FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Milenic, DE
Wong, KJ
Baidoo, KE
Ray, GL
Garmestani, K
Williams, M
Brechbiel, MW
AF Milenic, Diane E.
Wong, Karen J.
Baidoo, Kwamena E.
Ray, Geoffrey L.
Garmestani, Kayhan
Williams, Mark
Brechbiel, Martin W.
TI Cetuximab: Preclinical Evaluation of a Monoclonal Antibody Targeting
EGFR for Radioimmunodiagnostic and Radioimmunotherapeutic Applications
SO CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS
LA English
DT Article
DE monoclonal antibody; EGFR; radioimmunodiagnosis; radioimmunotherapy
ID EPIDERMAL-GROWTH-FACTOR; RECEPTOR-POSITIVE TUMORS; NUDE-MICE BEARING;
COLORECTAL-CANCER; CARCINOMA XENOGRAFTS; ANTITUMOR-ACTIVITY; IN-VIVO;
BIODISTRIBUTION; EXPRESSION; PET
AB The monoclonal antibody, cetuximab, binds to epidermal growth-factor receptor and thus provides all. opportunity to create both imaging and therapies that target this receptor. The potential of cetuximab as a radioimmunoconjugate, using the acyclic bifunctional chelator, CHX-A"-DTPA, was investigated. The pharmacokinetic behavior in the blood was determined in mice with and without tumors. Tumor targeting and scintigraphic imaging were evaluated in mice bearing xenografts of LS-174T (colorectal), SHAW (pancreatic), SKOV3 (ovarian), DU145 (prostate), and HT-29 (colorectal). Excellent tumor targeting was observed in each of the models with peak tumor uptakes of 59.8 +/- 18.1, 22.5 +/- 4.7, 33.3 +/- 5.7, 18.2 +/- 7.8, and 41.7 +/- 10.8 injected dose per gram (%ID/g) at 48-72 hours, respectively. In contrast, the highest tumor %ID/g obtained in mice bearing melanoma (A375) xenografts was 6.3 +/- 1.1 at 72 hours. The biodistribution of (111)In-cetuximab was also evaluated in nontumor-bearing mice. The highest %ID/g was observed in the liver (9.3 +/- 1.3 at 24 hours) and the salivary glands (8.1 +/- 2.8 at 72 hours). Scintigraphy showed excellent tumor targeting at 24 hours. Blood pool was evident, as expected, but cleared over time. At 168 hours, the tumor was clearly discernible with negligible background.
C1 [Milenic, Diane E.; Baidoo, Kwamena E.; Ray, Geoffrey L.; Garmestani, Kayhan; Brechbiel, Martin W.] NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Wong, Karen J.; Williams, Mark] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Milenic, DE (reprint author), NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, Ctr Canc Res,NIH, Bldg 10,Room 1B40,10 Ctr Dr,MSC-1088, Bethesda, MD 20892 USA.
EM dm71q@nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research (Bethesda,
MD)
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research (Bethesda,
MD).
NR 40
TC 43
Z9 44
U1 0
U2 8
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1084-9785
J9 CANCER BIOTHER RADIO
JI Cancer Biother. Radiopharm.
PD OCT
PY 2008
VL 23
IS 5
BP 619
EP 631
DI 10.1089/cbr.2008.0493
PG 13
WC Oncology; Medicine, Research & Experimental; Pharmacology & Pharmacy;
Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Research & Experimental Medicine; Pharmacology & Pharmacy;
Radiology, Nuclear Medicine & Medical Imaging
GA 380JR
UT WOS:000261462500010
PM 18999934
ER
PT J
AU Chiu, BCH
Dave, BJ
Ward, MH
Fought, AJ
Hou, LF
Jain, S
Gapstur, S
Evens, AM
Zahm, SH
Blair, A
Weisenburger, DD
AF Chiu, Brian C. -H.
Dave, Bhavana J.
Ward, Mary H.
Fought, Angela J.
Hou, Lifang
Jain, Smrati
Gapstur, Susan
Evens, Andrew M.
Zahm, Shelia Hoar
Blair, Aaron
Weisenburger, Dennis D.
TI Dietary factors and risk of t(14;18)-defined subgroups of non-Hodgkin
lymphoma
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE lymphoma; non-Hodgkin; chromosomal aberrations; diet; risk factors;
epidemiology
ID CHROMOSOMAL TRANSLOCATIONS; MOLECULAR PATHOGENESIS; DRINKING-WATER;
UNITED-STATES; SUBTYPES; NITRATE; GENOTOXICITY; LYMPHOCYTES; NITRITE;
CANCER
AB Objective To evaluate the associations between diet and non-Hodgkin lymphoma (NHL) according to t(14;18) status, one of the most common chromosomal abnormalities in NHL, as t(14;18)-positive NHL represents a genetically more homogeneous group than NHL overall.
Methods We determined the presence of the t(14;18)(q32;q21) by fluorescence in situ hybridization in 172 of 175 tumor blocks from a population-based, case-control study conducted in Nebraska during 1983-1986. Information on the frequency of consumption as an adult of 30 food items was derived from the parent case-control study. Dietary factors in 60 t(14;18)-positive and 87 t(14;18)-negative cases were compared with 1,075 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using polytomous logistic regression.
Results The risk of t(14;18)-positive NHL for the highest versus the lowest approximate tertile of intake was elevated for milk (OR = 2.2; 1.0-5.0) and dietary nitrite (OR = 2.8; 1.3-6.1), whereas coffee consumption was inversely associated with risk (OR = 0.4; 0.2-0.7). We also found inverse associations between the intake of fish (OR = 0.5; 0.3-1.0) and carotene (OR = 0.5; 0.2-0.9) and risk of t(14;18)-negative NHL. There was no association between the intake of meats, vegetables, protein, or vitamin C and risk of either t(14;18)-positive or t(14;18)-negative NHL.
Conclusions We observed differences in associations between diet and t(14;18)-defined subgroups of NHL. These findings should be interpreted cautiously because of the small sample.
C1 [Chiu, Brian C. -H.; Fought, Angela J.; Hou, Lifang; Gapstur, Susan] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Chiu, Brian C. -H.; Gapstur, Susan; Evens, Andrew M.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
[Dave, Bhavana J.; Jain, Smrati] Univ Nebraska Med Ctr, Munroe Meyer Inst Genet & Rehabil, Omaha, NE USA.
[Dave, Bhavana J.; Weisenburger, Dennis D.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
[Ward, Mary H.; Zahm, Shelia Hoar; Blair, Aaron] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Evens, Andrew M.] Northwestern Univ, Feinberg Sch Med, Dept Med, Div Hematol,Oncol Lymphoma Program, Chicago, IL 60611 USA.
RP Chiu, BCH (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, 680 N Lake Shore Dr,Suite 1102, Chicago, IL 60611 USA.
EM bchiu@northwestern.edu
RI Zahm, Shelia/B-5025-2015
FU National Cancer Institute (NCI) [CA94770, CA100555, CA132153]; NIH; NCI
[K23 CA109613]
FX This research was supported by grants CA94770, CA100555, and CA132153
from the National Cancer Institute (NCI) and, in part, by the Intramural
Research Program of the NIH (Division of Cancer Epidemiology and
Genetics of the NCI). Dr. Evens was supported in part by an NCI award
(K23 CA109613). The authors thank Mr. Martin Bast of the Nebraska
Lymphoma Registry and Tissue Bank for coordinating the retrieval of the
tumor blocks.
NR 41
TC 16
Z9 16
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2008
VL 19
IS 8
BP 859
EP 867
DI 10.1007/s10552-008-9148-3
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 350QL
UT WOS:000259368100007
PM 18386141
ER
PT J
AU Sharifi, N
Hurt, EM
Farrar, WL
AF Sharifi, Nima
Hurt, Elaine M.
Farrar, William L.
TI Androgen receptor expression in prostate cancer stem cells: is there a
conundrum?
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
ID AMPLIFICATION; THERAPY; BIOLOGY
AB Androgen deprivation therapy (ADT) is standard frontline therapy for metastatic prostate cancer. However, prostate cancer progresses to a castrate-resistant state. The response of prostate cancer to androgen deprivation is mediated by the androgen receptor (AR). Castrate-resistant disease is marked by a gain-of-function in AR and AR reactivation. The stem cell hypothesis of cancer would therefore predict that AR should be expressed in the prostate cancer stem cell, since genetic selection for gain-of-function changes in AR, such as AR gene amplification, should occur at the level of the stem cell population. Initial reports characterizing prostate cancer stem cells suggest that AR is not expressed in this population, which is an apparent conundrum. Here, we examined the CD44+/24- LNCaP putative stem cell population by in-cell Western and show that AR is expressed at the protein level. Our findings suggest that at least a subset of prostate cancers express AR in the putative stem cell population.
C1 [Sharifi, Nima; Hurt, Elaine M.; Farrar, William L.] NCI, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res, Frederick, MD 21702 USA.
[Sharifi, Nima] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Sharifi, N (reprint author), NCI, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res, Frederick, MD 21702 USA.
EM galanthus7@yahoo.com
FU NIH; National Cancer Institute
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute. The content of this publication
does not necessarily reflect the views or policies of the Department of
Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the US Government.
NR 11
TC 11
Z9 11
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD OCT
PY 2008
VL 62
IS 5
BP 921
EP 923
DI 10.1007/s00280-007-0659-5
PG 3
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 338SB
UT WOS:000258527900021
PM 18075739
ER
PT J
AU Hsing, AW
Chu, LW
Stanczyk, FZ
AF Hsing, Ann W.
Chu, Lisa W.
Stanczyk, Frank Z.
TI Androgen and prostate cancer: Is the hypothesis dead?
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID HORMONE-BINDING GLOBULIN; ENDOGENOUS SEX-HORMONES; DEPRIVATION THERAPY;
RISK LOCUS; MOLECULAR EPIDEMIOLOGY; TOTAL TESTOSTERONE; METABOLIC
SYNDROME; CHROMOSOME 8Q24; RECEPTOR GENE; MEN
AB Data from animal, clinical, and prevention studies support the role of androgen in prostate cancer growth, proliferation, and progression. However, results serum-based epidemiologic studies in humans have been inconclusive. Part of the inconsistency in these findings stems from differences in study population, assay accuracy, intraperson variation, and limited sample size. Recently, data from a large pooled analysis of 18 prospective studies (3,886 cases and 6,438 healthy controls) showed no association between serum androgen and prostate cancer risk. It is not surprising that the pooled analysis did not find a positive link between circulating levels of total testosterone and prostate cancer risk because, individually, few of the 18 studies included in the pooled analysis reported a substantial positive association. The null result, however,, does not pronounce a death sentence for the androgen hypothesis; rather, it underscores the importance of a better understanding of androgen action within the prostate, including the relationship between tissue and serum levels of androgen. In this commentary, we explain why circulating levels of testosterone may not reflect androgen action in the prostate and why tissue levels of androgen, in particular dihydrotestosterone, and the androgen receptor and its coregulators are critical to androgen action in the prostate and should be incorporated in future studies. It is timely to integrate system thinking into our research and use an interdisciplinary approach that involves different disciplines, including epidemiology, endocrinology, pathology, and molecular biology, to help dissect the complex interplay between sex steroids and genetic and lifestyle factors in prostate cancer etiology.
C1 [Hsing, Ann W.; Chu, Lisa W.] NCI, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Chu, Lisa W.] NCI, NIH, Off Prevent Oncol, Bethesda, MD 20892 USA.
[Stanczyk, Frank Z.] Univ So Calif, Dept Obstet & Gynecol, Keck Sch Med, Los Angeles, CA 90089 USA.
[Stanczyk, Frank Z.] Univ So Calif, Dept Prevent Med, Keck Sch Med, Los Angeles, CA 90089 USA.
RP Hsing, AW (reprint author), NCI, NIH, Div Canc Epidemiol & Genet, Execut Plaza S 5024,MSC 7234,6120 Execut Blvd, Bethesda, MD 20892 USA.
EM hsinga@mail.nih.gov
FU Intramural NIH HHS
NR 51
TC 45
Z9 46
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2008
VL 17
IS 10
BP 2525
EP 2530
DI 10.1158/1055-9965.EPI-08-0448
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 360IK
UT WOS:000260051000002
PM 18842992
ER
PT J
AU Cuschieri, K
Wentzensen, N
AF Cuschieri, Kate
Wentzensen, Nicolas
TI Human papillomavirus mRNA and p16 detection as biomarkers for the
improved diagnosis of cervical neoplasia
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Review
ID LIQUID-BASED CYTOLOGY; POLYMERASE-CHAIN-REACTION; ATYPICAL
SQUAMOUS-CELLS; 2-YEAR FOLLOW-UP; INTRAEPITHELIAL NEOPLASIA; P16(INK4A)
EXPRESSION; HIGH-RISK; UTERINE CERVIX; PAP-SMEAR; UNDETERMINED
SIGNIFICANCE
AB Human papillomavirus (HPV) infection of the genital tract is very common and normally follows a benign clinical course; however, in an unfortunate minority of infected individuals, it can cause disease that sometimes leads to cancer. It is accepted that HPV DNA testing has a role in the management of cervical disease both in a prevaccination and postvaccination era; however, to improve the specificity of this approach, there is a requirement to develop and validate tools/assays that can identify women at risk for progressive disease. There is evidence to suggest that detection of viral gene expression both directly and indirectly may constitute a more specific approach for delineating clinically significant infection compared with HPV DNA-based assays. HPV oncogene expression and evidence of its deregulation can be monitored through direct detection of viral mRNA transcripts or through detection of the cellular protein p16. For both approaches, commercial assays have been introduced and numerous studies have been conducted. The present article describes the scientific theory underpinning these approaches, their amenability to routine-diagnostic specimens/settings, and the clinical data that has been garnered through their application thus far. Currently, there is promising data indicating that HPV mRNA and p16 might play an important role in future cervical cancer screening scenarios. Still, large randomized studies are necessary to confirm the preliminary data.
Methods: PubMed and OVID were interrogated with search terms "HPV RNA;" "HPV mRNA;" "HPV transcript-detection, testing, and methods;" "p16" AND "cervical cancer;" "p16" AND "CIN;" "p16" AND "histology"; "p16" AND "cytology;" "p16;" and "screening.".
C1 [Cuschieri, Kate] Royal Infirm Edinburgh NHS Trust, Specialist Virol Ctr, Edinburgh EH16 4SA, Midlothian, Scotland.
[Wentzensen, Nicolas] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Cuschieri, K (reprint author), Royal Infirm Edinburgh NHS Trust, Specialist Virol Ctr, Edinburgh EH16 4SA, Midlothian, Scotland.
EM Kate.Cuschieri@luht.scot.nhs.uk
FU Intramural NIH HHS [ZIA CP010124-14]
NR 88
TC 130
Z9 144
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2008
VL 17
IS 10
BP 2536
EP 2545
DI 10.1158/1055-9965.EPI-08-0306
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 360IK
UT WOS:000260051000004
PM 18842994
ER
PT J
AU Reed, GA
Sunega, JM
Sullivan, DK
Gray, JC
Mayo, MS
Crowell, JA
Hurwitz, A
AF Reed, Gregory A.
Sunega, Jean M.
Sullivan, Debra K.
Gray, John C.
Mayo, Matthew S.
Crowell, James A.
Hurwitz, Aryeh
TI Single-dose pharmacokinetics and tolerability of absorption-enhanced 3,3
'-diindolylmethane in healthy subjects
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID DIETARY INDOLE-3-CARBINOL; RAINBOW-TROUT; MAMMARY CARCINOGENESIS;
BREAST-CANCER; RATS; MICE; CHEMOPREVENTION; WOMEN; 3,3-DIINDOLYLMETHANE;
INHIBITION
AB We have completed a single ascending dose clinical study of the proposed chemopreventive agent 3,3'-diindolylmethane (DIM). The study agent was nutritional-grade, absorption-enhanced BioResponse 3,3'-diindolylmethane (BR-DIM). We determined the safety, tolerability, and pharmacokinetics of single doses of BR-DIM in drug-free, non-smoking, healthy men and women. Groups of four subjects were enrolled for each dose level. After randomization, one subject in each group received placebo whereas three received active BR-DIM. The doses administered were 50,100,150,200, and 300 mg, with the 300-mg dose repeated in an additional group. No BR-DIM-related adverse effects were reported at doses up to 200 mg. At the 300-mg dose, one of six subjects reported mild nausea and headache and one also reported vomiting. Only the latter effect was judged as probably related to the study agent. Analysis of serial plasma samples showed that only one subject at the 50-mg dose had detectable concentrations of DIM. The single 100-mg dose of BR-DIM resulted in a mean maximum plasma concentration (C-max) Of 32 ng/mL and a mean area under the curve (AUC) of 128 h ng/mL, and a single 200-mg dose produced a mean Cmax of 104 ng/mL and a mean AUC of 553 h ng/mL. The single 300-mg dose of BR-DIM resulted in a mean C-max. of 108 ng/mL and a mean AUC of 532 h ng/mL. We conclude that BR-DIM is well tolerated at single doses of up to 200 mg, and that increasing the dose to 300 mg did not result in an increase in C-max.
C1 [Reed, Gregory A.; Hurwitz, Aryeh] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Kansas City, KS 66160 USA.
[Reed, Gregory A.; Sunega, Jean M.; Hurwitz, Aryeh] Univ Kansas, Med Ctr, Dept Internal Med, Kansas City, KS 66160 USA.
[Sullivan, Debra K.] Univ Kansas, Med Ctr, Dept Nutr & Dietet, Kansas City, KS 66160 USA.
[Mayo, Matthew S.] Univ Kansas, Med Ctr, Dept Biostat, Kansas City, KS 66160 USA.
