FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU ALLEN, AC
   ROBLES, J
   DOVENSKI, W
   CALDERON, S
AF ALLEN, AC
   ROBLES, J
   DOVENSKI, W
   CALDERON, S
TI PCP - A REVIEW OF SYNTHETIC METHODS FOR FORENSIC CLANDESTINE
   INVESTIGATION
SO FORENSIC SCIENCE INTERNATIONAL
LA English
DT Article
DE PHENCYCLIDINE; SYNTHETIC METHODS; REVIEW
ID PHENCYCLIDINE DERIVATIVES; ANALOGS
AB A review of the synthetic routes to phencyclidine (PCP, 1-(1-phenylcyclohexyl)piperidine) available in the open literature is presented. The emphasis herein is directed toward the forensic investigation of clandestine PCP laboratories. Six published synthetic routes to PCP/analogs are discussed. Each method is rated for overall yield, degree of difficulty and potential hazard, in order to assist the forensic chemist in evaluation of a particular clandestine operation. One clandestine recipe is illustrated and discussed.
C1 INST DENT RES,DEPT ARMY,FT GEORGE G MEADE,MD.
RP ALLEN, AC (reprint author), NIDA,ADDICT RES CTR,DRUG DEV GRP,POB 5180,BALTIMORE,MD 21224, USA.
NR 53
TC 4
Z9 4
U1 1
U2 4
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0379-0738
J9 FORENSIC SCI INT
JI Forensic Sci.Int.
PD OCT
PY 1993
VL 61
IS 2-3
BP 85
EP 100
DI 10.1016/0379-0738(93)90217-X
PG 16
WC Medicine, Legal
SC Legal Medicine
GA MV389
UT WOS:A1993MV38900002
PM 8307527
ER

PT J
AU KODAVANTI, PRS
   MUNDY, WR
   TILSON, HA
   HARRY, GJ
AF KODAVANTI, PRS
   MUNDY, WR
   TILSON, HA
   HARRY, GJ
TI EFFECTS OF SELECTED NEUROACTIVE CHEMICALS ON CALCIUM TRANSPORTING
   SYSTEMS IN RAT CEREBELLUM AND ON SURVIVAL OF CEREBELLAR GRANULE CELLS
SO FUNDAMENTAL AND APPLIED TOXICOLOGY
LA English
DT Article
ID ALUMINUM INTERACTION; NEUROBLASTOMA-CELLS; BRAIN CALCIUM; NEUROTOXICITY;
   SYNAPTOSOMES; INHIBITION; PYRETHROIDS; CHLORPROMAZINE; CHANNELS; CULTURE
C1 NIEHS, DIV INTRAMURAL RES, RES TRIANGLE PK, NC 27709 USA.
RP KODAVANTI, PRS (reprint author), US EPA, HLTH EFFECTS RES LAB, DIV NEUROTOXICOL, CELLULAR & MOLEC TOXICOL BRANCH, RES TRIANGLE PK, NC 27711 USA.
NR 54
TC 38
Z9 38
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 0272-0590
J9 FUND APPL TOXICOL
JI Fundam. Appl. Toxicol.
PD OCT
PY 1993
VL 21
IS 3
BP 308
EP 316
DI 10.1006/faat.1993.1103
PG 9
WC Toxicology
SC Toxicology
GA MC193
UT WOS:A1993MC19300006
PM 8258384
ER

PT J
AU MORGAN, DL
   MAHLER, JF
   DILL, JA
   PRICE, HC
   OCONNOR, RW
   ADKINS, B
AF MORGAN, DL
   MAHLER, JF
   DILL, JA
   PRICE, HC
   OCONNOR, RW
   ADKINS, B
TI STYRENE INHALATION TOXICITY STUDIES IN MICE .2. SEX-DIFFERENCES IN
   SUSCEPTIBILITY OF B6C3F1 MICE
SO FUNDAMENTAL AND APPLIED TOXICOLOGY
LA English
DT Article
ID GLUTATHIONE; METABOLISM; RAT; OXIDE; MOUSE; LIVER
C1 PACIFIC NW LAB, RICHLAND, WA 99352 USA.
   MANTECH ENVIRONM TECHNOL INC, RES TRIANGLE PK, NC 27709 USA.
RP MORGAN, DL (reprint author), NIEHS, MD IF-00, RES TRIANGLE PK, NC 27709 USA.
NR 30
TC 27
Z9 27
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0272-0590
J9 FUND APPL TOXICOL
JI Fundam. Appl. Toxicol.
PD OCT
PY 1993
VL 21
IS 3
BP 317
EP 325
DI 10.1006/faat.1993.1104
PG 9
WC Toxicology
SC Toxicology
GA MC193
UT WOS:A1993MC19300007
PM 8258385
ER

PT J
AU MORGAN, DL
   MAHLER, JF
   DILL, JA
   PRICE, HC
   OCONNOR, RW
   ADKINS, B
AF MORGAN, DL
   MAHLER, JF
   DILL, JA
   PRICE, HC
   OCONNOR, RW
   ADKINS, B
TI STYRENE INHALATION TOXICITY STUDIES IN MICE .3. STRAIN DIFFERENCES IN
   SUSCEPTIBILITY
SO FUNDAMENTAL AND APPLIED TOXICOLOGY
LA English
DT Article
ID STYRENE-7,8-OXIDE
C1 PACIFIC NW LAB, RICHLAND, WA 99352 USA.
   MANTECH ENVIRONM TECHNOL INC, RES TRIANGLE PK, NC 27709 USA.
RP MORGAN, DL (reprint author), NIEHS, MD IF-00, RES TRIANGLE PK, NC 27709 USA.
NR 19
TC 33
Z9 33
U1 0
U2 1
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0272-0590
J9 FUND APPL TOXICOL
JI Fundam. Appl. Toxicol.
PD OCT
PY 1993
VL 21
IS 3
BP 326
EP 333
DI 10.1006/faat.1993.1105
PG 8
WC Toxicology
SC Toxicology
GA MC193
UT WOS:A1993MC19300008
PM 8258386
ER

PT J
AU PISEGNA, JR
   SLIMAK, GG
   DOPPMAN, JL
   STRADER, DB
   METZ, DC
   BENYA, RV
   ORBUCH, M
   FISHBEYN, VA
   FRAKER, DL
   NORTON, JA
   MATON, PN
   JENSEN, RT
AF PISEGNA, JR
   SLIMAK, GG
   DOPPMAN, JL
   STRADER, DB
   METZ, DC
   BENYA, RV
   ORBUCH, M
   FISHBEYN, VA
   FRAKER, DL
   NORTON, JA
   MATON, PN
   JENSEN, RT
TI AN EVALUATION OF HUMAN RECOMBINANT ALPHA-INTERFERON IN PATIENTS WITH
   METASTATIC GASTRINOMA
SO GASTROENTEROLOGY
LA English
DT Article
ID ZOLLINGER-ELLISON SYNDROME; ISLET-CELL CARCINOMA; FLUOROURACIL;
   STREPTOZOTOCIN; CHEMOTHERAPY; RESECTION; TUMORS
C1 NIDDKD,DIGEST DIS BRANCH,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892.
   NCI,SURG METAB SECT,BETHESDA,MD 20892.
   NIH,DEPT RADIOL,CTR CLIN,BETHESDA,MD 20892.
NR 19
TC 29
Z9 29
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 1993
VL 105
IS 4
BP 1179
EP 1183
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LZ246
UT WOS:A1993LZ24600029
PM 8405864
ER

PT J
AU ALMOUZNI, G
   WOLFFE, AP
AF ALMOUZNI, G
   WOLFFE, AP
TI REPLICATION-COUPLED CHROMATIN ASSEMBLY IS REQUIRED FOR THE REPRESSION OF
   BASAL TRANSCRIPTION IN-VIVO
SO GENES & DEVELOPMENT
LA English
DT Article
DE CHROMATIN ASSEMBLY; DNA SYNTHESIS; BASAL TRANSCRIPTION; TRANSCRIPTIONAL
   ACTIVATOR; CHROMATIN-MEDIATED REPRESSION; REPLICATION
ID RNA POLYMERASE-II; REGULARLY SPACED NUCLEOSOMES; SV40 DNA-REPLICATION;
   XENOPUS-OOCYTES; ACTIVE CHROMATIN; GENES INVIVO; INVITRO; COMPLEX; EGGS;
   GAL4
AB The chromatin assembly process coupled to DNA synthesis in the Xenopus oocyte nucleus is significantly more repressive toward basal transcription than chromatin assembly on duplex DNA. We show that chromatin assembly concurrent with DNA synthesis over the promoter region itself is causal for repression. However, the trans-activator Gal4-VP16 both relieves repression and activates transcription regardless of the chromatin assembly pathway. This activation is independent of whether Gal4-VP16 addition occurs before or after chromatin assembly. We propose that replication-coupled chromatin assembly represents a general mechanism to direct the efficient repression of basal transcription. However transcription induction by a specific activator, Gal4-VP16, occurs independent of this chromatin-mediated repression.
C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892.
NR 67
TC 138
Z9 138
U1 0
U2 0
PU COLD SPRING HARBOR LAB PRESS
PI PLAINVIEW
PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724
SN 0890-9369
J9 GENE DEV
JI Genes Dev.
PD OCT
PY 1993
VL 7
IS 10
BP 2033
EP 2047
DI 10.1101/gad.7.10.2033
PG 15
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA MB745
UT WOS:A1993MB74500016
PM 8406006
ER

PT J
AU KAWAKAMI, K
   PANDE, S
   FAIOLA, B
   MOORE, DP
   BOEKE, JD
   FARABAUGH, PJ
   STRATHERN, JN
   NAKAMURA, Y
   GARFINKEL, DJ
AF KAWAKAMI, K
   PANDE, S
   FAIOLA, B
   MOORE, DP
   BOEKE, JD
   FARABAUGH, PJ
   STRATHERN, JN
   NAKAMURA, Y
   GARFINKEL, DJ
TI A RARE TRANSFER RNA-ARG(CCU) THAT REGULATES TY1 ELEMENT RIBOSOMAL
   FRAMESHIFTING IS ESSENTIAL FOR TY1 RETROTRANSPOSITION IN
   SACCHAROMYCES-CEREVISIAE
SO GENETICS
LA English
DT Article
ID VIRUS-LIKE PARTICLES; STRANDED-RNA VIRUS; POL FUSION PROTEIN;
   ESCHERICHIA-COLI; YEAST; TRANSPOSITION; GENES; DNA; SEQUENCES; SITE
AB Translation of the yeast retrotransposon Tyl TYA1(gag)-TYB1(pol) gene occurs by a + 1 ribosomal frameshifting event at the sequence CUU AGG C. Because overexpression of a low abundance tRNA-Arg(CCU) encoded by the HSX1 gene resulted in a reduction in Ty1 frameshifting, it was suggested that a translational pause at the AGG-Arg codon is required for optimum frameshifting. The present work shows that the absence of tRNA-Arg(CCU) affects Ty1 transposition, translational frameshifting, and accumulation of mature TYB1 proteins. Transposition of genetically tagged Ty1 elements decreases at least 50-fold and translational frameshifting increases 3-17-fold in cells lacking tRNA-Arg(CCU). Accumulation of Ty1-integrase and Ty1-reverse transcriptase/ribonuclease H is defective in an hsx1 mutant. The defect in Ty1 transposition is complemented by the wild-type HSX1 gene or a mutant tRNA-Arg(UCU) gene containing a C for T substitution in the first position of the anticodon. Overexpression of TYA 1 stimulates Ty 1 transposition 50-fold above wild-type levels when the level of transposition is compared in isogenic hsx1 and HSX1 strains. Thus, the HSX1 gene determines the ratio of the TYA 1 to TYA 1 -TYB 1 precursors required for protein processing or stability, and keeps expression of TYB1 a rate-limiting step in the retrotransposition cycle.
C1 UNIV MARYLAND, DEPT BIOL SCI, CATONSVILLE, MD 21228 USA.
   NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, FREDERICK, MD 21701 USA.
   JOHNS HOPKINS UNIV, SCH MED, DEPT MOLEC BIOL & GENET, BALTIMORE, MD 21205 USA.
RP UNIV TOKYO, INST MED SCI, DEPT TUMOR BIOL, TOKYO 108, JAPAN.
FU NCI NIH HHS [N01-CO-74101]; NIGMS NIH HHS [GM 29480, GM 36481]
NR 43
TC 91
Z9 92
U1 0
U2 0
PU GENETICS SOCIETY AMERICA
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 0016-6731
EI 1943-2631
J9 GENETICS
JI Genetics
PD OCT
PY 1993
VL 135
IS 2
BP 309
EP 320
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA LZ432
UT WOS:A1993LZ43200007
PM 8243996
ER

PT J
AU HOLBECK, SL
   SMITH, GR
AF HOLBECK, SL
   SMITH, GR
TI STALKING THE ELUSIVE RECOMBINATION INTERMEDIATE - RESPONSE
SO GENETICS
LA English
DT Letter
ID DNA HETEROLOGIES
C1 FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104.
RP HOLBECK, SL (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702, USA.
NR 7
TC 1
Z9 1
U1 0
U2 0
PU GENETICS
PI BALTIMORE
PA 428 EAST PRESTON ST, BALTIMORE, MD 21202
SN 0016-6731
J9 GENETICS
JI Genetics
PD OCT
PY 1993
VL 135
IS 2
BP 611
EP 611
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LZ432
UT WOS:A1993LZ43200031
ER

PT J
AU JABS, EW
   LI, X
   LOVETT, M
   YAMAOKA, LH
   TAYLOR, E
   SPEER, MC
   COSS, C
   CADLE, R
   HALL, B
   BROWN, K
   KIDD, KK
   DOLGANOV, G
   POLYMEROPOULOS, MH
   MEYERS, DA
AF JABS, EW
   LI, X
   LOVETT, M
   YAMAOKA, LH
   TAYLOR, E
   SPEER, MC
   COSS, C
   CADLE, R
   HALL, B
   BROWN, K
   KIDD, KK
   DOLGANOV, G
   POLYMEROPOULOS, MH
   MEYERS, DA
TI GENETIC AND PHYSICAL MAPPING OF THE TREACHER-COLLINS SYNDROME LOCUS WITH
   RESPECT TO LOCI IN THE CHROMOSOME-5Q3 REGION
SO GENOMICS
LA English
DT Article
ID DINUCLEOTIDE REPEAT POLYMORPHISM; RADIATION HYBRID MAP; GROWTH-FACTOR;
   LONG ARM; DISEASE LOCUS; DNA; RECEPTOR; LINKAGE; YEAST; CONSTRUCTION
C1 JOHNS HOPKINS UNIV,SCH MED,CTR MED GENET,DEPT MED,BALTIMORE,MD 21205.
   UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78285.
   UNIV TEXAS,SW MED CTR,MCDERMOTT CTR,SAN ANTONIO,TX 78285.
   DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC 27710.
   UNIV KENTUCKY,DEPT PEDIAT,LEXINGTON,KY 40506.
   YESHIVA UNIV ALBERT EINSTEIN COLL MED,DIV REPROD GENET,BRONX,NY 10461.
   MONTEFIORE MED CTR,BRONX,NY 10467.
   YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06510.
   GENELABS INC,REDWOOD CITY,CA.
   ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,BIOCHEM GENET LAB,WASHINGTON,DC 20032.
RP JABS, EW (reprint author), JOHNS HOPKINS UNIV,SCH MED,CTR MED GENET,DEPT PEDIAT,CMSC 10-04,600 N WOLFE ST,BALTIMORE,MD 21287, USA.
OI Jabs, Ethylin/0000-0001-8983-5466
FU NCRR NIH HHS [RR00052]; NICHD NIH HHS [HD24061]; NIDCR NIH HHS [DE10180]
NR 29
TC 24
Z9 24
U1 0
U2 2
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD OCT
PY 1993
VL 18
IS 1
BP 7
EP 13
DI 10.1006/geno.1993.1420
PG 7
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA MB019
UT WOS:A1993MB01900002
PM 8276417
ER

PT J
AU WEBB, GC
   JENKINS, NA
   LARGAESPADA, DA
   COPELAND, NG
   FERNANDEZ, CS
   BOWTELL, DDL
AF WEBB, GC
   JENKINS, NA
   LARGAESPADA, DA
   COPELAND, NG
   FERNANDEZ, CS
   BOWTELL, DDL
TI MAMMALIAN HOMOLOGS OF THE DROSOPHILA SON OF SEVENLESS GENE MAP TO MURINE
   CHROMOSOME-17 AND CHROMOSOME-12 AND TO HUMAN CHROMOSOME-2 AND
   CHROMOSOME-14, RESPECTIVELY
SO GENOMICS
LA English
DT Article
ID PROTEIN-TYROSINE KINASE; MOUSE CHROMOSOMES; LOCALIZATION; LINKAGE;
   CANCER; LOCUS; CHAIN; RAS
C1 UNIV MELBOURNE,HOWARD FLOREY INST EXPTL PHYSIOL & MED,PARKVILLE,VIC 3052,AUSTRALIA.
   QUEEN ELIZABETH HOSP,DEPT GENET,WOODVILLE,SA 5011,AUSTRALIA.
   NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702.
RI Largaespada, David/C-9832-2014; Bowtell, David/H-1007-2016
OI Bowtell, David/0000-0001-9089-7525
FU NCI NIH HHS [N01-CO-74101]; Wellcome Trust
NR 22
TC 27
Z9 27
U1 0
U2 1
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD OCT
PY 1993
VL 18
IS 1
BP 14
EP 19
DI 10.1006/geno.1993.1421
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA MB019
UT WOS:A1993MB01900003
PM 8276400
ER

PT J
AU VOLZ, A
   KORGE, BP
   COMPTON, JG
   ZIEGLER, A
   STEINERT, PM
   MISCHKE, D
AF VOLZ, A
   KORGE, BP
   COMPTON, JG
   ZIEGLER, A
   STEINERT, PM
   MISCHKE, D
TI PHYSICAL MAPPING OF A FUNCTIONAL CLUSTER OF EPIDERMAL DIFFERENTIATION
   GENES ON CHROMOSOME-1Q21
SO GENOMICS
LA English
DT Article
ID EPIDERMOLYSIS-BULLOSA SIMPLEX; HUMAN INVOLUCRIN GENE; HUMAN LORICRIN
   GENE; HUMAN SKIN INVIVO; BINDING PROTEINS; RETINOIC ACID; CRABP-II;
   CORNIFIED ENVELOPE; PROFILAGGRIN GENE; 2 FAMILIES
C1 FREE UNIV BERLIN,KLINIKUM RUDOLF VIRCHOW,INST EXPTL ONKOL & TRANSPLANTAT MED,SPANDAUER DAMM 130,D-14050 BERLIN,GERMANY.
   NIAMS,SKIN BIOL BRANCH,BETHESDA,MD.
NR 56
TC 114
Z9 115
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD OCT
PY 1993
VL 18
IS 1
BP 92
EP 99
DI 10.1006/geno.1993.1430
PG 8
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA MB019
UT WOS:A1993MB01900012
PM 8276421
ER

PT J
AU AVRAHAM, KB
   CHO, BC
   GILBERT, D
   FUJII, H
   OKAMOTO, K
   SHIMAZAKI, T
   ITO, T
   SHOJI, H
   WAKAMATSU, Y
   KONDOH, H
   TAKAHASHI, N
   MURAMATSU, M
   HAMADA, H
   COPELAND, NG
   JENKINS, NA
AF AVRAHAM, KB
   CHO, BC
   GILBERT, D
   FUJII, H
   OKAMOTO, K
   SHIMAZAKI, T
   ITO, T
   SHOJI, H
   WAKAMATSU, Y
   KONDOH, H
   TAKAHASHI, N
   MURAMATSU, M
   HAMADA, H
   COPELAND, NG
   JENKINS, NA
TI MURINE CHROMOSOMAL LOCATION OF 4 CLASS-III POU TRANSCRIPTION FACTORS
SO GENOMICS
LA English
DT Note
ID GENETIC-LINKAGE MAP; EXPRESSION; BRAIN
C1 NCI,FCRDC,ALB BRP,MAMMALIAN GENET LAB,POB B,BLDG 539,FREDERICK,MD 21702.
   UNIV TOKYO,FAC MED,DEPT BIOCHEM,BUNKYO KU,TOKYO 113,JAPAN.
   NAGOYA UNIV,SCH SCI,DEPT MOLEC BIOL,CHIKUSA KU,NAGOYA,AICHI 464,JAPAN.
RI Shimazaki, Takuya/L-1159-2013
OI Shimazaki, Takuya/0000-0002-3936-2098
FU NCI NIH HHS [N01-CO-74101]
NR 16
TC 18
Z9 18
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD OCT
PY 1993
VL 18
IS 1
BP 131
EP 133
DI 10.1006/geno.1993.1436
PG 3
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA MB019
UT WOS:A1993MB01900018
PM 8276397
ER

PT J
AU GEARING, DP
   DRUCK, T
   HUEBNER, K
   OVERHAUSER, J
   GILBERT, DJ
   COPELAND, NG
   JENKINS, NA
AF GEARING, DP
   DRUCK, T
   HUEBNER, K
   OVERHAUSER, J
   GILBERT, DJ
   COPELAND, NG
   JENKINS, NA
TI THE LEUKEMIA INHIBITORY FACTOR-RECEPTOR (LIFR) GENE IS LOCATED WITHIN A
   CLUSTER OF CYTOKINE RECEPTOR LOCI ON MOUSE CHROMOSOME-15 AND HUMAN
   CHROMOSOME-5P12-P13
SO GENOMICS
LA English
DT Note
ID IL-6 SIGNAL TRANSDUCER; GROWTH-HORMONE; LINKAGE MAP; RESPECT; GP130;
   CELLS
C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,JEFFERSON CANC INST,PHILADELPHIA,PA 19107.
   THOMAS JEFFERSON UNIV,JEFFERSON INST MOLEC MED,DEPT BIOCHEM & MOLEC BIOL,PHILADELPHIA,PA 19107.
   NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702.
RP GEARING, DP (reprint author), IMMUNEX RES & DEV CORP,51 UNIV ST,SEATTLE,WA 98101, USA.
FU NCI NIH HHS [CA 21124, CA 39860]; NHGRI NIH HHS [HG000236]
NR 13
TC 29
Z9 30
U1 0
U2 1
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0888-7543
J9 GENOMICS
JI Genomics
PD OCT
PY 1993
VL 18
IS 1
BP 148
EP 150
DI 10.1006/geno.1993.1441
PG 3
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA MB019
UT WOS:A1993MB01900023
PM 8276403
ER

PT J
AU WEINGARTNER, HJ
   KAWAS, C
   RAWLINGS, R
   SHAPIRO, M
AF WEINGARTNER, HJ
   KAWAS, C
   RAWLINGS, R
   SHAPIRO, M
TI CHANGES IN SEMANTIC MEMORY IN EARLY-STAGE ALZHEIMERS-DISEASE PATIENTS
SO GERONTOLOGIST
LA English
DT Article
DE SEMANTIC MEMORY; AGING; ALZHEIMERS DISEASE
ID IMPAIRMENT; KNOWLEDGE; DEMENTIA; MODELS; FAILURE
AB The types and number of exemplars of categories that are retrieved from semantic memory differentiate elderly normal controls and early stage Alzheimer's disease (AD) patients. Elderly normal controls generated more uncommon exemplars from closed semantic categories (fruits and vegetables) than did AD patients 2 1/2 years prior to the presumed onset of AD. AD patients, however, were just as productive as elderly normal controls in generating associations to open categories (letters). The findings suggest that one of the early cognitive symptoms of AD is changes in availability of uncommon exemplars of semantic networks.
C1 JOHNS HOPKINS UNIV,DEPT NEUROL,BALTIMORE,MD 21218.
RP WEINGARTNER, HJ (reprint author), NIAAA,CLIN STUDIES LAB,COGNIT NEUROSCI SECT,BLDG 10 3B19,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 30
TC 28
Z9 28
U1 1
U2 3
PU GERONTOLOGICAL SOCIETY AMER
PI WASHINGTON
PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 1993
VL 33
IS 5
BP 637
EP 643
PG 7
WC Gerontology
SC Geriatrics & Gerontology
GA MA570
UT WOS:A1993MA57000007
PM 8225008
ER

PT J
AU LANDS, WEM
AF LANDS, WEM
TI LETTERS TO THE GLYCO-FORUM - DO ALCOHOL AND COMPLEX CARBOHYDRATES MIX
SO GLYCOBIOLOGY
LA English
DT Editorial Material
ID DEFICIENT TRANSFERRIN; SERUM TRANSFERRIN; ETHANOL; GANGLIOSIDES;
   MEMBRANES
RP LANDS, WEM (reprint author), NIAAA,DIV BASIC RES,BETHESDA,MD 20892, USA.
NR 18
TC 4
Z9 4
U1 0
U2 0
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0959-6658
J9 GLYCOBIOLOGY
JI Glycobiology
PD OCT
PY 1993
VL 3
IS 5
BP 415
EP 416
DI 10.1093/glycob/3.5.415
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA ME111
UT WOS:A1993ME11100002
PM 8286850
ER

PT J
AU LEE, JW
   PIZZO, PA
AF LEE, JW
   PIZZO, PA
TI MANAGEMENT OF THE CANCER-PATIENT WITH FEVER AND PROLONGED NEUTROPENIA
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Review
ID COLONY-STIMULATING FACTOR; BONE-MARROW TRANSPLANTATION;
   ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PNEUMOCYSTIS-CARINII PNEUMONIA;
   PLACEBO-CONTROLLED TRIAL; INVASIVE PULMONARY ASPERGILLOSIS; PREVENT
   CYTOMEGALOVIRUS DISEASE; AMPHOTERICIN-B THERAPY; CELL LUNG-CANCER;
   ACUTE-LEUKEMIA
C1 NCI,PEDIAT BRANCH,INFECT DIS RES LAB,BLDG 10,ROOM 13N240,BETHESDA,MD 20892.
   NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,BETHESDA,MD 20892.
   UNIFORMED SERV UNIV HLTH SCI,DEPT PEDIAT,BETHESDA,MD 20814.
NR 170
TC 17
Z9 17
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0889-8588
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD OCT
PY 1993
VL 7
IS 5
BP 937
EP 960
PG 24
WC Oncology; Hematology
SC Oncology; Hematology
GA LZ421
UT WOS:A1993LZ42100003
PM 8226567
ER

PT J
AU WALSH, TJ
AF WALSH, TJ
TI MANAGEMENT OF IMMUNOCOMPROMISED PATIENTS WITH EVIDENCE OF AN INVASIVE
   MYCOSIS
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Review
ID BONE-MARROW TRANSPLANTATION; COLONY-STIMULATING FACTOR;
   LIPOSOMAL-AMPHOTERICIN-B; GRANULOCYTOPENIC CANCER-PATIENTS;
   HOSPITAL-ACQUIRED CANDIDEMIA; SYSTEMIC FUNGAL-INFECTIONS; CENTRAL
   NERVOUS-SYSTEM; ACUTE-LEUKEMIA; DISSEMINATED CANDIDIASIS; RISK-FACTORS
RP WALSH, TJ (reprint author), NCI,INFECT DIS SECT,PEDIAT BRANCH,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, USA.
NR 112
TC 30
Z9 30
U1 0
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0889-8588
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD OCT
PY 1993
VL 7
IS 5
BP 1003
EP 1026
PG 24
WC Oncology; Hematology
SC Oncology; Hematology
GA LZ421
UT WOS:A1993LZ42100005
PM 8226563
ER

PT J
AU PIZZO, PA
AF PIZZO, PA
TI INFECTIOUS COMPLICATIONS IN THE IMMUNOCOMPROMISED HOST-II - PREFACE
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Editorial Material
RP PIZZO, PA (reprint author), NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, 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 0889-8588
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD OCT
PY 1993
VL 7
IS 5
BP R9
EP R10
PG 2
WC Oncology; Hematology
SC Oncology; Hematology
GA LZ421
UT WOS:A1993LZ42100001
ER

PT J
AU NORMAN, JE
   BEEBE, GW
   HOFFNAGLE, JH
   SEEFF, LB
AF NORMAN, JE
   BEEBE, GW
   HOFFNAGLE, JH
   SEEFF, LB
TI MORTALITY FOLLOW-UP OF THE 1942 EPIDEMIC OF HEPATITIS-B IN THE
   UNITED-STATES-ARMY
SO HEPATOLOGY
LA English
DT Article
ID PRIMARY HEPATOCELLULAR-CARCINOMA; CHRONIC LIVER-DISEASE;
   VIRUS-INFECTION; VIRAL-HEPATITIS; CARRIER STATE; CIRRHOSIS; CANCER; DNA
AB The hypothesis that adult infection with the hepatitis B virus in the United States leads to a carrier state with a high risk of primary liver cancer was tested in two ways: (a) a cohort mortality study of U.S. Army veterans given yellow fever vaccine contaminated with hepatitis B virus in 1942 and controls and (b) a case-control study comparing veterans with hepatocellular carcinoma in Veterans Affairs hospitals with matched controls with respect to receipt of contaminated vaccine in 1942. Three groups totaling 69,988 men were the subjects of the cohort study: group 1 comprised men hospitalized with hepatitis in 1942, group 2 comprised men subclinically infected in 1942 and group 3 comprised controls who entered service after the contaminated vaccine was discontinued. Hepatocellular carcinoma cases (n = 24) and control subjects (n = 63) derived from Veterans Affairs hospital discharge files were the subjects of the case-control study. Group comparisons of death rates from liver cancer were refined by expert review of records to select hepatocellular carcinoma from among all causes of death so diagnosed in the cohort study. Slightly excess mortality was found for hepatocellular carcinoma in group 2 (subclinical hepatitis B) but not for group 1 (overt hepatitis B) compared with group 3 (controls) (p = 0.08). Mortality from nonalcoholic chronic liver disease was less in group 2 than in group 3. In the case-control study, the relative risk for hepatocellular carcinoma conferred by receipt of contaminated vaccine was estimated as 3.3 (p = 0.06). We conclude from the cohort study that immunocompetent adult males rarely become carriers after hepatitis B virus infection, probably far less often than the frequently assumed rate of 5% to 10%. The small excess liver cancer mortality seen in the cohort study and the results of the case-control study are consistent, nevertheless, with the now well-established etiological role of hepatitis B virus infection in liver cancer.
C1 NATL ACAD SCI, INST MED, MED FOLLOW UP AGCY, WASHINGTON, DC 20418 USA.
   NIH, BETHESDA, MD 20892 USA.
   VET AFFAIRS MED CTR, WASHINGTON, DC 20422 USA.
   GEORGETOWN UNIV, SCH MED, WASHINGTON, DC 20057 USA.
FU NCI NIH HHS [N01-CP-31021, N01-CP-61012]
NR 32
TC 26
Z9 27
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP 790
EP 797
DI 10.1002/hep.1840180407
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA MA114
UT WOS:A1993MA11400006
PM 8406352
ER

PT J
AU MARTIN, JL
   KENNA, JG
   MARTIN, BM
   THOMASSEN, D
   REED, GF
   POHL, LR
AF MARTIN, JL
   KENNA, JG
   MARTIN, BM
   THOMASSEN, D
   REED, GF
   POHL, LR
TI HALOTHANE HEPATITIS PATIENTS HAVE SERUM ANTIBODIES THAT REACT WITH
   PROTEIN DISULFIDE-ISOMERASE
SO HEPATOLOGY
LA English
DT Article
ID ENDOPLASMIC-RETICULUM; METABOLIC BASIS; LIVER; ANTIGENS; HEPATOTOXICITY;
   AUTOANTIBODIES; HEPATOCYTES; NEOANTIGENS; SEQUENCE; MICE
AB Clinical and laboratory evidence suggests that the fulminant liver failure sometimes associated with the inhalation anesthetic halothane may be an immune-mediated toxicity. Most importantly, the vast majority of patients with a clinical diagnosis of halothane hepatitis have serum antibodies. which react with one or more specific liver microsomal proteins that have been covalently altered by the trifluoroacetyl chloride metabolite of halothane. The serum antibodies are specific to halothane hepatitis patients and are not seen in sera of patients with other types of liver pathology. In this study, a 57-kD trifluoroacetylated liver microsomal neoantigen associated with halothane hepatitis and native 57-kD protein were purified from liver microsomes of halothane-treated and -untreated rats, respectively. When the purified trifluoroacetylated 57-kD and native 57-kD proteins were used as test antigens in an enzyme-linked immunosorbent assay, serum antibodies from halothane hepatitis patients (n = 40) reacted with both of these proteins to a significantly greater extent than did serum antibodies from control patients (n = 32). On the basis of its apparent monomeric molecular mass, isoelectric point and NH2-terminal amino acid and tryptic peptide sequences. the 57-kD protein has been identified as rat liver protein disulfide isomerase. Antibodies raised against rat liver protein disulfide isomerase also reacted with a protein of approximately 58-kD in human liver microsomes.  The results of this investigation suggest that trifluoroacetylated protein disulfide isomerase is one of the immunogens associated with halothane hepatitis. In certain patients it might lead either to specific antibodies or, possibly, to specific T cells, which could be responsible for halothane hepatitis.
C1 JOHNS HOPKINS MED INST,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21287.
   NIAID,EPIDEMIOL & BIOMETRY BRANCH,BETHESDA,MD 20892.
   NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892.
RP MARTIN, JL (reprint author), NHLBI,CHEM PHARMACOL LAB,BLDG 10 ROOM 8N-115,BETHESDA,MD 20892, USA.
NR 32
TC 66
Z9 67
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP 858
EP 863
DI 10.1002/hep.1840180417
PG 6
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA MA114
UT WOS:A1993MA11400016
PM 8406360
ER

PT J
AU BACON, BR
   REBHOLZ, AE
   FRIED, M
   DIBISCEGLIE, AM
AF BACON, BR
   REBHOLZ, AE
   FRIED, M
   DIBISCEGLIE, AM
TI BENEFICIAL EFFECT OF IRON REDUCTION THERAPY IN PATIENTS WITH CHRONIC
   HEPATITIS-C WHO FAILED TO RESPOND TO INTERFERON-ALPHA
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 ST LOUIS UNIV,HLTH SCI CTR,DIV GASTROENTEROL,ST LOUIS,MO 63103.
   NIH,LIVER DIS SECT,BETHESDA,MD 20892.
NR 0
TC 39
Z9 39
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A150
EP A150
DI 10.1016/0270-9139(93)92127-L
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500373
ER

PT J
AU BATTEGAY, M
   SIMPSON, L
   SALLIE, R
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
AF BATTEGAY, M
   SIMPSON, L
   SALLIE, R
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
TI HEPATITIS DELTA-VIRUS (HDV) RNA IN SERUM OF PATIENTS WITH CHRONIC
   DELTA-HEPATITIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIH,LIVER DIS SECT,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A223
EP A223
DI 10.1016/0270-9139(93)92414-U
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500660
ER

PT J
AU BERGASA, NV
   MUKEERJE, E
   KLEINER, D
   JONES, EA
AF BERGASA, NV
   MUKEERJE, E
   KLEINER, D
   JONES, EA
TI METHOTREXATE (MTX) THERAPY IS ASSOCIATED WITH DECREASED BILE DUCTULAR
   PROLIFERATION IN CHOLESTATIC RAT LIVERS FROM BILE-DUCT RESECTION -
   IMPLICATION ON HEPATIC ENDOGENOUS OPIOIDS
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIDDKD,LIVER DIS SECT,BETHESDA,MD.
   NCI,DEPT CLIN PATHOL,BETHESDA,MD 20892.
NR 1
TC 0
Z9 0
U1 0
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A296
EP A296
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500948
ER

PT J
AU BERGASA, NV
   ALLING, DW
   TALBOT, TL
   CHIA, SC
   SOUPPAYA, M
   CONJEEVARAM, H
   SALLIE, R
   YURDAYDIN, C
   WELLS, M
   SWAIN, MG
   DIBISCEGLIE, AM
   HOOFNAGLE, JH
   JONES, EA
AF BERGASA, NV
   ALLING, DW
   TALBOT, TL
   CHIA, SC
   SOUPPAYA, M
   CONJEEVARAM, H
   SALLIE, R
   YURDAYDIN, C
   WELLS, M
   SWAIN, MG
   DIBISCEGLIE, AM
   HOOFNAGLE, JH
   JONES, EA
TI NALMEFENE THERAPY IS ASSOCIATED WITH THE RELIEF OF THE PRURITUS OF
   CHOLESTASIS - RESULTS OF A DOUBLE-BLIND RANDOMIZED PLACEBO-CONTROLLED
   TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIDDK,LIVER DIS,BETHESDA,MD.
   NIAID,DIV INTRAMURAL RES,BETHESDA,MD 20892.
   NIH,APPL CLIN ENGN SECT,BETHESDA,MD 20892.
NR 1
TC 10
Z9 10
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A177
EP A177
DI 10.1016/0270-9139(93)92233-P
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500479
ER

PT J
AU BERGASA, NV
   VERGALLA, J
   SWAIN, MG
   JONES, EA
AF BERGASA, NV
   VERGALLA, J
   SWAIN, MG
   JONES, EA
TI THE CONTENT OF PROENKEPHALIN-DERIVED OPIOIDS IS INCREASED IN THE LIVER
   OF RATS WITH CHOLESTASIS FROM BILE-DUCT RESECTION (BDR)
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIDDK,LIVER DIS SECT,BETHESDA,MD.
NR 1
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A140
EP A140
DI 10.1016/0270-9139(93)92087-G
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500333
ER

PT J
AU CHUNG, YH
   MCMAHON, B
   LANIER, A
   PARKINSON, AJ
   ZANIS, C
   DIBISCEGLIE, AM
AF CHUNG, YH
   MCMAHON, B
   LANIER, A
   PARKINSON, AJ
   ZANIS, C
   DIBISCEGLIE, AM
TI ABSENCE OF HEPATITIS-C VIRAL (HCV) INFECTION IN ALASKA PATIENTS WITH
   HEPATOCELLULAR-CARCINOMA (HCC) NOT RELATED TO HEPATITIS-B
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
   ALASKA NATIVE MED CTR,ANCHORAGE,AK.
   ARCTIC INVESTIGAT PROGRAM,ANCHORAGE,AK.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A82
EP A82
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500102
ER

PT J
AU CONJEEVARAM, H
   BALOW, JE
   AUSTIN, H
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
AF CONJEEVARAM, H
   BALOW, JE
   AUSTIN, H
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
TI LONG-TERM FOLLOW-UP OF HEPATITIS-B VIRUS (HBV) RELATED
   GLOMERULONEPHRITIS TREATED WITH ALPHA-INTERFERON
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIH,LIVER & KIDNEY DIS SECT,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A146
EP A146
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500359
ER

PT J
AU CONJEEVARAM, HS
   KLEINER, DE
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
AF CONJEEVARAM, HS
   KLEINER, DE
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
TI GROUND GLASS HEPATOCYTES IN CHRONIC HEPATITIS-B - QUANTITATION AND
   CLINICAL-SIGNIFICANCE
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIDDR,LIVER DIS SECT,BETHESDA,MD.
   NCI,PATHOL LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A227
EP A227
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500678
ER

PT J
AU DEVOID, DE
   MINKOFF, H
   GOEDERT, J
   BISWAS, R
   DIBISCEGLIE, AM
AF DEVOID, DE
   MINKOFF, H
   GOEDERT, J
   BISWAS, R
   DIBISCEGLIE, AM
TI PERINATAL TRANSMISSION OF HEPATITIS-C
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 UNESCO,DEPT PEDIAT,F-75700 PARIS,FRANCE.
   NIH,LIVER DIS SECT,BETHESDA,MD 20892.
   NIH,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892.
   SUNY HLTH SCI CTR,NEW YORK,NY.
   US FDA,CBER,HEPATITIS LAB,ROCKVILLE,MD 20857.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A229
EP A229
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500687
ER

PT J
AU DIBISCEGLIE, AM
   FRIED, MW
   SWAIN, MG
   BERGASA, NV
   YURDAYDIN, C
   SIMPSON, LH
   SALLIE, R
   CONJEEVARAM, H
   KLEINER, D
   PARK, Y
   HOOFNAGLE, JH
AF DIBISCEGLIE, AM
   FRIED, MW
   SWAIN, MG
   BERGASA, NV
   YURDAYDIN, C
   SIMPSON, LH
   SALLIE, R
   CONJEEVARAM, H
   KLEINER, D
   PARK, Y
   HOOFNAGLE, JH
TI RANDOMIZED, DOUBLE-BLIND PLACEBO-CONTROLLED TRIAL OF RIBAVIRIN THERAPY
   FOR CHRONIC HEPATITIS-C
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIH,LIVER DIS SECT,BETHESDA,MD 20892.
   NIH,PATHOL LAB,BETHESDA,MD 20892.
NR 0
TC 11
Z9 11
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A93
EP A93
DI 10.1016/0270-9139(93)91899-4
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500145
ER

PT J
AU FARCI, P
   ALTER, HJ
   WONG, D
   SHAPIRO, M
   PURCELL, RH
AF FARCI, P
   ALTER, HJ
   WONG, D
   SHAPIRO, M
   PURCELL, RH
TI PREVENTION OF HCV INFECTION IN CHIMPANZEES FOLLOWING ANTIBODY-MEDIATED
   IN-VITRO NEUTRALIZATION
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIAID,INFECT DIS LAB,ROCKVILLE,MD 20850.
   NIH,DEPT TRANSFUS MED,BETHESDA,MD 20892.
   BIOQUAL INC,ROCKVILLE,MD 20850.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A111
EP A111
DI 10.1016/0270-9139(93)91973-V
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500218
ER

PT J
AU FARSHID, M
   TABOR, E
AF FARSHID, M
   TABOR, E
TI LOCALIZING MUTATIONS IN THE RB TUMOR-SUPPRESSOR GENE IN HUMAN
   HEPATOCELLULAR-CARCINOMA CELL-LINES BY SINGLE-STRAND CONFORMATION
   POLYMORPHISM
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A183
EP A183
DI 10.1016/0270-9139(93)92259-3
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500504
ER

PT J
AU FUJIO, K
   EVARTS, RP
   HU, ZY
   MARSDEN, ER
   THORGEIRSSON, SS
AF FUJIO, K
   EVARTS, RP
   HU, ZY
   MARSDEN, ER
   THORGEIRSSON, SS
TI INVOLVEMENT OF STEM-CELL FACTOR AND ITS RECEPTOR, C-KIT, IN
   LIVER-REGENERATION VIA THE HEPATIC STEM-CELL COMPARTMENT
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A161
EP A161
DI 10.1016/0270-9139(93)92173-W
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500418
ER

PT J
AU HERION, D
   GEORGE, DT
   ECKARDT, MJ
   BEAMES, M
   DIBISCEGLIE, AM
AF HERION, D
   GEORGE, DT
   ECKARDT, MJ
   BEAMES, M
   DIBISCEGLIE, AM
TI PREVALENCE AND SIGNIFICANCE OF HEPATITIS-C VIRIAL (HCV) INFECTION AMONG
   ALCOHOLICS WITHOUT EVIDENCE OF LIVER-DISEASE
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIAAA,CLIN STUDIES LAB,BETHESDA,MD.
   NIDDK,LIVER DIS SECT,BETHESDA,MD.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A235
EP A235
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500711
ER

PT J
AU HSIA, CC
   THORGEIRSSON, SS
   TABOR, E
AF HSIA, CC
   THORGEIRSSON, SS
   TABOR, E
TI DETECTION OF HEPATITIS-B SURFACE-ANTIGEN (HBSAG) AND TRANSFORMING
   GROWTH-FACTOR-ALPHA (TGF-ALPHA) IN OVAL CELLS OF NONTUMOROUS LIVER IN
   PATIENTS WITH HEPATOCELLULAR-CARCINOMA (HCC)
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A185
EP A185
DI 10.1016/0270-9139(93)92268-5
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500514
ER

PT J
AU HU, ZG
   EVARTS, RP
   FUJIO, K
   MARSDEN, ER
   THORGEIRSSON, SS
AF HU, ZG
   EVARTS, RP
   FUJIO, K
   MARSDEN, ER
   THORGEIRSSON, SS
TI EXPRESSION OF TRANSFORMING GROWTH-FACTOR-ALPHA EPIDERMAL GROWTH-FACTOR
   RECEPTOR, HEPATOCYTE GROWTH FACTOR/C-MET, ACIDIC FIBROBLAST
   GROWTH-FACTOR FIBROBLAST GROWTH-FACTOR RECEPTORS DURING
   HEPATOCARCINOGENESIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A160
EP A160
DI 10.1016/0270-9139(93)92170-5
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500416
ER

PT J
AU KLEINER, DE
   CONJEEVARAM, H
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
AF KLEINER, DE
   CONJEEVARAM, H
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
TI DISTINCTIVE HISTOPATHOLOGICAL FEATURES OF CHRONIC HEPATITIS-B IN
   CHILDREN
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIH,PATHOL LAB,BETHESDA,MD 20892.
   NIH,LIVER DIS SECT,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A118
EP A118
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500246
ER

PT J
AU LOREAL, O
   LHELGOUALCH, A
   LIETARD, J
   UTANI, A
   YAMADA, Y
   GUILLOUZO, A
   CLEMENT, B
AF LOREAL, O
   LHELGOUALCH, A
   LIETARD, J
   UTANI, A
   YAMADA, Y
   GUILLOUZO, A
   CLEMENT, B
TI ABSENCE OF CORRELATION BETWEEN LAMININ DEPOSITION AND EXPRESSION OF
   B2-LAMININ, S-LAMININ, AND M-LAMININ GENES IN ITO CELL AND HEPATOCYTE
   PRIMARY CULTURES
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 HOP PONTCHAILLOU,INSERM,U49,F-35033 RENNES,FRANCE.
   NIDR,DEV BIOL LAB,BETHESDA,MD 20892.
RI Loreal, Olivier/G-3366-2013
NR 0
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A147
EP A147
DI 10.1016/0270-9139(93)92116-H
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500363
ER

PT J
AU MAHANEY, K
   BRANTLY, M
   REDWINE, J
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
AF MAHANEY, K
   BRANTLY, M
   REDWINE, J
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
TI ALPHA-1-ANTITRYPSIN (AAT) LEVELS AND PHENOTYPES AND PROGRESSION OF
   LIVER-DISEASE IN CHRONIC VIRAL-HEPATITIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD.
   NIDDK,LIVER DIS SECT,BETHESDA,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A272
EP A272
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500856
ER

PT J
AU MAHANEY, K
   DIBISCEGLIE, AM
   HOOFNAGLE, JH
   SALLIE, R
AF MAHANEY, K
   DIBISCEGLIE, AM
   HOOFNAGLE, JH
   SALLIE, R
TI GENOMIC VARIABILITY OF THE HEPATITIS-C VIRUS (HCV) - DEVELOPMENT OF
   MUTATIONS DURING ANTIVIRAL THERAPY
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIH,LIVER DIS SECT,BETHESDA,MD 20892.
   US FDA,HEPATITIS RES LAB,BETHESDA,MD 20014.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A92
EP A92
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500144
ER

PT J
AU MANGIA, A
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
AF MANGIA, A
   HOOFNAGLE, JH
   DIBISCEGLIE, AM
TI SERUM HBV DNA LEVELS CORRELATE WITH THE PRESENCE OF HEPATIC-INJURY IN
   PATIENTS WITH CHRONIC HEPATITIS-B SERONEGATIVE FOR HBEAG
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIH,LIVER DIS SECT,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A115
EP A115
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500234
ER

PT J
AU MASON, A
   WICK, M
   SWANSON, P
   LIE, J
   ADAMS, E
   HEBERT, B
   PERRILLO, R
AF MASON, A
   WICK, M
   SWANSON, P
   LIE, J
   ADAMS, E
   HEBERT, B
   PERRILLO, R
TI DETECTION OF HEPATITIS-B VIRUS (HBV) REPLICATION IN THE EXTRAHEPATIC
   TISSUES OF PATIENTS WITH HBV-RELATED SYNDROMES
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 VAMC,GASTROENTEROL SECT,ST LOUIS,MO.
   WASHINGTON UNIV,DEPT PATHOL,ST LOUIS,MO 63130.
   WASHINGTON UNIV,DEPT INTERNAL MED,ST LOUIS,MO 63130.
   UNIV CALIF DAVIS,DEPT PATHOL,DAVIS,CA 95616.
   NIAMS,BETHESDA,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A116
EP A116
DI 10.1016/0270-9139(93)91994-4
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500240
ER

PT J
AU MUKERJEE, E
   BERGASA, NV
   JONES, EA
AF MUKERJEE, E
   BERGASA, NV
   JONES, EA
TI DIMETHYL PROSTAGLANDIN-E2 (DMPGE2) TREATMENT DOES NOT CHANGE THE
   NATURAL-HISTORY OF THIOACETAMIDE (TAA)-INDUCED HEPATOCELLULAR NECROSIS
   IN RATS - A STEREOLOGICAL STUDY
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIDDKD,LIVER DIS SECT,BETHESDA,MD.
NR 1
TC 0
Z9 0
U1 1
U2 2
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A318
EP A318
DI 10.1016/0270-9139(93)92796-3
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99501041
ER

PT J
AU OLYNYK, J
   REDDY, R
   DIBISCEGLIE, AM
   JEFFERS, LJ
   PARKER, T
   RADICK, J
   SCHIFF, ER
   BACON, BR
AF OLYNYK, J
   REDDY, R
   DIBISCEGLIE, AM
   JEFFERS, LJ
   PARKER, T
   RADICK, J
   SCHIFF, ER
   BACON, BR
TI HEPATIC IRON CONCENTRATION AS A PREDICTOR OF RESPONSE TO
   ALPHA-INTERFERON THERAPY IN CHRONIC HEPATITIS-C
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 ST LOUIS UNIV,HLTH SCI CTR,DIV GASTROENTEROL & HEPATOL,ST LOUIS,MO 63103.
   UNIV MIAMI,CTR LIVER DIS,MIAMI,FL 33152.
   NIH,LIVER STUDIES SECT,BETHESDA,MD 20892.
NR 2
TC 11
Z9 11
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A90
EP A90
DI 10.1016/0270-9139(93)91887-X
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500133
ER

PT J
AU PREISEGGER, KH
   BISGAARD, HC
   NAGY, P
   THORGEIRSSON, SS
AF PREISEGGER, KH
   BISGAARD, HC
   NAGY, P
   THORGEIRSSON, SS
TI MALLORY BODY FORMATION IS ASSOCIATED WITH KERATIN-14 EXPRESSION IN
   MURINE LIVER
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A192
EP A192
DI 10.1016/0270-9139(93)92296-C
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500542
ER

PT J
AU SALLIE, R
   NIZETIC, D
   JONES, EA
AF SALLIE, R
   NIZETIC, D
   JONES, EA
TI THE HEMOCHROMATOSIS GENE - IDENTIFICATION OF CANDIDATE COSMID DNA/CDNA
   CLONES BY SEQUENTIAL SUBTRACTIVE AND BOOLEAN HYBRIDIZATION
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND.
   NIDDK,LIVER DIS SECT,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A275
EP A275
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500870
ER

PT J
AU SALLIE, R
   NIZETIC, D
   JONES, EA
AF SALLIE, R
   NIZETIC, D
   JONES, EA
TI THE WILSONS-DISEASE GENE - IDENTIFICATION OF CANDIDATE COSMID DNA/CDNA
   CLONES BY SEQUENTIAL SUBTRACTIVE AND BOOLEAN HYBRIDIZATION
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIDDK,LIVER DIS SECT,BETHESDA,MD 20892.
   IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A275
EP A275
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500869
ER

PT J
AU SALLIE, R
   CHIA, SC
   HOOFNAGLE, J
   DIBISCEGLIE, AM
   FEINSTONE, SM
AF SALLIE, R
   CHIA, SC
   HOOFNAGLE, J
   DIBISCEGLIE, AM
   FEINSTONE, SM
TI THE 5' END OF HCV - CHARACTERIZATION BY END-TO-END RNA LIGATION-MEDIATED
   POLYMERASE CHAIN-REACTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIDDK,LIVER DIS SECT,BETHESDA,MD 20892.
   US FDA,CBER,HEPATITIS LAB,BETHESDA,MD 20205.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A78
EP A78
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500085
ER

PT J
AU STRAIN, AJ
   MCGUINNESS, G
   GARDNER, M
   RUBIN, JS
   AARONSON, SA
AF STRAIN, AJ
   MCGUINNESS, G
   GARDNER, M
   RUBIN, JS
   AARONSON, SA
TI MODULATION OF KERATINOCYTE GROWTH-FACTOR AND FIBROBLAST GROWTH-FACTOR
   ACTIVITY IN PRIMARY RAT AND HUMAN HEPATOCYTES BY HEPARIN
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 QUEEN ELIZABETH HOSP,LIVER UNIT,BIRMINGHAM B15 2TH,W MIDLANDS,ENGLAND.
   NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A161
EP A161
DI 10.1016/0270-9139(93)92171-U
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500417
ER

PT J
AU SWAIN, MG
AF SWAIN, MG
TI PROINFLAMMATORY CYTOKINE-INDUCED ACTIVATION OF THE
   HYPOTHALAMIC-PITUITARY-ADRENAL (HPA) AXIS IS ALTERED IN RATS WITH ACUTE
   CHOLESTASIS - ADRENAL-RESPONSE TO TNF-ALPHA
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NIH,LIVER DIS SECT,BETHESDA,MD 20892.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A171
EP A171
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500456
ER

PT J
AU TABOR, E
   HSIA, CC
   MUCHMORE, E
AF TABOR, E
   HSIA, CC
   MUCHMORE, E
TI HEPATOCELLULAR-CARCINOMA (HCC) IN 2 CHIMPANZEES - STUDIES OF
   TRANSFORMING GROWTH-FACTOR-ALPHA (TGF-ALPHA) AND P53, AND DETECTION OF
   OVAL CELLS
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
   NYU,MED CTR,LEMSIP,TUXEDO PK,NY.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A194
EP A194
DI 10.1016/0270-9139(93)92303-H
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500548
ER

PT J
AU YUWEN, H
   BAYLEY, AC
   CAIRNS, J
   TABOR, E
AF YUWEN, H
   BAYLEY, AC
   CAIRNS, J
   TABOR, E
TI SEQUENCE VARIATION OF THE HEPATITIS-C VIRUS (HCV) 5'-NONCODING REGION IN
   THE SERA OF HEPATOCELLULAR-CARCINOMA (HCC) PATIENTS
SO HEPATOLOGY
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
   UNIV TEACHING HOSP,LUSAKA,ZAMBIA.
   ST FRANCIS HOSP,KATETE,ZAMBIA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 1993
VL 18
IS 4
BP A79
EP A79
DI 10.1016/0270-9139(93)91846-K
PN 2
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA LY995
UT WOS:A1993LY99500092
ER

PT J
AU ANDERSON, WF
AF ANDERSON, WF
TI MUSINGS ON THE STRUGGLE .4. AFTERMATH OF THE RAC MEETING
SO HUMAN GENE THERAPY
LA English
DT Editorial Material
C1 USC,SCH MED,NORRIS CANC CTR,LOS ANGELES,CA 90033.
RP ANDERSON, WF (reprint author), NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892, USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 1993
VL 4
IS 5
BP 555
EP 556
DI 10.1089/hum.1993.4.5-555
PG 2
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA MD263
UT WOS:A1993MD26300001
PM 8280793
ER

PT J
AU CORNETTA, K
   NGUYEN, N
   MORGAN, RA
   MUENCHAU, DD
   HARTLEY, JW
   BLAESE, RM
   ANDERSON, WF
AF CORNETTA, K
   NGUYEN, N
   MORGAN, RA
   MUENCHAU, DD
   HARTLEY, JW
   BLAESE, RM
   ANDERSON, WF
TI INFECTION OF HUMAN-CELLS WITH MURINE AMPHOTROPIC REPLICATION-COMPETENT
   RETROVIRUSES
SO HUMAN GENE THERAPY
LA English
DT Article
ID MEDIATED GENE-TRANSFER; LEUKEMIA VIRUSES; SEQUENCES; THERAPY; FRIEND;
   EXPRESSION; VECTORS; REGION; ASSAY; MICE
AB Replication of the murine wild-type 4070A amphotropic retrovirus and a recombinant amphotropic replication-competent retrovirus arising from the PA12 packaging cell line varied considerably among the primate cell types tested. Medium from infected primate fibroblasts and endothelial cells contained the highest viral titers [10(4)-10(5) focus-forming units (ffu)/ml], while most hematopoietic cell lines, such as K562 and MOLT4, were associated with viral titers in the range of 10(-3)-10(4) ffu/ml. Interestingly, HTLV-1-transformed T cell lines (TJF-2 and HM) and primary tumor infiltrating lymphocytes (TIL) had very low viral titer (0-10(1) ffu/ml). The low production of virus was not due to low infectivity and, in contrast to the virus, retroviral vectors were expressed without difficulty. Because screening for replication-competent retrovirus (RCR) is an important component of human retroviral-mediated gene therapy clinical protocols, a variety of assays were tested for their ability to detect RCR in virus-exposed cell lines. A biologic assay (3T3 amplification) and polymerase chain reaction (PCR) for the 4070A viral envelope are effective screening methods for RCR, even in cell lines associated with low virus production.
C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892.
   NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892.
   NCI,METAB BRANCH,CELLULAR IMMUNOL SECT,BETHESDA,MD 20892.
   GILEAD SCI INC,FOSTER CITY,CA 94404.
   USC,SCH MED,NORRIS CANC CTR,LOS ANGELES,CA 90033.
RP CORNETTA, K (reprint author), INDIANA UNIV,HEMATOL ONCOL SECT,IB 442,975 W WALNUT ST,INDIANAPOLIS,IN 46202, USA.
NR 28
TC 39
Z9 40
U1 0
U2 0
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 1993
VL 4
IS 5
BP 579
EP 588
DI 10.1089/hum.1993.4.5-579
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA MD263
UT WOS:A1993MD26300004
PM 8280796
ER

PT J
AU BADMAN, DG
   SCHECHTER, AN
AF BADMAN, DG
   SCHECHTER, AN
TI NIDDK SYMPOSIUM ON THE IMPACT OF MOLECULAR-GENETICS ON THE TREATMENT OF
   GENETIC-DISEASES
SO HUMAN GENE THERAPY
LA English
DT Editorial Material
RP BADMAN, DG (reprint author), NIDDK,DIV KIDNEY UROL & HEMATOL DIS,WESTWOOD BLDG,RM 3A05,5333 WESTBARD AVE,BETHESDA,MD 20892, USA.
OI Schechter, Alan N/0000-0002-5235-9408
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 1993
VL 4
IS 5
BP 635
EP 642
DI 10.1089/hum.1993.4.5-635
PG 8
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA MD263
UT WOS:A1993MD26300010
PM 8280801
ER

PT J
AU WALKER, R
   BLAESE, RM
   CARTER, CS
   CHANG, L
   KLEIN, H
   LANE, HC
   LEITMAN, SF
   MULLEN, CA
   LARSON, M
AF WALKER, R
   BLAESE, RM
   CARTER, CS
   CHANG, L
   KLEIN, H
   LANE, HC
   LEITMAN, SF
   MULLEN, CA
   LARSON, M
TI A STUDY OF THE SAFETY AND SURVIVAL OF THE ADOPTIVE TRANSFER OF
   GENETICALLY MARKED SYNGENEIC LYMPHOCYTES IN HIV-INFECTED IDENTICAL-TWINS
SO HUMAN GENE THERAPY
LA English
DT Article
ID TUMOR-INFILTRATING LYMPHOCYTES; BONE-MARROW TRANSPLANTATION;
   PLACEBO-CONTROLLED TRIAL; AIDS-RELATED COMPLEX; ACQUIRED
   IMMUNODEFICIENCY SYNDROME; HUMAN-GENE THERAPY; DOUBLE-BLIND;
   AZIDOTHYMIDINE AZT; ZIDOVUDINE AZT; VIRUS TYPE-1
AB This phase I/II pilot project will evaluate the survival, tolerance, safety, and efficacy of infusions of activated, gene marked, syngeneic T lymphocytes obtained from HIV seronegative identical twins on the functional immune status of HIV infected twin recipients. T cells from each seronegative twin will be obtained by periodic apheresis, separated into CD4 and CD8 enriched populations by monoclonal antibody affinity binding techniques, induced to polyclonal proliferation with anti-CD3 and rIL-2 stimulation, transduced with distinctive neoR retroviral vectors, and expanded 10-1,000 fold in numbers during approximately 2 weeks of culture. These marked T cell fractions will then be infused into the seropositive twins and the survival of the uniquely marked T cell populations will be monitored by vector-specific PCR, while the recipients' functional immune status is monitored by standard in vitro and in vivo testing protocols. A total of 3 cycles of treatment will be given at intervals of 6 weeks between infusions.
C1 NCI,DCBD,BETHESDA,MD 20892.
RP WALKER, R (reprint author), NIAID,LIR,BETHESDA,MD 20892, USA.
NR 45
TC 22
Z9 22
U1 0
U2 0
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 1993
VL 4
IS 5
BP 659
EP 680
DI 10.1089/hum.1993.4.5-659
PG 22
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine
GA MD263
UT WOS:A1993MD26300012
PM 8280803
ER

PT J
AU SZYMANSKI, SC
   HUMMERICH, H
   LATIF, F
   LERMAN, MI
   ROHRBORN, G
   SCHRODER, E
AF SZYMANSKI, SC
   HUMMERICH, H
   LATIF, F
   LERMAN, MI
   ROHRBORN, G
   SCHRODER, E
TI LONG-RANGE RESTRICTION MAP OF THE VONHIPPEL-LINDAU GENE REGION ON HUMAN
   CHROMOSOME-3P
SO HUMAN GENETICS
LA English
DT Article
ID DELETION MAPPING PANEL; LINKAGE ANALYSIS; DNA FRAGMENTS; CPG ISLANDS;
   CELL-LINES; DISEASE; LOCALIZATION; LOCUS; METHYLATION
AB Von Hippel-Lindau disease is a heritable tumour syndrome caused by the loss of the function of a tumour suppressor gene on the short arm of human chromosome 3. The interval RAF1-D3S18 (3p25-3p26) has been identified by genetic linkage studies to harbour the von Hippel-Lindau gene. We have constructed a long range restriction map of this region and have succeeded in demonstrating the physical linkage of loci D3S726 (DNA probe LIB31-38), D3S18 (c-LIB-1, L162E5), D3S601 (LIB19-63) and D3S587 (LIB12-48). Since multipoint analysis has located D3S601 proximal to D3S726, the physical map should be oriented with D3S726 towards the telomere. The order and distances of probes within the von Hippel-Lindau gene region is as follows: telomere - LIB31-38 - (<280 kb) - c-LIB-1 - (overlapping) - L162E5 - (900-1600 kb) - (LIB19-63, LIB12-48) - centromere. In tissues that included blood, semen and Epstein-Barr-virus-transformed lymphocytes, we detected a putative CpG island flanking D3S18.
C1 IMPERIAL CANC RES FUND,GENOME ANAL LAB,LONDON WC2A 3PX,ENGLAND.
   NCI,FREDERICK CANC RES & DEV,IMMUNOBIOL LAB,FREDERICK,MD 21701.
   UNIV DUSSELDORF,DEPT MED,INST HUMAN GENET & ANTHROPOL,D-40225 DUSSELDORF,GERMANY.
RP SZYMANSKI, SC (reprint author), UNIV ESSEN GESAMTHSCH,SCH MED,DEPT INTERNAL MED CANC RES,HUFELANDSTR 55,D-45147 ESSEN,GERMANY.
NR 32
TC 4
Z9 4
U1 0
U2 5
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0340-6717
J9 HUM GENET
JI Hum. Genet.
PD OCT
PY 1993
VL 92
IS 3
BP 282
EP 288
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA MB308
UT WOS:A1993MB30800010
PM 8406436
ER

PT J
AU BECKER, KG
   SWERGOLD, GD
   OZATO, K
   THAYER, RE
AF BECKER, KG
   SWERGOLD, GD
   OZATO, K
   THAYER, RE
TI BINDING OF THE UBIQUITOUS NUCLEAR TRANSCRIPTION FACTOR YY1 TO A CIS
   REGULATORY SEQUENCE IN THE HUMAN LINE-1 TRANSPOSABLE ELEMENT
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID POLYMERASE-II; CELL-LINE; DNA; PROTEIN; IDENTIFICATION; CARCINOMA;
   FAMILY; LONG; RNA; INSERTION
AB The first step of the currently favored model for the mechanism of transposition of the human LINE-1 element involves the synthesis of full length LINE-1 mRNA. Previous work demonstrated that the 5'-terminal 100 base pairs of the human LINE-1 element (L1Hs) has an important role in regulating it's expression. Here we report further deletion analysis revealing the presence of a cis regulatory element overlapping the region between base pairs + 12 and + 18. Oligonucleotides containing this sequence form a specific complex with a nuclear protein extracted from NTera2D1 and Jurkat cells, and with recombinant YY1 produced in E. coli. The complex is competed by YY1 binding sites found in other genes, and is ablated by anti-YY1 serum. These results suggest that YY1 is involved in the regulation of Ll Hs transcription and therefore transposition.
C1 NIAID,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892.
   NCI,BIOCHEM LAB,BETHESDA,MD 20892.
OI Becker, Kevin/0000-0002-6794-6656
NR 39
TC 78
Z9 79
U1 0
U2 0
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD OCT
PY 1993
VL 2
IS 10
BP 1697
EP 1702
DI 10.1093/hmg/2.10.1697
PG 6
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA MC223
UT WOS:A1993MC22300028
PM 8268924
ER

PT J
AU RICHARDS, FM
   LATIF, F
   LERMAN, MI
   ZBAR, B
   MAHER, ER
AF RICHARDS, FM
   LATIF, F
   LERMAN, MI
   ZBAR, B
   MAHER, ER
TI TAQI AND PSTI RFLPS IN THE VONHIPPEL-LINDAU DISEASE GENE (VHL)
SO HUMAN MOLECULAR GENETICS
LA English
DT Note
C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702.
RP RICHARDS, FM (reprint author), UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE CB2 1QP,ENGLAND.
NR 1
TC 5
Z9 5
U1 0
U2 5
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD OCT
PY 1993
VL 2
IS 10
BP 1750
EP 1750
DI 10.1093/hmg/2.10.1750
PG 1
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA MC223
UT WOS:A1993MC22300053
PM 7903582
ER

PT J
AU BULLETTI, C
   PREFETTO, RA
   BAZZOCCHI, G
   ROMERO, R
   MIMMI, P
   POLLI, V
   LANFRANCHI, GA
   LABATE, AMM
   FLAMIGNI, C
AF BULLETTI, C
   PREFETTO, RA
   BAZZOCCHI, G
   ROMERO, R
   MIMMI, P
   POLLI, V
   LANFRANCHI, GA
   LABATE, AMM
   FLAMIGNI, C
TI ELECTROMECHANICAL ACTIVITIES OF HUMAN UTERI DURING EXTRACORPOREAL
   PERFUSION WITH OVARIAN-STEROIDS
SO HUMAN REPRODUCTION
LA English
DT Article
DE ELECTROMECHANICAL ACTIVITIES; OVARIAN STEROIDS; UTERUS
ID DYSMENORRHEA; PARTURITION; RESPONSES; WOMEN
AB A new experimental system was designed to study human uterine activities based on the extra-corporeal perfusion of isolated human uteri. Electromechanical activities in the uterine wall were recorded using bipolar silver-silver electrodes, endoluminal pressure catheters and a dedicated acquisition, storage and analytical system. The electrical signals recorded were isolated spikes and rhythmic activities; the last being primarily associated with organized mechanical events. Perfusion media containing 17beta-oestradiol alone or with progesterone were used for those uteri obtained during proliferative (n = 5) or secretory (n = 5) phases of the menstrual cycle, respectively. Progesterone caused a reduction of frequency (P < 0.001) and duration (P < 0.001) of the rhythmic electrical activity, and decreased the endoluminal pressure at both detection sites (P < 0.01). 17beta-Oestradiol increased both frequency (P < 0.001) and duration (P < 0.001) of the rhythmic electrical activity as well as the endoluminal pressure at two different detection sites (3 and 5 cm from the fundus) (P < 0.05). Significant differences between the fundus and cervix sites in the uterine wall were detected. In conclusion, uterine perfusion would be useful to examine the effects of uterotonic and tocolytic drugs before administration to humans, at no risk to the patients. Oestrogens increase and progesterone decreases both electrical and mechanical uterine activities.
C1 UNIV BOLOGNA,BELLARIA HOSP,DEPT MED,I-40100 BOLOGNA,ITALY.
   WAYNE STATE UNIV,HUTZEL HOSP,DEPT OBSTET & GYNAECOL,DETROIT,MI 48201.
   NICHHD,PERINATOL BRANCH,DETROIT,MI.
   UNIV BOLOGNA,DEPT MED & GASTROENTEROL,I-40138 BOLOGNA,ITALY.
RP BULLETTI, C (reprint author), UNIV BOLOGNA,DEPT OBSTET & GYNAECOL,REPROD MED UNIT,VIA MASSARENTI 13,I-40138 BOLOGNA,ITALY.
NR 30
TC 42
Z9 42
U1 0
U2 0
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0268-1161
J9 HUM REPROD
JI Hum. Reprod.
PD OCT
PY 1993
VL 8
IS 10
BP 1558
EP 1563
PG 6
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA MA952
UT WOS:A1993MA95200007
PM 8300807
ER

PT J
AU KUMANYIKA, SK
   HEBERT, PR
   CUTLER, JA
   LASSER, VI
   SUGARS, CP
   STEFFENBATEY, L
   BREWER, AA
   CAMERON, M
   SHEPEK, LD
   COOK, NR
   MILLER, ST
AF KUMANYIKA, SK
   HEBERT, PR
   CUTLER, JA
   LASSER, VI
   SUGARS, CP
   STEFFENBATEY, L
   BREWER, AA
   CAMERON, M
   SHEPEK, LD
   COOK, NR
   MILLER, ST
TI FEASIBILITY AND EFFICACY OF SODIUM REDUCTION IN THE TRIALS OF
   HYPERTENSION PREVENTION, PHASE-I
SO HYPERTENSION
LA English
DT Article
DE HYPERTENSION, SODIUM-DEPENDENT; BLOOD PRESSURE; SODIUM, DIETARY; PRIMARY
   PREVENTION; BLACKS; WOMEN
ID LOWER BLOOD-PRESSURE; MILD HYPERTENSION; SALT REDUCTION; OBSERVATIONAL
   DATA; FINAL REPORT; DIETARY; RESTRICTION; POPULATIONS
AB Phase I of the Trials of Hypertension Prevention was a multicenter, randomized trial of the feasibility and efficacy of seven nonpharmacologic interventions, including sodium reduction, in lowering blood pressure in 30- to 54-year-old individuals with a diastolic blood pressure of 80 to 89 mm Hg. Six centers tested an intervention designed to reduce dietary sodium to 80 mmol (1800 mg)/24 h with a total of 327 active intervention and 417 control subjects. The intervention consisted of eight group and two one-to-one meetings during the first 3 months, followed by less-intensive counseling and support for the duration of the study. The mean net decrease in sodium excretion was 43.9 mmol/24 h at 18 months. Women had lower sodium intake at baseline and were therefore more likely to decrease to less than 80 mmol/24 h. Black subjects were less likely to decrease to less than 80 mmol/d, independent of sex or baseline sodium excretion. The mean (95% confidence interval) net decrease associated with treatment was -2.1 (-3.3, -0.8) mm Hg for systolic blood pressure and -1.2 (-2.0, -0.3) mm Hg for diastolic blood pressure at 18 months (both P<.01). Multivariate analyses indicated a larger systolic blood pressure effect in women (-4.44 versus -1.23 mm Hg in men), adjusted for age, race, baseline blood pressure, and baseline 24-hour urinary sodium excretion (P=.02). Dose-response analyses indicated an adjusted decrease of -1.4 mm Hg for systolic blood pressure and -0.9 mm Hg for diastolic blood pressure for a decrease of 100 mmol/24 h in 18-month sodium excretion. These results support the utility of sodium reduction as a population strategy for hypertension prevention and raise questions about possible differences in dose response associated with gender and initial level of sodium intake.
C1 JOHNS HOPKINS UNIV, SCH HYG & PUBL HLTH, DEPT EPIDEMIOL, BALTIMORE, MD 21218 USA.
   HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA.
   BRIGHAM & WOMENS HOSP, DEPT MED, CHANNING LAB, BOSTON, MA 02115 USA.
   NHLBI, DIV EPIDEMIOL & CLIN APPLICAT, PREVENT & DEMONSTRAT RES BRANCH, BETHESDA, MD 20892 USA.
   UNIV MED & DENT NEW JERSEY, NEW JERSEY MED SCH, DEPT MED, PREVENT CARDIOL PROGRAM, NEWARK, NJ 07103 USA.
   UNIV CALIF DAVIS, DEPT INTERNAL MED, DAVIS, CA 95616 USA.
   UNIV MISSISSIPPI, JACKSON, MS 39216 USA.
   ST LOUIS UNIV, SCH MED, ST LOUIS, MO 63104 USA.
FU NHLBI NIH HHS [HL-37849, HL-37852, HL-37854]
NR 36
TC 67
Z9 69
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD OCT
PY 1993
VL 22
IS 4
BP 502
EP 512
PG 11
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA MA428
UT WOS:A1993MA42800005
PM 8406655
ER

PT J
AU MATZINGER, P
AF MATZINGER, P
TI WHY POSITIVE SELECTION
SO IMMUNOLOGICAL REVIEWS
LA English
DT Review
ID MAJOR HISTOCOMPATIBILITY COMPLEX; CELL ANTIGEN RECEPTOR; MHC CLASS-I;
   LYMPHOCYTE-T PRECURSORS; SELF-TOLERANCE; TRANSGENIC MICE; REPERTOIRE
   SELECTION; THYMIC SELECTION; INVIVO INDUCTION; FOREIGN ANTIGEN
RP MATZINGER, P (reprint author), NIAID,MOLEC & CELLULAR IMMUNOL LAB,BETHESDA,MD 20892, USA.
NR 107
TC 50
Z9 50
U1 0
U2 2
PU MUNKSGAARD INT PUBL LTD
PI COPENHAGEN
PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
SN 0105-2896
J9 IMMUNOL REV
JI Immunol. Rev.
PD OCT
PY 1993
VL 135
BP 81
EP 117
DI 10.1111/j.1600-065X.1993.tb00645.x
PG 37
WC Immunology
SC Immunology
GA MH392
UT WOS:A1993MH39200004
PM 8282319
ER

PT J
AU SONG, L
   ADLER, WH
   CHUNG, S
   KIM, YH
   TENBROOK, J
   COLLINS, GD
   NAGEL, JE
AF SONG, L
   ADLER, WH
   CHUNG, S
   KIM, YH
   TENBROOK, J
   COLLINS, GD
   NAGEL, JE
TI CONCURRENT STRONG TYROSINE PHOSPHORYLATION OF A 42,000 MW ERK AND A
   100,000 MW PROTEIN IS ASSOCIATED WITH IL-2 PRODUCTION IN HUMAN JURKAT
   T-CELLS
SO IMMUNOLOGY
LA English
DT Article
ID HUMAN LYMPHOCYTES-T; MAP-2 KINASE; 3T3-L1 CELLS; ACTIVATION; CD2;
   RECEPTOR; STIMULATION; ANTIBODIES; LINE; PHOSPHATASE
AB The tyrosine phosphorylated protein(s) responsible for the signalling for interleukin-2 (IL-2) production has not been clearly defined. In this study, the relationship between IL-2 production and the protein tyrosine phosphorylation pattern of human Jurkat T cells was investigated using phosphotyrosine immunoblotting analysis. With anti-CD3 or anti-CD2 activation the cells showed only a low (anti-CD3) or a moderate (anti-CD2) level of tyrosine phosphorylation of a 42,000 MW external signal-regulated kinase (ERK), which was accompanied by undetectable (anti-CD3) or low level (anti-CD2) IL-2 production. In the presence of phorbol myristate acetate (PMA), large amounts of IL-2 were induced by both anti-CD3 and anti-CD2 stimulation, which was accompanied by strong concurrent tyrosine phosphorylation of the 42,000 MW ERK and a 100,000 MW protein. PMA alone, which induced high levels of tyrosine phosphorylation of the ERK protein, neither induced any detectable IL-2 nor increased the level of tyrosine phosphorylation of the 100,000 MW protein. These observations suggest that concurrent tyrosine phosphorylation of the 42,000 MW ERK and a 100,000 MW protein may be required for IL-2 production.
RP SONG, L (reprint author), NIA,GERONTOL RES CTR,CLIN IMMUNOL SECT,4940 EASTERN AVE,BALTIMORE,MD 21224, USA.
NR 26
TC 5
Z9 5
U1 0
U2 0
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL
SN 0019-2805
J9 IMMUNOLOGY
JI Immunology
PD OCT
PY 1993
VL 80
IS 2
BP 222
EP 228
PG 7
WC Immunology
SC Immunology
GA LZ829
UT WOS:A1993LZ82900010
PM 7903276
ER

PT J
AU MAKINO, M
   WINKLER, DF
   WUNDERLICH, J
   HARTLEY, JW
   MORSE, HC
   HOLMES, KL
AF MAKINO, M
   WINKLER, DF
   WUNDERLICH, J
   HARTLEY, JW
   MORSE, HC
   HOLMES, KL
TI HIGH EXPRESSION OF NK-11 ANTIGEN IS INDUCED BY INFECTION WITH MURINE
   AIDS VIRUS
SO IMMUNOLOGY
LA English
DT Article
ID RETROVIRUS-INDUCED IMMUNODEFICIENCY; NATURAL-KILLER CELLS; C57BL/6 MICE;
   SYNDROME MAIDS; T-CELLS; MOUSE; INDUCTION; INTERLEUKIN-2; SPECIFICITY;
   RESISTANCE
AB Spleen cells from mice infected with LP-BM5 MuLV, a causative agent of murine acquired immunodeficiency syndrome (MAIDS), were tested for frequency of NK-1.1+ cells and natural killer (NK) activity. During the first 3 weeks following infection, NK activity was well conserved, but by 9-12 weeks post-infection (p.i.), killer activity was depressed: however, the frequency of NK-1.1+ cells increased within 4 weeks of infection and remained elevated thereafter, even following the decline in functional killing activity. Since the absolute number of NK-1.1 + cells increased after infection, the ability of each NK-1.1+ cell to kill the targets seems drastically impaired. Extraordinary expansion of NK-1.1-positive cells was induced by infection with LP-BM 5-defective virus (BM5def), a crucial element for MAIDS induction, but not with a helper non-pathogenic virus. With advance of MAIDS the NK-1.1 antigen (Ag) was preferentially expressed on B220+ and Thy-1+ cells, in contrast to CD4+ and CD8+ cells, and among activated large cells a higher proportion was NK-1.1- than NK-1.1-. Mice with graft-versus-host disease (GVHD) due to class II major histocompatibility complex (MHC) Ag disparity showed a high frequency of NK-1.1 expression in association with other phenotypic alterations, very similar to those seen in mice with MAIDS. In contrast, B6-lpr/lpr mice developed similar activation of B cells but did not exhibit enhanced expression of the NK-1.1 marker. Thus, enhanced expression of the NK-1.1 Ag might be associated with chronic activation of lymphocytes through a common but not universal pathway.
C1 NIH,IMMUNOPATHOL LAB,BETHESDA,MD 20892.
   NIH,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892.
   NIH,BIOL RESOURCES BRANCH,BETHESDA,MD 20892.
RP MAKINO, M (reprint author), NATL INST HLTH,DEPT BACTERIAL & BLOOD PROD,1-23-1 TOYAMA,SHINJUKU KU,TOKYO 162,JAPAN.
OI Morse, Herbert/0000-0002-9331-3705
FU NIAID NIH HHS [N0I AI-72622]
NR 27
TC 16
Z9 16
U1 0
U2 0
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL
SN 0019-2805
J9 IMMUNOLOGY
JI Immunology
PD OCT
PY 1993
VL 80
IS 2
BP 319
EP 325
PG 7
WC Immunology
SC Immunology
GA LZ829
UT WOS:A1993LZ82900025
PM 8262561
ER

PT J
AU ADHYA, S
AF ADHYA, S
TI A REGULATORY APPARATUS WITH DNA LOOPING
SO INDIAN JOURNAL OF BIOCHEMISTRY & BIOPHYSICS
LA English
DT Review
ID ESCHERICHIA-COLI; GALACTOSE OPERON; RNA-POLYMERASE; GAL OPERON;
   REPRESSOR; TRANSCRIPTION; BINDING; GENE; PROMOTER; COMMUNICATION
RP ADHYA, S (reprint author), NCI,MOLEC BIOL LAB,BETHESDA,MD 20892, USA.
NR 36
TC 0
Z9 0
U1 0
U2 0
PU COUNCIL SCIENTIFIC INDUSTRIAL RESEARCH
PI NEW DELHI
PA PUBL & INFO DIRECTORATE, NEW DELHI 110012, INDIA
SN 0301-1208
J9 INDIAN J BIOCHEM BIO
JI Indian J. Biochem. Biophys.
PD OCT
PY 1993
VL 30
IS 5
BP 247
EP 251
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA MG720
UT WOS:A1993MG72000001
PM 8144166
ER

PT J
AU TAMISLEMONDA, CS
   BORNSTEIN, MH
AF TAMISLEMONDA, CS
   BORNSTEIN, MH
TI ANTECEDENTS OF EXPLORATORY COMPETENCE AT ONE-YEAR
SO INFANT BEHAVIOR & DEVELOPMENT
LA English
DT Article
DE SYMBOLIC PLAY; EXPLORATION; HABITUATION
ID INDIVIDUAL-DIFFERENCES; UNITED-STATES; NATURALISTIC EXCHANGES; INFANT
   INTERACTION; MOTHER-INFANT; SAMPLE-SIZE; FREE PLAY; ATTENTION; LANGUAGE;
   CHILD
AB The start of the 2nd year is a period of transition and substantial variability among toddlers in play and attention abilities. This longitudinal study examined the antecedents of variation among 13-month-old toddlers in these exploratory competencies in the infants' own information-processing abilities at 5 months (indexed by visual fixation in the laboratory), the infants' vocal and exploratory activities at 5 months (measured during naturalistic observation in the home), mothers' stimulation of infants at 5 months, and mothers' IQ. Infant visual fixation and maternal IQ predicted toddler symbolic play; furthermore, infant visual fixation, infant activity, and maternal IQ predicted toddler attention span. In contrast, mothers' early stimulation did not predict ploy or attention in toddlers. Structural equation modeling was used to assess prediction of the three significant antecedents (infant visual fixation, infant activity, and maternal IQ) to toddlers' exploratory competence, a latent variable representing the shared variance between play and attention. Together, the three predictors accounted for 50% of the variance in toddler exploratory competence. These data broaden the scope of infant and mother prediction beyond toddler verbal-representational abilities to encompass domains of toddler exploration.
C1 NICHHD,BETHESDA,MD 20892.
RP TAMISLEMONDA, CS (reprint author), NYU,DEPT APPL PSYCHOL,239 GREENE ST,5TH FLOOR,NEW YORK,NY 10003, USA.
NR 71
TC 11
Z9 11
U1 1
U2 3
PU ABLEX PUBL CORP
PI NORWOOD
PA 355 CHESTNUT ST, NORWOOD, NJ 07648
SN 0163-6383
J9 INFANT BEHAV DEV
JI Infant Behav. Dev.
PD OCT-DEC
PY 1993
VL 16
IS 4
BP 423
EP 439
DI 10.1016/0163-6383(93)80002-P
PG 17
WC Psychology, Developmental
SC Psychology
GA MP943
UT WOS:A1993MP94300002
ER

PT J
AU MANNING, DS
   STEWART, SJ
AF MANNING, DS
   STEWART, SJ
TI EXPRESSION OF THE MAJOR OUTER-MEMBRANE PROTEIN OF CHLAMYDIA-TRACHOMATIS
   IN ESCHERICHIA-COLI
SO INFECTION AND IMMUNITY
LA English
DT Article
ID MURAMIC ACID; GENES
AB The major outer membrane protein (MOMP) of Chlamydia trachomatis was expressed in Escherichia coli. To assess whether it assembled into a conformationally correct structure at the cell surface, we characterized the recombinant MOMP (rMOMP) by Western immunoblot analysis, indirect immunofluorescence, and immunoprecipitation with monoclonal antibodies (MAbs) that recognize contiguous and conformational MOMP epitopes. Western blot analysis showed that most of the rMOMP comigrated with authentic monomer MOMP, indicating that its signal peptide was recognized and cleaved by E. coli. The rMOMP could not be detected on the cell surface of viable or formalin-killed E. coli organisms by indirect immunofluorescence staining with a MAb specific for a MOMP contiguous epitope. In contrast, the same MAb readily stained rMOMP-expressing E. coli cells that had been permeablized by methanol fixation. A MAb that recognizes a conformational MOMP epitope and reacted strongly with formalin- or methanol-fixed elementary bodies failed to stain formalin- or methanol-fixed E. coli expressing rMOMP. Moreover, this MAb did not immunoprecipitate rMOMP from expressing E. coli cells even though it precipitated the authentic protein from lysates of C. trachomatis elementary bodies. Therefore we concluded that rMOMP was not localized to the E. coli cell surface and was not recognizable by a conformation-dependent antibody. These results indicate that rMOMP expressed by E. coli is unlikely to serve as an accurate model of MOMP structure and function. They also question the utility of rMOMP as a source of immunogen for eliciting neutralizing antibodies against conformational antigenic sites of the protein.
RP MANNING, DS (reprint author), NIAID,ROCKY MT LABS,INTRACELLULAR PARASITES LAB,HAMILTON,MT 59840, USA.
NR 19
TC 8
Z9 8
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD OCT
PY 1993
VL 61
IS 10
BP 4093
EP 4098
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA LZ264
UT WOS:A1993LZ26400011
PM 8406797
ER

PT J
AU MURDIN, AD
   SU, H
   MANNING, DS
   KLEIN, MH
   PARNELL, MJ
   CALDWELL, HD
AF MURDIN, AD
   SU, H
   MANNING, DS
   KLEIN, MH
   PARNELL, MJ
   CALDWELL, HD
TI A POLIOVIRUS HYBRID EXPRESSING A NEUTRALIZATION EPITOPE FROM THE MAJOR
   OUTER-MEMBRANE PROTEIN OF CHLAMYDIA-TRACHOMATIS IS HIGHLY IMMUNOGENIC
SO INFECTION AND IMMUNITY
LA English
DT Article
ID PROTECTIVE MONOCLONAL-ANTIBODIES; ANTIGENIC HYBRID; PEPTIDE-SYNTHESIS;
   ANIMAL-MODEL; AMINO-ACID; VACCINES; RESOLUTION; INFECTIONS; DOMAINS;
   MONKEYS
AB Trachoma and sexually transmitted diseases caused by Chlamydia trachomatis are major health problems worldwide. Epitopes on the major outer membrane protein (MOMP) of C. trachomatis have been identified as important targets for the development of vaccines. In order to examine the immunogenicity of a recombinant vector expressing a chlamydial epitope, a poliovirus hybrid was constructed in which part of neutralization antigenic site I of poliovirus type 1 Mahoney (PV1-M) was replaced by a sequence from variable domain I of the MOMP of C. trachomatis serovar A. The chlamydial sequence included the neutralization epitope VAGLEK. This hybrid was viable, grew very well compared with PV1-M, and expressed both poliovirus and chlamydial antigenic determinants. When inoculated into rabbits, this hybrid was highly immunogenic, inducing a strong response against both PV1-M and C. trachomatis serovar A. Antichlamydia titers were 10- to 100-fold higher than the titers induced by equimolar amounts of either purified MOMP or a synthetic peptide expressing the VAGLEK epitope. Furthermore, rabbit antisera raised against this hybrid neutralized chlamydial infectivity both in vitro, for hamster kidney cells, and passively in vivo, for conjunctival epithelia of cynomolgus monkeys. Because poliovirus infection induces a strong mucosal immune response in primates and humans, these results indicate that poliovirus-chlamydia hybrids could become powerful tools for the study of mucosal immunity to chlamydial infection and for the development of recombinant chlamydial vaccines.
C1 NIAID,ROCKY MT LABS,INTRACELLULAR PARASITES LAB,HAMILTON,MT 59840.
RP MURDIN, AD (reprint author), CONNAUGHT CTR BIOTECHNOL RES,1755 STEELES AVE W,N YORK M2R 3T4,ON,CANADA.
NR 53
TC 17
Z9 18
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD OCT
PY 1993
VL 61
IS 10
BP 4406
EP 4414
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA LZ264
UT WOS:A1993LZ26400055
PM 7691749
ER

PT J
AU PETTINELLI, CB
   SCHNITTMAN, SM
AF PETTINELLI, CB
   SCHNITTMAN, SM
TI TREATMENT RESEARCH PRIORITIES FOR HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION
SO INFECTIOUS AGENTS AND DISEASE-REVIEWS ISSUES AND COMMENTARY
LA English
DT Review
DE HIV-1; AIDS; ANTIRETROVIRAL THERAPIES; IMMUNE-BASED THERAPIES; ACUTE HIV
   INFECTION
ID IMMUNE-DEFICIENCY SYNDROME; PRIMARY HIV-1 INFECTION; AIDS-RELATED
   COMPLEX; REVERSE-TRANSCRIPTASE INHIBITORS; ALPHA-INTERFERON THERAPY;
   LYMPHOCYTE-T RESPONSES; KAPOSIS-SARCOMA; TYPE-1 INFECTION;
   LYMPHOBLASTOID INTERFERON; RECOMBINANT INTERLEUKIN-2
AB Viral infections such as with the human immunodeficiency virus (HIV) present difficult challenges for the development of effective antiviral therapies. These viruses depend on the host cell machinery for their existence, and interference with these processes typically interferes with other important host physiology. HIV presents other challenges as well because of its inherent pathogenic destruction of the immune system. It is the goal of HIV therapeutics to attempt to cure HIV infection, or if that is not possible, to stop HIV disease progression while preserving a high quality of life for HIV-infected individuals. This may be achieved through an effective combination of interference with the viral life cycle and the pathogenic processes, and by slowing or reversing the immunologic dysfunction that leads to the complications of HIV infection. Unprecedented progress has been made in understanding the virus and HIV disease pathogenesis. This knowledge has led to the identification of viral features that have become targets for therapeutic intervention. This article reviews the most important priorities of HIV treatment research for adult HIV-infected patients for the immediate future. These priorities include the following: development of new antiretroviral compounds and their application as both monotherapies and in combination therapy approaches; immune-based therapeutic approaches; and research and treatment for acute or primary HIV infections.
C1 NIAID,DIV AIDS,ROCKVILLE,MD.
NR 134
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 1056-2044
J9 INFECT AGENT DIS
JI Infect. Agents Dis.-Rev. Issues Comment.
PD OCT
PY 1993
VL 2
IS 5
BP 291
EP 303
PG 13
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA NC594
UT WOS:A1993NC59400001
PM 8173814
ER

PT J
AU BROWNSON, RC
   ALAVANJA, MCR
   HOCK, ET
AF BROWNSON, RC
   ALAVANJA, MCR
   HOCK, ET
TI RELIABILITY OF PASSIVE SMOKE EXPOSURE HISTORIES IN A CASE-CONTROL STUDY
   OF LUNG-CANCER
SO INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
ID ENVIRONMENTAL TOBACCO-SMOKE
AB Despite the growing number of studies on the health effects of passive smoke exposure, few data exist on the quality of questionnaire data on passive smoking. To measure the reliability of passive smoking histories, re-interviews were conducted for 110 subjects (37 cases and 73 controls) as part of a larger study of lung cancer among non-smoking women in Missouri. Agreement was high both for parental smoking status (94% concordance; kappa = 0.82) and for spousal smoking status (84% concordance; kappa = 0.67). Concordance also was relatively high for cigarette pack-years of exposure due to the parents or spouse. Reliability tended to be somewhat higher among controls than among cases, and for exposure due to a parent or spouse than for that due to other household members. Questions on the perceived harmfulness of passive smoke exposure showed no differences between cases and controls. These findings indicate a high degree of repeatability in responses regarding passive smoking, but also suggest the potential for misclassification of passive smoke exposure status, the desirability of standardized questions on passive smoking, and the need for additional studies of reliability and validity.
C1 INFORMAT MANAGEMENT SERV INC,ROCKVILLE,MD.
   NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892.
RP BROWNSON, RC (reprint author), MISSOURI DEPT HLTH,DIV CHRON DIS PREVENT & HLTH PROMOT,201 BUSINESS LOOP 70 W,COLUMBIA,MO 65203, USA.
FU NCI NIH HHS [N01-CP7-1096-01, N01-CP7-1096-02]
NR 25
TC 37
Z9 37
U1 0
U2 0
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0300-5771
J9 INT J EPIDEMIOL
JI Int. J. Epidemiol.
PD OCT
PY 1993
VL 22
IS 5
BP 804
EP 808
DI 10.1093/ije/22.5.804
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA MJ331
UT WOS:A1993MJ33100006
PM 8282458
ER

PT J
AU SUZUKI, H
   ROMANOSPICA, V
   GEORGIOU, P
   FISHER, RJ
   PAPAS, TS
   BHAT, N
AF SUZUKI, H
   ROMANOSPICA, V
   GEORGIOU, P
   FISHER, RJ
   PAPAS, TS
   BHAT, N
TI CHARACTERIZATION OF ECTOPICALLY-EXPRESSED ETS1 IN HUMAN COLON-CANCER
   CELLS - INDUCTION OF PUTATIVE ETS1-TARGET GENE
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE ETS1; COLON CANCER CELLS; DNA BINDING; CELL BACKGROUND
ID SEQUENCE-SPECIFIC BINDING; LONG TERMINAL REPEAT; DNA-BINDING; C-FOS;
   TRANSCRIPTION FACTOR; C-ETS-1 PROTOONCOGENE; RESPONSE ELEMENT;
   LEUKEMIA-VIRUS; PROTO-ONCOGENE; FAMILY
AB We have previously shown that the ETS1 gene is expressed in a tissue-specific manner, and encodes a transcription factor, that may be involved in lymphocyte development, activation and proliferation. To understand the ETS1 function in non-lymphoid cells, we have ectopically expressed ETS1 protein in a human colon cancer cell line, and studied its biochemical properties. The 51 kDa ETS1 protein expressed in transfected cells localized in both the nucleus and the cytoplasm, has similar biochemical properties compared to ETS1 protein expressed in lymphoid cells. The ectopically expressed ETS1 binds to the DNA in sequence-specific manner and the binding activity is affected by the flanking sequences outside the 'GGA' core. Our results also demonstrate that the DNA-binding activity of full-length ETS1 is similar in lymphoid and non-lymphoid cells. The ETS1 expressed in DLD-1 cells is biologically active since it induces a 54.5 kDa polypeptide, whose expression level correlates with the expression of ETS1 in DLD-1 cells.
C1 NCI,MOLEC ONCOL LAB,POB B,FREDERICK,MD 21702.
   INC DYNCORP,PROGRAM RESOURCES,FREDERICK,MD 21702.
RI Fisher, Robert/B-1431-2009
NR 52
TC 11
Z9 11
U1 0
U2 2
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 OCT
PY 1993
VL 3
IS 4
BP 565
EP 573
PG 9
WC Oncology
SC Oncology
GA LX916
UT WOS:A1993LX91600003
PM 21573401
ER

PT J
AU ALLENHOFFMANN, BL
   SCHLOSSER, SJ
   RHIM, JS
AF ALLENHOFFMANN, BL
   SCHLOSSER, SJ
   RHIM, JS
TI USE OF RHEK-1 IMMORTALIZED HUMAN KERATINOCYTES FOR DETECTION OF INDUCED
   MUTATION AT THE HYPOXANTHINE-GUANINE PHOSPHORIBOSYLTRANSFERASE LOCUS
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE KERATINOCYTE; HYPOXANTHINE-GUANINE PHOSPHORIBOSYLTRANSFERASE;
   MUTAGENICITY TEST; POLYCYCLIC AROMATIC HYDROCARBONS
ID HUMAN EPIDERMAL-KERATINOCYTES; EPITHELIAL-CELLS INVITRO; NEOPLASTIC
   TRANSFORMATION; CHEMICAL CARCINOGENS; IONIZING-RADIATION; METABOLISM;
   BENZO(A)PYRENE; FIBROBLASTS; MUTAGENESIS; INDUCTION
AB We report here the use of a nontumorigenic, immortalized human keratinocyte line, RHEK-1, for the detection of rare mutations induced at the hypoxanthine-guanine phosphoribosyltransferase locus. RHEK-1 keratinocytes were used as a prototype to determine mutagen treatment conditions, plating density, and phenotypic expression time for maximum recovery of thioguanine-resistant mutants. Mutation frequency was measured after exposure to ionizing radiation or to polycyclic aromatic hydrocarbons. 7,12-Dimethylbenz[a]-anthracene and benzo[a]pyrene caused almost no cytotoxicity, but induced thioguanine-resistant mutants at frequencies as much as 30 to 40-fold higher than the median spontaneous frequency of 7 x 10(-6). X-irradiation was also an efficient mutagen in RHEK-1 keratinocytes. The mutants were aminopterin-sensitive and possessed no measurable hypoxanthine-guanine phosphoribosyltransferase activity. The RHEK-1 human epithelial cell line is therefore useful for the study of induced mutation at a defined genetic locus as well as being an important model for the investigation, of molecular, cellular and genetic mechanisms of neoplastic transformation in human stratified squamous epithelia.
C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892.
RP ALLENHOFFMANN, BL (reprint author), UNIV WISCONSIN,DEPT PATHOL,5638 MED SCI CTR,1300 UNIV AVE,MADISON,WI 53706, USA.
NR 42
TC 1
Z9 1
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 OCT
PY 1993
VL 3
IS 4
BP 619
EP 625
PG 7
WC Oncology
SC Oncology
GA LX916
UT WOS:A1993LX91600011
PM 21573409
ER

PT J
AU YASUDA, D
   IGUCHI, H
   IKEDA, Y
   NISHIMURA, S
   STEEG, PS
   MISAWA, T
   NAWATA, H
   KONO, A
AF YASUDA, D
   IGUCHI, H
   IKEDA, Y
   NISHIMURA, S
   STEEG, PS
   MISAWA, T
   NAWATA, H
   KONO, A
TI POSSIBLE ASSOCIATION OF NM23 GENE-EXPRESSION AND KI-RAS POINT MUTATIONS
   WITH METASTATIC POTENTIAL IN HUMAN PANCREATIC CANCER-DERIVED CELL-LINES
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE NM23 GENE; KI-RAS MUTATION; METASTASIS; PANCREATIC CANCER
ID NUDE-MICE; TUMOR; ESTABLISHMENT; CARCINOMA; POLYMERASE; CULTURE; SITES
AB Nm23 gene expression and Ki-ras point mutations of eight human pancreatic cancer-derived cell lines with different metastatic capabilities were studied. Nm23 gene expression was significantly reduced in the cell lines with a high metastatic potential as compared with those with a low meta static potential (p<0.05). The same mutation at codon 12 of the Ki-ras gene (Gly12 to Asp12) was found in all cell lines with a high metastatic potential. These findings suggest a possible association of metastatic potential with Nm23 gene expression as well as the mutation of Ki-ras gene in human pancreatic cancer.
C1 NATL KYUSHU CANC CTR,RES INST,FUKUOKA,JAPAN.
   NATL CANC CTR,RES INST,DIV BIOL,TOKYO 104,JAPAN.
   NIH,PATHOL LAB,BETHESDA,MD 20892.
RP YASUDA, D (reprint author), KYUSHU UNIV,FAC MED,DEPT INTERNAL MED 3,FUKUOKA 812,JAPAN.
NR 25
TC 7
Z9 7
U1 0
U2 1
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 OCT
PY 1993
VL 3
IS 4
BP 641
EP 644
PG 4
WC Oncology
SC Oncology
GA LX916
UT WOS:A1993LX91600014
PM 21573412
ER

PT J
AU SATO, S
AF SATO, S
TI ALDOSE REDUCTASE THE MAJOR PROTEIN ASSOCIATED WITH NAPHTHALENE
   DIHYDRODIOL DEHYDROGENASE-ACTIVITY IN RAT LENS
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
DE CATARACT; NAPHTHALENE; ALDOSE REDUCTASE; ALDOSE REDUCTASE INHIBITORS;
   DIHYDRODIOL DEHYDROGENASE
ID ALDEHYDE REDUCTASE; 3-ALPHA-HYDROXYSTEROID DEHYDROGENASE; MULTIPLE
   FORMS; LIVER CYTOSOL; CATARACT; PURIFICATION; INHIBITION; IDENTITY;
   INVITRO; KIDNEY
AB Purpose. Recent studies have indicated that certain aldose reductase inhibitors prevent the formation of cataracts in naphthalene-fed rats. The study was designed to investigate whether aldose reductase itself is involved in the metabolism of naphthalene in the lens and the mechanism of this cataract formation.
   Methods. Aldose reductase was purified from whole rat lens using a series of chromatographic steps that include gel filtration, affinity chromatography, and chromatofocusing. The dehydrogenase activity of the purified enzyme was evaluated with 1,2-dihydro-1,2-dihydroxynaphthalene (naphthalene dihydrodiol) as substrate. The same dehydrogenase activity was also examined with the recombinant protein obtained from rat lens aldose reductase clone.
   Results. Throughout the purification steps, dehydrogenase activity with naphthalene dihydrodiol as substrate coeluted with aldose reductase activity assayed with DL-glyceraldehyde as substrate. The purified aldose reductase, which appeared as a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, displayed dehydrogenase activity with naphthalene dihydrodiol as a substrate similar to that observed with the crude extract from whole rat lens. Recombinant protein from rat lens aldose reductase clone also displayed dehydrogenase activity similar to that observed with purified rat lens aldose reductase. Both the reductase and dehydrogenase activities of purified aldose reductase were inhibited by aldose reductase inhibitors. However, inhibition of dehydrogenase activity was less than reductase activity. Aldehyde reductase, an another nicotinamide adenine dinucleotide phosphate-dependent reductase, also displayed dihydrodiol dehydrogenase activity with naphthalene dihydrodiol and this activity was also inhibited by aldose reductase inhibitors.
   Conclusions. Aldose reductase displays dehydrogenase activity in addition to reductase activity. In rat lens aldose reductase is a major protein associated with naphthalene dihydrodiol dehydrogenase activity. This suggests that aldose reductase is linked to 1,2-dihydroxynaphthalene formation in rat lens and the subsequent formation of cataracts in naphthalene-fed rats.
RP SATO, S (reprint author), NEI,OCULAR THERAPEUT LAB,BLDG 10,RM 10B09,BETHESDA,MD 20892, USA.
NR 24
TC 11
Z9 11
U1 0
U2 2
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD OCT
PY 1993
VL 34
IS 11
BP 3172
EP 3178
PG 7
WC Ophthalmology
SC Ophthalmology
GA MB601
UT WOS:A1993MB60100016
PM 8407226
ER

PT J
AU WEST, S
   MUNOZ, B
   BOBO, L
   QUINN, TC
   MKOCHA, H
   LYNCH, M
   MMBAGA, BBO
   VISCIDI, R
AF WEST, S
   MUNOZ, B
   BOBO, L
   QUINN, TC
   MKOCHA, H
   LYNCH, M
   MMBAGA, BBO
   VISCIDI, R
TI NONOCULAR CHLAMYDIA INFECTION AND RISK OF OCULAR REINFECTION AFTER MASS
   TREATMENT IN A TRACHOMA HYPERENDEMIC AREA
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
DE TRACHOMA; CHLAMYDIA; INFECTION
ID ENZYME-IMMUNOASSAY; CENTRAL TANZANIA; EPIDEMIOLOGY; DIAGNOSIS
AB Purpose. The presence of nasal discharge on a child's face increases the risk of active trachoma, suggesting that Chlamydia trachomatis in nasal secretions may be a possible source of ocular reinfection. The prevalence of chlamydia in nasal secretions and the risk of reinfection after mass treatment was investigated in a hyperendemic area of Tanzania.
   Methods. In one village a total of 232 children aged 1 to 7 years were followed before and after mass treatment. Clinical trachoma, and microbiologic evidence of chlamydia, were assessed at baseline, 2 and 4 weeks into mass treatment, and 4 weeks after treatment stopped. The presence of chlamydia in ocular and nasal secretions was determined by polymerase chain reaction-enzyme immunoassay techniques.
   Results. Of the 232 children, 59% had clinical trachoma and 27% had nasal specimens positive for chlamydia. Children with positive ocular chlamydia specimens and/or clinical trachoma were significantly more likely to have positive nasal specimens. At the end of mass treatment, only 4% of children had positive ocular specimens. However, 1 month after treatment stopped, the incidence of new infection was 2 1%. The rate of new ocular infections in those who had-negative ocular specimens after treatment was similar between those who had positive and those who had negative nasal specimens at baseline. Positive ocular specimens at baseline was not a predictor of risk of new infection after treatment (odds ratio = 1. 18, 95% confidence interval = 0.58, 2.40), suggesting these new infections were not the result of latent or persistent organism.
   Conclusions. These data do not support a role for nasal secretions in causing reinfection after treatment. One mass topical treatment alone is unlikely to be effective in trachoma hyperendemic areas as shown by the rapid re-emergence of infection.
C1 JOHNS HOPKINS UNIV,DANA CTR PREVENT OPHTHALMOL,BALTIMORE,MD 21218.
   JOHNS HOPKINS UNIV,DEPT PEDIAT,EUDOWOOD DIV INFECT DIS,BALTIMORE,MD 21218.
   NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892.
   KONGWA TRACHOMA PROJECT,KONGWA,TANZANIA.
   HELEN KELLER INT,NEW YORK,NY.
FU NIAID NIH HHS [2 P01 AI 16959-09, N01 AI 52579]
NR 12
TC 31
Z9 31
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD OCT
PY 1993
VL 34
IS 11
BP 3194
EP 3198
PG 5
WC Ophthalmology
SC Ophthalmology
GA MB601
UT WOS:A1993MB60100019
PM 8407229
ER

PT J
AU JENSEN, PS
   KORETZ, D
   LOCKE, BZ
   SCHNEIDER, S
   RADKEYARROW, M
   RICHTERS, JE
   RUMSEY, JM
AF JENSEN, PS
   KORETZ, D
   LOCKE, BZ
   SCHNEIDER, S
   RADKEYARROW, M
   RICHTERS, JE
   RUMSEY, JM
TI CHILD AND ADOLESCENT PSYCHOPATHOLOGY RESEARCH - PROBLEMS AND PROSPECTS
   FOR THE 1990S
SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY
LA English
DT Article
AB In November 1990 the National Institute of Mental Health (NIMH) convened a special conference of over 100 scientists and leaders to outline specific strategies and research initiatives that should be developed to implement the recently released National Plan for Research on Child and Adolescent Mental Disorders. Participants included journal editors, educators from psychology and psychiatry, representatives from private foundations, and leaders of research program areas in public funding agencies. Critical knowledge gaps were identified in five areas of child and adolescent psychopathology, including depression, attention deficit hyperactivity disorder, conduct disorder, the anxiety disorders, and the developmental disorders. For each of these areas, special emphasis was placed on developing new ideas and obtaining critical input from other areas of investigation. This report summarizes the identified research gaps and recommends research initiatives to implement the National Plan, as outlined by the conference participants.
RP JENSEN, PS (reprint author), NIMH,CHILD & ADOLESCENT DISORDERS RES BRANCH,ROOM 18C-17,ROCKVILLE,MD 20857, USA.
OI Richters, John/0000-0002-6780-1828; Jensen, Peter/0000-0003-2387-0650
NR 4
TC 35
Z9 36
U1 0
U2 1
PU PLENUM PUBL CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
SN 0091-0627
J9 J ABNORM CHILD PSYCH
JI J. Abnorm. Child Psychol.
PD OCT
PY 1993
VL 21
IS 5
BP 551
EP 580
DI 10.1007/BF00916319
PG 30
WC Psychology, Clinical; Psychology, Developmental
SC Psychology
GA MG536
UT WOS:A1993MG53600006
PM 7507503
ER

PT J
AU TSAI, CC
   FOLLIS, KE
   GRANT, RF
   NOLTE, RE
   BARTZ, CR
   BENVENISTE, RE
   SAGER, PR
AF TSAI, CC
   FOLLIS, KE
   GRANT, RF
   NOLTE, RE
   BARTZ, CR
   BENVENISTE, RE
   SAGER, PR
TI EFFECT OF DOSING FREQUENCY ON ZDV PROPHYLAXIS IN MACAQUES INFECTED WITH
   SIMIAN IMMUNODEFICIENCY VIRUS
SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE ANTIVIRAL EFFECT; ZIDOVUDINE; PROPHYLAXIS; DOSING FREQUENCY; SIV
ID PLACEBO-CONTROLLED TRIAL; RHESUS-MONKEYS; DOUBLE-BLIND; ZIDOVUDINE; SIV;
   AIDS; AZIDOTHYMIDINE; LENTIVIRUSES; SEQUENCE; THERAPY
AB The effect of dosing frequency on zidovudine (ZDV) prophylaxis against simian immunodeficiency virus (SIV) infection was examined in long-tailed macaque monkeys (Macaca fascicularis). The results indicate that dosing frequency is extremely important for drug efficacy. The monkeys were divided into three groups based on dosing frequencies of 6-, 8-, or 12-h intervals. All were given a total daily dose of 100 mg/kg of ZDV. The drug was administered subcutaneously starting 24 h before SIV inoculation, and treatment continued for an additional 28 days. With the total daily dose held constant, ZDV was most therapeutic when administered at 12-h intervals, less effective at 8-h intervals, and least effective at 6-h intervals. These results indicate that early ZDV treatment based on infrequent but high dosages may increase the antiretroviral effect of the drug. These findings could serve as a model for ZDV chemoprophylaxis in humans. In cases involving accidental exposure to SIV or human immunodeficiency virus (HIV-1 or HIV-2), immediate, high-dosage therapies may be most therapeutic.
C1 UNIV WASHINGTON, REG PRIMATE RES CTR, SEATTLE, WA 98195 USA.
   NCI, VIRAL CARCINOGENESIS LAB, FREDERICK, MD 21701 USA.
   NIAID, DEV THERAPEUT BRANCH, BETHESDA, MD 20892 USA.
FU NCRR NIH HHS [RR00166]; NIAID NIH HHS [NIAID NO1-AI-15120]
NR 29
TC 30
Z9 30
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 J ACQ IMMUN DEF SYND
JI J. Acquir. Immune Defic. Syndr.
PD OCT
PY 1993
VL 6
IS 10
BP 1086
EP 1092
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA MC829
UT WOS:A1993MC82900002
PM 8410666
ER

PT J
AU MOFENSON, LM
   BETHEL, J
   MOYE, J
   FLYER, P
AF MOFENSON, LM
   BETHEL, J
   MOYE, J
   FLYER, P
TI EFFECT OF INTRAVENOUS IMMUNOGLOBULIN (IVIG) ON CD4+ LYMPHOCYTE DECLINE
   IN HIV-INFECTED CHILDREN IN A CLINICAL-TRIAL OF IVIG INFECTION
   PROPHYLAXIS
SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY
LA English
DT Article
DE INTRAVENOUS IMMUNOGLOBULIN; CD4+ LYMPHOCYTES; DECLINE; INFECTION
   PROPHYLAXIS; HUMAN IMMUNODEFICIENCY VIRUS; CHILDREN
ID HUMAN-IMMUNODEFICIENCY-VIRUS; GAMMA-GLOBULIN; IMMUNE GLOBULIN;
   HEALTHY-CHILDREN; PERIPHERAL-BLOOD; THERAPY; SUBSETS; ZIDOVUDINE;
   INVIVO; CELLS
AB Our objective was to evaluate the effect of intravenous immunoglobulin (IVIG) on absolute CD4+ lymphocyte count (CD4+ count) trends in human immunodeficiency virus- (HIV) infected children enrolled in a trial of IVIG for infection prophylaxis. To that end, we conducted a randomized, double-blind, outpatient trial comparing subjects treated with 400 mg per kilogram of IVIG every 28 days with those given 0.1% albumin placebo. CD4+ counts were measured at entry and every 12 weeks. Twenty-eight clinical centers in mainland United States and Puerto Rico participated. Previous reports showed IVIG efficacy for infection prophylaxis in 313 patients with entry CD4+ counts of greater-than-or-equal-to 0.20 x 10(9)/L (greater-than-or-equal-to 200/mm3). Two hundred and seventy-seven (89%) of these 313 children had three or more CD4+ counts measured during the trial and were included in evaluation of CD4+ count trends. Rates of CD4+ count decline, as measured by regression slopes, were compared between IVIG and placebo groups using generalized linear models, comparing unadjusted, age-adjusted, and standardized age-adjusted data. Potential covariate effects were assessed by modeling change in CD4+ count in terms of log change between successive measurements. Age-adjusted slope analysis showed slowing of CD4+ count decline by 13.5 cells/mm3 per month in IVIG compared with placebo recipients (95% confidence interval, 3.1-23.9, p = 0.012). Modeling log change between measurements documented a beneficial effect of IVIG that was cumulative over time and independent of other therapies. Occurrence of serious bacterial infection in the interval before CD4+ count measurement or death was independently associated with more rapid CD4+ count decline (p = 0.01 and p = 0.008, respectively). Zidovudine therapy was associated with a transient increase in CD4+ count. Benefits of IVIG include slowing of CD4+ count decline as well as previously reported reductions in serious and minor bacterial and viral infections in subjects with entry CD4+ counts of greater-than-or-equal-to 0.20 x 10(9)/L. This finding provides corroboration for the hypothesis that immunologic mechanisms contribute to the pathogenesis of CD4+ decline in HIV infection.
C1 WESTAT CORP,ROCKVILLE,MD.
RP MOFENSON, LM (reprint author), NICHHD,CTR RES MOTHERS & CHILDREN,BETHESDA,MD 20892, USA.
OI Mofenson, Lynne/0000-0002-2818-9808
NR 49
TC 43
Z9 43
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 1077-9450
J9 J ACQ IMMUN DEF SYND
JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol.
PD OCT
PY 1993
VL 6
IS 10
BP 1103
EP 1113
PG 11
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA MC829
UT WOS:A1993MC82900004
PM 8105072
ER

PT J
AU WIKTOR, SZ
   PATE, EJ
   MURPHY, EL
   PALKER, TJ
   CHAMPEGNIE, E
   RAMLAL, A
   CRANSTON, B
   HANCHARD, B
   BLATTNER, WA
AF WIKTOR, SZ
   PATE, EJ
   MURPHY, EL
   PALKER, TJ
   CHAMPEGNIE, E
   RAMLAL, A
   CRANSTON, B
   HANCHARD, B
   BLATTNER, WA
TI MOTHER-TO-CHILD TRANSMISSION OF HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I
   (HTLV-I) IN JAMAICA - ASSOCIATION WITH ANTIBODIES TO ENVELOPE
   GLYCOPROTEIN (GP46) EPITOPES
SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY
LA English
DT Article
DE HTLV-I; MOTHER-TO-CHILD TRANSMISSION; BREAST-FEEDING; ANTIBODY TITER;
   ENVELOPE PROTEINS
ID HUMAN-IMMUNODEFICIENCY-VIRUS; HUMAN MONOCLONAL-ANTIBODY; LEUKEMIA-VIRUS;
   MATERNAL ANTIBODIES; SYNTHETIC PEPTIDES; CARRIER MOTHERS;
   IDENTIFICATION; INFECTION; INDUCTION; REGIONS
AB To study mother-to-child transmission of HTLV-1 in Jamaica, we screened antenatal patients in Kingston, Jamaica, from 1983 to 1985. Of 2,329 women, 81 (3.5%) were HTLV-1 seropositive. Two to three years later, 36 seropositive mothers were recontacted, and blood was drawn from them and their children. All sera were tested for HTLV-1 antibodies, and mother's sera were additionally tested for HTLV-1 whole-virus antibody titer, syncytium-inhibition neutralizing antibody titer, and titers to six synthetic peptides from the HTLV-1 envelope glycoprotein gp46. Seventeen of 74 (23%) [95% confidence interval (CI) 15-34%] children were seropositive. HTLV-1 transmission was associated with breast-feeding duration > 6 months [relative risk (RR) 3.2; CI 0.4-22.1], maternal age > 30 years (RR 2.8; CI 1.0-7.8), and higher maternal whole-virus antibody titer (RR 3.3; CI 1.3-8.5). After controlling for higher whole-virus antibody titer, transmission remained associated with higher titer of neutralizing antibody and higher titer of antibody to the peptide sp4a1, corresponding to amino acids 196-209 of the gp46 envelope glycoprotein. We conclude that mother-to-child transmission of HTLV-1 in Jamaica is associated with longer duration of breast-feeding, older age, and higher HTLV-1 antibody titer, in particular to a certain immunogenic portion of the gp46 envelope glycoprotein.
C1 NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892.
   UNIV W INDIES,DEPT CHILD HLTH,KINGSTON 7,JAMAICA.
   UNIV W INDIES,DEPT PATHOL,KINGSTON 7,JAMAICA.
   UCSF,DEPT LAB MED,SAN FRANCISCO,CA.
   DUKE UNIV,DEPT CHEM,DURHAM,NC 27706.
FU NCI NIH HHS [NCI RO1-CA40660, NCI NO1-CP-31006]
NR 34
TC 33
Z9 33
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 1077-9450
J9 J ACQ IMMUN DEF SYND
JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol.
PD OCT
PY 1993
VL 6
IS 10
BP 1162
EP 1167
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA MC829
UT WOS:A1993MC82900013
PM 7692038
ER

PT J
AU LEIBENLUFT, E
AF LEIBENLUFT, E
TI DO GONADAL-STEROIDS REGULATE CIRCADIAN-RHYTHMS IN HUMANS
SO JOURNAL OF AFFECTIVE DISORDERS
LA English
DT Article
DE CIRCADIAN RHYTHMS; ESTROGEN; SLEEP; GENDER DIFFERENCES; MOOD DISORDER;
   MENOPAUSE
ID CENTRAL NERVOUS-SYSTEM; FEMALE RAT; MENSTRUAL-CYCLE; TESTOSTERONE
   REPLACEMENT; LOCOMOTOR-ACTIVITY; RUNNING RHYTHMS; SEX-DIFFERENCES;
   SLEEP; ESTRADIOL; HAMSTER
AB While a number of studies demonstrate that gonadal steroids regulate circadian rhythms in animals, the issue has received little attention in humans. The question is relevant to our understanding of gender differences in the phenomenology of depression, and of changes in the sleep-activity cycle that are seen in affective illness and during the menopause. In this paper, the literature demonstrating that gonadal steroids regulate circadian rhythms in animals is reviewed, along with the limited human literature. A hypothesis is forwarded suggesting that, in humans, estrogen shortens the circadian period, lengthens the sleep phase, advances sleep onset, and consolidates sleep. A study in progress is described which is designed to test the effects of the hypogonadal state, estrogen, and progesterone on circadian rhythms in women.
RP LEIBENLUFT, E (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,BLDG 10,ROOM 4S-239,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 64
TC 32
Z9 32
U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0327
J9 J AFFECT DISORDERS
JI J. Affect. Disord.
PD OCT-NOV
PY 1993
VL 29
IS 2-3
BP 175
EP 181
DI 10.1016/0165-0327(93)90031-E
PG 7
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA MK592
UT WOS:A1993MK59200008
PM 8300976
ER

PT J
AU FRIEDMAN, BS
   SANTIAGO, ML
   BERKEBILE, C
   METCALFE, DD
AF FRIEDMAN, BS
   SANTIAGO, ML
   BERKEBILE, C
   METCALFE, DD
TI COMPARISON OF AZELASTINE AND CHLORPHENIRAMINE IN THE TREATMENT OF
   MASTOCYTOSIS
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE MASTOCYTOSIS; ANTIHISTAMINES; MAST CELLS; HISTAMINE; CLINICAL TRIAL
ID ALLERGIC HISTAMINE-RELEASE; PERITONEAL MAST-CELLS; SYSTEMIC
   MASTOCYTOSIS; DOUBLE-BLIND; INHIBITION; ANTIHISTAMINES; EFFICACY; TRIAL;
   DRUGS
AB Background: Azelastine, a novel antiallergic medication, was compared with chlorpheniramine maleate for efficacy and safety in the treatment of systemic mastocytosis.
   Methods: Fifteen subjects with mastocytosis participated in a double-blind, randomized, three-period, crossover trial, which compared an azelastine regimen of 4 mg or 8 mg every 12 hours with a chlorpheniramine regimen of 12 mg every 12 hours. Response to therapy was assessed by daily symptom scores, extinction dilution skin tests, plasma histamine levels, and global evaluations.
   Results: Subjects' mean wheal area responses provoked by histamine or morphine sulfate were significantly lowered by azelastine when compared with chlorpheniramine. Plasma histamine levels in subjects receiving azelastine or chlorpheniramine were not significantly different. There were no significant differences between azelastine and chlorpheniramine in individual symptom scores or global evaluations except that azelastine at both doses significantly relieved pruritus and at 4 mg significantly relieved abdominal pain and that chlorpheniramine was associated with less fatigue in comparison to azelastine at 8 mg.
   Conclusions: It thus appears that azelastine is superior to chlorpheniramine in suppressing skin responses to histamine and morphine sulfate and in suppressing pruritus in patients with mastocytosis. However, when all parameters are considered, neither drug is clearly superior for the treatment of patients with mastocytosis.
C1 NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BLDG 10,ROOM 11C210,BETHESDA,MD 20892.
NR 14
TC 22
Z9 23
U1 0
U2 0
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 1993
VL 92
IS 4
BP 520
EP 526
DI 10.1016/0091-6749(93)90076-R
PG 7
WC Allergy; Immunology
SC Allergy; Immunology
GA MC590
UT WOS:A1993MC59000004
PM 8104966
ER

PT J
AU SRIRAMARAO, P
   PRAKASH, O
   METCALFE, DD
   RAO, PVS
AF SRIRAMARAO, P
   PRAKASH, O
   METCALFE, DD
   RAO, PVS
TI THE USE OF MURINE POLYCLONAL ANTIIDIOTYPIC ANTIBODIES AS SURROGATE
   ALLERGENS IN THE DIAGNOSIS OF PARTHENIUM HYPERSENSITIVITY
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE ANTIIDIOTYPIC ANTIBODIES; PARTHENIUM; SKIN TESTS; RHINITIS; ALLERGY;
   ALLERGENS; IGE
ID HUMAN IMMUNE-RESPONSE; HOUSE DUST MITE; IGE ANTIBODIES; RYE-I;
   DERMATOPHAGOIDES-PTERONYSSINUS; IMMEDIATE HYPERSENSITIVITY;
   ANTIIDIOTYPIC ANTIBODY; MONOCLONAL-ANTIBODIES; HUMAN-SERA; IMMUNOTHERAPY
AB Background: Anti-idiotypic antibodies (Ab-2), which are the mirror images of idiotypic antibodies (Ab-1), may be useful as diagnostic reagents and for use as immunogen to induce antigen-specific immune responses.
   Methods and Results: To explore the biologic potential of Ab-2 as diagnostic reagents in allergic diseases, murine mouse (m) Ab-2 were raised by immunizing Balb/c mice with affinity purified rabbit (r) Ab-1 specific for the pollen of Parthenium hysterophorus, an allergenic weed that grows wild on the Indian subcontinent and in Australia, Mexico, and the southern United States. Affinity purified Parthenium-specific human (h)AB-1 could successfully inhibit the binding of mAb-2 to immobilized rAb-1. Further, Balb/c mice immunized with mAb-2 induced Parthenium-specific anti-anti-idiotypic IgE and IgG antibodies. Specificity of the Ab-2 was confirmed by the ability of Parthenium pollen extracts to inhibit the binding of allergen-specific IgE and IgG Ab-1 in the sera of patients with rhinitis to immobilized mAb-2. Parthenium-sensitive patients with rhinitis who had positive results on skin prick tests to Parthenium pollen extracts also responded with a positive skin reaction to mAb-2.
   Conclusion: Our data demonstrate that Parthenium-specific mAb-2 may be of value as surrogate allergens in allergen standardization and for in vitro diagnosis.
C1 NIAID,CLIN INVEST,MAST CELL PHYSIOL SECT LAB,BETHESDA,MD 20892.
   INDIAN INST SCI,DEPT BIOCHEM,IMMUNOL & ALLERG DIS LAB,BANGALORE 560012,KARNATAKA,INDIA.
   ST MARTHAS HOSP,DEPT MED,BANGALORE,INDIA.
NR 42
TC 2
Z9 3
U1 0
U2 1
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 1993
VL 92
IS 4
BP 567
EP 580
DI 10.1016/0091-6749(93)90081-P
PG 14
WC Allergy; Immunology
SC Allergy; Immunology
GA MC590
UT WOS:A1993MC59000009
PM 8409117
ER

PT J
AU CONE, EJ
   HOLICKY, BA
   GRANT, TM
   DARWIN, WD
   GOLDBERGER, BA
AF CONE, EJ
   HOLICKY, BA
   GRANT, TM
   DARWIN, WD
   GOLDBERGER, BA
TI PHARMACOKINETICS AND PHARMACODYNAMICS OF INTRANASAL SNORTED HEROIN
SO JOURNAL OF ANALYTICAL TOXICOLOGY
LA English
DT Article
RP CONE, EJ (reprint author), NIDA,ARC,POB 5180,BALTIMORE,MD 21224, USA.
NR 12
TC 45
Z9 48
U1 0
U2 2
PU PRESTON PUBLICATIONS INC
PI NILES
PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648
SN 0146-4760
J9 J ANAL TOXICOL
JI J. Anal. Toxicol.
PD OCT
PY 1993
VL 17
IS 6
BP 327
EP 337
PG 11
WC Chemistry, Analytical; Toxicology
SC Chemistry; Toxicology
GA LZ152
UT WOS:A1993LZ15200003
PM 8271778
ER

PT J
AU KATO, K
   HILLSGROVE, M
   WEINHOLD, L
   GORELICK, DA
   DARWIN, WD
   CONE, EJ
AF KATO, K
   HILLSGROVE, M
   WEINHOLD, L
   GORELICK, DA
   DARWIN, WD
   CONE, EJ
TI COCAINE AND METABOLITE EXCRETION IN SALIVA UNDER STIMULATED AND
   NONSTIMULATED CONDITIONS
SO JOURNAL OF ANALYTICAL TOXICOLOGY
LA English
DT Article
ID ECGONINE METHYL-ESTER; URINARY-EXCRETION; DRUGS; BENZOYLECGONINE;
   PLASMA; HUMANS
C1 NIDA,ARC,POB 5180,BALTIMORE,MD 21224.
NR 13
TC 65
Z9 67
U1 0
U2 8
PU PRESTON PUBLICATIONS INC
PI NILES
PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648
SN 0146-4760
J9 J ANAL TOXICOL
JI J. Anal. Toxicol.
PD OCT
PY 1993
VL 17
IS 6
BP 338
EP 341
PG 4
WC Chemistry, Analytical; Toxicology
SC Chemistry; Toxicology
GA LZ152
UT WOS:A1993LZ15200004
PM 8271779
ER

