION AB The effects of vitamin E deficiency on diaphragm function were studied at rest and after resistive breathing (RB) in Sprague-Dawley rats (wt 300-400 g). The animals were pair fed a vitamin E-deficient diet (E-def) or a matched vitamin E-sufficient diet (E-suf). Each diet group was then further subdivided into a group that breathed unimpeded (control) and a second group that breathed through an inspiratory resistor until the animals were unable to sustain 70% of their maximum airway pressure. Diaphragm samples were obtained for analysis of thiobarbituric acid-reactive substances, glutathione (GSH) concentrations, and glutathione disulfide (GSSG) concentrations. In vitro isometric contractile studies were also performed and included twitch (P(t)) and maximum tetanic (P(o)) tensions, force-frequency curves, fatigue index, and recovery index. P(t) was significantly reduced in the E-suf RB group as well as both of the E-def groups. P(o) was also significantly reduced in both E-def groups. The E-def rats subjected to RB showed a significant decrease in tension at both high and low frequencies compared with the E-suf rats. Concentrations of diaphragm thiobarbituric acid-reactive substances were significantly increased in both E-def groups. RB in both E-suf and E-def rats resulted in increases in diaphragm concentrations of GSSG and decreases in the GSH/GSSG ratios. We conclude that reduction of contractile function, lipid peroxidation, and activation of the GSH redox cycle occur with RB and that these effects are significantly increased in the presence of vitamin E deficiency. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP ANZUETO, A (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 NR 36 TC 29 Z9 30 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JAN PY 1993 VL 74 IS 1 BP 267 EP 271 PG 5 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA KJ480 UT WOS:A1993KJ48000036 PM 8444702 ER PT J AU CHEN, TY WARREN, HS GREENE, E BLACK, KM FROSTELL, CG ROBINSON, DR ZAPOL, WM AF CHEN, TY WARREN, HS GREENE, E BLACK, KM FROSTELL, CG ROBINSON, DR ZAPOL, WM TI PROTECTIVE EFFECTS OF ANTI-O POLYSACCHARIDE AND ANTI-LIPID A MONOCLONAL-ANTIBODIES ON PULMONARY HEMODYNAMICS SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE LIPOPOLYSACCHARIDE; ENDOTOXIN; THROMBOXANE; SHEEP; PULMONARY HYPERTENSION ID GRAM-NEGATIVE BACTEREMIA; MUTANT ESCHERICHIA-COLI; LIPOPOLYSACCHARIDE LPS; SEPTIC SHOCK; INTERLEUKIN-1 INDUCTION; SALMONELLA-MINNESOTA; CROSS-REACTIVITY; BINDING-PROTEIN; AWAKE SHEEP; ENDOTOXIN AB Monoclonal antibodies (MAbs) directed to endotoxin can protect in some animal models against the pathophysiological effects of endotoxin infusion. When 0.02 mug/kg of lipopolysaccharide (LPS) derived from Escherichia coli O111:B4 was incubated in vitro for 2 h with the murine immunoglobulin G MAb, 5B10, directed against the 0-polysaccharide antigenic domain of E. coli O111:B4 and then the mixture was infused into sheep, we noted significant protection. The second temperature peak was decreased (P < 0.05 vs. LPS control). The acute pulmonary arterial pressure elevation was diminished (mean peak pulmonary arterial pressure 23.2 +/- 2.5 mmHg, P < 0.05 vs. LPS control), and the peak plasma thromboxane B2 level was reduced (mean peak thromboxane B2 level 0.50 +/- 0.15 ng/ml, P < 0.05 vs. LPS control). In contrast, preincubation of the LPS with a human immunoglobulin M MAb, HA-1A, directed against the core glycolipid of the LPS molecule provided no protective effects in this sheep model. This finding is in agreement with recent studies reporting HA-IA may bind to antibiotic-treated bacteria but not to purified smooth LPS. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. RP ZAPOL, WM (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-42397]; NIAID NIH HHS [AI-28465]; NIAMS NIH HHS [AR-79427] NR 34 TC 9 Z9 9 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JAN PY 1993 VL 74 IS 1 BP 423 EP 427 PG 5 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA KJ480 UT WOS:A1993KJ48000058 PM 8444723 ER PT J AU HALL, SD KANE, MF KOLODNER, RD AF HALL, SD KANE, MF KOLODNER, RD TI IDENTIFICATION AND CHARACTERIZATION OF THE ESCHERICHIA-COLI RECT PROTEIN, A PROTEIN ENCODED BY THE RECE REGION THAT PROMOTES RENATURATION OF HOMOLOGOUS SINGLE-STRANDED-DNA SO JOURNAL OF BACTERIOLOGY LA English DT Article ID GENETIC-RECOMBINATION; BACTERIOPHAGE-LAMBDA; EXONUCLEASE-VIII; BETA-PROTEIN; PLASMID RECOMBINATION; RAC PROPHAGE; K-12; MUTATIONS; SUPPRESSION; MUTANTS AB Recombination of plasmid DNAs and recombination of bacteriophage lambda red mutants in recB recC sbcA Escherichia coli mutants, in which the recE region is expressed, do not require recA. The recE gene is known to encode exonuclease VIII (exoVIII), which is an ATP-independent exonuclease involved in the RecE pathway of recombination. A 33,000-molecular-weight (MW) protein was observed to be coexpressed with both exoVIII and a truncated version of exoVIII, pRac3 exo, when they were overproduced under the control of strong promoters. We have purified this 33,000-MW protein (p33) and demonstrated by protein sequence analysis that it is encoded by the same coding sequence that encodes the C-terminal 33,000-MW portion of exoVIII. p33 is expressed independently of exoVIII but is probably translated from the same mRNA. p33 was found to bind to single-stranded DNA and also to promote the renaturation of complementary single-stranded DNA. It appears that p33 is functionally analogous to the bacteriophage lambda beta protein, which may explain why RecE pathway recombination does not require recA. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. FU NIGMS NIH HHS [GM26017] NR 55 TC 76 Z9 79 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 1993 VL 175 IS 1 BP 277 EP 287 PG 11 WC Microbiology SC Microbiology GA KE618 UT WOS:A1993KE61800034 PM 8416902 ER PT J AU GOTO, Y KOGURE, E TAKAGI, T AIMOTO, S AOBA, T AF GOTO, Y KOGURE, E TAKAGI, T AIMOTO, S AOBA, T TI MOLECULAR-CONFORMATION OF PORCINE AMELOGENIN IN SOLUTION - 3 FOLDING UNITS AT THE N-TERMINAL, CENTRAL, AND C-TERMINAL REGIONS SO JOURNAL OF BIOCHEMISTRY LA English DT Article ID BOVINE TOOTH ENAMEL; MINERAL INTERACTION; CIRCULAR-DICHROISM; PROTEIN AB Circular dichroism (CD) studies were conducted to gain a better insight into the conformation of amelogenins, which were isolated from developing enamel of piglets. The intact porcine amelogenin and its degraded products were purified chromatographically. The 25-residue peptide corresponding to the segment at the C-terminus was synthesized. CD spectra of these samples were measured at pH 5.0-5.3 in the temperature range between 4 and 90-degrees-C. The most remarkable finding was that the CD spectrum of the intact amelogenin was accounted for by the sum of the spectra of the three fragments at the N-terminal, central, and C-terminal regions, supporting the hypothesis that the structure of the whole protein consists of discrete folding units. Furthermore, low-angle laser light scattering analysis provided evidence that the 20 kDa amelogenin, the most abundant extracellular matrix protein in forming enamel tissue, exists in a monomeric form at pH 5.3 and 25-degrees-C. It was tentatively concluded that the N-terminal region contains beta-sheet structures, while the spectral characteristics of the C-terminal region are similar to those of a random coil conformation. The conformation of the central region was characterized by a strong negative ellipticity at 203 nm, although its nature remains to be defined. C1 FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115. OSAKA UNIV,FAC SCI,DEPT BIOL,TOYONAKA,OSAKA 530,JAPAN. OSAKA UNIV,INST PROT RES,SUITA,OSAKA 565,JAPAN. FU NIDCR NIH HHS [DE07623] NR 20 TC 34 Z9 35 U1 0 U2 2 PU JAPANESE BIOCHEMICAL SOC PI TOKYO PA ISHIKAWA BLDG-3F 25-16 HONGO-5-CHOME, TOKYO TOKYO 113, JAPAN SN 0021-924X J9 J BIOCHEM-TOKYO JI J. Biochem. (Tokyo) PD JAN PY 1993 VL 113 IS 1 BP 55 EP 60 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KR549 UT WOS:A1993KR54900011 PM 8454575 ER PT J AU JAMES, SP SCHMALZRIED, TP MCGARRY, FJ HARRIS, WH AF JAMES, SP SCHMALZRIED, TP MCGARRY, FJ HARRIS, WH TI EXTENSIVE POROSITY AT THE CEMENT FEMORAL PROSTHESIS INTERFACE - A PRELIMINARY-STUDY SO JOURNAL OF BIOMEDICAL MATERIALS RESEARCH LA English DT Article ID FINITE-ELEMENT; COMPONENTS AB This study is the first description of the extensive porosity which is preferentially located at the cement-prosthesis interface of cemented femoral components of total hip replacements. The observation is important because the interfacial porosity may decrease the strength of the cement-femoral prosthesis interface and jeopardize the mechanical integrity of the cement mantle. We examined the cement-metal interfaces from a multiplicity of in vivo and in vitro specimens using both optical and scanning electron microscopy. These samples included several stem designs, implants made from either Co-Cr or Ti alloy, implants made with a variety of surface finishes and both centrifuged and uncentrifuged cement. All in vivo and in vitro samples had marked porosity in the cement focally concentrated at the cement-metal interface. The amount of porosity at the interface greatly exceeded the amount of general porosity found throughout the bulk cement. Centrifuging did not affect the interfacial porosity, and neither did alloy nor surface finish. The presence of these pores may be explained by the rheological characteristics of the cement. C1 MIT,DEPT MAT SCI & ENGN,CAMBRIDGE,MA 02139. HARBOR UCLA MED CTR,TORRANCE,CA 90509. JOINT REPLACEMENT INST,LOS ANGELES,CA 90007. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 14 TC 57 Z9 57 U1 0 U2 4 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9304 J9 J BIOMED MATER RES JI J. Biomed. Mater. Res. PD JAN PY 1993 VL 27 IS 1 BP 71 EP 78 DI 10.1002/jbm.820270110 PG 8 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA KC876 UT WOS:A1993KC87600009 PM 8421001 ER PT J AU HEALY, WL SILISKI, JM INCAVO, SJ AF HEALY, WL SILISKI, JM INCAVO, SJ TI OPERATIVE TREATMENT OF DISTAL FEMORAL FRACTURES PROXIMAL TO TOTAL KNEE REPLACEMENTS SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article AB Twenty fractures of the distal part of the femur proximal to a total knee replacement were treated operatively by members of the New England Trauma Study Group. Notching of the anterior aspect of the femoral cortex was associated with only two of these fractures, and none of the knee prostheses was loose at the time of the fracture. All twenty fractures were treated with open reduction and stable internal fixation, and the operation on fifteen fractures was supplemented with bone grafts. Every fracture healed, and eighteen healed after a mean of sixteen weeks (range, six to forty weeks). Union of the other two fractures was delayed, but repeat open reduction and internal fixation combined with autogenous bone-grafting resulted in union. After operative treatment, the patients returned to the level of activity that they had had before the fracture. The pre-existing tibiofemoral alignment and range of motion of the knee were also restored. At the time of follow-up, the average clinical rating of the Knee Society for all twenty knees had not decreased compared with the score before the fracture. C1 LAHEY CLIN FDN,MED CTR,DEPT ORTHOPAED SURG,BURLINGTON,MA 01805. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. UNIV VERMONT,SCH MED,MED CTR HOSP,DEPT ORTHOPAED SURG,BURLINGTON,VT 05405. NR 22 TC 98 Z9 100 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 1993 VL 75A IS 1 BP 27 EP 34 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA KH729 UT WOS:A1993KH72900004 PM 8419387 ER PT J AU BARRACK, RL HARRIS, WH AF BARRACK, RL HARRIS, WH TI THE VALUE OF ASPIRATION OF THE HIP-JOINT BEFORE REVISION TOTAL HIP-ARTHROPLASTY SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID DEEP INFECTION; REPLACEMENT; SEPSIS AB The role of aspiration of the hip joint before revision of a total hip arthroplasty remains controversial. To address this issue, we reviewed the results of 270 consecutive hips in which aspiration had been attempted before revision procedures that were performed between 1980 and 1988. All hips had intraoperative findings and clinical follow-up of at least two years to confirm the presence or absence of infection. Only six (2 per cent) of the 270 hips were determined to be infected. Aspiration had been attempted in all six hips, but fluid could be obtained from only four. All six hips also had clinical or radiographic signs, or both, of infection, including increasing pain within three years after the arthroplasty (four hips), inability of the patient to attain pain-free status after the original procedure (four hips), radiographic findings compatible with infection (six hips), and a positive finding on culture of a specimen obtained from a previous aspiration (two hips). Because of these factors, aspiration was attempted a second time in four of the six hips and a third time in three of the four. The four hips from which fluid could be obtained had a total of ten successful aspirations; the cultures of specimens obtained from six of these procedures were positive and those from four were negative. The appearance of the capsular tissue at the time of the operation suggested infection in five of the six infected hips. Histological sections were positive for inflammation in all six: there was acute inflammation only in one, chronic inflammation only in two, and acute and chronic inflammation in three. No organisms were seen on gram stains of specimens from any of the six infected hips. Of the 254 hips that did not have an infection and had been aspirated successfully, thirty-two (13 per cent) had a false-positive result on culture of a specimen of the aspiration fluid. Only two (6 per cent) of the thirty-four hips that had a positive result on culture of fluid from the initial aspiration had a true-positive result. No hip had a true-positive result on culture of fluid that had been aspirated preoperatively without also having clinical and radiographic evidence of infection. On the basis of these findings, we recommend that aspiration be performed in selected patients rather than routinely. It also should be performed only if a detailed clinical history suggests infection or if radiographs demonstrate focal lysis, aggressive non-focal lysis, or periostitis. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 42 TC 136 Z9 139 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 1993 VL 75A IS 1 BP 66 EP 76 PG 11 WC Orthopedics; Surgery SC Orthopedics; Surgery GA KH729 UT WOS:A1993KH72900009 PM 8419393 ER PT J AU MANKIN, HJ AF MANKIN, HJ TI GAUCHERS-DISEASE - A NOVEL TREATMENT AND AN IMPORTANT BREAKTHROUGH SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Editorial Material ID GLUCOCEREBROSIDASE; SEQUENCE; THERAPY; BONE RP MANKIN, HJ (reprint author), MASSACHUSETTS GEN HOSP,FRUIT ST,BOSTON,MA 02114, USA. NR 18 TC 3 Z9 3 U1 0 U2 0 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 1993 VL 75 IS 1 BP 2 EP 3 PG 2 WC Orthopedics; Surgery SC Orthopedics; Surgery GA KH160 UT WOS:A1993KH16000001 PM 8421025 ER PT J AU ANNER, BM HAUPERT, GT AF ANNER, BM HAUPERT, GT TI USE OF 2-SIDED BIFUNCTIONAL LIPOSOMES IN THE STUDY OF A HYPOTHALAMIC NA,K-ATPASE INHIBITOR SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article; Proceedings Paper CT SATELLITE MEETING ON NATRIURETIC FACTORS AND HYPERTENSION, AT THE 14TH SCIENTIFIC MEETING OF THE INTERNATIONAL-SOC-OF-HYPERTENSION CY JUN 19-20, 1992 CL SEVILLA, SPAIN SP INT SOC HYPERTENS, FONDO INVESTIGAC SANITARIA, MARION MERRELL DOW, BRISTOL MYERS SQUIBB, KNOLL, MERCK SHARP & DOHME, PFIZER, SK&F, LABS SERVIER, LAB ESTEVE DE NA,K-ATPASE; 2-SIDED BIFUNCTIONAL LIPOSOMES; SIDE OF HYPOTHALAMIC INHIBITOR ACTION; MEMBRANE PERMEABILITY; INHIBITOR TITRATION ID INTRAMEMBRANE PARTICLE FORMATION; SODIUM-TRANSPORT INHIBITOR; K+-ATPASE INHIBITOR; (NA++K+)-ATPASE LIPOSOMES; NATRIURETIC HORMONE; ALPHA-SUBUNIT; NA+; NA+,K+-TRANSPORT AB Two-sided bifunctional (ATP-filled) Na,K-ATPase liposomes have been developed as a result of knowledge about the average liposome diameter and volume, the liposome size distribution, the average number of Na,K-ATPase molecules reconstituted per liposome, and the orientation of the reconstituted Na,K-ATPase molecules. The addition of 5-10 muM external Rb-86 to the liposomes containing 50 mM encapsulated ATP provoked an impressive Rb-86 accumulation by the cell-like-oriented pumps. The successive addition of external ATP activated the pumps in the reversed orientation of the same liposome, leading to total extrusion of the previously accumulated Rb-86. An inhibitor extracted from bovine hypothalamus (hypothalamic inhibitory factor) inhibited the cell-like-oriented population, i.e., acted like an extracellular inhibitor at 30 nM. Conversely, at 75 nM, the reversed pump population was also blocked, indicating that the inhibitor either traversed the membrane or was able to act also at the intracellular enzyme side at a higher concentration. Thus, the side of action as well as the membrane permeability of structurally unknown endogenous Na,K-ATPase inhibitors can be determined simultaneously in a single suspension of two-sided bifunctional Na,K-ATPase liposomes. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RENAL UNIT,BOSTON,MA 02114. RP ANNER, BM (reprint author), UNIV GENEVA,MED CTR,SCH MED,DIV CLIN PHARMACOL,EXPTL THERAPEUT LAB,CH-1211 GENEVA 4,SWITZERLAND. NR 15 TC 5 Z9 5 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. PY 1993 VL 22 SU 2 BP S51 EP S53 DI 10.1097/00005344-199322002-00017 PG 3 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA MC235 UT WOS:A1993MC23500017 PM 7508028 ER PT J AU JANSSENS, SP KACHORIS, C PARKER, WL HALES, CA HAUPERT, GT AF JANSSENS, SP KACHORIS, C PARKER, WL HALES, CA HAUPERT, GT TI HYPOTHALAMIC NA+,K+-ATPASE INHIBITOR CONSTRICTS PULMONARY-ARTERIES OF SPONTANEOUSLY HYPERTENSIVE RATS SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article; Proceedings Paper CT SATELLITE MEETING ON NATRIURETIC FACTORS AND HYPERTENSION, AT THE 14TH SCIENTIFIC MEETING OF THE INTERNATIONAL-SOC-OF-HYPERTENSION CY JUN 19-20, 1992 CL SEVILLA, SPAIN SP INT SOC HYPERTENS, FONDO INVESTIGAC SANITARIA, MARION MERRELL DOW, BRISTOL MYERS SQUIBB, KNOLL, MERCK SHARP & DOHME, PFIZER, SK&F, LABS SERVIER, LAB ESTEVE DE PULMONARY HYPERTENSION; ISOLATED PULMONARY ARTERY; SPONTANEOUSLY HYPERTENSIVE RAT; NA+,K+-ATPASE INHIBITION; ENDOGENOUS DIGITALIS ID SODIUM-TRANSPORT INHIBITOR; ADRENERGIC NEUROEFFECTOR INTERACTION; BLOOD-VESSEL WALL; SMOOTH-MUSCLE; ATPASE INHIBITOR; K+-ATPASE; CONTRACTILITY; OUABAIN; CALCIUM; NA+ AB Hypothalamic inhibitory factor (HIF) is an endogenous high-affinity inhibitor of Na+,K+-ATPase with ouabain-like properties and has been implicated in the pathogenesis of genetic systemic hypertension. We wondered whether HIF might also be associated with the recently demonstrated pulmonary hypertension of spontaneously hypertensive rats (SHRs). We compared HIF effects on the contractility of isolated 2- to 3-mm pulmonary artery (PA) rings from SHRs and age-matched normotensive Sprague-Dawley (SD) rats. HIF caused a reversible, concentration-dependent increase in tension in PA rings of SHR and SD rats, whereas ouabain did not. PA tension development with HIF (4 nM final concentration) was significantly higher in SHRs than in SD rats: 308 +/- 56 mg (mean +/- SE) vs. 137 +/- 26, respectively, p < 0.05. Abdominal aortic contractions induced by HIF did not differ between SHRs and SD rats. In SHRs, but not SD rats, the effect on PA rings was significantly greater than on aortic rings. In all cases, contraction was abolished by phentolamine but was unaffected by calcium-channel blockade using verapamil. HIF-induced tension development required external Ca2+. We conclude that PA rings from SHRs are more sensitive to Na+,K+-ATPase inhibitory effects of HIF than PA rings from SD rats, which may contribute to the observed pulmonary hypertension in SHR. Local modulation of the Na+,K+-ATPase-adrenergic neuroeffector interaction may be the vasoconstrictive mechanism of action of HIF in these vessels. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,RENAL UNIT,BOSTON,MA 02114. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,PRINCETON,NJ. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,PULM CRIT CARE UNIT,BOSTON,MA 02114. FU FIC NIH HHS [IF05TWO4379-1]; NHLBI NIH HHS [HL 39150] NR 23 TC 11 Z9 11 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. PY 1993 VL 22 SU 2 BP S42 EP S46 DI 10.1097/00005344-199322002-00015 PG 5 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA MC235 UT WOS:A1993MC23500015 PM 7508026 ER PT J AU VANDESTOLPE, A KARPERIEN, M LOWIK, CWGM JUPPNER, H SEGRE, GV ABOUSAMRA, AB DELAAT, SW DEFIZE, LHK AF VANDESTOLPE, A KARPERIEN, M LOWIK, CWGM JUPPNER, H SEGRE, GV ABOUSAMRA, AB DELAAT, SW DEFIZE, LHK TI PARATHYROID HORMONE-RELATED PEPTIDE AS AN ENDOGENOUS INDUCER OF PARIETAL ENDODERM DIFFERENTIATION SO JOURNAL OF CELL BIOLOGY LA English DT Article ID TERATOCARCINOMA STEM-CELLS; MOUSE EMBRYOS; RETINOIC ACID; ADULT TISSUES; MESSENGER-RNA; LOCALIZATION; RAT; PREIMPLANTATION; RESPONSES; RECEPTOR AB Parathyroid hormone related peptide (PTHrP), first identified in tumors from patients with the syndrome of ''Humoral Hypercalcemia of Malignancy,'' can replace parathyroid hormone (PTH) in activating the PTH-receptor in responsive cells. Although PTHrP expression is widespread in various adult and fetal tissues, its normal biological function is as yet unknown. We have examined the possible role of PTHrP and the PTH/PTHrP-receptor in early mouse embryo development. Using F9 embryonal carcinoma (EC) cells and ES-5 embryonic stem (ES) cells as in vitro models, we demonstrate that during the differentiation of these cells towards primitive and parietal endoderm-like phenotypes, PTH/PTHrP-receptor mRNA is induced. This phenomenon is correlated with the appearance of functional adenylate cyclase coupled PTH/PTHrP-receptors. These receptors are the mouse homologues of the recently cloned rat bone and opossum kidney PTH/PTHrP-receptors. Addition of exogenous PTH or PTHrP to RA-treated EC or ES cells is an efficient replacement for dBcAMP in inducing full parietal endoderm differentiation. Endogenous PTHrP is detectable at very low levels in undifferentiated EC and ES cells, and is up-regulated in their primitive and parietal endoderm-like derivatives as assessed by immunofluorescence. Using confocal laser scanning microscopy on preimplantation mouse embryos, PTHrP is detected from the late morula stage onwards in developing trophectoderm cells, but not in inner cell mass cells. In blastocyst stages PTHrP is in addition found in the first endoderm derivatives of the inner cell mass. Together these results indicate that the PTH/PTHrP-receptor signalling system serves as a para- or autocrine mechanism for parietal endoderm differentiation in the early mouse embryo, thus constituting the earliest hormone receptor system involved in embryogenesis defined to date. C1 LEIDEN UNIV HOSP,DEPT ENDOCRINOL,2333 AA LEIDEN,NETHERLANDS. UNIV UTRECHT,DEPT MOLEC CELL BIOL,UTRECHT,NETHERLANDS. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. RP VANDESTOLPE, A (reprint author), NETHERLANDS INST DEV BIOL,HUBRECHT LAB,UPPSALALAAN 8,3584 CT UTRECHT,NETHERLANDS. OI Abou-Samra, Abdul/0000-0001-8735-1142 NR 33 TC 97 Z9 98 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD JAN PY 1993 VL 120 IS 1 BP 235 EP 243 DI 10.1083/jcb.120.1.235 PG 9 WC Cell Biology SC Cell Biology GA KE650 UT WOS:A1993KE65000024 PM 8380175 ER PT J AU CHAN, BMC HEMLER, ME AF CHAN, BMC HEMLER, ME TI MULTIPLE FUNCTIONAL FORMS OF THE INTEGRIN VLA-2 CAN BE DERIVED FROM A SINGLE ALPHA(2) CDNA CLONE - INTERCONVERSION OF FORMS INDUCED BY AN ANTI-BETA(1) ANTIBODY SO JOURNAL OF CELL BIOLOGY LA English DT Article ID EXTRACELLULAR-MATRIX RECEPTORS; HUMAN FIBRONECTIN RECEPTOR; MEDIATED CELL-ADHESION; PLATELET GPIIB-IIIA; MONOCLONAL-ANTIBODY; T-CELLS; CYTOPLASMIC DOMAIN; BETA-SUBUNIT; COLLAGEN RECEPTOR; LAMININ RECEPTOR AB The integrin VLA-2 was previously found to bind to either collagen alone, or collagen plus laminin, but the mechanism for this cell-specific functional difference was unknown. Here we transfected VLA-2 alpha2 subunit cDNA into K562 cells and obtained VLA-2 (called Form-O) which bound to neither collagen nor laminin. We then used a Matrigel selection procedure to enrich for a minor subpopulation of K562 cells stably expressing a form of VLA-2 (Form-C) that bound to collagen but not laminin. In contrast, the same alpha2 cDNA transfected into RD cells yielded VLA-2 (Form-CL) which bound to both collagen and laminin. These Form-O, -C, and -CL activities were stably expressed during extended cell culture, and could not be qualitatively altered by adding phorbol esters or by exchanging the resident divalent cations. However, addition of stimulatory anti-beta1 antibodies (TS2/16, A-1A5) rapidly converted VLA-2 Form-O and Form-C into Form-CL. Anti-beta1 antibody stimulation of VLA-2 activity was observed not only on whole cells, but also with solubilized receptors. These results suggest (a) that the ligand binding specificity of VLA-2 can be determined by its cellular environment, rather than by variations in the primary sequence of the alpha2 subunit, (b) that stably inactive or partly active VLA-2 can be rapidly converted to a fully active form through conformational changes initiated at a nonligand binding site on the beta1 subunit, and (c) that the mechanisms for VLA-2 stimulation by phorbol ester and by antibody are quite distinct, because the latter does not require an intact cell. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NIGMS NIH HHS [GM46526, GM38903] NR 63 TC 144 Z9 144 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD JAN PY 1993 VL 120 IS 2 BP 537 EP 543 DI 10.1083/jcb.120.2.537 PG 7 WC Cell Biology SC Cell Biology GA KH215 UT WOS:A1993KH21500023 PM 8421065 ER PT J AU DIAMOND, MS SPRINGER, TA AF DIAMOND, MS SPRINGER, TA TI A SUBPOPULATION OF MAC-1 (CD11B/CD18) MOLECULES MEDIATES NEUTROPHIL ADHESION TO ICAM-1 AND FIBRINOGEN SO JOURNAL OF CELL BIOLOGY LA English DT Article ID FUNCTION-ASSOCIATED ANTIGEN-1; INCREASED SURFACE EXPRESSION; MEMBRANE GLYCOPROTEIN-IIB; REDUCES ORGAN INJURY; PLATELET GPIIB-IIIA; MONOCLONAL-ANTIBODY; LEUKOCYTE ADHESION; CELL-SURFACE; POLYMORPHONUCLEAR LEUKOCYTES; TRANSENDOTHELIAL MIGRATION AB We report that a subpopulation (10%) of the Mac-1 (CD11b/CD18) molecules on activated neutrophils mediates adhesion to ICAM-1 and fibrinogen. We describe a novel mAb (CBRM1/5) that binds to an activation-specific neoepitope on a subset of Mac-1 molecules on neutrophils and monocytes after stimulation with chemoattractants or phorbol esters but does not recognize Mac-1 on resting myeloid cells. CBRM1/5 immunoprecipitates a subpopulation of Mac-1 molecules from detergent lysates of neutrophils, binds to immunoaffinity-purified Mac-1, and localizes to the I domain on the alpha chain of Mac-1. Because CBRM1/5 recognizes a fraction of Mac-1 on activated neutrophils, but still blocks Mac-1-dependent adhesion to fibrinogen and ICAM-1, we suggest that only a small subset of Mac-1 molecules is competent to mediate adhesion. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA. RP DIAMOND, MS (reprint author), HARVARD UNIV,SCH MED,COMM CELL & DEV BIOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA31799]; NIGMS NIH HHS [T32-GM07753-11, T32 GM007753] NR 87 TC 453 Z9 456 U1 2 U2 10 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD JAN PY 1993 VL 120 IS 2 BP 545 EP 556 DI 10.1083/jcb.120.2.545 PG 12 WC Cell Biology SC Cell Biology GA KH215 UT WOS:A1993KH21500024 PM 7678422 ER PT J AU STOW, JL DEALMEIDA, JB AF STOW, JL DEALMEIDA, JB TI DISTRIBUTION AND ROLE OF HETEROTRIMERIC G-PROTEINS IN THE SECRETORY PATHWAY OF POLARIZED EPITHELIAL-CELLS SO JOURNAL OF CELL SCIENCE LA English DT Article DE G PROTEINS; SECRETION; GOLGI; VESICLE TRAFFICKING ID GTP-BINDING PROTEINS; HEPARAN-SULFATE PROTEOGLYCAN; BETA-GAMMA-SUBUNITS; PERTUSSIS-TOXIN; GOLGI MEMBRANES; BASEMENT-MEMBRANE; ADENYLYL CYCLASE; BREFELDIN-A; ENDOPLASMIC-RETICULUM; ALPHA-SUBUNITS AB The movement of newly synthesized proteins in the constitutive secretory pathway, from their site of synthesis in the endoplasmic reticulum to the cell surface or to intracellular destinations, requires an orderly sequence of transport steps between membrane-bound compartments. Until recently, the trafficking and secretion of proteins through this pathway was thought to occur as a relatively automatic, unregulated series of events. Recent studies show that protein trafficking in the constitutive secretory pathway requires GTP hydrolysis by families of GTP-binding proteins (G proteins), which at multiple steps potentially provide regulation and specificity for protein trafficking. Many monomeric G proteins are known to be localized and functional on membrane compartments in the constitutive secretory pathway. Now, members of the heterotrimeric G protein family have also been localized on intracellular membranes and compartments such as the Golgi complex. We have studied the localization and targeting of G alpha subunits to distinct membrane domains in polarized epithelial cells. The distribution of different G alpha subunits on very specific membrane domains in cultured epithelial cells, and in epithelial cells of the kidney cortex, is highly suggestive of roles for these G proteins in intracellular trafficking pathways. One of these G protein subunits, G alpha(i-3), was localized on Golgi membranes. Studies on LLC-PK1 cells overexpressing G alpha(i-3) provided evidence for its functional role in regulating the transport of a constitutively secreted heparan sulfate proteoglycan through the Golgi complex. Inhibition or activation of heterotrimeric G proteins by pertussis toxin or by aluminium fluoride respectively, have provided further evidence for regulation of intracellular transport by pertussis toxin-sensitive G proteins. Although the functions of Golgi-associated G proteins are not yet understood at the molecular level, heterotrimeric G proteins have been implicated in the binding of cytosolic coat proteins and vesicle formation on Golgi membranes. Future studies will elucidate how multiple G proteins, of both the heterotrimeric and monomeric families, are involved in the regulation of Golgi function and protein trafficking in the secretory pathway. subunits on very specific membrane domains in cultured epithelial C1 MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02129 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02129 USA. RP STOW, JL (reprint author), MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02129 USA. OI Stow, Jennifer/0000-0002-5409-9101 NR 51 TC 5 Z9 5 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PY 1993 SU 17 BP 33 EP 39 PG 7 WC Cell Biology SC Cell Biology GA MW455 UT WOS:A1993MW45500007 ER PT J AU BROWN, D SABOLIC, I AF BROWN, D SABOLIC, I TI ENDOSOMAL PATHWAYS FOR WATER CHANNEL AND PROTON PUMP RECYCLING IN KIDNEY EPITHELIAL-CELLS SO JOURNAL OF CELL SCIENCE LA English DT Article DE KIDNEY; IMMUNOCYTOCHEMISTRY; PROTON PUMP; WATER CHANNEL; PRINCIPAL CELL; INTERCALATED CELL; COLLECTING DUCT ID VACUOLAR H+-ATPASE; DUCT PRINCIPAL CELLS; TOAD URINARY-BLADDER; COLLECTING DUCT; RAT-KIDNEY; ANTIDIURETIC-HORMONE; INTERCALATED CELLS; MEMBRANE-PROTEINS; TURTLE BLADDER; ACTIN-FILAMENTS AB The plasma membrane composition of virtually all eukaryotic cells is maintained and continually modified by the recycling of specific protein and lipid components. In the kidney collecting duct, urinary acidification and urinary concentration are physiologically regulated at the cellular level by the shuttling of proton pumps and water channels between intracellular vesicles and the plasma membrane of highly specialized cell types. In the intercalated cell, hydrogen ion secretion into the urine is modulated by the recycling of vesicles carrying a proton pumping ATPase to and from the plasma membrane. In the principal cell, the antidiuretic hormone, vasopressin, induces the insertion of vesicles that contain proteinaceous water channels into the apical cell membrane, thus increasing the permeability to water of the epithelial layer. In both cell types, 'coated' carrier vesicles are involved in this process, but whereas clathrin-coated vesicles are involved in the endocytotic phase of water channel recycling, the transporting vesicles in intercalated cells are coated with the cytoplasmic domains of the proton pumping ATPase. By a combination of morphological and functional techniques using FITC-dextran as an endosomal marker, we have shown that recycling endosomes from intercalated cells are acidifying vesicles but that they do not contain water channels. In contrast, principal cell vesicles that recycle water channels do not acidify their lumens in response to ATP. These non-acidic vesicles lack functionally important subunits of the vacuolar proton ATPase, including the 16 kDa proteolipid that forms the transmembrane proton pore. Because these endosomes are directly derived via clathrin-mediated endocytosis, our results indicate that endocytotic clathrin-coated vesicles are non-acidic compartments in principal cells. In contrast, recycling vesicles in intercalated cells contain large numbers of proton pumps, arranged in hexagonally packed arrays on the vesicle membrane. These pumps are inserted into the apical plasma membrane of A-type (acid-secreting) intercalated cells, and the baselateral plasma membrane of B-type (bicarbonate-secreting) cells in the collecting duct. Both apical and baselateral targeting of H+-ATPase-containing vesicles in these cells may be directed by microtubules, because polarized insertion of the pump into both membrane domains is disrupted by microtubule depolymerizing agents. However, the basolateral localization of other transporting proteins in intercalated cells, including the band 3-like anion exchanger and facilitated glucose transporters, is not affected by microtubule disruption. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP BROWN, D (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114, USA. NR 91 TC 7 Z9 7 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 1993 SU 17 BP 49 EP 59 PG 11 WC Cell Biology SC Cell Biology GA MW455 UT WOS:A1993MW45500009 ER PT J AU KOPANS, DB AF KOPANS, DB TI BREAST IMAGING AND BREAST-CANCER PREVENTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT Workshop on Chemoprevention of Breast Cancer CY OCT 06-10, 1993 CL LAKE TAHOE, CA SP NCI, CHEMOPREVENTION INVESTIGAT DRUG UNIT, DIV CANC PREVENT & CONTROL DE BREAST CANCER; BREAST IMAGING; CHEMOPREVENTION; DETECTION; MAMMOGRAPHY ID REPLACEMENT THERAPY; MAMMOGRAPHY AB Earlier detection of breast cancer through periodic screening is the only currently available intervention likely to reduce breast cancer-related mortality in the near term; prevention would be preferable. The alteration of proliferative changes and the assessment of intermediate endpoints may establish some interventions as more likely than others to interrupt the progression to lethal cancer. However, since not all breast cancers are fatal, the endpoint that will ultimately be accepted as proof of prevention success will be a reduction in breast cancer mortality. Methods of detection and monitoring must be carefully tailored so that the influences of the detection techniques do not alter the prevention results. (C) 1993 Wiley-Liss, Inc. RP KOPANS, DB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,100 BLOSSOM ST,BOSTON,MA 02114, USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1993 SU 17G BP 92 EP 95 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE169 UT WOS:A1993NE16900017 ER PT J AU SMITH, HS LU, Y DENG, GR MARTINEZ, O KRAMS, S LJUNG, BM THOR, A LAGIOS, M AF SMITH, HS LU, Y DENG, GR MARTINEZ, O KRAMS, S LJUNG, BM THOR, A LAGIOS, M TI MOLECULAR ASPECTS OF EARLY STAGES OF BREAST-CANCER PROGRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT Workshop on Chemoprevention of Breast Cancer CY OCT 06-10, 1993 CL LAKE TAHOE, CA SP NCI, CHEMOPREVENTION INVESTIGAT DRUG UNIT, DIV CANC PREVENT & CONTROL DE IMMUNE SURVEILLANCE; LOSS OF HETEROZYGOSITY; ONCOGENE; P53; TUMOR SUPPRESSOR GENE ID WILD-TYPE P53; TUMOR SUPPRESSOR GENE; CELL-CYCLE CONTROL; A MOUSE CELLS; ALLELE LOSSES; MUTANT P53; SV40-TRANSFORMED CELLS; CARCINOMA INSITU; NORMAL 3T3; SHORT ARM AB It is clear that breast cancer progression is associated with inactivation of a number of different recessive oncogenes. The most widely evaluated tumor suppressor gene, p53, is mutated in approximately 30-50% of sporadic breast cancers. Mutations usually occur early in malignant progression. Loss of heterozygosity (LOH) studies have identified numerous chromosomal regions where other recessive oncogenes relevant to breast cancer may be located. Each LOH is seen in a varying proportion of breast cancers and may appear either early or late in progression. High-grade ductal carcinoma in situ (DCIS) and invasive carcinoma have similar genetic lesions, showing that aberrations can occur before invasive disease. Direct evidence that the same aberrations can be acquired later in progression comes from a study of multiple metastases from the same patient; other studies found that primary invasive cancers are characterized by marked intratumor heterogeneity for each lesion examined. The model we propose to account for these results hypothesizes that multiple genetic lesions can accomplish each phenotype required for malignancy (i.e., dysregulated proliferation, invasion, angiogenesis, etc.) and that, for a given tumor, at least one aberrant gene for each phenotypic change is stochastically selected. Biological heterogeneity of breast cancer results from the stochastic acquisition of various genetic aberrations. We further propose that the lymphocytic reaction in high-grade DCIS may select for aggressive tumor subpopulations capable of escaping immune surveillance. Another aspect of tumor heterogeneity may be the multiple mechanisms employed by various tumors to escape immune surveillance. (C) 1993 Wiley-Liss, Inc. C1 CALIF PACIFIC MED CTR,GERALDINE BRUSH CANC RES INST,SAN FRANCISCO,CA 94115. UNIV CALIF SAN FRANCISCO,DEPT PATHOL,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 89 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1993 SU 17G BP 144 EP 152 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE169 UT WOS:A1993NE16900027 ER PT J AU NOZAKI, K MOSKOWITZ, MA MAYNARD, KI KOKETSU, N DAWSON, TM BREDT, DS SNYDER, SH AF NOZAKI, K MOSKOWITZ, MA MAYNARD, KI KOKETSU, N DAWSON, TM BREDT, DS SNYDER, SH TI POSSIBLE ORIGINS AND DISTRIBUTION OF IMMUNOREACTIVE NITRIC-OXIDE SYNTHASE-CONTAINING NERVE-FIBERS IN CEREBRAL-ARTERIES SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE NITRIC OXIDE SYNTHASE; NITRIC OXIDE; CEREBRAL ARTERY; VASOACTIVE INTESTINAL POLYPEPTIDE; SPHENOPALATINE GANGLION; PARASYMPATHETIC ID VASOACTIVE INTESTINAL POLYPEPTIDE; GENE-RELATED PEPTIDE; SMOOTH-MUSCLE CELLS; STORING SUBSTANCE-P; RELAXING FACTOR; L-ARGININE; RAT; SPHENOPALATINE; RELAXATION; PATHWAYS AB The distribution of perivascular nerve fibers expressing nitric oxide synthase (NOS)-immunoreactivity was examined in Sprague-Dawley and Long-Evans rats using affinity-purified rabbit antisera raised against NOS from rat cerebellum. NOS immunoreactivity was expressed within the endothelium and adventitial nerve fibers in both rat strains. Labeled axons were abundant and dense in the proximal anterior and middle cerebral arteries, but were less numerous in the caudal circle of Willis and in small pia arteries. The sphenopalatine ganglia were the major source of positive fibers in these vessels. Sectioning postganglionic parasympathetic fibers from both sphenopalatine ganglia reduced the density of NOS-immunoreactive (IR) nerve fibers by >75% in the rostral circle of Willis. Moreover, NOS-IR was present in 70-80% of sphenopalatine ganglion cells. Twenty percent of these neurons also contained vasoactive intestinal polypeptide (VIP)-immunoreactivity. By contrast, the superior cervical ganglia did not contain NOS-IR cells. In the trigeminal ganglion, NO-IR neurons were found chiefly within the ophthalmic division; approximately 10-15% of neurons were positively labeled. Colocalization with calcitonin gene-related peptide (CGRP) was not observed. Sectioning the major trigeminal branch innervating the circle of Willis decreased positive fibers by less-than-or-equal-to 25% in the ipsilateral vessels. In the nodose ganglion, 20-30% of neurons contained NOS-immunoreactivity, whereas less than 1% were in the C2 and C3 dorsal root ganglia. Three human circles of Willis obtained at autopsy showed sparse immunoreactive fibers, chiefly within vessels of the posterior circulation. Postmortem delay accounted for some of the reduced density. Our findings indicate that nerve fibers innervating cerebral arteries may serve as a nonendothelial source of the vasodilator nitric oxide (NO). The coexistence of NOS and VIP within sphenopalatine ganglion cells raises the possibility that two vasodilatory agents, one, a highly diffusable short-lived, low-molecular-weight molecule, and the other, a polar 28 amino acid-containing peptide, may serve as coneuromediators within the cerebral circulation. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL,BALTIMORE,MD 21205. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC SCI,BALTIMORE,MD 21205. RP MOSKOWITZ, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,STROKE RES LAB,32 FRUIT ST,BOSTON,MA 02114, USA. RI Moskowitz, Michael/D-9916-2011 FU NIDA NIH HHS [DA-00266]; NINDS NIH HHS [NS 10828, NS 26361] NR 32 TC 332 Z9 334 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1993 VL 13 IS 1 BP 70 EP 79 PG 10 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA KE730 UT WOS:A1993KE73000007 PM 7678014 ER PT J AU LAFLECHE, G ALBERT, MS MILLER, L RICHARDS, M BYLSMA, FW STERN, Y AF LAFLECHE, G ALBERT, MS MILLER, L RICHARDS, M BYLSMA, FW STERN, Y TI PREDICTORS OF FUNCTIONAL STATUS IN MILD ALZHEIMERS-DISEASE (AD) SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,BALTIMORE,MD 21287. NEUROL INST,NEW YORK,NY 10032. MASSACHUSETTS GEN HOSP,CNYM,DEPT PSYCHIAT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 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 1993 VL 15 IS 1 BP 32 EP 33 PG 2 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA KL806 UT WOS:A1993KL80600073 ER PT J AU COOPER, JB CULLEN, DJ EICHHORN, JH PHILIP, JH HOLZMAN, RS AF COOPER, JB CULLEN, DJ EICHHORN, JH PHILIP, JH HOLZMAN, RS TI ADMINISTRATIVE GUIDELINES FOR RESPONSE TO AN ADVERSE ANESTHESIA EVENT SO JOURNAL OF CLINICAL ANESTHESIA LA English DT Article DE ANESTHESIA, COMPLICATIONS FROM; OUTCOME; QUALITY ASSURANCE; RISK MANAGEMENT AB The Risk Management Committee of the Harvard Medical School's Department of Anaesthesia developed a set of guidelines recommending administrative actions that should be taken immediately following an adverse anesthesia event. The guidelines are intended to limit patient injury from a specific event associated with anesthesia and to ensure that the causes of the event are identified to prevent recurrence. The guidelines direct the primary anesthetist to concentrate on continuing care but quickly notify someone in a leadership position, who would become the ''incident supervisor. '' The incident supervisor would be knowledgeable of the details of the protocol and direct activities for ensuring appropriate medical care, sequestration of equipment, documentation of information, and contact of other appropriate administrative personnel. Experience with the guidelines has shown that they can be effective if applied but that it is difficult to do that consistently in our large medical centers. RP COOPER, JB (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 14 Z9 14 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0952-8180 J9 J CLIN ANESTH JI J. Clin. Anesth. PD JAN-FEB PY 1993 VL 5 IS 1 BP 79 EP 84 DI 10.1016/0952-8180(93)90095-V PG 6 WC Anesthesiology SC Anesthesiology GA KL136 UT WOS:A1993KL13600017 PM 8442975 ER PT J AU CALIGIURI, MA MURRAY, C ROBERTSON, MJ WANG, E COCHRAN, K CAMERON, C SCHOW, P ROSS, ME KLUMPP, TR SOIFFER, RJ SMITH, KA RITZ, J AF CALIGIURI, MA MURRAY, C ROBERTSON, MJ WANG, E COCHRAN, K CAMERON, C SCHOW, P ROSS, ME KLUMPP, TR SOIFFER, RJ SMITH, KA RITZ, J TI SELECTIVE MODULATION OF HUMAN NATURAL-KILLER-CELLS INVIVO AFTER PROLONGED INFUSION OF LOW-DOSE RECOMBINANT INTERLEUKIN-2 SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE IL-2; NATURAL KILLER CELLS; IMMUNOTHERAPY; IL-2 RECEPTOR; CYTOTOXICITY ID TUMOR NECROSIS FACTOR; CANCER-PATIENTS; FUNCTIONAL CONSEQUENCES; MARROW PRECURSORS; HUMAN-MONOCYTES; NK CELLS; RECEPTOR; IL-2; ACTIVATION; EXPRESSION AB The immunologic consequences of prolonged infusions of rIL-2 in doses that produce physiologic serum concentrations of this cytokine were investigated. rIL-2 in doses of 0.5-6.0 x 10(6) U/m2 per d (3.3-40 mug/m2 per d) was administered by continuous intravenous infusion for 90 consecutive days to patients with advanced cancer. IL-2 concentrations (25+/-25 and 77+/-64 pM, respectively) that selectively saturate high-affinity IL-2 receptors (IL-2R) were achieved in the serum of patients receiving rIL-2 infusions of 10 mug/M2 per d and 30 mug/m2 per d. A gradual, progressive expansion of natural killer (NK) cells was seen in the peripheral blood of these patients with no evidence of a plateau effect during the 3 mo of therapy. A preferential expansion of CD56bright NK cells was consistently evident. NK cytotoxicity against tumor targets was only slightly enhanced at these dose levels. However, brief incubation of these expanded NK cells with IL-2 in vitro induced potent lysis of NK-sensitive, NK-resistant, and antibody-coated targets. Infusions of rIL-2 at 40 mug/m2 per d produced serum IL-2 levels (345+/-381 pM) sufficient to engage intermediate affinity IL-2R p75, which is constitutively expressed by human NK cells. This did not result in greater NK cell expansion compared to the lower dose levels, but did produce in vivo activation of NK cytotoxicity, as evidenced by lysis of NK-resistant targets. There was no consistent change in the numbers of CD56- CD3+ T cells, CD56+ CD3+ MHC-unrestricted T cells, or B cells during infusions of rIL-2 at any of the dosages used. This study demonstrates that prolonged infusions of rIL-2 in doses that saturate only high affinity IL-2R can selectively expand human NK cells for an extended period of time with only minimal toxicity. Further activation of NK cytolytic activity can also be achieved in vivo, but it requires concentrations of IL-2 that bind intermediate affinity IL-2R p75. Clinical trials are underway attempting to exploit the differing effects of various concentrations of IL-2 on human NK cells in vivo. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT MED,HANOVER,NH 03756. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT MED,BUFFALO,NY 14263. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT MOLEC MED & IMMUNOL,BUFFALO,NY 14263. FU NCI NIH HHS [CA01572, CA41619]; NIAID NIH HHS [AI17643] NR 49 TC 190 Z9 196 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1993 VL 91 IS 1 BP 123 EP 132 DI 10.1172/JCI116161 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KK042 UT WOS:A1993KK04200021 PM 7678599 ER PT J AU FRAGOSO, G VALDEZ, F ROSENSTEIN, Y GOVEZENSKY, T LARRALDE, C SCIUTTO, E AF FRAGOSO, G VALDEZ, F ROSENSTEIN, Y GOVEZENSKY, T LARRALDE, C SCIUTTO, E TI IMMUNOENZYMATIC ASSAY THAT MEASURES THE EXPRESSION OF MURINE HISTOCOMPATIBILITY ANTIGENS IN MACROPHAGES AND LYMPHOCYTES SO JOURNAL OF CLINICAL LABORATORY ANALYSIS LA English DT Article DE MHC-ELISA; H-2 ANTIGENS; SURFACE ANTIGENS ID MOUSE MHC ANTIGENS; MONOCLONAL-ANTIBODIES; CELL-CYCLE; CRASSICEPS CYSTICERCOSIS; ENZYME-IMMUNOASSAY; SURFACE; ELISA; QUANTITATION; COMPLEX AB A convenient-simple, sensitive, rapid and reproducible enzyme immunoassay to measure H-2 particulated and solubilized cellular antigens is described. Cellular antigens were measured by ELISA through the binding of specific biotinylated antibodies and streptoavidin-peroxidase conjugate to cells in suspension. Endogenous peroxidase activity of activated cells was inhibited by addition of sodium azide and H2O2 in acid conditions. The assay proved capable of distinguishing between two cell lines (EL-4/H-2 b and P815/H-2d) and even between the cells of three congenic mouse strains (BALB/B, H-2b , BALB/c, H-2d, and BALB/K, H-2k) and was sensitive to as few as 2.5 x 10(4) cells/well. Results were comparable to those obtained with FACS. An inhibition version of this assay was found to be very useful for the detection of H-2 antigens present in whole antigen cells extracts. (C) 1993 Wiley-Liss. Inc. C1 Univ Nacl Autonoma Mexico, INST INVEST BIOMED, APDO POSTAL 70228, MEXICO CITY 04510, DF, MEXICO. DANA FARBER INST, BOSTON, MA USA. NR 24 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0887-8013 J9 J CLIN LAB ANAL JI J. Clin. Lab. Anal. PY 1993 VL 7 IS 6 BP 348 EP 352 DI 10.1002/jcla.1860070609 PG 5 WC Medical Laboratory Technology SC Medical Laboratory Technology GA MD085 UT WOS:A1993MD08500008 PM 8277358 ER PT J AU SIMON, BA LOVICH, MA SIMS, N COOPER, JB AF SIMON, BA LOVICH, MA SIMS, N COOPER, JB TI THE TIME HAS COME FOR EVOLUTION FROM THE CIRCLE BREATHING SYSTEM SO JOURNAL OF CLINICAL MONITORING LA English DT Article DE EQUIPMENT, ANESTHESIA MACHINE ID ANESTHESIA C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,ANESTHESIA BIOENGN UNIT,BOSTON,MA 02114. NR 9 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0748-1977 J9 J CLIN MONITOR JI J. Clin. Monit. PD JAN PY 1993 VL 9 IS 1 BP 60 EP 63 DI 10.1007/BF01627639 PG 4 WC Anesthesiology SC Anesthesiology GA KG910 UT WOS:A1993KG91000011 PM 8463807 ER PT J AU CANELLOS, GP DEMETRI, GD AF CANELLOS, GP DEMETRI, GD TI MYELOSUPPRESSION AND CONVENTIONAL CHEMOTHERAPY - WHAT PRICE, WHAT BENEFIT SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID COLONY-STIMULATING FACTOR; NEUTROPENIA; CARCINOMA; CANCER C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 11 TC 9 Z9 9 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1993 VL 11 IS 1 BP 1 EP 2 PG 2 WC Oncology SC Oncology GA KF531 UT WOS:A1993KF53100001 PM 8418220 ER PT J AU CUMMINGS, FJ GRAY, R TORMEY, DC DAVIS, TE VOLK, H HARRIS, J FALKSON, G BENNETT, JM AF CUMMINGS, FJ GRAY, R TORMEY, DC DAVIS, TE VOLK, H HARRIS, J FALKSON, G BENNETT, JM TI ADJUVANT TAMOXIFEN VERSUS PLACEBO IN ELDERLY WOMEN WITH NODE-POSITIVE BREAST-CANCER - LONG-TERM FOLLOW-UP AND CAUSES OF DEATH SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID COOPERATIVE-ONCOLOGY-GROUP; POSTMENOPAUSAL WOMEN; CLINICAL-TRIALS; THERAPY; CHEMOTHERAPY C1 BROWN UNIV,PROVIDENCE,RI 02912. ROGER WILLIAMS GEN HOSP,PROVIDENCE,RI 02908. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV WISCONSIN,CTR COMPREHENS CANC,MADISON,WI 53706. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. UNIV PRETORIA,PRETORIA,SOUTH AFRICA. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. FU NCI NIH HHS [CA 06594, CA 14144, CA 14548] NR 29 TC 89 Z9 89 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1993 VL 11 IS 1 BP 29 EP 35 PG 7 WC Oncology SC Oncology GA KF531 UT WOS:A1993KF53100006 PM 8418238 ER PT J AU ABNER, AL RECHT, A EBERLEIN, T COME, S SHULMAN, L HAYES, D CONNOLLY, JL SCHNITT, SJ SILVER, B HARRIS, JR AF ABNER, AL RECHT, A EBERLEIN, T COME, S SHULMAN, L HAYES, D CONNOLLY, JL SCHNITT, SJ SILVER, B HARRIS, JR TI PROGNOSIS FOLLOWING SALVAGE MASTECTOMY FOR RECURRENCE IN THE BREAST AFTER CONSERVATIVE SURGERY AND RADIATION-THERAPY FOR EARLY-STAGE BREAST-CANCER SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID LOCAL RECURRENCE; RADIOTHERAPY; IRRADIATION; LUMPECTOMY; CARCINOMA C1 HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT HEMATOL ONCOL,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BREAST EVALUAT,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02215. RP ABNER, AL (reprint author), BETH ISRAEL HOSP,DEPT RADIAT ONCOL,JOINT CTR RADIAT THERAPY,50 BINNEY ST,BOSTON,MA 02215, USA. NR 18 TC 131 Z9 134 U1 0 U2 2 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 1993 VL 11 IS 1 BP 44 EP 48 PG 5 WC Oncology SC Oncology GA KF531 UT WOS:A1993KF53100008 PM 8418240 ER PT J AU WEST, DC SHAMBERGER, RC MACKLIS, RM KOZAKEWICH, HPW WAYNE, AS KREISSMAN, SG KORF, BR LAVALLY, B GRIER, HE AF WEST, DC SHAMBERGER, RC MACKLIS, RM KOZAKEWICH, HPW WAYNE, AS KREISSMAN, SG KORF, BR LAVALLY, B GRIER, HE TI STAGE-III NEUROBLASTOMA OVER 1 YEAR OF AGE AT DIAGNOSIS - IMPROVED SURVIVAL WITH INTENSIVE MULTIMODALITY THERAPY INCLUDING MULTIPLE ALKYLATING-AGENTS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID PEDIATRIC-ONCOLOGY-GROUP; CANCER-STUDY-GROUP; N-MYC ONCOGENE; IV NEURO-BLASTOMA; CHILDRENS-CANCER; GENE AMPLIFICATION; EXPERIENCE C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV NEUROL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV GENET,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIAT ONCOL,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP WEST, DC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 24 TC 32 Z9 32 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1993 VL 11 IS 1 BP 84 EP 90 PG 7 WC Oncology SC Oncology GA KF531 UT WOS:A1993KF53100014 PM 8418247 ER PT J AU COOPER, MR DEAR, K MCINTYRE, OR OZER, H ELLERTON, J CANELLOS, G BERNHARDT, B DUGGAN, D FARAGHER, D SCHIFFER, C AF COOPER, MR DEAR, K MCINTYRE, OR OZER, H ELLERTON, J CANELLOS, G BERNHARDT, B DUGGAN, D FARAGHER, D SCHIFFER, C TI A RANDOMIZED CLINICAL-TRIAL COMPARING MELPHALAN PREDNISONE WITH OR WITHOUT INTERFERON ALFA-2B IN NEWLY DIAGNOSED PATIENTS WITH MULTIPLE-MYELOMA - A CANCER AND LEUKEMIA GROUP-B STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ALPHA-INTERFERON; INVITRO; ASSAY C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. DARTMOUTH COLL,HITCHCOCK MED CTR,HANOVER,NH 03756. UNIV N CAROLINA,CHAPEL HILL,NC 27514. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. CORNELL UNIV,MED CTR,NEW YORK HOSP,NEW YORK,NY 10021. SUNY HLTH SCI CTR,SYRACUSE,NY. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. UNIV MARYLAND,CTR CANC,BALTIMORE,MD 21201. RP COOPER, MR (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,CTR COMPREHENS CANC,300 S HAWTHORNE RD,WINSTON SALEM,NC 27103, USA. FU NCI NIH HHS [CA 04326, CA 03927, CA 33601] NR 23 TC 92 Z9 92 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1993 VL 11 IS 1 BP 155 EP 160 PG 6 WC Oncology SC Oncology GA KF531 UT WOS:A1993KF53100024 PM 8418228 ER PT J AU RECHT, A COLEMAN, CN HARRIS, JR COME, SE GELMAN, RS AF RECHT, A COLEMAN, CN HARRIS, JR COME, SE GELMAN, RS TI TIMING OF RADIOTHERAPY IN THE TREATMENT OF EARLY-STAGE BREAST-CANCER - REPLY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP RECHT, A (reprint author), HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115, USA. NR 1 TC 8 Z9 8 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1993 VL 11 IS 1 BP 192 EP 193 PG 2 WC Oncology SC Oncology GA KF531 UT WOS:A1993KF53100029 ER PT J AU LIBERMAN, MC AF LIBERMAN, MC TI CENTRAL PROJECTIONS OF AUDITORY-NERVE FIBERS OF DIFFERING SPONTANEOUS RATE .2. POSTEROVENTRAL AND DORSAL COCHLEAR NUCLEI SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE INTRACELLULAR LABEL; COCHLEA; SENSORY; BRAIN-STEM ID SPHERICAL BUSHY CELLS; SINGLE UNIT-ACTIVITY; RESPONSE PROPERTIES; PHYSIOLOGICAL-PROPERTIES; HORSERADISH-PEROXIDASE; FUNCTIONAL-PROPERTIES; FINE-STRUCTURE; CAT; ORGANIZATION; NEURONS AB Response properties of auditory nerve fibers (ANFs), including threshold sensitivity, vary systematically with spontaneous discharge rate (SR) (Liberman, M.C.: J. Acoust. Soc Amer. 63:442-455, 1978). Thus, an understanding of the mechanisms underlying signal transformation in the cochlear nucleus (CN) must include a description of any SR-based difference in ANF projections. This study is the second of a pair describing the CN projections of intracellularly labeled ANFs of known SR, the first of which summarized projection to the anteroventral CN (Liberman, M.C.: J. Comp. Neurol. 313:240-258, 1991). For each swelling from each labeled fiber, the position (within CN subdivisions), the size, and the type of cell contacted (if determinable) was noted: roughly one in four labeled swellings appeared in intimate contact with the soma or proximal dendrites of a CN cell. In all such cases, cell size and swelling size were measured. As reported for auteroventral cochlear nucleus, the ANF innervation of the small-cell regions of posteroventral CN (PVCN) was almost exclusively by low- and medium-SR fibers. Other significant SR-based trends in ANF projections included 1) a tendency for high-SR fibers to contact larger cells in PVCN, 2) a meager projection of low- and medium-SR fibers to octopus cells, and 3) a tendency in the dorsal CN (DCN) for low-SR terminals to end closer to the fusiform cell layer than high-SR terminals. There were no significant SR-based difference in ANF swelling sizes in any subdivision. A consideration of the average cell sizes, ANF swelling sizes and estimated numbers of ANFs of different CF and SR converging on each CN cell help explain some of the differences in response transformation associated with different cell types in the CN. C1 HARVARD UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,BOSTON,MA 02114. RP LIBERMAN, MC (reprint author), HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115, USA. FU NIDCD NIH HHS [DC00188] NR 60 TC 70 Z9 70 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD JAN 1 PY 1993 VL 327 IS 1 BP 17 EP 36 DI 10.1002/cne.903270103 PG 20 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA KD903 UT WOS:A1993KD90300002 PM 8432906 ER PT J AU ROSEN, BR BRADY, TJ AF ROSEN, BR BRADY, TJ TI FUTURE USES OF MR-IMAGING AGENTS SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article; Proceedings Paper CT SYMP ON GADOLINIUM CONTRAST AGENTS IN NEURO-MRI : CLINICAL AND ECONOMIC CONSIDERATIONS CY FEB 29, 1992 CL NEW YORK, NY SP TEMPLE UNIV SCH MED, SANOFI WINTHROP DE BRAIN; DYSPROSIUM; GADOLINIUM; HEMODYNAMICS; MAGNETIC RESONANCE IMAGING; MAGNETIC SUSCEPTIBILITY CONTRAST; MIONS; MYOCARDIAL INFARCTION; SUPERPARAMAGNETIC IRON OXIDES; TARGET-SPECIFIC IMAGING ID SUPERPARAMAGNETIC IRON-OXIDE; CONTRAST AGENTS AB Existing paramagnetic agents and novel superparamagnetic pharmaceuticals under development promise to advance substantially the frontiers of MR imaging. Used in conjunction with ultrafast MR techniques, such as echoplanar imaging and turboFLASH (fast low-angle shot), relaxivity agents (e.g., dysprosium, gadolinium), which alter T1 characteristics of tissue protons they act on, can be used to generate quantitative maps of dynamic blood-brain barrier permeability as well as regional hemodynamic profiles of diseased heart and other organs. In addition, the magnetic susceptibility (T2*)-altering effects of gadolinium can be exploited to map regional cerebral blood volume during task-activated and pathologic brain states. Magnetic susceptibility agents, such as monocrystalline iron oxide nanoparticles (MIONs), allow the advantages of scintigraphy to be joined with the high spatial resolution of MR imaging. Not only can these magnetopharmaceutical preparations serve as hemodynamic markers, they have already enabled function-specific imaging at the cellular level under diverse pathologic conditions. C1 MASSACHUSETTS GEN HOSP,NMR CTR,DEPT RADIOL,13TH ST,BLDG 149,BOSTON,MA 02129. NR 18 TC 7 Z9 7 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PY 1993 VL 17 SU 1 BP S36 EP S42 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LC677 UT WOS:A1993LC67700008 PM 8486829 ER PT J AU WOLF, GL AF WOLF, GL TI ECONOMIC REIMBURSEMENT ISSUES IN MR-IMAGING WITH GADOLINIUM CONTRAST AGENTS SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article; Proceedings Paper CT SYMP ON GADOLINIUM CONTRAST AGENTS IN NEURO-MRI : CLINICAL AND ECONOMIC CONSIDERATIONS CY FEB 29, 1992 CL NEW YORK, NY SP TEMPLE UNIV SCH MED, SANOFI WINTHROP DE COST EFFECTIVENESS; DIAGNOSTIC MERIT; GADODIAMIDE; GADOLINIUM; GADOPENTETATE DIMEGLUMINE; GADOTERIDOL; REIMBURSEMENT ID RESONANCE AB Implementation of an accurate, reliable index of cost effectiveness would help to advance technology assessment and reimbursement of MR imaging procedures, including gadolinium enhancement. To this end, an objective, consensual measure that satisfies the need for ''gold-standard'' confirmation of diagnostic impressions in routine clinical practice and limits interpreter bias has been developed. Eponymously termed Diagnostic Merit, this barometer is expressed as the percentage of independent judges confirming diagnostic impressions entered by case-blinded radiologists assigned unenhanced and enhanced image sets for interpretation. The judges, who are informed of clinical indications, clinical follow-up, and unblinded diagnostic interpretation of the MR scans, confirm only those case-blind interpretations deemed ''close enough for diagnostic utility'' to actual clinical profiles. According to this method, gadopentetate dimeglumine has been shown to be cost effective by promoting optimal diagnostic performance. This improvement in utility offsets the cost of the gadolinium contrast agent. Efficacies of gadodiamide and gadoteridol, two other contrast agents in development, have been demonstrated by other measures but are probably also evaluable through the Diagnostic Merit method. CPT-4 codes for contrast-enhanced MR imaging are reviewed. RP WOLF, GL (reprint author), MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,13TH ST,BLDG 149,BOSTON,MA 02129, USA. NR 11 TC 1 Z9 1 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. PY 1993 VL 17 SU 1 BP S43 EP S48 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LC677 UT WOS:A1993LC67700009 PM 8486830 ER PT J AU SKOBE, Z HEELEY, JD DOBECK, JM PROSTAK, KS MARAVELIS, L STERN, DN AF SKOBE, Z HEELEY, JD DOBECK, JM PROSTAK, KS MARAVELIS, L STERN, DN TI COMPARISON OF RATES OF ENAMEL SYNTHESIS IN IMPEDED AND UNIMPEDED RAT INCISORS SO JOURNAL OF DENTAL RESEARCH LA English DT Article AB Periodic intubations of rats with solutions of fluoride (F) lead to the appearance of bands of disrupted pigmentation in continuously erupting incisors. Distances between fluorotic bands reflect time intervals between intubations. In this experiment, the periodicity of fluorotic banding was used for estimation of the rate of enamel synthesis in impeded and unimpeded rat incisors. Rats kept on a low-F diet and distilled water were intubated two or four times per week with 2 mg NaF/150 g body weight. In a group of rats, one of the mandibular incisors was cut at the gingival margin after two weeks, and intubations were continued for an additional two weeks. In another group of F-intubated rats, incisors were cut or notched at the gingival margin twice, six days apart. Control rats either received the same periodic F intubations or were maintained on the low-F diet without intubation. Measurements of spacing between fluorotic bands were identical in impeded and unimpeded teeth, even though the latter erupted at a faster rate. In unimpeded mandibular incisors, there was a significant elongation of the secretory zone and a shortening of the pigmentation zone, resulting in reduced pigmentation intensity of the erupted portions of the teeth. The results show that the rate of enamel synthesis is independent of the eruption rate. RP SKOBE, Z (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NCRR NIH HHS [RR-05483]; NIDCR NIH HHS [DE-04230, DE-07463] NR 14 TC 4 Z9 4 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD JAN PY 1993 VL 72 IS 1 BP 46 EP 50 DI 10.1177/00220345930720010601 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KG630 UT WOS:A1993KG63000007 PM 8418106 ER PT J AU SANCHEZ, MJ GUTIERREZRAMOS, JC FERNANDEZ, E LEONARDO, E LOZANO, J MARTINEZ, C TORIBIO, ML AF SANCHEZ, MJ GUTIERREZRAMOS, JC FERNANDEZ, E LEONARDO, E LOZANO, J MARTINEZ, C TORIBIO, ML TI PUTATIVE PRETHYMIC T-CELL PRECURSORS WITHIN THE EARLY HUMAN EMBRYONIC LIVER - A MOLECULAR AND FUNCTIONAL-ANALYSIS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID THYMIC EPITHELIAL-CELLS; HEMATOPOIETIC PROGENITOR CELLS; STIMULATORY FACTOR-I; MONOCLONAL-ANTIBODIES; INTERLEUKIN-2 RECEPTOR; SURFACE-ANTIGENS; HUMAN THYMOCYTES; HUMAN-MONOCYTES; FETAL LIVER; EXPRESSION AB Hematopoietic cells present in the liver in early human fetal life were characterized by phenotypic analysis using a broad panel of monoclonal antibodies. Expression of very late antigen 4 and leukocyte function-associated antigen 3 cell adhesion receptors and 4F2 cell activation molecules was found in all fetal liver hematopoietic cells before acquisition of T cell-, B cell-, or myeloid-specific surface markers, and before the time of intrathymic colonization. Molecular studies showed that expression of the interleukin 2 receptor beta (IL-2Rbeta) also occurred in the embryonic liver at this early ontogenic stage. In contrast, no expression of IL-2Ralpha or IL-2 transcripts was found in fetal liver cells, whereas transcription of the IL-4 gene was detected in a small fetal liver cell subset. Putative T cell precursors were identified among the hematopoietic fetal liver cells by the expression of genes encoding the gamma, delta, epsilon, and zeta invariant chains of the CD3-T cell receptor (TCR) complex. However, no transcription of the polymorphic alpha and beta TCR genes was detected. Functional in vitro assays further demonstrated that fetal liver hematopoietic cells from those early embryos were capable of proliferating in response to T cell growth factors, including IL-4 and IL-2. However, whereas IL-4-induced proliferation paralleled the appearance in vitro of CD45+CD7-CD4dull cells expressing the CD14 myeloid antigen, as well as of CD34+ primitive hematopoietic progenitors, differentiation into CD45+CD7+CD8+CD3- immature T cells was observed when using IL-2. Moreover, coculture with thymic epithelial cell monolayers provided additional evidence that early fetal liver hematopoietic cells may include very primitive T cell precursors, which were able to differentiate in vitro into TCR alpha/beta+ mature T cells. Therefore, our results indicate that, after triggering of the T cell-specific maturation program in primitive fetal liver hematopoietic progenitors, specific signals provided intrathymically by epithelial cells may fulfill the requirements to drive terminal differentiation of prethymically committed T cell precursors. C1 UNIV AUTONOMA MADRID,CSIC,CTR BIOL MOLEC SEVERO OCHOA,CAMPUS CANTOBLANCO,E-28049 MADRID,SPAIN. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. CLIN PUERTA DE HIERRO,E-28035 MADRID,SPAIN. RI Sanchez, Maria Jose/P-4716-2016; Toribio, Maria L/C-2039-2017 OI Sanchez, Maria Jose/0000-0003-3464-6224; Toribio, Maria L/0000-0002-8637-0373 NR 78 TC 38 Z9 38 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1993 VL 177 IS 1 BP 19 EP 33 DI 10.1084/jem.177.1.19 PG 15 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KE652 UT WOS:A1993KE65200003 PM 8418199 ER PT J AU WARREN, HS AMATO, SF FITTING, C BLACK, KM LOISELLE, PM PASTERNACK, MS CAVAILLON, JM AF WARREN, HS AMATO, SF FITTING, C BLACK, KM LOISELLE, PM PASTERNACK, MS CAVAILLON, JM TI ASSESSMENT OF ABILITY OF MURINE AND HUMAN ANTILIPID-A MONOCLONAL-ANTIBODIES TO BIND AND NEUTRALIZE LIPOPOLYSACCHARIDE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TUMOR-NECROSIS-FACTOR; GRAM-NEGATIVE BACTEREMIA; ESCHERICHIA-COLI J5; SEPTIC SHOCK; SALMONELLA-MINNESOTA; ROUGH MUTANTS; BACTERIAL LIPOPOLYSACCHARIDE; RABBIT ANTISERA; IGM ANTIBODY; ENDOTOXIN AB The use of monoclonal antibodies (mAbs) directed to lipid A for the therapy of gram-negative sepsis is controversial. In an attempt to understand their biologic basis of action, we used a fluid-phase radioimmunoassay to measure binding between bacterial lipopolysaccharide (LPS) and two IgM mAbs directed to lipid A that are being evaluated for the treatment of gram-negative bacterial sepsis. Both antibodies bound H-3-LPS prepared from multiple strains of gram-negative bacteria when large excesses of antibody were used, although binding was modest and only slightly greater than control preparations. We also studied the ability of each anti-lipid A antibody to neutralize some of the biological effects of LPS in vitro. Despite large molar excesses, neither antibody neutralized LPS as assessed by the limulus lysate test, by a mitogenic assay for murine splenocytes, or by the production of cytokines interleukin (IL)-1, IL-6, or tumor necrosis factor from human monocytes in culture medium or in whole blood. Our experiments do not support the hypothesis that either of these anti-lipid A mAbs function by neutralizing the toxic effects of LPS. C1 MASSACHUSETTS GEN HOSP,DEPT CHILDRENS SERV,INFECT DIS UNIT,BOSTON,MA 02129. SHRINERS BURN INST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. INST PASTEUR,IMMUNOALLERGY UNIT,F-75724 PARIS,FRANCE. RP WARREN, HS (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,INFECT DIS UNIT,E 149 13TH ST,5TH FLOOR,BOSTON,MA 02129, USA. FU NIAID NIH HHS [R29AI-28943-03] NR 54 TC 119 Z9 122 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1993 VL 177 IS 1 BP 89 EP 97 DI 10.1084/jem.177.1.89 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KE652 UT WOS:A1993KE65200009 PM 8418211 ER PT J AU SYKES, M ABRAHAM, VS HARTY, MW PEARSON, DA AF SYKES, M ABRAHAM, VS HARTY, MW PEARSON, DA TI IL-2 REDUCES GRAFT-VERSUS-HOST DISEASE AND PRESERVES A GRAFT-VERSUS-LEUKEMIA EFFECT BY SELECTIVELY INHIBITING CD4+ T-CELL ACTIVITY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID BONE-MARROW TRANSPLANTATION; II H-2 DIFFERENCES; MAJOR HISTOCOMPATIBILITY BARRIERS; CHRONIC MYELOGENOUS LEUKEMIA; SYNGENEIC LYMPHOMA; LYMPHOCYTES-T; INTERLEUKIN-2; MICE; DEPLETION; INVIVO AB We have recently demonstrated, in a fully MHC-mismatched murine bone marrow transplantation model, that administration of a short course of high dose IL-2 markedly diminishes graft-vs-host disease (GVHD) without compromising alloengraftment or the graft-vs-leukemia (GVL) effect of allogeneic T cells. We have now evaluated the mechanism of the dissociation of GVL and GVHD observed in this model. We demonstrate that CD4+ T cells were required to produce severe, acute GVHD in the fully MHC-mismatched plus minor histocompatibility Ag-mismatched A/J-->B10 strain combination. The GVHD-producing activity of A/J CD4+ T cells administered without CD8+ T cells was inhibited by IL-2 treatment. In contrast, CD8+ T cells alone mediated the GVL effect observed in the EL4 leukemia/lymphoma model, and CD4+ cells did not contribute to this effect. This CD8-mediated GVL activity was not inhibited by IL-2 treatment. Because naive A/J CD8+ T cells administered without CD4+ T cells did not produce acute GVHD, we were unable to evaluate the effect of IL-2 in this model. However, when A/J donors were presensitized with B10 skin grafts, CD4-depleted A/J spleen cells were capable of causing acute GVHD in B10 recipients. This CD8-mediated GVHD was not inhibited by treatment with IL-2. However, IL-2 did partially inhibit the GVHD produced by nondepleted presensitized A/J spleen cells, probably due to selective inhibition of the function of presensitized A/J CD4+ T cells. The dissociation of GVHD and GVL against the EL4 leukemia/lymphoma in IL-2-treated mice can therefore be explained by selective inhibition by IL-2 of CD4 activity. C1 NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,CTR TRANSPLANTAT RES BIOL,BOSTON,MA 02129. FU NCI NIH HHS [R01CA55290] NR 46 TC 114 Z9 116 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 1993 VL 150 IS 1 BP 197 EP 205 PG 9 WC Immunology SC Immunology GA KE757 UT WOS:A1993KE75700023 PM 8093257 ER PT J AU KAPLAN, E DINARELLO, CA WAKABAYASHI, G BURKE, JF CONNOLLY, RS GELFAND, JA AF KAPLAN, E DINARELLO, CA WAKABAYASHI, G BURKE, JF CONNOLLY, RS GELFAND, JA TI INTERLEUKIN-1 PRETREATMENT PROTECTS AGAINST ENDOTOXIN-INDUCED HYPOTENSION IN RABBITS - ASSOCIATION WITH DECREASED TUMOR-NECROSIS-FACTOR LEVELS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID BINDING-PROTEIN; LIPOPOLYSACCHARIDE; CACHECTIN; MORTALITY; RECEPTOR; SHOCK AB Rabbits were infused with either low-dose recombinant human interleukin (IL)-1beta or vehicle 16 h prior to receiving lipopolysaccharide (LPS). In controls pretreated with vehicle, mean arterial pressure decreased to 68% of the baseline value by 90 min after LPS infusion and remained low for the duration of the study period. In IL-1-pretreated animals, a similar decrease in mean arterial pressure to 69% was observed at 60 min but returned to 90% of baseline after 180 min (P < .05). IL-1-pretreated animals showed no significant rise in serum tumor necrosis factor after LPS infusion compared with vehicle-treated animals (P < .05). Rabbits were pretreated as above with IL-1 and, 40 h later, plasma was transfused into a second group of rabbits just prior to LPS infusion. An infusion of post-IL-1 plasma did not reduce LPS-induced hypotension. Thus, pretreatment with IL-1 reduces the hypotension in response to LPS by a mechanism that is not plasma-mediated but that is associated with reduced serum tumor necrosis factor levels. C1 TUFTS UNIV,NEW ENGLAND MED CTR,DEPT MED,DIV GEOG MED & INFECT DIS,750 WASHINGTON ST,NEMCH 480,BOSTON,MA 02111. TUFTS UNIV,NEW ENGLAND MED CTR,DEPT SURG,DIV GEOG MED & INFECT DIS,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. KEIO UNIV,SCH MED,DEPT SURG,TOKYO 108,JAPAN. FU NIAID NIH HHS [AI-15614]; NIGMS NIH HHS [GM-21700, GM-07035] NR 16 TC 9 Z9 9 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 1993 VL 167 IS 1 BP 244 EP 247 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KE846 UT WOS:A1993KE84600042 PM 8418176 ER PT J AU BOUSTANY, RM FILIPEK, P AF BOUSTANY, RM FILIPEK, P TI SEIZURES, DEPRESSION AND DEMENTIA IN TEENAGERS WITH BATTEN-DISEASE SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL SYMP ON THE NEURONAL CEROID-LIPOFUSCINOSIS ( BATTEN DISEASE ) CY JUN 11-13, 1992 CL HAMBURG, GERMANY C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. RP BOUSTANY, RM (reprint author), DUKE UNIV,MED CTR,DEPT PEDIAT,BOX 3533,DURHAM,NC 27710, USA. NR 7 TC 14 Z9 14 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1993 VL 16 IS 2 BP 252 EP 255 DI 10.1007/BF00710257 PG 4 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA LM407 UT WOS:A1993LM40700011 PM 8411973 ER PT J AU MITCHISON, HM WILLIAMS, RE MCKAY, TR CALLEN, DF THOMPSON, AD MULLEY, JC STALLINGS, RL HILDEBRAND, CE MOYZIS, RK JARVELA, I PELTONEN, L HAINES, J SUTHERLAND, GR GARDINER, RM AF MITCHISON, HM WILLIAMS, RE MCKAY, TR CALLEN, DF THOMPSON, AD MULLEY, JC STALLINGS, RL HILDEBRAND, CE MOYZIS, RK JARVELA, I PELTONEN, L HAINES, J SUTHERLAND, GR GARDINER, RM TI REFINED GENETIC-MAPPING OF JUVENILE-ONSET NEURONAL CEROID-LIPOFUSCINOSIS ON CHROMOSOME-16 SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL SYMP ON THE NEURONAL CEROID-LIPOFUSCINOSIS ( BATTEN DISEASE ) CY JUN 11-13, 1992 CL HAMBURG, GERMANY ID DISEASE C1 NATL PUBL HLTH INST,MOL GENET LAB,SF-00300 HELSINKI,FINLAND. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,BOSTON,MA 02129. ADELAIDE CHILDRENS HOSP INC,DEPT CYTOGENET & MOLEC GENET,ADELAIDE,SA 5006,AUSTRALIA. LOS ALAMOS NATL LAB,CTR HUMAN GENOME STUDIES,LOS ALAMOS,NM 87545. RP MITCHISON, HM (reprint author), UCL,SCH MED,RAYNE INST,DEPT PAEDIAT,5 UNIV ST,LONDON WC1E 6JJ,ENGLAND. RI Stallings, Raymond/A-7213-2008; Sutherland, Grant/D-2606-2012; Callen, David/G-1975-2012; Jarvela, Irma/L-5836-2013; OI Callen, David/0000-0002-6189-9991 NR 8 TC 9 Z9 9 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1993 VL 16 IS 2 BP 339 EP 341 DI 10.1007/BF00710278 PG 3 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA LM407 UT WOS:A1993LM40700032 PM 8105142 ER PT J AU PRENCE, EM NATOWICZ, MR AF PRENCE, EM NATOWICZ, MR TI UNUSUAL BIOCHEMICAL PRESENTATION OF GM1 GANGLIOSIDOSIS - MARKEDLY ELEVATED LEVELS OF MULTIPLE PLASMA LYSOSOMAL-ENZYME ACTIVITIES SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Note C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV BIOCHEM,WALTHAM,MA 02554. HARVARD UNIV,SCH MED,DEPT NEUROSURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP PRENCE, EM (reprint author), EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MED GENET,WALTHAM,MA 02554, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1993 VL 16 IS 5 BP 897 EP 898 DI 10.1007/BF00714288 PG 2 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA MC266 UT WOS:A1993MC26600017 PM 8295410 ER PT J AU ROSENMAN, SJ GANJI, AA TEDDER, TF GALLATIN, WM AF ROSENMAN, SJ GANJI, AA TEDDER, TF GALLATIN, WM TI SYN-CAPPING OF HUMAN LYMPHOCYTE-T ADHESION ACTIVATION MOLECULES AND THEIR REDISTRIBUTION DURING INTERACTION WITH ENDOTHELIAL-CELLS SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE CYTOSKELETON; EXTRAVASATION; IMMUNOFLUORESCENCE; CONFOCAL ID LEUKOCYTE ADHESION; TRANSENDOTHELIAL MIGRATION; DIFFERENTIATION ANTIGENS; MONOCLONAL-ANTIBODIES; DISTINCT EPITOPES; PHORBOL ESTER; ACTIVATION; SURFACE; RECEPTOR; ASSOCIATION AB Lymphocyte-endothelial cell interactions are mediated in part by multiple lymphocyte surface adhesion/activation molecules and their cognate ligands. We investigated the surface localization of several of these molecules implicated in T cell adhesion and transendothelial migration mechanisms to determine if spatial regulation of their distribution contributes to these processes. T lymphocyte suspensions were stained to define distribution, ability to be aggregated into energy-dependent caps, and potential cocapping of several adhesion structures. CD2, CD44, L-selectin (LAM-1, LECCAM-1), and CD11a/CD18 (LFA-1) exhibited uniform distribution on the T cell surface by direct immunofluorescence but formed caps in an energy-dependent, and therefore cytoskeletally driven, manner when examined by indirect immunofluorescence. CD2 was shown to syn-cap (unidirectionally cocap) with CD44 and CD11a/CD18 (LFA-1), an observation potentially related to functional cooperation among these molecules in T cell activation. T cells were also added to endothelial cell monolayers to assess, in a physiologically relevant context, potential surface molecule reorganization. Lymphocytes co-cultured with human umbilical vein endothelial cells (HUVEC) underwent a profound shape change, from essentially round cells to polarized cells bearing pseudopodia. Immunofluorescent localization of T cell adhesion/activation molecules using confocal microscopy revealed the redistribution of CD2, CD44, and L-selectin to the pseudopod. In contrast, CD11a/CD18 remained globally distributed on the cell surface, even in severely deformed cells. Both lymphocyte shape change and membrane molecule redistribution appear to be cell-cell contact-dependent phenomena requiring intact, viable endothelial cells. Mechanisms that control these events may be critical to lymphocyte recirculation and inflammation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP ROSENMAN, SJ (reprint author), ICOS CORP,22021 20TH AVE SE,BOTHELL,WA 98021, USA. NR 57 TC 59 Z9 60 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD JAN PY 1993 VL 53 IS 1 BP 1 EP 10 PG 10 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA KK631 UT WOS:A1993KK63100001 PM 7678845 ER PT J AU PRICE, P SCADDEN, D JOHNSON, P WALKER, B AF PRICE, P SCADDEN, D JOHNSON, P WALKER, B TI CYTOTOXIC CD8 T-CELLS CULTURED FROM HIV-1 PATIENTS PRODUCE GM-CSF, GAMMA-IFN, TNF-ALPHA, IL2, IL3 AND IL4 FOLLOWING STIMULATION WITH COGNATE PEPTIDES SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 UNIV WESTERN AUSTRALIA,DEPT MICROBIOL,NEDLANDS,WA 6009,AUSTRALIA. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 44 EP 44 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500065 ER PT J AU TEDDER, TF LUSCINSKAS, FW SAUNDERS, KB AF TEDDER, TF LUSCINSKAS, FW SAUNDERS, KB TI REGULATION OF LEUKOCYTE-ENDOTHELIUM INTERACTIONS THROUGH L-SELECTIN SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT IMMUNOL,DURHAM,NC 27710. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 104 EP 104 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500423 ER PT J AU BLUMENFELD, A AXELROD, FB TROFATTER, JA MAAYAN, C LUCENTE, DE SLAUGENHAUPT, SA LIEBERT, CB OZELIUS, LJ HAINES, JL BREAKEFIELD, XO GUSELLA, JF AF BLUMENFELD, A AXELROD, FB TROFATTER, JA MAAYAN, C LUCENTE, DE SLAUGENHAUPT, SA LIEBERT, CB OZELIUS, LJ HAINES, JL BREAKEFIELD, XO GUSELLA, JF TI EXCLUSION OF FAMILIAL DYSAUTONOMIA FROM MORE THAN 60-PERCENT OF THE GENOME SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID DINUCLEOTIDE REPEAT POLYMORPHISM; GENETIC-LINKAGE MAP; NERVE GROWTH-FACTOR; DNA POLYMORPHISMS; TRK PROTOONCOGENE; RECEPTOR AB Familial dysautonomia (FD) is a recessive neurological disorder that affects the development of the sensory and autonomic nervous system. The gene defect appears to be limited to the Ashkenazi Jewish population, where the carrier frequency is 1 in 30. One hundred and ninety-one marker loci representing all autosomes were tested for linkage with the FD genetic defect in 23 families. A combination of pairwise and multipoint analyses excluded the FD gene from at least 60% of the autosomal genome. The program EXCLUDE predicted regions of chromosomes 2, 4, 5q, 9, or 10 as the most promising locations for future analyses. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. NYU,SCH MED,DEPT PEDIAT,NEW YORK,NY 10016. HADASSAH UNIV HOSP,DEPT PEDIAT,JERUSALEM,ISRAEL. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00317, HG00169, HG00324] NR 27 TC 5 Z9 5 U1 0 U2 4 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD JAN PY 1993 VL 30 IS 1 BP 47 EP 52 DI 10.1136/jmg.30.1.47 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA KK182 UT WOS:A1993KK18200006 PM 8093738 ER PT J AU JIMENEZHAKIM, E ELAZOUZI, M BLACK, PM AF JIMENEZHAKIM, E ELAZOUZI, M BLACK, PM TI THE EFFECT OF PROLACTIN AND BOMBESIN ON THE GROWTH OF MENINGIOMA-DERIVED CELLS IN MONOLAYER-CULTURE SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE BOMBESIN; PROLACTIN; GROWTH FACTORS; MENINGIOMA; BRAIN NEOPLASMS ID GASTRIN-RELEASING PEPTIDE; BREAST-CANCER; LUNG-CANCER; STIMULATION; RECEPTORS; CARCINOMA; ESTROGEN; INVITRO; IMMUNOREACTIVITY; PROGESTERONE AB Meningioma growth is thought to be stimulated by the sex hormones progesterone and possibly estrogen. We report here stimulation of growth of meningioma-derived cells in culture by prolactin. Fourteen human tumors taken from surgery were initially grown in Ham's medium F10 with 15 % fetal calf serum. The tumors were then trypsinized and resuspended in medium in a multi-well plate with either prolactin or bombesin; the cells were incubated for 1 week, washed, and resuspended for cell counting. The growth-stimulating effect of prolactin at 10 and 200 mu g/ml was compared with bombesin at 5 mM/ml or 15 mM/ml. A growth index compared cell count in the experimental well to the control well; growth at the rate of the control well was given an index of 1.0. The tumors included 7 meningiomas and 7 other neoplasms (3 astrocytomas, an ependymoma, a pineoblastoma, a hemangiopericytoma, and a metastatic adenocarcinoma). For meningiomas incubated in 10 mu g/ ml prolactin, the growth index was 3.08; for those incubated in 200 mu g/ml prolactin, it was 2.28. Bombesin indices were 1.7 and 1.2 at 5 mM/ml and 15 mM/ml, respectively. By 2-tailed t-testing both prolactin concentrations stimulated the growth of meningiomas significantly (P less than or equal to 0.02), while bombesin did not. Neither peptide enhanced the growth of the other tumors tested. C1 CHILDRENS HOSP,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CTR BRAIN TUMOR,BOSTON,MA. DANA FARBER CANC INST,BOSTON,MA. BRIGHAM & WOMENS HOSP,NEUROSURG SERV,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 48 TC 12 Z9 12 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1993 VL 16 IS 3 BP 185 EP 190 DI 10.1007/BF01057032 PG 6 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA ME927 UT WOS:A1993ME92700001 PM 8301342 ER PT J AU DEEN, DF CHIARODO, A GRIMM, EA FIKE, JR ISRAEL, MA KUN, LE LEVIN, VA MARTON, LJ PACKER, RJ PEGG, AE ROSENBLUM, ML SUIT, HD WALKER, MD WIKSTRAND, CJ WILSON, CB WONG, AJ YUNG, WKA AF DEEN, DF CHIARODO, A GRIMM, EA FIKE, JR ISRAEL, MA KUN, LE LEVIN, VA MARTON, LJ PACKER, RJ PEGG, AE ROSENBLUM, ML SUIT, HD WALKER, MD WIKSTRAND, CJ WILSON, CB WONG, AJ YUNG, WKA TI BRAIN-TUMOR WORKING GROUP-REPORT ON THE 9TH INTERNATIONAL-CONFERENCE ON BRAIN-TUMOR RESEARCH AND THERAPY SO JOURNAL OF NEURO-ONCOLOGY LA English DT Review DE BRAIN TUMOR RESEARCH; BRAIN TUMOR THERAPY; POLYAMINES CELL KINETICS; RADIATION NECROSIS ID CENTRAL NERVOUS-SYSTEM; HYPERFRACTIONATED RADIATION-THERAPY; GROWTH-FACTOR RECEPTOR; PHASE-I-II; MALIGNANT GLIOMAS; GLIOBLASTOMA-MULTIFORME; MONOCLONAL-ANTIBODY; RECURRENT GLIOMAS; ALPHA-DIFLUOROMETHYLORNITHINE; PROGNOSTIC IMPORTANCE AB Proceedings of the 9th International Conference on Brain Tumor Research and Therapy: 1. Introduction; 2. Surgery; 3. Radiation therapy; 4. Chemotherapy; 5. Immunotherapy; 6. Growth-regulatory alterations; 7. Molecular genetics; 8. Brain tumor invasion; 9. Normal tissue damage; 10. Polyamines. C1 UNIV CALIF SAN FRANCISCO, SAN FRANCISCO, CA 94143 USA. NCI, BETHESDA, MD 20892 USA. UNIV TEXAS, MD ANDERSON CANC CTR, HOUSTON, TX USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN USA. CHILDRENS NATL MED CTR, WASHINGTON, DC USA. PENN STATE UNIV, MILTON S HERSHEY MED CTR, HERSHEY, PA 17033 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA USA. NINCDS, BETHESDA, MD USA. DUKE UNIV, DURHAM, NC USA. FOX CHASE CANC CTR, PHILADELPHIA, PA 19111 USA. NR 149 TC 46 Z9 46 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1993 VL 16 IS 3 BP 243 EP 272 DI 10.1007/BF01057041 PG 30 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA ME927 UT WOS:A1993ME92700010 PM 7905510 ER PT J AU SWEADNER, KJ AF SWEADNER, KJ TI NA,K-ATPASE ISOFORM EXPRESSION AND PROPERTIES IN ASTROCYTES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S245 EP S245 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500964 ER PT J AU BROUILLET, E JENKINS, BG HYMAN, BT FERRANTE, RJ KOWALL, NW SRIVASTAVA, R ROY, DS ROSEN, BR BEAL, MF AF BROUILLET, E JENKINS, BG HYMAN, BT FERRANTE, RJ KOWALL, NW SRIVASTAVA, R ROY, DS ROSEN, BR BEAL, MF TI AGE-DEPENDENT VULNERABILITY OF THE STRIATUM TO THE MITOCHONDRIAL TOXIN 3-NITROPROPIONIC ACID SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE EXCITOTOXICITY; MITOCHONDRIA; HUNTINGTONS DISEASE; AGING; NEURODEGENERATIVE DISEASES; STRIATUM ID HUNTINGTONS-DISEASE; SPINY NEURONS; LESIONS; MECHANISM; GLUTAMATE; RECEPTOR AB The mechanisms of delayed onset and cell death in Huntington's disease (HD) are unknown. One possibility is that a genetic defect in energy metabolism may result in slow excitotoxic neuronal death. Therefore, we examined the effects of age on striatal lesions produced by local administration of the mitochondrial toxin 3-nitropropionic acid in rats. In vivo chemical shift magnetic resonance imaging showed marked increases in striatal lactate concentrations that significantly correlated with increasing age. Histologic and neurochemical studies showed a striking age dependence of the lesions, with 4- and 12-month-old animals being much more susceptible than 1-month-old animals. Continuous systemic administration of low doses of 3-nitropropionic acid for 1 month resulted in striatal lesions showing growth-related changes in dendrites of striatal spiny neurons using the Golgi technique. These results show that a known mitochondrial toxin can produce selective axon-sparing striatal lesions showing both the age dependence and striatal spiny neuron dendritic changes that characterize HD. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,NEUROPATHOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,CTR NMR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Kowall, Neil/G-6364-2012; Brouillet, Emmanuel/B-4784-2014 OI Kowall, Neil/0000-0002-6624-0213; Brouillet, Emmanuel/0000-0001-6322-7403 FU NINDS NIH HHS [NS10828]; PHS HHS [16367] NR 21 TC 281 Z9 285 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1993 VL 60 IS 1 BP 356 EP 359 DI 10.1111/j.1471-4159.1993.tb05859.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KD041 UT WOS:A1993KD04100044 PM 8417157 ER PT J AU YU, JS PANDEY, JP MASSACESI, L LINCOLN, R USUKU, K SEBOUN, E HAUSER, SL AF YU, JS PANDEY, JP MASSACESI, L LINCOLN, R USUKU, K SEBOUN, E HAUSER, SL TI SEGREGATION OF IMMUNOGLOBULIN HEAVY-CHAIN CONSTANT REGION GENES IN MULTIPLE-SCLEROSIS SIBLING PAIRS SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Note DE MULTIPLE SCLEROSIS; IGH GENES; GM ALLOTYPES ID FRAGMENT-LENGTH-POLYMORPHISM; GM ALLOTYPES; SUSCEPTIBILITY; SEVERITY; IGG1; CSF C1 MASSACHUSETTS GEN HOSP,NEUROIMMUNOL UNIT,BOSTON,MA 02114. MED UNIV S CAROLINA,DEPT MICROBIOL & IMMUNOL,CHARLESTON,SC 29425. RI Hauser, Stephen/J-2978-2016; OI Massacesi, Luca/0000-0001-5083-372X FU NIMH NIH HHS [1-T32-MH 18882]; NINDS NIH HHS [NS26799] NR 30 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD JAN PY 1993 VL 42 IS 1 BP 113 EP 116 DI 10.1016/0165-5728(93)90218-N PG 4 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA KJ766 UT WOS:A1993KJ76600013 PM 8423203 ER PT J AU LOUIS, DN VONDEIMLING, A CHUNG, RY RUBIO, MP WHALEY, JM EIBL, RH OHGAKI, H WIESTLER, OD THOR, AD SEIZINGER, BR AF LOUIS, DN VONDEIMLING, A CHUNG, RY RUBIO, MP WHALEY, JM EIBL, RH OHGAKI, H WIESTLER, OD THOR, AD SEIZINGER, BR TI COMPARATIVE-STUDY OF P53 GENE AND PROTEIN ALTERATIONS IN HUMAN ASTROCYTIC TUMORS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE AGE; ASTROCYTOMA; GLIOBLASTOMA MULTIFORME; IMMUNOHISTOCHEMISTRY; P53 GENE; P53 PROTEIN; SEX ID HUMAN PAPILLOMAVIRUS TYPE-16; CARCINOMA CELL-LINES; BREAST-CANCER; MUTANT P53; WILD-TYPE; ACTIVATING MUTATIONS; GEL-ELECTROPHORESIS; GROWTH-REGULATION; BINDING-PROTEIN; LUNG-CANCER AB The p53 gene is a tumor suppressor gene involved in many common malignancies, including astrocytomas. Genetic analysis of the p53 gene and immunohistochemistry of the p53 protein have each been used to screen astrocytomas. To compare these methods, we performed immunohistochemistry with the monoclonal antibody PAb 1801 and single-strand conformational polymorphism (SSCP) with sequence analysis on 34 astrocytic tumors (WHO grades II, III and IV). Seven cases had detectable p53 protein and gene mutations, while twelve cases had neither detectable protein nor gene mutations. Four tumors had frameshift mutations in the p53 gene that were not revealed by immunohistochemistry. One tumor had a genetic polymorphism and no detectable p53 protein. Ten tumors had p53 protein accumulation but no mutations by SSCP; these cases may represent p53 mutations outside of the conserved exons or elevated levels of wild-type p53 protein. Thus, some p53 mutations are missed with PAb 1801 immunohistochemistry alone. p53 immunohistochemistry, however, may reveal p53 accumulation independent of mutations in the conserved portions of the gene. Finally, we suggest that glioblastomas with p53 mutations in the conserved region of the gene may be a subset that are more common in women and in younger patients. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOLEC NEURORONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV ZURICH,DEPT NEUROPATHOL,CH-8006 ZURICH,SWITZERLAND. RI Rubio, Mari-Paz/K-4364-2014; von Deimling, Andreas/F-7774-2013 OI Rubio, Mari-Paz/0000-0003-3963-5903; von Deimling, Andreas/0000-0002-5863-540X FU NCI NIH HHS [CA 09144, P01 CA 44768]; NIGMS NIH HHS [T32 GM007753, T32 GMO 7753-12] NR 57 TC 179 Z9 180 U1 0 U2 2 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD JAN PY 1993 VL 52 IS 1 BP 31 EP 38 DI 10.1097/00005072-199301000-00005 PG 8 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA KG152 UT WOS:A1993KG15200005 PM 8381161 ER PT J AU GOLDEN, JA SCHOENE, WC AF GOLDEN, JA SCHOENE, WC TI CENTRAL-NERVOUS-SYSTEM MALFORMATIONS IN TRISOMY-9 SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE AGENESIS OF THE CORPUS CALLOSUM; DANDY-WALKER MALFORMATION; HIPPOCAMPUS; MYELOMENINGOCELE; TRISOMY-9 ID MULTIPLE CONGENITAL ANOMALIES; DANDY-WALKER SYNDROME; MOSAICISM AB Trisomy 21, 18 and 13 are the most common varieties of autosomal trisomy recognized at birth; most of the others lead to spontaneous abortions in the first trimester. Trisomy 9, a rare trisomy, is compatible with life, but, unlike trisomy 21, 18 and 13, the range of manifestations has not been well catalogued. Central nervous system abnormalities have been reported in the majority of cases, usually including a dilated fourth ventricle and malformed cerebellum. The posterior fossa malformation closely resembles the descriptions of the Dandy-Walker malformation leading some to suggest this designation, while others have suggested that the features are unique to trisomy 9. Two cases of trisomy 9 are presented in this report which extend the range of neuropathologic manifestations in this cytogenetic disorder. The first infant had cortical migration abnormalities, anomalous hippocampal formation, simplified inferior olivary nuclei, germinal matrix cysts, mild ventriculomegaly, syringomyelia, and a large myelomeningocele without a Chiari type II malformation. The fourth ventricle was normal in size and the cerebellum unremarkable. The second infant had a cystically dilated fourth ventricle and widely separated cerebellar hemispheres with an intact cerebellar vermis, the features of which we felt were compatible with the Dandy-Walker malformation. In addition, agenesis of the corpus callosum, anomalous hippocampal formation, subpial glial nodules and mild ventriculomegaly were present. These cases extend the range of malformations that may be associated with trisomy 9, and raise the differential diagnosis of trisomy 9 when these malformations are identified. Furthermore, the malformation of the posterior fossa cystic enlargement of the fourth ventricle and lateral separation of the cerebellar hemispheres is compared with published descriptions of the Dandy-Walker malformation. This malformation in cases of trisomy 9 fulfill the criteria for the Dandy-Walker malformation as described in infants with presumably normal karyotypes. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV WOMENS & PERINATAL PATHOL,BOSTON,MA 02115. RP GOLDEN, JA (reprint author), MASSACHUSETTS GEN HOSP,CHARLES S KUBIK LAB NEUROPATHOL,DEPT PATHOL,WARREN 3,BOSTON,MA 02114, USA. NR 22 TC 16 Z9 17 U1 0 U2 1 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD JAN PY 1993 VL 52 IS 1 BP 71 EP 77 DI 10.1097/00005072-199301000-00009 PG 7 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA KG152 UT WOS:A1993KG15200009 PM 8426188 ER PT J AU FISCHMAN, AJ ALPERT, NM AF FISCHMAN, AJ ALPERT, NM TI FDG-PET IN ONCOLOGY - THERES MORE TO IT THAN LOOKING AT PICTURES SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID POSITRON EMISSION TOMOGRAPHY; EXTREMITY MUSCULOSKELETAL TUMORS; EXPERIMENTAL CEREBRAL-ISCHEMIA; METASTATIC BREAST-CARCINOMA; LUMPED CONSTANT; GLUCOSE-UTILIZATION; FLOW-CYTOMETRY; NECK TUMORS; CANCER; F-18 C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 43 TC 59 Z9 60 U1 0 U2 1 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JAN PY 1993 VL 34 IS 1 BP 6 EP 11 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KE715 UT WOS:A1993KE71500006 PM 8418272 ER PT J AU BARR, SJ ZALESKE, DJ MANKIN, HJ AF BARR, SJ ZALESKE, DJ MANKIN, HJ TI PHYSEAL REPLACEMENT WITH CULTURED CHONDROCYTES OF VARYING DEVELOPMENTAL TIME - FAILURE TO RECONSTRUCT A FUNCTIONAL OR STRUCTURAL PHYSIS SO JOURNAL OF ORTHOPAEDIC RESEARCH LA English DT Article ID MURINE MODEL; REGIONS; LIMBS AB Reconstruction of physeal regions excised from the distal femoral chondroepiphysis was attempted in a murine model. Cultured chondrocytes of varying developmental time from the same inbred strain of mice were used for replacement. Vascularity, matrix formation, and cell division, as well as growth, were assessed. The cultured chondrocytes did not produce growth. Consistent with this, cell division, as assessed with incorporation of tritiated thymidine, was not normal. However, the cultured chondrocytes did receive a nutritional supply from the host and did continue matrix formation after transplantation. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,ACC 507,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIAMS NIH HHS [AR39380] NR 16 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 JAN PY 1993 VL 11 IS 1 BP 10 EP 19 DI 10.1002/jor.1100110103 PG 10 WC Orthopedics SC Orthopedics GA KJ772 UT WOS:A1993KJ77200002 PM 8423511 ER PT J AU KHILNANI, P MUNOZ, R SALEM, M GELB, C TODRES, ID CHERNOW, B AF KHILNANI, P MUNOZ, R SALEM, M GELB, C TODRES, ID CHERNOW, B TI HORMONAL RESPONSES TO SURGICAL STRESS IN CHILDREN SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article DE STRESS; SURGICAL; PEDIATRIC; HORMONAL RESPONSE ID THYROID-FUNCTION; HUMAN PROLACTIN; GROWTH-HORMONE; ANESTHESIA; SURGERY; PLASMA; RADIOIMMUNOASSAY; CORTISOL C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA CRIT CARE,BOSTON,MA 02114. NR 23 TC 26 Z9 26 U1 0 U2 0 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 JAN PY 1993 VL 28 IS 1 BP 1 EP 4 DI 10.1016/S0022-3468(05)80343-4 PG 4 WC Pediatrics; Surgery SC Pediatrics; Surgery GA KG664 UT WOS:A1993KG66400001 PM 8429460 ER PT J AU HABER, J WATTLES, J CROWLEY, M MANDELL, R JOSHIPURA, K KENT, RL AF HABER, J WATTLES, J CROWLEY, M MANDELL, R JOSHIPURA, K KENT, RL TI EVIDENCE FOR CIGARETTE-SMOKING AS A MAJOR RISK FACTOR FOR PERIODONTITIS SO JOURNAL OF PERIODONTOLOGY LA English DT Article DE TOBACCO ADVERSE EFFECTS; DIABETES-MELLITUS; RISK FACTORS ID TOBACCO SMOKERS; ORAL HYGIENE; DISEASE; INDIVIDUALS; THERAPY; SUBSETS; HEALTH AB THE ROLE OF SMOKING as a risk factor for periodontitis was assessed separately in diabetic and nondiabetic study groups. Subject listings stratified for age (19 to 40 years) and sex were obtained for subjects with insulin-dependent diabetes mellitus (IDDM) and nondiabetic subjects. For both the IDDM group (n = 132) and the nondiabetic group (n = 95), age and sex stratified samples were constructed by random selection of subjects from each subject listing. Patients were recruited by phone, examined, and their medical and dental histories obtained. Among nondiabetic subjects, the prevalence of periodontitis was markedly higher among current smokers compared with never smokers (P less-than-or-equal-to 0.005) in both the 19 to 30 year-old (46% vs. 12%) and 31 to 40 year-old groups (88% vs. 33%). The subject mean percent of sites with gingival pocket depth greater-than-or-equal-to 4 mm was higher among current smokers than never smokers (P = 0.001) in the 19 to 30 (8.2% vs. 3.4%) and 31 to 40 (14.3% vs. 4.3%) age groups. The effects of smoking among IDDM subjects were similar to that observed in the nondiabetic population. There were no differences between current and never smokers in the proportion of sites positive for plaque. Attributable risk percents from prevalence data suggest that among nondiabetic subjects, a large proportion, perhaps as much as 51% of the periodontitis in the 19 to 30 year old group and 32% of the periodontitis in the 31 to 40 year old group, is associated with smoking. These findings suggest that smokers are a high risk group for periodontitis, and that smoking may be the single most important environmental risk factor for periodontitis. C1 TUFTS UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02111. TUFTS UNIV,SCH DENT MED,DEPT ORAL PATHOL,BOSTON,MA 02111. FORSYTH DENT CTR,DEPT MICROBIOL,BOSTON,MA 02115. FORSYTH DENT CTR,DEPT BIOSTAT,BOSTON,MA 02115. RP HABER, J (reprint author), TUFTS UNIV,SCH MED,DEPT ORAL PATHOL,1 KNEELAND ST,BOSTON,MA 02111, USA. RI de la Flor, Maria/B-9212-2015 FU NIDCR NIH HHS [DE04881, DE08463] NR 44 TC 353 Z9 371 U1 8 U2 19 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD JAN PY 1993 VL 64 IS 1 BP 16 EP 23 DI 10.1902/jop.1993.64.1.16 PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KJ144 UT WOS:A1993KJ14400002 PM 8426285 ER PT J AU LOCKE, JL AF LOCKE, JL TI LEARNING TO SPEAK SO JOURNAL OF PHONETICS LA English DT Article ID PERCEPTION; SPEECH; LANGUAGE; INFANTS RP LOCKE, JL (reprint author), MASSACHUSETTS GEN HOSP,101 MERRIMAC ST,BOSTON,MA 02114, USA. NR 31 TC 3 Z9 4 U1 0 U2 3 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0095-4470 J9 J PHONETICS JI J. Phon. PD JAN-APR PY 1993 VL 21 IS 1-2 BP 141 EP 146 PG 6 WC Linguistics; Language & Linguistics SC Linguistics GA KU242 UT WOS:A1993KU24200010 ER PT J AU ZACHAZEWSKI, JE RILEY, PO KREBS, DE AF ZACHAZEWSKI, JE RILEY, PO KREBS, DE TI BIOMECHANICAL ANALYSIS OF BODY-MASS TRANSFER DURING STAIR ASCENT AND DESCENT OF HEALTHY-SUBJECTS SO JOURNAL OF REHABILITATION RESEARCH AND DEVELOPMENT LA English DT Article DE CENTER OF MASS; CENTER OF PRESSURE; GAIT; GROUND REACTION FORCES; STAIRS AB The purposes of this study were to: 1) assess whole body center of mass (CM) motion in the frontal, sagittal, and transverse planes; 2) compare CM displacement with center of pressure (CP); and, 3) further define the stance and swing subphases of stair ascent (SA) and stair descent (SD) based on critical CM, CP, and ground reaction force (GRF) events. SA and SD were analyzed on a convenience sample of 11 subjects. Unpaced data were collected from 28 SA trials and 24 SD trials utilizing a bilateral SELSPOT II(T)/TRACK(C) data acquisition system and two Kistler force plates at a sampling frequency of 153 Hz. Twenty-six discrete data points were chosen from each trial for analysis. Each identified point detailed the intersection, separation, maximum or minimum value of CM, CP, or GRF in all three planes. Specific phases of SA and SD are presented and described. The actions of CM, CP, and GRF are presented during each phase. Results further refine the phases originally described by McFayden and Winter. Subtle differences in phases and duration of single and double support are demonstrated between SA and SD. Based on these results, it is apparent that SD is a more dynamic process with greater inherent instability. Knowledge of SA and SD phases and CM/CP dynamics in healthy, normal subjects will permit comparison with patients exhibiting various pathologies. Such comparison should facilitate the development of appropriate intervention strategies. C1 MGH THERAPY SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BIOMOT LAB,BOSTON,MA 02114. RP ZACHAZEWSKI, JE (reprint author), MGH INST HLTH PROFESS,101 MERRIMAC ST,BOSTON,MA 02114, USA. RI Riley, Patrick/B-3053-2009 NR 16 TC 68 Z9 68 U1 1 U2 7 PU JOURNAL REHAB RES & DEV PI BALTIMORE PA DEPT OF VETERANS AFFAIRS REHABIL RES & DEVELOP CTR 103 SOUTH GAY STREET, BALTIMORE, MD 21202-4051 SN 0007-506X J9 J REHABIL RES DEV JI J. Rehabil. Res. Dev. PY 1993 VL 30 IS 4 BP 412 EP 422 PG 11 WC Rehabilitation SC Rehabilitation GA MR325 UT WOS:A1993MR32500007 PM 8158557 ER PT J AU CARLSON, KJ DRETLER, SP ROTH, RA HATZIANDREU, E GLADSTONE, K MULLEY, AG AF CARLSON, KJ DRETLER, SP ROTH, RA HATZIANDREU, E GLADSTONE, K MULLEY, AG TI EXTRACORPOREAL SHOCK-WAVE LITHOTRIPSY AND PERCUTANEOUS NEPHROSTOLITHOTOMY FOR URINARY CALCULI - COMPARISON OF IMMEDIATE AND LONG-TERM EFFECTS SO JOURNAL OF STONE DISEASE LA English DT Article AB Extracorporeal shock wave lithotripsy and percutaneous nephrostolithotomy have become widely used technologies for removal of urinary calculi, despite a lack of adequate evaluative studies. The possibility of long-term adverse effects of these treatments has been raised, particularly an increase in stone recurrence and development of hypertension following extracorporeal shock wave lithotripsy. We conducted a retrospective study of 1,000 patients treated with extracorporeal shock wave lithotripsy or percutaneous nephrostolithotomy for upper tract stone disease to assess immediate effectiveness and complications, with prospective follow-up to assess stone recurrence and development of hypertension. The effectiveness of each treatment (defined in terms of patients rendered stone-free or having only fragments at discharge) was similar for most stone types. While stone recurrence rates in the first 2 years after treatment were similar in the two groups, cumulative recurrence at 3 years was higher following extracorporeal shock wave lithotripsy compared to percutaneous nephrostolithotomy (39% vs. 23%, p = 0.04). However, logistic regression and Kaplan-Meier analyses showed no significant difference in clinically evident recurrence for patients treated with extracorporeal shock wave lithotripsy. Cumulative incidence of clinically evident stone recurrence did not differ significantly between patients with fragments at discharge (20%) and patients rendered stone-free (15%) (p = 0.24). There was no difference in the development of new hypertension requiring medical treatment. Our findings indicate that extracorporeal shock wave lithotripsy is effective and associated with lower short-term morbidity than percutaneous nephrostolithotomy. Stone fragments left behind by lithotripsy do not appear to confer significant risk of early stone recurrence. Further study is necessary to define long-term risk of recurrence following extracorporeal shock wave lithotripsy. RP CARLSON, KJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. FU AHRQ HHS [HS 05604] NR 0 TC 4 Z9 4 U1 0 U2 0 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 1059-9509 J9 J STONE DIS PD JAN PY 1993 VL 5 IS 1 BP 8 EP 18 PG 11 WC Gastroenterology & Hepatology; Urology & Nephrology SC Gastroenterology & Hepatology; Urology & Nephrology GA LW644 UT WOS:A1993LW64400003 PM 10148257 ER PT J AU GOLD, J SHERA, D CLARKSON, B AF GOLD, J SHERA, D CLARKSON, B TI PRIVATE PSYCHIATRIC-HOSPITALIZATION OF CHILDREN - PREDICTORS OF LENGTH OF STAY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE HOSPITALIZATION; LENGTH OF STAY; CHILD PSYCHIATRY; DIAGNOSIS RELATED GROUPS ID DIAGNOSIS-RELATED GROUPS; GLOBAL ASSESSMENT SCALE; CHILDHOOD DISORDER DRG; PROSPECTIVE PAYMENT; INPATIENT TREATMENT; DSM-III; RELIABILITY; AXIS; VALIDITY; MODEL AB Objective. To quantitatively identify predictors and determinants of length of psychiatric hospital stay for children. Method: Forty-seven demographic, psychosocial stressor, psychopathology, and disposition variables were statistically reviewed as correlates of length of stay in 100 consecutive discharges from a child psychiatry inpatient service (age range 4-12) in a private hospital. Those with strong statistical significance were then analyzed by multiple regression. Results: Greater severity of psychopathology (measured by the Children's Global Assessment Scale), greater severity of psychosocial stressors (by Axis IV scale), diagnosis of post-traumatic stress disorder, special educational and out-of-home dispositions, and severe tantrums in hospital all strongly predicted longer hospital stay. Diagnosis of adjustment disorder predicted shorter stay. Together these variables explained 57% of the total variance in length of stay. Conclusions. The most powerful of these predictor variables could potentially be measured at the time of admission, thus permitting accurate prediction of length of stay. A set of models was generated for this purpose. C1 WESTWOOD LODGE HOSP,WESTWOOD,MA. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BIOSTAT UNIT,BOSTON,MA 02114. NR 31 TC 28 Z9 30 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1993 VL 32 IS 1 BP 135 EP 143 DI 10.1097/00004583-199301000-00020 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KD791 UT WOS:A1993KD79100019 PM 8428866 ER PT J AU FARAONE, SV BIEDERMAN, J SPRICHBUCKMINSTER, S CHEN, W TSUANG, MT AF FARAONE, SV BIEDERMAN, J SPRICHBUCKMINSTER, S CHEN, W TSUANG, MT TI EFFICIENCY OF DIAGNOSTIC-CRITERIA FOR ATTENTION-DEFICIT DISORDER - TOWARD AN EMPIRICAL-APPROACH TO DESIGNING AND VALIDATING DIAGNOSTIC ALGORITHMS SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE ATTENTION DEFICIT DISORDER; DIAGNOSTIC EFFICIENCY; COMORBIDITY; FAMILY STUDY ID DSM-III-R; AUTISTIC DISORDER; FIELD TRIAL; CONDUCT; FAMILY AB Using structured psychiatric interviews, 73 attention deficit disorder (ADD) patients, 26 psychiatric control patients, 26 normal controls, and all available first degree relatives of these index children were examined. ADD subgroups with and without comorbid psychiatric disorders did not differ on rates of specific ADD symptoms. The construct of ADD is internally consistent as measured by Cronbach's alpha. The diagnostic efficiency of individual items is presented. A receiver operating characteristic-based procedure is used to create an ADD diagnostic algorithm that is more efficient in discriminating ADD children from controls than the DSM-III-based clinical diagnosis. Cross-validation with family study data shows this procedure to be superior to the procedure used for the DSM-III-R diagnosis. The results show that proponents of conditional probability and receiver operating characteristic analyses are correct in asserting that the examination of symptom combinations may result in better diagnostic algorithms. C1 MASSACHUSETTS GEN HOSP,PEDIATR PSYCHOPHARMACOL UNIT ACC725,CHILD PSYCHIAT SERV,FRUIT ST,BOSTON,MA 02114. BROCKTON W ROXBURY VET ADM MED CTR,PSYCHIAT SERV,BROCKTON,MA. HARVARD UNIV,SCH MED & PUBL HLTH,JOINT PROGRAM PSYCHIAT EPIDEMIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [R01 MH-41314-01A2] NR 17 TC 25 Z9 25 U1 2 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1993 VL 32 IS 1 BP 166 EP 174 DI 10.1097/00004583-199301000-00024 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KD791 UT WOS:A1993KD79100023 PM 7679093 ER PT J AU BIEDERMAN, J BALDESSARINI, RJ WRIGHT, V KEENAN, K FARAONE, S AF BIEDERMAN, J BALDESSARINI, RJ WRIGHT, V KEENAN, K FARAONE, S TI A DOUBLE-BLIND PLACEBO CONTROLLED-STUDY OF DESIPRAMINE IN THE TREATMENT OF ADD .3. LACK OF IMPACT OF COMORBIDITY AND FAMILY HISTORY FACTORS ON CLINICAL-RESPONSE SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE ATTENTION DEFICIT DISORDER; DESIPRAMINE; CHILDREN; ADOLESCENTS; COMORBIDITY ID ATTENTION-DEFICIT DISORDER; AGGRESSIVE NONCOMPLIANT FEATURES; HYPERACTIVITY DISORDER; CHILDREN; METHYLPHENIDATE; INTERVIEW; BOYS; ANXIETY; CONDUCT; PARENTS AB A 6-week randomized, double-blind, placebo controlled trial of desipramine (DMI) in daily doses averaging 4 to 5 mg/kg for the treatment of children and adolescents with attention deficit disorder with hyperactivity (ADDH) was further analyzed. Investigators examined whether comorbidity of ADDH with conduct disorder, major depression, an anxiety disorder, or a family history of ADDH predicted response to DMI treatment. There was a highly significant effect of treatment with DMI in outcome assessments, but responses to DMI were indistinguishable in ADDH patients with and without a comorbid disorder or familial ADDH. Cases of ''pure'' ADDH (lacking comorbidity with depression, anxiety, or conduct disorder and having a positive family history of ADDH) showed a trend toward lesser placebo responses and a corresponding greater DMI-placebo difference. These findings suggest that (1) DMI is effective in simple, noncomorbid cases, (2) DMI is not selective for comorbid cases, but (3) a response to DMI can be obtained even in complex cases of ADDH with associated comorbidity. C1 MCLEAN HOSP,MAILMAN RES CTR,PSYCHIATR RES LABS,BELMONT,MA 02178. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PEDIATR PSYCHOPHARMACOL UNIT,ACC725,15 PARKMAN ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH-31154, MH-36224, MH-47370] NR 37 TC 40 Z9 40 U1 2 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1993 VL 32 IS 1 BP 199 EP 204 DI 10.1097/00004583-199301000-00028 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KD791 UT WOS:A1993KD79100027 PM 8428872 ER PT J AU SPENCER, T BIEDERMAN, J WILENS, T STEINGARD, R GEIST, D AF SPENCER, T BIEDERMAN, J WILENS, T STEINGARD, R GEIST, D TI NORTRIPTYLINE TREATMENT OF CHILDREN WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER AND TIC DISORDER OR TOURETTES-SYNDROME SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE NORTRIPTYLINE; TOURETTES SYNDROME; ATTENTION-DEFICIT HYPERACTIVITY DISORDER ID DOUBLE-BLIND; GILLES; DESIPRAMINE; IMIPRAMINE; METHYLPHENIDATE; ADOLESCENTS; PLASMA AB Although as many as 50% of patients with Tourette's syndrome (TS) also meet diagnostic criteria for Attention-deficit Hyperactivity Disorder (ADHD), until recently little attention has been paid to ADHD symptoms in the assessment of therapeutic outcome of TS or patients with chronic motor tics (CMT). Because antipsychotics are of limited value in controlling the symptoms of ADHD and stimulants can exacerbate tics, alternative treatments for patients with chronic tic disorder (CTD) (TS or CMT) plus ADHD (CTD + ADHD) patients are direly needed. We examined the efficacy of the tricyclic antidepressant nortriptyline in the treatment of pediatric patients with CTD + ADHD ascertained from systematic chart reviews of all subjects with this diagnosis treated with nortriptyline. Of the 12 identified patients, 67% had significant improvement in CTD symptomatology and 92% significantly improved ADHD symptoms without major adverse effects over an average follow-up period of 19 months. Although the conclusions from this retrospective report can be only seen as preliminary until replicated in a controlled investigation, the magnitude and persistence of the response is encouraging and suggest a therapeutic role for nortriptyline in the treatment of CTD + ADHD patients. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SPENCER, T (reprint author), MASSACHUSETTS GEN HOSP,PEDIATR PSYCHOPHARMACOL UNIT ACC-725,FRUIT ST,BOSTON,MA 02114, USA. NR 49 TC 51 Z9 51 U1 2 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1993 VL 32 IS 1 BP 205 EP 210 DI 10.1097/00004583-199301000-00029 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KD791 UT WOS:A1993KD79100028 PM 8428873 ER PT J AU SPENCER, T BIEDERMAN, J STEINGARD, R WILENS, T AF SPENCER, T BIEDERMAN, J STEINGARD, R WILENS, T TI BUPROPION EXACERBATES TICS IN CHILDREN WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER AND TOURETTES-SYNDROME SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE BUPROPION; TOURETTES SYNDROME; ADHD ID STIMULANTS; CLONIDINE; DESIPRAMINE AB Concerns have been raised regarding the development of tics in some children with attention-deficit hyperactivity disorder (ADHD) receiving stimulants. Because in many patients with Tourette's syndrome (TS) the ADHD symptoms are the major source of disability, alternative nonstimulant treatments are needed. Initial reports on bupropion have suggested that it may be an effective alternative in children and adults with ADHD. The value of bupropion as an alternative treatment for patients with comorbid TS and ADHD is determined by the question of association with exacerbation of tics. The purpose of this study was to examine an apparent association with exacerbation of tics in patients with comorbid TS and ADHD. A careful retrospective analysis was conducted of clinic cases of patients who all had comorbid TS and ADHD treated with bupropion. We present four cases of children with ADHD and comorbid TS treated with bupropion in whom tics were exacerbated by this medicine. This series suggests that bupropion may not be an appropriate alternative to stimulants in the treatment of ADHD in TS. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SPENCER, T (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT ACC-725,FRUIT ST,BOSTON,MA 02114, USA. NR 31 TC 36 Z9 36 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1993 VL 32 IS 1 BP 211 EP 214 DI 10.1097/00004583-199301000-00030 PG 4 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA KD791 UT WOS:A1993KD79100029 PM 8428875 ER PT J AU AHMED, AR AF AHMED, AR TI TOPICAL CYCLOSPORINE FOR CICATRICIAL PEMPHIGOID - REPLY SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Letter ID MEMBRANE RP AHMED, AR (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD JAN PY 1993 VL 28 IS 1 BP 134 EP 135 PG 2 WC Dermatology SC Dermatology GA KF423 UT WOS:A1993KF42300043 ER PT J AU MODY, FV BUXTON, DB ARAUJO, LI FISHBEIN, ME SELIN, CE SCHELBERT, HR SCHWAIGER, M AF MODY, FV BUXTON, DB ARAUJO, LI FISHBEIN, ME SELIN, CE SCHELBERT, HR SCHWAIGER, M TI BLOOD FLOW-DEPENDENT UPTAKE OF IN-111 MONOCLONAL ANTIMYOSIN ANTIBODY IN CANINE ACUTE MYOCARDIAL-INFARCTION SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID EMISSION COMPUTED-TOMOGRAPHY; MYOSIN-SPECIFIC ANTIBODY; CREATINE KINASE-MB; CARDIAC MYOSIN; SIZE; QUANTIFICATION; REPERFUSION; PYROPHOSPHATE; FRAGMENTS; OCCLUSION AB Objectives. The relation of myocardial blood flow and indium-111 (In-111) antimyosin antibody uptake was studied by inducing myocardial infarction in 18 dogs, 8 with closed chest left anterior descending artery balloon occlusion for 3 h followed by reperfusion (group A) and 10 dogs with open chest left anterior descending artery ligation (without reperfusion, group B). Background. The relation of antimyosin uptake to myocardial injury has been documented. However, its relation to tracer delivery by myocardial blood flow has not been studied and has been assumed to be independent. Methods. Indium-111 antimyosin antibody, 2 mCi, was injected 20 min after reperfusion and 3 h after coronary artery ligation in groups A and B, respectively. Regional blood flows were determined by radiolabeled microspheres during occlusion and 24 h later in both groups. On day 2, dogs were killed after risk zone delineation with gentian violet. The heart was excised and stained with triphenyltetrazolium chloride solution and graded for increasing severity of tissue injury based on extent of staining. Microsphere activity and In-111 antimyosin activity were measured in control tissue (grade 1), noninfarct tissue at risk (grade 2), mixed tissue (grade 3), infarct tissue (grade 4) and hemorrhagic infarct tissue (grade 5, present only in group A dogs). Count activity was normalized to that of the mean value in control tissue (grade 1) and expressed as a ratio of activity. Results. Indium-111 antimyosin activity was high in triphenyltetrazolium chloride grade 4 tissue in both groups but was attenuated in grade 4 tissue in group B dogs (10.6 +/- 5.1 vs. 5.0 +/-4.5; p < 0.05 group A vs. group B), which had lower blood flow on day 2 (0.51 +/- 0.36 vs. 0.23 vs. 0.22; p < 0.01). Normalizing In-111 antimyosin activity for blood flow on day 2 resulted in equivalent In-111 antimyosin uptake for infarct tissue (32.6 +/- 21.6 vs. 36.6 +/- 29.8 for group A vs. group B; p = NS). Conclusions. Thus, In-111 antimyosin uptake is a specific marker of necrotic tissue with a high signal ratio in reperfused tissue. However, its uptake is dependent on residual blood flow in the infarct territory. Indium-111 antimyosin could potentially serve as a suitable tracer for infarct sizing if myocardial blood flow in the same region were factored simultaneously. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT RADIOL SCI,DIV NUCL MED & BIOPHYS,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,BIOMED & ENVIRONM SCI,NUCL MED LAB,LOS ANGELES,CA 90024. RP MODY, FV (reprint author), W LOS ANGELES WADSWORTH VET AFFAIRS MED CTR,DIV CARDIOL,691W111E,LOS ANGELES,CA 90073, USA. FU NHLBI NIH HHS [HL33177, HL29845] NR 23 TC 5 Z9 5 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 JAN PY 1993 VL 21 IS 1 BP 233 EP 239 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KG398 UT WOS:A1993KG39800033 PM 7678020 ER PT J AU HUTTER, AM AF HUTTER, AM TI PRESIDENTS PAGE - ACCESS TO CARDIOVASCULAR CARE SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Editorial Material RP HUTTER, AM (reprint author), MASSACHUSETTS GEN HOSP,ACC BLDG,SUITE 467,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JAN PY 1993 VL 21 IS 1 BP 276 EP 276 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KG398 UT WOS:A1993KG39800040 ER PT J AU LJUNG, GM AF LJUNG, GM TI ON OUTLIER DETECTION IN TIME-SERIES SO JOURNAL OF THE ROYAL STATISTICAL SOCIETY SERIES B-METHODOLOGICAL LA English DT Article DE AUTOREGRESSIVE MOVING AVERAGE PROCESS; DELETION DIAGNOSTICS; INTERPOLATION; LIKELIHOOD FUNCTION; MISSING VALUES; OUTLIER DETECTION; STUDENTIZED RESIDUALS; TIME SERIES ID MOVING AVERAGE MODELS; MISSING OBSERVATIONS; LIKELIHOOD FUNCTION; MAXIMUM-LIKELIHOOD; ALGORITHM AB The estimation and detection of outliers in a time series generated by a Gaussian autoregressive moving average process is considered. It is shown that the estimation of additive outliers is directly related to the estimation of missing or deleted observations. A recursive procedure for computing the estimates is given. Likelihood ratio and score criteria for detecting additive outliers are examined and are shown to be closely related to the leave-k-out diagnostics studied by Bruce and Martin. The procedures are contrasted with those appropriate for innovational outliers. RP LJUNG, GM (reprint author), MASSACHUSETTS GEN HOSP,DEPT MATH,ROOM 2-332,77 MASSACHUSETTS AVE,BOSTON,MA 02114, USA. NR 24 TC 43 Z9 43 U1 1 U2 3 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0035-9246 J9 J ROY STAT SOC B MET JI J. R. Stat. Soc. Ser. B-Methodol. PY 1993 VL 55 IS 2 BP 559 EP 567 PG 9 WC Statistics & Probability SC Mathematics GA KW965 UT WOS:A1993KW96500020 ER PT J AU ROWAN, AB FOY, DW AF ROWAN, AB FOY, DW TI POSTTRAUMATIC-STRESS-DISORDER IN CHILD SEXUAL ABUSE SURVIVORS - A LITERATURE-REVIEW SO JOURNAL OF TRAUMATIC STRESS LA English DT Article DE PTSD; CHILD SEXUAL ABUSE; EXPOSURE ID IMPACT; INCEST; RAPE; VICTIMS; WOMEN AB Research to date has failed to identify a unique syndrome describing the sequelae of child sexual abuse (CSA). Recently, however, some researchers have suggested Post-Traumatic Stress Disorder as the diagnosis which best fits the syndrome commonly seen in CSA survivors. Research examining the consequences of CSA in terms of the applicability of a PTSD diagnosis is reviewed. Additionally, based on findings of significant relationships between PTSD and traumatic exposure in other trauma groups, this review also examines studies which have investigated relationships between exposure and symptom development among CSA survivors. Finally, conclusions regarding the applicability of PTSD to CSA survivors and suggestions for future research are offered. C1 W LOS ANGELES VA MED CTR,BRENTWOOD DIV,BRENTWOOD,CA. RP ROWAN, AB (reprint author), FULLER THEOL SEMINARY,GRAD SCH PSYCHOL,PASADENA,CA 91101, USA. NR 38 TC 79 Z9 79 U1 1 U2 5 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0894-9867 J9 J TRAUMA STRESS JI J. Trauma Stress PD JAN PY 1993 VL 6 IS 1 BP 3 EP 20 DI 10.1002/jts.2490060103 PG 18 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA KR236 UT WOS:A1993KR23600001 ER PT J AU GREGOIRE, M KANTOFF, P DEWOLF, WC AF GREGOIRE, M KANTOFF, P DEWOLF, WC TI SYNCHRONOUS ADENOCARCINOMA AND TRANSITIONAL CELL-CARCINOMA OF THE BLADDER ASSOCIATED WITH AUGMENTATION - CASE-REPORT AND REVIEW OF THE LITERATURE SO JOURNAL OF UROLOGY LA English DT Article DE BLADDER NEOPLASMS; ADENOCARCINOMA; CARCINOMA, TRANSITIONAL CELL ID TRANSGENIC MICE; ORNITHINE DECARBOXYLASE; GROWTH-FACTORS; RAS ONCOGENES; HUMAN-COLON; URETEROSIGMOIDOSTOMY; TUMOR; CANCER; CARCINOGENESIS; TUMORIGENESIS AB We report a case of synchronous transitional cell carcinoma and adenocarcinoma in an augmented bladder 8 years after cecocystoplasty. We discuss the clinical presentation as well as current clinical and basic research concepts, and suggest that the anastomotic zone in such cases may be at risk for malignant transformation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. RP GREGOIRE, M (reprint author), BETH ISRAEL HOSP,DIV UROL,BOSTON,MA 02215, USA. NR 38 TC 34 Z9 34 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD JAN PY 1993 VL 149 IS 1 BP 115 EP 118 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA KE259 UT WOS:A1993KE25900039 PM 8417189 ER PT J AU JOHNSON, RP TROCHA, A BUCHANAN, TM WALKER, BD AF JOHNSON, RP TROCHA, A BUCHANAN, TM WALKER, BD TI RECOGNITION OF A HIGHLY CONSERVED REGION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GP120 BY AN HLA-CW4-RESTRICTED CYTOTOXIC LYMPHOCYTE-T CLONE SO JOURNAL OF VIROLOGY LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; CYTO-TOXIC RESPONSES; SYNTHETIC PEPTIDES; SEROPOSITIVE INDIVIDUALS; ENVELOPE GLYCOPROTEIN; FINE SPECIFICITY; CELL RECOGNITION; INFLUENZA-VIRUS; HIV-1; INFECTION AB Human immunodeficiency virus type 1 (HIV-1) isolates exhibit extensive sequence variation, particularly in the gp120 subunit of the envelope glycoprotein, and the degree of this variation has raised questions as to whether conserved regions of the HIV-1 envelope can be recognized by the host immune response. A CD8+ cytotoxic T-lymphocyte (CTL) clone specific for the HIV-1 envelope was derived by culturing peripheral blood mononuclear cells from an HIV-1 seropositive subject in the presence of a CD3-specific monoclonal antibody, interleukin-2, and irradiated allogeneic peripheral blood mononuclear cells. Lysis of target cells was restricted by an HLA-C molecule, Cw4, which has not been previously shown to present viral antigen to CTL. Mapping of the specificity of this CTL clone by using synthetic HIV-1 peptides localized the epitope to an 8-amino-acid region of gp120 (amino acids 376 to 383) which is conserved among approximately 90% of sequenced viral isolates. Examination of the recognition of variant peptides by this CTL clone demonstrated that a single, nonconservative amino acid substitution within the 8-amino-acid minimal epitope could abrogate lysis of targets incubated with the variant peptide. The identification of a CTL epitope in a highly conserved region of gp120 documents the ability of cellular immune responses of infected persons to respond to relatively invariant portions of this highly variable envelope glycoprotein. However, the ability of even a single-amino-acid change in gp120 to abolish lysis by CTL supports the hypothesis that sequence variation in HIV-1 may serve as a mechanism of immune escape. In addition, the identification of an HLA-C molecule presenting viral antigen to CTL supports a functional role for these molecules. C1 UNIV WASHINGTON,SEATTLE,WA 98144. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JOHNSON, RP (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114, USA. FU NIAID NIH HHS [AI-28568, AI-30914, AI-26463] NR 53 TC 90 Z9 90 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 JAN PY 1993 VL 67 IS 1 BP 438 EP 445 PG 8 WC Virology SC Virology GA KB970 UT WOS:A1993KB97000050 PM 7677956 ER PT J AU ABBOUD, HE SCHENA, FP COHEN, JJ STERZEL, RB STRIKER, G GESUALDO, L FINE, LG STRIKER, L PETEN, E THOMSON, N CAMERON, S BORSATTI, A RUBINKELLY, VE REMUZZI, G AF ABBOUD, HE SCHENA, FP COHEN, JJ STERZEL, RB STRIKER, G GESUALDO, L FINE, LG STRIKER, L PETEN, E THOMSON, N CAMERON, S BORSATTI, A RUBINKELLY, VE REMUZZI, G TI GROWTH-FACTORS IN GLOMERULONEPHRITIS SO KIDNEY INTERNATIONAL LA English DT Discussion ID TUMOR-NECROSIS-FACTOR; GLOMERULAR MESANGIAL CELLS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MEMBRANE ATTACK COMPLEX; FACTOR-I; FACTOR-BETA; GENE-EXPRESSION; PDGF RECEPTOR; ENDOTHELIAL-CELLS; MESSENGER-RNA C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. UNIV BARI, DIV NEPHROL, I-70124 BARI, ITALY. SUNY STONY BROOK, STONY BROOK, NY 11794 USA. UNIV ERLANGEN NURNBERG, W-8520 ERLANGEN, GERMANY. NIH, DIV KIDNEY UROL & HEMATOL DIS, BETHESDA, MD 20892 USA. UNIV COLL & MIDDLESEX SCH MED, DEPT MED, LONDON, ENGLAND. NIDDKD, BETHESDA, MD USA. UNIV HOSP PADOVA, DIV NEPHROL, PADUA, ITALY. MONASH UNIV, QUEEN VICTORIA MED CTR, MELBOURNE, VIC 3004, AUSTRALIA. GUYS HOSP, LONDON SE1 9RT, ENGLAND. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. MARIO NEGRI INST PHARMACOL RES, KIDNEY DIS LAB, I-20157 MILAN, ITALY. RP ABBOUD, HE (reprint author), UNIV TEXAS, HLTH SCI CTR, DIV NEPHROL, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. RI Schena, Francesco /K-6982-2016 OI Schena, Francesco /0000-0001-7927-5207 FU NIDDK NIH HHS [DK 43988, DK 33665] NR 156 TC 198 Z9 200 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1993 VL 43 IS 1 BP 252 EP 267 DI 10.1038/ki.1993.39 PG 16 WC Urology & Nephrology SC Urology & Nephrology GA KC891 UT WOS:A1993KC89100039 PM 8433565 ER PT J AU BELL, DA SCULLY, RE AF BELL, DA SCULLY, RE TI EARLY DENOVO OVARIAN-CARCINOMA - A STUDY OF 14 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A72 EP A72 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200423 ER PT J AU CASTAGNARO, M YANDELL, D HIORT, O NABER, S OLEARY, M MEARES, E WOLFE, H AF CASTAGNARO, M YANDELL, D HIORT, O NABER, S OLEARY, M MEARES, E WOLFE, H TI P53 AND ANDROGEN RECEPTOR GENES ANALYSIS IN HUMAN PROSTATE-CANCER SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NEW ENGLAND CTR HOSP,BOSTON,MA. UNIV TURIN,SCH VET MED,I-10124 TURIN,ITALY. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A57 EP A57 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200333 ER PT J AU CENTENO, BA SOBEZAK, ML PREFFER, FL COLVIN, RB SHIPLEY, WU AF CENTENO, BA SOBEZAK, ML PREFFER, FL COLVIN, RB SHIPLEY, WU TI RADIATION-THERAPY AND LOCAL-CONTROL IN PROSTATE-CANCER - PROLIFERATIVE FRACTION AND DNA PLOIDY BY FLOW-CYTOMETRY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A57 EP A57 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200334 ER PT J AU DUNCAN, LM BOUFFARD, D HOWARD, C MIHM, MC BYERS, HR AF DUNCAN, LM BOUFFARD, D HOWARD, C MIHM, MC BYERS, HR TI INTEGRIN VLA-2 AND ALPHA-ACTININ DISTRIBUTION IN MELANOCYTIC PROLIFERATIONS INSITU SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A33 EP A33 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200191 ER PT J AU EICHHORN, JH SCULLY, RE AF EICHHORN, JH SCULLY, RE TI OVARIAN-TUMORS RESEMBLING SALIVARY-GLAND NEOPLASMS - A STUDY OF 14 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A73 EP A73 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200429 ER PT J AU FANBURG, JC MEIS, JM ROSENBERG, AE AF FANBURG, JC MEIS, JM ROSENBERG, AE TI MAFFUCCIS-SYNDROME - MULTIPLE ENCHONDROMAS AND SPINDLE CELL HEMANGIOENDOTHELIOMAS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. UNIV VERMONT,BURLINGTON,VT 05405. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A6 EP A6 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200028 ER PT J AU FERRY, JA HARRIS, NL YOUNG, RH SCULLY, RE AF FERRY, JA HARRIS, NL YOUNG, RH SCULLY, RE TI MALIGNANT-LYMPHOMA OF THE TESTIS, EPIDIDYMIS AND SPERMATIC CORD - A CLINICOPATHOLOGICAL STUDY OF 65 CASES WITH IMMUNOPHENOTYPIC ANALYSIS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A89 EP A89 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200526 ER PT J AU GOULART, RA MARK, EJ ROSEN, S AF GOULART, RA MARK, EJ ROSEN, S TI EXTRAVASCULAR MANIFESTATIONS OF WEGENER GRANULOMATOSIS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 BETH ISRAEL HOSP,DEPT PATHOL,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A123 EP A123 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200724 ER PT J AU HSI, ED ZUKERBERG, LR SCHNITZER, B HARRIS, NL AF HSI, ED ZUKERBERG, LR SCHNITZER, B HARRIS, NL TI DEVELOPMENT OF EXTRASALIVARY GLAND LYMPHOMA IN MYOEPITHELIAL SIALADENITIS (BENIGN LYMPHOEPITHELIAL LESION) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV MICHIGAN,ANN ARBOR,MI 48109. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A92 EP A92 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200543 ER PT J AU KUPRYJANCZYK, J BEAUCHAMP, R BELL, D YANDELL, DW THOR, A AF KUPRYJANCZYK, J BEAUCHAMP, R BELL, D YANDELL, DW THOR, A TI P53 GENE ALTERATIONS AND P53 PROTEIN EXPRESSION IN OVARIAN CANCERS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A75 EP A75 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200441 ER PT J AU LAUER, E YANDELL, D CASTAGNARO, M ALMAN, B GOLDBERG, M NABER, S WOLFE, H AF LAUER, E YANDELL, D CASTAGNARO, M ALMAN, B GOLDBERG, M NABER, S WOLFE, H TI MOLECULAR GENETIC AND IMMUNOHISTOCHEMICAL ANALYSIS OF TUMOR SUPPRESSOR GENES P53 AND RB IN FIBROMATOSIS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NEW ENGLAND MED CTR,HOSP,BOSTON,MA 02111. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A8 EP A8 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200037 ER PT J AU MATIASGUIU, X PRAT, J YOUNG, RH CAPEN, CC DELELLIS SCULLY, RE AF MATIASGUIU, X PRAT, J YOUNG, RH CAPEN, CC DELELLIS SCULLY, RE TI HUMAN PARATHYROID-HORMONE RELATED PROTEIN (PTHRP) IN OVARIAN SMALL-CELL CARCINOMAS - AN IMMUNOHISTOCHEMICAL STUDY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HOSP SANTA CRUZ & SAN PABLO,BARCELONA,SPAIN. OHIO STATE UNIV,COLUMBUS,OH 43210. TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RI Prat, Jaime/G-4679-2011 NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A76 EP A76 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200445 ER PT J AU MATSUBARA, O TAMURA, A DOI, N KASUGA, T MARK, EJ AF MATSUBARA, O TAMURA, A DOI, N KASUGA, T MARK, EJ TI SIGNIFICANCE OF PALISADING GRANULOMA AND LEUKOCYTOCLASTIC VASCULITIS IN NASAL BIOPSY OF WEGENER (PATHERGIC) GRANULOMATOSIS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 TOKYO MED & DENT UNIV,TOKYO 113,JAPAN. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A82 EP A82 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200482 ER PT J AU OCONNELL, JX RENARD, LG LIEBSCH, NJ EFIRD, JT ROSENBERG, AE AF OCONNELL, JX RENARD, LG LIEBSCH, NJ EFIRD, JT ROSENBERG, AE TI BASE OF SKULL CHORDOMA - A CLINICOPATHOLOGICAL STUDY OF 60 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A9 EP A9 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200048 ER PT J AU OCONNELL, JX MANGHAN, DC MANKIN, HJ ROSENBERG, AE AF OCONNELL, JX MANGHAN, DC MANKIN, HJ ROSENBERG, AE TI SMALL-CELL OSTEOSARCOMA - AN IMMUNOHISTOCHEMICAL AND FLOW CYTOMETRIC STUDY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A9 EP A9 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200047 ER PT J AU QUINTANILLA, L MULLERHERMELINK, HK WILKINS, EW FERRY, JA HUG, E CHOI, N HARRIS, NL AF QUINTANILLA, L MULLERHERMELINK, HK WILKINS, EW FERRY, JA HUG, E CHOI, N HARRIS, NL TI THYMOMA - HISTOGENETIC CLASSIFICATION PREDICTS OUTCOME SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV WURZBURG,W-8700 WURZBURG,GERMANY. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A98 EP A98 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200577 ER PT J AU QUINTANILLAMARTINEZ, L PREFFER, FI RUBIN, D HARRIS, NL AF QUINTANILLAMARTINEZ, L PREFFER, FI RUBIN, D HARRIS, NL TI CD20+ T-CELL LYMPHOMA - EXPANSION OF A NORMAL SUBSET OF CD20+ T-CELLS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A98 EP A98 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200578 ER PT J AU ROSENBERG, AE BROWN, GA BHAN, AK LEE, JM AF ROSENBERG, AE BROWN, GA BHAN, AK LEE, JM TI CHONDROID CHORDOMA - A VARIANT OF CHORDOMA - A MORPHOLOGICAL AND IMMUNOHISTOCHEMICAL STUDY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A10 EP A10 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200053 ER PT J AU RUIZ, P NASSIRI, M TEDDER, TF VICIANA, AL AF RUIZ, P NASSIRI, M TEDDER, TF VICIANA, AL TI ADHESION MOLECULE AND HOMING RECEPTOR EXPRESSION DURING ACUTE HEPATIC ALLOGRAFT-REJECTION SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV MIAMI,SCH MED,MIAMI,FL 33152. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RI Nassiri, Mehdi/G-9707-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A125 EP A125 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200735 ER PT J AU SUSTER, S WONG, TY AF SUSTER, S WONG, TY TI ON THE DISCRIMINATORY VALUE OF ANTI-HPCA-1 (CD-34) IN THE DIFFERENTIAL-DIAGNOSIS OF BENIGN AND MALIGNANT CUTANEOUS VASCULAR PROLIFERATIONS - A COMPARATIVE IMMUNOHISTOCHEMICAL STUDY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MT SINAI MED CTR,DEPT PATHOL,MIAMI BEACH,FL 33140. MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A37 EP A37 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200211 ER PT J AU TAMURA, A MATSUBARA, O KASUGA, T MARK, EJ AF TAMURA, A MATSUBARA, O KASUGA, T MARK, EJ TI LUNG PATHOLOGY IN MARFAN-SYNDROME SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 TOKYO MED & DENT UNIV,TOKYO 113,JAPAN. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A135 EP A135 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200795 ER PT J AU ZERBINI, C GELBER, RD WEINBERG, D SALLAN, SE KUPSKY, W TARBELL, NJ AF ZERBINI, C GELBER, RD WEINBERG, D SALLAN, SE KUPSKY, W TARBELL, NJ TI PROGNOSTIC FACTORS IN MEDULLOBLASTOMA INCLUDING DNA PLOIDY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,DANA FARBER CANC INST,CAMBRIDGE,MA 02138. HARVARD UNIV,DEPT BIOSTAT,CAMBRIDGE,MA 02138. UNIV SAO PAULO,SCH MED,SAO PAULO,BRAZIL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A128 EP A128 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200757 ER PT J AU KOZAKEWICH, H PEREZATAYDE, A JUNG, WH SHAMBERGER, R HOFFER, F DILLER, L AF KOZAKEWICH, H PEREZATAYDE, A JUNG, WH SHAMBERGER, R HOFFER, F DILLER, L TI CYSTIC ADRENAL NEUROBLASTOMA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP P6 EP P6 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200875 ER PT J AU EAVEY, RD AF EAVEY, RD TI ABNORMALITIES OF THE NEONATAL EAR - OTOSCOPIC OBSERVATIONS, HISTOLOGIC OBSERVATIONS, AND A MODEL FOR CONTAMINATION OF THE MIDDLE-EAR BY CELLULAR CONTENTS OF AMNIOTIC-FLUID SO LARYNGOSCOPE LA English DT Review ID ACUTE OTITIS-MEDIA; INTENSIVE-CARE UNIT; CHLAMYDIA-TRACHOMATIS; MECONIUM ASPIRATION; EUSTACHIAN-TUBE; TEMPORAL BONES; INNER-EAR; INFANTS; MESENCHYME; INFLAMMATION AB It is unknown whether childhood ear disease could be present long before symptoms provoke an initial otoscopic examination. A newborn middle ear might or might not start in a pristine, privileged state. The clinician evaluating later infant and childhood ear disease is often unaware of the status of a patient's ear from the neonatal period, the earliest time at which the tympanic membrane can be evaluated. Adding to the physician's handicap, normative otoscopic and histologic data on the neonatal ear are incomplete. In order to test the hypothesis that disease in the neonatal middle ear may be more common than is generally appreciated, the population of critically ill neonates was selected for study since this group can provide both clinical as well as histologic data. This manuscript is divided into three parts. Clinically, otoscopic observations were analyzed on infants in an intensive care unit. Histologically, neonatal temporal bones were studied for normal anatomy and pathology of the middle ear and antrum. Experimentally, an animal study was performed to evaluate the potential effect of amniotic fluid cellular contents aspirated into the middle ear. I. Clinical Otoscopic Observations. Daily otoscopic examination was conducted on 44 neonates in an intensive care unit. Specific parameters of the otoscopic examination were evaluated to compare with the normal, translucent tympanic membrane of the older child. The otoscopic appearance was found to be abnormal in 97.7% of neonatal ears. Of the otoscopic parameters evaluated, right ears averaged 2.6 abnormalities and left ears averaged 2.5 otoscopic abnormalities. The otoscopic appearance of the neonate in the neonatal intensive care unit is nearly universally abnormal. II. Temporal Bone Histologic Observations. One hundred eleven temporal bones from 56 neonates were collected for histologic study by light microscopy. Mesenchyme filling more than 60% of the middle ear space was found in 13 bones. Amniotic fluid cellular content was detected in 90 bones. Purulent otitis media was detected in 24 bones. Varying amounts of blood were found in the middle ear space of 34 bones. Only 7 of the bones had no significant middle ear abnormality. It is concluded that in the critically ill neonate, the middle ear and antrum usually contain cellular or fluid material, often in significant volume, that would not be considered normal in the older patient. III. An Animal Model Simulating Contamination of the Middle Ear by Cellular Contents of Amniotic Fluid. In human neonatal ears the histologic residue of refluxed amniotic fluid, keratinized epithelial cells and lanugo hair, initiates a foreign-body giant-cell reaction with granulation tissue formation. It was hypothesized that this residue might not be evacuated easily and potentially could persist as an inflammatory nidus. An animal model was designed to determine if the human findings could be reproduced and to analyze the host reaction over 2 months. An aliquot of autologous, sterilized hair and keratinized epithelial cells was placed into the left bulla of seven gerbils. The contralateral bulla underwent saline instillation as a control. The animals were killed from time 0 to 63 days. By 1 week, the experimental ear with keratin demonstrated not only hair but angioneogenesis with granulation tissue, blood, and proteinaceous precipitate. This pattern persisted so that at 63 days the keratinized cellular elements were still present. In addition, further pathologic changes including osteoneogenesis and cholesterol granuloma were found. Control ears were unremarkable. It is concluded that the foreign-body reaction provoked by autologous keratin in this model provided histologic findings similar to that seen in the human neonatal temporal bones and that, by 2 months, this material had not been eliminated but was still producing a foreign-body reaction. These studies demonstrate that the otoscopic appearance of the critically ill neonate is distinct from the typical tympanic membrane appearance of the older child, that the ear is subject to several significant pathologic conditions, and that such pathology might not spontaneously and quickly improve. Therefore, vigilant otologic attention is warranted even for the youngest patients. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. RP EAVEY, RD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 112 TC 28 Z9 32 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD JAN PY 1993 VL 103 IS 1 BP 1 EP 31 PN 2 PG 31 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA KG365 UT WOS:A1993KG36500001 PM 8419727 ER PT J AU KUNG, RTV STEWART, RB ZELT, DT LITALIEN, GJ LAMURAGLIA, GM AF KUNG, RTV STEWART, RB ZELT, DT LITALIEN, GJ LAMURAGLIA, GM TI ABSORPTION CHARACTERISTICS AT 1.9 MU-M - EFFECT ON VASCULAR WELDING SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE BURST STRENGTH; OPTICAL PENETRATION DEPTH; VESSEL WALL THICKNESS ID LASER AB A 1.9 mum laser was used to investigate the acute weld strengths for anastomoses of rat and rabbit aortas and femoral arteries. The wall thicknesses for these vessels approximately matched the optical absorption depth of 125 mum for 1.9 mum radiation in vascular tissues. A low power (150 mW) 1.9 mum laser was used. Laser power was delivered through silica fiber optics for manual control. The fiber tip was held approximately 1 mm from the, target resulting in a laser spot size of 0.7 mm at the tissue. The linear delivery rate was approximately 0.3 mm/sec. Acute burst pressures of the welds showed a linear correlation with the reciprocal of the vessel radius. These results suggest that the product of the weld strength times the optical absorption depth is constant over the range of vessel sizes studied. A weld strength for a weld thickness equal to the optical absorption depth was determined to be 4 x 10(6) dynes/cm2, which is comparable to the strength of sutured anastomoses. These acute studies suggest that a laser wavelength with absorption depth in tissue matched to the vessel wall thickness should yield optimum welds. Therefore, a laser operating near 1.9 mum is suitable for small vessel welding. C1 MASSACHUSETTS GEN HOSP,DIV VASC SURG,BOSTON,MA 02114. RP KUNG, RTV (reprint author), ABIOMED INC,33 CHERRY HILL DR,DANVERS,MA 01923, USA. FU NHLBI NIH HHS [K-08HL02583-01, R43-HL45390] NR 11 TC 27 Z9 27 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 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1993 VL 13 IS 1 BP 12 EP 17 DI 10.1002/lsm.1900130105 PG 6 WC Dermatology; Surgery SC Dermatology; Surgery GA KJ791 UT WOS:A1993KJ79100002 PM 8426519 ER PT J AU MITCHELL, DC PRINCE, MR FRISOLI, JK SMITH, RE WOOD, RFM AF MITCHELL, DC PRINCE, MR FRISOLI, JK SMITH, RE WOOD, RFM TI BETA CAROTENE UPTAKE INTO ATHEROSCLEROTIC PLAQUE - ENHANCED STAINING AND PREFERENTIAL ABLATION WITH THE PULSED DYE-LASER SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE ATHEROSCLEROSIS; CAROTENOIDS; LASER-ANGIOPLASTY ID CANTHAXANTHIN RETINOPATHY; MACULOPATHY AB The yellow color of atherosclerotic plaque is due to the presence of carotenoids, which absorb light between 430-530 nm and account for the preferential ablation of plaque by the pulsed dye laser operating at 480 nm. This study was designed to examine tissue uptake of beta-carotene and the effect of uptake on arterial plaque ablation. Forty-two atherosclerotic NZW rabbits were given intravenous beta-carotene at a dose of 40 mg/kg, twice weekly and killed between 1 hour and 28 days after the initial injection. beta-carotene was not detected in control specimens but was significantly greater in plaque than in normal wall at all time points following beta-carotene injection (P < 0.04 Mann Whitney U test). The ablation threshold was significantly lower in beta-carotene treated plaque than in untreated plaque or normal arterial wall (P < 0.01, Fisher's exact test). In this model beta-carotene is preferentially taken up into arterial plaque, resulting in increased absorption of laser radiation at 480 nm and enhanced tissue ablation. C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RP MITCHELL, DC (reprint author), ST BARTHOLOMEWS HOSP,PROFESSORIAL SURG UNIT,LONDON EC1A 7BE,ENGLAND. FU NHLBI NIH HHS [HL46384] NR 18 TC 7 Z9 8 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 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1993 VL 13 IS 2 BP 149 EP 157 DI 10.1002/lsm.1900130202 PG 9 WC Dermatology; Surgery SC Dermatology; Surgery GA KU389 UT WOS:A1993KU38900001 PM 7681923 ER PT J AU SCHWENGEL, RH GREGORY, KW HEARNE, SE SCOTT, HJ BEAUMAN, GJ MERGNER, WJ CAPLIN, JL ZISKIND, AA AF SCHWENGEL, RH GREGORY, KW HEARNE, SE SCOTT, HJ BEAUMAN, GJ MERGNER, WJ CAPLIN, JL ZISKIND, AA TI CHARACTERIZATION OF PULSED-DYE LASER-MEDIATED VASODILATATION IN A RABBIT FEMORAL-ARTERY MODEL OF VASOCONSTRICTION SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE VASCULAR REACTIVITY; SUBARACHNOID HEMORRHAGE; ANESTHETIZED RABBIT ID ENDOTHELIUM-INDEPENDENT RELAXATION; ULTRAVIOLET-RADIATION; SMOOTH-MUSCLE; ANGIOPLASTY; IRRADIATION; VASOSPASM; TENSION; AORTA AB Vasoconstriction is a clinical problem associated with invasive vascular procedures, microvascular reconstruction and subarachnoid hemorrhage. We sought to characterize the ability of pulsed-dye laser irradiation to reverse and prevent vasoconstriction in an anesthetized rabbit model of surgically and pharmacologically induced vasoconstriction. Five groups of experiments were performed to study the effect of pulsed-dye laser irradiation delivered through a 320 mum core ball-tip fiber into the femoral artery. The studies demonstrated that pulsed-dye irradiation can reproducibly cause vascular dilatation. The zone of vasodilatation propagated equally proximal and distal to the site of irradiation within the vessel. When saline was infused into the vessel to replace flowing blood during delivery of laser irradiation, no significant vasodilatation occurred. After laser irradiation reversed surgical and pharmacologic vasoconstriction, the vessel was resistant to further pharmacologic vasoconstriction. This resistance to pharmacologic vasoconstriction did not occur if the vessel was pharmacologically predilated before delivery of laser irradiation. Pathologic analysis of the vessels revealed endothelial damage and mild to moderate medial necrosis, most significant at the site of energy delivery. These studies provide characterization of pulsed-dye laser-mediated vasodilatation in an in vivo model. Delivery of pulsed- dye laser energy has potential clinical application and warrants further investigation. C1 UNIV MARYLAND,SCH MED,DIV CARDIOL,22 S GREENE ST,RM N3W77,BALTIMORE,MD 21201. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. NR 25 TC 11 Z9 11 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 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1993 VL 13 IS 3 BP 284 EP 295 DI 10.1002/lsm.1900130305 PG 12 WC Dermatology; Surgery SC Dermatology; Surgery GA LE065 UT WOS:A1993LE06500004 PM 8515668 ER PT J AU BHATTA, N ISAACSON, K FLOTTE, T SCHIFF, I ANDERSON, RR AF BHATTA, N ISAACSON, K FLOTTE, T SCHIFF, I ANDERSON, RR TI INJURY AND ADHESION FORMATION FOLLOWING OVARIAN WEDGE RESECTION WITH DIFFERENT THERMAL SURGICAL MODALITIES SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE ADHESIONS; ACUTE THERMAL DAMAGE; BLEEDING; CHARRING; ELECTROCAUTERY; LASERS ID CARBON-DIOXIDE LASER; TISSUE; CO2-LASER AB The purpose of this study is to determine the role of bleeding, acute thermal damage, and charring in adhesion formation. Postoperative adhesions were compared following ovarian wedge resection in 48 rabbits using different lasers, electrosurgery, and scalpel. Twelve ovaries were sectioned per modality, in randomized pairs. Acute thermal injury as assessed by histology, bleeding, and charring differed amonge the modalities used. Adhesions were assessed 4 weeks later, by an investigator completely blinded of the treatment protocol. The adhesion scores were 11.6 +/- 8.0 with pulsed Er:YAG laser; 11.9 +/- 7.5 with scalpel; 8.3 +/- 9.3 with electrocautery; 6.7 +/- 8.8 with a continuous (c.w.) Nd:YAG laser; 5.3 +/- 4.8 with c.w. CO2 laser; 3.1 +/- 2.7 with pulsed CO2 laser; 1.7 +/- 1.8 with pulsed Ho:YAG laser; and 0.8 +/- 1.5 in the control (no resection) group. Ho:YAG, Nd:YAG, and electrocautery were completely hemostatic. Bleeding was minimal with the CO2 lasers. Er:YAG and scalpel caused maximum bleeding, requiring hemostatic measures to prevent exanguination. Charring occurred with electrocautery, CO2 laser, and Nd:YAG laser. Bleeding and charring correlated with adhesion formation, but the histological depth of thermal damage did not. The Ho:YAG laser is a hemostatic, fiber-optic compatible laser causing significantly fewer adhesions (P<0.04) than scalpel, electrocautery, Nd: YAG, Er:YAG, and c.w. CO2 lasers. Clinical use of the Ho:YAG laser, and the role of carbonization in promoting adhesions, deserve further study. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT GYNECOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. RP BHATTA, N (reprint author), MASSACHUSETTS GEN HOSP,CTR LASER,WELLMAN 2,BOSTON,MA 02114, USA. NR 16 TC 12 Z9 13 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 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1993 VL 13 IS 3 BP 344 EP 352 DI 10.1002/lsm.1900130311 PG 9 WC Dermatology; Surgery SC Dermatology; Surgery GA LE065 UT WOS:A1993LE06500010 PM 8515673 ER PT B AU LI, FP GARBER, JE FRIEND, SH STRONG, LC PATENAUDE, AF JUENGST, ET REILLY, PR CORREA, P FRAUMENI, JF AF LI, FP GARBER, JE FRIEND, SH STRONG, LC PATENAUDE, AF JUENGST, ET REILLY, PR CORREA, P FRAUMENI, JF GP SUFFOLK UNIVERSITY LAW SCHOOL TI RECOMMENDATIONS ON PREDICTIVE TESTING FOR GERM-LINE P53 MUTATIONS AMONG CANCER-PRONE INDIVIDUALS SO LAW AND SCIENCE AT THE CROSSROADS: BIOMEDICAL TECHNOLOGY, ETHICS, PUBLIC POLICY AND THE LAW LA English DT Proceedings Paper CT Conference on Law and Science at the Crossroads: Biomedical Technology, Ethics, Public Policy and the Law CY OCT 21-22, 1993 CL BOSTON, MA SP SUFFOLK UNIV LAW SCH, UNIV MASSACHUSETTS MED CTR, OFF CONTINUING EDUC C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SUFFOLK UNIV LAW SCHOOL PI BOSTON PA ADVANCED LEGAL STUDIES, 41 TEMPLE STREET, BOSTON, MA 02114 PY 1993 BP 127 EP 131 PG 5 WC Law; Social Sciences, Biomedical SC Government & Law; Biomedical Social Sciences GA BZ93T UT WOS:A1993BZ93T00019 ER PT J AU GRIBBEN, JG NADLER, LM AF GRIBBEN, JG NADLER, LM TI BONE-MARROW PURGING FOR AUTOLOGOUS BONE-MARROW TRANSPLANTATION SO LEUKEMIA & LYMPHOMA LA English DT Article; Proceedings Paper CT Meeting on Leukemia...The Next Question CY MAR 24-27, 1993 CL HOUSTON, TX DE PURGING; MONOCLONAL ANTIBODIES; LEUKEMIA; LYMPHOMA AB High dose therapy with the resulting myeloablation rescued by infusion of autologous bone marrow (ABMT) has become a major treatment option for an increasing number of patients with hematologic and solid tumors. ABMT has several potential advantages over allogeneic transplantation. However, the major obstacle to the use of ABMT is that the infusion of occult tumor cells harbored within the harvested marrow would result in more rapid relapse of disease. To minimize the effects of the infusion of significant numbers of malignant cells, marrow for ABMT is obtained when the patient is either in complete remission or when there is no histologic evidence of bone marrow infiltration of disease. There is increasing evidence that minimal numbers of malignant cells can be detected within the remission marrow of these patients, particularly when assessed by sensitive clonogenic assays or polymerase chain reaction amplification. A variety of methods, pharmacologic and immunologic have been developed to ''purge'' malignant cells from the marrow. The aim of purging is to eliminate any contaminating malignant cells and leave intact the hematopoietic stem cells that are necessary for engraftment. Although the rationale for removing any contaminating cells from the autologous marrow appears compelling, the issue of purging remains highly controversial. Intense argument persists as to whether attempts to remove residual tumor cells from the harvested bone marrow have contributed to improving disease-free survival in these patients. To date there have been no clinical trials testing the efficacy of purging by comparison of infusion of purged versus unpurged autologous bone marrow. This is due primarily to the large number of patients that would be required for such studies. In addition, the finding that the majority of patients who relapse after autologous BMT do so at sites of prior disease has led to the widespread view that purging of autologous marrow could contribute little to subsequent outcome after autologous BMT. The pre-clinical and clinical experience of in vitro marrow purging will be reviewed. RP GRIBBEN, JG (reprint author), HARVARD UNIV,SCH MED,DEPT MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 16 Z9 16 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-8194 J9 LEUKEMIA LYMPHOMA JI Leuk. Lymphoma PY 1993 VL 11 SU 2 BP 141 EP 148 DI 10.3109/10428199309064274 PG 8 WC Oncology; Hematology SC Oncology; Hematology GA MQ775 UT WOS:A1993MQ77500022 PM 8124225 ER PT J AU VANETTEN, RA AF VANETTEN, RA TI DISEASE PROGRESSION IN A MURINE MODEL OF BCR/ABL LEUKEMOGENESIS SO LEUKEMIA & LYMPHOMA LA English DT Article; Proceedings Paper CT 2ND INTERNATIONAL CONF ON CHRONIC MYELOID LEUKEMIA CY OCT 04-07, 1992 CL BOLOGNA, ITALY DE MURINE MODEL; BCR-ABL; LEUKEMIA; DISEASE PROGRESSION AB We have developed a system for expressing bcr/abl genes in the mouse hematopoietic system utilizing retroviral gene transfer and bone marrow transplantation. Expression of the P210bcr/abl gene in mice gives rise to a spectrum of hematological malignancies, most prominently a myeloproliferative syndrome which closely resembles human chronic myelogenous leukemia (CML). Studies of this system and related systems in other laboratories have begun to yield insights into the pathophysiology of the human bcr/abl leukemias. The CML-like syndrome appears to be a consequence of infection of a multipotential hematopoietic progenitor target cell. The leukemic clone is difficult to transplant to secondary recipients, but undergoes evolution to acute leukemia. The P190 form of bcr/abl appears to be more potent in leukemogenesis than P210, but may also be associated with a CML-like picture upon infection of a multipotential target cell. There may be a spectrum of different chronic phase duration associated with different Bcr/Abl proteins, with bcr sequences influencing the rate of disease progression. In mice, duplication or alterations of the bcr/abl gene itself may constitute a major mechanism of disease progression. RP VANETTEN, RA (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,CTR BLOOD RES,BOSTON,MA 02115, USA. NR 0 TC 5 Z9 5 U1 1 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-8194 J9 LEUKEMIA LYMPHOMA JI Leuk. Lymphoma PY 1993 VL 11 SU 1 BP 239 EP 242 DI 10.3109/10428199309047893 PG 4 WC Oncology; Hematology SC Oncology; Hematology GA MA145 UT WOS:A1993MA14500041 PM 8251903 ER PT J AU TOJO, K ABOUSAMRA, AB AF TOJO, K ABOUSAMRA, AB TI CORTICOTROPIN-RELEASING FACTOR (CRF) STIMULATES CA-45(2+) UPTAKE IN THE MOUSE CORTICOTROPH CELL-LINE ATT-20 SO LIFE SCIENCES LA English DT Article ID DEPENDENT PROTEIN-KINASE; ANTERIOR-PITUITARY CELLS; CALCIUM CHANNELS; ADRENOCORTICOTROPIN RELEASE; RAT PITUITARY; TUMOR-CELLS; ADENYLYL CYCLASE; HORMONE-RELEASE; BETA-ENDORPHIN; ACTH RELEASE AB Corticotropin-releasing factor (CRF) stimulates adrenocorticotropin (ACTH) release via the adenylate cyclase/cAMP-dependent protein kinase system. Because calcium is necessary for receptor-mediated release of ACTH, we have examined the effect of CRF on Ca-45(2+) uptake in a corticotroph cell line model, AtT-20. Treatment of AtT-20 cells with CRF (10(-9) - 10(-6) M) resulted in dose- and time-dependent increases in Ca-45(2+) uptake, up to 2.2-fold above control values. The effect was statistically significant at 1 min and persisted for at least 10 min. Treatment with forskolin (1-30 muM), 8-Br-cAMP (0.5 mM), cholera toxin (CT, 100 ng/ml) and K+ (20 mM) also increased cell-associated Ca-45(2+). The effect of K+ was completely blocked by nifedipine (100 muM), whereas the effects of CRF (10(-8) M) were only partially inhibited by this calcium channel antagonist. These data suggested a role of voltage-dependent calcium channels in Ca-45(2+) uptake. Short term pretreatment (1-2 h) of AtT-20 cells with CRF (10(-8) M) significantly desensitized both CRF-stimulated cAMP accumulation and ACTH release, but did not attenuate CRF-stimulated Ca-45(2+) uptake. Pretreatment with CRF (10(-8) M) for 4 h did not alter CT- or forskolin-stimulated cAMP accumulation and ACTH release. This suggests that the molecular mechanisms of desensitization are proximal to adenylate cyclase. Conversely, long term pretreatment (24 h) of AtT-20 cells with CRF (10(-8) M) induced significant desensitization of CRF-stimulated Ca-45(2+) uptake. These results indicate that CRF stimulates calcium uptake in AtT-20 cells via cAMP-dependent and cAMP-independent mechanisms, and that the cellular mechanisms involved in desensitization of cAMP accumulation and ACTH release and those involved in desensitization of calcium uptake are qualitatively different. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BULFINCH 3,FRUIT ST,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON UNIT,BOSTON,MA 02114. NR 37 TC 5 Z9 5 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 52 IS 7 BP 621 EP 630 DI 10.1016/0024-3205(93)90453-A PG 10 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KK518 UT WOS:A1993KK51800003 PM 8381502 ER PT J AU LIVINGSTON, EH GUTH, PH AF LIVINGSTON, EH GUTH, PH TI ANTISECRETORY AND CYTOPROTECTIVE DOSES OF ENPROSTIL DO NOT ALTER GASTRIC-MUCOSAL BLOOD-FLOW SO LIFE SCIENCES LA English DT Article ID HYDROGEN GAS CLEARANCE; 16,16-DIMETHYL PROSTAGLANDIN-E2; ACID SECRETION; RAT DUODENUM; PROSTACYCLIN; PGE2; CIMETIDINE; ULCERATION; DAMAGE; INDOMETHACIN AB Prostaglandins of the E series are antisecretory and cytoprotective. Cytoprotection occurs in the deep but not superficial gastric mucosa. It has been hypothesized that the mechanism of cytoprotection involves increased gastric mucosal blood flow (GMBF). However, basal and stimulated gastric mucosal blood flow is greater in the deep than superficial corpus mucosa. The purpose of this study was to investigate the effect of a prostaglandin E2 analog, enprostil, on GMBF in the deep mucosa, where cytoprotection is observed, in both antisecretory and cytoprotective doses. Gastric mucosal blood flow in the deep half of the mucosa was measured by the hydrogen gas clearance method before, during and after intragastric perfusion of enprostil, 0.1-100 mug/kg, in urethane anesthetized rats. Enprostil did not alter GMBF in any of the doses tested. Therefore, the cytoprotective action of enprostil is mediated by factors other than a primary increase in GMBF. C1 W LOS ANGELES VET AFFAIRS MED CTR, SURG SERV, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, MED SERV, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, RES SERV, LOS ANGELES, CA 90073 USA. CTR ULCER RES & EDUC, LOS ANGELES, CA 90073 USA. RP LIVINGSTON, EH (reprint author), UNIV CALIF LOS ANGELES, SCH MED, DEPT SURG, 10833 LE CONTE AVE, 72-215 CHS, LOS ANGELES, CA 90024 USA. NR 47 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 52 IS 20 BP 1621 EP 1628 DI 10.1016/0024-3205(93)90043-3 PG 8 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KX649 UT WOS:A1993KX64900004 PM 8483391 ER PT J AU SCHAFFER, BK LINKER, C PAPISOV, M TSAI, E NOSSIFF, N SHIBATA, T BOGDANOV, A BRADY, TJ WEISSLEDER, R AF SCHAFFER, BK LINKER, C PAPISOV, M TSAI, E NOSSIFF, N SHIBATA, T BOGDANOV, A BRADY, TJ WEISSLEDER, R TI MION-ASF - BIOKINETICS OF AN MR RECEPTOR AGENT SO MAGNETIC RESONANCE IMAGING LA English DT Article DE MAGNETICS; MAGNETISM; MRI; CONTRAST AGENT; IRON OXIDE; ASIALOFETUIN; ASIALOGLYCOPROTEIN; RECEPTOR AB Receptor-directed MR contrast agents are currently being designed to improve sensitivity and specificity of MR imaging and to provide for functional MR imaging. In the current study we have synthesized a conjugate of asialofetuin (ASF), a bovine plasma protein with a known, high affinity f or the hepatic asialoglycoprotein receptor, and a well defined, single crystal superparamagnetic label (monocrystalline iron oxide nanoparticle, MION). MION-ASF is cleared f rom the circulation more than 300 times faster than MION, has a 3.7 times higher hepatic accumulation, increases liver R2 relaxivity 2.8-fold compared to MION, and accumulates in hepatocytes unlike MION, which accumulates only in macrophages. Competition assays indicate that receptor-mediated hepatocyte uptake can be competitively blocked and that this effect can be demonstrated by imaging. These studies indicate that sensitive iron oxide based probes can be developed for functional MR imaging. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. FU NCI NIH HHS [1ROI CA54886-01] NR 0 TC 48 Z9 48 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0730-725X J9 MAGN RESON IMAGING JI Magn. Reson. Imaging PY 1993 VL 11 IS 3 BP 411 EP 417 DI 10.1016/0730-725X(93)90074-N PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LA779 UT WOS:A1993LA77900013 PM 7685055 ER PT J AU GARRIDO, L KWONG, KK PFLEIDERER, B CRAWLEY, AP HULKA, CA WHITMAN, GL KOPANS, DB AF GARRIDO, L KWONG, KK PFLEIDERER, B CRAWLEY, AP HULKA, CA WHITMAN, GL KOPANS, DB TI ECHO-PLANAR CHEMICAL-SHIFT IMAGING OF SILICONE GEL PROSTHESES SO MAGNETIC RESONANCE IMAGING LA English DT Article DE ECHO-PLANAR IMAGING; CHEMICAL SHIFT IMAGING; SILICONE; BREAST PROSTHESES; MIGRATION AB We have developed an echo-planar (EP) proton chemical shift imaging (CSI) MR technique that allow us to discriminate the polydimethylsiloxane (PDMS, silicone) proton MR signal from that of the fat and water protons found in tissues, in order to map the distribution of PDMS in humans who have silicone gel prostheses. Silicone gel-filled prosthetic implants induce histologic changes in the surrounding tissue which are attributed to the leakage of free PDMS from the prosthesis. The T2 relaxation measurements of three silicone gels show that there are two components in them, each with a different degree of molecular mobility. The presence of free silicone is confirmed by chloroform extraction, which removed 14-28% of the material. This free polymer present in the gel can pass through the intact or ruptured membrane of the implant into the surrounding tissue. Our preliminary imaging results indicate that EP-CSI MR might be useful as a diagnostic technique for implant malfunction. RP GARRIDO, L (reprint author), MASSACHUSETTS GEN HOSP,CTR NMR,149 13TH ST,BOSTON,MA 02129, USA. RI Garrido, Leoncio/K-3092-2014 OI Garrido, Leoncio/0000-0002-7587-1260 NR 0 TC 9 Z9 9 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0730-725X J9 MAGN RESON IMAGING JI Magn. Reson. Imaging PY 1993 VL 11 IS 5 BP 625 EP 634 DI 10.1016/0730-725X(93)90004-W PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA LK597 UT WOS:A1993LK59700004 PM 8345777 ER PT J AU ZIMMER, W YUCEL, EK AF ZIMMER, W YUCEL, EK TI MESENTERIC VARICES - EVALUATION WITH COLOR-FLOW DOPPLER AND MAGNETIC-RESONANCE ANGIOGRAPHY SO MAGNETIC RESONANCE IMAGING LA English DT Note DE PORTAL HYPERTENSION; VENOGRAPHY; VARICES AB Varix formation is a well recognized complication of portal hypertension. Rarely, varices may form in the distribution of the mesenteric veins. We present a case of mesenteric varices evaluated by color flow Doppler ultrasound and magnetic resonance angiography. RP ZIMMER, W (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0730-725X J9 MAGN RESON IMAGING JI Magn. Reson. Imaging PY 1993 VL 11 IS 7 BP 1063 EP 1066 DI 10.1016/0730-725X(93)90227-5 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MB034 UT WOS:A1993MB03400019 PM 8231672 ER PT S AU CADAY, CG SKLAR, RM BERLOVE, DJ KEMMOU, A BROWN, RH FINKLESTEIN, SP AF CADAY, CG SKLAR, RM BERLOVE, DJ KEMMOU, A BROWN, RH FINKLESTEIN, SP BE Johnnessen, JN TI POLYUBIQUITIN GENE-EXPRESSION FOLLOWING CEREBRAL-ISCHEMIA SO MARKERS OF NEURONAL INJURY AND DEGENERATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON MARKERS OF NEURONAL INJURY AND DEGENERATION CY APR 22-24, 1992 CL BETHESDA, MD SP SIGMA XI, ALCOHOL DRUG ABUSE & MENTAL HLTH ADM, FDA, NIOSH, NIH, US EPA RP CADAY, CG (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,CNS GROWTH FACTOR RES LAB,BOSTON,MA 02114, USA. FU NIA NIH HHS [NIA AG-08207]; NINDS NIH HHS [NINDS NS-10828] NR 0 TC 6 Z9 6 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-795-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 679 BP 188 EP 194 DI 10.1111/j.1749-6632.1993.tb18298.x PG 7 WC Neurosciences SC Neurosciences & Neurology GA BY50G UT WOS:A1993BY50G00015 PM 8390143 ER PT J AU COULL, BM CLARK, WM AF COULL, BM CLARK, WM TI ABNORMALITIES OF HEMOSTASIS IN ISCHEMIC STROKE SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID PROTEIN-S DEFICIENCY; THROMBOTIC THROMBOCYTOPENIC PURPURA; SICKLE-CELL DISEASE; PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA; SYSTEMIC LUPUS-ERYTHEMATOSUS; OCCLUSIVE CEREBROVASCULAR-DISEASE; CEREBRAL VENOUS THROMBOSIS; INDEPENDENT RISK FACTOR; PATENT FORAMEN OVALE; ANTICARDIOLIPIN ANTIBODIES C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP COULL, BM (reprint author), OREGON HLTH SCI UNIV,DEPT NEUROL,L-226,3181 SW SAM JACKSON PK DR,PORTLAND,OR 97201, USA. FU NINDS NIH HHS [2PO1 NS17493-09] NR 122 TC 25 Z9 26 U1 0 U2 0 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 JAN PY 1993 VL 77 IS 1 BP 77 EP 94 PG 18 WC Medicine, General & Internal SC General & Internal Medicine GA KG314 UT WOS:A1993KG31400006 PM 8419725 ER PT J AU CAROFF, SN MANN, SC AF CAROFF, SN MANN, SC TI NEUROLEPTIC MALIGNANT SYNDROME SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID ELECTROCONVULSIVE-THERAPY; LETHAL CATATONIA; HYPERTHERMIA; METABOLISM; PATHOLOGY; FREQUENCY; BRAIN; RISK C1 DEPT VET AFFAIRS MED CTR,INPATIENT PSYCHIAT UNIT,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. RP CAROFF, SN (reprint author), DEPT VET AFFAIRS MED CTR 116A,GEN PSYCHIAT SECT,UNIV AVE,PHILADELPHIA,PA 19104, USA. NR 48 TC 266 Z9 272 U1 1 U2 4 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 JAN PY 1993 VL 77 IS 1 BP 185 EP 202 PG 18 WC Medicine, General & Internal SC General & Internal Medicine GA KG314 UT WOS:A1993KG31400012 PM 8093494 ER PT J AU HENDRICK, GK GJINOVCI, A BAXTER, LA MOJSOV, S WOLLHEIM, CB HABENER, JF WEIR, GC AF HENDRICK, GK GJINOVCI, A BAXTER, LA MOJSOV, S WOLLHEIM, CB HABENER, JF WEIR, GC TI GLUCAGON-LIKE PEPTIDE-I-(7-37) SUPPRESSES HYPERGLYCEMIA IN RATS SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID PEPTIDE-I; PREPROGLUCAGON GENE; INSULIN-SECRETION; CHINOOK SALMON; PANCREAS; INCRETIN; RELEASE; GLUCOSE; HUMANS; INTESTINE C1 HARVARD UNIV,JOSLIN DIABET CTR,SCH MED,1 JOSLIN PL,BOSTON,MA 02215. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,BOSTON,MA 02215. UNIV GENEVA,DEPT MED,DIV CLIN BIOCHEM,CH-1211 GENEVA 4,SWITZERLAND. MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. FU NIADDK NIH HHS [AM-30834]; NIDDK NIH HHS [DK-P30-36836, DK-35449] NR 27 TC 28 Z9 28 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD JAN PY 1993 VL 42 IS 1 BP 1 EP 6 DI 10.1016/0026-0495(93)90163-I PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KF999 UT WOS:A1993KF99900001 PM 8446036 ER PT J AU PARK, E SHINOHARA, N ARN, JS SHARROW, SO WANECK, GL SACKS, DH AF PARK, E SHINOHARA, N ARN, JS SHARROW, SO WANECK, GL SACKS, DH TI ANTIGENIC HETEROGENEITY OF QA-2 ANTIGENS IN C57BL/6 SO MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE QA-2; MHC CLASS-I ANTIGEN; PI LINKAGE; HETEROGENEITY; MULTIGENE ID MAJOR HISTOCOMPATIBILITY COMPLEX; N-ACETYLGLUCOSAMINIDASE-F; FUNCTIONAL LYMPHOCYTES-T; CLASS-I GENES; MONOCLONAL-ANTIBODIES; TRANSPLANTATION ANTIGENS; EXPRESSION; MOUSE; REGION; IDENTIFICATION AB The Qa-2 antigens are class I-like molecules encoded by genes mapped telomeric to the H-2D region on chromosome 17 in the mouse. A panel of 8 new monoclonal anti-Qa-2 antibodies derived from a C3H.KBR anti-C3H. SW immunization was studied. Immunoprecipitation of I-125-labeled C57BL/6 splenocyte antigens showed that all of these antibodies precipitated 40 kDa molecules which could be completely precleared by the monoclonal antibody 20-8-4, which had previously been shown to crossreact with Qa-2. One of the monoclonal antibodies (1-12-1), however, was found not to completely preclear Qa-2 antigens precipitable by the other 7 antibodies or by 20-8-4, suggesting the existence of at least two different species of Qa-2 molecules. Cell lines transfected with Q7 or Q9 genes were reactive with all 9 antibodies and the Qa-2 antigens expressed on surface membranes of these cells were completely precleared by both 20-8-4 and 1-12-1. Therefore, the observed heterogeneity of these molecules cannot be explained by an antigenic difference between the Q7 and Q9 gene products. 2D gel analyses showed identical pI spectra between Qa-2 molecules precipitated with 20-8-4 and 1-12-1. In addition, all of the monoclonal antibodies reacted with labeled antigen preparations following treatment with Endo F or neuraminidase, indicating that carbohydrate moieties are probably not responsible for the antigenic difference between the two species of Qa-2 antigen. C1 NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 43 TC 1 Z9 1 U1 0 U2 0 PU CENTER ACADEMIC PUBL JAPAN PI TOKYO PA 4-16 YAYOI 2-CHOME, BUNKYO-KU, TOKYO 113, JAPAN SN 0385-5600 J9 MICROBIOL IMMUNOL JI Microbiol. Immunol. PY 1993 VL 37 IS 9 BP 743 EP 752 PG 10 WC Immunology; Microbiology SC Immunology; Microbiology GA LX329 UT WOS:A1993LX32900010 PM 8271976 ER PT S AU MOSKOWITZ, MA MORIKAWA, E HUANG, ZH ROSENBLATT, S YOSHIDA, T IRIKURA, K DALKARA, T MAIESE, K KOZNIEWSKA, E AF MOSKOWITZ, MA MORIKAWA, E HUANG, ZH ROSENBLATT, S YOSHIDA, T IRIKURA, K DALKARA, T MAIESE, K KOZNIEWSKA, E BE Tomita, M Mchedlishvili, F Rosenblum, W Heiss, WD Fukuuchi, Y TI L-ARGININE INFUSION PROMOTES NITRIC OXIDE-DEPENDENT VASODILATION IN THE RAT CEREBROVASCULATURE SO MICROCIRCULATORY STASIS IN THE BRAIN SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT Symposium on Microcirculatory Stasis in the Brain CY MAY 20-21, 1993 CL TOKYO, JAPAN SP JAPAN HEART FDN ID FOCAL CEREBRAL-ISCHEMIA; ENDOTHELIAL-CELLS; ARTERY OCCLUSION; BLOOD-FLOW C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CORNELL UNIV,COLL MED,DEPT NEUROL & NEUROSCI,NEW YORK,NY 10021. UNIV CALIF SAN FRANCISCO,DEPT NEURORADIOL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. RP MOSKOWITZ, MA (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114, USA. NR 15 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-89669-4 J9 INT CONGR SER PY 1993 VL 1031 BP 287 EP 295 PG 9 WC Neurosciences; Pathology; Physiology SC Neurosciences & Neurology; Pathology; Physiology GA BZ68Q UT WOS:A1993BZ68Q00033 ER PT S AU STAUB, F WINKLER, A PETERS, J KEMPSKI, O BAETHMANN, A CHOI, DW POVLISHOCK, JT MOSKOWITZ, MA BUSIJA, DW SCHMIDSCHONBEIN, GW AF STAUB, F WINKLER, A PETERS, J KEMPSKI, O BAETHMANN, A CHOI, DW POVLISHOCK, JT MOSKOWITZ, MA BUSIJA, DW SCHMIDSCHONBEIN, GW BE Tomita, M Mchedlishvili, F Rosenblum, W Heiss, WD Fukuuchi, Y TI SWELLING AND DAMAGE OF GLIAL-CELLS BY ARACHIDONIC-ACID SO MICROCIRCULATORY STASIS IN THE BRAIN SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT Symposium on Microcirculatory Stasis in the Brain CY MAY 20-21, 1993 CL TOKYO, JAPAN SP JAPAN HEART FDN ID UNSATURATED FATTY-ACIDS; ASCITES TUMOR-CELLS; BRAIN EDEMA; LIPID-PEROXIDATION; RADICAL FORMATION; VOLUME REGULATION; RAT-BRAIN; INVITRO; PROSTAGLANDINS; LEUKOTRIENES C1 UNIV MAINZ,INST NEUROSURG PATHOPHYSIOL,W-6500 MAINZ,GERMANY. WASHINGTON UNIV,SCH MED,DEPT NEUROL,ST LOUIS,MO 63110. VIRGINIA COMMONWEALTH UNIV,SCH BASIC HLTH SCI,DEPT ANAT,RICHMOND,VA 23298. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MGH,BOSTON,MA 02114. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PHYSIOL,WINSTON SALEM,NC 27157. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PHARMACOL,WINSTON SALEM,NC 27157. INST BIOMED ENGN,LA JOLLA,CA 92093. RP STAUB, F (reprint author), UNIV MUNICH,KLINIKUM GROSSHADERN,INST SURG RES,MARCHIONINISTR 15,W-8000 MUNICH 70,GERMANY. NR 26 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-89669-4 J9 INT CONGR SER PY 1993 VL 1031 BP 311 EP 318 PG 8 WC Neurosciences; Pathology; Physiology SC Neurosciences & Neurology; Pathology; Physiology GA BZ68Q UT WOS:A1993BZ68Q00036 ER PT J AU EPSTEIN, AM BLUMENTHAL, D AF EPSTEIN, AM BLUMENTHAL, D TI PHYSICIAN-PAYMENT REFORM - PAST AND FUTURE SO MILBANK QUARTERLY LA English DT Article ID MEDICARE; OUTCOMES AB Medicare's decision to compensate physicians using a fee schedule based on the relative value of their services was an attempt to rationalize fee-for-service payment of physicians. Reformers hoped also to control the costs of care, improve its quality, and protect access to health services among Medicare beneficiaries. A close examination of the system's provisions indicates, however, that the reform does not address many fundamental problems that have plagued physician payment under Medicare in the past. In the cost area, for example, the new fee schedule docs not affect such factors as the basic incentives built into fee-for-service medicine and the explosion of new medical technologies. The failure of the program to achieve its goals in cost containment and other areas could result in abandonment of fee-for-service compensation of physicians under Medicare. C1 MASSACHUSETTS GEN HOSP,HLTH POLICY RES & DEV UNIT,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NR 38 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL PUBLISHERS PI CAMBRIDGE PA 350 MAIN STREET, STE 6, CAMBRIDGE, MA 02148-5023 SN 0887-378X J9 MILBANK Q JI Milbank Q. PY 1993 VL 71 IS 2 BP 193 EP 215 DI 10.2307/3350398 PG 23 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA LH556 UT WOS:A1993LH55600001 PM 8510600 ER PT B AU YOUNG, AB AF YOUNG, AB BE WAXMAN, SG TI ROLE OF EXCITOTOXINS IN HEREDITODEGENERATIVE NEUROLOGIC DISEASES SO MOLECULAR AND CELLULAR APPROACHES TO THE TREATMENT OF NEUROLOGICAL DISEASE SE RESEARCH PUBLICATIONS : ASSOCIATION FOR RESEARCH IN NERVOUS AND MENTAL DISEASE LA English DT Proceedings Paper CT SYMP ON MOLECULAR AND CELLULAR APPROACHES TO THE TREATMENT OF BRAIN DISEASE CY DEC 06-07, 1991 CL NEW YORK, NY SP ASSOC RES NERVOUS & MENTAL DIS RP YOUNG, AB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,NEUROL SERV,BOSTON,MA 02114, USA. FU NIA NIH HHS [AG08671]; NINDS NIH HHS [NS19613] NR 0 TC 11 Z9 11 U1 0 U2 1 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-953-4 J9 RES P ARNMD PY 1993 VL 71 BP 175 EP 189 PG 15 WC Biochemistry & Molecular Biology; Neurosciences; Pathology SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pathology GA BX06V UT WOS:A1993BX06V00010 PM 8093331 ER PT J AU SCHWEIGHOFFER, F CAI, H CHEVALLIERMULTON, MC FATH, I COOPER, G TOCOUE, B AF SCHWEIGHOFFER, F CAI, H CHEVALLIERMULTON, MC FATH, I COOPER, G TOCOUE, B TI THE SACCHAROMYCES-CEREVISIAE SDC25 C-DOMAIN GENE-PRODUCT OVERCOMES THE DOMINANT INHIBITORY ACTIVITY OF HA-RAS ASN-17 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID GUANINE-NUCLEOTIDE EXCHANGE; GTPASE ACTIVATING PROTEIN; SIGNAL-TRANSDUCTION; GAP; P21; CELLS; GDP; MUTATION; MUTANTS; PHOSPHORYLATION AB The carboxy-terminal part of the Saccharomyces cerevisiae SDC25 gene product (SDC25 C domain) can elicit activation of mammalian Ras proteins. Specifically, SDC25 C domain functions as an exchange factor for cellular Ras proteins in CHO cells. In this study, we used the dominant inhibitory Ha-Ras Asn-17 mutant and SDC25 C domain to further investigate the interaction between cellular Ras proteins and their putative endogenous guanine nucleotide-releasing factors. Transcription from the polyomavirus thymidine kinase gene (Py tk) promoter is strongly inhibited by the expression of Ha-Ras Asn-17 in NIH 3T3 cells. Coexpression of SDC25 C domain overcomes the negative effect of the Ras mutant on the Py tk promoter. On the other hand, transactivation of the Ras-responsive element of the Py tk promoter induced by SDC25 C domain is lost upon coexpression of increasing amounts of Ha-Ras Asn-17. In addition, coexpression of SDC25 C domain overcomes the inhibition of proliferation of NIH 3T3 cells caused by Ha-Ras Asn-17. These results are consistent with the idea that the Ha-Ras Asn-17 mutant functions by titrating an upstream activator of cellular Ras proteins. C1 RHONE POULENC RORER,13 QUAI JULES GUESDE,BP 14,F-94403 VITRY,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [R0I CAI8689] NR 42 TC 61 Z9 61 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JAN PY 1993 VL 13 IS 1 BP 39 EP 43 PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KD785 UT WOS:A1993KD78500005 PM 8380225 ER PT J AU LUDLOW, JW GLENDENING, CL LIVINGSTON, DM DECAPRIO, JA AF LUDLOW, JW GLENDENING, CL LIVINGSTON, DM DECAPRIO, JA TI SPECIFIC ENZYMATIC DEPHOSPHORYLATION OF THE RETINOBLASTOMA PROTEIN SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SUSCEPTIBILITY GENE-PRODUCT; SV40 LARGE-T; CELL-CYCLE; RB PROTEIN; PHOSPHORYLATION; MITOSIS; PHOSPHATASE-1; FIBROBLASTS; DROSOPHILA; EXPRESSION AB The retinoblastoma gene product (RB) undergoes cell cycle-dependent phosphorylation and dephosphorylation. Pulse-chase experiments revealed that the change in RB gel electrophoretic migration which occurs near mitosis is due to enzymatic dephosphorylation (J. W. Ludlow, J. Shon, J. M. Pipas, D. M. Livingston, and J. A. DeCaprio, Cell 60:387-396, 1990). To determine the precise timing of RB dephosphorylation and whether a specific phosphatase is active in this process, we have utilized a nocodazole block and release protocol which allows a large population of cells to progress synchronously through mitosis. In such experiments, RB dephosphorylation began during anaphase and continued until complete dephosphorylation was apparent in the ensuing G1 period. In addition, late mitotic cell extracts were capable of dephosphorylating RB in vitro. This RB-specific mitotic phosphatase activity was more active in anaphase extracts than in pro- or metaphase extracts, which is consistent with the results obtained in vivo. Okadaic acid and protein phosphatase inhibitors 1 and 2 inhibited this specific RB phosphatase activity. These results suggest a role for serine and threonine phosphoprotein phosphatase type 1 in the late mitotic dephosphorylation of RB. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA-08616-02, K11 CA01385-03] NR 44 TC 235 Z9 236 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JAN PY 1993 VL 13 IS 1 BP 367 EP 372 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KD785 UT WOS:A1993KD78500039 PM 8380224 ER PT J AU MAJOCHA, RE TATE, B MAROTTA, CA AF MAJOCHA, RE TATE, B MAROTTA, CA TI PC12 CELLS RELEASE STIMULATORY FACTORS AFTER TRANSFECTION WITH BETA/A4-C-TERMINAL DNA OF THE ALZHEIMER AMYLOID PRECURSOR PROTEIN SO MOLECULAR AND CHEMICAL NEUROPATHOLOGY LA English DT Article DE AMYLOID; ALZHEIMER DISEASE; PC12 CELLS; NEURITE EXTENSION; TRANSFECTION ID FIBROBLAST GROWTH-FACTORS; MESSENGER-RNA; BETA-PROTEIN; NEURITE OUTGROWTH; MOLECULAR-CLONING; DISEASE; LAMININ; BRAIN; CDNA; NEURONS AB The beta/A4 region of the amyloid precursor protein (APP) accumulates in brains of victims of Alzheimer disease (AD) where it is a major component of senile plaques. We examined the pathophysiological consequences of overexpression of the beta/A4-C-terminal DNA in PC12 cells. Serum-free conditioned media (SFCM) from positive transfectants stimulated control PC12 cells to extend neurites and increase in size. Unlike the factor that affected cell size, neurite lengthening activity was significantly decreased after immunoabsorption with anti-beta/A4 monoclonal antibodies (MAb) and changes in pH. The data support the view that among the consequences of beta/A4-C-terminal DNA overexpression in PC12 cells is the release of factors that stimulate nontransfected cells to undergo morphological transformations that include differentiation to a neuronal phenotype. It is hypothesized that similar activities that may contribute to the molecular pathophysiology of the disorder may be present in the AD brain. C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,NEUROBIOL LAB,BOSTON,MA 02114. FU NIA NIH HHS [P01 AG 02126] NR 42 TC 2 Z9 2 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 1044-7393 J9 MOL CHEM NEUROPATHOL JI Mol. Chem. Neuropathol. PD JAN-FEB PY 1993 VL 18 IS 1-2 BP 99 EP 113 PG 15 WC Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA KQ791 UT WOS:A1993KQ79100007 PM 8466596 ER PT S AU BROWN, RH AF BROWN, RH BE Higashida, H Yoshioka, T Mikoshiba, K TI ION-CHANNEL MUTATIONS IN PERIODIC PARALYSIS AND RELATED MYOTONIC DISEASES SO MOLECULAR BASIS OF ION CHANNELS AND RECEPTORS INVOLVED IN NERVE EXCITATION, SYNAPTIC TRANSMISSION AND MUSCLE CONTRACTION: IN MEMORY OF PROFESSOR SHOSAKU NUMA SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Molecular Basis of Ion Channels and Receptors Involved in Nerve Excitation Synaptic Transmission and Muscle Contraction (In Memory of Professor Shosaku Numa) CY JAN 12-15, 1993 CL TOKYO, JAPAN SP NEW YORK ACAD SCI ID MUSCLE SODIUM-CHANNEL; ADYNAMIA EPISODICA HEREDITARIA; ALPHA-SUBUNIT GENE; PARAMYOTONIA-CONGENITA; CHLORIDE CHANNEL; INACTIVATION; MEMBRANE; LOCUS; CONDUCTANCE; WEAKNESS RP BROWN, RH (reprint author), MASSACHUSETTS GEN HOSP EAST,HARVARD MED SCH,DEPT NEUROL,DAY NEUROMUSCULAR RES LAB,CNY-6,BOSTON,MA 02112, USA. RI Mikoshiba, Katsuhiko/N-7943-2015 FU NIAMS NIH HHS [5ROI-AR41025-02] NR 51 TC 8 Z9 8 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-823-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 707 BP 305 EP 316 DI 10.1111/j.1749-6632.1993.tb38061.x PG 12 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences; Physiology SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology; Physiology GA BZ86C UT WOS:A1993BZ86C00025 PM 9137561 ER PT J AU STARR, DZ AF STARR, DZ TI A HOSPITAL EXPERIENCE SO MOUNT SINAI JOURNAL OF MEDICINE LA English DT Article AB This article is an account of the author's experience and observations on having been incorrectly diagnosed as having a myocardial infarction and having been admitted to a coronary intensive care unit. The article touches on the rigidities of medical thinking, how one can come to believe what is not true, how to be an ''exceptional patient,'' how medical care feels from the other side, and other relevant observations. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BOSTON UNIV,SCH MED,BOSTON,MA 02118. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MOUNT SINAI HOSPITAL PI NEW YORK PA BOX 1094 ONE GUSTAVE L LEVY PLACE ATTN: CIRCULATION ASST, NEW YORK, NY 10029-6574 SN 0027-2507 J9 MT SINAI J MED JI Mt. Sinai J. Med. PD JAN PY 1993 VL 60 IS 1 BP 76 EP 78 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA KJ486 UT WOS:A1993KJ48600018 PM 8426602 ER PT J AU THE, I MURTHY, AE HANNIGAN, GE JACOBY, LB MENON, AG GUSELLA, JF BERNARDS, A AF THE, I MURTHY, AE HANNIGAN, GE JACOBY, LB MENON, AG GUSELLA, JF BERNARDS, A TI NEUROFIBROMATOSIS TYPE-1 GENE-MUTATIONS IN NEUROBLASTOMA SO NATURE GENETICS LA English DT Article ID RAS GENE; VONRECKLINGHAUSEN NEUROFIBROMATOSIS; NEURO-BLASTOMA; N-MYC; PROTEIN; CHROMOSOME-17; TRANSLOCATION; AMPLIFICATION; ACTIVATION; SEQUENCE AB The introduction of human chromosome 17 suppresses the tumourigenicity of a neuroblastoma cell line in the absence of any effects on in vitro growth and the neurofibromatosis type 1 (NF1) gene may be responsible. Here we report that 4 out of 10 human neuroblastoma lines express little or no neurofibromin and that two of these lines show evidence of NF1 mutations, providing further proof that NF1 mutations occur in tumours that are not commonly found in NF1 patients. We also show that NF1 deficient neuroblastomas show only moderately elevated ras-GTP levels, in contrast to NF1 tumour cells, indicating that neurofibromin contributes differently to the negative regulation of ras in different cell types. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,MGH E,BLDG 149,13TH ST,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. RI The, Inge/B-8884-2011; Hannigan, Greg/A-5092-2009 FU NCI NIH HHS [CA51410]; NINDS NIH HHS [NS22224] NR 34 TC 130 Z9 131 U1 0 U2 2 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD JAN PY 1993 VL 3 IS 1 BP 62 EP 66 DI 10.1038/ng0193-62 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA KF372 UT WOS:A1993KF37200014 PM 8490657 ER PT J AU MACIEJEWSKI, BA SKATES, S ZAJUSZ, A LANGE, D AF MACIEJEWSKI, BA SKATES, S ZAJUSZ, A LANGE, D TI IMPORTANCE OF TUMOR SIZE AND REPOPULATION FOR RADIOCURABILITY OF SKIN-CANCER SO NEOPLASMA LA English DT Article DE SKIN CANCER; DOSE FRACTIONATION; TUMOR SIZE; REPOPULATION ID DOSE-RESPONSE; RADIOTHERAPY; FRACTIONATION; IRRADIATION; VOLUME; TIME AB Data on 946 skin cancers treated by radiation were used to estimate the importance of repopulation. Six different treatment regimes were used from a single dose to 74 Gy given in 47 fractions. High local control of the small skin cancers (L1 cm) was independent of dose fractionation. For large tumors, only 74 Gy in 47 fractions was the optimal treatment. Time factor analysis showed a steep increase in the NTD50 values between day 28 and 65 of treatment. This implies that tumor clonogen repopulation starts around 4 weeks of treatment The present results showed a three-component dose response curve instead of the two-component curves which were found for head and neck and bladder cancer. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,DEPT RADIAT MED,BOSTON,MA 02114. RP MACIEJEWSKI, BA (reprint author), M SKLODOWSKA CURIE MEM INST,CTR ONCOL,PL-44101 GLIWICE,POLAND. NR 15 TC 8 Z9 8 U1 0 U2 0 PU SLOVAK ACADEMIC PRESS LTD PI BRATISLAVA PA PO BOX 57, NAM SLOBODY 6, 810 05 BRATISLAVA, SLOVAKIA SN 0028-2685 J9 NEOPLASMA JI Neoplasma PY 1993 VL 40 IS 1 BP 51 EP 54 PG 4 WC Oncology SC Oncology GA KP236 UT WOS:A1993KP23600010 PM 8350948 ER PT B AU KOWALL, NW MCKEE, AC AF KOWALL, NW MCKEE, AC BE SEIL, FJ TI THE HISTOPATHOLOGY OF NEURONAL DEGENERATION AND PLASTICITY IN ALZHEIMER-DISEASE SO NEURAL INJURY AND REGENERATION SE ADVANCES IN NEUROLOGY LA English DT Proceedings Paper CT 4TH INTERNATIONAL SYMP ON NEURAL REGENERATION CY DEC 11-15, 1991 CL PACIFIC GROVE, CA SP US DEPT VET AFFAIRS, MED RES SERV, PARALYZED VET AMER, SPINAL CORD RES FDN, NINDS, NICHD, NIA, AMER PARALYSIS ASSOC, ALZHEIMERS ASSOC RP KOWALL, NW (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NIA NIH HHS [AG 05134]; NINDS NIH HHS [NS 25588] NR 0 TC 11 Z9 12 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-948-8 J9 ADV NEUROL JI Adv.Neurol. PY 1993 VL 59 BP 5 EP 33 PG 29 WC Clinical Neurology; Neurosciences; Pathology; Physiology SC Neurosciences & Neurology; Pathology; Physiology GA BX06U UT WOS:A1993BX06U00002 PM 8420123 ER PT J AU REBECK, GW HYMAN, BT AF REBECK, GW HYMAN, BT TI NEUROANATOMICAL CONNECTIONS AND SPECIFIC REGIONAL VULNERABILITY IN ALZHEIMERS-DISEASE SO NEUROBIOLOGY OF AGING LA English DT Note ID PRECURSOR MESSENGER-RNAS; DIFFERENTIAL EXPRESSION; QUANTITATIVE-ANALYSIS; PYRAMIDAL NEURONS; VISUAL-CORTEX; PROTEIN GENE; HUMAN-BRAIN; PATHOLOGY; RECOGNITION; IMPAIRMENT RP REBECK, GW (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,WARREN 407,BOSTON,MA 01228, USA. NR 37 TC 21 Z9 21 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD JAN-FEB PY 1993 VL 14 IS 1 BP 45 EP 47 DI 10.1016/0197-4580(93)90019-8 PG 3 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA KK329 UT WOS:A1993KK32900005 PM 8450931 ER PT J AU DUFFY, FH MCANULTY, GB ALBERT, MS AF DUFFY, FH MCANULTY, GB ALBERT, MS TI THE PATTERN OF AGE-RELATED DIFFERENCES IN ELECTROPHYSIOLOGICAL ACTIVITY OF HEALTHY-MALES AND FEMALES SO NEUROBIOLOGY OF AGING LA English DT Article DE AGING, HEALTHY ADULTS; AGING, GENDER DIFFERENCE; AGING, EEG AND EVOKED POTENTIALS ID BRAIN ELECTRICAL-ACTIVITY; EEG AMPLITUDES; ELDERLY ADULTS; ELECTROENCEPHALOGRAM; DISTRIBUTIONS; PARAMETERS; NORMALITY; DEMENTIA AB Age-related differences in quantified electrophysiological measures were examined in 202 subjects (109 females; 93 males) ages 30-80 all of whom were judged to be optimally healthy on a wide variety of criteria. The study utilized both absolute and relative measures from EEG spectral analysis as well as additional measures from long latency-evoked potentials. The same findings were noted for the 109 newly studied females as were reported for 63 previously studied male subjects. Results indicate that there is a broad trend for decreased EEG slow and increased fast activity with age, however, some of the measures change linearly and others are best represented by nonlinear functions. There is no decade where activities remain stable- Overall the pattern of change for males and females is similar, however, gender differences in both the EEG and EP data were present. The females had higher magnitudes for almost all absolute spectral and fast relative spectral measures. However. females demonstrated lower absolute alpha amplitude, lower relative slow activity, and lower late-latency EP data. Moreover, the absolute slow activity measure showed a gender X age interaction, indicating that the females had a different change in pattern of activity with increasing age than the males. Thus, gender-related findings were complex and could not be expressed as simple differences in overall amplitude. Age-related change is not a simple linear process but differs for differing EEG spectral bands, relative, and absolute spectral measures and for males and females. The overall findings contradict the common wisdom that EEG and alpha slow with age and that age related EEG change is on a continuum with findings in Alzheimer's disease where increased slowing predominates. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02115. RP DUFFY, FH (reprint author), HARVARD UNIV,SCH MED,HOSP,DEPT NEUROL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIA NIH HHS [P01-AG-4953] NR 32 TC 64 Z9 66 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD JAN-FEB PY 1993 VL 14 IS 1 BP 73 EP 84 DI 10.1016/0197-4580(93)90025-7 PG 12 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA KK329 UT WOS:A1993KK32900011 PM 8450936 ER PT J AU GABRIEL, SM HUNNICUT, EH MILLARD, WJ BADGER, TM NATHANSON, JA AF GABRIEL, SM HUNNICUT, EH MILLARD, WJ BADGER, TM NATHANSON, JA TI INFLUENCE OF INVIVO REPRODUCTIVE ENDOCRINE STATE ON GROWTH HORMONE-RELEASING FACTOR STIMULATED ADENYLATE-CYCLASE ACTIVITY IN ANTERIOR-PITUITARY FRAGMENTS SO NEUROENDOCRINOLOGY LA English DT Article DE ESTROGEN; TESTOSTERONE; GROWTH HORMONE RELEASING FACTOR; ADENYLATE CYCLASE; GROWTH HORMONE ID (GH)-RELEASING FACTOR; FACTOR INVITRO; RAT PITUITARY; FEMALE RATS; SEX; ESTROGEN; SOMATOSTATIN; TESTOSTERONE; CELLS; SECRETION AB The growth hormone releasing factor (GRF) stimulated adenylate cyclase activity was evaluated in membrane fractions of anterior pituitary glands from male and female rats and in gonadectomized rats following in vivo gonadal steroid treatments. The baseline adenylate cyclase activity was lower in random estrous cycle female rats as compared with males. When estrous cycle phases were evaluated, diestrus 1 females had a lower basal activity as compared with males, while proestrus females were similar to males. The maximal stimulation of adenylate cyclase activity by GRF (i.e. V(max)) was lower in random estrous cycle female rats than in males. This lower V(max), relative to males, was more pronounced in diestrus 1 than in proestrus females. There was little difference in the ED50 for GRF-stimulated adenylate cyclase activity among these groups. The adenylate cyclase activity was altered 1 week after gonadectomy or 1 week after gonadectomy plus simultaneous in vivo gonadal steroid treatment. The expression of data as a function of whole tissue (content) or as a function of protein (concentration) influenced magnitude and direction of these treatment effects. This may reflect the proliferation of nonsomatotroph cell populations and altered protein synthetic activity following reproductive endocrine manipulations. When expressed as a whole tissue content, the baseline adenylate cyclase activity was unchanged after gonadectomy when compared to same-sex, gonadal-intact cohorts. However, an increase in the V(max) for GRF-stimulated adenylate cyclase activity was found in gonadectomized rats relative to sham-operated, gonadal-intact cohorts. When the same data were calculated relative to protein concentration, a decrease in baseline was found following orchidectomy, but not following ovariectomy, when compared to sham-operated, gonadal-intact cohorts. The corresponding V(max) for these groups, expressed as a concentration, decreased after orchidectomy, but increased after ovariectomy. Gonadectomy plus estrogen treatment decreased both baseline and V(max) for GRF-stimulated adenylate cyclase activity. This potent decrease was evident when compared to either same-sex, gonadectomized, or gonadal-intact cohorts for both forms of data expression. Basal and maximally stimulated adenylate cyclase activities following ovariectomy plus testosterone treatment were similar to gonadal-intact females when the data were expressed as a content, but similar to ovariectomized rats when the same data were expressed as a concentration. None of the above treatments significantly altered the ED50 for GRF-stimulated adenylate cyclase activity. These data indicate sex differences for in vitro basal and GRF-stimulated adenylate cyclase activity in rat anterior pituitary membranes. With heterotypic in vivo steroid treatment, estrogen was inhibitory, while testosterone partially was stimulatory to basal and GRF-stimulated adenylate cyclase activity. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. FU NICHD NIH HHS [HD22199]; NIDDK NIH HHS [DK07561]; NIMH NIH HHS [MH45480] NR 40 TC 3 Z9 3 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD JAN PY 1993 VL 57 IS 1 BP 63 EP 69 DI 10.1159/000126343 PG 7 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA KU368 UT WOS:A1993KU36800010 PM 8479617 ER PT J AU DROPCHO, EJ KLINE, LB RISER, J AF DROPCHO, EJ KLINE, LB RISER, J TI ANTINEURONAL (ANTI-RI) ANTIBODIES IN A PATIENT WITH STEROID-RESPONSIVE OPSOCLONUS-MYOCLONUS SO NEUROLOGY LA English DT Note ID NEOPLASTIC CEREBELLAR DEGENERATION; NERVOUS-SYSTEM; CANCER; ADULTS AB A 45-year-old woman developed opsoclonus, myoclonus, and severe truncal and gait ataxia. Serum and CSF contained IgG antibodies that appear to be identical to ''anti-Ri'' antibodies associated with paraneoplastic opsoclonus and ataxia. The patient had a fluctuating course with exacerbations that responded well to corticosteroids and later to cyclophosphamide. Her anti-Ri antibody titer has declined significantly but still remains high. After more than 3 years of follow-up, no neoplasm has been detected. C1 UNIV ALABAMA,DEPT OPHTHALMOL,BIRMINGHAM,AL 35294. BIRMINGHAM VET AFFAIRS MED CTR,BIRMINGHAM,AL. BROOKWOOD MED CTR,BIRMINGHAM,AL. RP DROPCHO, EJ (reprint author), UNIV ALABAMA,DEPT NEUROL,UAB STN,BIRMINGHAM,AL 35294, USA. NR 10 TC 74 Z9 74 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1993 VL 43 IS 1 BP 207 EP 211 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA KJ189 UT WOS:A1993KJ18900036 PM 8423887 ER PT J AU GORMAN, DG UNUTZER, J AF GORMAN, DG UNUTZER, J TI BRODMANN MISSING NUMBERS SO NEUROLOGY LA English DT Article C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, PSYCHIAT SERV, BEHAV NEUROSCI SECT, LOS ANGELES, CA USA. RP GORMAN, DG (reprint author), LOVELACE MED CTR, DEPT NEUROL, 5400 GIBSON BLVD SE, ALBUQUERQUE, NM 87108 USA. NR 9 TC 9 Z9 9 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1993 VL 43 IS 1 BP 226 EP 227 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA KJ189 UT WOS:A1993KJ18900043 PM 8423895 ER PT J AU GOTO, J FIGLEWICZ, DA HAINES, JL BROWN, RH KHODR, N ROULEAU, GA AF GOTO, J FIGLEWICZ, DA HAINES, JL BROWN, RH KHODR, N ROULEAU, GA TI THE GLYCINAMIDE RIBONUCLEOTIDE TRANSFORMYLASE (GART) GENE IS NOT RESPONSIBLE FOR FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS SO NEUROMUSCULAR DISORDERS LA English DT Article DE FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS; GLYCINAMIDE RIBONUCLEOTIDE TRANSFORMYLASE; CHROMOSOME-21 ID MOTOR NEURON DISEASE; HUMAN CHROMOSOME-21; WOBBLER MOUSE; LINKAGE; RECOMBINATION AB Though the nature of the underlying metabolic defect which leads to amyotrophic lateral sclerosis (ALS) remains obscure, certain biochemical anomalies have been found, such as, reduced RNA content in ALS motor neurons. Recently, a gene causing the familial form of ALS (FALS) has been assigned to an interval of approximately 10 cM including the locus D21S58 on chromosome 21q22.1. This region includes the GART gene which encodes an enzyme catalyzing three steps in the de novo biosynthesis of purine nucleotides which are precursors for RNA. A defect of this gene might result in reduced RNA production and predispose to premature death of motor neurons. In order to test GART as a candidate we developed two highly informative DNA markers in this region and carried out linkage analyses for FALS. GART is excluded as a candidate for FALS. C1 MCGILL UNIV, CTR RES, MONTREAL H3G 1A4, PQ, CANADA. MCGILL UNIV, DEPT NEUROL, MONTREAL H3G 1A4, PQ, CANADA. UNIV TOKYO, SCH MED, INST BRAIN RES, TOKYO 113, JAPAN. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, NEUROGENET LAB, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DAY NEUROMUSCULAR LAB, BOSTON, MA 02114 USA. NR 17 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0960-8966 EI 1873-2364 J9 NEUROMUSCULAR DISORD JI Neuromusc. Disord. PY 1993 VL 3 IS 2 BP 157 EP 160 DI 10.1016/0960-8966(93)90008-8 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA LZ861 UT WOS:A1993LZ86100008 PM 8358240 ER PT J AU BONIFACIO, MJ EZZEDDINE, D SAKAKI, Y BREAKFIELD, XO SARAIVA, MJ AF BONIFACIO, MJ EZZEDDINE, D SAKAKI, Y BREAKFIELD, XO SARAIVA, MJ TI RETROVIRUS-MEDIATED GENE-TRANSFER OF TRANSTHYRETIN AND TRANSTHYRETIN METHIONINE-30 - A POTENTIAL TOOL FOR THE STUDY OF AMYLOIDOGENESIS SO NEUROMUSCULAR DISORDERS LA English DT Article DE TTR; AMYLOIDOSIS; RETROVIRUS; GENE TRANSFER ID FAMILIAL AMYLOIDOTIC POLYNEUROPATHY; TRANSGENIC MICE; MOUSE MODEL; CELL-LINES; EXPRESSION; THERAPY; SYSTEM; FIBROBLASTS; PREALBUMIN; DEFICIENCY AB Familial amyloidotic polyneuropathy (FAP) is a genetic disease characterized by systemic amyloid deposition particularly in the peripheral nervous system. These deposits are composed mainly of a mutant form of the serum protein transthyretin (TTR) having a methionine for valine substitution at position 30-TTR Met 30. The factors involved in the formation of these deposits are unknown. The existence of animal models for FAP should allow elucidation of these factors. As one approach to the development of animal models for amyloidogenesis in FAP, we have constructed recombinant retrovirus vectors, carrying the full length human cDNA for either TTR or TTR Met 30 under the control of the Moloney murine leukemia virus (MoMLV) LTR element. After transfection of the packaging cell line, PSI2, viral stocks were used to infect a rat hepatoma cell line, H56, mouse fibroblast cell line, NIH3T3, and mouse primary fibroblasts. H56 cells efficiently secreted both TTR and TTR Met 30 as assessed by immunoprecipitation and ELISA, whereas NIH3T3 fibroblasts appeared not to release these proteins under the conditions tested. Primary fibroblasts secreted the mutant protein as assessed by ELISA. These genetically modified cells can be grafted into animals for in vivo study of amyloidogenesis, as well as be used in culture to investigate factors that might regulate the rate of amyloid deposition. C1 HOSP DE SANTO ANTONIO, CTR ESTUDOS PARAMILOIDOSE, OPORTO, PORTUGAL. UNIV OPORTO, INST CIENCIAS BIOMED ABEL SALAZAR, OPORTO, PORTUGAL. MASSACHUSETTS GEN HOSP, CTR NEUROSCI, E CHARLESTOWN, MA USA. HARVARD UNIV, SCH MED, NEUROSCI PROGRAM, BOSTON, MA 02115 USA. UNIV TOKYO, INST MED SCI, TOKYO 113, JAPAN. RI Saraiva, Maria Joao/K-3907-2013 OI Saraiva, Maria Joao/0000-0002-3360-6899 FU NINDS NIH HHS [R01NS24279]; PHS HHS [P01N52590] NR 36 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0960-8966 EI 1873-2364 J9 NEUROMUSCULAR DISORD JI Neuromusc. Disord. PY 1993 VL 3 IS 4 BP 275 EP 282 DI 10.1016/0960-8966(93)90020-K PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA MH202 UT WOS:A1993MH20200004 PM 8268724 ER PT J AU KOVACHICH, GB FRAZER, A ARONSON, CE AF KOVACHICH, GB FRAZER, A ARONSON, CE TI EFFECT OF CHRONIC ADMINISTRATION OF ANTIDEPRESSANTS ON ALPHA-2-ADRENOCEPTORS IN THE LOCUS-CERULEUS AND ITS PROJECTION FIELDS IN RAT-BRAIN DETERMINED BY QUANTITATIVE AUTORADIOGRAPHY SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE ALPHA-2-ADRENOCEPTORS; H-3-IDAZOXAN; LOCUS COERULEUS; ANTIDEPRESSANTS ID ALPHA-2 ADRENOCEPTOR HETEROGENEITY; NORADRENERGIC NEURONS; H-3 RAUWOLSCINE; PRESYNAPTIC RECEPTORS; FILM AUTORADIOGRAPHY; ANTAGONIST BINDING; AMINE METABOLISM; HIGH-AFFINITY; SITES; INHIBITION AB The density of alpha2-adrenoceptors, using H-3-idazoxan as the radioligand, was determined by quantitative autoradiography in the locus coeruleus and in 13 noradrenergic projection fields following chronic administration of drugs acting on noradrenergic and/or serotonergic neurons. Protriptyline, an inhibitor of the uptake of norepinephrine, and mianserin, an alpha2-adrenoceptor antagonist, reduced the binding of H-3-idazoxan only in the locus coeruleus. Phenelzine, an inhibitor of both type A and type B monoamine oxidase (MAO), reduced the binding of H-3-idazoxan in the locus coeruleus and in several areas with noradrenergic innervation from tegmental cell bodies. Clorgyline, a selective inhibitor of type A MAO, had no effect. Of the two selective inhibitors of serotonin uptake, citalopram caused a modest increase in binding only in one terminal field area, whereas sertraline had no effect. Although these antidepressants did not produce consistent effects on alpha2-adrenoceptors, protriptyline, mianserin, and phenelzine were similar in that they all decreased the binding of H-3-idazoxan in the locus coeruleus without widely affecting its binding in the coerulean terminal fields. Deprenyl, a selective inhibitor of type B MAO, the only drug in this study without proven antidepressant efficacy, differed from all other drugs in that it decreased the binding of H-3-idazoxan both in the locus coeruleus as well as in most terminal fields with primarily coerulean noradrenergic innervation. C1 UNIV PENN,DEPT VET AFFAIRS MED CTR,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH VET MED,PHARMACOL LAB,PHILADELPHIA,PA 19104. UNIV PENN,SCH VET MED,TOXICOL LAB,PHILADELPHIA,PA 19104. FU NIMH NIH HHS [MH29094] NR 55 TC 37 Z9 38 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD JAN PY 1993 VL 8 IS 1 BP 57 EP 65 PG 9 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA KD906 UT WOS:A1993KD90600007 PM 8093834 ER PT J AU BOSSI, SR SIMPSON, JR ISACSON, O AF BOSSI, SR SIMPSON, JR ISACSON, O TI AGE DEPENDENCE OF STRIATAL NEURONAL DEATH CAUSED BY MITOCHONDRIAL DYSFUNCTION SO NEUROREPORT LA English DT Article DE 3-NITROPROPIONIC ACID; MITOCHONDRIA; CENTRAL NERVOUS SYSTEM; AGING; HUNTINGTONS DISEASE; ALZHEIMERS DISEASE; DIAGNOSTIC TESTS; METABOLISM; STRIATUM; NEUROTOXICITY ID 3-NITROPROPIONIC ACID; HUNTINGTONS-DISEASE; BRAIN-LESIONS; RATS AB SEVERAL lines of evidence point to a decline in mitochondrial efficiency with age. The relationship between age and sensitivity to Huntington disease-like neuronal death in the striatum induced by the mitochondrial inhibitor 3-nitropropionic acid (3-NP) was examined. 3-NP has been shown to cause degeneration of striatum, hippocampus, and thalamus in rat and of caudate-putamen in humans. We administered single doses of 3-NP intraperitoneally to rats of various ages. Animals older than 4 months exhibited a far greater susceptibility to striatal neurotoxicity and mortality compared with younger animals. These results are discussed in the context of age-dependent metabolic impairment, which may be a key factor in the etiology of neurodegenerative disorders such as Huntington's disease and Alzheimer's disease. C1 MCLEAN HOSP,NEUROREGENERAT LAB,BELMONT,MA 02178. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. FU NINDS NIH HHS [NS29178, NS30064] NR 18 TC 67 Z9 67 U1 0 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD JAN PY 1993 VL 4 IS 1 BP 73 EP 76 DI 10.1097/00001756-199301000-00019 PG 4 WC Neurosciences SC Neurosciences & Neurology GA KN461 UT WOS:A1993KN46100019 PM 8453041 ER PT S AU HALLER, DG LEFKOPOULOU, M MACDONALD, JS MAYER, RS AF HALLER, DG LEFKOPOULOU, M MACDONALD, JS MAYER, RS BE Rustum, YM TI SOME CONSIDERATIONS CONCERNING THE DOSE AND SCHEDULE OF 5FU AND LEUCOVORIN - TOXICITIES OF 2 DOSE SCHEDULES FROM THE INTERGROUP COLON ADJUVANT TRIAL (INT-0089) SO NOVEL APPROACHES TO SELECTIVE TREATMENTS OF HUMAN SOLID TUMORS: LABORATORY AND CLINICAL CORRELATION SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT International Symposium on Novel Approaches to Selective Treatments of Human Tumors: Laboratory and Clinical Correlation CY SEP 10-12, 1992 CL BUFFALO, NY C1 DANA FARBER CANC CTR,BOSTON,MA. TEMPLE UNIV,PHILADELPHIA,PA. RP HALLER, DG (reprint author), UNIV PENN,CTR CANC,PHILADELPHIA,PA 19104, USA. NR 0 TC 10 Z9 10 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44592-1 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1993 VL 339 BP 51 EP 54 PG 4 WC Oncology; Medicine, General & Internal; Pharmacology & Pharmacy SC Oncology; General & Internal Medicine; Pharmacology & Pharmacy GA BZ51M UT WOS:A1993BZ51M00006 PM 8178728 ER PT J AU LIVNI, E BABICH, J ALPERT, NM LIU, YY THOM, E CLEELAND, R PROSSER, BL CORREIA, JA STRAUSS, HW RUBIN, RH FISCHMAN, AJ AF LIVNI, E BABICH, J ALPERT, NM LIU, YY THOM, E CLEELAND, R PROSSER, BL CORREIA, JA STRAUSS, HW RUBIN, RH FISCHMAN, AJ TI SYNTHESIS AND BIODISTRIBUTION OF F-18 LABELED FLEROXACIN SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article ID INVITRO ACTIVITY; PHARMACOKINETICS; TISSUE; PENETRATION; RO-23-6240; QUINOLONE; AM-833; URINE AB [F-18]Fleroxacin (6,8-difluoro-1,4-dihydro-1-(2-[F-18]fluoroethyl)-4-oxo-7-(4-methyl-1-piperazinyl)-3-quinolinecarboxylic acid) was synthesized from its methylsulfonyl ester precursor. 6.7,8-Trifluoro-4-hydroxy-quinoline-3-carboxylic acid ethyl ester (Ro 19-7423) was alkylated with 2-bromoethanol to produce 6,7,8-trifluoro-1,4-dihydro-1-(2-hydroxyethyl)-4-oxo-3-quinolinecarboxylic acid ethyl ester in 76% yield which was then condensed with 1-methyl-piperazine to produce 6,8-difluoro-1,4-dihydro-1-(2-hydroxy-ethyl)-7-(4-methyl-1-piperazinyl)4-oxo-3-quinolinecarboxylic acid ethyl ester in 67% yield. This product was reacted with methanesulfonyl chloride to produce the mesylate precursor of fleroxacin in 66% yield. Nucleophilic substitution of the mesylate with F-18 in the presence of Kryptofix(R) 2.2.2 followed by basic hydrolysis produced [F-18]fleroxacin with a radiochemical yield of 5-8% [EOS] within 90 min, The pattern of biodistribution of [F-18]fleroxacin was similar to the C-14-labeled drug. C1 MASSACHUSETTS GEN HOSP,MED SERV,CLIN INVEST PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. RP LIVNI, E (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 22 TC 13 Z9 15 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD JAN PY 1993 VL 20 IS 1 BP 81 EP 87 DI 10.1016/0969-8051(93)90139-L PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KC913 UT WOS:A1993KC91300010 PM 8461883 ER PT B AU SMITH, RJ AF SMITH, RJ BE Gussler, JD Silverman, E TI GLUTAMINE - CONDITIONALLY ESSENTIAL SO NUTRITIONAL ESSENTIALITY: A CHANGING PARADIGM: REPORT OF THE TWELFTH ROSS CONFERENCE ON MEDICAL RESEARCH LA English DT Proceedings Paper CT 12th Ross Conference on Medical Research CY DEC 05-07, 1992 CL CAREFREE, AZ SP ROSS PROD DIV, ABBOTT LABS C1 JOSLIN DIABET CTR,METAB SECT,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ROSS PRODUCTS DIV ABBOTT LABORATORIES PI COLUMBUS PA COLUMBUS, OH 43215-1724 PY 1993 BP 46 EP 51 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA BA42H UT WOS:A1993BA42H00009 ER PT J AU WORDEN, JW SILVERMAN, PS AF WORDEN, JW SILVERMAN, PS TI GRIEF AND DEPRESSION IN NEWLY WIDOWED PARENTS WITH SCHOOL-AGE-CHILDREN SO OMEGA-JOURNAL OF DEATH AND DYING LA English DT Article ID SYMPTOMS AB The objectives of this study were to examine depression levels found in newly widowed parents with school age children and to distinguish bereavement dysphoria from clinical depression. A community based sample of seventy bereaved families with school-age children were assessed four months after the death and at the first anniversary. Parents were assessed with the CES-D depression scale [1], and the Impact of Events Scale [2], and the Family Inventory of Life Events [3]. The results indicate that 56 percent of the parents had high CES-D scores (> 16) at four months and 44 percent had high scores at one year. Early depression was a strong predictor of later depression. Higher depression levels were associated with more family life changes (FILE), limited income, lack of peer support, more younger children, and difficulty mobilizing support. Few parents with high CES-D scores selected the low self-esteem items suggesting more of a grief response than depression. Those who selected the low esteem items looked more clinically depressed than those who did not. In conclusion, it is important to distinguish between clinical depression and grief reactions since both share similar characteristics. This distinction is especially critical when planning appropriate interventions to assist the bereaved in coping with the loss. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WORDEN, JW (reprint author), MASSACHUSETTS GEN HOSP,CHILD BEREAVEMENT STUDY,BOSTON,MA 02114, USA. NR 27 TC 8 Z9 8 U1 1 U2 3 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0030-2228 J9 OMEGA-J DEATH DYING JI Omega-J. Death Dying PY 1993 VL 27 IS 3 BP 251 EP 261 PG 11 WC Psychology, Multidisciplinary; Social Sciences, Biomedical SC Psychology; Biomedical Social Sciences GA LX934 UT WOS:A1993LX93400005 ER PT J AU SNIJDERS, AJ HAASE, VH BERNARDS, A AF SNIJDERS, AJ HAASE, VH BERNARDS, A TI 4 TISSUE-SPECIFIC MOUSE LTK MESSENGER-RNAS PREDICT TYROSINE KINASES THAT DIFFER UPSTREAM OF THEIR TRANSMEMBRANE SEGMENT SO ONCOGENE LA English DT Article ID ENDOPLASMIC-RETICULUM; PROTEIN; RETENTION; GENE; GLYCOPROTEIN; SIGNAL; ER; IDENTIFICATION; EXPRESSION; TRANSPORT AB Two alternatively spliced mouse lymphocyte and brain ltk cDNAs predict small transmembrane tyrosine kinases that use CUG translational start codons and that differ upstream of their transmembrane segment. A recently isolated human neuroblastoma ltk cDNA, in contrast, includes a regular AUG start codon and predicts a more conventional receptor kinase with a larger N-terminal segment. This raised the suggestion that previous mouse cDNAs may have been aberrantly spliced or incomplete and questioned the significance of a recent study that localized the lymphoid ltk protein to the endoplasmic reticulum. Here we show that mice tissue-specifically express four ltk mRNAs. In addition to the two previously described lymphoid and brain mRNAs, we now describe two mRNAs from C1300 neuroblastoma cells that start with five exons which are absent from lymphoid or brain transcripts. The pair of C1300 mRNAs differ by the same alternatively spliced exon that distinguishes brain from lymphoid mRNAs and predict much larger receptor-type kinases that use regular AUG start codons. Our results also show that at least one of the larger, more conventional C1300 ltk receptors shares the endoplasmic reticulum localization of the shorter lymphoid protein. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC GENET LAB,BLDG 149,13TH ST,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Haase, Volker Hans/A-6758-2013 OI Haase, Volker Hans/0000-0002-7051-8994 NR 29 TC 15 Z9 18 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JAN PY 1993 VL 8 IS 1 BP 27 EP 35 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KN005 UT WOS:A1993KN00500004 PM 8380920 ER PT J AU MANOME, Y WEICHSELBAUM, RR KUFE, DW FINE, HA AF MANOME, Y WEICHSELBAUM, RR KUFE, DW FINE, HA TI EFFECT OF BCL-2 ON IONIZING-RADIATION AND 1-BETA-D-ARABINOFURANOSYLCYTOSINE-INDUCED INTERNUCLEOSOMAL DNA FRAGMENTATION AND CELL-SURVIVAL IN HUMAN MYELOID-LEUKEMIA CELLS SO ONCOLOGY RESEARCH LA English DT Article ID INDUCTION; APOPTOSIS; ELONGATION; TEMPLATE; DRUGS; DEATH; ACID AB 1-beta-D-Arabinofuranosylcytosine (ara-C) is an anti-leukemic agent that incorporates into cellular DNA leading to inhibition of DNA synthesis and loss of clonogenic survival. In contrast, ionizing radiation induces DNA damage through the generation of reactive oxygen intermediates. Although little is known of the specific determinants of ara-C and ionizing radiation-induced cytotoxicity, recent work has shown that both are capable of inducing internucleosomal DNA fragmentation in a pattern consistent with programmed cell death (apoptosis). In order to assess the importance of apoptosis in drug and ionizing radiation-induced cytotoxicity in the U-937 myelomonocytic cell line, we created cell lines that constitutively express a transfected bc1-2 gene. Bc1-2 was capable of inhibiting 40-50% of the ara-C and ionizing radiation-induced internucleosomal DNA fragmentation at all tested concentrations. However, cell survival following exposure to these agents was only increased in the bc1-2 transfectants at relatively low doses of ara-C and ionizing radiation. These data demonstrate that although bc1-2 is capable of inhibiting ara-C and ionizing radiation-induced DNA fragmentation in myeloid cells, it increases cell survival only at low doses of these agents. This suggests that apoptosis may be a less important mechanism of cytotoxicity at higher doses of ara-C and ionizing radiation than it is at lower doses. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. FU NCI NIH HHS [CA-55241, CA-29431] NR 15 TC 28 Z9 29 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0965-0407 J9 ONCOL RES JI Oncol. Res. PY 1993 VL 5 IS 3 BP 139 EP 144 PG 6 WC Oncology SC Oncology GA MB031 UT WOS:A1993MB03100005 PM 8260751 ER PT J AU MILLER, JW STINSON, WG FOLKMAN, J AF MILLER, JW STINSON, WG FOLKMAN, J TI REGRESSION OF EXPERIMENTAL IRIS NEOVASCULARIZATION WITH SYSTEMIC ALPHA-INTERFERON SO OPHTHALMOLOGY LA English DT Article ID RETINAL VEIN OCCLUSION; INHIBITION; ANGIOGENESIS; CELLS AB Background: Intraocular neovascularization leads to visual loss in many eye diseases, including diabetic retinopathy, age-related macular degeneration, and neovascular glaucoma. Current treatment relies on laser photocoagulation, involving the destruction of functional retinal tissue. A pharmacologic treatment directed at the newly growing vessels would represent a major advance. Methods: The authors investigated the effect of systemic alpha-interferon in an experimental model of iris neovascularization in cynomolgus monkeys. Alpha-interferon was administered systemically to animals with angiographically documented iris neovascularization. Results: Animals in the treatment group showed regression of neovascularization angiographically and histologically in eight of eight eyes. Control animals with documented iris neovascularization, followed without drug treatment, showed progression of the neovascularization in three of three eyes. Conclusion: Systemic alpha-interferon led to inhibition of neovascularization and regression of new vessels in an experimental model of iris neovascularization. This represents the first successful, controlled treatment of experimental neovascularization in the eye using a systemic drug directed specifically at the neovascular tissue. C1 HARVARD UNIV,SCH MED,CRIMINAL JUSTICE,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CHILDRENS HOSP,DEPT ANAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115. NR 18 TC 77 Z9 81 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 JAN PY 1993 VL 100 IS 1 BP 9 EP 14 PG 6 WC Ophthalmology SC Ophthalmology GA KJ661 UT WOS:A1993KJ66100014 PM 7679482 ER PT J AU TO, KW ADAMIAN, M JAKOBIEC, FA BERSON, EL AF TO, KW ADAMIAN, M JAKOBIEC, FA BERSON, EL TI OLIVOPONTOCEREBELLAR ATROPHY WITH RETINAL DEGENERATION - AN ELECTRORETINOGRAPHIC AND HISTOPATHOLOGIC INVESTIGATION SO OPHTHALMOLOGY LA English DT Article ID PIGMENT EPITHELIUM; RAT AB Background: Olivopontocerebellar atrophy is an uncommon disorder with variable clinical manifestations that affects the cerebellum, the spinocerebellar tracts, and other structures of the brainstem. A deficiency of glutamate dehydrogenase, which results in an excess of glutamate, has been suggested to play a role in the pathogenesis of olivopontocerebellar atrophy. In experimental animals, toxic levels of glutamate are known to cause a selective loss of the b-wave on electroretinographic (ERG) testing and a degeneration of the inner retinal layers. One of the subtypes of olivopontocerebellar atrophy, type II, according to Harding's classification, is associated with retinal degeneration. Methods: The authors describe the ophthalmologic and ERG findings in a family with olivopontocerebellar atrophy type II. Histopathologic study of an eye from a 6-year-old family member who died of severe neurologic deterioration secondary to olivopontocerebellar atrophy type II was performed. Results: Electroretinographic changes may be present in affected family members who are entirely asymptomatic and have a normal ophthalmologic evaluation. The changes on the ERG in one patient suggest that cone dysfunction is one of the subtle changes that may be seen in olivopontocerebellar atrophy type II. Our ERG results did not show a selective loss of the b-wave but instead showed a loss of both the a-wave and b-wave in affected family members. Results of light and electron microscopic examination showed diff use and extensive degeneration of the photoreceptors involving both rods and cones, the most prominent changes being present in the macula. An amorphous debris, presumably degenerated photoreceptors, was noted between the outer nuclear layer and retinal pigment epithelium. Conclusion: Patients with olivopontocerebellar atrophy type II have photoreceptor abnormalities as revealed in abnormal ERGs seen in many patients and histopathologic study of an autopsy eye from an affected 6-year-old boy. Our results do not support the hypothesis that glutamate toxicity may be responsible for the development of retinal degeneration in this condition. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,OPHTHALM PATHOL SERV,BOSTON,MA 02114. RP TO, KW (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114, USA. FU NEI NIH HHS [EYO2104] NR 19 TC 25 Z9 25 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 JAN PY 1993 VL 100 IS 1 BP 15 EP 23 PG 9 WC Ophthalmology SC Ophthalmology GA KJ661 UT WOS:A1993KJ66100015 PM 8433819 ER PT J AU WEINBERG, DV EGAN, KM SEDDON, JM AF WEINBERG, DV EGAN, KM SEDDON, JM TI ASYMMETRIC DISTRIBUTION OF ARTERIOVENOUS CROSSINGS IN THE NORMAL RETINA SO OPHTHALMOLOGY LA English DT Article ID VEIN OCCLUSION AB Background: Recently, there has been renewed interest in the orientation of the crossing retinal vessels at arteriovenous intersections, particularly as it relates to the risk of branch vein occlusion. Little is known about the distribution of the two types of crossings in the normal retina. Methods: The authors studied standard fundus photographs of 51 subjects without retinal disease. Arteriovenous crossings were analyzed for fundus location and relative orientation of the crossing vessels (vein-posterior- or vein-anterior). Findings: In the superotemporal quadrant, crossings were distributed closer to the optic disc (P < 0.001), and a greater proportion of crossings were vein-posterior (P = 0.01) than in the inferotemporal quadrant. As a result, within a 3-disc diameter (DD) radius of the optic disc, there were significantly more vein-posterior crossings in the superotemporal than in the inferotemporal quadrant (P < 0.001). Conclusion: These findings further define normal retinal vascular anatomy and may explain the predilection for branch retinal vein occlusions to occur in the superotemporal quadrant. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RETINA SERV,BOSTON,MA 02114. RP WEINBERG, DV (reprint author), NORTHWESTERN UNIV,SCH MED,DEPT OPHTHALMOL,WARD 2-186,303 E CHICAGO AVE,CHICAGO,IL 60611, USA. OI Weinberg, David/0000-0002-1974-9252 NR 8 TC 14 Z9 14 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 JAN PY 1993 VL 100 IS 1 BP 31 EP 36 PG 6 WC Ophthalmology SC Ophthalmology GA KJ661 UT WOS:A1993KJ66100017 PM 8433824 ER PT J AU FISH, DN GOULET, JA STEVENSON, T AF FISH, DN GOULET, JA STEVENSON, T TI CHRONIC OSTEOMYELITIS OF THE CALCANEUS - TREATMENT WITH A VASCULARIZED MUSCLE FLAP SO ORTHOPEDICS LA English DT Article RP FISH, DN (reprint author), MASSACHUSETTS GEN HOSP,ACC 514,BOSTON,MA 02114, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0147-7447 J9 ORTHOPEDICS JI Orthopedics PD JAN PY 1993 VL 16 IS 1 BP 81 EP 85 PG 5 WC Orthopedics SC Orthopedics GA KG022 UT WOS:A1993KG02200010 PM 8421664 ER PT J AU NEER, M SLOVIK, DM DALY, M POTTS, T NUSSBAUM, SR AF NEER, M SLOVIK, DM DALY, M POTTS, T NUSSBAUM, SR TI TREATMENT OF POSTMENOPAUSAL OSTEOPOROSIS WITH DAILY PARATHYROID-HORMONE PLUS CALCITRIOL SO OSTEOPOROSIS INTERNATIONAL LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON OSTEOPOROSIS CY NOV 05-07, 1991 CL KOBE, JAPAN ID TRABECULAR BONE; FRAGMENT; MASS RP NEER, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114, USA. NR 11 TC 9 Z9 9 U1 0 U2 0 PU SPRINGER-VERLAG LONDON LTD PI GODALMING PA SWEETAPPLE HOUSE CATTESHALL ROAD, GODALMING, SURREY, ENGLAND GU7 3DJ SN 0937-941X J9 OSTEOPOROSIS INT JI Osteoporosis Int. PY 1993 VL 3 SU 1 BP S204 EP S205 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KP881 UT WOS:A1993KP88100057 ER PT J AU KAWANISHI, DT SONG, SL FURMAN, S GROSS, J FRAME, R JOHNSTON, D PARSONNET, V ROTHBART, ST ZIMMERMAN, J WIDERHORN, J HASHIMOTO, KK BUCKINGHAM, TA GOLDIN, MD WIMER, EA DENKER, ST LIPTON, IH MALONEY, JD CASTLE, LW HARTHORNE, JW RUSKIN, JN GARAN, H MCGOVERN, BA GRIFFIN, JC SCHEINMAN, MM LESH, MD DORIAN, P NEWMAN, D DENES, P DAHL, W SAKSENA, S KROL, RB FOGOROS, RN AF KAWANISHI, DT SONG, SL FURMAN, S GROSS, J FRAME, R JOHNSTON, D PARSONNET, V ROTHBART, ST ZIMMERMAN, J WIDERHORN, J HASHIMOTO, KK BUCKINGHAM, TA GOLDIN, MD WIMER, EA DENKER, ST LIPTON, IH MALONEY, JD CASTLE, LW HARTHORNE, JW RUSKIN, JN GARAN, H MCGOVERN, BA GRIFFIN, JC SCHEINMAN, MM LESH, MD DORIAN, P NEWMAN, D DENES, P DAHL, W SAKSENA, S KROL, RB FOGOROS, RN TI CLINICAL OUTCOME FOLLOWING ICD REMOVAL SO PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY LA English DT Article; Proceedings Paper CT CARDIOSTIM 92 : CARDIAC PACING AND ELECTROPHYSIOLOGY CY JUN 17-20, 1992 CL NICE, FRANCE DE IMPLANTABLE CARDIOVERTER DEFIBRILLATOR; REMOVALS; SURVIVAL ID IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR; COMPLICATIONS; EXPERIENCE; SURVIVAL; EFFICACY AB The Bilitch ICD Registry includes 1,869 patients from 13 medical centers enrolled between March 1982 and April 1992. Of these, 95 patients had their units removed and not immediately replaced (77 males/18 females mean age 54.9 +/- 13.0 years, range 10-76). The mean duration of implanted ICD was 19.5 +/- 18.2 months, mean ejection fraction 30.1 +/- 11.7%. Coronary artery disease was present in 55 patients, absent in 30, and unknown in 10. The presenting clinical event was sudden death in 35 patients, symptomatic ventricular tachycardia in 34, other causes in 6, and unknown in 20. Reasons for ICD removal were: infection in 33 patients, cardiac transplant in 32, elective in 20, following battery depletion in 7, lead system failure in 2, and inappropriate shock in 1. Of all groups who had their ICD removed, the patients who had removal for cardiac transplantation had the highest incidence of appropriate ICD discharges while the device was implanted (43.8%). Of the 63 nontransplanted patients seven were lost to follow-up while alive. Of the 56 remaining, 17 died (1 cause unknown, 6 noncardiac, 3 sudden, 1 arrhythmic, 6 nonsudden nonarrhythmic cardiac death), 7 had an ICD reimplanted, and 32 are alive and well without an ICD. Follow-up for the 32 cardiac transplant patients: 2 were lost to follow-up while alive, 2 died of nonsudden nonarrhythmic death, and 28 are alive and well. The survival of patients who had their ICD removed and not reimplanted was not different from that of patients who never had their ICD removed up to 2 years. Thereafter, the survival without a device fell below that of those who never had their device removed. Summary: There is a high incidence of ICD discharges in the group undergoing ICD removal for cardiac transplantation. The most common cause of ICD removal was infection. The need for device reimplantation increases at 2 years following device removal. The ''elective'' device reimplantation does not compromise overall survival. C1 MONTEFIORE MED CTR,DEPT MED & SURG,BRONX,NY 10467. PACEMAKER CTR INC,NEWARK BETH ISRAEL MED CTR,NEWARK,NJ. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. ST LUKES HOSP,MILWAUKEE,WI 53215. TORONTO HOSP,TORONTO,ON,CANADA. CLEVELAND CLIN EDUC FDN,CLEVELAND,OH 44106. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,MOFFITT HOSP,SAN FRANCISCO,CA 94120. ST MICHAELS HOSP,TORONTO M5B 1W8,ONTARIO,CANADA. ST PAUL RAMSEY MED CTR,ST PAUL,MN 55101. EASTERN HEART INST,PASSAIC,NJ. ALLEGHENY GEN HOSP,PITTSBURGH,PA 15212. RP KAWANISHI, DT (reprint author), UNIV SO CALIF,SCH MED,CTR PACEMAKER,1355 SAN PABIO ST,1ST FLOOR,LOS ANGELES,CA 90033, USA. NR 10 TC 8 Z9 8 U1 1 U2 1 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 0147-8389 J9 PACE JI PACE-Pacing Clin. Electrophysiol. PD JAN PY 1993 VL 16 IS 1 BP 186 EP 192 DI 10.1111/j.1540-8159.1993.tb01559.x PN 2 PG 7 WC Cardiac & Cardiovascular Systems; Engineering, Biomedical SC Cardiovascular System & Cardiology; Engineering GA KJ384 UT WOS:A1993KJ38400011 PM 7681569 ER PT B AU COLE, DG AF COLE, DG BE Narabayashi, H Nagatsu, T Yanagisawa, N Mizuno, Y TI DOPAMINERGIC ACTIVATION OF FOS AND THE RAT MODEL OF PARKINSONS-DISEASE SO PARKINSONS DISEASE : FROM BASIC RESEARCH TO TREATMENT SE ADVANCES IN NEUROLOGY LA English DT Proceedings Paper CT 10TH INTERNATIONAL SYMP ON PARKINSONS DISEASE CY OCT 27-30, 1991 CL TOKYO, JAPAN SP WORLD FEDERAT NEUROL, RES COMM EXTRAPYRAMIDAL DIS, JAPAN INTRACTABLE DIS RES FDN RP COLE, DG (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-967-4 J9 ADV NEUROL JI Adv.Neurol. PY 1993 VL 60 BP 334 EP 337 PG 4 WC Biochemistry & Molecular Biology; Clinical Neurology; Pathology; Physiology SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pathology; Physiology GA BX37W UT WOS:A1993BX37W00050 PM 8380526 ER PT S AU RUPRECHT, RM FRATAZZI, C SHARMA, PL GREENE, MF PENNINCK, D WYAND, M AF RUPRECHT, RM FRATAZZI, C SHARMA, PL GREENE, MF PENNINCK, D WYAND, M BE Lyman, WD Rubinstein, A TI ANIMAL-MODELS FOR PERINATAL TRANSMISSION OF PATHOGENIC VIRUSES SO PEDIATRIC AIDS: CLINICAL, PATHOLOGIC, AND BASIC SCIENCE PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Pediatric Aids: Clinical, Pathologic, and Basic Science Perspectives CY NOV 18-21, 1992 CL WASHINGTON, DC SP NEW YORK ACAD SCI ID MOLONEY LEUKEMIA-VIRUS; SIMIAN IMMUNODEFICIENCY VIRUS; MATERNAL TRANSMISSION; RETROVIRAL DISEASE; GERM LINE; SPONGIFORM POLIOENCEPHALOMYELOPATHY; ANTIRETROVIRAL THERAPY; HIV-1 INFECTION; TRANSGENIC MICE; RHESUS-MONKEYS C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. TUFTS UNIV,SCH VET MED,DEPT SURG,N GRAFTON,MA 01536. TSI,MASON LABS,WORCESTER,MA 01608. RP RUPRECHT, RM (reprint author), DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [N01-AI-72664, R01-AI-32330, R01-AI25715] NR 43 TC 4 Z9 4 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-791-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 693 BP 213 EP 228 DI 10.1111/j.1749-6632.1993.tb26270.x PG 16 WC Immunology; Multidisciplinary Sciences; Pathology; Pediatrics; Virology SC Immunology; Science & Technology - Other Topics; Pathology; Pediatrics; Virology GA BZ45X UT WOS:A1993BZ45X00021 PM 8267266 ER PT J AU SHERIDAN, RL SHERIDAN, MG TOMPKINS, RG AF SHERIDAN, RL SHERIDAN, MG TOMPKINS, RG TI DISHWASHER EFFLUENT BURNS IN INFANTS SO PEDIATRICS LA English DT Note ID WATER SCALD BURNS; TAP WATER; PREVENTION; CHILDREN C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. SHRINERS BURN INST,BOSTON,MA. RP SHERIDAN, RL (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 16 TC 0 Z9 0 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JAN PY 1993 VL 91 IS 1 BP 142 EP 144 PG 3 WC Pediatrics SC Pediatrics GA KF835 UT WOS:A1993KF83500025 PM 8416479 ER PT J AU ROMERO, R KLEINMAN, RE AF ROMERO, R KLEINMAN, RE TI THROMBOCYTOPENIA ASSOCIATED WITH ACUTE HEPATITIS-B INFECTION SO PEDIATRICS LA English DT Note RP ROMERO, R (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,BOSTON,MA 02115, USA. NR 11 TC 8 Z9 9 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JAN PY 1993 VL 91 IS 1 BP 150 EP 152 PG 3 WC Pediatrics SC Pediatrics GA KF835 UT WOS:A1993KF83500030 PM 8416484 ER PT J AU PERRIN, JM STEIN, REK AF PERRIN, JM STEIN, REK TI SSI BENEFITS AND FUNCTIONAL ASSESSMENT - REPLY SO PEDIATRICS LA English DT Letter C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. RP PERRIN, JM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JAN PY 1993 VL 91 IS 1 BP 162 EP 163 PG 2 WC Pediatrics SC Pediatrics GA KF835 UT WOS:A1993KF83500041 ER PT J AU AOBA, T AF AOBA, T TI FORMATION OF CALCIUM PHOSPHATES IN DEVELOPING ENAMEL AS MODEL OF BIOMINERALIZATION SO PHOSPHORUS SULFUR AND SILICON AND THE RELATED ELEMENTS LA English DT Article; Proceedings Paper CT 12TH INTERNATIONAL CONF ON PHOSPHORUS CHEMISTRY CY JUL 06-10, 1992 CL TOULOUSE, FRANCE SP CNRS, MINIST AFFAIRES ETRANGERES FRANCE, MINIST EDUC NATL FRANCE, MINIST RECH & ESPACE FRANCE, CHAMBRE COMMERCE & IND TOULOUSE, CONSEIL REG MIDI PYRENEES, DIRECT REG RECH & TECHNOL MIDI PYRENEES, CNRS, LAB CHIM COORDINAT, MAIRIE TOULOUSE, TECHNOPOLE AGGLOMERAT TOULOUSE ID PORCINE AMELOGENESIS AB The stoichiometry and solubility of tooth enamel mineral at various developmental stages were determined on the basis of the model taking into account most putative ionic species occupying lattice positions. The enamel mineral, in common with other biominerals, is most adequately described as (Mg, Na)-containing calcium carbonatoapatites. An important finding was that changes in the stoichiometry and solubility of the enamel mineral take place with tissue development, suggesting that the nature and properties of the biomineral are modified markedly by possible changes in the microenvironments where the precipitation occurs. RP AOBA, T (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. NR 7 TC 1 Z9 1 U1 0 U2 2 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0308-664X J9 PHOSPHORUS SULFUR JI Phosphorus Sulfur Silicon Relat. Elem. PY 1993 VL 76 IS 1-4 BP 545 EP 548 PG 4 WC Chemistry, Inorganic & Nuclear; Chemistry, Organic SC Chemistry GA LZ880 UT WOS:A1993LZ88000073 ER PT J AU MAY, JW AF MAY, JW TI EXTRACORPOREAL-CIRCULATION FOR TISSUE-TRANSPLANTATION (IN THE CASE OF VENOUS FLAPS) - DISCUSSION SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Discussion RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,DIV PLAST & RECONSTRUCT SURG,LEVEL 4,SUITE 453,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD JAN PY 1993 VL 91 IS 1 BP 125 EP 126 PG 2 WC Surgery SC Surgery GA KE189 UT WOS:A1993KE18900018 ER PT J AU CASTILLO, L DEROJAS, TC CHAPMAN, TE VOGT, J BURKE, JF TANNENBAUM, SR YOUNG, VR AF CASTILLO, L DEROJAS, TC CHAPMAN, TE VOGT, J BURKE, JF TANNENBAUM, SR YOUNG, VR TI SPLANCHNIC METABOLISM OF DIETARY ARGININE IN RELATION TO NITRIC-OXIDE SYNTHESIS IN NORMAL ADULT MAN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE NITRATE; METABOLISM; DIET ID MAMMALIAN NITRATE BIOSYNTHESIS; GAS-CHROMATOGRAPHY; BIOLOGICAL-FLUIDS; MASS-SPECTROMETRY; AMINO-ACIDS; DERIVATIVES; RELEVANCE; NITROSAMINES; INTERMEDIATE; PHYSIOLOGY AB Urinary nitrate (NO3) is the stable end product of nitric oxide, which is formed, in turn, from a guanidino nitrogen of arginine. We have conducted two experiments, each in four healthy adult men receiving a low nitrate diet for 7-10 days, to investigate the in vivo conversion of arginine to nitrate. In the first study [guanidino-N-15(2) 5,5-H-2(2)]arginine was given on day 7 via a primed continuous intravenous infusion for 8 h. In the second study, the labeled arginine was given for 8 h by the intragastric route on day 7 and by the intravenous route on day 10. Measurement of (NO3)-N-15 output in urine collected for 24 h beginning at the time of the arginine tracer infusion revealed a more extensive transfer of N-15 when the arginine tracer was given intragastricly. From the comparative labeling of (NO3)-N-15 after administration of the tracer arginine via the intragastric and intravenous routes, we estimate that 16% +/- 2% of the daily production of nitrate arises from the metabolism of dietary arginine that is taken up during its ''first pass'' in the splanchnic region. Hence, nitric oxide production occurs, to a measurable extent, in this area in healthy subjects, raising the question as to how various pathophysiological states might alter the relations between exogenous and endogenous sources of arginine as precursors of NO. and the relative contributions made by various organs to whole body (NO.) NO3 formation. These results also raise important questions about the use of nitric oxide synthase inhibitors in animal and human studies. C1 MIT,CLIN RES CTR,HUMAN NUTR LAB,ROOM E18-613,CAMBRIDGE,MA 02139. MIT,DIV TOXICOL,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. FU NIDDK NIH HHS [DK 15856]; NIEHS NIH HHS [P30 ES002109, P30-ES02109]; NIGMS NIH HHS [GM02700 P01-CA26731] NR 39 TC 109 Z9 112 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 JAN 1 PY 1993 VL 90 IS 1 BP 193 EP 197 DI 10.1073/pnas.90.1.193 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KF407 UT WOS:A1993KF40700040 PM 8419922 ER PT J AU ABE, M KUFE, D AF ABE, M KUFE, D TI CHARACTERIZATION OF CIS-ACTING ELEMENTS REGULATING TRANSCRIPTION OF THE HUMAN DF3 BREAST CARCINOMA-ASSOCIATED ANTIGEN (MUC1) GENE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID EPITHELIAL TUMOR-ANTIGEN; MONOCLONAL-ANTIBODY DF3; CARCINOEMBRYONIC ANTIGEN; SEQUENCE-ANALYSIS; TANDEM REPEATS; LOCUS PUM; PROTEIN; CDNA; EXPRESSION; CLONING AB The present studies have examined the sequences responsible for regulating transcription of the human DF3 breast carcinoma-associated antigen (MUC1) gene. A region 1656 base pairs upstream to the DF3 transcription initiation site was fused to the chloramphenical acetyltransferase gene. Transient expression assays using a series of deleted constructs demonstrated that the region from position -618 contains the regulatory sequences necessary for DF3 transcription in human MCF-7 breast cancer cells. Further analysis with internal deletion vectors and heterologous promoter constructs indicated the involvement of cis-acting elements in the fragment extending from positions -598 to -485. By gel retardation and DNA footprinting, we have identified a protein in MCF-7 cells that recognizes sequences between positions -505 and -485. The results of Southwestern studies demonstrate that this protein has an apparent molecular mass of 45 kDa. Taken together, these results suggest that DF3 gene transcription is regulated by a previously undescribed transacting factor. RP ABE, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA38879] NR 41 TC 104 Z9 105 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 JAN 1 PY 1993 VL 90 IS 1 BP 282 EP 286 DI 10.1073/pnas.90.1.282 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KF407 UT WOS:A1993KF40700058 PM 8419933 ER PT J AU ABRAHAM, EH PRAT, AG GERWECK, L SENEVERATNE, T ARCECI, RJ KRAMER, R GUIDOTTI, G CANTIELLO, HF AF ABRAHAM, EH PRAT, AG GERWECK, L SENEVERATNE, T ARCECI, RJ KRAMER, R GUIDOTTI, G CANTIELLO, HF TI THE MULTIDRUG RESISTANCE (MDR1) GENE-PRODUCT FUNCTIONS AS AN ATP CHANNEL SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID BACTERIAL TRANSPORT PROTEINS; P-GLYCOPROTEIN EXPRESSION; PLASMA-MEMBRANE; TUMOR-CELLS; CYCLIC-AMP; ECTO-ATPASE; BINDING; VESICLES; TISSUES; CDNA AB The multidrug resistance (mdr1) gene product, P-glycoprotein, is responsible for the ATP-dependent extrusion of a variety of compounds, including chemotherapeutic drugs, from cells. The data presented here show that cells with increased levels of the P-glycoprotein release ATP to the medium in proportion to the concentration of the protein in their plasma membrane. Furthermore, measurements of whole-cell and single-channel currents with patch-clamp electrodes indicate that the P-glycoprotein serves as an ATP-conducting channel in the plasma membrane. These findings suggest an unusual role for the P-glycoprotein. C1 HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP ABRAHAM, EH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA22860]; NHLBI NIH HHS [HL08893] NR 53 TC 347 Z9 350 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 1 PY 1993 VL 90 IS 1 BP 312 EP 316 DI 10.1073/pnas.90.1.312 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KF407 UT WOS:A1993KF40700064 PM 7678345 ER PT J AU SCREMIN, OU JENDEN, DJ AF SCREMIN, OU JENDEN, DJ TI ACETYLCHOLINE TURNOVER AND RELEASE - THE INFLUENCE OF ENERGY-METABOLISM AND SYSTEMIC CHOLINE AVAILABILITY SO PROGRESS IN BRAIN RESEARCH LA English DT Review ID PLASMA CHOLINE; BRAIN CHOLINE; CEREBROSPINAL-FLUID; RAT-BRAIN; ISCHEMIA; TRANSPORT; NEURONS; EXCHANGE; OUTPUT; RABBIT C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT PHYSIOL, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PHARMACOL, LOS ANGELES, CA 90024 USA. RP SCREMIN, OU (reprint author), UNIV CALIF LOS ANGELES, W LOS ANGELES VET ADM MED CTR, SCH MED, LOS ANGELES, CA 90024 USA. NR 34 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 J9 PROG BRAIN RES JI Prog. Brain Res. PY 1993 VL 98 BP 191 EP 195 PG 5 WC Neurosciences SC Neurosciences & Neurology GA MA269 UT WOS:A1993MA26900024 ER PT S AU KRONENBERG, HM JUPPNER, H ABOUSAMRA, AB POTTS, JT SEGRE, G AF KRONENBERG, HM JUPPNER, H ABOUSAMRA, AB POTTS, JT SEGRE, G BE Mornex, R Jaffiol, C Leclere, J TI A COMMON RECEPTOR FOR PARATHYROID-HORMONE AND PARATHYROID HORMONE-LIKE PEPTIDE SO PROGRESS IN ENDOCRINOLOGY SE INTERNATIONAL CONGRESS, SYMPOSIUM AND SEMINAR SERIES LA English DT Proceedings Paper CT 9th International Congress of Endocrinology: Progress in Endocrinology CY SEP, 1992 CL NICE, FRANCE C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA SN 0969-2622 BN 1-85070-469-4 J9 I C S S PY 1993 VL 3 BP 357 EP 359 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA12S UT WOS:A1993BA12S00081 ER PT S AU ALEXANDERBRIDGES, M JHALA, U GARCIAJIMENEZ, C ZHAO, HF NIU, S BUGGS, C NIU, S AF ALEXANDERBRIDGES, M JHALA, U GARCIAJIMENEZ, C ZHAO, HF NIU, S BUGGS, C NIU, S BE Mornex, R Jaffiol, C Leclere, J TI IRE-ABP, A POTENTIAL REGULATOR OF THE SWITCH FROM THE FASTED TO THE RE-FED STATE SO PROGRESS IN ENDOCRINOLOGY SE INTERNATIONAL CONGRESS, SYMPOSIUM AND SEMINAR SERIES LA English DT Proceedings Paper CT 9th International Congress of Endocrinology: Progress in Endocrinology CY SEP, 1992 CL NICE, FRANCE C1 MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA SN 0969-2622 BN 1-85070-469-4 J9 I C S S PY 1993 VL 3 BP 783 EP 786 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA12S UT WOS:A1993BA12S00178 ER PT J AU HEYER, WD KOLODNER, RD AF HEYER, WD KOLODNER, RD TI ENZYMOLOGY OF HOMOLOGOUS RECOMBINATION IN SACCHAROMYCES-CEREVISIAE SO PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY, VOL 46 SE PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY LA English DT Review ID SINGLE-STRANDED-DNA; SITE-SPECIFIC ENDONUCLEASE; MEIOTIC GENE CONVERSION; CELL-FREE-EXTRACTS; EXCHANGE STIMULATORY FACTOR; CLEAVES HOLLIDAY JUNCTIONS; ENCODES THYMIDYLATE KINASE; HETERODUPLEX PLASMID DNA; YEAST MITOCHONDRIAL-DNA; TRANSFER PROTEIN-ALPHA C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. UNIV BERN,INST GEN MICROBIOL,CH-3012 BERN,SWITZERLAND. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NHGRI NIH HHS [HG00305]; NIGMS NIH HHS [GM29383] NR 212 TC 7 Z9 7 U1 1 U2 3 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0278-5846 J9 PROG NUCLEIC ACID RE PY 1993 VL 46 BP 221 EP 271 DI 10.1016/S0079-6603(08)61023-5 PG 51 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ69M UT WOS:A1993BZ69M00008 PM 8234785 ER PT J AU EDELBERG, JM LEE, YJ YOUNG, TN PIZZO, SV AF EDELBERG, JM LEE, YJ YOUNG, TN PIZZO, SV TI LIPOPROTEIN (A) - PURIFICATION AND KINETIC-ANALYSIS SO PROTEOLYTIC ENZYMES IN COAGULATION, FIBRINOLYSIS, AND COMPLEMENT ACTIVATION, PART B SE METHODS IN ENZYMOLOGY LA English DT Review ID CORONARY-ARTERY DISEASE; TISSUE PLASMINOGEN-ACTIVATOR; LOW-DENSITY-LIPOPROTEIN; LP(A) LIPOPROTEIN; HEART-DISEASE; APOLIPOPROTEIN(A); ATHEROSCLEROSIS; INHIBITION; HEPARIN; ALPHA-2-ANTIPLASMIN C1 DUKE UNIV,MED CTR,DEPT PATHOL,DURHAM,NC 27710. RP EDELBERG, JM (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114, USA. NR 49 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1993 VL 223 BP 272 EP 284 PG 13 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ58W UT WOS:A1993BZ58W00018 PM 8271958 ER PT J AU GUY, SM SMITH, GM BENTLER, PM AF GUY, SM SMITH, GM BENTLER, PM TI ADOLESCENT SOCIALIZATION AND USE OF LICIT AND ILLICIT SUBSTANCES - IMPACT ON ADULT HEALTH SO PSYCHOLOGY & HEALTH LA English DT Article DE ADOLESCENT-SUBSTANCE-USE; LOW-SOCIALIZATION; ADULT-HEALTH-OUTCOMES ID DRUG-USE; YOUNG ADULTHOOD; COVARIANCE-STRUCTURES; PERSONALITY STRUCTURE; SELF-REPORT; ALCOHOL; CONSEQUENCES; SCL-90; MODEL; VALIDATION AB This study examined the impact of adolescent substance use on young adult health. Longitudinal data from 825 participants were assessed when the participants were junior high school and high school students (1969-1973) and again in 1981. Latent variable models were used to determine what effect adolescent drug use had on later health. General substance use, which included tobacco, alcohol, stimulants, sedatives, and other hard drugs, had a small effect on adult health problems associated with substance use, and also predicted accidents related to substance use. In addition, the specific use of tobacco and cannabis in adolescence predicted later respiratory problems, while cigarette smoking during adolescence also predicted decreased physical hardiness. Lower adolescent socialization predicted post high school accidents (automobile and other) serious enough to require medical attention, and predicted increased psychosomatic and seizure symptoms, as well as general psychiatric distress. Implications of these results for the successful prevention or intervention of drug use are discussed. In addition to these results, gender differences are also examined. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP GUY, SM (reprint author), UNIV CALIF LOS ANGELES,DEPT PSYCHOL,LOS ANGELES,CA 90024, USA. NR 75 TC 9 Z9 9 U1 1 U2 3 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0887-0446 J9 PSYCHOL HEALTH JI Psychol. Health PY 1993 VL 8 IS 6 BP 463 EP 487 DI 10.1080/08870449308400449 PG 25 WC Public, Environmental & Occupational Health; Psychology, Multidisciplinary SC Public, Environmental & Occupational Health; Psychology GA MK870 UT WOS:A1993MK87000006 ER PT J AU KAHN, RS DAVIDSON, M AF KAHN, RS DAVIDSON, M TI SEROTONIN, DOPAMINE AND THEIR INTERACTIONS IN SCHIZOPHRENIA - AN EDITORIAL SO PSYCHOPHARMACOLOGY LA English DT Editorial Material ID CLOZAPINE; RECEPTORS RP KAHN, RS (reprint author), BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,13W KINGSBRIDGE RD,NEW YORK,NY 10468, USA. NR 17 TC 33 Z9 33 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PY 1993 VL 112 IS 1 SU S BP S1 EP S4 DI 10.1007/BF02245002 PG 4 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV406 UT WOS:A1993LV40600001 PM 7831437 ER PT J AU KAHN, RS SIEVER, L DAVIDSON, M GREENWALD, C MOORE, C AF KAHN, RS SIEVER, L DAVIDSON, M GREENWALD, C MOORE, C TI HALOPERIDOL AND CLOZAPINE TREATMENT AND THEIR EFFECT ON M-CHLOROPHENYLPIPERAZINE-MEDIATED RESPONSES IN SCHIZOPHRENIA - IMPLICATIONS FOR THE MECHANISM OF ACTION OF CLOZAPINE SO PSYCHOPHARMACOLOGY LA English DT Article DE CLOZAPINE; HALOPERIDOL; SCHIZOPHRENIA; M-CHLOROPHENYLPIPERAZINE ID META-CHLOROPHENYLPIPERAZINE; RAT-BRAIN; SEROTONIN FUNCTION; RECEPTORS; DOPAMINE; D2; CHLORPROMAZINE; ANTAGONISTS; RITANSERIN; SITES AB Since clozapine is, in contrast to conventional neuroleptics, effective in treatment refractory schizophrenic patients its mechanism of action may be different from that of typical neuroleptics. Clozapine has been shown to display the highest binding affinity of all neuroleptics to one of the serotonin (5-hydroxytryptamine, 5HT) receptor subtypes, i.e., the 5HT1c receptor. Furthermore, clozapine, in contrast to conventional neuroleptics, blocks the effect of 5HT agonists on ACTH and corticosterone release in animals. This study hypothesized that clozapine, but not haloperidol would block ACTH and prolactin release induced by the 5HT agonist, m-chlorophenylpiperazine (MCPP). MCPP (0.35 mg/kg PO) was administered after a 3-week drug-free period, after 5 weeks of haloperidol treatment (20 mg/day) and finally after 5 weeks of clozapine treatment (> 400 mg/day) in ten male schizophrenic patients. Clozapine, but not haloperidol, blocked the effect of MCPP on ACTH and prolactin release. These results suggest that clozapine, in contrast to haloperidol, is a functional 5HT antagonist. Since MCPP-induced ACTH and prolactin release may be (partially) 5HT1c mediated, these results suggest that clozapine is a potent antagonist at the 5HT1c receptor. RP KAHN, RS (reprint author), BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,130 W KINGSBRIDGE RD,NEW YORK,NY 10468, USA. NR 28 TC 27 Z9 27 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PY 1993 VL 112 IS 1 SU S BP S90 EP S94 DI 10.1007/BF02245012 PG 5 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV406 UT WOS:A1993LV40600011 PM 7831445 ER PT J AU HERZOG, DB SACKS, NR AF HERZOG, DB SACKS, NR TI BULIMIA-NERVOSA - COMPARISON OF TREATMENT RESPONDERS VS NONRESPONDERS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 32ND ANNUAL MEETING OF THE NEW CLINICAL DRUG EVALUATION UNIT CY MAY 26-29, 1992 CL BOCA RATON, FL SP NEW CLIN DRUG EVALUAT UNIT, NIMH, DIV CLIN & TREATMENT RES AB Though psychosocial and psychopharmacological treatments are effective in reducing bulimic symptomatology, bulimic patients often have unremitting behaviors and frequently relapse. The authors sought to identify factors that differentiate bulimic patients who improve while receiving treatment from those who do not. Ninety-eight treatment-seeking bulimic patients were studied as part of a prospective, naturalistic, longitudinal study of eating disorders. Bulimic patients who had drug treatment within the first 13 weeks were more likely to demonstrate sustained recovery over the course of the first year than those who did not have pharmacotherapy. This study suggests that drug therapy may have a differential effect on the outcome of bulimia nervosa; further study is necessary, however, to ascertain the presence of selection bias. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. RP HERZOG, DB (reprint author), MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,ACC 725,15 PARKMAN ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH-38333] NR 12 TC 8 Z9 8 U1 0 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 1 BP 121 EP 125 PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LN223 UT WOS:A1993LN22300016 PM 8378505 ER PT J AU JENIKE, MA AF JENIKE, MA TI OBSESSIVE-COMPULSIVE DISORDER - EFFICACY OF SPECIFIC TREATMENTS AS ASSESSED BY CONTROLLED TRIALS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article ID PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; CLOMIPRAMINE TREATMENT; BEHAVIORAL TREATMENT; RESPONSE PREVENTION; FOLLOW-UP; EXPOSURE; FLUVOXAMINE; NEUROSIS; RITUALS C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 63 TC 37 Z9 37 U1 0 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 4 BP 487 EP 499 PG 13 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA NV126 UT WOS:A1993NV12600006 PM 8084980 ER PT J AU STERN, TA PRAGER, LM CREMENS, MC AF STERN, TA PRAGER, LM CREMENS, MC TI AUTOGNOSIS ROUNDS FOR MEDICAL HOUSE STAFF SO PSYCHOSOMATICS LA English DT Article ID PATIENT; SUPPORT; RESIDENCY; CARE AB The authors describe the autognosis countertransference rounds for medical house staff at the Massachusetts General Hospital. At these rounds, which have been held weekly for more than a decade in the intensive care unit, countertransference phenomena and their relationship to medical practice are discussed. Methods that have facilitated the autognostic process are provided and highlighted by brief case examples. Participants at these rounds report that their self-awareness increases and the clinical care they provide often improves. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP STERN, TA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,WARREN 605,BOSTON,MA 02114, USA. NR 30 TC 16 Z9 16 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JAN-FEB PY 1993 VL 34 IS 1 BP 1 EP 7 PG 7 WC Psychiatry; Psychology SC Psychiatry; Psychology GA KF382 UT WOS:A1993KF38200001 PM 8426883 ER PT J AU RAUCH, SL JENIKE, MA AF RAUCH, SL JENIKE, MA TI NEUROBIOLOGICAL MODELS OF OBSESSIVE-COMPULSIVE DISORDER SO PSYCHOSOMATICS LA English DT Review ID GLUCOSE METABOLIC RATES; LA-TOURETTES SYNDROME; DOUBLE-BLIND; M-CHLOROPHENYLPIPERAZINE; CLOMIPRAMINE TREATMENT; SEROTONERGIC RESPONSIVITY; CONTROLLED TRIAL; HEALTHY-SUBJECTS; BASAL GANGLIA; FOLLOW-UP AB The authors review current neurobiological models of obsessive-compulsive disorder (OCD). The rationale for anatomically based models is outlined and selected brain regions of interest are discussed. The authors conclude that there is abundant evidence to implicate multiple brain regions as sites of abnormality in OCD. A review of neuropharmacological concepts related to the serotonergic (5-HT) hypothesis of OCD is also presented. The authors conclude that antiobsessional agents may well have therapeutic effects via the 5-HT system, yet there is little unequivocal evidence to suggest an underlying abnormality in the 5-HT system. A comprehensive neurobiological model of OCD must acknowledge the interrelationship between multiple transmitter systems and integrate anatomical with neuropharmacological concepts. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 104 TC 77 Z9 77 U1 3 U2 8 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JAN-FEB PY 1993 VL 34 IS 1 BP 20 EP 32 PG 13 WC Psychiatry; Psychology SC Psychiatry; Psychology GA KF382 UT WOS:A1993KF38200004 PM 8426888 ER PT J AU LEVITTE, SS AF LEVITTE, SS TI COEXISTENT HYPOMANIA AND SEVERE HYPOTHYROIDISM SO PSYCHOSOMATICS LA English DT Article ID BIPOLAR AFFECTIVE-DISORDER; THYROID-FUNCTION; LITHIUM; LEVOTHYROXINE C1 BAYLOR COLL MED,DEPT PSYCHIAT,HOUSTON,TX 77030. HOUSTON DEPT VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,HOUSTON,TX. NR 10 TC 7 Z9 8 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JAN-FEB PY 1993 VL 34 IS 1 BP 96 EP 97 PG 2 WC Psychiatry; Psychology SC Psychiatry; Psychology GA KF382 UT WOS:A1993KF38200014 PM 8426899 ER PT J AU LITTMAN, AB AF LITTMAN, AB TI REVIEW OF PSYCHOSOMATIC ASPECTS OF CARDIOVASCULAR-DISEASE SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Review DE CARDIOVASCULAR DISEASE; SMOKING; CHOLESTEROL; TYPE-A BEHAVIOR; DEPRESSIVE DISORDERS; ANXIETY DISORDERS; HOSTILITY; STRESS ID CORONARY-ARTERY DISEASE; A BEHAVIOR PATTERN; ACUTE MYOCARDIAL-INFARCTION; HEART-RATE-VARIABILITY; INDUCED ORTHOSTATIC HYPOTENSION; WESTERN COLLABORATIVE GROUP; TRICYCLIC ANTI-DEPRESSANTS; FACTOR INTERVENTION TRIAL; 25-YEAR FOLLOW-UP; MIDDLE-AGED MEN AB This review deals with the clinically most relevant psychosomatic aspects of cardiovascular disease. Smoking cessation, the role of physical activity in the prevention and rehabilitation of cardiac disease, the relationship of cholesterol to behavior, depression and heart disease, the pharmacotherapy of depression in this specific patient population, the psychiatric risk factors for coronary artery disease, and the treatment of hostility, stress and type A behavior are discussed. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LITTMAN, AB (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,CTR CARDIOVASC HLTH,BEHAV MED SER,FRUIT ST,BOSTON,MA 02114, USA. NR 170 TC 44 Z9 44 U1 2 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1993 VL 60 IS 3-4 BP 148 EP 167 PG 20 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MF446 UT WOS:A1993MF44600004 PM 8272474 ER PT J AU OTTO, MW YEO, RA AF OTTO, MW YEO, RA TI HEMISPHERIC ACTIVATION, AFFECTIVE JUDGMENTS, AND PAIN PERCEPTION SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Article DE PAIN; LATERALITY; EMOTIONAL PROCESSING; HEMISPHERIC ACTIVATION ID EMOTION; ASYMMETRIES; DEPRESSION AB This study utilized a unique contact lens method to examine the influence of right hemisphere processing on affective judgments and pain perception. Under conditions of unilateral visual stimulation, participants completed affective ratings of films and underwent a cold pressor pain task. The goal was to examine differences in affective judgments of films projected to one or the other hemisphere and to examine the influence of this unilateral visual stimulation on pain sensitivity. The results failed to replicate a previous finding of differential affective judgments under conditions of right and left visual stimulation. Nonetheless, in female subjects, unilateral visual stimulation was significantly associated with pain lateralization. This finding is discussed in terms of attentional processes in pain perception and limitations of the current lens design. C1 UNIV NEW MEXICO,DEPT PSYCHOL,ALBUQUERQUE,NM 87131. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 18 TC 3 Z9 3 U1 2 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1993 VL 60 IS 3-4 BP 186 EP 194 PG 9 WC Psychiatry; Psychology SC Psychiatry; Psychology GA MF446 UT WOS:A1993MF44600007 PM 8272477 ER PT J AU LITTMAN, AB FAVA, M MCKOOL, K LAMONFAVA, S PEGG, E AF LITTMAN, AB FAVA, M MCKOOL, K LAMONFAVA, S PEGG, E TI BUSPIRONE THERAPY FOR TYPE-A BEHAVIOR, HOSTILITY, AND PERCEIVED STRESS IN CARDIAC PATIENTS SO PSYCHOTHERAPY AND PSYCHOSOMATICS LA English DT Note DE BUSPIRONE; SEROTONIN; HOSTILITY; TYPE-A BEHAVIOR; STRESS; IRRITABILITY ID AGGRESSION; DISORDERS AB Hostility is considered to be a risk factor for coronary artery disease. Despite the findings of reduced serotonergic function and effectiveness of treatment with serotonergic agents in similar symptom complexes, there have been no attempts at using serotonergic psychopharmacologic agents to treat this population. We conducted an 8-week open trial of 10 type A, irritable men with coronary artery disease and no diagnosable psychiatric (axis I) condition to examine the effects of buspirone on these subjects. Buspirone appears to significantly reduce type A behavior, hostility, anxiety, impatience, and perceived stress. RP LITTMAN, AB (reprint author), MASSACHUSETTS GEN HOSP,CARDIOVASC HLTH SCI CTR,DEPT PSYCHIAT & PREVENT MED,DIV BEHAV MED,BOSTON,MA 02114, USA. NR 11 TC 8 Z9 8 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0033-3190 J9 PSYCHOTHER PSYCHOSOM JI Psychother. Psychosom. PY 1993 VL 59 IS 2 BP 107 EP 110 PG 4 WC Psychiatry; Psychology SC Psychiatry; Psychology GA LG645 UT WOS:A1993LG64500006 PM 8332702 ER PT S AU ALPERT, NM BERDICHEVSKY, D WEISE, S TANG, J RAUCH, SL AF ALPERT, NM BERDICHEVSKY, D WEISE, S TANG, J RAUCH, SL BE Uemura, K Lassen, NA Jones, T Kanno, I Hatazawa, J Miura, S Murakami, M Iida, H Fujita, H Inugami, A TI STEREOTAXIC TRANSFORMATION OF PET SCANS BY NONLINEAR LEAST-SQUARES SO QUANTIFICATION OF BRAIN FUNCTION: TRACER KINETICS AND IMAGE ANALYSIS IN BRAIN PET SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT International Symposium on Quantification of Brain Function (Brain PET 93 Akita) CY MAY 29-31, 1993 CL AKITA, JAPAN SP JAPANESE SOC CEREBRAL BLOOD FLOW & METAB, JAPANESE SOC NUCL MED, JAPAN BRAIN FDN, AKITA PREFECTURE, AKITA CITY, AKITA PREFECTURE CEREBROVASC MED FDN, AKITA RES INST BRAIN & BLOOD VESSELS, KEITOKUKAI FIJIWARA MEM HOSP, SEIRANKAI HONJOH DAIICHI HOSP ID LOCALIZATION RP ALPERT, NM (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 7 TC 28 Z9 28 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-89859-X J9 INT CONGR SER PY 1993 VL 1030 BP 459 EP 464 PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Neurosciences; Physiology SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ68P UT WOS:A1993BZ68P00052 ER PT S AU BELLIVEAU, JW AF BELLIVEAU, JW BE Uemura, K Lassen, NA Jones, T Kanno, I Hatazawa, J Miura, S Murakami, M Iida, H Fujita, H Inugami, A TI MRI TECHNIQUES FOR FUNCTIONAL MAPPING OF THE HUMAN BRAIN - INTEGRATION WITH PET, EEG/MEG AND INFRARED-SPECTROSCOPY SO QUANTIFICATION OF BRAIN FUNCTION: TRACER KINETICS AND IMAGE ANALYSIS IN BRAIN PET SE INTERNATIONAL CONGRESS SERIES LA English DT Review CT International Symposium on Quantification of Brain Function (Brain PET 93 Akita) CY MAY 29-31, 1993 CL AKITA, JAPAN SP JAPANESE SOC CEREBRAL BLOOD FLOW & METAB, JAPANESE SOC NUCL MED, JAPAN BRAIN FDN, AKITA PREFECTURE, AKITA CITY, AKITA PREFECTURE CEREBROVASC MED FDN, AKITA RES INST BRAIN & BLOOD VESSELS, KEITOKUKAI FIJIWARA MEM HOSP, SEIRANKAI HONJOH DAIICHI HOSP ID HUMAN VISUAL-CORTEX; CEREBRAL BLOOD-FLOW; POSITRON-EMISSION TOMOGRAPHY; HUMAN STRIATE CORTEX; MAGNETIC-SUSCEPTIBILITY; RETINOTOPIC ORGANIZATION; COGNITIVE NEUROSCIENCE; SENSORY STIMULATION; COMPUTED-TOMOGRAPHY; TUMOR ANGIOGENESIS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP BELLIVEAU, JW (reprint author), MASSACHUSETTS GEN HOSP,CTR MGH NMR,DEPT RADIOL,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 108 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-89859-X J9 INT CONGR SER PY 1993 VL 1030 BP 639 EP 667 PG 29 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Neurosciences; Physiology SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ68P UT WOS:A1993BZ68P00073 ER PT J AU NGUYEN, T BROWNELL, GL HOLDEN, SA KAHL, S MIURA, M TEICHER, BA AF NGUYEN, T BROWNELL, GL HOLDEN, SA KAHL, S MIURA, M TEICHER, BA TI SUBCELLULAR-DISTRIBUTION OF VARIOUS BORON-COMPOUNDS AND IMPLICATIONS FOR THEIR EFFICACY IN BORON NEUTRON-CAPTURE THERAPY BY MONTE-CARLO SIMULATIONS SO RADIATION RESEARCH LA English DT Article ID INVITRO; AGENTS; CELLS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. MIT,DEPT NUCL ENGN,CAMBRIDGE,MA 02139. MIT,WHITAKER COLL,CAMBRIDGE,MA 02139. UNIV CALIF SAN FRANCISCO,SCH PHARM,SAN FRANCISCO,CA 94143. BROOKHAVEN NATL LAB,DEPT MED,UPTON,NY 11973. FU NCI NIH HHS [R01-CA36508, R01-CA47379] NR 21 TC 35 Z9 36 U1 0 U2 0 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 JAN PY 1993 VL 133 IS 1 BP 33 EP 40 DI 10.2307/3578254 PG 8 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA KK623 UT WOS:A1993KK62300005 PM 8434111 ER PT J AU WEBER, AL AF WEBER, AL TI IMAGING OF CYSTS AND ODONTOGENIC-TUMORS OF THE JAW - DEFINITION AND CLASSIFICATION SO RADIOLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID KERATOCYST; AMELOBLASTOMA; MYXOMA C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WEBER, AL (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT RADIOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 41 TC 34 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 0033-8389 J9 RADIOL CLIN N AM JI Radiol. Clin. N. Am. PD JAN PY 1993 VL 31 IS 1 BP 101 EP 120 PG 20 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KG255 UT WOS:A1993KG25500009 PM 8419968 ER PT S AU KAHN, CR WHITE, MF SHOELSON, SE BACKER, JM ARAKI, E CHEATHAM, B CSERMELY, P FOLLI, F GOLDSTEIN, BJ HUERTAS, P ROTHENBERG, PL SAAD, MJA SIDDLE, K SUN, XJ WILDEN, PA YAMADA, K KAHN, SA AF KAHN, CR WHITE, MF SHOELSON, SE BACKER, JM ARAKI, E CHEATHAM, B CSERMELY, P FOLLI, F GOLDSTEIN, BJ HUERTAS, P ROTHENBERG, PL SAAD, MJA SIDDLE, K SUN, XJ WILDEN, PA YAMADA, K KAHN, SA BE Bardin, CW TI THE INSULIN-RECEPTOR AND ITS SUBSTRATE - MOLECULAR DETERMINANTS OF EARLY EVENTS IN INSULIN ACTION SO RECENT PROGRESS IN HORMONE RESEARCH, VOL 48 SE RECENT PROGRESS IN HORMONE RESEARCH LA English DT Article; Proceedings Paper CT 1991 Laurentian Hormone Conference CY 1991 CL PR ID GROWTH FACTOR-I; TYROSINE KINASE-ACTIVITY; NUCLEOTIDE REGULATORY PROTEINS; CATALYZED ADP-RIBOSYLATION; RAT HEPATOMA-CELLS; ATP-BINDING SITE; BETA-SUBUNIT; SIGNAL TRANSDUCTION; ALPHA-SUBUNIT; MONOCLONAL-ANTIBODIES C1 HARVARD UNIV,SCH MED,BOSTON,MA 02215. RP KAHN, CR (reprint author), BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215, USA. OI Kahn, Stacy/0000-0002-8001-6955; folli, franco/0000-0001-9824-5222 FU NIDDK NIH HHS [DK 31036, DK 33201] NR 208 TC 86 Z9 88 U1 0 U2 3 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0079-9963 BN 0-12-571148-4 J9 RECENT PROG HORM RES PY 1993 VL 48 BP 291 EP 339 PG 49 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BZ87T UT WOS:A1993BZ87T00012 PM 7680139 ER PT J AU SU, LH PARISSENTI, AM RIEDEL, H AF SU, LH PARISSENTI, AM RIEDEL, H TI FUNCTIONAL CARBOXYL-TERMINAL DELETION MAP OF PROTEIN KINASE-C-ALPHA SO RECEPTORS & CHANNELS LA English DT Article DE BAL31 DELETION; CDNA EXPRESSION; PHORBOL ESTER; SIGNAL TRANSDUCTION; TUMOR PROMOTER ID PHORBOL ESTER RECEPTOR; SACCHAROMYCES-CEREVISIAE; REGULATORY DOMAIN; YEAST-CELLS; ENDOTHELIAL-CELLS; CATALYTIC DOMAINS; GENE-EXPRESSION; CA-2+ CHANNELS; FAMILY; SEQUENCE AB The phorbol ester receptor protein kinase C (PKC) gene family encodes essential mediators of various eukaryotic cellular signals. Based on the predicted amino acid (aa) sequence homology of more than ten distinct PKC gene coding sequences, four highly conserved regions C1-C4 and five variable regions V1-V5 have been defined for the different PKC subtypes. Some of these regions, such as C1 and C3/V4/C4, have been correlated with specific PKC functions, such as activator binding and enzymatic activity, respectively, while the biological role of others is unknown. The biological significance of the PKC carboxyl terminus is unclear and the predicted boundary of the catalytic C4 region is controversial due to different interpretations of aa sequence comparisons. We explored the PKC alpha carboxyl terminal requirement for basic PKC function and mapped the boundary of the sequences essential for enzymatic activity based on functional criteria. cDNAs encoding normal and random carboxyl terminal truncations of bovine PKC alpha were introduced into Saccharomyces cerevisiae, allowing its rapid functional expression and characterization for catalytic as well as biological activity. We found that deletion of up to 11 carboxyl terminal aa still results in a phorbol ester-responsive, biologically active enzyme in vivo which is dependent on calcium and phospholipids for catalytic activation in vitro. Deletion of 15 and 23 aa results in marginal and total loss of catalytic activity, respectively, and in complete loss of biological activity for both truncations. Our findings indicate that at least 11 aa of the bovine PKC alpha carboxyl terminus are not essential for cofactor-dependent PKC function, thereby locating the boundary of sequences essential for enzymatic activity slightly upstream of this position, while aa sequence similarity between conventional PKC isoforms continues up to two aa from the PKC alpha carboxyl terminus. The yeast model should be valuable in defining the functional roles of various mammalian PKC domains. C1 JOSLIN DIABETES CTR,MOLEC BIOL SECT,1 JOSLIN PL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02215. NR 48 TC 18 Z9 18 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1060-6823 J9 RECEPTOR CHANNEL JI Recept. Channels PY 1993 VL 1 IS 1 BP 1 EP 9 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MU445 UT WOS:A1993MU44500001 PM 8081709 ER PT J AU DELIA, JA WEINRAUCH, LA GLEASON, RE DESILVA, RA NESTO, RW AF DELIA, JA WEINRAUCH, LA GLEASON, RE DESILVA, RA NESTO, RW TI PRELIMINARY SCREENING OF THE RELATIONSHIP OF SERUM-LIPIDS TO SURVIVAL OF CHRONIC DIALYSIS PATIENTS SO RENAL FAILURE LA English DT Article AB To assess the predictive value of serum lipid measurements in dialysis patients once the initial decrease on early dialysis had occurred, we obtained random serum cholesterol and triglyceride levels in stable, chronic dialysis patients who were then followed up to 9 years. Derived LDL (DLDL) was estimated by the Friedewald formula, calculated for all HDL levels between 30 and 45 mg/dL, and evaluated statistically against a panel of vascular disease markers, including clinical assessment for coronary, peripheral, and cerebrovascular disease; ECG, both standard and ambulatory; two-dimensional echocardiogram; and me&cations. Survival was calculated from entry (not dialysis onset) for 58 hemodialysis and 33 peritoneal dialysis patients. The 91 patients (49 males, 74 diabetics) were divided by cholesterol level (greater-than-or-equal-to 175 mg/dL = 53, < 175 = 38), triglyceride (greater-than-or-equal-to 175 mg/dL = 55, < 175 = 36), and DLDL (greater-than-or-equal-to 75 = 58, < 75 = 24). High total cholesterol was present in a larger proportion of females than low cholesterol, but groups were not different with respect to all vascular determinants, including survival (mean = 33.4 months vs. 43.2, p = NS). High vs. low triglyceride groups were not different with respect to vascular indicators, except for both incidence of abnormal standard ECG (69% vs. 42%, p < 0.05) and survivals (mean = 42.0 vs. 30.7, p < 0.05; 1 year = 80% vs. 56%, p < 0.01). High DLDL measurements identified a group with increased incidence of diabetes (88% vs. 67%, p < 0.05), female gender (53% vs. 25%, p < 0.01), coronary events (5% vs. 33%, p < 0.05), and cerebrovascular events (24% vs. 0%, p < 0.01), with a decreased mean survival (31.2 vs. 43.0 months, p < 0.01). These results suggest that DLDL levels in the ''normal'' range may be vasculopathic in a dialysis population. RP DELIA, JA (reprint author), HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT MED,JOSLIN DIABET CTR,BOSTON,MA 02215, USA. OI Weinrauch, Larry/0000-0003-1357-9528 NR 0 TC 9 Z9 9 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0886-022X J9 RENAL FAILURE JI Ren. Fail. PY 1993 VL 15 IS 2 BP 203 EP 209 DI 10.3109/08860229309046153 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA KU651 UT WOS:A1993KU65100011 PM 8469788 ER PT J AU THOMPSON, JP ANDERSON, TR BOERINGA, JA LEWIS, F PADILLA, FS AF THOMPSON, JP ANDERSON, TR BOERINGA, JA LEWIS, F PADILLA, FS TI THE HOMELESS - PSYCHOLOGICAL-ASPECTS OF THEIR REHABILITATION SO REVISTA LATINOAMERICANA DE PSICOLOGIA LA Spanish DT Article DE HOMELESS; VOCATIONAL COUNSELING; REHABILITATION ID COUNSELOR CHARACTERISTICS; PREFERENCES AB This paper discusses vocational rehabilitation approaches to counseling homeless people. The overall problem of homelessness is discussed. Definitions of homelessness are presented. General problems in counseling homeless people are reviewed. A discussion of counseling strategies follows with reference to: 1. sensitivity to cultural factors, 2. sensitivity to the homeless condition, 3. a review of empowerment approaches. The components of a comprehensive rehabilitation of homeless people, arc outlined. The importance of adequate housing and medical attention are stressed as key components of the rehabilitation of homeless people. The focus of the paper is on helping homeless people with disabilities. Traditional vocational assessment techniques such as vocational interest and aptitude testing is discussed within the context of working with homeless people. The necessity of formulating a comprehensive vocational plan is emphasized. Vocational rehabilitation resources available to homeless people are reviewed. C1 VET AFFAIRS MED CTR,HOUSTON,TX. RP THOMPSON, JP (reprint author), BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 19 TC 0 Z9 0 U1 1 U2 1 PU REV LATINOAMER PSICOL PI BOGOTA D.E. PA APARTADO 92621, BOGOTA D.E., COLOMBIA SN 0034-978X J9 REV LAT AM PSICOL JI Rev. Latinoam. Psicol. PY 1993 VL 25 IS 3 BP 365 EP 374 PG 10 WC Psychology, Multidisciplinary SC Psychology GA MU414 UT WOS:A1993MU41400002 ER PT S AU TAUBMAN, MA SMITH, DJ AF TAUBMAN, MA SMITH, DJ BE Malamud, D Tabak, L TI SIGNIFICANCE OF SALIVARY ANTIBODY IN DENTAL DISEASES SO SALIVA AS A DIAGNOSTIC FLUID SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SALIVA AS A DIAGNOSTIC FLUID CY OCT 22-25, 1992 CL PANAMA CITY BEACH, FL SP NEW YORK ACAD SCI, BLOCK DRUG, COLGATE PALMOLIVE, EPITOPE, NASA, NIDR, SALIVA DIAGNOST SYST, ABBOTT LABS, ENZYMATICS, HOFFMANN LA ROCHE RP TAUBMAN, MA (reprint author), FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE 04733, DE 07009, DE 03420] NR 0 TC 11 Z9 11 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-787-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 694 BP 202 EP 215 DI 10.1111/j.1749-6632.1993.tb18354.x PG 14 WC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology SC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology GA BZ06S UT WOS:A1993BZ06S00019 PM 8215056 ER PT J AU COUNTER, SA AF COUNTER, SA TI ELECTROMAGNETIC STIMULATION OF THE AUDITORY-SYSTEM - EFFECTS AND SIDE-EFFECTS SO SCANDINAVIAN AUDIOLOGY LA English DT Article DE MAGNETIC STIMULATION; MAGNETIC RESONANCE IMAGING; BRAIN-STEM AUDITORY EVOKED RESPONSES; HEARING LOSS; COCHLEA IMPLANT; IMPULSE NOISE; 8TH NERVE; DEAFNESS ID TRANSCRANIAL MAGNETIC STIMULATION; COCHLEAR IMPLANT PATIENTS; ELECTRICAL-STIMULATION; STAPEDIUS REFLEX; ACOUSTIC TRAUMA; FACIAL-NERVE; BRAIN-STIMULATION; MOTOR CORTEX; REGENERATION; FIELDS AB Extracranial electromagnetic stimulation (EMS) is a recently developed clinical technique which may be used in place of conventional transcutaneous electrical stimulation to activate the central and peripheral nervous systems. This technique is widely used in neurology and otolaryngology for non-invasive stimulation of the brain and facial nerve. EMS uses electromagnetic field pulses which pass unimpeded through the cranium and soft tissues to activate excitable membranes of volume conductors. In this series of studies, the effects and side-effects of electromagnetic stimulation on the auditory system of humans and experimental animals were investigated. In the first study, 18 profoundly hard-of-hearing and deaf patients who were candidates for cochlear implants were examined by non-invasive EMS in an effort to determine whether EMS could stimulate residual neurons in the cochlea, 8th nerve proper, or higher auditory brain centers, and evoke auditory sensations. The patients were stimulated with a magnetic coil positioned at the (1) auricle, (2) mastoid process, and (3) the temporal lobe area. EMS elicited auditory sensations in 26 ears (of 14 patients/subjects). The lowest threshold of auditory sensation (TAS) at each stimulus position was found to be at the 20 % EMS level, with a range of 20-50 % of the maximum level (2.0 Tesla), and with equal sensitivity in each coil position. There was no correlation between the EMS/TAS and the immediate postoperative psychoacoustic tests in ten patients receiving cochlear implants. A prominent side effect of EMS was found to be the high intensity, high frequency impulse noise generated by the coil which causes severe cochlear damage and permanent sensorineural hearing loss in experimental animals. Measurements of the sound pressure level (SPL) of the magnetic coil acoustic artifact (MCAA) at the tympanic membrane of the rabbit ear showed levels of up to 160 dB for maximum EMS. Measurements of the spectral content and SPL of the MCAA in the ear canal of life size models of the human cranium with the stimulating coil placed at standard clinical positions indicated that the major acoustic energy of the pulse is concentrated in the 2-5 kHz range, and that the SPL of the pulse at some positions may place persons at risk for hearing loss. Studies on computer simulated impulse noises showed that the peak sound pressure rather than the rise time (in the range 0.1 - 1.0 ms) determined the permanent threshold shift (PTS). The MCAA was more harmful than a 128 dB SPL continuous noise with 100 times more energy. The ear may be protected from the most damaging effects of the MCAA by the use of ear protectors. However, artifically activating the acoustic reflex with a contralateral broad band noise during exposure to the intense magnetic coil artifact reduced the PTS and protected the ear against noise-induced hearing loss. The findings on extensive and long term exposure of experimental animals to EMS showed no harmful effects on the brain or auditory system. It was concluded that EMS may induce sound perception in deaf ears and that the risk of acoustic trauma in normal ears due to the MCAA must be considered. It was further suggested that the EMS technique may be developed to be used in the selection of cochlea implant candidates and in stimulating surviving auditory neurons in deaf patients. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,CAMBRIDGE,MA 02138. OREBRO MED CTR HOSP,DEPT AUDIOL,OREBRO,SWEDEN. RP COUNTER, SA (reprint author), KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM 60,SWEDEN. NR 52 TC 0 Z9 0 U1 0 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0105-0397 J9 SCAND AUDIOL JI Scand. Audiol. PY 1993 VL 22 SU 37 BP 1 EP 32 PG 32 WC Otorhinolaryngology SC Otorhinolaryngology GA LU306 UT WOS:A1993LU30600001 ER PT J AU CRAIG, WA AF CRAIG, WA TI THE PHARMACOKINETICS OF CEFPIROME - RATIONALE FOR A 12-HOUR DOSING REGIMEN SO SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID MULTIPLE-DOSE PHARMACOKINETICS; HR 810; CEREBROSPINAL-FLUID; HEALTHY-VOLUNTEERS; CEPHALOSPORIN; PENETRATION; SINGLE; INFECTION; TISSUE AB Cefpirome is a new broad-spectrum beta-lactam antibiotic that exhibits minimal concentration dependent killing and produces prolonged postantibiotic effects only with Staphylococcus aureus. These pharmacodynamic characteristics suggest that the goal of optimal dosing regimens for cefpirome is to provide serum levels above the MIC of infecting pathogens for most of the dosing interval. Cefpirome has a half-life of 2.0 hours in normal volunteers that increases to 3.1 to 4.4 hours in elderly patients. Serum concentrations following 0.5, 1.0 and 2.0 grams of cefpirome are above the MIC of common pathogens for more than half of the dosing interval. For many of the Enterobacteriaceae, serum concentrations are above the MIC for over 12 hours. The drug distributes primarily into extracellular fluid and does provide potentially therapeutic concentrations in cerebrospinal fluid (CSF). The drug is eliminated primarily by the kidney and requires dosage modification when the creatinine clearance is below 50 ml/min. The half-life of the drug is not significantly altered in patients with cystic fibrosis and hepatic dysfunction. The integration of the drug's pharmacokinetic and pharmacodynamic characteristics support the use of a 12-hour dosing interval for the treatment of serious infection. C1 UNIV WISCONSIN,MADISON,WI 53706. RP CRAIG, WA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,2500 OVERLOOK TERR,MADISON,WI 53705, USA. NR 23 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 0036-5548 J9 SCAND J INFECT DIS JI Scand. J. Infect. Dis. PY 1993 SU 91 BP 33 EP 40 PG 8 WC Infectious Diseases SC Infectious Diseases GA MH453 UT WOS:A1993MH45300005 ER PT J AU SCHEIBEL, AB CONRAD, AS AF SCHEIBEL, AB CONRAD, AS TI HIPPOCAMPAL DYSGENESIS IN MUTANT MOUSE AND SCHIZOPHRENIC MAN - IS THERE A RELATIONSHIP SO SCHIZOPHRENIA BULLETIN LA English DT Article ID PYRAMIDAL CELL; DENTATE GYRUS; CEREBRAL-CORTEX; REELER MICE; AUTORADIOGRAPHIC ANALYSIS; PRENATAL EXPOSURE; RHESUS-MONKEY; ORIGIN; NEURONS; REGION AB A rapidly growing body of data points to structural alterations of the temporal lobe in a significant number of schizophrenic patients. At the histological level, these changes are most frequently seen in the hippocampus and entorhinal cortex, and a strong case can be made for attributing them to disturbed neuroembryogenesis. Archicortical components of the temporal lobe are now known to follow an unusually complex course of embryological development, and we suggest that the process may be especially vulnerable to interference. A number of autosomal mutant mice express anomalies of hippocampal development, some of which resemble caricatures of the more subtle alterations in schizophrenic patients. We have suggested that at least some schizophrenias may result from the impact of maternal exposure to influenza virus during the period of neuroblast migration into the hippocampal primordium in the presence of as yet unspecified patterns of genetically transmitted immuno-incompetence. Although this putative interaction of genetic and epigenetic factors in humans probably differs from the factors involved in the mutant mouse, study of the murine model may reveal those mechanisms of embryogenesis that are most likely to be disturbed in the temporal lobe of schizophrenic patients. C1 UNIV CALIF LOS ANGELES, MED CTR, BRAIN RES INST, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, MED CTR, DEPT NEUROL, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS CTR, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, MED CTR, DEPT ANAT & CELL BIOL, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, MED CTR, DEPT PSYCHIAT & BIOBEHAV SCI, LOS ANGELES, CA USA. NR 60 TC 45 Z9 45 U1 2 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1993 VL 19 IS 1 BP 21 EP 33 PG 13 WC Psychiatry SC Psychiatry GA KQ643 UT WOS:A1993KQ64300004 PM 8451611 ER PT J AU HOTAMISLIGIL, GS SHARGILL, NS SPIEGELMAN, BM AF HOTAMISLIGIL, GS SHARGILL, NS SPIEGELMAN, BM TI ADIPOSE EXPRESSION OF TUMOR-NECROSIS-FACTOR-ALPHA - DIRECT ROLE IN OBESITY-LINKED INSULIN RESISTANCE SO SCIENCE LA English DT Article ID RESPONSIVE GLUCOSE TRANSPORTER; LIPOPROTEIN-LIPASE ACTIVITY; SERINE PROTEASE HOMOLOG; SKELETAL-MUSCLE; MESSENGER-RNA; DECREASED EXPRESSION; 3T3-L1 ADIPOCYTES; DIABETES-MELLITUS; LIPID-METABOLISM; GENE-EXPRESSION AB Tumor necrosis factor-alpha (TNF-alpha) has been shown to have certain catabolic effects on fat cells and whole animals. An induction of TNF-alpha messenger RNA expression was observed in adipose tissue from four different rodent models of obesity and diabetes. TNF-alpha protein was also elevated locally and systemically. Neutralization of TNF-alpha in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. These results indicate a role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 42539] NR 80 TC 3996 Z9 4150 U1 36 U2 340 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 1 PY 1993 VL 259 IS 5091 BP 87 EP 91 DI 10.1126/science.7678183 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KE601 UT WOS:A1993KE60100035 PM 7678183 ER PT J AU MCKUSICK, KA QUAIFE, MA AF MCKUSICK, KA QUAIFE, MA TI CURRENT PROCEDURAL TERMINOLOGY CODING OF NUCLEAR-MEDICINE PROCEDURES SO SEMINARS IN NUCLEAR MEDICINE LA English DT Article C1 HARVARD UNIV,SCH MED,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02115. UNIV NEBRASKA,SCH MED,DEPT NUCL MED,OMAHA,NE 68182. UNIV NEBRASKA,MED CTR,OMAHA,NE 68105. RP MCKUSICK, KA (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114, 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 0001-2998 J9 SEMIN NUCL MED JI Semin. Nucl. Med. PD JAN PY 1993 VL 23 IS 1 BP 59 EP 66 DI 10.1016/S0001-2998(05)80062-5 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KK506 UT WOS:A1993KK50600007 PM 8469995 ER PT B AU MOSKOWITZ, MA NOZAKI, K AF MOSKOWITZ, MA NOZAKI, K BE Vanhoutte, PM Saxena, PR Paoletti, R Brunello, N TI 5-HT(1B/D)-RECEPTOR AGONISTS BLOCK C-FOS-LI WITHIN TRIGEMINAL NUCLEUS CAUDALIS IN RESPONSE TO NOXIOUS MENINGEAL STIMULATION SO SEROTONIN: FROM CELL BIOLOGY TO PHARMACOLOGY AND THERAPEUTICS SE MEDICAL SCIENCE SYMPOSIA SERIES LA English DT Proceedings Paper CT 2nd International Symposium on Serotonin from Cell Biology to Pharmacology and Therapeutics CY SEP 15-18, 1992 CL HOUSTON, TX SP SEROTONIN CLUB, GIOVANNI LORENZINI MED FDN, FONDAZIONE GIOVANNI LORENZINI C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-2518-4 J9 MED SCI SYMP SER PY 1993 VL 5 BP 33 EP 39 PG 7 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy; Physiology SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy; Physiology GA BZ51T UT WOS:A1993BZ51T00004 ER PT B AU BOEPPLE, PA MANSFIELD, MJ LANDY, H CROWLEY, WF AF BOEPPLE, PA MANSFIELD, MJ LANDY, H CROWLEY, WF BE Grave, GD Cutler, GB TI GNRH AGONIST THERAPY OF CENTRAL PRECOCIOUS PUBERTY - SHOULD THE GOAL BE COMPLETE PITUITARY-GONADAL SUPPRESSION SO SEXUAL PRECOCITY: ETIOLOGY, DIAGNOSIS, AND MANAGEMENT LA English DT Proceedings Paper CT CONF ON SEXUAL PRECOCITY CY OCT 28-31, 1990 CL AIRLIE, VA SP NICHD RP BOEPPLE, PA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PEDIAT,PEDIAT UNIT,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0078-7 PY 1993 BP 11 EP 26 PG 16 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA BZ01H UT WOS:A1993BZ01H00002 ER PT B AU BOEPPLE, PA MANSFIELD, MJ CRAWFORD, JD CRIGLER, JF BLIZZARD, RM CROWLEY, WF AF BOEPPLE, PA MANSFIELD, MJ CRAWFORD, JD CRIGLER, JF BLIZZARD, RM CROWLEY, WF BE Grave, GD Cutler, GB TI ANALYSIS OF GROWTH DATA IN CHILDREN WITH CENTRAL PRECOCIOUS PUBERTY - THE IMPACT OF LONG-TERM GNRH AGONIST THERAPY SO SEXUAL PRECOCITY: ETIOLOGY, DIAGNOSIS, AND MANAGEMENT LA English DT Proceedings Paper CT CONF ON SEXUAL PRECOCITY CY OCT 28-31, 1990 CL AIRLIE, VA SP NICHD RP BOEPPLE, PA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PEDIAT,PEDIAT UNIT,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0078-7 PY 1993 BP 69 EP 83 PG 15 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA BZ01H UT WOS:A1993BZ01H00008 ER PT B AU ADAMS, JM BOEPPLE, PA CROWLEY, WF AF ADAMS, JM BOEPPLE, PA CROWLEY, WF BE Grave, GD Cutler, GB TI THE USE OF ULTRASOUND IN THE EVALUATION OF CENTRAL PRECOCIOUS PUBERTY SO SEXUAL PRECOCITY: ETIOLOGY, DIAGNOSIS, AND MANAGEMENT LA English DT Proceedings Paper CT CONF ON SEXUAL PRECOCITY CY OCT 28-31, 1990 CL AIRLIE, VA SP NICHD RP ADAMS, JM (reprint author), MASSACHUSETTS GEN HOSP,REPROD ENDOCRINE UNIT,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0078-7 PY 1993 BP 167 EP 179 PG 13 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA BZ01H UT WOS:A1993BZ01H00016 ER PT J AU LOCKE, PA MACDONALD, ME SRINIDHI, J GILLIAM, TC TANZI, RE CONNEALLY, PM WEXLER, NS HAINES, JL GUSELLA, JF AF LOCKE, PA MACDONALD, ME SRINIDHI, J GILLIAM, TC TANZI, RE CONNEALLY, PM WEXLER, NS HAINES, JL GUSELLA, JF TI A GENETIC-LINKAGE MAP OF THE CHROMOSOME-4 SHORT ARM SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Article ID HUNTINGTONS-DISEASE; LONG ARM; LOCALIZATION; SUBUNIT; MARKER; D4S10 AB We have generated an 18-interval contiguous genetic linkage map of human chromosome 4 spanning the entire short arm and proximal long arm. Fifty-seven polymorphisms, representing 42 loci, were analyzed in the Venezuelan reference pedigree. The markers included seven genes (ADRA2C, ALB, GABRB1, GC, HOX7, IDUA, QDPR), one pseudogene (RAF1P1), and 34 anonymous DNA loci. Four loci were represented by microsatellite polymorphisms and one (GC) was expressed as a protein polymorphism. The remainder were genotyped based on restriction fragment length polymorphism. The sex-averaged map covered 123 cM. Significant differences in sex-specific rates of recombination were observed only in the pericentromeric and proximal long arm regions, but these contributed to different overall map lengths of 115 cM in males and 138 cM in females. This map provides 19 reference points along chromosome 4 that will be particularly useful in anchoring and seeding physical mapping studies and in aiding in disease studies. C1 COLUMBIA UNIV,DEPT PSYCHIAT,NEW YORK,NY 10031. COLUMBIA UNIV,DEPT NEUROL,NEW YORK,NY 10031. INDIANA UNIV,MED CTR,DEPT MED GENET,INDIANAPOLIS,IN 46202. COLUMBIA UNIV,DEPT NEUROL,NEW YORK,NY 10032. HEREDITARY DIS FDN,SANTA MONICA,CA 90401. HARVARD UNIV,DEPT GENET,BOSTON,MA 02115. RP LOCKE, PA (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114, USA. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00169]; NINDS NIH HHS [NS16367, NS22031] NR 26 TC 10 Z9 10 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD JAN PY 1993 VL 19 IS 1 BP 95 EP 101 DI 10.1007/BF01233958 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA KU991 UT WOS:A1993KU99100010 PM 8096345 ER EF