[Reed, Gregory A.; Sullivan, Debra K.; Gray, John C.; Mayo, Matthew S.; Hurwitz, Aryeh] Univ Kansas, Med Ctr, Kansas Masonic Canc Res Inst, Kansas City, KS 66160 USA.
[Crowell, James A.] NCI, Chemoprevent Agent Dev Res Grp, Bethesda, MD 20892 USA.
RP Reed, GA (reprint author), Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, MS 1018,3901 Rainbow Blvd, Kansas City, KS 66160 USA.
EM greed@kumc.edu
RI Mayo, Matthew/E-3774-2015
FU National Cancer Institute [N01-CN-35008]
FX National Cancer Institute contract N01-CN-35008.
NR 28
TC 47
Z9 51
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2008
VL 17
IS 10
BP 2619
EP 2624
DI 10.1158/1055-9965.EPI-08-0520
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 360IK
UT WOS:000260051000014
PM 18843002
ER
PT J
AU Colbert, LH
Graubard, BI
Michels, KB
Willett, WC
Forman, MR
AF Colbert, Lisa H.
Graubard, Barry I.
Michels, Karin B.
Willett, Walter C.
Forman, Michele R.
TI Physical activity during pregnancy and age at menarche of the daughter
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID EARLY-LIFE EXPOSURES; BREAST-CANCER; HEART-DISEASE; FETAL-GROWTH;
GLUCOSE-TOLERANCE; POSTNATAL-GROWTH; BIRTH-WEIGHT; IN-UTERO; RISK;
CHILDHOOD
AB In utero exposures have been proposed as possible determinants of later disease risk. Given that a later age at menarche is a breast cancer risk factor, and that higher childhood physical activity has been associated with a later menarcheal age, it is possible that a pregnant mother's activity may also influence this outcome. The purpose of this study was to determine if a mother's physical activity during pregnancy is related to their daughter's menarcheal age. Participants of the Nurses' Health Study 11 reported their age at menarche to the nearest year, whereas their mothers (n = 33,016) completed surveys regarding their health and lifestyle habits during their pregnancy with their daughters. Mothers reported their home, occupational, and leisure-time physical activities, as well as the activity of their daughters at ages 5 to 10 years. Using multiple linear regression analysis with adjustment for specific covariates including daughter's childhood body size, neither home nor occupational activity alone were associated with age at menarche of the daughter, but there was a direct association with leisure-time physical activity (P-trend < 0-001). Compared with women inactive in their leisure-time, women who were highly active had daughters with menarche 1.1 (95% confidence interval, 0.3-1.9) months later. Using a composite variable of both home and leisure-time activity, daughters of women who were highly active at home and in their leisure-time had daughters with menarche 3.1 (95% confidence interval, 0.4-5.9) months later than those who were highly inactive in both. Physical activity during pregnancy may be associated with a modest delay in menarcheal age in offspring.
C1 [Colbert, Lisa H.] Univ Wisconsin, Dept Kinesiol, Madison, WI 53706 USA.
[Colbert, Lisa H.] Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, Madison, WI 53706 USA.
[Graubard, Barry I.] NCI, Biostat Branch, Bethesda, MD 20892 USA.
[Michels, Karin B.; Willett, Walter C.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Michels, Karin B.] Brigham & Womens Hosp, Dept Obstet Gynecol & Reprod Biol, Obstet & Gynecol Epidemiol Ctr, Boston, MA 02115 USA.
[Michels, Karin B.] Harvard Univ, Sch Med, Dept Epidemiol, Boston, MA USA.
[Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Forman, Michele R.] Univ Texas Houston, MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
RP Colbert, LH (reprint author), Univ Wisconsin, Dept Kinesiol, 2000 Observ Dr, Madison, WI 53706 USA.
EM lhcolbert@education.wisc.edu
FU National Cancer Institute's Intramural Research Program [N02-RC-17027,
PO 263 MQ 411027]
FX National Cancer Institute's Intramural Research Program (M. Formao and
B. Graubard), N02-RC-17027 (W. Willett and K. Michels), and PO 263 MQ
411027 (W. Willett and K. Michels).
NR 34
TC 4
Z9 4
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2008
VL 17
IS 10
BP 2656
EP 2662
DI 10.1158/1055-9965.EPI-08-0194
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 360IK
UT WOS:000260051000019
PM 18843007
ER
PT J
AU Vo, TT
Gladen, BC
Cooper, GS
Baird, DD
Daniels, JL
Gammon, MD
Richardson, DB
AF Vo, Thao T.
Gladen, Beth C.
Cooper, Glinda S.
Baird, Donna D.
Daniels, Julie L.
Gammon, Marilie D.
Richardson, David B.
TI Dichlorodiphenyldichloroethane and polychlorinated biphenyls:
Intraindividual changes, correlations, and predictors in healthy women
from the Southeastern United States
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID POLYBROMINATED DIPHENYL ETHERS; NON-HODGKINS-LYMPHOMA; HUMAN
BREAST-MILK; ORGANOCHLORINE EXPOSURE; SERUM CONCENTRATIONS; NATURAL
MENOPAUSE; TIME TRENDS; HALF-LIVES; DDT LEVELS; PCB
AB Dichlorodiphenyldichloroethane (DDE) and polychlorinated biphenyls (PCB) are widespread environmental contaminants that have been postulated to increase the risk of diseases such as non-Hodgkin's lymphoma, breast cancer, as well as lead to early menopause. Studies assessing the effect of organochlorine exposure often can only measure organochlorine levels once, such as at study enrollment, which may not be an etiologically relevant time period. We assessed the temporal changes in DDE and PCBs and the predictors of those changes using interview data and DDE and PCB measures collected from 123 women who were enrolled in a baseline study from 1978 to 1982 and followed up in 2003 to 2004. Baseline and follow-up organochlorine levels were compared using Spearman correlations (r(s)), and predictors of the rate of change in log concentration were evaluated using linear regression models. Although serum concentrations dramatically declined (median follow-up to baseline concentration ratio was 16% for DDE and 45% for PCB), baseline and follow-up measures were strongly correlated for DDE (r(s) = 0.72) and moderately correlated for PCBs (r(s) = 0.43). Prediction of follow-up PCB levels was substantially improved (r(s) = 0.75) with data on initial concentration, length of lactation, baseline body mass index, and percent change in body fat, whereas DDE prediction improved slightly (r(s) = 0.83) with data on lactation and baseline body mass index. These findings suggest that a single organochlorine measure provides considerable information on relative ranking at distant times and that the predictive power can be improved, particularly for PCBs, with information on a few predictors.
C1 [Vo, Thao T.; Baird, Donna D.] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Gladen, Beth C.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Vo, Thao T.; Daniels, Julie L.; Gammon, Marilie D.; Richardson, David B.] Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC USA.
[Cooper, Glinda S.] US EPA, Washington, DC 20460 USA.
RP Baird, DD (reprint author), NIEHS, Epidemiol Branch, MD A3-05,Box 12233, Res Triangle Pk, NC 27709 USA.
EM baird@niehs.nih.gov
RI Baird, Donna/D-5214-2017
OI Baird, Donna/0000-0002-5544-2653
FU NIH; National Institute of Environmental Health Sciences
FX Grant support: Intramural Research Program of the NIH, National
Institute of Environmental Health Sciences.
NR 52
TC 15
Z9 15
U1 1
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2008
VL 17
IS 10
BP 2729
EP 2736
DI 10.1158/1055-9965.EPI-08-0379
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 360IK
UT WOS:000260051000028
PM 18843016
ER
PT J
AU Gaudet, MM
Chanock, S
Dunning, A
Driver, K
Brinton, LA
Lissowska, J
Peplonska, B
Pharoah, P
Garcia-Closas, M
AF Gaudet, Mia M.
Chanock, Stephen
Dunning, Alison
Driver, Kristy
Brinton, Louise A.
Lissowska, Jolanta
Peplonska, Beata
Pharoah, Paul
Garcia-Closas, Montserrat
TI HSD17B1 genetic variants and hormone receptor-defined breast cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID 17-BETA-HYDROXYSTEROID DEHYDROGENASES; CHINESE WOMEN; RISK;
POLYMORPHISMS; SUSCEPTIBILITY; TYPE-1; CYP17; CELLS; ASSAY; BIAS
AB HSD17B1 is an important candidate gene in breast cancer via its role in converting estrone to estradiol. A nonsynonymous G-to-A transition (rs605059) and an intronic C-to-A (rs676387) single-nucleotide polymorphism, which captured most common variation in HSD17B1, were evaluated in several breast cancer studies with inconclusive results. We followed up these findings in the Polish Breast Cancer Study (1,995 cases; 2,296 controls) and the British Studies of Epidemiology and Risk Factors in Cancer Heredity study (4,470 cases; 4,560 controls). Meta-analyses of published data and our own were also conducted among Caucasian women. Consistent with previous reports, we found little to no association with overall risk for heterozygotes and minor allele homozygotes compared with major allele homozygotes for rs605059 [summary odds ratios (95% confidence intervals), 0.93 (0.87-0.99) for GA and 0.96 (0.85-1.08), based on 11,762 cases and 14,329 controls from 10 studies] and for rs676387 [summary odds ratios (95% confidence intervals), 1.04 (0.97-1.12) and 1.12 (0.99-1.27), based on analyses of 11,074 cases and 13,605 controls from 8 studies]. Data from the Polish [n = 586 estrogen receptor-negative (ER-) cases] and British (n = 407) studies did not support the previous findings that ER- tumors were inversely associated with rs676387 AA genotype and positively associated with rs605059 GG genotype, based on subanalyses in 5 prospective cohorts with 354 ER- cases. In conclusion, it is unlikely that common genetic variation in HSD17B1 is associated with a moderate modulation in breast cancer risk overall; however, we cannot exclude the possibility of a very weak effect. Associations between HSD17B1 genotypes and risk for ER- breast cancer were inconsistent across studies and should be studied further.
C1 [Gaudet, Mia M.; Chanock, Stephen; Brinton, Louise A.; Lissowska, Jolanta; Garcia-Closas, Montserrat] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Chanock, Stephen] NCI, Core Genotype Facil, Adv Technol Ctr, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Dunning, Alison; Driver, Kristy; Pharoah, Paul] Univ Cambridge, Dept Oncol, Canc Res UK Human Canc Genet Res Grp, Cambridge, England.
[Lissowska, Jolanta] Ctr Canc, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta] M Sklodowska Curie Inst Oncol, Warsaw, Poland.
[Peplonska, Beata] Nofer Inst Occupat Med, Dept Occupat & Environm Epidemiol, Lodz, Poland.
RP Gaudet, MM (reprint author), 307 E 63rd St,3rd Floor, New York, NY 10021 USA.
EM gaudetm@mskcc.org
RI Peplonska, Beata/F-6004-2010; Garcia-Closas, Montserrat /F-3871-2015;
Brinton, Louise/G-7486-2015;
OI Garcia-Closas, Montserrat /0000-0003-1033-2650; Brinton,
Louise/0000-0003-3853-8562; Lissowska, Jolanta/0000-0003-2695-5799;
Dunning, Alison Margaret/0000-0001-6651-7166
FU National Cancer Institute, NIH; Department of Health and Human Services,
USA; Cancer Research UK
FX Grant support: The Polish study is funded by Intramural Research Program
of the National Cancer Institute, NIH, Department of Health and Human
Services, USA, and Studies of Epidemiology and Risk Factors in Cancer
Heredity is funded by a grant from Cancer Research UK.
NR 23
TC 5
Z9 6
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2008
VL 17
IS 10
BP 2766
EP 2772
DI 10.1158/1055-9965.EPT-07-2891
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 360IK
UT WOS:000260051000033
PM 18843021
ER
PT J
AU Smith, ER
Adams, SA
Das, IP
Bottai, M
Fulton, J
Hebert, JR
AF Smith, Emily Rose
Adams, Swann Arp
Das, Irene Prabhu
Bottai, Matteo
Fulton, Jeanette
Hebert, James R.
TI Breast cancer survival among economically disadvantaged women: The
influences of delayed diagnosis and treatment on mortality
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID INADEQUATE FOLLOW-UP; AFRICAN-AMERICAN; WHITE WOMEN; RACIAL-DIFFERENCES;
BLACK-WOMEN; CARCINOMA; STAGE; MAMMOGRAPHY; PROGNOSIS; RACE
AB Breast cancer affects thousands each year in the United States, and disproportionately affects certain subgroups. For example, the incidence of breast cancer in South Carolina is lower in African American compared with European American women by similar to 12% to 15%, but their mortality rate is twice as high as in European American women. The purpose of the study was to assess factors associated with breast cancer mortality between African American and European American women. Participants (n = 314) in South Carolina's Breast and Cervical Cancer Early Detection Program (SCBCCEDP), which provides breast cancer screening and treatment services, during the years 1996-2004 were included in the study. Data, including tumor characteristics, delay intervals, and race, were examined using the chi(2) test and the Wilcoxon rank-sum test. Cox regression modeling was used to assess the relationship between delay intervals and other factors. No racial differences were found in age at diagnosis, tumor characteristics, or delay intervals. Time delay intervals did not explain differences and mortality rates by race. Survival, however, was affected by prognostic factors as well as by a significant interaction between hormone-receptor status and race. Despite the excellent record of the SCBCCEDP in screening and diagnostic or treatment referrals, the racial disparities in breast cancer mortality continue to exist in South Carolina. These findings highlight the need for future research into the etiology of racial differences, and their impact on breast cancer survival.
C1 [Smith, Emily Rose; Adams, Swann Arp; Bottai, Matteo; Hebert, James R.] Univ S Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, Columbia, SC 29208 USA.
[Smith, Emily Rose; Adams, Swann Arp; Hebert, James R.] S Carolina Statewide Canc Prevent & Control Progr, Columbia, SC USA.
[Fulton, Jeanette] Palmetto Baptist Breast Hlth Ctr, Columbia, SC USA.
[Das, Irene Prabhu] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Smith, ER (reprint author), Scott & White Mem Healthcare, Aging & Care Res Program, Temple, TX USA.
EM esmith@swmail.sw.org
RI Arp Adams, Swann/C-7337-2015
OI Arp Adams, Swann/0000-0001-5779-6802
FU National Cancer Institute [1 U01 CA114601-01]; Centers for Disease
Control and Prevention's National Program of Cancer Registries
[U55CCU421931]; South Carolina Department of Health and Environmental
Control; National Cancer Prevention and Control Program [CCU421931-05]
FX Grant support: South Carolina Cancer Disparities Community Network
through grant number 1 U01 CA114601-01 from the National Cancer
Institute (Community Networks Program). The South Carolina Central
Cancer Registry is funded by the Centers for Disease Control and
Prevention's National Program of Cancer Registries, cooperative
agreement number U55CCU421931, and the South Carolina Department of
Health and Environmental Control. The South Carolina Breast and Cervical
Cancer Early Detection Program is under the National Cancer Prevention
and Control Program, cooperative agreement number CCU421931-05.
NR 62
TC 27
Z9 29
U1 1
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2008
VL 17
IS 10
BP 2882
EP 2890
DI 10.1158/1055-9965.EPI-08-0221
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 360IK
UT WOS:000260051000047
PM 18835941
ER
PT J
AU Szabo, E
AF Szabo, Eva
TI Assessing Efficacy in Early-Phase Cancer Prevention Trials: The Case of
Oral Premalignancy
SO CANCER PREVENTION RESEARCH
LA English
DT Editorial Material
ID CELL LUNG-CANCER; CHEMOPREVENTION TRIALS; COLORECTAL-CANCER;
FLUORESCENCE VISUALIZATION; CARDIOVASCULAR RISK; TASK-FORCE; END-POINTS;
CELECOXIB; LEUKOPLAKIA; DYSPLASIA
C1 NCI, Lung & Upper Aerodigest Canc Res Grp, Canc Prevent Div, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Szabo, E (reprint author), NCI, Lung & Upper Aerodigest Canc Res Grp, Canc Prevent Div, NIH,Dept Hlth & Human Serv, Room 2132,6130 Execut Blvd, Bethesda, MD 20892 USA.
EM szaboe@mail.nih.gov
NR 35
TC 7
Z9 7
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD OCT
PY 2008
VL 1
IS 5
BP 312
EP 315
DI 10.1158/1940-6207.CAPR-08-0171
PG 4
WC Oncology
SC Oncology
GA 420MK
UT WOS:000264293700003
PM 19138975
ER
PT J
AU Islami, F
Kamangar, F
AF Islami, Farhad
Kamangar, Farin
TI Helicobacter pylori and Esophageal Cancer Risk: A Meta-analysis
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; GASTROESOPHAGEAL-REFLUX DISEASE; GASTRIC
CARDIA; BARRETTS-ESOPHAGUS; INTESTINAL METAPLASIA; CAGA SEROPOSITIVITY;
COLORECTAL-CANCER; PANCREATIC-CANCER; UNITED-STATES; 5 CONTINENTS
AB We conducted this meta-analysis to examine the association between Helicobacter pylori and esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma. We searched the PubMed database, the ISI database, and the references of the selected articles. Case-control or nested case-control studies were selected if they used serology or endoscopic methods to detect H. pylori in the stomach and if control subjects were not restricted to upper gastrointestinal tract cancer or peptic ulcer disease patients. A total of 19 studies were used for this analysis. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using the DerSimonian-Laird method. Q statistics and I(2) statistics were calculated to examine heterogeneity. Subgroup analyses were conducted by CagA status. For EAC, the summary OR (95% CI) was 0.56 (0.46-0.68). There was little heterogeneity among studies (I(2) = 15%). Further analysis showed that colonization with CagA-positive strains was inversely associated with EAC risk (OR, 0.41; 95% CI, 0.28-0.62) but colonization with CagA-negative strains was not (OR, 1.08; 95% CI, 0.76-1.53). For esophageal squamous cell carcinoma, the summary OR (95% CI) was 1.10 (0.78-1.55). However, there was substantial heterogeneity among studies (I(2) = 73%), with statistically significant associations in both directions. Our results suggest an inverse association between CagA-positive H. pylori colonization and risk of EAC. The prominent decline of H. pylori colonization in the past few decades may be partly responsible for the recent increase in EAC incidence in Western countries.