PT J
AU GORAN, MI
   KASKOUN, MC
   CARPENTER, WH
   POEHLMAN, ET
   RAVUSSIN, E
   FONTVIEILLE, AM
AF GORAN, MI
   KASKOUN, MC
   CARPENTER, WH
   POEHLMAN, ET
   RAVUSSIN, E
   FONTVIEILLE, AM
TI ESTIMATING BODY-COMPOSITION OF YOUNG-CHILDREN BY USING BIOELECTRICAL
   RESISTANCE
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE FAT-FREE MASS; FAT MASS; TOTAL BODY WATER
ID IMPEDANCE; WATER; VALIDATION; FAT; PREDICTION; ADULTS; WEIGHT; BIRTH;
   MASS
AB It is currently unclear whether age-specific equations should be used for assessing body composition from bioelectrical resistance. Kushner et al. (Am. J. Clin. Nutr. 56: 835-839, 1992) showed that the relationship between height2/resistance and total body water (TBW) is robust across a wide age range, although uncertainty remained over the relationship in preschool children. We therefore cross-validated the Kushner equation for predicting total body water in 4- to 6-yr-old children in two independent laboratories. TBW was measured from (H2O)-O-18 dilution, and bioelectrical resistance and reactance were measured using an RJL 101A analyzer in 31 children (15 females, 16 males; 5 +/- 0.8 yr) studied in Burlington, Vermont, and 30 children (14 females, 16 males; 5 +/- 0.2 yr) studied in Phoenix, Arizona. There was no significant difference between TBW predicted from the Kushner equation and that measured in children in Burlington (11.76 +/- 2.00 vs. 11.91 +/- 2.46 kg, r = 0.94) or in Phoenix (11.53 +/- 1.64 vs. 11.66 +/- 1.90 kg; r = 0.94). The Kushner equation for TBW can be transformed into an equation for fat-free mass (FFM) by using published age- and gender-specific constants for the hydration of FFM: hydration of FFM = 76.9 - 0.25 age (yr) - 1.9 gender where female equals 0 and male equals 1. The intraclass reliability for estimates of fat mass and FFM with the use of bioelectrical resistance in an independent group of 26 children (5.0 +/- 0.8 yr, 20.2 +/- 3.0 kg) was >0.99 for duplicate observations performed 2 wk apart. We conclude that the relationship between TBW and height2/resistance in young children is robust across independent laboratories and that the Kushner equation relating these two variables is viable in young children.
C1 UNIV VERMONT,SIMS OBESITY NUTR RES CTR,BURLINGTON,VT 05405.
   NIH,CLIN DIABETES & NUTR SECT,PHOENIX,AZ 85016.
RP GORAN, MI (reprint author), UNIV VERMONT,DEPT MED,DIV ENDOCRINOL METAB & NUTR,BURLINGTON,VT 05405, USA.
FU NIA NIH HHS [KO4-AG-00564, R29-AG-07857]; NICHD NIH HHS [R55-HD-28720]
NR 25
TC 77
Z9 78
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 OCT
PY 1993
VL 75
IS 4
BP 1776
EP 1780
PG 5
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA MD352
UT WOS:A1993MD35200051
PM 8282631
ER

PT J
AU DESMET, MD
   BITAR, G
   ROBERGE, FG
   GERY, I
   NUSSENBLATT, RB
AF DESMET, MD
   BITAR, G
   ROBERGE, FG
   GERY, I
   NUSSENBLATT, RB
TI HUMAN S-ANTIGEN - PRESENCE OF MULTIPLE IMMUNOGENIC AND IMMUNOPATHOGENIC
   SITES IN THE LEWIS RAT
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
ID RETINOID-BINDING PROTEIN; EXPERIMENTAL AUTOIMMUNE UVEORETINITIS; IMMUNE
   RESPONSIVENESS; T-CELLS; IDENTIFICATION; UVEITIS; PINEALITIS; PEPTIDES;
   PHOTORECEPTORS; PROLIFERATION
RP DESMET, MD (reprint author), NEI,IMMUNOL LAB,BLDG 10,RM 10N112,BETHESDA,MD 20892, USA.
OI de Smet, Marc/0000-0002-9217-5603
NR 37
TC 45
Z9 46
U1 0
U2 0
PU ACADEMIC PRESS LTD
PI LONDON
PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
SN 0896-8411
J9 J AUTOIMMUN
JI J. Autoimmun.
PD OCT
PY 1993
VL 6
IS 5
BP 587
EP 599
DI 10.1006/jaut.1993.1048
PG 13
WC Immunology
SC Immunology
GA MF065
UT WOS:A1993MF06500006
PM 7694588
ER

PT J
AU FISCHER, D
   WOLFSON, H
   NUSSINOV, R
AF FISCHER, D
   WOLFSON, H
   NUSSINOV, R
TI SPATIAL, SEQUENCE-ORDER-INDEPENDENT STRUCTURAL COMPARISON OF ALPHA/BETA
   PROTEINS - EVOLUTIONARY IMPLICATIONS
SO JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS
LA English
DT Article
ID MOTIFS
AB We present a unique sequence-order independent approach which allows examination of three dimensional structures, searching for spatially similar substructural motifs. If the amino acids composing the motifs are contiguous in the primary chain, that is, they follow each other in the sequence, a common ancestor and a divergent evolutionary process may be implied. On the other hand, if the three-dimensional substructural motif consists of amino acids whose positions in the sequences vary between the different proteins, a convergent evolution might have taken place. Starting from different, ancient sequences, mutations may have occurred that brought about formation and conservation of a truly structural motif. Such a motif might be particularly suitable for fulfilling a specific function. Clearly, in order to be able to carry out such a task one needs a technique which allows comparisons of protein structures absolutely independent of their amino acid sequence-order. Our novel, efficient, computer vision based technique treats atoms (residues) as unconnected points in space, using strictly the atomic (either all atoms or only the Ca atoms) coordinates. The order of the residues is completely disregarded. Detection, cataloging and analysis of 'real' three-dimensional, sequence-order independent motifs in the crystallographic database is expected to be an invaluable tool for protein folding. Here we demonstrate the power of the technique by applying it to alpha/beta proteins. Our studies indicate that for some of the proteins, the 'classical' structural alignments (conserving the amino acid order) are the optimal ones. Nevertheless, for others, truly spatial (out of sequential-order) amino acid equivalencing results in a better geometrical match.
C1 TEL AVIV UNIV,FAC MED,SACKLER INST MOLEC MED,IL-69978 TEL AVIV,ISRAEL.
   TEL AVIV UNIV,SCH MATH SCI,DEPT COMP SCI,IL-69978 TEL AVIV,ISRAEL.
   NCI,FREDERICK CANC RES FACIL,PRI DYNACORP,MATH BIOL LAB,FREDERICK,MD 21702.
RI Wolfson, Haim/A-1837-2011
FU NCI NIH HHS [1-CO-74102]
NR 22
TC 4
Z9 4
U1 0
U2 0
PU ADENINE PRESS INC
PI GUILDERLAND
PA PO BOX 355/340, GUILDERLAND, NY 12084
SN 0739-1102
J9 J BIOMOL STRUCT DYN
JI J. Biomol. Struct. Dyn.
PD OCT
PY 1993
VL 11
IS 2
BP 367
EP &
PG 0
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA MF289
UT WOS:A1993MF28900011
PM 8286062
ER

PT J
AU BUCKWALTER, JA
   WOO, SLY
   GOLDBERG, VM
   HADLEY, EC
   BOOTH, F
   OEGEMA, TR
   EYRE, DR
AF BUCKWALTER, JA
   WOO, SLY
   GOLDBERG, VM
   HADLEY, EC
   BOOTH, F
   OEGEMA, TR
   EYRE, DR
TI CURRENT CONCEPTS REVIEW - SOFT-TISSUE AGING AND MUSCULOSKELETAL FUNCTION
SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME
LA English
DT Review
ID HUMAN ARTICULAR-CARTILAGE; AGE-RELATED-CHANGES; MEDIAL COLLATERAL
   LIGAMENT; ANTERIOR CRUCIATE LIGAMENT; HUMAN INTERVERTEBRAL-DISK; NUCLEUS
   PULPOSUS REGENERATION; HUMAN GROWTH-HORMONE; TENSILE PROPERTIES;
   SKELETAL-MUSCLE; DIABETES-MELLITUS
C1 UNIV PITTSBURGH,INST MUSCULOSKELETAL,PITTSBURGH,PA 15213.
   UNIV TEXAS,DEPT PHYSIOL & CELL BIOL,HOUSTON,TX 77225.
   UNIV IOWA HOSP & CLIN,DEPT ORTHOPAED,IOWA CITY,IA 52242.
   CASE WESTERN RESERVE UNIV,DEPT ORTHOPAED,CLEVELAND,OH 44106.
   NIA,BETHESDA,MD 20892.
FU NIAMS NIH HHS [R37 AR037318, R13 AR41458-01, R01 AR036794]
NR 181
TC 131
Z9 136
U1 0
U2 8
PU JOURNAL BONE JOINT SURGERY INC
PI NEEDHAM
PA 20 PICKERING ST, NEEDHAM, MA 02192
SN 0021-9355
J9 J BONE JOINT SURG AM
JI J. Bone Joint Surg.-Am. Vol.
PD OCT
PY 1993
VL 75A
IS 10
BP 1533
EP 1548
PG 16
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA ME011
UT WOS:A1993ME01100015
PM 8408143
ER

PT J
AU REDDY, SV
   SCARCEZ, T
   WINDLE, JJ
   LEACH, RJ
   HUNDLEY, JE
   CHIRGWIN, JM
   CHOU, JY
   ROODMAN, GD
AF REDDY, SV
   SCARCEZ, T
   WINDLE, JJ
   LEACH, RJ
   HUNDLEY, JE
   CHIRGWIN, JM
   CHOU, JY
   ROODMAN, GD
TI CLONING AND CHARACTERIZATION OF THE 5'-FLANKING REGION OF THE MOUSE
   TARTRATE-RESISTANT ACID-PHOSPHATASE GENE
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Article
ID MULTINUCLEATED CELLS; OSTEOCLAST PHENOTYPE; BONE-RESORPTION; SEQUENCE;
   PROMOTER; TYPE-5; TRANSCRIPTION; UTEROFERRIN; EXPRESSION; PROTEIN
AB Little information is available on the molecular mechanisms controlling osteoclastic bone resorption. We used tartrate-resistant acid phosphatase (TRAP) to begin to investigate the regulation of bone resorption at the molecular level. TRAP is expressed at high levels in osteoclasts and may play an important role in the bone resorptive process. Therefore, we isolated the murine TRAP gene from a mouse spleen genomic library and characterized its promoter. A restriction map was generated for the 17 kb TRAP insert. A 2 kb SmaI fragment, containing the 5'-flanking region, was subcloned and the nucleotide sequence determined. Sequence analysis of the SmaI fragment revealed the presence of numerous candidate transcription factor binding sequences, including those for AP1 and H-APF-1. The H-APF-1 site matches the consensus sequence for the IL-6-regulated transcription factor. An intron was identified at -1 to -393 bp relative to the ATG. The presence of an intron was confirmed by PCR analysis of RNA isolated from murine osteoclasts. Primer extension analysis indicated the presence of a transcription initiation site at -552 bp from the ATG. The region from -1846 to 2 bp relative to the ATG initiation codon drove the transient expression of a luciferase reporter gene when transfected into HRE H9 rabbit endometrial cells. PMA treatment of HRE H9 cells enhanced luciferase transcription approximately threefold. These data suggest that the TRAP promoter is complex and contains multiple regulatory elements. The availability of the TRAP promoter may also permit production of transgenic mice, which can be used to develop previously unavailable osteoclast cell lines.
C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284.
   UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284.
   UNIV TEXAS,HLTH SCI CTR,DEPT HEMATOL,SAN ANTONIO,TX 78284.
   CANC THERAPY & RES CTR S TEXAS,SAN ANTONIO,TX.
   UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284.
   UNIV TEXAS,HLTH SCI CTR,DEPT PEDIAT,SAN ANTONIO,TX 78284.
   NICHHD,BETHESDA,MD 20892.
OI Windle, Jolene/0000-0001-6690-385X
FU NIADDK NIH HHS [AM 35188]; NIAMS NIH HHS [AR 41336, AR 39539]
NR 30
TC 28
Z9 29
U1 0
U2 0
PU BLACKWELL SCIENCE INC
PI CAMBRIDGE
PA 238 MAIN ST, CAMBRIDGE, MA 02142
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD OCT
PY 1993
VL 8
IS 10
BP 1263
EP 1270
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA LY890
UT WOS:A1993LY89000014
PM 8256664
ER

PT J
AU ERZOUKI, HK
   BAUM, I
   GOLDBERG, SR
   SCHINDLER, CW
AF ERZOUKI, HK
   BAUM, I
   GOLDBERG, SR
   SCHINDLER, CW
TI COMPARISON OF THE EFFECTS OF COCAINE AND ITS METABOLITES ON
   CARDIOVASCULAR FUNCTION IN ANESTHETIZED RATS
SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
LA English
DT Article
DE COCAINE; COCAINE METABOLITES; ELECTROCARDIOGRAM; QRS; HEMODYNAMICS; RATS
ID URINARY-EXCRETION; HUMANS; COCAETHYLENE; CHANNELS; ALCOHOL
AB Hemodynamic and cardiac-electrophysiologic effects of cocaine and its metabolites were measured in 18 groups (n = 6 each) of anesthetized, artificially ventilated rats during continuous intravenous (i.v.) infusions at three different doses (0.15, 0.45, and 1.5 mg/kg/min). At the highest dose, cocaine decreased blood pressure (BP) and heart rate (HR), while QRS duration, an index of cocaine's local anesthetic effect, was increased. Cocaethylene, a metabolite produced after coadministration of cocaine and ethanol, had effects comparable to those of cocaine. The cocaine metabolite norcocaine produced a decrease in BP at the lower dose that reversed to a small increase at the higher dose. The highest dose of norcocaine clearly decreased HR and increased QRS duration. The increases in QRS duration observed for cocaine, cocaethylene, and norcocaine were reversed by sodium bicarbonate. The cocaine metabolites benzoylecgonine and ecgonine methyl ester increased BP at the higher doses without affecting either HR or QRS duration. These results suggest that the spectrum of effects produced by cocaine are not necessarily mimicked by its metabolites. In particular, accumulation of the persistent, active metabolites benzoylecgonine and ecgonine methyl ester may contribute to delayed-onset, cocaine-related toxicity.
RP ERZOUKI, HK (reprint author), NIDA,ADDICT RES CTR,BEHAV PHARMACOL & GENET SECT,PRECLIN PHARMACOL LAB,POB 5180,BALTIMORE,MD 21224, USA.
NR 41
TC 43
Z9 43
U1 3
U2 3
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0160-2446
J9 J CARDIOVASC PHARM
JI J. Cardiovasc. Pharmacol.
PD OCT
PY 1993
VL 22
IS 4
BP 557
EP 563
DI 10.1097/00005344-199310000-00008
PG 7
WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy
SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy
GA LZ144
UT WOS:A1993LZ14400007
PM 7505357
ER

PT J
AU DICKSTEIN, B
   VALVERIUS, EM
   WOSIKOWSKI, K
   SACEDA, M
   PEARSON, JW
   MARTIN, MB
   BATES, SE
AF DICKSTEIN, B
   VALVERIUS, EM
   WOSIKOWSKI, K
   SACEDA, M
   PEARSON, JW
   MARTIN, MB
   BATES, SE
TI INCREASED EPIDERMAL GROWTH-FACTOR RECEPTOR IN AN ESTROGEN-RESPONSIVE,
   ADRIAMYCIN-RESISTANT MCF-7 CELL-LINE
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
ID HUMAN-BREAST-CANCER; FACTOR-ALPHA; EPITHELIAL-CELLS; CARCINOMA-CELLS;
   PHENOL RED; EXPRESSION; CULTURE; BINDING; GENE; TUMORS
AB We examined the expression of the estrogen and epidermal growth factor (EGF) receptors in a drug-resistant subline of MCF-7 cells in order to study potential alterations in hormone dependence or in the growth factor pathway that could be related to the development of drug resistance in human breast cancer. The drug-resistant subline was derived from MCF-7 cells by selection with Adriamycin in the presence of the P-glycoprotein antagonist, verapamil, to prevent acquisition of the classical multidrug resistance phenotype. The Adriamycin-resistant cells retain estrogen-binding, estrogen-responsive monolayer growth, and estrogen-dependent tumorigenesis. Estrogen-binding studies demonstrate 1.4 x 10(6) sites per cell with unaltered affinity when compared to parental MCF-7 cells, which have 2.7 x 10(5) sites per cell. Ah increase in expression of EGF receptor, eight to 12-fold, occurred early in the selection for drug resistance, and appears to be unrelated to verapamil exposure, since cells maintained in Adriamycin without verapamil also have increased EGF receptor expression. Partially drug-sensitive revertants carried a verapamil, but out of Adriamycin, demonstrate a decline in EGF receptor expression. We postulate that activation of growth factor pathways in drug-resistant cells may enhance mechanisms of drug resistance, or provide mitogenic stimuli for cells to recover after damage by drug exposure. (C) 1993 Wiley-Liss, Inc.
C1 NCI,CLIN ONCOL PROGRAM,MED BRANCH,BETHESDA,MD 20892.
   NCI,BIOL RESPONSE MODIFIERS PROGRAM,EXPTL IMMUNOL LAB,BETHESDA,MD 20892.
   GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007.
RI Saceda, Miguel/A-1581-2008
NR 41
TC 38
Z9 38
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 0021-9541
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD OCT
PY 1993
VL 157
IS 1
BP 110
EP 118
DI 10.1002/jcp.1041570115
PG 9
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA MA272
UT WOS:A1993MA27200014
PM 8408230
ER

PT J
AU LARJAVA, H
   LYONS, JG
   SALO, T
   MAKELA, M
   KOIVISTO, L
   BIRKEDALHANSEN, H
   AKIYAMA, SK
   YAMADA, KM
   HEINO, J
AF LARJAVA, H
   LYONS, JG
   SALO, T
   MAKELA, M
   KOIVISTO, L
   BIRKEDALHANSEN, H
   AKIYAMA, SK
   YAMADA, KM
   HEINO, J
TI ANTI-INTEGRIN ANTIBODIES INDUCE TYPE-IV COLLAGENASE EXPRESSION IN
   KERATINOCYTES
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
ID TRANSFORMING GROWTH FACTOR-BETA-1; FIBRONECTIN RECEPTOR DISTRIBUTION;
   CULTURED HUMAN KERATINOCYTES; STROMELYSIN GENE-EXPRESSION;
   BASEMENT-MEMBRANE COLLAGEN; CELL-ADHESION RECEPTORS; HUMAN-SKIN;
   INTERSTITIAL COLLAGENASE; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION
AB During wound healing, pericellular proteolysis is thought to be essential for the detachment of keratinocytes from basement membrane and in their migration into the wound bed. We have characterized integrin-type cell adhesion/migration receptors in human mucosal keratinocytes and examined their function in the regulation of type IV collagenase gene expression. Two major integrins of the beta1 class, alpha2beta1 and alpha3beta1, were found to function as collagen and fibronectin receptors, respectively. Antibodies against beta1 and alpha3 integrin subunits were found to stimulate the expression of the 92 kDa type IV collagenase severalfold in a dose-dependent manner. Keratinocytes expressed also the 72 kDa type IV collagenase, the synthesis of which remained, however, unchanged in keratinocytes treated with anti-integrin antibodies. Stimulation of 92 kDa enzyme was found to be caused directly by antibody binding to integrins, since Fab-fragments of anti-beta1 antibodies alone were able to induce collagenase expression in the absence of secondary, clustering antibodies. Antibodies against alpha2beta1 integrin caused no stimulation. Keratinocytes seeded on different substrata (plastic, collagen, fibronectin, laminin, or vitronectin) showed equal induction of type IV collagenase expression. Expression of 92 kDa type IV collagenase could not be induced by peptides (GRGDS, GRGES), proteins (fibronectin, laminin, fibrinogen, albumin), or antibodies to fibronectin. We suggest that proteolytic processes around keratinocytes can be regulated by extracellular factors signalling through integrin-type receptors. (C) 1993 Wiley-Liss, Inc.
C1 UNIV TURKU, DEPT MED BIOCHEM, SF-20520 TURKU 52, FINLAND.
   UNIV ALABAMA, DEPT ORAL BIOL, BIRMINGHAM, AL 35294 USA.
   NIDR, DEV BIOL LAB, BETHESDA, MD 20892 USA.
   UNIV OULU, DEPT ORAL SURG, SF-90220 OULU, FINLAND.
RP LARJAVA, H (reprint author), UNIV TURKU, DEPT PERIODONT, SF-20520 TURKU 52, FINLAND.
RI Lyons, Guy/B-1319-2012; 
OI Lyons, Guy/0000-0002-4835-4663; Yamada, Kenneth/0000-0003-1512-6805
NR 72
TC 86
Z9 87
U1 0
U2 3
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0021-9541
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD OCT
PY 1993
VL 157
IS 1
BP 190
EP 200
DI 10.1002/jcp.1041570125
PG 11
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA MA272
UT WOS:A1993MA27200024
PM 8408237
ER

PT J
AU SCHIFFMANN, R
   MANNHEIM, GB
   STAFSTROM, CE
   HAMBURGER, SD
   HOLMES, GL
AF SCHIFFMANN, R
   MANNHEIM, GB
   STAFSTROM, CE
   HAMBURGER, SD
   HOLMES, GL
TI POSTERIOR-FOSSA ABNORMALITIES IN CHILDREN WITH INFANTILE SPASMS
SO JOURNAL OF CHILD NEUROLOGY
LA English
DT Article
ID DANDY-WALKER SYNDROME; POSITRON EMISSION TOMOGRAPHY; BRAIN-STEM
AB In order to explore possible pathophysiologic involvement of the brain stem in infantile spasms, we retrospectively compared clinical and electroencephalographic (EEG) features of 14 children with infantile spasms who had gross posterior fossa abnormalities on neuroimaging studies with 84 children with infantile spasms who had either normal neuroimaging (n = 19) or supratentorial abnormalities (n = 65). Children with posterior fossa abnormalities had lower mean initial and follow-up developmental quotients compared to those with normal imaging or supratentorial abnormalities alone. Age of onset of infantile spasms, latency to treatment, response to steroids, and follow-up EEG pattern were not significantly different among the three groups. Six children (6%) had Dandy-Walker cysts, an association rarely reported with infantile spasms. We conclude that the presence of posterior fossa abnormalities in patients with infantile spasms portends a relatively poor developmental outcome.
C1 HADASSAH UNIV HOSP,PEDIAT NEUROL UNIT,JERUSALEM,ISRAEL.
   TUFTS UNIV NEW ENGLAND MED CTR,DIV PEDIAT NEUROL,BOSTON,MA.
   NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892.
   HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115.
NR 23
TC 5
Z9 5
U1 0
U2 1
PU DECKER PERIODICALS INC
PI HAMILTON
PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA
SN 0883-0738
J9 J CHILD NEUROL
JI J. Child Neurol.
PD OCT
PY 1993
VL 8
IS 4
BP 360
EP 365
PG 6
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA MA260
UT WOS:A1993MA26000013
PM 7693798
ER

PT J
AU HERSHKOVITZ, E
   MARBACH, M
   BOSIN, E
   LEVY, J
   ROBERTS, CT
   LEROITH, D
   SCHALLY, AV
   SHARONI, Y
AF HERSHKOVITZ, E
   MARBACH, M
   BOSIN, E
   LEVY, J
   ROBERTS, CT
   LEROITH, D
   SCHALLY, AV
   SHARONI, Y
TI LUTEINIZING-HORMONE-RELEASING HORMONE ANTAGONISTS INTERFERE WITH
   AUTOCRINE AND PARACRINE GROWTH-STIMULATION OF MCF-7 MAMMARY-CANCER CELLS
   BY INSULIN-LIKE GROWTH-FACTORS
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID HUMAN-BREAST-CANCER; TERM TISSUE-CULTURE; POTENT ANTAGONISTS; FACTOR
   SECRETION; CARCINOMA; RECEPTORS; BINDING; PROLIFERATION; INHIBITION;
   MODULATION
AB Several studies have supported the idea that LH-releasing hormone (LHRH) antagonists have a direct effect on mammary tumor cells. In this study, we have evaluated the potential role of the insulin-like growth factors (IGFs) on the growth of MCF-7 mammary tumor cells and the effect of LHRH analogs on IGF action. The mitogenic effects of IGF-I, IGF-II, and insulin were compared. IGF-I was found to be 3 times more potent than IGF-II and 30 times more potent than insulin, suggesting that the effects of these growth factors are mediated by the IGF-I receptor. IGFs released by MCF-7 cells were measured by specific RIA after acid extraction and chromatography, so as to avoid the interference of IGF-binding proteins. MCF-7 cells secreted IGF-II, but not IGF-1. Estradiol (10(-9) mol/L) stimulated IGF-II release; this release preceded the effect of estradiol on cell growth. The LHRH antagonist [Ac-D-Nal(2)1,D-Phe(4Cl)2,D-Pal(3)3,D-Cit6,D-Ala10]LHRH (SB-75, CETRORELIX) inhbited basal, estrogen-induced, and IGF-induced growth. Moreover, this antagonist almost completely inhibited IGF-II release from MCF-7 cells. This effect preceeded the inhibition of tumor cell growth. We conclude that a LHRH antagonist can inhibit the growth of breast tumors by interfering with the autocrine action of IGF-II and by directly inhibiting the growth stimulatory effect of IGFs.
C1 BEN GURION UNIV NEGEV, FAC HLTH SCI, SOROKA MED CTR KUPAT HOLIM, DEPT CLIN BIOCHEM, IL-84105 BEER SHEVA, ISRAEL.
   NIDDKD, DIABET BRANCH, BETHESDA, MD 20892 USA.
   VET ADM MED CTR, INST ENDOCRINE POLYPEPTIDE & CANC, NEW ORLEANS, LA 70146 USA.
   TULANE UNIV, SCH MED, DEPT MED, NEW ORLEANS, LA 70112 USA.
RI Hershkovitz, Eli/F-1922-2012; 
OI Roberts, Charles/0000-0003-1756-5772; Schally,
   Andrew/0000-0003-1273-6747
NR 34
TC 54
Z9 55
U1 0
U2 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD OCT
PY 1993
VL 77
IS 4
BP 963
EP 968
DI 10.1210/jc.77.4.963
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA MC303
UT WOS:A1993MC30300015
PM 8408472
ER

PT J
AU IKEWAKI, K
   RADER, DJ
   SAKAMOTO, T
   NISHIWAKI, M
   WAKIMOTO, N
   SCHAEFER, JR
   ISHIKAWA, T
   FAIRWELL, T
   ZECH, LA
   NAKAMURA, H
   NAGANO, M
   BREWER, HB
AF IKEWAKI, K
   RADER, DJ
   SAKAMOTO, T
   NISHIWAKI, M
   WAKIMOTO, N
   SCHAEFER, JR
   ISHIKAWA, T
   FAIRWELL, T
   ZECH, LA
   NAKAMURA, H
   NAGANO, M
   BREWER, HB
TI DELAYED CATABOLISM OF HIGH-DENSITY-LIPOPROTEIN APOLIPOPROTEIN-A-I AND
   APOLIPOPROTEIN-A-II IN HUMAN CHOLESTERYL ESTER TRANSFER
   PROTEIN-DEFICIENCY
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE CHOLESTERYL ESTER TRANSFER PROTEIN; KINETICS; STABLE ISOTOPES; HIGH
   DENSITY LIPOPROTEINS; ATHEROSCLEROSIS
ID ISCHEMIC HEART-DISEASE; AMINO-ACID-SEQUENCE; HUMAN-PLASMA; FAMILIAL
   HYPERALPHALIPOPROTEINEMIA; DEUTERATED LEUCINE; STABLE ISOTOPES; B-100
   KINETICS; FAT DIET; APOA-I; METABOLISM
AB Deficiency of the cholesteryl ester transfer protein (CETP) in humans is characterized by markedly elevated plasma concentrations of HDL cholesterol and apoA-I. To assess the metabolism of HDL apolipoproteins in CETP deficiency, in vivo apolipoprotein kinetic studies were performed using endogenous and exogenous labeling techniques in two unrelated homozygotes with CETP deficiency, one heterozygote, and four control subjects. All study subjects were administered C-13(6)-labeled phenylalanine by primed constant infusion for up to 16 h. The fractional synthetic rates (FSRs) of apoA-I in two homozygotes with CETP deficiency (0.135, 0.134/d) were found to be significantly lower than those in controls (0.196+/-0.041/d, P < 0.01). Delayed apoA-I catabolism was confirmed by an exogenous radiotracer study in one CETP-deficient homozygote, in whom the fractional catabolic rate of I-125-apoA-I was 0.139/d (normal 0.216+/-0.018/d). The FSRs of apoA-II were also significantly lower in the homozygous CETP-deficient subjects (0.104, 0.112/d) than in the controls (0.170+/-0.023/d, P < 0.01). The production rates of apoA-land apoA-II were normal in both homozygous CETP-deficient subjects. The turnover of apoA-I and apoA-II was substantially slower in both HDL, and HDL3 in the CETP-deficient homozygotes than in controls. The kinetics of apoA-I and apoA-II in the CETP-deficient heterozygote were not different from those in controls. These data establish that homozygous CETP deficiency causes markedly delayed catabolism of apoA-I and apoA-II without affecting the production rates of these apolipoproteins.
C1 JIKEI UNIV,AOTO HOSP,SCH MED,DEPT INTERNAL MED,TOKYO,JAPAN.
   NATL DEF MED COLL,DEPT INTERNAL MED,SAITAMA,JAPAN.
   SAPPORO GEN HOSP,DEPT INTERNAL MED,HOKKAIDO,JAPAN.
RP IKEWAKI, K (reprint author), NHLBI,MOLEC DIS BRANCH,BLDG 10,ROOM 7N117,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 65
TC 122
Z9 123
U1 0
U2 2
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 OCT
PY 1993
VL 92
IS 4
BP 1650
EP 1658
DI 10.1172/JCI116750
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA MB166
UT WOS:A1993MB16600010
PM 8408618
ER

PT J
AU KING, CL
   MAHANTY, S
   KUMARASWAMI, V
   ABRAMS, JS
   REGUNATHAN, J
   JAYARAMAN, K
   OTTESEN, EA
   NUTMAN, TB
AF KING, CL
   MAHANTY, S
   KUMARASWAMI, V
   ABRAMS, JS
   REGUNATHAN, J
   JAYARAMAN, K
   OTTESEN, EA
   NUTMAN, TB
TI CYTOKINE CONTROL OF PARASITE-SPECIFIC ANERGY IN HUMAN LYMPHATIC
   FILARIASIS - PREFERENTIAL INDUCTION OF A REGULATORY T-HELPER TYPE-2
   LYMPHOCYTE SUBSET
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE LYMPHATIC FILARIASIS; TOLERANCE; T-HELPER SUBSETS; IL-10; ELISPOT
ID SCHISTOSOMA-MANSONI; INTERFERON-GAMMA; DOWN-REGULATION; BRUGIA-MALAYI;
   PROTECTIVE IMMUNITY; CELL PROLIFERATION; IGE RESPONSES; B-CELLS;
   ANTIGEN; INFECTION
AB The immunological mechanisms involved in maintenance of an asymptomatic microfilaremic state (MF) in patients with lymphatic filariasis remain undefined. MF patients have impaired filarial antigen (Ag)-specific lymphocyte proliferation and decreased frequencies (Fo) of Ag-specific T cells, and yet elevated serum IgE and antifilarial IgG4. To investigate the mechanism of Ag-specific anergy in MF patients in contrast to amicrofilaremic individuals with chronic lymphatic obstruction (CP), the Fo of Ag-specific lymphocytes from peripheral blood mononuclear cells secreting either IL-4 or IFN-gamma were assessed by filter spot enzyme-linked immunosorbent assay, and IL-10 and transforming growth factor-beta (TGF-beta) mRNA transcript levels were assessed by a semiquantitative reverse transcriptase polymerase chain reaction technique. The Fo of filaria-specific IL-4-secreting lymphocytes were equivalent in both MF (geometric mean [GM] = 1:11,700) and CP (GM = 1:29,300 P = 0.08), whereas the Fo of IFN-gamma-secreting lymphocytes were lower in MF (GM 1:39,300) than in CP (GM = 1:4,200, P < 0.01). When the ratio of IL4/IFN-gamma (T helper type 2 [Th2]/Th1)-secreting cells was examined, MF subjects showed a predominant Th2 response (8:1) compared with a Th1 response in CP individuals (1:4). mRNA transcript levels of IL-10 were also significantly elevated in MF compared with CP individuals (P < 0.01). Further, IL-10 and TGF-beta were shown to have a role in modulating the Ag-specific anergy among MF subjects, in that neutralizing anti-IL-10 or anti-TGF-beta significantly enhanced lymphocyte proliferation response (by 220-1,300%) to filarial Ags in MF individuals. These findings demonstrate that MF subjects respond to parasite antigen by producing a set of suppressive cytokines that may facilitate persistence of the parasite within humans while producing little clinical disease.
C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892.
   ANNA UNIV,TUBERCULOSIS RES CTR,MADRAS 600025,INDIA.
   ANNA UNIV,DEPT BIOTECHNOL,MADRAS 600025,INDIA.
   DNAX INC,RES INST,PALO ALTO,CA 94304.
RP KING, CL (reprint author), CASE WESTERN RESERVE UNIV,SCH MED,DIV GEOG MED,2109 ADELBERT RD,CLEVELAND,OH 44106, USA.
OI Mahanty, Siddhartha/0000-0003-1068-0524
NR 49
TC 225
Z9 229
U1 0
U2 5
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 OCT
PY 1993
VL 92
IS 4
BP 1667
EP 1673
DI 10.1172/JCI116752
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA MB166
UT WOS:A1993MB16600012
PM 8408619
ER

PT J
AU SPRAUL, M
   RAVUSSIN, E
   FONTVIEILLE, AM
   RISING, R
   LARSON, DE
   ANDERSON, EA
AF SPRAUL, M
   RAVUSSIN, E
   FONTVIEILLE, AM
   RISING, R
   LARSON, DE
   ANDERSON, EA
TI REDUCED SYMPATHETIC NERVOUS ACTIVITY - A POTENTIAL MECHANISM
   PREDISPOSING TO BODY-WEIGHT GAIN
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE SYMPATHETIC NERVOUS SYSTEM; MICRONEUROGRAPHY; BODY COMPOSITION; ENERGY
   EXPENDITURE; OBESITY
ID 24-HOUR ENERGY-EXPENDITURE; AGE-RELATED-CHANGES; INSULIN RESISTANCE;
   SYSTEM ACTIVITY; PIMA-INDIANS; SKELETAL-MUSCLE; FOOD-INTAKE; HUMANS;
   PLASMA; THERMOGENESIS
AB The sympathetic nervous system is recognized to play a role in the etiology of animal and possibly human obesity through its impact on energy expenditure and / or food intake. We, therefore, measured fasting muscle sympathetic nerve activity (MSNA) in the peroneal nerve and its relationship with energy expenditure and body composition in 25 relatively lean Pima Indian males (means+/-SD; 26+/-6 yr, 82+/-19 kg, 28+/-10% body fat) and 19 Caucasian males (29+/-5 yr, 81+/-13 kg, 24+/-9% body fat). 24-h energy expenditure, sleeping metabolic rate, and resting metabolic rate were measured in a respiratory chamber, whereas body composition was estimated by hydrodensitometry.
   Pima Indians had lower MSNA than Caucasians (23+/-6 vs 33+/-10 bursts/min, P = 0.0007). MSNA was significantly related to percent body fat in Caucasians (r = 0.55, P = 0.01) but not in Pimas. MSNA also correlated with energy expenditure adjusted for fat-free mass, fat mass, and age in Caucasians (r = 0.51, P = 0.03; r = 0.54, P = 0.02; and r = 0.53, P = 0.02 for adjusted 24-h energy expenditure, sleeping metabolic rate, and resting metabolic rate, respectively) but not in Pima Indians.
   In conclusion, the activity of the sympathetic nervous system is a determinant of energy expenditure in Caucasians. Individuals with low resting MSNA may be at risk for body weight gain resulting from a lower metabolic rate. A low resting MSNA and the lack of impact of MSNA on metabolic rate might play a role in the etiology of obesity in Pima Indians.
C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016.
   UNIV IOWA,COLL MED,DEPT ANESTHESIA,IOWA CITY,IA 52242.
   UNIV IOWA,COLL MED,CTR CARDIOVASC,IOWA CITY,IA 52242.
FU NHLBI NIH HHS [HL-43514, HL-44546]
NR 38
TC 218
Z9 221
U1 0
U2 5
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 OCT
PY 1993
VL 92
IS 4
BP 1730
EP 1735
DI 10.1172/JCI116760
PG 6
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA MB166
UT WOS:A1993MB16600020
PM 8408625
ER

PT J
AU KHALIL, N
   WHITMAN, C
   ZUO, L
   DANIELPOUR, D
   GREENBERG, A
AF KHALIL, N
   WHITMAN, C
   ZUO, L
   DANIELPOUR, D
   GREENBERG, A
TI REGULATION OF ALVEOLAR MACROPHAGE TRANSFORMING GROWTH-FACTOR-BETA
   SECRETION BY CORTICOSTEROIDS IN BLEOMYCIN-INDUCED PULMONARY INFLAMMATION
   IN THE RAT
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE PULMONARY FIBROSIS; INTERLEUKIN-1; TRANSFORMING GROWTH FACTOR-BETA(1);
   TRANSFORMING GROWTH FACTOR-BETA(2); TRANSFORMING GROWTH FACTOR-BETA(3)
ID FACTOR-BETA-1 GENE; EXPRESSION; FIBROSIS; INTERLEUKIN-1; COLLAGEN;
   INVITRO; RELEASE; GLUCOCORTICOIDS; STIMULATION; PROMOTER
AB In a model of pulmonary inflammation and fibrosis induced by the antineoplastic antibiotic, bleomycin, we previously demonstrated that TGF-beta was markedly elevated within 7 d of bleomycin administration. At the time of maximal TGF-beta production, TGF-beta1 was localized by immunohistochemistry to be present almost exclusively in alveolar macrophages. In this study, we have demonstrated that alveolar macrophages stimulated by bleomycin-induced injury secrete large quantities of biologically active TGF-beta1 when explanted into tissue culture. However, alveolar macrophages from normal saline-treated rats secrete small quantities of biologically inactive TGF-beta. In contrast, splenic macrophages secrete large quantities of inactive TGF-beta and are unaffected by the intratracheal bleomycin treatment. High doses of the corticosteroid methylprednisolone given intramuscularly before and concomitantly with bleomycin administration prevented the influx of alveolar macrophages into the lungs, diminishing both the number of macrophages present in the alveoli and the total lung content of TGF-beta. However, the rate of secretion of TGF-beta by alveolar macrophages recovered from the alveoli was unchanged after corticosteroid treatment. When activated alveolar macrophages were cultured in the presence of several concentrations of dexamethasone that completely suppressed IL-1 secretion, little effect on TGF-secretion was observed.
   The findings in this study demonstrate that during bleomycin-induced injury, alveolar macrophages not only secrete large quantities of active TGF-beta1, but are a predominant source of the enhanced TGF-beta response seen in this model. Furthermore, the alveolar macrophage secretion of TGF-beta is not inhibited by the presence of high concentrations of corticosteroids.
C1 NIH,CHEMOPREVENT LAB,BETHESDA,MD 20892.
RP KHALIL, N (reprint author), UNIV MANITOBA,MANITOBA INST CELL BIOL,DEPT MED,RESP DIS SECT,100 OLIVIA ST,WINNIPEG R3E 0V9,MANITOBA,CANADA.
NR 41
TC 144
Z9 151
U1 1
U2 2
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 OCT
PY 1993
VL 92
IS 4
BP 1812
EP 1818
DI 10.1172/JCI116771
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA MB166
UT WOS:A1993MB16600031
PM 7691887
ER

PT J
AU VAMVAKOPOULOS, NC
   CHROUSOS, GP
AF VAMVAKOPOULOS, NC
   CHROUSOS, GP
TI EVIDENCE OF DIRECT ESTROGENIC REGULATION OF HUMAN
   CORTICOTROPIN-RELEASING HORMONE GENE-EXPRESSION - POTENTIAL IMPLICATIONS
   FOR THE SEXUAL DIMORPHISM OF THE STRESS-RESPONSE AND IMMUNE INFLAMMATORY
   REACTION
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE CORTICOTROPIN-RELEASING HORMONE; GENE REGULATION; RECEPTORS, ESTROGEN;
   SEX CHARACTERISTICS
ID WALL INDUCED POLYARTHRITIS; PITUITARY-ADRENAL AXIS; CENTRAL
   NERVOUS-SYSTEM; DNA-BINDING; RAT-BRAIN; STEROID-HORMONE; HUMAN-PLACENTA;
   MESSENGER-RNA; FEMALE RATS; LEWIS RATS
AB Corticotropin-releasing hormone (CRH) plays major roles in coordination of the stress response and regulation of the immune/inflammatory reaction, two important functions associated with sexual dimorphism. Two overlapping segments of the 5' flanking region of the human (h) CRH gene, the proximal 0.9 kb (containing two perfect half-palindromic estrogen-responsive elements [EREs]) and the 2.4 kb (including the former and containing two additional perfect half-palindromic EREs), were examined for their ability to confer estrogen-mediated transcriptional enhancement to a homologous or heterologous promoter. The level of estrogen-induced transactivation by the 0.9- and 2.4-kb segments was determined by chloramphenicol acetyltransferase analysis in CV-1 cells cotransfected with estrogen receptor (ER) cDNA expression plasmids, and found to be respectively approximately 10% and 20% of that of the strongly estrogen-responsive Xenopus vitellogenin A2 enhancer. Gel retardation and immunoprecipitation demonstrated specific association between the perfect half-palindromic EREs of hCRH gene and the DNA binding domain of hER in vitro. These findings may constitute the basis of sexual dimorphism in the expression of the CRH gene in the central nervous system and periphery, and might shed light in existing gender differences in stress response and immune regulation.
RP VAMVAKOPOULOS, NC (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10N-240,BETHESDA,MD 20892, USA.
NR 61
TC 324
Z9 327
U1 0
U2 6
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 1993
VL 92
IS 4
BP 1896
EP 1902
DI 10.1172/JCI116782
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA MB166
UT WOS:A1993MB16600042
PM 8408641
ER

PT J
AU MURPHY, WJ
   BACK, TC
   CONLON, KC
   KOMSCHLIES, KL
   ORTALDO, JR
   SAYERS, TJ
   WILTROUT, RH
   LONGO, DL
AF MURPHY, WJ
   BACK, TC
   CONLON, KC
   KOMSCHLIES, KL
   ORTALDO, JR
   SAYERS, TJ
   WILTROUT, RH
   LONGO, DL
TI ANTITUMOR EFFECTS OF INTERLEUKIN-7 AND ADOPTIVE IMMUNOTHERAPY ON HUMAN
   COLON-CARCINOMA XENOGRAFTS
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE SCID HUMAN MOUSE; CYTOKINES; CANCER TREATMENT; T-CELLS; INTERLEUKIN-7
ID CYTOTOXIC LYMPHOCYTES-T; CELL GROWTH-FACTOR; KILLER-CELLS; EFFICACY;
   MODEL; MOUSE; IL-7
AB The antitumor properties of recombinant human IL-7 (rhIL-7) on a human tumor was evaluated by engrafting a human colon carcinoma into immunodeficient mice and then treating the mice with rhIL-7 and adoptively transferred human peripheral blood T cells. It was found that rhIL-7 alone had no effect on the survival of the tumor-bearing recipients. However, the combination of rhIL-7 and human T cells significantly promoted the survival of the recipients compared with mice receiving either treatment by itself. When the surviving mice were analyzed 6 mo later for the degree of human cell engraftment, the recipients receiving both rhIL-7 and human T cells had greater numbers of human CD8+ T cells in the spleens.  However, the human T cells recovered from the surviving mice showed low lytic activity against the tumor in vitro. Supernatants from human T cells cultured with the tumor and rhIL-7 in vitro were found to inhibit tumor growth and were demonstrated to contain high levels of IFN-gamma. Antibodies to IFN-gamma neutralized the growth inhibition of the tumor both in vitro and in vivo demonstrating that the in vivo mechanism underlying the antitumor effects of this regimen was partly dependent on the production of IFN-gamma by the T cells and not their cytolytic capability. Interestingly, systemic administration of rhIFN-gamma to tumor-bearing mice yielded little antitumor effect suggesting that adoptive immunotherapy with rhIL-7 was superior possibly because of the continuous local release of the cytokines. Therefore, rhIL-7 may be of clinical use as an antineoplastic agent and the human/mouse model is a potentially important preclinical model for in vivo evaluation of the efficacy of this and other immunotherapies.
C1 NCI,FREDERICK CANC RES & DEV CTR,EXPTL IMMUNOL LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702.
   NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702.
RP MURPHY, WJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,LEUKOCYTE BIOL LAB,BLDG 567,ROOM 141,FREDERICK,MD 21702, USA.
RI Sayers, Thomas/G-4859-2015
NR 17
TC 36
Z9 36
U1 0
U2 0
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 1993
VL 92
IS 4
BP 1918
EP 1924
DI 10.1172/JCI116785
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA MB166
UT WOS:A1993MB16600045
PM 8408644
ER

PT J
AU MEIER, CA
   PARKISON, C
   CHEN, A
   ASHIZAWA, K
   MEIERHEUSLER, SC
   MUCHMORE, P
   CHENG, SY
   WEINTRAUB, BD
AF MEIER, CA
   PARKISON, C
   CHEN, A
   ASHIZAWA, K
   MEIERHEUSLER, SC
   MUCHMORE, P
   CHENG, SY
   WEINTRAUB, BD
TI INTERACTION OF HUMAN BETA-1 THYROID-HORMONE RECEPTOR AND ITS MUTANTS
   WITH DNA AND RETINOID-X RECEPTOR-BETA T(3) RESPONSE ELEMENT DEPENDENT
   DOMINANT-NEGATIVE POTENCY
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
DE THYROID HORMONE RECEPTOR; GENERALIZED RESISTANCE TO THYROID HORMONE;
   T(3)-RESPONSE ELEMENT; RETINOID-X RECEPTOR; DOMINANT NEGATIVE ACTION
ID LIGAND-BINDING DOMAIN; GENERALIZED RESISTANCE; C-ERBA; RXR-BETA;
   TRANSCRIPTIONAL ACTIVATION; AUXILIARY PROTEIN; ACID RECEPTORS; GENE;
   TRIIODOTHYRONINE; KINDREDS
AB Mutations in the human beta thyroid hormone receptor (h-TRbeta) gene are associated with the syndrome of generalized resistance to thyroid hormone. We investigated the interaction of three h-TRbeta1 mutants representing different types of functional impairment (kindreds ED, OK, and PV) with different response elements for 3,3',5-triiodothyronine(T3)and with retinoid X receptor beta (RXPbeta). The mutant receptors showed an increased tendency to form homodimers on a palindromic T3-response element (TREpal), a direct repeat (DR + 4), and an inverted palindrome (TRElap). On TRElap, wild type TR binding was decreased by T3, while the mutant receptors showed a variably decreased degree of dissociation from TRElap in response to T3. The extent of dissociation was proportional to their T3 binding affinities. RXRbeta induced the formation of h-TRbeta1:RXRbeta heterodimers equally well for mutants and the wild type h-TRbeta1 on these T3 response elements. However, the T3-dependent increase in heterodimerization with RXRbeta was absent or reduced for the mutant TRs.
   Transient transfection studies indicated that the dominant negative potency was several-fold more pronounced on the TRElap as compared to TREpal or DR + 4. In CV-1 and HeLa cells, transfection of RXRbeta could not reverse the dominant negative action. These results demonstrate that the binding of mutant h-TRs to DNA, as well as their dominant negative potency, are TRE dependent. In addition, competition for DNA binding, rather than for limiting amounts of RXRbeta, is likely to mediate the dominant negative action.
C1 NIH,MOLEC & CELLULAR ENDOCRINOL BRANCH,BLDG 10,ROOM 8D14,BETHESDA,MD 20892.
   UNIV GENEVA,HOP CANTONAL,DEPT MED,DIV ENDOCRINOL,THYROID UNIT,CH-1211 GENEVA 4,SWITZERLAND.
   NCI,MOLEC BIOL LAB,BETHESDA,MD 20892.
NR 40
TC 81
Z9 81
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 OCT
PY 1993
VL 92
IS 4
BP 1986
EP 1993
DI 10.1172/JCI116793
PG 8
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA MB166
UT WOS:A1993MB16600053
PM 8408652
ER

PT J
AU HAMMER, S
   CRUMPACKER, C
   DAQUILA, R
   JACKSON, B
   LATHEY, J
   LIVNAT, D
   REICHELDERFER, P
AF HAMMER, S
   CRUMPACKER, C
   DAQUILA, R
   JACKSON, B
   LATHEY, J
   LIVNAT, D
   REICHELDERFER, P
TI USE OF VIROLOGICAL ASSAYS FOR DETECTION OF HUMAN-IMMUNODEFICIENCY-VIRUS
   IN CLINICAL-TRIALS - RECOMMENDATIONS OF THE AIDS CLINICAL-TRIALS GROUP
   VIROLOGY COMMITTEE
SO JOURNAL OF CLINICAL MICROBIOLOGY
LA English
DT Review
ID POLYMERASE CHAIN-REACTION; HIV-INFECTED INDIVIDUALS; PLACEBO-CONTROLLED
   TRIAL; BLOOD MONONUCLEAR-CELLS; P24 ANTIGEN; PERIPHERAL-BLOOD;
   IMMUNE-COMPLEXES; EARLY DIAGNOSIS; HOMOSEXUAL MEN; ZIDOVUDINE AZT
C1 NIAID,DIV AIDS,BETHESDA,MD 20892.
   NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215.
   HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115.
   BETH ISRAEL HOSP,CAMBRIDGE,MA.
   MASSACHUSETTS GEN HOSP,CAMBRIDGE,MA.
   CASE WESTERN RESERVE UNIV,DEPT CLIN PATHOL,CLEVELAND,OH 44106.
   UNIV CALIF SAN DIEGO,DEPT INFECT DIS,SAN DIEGO,CA 92103.
FU NIAID NIH HHS [NIAID UOI-AI25879, NIAID UOI-AI27659, NIAID UOI-AI27670]
NR 64
TC 62
Z9 62
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0095-1137
J9 J CLIN MICROBIOL
JI J. Clin. Microbiol.
PD OCT
PY 1993
VL 31
IS 10
BP 2557
EP 2564
PG 8
WC Microbiology
SC Microbiology
GA LY059
UT WOS:A1993LY05900001
PM 8253949
ER

PT J
AU MARCONI, RT
   SAMUELS, DS
   SCHWAN, TG
   GARON, CF
AF MARCONI, RT
   SAMUELS, DS
   SCHWAN, TG
   GARON, CF
TI IDENTIFICATION OF A PROTEIN IN SEVERAL BORRELIA SPECIES WHICH IS RELATED
   TO OSPC OF THE LYME-DISEASE SPIROCHETES
SO JOURNAL OF CLINICAL MICROBIOLOGY
LA English
DT Article
ID SIGNATURE NUCLEOTIDE ANALYSIS; MAJOR SURFACE-PROTEINS; MOLECULAR
   ANALYSIS; PHYLOGENETIC ANALYSIS; LINEAR PLASMIDS; NORTH-AMERICAN;
   BURGDORFERI; RNA; EXPRESSION; SEQUENCE
AB Using oligonucleotide probes which have previously been shown to be specific for the ospC gene found in the Lyme disease spirochete species Borrelia burgdorferi, B. garinii, and group VS461, we detected an ospC homolog in other Borrelia species including B. coriaceae, B. hermsii, B. anserina, B. turicatae, and B. parkeri. In contrast to the Lyme disease spirochetes, which carry the ospC gene on a 26-kb circular plasmid, we mapped the gene in other Borrelia species to linear plasmids which varied in size among the isolates tested. Some isolates carry multiple copies of the gene residing on linear plasmids of different sizes. The analyses conducted here also demonstrate that these Borrelia species contain a linear chromosome. Northern (RNA) blot analyses demonstrated that the gene is transcriptionally expressed in all species examined. High levels of transcriptional expression were observed in some B. hermsii isolates. Transcriptional start site analyses revealed that the length of the untranslated leader sequence was identical to that observed in the Lyme disease spirochete species. By Western blotting (immunoblotting) with antiserum (polyclonal) raised against the OspC protein of B. burgdorferi, we detected an immunoreactive protein of the same molecular weight as the OspC found in Lyme disease spirochete species. The results presented here demonstrate the presence of a protein that is genetically and antigenically related to OspC which is expressed in all species of the genus Borrelia tested.
RP MARCONI, RT (reprint author), NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840, USA.
RI Samuels, D Scott/B-7549-2012
OI Samuels, D Scott/0000-0001-8352-7593
NR 40
TC 53
Z9 53
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0095-1137
J9 J CLIN MICROBIOL
JI J. Clin. Microbiol.
PD OCT
PY 1993
VL 31
IS 10
BP 2577
EP 2583
PG 7
WC Microbiology
SC Microbiology
GA LY059
UT WOS:A1993LY05900004
PM 8253952
ER

PT J
AU SCHAUER, DB
   GHORI, N
   FALKOW, S
AF SCHAUER, DB
   GHORI, N
   FALKOW, S
TI ISOLATION AND CHARACTERIZATION OF FLEXISPIRA-RAPPINI FROM LABORATORY
   MICE
SO JOURNAL OF CLINICAL MICROBIOLOGY
LA English
DT Article
ID BACTERIUM; MUCOSA; GASTROENTERITIS; MICROORGANISMS; ULTRASTRUCTURE;
   ABORTION
AB A bacterium with an unusual ultrastructure and possessing a fusiform protoplasmic cylinder, spiral periplasmic fibers, and bipolar tufts of sheathed flagella was identified in the intestinal mucosae of laboratory mice. The organism was cultured under microaerophilic conditions and was found to rapidly hydrolyze urea. On the basis of 16S rRNA gene sequence analysis, the organism was shown to be ''Flexispira rappini.'' ''F. rappini'' is closely related to members of the genus Helicobacter and has been reported to be associated with human gastroenteritis and ovine abortion. ''F. rappini'' has not previously been observed in the gastrointestinal tracts of mice.
C1 STANFORD UNIV,MED CTR,SCH MED,DEPT MICROBIOL & IMMUNOL,STANFORD,CA 94305.
   NIAID,ROCKY MT LABS,HAMILTON,MT 59840.
FU NIDDK NIH HHS [DK38707-06]
NR 23
TC 89
Z9 90
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0095-1137
J9 J CLIN MICROBIOL
JI J. Clin. Microbiol.
PD OCT
PY 1993
VL 31
IS 10
BP 2709
EP 2714
PG 6
WC Microbiology
SC Microbiology
GA LY059
UT WOS:A1993LY05900028
PM 7504685
ER

PT J
AU COPPOLA, R
AF COPPOLA, R
TI STANDARD SPECIFICATION FOR TRANSFERRING DIGITAL NEUROPHYSIOLOGICAL DATA
   BETWEEN INDEPENDENT COMPUTER-SYSTEMS - COMMENT
SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY
LA English
DT Letter
RP COPPOLA, R (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,WASHINGTON,DC 20032, USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0736-0258
J9 J CLIN NEUROPHYSIOL
JI J. Clin. Neurophysiol.
PD OCT
PY 1993
VL 10
IS 4
BP 537
EP 537
DI 10.1097/00004691-199310000-00017
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA ML300
UT WOS:A1993ML30000018
PM 8308155
ER

PT J
AU WOLMARK, N
   ROCKETTE, H
   FISHER, B
   WICKERHAM, DL
   REDMOND, C
   FISHER, ER
   JONES, J
   MAMOUNAS, EP
   ORE, L
   PETRELLI, NJ
   SPURR, CL
   DIMITROV, N
   ROMOND, EH
   SUTHERLAND, CM
   KARDINAL, CG
   DEFUSCO, PA
   JOCHIMSEN, P
AF WOLMARK, N
   ROCKETTE, H
   FISHER, B
   WICKERHAM, DL
   REDMOND, C
   FISHER, ER
   JONES, J
   MAMOUNAS, EP
   ORE, L
   PETRELLI, NJ
   SPURR, CL
   DIMITROV, N
   ROMOND, EH
   SUTHERLAND, CM
   KARDINAL, CG
   DEFUSCO, PA
   JOCHIMSEN, P
TI THE BENEFIT OF LEUCOVORIN-MODULATED FLUOROURACIL AS POSTOPERATIVE
   ADJUVANT THERAPY FOR PRIMARY COLON-CANCER - RESULTS FROM NATIONAL
   SURGICAL ADJUVANT BREAST AND BOWEL PROJECT PROTOCOL C-03
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID ADVANCED COLORECTAL-CANCER; 5-FLUOROURACIL; VINCRISTINE; CHEMOTHERAPY;
   COMBINATION; LEVAMISOLE; CARCINOMA
RP WOLMARK, N (reprint author), NATL SURG ADJUVANT BREAST & BOWEL PROJECT, ROOM 914, SCAIFE HALL, 3550 TERRACE ST, PITTSBURGH, PA 15261 USA.
FU NCI NIH HHS [NCI-U10-CA-12027, NCI-U10-CA-37377]
NR 22
TC 480
Z9 489
U1 0
U2 4
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD OCT
PY 1993
VL 11
IS 10
BP 1879
EP 1887
PG 9
WC Oncology
SC Oncology
GA MC299
UT WOS:A1993MC29900008
PM 8410113
ER

PT J
AU HOROWITZ, ME
   KINSELLA, TJ
   WEXLER, LH
   BELASCO, J
   TRICHE, T
   TSOKOS, M
   STEINBERG, SM
   MCCLURE, L
   LONGO, DL
   STEIS, RG
   GLATSTEIN, E
   PIZZO, PA
   MISER, JS
AF HOROWITZ, ME
   KINSELLA, TJ
   WEXLER, LH
   BELASCO, J
   TRICHE, T
   TSOKOS, M
   STEINBERG, SM
   MCCLURE, L
   LONGO, DL
   STEIS, RG
   GLATSTEIN, E
   PIZZO, PA
   MISER, JS
TI TOTAL-BODY IRRADIATION AND AUTOLOGOUS BONE-MARROW TRANSPLANT IN THE
   TREATMENT OF HIGH-RISK EWINGS-SARCOMA AND RHABDOMYOSARCOMA
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID COMBINED MODALITY THERAPY; TERM FOLLOW-UP; YOUNG-ADULTS; INTERGROUP
   RHABDOMYOSARCOMA; MULTIMODAL THERAPY; LOCAL-CONTROL; CHILDREN;
   EXPERIENCE; REGIMEN; CELL
C1 NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892.
   CHILDRENS HOSP PHILADELPHIA,DIV ONCOL,PHILADELPHIA,PA.
   NCI,PATHOL LAB,BETHESDA,MD 20892.
   NCI,PEDIAT BRANCH,BETHESDA,MD 20892.
   NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892.
   NCI,MED BRANCH,BETHESDA,MD 20892.
NR 31
TC 132
Z9 132
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD OCT
PY 1993
VL 11
IS 10
BP 1911
EP 1918
PG 8
WC Oncology
SC Oncology
GA MC299
UT WOS:A1993MC29900013
PM 8410118
ER

PT J
AU REICHMAN, BS
   SEIDMAN, AD
   CROWN, JPA
   HEELAN, R
   HAKES, TB
   LEBWOHL, DE
   GILEWSKI, TA
   SURBONE, A
   CURRIE, V
   HUDIS, CA
   YAO, TJ
   KLECKER, R
   JAMISDOW, C
   COLLINS, J
   QUINLIVAN, S
   BERKERY, R
   TOOMASI, F
   CANETTA, R
   FISHERMAN, J
   ARBUCK, S
   NORTON, L
AF REICHMAN, BS
   SEIDMAN, AD
   CROWN, JPA
   HEELAN, R
   HAKES, TB
   LEBWOHL, DE
   GILEWSKI, TA
   SURBONE, A
   CURRIE, V
   HUDIS, CA
   YAO, TJ
   KLECKER, R
   JAMISDOW, C
   COLLINS, J
   QUINLIVAN, S
   BERKERY, R
   TOOMASI, F
   CANETTA, R
   FISHERMAN, J
   ARBUCK, S
   NORTON, L
TI PACLITAXEL AND RECOMBINANT HUMAN GRANULOCYTE-COLONY-STIMULATING FACTOR
   AS INITIAL CHEMOTHERAPY FOR METASTATIC BREAST-CANCER
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID PHASE-II TRIAL; TAXOL; AGENT; CELLS; RESISTANCE; TUBULIN; THERAPY;
   REINDUCTION; MECHANISM; CISPLATIN
C1 MEM SLOAN KETTERING CANC CTR,DEPT MED,DIV SOLID TUMOR ONCOL,BREAST & GYNECOL CANC MED SERV,NEW YORK,NY 10021.
   MEM SLOAN KETTERING CANC CTR,DEPT MED IMAGING,NEW YORK,NY 10021.
   BRISTOL MYERS SQUIBB PHARMACEUT RES INST,WALLINGFORD,CT.
   NCI,DIV CANC THERAPY,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD 20892.
   US FDA,DIV CLIN PHARMACOL,ROCKVILLE,MD 20857.
   MEM SLOAN KETTERING CANC CTR,DEPT EPIDEMIOL & BIOSTAT,NEW YORK,NY 10021.
FU NCI NIH HHS [1-CM07311, CA-09207-14]
NR 32
TC 260
Z9 261
U1 0
U2 7
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD OCT
PY 1993
VL 11
IS 10
BP 1943
EP 1951
PG 9
WC Oncology
SC Oncology
GA MC299
UT WOS:A1993MC29900017
PM 7691998
ER

PT J
AU SPARANO, JA
   FISHER, RI
   SUNDERLAND, M
   MARGOLIN, K
   ERNEST, ML
   SZNOL, M
   ATKINS, MB
   DUTCHER, JP
   MICETICH, KC
   WEISS, GR
   DOROSHOW, JH
   ARONSON, FR
   RUBINSTEIN, LV
   MIER, JW
AF SPARANO, JA
   FISHER, RI
   SUNDERLAND, M
   MARGOLIN, K
   ERNEST, ML
   SZNOL, M
   ATKINS, MB
   DUTCHER, JP
   MICETICH, KC
   WEISS, GR
   DOROSHOW, JH
   ARONSON, FR
   RUBINSTEIN, LV
   MIER, JW
TI RANDOMIZED PHASE-III TRIAL OF TREATMENT WITH HIGH-DOSE INTERLEUKIN-2
   EITHER ALONE OR IN COMBINATION WITH INTERFERON ALFA-2A IN PATIENTS WITH
   ADVANCED MELANOMA
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID METASTATIC MALIGNANT-MELANOMA; ACTIVATED KILLER-CELLS; CONTINUOUS
   INFUSION INTERLEUKIN-2; RECOMBINANT INTERLEUKIN-2; ALPHA-INTERFERON;
   CANCER-PATIENTS; THERAPY; INVIVO; ANTIGENS; TOXICITY
C1 UNIV TEXAS,HLTH SCI CTR,AUDI L MURPHY VET ADM MED CTR,SAN ANTONIO,TX 78284.
   NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD 20892.
   LOYOLA UNIV,MED CTR,MAYWOOD,IL 60153.
   UNIV CALIF SAN FRANCISCO,MED CTR,SAN FRANCISCO,CA 94143.
   CITY HOPE NATL MED CTR,DUARTE,CA 91010.
   TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA 02111.
   HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110.
RP SPARANO, JA (reprint author), MONTEFIORE MED CTR,ALBERT EINSTEIN CANC CTR,EXTRAMURAL IL2 WORKING GRP,111 E 210TH ST,BRONX,NY 10467, USA.
FU NCI NIH HHS [N01-CM73702, N01-CM73703, N01-CM73704]
NR 33
TC 135
Z9 137
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 OCT
PY 1993
VL 11
IS 10
BP 1969
EP 1977
PG 9
WC Oncology
SC Oncology
GA MC299
UT WOS:A1993MC29900020
PM 8410122
ER

PT J
AU BERTHOLD, CW
   DIONNE, RA
AF BERTHOLD, CW
   DIONNE, RA
TI CLINICAL-EVALUATION OF H(1)-RECEPTOR AND H(2)-RECEPTOR ANTAGONISTS FOR
   ACUTE POSTOPERATIVE PAIN
SO JOURNAL OF CLINICAL PHARMACOLOGY
LA English
DT Article
ID RECEPTOR ANTAGONIST; TERFENADINE; HISTAMINE; ANALGESIA; HYDROXYZINE; H-1
AB The acute analgesic activity of an H-1-histamine antagonist, terfenadine 60 mg, and an H-2-histamine antagonist, ranitidine 150 mg, were compared with ibuprofen 600 mg and placebo in a double-blind, Placebo-controlled, parallel-group study. Treatments were administered to a total of 127 patients 1 hour before oral surgery. Analgesia was assessed every 30 minutes for 240 minutes after surgery. Analgesic efficacy was compared using the following standard pain intensity scales: visual analog scale, category, graphic rating, and global evaluation. Ibuprofen was significantly better than all other treatments for all measures of analgesic activity. The effects of terfenadine and ranitidine were similar to placebo. These data indicate that pretreatments with a single dose of a histamine receptor antagonist specific for either the H-1- or H-2-receptor does not produce analgesia in an oral surgery model of acute pain with overall assay sensitivity, suggesting that antihistamines that act primarily at peripheral sites are devoid of analgesic activity. These data contrast with other studies that have demonstrated analgesia using centrally acting antihistamines such as hydroxyzine, phenyltoloxamine, or orphenadrine.
C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,CLIN PHARMACOL UNIT,BLDG 10,BETHESDA,MD 20892.
NR 26
TC 9
Z9 9
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0091-2700
J9 J CLIN PHARMACOL
JI J. Clin. Pharmacol.
PD OCT
PY 1993
VL 33
IS 10
BP 944
EP 948
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA MA786
UT WOS:A1993MA78600009
PM 8227466
ER

PT J
AU WATKINS, JT
   LEBER, WR
   IMBER, SD
   COLLINS, JF
   ELKIN, I
   PILKONIS, PA
   SOTSKY, SM
   SHEA, MT
   GLASS, DR
AF WATKINS, JT
   LEBER, WR
   IMBER, SD
   COLLINS, JF
   ELKIN, I
   PILKONIS, PA
   SOTSKY, SM
   SHEA, MT
   GLASS, DR
TI TEMPORAL COURSE OF CHANGE OF DEPRESSION
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
ID COLLABORATIVE RESEARCH-PROGRAM; PSYCHOTHERAPY; DRUGS
AB Two hundred fifty moderately to severely depressed outpatients were randomly assigned to 16 weeks of cognitive-behavioral therapy, interpersonal psychotherapy, imipramine plus clinical management (IMI-CM), or pill placebo plus clinical management. Two hundred thirty-nine patients actually began treatment. The most rapid change in depressive symptoms occurred in the IMI-CM condition, which achieved significantly better results than the other treatments at 8 and 12 weeks on 1 or more variables. Change over the course of treatment on variables hypothesized to be most specifically affected by the respective treatments was found only in the case of pharmacotherapy, in which imipramine produced significantly greater changes on the endogenous measure at 8 and 12 weeks.
C1 UNIV OKLAHOMA HLTH SCI CTR,HLTH SCI CTR,DEPT PSYCHIAT & BEHAV SCI,OKLAHOMA CITY,OK 73190.
   UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA 15261.
   WESTERN PSYCHIAT INST & CLIN,PITTSBURGH,PA 15261.
   VET ADM MED CTR,COOPERAT STUDIES PROGRAM COORDINATING CTR,PERRY POINT,MD 21902.
   NIMH,MOOD ANXIETY & PERSONAL DISORDERS RES BRANCH,BETHESDA,MD 20892.
   GEORGE WASHINGTON UNIV,MED CTR,DEPT PSYCHIAT & BEHAV SCI,WASHINGTON,DC 20037.
FU NIMH NIH HHS [MH 33760, MH 33753, MH 33762]
NR 20
TC 47
Z9 47
U1 0
U2 2
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD OCT
PY 1993
VL 61
IS 5
BP 858
EP 864
DI 10.1037//0022-006X.61.5.858
PG 7
WC Psychology, Clinical
SC Psychology
GA MC038
UT WOS:A1993MC03800017
PM 8245283
ER

PT J
AU LI, SH
   KINGMAN, A
   FORTHOFER, R
   SWANGO, P
AF LI, SH
   KINGMAN, A
   FORTHOFER, R
   SWANGO, P
TI COMPARISON OF TOOTH SURFACE-SPECIFIC DENTAL-CARIES ATTACK PATTERNS IN
   UNITED-STATES SCHOOLCHILDREN FROM 2 NATIONAL SURVEYS
SO JOURNAL OF DENTAL RESEARCH
LA English
DT Article
ID RATES
AB The 1979-1980 and the 1986-1987 National Institute of Dental Research (NIDR) surveys of school-aged children revealed that virtually all tooth surfaces experienced a decrease in caries prevalence during the inter-survey period. Overall, there was a 28% decrease in the proportion of tooth surfaces attacked by caries for the primary dentition between the two surveys. The decrease for primary incisors was numerically small (5 surfaces per thousand surfaces at risk) and not statistically significant, whereas decreases in the canines and primary molars were considerably larger (23 surfaces per thousand) and statistically significant. For the permanent dentition, the overall decrease in the proportion of surfaces attacked was 35% during the 1979-87 period. Differences between the two surveys in the proportions of surfaces with caries were largest for pit and fissure surfaces (56 surfaces per thousand), followed by those for posterior approximal surfaces (14 surfaces per thousand) and all other smooth surfaces (5 surfaces per thousand). Almost all of these differences were statistically significant, except for some surfaces which experienced very few caries.
C1 NIDR,EPIDEMIOL & ORAL DIS PREVENT PROGRAM,BETHESDA,MD 20892.
NR 14
TC 41
Z9 41
U1 0
U2 0
PU AMER ASSOC DENTAL RESEARCH
PI ALEXANDRIA
PA 1619 DUKE ST, ALEXANDRIA, VA 22314
SN 0022-0345
J9 J DENT RES
JI J. Dent. Res.
PD OCT
PY 1993
VL 72
IS 10
BP 1398
EP 1405
DI 10.1177/00220345930720100901
PG 8
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA MA597
UT WOS:A1993MA59700009
PM 8408882
ER

PT J
AU SAITO, K
   KURODA, A
   TANAKA, H
   YOSHIDA, A
   YOSHIDA, H
   FERRANS, VJ
AF SAITO, K
   KURODA, A
   TANAKA, H
   YOSHIDA, A
   YOSHIDA, H
   FERRANS, VJ
TI DIFFERENTIAL SENSITIVITY OF RAT CARDIAC SARCOLEMMA AND MITOCHONDRIA TO
   DAMAGE-INDUCED BY LIPID-PEROXIDATION
SO JOURNAL OF ELECTRON MICROSCOPY
LA English
DT Article
DE FREE RADICAL; CUMENE HYDROPEROXIDE; ULTRASTRUCTURE; SARCOLEMMA;
   MITOCHONDRIA
ID CUMENE HYDROPEROXIDE; MICROSOMAL-ENZYMES; FREE-RADICALS; HEART;
   LANTHANUM; ISCHEMIA; INJURY; REPERFUSION; PERMEABILITY; MYOCARDIUM
AB It is well known that the sarcolemma is the organelle most susceptible to lipid peroxidative attack in the isolated membrane preparations. To determine whether this also occurs in the intact heart, we studied the effect of cumene hydroperoxide, an agent capable of initiating lipid peroxidation, on the ultrastructure and lanthanum (La) staining of isolated rat hearts perfused with HEPES buffer (pH 7.4) containing: 140mM NaCl, 5mM KCl, 1mM MgCl2, 3 mM HEPES, 1.5mM CaCl2 and 11mM glucose. No ultrastructural alterations or intracellular deposits of La were observed in myocytes of rats perfused with HEPES buffer. Perfusion with cumene hydroperoxide (0.5mM) for 30 min induced a release of malondialdehyde-like substance in the perfusate and a spectrum of myocardial ultrastructural alterations. La was always observed only outside the sarcolemma in myocytes with moderate damage consisting of clearing of the mitochondrial matrix and slight margination of chromatin in the nuclei. Intracellular La was found in myocytes with severe and irreversible damages consisting of fragmentation of cristae and electron-dense amorphous particles in mitochondria. La was deposited on the outer surface of the mitochondrial membranes, lipid droplets and myofilaments. These data suggest that mitochondria are more susceptible than is the sarcolemma to lipid peroxidation induced by cumene hydroperoxide in the beating rat heart.
C1 KAGOSHIMA UNIV, FAC MED, DEPT INTERNAL MED 1, KAGOSHIMA, KAGOSHIMA 890, JAPAN.
   KAGOSHIMA UNIV, FAC MED, DEPT PATHOL 1, KAGOSHIMA, KAGOSHIMA 890, JAPAN.
   NHLBI, PATHOL BRANCH, ULTRASTRUCT SECT, BETHESDA, MD USA.
RP NATL INST FITNESS & SPORTS, CTR HLTH SERV, 1 SHIROMIZU, KANOYA, KAGOSHIMA 89123, JAPAN.
NR 23
TC 1
Z9 1
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0022-0744
EI 1477-9986
J9 J ELECTRON MICROSC
JI J. Electron Microsc.
PD OCT
PY 1993
VL 42
IS 5
BP 305
EP 309
PG 5
WC Microscopy
SC Microscopy
GA MH363
UT WOS:A1993MH36300003
PM 7508971
ER

PT J
AU SMITH, JJ
   CAPUCO, AV
   MATHER, IH
   VONDERHAAR, BK
AF SMITH, JJ
   CAPUCO, AV
   MATHER, IH
   VONDERHAAR, BK
TI RUMINANTS EXPRESS A PROLACTIN RECEPTOR OF M(R) 33 000-36 000 IN THE
   MAMMARY-GLAND THROUGHOUT PREGNANCY AND LACTATION
SO JOURNAL OF ENDOCRINOLOGY
LA English
DT Article
ID HUMAN GROWTH-HORMONE; MONOCLONAL-ANTIBODIES; PARTIAL-PURIFICATION;
   LACTOGENIC HORMONES; MOLECULAR-CLONING; CLEAVED PROLACTIN; OVINE
   PROLACTIN; GENE-EXPRESSION; RAT PROLACTIN; 16K FORMS
AB Developmental variation in the expression of the prolactin receptor in the ruminant mammary gland was investigated. Affinity chromatography revealed that bovine prolactin and human GH each bound to the same mammary gland proteins, yielding fractions enriched in binding activity and a protein of M(r) 36 000, assumed to be a bovine prolactin receptor. Affinity cross-linking of I-125-labelled human GH to mammary microsomes confirmed that the M(r) 36 000 protein was a bovine prolactin receptor. Binding assays of receptors in microsomes from the mammary tissue of cows and ewes at various stages of the lactational/reproductive cycle indicated developmental regulation of receptor concentration, but not receptor type, as no other bovine prolactin receptor type was detected by affinity cross-linking. These results suggest that differences in the response to prolactin in the mammary gland at various developmental stages in ruminants are not due to the expression of different forms of the prolactin receptor, and the lack of a prolactin effect on established lactation in ruminants is not due to the absence of the M(r) 36 000 form of the prolactin receptor.
C1 USDA ARS,LPSI,MILK SECRET & MASTITIS LAB,BELTSVILLE,MD 20705.
   UNIV MARYLAND,DEPT ANIM SCI,COLL PK,MD 20742.
   NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892.
NR 52
TC 7
Z9 8
U1 1
U2 4
PU J ENDOCRINOLOGY LTD
PI BRISTOL
PA 17/18 THE COURTYARD, WOODLANDS, ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ
SN 0022-0795
J9 J ENDOCRINOL
JI J. Endocrinol.
PD OCT
PY 1993
VL 139
IS 1
BP 37
EP 49
DI 10.1677/joe.0.1390037
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA MH227
UT WOS:A1993MH22700005
PM 8254292
ER

PT J
AU ZUNIGAPFLUCKER, JC
   SCHWARTZ, HL
   LENARDO, MJ
AF ZUNIGAPFLUCKER, JC
   SCHWARTZ, HL
   LENARDO, MJ
TI GENE-TRANSCRIPTION IN DIFFERENTIATING IMMATURE T-CELL RECEPTOR(NEG)
   THYMOCYTES RESEMBLES ANTIGEN-ACTIVATED MATURE T-CELLS
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID LYMPHOCYTES-T; EXPRESSION; THYMUS; MOUSE; EVENTS; SUBPOPULATIONS;
   MATURATION; ONTOGENY; SIGNALS; MARKER
AB Early in ontogeny thymocytes have a surface marker phenotype that resembles activated mature T cells but they lack expression of the T cell receptor (TCR) complex. We have made preparations of day 14/15 triple negative fetal thymocytes that exhibit the activated T lymphocyte markers CD25, intercellular adhesion molecule 1, Ly-6A/E, CD44, and heat stable antigen and are rapidly proliferating as evidenced by flow cytometric examination of BrdU incorporation. We found that binding activities of the gene regulators nuclear factor (NF)-kappaB, the NF-kappaB p50 homodimer complex, nuclear factor of activated T cells (NF-AT), oct-1, oct-2, activator protein 1 (AP-1), and serum response factor (SRF), are all present in these early thymocytes. Whereas the octamer factors and SRF persist during ontogeny, NF-kappaB, NF-AT, and AP-1 decrease and are undetectable in the adult thymus. Transfection of disaggregated thymocytes by electroporation or intact thymic lobes by gold-particle bombardment revealed that reporter constructs for NF-kappaB, NF-AT, AP-1, octamer factors and, to a small extent, the TCR-alpha enhancer were active in early thymocyte development. We rigorously eliminated the possibility that these transcriptional events were due to minor populations of TCR+ cells by showing that these reporter constructs were also active in recombinase activating gene (RAG)-/- thymocytes that are incapable of completing TCR gene rearrangement, and predominantly contain cells that have an activated phenotype. Thus, transcriptional events that are usually triggered by antigen stimulation in mature T cells take place early in thymic ontogeny in the absence of the TCR. Our analysis suggests that there are striking regulatory similarities but also important differences between the activation processes that take place in antigen-stimulated mature T cells and thymic progenitor cells.
RP ZUNIGAPFLUCKER, JC (reprint author), NIAID,IMMUNOL LAB,BLDG 10,RM 11D09,BETHESDA,MD 20892, USA.
RI Zuniga-Pflucker, Juan/H-1295-2012; 
OI Zuniga-Pflucker, Juan Carlos/0000-0003-2538-3178
NR 54
TC 51
Z9 51
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 OCT 1
PY 1993
VL 178
IS 4
BP 1139
EP 1149
DI 10.1084/jem.178.4.1139
PG 11
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA LY323
UT WOS:A1993LY32300001
PM 8376926
ER

PT J
AU STANLEY, SK
   MCCUNE, JM
   KANESHIMA, H
   JUSTEMENT, JS
   SULLIVAN, M
   BOONE, E
   BASELER, M
   ADELSBERGER, J
   BONYHADI, M
   ORENSTEIN, J
   FOX, CH
   FAUCI, AS
AF STANLEY, SK
   MCCUNE, JM
   KANESHIMA, H
   JUSTEMENT, JS
   SULLIVAN, M
   BOONE, E
   BASELER, M
   ADELSBERGER, J
   BONYHADI, M
   ORENSTEIN, J
   FOX, CH
   FAUCI, AS
TI HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION OF THE HUMAN THYMUS AND
   DISRUPTION OF THE THYMIC MICROENVIRONMENT IN THE SCID-HU MOUSE
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID IMMUNE-DEFICIENCY SYNDROME; CD4+ T-CELLS; EPITHELIAL-CELLS;
   MONOCLONAL-ANTIBODIES; HIV-INFECTION; LYMPHOCYTES-T; BONE-MARROW;
   TYPE-1; PATHOGENESIS; MODEL
AB Infection with the human immunodeficiency virus (HIV) results in immunosuppression and depletion of circulating CD4+ T cells. Since the thymus is the primary organ in which T cells mature it is of interest to examine the effects of HIV infection in this tissue. HIV infection has been demonstrated in the thymuses of infected individuals and thymocytes have been previously demonstrated to be susceptible to HIV infection both in vivo, using the SCID-hu mouse, and in vitro. The present study sought to determine which subsets of thymocytes were infected in the SCID-hu mouse model and to evaluate HIV-related alterations in the thymic microenvironment. Using two different primary HIV isolates, infection was found in CD4+/CD8+ double positive thymocytes as well as in both the CD4+ and CD8+ single positive subsets of thymocytes. The kinetics of infection and resulting viral burden differed among the three thymocyte subsets and depended on which HIV isolate was used for infection. Thymic epithelial (TE) cells were also shown to endocytose virus and to often contain copious amounts of viral RNA in the cytoplasm by in situ hybridization, although productive infection of these cells could not be definitively shown. Furthermore, degenerating TE cells were observed even without detection of HIV in the degenerating cells. Two striking morphologic patterns of infection were seen, involving either predominantly thymocyte infection and depletion, or TE cell involvement with detectable cytoplasmic viral RNA and/or TE cell toxicity. Thus, a variety of cells in the human thymus is susceptible to HIV infection, and infection with HIV results in a marked disruption of the thymic microenvironment leading to depletion of thymocytes and degeneration of TE cells.
C1 GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC 20037.
   SYSTEMIX INC,NEW ENTERPRISE RES DIV,PALO ALTO,CA 94303.
   PRI DYNCORP,FREDERICK,MD 21702.
   MOLEC HISTOL INC,GAITHERSBURG,MD 20879.
RP STANLEY, SK (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 6A11,BETHESDA,MD 20892, USA.
NR 42
TC 230
Z9 230
U1 1
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 OCT 1
PY 1993
VL 178
IS 4
BP 1151
EP 1163
DI 10.1084/jem.178.4.1151
PG 13
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA LY323
UT WOS:A1993LY32300002
PM 8376927
ER

PT J
AU SAWASDIKOSOL, S
   HAGUE, BF
   ZHAO, TM
   BOWERS, FS
   SIMPSON, RM
   ROBINSON, M
   KINDT, TJ
AF SAWASDIKOSOL, S
   HAGUE, BF
   ZHAO, TM
   BOWERS, FS
   SIMPSON, RM
   ROBINSON, M
   KINDT, TJ
TI SELECTION OF RABBIT CD4-CD8- T-CELL RECEPTOR-GAMMA/DELTA CELLS BY
   IN-VITRO TRANSFORMATION WITH HUMAN T-LYMPHOTROPIC VIRUS-I
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID TROPICAL SPASTIC PARAPARESIS; LEUKEMIA-LIKE DISEASE; HTLV-I;
   MONOCLONAL-ANTIBODIES; GEL-ELECTROPHORESIS; GAMMA-DELTA; B-CELLS;
   INFECTION; GENE; PATIENT
AB In vitro transformation of rabbit peripheral blood mononuclear cells (PBMC) with human T lymphotropic virus-I (HTLV)-infected human or rabbit cells resulted in CD4-CD8- cell lines, some of which caused acute leukemia when injected into rabbits. Structural analyses of the from cell lines with diverse pathogenic effects provided no clear correlation with lethality. The rabbit lines were provisionally designated T cells because they express interleukin 2R (IL-2R) and CD5 and lack surface immunoglobulin, but none express functional T cell receptor (TCR) alpha or beta transcripts. A more detailed characterization of the HTLV-I-infected cells was required to determine cell lineage and its potential influence on pathogenic consequences. Probes for rabbit TCRgamma and delta genes were derived and used to detect gamma and delta TCR RNA transcripts, identifying the in vitro transformed lines as gamma/delta T cells. CD4+ and CD8+ lines were derived from PBMC of HTLV-1-infected rabbits and CD4+ TCR-alpha/beta HTLV-I lines were derived from rabbit thymus, eliminating the possibility that the HTLV-I isolates used here transform only CD4-CD8- TCR-gamma/delta cells. The percentage of gamma/delta cells in rabbit PBMC is relatively high (23% in adult rabbits); this with diminution of CD4+ and CD8+ cells in IL-2-supplemented PBMC or thymocyte cultures may account for selection of rabbit HTLV-I-infected gamma/delta T cell lines in vitro. The availability of well-characterized T cell lines with diverse in vivo effects in the rabbit HTLV-I disease model allows evaluation of roles played by cell type in HTLV-I-mediated disease.
C1 NIAID,IMMUNOGENET LAB,TWINBROOK II FACIL,12441 PARKLAWN DR,ROCKVILLE,MD 20852.
NR 49
TC 34
Z9 34
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 OCT 1
PY 1993
VL 178
IS 4
BP 1337
EP 1345
DI 10.1084/jem.178.4.1337
PG 9
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA LY323
UT WOS:A1993LY32300018
PM 8376938
ER

PT J
AU CHU, CC
   MAX, EE
   PAUL, WE
AF CHU, CC
   MAX, EE
   PAUL, WE
TI DNA REARRANGEMENT CAN ACCOUNT FOR IN-VITRO SWITCHING TO IGG1
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID POLYMERASE CHAIN-REACTION; B-LYMPHOBLASTOID CELLS; TRANS-MESSENGER RNA;
   MONOCLONAL-ANTIBODIES; CIRCULAR DNA; HEAVY-CHAINS; IGH LOCI;
   RECOMBINATION; ISOTYPE; EXPRESSION
AB During immune responses, B lymphocytes may switch from the expression of immunoglobulin M (IgM) to the expression of another isotype (e.g., IgG, IgE, IgA). In stable hybridomas and myelomas expressing a ''switched'' (S) isotype, DNA deletions between Smu and a ''downstream' S region (S region recombination) have been found. In primary B cells, studies of the molecular basis of switching have been limited by the ability to sensitively quantitate the amount of DNA deletion; such studies would be of interest because other nondeletional mechanisms (trans-splicing, alternative processing of a long transcript) have been proposed to account for isotype switching in certain circumstances. We have applied the digestion-circularization polymerase chain reaction (DC-PCR) technique to measure the amount of S region recombination that occurs in the course of class switching in primary B lymphocytes. Resting B cells were cultured in lipopolysaccharide (LPS) and interleukin 4 (IL-4) to stimulate switching to IgG1. These cells begin to express membrane IgG1 at day 2.5 of culture and reach maximum expression by day 4.5. DNA was prepared from cultured cells and analyzed for Smu-Sgamma1 rearrangement by DC-PCR. Chimeric switch regions, indicating Smu-Sgamma1 recombination, were detected in amounts that, in most cases, correlated with surface expression. Furthermore, when cells were sorted on the basis of surface IgG1 expression, a mean of at least one Smu-Sgamma1 rearrangement per cell was seen in five out of seven experiments. In general, the IgG1+ cells obtained at 4.5 and 5.5 d of culture had close to 2 Smu-Sgamma1 rearrangements per cell. In IgG1- cells, Smu-Sgamma1 rearrangements were detectable, but at frequencies substantially lower that in IgG1+ cells. Thus, these results indicate that DNA deletion accompanies class switching in normal B cells stimulated with LPS and IL-4.
C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892.
   US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD 20892.
NR 31
TC 24
Z9 26
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 OCT 1
PY 1993
VL 178
IS 4
BP 1381
EP 1390
DI 10.1084/jem.178.4.1381
PG 10
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA LY323
UT WOS:A1993LY32300022
PM 8376941
ER

PT J
AU PUCILLO, C
   CEPEDA, R
   HODES, RJ
AF PUCILLO, C
   CEPEDA, R
   HODES, RJ
TI EXPRESSION OF A MHC CLASS-II TRANSGENE DETERMINES BOTH SUPERANTIGENICITY
   AND SUSCEPTIBILITY TO MAMMARY-TUMOR VIRUS-INFECTION
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Note
ID T-CELLS; CLONAL DELETION; B-CELLS; MICE; MOUSE; GENES; SELECTION; THYMUS
AB Milk-borne mouse mammary tumor virus (MMTV) is a type B retrovirus that induces mammary carcinoma. Infectious MMTV, as well as genomically integrated mouse mammary proviruses, encode superantigens that are recognized by T cells that express appropriate T cell receptor Vbeta products. To determine the relationship between the superantigenic property of milk-borne MMTV and its in vivo infectivity, mice which were either positive or negative for expression of a transgene-encoded EalphaEbeta class II major histocompatibility complex (MHC) product were exposed to milk borne C3H MMTV. Superantigen-mediated deletion of Vbeta14-expressing T cells occurred only in Ealpha transgene-positive mice, indicating that the deletion was EalphaEbeta dependent. When mice were analyzed for viral infection by assaying viral p28 in the milk of recipient females, significant p28 levels were found only in EalphaEbeta transgene-positive mice. Similarly, the presence of C3H MMTV LTR mRNA in mammary glands, as detected by PCR, paralleled p28 levels. These findings indicate that Ealpha expression or the Ealpha-dependent T cell response to viral superantigen is causally related to susceptibility to MMTV infection, and that lack of a permissive class II product can protect mice from virus infection.
RP PUCILLO, C (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM 4B17,BETHESDA,MD 20892, USA.
RI Pucillo, Carlo/A-5515-2008; 
OI Pucillo, Carlo/0000-0002-4872-6156
NR 23
TC 35
Z9 35
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 OCT 1
PY 1993
VL 178
IS 4
BP 1441
EP 1445
DI 10.1084/jem.178.4.1441
PG 5
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA LY323
UT WOS:A1993LY32300029
PM 8397273
ER

PT J
AU SAMUELS, DS
   MARCONI, RT
   GARON, CF
AF SAMUELS, DS
   MARCONI, RT
   GARON, CF
TI VARIATION IN THE SIZE OF THE OSPA-CONTAINING LINEAR PLASMID, BUT NOT THE
   LINEAR CHROMOSOME, AMONG THE 3 BORRELIA SPECIES ASSOCIATED WITH
   LYME-DISEASE
SO JOURNAL OF GENERAL MICROBIOLOGY
LA English
DT Article
ID PHYLOGENETIC ANALYSIS; MOLECULAR ANALYSIS; NORTH-AMERICAN; SP-NOV;
   BURGDORFERI; PROTEINS; AGENT; DNA; IDENTIFICATION; HETEROGENEITY
AB The aetiological agents of Lyme disease form a phylogenetically heterogeneous group, composed of three species, Borrelia burgdorferi, Borrelia garinii, and group VS461. We have compared the sizes of the linear plasmid that carries the genes encoding the major outer-surface proteins OspA and OspB as well as the size and structure of the chromosome among the Lyme disease spirochaetes. We have found differences in the sizes of the ospA-containing plasmids, but not the linear chromosomes among the three species. The ospA-containing plasmid size of 50 kb in B. burgdorferi isolates is significantly smaller than the size of 55 kb in B. garinii isolates and 56 kb in group VS461 isolates. The chromosome was found to be linear in all three Borrelia species. but not significantly different in size.
RP SAMUELS, DS (reprint author), NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840, USA.
RI Samuels, D Scott/B-7549-2012
OI Samuels, D Scott/0000-0001-8352-7593
NR 45
TC 34
Z9 35
U1 0
U2 1
PU SOC GENERAL MICROBIOLOGY
PI READING
PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS
SN 0022-1287
J9 J GEN MICROBIOL
JI J. Gen. Microbiol.
PD OCT
PY 1993
VL 139
BP 2445
EP 2449
PN 10
PG 5
WC Microbiology
SC Microbiology
GA MC996
UT WOS:A1993MC99600018
PM 8254314
ER

PT J
AU FENDLER, K
   JARUSCHEWSKI, S
   HOBBS, A
   ALBERS, W
   FROEHLICH, JP
AF FENDLER, K
   JARUSCHEWSKI, S
   HOBBS, A
   ALBERS, W
   FROEHLICH, JP
TI PRE-STEADY-STATE CHARGE TRANSLOCATION IN NAK-ATPASE FROM EEL ELECTRIC
   ORGAN
SO JOURNAL OF GENERAL PHYSIOLOGY
LA English
DT Article
ID CURRENT-VOLTAGE RELATIONSHIP; PLANAR BILAYER-MEMBRANES; PIG VENTRICULAR
   MYOCYTES; SODIUM-POTASSIUM PUMP; (NA+ + K+)-ATPASE; NA+/K+-ATPASE; NA/K
   PUMP; CONFORMATIONAL TRANSITIONS; MICROSCOPIC ANALYSIS; LIPID-MEMBRANES
AB Time-resolved measurements of charge translocation and phosphorylation kinetics during the pre-steady state of the NaK-ATPase reaction cycle are presented. NaK-ATPase-containing microsomes prepared from the electric organ of Electrophorus electricus were adsorbed to planar lipid bilayers for investigation of charge translocation, while rapid acid quenching was used to study the concomitant enzymatic partial reactions involved in phosphoenzyme formation. To facilitate comparison of these data, conditions were standardized with respect to pH (6.2), ionic composition, and temperature (24-degrees-C). The different phases of the current generated by the enzyme are analyzed under various conditions and compared with the kinetics of phosphoenzyme formation. The slowest time constant (tau3(-1) almost-equal-to 8 s-1) is related to the influence of the capacitive coupling of the adsorbed membrane fragments on the electrical signal. The relaxation time associated with the decaying phase of the electrical signal (tau2(-1) = 10-70 s-1) depends on ATP and caged ATP concentration. It is assigned to the ATP and caged ATP binding and exchange reaction. A kinetic model is proposed that explains the behavior of the relaxation time at different ATP and caged ATP concentrations. Control measurements with the rapid mixing technique confirm this assignment. The rising phase of the electrical signal was analyzed with a kinetic model based on a condensed Albers-Post cycle. Together with kinetic information obtained from rapid mixing studies, the analysis suggests that electroneutral ATP release, ATP and caged ATP binding, and exchange and phosphorylation are followed by a fast electrogenic E1P --> E2P transition. At 24-degrees-C and pH 6.2, the rate constant for the E1P --> E2P transition in NaK-ATPase from eel electric organ is greater-than-or-equal-to 1,000 s-1.
C1 NIA,BALTIMORE,MD 21224.
   NINCDS,BETHESDA,MD 20892.
RP FENDLER, K (reprint author), MAX PLANCK INST BIOPHYS,KENNEDYALLEE 70,D-60596 FRANKFURT,GERMANY.
NR 62
TC 65
Z9 65
U1 1
U2 7
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021
SN 0022-1295
J9 J GEN PHYSIOL
JI J. Gen. Physiol.
PD OCT
PY 1993
VL 102
IS 4
BP 631
EP 666
DI 10.1085/jgp.102.4.631
PG 36
WC Physiology
SC Physiology
GA ME924
UT WOS:A1993ME92400002
PM 8270908
ER

PT J
AU COHEN, GD
AF COHEN, GD
TI AFRICAN-AMERICAN ISSUES IN GERIATRIC PSYCHIATRY - A PERSPECTIVE ON
   RESEARCH OPPORTUNITIES
SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY
LA English
DT Article
ID DISORDERS
AB Racial, ethnic, and cultural factors influencing mental health in later life are important to study in their own right However, they also offer an opportunity to expand our understanding of mental health and mental illness in older adults independent of race, ethnicity, or culture. Any time an opportunity arises to examine a problem from a different perspective, chances increase that new light will be shed on the problem. For example, while suicide is greatest in older Americans compared with any other US population group, it is less frequent in older blacks than older whites. Why? Among the different theories that have been advanced, one holds that older African Americans in reaching later life have surmounted more threats to self-esteem (compared with whites) and are thereby better adapted to new challenges associate with aging.1 Still, the discrepancy in suicide rates between older blacks and whites remains an important research question. In studying suicide with attention to racial and ethnic variables, the opportunity presents itself to gain a more fundamental understanding of suicide itself-to the benefit of all older adults, indeed to the benefit of all age groups.
   This paper focuses on some African American issues pertinent to geriatric psychiatry and identifies areas for further research. In addition to a selected literature review, the author draws on his own research from a 20-year longitudinal study, initiated in 1971, of a senior citizens' apartment building in Washington, DC, with a predominantly African American population.2 (1 = Group for the Advancement of Psychiatry, Committee on Cultural Psychiatry: Suicide and Ethnicity in the United States, New York, Bruner/Mazel, 1989; and 2 = Cohen GD: Lessons from longitudinal studies of mentally ill and mentally healthy elderly: A 17-year perspective, in Bergener M, Finkel SI (eds): Clinical and Scientific Psychogeriatrics, Vol. 1. New York, Springer, 1990.)
C1 NIA,DHHS,BETHESDA,MD 20892.
NR 25
TC 5
Z9 5
U1 1
U2 1
PU DECKER PERIODICALS INC
PI HAMILTON
PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA
SN 0891-9887
J9 J GERIATR PSYCH NEUR
JI J. Geriatr. Psychiatry Neurol.
PD OCT-DEC
PY 1993
VL 6
IS 4
BP 195
EP 199
PG 5
WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry
SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry
GA MA734
UT WOS:A1993MA73400002
PM 8251045
ER

PT J
AU MARQUEZ, VE
   LIM, BB
   DRISCOLL, JS
   SNOEK, R
   BALZARINI, J
   IKEDA, S
   ANDREI, G
   DECLERCQ, E
AF MARQUEZ, VE
   LIM, BB
   DRISCOLL, JS
   SNOEK, R
   BALZARINI, J
   IKEDA, S
   ANDREI, G
   DECLERCQ, E
TI CYCLOPENTENE CARBOCYCLIC NUCLEOSIDES RELATED TO THE ANTITUMOR NUCLEOSIDE
   CLITOCINE AND THEIR CONVERSION TO 8-AZA-NEPLANOCIN ANALOGS - SYNTHESIS
   AND ANTIVIRAL ACTIVITY
SO JOURNAL OF HETEROCYCLIC CHEMISTRY
LA English
DT Article
ID NEPLANOCIN; VIRUS
AB Synthesis of the cyclopentene carbocyclic analogue of the naturally occurring nucleoside clitocine (1) is reported. Starting with racemic cyclopentenylamine (10), the heterocyclic moieties of the clitocine analogue 4 and related 1,6-dihydro-6-oxo, 5, and 2-amino-1,6-dihydro-6-oxo, 6, analogues were constructed. These compounds were respectively converted to 8-aza-neplanocin A (7), 8-aza-neplanocin D (8, the inosine analogue), and the corresponding 8-aza-guanosine analogue 9 after reduction of the nitro group followed by nitrous acid cyclization. Extensive antiviral evaluation revealed that only 8-aza-neplanocin A (7) had enough antiviral activity to warrant further studies. This compound showed weak antiviral activity against HSV-1, HSV-2, and the thymidine kinase deficient (TK-) HSV-1. However, it displayed good antiviral activity against human cytomegalovirus (HCMV) at a concentration of 0.40-2.50 mu g/lml, well below the cytotoxicity threshold. This activity profile is consistent with a mechanism of action involving the inhibition of the enzyme adenosylhomo-cysteine hydrolase.
C1 KATHOLIEKE UNIV LEUVEN,REGA INST,B-3000 LOUVAIN,BELGIUM.
RP MARQUEZ, VE (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892, USA.
NR 13
TC 12
Z9 12
U1 1
U2 1
PU HETERO CORPORATION
PI TAMPA
PA BOX 20285, TAMPA, FL 33622-0285
SN 0022-152X
J9 J HETEROCYCLIC CHEM
JI J. Heterocycl. Chem.
PD OCT-NOV
PY 1993
VL 30
IS 5
BP 1393
EP 1398
PG 6
WC Chemistry, Organic
SC Chemistry
GA MM424
UT WOS:A1993MM42400037
ER

PT J
AU RUTHERFORD, AV
   WILLINGHAM, MC
AF RUTHERFORD, AV
   WILLINGHAM, MC
TI ULTRASTRUCTURAL-LOCALIZATION OF DAUNOMYCIN IN MULTIDRUG-RESISTANT
   CULTURED-CELLS WITH MODULATION OF THE MULTIDRUG TRANSPORTER
SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
LA English
DT Note
DE FLUORESCENCE PHOTOCONVERSION; MULTIDRUG RESISTANCE; DAUNOMYCIN; ELECTRON
   MICROSCOPY; AUTOFLUORESCENCE; NUCLEUS; LYSOSOMES
ID CYTOFLUORESCENCE LOCALIZATION; DAUNORUBICIN; ADRIAMYCIN; MICROSCOPY
AB We localized the chemotherapeutic drug daunomycin inside cultured cells by taking advantage of its inherent fluorescence. Multidrug-resistant cultured cells, in which the accumulation of daunomycin can be reversibly controlled with verapamil to block the multidrug transporter, were incubated in daunomycin and verapamil and the accumulated daunomycin was visualized with epifluorescence optics. After fixation under a variety of different conditions to make cells permeable to diaminobenzidine (DAB), the internal daunomycin was illuminated under the fluorescence microscope in the presence of DAB. Photooxidation of DAB in sites of fluorescing daunomycin (photoconversion) resulted in intracellular deposition of oxidized DAB product. These sites were then visualized by transmission electron microscopy. In cells in which the multidrug transporter was inhibited by verapamil, daunomycin was localized in the nucleus of cells by mild fixation conditions such as formaldehyde. Increasing amounts of glutaraldehyde in the fixative caused apparent quenching of the nuclear fluorescence but still allowed fluorescence to occur in other cell organelles, which were then well preserved. Daunomycin was found in the nuclear envelope, the endoplasmic reticulum, and in lysosomes in cells in which the multidrug transporter was inhibited. Lysosomal accumulation has been previously described and was expected because of the known accumulation of positively charged molecules in organelles with low pH. However, the accumulation of daunomycin in the nuclear envelope and endoplasmic reticulum has not been previously observed. These results dearly demonstrate the utility of fluorescence photoconversion methodology for the high-resolution ultrastructural localization of fluorescent materials.
C1 NCI,MOLEC BIOL LAB,ULTRASTRUCT CYTOCHEM SECT,BETHESDA,MD 20892.
NR 14
TC 43
Z9 44
U1 0
U2 0
PU HISTOCHEMICAL SOC INC
PI NEW YORK
PA MT SINAI MEDICAL CENTER 19 EAST 98TH ST SUTIE 9G, NEW YORK, NY 10029
SN 0022-1554
J9 J HISTOCHEM CYTOCHEM
JI J. Histochem. Cytochem.
PD OCT
PY 1993
VL 41
IS 10
BP 1573
EP 1577
PG 5
WC Cell Biology
SC Cell Biology
GA LX775
UT WOS:A1993LX77500015
PM 7902372
ER

PT J
AU KITANI, A
   STROBER, W
AF KITANI, A
   STROBER, W
TI REGULATION OF C-GAMMA SUBCLASS GERM-LINE TRANSCRIPTS IN HUMAN
   PERIPHERAL-BLOOD B-CELLS
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID CONSTANT-REGION GENES; HEAVY-CHAIN TRANSCRIPTS; STIMULATORY FACTOR-I;
   EPSILON-TRANSCRIPTS; INTERFERON-GAMMA; IGE PRODUCTION; LYMPHOCYTES-B;
   IFN-GAMMA; INDUCTION; INTERLEUKIN-4
AB In the present study we investigated the early steps of human IgG subclass differentiation by defining the conditions necessary for IgG subclass-specific production of germ-line transcripts in human peripheral blood B cells. Constant region of gamma-globulin (Cgamma) subclass germ-line transcripts were measured using newly developed reverse transcription and polymerase chain reaction (RT-PCR) assays that were shown to be Cgamma subclass-specific germ-line transcripts by size of the amplification products obtained before and after digestion with appropriate endonucleases (NarI and NcoI). In initial studies we found that Cgamma1 and Cgamma2 germ-line transcripts were constitutively expressed in total peripheral blood B cells, but not in high density sIgM+(sIgG-) B cells prepared with Percoll density gradients and magnetic beads separation techniques; the latter cells were therefore used throughout this study. Induction of germ-line transcripts (germ-line Cgamma1 transcript) was noted in stimulated B cells (SAC plus IL-2) at 6 h; thus, the appearance of germ-line transcripts could not be attributed to preferential growth of B cells expressing germ-line transcripts. In subsequent studies we found that induction of germ-line transcripts for the various IgG subclasses fell into two patterns. Induction of Cgamma3 and Cgamma1 germ-line transcripts, transcripts of genes in the first human duplication unit, generally required a proliferative stimulus (Staphylococcus aureus Cowan I, SAC) and was brought about by SAC plus IL-4 (Cgamma3 germ-line transcripts) and SAC alone or SAC plus IL-2 (Cgamma1 germ-line transcripts); in contrast, induction of Cgamma2 and Cgamma4 germ-line transcripts, transcripts of genes in the second duplication unit, was accomplished with cytokines alone: IFN-gamma (Cgamma2 germ-line transcripts) and IL-4 (Cgamma4 germ-line transcripts), and was not augmented by addition of a proliferative stimulus. Finally, we found that IFN-gamma inhibited IL-4-induced Cgamma3 and Cgamma4 germ-line transcripts (with or without SAC). These findings establish that the various human IgG subclasses manifest distinct requirements for the regulation of early steps in isotype differentiation. In addition, they suggest that human Cgamma genes exhibit patterns of regulation related to their respective duplication units.
RP KITANI, A (reprint author), NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BLDG 10,ROOM 11N250,BETHESDA,MD 20892, USA.
NR 47
TC 112
Z9 112
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 1993
VL 151
IS 7
BP 3478
EP 3488
PG 11
WC Immunology
SC Immunology
GA LZ636
UT WOS:A1993LZ63600008
PM 8376788
ER

PT J
AU GAZZINELLI, RT
   ELTOUM, I
   WYNN, TA
   SHER, A
AF GAZZINELLI, RT
   ELTOUM, I
   WYNN, TA
   SHER, A
TI ACUTE CEREBRAL TOXOPLASMOSIS IS INDUCED BY IN-VIVO NEUTRALIZATION OF
   TNF-ALPHA AND CORRELATES WITH THE DOWN-REGULATED EXPRESSION OF INDUCIBLE
   NITRIC-OXIDE SYNTHASE AND OTHER MARKERS OF MACROPHAGE ACTIVATION
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TUMOR-NECROSIS-FACTOR; RETROVIRUS-INDUCED IMMUNODEFICIENCY; INHIBITS
   CYTOKINE PRODUCTION; IMMUNE-DEFICIENCY SYNDROME; IFN-GAMMA;
   OPPORTUNISTIC INFECTIONS; GONDII INFECTION; NITROGEN-OXIDES;
   MESSENGER-RNA; L-ARGININE
AB C57BL/6 mice infected with the ME-49 strain of Toxoplasma gondii develop a progressive encephalitis culminating in 100% mortality between 12 and 15 wk after intraperitoneal inoculation of the parasite. Moreover, when injected at 4 wk after infection with anti-IFN-gamma mAb, progression of toxoplasmic encephalitis is markedly accelerated, resulting in death of the animals by 9 to 12 days posttreatment. In this study, we investigated the expression of mRNAs encoding cytokines as well as lymphocyte and macrophage markers during the development of toxoplasmic encephalitis. High levels of lymphocyte CD4 and CD8 surface Ag transcript were detected in the brains of mice throughout the infection. In addition from 2 to 4 wk we found elevations of Th1 (IFN-gamma and IL-2) but not of Th2 (IL-4 and IL-5) cytokine mRNAs. The elevation in Th1 cytokines was accompanied by increases in the expression of monokine (IL-1, IL-6, IL-10, granulocyte macrophage-colony stimulating factor [GM-CSF], and TNF-alpha) mRNAs, as well as markers expressed by activated macrophages (major histocmpatibility class II [Ia], inducible nitric oxide synthase [iNOS] and macrophage activation gene 1 [Mag-1]). Interestingly, after 8 wk of infection with T. gondii we observed a dramatic decrease of Th1 cytokine and most monokine (IL-1, IL-6, GM-CSF, and TNF-alpha) as well as Mag-1 and iNOS mRNA levels. This down-regulation was associated with enhanced necrosis and neutrophilic infiltrates in the brain accompanied by increased expression of genes expressed specifically by the tachyzoite stage of T. gondii (T. gondii surface antigen 1 [SAG-1] and T. gondii surface antigen 2 [SAG-2]). Similarly, in mice chronically infected with T gondii and treated with anti-IFN-gamma mAb the resulting pathology was associated with decreased expression of TNF-alpha and iNOS and increased expression of SAG-1 and SAG-2. Moreover, treatment with anti-TNF-alpha mAb also resulted in enhanced pathology, which correlated with low levels of iNOS mRNA and high levels of tachyzoite-specific mRNAs. Together these results suggest that reactivation of T. gondii results from a down-regulation of IFN-gamma and TNF-alpha expression leading to decreased macrophage or microglial cell activation, release of parasite growth, and subsequent tissue damage.
RP GAZZINELLI, RT (reprint author), NIAID,LPD,BLDG 4,RM 126,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
RI Wynn, Thomas/C-2797-2011
NR 37
TC 273
Z9 281
U1 0
U2 4
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 1993
VL 151
IS 7
BP 3672
EP 3681
PG 10
WC Immunology
SC Immunology
GA LZ636
UT WOS:A1993LZ63600027
PM 7690809
ER

PT J
AU MAHANTY, S
   KING, CL
   KUMARASWAMI, V
   REGUNATHAN, J
   MAYA, A
   JAYARAMAN, K
   ABRAMS, JS
   OTTESEN, EA
   NUTMAN, TB
AF MAHANTY, S
   KING, CL
   KUMARASWAMI, V
   REGUNATHAN, J
   MAYA, A
   JAYARAMAN, K
   ABRAMS, JS
   OTTESEN, EA
   NUTMAN, TB
TI IL-4-SECRETING AND IL-5-SECRETING LYMPHOCYTE POPULATIONS ARE
   PREFERENTIALLY STIMULATED BY PARASITE-DERIVED ANTIGENS IN HUMAN TISSUE
   INVASIVE NEMATODE INFECTIONS
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID T-CELL SUBSETS; SCHISTOSOMA-MANSONI; CYTOKINE PRODUCTION; LYMPHOKINE
   SECRETION; HELMINTH INFECTIONS; FUNCTIONAL SUBSETS; INTERFERON-GAMMA;
   ACCESSORY CELLS; DOWN-REGULATION; TH2 RESPONSES
AB Helminth infections in humans and animals are associated with strong T helper 2 (Th2) responses. To determine whether parasite-derived Ag preferentially expand a Th2-like cell population, a filter immunoplaque assay was used to enumerate the frequencies (F0) of PBMC and CD4+-enriched PBMC from individuals with helminth infections secreting selected cytokines in response to parasite-derived (PAg) and nonparasite antigens (NPAg). In 20 individuals with lymphatic filariasis, frequency analysis of PBMC secreting IL-4 and IFN-gamma indicated that the F0 of PAg-specific IL-4-secreting cel Is (geometric mean F0 (GM): 1/12,100) was 57-fold higher than the corresponding F0 of NPAg-reactive cells (GM: 1/692,000; p < 0.02). In marked contrast, the F0 of IFN-gamma-secreting cells responding to PAg (GM: 1/2,700) did not differ from those of cells specific for NPAg (GM: 1/3,400; p = 0.83). In another group of helminth-infected individuals, the F0 of highly enriched CD4+ cells secreting IL-4 and IL-5 in response to PAg (GMs: 1/2,600 and 1/5,600 CD4+ cells, respectively) were also found to be significantly higher than those specific for NPAg (GMs: 1/291,000 and 1/303,000 CD4+; p < 0.05 and p < 0.01, respectively), whereas the corresponding F0 of IFN-gamma- and granulocyte-macrophage-CSF-secreting cells were equivalent for PAg and NPag. Furthermore, the proportion of PAg-specific IL-4- and IL-5-secreting CD4+ cells relative to all cells secreting the given cytokine were approximately 29-fold higher than the proportion of NPAg-specific cells secreting these cytokines. Again, the corresponding proportions of Ag-specific IFN-gamma and GM-CSF-secreting CD4+ cells were equivalent for PAg and NPAg. Thus, in this ex vivo system, a circulating population of IL-4- and IL-5-secreting (Th2-like) cells has been shown to exist in humans; PAg appears to expand these cells preferentially.
C1 TB RES CTR,MADRAS,INDIA.
   ANNA UNIV,CTR BIOTECHNOL,MADRAS,INDIA.
   DNAX RES INST MOLEC & CELLULAR BIOL INC,RES INST,PALO ALTO,CA 94303.
RP MAHANTY, S (reprint author), NIAID,PARASIT DIS LAB,BLDG 4,ROOM B1-05,BETHESDA,MD 20892, USA.
OI Mahanty, Siddhartha/0000-0003-1068-0524
NR 58
TC 70
Z9 71
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 1993
VL 151
IS 7
BP 3704
EP 3711
PG 8
WC Immunology
SC Immunology
GA LZ636
UT WOS:A1993LZ63600030
PM 8376801
ER

PT J
AU MEKORI, YA
   OH, CK
   METCALFE, DD
AF MEKORI, YA
   OH, CK
   METCALFE, DD
TI IL-3-DEPENDENT MURINE MAST-CELLS UNDERGO APOPTOSIS ON REMOVAL OF IL-3 -
   PREVENTION OF APOPTOSIS BY C-KIT LIGAND
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID HEMATOPOIETIC GROWTH-FACTOR; TYROSINE KINASE-ACTIVITY; SIGNAL
   TRANSDUCTION; BONE-MARROW; MESSENGER-RNA; STEEL FACTOR; SI-LOCUS;
   RECEPTOR; MOUSE; DEATH
AB It is well established that mast cell proliferation and maturation are regulated by two principle cytokines, IL-3 and the c-kit ligand stem cell factor (SCF). Little is known, however, how these two processes are negatively regulated and thus, how mast cell number is controlled in normal or pathologic processes. In this study we hypothesized that IL-3-dependent mast cells would undergo programmed cell death (apoptosis) on removal of IL-3 as was shown with other growth factor-dependent hemopoietic cells. Apoptotic changes were analyzed using light microscopy, fluorescent staining with acridine orange, flow cytometric analysis, and DNA electrophoresis. We could demonstrate that elimination of IL-3 from either primary bone marrow-derived cultured mast cell cultures (BMCMC) or from the growth factor-dependent mast cell line MCP5 resulted in the characteristic changes of apoptosis including condensed chromatin, fragmented nuclei, cellular vacuolization, typical pattern of propidium iodide or Hoechst 33342 uptake by flow cytometry, and the characteristic 200 bp ''ladder'' pattern of DNA cleavage. These events were prevented by SCF, an action that was in part mediated by tyrosine kinases, in that the tyrosine kinase inhibitor herbimycin inhibited the action of SCF in preventing apoptosis in IL-3-deprived cells. By using anti c-kit mAb and IL-3-dependent BMCMC obtained from W/W(v) mice homozygous for mutation at the w locus that encodes the c-kit receptor, we could also show that SCF exerted its effect via c-kit. Neither dexamethasone nor cyclosporin A inhibited the ''rescue'' effect of SCF, suggesting that ''rescue'' was mediated by SCF and not through the induction of other cytokines. Thus, IL-3-dependent mast cells undergo apoptosis on removal of IL-3, an event that is prevented by the addition of SCF through its ligand c-kit, thus demonstrating how these principle mast cell growth factors may act in concert to regulate mast cell number under physiologic conditions.
C1 MEIR HOSP,DEPT MED,KEFAR SAVA,ISRAEL.
   TEL AVIV UNIV,SACKLER SCH MED,TEL AVIV,ISRAEL.
RP MEKORI, YA (reprint author), NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BLDG 10,ROOM 11C210,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 62
TC 169
Z9 169
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 1993
VL 151
IS 7
BP 3775
EP 3784
PG 10
WC Immunology
SC Immunology
GA LZ636
UT WOS:A1993LZ63600038
PM 7690814
ER

PT J
AU KOENIG, S
   WOODS, RM
   BREWAH, YA
   NEWELL, AJ
   JONES, GM
   BOONE, E
   ADELSBERGER, JW
   BASELER, MW
   ROBINSON, SM
   JACOBSON, S
AF KOENIG, S
   WOODS, RM
   BREWAH, YA
   NEWELL, AJ
   JONES, GM
   BOONE, E
   ADELSBERGER, JW
   BASELER, MW
   ROBINSON, SM
   JACOBSON, S
TI CHARACTERIZATION OF MHC CLASS-I RESTRICTED CYTOTOXIC T-CELL RESPONSES TO
   TAX IN HTLV-1 INFECTED PATIENTS WITH NEUROLOGIC DISEASE
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TROPICAL SPASTIC PARAPARESIS; TOXIC LYMPHOCYTES-T; VIRUS TYPE-I;
   AUTOIMMUNE ENCEPHALOMYELITIS; PEPTIDES; RECOGNITION; REPLICATION;
   ANTIBODIES; PROTEINS; MOLECULE
AB To understand the nature of the cytotoxic T cell response generated in human T lymphotropic virus type 1 (HTLV-1)-infected patients with HTLV-1 -associated myelopathy/tropical spastic paraparesis, we cloned CTL from the peripheral blood and cerebrospinal fluid from patients with neurologic diseases and demonstrated the presence of HLA-A2, A3, and B14 restricted responses to the HTLV-1 p40x (tax) protein. We identified the minimal amino acid residues within the epitopes required for binding and recognition by HLA-A2- and B14-restricted CTL, identified the critical residues within the peptide sequence defining the HLA-A2-restricted response, and demonstrated that CTL can lyse T cells infected with HTLV-1. This study shows that the CTL response to HTLV-1 tax in patients with neurologic diseases is heterogenous in nature and is not confined to patients of a single HLA haplotype or to a specific region of the tax protein.
C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892.
   NINCDS,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892.
   FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21701.
RP KOENIG, S (reprint author), MEDIMMUNE INC,DEPT IMMUNOL,GAITHERSBURG,MD 20878, USA.
FU NCI NIH HHS [N01-CO-74102]
NR 33
TC 66
Z9 66
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 1993
VL 151
IS 7
BP 3874
EP 3883
PG 10
WC Immunology
SC Immunology
GA LZ636
UT WOS:A1993LZ63600047
PM 7690819
ER

PT J
AU VIA, CS
   TSOKOS, GC
   BERMAS, B
   CLERICI, M
   SHEARER, GM
AF VIA, CS
   TSOKOS, GC
   BERMAS, B
   CLERICI, M
   SHEARER, GM
TI T-CELL-ANTIGEN-PRESENTING CELL-INTERACTIONS IN HUMAN SYSTEMIC
   LUPUS-ERYTHEMATOSUS - EVIDENCE FOR HETEROGENEOUS EXPRESSION OF MULTIPLE
   DEFECTS
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID MIXED LYMPHOCYTE REACTIONS; MRL-LPR/LPR MICE; HOST DISEASE; HELPER;
   INTERLEUKIN-2; INVITRO; ACTIVATION; ANTIBODY; L3T4+; MHC
AB To assess interactions between T cells and APC in patients with SLE, PBL were stimulated in vitro and IL-2 production measured after stimulation with either a MHC-self-restricted Ag (influenza A virus) or an Ag which can use both MHC-self-restricted or unrestricted T cell activation pathways (HLA-alloantigen). SLE patients (n = 26) and controls (n = 8) were categorized as responder (+) or nonresponder (-) for each stimulus and grouped according to their paired response pattern. All controls responded to both influenza virus (Flu) or alloantigen (Allo) and were categorized as +/+. In contrast, SLE patient response patterns were heterogeneous with no evidence for a single SLE-associated defect. Instead, SLE patient responses fell into one of three different patterns: a) normal responses to both Flu and Allo (+/+), observed in nine (35%) patients; b) defective responses to Flu but intact Allo responses (-/+) observed in 12 (46%) SLE patients; and c) defective responses to both Flu and Allo (-/-), observed in five (19%) SLE patients. There was no statistically significant correlation between immune response pattern and the use of immunosuppressants. Further analysis of -/- SLE patients indicated defects in APC function and in both CD4+ and CD8+ T cell function. In contrast, cell depletion and add-back studies in -/+ SLE patients demonstrated defects in APC function only. Thus, similar to the well recognized clinical heterogeneity among SLE patients, our data support the concept that SLE patients are heterogeneous with respect to in vitro T cell-APC function, exhibiting responses ranging from normal function to defects in APC and in both T cell subsets. Prospective studies are in progress to determine the clinical relevance of these observations.
C1 DEPT VET AFFAIRS,BALTIMORE,MD 21201.
   UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814.
   NIDDKD,KIDNEY DIS SECT,BETHESDA,MD 20892.
RP VIA, CS (reprint author), UNIV MARYLAND,SCH MED,DEPT MED,DIV RHEUMATOL,MSTF 8-34,BALTIMORE,MD 21201, USA.
NR 43
TC 58
Z9 61
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 1993
VL 151
IS 7
BP 3914
EP 3922
PG 9
WC Immunology
SC Immunology
GA LZ636
UT WOS:A1993LZ63600051
PM 8376810
ER

PT J
AU RESTIFO, NP
   KAWAKAMI, Y
   MARINCOLA, F
   SHAMAMIAN, P
   TAGGARSE, A
   ESQUIVEL, F
   ROSENBERG, SA
AF RESTIFO, NP
   KAWAKAMI, Y
   MARINCOLA, F
   SHAMAMIAN, P
   TAGGARSE, A
   ESQUIVEL, F
   ROSENBERG, SA
TI MOLECULAR MECHANISMS USED BY TUMORS TO ESCAPE IMMUNE RECOGNITION -
   IMMUNOGENETHERAPY AND THE CELL BIOLOGY OF MAJOR HISTOCOMPATIBILITY
   COMPLEX CLASS-I
SO JOURNAL OF IMMUNOTHERAPY
LA English
DT Article
DE MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I; TUMOR; ANTIGEN PROCESSING;
   ANTIGEN PRESENTATION; CD8+ T-CELLS; VACCINIA VIRUS, RECOMBINANT
ID INFILTRATING LYMPHOCYTES; DEFECTIVE PRESENTATION; ANTIGEN PRESENTATION;
   INTERFERON-GAMMA; VIRAL PEPTIDES; MHC MOLECULES; T-CELLS; MELANOMA;
   SELF; IMMUNOTHERAPY
AB In this article, we explore the hypothesis that tumor cells can escape recognition by CD8+ T cells via deficiencies in antigen processing and presentation. Aspects of the molecular and cellular biology of major histocompatibility complex class I are reviewed. Evidence for histology-specific molecular mechanisms in the antigen-processing and -presentation deficiencies observed in some human and murine tumors is presented. Mechanisms identified include down-regulation of antigen processing, loss of functional beta2-microglobulin, and deletion of specific alpha-chain alleles. Finally, we discuss studies using an antigen-presentation-deficient mouse tumor as a model for the immunogenetherapy of an antigen-presentation deficiency.
C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892.
RP RESTIFO, NP (reprint author), NCI,DIV CANC TREATMENT,SURG BRANCH,BLDG 10 ROOM 2B42,BETHESDA,MD 20892, USA.
RI Restifo, Nicholas/A-5713-2008; Kawakami, Yutaka /E-7429-2013; 
OI Kawakami, Yutaka /0000-0003-4836-2855; Restifo, Nicholas
   P./0000-0003-4229-4580
FU Intramural NIH HHS [NIH0010139353, Z01 BC010763-01, Z99 TW999999]
NR 35
TC 104
Z9 106
U1 0
U2 4
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 1053-8550
J9 J IMMUNOTHER
JI J. Immunother.
PD OCT
PY 1993
VL 14
IS 3
BP 182
EP 190
DI 10.1097/00002371-199310000-00004
PG 9
WC Oncology; Immunology; Medicine, Research & Experimental
SC Oncology; Immunology; Research & Experimental Medicine
GA MC307
UT WOS:A1993MC30700004
PM 8297900
ER

PT J
AU BENNINK, JR
   ANDERSON, R
   BACIK, I
   COX, J
   DAY, P
   DENG, YP
   LAPHAM, C
   LINK, H
   RUSS, G
   YEWDELL, JW
AF BENNINK, JR
   ANDERSON, R
   BACIK, I
   COX, J
   DAY, P
   DENG, YP
   LAPHAM, C
   LINK, H
   RUSS, G
   YEWDELL, JW
TI ANTIGEN-PROCESSING - WHERE TUMOR-SPECIFIC T-CELL RESPONSES BEGIN
SO JOURNAL OF IMMUNOTHERAPY
LA English
DT Article
DE ANTIGEN PROCESSING; CYTOTOXIC T-LYMPHOCYTES; RECOMBINANT VACCINIA VIRUS;
   MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I MOLECULE
ID TOXIC LYMPHOCYTES-T; CLASS-II REGION; DEFECTIVE PRESENTATION;
   ENDOPLASMIC-RETICULUM; ENDOGENOUS ANTIGENS; HLA-A2 MOLECULES; SIGNAL
   SEQUENCE; INFECTED CELLS; MHC; PROTEIN
AB It is well established that tumor-specific CD8+ T cells have the capacity to prevent and cure malignancies in animals under experimental conditions. This has raised expectations that it will prove possible to achieve similar successes with human cancers. CD8+ T cells recognize peptides of 8-10 residues derived from cytosolic proteins that are bound to the class I molecules of the major histocompatibility complex. To most effectively manipulate the T-cell response to tumor cells, it is essential to understand the means by which the peptide-class I complex is created in cells. An overview of this process is provided with an emphasis toward the recent findings made by our laboratory.
RP BENNINK, JR (reprint author), NIAID,VIRAL DIS LAB,BETHESDA,MD 20892, USA.
RI yewdell, jyewdell@nih.gov/A-1702-2012
NR 42
TC 18
Z9 18
U1 0
U2 1
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 1053-8550
J9 J IMMUNOTHER
JI J. Immunother.
PD OCT
PY 1993
VL 14
IS 3
BP 202
EP 208
DI 10.1097/00002371-199310000-00006
PG 7
WC Oncology; Immunology; Medicine, Research & Experimental
SC Oncology; Immunology; Research & Experimental Medicine
GA MC307
UT WOS:A1993MC30700006
PM 8297901
ER

PT J
AU COHEN, PA
   KIM, H
   FOWLER, DH
   GRESS, RE
   JAKOBSEN, MK
   ALEXANDER, RB
   MULE, JJ
   CARTER, C
   ROSENBERG, SA
AF COHEN, PA
   KIM, H
   FOWLER, DH
   GRESS, RE
   JAKOBSEN, MK
   ALEXANDER, RB
   MULE, JJ
   CARTER, C
   ROSENBERG, SA
TI USE OF INTERLEUKIN-7, INTERLEUKIN-2, AND INTERFERON-GAMMA TO PROPAGATE
   CD4+ T-CELLS IN CULTURE WITH MAINTAINED ANTIGEN-SPECIFICITY
SO JOURNAL OF IMMUNOTHERAPY
LA English
DT Article
DE INTERLEUKIN-7; INTERFERON-GAMMA; CD4+ T-CELLS; DENDRITIC CELLS
ID TUMOR-INFILTRATING LYMPHOCYTES; MURINE TUMOR; CLONES; IMMUNOTHERAPY;
   MELANOMA
AB In contrast to CD8+ T cells. it has been difficult to establish consistently satisfactory conditions for the bulk culture of antitumor CD4+ T cells in either mice or humans. This difficulty is not limited to tumor antigen, since similar problems are encountered growing CD4+ T cells that recognize alloantigen, tetanus, or candida. Four basic findings are reviewed in this article, stemming from work with identical results in both human and mouse. (a) Although CD4+ T cells initially proliferate after exposure to appropriate antigen-presenting cells (APCs), such proliferation is not sustained; however, expansion of CD4- T cells can be achieved with the addition of recombinant interleukin-2 (rIL2) or rIL-7. (b) Specific CD4+ responses to antigens are often better sustained with exogenous IL-7 than with exogenous IL-2. (c) Adding rIL-7 or rIL-2 permits sustained CD4+ T-cell proliferation, but subsequent culture restimulation is complicated by high background reactivity to APCs whether APCs are antigen pulsed or not; this problem can be overcome by addition of exogenous interferon-gamma (IFN-gamma) to the CD4+ cultures. (d) In certain instances proliferation is paradoxically impaired by reexposure to specific antigen, possibly reflecting apoptosis; this problem is also overcome by addition of rINF-gamma to culture. We conclude that combinations of exogenous IL-7, IL-2, and IFN-gamma with APC restimulation can be used to sustain antigen-specific CD4+ T cells in culture. Using these techniques, antitumor CD4+ T cells were propagated from the peripheral blood of two tumor-bearing patients.
C1 NIH,DIV CANC BIOL & DIAG,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892.
   NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892.
   SYSTEM INC,PALO ALTO,CA.
RP COHEN, PA (reprint author), NCI,SURG BRANCH,CLIN ONCOL PROGRAM,BLDG 10,ROOM 2B46,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 19
TC 27
Z9 27
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 1053-8550
J9 J IMMUNOTHER
JI J. Immunother.
PD OCT
PY 1993
VL 14
IS 3
BP 242
EP 252
DI 10.1097/00002371-199310000-00012
PG 11
WC Oncology; Immunology; Medicine, Research & Experimental
SC Oncology; Immunology; Research & Experimental Medicine
GA MC307
UT WOS:A1993MC30700012
PM 7507711
ER