C1 [Kamangar, Farin] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Islami, Farhad] Univ Tehran Med Sci, Digest Dis Res Ctr, Tehran, Iran.
[Islami, Farhad] IARC, Environm & Canc Grp, Lyon, France.
[Islami, Farhad] Kings Coll London, Thames Canc Registry, London WC2R 2LS, England.
RP Kamangar, F (reprint author), NCI, Div Canc Epidemiol & Genet, Room 3034,6120 Execut Blvd, Bethesda, MD 20892 USA.
EM kamangaf@mail.nih.gov
FU National Cancer Institute; NIH
FX Grant support: National Cancer Institute, NIH.
NR 81
TC 150
Z9 151
U1 2
U2 12
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD OCT
PY 2008
VL 1
IS 5
BP 329
EP 338
DI 10.1158/1940-6207.CAPR-08-0109
PG 10
WC Oncology
SC Oncology
GA 420MK
UT WOS:000264293700005
PM 19138977
ER
PT J
AU Adams, L
Roth, MJ
Abnet, CC
Dawsey, SP
Qiao, YL
Wang, GQ
Wei, WQ
Lu, N
Dawsey, SM
Woodson, K
AF Adams, Lisa
Roth, Mark J.
Abnet, Christian C.
Dawsey, Sonja P.
Qiao, You-Lin
Wang, Guo-Qing
Wei, Wen-Qiang
Lu, Ning
Dawsey, Sanford M.
Woodson, Karen
TI Promoter Methylation in Cytology Specimens as an Early Detection Marker
for Esophageal Squamous Dysplasia and Early Esophageal Squamous Cell
Carcinoma
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID PRECURSOR LESIONS; ASYMPTOMATIC ADULTS; LINXIAN; CHINA; BALLOON; CANCER;
POPULATION; SAMPLERS
AB The incidence of esophageal squamous cell carcinoma (ESCC) is very high in northern China. This cancer has a very poor prognosis, mostly because it is usually diagnosed at a late stage. Detection at an earlier stage can dramatically improve prognosis. Microscopic evaluation of esophageal balloon cytology (EBC) specimens has been the most common method for early detection of ESCC, but this technique is limited by low sensitivity and specificity. The use of molecular markers may improve these screening characteristics. This study evaluates whether measurement of gene methylation in EBC specimens may have utility for the detection of esophageal squamous dysplasia and early ESCC. We evaluated the presence of methylation in eight genes shown to be methylated in ESCC in previous studies in EBC specimens from 147 patients with endoscopic biopsy diagnoses ranging from normal mucosa to severe squamous dysplasia. Methylation status was determined using quantitative methylation-specific PCR techniques. The sensitivity and specificity of methylation of each individual gene and of combinations of these genes to detect biopsy-proven high-grade (moderate or severe) squamous dysplasia were determined. For individual genes, the sensitivities ranged from 9% to 34% and the specificities ranged from 77% to 99%. Using a panel of four genes (AHRR, p16INK4a, MT1G, and CLDN3) resulted in sensitivity and specificity of 50% and 68%, respectively. This study suggests that evaluation of gene methylation in EBC samples may have utility for early detection of esophageal squamous dysplasia and early ESCC; however, identification of more sensitive methylation markers will be required for development of a clinically useful screening test.
C1 [Roth, Mark J.; Abnet, Christian C.; Dawsey, Sanford M.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Adams, Lisa; Dawsey, Sonja P.; Woodson, Karen] NCI, Genet Branch, Ctr Canc Res, NIH, Rockville, MD 20852 USA.
[Qiao, You-Lin; Wei, Wen-Qiang] Chinese Acad Med Sci, Dept Canc Epidemiol, Beijing 100037, Peoples R China.
[Wang, Guo-Qing] Chinese Acad Med Sci, Dept Endoscopy, Beijing 100037, Peoples R China.
[Lu, Ning] Chinese Acad Med Sci, Dept Pathol, Inst Canc, Beijing 100037, Peoples R China.
RP Roth, MJ (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS 320 MSC 7232, Rockville, MD 20852 USA.
EM mr166i@nih.gov
RI Qiao, You-Lin/B-4139-2012; Abnet, Christian/C-4111-2015;
OI Qiao, You-Lin/0000-0001-6380-0871; Abnet, Christian/0000-0002-3008-7843;
Dawsey, Sonja/0000-0003-1605-3994
FU Intramural NIH HHS [Z01 CP000185-03]
NR 16
TC 23
Z9 26
U1 1
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD OCT
PY 2008
VL 1
IS 5
BP 357
EP 361
DI 10.1158/1940-6207.CAPR-08-0061
PG 5
WC Oncology
SC Oncology
GA 420MK
UT WOS:000264293700008
PM 19137073
ER
PT J
AU Mazan-Mamczarz, K
Hagner, PR
Dai, BJ
Wood, WH
Zhang, YQ
Becker, KG
Liu, ZQ
Gartenhaus, RB
AF Mazan-Mamczarz, Krystyna
Hagner, Patrick R.
Dai, Bojie
Wood, William H.
Zhang, Yongqing
Becker, Kevin G.
Liu, Zhenqui
Gartenhaus, Ronald B.
TI Identification of transformation-related pathways in a breast epithelial
cell model using a ribonomics approach
SO CANCER RESEARCH
LA English
DT Article
ID MESSENGER-RNA STABILITY; PROTEIN HUR; BINDING; TRANSLATION; AUF1; TIAR
AB The aberrant expression of many genes is a common feature in the malignant transformation of cells. In mammalian cells, posttranscriptional gene regulatory processes are emerging as critical determinants controlling gene expression both in physiologic and pathologic conditions. These regulatory mechanisms are directed primarily by the interaction of mRNAs with specific RNA-binding proteins (RBP). There is an emerging body of data demonstrating that two RBPs, AUF1 and HuR, can antagonistically affect the posttranscriptional fate of target mRNAs, as well as concurrently bind to common target transcripts. Employing MCT-1 oncogene-mediated transformation of immortalized breast epithelial MCF10A cells, we characterized the largely reciprocal association of these two RBPs with target mRNAs and their influence on protein expression vis-a-vis cellular transformation. Using a ribonomics approach, we identified mRNAs from cancer-related pathways whose association with AUF1 and/or HuR were altered when comparing immortalized with transformed MCF10A cells. Significantly, we were able to show that knockdown of HuR expression using RNA interference reduced anchorage-independent growth capacity in transformed MCF10A cells and decreased protein expression of a number of validated target genes. Our data show that the global alterations in binding of HuR and AUF1 with target transcripts have a critical role in posttranscriptional regulation of genes encoding proteins involved in breast epithelial cell transformation. These findings further support the feasibility of using a ribonomics approach for the identification of cancer-related pathways.
C1 [Mazan-Mamczarz, Krystyna; Hagner, Patrick R.; Dai, Bojie; Liu, Zhenqui; Gartenhaus, Ronald B.] Univ Maryland, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Wood, William H.; Zhang, Yongqing; Becker, Kevin G.] NIA, Gene Express & Genom Unit, NIH, Baltimore, MD 21224 USA.
RP Gartenhaus, RB (reprint author), Univ Maryland, Marlene & Stewart Greenebaum Canc Ctr, 9-011 BRB,655 W Baltimore St, Baltimore, MD 21201 USA.
EM rgartenhaus@som.umaryland.edu
OI Becker, Kevin/0000-0002-6794-6656
FU Department of Veterans Affairs; Flight Attendant Research Institute
FX Grant support: Merit Review Award from the Department of Veterans
Affairs (R.B. Gartenhaus) and Clinical Innovator Award from the Flight
Attendant Research Institute (R.B. Gartenhaus).
NR 20
TC 24
Z9 24
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD OCT 1
PY 2008
VL 68
IS 19
BP 7730
EP 7735
DI 10.1158/0008-5472.CAN-08-2393
PG 6
WC Oncology
SC Oncology
GA 360AR
UT WOS:000260029900006
PM 18829526
ER
PT J
AU Qin, HR
Kim, HJ
Kim, JY
Hurt, EM
Klarmann, GJ
Kawasaki, BT
Serrat, MAD
Farrar, WL
AF Qin, Haiyan R.
Kim, Han-Jong
Kim, Joon-Young
Hurt, Elaine M.
Klarmann, George J.
Kawasaki, Brian T.
Serrat, Maria A. Duhagon
Farrar, William L.
TI Activation of signal transducer and activator of transcription 3 through
a phosphomimetic serine 727 promotes prostate tumorigenesis independent
of tyrosine 705 phosphorylation
SO CANCER RESEARCH
LA English
DT Article
ID CANCER CELL-GROWTH; STAT3
AB Aberrantly activated signal transducer and activator of transcription 3 (Stat3) is implicated in the development of various human cancers. Y705 phosphorylation is conventionally thought to be required for Stat3 signal-dependent activation and seems to play an essential role in some malignancies. Recently, it was shown that Stat3 is activated through novel and noncanonical mechanisms, including phosphorylation at S727. Here, we investigate S727 phosphorylation of Stat3 and its subsequent effects in prostate cancer development, independent of Y705 phosphorylation, using mutated Stat3 in the human prostate cancer cell line LNCaP. We show mutation of S727 to the phosphomimetic residue Glu, and inactivation of Y705 (Y705F/S727E) resulted in a remarkable growth advantage in low-serum, enhanced anchorage-independent growth in soft agar, and increased tumorigenicity in nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice, possibly by direct activation of downstream proto-oncogenes c-myc, mcl-1, and survivin. Y705F/S727E mutant cells were more invasive than Y705F/S727A (inactivation of Y705 and S727) mutant cells, and more Y705F/S727E mutant Stat3 was localized in the nuclei relative to Y705F/S727A mutant Stat3 at the steady state. Furthermore, the Y705F/S727E but not the Y705F/S727A mutant induced anchorage-independent growth of noncancerous prostate epithelial cells (RWPE-1). We further show that Stat3 is phosphorylated at S727 in 65% of malignant prostate tissues (n = 20) relative to 25% of normal prostate tissues (n = 4). Moreover, there is a positive correlation between phosphoS727-Stat3 expression and Gleason score in these prostate cancer tissues (P = 0.05). Our data suggest for the first time that S727 phosphorylation is sufficient to activate Stat3, thereby driving prostate tumorigenesis independent of Y705 phosphorylation.
C1 [Qin, Haiyan R.; Hurt, Elaine M.; Kawasaki, Brian T.; Serrat, Maria A. Duhagon; Farrar, William L.] NCI, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
[Klarmann, George J.] NCI, Basic Res Program, Sci Applicat Int Corp Frederick Inc, NIH, Frederick, MD 21702 USA.
[Kim, Han-Jong; Kim, Joon-Young] Kyungpook Natl Univ, Sch Med, Dept Internal Med & Biochem & Cell Biol, Taegu, South Korea.
RP Qin, HR (reprint author), NCI, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res,NIH, 1050 Boyles St,Bldg 560,Room 21-81, Frederick, MD 21702 USA.
EM qinhaiyan@mail.nih.gov; farrar@mail.nciferf.gov
FU National Cancer Institute, NIH [N01-CO-12400]; Intramural Research
Program of the NIH; National Cancer Institute; Center for Cancer
Research
FX Grant support: National Cancer Institute, NIH, under contract
N01-CO-12400. Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research.
NR 20
TC 55
Z9 56
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD OCT 1
PY 2008
VL 68
IS 19
BP 7736
EP 7741
DI 10.1158/0008-5472.CAN-08-1125
PG 6
WC Oncology
SC Oncology
GA 360AR
UT WOS:000260029900007
PM 18829527
ER
PT J
AU Dai, CL
Tiwari, AK
Wu, CP
Su, XD
Wang, SR
Liu, DG
Ashby, CR
Huang, Y
Robey, RW
Liang, YJ
Chen, LM
Shi, CJ
Ambudkar, SV
Chen, ZS
Fu, LW
AF Dai, Chun-ling
Tiwari, Amit K.
Wu, Chung-Pu
Su, Xiao-dong
Wang, Si-Rong
Liu, Dong-geng
Ashby, Charles R., Jr.
Huang, Yan
Robey, Robert W.
Liang, Yong-ju
Chen, Li-ming
Shi, Cheng-Jun
Ambudkar, Suresh V.
Chen, Zhe-Sheng
Fu, Li-wu
TI Lapatinib (Tykerb, GW572016) reverses multidrug resistance in cancer
cells by inhibiting the activity of ATP-binding cassette subfamily B
member 1 and G member 2
SO CANCER RESEARCH
LA English
DT Article
ID TYROSINE KINASE INHIBITOR; HUMAN P-GLYCOPROTEIN; BREAST-CANCER;
IN-VITRO; PHASE-I; METHOTREXATE TRANSPORT; ACQUIRED MUTATIONS;
DRUG-RESISTANCE; CATALYTIC CYCLE; ABCG2
AB Lapatinib is active at the ATP-binding site of Lyrosine kinases that are associated with the human epidermal growth factor receptor (Her-1 or ErbB1) and Her-2. It is conceivable that lapatinib may inhibit the function of ATP-binding cassette (ABC) transporters by binding to their ATP-binding sites. The aim of this study was to investigate the ability of lapatinib to reverse tumor multidrug resistance (MDR) due to overexpression of ABC subfamily B member 1 (ABCB1) and ABC subfamily G member 2 (ABCG2) transporters. Our results showed that lapatinib significantly enhanced the sensitivity to ABCB1 or ABCG2 substrates in cells expressing these transporters, although a small synergetic effect was observed in combining lapatinib and conventional chemotherapeutic agents in parental sensitive MCF-7 or S1 cells. Lapatinib alone, however, did not significantly alter the sensitivity of non-ABCB1 or non-ABCG2 substrates in sensitive and resistant cells. Additionally, lapatinib significantly increased the accumulation of doxorubicin or mitoxantrone in ABCB1- or ABCG2-overexpressing cells and inhibited the transport of methotrexate and E(2)17 beta G by ABCG2. Furthermore, lapatinib stimulated the ATPase activity of both ABCB1 and ABCG2 and inhibited the photolabeling of ABCB1 or ABCG2 with [(125)I]iodoarylazidoprazosin in a concentration-dependent manner. However, lapatinib did not affect the expression of these transporters at mRNA or protein levels. Importantly, lapatinib also strongly enhanced the effect of paclitaxel on the inhibition of growth of the ABCB1-overexpressing KBv200 cell xenografts in nude mice. Overall, we conclude that lapatinib reverses ABCB1- and ABCG2-mediated MDR by directly inhibiting their transport function. These findings may be useful for cancer combinational therapy with lapatinib in the clinic.
C1 [Dai, Chun-ling; Su, Xiao-dong; Liu, Dong-geng; Huang, Yan; Liang, Yong-ju; Chen, Li-ming; Shi, Cheng-Jun; Fu, Li-wu] Sun Yat Sen Univ, State Key Lab Oncol S China, Ctr Canc, Guangzhou 510060, Guangdong, Peoples R China.
[Tiwari, Amit K.; Wang, Si-Rong; Ashby, Charles R., Jr.; Chen, Zhe-Sheng] St Johns Univ, Coll Pharm & Allied Hlth Profess, Dept Pharmaceut Sci, Jamaica, NY 11439 USA.
[Wu, Chung-Pu; Ambudkar, Suresh V.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Robey, Robert W.] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Fu, LW (reprint author), Sun Yat Sen Univ, State Key Lab Oncol S China, Ctr Canc, Guangzhou 510060, Guangdong, Peoples R China.
EM Chenz@stjohns.edu; Fulw@mail.sysu.edu.cn
RI Tiwari, Amit/A-3667-2012
OI Tiwari, Amit/0000-0002-7427-7155
FU China National Natural Sciences Foundation [30672407]; 863 Project
Foundation [2006AA09Z419]; St. John's University Tenure Track Faculty
Position Start-Up Funding [C-0531]; St. Johns University Seed
[579-1110]; Intramural Research Program, Center for Cancer Research,
National Cancer Institute, NIH
FX China National Natural Sciences Foundation No.30672407 (L-w. Fu); 863
Project Foundation No.2006AA09Z419 (L-w. Fu); St. John's University
Tenure Track Faculty Position Start-Up Funding No.C-0531 and St. Johns
University Seed Grant No.579-1110 (Z-S. Chen); and Intramural Research
Program, Center for Cancer Research, National Cancer Institute, NIH
(C-P. Wu, R.W. Robey, and SY. Ambudkar).
NR 50
TC 196
Z9 205
U1 0
U2 19
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD OCT 1
PY 2008
VL 68
IS 19
BP 7905
EP 7914
DI 10.1158/0008-5472.CAN-08-0499
PG 10
WC Oncology
SC Oncology
GA 360AR
UT WOS:000260029900027
PM 18829547
ER
PT J
AU Cao, L
Yu, YK
Darko, I
Currier, D
Mayeenuddin, LH
Wan, XL
Khanna, C
Helman, LJ
AF Cao, Liang
Yu, Yunkai
Darko, Isaac
Currier, Duane
Mayeenuddin, Linnia H.
Wan, Xiaolin
Khanna, Chand
Helman, Lee J.