PT J
AU NGUYEN, BYT
   SHAY, LE
   WYVILL, KM
   PLUDA, JM
   BRAWLEY, O
   COHEN, RB
   WHITCUP, SM
   VENZON, DJ
   BRODER, S
   YARCHOAN, R
AF NGUYEN, BYT
   SHAY, LE
   WYVILL, KM
   PLUDA, JM
   BRAWLEY, O
   COHEN, RB
   WHITCUP, SM
   VENZON, DJ
   BRODER, S
   YARCHOAN, R
TI A PILOT-STUDY OF SEQUENTIAL THERAPY WITH ZIDOVUDINE PLUS ACYCLOVIR,
   DIDEOXYINOSINE, AND DIDEOXYCYTIDINE IN PATIENTS WITH SEVERE
   HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID AIDS-RELATED COMPLEX; PNEUMOCYSTIS-CARINII PNEUMONIA; PLACEBO-CONTROLLED
   TRIAL; PHASE-I TRIAL; 2',3'-DIDEOXYINOSINE DDI; ANTIRETROVIRAL THERAPY;
   AZIDOTHYMIDINE AZT; HIV-INFECTION; HTLV-III/LAV; DOUBLE-BLIND
AB A pilot study was initiated to explore a sequential combination antiretroviral regimen in 21 patients with AIDS or advanced human immunodeficiency virus (HIV) infection, who had received little or no prior anti-HIV therapy. The mean entry CD4 cell count was 184/mm3. Patients received 3-week cycles consisting of zidovudine plus acyclovir, dideoxyinosine, and dideoxycytidine for 1 week each. Overall, the regimen was well tolerated for up to 3 years. The principal toxicities were anemia, nausea, and vomiting; 1 patient developed retinal lesions. The mean CD4 cell count reached a peak of 64 cells/mm3 above baseline at week 8 (P = .005 compared to baseline) and remained above baseline for >40 weeks. Patients also gained weight and had decreases in serum HIV p24 antigen. Eight patients developed opportunistic infections or tumors. Only 4 patients died during 3 years of follow-up. This regimen appears to be generally tolerable and to have anti-HIV activity. Additional studies will be needed, however, to learn how to best combine the available agents in patients with HIV infection.
C1 NCI,MED BRANCH,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892.
   NEI,CLIN BRANCH,BETHESDA,MD 20892.
RI Venzon, David/B-3078-2008
NR 49
TC 14
Z9 14
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD OCT
PY 1993
VL 168
IS 4
BP 810
EP 817
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA LY582
UT WOS:A1993LY58200002
PM 8397267
ER

PT J
AU KONKEL, ME
   MEAD, DJ
   CIEPLAK, W
AF KONKEL, ME
   MEAD, DJ
   CIEPLAK, W
TI KINETIC AND ANTIGENIC CHARACTERIZATION OF ALTERED PROTEIN-SYNTHESIS BY
   CAMPYLOBACTER-JEJUNI DURING CULTIVATION WITH HUMAN EPITHELIAL-CELLS
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID HEP-2 CELLS; EXPERIMENTAL-INFECTION; MAMMALIAN-CELLS; INVASION;
   SALMONELLA; ENTERITIS; COLI; EXPRESSION; VIRULENCE; ABILITY
AB Cultivation of Campylobacter jejuni with INT 407 cell monolayer cultures results in new or enhanced synthesis of a number of proteins compared with bacteria cultured in the absence of the epithelial cells. These proteins were detected within 60 min after the addition of the bacteria to the epithelial cell cultures, and their synthesis was temporally associated with an increase in C jejuni internalization. A rabbit antiserum raised against bacteria that were cultivated with INT 407 cells recognized nine proteins that were not recognized by an antiserum against C jejuni cultivated in medium alone. The former antiserum inhibited the internalization, but not the binding, of Campylobacter jejuni in a dose-dependent fashion. The results suggest that one or more of the proteins synthesized by C jejuni in response to cocultivation with epithelial cells plays a role in facilitating internalization.
C1 NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,903 S 4TH ST,HAMILTON,MT 59840.
NR 34
TC 30
Z9 30
U1 1
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD OCT
PY 1993
VL 168
IS 4
BP 948
EP 954
PG 7
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA LY582
UT WOS:A1993LY58200021
PM 8376841
ER

PT J
AU CLERICI, M
   YARCHOAN, R
   BLATT, S
   HENDRIX, CW
   AMMANN, AJ
   BRODER, S
   SHEARER, GM
AF CLERICI, M
   YARCHOAN, R
   BLATT, S
   HENDRIX, CW
   AMMANN, AJ
   BRODER, S
   SHEARER, GM
TI EFFECT OF A RECOMBINANT CD4-IGG ON IN-VITRO T-HELPER CELL-FUNCTION -
   DATA FROM A PHASE-I/II STUDY OF PATIENTS WITH AIDS
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Note
ID IMMUNODEFICIENCY-VIRUS TYPE-1; INFECTION; THERAPY; CD4; CHILDREN
AB Ten patients with AIDS were enrolled in a phase I/II protocol of recombinant CD4-IgG (rCD4-IgG) treatment. Patients' peripheral blood leukocytes (PBL) were tested before, during, and after therapy with rCD4-IgG for T helper (TH) cell function assessed by antigen- and mitogen-stimulated proliferation and interleukin-2 production in response to influenza A virus, allogeneic PBL (alloantigens), and phytohemagglutinin. Although clinical benefit was not evident, rCD4-IgG treatment was associated with rapid and potent improved TH cell function for two of three stimuli tested in 90% of the patients. These data are complemented by an in vitro experimental model that demonstrates the opposing immunologic effects of rgp120 and rCD4-IgG on TH cell function of PBL from uninfected individuals. Thus, restoration of TH cell function by rCD4-IgG in the absence of increased CD4 cell counts could be due to removal of an immunosuppressive factor, possibly gp 1 20. These findings suggest that rCD4-IgG can induce partial restoration of immune function in AIDS patients, even in the absence of apparent short-term clinical benefit.
C1 NCI,CLIN ONCOL PROGRAM,BETHESDA,MD 20892.
   HUMAN IMMUNODEFICIENCY VIRUS UNIT,LACKLAND AFB,TX.
   ARIEL PROJECT,NOVATO,CA.
RP CLERICI, M (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM 4B-17,BETHESDA,MD 20892, USA.
RI Hendrix, Craig/G-4182-2014
OI Hendrix, Craig/0000-0002-5696-8665
NR 15
TC 8
Z9 8
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD OCT
PY 1993
VL 168
IS 4
BP 1012
EP 1016
PG 5
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA LY582
UT WOS:A1993LY58200030
PM 8376811
ER

PT J
AU PARKER, RI
   BRAY, GL
   MCKEOWN, LP
   WHITE, JG
AF PARKER, RI
   BRAY, GL
   MCKEOWN, LP
   WHITE, JG
TI FAILURE TO MOBILIZE INTRACELLULAR CALCIUM IN RESPONSE TO THROMBIN IN A
   PATIENT WITH FAMILIAL THROMBOCYTOPATHY CHARACTERIZED BY
   MACROTHROMBOCYTOPENIA AND ABNORMAL PLATELET MEMBRANE COMPLEXES
SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE
LA English
DT Article
ID GLYCOPROTEIN-IB; VONWILLEBRAND-FACTOR; BLOOD-PLATELET; ACTIVATION;
   IDENTIFICATION; RECEPTOR; PATHWAY; DEFECT; GPIB; IX
AB We report a mother and son who were found to have macrothrombocytopenia, prolonged bleeding time, and abnormal platelet responses to thrombin. Transmission electron microscopy performed on the son's platelets demonstrated an unusual arrangement of membrane complexes formed by association of the open canalicular and dense tubular systems. Number and appearance of platelet alpha-granules, dense bodies, and mitochondria were normal. These platelets demonstrated normal agonist-induced Ca2+ flux in response to collagen and supranormal responses to arachidonic acid but displayed no increase in intracellular free Ca2+ in response to thrombin. Platelet surface glycoproteins IIb-IIIa, Ib, and granular membrane protein-140 measured by flourescence-activated flow cytometry, along with platelet content of von Willebrand factor and fibrinogen, were normal. The von Willebrand factor binding function of GP-Ib on these platelets was also normal. We believe that this family demonstrates a unique macrothrombocytopenia syndrome characterized by deficient Ca2+ mobilization in response to thrombin that is not related to a defect in GP-Ib.
C1 NIH,CTR CLIN,DEPT CLIN PATHOL,HEMATOL SERV,BETHESDA,MD 20892.
   GEORGE WASHINGTON UNIV,CHILDRENS NATL MED CTR,DEPT PEDIAT,DEPT HEMATOL ONCOL,WASHINGTON,DC 20052.
   UNIV MINNESOTA,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455.
   UNIV MINNESOTA,DEPT PEDIAT,MINNEAPOLIS,MN 55455.
NR 30
TC 2
Z9 2
U1 0
U2 0
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0022-2143
J9 J LAB CLIN MED
JI J. Lab. Clin. Med.
PD OCT
PY 1993
VL 122
IS 4
BP 441
EP 449
PG 9
WC Medical Laboratory Technology; Medicine, General & Internal; Medicine,
   Research & Experimental
SC Medical Laboratory Technology; General & Internal Medicine; Research &
   Experimental Medicine
GA MF814
UT WOS:A1993MF81400014
PM 8228559
ER

PT J
AU WANG, MH
   SKEEL, A
   YOSHIMURA, T
   COPELAND, TD
   SAKAGUCHI, K
   LEONARD, EJ
AF WANG, MH
   SKEEL, A
   YOSHIMURA, T
   COPELAND, TD
   SAKAGUCHI, K
   LEONARD, EJ
TI ANTIBODIES TO MACROPHAGE STIMULATING PROTEIN (MSP) - SPECIFICITY,
   EPITOPE INTERACTIONS, AND IMMUNOASSAY OF MSP IN HUMAN SERUM
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE KRINGLE; HEPATOCYTE GROWTH FACTOR; ELISA
ID HEPATOCYTE GROWTH-FACTOR; AMINO-ACID-SEQUENCE; IDENTIFICATION;
   PROTHROMBIN; HOMOLOGY
AB Macrophage stimulating protein (MSP) is a member of a family of proteins characterized by a triple disulfide loop structure (kringle). We developed antibodies to human MSP for detection in Western blots, quantification in biological fluids, and neutralization of activity. Immunogens included native MSP, reduced and alkylated alpha and beta chains, and peptides of MSP regions with minimal sequence similarity to other kringle proteins. We found three antibody categories based on interaction with the following types of epitope: primary sequence, discontinuous (dependent on disulfide bonds), and cryptic (not exposed in native MSP). None of the antibodies reacted with related kringle proteins. A specific sandwich ELISA was developed for measuring human MSP. The mean serum concentration was 4 nM. Serum MSP did not increase over a 24-h period in response to intravenous lipopolysaccharide, indicating that MSP is not an acute phase protein. These findings are consistent with the hypothesis that regulation of MSP activity is by conversion of pro-MSP to MSP rather than by rapid changes in rates of synthesis.
C1 NCI,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LABS,BASIC RES PROGRAM,FREDERICK,MD 21701.
   NCI,CELL BIOL LAB,CHEM SECT,BETHESDA,MD 20892.
RP WANG, MH (reprint author), NCI,FCRDC,IMMUNOBIOL LAB,IMMUNOPATHOL SECT,BLDG 560,ROOM 12-71,FREDERICK,MD 21702, USA.
FU NCI NIH HHS [N01-CO-74101]
NR 18
TC 30
Z9 31
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 OCT
PY 1993
VL 54
IS 4
BP 289
EP 295
PG 7
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA MA318
UT WOS:A1993MA31800004
PM 7691976
ER

PT J
AU TOFTS, PS
   BERKOWITZ, BA
AF TOFTS, PS
   BERKOWITZ, BA
TI RAPID MEASUREMENT OF CAPILLARY-PERMEABILITY USING THE EARLY PART OF THE
   DYNAMIC GD-DTPA MRI ENHANCEMENT CURVE
SO JOURNAL OF MAGNETIC RESONANCE SERIES B
LA English
DT Article
ID BRAIN-BARRIER PERMEABILITY; GADOLINIUM-DTPA; MULTIPLE-SCLEROSIS;
   CONTRAST AGENT; INJECTION; COMPLEX
C1 NIEHS,RES TRIANGLE PK,NC 27709.
RP TOFTS, PS (reprint author), INST NEUROL,QUEEN SQ,LONDON WC1N 3BG,ENGLAND.
RI Tofts, Paul/C-8517-2009
OI Tofts, Paul/0000-0002-8552-2419
NR 16
TC 32
Z9 32
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 1064-1866
J9 J MAGN RESON SER B
JI J. Magn. Reson. Ser. B
PD OCT
PY 1993
VL 102
IS 2
BP 129
EP 136
DI 10.1006/jmrb.1993.1075
PG 8
WC Physics, Atomic, Molecular & Chemical
SC Physics
GA MB743
UT WOS:A1993MB74300001
ER

PT J
AU POSSE, S
   CUENOD, CA
   LEBIHAN, D
AF POSSE, S
   CUENOD, CA
   LEBIHAN, D
TI MOTION ARTIFACT COMPENSATION IN H-1 SPECTROSCOPIC IMAGING BY SIGNAL
   TRACKING
SO JOURNAL OF MAGNETIC RESONANCE SERIES B
LA English
DT Note
ID MAGNETIC-RESONANCE SPECTRA; HUMAN-BRAIN; STIMULATED ECHOES; MR
   SPECTROSCOPY; TUMORS
C1 NIH,DIAGNOST RADIOL RES LAB,BETHESDA,MD 20892.
RP POSSE, S (reprint author), NIH,DEPT DIAGNOST RADIOL,BLDG 10,ROOM 1C660,BETHESDA,MD 20892, USA.
NR 31
TC 23
Z9 23
U1 0
U2 1
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 1064-1866
J9 J MAGN RESON SER B
JI J. Magn. Reson. Ser. B
PD OCT
PY 1993
VL 102
IS 2
BP 222
EP 227
DI 10.1006/jmrb.1993.1088
PG 6
WC Physics, Atomic, Molecular & Chemical
SC Physics
GA MB743
UT WOS:A1993MB74300014
ER

PT J
AU VUISTER, GW
   BAX, A
AF VUISTER, GW
   BAX, A
TI MEASUREMENT OF 2-BOND AND 3-BOND PROTON TO METHYL-CARBON J-COUPLINGS IN
   PROTEINS UNIFORMLY ENRICHED WITH C-13
SO JOURNAL OF MAGNETIC RESONANCE SERIES B
LA English
DT Note
ID IMPROVED LINEAR PREDICTION; NMR-SPECTROSCOPY; CONSTANTS; SPECTRA;
   SIGNALS; N-15
RP VUISTER, GW (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA.
NR 29
TC 29
Z9 29
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 1064-1866
J9 J MAGN RESON SER B
JI J. Magn. Reson. Ser. B
PD OCT
PY 1993
VL 102
IS 2
BP 228
EP 231
DI 10.1006/jmrb.1993.1089
PG 4
WC Physics, Atomic, Molecular & Chemical
SC Physics
GA MB743
UT WOS:A1993MB74300015
ER

PT J
AU WILL, K
   REISS, J
   DEAN, M
   SCHLOSSER, M
   SLOMSKI, R
   SCHMIDTKE, J
   STUHRMANN, M
AF WILL, K
   REISS, J
   DEAN, M
   SCHLOSSER, M
   SLOMSKI, R
   SCHMIDTKE, J
   STUHRMANN, M
TI CFTR TRANSCRIPTS ARE UNDETECTABLE IN LYMPHOCYTES AND RESPIRATORY
   EPITHELIAL-CELLS OF A CF PATIENT HOMOZYGOUS FOR THE NONSENSE MUTATION
   R553X
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
ID CYSTIC-FIBROSIS GENE; COMMON MUTATION; CONDUCTANCE; IDENTIFICATION;
   EXPRESSION; RESISTANCE; DNA; DEFICIENCY; GENOTYPE; SEQUENCE
AB In order to analyse the influence of the nonsense mutation R553X on CFTR gene expression, transcripts from epithelial cells and lymphocytes were examined from nine subjects (one CF patient homozygous for R553X, one CF patient compound heterozygous for R553X/DELTAF508, four CF carriers heterozygous for R553X, one CF carrier with the genotype DELTAF508/N, and two uncharacterised normal adults). After reverse transcription of the region from exons 10 to 13 to cDNA, fragments of the expected size were amplified from all heterozygous and normal subjects. In three subjects an additional alternatively spliced product was observed, which was found to contain a termination codon. In repeated experiments it was not possible to detect any CFTR mRNA in cells derived from the R553X homozygous patient. Furthermore, in subjects heterozygous for R553X we could not detect by hybridisation with a specific oligonucleotide probe and direct sequencing any CFTR mRNA derived from the R553X allele. However, the wild type product was present in all of these subjects. Our results support the view that nonsense mutations in the CFTR gene can lead to a reduction or absence of cytoplasmic CFTR mRNA.
C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,BLDG 560,RM 21-19,FREDERICK,MD 21702.
   HANNOVER MED SCH,INST HUMAN GENET,W-3000 HANNOVER 61,GERMANY.
   UNIV GOTTINGEN,INST HUMAN GENET,W-3400 GOTTINGEN,GERMANY.
RI Dean, Michael/G-8172-2012
OI Dean, Michael/0000-0003-2234-0631
NR 30
TC 13
Z9 13
U1 0
U2 0
PU BRITISH MED JOURNAL PUBL GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR
SN 0022-2593
J9 J MED GENET
JI J. Med. Genet.
PD OCT
PY 1993
VL 30
IS 10
BP 833
EP 837
DI 10.1136/jmg.30.10.833
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA MA906
UT WOS:A1993MA90600009
PM 7693946
ER

PT J
AU DAHL, SP
   KIMBERLING, WJ
   GORIN, MB
   WESTON, MD
   FURMAN, JMR
   PIKUS, A
   MOLLER, C
AF DAHL, SP
   KIMBERLING, WJ
   GORIN, MB
   WESTON, MD
   FURMAN, JMR
   PIKUS, A
   MOLLER, C
TI GENETIC-HETEROGENEITY OF USHER SYNDROME TYPE-II
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
ID LINKAGE; CHROMOSOME-1Q; LOCALIZATION; CONSORTIUM
AB Usher syndrome is an autosomal recessive disorder characterised by retinitis pigmentosa and congenital sensorineural hearing loss. A gene for Usher syndrome type II (USH2) has been localised to chromosome 1q32-q41. DNA from a family with four of seven sibs affected with clinical characteristics of Usher syndrome type II was genotyped using markers spanning the 1q32-1q41 region. These included D1S70 and D1S81, which are believed to flank USH2. Genotypic results and subsequent linkage analysis indicated non-linkage of this family to these markers. The A test analysis for heterogeneity with this family and 32 other Usher type II families was statistically significant at p<0.05. Further clinical evaluation of this family was done in light of the linkage results to determine if any phenotypic characteristics would allow for clinical identification of the unlinked type. No clear phenotypic differences were observed; however, this unlinked family may represent a previously unreported subtype of Usher type II characterised by a milder form of retinitis pigmentosa and mild vestibular abnormalities. Heterogeneity of Usher syndrome type II complicates efforts to isolate and clone Usher syndrome genes using linkage analysis and limits the use of DNA markers in early detection of Usher type II.
C1 BOYS TOWN NATL RES HOSP,DEPT GENET,555 N 30 ST,OMAHA,NE 68131.
   EYE & EAR INST PITTSBURGH,PITTSBURGH,PA.
   NIDOCD,BETHESDA,MD.
   LINKOPING UNIV,S-58183 LINKOPING,SWEDEN.
NR 17
TC 24
Z9 24
U1 0
U2 0
PU BRITISH MED JOURNAL PUBL GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR
SN 0022-2593
J9 J MED GENET
JI J. Med. Genet.
PD OCT
PY 1993
VL 30
IS 10
BP 843
EP 848
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA MA906
UT WOS:A1993MA90600011
ER

PT J
AU CARROLL, FI
   GRAY, JL
   ABRAHAM, P
   KUZEMKO, MA
   LEWIN, AH
   BOJA, JW
   KUHAR, MJ
AF CARROLL, FI
   GRAY, JL
   ABRAHAM, P
   KUZEMKO, MA
   LEWIN, AH
   BOJA, JW
   KUHAR, MJ
TI 3-ARYL-2-(3'-SUBSTITUTED-1',2',4'-OXADIAZOL-5'-YL)TROPANE ANALOGS OF
   COCAINE - AFFINITIES AT THE COCAINE BINDING-SITE AT THE DOPAMINE,
   SEROTONIN, AND NOREPINEPHRINE TRANSPORTERS
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID LIGAND-BINDING; H-3 NISOXETINE; INHIBITION; RECEPTOR; RADIOLIGAND;
   ISOMERS; ESTERS; POTENT; INVIVO; BRAIN
AB Previous studies have shown that 3beta-(substituted phenyl)tropan-2beta-carboxylic acid esters possess high affinity for the cocaine binding site on the dopamine transporter both in vitro and in vivo and inhibit dopamine uptake in vitro. Since 1,2,4-oxadiazoles are excellent bioisosteres of ester groups, we have prepared several 3beta-(substituted phenyl)-2beta-(3-substituted 1',2',4'-oxadiazol-5'-yl)tropanes (5b-h) and all four stereoisomers of (1R,5S)-3 phenyl-2-(3-methyl-1',2',4'-oxadiazol-5'-yl)tropane (5a and 6-8).  The 3alpha-phenyl-2alpha-(3'-methyl-1',2',4'-oxadiazole) isomer 7 was prepared from a stereoselective addition of phenyllithium to (1R,5S)-2-(3'-methyl-1',2',4'-oxadizol-5-yl)-8-methyl-8-azabicyclo[3.2.1]oct-2-ene(11).  The binding affinities for 5a-h and 6-8 at the dopamine, serotonin, and norepinephrine transporters were obtained. In general these bioisosteres showed potencies for the dopamine transporter similar to those of their parent esters.  3beta-(4'-Chlorophenyl)-2beta-(3'-phenyl-1',2',4'-oxadiazol-5'-yl)tropane (5d) was the most potent analogue with an IC50 of 1.62 nM. However, 3beta-(4'-chlorophenyl)-2beta-(3'-methoxyphenyl-1',2',4'-oxadiazol-5'-yl)tropane (5e) with an IC50 of 1.81 nM was the most selective analogue for the dopamine transporter showing NE/DA and 5-HT/DA ratios of 461 and 186, respectively. The cis- and trans-3alpha-phenyl-2-(3'-methyl-1',2',4'-oxadiazol-5'-yl)tropanes (7 and 8), which exist in a boat conformation, have IC50 values only slightly greater than that of the 3beta,2beta-isomer (5a) which possesses the cocaine stereochemistry.
C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224.
RP CARROLL, FI (reprint author), RES TRIANGLE INST,POB 12194,RES TRIANGLE PK,NC 27709, USA.
FU NIDA NIH HHS [DA05477]
NR 32
TC 118
Z9 118
U1 0
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD OCT 1
PY 1993
VL 36
IS 20
BP 2886
EP 2890
DI 10.1021/jm00072a007
PG 5
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA MA321
UT WOS:A1993MA32100007
PM 8411004
ER

PT J
AU SMYTH, MS
   STEFANOVA, I
   HARTMANN, F
   HORAK, ID
   OSHEROV, N
   LEVITZKI, A
   BURKE, TR
AF SMYTH, MS
   STEFANOVA, I
   HARTMANN, F
   HORAK, ID
   OSHEROV, N
   LEVITZKI, A
   BURKE, TR
TI NON-AMINE BASED ANALOGS OF LAVENDUSTIN-A AS PROTEIN-TYROSINE KINASE
   INHIBITORS
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID GROWTH-FACTOR-RECEPTOR; STYRYL-BASED INHIBITORS; EGF-RECEPTOR; SIGNAL
   TRANSDUCTION; TYRPHOSTINS; ERBSTATIN; AGENTS
AB The fermentation product lavendustin A (1) is a protein-tyrosine kinase (PTK) inhibitor whose active pharmacophore has previously been shown to reside in the more simplified salicyl-containing benzylamine 2. Amine 2 bears some structural resemblance to two other natural product PTK inhibitors, erbstatin (3) and piceatannol (4). Non-amine containing analogues of 2 were therefore synthesized which incorporated additional aspects of either erbstatin or piceatannol. Examination of these inhibitors in immunoprecipitated p56lck, epidermal growth factor receptor (EGFR), and c-erb B-2/HER 2/neu PTK preparations showed that compound 12 (IC50 = 60 nM) was one of the most potent p56lck inhibitors reported to date. These results demonstrate that nitrogen is not an essential component of the lavendustin A pharmacophore 2 and that 1,2-diarylethanes and -ethenes bearing a salicyl moiety appear to be valuable structural motifs for the construction of extremely potent PTK inhibitors.
C1 NIH,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BLDG 37,ROOM 5C06,BETHESDA,MD 20892.
   NCI,DIV CANC BIOL DIAG & CTR,METAB BRANCH,BETHESDA,MD 20892.
   HEBREW UNIV JERUSALEM,DEPT BIOL CHEM,IL-91904 JERUSALEM,ISRAEL.
RI Burke, Terrence/N-2601-2014
NR 26
TC 38
Z9 40
U1 0
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD OCT 1
PY 1993
VL 36
IS 20
BP 3010
EP 3014
DI 10.1021/jm00072a022
PG 5
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA MA321
UT WOS:A1993MA32100022
PM 8105084
ER

PT J
AU SMYTH, MS
   STEFANOVA, I
   HORAK, ID
   BURKE, TR
AF SMYTH, MS
   STEFANOVA, I
   HORAK, ID
   BURKE, TR
TI HYDROXYLATED 2-(5'-SALICYL)NAPHTHALENES AS PROTEIN-TYROSINE KINASE
   INHIBITORS
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID SIGNAL TRANSDUCTION; EGF-RECEPTOR; DERIVATIVES; TYRPHOSTINS; AGENTS
AB The salicyl group figures prominently in several potent protein-tyrosine kinase (PTK) inhibitors, including the fermentation product lavendustin A (3), the salicylsulfonyl nitrostyryl 30, and our recently reported salicyl-containing stilbene 7. Taking compound 7 and the isomeric 8 as lead structures, bicyclic nuclei 9-12 were prepared as conformationally constrained mimetics in which the hydroxyphenyl rings of 7 and 8 are held coplanar with the stilbene ethylene bridge. A similar approach with styryl-based PTK inhibitors of structure 1 previously yielded analogues 2 with enhanced potency.  In the present case, however, the resulting salicyl-containing bicyclics exhibited extremely poor inhibitory potency when examined against autophosphorylation of immunoprecipitated p56lck PTK preparations. The implications of these results are discussed as they relate to the potential ways in which salicyl-containing stilbenes may be oriented relative to styryl-based inhibitors of type 1 and to an emerging class of potent aryl-substituted bicyclic inhibitors exemplified by compound 31.
C1 NIH,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BLDG 37,ROOM 5C06,BETHESDA,MD 20892.
   NCI,DIV CANC BIOL DIAG & CTR,METAB BRANCH,BETHESDA,MD 20892.
RI Burke, Terrence/N-2601-2014
NR 24
TC 27
Z9 27
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD OCT 1
PY 1993
VL 36
IS 20
BP 3015
EP 3020
DI 10.1021/jm00072a023
PG 6
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA MA321
UT WOS:A1993MA32100023
PM 8411019
ER

PT J
AU AIDA, K
   NEGISHI, M
AF AIDA, K
   NEGISHI, M
TI A TRANS-ACTING LOCUS REGULATES TRANSCRIPTIONAL REPRESSION OF THE
   FEMALE-SPECIFIC STEROID 15-ALPHA-HYDROXYLASE GENE IN MALE-MICE
SO JOURNAL OF MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID TISSUE-SPECIFIC EXTINGUISHER; GROWTH-HORMONE; MOUSE-LIVER; TESTOSTERONE
   16-ALPHA-HYDROXYLASE; POSTTRANSCRIPTIONAL REGULATION; PROTEIN-KINASE;
   TSE1 ENCODES; EXPRESSION; CYTOCHROME-P-450; P-45015-ALPHA
AB Steroid 15 alpha-hydroxylase (P450(15)alpha) is a female-specific enzyme in the livers of many inbred mice including DBA/2J. Run-on assays using liver nuclei from GH-deficient Little mice indicated that the P450(15)alpha gene is transcriptionally repressed by GH in male mice. BALB/cJ is a variant strain in which the gene is expressed in the males as well as in the females. Genetic crosses between DBA/2J and BALB/cJ indicated that expression of the P450(15)alpha, gene in BALB/cJ males is inherited as a recessive trait and is regulated by a single locus. The parental origin of the P450(15)alpha genes, determined using restriction site polymorphism in the exons of the P450(15)alpha genes, divided the F2 males expressing the P450(15)alpha gene into three phenotypes at a ratio of 1:1:2, the individuals expressing the gene from only BALB/cJ or DBA/2J and the individuals expressing the genes from both parents respectively. The results indicate that the repression of the P450(15)alpha gene in male mice is regulated by a trans-acting regulatory locus between the DBA/2J and BALB/cJ pairs. Because hypophysectomy derepressed the P450(15)alpha gene in F1 males and GH repressed the gene in hypophysectomized F1 males, the hormone appears to regulate gene repression through a trans-acting locus, named GH-dependent repression, GDR.
C1 NIEHS,PHARMACOGENET SECT,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709.
NR 30
TC 17
Z9 17
U1 0
U2 0
PU J ENDOCRINOLOGY LTD
PI BRISTOL
PA 17/18 THE COURTYARD, WOODLANDS, ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ
SN 0952-5041
J9 J MOL ENDOCRINOL
JI J. Mol. Endocrinol.
PD OCT
PY 1993
VL 11
IS 2
BP 213
EP 222
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA MG255
UT WOS:A1993MG25500010
PM 8297477
ER

PT J
AU CRAGG, GM
   SCHEPARTZ, SA
   SUFFNESS, M
   GREVER, MR
AF CRAGG, GM
   SCHEPARTZ, SA
   SUFFNESS, M
   GREVER, MR
TI THE TAXOL SUPPLY CRISIS - NEW NCI POLICIES FOR HANDLING THE LARGE-SCALE
   PRODUCTION OF NOVEL NATURAL PRODUCT ANTICANCER AND ANTI-HIV AGENTS
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID PRACTICAL APPROACH; TAXUS-BREVIFOLIA; PHASE-II; EFFICIENT; ANALOGS
AB Over the past 30 years, the National Cancer Institute has been involved in the preclinical and/or clinical evaluation of the majority of those agents approved for the treatment of cancer. Many of the new agents under consideration in the NCI program are either natural products or derivatives of natural product leads, and of critical importance to their development is the issue of drug supply. In responding to the drug supply crisis which emerged with the demonstration of the clinical efficacy of taxol, the NCI has identified several important lessons for those interested in natural product drug discovery and development. As a result, the NCI has developed plans to avert similar supply crises in the future by initiating exploratory research projects for large-scale production of promising agents at the earliest possible point following the demonstration of confirmed antitumor activity. These plans, together with a review of the development of taxol, are presented in this paper.
C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892.
NR 33
TC 158
Z9 187
U1 3
U2 16
PU AMER SOC PHARMACOGNOSY
PI CINCINNATI
PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD OCT
PY 1993
VL 56
IS 10
BP 1657
EP 1668
DI 10.1021/np50100a001
PG 12
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA ME510
UT WOS:A1993ME51000001
PM 7903979
ER

PT J
AU PETTIT, GR
   PETTIT, GR
   BACKHAUS, RA
   BOYD, MR
   MEEROW, AW
AF PETTIT, GR
   PETTIT, GR
   BACKHAUS, RA
   BOYD, MR
   MEEROW, AW
TI ANTINEOPLASTIC AGENTS .256. CELL-GROWTH INHIBITORY ISOCARBOSTYRILS FROM
   HYMENOCALLIS
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID LINES
AB The bulbs of Hymenocallis littoralis, collected in Hawaii and horticulturally grown in Arizona, and bulbs of Hymenocallis caribaea and Hymenocallis latifolia, collected in Singapore, were found to contain a cytotoxic, isocarbostyril-type biosynthetic product, 7-deoxy-trans-dihydronarciclasine [2]. This new compound inhibited the cytopathicity and/or replication of various viruses. Companion cytotoxic constituents of H. littoralis and Hymenocallis sp. were found to be pancratistatin [1), narciclasine [5], and 7-deoxynarciclasine [4). These four compounds, along with four other closely related compounds, were comparatively evaluated in the National Cancer Institute's in vitro cytocoxicity panel. Although there were striking differences in overall potency, some of the compounds shared a highly characteristic differential cytotoxicity profile against the 60 diverse human rumor cell lines comprising the NCI panel. As a group, the melanoma subpanel lines were most sensitive; certain individual lines within other subpanels (eg., NSC lung, colon, brain, renal) were as much as a thousand-fold of more sensitive than the less sensitive lines.
C1 ARIZONA STATE UNIV,DEPT BOT,TEMPE,AZ 85287.
   NCI,FREDERICK CANC RES & DEV CTR,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702.
   UNIV FLORIDA,FORT LAUDERDALE RES & EDUC CTR,IFAS,FT LAUDERDALE,FL 33314.
RP PETTIT, GR (reprint author), ARIZONA STATE UNIV,DEPT CHEM,CANC RES INST,TEMPE,AZ 85287, USA.
FU NCI NIH HHS [CA-16049-05-12, CA-44344-01A1-02-05]; NIAID NIH HHS
   [AI25696-02-05]
NR 22
TC 101
Z9 105
U1 5
U2 14
PU AMER SOC PHARMACOGNOSY
PI CINCINNATI
PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD OCT
PY 1993
VL 56
IS 10
BP 1682
EP 1687
DI 10.1021/np50100a004
PG 6
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA ME510
UT WOS:A1993ME51000004
PM 8277308
ER

PT J
AU BEUTLER, JA
   CARDELLINA, JH
   GRAY, GN
   PRATHER, TR
   SHOEMAKER, RH
   BOYD, MR
   LIN, CM
   HAMEL, E
   CRAGG, GM
AF BEUTLER, JA
   CARDELLINA, JH
   GRAY, GN
   PRATHER, TR
   SHOEMAKER, RH
   BOYD, MR
   LIN, CM
   HAMEL, E
   CRAGG, GM
TI 2 NEW CYTOTOXIC CHALCONES FROM CALYTHROPSIS-AUREA
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID TUMOR-CELL-LINES; ANTIMITOTIC AGENTS
AB The crude extract of Calythropsis aurea (Myrtaceae) produced a pattern of differential cytotoxicity in the NCI 60 cell line assay which was similar to those of known tubulin-interactive compounds. Cytotoxicity-guided fractionation led to the isolation of two new chalcones, calythropsin [1] and dihydrocalythropsin (2], which were responsible for the activity. Calythropsin was demonstrated to have a weak effect on mitosis, and presumably also on tubulin polymerization.
C1 NCI,DIV CANC TREATMENT,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702.
   NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,NAT PROD BRANCH,FREDERICK,MD 21702.
   NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,FREDERICK,MD 21702.
RI Beutler, John/B-1141-2009
OI Beutler, John/0000-0002-4646-1924
NR 9
TC 14
Z9 16
U1 0
U2 2
PU AMER SOC PHARMACOGNOSY
PI CINCINNATI
PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD OCT
PY 1993
VL 56
IS 10
BP 1718
EP 1722
DI 10.1021/np50100a009
PG 5
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA ME510
UT WOS:A1993ME51000009
PM 8277311
ER

PT J
AU BEUTLER, JA
   CARDELLINA, JH
   PRATHER, T
   SHOEMAKER, RH
   BOYD, MR
   SNADER, KM
AF BEUTLER, JA
   CARDELLINA, JH
   PRATHER, T
   SHOEMAKER, RH
   BOYD, MR
   SNADER, KM
TI A CYTOTOXIC BETA-CARBOLINE FROM THE BRYOZOAN CATENICELLA-CRIBRARIA
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
AB 1-Vinyl-8-hydroxy-beta-carboline was identified as the cytotoxic constituent of the bryozoans Catenicella cribraria and Cribricellina cribraria. Literature nmr data for this previously known compound, now reported from a new source, were corrected.
C1 NCI,DIV CANC TREATMENT,DRUG DISCOVERY RES & DEV LAB,BLDG 1052,FREDERICK,MD 21702.
   NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,NAT PROD BRANCH,FREDERICK,MD 21702.
RI Beutler, John/B-1141-2009
OI Beutler, John/0000-0002-4646-1924
NR 5
TC 8
Z9 9
U1 0
U2 5
PU AMER SOC PHARMACOGNOSY
PI CINCINNATI
PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD OCT
PY 1993
VL 56
IS 10
BP 1825
EP 1826
DI 10.1021/np50100a026
PG 2
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA ME510
UT WOS:A1993ME51000026
PM 8277321
ER

PT J
AU KAROUM, F
   CHRAPUSTA, SJ
   EGAN, MF
   WYATT, RJ
AF KAROUM, F
   CHRAPUSTA, SJ
   EGAN, MF
   WYATT, RJ
TI ABSENCE OF 6-HYDROXYDOPAMINE IN THE RAT-BRAIN AFTER TREATMENT WITH
   STIMULANTS AND OTHER DOPAMINERGIC AGENTS - A MASS FRAGMENTOGRAPHIC STUDY
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE 6-HYDROXYDOPAMINE; DOPAMINE; METHAMPHETAMINE; AMPHETAMINE;
   PSYCHOSTIMULANT; STIMULANT; RAT; BLOOD-BRAIN BARRIER
ID HYDROGEN-PEROXIDE; METHYLAMPHETAMINE; METHAMPHETAMINE; GENERATION;
   METABOLISM; MECHANISM; ACID
AB Formation of 6-hydroxydopamine (6-OHDA) from dopamine has been hypothesized to mediate neuro-degeneration induced by some psychostimulants. Although the emergence of a 6-OHDA-like substance was reported in the striatum of methamphetamine-treated rats, this substance has not been identified by a direct approach. We used mass fragmentography to search for 6-OHDA in the rat frontal cortex and striatum after the administration of a number of drugs including 3,4-dihydroxyphenyl-L-alanine, methamphetamine, amphetamine, and cocaine, all of which increase synaptic dopamine. No 6-OHDA was detected after the acute systemic administration of these agents. Intraventricular administration of 6-OHDA (10 mug/rat) produced measurable concentrations of 6-OHDA that were higher in the striatum than in the frontal cortex. Intraventricular administration of 2,4,5-trihydroxyphenyl-D,L-alanine (6-OHDOPA; 10 mug/rat) produced similar concentrations of 6-OHDA in both regions. Pargyline, but not carbidopa (alpha-methyldopahydrazine), enhanced the effect of intraperitoneal 6-OHDOPA administration (80 mg/kg). We conclude that (1) 6-OHDOPA can cross the blood-brain barrier and is converted to 6-OHDA in the brain, (2) 6-OHDA is a substrate for monoamine oxidase(s) and therefore a search for its purported deaminated metabolite is warranted, and (3) acute treatment with the above stimulants either does not lead to the formation of 6-OHDA or produces concentrations below the detection limit of the assay (< 34 pg/mg of protein).
RP KAROUM, F (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,WASHINGTON,DC 20032, USA.
NR 17
TC 32
Z9 32
U1 1
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 OCT
PY 1993
VL 61
IS 4
BP 1369
EP 1375
DI 10.1111/j.1471-4159.1993.tb13630.x
PG 7
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA LY325
UT WOS:A1993LY32500021
PM 8104232
ER

PT J
AU LASLOP, A
   STEINER, HJ
   EGGER, C
   WOLKERSDORFER, M
   KAPELARI, S
   HOGUEANGELETTI, R
   ERICKSON, JD
   FISCHERCOLBRIE, R
   WINKLER, H
AF LASLOP, A
   STEINER, HJ
   EGGER, C
   WOLKERSDORFER, M
   KAPELARI, S
   HOGUEANGELETTI, R
   ERICKSON, JD
   FISCHERCOLBRIE, R
   WINKLER, H
TI GLYCOPROTEIN-III (CLUSTERIN, SULFATED GLYCOPROTEIN-2) IN ENDOCRINE,
   NERVOUS, AND OTHER TISSUES - IMMUNOCHEMICAL CHARACTERIZATION,
   SUBCELLULAR-LOCALIZATION, AND REGULATION OF BIOSYNTHESIS
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE CLUSTERIN; LARGE DENSE-CORE VESICLES; ADRENAL MEDULLA; PITUITARY GLAND
ID ADRENAL CHROMAFFIN GRANULES; MESSENGER-RNA LEVELS; DOPAMINE
   BETA-HYDROXYLASE; CHROMOGRANIN-B; IMMUNOLOGICAL CHARACTERIZATION;
   SECRETORY GRANULES; SECRETOGRANIN-II; EXOCYTOTIC EXPOSURE;
   CARBOXYPEPTIDASE-H; MOLECULAR-CLONING
AB Specific antisera were raised against the A and B chains of glycoprotein III. Immunoblotting revealed that in adrenal medulla both chains migrate very closely together in two-dimensional electrophoresis. Both chains with slightly differing molecular sizes are found in several endocrine tissues and in brain, kidney, liver, and serum. The mRNA has an analogous widespread distribution. In primary cultures of chromaffin cells the level of message becomes significantly increased by treatment with histamine or 12-O-tetradecanoylphorbol 13-acetate/forskolin. However, the increase is small when compared with that of secretogranin II. The subcellular localization of glycoprotein III in endocrine organs and in the posterior pituitary was investigated by subcellular fractionation and immunoelectron microscopy. Glycoprotein III was found to be confined to the large dense-core vesicles of these organs. For a discussion of the function of glycoprotein III, its localization in these organelles has to be taken into account.
C1 UNIV INNSBRUCK, DEPT PHARMACOL, PETER MAYR STR 1A, A-6020 INNSBRUCK, AUSTRIA.
   YESHIVA UNIV ALBERT EINSTEIN COLL MED, DEPT DEV BIOL & CANC, BRONX, NY 10461 USA.
   UNIV INNSBRUCK, DEPT PATHOL, A-6020 INNSBRUCK, AUSTRIA.
   NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA.
NR 51
TC 27
Z9 27
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3042
J9 J NEUROCHEM
JI J. Neurochem.
PD OCT
PY 1993
VL 61
IS 4
BP 1498
EP 1505
DI 10.1111/j.1471-4159.1993.tb13645.x
PG 8
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA LY325
UT WOS:A1993LY32500036
PM 8377000
ER

PT J
AU GOLDSTEIN, DS
   GARTY, M
   BAGDY, G
   SZEMEREDI, K
   STERNBERG, EM
   LISTWAK, S
   PACAK, K
   DEKASTAROSTA, A
   HOFFMAN, A
   CHANG, PC
   STULL, R
   GOLD, PW
   KOPIN, IJ
AF GOLDSTEIN, DS
   GARTY, M
   BAGDY, G
   SZEMEREDI, K
   STERNBERG, EM
   LISTWAK, S
   PACAK, K
   DEKASTAROSTA, A
   HOFFMAN, A
   CHANG, PC
   STULL, R
   GOLD, PW
   KOPIN, IJ
TI ROLE OF CRH IN GLUCOPENIA-INDUCED ADRENOMEDULLARY ACTIVATION IN RATS
SO JOURNAL OF NEUROENDOCRINOLOGY
LA English
DT Article
DE ACTH; EPINEPHRINE; STRESS; HYPOGLYCEMIA; CORTICOTROPIN-RELEASING HORMONE
ID CORTICOTROPIN-RELEASING FACTOR; INSULIN-INDUCED HYPOGLYCEMIA;
   SYMPATHETIC NERVOUS-SYSTEM; ADRENAL-MEDULLARY RESPONSES; HYPOPHYSEAL
   PORTAL BLOOD; ARGININE VASOPRESSIN; BETA-ENDORPHIN; PLASMA
   DIHYDROXYPHENYLALANINE; GENE-EXPRESSION; LEWIS RATS
AB Acute glucoprivation profoundly stimulates hypothalamic-pituitary-adrenocortical (HPA) and adrenomedullary outflows. Whether these responses reflect a single central mechanism regulated by corticotropin-releasing hormone (CRH) has been unclear. This study examined the role of endogenous CRH in HPA and adrenomedullary responses to hypoglycemia in Sprague-Dawley rats, by using anti-CRH immune serum or a CRH antagonist (alpha-helical h/r CRH9-41, and in Lewis rats, a strain characterized by deficient hypothalamic CRH responses during stress. In conscious Sprague-Dawley rats with indwelling arterial and venous cannulas, insulin (0.3 U/kg) was injected iv, and responses of serum glucose concentrations and plasma levels of corticotropin (ACTH) and catechols (including epinephrine, EPI; norepinephrine, NE; dihydroxyphenylalanine, DOPA; dihydroxyphenylglycol, DHPG; and dihydroxyphenylacetic acid, DOPAC) were assessed, with or without pretreatment with anti-CRH immune serum (0.5 or 1.0 ml iv or 10 mul icv) or alpha-helical h/r CRH9-41, (130 nmol iv or 13 nmol icv). Responses to insulin (1.0 U/kg iv) were also measured in conscious juvenile Lewis and Fischer 344/N rats. Insulin-induced hypoglycemia markedly increased plasma levels of EPI and ACTH in all groups. Pretreatment iv with 1.0 ml of anti-CRH immune serum blocked the ACTH response to insulin but failed to attenuate the EPI response. Alpha-helical h/r CRH9-41, whether given iv or icv, failed to alter ACTH or EPI responses to insulin, although the antagonist did block EPI responses to icv CRH. Hypoglycemia elicited similar increments in ACTH levels in Lewis rats and Fischer 344/N control rats; and although Lewis rats had lower baseline EPI and smaller responses of NE, DHPG, DOPA, and DOPAC levels, the groups did not differ in proportionate increments in EPI levels. The results indicate that the ACTH response to hypoglycemia depends on availability of CRH outside the blood-brain barrier-presumably in the pituitary gland. The findings with icv alpha-helical h/r CRH9-41 can be explained by failure of the antagonist to reach effective concentrations at central sites of action of endogenous CRH, or by mechanisms other than CRH release determining the adrenomedullary response to hypoglycemia. Lewis rats seem to have less adrenomedullary secretion at baseline and smaller responses of NE synthesis and release during hypoglycemia than do Fischer 344/N rats. Neurochemical evidence for differential adrenomedullary and sympathoneural responses during hypoglycemia in all three rat strains is inconsistent with Cannon's view of a functionally unitary sympathoadrenal system. Since Lewis and Fischer 344/N rats had similar proportionate responses of both ACTH and EPI levels during hypoglycemia, either Lewis rats have deficient CRH responses to some stressors but not to others, or else pituitary-adrenocortical and adrenomedullary responses in this setting depend on mechanisms other than CRH release in the brain. Both explanations are inconsistent with the doctrine of non-specificity, the main tenet of Selye's stress theory.
C1 BEILINSON MED CTR,DEPT MED,IL-49100 PETAH TIQWA,ISRAEL.
   NATL INST PSYCHIAT & NEUROL,EXPTL MED LAB,BUDAPEST,HUNGARY.
   EGIS PHARMACEUT,DEPT PHARMACOL,BUDAPEST,HUNGARY.
   NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892.
   NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892.
   NHLBI,HYPERTENS ENDOCRINE BRANCH,BETHESDA,MD 20892.
   ACAD ZIEKENHUIS LEIDEN,DEPT NEPHROL,LEIDEN,NETHERLANDS.
RP GOLDSTEIN, DS (reprint author), NINCDS,CLIN NEUROSCI BRANCH,BLDG 10,ROOM SN262,BETHESDA,MD 20892, USA.
NR 50
TC 28
Z9 28
U1 0
U2 0
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL
SN 0953-8194
J9 J NEUROENDOCRINOL
JI J. Neuroendocrinol.
PD OCT
PY 1993
VL 5
IS 5
BP 475
EP 486
DI 10.1111/j.1365-2826.1993.tb00511.x
PG 12
WC Endocrinology & Metabolism; Neurosciences
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA LZ751
UT WOS:A1993LZ75100002
PM 8680414
ER

PT J
AU AGUILERA, G
   KISS, A
AF AGUILERA, G
   KISS, A
TI ACTIVATION OF MAGNOCELLULAR VASOPRESSIN RESPONSES TO NONOSMOTIC STRESS
   AFTER CHRONIC ADRENAL DEMEDULLATION IN RATS
SO JOURNAL OF NEUROENDOCRINOLOGY
LA English
DT Article
DE VASOPRESSIN; HYPOTHALAMUS; ADRENAL MEDULLA; STRESS
ID CORTICOTROPIN-RELEASING-FACTOR; AUTORADIOGRAPHIC IDENTIFICATION;
   ALPHA-1-ADRENERGIC RECEPTORS; FACTOR NEURONS; PITUITARY; SECRETION;
   LOCALIZATION; ADRENOCORTICOTROPIN; IMMOBILIZATION; DEXAMETHASONE
AB Increases in plasma VP in response to osmotic stimulation are critical for water conservation, while VP released into the pituitary portal circulation is an important regulator of ACTH secretion and does not contribute to plasma VP levels. The role of the adrenal medulla in the specificity of these responses was studied in rats subjected to osmotic and non-osmotic stress two months following adrenal demedullation or sham operation. Basal and stimulated plasma corticosterone, aldosterone, ACTH and PRA levels in adrenal demedullated rats were similar to those in the sham operated groups indicating recovery of adrenocortical function. Basal plasma VP levels were similar in sham operated controls and adrenal demedullated rats (0.93+/-0.13 and 1.0+/-0.1 pg/ml, respectively) and rose to comparable levels in both groups following 48 h osmotic stimulation by water deprivation (14.4+/-1.3 and 20.7+/-3.4, respectively). On the other hand, while in sham operated rats, immobilization for 15 min, a non-osmotic stress, had no effect on plasma VP levels in control or water deprived (2.0+/-0.9 and 15.0+/-2.7 pg/ml), in adrenal demedullated rats, caused dramatic increases in plasma VP from 1.0+/-0.1 to 126.0+/-29.9 pg/ml in controls, and from 20.7+/-3.4 to 155+/-37 pg/ml in water deprived rats. Intraperitoneal hypertonic saline injection, a combination of osmotic and painful stress, caused much higher increases in plasma VP in adrenal demedullated rats (138.0+/-22.1 compared with 34.7+/-3.7 pg/ml in sham operated rats). Water deprivation potentiated this response to 70.0+/-8.3 and 295+/-24 pg/ml in sham operated and adrenal demedullated rats, respectively. VP mRNA measured by in situ hybridization, and irVP measured by immunohistochemistry, were elevated in magnocellular neurones in the hypothalamus of adrenal demedullated rats. The demonstration of marked plasma VP responses to non-osmotic stimuli in adrenal demedullated rats, suggests a modulatory role for the adrenal medulla in the specificity of the secretory responses of the magnocellular and parvicellular vasopressinergic systems.
RP AGUILERA, G (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, ENDOCRINE PHYSIOL SECT, BLDG 10, RM 10N262, BETHESDA, MD 20892 USA.
NR 35
TC 8
Z9 8
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-8194
J9 J NEUROENDOCRINOL
JI J. Neuroendocrinol.
PD OCT
PY 1993
VL 5
IS 5
BP 501
EP 507
DI 10.1111/j.1365-2826.1993.tb00514.x
PG 7
WC Endocrinology & Metabolism; Neurosciences
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA LZ751
UT WOS:A1993LZ75100005
PM 8680417
ER

PT J
AU KORTE, M
   RAUSCHECKER, JP
AF KORTE, M
   RAUSCHECKER, JP
TI AUDITORY SPATIAL TUNING OF CORTICAL-NEURONS IS SHARPENED IN CATS WITH
   EARLY BLINDNESS
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Note
ID ANTERIOR ECTOSYLVIAN SULCUS; SUPERIOR COLLICULUS; CORTEX; FIELD;
   SENSITIVITY; LOCATION; AREA
AB 1. The specificity for the location of a sound source in azimuth was measured in single neurons of the anterior ectosylvian (AE) region of the cat's cortex, which includes the anterior auditory field (AAF) and the anterior ectosylvian auditory field (AEA).
   2. The influence of visual experience on auditory spatial tuning of these neurons was determined by comparing responses in cats with binocular deprivation from birth with those in normal control cats.
   3. Spatial tuning was measured under near free-field conditions by presenting broadband sounds through a speaker in seven different azimuthal locations, from -60 to +60-degrees at 20-degrees intervals. Elevation was constant at the cats' ears.
   4. In normal cats, a little over one-half of the neurons in the AE region (82/146 = 56%) showed some degree of azimuthal spatial tuning, as defined by at least a 2:1 ratio of responses between best and worst location. The rest (44%) were omnidirectional.
   5. In binocularly deprived cats, a significantly higher proportion (70/82 = 86%) of the neurons in the AE region were spatially tuned. Only 14% were omnidirectional. Median spatial tuning width was significantly sharper than in normal cats.
   6. We conclude that visual deprivation from birth induces intermodal changes that enhance the response specificity of neurons in the auditory cortex. These modifications may constitute the neural basis of behavioral compensation for early blindness.
C1 NIMH,NEUROPHYSIOL LAB,UNIT NEUROETHOL,POB 608,POOLESVILLE,MD 20837.
   MAX PLANCK INST BIOL CYBERNET,W-7400 TUBINGEN,GERMANY.
RI Rauschecker, Josef/A-4120-2013
NR 17
TC 95
Z9 97
U1 0
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-3077
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD OCT
PY 1993
VL 70
IS 4
BP 1717
EP 1721
PG 5
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA MC013
UT WOS:A1993MC01300042
PM 8283227
ER

PT J
AU RAUSCHECKER, JP
   KORTE, M
AF RAUSCHECKER, JP
   KORTE, M
TI AUDITORY COMPENSATION FOR EARLY BLINDNESS IN CAT CEREBRAL-CORTEX
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE CROSS-MODAL PLASTICITY; VISUAL DEPRIVATION; SENSORY COMPENSATION;
   MULTIMODAL PROCESSING; ANTERIOR ECTOSYLVIAN CORTEX
ID ANTERIOR ECTOSYLVIAN SULCUS; SUPRASYLVIAN VISUAL-CORTEX; SUPERIOR
   COLLICULUS; SOMATOSENSORY CORTEX; HEBB SYNAPSES; FIELD; AREA;
   ORGANIZATION; CONNECTIONS; DEPRIVATION
AB Single-neuron activity was recorded in the caudal part of the anterior ectosylvian (AE) cortex of cats that had been deprived of vision for several years by means of binocular lid suture shortly after birth and in normal control animals. Over 300 neurons were tested in each group with auditory, visual, and somatosensory stimuli.
   We confirmed the existence of an anterior ectosylvian visual area (AEV) in the fundus and ventral bank of the AE sulcus. Neurons in AEV had purely visual responses in normal cats. In visually deprived cats, by contrast, only a minority of cells in this area still responded to visual stimulation. Instead, most cells reacted vigorously to auditory and, to some extent, somatosensory stimuli. The few remaining visual neurons were also driven by auditory or somatosensory stimuli. No increase in the number of unresponsive neurons was found. It appears, therefore, that a cortical region that normally represents visual activity can become driven by auditory or somatosensory activity as a result of visual deprivation. Our results imply that early blindness causes compensatory increases in the amount of auditory cortical representation, possibly by an expansion of nonvisual areas into previously visual territory. In particular, they provide evidence for the existence of neural mechanisms for intermodal compensatory plasticity in the cerebral cortex of young animals. The changes described here may also provide the neural basis for a behavioral compensation for early blindness described elsewhere.
C1 MAX PLANCK INST BIOL CYBERNET,W-7400 TUBINGEN,GERMANY.
RP RAUSCHECKER, JP (reprint author), NIMH,NEUROPHYSIOL LAB,POB 608,POOLESVILLE,MD 20837, USA.
RI Rauschecker, Josef/A-4120-2013
NR 56
TC 159
Z9 160
U1 0
U2 4
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD OCT
PY 1993
VL 13
IS 10
BP 4538
EP 4548
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA MB164
UT WOS:A1993MB16400035
PM 8410202
ER

PT J
AU MURRAY, EA
   GAFFAN, D
   MISHKIN, M
AF MURRAY, EA
   GAFFAN, D
   MISHKIN, M
TI NEURAL SUBSTRATES OF VISUAL STIMULUS STIMULUS ASSOCIATION IN
   RHESUS-MONKEYS
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE MEMORY; AMYGDALA; HIPPOCAMPUS; ENTORHINAL CORTEX; PERIRHINAL CORTEX;
   AMNESIA
ID FORNIX TRANSECTION; HIPPOCAMPAL-FORMATION; MEMORY; AMYGDALA; CORTEX;
   REWARD; DISCONNECTION; RECOGNITION; DEFICITS; AMNESIA
AB Rhesus monkeys learned 10 visual stimulus-stimulus association, or paired associates. They then received bilateral removals of either the amygdaloid complex and underlying cortex, the hippocampal formation and underlying cortex, or both combined, or they were retained as unoperated controls. After surgery or rest, the monkeys were tested for their retention of the preoperatively learned set of paired associates, as well as for their ability to learn new associations of the same type. Both unoperated controls and hippocampectomized monkeys relearned the preoperatively trained set of paired associates almost immediately. By contrast, monkeys with amygdala removals were moderately retarded in relearning, and monkeys with combined amygdala and hippocampal ablations were severely retarded. When confronted with new sets of visual stimuli, monkeys with amygdala removals or hippocampal removals learned new sets of paired associates at the same rate as the controls, whereas monkeys with the combined ablation were again profoundly retarded. Only one monkey with the combined lesion was able to learn new stimulus-stimulus associations to criterion, and then only after extensive training, despite the ability of all three animals in this group to perform delayed matching-to-sample with the same stimuli and the same intratrial delays as those used in the paired associate task. At the end of the main experiment, two of the unoperated controls received bilateral ablations of the rhinal cortex. These monkeys showed the same level of difficulty in learning new paired associates as the animals in the main experiment that had received the combined amygdala plus hippocampal ablations. The results implicate the medial temporal lobe, and particularly the rhinal cortex, in the formation of stimulus-stimulus associative memories.
C1 UNIV OXFORD,DEPT EXPTL PSYCHOL,OXFORD,ENGLAND.
RP MURRAY, EA (reprint author), NIMH,NEUROPHYSIOL LAB,BLDG 49,ROOM 1B80,BETHESDA,MD 20892, USA.
OI Murray, Elisabeth/0000-0003-1450-1642
NR 27
TC 236
Z9 237
U1 1
U2 5
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD OCT
PY 1993
VL 13
IS 10
BP 4549
EP 4561
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA MB164
UT WOS:A1993MB16400036
PM 8410203
ER

PT J
AU KUNWAR, S
   PAI, LH
   PASTAN, I
AF KUNWAR, S
   PAI, LH
   PASTAN, I
TI CYTOTOXICITY AND ANTITUMOR EFFECTS OF GROWTH FACTOR-TOXIN FUSION
   PROTEINS ON HUMAN GLIOBLASTOMA-MULTIFORME CELLS
SO JOURNAL OF NEUROSURGERY
LA English
DT Article
DE GLIOBLASTOMA MULTIFORME; GROWTH FACTOR; PSEUDOMONAS EXOTOXIN-A;
   CYTOTOXICITY; BRAIN NEOPLASM
ID PSEUDOMONAS EXOTOXIN-A; HUMAN-MALIGNANT GLIOMA; FACTOR RECEPTORS;
   BRAIN-TUMORS; FACTOR-I; CHIMERIC TOXINS; FACTOR-ALPHA; INSULIN;
   EXPRESSION; ANTIBODY
AB The prognosis of glioblastoma multiforme remains poor despite advances in treatment by surgery, irradiation, and chemotherapy. Many malignant gliomas overexpress growth factor receptors. The possibility of targeting these receptors with selective cytotoxic molecules constructed by fusing deoxyribonucleic acid (DNA)-encoding mutant forms of Pseudomonas exotoxin A (PE) with complementary DNA-encoding growth factors was investigated. Several recombinant toxins have been produced, including those in which transforming growth factor (TGF)-alpha, insulin-like growth factor (IGF)-I, and acidic fibroblast growth factor (FGF) were fused to mutant forms of PE lacking the native cell-binding domain. These recombinant proteins are cytotoxic to cells that express specific cell-surface receptors. The cytotoxic activity of TGF-alpha, IGF-I, and acidic FGF chimeric toxins was tested in vitro against human glioblastoma cell lines. Each recombinant toxin exhibited potent and specific killing of cells. The TGF-alpha-PE40 construct was cytotoxic to seven of the eight cell lines and was active at concentrations as low as 0.5 ng/ml (1.1 x 10(-11) M). The acidic FGF-PE40 toxin was also active on seven of the eight cell lines but was 50-fold less active than the TGF-alpha-PE40. The IGF-I-PE40 construct was active on only two cell lines. To determine the possible therapeutic effect in animal TGF-alpha-PE40 was administered to nude mice bearing subcutaneous human glioblastoma xenografts. The animals were treated for 7 days via a continuous infusion pump placed in the peritoneal cavity. A constant serum level of TGF-alpha-PE40 was achieved that was nontoxic to the mice yet caused a reduction in tumor volume and retarded growth beyond the treatment period. The overexpression of the epidemal growth factor receptor in glioblastomas multiforme and the potency and specificity of the TGF-alpha-PE40 construct designed to target this receptor suggests that TGF-alpha-PE40 has the potential to be an effective antitumor agent for the adjuvant therapy of these carcinomas.
C1 NCI,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,37-4E16,BETHESDA,MD 20892.
NR 41
TC 41
Z9 41
U1 0
U2 1
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI CHARLOTTESVILLE
PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903
SN 0022-3085
J9 J NEUROSURG
JI J. Neurosurg.
PD OCT
PY 1993
VL 79
IS 4
BP 569
EP 576
DI 10.3171/jns.1993.79.4.0569
PG 8
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA LZ628
UT WOS:A1993LZ62800014
PM 7692018
ER

PT J
AU SHENKER, A
   WEINSTEIN, LS
   MORAN, A
   PESCOVITZ, OH
   CHAREST, NJ
   BONEY, CM
   VANWYK, JJ
   MERINO, MJ
   FEUILLAN, PP
   SPIEGEL, AM
AF SHENKER, A
   WEINSTEIN, LS
   MORAN, A
   PESCOVITZ, OH
   CHAREST, NJ
   BONEY, CM
   VANWYK, JJ
   MERINO, MJ
   FEUILLAN, PP
   SPIEGEL, AM
TI SEVERE ENDOCRINE AND NONENDOCRINE MANIFESTATIONS OF THE MCCUNE-ALBRIGHT
   SYNDROME-ASSOCIATED WITH ACTIVATING MUTATIONS OF STIMULATORY G-PROTEIN
   G(S)
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID POLYOSTOTIC FIBROUS DYSPLASIA; CYCLIC-AMP; ALPHA-SUBUNIT; CUSHING
   SYNDROME; PLASMA-MEMBRANE; CELLS; MECHANISM; DIFFERENTIATION;
   HYPERTHYROIDISM; DEGRADATION
AB McCune-Albright syndrome (MCAS) is a sporadic disease classically including polyostotic fibrous dysplasia, cafe au lait spots, sexual precocity, and other hyperfunctional endocrinopathies. An activating missense mutation in the gene for the alpha subunit of G(s), the G protein that stimulates cyclic adenosine monophosphate formation, has been reported to be present in these patients. The mutation is found in variable abundance in different affected endocrine and nonendocrine tissues, consistent with the mosaic distribution of abnormal cells generated by a somatic cell mutation early in embryogenesis. We describe three patients with MCAS who had profound endocrine and nonendocrine-disease and who died in childhood. Two of the patients were severely ill neonates whose complex symptoms did not immediately suggest MCAS. A mutation of residue Arg201 of G(s)alpha was found in affected tissues from all three children. A review of the literature and unpublished case histories emphasizes the existence of other patients with severe and unusual clinical manifestations. We conclude that the manifestations of MCAS are more extensive than is generally appreciated, and may include hepatobiliary disease, cardiac disease, other nonendocrine abnormalities, and sudden or premature death.
C1 NCI, PATHOL LAB, BETHESDA, MD 20892 USA.
   NICHHD, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA.
   UNIV MINNESOTA, DEPT PEDIAT, MINNEAPOLIS, MN 55455 USA.
   UNIV N CAROLINA, DEPT PEDIAT, CHAPEL HILL, NC 27514 USA.
   INDIANA UNIV, SCH MED, DEPT PEDIAT, INDIANAPOLIS, IN 46202 USA.
   YALE UNIV, SCH MED, DEPT PEDIAT, NEW HAVEN, CT 06510 USA.
RP SHENKER, A (reprint author), NIDDKD, MOLEC PATHOPHYSIOL BRANCH, ROOM 8C-101, BLDG 10, BETHESDA, MD 20892 USA.
RI Weinstein, Lee/I-5575-2015
NR 65
TC 185
Z9 191
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
EI 1097-6833
J9 J PEDIATR-US
JI J. Pediatr.
PD OCT
PY 1993
VL 123
IS 4
BP 509
EP 518
DI 10.1016/S0022-3476(05)80943-6
PG 10
WC Pediatrics
SC Pediatrics
GA MA725
UT WOS:A1993MA72500002
PM 8410501
ER

PT J
AU POWERS, WF
   CLEMENS, JD
AF POWERS, WF
   CLEMENS, JD
TI PROGNOSTIC IMPLICATIONS OF AGE AT DETECTION OF AIR LEAK IN
   VERY-LOW-BIRTH-WEIGHT INFANTS REQUIRING VENTILATORY SUPPORT
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID CHRONIC LUNG-DISEASE; BRONCHOPULMONARY DYSPLASIA; OUTCOMES
AB Study objective: To measure the association between the development of air leak (pneumothorax or pulmonary interstitial emphysema) during the first 27 postnatal days and neonatal death or chronic lung disease, as determined on day 28, among very low birth weight infants who required mechanical ventilation from the first day of life.
   Design: Prospective, multicenter cohort study.
   Patients: Two hundred sixty inborn, very low birth weight (504 to 1500 gm) infants given ventilatory support from the first day of life.
   Results: The risk of an adverse outcome (death or chronic lung disease) changed with postnatal age at the time of diagnosis of the air leak. The association between air leak and an adverse outcome, as measured by gestational age-adjusted odds ratio (95% confidence interval), was 13.9 (i.7 to 114.6) for those in whom an air leak developed on day 0 or 1 (early), decreased to 1.7 (0.7 to 4.1) for those whose air leak developed on day 2 or 3 (intermediate), and increased to 16.6 (2.1 to 130.4) for those whose air leak developed on days 4 to 27 (late). The association with neonatal death showed even more striking fluctuations with postnatal age at occurrence of an air leak, ranging from an odds ratio of 40.3 (3.5 to 464.8) for the early group to 7.5 (2.3 to 25.0) for the intermediate group and 78.3 (6.9 to 889.5) for the late group.
   Conclusions: Air leak in newborn infants requiring mechanical ventilation is associated with increased risks of death or future morbidity, but the magnitude of these risks changes with postnatal age at the time of diagnosis of the air leak. Failure to consider the age at which the air leak is detected may miss changes in its prognostic implications and may partly explain inconsistent results in previous studies.
C1 NICHHD, DIV EPIDEMIOL STAT & PREVENT RES, BETHESDA, MD 20892 USA.
NR 21
TC 19
Z9 21
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
EI 1097-6833
J9 J PEDIATR-US
JI J. Pediatr.
PD OCT
PY 1993
VL 123
IS 4
BP 611
EP 617
DI 10.1016/S0022-3476(05)80964-3
PG 7
WC Pediatrics
SC Pediatrics
GA MA725
UT WOS:A1993MA72500022
PM 8410519
ER

PT J
AU PAYZA, K
   AKAR, CA
   YANG, HYT
AF PAYZA, K
   AKAR, CA
   YANG, HYT
TI NEUROPEPTIDE FF RECEPTORS - STRUCTURE-ACTIVITY RELATIONSHIP AND EFFECT
   OF MORPHINE
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID RAT SPINAL-CORD; STRESS-INDUCED ANALGESIA; MODULATING PEPTIDE;
   INHIBITORY INFLUENCES; BRAIN; FMRFAMIDE; FLFQPQRFAMIDE; BINDING;
   FLFQPQRF-NH2; NOCICEPTION
AB Neuropeptide FF (FLFQPQRFamide, NPFF) is an octapeptide implicated in morphine analgesia, tolerance and dependence. Many of the behavioral effects of NPFF have also been observed with the invertebrate neuropeptide Phe-Met-Arg-Phe-amide (FMRFamide), which binds to NPFF receptors because of its low homology to the C-terminal portion of NPFF. A competitive ligand binding assay was used to characterize NPFF receptors in rat spinal cord and a strong requirement was found for the C-terminal Arg-Phe-amide. It was found that FMRFamide (K(i):= 1.8 nM) bound with lower affinity than NPFF (0.26 nM) but it was about 7-fold more potent than PQRFamide (12 nM). This finding explains the similar bioactivities of NPFF and FMRFamide. The Gln2 appeared to be the cause of the relatively low potency of PQRFamide, based on the binding specificity of NPFF receptors for a series of FMRFamide analogs. In contrast to the Arg-Pheamide, substitutions at the first and second positions of FMRFamide were generally tolerated, with the most potent analogs being PMRFamide (K(i) = 0.54 nM), FFRFamide (0.25 nM) and FWRFamide (0.42 nM). Among the most potent ligands was a pentapeptide containing a photoreactive Phe analog, D-Tyr-(p-benzoyl-Phe)-norLeu-Arg-Phe-amide K(i) = 0.23 nM). It was found that dansyl-PQRFamide and dansyl-RFamide also bound to NPFF receptors with K(i) values of 6.1 and 73 nM, respectively. The radioligand binding and G-protein coupling of NPFF receptors were not altered by chronic morphine treatment.
RP PAYZA, K (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,BIOCHEM GENET LAB,NEUROPEPTIDES SECT,WASHINGTON,DC 20032, USA.
NR 34
TC 50
Z9 50
U1 0
U2 2
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 1993
VL 267
IS 1
BP 88
EP 94
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA MD942
UT WOS:A1993MD94200012
PM 8229791
ER

PT J
AU IZENWASSER, S
   BUZAS, B
   COX, BM
AF IZENWASSER, S
   BUZAS, B
   COX, BM
TI DIFFERENTIAL REGULATION OF ADENYLYL-CYCLASE ACTIVITY BY MU AND DELTA
   OPIOIDS IN RAT CAUDATE-PUTAMEN AND NUCLEUS-ACCUMBENS
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID RECEPTOR-MEDIATED INHIBITION; ADENOSINE 3'-5'-CYCLIC MONOPHOSPHATE;
   CHRONIC OPIATE-REGULATION; BRAIN MEMBRANES; POSSIBLE INVOLVEMENT;
   BETA-FUNALTREXAMINE; E PROSTAGLANDINS; PRIMARY CULTURES;
   CROSS-TOLERANCE; NG108-15 CELLS
AB The regulation of adenylyl cyclase by opioid receptor types was characterized in the rat nucleus accumbens, a brain region that is involved in the reinforcing effects of drugs of abuse, and in the caudate putamen, a region not implicated in drug reinforcement. Both mu and delta opioid ligands inhibited adenylyl cyclase activity in the nucleus accumbens and in the caudate putamen of rat, whereas the kappa agonist, U69,593 (5alpha,7alpha,8alpha)-(+)-N-methyl-N-[7-(1-(pyrrolidinyl)-1-oxaspiro[4,5]dec-8-yl]-benzeneacetamide, was ineffective. The mu agonists, DAMGO and Tyr-D-Arg-Phe-Sar, were more potent inhibitors of the enzyme in caudate putamen than in nucleus accumbens. The delta-selective agonists, DSLET and [D-Ala2]-deltorphin II more potently inhibited adenylyl cyclase in nucleus accumbens than in caudate putamen. Inhibition of the enzyme by DAMGO and Tyr-D-Arg-Phe-Sar was antagonized by the mu-selective competitive antagonist, CTOP D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2, and the noncompetitive mu antagonists, beta-funaltrexamine and naloxonazine. Inhibition of adenylyl cyclase activity by the delta-selective ligands, DPDPE, DSLET and [D-Ala2]-deltorphin II was unaffected by these antagonists. Conversely, the de/ta-selective antagonists, ICI 174,864 N-allyl2-Tyr-(alpha-aminisobutyric acid)2-Phe-Leu-OH and naltrindole, blocked the effects of the delta but not the mu opioid ligands. Adenylyl cyclase activity in nucleus accumbens and in caudate putamen is subject to regulation by both mu and delta opioid receptors.
C1 UNIFORMED SERV UNIV HLTH SCI,DEPT PHARMACOL,BETHESDA,MD 20814.
RP IZENWASSER, S (reprint author), NIDA,ADDICT RES CTR,PSYCHOBIOL SECT,PO 5180,BALTIMORE,MD 21224, USA.
RI Izenwasser, Sari/G-9193-2012
FU NIDA NIH HHS [DA 03102]
NR 41
TC 34
Z9 34
U1 0
U2 1
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 1993
VL 267
IS 1
BP 145
EP 152
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA MD942
UT WOS:A1993MD94200021
PM 7901389
ER

PT J
AU TELLA, SR
   SCHINDLER, CW
   GOLDBERG, SR
AF TELLA, SR
   SCHINDLER, CW
   GOLDBERG, SR
TI COCAINE - CARDIOVASCULAR EFFECTS IN RELATION TO INHIBITION OF PERIPHERAL
   NEURONAL MONOAMINE UPTAKE AND CENTRAL STIMULATION OF THE SYMPATHOADRENAL
   SYSTEM
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID CONSCIOUS SQUIRREL-MONKEYS; CENTRAL-NERVOUS-SYSTEM; RATS;
   NOREPINEPHRINE; MECHANISMS; ABUSE; DOGS; DESIPRAMINE; RESPONSES; RELEASE
AB Cocaine (0.03-5.6 mg/kg i.v.) produced a dose-dependent and prolonged increase in mean arterial blood pressure and heart rate in conscious rats. The 0.3 and 1 mg/kg doses of cocaine potentiated the pressor response to exogenous norepinephrine (0.2 mug/kg), whereas lower (0.03 and 0.1 mg/kg) and higher (3 and 5.6 mg/kg) doses were ineffective. Desipramine (0.03-1 mg/kg), a prototype norepinephrine uptake blocker, did not alter blood pressure or heart rate. Nisoxetine (0.01 -1 mg/kg), another norepinephrine selective uptake blocker, produced a small and brief (<5 min) pressor response, but no tachycardiac response. Unlike cocaine, both desipramine and nisoxetine produced a dose-dependent potentiation of the pressor response to norepinephrine with the maximal potentiation exceeding that of cocaine. Plasma norepinephrine and epinephrine levels were increased by cocaine (3 mg/kg), but not by nisoxetine (1 mg/kg). Chemical sympathectomy by 6-hydroxydopamine selectively antagonized cocaine-induced increases in both blood pressure and plasma norepinephrine levels, but did not alter cocaine-induced increases in heart rate or plasma epinephrine levels; the converse was the case with adrenal demedullation. Both the combination of chemical sympathectomy and adrenal demedullation and pretreatment with chlorisondamine (10 mg/kg) antagonized cocaine-induced pressor and tachycardiac effects and cocaine-induced increases in plasma epinephrine and norepinephrine levels. In the control group, cocaine (3 mg/kg) produced a biphasic increase in blood pressure consisting of an early peak increase of 52 +/- 2.5 mm Hg 15 sec after its injection followed by a quick and partial recovery to an increase of 20.5 +/- 3.3 mm Hg at 1 min which gradually declined to base-line values in about 30 min. Prazosin (1 mg/kg) pretreatment decreased the magnitude of the initial peak pressor response produced by cocaine and reversed the sustained pressor response to cocaine to a depressor response; the reversal of the pressor response to cocaine to a depressor response by prazosin was not seen after erythro-dl-1-(7-methylindan-4-yloxy)-3-isopropylaminobutan-2-ol (ICI 118,551) (3 mg/kg) treatment or adrenal demedullation. Treatment with ICI 118,551 alone enhanced the magnitude of the sustained phase of the pressor response to cocaine. These results indicate that inhibition of peripheral sympathetic neuronal amine uptake mechanism by cocaine is not critical for initiating its pressor, tachycardiac and plasma catecholamine increasing effects in conscious rats and that central stimulation of sympathoadrenal neural axis activity plays an important role in these effects. The data further suggest that peak pressor effects of cocaine are mediated by norepinephrine of sympathetic neural origin and peak tachycardiac effects of cocaine are mediated by epinephrine of adrenal medullary origin. Cocaine also produces a beta-2 adrenoceptor-mediated depressor response through the release of epinephrine from the adrenal medulla which in turn modulates its alpha-1 adrenoceptor-mediated pressor response.
RP TELLA, SR (reprint author), NIDA,ADDICT RES CTR,PRECLIN PHARMACOL LAB,BEHAV PHARMACOL & GENET SECT,POB 5180,BALTIMORE,MD 21224, USA.
NR 57
TC 46
Z9 47
U1 3
U2 6
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 1993
VL 267
IS 1
BP 153
EP 162
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA MD942
UT WOS:A1993MD94200022
PM 8229742
ER

PT J
AU COTE, TE
   IZENWASSER, S
   WEEMS, HB
AF COTE, TE
   IZENWASSER, S
   WEEMS, HB
TI NALTREXONE-INDUCED UP-REGULATION OF MU-OPIOID RECEPTORS ON 7315C CELL
   AND BRAIN MEMBRANES - ENHANCEMENT OF OPIOID EFFICACY IN INHIBITING
   ADENYLYL-CYCLASE
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID OPIATE RECEPTOR; UP-REGULATION; POTASSIUM CHANNELS; SUPER-SENSITIVITY;
   BINDING PROTEINS; ANTAGONIST; MORPHINE; NALOXONE; SYSTEMS; AGONIST
AB The effect of chronic naltrexone administration on the expression of mu opioid receptors on 7315c tumor cells was examined. Osmotic minipumps containing either saline or naltrexone were subcutaneously implanted into Buffalo rats that had been injected intraperitoneally with 7315c cells. Fourteen days after the pumps were implanted, 7315c tissue and brain tissue were removed and examined for their ability to bind      [H-3]DAMGO and to respond to morphine (or DAMGO) and guanosine 5'-O-(3-thiotriphosphate) in an adenylyl cyclase assay. Naltrexone treatment caused a doubling in the density of [H-3]DAMGO binding sites in both whole brain membranes and the 7315c cell membranes. Naltrexone treatment may have slightly diminished the affinity of mu opioid receptors for [H-3]DAMGO (by 1.5- to 2-fold), but the precision of the assay was inadequate to determine whether this difference was significant. Naltrexone treatment also had no effect on the potency or efficacy of guanosine 5'-O-(3-thiotriphosphate) in diminishing [H-3]DAMGO binding to either whole brain or 7315c cell membranes. The influence of naltrexone treatment on opioid inhibition of adenylyl cyclase activity was also investigated in both tissues. In 7315c membranes, naltrexone treatment caused a 40% increase in the efficacy (maximal effect) of morphine but had no effect on the potency (IC50) Of morphine in inhibiting forskolin-stimulated adenylyl cyclase activity. In whole brain membranes from control rats, DAMGO failed to affect significantly forskolin-stimulated adenylyl cyclase. However, in whole brain membranes from naltrexone-treated rats, DAMGO caused a 30% inhibition of forskolin-stimulated adenylyl cyclase activity. Finally, naltrexone had no effect on either the potency or efficacy of guanosine 5'-O-(3-thiotriphosphate) in inhibiting forskolin-stimulated adenylyl cyclase activity in either 7315c cell membranes or whole brain membranes.
C1 NIDA,ADDICT RES CTR,PSYCHOBIOL SECT,BALTIMORE,MD.
RP COTE, TE (reprint author), UNIFORMED SERV UNIV HLTH SCI,DEPT PHARMACOL,4301 JONES BRIDGE RD,BETHESDA,MD 20814, USA.
RI Izenwasser, Sari/G-9193-2012
NR 26
TC 21
Z9 23
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 1993
VL 267
IS 1
BP 238
EP 244
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA MD942
UT WOS:A1993MD94200033
PM 8229750
ER

PT J
AU WITKIN, JM
   NEWMAN, AH
   NOWAK, G
   KATZ, JL
AF WITKIN, JM
   NEWMAN, AH
   NOWAK, G
   KATZ, JL
TI ROLE OF DOPAMINE-D(1) RECEPTORS IN THE LETHAL EFFECTS OF COCAINE AND A
   QUATERNARY METHIODIDE ANALOG
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID SQUIRREL-MONKEYS; CARDIOVASCULAR FUNCTION; CONSCIOUS RATS; SCH 23390;
   ANTAGONIST; SCH-23390; AGONIST; INTOXICATION; BENZAZEPINE;
   METHAMPHETAMINE
AB Acute cocaine overdose can result in convulsions and death although the mechanisms associated with this toxicity are poorly understood. The role of D1 receptors in the central and peripheral actions in cocaine were investigated by comparisons of cocaine with the stable charged cocaine analog, cocaine methiodide. Both cocaine and cocaine methiodide produced dose-related increases in lethality in male, Swiss Webster mice, with cocaine methiodide being slightly more potent than cocaine; however, only cocaine produced convulsions. Several dopamine D1 antagonists ([R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tet-rahydro-1H-3-benzazephine] (SCH 23390), [(-)-trans-6,7,7a,8, 9,13b-hexahydro-3-chloro-2-hydroxy-N-methyl-5H-benzo-[d]naptho-{2-1-b}azepine (SCH 39166), 1-(2-bromo-4,5-dime-thoxybenzyl)-7-hydroxy-6-methoxy-2-methyl-1,2,3,4-tetrahy-droisoquinoline HBr (A-69024), [R-(+)-7-bromo-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine] (SK F83566)) produced dose-dependent protection against the lethal effects of both compounds. Protection against cocaine methiodide-induced lethality was conferred by lower doses of the D1 antagonists than those effective against cocaine. Stereoselectivity of this effect was demonstrated by the lack of activity of the inactive enantiomer of SCH 23390. The D2 antagonist haloperidol was ineffective against either cocaine- or cocaine methiodide-induced lethality. Lethal effects of the nondopaminergic local anesthetic, lidocaine, were not influenced by prior treatment with D1 antagonists. Lethal effects of cocaine were enhanced by both centrally and peripherally acting D1 agonists but not by the D2 agonist quinpirole. Cocaine methiodide-induced lethality was also enhanced by the peripherally active DA1 agonist, fenoldopam. These results establish an important role for D1 but not D2 receptors in the lethal effects of acutely administered cocaine and suggest that peripheral loci may be one pathophysiological target.
C1 NIDA,ADDICT RES CTR,PSYCHOBIOL SECT,BALTIMORE,MD 21224.
   NIDDKD,NEUROSCI LAB,BETHESDA,MD.
RP WITKIN, JM (reprint author), NIDA,ADDICT RES CTR,DRUG DEV GRP,POB 5180,BALTIMORE,MD 21224, USA.
NR 54
TC 31
Z9 31
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 1993
VL 267
IS 1
BP 266
EP 274
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA MD942
UT WOS:A1993MD94200037
PM 7901394
ER

PT J
AU WALKER, EA
   BUTELMAN, ER
   DECOSTA, BR
   WOODS, JH
AF WALKER, EA
   BUTELMAN, ER
   DECOSTA, BR
   WOODS, JH
TI OPIOID THERMAL ANTINOCICEPTION IN RHESUS-MONKEYS - RECEPTOR MECHANISMS
   AND TEMPERATURE DEPENDENCY
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID APPARENT PA2 ANALYSIS; ANTAGONISTIC ACTIONS; NOR-BINALTORPHIMINE;
   MORPHINE; AGONIST; DIFFERENTIATION; PIGEONS; SALINE
AB The antinociceptive effects of the opioid agonists etonitazene and alfentanil, as well as the agonist/antagonists nalbuphine, [(1)-beta-2'-hydroxy-2,9-dimethyl-5-phenyl-6,7-benzomorphan (GPA 1657)] and profadol were studied in the warm water (48-degrees and 55-degrees-C) tail-withdrawal assay in rhesus monkeys. Etonitazene and alfentanil produced dose-dependent increases in tail-withdrawal latency up to the maximum possible latency of 20 sec in 48-degrees- and 55-degrees-C water. Nalbuphine, GPA 1657 and profadol produced the maximum possible effect only at 48-degrees-C, and were ineffective at 55-degrees-C. The opioid antagonist quadazocine produced a dose-dependent antagonism of all agonists except profadol. In a Schild plot analysis, apparent pA2 values for quadazocine with alfentanil, etonitazene and nalbuphine were homogeneous (7.3-7.7 mol/kg), suggesting their effects were probably mediated by mu opioid receptors. The apparent pA2 value for GPA 1657 was significantly lower (6.2 mol/kg), suggesting GPA 1657 may have produced antinociception by a non mu receptor-mediated mechanism. The selective delta antagonist naltrindole (0.32-1.0 mg/kg) antagonized the antinociceptive effect of GPA 1657. The kappa-selective antagonist nor-binaltorphimine (nor-BNI, 3.2 mg/kg) caused a small rightward shift in the GPA 1657 dose-effect curve. Nalbuphine, GPA 1657 or profadol produced a rightward shift in the alfentanil dose-effect curve in 55-degrees-C water, consistent with possible low-efficacy mu agonist effects of these compounds. These studies suggest agonists may be differentiated based on antinociceptive effectiveness, receptor selectivity and intrinsic efficacy in the rhesus monkey tail-withdrawal procedure.
C1 UNIV MICHIGAN,DEPT PHARMACOL,ANN ARBOR,MI 48109.
   UNIV MICHIGAN,DEPT PSYCHOL,ANN ARBOR,MI 48109.
   NIDDK,BETHESDA,MD.
FU NIDA NIH HHS [DA00254]
NR 42
TC 81
Z9 81
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 1993
VL 267
IS 1
BP 280
EP 286
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA MD942
UT WOS:A1993MD94200039
PM 7901396
ER

PT J
AU PRESTON, KL
   SULLIVAN, JT
   BERGER, P
   BIGELOW, GE
AF PRESTON, KL
   SULLIVAN, JT
   BERGER, P
   BIGELOW, GE
TI EFFECTS OF COCAINE ALONE AND IN COMBINATION WITH MAZINDOL IN HUMAN
   COCAINE ABUSERS
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID DOPAMINE; BROMOCRIPTINE; ANORECTICS; MONKEYS
AB Mazindol is a catecholamine reuptake inhibitor that blocks binding of cocaine at the dopamine reuptake site. This study was conducted to determine whether the acute administration of mazindol modulates the pharmacological effects of intravenous cocaine in humans. In a crossover study, twelve acute drug conditions were tested in randomized order under double-blind, double-dummy conditions in eight cocaine abusers. Cocaine (0, 12.5, 25 and 50 mg, i.v.) was administered in combination with mazindol (0, 1 and 2 mg given orally 2 hr before the cocaine injection). Physiological and subject- and observer-rated responses were measured. Cocaine and mazindol alone both significantly increased heart rate and blood pressure. Cocaine increased ratings on stimulant-like subjective effect measures, including desire for cocaine; mazindol had mild, stimulant-like subjective effects. There were significant interactions between the effects of cocaine and mazindol on heart rate and blood pressure, with combinations producing significantly larger and more sustained increases compared with cocaine alone. There was no evidence that mazindol substantially altered the magnitude or profile of the subjective effects of cocaine, including cocaine-induced craving for cocaine. These results do not support the utility of acute administration of mazindol in the treatment of cocaine abusers through a mechanism of modulation of cocaine's subjective effects. Furthermore, mazindol treatment may increase the cardiovascular risks of cocaine.
C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205.
   JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205.
   UNIV CALIF SAN FRANCISCO,DEPT PSYCHIAT,SAN FRANCISCO,CA 94143.
RP PRESTON, KL (reprint author), NIDA,ADDICT RES CTR,CLIN TRIALS SECT,POB 5180,BALTIMORE,MD 21224, USA.
RI Preston, Kenzie/J-5830-2013
OI Preston, Kenzie/0000-0003-0603-2479
FU NIDA NIH HHS [DA-05196, DA-06120, K05 DA-00050]
NR 20
TC 62
Z9 63
U1 1
U2 1
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 1993
VL 267
IS 1
BP 296
EP 307
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA MD942
UT WOS:A1993MD94200041
PM 8229755
ER

PT J
AU VANDERAH, TW
   WILD, KD
   TAKEMORI, AE
   SULTANA, M
   PORTOGHESE, PS
   BOWEN, WD
   HRUBY, VJ
   MOSBERG, HI
   PORRECA, F
AF VANDERAH, TW
   WILD, KD
   TAKEMORI, AE
   SULTANA, M
   PORTOGHESE, PS
   BOWEN, WD
   HRUBY, VJ
   MOSBERG, HI
   PORRECA, F
TI MODULATION OF MORPHINE ANTINOCICEPTION BY SWIM-STRESS IN THE MOUSE -
   INVOLVEMENT OF SUPRASPINAL OPIOID DELTA(2) RECEPTORS
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID MU-MEDIATED ANTINOCICEPTION; BINDING-SITES; NALTRINDOLE
   5'-ISOTHIOCYANATE; DIFFERENTIAL ANTAGONISM; INDUCED ANALGESIA;
   KAPPA-AGONISTS; MICE; INVIVO; PEPTIDES; AFFINITY
AB The present study evaluated the effect of a brief exposure of mice to cold-water swim-stress (CWSS) on the antinociceptive potency of i.c.v. given morphine. No significant antinociceptive response could be demonstrated in the warm-water tail-flick test, 10 min after a 30-sec exposure of mice to water at 5-degrees-C. However, the i.c.v. morphine dose-response curve in mice exposed to CWSS was displaced significantly to the left when compared to that obtained in control (i.e., non-CWSS-exposed) mice. Although coadministration of the delta antagonist, N,N-diallyl-Tyr-Aib-Aib-Phe-Leu-OH 1 (ICI 174,864), with i.c.v. morphine did not produce antagonism of the antinociceptive action of this mu opiate, the leftward displacement of the i.c.v. morphine dose-response curve seen in CWSS-exposed mice was blocked in ICI 174,864-treated mice suggesting involvement of opioid delta receptors in the modulatory effect. Pretreatment of mice with the delta-1 antagonist, [D-Ala2, Leu5, Cys6] enkephalin, did not antagonize the antinociception of morphine and further did not antagonize the leftward displacement produced by exposure to CWSS. Pretreatment of mice with the delta-2 antagonist, 5'-isothiocyanate, also did not antagonize the antinociceptive effects of morphine but blocked the leftward displacement in the morphine dose-response curve associated with CWSS, suggesting involvement of an opioid delta-2 receptor in this effect. Pretreatment of mice with the mu antagonist, beta-funaltrexamine, produced a significant antagonism of the morphine antinociceptive effect as seen by a rightward displacement of the morphine dose-effect curve. Further, in these beta-funaltrexamine-pretreated mice, exposure to CWSS did not result in an enhancement of morphine potency. Finally, i.c.v. pretreatment of mice with antibodies raised against [Leu5]enkephalin, but not antibodies against [Met5]enkephalin, blocked the modulatory action produced by exposure to CWSS; both antibodies to [Met5]enkephalin or [Leu5]enkephalin did not alter the morphine response directly. These data suggest that modulation of morphine potency by exposure to CWSS involves activation of an opioid delta-2 receptor which may be functionally and/or physically associated with opioid mu receptors. Additionally, the modulatory action appears to be produced in the brain by release of a [Leu5] enkephalin-like molecule. Finally, these observations may provide, in part, a physiological basis for the observed increase in analgesic effectiveness of morphine in situations of stress.
C1 UNIV ARIZONA,ARIZONA HLTH SCI CTR,COLL MED,DEPT PHARMACOL,TUCSON,AZ 85724.
   UNIV ARIZONA,ARIZONA HLTH SCI CTR,DEPT CHEM,TUCSON,AZ 85724.
   UNIV MICHIGAN,COLL PHARM,ANN ARBOR,MI 48109.
   UNIV MINNESOTA,DEPT PHARMACOL,MINNEAPOLIS,MN 55455.
   UNIV MINNESOTA,DEPT MED CHEM,MINNEAPOLIS,MN 55455.
   NIDDKD,MED CHEM LAB,RECEPTOR BIOCHEM & PHARMACOL UNIT,BETHESDA,MD.
FU NIDA NIH HHS [DA 00118]
NR 46
TC 36
Z9 36
U1 1
U2 1
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 1993
VL 267
IS 1
BP 449
EP 455
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA MD942
UT WOS:A1993MD94200059
PM 8229774
ER

PT J
AU VYKLICKY, L
AF VYKLICKY, L
TI CALCIUM-MEDIATED MODULATION OF N-METHYL-D-ASPARTATE (NMDA) RESPONSES IN
   CULTURED RAT HIPPOCAMPAL-NEURONS
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Article
ID EXCITATORY AMINO-ACIDS; SPINAL-CORD NEURONS; RECEPTOR DESENSITIZATION;
   DIVALENT-CATIONS; ACTIVATION; GLYCINE; CHANNELS; VOLTAGE; CALPAIN;
   PHOSPHORYLATION
AB 1. Agonist-independent (inactivation) and agonist-induced (desensitization) refractory states of N-methyl-D-aspartate (NMDA) receptors were studied on cultured rat hippocampal neurones using whole-cell and inside-out patch-clamp techniques and a fast perfusion system.
   2. Shortly after whole-cell formation, application of 100 mum NMDA in the presence of 10 mum glycine and 0.2 mm [Ca2+]o induced membrane currents that desensitized by 23 %. Repeated application of NMDA at 30 s intervals resulted in a progressive increase in the degree and rate of onset of NMDA receptor desensitization.
   3. Test responses to NMDA recorded in the presence of 0.2 mm [Ca2+]o were reversibly inactivated by 60 % following a train of ten 1 s applications of NMDA delivered at 0.5 Hz in the presence of 2 mm [Ca2+]o; similar results were obtained with 2 mm [Sr2+]o and 2 mm [Ba2+]o. In the presence of Ca2+ or Sr2+, desensitization during the train of responses to NMDA increased by 14 and 19 % respectively, while with Ba2+ there was no increase in desensitization.
   4. In the presence of 0.2 mm [Ca2+]o at a holding potential of -60 mV, or in the presence of 2 mm [Ca2+]o at a holding potential of + 50 mV, a train of ten applications of NMDA failed to induce either inactivation or an increase in desensitization of test responses to NMDA. These results suggest an important role for [Ca2+]o in the induction of both inactivation and desensitization of NMDA receptors.
   5. Increasing the intracellular calcium concentration, [Ca2+]i, via repeated activation of voltage-gated Ca+ channels, resulted in a reversible inactivation of test responses to NMDA by 35 % but failed to increase desensitization. In neurones dialysed with intracellular solution containing 2-5 mm Ca2+ NMDA receptor desensitization was similar to that in neurones dialysed with 10 nm Ca2+.
   6. Block of NMDA receptor-channels by 2 MM [Mg2+]o during the train application of NMDA prevented the induction of both inactivation and desensitization. In contrast 3 mm [Mg2+]i was ineffective.
   7. The magnitude of both inactivation and desensitization of NMDA receptors was not affected by intracellular dialysis of ATP, the non-hydrolysable ATP analogue 5'-adenylylimido-diphosphate (AMP-PNP), different Ca2+ chelators (EGTA or BAPTA), the Ca2+-activated protease inhibitor (leupeptin), dithiothreitol, or the phosphatase inhibitors (okadaic acid and a calcineurin inhibitor).
   8. Application of 2.5 mM Ca2+ to the cytoplasmic side of inside-out patches induced inactivation of NMDA responses similar in magnitude to the inactivation seen in whole-cell recording. Complete recovery from inactivation was, however, much faster (20 s) for inside-out patches than for whole-cell responses (usually 5-10 min).
   9. These results suggest two distinct mechanisms for modulation of NMDA receptors by intracellular Ca2+. Desensitization of NMDA receptors is induced when both [Ca2+]i is increased and NMDA receptors activated by agonist. Inactivation of NMDA receptors is produced by increased levels of [Ca2+]i and does not require NMDA receptor activation for induction.
C1 NICHHD,CELLULAR & MOLEC NEUROPHYSIOL LAB,BETHESDA,MD 20892.
RP VYKLICKY, L (reprint author), ACAD SCI CZECH REPUBL,INST PHYSIOL,VIDENSKA 1083,CS-14220 PRAGUE 4,CZECHOSLOVAKIA.
RI Vyklicky, Ladislav/C-1851-2012
OI Vyklicky, Ladislav/0000-0002-0015-0098
NR 42
TC 91
Z9 92
U1 0
U2 2
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211
SN 0022-3751
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD OCT
PY 1993
VL 470
BP 575
EP 600
PG 26
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA MD558
UT WOS:A1993MD55800035
PM 8308745
ER

PT J
AU KNOX, SS
   FOLLMANN, D
AF KNOX, SS
   FOLLMANN, D
TI GENDER DIFFERENCES IN THE PSYCHOSOCIAL VARIANCE OF FRAMINGHAM AND
   BORTNER TYPE-A MEASURES
SO JOURNAL OF PSYCHOSOMATIC RESEARCH
LA English
DT Article
ID HEART-DISEASE; BEHAVIOR; SCALE
AB The object of the present study was to determine whether the non-genetic variance of a Type A scale composed of Framingham and Bortner items had gender specific psychosocial components. The study was performed on a group of Swedish twins so that variance explained by heritability for Type A could first be removed from the equation. The overall Type A score had been found to relate to self-reported CHD in this population. The dependent variable was the standardized score residual remaining after removing the genetic variance (i.e., that explained by co-twin score and zygosity). Multiple regression analyses revealed that there were differences in the psychosocial components of the Type A residual in men and women. These results are discussed in terms of culturally accepted gender roles and their possible implications for health endpoints.
RP KNOX, SS (reprint author), NHLBI,BEHAV MED SECT,FED BLDG,ROOM 216,BETHESDA,MD 20892, USA.
FU NIA NIH HHS [AG-04563]
NR 29
TC 2
Z9 2
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0022-3999
J9 J PSYCHOSOM RES
JI J. Psychosomat. Res.
PD OCT
PY 1993
VL 37
IS 7
BP 709
EP 716
DI 10.1016/0022-3999(93)90099-2
PG 8
WC Psychiatry
SC Psychiatry
GA MA304
UT WOS:A1993MA30400003
PM 8229902
ER

PT J
AU BOUMPAS, DT
   SCOTT, DE
   BALOW, JE
AF BOUMPAS, DT
   SCOTT, DE
   BALOW, JE
TI NEUROPSYCHIATRIC LUPUS - A CASE FOR GUARDED OPTIMISM
SO JOURNAL OF RHEUMATOLOGY
LA English
DT Editorial Material
ID NERVOUS-SYSTEM DISEASE; INTRAVENOUS CYCLOPHOSPHAMIDE; TRANSVERSE
   MYELITIS; BRAIN-LESIONS; ERYTHEMATOSUS; PROGNOSIS
C1 NIAMSD,BETHESDA,MD 20892.
RP BOUMPAS, DT (reprint author), NIDDKD,BLDG 10,ROOM 3N112,BETHESDA,MD 20892, USA.
NR 23
TC 15
Z9 15
U1 0
U2 0
PU J RHEUMATOL PUBL CO
PI TORONTO
PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA
SN 0315-162X
J9 J RHEUMATOL
JI J. Rheumatol.
PD OCT
PY 1993
VL 20
IS 10
BP 1641
EP 1643
PG 3
WC Rheumatology
SC Rheumatology
GA MG978
UT WOS:A1993MG97800002
PM 8295171
ER

PT J
AU KOGAN, V
   KUHLMAN, MR
   COUTANT, RW
   LEWIS, RG
AF KOGAN, V
   KUHLMAN, MR
   COUTANT, RW
   LEWIS, RG
TI AEROSOL FILTRATION BY SORBENT BEDS
SO JOURNAL OF THE AIR & WASTE MANAGEMENT ASSOCIATION
LA English
DT Article
ID MEDIA; FOAM; DUST
AB Fixed beds of sorbent media are used for the evaluation of polynuclear aromatic hydrocarbons (PAH) present in air. Two-stage sampling and separate extraction and analyses of PAH associated with aerosol particles and those present in the vapor state are usually performed. The ability of commonly used sorbents to retain particulate matter introduces a potential for reducing the time and cost of PAH evaluation procedures.
   The filtration efficiency of three sorbent media, Florisil, XAD-2, and polyurethane foam (PUF), for particles in 0.1 to 1 mum size range was studied using air flow rates from 4 to 250 L/min through a PS-1 sorbent cartridge. Theoretical considerations were used to identify the principal filtration mechanisms and to assess the predictability of the aerosol filtration performance of sorbent filters. The results of this study indicate XAD-2 to be an efficient filtration medium owing to the electrostatic enhancement of capturing and retaining aerosol particles.
   As a result of theoretical considerations, Brownian diffusion and inertial deposition were found to be major filtration mechanisms accompanied by electrostatic effects. While the efficiency of the diffusional deposition mechanism was reasonably well predicted with available theories, modeling of submicron particle impaction at higher fluid velocities appeared to be inadequate. Further developments are suggested to improve our understanding of filtration phenomena in sorbent beds under high flow rate conditions.
C1 NIEHS,ATMOSPHER RES & EXPOSURE ASSESSMENT LAB,AMBIENT METHODS RES BRANCH,RES TRIANGLE PK,NC 27709.
RP KOGAN, V (reprint author), BATTELLE MEM INST,505 KING AVE,COLUMBUS,OH 43201, USA.
NR 18
TC 7
Z9 9
U1 0
U2 1
PU AIR & WASTE MANAGEMENT ASSOC
PI PITTSBURGH
PA PO BOX 2861, PITTSBURGH, PA 15230
SN 1047-3289
J9 J AIR WASTE MANAGE
JI J. Air Waste Manage. Assoc.
PD OCT
PY 1993
VL 43
IS 10
BP 1367
EP 1373
PG 7
WC Engineering, Environmental; Environmental Sciences; Meteorology &
   Atmospheric Sciences
SC Engineering; Environmental Sciences & Ecology; Meteorology & Atmospheric
   Sciences
GA MB776
UT WOS:A1993MB77600005
ER

PT J
AU PETERS, RW
   ZOBLE, RG
   LIEBSON, PR
   PAWITAN, Y
   BROOKS, MM
   PROSCHAN, M
AF PETERS, RW
   ZOBLE, RG
   LIEBSON, PR
   PAWITAN, Y
   BROOKS, MM
   PROSCHAN, M
TI IDENTIFICATION OF A SECONDARY PEAK IN MYOCARDIAL-INFARCTION ONSET 11 TO
   12 HOURS AFTER AWAKENING - THE CARDIAC-ARRHYTHMIA SUPPRESSION TRIAL
   (CAST) EXPERIENCE
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
ID CIRCADIAN VARIATION; MORNING INCREASE; DEATH; FREQUENCY; TIME; TRIGGERS;
   STROKE; RISK
AB Objectives. The purpose of this study was to assess the relation between the time of awakening and the time of onset of acute myocardial infarction.
   Background. Previous investigation has shown the onset of symptoms of acute myocardial infarction to have a primary peak 1 to 2 h after awakening. In studies not corrected for time of awakening, there appears to be a late afternoon/early evening peak, but data correlating the onset of symptoms with awakening have been limited by small numbers of patients, perhaps precluding identification of a secondary peak.
   Methods. In the Cardiac Arrhythmia Suppression Trial (CAST), 3,549 patients had a documented myocardial infarction and entered antiarrhythmic drug titration. Of these, 3,309 had data on the onset of symptoms relative to the time of awakening and form the basis of this report.
   Results. A total of 870 patients (26.3%) were awakened by symptoms. Of the remaining 2,439 patients who were not awakened by symptoms, 798 (32.7%) experienced the onset of symptoms in the lst 4 h after awakening (with the highest number in the 1st h), after which the incidence of symptom onset decreased in a linear fashion, with a secondary peak 11 to 12 h after awakening. Both peaks are statistically significant. A similar pattern was seen in most of the subgroups examined (based on age, gender and various other demographic characteristics).
   Conclusions. Analysis of the very large CAST data base confirms the relation between awakening and onset of symptoms of myocardial infarction, suggesting involvement of the morning catecholamine surge. A secondary peak in symptom onset, occurring 11 to 12 h after awakening, is a new observation and may relate to ingestion of the evening meal or other trigger factors concentrated in those hours.
C1 UNIV MARYLAND, College Pk, MD 20742 USA.
   JAMES A HALEY DEPT VET AFFAIRS MED CTR, DEPT MED, TAMPA, FL USA.
   UNIV S FLORIDA, TAMPA, FL 33620 USA.
   RUSH MED COLL, CHICAGO, IL 60612 USA.
   UNIV WASHINGTON, DEPT BIOSTAT, SEATTLE, WA 98195 USA.
   NHLBI, BIOSTAT RES BRANCH, BETHESDA, MD 20892 USA.
RP PETERS, RW (reprint author), BALTIMORE DEPT VET AFFAIRS MED CTR, DEPT MED, 10 N GREENE ST, BALTIMORE, MD 21218 USA.
OI Brooks, Maria/0000-0002-2030-7873
NR 22
TC 38
Z9 38
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
EI 1558-3597
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD OCT
PY 1993
VL 22
IS 4
BP 998
EP 1003
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA MQ362
UT WOS:A1993MQ36200006
PM 8409074
ER

PT J
AU BIKKINA, M
   LARSON, MG
   LEVY, D
AF BIKKINA, M
   LARSON, MG
   LEVY, D
TI ASYMPTOMATIC VENTRICULAR ARRHYTHMIAS AND MORTALITY RISK IN SUBJECTS WITH
   LEFT-VENTRICULAR HYPERTROPHY
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
ID CORONARY-ARTERY DISEASE; ANGINA-PECTORIS; HEART-DISEASE; HYPERTENSION;
   MASS; DETERMINANTS; CRITERIA; MEN
AB Objectives. The purpose of this study was to evaluate the long-term prognostic role of asymptomatic ventricular arrhythmias in original Framingham Heart Study subjects and Framingham Offspring Study subjects who had echocardiographic evidence of left ventricular hypertrophy.
   Background. Echocardiographically determined left ventricular hypertrophy is associated with increased risk for ventricular arrhythmias. There are no population-based data available with regard to the long-term prognostic implications of asymptomatic ventricular arrhythmias in subjects with left ventricular hypertrophy.
   Methods. In a population-based cohort study, we studied 224 men and 393 women with echocardiographically determined left ventricular hypertrophy who were free of coronary heart disease and had 1-h ambulatory electrocardiograms at the baseline examination. The age-adjusted prevalence of complex or frequent ventricular arrhythmias (>30 ventricular premature beats/h, multiform premature complexes, couplets, ventricular tachycardia or R on T ventricular premature complexes) was 28% (51 of 224) in men and 17% (71 of 393) in women. The mean follow-up period was 5.7 years for cohort and 4.5 years for offspring subjects.
   Results. In men with complex or frequent arrhythmias, the 6-year cumulative incidence of all-cause mortality was 38%, whereas in those free of arrhythmia it was 12%; corresponding values in women were 22% and 11%. The cumulative incidence of myocardial infarction or death due to coronary heart disease was 20% for men with and 10% for men without arrhythmia, but in women little difference was noted (5% vs. 4%). After adjustment for age and gender in a Cox proportional hazards model, subjects with complex or frequent arrhythmia were at increased risk for all-cause mortality (hazard ratio 1.80, 95% confidence interval [CI] 1.13 to 2.87, p = 0.013). After adjusting for eight clinical covariates, the increased risk for all-cause mortality remained marginally significant (hazard ratio 1.62, 95% CI 0.98 to 2.68, p = 0.058). No significant increased risk was noted for myocardial infarction or death due to coronary heart disease.
   Conclusions. In subjects with left ventricular hypertrophy, the presence of asymptomatic ventricular arrhythmias was associated with higher mortality, which was statistically significant after adjusting for age and gender and marginally significant after taking into account other covariates.
C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,5 THURBER ST,FRAMINGHAM,MA 01701.
   NHLBI,BETHESDA,MD 20892.
   BOSTON UNIV,SCH MED,DIV EPIDEMIOL,BOSTON,MA 02118.
   BOSTON UNIV,SCH MED,DIV PREVENT MED,BOSTON,MA 02118.
   BETH ISRAEL HOSP,DIV CARDIOL,BOSTON,MA 02215.
   BETH ISRAEL HOSP,DIV CLIN EPIDEMIOL,BOSTON,MA 02215.
NR 31
TC 104
Z9 104
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD OCT
PY 1993
VL 22
IS 4
BP 1111
EP 1116
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA MQ362
UT WOS:A1993MQ36200022
PM 8409049
ER

PT J
AU GARG, R
   PACKER, M
   PITT, B
   YUSUF, S
AF GARG, R
   PACKER, M
   PITT, B
   YUSUF, S
TI HEART-FAILURE IN THE 1990S - EVOLUTION OF A MAJOR PUBLIC-HEALTH PROBLEM
   IN CARDIOVASCULAR MEDICINE
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Editorial Material
ID MYOCARDIAL-INFARCTION; MORTALITY; ENALAPRIL; TRIAL
C1 COLUMBIA UNIV COLL PHYS & SURG,DIV CIRCULATORY PHYSIOL,NEW YORK,NY.
   UNIV MICHIGAN,SCH MED,DIV CARDIOL,ANN ARBOR,MI.
   MCMASTER UNIV,DIV CARDIOL,HAMILTON,ON,CANADA.
RP GARG, R (reprint author), NHLBI,CLIN TRIALS BRANCH,DIV EPIDEMIOL & CLIN APPLICAT,FED BLDG,ROOM 5C10,BETHESDA,MD 20892, USA.
NR 14
TC 104
Z9 106
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD OCT
PY 1993
VL 22
IS 4
SU A
BP A3
EP A5
PG 3
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA MR869
UT WOS:A1993MR86900001
PM 8376694
ER

PT J
AU GARG, R
   YUSUF, S
AF GARG, R
   YUSUF, S
TI CURRENT AND ONGOING RANDOMIZED TRIALS IN HEART-FAILURE AND
   LEFT-VENTRICULAR DYSFUNCTION
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article; Proceedings Paper
CT Symposium on Mechanisms and Management of Heart Failure: Implications of
   Clinical Trials for Clinical Practice
CY APR 27-28, 1992
CL BETHESDA, MD
SP NHLBI
ID MORTALITY
AB Several large randomized trials have been completed recently and provided valuable information on the effects of various interventions in heart failure and left ventricular dysfunction. A review of ongoing randomized trials showed that there were 19 major trials addressing the effect of treatments on exercise tolerance, morbidity or mortality. Although it is hoped that these trials will answer many questions, they will also raise additional questions. Therefore, these remaining questions will need to be answered by future clinical trials,
C1 HAMILTON GEN HOSP,HAMILTON,ON,CANADA.
RP GARG, R (reprint author), NHLBI,CLIN TRIALS BRANCH,DIV EPIDEMIOL & CLIN APPLICAT,7550 WISCONSIN AVE,BETHESDA,MD 20892, USA.
NR 6
TC 7
Z9 7
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD OCT
PY 1993
VL 22
IS 4
SU A
BP A194
EP A197
PG 4
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA MR869
UT WOS:A1993MR86900037
PM 8104204
ER

PT J
AU HO, KKL
   PINSKY, JL
   KANNEL, WB
   LEVY, D
AF HO, KKL
   PINSKY, JL
   KANNEL, WB
   LEVY, D
TI THE EPIDEMIOLOGY OF HEART-FAILURE - THE FRAMINGHAM-STUDY
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article; Proceedings Paper
CT Symposium on Mechanisms and Management of Heart Failure: Implications of
   Clinical Trials for Clinical Practice
CY APR 27-28, 1992
CL BETHESDA, MD
SP NHLBI
ID UNITED-STATES; SYSTOLIC FUNCTION; PREVALENCE; MORTALITY; POPULATION;
   DYSFUNCTION; DISEASE
AB Congestive heart failure has become an increasingly frequent reason for hospital admission during the last 2 decades and clearly represents a major health problem. Data from the Framingham Heart Study indicate that the incidence of congestive heart failure increases with age and is higher in men than in women. Hypertension and coronary heart disease are the two most common conditions predating its onset. Diabetes mellitus and electrocardiographic left ventricular hypertrophy are also associated with an increased risk of heart failure. During the 1980s, the annual age-adjusted incidence of congestive heart failure among persons aged greater than or equal to 45 years was 7.2 cases/1,000 in men and 4.7 cases/1,000 in women, whereas the age adjusted prevalence of overt heart failure was 24/1,000 in men and 25/1,000 in women. Despite improved treatments far ischemic heart disease and hypertension, the age-adjusted incidence of heart failure has declined by only 11%/calendar decade in men and by 17%/calendar decade in women during a 40-year period of observation. In addition, congestive heart failure remains highly lethal, with a median survival time of 1.7 gears in men and 3.2 years in women and a 5-year survival rate of 25% in men and 38% in women.
C1 NHLBI,FRAMINGHAM HEART STUDY,FRAMINGHAM,MA 01701.
   BETH ISRAEL HOSP,CHARLES A DANA RES INST,BOSTON,MA 02215.
   BETH ISRAEL HOSP,DEPT MED,DIV CARDIOVASC,HARVARD THORNDIKE LAB,BOSTON,MA 02215.
   HARVARD UNIV,SCH MED,BOSTON,MA.
   NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892.
   BOSTON UNIV HOSP,DEPT EPIDEMIOL & PREVENT MED,BOSTON,MA.
   BOSTON UNIV,SCH MED,BOSTON,MA 02118.
FU NHLBI NIH HHS [5T32 HL 07374-13, N01-HC-38038]
NR 38
TC 560
Z9 632
U1 4
U2 26
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD OCT
PY 1993
VL 22
IS 4
SU A
BP A6
EP A13
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA MR869
UT WOS:A1993MR86900002
PM 8376698
ER

PT J
AU PITT, B
   BOURASSA, MG
   COLUCCI, WS
   HO, KKL
   PACKER, M
   POOLEWILSON, PA
   SMITH, TW
   YUSUF, S
AF PITT, B
   BOURASSA, MG
   COLUCCI, WS
   HO, KKL
   PACKER, M
   POOLEWILSON, PA
   SMITH, TW
   YUSUF, S
TI MECHANISMS AND MANAGEMENT OF HEART-FAILURE - IMPLICATIONS OF
   CLINICAL-TRIALS FOR CLINICAL-PRACTICE - PROCEEDINGS OF A SYMPOSIUM
   SPONSORED BY THE NATIONAL-HEART-LUNG-AND-BLOOD-INSTITUTE .2. NEW
   INSIGHTS INTO THE EPIDEMIOLOGY AND PATHOPHYSIOLOGY OF HEART-FAILURE -
   DISCUSSION-I
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Discussion
C1 MONTREAL HEART INST,MONTREAL H1T 1C8,PQ,CANADA.
   BRIGHAM & WOMENS HOSP,DIV CARDIOVASC,BOSTON,MA 02115.
   BETH ISRAEL HOSP,CHARLES A DANA RES INST,BOSTON,MA 02215.
   BETH ISRAEL HOSP,DEPT MED,DIV CARDIOVASC,HARVARD THORNDIKE LAB,BOSTON,MA 02215.
   HARVARD UNIV,SCH MED,BOSTON,MA.
   NHLBI,FRAMINGHAM HEART STUDY,FRAMINGHAM,MA.
   COLUMBIA UNIV COLL PHYS & SURG,DIV CIRCULATORY PHYSIOL,NEW YORK,NY.
   NATL HEART & LUNG INST,LONDON SW3 6LY,ENGLAND.
   ROYAL BROMPTON HOSP,LONDON SW3 6LY,ENGLAND.
   BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOL,BOSTON,MA 02115.
   MCMASTER UNIV,DIV CARDIOL,HAMILTON,ON,CANADA.
RP PITT, B (reprint author), UNIV MICHIGAN,SCH MED,DIV CARDIOL,ANN ARBOR,MI, USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD OCT
PY 1993
VL 22
IS 4
SU A
BP A20
EP A21
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA MR869
UT WOS:A1993MR86900004
ER

PT J
AU LIPTON, JA
   SHIP, JA
   LARACHROBINSON, D
AF LIPTON, JA
   SHIP, JA
   LARACHROBINSON, D
TI ESTIMATED PREVALENCE AND DISTRIBUTION OF REPORTED OROFACIAL PAIN IN THE
   UNITED-STATES
SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION
LA English
DT Article
ID NUTRITION EXAMINATION SURVEY; BURNING MOUTH SYNDROME; MANDIBULAR
   DYSFUNCTION; GENERAL-POPULATION; FACIAL-PAIN; TEMPOROMANDIBULAR
   DISORDERS; SYMPTOMS; EPIDEMIOLOGY; COMPLAINTS; EXPERIENCE
AB This paper presents the first estimates of the prevalence and distribution of several types of mouth and face pains for the U.S. adult, civilian population.
C1 NIDR,BETHESDA,MD 20892.
   UNIV MICHIGAN,SCH DENT,DEPT ORAL MED PATHOL SURG,ANN ARBOR,MI 48109.
NR 49
TC 381
Z9 399
U1 1
U2 17
PU AMER DENTAL ASSN
PI CHICAGO
PA 211 E CHICAGO AVE, CHICAGO, IL 60611
SN 0002-8177
J9 J AM DENT ASSOC
JI J. Am. Dent. Assoc.
PD OCT
PY 1993
VL 124
IS 10
BP 115
EP 121
PG 7
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA MC035
UT WOS:A1993MC03500021
PM 8409001
ER

PT J
AU BILD, DE
   FITZPATRICK, A
   FRIED, LP
   WONG, ND
   HAAN, MN
   LYLES, M
   BOVILL, E
   POLAK, JF
   SCHULZ, R
AF BILD, DE
   FITZPATRICK, A
   FRIED, LP
   WONG, ND
   HAAN, MN
   LYLES, M
   BOVILL, E
   POLAK, JF
   SCHULZ, R
TI AGE-RELATED TRENDS IN CARDIOVASCULAR MORBIDITY AND PHYSICAL FUNCTIONING
   IN THE ELDERLY - THE CARDIOVASCULAR HEALTH STUDY
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
ID VENTRICULAR EJECTION FRACTION; CORONARY-ARTERY DISEASE; LIFE EXPECTANCY;
   VITAL CAPACITY; HEART-DISEASE; POPULATION; INFARCTION; DISABILITY;
   ISSUES; IMPACT
AB Objective: To describe relationships between age and subclinical cardiovascular disease, manifest chronic disease, and physical functioning and limitations among persons aged 65 years and older, with emphasis on the ''oldest old,'' those 85 years and older.
   Design: Observational population-based study Setting: Four U.S. communities: Forsyth County, North Carolina; Sacramento County, California; Washington County, Maryland; and Pittsburgh, Pennsylvania.
   Participants: 5,201 men and women aged 65 years and older.
   Measurements: Demographic data; histories of cardiovascular disease (CVD), chronic lung disease, arthritis, diabetes, and hypertension; measures of subclinical disease including arm and ankle blood pressures, internal carotid wall thickness and stenosis, ejection fraction, left ventricular mass, fractional shortening, and diastolic function, electrocardiographic left ventricular hypertrophy and cardiac injury score, forced expiratory flow and volume; functional status including self-reported physical functioning, hearing and sight limitations and health status, and performance-based measures of function. These variables were examined among men and women in three age groups: 65-74 years, 75-84 years, and 85+ years. Subgroups of participants with and without manifest CVD were also examined.
   Main Results: In women, the prevalence of CVD and other chronic conditions increased with age, and the highest rates occurred among those 85 years and older. In men, prevalence rateS increased between the two younger groups, but the oldest group had lower than expected rates for coronary heart disease, cerebrovascular disease, hypertension, and chronic lung disease. In contrast, there were strong age-related linear trends in most of the subclinical measures of blood pressure atherosclerosis and pulmonary function and in virtually all measures of functional status in both gender groups across the age range. There was a particularly marked decline in functional status between the two older age groups. While subclinical disease was greater and functional status was poorer among those with manifest CVD, with few exceptions, age-related trends were not significantly different between the two groups.
   Conclusions: Lower than expected prevalence rates of CVD among those aged 85 years and older, particularly among men, in this study of community-dwelling elderly may represent selection bias or a real plateauing in disease prevalence with age. However, subclinical disease appears to increase and functional status to decline across the age range in both men and women regardless of the presence of CVD. The apparent increase in subclinical disease with age indicates potential for CVD prevention after age 65.
C1 UNIV WASHINGTON,DEPT BIOSTAT,SEATTLE,WA 98195.
   JOHNS HOPKINS UNIV,DEPT MED,BALTIMORE,MD 21218.
   UNIV CALIF IRVINE,PREVENT CARDIOL PROGRAM,IRVINE,CA 92717.
   UNIV CALIF DAVIS,DEPT COMMUNITY & INT HLTH,DAVIS,CA 95616.
   WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT INTERNAL MED,WINSTON SALEM,NC 27103.
   UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405.
   BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115.
   UNIV PITTSBURGH,DEPT PSYCHIAT,PITTSBURGH,PA 15260.
   UNIV PITTSBURGH,UNIV CTR SOCIAL & URBAN RES,PITTSBURGH,PA 15260.
RP BILD, DE (reprint author), NHLBI,DECA,7550 WISCONSIN AVE,FED BLDG,ROOM 300,BETHESDA,MD 20892, USA.
FU NHLBI NIH HHS [N01-HC-85079, N01-HC-85086]
NR 32
TC 61
Z9 63
U1 0
U2 3
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD OCT
PY 1993
VL 41
IS 10
BP 1047
EP 1056
PG 10
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA MA326
UT WOS:A1993MA32600005
PM 8409149
ER

PT J
AU OUSLANDER, JG
   PALMER, MH
   ROVNER, BW
   GERMAN, PS
AF OUSLANDER, JG
   PALMER, MH
   ROVNER, BW
   GERMAN, PS
TI URINARY-INCONTINENCE IN NURSING-HOMES - INCIDENCE, REMISSION AND
   ASSOCIATED FACTORS
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
ID LONG-TERM CARE; MANAGEMENT; POPULATION; DYSFUNCTION; DEPRESSION;
   PREVALENCE; PATTERNS
AB Objective: To determine the incidence and remission rates of daytime urinary incontinence (UI) in a cohort of newly admitted nursing home (NH) residents.
   Design: Prospective cohort study.
   Setting: Eight proprietary NHs in Maryland.
   Subjects: Four hundred thirty new admissions age 65 or older who were participants in a larger prospective study of mental morbidity and adjustment to the NH.
   Measures: Nurses aides' reports of continence status, psychiatric examinations, and nursing staff assessments of mobility at 2 weeks, 2 months, and 1 year after NH admission. Results: The prevalence of daytime UI at admission was 39% in both females and males. Among the 293 members (68%) of the admission cohort remaining in the NHs 2 months after admission, the incidence of daytime UI was 27% (21% in females, 51% in males); daytime UI resolved in 23% (24% in females, 20% in males). Among the 178 members (41%) of the admission cohort remaining in the NHs 1 year after admission, the incidence of daytime UI between 2 months and 1 year after admission was 19% (16% in females, 46% in males); daytime UI resolved in 22% (23% in females, 14% in males). The continence status of about two-thirds of residents remaining in the NH at 1 year after admission was stable over time: 22% had daytime UI, and 42% were continent at all three data collection points. The development of daytime UI was associated with male sex, the diagnosis of dementia, fecal incontinence, and the inability to ambulate or transfer independently. Resolution of daytime UI was associated with the absence of these characteristics.
   Conclusions: Despite limitations attributable to the method of defining UI and potential biases related to the attrition of the admission cohort over time, this is the first large prospective study to examine the incidence and remission patterns of daytime UI among NH residents. The strong association between UI and dementia was validated for the first time by direct psychiatric examinations. Sex and mobility are also closely associated with the development and remission of UI in this setting. This study provides some valuable data that can be used to assess the impacts of the recently developed Resident Assessment Protocol for UI and Agency for Health Care Policy and Research Clinical Practice Guidelines.
C1 UNIV CALIF LOS ANGELES, SCH MED, MULTICAMPUS PROGRAM GERIATR MED & GERONTOL, LOS ANGELES, CA USA.
   NATL CTR NURSING RES, BETHESDA, MD USA.
   HAHNEMAN SCH MED, WILLS GERIATR PSYCHIAT PROGRAM, PHILADELPHIA, PA USA.
   JOHNS HOPKINS SCH HYG & PUBL HLTH, BALTIMORE, MD USA.
RP OUSLANDER, JG (reprint author), JEWISH HOME AGING, 18855 VICTORY BLVD, RESEDA, CA 91335 USA.
FU NIA NIH HHS [AG-05146]; NIMH NIH HHS [R01MH41570]
NR 35
TC 74
Z9 77
U1 4
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD OCT
PY 1993
VL 41
IS 10
BP 1083
EP 1089
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA MA326
UT WOS:A1993MA32600010
PM 8409154
ER

PT J
AU GONZALEZ, FJ
   GELBOIN, HV
AF GONZALEZ, FJ
   GELBOIN, HV
TI ROLE OF HUMAN CYTOCHROME-P-450S IN RISK ASSESSMENT AND SUSCEPTIBILITY TO
   ENVIRONMENTALLY BASED DISEASE
SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH
LA English
DT Article; Proceedings Paper
CT 31ST HANFORD SYMP ON HEALTH AND THE ENVIRONMENT
CY OCT 20-23, 1992
CL RICHLAND, WA
SP US DOE, BATTELLE, PACIFIC NW LABS, UNIV WASHINGTON SCH PUBLIC HLTH AND COMMUNITY MED, DEPT ENVIRONM HLTH, NIEHS
ID LUNG-CANCER; METABOLIC-ACTIVATION; BREATH TEST; GENE; POLYMORPHISM;
   OXIDATION; CAFFEINE; LINE; NITROSAMINE; EXPRESSION
AB Cytochromes P-450 (P-450s) are a large group of heme-containing proteins that carry out oxidation of numerous chemicals. In mammals, a limited number of P-450s are involved in metabolic pathways of steroid synthesis, while most of these enzymes are involved in metabolism of foreign compounds. The principal beneficial function of P-450s is to convert chemicals into derivatives that can be easily eliminated from the body. This generally occurs through P-450-mediated oxidations of hydrophobic substances followed by conjugation reactions. For many foreign compounds, P-450 metabolism results in production of ''activated'' metabolites that can cause cell death and gene mutations. During the past several years, it has become widely recognized that marked species differences occur among the foreign compound-metabolizing P-450s. In addition to this interspecies variability in metabolism, marked intraspecies variability, frequently referred to as drug oxidation polymorphisms, occurs in virtually all mammals examined to date. Based on these observations, it is necessary to develop new human P-450-based systems that can be used to study foreign compound metabolism in order to predict human risk. This is being accomplished by use of cDNA-directed expression in B lymphoblastoid cells. These cells can be used to predict how humans will metabolize a chemical and whether it will be metabolically activated to a toxic or mutagenic metabolite. To study human P-450 polymorphisms, polymerase chain reaction (PCR) assays have been developed for diagnosis of known mutant P-450 genes. Molecular probes are also being used to screen populations for levels of expression of carcinogen-activating P-450s in an effort to determine whether expression of certain P-450 forms is associated with increased risk for development of environmentally based disease.
RP GONZALEZ, FJ (reprint author), NCI, BLDG 37, ROOM 3E24, BETHESDA, MD 20892 USA.
NR 44
TC 47
Z9 49
U1 0
U2 0
PU TAYLOR & FRANCIS
PI BRISTOL
PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598
SN 0098-4108
J9 J TOXICOL ENV HEALTH
JI J. Toxicol. Environ. Health
PD OCT-NOV
PY 1993
VL 40
IS 2-3
BP 289
EP 308
PG 20
WC Environmental Sciences; Public, Environmental & Occupational Health;
   Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health; Toxicology
GA MJ197
UT WOS:A1993MJ19700014
PM 8230303
ER

PT J
AU OKUDA, M
   UMEDA, A
   MATSUMOTO, Y
   MOMOI, Y
   WATARI, T
   GOITSUKA, R
   OBRIEN, SJ
   TSUJIMOTO, H
   HASEGAWA, A
AF OKUDA, M
   UMEDA, A
   MATSUMOTO, Y
   MOMOI, Y
   WATARI, T
   GOITSUKA, R
   OBRIEN, SJ
   TSUJIMOTO, H
   HASEGAWA, A
TI MOLECULAR-CLONING AND CHROMOSOMAL MAPPING OF FELINE P53 TUMOR-SUPPRESSOR
   GENE
SO JOURNAL OF VETERINARY MEDICAL SCIENCE
LA English
DT Article
DE CHROMOSOMAL MAPPING; FELINE; MOLECULAR CLONING; P53 TUMOR SUPPRESSOR
   GENE
ID LEUKEMIA-VIRUS; DOMESTIC CAT; CELL-LINE; SV40-TRANSFORMED CELLS;
   NUCLEOTIDE-SEQUENCE; NUCLEAR ONCOPROTEIN; MYC GENE; C-MYC; MUTATIONS;
   ANTIGEN
AB Alterations of the p53 tumor suppressor gene have been observed in a variety of human and mouse tumors. For investigation of the role of this gene in tumors in cats, feline p53 cDNA was molecularly cloned by PCR amplifications using primers based on the sequences conserved among several species. The cloned cDNA appeared to cover approximately 90% of the open reading frame of the feline p53 gene and had characteristic structures in common with the p53 genes of several other species. The amino acid sequence similarities of the feline p53 with the human, mouse, rat and chicken counterparts were 82.9%, 75.6%, 76.5% and 57.2% respectively. Moreover, using a panel of feline x rodent somatic cell hybrids, the feline p53 gene was assigned to feline chromosome E1. These data will be useful for determining the role of the p53 tumor suppressor gene in feline tumors.
C1 NATL INST ANIM HLTH,IMMUNE CYTOL LAB,IBARAKI 305,JAPAN.
   NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702.
RP OKUDA, M (reprint author), UNIV TOKYO,FAC AGR,DEPT VET INTERNAL MED,TOKYO 113,JAPAN.
NR 38
TC 23
Z9 24
U1 2
U2 2
PU JAPAN SOC VET SCI
PI TOKYO
PA UNIV TOKYO, 1-1-1 YAYOI, BUNKYO-KU, TOKYO 103, JAPAN
SN 0916-7250
J9 J VET MED SCI
JI J. Vet. Med. Sci.
PD OCT
PY 1993
VL 55
IS 5
BP 801
EP 805
PG 5
WC Veterinary Sciences
SC Veterinary Sciences
GA MD735
UT WOS:A1993MD73500018
PM 8286534
ER

PT J
AU VILLENEUVE, L
   JIANG, XY
   TURMEL, C
   KOZAK, CA
   JOLICOUER, P
AF VILLENEUVE, L
   JIANG, XY
   TURMEL, C
   KOZAK, CA
   JOLICOUER, P
TI LONG-RANGE MAPPING OF MIS-2, A COMMON PROVIRUS INTEGRATION SITE
   IDENTIFIED IN MURINE LEUKEMIA VIRUS-INDUCED THYMOMAS AND LOCATED 160
   KILOBASE PAIRS DOWNSTREAM OF MYB
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID T-CELL LYMPHOMAS; C-MYB; PLASMACYTOID LYMPHOSARCOMAS; DISEASE
   SPECIFICITY; NUCLEOTIDE-SEQUENCE; VIRAL INTEGRATION; RAT THYMOMAS;
   MOLONEY; MOUSE; DNA
AB The nondefective Moloney murine leukemia virus (MuLV) induces clonal or oligoclonal T-cell tumors in mice or rats. The proviruses of these nondefective MuLVs have been shown to act as insertion mutagens most frequently activating an adjacent cellular gene involved in cell growth control. Mutations by provirus insertions, recognized as common provirus integration sites, have been instrumental in identifying novel cellular genes involved in tumor formation. We have searched for new common provirus integration sites in Moloney MuLV-induced thymomas. Using cellular sequences flanking a provirus cloned from one of these tumors, we found one region, designated Mis-2, which was the target of provirus integration in a low (3%) percentage of these tumors. Mis-2 was mapped on mouse chromosome 10, approximately 160 kbp downstream of myb. The Mis-2 region may contain a novel gene involved in tumor development.
C1 INST RECH CLIN MONTREAL,MOLEC BIOL LAB,MONTREAL H2W 1R7,QUEBEC,CANADA.
   XEROX RES CTR CANADA LTD,MISSISSAUGA L5K 2L1,ONTARIO,CANADA.
   NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892.
   UNIV MONTREAL,DEPT MICROBIOL & IMMUNOL,MONTREAL H3C 3J7,QUEBEC,CANADA.
   MCGILL UNIV,DEPT EXPTL MED,MONTREAL H3G 1A4,PQ,CANADA.
NR 37
TC 15
Z9 15
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 5733
EP 5739
PG 7
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000004
PM 8371338
ER

PT J
AU KECK, JG
   KOVACS, GR
   MOSS, B
AF KECK, JG
   KOVACS, GR
   MOSS, B
TI OVEREXPRESSION, PURIFICATION, AND LATE TRANSCRIPTION FACTOR ACTIVITY OF
   THE 17-KILODALTON PROTEIN ENCODED BY THE VACCINIA VIRUS A1L-GENE
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID METAL CHELATE ADSORBENT; RNA-POLYMERASE; INTERMEDIATE GENE; EXPRESSION
   SYSTEM; DNA-REPLICATION; FOREIGN GENES; PROMOTERS; IDENTIFICATION;
   SEQUENCE; VECTORS
AB The A1L, A2L, and G8R open reading frames (ORFs) were previously shown by transfection assays to encode transactivators of late gene expression. We now present evidence that the 17-kDa protein product of the A1L gene can function in vitro as a transcription factor. Simultaneous overexpression of the transactivators was achieved by coinfecting HeLa cells with one recombinant vaccinia virus that encodes the bacteriophage T7 RNA polymerase and three recombinant vaccinia viruses that contain copies of A1L, A2L, and G8R ORFs regulated by T7 promoters. Extracts from the recombinant virus-infected cells exhibited greatly enhanced late in vitro transcription activity and served as a source of factors. The 17-kDa product of the A1L ORF represented approximately 8% of the ammonium sulfate-precipitated cell protein and copurified with a late transcription factor activity. The transcription factor activity could be specifically immunodepleted with immobilized antibody to the bacterially expressed A1L-encoded protein, providing additional evidence for its identity and role. A sequence encoding six consecutive histidines was added to the AIL ORF, which was then incorporated into the genome of a baculovirus expression vector. The 17-kDa protein, synthesized in insect cells and purified by binding to an Ni2+-chelating affinity column, could replace the vaccinia virus-overexpressed 17-kDa protein in transcription assays. In addition to the 17-kDa product of the A1L gene, which was named vaccinia virus late transcription factor 2, the proteins that stimulate specific transcription of late promoter-regulated templates included the viral multisubunit RNA polymerase, vaccinia virus late transcription factor 1 (the product of the G8R ORF), and at least one other partially purified protein.
C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892.
NR 42
TC 31
Z9 32
U1 1
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 5740
EP 5748
PG 9
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000005
PM 8371339
ER

PT J
AU KECK, JG
   FEIGENBAUM, F
   MOSS, B
AF KECK, JG
   FEIGENBAUM, F
   MOSS, B
TI MUTATIONAL ANALYSIS OF A PREDICTED ZINC-BINDING MOTIF IN THE
   26-KILODALTON PROTEIN ENCODED BY THE VACCINIA VIRUS A2L-GENE -
   CORRELATION OF ZINC-BINDING WITH LATE TRANSCRIPTIONAL TRANSACTIVATION
   ACTIVITY
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RNA-POLYMERASE; DNA-REPLICATION; LATE GENES; EXPRESSION
AB Transient transfection assays indicated that A2L is one of three vaccinia virus intermediate genes that are required for the transcriptional transactivation of viral late genes. We have expressed the A2L open reading frame in Escherichia coli and shown by blotting experiments that the 26-kDa protein binds zinc, a property predicted by the presence of a CX2CX13CX2C zinc finger motif. The specificity for zinc binding was demonstrated by competition with other metals. The role of the sequence motif in zinc binding was established by analysis of a series of mutations, including truncations and conservative single amino acid substitutions. Mutations that reduced zinc binding in vitro prevented the ability of A2L to transactivate late genes in vivo.
C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892.
NR 26
TC 17
Z9 18
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 5749
EP 5753
PG 5
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000006
PM 8371340
ER

PT J
AU BLOOM, ME
   BERRY, BD
   WEI, W
   PERRYMAN, S
   WOLFINBARGER, JB
AF BLOOM, ME
   BERRY, BD
   WEI, W
   PERRYMAN, S
   WOLFINBARGER, JB
TI CHARACTERIZATION OF CHIMERIC FULL-LENGTH MOLECULAR CLONES OF ALEUTIAN
   MINK DISEASE PARVOVIRUS (ADV) - IDENTIFICATION OF A DETERMINANT
   GOVERNING REPLICATION OF ADV IN CELL-CULTURE
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID FELINE PANLEUKOPENIA VIRUS; NONSTRUCTURAL PROTEIN NS2; AMINO-ACID
   SUBSTITUTIONS; CANINE HOST RANGE; MINUTE VIRUS; NUCLEOTIDE-SEQUENCE;
   INFECTED MINK; INTERSTITIAL PNEUMONIA; 5'-TERMINAL PALINDROME;
   MONOCLONAL-ANTIBODIES
AB The ADV-G strain of Aleutian mink disease parvovirus (ADV) is nonpathogenic for mink but replicates permissively in cell culture, whereas the ADV-Utah 1 strain is highly pathogenic for mink but replicates poorly in cell culture. In order to relate these phenotypic differences to primary genomic features, we constructed a series of chimeric plasmids between a full-length replication-competent molecular clone of ADV-G and subgenomic clones of ADV-Utah 1 representing map units (MU) 15 to 88. After transfection of the plasmids into cell culture and serial passage of cell lysates, we determined that substitution of several segments of the ADV-Utah 1 genome (MU 15 to 54 and 65 to 73) within an infectious ADV-G plasmid did not impair the ability of these constructs to yield infectious virus in vitro. Like ADV-G, the viruses derived from these replication-competent clones caused neither detectable viremia 10 days after inoculation nor any evidence of Aleutian disease in adult mink. On the other hand, other chimeric plasmids were incapable of yielding infectious virus and were therefore replication defective in vitro. The MU 54 to 65 EcoRI-EcoRV fragment of ADV-Utah 1 was the minimal segment capable of rendering ADV-G replication defective. Substitution of the ADV-G EcoRI-EcoRV fragment into a replication-defective clone restored replication competence, indicating that this 0.53-kb portion of the genome, wholly located within shared coding sequences for the capsid proteins VP1 and VP2, contained a determinant that governs replication in cell culture. When cultures of cells were studied 5 days after transfection with replication-defective clones, rescue of dimeric replicative form DNA and single-stranded progeny DNA could not be demonstrated. This defect could not be complemented by cotransfection with a replication-competent construction.
RP BLOOM, ME (reprint author), NATL INST ALLERGY & INFECT DIS,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA.
NR 82
TC 31
Z9 32
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 5976
EP 5988
PG 13
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000033
PM 8396664
ER

PT J
AU LODMELL, DL
   ESPOSITO, JJ
   EWALT, LC
AF LODMELL, DL
   ESPOSITO, JJ
   EWALT, LC
TI RABIES VIRUS ANTINUCLEOPROTEIN ANTIBODY PROTECTS AGAINST RABIES VIRUS
   CHALLENGE IN-VIVO AND INHIBITS RABIES VIRUS-REPLICATION IN-VITRO
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MONOCLONAL-ANTIBODIES; T-CELL; GLYCOPROTEIN; VACCINATION; NUCLEOPROTEIN;
   RECOMBINANTS; SKUNKS; MOUSE; MICE; STRAINS
AB We previously reported that A/WySnJ mice vaccinated via a tail scratch with a recombinant raccoon poxvirus (RCN) expressing the rabies virus internal structural nucleoprotein (N) (RCN-N) were protected against a street rabies virus (D. L. Lodmell, J. W. Sumner, J. J. Esposito, W. J. Bellini, and L. C. Ewalt, J. Virol. 65:3400-3405, 1991). To improve our understanding of the mechanism(s) of this protection, we investigated whether sera of A/WySnj mice that had been vaccinated with RCN-N but not challenged with street rabies virus had anti-rabies virus activity. In vivo studies illustrated that mice inoculated in the footpad with preincubated mixtures of anti-N sera and virus were protected. In addition, anti-N sera inoculated into the site of virus challenge protected mice. The antiviral activity of anti-N sera was also demonstrated in vitro. Infectious virus was not detected in cultures 24 h following infection with virus that had been preincubated with anti-N sera. At later time points, infectious virus was detected, but inhibition of viral production was consistently greater-than-or-equal-to 99% compared with control cultures. The protective and antiviral inhibitory activity of the anti-N sera was identified as anti-N antibody by several methods. First, absorption of anti-N sera with goat anti-mouse immunoglobulin serum, but not normal goat serum, removed the activity. Second, radioimmuno-precipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of sucrose density gradient-fractionated anti-N sera showed that antiviral activity was present only in the fraction containing anti-N antibody. Finally, absorption of anti-N sera with insect cells infected with a baculovirus expressing the N protein removed the protective activity. These data indicate that anti-N antibody is a component of the resistance to rabies virus infections.
C1 CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV VIRAL & RICKETTSIAL DIS,ATLANTA,GA 30333.
RP LODMELL, DL (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA.
NR 31
TC 28
Z9 36
U1 1
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 6080
EP 6086
PG 7
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000043
PM 8371354
ER

PT J
AU DITTMER, J
   GITLIN, SD
   REID, RL
   BRADY, JN
AF DITTMER, J
   GITLIN, SD
   REID, RL
   BRADY, JN
TI TRANSACTIVATION OF THE P2 PROMOTER OF PARATHYROID HORMONE-RELATED
   PROTEIN BY HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I TAX1 - EVIDENCE FOR
   THE INVOLVEMENT OF TRANSCRIPTION FACTOR ETS1
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID LONG TERMINAL REPEAT; NF-KAPPA-B; LEUKEMIA-VIRUS; HUMORAL HYPERCALCEMIA;
   21-BASE-PAIR REPEATS; GENE-EXPRESSION; ACTIVATOR TAX; HUMAN-TUMOR;
   IDENTIFICATION; PEPTIDE
AB Expression of the parathyroid hormone-related protein (PTHrP), a protein that plays a primary role in the development of the humoral hypercalcemia of malignancy, is regulated by two distinct promoters, P1 and P2. PTHrP is overexpressed in lymphocytes from adult T-cell leukemia patients. We now demonstrate that in the human T-cell lymphotropic virus type I-transformed cell line MT-2, RNA synthesis is initiated primarily at the P2 promoter. Furthermore, in cotransfection experiments, Tax1 transactivates the P2 promoter 10- to 12-fold. By using deletion and site-specific point mutations, we have identified a promoter-proximal sequence (positions -72 to -40) which is important for Tax1 transactivation. The PTHrP promoter-proximal element contains two potential overlapping Ets1 binding sites, EBS I and EBS II. Gel shift analysis demonstrated that Ets1 binds specifically to both EBS I and EBS II. Mutation of the consensus GGAA core motif in EBS I abolished binding and Tax1 transactivation in Jurkat lymphocytes. In Ets1-deficient cells, cotransfection of Tax, and Ets1 expression plasmids stimulates PTHrP promoter activity. In the absence of Ets1, minimal transactivation of the PTHrP promoter is observed. These data suggest that Ets1 binds to EBS I and cooperates with Tax, to transactivate the PTHrP P2 promoter.
C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892.
RI Dittmer, Juergen/G-1160-2011
NR 68
TC 60
Z9 60
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 6087
EP 6095
PG 9
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000044
PM 8371355
ER

PT J
AU JEANG, KT
   CHUN, R
   LIN, NH
   GATIGNOL, A
   GLABE, CG
   FAN, H
AF JEANG, KT
   CHUN, R
   LIN, NH
   GATIGNOL, A
   GLABE, CG
   FAN, H
TI IN-VITRO AND IN-VIVO BINDING OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TAT
   PROTEIN AND SP1 TRANSCRIPTION FACTOR
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID LONG TERMINAL REPEAT; RNA POLYMERASE-II; TRANS-ACTIVATOR GENE; HIV-1
   TAT; MESSENGER-RNA; HTLV-III; REGULATORY SEQUENCES; RESPONSIVE SEQUENCE;
   CELLULAR PROTEINS; NASCENT RNA
AB Recent genetic experiments have suggested that tat transactivation of the human immunodeficiency virus type 1 (HIV-1) long terminal repeat requires functional upstream enhancer sequences-Spl sites, in particular. In these experiments, HeLa cell nuclear extracts were passed over affinity matrices containing chemically synthesized or bacterially expressed HIV-1 Tat. Assay of material that bound to and eluted from the Tat matrices revealed the presence of the Sp1 transcription factor. Other transcription factors (Oct and NF-kappaB) also bound to Tat matrices but with less efficiency-in parallel with the lower capacities of these binding motifs to confer Tat responsiveness on a basal HIV-1 promoter compared with Sp1 sites. Passage of nuclear extracts over matrices containing other neutral proteins, including bovine serum albumin, ovalbumin, and lysozyme, revealed no or reduced binding. Cross-linking experiments indicated that the purified Spl and Tat proteins can form multimeric complexes in the absence of other proteins. The region of Tat responsible for Sp1 binding was localized to a region encompassing residues 30 to 62. Immunoprecipitation experiments with HIV-1-infected T lymphocytes indicated coimmunoprecipitation of Tat and Sp1. These experiments extend previous genetic experiments and suggest a direct interaction between Tat and Sp1 during transactivation.
C1 UNIV CALIF IRVINE,DEPT MOLEC BIOL & BIOCHEM,IRVINE,CA 92717.
   UNIV CALIF IRVINE,CANC RES INST,IRVINE,CA 92717.
   NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892.
RI Jeang, Kuan-Teh/A-2424-2008; Chun, Rene/A-9415-2010
OI Chun, Rene/0000-0002-0190-0807
FU NIAID NIH HHS [K08 AI081545]
NR 74
TC 214
Z9 214
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 6224
EP 6233
PG 10
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000058
PM 7690421
ER

PT J
AU KELLER, R
   PEDEN, K
   PAULOUS, S
   MONTAGNIER, L
   CORDONNIER, A
AF KELLER, R
   PEDEN, K
   PAULOUS, S
   MONTAGNIER, L
   CORDONNIER, A
TI AMINO-ACID CHANGES IN THE 4TH CONSERVED REGION OF
   HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-2 STRAIN HIV-2(ROD) ENVELOPE
   GLYCOPROTEIN MODULATE FUSION
SO JOURNAL OF VIROLOGY
LA English
DT Note
ID RECEPTOR-BINDING; GP120; CD4; TROPISM; GENE; IDENTIFICATION; RETROVIRUS;
   DOMAINS; HIV-1
AB The fourth conserved region (C4) of human immunodeficiency virus type 1 (HIV-1) surface glycoprotein has been shown to participate in CD4 binding and to influence viral tropism (A. Cordonnier, L. Montagnier, and M. Emerman, Nature [London] 340:571-574, 1989). To define the role of the corresponding region of HIV-2, we introduced single amino acid changes into the C4 sequence of HIV-2ROD. The effects of these mutations on glycoprotein function and on virus infectivity have been examined. We have shown that the tryptophan residue at position 428 is necessary primarily for CD4 binding. The isoleucine residue at position 421 is necessary for the establishment of productive infection in the promonocytic cell line U937, while it is dispensable to some extent for infection of primary T lymphocytes or the lymphocytic cell line SUP-T1. This replication defect correlated with the failure of the Ile-421-to-Thr (Ile-421-Thr) mutant glycoprotein to form syncytia in U937 cells. DNA analysis of revertant viruses revealed that a strong selective pressure was exerted on residue 421 of the surface glycoprotein to allow HIV-2 infection of U937 cells. These results demonstrate that this region of HIV-2 plays an important role in determining fusion efficiency in a cell-dependent manner and consequently can influence viral tropism.
C1 INST PASTEUR,CNRS,UNITE ONCOL VIRALE,UA 1157,F-75724 PARIS 15,FRANCE.
   NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892.
NR 23
TC 18
Z9 18
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 6253
EP 6258
PG 6
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000062
PM 8371358
ER

PT J
AU CAUGHEY, B
   ERNST, D
   RACE, RE
AF CAUGHEY, B
   ERNST, D
   RACE, RE
TI CONGO RED INHIBITION OF SCRAPIE AGENT REPLICATION
SO JOURNAL OF VIROLOGY
LA English
DT Note
ID PRION PROTEIN; INCUBATION PERIOD; PRP ACCUMULATION; DEXTRAN SULFATE;
   INFECTION; FIBRILS; IDENTIFICATION; POLYANIONS; BRAIN; MICE
AB Congo red inhibits the accumulation of protease-resistant PrP in scrapie-infected mouse neuroblastoma cells. Here we show that Congo red also inhibits the replication of scrapie infectivity in these cells. This observation is consistent with the idea that protease-resistant PrP is a vital component of the scrapie agent or that agent replication depends on the presence of protease-resistant PrP in the cell.
RP CAUGHEY, B (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA.
NR 24
TC 103
Z9 107
U1 0
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 6270
EP 6272
PG 3
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000065
PM 8103804
ER

PT J
AU SPALHOLZ, BA
AF SPALHOLZ, BA
TI IMPORTANCE OF THE BOVINE PAPILLOMAVIRUS P(2443) PROMOTER IN THE
   REGULATION OF E2 AND E5 EXPRESSION
SO JOURNAL OF VIROLOGY
LA English
DT Note
ID OPEN READING FRAMES; TRANSCRIPTIONAL REGULATION; TRANSFORMING REGION;
   TRANS-ACTIVATION; GENE-EXPRESSION; TYPE-1 ENCODES; BINDING-SITES;
   REPLICATION; CELLS; E1
AB The full-length bovine papillomavirus E2 gene product (E2TA), which has a direct role in DNA replication and functions as a transcriptional activator, can be expressed from an unspliced mRNA transcribed from the P2443 promoter or from spliced mRNAs transcribed from other upstream promoters. The regulation of E2 expression from these promoters is still in question. In the background of wild-type protein coding sequences, this study identified the P2443 promoter as the major source of E2TA as well as E5 expression in C127 cells.
RP SPALHOLZ, BA (reprint author), NCI,TUMOR VIRUS BIOL LAB,BLDG 41,ROOM D505,BETHESDA,MD 20892, USA.
NR 47
TC 4
Z9 4
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 1993
VL 67
IS 10
BP 6278
EP 6284
PG 7
WC Virology
SC Virology
GA LX120
UT WOS:A1993LX12000067
PM 8396681
ER

PT J
AU DONOVAN, JC
   MAYO, JG
   RICE, JM
   WARD, JM
   FOX, JG
AF DONOVAN, JC
   MAYO, JG
   RICE, JM
   WARD, JM
   FOX, JG
TI HELICOBACTER-ASSOCIATED HEPATITIS OF MICE
SO LABORATORY ANIMAL SCIENCE
LA English
DT Letter
C1 NCI,FREDERICK,MD 21701.
   MIT,CAMBRIDGE,MA 02139.
RP DONOVAN, JC (reprint author), NCI,BETHESDA,MD 20892, USA.
NR 1
TC 10
Z9 10
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI CORDOVA
PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018
SN 0023-6764
J9 LAB ANIM SCI
JI Lab. Anim. Sci.
PD OCT
PY 1993
VL 43
IS 5
BP 403
EP 403
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA MF111
UT WOS:A1993MF11100001
PM 8277716
ER

PT J
AU TSAI, CC
   FOLLIS, KE
   GRANT, RF
   NOLTE, RE
   WU, HN
   BENVENISTE, RE
AF TSAI, CC
   FOLLIS, KE
   GRANT, RF
   NOLTE, RE
   WU, HN
   BENVENISTE, RE
TI INFECTIVITY AND PATHOGENESIS OF TITERED DOSAGES OF SIMIAN
   IMMUNODEFICIENCY VIRUS EXPERIMENTALLY INOCULATED INTO LONGTAILED
   MACAQUES (MACACA-FASCICULARIS)
SO LABORATORY ANIMAL SCIENCE
LA English
DT Article
ID T-CELL; CERCOCEBUS-ATYS; RETROVIRUS; MONKEYS; HTLV; LENTIVIRUS; SIV;
   MANGABEYS; LYMPHOMA; BABOONS
AB The 50% macaque infectious dose (MID50) and pathogenesis of uncloned simian immunodeficiency virus (isolated from a pigtailed macaque, SIV(mne)) was determined in longtailed macaques (Macaca fascicularis). Five pairs of macaques were inoculated with 10-fold dilutions of the virus stock, and one macaque was mock-infected. The virologic and clinical status of these macaques was monitored for up to 80 weeks. The MID50 Of SIV(mne) was determined to be 10(2) cell culture infectious dose of the original virus stock. In order to test the infectivity and pathogenesis of an established viral dose, six additional macaques were inoculated with 10x MID50 (10(3) cell culture infectious dose) of the SIV(mne). The virologic and clinical status of these macaques was monitored for 40 weeks. All of the macaques inoculated with 10x MID50 or greater became infected as evidenced by seroconversion and consistent virus isolation from peripheral blood mononuclear cells. Macaques infected with SIV(mne) had an initial sharp decrease in CD2, CD20, CD4, CD8, and CD4CD29 lymphocyte subsets, whereas the CD4:CD8 ratio increased. Viremic macaques developed persistent slight to moderate peripheral lymphadenopathy approximately 3 to 4 weeks after inoculation. Four macaques subsequently died of AIDS-like disease at 29, 33, 42, and 80 weeks after inoculation. Data obtained from the viral titration study and the acute infection model will aid in the development of animal trials to evaluate antiretroviral therapies and preventive vaccines against human immunodeficiency virus infection.
C1 NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701.
RP TSAI, CC (reprint author), UNIV WASHINGTON,REG PRIMATE RES CTR,SEATTLE,WA 98195, USA.
FU NCRR NIH HHS [RR00166]; NIAID NIH HHS [N01-AI-15120]
NR 20
TC 17
Z9 17
U1 0
U2 1
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI CORDOVA
PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018
SN 0023-6764
J9 LAB ANIM SCI
JI Lab. Anim. Sci.
PD OCT
PY 1993
VL 43
IS 5
BP 411
EP 416
PG 6
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA MF111
UT WOS:A1993MF11100004
PM 8277718
ER

PT J
AU THIGPEN, JE
   LOCKLEAR, J
   ROMINES, C
   TAYLOR, KA
   YEARBY, W
   STOKES, WS
AF THIGPEN, JE
   LOCKLEAR, J
   ROMINES, C
   TAYLOR, KA
   YEARBY, W
   STOKES, WS
TI A STANDARD PROCEDURE FOR MEASURING PELLET HARDNESS OF RODENT DIETS
SO LABORATORY ANIMAL SCIENCE
LA English
DT Article
AB A Chatillon Model TCM-200 test stand with exchangeable flat horizontal or concave receptacle bases and a DFI-200 gauge load cell with multiple types of upper exchangeable test jaws (large round-flat, medium round-flat, chisel, bullet, and cone-shaped) were compared by using preautoclaved and autoclaved NIH-31 rodent diet pellets to determine which type of hardness testing system would give the most accurate and reproducible results for measuring pellet hardness. The type and size of the contact area of the upper jaws significantly affected the force required to break the pellets. Significant differences were observed between the flat-horizontal and concave receptacle bases in the force required to break the pellets when using the two round-flat upper jaws. In contrast, similar results were obtained with both bases when the bullet, chisel, or cone-shaped upper jaws were used. Autoclaved pellets were 69.4% (range, 49 to 94%) harder than preautoclaved pellets. These results suggest that different testing systems can be used for measuring pellet hardness and that a standard procedure must be used in order to compare pellet hardness results between different testing laboratories. It was concluded that the flat-horizontal base and the larger round-flat end upper jaw gave the most reproducible results for measuring pellet hardness.
RP THIGPEN, JE (reprint author), NIEHS,COMPARAT MED BRANCH,RES TRIANGLE PK,NC 27709, USA.
NR 8
TC 3
Z9 3
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI CORDOVA
PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018
SN 0023-6764
J9 LAB ANIM SCI
JI Lab. Anim. Sci.
PD OCT
PY 1993
VL 43
IS 5
BP 488
EP 491
PG 4
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA MF111
UT WOS:A1993MF11100018
PM 8277732
ER

PT J
AU DIXON, D
   GOELZ, MF
   LOCKLEAR, J
   MYERS, PH
   THIGPEN, JE
AF DIXON, D
   GOELZ, MF
   LOCKLEAR, J
   MYERS, PH
   THIGPEN, JE
TI DIAGNOSTIC EXERCISE - GASTRITIS IN ATHYMIC NUDE-MICE
SO LABORATORY ANIMAL SCIENCE
LA English
DT Article
ID CANDIDIASIS; IMMUNITY
C1 NIEHS,COMPARAT MED BRANCH,RES TRIANGLE PK,NC 27709.
RP DIXON, D (reprint author), NIEHS,EXPTL PATHOL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA.
FU NCRR NIH HHS [RR00301]
NR 11
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI CORDOVA
PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018
SN 0023-6764
J9 LAB ANIM SCI
JI Lab. Anim. Sci.
PD OCT
PY 1993
VL 43
IS 5
BP 497
EP 499
PG 3
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA MF111
UT WOS:A1993MF11100021
PM 8277735
ER

PT J
AU MCWILLIAMS, TS
   WAGGIE, KS
   LUZARRAGA, MB
   FRENCH, AW
   ADAMS, RJ
AF MCWILLIAMS, TS
   WAGGIE, KS
   LUZARRAGA, MB
   FRENCH, AW
   ADAMS, RJ
TI CORYNEBACTERIUM SPECIES-ASSOCIATED KERATOCONJUNCTIVITIS IN AGED MALE
   C57BL/6J MICE
SO LABORATORY ANIMAL SCIENCE
LA English
DT Article
ID CORYNEFORM
C1 NIA,GERONTOL RES CTR,RES RESOURCES BRANCH,ANIM RESOURCES SECT,BALTIMORE,MD 21224.
RP MCWILLIAMS, TS (reprint author), JOHNS HOPKINS UNIV,SCH MED,DIV COMPARAT MED,BALTIMORE,MD 21205, USA.
FU NCRR NIH HHS [RR07002, RR00130]
NR 8
TC 5
Z9 5
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI CORDOVA
PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018
SN 0023-6764
J9 LAB ANIM SCI
JI Lab. Anim. Sci.
PD OCT
PY 1993
VL 43
IS 5
BP 509
EP 512
PG 4
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA MF111
UT WOS:A1993MF11100025
PM 8277739
ER

PT J
AU LEBIHAN, D
   TURNER, R
   MOSELEY, ME
   HYDE, JS
AF LEBIHAN, D
   TURNER, R
   MOSELEY, ME
   HYDE, JS
TI FUNCTIONAL MRI OF THE BRAIN - A REPORT ON THE SMRM SMRI WORKSHOP HELD IN
   ARLINGTON, VIRGINIA JUNE 17-19, 1993
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Editorial Material
C1 NIH,CARDIAC ENERGET LAB,BETHESDA,MD 20892.
   STANFORD UNIV,DEPT RADIOL,STANFORD,CA 94305.
   MED COLL WISCONSIN,BIOPHYS RES INST,MILWAUKEE,WI 53226.
RP LEBIHAN, D (reprint author), NIH,DEPT DIAGNOST RADIOL,BLDG 10,ROOM 1C 660,BETHESDA,MD 20892, USA.
RI Turner, Robert/C-1820-2008
NR 0
TC 2
Z9 2
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0740-3194
J9 MAGNET RESON MED
JI Magn.Reson.Med.
PD OCT
PY 1993
VL 30
IS 4
BP 405
EP 408
DI 10.1002/mrm.1910300402
PG 4
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA MA378
UT WOS:A1993MA37800001
ER

PT J
AU DUYN, JH
   MOONEN, CTW
AF DUYN, JH
   MOONEN, CTW
TI FAST PROTON SPECTROSCOPIC IMAGING OF HUMAN BRAIN USING MULTIPLE
   SPIN-ECHOES
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE PROTON SPECTROSCOPIC IMAGING; BRAIN, MR; FAST MR IMAGING
ID NMR-SPECTROSCOPY; MR; RELAXATION; INVIVO
AB We introduce a multi-echo multi-slice MR proton spectroscopic imaging method, which allows for a dramatic reduction of the measurement time by acquiring multiple spin-echoes within a single repetition time.  In the multi-echo multi-slice experiment discussed in this paper, a threefold reduction in measurement time is obtained by sacrificing some spectral resolution. Signal-to-noise ratio and spatial resolution are preserved. Metabolite images of N-acetyl aspartate, and total choline + total creatine from multiple slices through the human brain are presented and compared with images obtained with a conventional single-echo multi-slice method.
C1 NIH,INVIVO NMR RES CTR,NCRR,BEIP,BETHESDA,MD 20892.
RP DUYN, JH (reprint author), NIH,DIAGNOST RADIOL RES LAB,BLDG 10,ROOM B1N 256,BETHESDA,MD 20892, USA.
RI Duyn, Jozef/F-2483-2010
NR 26
TC 118
Z9 119
U1 0
U2 7
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0740-3194
J9 MAGNET RESON MED
JI Magn.Reson.Med.
PD OCT
PY 1993
VL 30
IS 4
BP 409
EP 414
DI 10.1002/mrm.1910300403
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA MA378
UT WOS:A1993MA37800002
PM 8255188
ER

PT J
AU NAGY, IZ
   OHTA, M
   KITANI, K
   CUTLER, RG
AF NAGY, IZ
   OHTA, M
   KITANI, K
   CUTLER, RG
TI THE EFFECT OF CALORIC RESTRICTION ON THE LATERAL DIFFUSION CONSTANT OF
   HEPATOCYTE MEMBRANE-PROTEINS IN C57BL/6 MALE-MICE OF DIFFERENT AGES -
   FRAP STUDIES ON LIVER SMEARS
SO MECHANISMS OF AGEING AND DEVELOPMENT
LA English
DT Article
ID FLUORESCENCE RECOVERY; PLASMA-MEMBRANE; FOOD RESTRICTION; DIETARY
   RESTRICTION; RAT-LIVER; DEPENDENT DECREASE; FISCHER-344 RAT; MOBILITY;
   AUTOFLUORESCENCE; MANIPULATION
AB The lateral mobility of proteins in hepatocyte plasma membranes was compared in calorically restricted and ad libitum (AL)-fed C57BL/6 male mice in age groups from 7 to 28 months. Caloric restriction was achieved by means of the every-other-day (EOD) feeding regimen, maintained for various periods from 1 to 15 months. Protein lateral diffusion constant (D) in hepatocyte membranes was measured by means of fluorescence recovery after photobleaching (FRAP) in liver smears. The peroxide-induced autofluorescence (PIAF) was utilized as a fluorescent label. A mild (1 mM for 10 min) H2O2 treatment of liver smears produces oxidation of riboflavin that is bound to all proteins of the cell membrane. Using this technique, the average lateral diffusion constant (D) and the fractional recovery (FR) of these proteins can be measured. EOD feeding resulted in a significant decrease in body weights and also a significant increase in the values of D in all age groups after 1 month of EOD feeding. After 3.5 months of EOD feeding a further increase of D was observed (up to about 15%). Nevertheless no further change in D occurred if the EOD feeding was maintained for 6.5 or even 15 months. The negative linear age correlation of D observed in the AL-fed animals was present also under the EOD feeding; however, the whole regression equation shifted towards higher values. These experiments indicate that caloric restriction influences the lateral diffusion constant of membrane proteins in hepatocytes. The results are interpreted as a result of an increased protein turnover caused by the caloric restriction.
C1 TOKYO METROPOLITAN GERIATR HOSP & INST GERONTOL,DEPT CLIN PHYSIOL,ITABASHI KU,TOKYO 173,JAPAN.
   NIA,GERONTOL RES CTR,BALTIMORE,MD 21224.
RP NAGY, IZ (reprint author), DEBRECEN UNIV MED,SCH MED,VERZAR INT LAB EXPTL GERONTOL,HUNGARIAN SECT,H-4012 DEBRECEN,HUNGARY.
NR 40
TC 5
Z9 5
U1 0
U2 0
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0047-6374
J9 MECH AGEING DEV
JI Mech. Ageing. Dev.
PD OCT 1
PY 1993
VL 71
IS 1-2
BP 85
EP 96
PG 12
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA MD032
UT WOS:A1993MD03200008
PM 8309285
ER

PT J
AU LOCKWICH, T
   DUNIGAN, CD
   SHAMOO, AE
AF LOCKWICH, T
   DUNIGAN, CD
   SHAMOO, AE
TI UNCOUPLING OF OCCLUSION FROM ATP HYDROLYSIS ACTIVITY IN
   SARCOPLASMIC-RETICULUM (CA2++MG2+)-ATPASE
SO MEMBRANE BIOCHEMISTRY
LA English
DT Article
DE UNCOUPLING; SARCOPLASMIC RETICULUM; (CA(2+)+MG(2+))-ATPASE; TRYPSIN
ID CA-2+,MG-2+-ADENOSINE TRIPHOSPHATASE; CALCIUM-TRANSPORT; TRYPTIC
   DIGESTION; CA2+ TRANSPORT; CA-2+; CA-2+-ATPASE; CA2+-ATPASE;
   SUSCEPTIBILITY; TEMPERATURE; MEMBRANES
AB The uncoupling of Ca2+ transport from ATP hydrolysis in the sarcoplasmic reticulum (Ca2++Mg2+)-ATPase by trypsin digestion was re-investigated by comparing ATPase activity with the ability of the enzyme to occlude Eu3+ (a transport parameter) after various tryptic digests. With this method, I e-examination of uncoupling by tryptic digest of the ATPase revealed that TD2 cleavage (Arg-198) had no effect on either occlusion or ATPase activity. Digestion past TD2 in the presence of 5 mM Ca2+ and at 25 degrees C resulted in the loss of about 70% of the ATPase activity, but no loss of occlusion. Digestion past TD2 in the presence of 5 mM Ca2+, 3 mM ATP, and at 25 degrees C resulted in a partially uncoupled enzyme complex which retained about 50% of the ATPase activity, but completely lost the ability to occlude Eu3+. Digest past TD2 in the presence of 5 mM Ca2+ and 3 mM AMP-PNP (a non-hydrolyzable ATP analog) at 25 degrees C resulted in no loss of occlusion,, thus revealing the absolute requirement of ATP during the digest to eliminate occlusion. From these findings we conclude that uncoupling of Ca2+ transport from ATPase activity is possible by tryptic digestion of the (Ca2+ +Mg2+)-ATPase. Interestingly, only after phosphorylation of the enzyme do the susceptible bond(s) which lead to the loss of occlusion become exposed to trypsin.
C1 UNIV BALTIMORE,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21201.
RP LOCKWICH, T (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892, USA.
NR 33
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS
PI BRISTOL
PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598
SN 0149-046X
J9 MEMBRANE BIOCHEM
PD OCT-DEC
PY 1993
VL 10
IS 4
BP 191
EP 201
DI 10.3109/09687689309150267
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA MZ572
UT WOS:A1993MZ57200001
PM 8007838
ER

PT J
AU OLIVARES, E
   ARISPE, N
   ROJAS, E
AF OLIVARES, E
   ARISPE, N
   ROJAS, E
TI PROPERTIES OF THE RYANODINE RECEPTOR PRESENT IN THE
   SARCOPLASMIC-RETICULUM FROM LOBSTER SKELETAL-MUSCLE
SO MEMBRANE BIOCHEMISTRY
LA English
DT Article
DE E-C COUPLING; CALCIUM RELEASE CHANNEL; CRUSTACEAN MUSCLE
ID CA-2+ RELEASE CHANNEL; INDUCED CALCIUM RELEASE; TERMINAL CISTERNAE;
   BINDING-SITES; CONTRACTION; COMPLEX; TETRACAINE; PROTEINS; VESICLES;
   FIBERS
AB Microsomal sarcoplasmic reticulum (SR) fractions from lobster skeletal muscle were found to bind [H-3]-ryanodine. [H-3]-ryanodine binding was enhanced by AMP, Ca2+ and caffeine, and significantly diminished by ATP, Ba2+ and Sr2+. Furthermore, dantrolene and ruthenium red, two classical inhibitors of Ca2+ release from the SR, blocked [H-3]-ryanodine binding. Similarly, tetracaine, known to block the charge movement associated with excitation-contraction coupling in vertebrate muscle, inhibited the binding of the alkaloid. Our lobster SR preparation exhibited a single high-affinity ryanodine binding site (K-d = 6.6 nM, B-max = 10 pmol/mg protein). Since SDS-PAGE of the SR proteins revealed a major band c. 565 kDa which comigrated with the putative ryanodine receptor from both rat and chicken skeletal muscle, we concluded that lobster skeletal muscle is equipped with the 565 kDA ryanodine receptor. Finally, incorporation of the SR microsomal fraction from lobster into planar bilayer membranes revealed the presence of a ryanodine-sensitive Ca2+ channel activity (160 pS in symmetrical 200 mM CsCl solutions). We concluded that both the crustacean and vertebrate skeletal muscle ryanodine receptor share the relevant properties such as molecular weight and affinity for ryanodine and inositol 1,4,5 triphosphate. However, there are important differences between the two receptors including differential effects of the alkaloid on the Ca2+ release channel and modulation of the receptor by nucleotides.
C1 NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892.
NR 43
TC 14
Z9 14
U1 0
U2 0
PU TAYLOR & FRANCIS
PI BRISTOL
PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598
SN 0149-046X
J9 MEMBRANE BIOCHEM
PD OCT-DEC
PY 1993
VL 10
IS 4
BP 221
EP 235
DI 10.3109/09687689309150270
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA MZ572
UT WOS:A1993MZ57200004
PM 7516463
ER

PT J
AU SEGARS, JH
   NAGATA, T
   BOURS, V
   MEDIN, JA
   FRANZOSO, G
   BLANCO, JCG
   DREW, PD
   BECKER, KG
   AN, JB
   TANG, T
   STEPHANY, DA
   NEEL, B
   SIEBENLIST, U
   OZATO, K
AF SEGARS, JH
   NAGATA, T
   BOURS, V
   MEDIN, JA
   FRANZOSO, G
   BLANCO, JCG
   DREW, PD
   BECKER, KG
   AN, JB
   TANG, T
   STEPHANY, DA
   NEEL, B
   SIEBENLIST, U
   OZATO, K
TI RETINOIC ACID INDUCTION OF MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I
   GENES IN NTERA-2 EMBRYONAL CARCINOMA-CELLS INVOLVES INDUCTION OF
   NF-KAPPA-B (P50-P65) AND RETINOIC ACID RECEPTOR BETA-RETINOID X
   RECEPTOR-BETA HETERODIMERS
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID TISSUE-SPECIFIC EXPRESSION; DNA-BINDING PROTEIN; TRANSCRIPTION FACTOR;
   TERATOCARCINOMA CELLS; REGULATORY ELEMENT; THYROID-HORMONE; STEM-CELLS;
   DIFFERENTIAL EXPRESSION; NUCLEAR RECEPTORS; REL ONCOGENE
AB Retinoic acid (RA) treatment of human embryonal carcinoma (EC) NTera-2 (NT2) cells induces expression of major histocompatibility complex (MHC) class I and beta-2 microglobulin surface molecules. We found that this induction was accompanied by increased levels of MHC class I mRNA, which was attributable to the activation of the two conserved upstream enhancers, region I (NF-kappaB like) and region II. This activation coincided with the induction of nuclear factor binding activities specific for the two enhancers. Region I binding activity was not present in undifferentiated NT2 cells, but binding of an NF-kappaB heterodimer, p50-p65, was induced following RA treatment. The p50-p65 heterodimer was produced as a result of de novo induction of p50 and p65 mRNAs. Region II binding activity was present in undifferentiated cells at low levels but was greatly augmented by RA treatment because of activation of a nuclear hormone receptor heterodimer composed of the retinoid X receptor (RXRbeta) and the RA receptor (RARbeta). The RXRbeta-RARbeta heterodimer also bound RA responsive elements present in other genes which are likely to be involved in RA triggering of EC cell differentiation. Furthermore, transfection of p50 and p65 into undifferentiated NT2 cells synergistically activated region I-dependent MHC class I reporter activity. A similar increase in MHC class I reporter activity was demonstrated by cotransfection of RXRbeta and RARbeta. These data show that following RA treatment, heterodimers of two transcription factor families are induced to bind to the MHC enhancers, which at least partly accounts for RA induction of MHC class I expression in NT2 EC cells.
C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892.
   NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892.
   NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892.
   NINCDS,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892.
   HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,MOLEC MED UNIT,BOSTON,MA 02215.
NR 79
TC 69
Z9 70
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 OCT
PY 1993
VL 13
IS 10
BP 6157
EP 6169
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA LY424
UT WOS:A1993LY42400022
PM 8413217
ER

PT J
AU LIN, JX
   BHAT, NK
   JOHN, S
   QUEALE, WS
   LEONARD, WJ
AF LIN, JX
   BHAT, NK
   JOHN, S
   QUEALE, WS
   LEONARD, WJ
TI CHARACTERIZATION OF THE HUMAN INTERLEUKIN-2 RECEPTOR BETA-CHAIN GENE
   PROMOTER - REGULATION OF PROMOTER ACTIVITY BY ETS GENE-PRODUCTS
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID LONG TERMINAL REPEAT; SEQUENCE-SPECIFIC BINDING; IL-2 RECEPTOR;
   ALPHA-CHAIN; DNA-BINDING; PROTEIN INTERACTIONS; MOLECULAR-CLONING; CELL
   GROWTH; IDENTIFICATION; EXPRESSION
AB The interleukin-2 receptor (IL-2R) beta chain (IL-2Rbeta) is an essential signaling component of high- and intermediate-affinity IL-2Rs. Our laboratory previously reported that a DNA fragment containing 857 bp of 5'-flanking sequence of the human IL-2Rbeta gene exhibited promoter activity. We have now further characterized the promoter and delineated cis-acting regulatory regions. The region downstream of -363 is critical for basal and phorbol myristate acetate-inducible IL-2Rbeta promoter activity and contains at least three enhancer-like regions. Among them, the -56 to -34 enhancer was the most potent and had high-level activity in two T-cell lines but not in nonlymphoid HeLaS3 and MG63 cells. This enhancer contains a GGAA Ets binding site which bound two Ets family proteins, Ets-1 and GA-binding protein in vitro. Mutation of the Ets motif strongly diminished both promoter and enhancer activities. We conclude that this Ets binding site plays a key role in regulating basal and phorbol myristate acetate-inducible IL-2Rbeta promoter activity and may also contribute to tissue-specific expression of the IL-2Rbeta gene.
C1 NHLBI,PULM & MOLEC IMMUNOL SECT,OFF DIRECTOR,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892.
   NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702.
   PROGRAM RESOURCES INC DYNCORP,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702.
NR 51
TC 68
Z9 68
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 OCT
PY 1993
VL 13
IS 10
BP 6201
EP 6210
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA LY424
UT WOS:A1993LY42400026
PM 8413220
ER

PT J
AU COHEN, BD
   LOWY, DR
   SCHILLER, JT
AF COHEN, BD
   LOWY, DR
   SCHILLER, JT
TI THE CONSERVED C-TERMINAL DOMAIN OF THE BOVINE PAPILLOMAVIRUS E5
   ONCOPROTEIN CAN ASSOCIATE WITH AN ALPHA-ADAPTIN-LIKE MOLECULE - A
   POSSIBLE LINK BETWEEN GROWTH-FACTOR RECEPTORS AND VIRAL TRANSFORMATION
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID COATED VESICLE PROTEINS; POLYOMA-VIRUS; CLATHRIN; INTERNALIZATION;
   POLYPEPTIDE; COMPLEX; ENCODES; GENE
AB The bovine papillomavirus E5 gene encodes an oncoprotein that can independently transform rodent fibroblasts. This small 44-amino-acid protein is thought to function through the activation of growth factor receptors. E5 activation of the epidermal growth factor receptor results in an increase in the number of activated receptors at the cell surface. This finding suggests that E5 may act by inhibiting the normal down regulation of activated epidermal growth factor receptor via coated pit-mediated endocytosis. We have constructed a fusion protein consisting of glutathione S-transferase and the conserved C-terminal domain of E5 (GST-E5) in order to identify E5-associated cellular proteins that may be involved in its transforming activity. We have identified a 125-kDa cellular protein with a strong associated serine kinase activity that specifically associated with GST-E5 in the reduced form but not with GST-E5 fusions that contained changes in several conserved amino acids. Microsequence and biochemical analyses suggest that p125 is a novel member of the alpha-adaptin family. Since alpha-adaptins have previously been shown to be involved in coated pit-mediated cell surface receptor endocytosis and down regulation, these results suggest that p125 may be an alpha-adaptin-like molecule involved in growth factor receptor down regulation and that E5 may act by inhibiting its activity.
C1 NCI,CELLULAR ONCOL LAB,BLDG 37,ROOM 1B-26,BETHESDA,MD 20892.
FU NCI NIH HHS [TA-CA-B046]
NR 27
TC 32
Z9 33
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 OCT
PY 1993
VL 13
IS 10
BP 6462
EP 6468
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA LY424
UT WOS:A1993LY42400052
PM 8413245
ER

PT J
AU FLANDERS, KC
   LUDECKE, G
   RENZING, J
   HAMM, C
   CISSEL, DS
   UNSICKER, K
AF FLANDERS, KC
   LUDECKE, G
   RENZING, J
   HAMM, C
   CISSEL, DS
   UNSICKER, K
TI EFFECTS OF TGF-BETA-S AND BFGF ON ASTROGLIAL CELL-GROWTH AND
   GENE-EXPRESSION IN-VITRO
SO MOLECULAR AND CELLULAR NEUROSCIENCE
LA English
DT Article
ID PLASMINOGEN-ACTIVATOR INHIBITOR; COMPLEMENTARY-DNA CLONING; HUMAN-LUNG
   FIBROBLASTS; MESSENGER-RNA; NERVOUS-SYSTEM; ADULT TISSUES; RAT-BRAIN;
   EXTRACELLULAR-MATRIX; ASTROCYTE CULTURES; CARCINOMA-CELLS
C1 UNIV HEIDELBERG, DEPT ANAT & CELL BIOL, D-69120 HEIDELBERG, GERMANY.
RP FLANDERS, KC (reprint author), NCI, CHEMOPREVENT LAB, BETHESDA, MD 20892 USA.
NR 77
TC 52
Z9 52
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1044-7431
J9 MOL CELL NEUROSCI
JI Mol. Cell. Neurosci.
PD OCT
PY 1993
VL 4
IS 5
BP 406
EP 417
DI 10.1006/mcne.1993.1051
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA LX930
UT WOS:A1993LX93000003
PM 19912947
ER

PT J
AU KUSIAK, JW
   NORTON, DD
AF KUSIAK, JW
   NORTON, DD
TI A SPLICE VARIANT OF THE N-METHYL-D-ASPARTATE (NMDAR1) RECEPTOR
SO MOLECULAR BRAIN RESEARCH
LA English
DT Article
DE NMDA; NMDA RECEPTOR; LIGAND-GATED ION CHANNEL; ALTERNATIVE SPLICING;
   REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; GENE STRUCTURE
ID NICOTINIC ACETYLCHOLINE-RECEPTOR; GLUTAMATE-OPERATED CHANNELS;
   ALPHA-SUBUNIT; MOLECULAR-CLONING; FUNCTIONAL EXPRESSION; EXTRACELLULAR
   ATP; XENOPUS OOCYTES; BINDING SUBUNIT; ION CHANNELS; CLONED CDNAS
AB A splice variant of the NMDA receptor (NMDAR1) was discovered containing a deletion of 37 amino acids near the carboxyl tail and has been designated NMDAR1b. The III nucleotides corresponding to the deleted amino acid sequence were found in a separate exon bounded by consensus intron/exon junction sequences in rat genomic DNA. A partial restriction map of genomic DNA bounding this region placed the deleted exon approximately 600 base pairs (bp) downstream of the upstream exon. RT/PCR analysis of RNA from different brain regions showed that the deletion variant is more abundantly expressed in the brain stem and cerebellum while the full-length form is expressed more abundantly in the olfactory bulb, striatum, hippocampus, and cortex. Northern analysis of poly(A)+ RNA from different brain regions with probes specific for the deleted exon (i.e., full-length form) and for the splice junction (deletion form) indicated approximately 4.4 kb transcripts. The probe for the deleted exon hybridized to transcripts in olfactory bulb, cortex, striatum, and hippocampus while the splice junction probe hybridized most strongly to transcripts in cerebellum. The results suggest an interesting rostral to caudal shift in the expression of splice variants of the NMDAR1 which may signify important functional differences in native forms of NMDA receptors.
RP KUSIAK, JW (reprint author), NIA,FS KEY MED CTR,BIOL CHEM LAB,MOLEC NEUROBIOL UNIT,BALTIMORE,MD 21224, USA.
NR 46
TC 18
Z9 18
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0169-328X
J9 MOL BRAIN RES
JI Mol. Brain Res.
PD OCT
PY 1993
VL 20
IS 1-2
BP 64
EP 70
DI 10.1016/0169-328X(93)90110-B
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA LY418
UT WOS:A1993LY41800006
ER

PT J
AU PERSICO, AM
   SCHINDLER, CW
   OHARA, BF
   BRANNOCK, MT
   UHL, GR
AF PERSICO, AM
   SCHINDLER, CW
   OHARA, BF
   BRANNOCK, MT
   UHL, GR
TI BRAIN TRANSCRIPTION FACTOR EXPRESSION - EFFECTS OF ACUTE AND CHRONIC
   AMPHETAMINE AND INJECTION STRESS
SO MOLECULAR BRAIN RESEARCH
LA English
DT Article
DE TRANSCRIPTION FACTOR; IMMEDIATE-EARLY GENE; C-FOS; AMPHETAMINE;
   TOLERANCE; SENSITIZATION; STRESS
ID IMMEDIATE-EARLY GENE; C-FOS EXPRESSION; SERUM GROWTH-FACTORS;
   DNA-BINDING ACTIVITY; RAT-BRAIN; MESSENGER-RNAS; SUPRACHIASMATIC
   NUCLEUS; DISCRIMINATIVE STIMULUS; RECEPTOR ACTIVATION; CEREBRAL-CORTEX
AB Amphetamine influences behaviors and the expression of transcription factor genes in the central nervous system (CNS). A single d-amphetamine dose (7.5 mg/kg, i.p.) enhances behavioral sterotypy and augments brain expression of c-fos, fos-B, fra-1, zif 268, jun-B, and c-jun by 2-11 fold. When the single amphetamine dose is preceeded by 28 saline injections over 14 days, it is half as effective in enhancing expression of these genes. Rats injected with 7.5 mg/kg i.p. twice daily for 2 weeks and sacrificed after the last injection reveal further attenuation or abolition of the amphetamine-induced mRNA upregulation. These stigmata of 'tolerance' in gene expression display partial overlap with behavioral tolerance, manifest as changes in locomotor activity. Rats receiving low (2 mg/kg) amphetamine challenge doses following the 2-week 7.5 mg/kg b.i.d. amphetamine treatment show tolerance to the locomotor activating effects of the drug; no tolerance is evident following a high (7.5 mg/kg) challenge dose. These data suggest that amphetamine-induced alterations in brain transcription factor gene expression can display 'tolerance' and possibly 'cross-tolerance' with the stress caused by i.p. injection.
C1 NIDA,ARC,MOLEC NEUROBIOL BRANCH,BOX 5180,BALTIMORE,MD 21224.
   NIDA,ARC,BEHAV PHARMACOL & GENET SECT,BALTIMORE,MD 21224.
   JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL & NEUROSCI,BALTIMORE,MD 21205.
NR 77
TC 94
Z9 95
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0169-328X
J9 MOL BRAIN RES
JI Mol. Brain Res.
PD OCT
PY 1993
VL 20
IS 1-2
BP 91
EP 100
DI 10.1016/0169-328X(93)90113-4
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA LY418
UT WOS:A1993LY41800009
ER

PT J
AU SALBERT, G
   FANJUL, A
   PIEDRAFITA, FJ
   LU, XP
   KIM, SJ
   TRAN, P
   PFAHL, M
AF SALBERT, G
   FANJUL, A
   PIEDRAFITA, FJ
   LU, XP
   KIM, SJ
   TRAN, P
   PFAHL, M
TI RETINOIC ACID RECEPTORS AND RETINOID-X RECEPTOR-ALPHA DOWN-REGULATE THE
   TRANSFORMING GROWTH FACTOR-BETA(1) PROMOTER BY ANTAGONIZING AP-1
   ACTIVITY
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID T-CELL LEUKEMIA; THYROID-HORMONE; FACTOR-BETA; TGF-BETA; NUCLEAR
   RECEPTORS; GLUCOCORTICOID RECEPTOR; EXTRACELLULAR-MATRIX; POTENTIAL
   MECHANISM; TARGET SEQUENCES; GENE-EXPRESSION
AB Overexpression of the multifunctional growth factor transforming growth factor-beta1 (TGFbeta1) has been connected to numerous diseases in human. TGFbeta1 expression is largely governed by three AP-1 binding sites located in two different promoters of this gene. We have examined the ability of retinoid receptors to inhibit the activity of the two promoters (especially the promoter 1) by cotransfection assays in the hepatocellular carcinoma cell line HepG2. When the TGFbeta1 promoter activity is induced by 12-O-tetradecanoyl phorbol-13-acetate (an activator of AP-1-controlled gene transcription), this activity can be strongly repressed by retinoic acid receptor-alpha (RARalpha), RARbeta, or retinoid X receptor-alpha (RXRalpha) as well as other members of the nuclear receptor family. Repression was hormone dependent and a function of receptor concentration. Heterodimerization of RARa or RARbeta with RXRalpha did not modify the inhibition activities of these receptors, indicating that heterodimer formation is not required for antagonizing of AP-1 activity. On further examining the anti-AP-1 activity of RXRalpha we observed that three different AP-1-controlled promoters (TGFbeta1, collagenase, and cFos) can be inhibited. Using gel shift assays, we demonstrated that RXRalpha inhibits Jun and Fos DNA binding and that 9-cis RA enhances this inhibition, suggesting that a mechanism involving direct protein-protein interaction between RXR and AP-1 components mediates the inhibitory effect observed in vivo. Transfection analyses with RXRalpha point mutations revealed that residues L422, C432, and, to a lesser extent, residues L418 and L430, are involved in ligand-induced anti-AP1 activity of RXRalpha in vivo. Thus both types of retinoid receptors can inhibit AP-1-activated promoters, including the TGFbeta1 gene promoter, via a mechanism that involves protein-protein interaction.
C1 LA JOLLA CANC RES FDN, 10901 N TORREY PINES RD, LA JOLLA, CA 92037 USA.
   NCI, CHEMOPREVENT LAB, BETHESDA, MD 20892 USA.
FU NCI NIH HHS [CA-55681]
NR 66
TC 158
Z9 159
U1 0
U2 2
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD OCT
PY 1993
VL 7
IS 10
BP 1347
EP 1356
DI 10.1210/me.7.10.1347
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA MD616
UT WOS:A1993MD61600013
PM 8264664
ER

PT J
AU GRILLI, M
   CHENTRAN, A
   LENARDO, MJ
AF GRILLI, M
   CHENTRAN, A
   LENARDO, MJ
TI TUMOR-NECROSIS-FACTOR-ALPHA MEDIATES A T-CELL RECEPTOR-INDEPENDENT
   INDUCTION OF THE GENE REGULATORY FACTOR NF-KAPPA-B IN T-LYMPHOCYTES
SO MOLECULAR IMMUNOLOGY
LA English
DT Article
ID DNA-BINDING SUBUNIT; ANTIGEN-PRESENTING CELLS; CLONAL ANERGY;
   MESSENGER-RNA; REL ONCOGENE; ACTIVATION; EXPRESSION; PROTEIN;
   TRANSCRIPTION; CLONING
AB We investigated the molecular basis of the ability of DCEK experimental antigen-presenting cells (APCs) to induce the nuclear form of the transcription factor NF-kappaB in T lymphocytes without engagement of the T cell receptor. We found that NF-kappaB induction did not require contact between the APCs and T lymphocytes and could be achieved by medium conditioned by the APCs. The APCs were found to express low levels of mRNA for TNFalpha. The addition of antibody against TNFalpha blocked the ability of APCs to induce NF-kappaB. These observations were extended by the finding that NF-kappaB was also induced in T lymphocytes separated by a membrane from a mixture of T lymphocytes, splenic APCs and antigen by a TNFalpha-dependent mechanism. Together, these findings suggest that induction of NF-kappaB in antigenically stimulated or 'bystander' T cells may take place through stimulation by TNFalpha as well as in response to T cell receptor occupancy.
C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892.
NR 43
TC 7
Z9 7
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD OCT
PY 1993
VL 30
IS 14
BP 1287
EP 1294
DI 10.1016/0161-5890(93)90045-D
PG 8
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA MA376
UT WOS:A1993MA37600009
PM 8413329
ER

PT J
AU HEINEMANN, JA
   ANKENBAUER, RG
AF HEINEMANN, JA
   ANKENBAUER, RG
TI RETROTRANSFER OF INCP PLASMID R751 FROM ESCHERICHIA-COLI MAXICELLS -
   EVIDENCE FOR THE GENETIC SUFFICIENCY OF SELF-TRANSFERABLE PLASMIDS FOR
   BACTERIAL CONJUGATION
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID ANTIBIOTIC-RESISTANCE; EVOLUTION; DNA; IDENTIFICATION; PRODUCT; ORIGIN;
   SEX
AB Gene transfer between organisms is a prime contributor to evolution. Bacterial conjugation is probably the most important mechanism by which genes are spread among prokaryotes and perhaps also contributes to eukaryotic evolution. Conjugation is mediated by plasmids. The mechanism of conjugation remains ill-understood despite progress in the identification, mapping and sequencing of genes required for plasmid transmission. All conjugation-specific genes (those required only for DNA transfer and establishment) identified to date map to plasmids. We found that IncP plasmids could enter and subsequently convert maxicells, which are trapped in a metabolic state that prevents de novo expression of chromosomal genes, into conjugative donors. This suggests that IncP plasmids encode not only necessary functions but indeed all functions specific to DNA transmission. Thus, like viruses, plasmids can convert non-viable cells into gene vectors.
RP HEINEMANN, JA (reprint author), NIAID,LMSF,ROCKY MT LABS,HAMILTON,MT 59840, USA.
NR 39
TC 22
Z9 23
U1 0
U2 0
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD OCT
PY 1993
VL 10
IS 1
BP 57
EP 62
DI 10.1111/j.1365-2958.1993.tb00903.x
PG 6
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA MB916
UT WOS:A1993MB91600007
PM 7968518
ER

PT J
AU OPPENHEIM, AB
   RUDD, KE
   MENDELSON, I
   TEFF, D
AF OPPENHEIM, AB
   RUDD, KE
   MENDELSON, I
   TEFF, D
TI INTEGRATION HOST FACTOR BINDS TO A UNIQUE CLASS OF COMPLEX REPETITIVE
   EXTRAGENIC DNA-SEQUENCES IN ESCHERICHIA-COLI
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID MESSENGER-RNA STABILITY; PALINDROMIC SEQUENCES; GENE-EXPRESSION;
   SALMONELLA-TYPHIMURIUM; REP SEQUENCES; FACTOR IHF; PROTEIN; FAMILY;
   TRANSCRIPTION; INVIVO
AB Interspersed repeated DNA sequences are characteristic features of both prokaryotic and eukaryotic genomes. REP sequences are defined as conserved repetitive extragenic palindromic sequences and are found in Escherichia coli, Salmonella typhimurium and other closely related enteric bacteria. These REP sequences may participate in the folding of the bacterial chromosome. In this work we describe a unique class of 28 conserved complex REP clusters, about 100 bp long, in which two inverted REPs are separated by a singular integration host factor (IHF) recognition sequence. We term these sequences RIP (for repetitive IHF-binding palindromic) elements and demonstrate that IHF binds to them specifically. It is estimated that there are about 70 RIP elements in E. coli. Our analysis shows that the RIP elements are evenly distributed around the bacterial chromosome. The possible function of the RIP element is discussed.
C1 NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894.
RP OPPENHEIM, AB (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT MOLEC GENET,IL-91010 JERUSALEM,ISRAEL.
NR 49
TC 47
Z9 47
U1 0
U2 1
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD OCT
PY 1993
VL 10
IS 1
BP 113
EP 122
DI 10.1111/j.1365-2958.1993.tb00908.x
PG 10
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA MB916
UT WOS:A1993MB91600012
PM 7968507
ER

PT J
AU HINNEBUSCH, AG
AF HINNEBUSCH, AG
TI GENE-SPECIFIC TRANSLATIONAL CONTROL OF THE YEAST GCN4 GENE BY
   PHOSPHORYLATION OF EUKARYOTIC INITIATION FACTOR-II
SO MOLECULAR MICROBIOLOGY
LA English
DT Review
ID TRANSFER-RNA-SYNTHETASES; AMINO-ACID BIOSYNTHESIS; POLYPEPTIDE-CHAIN
   INITIATION; ACTIVATED PROTEIN-KINASE; OPEN READING FRAMES;
   SACCHAROMYCES-CEREVISIAE; MESSENGER-RNA; TRANSCRIPTIONAL ACTIVATOR;
   EIF-2-ALPHA KINASE; ESCHERICHIA-COLI
AB Phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF-2alpha) is one of the best-characterized mechanisms for down-regulating total protein synthesis in mammalian cells in response to various stress conditions. Recent work indicates that regulation of the GCN4 gene of Saccharomyces cerevisiae by amino acid availability represents a gene-specific case of translational control by phosphorylation of eIF-2alpha. Four short open reading frames in the leader of GCN4 mRNA (uORFs) restrict the flow of scanning ribosomes from the cap site to the GCN4 initiation codon. When amino acids are abundant, ribosomes translate the first uORF and reinitiate at one of the remaining uORFs in the leader, after which they dissociate from the mRNA. Under conditions of amino acid starvation, many ribosomes which have translated uORF1 fail to reinitiate at uORFs 2-4 and utilize the GCN4 start codon instead. Failure to reinitiate at uORFs 2-4 in starved cells results from a reduction in the GTP-bound form of eIF-2 that delivers charged initiator tRNA(i)Met to the ribosome. When the levels of eIF-2.GTP.Met-tRNA(i)Met ternary complexes are low, many ribosomes will not rebind this critical initiation factor following translation of uORF1 until after scanning past uORF4, but before reaching GCN4. Phosphorylation of eIF-2 by the protein kinase GCN2 decreases the concentration of eIF-2.GTP.Met-tRNA(i)Met complexes by inhibiting the guanine nucleotide exchange factor for eIF-2, which is the same mechanism utilized in mammalian cells to inhibit total protein synthesis by phosphorylation of eIF-2.
RP HINNEBUSCH, AG (reprint author), NICHHD,MOLEC GENET LAB,MOLEC GENET LOWER EUKARYOTES SECT,BETHESDA,MD 20892, USA.
NR 55
TC 90
Z9 90
U1 0
U2 10
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD OCT
PY 1993
VL 10
IS 2
BP 215
EP 223
DI 10.1111/j.1365-2958.1993.tb01947.x
PG 9
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA MD250
UT WOS:A1993MD25000001
PM 7934812
ER

PT J
AU WEICKERT, MJ
   ADHYA, S
AF WEICKERT, MJ
   ADHYA, S
TI THE GALACTOSE REGULON OF ESCHERICHIA-COLI
SO MOLECULAR MICROBIOLOGY
LA English
DT Review
ID ACCEPTING CHEMOTAXIS PROTEIN; GENE ACTIVATOR PROTEIN; GAL REPRESSOR;
   RNA-POLYMERASE; NUCLEOTIDE-SEQUENCE; TRANSPORT-SYSTEM; POSITIVE CONTROL;
   L-ARABINOSE; DNA; OPERON
AB Galactose transport and metabolism in Escherichia coli involves a multicomponent amphibolic pathway Galactose transport is accomplished by two different galactose-specific transport systems. At least four of the genes and operons involved in galactose transport and metabolism have promoters containing similar regulatory sequences. These sequences are recognized by at least three regulators, Gal repressor (GalR), Gal isorepressor (GalS) and cAMP receptor protein (CRP), which modulate transcription from these promoters. The negative regulators, GalR and GalS, discriminate between utilization of the high-affinity (regulated by GalS) and low-affinity (regulated by GalR) transport systems, and modulate the expression of genes for galactose metabolism in an overlapping fashion. GalS is itself autogenously regulated and CRP dependent, while the gene for GalR is constitutive. The gal operon encoding the enzymes for galactose metabolism has two promoters regulated by CRP in opposite ways; one (P1) is stimulated and the other (P2) inhibited by CRP. Both promoters are strongly repressed by GalR but weakly by GalS. All but one of the constituent promoters of the gal regulon have two operators. The gal regulon has the potential to coordinate galactose metabolism and transport in a highly efficient manner, under a wide variety of conditions of galactose availability.
C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892.
   SOMATOGEN INC,5797 CENT AVE,BOULDER,CO 80301.
NR 59
TC 81
Z9 81
U1 2
U2 10
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD OCT
PY 1993
VL 10
IS 2
BP 245
EP 251
DI 10.1111/j.1365-2958.1993.tb01950.x
PG 7
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA MD250
UT WOS:A1993MD25000004
PM 7934815
ER

PT J
AU BAI, RL
   CICHACZ, ZA
   HERALD, CL
   PETTIT, GR
   HAMEL, E
AF BAI, RL
   CICHACZ, ZA
   HERALD, CL
   PETTIT, GR
   HAMEL, E
TI SPONGISTATIN-1, A HIGHLY CYTOTOXIC, SPONGE-DERIVED, MARINE NATURAL
   PRODUCT THAT INHIBITS MITOSIS, MICROTUBULE ASSEMBLY, AND THE BINDING OF
   VINBLASTINE TO TUBULIN
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID ANTINEOPLASTIC AGENTS; ANTIMITOTIC AGENTS; PHOMOPSIN-A; DOLASTATIN-10;
   NUCLEOTIDE; SITE; POLYMERIZATION; ANTIBIOTICS; COMPONENT; DOMAIN
AB A highly cytotoxic macrocyclic lactone polyether has been isolated from a Spongia species and named spongistatin 1. With L1210 murine leukemia cells an IC50 value for cell proliferation of 20 pm was obtained, and an increase in the mitotic index concordant with the decrease in cell number was observed. Kangaroo rat kidney PtK1 cells were examined by indirect immunofluorescence with a spongistatin 1 concentration that caused 50% reduction in cellular protein (0.3 nm) and with a 10-fold higher concentration. These cells displayed mitotic and nuclear aberrations at both concentrations, and intracellular microtubules were reduced in number at the lower concentration and disappeared at the higher. Similar changes in PtK1 cells were observed after treatment with equivalent toxic concentrations of the antimitotic agents colchicine, vinblastine, halichondrin B, and dolastatin 10. Spongistatin 1 inhibited the glutamate-induced polymerization of purified tubulin (IC50 value of 3.6 muM versus 2.1 muM for dolastatin 10 and vinblastine and 5.2 muM for halichondrin B). Spongistatin 1 had no effect on the binding of colchicine to tubulin, but it was a potent inhibitor of the binding of vinblastine and GTP to tubulin. In initial experiments with 5 muM tubulin and 5 Am vinblastine, spongistatin 1 and dolastatin 10 both had IC50 values of 2 muM, whereas halichondrin B had an IC50 value of 5 muM. Spongistatin 1 thus represents a new member of the group of complex natural products that inhibit mitosis by binding in the Vinca alkaloid domain of tubulin.
C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BLDG 37,ROOM 5C25,BETHESDA,MD 20892.
   ARIZONA STATE UNIV,CANC RES INST,TEMPE,AZ 85297.
   ARIZONA STATE UNIV,DEPT CHEM,TEMPE,AZ 85297.
NR 28
TC 113
Z9 115
U1 0
U2 4
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD OCT
PY 1993
VL 44
IS 4
BP 757
EP 766
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA ME531
UT WOS:A1993ME53100011
PM 8232226
ER

PT J
AU PODDEVIN, B
   RIOU, JF
   LAVELLE, F
   POMMIER, Y
AF PODDEVIN, B
   RIOU, JF
   LAVELLE, F
   POMMIER, Y
TI DUAL TOPOISOMERASE-I AND TOPOISOMERASE-II INHIBITION BY INTOPLICINE
   (RP-60475), A NEW ANTITUMOR AGENT IN EARLY CLINICAL-TRIALS
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID DNA STRAND BREAKS; HAMSTER CELLS RESISTANT; CULTURED L1210 CELLS;
   ANTINEOPLASTIC AGENTS; INTERCALATING AGENTS; REUNION REACTION;
   ACTINOMYCIN-D; DRUG-ACTION; CAMPTOTHECIN; CLEAVAGE
AB The mechanisms of action of intoplicine (RP-60475), a 7H-benzo[e]pyrido[4,3-b]indole derivative that is presently in early clinical trials, have been investigated. Intoplicine induced both topoisomerase I- and II-mediated DNA strand breaks, using purified topoisomerases. The topoisomerase cleavage site patterns induced by intoplicine were unique, relative to those of camptothecin, 4'-(9-acridinylamino)methanesulfon-m-anisidide (m-AMSA), and other known topoisomerase inhibitors. Both topoisomerase I- and II-induced DNA breaks decreased at drug concentrations higher than 1 muM, which is consistent with the DNA-intercalating activity of intoplicine. DNA damage was investigated in KB cells in culture by using alkaline elution. Intoplicine induced single-strand breaks (SSB) in a bell-shaped manner with respect to drug concentration (maximum frequency at 1 muM almost-equal-to 220 rad-equivalents). SSB formation was fast, whereas reversal after drug removal was slow. Similar bell-shaped curves were obtained for DNA double-strand breaks (DSB) and DNA-protein cross-links. SSB and DNA-protein cross-link frequencies were approximately equal, and no protein-free breaks were detectable, indicating the protein concealment of the breaks, as expected for topoisomerase inhibition. Comparison of SSB and DSB frequencies indicated that intoplicine produced a significant amount of SSB not related to DSB, which is consistent with concomitant inhibition of both DNA topoisomerases I and II in cells. Data derived from resistant cell lines indicated that multidrug-resistant cells were cross-resistant to intoplicine but that m-AMSA- and camptothecin-resistant cells were sensitive to intoplicine. Hence, intoplicine might circumvent topoisomerase I-mediated and topoisomerase II-mediated resistance by poisoning both enzymes simultaneously.
C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BLDG 37,ROOM 5C25,BETHESDA,MD 20892.
   RHONE POULENC RORER SA,F-94403 VITRY,FRANCE.
NR 44
TC 71
Z9 72
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD OCT
PY 1993
VL 44
IS 4
BP 767
EP 774
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA ME531
UT WOS:A1993ME53100012
PM 8232227
ER

PT J
AU ORBUCH, M
   TAYLOR, JE
   COY, DH
   MROZINSKI, JE
   MANTEY, SA
   BATTEY, JF
   MOREAU, JP
   JENSEN, RT
AF ORBUCH, M
   TAYLOR, JE
   COY, DH
   MROZINSKI, JE
   MANTEY, SA
   BATTEY, JF
   MOREAU, JP
   JENSEN, RT
TI DISCOVERY OF A NOVEL CLASS OF NEUROMEDIN B-RECEPTOR ANTAGONISTS,
   SUBSTITUTED SOMATOSTATIN ANALOGS
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID GASTRIN-RELEASING PEPTIDE; BOMBESIN-LIKE PEPTIDES; PANCREATIC
   ACINAR-CELLS; GROWTH-FACTORS; CANCER CELLS; LUNG-CANCER; 3T3 CELLS;
   BINDING; CLONING; NEUROPEPTIDES
AB Bombesin-related peptides have widespread activities in the central nervous system and peripheral tissues. Recent studies show two subtypes of receptors; a gastrin-releasing peptide (GRP) receptor subtype and a neuromedin B (NMB) receptor subtype exist. In contrast to the GRP receptor, no antagonists exist for the NMB receptor. In the present study we report that certain somatostatin (SS) octapeptide analogues function as selective NMB receptor antagonists. The most potent analogue, D-Nal-Cys-Tyr-D-Trp-Lys-Val-Cys-Nal-NH2, inhibited binding of I-125-[D-Tyr(o)]NMB to NMB receptor-transfected 3T3 cells and C6 cells. This analogue had 100-fold lower affinity for GRP receptors. Structure-function studies were performed by synthesizing 18 structurally related SS octapeptide analogues; each of these analogues, but not native SS-1 4 or SS-28, also inhibited binding to NMB receptors. The stereochemistry at positions 1, 2, 7, and 8, the hydrophobicity and ring size of the substitution in positions 1, 3, and 4, and the basicity of the group in position 5 were all important in determining NMB receptor affinity. No SS octapeptide analogue increased [H-3]inositol phosphates in NMB receptor-transfected cells; however, each analogue inhibited NMB-stimulated increases. The most potent analogue, D-Nal-Cys-Tyr-D-Trp-Lys-Val-Cys-Nal-NH2, caused a parallel rightward shift of the NMB dose-response curve, the Schild plot slope was not significantly different from unity, and the affinity was 230 nm. SS octapeptide analogues also interacted with SS receptors and mu-opioid receptors; however, there was no correlation between the affinities of the analogues for these receptors and their affinities for NMB receptors, demonstrating that these activities can be separated. The results demonstrate for the first time a class of antagonists with >100-fold selectivity for NMB versus GRP receptors. Because the structural requirements for determining NMB, SS, and mu-opioid receptor activity differ, it is likely that highly selective, specific, high affinity NMB receptor antagonists can now be developed that will be useful in defining the role of NMB in various physiological processes.
C1 NIDDKD,DIGEST DIS BRANCH,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892.
   BIOMEASURE INC,MILFORD,MA 01757.
   NCI,BIOL CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892.
   TULANE UNIV,SCH MED,PEPTIDE RES LABS,NEW ORLEANS,LA 70112.
FU NCI NIH HHS [CA45153]
NR 42
TC 46
Z9 46
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD OCT
PY 1993
VL 44
IS 4
BP 841
EP 850
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA ME531
UT WOS:A1993ME53100021
PM 7901752
ER

PT J
AU LI, CY
   AGUAYO, L
   PEOPLES, RW
   WEIGHT, FF
AF LI, CY
   AGUAYO, L
   PEOPLES, RW
   WEIGHT, FF
TI ETHANOL INHIBITS A NEURONAL ATP-GATED ION-CHANNEL
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID BULLFROG SENSORY NEURONS; HIPPOCAMPAL-NEURONS; ACTIVATED CHANNELS; MOUSE
   HIPPOCAMPAL; MAMMALIAN NEURONS; RAT; RECEPTORS; CURRENTS; GLYCINE;
   VOLTAGE
AB The cellular mechanisms by which ethanol affects nervous system function are poorly understood. However, evidence has been accumulating that ethanol can affect the function of neurotransmitter-gated ion channels. Extracellular ATP has recently been reported to produce excitatory actions in the peripheral and central nervous systems by activating ligand-gated ion channels. We studied the effect of ethanol on membrane ion current activated by extracellular ATP in isolated bullfrog dorsal root ganglion neurons, by means of the whole-cell patch-clamp technique. The amplitude of the ATP-activated current was decreased by ethanol in a concentration-dependent manner over the range of 3-500 mm. The average inhibition of 1 mum ATP-activated current by 100 mM ethanol was 64 +/- 3%, and the concentration of ethanol that produced 50% inhibition was 68 mm. Ethanol inhibition of ATP-activated current was not dependent on membrane potential from -80 to +40 mV, and ethanol did not change the reversal potential of ATP-activated current. Ethanol (100 or 400 mm) shifted the ATP concentration-response curve to the right, increasing the EC50 for ATP from 3.0 mum to 6.0 mum or 22.3 mum, respectively, but did not reduce the maximal response to ATP. The results suggest that ethanol inhibits ATP-activated current by increasing the apparent dissociation constant for the ATP receptor.
RP LI, CY (reprint author), NIAAA,MOLEC & CELLULAR NEUROBIOL LAB,12501 WASHINGTON AVE,ROCKVILLE,MD 20852, USA.
NR 28
TC 47
Z9 49
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD OCT
PY 1993
VL 44
IS 4
BP 871
EP 875
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA ME531
UT WOS:A1993ME53100025
PM 8232236
ER

PT J
AU BENNETT, GJ
AF BENNETT, GJ
TI AN ANIMAL-MODEL OF NEUROPATHIC PAIN - A REVIEW
SO MUSCLE & NERVE
LA English
DT Article; Proceedings Paper
CT INTERNATIONAL SYMP ON NEUROPATHIC PAIN
CY OCT   18, 1992
CL CHARLESTON, SC
SP AMER ASSOC ELECTRODIAGNOST MED
DE ANIMAL MODELS; CAUSALGIA; PERIPHERAL NEUROPATHY; NEUROPATHIC PAIN;
   SYMPATHECTOMY
ID SCIATIC-NERVE INJURY; EXPERIMENTAL PERIPHERAL NEUROPATHY; EXPERIMENTAL
   ANESTHESIA DOLOROSA; SPONTANEOUS DISCHARGE; CONSTRICTION INJURY;
   AFFERENT INPUT; SPINAL-CORD; RAT MODEL; MONONEUROPATHY; BEHAVIOR
AB Recent work has succeeded in producing models of painful peripheral neuropathies in laboratory animals. There is evidence that the animals experience both abnormal spontaneous pain and abnormal evoked pains (allodynia and hyperalgesia). Experimental analyses of these models have demonstrated potential pathophysiologic mechanisms in both the peripheral and central nervous systems; it is likely that the model neuropathic pain syndromes are due to several different mechanisms. One line of evidence suggests that these pain states gradually become centralized due to an excitotoxic effect on spinal cord dorsal horn inhibitory interneurons. The role of the sympathetic nervous system appears to vary, depending on the type of nerve injury and the temporal evolution of the syndrome. There is evidence indicating that the abnormality of cutaneous temperature regulation that often accompanies painful peripheral neuropathy is not necessarily due to the activity of sympathetic vasomotor efferents.  (C) 1993 John Wiley & Sons, Inc.
RP BENNETT, GJ (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 30,ROOM B-20,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 36
TC 107
Z9 109
U1 1
U2 7
PU JOHN WILEY & SONS INC
PI NEW YORK
PA 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0148-639X
J9 MUSCLE NERVE
JI Muscle Nerve
PD OCT
PY 1993
VL 16
IS 10
BP 1040
EP 1048
DI 10.1002/mus.880161007
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA LY390
UT WOS:A1993LY39000006
PM 8413357
ER

PT J
AU OLLER, AR
   FIJALKOWSKA, IJ
   SCHAAPER, RM
AF OLLER, AR
   FIJALKOWSKA, IJ
   SCHAAPER, RM
TI THE ESCHERICHIA-COLI GALK2 PAPILLATION ASSAY - ITS SPECIFICITY AND
   APPLICATION TO 7 NEWLY ISOLATED MUTATOR STRAINS
SO MUTATION RESEARCH
LA English
DT Article
DE GALK2 GENE; PAPILLATION ASSAY; ESCHERICHIA-COLI MUTATOR STRAINS; DNA
   POLYMERASE; EXONUCLEOLYTIC PROOFREADING; DNAE GENE; DNAQ GENE
ID DNA POLYMERASE-III; MISMATCH REPAIR; MUTD5; MUTAGENESIS; GENE; MUTANTS;
   REPLICATION; SATURATION; HOLOENZYME; MECHANISMS
AB The Escherichia coli dnaE and dnaQ genes encode, respectively, the alpha (polymerase) and epsilon (proofreading) subunits of DNA polymerase III. Mutations in these genes resulting in mutator or antimutator phenotypes provide important tools to understand the mechanisms by which mutations occur. One way to isolate such strains is the use of papillation assays. We used one such assay based on the reversion of the galK2 allele in cells grown on MacConkey-Gal plates. Here, we describe the identification of the galK2 mutation and its possible reversion pathways, and the characterization of 7 mutators isolated using this system. 1 mutator resided in dnaE and 6 in dnaQ. Sequencing of the galK2 allele revealed a G . C --> T . A transversion at base pair 571 that changed a glu codon (GAA) to a stop codon (TAA). The analysis of 319 revertants showed that a Gal+ phenotype can be achieved by A . T --> G . C transition, A . T --> T . A transversion and A . T --> C . G transversion. We characterized the mutator phenotypes of the newly isolated mutators by determining (i) their mutation frequencies to resistance to rifampicin and nalidixic acid in both wild-type and mutL backgrounds, (ii) their temperature sensitivity and medium dependence and (iii) their mutational specificity (by analyzing the nature of galK revertants). Based on the genomic locations of their mutations, specificity of reversion pathways and magnitude of mutator effects, the mutators can be grouped into 3 classes. These classes may represent different mutational mechanisms that include defective base insertion, defective proofreading and interference with the postreplicative mismatch-repair system.
C1 NIEHS,MOLEC GENET LAB,POB 12233,111 TW ALEXANDER DR,RES TRIANGLE PK,NC 27709.
RI Fijalkowska, Iwona/I-7796-2016
NR 41
TC 16
Z9 17
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0921-8262
J9 MUTAT RES
PD OCT
PY 1993
VL 292
IS 2
BP 175
EP 185
DI 10.1016/0165-1161(93)90145-P
PG 11
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA LY932
UT WOS:A1993LY93200010
PM 7692254
ER

PT J
AU GENAZZANI, AD
   MICIELI, G
   MARTIGNONI, E
   FACCHINETTI, F
   RODBARD, D
   NAPPI, G
AF GENAZZANI, AD
   MICIELI, G
   MARTIGNONI, E
   FACCHINETTI, F
   RODBARD, D
   NAPPI, G
TI DERANGEMENT OF LH EPISODIC SECRETION IN CLUSTER HEADACHE SUFFERERS
SO NEUROENDOCRINOLOGY LETTERS
LA English
DT Article
ID LUTEINIZING-HORMONE; TESTOSTERONE LEVELS; MELATONIN; PROLACTIN; CORTISOL
AB In patients with cluster headache (CH) testosterone plasma levels have been consinstently reported to be lower than in normal males. Thus, we studied LH pulsatile secretory pattern in a group of 29 males suffering from CH. Ten of them were studied longitudinally, while 19 were studied cross-sectionally only during active (n=9) or attack free (n=10) phases. Nine healthy, age-matched males were studied as reference group. All subjects underwent a pulsatility study of 6 hours, sampling every 15 minutes.
   CH patients resulted to have a lower LH pulsatile release both during active (3.6+/-0.9 peaks/6h, p<0.0001) and attack free (4.1+/-0.9 peaks/6h, p<0.004) phases than normal males (5.2+/-0.6 peaks/6h). When longitudinally studied, CH patients (n=10) showed lower LH secretory episodes during the active than during the attack free phase (3.3+/-0.9 and 4.1+/-0.7 peaks/6h, p<0.05). Testosterone plasma levels did not differ between active and free phases (4.3+/-1 and 4.7+/-0.8 ng/ml, respectively), while, in patients they were significantly lower than in controls (6.8+/-0.9 ng/ml, p<0.01)).
   These data demonstrate an impaired function of the hypothalamo-pituitary axis possibly due to an overactivity of the opioid neuromodulation.
C1 UNIV CTR ADAPT DISORDERS & HEADACHE,PAVIA,ITALY.
   NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892.
RP GENAZZANI, AD (reprint author), UNIV MODENA,DEPT OBSTET & GYNECOL,I-41100 MODENA,ITALY.
RI Facchinetti, Fabio/K-9929-2014
OI Facchinetti, Fabio/0000-0003-4694-9564
NR 21
TC 0
Z9 0
U1 0
U2 0
PU BRAIN RESEARCH PROMOTION,
PI LONDON
PA 10 DEENA CLOSE, QUEENS DRIVE, LONDON, ENGLAND W3 OHR
SN 0172-780X
J9 NEUROENDOCRINOL LETT
JI Neuroendocrinol. Lett.
PD OCT-DEC
PY 1993
VL 15
IS 5-6
BP 443
EP 449
PG 7
WC Endocrinology & Metabolism; Neurosciences
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA MB139
UT WOS:A1993MB13900013
ER

PT J
AU PATTERSON, MC
   HOROWITZ, M
   ABEL, RB
   CURRIE, JN
   YU, KT
   KANESKI, C
   HIGGINS, JJ
   ONEILL, RR
   FEDIO, P
   PIKUS, A
   BRADY, RO
   BARTON, NW
AF PATTERSON, MC
   HOROWITZ, M
   ABEL, RB
   CURRIE, JN
   YU, KT
   KANESKI, C
   HIGGINS, JJ
   ONEILL, RR
   FEDIO, P
   PIKUS, A
   BRADY, RO
   BARTON, NW
TI ISOLATED HORIZONTAL SUPRANUCLEAR GAZE PALSY AS A MARKER OF SEVERE
   SYSTEMIC INVOLVEMENT IN GAUCHERS-DISEASE
SO NEUROLOGY
LA English
DT Article
ID GLUCOCEREBROSIDASE GENE; MUTATION
AB Type 3 neuronopathic Gaucher's disease (GD3) is phenotypically heterogeneous. In many GD3 patients, progressive myoclonus and dementia dominate the illness, with death secondary to progressive CNS disease. We have designated this group as GD3a. We studied 14 children with Gaucher's disease, isolated horizontal supranuclear gaze palsy, and aggressive systemic disease, and designated this group as GD3b. In comparison with 13 children with type 1 non-neuronopathic Gaucher's disease, the GD3b children presented earlier, and were shorter, underweight, and more prone to cardiopulmonary, hepatic, and skeletal complications. One-half of the children died in childhood or adolescence of systemic complications. Patients with at least one copy of the mutation that causes substitution of asparagine for serine at amino acid 370 of glucocerebrosidase did not develop neurologic signs. Patients homoallelic for the mutation causing substitution of leucine for proline at position 444 had severe systemic disease; neurologic signs were frequently, but not invariably, present. Early diagnosis and timely enzyme replacement therapy promise to improve the prognosis in GD3b.
C1 NINCDS,DMNB,BLDG 10,ROOM 3D03,9000 ROCKVILLE PIKE,BETHESDA,MD 20892.
   NIDOCD,AUDIOL SECT,BETHESDA,MD.
   MENTAL HLTH RES INST,MELBOURNE,AUSTRALIA.
   NINCDS,MED NEUROL BRANCH,BETHESDA,MD 20892.
   NINCDS,BIOMETRY & FIELD STUDIES BRANCH,BETHESDA,MD 20892.
   TEL AVIV UNIV,IL-69978 TEL AVIV,ISRAEL.
OI Kaneski, Christine/0000-0003-1453-2502; Patterson,
   Marc/0000-0002-1116-126X
NR 27
TC 84
Z9 84
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD OCT
PY 1993
VL 43
IS 10
BP 1993
EP 1997
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA MC704
UT WOS:A1993MC70400022
PM 8413956
ER

PT J
AU BHATIA, S
   BOOKHEIMER, SY
   GAILLARD, WD
   THEODORE, WH
AF BHATIA, S
   BOOKHEIMER, SY
   GAILLARD, WD
   THEODORE, WH
TI MEASUREMENT OF WHOLE TEMPORAL-LOBE AND HIPPOCAMPUS FOR MR VOLUMETRY -
   NORMATIVE DATA
SO NEUROLOGY
LA English
DT Article
ID INTRACTABLE PARTIAL EPILEPSY; NEURON LOSS; PATHOLOGICAL CORRELATIONS;
   ALZHEIMERS-DISEASE; HUMAN-BRAIN; SEIZURES; CT; SCLEROSIS; ASYMMETRY;
   IMAGES
AB We measured the volumes of the entire length of temporal lobe and hippocampal formation from coronal images in 29 healthy young adults to take into account normal side-to-side variation. Although whole-brain, temporal lobe, and left hippocampal volumes were significantly smaller in women, normalizing measurements for the whole brain eliminated intersex temporal lobe and hippocampal differences. There was a weak but significant inverse correlation between age and normalized hippocampal, but not temporal lobe or whole-brain, volume. In contrast to previous studies, we found no significant side-to-side differences in the sizes of temporal lobes or hippocampi. When performing MR volumetry, it is important to include the entire length of the hippocampal formation.
C1 NIH,EPILEPSY RES BRANCH,BLDG 10,ROOM 5C 207,BETHESDA,MD 20892.
NR 37
TC 100
Z9 102
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 OCT
PY 1993
VL 43
IS 10
BP 2006
EP 2010
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA MC704
UT WOS:A1993MC70400024
PM 8413958
ER

PT J
AU LABUDA, MC
   FLETCHER, NA
   KORCZYN, AD
   INZELBERG, R
   HARDING, AE
   PAULS, DL
AF LABUDA, MC
   FLETCHER, NA
   KORCZYN, AD
   INZELBERG, R
   HARDING, AE
   PAULS, DL
TI GENOMIC IMPRINTING AND ANTICIPATION IN IDIOPATHIC TORSION DYSTONIA
SO NEUROLOGY
LA English
DT Article
ID AUTOSOMAL DOMINANT INHERITANCE; HUNTINGTON DISEASE; SEGREGATION
   ANALYSIS; ASHKENAZI JEWS; ONSET; AGE; GENE
AB Idiopathic torsion dystonia (ITD) is a dominantly inherited disorder with variable penetrance and expressivity. Factors affecting the penetrance of the ITD gene have not yet been identified. The present study used four published series of cases to test specific hypotheses regarding factors that could affect the expression of ITD. Among the combined 253 families, transmission of ITD did not depend on either the sex of the affected offspring or that of the transmitting parent. Furthermore, neither the specific type of dystonia manifested, the site at which clinical signs of dystonia first appeared, nor age of onset differed significantly as a function of the gender of the transmitting parent. However, in familial cases of later onset (age greater-than-or-equal-to 20 years), nearly all involved a transmitting mother. There is evidence for consistency of age of onset within the subset of Jewish families. Although anticipation effects are apparent, sampling bias cannot be ruled out.
C1 TEL AVIV UNIV,SACKLER FAC MED,IL-69978 TEL AVIV,ISRAEL.
   UNIV LONDON,INST NEUROL,DEPT CLIN NEUROL,LONDON,ENGLAND.
   NIDA,ADDICT RES CTR,BALTIMORE,MD.
   YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06510.
   YALE UNIV,SCH MED,CTR CHILD STUDY,NEW HAVEN,CT 06510.
RI Korczyn, Amos/C-3461-2017
OI Korczyn, Amos/0000-0003-0125-2579
NR 31
TC 6
Z9 6
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD OCT
PY 1993
VL 43
IS 10
BP 2040
EP 2043
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA MC704
UT WOS:A1993MC70400032
PM 8413963
ER

PT J
AU ANGELI, SJ
   MURRAY, EA
   MISHKIN, M
AF ANGELI, SJ
   MURRAY, EA
   MISHKIN, M
TI HIPPOCAMPECTOMIZED MONKEYS CAN REMEMBER ONE PLACE BUT NOT 2
SO NEUROPSYCHOLOGIA
LA English
DT Article
ID FORNIX TRANSECTION; MEMORY; HIPPOCAMPUS; LESIONS; AMYGDALECTOMY;
   ABLATIONS; AMNESIA; OBJECTS; REMOVAL; TASKS
AB In an earlier study by PARKINSON et al. (J. Neurosci. 8, 4159-4167, 1988 [26]), hippocampectomized monkeys were found to be impaired on a task in which they were required to remember the spatial positions of trial-unique objects overlying two of the wells in a three-well test tray. There were two types of trial in the task. One type (object-place) required memory for the conjunction of object quality and object location, whereas the other (place only) required memory only for the location of the objects, i.e. independent of object quality. The hippocampectomized monkeys performed at near chance levels on both types of trials. The present study sought to determine whether the poor performance of the hippocampectomized monkeys on the place-only trials, which closely resembled spatial delayed response (an ability that is unaffected by hippocampectomy when similarly short delays are used), could have been due to interference from the simultaneous training they had received on the object-place trials. To this end, we examined the effect of hippocampal removals on performance of the ''place-only'' trial type when that was the only training given. The hippocampectomized monkeys in the present study were found to be just as severely impaired as those in the earlier study, thus ruling out the possible explanation outlined above. Since performance on this modified version of spatial delayed response, unlike performance on the classical version with the same delay, is critically dependent on the hippocampus, it appears that monkeys with hippocampectomy can remember one place after a short delay but not two.
C1 NIMH,NEUROPSYCHOL LAB,BLDG 49,ROOM 1B80,BETHESDA,MD 20892.
NR 29
TC 95
Z9 96
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0028-3932
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD OCT
PY 1993
VL 31
IS 10
BP 1021
EP 1030
DI 10.1016/0028-3932(93)90030-4
PG 10
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA MD852
UT WOS:A1993MD85200003
PM 8290020
ER

PT J
AU JUCKER, M
   WALKER, LC
   KIBBEY, MC
   KLEINMAN, HK
   INGRAM, DK
AF JUCKER, M
   WALKER, LC
   KIBBEY, MC
   KLEINMAN, HK
   INGRAM, DK
TI LOCALIZATION OF A LAMININ-BINDING PROTEIN IN BRAIN
SO NEUROSCIENCE
LA English
DT Article
ID AMYLOID PRECURSOR PROTEIN; CENTRAL-NERVOUS-SYSTEM; BASEMENT-MEMBRANE
   COMPONENTS; NEURITE OUTGROWTH; SYNTHETIC PEPTIDE; RAT-BRAIN; A-CHAIN;
   NEUROMUSCULAR-JUNCTION; MONOCLONAL-ANTIBODIES; GROWTH-FACTOR
AB A 110,000 mol.wt laminin-binding protein from newborn mouse brain recognizes a neurite promoting laminin A chain site and is related to the beta-amyloid precursor protein. In the present study, we examined the expression of 110,000 mol.wt laminin-binding protein in brains of adult mice, rats, and non-human primates. Essentially identical immunoreactivities were observed across species with distinct staining of cortical pyramidal neurons with apical dendrites, cerebellar basket cell axons, hippocampal mossy fibers, and fine labeling of processes throughout the brain. Colocalization of immunoreactivities to 110,000 mol.wt laminin-binding protein and to laminin in neurons of the adult rat brain was observed. Electron microscopy demonstrated that 110,000 mol.wt laminin-binding protein-like immunoreactivity is intracellular and is possibly associated with the neuronal cytoskeleton. Western blot analysis revealed that anti-110,000 mol.wt laminin-binding protein also recognizes a 140,000 mol.wt protein in the pellet, in addition to the 110,000 mol.wt protein in the Triton soluble extract. Antibody fractions specific to the two reactive protein species (110,000 mol.wt and 140,000 mol.wt) exhibited cross-reactivity on immunoblots and revealed similar immunohistochemical staining in adult brain. Results suggest a significant interaction between laminin-like molecules and 110,000 mol.wt laminin-binding protein-like molecules in normal brain function, in response to CNS injury and possibly in the pathogenesis of Alzheimer's disease.
C1 NIA,CELLULAR & MOLEC BIOL LAB,GERONTOL RES CTR,BETHESDA,MD 20892.
   JOHNS HOPKINS UNIV,SCH MED,NEUROPATHOL LAB,BALTIMORE,MD 21205.
   NIDR,DEV BIOL LAB,BETHESDA,MD 20892.
RP JUCKER, M (reprint author), SWISS FED INST TECHNOL,DEPT NEUROBIOL,CH-8093 ZURICH,SWITZERLAND.
RI Walker, L/J-6541-2015
OI Walker, L/0000-0001-9166-3261
NR 61
TC 17
Z9 17
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0306-4522
J9 NEUROSCIENCE
JI Neuroscience
PD OCT
PY 1993
VL 56
IS 4
BP 1009
EP 1022
DI 10.1016/0306-4522(93)90147-8
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA MB766
UT WOS:A1993MB76600021
PM 8284032
ER

PT J
AU YANO, T
   SANDER, CA
   CLARK, HM
   DOLEZAL, MV
   JAFFE, ES
   RAFFELD, M
AF YANO, T
   SANDER, CA
   CLARK, HM
   DOLEZAL, MV
   JAFFE, ES
   RAFFELD, M
TI CLUSTERED MUTATIONS IN THE 2ND EXON OF THE MYC GENE IN SPORADIC
   BURKITT-LYMPHOMA
SO ONCOGENE
LA English
DT Article
ID HUMAN C-MYC; CASEIN KINASE-II; PHOSPHORYLATION SITE;
   NUCLEOTIDE-SEQUENCE; SOMATIC MUTATION; PROTEIN-KINASE; 1ST EXON;
   ONCOGENE; TRANSCRIPTION; REGION
AB The primary tumors from 15 untreated patients with Burkitt's lymphoma were analysed for abnormalities in the coding region of the MYC gene by single stranded conformational polymorphism (SSCP) analysis followed by DNA sequencing. Fourteen of the 15 tumors had one or more clonal mutations. Forty one mutations were found in the second exon; only one occurred in the third exon. Seven tumors had mutations that clustered in a region spanning amino acids 38-63. Four of these possessed mutations that altered prolines at positions 57 (3), 60 (1), and 63 (1). Seven tumors were mutated in the central portions of the second exon. These occurred at position 95 (2), position 115 (2), position 137 (1), and position 138 (3). Analysis of the published sequences from five lymphoma cell lines and one primary tumor showed a similar clustering of mutations, with all six having mutations in codons between positions 38-63. The regions where mutations occurred have been associated with a variety of properties, including transcriptional activation and cellular transformation. The number and location of mutations showed no correlation with either chromosome 8 or chromosome 14 breakpoints or with the Epstein-Bar virus positivity of the tumors. This unexpected, frequent occurrence of clustered mutations in the second exon of the MYC gene suggests a rote for the mutated MYC proteins in the pathogenesis of Burkitt's lymphoma, possibly through altered interactions of this domain with other cellular factors.
C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,BLDG 10,ROOM 2N110,BETHESDA,MD 20892.
NR 41
TC 89
Z9 91
U1 0
U2 1
PU STOCKTON PRESS
PI BASINGSTOKE
PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD OCT
PY 1993
VL 8
IS 10
BP 2741
EP 2748
PG 8
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA LX343
UT WOS:A1993LX34300015
PM 8397370
ER

PT J
AU KNUTTEL, A
   SCHMITT, JM
AF KNUTTEL, A
   SCHMITT, JM
TI STATIONARY DEPTH-PROFILING REFLECTOMETER BASED ON LOW-COHERENCE
   INTERFEROMETRY
SO OPTICS COMMUNICATIONS
LA English
DT Article
ID FOURIER-TRANSFORM SPECTROMETER; TIME-DOMAIN REFLECTOMETER; PHOTODIODE
   ARRAY; RESOLUTION
AB Described is a new optical reflectometer based on low-coherence interferometry that employs no moving parts. Depth profiling up to a maximum free-space distance of 300 mum ( 150 mum depth) was achieved with a spatial resolution of 23 mum. In a proof-of-principle application, the thickness of a thin plastic film was determined.
RP KNUTTEL, A (reprint author), NIH,BETHESDA,MD 20892, USA.
NR 17
TC 4
Z9 4
U1 2
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0030-4018
J9 OPT COMMUN
JI Opt. Commun.
PD OCT 1
PY 1993
VL 102
IS 3-4
BP 193
EP 198
DI 10.1016/0030-4018(93)90380-N
PG 6
WC Optics
SC Optics
GA LX577
UT WOS:A1993LX57700001
ER

PT J
AU CAVEDON, K
   LONDON, J
AF CAVEDON, K
   LONDON, J
TI ADHESION DEGRADATION - A POSSIBLE FUNCTION FOR A PREVOTELLA-LOESCHEII
   PROTEASE
SO ORAL MICROBIOLOGY AND IMMUNOLOGY
LA English
DT Article
DE PROTEASE ACTIVITY; FIMBRIA-ASSOCIATED ADHESIN; ISOELECTRIC FOCUSING;
   PREVOTELLA-LOESCHEII
ID FIMBRIA-ASSOCIATED ADHESINS; BACTEROIDES-LOESCHEII;
   ACTINOMYCES-VISCOSUS; EUKARYOTIC CELLS; PROTEINS; GINGIVALIS;
   INHIBITION; VIRULENCE; PK1295
AB Prevotella loescheii PK1295 produces at least 3 proteases that are separable by isoelectric focusing. One of these proteases, an enzyme with an isoelectric point at 8.5 and an M(r) of 36,000, hydrolyzes the fimbria-associated adhesin on P loescheii responsible for coaggregation with Streptococcus oralis 34, as well as gelatin, casein and fibrin. The action of this protease may contribute to the detachment of P. loescheii from its streptococcal coaggregation partner and provide a mechanism for bacterial relocation in dental plaque.
C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892.
NR 18
TC 6
Z9 6
U1 0
U2 0
PU MUNKSGAARD INT PUBL LTD
PI COPENHAGEN
PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
SN 0902-0055
J9 ORAL MICROBIOL IMMUN
JI Oral Microbiol. Immunol.
PD OCT
PY 1993
VL 8
IS 5
BP 283
EP 287
DI 10.1111/j.1399-302X.1993.tb00575.x
PG 5
WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology
SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology
GA LX575
UT WOS:A1993LX57500005
PM 7903444
ER

PT J
AU THOMAS, DA
   ANTON, F
   KENSHALO, DR
   WILLIAMS, GM
   DUBNER, R
AF THOMAS, DA
   ANTON, F
   KENSHALO, DR
   WILLIAMS, GM
   DUBNER, R
TI NORADRENERGIC AND OPIOID SYSTEMS INTERACT TO ALTER THE DETECTION OF
   NOXIOUS THERMAL STIMULI AND FACIAL SCRATCHING IN MONKEYS
SO PAIN
LA English
DT Article
DE BRAIN STEM; NUCLEUS CAUDALIS; NOCICEPTION; BEHAVIOR; RHESUS; PRURITUS;
   (MONKEYS)
ID ALPHA-ADRENERGIC AGONISTS; TOOTH-PULP SENSATIONS; MEDULLARY DORSAL HORN;
   PERCEIVED INTENSITY; INTRATHECAL MORPHINE; CROSS-TOLERANCE;
   BLOOD-PRESSURE; OPIATE; ANTINOCICEPTION; CLONIDINE
AB We examined the ability of the alpha2-adrenoceptor agonist, ST-91, microinjected into the medullary dorsal horn (MDH), to diminish the sensory-discriminative features of noxious heat stimuli in awake behaving monkeys. Two monkeys performed a noxious thermal detection task and the time to detection of small increases in heat served as a measure of the perceived intensity of pain. ST-91 microinjected into the MDH (1.0, 3.0, 10.0 and 30.0 mug/0.4 mul) produced dose-dependent increases in detection time to graded temperature increases (0.4-1.0-degrees-C) from a noxious 46-degrees-C base line. These dose-dependent effects were attenuated by the systemic administration of the alpha2-adrenoceptor antagonist, idazoxan (2.0 mg/kg, i.m.), but not by the alpha1-adrenoceptor antagonist, prazosin (0.5 mg/kg, i.m.) or the opioid-receptor antagonist, naloxone (0.5 mg/kg, i.m.). The effect of ST-91 on detection latency of thermal stimuli was not the result of alterations in attentional, motivational or motoric aspects of the monkeys' behavior, because detection of visual stimuli and non-noxious temperature coolings (36.0-34.5-degrees-C) in a similar paradigm were not consistently altered. Microinjection of morphine (3.0 mg) into the MDH also increased detection latency of the noxious heat stimuli. Systemic administration of the opioid-receptor antagonist, naloxone (0.5 mg/kg), and the alpha2-adrenoceptor antagonist, idazoxan (2.0 mg/kg, i.m.) attenuated these effects of morphine. In a separate experiment, morphine (5.0 mug) microinjected into the MDH induced facial scratching behavior. Idazoxan (2.0 mg/kg) was effective at attenuating this scratching behavior. We have thus shown participation of MDH alpha2-adrenoceptors in the process underlying the perception of the intensity of noxious thermal stimulation in monkeys. Further, opioid and noradrenergic systems interacted in the noxious heat detection paradigm and a paradigm where facial scratching behavior was studied.
RP THOMAS, DA (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 49,ROOM 1A11,BETHESDA,MD 20892, USA.
NR 36
TC 12
Z9 12
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
J9 PAIN
JI Pain
PD OCT
PY 1993
VL 55
IS 1
BP 63
EP 70
DI 10.1016/0304-3959(93)90185-R
PG 8
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA MC115
UT WOS:A1993MC11500004
PM 7904058
ER

PT J
AU ROCKEN, M
   SHEVACH, EM
AF ROCKEN, M
   SHEVACH, EM
TI DO PARASITIC INFECTIONS BREAK T-CELL TOLERANCE AND TRIGGER
   AUTOIMMUNE-DISEASE
SO PARASITOLOGY TODAY
LA English
DT Article
ID TRANSGENIC MICE; INTERLEUKIN-2; LYMPHOCYTES; REPERTOIRE; RESPONSES;
   MALARIA
AB Burnet and Fenner originally defined 'tolerance' as 'unresponsiveness against self'1. It is now generally accepted that the phenomenon of tolerance is required to protect on individual from potentially autoreactive cells. Recent experiments have independently shown that parasite infection2 or interleukin 2 (IL-2)3,4 can reverse an established T-cell tolerance in vivo, Breaking T-cell tolerance restores the capacity of T cells to be stimulated by their specific antigen2 and, in the case of a self-antigen, may be followed by autoimmune disease3,4. In this review, Martin Rocken and Ethan Shevach briefly describe the potential pathways for generating T-cell tolerance in vivo, and focus on recently described mechanisms by which parasitic infections may circumvent or abrogate the tolerant state.
C1 UNIV MUNICH,DEPT DERMATOL,W-8000 MUNICH 2,GERMANY.
RP ROCKEN, M (reprint author), NIAID,IMMUNOL LAB,BETHESDA,MD 20892, USA.
NR 31
TC 9
Z9 9
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB
SN 0169-4758
J9 PARASITOL TODAY
JI Parasitol. Today
PD OCT
PY 1993
VL 9
IS 10
BP 377
EP 380
DI 10.1016/0169-4758(93)90087-V
PG 4
WC Parasitology
SC Parasitology
GA LX693
UT WOS:A1993LX69300012
PM 15463673
ER

PT J
AU BLAESE, RM
   MULLEN, CA
   RAMSEY, WJ
AF BLAESE, RM
   MULLEN, CA
   RAMSEY, WJ
TI STRATEGIES FOR GENE-THERAPY
SO PATHOLOGIE BIOLOGIE
LA English
DT Article
DE RETROVIRAL VECTORS; ADENOSINE DEAMINASE; SEVERE COMBINED
   IMMUNODEFICIENCY; HERPES THYMIDINE KINASE; SUICIDE GENES
ID BONE-MARROW TRANSPLANTATION; LYMPHOCYTES; RETROVIRUS; DISEASES; CELLS
AB The use of retroviral-mediated gene transfer to introduce a DNA label into T cells (TIL) being used in the immunotherapy of patients with malignant melanoma finally opened the door to the clinical application of gene therapy for a wide variety of inherited and acquired diseases. The gene therapy trial for ADA deficiency SCID has demonstrated that long term stable expression of exogenous genes can be achieved in human T lymphocytes using retroviral vectors for ex vivo treatment and that significant immune reconstitution can be achieved in these patients following periodic infusions with ADA gene-corrected autologous T cells. Newer clinical applications include the insertion of genes into CD34 enriched stem cell populations, the testing of autologous tumor vaccines employing cytokine gene-modified tumor cells and the direct transfer of the herpes thymidine kinase gene into brain tumors in situ in order to render those tumors sensitive to treatment with the ordinarily non-cytotoxic drug ganciclovir.
RP BLAESE, RM (reprint author), NCI,METAB BRANCH,CELLULAR IMMUNOL SECT,BLDG 10,ROOM 6B05,BETHESDA,MD 20892, USA.
NR 19
TC 17
Z9 17
U1 0
U2 1
PU EXPANSION SCI FRANCAISE
PI PARIS
PA 31 BLVD LATOUR MAUBOURG, 75007 PARIS, FRANCE
SN 0369-8114
J9 PATHOL BIOL
JI Pathol. Biol.
PD OCT
PY 1993
VL 41
IS 8
BP 672
EP 676
PG 5
WC Pathology
SC Pathology
GA MD051
UT WOS:A1993MD05100004
PM 8290310
ER

PT J
AU ROSENFELD, MA
   RONALD, G
   CRYSTAL, RG
AF ROSENFELD, MA
   RONALD, G
   CRYSTAL, RG
TI GENE-THERAPY FOR PULMONARY-DISEASES
SO PATHOLOGIE BIOLOGIE
LA English
DT Article
DE GENE; LUNG; EPITHELIAL; VECTOR; GENE THERAPY
ID CYSTIC-FIBROSIS GENE; ADENOVIRUS-MEDIATED TRANSFER; CONDUCTANCE
   REGULATOR GENE; ALPHA-1-ANTITRYPSIN DEFICIENCY; EPITHELIAL-CELLS;
   EXPRESSION; IDENTIFICATION; INVIVO; EMPHYSEMA; VECTORS
AB The common fatal hereditary disorders, alpha 1-antitrypsin (alpha1AT) deficiency and cystic fibrosis (CF), are clinical models for the common lung diseases, emphysema and chronic bronchitis, respectively. Both are potentially amenable to therapeutic intervention by gene therapy, in which the relevant gene is used to modify cells of the affected individual. Although the gene therapy strategies for these diseases are conceptually quite different, a promising approach for both is the in vivo administration of a recombinant replication deficient adenovirus vector containing a normal copy of the abnormal gene. If the goal is to express the normal extracellular anti-protease alpha1AT, the route of administration could be directly into the lung, liver or vascular endothelium. If the goal is to express the normal transmembrane protein defective in CF epithelial cells, the new gene will need to be delivered directly to the affected cells. The feasibility of these approaches has been demonstrated in vitro and in vivo in experimental animals.
RP ROSENFELD, MA (reprint author), NHLBI,PULM BRANCH,BETHESDA,MD 20892, USA.
NR 23
TC 17
Z9 17
U1 0
U2 1
PU EXPANSION SCI FRANCAISE
PI PARIS
PA 31 BLVD LATOUR MAUBOURG, 75007 PARIS, FRANCE
SN 0369-8114
J9 PATHOL BIOL
JI Pathol. Biol.
PD OCT
PY 1993
VL 41
IS 8
BP 677
EP 680
PG 4
WC Pathology
SC Pathology
GA MD051
UT WOS:A1993MD05100005
PM 8290311
ER

PT J
AU CARDENAS, MP
   SIMONSMORTON, BG
AF CARDENAS, MP
   SIMONSMORTON, BG
TI THE EFFECT OF ANTICIPATORY GUIDANCE ON MOTHERS SELF-EFFICACY AND
   BEHAVIORAL INTENTIONS TO PREVENT BURNS CAUSED BY HOT TAP WATER
SO PATIENT EDUCATION AND COUNSELING
LA English
DT Article
DE ANTICIPATORY GUIDANCE; ADHERENCE; INFORMATIONAL CARTOON; BURNS;
   HISPANICS; TAP WATER
ID WELL-CHILD CARE; SCALD BURNS; PARENTS
AB An informational cartoon was developed and tested in a low-socioeconomic population composed mainly of Hispanics attending the Ripley Health Clinic in Houston, TX. The informational cartoon illustrated how scald injuries can be prevented by adjusting the water heater thermostal. Self-efficacy, intention, knowledge, attitude and social desirability were measured Days were the randomization units. Over a 2-week period, five clinic days were randomly allocated to control and five to the intervention condition. During the control days, mothers in the pediatric department received only a posttest. During the intervention days mothers received the informational cartoon and posttest. Significant posttest differences between groups were found for self-efficacy (P < 0.004), intention (P < 0.001), knowledge (P < 0.001) and attitude (P < 0.03). The results support the hypothesis that the informational cartoon affected the target outcomes.
C1 NICHHD,DESPR,6100 EXECUT BLVD,ROOM 7B05,BETHESDA,MD 20892.
   UNIV TEXAS,MED BRANCH,DEPT FAMILY MED,GALVESTON,TX 77550.
OI Simons-Morton, Bruce/0000-0003-1099-6617
NR 21
TC 8
Z9 8
U1 0
U2 0
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0738-3991
J9 PATIENT EDUC COUNS
JI Patient Educ. Couns.
PD OCT
PY 1993
VL 21
IS 3
BP 117
EP 123
DI 10.1016/0738-3991(93)90069-9
PG 7
WC Public, Environmental & Occupational Health; Social Sciences,
   Interdisciplinary
SC Public, Environmental & Occupational Health; Social Sciences - Other
   Topics
GA ME602
UT WOS:A1993ME60200001
ER

PT J
AU DIEFFENBACH, CW
   DVEKSLER, GS
AF DIEFFENBACH, CW
   DVEKSLER, GS
TI PCR PRIMER - A MANUAL SUPPLEMENT - INTRODUCTION
SO PCR-METHODS AND APPLICATIONS
LA English
DT Editorial Material
C1 UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814.
RP DIEFFENBACH, CW (reprint author), NIAID,DIV AIDS,BETHESDA,MD 20892, USA.
NR 0
TC 5
Z9 5
U1 0
U2 3
PU COLD SPRING HARBOR LAB PRESS
PI PLAINVIEW
PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724
SN 1054-9803
J9 PCR METH APPL
JI PCR-Methods Appl.
PD OCT
PY 1993
VL 3
IS 2
BP S1
EP S1
PG 1
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA MD191
UT WOS:A1993MD19100012
ER

PT J
AU DIEFFENBACH, CW
   DVEKSLER, GS
AF DIEFFENBACH, CW
   DVEKSLER, GS
TI SETTING UP A PCR LABORATORY
SO PCR-METHODS AND APPLICATIONS
LA English
DT Article
ID URACIL-DNA GLYCOSYLASE; CONTAMINATION
C1 UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814.
RP DIEFFENBACH, CW (reprint author), NIAID,DIV AIDS,BETHESDA,MD 20892, USA.
NR 9
TC 27
Z9 27
U1 0
U2 2
PU COLD SPRING HARBOR LAB PRESS
PI PLAINVIEW
PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724
SN 1054-9803
J9 PCR METH APPL
JI PCR-Methods Appl.
PD OCT
PY 1993
VL 3
IS 2
BP S2
EP S7
PG 6
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA MD191
UT WOS:A1993MD19100013
PM 8268784
ER

PT J
AU ROBBINS, JB
   PITTMAN, M
   TROLLFORS, B
   LAGERGARD, TA
   TARANGER, J
   SCHNEERSON, R
AF ROBBINS, JB
   PITTMAN, M
   TROLLFORS, B
   LAGERGARD, TA
   TARANGER, J
   SCHNEERSON, R
TI PRIMUM-NON-NOCERE - A PHARMACOLOGICALLY INERT PERTUSSIS TOXOID ALONE
   SHOULD BE THE NEXT PERTUSSIS-VACCINE
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Review
DE PERTUSSIS; PERTUSSIS TOXOID; VACCINE
ID LYMPHOCYTOSIS-PROMOTING FACTOR; ISLET-ACTIVATING PROTEIN; OUTER-MEMBRANE
   PROTEIN; BORDETELLA ADENYLATE-CYCLASE; COMPONENT DTP VACCINE; HAMSTER
   OVARY CELLS; INFLUENZAE TYPE-B; WHOLE-CELL; WHOOPING-COUGH; FILAMENTOUS
   HEMAGGLUTININ
C1 GOTHENBURG UNIV,DEPT PEDIAT,S-41124 GOTHENBURG,SWEDEN.
   GOTHENBURG UNIV,DEPT MICROBIOL & IMMUNOL,S-41124 GOTHENBURG,SWEDEN.
   US FDA,CTR BIOL RES & REVIEW,BETHESDA,MD 20014.
RP ROBBINS, JB (reprint author), NICHHD,LAB & DEV & MOLEC IMMUN,BLDG 6,ROOM 145,BETHESDA,MD 20892, USA.
NR 239
TC 39
Z9 39
U1 0
U2 1
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0891-3668
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD OCT
PY 1993
VL 12
IS 10
BP 795
EP 807
DI 10.1097/00006454-199310000-00001
PG 13
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA MB703
UT WOS:A1993MB70300001
PM 8284114
ER

PT J
AU SIMONDS, RJ
   CHANOCK, S
AF SIMONDS, RJ
   CHANOCK, S
TI MEDICAL ISSUES RELATED TO CARING FOR HUMAN IMMUNODEFICIENCY
   VIRUS-INFECTED CHILDREN IN AND OUT OF THE HOME
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Editorial Material
DE HUMAN IMMUNODEFICIENCY VIRUS INFECTION; HUMAN IMMUNODEFICIENCY VIRUS
   TRANSMISSION; CHILDREN; INFECTION CONTROL; DAY CARE; EDUCATION;
   ATHLETICS; HOME
ID AIDS-RELATED COMPLEX; HOUSEHOLD CONTACTS; HTLV-III; HIV-INFECTION;
   SEROPOSITIVE HEMOPHILIACS; TYPE-1 HIV-1; HETEROSEXUAL PARTNERS;
   ANABOLIC-STEROIDS; SEXUAL PARTNERS; ANTIBODY STATUS
C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892.
RP SIMONDS, RJ (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV HIV AIDS,1600 CLIFTON RD,MAILSTOP E-45,ATLANTA,GA 30333, USA.
NR 76
TC 21
Z9 21
U1 0
U2 0
PU WILLIAMS & WILKINS
PI BALTIMORE
PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436
SN 0891-3668
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD OCT
PY 1993
VL 12
IS 10
BP 845
EP 852
DI 10.1097/00006454-199310000-00010
PG 8
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA MB703
UT WOS:A1993MB70300010
PM 8284122
ER

PT J
AU SCHWEIKL, H
   TAYLOR, JA
   KITAREEWAN, S
   LINKO, P
   NAGORNEY, D
   GOLDSTEIN, JA
AF SCHWEIKL, H
   TAYLOR, JA
   KITAREEWAN, S
   LINKO, P
   NAGORNEY, D
   GOLDSTEIN, JA
TI EXPRESSION OF CYP1A1 AND CYP1A2 GENES IN HUMAN LIVER
SO PHARMACOGENETICS
LA English
DT Article
ID MICROSOMAL CYTOCHROME-P-450 ENZYMES; POLYMERASE CHAIN-REACTION;
   MESSENGER-RNA; CHROMOSOMAL LOCALIZATION; RAT; METABOLISM; QUANTITATION;
   SEQUENCE; 2-ACETYLAMINOFLUORENE; PURIFICATION
AB Immunoblot analysis of human livers using a monospecific antibody to rat CYP1A2 demonstrated that the expression of CYP1A2 protein is highly variable in human liver. Quantitative PCR analysis was then employed to examine the interindividual variability of both CYP1A1 and CYP1A2 mRNAs in human liver. Hepatic content of CYP1A2 mRNA correlated significantly with levels of CYP1A2 protein as analysed by immunoblot analysis (r = 0.58; p < 0.01). CYP1A2 mRNA content varied >40-fold among individuals while CYP1A1 content varied >20-fold. CYP1A2 mRNA was higher than CYP1A1 mRNA (approximately two to 30-fold) in livers of different individuals. The individual with the highest CYP1A1 and CYP1A2 mRNA amounts was a current smoker, but mRNA expression in two other smokers was within the range observed among nonsmokers. The expression of the two CYP1A mRNAs correlated highly (r = 0. 72; p < 0.0005) when smokers were included, but the correlation was less significant (r = 0.62; p < 0.05) in nonsmokers. We amplified a full-length CYP1A2 cDNA clone by PCR from a liver which expressed extremely low amounts of CYP1A2 protein. Sequence analysis indicated that exon 4 was missing in this clone, but no other sequence changes were found. PCR analysis demonstrated that both the normally spliced mRNA and abnormally spliced mRNA could be detected in all human livers examined, but the normally spliced mRNA was more abundant than the splice variant. Therefore, sequence changes in the coding region of CYP1A2 did not account for the poor expression of CYP1A2 in this individual.
C1 NIEHS,BIOCHEM RISK ANAL LAB,POB 12233,RES TRIANGLE PK,NC 27709.
   NIEHS,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC 27709.
   MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905.
RI Goldstein, Joyce/A-6681-2012; Schweikl, Helmut/C-2998-2013; 
OI taylor, jack/0000-0001-5303-6398
NR 42
TC 124
Z9 127
U1 0
U2 8
PU CHAPMAN HALL LTD
PI LONDON
PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN
SN 0960-314X
J9 PHARMACOGENETICS
JI Pharmacogenetics
PD OCT
PY 1993
VL 3
IS 5
BP 239
EP 249
DI 10.1097/00008571-199310000-00003
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
   & Pharmacy
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
   & Pharmacy
GA MG989
UT WOS:A1993MG98900003
PM 8287062
ER