TI Addiction to elevated insulin-like growth factor I receptor and initial
modulation of the AKT pathway define the responsiveness of
rhabdomyosarcoma to the targeting antibody
SO CANCER RESEARCH
LA English
DT Article
ID BREAST-CANCER-CELLS; ANTITUMOR-ACTIVITY; IGF-1 RECEPTOR; HEMATOLOGIC
MALIGNANCIES; SOMATOMEDIN RECEPTOR; MONOCLONAL-ANTIBODY; FACTOR (IGF)-I;
SOLID TUMORS; INHIBITION; THERAPY
AB Insulin-like growth factor I receptor (IGF-IR) and its ligands are overexpressed by tumors, mediating proliferation and protecting against stress-induced apoptosis. Accordingly, there has been a considerable amount of interest in developing therapeutic agents against IGF-IR. IGF-IR is believed to be ubiquitously expressed without detectable mutation or amplification in cancer. We explored the determinants of cellular response to a humanized anti-IGF-IR antibody. Our results showed a large variation in IGF-IR levels in rhabdomyosarcoma tumor specimens that were comparable with those in rhabdomyosarcoma cell lines. In vitro analysis revealed a direct and very significant correlation between elevated IGF-IR levels and antiproliferative effects of the antibody and defined a receptor number that would predict sensitivity. Our data further suggested a strong dependence on IGF-IR for AKT signaling in cells with elevated IGF-IR. The sensitivity of the high IGF-IR-expressing cells was blocked with a constitutively active AKT. The extracellular signal-regulated kinase pathway was not affected by the antibody. In vivo studies showed that anti-IGF-IR had single-agent antitumor activity; furthermore, predictions of responses based on IGF-IR levels were accurate. In vivo biomarker anyalsis suggested that h7C10 down-regulated both IGF-IR and p-AKT initially, concordant with antitumor activity. Subsequent progression of tumors was associated with reactivation of p-AKT despite sustained suppression of IGF-IR. These results identified the first predictive biomarker for anti-IGF-IR therapies in cancer.
C1 [Cao, Liang; Yu, Yunkai; Mayeenuddin, Linnia H.] NCI, Genet Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Darko, Isaac; Currier, Duane; Wan, Xiaolin; Khanna, Chand; Helman, Lee J.] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Yu, Yunkai; Mayeenuddin, Linnia H.] NCI, Lab Proteom & Analyt Technol, Sci Applicat Int Corp, Frederick Inc, Frederick, MD 21701 USA.
RP Cao, L (reprint author), NCI, Genet Branch, Ctr Canc Res, 37 Convent Dr,MSC 4265, Bethesda, MD 20892 USA.
EM caoli@mail.nih.gov
FU NIH [N01-CO-12400]; NCI Center for Cancer Research; NCI
FX Intramural Research Program of the NIH, NCI Center for Cancer Research.
This project was also funded in part with federal funds from the NCI,
NIH, under contract N01-CO-12400. The content of this publication does
not necessarily reflect the views or policies of the Department of
Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. Government.
NR 40
TC 103
Z9 107
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD OCT 1
PY 2008
VL 68
IS 19
BP 8039
EP 8048
DI 10.1158/0008-5472.CAN-08-1712
PG 10
WC Oncology
SC Oncology
GA 360AR
UT WOS:000260029900042
PM 18829562
ER
PT J
AU Hosgood, HD
Menashe, I
Shen, M
Yeager, M
Yuenger, J
Rajaraman, P
He, XZ
Chatterjee, N
Caporaso, NE
Zhu, Y
Chanock, SJ
Zheng, TZ
Lan, Q
AF Hosgood, H. Dean, III
Menashe, Idan
Shen, Min
Yeager, Meredith
Yuenger, Jeff
Rajaraman, Preetha
He, Xingzhou
Chatterjee, Nilanjan
Caporaso, Neil E.
Zhu, Yong
Chanock, Stephen J.
Zheng, Tongzhang
Lan, Qing
TI Pathway-based evaluation of 380 candidate genes and lung cancer
susceptibility suggests the importance of the cell cycle pathway
SO CARCINOGENESIS
LA English
DT Article
ID COAL COMBUSTION EMISSIONS; EPIDERMAL-GROWTH-FACTOR; XUAN-WEI; GENOMEWIDE
ASSOCIATION; CHINA; RISK; EPIDEMIOLOGY; POLYMORPHISM; POPULATION;
CARCINOMAS
AB Common genetic variation may play an important role in altering lung cancer risk. We conducted a pathway-based candidate gene evaluation to identify genetic variations that may be associated with lung cancer in a population-based case-control study in Xuan Wei, China (122 cases and 111 controls). A total of 1260 single-nucleotide polymorphisms (SNPs) in 380 candidate genes for lung cancer were successfully genotyped and assigned to one of 10 pathways based on gene ontology. Logistic regression was used to assess the marginal effect of each SNP on lung cancer susceptibility. The minP test was used to identify statistically significant associations at the gene level. Important pathways were identified using a test of proportions and the rank truncated product methods. The cell cycle pathway was found as the most important pathway (P = 0.044) with four genes significantly associated with lung cancer (PLA2G6 minP = 0.001, CCNA2 minP = 0.006, GSK3 beta minP = 0.007 and EGF minP = 0.013), after adjusting for multiple comparisons. Interestingly, most cell cycle genes that were associated with lung cancer in this analysis were concentrated in the AKT signaling pathway, which is essential for regulation of cell cycle progression and cellular survival, and may be important in lung cancer etiology in Xuan Wei. These results should be viewed as exploratory until they are replicated in a larger study.
C1 [Hosgood, H. Dean, III; Menashe, Idan; Shen, Min; Yeager, Meredith; Yuenger, Jeff; Rajaraman, Preetha; Chatterjee, Nilanjan; Caporaso, Neil E.; Chanock, Stephen J.; Lan, Qing] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Hosgood, H. Dean, III; Zhu, Yong; Zheng, Tongzhang] Yale Univ, Dept Epidemiol & Publ Hlth, Sch Med, New Haven, CT 06520 USA.
[He, Xingzhou] Chinese Ctr Dis Control & Prevent, Beijing, Peoples R China.
RP Hosgood, HD (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM hosgoodd@mail.nih.gov
FU Intramural National Cancer Institute [N01-CO-12400]; Yale
University-National Cancer Institute Partnership Predoctoral Fellowship
Training Program [NCI TU2 CA105666]
FX Intramural National Cancer Institute (N01-CO-12400) program; Yale
University-National Cancer Institute Partnership Predoctoral Fellowship
Training Program (NCI TU2 CA105666).
NR 40
TC 39
Z9 42
U1 1
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD OCT
PY 2008
VL 29
IS 10
BP 1938
EP 1943
DI 10.1093/carcin/bgn178
PG 6
WC Oncology
SC Oncology
GA 356HD
UT WOS:000259768400011
PM 18676680
ER
PT J
AU Figueroa, JD
Malats, N
Garcia-Closas, M
Real, FX
Silverman, D
Kogevinas, M
Chanock, S
Welch, R
Dosemeci, M
Lan, Q
Tardon, A
Serra, C
Carrato, A
Garcia-Closas, R
Castano-Vinyals, G
Rothman, N
AF Figueroa, Jonine D.
Malats, Nuria
Garcia-Closas, Montserrat
Real, Francisco X.
Silverman, Debra
Kogevinas, Manolis
Chanock, Stephen
Welch, Robert
Dosemeci, Mustafa
Lan, Qing
Tardon, Adonina
Serra, Consol
Carrato, Alfredo
Garcia-Closas, Reina
Castano-Vinyals, Gemma
Rothman, Nathaniel
TI Bladder cancer risk and genetic variation in AKR1C3 and other
metabolizing genes
SO CARCINOGENESIS
LA English
DT Article
ID OXIDOREDUCTASE(1) DT-DIAPHORASE; SINGLE-NUCLEOTIDE POLYMORPHISMS;
ALDO-KETO REDUCTASES; ASSOCIATION; EXPRESSION; EXPOSURE; CELLS; LUNG;
CARCINOGENESIS; EPIDEMIOLOGY
AB Aromatic amines (AAs) and polycyclic aromatic hydrocarbons (PAHs) are carcinogens present in tobacco smoke and functional polymorphisms in NAT2 and GSTM1 metabolizing genes are associated with increased bladder cancer risk. We evaluated whether genetic variation in other candidate metabolizing genes are also associated with risk. Candidates included genes that control the transcription of metabolizing genes [aryl hydrocarbon receptor (AHR), AHRR and aryl hydrocarbon nuclear translocator (ARNT)] and genes that activate/detoxify AA or PAH (AKR1C3, CYP1A1, CYP1A2, CYP1B1, CYP3A4, EPHX1, EPHX2, NQO1, MPO, UGT1A4, SULT1A1 and SULT1A2). Using genotype data from 1150 cases of urothelial carcinomas and 1149 controls from the Spanish Bladder Cancer Study, we estimated odds ratios (ORs) and 95% confidence intervals (CIs) adjusting for age, gender, region and smoking status. Based on a test for trend, we observed 10 non-redundant single-nucleotide polymorphisms (SNPs) in five genes (AKR1C3, ARNT, CYP1A1, CYP1B1 and SULT1A2) significantly associated with bladder cancer risk. We observed an inverse association with risk for the AKR1C3 promoter SNP rs1937845 [OR (95% CI) for heterozygote and homozygote variant compared with common homozygote genotype were 0.86 (0.70-1.06) and 0.74 (0.57-0.96), respectively; P for trend = 0.02]. Interestingly, genetic variation in this region has been associated with lung, non-Hodgkin lymphoma and prostate cancer risk. Analysis of additional SNPs to capture most (similar to 90%) of common genetic variation in AKR1C3 and haplotype walking analyses based on all AKR1C3 SNPs (n = 25) suggest two separate regions associated with bladder cancer risk. These results indicate that genetic variation in carcinogen-metabolizing genes, particularly AKR1C3, could be associated with bladder cancer risk.
C1 [Figueroa, Jonine D.; Garcia-Closas, Montserrat; Silverman, Debra; Chanock, Stephen; Dosemeci, Mustafa; Lan, Qing; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Malats, Nuria; Kogevinas, Manolis; Castano-Vinyals, Gemma] Ctr Res Environm Epidemiol, Barcelona, Spain.
[Real, Francisco X.; Castano-Vinyals, Gemma] Inst Municipal Invest Med, Unitat Biol Cellular & Mol, E-08003 Barcelona, Spain.
[Real, Francisco X.] Univ Pompeu Fabra, Dept Ciencies Expt & Salut, Barcelona, Spain.
[Kogevinas, Manolis] Sch Med, Iraklion, Greece.
[Chanock, Stephen; Welch, Robert] NCI, Core Genotype Facil, Adv Technol Ctr, Gaithersburg, MD USA.
[Tardon, Adonina] Univ Oviedo, Oviedo, Spain.
[Carrato, Alfredo] Elche Univ Hosp, Dept Med Oncol, Elche, Spain.
[Garcia-Closas, Reina] Hop Univ Canarias, Unidad Invest, San Cristobal la Laguna, Spain.
RP Figueroa, JD (reprint author), NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM figueroaj@mail.nih.gov
RI Serra, C/E-6879-2014; Garcia-Closas, Montserrat /F-3871-2015; Malats,
Nuria/H-7041-2015; Kogevinas, Manolis/C-3918-2017; Real, Francisco
X/H-5275-2015;
OI Serra, C/0000-0001-8337-8356; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Malats, Nuria/0000-0003-2538-3784; Real, Francisco
X/0000-0001-9501-498X; Castano-Vinyals, Gemma/0000-0003-4468-1816
FU National Institutes of Health; National Cancer Institute, Division of
Cancer Epidemiology and Genetics; FIS/Spain [00/0745, G03/174, G03/160,
C03/09, C03/10]
FX National Institutes of Health; National Cancer Institute, Division of
Cancer Epidemiology and Genetics; FIS/Spain (00/0745, G03/174, G03/160,
C03/09 and C03/10).
NR 43
TC 54
Z9 57
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD OCT
PY 2008
VL 29
IS 10
BP 1955
EP 1962
DI 10.1093/carcin/bgn163
PG 8
WC Oncology
SC Oncology
GA 356HD
UT WOS:000259768400014
PM 18632753
ER
PT J
AU Wang, TTY
Hudson, TS
Wang, TC
Remsberg, CM
Davies, NM
Takahashi, Y
Kim, YS
Seifried, H
Vinyard, BT
Perkins, SN
Hursting, SD
AF Wang, Thomas T. Y.
Hudson, Tamaro S.
Wang, Tien-Chung
Remsberg, Connie M.
Davies, Neal M.
Takahashi, Yoko
Kim, Young S.
Seifried, Harold
Vinyard, Bryan T.
Perkins, Susan N.
Hursting, Stephen D.
TI Differential effects of resveratrol on androgen-responsive LNCaP human
prostate cancer cells in vitro and in vivo
SO CARCINOGENESIS
LA English
DT Article
ID PHOSPHOINOSITIDE 3-KINASE PATHWAY; CHEMOPREVENTIVE AGENT;
ESTROGEN-RECEPTORS; EXPRESSION; GROWTH; APOPTOSIS; GENES; PROLIFERATION;
MICE; PHYTOCHEMICALS
AB Resveratrol is a phytochemical that has been under consideration for use as a prostate cancer chemopreventive agent. However, the efficacy, as well as the mechanisms of action of resveratrol on prostate cancer prevention, remains largely unknown. This study seeks to address these questions and examine the cancer preventive effects of resveratrol using complementary human LNCaP prostate cancer cell culture and xenograft models. In cultured LNCaP cells, we found that resveratrol inhibited cell growth. The growth inhibitory effects of resveratrol appeared to be through modulation of both androgen-and estrogen-mediated events. Global gene expression analysis using microarrays identified androgen-responsive genes as a group of genes universally affected by resveratrol in LNCaP cells in vitro. The effect of resveratrol on expression of these genes appeared to be through inhibition of bothandrogen-and estrogen-mediated transcription. In a xenograft model, resveratrol delayed LNCaP tumor growth and inhibited expression of a marker for steroid hormone responses. However, exposure to resveratrol also led to increased angiogenesis and inhibition of apoptosis in the xenograft. In summary, resveratrol may act through modulation of steroid hormone-dependent pathways to inhibit prostate cancer cell growth in both culture and xenografts, but exposure in vivo may be of concern.
C1 [Wang, Thomas T. Y.] ARS, Diet Genom & Immunol Lab, Beltsville Human Nutr Res Ctr, USDA, Beltsville, MD 20705 USA.
[Hudson, Tamaro S.] NCI, Lab Cellular Regulat & Carcinogenesis, NIH, Bethesda, MD 20892 USA.
[Wang, Tien-Chung] Univ Maryland, Dept Nutr & Food Sci, College Pk, MD 20742 USA.
[Remsberg, Connie M.; Davies, Neal M.] Washington State Univ, Dept Pharmaceut Sci, Pullman, WA 99164 USA.
[Remsberg, Connie M.; Davies, Neal M.] Washington State Univ, Pharmacol & Toxicol Grad Program, Coll Pharm, Pullman, WA 99164 USA.
[Takahashi, Yoko] Natl Food Res Inst, Tsukuba, Ibaraki 3058642, Japan.
[Kim, Young S.; Seifried, Harold] NCI, Nutr Sci Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Vinyard, Bryan T.] ARS, USDA, Biometr Consulting Serv, Beltsville Area, Beltsville, MD 20705 USA.
[Perkins, Susan N.; Hursting, Stephen D.] Univ Texas Austin, Div Nutr Sci, Austin, TX 78712 USA.
[Hursting, Stephen D.] MD Anderson Canc Ctr, Dept Carcinogenesis, Smithville, TX 78957 USA.
RP Wang, TTY (reprint author), ARS, Diet Genom & Immunol Lab, Beltsville Human Nutr Res Ctr, USDA, 10300 Baltimore Ave,Bldg 307C,Room 132, Beltsville, MD 20705 USA.
EM tom.wang@ars.usda.gov
RI Davies, Neal/J-5811-2013
FU United States Department of Agriculture [1235-51530-052-00]; National
Cancer Institute; National Institute of Environmental Health Sciences
[P30ES007784]
FX USA appropriated funds to United States Department of Agriculture
project number 1235-51530-052-00 to T. T. Y. W., T.-C. W and B. V.;
National Cancer Institute to T. S. H., Y. S. K. and H. S.; National
Institute of Environmental Health Sciences to S. D. H. and S. N. P.
(P30ES007784).
NR 48
TC 47
Z9 51
U1 0
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD OCT
PY 2008
VL 29
IS 10
BP 2001
EP 2010
DI 10.1093/carcin/bgn131
PG 10
WC Oncology
SC Oncology
GA 356HD
UT WOS:000259768400021
PM 18586690
ER
PT J
AU Campa, F
Randazzo, PA
AF Campa, Fanny
Randazzo, Paul A.
TI Arf GTPase-activating proteins and their potential role in cell
migration and invasion
SO CELL ADHESION & MIGRATION
LA English
DT Article
DE Arf GAP; Arf; effector; ADP-ribosylation factor; GTPase-activating
protein; focal adhesions; podosomes; invadopodia; cell migration
AB Cell migration is central to normal physiology in embryogenesis, the inflammatory response and wound healing. In addition, the acquisition of a motile and invasive phenotype is an important step in the development of tumors and metastasis. Arf GTPase-activating proteins (GAPs) are nonredundant regulators of specialized membrane surfaces implicated in cell migration. Part of Arf GAP function is mediated by regulating the ADP ribosylation factor (Arf) family GTP-binding proteins. However, Arf GAPs can also function independently of their GAP enzymatic activity, in some cases working as Arf effectors. In this commentary, we discuss examples of Arf GAPs that function either as regulators of Arfs or independently of the GTPase activity to regulate membrane structures that mediate cell adhesion and movement.