PT J
AU ROTHMAN, N
   HAYES, RB
   BI, WF
   CAPORASO, N
   BROLY, F
   WOOSLEY, RL
   YIN, SN
   FENG, PW
   YOU, XJ
   MEYER, UA
AF ROTHMAN, N
   HAYES, RB
   BI, WF
   CAPORASO, N
   BROLY, F
   WOOSLEY, RL
   YIN, SN
   FENG, PW
   YOU, XJ
   MEYER, UA
TI CORRELATION BETWEEN N-ACETYLTRANSFERASE ACTIVITY AND NAT2 GENOTYPE IN
   CHINESE MALES
SO PHARMACOGENETICS
LA English
DT Article
ID AROMATIC AMINE ACETYLTRANSFERASE; ETHANOL-INDUCED INCREASE;
   COLORECTAL-CANCER; HUMAN LIVER; ACETYLATION; PHENOTYPE; DAPSONE;
   HYDROXYLATION; PHARMACOKINETICS; CARCINOGENESIS
AB Eighty-four healthy Chinese male control subjects derived from an occupation-based case-control study of bladder cancer were evaluated for hepatic N-acetyltransferase activity by dapsone and for NAT2 genotype using allele-specific amplification of peripheral leukocyte DNA by the polymerase chain reaction. Fifty-nine percent of the overall variation in acetylation activity was explained by genotype (p < 0.0001). The remaining variation in acetylation was not associated with dapsone N-hydroxylation activity, age, current smoking status, or weight in the study population, or within any genotype subgroup. Although acetylation activity in the homozygous mutant group did not overlap with the other genotype categories, there was moderate overlap in acetylation between the heterozygous mutant and wildtype groups, and substantial variation in acetylation within them. Considering all subjects with the identical NAT2 genotype as phenotypically similar and all subjects with differing NAT2 genotypes as phenotypically distinct may result in misclassification of metabolic risk factors in epidemiological investigations. As such, it would seem prudent, where possible, to collect both acetylation phenotype and NAT2 genotype data, since the advantages and limitations of these two sources of information complement, and serve to assess the accuracy of each other.
C1 CHINESE ACAD PREVENT MED,BEIJING,PEOPLES R CHINA.
   TIANJIN BUR CHEM IND,INST LABOR HYG,TIANJIN,PEOPLES R CHINA.
   SHANGHAI INST OCCUPAT MED,SHANGHAI,PEOPLES R CHINA.
   UNIV BASEL,BIOCTR,DEPT PHARMACOL,CH-4056 BASEL,SWITZERLAND.
   GEORGETOWN UNIV,SCH MED,DEPT PHARMACOL,WASHINGTON,DC 20057.
RP ROTHMAN, N (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,EPN 418,BETHESDA,MD 20892, USA.
NR 33
TC 63
Z9 63
U1 2
U2 2
PU CHAPMAN HALL LTD
PI LONDON
PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN
SN 0960-314X
J9 PHARMACOGENETICS
JI Pharmacogenetics
PD OCT
PY 1993
VL 3
IS 5
BP 250
EP 255
DI 10.1097/00008571-199310000-00004
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
   & Pharmacy
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
   & Pharmacy
GA MG989
UT WOS:A1993MG98900004
PM 8287063
ER

PT J
AU YOKOTA, H
   TAMURA, S
   FURUYA, H
   KIMURA, S
   WATANABE, M
   KANAZAWA, I
   KONDO, I
   GONZALEZ, FJ
AF YOKOTA, H
   TAMURA, S
   FURUYA, H
   KIMURA, S
   WATANABE, M
   KANAZAWA, I
   KONDO, I
   GONZALEZ, FJ
TI EVIDENCE FOR A NEW VARIANT CYP2D6 ALLELE CYP2D6J IN A JAPANESE
   POPULATION ASSOCIATED WITH LOWER IN-VIVO RATES OF SPARTEINE METABOLISM
SO PHARMACOGENETICS
LA English
DT Article
ID DRUG-METABOLISM; GENETIC-POLYMORPHISM; POOR METABOLIZERS; DEBRISOQUINE;
   OXIDATION; HYDROXYLATION; MUTATIONS; CHINESE; COMMON; DEFECT
AB A group of Japanese subjects were phenotyped for CYP2D6 activity by administration of sparteine and determination of urine metabolic ratios (MR). The CYP2D6 alleles from two subjects having a high MR, characteristic of slower rates of sparteine metabolism, were cloned in lambdaEMBL3 and subjected to sequence analysis. One individual possessed a CYP2D6B allele, typically found in Caucasians, that is inactive due to an altered 3' splice recognition site and other potentially disruptive mutations. The second allele from this individual was identical to the wild type normal Caucasian CYP2D6 allele except for C188T and G4268C base differences in exons 1 and 9, respectively, that result in P34S and S486T amino acid substitutions. This allele was designated CYP2D6J. The second individual possessed two CYP2D6J alleles. PCR assays were performed to detect this allele and other alleles from a group of subjects exhibiting low rates of sparteine metabolism, i.e. with MRs > 1.5. Eleven CYP2D6J alleles were detected in 14 subjects exhibiting low rates of metabolism and including four individuals who were homozygous for this variant and had very low rates of sparteine metabolism (MRs > 2.5). In contrast, only two CYP2D6J alleles were found in 14 subjects having MRs of < 1.0. These data suggest that CYP2D6J encodes an enzyme having lower rates of sparteine metabolism.
C1 NCI,MOLEC CARCINOGENESIS LAB,BLDG 37,ROOM 3E24,BETHESDA,MD 20892.
   UNIV TOKYO,INST BRAIN RES,BUNKYO KU,TOKYO 113,JAPAN.
   EHIME UNIV,DEPT HYG,SHIGENOBU,EHIME 79102,JAPAN.
NR 25
TC 132
Z9 137
U1 0
U2 0
PU CHAPMAN HALL LTD
PI LONDON
PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN
SN 0960-314X
J9 PHARMACOGENETICS
JI Pharmacogenetics
PD OCT
PY 1993
VL 3
IS 5
BP 256
EP 263
DI 10.1097/00008571-199310000-00005
PG 8
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
   & Pharmacy
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
   & Pharmacy
GA MG989
UT WOS:A1993MG98900005
PM 8287064
ER

PT J
AU LI, R
   WING, LL
   WYATT, RJ
   KIRCH, DG
AF LI, R
   WING, LL
   WYATT, RJ
   KIRCH, DG
TI EFFECTS OF HALOPERIDOL, LITHIUM, AND VALPROATE ON PHOSPHOINOSITIDE
   TURNOVER IN RAT-BRAIN
SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
LA English
DT Article
DE HALOPERIDOL; LITHIUM; VALPROATE; INOSITOL PHOSPHATES; FRONTAL CORTEX;
   STRIATUM
ID INOSITOL PHOSPHOLIPID HYDROLYSIS; STRIATAL SLICES; CEREBRAL-CORTEX;
   STIMULATION; RECEPTORS; AGONIST; CHLORPROMAZINE; METABOLISM; PHOSPHATES;
   INCREASES
AB The effects of acute, subacute, and chronic treatment with haloperidol, lithium, and valproate on inositol phosphate (IP) formation were examined. Acute treatment with haloperidol or the combination of haloperidol and lithium significantly reduced IP basal cortical levels. Subacute (three days) treatment with lithium decreased the IP basal level in the frontal cortex. Chronic treatment with haloperidol (14 and 28 days) caused a significant attenuation of carbachol-sensitive IP accumulation in the frontal cortex and striatum and a significant decrease in norepinephrine (NE)-induced IP formation in the frontal cortex (14 and 28 days) and striatum (28 days). Lithium treatment for 14 days produced a significant reduction in the IP basal cortical value, and a significant reduction in cortical carbachol- and NE-induced IP formation was found after 28 days of lithium treatment. The combination of haloperidol and lithium for 28 days decreased the striatal carbachol- and cortical NE-induced IP accumulation and caused a significant increase in NE-sensitive IP formation in the striatum at 14 days. Valproate treatment for 28 days was associated with a significant attenuation in striatal agonist-stimulated IP formation. Therefore, three drugs with different specificities for primary neurotransmitters may have common effects on second-messenger systems.
C1 NIMH,NEUROSCI CTR ST ELIZABETHS,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032.
   NIMH,DIV INTRAMURAL RES,BETHESDA,MD 20892.
NR 38
TC 26
Z9 26
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0091-3057
J9 PHARMACOL BIOCHEM BE
JI Pharmacol. Biochem. Behav.
PD OCT
PY 1993
VL 46
IS 2
BP 323
EP 329
DI 10.1016/0091-3057(93)90360-6
PG 7
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA MD466
UT WOS:A1993MD46600011
PM 8265687
ER

PT J
AU GRANSTEIN, RD
   MORISON, WL
   KRIPKE, ML
AF GRANSTEIN, RD
   MORISON, WL
   KRIPKE, ML
TI CARCINOGENICITY OF COMBINED ULTRAVIOLET-B RADIATION AND PSORALEN PLUS
   ULTRAVIOLET-A IRRADIATION TREATMENT OF MICE
SO PHOTODERMATOLOGY PHOTOIMMUNOLOGY & PHOTOMEDICINE
LA English
DT Article
DE UVB, PUVA; SKIN CANCER
ID ORAL METHOXSALEN; PSORIASIS; PHOTOCHEMOTHERAPY; RISK
AB Psoralen plus ultraviolet A (PUVA) therapy and UVB phototherapy are frequently used in the treatment of psoriasis and other skin diseases. Both treatments are thought to be carcinogenic, but little is known about their interaction in the induction of skin cancer. Tumors induced in mice treated with both PUVA and UVB, either given sequentially or concurrently, seemed to be more antigenic as a group than tumors treated by PUVA alone, as determined by their lower frequency of growth when transplanted into naive mice. In this study, we treated C3H mice with a subcarcinogenic dose of UVB radiation for 4 weeks, followed by PUVA treatment for 41 weeks (sequential experiment) or with both UVB radiation (minimal carcinogenic dose) and PUVA for 41 weeks (concurrent experiment) and monitored the development of skin cancers. Although a few tumors appeared earlier in the groups treated with both UVB and PUVA in both experiments, no significant differences were observed in the rate of tumor development in mice treated with UVB and PUVA versus those treated with PUVA alone.
C1 NCI,FREDERICK RES FACIL,FREDERICK,MD 21701.
   JOHNS HOPKINS MED INST,BALTIMORE,MD 21205.
   MD ANDERSON CANC CTR,HOUSTON,TX.
RP GRANSTEIN, RD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA.
NR 10
TC 1
Z9 1
U1 0
U2 0
PU MUNKSGAARD INT PUBL LTD
PI COPENHAGEN
PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
SN 0905-4383
J9 PHOTODERMATOL PHOTO
JI Photodermatol. Photoimmunol. Photomed.
PD OCT
PY 1993
VL 9
IS 5
BP 198
EP 202
PG 5
WC Dermatology
SC Dermatology
GA MA680
UT WOS:A1993MA68000002
ER

PT J
AU PRITCHARD, JB
   MILLER, DS
AF PRITCHARD, JB
   MILLER, DS
TI MECHANISMS MEDIATING RENAL SECRETION OF ORGANIC-ANIONS AND CATIONS
SO PHYSIOLOGICAL REVIEWS
LA English
DT Review
ID BRUSH-BORDER MEMBRANE; PARA-AMINOHIPPURATE TRANSPORT; XENOPUS-LAEVIS
   OOCYTES; BILE-ACID TRANSPORT; RABBIT PROXIMAL TUBULE; LIVER CANALICULAR
   MEMBRANE; MULTIDRUG-RESISTANCE GENE; ATP-DEPENDENT TRANSPORT;
   BLOOD-BRAIN-BARRIER; RAT CHOROID-PLEXUS
C1 NIEHS, CELLULAR & MOLEC PHARMACOL LAB, INTRACELLULAR REGULAT SECT, RES TRIANGLE PK, NC 27709 USA.
RP NIEHS, CELLULAR & MOLEC PHARMACOL LAB, COMPARAT MEMBRANE PHARMACOL SECT, RES TRIANGLE PK, NC 27709 USA.
NR 368
TC 446
Z9 449
U1 0
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0031-9333
EI 1522-1210
J9 PHYSIOL REV
JI Physiol. Rev.
PD OCT
PY 1993
VL 73
IS 4
BP 765
EP 796
PG 32
WC Physiology
SC Physiology
GA MC109
UT WOS:A1993MC10900004
PM 8415925
ER

PT J
AU KRAMLIK, SK
   ALTEMUS, M
   CASTONGUAY, TW
AF KRAMLIK, SK
   ALTEMUS, M
   CASTONGUAY, TW
TI THE EFFECTS OF THE ACUTE ADMINISTRATION OF RU-486 ON DIETARY-FAT
   PREFERENCE IN FASTED LEAN AND OBESE MEN
SO PHYSIOLOGY & BEHAVIOR
LA English
DT Article
DE HUMAN OBESITY; GLUCOCORTICOID; CORTISOL; RU-486; FOOD INTAKE; DIETARY
   PREFERENCES
ID ZUCKER RATS; FOOD-INTAKE; RU 486; CORTISOL; GLUCOCORTICOIDS;
   ADRENOCORTICOTROPIN; ADRENALECTOMY; SECRETION; WOMEN
AB The effects of RU 486, a potent glucocorticoid antagonist, on dietary fat preference were explored in obese men and lean controls in a double-blind crossover study. An oral 10 mg/kg dose of RU 486 or placebo was administered at midnight the second night of a 48-h hospital stay. Macronutrient and caloric intakes were calculated each day and a taste test of six commercial dairy products (fat content by weight < 0.5%, 2.0%, 3.3%, 10.5%, 18%, and 36%) was performed. Dairy products were judged for pleasantness, creaminess, and overall preference. Subjects were then asked to consume their favorite dairy product until sated. Urinary free cortisol (UFC) and plasma adrenocorticotropic hormone (ACTH), cortisol, insulin, and glucose were determined. Intake of a self-selected diet was recorded. As expected, in response to RU 486, UFC increased from 120 +/- 25 mug/24 h to 297 +/- 73 mug/24 h (p < 0.05) in obese men and from 81 +/- 10 mug/24 h to 357 +/- 109 mug/24 h (p < 0.05) in lean men. Plasma cortisol increased from 26.1 +/- 1.1 mug/dl to 31.8 +/- 1.0 mug/dl (p < 0.05) in obese men and from 26.1 +/- 1.7 mug/dl to 32.2 +/- 1.7 mug/dl (p < 0.05) in lean men. Plasma insulin was significantly higher in obese 24.6 +/- 3.2 muIU/ml than in lean men 12.8 +/- 1.1 muIU/ml (p = 0.0001) but was unaffected by RU 486. RU 486 did not decrease fat intake in either obese or lean men. However, in obese men UFC was significantly correlated with fat intake from the overall preferred product in the taste test (r = 0.84, p < 0.05) and with fat intake during the following 24 h. This correlation was lost after RU 486 administration in obese men and was not seen in either condition in lean men. Although RU 486 did not alter fat intake in obese or lean men, correlations between UFC and both measures of fat intake in obese men suggest that cortisol may play a role in the pathophysiology of obesity.
C1 UNIV MARYLAND,DEPT NUTR & FOOD SCI,COLL PK,MD 20742.
   NIMH,BETHESDA,MD 20982.
OI Castonguay, Thomas/0000-0003-1176-5095
FU NIDDK NIH HHS [DK 42446]
NR 33
TC 8
Z9 8
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0031-9384
J9 PHYSIOL BEHAV
JI Physiol. Behav.
PD OCT
PY 1993
VL 54
IS 4
BP 717
EP 724
DI 10.1016/0031-9384(93)90082-Q
PG 8
WC Psychology, Biological; Behavioral Sciences
SC Psychology; Behavioral Sciences
GA LW922
UT WOS:A1993LW92200015
PM 8248349
ER

PT J
AU FERRIS, CF
   DELVILLE, Y
   GRZONKA, Z
   LUBERNAROD, J
   INSEL, TR
AF FERRIS, CF
   DELVILLE, Y
   GRZONKA, Z
   LUBERNAROD, J
   INSEL, TR
TI AN IODINATED VASOPRESSIN (V1) ANTAGONIST BLOCKS FLANK MARKING AND
   SELECTIVELY LABELS NEURAL BINDING-SITES IN GOLDEN-HAMSTERS
SO PHYSIOLOGY & BEHAVIOR
LA English
DT Article
DE ANTERIOR HYPOTHALAMUS; PARAVENTRICULAR NUCLEUS; AMYGDALOID COMPLEX; MAIN
   OLFACTORY BULBS; ACCESSORY OLFACTORY BULBS; VOMERONASAL PATHWAY
ID PAPEZ CIRCUIT; MAGNOCELLULAR NEURONS; SOCIAL MEMORY; SCENT MARKING;
   BEHAVIOR; HYPOTHALAMUS; RATS; MICROINJECTION; BRAIN; AREA
AB An arginine-vasopressin (AVP) derivative, [d(CH2)5,Sar7]AVP (SAVP), has been characterized as an antagonist to vasopressin V1 receptors. Using AVP-dependent flank-marking behavior as a bioassay, it was possible to verify that iodinated SAVP (I-SAVP) retains biological activity within the central nervous system, as the antagonist blocked the behavior. Furthermore, I-125-SAVP was used to localize specific V1 binding sites in the brain. The resulting binding was localized to discrete anatomical sites, and highly specific to V1-like receptors. While we confirmed previous findings using H-3-AVP in golden hamsters, we also identified binding in many areas previously unreported (e.g., arcuate and paraventricular nuclei of the hypothalamus, tenia tecta, posteromedial cortical nucleus of the amygdala, and zona incerta), suggesting that I-125-SAVP provides a greater level of resolution. In addition, specific binding was observed in the lateral septum, anterior hypothalamus, and midbrain central gray, areas that have previously been shown to trigger flank marking in response to AVP microinjection. The presence of AVP binding sites in limbic and mesencephalic areas involved in the regulation of flank marking suggests that this neuropeptide may play an important role as a neurotransmitter at multiple levels in the neural circuits controlling this behavior.
C1 UNIV GDANSK,INST CHEM,PL-80925 GDANSK,POLAND.
   UNIV MASSACHUSETTS,MED CTR,DEPT UROL,WORCESTER,MA 01605.
   NIMH,NEUROPHYSIOL LAB,POOLESVILLE,MD.
RP FERRIS, CF (reprint author), UNIV MASSACHUSETTS,MED CTR,DEPT PSYCHIAT,BEHAV NEUROSCI LAB,55 LAKE AVE N,WORCESTER,MA 01655, USA.
NR 31
TC 54
Z9 55
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0031-9384
J9 PHYSIOL BEHAV
JI Physiol. Behav.
PD OCT
PY 1993
VL 54
IS 4
BP 737
EP 747
DI 10.1016/0031-9384(93)90085-T
PG 11
WC Psychology, Biological; Behavioral Sciences
SC Psychology; Behavioral Sciences
GA LW922
UT WOS:A1993LW92200018
PM 8248352
ER

PT J
AU CHO, MH
   SHEARS, SB
   BOSS, WF
AF CHO, MH
   SHEARS, SB
   BOSS, WF
TI CHANGES IN PHOSPHATIDYLINOSITOL METABOLISM IN RESPONSE TO HYPEROSMOTIC
   STRESS IN DAUCUS-CAROTA L CELLS GROWN IN SUSPENSION-CULTURE
SO PLANT PHYSIOLOGY
LA English
DT Article
ID POLYPHOSPHOINOSITIDE PHOSPHOLIPASE-C; PLASMA-MEMBRANE ATPASE;
   INOSITOL-CONTAINING LIPIDS; PROTEIN KINASE-C; PHOSPHOINOSITIDE KINASES;
   DIACYLGLYCEROL KINASE; DUNALIELLA-SALINA; HUMAN-PLATELET; HIGHER-PLANTS;
   OKADAIC ACID
AB Carrot (Daucus carota L.) cells plasmolyzed within 30 s after adding sorbitol to increase the osmotic strength of the medium from 0.2 to 0.4 or 0.6 osmolal. However, there was no significant change in the polyphosphorylated inositol phospholipids or inositol phosphates or in inositol phospholipid metabolism within 30 s of imposing the hyperosmotic stress. Maximum changes in phosphatidylinositol 4-monophosphate (PIP) metabolism were detected at 5 min, at which time the cells appeared adjust to the change in osmoticum. There was a 30% decrease in [H-3]inositol-labeled PIP. The specific activity of enzymes involved in the metabolism of the inositol phospholipids also changed. The plasma membrane phosphatidylinositol ( PI) kinase decreased 50% and PIP-phospholipase C (PIP-PLC) increased 60% compared with the control values after 5 min of hyperosmotic stress. The PIP-PLC activity recovered to control levels by 10 min; however, the PI kinase activity remained below the control value, suggesting that the cells had reached a new steady state with regard to PIP biosynthesis. If cells were pretreated with okadaic acid, the protein phosphatase 1 and 2A inhibitor, the differences in enzyme activity resulting from the hyperosmotic stress were no longer evident, suggesting that an okadaic acid-sensitive phosphatase was activated in response to hyperosmotic stress. Our work suggests that, in this system, PIP is not involved in the initial response to hyperosmotic stress but may be involved in the recovery phase.
C1 N CAROLINA STATE UNIV,DEPT BOT,RALEIGH,NC 27695.
   NATL INST ENVIRONM HLTH SCI,CELLULAR & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709.
NR 73
TC 52
Z9 57
U1 0
U2 2
PU AMER SOC PLANT PHYSIOLOGISTS
PI ROCKVILLE
PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855
SN 0032-0889
J9 PLANT PHYSIOL
JI Plant Physiol.
PD OCT
PY 1993
VL 103
IS 2
BP 637
EP 647
DI 10.1104/pp.103.2.637
PG 11
WC Plant Sciences
SC Plant Sciences
GA MB642
UT WOS:A1993MB64200042
PM 8029337
ER

PT J
AU BEARD, WL
   HAYES, HM
AF BEARD, WL
   HAYES, HM
TI RISK-FACTORS FOR LARYNGEAL HEMIPLEGIA IN THE HORSE
SO PREVENTIVE VETERINARY MEDICINE
LA English
DT Article
ID COMBINATION; TABLES
AB Hospital data from the Veterinary Medical Data Base were obtained for January 1970 to June 1986. Data were from 18 North American veterinary teaching hospitals. Patients diagnosed with laryngeal hemiplegia were identified. In order to determine the frequency of diagnosis, statistics were gathered for patient-years-at-risk. The independant risks of age, sex, and breed on the hospital prevalence were determined. Laryngeal hemiplegia was diagnosed in 2798 horses representing 29 breeds. The male risk compared with females (OR = 1) was 2.7. Laryngeal hemiplegia was diagnosed significantly more often in three breeds of draft horses, Thoroughbreds, and American Saddlebreds; and significantly less often in Arabians, Appaloosas, American Paints, and American QuarteT Horses. Standard bred horses and Tennessee Walking Horses were seen about as frequently as they were represented in the hospital population. Using the proportion of cases-to-population seen at 2-3 years of age as the standard reference point (OR = 1), Thoroughbreds showed a peak hospital prevalence at 2-3 years of age; thereafter their cause specific accession rate decreased. Other breeds, particularly the draft horses, showed an increasing rate of diagnosis over 3 years of age. The peak age of diagnosis for draft animals was 7-9 years; for the Standardbred and the American Quarter Horse, it was 4-6 years.
C1 NCI,ENVIRONM EPIDEMIOL BRANCH,ROCKVILLE,MD 20892.
RP BEARD, WL (reprint author), OHIO STATE UNIV,DEPT VET CLIN SCI,601 VERNON L THARP ST,COLUMBUS,OH 43210, USA.
NR 14
TC 4
Z9 4
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-5877
J9 PREV VET MED
JI Prev. Vet. Med.
PD OCT
PY 1993
VL 17
IS 1-2
BP 57
EP 63
DI 10.1016/0167-5877(93)90055-X
PG 7
WC Veterinary Sciences
SC Veterinary Sciences
GA MD618
UT WOS:A1993MD61800007
ER

PT J
AU WESTERGAARD, GC
   SUOMI, SJ
AF WESTERGAARD, GC
   SUOMI, SJ
TI USE OF A TOOL-SET BY CAPUCHIN MONKEYS (CEBUS-APELLA)
SO PRIMATES
LA English
DT Note
DE CAPUCHIN; CEBUS APELLA; MONKEY; NUT-CRACKING; TOOL-SET; TOOL-USE
ID MANUFACTURE; HAMMERS
AB The purpose of this study was to examine the use of a tool-set by capuchin monkeys (Cebus apella). Capuchins were presented with an apparatus designed to accommodate the use of pounding tools to crack walnuts and the use of probing tools to loosen and extract the inner meat. Three capuchins used stones and sticks sequentially for these purposes. The capuchins' behavior was similar in form and function to behavior that has been reported for chimpanzees in analogous situations. These results provide further evidence of the extensive tool-using capabilities of capuchin monkeys and are consistent with a hypothesis of cross-species continuity in the skillful use of tools by primates.
C1 NICHHD,BETHESDA,MD 20892.
NR 13
TC 22
Z9 22
U1 1
U2 6
PU JAPAN MONKEY CENTRE
PI INUYAMA AICHI
PA PRIMATES, EDITORIAL OFFICE, INUYAMA AICHI 484, JAPAN
SN 0032-8332
J9 PRIMATES
JI Primates
PD OCT
PY 1993
VL 34
IS 4
BP 459
EP 462
DI 10.1007/BF02382655
PG 4
WC Zoology
SC Zoology
GA MK543
UT WOS:A1993MK54300005
ER

PT J
AU PAUL, A
   KUESTER, J
   TIMME, A
   ARNEMANN, J
AF PAUL, A
   KUESTER, J
   TIMME, A
   ARNEMANN, J
TI THE ASSOCIATION BETWEEN RANK, MATING EFFORT, AND REPRODUCTIVE SUCCESS IN
   MALE BARBARY MACAQUES (MACACA-SYLVANUS)
SO PRIMATES
LA English
DT Article
DE BARBARY MACAQUES; PATERNITY; RANK; MATING EFFORT; SPERM COMPETITION;
   REPRODUCTIVE SUCCESS
ID MALE SAVANNA BABOONS; RHESUS-MONKEYS; SEXUAL-BEHAVIOR; SPERM
   COMPETITION; DOMINANCE RANK; SOCIAL RANK; PATERNITY; PRIMATES; MULATTA;
   DETERMINANTS
AB The association between social rank, mating effort, and reproductive success of male Barbary macaques (Macaca sylvanus) has been evaluated by longterm behavioral observations and subsequent paternity determination via oligonucleotide DNA fingerprinting in a large semifree-ranging group. All offspring born between 1985 and 1988 that survived to at least 1 year of age (n=75) were available for paternity testing. The exclusion of all but one of the potential fathers from paternity was possible in 70 cases (93%). Mating activities were recorded using ad lib. and focal female sampling techniques. The analysis of male mating effort was restricted to the most likely days of conception. Male rank correlated significantly with male mating success in all four breeding seasons and with male reproductive success in three of the four seasons. Mating success and reproductive success also showed a significant correlation, with the exception of one breeding season, in which the proportion of males per fertilizable female was especially high. Poor mating success was almost always associated with poor reproductive success, while good mating success was less predictive for a male's actual reproductive success. This was apparently a consequence of sperm competition, resulting from the promiscuous mating system. Male mating success is not necessarily an unreliable indicator for reproductive success, provided that sufficient sample sizes are available and that conception periods can be determined. Sperm competition and other factors may weaken the association, however.
C1 UNIV BONN,INST ZOOL,ETHOL ABT,D-53115 BONN,GERMANY.
   NIH,CTR ANIM,COMPARAT ETHOL LAB,POOLESVILLE,MD 20837.
   UNIV FRANKFURT KLINIKUM,INST HUMANGENET,D-60596 FRANKFURT,GERMANY.
RP PAUL, A (reprint author), UNIV GOTTINGEN,INST ANTHROPOL,BURGERSTR 50,D-37073 GOTTINGEN,GERMANY.
NR 54
TC 56
Z9 59
U1 2
U2 8
PU JAPAN MONKEY CENTRE
PI INUYAMA AICHI
PA PRIMATES, EDITORIAL OFFICE, INUYAMA AICHI 484, JAPAN
SN 0032-8332
J9 PRIMATES
JI Primates
PD OCT
PY 1993
VL 34
IS 4
BP 491
EP 502
DI 10.1007/BF02382660
PG 12
WC Zoology
SC Zoology
GA MK543
UT WOS:A1993MK54300010
ER

PT J
AU JAHANGEER, S
   RODBELL, M
AF JAHANGEER, S
   RODBELL, M
TI THE DISAGGREGATION THEORY OF SIGNAL-TRANSDUCTION REVISITED - FURTHER
   EVIDENCE THAT G-PROTEINS ARE MULTIMERIC AND DISAGGREGATE TO MONOMERS
   WHEN ACTIVATED
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID GTP-BINDING PROTEINS; REGULATORY PROTEINS; ADENYLYL CYCLASE;
   GUANINE-NUCLEOTIDES; GLUCAGON RECEPTOR; OCTYL GLUCOSIDE; ALPHA-SUBUNIT;
   HYDROLYSIS; ANTIBODIES; MEMBRANES
AB We have compared the sedimentation rates on sucrose gradients of the heterotrimeric GTP-binding regulatory (G) proteins G(s), G(o), G(i), and G(q) extracted from rat brain synaptoneurosomes with Lubrol and digitonin. The individual alpha and beta subunits were monitored with specific antisera. In all cases, both subunits cosedimented, indicating that the subunits are likely complexed as heterotrimers. When extracted with Lubrol all of the G proteins sedimented with rates of about 4.5 S (consistent with heterotrimers) whereas digitonin extracted 60% of the G proteins with peaks at 11 S; 40% pelleted as larger structures. Digitonin-extracted G(i) was cross-linked by p-phenylenedimaleimide, yielding structures too large to enter polyacrylamide gels. No cross-linking of Lubrol-extracted G(i) occurred. Treatment of the membranes with guanosine 5'-[gamma-thio]triphosphate and Mg2+ yielded digitonin-extracted structures with peak sedimentation values of 8.5 S-i.e., comparable to that of purified G(o) in digitonin and considerably larger than the Lubrol-extracted 2S structures representing the separated alpha and betagamma subunits formed by the actions of guanosine 5'-[gamma-thio]triphosphate. It is concluded that the multimeric structures of G proteins in brain membranes are at least partially preserved in digitonin and that activation of these structures in membranes yields monomers of G proteins rather than the disaggregated products (alpha and betagamma complexes) observed in Lubrol. It is proposed that hormones and GTP affect the dynamic interplay between multimeric G proteins and receptors in a fashion analogous to the actions of ATP on the dynamic interactions between myosin and actin filaments. Signal transduction is mediated by activated monomers released from the multimers during the activation process.
RP JAHANGEER, S (reprint author), NIEHS,CELLULAR & MOLEC PHARMACOL LAB,SIGNAL TRANSDUCT SECT,RES TRIANGLE PK,NC 27709, USA.
NR 35
TC 58
Z9 58
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 OCT 1
PY 1993
VL 90
IS 19
BP 8782
EP 8786
DI 10.1073/pnas.90.19.8782
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA595
UT WOS:A1993MA59500007
PM 8415607
ER

PT J
AU GAO, WY
   CARA, A
   GALLO, RC
   LORI, F
AF GAO, WY
   CARA, A
   GALLO, RC
   LORI, F
TI LOW-LEVELS OF DEOXYNUCLEOTIDES IN PERIPHERAL-BLOOD LYMPHOCYTES - A
   STRATEGY TO INHIBIT HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 REPLICATION
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE HYDROXYUREA; DNTP; THERAPY
ID REVERSE-TRANSCRIPTASE; ACTIVATION; VIRIONS
AB Human immunodeficiency virus type 1 (HIV-1) viral DNA synthesis in quiescent and activated peripheral blood lymphocytes (PBLs) was studied. Incomplete viral DNA (previously demonstrated to be associated with HIV-1 virions) is carried by HIV-1 virions into quiescent and activated PBLS, contributing to the formation of an early viral DNA pool in these cells. The viral DNA is subsequently completed but only extremely slowly and inefficiently in quiescent PBLs compared to that in stimulated PBLs. We find that this correlates with significantly lower levels of dNTP substrates in quiescent compared to activated PBLs. At these low dNTP concentrations, HIV-1 reverse transcriptase acts in a partially distributive manner. Increasing dNTP concentrations from the levels of quiescent PBLs to the levels of activated pBLs the processive action of reverse transcriptase, which in turn stimulates rapid and efficient formation of full-length DNA. Furthermore, hydroxyurea treatment of stimulated PBLs decreases the dNTP levels and the DNA synthesis rate to levels comparable to quiescent PBLs. Our data therefore indicate that low levels of dNTP may explain why HIV-1 DNA is synthesized slowly and inefficiently in quiescent PBLs and suggest that pharmacologic induction of low dNTP levels represents a therapeutic approach for inhibition of HIV-1 replication.
C1 NCI,TUMOR CELL BIOL LAB,BLDG 37,ROOM 6A09,BETHESDA,MD 20892.
   NCI,MED CHEM LAB,BETHESDA,MD 20892.
RI Cara, Andrea/M-4865-2015
OI Cara, Andrea/0000-0003-4967-1895
NR 17
TC 276
Z9 279
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 1
PY 1993
VL 90
IS 19
BP 8925
EP 8928
DI 10.1073/pnas.90.19.8925
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA595
UT WOS:A1993MA59500036
PM 7692440
ER

PT J
AU JING, TW
   JEFFREY, AM
   DEROSE, JA
   LYUBCHENKO, YL
   SHLYAKHTENKO, LS
   HARRINGTON, RE
   APPELLA, E
   LARSEN, J
   VAUGHT, A
   REKESH, D
   LU, FX
   LINDSAY, SM
AF JING, TW
   JEFFREY, AM
   DEROSE, JA
   LYUBCHENKO, YL
   SHLYAKHTENKO, LS
   HARRINGTON, RE
   APPELLA, E
   LARSEN, J
   VAUGHT, A
   REKESH, D
   LU, FX
   LINDSAY, SM
TI STRUCTURE OF HYDRATED OLIGONUCLEOTIDES STUDIED BY IN-SITU
   SCANNING-TUNNELING-MICROSCOPY
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID PROBE MICROSCOPY; DNA; SURFACE; WATER; MOLECULES; GRAPHITE; AU(111)
AB We have used the scanning tunneling microscope (STM) to image several synthetic oligonucleotides adsorbed onto a positively charged Au(111) electrode. The molecules were deposited and imaged in aqueous electrolyte under potential control, a procedure that eliminated the problem of the substrate artifacts that had limited some previous STM studies. Experiments were carried out with two types of single-stranded molecules (11 and 20 bases long) and three types of double-stranded molecules (20 and 61 base pairs and 31 bases with 25 bases paired and 6-base ''sticky'' ends). The molecules lie along symmetry directions on the reconstructed (23 x square-root 3) gold surface, and length measurements indicate that they adopt simple base-stacked structures. The base stacking distances are, within experimental uncertainty, equal to the 0.33 nm measured for polymeric aggregates of stacked purines by direct imaging in identical conditions. The images show features consistent with helical structures. Double helices have a major-groove periodicity that is consistent with a 36-degrees twist. The single helices appear to be more tightly twisted. A simple tunneling model of STM contrast generates good agreement between measured and calculated images.
C1 ARIZONA STATE UNIV,DEPT PHYS & ASTRON,TEMPE,AZ 85287.
   ARIZONA STATE UNIV,DEPT MICROBIOL,TEMPE,AZ 85287.
   COLUMBIA UNIV COLL PHYS & SURG,DEPT MED BIOCHEM,NEW YORK,NY 10032.
   COLUMBIA UNIV COLL PHYS & SURG,DIV ENVIRONM SCI,NEW YORK,NY 10032.
   UNIV NEVADA,DEPT BIOCHEM,RENO,NV 89557.
   NCI,CELL BIOL LAB,BETHESDA,MD 20892.
FU NCI NIH HHS [CA21111]; NHGRI NIH HHS [R55 HG00656]; NIGMS NIH HHS [R01
   GM33435]
NR 39
TC 37
Z9 40
U1 0
U2 8
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 1
PY 1993
VL 90
IS 19
BP 8934
EP 8938
DI 10.1073/pnas.90.19.8934
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA595
UT WOS:A1993MA59500038
PM 8415633
ER

PT J
AU CLARK, J
   MOORE, L
   KRASINSKAS, A
   WAY, J
   BATTEY, J
   TAMKUN, J
   KAHN, RA
AF CLARK, J
   MOORE, L
   KRASINSKAS, A
   WAY, J
   BATTEY, J
   TAMKUN, J
   KAHN, RA
TI SELECTIVE AMPLIFICATION OF ADDITIONAL MEMBERS OF THE ADP-RIBOSYLATION
   FACTOR (ARF) FAMILY - CLONING OF ADDITIONAL HUMAN AND DROSOPHILA
   ARF-LIKE GENES
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID GTP-BINDING PROTEINS; CHOLERA-TOXIN; SACCHAROMYCES-CEREVISIAE;
   ENDOPLASMIC-RETICULUM; REGULATORY COMPONENT; ADENYLATE-CYCLASE;
   MOLECULAR-CLONING; MAMMALIAN-CELLS; EXPRESSION; COFACTOR
AB The ADP-ribosylation factor (ARF) family is one of four subfamilies of the RAs superfamily of low molecular weight GTP-binding proteins (G proteins). Highly degenerate oligonucleotides encoding two conserved regions were used in a PCR reaction to amplify cDNAs encoding each of the known ARF proteins and eight addition cDNA fragments encoding previously unreported human members of the ARF family. Additional sequences were obtained from yeast or fly libraries by using this technique. These oligonucleotides specifically amplify members of the ARF family but not the structurally related G protein alpha subunits or members of the other three subfamilies of the RAS superfamily. Fragments obtained by PCR were used to obtain full-length sequences encoding highly homologous ARF-like (ARL) gene products from human and Drosophila melanogaster libraries, termed ARL2 and Arl84F, respectively. The encoded proteins are each 184 amino acids long and am 76% identical, with 40-45% identity to human ARF1 and Drosophila arf-like (arl) proteins. These genes appear to be generally expressed in human tissues and during Drosophila development. The purified human ARL2 protein differed in several biochemical properties from human ARF proteins, including the complete absence of ARF activity. Thus, the ARF family of low molecular weight GTP-binding proteins includes at least 15 distinct but structurally conserved members, including both the functionally conserved ARF proteins and the functionally disparate ARL proteins. The latter proteins currently comprise two distinct gene products in Drosophila (arl and ARL84F) and one in man (ARL2).
C1 NCI, DIV CANC TREATMENT,DEV THERAPEUT PROGRAM, BIOL CHEM LAB,BLDG 37,ROOM 5D-02, BETHESDA, MD 20892 USA.
   UNIV CALIF SANTA CRUZ, DEPT BIOL, SINSHEIMER LABS 323, SANTA CRUZ, CA 95064 USA.
NR 34
TC 114
Z9 118
U1 1
U2 3
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 1
PY 1993
VL 90
IS 19
BP 8952
EP 8956
DI 10.1073/pnas.90.19.8952
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA595
UT WOS:A1993MA59500042
PM 8415637
ER

PT J
AU JIANG, W
   ZHANG, YJ
   KAHN, SM
   HOLLSTEIN, MC
   SANTELLA, RM
   LU, SH
   HARRIS, CC
   MONTESANO, R
   WEINSTEIN, IB
AF JIANG, W
   ZHANG, YJ
   KAHN, SM
   HOLLSTEIN, MC
   SANTELLA, RM
   LU, SH
   HARRIS, CC
   MONTESANO, R
   WEINSTEIN, IB
TI ALTERED EXPRESSION OF THE CYCLIN D1 AND RETINOBLASTOMA GENES IN HUMAN
   ESOPHAGEAL CANCER
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE GENE AMPLIFICATION; CELL CYCLE
ID CARCINOMA CELL-LINES; CANDIDATE ONCOGENE; CHROMOSOME 11Q13; RAS
   MUTATIONS; NO EVIDENCE; PROTEIN; PRODUCT; TUMORS; COAMPLIFICATION;
   HETEROZYGOSITY
AB We have examined DNA from four hu an esophageal carcinoma cell lines and 50 primary esophageal carcinomas obtained from China, Italy, and France for amplification of the cyclin D1 gene. We also examined 36 of these 50 carcinomas for expression of the cyclin D1 and retinoblastoma (RB) proteins by immunohistochemistry. We found a 3- to 10-fold amplification of the cyclin D1 gene in 16 of the 50 (32%) tumors and in two of the four cell lines. Cyclin D1 protein was overexpressed in 12 of 13 tumors and the two cell lines that showed gene amplification when compared to normal controls. Studies on RB protein expression indicated that 6 of the 36 (17%) tumor samples examined and one cell line did not show detectable expression of this protein. The tumors and cell lines that had cyclin D1 gene amplification and overexpression exhibited normal levels of expression of R.B protein. By contrast, the tumors and cell line that did not appear to express the RB protein did not show amplification of the cyclin D1 gene and expressed only low levels of the cyclin D1 protein (P = 0.03). These results suggest that the inhibitory effect of RB on cell cycle progression can be abrogated during tumor development either by loss of expression of the RB gene or by increased expression of the cyclin D1 gene.
C1 COLUMBIA UNIV COLL PHYS & SURG,CTR COMPREHENS CANC,NEW YORK,NY 10032.
   CHINESE ACAD MED SCI,INST CANC,BEIJING,PEOPLES R CHINA.
   NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892.
   COLUMBIA UNIV COLL PHYS & SURG,INST CANC RES,NEW YORK,NY 10032.
   INT AGCY RES CANC,F-69372 LYON,FRANCE.
FU NCI NIH HHS [CA02111]
NR 46
TC 379
Z9 389
U1 2
U2 6
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 1
PY 1993
VL 90
IS 19
BP 9026
EP 9030
DI 10.1073/pnas.90.19.9026
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA595
UT WOS:A1993MA59500057
PM 8415648
ER

PT J
AU STEINBACH, PJ
   BROOKS, BR
AF STEINBACH, PJ
   BROOKS, BR
TI PROTEIN HYDRATION ELUCIDATED BY MOLECULAR-DYNAMICS SIMULATION
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE DEVIATION FROM X-RAY CRYSTAL STRUCTURE; FLUCTUATION; DIHEDRAL
   TRANSITIONS; GLASS TRANSITION
ID NEUTRON-SCATTERING; LOW-TEMPERATURE; MYOGLOBIN; ENVIRONMENT; TRANSITION;
   WATER; DEPENDENCE; CRYSTALS; LYSOZYME; SOLVENT
AB Molecular dynamics (MD) simulations covering a wide range of hydration indicate that myoglobin is fully hydrated by 350 water molecules, in agreement with experiment. These waters, originally placed uniformly about the protein, form clusters that hydrate every charged group throughout the entire simulation. Some atoms in charged groups are hydrated by two water layers while 37% of the protein surface remains uncovered. The locations of the 350 waters are consistent with those of crystallographic waters resolved by x-ray and neutron diffraction. Hydration by 350 waters at 300 K stabilizes the conformation of carboxymyoglobin measured by x-ray diffraction throughout the entire protein, halves the rate of torsional transitions, and promotes alternative conformations for surface atoms. The glass transition observed experimentally in hydrated myoglobin near 220 K is also seen in the simulations and correlates with an increase in the number of dihedral angles undergoing transitions. The anharmonic protein motion above 220 K is enhanced by protein hydration.
C1 NIH, DIV COMP RES & TECHNOL, STRUCT BIOL LAB, BETHESDA, MD 20892 USA.
NR 27
TC 214
Z9 218
U1 2
U2 14
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 1
PY 1993
VL 90
IS 19
BP 9135
EP 9139
DI 10.1073/pnas.90.19.9135
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA595
UT WOS:A1993MA59500079
PM 8415667
ER

PT J
AU KOZASA, T
   HEPLER, JR
   SMRCKA, AV
   SIMON, MI
   RHEE, SG
   STERNWEIS, PC
   GILMAN, AG
AF KOZASA, T
   HEPLER, JR
   SMRCKA, AV
   SIMON, MI
   RHEE, SG
   STERNWEIS, PC
   GILMAN, AG
TI PURIFICATION AND CHARACTERIZATION OF RECOMBINANT-G(16-ALPHA) FROM SF9
   CELLS - ACTIVATION OF PURIFIED PHOSPHOLIPASE-C ISOZYMES BY G-PROTEIN
   ALPHA-SUBUNITS
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID BETA-GAMMA-SUBUNITS; BINDING PROTEIN; BOVINE BRAIN; EXPRESSION
AB A cDNA encoding G16alpha, the alpha subunit of a heterotrimeric guanine nucleotide-binding protein, was expressed in Sf9 cells using recombinant baculovirus. G16alpha in membrane extracts of Sf9 cells activated phospholipase C-beta1 (PLC-beta1) in the presence of guanosine 5'-[gamma-thio]triphosphate; the system could not be activated by Al3+, Mg2+, and F-. The G16alpha in the cytosolic fraction of Sf9 cells did not stimulate PLC-beta1. Concurrent expression of the G-protein betagamma subunit complex increased the amount of G16alpha. in Sf9 cell membranes. The guanosine 5'-[gamma-thio]triphosphate-activated form of G16alpha was purified from cholate extracts of membranes from cells expressing G16alpha, and the G-protein beta2 and gamma2 subunits. G16alpha activated PLC-beta1, PLC-beta2, and PLC-beta3 in a manner essentially indistinguishable from that of G(qalpha).  G16alpha-mediated activation of PLC-beta1 and PLC-beta3 greatly exceeded that of PLC-beta2. G16alpha did not activate PLC-gamma1 or PLC-delta1. Thus, two distantly related members of the G(qalpha) family, G(qalpha) and G16alpha, have the same ability to activate the known isoforms of PLC-beta.
C1 UNIV TEXAS,SW MED CTR,DEPT PHARMACOL,DALLAS,TX 75235.
   NHLBI,BETHESDA,MD 20892.
   CALTECH,DEPT BIOL,PASADENA,CA 91125.
FU NIGMS NIH HHS [GM31954, GM34236, GM34497]
NR 27
TC 70
Z9 71
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 OCT 1
PY 1993
VL 90
IS 19
BP 9176
EP 9180
DI 10.1073/pnas.90.19.9176
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA595
UT WOS:A1993MA59500088
PM 8415674
ER

PT J
AU HAYES, F
   AUSTIN, SJ
AF HAYES, F
   AUSTIN, SJ
TI SPECIFICITY DETERMINANTS OF THE P1 AND P7 PLASMID CENTROMERE ANALOGS
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE PARTITION; SEGREGATION; PROTEIN-DNA INTERACTIONS; PARS; INTEGRATION HOST
   FACTOR
ID INTEGRATION HOST FACTOR; UNIT-COPY MINIPLASMIDS; ESCHERICHIA-COLI;
   PARTITION SYSTEM; DAUGHTER CELLS; SITE; SEQUENCE; PROTEINS; BINDING;
   VECTORS
AB The cis-acting parS sites of P1 and P7 are similar in sequence and promote active partition of their respective plasmid prophages to daughter cells when the cognate Par proteins are supplied. Forty of the 94 relevant bases differ between the P1 and P7 parS sites, and the protein-site interactions show complete species specificity. A method was developed to predict which subset of the differing parS bases is responsible. When the four Pl bases thus identified were substituted into the P7 parS site, a complete switch to P1 specificity was observed. The P1-specific bases constitute two CG dinucleotide elements situated 66 bp apart. They lie within repeats of the TCGCCA sequence implicated in secondary contacts with the P1 ParB protein. The equivalent TC dinucleotides in the P7 site were found to be involved in P7 specificity. However, three other P7 bases can also contribute, including two in the heptamer repeats primarily responsible for ParB binding, and the P7-specific information shows some redundancy. The motifs containing the specificity dinucleotides and the primary ParB binding (heptamer) sites bear no obvious relationship of spacing or orientation to each other. For the ParB protein to contact both types of motif at the same time, the topology of the interaction must be complex.
C1 NCI,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LABS,BASIC RES PROGRAM,CHROMOSOME BIOL LAB,FREDERICK,MD 21702.
FU NCI NIH HHS [N01-CO-74101]
NR 26
TC 33
Z9 33
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 1
PY 1993
VL 90
IS 19
BP 9228
EP 9232
DI 10.1073/pnas.90.19.9228
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA595
UT WOS:A1993MA59500099
PM 8415682
ER

PT J
AU LAZARUS, LH
   ATTILA, M
AF LAZARUS, LH
   ATTILA, M
TI THE TOAD, UGLY AND VENOMOUS, WEARS YET A PRECIOUS JEWEL IN HIS SKIN
SO PROGRESS IN NEUROBIOLOGY
LA English
DT Review
ID XENOPUS-LAEVIS SKIN; AMINO-ACID-SEQUENCE; PORCINE SPINAL-CORD;
   D-ASPARTIC ACID; CORTICOTROPIN-RELEASING FACTOR; DELTA-OPIOID RECEPTORS;
   ALPHA-AMIDATING ENZYME; BOMBESIN-LIKE PEPTIDE; SMALL-CELL CARCINOMA;
   OPIATE-LIKE PEPTIDE
RP NIEHS, INTEGRAT BIOL LAB, PEPTIDE NEUROCHEM SECT, RES TRIANGLE PK, NC 27709 USA.
NR 338
TC 180
Z9 186
U1 1
U2 19
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0301-0082
J9 PROG NEUROBIOL
JI Prog. Neurobiol.
PD OCT
PY 1993
VL 41
IS 4
BP 473
EP 507
DI 10.1016/0301-0082(93)90027-P
PG 35
WC Neurosciences
SC Neurosciences & Neurology
GA LQ436
UT WOS:A1993LQ43600003
PM 8210414
ER

PT J
AU DEMITRACK, MA
   PUTNAM, FW
   RUBINOW, DR
   PIGOTT, TA
   ALTEMUS, M
   KRAHN, DD
   GOLD, PW
AF DEMITRACK, MA
   PUTNAM, FW
   RUBINOW, DR
   PIGOTT, TA
   ALTEMUS, M
   KRAHN, DD
   GOLD, PW
TI RELATION OF DISSOCIATIVE PHENOMENA TO LEVELS OF CEREBROSPINAL-FLUID
   MONOAMINE METABOLITES AND BETA-ENDORPHIN IN PATIENTS WITH EATING
   DISORDERS - A PILOT-STUDY
SO PSYCHIATRY RESEARCH
LA English
DT Article
DE DISSOCIATION; HYPNOTIZABILITY; ANOREXIA NERVOSA; BULIMIA; HOMOVANILLIC;
   ACID; 5-HYDROXYINDOLEACETIC ACID
ID MULTIPLE PERSONALITY-DISORDER; ANOREXIA-NERVOSA; OPTICAL-DIFFERENCES;
   SEXUAL ABUSE; BULIMIA; HYPNOTIZABILITY
AB Dissociation is made manifest by a failure to integrate thoughts, feelings, memories, and actions into a unified sense of consciousness. Although dissociation is presumed to be a special state of consciousness manifested by state-dependent memory and physiology, the psychobiology of dissociation is poorly understood. In this study, we examined cerebrospinal fluid levels of the major monoamine metabolites and beta-endorphin in patients with eating disorders (11 with anorexia nervosa, 16 with bulimia nervosa), while they were acutely ill. Dissociative capacity was measured using the Dissociative Experiences Scale (DES). We provide evidence that neurochemical changes in dopaminergic, serotonergic, and opioid systems may be associated with the clinical expression of dissociation in patients with eating disorders during the acute phase of their illness. These preliminary results are compatible with previous studies of neurochemical disturbances in the eating disorders and suggest that future work in dissociation should specifically include examination of these neurobiologic systems.
C1 NIMH,DEV PSYCHOL LAB,DISSOCIAT DISORDERS UNIT,BETHESDA,MD 20892.
   NIMH,BIOL PSYCHIAT BRANCH,BEHAV ENDOCRINOL SECT,BETHESDA,MD 20892.
   GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC.
   NIMH,CLIN SCI LAB,BETHESDA,MD 20892.
   UNIV WISCONSIN,DEPT PSYCHIAT,MADISON,WI 53706.
   NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892.
RP DEMITRACK, MA (reprint author), UNIV MICHIGAN,SCH MED,DEPT PSYCHIAT,MICHIGAN EATING DISORDERS PROGRAM,1500 E MED CTR DR,ANN ARBOR,MI 48109, USA.
RI Demitrack, Mark/I-7697-2013
NR 35
TC 22
Z9 23
U1 1
U2 2
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0165-1781
J9 PSYCHIAT RES
JI Psychiatry Res.
PD OCT
PY 1993
VL 49
IS 1
BP 1
EP 10
DI 10.1016/0165-1781(93)90026-D
PG 10
WC Psychiatry
SC Psychiatry
GA MQ005
UT WOS:A1993MQ00500001
PM 7511247
ER

PT J
AU CASANOVA, MF
   CAROSELLA, NW
   GOLD, JM
   KLEINMAN, JE
   WEINBERGER, DR
   POWERS, RE
AF CASANOVA, MF
   CAROSELLA, NW
   GOLD, JM
   KLEINMAN, JE
   WEINBERGER, DR
   POWERS, RE
TI A TOPOGRAPHICAL STUDY OF SENILE PLAQUES AND NEUROFIBRILLARY TANGLES IN
   THE HIPPOCAMPI OF PATIENTS WITH ALZHEIMERS-DISEASE AND COGNITIVELY
   IMPAIRED PATIENTS WITH SCHIZOPHRENIA
SO PSYCHIATRY RESEARCH
LA English
DT Review
DE NEUROPATHOLOGY; DEMENTIA; SENILE PLAQUES; NEUROFIBRILLARY TANGLES
ID DOPAMINE NERVE-TERMINALS; GRANULOVACUOLAR DEGENERATION; LIMBIC SYSTEM;
   DEMENTIA; PATHOLOGY; BRAIN; CORTEX; CONNECTIONS; DYSFUNCTION; DISORDERS
AB Neuropsychological testing of elderly schizophrenic patients reveals that a significant portion of this population exhibit varying degrees of cognitive impairment. Since Alzheimer's disease is the most common cause of dementia in geriatric patients, we investigated whether the cognitive decline observed in schizophrenia is the result of degenerative changes analogous to those characteristic of Alzheimer's disease. For this purpose, the number and distribution of senile plaques and neurofibrillary tangles were mapped in the hippocampi of 10 cognitively impaired schizophrenic patients, 10 patients with Alzheimer's disease, and IO patients with dementia not attributed to either schizophrenia or Alzheimer's disease. In Alzheimer's disease, degenerative changes invariably predominated in the CA1 subfield, subiculum, and proisocortex. By contrast, findings characteristic of Alzheimer's disease were virtually never observed in the hippocampi of schizophrenic and other cognitively impaired patients. In some patients with Alzheimer's disease, the presence of senile plaques in the molecular layer of the dentate gyrus suggested the existence of an underlying entorhinal cortex lesion. Similar dentate gyrus pathology was never found in any of the other patients. The authors conclude that cognitive impairment in schizophrenia is not the result of degenerative changes analogous to those found in Alzheimer's disease.
C1 MED COLL GEORGIA,AUGUSTA,GA 30912.
   AUGUSTA VET AFFAIRS HOSP,AUGUSTA,GA.
   ST ELIZABETH HOSP,NIMH,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC.
   UNIV ALABAMA,BRAIN RESOURCE PROGRAM,BIRMINGHAM,AL.
   NIMH,BRAIN BANK UNIT,WASHINGTON,DC.
NR 106
TC 39
Z9 39
U1 0
U2 3
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0165-1781
J9 PSYCHIAT RES
JI Psychiatry Res.
PD OCT
PY 1993
VL 49
IS 1
BP 41
EP 62
DI 10.1016/0165-1781(93)90029-G
PG 22
WC Psychiatry
SC Psychiatry
GA MQ005
UT WOS:A1993MQ00500004
PM 8140181
ER

PT J
AU MARENCO, S
   COPPOLA, R
   DANIEL, DG
   ZIGUN, JR
   WEINBERGER, DR
AF MARENCO, S
   COPPOLA, R
   DANIEL, DG
   ZIGUN, JR
   WEINBERGER, DR
TI REGIONAL CEREBRAL BLOOD-FLOW DURING THE WISCONSIN CARD SORTING TEST IN
   NORMAL SUBJECTS STUDIED BY XE-133 DYNAMIC SPECT - COMPARISON OF ABSOLUTE
   VALUES, PERCENT DISTRIBUTION VALUES, AND COVARIANCE ANALYSIS
SO PSYCHIATRY RESEARCH-NEUROIMAGING
LA English
DT Article
DE SINGLE PHOTON EMISSION COMPUTED TOMOGRAPHY; MATCHING-TO-SAMPLE TASK;
   NEUROPSYCHOLOGY; FRONTAL LOBES
ID DORSOLATERAL PREFRONTAL CORTEX; EMISSION COMPUTED-TOMOGRAPHY; INERT-GAS
   CONCENTRATIONS; PHYSIOLOGIC DYSFUNCTION; XE-133 INHALATION;
   SCHIZOPHRENIA; BRAIN; ATTENTION; DEMENTIA
AB We studied regional cerebral blood flow (rCBF) by xenon-133 dynamic single photon emission computed tomography (SPECT) in 17 normal volunteers who were performing the Wisconsin Card Sorting Test (WCST), a task that is particularly sensitive to disturbance of the prefrontal cortex, and a simple matching-to-sample task (BAR) as a sensorimotor control. Three methods for statistical analysis of regional ''subtraction'' data were used: absolute rCBF values, percent distribution values, and means adjusted for global CBF changes (covariance analysis). The absolute values had high variance, due to the combination of interindividual differences in global flow and intra-individual variation, and showed no statistically significant regional changes. This variation was greatly reduced by percent values and covariance analysis, which had quite similar outcomes. With both methods, significant increases of rCBF during the WCST as compared with the BAR were seen-in the right anterior dorsolateral prefrontal and left occipital cortices, and reduction of rCBF in the left pararolandic region. Moreover, significant correlations with performance were found in the medial regions of the frontal lobes, with opposite trends for the right and left hemisphere. The posterior dorsolateral prefrontal region showed a negative correlation with sensory-motor frequency, an index related to the task's difficulty. These results are consistent with previous findings using other rCBF techniques and confirm the statistical advantage of normalization and covariance methods, which yield practically identical results, at least in this analysis based on regions of interest.
C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032.
RI Marenco, Stefano/A-2409-2008
OI Marenco, Stefano/0000-0002-2488-2365
NR 37
TC 63
Z9 63
U1 0
U2 0
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0925-4927
J9 PSYCHIAT RES-NEUROIM
JI Psychiatry Res. Neuroimaging
PD OCT
PY 1993
VL 50
IS 3
BP 177
EP 192
DI 10.1016/0925-4927(93)90029-H
PG 16
WC Clinical Neurology; Neuroimaging; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA MA858
UT WOS:A1993MA85800004
PM 8272453
ER

PT J
AU IIJIMA, S
   GREIG, NH
   GAROFALO, P
   SPANGLER, EL
   HELLER, B
   BROSSI, A
   INGRAM, DK
AF IIJIMA, S
   GREIG, NH
   GAROFALO, P
   SPANGLER, EL
   HELLER, B
   BROSSI, A
   INGRAM, DK
TI PHENSERINE - A PHYSOSTIGMINE DERIVATIVE THAT IS A LONG-ACTING INHIBITOR
   OF CHOLINESTERASE AND DEMONSTRATES A WIDE DOSE RANGE FOR ATTENUATING A
   SCOPOLAMINE-INDUCED LEARNING IMPAIRMENT OF RATS IN A 14-UNIT T-MAZE
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE ACETYLCHOLINE; MEMORY; AGING; ALZHEIMERS DISEASE; ANTICHOLINERGICS
ID FIMBRIA-FORNIX LESIONS; ALZHEIMERS-DISEASE; HEPTYL-PHYSOSTIGMINE;
   CHOLINERGIC SYSTEM; RETENTION PERFORMANCE; YOUNG-RATS; AGED RATS;
   MEMORY; TETRAHYDROAMINOACRIDINE; DEMENTIA
AB Phenserine ((-)-N-phenylcarbamoyl eseroline), a carbamate analog of physostigmine (Phy), is a long-acting inhibitor of cholinesterase. We have assessed the potential clinical value of phenserine for cholinomimetic therapy of cognitive impairments associated with aging and Alzheimer's disease by evaluating its duration of in vivo activity against rat plasma acetylcholinesterase (AChE) and its effect on attenuating a scopolamine-induced impairment in learning performance of young rats in a shock-motivated 14-unit T-maze. Phenserine achieved maximum AChE inhibition of 73.5% at 5 min and maintained a high and relatively constant inhibition for more than 8 h. For analysis of effects on learning performance, 69, 3-month-old male Fischer-344 rats were pretrained in a straight runway to avoid electric footshock. On the following day, each animal received 15 trials in the 14-unit T-maze. Sixty minutes prior to the maze training, each rat received the first IP injection of either vehicle (Tween 80, ethanol and 0.9% NaCl) or phenserine at 1.5, 3.0, 4.0, 5.0, 7.5, or 10.0 mg/kg. Then 30 min prior to the training, each animal received a second IP injection of either 0.9% NaCl or scopolamine hydrochloride (0.75 mg/kg; SCOP). Compared to the vehicle-SCOP group, all but the 7.5 mg/kg dose of phenserine significantly ameliorated error performance, runtime, shock frequency and shock duration in SCOP-treated rats at the final block of three trials. Appearing to have a long effect and a wide therapeutic window, phenserine deserves further study as a cognitive enhancer.
C1 NIA,GERONTOL RES CTR,CELLULAR & MOLEC BIOL LAB,MOLEC PHYSIOL & GENET SECT,BALTIMORE,MD 21224.
   NIA,NEUROSCI LAB,BETHESDA,MD 20892.
   NIDDKD,STRUCT BIOL LAB,NAT PROD SECT,BETHESDA,MD 20892.
NR 38
TC 27
Z9 27
U1 1
U2 4
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 1993
VL 112
IS 4
BP 415
EP 420
DI 10.1007/BF02244888
PG 6
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA ME588
UT WOS:A1993ME58800003
PM 7871051
ER

PT J
AU SONCRANT, TT
   RAFFAELE, KC
   ASTHANA, S
   BERARDI, A
   MORRIS, PP
   HAXBY, JV
AF SONCRANT, TT
   RAFFAELE, KC
   ASTHANA, S
   BERARDI, A
   MORRIS, PP
   HAXBY, JV
TI MEMORY IMPROVEMENT WITHOUT TOXICITY DURING CHRONIC, LOW-DOSE INTRAVENOUS
   ARECOLINE IN ALZHEIMERS-DISEASE
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE ARECOLINE; ALZHEIMERS DISEASE; MEMORY
ID CHOLINERGIC AGONIST ARECOLINE; ORAL PHYSOSTIGMINE; SENILE DEMENTIA;
   DOUBLE-BLIND; LECITHIN; ASYMMETRIES; INFUSIONS; RECEPTORS; THERAPY;
   TRIALS
AB Arecoline, a cholinergic agonist, administered at low doses by continuous intravenous infusion for up to 2 weeks, significantly and replicably improved memory in five of nine subjects with mild-moderate Alzheimer's disease. During dose finding, performance on a verbal memory task improved with an inverted U-shaped relation to dose. Six of nine subjects were classified as responders. During blinded, placebo-controlled, individualized optimal dosing for 5 days, verbal memory again improved in five of six responders but not in any non-responder. No adverse drug effects occurred. Arecoline, and possibly other cholinergic agonists, can safely improve memory in Alzheimer's disease at doses much lower than previously studied.
RP SONCRANT, TT (reprint author), NIA,NEUROSCI LAB,PHARMACOL & PHARMACOKINET UNIT,10-6C103,BETHESDA,MD 20892, USA.
NR 42
TC 49
Z9 50
U1 2
U2 2
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 1993
VL 112
IS 4
BP 421
EP 427
DI 10.1007/BF02244889
PG 7
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA ME588
UT WOS:A1993ME58800004
PM 7871052
ER

PT J
AU HOMMER, D
   WEINGARTNER, H
   BREIER, A
AF HOMMER, D
   WEINGARTNER, H
   BREIER, A
TI DISSOCIATION OF BENZODIAZEPINE-INDUCED AMNESIA FROM SEDATION BY
   FLUMAZENIL PRETREATMENT
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE BENZODIAZEPINE; FLUMAZENIL; MEMORY; ATTENTION; SEDATION
ID MULTIPLE MEMORY-SYSTEMS; DIAZEPAM; PSYCHOMOTOR; PERFORMANCE; ANTAGONIST;
   RO-15-1788; RECEPTORS; EXPLICIT; REVERSAL; BRAIN
AB AThe human amnestic syndrome associated with lesions of the hippocampus and amygdala is characterized by a selective impairment of recent (explicit, episodic) memory. Benzodiazepine (BZ) treated normal subjects demonstrate similar, marked impairments in episodic memory, but in addition, BZ also induces sedation and inattention. Thus, the amnestic effects of BZ may be secondary to drug-induced sedation. However, when subjects were pretreated with the specific BZ receptor antagonist, flumazenil, the sedative and attentional effects of diazepam were blocked, but a marked impairment in episodic memory still occurred. This demonstrates that, using neuropharmacological, methods, it is possible to produce a dissociation of memory impairment from inattention and sedation. Such distinct patterns of cognitive dysfunction may serve as models for clinical cognitive syndromes.
C1 UNIV MARYLAND,SCH MED,DEPT PSYCHIAT,MARYLAND PSYCHIAT RES CTR,BALTIMORE,MD 21201.
RP HOMMER, D (reprint author), NIAAA,CLIN SCI LAB,BLDG 10,ROOM 3B19,9000 ROCKVILLE PIKE,BETHESDA,MD 20894, USA.
NR 33
TC 43
Z9 43
U1 0
U2 1
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 1993
VL 112
IS 4
BP 455
EP 460
DI 10.1007/BF02244894
PG 6
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA ME588
UT WOS:A1993ME58800009
PM 7871057
ER

PT J
AU TELLA, SR
   GOLDBERG, SR
AF TELLA, SR
   GOLDBERG, SR
TI MONOAMINE UPTAKE INHIBITORS ALTER COCAINE PHARMACOKINETICS
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE COCAINE; BENZOYLECGONINE; PLASMA LEVELS; UPTAKE INHIBITION; MONOAMINES;
   NOREPINEPHRINE; SEROTONIN; DOPAMINE
ID DOPAMINE DEPLETION HYPOTHESIS; BINDING-SITES; STRUCTURAL REQUIREMENTS;
   REUPTAKE INHIBITORS; MOUSE-BRAIN; RAT-BRAIN; ABUSE; DESIPRAMINE;
   BROMOCRIPTINE; SEROTONIN
AB The time course of change in plasma levels of cocaine and its major metabolite benzoylecgonine following 3 mg/kg IV cocaine and the pharmacokinetic interaction between cocaine and several monoamine uptake inhibitors were investigated in conscious rats implanted with arterial and venous cannulae. The IV bolus administration of 3 mg/kg cocaine resulted in plasma levels of 1276 +/- 53 ng/ml cocaine at 0.5 min following its injection and the levels then rapidly declined to 768 +/- 110 ng/ml by 2 min. Thereafter, the decline of plasma cocaine levels was relatively slow. Plasma benzoylecgonine levels were similar at 0.5 and 2 min following cocaine injection but increased gradually over the next 25 min. Pretreatment with the norepinephrine-selective ve uptake inhibitors desipramine and nisoxetine, the serotonin-selective uptake inhibitor fluoxetine or the dopamine-selective uptake inhibitor GBR 12909 all enhanced plasma levels of cocaine after a 3 mg/kg IV bolus injection at 0.5, but not at 5 min after injection. The enhancement of plasma cocaine levels by GBR 12909 was of greater magnitude than that produced by desipramine, nisoxetine or fluoxetine. These agents, with the exception of the high dose (10 mg/kg) of GBR 12909, did not significantly alter plasma levels of benzoylecgonine measured at either 0.5 or 5 min following cocaine injection. These results indicate that monoamine uptake inhibitors can alter or interfere with the pharmacokinetics of cocaine and that this interaction is not due to a change in the biotransformation of cocaine. It is suggested that the central monoamine uptake sites serving as rapid distribution sites for cocaine may play a role in this pharmacokinetic interaction.
C1 GEORGETOWN UNIV,SCH MED,DEPT PHARMACOL,WASHINGTON,DC 20007.
RP TELLA, SR (reprint author), NIDA,ADDICT RES CTR,BEHAV PHARMACOL & GENET SECT,PRECLIN PHARMACOL LAB,POB 5180,BALTIMORE,MD 21224, USA.
NR 37
TC 16
Z9 16
U1 3
U2 3
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 1993
VL 112
IS 4
BP 497
EP 502
DI 10.1007/BF02244900
PG 6
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA ME588
UT WOS:A1993ME58800015
PM 7871063
ER

PT J
AU KIMES, AS
   VAUPEL, DB
   LONDON, ED
AF KIMES, AS
   VAUPEL, DB
   LONDON, ED
TI ATTENUATION OF SOME SIGNS OF OPIOID WITHDRAWAL BY INHIBITORS OF
   NITRIC-OXIDE SYNTHASE
SO PSYCHOPHARMACOLOGY
LA English
DT Note
DE NITRIC OXIDE SYNTHASE INHIBITOR; MORPHINE; DEPENDENCE; WITHDRAWAL;
   L-N-G-NITROARGININE; RATS; OPIOID WITHDRAWAL
ID MORPHINE-WITHDRAWAL; OPIATE-WITHDRAWAL; TOLERANCE; INVITRO; INVIVO
AB Effects of nitric oxide synthase (NOS) inhibitors (L-N-G-nitroarginine, L-N-G-nitroarginine methyl ester) on precipitated opioid withdrawal were studied in morphine-dependent rats given naloxone, in order to assess the involvement of nitric oxide (NO) in opioid dependence. L-N-G-Nitroarginine (7.5mg/kg, IP, 1 h before naloxone or b.i.d. on days 4-7 of an 8-day morphine treatment) reduced wet dog shakes and weight loss; when given by osmotic pumps (15 mg/kg per day), the drug reduced wet dog shakes but not weight loss. L-N-G-Nitroarginine methyl ester (60 mg/kg, 1 h before naloxone) also reduced wet dog shakes and weight loss. The results indicate that NOS inhibitors warrant further study as potential treatments of the opioid withdrawal syndrome.
C1 JOHNS HOPKINS MED INST,DEPT RADIOL,BALTIMORE,MD 21205.
   UNIV MARYLAND,SCH MED,DEPT PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21201.
RP KIMES, AS (reprint author), NIDA,ADDICT RES CTR,NEUROIMAGING & DRUG ACT SECT,POB 5180,BALTIMORE,MD 21224, USA.
NR 11
TC 79
Z9 80
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
PD OCT
PY 1993
VL 112
IS 4
BP 521
EP 524
DI 10.1007/BF02244904
PG 4
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA ME588
UT WOS:A1993ME58800019
PM 7532866
ER

PT J
AU NAGLER, RM
   BAUM, BJ
   FOX, PC
AF NAGLER, RM
   BAUM, BJ
   FOX, PC
TI ACUTE EFFECTS OF X-IRRADIATION ON THE FUNCTION OF RAT SALIVARY-GLANDS
SO RADIATION RESEARCH
LA English
DT Article
ID PAROTID-GLAND; ACINAR-CELLS; SUBMANDIBULAR-GLAND; RADIATION-INJURY;
   RADIOSENSITIVITY
RP NAGLER, RM (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892, USA.
NR 37
TC 47
Z9 49
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 OCT
PY 1993
VL 136
IS 1
BP 42
EP 47
DI 10.2307/3578638
PG 6
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
   Nuclear Medicine & Medical Imaging
GA MD360
UT WOS:A1993MD36000006
PM 8210337
ER

PT J
AU DOPPMAN, JL
AF DOPPMAN, JL
TI PARAPLEGIA AFTER SURGERY FOR THORACOABDOMINAL ANEURYSMS - RUSSIAN
   ROULETTE FOR THE VASCULAR SURGEON
SO RADIOLOGY
LA English
DT Editorial Material
DE ANEURYSM, AORTIC; ANGIOGRAPHY, PREOPERATIVE; ARTERIES, SPINAL;
   EDITORIALS; RADIOLOGY AND RADIOLOGISTS, IATROGENIC INJURY
ID AVOID ISCHEMIA; ADJUNCTS
RP DOPPMAN, JL (reprint author), NIH,DEPT RADIOL,BLDG 10,RM 1C660,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 11
TC 8
Z9 8
U1 0
U2 0
PU RADIOLOGICAL SOC NORTH AMER
PI EASTON
PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD OCT
PY 1993
VL 189
IS 1
BP 27
EP 28
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA LY023
UT WOS:A1993LY02300004
PM 8372203
ER

PT J
AU FULHAM, MJ
   MELISI, JW
   NISHIMIYA, J
   DWYER, AJ
   DICHIRO, G
AF FULHAM, MJ
   MELISI, JW
   NISHIMIYA, J
   DWYER, AJ
   DICHIRO, G
TI NEUROIMAGING OF JUVENILE PILOCYTIC ASTROCYTOMAS - AN ENIGMA
SO RADIOLOGY
LA English
DT Article
DE BRAIN NEOPLASMS; BRAIN NEOPLASMS; BRAIN NEOPLASMS, MR; BRAIN NEOPLASMS,
   RADIONUCLIDE STUDIES
ID POSITRON EMISSION TOMOGRAPHY; MONOCLONAL-ANTIBODY KI-67;
   HUMAN-BRAIN-TUMORS; NERVOUS-SYSTEM TUMORS; GLUCOSE-TRANSPORTER; HUMAN
   GLIOMAS; CEREBELLAR ASTROCYTOMA; CEREBRAL HEMISPHERES;
   BROMODEOXYURIDINE; RECURRENCE
AB PURPOSE: To present the imaging, metabolic, and clinical data obtained in five patients with juvenile pilocytic astrocytomas (JPAs) and discuss the paradoxical neuroimaging findings.
   MATERIALS AND METHODS: Five patients with JPAs who had undergone structural imaging and fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) were studied. Normalized glucose utilization rates (GURs) in the tumor were compared with GURs in histopathologically verified low-grade astrocytomas and high-grade tumors.
   RESULTS: All JPAs enhanced markedly after administration of contrast medium. Their glucose metabolism was significantly (P < .001) higher than that of low-grade astrocytomas and was similar to that of anaplastic astrocytomas. All patients with JPAs were in stable condition and showed no evidence of disease progression despite contrast enhancement and high tumoral glucose metabolism.
   CONCLUSION: The paradoxical FDG PET findings and enhancement at structural imaging might reflect the unusual vascularity of pilocytic tumors, and the increased GUR might be related to expression of the glucose transporter.
C1 NINCDS,NEUROIMAGING BRANCH,RM 1C451,BLDG 10,9000 ROCKVILLE PIKE,BETHESDA,MD 20892.
   NINCDS,CLIN NEUROPHARMACOL SECT,BETHESDA,MD 20892.
   NIH,CTR CLIN,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892.
NR 53
TC 65
Z9 66
U1 0
U2 1
PU RADIOLOGICAL SOC NORTH AMER
PI EASTON
PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD OCT
PY 1993
VL 189
IS 1
BP 221
EP 225
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA LY023
UT WOS:A1993LY02300043
PM 8372197
ER

PT J
AU MELNICK, RL
AF MELNICK, RL
TI CRITIQUE DOES NOT VALIDATE ASSUMPTIONS IN THE MODEL ON ALPHA-2U-GLOBULIN
   AND RENAL CARCINOGENESIS
SO REGULATORY TOXICOLOGY AND PHARMACOLOGY
LA English
DT Note
ID FEMALE FISCHER-344 RATS; NEPHROPATHY
RP MELNICK, RL (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA.
NR 11
TC 13
Z9 13
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 0273-2300
J9 REGUL TOXICOL PHARM
JI Regul. Toxicol. Pharmacol.
PD OCT
PY 1993
VL 18
IS 2
BP 365
EP 368
DI 10.1006/rtph.1993.1062
PG 4
WC Medicine, Legal; Pharmacology & Pharmacy; Toxicology
SC Legal Medicine; Pharmacology & Pharmacy; Toxicology
GA MC736
UT WOS:A1993MC73600014
PM 7506437
ER

PT J
AU KEEGAN, AD
   WANG, LM
   PAUL, WE
   PIERCE, JH
AF KEEGAN, AD
   WANG, LM
   PAUL, WE
   PIERCE, JH
TI CHARACTERIZATION OF THE INTERLEUKIN-4 RECEPTOR - STRUCTURE AND
   SIGNAL-TRANSDUCTION PATHWAYS
SO RESEARCH IN IMMUNOLOGY
LA English
DT Article
ID STIMULATORY FACTOR-I; PROTEIN TYROSINE PHOSPHORYLATION; MURINE
   LYMPHOCYTES-B; CELL GROWTH-FACTOR; HIGH-AFFINITY; MOLECULAR-CLONING;
   IL-4 RECEPTOR; FC-EPSILON; T-CELLS; EXPRESSION
C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892.
RP KEEGAN, AD (reprint author), NIAID,IMMUNOL LAB,BETHESDA,MD 20892, USA.
NR 53
TC 4
Z9 4
U1 0
U2 1
PU EDITIONS SCIENTIFIQUES ELSEVIER
PI PARIS CEDEX 15
PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE
SN 0923-2494
J9 RES IMMUNOL
JI Res. Immunol.
PD OCT
PY 1993
VL 144
IS 8
BP 590
EP 596
DI 10.1016/S0923-2494(05)80008-2
PG 7
WC Immunology
SC Immunology
GA MN101
UT WOS:A1993MN10100008
PM 8303078
ER

PT J
AU OSWALD, IP
   WYNN, TA
   WILLIAMS, ME
   ELTOUM, I
   CHEEVER, AW
   JAMES, SL
   SHER, A
AF OSWALD, IP
   WYNN, TA
   WILLIAMS, ME
   ELTOUM, I
   CHEEVER, AW
   JAMES, SL
   SHER, A
TI REGULATORY AND IMMUNOPATHOLOGICAL ROLES OF IL4 IN EXPERIMENTAL
   SCHISTOSOMIASIS
SO RESEARCH IN IMMUNOLOGY
LA English
DT Article
ID TUMOR-NECROSIS-FACTOR; T-CELL SUBSETS; DOWN-REGULATION; INTERLEUKIN-4;
   CYTOKINES; MANSONI; ACTIVATION; IMMUNITY; GAMMA; IL-4
RP OSWALD, IP (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA.
RI Wynn, Thomas/C-2797-2011; OSWALD, Isabelle/A-8497-2013; 
OI OSWALD, Isabelle/0000-0001-9918-277X
NR 28
TC 2
Z9 2
U1 0
U2 2
PU EDITIONS SCIENTIFIQUES ELSEVIER
PI PARIS CEDEX 15
PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE
SN 0923-2494
J9 RES IMMUNOL
JI Res. Immunol.
PD OCT
PY 1993
VL 144
IS 8
BP 643
EP 648
DI 10.1016/S0923-2494(05)80020-3
PG 6
WC Immunology
SC Immunology
GA MN101
UT WOS:A1993MN10100020
PM 8303083
ER

PT J
AU ZHOU, GX
   SCHMITT, JM
   ELLICOTT, CE
AF ZHOU, GX
   SCHMITT, JM
   ELLICOTT, CE
TI SENSITIVE DETECTION OF OPTICAL-ROTATION IN LIQUIDS BY REFLECTION
   POLARIMETRY
SO REVIEW OF SCIENTIFIC INSTRUMENTS
LA English
DT Article
ID DIODES
AB We describe a sensitive polarimeter for measuring optical rotation induced by chiral molecules in solution that operates in the reflectance mode. A polarized light beam is made to pass through a liquid sample two or more times before detection by reflecting the beam from the surface of the sample container. The optical activity of the sample is measured using a differential polarization detector. Our results show that, for certain initial polarization states and angular orientations of the beam with respect to the glass interfaces, high sensitivity to changes in the concentration of the sample can be achieved. Results of a theoretical analysis of the technique were confirmed by experiments in which optical rotation of glucose in water was measured using a simple apparatus that employs a light-emitting diode source. Glucose sensing in vivo and on-line monitoring of industrial processes using integrated optoelectronic sensors are discussed as potential applications.
C1 NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 10,BETHESDA,MD 20892.
   JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205.
NR 19
TC 6
Z9 6
U1 0
U2 8
PU AMER INST PHYSICS
PI WOODBURY
PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999
SN 0034-6748
J9 REV SCI INSTRUM
JI Rev. Sci. Instrum.
PD OCT
PY 1993
VL 64
IS 10
BP 2801
EP 2807
DI 10.1063/1.1144366
PG 7
WC Instruments & Instrumentation; Physics, Applied
SC Instruments & Instrumentation; Physics
GA MC137
UT WOS:A1993MC13700012
ER

PT J
AU WILLIAMSON, CK
   KNUTTEL, A
   KNUTSON, JR
AF WILLIAMSON, CK
   KNUTTEL, A
   KNUTSON, JR
TI A SIMPLE INTERNALLY MIXED PHOTOMULTIPLIER WITH GHZ RESPONSE
SO REVIEW OF SCIENTIFIC INSTRUMENTS
LA English
DT Article
AB A small head-on photomultiplier (HR2247) with ''half photocathode gating'' is being used for detection in a superheterodyne mixing scheme. The HR2247 has a spectral range of 160-650 nm, a frequency response to 1 GHz and is inexpensive. A gate mesh covers part of the photocathode surface. Internal mixing is accomplished by applying a rf signal to the gate mesh. A fiber-optic/objective assembly mounted on an X-Y stage scans the position of the incident laser beam on the mesh. In order to evaluate the suitability of the HR2247 for practical fluorescence and imaging experiments, the photocathode surface was mapped at 41, 205, 410, 615, and 820 MHz modulation frequencies for variations in phase and modulation. The mixed signal at any point on the gate mesh can be optimized by adjusting the potential at the gate mesh.
RP WILLIAMSON, CK (reprint author), NHLBI,CELL BIOL LAB,BETHESDA,MD 20892, USA.
NR 4
TC 2
Z9 2
U1 0
U2 0
PU AMER INST PHYSICS
PI WOODBURY
PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999
SN 0034-6748
J9 REV SCI INSTRUM
JI Rev. Sci. Instrum.
PD OCT
PY 1993
VL 64
IS 10
BP 3014
EP 3017
DI 10.1063/1.1144349
PG 4
WC Instruments & Instrumentation; Physics, Applied
SC Instruments & Instrumentation; Physics
GA MC137
UT WOS:A1993MC13700048
ER

PT J
AU KOHN, MC
   PORTIER, CJ
AF KOHN, MC
   PORTIER, CJ
TI EFFECTS OF THE MECHANISM OF RECEPTOR-MEDIATED GENE-EXPRESSION ON THE
   SHAPE OF THE DOSE-RESPONSE CURVE
SO RISK ANALYSIS
LA English
DT Article
DE PHARMACODYNAMIC MODELING; DOSE RESPONSE MECHANISMS; RECEPTOR-MEDIATED
   GENE EXPRESSION; TOXICITY THRESHOLDS
AB A mathematical model of receptor-mediated gene expression that includes receptor binding of natural and xenobiotic ligands, protein synthesis and degradation, and metabolism of the xenobiotic ligand was created to identify the determinants of the shape of the dose-response profile. Values of the model's parameters were varied to reflect alternative mechanisms of expression of the protein. These assumptions had dramatic effects on the computed response to a bolus dose of the xenobiotic ligand. If all processes in the model exhibit hyperbolic kinetics, the dose-response curves can appear sigmoidal but actually be linear with a positive slope at low doses. The slope of the curve only approached zero at low dose, indicative of a threshold for response, if binding of the xenobiotic ligand to the receptor exhibited positive cooperativity (ligand binding at one site increases the affinity for ligand at another binding site on the receptor). Positive cooperativity in the rate-limiting step of protein synthesis produced dose-response curves which were ''U-shaped'' at low doses, also indicative of a threshold. Positive cooperativity in the metabolism of the xenobiotic ligand produced dose-response curves that increased more rapidly than linearly with increasing dose. The model illustrates the fact that response cannot be predicted from qualitative mechanistic arguments alone; any assessment of risk to health from xenobiotic chemicals must be based on a detailed quantitative examination of the kinetic behavior of each chemical species individually.
RP KOHN, MC (reprint author), NIEHS,STAT & BIOMATH BRANCH,POB 12233,RES TRIANGLE PK,NC 27709, USA.
RI Portier, Christopher/A-3160-2010
OI Portier, Christopher/0000-0002-0954-0279
NR 7
TC 21
Z9 21
U1 0
U2 1
PU PLENUM PUBL CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
SN 0272-4332
J9 RISK ANAL
JI Risk Anal.
PD OCT
PY 1993
VL 13
IS 5
BP 565
EP 572
DI 10.1111/j.1539-6924.1993.tb00016.x
PG 8
WC Public, Environmental & Occupational Health; Mathematics,
   Interdisciplinary Applications; Social Sciences, Mathematical Methods
SC Public, Environmental & Occupational Health; Mathematics; Mathematical
   Methods In Social Sciences
GA MH191
UT WOS:A1993MH19100015
PM 8259447
ER

PT J
AU COLLINS, F
   GALAS, D
AF COLLINS, F
   GALAS, D
TI A NEW 5-YEAR PLAN FOR THE UNITED-STATES HUMAN GENOME PROJECT
SO SCIENCE
LA English
DT Article
C1 US DOE,OFF HLTH & ENVIRONM RES,WASHINGTON,DC 20585.
RP COLLINS, F (reprint author), NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892, USA.
NR 3
TC 231
Z9 237
U1 0
U2 6
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD OCT 1
PY 1993
VL 262
IS 5130
BP 43
EP 46
DI 10.1126/science.8211127
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LZ635
UT WOS:A1993LZ63500021
PM 8211127
ER

PT J
AU COPELAND, NG
   JENKINS, NA
   GILBERT, DJ
   EPPIG, JT
   MALTAIS, LJ
   MILLER, JC
   DIETRICH, WF
   WEAVER, A
   LINCOLN, SE
   STEEN, RG
   STEIN, LD
   NADEAU, JH
   LANDER, ES
AF COPELAND, NG
   JENKINS, NA
   GILBERT, DJ
   EPPIG, JT
   MALTAIS, LJ
   MILLER, JC
   DIETRICH, WF
   WEAVER, A
   LINCOLN, SE
   STEEN, RG
   STEIN, LD
   NADEAU, JH
   LANDER, ES
TI A GENETIC-LINKAGE MAP OF THE MOUSE - CURRENT APPLICATIONS AND
   FUTURE-PROSPECTS
SO SCIENCE
LA English
DT Article
ID MAJOR HISTOCOMPATIBILITY COMPLEX; FRAGMENT LENGTH POLYMORPHISMS;
   RECOMBINANT CONGENIC STRAINS; TYROSINASE-RELATED PROTEIN; HUMAN
   PRADER-WILLI; COAT COLOR LOCUS; RETINAL DEGENERATION; POINT MUTATION;
   MESSENGER-RNA; W-LOCUS
AB Technological advances have made possible the development of high-resolution genetic linkage maps for the mouse. These maps in turn offer exciting prospects for understanding mammalian genome evolution through comparative mapping, for developing mouse models of human disease, and for identifying the function of all genes in the organism.
C1 WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142.
   MIT,DEPT BIOL,CAMBRIDGE,MA 02139.
   JACKSON LAB,BAR HARBOR,ME 04609.
RP COPELAND, NG (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702, USA.
FU NCI NIH HHS [N01-CO-74101]; NHGRI NIH HHS [HG00198]
NR 137
TC 552
Z9 557
U1 1
U2 5
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD OCT 1
PY 1993
VL 262
IS 5130
BP 57
EP 66
DI 10.1126/science.8211130
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LZ635
UT WOS:A1993LZ63500024
PM 8211130
ER

PT J
AU BROWN, KE
   ANDERSON, SM
   YOUNG, NS
AF BROWN, KE
   ANDERSON, SM
   YOUNG, NS
TI ERYTHROCYTE-P ANTIGEN - CELLULAR RECEPTOR FOR B19 PARVOVIRUS
SO SCIENCE
LA English
DT Article
ID VIRUS; INFECTION; ANTIBODIES; GLOBOSIDE; SYSTEM; FETUS; CELLS
AB The pathogenic human parvovirus B19 replicates only in erythroid progenitor cells. This virus was shown to bind to blood-group P antigen, as measured by hemagglutination. Erythrocytes lacking P antigen were not agglutinated with B19. Purified P antigen (globoside) blocked the binding of the virus to erythroid cells and the infectivity of the virus in a hematopoietic colony assay. Target cells were protected from infection by preincubation with monoclonal antibody to globoside. Knowledge of a parvovirus receptor has implications for understanding the pathogenesis of parvovirus infections and for the use of parvoviruses in gene therapy.
RP BROWN, KE (reprint author), NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892, USA.
NR 26
TC 519
Z9 545
U1 2
U2 9
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD OCT 1
PY 1993
VL 262
IS 5130
BP 114
EP 117
DI 10.1126/science.8211117
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LZ635
UT WOS:A1993LZ63500036
PM 8211117
ER

PT J
AU AKIYAMA, SK
   YAMADA, KM
AF AKIYAMA, SK
   YAMADA, KM
TI ADHESION MOLECULES IN CANCER .2. INTRODUCTION
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Editorial Material
RP AKIYAMA, SK (reprint author), NIDR,DEV BIOL LAB,BETHESDA,MD 20892, USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD
PI LONDON
PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
SN 1044-579X
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD OCT
PY 1993
VL 4
IS 5
BP 267
EP 267
PG 1
WC Oncology
SC Oncology
GA MA628
UT WOS:A1993MA62800001
ER

PT J
AU OLDEN, K
AF OLDEN, K
TI ADHESION MOLECULES AND INHIBITORS OF GLYCOSYLATION IN CANCER
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Article
DE MALIGNANT; METASTASIS; ADHESION; GLYCOSYLATION
ID ASPARAGINE-LINKED OLIGOSACCHARIDES; CELL-SURFACE PROPERTIES; HUMAN
   HEPATOMA-CELLS; BLOOD-BORNE ARREST; TUMOR-CELLS; PROTEIN GLYCOSYLATION;
   SECRETORY GLYCOPROTEINS; CARBOHYDRATE MOIETIES; ENDOPLASMIC-RETICULUM;
   PROCESSING INHIBITORS
C1 NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709.
RP OLDEN, K (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA.
NR 76
TC 17
Z9 17
U1 1
U2 1
PU ACADEMIC PRESS LTD
PI LONDON
PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
SN 1044-579X
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD OCT
PY 1993
VL 4
IS 5
BP 269
EP 276
PG 8
WC Oncology
SC Oncology
GA MA628
UT WOS:A1993MA62800002
PM 8257778
ER

PT J
AU SOBEL, ME
AF SOBEL, ME
TI DIFFERENTIAL EXPRESSION OF THE 67 KDA LAMININ RECEPTOR IN CANCER
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Article
DE ADENOCARCINOMA; BASEMENT MEMBRANE; LAMININ; NONINTEGRIN; 67 KDA LAMININ
   RECEPTOR
ID HUMAN COLON-CARCINOMA; MESSENGER-RNA; EXTRACELLULAR-MATRIX; BINDING
   PROTEIN; MONOCLONAL-ANTIBODIES; RIBOSOMAL-PROTEIN; EMBRYONIC RETINA;
   TUMOR-CELLS; PROGRESSION; METASTASIS
RP SOBEL, ME (reprint author), NCI,PATHOL LAB,MOLEC PATHOL SECT,BETHESDA,MD 20892, USA.
NR 51
TC 55
Z9 57
U1 0
U2 3
PU ACADEMIC PRESS LTD
PI LONDON
PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
SN 1044-579X
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD OCT
PY 1993
VL 4
IS 5
BP 311
EP 317
PG 7
WC Oncology
SC Oncology
GA MA628
UT WOS:A1993MA62800007
PM 8257781
ER

PT J
AU YEWDELL, JW
   BENNINK, JR
AF YEWDELL, JW
   BENNINK, JR
TI ANTIGEN-PROCESSING - A CRITICAL FACTOR IN RATIONAL VACCINE DESIGN
SO SEMINARS IN HEMATOLOGY
LA English
DT Article; Proceedings Paper
CT SYMP ON RECENT ADVANCES IN VACCINE DEVELOPMENT AND DELIVERY, ADHESION
   MOLECULES IN THE IMMUNE RESPONSE, AND BONE MARROW TRANSPLANTATION
CY JAN 08-09, 1993
CL PALM BEACH, FL
SP MILES INC PHARM DIV, BIOL PROD
ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-I MOLECULES; RESTRICTED
   LYMPHOCYTES-T; PROTEASOME SUBUNITS; PEPTIDES; MHC; TRANSPORTER;
   POLYMORPHISM; RECOGNITION; SEQUENCE
RP YEWDELL, JW (reprint author), NIAID,VIRAL DIS LAB,BETHESDA,MD 20892, USA.
RI yewdell, jyewdell@nih.gov/A-1702-2012
NR 28
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 0037-1963
J9 SEMIN HEMATOL
JI Semin. Hematol.
PD OCT
PY 1993
VL 30
IS 4
SU 4
BP 26
EP 34
PG 9
WC Hematology
SC Hematology
GA MF180
UT WOS:A1993MF18000004
PM 8303307
ER

PT J
AU SHAW, S
AF SHAW, S
TI REGULATION OF T-CELL ADHESION TO ENDOTHELIUM
SO SEMINARS IN HEMATOLOGY
LA English
DT Article; Proceedings Paper
CT SYMP ON RECENT ADVANCES IN VACCINE DEVELOPMENT AND DELIVERY, ADHESION
   MOLECULES IN THE IMMUNE RESPONSE, AND BONE MARROW TRANSPLANTATION
CY JAN 08-09, 1993
CL PALM BEACH, FL
SP MILES INC PHARM DIV, BIOL PROD
ID CYTOKINE FAMILY; LYMPHOCYTES-T; MEMORY; RECOGNITION; SUBSETS;
   GLYCOSAMINOGLYCANS; SIMILARITIES; EXPRESSION; ACTIVATION; MOLECULES
RP SHAW, S (reprint author), NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892, USA.
NR 29
TC 6
Z9 6
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0037-1963
J9 SEMIN HEMATOL
JI Semin. Hematol.
PD OCT
PY 1993
VL 30
IS 4
SU 4
BP 56
EP 65
PG 10
WC Hematology
SC Hematology
GA MF180
UT WOS:A1993MF18000007
PM 8303311
ER

PT J
AU RABKIN, CS
   DEVESA, SS
   ZAHM, SH
   GAIL, MH
AF RABKIN, CS
   DEVESA, SS
   ZAHM, SH
   GAIL, MH
TI INCREASING INCIDENCE OF NON-HODGKINS-LYMPHOMA
SO SEMINARS IN HEMATOLOGY
LA English
DT Article
ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; CELL LEUKEMIA-LYMPHOMA; TRANSPLANT
   RECIPIENTS; IMMUNE SURVEILLANCE; UNITED-STATES; CANCER; TRENDS; RISK;
   MORTALITY; WORKERS
RP RABKIN, CS (reprint author), NCI,EPIDEMIOL & BIOSTATIST PROGRAM,VIRAL EPIDEMIOL SECT,6130 EXECUT BLVD,EPN-434,ROCKVILLE,MD 20852, USA.
RI Zahm, Shelia/B-5025-2015
NR 70
TC 62
Z9 63
U1 1
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0037-1963
J9 SEMIN HEMATOL
JI Semin. Hematol.
PD OCT
PY 1993
VL 30
IS 4
BP 286
EP 296
PG 11
WC Hematology
SC Hematology
GA ME787
UT WOS:A1993ME78700003
PM 8266115
ER

PT J
AU CHESON, BD
AF CHESON, BD
TI INDOLENT B-CELL LYMPHOMAS - LESSONS LEARNED - INTRODUCTION
SO SEMINARS IN ONCOLOGY
LA English
DT Editorial Material
RP CHESON, BD (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,CLIN INVEST BRANCH,MED SECT,BETHESDA,MD 20892, 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 0093-7754
J9 SEMIN ONCOL
JI Semin. Oncol.
PD OCT
PY 1993
VL 20
IS 5
SU 5
BP 1
EP 2
PG 2
WC Oncology
SC Oncology
GA MF182
UT WOS:A1993MF18200001
ER

PT J
AU JAFFE, ES
   RAFFELD, M
   MEDEIROS, LJ
AF JAFFE, ES
   RAFFELD, M
   MEDEIROS, LJ
TI HISTOPATHOLOGIC SUBTYPES OF INDOLENT LYMPHOMAS - CARICATURES OF THE
   MATURE B-CELL SYSTEM
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; NON-HODGKINS-LYMPHOMAS; IMMUNOGLOBULIN
   GENE REARRANGEMENTS; MANTLE-ZONE LYMPHOMA; EPSTEIN-BARR-VIRUS; NODULAR
   HISTIOCYTIC LYMPHOMA; LOW-GRADE LYMPHOMA; MALIGNANT-LYMPHOMA;
   INTERMEDIATE DIFFERENTIATION; FOLLICULAR LYMPHOMA
C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,BETHESDA,MD 20892.
   BROWN UNIV,RHODE ISL HOSP,DEPT PATHOL,PROVIDENCE,RI 02903.
NR 141
TC 22
Z9 22
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0093-7754
J9 SEMIN ONCOL
JI Semin. Oncol.
PD OCT
PY 1993
VL 20
IS 5
SU 5
BP 3
EP 30
PG 28
WC Oncology
SC Oncology
GA MF182
UT WOS:A1993MF18200002
PM 8211205
ER

PT J
AU CHESON, BD
AF CHESON, BD
TI NEW CHEMOTHERAPEUTIC-AGENTS FOR THE TREATMENT OF LOW-GRADE
   NON-HODGKINS-LYMPHOMAS
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID PHASE-II TRIAL; CHRONIC LYMPHOCYTIC-LEUKEMIA; SOUTHWEST-ONCOLOGY-GROUP;
   ADVANCED MALIGNANT-LYMPHOMA; PREVIOUSLY TREATED PATIENTS; BONE-MARROW
   TRANSPLANTATION; GROUP-B STUDY-8552; FLUDARABINE PHOSPHATE;
   CLINICAL-TRIALS; COMBINATION CHEMOTHERAPY
RP CHESON, BD (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,EXECUT PLAZA N,ROOM 741,BETHESDA,MD 20892, USA.
NR 121
TC 10
Z9 10
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0093-7754
J9 SEMIN ONCOL
JI Semin. Oncol.
PD OCT
PY 1993
VL 20
IS 5
SU 5
BP 96
EP 110
PG 15
WC Oncology
SC Oncology
GA MF182
UT WOS:A1993MF18200008
PM 8105539
ER

PT J
AU PARKINSON, DR
   SZNOL, M
   CHESON, BD
AF PARKINSON, DR
   SZNOL, M
   CHESON, BD
TI BIOLOGIC THERAPIES FOR LOW-GRADE LYMPHOMAS
SO SEMINARS IN ONCOLOGY
LA English
DT Article
ID NON-HODGKINS-LYMPHOMA; CHRONIC LYMPHOCYTIC-LEUKEMIA; B-CELL LYMPHOMA;
   HUMAN-LEUKOCYTE INTERFERON; ANTI-IDIOTYPE ANTIBODY; RECOMBINANT
   LEUKOCYTE; MALIGNANT-LYMPHOMA; PHASE-II; INTERLEUKIN-4; CHEMOTHERAPY
RP PARKINSON, DR (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,INVEST DRUG BRANCH,6130 EXECUT BLVD,BETHESDA,MD 20892, USA.
NR 48
TC 6
Z9 6
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0093-7754
J9 SEMIN ONCOL
JI Semin. Oncol.
PD OCT
PY 1993
VL 20
IS 5
SU 5
BP 111
EP 117
PG 7
WC Oncology
SC Oncology
GA MF182
UT WOS:A1993MF18200009
PM 8211201
ER

PT J
AU PERSICO, AM
   SMITH, SS
   UHL, GR
AF PERSICO, AM
   SMITH, SS
   UHL, GR
TI D2-RECEPTOR GENE VARIANTS AND SUBSTANCE-ABUSE LIABILITY
SO SEMINARS IN THE NEUROSCIENCES
LA English
DT Article
DE D2-DOPAMINE RECEPTOR; GENETIC ASSOCIATION; LINKAGE DISEQUILIBRIUM;
   ALCOHOLISM; SUBSTANCE ABUSE
ID DOPAMINE RECEPTOR GENE; D2-DOPAMINE RECEPTOR; ALLELIC ASSOCIATION;
   SEVERE ALCOHOLISM; DRUG-ABUSE; D2; RFLP; SYSTEM; LOCUS; RATS
C1 NIDA,ADDICT RES CTR,MOLEC NEUROBIOL BRANCH,BALTIMORE,MD 21224.
NR 40
TC 2
Z9 2
U1 0
U2 0
PU ACADEMIC PRESS LTD
PI LONDON
PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
SN 1044-5765
J9 SEMIN NEUROSCI
JI Semin. Neurosci.
PD OCT
PY 1993
VL 5
IS 5
BP 377
EP 382
DI 10.1016/S1044-5765(05)80046-6
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA ME216
UT WOS:A1993ME21600010
ER

PT J
AU FRANKEL, P
   KIEMEL, T
AF FRANKEL, P
   KIEMEL, T
TI RELATIVE PHASE-BEHAVIOR OF 2 SLOWLY COUPLED OSCILLATORS
SO SIAM JOURNAL ON APPLIED MATHEMATICS
LA English
DT Article
DE PHASE BEHAVIOR; OSCILLATORS; AVERAGING; INVARIANT MANIFOLD
ID DYNAMICS; PATTERNS
AB Two oscillators coupled via slowly varying scalars are investigated. It is shown that the dynamics of the slow variables is approximated by a two-dimensional averaged system. If the oscillators.have similar frequencies at a fixed point of the averaged system, then the relative phase behavior of the oscillators is approximated by a three-dimensional flow. Under the stronger assumption that the oscillators themselves are similar and that the fixed point of the averaged system is symmetric, hyperbolic, and stable, a further reduction to a flow on a cylinder is possible. This cylinder flow is computed for an example in which phase entrainment, relative phase oscillations, and bidirectional wrapping of relative phase are demonstrated.
C1 NIDDKD,MATH RES BRANCH,BETHESDA,MD 20892.
   BROWN UNIV,DEPT APPL MATH,PROVIDENCE,RI 02912.
NR 15
TC 7
Z9 7
U1 0
U2 1
PU SIAM PUBLICATIONS
PI PHILADELPHIA
PA 3600 UNIV CITY SCIENCE CENTER, PHILADELPHIA, PA 19104-2688
SN 0036-1399
J9 SIAM J APPL MATH
JI SIAM J. Appl. Math.
PD OCT
PY 1993
VL 53
IS 5
BP 1436
EP 1446
DI 10.1137/0153067
PG 11
WC Mathematics, Applied
SC Mathematics
GA MB784
UT WOS:A1993MB78400010
ER

PT J
AU MUNTANER, C
   PULVER, AE
   MCGRATH, J
   EATON, WW
AF MUNTANER, C
   PULVER, AE
   MCGRATH, J
   EATON, WW
TI WORK-ENVIRONMENT AND SCHIZOPHRENIA - AN EXTENSION OF THE AROUSAL
   HYPOTHESIS TO OCCUPATIONAL SELF-SELECTION
SO SOCIAL PSYCHIATRY AND PSYCHIATRIC EPIDEMIOLOGY
LA English
DT Article
ID PSYCHIATRIC-DISORDERS; SOCIOECONOMIC-STATUS; SOCIAL-CLASS; RISK; GENDER
AB The present study investigated a possible mechanism underlying the occupational self-selection of future schizophrenic patients prior to their first admission. More precisely, we explored whether schizophrenic patients are more likely than other psychotic patients to work in environments with a low potential for arousal (low complexity environments) in the last full-time job that preceded their hospitalization. All first admissions with psychotic symptoms to 15 hospitals providing inpatient psychiatric services in the Baltimore-Washington area were surveyed during a 6-year period. Patients diagnosed with schizophrenia were compared to patients diagnosed with bipolar disorder and other psychotic disorders to evaluate the suspected association. Study participants were assessed with a modified version of the Diagnostic Interview Schedule. Standard survey questions were used to assess occupational background. A measure based on the dictionary of occupational titles (DOT) was used to estimate the degree of complexity to which patients had been exposed in their last full-time occupation. Data were analyzed using multinomial logistic regression. After adjustment for age, gender, marital status, unemployment, socioeconomic status, hospital type, and physical demands and hazards on the job, patients with schizophrenia were more likely to have been working in low complexity environments in their last full-time jobs (e.g., janitors, gardeners, guards) than patients with bipolar disorder or with other psychotic disorders. Alternative explanations and potential implications regarding which work environments might be best suited to the social behavior of patients with schizophrenia are examined.
C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MENTAL HYG,BALTIMORE,MD 21205.
   JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205.
RP MUNTANER, C (reprint author), NIMH,SOCIOENVIRONM STUDIES LAB,BETHESDA,MD 20892, USA.
RI Muntaner, C/A-5043-2010
FU NIMH NIH HHS [R01MH35712]
NR 51
TC 14
Z9 14
U1 0
U2 2
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0933-7954
J9 SOC PSYCH PSYCH EPID
JI Soc. Psychiatry Psychiatr. Epidemiol.
PD OCT
PY 1993
VL 28
IS 5
BP 231
EP 238
PG 8
WC Psychiatry
SC Psychiatry
GA MC911
UT WOS:A1993MC91100005
PM 8284736
ER

PT J
AU CHEN, R
   CONNELLY, RR
   MANTEL, N
AF CHEN, R
   CONNELLY, RR
   MANTEL, N
TI ANALYZING POST-ALARM DATA IN A MONITORING-SYSTEM IN ORDER TO ACCEPT OR
   REJECT THE ALARM
SO STATISTICS IN MEDICINE
LA English
DT Article
AB In a disease monitoring system embracing several diseases and communities, alarms indicating a significant increase in disease incidence will frequently occur even though the false alarm rate has been set quite low. An approach is presented by which an alarm is determined as either confirmed or rejected according to data observed subsequent to the alarm. The suggested procedure is expected to weed out a substantial proportion (say about 75 per cent) of the false alarms at the expense of some delay in detecting a true alarm.
C1 NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,BETHESDA,MD 20892.
   AMER UNIV,DEPT MATH & STAT,BETHESDA,MD 20814.
RP CHEN, R (reprint author), ISRAEL INST BIOL RES,DEPT APPL MATH,POB 19,IL-70450 NESS ZIONA,ISRAEL.
RI Chen, Robert/B-3899-2009
OI Chen, Robert/0000-0002-8371-8629
NR 8
TC 16
Z9 16
U1 1
U2 1
PU JOHN WILEY & SONS LTD
PI W SUSSEX
PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD OCT
PY 1993
VL 12
IS 19-20
BP 1807
EP 1812
DI 10.1002/sim.4780121908
PG 6
WC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Medicine, Research &
   Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Research & Experimental
   Medicine; Mathematics
GA MC579
UT WOS:A1993MC57900007
PM 8272662
ER

PT J
AU ETTINGHAUSEN, SE
AF ETTINGHAUSEN, SE
TI COLLAGENOUS COLITIS, EOSINOPHILIC COLITIS, AND NEUTROPENIC COLITIS
SO SURGICAL CLINICS OF NORTH AMERICA
LA English
DT Review
ID CLOSTRIDIUM-SEPTICUM INFECTION; NONSTEROIDAL ANTIINFLAMMATORY DRUGS;
   LYMPHOCYTIC MICROSCOPIC COLITIS; BONE-MARROW TRANSPLANTATION; LONG-TERM
   SURVIVAL; ACUTE-LEUKEMIA; SURGICAL-MANAGEMENT; GASTROINTESTINAL-TRACT;
   MYELOGENOUS LEUKEMIA; RHEUMATOID-ARTHRITIS
RP ETTINGHAUSEN, SE (reprint author), NCI,SURG BRANCH,BLDG 10,ROOM 2B56,BETHESDA,MD 20892, USA.
NR 136
TC 42
Z9 42
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0039-6109
J9 SURG CLIN N AM
JI Surg. Clin.-North Am.
PD OCT
PY 1993
VL 73
IS 5
BP 993
EP 1016
PG 24
WC Surgery
SC Surgery
GA LZ145
UT WOS:A1993LZ14500008
PM 8378836
ER

PT J
AU WONG, DF
   YUNG, B
   DANNALS, RF
   SHAYA, EK
   RAVERT, HT
   CHEN, CA
   CHAN, B
   FOLIO, T
   SCHEFFEL, U
   RICAURTE, GA
   NEUMEYER, JL
   WAGNER, HN
   KUHAR, MJ
AF WONG, DF
   YUNG, B
   DANNALS, RF
   SHAYA, EK
   RAVERT, HT
   CHEN, CA
   CHAN, B
   FOLIO, T
   SCHEFFEL, U
   RICAURTE, GA
   NEUMEYER, JL
   WAGNER, HN
   KUHAR, MJ
TI IN-VIVO IMAGING OF BABOON AND HUMAN DOPAMINE TRANSPORTERS BY POSITRON
   EMISSION TOMOGRAPHY USING [C-11] WIN-35,428
SO SYNAPSE
LA English
DT Article
DE PET; DOPAMINE TRANSPORTER; DOPAMINE REUPTAKE SITE; COCAINE
ID COCAINE BINDING-SITES; PARKINSONS-DISEASE; REUPTAKE SITES;
   NERVOUS-SYSTEM; H-3 WIN-35,428; PRIMATE BRAIN; I-125 RTI-55; MONKEY
   BRAIN; RECEPTORS; ANALOGS
AB [C-11]WIN 35,428 was evaluated as a specific in vivo radioligand for the dopamine transporter site by PET scanning in nonhuman primates and humans. In studies with a baboon (Papio anubis), [C-11]WIN 35,428 accumulated in brain regions containing dopamine transporters, i.e., the striata. This accumulation was partially blocked by prior administration of (-)cocaine (4 mg/kg, i.v.). Placement of a unilateral lesion of dopamine-containing nerve terminals with MPTP resulted in a unilateral reduction in [C-11]WIN 35,428 accumulation in the striatum on the side of the lesion. Imaging of D2 dopamine receptors with [C-11]NMSP in the same MPTP-treated animals showed much less reduction in the postsynaptic D2 dopamine receptors as compared to the much larger reduction in the dopamine transporters labeled with [C-11]WIN 35,428.
   A total of ten normal human volunteers (five males and five females) with ages ranging from 19 to 81 years were studied. The caudate/cerebellar and putamen/cerebellar ratios ranged from 4.4 to 5.7 90 min after injection of the tracer. Preliminary kinetic modeling with arterial plasma sampling resulted in an average binding potential (k3/k4) of 4.98 in the caudate nucleus and 5.13 in putamen. To demonstrate in vivo blockade with dopamine reuptake inhibitors, two subjects received prior oral doses of 6 mg mazindol. Subject 5 had significant reductions of 29% in the caudate/cerebellar ratio at 90 min, 35% in the putamen/cerebellar ratio at 90 min, 45% in the caudate k3/k4 ratio from 6.7 to 3.7, and 46% in the putamen k3/k4 from 4.7 to 2.5. Subject 8 had significant reductions of 20% in both the caudate/cerebellar ratio and the putamen/cerebellar ratio at 90 min.
   During the human PET studies, a number of neuropsychological tests and physiological measurements were performed. No significant changes were found after administration of the [C-11]WIN 35,428 alone. Taken together, these data indicate that [C-11]WIN 35,428 is a promising radioligand for future studies of neuropsychiatric disorders that involve the dopamine transporter site.   (C) 1993 Wiley-Liss, Inc.
C1 NIDA,ARC,BALTIMORE,MD 21224.
   JOHNS HOPKINS UNIV,DEPT RADIOL,DIV NUCL MED,BALTIMORE,MD 21205.
   JOHNS HOPKINS UNIV,DEPT ENVIRONM HLTH SCI,DIV RADIAT HLTH SCI,BALTIMORE,MD 21205.
   JOHNS HOPKINS UNIV,DEPT NEUROL,BALTIMORE,MD 21205.
   JOHNS HOPKINS MED INST,BALTIMORE,MD 21205.
   RES BIOCHEM INC,NATICK,MA 01760.
FU NCI NIH HHS [CA-32845]; NICHD NIH HHS [HD-24061]; NINDS NIH HHS
   [NS-15080]
NR 46
TC 131
Z9 134
U1 2
U2 2
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0887-4476
J9 SYNAPSE
JI Synapse
PD OCT
PY 1993
VL 15
IS 2
BP 130
EP 142
DI 10.1002/syn.890150205
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA LZ546
UT WOS:A1993LZ54600004
PM 8259524
ER

PT J
AU KIESEWETTER, DO
AF KIESEWETTER, DO
TI ASYMMETRIC-SYNTHESIS OF BENZILIC ACID ANALOGS USING 8-PHENYLMENTHOL AS A
   CHIRAL AUXILIARY
SO TETRAHEDRON-ASYMMETRY
LA English
DT Article
ID POTENTIAL RADIOPHARMACEUTICALS; NUCLEOPHILIC-ADDITION; INDUCTION;
   INVITRO; INVIVO
AB Our program on the synthesis of F-18-labeled muscarinic receptor ligands required the preparation of chiral fluoroalkyl benzilic acids. An enantioselective synthesis of substituted benzilic acids was achieved using 8-phenylmenthol as the chiral auxiliary. Grignard addition to the si face of 8-phenylmenthyl benzoylformate 7 proceeded with high selectivity. The results of the chiral induction support assignments of the chirality of benzilic acids previously resolved by crystallization. The method was used to synthesize (R)-quinuclidinyl-(R)-(4-iodo)benzilate, which proved identical to an authentic sample. In addition, the method allows the preparation of (R)- and (S)-fluoroethyl benzilic acids in a stereoselective manner.
RP KIESEWETTER, DO (reprint author), NIMH,WARREN GRANT MAGNUSON CLIN CTR,DEPT POSITRON EMISS TOMOG,BLDG 10,BETHESDA,MD 20892, USA.
NR 16
TC 17
Z9 17
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0957-4166
J9 TETRAHEDRON-ASYMMETR
JI Tetrahedron: Asymmetry
PD OCT
PY 1993
VL 4
IS 10
BP 2183
EP 2198
DI 10.1016/S0957-4166(00)80069-5
PG 16
WC Chemistry, Inorganic & Nuclear; Chemistry, Organic; Chemistry, Physical
SC Chemistry
GA MB857
UT WOS:A1993MB85700017
ER

PT J
AU JESCHKE, T
   WENSBO, D
   ANNBY, U
   GRONOWITZ, S
   COHEN, LA
AF JESCHKE, T
   WENSBO, D
   ANNBY, U
   GRONOWITZ, S
   COHEN, LA
TI A NOVEL-APPROACH TO BZ-SUBSTITUTED TRYPTOPHANS VIA PD-CATALYZED COUPLING
   ANNULATION
SO TETRAHEDRON LETTERS
LA English
DT Article
AB The Pd-catalysed preparation of bz-substituted tryptophans and their derivatives, starting from 2-iodoanilines and gamma,delta-acetylenic amino acid derivatives, is reported.
C1 LUND UNIV,CTR CHEM,DIV ORGAN CHEM 1,POB 124,S-22100 LUND,SWEDEN.
   NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD 20892.
NR 13
TC 70
Z9 70
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB
SN 0040-4039
J9 TETRAHEDRON LETT
JI Tetrahedron Lett.
PD OCT 1
PY 1993
VL 34
IS 40
BP 6471
EP 6474
DI 10.1016/0040-4039(93)85073-6
PG 4
WC Chemistry, Organic
SC Chemistry
GA MA327
UT WOS:A1993MA32700032
ER

PT J
AU JOHNSTON, LA
   DONOGHUE, AM
   OBRIEN, SJ
   WILDT, DE
AF JOHNSTON, LA
   DONOGHUE, AM
   OBRIEN, SJ
   WILDT, DE
TI INFLUENCE OF CULTURE-MEDIUM AND PROTEIN SUPPLEMENTATION ON IN-VITRO
   OOCYTE MATURATION AND FERTILIZATION IN THE DOMESTIC CAT
SO THERIOGENOLOGY
LA English
DT Article
DE CAT; OOCYTE MATURATION; FERTILIZATION; EMBRYO
ID FOLLICULAR OOCYTES; DEVELOPMENTAL COMPETENCE; MATURED INVITRO; CAPACITY;
   EMBRYOS
AB Domestic cat oocytes were cultured either in Waymouth MB 753/1 Medium (WAY) or in Eagle's Minimum Essential Medium (MEM) containing FSH, LH and estradiol-17beta and supplemented with one of the following: 5% fetal calf serum (FCS); 4 mg/ml bovine serum albumin (BSA); or 3 mg/ml polyvinylalcohol (PVA, a non-protein control). The oocytes were evaluated for: nuclear maturation after 48 hours of culture (in vitro maturation, IVM); fertilization and cleavage 24 to 30 hours postinsemination (in vitro fertilization, IVF); and early embryo development 48 hours postinsemination. Maturation rates were similar (P>0.05) for WAY + BSA (29.4%), MEM + BSA (46.7%) and MEM + PVA (43.3%), but were different (P<0.05) from the other treatments (range, WAY + FCS, 9.6% to WAY + PVA, 14.9%). Fertilization and cleavage rates were also similar (P>0.05) for WAY + BSA (51.4%, 30.5%), MEM + BSA (45.8%, 40.1%) and MEM + PVA (56.1%, 37.4%) and were greater (P<0.05) than all other treatments. These IVM/IVF oocytes were capable of culturing beyond 2-cells, with the highest proportion of 4- and 8- cell embryos forming in WAY and MEM media in the presence of BSA or in MEM medium containing PVA. In the domestic cat IVM/IVF system: both the type of culture medium and protein supplement influence the proportion of oocytes reaching Metaphase II; the type of protein supplement has a more significant (P<0.05) impact than medium on fertilization, cleavage and early embryo development; and nuclear maturation and fertilization in vitro can proceed in this species in the absence of supplementary protein.
C1 HENRY DOORLY ZOO,OMAHA,NE 68107.
   NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701.
RP JOHNSTON, LA (reprint author), SMITHSONIAN INST,NATL ZOOL PK,WASHINGTON,DC 20008, USA.
NR 27
TC 22
Z9 22
U1 3
U2 6
PU BUTTERWORTH-HEINEMANN
PI WOBURN
PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084
SN 0093-691X
J9 THERIOGENOLOGY
JI Theriogenology
PD OCT
PY 1993
VL 40
IS 4
BP 829
EP 839
DI 10.1016/0093-691X(93)90218-T
PG 11
WC Reproductive Biology; Veterinary Sciences
SC Reproductive Biology; Veterinary Sciences
GA LZ874
UT WOS:A1993LZ87400017
PM 16727364
ER

PT J
AU HOLROYD, KJ
   BUHL, R
   BOROK, Z
   ROUM, JH
   BOKSER, AD
   GRIMES, GJ
   CZERSKI, D
   CANTIN, AM
   CRYSTAL, RG
AF HOLROYD, KJ
   BUHL, R
   BOROK, Z
   ROUM, JH
   BOKSER, AD
   GRIMES, GJ
   CZERSKI, D
   CANTIN, AM
   CRYSTAL, RG
TI CORRECTION OF GLUTATHIONE DEFICIENCY IN THE LOWER RESPIRATORY-TRACT OF
   HIV-SEROPOSITIVE INDIVIDUALS BY GLUTATHIONE AEROSOL TREATMENT
SO THORAX
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; INFECTION; CELLS; DYSFUNCTION; PREVENTION;
   METABOLISM; THERAPY; DAMAGE; LAVAGE
AB Background-Concentrations of glutathione, a ubiquitous tripeptide with immune enhancing and antioxidant properties, are decreased in the blood and lung epithelial lining fluid of human immunodeficiency virus (HIV) seropositive individuals. Since the lung is the most common site of infection in those who progress to AIDS it is rational to consider whether it is possible to safely augment glutathione levels in the epithelial lining fluid of HIV seropositive individuals, thus potentially improving local host defence.
   Methods-Purified reduced glutathione was delivered by aerosol to HIV seropositive individuals (n = 14) and the glutathione levels in lung epithelial lining fluid were compared before and at one, two, and three hours after aerosol administration.
   Results-Before treatment total glutathione concentrations in the epithelial lining fluid were approximately 60% of controls. After three days of twice daily doses each of 600 mg reduced glutathione, total glutathione levels in the epithelial lining fluid increased and remained in the normal range for at least three hours after treatment. Strikingly, even though >95% of the glutathione in the aerosol was in its reduced form, the percentage of oxidised glutathione in epithelial lining fluid increased from 5% before treatment to about 40% three hours after treatment, probably reflecting the use of glutathione as an antioxidant in vivo. No adverse effects were observed.
   Conclusions-It is feasible and safe to use aerosolised reduced glutathione to augment the deficient glutathione levels of the lower respiratory tract of HIV seropositive individuals. It is rational to evaluate further the efficacy of this tripeptide in improving host defence in HIV seropositive individuals.
C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892.
   NIH,DEPT PHARM,BETHESDA,MD 20892.
   CHU SHERBROOKE,SERV PNEUMOL,SHERBROOKE J1H 5N4,QUEBEC,CANADA.
NR 40
TC 31
Z9 31
U1 0
U2 1
PU BRITISH MED JOURNAL PUBL GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR
SN 0040-6376
J9 THORAX
JI Thorax
PD OCT
PY 1993
VL 48
IS 10
BP 985
EP 989
DI 10.1136/thx.48.10.985
PG 5
WC Respiratory System
SC Respiratory System
GA MC998
UT WOS:A1993MC99800008
PM 8256245
ER

PT J
AU KLEIN, HG
AF KLEIN, HG
TI IT SEEMED A PITY TO THROW AWAY THE RED-CELLS - SELECTIVE COMPONENT
   COLLECTION
SO TRANSFUSION
LA English
DT Editorial Material
RP KLEIN, HG (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892, USA.
NR 15
TC 9
Z9 9
U1 0
U2 0
PU AMER ASSOC BLOOD BANKS
PI BETHESDA
PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749
SN 0041-1132
J9 TRANSFUSION
JI Transfusion
PD OCT
PY 1993
VL 33
IS 10
BP 788
EP 790
DI 10.1046/j.1537-2995.1993.331094054611.x
PG 3
WC Hematology
SC Hematology
GA MF033
UT WOS:A1993MF03300001
PM 8236416
ER

PT J
AU CADEDDU, JA
   PEARSON, JD
   PARTIN, AW
   EPSTEIN, JI
   CARTER, HB
AF CADEDDU, JA
   PEARSON, JD
   PARTIN, AW
   EPSTEIN, JI
   CARTER, HB
TI RELATIONSHIP BETWEEN CHANGES IN PROSTATE-SPECIFIC ANTIGEN AND PROGNOSIS
   OF PROSTATE-CANCER
SO UROLOGY
LA English
DT Article
ID ROUNDNESS FACTOR MEASUREMENT; NUCLEAR ROUNDNESS; ADENOCARCINOMA;
   DISEASE; MORPHOMETRY; CARCINOMA; SYSTEM; MARKER; SERUM; MEN
AB Changes in prostate-specific antigen (PSA), used to estimate PSA doubling times, may reflect prostate cancer growth. To determine if PSA doubling time prior to diagnosis predicted outcome in men with prostate cancer, we evaluated 16 men with prostate cancer who had (1) serial PSA determinations (mean 9.9) on frozen sera from twelve to twenty-six years before diagnosis; (2) at least five years of follow-up in those subjects without metastatic disease (range 5.5-12.3 years); and (3) archival material from diagnosis available for pathologic evaluation. PSA doubling time prior to diagnosis was investigated with relation to patient outcome (regardless of treatment) and the known predictors of tumor behavior, Gleason score and nuclear morphometry. In 5 of 16 men who had evidence of metastatic disease at diagnosis, metastasis developed or they died of prostate cancer during follow-up (group 1). Eleven of 16 had no evidence of metastatic disease during follow-up (group 2). Both Gleason score and variance of nuclear roundness (VNR) were significantly greater for group 1 (p < 0.05). There was no significant difference between the two groups with respect to PSA doubling time, and the PSA level at diagnosis did not correlate with the development of metastatic disease. One of 5 men with no PSA level greater than 4.0 ng/mL prior to diagnosis died within two years of diagnosis. These data suggest that (1) a normal PSA at diagnosis does not exclude an aggressive cancer, and (2) changes in PSA that occur before the diagnosis of prostate cancer may not always predict outcome. Since PSA level is influenced by tumor grade, an inability to correct PSA for tumor grade could have influenced the results.
C1 JOHNS HOPKINS UNIV HOSP, SCH MED,JAMES BUCHANAN BRADY UROL INST,DEPT UROL, 600 N WOLFE ST, BALTIMORE, MD 21287 USA.
   JOHNS HOPKINS UNIV HOSP, SCH MED, JAMES BUCHANAN BRADY UROL INST, DEPT PATHOL, BALTIMORE, MD 21287 USA.
   NIA, RES CTR, LONGITUDINAL STUDIES BRANCH, BALTIMORE, MD 21224 USA.
NR 25
TC 24
Z9 24
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0090-4295
EI 1527-9995
J9 UROLOGY
JI Urology
PD OCT
PY 1993
VL 42
IS 4
BP 383
EP 389
DI 10.1016/0090-4295(93)90362-E
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA MC625
UT WOS:A1993MC62500008
PM 7692658
ER

PT J
AU LEWIS, MG
   ELKINS, WR
   MCCUTCHAN, FE
   BENVENISTE, RE
   LAI, CY
   MONTEFIORI, DC
   BURKE, DS
   EDDY, GA
   SHAFFERMAN, A
AF LEWIS, MG
   ELKINS, WR
   MCCUTCHAN, FE
   BENVENISTE, RE
   LAI, CY
   MONTEFIORI, DC
   BURKE, DS
   EDDY, GA
   SHAFFERMAN, A
TI PASSIVELY TRANSFERRED ANTIBODIES DIRECTED AGAINST CONSERVED REGIONS OF
   SIV ENVELOPE PROTECT MACAQUES FROM SIV INFECTION
SO VACCINE
LA English
DT Article
DE ENVELOPE PEPTIDE VACCINE; NEUTRALIZING ANTIBODIES; HUMAN
   IMMUNODEFICIENCY VIRUS
ID IMMUNODEFICIENCY-VIRUS TYPE-1; MONOCLONAL-ANTIBODIES; RECOMBINANT GP160;
   HIV-INFECTION; VACCINE; IDENTIFICATION; GLYCOPROTEIN; IMMUNIZATION;
   PREVENTION; SEQUENCES
AB Inactivated plasma collected from either SIV-infected or peptide-vaccinated macaques was transferred into 17 naive rhesus monkeys. Two additional macaques received normal plasma and served as controls. Following transfer all 19 monkeys were inoculated with SIV. While the controls became infected and were virus-isolation-positive, 3 of 6 recipients of SIV peptide vaccine plasma and 9 of 11 recipients of SIV-infected monkey plasma were protected. None of the 12 protected animals became virus-isolation-positive or seroconverted within 100 days of follow-up. One, however was SIV-PCR-positive. All 12 protected animals were rechallenged 100 days after the initial inoculation; 8 became infected and yielded virus as expected, but 4 remained uninfected. One of the latter was the SIV-PCR-positive monkey mentioned above, suggesting that cryptic SIV infection may be of significance in immunological protection. The results demonstrate that envelope anti-peptide antibodies have similar protective potential in vivo as antibodies directed to the whole virus. In vitro neutralization competition assays performed with sera from vaccinated macaques in the presence of the free peptides suggest that of the four conserved envelope peptides of the vaccine, the two originating from gp41 rather than the two from gp120 are responsible for inducing the neutralizing anti-syncytial activity.
C1 NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702.
   WALTER REED ARMY INST RES,DIV RETROVIROL,ROCKVILLE,MD 20852.
   ISRAEL INST BIOL RES,DEPT BIOCHEM,IL-70450 NESS ZIONA,ISRAEL.
   NIAID,INFECT DIS LAB,ROCKVILLE,MD 20852.
   VANDERBILT UNIV,MED CTR,SCH MED,DEPT PATHOL,NASHVILLE,TN 37232.
RP LEWIS, MG (reprint author), HENRY M JACKSON FDN RES LAB,1500E GUDE DR,ROCKVILLE,MD 20852, USA.
OI /0000-0002-5704-8094
NR 38
TC 63
Z9 64
U1 0
U2 1
PU BUTTERWORTH-HEINEMANN LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB
SN 0264-410X
J9 VACCINE
JI Vaccine
PD OCT
PY 1993
VL 11
IS 13
BP 1347
EP 1355
DI 10.1016/0264-410X(93)90106-8
PG 9
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA MC984
UT WOS:A1993MC98400013
PM 7507625
ER

PT J
AU SKARLATOS, SI
   RAO, R
   DICKENS, BF
   KRUTH, HS
AF SKARLATOS, SI
   RAO, R
   DICKENS, BF
   KRUTH, HS
TI PHOSPHOLIPID LOSS IN DYING PLATELETS
SO VIRCHOWS ARCHIV B-CELL PATHOLOGY INCLUDING MOLECULAR PATHOLOGY
LA English
DT Article
DE PHOSPHOLIPID; CHOLESTEROL; PHOSPHOLIPASE; CELL DEATH; CELL INJURY
ID CELL INJURY; MEMBRANE DYSFUNCTION; CHOLESTEROL; DEGRADATION;
   ACCUMULATION; ISCHEMIA; RAT; SPHINGOMYELIN; PARTICLES
AB The death of a cell results in a large amount of membrane lipid, predominantly phospholipids and cholesterol, that must be eliminated. In this study, we have examined what happens to phospholipids in dying rat platelets. Rat platelets were incubated for up to three days following their activation with thrombin. Platelet death occurred during the first day of incubation. This was indicated by a complete loss of platelet lactate dehydrogenase into the incubation medium. The platelets progressively lost over one-half of their phospholipid content during the three days of incubation. Cholesterol and sphingomyelin (the phospholipid with the highest affinity for cholesterol) were not lost during the same period. Our findings suggest that significant degradation of cellular non-sphingomyelin phospholipid can be triggered by cell death. The preservation of sphingomyelin in dying platelets, may be an adaptive response to maintain cholesterol in a solubilized state within dying cells.
C1 NIH,EXPTL ATHEROSCLEROSIS SECT,BLDG 10,ROOM 5N-113,BETHESDA,MD 20892.
   GEORGE WASHINGTON UNIV,DIV EXPTL,WASHINGTON,DC.
NR 30
TC 6
Z9 6
U1 0
U2 0
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0340-6075
J9 VIRCHOWS ARCH B
JI Virchows Arch. B-Cell Molec. Pathol.
PD OCT
PY 1993
VL 64
IS 4
BP 241
EP 245
DI 10.1007/BF02915118
PG 5
WC Pathology
SC Pathology
GA MD856
UT WOS:A1993MD85600006
PM 8287120
ER

PT J
AU MENENDEZARIAS, L
   GOTTE, D
   OROSZLAN, S
AF MENENDEZARIAS, L
   GOTTE, D
   OROSZLAN, S
TI MOLONEY MURINE LEUKEMIA-VIRUS PROTEASE - BACTERIAL EXPRESSION AND
   CHARACTERIZATION OF THE PURIFIED ENZYME
SO VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-1 PROTEINASE; POL POLYPROTEINS;
   ESCHERICHIA-COLI; GAG GENE; INHIBITORS; PURIFICATION; MATURATION;
   CLEAVAGE; INFECTIVITY
C1 NCI, FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM, MOLEC VIROL & CARCINOGENESIS LAB, FREDERICK, MD 21702 USA.
RI Menendez Arias, Luis /G-2436-2016; Menendez Arias, Luis/N-7447-2016
OI Menendez Arias, Luis/0000-0002-1251-6640
FU NCI NIH HHS [N01-CO-74101]
NR 39
TC 28
Z9 28
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD OCT
PY 1993
VL 196
IS 2
BP 557
EP 563
DI 10.1006/viro.1993.1511
PG 7
WC Virology
SC Virology
GA LY071
UT WOS:A1993LY07100018
PM 8372434
ER

PT J
AU CHEN, W
   DRILLIEN, R
   SPEHNER, D
   BULLER, RML
AF CHEN, W
   DRILLIEN, R
   SPEHNER, D
   BULLER, RML
TI IN-VITRO AND IN-VIVO STUDY OF THE ECTROMELIA VIRUS HOMOLOG OF THE
   VACCINIA VIRUS K1L HOST-RANGE GENE
SO VIROLOGY
LA English
DT Article
ID CYCLE CONTROL PROTEINS; HAMSTER OVARY CELLS; ESCHERICHIA-COLI; SEQUENCE;
   REPLICATION; EXPRESSION; VECTORS; DNA; MULTIPLICATION; BACTERIOPHAGE
C1 NIAID,VIRAL DIS LAB,BLDG 4,ROOM 137,9000 ROCKVILLE PIKE,BETHESDA,MD 20892.
   FAC MED STRASBOURG,INST VIROL,INSERM,U74,F-67000 STRASBOURG,FRANCE.
   FAC MED STRASBOURG,INST VIROL,ULP SYNTHELABO,COMMUN LAB,F-67000 STRASBOURG,FRANCE.
NR 41
TC 16
Z9 17
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0042-6822
J9 VIROLOGY
JI Virology
PD OCT
PY 1993
VL 196
IS 2
BP 682
EP 693
DI 10.1006/viro.1993.1525
PG 12
WC Virology
SC Virology
GA LY071
UT WOS:A1993LY07100032
PM 8372441
ER

PT J
AU TSUJIMOTO, H
   FULTON, R
   NISHIGAKI, K
   MATSUMOTO, Y
   HASEGAWA, A
   TSUJIMOTO, A
   CEVARIO, S
   OBRIEN, SJ
   TERRY, A
   ONIONS, D
   NEIL, JC
AF TSUJIMOTO, H
   FULTON, R
   NISHIGAKI, K
   MATSUMOTO, Y
   HASEGAWA, A
   TSUJIMOTO, A
   CEVARIO, S
   OBRIEN, SJ
   TERRY, A
   ONIONS, D
   NEIL, JC
TI A COMMON PROVIRAL INTEGRATION REGION, FIT-1, IN T-CELL TUMORS INDUCED BY
   MYC-CONTAINING FELINE LEUKEMIA VIRUSES
SO VIROLOGY
LA English
DT Note
ID TRANSGENIC MICE; C-MYC; GENE; LYMPHOMAGENESIS; ORGANIZATION; EXPRESSION;
   SEQUENCES; ONCOGENES; ADJACENT
C1 UNIV GLASGOW,DEPT VET PATHOL,MOLEC ONCOL LAB,GLASGOW G61 1QH,SCOTLAND.
   UNIV TOKYO,DEPT VET INTERNAL MED,TOKYO 113,JAPAN.
   BEATSON INST CANC RES,GLASGOW G61 1BD,SCOTLAND.
   NATL CANC CTR,RES INST,TOKYO 104,JAPAN.
   NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21202.
NR 20
TC 22
Z9 22
U1 0
U2 2
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0042-6822
J9 VIROLOGY
JI Virology
PD OCT
PY 1993
VL 196
IS 2
BP 845
EP 848
DI 10.1006/viro.1993.1544
PG 4
WC Virology
SC Virology
GA LY071
UT WOS:A1993LY07100051
PM 8396812
ER

PT J
AU STOKES, A
   TIERNEY, EL
   SARRIS, CM
   MURPHY, BR
   HALL, SL
AF STOKES, A
   TIERNEY, EL
   SARRIS, CM
   MURPHY, BR
   HALL, SL
TI THE COMPLETE NUCLEOTIDE-SEQUENCE OF 2 COLD-ADAPTED,
   TEMPERATURE-SENSITIVE ATTENUATED MUTANT VACCINE VIRUSES (CP12 AND CP45)
   DERIVED FROM THE JS STRAIN OF HUMAN PARAINFLUENZA VIRUS TYPE-3 (PIV3)
SO VIRUS RESEARCH
LA English
DT Article
DE COLD-ADAPTED VACCINE VIRUS; HUMAN PARAINFLUENZA VIRUS TYPE-3, STRAIN JS;
   NUCLEOTIDE SEQUENCE
ID ORAL POLIOVIRUS VACCINE; SENDAI VIRUS; RNA; IDENTIFICATION;
   GLYCOPROTEIN; PROTEIN; GENOME; GENE; HN
AB Two cold-passaged mutant vaccine viruses (cp12 and cp45) derived from the JS wild-type (wt) strain of human parainfluenza virus type 3 (PIV3) have been sequenced. These mutant viruses display the cold-adapted (ca), temperature-sensitive (ts), and attenuation (att) phenotypes. Sequence data indicate that both cp12 and cp45 sustained nucleotide substitutions during cold passage and subsequent cloning. Fifteen nucleotide changes were present in Cp12 and 18 in cp45. Of these changes, some were present in the sequence of the prototype wt strain (Wash/47885/57) or were non-coding changes present in the open reading frames (ORFs). These were considered unlikely to be of significance in contributing to phenotypic differences between the mutants and the JS wt. There were nine remaining changes in cp12 and eight in cp45 that would most likely contribute to their phenotypes. For cp12, two were non-coding changes in regulatory regions, one in the 3' genome leader and one in the NP gene transcription start signal. The remaining seven changes resulted in amino acid substitutions in NP, F, HN, and L. For cp45, two mutations were in a non-coding regulatory region, the 3' genome leader. The remaining six changes resulted in amino acid substitutions in F, HN, and L. Only one amino acid substitution was conserved between cp12 and cp45 (a valine to alanine change at position 384 of the HN gene). These results should prove useful in the future in understanding the genetic basis of attenuation of the cold-passaged PIV3 candidate vaccine viruses.
C1 NIAID,INFECT DIS LAB,BETHESDA,MD 20892.
NR 32
TC 25
Z9 26
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-1702
J9 VIRUS RES
JI Virus Res.
PD OCT
PY 1993
VL 30
IS 1
BP 43
EP 52
DI 10.1016/0168-1702(93)90014-E
PG 10
WC Virology
SC Virology
GA MA620
UT WOS:A1993MA62000004
PM 8266719
ER

PT J
AU SENKEVICH, TG
   MURAVNIK, GL
   POZDNYAKOV, SG
   CHIZHIKOV, VE
   RYAZANKINA, OI
   SHCHELKUNOV, SN
   KOONIN, EV
   CHERNOS, VI
AF SENKEVICH, TG
   MURAVNIK, GL
   POZDNYAKOV, SG
   CHIZHIKOV, VE
   RYAZANKINA, OI
   SHCHELKUNOV, SN
   KOONIN, EV
   CHERNOS, VI
TI NUCLEOTIDE-SEQUENCE OF XHOI O FRAGMENT OF ECTROMELIA VIRUS-DNA REVEALS
   SIGNIFICANT DIFFERENCES FROM VACCINIA VIRUS
SO VIRUS RESEARCH
LA English
DT Article
DE ECTROMELIA VIRUS; POXVIRUS; GENE FAMILY; TRANSCRIPTION FACTOR; VIRUS
   EVOLUTION
ID SHOPE FIBROMA VIRUS; ZINC FINGERS; ENCODES; PROTEINS; FAMILY; GENE;
   DROSOPHILA; PROMOTERS
AB The nucleotide sequence of the 3913 base pair XhoI O fragment located in an evolutionary variable region adjacent to the right end of the genome of ectromelia virus (EMV) was determined. The sequence contains two long open reading frames coding for putative proteins of 559 amino acid residues (p65) and 344 amino acid residues (p39). Amino acid database searches showed that p39 is closely related to vaccinia virus (VV), strain WR, B22R gene product (C12L gene product of strain Copenhagen), which belongs to the family of serine protease inhibitors (serpins). Despite the overall high conservation, differences were observed in the sequences of p39, B22R, and C12L in the site known to interact with proteases in other serpins, suggesting that the serpins of EMV and two strains of VV may all inhibit proteases with different specificities.
   The gene coding for the ortholog of p65 is lacking in the Copenhagen strain of vaccinia virus; the WR strain contains a truncated variant of this gene (B21R) potentially coding for a small protein (p16) corresponding to the C-terminal region of p65. p65 is a new member of the family of poxvirus proteins including vaccinia virus proteins A55R, C2L and F3L, and a group of related proteins of leporipoxviruses, Shope fibroma and myxoma viruses (T6, T8, T9, M9). These proteins are homologous to the Drosophila protein Kelch involved in egg development. Both Kelch protein and the related poxvirus proteins contain two distinct domains. The N-terminal domain is related to the similarly located domains of transcription factors Ttk, Br-C (Drosophila), and KUP (human), and GCL protein involved in early development in Drosophila. The C-terminal domain consists of an array of four to five imperfect repeats and is related to human placental protein MIPP. Phylogenetic analysis of the family of poxvirus proteins showed that their genes have undergone a complex succession of duplications, and complete or partial deletions.
C1 NIH, NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BLDG 38A, BETHESDA, MD 20892 USA.
   ACAD MED SCI MOSCOW, INST VIRAL PREPARAT, MOSCOW 109088, RUSSIA.
   SPU VECTOR, MOLEC BIOL RES INST, KOLTZOVO, RUSSIA.
NR 33
TC 31
Z9 31
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-1702
EI 1872-7492
J9 VIRUS RES
JI Virus Res.
PD OCT
PY 1993
VL 30
IS 1
BP 73
EP 88
DI 10.1016/0168-1702(93)90017-H
PG 16
WC Virology
SC Virology
GA MA620
UT WOS:A1993MA62000007
PM 8266721
ER

PT J
AU MUNTANER, C
   EATON, WW
   GARRISON, R
AF MUNTANER, C
   EATON, WW
   GARRISON, R
TI DIMENSIONS OF THE PSYCHOSOCIAL WORK-ENVIRONMENT IN A SAMPLE OF THE
   UNITED-STATES METROPOLITAN POPULATION
SO WORK AND STRESS
LA English
DT Article
ID JOB DECISION LATITUDE; OF-MENTAL-HEALTH; OCCUPATIONAL STRESS;
   CARDIOVASCULAR-DISEASE; STRAIN; RISK; ORGANIZATION; MORTALITY; POSITION;
   SUPPORT
AB The present study investigates the dimensional structure of die psychosocial work environment as assessed by Karasek's job characteristics scales and a set of factorial scales derived from the Dictionary of Occupational Titles (DOT) observers' ratings of occupational characteristics for census occupations. Scale scores on the Karasek and DOT were linked to information on occupation from die Epidemiologic Catchment Area (ECA) study sample. Scale intercorrelations and factor analysis were performed on those ECA subjects who reported ever having a full-time job (n=11,789). DOTs Substantive Complexity scale was positively correlated with Karasek's Skill Discretion and Decision Authority scales, and DOT's Physical Demands and Hazards scale was positively correlated with Karasek's Physical Demands scale. In addition, the DOT system compared to the Karasek system seems to assess psychosocial work domains less characteristic of traditional industrial jobs (interpersonal stress, expressive work). The content validity of the Karasek scales might be increased with the assessment of these domains. Giving support to Karasek's Demand/Control Model, the factor structure of the psychosocial work environment in the probability sample of five US metropolitan populations yielded two major dimensions: Control, and Physical Demands.
C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD 21218.
RP MUNTANER, C (reprint author), NATL INST MENTAL HLTH,LAB SOCIO ENVIRONM STUDIES,BETHESDA,MD 20892, USA.
RI Muntaner, C/A-5043-2010
NR 44
TC 24
Z9 24
U1 1
U2 7
PU TAYLOR & FRANCIS LTD
PI LONDON
PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE
SN 0267-8373
J9 WORK STRESS
JI Work Stress
PD OCT-DEC
PY 1993
VL 7
IS 4
BP 351
EP 363
DI 10.1080/02678379308257074
PG 13
WC Psychology, Applied
SC Psychology
GA ND729
UT WOS:A1993ND72900006
ER

PT J
AU ROCCO, V
   DALY, MJ
   MATRE, V
   LICHTEN, M
   NICOLAS, A
AF ROCCO, V
   DALY, MJ
   MATRE, V
   LICHTEN, M
   NICOLAS, A
TI IDENTIFICATION OF 2 DIVERGENTLY TRANSCRIBED GENES CENTROMERE-PROXIMAL TO
   THE ARG4 LOCUS ON CHROMOSOME-VIII OF SACCHAROMYCES-CEREVISIAE
SO YEAST
LA English
DT Note
DE YEAST; SACCHAROMYCES CEREVISIAE; CHROMOSOME VIII; ARG4; MEIOSIS; SH3
   DOMAIN
ID MANGANESE-SUPEROXIDE-DISMUTASE; NUCLEOTIDE-SEQUENCE; YEAST; PROTEIN;
   DNA; CONVERSION; MEIOSIS
AB We have sequenced a 3296 bp segment of the chromosome Vm adjacent to the 3' end of the ARG4 gene. This segment contains two divergently oriented open reading frames (YSC83 and YSC84). Northern blot analysis showed the presence of transcripts corresponding to these two open reading frames in vegetative cells. Levels of these transcripts increase five to ten-fold during sporulation. These two genes are not essential for vegetative growth or sporulation. Analysis of the putative protein products on the SwissProt database revealed that the C-terminal region of the Ysc84 protein contains a putative SH3 domain.
C1 UNIV PARIS 11,INST GENET & MICROBIOL,CNRS,URA 1354,F-91405 ORSAY,FRANCE.
   NCI,BIOCHEM LAB,DCBDC,BETHESDA,MD 20892.
RI Lichten, Michael/C-5795-2013
OI Lichten, Michael/0000-0001-9707-2956
NR 28
TC 7
Z9 9
U1 0
U2 6
PU JOHN WILEY & SONS LTD
PI W SUSSEX
PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD
SN 0749-503X
J9 YEAST
JI Yeast
PD OCT
PY 1993
VL 9
IS 10
BP 1111
EP 1120
DI 10.1002/yea.320091012
PG 10
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Microbiology; Mycology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Microbiology; Mycology
GA ME207
UT WOS:A1993ME20700011
PM 8256520
ER

PT J
AU BILD, DE
   WILLIAMS, RR
   BREWER, HB
   HERD, JA
   PEARSON, TA
   STEIN, E
AF BILD, DE
   WILLIAMS, RR
   BREWER, HB
   HERD, JA
   PEARSON, TA
   STEIN, E
TI IDENTIFICATION AND MANAGEMENT OF HETEROZYGOUS FAMILIAL
   HYPERCHOLESTEROLEMIA - SUMMARY AND RECOMMENDATIONS FROM AN NHLBI
   WORKSHOP
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Editorial Material
ID II HYPERLIPOPROTEINEMIA; HEART-DISEASE
AB Heterozygous familial hypercholesterolemia (hFH) is one of the most common monogenic disorders with serious health consequences, affecting approximately 1 in 500 persons in the United States.  Persons with hFH generally manifest elevations of low density lipoprotein (LDL) cholesterol throughout their lives and have a markedly increased risk of death from coronary artery disease. The hypercholesterolemia of hFH is responsive to medication and diet, and, if detected early, aggressive LDL cholesterol control may prevent or substantially delay cardiovascular disease. However, evidence suggests that many persons with hFH are undetected and inadequately treated.  On July 20-21, 1992, the National Heart, Lung, and Blood Institute sponsored a workshop to assess the current understanding of the diagnosis and management of hFH, to emphasize recommendations for identification and management that are known to be effective, and to identify opportunities and needs for intervention and research.
C1 UNIV UTAH,CARDIOVASC GENET RES CLIN,SALT LAKE CITY,UT 84112.
   NHLBI,DIV INTRAMURAL RES,MOLEC DIS BRANCH,BETHESDA,MD 20892.
   BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030.
   COLUMBIA UNIV,MARY IMOGENE BASSETT RES INST,COOPERSTOWN,NY.
   CHRIST HOSP,CARDIOVASC RES CTR,CINCINNATI,OH 45219.
RP BILD, DE (reprint author), NHLBI,DECA,CLIN & GENET EPIDEMIOL BRANCH,7550 WISCONSIN AVE,ROOM 300,BETHESDA,MD 20892, USA.
NR 23
TC 12
Z9 12
U1 0
U2 0
PU EXCERPTA MEDICA INC
PI NEW YORK
PA 245 WEST 17TH STREET, NEW YORK, NY 10011
SN 0002-9149
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD SEP 30
PY 1993
VL 72
IS 10
BP D1
EP D5
DI 10.1016/0002-9149(93)90002-T
PG 5
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA LZ360
UT WOS:A1993LZ36000001
PM 8105671
ER

PT J
AU HOEG, JM
AF HOEG, JM
TI HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA - A PARADIGM FOR PHENOTYPIC
   VARIATION
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article; Proceedings Paper
CT WORKSHOP ON IDENTIFICATION AND MANAGEMENT OF HETEROZYGOUS FAMILIAL
   HYPERCHOLESTEROLEMIA
CY JUL 20-21, 1992
CL NHLBI, BETHESDA, MD
SP NHLBI
HO NHLBI
ID RECEPTOR; DISEASE; GENE
AB Most, if not all, inborn errors of metabolism manifest phenotypic heterogeneity in their clinical presentation.  The term ''penetrance'' has been used to describe the degree to which a given genotype expresses itself in the phenotype of the individual.  Although many explanations for this phenomenon have been put forward, the molecular bases for this have been difficult to define. The investigation of the disease familial hypercholesterolemia (FH) has been used as a paradigm at many different levels.  This condition, in which a wide variety of mutations in the low density lipoprotein (LDL) receptor gene leads to elevated concentrations of LDL particles has a wide array of clinical manifestations that are variably expressed in both patients who are heterozygous and homozygous for mutations at the LDL receptor allele.  Progress in understanding lipoprotein metabolism, atherogenesis, and the development of molecular biology and transgenic expression techniques coverage to utilize homozygous FH as a paradigm for understanding the molecular basis of penetrance.  Elucidation of the key factor in altering the clinical features expressed by patients with FH have theoretical implications in understanding the polygenic nature of atherosclerosis as well as practical ramifications in the treatment of patients with FH.
RP HOEG, JM (reprint author), NHLBI,MOLEC DIS BRANCH,CELL BIOL SECT,BLDG 10,ROOM 7N117,BETHESDA,MD 20892, USA.
NR 17
TC 21
Z9 21
U1 0
U2 0
PU EXCERPTA MEDICA INC
PI NEW YORK
PA 245 WEST 17TH STREET, NEW YORK, NY 10011
SN 0002-9149
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD SEP 30
PY 1993
VL 72
IS 10
BP D11
EP D14
DI 10.1016/0002-9149(93)90004-V
PG 4
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA LZ360
UT WOS:A1993LZ36000003
PM 8213490
ER

PT J
AU DAVIS, CD
   ADAMSON, RH
   SNYDERWINE, EG
AF DAVIS, CD
   ADAMSON, RH
   SNYDERWINE, EG
TI STUDIES ON THE MUTAGENIC ACTIVATION OF HETEROCYCLIC AMINES BY CYNOMOLGUS
   MONKEY, RAT AND HUMAN MICROSOMES SHOW THAT CYNOMOLGUS MONKEYS HAVE A LOW
   CAPACITY TO N-OXIDIZE THE QUINOXALINE-TYPE HETEROCYCLIC AMINES
SO CANCER LETTERS
LA English
DT Article
DE AMINOIMIDAZOAZAARENES; QUINOLINES; QUINOXALINES; MUTAGENICITY
ID SALMONELLA-TYPHIMURIUM TA98; HUMAN-LIVER MICROSOMES;
   METABOLIC-ACTIVATION; AROMATIC-AMINES; FOOD; BINDING;
   2-AMINO-3-METHYLIMIDAZO<4,5-F>QUINOLINE; PURIFICATION; FRACTIONS; MEIQ
AB A number of mutagens and carcinogens have been isolated from cooked meats. In the current study we investigated the ability of hepatic microsomes from cynomolgus monkeys, Fischer-344 rats and humans to metabolically activate these compounds. Monkeys had almost no capacity to activate the quinoxaline-type compounds to mutagens in the Ames test relative to rats and humans but were able to activate the quinoline, pyridoindole and pyridoimidazole compounds. Differences in the mutagenicity of the quinoline and quinoxaline compounds by monkeys and rats was related to differences in cytochrome P-450-mediated N-oxidation between the species. This suggests that monkeys and rats may have different hepatic cytochrome P-450 isozymes, which are important for the metabolic activation of quinolines and quinoxalines, or that the orthologous monkey cytochromes show a select substrate specificity for the quinolines over the quinoxalines.
C1 NCI,DIV CANC ETIOL,OFF DIRECTOR,BETHESDA,MD 20892.
RP DAVIS, CD (reprint author), NCI,DIV CANC ETIOL,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892, USA.
NR 33
TC 22
Z9 22
U1 1
U2 1
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD SEP 30
PY 1993
VL 73
IS 2-3
BP 95
EP 104
DI 10.1016/0304-3835(93)90250-D
PG 10
WC Oncology
SC Oncology
GA ME033
UT WOS:A1993ME03300004
PM 8221635
ER

PT J
AU ADHYA, S
   GOTTESMAN, M
   GARGES, S
   OPPENHEIM, A
AF ADHYA, S
   GOTTESMAN, M
   GARGES, S
   OPPENHEIM, A
TI PROMOTER RESURRECTION BY ACTIVATORS - A MINIREVIEW
SO GENE
LA English
DT Review
DE RNA POLYMERASE; SIGMA FACTORS; ACTIVATORS; CRP; IHF
ID COLI RNA-POLYMERASE; INTEGRATION HOST FACTOR; AMP RECEPTOR PROTEIN;
   ESCHERICHIA-COLI; COLIPHAGE-LAMBDA; TRANSCRIPTIONAL ACTIVATOR; GALACTOSE
   OPERON; POSITIVE CONTROL; ALPHA-SUBUNIT; LAC PROMOTER
AB Frequently, in nature, defective promoters can be resurrected by activator proteins in response to cellular demands. The activators bind to nearby DNA sites for action. Various protein-protein and DNA-protein contacts involving activators, RNA polymerase, and different segments of DNA in and around a defective promoter form a DNA-multiprotein complex (cage) which enhances transcription.
C1 COLUMBIA UNIV COLL PHYS & SURG,INST CANC RES,NEW YORK,NY 10032.
   HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT MOLEC GENET,IL-91010 JERUSALEM,ISRAEL.
RP ADHYA, S (reprint author), NCI,MOLEC BIOL LAB,BLDG 37,ROOM 2E16,BETHESDA,MD 20892, USA.
NR 50
TC 23
Z9 23
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
J9 GENE
JI Gene
PD SEP 30
PY 1993
VL 132
IS 1
BP 1
EP 6
DI 10.1016/0378-1119(93)90507-Y
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA MC180
UT WOS:A1993MC18000001
PM 8406030
ER

PT J
AU PATTERSON, TA
   COSTANTINO, N
   DASGUPTA, S
   COURT, DL
AF PATTERSON, TA
   COSTANTINO, N
   DASGUPTA, S
   COURT, DL
TI IMPROVED BACTERIAL HOSTS FOR REGULATED EXPRESSION OF GENES FROM
   LAMBDA-P(L) PLASMID VECTORS
SO GENE
LA English
DT Note
DE LAMBDA-PROPHAGE; PROMOTER; TRANSCRIPTION ANTITERMINATION; BIOA DELETION;
   REX
ID ESCHERICHIA-COLI K-12; HIGH-LEVEL EXPRESSION; PHAGE-LAMBDA; BIO OPERON;
   CONSTRUCTION; PROMOTERS; REPRESSOR; SEQUENCES; PKC30; MAP
AB The construction and use of a set of Escherichia coli strains with defective lambda prophages that facilitate expression of genes cloned in lambda p(L)-plasmid vectors is described. These bacteria allow high and regulated expression of such genes, whereas a kanamycin-resistance marker (Km(R)) on the prophage allows easy identification and genetic transfer from strain to strain. Optimal conditions for examining gene expression with the PL-vector systems using these strains are discussed.
C1 NCI,FREDERICK CANC RES & DEV CTR,CHROMOSOME BIOL LAB,ABL BASIC RES PROGRAM,POB B,FREDERICK,MD 21702.
FU NCI NIH HHS [N01-CO-74101]
NR 23
TC 24
Z9 24
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
J9 GENE
JI Gene
PD SEP 30
PY 1993
VL 132
IS 1
BP 83
EP 87
DI 10.1016/0378-1119(93)90517-7
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA MC180
UT WOS:A1993MC18000011
PM 8406046
ER

PT J
AU HACKSTADT, T
   BRICKMAN, TJ
   BARRY, CE
   SAGER, J
AF HACKSTADT, T
   BRICKMAN, TJ
   BARRY, CE
   SAGER, J
TI DIVERSITY IN THE CHLAMYDIA-TRACHOMATIS HISTONE HOMOLOG HC2
SO GENE
LA English
DT Note
DE HISTONE-LIKE PROTEIN; INTRACELLULAR PARASITE; NUCLEOTIDE SEQUENCE;
   SEROVAR
ID PROTEIN-BLOTTING PROCEDURE; PSEUDOMONAS-AERUGINOSA; GENE; DNA; H1;
   IDENTIFICATION; PURIFICATION; BIND
AB Chlamydia trachomatis elementary bodies contain two developmentally expressed histone H1 homologues. An 18-kDa histone homologue, Hcl, is conserved among C. trachomatis serovars and C. psittaci. The other histone homologue, Hc2 (encoded by hctB), varies in size between C. trachomatis serovars but is present in reduced amounts or absent from C. psittaci. The variation in Hc2 size among C. trachomatis serovars was found to be due to internal deletions from a region of the hctB gene encoding lysine- and alanine-rich pentameric repeats.
RP HACKSTADT, T (reprint author), NIAID,ROCKY MT LABS,INTRACELLULAR PARASITES LAB,HAMILTON,MT 59840, USA.
RI Barry, III, Clifton/H-3839-2012
NR 21
TC 26
Z9 28
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
J9 GENE
JI Gene
PD SEP 30
PY 1993
VL 132
IS 1
BP 137
EP 141
DI 10.1016/0378-1119(93)90526-9
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA MC180
UT WOS:A1993MC18000020
PM 8406036
ER

PT J
AU GREGOR, P
   OHARA, BF
   YANG, XD
   UHL, GR
AF GREGOR, P
   OHARA, BF
   YANG, XD
   UHL, GR
TI EXPRESSION AND NOVEL SUBUNIT ISOFORMS OF GLUTAMATE-RECEPTOR GENES GLUR5
   AND GLUR6
SO NEUROREPORT
LA English
DT Article
DE HUMAN GLUTAMATE RECEPTOR GLUR5; KAINATE RECEPTOR ISOFORMS; GENE
   EXPRESSION; GLUTAMATE RECEPTORS IN BRAIN DEVELOPMENT
ID KAINATE-BINDING SUBUNIT; HIGH-AFFINITY KAINATE; CLONING; BRAIN;
   CHANNELS; DOMOATE; PROTEIN; CDNA
AB MOLECULAR heterogeneity of kainate-selective glutamate receptor subunits GluR5 and GluR6 was revealed by identification of a human cDNA, GluR5-1d, and a murine cDNA, GluR6-2, that each encode subunits with novel carboxy-terminal sequences. Both GluR5-1d and GluR6-2 appear to be generated by alternative splicing at analogous sites 14 codons following the fourth putative transmembrane segment. The principal transcripts of GluR5 and GluR6 were detected by Northern analyses of several regions of mammalian brains as 4 and 6 kb bands, respectively. Potential roles for these receptors in development are indicated by detection of their mRNAs in mouse embryos of 11 days gestation. These findings add to the description of the remarkable diversity of glutamate receptor gene expression.
C1 STANFORD UNIV,DEPT BIOL SCI,SLEEP RES CTR,STANFORD,CA 94305.
   JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205.
   JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205.
RP GREGOR, P (reprint author), NIDA,ADDICT RES CTR,MOLEC NEUROBIOL BRANCH,POB 5180,BALTIMORE,MD 21224, USA.
FU NICHD NIH HHS [HD29732]
NR 24
TC 54
Z9 58
U1 1
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 SEP 30
PY 1993
VL 4
IS 12
BP 1343
EP 1346
DI 10.1097/00001756-199309150-00014
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA MA668
UT WOS:A1993MA66800014
PM 8260617
ER

PT J
AU SHAMOON, H
   DUFFY, H
   FLEISCHER, N
   ENGEL, S
   SAENGER, P
   STRELZYN, M
   LITWAK, M
   WYLIEROSETT, J
   FARKASH, A
   GEIGER, D
   ENGEL, H
   FLEISCHMAN, J
   POMPI, D
   GINSBERG, N
   GLOVER, M
   BRISMAN, M
   WALKER, E
   THOMASHUNIS, A
   GONZALEZ, J
   GENUTH, S
   BROWN, E
   DAHMS, W
   PUGSLEY, P
   MAYER, L
   KERR, D
   LANDAU, B
   SINGERMAN, L
   RICE, T
   NOVAK, M
   SMITHBREWER, S
   MCCONNELL, J
   DROTAR, D
   WOODS, D
   KATIRGI, B
   LITVENE, M
   BROWN, C
   LUSK, M
   CAMPBELL, R
   LACKAYE, M
   RICHARDSON, M
   LEVY, B
   CHANG, S
   HEINHEINEMANN, M
   BARRON, S
   ASTOR, L
   LEBECK, D
   BRILLON, D
   DIAMOND, B
   VASILASDWOSKIN, A
   LAURENZI, B
   FOLDI, N
   RUBIN, M
   FLYNN, T
   REPPUCCI, V
   HEISE, C
   SANCHEZ, A
   WHITEHOUSE, F
   KRUGER, D
   KAHKONEN, D
   FACHNIE, J
   FISK, J
   CAREY, J
   COX, M
   AHMAD, B
   ANGUS, E
   CAMPBELL, H
   FIELDS, D
   CROSWELL, M
   BASHA, K
   CHUNG, P
   SCHOENHERR, A
   MOBLEY, M
   MARCHIORI, K
   FRANCIS, J
   KELLY, J
   ETZWILER, D
   CALLAHAN, P
   HOLLANDER, P
   CASTLE, G
   BERGENSTAL, R
   SPENCER, M
   NELSON, J
   BEZECNY, L
   ROETHKE, C
   ORBAN, M
   ULRICH, C
   GILL, L
   MORGAN, K
   LAECHELT, J
   TAYLOR, F
   FREKING, D
   TOWEY, A
   LIEPPMAN, M
   RAKES, S
   MANGUM, J
   COOPER, N
   UPHAM, P
   JACOBSON, A
   CROWELL, S
   WOLFSDORF, J
   BEASER, R
   GANDA, O
   ROSENZWEIG, J
   STEWART, C
   HALFORD, B
   FRIEDLANDER, E
   TARSY, D
   ARRIGG, P
   SHARUK, G
   SHAH, S
   WU, G
   CAVALLERANO, J
   POOLE, R
   SILVER, P
   CAVICCHI, R
   FLEMING, D
   MARCUS, J
   GRIFFITHS, C
   CAPPELLA, N
   NATHAN, D
   LARKIN, M
   GODINE, J
   LYNCH, J
   NORMAN, D
   MCKITRICK, C
   HAGGEN, C
   DELAHANTY, L
   ANDERSON, E
   LOU, P
   TAYLOR, C
   CROS, D
   FOLINO, K
   BRINK, S
   ABBOTT, K
   SICOTTE, K
   SERVICE, FJ
   SCHMIDT, A
   RIZZA, R
   ZIMMERMAN, B
   SCHWENK, W
   MORTENSON, J
   ZIEGLER, G
   LUCAS, A
   HANSON, N
   SELLNOW, S
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   STEIN, D
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   WOODWICK, R
   TACKMANN, R
   TRAUTMANN, J
   ROSTVOLD, J
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   DAUBE, J
   COLLIGAN, R
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   KING, J
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   BILLINGS, D
   DABNEY, Y
   BUSE, J
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   VALE, S
   THOMPSON, T
   BOHM, B
   LYONS, T
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   RICE, A
   MOLITCH, M
   SCHAEFER, B
   JOHNSON, C
   LYONS, J
   METZGER, B
   COHEN, B
   NISHIDA, T
   PARQUE, K
   YUSIM, V
   MOORE, M
   JAMPOL, L
   DINEEN, K
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   WEINBERG, D
   LOOSE, I
   KUSHNER, M
   MORRISON, A
   JALBERT, A
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   LEUNG, S
   BEGG, I
   JOHNSON, D
   LALANI, S
   KENNEDY, T
   MEADOWS, G
   KOLTERMAN, O
   LORENZI, G
   JONES, K
   GOLDBAUM, M
   SWENSON, M
   LYON, R
   GIOTTA, M
   KADLEC, K
   REED, R
   KIRSCH, L
   GOODMAN, J
   CAHILL, S
   CLARK, T
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   GLORIA, R
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   GRANT, J
   GRASSE, B
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   KIMURA, A
   STONE, E
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   FOUNTAIN, C
   KARAKAS, S
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   MONTAGUE, P
   KEYSER, D
   MENNEN, S
   DOGGETT, C
   ROSE, G
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   GASH, L
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AF SHAMOON, H
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   FARKASH, A
   GEIGER, D
   ENGEL, H
   FLEISCHMAN, J
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   GLOVER, M
   BRISMAN, M
   WALKER, E
   THOMASHUNIS, A
   GONZALEZ, J
   GENUTH, S
   BROWN, E
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   PUGSLEY, P
   MAYER, L
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   SINGERMAN, L
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   SMITHBREWER, S
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   BROWN, C
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   CAMPBELL, R
   LACKAYE, M
   RICHARDSON, M
   LEVY, B
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   HEINHEINEMANN, M
   BARRON, S
   ASTOR, L
   LEBECK, D
   BRILLON, D
   DIAMOND, B
   VASILASDWOSKIN, A
   LAURENZI, B
   FOLDI, N
   RUBIN, M
   FLYNN, T
   REPPUCCI, V
   HEISE, C
   SANCHEZ, A
   WHITEHOUSE, F
   KRUGER, D
   KAHKONEN, D
   FACHNIE, J
   FISK, J
   CAREY, J
   COX, M
   AHMAD, B
   ANGUS, E
   CAMPBELL, H
   FIELDS, D
   CROSWELL, M
   BASHA, K
   CHUNG, P
   SCHOENHERR, A
   MOBLEY, M
   MARCHIORI, K
   FRANCIS, J
   KELLY, J
   ETZWILER, D
   CALLAHAN, P
   HOLLANDER, P
   CASTLE, G
   BERGENSTAL, R
   SPENCER, M
   NELSON, J
   BEZECNY, L
   ROETHKE, C
   ORBAN, M
   ULRICH, C
   GILL, L
   MORGAN, K
   LAECHELT, J
   TAYLOR, F
   FREKING, D
   TOWEY, A
   LIEPPMAN, M
   RAKES, S
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   COOPER, N
   UPHAM, P
   JACOBSON, A
   CROWELL, S
   WOLFSDORF, J
   BEASER, R
   GANDA, O
   ROSENZWEIG, J
   STEWART, C
   HALFORD, B
   FRIEDLANDER, E
   TARSY, D
   ARRIGG, P
   SHARUK, G
   SHAH, S
   WU, G
   CAVALLERANO, J
   POOLE, R
   SILVER, P
   CAVICCHI, R
   FLEMING, D
   MARCUS, J
   GRIFFITHS, C
   CAPPELLA, N
   NATHAN, D
   LARKIN, M
   GODINE, J
   LYNCH, J
   NORMAN, D
   MCKITRICK, C
   HAGGEN, C
   DELAHANTY, L
   ANDERSON, E
   LOU, P
   TAYLOR, C
   CROS, D
   FOLINO, K
   BRINK, S
   ABBOTT, K
   SICOTTE, K
   SERVICE, FJ
   SCHMIDT, A
   RIZZA, R
   ZIMMERMAN, B
   SCHWENK, W
   MORTENSON, J
   ZIEGLER, G
   LUCAS, A
   HANSON, N
   SELLNOW, S
   PACH, J
   STEIN, D
   EICKHOFF, B
   WOODWICK, R
   TACKMANN, R
   TRAUTMANN, J
   ROSTVOLD, J
   LINK, T
   DYCK, P
   DAUBE, J
   COLLIGAN, R
   WINDEBANK, A
   KING, J
   COLWELL, J
   WOOD, D
   MAYFIELD, R
   PICKET, J
   CHITWOOD, M
   BILLINGS, D
   DABNEY, Y
   BUSE, J
   KING, L
   VALE, S
   THOMPSON, T
   BOHM, B
   LYONS, T
   HERMAYER, K
   RICE, A
   MOLITCH, M
   SCHAEFER, B
   JOHNSON, C
   LYONS, J
   METZGER, B
   COHEN, B
   NISHIDA, T
   PARQUE, K
   YUSIM, V
   MOORE, M
   JAMPOL, L
   DINEEN, K
   STAHL, J
   RICHINE, L
   WEINBERG, D
   LOOSE, I
   KUSHNER, M
   MORRISON, A
   JALBERT, A
   TILDESLEY, H
   LEUNG, S
   BEGG, I
   JOHNSON, D
   LALANI, S
   KENNEDY, T
   MEADOWS, G
   KOLTERMAN, O
   LORENZI, G
   JONES, K
   GOLDBAUM, M
   SWENSON, M
   LYON, R
   GIOTTA, M
   KADLEC, K
   REED, R
   KIRSCH, L
   GOODMAN, J
   CAHILL, S
   CLARK, T
   ABRAM, R
   SAYNER, L
   OCHABSKI, R
   GLORIA, R
   BIRCHLER, G
   GRANT, J
   GRASSE, B
   CHRISTLE, L
   ABREU, B
   GRANT, I
   HEATON, R
   ZEITLER, R
   SIVITZ, W
   BAYLESS, M
   SCHROTT, H
   OLSON, N
   TINDAL, B
   SNETSELAAR, L
   MUELLER, D
   DUDLER, A
   SWARTZENDRUBER, J
   HOFFMAN, R
   MACINDOE, J
   KRAMER, J
   WEINGEIST, T
   KIMURA, A
   STONE, E
   GROUT, T
   FOUNTAIN, C
   KARAKAS, S
   VOGEL, C
   MONTAGUE, P
   KEYSER, D
   MENNEN, S
   DOGGETT, C
   ROSE, G
   DEVET, K
   MUHLE, P
   KOWARSKI, A
   OSTROWSKI, D
   LEVIN, P
   CHALEW, S
   HYLTON, J
   YOUNGHYMAN, D
   BARLOW, M
   MAYER, R
   ELMAN, M
   LAKHANPAL, V
   WEINER, B
   MILLAR, M
   BLUM, S
   BUIE, W
   MACE, B
   GREENE, D
   MARTIN, C
   FLOYD, J
   DUNN, F
   HENRY, D
   BENNETT, S
   LASICHAK, A
   VINE, A
   ALBERS, J
   SANDFORD, T
   LOFTIN, J
   STEVENS, M
   ELNER, S
   MARTONYI, C
   MCIVER, F
   STANLEY, S
   WILLIS, J
   RYAN, K
   SPIEGELBERG, T
   NALEPA, S
   GLASGOW, B
   CHAN, E
   DOTIMAS, P
   BANTLE, J
   MECH, M
   BALLES, M
   KENNEDY, W
   KHAN, M
   KNOBLOCH, W
   KWONG, C
   MCKENZIE, L
   OLSON, J
   RAMSAY, R
   ROBINER, W
   WARHOL, R
   GENIA, A
   MCDONOUGH, G
   MCMICHAEL, B
   PHILIPH, D
   PONWITH, L
   SAHINEN, R
   STINSON, E
   VERNESS, J
   FIMREITE, L
   STEIN, J
   GOLDSTEIN, D
   HALL, M
   BURNS, T
   KLACHKO, D
   GIANGIACOMO, J
   RAWLINGS, S
   ASTON, L
   ENGLAND, J
   WIEDMEYER, H
   DAUGHERTY, M
   LIGHTFOOT, M
   WILSON, R
   WILSON, R
   GRIFFING, G
   GARDNER, D
   CONWAY, R
   BLINDER, K
   BROWNLEEDUFFECK, M
   PALMER, N
   GASH, L
   SCHADE, D
   JOHANNES, C
   REIDY, R
   BICKNELL, J
   VOGEL, A
   DRUMM, D
   BOYLE, P
   BURGE, M
   JONES, N
   CANADY, J
   NICKELL, D
   BAKER, L
   ILVESCORRESSEL, P
   SCHWARTZ, S
   BRAUNSTEIN, S
   MCBRIDE, J
   BRUCKER, A
   RENDLE, L
   BROWN, M
   SLADKY, J
   MASCHAKCAREY, B
   LAWLEY, D
   NYBERG, W
   WEENEY, L
   SANDBURG, E
   BYRD, S
   AGUADO, E
   MULHOLLAND, N
   CAHN, D
   SUSCAVAGE, M
   EGLER, J
   VAUGHNNORTON, M
   COLLINS, C
   MAMENISKIS, H
   DRASH, A
   WESCHE, J
   BRATKOWSKI, M
   BECKER, D
   ARSLANIAN, S
   DOFT, B
   LOBES, L
   RINKOFF, J
   WARNICKI, J
   CURTIN, D
   STEINBERG, D
   VAGSTAD, G
   RYAN, C
   HARRIS, F
   STERANCHAK, L
   ARCH, J
   KELLY, K
   OSTROSKA, P
   GUILIANI, M
   GOOD, M
   WILLIAMS, T
   OLSEN, K
   CAMPBELL, A
   SHIPE, C
   CONWIT, R
   FINEGOLD, D
   ZAUCHA, M
   MALONE, J
   GROVE, N
   MCMILLAN, D
   BABIONE, L
   DECLUE, T
   PAVAN, P
   KORTHALS, J
   SOLC, H
   MANGIONE, A
   KITABCHI, A
   TAYLOR, L
   JONES, L
   PITTS, K
   BERTORINI, T
   BITTLE, J
   BURGHEN, G
   FISHER, J
   HUGHES, T
   LINN, J
   MEYER, D
   MURPHY, W
   JUSTICE, M
   SHERMAN, A
   WRIGHT, L
   MURPHY, L
   RASKIN, P
   STROWIG, S
   BASCO, M
   CERCONE, S
   RAMIREZ, L
   ANAND, R
   WILSON, C
   GREENLEE, R
   ANDERSON, W
   MENDELSON, E
   VANACEK, P
   HOWARD, J
   OUSLEY, C
   YATES, B
   CONGER, D
   MAGUIRE, B
   BIGGS, M
   NEWTON, B
   SHERILL, K
   ZINMAN, B
   BARNIE, A
   EHRLICH, R
   DANEMAN, D
   PERLMAN, K
   LEITER, L
   GOTTESMAN, I
   DEVENYI, R
   MORTIMER, C
   MOFFAT, K
   GORDON, A
   FERGUSON, R
   CAMELON, K
   SIMKINS, S
   LITTLEFIELD, C
   RODIN, G
   HARTLEY, K
   KWAN, J
   GNANAPANDITHEN, D
   ROGERS, S
   HAYE, L
   ROSE, J
   MEZEI, S
   BUNPHY, B
   MACLEAN, S
   MACKEEN, L
   MANDELCORN, M
   NELLIS, P
   RUTTAN, L
   WILSONSMITH, D
   PALMER, J
   GINSBERG, J
   HIRSCH, I
   KINYOUN, J
   DOERR, H
   MAUSETH, R
   SWEENEY, K
   VANOTTINGHAM, L
   THOMSON, L
   GREENBAUM, C
   SAMESHIMA, L
   FARKASHIRSCH, R
   ROSENBAUM, G
   RUBNER, N
   BROWN, T
   KRAFT, G
   BROECKEL, J
   KARLSEN, M
   KHAKPOUR, D
   RAMIREZ, M
   SMIT, B
   MIX, L
   DUPRE, J
   COLBY, P
   RODGER, W
   HRAMIAK, I
   JENNER, M
   CANNY, C
   BROWN, W
   SMITH, T
   HARTH, J
   BONDY, S
   BEATH, S
   MCCABE, S
   GOUCHIE, C
   BLANCHARD, K
   MCCALLUM, J
   JUNG, S
   SUETANG, A
   LORENZ, R
   LIPPS, J
   MCRAE, J
   MAY, J
   MAY, M
   CAMPBELL, P
   FEMAN, S
   KILROY, A
   PULLIAM, C
   SCHLUNDT, D
   JANNASCH, K
   DAVIS, D
   CULLEN, N
   ADKINS, T
   SNELL, M
   VIRTS, K
   QUESENBERRY, L
   SANTIAGO, J
   LEVANDOSKI, L
   WHITE, N
   MCGILL, J
   BUBB, J
   SCHMIDT, L
   STRASBERG, Y
   CASSO, M
   NOETZEL, M
   OLK, R
   BONIUK, I
   GRAND, M
   THOMAS, M
   WILLIAMS, D
   NOBEL, G
   KACIZAK, R
   ORT, E
   DAHL, J
   BREEDING, L
   HOFFMEYER, G
   BILYEU, P
   BLANK, J
   WALTERS, C
   BODNAR, J
   RODRIGUEZ, P
   ERICKSON, M
   HEDRICK, S
   TAMBORLANE, W
   AHERN, J
   SHERWIN, R
   GATCOMB, P
   STOESSEL, K
   HELD, N
   EBERSOLE, J
   SCANLON, I
   LOUARD, R
   WILDSTEIN, C
   BILODEAU, D
   FONG, K
   OTTAVIANO, D
   LARSON, C
   CROFFORD, OB
   LACHIN, J
   CLEARY, P
   THOMPSON, D
   KENNY, D
   LAN, S
   LAN, G
   BRENNEMAN, A
   OWEN, W
   ADAMS, K
   ARNOLD, D
   CAMPANELL, R
   LORING, N
   SCHEIRER, P
   BECKER, D
   LAMAS, D
   DUNEGAN, C
   VEERAMACHANENI, H
   WILLIAMS, C
   ABDULBAAQIY, S
   KASSOFF, A
   ADAMS, K
   GRANT, I
   HEATON, R
   DORMAN, J
   SPIELMAN, R
   KLEIN, R
   SIEBERT, C
   SILVERMAN, R
   PFEIFER, M
   SCHUMER, M
   MORAN, M
   FARQUHAR, J
   ENGLAND, J
   WIEDMEYER, H
   ROHLFING, C
   DAVIS, M
   HUBBARD, L
   MAGLI, Y
   THOMAS, S
   ONOFREY, J
   JENSEN, K
   BROTHERS, R
   ANSAY, S
   ARMSTRONG, J
   BADAL, D
   VANDERHOOFYOUNG, M
   ESSER, B
   GEITHMAN, P
   HURLBURT, D
   REIMERS, J
   KEWLEY, K
   MINER, K
   STEFFES, M
   BUCKSA, J
   RYAN, C
   CATANZARO, R
   LUKES, A
   BAGOVICH, G
   WOODFILL, T
   CROW, R
   HUGHLETT, J
   SWANSON, C
   BUZZARD, I
   STEVENS, M
   SIELAFF, B
   PICKERING, B
   SCHAKEL, S
   HERMAN, W
   DASBACH, E
   SONGER, T
   JANES, G
   DEEB, L
   EWART, R
   ORCHARD, T
   CLARK, C
   CUTTER, G
   DAVIS, M
   DEMETS, D
   FERRIS, F
   FURBERG, C
   HORTON, E
   KEEN, J
   LOCKWOOD, D
   PALMBERG, P
   ROURKE, B
   TSIATIS, A
   LEVY, R
   FRANK, R
   GRIZZLE, J
   RUBENSTEIN, A
   SCHNEIDER, J
   SKYLER, J
   NATHAN, DM
   GENUTH, S
   LACHIN, J
   CLEARY, P
   CROFFORD, O
   DAVIS, M
   RAND, L
   SIEBERT, C
TI THE EFFECT OF INTENSIVE TREATMENT OF DIABETES ON THE DEVELOPMENT AND
   PROGRESSION OF LONG-TERM COMPLICATIONS IN INSULIN-DEPENDENT
   DIABETES-MELLITUS
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID GLUCOSE CONTROL; METABOLIC CONTROL; GLYCEMIC CONTROL; RETINOPATHY; AGE;
   PREVALENCE; DIAGNOSIS; INFUSION; RISK
AB Background. Long-term microvascular and neurologic complications cause major morbidity and mortality in patients with insulin-dependent diabetes mellitus (IDDM). We examined whether intensive treatment with the goal of maintaining blood glucose concentrations close to the normal range could decrease the frequency and severity of these complications.
   Methods. A total of 1441 patients with IDDM - 726 with no retinopathy at base line (the primary-prevention cohort) and 715 with mild retinopathy (the secondary-intervention cohort) were randomly assigned to intensive therapy administered either with an external insulin pump or by three or more daily insulin injections and guided by frequent blood glucose monitoring or to conventional therapy with one or two daily insulin injections. The patients were followed for a mean of 6.5 years, and the appearance and progression of retinopathy and other complications were assessed regularly.
   Results. In the primary-prevention cohort, intensive therapy reduced the adjusted mean risk for the development of retinopathy by 76 percent (95 percent confidence interval, 62 to 85 percent), as compared with conventional therapy. In the secondary-intervention cohort, intensive therapy slowed the progression of retinopathy by 54 percent (95 percent confidence interval, 39 to 66 percent) and reduced the development of proliferative or severe nonproliferative retinopathy by 47 percent (95 percent confidence interval, 14 to 67 percent). In the two cohorts combined, intensive therapy reduced the occurrence of microalbuminuria (urinary albumin excretion of greater-than-or-equal-to 40 mg per 24 hours) by 39 percent (95 percent confidence interval, 21 to 52 percent), that of albuminuria (urinary albumin excretion of greater-than-or-equal-to 300 mg per 24 hours) by 54 percent (95 percent confidence interval, 19 to 74 percent), and that of clinical neuropathy by 60 percent (95 percent confidence interval, 38 to 74 percent). The chief adverse event associated with intensive therapy was a two-to-threefold increase in severe hypoglycemia.
   Conclusions. Intensive therapy effectively delays the onset and slows the progression of diabetic retinopathy, nephropathy, and neuropathy in patients with IDDM.
C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED, BRONX, NY 10461 USA.
   CASE WESTERN RESERVE UNIV, CLEVELAND, OH 44106 USA.
   CORNELL UNIV, MED CTR, NEW YORK, NY 10021 USA.
   HENRY FORD HOSP, DETROIT, MI 48202 USA.
   INT DIABET CTR, MINNEAPOLIS, MN USA.
   JOSLIN DIABET CTR, BOSTON, MA USA.
   MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA.
   MAYO CLIN & MAYO FDN, ROCHESTER, MN 55905 USA.
   MED UNIV S CAROLINA, CHARLESTON, SC 29425 USA.
   NORTHWESTERN UNIV, EVANSTON, IL 60201 USA.
   UNIV BRITISH COLUMBIA, VANCOUVER V6T 1W5, BC, CANADA.
   UNIV CALIF SAN DIEGO, LA JOLLA, CA 92093 USA.
   UNIV IOWA, IOWA CITY, IA 52242 USA.
   UNIV MARYLAND, SCH MED, BALTIMORE, MD 21201 USA.
   UNIV MICHIGAN, ANN ARBOR, MI 48109 USA.
   UNIV MINNESOTA, CENT BIOCHEM LAB, MINNEAPOLIS, MN 55455 USA.
   UNIV MISSOURI, CENT BACKUP LAB HBAIC, COLUMBIA, MO 65201 USA.
   UNIV NEW MEXICO, SCH MED, ALBUQUERQUE, NM 87131 USA.
   UNIV PENN, CHILDRENS HOSP, PHILADELPHIA, PA 19104 USA.
   UNIV PITTSBURGH, PITTSBURGH, PA 15260 USA.
   UNIV S FLORIDA, TAMPA, FL 33620 USA.
   UNIV TENNESSEE, KNOXVILLE, TN 37996 USA.
   UNIV TEXAS, SW MED CTR, DALLAS, TX 75230 USA.
   UNIV TORONTO, TORONTO M5S 1A1, ONTARIO, CANADA.
   UNIV WASHINGTON HOSP, SEATTLE, WA 98105 USA.
   UNIV WESTERN ONTARIO, LONDON N6A 3K7, ONTARIO, CANADA.
   VANDERBILT UNIV, NASHVILLE, TN 37240 USA.
   WASHINGTON UNIV, ST LOUIS, MO 63130 USA.
   YALE UNIV, SCH MED, NEW HAVEN, CT 06510 USA.
   NIDDKD, PROGRAM OFF, BETHESDA, MD USA.
   SO ILLINOIS UNIV, CENT AUTONOM CODING UNIT, CARBONDALE, IL 62901 USA.
   UNIV WISCONSIN, CENT FUNDUS PHOTOG READING CTR, MADISON, WI 53706 USA.
   WESTERN PSYCHIAT INST & CLIN, CENT NEUROBEHAV CODING UNIT, PITTSBURGH, PA 15261 USA.
   UNIV MINNESOTA, CENT ECG READING UNIT, MINNEAPOLIS, MN 55455 USA.
   UNIV MINNESOTA, CENT NUTR CODING UNIT, MINNEAPOLIS, MN 55455 USA.
RP SHAMOON, H (reprint author), DCCT, RES GRP, BOX NDIC DCCT, BETHESDA, MD 20892 USA.
RI Rice, Treva/D-1385-2009; Hoffman, Robert/E-3252-2011; Walters,
   Carl/D-5714-2012; Zinman, Bernard/E-7266-2013
NR 43
TC 11134
Z9 11411
U1 87
U2 621
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD SEP 30
PY 1993
VL 329
IS 14
BP 977
EP 986
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA LY587
UT WOS:A1993LY58700001
ER

PT J
AU LUFT, BJ
   HAFNER, R
   KORZUN, AH
   LEPORT, C
   ANTONISKIS, D
   BOSLER, EM
   BOURLAND, DD
   UTTAMCHANDANI, R
   FUHRER, J
   JACOBSON, J
   MORLAT, P
   VILDE, JL
   REMINGTON, JS
AF LUFT, BJ
   HAFNER, R
   KORZUN, AH
   LEPORT, C
   ANTONISKIS, D
   BOSLER, EM
   BOURLAND, DD
   UTTAMCHANDANI, R
   FUHRER, J
   JACOBSON, J
   MORLAT, P
   VILDE, JL
   REMINGTON, JS
TI TOXOPLASMIC ENCEPHALITIS IN PATIENTS WITH THE
   ACQUIRED-IMMUNODEFICIENCY-SYNDROME
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID CENTRAL-NERVOUS-SYSTEM; AIDS; PYRIMETHAMINE; THERAPY; LESIONS;
   SULFADIAZINE; CLINDAMYCIN; EFFICACY
AB Background. In patients with the acquired immunodeficiency syndrome (AIDS), toxoplasmic encephalitis is usually a presumptive diagnosis based on the clinical manifestations, a positive antitoxoplasma-antibody titer, and characteristic neuroradiologic abnormalities. A response to specific therapy helps to confirm the diagnosis, but it is unclear how rapid the response should be. We studied the course of patients treated for acute toxoplasmic encephalitis and evaluated objective clinical criteria for this empirical diagnosis.
   Methods. A quantifiable neurologic assessment was used prospectively to evaluate the clinical outcome of patients with AIDS and toxoplasmic encephalitis who were treated with oral clindamycin (600 mg four times a day) and pyrimethamine (75 mg every day) for six weeks.
   Results. Thirty-five of 49 patients (71 percent) responded to therapy, and 30 of these (86 percent) had improvement by day 7. Thirty-two of those with a response (91 percent) improved with respect to at least half of their base-line abnormalities by day 14. Improvement in neurologic abnormalities within 7 to 14 days after the start of therapy was strongly associated with the neurologic response at 6 weeks. The four patients in whom treatment failed and the two patients with lymphoma had progressing neurologic abnormalities or new abnormalities during the first 12 days of therapy. Nonlocalizing abnormalities (headache and seizure) improved regardless of the clinical outcome.
   Conclusions. Oral clindamycin and pyrimethamine are an effective treatment for toxoplasmic encephalitis. Patients who have early neurologic deterioration despite treatment or who do not improve neurologically after 10 to 14 days of appropriate antitoxoplasma therapy should be considered candidates for brain biopsy.
C1 NIAID,DIV AIDS,BETHESDA,MD 20892.
   HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115.
   GRP HOSP BICHAT CLAUDE BERNARD,PARIS,FRANCE.
   UNIV SO CALIF,LOS ANGELES CTY MED CTR,LOS ANGELES,CA 90033.
   UNIV MIAMI,MIAMI,FL 33152.
   MT SINAI MED CTR,NEW YORK,NY 10029.
   HOP PELLEGRIN,F-33076 BORDEAUX,FRANCE.
   PALO ALTO MED RES FDN,PALO ALTO,CA 94301.
RP LUFT, BJ (reprint author), SUNY,DIV INFECT DIS,STONY BROOK,NY 11794, USA.
OI Luft, Benjamin/0000-0001-9008-7004
FU NIAID NIH HHS [AI-04717, UO1AI-131808]
NR 12
TC 285
Z9 293
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 SEP 30
PY 1993
VL 329
IS 14
BP 995
EP 1000
DI 10.1056/NEJM199309303291403
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA LY587
UT WOS:A1993LY58700003
PM 8366923
ER

PT J
AU STEINERT, PM
   MAREKOV, LN
   PARRY, DAD
AF STEINERT, PM
   MAREKOV, LN
   PARRY, DAD
TI CONSERVATION OF THE STRUCTURE OF KERATIN INTERMEDIATE FILAMENTS -
   MOLECULAR MECHANISM BY WHICH DIFFERENT KERATIN MOLECULES INTEGRATE INTO
   PREEXISTING KERATIN INTERMEDIATE FILAMENTS DURING DIFFERENTIATION
SO BIOCHEMISTRY
LA English
DT Article
ID MOUSE EPIDERMAL-CELLS; COILED-COIL; INVITRO; CYTOKERATINS; POLYPEPTIDES;
   HETERODIMER; NETWORKS; DYNAMICS
AB During development and differentiation, the intermediate filament component of the cytoskeleton of many cells and tissues is rebuilt by a dynamic exchange process in which one set of protein chains is replaced by another, without recourse to creation of a new network. One major example is the replacement of keratin 5/keratin 14 (K5/K14) keratin intermediate filaments (KIFs) by K1/K10 KIFs during terminal differentiation in the epidermis. The present work was undertaken to explore how this may occur. We have induced lysine-lysine cross-links with disulfosuccinimidyl tartrate in K5/K14 KIFs in order to determine the axial dimensions and relative axial alignments of the K5/K14 molecules. Many of the cross-links induced in subfilamentous oligomers containing one, two, or three molecules were also found in the intact KIF, indicating that the body of data thus generated provides physiologically relevant information on the structural organization in the KIF. A least-squares analysis using as data the positions of lysine residues involved in 23 induced cross-links has allowed the axial alignments of the various coiled-coil segments in the rod domain to be determined. Three modes of antiparallel alignment of two neighboring molecules were found: A11 (staggered by -16.7 nm), A22 (staggered by 28.8 nm), and A12 (almost in register; staggered by only 0.3 nm). Since the axial repeat length is about 1 nm less than the molecular length, the data require a fourth mode of molecule alignment, termed A(CN), in which similarly directed molecules are overlapped by the equivalent of about 5-10 residues.  Interestingly, these axial alignments and dimensions are essentially identical to those adduced previously for K1/K10 KIF [Steinert, P. M., Marekov, L. N., Fraser, R. D. B., & Parry, D. A. D. (1993) J. Mol. Biol. 230, 436-452], thus indicating that the two types of KIF have conserved structures.  Accordingly, our new data suggest that exchange of the K5/K14 molecules by K1/K10 molecules can occur simply because both have the same linear dimensions and axial configurations. Further work will be necessary to determine whether the lack of assembly compatibility of molecules in other IF systems is due to variations in their axial dimensions and alignments.
C1 MASSEY UNIV,DEPT PHYS & BIOPHYS,PALMERSTON NORTH,NEW ZEALAND.
RP STEINERT, PM (reprint author), NIAMSD,SKIN BIOL BRANCH,BLDG 6,ROOM 425,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 52
TC 57
Z9 57
U1 0
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD SEP 28
PY 1993
VL 32
IS 38
BP 10046
EP 10056
DI 10.1021/bi00089a021
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LZ638
UT WOS:A1993LZ63800021
PM 7691168
ER

PT J
AU HANSON, RL
   NELSON, RG
   MCCANCE, DR
   BEART, JA
   CHARLES, MA
   PETTITT, DJ
   KNOWLER, WC
AF HANSON, RL
   NELSON, RG
   MCCANCE, DR
   BEART, JA
   CHARLES, MA
   PETTITT, DJ
   KNOWLER, WC
TI COMPARISON OF SCREENING-TESTS FOR NON-INSULIN-DEPENDENT
   DIABETES-MELLITUS
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID FASTING PLASMA-GLUCOSE; LIQUID-CHROMATOGRAPHIC ASSAY; GLYCOSYLATED
   HEMOGLOBIN; TOLERANCE TEST; PIMA-INDIANS; FRUCTOSAMINE; POPULATION;
   DIAGNOSIS; INTOLERANCE; UTILITY
AB Background: Screening for non-insulin-dependent diabetes mellitus (NIDDM) can be useful in clinical practice and in epidemiologic and genetic studies but the available information for choosing between screening methods is limited. In this study, characteristics of several screening tests for NIDDM were compared.
   Methods: Among Pima Indians participating in an epidemiologic study, the sensitivity and specificity for detecting NIDDM of fasting plasma glucose (FPG) levels and two measures of glycated hemoglobin (HbA1 or HbA1c) were compared in 2092 fasting subjects. Glycated hemoglobin, quantitative glycosuria, and dipstick glycosuria were compared in 237 nonfasting subjects. Diabetes was diagnosed using an oral glucose tolerance test if the 2-hour postload venous plasma glucose concentration was 11.1 mmol/L (200 mg/dL) or greater- The area under the relative operating characteristic curve was used to compare tests.
   Results: In fasting subjects, the sensitivity for detecting diabetes with 98% specificity was 78.8% for HbA, level of 7.5% or greater, 80.3% for HbA1c level of 6.3% or greater, and 88.0% for FPG level of 6.83 mmol/L (123 mg/dL) or greater. By relative operating characteristic analysis, there were no significant differences between FPG and HbA1c, but FPG was significantly more sensitive than HbA1. In nonfasting subjects the sensitivity at 98% specificity was 92.9% for HbA, level of 7.3% or greater, 80.6% for quantitative urine glucose level of 1.94 mmol/L (35 mg/dL) or greater, and 64.3% for trace or greater of dipstick glycosuria. The area under the relative operating characteristic curve was significantly greater for glycated hemoglobin than for either measure of glycosuria.
   Conclusions: Although FPG has the best screening properties, HbA1c, HbA1, and quantitative urine glucose also provide high specificity, and approximately 80% sensitivity in detecting NIDDM. The choice of a particular method could depend on cost, convenience, and availability.
RP HANSON, RL (reprint author), NIDDKD,DIABET & ARTHRITIS EPIDEMIOL SECT,PHOENIX,AZ, USA.
RI Nelson, Robert/B-1470-2012; Hanson, Robert/O-3238-2015
OI Hanson, Robert/0000-0002-4252-7068
FU NIDDK NIH HHS [N01-DK-6-2285]
NR 41
TC 71
Z9 72
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD SEP 27
PY 1993
VL 153
IS 18
BP 2133
EP 2140
DI 10.1001/archinte.153.18.2133
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA LY471
UT WOS:A1993LY47100007
PM 8379805
ER

PT J
AU NICHOLLS, PJ
   JOHNSON, VG
   BLANFORD, MD
   ANDREW, SM
AF NICHOLLS, PJ
   JOHNSON, VG
   BLANFORD, MD
   ANDREW, SM
TI AN IMPROVED METHOD FOR GENERATING SINGLE-CHAIN ANTIBODIES FROM
   HYBRIDOMAS
SO JOURNAL OF IMMUNOLOGICAL METHODS
LA English
DT Article
DE SINGLE-CHAIN ANTIBODY; VARIABLE REGION; ANTIBODY FRAGMENT; CLONING;
   HYBRIDOMA; IN-VITRO EXPRESSION
ID IMMUNOGLOBULIN VARIABLE DOMAINS; ESCHERICHIA-COLI; ANTIGEN-BINDING;
   PSEUDOMONAS EXOTOXIN; DIPHTHERIA-TOXIN; REGION GENES; CLONING; FV;
   RECEPTOR; CONSTRUCTION
AB Cloning the correct V(L) kappa gene from hybridomas derived from MOPC-21 can be problematic because such cell lines variably express a transcript which is aberrantly rearranged at the VJ recombination site. Cellular levels of the aberrant transcript can exceed that of productive light chain RNA, so a large proportion of the V(L) gene-derived products obtained on PCR amplification of hybridoma cDNA may not encode a functional protein. We have developed a method in which antibody variable region genes are recovered from hybridoma cDNA using a unique set of V gene family-specific primers; the V region genes are then spliced by PCR, in the form 5'-V(L)-LINKER-V(H)-3' (where the linker encodes [GlyGlyGlyGlySer]3), and cloned into an expression vector under control of T7 RNA polymerase. Plasmid DNA is isolated from colonies, and the insert is expressed in an in vitro rabbit reticulocyte lysate-based coupled transcription/translation system, in a microtiter plate format. Since aberrantly rearranged V(L) kappa genes contain a translation termination codon at amino acid position 105, only constructs containing the correctly rearranged gene produce a protein of the predicted size. We demonstrate the method by producing the single-chain form of OKT9, a murine IgG1 which binds to the human transferrin receptor, and extend the results to show thal the protein generated by the in vitro expression system retains the antigen binding properties of the parent antibody. Our method will be generally useful for screening single-chain antibodies for function prior to large scale production in vivo.
C1 NINCDS, SURG NEUROL BRANCH, BIOCHEM SECT, BETHESDA, MD 20892 USA.
   FDA, CBER, DIV BACTERIAL PROD, BACTERIAL TOXINS LAB, BETHESDA, MD 20892 USA.
   NCI, EXPTL IMMUNOL BRANCH, BETHESDA, MD 20892 USA.
NR 28
TC 41
Z9 42
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-1759
EI 1872-7905
J9 J IMMUNOL METHODS
JI J. Immunol. Methods
PD SEP 27
PY 1993
VL 165
IS 1
BP 81
EP 91
DI 10.1016/0022-1759(93)90109-K
PG 11
WC Biochemical Research Methods; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA MB511
UT WOS:A1993MB51100010
PM 8409471
ER

PT J
AU MISCHAK, H
   PIERCE, JH
   GOODNIGHT, J
   KAZANIETZ, MG
   BLUMBERG, PM
   MUSHINSKI, JF
AF MISCHAK, H
   PIERCE, JH
   GOODNIGHT, J
   KAZANIETZ, MG
   BLUMBERG, PM
   MUSHINSKI, JF
TI PHORBOL ESTER-INDUCED MYELOID DIFFERENTIATION IS MEDIATED BY PROTEIN
   KINASE-C-ALPHA AND KINASE-C-DELTA AND NOT BY PROTEIN KINASE-C-BETA-II,
   KINASE-C-DELTA, KINASE-C-ZETA, AND KINASE-C-ETA
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LEUKEMIA-CELL LINE; HEMATOPOIETIC-CELLS; RAT-BRAIN; EXPRESSION; HL-60;
   FAMILY; ACTIVATION; NPKC; PROLIFERATION; FIBROBLASTS
AB It is generally accepted that the multiple, similar protein kinase C (PKC) isozymes are responsible for different specialized physiological processes, but evidence that directly assigns specific functions to specific isozymes is scarce. To test whether specific PKC isozymes are involved in myeloid differentiation, we have studied the effect of overexpression of PKC-alpha, -betaII, -delta, -epsilon, -zeta and -eta in 32D, a mouse myeloid progenitor cell line that does not differentiate in response to 12-O-tetradecanoylphorbol-13-acetate (TPA). No significant morphological or phenotypic changes could be observed in unstimulated cells that overexpress any of these isozymes. However, the cell lines that overexpressed PKC-alpha or -delta had acquired the ability to become mature macrophages 2-6 h after TPA stimulation. The overexpression of PKC-betaII, -epsilon, -zeta, or -eta, in contrast, did not permit TPA-induced differentiation. These results indicate that only these two members of the PKC gene family can participate in TPA-induced myeloid differentiation.
C1 NCI,GENET LAB,BLDG 37,RM 2B26,BETHESDA,MD 20892.
   NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892.
   NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT,BETHESDA,MD 20892.
RI Mischak, Harald/E-8685-2011
NR 37
TC 255
Z9 257
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 SEP 25
PY 1993
VL 268
IS 27
BP 20110
EP 20115
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY019
UT WOS:A1993LY01900031
PM 8376369
ER

PT J
AU SAFAR, J
   ROLLER, PP
   GAJDUSEK, DC
   GIBBS, CJ
AF SAFAR, J
   ROLLER, PP
   GAJDUSEK, DC
   GIBBS, CJ
TI CONFORMATIONAL TRANSITIONS, DISSOCIATION, AND UNFOLDING OF SCRAPIE
   AMYLOID (PRION) PROTEIN
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CIRCULAR-DICHROISM SPECTRA; MOLTEN GLOBULE STATE; SECONDARY STRUCTURE;
   PRECURSOR PROTEIN; LIPOSOMES; ABSORPTION; PURIFICATION; INFECTIVITY;
   TRYPTOPHAN; PEPTIDE
AB The infectious form of the scrapie amyloid (prion) precursor, PrP(Sc), is a host-derived protein and a component of the infectious agent causing scrapie. PrP(Sc) and the carboxyl-terminal proteinase K resistant core, PrP27-30, have the potential to form amyloid as a result of a post-translational event or conformational abnormality. We have studied the conformational transitions of both proteins reconstituted into liposomes, associated in solid state in thin films, and dissociated by guanidine HCl. The secondary structure of PrP(sc) in liposomes deduced from analysis of circular dichroism spectra contained approximately 34% beta-sheets, approximately 20% alpha-helix, and approximately 46%  beta-turns and random coil. Cleavage of the amino-terminal region of PrP(Sc) resulted in all-beta PrP27-30, with an estimated approximately 43% beta-sheet, no alpha-helix, and approximately 57% beta-turns and random coil. The PrP(Sc) associated in thin films with a tertiary structure perturbation corresponding to unfolding, while the secondary structure was preserved. The PrP27-30 assembled into the solid state with a similar perturbation of tertiary structure but with a large increase in the beta-sheet content, probably due to an intermolecular alignment of the external beta-sheets, or to a secondary structure transition, or both. The various conformational states had little or no impact on infectivity. Equilibrium dissociation and unfolding demonstrated a greater resistance of PrP27-30 to denaturation. The dissociated monomers unfolded through intermediate(s), suggesting the presence of protein domains with distinct secondary structure stabilities. The results provide experimental evidence for the beta-sheet type assembly of scrapie amyloid PrP27-30 in the solid state and demonstrate the importance of amino-terminal cleavage in the stability and alignment of the amyloid-forming monomers.
C1 NCI,DIV CANC TREATMENT,MEDICINAL CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892.
RP SAFAR, J (reprint author), NINCDS,CENT NERVOUS SYST STUDIES LAB,BLDG 36,RM 4A-15,BETHESDA,MD 20892, USA.
RI Safar, Jiri/G-6512-2013
NR 58
TC 309
Z9 317
U1 3
U2 17
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 SEP 25
PY 1993
VL 268
IS 27
BP 20276
EP 20284
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY019
UT WOS:A1993LY01900055
PM 8104185
ER

PT J
AU BENYA, RV
   FATHI, Z
   BATTEY, JF
   JENSEN, RT
AF BENYA, RV
   FATHI, Z
   BATTEY, JF
   JENSEN, RT
TI SERINES AND THREONINES IN THE GASTRIN-RELEASING PEPTIDE RECEPTOR
   CARBOXYL-TERMINUS MEDIATE INTERNALIZATION
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BETA-ADRENERGIC-RECEPTOR; BOMBESIN-LIKE PEPTIDES;
   CENTRAL-NERVOUS-SYSTEM; SWISS 3T3 CELLS; BETA-2-ADRENERGIC RECEPTOR;
   PHOSPHORYLATION SITE; CYTOPLASMIC DOMAIN; DOWN-REGULATION; BINDING;
   SEQUESTRATION
AB Most seven-transmembrane G-protein-coupled receptors are rapidly internalized after binding agonist, but the general amino acid recognition sequences mediating this phenomenon have not been identified. In this study, components of the gastrin-releasing peptide receptor (GRP-R) regulating internalization were identified. Four GRP-R mutants with stop codons placed at variable distances distal to the putative palmitoylation sites Cys340-341 were transiently expressed in CHOP fibroblasts. A construct with a minimal carboxyl tail deletion, T375, bound and internalized agonist similarly to wild type receptor. Progressively larger truncations of the carboxyl terminus, however, increasingly impaired GRP-R-mediated internalization without altering receptor-agonist affinity. Three additional constructs were created: one with the putative palmitoylation sites replaced with Ala (CC340-341 AA), one with the carboxyl-terminal protein kinase C-consensus sequence converted to Ala (TS360-361AA), and one with all Ser and Thr distal to Cys341 converted to Ala, Asn, or Gly (JF1). All constructs bound agonist similarly to wild type receptor. CC340-341AA internalized similarly to native receptor (93 +/- 3% of wild type by 60 min), whereas internalization of TS360-361AA was partially attenuated (64 +/- 2% of wild type by 60 min). JF1, however, internalized as poorly as T346, with only 16 +/- 2% of the wild type receptors internalized by 60 min. To assess G-protein coupling, selected receptor constructs were stably transfected into Balb fibroblasts, and phosphoinositol hydrolysis was determined. The largest GRP-R truncation, T346, increased total inositol phosphates (EC50 = 2.9 +/- 0.9 nm) similarly to wild type receptor (EC50 = 5.1 +/- 2.2 nm), as did  CC340-341AA (EC50 = 5.4 +/- 1.5 nm) and TS360-361AA (EC50 = 3.1 +/- 1.2 nM). These data demonstrate that the multiple Ser and Thr located within the GRP-R carboxyl terminus distal to Cys341, including but not limited to those within the protein kinase C-concensus sequence, specifically regulate GRP-R internalization rates independent of receptor-G-protein coupling.
C1 NIDDKD,DIGEST DIS BRANCH,BLDG 10,9C-103,BETHESDA,MD 20892.
   NCI,BIOL CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892.
NR 48
TC 91
Z9 92
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 25
PY 1993
VL 268
IS 27
BP 20285
EP 20290
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY019
UT WOS:A1993LY01900056
PM 8397203
ER

PT J
AU SHI, YB
   BROWN, DD
AF SHI, YB
   BROWN, DD
TI THE EARLIEST CHANGES IN GENE-EXPRESSION IN TADPOLE INTESTINE INDUCED BY
   THYROID-HORMONE
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RECEPTOR BETA GENES; XENOPUS-LAEVIS; AMPHIBIAN METAMORPHOSIS; LARVAL
AB Genes induced by thyroid hormone (TH) to change their expression in the Xenopus laevis gastrointestinal (GI) tract have been isolated using a subtractive hybridization method. An exhaustive search for down-regulated genes identified a single gene. Thirty-two different cDNA fragments derived from the up-regulated mRNA of tadpole intestine 18 h after addition of TH were cloned. They map to no more than 22 distinct genes. The isolation of multiple cDNA fragments derived from a single mRNA indicates that the complexity of up-regulated genes is limited. Both ubiquitous and intestine-specific up-regulated genes were found in this screen. The majority of these genes respond directly to TH induction as judged by the resistance of up-regulation to inhibitors of protein synthesis. The biological significance of these genes is supported by their dramatic regulation in the GI tract during spontaneous metamorphosis.
C1 CARNEGIE INST WASHINGTON,DEPT EMBRYOL,BALTIMORE,MD 21210.
RP SHI, YB (reprint author), NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892, USA.
NR 37
TC 154
Z9 156
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 25
PY 1993
VL 268
IS 27
BP 20312
EP 20317
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY019
UT WOS:A1993LY01900060
PM 7690754
ER

PT J
AU MANTILE, G
   MIELE, L
   CORDELLAMIELE, E
   SINGH, G
   KATYAL, SL
   MUKHERJEE, AB
AF MANTILE, G
   MIELE, L
   CORDELLAMIELE, E
   SINGH, G
   KATYAL, SL
   MUKHERJEE, AB
TI HUMAN CLARA CELL 10-KDA PROTEIN IS THE COUNTERPART OF RABBIT UTEROGLOBIN
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ANTIINFLAMMATORY PEPTIDES ANTIFLAMMINS; BACTERIOPHAGE-T7 RNA-POLYMERASE;
   PLATELET-ACTIVATING-FACTOR; DISULFIDE BOND FORMATION; HIGH-LEVEL
   EXPRESSION; PHOSPHOLIPASE-A2 ACTIVITY; PANCREATIC PHOSPHOLIPASE-A2;
   QUATERNARY STRUCTURE; ESCHERICHIA-COLI; LIPOCORTIN-I
AB Human Clara cell 10-kDa protein has been suggested to be a counterpart of rabbit uteroglobin, an immunomodulatory and antiinflammatory secretory protein. Since this human protein is not readily available in substantial quantity for detailed characterization of its biochemical, biological, and pharmacological properties, we sought to express it in Escherichia coli in order to study its structure-function relationship. However, bacterial overproduction of homodimeric proteins with interchain disulfide bonds, such as Clara cell 10-kDa protein, was thought to be impossible until we achieved expression of native uteroglobin (Miele, L., Cordella-Miele, E., and Mukherjee, A. B. (1990) J. Biol. Chem. 265, 6427-6435). Here, we report high level production of recombinant native dimeric human Clara cell 10-kDa protein in E. coli and its characterization. Recombinant human Clara cell 10-kDa protein forms its disulfide bonds within the bacterial cytoplasm. The purified protein possesses two of the most important activities characteristic of uteroglobin: (i) it is an excellent substrate of transglutaminase, and (ii) it is a potent inhibitor of porcine pancreatic and, more importantly, human synovial phospholipase A2. These results demonstrate that human Clara cell 10-kDa protein and rabbit uteroglobin have very similar biochemical properties. Our data suggest that this protein may possess immunomodulatory and antiinflammatory activities of potential physiological and pharmacological importance.
C1 NICHHD, DEV GENET SECT,HUMAN GENET BRANCH,BLDG 10,RM 95242, BETHESDA, MD 20892 USA.
   UNIV PITTSBURGH, SCH MED, DEPT PATHOL, PITTSBURGH, PA 15261 USA.
NR 75
TC 121
Z9 124
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 25
PY 1993
VL 268
IS 27
BP 20343
EP 20351
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY019
UT WOS:A1993LY01900064
PM 8104186
ER

PT J
AU MALHOTRA, P
   MANOHAR, CF
   SWAMINATHAN, S
   TOYAMA, R
   DHAR, R
   REICHEL, R
   THIMMAPAYA, B
AF MALHOTRA, P
   MANOHAR, CF
   SWAMINATHAN, S
   TOYAMA, R
   DHAR, R
   REICHEL, R
   THIMMAPAYA, B
TI E2F SITE ACTIVATES TRANSCRIPTION IN FISSION YEAST
   SCHIZOSACCHAROMYCES-POMBE AND BINDS TO A 30-KDA TRANSCRIPTION FACTOR
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID INDUCIBLE ADENOVIRUS PROMOTER; RETINOBLASTOMA GENE-PRODUCT;
   DNA-SYNTHESIS GENES; CELL-CYCLE CONTROL; SACCHAROMYCES-CEREVISIAE;
   BUDDING YEAST; PROTEIN; SEQUENCE; COMPLEX; IDENTIFICATION
AB The mammalian transcription factor E2F binds to several cellular proteins including Rb, p107, cyclin A, cyclin E, and p33cdk2 protein kinase in a stage-specific manner during cell cycle. Its recognition sequence, TTTCGCGC, is present in two of the human adenovirus early promoters and in several promoters of cellular genes whose products are implicated in the control of cell proliferation. These observations suggest that E2F may play an important role in cell-cycle regulation and prompted us to ask whether E2F-like activities are present in yeast. We found that the E2F motif can function as an activating sequence in Schizosaccharomyces pombe when cloned upstream of a reporter gene. Consistent with this, the expression of adenovirus E2 promoter in S. pombe was dependent on both E2F motifs of this promoter. A protein, spE2F, that binds to the E2F site was partially purified from S. pombe using DNA-affinity chromatography. The binding specificity of this protein was compared to that of human E2F using a number of mutant E2F sites as competitors. These studies showed that spE2F recognizes a sequence closely related to the E2F site. Ultraviolet cross-linking and Southwestern blot studies indicated that the molecular size of spE2F is 30 kDa. Previous studies have shown that a cis-acting element, ACGCGTNA, also called MluI cell cycle box, or MCB, is critical for the regulated expression of cell cycle related genes both in fission and budding yeast. In S. pombe, the cdc10 gene product binds to this element and controls the cell cycle related genes. Electrophoretic mobility shift assays and molecular size determination studies indicated that spE2F is different from that encoded by cdc10. Thus, our studies suggest that spE2F is a novel transcription factor. We discuss these results in light of recent observations about the periodically expressed genes involved in the cell cycle progression in yeast.
C1 NORTHWESTERN UNIV,SCH MED,DEPT MICROBIOL IMMUNOL,CHICAGO,IL 60611.
   NCI,MOLEC VIROL LAB,BETHESDA,MD 20892.
   CHICAGO MED SCH,DEPT PHARMACOL & MOLEC BIOL,N CHICAGO,IL 60064.
OI Swaminathan, Sathyamangalam/0000-0002-4388-2248
FU NIAID NIH HHS [AI 18029, AI 20156]
NR 63
TC 11
Z9 11
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 SEP 25
PY 1993
VL 268
IS 27
BP 20392
EP 20401
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY019
UT WOS:A1993LY01900071
PM 8376397
ER

PT J
AU CAMAIONI, A
   HASCALL, VC
   YANAGISHITA, M
   SALUSTRI, A
AF CAMAIONI, A
   HASCALL, VC
   YANAGISHITA, M
   SALUSTRI, A
TI EFFECTS OF EXOGENOUS HYALURONIC-ACID AND SERUM ON MATRIX ORGANIZATION
   AND STABILITY IN THE MOUSE CUMULUS CELL-OOCYTE COMPLEX
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ALPHA-TRYPSIN INHIBITOR; MURAL GRANULOSA-CELLS; PLASMINOGEN-ACTIVATOR;
   EXTRACELLULAR-MATRIX; ACROSOME REACTION; GOLDEN-HAMSTER; ZONA PELLUCIDA;
   RAT OOCYTES; INVITRO; FERTILIZATION
AB Compact cumulus cell-oocyte complexes (COCs) isolated from preovulatory mouse follicles undergo expansion in vitro when high levels of hyaluronic acid (HA) are synthesized and organized into an extracellular matrix. We studied the effects of fetal bovine serum (FBS) and of exogenous HA and HA-oligomers on the expansion process. Maximum retention of HA in the COC matrix, and hence complete COC expansion, occurs when 1% FBS is continuously present during the first 18 h of culture. Irrespective of the culture time, HA synthesized when serum is absent is primarily in the medium, whereas HA synthesized when serum is present is primarily in the cell matrix. These findings support the hypothesis that the serum factor, identified as an inter-alpha-trypsin inhibitor by Chen et al. (Chen, L., Mao, S. J., and Larsen, W. J. (1992) J. Biol. Chem. 267, 12380-12386), is a structural component of the matrix. Addition of exogenous HA or of HA oligomers of decasaccharide size (GlcUA-GlcNAc)5 or larger effectively displaces endogenously synthesized HA from the matrix into the medium, thereby preventing COC expansion. Addition of exogenous chondroitin sulfate affects neither matrix organization nor COC expansion, thus indicating specificity of the binding of some structural component(s) to HA. Fully expanded, COCs disassemble when cultured longer than 18 h, a process which occurs also in vivo and which correlates with loss of oocyte fertilizability both in vivo and in vitro. This process involves release of macromolecular HA from the matrix into the medium, with loss of 50% of the HA in the first 8 h of incubation after full expansion. The release is not facilitated when HA oligomers, long enough to prevent matrix formation, are added to the culture medium after the COCs are fully expanded. This suggests that cooperative binding to HA of either the serum factor, an endogenously synthesized factor(s), or both is required to stabilize the fully expanded COC matrix.
C1 NIDR, BONE RES BRANCH, BLDG 30, RM 106, BETHESDA, MD 20892 USA.
   UNIV ROMA TOR VERGATA, FAC MED, DEPT SANITA PUBBL & BIOL CELLULARE, I-00173 ROME, ITALY.
OI SALUSTRI, ANTONIETTA/0000-0002-8731-1041; CAMAIONI,
   ANTONELLA/0000-0002-7059-2617
NR 37
TC 95
Z9 97
U1 1
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 25
PY 1993
VL 268
IS 27
BP 20473
EP 20481
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY019
UT WOS:A1993LY01900080
PM 8376402
ER

PT J
AU ZIMMERMAN, PA
   CARRINGTON, MN
   NUTMAN, TB
AF ZIMMERMAN, PA
   CARRINGTON, MN
   NUTMAN, TB
TI EXPLOITING STRUCTURAL DIFFERENCES AMONG HETERODUPLEX MOLECULES TO
   SIMPLIFY GENOTYPING THE DQA1 AND DQB1 ALLELES IN HUMAN LYMPHOCYTE TYPING
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID CLASS-II REGION; HLA; DNA; AMPLIFICATION; RECOGNITION; ANTIGENS;
   RECOMBINATION; POLYMORPHISM; ASSOCIATION; POLYMERASE
AB A novel approach to DNA probe hybridization and heteroduplex analysis, termed directed heteroduplex analysis (DHDA) is presented here to illustrate its utility in simplification of human lymphocyte antigen (HLA)-typing. By strategic labeling of single-stranded probe sequences, DHDA allows the identification of specific heteroduplex structures that contribute to the differentiation of DQA1 and DQB1 alleles. Because of the high degree of polymorphism among major histocompatibility complex class II second exon sequences, this analysis of 50 different heteroduplex molecules provides evidence of the importance of unpaired bases and mismatched base pairs and their effect on heteroduplex electrophoretic-mobility differences. This strategy is further used to genotype accurately a family for DQA1 which was previously analyzed by sequence specific oligonucleotide (SSO) probe hybridization. To differentiate by SSO-typing among the DQA1 and DQB1 alleles analyzed in this study requires the use of 23 different probes. Equivalent results are obtained by DHDA using only three probes. Therefore, this study suggests that accurate HLA-typing can be simplified by DHDA. Additionally, DHDA may be useful for differentiation of DNA sequence polymorphisms in other genetic systems.
C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702.
RP ZIMMERMAN, PA (reprint author), NIAID,PARASIT DIS LAB,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA.
NR 31
TC 34
Z9 34
U1 0
U2 0
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP 25
PY 1993
VL 21
IS 19
BP 4541
EP 4547
DI 10.1093/nar/21.19.4541
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA MB070
UT WOS:A1993MB07000015
PM 8233788
ER

PT J
AU JAFFREY, SR
   HAILE, DJ
   KLAUSNER, RD
   HARFORD, JB
AF JAFFREY, SR
   HAILE, DJ
   KLAUSNER, RD
   HARFORD, JB
TI THE INTERACTION BETWEEN THE IRON-RESPONSIVE ELEMENT-BINDING PROTEIN AND
   ITS COGNATE RNA IS HIGHLY DEPENDENT UPON BOTH RNA SEQUENCE AND STRUCTURE
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID RECEPTOR MESSENGER-RNA; TRANSFERRIN RECEPTOR; SECONDARY STRUCTURE;
   REGULATORY REGION; TAR RNA; REV PROTEIN; FERRITIN; DETERMINANT;
   EXPRESSION; BULGE
AB To assess the influence of RNA sequence/structure on the interaction RNAs with the iron-responsive element binding protein (IRE-BP), twenty eight altered RNAs were tested as competitors for an RNA corresponding to the ferritin H chain IRE. All changes in the loop of the predicted IRE hairpin and in the unpaired cytosine residue characteristically found in IRE stems significantly decreased the apparent affinity of the RNA for the IRE-BP. Similarly, alteration in the spacing and/or orientation of the loop and the unpaired cytosine of the stem by either increasing or decreasing the number of base pairs separating them significantly reduced efficacy as a competitor. It is inferred that the IRE-BP forms multiple contacts with its cognate RNA, and that these contacts, acting in concert, provide the basis for the high affinity of this interaction.
C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892.
NR 29
TC 96
Z9 95
U1 1
U2 1
PU OXFORD UNIV PRESS UNITED KINGDOM
PI OXFORD
PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP 25
PY 1993
VL 21
IS 19
BP 4627
EP 4631
DI 10.1093/nar/21.19.4627
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA MB070
UT WOS:A1993MB07000029
PM 8233801
ER

PT J
AU RODRIGUEZ, JB
   MARQUEZ, VE
   NICKLAUS, MC
   BARCHI, JJ
AF RODRIGUEZ, JB
   MARQUEZ, VE
   NICKLAUS, MC
   BARCHI, JJ
TI SYNTHESIS OF CYCLOPROPANE-FUSED DIDEOXYCARBOCYCLIC NUCLEOSIDES
   STRUCTURALLY RELATED TO NEPLANOCIN-C
SO TETRAHEDRON LETTERS
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; CARBOCYCLIC ANALOGS; CONFORMATION
AB The syntheses of five novel carbocyclic dideoxynucleosides with a bicyclo[3.1.0]hexane skeleton was accomplished via a Mitsunobu-type coupling reaction with various heterocyclic bases. These compounds appear to prefer a typical nucleoside northern conformation.
C1 NCI, DIV CANC TREATMENT, DEV THERAPEUT PROGRAM, MED CHEM LAB, BETHESDA, MD 20892 USA.
RI Nicklaus, Marc/N-4183-2014; Barchi Jr., Joseph/N-3784-2014; 
OI Rodriguez, Juan Bautista/0000-0002-5180-096X
NR 21
TC 71
Z9 71
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0040-4039
J9 TETRAHEDRON LETT
JI Tetrahedron Lett.
PD SEP 24
PY 1993
VL 34
IS 39
BP 6233
EP 6236
DI 10.1016/S0040-4039(00)73718-X
PG 4
WC Chemistry, Organic
SC Chemistry
GA LY750
UT WOS:A1993LY75000019
ER

PT J
AU COWLEN, MS
   ELING, TE
AF COWLEN, MS
   ELING, TE
TI EFFECTS OF PROSTAGLANDINS AND HYDROXYOCTADECADIENOIC ACID ON EPIDERMAL
   GROWTH FACTOR-DEPENDENT DNA-SYNTHESIS AND C-MYC PROTOONCOGENE EXPRESSION
   IN SYRIAN-HAMSTER EMBRYO CELLS
SO BIOCHIMICA ET BIOPHYSICA ACTA
LA English
DT Article
DE EPIDERMAL GROWTH FACTOR; PROTOONCOGENE; DNA SYNTHESIS; C-MYC EXPRESSION;
   FATTY ACID METABOLITE; MITOGENIC RESPONSE; (SHE CELL)
ID TUMOR-SUPPRESSOR GENE; ARACHIDONIC-ACID; MITOGENIC RESPONSE;
   MESSENGER-RNA; METABOLISM; PROLIFERATION; FIBROBLASTS; INHIBITION;
   CONVERSION; MODULATION
AB Epidermal growth factor (EGF) stimulates DNA synthesis in quiescent Syrian hamster embryo (SHE) cells. Work in the present authors' laboratory has shown that the formation of 9- and 13-hydroxyoctadecadienoic acid (HODEs), 15-lipoxygenase-derived metabolites of linoleic acid, are involved in the mitogenic response to EGF in these cells (Glasgow et al. (1992) J. Biol. Chem. 267, 10771-10779). SHE cells also produce prostaglandin E2 (PGE2) and prostaglandin F2alpha (PGF2alpha). We now report the effects of HODEs and prostaglandins on EGF-dependent expression of the growth-related proto-oncogene c-myc in SHE cells. Treatment of cells with eicosatetraynoic acid (ETYA), which blocks EGF-dependent HODE formation, inhibited the mitogenic response to EGF, while exogenous 13-HODE potentiated EGF-dependent DNA synthesis. However, neither ETYA or 13-HODE altered the accumulation of c-myc mRNA in response to EGF. In contrast, PGE2 inhibited EGF-induced DNA synthesis and down-regulated EGF-stimulated c-myc mRNA accumulation in a dose-dependent manner, whereas PGF2alpha had no effect on these responses. PGE2, but not PGF2alpha, induced a rapid increase in cAMP formation, and both forskolin and 8-(4-chlorophenylthio)-cAMP mimicked the inhibitory effects of PGE2 on EGF-dependent DNA synthesis and c-myc mRNA accumulation, suggesting that the involvement of cAMP. The results indicate that the modulation of EGF-dependent DNA synthesis by PGE2, but not by HODEs, is associated with altered expression of the proto-oncogene c-myc in SHE cells.
RP ELING, TE (reprint author), NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA.
NR 26
TC 23
Z9 23
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-3002
J9 BIOCHIM BIOPHYS ACTA
PD SEP 23
PY 1993
VL 1174
IS 3
BP 234
EP 240
DI 10.1016/0167-4781(93)90192-G
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA LZ195
UT WOS:A1993LZ19500002
PM 8373802
ER

PT J
AU KLEBANOFF, MA
   READ, JS
   MILLS, JL
   SHIONO, PH
AF KLEBANOFF, MA
   READ, JS
   MILLS, JL
   SHIONO, PH
TI THE RISK OF CHILDHOOD-CANCER AFTER NEONATAL EXPOSURE TO VITAMIN-K
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
AB Background. Two recent studies have found that infants who received intramuscular vitamin K were at twice the expected risk tor cancer during childhood. Since nearly all newborns in the United States receive this drug, the public health implications ot this association, it confirmed, would be substantial.
   Methods. We examined the relation between vitamin K and cancer in a nested case-control study that used data from the Collaborative Perinatal Project, a multicenter, prospective study of pregnancy, delivery, and childhood. Among 54,795 children born from 1959 through 1966, 48 cases ot cancer were diagnosed after the first day ot lite and before the eighth birthday. Each case child was matched with five randomly selected controls whose last study visit occurred at or after the age when the case child's cancer was diagnosed. Exposure to vitamin K was determined from study forms and medical records.
   Results. Vitamin K had been administered to 68 percent of the 44 case children and 71 percent of the 226 controls for whom data were available (matched odds ratio, 0.84; 95 percent confidence interval, 0.41 to 1.71). The odds ratio was 0.47 (95 percent confidence interval, 0.14 to 1.55) for leukemia and 1.08 (95 percent confidence interval, 0.45 to 2.61) for other cancers. Sequential adjustment for potential confounding factors did not change the results substantially.
   Conclusions. We found no association between exposure to vitamin K and an increased risk of any childhood cancer or of all childhood cancers combined, although a slightly increased risk could not be ruled out. The benefits of neonatal vitamin K prophylaxis against hemorrhagic disease have been well described. Unless other evidence supporting an association between vitamin K and cancer appears, there is no reason to abandon the routine administration of vitamin K to newborns.
C1 DAVID & LUCILE PACKARD FDN,CTR FUTURE CHILDREN,LOS ALTOS,CA.
RP KLEBANOFF, MA (reprint author), NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,6100 BLDG,RM 7B03,BETHESDA,MD 20892, USA.
NR 17
TC 86
Z9 87
U1 5
U2 7
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD SEP 23
PY 1993
VL 329
IS 13
BP 905
EP 908
DI 10.1056/NEJM199309233291301
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA LX751
UT WOS:A1993LX75100001
PM 8361503
ER

PT J
AU HAUSER, P
   ZAMETKIN, AJ
   WEINTRAUB, B
AF HAUSER, P
   ZAMETKIN, AJ
   WEINTRAUB, B
TI ATTENTION-DEFICIT HYPERACTIVITY DISORDER - REPLY
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
RP HAUSER, P (reprint author), NIH, BETHESDA, MD 20892 USA.
NR 4
TC 0
Z9 0
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD SEP 23
PY 1993
VL 329
IS 13
BP 967
EP 967
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA LX751
UT WOS:A1993LX75100023
ER

PT J
AU LOCKWICH, T
   MERTZ, LM
   AMBUDKAR, IS
AF LOCKWICH, T
   MERTZ, LM
   AMBUDKAR, IS
TI INVOLVEMENT OF CARBOXYL GROUPS IN THE DIVALENT-CATION PERMEABILITY OF
   RAT PAROTID-GLAND BASOLATERAL PLASMA-MEMBRANE
SO MOLECULAR AND CELLULAR BIOCHEMISTRY
LA English
DT Article
DE PLASMA MEMBRANE; MEMBRANE PERMEABILITY; MEMBRANE CARBOXYL GROUPS;
   PAROTID GLAND
ID ACINAR-CELLS; CALCIUM ENTRY; MAST-CELLS; ACTIVATION; INFLUX; CA-2+;
   CARBACHOL; VESICLES; POOL; PH
AB Divalent cation permeability of rat parotid gland basolateral plasma membranes was examined in dispersed parotid acini (by Ca2+ or Mn2+ entry) and in isolated basolateral plasma membrane vesicles (BLMV, by Ca-45(2+) influx). Mn2+ entry (fura2 quenching) was about 1.6 fold higher in internal Ca2+ pool-depleted acini (Ca2+-depl acini) than in unstimulated cells. Mn2+ entry into Ca2+-depl acini was increased at external pH > 7.4 and decreased at pH < 7.4. Pretreatment of Ca2+-depl acini with the relatively hydrophobic carboxylic group reagent, N,N'-dicyclohexylcarbodiimide de (DCCD, 50 mu M for 30 min) resulted in the inhibition of Mn2+ entry into Ca2+-depl acini to unstimulated levers. Another hydrophobic carboxyl group reagent, N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) and the relatively hydrophilic carboxyl group reagents, 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC) and 1-cyclohexyl-3-(2-morpholinoethyl)carbodiimide (CMCD) did not affect Mn2+ entry.
   Similar to the effects in intact acini, Ca2+ influx into BLMV was decreased when the external pH was lowered below 7.4. Also DCCD (5 mM, 30 min), but not EEDQ, decreased (40%) Ca2+ influx in BLMV. However, unlike in acini, the hydrophilic reagents, EDC, EAC, and CMCD decreased Ca2+ permeability in BLMV and the effects were nonadditive with the decrease induced by DCCD. The aggregate effects of carboxyl group reagents on the Ca2+ and Mn2+ permeability in BLMV and intact acini, respectively, suggest that a critical carboxyl group (most likely accessible from the cytoplasmic side of the plasma membrane) is involved in divalent cation flux in rat parotid acinar cells.
C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892.
NR 26
TC 6
Z9 6
U1 0
U2 1
PU KLUWER ACADEMIC PUBL
PI DORDRECHT
PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS
SN 0300-8177
J9 MOL CELL BIOCHEM
JI Mol. Cell. Biochem.
PD SEP 22
PY 1993
VL 126
IS 2
BP 143
EP 150
DI 10.1007/BF00925692
PG 8
WC Cell Biology
SC Cell Biology
GA MM025
UT WOS:A1993MM02500007
PM 8302292
ER

PT J
AU BEARD, WA
   WILSON, SH
AF BEARD, WA
   WILSON, SH
TI KINETIC-ANALYSIS OF TEMPLATE.PRIMER INTERACTIONS WITH RECOMBINANT FORMS
   OF HIV-1 REVERSE-TRANSCRIPTASE
SO BIOCHEMISTRY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; STEADY-STATE KINETICS; RNASE-H ACTIVITIES;
   PRIMER BINDING; DNA-POLYMERASE; DOMAIN-STRUCTURE; ACTIVE-SITE;
   MECHANISM; 3'-AZIDO-3'-DEOXYTHYMIDINE; PROCESSIVITY
AB The reverse transcriptase (RT) from the human immunodeficiency virus (HIV) exists predominantly as a heterodimer (p66/p51), but can also form a homodimer of p66 subunits (p66/p66). RT binds to template-primer (T/P) tightly to form the first complex in the reaction sequence poised to conduct DNA synthesis upon the addition of dNTP and Mg2+. We have made use of this property to kinetically analyze poly(rA)-(dT)n interactions with recombinant homo- and heterodimeric HIV-1 RT derived from HXB2R proviral DNA. A T/P challenge assay was used to quantitatively follow RT-T/P complex formation. The homo- and heterodimeric forms of RT bound to poly(rA)-(dT)16 in a kinetically similar fashion. There was no more than a 2-fold difference in k(cat) or for any T/P parameter examined: K(m), K(d), k(on), k(off) determined from a binary complex or from a complex incorporating fTMP, processivity, and stoichiometry of binding. In contrast, it was found that the T/P K(m) with heterodimeric RT derived from the NY5 strain was significantly greater than that determined for HXB2R enzyme, indicating that a kinetic diversity exists between RT derived from different viral strains. Since HXB2R RT binds to poly(rA)-(dT)16 tightly, K(d) < 1 nM, active-site titrations are facilitated. At saturation, one T/P binds per two polypeptides, suggesting that RT binds substrate productively as a dimer and that if monomers are present they must rapidly form dimers in the presence of T/P. In contrast, when the template to primer nucleotide ratio was diminished, the apparent number of T/P binding sites increased to 2 per dimer. The K(d) for poly(rA)-(dT)n was dependent on the length of the primer, with short primers binding with a lower affinity primarily due to a more rapid dissociation rate constant. The dissociation reaction could often be better fitted to a double-exponential decay, suggesting that multiple conformations of the RT-T/P complex exist.
C1 UNIV TEXAS, MED BRANCH, SEALY CTR MOLEC SCI, GALVESTON, TX 77550 USA.
   NCI, BIOCHEM LAB, BETHESDA, MD 20892 USA.
NR 43
TC 53
Z9 53
U1 0
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD SEP 21
PY 1993
VL 32
IS 37
BP 9745
EP 9753
DI 10.1021/bi00088a029
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY294
UT WOS:A1993LY29400029
PM 7690592
ER

PT J
AU BAUM, BJ
AF BAUM, BJ
TI PRINCIPLES OF SALIVA SECRETION
SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article
ID PAROTID ACINAR-CELLS; DEPENDENT PROTEIN-KINASE; ALPHA-AMYLASE RELEASE;
   CYCLIC-AMP; SIGNAL TRANSDUCTION; EXOCRINE SECRETION; MUCIN SECRETION;
   CALCIUM ENTRY; RAT; EXOCYTOSIS
RP BAUM, BJ (reprint author), NIDR, CLIN INVEST & PATIENT CARE BRANCH, BETHESDA, MD 20892 USA.
NR 44
TC 7
Z9 7
U1 0
U2 6
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 E 63RD ST, NEW YORK, NY 10021 USA
SN 0077-8923
J9 ANN NY ACAD SCI
JI Ann.NY Acad.Sci.
PD SEP 20
PY 1993
VL 694
BP 17
EP 23
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA264
UT WOS:A1993MA26400003
ER

PT J
AU TURNER, RJ
AF TURNER, RJ
TI MECHANISMS OF FLUID SECRETION BY SALIVARY-GLANDS
SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article
ID PAROTID ACINAR-CELLS; ACTIVATED POTASSIUM CHANNELS; AGONIST-INDUCED
   ACTIVATION; NA+/H+ EXCHANGE; ION-TRANSPORT; RAT; CALCIUM; DUCTS; HCO3
RP TURNER, RJ (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892, USA.
NR 33
TC 50
Z9 51
U1 0
U2 1
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 E 63RD ST, NEW YORK, NY 10021
SN 0077-8923
J9 ANN NY ACAD SCI
JI Ann. N.Y. Acad. Sci.
PD SEP 20
PY 1993
VL 694
BP 24
EP 35
DI 10.1111/j.1749-6632.1993.tb18339.x
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA264
UT WOS:A1993MA26400004
PM 8215060
ER

PT J
AU CONE, EJ
AF CONE, EJ
TI SALIVA TESTING FOR DRUGS OF ABUSE
SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article
ID PERFORMANCE LIQUID-CHROMATOGRAPHY; GAS-CHROMATOGRAPHY;
   MASS-SPECTROMETRY; ETHANOL CONCENTRATIONS; PAROTID-SALIVA; CAFFEINE
   CLEARANCE; HEALTHY-VOLUNTEERS; SEMINAL STAINS; SERUM CAFFEINE; MIXED
   SALIVA
RP CONE, EJ (reprint author), NIDA,ADDICT RES CTR,BALTIMORE,MD 21224, USA.
NR 134
TC 107
Z9 110
U1 0
U2 6
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 E 63RD ST, NEW YORK, NY 10021
SN 0077-8923
J9 ANN NY ACAD SCI
JI Ann. N.Y. Acad. Sci.
PD SEP 20
PY 1993
VL 694
BP 91
EP 127
DI 10.1111/j.1749-6632.1993.tb18346.x
PG 37
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA264
UT WOS:A1993MA26400011
PM 8215090
ER

PT J
AU FOX, PC
AF FOX, PC
TI SALIVARY MONITORING IN ORAL-DISEASES
SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article
ID CYSTIC-FIBROSIS PATIENTS; PSEUDOMONAS-AERUGINOSA; DIABETES-MELLITUS;
   GLAND FUNCTION; AGGREGATION
RP FOX, PC (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,CLIN INVEST SECT,BETHESDA,MD 20892, USA.
NR 21
TC 15
Z9 15
U1 0
U2 0
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 E 63RD ST, NEW YORK, NY 10021
SN 0077-8923
J9 ANN NY ACAD SCI
JI Ann. N.Y. Acad. Sci.
PD SEP 20
PY 1993
VL 694
BP 234
EP 237
DI 10.1111/j.1749-6632.1993.tb18356.x
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA264
UT WOS:A1993MA26400021
PM 8215058
ER

PT J
AU ATKINSON, JC
AF ATKINSON, JC
TI THE ROLE OF SALIVARY MEASUREMENTS IN THE DIAGNOSIS OF SALIVARY
   AUTOIMMUNE-DISEASES
SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
LA English
DT Article
ID PRIMARY SJOGRENS-SYNDROME; SYSTEMIC SICCA SYNDROME; HOST-DISEASE;
   RHEUMATOID FACTORS; IMMUNOGLOBULIN-A; GLAND DISEASE; WHOLE SALIVA;
   SIALOCHEMISTRY; LACTOFERRIN; BIOPSY
RP ATKINSON, JC (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892, USA.
NR 51
TC 22
Z9 22
U1 0
U2 0
PU NEW YORK ACAD SCIENCES
PI NEW YORK
PA 2 E 63RD ST, NEW YORK, NY 10021
SN 0077-8923
J9 ANN NY ACAD SCI
JI Ann. N.Y. Acad. Sci.
PD SEP 20
PY 1993
VL 694
BP 238
EP 251
DI 10.1111/j.1749-6632.1993.tb18357.x
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA MA264
UT WOS:A1993MA26400022
PM 8215059
ER

PT J
AU PAPP, PP
   CHATTORAJ, DK
   SCHNEIDER, TD
AF PAPP, PP
   CHATTORAJ, DK
   SCHNEIDER, TD
TI INFORMATION ANALYSIS OF SEQUENCES THAT BIND THE REPLICATION INITIATOR
   REPA
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE DNA-PROTEIN INTERACTIONS; DNA REPLICATION; INFORMATION THEORY; SEQUENCE
   LOGO
ID P1 PLASMID REPLICATION; GENE ACTIVATOR PROTEIN; ESCHERICHIA-COLI K-12;
   GAMMA-DELTA-RESOLVASE; LAMBDA-REPRESSOR; REGULATORY PROTEINS; ARGININE
   REPRESSOR; DNA RECOGNITION; RNA-POLYMERASE; TRP REPRESSOR
C1 NCI,FCRDC,MATH BIOL LAB,POB B,FREDERICK,MD 21702.
   NCI,BIOCHEM LAB,BETHESDA,MD 20892.
RI Papp, Peter/A-6907-2013; 
OI Schneider, Thomas/0000-0002-9841-1531
NR 56
TC 49
Z9 49
U1 0
U2 0
PU ACADEMIC PRESS LTD
PI LONDON
PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
SN 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD SEP 20
PY 1993
VL 233
IS 2
BP 219
EP 230
DI 10.1006/jmbi.1993.1501
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY295
UT WOS:A1993LY29500003
PM 8377199
ER

PT J
AU SAUNDERS, AM
   SCHMADER, K
   BREITNER, JCS
   BENSON, MD
   BROWN, WT
   GOLDFARB, L
   GOLDGABER, D
   MANWARING, MG
   SZYMANSKI, MH
   MCCOWN, N
   DOLE, KC
   SCHMECHEL, DE
   STRITTMATTER, WJ
   PERICAKVANCE, MA
   ROSES, AD
AF SAUNDERS, AM
   SCHMADER, K
   BREITNER, JCS
   BENSON, MD
   BROWN, WT
   GOLDFARB, L
   GOLDGABER, D
   MANWARING, MG
   SZYMANSKI, MH
   MCCOWN, N
   DOLE, KC
   SCHMECHEL, DE
   STRITTMATTER, WJ
   PERICAKVANCE, MA
   ROSES, AD
TI APOLIPOPROTEIN-E-EPSILON-4 ALLELE DISTRIBUTIONS IN LATE-ONSET
   ALZHEIMERS-DISEASE AND IN OTHER AMYLOID-FORMING DISEASES
SO LANCET
LA English
DT Note
AB The frequency of the allele for apolipoprotein E type 4 (epsilon4) is increased in late-onset familial and sporadic Alzheimer's disease (AD). We have examined epsilon4 frequencies in. four distinct, normal, elderly control groups and, most importantly, in patients with amyloid-forming diseases whose epsilon4 distributions were not previously known (Creutzfeldt-Jakob disease, familial amyloidotic polyneuropathy, Down's syndrome). There were no differences between any of these controls and published control series, cementing the relevance of epsilon4 for late-onset AD. The increase in late-onset AD was confirmed in two new series.
C1 DUKE UNIV,MED CTR,BRYAN ALZHEIMERS DIS RES CTR,DIV NEUROL,DURHAM,NC 27710.
   SUNY,DEPT PSYCHIAT,STONY BROOK,NY 11794.
   INDIANA UNIV,SCH MED,INDIANAPOLIS,IN 46202.
   NIH,BETHESDA,MD 20892.
   NEW YORK STATE INST BASIC RES DEV DISABIL,STATEN ISL,NY 10314.
FU NCRR NIH HHS [M01-RR-30]; NIA NIH HHS [AG05128, AGO7922, U24 AG021886]
NR 6
TC 438
Z9 443
U1 0
U2 5
PU LANCET LTD
PI LONDON
PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL
SN 0140-6736
J9 LANCET
JI Lancet
PD SEP 18
PY 1993
VL 342
IS 8873
BP 710
EP 711
DI 10.1016/0140-6736(93)91709-U
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA LX469
UT WOS:A1993LX46900010
PM 8103823
ER

PT J
AU BROUARD, A
   PELAPRAT, D
   BOJA, JW
   CARROLL, FI
   VIAL, M
   KUHAR, MJ
   ROSTENE, W
AF BROUARD, A
   PELAPRAT, D
   BOJA, JW
   CARROLL, FI
   VIAL, M
   KUHAR, MJ
   ROSTENE, W
TI POTENT COCAINE ANALOGS INHIBIT [H-3] DOPAMINE UPTAKE IN RAT
   MESENCEPHALIC CELLS IN PRIMARY CULTURES - PHARMACOLOGICAL SELECTIVITY OF
   EMBRYONIC COCAINE SITES
SO DEVELOPMENTAL BRAIN RESEARCH
LA English
DT Article
DE COCAINE; DOPAMINE; CELL CULTURE; BRAIN; MESENCEPHALON
ID DOPAMINERGIC-NEURONS; LIGAND-BINDING; INVITRO; TRANSPORTERS; RECEPTORS;
   BRAIN
AB The cellular localization of the cocaine binding sites in primary cultures of embryonic rat mesencephalic cells was previously reported to differ from that observed in adult rat brain. In order to know whether this different localization was associated with a different pharmacological selectivity, we tested the effect of new cocaine analogs on tritiated dopamine ([H-3]DA) uptake in primary cultures of rat embryonic mesencephalic cells. In these cultures, [H-3]DA was taken up by a nomifensine-sensitive, but desipramine and fluoxetine-insensitive process, reflecting selective uptake by the dopaminergic transporter. 3beta-(4-Chlorophenyl)tropan-2beta-carboxylic acid methyl ester (RTI-COC-31) was by far the most potent inhibitor of the [H-3]DA uptake, presenting an IC50 of 3.8 nM, while the corresponding analog with an unsubstituted phenyl ring (WIN 35,065-2) was 38 times less potent. The enantiomer of WIN 35,065-2, namely WIN 35,065-3, was 30 times less potent than the former. A similar pattern was found for the relative ability of these compounds to inhibit binding of the radiolabeled cocaine derivative [I-125]RTI-55 to membranes prepared from mesencephalic cultures. The order of potencies found for the three cocaine analogs on mesencephalic cultures was similar to that previously obtained in [H-3] WIN 35,428 binding experiments and [H-3]DA uptake inhibition in adult rat striatum, suggesting that the pharmacological selectivity of cocaine sites functionally related to the DA transporter in cultured embryonic neurons does not differ from that obtained in adult rat brain.
C1 HOP ST ANTOINE,INSERM,U339,184 RUE FAUBOURG ST ANTOINE,F-75571 PARIS 12,FRANCE.
   NIDA,NEUROSCI BRANCH,ADDICT RES CTR,BALTIMORE,MD 21224.
   RES TRIANGLE INST,RES TRIANGLE PK,NC 27709.
RI Rostene, William/F-2754-2017
NR 19
TC 7
Z9 7
U1 2
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-3806
J9 DEV BRAIN RES
JI Dev. Brain Res.
PD SEP 17
PY 1993
VL 75
IS 1
BP 13
EP 17
DI 10.1016/0165-3806(93)90060-N
PG 5
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA LX618
UT WOS:A1993LX61800002
PM 8222207
ER

PT J
AU CUSHMAN, M
   HE, HM
   LIN, CM
   HAMEL, E
AF CUSHMAN, M
   HE, HM
   LIN, CM
   HAMEL, E
TI SYNTHESIS AND EVALUATION OF A SERIES OF BENZYLANILINE HYDROCHLORIDES AS
   POTENTIAL CYTOTOXIC AND ANTIMITOTIC AGENTS ACTING BY INHIBITION OF
   TUBULIN POLYMERIZATION
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID STEGANACIN CONGENERS; ANTITUBULIN ACTIVITY; ANALOGS; THIOCOLCHICINE;
   DERIVATIVES; ETHER
AB Although certain substituted cis-stilbenes have displayed potent tubulin polymerization inhibitory activity and significant cytotoxicities in cancer cell cultures, these compounds have limited aqueous solubility and are therefore difficult to formulate for in vivo evaluation. A series of water-soluble N-(3,4,5-trimethoxybenzyl)aniline salts has therefore been synthesized in which the olefinic bridge of the stilbenes is replaced by an aminomethylene hydrochloride moiety. A relationship was found between the size of the substituent in the 4-position of the aniline ring and both antitubulin activity and cytotoxicity, such that the smaller the substituent, the greater the potency. The most promising of the newly synthesized compounds was 4-methyl-N-(3,4,5-trimethoxybenzyl)aniline hydrochloride, with an IC50 value of 3.5 muM for inhibition of tubulin polymerization and cytotoxicity for a wide variety of cancer cell lines. The cytotoxicities of the benzylaniline hydrochlorides correlated remarkably well with their antitubulin activities.
C1 NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892.
RP CUSHMAN, M (reprint author), PURDUE UNIV,DEPT MED CHEM & PHARMACOGNOSY,W LAFAYETTE,IN 47907, USA.
FU NCI NIH HHS [N01-CM-17512]
NR 27
TC 52
Z9 52
U1 0
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD SEP 17
PY 1993
VL 36
IS 19
BP 2817
EP 2821
DI 10.1021/jm00071a012
PG 5
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA LZ482
UT WOS:A1993LZ48200012
PM 8410995
ER

PT J
AU BROOKES, N
   TURNER, RJ
AF BROOKES, N
   TURNER, RJ
TI EXTRACELLULAR POTASSIUM REGULATES THE GLUTAMINE CONTENT OF ASTROCYTES -
   MEDIATION BY INTRACELLULAR PH
SO NEUROSCIENCE LETTERS
LA English
DT Article
DE AMMONIUM; GLUTAMATE; HYPERAMMONEMIA; GLUTAMINE SYNTHETASE; TRANSPORT;
   MOUSE
ID CEREBRAL-CORTEX; NERVOUS-SYSTEM; BRAIN; METABOLISM; CELLS; MOUSE;
   RELEASE
AB Based upon previous evidence that glutamine formation in astrocytes is pH-sensitive and that raised extracellular K+ alkalinizes astrocytic cytoplasm, it was hypothesized that extracellular K+ might regulate glutamine formation. In this study, the free glutamine content of mouse cerebral astrocytes incubated with 0.1 mM glutamate and 0.1 mM ammonium increased by 80-90% when the extracellular K+ concentration was raised from 3 to 12 mM. The corresponding K+-induced intracellular alkalinization of +0.13 pH units only partially reversed a glutamate-induced intracellular acidification of -0.24 pH units. By comparison, adjustment of extracellular pH from 7.4 to 7.8 shifted intracellular pH by + 0.25 pH units, fully reversing the glutamate-induced acidification and increasing glutamine content by 120-180%. The effect of K+ on intracellular pH increased to + 0.25 pH units in bicarbonate-buffered solution, suggesting that the regulation of glutamine formation by extracellular K+ is enhanced in the presence of bicarbonate.
C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892.
RP BROOKES, N (reprint author), UNIV MARYLAND,SCH MED,DEPT PHARMACOL & EXPTL THERAPEUT,655 W BALTIMORE ST,BALTIMORE,MD 21201, USA.
FU NIEHS NIH HHS [ES03928]
NR 23
TC 20
Z9 20
U1 0
U2 0
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0304-3940
J9 NEUROSCI LETT
JI Neurosci. Lett.
PD SEP 17
PY 1993
VL 160
IS 1
BP 73
EP 76
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA LX946
UT WOS:A1993LX94600019
PM 8247337
ER

PT J
AU WANG, LM
   MYERS, MG
   SUN, XJ
   AARONSON, SA
   WHITE, M
   PIERCE, JH
AF WANG, LM
   MYERS, MG
   SUN, XJ
   AARONSON, SA
   WHITE, M
   PIERCE, JH
TI IRS-1 - ESSENTIAL FOR INSULIN-STIMULATED AND IL-4-STIMULATED MITOGENESIS
   IN HEMATOPOIETIC-CELLS
SO SCIENCE
LA English
DT Article
ID TYROSINE KINASE-ACTIVITY; GTPASE-ACTIVATING PROTEIN;
   SIGNAL-TRANSDUCTION; PHOSPHATIDYLINOSITOL 3'-KINASE; JUXTAMEMBRANE
   REGION; ATP-BINDING; RECEPTOR; PHOSPHORYLATION; GROWTH; RAS
AB Although several interleukin-3 (IL-3)-dependent cell lines proliferate in response to IL-4 or insulin, the 32D line does not. Insulin and IL-4 sensitivity was restored to 32D cells by expression of IRS-1, the principal substrate of the insulin receptor. Although 32D cells possessed receptors for both factors, they lacked the IRS-1-related protein, 4PS, which becomes phosphorylated by tyrosine in insulin- or IL-4-responsive lines after stimulation. These results indicate that factors that bind unrelated receptors can use similar mitogenic signaling pathways in hematopoietic cells and that 4PS and IRS-1 are functionally similar proteins that are essential for insulin- and IL-4-induced proliferation.
C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892.
   HARVARD UNIV,SCH MED,DEPT MED,JOSLIN DIABET CTR,BOSTON,MA 02115.
FU NIDDK NIH HHS [DK-43808]
NR 31
TC 402
Z9 403
U1 0
U2 2
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD SEP 17
PY 1993
VL 261
IS 5128
BP 1591
EP 1594
DI 10.1126/science.8372354
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LX474
UT WOS:A1993LX47400034
PM 8372354
ER

PT J
AU LIOTTA, LA
AF LIOTTA, LA
TI MOLECULAR AND CELLULAR ASPECTS OF BASEMENT-MEMBRANES - ROHRBACH,DH,
   TIMPL,R
SO SCIENCE
LA English
DT Book Review
RP LIOTTA, LA (reprint author), NCI,PATHOL LAB,BETHESDA,MD 20892, USA.
NR 1
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD SEP 17
PY 1993
VL 261
IS 5128
BP 1611
EP 1613
DI 10.1126/science.261.5128.1611
PG 3
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LX474
UT WOS:A1993LX47400038
PM 17798120
ER

PT J
AU KUNKEL, TA
AF KUNKEL, TA
TI NUCLEOTIDE REPEATS - SLIPPERY DNA AND DISEASES
SO NATURE
LA English
DT Editorial Material
ID MISMATCH REPAIR; ERRORS
RP KUNKEL, TA (reprint author), NIEHS,MOLEC GENET LAB E301,RES TRIANGLE PK,NC 27709, USA.
NR 10
TC 196
Z9 199
U1 1
U2 5
PU MACMILLAN MAGAZINES LTD
PI LONDON
PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW
SN 0028-0836
J9 NATURE
JI Nature
PD SEP 16
PY 1993
VL 365
IS 6443
BP 207
EP 208
DI 10.1038/365207a0
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LX471
UT WOS:A1993LX47100029
PM 8371775
ER

PT J
AU EWIGMAN, BG
   CRANE, JP
   FRIGOLETTO, FD
   LEFEVRE, ML
   BAIN, RP
   MCNELLIS, D
AF EWIGMAN, BG
   CRANE, JP
   FRIGOLETTO, FD
   LEFEVRE, ML
   BAIN, RP
   MCNELLIS, D
TI EFFECT OF PRENATAL ULTRASOUND SCREENING ON PERINATAL OUTCOME
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID RANDOMIZED CONTROLLED TRIAL; TWIN PREGNANCY; RISK POPULATION; FETAL
   GROWTH; GESTATION; FETUSES; VIEW
AB Background. Many clinicians advocate routine ultrasound screening during pregnancy to detect congenital anomalies, multiple-gestation pregnancies, fetal growth disorders, placental abnormalities, and errors in the estimation of gestational age. However, it is not known whether the detection of these conditions through screening leads to interventions that improve perinatal outcome.
   Methods. We conducted a randomized trial involving 15,151 pregnant women at low risk for perinatal problems to determine whether ultrasound screening decreased the frequency of adverse perinatal outcomes. The women randomly assigned to the ultrasound-screening group underwent one sonographic examination at 15 to 22 weeks of gestation and another at 31 to 35 weeks. The women in the control group underwent ultrasonography only for medical indications, as identified by their physicians. Adverse perinatal outcome was defined as fetal death, neonatal death, or neonatal morbidity such as intraventricular hemorrhage.
   Results. The mean numbers of sonograms obtained per woman in the ultrasound-screening and control groups were 2.2 and 0.6, respectively. The rate of adverse perinatal outcome was 5.0 percent among the infants of the women in the ultrasound-screening group and 4.9 percent among the infants of the women in the control group (relative risk, 1.0; 95 percent confidence interval, 0.9 to 1.2; P = 0.85). The rates of preterm delivery and the distribution of birth weights were nearly identical in the two groups. The ultrasonographic detection of congenital anomalies had no effect on perinatal outcome. There were no significant differences between the groups in perinatal outcome in the subgroups of women with post-date pregnancies, multiple-gestation pregnancies, or infants who were small for gestational age.
   Conclusions. Screening ultrasonography did not improve perinatal outcome as compared with the selective use of ultrasonography on the basis of clinician judgment.
C1 WASHINGTON UNIV,SCH MED,DEPT OBSTET & GYNECOL,ST LOUIS,MO 63110.
   HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02115.
   GEORGE WASHINGTON UNIV,CTR BIOSTAT,ROCKVILLE,MD.
   NICHHD,BETHESDA,MD 20892.
RP EWIGMAN, BG (reprint author), UNIV MISSOURI,HLTH SCI CTR MA303,SCH MED,DEPT FAMILY & COMMUNITY MED,1 HOSP DR,COLUMBIA,MO 65212, USA.
FU NICHD NIH HHS [HD 19897, HD 21017, HD 21140]
NR 33
TC 428
Z9 438
U1 0
U2 8
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD SEP 16
PY 1993
VL 329
IS 12
BP 821
EP 827
DI 10.1056/NEJM199309163291201
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA LW551
UT WOS:A1993LW55100001
PM 8355740
ER