C1 [Campa, Fanny; Randazzo, Paul A.] NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA.
RP Randazzo, PA (reprint author), NCI, Cellular & Mol Biol Lab, Bldg 37,Rm 2042B,37 Convent Dr, Bethesda, MD 20892 USA.
EM randazzp@mail.nih.gov
FU National Cancer Institute, National Institutes of Health, Department of
Health and Human Services, USA
FX This work was supported by the Intramural Program at the National Cancer
Institute, National Institutes of Health, Department of Health and Human
Services, USA.
NR 30
TC 3
Z9 5
U1 2
U2 4
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1933-6918
J9 CELL ADHES MIGR
JI Celll Adhes. Migr.
PD OCT-DEC
PY 2008
VL 2
IS 4
BP 258
EP 262
DI 10.4161/cam.2.4.6959
PG 5
WC Cell Biology
SC Cell Biology
GA V21VC
UT WOS:000208234100012
PM 19262159
ER
PT J
AU Fowler, BA
Conner, EA
Yamauchi, H
Wang, G
Whittaker, MH
AF Fowler, Bruce A.
Conner, E. A.
Yamauchi, H.
Wang, G.
Whittaker, M. H.
TI Proteomic and metabolomic biomarkers for assessing low dose toxic trace
element interactions: an overview
SO CELL BIOLOGY AND TOXICOLOGY
LA English
DT Article; Proceedings Paper
CT European-Tissue-Culture-Society Workshop
CY APR 19, 2007
CL Univ Coll London, London, ENGLAND
SP European Tissue Culture Soc
HO Univ Coll London
ID METHYL MERCURY EXPOSURE; III-V SEMICONDUCTORS; RAT-KIDNEY; LEAD;
ARSENATE; INDIUM; EXCRETION; CADMIUM; GALLIUM; METAL
C1 [Fowler, Bruce A.] ATSDR, Div Toxicol & Environm Med, Atlanta, GA USA.
[Conner, E. A.] NCI, Bethesda, MD 20892 USA.
[Yamauchi, H.] Kitasato Univ, Kanagawa, Japan.
[Wang, G.] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Whittaker, M. H.] Tox Serv, Washington, DC USA.
RP Fowler, BA (reprint author), ATSDR, Div Toxicol & Environm Med, Atlanta, GA USA.
EM bxf9@cdc.gov
NR 20
TC 0
Z9 0
U1 2
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0742-2091
J9 CELL BIOL TOXICOL
JI Cell Biol. Toxicol.
PD OCT
PY 2008
VL 24
IS 5
BP 440
EP 442
PG 3
WC Cell Biology; Toxicology
SC Cell Biology; Toxicology
GA 340OF
UT WOS:000258654200010
ER
PT J
AU Peng, YW
Chen, ZG
Yu, WH
Zhou, QF
Xu, L
Mao, FF
Huang, G
Zhang, XM
Li, SN
Lahn, BT
Xiang, AP
AF Peng, Yanwen
Chen, Zhenguang
Yu, Weihua
Zhou, Qifeng
Xu, Lin
Mao, Frank Fuxiang
Huang, Gang
Zhang, Xiuming
Li, Shunong
Lahn, Bruce T.
Xiang, Andy Peng
TI Effects of thymic polypeptides on the thymopoiesis of mouse embryonic
stem cells
SO CELL BIOLOGY INTERNATIONAL
LA English
DT Article
DE Embryonic stem (ES) cells; T cells; Thymopentin (TP5); Thymosin alpha-1
(T alpha-1); Thymopeptides
ID IN-VITRO; NOTCH
AB The thymus provides a unique cellular and hormonic microenvironment for the development of immunocompetent T cells. Thymic polypeptides have been widely used clinically for the treatment of tumors, infectious diseases and immune deficiency diseases. They have already shown the ability to stimulate the maturation of hematopoietic stem cells towards the CD3+CD4+ T cell lineage. However, their effects on the thymopoiesis of embryonic stem cells are still unexplored.
In this paper, we compared the effects of three thymic polypeptides, thymopentin (TP5), thymosin alpha-1 (T alpha-1) and thymopeptides on the in vitro thymopoiesis of mouse embryonic stem (ES) cells. Using the embryoid body induction system, we found that both T alpha-1 and thymopeptides effectively induced ES cells to differentiate sequentially into the CD3+ and CD4+/CD8+ T cells. These T cells had T cell receptor (TCR) V beta gene rearrangement and most were TCR alpha beta T cells. We also found that the expression of the Notch receptor and its ligands Delta-like-1 and Delta-like-4 gradually increased during the induction. However, TP5 failed to induce the T cell differentiation of the ES cells.
In summary, this is the first report to demonstrate that T alpha-1 can stimulate the T cell early stage differentiation from ES cells using the embryoid body protocol. These findings provide a powerful model for studying T cell development and may open new venues for the clinical application of T alpha-1. (c) 2008 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.
C1 [Peng, Yanwen; Yu, Weihua; Xu, Lin; Mao, Frank Fuxiang; Zhang, Xiuming; Li, Shunong; Lahn, Bruce T.; Xiang, Andy Peng] Sun Yat Sen Univ, Ctr Stem Cell Biol & Tissue Engn, Guangzhou 510080, Guangdong, Peoples R China.
[Peng, Yanwen; Xu, Lin] Sun Yat Sen Univ, Sch Preclin Med, Dept Immunol, Guangzhou 510080, Guangdong, Peoples R China.
[Zhou, Qifeng] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Chen, Zhenguang; Huang, Gang] Sun Yat Sen Univ, Affiliated Hosp 1, Guangzhou 510080, Guangdong, Peoples R China.
RP Xiang, AP (reprint author), Sun Yat Sen Univ, Ctr Stem Cell Biol & Tissue Engn, 74 Zhongshan Rd 2, Guangzhou 510080, Guangdong, Peoples R China.
EM xiangp@mail.sysu.edu.cn
FU Key Scientific and Technological Projects of Guangdong Province
[2007A032100003, 2005A30201001]; Natural Science Foundation of Guangdong
Province [4203002]; Key Scientific and Technological Projects of
Guangzhou City [2006Z2-E4071]
FX This work was supported by the Key Scientific and Technological Projects
of Guangdong Province (2007A032100003, 2005A30201001), Natural Science
Foundation of Guangdong Province (4203002), and the Key Scientific and
Technological Projects of Guangzhou City (2006Z2-E4071).
NR 22
TC 10
Z9 13
U1 0
U2 14
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 1065-6995
J9 CELL BIOL INT
JI Cell Biol. Int.
PD OCT
PY 2008
VL 32
IS 10
BP 1265
EP 1271
DI 10.1016/j.cellbi.2008.07.011
PG 7
WC Cell Biology
SC Cell Biology
GA 369CT
UT WOS:000260671800011
PM 18692582
ER
PT J
AU Baranovskiy, AG
Babayeva, ND
Liston, VG
Rogozin, IB
Koonin, EV
Pavlov, YI
Vassylyev, DG
Tahirov, TH
AF Baranovskiy, Andrey G.
Babayeva, Nigar D.
Liston, Victoria G.
Rogozin, Igor B.
Koonin, Eugene V.
Pavlov, Youri I.
Vassylyev, Dmitry G.
Tahirov, Tahir H.
TI X-ray structure of the complex of regulatory subunits of human DNA
polymerase delta
SO CELL CYCLE
LA English
DT Article
DE DNA polymerase delta; Pol delta; p50; p66; Pol31; Pol32; OB; Myb;
phosphodiesterase; human; yeast
ID REPLICATION PROTEIN-A; IN-VIVO; CATALYTIC SUBUNIT; REV1 PROTEIN;
POL-ETA; ROLES; DOMAINS; CDC27; EPSILON; BINDING
AB The eukaryotic DNA polymerase delta (Pol delta) participates in genome replication, homologous recombination, DNA repair and damage tolerance. Regulation of the plethora of Pol delta functions depends on the interaction between the second (p50) and third (p66) non-catalytic subunits. We report the crystal structure of p50.p66(N) complex featuring oligonucleotide binding and phosphodiesterase domains in p50 and winged helix-turn-helix N-terminal domain in p66. Disruption of the interaction between the yeast orthologs of p50 and p66 by strategic amino acid changes leads to cold-sensitivity, sensitivity to hydroxyurea and to reduced UV mutagenesis, mimicking the phenotypes of strains where the third subunit of Pol delta is absent. The second subunits of all B family replicative DNA polymerases in archaea and eukaryotes, except Pol delta, share a three-domain structure similar to p50.p66(N), raising the possibility that a portion of the gene encoding p66 was derived from the second subunit gene relatively late in evolution.
C1 [Baranovskiy, Andrey G.; Babayeva, Nigar D.; Liston, Victoria G.; Pavlov, Youri I.; Tahirov, Tahir H.] Univ Nebraska Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA.
[Rogozin, Igor B.; Koonin, Eugene V.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Vassylyev, Dmitry G.] Univ Alabama, Sch Med & Dent, Dept Biochem & Mol Genet, Birmingham, AL USA.
RP Tahirov, TH (reprint author), Univ Nebraska Med Ctr, Eppley Inst Res Canc & Allied Dis, 987696 Nebraska Med Ctr,668 S 41st St,Lied Transp, Omaha, NE 68198 USA.
EM ttahirov@unmc.edu
RI Vassylyev, Dmitry/A-9005-2008
FU Cancer Center [P30CA036727]; UNMC Eppley Cancer Center [LB595]; NE DHHS
[LB506]; NIH [GM74252, GM74840]; National Library of Medicine at
National Institutes of Health/DHHS
FX We thank P. V. Shcherbakova, D. Bugreev and E. I. Stepchenkova for
critical reading the manuscript, K. Spitler and E. I. Stepchenkova for
the construction of the pRS306-POL31C vector, D. Bugreev for discussion
of protein expression and purification approaches, J. Lovelace and G. E.
Borgstahl for the maintenance and management of the Eppley Institute's
X-ray Crystallography facility. The primers were synthesized in the
Eppley Institute's Molecular Biology Core facility. Both facilities are
supported by the Cancer Center Support Grant P30CA036727. This work is
funded in part by UNMC Eppley Cancer Center Pilot Projects LB595 to Y.
I. P. and T. H. T., in part by the 2008 NE DHHS grant LB506 to Y. I. P.,
and in part by the NIH grants GM74252 and GM74840 to D. G. V. I. B. R.
and E. V. K. were supported by the Intramural Research Program of the
National Library of Medicine at National Institutes of Health/DHHS.
NR 48
TC 39
Z9 41
U1 1
U2 4
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD OCT 1
PY 2008
VL 7
IS 19
BP 3026
EP 3036
DI 10.4161/cc.7.19.6720
PG 11
WC Cell Biology
SC Cell Biology
GA 363JG
UT WOS:000260263000016
PM 18818516
ER
PT J
AU Long, JM
Bell, CW
Fagg, WS
Kushman, ME
Becker, KG
McCubrey, JA
Farwell, MA
AF Long, Jacquelyn M.
Bell, Charles W.
Fagg, W. Samuel
Kushman, Mary E.
Becker, Kevin G.
McCubrey, James A.
Farwell, Mary A.
TI Microarray and pathway analysis reveals decreased CDC25A and increased
CDC42 associated with slow growth of BCL2 overexpressing immortalized
breast cell line
SO CELL CYCLE
LA English
DT Article
DE Bcl-2; MCF10A; colchicine; microarray; qRT-PCR; PAGE; IPA
ID GENE SET ENRICHMENT; CYCLE PROGRESSION; RHO-GTPASES; EPITHELIAL-CELLS;
EXPRESSION; CANCER; DEATH; APOPTOSIS; PROTEIN; INHIBITION
AB Bcl-2 is an anti-apoptotic protein that is frequently overexpressed in cancer cells but its role in carcinogenesis is not clear. We are interested in how Bcl-2 expression affects non-cancerous breast cells and its role in the cell cycle. We prepared an MCF10A breast epithelial cell line that stably overexpressed Bcl-2. We analyzed the cells by flow cytometry after synchronization, and used cDNA microarrays with quantitative reverse-transcription PCR (qRT-PCR) to determine differences in gene expression. The microarray data was subjected to two pathway analysis tools, parametric analysis of gene set enrichment (PAGE) and ingenuity pathway analysis (IPA), and western analysis was carried out to determine the correlation between mRNA and protein levels. The MCF10A/Bcl-2 cells exhibited a slow-growth phenotype compared to control MCF10A/Neo cells that we attributed to a slowing of the G(1)-S cell cycle transition. A total of 363 genes were differentially expressed by at least two-fold, 307 upregulated and 56 downregulated. PAGE identified 22 significantly changed gene sets. The highest ranked network of genes identified by IPA contained 24 genes. Genes that were chosen for further analysis were confirmed by qRT-PCR, however, the western analysis did not always confirm differential expression of the proteins. Downregulation of the phosphatase CDC25A could solely be responsible for the slow growth phenotype in MCF10A/Bcl-2 cells. Increased levels of GTPase Cdc42 could be adding to this effect. PAGE and IPA are valuable tools for microarray analysis, but protein expression results do not always follow mRNA expression results.
C1 [Long, Jacquelyn M.; Bell, Charles W.; Fagg, W. Samuel; Farwell, Mary A.] E Carolina Univ, Dept Biol, Greenville, NC 27858 USA.
[Kushman, Mary E.] Univ Penn, Dept Pharmacol, Philadelphia, PA 19104 USA.
[Kushman, Mary E.] Ctr Excellence Environm Toxicol, Philadelphia, PA USA.
[Becker, Kevin G.] NIA, NIH, Gene Express & Genom Unit, Res Resources Branch, Baltimore, MD 21224 USA.
[McCubrey, James A.] E Carolina Univ, Brody Sch Med, Dept Microbiol & Immunol, Greenville, NC USA.
RP Farwell, MA (reprint author), E Carolina Univ, Dept Biol, Greenville, NC 27858 USA.
EM farwellm@ecu.edu
OI Becker, Kevin/0000-0002-6794-6656; McCubrey, James/0000-0001-6027-3156
FU NIH; National Institute on Aging; National Cancer Institute
[1R15CA87810-01, R01CA098195]; Developmental Studies Hybdridoma Band
FX The authors would like to thank Megan Hadden for help with the
microarray hybridization and Matthew M. Smith for technical assistance.
This research was supported in part by the Intramural Research Program
of the NIH, National Institute on Aging, and in part by grants from the
National Cancer Institute (1R15CA87810-01) to MAF and (R01CA098195) to
JAM. The TGF beta 3 and Fn1 antibodies developed by Raymond Runyan and
Robert J. Klebe, respectively, were obtained from the Developmental
Studies Hybdridoma Band developed under the auspices of the NICHD and
maintained by The University of Iowa, Department of Biological Sciences,
Iowa City, IA 52242.
NR 73
TC 3
Z9 3
U1 0
U2 3
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD OCT 1
PY 2008
VL 7
IS 19
BP 3062
EP 3073
DI 10.4161/cc.7.19.6761
PG 12
WC Cell Biology
SC Cell Biology
GA 363JG
UT WOS:000260263000020
PM 18838868
ER
PT J
AU BoseDasgupta, S
Das, BB
Sengupta, S
Ganguly, A
Roy, A
Dey, S
Tripathi, G
Dinda, B
Majumder, HK
AF BoseDasgupta, S.
Das, B. B.
Sengupta, S.
Ganguly, A.
Roy, A.
Dey, S.
Tripathi, G.
Dinda, B.
Majumder, H. K.
TI The caspase-independent algorithm of programmed cell death in Leishmania
induced by baicalein: the role of LdEndoG, LdFEN-1 and LdTatD as a DNA
'degradesome'
SO CELL DEATH AND DIFFERENTIATION
LA English
DT Article
DE Leishmania; baicalein; topoisomerase IB; caspase-independent; LdEndoG
ID ENDONUCLEASE-G; APOPTOTIC NUCLEASES; OXIDATIVE STRESS; TOPOISOMERASE-I;
CYCLOPHILIN-A; DONOVANI; FRAGMENTATION; CAMPTOTHECIN; MITOCHONDRIA;
DEGRADATION
AB In the post-genomic perspective, the quest of programmed cell death (PCD) mechanisms in kinetoplastid parasites lies in the identification and characterization of cell death executer proteins. Here, we show that baicalein (BLN), a potent topoisomerase IB inhibitor, generates an oxidative stress in the parasites leading to altered physiological and morphological parameters, which are characteristic of PCD. For the first time we elucidate that, caspase-independent activation of a novel effector molecule, endonuclease G (LdEndoG), mediates BLN-induced cell death. Functional characterization of LdEndoG identifies Flap endonuclease-1 (LdFEN-1) and LdTatD-like nuclease as other effector molecules. BLN treatment translocates LdEndoG from mitochondria to nucleus, where it forms separate complexes with LdFEN-1 and LdTatD to constitute a DNA 'degradesome' unique to these parasites. Conditional antisense knockdown of LdEndoG provides protection against PCD. This knowledge paves the path toward a better understanding of the PCD pathway in simpler systems, which could be exploited in anti-leishmanial chemotherapy.
C1 [BoseDasgupta, S.; Sengupta, S.; Ganguly, A.; Roy, A.; Majumder, H. K.] Indian Inst Chem Biol, Mol Parasitol Lab, Infect Dis & Immunol Div, Kolkata 700032, W Bengal, India.
[Das, B. B.] NCI, Ctr Canc Res, Mol Pharmacol Lab, Bethesda, MD 20892 USA.
[Dey, S.] Indian Inst Chem Biol, Elect Microscopy Div, Kolkata, India.
[Tripathi, G.] Indian Inst Chem Biol, Div Cellular Physiol, Kolkata, India.