PT J
AU LOWREY, CH
   NIENHUIS, AW
AF LOWREY, CH
   NIENHUIS, AW
TI TREATMENT WITH AZACITIDINE OF PATIENTS WITH END-STAGE BETA-THALASSEMIA
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Note
ID SICKLE-CELL-ANEMIA; FETAL HEMOGLOBIN PRODUCTION; GAMMA-GLOBIN SYNTHESIS;
   5-AZACYTIDINE; ALLOANTIBODIES; DISEASE; HBF
C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892.
RP LOWREY, CH (reprint author), DARTMOUTH HITCHCOCK MED CTR,DEPT MED,HEMATOL & ONCOL SECT,1 MED CTR DR,LEBANON,NH 03756, USA.
NR 27
TC 90
Z9 91
U1 0
U2 1
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD SEP 16
PY 1993
VL 329
IS 12
BP 845
EP 848
DI 10.1056/NEJM199309163291205
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA LW551
UT WOS:A1993LW55100005
PM 7689171
ER

PT J
AU MASUR, H
AF MASUR, H
TI RECOMMENDATIONS ON PROPHYLAXIS AND THERAPY FOR DISSEMINATED
   MYCOBACTERIUM-AVIUM COMPLEX DISEASE IN PATIENTS INFECTED WITH THE
   HUMAN-IMMUNODEFICIENCY-VIRUS
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID IMMUNE-DEFICIENCY-SYNDROME; INTRACELLULARE BACTEREMIA; NATURAL-HISTORY;
   AIDS; CLARITHROMYCIN; CIPROFLOXACIN; ETHAMBUTOL; IDENTIFICATION;
   EPIDEMIOLOGY; CLOFAZIMINE
RP MASUR, H (reprint author), NIH,BETHESDA,MD 20892, USA.
NR 33
TC 268
Z9 270
U1 0
U2 2
PU MASS MEDICAL SOC
PI BOSTON
PA 10 SHATTUCK, BOSTON, MA 02115
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD SEP 16
PY 1993
VL 329
IS 12
BP 898
EP 904
DI 10.1056/NEJM199309163291228
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA LW551
UT WOS:A1993LW55100037
PM 8395019
ER

PT J
AU ELIAS, MF
   WOLF, PA
   DAGOSTINO, RB
   COBB, J
   WHITE, LR
AF ELIAS, MF
   WOLF, PA
   DAGOSTINO, RB
   COBB, J
   WHITE, LR
TI UNTREATED BLOOD-PRESSURE LEVEL IS INVERSELY RELATED TO
   COGNITIVE-FUNCTIONING - THE FRAMINGHAM-STUDY
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE ANTIHYPERTENSIVE AGENTS; BLOOD PRESSURE; COGNITION; HYPERTENSION
ID PERFORMANCE; HYPERTENSION; MEN
AB It was hypothesized that blood pressure would be inversely related to cognitive functioning, if unconfounded with antihypertensive medication and measured over many occasions prior to neuropsychological testing. For stroke-free Framingham Study participants aged 55-88 years (n = 1,702), blood pressure levels were averaged over five biennial examinations (1956-1964) when few hypertensives were being treated, and examined in relation to neuropsychological tests administered between 1976 and 1978. With age, education, occupation, cigarette smoking, alcohol consumption, and gender controlled, blood pressure levels and chronicity of hypertension were inversely related to the composite score and measures of attention and memory. This was true for the full sample, for a subsample untreated during blood pressure measurement (n = 1,485), and for a subsample untreated throughout the entire study period (n = 1,038). For example, decline per 10 mmHg increment in blood pressure ranged from -0.04 to -0.07 standard score units (z) for the composite score. A negative finding previously was most likely due to blood pressure measurement concurrently with neuropsychological testing, or too few measurements. Hypertension-associated pathogenic processes may cause mild cognitive impairment, but other mechanisms need to be considered.
C1 UNIV HOSP BOSTON, EVANS MEM DEPT CLIN RES, PREVENT MED & EPIDEMIOL SECT, BOSTON, MA 02118 USA.
   UNIV HOSP BOSTON, DEPT MED, BOSTON, MA 02118 USA.
   NIA, HONOLULU HEART & AGING STUDY, KUAKINI MED CTR, HONOLULU, HI USA.
   BOSTON UNIV, SCH MED, DEPT NEUROL, BOSTON, MA 02118 USA.
   BOSTON UNIV, DEPT MATH, BOSTON, MA 02215 USA.
RP ELIAS, MF (reprint author), UNIV MAINE, DEPT PSYCHOL, LITTLE HALL, ORONO, ME 04469 USA.
FU NIA NIH HHS [1-R01-AG08122-05, 5-R37-AG03055-11]; NINDS NIH HHS
   [2-R01-NS-17950-11]
NR 30
TC 429
Z9 450
U1 4
U2 16
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD SEP 15
PY 1993
VL 138
IS 6
BP 353
EP 364
PG 12
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA MA341
UT WOS:A1993MA34100001
PM 8213741
ER

PT J
AU EASTERBROOK, PJ
   CHMIEL, JS
   HOOVER, DR
   SAAH, AJ
   KASLOW, RA
   KINGSLEY, LA
   DETELS, R
AF EASTERBROOK, PJ
   CHMIEL, JS
   HOOVER, DR
   SAAH, AJ
   KASLOW, RA
   KINGSLEY, LA
   DETELS, R
TI RACIAL AND ETHNIC-DIFFERENCES IN HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1
   (HIV-1) SEROPREVALENCE AMONG HOMOSEXUAL AND BISEXUAL MEN
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE BLACKS; ETHNIC GROUPS; HISPANIC AMERICANS; HIV-1; RISK FACTORS
ID INTRAVENOUS-DRUG-USERS; MULTICENTER AIDS COHORT; NEW-YORK-CITY;
   SAN-FRANCISCO; UNITED-STATES; RISK-FACTORS; INFECTION; ABUSERS;
   ASSOCIATION; SEROPOSITIVITY
AB To determine whether the excess prevalence of human immunodeficiency virus type 1 (HIV-1) infection in US black and Hispanic homosexual men relative to white men can be explained by differences in sociodemographic factors, history of sexually transmitted diseases, or sexual and drug-use behaviors, the authors conducted a cross-sectional analysis of baseline HIV-1 seroprevalence and HIV-1 risk factors among 4,475 non-Hispanic white, 234 Hispanic white, and 194 black homosexual men from four centers in the United States (Baltimore/Washington, DC, Pittsburgh, Chicago, and Los Angeles). HIV-1 seroprevalence was significantly higher in Hispanic men (50%; odds ratio (OR) = 1.83,95% confidence interval (CI) 1.41-2.39) and black men (47%; OR = 1.62,95% CI 1.21-2.16) compared with white men (35%). Both Hispanic and black men more frequently reported a history of sexually transmitted diseases. Overall, Hispanics had the highest risk profile and blacks the lowest risk profile with respect to certain high-risk sexual behaviors (e.g., receptive anal intercourse and use of anonymous sexual partners) and recreational drug. use. After multivariate adjustment, black race remained a significant independent risk factor for HIV-1 seropositivity (OR = 1.60, 95% CI 1.132. 26), but Hispanic ethnicity was no longer statistically significant (OR = 1.17, 95% CI 0.82-1.69). Most of the excess HIV-1 prevalent infection among Hispanics was explained by their predominant recruitment from Los Angeles-the study center with the highest HIV-1 seroprevalence-and their greater prevalence of a history of sexually transmitted diseases and certain high-risk sexual practices. By contrast, adjustment for these same risk behaviors failed to explain the observed black-white differences in HIV-1 seroprevalence, and further studies are needed to elucidate the reasons for these unexplained racial differences. HIV-1 educational programs for homosexual men should take into account the behavioral differences that exist between white and minority racial/ethnic groups.
C1 JOHNS HOPKINS SCH HYG & PUBL HLTH,BALTIMORE,MD.
   NORTHWESTERN UNIV,CHICAGO,IL 60611.
   NIAID,BETHESDA,MD 20892.
   UNIV PITTSBURGH,SCH PUBL HLTH,PITTSBURGH,PA 15260.
   UNIV CALIF LOS ANGELES,SCH PUBL HLTH,LOS ANGELES,CA 90024.
FU NIAID NIH HHS [N01-AI72631, N01-AI-72634, N01-AI-72632]
NR 38
TC 46
Z9 46
U1 0
U2 0
PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH
PI BALTIMORE
PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD SEP 15
PY 1993
VL 138
IS 6
BP 415
EP 429
PG 15
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA MA341
UT WOS:A1993MA34100007
PM 8213747
ER

PT J
AU YANNUZZI, LA
   SORENSON, JA
   SOBEL, RS
   DALY, JR
   DEROSA, JT
   SEDDON, JM
   GRAGOUDAS, ES
   PULIAFITO, CA
   GELLES, E
   GONET, R
   BURTON, TC
   ROLNICK, C
   FLOM, T
   HALLER, J
   PUSIN, S
   CASSEL, G
   APPLEGATE, CA
   SEIGEL, D
   SPERDUTO, RD
   HILLER, R
   MOWERY, R
   CHEW, E
   CULVER, J
   METZGER, K
   KALBFLEISCH, N
   ZARLING, D
   FARBER, MD
   BLAIR, N
   STELMACK, T
   AXELROD, A
   WAITR, SE
   CROSS, A
   TAMBOLI, A
   DUNN, M
   SEDDON, JM
   SHAMBAN, K
   LENTO, D
AF YANNUZZI, LA
   SORENSON, JA
   SOBEL, RS
   DALY, JR
   DEROSA, JT
   SEDDON, JM
   GRAGOUDAS, ES
   PULIAFITO, CA
   GELLES, E
   GONET, R
   BURTON, TC
   ROLNICK, C
   FLOM, T
   HALLER, J
   PUSIN, S
   CASSEL, G
   APPLEGATE, CA
   SEIGEL, D
   SPERDUTO, RD
   HILLER, R
   MOWERY, R
   CHEW, E
   CULVER, J
   METZGER, K
   KALBFLEISCH, N
   ZARLING, D
   FARBER, MD
   BLAIR, N
   STELMACK, T
   AXELROD, A
   WAITR, SE
   CROSS, A
   TAMBOLI, A
   DUNN, M
   SEDDON, JM
   SHAMBAN, K
   LENTO, D
TI RISK-FACTORS FOR BRANCH RETINAL VEIN OCCLUSION
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID ALCOHOL-CONSUMPTION; HEART-DISEASE; PRESSURE; OBESITY
AB The objective of our clinic-based case-control study was to identify risk factors for branch retinal vein occlusion. Between 1986 and 1990 data were obtained at five clinical centers from 270 patients with branch retinal vein occlusion and 1,142 controls. Data were collected from interviews, clinical examinations, and laboratory analyses of blood specimens. An increased risk of branch retinal vein occlusion was found in persons with a history of systemic hypertension, a history of cardiovascular disease, an increased body mass index at 20 years of age, a history of glaucoma, and higher serum levels of alpha2-globulin. Risk of branch retinal vein occlusion decreased with higher levels of alcohol consumption and high-density lipoprotein cholesterol. The data suggest a cardiovascular risk profile for patients with branch retinal vein occlusion and indicate that 50% of patients with branch retinal vein occlusion may be attributable to hypertension. Our findings support current public health recommendations to diagnose and treat hypertension, reduce weight, increase physical activity, and maximize serum high-density lipoprotein levels.
C1 NEI,BETHESDA,MD 20892.
   MANHATTAN EYE EAR & THROAT HOSP,NEW YORK,NY 10021.
   HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115.
   ORKAND CORP,CTR COORDINATING,SILVER SPRING,MD.
   PHOTOG READING CTR,BOSTON,MA.
NR 27
TC 128
Z9 132
U1 0
U2 1
PU OPHTHALMIC PUBL CO
PI CHICAGO
PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD SEP 15
PY 1993
VL 116
IS 3
BP 286
EP 296
PG 11
WC Ophthalmology
SC Ophthalmology
GA LW157
UT WOS:A1993LW15700003
ER

PT J
AU YU, YM
   SKLAR, MM
   NISSLEY, SP
   REDDI, AH
AF YU, YM
   SKLAR, MM
   NISSLEY, SP
   REDDI, AH
TI CHANGES IN THE EXPRESSION OF INSULIN-LIKE GROWTH FACTOR-II
   MANNOSE-6-PHOSPHATE RECEPTOR DURING ENDOCHONDRAL BONE-DEVELOPMENT
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
ID MANNOSE 6-PHOSPHATE RECEPTOR; MESSENGER-RNA; LIVER-REGENERATION;
   DEVELOPING RAT; FACTOR-BETA; PROTEIN; LOCALIZATION; FIBROBLASTS;
   BINDING; CELLS
C1 NIDR,BONE CELL BIOL SECT,BETHESDA,MD 20892.
   NCI,METAB BRANCH,BETHESDA,MD 20892.
NR 35
TC 8
Z9 9
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD SEP 15
PY 1993
VL 195
IS 2
BP 516
EP 524
DI 10.1006/bbrc.1993.2076
PG 9
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA LW469
UT WOS:A1993LW46900002
PM 8373392
ER

PT J
AU MONTPIED, P
   WELLER, M
   PAUL, SM
AF MONTPIED, P
   WELLER, M
   PAUL, SM
TI N-METHYL-D-ASPARATE RECEPTOR AGONISTS DECREASE PROTOONCOGENE BCL-2
   MESSENGER-RNA EXPRESSION IN CULTURED RAT CEREBELLAR GRANULE NEURONS
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
ID PROGRAMMED CELL-DEATH; NERVE GROWTH-FACTOR; D-ASPARTATE RECEPTOR;
   SYMPATHETIC NEURONS; FACTOR DEPRIVATION; PROTEIN-SYNTHESIS; PC12 CELLS;
   APOPTOSIS; GLUTAMATE; PREVENTION
C1 NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BETHESDA,MD 20892.
NR 25
TC 31
Z9 31
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD SEP 15
PY 1993
VL 195
IS 2
BP 623
EP 629
DI 10.1006/bbrc.1993.2091
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA LW469
UT WOS:A1993LW46900017
PM 8103985
ER

PT J
AU DOHLMAN, JG
   LUPAS, A
   CARSON, M
AF DOHLMAN, JG
   LUPAS, A
   CARSON, M
TI LONG CHARGE-RICH ALPHA-HELICES IN SYSTEMIC AUTOANTIGENS
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
ID SMALL NUCLEAR RIBONUCLEOPROTEIN; B-CELL EPITOPES; 3-DIMENSIONAL
   STRUCTURE; T-CELLS; PROTEIN; ANTIGEN; BINDING; VIRUS; COMPLEX; SITES
C1 MAX PLANCK INST BIOCHEM,W-8033 MARTINSRIED,GERMANY.
   UNIV ALABAMA,MED CTR,CTR MACROMOLEC CRYSTALLOG,BIRMINGHAM,AL 35294.
RP DOHLMAN, JG (reprint author), NIAMS,CONNECT TISSUE DIS SECT,BLDG 10,RM 9N244,BETHESDA,MD 20892, USA.
FU NIAID NIH HHS [P30 AI27767]; NIAMS NIH HHS [5T32AR0745007]
NR 34
TC 56
Z9 57
U1 0
U2 0
PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD SEP 15
PY 1993
VL 195
IS 2
BP 686
EP 696
DI 10.1006/bbrc.1993.2100
PG 11
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA LW469
UT WOS:A1993LW46900026
PM 8373407
ER

PT J
AU VOSTAL, JG
   SHULMAN, NR
AF VOSTAL, JG
   SHULMAN, NR
TI VINCULIN IS A MAJOR PLATELET PROTEIN THAT UNDERGOES CA2+-DEPENDENT
   TYROSINE PHOSPHORYLATION
SO BIOCHEMICAL JOURNAL
LA English
DT Article
ID GLYCOPROTEIN-IIB; RABBIT PLATELETS; KINASE; THROMBIN; TALIN; CELLS; IIIA
AB When intracellular Ca2+ pools are released during platelet stimulation by thrombin, elevation of platelet cytosolic Ca2+ concentration induces tyrosine phosphorylation of a 130 kDa protein, and refilling the pools mediates dephosphorylation of this protein [Vostal, Jackson and Shulman (1991) J. Biol. Chem. 266, 16911-16916]. In the present work the 130 kDa protein was identified as vinculin by the following criteria. (1) It is detected on protein immunoblots of thrombin-activated platelets by both monoclonal anti-phosphotyrosine and anti-vinculin antibodies. (2) Removal of N-linked sugars with peptide-N-glycosidase or reduction did not change the molecular mass of vinculin or of the 130 kDa protein on SDS/PAGE. (3) The 130 kDa tyrosine-phosphorylated protein associates with Triton-soluble fraction of platelets as does vinculin. (4) The 130 kDa protein immunoprecipitated by anti-vinculin monoclonal antibody reacts with anti-phosphotyrosine antibody; when immunoprecipitated by anti-phosphotyrosine antibody it reacts with anti-vinculin antibody. (5) The 130 kDa tyrosine-phosphorylated protein and vinculin focus isoelectrically at pI 5.4-5.8. Our finding that vinculin is a major platelet protein that undergoes Ca2+-dependent tyrosine phosphorylation during platelet activation may provide clues to the function of this protein.
C1 NIDDKD,CLIN HEMATOL BRANCH,BETHESDA,MD 20892.
RP VOSTAL, JG (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL,BETHESDA,MD 20892, USA.
NR 28
TC 37
Z9 37
U1 0
U2 0
PU PORTLAND PRESS
PI LONDON
PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD SEP 15
PY 1993
VL 294
BP 675
EP 680
PN 3
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LY645
UT WOS:A1993LY64500010
PM 7691054
ER

PT J
AU WALDMANN, TA
   WHITE, JD
   GOLDMAN, CK
   TOP, L
   GRANT, A
   BAMFORD, R
   ROESSLER, E
   HORAK, ID
   ZAKNOEN, S
   KASTENSPORTES, C
   ENGLAND, R
   HORAK, E
   MISHRA, B
   DIPRE, M
   HALE, P
   FLEISHER, TA
   JUNGHANS, RP
   JAFFE, ES
   NELSON, DL
AF WALDMANN, TA
   WHITE, JD
   GOLDMAN, CK
   TOP, L
   GRANT, A
   BAMFORD, R
   ROESSLER, E
   HORAK, ID
   ZAKNOEN, S
   KASTENSPORTES, C
   ENGLAND, R
   HORAK, E
   MISHRA, B
   DIPRE, M
   HALE, P
   FLEISHER, TA
   JUNGHANS, RP
   JAFFE, ES
   NELSON, DL
TI THE INTERLEUKIN-2 RECEPTOR - A TARGET FOR MONOCLONAL-ANTIBODY TREATMENT
   OF HUMAN T-CELL LYMPHOTROPHIC VIRUS-I-INDUCED ADULT T-CELL LEUKEMIA
SO BLOOD
LA English
DT Article
ID TAC ANTIGEN; IL-2 RECEPTOR; EXPRESSION; IMMUNOGLOBULIN; LYMPHOMA;
   THERAPY; GENE; IMMUNOTHERAPY; REARRANGEMENT; SPECIFICITY
C1 NCI,PATHOL LAB,BETHESDA,MD 20892.
   NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT CLIN PATHOL,BETHESDA,MD 20892.
RP WALDMANN, TA (reprint author), NCI,METAB BRANCH,BLDG 10,RM 4N115,BETHESDA,MD 20892, USA.
NR 45
TC 149
Z9 152
U1 0
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0006-4971
J9 BLOOD
JI Blood
PD SEP 15
PY 1993
VL 82
IS 6
BP 1701
EP 1712
PG 12
WC Hematology
SC Hematology
GA LY151
UT WOS:A1993LY15100003
PM 8400227
ER

PT J
AU YANO, T
   SANDER, CA
   ANDRADE, RE
   GAUWERKY, CE
   CROCE, CM
   LONGO, DL
   JAFFE, ES
   RAFFELD, M
AF YANO, T
   SANDER, CA
   ANDRADE, RE
   GAUWERKY, CE
   CROCE, CM
   LONGO, DL
   JAFFE, ES
   RAFFELD, M
TI MOLECULAR ANALYSIS OF THE BCL-3 LOCUS AT CHROMOSOME-17Q22 IN B-CELL
   NEOPLASMS
SO BLOOD
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; HUMAN FOLLICULAR LYMPHOMA; TRANSCRIPTIONAL
   UNIT; ONCOGENE LOCUS; P53 GENE; MYC; REARRANGEMENTS; TRANSLOCATION;
   BREAKPOINT; EVOLUTION
C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,BLDG 10,RM 2N110,BETHESDA,MD 20892.
   THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,PHILADELPHIA,PA 19107.
   NCI,FREDERICK CANC RES FACIL,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701.
NR 20
TC 14
Z9 14
U1 0
U2 0
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0006-4971
J9 BLOOD
JI Blood
PD SEP 15
PY 1993
VL 82
IS 6
BP 1813
EP 1819
PG 7
WC Hematology
SC Hematology
GA LY151
UT WOS:A1993LY15100016
PM 8400234
ER

PT J
AU MILLER, JL
   WALSH, CE
   NEY, PA
   SAMULSKI, RJ
   NIENHUIS, AW
AF MILLER, JL
   WALSH, CE
   NEY, PA
   SAMULSKI, RJ
   NIENHUIS, AW
TI SINGLE-COPY TRANSDUCTION AND EXPRESSION OF HUMAN GAMMA-GLOBIN IN K562
   ERYTHROLEUKEMIA-CELLS USING RECOMBINANT ADENOASSOCIATED VIRUS VECTORS -
   THE EFFECT OF MUTATIONS IN NF-E2 AND GATA-1 BINDING MOTIFS WITHIN THE
   HYPERSENSITIVITY SITE-2 ENHANCER
SO BLOOD
LA English
DT Article
ID LOCUS-CONTROL REGION; DOMINANT CONTROL REGION; PROTEIN DNA INTERACTIONS;
   HS-II ENHANCER; GENE-EXPRESSION; ADENOASSOCIATED VIRUS; ACTIVATING
   REGION; ERYTHROID-CELLS; NUCLEAR-PROTEIN; MAMMALIAN-CELLS
C1 NHLBI, CLIN HEMATOL BRANCH, BLDG 10, RM 7C103, BETHESDA, MD 20892 USA.
   UNIV PITTSBURGH, DEPT BIOL SCI, PITTSBURGH, PA 15260 USA.
FU NHLBI NIH HHS [HL 48347-03]
NR 38
TC 46
Z9 46
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD SEP 15
PY 1993
VL 82
IS 6
BP 1900
EP 1906
PG 7
WC Hematology
SC Hematology
GA LY151
UT WOS:A1993LY15100026
PM 8400240
ER

PT J
AU UMEMURA, T
   TOKUMO, K
   SIRMA, H
   GEBHARDT, R
   POIRIER, MC
   WILLIAMS, GM
AF UMEMURA, T
   TOKUMO, K
   SIRMA, H
   GEBHARDT, R
   POIRIER, MC
   WILLIAMS, GM
TI DOSE-RESPONSE EFFECTS OF 2-ACETYLAMINOFLUORENE ON DNA-DAMAGE,
   CYTOTOXICITY, CELL-PROLIFERATION AND NEOPLASTIC CONVERSION IN RAT-LIVER
SO CANCER LETTERS
LA English
DT Article
DE ACETYLAMINOFLUORENE; DNA DAMAGE; CELL PROLIFERATION; NEOPLASTIC
   CONVERSION; RAT LIVER
ID ALTERED FOCI; GLUTAMINE-SYNTHETASE; ADDUCT FORMATION; CHEMICAL
   CARCINOGENS; IRON ACCUMULATION; REMOVAL; INITIATION; RESISTANT;
   PROMOTION; LESIONS
AB This study measured the effect of precise doses of 2-acetylaminofluorene (AAF) in inducing DNA damage, functional changes and neoplastic conversion in rat liver. Groups of male F344 rats at 9 weeks of age were exposed to cumulative doses of 0.5 or 2.0 mmol AAF per kg body weight given by gavage daily 5 days per week over an 8-week period and maintained with no further exposure for up to 8 weeks. Administration of AAF resulted in the formation of N-deoxyguanosin-(8-yl)-2-aminofluorene in liver DNA in relationship to dose. In centrilobular hepatocytes the zone of glutamine synthetase-expressing cells was reduced by exposure. By 8 weeks, but not at 4 weeks, the higher of the two doses of AAF provoked an increase in cell proliferation measured by immunohistochemical incorporation of bromode-oxyuridine. Altered hepatocellular foci expressing the placental form of glutathione transferase were induced by the high dose of AAF at 4 weeks, but not at the low dose. At 8 weeks the incidence of foci at the high dose was 79 times that induced by the low dose. These foci were highly proliferative. In animals exposed to AAF for 8 weeks and maintained for 4 weeks with no exposure, DNA adducts decreased by 80% and cell proliferation subsided by 80%, although the glutamine synthetase zone remained diminished. After discontinuation of AAF, the number of foci diminished by 50% and their proliferation subsided by 80% at 4 weeks, indicating a phenotypic reversion of many foci. With this protocol of administration of precise doses of AAF, we have established non-linearity of effects and a lack of correlation between DNA adduct formation and induction of cellular lesions. We suggest that doses in the range of those reported can be used to study the contribution of epigenetic and genotoxic effects in carcinogenesis and to study threshold events.
C1 AMER HLTH FDN,DIV PATHOL & TOXICOL,1 DANA RD,VALHALLA,NY 10595.
   NATL INST HYG SCI,DIV TOXICOL,TOKYO 158,JAPAN.
   HIROSHIMA UNIV,SCH MED,DEPT INTERNAL MED 1,HIROSHIMA 730,JAPAN.
   UNIV TUBINGEN,INST PHYSIOL CHEM,W-7400 TUBINGEN 1,GERMANY.
   NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892.
NR 49
TC 52
Z9 53
U1 0
U2 0
PU ELSEVIER SCI IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD SEP 15
PY 1993
VL 73
IS 1
BP 1
EP 10
DI 10.1016/0304-3835(93)90181-8
PG 10
WC Oncology
SC Oncology
GA MB800
UT WOS:A1993MB80000001
PM 8402592
ER

PT J
AU LAN, MS
   RUSSELL, EK
   LU, J
   JOHNSON, BE
   NOTKINS, AL
AF LAN, MS
   RUSSELL, EK
   LU, J
   JOHNSON, BE
   NOTKINS, AL
TI IA-1, A NEW MARKER FOR NEUROENDOCRINE DIFFERENTIATION IN HUMAN
   LUNG-CANCER CELL-LINES
SO CANCER RESEARCH
LA English
DT Note
ID L-DOPA DECARBOXYLASE; CHROMOGRANIN-A; CYTOGENETIC ABNORMALITIES;
   SUPPLEMENTED MEDIUM; CARCINOMA; GROWTH; ESTABLISHMENT; ENDOCRINE; TUMORS
AB IA-1 is a recently isolated novel complementary DNA which encodes a protein of 510 amino acids that contains both a zinc ringer DNA-binding domain and a putative prohormone domain. mRNA expression of IA-1 has been found thus far only in tumors of neuroendocrine origin. In this report we describe the expression of IA-1 mRNA in a panel of 64 human lung cancer cell lines. IA-1 mRNA was detected by Northern blot analysis in 97% (30 of 31) of small cell lung cancer cell lines. In contrast, IA-1 mRNA was detected in only 13% (4 of 30) of non-small cell lung cancer cell lines. Nine of the 30 (30%) expressed either chromogranin A mRNA or produced L-dopa decarboxylase. Four of these 9 (44%) had detectable levels of IA-1 mRNA. In most of the lung cancer cell lines examined, IA-1 showed high concordance with the other neuroendocrine markers, L-dopa decarboxylase, and chromogranin A. The one exception was a variant small cell lung cancer cell line which expressed low or nondetectable levels of L-dopa decarboxylase. IA-1 is a candidate marker of neuroendocrine differentiation of human lung tumors.
C1 USN,NATL MED CTR,NCI,NAVY ONCOL BRANCH,BETHESDA,MD 20889.
RP LAN, MS (reprint author), NIDR,ORAL MED LAB,BLDG 30,ROOM 121,BETHESDA,MD 20892, USA.
NR 24
TC 48
Z9 48
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 SEP 15
PY 1993
VL 53
IS 18
BP 4169
EP 4171
PG 3
WC Oncology
SC Oncology
GA LW553
UT WOS:A1993LW55300010
PM 8364910
ER

PT J
AU KAMESAKI, S
   KAMESAKI, H
   JORGENSEN, TJ
   TANIZAWA, A
   POMMIER, Y
   COSSMAN, J
AF KAMESAKI, S
   KAMESAKI, H
   JORGENSEN, TJ
   TANIZAWA, A
   POMMIER, Y
   COSSMAN, J
TI BCL-2 PROTEIN INHIBITS ETOPOSIDE-INDUCED APOPTOSIS THROUGH ITS EFFECTS
   ON EVENTS SUBSEQUENT TO TOPOISOMERASE II-INDUCED DNA STRAND BREAKS AND
   THEIR REPAIR
SO CANCER RESEARCH
LA English
DT Article
ID PROGRAMMED CELL-DEATH; CHINESE-HAMSTER CELLS; CYTO-TOXICITY; ANTICANCER
   DRUGS; GENE-TRANSFER; CLEAVAGE; FRAGMENTATION; DAMAGE; LINE; P53
AB Previous studies have shown that bcl-2 overexpression can inhibit apoptosis induced by DNA-damaging agents widely used in cancer chemotherapy, including X-irradiation, alkylating agents (hydroperoxycyclophosphamide, etc.), and topoisomerase II inhibitors (etoposide, etc.). However, little is known about the mechanism by which bcl-2 overexpression inhibits apoptosis triggered by these agents. In this study, we examined whether bcl-2 overexpression could have effects on etoposide-induced DNA damage and its repair. For these experiments, we developed CH31 clones (mouse B-cells) stably transfected with human bcl-2 sense plasmids and compared these clones with a parental CH31 clone or CH31 clones with antisense plasmids. Overexpression of bcl-2 protein inhibited etoposide-induced apoptosis and cytotoxicity. However, there was no or little difference in the production and repair of DNA-protein cross-links, DNA single-strand breaks, and double-strand breaks among a parental CH31 clone and CH31 clones with human bcl-2 sense or antisense plasmids. These findings indicate that (a) apoptosis or cytotoxicity induced by etoposide can be separated into early events (formation of double-strand breaks, DNA single-strand breaks, and double-strand breaks) and later events (secondary DNA fragmentation or cell death) and (b) bcl-2 inhibits apoptosis and cytotoxicity induced by etoposide at some steps between these events.
C1 GEORGETOWN UNIV,SCH MED,DEPT PATHOL,3900 RESERVOIR RD NW,WASHINGTON,DC 20007.
   GEORGETOWN UNIV,SCH MED,DEPT RADIAT MED,WASHINGTON,DC 20007.
   NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,BETHESDA,MD 20892.
FU NCI NIH HHS [CA-48716]
NR 40
TC 243
Z9 246
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 SEP 15
PY 1993
VL 53
IS 18
BP 4251
EP 4256
PG 6
WC Oncology
SC Oncology
GA LW553
UT WOS:A1993LW55300023
PM 8395979
ER

PT J
AU TAKAGI, H
   SHARP, R
   TAKAYAMA, H
   ANVER, MR
   WARD, JM
   MERLINO, G
AF TAKAGI, H
   SHARP, R
   TAKAYAMA, H
   ANVER, MR
   WARD, JM
   MERLINO, G
TI COLLABORATION BETWEEN GROWTH-FACTORS AND DIVERSE CHEMICAL CARCINOGENS IN
   HEPATOCARCINOGENESIS OF TRANSFORMING GROWTH-FACTOR-ALPHA TRANSGENIC MICE
SO CANCER RESEARCH
LA English
DT Article
ID LIVER EPITHELIAL-CELLS; 2-ACETYLAMINOFLUORENE-INDUCED HEPATIC
   TUMORIGENESIS; ENZYME-ALTERED FOCI; RAT-LIVER; FACTOR RECEPTOR;
   TGF-ALPHA; HEPATOCELLULAR-CARCINOMA; PHENOBARBITAL PROMOTION;
   POLYOMA-VIRUS; EXPRESSION
AB Transforming growth factor alpha (TGF-alpha) has been shown to induce liver tumors within 1 year in transgenic male mice in which this potent mitogen is overexpressed. To determine more precisely how TGF-alpha participates in multistep tumorigenesis of the liver, genotoxic (diethylnitrosamine or dimethylnitrosamine) and nongenotoxic (phenobarbital) chemical carcinogens were administered independently to TGF-alpha transgenic mice [line MT42 on a Crl:CD-1(ICR)BR background]. TGF-alpha overexpression dramatically accelerated carcinogen-induced hepatocarcinogenesis in MT42 males but not females. Interestingly, all three chemical agents were found to enhance strongly both hepatic tumor formation and progression in TGF-alpha transgenic male mice. In this study 100%, 90%, and 78% of transgenic males exposed to diethylnitrosamine, dimethylnitrosamine or phenobarbital, respectively, developed tumors between 24 and 32 weeks of age. Moreover, approximately 70% of tumor-bearing transgenic mice from each treatment group had hepatocellular carcinomas; no malignant lesions were found in any carcinogen-treated or untreated nontransgenic mice or in untreated MT42 mice at this age. These results demonstrate that chemical agents as diverse as nitrosamines and phenobarbital act as cocarcinogens with TGF-alpha in the livers of these transgenic mice, indicating that TGF-alpha possesses the unique ability to complement both initiation and promotion in hepatocarcinogenesis. Furthermore, because carcinogen-induced malignant conversion was restricted to transgenic mice, constitutive TGF-alpha overexpression may promote liver tumor progression as well.
C1 NCI,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BLDG 37,ROOM 2E24,BETHESDA,MD 20892.
   NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,PATHOL HISTOTECHNOL LAB,FREDERICK,MD 21702.
   NCI,OFF LAB ANIM SCI,VET & TUMOR PATHOL SECT,FREDERICK,MD 21702.
FU NCI NIH HHS [N01-CO-74102]
NR 67
TC 51
Z9 51
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W.,
   PHILADELPHIA, PA 19106
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD SEP 15
PY 1993
VL 53
IS 18
BP 4329
EP 4336
PG 8
WC Oncology
SC Oncology
GA LW553
UT WOS:A1993LW55300035
PM 8364928
ER

PT J
AU LEWIN, AH
   SKOLNICK, P
   MARVIZON, JC
   PAUL, IA
   BOWEN, JP
AF LEWIN, AH
   SKOLNICK, P
   MARVIZON, JC
   PAUL, IA
   BOWEN, JP
TI REQUIREMENTS FOR HIGH-AFFINITY BINDING OF GLYCINE ANALOGS TO THE GLYCINE
   SITE OF THE NMDA RECEPTOR COMPLEX
SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION
LA English
DT Article
DE STRYCHNINE-INSENSITIVE GLYCINE SITE; NMDA RECEPTOR COMPLEX; (HIGH
   AFFINITY)
ID CENTRAL NERVOUS-SYSTEM; AMINO-ACID RECEPTORS; STRUCTURAL REQUIREMENTS;
   ANTICONVULSANT MK-801; MODULATORY SITE; XENOPUS OOCYTES; H-3 GLYCINE;
   RAT-BRAIN; ASPARTATE; ANTAGONIST
AB Correlation of the isopotential contours of the optimized conformations of a series of alpha-amino acids, in their neutral zwitterionic forms, with their potencies to inhibit [H-3]glycine binding and to enhance [H-3]10,11-dihydro-5-methyl-5H-dibenzo[a,d]cyclohepten-5,10-imine ([H-3]MK-801) binding, leads to the following conclusions: (a) steric congestion at the amino group is detrimental to binding potency; (b) a zwitterionic amino acid is required for high affinity to the receptor; (c) a conformation in which the carboxylate group is at a 90-degrees dihedral angle to the ammonium nitrogen is preferred for high affinity; and (d) placing the carbon backbone of the zwitterionic alpha-amino acid, in its preferred conformation, above the plane defined by the ammonium nitrogen and the carboxylate oxygen atoms, and viewing the molecule along the nitrogen to carboxylate carbon axis, there is a space forbidden to the ligand (receptor-required-space) to the left.
C1 NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892.
   UNIV GEORGIA,COMPUTAT CTR MOLEC STRUCT & DESIGN,DEPT CHEM,ATHENS,GA 30602.
RP LEWIN, AH (reprint author), RES TRIANGLE INST,POB 12194,RES TRIANGLE PK,NC 27709, USA.
FU DS NIH HHS [NINDS 5 R01 27859]
NR 40
TC 5
Z9 5
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0922-4106
J9 EUR J PHARM-MOLEC PH
JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect.
PD SEP 15
PY 1993
VL 247
IS 1
BP 1
EP 10
DI 10.1016/0922-4106(93)90131-R
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA LZ242
UT WOS:A1993LZ24200001
PM 8258354
ER

PT J
AU WONG, G
   GU, ZQ
   DECOSTA, B
   SKOLNICK, P
AF WONG, G
   GU, ZQ
   DECOSTA, B
   SKOLNICK, P
TI LABELING OF DIAZEPAM-SENSITIVE AND DIAZEPAM-INSENSITIVE BENZODIAZEPINE
   RECEPTORS WITH [H-3]
   TERT-BUTYL-8-CHLORO-5,6-DIHYDRO-5-METHYL-6-OXO-4H-IMIDAZO[1,5-A][1,4]BEN
   ZODIAZEPINE 3-CARBOXYLATE (ZG-63)
SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION
LA English
DT Article
DE GABA(A) RECEPTOR; GABA (GAMMA-AMINOBUTYRIC ACID); DIAZEPAM-INSENSITIVE
   BENZODIAZEPINE RECEPTOR; ZG-63
ID GABA-A RECEPTORS; ALCOHOL ANTAGONIST; BINDING-SITES; RO-15-4513 BINDING;
   H-3 RO-15-4513; RAT; PHARMACOLOGY; ETHANOL; SUBUNIT;
   IMIDAZOBENZODIAZEPINE
AB A diazepam-insensitive subtype of benzodiazepine receptor has been identified in the cerebella of several species, including man. t-Butyl-8-chloro-5,6-dihydro-5-methyl-6-oxo-4H-imidazo[1,5-a][1,4]benzodiazepine 3-carboxylate (ZG-63) was recently described as a selective, high affinity ligand at diazepam-insensitive benzodiazepine receptors. This compound was tritiated, and its properties as a radioligand evaluated in rat brain membranes. Consistent with the high affinity and selectivity described for the non-radioactive form of this compound, saturation analyses    of [H-3]ZG-63 binding to cerebellar diazepam-insensitive and other, diazepam-sensitive benzodiazepine receptors revealed K(d) values of 2.6 +/- 0.2 nM and 10.6 +/- 1.4 nM, respectively. The density (B(max)) of cerebellar diazepam-insensitive receptors labelled with   [H-3]ZG-63 was not significantly different from values obtained with the prototypical diazepam-insensitive receptor ligand    [H-3]Ro 15-4513, representing approximately 30% of total cerebellar benzodiazepine receptors. [H-3]ZG-63 also labelled cortical diazepam-sensitive benzodiazepine receptors, with B(max) values that were not significantly different from those obtained with [H-3]flunitrazepam. Diazepam-insensitive benzodiazepine receptors in rat cerebral cortex could be detected with   [H-3]ZG-63, but the densities of these sites are a very minor component (less-than-or-equal-to 5%) of total benzodiazepine receptors. In the presence of GABA,          [H-3]ZG-63 behaved as a 'gamma-aminobutyric acid (GABA) -positive', 'GABA-negative', and 'GABA-neutral' ligand at cortical diazepam-sensitive receptors, cerebellar diazepam-sensitive receptors, and cerebellar diazepam-insensitive benzodiazepine receptors, respectively. This profile differs from the prototype diazepam-insensitive receptor ligand, [H-3]Ro 15-4513. Competition studies demonstrated a very high correlation (r2 = 0.98; P < 0.002) between the potencies of a series of benzodiazepine receptor ligands to inhibit       [H-3]ZG-63 and   [H-3]Ro 15-4513 binding to cerebellar diazepam-insensitive receptors. The high affinity and selectivity of [H-3]ZG-63 for diazepam-insensitive receptors (diazepam-insensitive/diazepam-sensitive ratio of approximately 0.25) together with a GABA-shift profile which differs from Ro 15-4513 suggests that this compound may be useful in elucidating the function(s) of this benzodiazepine receptor subtype.
C1 NIDDKD,MED CHEM LAB,BETHESDA,MD 20892.
RP WONG, G (reprint author), NIDDKD,NEUROSCI LAB,BLDG 8,RM 111,BETHESDA,MD 20892, USA.
NR 34
TC 10
Z9 10
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0922-4106
J9 EUR J PHARM-MOLEC PH
JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect.
PD SEP 15
PY 1993
VL 247
IS 1
BP 57
EP 63
DI 10.1016/0922-4106(93)90137-X
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA LZ242
UT WOS:A1993LZ24200007
PM 8258361
ER

PT J
AU NOWAK, G
   PAUL, IA
   POPIK, P
   YOUNG, A
   SKOLNICK, P
AF NOWAK, G
   PAUL, IA
   POPIK, P
   YOUNG, A
   SKOLNICK, P
TI CA2+ ANTAGONISTS EFFECT AN ANTIDEPRESSANT-LIKE ADAPTATION OF THE NMDA
   RECEPTOR COMPLEX
SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION
LA English
DT Note
DE NIMODIPINE; BAY-K8644; STRYCHNINE-INSENSITIVE GLYCINE RECEPTORS
ID BEHAVIORAL DESPAIR
AB Chronic, but not acute treatment of mice with nimodipine and diltiazem produce significant increases in the IC50 of glycine to inhibit [H-3]5,7-dichlorokynurenic acid binding in cerebral cortex. Such adaptive changes in the ligand binding properties of the NMDA receptor complex are also manifested following chronic treatment with antidepressants from every principal therapeutic class. These findings indicate voltage-dependent calcium channel antagonists would be strong candidates for rigorous clinical trials in depressive disorders.
C1 NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892.
RI Popik, Piotr/R-5383-2016
OI Popik, Piotr/0000-0003-0722-1263
NR 7
TC 18
Z9 18
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0922-4106
J9 EUR J PHARM-MOLEC PH
JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect.
PD SEP 15
PY 1993
VL 247
IS 1
BP 101
EP 102
DI 10.1016/0922-4106(93)90144-X
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA LZ242
UT WOS:A1993LZ24200014
PM 8258355
ER

PT J
AU KANTOROW, M
   BECKER, K
   SAX, CM
   OZATO, K
   PIATIGORSKY, J
AF KANTOROW, M
   BECKER, K
   SAX, CM
   OZATO, K
   PIATIGORSKY, J
TI BINDING OF TISSUE-SPECIFIC FORMS OF ALPHA-A-CRYBP1 TO THEIR REGULATORY
   SEQUENCE IN THE MOUSE ALPHA-A-CRYSTALLIN-ENCODING GENE - DOUBLE-LABEL
   IMMUNOBLOTTING OF UV-CROSS-LINKED COMPLEXES
SO GENE
LA English
DT Article
DE RECOMBINANT DNA; EYE LENS; NF-KAPPA-B TRANSCRIPTION FACTOR; WESTERN
   ANALYSIS
ID NF-KAPPA-B; MAJOR HISTOCOMPATIBILITY COMPLEX; PROTEIN; LENS; DNA;
   PROMOTER; EXPRESSION; ACTIVATION; RECOGNIZE; SUBUNITS
AB The alphaA-CRYBP1 regulatory sequence (alphaA-CRYBP1RS), at nucleotides -66 to -57 of the mouse alphaA-crystallin-encoding gene (alphaA-CRY) promoter, is an important control element involved in the regulation of mouse alphaA-CRY expression. The gene encoding a protein (alphaA-CRYBP1) that specifically binds to the alphaA-CRYBP1RS sequence has been cloned from a cultured mouse lens cell line. In the present study, we have used an antibody (specific to the alphaA-CRYBP1 protein and made against a synthetic peptide) to directly identify UV-crosslinked protein-DNA complexes via a double-label immunoblotting technique. Multiple alphaA-CRYBP1 antigenically related proteins interacted with alphaA-CRYBP1RS in nuclear extracts from both a cloned mouse lens cell line (alphaTN4-1) that expresses alphaA-CRY and a mouse fibroblast line (L929) that does not express the gene. Two sizes (50 kDa and 90 kDa) of proteins reacting with the alphaA-CRYBP1-specific Ab were detected in both cell lines and, in addition, a > 200-kDa protein reacting with the Ab was unique to the fibroblast line. Thus, alphaA-CRYBP1 antigenically related proteins interact with alphaA-CRYBP1RS regardless of alphaA-CRY expression. Moreover, differential processing of the alphaA-CRYBP1 protein and/or alternative splicing of the alphaA-CRY transcript may affect expression of alphaA-CRY.
C1 NEI,MOLEC & DEV BIOL LAB,BLD 6,RM 203,BETHESDA,MD 20892.
   NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892.
NR 33
TC 16
Z9 16
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
J9 GENE
JI Gene
PD SEP 15
PY 1993
VL 131
IS 2
BP 159
EP 165
DI 10.1016/0378-1119(93)90289-F
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA MA233
UT WOS:A1993MA23300001
PM 8406008
ER

PT J
AU SUN, Y
   HEGAMYER, G
   COLBURN, NH
AF SUN, Y
   HEGAMYER, G
   COLBURN, NH
TI SEQUENCE OF MANGANESE SUPEROXIDE DISMUTASE-ENCODING CDNAS FROM MULTIPLE
   MOUSE ORGANS
SO GENE
LA English
DT Note
DE RECOMBINANT DNA; REVERSE TRANSCRIPTASE; PCR; MITOCHONDRIAL ENZYME
ID DNA
AB Manganese superoxide dismutase (MnSOD)-encoding cDNAs from multiple mouse organs, including liver, kidney, brain, spleen and heart, show three sequence differences compared with the previously published mouse placenta MnSOD cDNA. The differences cause substitutions of Val-7-->Gly (GTG-->GGT) and Met114-->Val (ATG-->GTG) and a G746 deletion in the 3' untranslated region. The analysis, by reverse transcriptase-polymerase chain reaction-direct sequencing, of BALB/c mouse placenta RNA revealed the same sequence in the placenta MnSOD as that from multiple mouse organs. The data presented will be useful for wild-type sequence verification and possible point mutation detection.
RP SUN, Y (reprint author), NCI,FCRDC,LVC,CELL BIOL SECT,BLDG 560,RM 21-89,FREDERICK,MD 21702, USA.
NR 7
TC 8
Z9 9
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
J9 GENE
JI Gene
PD SEP 15
PY 1993
VL 131
IS 2
BP 301
EP 302
DI 10.1016/0378-1119(93)90311-P
PG 2
WC Genetics & Heredity
SC Genetics & Heredity
GA MA233
UT WOS:A1993MA23300023
PM 8406027
ER

PT J
AU BLOT, WJ
   DEVESA, SS
   FRAUMENI, JF
AF BLOT, WJ
   DEVESA, SS
   FRAUMENI, JF
TI CONTINUING CLIMB IN RATES OF ESOPHAGEAL ADENOCARCINOMA - AN UPDATE
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
RP BLOT, WJ (reprint author), NCI,BETHESDA,MD 20892, USA.
NR 2
TC 351
Z9 354
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD SEP 15
PY 1993
VL 270
IS 11
BP 1320
EP 1320
DI 10.1001/jama.270.11.1320
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA LW345
UT WOS:A1993LW34500027
PM 8360967
ER

PT J
AU NISHIMURA, H
   ZARNOWSKI, MJ
   SIMPSON, IA
AF NISHIMURA, H
   ZARNOWSKI, MJ
   SIMPSON, IA
TI GLUCOSE-TRANSPORTER RECYCLING IN RAT ADIPOSE-CELLS - EFFECTS OF
   POTASSIUM-DEPLETION
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RECEPTOR-MEDIATED ENDOCYTOSIS; COATED PIT FORMATION; FACTOR-II BINDING;
   PLASMA-MEMBRANE; POTENTIAL MECHANISM; STIMULATORY ACTION; 3T3-L1
   ADIPOCYTES; CLATHRIN LATTICES; INSULIN-RECEPTORS; TRANSLOCATION
AB Depletion of intracellular potassium (K+) induced a 4-fold increase in basal and 1 muM phorbol-12-myristate-13-acetate (PMA)-stimulated 3-O-methylglucose transport in rat adipose cells. K+ depletion had no effect on the maximum insulin (0.7 muM)-stimulated transport rate but enhanced the sensitivity to insulin 3-fold (EC50= 0.05 versus 0.15 nM) by a mechanism that did not result from changes in the insulin receptor binding, autophosphorylation, or tyrosine kinase activity. Western blotting analysis revealed that K+ depletion induced a 2.2-fold increase in GLUT4 in plasma membranes from basal cells, enhanced the PMA-stimulated GLUT4 translocation by 4-fold, and increased the 5-fold insulin-stimulated GLUT4 translocation by 15%, indicating the presence of an inactive GLUT4 intermediate. The time course for insulin's stimulation of transport activity was accelerated by K+ depletion (t1/2 = 3 versus 1.5 min). Conversely, the reversal of transport activity, on removal of insulin, was delayed (t1/2 = 11 versus 22 min). The corresponding t1/2 values for the loss of GLUT4 were 22 min in control cells and 40 min in K+-depleted cells, again indicating the existence of an inactive intermediate. Photolabeling intact cells with the impermeant, exofacial photolabel 2-N-4-(1-azi-2,2,2-trifluoroethyl)benzoyl-1,3-bis(D-mannos-4-yloxy)-2-propylamine in the continuous presence of insulin revealed that K+ depletion had no effect on the GLUT4 externalization rate but halved the rate of internalization. K+ depletion elicited entirely analogous effects on the recycling of insulin-like growth factor II/mannose 6-phosphate receptor, strongly supporting the involvement of a coated pit mechanism in the recycling of GLUT4 transporters. An inactive conformation of GLUT4 has been detected in plasma membranes from insulin-stimulated cells, which is enhanced by K+ depletion, suggesting a limitation in the adipose cells' capacity to express active GLUT4 transporters.
C1 NIDDK,DIABET BRANCH,EDMNS,BLDG 10,RM 5N102,BETHESDA,MD 20892.
NR 45
TC 34
Z9 34
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 SEP 15
PY 1993
VL 268
IS 26
BP 19246
EP 19253
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LW819
UT WOS:A1993LW81900018
PM 7690030
ER

PT J
AU ENGLANDER, EW
   WOLFFE, AP
   HOWARD, BH
AF ENGLANDER, EW
   WOLFFE, AP
   HOWARD, BH
TI NUCLEOSOME INTERACTIONS WITH A HUMAN ALU ELEMENT - TRANSCRIPTIONAL
   REPRESSION AND EFFECTS OF TEMPLATE METHYLATION
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RNA POLYMERASE-III; TUMOR VIRUS PROMOTER; CPG BINDING-PROTEIN; DNA
   METHYLATION; INHIBITS TRANSCRIPTION; REGULATORY NUCLEOSOME; CHROMATIN
   STRUCTURE; GENE-EXPRESSION; SEQUENCE; ORGANIZATION
AB Alu interspersed repetitive elements possess internal RNA polymerase III promoters which are strongly transcribed in vitro, yet these elements are nearly silent in somatic cells. To examine whether repression by chromatin proteins could contribute to the low level of Alu expression, a conserved Alu element from the fourth intron of the human alpha-fetoprotein gene was reconstituted with purified octamer or tetramer particles. Analysis of reconstitutes revealed that this Alu element directed translational and rotational positioning of octamers as well as tetramers. In vitro transcription experiments with reconstituted templates demonstrated that RNA polymerase III-dependent transcription of the Alu element was profoundly repressed by positioned octamer particles. Furthermore, complete CpG methylation of this template enhanced the capacity of tetramers to repress transcription.
C1 NICHHD,MOLEC GROWTH REGULAT LAB,BLDG 6,RM 416,BETHESDA,MD 20892.
   NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892.
NR 66
TC 89
Z9 90
U1 1
U2 3
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 SEP 15
PY 1993
VL 268
IS 26
BP 19565
EP 19573
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LW819
UT WOS:A1993LW81900065
PM 8366099
ER

PT J
AU YU, BW
   ICHINOSE, I
   BONHAM, MA
   ZAJAC-KAYE, M
AF YU, BW
   ICHINOSE, I
   BONHAM, MA
   ZAJAC-KAYE, M
TI SOMATIC MUTATIONS IN C-MYC INTRON-I CLUSTER IN DISCRETE DOMAINS THAT
   DEFINE PROTEIN-BINDING SEQUENCES
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LYMPHOMA CELL-LINE; HEAVY-CHAIN LOCUS; BURKITT-LYMPHOMA; CHROMATIN
   STRUCTURE; TRANSCRIPTION INITIATION; VARIANT TRANSLOCATION;
   TRANS-ACTIVATION; 1ST EXON; GENE; PROMOTER
AB The activated c-myc allele in Burkitt's lymphoma tumor cells is associated with a clustering of somatic mutations within intron I near the exon I boundary. We have identified several discrete protein binding sites within this region of c-myc intron I designated as myc intron factor-1 (MIF-1), MIF-2, and MIF-3. In addition to our previous characterization of a 20-nucleotide binding site for MIF-1, we now have identified adjacent 20-nucleotide and 34-nucleotide binding sites for MIF-2 and MIF-3, respectively. All three elements are protected from exonuclease digestion by nuclear protein extracts, and each gives rise to a distinct migration pattern on mobility shift assays. In addition, MIF-1, 2, and 3 share a 5-nucleotide (TTATG) internal sequence, which may account for cross-competition of these binding sites in the exonuclease protection experiment. Deletion mutant analyses showed that selective removal of the MIF-3 binding site alone was sufficient to enhance chloramphenicol acetyltransferase reporter activity similar to that observed with larger deletions of myc intron I. We have demonstrated that somatic mutations in activated c-myc alleles are frequently clustered in discrete domains that define protein recognition sequences.
C1 NCI, BIOL CHEM LAB, BLDG 37-5D02, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA.
   NCI, MED BRANCH, BETHESDA, MD 20892 USA.
NR 46
TC 31
Z9 31
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 SEP 15
PY 1993
VL 268
IS 26
BP 19586
EP 19592
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LW819
UT WOS:A1993LW81900068
PM 8366102
ER

PT J
AU WANGE, RL
   MALEK, SN
   DESIDERIO, S
   SAMELSON, LE
AF WANGE, RL
   MALEK, SN
   DESIDERIO, S
   SAMELSON, LE
TI TANDEM SH2 DOMAINS OF ZAP-70 BIND TO T-CELL ANTIGEN RECEPTOR-ZETA AND
   CD3-EPSILON FROM ACTIVATED JURKAT T-CELLS
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PROTEIN-TYROSINE KINASE; SIGNAL TRANSDUCTION; PDGF RECEPTOR; CHAIN;
   PHOSPHORYLATION; ASSOCIATION; CD4; LYMPHOCYTES; INDUCTION; P59FYN
AB A proximal and critical biochemical event upon T cell antigen receptor (TCR) stimulation is the activation of a protein tyrosine kinase (PTK) pathway. ZAP-70, a PTK of the p72syk family, associates with phosphorylated TCR subunits upon TCR stimulation. Here we report that the tandem SH2 domains of ZAP-70, expressed as a fusion protein, bind to tyrosine-phosphorylated CD3epsilon and TCRzeta from activated Jurkat T cell lysates. The single N- and C-terminal SH2 domains of ZAP-70, expressed separately, do not bind these TCR subunits. In comparison to fusion proteins containing SH2 domains from other proteins, the tandem SH2 domains of ZAP-70 demonstrate a remarkably restricted repertoire of protein binding, binding only TCRzeta and CD3epsilon. ZAP-70 is also recovered in the binding assay, but this is likely to be a consequence of its interaction with multiple SH2 binding sites on the zeta-zeta and CD3epsilon-containing dimers.
C1 JOHNS HOPKINS UNIV,SCH MED,HOWARD HUGHES MED INST,BALTIMORE,MD 21205.
   JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205.
RP WANGE, RL (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA.
NR 37
TC 249
Z9 250
U1 2
U2 4
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 SEP 15
PY 1993
VL 268
IS 26
BP 19797
EP 19801
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LW819
UT WOS:A1993LW81900096
PM 8366117
ER

PT J
AU HARADA, N
   SANTOSARGUMEDO, L
   CHANG, R
   GRIMALDI, JC
   LUND, FE
   BRANNAN, CI
   COPELAND, NG
   JENKINS, NA
   HEATH, AW
   PARKHOUSE, RME
   HOWARD, M
AF HARADA, N
   SANTOSARGUMEDO, L
   CHANG, R
   GRIMALDI, JC
   LUND, FE
   BRANNAN, CI
   COPELAND, NG
   JENKINS, NA
   HEATH, AW
   PARKHOUSE, RME
   HOWARD, M
TI EXPRESSION CLONING OF A CDNA-ENCODING A NOVEL MURINE B-CELL ACTIVATION
   MARKER - HOMOLOGY TO HUMAN-CD38
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID HUMAN LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; CD38 MOLECULE;
   DIFFERENTIATION; ANTIGEN; INTERLEUKIN-4; PROLIFERATION; DETERMINANTS;
   THYMOCYTES; RECEPTOR
AB A rat mAb (NIM-R5) has recently been prepared against a novel murine B cell activation marker. We report here isolation of a cDNA (I-19) encoding the B cell-derived protein recognized by NIM-R5 antibody. This cDNA contains an open reading frame that encodes a polypeptide of 304 amino acids with a predicted molecular weight of 34,500. The existence of a 22-amino acid hydrophobic region located 23 amino acids from the amino terminal of the deduced protein, together with four potential N-linked glycosylation sites, characterize the deduced protein encoded by I-19 cDNA as a typical type II transmembrane glycoprotein. Although I-19 cDNA appears to encode a novel murine protein, its nucleotide sequence and deduced amino acid sequence show approximately 70% homology to the previously reported sequence of human CD38, suggesting that I-19 cDNA encodes either the mouse homologue of CD38 or a closely related protein. Northern blot analysis of the expression of this cDNA product in a variety of cell types, together with immunoprecipitation of the recombinant protein expressed in BaF3 cells, indicated that I-19 cDNA encodes not only the epitope recognized by NIM-R5 but also a protein that is indistinguishable biochemically and in terms of distribution from the murine B cell activation marker recognized by NIM-R5 antibody. Chromosomal mapping studies have localized this locus to the proximal region of mouse chromosome 5. We anticipate that the availability of probes for the murine B cell activation marker recognized by NIM-R5, and the recombinant protein itself, will greatly aid efforts to define the role of this molecule in murine B cell development.
C1 DNAX RES INST MOLEC & CELLULAR BIOL INC,901 CALIF AVE,PALO ALTO,CA 94304.
   NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702.
   INST ANIM HLTH,PIRBRIGHT LAB,PIRBRIGHT GU24 ONF,SURREY,ENGLAND.
OI Parkhouse, Michael/0000-0001-5967-3291; Santos-Argumedo,
   Leopoldo/0000-0002-4772-0713
FU NCI NIH HHS [N01-CO-74101]
NR 38
TC 100
Z9 101
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD SEP 15
PY 1993
VL 151
IS 6
BP 3111
EP 3118
PG 8
WC Immunology
SC Immunology
GA LY492
UT WOS:A1993LY49200020
PM 8376770
ER

PT J
AU SYLVESTER, I
   SUFFREDINI, AF
   BOUJOUKOS, AJ
   MARTICH, GD
   DANNER, RL
   YOSHIMURA, T
   LEONARD, EJ
AF SYLVESTER, I
   SUFFREDINI, AF
   BOUJOUKOS, AJ
   MARTICH, GD
   DANNER, RL
   YOSHIMURA, T
   LEONARD, EJ
TI NEUTROPHIL ATTRACTANT PROTEIN-1 AND MONOCYTE CHEMOATTRACTANT PROTEIN-1
   IN HUMAN SERUM - EFFECTS OF INTRAVENOUS LIPOPOLYSACCHARIDE ON FREE
   ATTRACTANTS, SPECIFIC IGG AUTOANTIBODIES AND IMMUNE-COMPLEXES
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID NECROSIS-FACTOR; ANTIBODIES; CYTOKINE; INTERLEUKIN-8; EXPRESSION
AB We recently found that normal human sera contain IgG antibodies against two chemoattractants, neutrophil attractant protein-1 (NAP-1/IL-8) and monocyte chemoattractant protein-1 (MCP-1), as well as immune complexes of these proteins. Intravenously administered LPS was reported to cause a sharp rise in serum NAP-1 concentration. Our study was designed to determine if LPS also caused an increase in MCP-1 and to measure associated changes in concentrations of antibody and immune complex. LPS caused a rise to a peak within 2 to 3 h in serum concentrations of free NAP-1 and MCP-1, followed by an almost equally rapid fall toward base-line levels by about 5 h postinjection. MCP-1 concentration in sera from the 11 subjects rose to a peak of 330 +/- 52 pM. The peak value for NAP-1 was 80 +/- 11 pM. In 10 of the 11 subjects, free IgG autoantibody to MCP-1 decreased from a mean pre-LPS value of 1820 +/- 660 pM to a mean low of 53% of the respective initial values. Corresponding data for IgG anti-NAP-1 were a pre-LPS concentration of 216 +/- 7 pM, which decreased to a mean low of 44% of the respective initial values. The finding in some subjects of a rapid rise in free antibody after the nadir suggests the possibility of acute regulation of autoantibody secretion rates. Although the results suggested that LPS-induced chemoattractant combined with free antibody, serum concentrations of MCP-1-IgG or NAP-1-IgG did not increase, which points to an as yet unknown mechanism for trapping and elimination of the immune complexes.
C1 NCI,FCRDC,IMMUNOBIOL LAB,IMMUNOPATHOL SECT,BLDG 560,RM 12-17,FREDERICK,MD 21702.
   NIH,WARREN G MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BETHESDA,MD 20892.
   NCI,FCRDC,DYN CORP PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702.
FU NCI NIH HHS [N01-CO-74102]
NR 17
TC 79
Z9 79
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD SEP 15
PY 1993
VL 151
IS 6
BP 3292
EP 3298
PG 7
WC Immunology
SC Immunology
GA LY492
UT WOS:A1993LY49200040
PM 8376779
ER

PT J
AU HOOKS, JJ
   PERCOPO, C
   WANG, Y
   DETRICK, B
AF HOOKS, JJ
   PERCOPO, C
   WANG, Y
   DETRICK, B
TI RETINA AND RETINAL-PIGMENT EPITHELIAL-CELL AUTOANTIBODIES ARE PRODUCED
   DURING MURINE CORONAVIRUS RETINOPATHY
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID EXPERIMENTAL AUTOIMMUNE UVEITIS; VIRUS B3-INDUCED MYOCARDITIS; HUMAN
   SYMPATHETIC OPHTHALMIA; PARANEOPLASTIC RETINOPATHY; MOLECULAR MIMICRY;
   STRAIN JHM; S-ANTIGEN; EXPRESSION; ANTIBODIES; DEMYELINATION
AB The murine coronavirus, mouse hepatitis virus (MHV), JHM strain, induces a biphasic retinal disease in adult BALB/c mice. In the early phase of the disease, day 1 to 7, a retinal vasculitis is noted and is associated with the presence of virus particles. In the late phase of the disease, day 10 to 140, a retinal degeneration is observed and is associated with the absence of both virus particles and inflammatory cells. We show that the retinal degenerative process is also associated with the presence of antiretinal autoantibodies. In total, 22 of 23 sera collected from 10 to 70 days after JHM virus inoculation contained antiretinal autoantibodies. These autoantibodies are not found in sera from normal or mock-injected mice. Antibodies to retinal tissue were identified as two distinct patterns of immunoperoxidase staining on frozen sections of normal rat eyes, retinal autoantibodies and retinal pigment epithelium (RPE) autoantibodies. The antiretinal autoantibodies first appeared as IgM class antibodies that shifted to IgG class autoantibodies. The anti-RPE cell autoantibodies were predominantly of the IgG class. Sera that were positive for these autoantibodies did not stain with liver or kidney sections but 2 of 3 did react with rat brain sections. A second mouse strain, CD-1, was also evaluated because these animals respond to JHM virus inoculation by developing only the early phase of this disease, i.e. vasculitis. On day 10 postinoculation, the retina architecture has a normal appearance. In these mice, which are free of a retinal degeneration, antiretinal autoantibodies are not produced. However, just as is noted in the BALB/c mice, antivirus neutralizing antibodies are produced in the infected CD-1 mice. These findings suggest a role for autoimmunity in the pathogenesis of murine coronavirus induced retinal degeneration. This study establishes an animal model for the study of humoral autoimmune responses in human retinal degenerations.
C1 GEORGE WASHINGTON UNIV, MED CTR, DEPT PATHOL, WASHINGTON, DC 20052 USA.
RP HOOKS, JJ (reprint author), NEI, IMMUNOL LAB, IMMUNOL & VIROL SECT, BETHESDA, MD 20892 USA.
NR 53
TC 28
Z9 28
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD SEP 15
PY 1993
VL 151
IS 6
BP 3381
EP 3389
PG 9
WC Immunology
SC Immunology
GA LY492
UT WOS:A1993LY49200049
PM 8397257
ER

PT J
AU MURPHY, WJ
   REYNOLDS, CW
   TIBERGHIEN, P
   LONGO, DL
AF MURPHY, WJ
   REYNOLDS, CW
   TIBERGHIEN, P
   LONGO, DL
TI NATURAL-KILLER-CELLS AND BONE-MARROW TRANSPLANTATION
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Review
ID VERSUS-HOST DISEASE; ANTI-ASIALO GM1; LARGE GRANULAR LYMPHOCYTES;
   COLONY-STIMULATING FACTOR; NK-CELLS; T-CELL; GRAFT-REJECTION; HYBRID
   RESISTANCE; EFFECTOR-CELLS; DONOR ORIGIN
AB Bone marrow transplantation is currently used in the treatment of a variety of neoplastic and nonneoplastic diseases. However, significant obstacles still limit the efficacy of this procedure. These include the occurrence of graft-versus-host disease, the failure of the marrow to engraft, the susceptibility of patients to opportunistic infections during the period of immunodeficiency after transplantation before full recovery of immune function, and finally, the recurrence of the cancer. Natural killer (NK) cells are lymphoid cells responsible for mediating a variety of immunologic and homeostatic functions. Initially described almost 20 years ago, the full range of functions carried out by these enigmatic cells continues to unfold. NK cells may be both beneficial and deleterious in bone marrow transplantation, depending on their genotype and activation status. Resting host-derived NK cells appear capable of mediating resistance to both autologous and allogeneic bone marrow cell grafts. At the other end of the spectrum, the transfer of activated NK cells of donor type appears to produce multiple beneficial effects during both syngeneic and allogeneic bone marrow transplantation. Here, we review and attempt to reconcile the literature concerning the basic biology of NK cells and their effects on hematopoiesis, both in vitro and in vivo. We also discuss the current issues in bone marrow transplantation and the potential role NK cells may play in determining the outcome of the marrow graft, the occurrence of graft-versus-host disease, and the generation of a graft-versus-tumor response when bone marrow transplantation is used for the treatment of cancer.
RP MURPHY, WJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702, USA.
FU NCI NIH HHS [N01CO74102]
NR 104
TC 52
Z9 53
U1 0
U2 0
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD SEP 15
PY 1993
VL 85
IS 18
BP 1475
EP 1482
DI 10.1093/jnci/85.18.1475
PG 8
WC Oncology
SC Oncology
GA LW561
UT WOS:A1993LW56100011
PM 8360930
ER

PT J
AU BLOT, WJ
   LI, JY
   TAYLOR, PR
   GUO, WD
   DAWSEY, S
   WANG, GQ
   YANG, CS
   ZHENG, SF
   GAIL, M
   LI, GY
   YU, Y
   LIU, BQ
   TANGREA, J
   SUN, YH
   LIU, FS
   FRAUMENI, JF
   ZHANG, YH
   LI, B
AF BLOT, WJ
   LI, JY
   TAYLOR, PR
   GUO, WD
   DAWSEY, S
   WANG, GQ
   YANG, CS
   ZHENG, SF
   GAIL, M
   LI, GY
   YU, Y
   LIU, BQ
   TANGREA, J
   SUN, YH
   LIU, FS
   FRAUMENI, JF
   ZHANG, YH
   LI, B
TI NUTRITION INTERVENTION TRIALS IN LINXIAN, CHINA - SUPPLEMENTATION WITH
   SPECIFIC VITAMIN MINERAL COMBINATIONS, CANCER INCIDENCE, AND
   DISEASE-SPECIFIC MORTALITY IN THE GENERAL-POPULATION
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID DOUBLE-BLIND INTERVENTION; ESOPHAGEAL CANCER; BETA-CAROTENE; RIBOFLAVIN
   DEFICIENCY; STOMACH-CANCER; GASTRIC-CANCER; BLOOD-PRESSURE; HIGH-RISK;
   SELENIUM; MICRONUCLEI
AB Background: Epidemiologic evidence indicates that diets high in fruits and vegetables are associated with a reduced risk of several cancers, including cancers of the esophagus and stomach. Vitamins and minerals in these foods may contribute to the reduced cancer risk. The people of Linxian County, China, have one of the world's highest rates of esophageal/gastric cardia cancer and a persistently low intake of several micronutrients. Purpose: We sought to determine if dietary supplementation with specific vitamins and minerals can lower mortality from or incidence of cancer as well as mortality from other diseases in Linxian. Methods: Individuals of ages 40-69 were recruited in 1985 from four Linxian communes. Mortality and cancer incidence during March 1986-May 1991 were ascertained for 29584 adults who received daily vitamin and mineral supplementation throughout this period. The subjects were randomly assigned to intervention groups according to a one-half replicate of a 24 factorial experimental design. This design enabled testing for the effects of four combinations of nutrients: (A) retinol and zinc; (B) riboflavin and niacin; (C) vitamin C and molybdenum; and (D) beta carotene, vitamin E, and selenium. Doses ranged from one to two times U.S. Recommended Daily Allowances. Results: A total of 2127 deaths occurred among trial participants during the intervention period. Cancer was the leading cause of death, with 32% of all deaths due to esophageal or stomach cancer, followed by cerebrovascular disease (25%). Significantly (P = .03) lower total mortality (relative risk [RR] = 0.91; 95% confidence interval [CI] = 0.84-0.99) occurred among those receiving supplementation with beta carotene, vitamin E, and selenium. The reduction was mainly due to lower cancer rates (RR = 0.87; 95% CI = 0.75-1.00), especially stomach cancer (RR = 0.79; 95% CI = 0.64-0.99), with the reduced risk beginning to arise about 1-2 years after the start of supplementation with these vitamins and minerals. No significant effects on mortality rates from all causes were found for supplementation with retinol and zinc, riboflavin and niacin, or vitamin C and molybdenum. Patterns of cancer incidence, on the basis of 1298 cases, generally resembled those for cancer mortality. Conclusions: The findings indicate that vitamin and mineral supplementation of the diet of Linxian adults, particularly with the combination of beta carotene, vitamin E, and selenium, may effect a reduction in cancer risk in this population. Implications: The results on their own are not definitive, but the promising findings should stimulate further research to clarify the potential benefits of micronutrient supplements.
C1 CHINESE ACAD MED SCI,INST CANC,BEIJING,PEOPLES R CHINA.
RP BLOT, WJ (reprint author), NCI,DIV CANC ETIOL,BIOSTAT BRANCH,6130 EXECUT BLVD,ROCKVILLE,MD 20852, USA.
NR 55
TC 1216
Z9 1252
U1 7
U2 72
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD SEP 15
PY 1993
VL 85
IS 18
BP 1483
EP 1492
DI 10.1093/jnci/85.18.1483
PG 10
WC Oncology
SC Oncology
GA LW561
UT WOS:A1993LW56100012
PM 8360931
ER

PT J
AU LI, JY
   TAYLOR, PR
   LI, B
   DAWSEY, S
   WANG, GQ
   ERSHOW, AG
   GUO, WD
   LIU, SF
   YANG, CS
   SHEN, Q
   WANG, W
   MARK, SD
   ZOU, XN
   GREENWALD, P
   WU, YP
   BLOT, WJ
AF LI, JY
   TAYLOR, PR
   LI, B
   DAWSEY, S
   WANG, GQ
   ERSHOW, AG
   GUO, WD
   LIU, SF
   YANG, CS
   SHEN, Q
   WANG, W
   MARK, SD
   ZOU, XN
   GREENWALD, P
   WU, YP
   BLOT, WJ
TI NUTRITION INTERVENTION TRIALS IN LINXIAN, CHINA - MULTIPLE VITAMIN
   MINERAL SUPPLEMENTATION, CANCER INCIDENCE, AND DISEASE-SPECIFIC
   MORTALITY AMONG ADULTS WITH ESOPHAGEAL DYSPLASIA
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID BLOOD-PRESSURE; BETA-CAROTENE; CARCINOGENESIS; ANTIOXIDANTS; VEGETABLES;
   FRUIT; RATS
AB Background: A number of vitamins and minerals have been shown to influence carcinogenesis in experimental animals. In humans, epidemiologic evidence suggests that intake of fruits and vegetables may reduce risk of esophageal and other cancers. Vitamins and minerals in these foods may contribute to the reduced cancer risk. The people of Linxian, China, have persistently low intake of multiple nutrients and exhibit one of the world's highest rates of esophageal/gastric cardia cancer, with an exceptionally high risk of esophageal dysplasia. Purpose: To determine whether supplementation with multiple vitamins and minerals may reduce esophageal/gastric cardia cancer among persons with esophageal dysplasia, we conducted a 6-year prospective intervention trial in Linxian. Methods: Mortality and cancer incidence were ascertained from May 1985 through May 1991 for 3318 persons with cytologic evidence of esophageal dysplasia who were randomly assigned to receive, throughout that period, daily supplementation with 14 vitamins and 12 minerals or placebo. Doses were typically two to three times U.S. Recommended Daily Allowances. Compliance was assessed by counting unused pills monthly for all trial participants and by assaying nutrient levels in blood collected from samples of individuals randomly selected without replacement every 3 months throughout the trial. Cancers were identified through routine surveillance and by special cytology and endoscopy screenings after 21/2 years and 6 years. Results: A total of 324 deaths occurred during the 6-year intervention period; 167 occurred in the control (placebo) group and 157 occurred in the supplement group. Cancer was the leading cause of death (54% of all deaths); 18% were due to cerebrovascular diseases and 29% to other causes. Cumulative esophageal/gastric cardia death rates were 8% lower (relative risk [RR] = 0.92; 95% confidence interval [CI] = 0.67-1.28) among individuals receiving supplements rather than placebo, a nonsignificant (P>.10) difference. Risk of total mortality was 7% lower (RR = 0.93; 95% CI = 0.75-1.16; P>.10), total cancer 4% lower (RR = 0.96; 95% CI = 0.71-1.29; P>.10), cerebrovascular disease 38% lower (RR = 0.62; 95% CI = 0.37-1.06; P = .08), and other diseases 12% higher (RR = 1.12; 95% CI = 0.74-1.69; P>.10) among the treated group. Cumulative cancer incidence rates were nearly the same in the two groups. Conclusions: No substantial short-term beneficial effect on incidence or mortality for this type of cancer occurred following daily supplementation with multiple vitamins and minerals among adults with precancerous lesions of the esophagus. Implications: Although no statistically significant short-term benefits were observed, longer follow-up should be more informative about the effectiveness of this 6-year supplementation on cancer and other diseases among individuals with esophageal dysplasia.
C1 NCI,DIV CANC ETIOL,BIOSTAT BRANCH,6130 EXECUT BLVD,ROCKVILLE,MD 20852.
   CHINESE ACAD MED SCI,INST CANC,BEIJING,PEOPLES R CHINA.
   NHLBI,BETHESDA,MD 20892.
   RUTGERS UNIV,PISCATAWAY,NJ 08854.
   HENAN MED UNIV,ZHENGZHOU,PEOPLES R CHINA.
NR 30
TC 310
Z9 316
U1 0
U2 4
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD SEP 15
PY 1993
VL 85
IS 18
BP 1492
EP 1498
DI 10.1093/jnci/85.18.1492
PG 7
WC Oncology
SC Oncology
GA LW561
UT WOS:A1993LW56100013
PM 8360932
ER

PT J
AU KOHLER, MF
   MARKS, JR
   WISEMAN, RW
   JACOBS, IJ
   DAVIDOFF, AM
   CLARKEPEARSON, DL
   SOPER, JT
   BAST, RC
   BERCHUCK, A
AF KOHLER, MF
   MARKS, JR
   WISEMAN, RW
   JACOBS, IJ
   DAVIDOFF, AM
   CLARKEPEARSON, DL
   SOPER, JT
   BAST, RC
   BERCHUCK, A
TI SPECTRUM OF MUTATION AND FREQUENCY OF ALLELIC DELETION OF THE P53 GENE
   IN OVARIAN-CANCER
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Note
ID TUMOR-SUPPRESSOR GENE; BREAST-CANCER; TP53 GENE; POLYMORPHISM;
   OVEREXPRESSION; CHROMOSOME-17; MUTAGENESIS; CARCINOMA; NEOPLASMS; LOSSES
AB Background: The p53 gene encodes a nuclear phosphoprotein present in low levels in normal human cells. The wild-type form of this protein functions to restrain inappropriate cellular proliferation. Approximately one half of human epithelial ovarian cancers have mutations in the p53 gene and overexpress the mutant protein product. Deletion of one allele of the p53 gene also frequently occurs in these cancers. Purpose: We sought to define the spectrum of mutations in the p53 gene in epithelial ovarian cancer with respect to both the specific codons involved and the type of mutations observed. We also examined the frequency of allelic deletion of the p53 gene in cancers containing p53 gene mutations. Methods: Tissue samples from the epithelial ovarian cancers of 62 patients were obtained during initial laparotomy. Histologic examination was done to ensure that the experimental samples used in this study contained more than 75% cancer cells. Total RNA was extracted from these samples and separately from matched control noncancerous regions of the surgical specimen or white blood cells. The purified RNAs were reverse transcribed to generate cDNA copies of exons 4-10 of the p53 gene. Two rounds of polymerase chain reaction (PCR) were conducted to produce enough template for DNA sequence analysis of the regions of interest within the p53 gene. Dideoxy sequencing of at least two independent productions of each amplified DNA template was done to confirm the validity of the mutations found. Allelic deletions were identified by PCR and gel electrophoretic techniques to examine three polymorphisms within the p53 gene in cancer-normal DNA pairs. Results: We identified 45 mutations in exons 5-8 of the p53 gene, where mutations frequently have been found in other cancer types. An additional mutation was identified in exon 4. Overall, 72% of the mutations were transitions, 24% transversions, and 4% microdeletions. Allelic deletion of the other p53 allele was seen in 67% of ovarian cancers in which a p53 mutation was present. Germ-line p53 mutations were not found in any patients whose cancers had p53 mutations. Conclusions and Implications: Like p53 mutations in other types of human cancers, those in epithelial ovarian cancers are diverse and occur frequently in exons 5-8. The predominance of transition mutations suggests that p53 mutations in ovarian cancer arise because of spontaneous errors in DNA synthesis and repair rather than the direct interaction of carcinogens with DNA. These molecular data are consistent with data from epidemiologic studies that have failed to demonstrate a convincing relationship between exposure to environmental carcinogens and the development of ovarian cancer.
C1 DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DIV GYNECOL ONCOL,BOX 3079,DURHAM,NC 27710.
   DUKE UNIV,MED CTR,DEPT MED & IMMUNOL,DURHAM,NC 27710.
   DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710.
   DUKE COMPREHENS CANC CTR,DURHAM,NC.
   NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709.
RI Bast, Robert/E-6585-2011; Jacobs, Ian/F-1743-2013
OI Bast, Robert/0000-0003-4621-8462; Jacobs, Ian/0000-0002-8112-4624
FU NCI NIH HHS [CA55640]
NR 41
TC 182
Z9 183
U1 0
U2 4
PU NATL CANCER INSTITUTE
PI BETHESDA
PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD SEP 15
PY 1993
VL 85
IS 18
BP 1513
EP 1519
DI 10.1093/jnci/85.18.1513
PG 7
WC Oncology
SC Oncology
GA LW561
UT WOS:A1993LW56100016
PM 8360934
ER

PT J
AU CAO, XQ
   KOZAK, CA
   LIU, YJ
   NOGUCHI, M
   OCONNELL, E
   LEONARD, WJ
AF CAO, XQ
   KOZAK, CA
   LIU, YJ
   NOGUCHI, M
   OCONNELL, E
   LEONARD, WJ
TI CHARACTERIZATION OF CDNAS ENCODING THE MURINE INTERLEUKIN-2 RECEPTOR
   (IL-2R) GAMMA-CHAIN - CHROMOSOMAL MAPPING AND TISSUE-SPECIFICITY OF
   IL-2R GAMMA-CHAIN EXPRESSION
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID BETA-CHAIN; NUCLEOTIDE-SEQUENCE; CELLS; COMPLEX; BINDING; INVOLVEMENT;
   COMPONENT; DISTINCT; CLONING; GENE
AB The IL-2R gamma chain (IL-2Rgamma) is an essential component of high- and intermediate-affinity IL-2Rs, playing critical roles for ligand binding and internalization. Recently, our laboratory has demonstrated that IL-2Rgamma mutation results in X chromosome-linked severe combined immunodeficiency in humans, suggesting that IL-2Rgamma plays a vital role in thymic maturation of human T cells. We now report the isolation and characterization of cDNAs encoding murine IL-2Rgamma. The open reading frame encodes 369 aa, identical in length to that encoded by the human IL-2Rgamma cDNA. Murine IL-2Rgamma and human IL-2Rgamma have 69% and 70% identity at the nucleotide and amino acid levels, respectively. As expected, the murine IL-2Rgamma retains the WSXWS motif and four cysteine residues characteristic of cytokine receptor superfamily members. IL-2Rgamma mRNA distribution shows significant tissue specificity, with particularly high-level expression in spleen and thymus, and higher expression in single-positive (CD4+8- or CD4-8+)-enriched thymocytes than in double-negative (CD4-8-) thymocytes. Finally, we have localized the murine IL-2Rgamma gene, Il2rg, to the X chromosome between Rsvp and Plp and demonstrated that a defect in IL-2Rgamma is not responsible for the X chromosome-linked xid mutation, which maps to this same region. The cloning of the murine IL-2Rgamma cDNA will facilitate the investigation of the role of this protein in lymphocyte function and thymic development.
C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892.
   NIAID,CELLULAR & MOLEC IMMUNOL LAB,BETHESDA,MD 20892.
RP CAO, XQ (reprint author), NHLBI,PULM & MOLEC IMMUNOL SECT,INTRAMURAL RES PROGRAM,OFF DIRECTOR,BETHESDA,MD 20892, USA.
NR 42
TC 55
Z9 58
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD SEP 15
PY 1993
VL 90
IS 18
BP 8464
EP 8468
DI 10.1073/pnas.90.18.8464
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LX750
UT WOS:A1993LX75000035
PM 8378320
ER

PT J
AU LI, BQ
   SUBLESKI, M
   SHALLOWAY, D
   KUNG, HF
   KAMATA, T
AF LI, BQ
   SUBLESKI, M
   SHALLOWAY, D
   KUNG, HF
   KAMATA, T
TI MITOGENIC ACTIVATION OF THE RAS GUANINE-NUCLEOTIDE EXCHANGE FACTOR IN
   NIH 3T3 CELLS INVOLVES PROTEIN-TYROSINE PHOSPHORYLATION
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID SACCHAROMYCES-CEREVISIAE; SIGNAL-TRANSDUCTION; KINASE-ACTIVITY;
   GROWTH-FACTOR; IDENTIFICATION; GTPASE; P21RAS; CDC25; GENE; STIMULATION
AB We report biochemical evidence that epidermal growth factor and platelet-derived growth factor stimulate the Ras guanine nucleotide exchange factor activity in quiescent NIH 3T3 cells. Moreover, the exchange activity is constitutively enhanced in NIH 3T3 cells transformed by Src and ErbB2 oncogenic tyrosine protein kinases (TPKs), whereas transformation by oncogenic Mos and Raf does not alter the activity. GTPase-activating protein activity was not affected under these conditions. Overexpression of pp60c-Src mutants containing activated and suppressor TPK mutations resulted in stimulation and inhibition of the exchange factor activity, respectively. A TPK inhibitor, genistein, prevented the activation of the exchange factor in epidermal growth factor/platelet-derived growth factor-treated cells and src-transformed cells. Furthermore, the exchange factor activity bound to an antiphosphotyrosine antibody immunoaffinity column. These findings suggest that the guanine nucleotide exchange factor, but not GTPase-activating protein, plays a major role in the Ras activation in cell proliferation initiated by growth factor receptor TPKs and malignant transformation by oncogenic TPKs and that tyrosine phosphorylation of either the exchange factor or a tightly bound protein(s) may mediate the activation of the exchange factor by these TPKs.
C1 PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702.
   NCI,FREDERICK CANC RES & DEV CTR,BIOCHEM PHYSIOL LAB,FREDERICK,MD 21702.
   CORNELL UNIV,DEPT PATHOL,BIOCHEM MOLEC & CELLULAR BIOL SECT,ITHACA,NY 14853.
NR 45
TC 23
Z9 25
U1 0
U2 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD SEP 15
PY 1993
VL 90
IS 18
BP 8504
EP 8508
DI 10.1073/pnas.90.18.8504
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LX750
UT WOS:A1993LX75000043
PM 8104337
ER

PT J
AU ROCHE, PA
   TELETSKI, CL
   STANG, E
   BAKKE, O
   LONG, EO
AF ROCHE, PA
   TELETSKI, CL
   STANG, E
   BAKKE, O
   LONG, EO
TI CELL-SURFACE HLA-DR INVARIANT CHAIN COMPLEXES ARE TARGETED TO ENDOSOMES
   BY RAPID INTERNALIZATION
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE ENDOCYTOSIS; MAJOR HISTOCOMPATIBILITY COMPLEX
ID MHC CLASS-II; MONOCLONAL-ANTIBODIES; INTRACELLULAR-TRANSPORT; PEPTIDE
   COMPLEXES; MOLECULES; ANTIGEN; EXPRESSION; ENDOCYTOSIS; BINDING;
   COMPARTMENTS
AB Class II molecules of the major histocompatibility complex (MHC) bind peptides derived from protein antigens delivered into endocytic compartments and present these peptides to CD4+ T cells. The precursors to functional MHC class II molecules loaded with peptides are complexes of the invariant chain associated with class II alphabeta heterodimers. Targeting of newly synthesized MHC class II molecules to endosomes is mediated by the invariant chain, but the intracellular transport route is not known. This study demonstrates that in a human B-cell line a large population of MHC class II-invariant chain complexes reaches endosomes by rapid internalization from the cell surface. Quantitation of cell surface MHC class II-invariant chain complexes and of their surface half-life revealed that 3000 complexes internalized per minute into endosomes. This highly efficient endocytosis was mediated by the cytoplasmic tail of the invariant chain. After internalization, the invariant chain dissociated from the MHC class II-invariant chain complexes. This pathway may represent an important mechanism for loading class II molecules with immunogenic peptides from several endocytic compartments.
C1 UNIV OSLO,DEPT BIOL,N-0316 OSLO,NORWAY.
RP ROCHE, PA (reprint author), NIAID,IMMUNOGENET LAB,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA.
RI Long, Eric/G-5475-2011
OI Long, Eric/0000-0002-7793-3728
NR 34
TC 187
Z9 188
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 SEP 15
PY 1993
VL 90
IS 18
BP 8581
EP 8585
DI 10.1073/pnas.90.18.8581
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LX750
UT WOS:A1993LX75000059
PM 8397411
ER

PT J
AU BURMESTER, JK
   QIAN, SW
   ROBERTS, AB
   HUANG, A
   AMATAYAKULCHANTLER, S
   SUARDET, L
   ODARTCHENKO, N
   MADRI, JA
   SPORN, MB
AF BURMESTER, JK
   QIAN, SW
   ROBERTS, AB
   HUANG, A
   AMATAYAKULCHANTLER, S
   SUARDET, L
   ODARTCHENKO, N
   MADRI, JA
   SPORN, MB
TI CHARACTERIZATION OF DISTINCT FUNCTIONAL DOMAINS OF TRANSFORMING
   GROWTH-FACTOR-BETA
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE CHIMERA; RECEPTOR; ALPHA-2-MACROGLOBULIN; HEART; COLON CANCER
ID ENDOTHELIAL-CELLS; CRYSTAL-STRUCTURE; RECEPTOR SYSTEM; 2 FORMS; BINDING;
   LINES; GROWTH-FACTOR-BETA-2; RESPONSIVENESS; FACTOR-BETA-2; INHIBITION
AB Three distinct isoforms of transforming growth factor beta (TGF-beta) are expressed in mammalian cells. Although many cells respond equivalently to all three isoforms, certain cells respond selectively. Using chimeric proteins in which selected regions of the different isoforms were interchanged, we have identified two distinct functional domains of TGF-beta involved in determining the biological potencies and functions of the molecule. The first domain is important for determining whether TGF-beta can be sequestered by alpha2-macroglobulin. By replacing aa 45 and 47 of TGF-beta2 with the corresponding amino acids of TGF-beta1, sequestration of the TGF-beta molecule by alpha2-macroglobulin was markedly reduced. The second domain is functionally different from the alpha2-macroglobulin sequestration site and is important for determining the potency of TGF-beta to inhibit growth of the LS513 human colorectal cancer cell line. Neither the TGF-beta2/beta1-(40-47) replacement construct nor a chimera containing aa 1-39 of TGF-beta2, aa 40-82 of TGF-beta1, and aa 83-112 of TGF-beta2 was equivalent to TGF-beta1 in inhibiting growth of LS513 cells. This fact suggests that additional amino acids outside of the aa 40-82 region are required to specify TGF-beta1 activity with these cells.
C1 NIH,CHEMOPREVENT LAB,BETHESDA,MD 20892.
   SWISS INST CANC RES,CH-1066 EPALINGES,SWITZERLAND.
   YALE UNIV,NEW HAVEN,CT 06413.
RP BURMESTER, JK (reprint author), MARSHFIELD MED RES & EDUC FDN,MARSHFIELD,WI 54449, USA.
FU NHLBI NIH HHS [R01-HL-28373]
NR 31
TC 43
Z9 43
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 SEP 15
PY 1993
VL 90
IS 18
BP 8628
EP 8632
DI 10.1073/pnas.90.18.8628
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LX750
UT WOS:A1993LX75000069
PM 7690965
ER

PT J
AU WALLACE, W
   AHLERS, ST
   GOTLIB, J
   BRAGIN, V
   SUGAR, J
   GLUCK, R
   SHEA, PA
   DAVIS, KL
   HAROUTUNIAN, V
AF WALLACE, W
   AHLERS, ST
   GOTLIB, J
   BRAGIN, V
   SUGAR, J
   GLUCK, R
   SHEA, PA
   DAVIS, KL
   HAROUTUNIAN, V
TI AMYLOID PRECURSOR PROTEIN IN THE CEREBRAL-CORTEX IS RAPIDLY AND
   PERSISTENTLY INDUCED BY LOSS OF SUBCORTICAL INNERVATION
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE NUCLEUS BASALIS OF MEYNERT; RAT
ID ALZHEIMERS-DISEASE; NUCLEUS BASALIS; RATS; RECEPTOR
AB Lesions of the cholinergic nucleus basalis of Meynert elevate the ex vivo synthesis of beta amyloid precursor protein (beta-APP) in the cerebral cortex, a major projection region. We have found that this elevation is reflected by increased levels of beta-APP mRNA. The induction is rapid (occurring 60 min after placement of the lesion) and persistent (remaining for at least 45 days after lesioning). Two other subcortical lesions, which result in reductions of cortical adrenergic and serotonergic innervation, similarly induced cortical beta-APP. The beta-APP induction is reversible and does not require loss of the subcortical neurons. Infusion of lidocaine, a calcium antagonist that disrupts neurotransmitter release, into the nucleus basalis of Meynert leads to the temporary reduction of released acetylcholine in the cortex. In this model, beta-APP mRNA levels are elevated shortly after the infusion of lidocaine (90 min) but return to preinfusion levels 7 days after the lidocaine treatment. However, metabolic stresses of the brain, including chronic physostigmine, glucocorticoid, and diabetogenic treatments, fail to induce the beta-APP response. These results suggest that the induction of beta-APP is a specific response to the loss of functional innervation in the cortex. Importantly, these studies show that cortical beta-APP is induced by lesions that mimic the neurochemical deficits most frequently observed in Alzheimer disease.
C1 USN,MED RES INST,THERMAL STRESS ADAPTAT PROGRAM,BETHESDA,MD 20889.
   CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029.
   VET AFFAIRS MED CTR,BRONX,NY 10468.
RP WALLACE, W (reprint author), ST ELIZABETH HOSP,CTR NEUROSCI,NATL INST MENTAL HLTH,WASHINGTON,DC 20032, USA.
NR 15
TC 103
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 SEP 15
PY 1993
VL 90
IS 18
BP 8712
EP 8716
DI 10.1073/pnas.90.18.8712
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LX750
UT WOS:A1993LX75000086
PM 8378353
ER

PT J
AU UCHIDA, K
   SZWEDA, LI
   CHAE, HZ
   STADTMAN, ER
AF UCHIDA, K
   SZWEDA, LI
   CHAE, HZ
   STADTMAN, ER
TI IMMUNOCHEMICAL DETECTION OF 4-HYDROXYNONENAL PROTEIN ADDUCTS IN OXIDIZED
   HEPATOCYTES
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID LIPID-PEROXIDATION; GLUTATHIONE TRANSFERASE; LIVER;
   4-HYDROXYALK-2-ENALS; 4-HYDROXYALKENALS; PRODUCTS
AB We report here the development of an immunochemical procedure that uses an antibody specific to the 4-hydroxynonenal (HNE) moiety for the detection of HNE-protein adducts. The HNE-specific antibody was prepared by immunizing rabbits with a HNE-keyhole limpet hemocyanin conjugate and purifying the rabbit serum on an affinity gel prepared by covalent attachment of a HNE-conjugated heptapeptide. When various preparations of glyceraldehyde-3-phosphate dehydrogenase containing 0-7.0 equivalent of HNE-histidine residues per subunit were obtained by incubating samples of glyceraldehyde-3-phosphate dehydrogenase with increased amounts of HNE and subjected to immunoblotting with the HNE-specific antibody, the intensities of the blots were directly proportional to the number of HNE-histidine adducts as measured directly by amino acid analysis. Binding of the HNE-conjugated glyceraldehyde-3-phosphate dehydrogenase to the HNE-specific antibody could be completely inhibited by HNE-N-acetylhistidine, HNE-N-acetyllysine, or HNE-glutathione, suggesting that the antigenic determinant recognized by the antibody is the HNE moiety, not the HNE-amino add conjugates, such as HNE-histidine, HNE-lysine, and HNE-cysteine. The utility of the HNE-specific antibody was demonstrated by its ability to react selectively with a number of HNE-protein adducts in immunoblot analyses of crude homogenates of rat liver hepatocytes that had been exposed to HNE or oxidative stresses with tert-butylhydroperoxide or metal-ion-catalyzed oxidation systems.
C1 NHLBI,BIOCHEM LAB,9000 ROCKVILLE PIKE,BLDG 3,ROOM 222,BETHESDA,MD 20892.
NR 23
TC 305
Z9 312
U1 1
U2 9
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD SEP 15
PY 1993
VL 90
IS 18
BP 8742
EP 8746
DI 10.1073/pnas.90.18.8742
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LX750
UT WOS:A1993LX75000092
PM 8378358
ER

PT J
AU MARK, SD
   ROBINS, JM
AF MARK, SD
   ROBINS, JM
TI ESTIMATING THE CAUSAL EFFECT OF SMOKING CESSATION IN THE PRESENCE OF
   CONFOUNDING FACTORS USING A RANK PRESERVING STRUCTURAL FAILURE TIME
   MODEL
SO STATISTICS IN MEDICINE
LA English
DT Article
ID CORONARY HEART-DISEASE; FACTOR INTERVENTION TRIAL; CIGARETTE-SMOKING;
   PROPENSITY SCORE; ARTERY DISEASE; CASS REGISTRY; RISK; MORTALITY;
   INFERENCE; SMOKERS
AB Estimating the causal effect of quitting smoking on time to death or first myocardial infarction requires that one control for the differences in risk factors between individuals who elect to quite at each time t versus those who elect to continue smoking at time t. In this paper we examine the limitations of standard time varying Cox proportional hazards models to yield tests and estimates of this effect. Implementing the method of G-estimation proposed by Robins, we perform an observational analysis of data from the Multiple Risk Factor Intervention Trial (MRFIT) and estimate the causal effect of cigarette cessation while controlling for such time varying confounders as angina. We reject the null hypothesis of no effect of quitting on time to failure, and estimate that by quitting smoking, an individual increases by 50 per cent his time to death or first myocardial infarction (MI).
C1 HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115.
   HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115.
RP MARK, SD (reprint author), NCI,EPIDEMIOL METHODS SECT,6130 EXECUT BLVD,EPN 403,ROCKVILLE,MD 20892, USA.
FU NCI NIH HHS [NCI5T32CA09001]; NIAID NIH HHS [R01AI32475]; NIEHS NIH HHS
   [5R01ESO3405]
NR 50
TC 47
Z9 48
U1 0
U2 5
PU JOHN WILEY & SONS LTD
PI W SUSSEX
PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD SEP 15
PY 1993
VL 12
IS 17
BP 1605
EP 1628
DI 10.1002/sim.4780121707
PG 24
WC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Medicine, Research &
   Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Research & Experimental
   Medicine; Mathematics
GA LY084
UT WOS:A1993LY08400006
PM 8235180
ER

PT J
AU BYAR, DP
   HERZBERG, AM
   TAN, WY
AF BYAR, DP
   HERZBERG, AM
   TAN, WY
TI INCOMPLETE FACTORIAL-DESIGNS FOR RANDOMIZED CLINICAL-TRIALS
SO STATISTICS IN MEDICINE
LA English
DT Article
AB Recently there has been increased interest in considering factorial designs for randomized clinical trials when one wishes to study two or more treatments. Such designs may offer impressive gains in efficiency compared with a series of trials studying one treatment at a time. This is especially true when the treatments do not interact with one another. If interactions are of special interest, factorial designs provide one sensible approach for studying them, but larger sample sizes would be required because tests for interactions have lower power than those for main effects. In trials designed to test putative agents for preventing cancer, interactions may be of less interest so that fractions of higher-order factorial designs might be appropriate. Sometimes it may not be reasonable, interesting, feasible, or ethical to study all treatment combinations required in a complete or fractional factorial design, yet one may want to preserve some of the factorial structure to increase efficiency and to aid understanding. For such situations, incomplete factorial designs are proposed. Although not all of the advantages of full factorial designs are preserved, such designs may provide reasonable compromises for certain situations.
C1 QUEENS UNIV,DEPT MATH & STAT,KINGSTON K7L 3N6,ONTARIO,CANADA.
   MEMPHIS STATE UNIV,DEPT MATH SCI,MEMPHIS,TN 38152.
   NCI,BETHESDA,MD 20892.
NR 9
TC 18
Z9 18
U1 1
U2 3
PU JOHN WILEY & SONS LTD
PI W SUSSEX
PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD SEP 15
PY 1993
VL 12
IS 17
BP 1629
EP 1641
DI 10.1002/sim.4780121708
PG 13
WC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Medicine, Research &
   Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Research & Experimental
   Medicine; Mathematics
GA LY084
UT WOS:A1993LY08400007
PM 8235181
ER

PT J
AU ZORAD, S
   TSUTSUMI, K
   BHATIA, AJ
   SAAVEDRA, JM
AF ZORAD, S
   TSUTSUMI, K
   BHATIA, AJ
   SAAVEDRA, JM
TI LOCALIZATION AND CHARACTERISTICS OF ATRIAL-NATRIURETIC-PEPTIDE RECEPTORS
   IN PRENATAL AND POSTNATAL RAT-BRAIN
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE AUTORADIOGRAPHY; CEREBRAL CORTEX; DEVELOPMENT; NATRIURETIC PEPTIDE
   RECEPTORS
ID BINDING-SITES; CHOROID-PLEXUS; SUBTYPES; AUTORADIOGRAPHY; FAMILY;
   SYSTEM; AREAS; CNP
AB We studied the expression of atrial natriuretic peptide (ANP) receptor subtypes during development in the rat forebrain, using quantitative autoradiography. Highest ANP binding was observed in the cortical neuroepithelium at embryonic day 17. Lower ANP binding was found in cingulate and frontal cortices at postnatal day 10, but none was detectable at 8 weeks of age. In the neuroepithelium of the embryonic rat, binding was displaced with a potency of rat ANP-(1-28) (rANP) > porcine type-C natriuretic peptide (pCNP-22) = rat ANP fragment C-ANP-(4-23) (rC-ANP-(4-23)) = rat brain natriuretic peptide (rBNP-32), different from that of any of the well-characterized (ANP(A), ANP(B), and ANP(C)) natriuretic peptide receptors. The present results support the hypothesis of a role for ANP during brain maturation and indicate that the ANP receptors highly expressed in the embryonic neuroepithelium may belong to a new ANP receptor subtype not yet characterized.
C1 NIMH,CLIN SCI LAB,PHARMACOL SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2D-45,BETHESDA,MD 20892.
NR 24
TC 12
Z9 13
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-2999
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD SEP 14
PY 1993
VL 241
IS 2-3
BP 195
EP 200
DI 10.1016/0014-2999(93)90203-T
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA LX542
UT WOS:A1993LX54200009
PM 8243555
ER

PT J
AU ATOR, NA
   GRANT, KA
   PURDY, RH
   PAUL, SM
   GRIFFITHS, RR
AF ATOR, NA
   GRANT, KA
   PURDY, RH
   PAUL, SM
   GRIFFITHS, RR
TI DRUG DISCRIMINATION ANALYSIS OF ENDOGENOUS NEUROACTIVE STEROIDS IN RATS
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE NEUROACTIVE STEROIDS; BEHAVIOR; DRUG DISCRIMINATION; BENZODIAZEPINES;
   PENTOBARBITAL; ETHANOL
ID GABA-RECEPTOR; LORAZEPAM; BABOONS; CHLORDIAZEPOXIDE; ANXIOLYTICS
AB Rats were trained in a two-lever procedure to discriminate either pentobarbital (10 mg/kg), ethanol (1.5 g/kg), diazepam (1 mg/kg), or lorazepam (I mg/kg) from the no-drug condition. Consistent with previous reports, rats in the pentobarbital, ethanol, and diazepam training conditions all showed complete dose-dependent generalization to pentobarbital under test conditions, but rats trained to discriminate lorazepam did not. Administration of the neuroactive steroids 3alpha,21-dihydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THDOC) and 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-P) also produced complete generalization in rats trained to discriminate pentobarbital, ethanol, and diazepam, but not in rats trained to discriminate lorazepam. These results further indicate the specificity of the lorazepam training condition and are consistent with neurochemical data indicating that these neuroactive steroids are similar to barbiturates in modulating gamma-aminobutyric acid (GABA)A receptors. In the context of previous data, the results from the four training groups suggest that the discriminative-stimulus effects of the neuroactive steroids are sedative/anxiolytic in nature and probably mediated through a non-benzodiazepine GABA(A) site.
C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205.
   JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205.
   NIAAA,DIV INTRAMURAL CLIN & BIOL RES,ROCKVILLE,MD 20852.
   SW FDN BIOMED RES,DEPT ORGAN CHEM,SAN ANTONIO,TX 78284.
   NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BETHESDA,MD 20892.
RP ATOR, NA (reprint author), BEHAV BIOL RES CTR,HOPKINS BAYVIEW RES CAMPUS,5510 NATHAN SHOCK DR,SUITE 3000-DBB,BALTIMORE,MD 21224, USA.
FU NIAAA NIH HHS [AA 09346]; NIDA NIH HHS [DA 04133]
NR 24
TC 107
Z9 110
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-2999
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD SEP 14
PY 1993
VL 241
IS 2-3
BP 237
EP 243
DI 10.1016/0014-2999(93)90208-Y
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA LX542
UT WOS:A1993LX54200014
PM 7902289
ER

PT J
AU KARUPIAH, G
   XIE, QW
   BULLER, RML
   NATHAN, C
   DUARTE, C
   MACMICKING, JD
AF KARUPIAH, G
   XIE, QW
   BULLER, RML
   NATHAN, C
   DUARTE, C
   MACMICKING, JD
TI INHIBITION OF VIRAL REPLICATION BY INTERFERON-GAMMA-INDUCED NITRIC-OXIDE
   SYNTHASE
SO SCIENCE
LA English
DT Article
ID VACCINIA VIRUS; RIBONUCLEOTIDE REDUCTASE; PROTEIN-KINASE; CELLS;
   MACROPHAGES; BIOCHEMISTRY; MECHANISM; ARGINASE; PRODUCT; SYSTEM
AB Interferons (IFNs) induce antiviral activity in many cell types. The ability of IFN-gamma to inhibit replication of ectromelia, vaccinia, and herpes simplex-1 viruses in mouse macrophages correlated with the cells' production of nitric oxide (NO). Viral replication was restored in IFN-gamma-treated macrophages exposed to inhibitors of NO synthase. Conversely, epithelial cells with no detectable NO synthesis restricted viral replication when transfected with a complementary DNA encoding inducible NO synthase or treated with organic compounds that generate NO. In mice, an inhibitor of NO synthase converted resolving ectromelia virus infection into fulminant mousepox. Thus, induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma.
C1 CORNELL UNIV,MED CTR,COLL MED,DEPT MED,DIV HEMATOL ONCOL,BEATRICE & SAMUEL A SEAVER LAB,NEW YORK,NY 10021.
RP KARUPIAH, G (reprint author), NIAID,VIRAL DIS LAB,BETHESDA,MD 20892, USA.
RI Karupiah, Gunasegaran/J-4707-2013
FU NCI NIH HHS [CA43610]
NR 40
TC 688
Z9 702
U1 1
U2 7
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD SEP 10
PY 1993
VL 261
IS 5127
BP 1445
EP 1448
DI 10.1126/science.7690156
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LW549
UT WOS:A1993LW54900032
PM 7690156
ER

PT J
AU RABKIN, CS
   BIGGAR, RJ
   BAPTISTE, MS
   ABE, T
   KOHLER, BA
   NASCA, PC
AF RABKIN, CS
   BIGGAR, RJ
   BAPTISTE, MS
   ABE, T
   KOHLER, BA
   NASCA, PC
TI CANCER INCIDENCE TRENDS IN WOMEN AT HIGH-RISK OF
   HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) INFECTION
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
ID HUMAN PAPILLOMAVIRUS INFECTION; INVASIVE CERVICAL-CANCER; NON-HODGKINS
   LYMPHOMA; KAPOSIS-SARCOMA; LATIN-AMERICA; SYNDROME AIDS; DISEASE;
   EPIDEMIOLOGY; MALIGNANCIES; NEOPLASIA
AB To determine the types and rates of tumors which may be associated with HIV infection in women, we used cancer incidence data from New York and northern New Jersey. We examined changes in incidence of selected cancers in women aged 20-49 years and compared groups differing in incidence of AIDS. Black women were compared to white women in New York City and in the remainder of New York State; for cervical cancer, rates were also compared for Blacks and Whites in northern New Jersey. The incidence of Kaposi's sarcoma in women increased in New York City, beginning in 1982 for Blacks and in 1984 for Whites, but remained stable in the remainder of New York State. The incidence of non-Hodgkin's lymphoma in New York women doubled in Blacks after 1982 whereas incidence trends in Whites were unchanged. No consistent variation was seen in the incidence of Hodgkin's disease. Cervical cancer in New York and northern New Jersey Blacks declined over the same period by approximately 40% for invasive tumors and 50% for in situ lesions. The HIV epidemic is associated with substantial excesses of Kaposi's sarcoma and non-Hodgkin's lymphoma in women. The absence of Kaposi's sarcoma in upstate New York women suggests the existence of a geographically restricted co-factor(s) for Kaposi's sarcoma in addition to HIV. If HIV affected cervical cancer incidence through 1988, its impact was small compared to the striking decreases which followed widespread adoption of Papanicolaou screening. (C) 1993 Wiley-Liss, Inc.
C1 NEW YORK STATE DEPT HLTH,BUR CANC EPIDEMIOL,ALBANY,NY 12237.
   NEW JERSEY STATE DEPT HLTH,DIV EPIDEMIOL ENVIRONM & OCCUPAT HLTH SERV,TRENTON,NJ 08625.
RP RABKIN, CS (reprint author), NCI,DIV CANC ETIOL,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA.
NR 27
TC 54
Z9 54
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD SEP 9
PY 1993
VL 55
IS 2
BP 208
EP 212
DI 10.1002/ijc.2910550207
PG 5
WC Oncology
SC Oncology
GA LX665
UT WOS:A1993LX66500006
PM 8370617
ER

PT J
AU LOLLINI, PL
   BOSCO, MC
   CAVALLO, F
   DEGIOVANNI, C
   GIOVARELLI, M
   LANDUZZI, L
   MUSIANI, P
   MODESTI, A
   NICOLETTI, G
   PALMIERI, G
   SANTONI, A
   YOUNG, HA
   FORNI, G
   NANNI, P
AF LOLLINI, PL
   BOSCO, MC
   CAVALLO, F
   DEGIOVANNI, C
   GIOVARELLI, M
   LANDUZZI, L
   MUSIANI, P
   MODESTI, A
   NICOLETTI, G
   PALMIERI, G
   SANTONI, A
   YOUNG, HA
   FORNI, G
   NANNI, P
TI INHIBITION OF TUMOR-GROWTH AND ENHANCEMENT OF METASTASIS AFTER
   TRANSFECTION OF THE GAMMA-INTERFERON GENE
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
ID REDUCED TUMORIGENICITY; MELANOMA-CELLS; EXPRESSION; IMMUNITY; MICE;
   ANTIGENS; ABILITY
AB Cells from the spontaneous metastatic TS/A mammary adenocarcinoma of a BALB/c mouse were transfected with the murine gamma-interferon (IFN-gamma) gene. Six clones (IFN-gamma clones) releasing between 2 and 6,000 international units (IU) of IFN-gamma/ml culture medium, were compared to TS/A parental cells (TS/A-pc) and to cells transfected with neomycin resistance gene only (NEO cells). Autocrine IFN-gamma up-regulated membrane expression of H-2 class-1 and Ly-6 glycoproteins, but did not alter cellular proliferation in vitro. All IFN-gamma clones gave rise to progressive tumors with a growth rate significantly slower than that of tumors induced by TS/A-pc and NEO cells, and inversely correlated with the amount of IFN-gamma secreted. TS/A-pc and NEO tumors displayed a marginal reactive infiltrate, whereas those formed by IFN-gamma clones were massively infiltrated mostly by macrophages. In T- and NK-deficient mice the growth of tumors formed by IFN-gamma clones was not enhanced. In vitro tests showed that IFN-gamma clone cells were markedly more lysed by macrophages than TS/A-pc and NEO cells, while they remained poorly sensitive to NK and LAK cells. These data as a whole suggest that the development of solid tumors by IFN-gamma clones is primarily hampered by macrophages and not by T-lymphocytes or NK cells. When spontaneous metastatic ability was compared, 2 IFN-gamma clones releasing 2-4 IFN-gamma IU/ml were significantly more metastatic, while most IFN-gamma clones appeared to be as metastatic as NEO cells. By contrast, following intravenous challenge, all IFN-gamma clones produced 5-10 times more experimental metastases than NEO cells. The higher metastatic ability of IFN-gamma clones was attributed to increased resistance to NK cells since, in NK-depleted BALB/c mice, metastatic spread of IFN-gamma clones was not enhanced, whereas a 50-fold increase in the number of metastases was found upon injection of NEO cells. (C) 1993 Wiley-Liss, Inc.
C1 NCI,FREDERICK CANC RES & DEV CTR,BRMP,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21701.
   UNIV G DANNUNZIO,IST PATOL UMANA & MED SOCIALE,CHIETI,ITALY.
   NCI,FREDERICK CANC RES & DEV CTR,BRMP,EXPTL IMMUNOL LAB,FREDERICK,MD 21701.
   IST,SEZ BIOTECNOL,GENOA,ITALY.
   CNR,CTR IMMUNOGENET & ISTOCOMPATIBIL,TURIN,ITALY.
   UNIV ROME,DIPARTIMENTO MED SPERIMENTALE,I-00100 ROME,ITALY.
RP LOLLINI, PL (reprint author), UNIV BOLOGNA,IST CANCEROL,VIALE FILOPANTI 22,I-40126 BOLOGNA,ITALY.
RI Lollini, Pier Luigi/A-7644-2008; De Giovanni, Carla/B-1312-2009;
   Cavallo, Federica/C-5666-2011; Palmieri, Gabriella/Q-1761-2015; Bosco,
   Maria Carla/J-7928-2016; 
OI Lollini, Pier Luigi/0000-0003-1702-4108; Cavallo,
   Federica/0000-0003-4571-1060; Palmieri, Gabriella/0000-0002-1467-1417;
   Bosco, Maria Carla/0000-0003-1857-7193; Nanni,
   Patrizia/0000-0001-5319-0803
NR 23
TC 82
Z9 82
U1 1
U2 4
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD SEP 9
PY 1993
VL 55
IS 2
BP 320
EP 329
DI 10.1002/ijc.2910550224
PG 10
WC Oncology
SC Oncology
GA LX665
UT WOS:A1993LX66500023
PM 8370628
ER

PT J
AU KIRSCHSTEIN, R
AF KIRSCHSTEIN, R
TI SLEEP RESEARCH HAS BROAD SWEEP
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
RP KIRSCHSTEIN, R (reprint author), NIH,BETHESDA,MD 20892, USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD SEP 8
PY 1993
VL 270
IS 10
BP 1172
EP 1172
DI 10.1001/jama.270.10.1172
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA LV649
UT WOS:A1993LV64900005
PM 8355369
ER

PT J
AU YESALIS, CE
   KENNEDY, NJ
   KOPSTEIN, AN
   BAHRKE, MS
AF YESALIS, CE
   KENNEDY, NJ
   KOPSTEIN, AN
   BAHRKE, MS
TI ANABOLIC-ANDROGENIC STEROID USE IN THE UNITED-STATES
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID DRUG-USE; DEPENDENCE; SCHOOL; SYMPTOMS; MEN
AB Objective.- To estimate the size of the anabolic-androgenic steroid (AAS) user population in the United States, to examine characteristics of AAS users, and to explore the association between AAS use and the use of other illicit drugs as well as self-reported aggressive behaviors.
   Design.- A cross-sectional study using data from the 1991 National Household Survey on Drug Abuse.
   Study Population.- The survey covered the population aged 12 years and older living in households in the United States. The results of the survey were based on personal interviews combined with self-administered questionnaires from 32 594 respondents. These respondents were randomly selected by means of a stratified multistage area sample of the household population.
   Results.- Estimates based on data from the National Household Survey on Drug Abuse indicated that there are more than 1 million current or former AAS users in this country, with more than half of the lifetime user population being 26 years of age or older. More than 300 000 individuals used AAS in the past year. Males had higher levels of AAS use during their lifetime than females (0.9% and 0.1%, respectively; P<.01). The median age of first use of AAS for the study population was 18 years; for 12- to 17-year-olds, the median age of initiation was 15 years. Among 12- to 34-year-olds, AAS use was significantly and positively associated with the use of other illicit drugs (P<.05), cigarettes (12- to 17-year-olds only; P<.01), and alcohol (P<.01). Furthermore, AAS use is highly correlated with self-reported aggressive behavior (P<.01) and crimes against property (P<.01).
   Conclusions.- These results indicate that AAS use impacts a large number of men and women from various racial and age groups across the nation. While causal inferences cannot be made regarding the associations between AAS use and use of other drugs as well as antisocial behavior, these findings should enhance our ability to profile the typical AAS user.
C1 CTR SUBST ABUSE PREVENT, POLICY & PLANNING UNIT, ROCKVILLE, MD USA.
   NIDA, STAT & ANAL BRANCH, ROCKVILLE, MD USA.
   UNIV ILLINOIS, DEPT EPIDEMIOL & BIOSTAT, CHICAGO, IL 60680 USA.
RP YESALIS, CE (reprint author), PENN STATE UNIV, DEPT HLTH POLICY & ADM, 115 HENDERSON BLDG, UNIV PK, PA 16802 USA.
NR 67
TC 228
Z9 234
U1 3
U2 18
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD SEP 8
PY 1993
VL 270
IS 10
BP 1217
EP 1221
DI 10.1001/jama.270.10.1217
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA LV649
UT WOS:A1993LV64900027
PM 8355384
ER

PT J
AU EPLER, KS
   ZIEGLER, RG
   CRAFT, NE
AF EPLER, KS
   ZIEGLER, RG
   CRAFT, NE
TI LIQUID-CHROMATOGRAPHIC METHOD FOR THE DETERMINATION OF CAROTENOIDS,
   RETINOIDS AND TOCOPHEROLS IN HUMAN SERUM AND IN FOOD
SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS
LA English
DT Article
ID DIODE-ARRAY DETECTION; BETA-CAROTENE; REVERSED-PHASE; ALPHA-TOCOPHEROL;
   HUMAN-PLASMA; CIS-ISOMERS; SEPARATION; IDENTIFICATION; ADSORPTION; HPLC
AB A liquid chromatographic (LC) method has been developed for the quantitative measurement of the six major carotenoids in human serum (lutein, zeaxanthin, beta-cryptoxanthin, lycopene, alpha-carotene, and beta-carotene) as well as retinol, retinyl palmitate, alpha-tocopherol, gamma-tocopherol, and delta-tocopherol. Several polar carotenoids, 2',3'-anhydrolutein, alpha-cryptoxanthin, and geometric isomers of lycopene and beta-carotene are also separated. Retinoids and carotenoids are monitored using a programmable ultraviolet-visible detector, while tocopherols are monitored using a fluorescence detector. The method uses a gradient containing acetonitrile, methanol, and ethyl acetate. Ammonium acetate is introduced with the methanol to minimize carotenoid losses on the LC column aggravated by the use of acetonitrile and ethyl acetate. The method is also applicable to the analysis of foods.
C1 NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892.
RP EPLER, KS (reprint author), US TECHNOL ADM,NATL INST STANDARDS & TECHNOL,ORGAN ANALYT RES DIV,CHEM SCI & TECHNOL LAB,GAITHERSBURG,MD 20899, USA.
FU NCI NIH HHS [Y01-CP9-0513]
NR 27
TC 137
Z9 139
U1 0
U2 9
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 SEP 8
PY 1993
VL 619
IS 1
BP 37
EP 48
DI 10.1016/0378-4347(93)80444-9
PG 12
WC Chemistry, Analytical
SC Chemistry
GA LX510
UT WOS:A1993LX51000005
PM 8245162
ER

PT J
AU BRYANT, SD
   SALVADORI, S
   ATTILA, M
   LAZARUS, LH
AF BRYANT, SD
   SALVADORI, S
   ATTILA, M
   LAZARUS, LH
TI TOPOGRAPHICAL CONFORMATIONS OF THE DELTORPHINS PREDICATE DELTA-OPIOID
   RECEPTOR AFFINITY
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Note
ID SELECTIVITY; PEPTIDES; ANALOGS; REQUIREMENTS; DERMENKEPHALIN; SEQUENCE;
   LIGANDS; BINDING; ADDRESS; NMR
C1 UNIV FERRARA,DEPT PHARMACEUT SCI,I-44100 FERRARA,ITALY.
RP BRYANT, SD (reprint author), NIEHS,PEPTIDE NEUROCHEM SECT,INTEGRAT BIOL LAB,RES TRIANGLE PK,NC 27709, USA.
NR 25
TC 20
Z9 21
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD SEP 8
PY 1993
VL 115
IS 18
BP 8503
EP 8504
DI 10.1021/ja00071a092
PG 2
WC Chemistry, Multidisciplinary
SC Chemistry
GA LX752
UT WOS:A1993LX75200092
ER

PT J
AU BATES, SE
   LEE, JS
   DICKSTEIN, B
   SPOLYAR, M
   FOJO, AT
AF BATES, SE
   LEE, JS
   DICKSTEIN, B
   SPOLYAR, M
   FOJO, AT
TI DIFFERENTIAL MODULATION OF P-GLYCOPROTEIN TRANSPORT BY PROTEIN-KINASE
   INHIBITION
SO BIOCHEMISTRY
LA English
DT Article
ID CARCINOMA CELL-LINES; MULTIDRUG RESISTANCE; PHORBOL ESTERS; C-ZETA;
   MEMBRANE GLYCOPROTEIN; CALPHOSTIN-C; CANCER-CELLS; HL60 CELLS;
   PHOSPHORYLATION; EXPRESSION
AB Previous studies of P-glycoprotein have demonstrated that its function can be modulated by phosphorylation. In the present study, inhibition of protein kinase C with calphostin C or stauroporine or prolonged treatment with the phorbol ester TPA decreased phosphorylation of P-glycoprotein, and impaired transport of vinblastine. Calphostin C also inhibited transport of actinomycin D, vincristine, rhodamine, and azidopine in SW620 Ad300 multidrug-resistant human colon carcinoma cells. Photoaffinity labeling of P-glycoprotein with azidopine was decreased by calphostin C, suggesting that dephosphorylation alters the affinity of P-glycoprotein for its substrates. Impaired transport of rhodamine in normal T lymphocytes treated with staurosporine demonstrates that modulation of P-glycoprotein function is not limited to cells selected for drug resistance in vitro. Transport of P-glycoprotein antagonists in SW620 Ad300 cells was also affected by calphostin C. Cyclosporin A transport decreased, while verapamil transport increased. Cyclosporin A in calphostin C-treated cells resulted in additive P-glycoprotein antagonism, while no additive effect could be demonstrated with verapamil, suggesting that the increase in verapamil transport makes it a poorer P-glycoprotein antagonist. These studies suggest that transport by P-glycoprotein is a dynamic process which can be modulated by phosphorylation, and that antagonists may block P-glycoprotein differently in different phosphorylation states.
RP BATES, SE (reprint author), NCI,MED BRANCH,BLDG 10,ROOM 12N226,BETHESDA,MD 20892, USA.
NR 41
TC 96
Z9 98
U1 0
U2 0
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD SEP 7
PY 1993
VL 32
IS 35
BP 9156
EP 9164
DI 10.1021/bi00086a022
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LW440
UT WOS:A1993LW44000022
PM 7690250
ER

PT J
AU GOODWIN, FK
   MORRISON, AR
AF GOODWIN, FK
   MORRISON, AR
TI IN ANIMAL RIGHTS DEBATE, THE ONLY VALID MODERATES ARE RESEARCHERS
SO SCIENTIST
LA English
DT Editorial Material
AB There is no ''middle ground'' in the debate between scientists and animal rights defenders absent the acceptance of the necessity for the use of animals in research, say National Institute of Mental Health director Frederick K. Goodwin and University of Pennsylvania anatomy professor Adrian Morrison.
C1 UNIV PENN,PHILADELPHIA,PA 19104.
RP GOODWIN, FK (reprint author), NIMH,PROGRAM ANIM RES ISSUES,ROCKVILLE,MD 20857, USA.
NR 3
TC 3
Z9 3
U1 0
U2 0
PU SCIENTIST INC
PI PHILADELPHIA
PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104
SN 0890-3670
J9 SCIENTIST
JI Scientist
PD SEP 6
PY 1993
VL 7
IS 17
BP 12
EP 12
PG 1
WC Information Science & Library Science; Multidisciplinary Sciences
SC Information Science & Library Science; Science & Technology - Other
   Topics
GA LV433
UT WOS:A1993LV43300007
ER

PT J
AU KENYON, K
   MODI, WS
   CONTENTE, S
   FRIEDMAN, RM
AF KENYON, K
   MODI, WS
   CONTENTE, S
   FRIEDMAN, RM
TI A NOVEL HUMAN CDNA WITH A PREDICTED PROTEIN SIMILAR TO LYSYL OXIDASE
   MAPS TO CHROMOSOME-15Q24-Q25
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Note
ID AMINO-ACID-SEQUENCE; MARFAN-SYNDROME; MESSENGER-RNA; GENE; LOCALIZATION;
   ASSIGNMENT; CLONING; INSITU
AB A novel human cDNA with a predicted protein homologous to the carboxyl end of lysyl oxidase, an extracellular enzyme involved in the maturation of collagen and elastin, has been isolated. The homology to lysyl oxidase begins exactly at the position of the exon 1/exon 2 boundary in the mouse gene (Contente, S., Csiszar, K., Kenyon, K., and Friedman, R. M. (1993) Genomics 16, 395-400). This lysyl oxidase-like gene, which appears to be no larger than 22.1 kilobases, codes for a single poly-adenylated RNA species of 2.48 kilobases and has been mapped to chromosome 15q24-q25.
C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702.
RP KENYON, K (reprint author), UNIFORMED SERV UNIV HLTH SCI,DEPT PATHOL,BETHESDA,MD 20814, USA.
FU NCI NIH HHS [R01 CA37351]
NR 25
TC 80
Z9 83
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 5
PY 1993
VL 268
IS 25
BP 18435
EP 18437
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LV659
UT WOS:A1993LV65900010
PM 7689553
ER