[Dinda, B.] Tripura Univ, Dept Chem, Suryamaninagar, Tripura, India.
RP Majumder, HK (reprint author), Indian Inst Chem Biol, Mol Parasitol Lab, Infect Dis & Immunol Div, 4 Raja SC Mullick Rd, Kolkata 700032, W Bengal, India.
EM hkmajumder@iicb.res.in
FU Department of Biotechnology, Government of India
[BT/PR6399/BRB/10/434/05]; CSIR, Government of India
FX We are grateful to Professor S Roy, Director, IICB, for his interest in
this work. We thank Professor GAM Cross for gifting the Leismania
transfection vectors. We thank Arunima Biswas for her help in flow
cytometry. This study was supported by the grant from Department of
Biotechnology, Government of India (BT/PR6399/BRB/10/434/05) to HKM. SBD
was supported by a Senior Research Fellowship from CSIR, Government of
India.
NR 34
TC 29
Z9 30
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1350-9047
EI 1476-5403
J9 CELL DEATH DIFFER
JI Cell Death Differ.
PD OCT
PY 2008
VL 15
IS 10
BP 1629
EP 1640
DI 10.1038/cdd.2008.85
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 348OF
UT WOS:000259219100010
PM 18566607
ER
PT J
AU Garg, H
Blumenthal, R
AF Garg, H.
Blumenthal, R.
TI Role of HIV Gp41 mediated fusion/hemifusion in bystander apoptosis
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Review
DE HIV-1; Env; pathogenesis; fusion; hemifusion; apoptosis; gp41; CD4 cells
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TYPE-1 ENVELOPE GLYCOPROTEIN; T-CELL
DEPLETION; HUMAN LYMPHOID-TISSUE; ENFUVIRTIDE RESISTANCE MUTATIONS;
ACTIVE ANTIRETROVIRAL THERAPY; CHEMOKINE RECEPTOR CXCR4; INFECTION
IN-VITRO; ZIPPER-LIKE DOMAIN; SCID-HU MICE
AB Mechanisms of HIV-mediated CD4+ T cell loss leading to immunodeficiency are amongst the most extensively studied yet unanswered questions in HIV biology. The level of CD4+ T cell depletion in HIV infected patients far exceeds the number of infected T cells, suggesting an indirect mechanism of HIV pathogenesis termed bystander cell death. Evidence is accumulating that the HIV envelope glycoprotein (Env) is a major determinant of HIV pathogenesis and plays a critical role in bystander cell death. The complex structure and function of HIV Env makes the determination of the mechanism of Env-mediated apoptosis more complex than previously thought. This review will examine the complex relationship between HIV Env phenotype, coreceptor expression and immune activation in determining HIV pathogenesis. We review data here corresponding to the role of HIV Env hemifusion activity in HIV pathogenesis and how it interplays with other AIDS associated factors such as chemokine receptor expression and immune activation.
C1 [Garg, H.; Blumenthal, R.] NCI, Membrane Struct & Funct Sect, Ctr Canc Res, Nanobiol Program,Natl Inst Hlth, Frederick, MD 21702 USA.
RP Blumenthal, R (reprint author), NCI, Membrane Struct & Funct Sect, Ctr Canc Res, Nanobiol Program,Natl Inst Hlth, POB B,Bldg 469,Room 152,Miller Dr, Frederick, MD 21702 USA.
EM blumenthalr@mail.nih.gov
FU Intramural Research Program of the NIH; National Cancer Institute;
Center for Cancer Research
FX This research was supported, in part, by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research.
NR 125
TC 27
Z9 27
U1 0
U2 4
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1420-682X
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD OCT
PY 2008
VL 65
IS 20
BP 3134
EP 3144
DI 10.1007/s00018-008-8147-6
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 360UO
UT WOS:000260083600003
PM 18500445
ER
PT J
AU Bavelier, D
Newman, AJ
Mukherjee, M
Hauser, P
Kemeny, S
Braun, A
Boutla, M
AF Bavelier, D.
Newman, A. J.
Mukherjee, M.
Hauser, P.
Kemeny, S.
Braun, A.
Boutla, M.
TI Encoding, rehearsal, and recall in signers and speakers: Shared network
but differential engagement
SO CEREBRAL CORTEX
LA English
DT Article
DE American Sign Language; deafness; fMRI; short-term memory
ID SHORT-TERM-MEMORY; VERBAL WORKING-MEMORY; EVENT-RELATED FMRI; DEAF
SIGNERS; PARIETAL CORTEX; FUNCTIONAL MRI; SERIAL-RECALL; LANGUAGE;
SPEECH; MAINTENANCE
AB Short-term memory (STM), or the ability to hold verbal information in mind for a few seconds, is known to rely on the integrity of a frontoparietal network of areas. Here, we used functional magnetic resonance imaging to ask whether a similar network is engaged when verbal information is conveyed through a visuospatial language, American Sign Language, rather than speech. Deaf native signers and hearing native English speakers performed a verbal recall task, where they had to first encode a list of letters in memory, maintain it for a few seconds, and finally recall it in the order presented. The frontoparietal network described to mediate STM in speakers was also observed in signers, with its recruitment appearing independent of the modality of the language. This finding supports the view that signed and spoken STM rely on similar mechanisms. However, deaf signers and hearing speakers differentially engaged key structures of the frontoparietal network as the stages of STM unfold. In particular, deaf signers relied to a greater extent than hearing speakers on passive memory storage areas during encoding and maintenance, but on executive process areas during recall. This work opens new avenues for understanding similarities and differences in STM performance in signers and speakers.
C1 [Bavelier, D.; Mukherjee, M.; Boutla, M.] Univ Rochester, Brain & Cognit Sci Dept, Rochester, NY 14627 USA.
[Bavelier, D.; Mukherjee, M.; Boutla, M.] Univ Rochester, Rochester Ctr Brain Imaging, Rochester, NY 14627 USA.
[Newman, A. J.] Dalhousie Univ, Halifax, NS B3H 4J1, Canada.
[Hauser, P.] Natl Tech Inst Deaf, Dept Res & Teacher Educ, Rochester, NY 14623 USA.
[Kemeny, S.; Braun, A.] Natl Inst Deafness & Commun Disorder, Bethesda, MD 20892 USA.
RP Bavelier, D (reprint author), Univ Rochester, Brain & Cognit Sci Dept, RC Box 270268, Rochester, NY 14627 USA.
EM daphne@bcs.rochester.edu
OI Bavelier, Daphne/0000-0002-5904-1240
FU National Institutes of Health [DC04418]; The James S. McDonnell
Foundation; Canadian Institutes of Health Research
FX This research was supported by the National Institutes of Health
(DC04418 to D. B.); The James S. McDonnell Foundation (to D. B.); the
Canadian Institutes of Health Research (to A. N.).
NR 63
TC 18
Z9 18
U1 2
U2 7
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
J9 CEREB CORTEX
JI Cereb. Cortex
PD OCT
PY 2008
VL 18
IS 10
BP 2263
EP 2274
DI 10.1093/cercor/bhm248
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 350BF
UT WOS:000259326700004
PM 18245041
ER
PT J
AU Sarpal, D
Buchsbaum, BR
Kohn, PD
Kippenhan, JS
Mervis, CB
Morris, CA
Meyer-Lindenberg, A
Berman, KF
AF Sarpal, Deepak
Buchsbaum, Bradley R.
Kohn, Philip D.
Kippenhan, J. Shane
Mervis, Carolyn B.
Morris, Colleen A.
Meyer-Lindenberg, Andreas
Berman, Karen Faith
TI A genetic model for understanding higher order visual processing:
Functional interactions of the ventral visual stream in Williams
syndrome
SO CEREBRAL CORTEX
LA English
DT Article
DE amygdala; fMRI; functional connectivity; fusiform gyrus; intraparietal
sulcus; parahippocampal gyrus
ID FUSIFORM FACE AREA; PARAHIPPOCAMPAL PLACE AREA; SURFACE-BASED ANALYSIS;
CORTICAL SURFACE; VISUOSPATIAL CONSTRUCTION; COGNITIVE NEUROSCIENCE;
COORDINATE SYSTEM; SPATIAL DEFICITS; NEURAL BASIS; BRAIN
AB Williams syndrome (WS) is a rare neurodevelopmental disorder caused by a 1.6 Mb microdeletion on chromosome 7q11.23 and characterized by hypersocial personality and prominent visuospatial construction impairments. Previous WS studies have identified functional and structural abnormalities in the hippocampal formation, prefrontal regions crucial for amygdala regulation and social cognition, and the dorsal visual stream, notably the intraparietal sulcus (IPS). Although aberrant ventral stream activation has not been found in WS, object-related visual information that is processed in the ventral stream is a critical source of input into these abnormal regions. The present study, therefore, examined neural interactions of ventral stream areas in WS. Using a passive face- and house-viewing paradigm, activation and functional connectivity of stimulus-selective regions in fusiform and parahippocampal gyri, respectively, were investigated. During house viewing, significant activation differences were observed between participants with WS and a matched control group in IPS. Abnormal functional connectivity was found between parahippocampal gyrus and parietal cortex and between fusiform gyrus and a network of brain regions including amygdala and portions of prefrontal cortex. These results indicate that abnormal upstream visual object processing may contribute to the complex cognitive/behavioral phenotype in WS and provide a systems-level characterization of genetically mediated abnormalities of neural interactions.
C1 [Sarpal, Deepak; Buchsbaum, Bradley R.; Kohn, Philip D.; Kippenhan, J. Shane; Meyer-Lindenberg, Andreas; Berman, Karen Faith] NIMH, Sect Integrat Neuroimaging, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program,NIH,DHHS, Bethesda, MD 20892 USA.
[Mervis, Carolyn B.] Univ Louisville, Dept Psychol & Brain Sci, Neurodev Sci Lab, Louisville, KY 40292 USA.
[Morris, Colleen A.] Univ Nevada, Sch Med, Dept Pediat, Reno, NV 89102 USA.
[Meyer-Lindenberg, Andreas] NIMH, Unit Syst Neurosci Psychiat, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program,NIH,DHHS, Bethesda, MD 20892 USA.
RP Berman, KF (reprint author), 10-4C101,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM karen.berman@nih.gov
RI Sarpal, Deepak/O-5630-2014; Meyer-Lindenberg, Andreas/H-1076-2011
OI Meyer-Lindenberg, Andreas/0000-0001-5619-1123
FU National Institute of Mental Health Intramural Research Program;
National Institute of Neurological Disorders and Stroke [NS35102]
FX National Institute of Mental Health Intramural Research Program;
National Institute of Neurological Disorders and Stroke (NS35102 to C.
B. M.).
NR 57
TC 25
Z9 26
U1 1
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
EI 1460-2199
J9 CEREB CORTEX
JI Cereb. Cortex
PD OCT
PY 2008
VL 18
IS 10
BP 2402
EP 2409
DI 10.1093/cercor/bhn004
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 350BF
UT WOS:000259326700018
PM 18308711
ER
PT J
AU Dietz, BM
Liu, DT
Hagos, GK
Yao, P
Schinkovitz, A
Pro, SM
Deng, SX
Farnsworth, NR
Pauli, GF
van Breemen, RB
Bolton, JL
AF Dietz, Birgit M.
Liu, Dongting
Hagos, Ghenet K.
Yao, Ping
Schinkovitz, Andreas
Pro, Samuel M.
Deng, Shixin
Farnsworth, Norman R.
Pauli, Guido F.
van Breemen, Richard B.
Bolton, Judy L.
TI Angelica sinensis and Its Alkylphthalides Induce the Detoxification
Enzyme NAD(P)H: Quinone Oxidoreductase 1 by Alkylating Keap1
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Article
ID ANTIOXIDANT RESPONSIVE ELEMENT; TRANSCRIPTION FACTOR NRF2; PERFORMANCE
LIQUID-CHROMATOGRAPHY; CANCER CHEMOPREVENTIVE ACTIVITY; UMBELLIFEROUS
MEDICINAL-PLANTS; BROCCOLI SPROUT EXTRACTS; Z-LIGUSTILIDE;
HYDROGEN-PEROXIDE; MASS-SPECTROMETRY; OXIDATIVE STRESS
AB The roots of Angelica sinensis (Oliv.) Diels (Dang Gui; Apiaceae) have a long history in traditional Chinese medicine as a remedy for women's disorders and are often called "lady's ginseng". Currently, extracts of A. sinensis are commonly included in numerous dietary supplements used for women's health and as antiaging products. In the present study, we examined the potential chemopreventive activity of A. sinensis extracts by measuring the relative ability to induce the detoxification enzyme, NAD(P)H:quinone oxidoreductase 1 (NQO1). The lipophilic partitions showed strong NQO1 induction with concentrations to double the enzyme activity (CD) of 5.5 +/- 0.7 (petroleum ether) and 3.9 +/- 0.5 mu g/mL (chloroform). Fractionation led to the isolation of phenolic esters and alkylphthalides, especially Z-ligustilide, the main lipophilic compound, which showed strong NQO1 inducing properties (CD = 6.9 +/- 1.9 mu M). Transcription of many detoxifying enzymes is regulated through the antioxidant response element (ARE) and its transcription factor Nrf2, which is repressed under basal conditions by Keap1. However, exposure to electrophilic inducers that alkylate Keap1 results in higher concentrations of free Nrf2 and ARE activation. The ARE reporter activity was therefore analyzed in HepG2-ARE-C8 cells after incubation with lipophilic extracts of A. sinensis or ligustilide for 24 h. Under these conditions, both the extract and the ligustilide increased ARE-luciferase reporter activity in a dose-dependent manner. Incubation of ligustilide with GSH and subsequent LC-MS-MS analysis revealed that ligustilide as well as oxidized ligustilide species covalently modified GSH. In addition, using MALDI-TOF mass spectrometry and LC-MS-MS, it was demonstrated that the lipophilic extracts, ligustilide, and monooxygenated. ligustilide alkylated important cysteine residues in human Keap1 protein, thus activating Nrf2 and transcription of ARE regulated genes. These observations suggest that A. sinensis dietary supplements standardized to ligustilide have potential as chemopreventive agents through induction of detoxification enzymes.
C1 [Pro, Samuel M.] Univ Illinois, Inst TB Res, Chicago, IL 60612 USA.
[Dietz, Birgit M.; Liu, Dongting; Hagos, Ghenet K.; Yao, Ping; Schinkovitz, Andreas; Deng, Shixin; Farnsworth, Norman R.; Pauli, Guido F.; van Breemen, Richard B.; Bolton, Judy L.] Univ Illinois, Dept Med Chem & Pharmacognosy, NIH, Ctr Bot Dietary Supplements Res, Chicago, IL 60612 USA.
RP Dietz, BM (reprint author), Univ Illinois, Dept Med Chem & Pharmacognosy, NIH, Ctr Bot Dietary Supplements Res, 833 S Wood St,M-C 781, Chicago, IL 60612 USA.
EM birgitd@uic.edu
RI Zhu, Likun/D-5333-2009;
OI Deng, Shixin/0000-0002-3947-7629; Pauli, Guido/0000-0003-1022-4326
FU Searle Funds at The Chicago Community Trust; NIH [P50 AT00155]; National
Center for Complementary and Alternative Medicine
FX e thank Dr. J. P. Whitlock, Jr. (Stanford University, Stanford, CA) for
providing the Hepa1c1c7 cells and Drs. Tan Kong, C. Chen (Rutgers
University, Piscataway, NJ), and W. E. Fahl (University of
Wisconsin-Madison, Madison, WI) for kindly supplying the HepG2-ARE-C8
cells. We are also grateful to Drs. A. L. Eggler, A. D. Mesecar, and D.
Lankin (UIC, Chicago, IL) for kindly providing the Keap1 protein and
helpful discussions, respectively, and to the Chicago Biomedical
Consortium for access to the LTQ-FT ICR mass spectrometer, which was
purchased with a grant from The Searle Funds at The Chicago Community
Trust. This study was funded by NIH Grant P50 AT00155 jointly provided
to the UIC/NIH Center for Botanical Dietary Supplements Research by the
Office of Dietary Supplements and the National Center for Complementary
and Alternative Medicine. Its contents are solely the responsibility of
the authors and do not necessarily represent the official views of the
National Center for Complementary and Alternative Medicine, the Office
of Dietary Supplements, or the National Institutes of Health.
NR 85
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PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0893-228X
J9 CHEM RES TOXICOL
JI Chem. Res. Toxicol.
PD OCT
PY 2008
VL 21
IS 10
BP 1939
EP 1948
DI 10.1021/tx8001274
PG 10
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA 361SV
UT WOS:000260148300009
PM 18808158
ER
PT J
AU Bagley, J
Belluscio, L
AF Bagley, Joshua
Belluscio, Leonardo
TI Molecular Guidance of Newborn RMS Neurons from the Subventricular Zone
to the Olfactory Bulb
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Bagley, Joshua; Belluscio, Leonardo] NINDS, Dev Neural Plast Unit, NIH, Bethesda, MD 20892 USA.
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PD OCT
PY 2008
VL 33
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GA 359GE
UT WOS:000259973600519
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PT J
AU Bath, KG
Carim-Todd, L
Tessarollo, L
Lee, FS
AF Bath, Kevin G.
Carim-Todd, Laura
Tessarollo, Lino
Lee, Francis S.
TI Genetic Ablation of Atruncated TRKB Isoform (TRKB.T1) Increases Adult
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SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Bath, Kevin G.; Lee, Francis S.] Weill Cornell Med Coll, New York, NY USA.
[Carim-Todd, Laura; Tessarollo, Lino] Natl Canc Inst, Gene Targeting Facil, Frederick, MD USA.
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PD OCT
PY 2008
VL 33
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GA 359GE
UT WOS:000259973600464
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PT J
AU Chen, WG
AF Chen, Wen G.