PT J
AU TAIRA, M
   HOCKMAN, SC
   CALVO, JC
   TAIRA, M
   BELFRAGE, P
   MANGANIELLO, VC
AF TAIRA, M
   HOCKMAN, SC
   CALVO, JC
   TAIRA, M
   BELFRAGE, P
   MANGANIELLO, VC
TI MOLECULAR-CLONING OF THE RAT ADIPOCYTE HORMONE-SENSITIVE CYCLIC
   GMP-INHIBITED CYCLIC-NUCLEOTIDE PHOSPHODIESTERASE
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CAMP PHOSPHODIESTERASE; FAT-CELLS; AMP PHOSPHODIESTERASE; INSULIN;
   LIPOLYSIS; TISSUE
AB Two distinct but related cGMP-inhibited cyclic nucleotide phosphodiesterase (cGI PDE) cDNAs were cloned from rat adipose tissue cDNA libraries. The open reading frame (3324 base pairs) of RcGIP1 encodes 1108 amino acids, including a hydrophobic membrane-association domain in the NH2-terminal portion and, in the COOH-terminal portion, a putative catalytic domain conserved among all mammalian PDEs which is preceded by a putative regulatory domain that contains three consensus cAMP-dependent protein kinase phosphorylation sites and followed by a hydrophilic COOH-terminal domain. The carboxyl-terminal portion including the conserved domain was expressed as a glutathione S-transferase fusion protein and exhibited cAMP PDE activity which was inhibited by cilostamide, a specific cGI PDE inhibitor. RcGIP1 cDNA hybridizes strongly with RNA from isolated adipocytes, and its mRNA increases dramatically during differentiation of 3T3-L1 adipocytes.
   The deduced sequence of the second partial cDNA clone (RcGIP2 clone 53B) is highly homologous to the corresponding region of human cardiac cGI PDE cDNA. RcGIP2 cDNA hybridized strongly with rat cardiac tissue RNA and weakly if at all with RNA from rat adipocytes or 3T3-L1 fibroblasts or adipocytes. We suggest that RcGIP1 represents the hormone-sensitive, membrane-associated rat adipocyte cGI PDE and RcGIP2, a cGI PDE from vascular elements in rat adipose tissue.
C1 NIDR, BONE RES BRANCH, BETHESDA, MD 20892 USA.
   NICHHD, MOLEC GENET LAB, BETHESDA, MD 20892 USA.
   CHIBA UNIV, SCH MED, DEPT INTERNAL MED 2, CHIBA 280, JAPAN.
   CHIBA UNIV, SCH MED, DEPT BIOCHEM, CHIBA 280, JAPAN.
   LUND UNIV, SCH MED, DEPT PHYSIOL CHEM, S-22100 LUND, SWEDEN.
RP TAIRA, M (reprint author), NHLBI, CELLULAR METAB LAB, RM 5N-307, BLDG 10, BETHESDA, MD 20892 USA.
NR 30
TC 110
Z9 112
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD SEP 5
PY 1993
VL 268
IS 25
BP 18573
EP 18579
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LV659
UT WOS:A1993LV65900033
PM 8395509
ER

PT J
AU BRESNICK, EH
   FELSENFELD, G
AF BRESNICK, EH
   FELSENFELD, G
TI EVIDENCE THAT THE TRANSCRIPTION FACTOR USF IS A COMPONENT OF THE HUMAN
   BETA-GLOBIN LOCUS-CONTROL REGION HETEROMERIC PROTEIN COMPLEX
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID DOMINANT CONTROL REGION; MAJOR LATE PROMOTER; PORPHOBILINOGEN DEAMINASE
   GENE; CELL GLUCOCORTICOID RECEPTOR; HIGH-LEVEL EXPRESSION; HEAT-SHOCK
   PROTEIN; DNA-BINDING; CHROMATIN STRUCTURE; ERYTHROID PROMOTER;
   ACTIVATION REGION
AB The human locus control region (LCR) consists of four DNase I hypersensitive sites upstream of the epsilon-globin gene and is intimately involved in globin gene transcription. We have used DNase I footprinting with K562 erythroleukemia cell extracts to identify protein components of the minimal LCR element, hypersensitive site 2. Six major regions of protection were observed, and the occupation of two regions (sites II and V) was strongly temperature-dependent. Fractionation of K562 nuclear proteins revealed a single major protein that bound tightly to site II. An E-box was necessary for high affinity binding to DNA. We used antibodies and recombinant USF protein to prove that the helix-loop-helix transcription factor USF is the only detectible component in K562 cells that binds to this site. Despite significant differences between site II and a canonical USF-binding site, the USF binding affinity was comparable for the two sites. In both cases the interaction with the E-box of either wild-type USF or a approximately 15-kDa minimal USF DNA binding polypeptide displays an unusual positive temperature dependence, consistent with the observed footprinting behavior. The results show that a relatively ubiquitous factor, not confined to erythroid cells, is an important part of the complex of proteins bound at hypersensitive site 2 of the LCR in K562 cells.
C1 NIDDKD,MOLEC BIOL LAB,BLDG 5,RM 214,BETHESDA,MD 20892.
NR 56
TC 87
Z9 87
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 SEP 5
PY 1993
VL 268
IS 25
BP 18824
EP 18834
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA LV659
UT WOS:A1993LV65900069
PM 8360172
ER

PT J
AU TAKASHIMA, H
   WALKER, BR
   CANNONSPOOR, HE
   FREED, WJ
AF TAKASHIMA, H
   WALKER, BR
   CANNONSPOOR, HE
   FREED, WJ
TI KAINIC ACID LESIONS INCREASE REAFFERENTATION OF THE STRIATUM BY
   SUBSTANTIA-NIGRA GRAFTS
SO BRAIN RESEARCH
LA English
DT Article
DE TRANSPLANTATION; SUBSTANTIA-NIGRA; NEURITE; BRAIN INJURY; FLUORESCENCE
   HISTOCHEMISTRY; KAINIC ACID; EXCITOTOXIC LESION
ID FIBROBLAST GROWTH-FACTOR; DOPAMINERGIC-NEURONS INVITRO; ADULT-RAT
   HIPPOCAMPUS; MESENCEPHALIC NEURONS; DENERVATED STRIATUM; PRIMARY
   CULTURE; MESSENGER-RNA; BRAIN GRAFTS; SURVIVAL; LAMININ
AB Effects of kainic acid lesions of the striatum on reafferentation of the striatum produced by intraventricular substantia nigra (SN) grafts were investigated. Rats with unilateral 6-hydroxydopamine lesions of the SN received intrastriatal kainic acid lesions or sham lesions, and then received fetal (E16) SN or sciatic nerve grafts in the lateral ventricle. The depth of reafferentation of the striatum by catecholaminergic neurites from SN grafts was significantly increased in rats with kainic acid-induced striatal lesions, as compared to the sham-lesioned controls. No reafferentation was seen in the control animals with sciatic nerve grafts. These data suggest that striatal injury promotes the growth of dopaminergic neurites from SN grafts.
C1 NIMH,NEUROSCI CTR ST ELIZABETHS,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032.
NR 55
TC 7
Z9 7
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD SEP 3
PY 1993
VL 621
IS 1
BP 71
EP 78
DI 10.1016/0006-8993(93)90299-3
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA LU745
UT WOS:A1993LU74500009
PM 8221075
ER

PT J
AU SCHNEIDER, RJ
   FRIEDMAN, DP
   MISHKIN, M
AF SCHNEIDER, RJ
   FRIEDMAN, DP
   MISHKIN, M
TI A MODALITY-SPECIFIC SOMATOSENSORY AREA WITHIN THE INSULA OF THE
   RHESUS-MONKEY
SO BRAIN RESEARCH
LA English
DT Note
DE RHESUS MONKEY; GRANULAR INSULA; SINGLE UNIT; SOMATOSENSORY; BILATERAL
   RECEPTIVE FIELD
ID M FASCICULARIS; CORTEX; NEURONS; MACAQUE; SYSTEM; FIELDS; SERIAL
AB Response properties of neurons in the monkey's granular insula (Ig) were examined with somatic, auditory, visual, and gustatory stimuli. Results indicate that a major portion of Ig is a somatic processing area exclusively, with units that have large and often bilateral receptive fields, consistent with the view that this area serves as a higher-order, modality-specific link in the somatosensory-limbic pathway.
C1 NIMH,NEUROPSYCHOL LAB,BLDG 49,ROOM 1B80,BETHESDA,MD 20892.
NR 16
TC 119
Z9 119
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD SEP 3
PY 1993
VL 621
IS 1
BP 116
EP 120
DI 10.1016/0006-8993(93)90305-7
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA LU745
UT WOS:A1993LU74500015
PM 8221062
ER

PT J
AU FREO, U
   DAM, M
   PIZZOLATO, G
   PIETRINI, P
   SONCRANT, TT
   BATTISTIN, L
AF FREO, U
   DAM, M
   PIZZOLATO, G
   PIETRINI, P
   SONCRANT, TT
   BATTISTIN, L
TI THE MONOSIALOGANGLIOSIDE GM(1) DOSE-DEPENDENTLY REDUCES REGIONAL
   CEREBRAL METABOLIC RATES FOR GLUCOSE IN AWAKE RATS
SO BRAIN RESEARCH
LA English
DT Note
DE MONOSIALOGANGLIOSIDE GM(1); GLUCOSE METABOLIC RATE; CEREBRAL METABOLISM;
   EXCITATORY AMINO ACID; HIPPOCAMPUS
ID GM1 GANGLIOSIDE TREATMENT; D-ASPARTATE ANTAGONISTS; AMINO-ACID
   RECEPTORS; NEURONS; NMDA; CATS; NEUROTOXICITY; PHENCYCLIDINE; HISTOLOGY;
   RECOVERY
AB Using the quantitative autoradiographic [C-14]2-deoxyglucose technique, regional cerebral metabolic rates for glucose (rCMRglc) were measured in awake male Fischer-344 rats at 1, 2, 3, 4 and 6 h after administration of GM, 30 mg/kg and at 3 h after GM1 150 or 300 mg/kg. GM1 is a natural compound that is able to prevent neuron degeneration induced by exposure to excitatory amino acids in vitro and by ischemia or neurotoxins in vivo. GM1 30 mg/kg, a dose very effective in preventing excitatory amino acid-induced neurotoxicity, produced minimal rCMRglc change over a 6 h period. GM1 150 and 300 mg/kg reduced rCMRglc, in 14 (31%) and in 29 (64%) brain regions, respectively. Maximal metabolic effects occurred in hippocampal areas which possess, in specific subfields, the highest brain concentrations of different excitatory amino acid receptor subtypes. This finding suggests an effect by GM1 on postreceptor mechanisms common to different excitatory amino acids.
C1 CLIN MALATTIE NERVOSE & MENTALI, PADUA, ITALY.
   CLIN PSICHIAT 1, PISA, ITALY.
RP FREO, U (reprint author), NIA, NEUROSCI LAB, PHARMACOL & PHARMACOKINET UNIT, BLDG 10, ROOM 6C414, BETHESDA, MD 20892 USA.
NR 30
TC 1
Z9 1
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD SEP 3
PY 1993
VL 621
IS 1
BP 175
EP 179
DI 10.1016/0006-8993(93)90317-G
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA LU745
UT WOS:A1993LU74500027
PM 8106115
ER

PT J
AU JACOBSON, KA
   SHI, D
   GALLORODRIGUEZ, C
   MANNING, M
   MULLER, C
   DALY, JW
   NEUMEYER, JL
   KIRIASIS, L
   PFLEIDERER, W
AF JACOBSON, KA
   SHI, D
   GALLORODRIGUEZ, C
   MANNING, M
   MULLER, C
   DALY, JW
   NEUMEYER, JL
   KIRIASIS, L
   PFLEIDERER, W
TI EFFECT OF TRIFLUOROMETHYL AND OTHER SUBSTITUENTS ON ACTIVITY OF
   XANTHINES AT ADENOSINE RECEPTORS
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID A2-ADENOSINE RECEPTORS; A1-ADENOSINE RECEPTORS; ANTAGONISTS; POTENT;
   ANALOGS; 1,3-DIPROPYL-8-PHENYLXANTHINE; INHIBITION; BINDING; AGONIST;
   BRAIN
AB An aryl p-(trifluoromethyl) substituent increases the affinity of 1,3-disubstituted 8-phenylxanthines at A2a-adenosine receptors, while having little effect on affinity at Al-adenosine receptors. In contrast, an aryl p-(trifluoromethyl) substituent has little effect on affinity of 3,7-disubstituted and 1,3,7-trisubstituted 8-phenylxanthines. An aryl p-sulfo substituent reduces affinity of all 8-phenylxanthines at A1-and A2a-adenosine receptors. An 8-(trifluoromethyl) substituent markedly reduces affinity of 1,3-dialkylxanthines at both A1- and A2a-adenosine receptors. In contrast, 8-(trifluoromethyl)caffeine retains affinity for A2a-adenosine receptors, but does lose affinity for A1-adenosine receptors. 8-Bromo-, 8-acryl-, and 8-pent-1-enylcaffeines are also selective for A2-adenosine receptors, while 8-cyclobutylcaffeine is nonselective. 8-[trans-2-(tert-butyloxycarbonyl)vinylcaffeine is 20-fold selective for Aza vs A1 receptors.
C1 RES BIOCHEM INT,NATICK,MA 01760.
   UNIV CONSTANCE,FAC CHEM,W-7750 CONSTANCE,GERMANY.
RP JACOBSON, KA (reprint author), NIH,BIOORGAN CHEM LAB,BETHESDA,MD 20892, USA.
RI Gallo-Rodriguez, Carola/E-1732-2012; Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999]
NR 25
TC 41
Z9 42
U1 0
U2 0
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD SEP 3
PY 1993
VL 36
IS 18
BP 2639
EP 2644
DI 10.1021/jm00070a007
PG 6
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA LW550
UT WOS:A1993LW55000007
PM 8410976
ER

PT J
AU HAMER, D
   HU, S
   MAGNUSON, V
   HU, N
   PATTATUCCI, A
AF HAMER, D
   HU, S
   MAGNUSON, V
   HU, N
   PATTATUCCI, A
TI GENETICS AND MALE SEXUAL ORIENTATION - RESPONSE
SO SCIENCE
LA English
DT Letter
RP HAMER, D (reprint author), NCI,BIOCHEM LAB,BETHESDA,MD 20892, USA.
NR 0
TC 2
Z9 2
U1 1
U2 7
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005
SN 0036-8075
J9 SCIENCE
JI Science
PD SEP 3
PY 1993
VL 261
IS 5126
BP 1259
EP 1259
DI 10.1126/science.261.5126.1259
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LV656
UT WOS:A1993LV65600004
PM 17731839
ER

PT J
AU HARATA, K
   RAO, CT
   PITHA, J
AF HARATA, K
   RAO, CT
   PITHA, J
TI CRYSTAL-STRUCTURE OF 6-0-[(R)-2-HYDROXYPROPYL]CYCLOMALTOHEPTAOSE AND
   6-0-[(S)-2-HYDROXYPROPYL]CYCLOMALTOHEPTAOSE
SO CARBOHYDRATE RESEARCH
LA English
DT Article
ID BETA-CYCLODEXTRIN; DERIVATIVES; COMPLEXES; DRUGS
AB Crystal structures of 6-O-[(R)-2-hydroxypropyl]- and 6-O-[(S)-2-hydroxypropyl)-cyclomaltoheptaose were determined by X-ray analysis. In both structures, the 2-hydroxypropyl group is inserted into the macrocyclic cavity of the next molecule related by the two-fold screw axis, and a helically extended polymeric structure is formed by repetition of the intermolecular inclusion. The hydroxyl group of the substituent group penetrates through the macrocyclic ring from the secondary hydroxyl side and is linked to an HO-6 group by a hydrogen bond. Comparison of intermolecular contacts of the substituent group indicates that the (S)-2-hydroxypropyl group is better fitted to the cavity than the (R)-2-hydroxypropyl group.
C1 RES INST POLYMERS & TEXT,TSUKUBA,IBARAKI 305,JAPAN.
   NIA,GRC,BALTIMORE,MD 21224.
NR 19
TC 33
Z9 34
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0008-6215
J9 CARBOHYD RES
JI Carbohydr. Res.
PD SEP 2
PY 1993
VL 247
BP 83
EP 98
DI 10.1016/0008-6215(93)84243-Y
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA LX562
UT WOS:A1993LX56200008
PM 8221734
ER

PT J
AU SHARP, D
   BLINDERMAN, L
   COMBS, KA
   KIENZLE, B
   RICCI, B
   WAGERSMITH, K
   GIL, CM
   TURCK, CW
   BOUMA, ME
   RADER, DJ
   AGGERBECK, LP
   GREGG, RE
   GORDON, DA
   WETTERAU, JR
AF SHARP, D
   BLINDERMAN, L
   COMBS, KA
   KIENZLE, B
   RICCI, B
   WAGERSMITH, K
   GIL, CM
   TURCK, CW
   BOUMA, ME
   RADER, DJ
   AGGERBECK, LP
   GREGG, RE
   GORDON, DA
   WETTERAU, JR
TI CLONING AND GENE DEFECTS IN MICROSOMAL TRIGLYCERIDE TRANSFER PROTEIN
   ASSOCIATED WITH ABETALIPOPROTEINEMIA
SO NATURE
LA English
DT Article
ID HEP G2 CELLS; APOLIPOPROTEIN-B; INTRACELLULAR DEGRADATION; DISULFIDE
   ISOMERASE; SECRETION; LIPOPROTEINS; COMPLEX; SITES
AB THE microsomal triglyceride transfer protein (MTP), which catalyses the transport of triglyceride, cholesteryl ester and phospholipid between phospholipid surfaces, is a heterodimer composed of the multifunctional protein, protein disulphide isomerase, and a unique large subunit with an apparent M(r) of 88K (refs 1-3).  It is isolated as a soluble protein from the lumen of the microsomal fraction of liver and intestine4. The large subunit of MTP was not detectable in four unrelated subjects with abetatipoproteinaemia5, a rare autosomal recessive disease characterized by a defect in the assembly or secretion of plasma lipoproteins that contain apolipoprotein B (ref. 6). We report here the isolation and sequencing of complementary DNA encoding the large subunit of MTP. A comparison of this sequence to corresponding genomic sequences from two abetatipoproteinaemic subjects revealed a homozygous frameshift mutation in one subject and a homozygous nonsense mutation in the other. The results indicate that a defect in the gene for die large subunit of MTP is the proximal cause of abetalipoproteinaemia in these two subjects, and that MTP is required for the secretion of plasma lipoproteins that contain apolipoprotein B.
C1 BRISTOL MYERS SQUIBB,DEPT METAB DIS,PRINCETON,NJ 08543.
   UNIV CINCINNATI,DEPT PHARMACOL & CELL BIOPHYS,CINCINNATI,OH 45267.
   UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,DEPT MED,SAN FRANCISCO,CA 94143.
   UNIV PARIS 07,INSERM,U327,F-75018 PARIS,FRANCE.
   NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892.
   CNRS,CTR GENET MOLEC,F-91198 GIF SUR YVETTE,FRANCE.
NR 17
TC 331
Z9 338
U1 0
U2 3
PU MACMILLAN MAGAZINES LTD
PI LONDON
PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW
SN 0028-0836
J9 NATURE
JI Nature
PD SEP 2
PY 1993
VL 365
IS 6441
BP 65
EP 69
DI 10.1038/365065a0
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA LV646
UT WOS:A1993LV64600055
PM 8361539
ER

PT J
AU JORDAN, EK
   HEYES, MP
AF JORDAN, EK
   HEYES, MP
TI VIRUS ISOLATION AND QUINOLINIC ACID IN PRIMARY AND CHRONIC SIMIAN
   IMMUNODEFICIENCY VIRUS-INFECTION
SO AIDS
LA English
DT Article
DE QUINOLINIC ACID; CEREBROSPINAL FLUID; SIMIAN IMMUNODEFICIENCY VIRUS;
   SERUM; PERIPHERAL BLOOD MONONUCLEAR CELLS
ID PRIMARY HIV INFECTION; SIV BRAIN INFECTION; CEREBROSPINAL-FLUID;
   RHESUS-MONKEYS; NERVOUS-SYSTEM; IMMATURE HOST; HTLV-III; AIDS; PLASMA;
   INTERFERON
AB Objective: In this 2.5-year study of simian immunodeficiency virus (SIV(sm)) infection in rhesus monkeys, quinolinic acid (QUIN) levels and virus isolation determinations were made in serial cerebrospinal fluid (CSF) and blood samples to evaluate the relationship between these parameters over the course of infection.
   Methods: Eight rhesus monkeys were inoculated in the saphenous vein with SIV(sm). Four animals were maintained as uninoculated controls. CSF and blood samples were obtained every 1-4 weeks over the course of study. SIV isolation was determined in H9 cells for the CSF and in primary rhesus lymphocyte co-cultures for peripheral blood mononuclear cells (PBMC). QUIN was quantitated in CSF and serum by electron-capture negative chemical ionization gas chromatography mass spectrometry.
   Results: All SIV-inoculated animals became CSF and PBMC isolation-positive by 1-3 weeks post-inoculation. Control animals remained SIV-negative. One SIV-positive animal was humanely euthanized at 2 weeks post-inoculation. The three SIV-inoculated animals that were CSF isolation-negative after the fifth week post-inoculation maintained CSF QUIN values < 100 nM, remained CSF and PBMC isolation-negative, and clinically healthy in the chronic course of disease. In contrast, the four SIV-inoculated animals that were CSF isolation-positive 6-8 weeks post-inoculation had CSF QUIN levels as high as 153-565 nM during the second month post-inoculation and remained CSF virus isolation-negative, persistently PBMC isolation-positive, and experienced clinical symptoms of SIV in the chronic course of disease. Three of these four animals have succumbed to SIV infection.
   Discussion: Initial QUIN responses and viral isolation status in the first month post-inoculation were consistent among SIV-inoculated animals with CSF and serum QUIN values significantly higher than those of controls. A divergence within the SIV-inoculated group of animals became apparent within the second month of primary SIV infection and was maintained throughout the course of infection. Persistent PBMC viral isolation and marked elevations of QUIN were linked to symptomatic disease and a poor prognosis for survival. Predominantly negative PBMC viral isolation and slight, but significant, elevations of QUIN were linked to asymptomatic disease with a favorable prognosis for survival.
C1 NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BETHESDA,MD 20892.
RP JORDAN, EK (reprint author), NINCDS,ANIM HLTH & CARE SECT,RM 4A-19,BLDG 36,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 52
TC 11
Z9 11
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
PD SEP
PY 1993
VL 7
IS 9
BP 1173
EP 1179
DI 10.1097/00002030-199309000-00004
PG 7
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA LV706
UT WOS:A1993LV70600004
PM 8216973
ER

PT J
AU NELSON, AM
   PERRIENS, JH
   KAPITA, B
   OKONDA, L
   LUSAMUNO, N
   KALENGAYI, MR
   ANGRITT, P
   QUINN, TC
   MULLICK, FG
AF NELSON, AM
   PERRIENS, JH
   KAPITA, B
   OKONDA, L
   LUSAMUNO, N
   KALENGAYI, MR
   ANGRITT, P
   QUINN, TC
   MULLICK, FG
TI A CLINICAL AND PATHOLOGICAL COMPARISON OF THE WHO AND CDC CASE
   DEFINITIONS FOR AIDS IN KINSHASA, ZAIRE - IS PASSIVE SURVEILLANCE VALID
SO AIDS
LA English
DT Article
DE AIDS; AIDS SURVEILLANCE; CLINICAL CASE DEFINITION; AUTOPSY;
   HISTOPATHOLOGY; AFRICA; ZAIRE
ID TUBERCULOSIS; AFRICA
AB Objectives: To compare the specificity of the World Health Organization (WHO) and Centers for Disease Control and Prevention (CDC) case definitions for AIDS in autopsy cases from Zaire.
   Setting: Mama Yemo Hospital and University Hospital morgues in Kinshasa, and Karawa Hospital in Equateur Region, Zaire.
   Methods: Autopsy cases with a clinical diagnosis of AIDS on the death certificate or chart were studied. Evaluation included post-mortem HIV-1 serology, chart review for specific AIDS-related symptoms and signs, and application of WHO and CDC case criteria to the clinical and autopsy diagnoses.
   Results: Of the 68 diagnosed AIDS cases, 98% fulfilled WHO criteria for AIDS and 93% fulfilled both WHO and CDC criteria. All cases fulfilling both criteria were HIV-1-seropositive. Opportunistic infections accounted for 84% of CDC AIDS-defining conditions. Disseminated tuberculosis was the most frequent (41%) specific diagnosis; Pneumocystis carinii pneumonia was rare (<2%).
   Conclusions: There was good concordance between WHO and CDC case definitions. A diagnosis of AIDS on the chart or death certificate is adequate for surveillance purposes in this population.
C1 PROJET SIDA,KINSHASA,ZAIRE.
   AMER REGISTRY PATHOL,WASHINGTON,DC.
   INST TROP MED,ANTWERP,BELGIUM.
   MAMA YEMO HOSP,KINSHASA,ZAIRE.
   UNIV HOSP KINSHASA,KINSHASA,ZAIRE.
   JOHNS HOPKINS UNIV,NIAID,BALTIMORE,MD 21218.
RP NELSON, AM (reprint author), ARMED FORCES INST PATHOL,DIV AIDS PATHOL,WASHINGTON,DC 20306, USA.
NR 15
TC 41
Z9 41
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
PD SEP
PY 1993
VL 7
IS 9
BP 1241
EP 1245
DI 10.1097/00002030-199309000-00014
PG 5
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA LV706
UT WOS:A1993LV70600014
PM 8216982
ER

PT J
AU BRIGGS, NC
   NATOLI, C
   TINARI, N
   DEGIDIO, M
   GOEDERT, JJ
   IACOBELLI, S
AF BRIGGS, NC
   NATOLI, C
   TINARI, N
   DEGIDIO, M
   GOEDERT, JJ
   IACOBELLI, S
TI A 90-KDA PROTEIN SERUM MARKER FOR THE PREDICTION OF PROGRESSION TO AIDS
   IN A COHORT OF HIV-1+ HOMOSEXUAL MEN
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TUMOR-ASSOCIATED ANTIGEN; PROGNOSTIC
   VALUE; BREAST-CANCER; INFECTION; ANTIBODY; NEOPTERIN; LEVEL; RISK; 90K
AB Levels of a 90-kDa protein (90K), recently reported as a possible marker of HIV-1 infection, were serially examined in a group of HIV-1-infected (HIV-1+) and uninfected (HIV-1-) subjects drawn from the same cohort of homosexual men. The first phase of the study included 61 HIV-1+ AIDS-free subjects 4 years (+/- 6 months) postseroconversion and 75 contemporaneous uninfected subjects. Two years later, a subset of 35 HIV-1+ AIDS-free subjects and 72 HIV-1 controls was examined. Mean 90K levels for HIV-1+ subjects were significantly higher than for contemporaneous HIV-1- subjects both 4 and 6 years postseroconversion (p < 0.0001). A significantly more rapid progression to AIDS was seen in HIV-1+ subjects with high 90K levels both 4 years (p = 0.01) and 6 years (p = 0.003) postseroconversion. Four years postseroconversion, 90K was significantly correlated with CD8 cell percent, interferon, neopterin, and beta2-microglobulin (p < 0.05). Two years later, significant correlations were seen between 90K levels and CD4 cell percent, CD4 cell number, and beta2-microglobulin (p < 0. 05). Stepwise-stepdown regression modeling using 90K, CD4 cell percent, interferon, and beta2-microglobulin levels 4 years postseroconversion showed that the predictive value of a trivariate model of 90K-interferon-CD4 percent was better than any univariate or bivariate model. We conclude that the 90K protein may be a useful predictor of progression to AIDS in HIV-1+ patients, particularly in combination with the established markers of CD4 cell percent and interferon.
C1 UNIV G DANNUNZIO, CATTEDRA ONCOL MED, I-66100 CHIETI, ITALY.
RP NCI, DIV CANC ETIOL, EPIDEMIOL & BIOSTAT PROGRAM, VIRAL EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA.
RI Natoli, Clara/E-1378-2013
OI Natoli, Clara/0000-0001-7295-0230
FU NCI NIH HHS [N01-CP-95612]
NR 23
TC 27
Z9 28
U1 0
U2 3
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD SEP
PY 1993
VL 9
IS 9
BP 811
EP 816
DI 10.1089/aid.1993.9.811
PG 6
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA MB204
UT WOS:A1993MB20400002
PM 7504933
ER

PT J
AU ARYA, SK
AF ARYA, SK
TI HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-2 (HIV-2) TRANSACTIVATOR (TAT) -
   FUNCTIONAL DOMAINS AND THE SEARCH FOR TRANSDOMINANT NEGATIVE MUTANTS
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
ID LONG TERMINAL REPEAT; GENE-EXPRESSION; MUTATIONAL ANALYSIS;
   TRANSCRIPTIONAL INITIATION; RESPONSIVE SEQUENCE; RNA RECOGNITION; BASIC
   DOMAIN; HTLV-III; PROTEIN; TRANSACTIVATION
AB Human immunodeficiency virus type 2 (HIV-2) trans-activator (Tat) is an important trans-regulator of viral gene expression. It differs from the related HIV-1 Tat in certain aspects of its structure and function. HIV-2 Tat is composed of 130 amino acids versus 86 amino acids for HIV-1 Tat. Apart from certain conserved regions, there is little homology between the two Tats. They also differ in their ability to trans-activate HIV-2 and HIV-1 long terminal repeat (LTR)-directed gene expression. As an aid to understanding its mechanism of action, the functional domains important for HIV-2 Tat trans-activation of HIV-2 and HIV-1 LTR-directed gene expression were investigated. Like HIV-1 Tat, HIV-2 Tat contains conserved cysteine- and arginine-rich domains important for its function. However, HIV-2 Tat differs from HIV-1 Tat in that about 20% of the HIV-2 Tat at the amino terminus was not essential for its trans-activation function while HIV-1 Tat amino terminus is reportedly a part of its activation domain. Similarly, about 30% of the protein at the carboxy terminus of HIV-2 Tat was not essential. A domain critical for HIV-2 Tat-mediated trans-activation was located just upstream of the cysteine-rich domain. This segment is predicted to adopt an alpha-helical conformation and also contains acidic amino acid residues; thus, it may resemble amphipathic helix-type activation domains found in some transcriptional factors. A region with predicted hydrophobic alpha-helical character located between the cysteine- and arginine-rich domains was also important for HIV-2 Tat function. HIV-2 Tat mutants that were analogs of HIV-1 Tat trans-dominant negative mutants did not display such a phenotype.
RP ARYA, SK (reprint author), NCI,TUMOR CELL BIOL LAB,BLDG 37,ROOM 6A09,BETHESDA,MD 20892, USA.
NR 48
TC 13
Z9 13
U1 0
U2 1
PU MARY ANN LIEBERT INC PUBL
PI LARCHMONT
PA 2 MADISON AVENUE, LARCHMONT, NY 10538
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD SEP
PY 1993
VL 9
IS 9
BP 839
EP 848
DI 10.1089/aid.1993.9.839
PG 10
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA MB204
UT WOS:A1993MB20400006
PM 8257633
ER

PT J
AU NIU, MT
   JERMANO, JA
   REICHELDERFER, P
   SCHNITTMAN, SM
AF NIU, MT
   JERMANO, JA
   REICHELDERFER, P
   SCHNITTMAN, SM
TI SUMMARY OF THE NATIONAL-INSTITUTES-OF-HEALTH WORKSHOP ON PRIMARY
   HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
ID PERSISTENT GENERALIZED LYMPHADENOPATHY; HIV-1 BIOLOGICAL PHENOTYPE;
   PROGRAMMED CELL-DEATH; PROPHYLACTIC ZIDOVUDINE; RHESUS-MONKEYS; AIDS;
   3'-AZIDO-3'-DEOXYTHYMIDINE; DISEASE; FAILURE; THERAPY
AB A Workshop on primary human immunodeficiency virus type 1 (HIV-1) infection sponsored by the National Institute of Allergy and Infectious Diseases (NIAID) and the Office of AIDS Research (OAR) of the National Institutes of Health (NIH) was held February 25-26, 1993 in Bethesda, Maryland. The major goals of this scientific meeting were to bring together researchers and infectious disease specialists who have expertise in primary HIV-1 infection (PHI) to review the pathogenesis of PHI, the treatment experience of PHI in humans and of early retroviral infection in animal models, and to devise theoretical and operational strategies for future clinical trials relating to therapeutic intervention of PHI. The proceedings of this workshop are timely and serve to further the development of innovative strategies for the treatment of HIV-1 infection.
RP NIU, MT (reprint author), NIAID,DIV AIDS,CLIN RES PROGRAM,MED BRANCH,6003 EXECUT BLVD,BETHESDA,MD 20892, USA.
NR 37
TC 28
Z9 29
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 SEP
PY 1993
VL 9
IS 9
BP 913
EP 924
DI 10.1089/aid.1993.9.913
PG 12
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA MB204
UT WOS:A1993MB20400015
PM 7903045
ER

PT J
AU GUO, HG
   REITZ, MS
   GALLO, RC
   KO, YC
   CHANG, KSS
AF GUO, HG
   REITZ, MS
   GALLO, RC
   KO, YC
   CHANG, KSS
TI A NEW SUBTYPE OF HIV-1 GAG SEQUENCE DETECTED IN TAIWAN
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Note
C1 CHANG GUNG MED COLL,GRAD INST CLIN MED,TAYUAN,TAIWAN.
   NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892.
   KACHSIUNG MED COLL,SCH PUBL HLTH,KACHSIUNG,TAIWAN.
NR 7
TC 10
Z9 10
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 SEP
PY 1993
VL 9
IS 9
BP 925
EP 927
DI 10.1089/aid.1993.9.925
PG 3
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA MB204
UT WOS:A1993MB20400016
PM 8257639
ER

PT J
AU WEINBERG, CR
AF WEINBERG, CR
TI REPRODUCTIVE FACTORS AND RISK OF MYOCARDIAL-INFARCTION
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Letter
ID HEART-DISEASE; IRON
RP WEINBERG, CR (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA.
NR 5
TC 1
Z9 1
U1 0
U2 0
PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH
PI BALTIMORE
PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD SEP 1
PY 1993
VL 138
IS 5
BP 351
EP 351
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA LW583
UT WOS:A1993LW58300010
PM 8356975
ER

PT J
AU MAHER, ER
   RICHARDS, FM
   CROSSEY, PA
   LATIF, F
   FOSTER, K
   LINEHAN, M
   AFFARA, NA
   LERMAN, M
   ZBAR, B
   FERGUSONSMITH, MA
AF MAHER, ER
   RICHARDS, FM
   CROSSEY, PA
   LATIF, F
   FOSTER, K
   LINEHAN, M
   AFFARA, NA
   LERMAN, M
   ZBAR, B
   FERGUSONSMITH, MA
TI MOLECULAR-GENETIC ANALYSIS IN THE MANAGEMENT OF VONHIPPEL-LINDAU (VHL)
   DISEASE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NCI,SURG BRANCH,BETHESDA,MD 20892.
   UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE,ENGLAND.
   NCI,FREDERICK CANC RES FACIL,IMMUNOBIOL LAB,FREDERICK,MD 21701.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 16
EP 16
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500014
ER

PT J
AU BOYD, J
   KOHLER, MF
   BERCHUCK, A
   WATSON, P
   LYNCH, HT
   RISINGER, JI
AF BOYD, J
   KOHLER, MF
   BERCHUCK, A
   WATSON, P
   LYNCH, HT
   RISINGER, JI
TI MICROSATELLITE INSTABILITY IN SPORADIC ENDOMETRIAL CARCINOMAS AND THOSE
   ASSOCIATED WITH HNPCC
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIEHS,RES TRIANGLE PK,NC 27709.
   DUKE UNIV,DURHAM,NC 27706.
   CREIGHTON UNIV,OMAHA,NE 68178.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 22
EP 22
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500022
ER

PT J
AU RICHARDS, FM
   CROSSEY, PA
   LATIF, F
   FOSTER, K
   LINEHAN, M
   AFFARA, NA
   LERMAN, M
   ZBAR, B
   FERGUSONSMITH, MA
   MAHER, ER
AF RICHARDS, FM
   CROSSEY, PA
   LATIF, F
   FOSTER, K
   LINEHAN, M
   AFFARA, NA
   LERMAN, M
   ZBAR, B
   FERGUSONSMITH, MA
   MAHER, ER
TI FREQUENT GERMLINE DELETIONS IN VONHIPPEL-LINDAU DISEASE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE,ENGLAND.
   NCI,FREDERICK CANC RES FACIL,IMMUNOBIOL LAB,FREDERICK,MD 21701.
   NCI,SURG BRANCH,BALTIMORE,MD 21211.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 24
EP 24
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500026
ER

PT J
AU CROSSEY, PA
   RICHARDS, FM
   LATIF
   FOSTER, K
   LINEHAN, M
   AFFARA, NA
   LERMAN, M
   ZBAR, B
   FERGUSONSMITH, MA
   MAHER, ER
AF CROSSEY, PA
   RICHARDS, FM
   LATIF
   FOSTER, K
   LINEHAN, M
   AFFARA, NA
   LERMAN, M
   ZBAR, B
   FERGUSONSMITH, MA
   MAHER, ER
TI MOLECULAR CHARACTERIZATION OF GERMLINE MUTATIONS IN THE VONHIPPEL-LINDAU
   DISEASE GENE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NCI,FREDERICK CANC RES FACIL,IMMUNOBIOL LAB,FREDERICK,MD 21701.
   UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE,ENGLAND.
   NCI,SURG BRANCH,BALTIMORE,MD 21211.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 25
EP 25
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500024
ER

PT J
AU GAILANI, M
   DEAN, M
   MYERS, JC
   CHIDAMBARAM, A
   LEFFELL, D
   SIU, V
   BALE, A
AF GAILANI, M
   DEAN, M
   MYERS, JC
   CHIDAMBARAM, A
   LEFFELL, D
   SIU, V
   BALE, A
TI EVALUATION OF COL15A1 AS A CANDIDATE GENE FOR GORLIN SYNDROME
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 YALE UNIV,NEW HAVEN,CT 06520.
   NCI,FREDERICK CANC RES FACIL,FREDERICK,MD 21701.
   UNIV PENN,PHILADELPHIA,PA 19104.
   N YORK GEN HOSP,N YORK M2K 1E1,ONTARIO,CANADA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 31
EP 31
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500030
ER

PT J
AU CHUNG, MY
   RANUM, LPW
   DUVICK, LA
   GOLDFARB, L
   ZOGHBI, HY
   ORR, HT
AF CHUNG, MY
   RANUM, LPW
   DUVICK, LA
   GOLDFARB, L
   ZOGHBI, HY
   ORR, HT
TI ANALYSIS OF THE TRINUCLEOTIDE CAG REPEAT IN SPINOCEREBELLAR ATAXIA
   TYPE-1 SUGGESTS THAT CONVERSION FROM AN INTERRUPTED TO A HOMOGENEOUS
   REPEAT LEADS TO INSTABILITY
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 UNIV MINNESOTA,MINNEAPOLIS,MN 55455.
   BAYLOR COLL MED,HOUSTON,TX 77030.
   NIH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 84
EP 84
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500084
ER

PT J
AU ROSS, CA
   LI, SH
   YOUNG, WS
   SCHILLING, G
   LI, XJ
   STINE, OC
   MARGOLIS, RL
   WAGSTER, MV
   RANEN, NG
   HEDREEN, JC
   FOLSTEIN, SE
AF ROSS, CA
   LI, SH
   YOUNG, WS
   SCHILLING, G
   LI, XJ
   STINE, OC
   MARGOLIS, RL
   WAGSTER, MV
   RANEN, NG
   HEDREEN, JC
   FOLSTEIN, SE
TI EXPRESSION OF IT-15 AND LACK OF REDUCTION IN HUNTINGTONS-DISEASE (HD)
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,MOLEC NEUROBIOL LAB,BALTIMORE,MD 21205.
   JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205.
   JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205.
   NIMH,CELL BIOL LAB,BETHESDA,MD 20892.
RI Young, W Scott/A-9333-2009
OI Young, W Scott/0000-0001-6614-5112
NR 0
TC 3
Z9 3
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 85
EP 85
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500087
ER

PT J
AU KIESEWETTER, S
   MACEK, M
   CURRISTIN, S
   CHU, C
   GRAHAM, C
   SHRIMPTON, AE
   DEARCE, M
   ZIELENSKI, J
   MICKLE, J
   AMOS, J
   HIGHSMITH, WE
   SHUBER, A
   WITT, D
   CRYSTAL, RG
   CUTTING, GR
AF KIESEWETTER, S
   MACEK, M
   CURRISTIN, S
   CHU, C
   GRAHAM, C
   SHRIMPTON, AE
   DEARCE, M
   ZIELENSKI, J
   MICKLE, J
   AMOS, J
   HIGHSMITH, WE
   SHUBER, A
   WITT, D
   CRYSTAL, RG
   CUTTING, GR
TI THE CFTR MUTATION R117H PRODUCES DIFFERENT PHENOTYPES DEPENDING ON
   GENETIC BACKGROUND
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
   JOHNS HOPKINS UNIV,BALTIMORE,MD 21218.
   REG GENET CTR,BELFAST,NORTH IRELAND.
   UNIV EDINBURGH,EDINBURGH EH8 9YL,MIDLOTHIAN,SCOTLAND.
   KAISER PERMANENTE,SAN JOSE,CA.
   UNIV DUBLIN TRINITY COLL,DUBLIN 2,IRELAND.
   HOSP SICK CHILDREN,TORONTO M5G 1X8,ONTARIO,CANADA.
   BOSTON UNIV,SCH MED,BOSTON,MA 02118.
   N CAROLINA MEM HOSP,CHAPEL HILL,NC 27514.
   INTEGRATED GENET INC,FRAMINGHAM,MA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 86
EP 86
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500085
ER

PT J
AU MCKINNEY, C
   SIDRANSKY, E
   MARTIN, BM
   ELIASON, W
   GALDZICKA, M
   CHO, M
   LEE, S
   GILBERT, C
   SHORR, R
   GINNS, EI
AF MCKINNEY, C
   SIDRANSKY, E
   MARTIN, BM
   ELIASON, W
   GALDZICKA, M
   CHO, M
   LEE, S
   GILBERT, C
   SHORR, R
   GINNS, EI
TI POLYETHYLENE-GLYCOL MODIFIED GLUCOCEREBROSIDASE - RESULTS FROM
   PRECLINICAL STUDIES
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892.
   ENZON INC,DEPT RES & DEV,PISCATHWAY,NJ.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 103
EP 103
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500104
ER

PT J
AU STAMATOYANNOPOULOS, JA
   LOWREY, CH
   NIENHUIS, AW
AF STAMATOYANNOPOULOS, JA
   LOWREY, CH
   NIENHUIS, AW
TI CHROMATIN STRUCTURE OF AN ENHANCER ELEMENT - RELATION BETWEEN REGULATORY
   FACTOR-BINDING AND HYPERSENSITIVE SITE FORMATION
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIH,CLIN HEMATOL BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 232
EP 232
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500232
ER

PT J
AU TAGLE, DA
   VALDES, J
   SWAROOP, M
   BLANCHARDMCQUATE, K
   COLLINS, FS
AF TAGLE, DA
   VALDES, J
   SWAROOP, M
   BLANCHARDMCQUATE, K
   COLLINS, FS
TI EVOLUTIONARY CONSERVATION OF THE HUNTINGTONS-DISEASE GENE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 UNIV MICHIGAN,MED CTR,ANN ARBOR,MI 48109.
   NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 237
EP 237
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500237
ER

PT J
AU LIU, P
   TARLE, SA
   HAJRA, A
   CLAXTON, DF
   MARLTON, P
   FREEDMAN, M
   SICILIANO, MJ
   COLLINS, FS
AF LIU, P
   TARLE, SA
   HAJRA, A
   CLAXTON, DF
   MARLTON, P
   FREEDMAN, M
   SICILIANO, MJ
   COLLINS, FS
TI A FUSION BETWEEN TRANSCRIPTION FACTOR CBF-BETA-PEBP2-BETA AND A MYOSIN
   HEAVY-CHAIN IS GENERATED BY THE CHROMOSOME-16 INVERSION IN ACUTE
   MYELOMONOCYTIC LEUKEMIA M4EO
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,ANN ARBOR,MI 48109.
   UNIV MICHIGAN,MED CTR,DEPT HUMAN GENET,ANN ARBOR,MI 48109.
   UNIV MICHIGAN,MED CTR,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109.
   UNIV TEXAS,M D ANDERSON CANC CTR,DEPT HEMATOL,HOUSTON,TX 77030.
   UNIV TEXAS,M D ANDERSON CANC CTR,DEPT MOLEC GENET,HOUSTON,TX 77030.
   NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892.
RI Marlton, Paula/F-3026-2011; Liu, Paul/A-7976-2012
OI Liu, Paul/0000-0002-6779-025X
NR 0
TC 0
Z9 0
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 243
EP 243
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500243
ER

PT J
AU BALE, SJ
   COMPTON, JG
   CHIPEV, CC
   YANG, JM
   STEINERT, PM
   DIGIOVANNA, JJ
AF BALE, SJ
   COMPTON, JG
   CHIPEV, CC
   YANG, JM
   STEINERT, PM
   DIGIOVANNA, JJ
TI DISTINCT CLINICAL PHENOTYPES IN EPIDERMOLYTIC HYPERKERATOSIS (EH) -
   CORRELATION WITH MUTATIONS IN KERATIN-1 OR KERATIN-10
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD.
   NCI,DERMATOL BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 247
EP 247
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500248
ER

PT J
AU BRAUCH, H
   MASEK, O
   KOOP, H
   LERMAN, MI
   HOFLER, H
AF BRAUCH, H
   MASEK, O
   KOOP, H
   LERMAN, MI
   HOFLER, H
TI CHROMOSOME-3P HAPLOTYPE ANALYSIS IN 2 SLOVAKIAN PEDIGREES WITH
   VONHIPPEL-LINDAU DISEASE - PRESYMPTOMATIC DIAGNOSIS OF GENE CARRIERS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 MISSION RES INC,MOLEC PATHOL LAB,D-81675 MUNICH,GERMANY.
   NCI,FCRDC,IMMUNOBIOL LAB,FREDERICK,MD 21702.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 277
EP 277
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500278
ER

PT J
AU DEAN, M
   CHIDAMBARAM, A
   GAILANI, M
   STEWART, C
   GERRARD, B
   CHUMAKOV, I
   BALE, SJ
   GOLDSTEIN, A
   BALE, A
AF DEAN, M
   CHIDAMBARAM, A
   GAILANI, M
   STEWART, C
   GERRARD, B
   CHUMAKOV, I
   BALE, SJ
   GOLDSTEIN, A
   BALE, A
TI GENETIC-ANALYSIS OF THE NEVOID BASAL-CELL CARCINOMA SYNDROME (NBCCS)
   LOCUS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NCI,FCRDC,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701.
   NCI,FCRDC,BCDP,PRI,DYNCORP,FREDERICK,MD 21701.
   YALE UNIV,NEW HAVEN,CT 06520.
   GENETHON,EVRY,FRANCE.
   NIAMS,GENET STUDIES SECT,BETHESDA,MD.
   NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 285
EP 285
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500285
ER

PT J
AU FRIEDMAN, E
   ADAMS, EF
   HOOG, A
   GEJMAN, PV
   CARSON, E
   LARSSON, C
   DEMARCO, L
   WERNER, S
   FAHLBUSCH, R
   NORDENSKJOLD, M
AF FRIEDMAN, E
   ADAMS, EF
   HOOG, A
   GEJMAN, PV
   CARSON, E
   LARSSON, C
   DEMARCO, L
   WERNER, S
   FAHLBUSCH, R
   NORDENSKJOLD, M
TI NORMAL STRUCTURAL DOPAMINE TYPE-2 RECEPTOR GENE IN PROLACTIN-SECRETING
   AND OTHER PITUITARY-TUMORS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 KAROLINSKA HOSP,S-10401 STOCKHOLM 60,SWEDEN.
   KOPFKLINIKUM,ERLANGEN,GERMANY.
   NIMH,BETHESDA,MD 20892.
   UFMG,BELO HORIZON,BRAZIL.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 300
EP 300
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500299
ER

PT J
AU LATIF, F
   GNARRA, J
   TORY, K
   YAO, M
   DUH, FM
   CHEN, F
   DEAN, M
   GLAVAC, D
   MAHER, ER
   LINEHAN, WM
   LERMAN, MI
   ZBAR, B
AF LATIF, F
   GNARRA, J
   TORY, K
   YAO, M
   DUH, FM
   CHEN, F
   DEAN, M
   GLAVAC, D
   MAHER, ER
   LINEHAN, WM
   LERMAN, MI
   ZBAR, B
TI FREQUENT GERMLINE AND SPORADIC RENAL-CELL CARCINOMA MUTATIONS IN
   VONHIPPEL-LINDAU DISEASE TUMOR-SUPPRESSOR GENE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NCI,FCRDC,IMMUNOBIOL LAB,FREDERICK,MD 21702.
   NCI,FCRDC,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21702.
   NCI,SURG BRANCH,BETHESDA,MD 20892.
   UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE CB2 1QP,ENGLAND.
   NCI,FCRDC,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 318
EP 318
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500317
ER

PT J
AU TORY, K
   SCHMIDT, L
   CHEN, F
   LI, H
   HUI, M
   GNARRA, J
   LATIF, F
   DUH, F
   LINEHAN, M
   LERMAN, M
   ZBAR, B
AF TORY, K
   SCHMIDT, L
   CHEN, F
   LI, H
   HUI, M
   GNARRA, J
   LATIF, F
   DUH, F
   LINEHAN, M
   LERMAN, M
   ZBAR, B
TI MUTATION ANALYSIS OF THE VONHIPPEL-LINDAU DISEASE (VHL) GENE IN
   CARCINOMAS OF THE KIDNEY LUNG, BREAST AND OVARY
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD.
   NCI,IMMUNOBIOL LAB,FREDERICK,MD 21701.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 378
EP 378
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500377
ER

PT J
AU BAUMBACH, L
   BHASKAR, A
   HOFFMAN, E
   EDWARDS, J
   HEJTMANICK, JF
   BEST, B
AF BAUMBACH, L
   BHASKAR, A
   HOFFMAN, E
   EDWARDS, J
   HEJTMANICK, JF
   BEST, B
TI X-LINKED INFANTILE LETHAL ANTERIOR HORN CELL DISEASE PROVIDES EVIDENCE
   FOR GENETIC-HETEROGENEITY WITHIN THE PROXIMAL SPINAL MUSCULAR ATROPHIES
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 UNIV MIAMI,MIAMI,FL 33152.
   UNIV PITTSBURGH,PITTSBURGH,PA 15260.
   UNIV S CAROLINA,COLUMBIA,SC 29208.
   NIH,BETHESDA,MD 20892.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 399
EP 399
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500399
ER

PT J
AU RAO, PA
   PICKAR, D
   GEJMAN, PV
   RAM, A
   GERSHON, ES
   GELERNTER, J
AF RAO, PA
   PICKAR, D
   GEJMAN, PV
   RAM, A
   GERSHON, ES
   GELERNTER, J
TI ALLELIC VARIATION IN THE D4 DOPAMINE-RECEPTOR GENE (DRD4) DOES NOT
   PREDICT RESPONSE TO CLOZAPINE IN SCHIZOPHRENIC SUBJECTS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 WEST HAVEN DVAMC,W HAVEN,CT.
   YALE UNIV,SCH MED,NEW HAVEN,CT 06510.
   NIMH,EXP THER BRANCH,BETHESDA,MD 20892.
   NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 492
EP 492
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500491
ER

PT J
AU AKSENTIJEVICH, I
   PRAS, E
   GRUBERG, L
   SHEN, Y
   HOLMAN, K
   HELLING, S
   PROSEN, L
   SUTHERLAND, GR
   RICHARDS, RI
   DEAN, M
   PRAS, M
   KASTNER, DL
AF AKSENTIJEVICH, I
   PRAS, E
   GRUBERG, L
   SHEN, Y
   HOLMAN, K
   HELLING, S
   PROSEN, L
   SUTHERLAND, GR
   RICHARDS, RI
   DEAN, M
   PRAS, M
   KASTNER, DL
TI FAMILIAL MEDITERRANEAN FEVER (FMF) IN MOROCCAN JEWS - DEMONSTRATION OF A
   FOUNDER EFFECT BY EXTENDED HAPLOTYPE ANALYSIS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID MARKER LOCI D9S5; LINKAGE DISEQUILIBRIUM; FRIEDREICH ATAXIA; HUMAN
   CHROMOSOME-16; GENETIC-ANALYSIS; ASHKENAZI JEWS; SHORT ARM; DISEASE;
   HOMOGENEITY; MAP
AB Familial Mediterranean fever (FMF) is an autosomal recessive disease causing attacks of fever and serositis. The FMF gene (designated ''MEF'') is on 16p, with the gene order 16cen-D16S80-MEF-D16S94-D16S283-D16S291-16pter. Here we report the association of FMF susceptibility with alleles at D16S94, D16S283, and D16S291 among 31 non-Ashkenazi Jewish families (14 Moroccan, 17 non-Moroccan). We observed highly significant associations at D16S283 and D16S291 among the Moroccan families. For the non-Moroccans, only the allelic association at D16S94 approached statistical significance. Haplotype analysis showed that 18/25 Moroccan FMF chromosomes, versus 0/21 noncarrier chromosomes, bore a specific haplotype for D16S94-D16S283-D16S291. Among non-Moroccans this haplotype was present in 6/26 FMF chromosomes versus 1/28 controls. Both groups of families are largely descended from Jews who fled the Spanish Inquisition. The strong haplotype association seen among the Moroccans is most likely a founder effect, given the recent origin and genetic isolation of the Moroccan Jewish community. The lower haplotype frequency among non-Moroccan carriers may reflect differences both in history and in population genetics.
C1 NIAMSO,ARTHRITIS & RHEUMATISM BRANCH,BLDG 6,ROOM 112,BETHESDA,MD 20892.
   CHAIM SHEBA MED CTR,DEPT MED F,IL-52621 TEL HASHOMER,ISRAEL.
   CHAIM SHEBA MED CTR,HELLER INST MED RES,IL-52621 TEL HASHOMER,ISRAEL.
   ADELAIDE CHILDRENS HOSP INC,DEPT CYTOGENET & MOLEC GENET,ADELAIDE,SA 5006,AUSTRALIA.
   NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701.
RI Sutherland, Grant/D-2606-2012; Dean, Michael/G-8172-2012
OI Dean, Michael/0000-0003-2234-0631
NR 27
TC 30
Z9 30
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
BP 644
EP 651
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA LU559
UT WOS:A1993LU55900008
PM 8102507
ER

PT J
AU MAROULAKOU, I
   GARRETT, LJ
   ANVER, MR
   PAPAS, TS
   GREEN, JE
AF MAROULAKOU, I
   GARRETT, LJ
   ANVER, MR
   PAPAS, TS
   GREEN, JE
TI CHONDRODYSPLASIA AND MULTIPLE TUMORS IN MICE CARRYING A HORMONAL
   RESPONSIVE PROMOTER-TAG TRANSGENE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD 21701.
   PRI DYNCORP,PATHOL HISTOTECHNOL LAB,FREDERICK,MD.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 646
EP 646
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500645
ER

PT J
AU BOLES, DJ
   PROIA, RL
AF BOLES, DJ
   PROIA, RL
TI PROCESSING OF HEXA MESSENGER-RNA IN THE PRESENCE OF THE 4BP INSERTION
   COMMONLY FOUND IN TAY-SACHS-DISEASE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIH,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892.
RI Proia, Richard/A-7908-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 667
EP 667
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500667
ER

PT J
AU CHOU, JY
   SHELLY, LL
   LEI, KJ
   PAN, CJ
AF CHOU, JY
   SHELLY, LL
   LEI, KJ
   PAN, CJ
TI CHARACTERIZATION OF A COMPLEMENTARY-DNA ENCODING MURINE
   GLUCOSE-6-PHOSPHATASE - THE ENZYME-DEFICIENT IN GLYCOGEN-STORAGE-DISEASE
   TYPE 1A
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 670
EP 670
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500671
ER

PT J
AU SCHNEIDER, MC
   WATERBURY, G
   WEINSTATSASLOW, D
   BARTON, NJ
   SOMLO, S
   GERMINO, GG
   REEDERS, ST
AF SCHNEIDER, MC
   WATERBURY, G
   WEINSTATSASLOW, D
   BARTON, NJ
   SOMLO, S
   GERMINO, GG
   REEDERS, ST
TI STRUCTURE OF 3 DISTINCT GENES THAT ENCODE WD-40 MOTIFS IN THE PKD1
   REGION
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 YALE UNIV,NEW HAVEN,CT 06520.
   NIH,BETHESDA,MD 20892.
   ALBERT EINSTEIN COLL MED,BRONX,NY.
   JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 727
EP 727
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500727
ER

PT J
AU VALDES, J
   TAGLE, D
   ELMER, L
   COLLINS, F
AF VALDES, J
   TAGLE, D
   ELMER, L
   COLLINS, F
TI ANALYSIS OF ALTERNATIVE SPLICING PATTERNS OF THE HUNTINGTON DISEASE GENE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 UNIV MICHIGAN,ANN ARBOR,MI 48109.
   NIH,NATL CTR MED GENOME RES,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 737
EP 737
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500735
ER

PT J
AU FELLEYBOSCO, E
   WESTON, A
   CAWLEY, HM
   BENNETT, WP
   HARRIS, CC
AF FELLEYBOSCO, E
   WESTON, A
   CAWLEY, HM
   BENNETT, WP
   HARRIS, CC
TI FUNCTIONAL-STUDIES OF A GERM-LINE POLYMORPHISM AT CODON-47 WITHIN THE
   P53 GENE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID WILD-TYPE P53; CELLULAR TUMOR-ANTIGEN; HUMAN LUNG-CANCER; ACTIVATING
   MUTATIONS; SUPPRESSOR GENE; CELLS; TRANSFORMATION; PROTEIN; GROWTH;
   EXPRESSION
AB A rare germ-line polymorphism in codon 47 of the p53 gene replaces the wild-type proline (CCG) with a serine (TCG). Restriction analysis of 101 human samples revealed the frequency of the rare allele to be 0% (n = 69) in Caucasians and 4.7% (3/64, n = 32) among African-Americans. To investigate the consequence of this amino acid substitution, a cDNA construct (p53 mut47ser) containing the mutation was introduced into a lung adenocarcinoma cell line (Calu-6) that does not express p53. A growth suppression similar to that obtained after introduction of a wild-type p53 cDNA construct was observed, in contrast to the result obtained by introduction of p53 mut143ala. Furthermore, expression of neither p53 mut47ser nor wild-type p53 was tolerated by growing cells. In transient expression assays, both mut47ser and wild-type p53 activated the expression of a reporter gene linked to a p53 binding sequence (PG13-CAT) and inhibited the expression of the luciferase gene under the control of the Rous sarcoma virus promoter (RSVluc). In the same assay, mut143ala did not activate the expression of PG13-CAT and produced only a slight inhibitory effect on RSVluc. These findings indicate that the p53 variant with a serine at codon 47 should be considered as a rare germ-line polymorphism that does not alter the growth-suppression activity of p53.
C1 NCI,HUMAN CARCINOGENESIS LAB,BLDG 37,ROOM 2C09,BETHESDA,MD 20892.
RI Felley-Bosco, Emanuela/E-7484-2017
OI Felley-Bosco, Emanuela/0000-0002-3408-0294
NR 30
TC 75
Z9 75
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
BP 752
EP 759
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA LU559
UT WOS:A1993LU55900019
PM 8352280
ER

PT J
AU STRUEWING, JP
   LERMAN, CE
   KASE, R
   GIAMBARRESI, T
   TUCKER, MA
AF STRUEWING, JP
   LERMAN, CE
   KASE, R
   GIAMBARRESI, T
   TUCKER, MA
TI PREDICTED UPTAKE AND IMPACT OF GENETIC TESTING IN INHERITED
   BREAST-OVARIAN CANCER FAMILIES
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892.
   FOX CHASE CANC CTR,CHELTENHAM,PA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 766
EP 766
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500767
ER

PT J
AU CITRON, BA
   KAUFMAN, S
   MILSTIEN, S
   NAYLOR, EW
   GREENE, CL
   DAVIS, MD
AF CITRON, BA
   KAUFMAN, S
   MILSTIEN, S
   NAYLOR, EW
   GREENE, CL
   DAVIS, MD
TI MUTATION IN THE 4A-CARBINOLAMINE DEHYDRATASE GENE LEADS TO MILD
   HYPERPHENYLALANINEMIA WITH DEFECTIVE COFACTOR METABOLISM
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID AMINO-ACID HYDROXYLASES; PHENYLALANINE-HYDROXYLASE; 7-SUBSTITUTED
   PTERINS; RAT-LIVER; PROTEIN; 7-TETRAHYDROBIOPTERIN; TETRAHYDROBIOPTERIN;
   PHENYLKETONURIA; DEFICIENCY; STIMULATOR
AB Hyperphenylalaninemias represent a major class of inherited metabolic disorders. They are most often cause by mutations in the phenylalanine hydroxylase gene and, less frequently but with usually more serious consequences, in genes necessary for the synthesis and regeneration of the cofactor, tetrahydrobiopterin. This cofactor is absolutely required for all aromatic amino acid hydroxylations, and, recently, nitric oxide production from L-arginine has also been found to be dependent on tetrahydrobiopterin. Phenylalanine hydroxylase catalyzes a coupled reaction in which phenylalanine is converted to tyrosine and in which tetrahydrobiopterin is converted to the unstable carbinolamine, 4a-hydroxytetrahydrobiopterin. The enzyme, carbinolamine dehydratase, catalyzes the dehydration of the carbinolamine to quinonoid dihydropterin. A decreased rate of dehydration of this compound has been hypothesized to be responsible for the production of 7-biopterin found in certain mildly hyperphenylalaninemic individuals. We have now identified nonsense and missense mutations in the 4a-carbinolamine dehydratase gene in a hyperphenylalaninemic child who excretes large amounts of 7-biopterin. This finding is consistent with the role of the carbinolamine dehydratase in the phenylalanine hydroxylation reaction. Together with previously identified inherited disorders in phenylalanine hydroxylase and dihydropteridine reductase, there are now identified mutations in the three enzymes involved in the phenylalanine hydroxylation system. In addition, the genetics of this system may have broader implications, since the product of the dehydratase gene has previously been shown to play an additional role (as dimerization cofactor for hepatocyte nuclear factor-1alpha) in the regulation of transcription, through interaction with hepatocyte nuclear factor-1alpha.
C1 UNIV PITTSBURGH,DEPT HUMAN GENET,PITTSBURGH,PA 15260.
   UNIV COLORADO,CHILDRENS HOSP,DEPT PEDIAT,DENVER,CO 80202.
RP CITRON, BA (reprint author), NIMH,NEUROCHEM LAB,BLDG 36,ROOM 3D30,BETHESDA,MD 20892, USA.
NR 36
TC 52
Z9 53
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
BP 768
EP 774
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA LU559
UT WOS:A1993LU55900021
PM 8352282
ER

PT J
AU ADAMSON, MD
   KENNEDY, J
   PETRONIS, A
   DEAN, M
   VIRKKUNEN, M
   LINNOILA, M
   GOLDMAN, D
AF ADAMSON, MD
   KENNEDY, J
   PETRONIS, A
   DEAN, M
   VIRKKUNEN, M
   LINNOILA, M
   GOLDMAN, D
TI DRD4 DOPAMINE-RECEPTOR ALLELE FREQUENCIES IN VARIOUS POPULATIONS AND
   RELATIONSHIP TO CSF HOMOVANILLIC-ACID (HVA) LEVELS IN FINNS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIAAA, NEUROGENET LAB, BETHESDA, MD USA.
   CLARKE INST PSYCHIAT, TORONTO M5T 1R8, ONTARIO, CANADA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
EI 1537-6605
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 772
EP 772
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500771
ER

PT J
AU MCDOWELL, GA
   BLITZER, MG
AF MCDOWELL, GA
   BLITZER, MG
TI TAY-SACHS GENES IN ACADIANS - REPLY
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Letter
C1 UNIV MARYLAND,SCH MED,DEPT PEDIAT,DIV HUMAN GENET,BALTIMORE,MD 21201.
   UNIV MARYLAND,SCH MED,DEPT OBSTET & GYNECOL,DIV HUMAN GENET,BALTIMORE,MD 21201.
RP MCDOWELL, GA (reprint author), NICHHD,HUMAN BIOCHEM GENET SECT,BETHESDA,MD 20892, USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
BP 782
EP 783
PG 2
WC Genetics & Heredity
SC Genetics & Heredity
GA LU559
UT WOS:A1993LU55900027
ER

PT J
AU GOLDSTEIN, AM
   FRASER, MC
   TUCKER, MA
AF GOLDSTEIN, AM
   FRASER, MC
   TUCKER, MA
TI RISK-FACTORS FOR FAMILIAL MELANOMA
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NCI,BETHESDA,MD 20892.
RI Tucker, Margaret/B-4297-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 808
EP 808
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500806
ER

PT J
AU PETTY, EM
   GREEN, J
   TAGGART, RT
   MARX, SJ
   BALE, AE
AF PETTY, EM
   GREEN, J
   TAGGART, RT
   MARX, SJ
   BALE, AE
TI LINKAGE DISEQUILIBRIUM SUGGESTS A FOUNDER EFFECT FOR THE PROLACTINOMA
   VARIANT OF MULTIPLE ENDOCRINE NEOPLASIA TYPE-1 (MEN-1 BURIN)
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIDDK,BETHESDA,MD.
   WAYNE STATE UNIV,DETROIT,MI 48202.
   YALE UNIV,SCH MED,NEW HAVEN,CT 06510.
   MEM UNIV NEWFOUNDLAND,ST JOHNS A1C 5S7,NEWFOUNDLAND,CANADA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 843
EP 843
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500844
ER

PT J
AU CHARNAS, L
   BLANCHARD, N
   OSHIMA, M
   NUSSBAUM, R
AF CHARNAS, L
   BLANCHARD, N
   OSHIMA, M
   NUSSBAUM, R
TI ALTERNATIVE SPLICING AND TRANSCRIPT HETEROGENEITY OF OCRL, THE GENE
   CAUSING THE OCULOCEREBRORENAL SYNDROME OF LOWE, OCCURS IN THE
   NERVOUS-SYSTEM
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD.
   NICHHD,GROWTH FACTORS SECT,BETHESDA,MD.
   UNIV PENN,SCH MED,DEPT HUMAN GENET,PHILADELPHIA,PA 19104.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 894
EP 894
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500896
ER

PT J
AU LAMARCA, ME
   YOSHIKAWA, H
   MCKINNEY, CE
   STUBBLEFIELD, BK
   WINFIELD, S
   CARMON, L
   MARTIN, BM
   SIDRANSKY, E
   GINNS, EI
AF LAMARCA, ME
   YOSHIKAWA, H
   MCKINNEY, CE
   STUBBLEFIELD, BK
   WINFIELD, S
   CARMON, L
   MARTIN, BM
   SIDRANSKY, E
   GINNS, EI
TI TARGETING THE COMMON N370S GAUCHER POINT MUTATION TO THE
   GLUCOCEREBROSIDASE GENE IN MURINE EMBRYONIC STEM-CELLS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 917
EP 917
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500917
ER

PT J
AU RABEN, N
   SHERMAN, J
   NICASTRI, C
   ADAMS, E
   ARGOV, Z
   NAKAJINIA, H
   PLOTZ, P
AF RABEN, N
   SHERMAN, J
   NICASTRI, C
   ADAMS, E
   ARGOV, Z
   NAKAJINIA, H
   PLOTZ, P
TI A LIMITED NUMBER OF MUTATIONS IN THE PHOSPHOFRUCTOKINASE GENE IN
   ASHKENAZI JEWISH PATIENTS WITH GLYCOGENOSIS-VII (TARUI DISEASE)
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 942
EP 942
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500944
ER

PT J
AU SIDRANSKY, E
   GINNS, EI
   ELIAS, PM
   CARMON, L
   HOLLERAN, WM
AF SIDRANSKY, E
   GINNS, EI
   ELIAS, PM
   CARMON, L
   HOLLERAN, WM
TI SEVERE GAUCHER DISEASE IN NEONATAL MICE AND HUMANS RESULTS IN SKIN
   ABNORMALITIES
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892.
   UNIV CALIF SAN FRANCISCO,DEPT DERMATOL,SAN FRANCISCO,CA 94143.
   VET ADM MED CTR,DERM SERV,SAN FRANCISCO,CA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 951
EP 951
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500949
ER

PT J
AU AYYAGARI, R
   SMITH, RJH
   LEE, EC
   KIMBERLING, WJ
   DAIGER, SP
   PELIAS, MZ
   KEATS, BJB
   JAY, M
   BIRD, A
   REARDON, W
   GUEST, M
   HEJTMANCIK, JF
AF AYYAGARI, R
   SMITH, RJH
   LEE, EC
   KIMBERLING, WJ
   DAIGER, SP
   PELIAS, MZ
   KEATS, BJB
   JAY, M
   BIRD, A
   REARDON, W
   GUEST, M
   HEJTMANCIK, JF
TI USHER SYNDROME TYPE-I IN THE FRENCH ACADIAN POPULATION - FINE MAPPING
   AND HAPLOTYPE ANALYSIS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NEI,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 970
EP 970
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33500970
ER

PT J
AU GOLDIN, LR
   WEEKS, DE
AF GOLDIN, LR
   WEEKS, DE
TI 2-LOCUS MODELS OF DISEASE - COMPARISON OF LIKELIHOOD AND NONPARAMETRIC
   LINKAGE METHODS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892.
   UNIV PITTSBURGH,PITTSBURGH,PA 15260.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1006
EP 1006
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501006
ER

PT J
AU KIMONIS, VE
   BALE, SJ
   DIGIOVANNA, JJ
   COMPTON, JG
AF KIMONIS, VE
   BALE, SJ
   DIGIOVANNA, JJ
   COMPTON, JG
TI LINKAGE OF PALMAR-PLANTAR HYPERKERATOSIS TO CHROMOSOME-12Q IN THE REGION
   OF THE TYPE-II KERATIN LOCI
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIAMDD,SKIN BIOL LAB,BETHESDA,MD 20892.
   NCI,DERMATOL BRANCH,BETHESDA,MD 20892.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1021
EP 1021
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501020
ER

PT J
AU LALWANI, AK
   BRISTER, R
   FEX, J
   GRUNDFAST, KM
   PLOPLIS, B
   AGUSTIN, TS
   SKARKA, H
   WILCOX, ER
AF LALWANI, AK
   BRISTER, R
   FEX, J
   GRUNDFAST, KM
   PLOPLIS, B
   AGUSTIN, TS
   SKARKA, H
   WILCOX, ER
TI A NEW NONSYNDROMIC X-LINKED SENSORINEURAL HEARING-LOSS LINKED TO
   XP11.3-21.1
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIDOCD,MOLEC BIOL LAB,BETHESDA,MD.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1027
EP 1027
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501026
ER

PT J
AU LEVY, E
   PRAS, E
   AKSENTIJEVICH, I
   PROSEN, L
   SWAIN, P
   KEITH, T
   SHEN, Y
   RICHARDS, RI
   DEAN, M
   PRAS, M
   KASTNER, DL
AF LEVY, E
   PRAS, E
   AKSENTIJEVICH, I
   PROSEN, L
   SWAIN, P
   KEITH, T
   SHEN, Y
   RICHARDS, RI
   DEAN, M
   PRAS, M
   KASTNER, DL
TI REFINED MAPPING OF THE GENE CAUSING FAMILIAL MEDITERRANEAN FEVER
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIAMS,ARB,BETHESDA,MD.
   COLLABORAT RES INC,WALTHAM,MA.
   ADELAIDE CHILDRENS HOSP INC,ADELAIDE,SA 5006,AUSTRALIA.
   NCI,FCRDC,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701.
   CHAIM SHEBA MED CTR,HELLER INST MED RES,IL-52621 TEL HASHOMER,ISRAEL.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1033
EP 1033
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501032
ER

PT J
AU TOWBIN, JA
   SIU, B
   ROBINSON, J
   MOSS, A
   AYYAGARI, R
   HEJTMANCIK, JF
AF TOWBIN, JA
   SIU, B
   ROBINSON, J
   MOSS, A
   AYYAGARI, R
   HEJTMANCIK, JF
TI GENETIC-HETEROGENEITY IN 22 FAMILIES WITH LONG QT SYNDROME
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 BAYLOR COLL MED,HOUSTON,TX 77030.
   UNIV ROCHESTER,ROCHESTER,NY 14627.
   NEI,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1092
EP 1092
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501094
ER

PT J
AU CHARLTON, P
   GUIDA, L
   COPELAND, N
   JENKINS, N
   MUNROE, D
   GREENBERG, F
   FIEDOREK, FT
   NICHOLLS, RD
AF CHARLTON, P
   GUIDA, L
   COPELAND, N
   JENKINS, N
   MUNROE, D
   GREENBERG, F
   FIEDOREK, FT
   NICHOLLS, RD
TI GENETIC APPROACH TO FUNCTION OF THE NEUROPEPTIDE GALANIN
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 UNIV N CAROLINA,CHAPEL HILL,NC 27514.
   UNIV FLORIDA,GAINESVILLE,FL 32611.
   CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106.
   NCI,FREDERICK,MD 21701.
   MIT,CAMBRIDGE,MA 02139.
   BAYLOR COLL MED,HOUSTON,TX 77030.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1137
EP 1137
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501137
ER

PT J
AU COMPTON, JG
   YANG, JM
   CHIPEV, CC
   DIGIOVANNA, JJ
   BALE, SJ
   STEINERT, PM
AF COMPTON, JG
   YANG, JM
   CHIPEV, CC
   DIGIOVANNA, JJ
   BALE, SJ
   STEINERT, PM
TI KERATIN MUTATIONS IN EPIDERMOLYTIC HYPERKERATOSIS (EH) PROVIDE A MODEL
   FOR KERATIN INTERMEDIATE FILAMENT INSTABILITY
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD.
   NCI,DERMATOL BRANCH,BETHESDA,MD 20892.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1146
EP 1146
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501145
ER

PT J
AU FARRER, LA
   ASHER, JH
   BALDWIN, CT
   FRIEDMAN, TB
   GREENBERG, J
   GRUNDFAST, KM
   LALWANI, AK
   MILUNSKY, A
   MORELL, R
   NEWTON, V
   RAMESAR, R
   RAO, VS
   AGUSTIN, TBS
   WILCOX, ER
   WINSHIP, I
   READ, AP
AF FARRER, LA
   ASHER, JH
   BALDWIN, CT
   FRIEDMAN, TB
   GREENBERG, J
   GRUNDFAST, KM
   LALWANI, AK
   MILUNSKY, A
   MORELL, R
   NEWTON, V
   RAMESAR, R
   RAO, VS
   AGUSTIN, TBS
   WILCOX, ER
   WINSHIP, I
   READ, AP
TI LOCUS HETEROGENEITY FOR WAARDENBURG SYNDROME IS NOT PREDICTIVE OF
   CLINICAL SUBTYPES
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 BOSTON UNIV,BOSTON,MA 02215.
   MICHIGAN STATE UNIV,E LANSING,MI 48824.
   UNIV CAPE TOWN,CAPE TOWN,SOUTH AFRICA.
   NIDCD,BETHESDA,MD.
   UNIV MANCHESTER,MANCHESTER M13 9PL,LANCS,ENGLAND.
RI Ramesar, Raj/I-6941-2015
OI Ramesar, Raj/0000-0001-5688-1634
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1156
EP 1156
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501156
ER

PT J
AU MARINI, JC
   WANG, Q
   LEWIS, MB
AF MARINI, JC
   WANG, Q
   LEWIS, MB
TI IDENTIFICATION OF AN IDENTICAL NON-LETHAL-ALPHA-1(I) MUTATION IN 2
   UNRELATED FAMILIES WITH WIDE VARIABILITY OF OSTEOGENESIS IMPERFECTA
   PHENOTYPE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1199
EP 1199
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501201
ER

PT J
AU POWELL, CM
   TAGGART, RT
   DRUMHELLER, TC
   WANGSA, D
   QIAN, C
   NELSON, LM
   WHITE, BJ
AF POWELL, CM
   TAGGART, RT
   DRUMHELLER, TC
   WANGSA, D
   QIAN, C
   NELSON, LM
   WHITE, BJ
TI MOLECULAR AND CYTOGENETIC STUDIES OF AN X - AUTOSOME TRANSLOCATION IN A
   PATIENT WITH PREMATURE OVARIAN FAILURE AND REVIEW OF OTHER CASES - IS
   THERE A POF2 GENE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIH,BETHESDA,MD 20892.
   CHILDRENS NATL MED CTR,WASHINGTON,DC.
   WAYNE STATE UNIV,DETROIT,MI 48202.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1215
EP 1215
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501215
ER

PT J
AU WANG, Q
   MARINI, JC
AF WANG, Q
   MARINI, JC
TI USE OF ANTISENSE OLIGONUCLEOTIDES DIRECTED AT MESSENGER-RNA AND GENOMIC
   DNA TO SELECTIVELY SUPPRESS PRODUCTION OF THE MUTANT ALPHA-2(I) CHAIN IN
   OSTEOGENESIS IMPERFECTA TYPE-IV FIBROBLASTS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1251
EP 1251
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501251
ER

PT J
AU GASTON, SM
   GREGOR, P
   OREGAN, JP
   YANG, X
   HAINES, JL
   PATTERSON, D
   BROWN, RH
   TANZI, RE
AF GASTON, SM
   GREGOR, P
   OREGAN, JP
   YANG, X
   HAINES, JL
   PATTERSON, D
   BROWN, RH
   TANZI, RE
TI YAC CONTIG MAPPING OF THE HUMAN GLUTAMATE-RECEPTOR GLUR5 SUBUNIT GENE ON
   CHROMOSOME-21Q22.1
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 HMS,MGH,GENET & AGING LAB,BOSTON,MA.
   NIDA,ARC,MOLEC NEUROBIOL SECT,BALTIMORE,MD.
   E ROOSEVELT INST CANC RES,DENVER,CO.
   HMS,MGH,DAY NEUROMUS RES CTR,BOSTON,MA.
   HMS,MGH,MOLEC NEUROGENET UNIT,BOSTON,MA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1292
EP 1292
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501290
ER

PT J
AU POLYMEROPOULOS, MH
   MERRIL, CR
AF POLYMEROPOULOS, MH
   MERRIL, CR
TI MAPPING OF 500 CDNAS AND THEIR DISTRIBUTION IN THE HUMAN GENOME
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIMH,BIOCHEM GENET LAB,WASHINGTON,DC 20032.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1346
EP 1346
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501344
ER

PT J
AU MEANEY, FJ
   KNUTSEN, T
   RIGGLE, SM
   CUNNINGHAM, GC
AF MEANEY, FJ
   KNUTSEN, T
   RIGGLE, SM
   CUNNINGHAM, GC
TI A COMPARISON AND EVALUATION OF 2 NATIONAL SURVEYS OF GENETIC SERVICES
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 ARIZONA DEPT HLTH SERV,PHOENIX,AZ.
   NIH,BETHESDA,MD 20892.
   CALIF DEPT HLTH SERV,BERKELEY,CA 94704.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1497
EP 1497
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501497
ER

PT J
AU CAO, Q
   CEDRONE, E
   BARRETT, C
   WANG, N
AF CAO, Q
   CEDRONE, E
   BARRETT, C
   WANG, N
TI SUPPRESSION OF IN-VITRO GROWTH OF OVARIAN-CARCINOMA CELLS BY
   MICROCELL-MEDIATED CHROMOSOME 11 TRANSFER
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 UNIV ROCHESTER,MED CTR,DEPT PEDIAT & PATHOL,ROCHESTER,NY 14642.
   NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1517
EP 1517
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501516
ER

PT J
AU GOLDMAN, D
   ENOCH, M
   ROHRBAUGH, JW
   LONG, JC
   DAVIS, EZ
   HARRIS, CR
   ELLINGSON, RJ
   ANDREASON, P
   MOORE, V
   VARNER, JL
   BROWN, GL
   ECKARDT, MJ
AF GOLDMAN, D
   ENOCH, M
   ROHRBAUGH, JW
   LONG, JC
   DAVIS, EZ
   HARRIS, CR
   ELLINGSON, RJ
   ANDREASON, P
   MOORE, V
   VARNER, JL
   BROWN, GL
   ECKARDT, MJ
TI GENETIC EPIDEMIOLOGY, RELATIONSHIP TO PSYCHOPATHOLOGY, AND VERTICAL
   TRANSMISSION OF ALPHA-EEG VARIANTS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIAAA,NEUROGENET LAB,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1546
EP 1546
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501545
ER

PT J
AU DING, JH
   ZHANG, H
   COONEY, DA
AF DING, JH
   ZHANG, H
   COONEY, DA
TI CDNA CLONING OF MOUSE CTP SYNTHASE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 DUKE UNIV,MED CTR,DURHAM,NC 27710.
   NCI,BETHESDA,MD 20892.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1634
EP 1634
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501636
ER

PT J
AU BRICARELLI, FD
   PERRONI, L
   PIERLUIG, M
   BARGIACCHI, S
   ARGUSTI, A
   BALDI, M
   PERFUMO, G
   EGEO, A
   CICCOLALLO, L
   STRIGINI, P
AF BRICARELLI, FD
   PERRONI, L
   PIERLUIG, M
   BARGIACCHI, S
   ARGUSTI, A
   BALDI, M
   PERFUMO, G
   EGEO, A
   CICCOLALLO, L
   STRIGINI, P
TI ORIGIN OF CHROMOSOME-21 NONDISJUNCTION - AN ITALIAN STUDY AND
   EPIDEMIOLOGIC COMPARISONS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 GALLIERA HOSP,GENOA,ITALY.
   NATL CANC INST,GENOA,ITALY.
RI Ciccolallo, Laura/F-5653-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1645
EP 1645
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501647
ER

PT J
AU STRIGINI, P
   PIERLUIGI, M
   BARGIACCHI, S
   PERFUMO, C
   ARGUSTI, A
   HEOUAINE, A
   BRICARELLI, FD
   PAOLUCCI, G
AF STRIGINI, P
   PIERLUIGI, M
   BARGIACCHI, S
   PERFUMO, C
   ARGUSTI, A
   HEOUAINE, A
   BRICARELLI, FD
   PAOLUCCI, G
TI GENETIC EPIDEMIOLOGY OF TRANSIENT LEUKEMIA AND ACUTE-LEUKEMIA IN
   DOWN-SYNDROME
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NATL CANC INST,GENOA,ITALY.
   GALLIERA HOSP,GENOA,ITALY.
   PEDIAT DEPT,BOLOGNA,ITALY.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1664
EP 1664
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501663
ER

PT J
AU HEINZMANN, C
   KOJIS, TL
   FLODMAN, P
   MULLEN, ML
   GONZALEZ, P
   RAO, PV
   KLISAK, I
   SPARKES, RS
   ZIGLER, JS
   SPENCE, MA
   BATEMAN, JB
AF HEINZMANN, C
   KOJIS, TL
   FLODMAN, P
   MULLEN, ML
   GONZALEZ, P
   RAO, PV
   KLISAK, I
   SPARKES, RS
   ZIGLER, JS
   SPENCE, MA
   BATEMAN, JB
TI LINKAGE RELATIONSHIPS OF ZETA-CRYSTALLIN ON HUMAN CHROMOSOME-1P22-1P31
   WITH HEREDITARY CATARACTS
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 UNIV CALIF LOS ANGELES, JULES STEIN EYE INST, DEPT OPHTHALMOL, LOS ANGELES, CA USA.
   UNIV CALIF LOS ANGELES JULES STEIN EYE INST, DEPT MED, LOS ANGELES, CA USA.
   UC IRVINE, DEPT PEDIAT, IRVINE, CA USA.
   NEI, BETHESDA, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1696
EP 1696
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501696
ER

PT J
AU MOIR, D
   SAXENA, R
   JONES, BF
   WEIFFENBACH, B
   CAPORASO, N
   RELLING, M
   EVANS, W
   SHAW, G
AF MOIR, D
   SAXENA, R
   JONES, BF
   WEIFFENBACH, B
   CAPORASO, N
   RELLING, M
   EVANS, W
   SHAW, G
TI IDENTIFICATION OF MUTATIONS IN THE CYP2D6 GENE THAT ALTER EXPRESSION OF
   DEBRISOQUINE-HYDROXYLASE
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 COLLABORAT RES INC, WALTHAM, MA USA.
   NCI, BETHESDA, MD 20892 USA.
   ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1740
EP 1740
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501739
ER

PT J
AU PERRY, RT
   GO, RCP
   HARRELL, LA
   ACTON, RT
AF PERRY, RT
   GO, RCP
   HARRELL, LA
   ACTON, RT
TI RARE DELETIONS IN THE HUMAN PRION PROTEIN GENE (PRNP) - A POSSIBLE
   SUSCEPTIBILITY GENE FOR ALZHEIMERS-DISEASE IN A SINGLE-FAMILY
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Meeting Abstract
C1 NIMH,GENET INITIAT,BETHESDA,MD 20892.
   UNIV ALABAMA,BIRMINGHAM,AL.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD SEP
PY 1993
VL 53
IS 3
SU S
BP 1748
EP 1748
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA LW335
UT WOS:A1993LW33501746
ER

PT J
AU SHARKEYMATHIS, PK
   KAUFFMAN, CA
   GRAYBILL, JR
   STEVENS, DA
   HOSTETLER, JS
   CLOUD, G
   DISMUKES, WE
   BENNETT, J
   BRADSHER, RW
   CHAPMAN, SW
   FISHER, JF
   KERKERING, TM
   MEDOFF, G
   PERFECT, JR
   PANKEY, GA
   REX, JH
   SAAG, MS
AF SHARKEYMATHIS, PK
   KAUFFMAN, CA
   GRAYBILL, JR
   STEVENS, DA
   HOSTETLER, JS
   CLOUD, G
   DISMUKES, WE
   BENNETT, J
   BRADSHER, RW
   CHAPMAN, SW
   FISHER, JF
   KERKERING, TM
   MEDOFF, G
   PERFECT, JR
   PANKEY, GA
   REX, JH
   SAAG, MS
TI TREATMENT OF SPOROTRICHOSIS WITH ITRACONAZOLE
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Article
ID PRIMARY PULMONARY SPOROTRICHOSIS; HIGH-DOSE KETOCONAZOLE;
   SPOROTHRIX-SCHENCKII; CUTANEOUS SPOROTRICHOSIS; SYSTEMIC SPOROTRICHOSIS;
   FUNGAL-INFECTIONS; AMPHOTERICIN-B; THERAPY; ARTHRITIS; EMPHASIS
AB PURPOSE: To describe the clinical presentation and outcomes of treatment with itraconazole in patients with sporotrichosis. METHODS: A culture for Sporothrix schenckii or compatible histopathology was required for inclusion in the study. Patients with both cutaneous and systemic sporotrichosis were treated. Patients received from 100 to 600 mg of itraconazole daily for 3 to 18 months. Patients were classified as responders or nonresponders. Responders were further classified as remaining on treatment, relapsed, or free of disease. Nonresponders included patients who failed to respond or progressed during treatment with itraconazole. RESULTS: Twenty-seven patients (mean age: 53 years) were treated with 30 courses of itraconazole. Diabetes mellitus and alcoholism were present in eight and seven patients, respectively. Sites of involvement included lymphocutaneous alone in 9 patients, articular/osseous in 15 (multifocal in 3), and lung in 3. Prior therapy was unsuccessful in 11 patients. Among the 30 courses, there were 25 responders and 5 nonresponders. All 5 nonresponders received at least 200 mg daily of itraconazole for durations that ranged from 6 to 18 months. Of the 25 responders, 7 relapsed 1 to 7 months after treatment durations of 6 to 18 months. Of the 7 who relapsed, 2 are responding to a second course. One responder was lost to follow-up after 10 months of treatment with itraconazole. Of the re 17 responders, 3 remain on treatment, and 14 are free of disease over follow-up durations of 6 to 42 months (mean: 17.6 months). Itraconazole was well tolerated with few side effects noted.
   CONCLUSIONS: These results document the efficacy of itraconazole in the treatment of cutaneous and systemic sporotrichosis.
C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284.
   DEPT VET AFFAIRS MED CTR,ANN ARBOR,MI.
   UNIV MICHIGAN,SCH MED,ANN ARBOR,MI 48104.
   SANTA CLARA VALLEY MED CTR,SAN JOSE,CA 95128.
   STANFORD UNIV,SCH MED,SAN JOSE,CA.
   UNIV ALABAMA,BIRMINGHAM,AL 35294.
   NIAID,MYCOSES STUDY GRP,BETHESDA,MD 20892.
   UNIV ARKANSAS MED SCI HOSP,LITTLE ROCK,AR 72205.
   UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216.
   MED COLL GEORGIA,AUGUSTA,GA 30912.
   VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298.
   WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110.
   DUKE UNIV,MED CTR,DURHAM,NC 27710.
   ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA 70121.
RP SHARKEYMATHIS, PK (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV INFECT DIS,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA.
FU NIAID NIH HHS [N01-AI-52562]
NR 36
TC 87
Z9 88
U1 1
U2 2
PU EXCERPTA MEDICA INC
PI NEW YORK
PA 245 WEST 17TH STREET, NEW YORK, NY 10011
SN 0002-9343
J9 AM J MED
JI Am. J. Med.
PD SEP
PY 1993
VL 95
IS 3
BP 279
EP 285
DI 10.1016/0002-9343(93)90280-3
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA LX046
UT WOS:A1993LX04600007
PM 8396321
ER

PT J
AU MILLER, DL
   DOPPMAN, JL
   CHANG, R
AF MILLER, DL
   DOPPMAN, JL
   CHANG, R
TI ANATOMY OF THE JUNCTION OF THE INFERIOR PETROSAL SINUS AND THE INTERNAL
   JUGULAR-VEIN
SO AMERICAN JOURNAL OF NEURORADIOLOGY
LA English
DT Article
DE SKULL, ANATOMY; VEINS, ANATOMY; VEINS, JUGULAR; FORAMINA, JUGULAR; DURAL
   SINUSES; VENOGRAPHY; CATHETERS AND CATHETERIZATION
AB PURPOSE: To evaluate the anatomy of the junction of the inferior petrosal sinus and the internal jugular vein. METHODS: Using a previously described classification system, we prospectively classified venous anatomy bilaterally in 135 of 136 persons consecutively undergoing inferior petrosal sinus sampling. RESULTS: Type IV anatomy, with no anastomosis between the inferior petrosal sinus and the internal jugular vein, was significantly less frequent in our series than in a previous series (1 versus 7%; P < .001). Venous anatomy did not differ significantly between the left and the right junctions or between men and women. Venous anatomy was symmetric in only 65% of subjects (86 of 133). We describe an uncommon variant anatomy, incomplete type IV, found in 4.5% of our subjects (six of 133), that may cause incorrect results of petrosal sinus sampling. CONCLUSION: Bilateral sampling of pituitary venous effluent can be accomplished by the methods described, despite the presence of either incomplete or true type IV venous anatomy. Bilateral petrosal sinus sampling is anatomically possible in 99% of persons.
C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892.
   GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20037.
NR 12
TC 40
Z9 40
U1 0
U2 0
PU AMER SOC NEURORADIOLOGY
PI OAK BROOK
PA 2210 MIDWEST RD, OAK BROOK, IL 60521
SN 0195-6108
J9 AM J NEURORADIOL
JI Am. J. Neuroradiol.
PD SEP-OCT
PY 1993
VL 14
IS 5
BP 1075
EP 1083
PG 9
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA LY600
UT WOS:A1993LY60000009
PM 8237683
ER

PT J
AU LEFEVRE, ML
   BAIN, RP
   EWIGMAN, BG
   FRIGOLETTO, FD
   CRANE, JP
   MCNELLIS, D
AF LEFEVRE, ML
   BAIN, RP
   EWIGMAN, BG
   FRIGOLETTO, FD
   CRANE, JP
   MCNELLIS, D
TI A RANDOMIZED TRIAL OF PRENATAL ULTRASONOGRAPHIC SCREENING - IMPACT ON
   MATERNAL MANAGEMENT AND OUTCOME
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE PRENATAL ULTRASONOGRAPHY; MASS SCREENING; PREGNANCY OUTCOME
ID EARLY-PREGNANCY; ULTRASOUND; ROUTINE
AB ObJECTIVES: This randomized clinical trial of 15,530 women was designed to test the hypothesis that screening ultrasonography in low-risk pregnancies would improve perinatal outcome. A secondary hypothesis addressed in this article was that screening ultrasonography would have a favorable impact on maternal management or outcome.
   STUDY DESIGN: Pregnant women without a specific indication for ultrasonographic examination in early pregnancy were randomly assigned to have either two screening sonograms or conventional obstetric care. Pregnancy interventions and maternal outcomes were compared in the two groups.
   RESULTS: No significant differences were found in maternal outcomes. Use of ultrasonography was markedly higher in the screened group. The rates of induced abortion, amniocentesis, tests of fetal well-being, external version, induction, and cesarean section and the distribution of total hospital days were similar in the two groups. Use of tocolytics and the rate of postdate pregnancy were both slightly lower in the screened group.
   CONCLUSION: Screening ultrasonography resulted in no clinically significant benefit.
C1 GEORGE WASHINGTON UNIV,CTR BIOSTAT,WASHINGTON,DC 20052.
   NICHHD,BETHESDA,MD 20892.
   HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02115.
   WASHINGTON UNIV,JEWISH HOSP ST LOUIS,DEPT OBSTET & GYNECOL,ST LOUIS,MO 63110.
RP LEFEVRE, ML (reprint author), UNIV MISSOURI,DEPT FAMILY & COMMUNITY MED,COLUMBIA,MO 65212, USA.
FU NICHD NIH HHS [HD 19897, HD 21017, HD 21140]
NR 20
TC 92
Z9 94
U1 0
U2 0
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD SEP
PY 1993
VL 169
IS 3
BP 483
EP 489
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA LY025
UT WOS:A1993LY02500001
PM 8372849
ER

PT J
AU JOHNSON, MD
   MAHON, KA
AF JOHNSON, MD
   MAHON, KA
TI DETECTION OF GENES THAT ARE DIFFERENTIALLY EXPRESSED DURING MOUSE
   EMBRYOGENESIS BY GENETIC TRAPPING STRATEGIES
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE EMBRYONIC DEVELOPMENT; GENE TRAPPING; INSERTIONAL MUTAGENESIS; EMBRYONIC
   STEM CELLS
ID EMBRYONIC STEM-CELLS; PLURIPOTENTIAL CELLS; LINES; RETROVIRUS;
   DROSOPHILA; PROMOTERS; REPORTER; INVITRO; MICE
AB OBJECTIVE: Our objective was to identify novel genes that are expressed in temporally and spatially restricted patterns during mouse embryonic development and organogenesis.
   STUDY DESIGN: Two genetic trapping reporter constructs that lack transcriptional regulatory sequences were introduced independently into transcriptionally active gene loci by electroporation into mouse embryonic stem cells. Patterns of host gene-reporter construct expression were investigated in differentiated embryonic stem cells, embryoid bodies, and chimeric embryos at various stages of development.
   RESULTS: Three patterns of host gene-reporter construct expression were observed from the developmental analysis of four vector-integrated cell lines. Reporter expression patterns reflecting developmental regulation, constitutive activity, and developmental inactivation of the host genes were observed.
   CONCLUSIONS: Two vector-integrated gene loci from cell lines CCE-1C1 and D3-B44 have expression patterns not previously described by genetic trapping. Molecular characterization of these interrupted genes will shed light on their developmental function.
C1 NICHHD,MAMMALIAN GENES & DEV LAB,DEV GENE REGULAT SECT,BETHESDA,MD 20892.
NR 23
TC 2
Z9 2
U1 0
U2 0
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD SEP
PY 1993
VL 169
IS 3
BP 683
EP 689
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA LY025
UT WOS:A1993LY02500039
PM 8372880
ER

PT J
AU KOHLER, MF
   NISHII, H
   HUMPHREY, PA
   SASKI, H
   MARKS, J
   BAST, RC
   CLARKEPEARSON, DL
   BOYD, J
   BERCHUCK, A
AF KOHLER, MF
   NISHII, H
   HUMPHREY, PA
   SASKI, H
   MARKS, J
   BAST, RC
   CLARKEPEARSON, DL
   BOYD, J
   BERCHUCK, A
TI MUTATION OF THE P53 TUMOR-SUPPRESSOR GENE IS NOT A FEATURE OF
   ENDOMETRIAL HYPERPLASIAS
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE P53; TUMOR-SUPPRESSOR GENE; ENDOMETRIAL HYPERPLASIA
ID POLYMERASE CHAIN-REACTION; BREAST-CANCER; PROTEIN; OVEREXPRESSION;
   CARCINOMA; DELETIONS; OCCUR; 17P
AB OBJECTIVE: Mutation and overexpression of the p53 gene occur in approximately 20% of endometrial carcinomas. To determine whether alteration of the p53 gene is an early event in endometrial carcinogenesis, we examined the p53 gene in endometrial hyperplasias.
   STUDY DESIGN: Genomic deoxyribonucleic acid was extracted from 117 endometrial hyperplasias (36 simple, 40 complex, 41 atypical) and 30 endometrial cancers. Exons 5 through 8 of the p53 gene were amplified by means of the polymerase chain reaction. Mutations in the p53 gene were sought with single-stranded conformation polymorphism analysis and confirmed by direct deoxyribonucleic acid sequencing.
   RESULTS: None of 117 endometrial hyperplasias were found to have mutations in the p53 gene, whereas mutations were seen in three of 30 (10%) endometrial cancers (p < 0.02). The p53 mutations seen in three cancers were confirmed by direct sequencing (codons 157, 180, 272).
   CONCLUSION: Because it does not appear to be a feature of endometrial hyperplasias, mutation of the p53 gene may represent a relatively late event in endometrial carcinogenesis.
C1 DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DIV GYNECOL ONCOL,BOX 3079,DURHAM,NC 27710.
   JIKEI UNIV SCH MED,DEPT OBSTET & GYNECOL,TOKYO 105,JAPAN.
   DUKE UNIV,MED CTR,DEPT PATHOL,DURHAM,NC 27710.
   DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710.
   DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710.
   DUKE UNIV,MED CTR,DEPT IMMUNOL,DURHAM,NC 27710.
   NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709.
RI Bast, Robert/E-6585-2011
OI Bast, Robert/0000-0003-4621-8462
NR 22
TC 51
Z9 51
U1 0
U2 0
PU MOSBY-YEAR BOOK INC
PI ST LOUIS
PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD SEP
PY 1993
VL 169
IS 3
BP 690
EP 694
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA LY025
UT WOS:A1993LY02500040
PM 8372881
ER

PT J
AU NGUYEN, TT
   DISTEFANO, JJ
   HUANG, LM
   YAMADA, H
   CAHNMANN, HJ
AF NGUYEN, TT
   DISTEFANO, JJ
   HUANG, LM
   YAMADA, H
   CAHNMANN, HJ
TI 5'-DEIODINASE AND 5-DEIODINASE ACTIVITIES IN ADULT-RAT CECUM AND
   LARGE-BOWEL CONTENTS INHIBITED BY INTESTINAL MICROFLORA
SO AMERICAN JOURNAL OF PHYSIOLOGY
LA English
DT Note
DE INTESTINAL BACTERIA; THYROID HORMONE; THYROXINE; TRIIODOTHYRONINE;
   DIIODOTHYROACETIC ACID; TRIIODOTHYROACETIC ACID; 5'-DEIODINASE;
   DECONTAMINATED; ANTIBIOTIC
AB Enzymatic mechanisms for deiodination of 3,5,3'-triiodothyronine or thyroxine in the phenolic ring (5'-deiodinase) or tyrosyl ring (5-deiodinase) are found in cells of many organs, including the intestinal wall. Deiodinases are highly active in intestinal tissue of developing rat fetuses and relatively inactive in adult intestinal cells, but little is known about these systems in the luminal contents of intestines. We have found both 5- and 5'-deiodinase activities in adult rat intestinal contents and have shown that their expression is inhibited by resident intestinal microflora, which are normally present in the adult but not in the fetus, possibly because they are bound by intestinal bacteria in the adult.
C1 NIDDKD,BETHESDA,MD 20205.
RP NGUYEN, TT (reprint author), UNIV CALIF LOS ANGELES,BIOCYBERNET LAB,LOS ANGELES,CA 90024, USA.
FU NIDDK NIH HHS [DK34839]
NR 7
TC 3
Z9 3
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814
SN 0002-9513
J9 AM J PHYSIOL
JI Am. J. Physiol.
PD SEP
PY 1993
VL 265
IS 3
BP E521
EP E524
PN 1
PG 4
WC Physiology
SC Physiology
GA MA184
UT WOS:A1993MA18400053
PM 8214060
ER

PT J
AU GOLDBERG, TE
   GOLD, JM
   GREENBERG, R
   GRIFFIN, S
   SCHULZ, SC
   PICKAR, D
   KLEINMAN, JE
   WEINBERGER, DR
AF GOLDBERG, TE
   GOLD, JM
   GREENBERG, R
   GRIFFIN, S
   SCHULZ, SC
   PICKAR, D
   KLEINMAN, JE
   WEINBERGER, DR
TI CONTRASTS BETWEEN PATIENTS WITH AFFECTIVE-DISORDERS AND PATIENTS WITH
   SCHIZOPHRENIA ON A NEUROPSYCHOLOGICAL TEST BATTERY
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID CARD SORTING TEST; COGNITIVE IMPAIRMENT; BIPOLAR DISORDER;
   PREFRONTAL-TYPE; DEPRESSION; MEMORY; DYSFUNCTION; RELIABILITY;
   INTELLIGENCE; NEUROLEPTICS
AB Objective: This study was designed to ascertain the degree and specificity of cognitive impairments in patients with schizophrenia and patients with affective disorders. Method: Cognitive function was assessed with a neuropsychological test battery in consecutively admitted patients with schizophrenia (N=57), unipolar depression (N=29), and bipolar disorder (N=16). Results: The performance of the schizophrenic group was significantly below that of the groups with affective disorders on measures of attention and psychomotor speed, verbal and visual memory, and problem solving and abstraction. IQ was lower in the schizophrenic group and appeared to have deteriorated from a normal premorbid level that was not different from that of the affective disorder groups, as determined by the Wide Range Achievement Test-Revised reading test, a putative measure of premorbid intelligence. When IQ was controlled, differences between the groups in problem solving and visual memory remained. Psychiatric symptoms bad a larger impact on test performance in the affective disorder groups than in the schizophrenic group. Conclusions: These results suggest that patients with schizophrenia perform systematically worse on cognitive measures than patients with affective disorders, which is consistent with their generally poorer outcome. The results also indicate that schizophrenia and affective disorders are qualitatively distinguishable in neuropsychological terms, given differences in apparent intellectual deterioration, profiles of cognitive impairment, and associations between cognitive performance and psychopathology.
C1 PSYCHIAT INST WASHINGTON DC,WASHINGTON,DC.
   CASE WESTERN RESERVE UNIV,DEPT PSYCHIAT,CLEVELAND,OH 44106.
   NIMH,INTRAMURAL RES PROGRAM,CLIN NEUROSCI LAB,WASHINGTON,DC 20032.
   NIMH,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032.
   NIMH,CLIN SERV BRANCH,WASHINGTON,DC 20032.
NR 74
TC 257
Z9 262
U1 6
U2 8
PU AMER PSYCHIATRIC ASSOCIATION
PI WASHINGTON
PA 1400 K ST NW, WASHINGTON, DC 20005
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD SEP
PY 1993
VL 150
IS 9
BP 1355
EP 1362
PG 8
WC Psychiatry
SC Psychiatry
GA LV197
UT WOS:A1993LV19700011
PM 8352346
ER

PT J
AU LICINIO, J
   SEIBYL, JP
   ALTEMUS, M
   CHARNEY, DS
   KRYSTAL, JH
AF LICINIO, J
   SEIBYL, JP
   ALTEMUS, M
   CHARNEY, DS
   KRYSTAL, JH
TI ELEVATED CSF LEVELS OF INTERLEUKIN-2 IN NEUROLEPTIC-FREE
   SCHIZOPHRENIC-PATIENTS
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Note
ID ABNORMALITIES; RECEPTORS; SIGNAL
AB Levels of CSF fluid interleukin-2, but not interleukin-1alpha, were found to be higher in 10 neuroleptic-free schizophrenic patients than in 1 0 healthy subjects matched for sex and age. Because interleukin-2 increases dopaminergic neurotransmission and participates in autoimmunity and cell growth, the authors postulate that elevated levels of central interleukin-2 might contribute to the increased dopaminergic neurotransmission, autoimmune phenomena, and abnormal brain morphology described in some patients with schizophrenia.
C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892.
RP LICINIO, J (reprint author), YALE UNIV,W HAVEN VET AFFAIRS MED CTR,SCH MED,DEPT PSYCHIAT,SCHIZOPHRENIA BIOL RES CTR,W HAVEN,CT 06516, USA.
RI Licinio, Julio/L-4244-2013
OI Licinio, Julio/0000-0001-6905-5884
NR 11
TC 157
Z9 167
U1 0
U2 3
PU AMER PSYCHIATRIC ASSOCIATION
PI WASHINGTON
PA 1400 K ST NW, WASHINGTON, DC 20005
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD SEP
PY 1993
VL 150
IS 9
BP 1408
EP 1410
PG 3
WC Psychiatry
SC Psychiatry
GA LV197
UT WOS:A1993LV19700021
PM 8102512
ER

PT J
AU SHOPLAND, DR
AF SHOPLAND, DR
TI SMOKING CONTROL IN THE 1990S - A NATIONAL-CANCER-INSTITUTE MODEL FOR
   CHANGE
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Editorial Material
RP SHOPLAND, DR (reprint author), NCI,SMOKING & TOBACCO CONTROL PROGRAM,EPN-241,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA.
NR 11
TC 18
Z9 18
U1 0
U2 0
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD SEP
PY 1993
VL 83
IS 9
BP 1208
EP 1210
DI 10.2105/AJPH.83.9.1208
PG 3
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA LV708
UT WOS:A1993LV70800004
PM 8362992
ER

PT J
AU KORN, EL
   GRAUBARD, BI
AF KORN, EL
   GRAUBARD, BI
TI BIAS IN WEIGHTED VS UNWEIGHTED ESTIMATES - REPLY
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Letter
RP KORN, EL (reprint author), NCI,BIOMETR RES BRANCH,EPN-739,BETHESDA,MD 20892, USA.
NR 3
TC 1
Z9 1
U1 0
U2 0
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD SEP
PY 1993
VL 83
IS 9
BP 1351
EP 1351
DI 10.2105/AJPH.83.9.1351-a
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA LV708
UT WOS:A1993LV70800042
ER

PT J
AU HERTELENDY, F
   ROMERO, R
   MOLNAR, M
   TODD, H
   BALDASSARE, JJ
AF HERTELENDY, F
   ROMERO, R
   MOLNAR, M
   TODD, H
   BALDASSARE, JJ
TI CYTOKINE-INITIATED SIGNAL-TRANSDUCTION IN HUMAN MYOMETRIAL CELLS
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article; Proceedings Paper
CT 40th Annual Meeting of the Society-for-Gynecologic-Investigation
CY MAR 31-APR 03, 1993
CL TORONTO, CANADA
SP SOC GYNECOL INVESTIGAT
DE IL-1 RECEPTORS; CAMP; PROSTAGLANDIN; FORSKOLIN; ILOPROST
ID CYCLIC-AMP; PROTEIN-KINASES; SMOOTH-MUSCLE; INTERLEUKIN-1; FIBROBLASTS
AB PROBLEM: The objectives of this study were to evaluate interleukin-1 (IL-1) binding and some postreceptor actions of this cytokine and tumor necrosis factor (TNF) in human myometrial cells (HMC).
   METHOD: Monolayer cultures of HMC were used to characterize binding and to measure cyclic (c)AMP, prostaglandin (PG)E2, and PGI2 production. Membrane preparations were used to assess ADP-ribosylation and for immunoblotting.
   RESULTS: HMC were found to specifically bind [I-125]IL-1 with an apparent K(d) of 2 x 10(-10))M. Incubation of HMC with IL-1 or TNF caused a time-dependent and dose-dependent accumulation of cAMP, as well as a significant potentiation of forskolin-promoted cAMP production. These cytokines also increase PGE2 and PGI2 output, independently of the activation of adenylyl cyclase. IL-1 treatment had no measurable effect either on cholera toxin-mediated and pertussis toxin-mediated ADP-ribosylation, or on the amount of G(i) proteins, as assessed by immunoblotting using a polyclonal antibody.
   CONCLUSIONS: It is suggested that IL-1 and TNF may activate one or more isoforms of the catalytic component of adenylyl cyclase, raising intracellular cAMP.
C1 ST LOUIS UNIV,SCH MED,DEPT PHARMACOL & PHYSIOL SCI,ST LOUIS,MO 63110.
   WAYNE STATE UNIV,DETROIT,MI 48202.
   NICHHD,PERINATOL BRANCH,BETHESDA,MD.
   SEMMELWEIS UNIV MED,INST PATHOPHYSIOL,H-1085 BUDAPEST 8,HUNGARY.
RP HERTELENDY, F (reprint author), ST LOUIS UNIV,SCH MED,DEPT OBSTET & GYNECOL,3635 VISTA AVE & GRAND BLVD,ST LOUIS,MO 63110, USA.
OI Molnar, Miklos/0000-0001-9231-782X
NR 28
TC 40
Z9 40
U1 0
U2 0
PU MUNKSGAARD INT PUBL LTD
PI COPENHAGEN
PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
SN 8755-8920
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD SEP-OCT
PY 1993
VL 30
IS 2-3
BP 49
EP 57
PG 9
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA MN381
UT WOS:A1993MN38100001
PM 8311930
ER

PT J
AU ROMERO, R
   YOON, BH
   KENNEY, JS
   GOMEZ, R
   ALLISON, AC
   SEHGAL, PB
AF ROMERO, R
   YOON, BH
   KENNEY, JS
   GOMEZ, R
   ALLISON, AC
   SEHGAL, PB
TI AMNIOTIC-FLUID INTERLEUKIN-6 DETERMINATIONS ARE OF DIAGNOSTIC AND
   PROGNOSTIC VALUE IN PRETERM LABOR
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article; Proceedings Paper
CT 40th Annual Meeting of the Society-for-Gynecologic-Investigation
CY MAR 31-APR 03, 1993
CL TORONTO, CANADA
SP SOC GYNECOL INVESTIGAT
DE AMNIOTIC FLUID; INTERLEUKIN-6; PRETERM LABOR
ID GAS-LIQUID-CHROMATOGRAPHY; INTRAAMNIOTIC INFECTION; MICROBIAL INVASION;
   PREMATURE RUPTURE; INTACT MEMBRANES; GLUCOSE-CONCENTRATION;
   CONGENITAL-SYPHILIS; WOMEN; PARTURITION; CHORIOAMNIONITIS
AB PROBLEM: The purpose of this study was to determine if amniotic fluid concentrations of the interleukin-6 (IL-6) are of value in diagnosis of microbial invasion of the amniotic cavity and in the prediction of failure of tocolysis, preterm delivery and perinatal morbidity and mortality.
   METHOD: Amniotic fluid was obtained by transabdominal amniocentesis from 146 consecutive patients admitted with the diagnosis of preterm labor and intact membranes. Fluid was cultured for aerobic and anaerobic bacteria as well as for mycoplasmas. Amniotic fluid IL-6 levels were measured using a monoclonal antibody-based enzyme-linked immunosorbent assay with a sensitivity of 0.03 ng/ml. Logistic regression and Cox's proportional hazards model were used to examine the effect of several variables on dichotomous outcomes or interval to delivery.
   RESULTS: Patients with a positive amniotic fluid culture had a significantly higher amniotic fluid IL,6 concentrations than patients with a negative culture (median 91.2 ng/ml, range 0.9 to 437 ng/ml versus median 0.4 ng/ml, range <0.3 to 195 ng/ml, respectively; P<.0001). An amniotic fluid IL-6 concentration of greater than or equal to 11.3 ng/ml had a sensitivity of 93.3% (14 of 15) and a specificity of 91.6% (120 of 131). All patients with an amniotic fluid IL-6 concentration above 11.3 ng/ml and a negative amniotic fluid culture (N = 11) delivered preterm and all placenta available for examination (N = 7) had histologic evidence of chorioamnionitis. Amniotic fluid concentrations of IL-6 were an independent predictor of preterm delivery, amniocentesis-to-delivery interval and neonatal morbidity and mortality. Moreover, IL-6 concentrations added significant information to the prediction of these outcomes to that provided only by clinical information such as cervical dilatation, gestational age at admission or at delivery.
   CONCLUSION: IL-6 is a sensitive and rapid test for the detection of microbial invasion of the amniotic cavity and for identifying women at risk for spontaneous preterm delivery and neonates at risk for morbidity and mortality.
C1 SEOUL NATL UNIV,DEPT OBSTET & GYNECOL,SEOUL 151,SOUTH KOREA.
   SYNTEX INC,INST IMMUNOL & BIOL SCI,PALO ALTO,CA 94304.
   NIH,PERINATOL BRANCH,BETHESDA,MD 20892.
   NEW YORK MED COLL,DEPT MICROBIOL & IMMUNOL,VALHALLA,NY 10595.
RP ROMERO, R (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,SCH MED,DEPT OBSTET & GYNECOL,4707 ST ANTOINE BLVD,DETROIT,MI 48201, USA.
RI Yoon, Bo Hyun/H-6344-2011
NR 44
TC 114
Z9 115
U1 0
U2 3
PU MUNKSGAARD INT PUBL LTD
PI COPENHAGEN
PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
SN 8755-8920
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD SEP-OCT
PY 1993
VL 30
IS 2-3
BP 167
EP 183
PG 17
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA MN381
UT WOS:A1993MN38100018
PM 8311926
ER

PT J
AU BAUMANN, P
   ROMERO, R
   BERRY, S
   GOMEZ, R
   MCFARLIN, B
   ARANEDA, H
   COTTON, DB
   FIDEL, P
AF BAUMANN, P
   ROMERO, R
   BERRY, S
   GOMEZ, R
   MCFARLIN, B
   ARANEDA, H
   COTTON, DB
   FIDEL, P
TI EVIDENCE OF PARTICIPATION OF THE SOLUBLE TUMOR-NECROSIS-FACTOR
   RECEPTOR-I IN THE HOST RESPONSE TO INTRAUTERINE INFECTION IN PRETERM
   LABOR
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article; Proceedings Paper
CT 40th Annual Meeting of the Society-for-Gynecologic-Investigation
CY MAR 31-APR 03, 1993
CL TORONTO, CANADA
SP SOC GYNECOL INVESTIGAT
DE SOLUBLE TUMOR NECROSIS FACTOR RECEPTOR-I; INTRAAMNIOTIC INFECTION;
   PARTURITION; PRETERM LABOR; CYTOKINES; TUMOR NECROSIS FACTOR-ALPHA
ID FACTOR-BINDING PROTEIN; AMNIOTIC-FLUID; HUMAN DECIDUA; FACTOR-ALPHA;
   MONOCLONAL-ANTIBODIES; BACTERIAL-ENDOTOXIN; MICROBIAL INVASION;
   MOLECULAR-CLONING; TNF RECEPTOR; IDENTIFICATION
AB PROBLEM: This study was conducted to determine whether: (1) the soluble tumor necrosis factor receptor I (sTNF-r I) is present in human amniotic fluid, neonatal urine, and the feto-maternal plasma; (2) there are changes in the concentration of the sTNF-r I in amniotic fluid with gestational age; and (3) microbial invasion of the amniotic cavity (in term and preterm parturition) is associated with changes in amniotic fluid sTNF-r I concentrations.
   METHOD: Amniotic fluid was retrieved by amniocentesis from 185 women classified into 11 groups according to gestational age (midtrimester, preterm gestation, and term), the presence or absence of labor, spontaneous rupture of membranes and microbial invasion of the amniotic cavity. sTNF-r I was assayed with a sensitive and enzyme-linked immunosorbent assay (ELISA) validated for amniotic fluid. In addition, sTNF-r I concentrations were determined in fetal blood obtained by cordocentesis in preterm gestations (N = 24) or at the time of delivery after spontaneous labor at term (N = 10). sTNF-r I concentrations were also measured in maternal venous and cord blood and neonatal urine (n = 13).
   RESULTS: sTNF-r I was found to be present in all amniotic fluid samples, maternal blood and fetal blood and neonatal urine samples; sTNF-r I concentrations were higher in the midtrimester than at term (mean +/- SD: 36.2 +/- 12.2 ng/ml versus mean +/- SD: 5.56 +/- 5.72 ng/ml [P < .05]); patients with preterm labor and microbial invasion of the amniotic cavity (with intact or with ruptured membranes) had significantly higher amniotic fluid concentrations of sTNF-r I than patients without microbial invasion; in the absence of microbial invasion, parturition (both term and preterm) was not associated with changes in amniotic fluid concentrations of sTNF-r I; neonatal urine contained the highest concentrations of sTNF-r I of all biological fluids assayed including maternal and neonatal/fetal blood and amniotic fluid.,
   CONCLUSIONS: It was concluded that sTNF-r I is a physiologic constitutent of amniotic fluid, as well as of the fetal and maternal plasma; that amniotic fluid sTNF-r I concentrations decrease as a function of gestional age and increases in the concentration of the sTNF-r I are part of the host response to intrauterine infection in preterm parturition.
C1 NICHHD,PERINATOL BRANCH,BETHESDA,MD 20892.
RP BAUMANN, P (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,SCH MED,DEPT OBSTET & GYNECOL,4707 ST ANTOINE BLVD,DETROIT,MI 48201, USA.
NR 31
TC 33
Z9 33
U1 0
U2 1
PU MUNKSGAARD INT PUBL LTD
PI COPENHAGEN
PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
SN 8755-8920
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD SEP-OCT
PY 1993
VL 30
IS 2-3
BP 184
EP 193
PG 10
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA MN381
UT WOS:A1993MN38100019
PM 8311927
ER

PT J
AU THEUER, CP
   PASTAN, I
AF THEUER, CP
   PASTAN, I
TI IMMUNOTOXINS AND RECOMBINANT TOXINS IN THE TREATMENT OF SOLID CARCINOMAS
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
AB Cancer remains the second most common cause of death in our society, and advanced disease is often refractory to surgical, chemotherapeutic, and radiologic interventions. One novel approach to cancer treatment involves targeting a cytotoxic agent to a cancer cell. Immunotoxins have been developed that contain a potent toxin (either Pseudomonas exotoxin, ricin toxin, or diphtheria toxin) coupled to a targeting moiety that directs the molecule to cells expressing a certain antigen. Chemically coupled immunotoxins have been developed over the past 12 years. These bind to and kill cells expressing many tumor-associated antigens. Initial clinical results were disappointing, but recent results have been more promising. Furthermore, newer immunotoxins have been developed that will soon be in clinical trials. Some of these are recombinant toxins that have been developed using techniques of genetic engineering. Transforming growth factor-alpha, acidic fibroblast growth factor, insulin-like growth factor-1, interleukin-2, interleukin-4, interleukin-6, the binding portions of monoclonal antibodies, and CD4 have been used to direct toxins to cancer cells or cells infected with the human immunodeficiency virus type 1. Efforts are under way to circumvent problems such as immunogenicity that may limit the clinical usefulness of immunotoxins.
C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BLDG 37,ROOM 4B27,BETHESDA,MD 20892.
NR 2
TC 20
Z9 21
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 SEP
PY 1993
VL 166
IS 3
BP 284
EP 288
DI 10.1016/S0002-9610(05)80975-4
PG 5
WC Surgery
SC Surgery
GA LX269
UT WOS:A1993LX26900011
PM 8368439
ER

PT J
AU BARKSDALE, SK
   MARINCOLA, FM
   JAFFE, G
AF BARKSDALE, SK
   MARINCOLA, FM
   JAFFE, G
TI CARCINOSARCOMA OF THE ADRENAL-CORTEX PRESENTING WITH MINERALOCORTICOID
   EXCESS
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Note
DE ADRENAL CARCINOSARCOMA; OSTEOSARCOMA; CHONDROSARCOMA; HYPERALDOSTERONISM
ID PRIMARY HYPER-ALDOSTERONISM; CARCINOMA
AB An adrenal carcinosarcoma is reported in a 79-year-old woman presenting with clinical signs of hyperaldosteronism. The tumor weighed 199 g and consisted of areas typical of adrenal carcinoma and areas of sarcoma. The sarcomatous component of the tumor showed osteogenic and chondroid differentiation. Vimentin stained both the carcinomatous and sarcomatous regions. Four months after resection, the patient developed metastases. This is the third reported case of adrenal carcinosarcoma and the only case in which hyperaldosteronism or bony differentiation was observed.
C1 NCI,DIV CANC TREATMENT,SURG BRANCH,BETHESDA,MD 20892.
RP BARKSDALE, SK (reprint author), NCI,DIAG & CTR,DIV CANC BIOL,PATHOL LAB,BLDG 10,ROOM 2N212,BETHESDA,MD 20892, USA.
NR 7
TC 18
Z9 19
U1 0
U2 0
PU LIPPINCOTT-RAVEN PUBL
PI PHILADELPHIA
PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106
SN 0147-5185
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD SEP
PY 1993
VL 17
IS 9
BP 941
EP 945
DI 10.1097/00000478-199309000-00012
PG 5
WC Pathology; Surgery
SC Pathology; Surgery
GA LT685
UT WOS:A1993LT68500012
PM 8352379
ER

PT J
AU CHORZELSKI, TP
   STEFANATO, CM
   STANLEY Jr
   BEUTNER, EH
   KORMAN, NJ
   OLSZEWSKA, M
   MACIEJOWSKA, E
   JABLONSKA, S
AF CHORZELSKI, TP
   STEFANATO, CM
   STANLEY, JR
   BEUTNER, EH
   KORMAN, NJ
   OLSZEWSKA, M
   MACIEJOWSKA, E
   JABLONSKA, S
TI ERYTHEMA ANNULARE-LIKE ACANTHOLYTIC DERMATOSIS (EAAD) - NONBULLOUS
   PEMPHIGUS OR A NEW ENTITY
SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES
LA English
DT Article
DE ERYTHEMA ANNULARE; ATYPICAL PEMPHIGUS; SUBSTRATE-SPECIFIC PEMPHIGUS
   ANTIBODIES
ID MULTIFORME; VULGARIS; DISEASE
AB This article describes a case of unusual annular erythema-like dermatosis, with histological features of pemphigus foliaceus (subcorneal acantholysis) and IgG antibodies in circulation and bound in vivo to the keratinocyte surface. The reactivity of the antibodies, restricted to human squamous epithelium, was unique, differing from that of all known forms of pemphigus. This also was confirmed by immunoprecipitation. The problem is that these circulating antibodies could be missed if not determined on human substrate. It is to be established whether such cases present a new type of pemphigus or a unknown dermatosis with an autoimmune response of a pemphigus type.
C1 WARSAW ACAD MED & HOSP, DEPT DERMATOL, KOSZYKOWA 82A, PL-02008 WARSAW, POLAND.
   NCI, DERMATOL BRANCH, BETHESDA, MD 20892 USA.
   SUNY Buffalo, SCH MED & BIOMED SCI, DEPT MICROBIOL, BUFFALO, NY 14260 USA.
   SUNY Buffalo, SCH MED & BIOMED SCI, DEPT DERMATOL, BUFFALO, NY 14260 USA.
NR 11
TC 6
Z9 6
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0002-9629
J9 AM J MED SCI
JI Am. J. Med. Sci.
PD SEP
PY 1993
VL 306
IS 3
BP 145
EP 150
DI 10.1097/00000441-199309000-00003
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA LW461
UT WOS:A1993LW46100003
PM 8128974
ER

PT J
AU KREUTZER, RD
   GROGL, M
   NEVA, FA
   FRYAUFF, DJ
   MAGILL, AJ
   ALEMANMUNOZ, MM
AF KREUTZER, RD
   GROGL, M
   NEVA, FA
   FRYAUFF, DJ
   MAGILL, AJ
   ALEMANMUNOZ, MM
TI IDENTIFICATION AND GENETIC COMPARISON OF LEISHMANIAL PARASITES CAUSING
   VISCEROTROPIC AND CUTANEOUS DISEASE IN SOLDIERS RETURNING FROM OPERATION
   DESERT-STORM
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID CULTIVATION; HEALTH; MEDIA
AB Six Leishmania major and seven L. tropica parasites were isolated and identified from participants in Operation Desert Shield/Storm. A complete enzyme analysis (21 enzymes) revealed that there was enzyme polymorphism among the isolates of each species group. Any one Desert Storm L. major isolate could differ from any other for 1-3 enzymes, and any L. tropica isolate could differ from any one other for up to eight enzymes. Enzyme polymorphism data from other L. major and L. tropica isolates from Africa and the Middle East region were obtained and combined with the Desert Storm data to produce population enzyme polymorphism estimates. Results from these population data indicated that L. major parasites could be expected to differ from each other for as many as eight enzymes and still be L. major and similarly, L. tropica isolates could differ for as many as 14 enzymes. These expected isolate variation extremes have not been observed among the isolates studied. All L. major and most L. tropica isolates were from patients who, as expected, presented with cutaneous disease, but the Desert Storm and two Kenyan patients infected with L. tropica presented with a viscerotropic disease, the symptoms of which are unlike those of classic visceral leishmaniasis. Such unrecognized presentation for these L. tropica-infected patients indicates that both parasite and patient can play critical roles in disease manifestations. The Desert Storm isolates are, as indicated, either L. major or L. tropica.
C1 WALTER REED ARMY INST RES,DIV EXPTL THERAPEUT,WASHINGTON,DC 20307.
   NIAID,PARASIT DIS LAB,BETHESDA,MD 20892.
   USN,RES UNIT 3,CAIRO,EGYPT.
   WALTER REED ARMY MED CTR,DEPT MED,INFECT DIS SERV,WASHINGTON,DC 20307.
   UNIV PANAMA,FAC MED,CTR INVEST ENFERMEDADES,DEPT MICROBIOL PARASITOL,PANAMA CITY,PANAMA.
RP KREUTZER, RD (reprint author), YOUNGSTOWN STATE UNIV,DEPT BIOL,YOUNGSTOWN,OH 44555, USA.
NR 13
TC 41
Z9 43
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD SEP
PY 1993
VL 49
IS 3
BP 357
EP 363
PG 7
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA LY612
UT WOS:A1993LY61200011
PM 8372957
ER

PT J
AU KITAZUME, E
   SATO, N
   SAITO, Y
   ITO, Y
AF KITAZUME, E
   SATO, N
   SAITO, Y
   ITO, Y
TI SEPARATION OF HEAVY-METALS BY HIGH-SPEED COUNTERCURRENT CHROMATOGRAPHY
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID BIOLOGICAL SAMPLES; SERIES; ELEMENTS; COLUMN
AB Separation of heavy metal elements such as Co, Cu, Fe(II), Fe(III), Mg, and Ni was performed with a high-speed CCC coil planet centrifuge equipped with a multilayer coil. The two-phase solvent systems used for the separation were composed of n-heptane containing bis(2-ethylhexyl) phosphoric acid (stationary phase) and diluted citric acid (mobile phase), where the distribution ratios of the elements can be optimized by selecting a proper acid concentration. The mobile phase was eluted through the column at a flow rate of 5.0 mL/min while the apparatus was rotated at 800 rpm. Continuous detection of the metal elements was effected by measurement of the emission intensity with direct current plasma atomic emission spectrometry (DCP-AES), where the elution curve was obtained by on-line monitoring of each emission signal. Each metal element was well resolved at high partition efficiencies ranging from 200 to 3600 theoretical plates.
C1 SHIMADZU CO LTD,ANALYT INSTRUMENTS RES LAB,NAKAGYO KU,KYOTO 604,JAPAN.
   NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892.
RP KITAZUME, E (reprint author), IWATE UNIV,COLL HUMANITIES & SOCIAL SCI,MORIOKA,IWATE 020,JAPAN.
NR 11
TC 12
Z9 12
U1 0
U2 2
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036
SN 0003-2700
J9 ANAL CHEM
JI Anal. Chem.
PD SEP 1
PY 1993
VL 65
IS 17
BP 2225
EP 2228
DI 10.1021/ac00065a010
PG 4
WC Chemistry, Analytical
SC Chemistry
GA LU634
UT WOS:A1993LU63400013
ER

EF