TI A Systems Approach to Studying the Chemosenses and Aging: Moving from
Populations to Mechanisms
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Chen, Wen G.] Natl Inst Aging, Bethesda, MD USA.
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PD OCT
PY 2008
VL 33
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GA 359GE
UT WOS:000259973600064
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PT J
AU Cummings, DM
Belluscio, L
AF Cummings, Diana M.
Belluscio, Leonardo
TI The Recovery of the Intrabulbar Map Following Unilateral Naris Closure
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Cummings, Diana M.; Belluscio, Leonardo] NINDS, Dev Neural Plast Unit, NIH, Bethesda, MD 20892 USA.
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PD OCT
PY 2008
VL 33
IS 8
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SC Behavioral Sciences; Food Science & Technology; Neurosciences &
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GA 359GE
UT WOS:000259973600592
ER
PT J
AU Davis, B
AF Davis, Barry
TI Special NIDCD Workshop: Ligand-Binding Properties of Taste and Smell
Receptors
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Davis, Barry] NIDCD, Taste & Smell Program, Bethesda, MD USA.
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GA 359GE
UT WOS:000259973600028
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PT J
AU Dotson, CD
Vigues, S
Shin, YK
Ott, SH
Elson, AET
Choi, HJ
Shaw, H
Egan, JM
Mitchell, BD
Steinle, NI
Munger, SD
AF Dotson, Cedrick D.
Vigues, Stephan
Shin, Yu-Kyong
Ott, Sandra H.
Elson, Amanda E. T.
Choi, Hyun Jin
Shaw, Hillary
Egan, Josephine M.
Mitchell, Braxton D.
Steinle, Nanette I.
Munger, Steven D.
TI A TAS2R9 Variant is Associated with Dysglycemia in Humans
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Dotson, Cedrick D.; Vigues, Stephan; Elson, Amanda E. T.; Choi, Hyun Jin; Munger, Steven D.] Univ Maryland, Dept Anat & Neurobiol, Baltimore, MD 21201 USA.
[Shin, Yu-Kyong; Egan, Josephine M.] NIA, NIH, Baltimore, MD 21224 USA.
[Ott, Sandra H.; Mitchell, Braxton D.; Steinle, Nanette I.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
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GA 359GE
UT WOS:000259973600162
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PT J
AU Fushan, A
Slack, J
Simons, C
Manichaikul, A
Drayna, D
AF Fushan, Alexey
Slack, Jay
Simons, Chris
Manichaikul, Ani
Drayna, Dennis
TI Allelic Variations Upstream of the T1R3 Gene Correlate with Sucrose
Sensitivities in Humans
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Fushan, Alexey; Manichaikul, Ani; Drayna, Dennis] NIDCD, Rockville, MD USA.
[Slack, Jay; Simons, Chris] Givaudan Flavors Corp, Cincinnati, OH USA.
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J9 CHEM SENSES
JI Chem. Senses
PD OCT
PY 2008
VL 33
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BP S146
EP S146
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SC Behavioral Sciences; Food Science & Technology; Neurosciences &
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GA 359GE
UT WOS:000259973600561
ER
PT J
AU Fushan, A
McKluskey, S
Simons, C
Slack, J
Drayna, D
AF Fushan, Alexey
McKluskey, Scott
Simons, Chris
Slack, Jay
Drayna, Dennis
TI Genetic Dissection of Human Taste Perception
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Fushan, Alexey; Drayna, Dennis] NIDCD, NIH, Rockville, MD USA.
[McKluskey, Scott; Simons, Chris; Slack, Jay] Givaudan Flavors Corp, Cincinnati, OH USA.
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J9 CHEM SENSES
JI Chem. Senses
PD OCT
PY 2008
VL 33
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BP S13
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WC Behavioral Sciences; Food Science & Technology; Neurosciences;
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SC Behavioral Sciences; Food Science & Technology; Neurosciences &
Neurology; Physiology
GA 359GE
UT WOS:000259973600054
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PT J
AU Hoffman, HJ
Davis, B
AF Hoffman, Howard J.
Davis, Barry
TI Perspectives on Future Community-Based or Nationally-Representative
Epidemiological Research Studies of Olfactory and Taste Impairment
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Hoffman, Howard J.; Davis, Barry] NIDCD, NIH, Bethesda, MD USA.
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PU OXFORD UNIV PRESS
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J9 CHEM SENSES
JI Chem. Senses
PD OCT
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VL 33
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BP S37
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SC Behavioral Sciences; Food Science & Technology; Neurosciences &
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GA 359GE
UT WOS:000259973600151
ER
PT J
AU Hoffman, HJ
Cruickshanks, KJ
Davis, B
AF Hoffman, Howard J.
Cruickshanks, Karen J.
Davis, Barry
TI Symposium on Epidemiological Studies of Taste and Smell
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Hoffman, Howard J.] NIDCD, Epidemiol & Biostat Program, DSP, NIH, Bethesda, MD USA.
[Davis, Barry] NIDCD, Taste & Smell Program, DSP, NIH, Bethesda, MD USA.
[Cruickshanks, Karen J.] Univ Wisconsin, Madison, WI 53706 USA.
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J9 CHEM SENSES
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PD OCT
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VL 33
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SC Behavioral Sciences; Food Science & Technology; Neurosciences &
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GA 359GE
UT WOS:000259973600143
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PT J
AU Ito, I
Ong, RC
Raman, B
Stopfer, M
AF Ito, Iori
Ong, Rose C.
Raman, Baranidharan
Stopfer, Mark
TI Sparse Odor Representation in the Mushroom Body and Associative Learning
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Ito, Iori; Ong, Rose C.; Raman, Baranidharan; Stopfer, Mark] NICHD, NIH, Bethesda, MD USA.
[Ong, Rose C.] Chinese Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China.
[Raman, Baranidharan] NIST, Gaithersburg, MD 20899 USA.
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GA 359GE
UT WOS:000259973600313
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PT J
AU McEwen, DP
Khanna, H
Swaroop, A
Martens, JR
AF McEwen, Dyke P.
Khanna, Hemant
Swaroop, Anand
Martens, Jeffrey R.
TI A Role for Retinitis Pigmentosa GTPase Regulator (RPGR) in Olfactory
Sensory Neurons
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [McEwen, Dyke P.; Martens, Jeffrey R.] Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48109 USA.
[Khanna, Hemant] Univ Michigan, Dept Ophthalmol, Ann Arbor, MI 48109 USA.
[Swaroop, Anand] NEI, NIH, Bethesda, MD 20892 USA.
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PT J
AU Nelson, TM
Lopezjimenez, ND
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Inoue, M
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Sullivan, SL
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Lopezjimenez, Nelson D.
Tessarollo, Lino
Inoue, Masashi
McCaughey, Stuart A.
Bachmanov, Alexander A.
Sullivan, Susan L.
TI Taste Function in pkd1l3 Knockout Mice
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Nelson, Theodore M.; McCaughey, Stuart A.; Bachmanov, Alexander A.] Monell Chem Senses Ctr, Philadelphia, PA 19104 USA.
[Lopezjimenez, Nelson D.; Sullivan, Susan L.] Natl Inst Deafness & Other Commun Disorders, Mol Biol Lab, NIH, Rockville, MD USA.
[Tessarollo, Lino] NCI, Mouse Canc Genet Program, Neural Dev Grp, Frederick, MD 21701 USA.
[Inoue, Masashi] Tokyo Univ Pharm & Life Sci, Dept Life Sci, Lab Cellular Neurobiol, Tokyo, Japan.
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PT J
AU Nguyen, M
Ryba, N
AF Nguyen, Minh
Ryba, Nick
TI Odorant Receptor Mis-Expression Alters Organization and Function of the
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LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Nguyen, Minh; Ryba, Nick] NIDCR, NIH, Bethesda, MD USA.
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GA 359GE
UT WOS:000259973600200
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PT J
AU Shin, YK
Martin, B
Golden, E
Dotson, CD
Maudsley, S
Kim, W
Jang, HJ
Mattson, MP
Drucker, DJ
Egan, JM
Munger, SD
AF Shin, Yu-Kyong
Martin, Bronwen
Golden, Erin
Dotson, Cedrick D.
Maudsley, Stuart
Kim, Wook
Jang, Hyeung-Jin
Mattson, Mark P.
Drucker, Daniel J.
Egan, Josephine M.
Munger, Steven D.
TI Modulation of Taste Sensitivity by GLP-1 Signaling in Taste Buds
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Shin, Yu-Kyong; Martin, Bronwen; Golden, Erin; Maudsley, Stuart; Kim, Wook; Jang, Hyeung-Jin; Mattson, Mark P.; Egan, Josephine M.] NIA, NIH, Baltimore, MD 21224 USA.
[Dotson, Cedrick D.; Munger, Steven D.] Univ Maryland, Sch Med, Dept Anat & Neurobiol, Baltimore, MD 21201 USA.
[Drucker, Daniel J.] Univ Toronto, Banting & Best Diabet Ctr, Toronto, ON M5G 1L5, Canada.
RI Mattson, Mark/F-6038-2012; jang, hyeung jin/C-8022-2013
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GA 359GE
UT WOS:000259973600567
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PT J
AU Slack, JP
McCluskey, TS
Simons, CT
Fushan, A
Drayna, D
AF Slack, Jay P.
McCluskey, T. Scott
Simons, Christopher T.
Fushan, Alex
Drayna, Dennis
TI Functional Analysis of Naturally Occurring Human Sweet Receptor Variants
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Slack, Jay P.; McCluskey, T. Scott; Simons, Christopher T.] Givaudan Flavors Corp, Cincinnati, OH USA.
[Fushan, Alex; Drayna, Dennis] NIDCD, Rockville, MD USA.
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GA 359GE
UT WOS:000259973600562
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PT J
AU Zhou, ZS
Belluscio, L
AF Zhou, Zhishang
Belluscio, Leonardo
TI Intrabulbar Projection Neurons Modulate Olfactory Bulb Output
SO CHEMICAL SENSES
LA English
DT Meeting Abstract
CT 15th International Symposium on Olfaction and Taste
CY JUL 21-26, 2008
CL San Francisco, CA
C1 [Zhou, Zhishang; Belluscio, Leonardo] NINDS, NIH, Bethesda, MD 20892 USA.
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VL 33
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GA 359GE
UT WOS:000259973600263
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PT J
AU Sengupta, K
Camps, J
Mathews, P
Barenboim-Stapleton, L
Nguyen, QT
Difilippantonio, MJ
Ried, T
AF Sengupta, Kundan
Camps, Jordi
Mathews, Priya
Barenboim-Stapleton, Linda
Nguyen, Quang Tri
Difilippantonio, Michael J.
Ried, Thomas
TI Position of human chromosomes is conserved in mouse nuclei indicating a
species-independent mechanism for maintaining genome organization
SO CHROMOSOMA
LA English
DT Article
ID ORDER CHROMATIN ARRANGEMENTS; GENE-EXPRESSION; CELL-NUCLEI; TERRITORY
ARRANGEMENTS; ARCHITECTURE; DENSITY; LOCALIZATION; CONSTRUCTION;
FIBROBLASTS; PRIMATES
AB The nonrandom positioning of chromosome territories in eukaryotic cells is largely correlated with gene density and is conserved throughout evolution. Gene-rich chromosomes are predominantly central, while gene-poor chromosomes are peripherally localized in interphase nuclei. We previously demonstrated that artificially introduced human chromosomes assume a position equivalent to their endogenous homologues in the diploid colon cancer cell line DLD-1. These chromosomal aneuploidies result in a significant increase in transcript levels, suggesting a relationship between genomic copy number, gene expression, and chromosome position. We previously proposed that each chromosome is marked by a "zip code" that determines its nonrandom position in the nucleus. In this paper, we investigated (1) whether mouse nuclei recognize such determinants of nuclear position on human chromosomes to facilitate their distinct partitioning and (2) if chromosome positioning and transcriptional activity remain coupled under these trans-species conditions. Using three-dimensional fluorescence in situ hybridization, confocal microscopy, and gene expression profiling, we show (1) that gene-poor and gene-rich human chromosomes maintain their divergent but conserved positions in mouse-human hybrid nuclei and (2) that a foreign human chromosome is actively transcribed in mouse nuclei. Our results suggest a species-independent conserved mechanism for the nonrandom positioning of chromosomes in the three-dimensional interphase nucleus.
C1 [Sengupta, Kundan; Camps, Jordi; Mathews, Priya; Barenboim-Stapleton, Linda; Nguyen, Quang Tri; Difilippantonio, Michael J.; Ried, Thomas] NCI, Sect Canc Genom, Genet Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Ried, T (reprint author), NCI, Sect Canc Genom, Genet Branch, Ctr Canc Res,NIH, 50 S Dr,Rm 1408, Bethesda, MD 20892 USA.
EM riedt@mail.nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research
FX We thank Stephen Wincovitch and Amalia Dutra (NHGRI/NIH) for use of the
confocal microscope and for valuable discussions. We thank Media
Cybernetics for help with 3D measurements and Buddy Chen, Tom Ellerman,
and Joseph Cheng for IT support. We are grateful to Sudhir Varma, NCI,
for critical comments and useful discussions on the manuscript. Hesed
Padilla-Nash kindly provided the chromosome arm-specific painting
probes. This research was supported in part by the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research.
NR 30
TC 9
Z9 9
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0009-5915
J9 CHROMOSOMA
JI Chromosoma
PD OCT
PY 2008
VL 117
IS 5
BP 499
EP 509
DI 10.1007/s00412-008-0171-7
PG 11
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 346KJ
UT WOS:000259067100008
PM 18563425
ER
PT J
AU O'Donnell, CJ
Nabel, EG
AF O'Donnell, Christopher J.
Nabel, Elizabeth G.
TI Cardiovascular Genomics, Personalized Medicine, and the National Heart,
Lung, and Blood Institute Part I: The Beginning of an Era
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE genetics; genomic studies
C1 [O'Donnell, Christopher J.] NHLBI, Ctr Populat Studies, Div Intramural Res, Bethesda, MD 20892 USA.
[O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Bethesda, MD 20892 USA.
[O'Donnell, Christopher J.; Nabel, Elizabeth G.] NHLBI, Off Director, Bethesda, MD 20892 USA.
RP O'Donnell, CJ (reprint author), NHLBI, Ctr Populat Studies, Div Intramural Res, 71 Mt Wayte Ave,2, Framingham, MA 01702 USA.
EM codonnell@nih.gov
FU Intramural NIH HHS [Z99 HL999999]
NR 42
TC 22
Z9 22
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1942-325X
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD OCT
PY 2008
VL 1
IS 1
BP 51
EP 57
DI 10.1161/CIRCGENETICS.108.813337
PG 7
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA V11AF
UT WOS:000207503800009
PM 20031542
ER
PT J
AU Scherer, E
Douek, D
McMichael, A
AF Scherer, E.
Douek, D.
McMichael, A.
TI 25 years of HIV research on virology, virus restriction,
immunopathogenesis, genes and vaccines
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Review
DE HIV; immunopathogenesis; meeting; restriction; vaccine
ID HUMAN-IMMUNODEFICIENCY-VIRUS; DEFICIENCY SYNDROME AIDS; T-CELL
DEPLETION; NEUTRALIZING ANTIBODIES; GASTROINTESTINAL-TRACT; VAGINAL
TRANSMISSION; MALE CIRCUMCISION; LEUKEMIA-VIRUS; REPLICATION; INFECTION
AB From 19 to 21 May 2008 an important meeting was held at the Pasteur Institute in Paris to mark the 25th Anniversary of the discovery of HIV as the aetiological agent of AIDS. This review summarizes the historical findings, recent work and future directions presented at this meeting.
C1 [Scherer, E.; McMichael, A.] Univ Oxford, Weatherall Inst Mol Med, Oxford, England.
[Douek, D.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Scherer, E (reprint author), John Radcliffe Hosp, MRC Human Immunol Unit, Weatherall Inst Mol Med, Oxford OX3 9DS, England.
EM erin.scherer@bioch.ox.ac.uk
NR 38
TC 9
Z9 10
U1 2
U2 9
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD OCT
PY 2008
VL 154
IS 1
BP 6
EP 14
DI 10.1111/j.1365-2249.2008.03750.x
PG 9
WC Immunology
SC Immunology
GA 346RL
UT WOS:000259086800002
PM 18761662
ER
PT J
AU Shott, JP
Iga, B
Makumbi, F
Luswata, C
Kagulire, C
Nammanda, J
Mills, LA
Serwadda, D
Quinn, TC
Reynolds, SJ
AF Shott, Joseph P.
Iga, Boaz
Makumbi, Fredrick
Luswata, Charles
Kagulire, Charles
Nammanda, Josephine
Mills, Lisa A.
Serwadda, David
Quinn, Thomas C.
Reynolds, Steven J.
TI CD4 stabilization tubes provide improved accuracy of absolute CD4 T-cell
counts compared to standard K-3 EDTA tubes in human immunodeficiency
virus immunologic monitoring in resource-poor settings
SO CLINICAL AND VACCINE IMMUNOLOGY
LA English
DT Article
AB CD4 stabilization tubes have the ability to ensure internal quality control in the human immunodeficiency virus (HIV) monitoring laboratory by maintaining accurate absolute CD4 T-cell counts for up to 6 days. Here, we assessed this technology for its use in an HIV clinical monitoring laboratory in a resource-poor setting in rural Uganda.
C1 [Shott, Joseph P.] SAIC Frederick Inc, NIAID, NIH, Rakai Hlth Sci Program, Kalisizo, Uganda.
[Shott, Joseph P.] NCI, SAIC Frederick,Inc, Clin Monitoring Res Program, Ft Detrick, MD 21702 USA.
[Shott, Joseph P.; Quinn, Thomas C.; Reynolds, Steven J.] NIAID, NIH, Bethesda, MD 20892 USA.
[Mills, Lisa A.; Quinn, Thomas C.; Reynolds, Steven J.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Makumbi, Fredrick; Serwadda, David] Makerere Univ, Sch Publ Hlth, Kampala, Uganda.
RP Shott, JP (reprint author), SAIC Frederick Inc, NIAID, NIH, Rakai Hlth Sci Program, POB 279, Kalisizo, Uganda.
EM ShottJ@mail.nih.gov
FU National Cancer Institute; National Institutes of Health [N01-CO-12400];
National Institute of Allergy and Infectious Diseases; Becton Dickinson
- East Africa
FX This project has been funded in part with federal funds from the
National Cancer Institute, National Institutes of Health, under contract
N01-CO-12400. This research was supported in part by the National
Institute of Allergy and Infectious Diseases and in part by Becton
Dickinson - East Africa. J. P. S. is employed by SAIC-Frederick, Inc.;
B. I., F. M., C. K., J. N., and C. L. are employed by the Rakai Health
Sciences Program; D. S. is employed by Makerere University; L. A. M. is
employed by Johns Hopkins Medical Institutions; and T. C. Q. and S. J.
R. are employed by the National Institutes of Allergy and Infectious
Diseases, NIH.; The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does the mention of trade names, commercial products, or
organizations imply endorsement by the U. S. government.; We thank Sarah
Kalibbala, Annet Christine Namuli, Gerald Makori, Betty Nyagah, John
Baptist Bwanika, and Noah Kiwanuka for helpful discussions and the
volunteers of the Rakai community cohort for their participation.
NR 1
TC 5
Z9 5
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1556-6811
J9 CLIN VACCINE IMMUNOL
JI Clin. Vaccine Immunol.
PD OCT
PY 2008
VL 15
IS 10
BP 1623
EP 1624
DI 10.1128/CVI.00176-08
PG 2
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 357BQ
UT WOS:000259821700018
PM 18753336
ER
PT J
AU Chau, CH
Rixe, O
McLeod, H
Figg, WD
AF Chau, Cindy H.
Rixe, Olivier
McLeod, Howard
Figg, William D.
TI Validation of Analytic Methods for Biomarkers Used in Drug Development
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID GASTROINTESTINAL STROMAL TUMORS; METASTATIC BREAST-CANCER; CHRONIC
MYELOID-LEUKEMIA; SURROGATE END-POINTS; BIOANALYTICAL METHOD VALIDATION;
MONOCLONAL-ANTIBODY; COLORECTAL-CANCER; IMATINIB; MUTATIONS; EFFICACY
AB The role of biomarkers in drug discovery and development has gained precedence over the years. As biomarkers become integrated into drug development and clinical trials, quality assurance and, in particular, assay validation become essential with the need to establish standardized guidelines for analytic methods used in biomarker measurements. New biomarkers can revolutionize both the development and use of therapeutics but are contingent on the establishment of a concrete validation process that addresses technology integration and method validation as well as regulatory pathways for efficient biomarker development. This perspective focuses on the general principles of the biomarker validation process with an emphasis on assay validation and the collaborative efforts undertaken by various sectors to promote the standardization of this procedure for efficient biomarker development.
C1 [McLeod, Howard] Univ N Carolina, Inst Pharmacogen & Individualized Therapy, Chapel Hill, NC 27599 USA.
[Chau, Cindy H.; Rixe, Olivier; Figg, William D.] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP McLeod, H (reprint author), Univ N Carolina, Inst Pharmacogen & Individualized Therapy, Campus Box 7360,3203 Kerr Hall, Chapel Hill, NC 27599 USA.
EM hmcleod@unc.edu; wdfigg@helix.nih.gov
RI Figg Sr, William/M-2411-2016
FU NIGMS NIH HHS [U01 GM063340, U01 GM063340-07]
NR 52
TC 100
Z9 101
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD OCT 1
PY 2008
VL 14
IS 19
BP 5967
EP 5976
DI 10.1158/1078-0432.CCR-07-4535
PG 10
WC Oncology
SC Oncology
GA 361QP
UT WOS:000260142500007
PM 18829475
ER
PT J
AU Simon, R
AF Simon, Richard
TI The Use of Genomics in Clinical Trial Design
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CELL LUNG-CANCER; GENE-EXPRESSION PROFILES; METASTATIC BREAST-CANCER;
DNA MICROARRAY DATA; TUMOR-MARKERS; AMERICAN-SOCIETY; MUTATIONS;
GEFITINIB; RECOMMENDATIONS; ONCOLOGY
AB Many cancer treatments benefit only a minority of patients who receive them. This results in an enormous burden on patients and on the health care system. The problem will become even greater with the increasing use of molecularly targeted agents whose benefits are likely to be more selective unless the drug development process is modified to include codevelopment of companion diagnostics. Whole genome biotechnology and decreasing costs of genome sequencing make it increasingly possible to achieve an era of predictive medicine in oncology therapeutics. The challenges are numerous and substantial but are not primarily technological. They involve organizing publicly funded diagnostics of deregulated pathways, adopting new paradigms for drug development, and developing incentives for industry to incur the complexity and expense of codevelopment of drugs and companion diagnostics. This article reviews some designs for phase III clinical trials that may facilitate movement to a more predictive oncology.
C1 NCI, Biometr Res Branch, Bethesda, MD 20892 USA.
RP Simon, R (reprint author), NCI, Biometr Res Branch, 9000 Rockville Pike,MSC 7434, Bethesda, MD 20892 USA.
EM rsimon@nih.gov
NR 58
TC 102
Z9 103
U1 3
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD OCT 1
PY 2008
VL 14
IS 19
BP 5984
EP 5993
DI 10.1158/1078-0432.CCR-07-4531
PG 10
WC Oncology
SC Oncology
GA 361QP
UT WOS:000260142500009
PM 18829477
ER
PT J
AU Sharifi, N
Hurt, EM
Thomas, SB
Farrar, WL
AF Sharifi, Nima
Hurt, Elaine M.
Thomas, Suneetha B.
Farrar, William L.
TI Effects of Manganese Superoxide Dismutase Silencing on Androgen Receptor
Function and Gene Regulation: Implications for Castration-Resistant
Prostate Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID TRANSCRIPTION FACTORS; SOLUBLE RECEPTOR; GROWTH-FACTOR; EXPRESSION;
CELLS; INTERLEUKIN-6; TESTOSTERONE; THERAPY; OVEREXPRESSION; SUPPRESSION
AB Purpose: Advanced prostate cancer is first treated with androgen deprivation therapy. However, tumors become resistant to and grow despite castrate levels of testosterone. Growth and proliferation of CRPC is mediated by gain-of-function changes in the AR and AR reactivation. Expression of manganese superoxide dismutase (SOD2), which regulates cellular ROS, is markedly down-regulated in CRPC when compared with hormone-responsive tumors.
Experimental Design: Here, we knocked down SOD2 expression in AR-expressing LNCaP prostate cancer cells and determined gene expression changes, transcription factor binding, and AR transcription activity in SOD2 knockdown cells.
Results: SOD2 knockdown results in an increase in ROS. Gene expression changes induced by SOD2 knockdown results in the up-regulation of genes that are also androgen responsive and 46% of genes up-regulated 2-fold by the androgen ligand R1881 are also up-regulated to the same extent with SOD2 knockdown. The induction of many of these genes with SOD2 knockdown, such as VEGFA and FKBP5, is reversible with the antioxidant N-acetylcysteine, suggesting that this mechanism is directly linked to ROS. Furthermore, an array for transcription factor DNA-binding activity shows that SOD2 knockdown induces DNA binding by several transcription factors, including AR. SOD2 knockdown-induced AR activation was confirmed by electrophoretic mobility shift assay and luciferase activity, and both were readily reversible with N-acetylcysteine.
Conclusions: These findings show that down-regulation of SOD2 induces AR activity in a ROS-dependent manner, and suggest that there may be a role for antioxidant therapy in CRPC.
C1 [Sharifi, Nima] Univ Texas SW Med Ctr Dallas, Div Hematol Oncol, Dallas, TX 75390 USA.
[Sharifi, Nima; Hurt, Elaine M.; Farrar, William L.] NCI, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res, Frederick, MD 21701 USA.
[Thomas, Suneetha B.] NCI, Basic Res Program, Sci Applicat Int Corp Frederick Inc, Frederick, MD 21701 USA.
RP Sharifi, N (reprint author), Univ Texas SW Med Ctr Dallas, Div Hematol Oncol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM nima.sharifi@utsouthwestern.edu
FU National Cancer Institute; NIH; N01-CO-12400
FX This publication has been funded in part with Federal funds from the
National Cancer Institute, NIH, under contract no. N01-CO-12400. This
research was supported in part by the Intramural Research Program of the
NIH, National Cancer Institute.
NR 37
TC 27
Z9 27
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD OCT 1
PY 2008
VL 14
IS 19
BP 6073
EP 6080
DI 10.1158/1078-0432.CCR-08-0591
PG 8
WC Oncology
SC Oncology
GA 361QP
UT WOS:000260142500018
PM 18829485
ER
PT J
AU Hortin, GL
Sviridov, D
Anderson, NL
AF Hortin, Glen L.
Sviridov, Denis
Anderson, N. Leigh
TI High-abundance polypeptides of the human plasma proteome comprising the
top 4 logs of polypeptide abundance
SO CLINICAL CHEMISTRY
LA English
DT Review
ID INDUSTRIAL-SCALE PROTEOMICS; HUMAN SERUM PROTEOME; MASS-SPECTROMETRY;
PROTEINS; CHROMATOGRAPHY; SEPARATION; DEPLETION; STANDARDIZATION;
QUANTIFICATION; DISEASE
AB CONTENT: We surveyed proteomic studies to identify candidates for high-abundance polypeptide chains. We searched the literature for information on the plasma concentrations of the most abundant components in healthy adults and for the molecular mass of the mature polypeptide chains in plasma. Because proteomic studies usually dissociate proteins into polypeptide chains or detect short peptide segments of proteins, we summarized data on individual peptide chains for proteins containing multiple subunits or polypeptides. We collected data on about 150 of the most abundant polypeptides in plasma. The abundant polypeptides span approximately the top 4 logs of concentration in plasma, from 650 to 0.06 mu mol/L on a molar basis or from about 50 000 to 1 mg/L mass abundance.
CONCLUSIONS: Data on the concentrations of the high-abundance peptide chains in plasma assist in understanding the composition of plasma and potential approaches for clinical laboratory or proteomic analysis of plasma proteins. Development of more extensive databases regarding the plasma concentrations of proteins in health and diseases would promote diagnostic and proteomic advances. (c) 2008 American Association for Clinical Chemistry.
C1 [Hortin, Glen L.; Sviridov, Denis] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Anderson, N. Leigh] Plasma Proteome Inst, Washington, DC USA.
RP Hortin, GL (reprint author), NIH, Dept Lab Med, Ctr Clin, Bldg 10,Room 2C-407,10 Ctr Dr, Bethesda, MD 20892 USA.
EM ghortin@mail.cc.nih.gov
FU NIH Clinical Center; Department of Health and Human Services; National
Cancer Institute's Clinical Proteomic Technology Assess for Cancer
Program [U24-CA126476]
FX Glen L Hortin, NIH Clinical Center, Department of Health and Human
Services; Leigh Anderson, National Cancer Institute's Clinical Proteomic
Technology Assess for Cancer Program (grant U24-CA126476).
NR 39
TC 134
Z9 137
U1 0
U2 12
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD OCT
PY 2008
VL 54
IS 10
BP 1608
EP 1616
DI 10.1373/clinchem.2008.108175
PG 9
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 358TH
UT WOS:000259939900006
PM 18687737
ER
PT J
AU Harris, KM
Lenz, P
Hankey, KG
MacVittie, T
Farese, A
Nakajima, K
Hasumi, K
Mann, DL
AF Harris, Kristina M.
Lenz, Petra
Hankey, Kim G.
MacVittie, Thomas
Farese, Ann
Nakajima, Kaori
Hasumi, Kenichiro
Mann, Dean L.
TI Products of anti-CD3/anti-CD28 activated lymphocytes induce
differentiation and maturation of dendritic cells and have adjuvant-like
activity in vitro and in vivo
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE dendritic cells; differentiation; conditioned medium; maturation; T cell
stimulation; CD3/CD28; vaccine adjuvant
ID MONOCYTE-CONDITIONED MEDIUM; T-CELLS; BLOOD MONOCYTES; CYTOKINES;
SUBSETS; ANTIGEN; MATURE; INTERFERON; CAPACITY; CPG
AB Dendritic cells (DC) orchestrate immune responses under direction of cytokines/ chemokines in their microenvironment. To investigate the influence of that generated during T cell activation, we stimulated peripheral blood mononuclear cells (PBMC) with anti-CD3 and anti-CD28 coated beads and tested cell-free culture supernatants (lymphocyte conditioned medium, LCM) for cytokine/chemokine composition and biologic activity. LCM contained a battery of mediators important in the biology of myeloid (mDC) and plasmacytoid (pDC) DC. LCM differentiated monocytes into functional immature mDC, and induced maturation of immature mDC. LCM also augmented maturation and IFN alpha-production of CpG-treated pDC. Functional activity of LCM-derived DC was confirmed by their ability to enhance in vitro recall T cell responses and substantially augment in vivo cellular and humoral immune responses to various vaccines in non-human primates. These results demonstrate that products of anti-CD3/anti-CD28 stimulated PBMC generate biologically active DC in vitro and function as a vaccine adjuvant in vivo. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Harris, Kristina M.; Hankey, Kim G.; Mann, Dean L.] Univ Maryland, Dept Pathol, Baltimore, MD 21201 USA.
[MacVittie, Thomas; Farese, Ann] Univ Maryland, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Lenz, Petra] NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA.
[Nakajima, Kaori; Hasumi, Kenichiro] Hasumi Int Res Fdn, Tokyo, Japan.
RP Mann, DL (reprint author), Room 700,10 S Pine St, Baltimore, MD 21201 USA.
EM dmann001@umaryland.edu
NR 44
TC 5
Z9 6
U1 0
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD OCT
PY 2008
VL 129
IS 1
BP 58
EP 68
DI 10.1016/j.clim.2008.06.003
PG 11
WC Immunology
SC Immunology
GA 351XM
UT WOS:000259459200009
PM 18691939
ER
PT J
AU Boasso, A
Hardy, AW
Landay, AL
Martinson, JL
Anderson, SA
Dolan, MJ
Clerici, M
Shearer, GM
AF Boasso, Adriano
Hardy, Andrew W.
Landay, Alan L.
Martinson, Jeffrey L.
Anderson, Stephanie A.
Dolan, Matthew J.
Clerici, Mario
Shearer, Gene M.
TI PDL-1 upregulation on monocytes and T cells by HIV via type I
interferon: Restricted expression of type I interferon receptor by
CCR5-expressing leukocytes
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE HIV-1; PDL-1; IFN-alpha; CCR5; T lymphocytes; monocytes; plasmacytoid
dendritic cells; antigen -presenting cells; proliferation
ID HUMAN-IMMUNODEFICIENCY-VIRUS; PLASMACYTOID DENDRITIC CELLS; CHRONIC
HEPATITIS-B; INFECTED INDIVIDUALS; LYMPHOID-TISSUE;
GASTROINTESTINAL-TRACT; VIRAL REPLICATION; SIV INFECTION; IFN-ALPHA;
ACTIVATION
AB The programmed death (PD)-1 interacts with its ligand (PDL-1) delivering a negative signal to T cells. During human immunodeficiency virus (HIV)-1 infection PD-1 and PDL-1 expressions are increased. Here we show that monocytes and CCR5(+) T cells of HIV-uninfected donors upregulated PDL-1 upon in vitro exposure to HIV. HIV-induced PDL-1 required interferon (IFN)-alpha, but not IFN-gamma, production. Inhibition of endocytosis, required for HIV-induced IFN-alpha production, prevented PDL-1 upregulation. IFN-alpha-inducing Toll-like receptor (TLR) agonists increased PDL-1 on monocytes and CCR5(+) T cells. CD80 and CD86 were also increased on monocytes and CCR5+ T cells after HIV exposure, but only CD80 was IFN-alpha-dependent. IFN-alpha-receptor subunit 2 (IFNAR2), was expressed only by CCR5(+) T cells and monocytes, explaining why these leukocytes responded to HIV-induced IFN-a. Finally, T cell proliferation was improved by PDL-1 blockade in HIV-treated PBMC. In the setting of HIV infection, IFN-a may negatively affect T cell responses by inducing PDL-1. K) 2008 (C) Elsevier Inc. All rights reserved.
C1 [Boasso, Adriano; Hardy, Andrew W.; Shearer, Gene M.] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Landay, Alan L.; Martinson, Jeffrey L.] Rush Univ, Med Ctr, Dept Immunol Microbiol, Chicago, IL 60612 USA.
[Anderson, Stephanie A.] Wilford Hall USAF Med Ctr, Infect Dis Clin Res Program, Henry M Jackson Fdn, Lackland AFB, TX 78236 USA.
[Dolan, Matthew J.] SAMMC, Infect Dis Clin Res Program, Henry M Jackson Fdn, Ft Sam Houston, TX 78234 USA.
[Clerici, Mario] Univ Milan, Dept Biomed Sci & Technol, I-20122 Milan, Italy.
[Clerici, Mario] Don C Gnocchi Fdn IRCCS, Lab Mol Med & Biotechnol, Milan, Italy.
RP Boasso, A (reprint author), Univ London Imperial Coll Sci Technol & Med, Chelsea & Westminster Hosp, Fac Med, Dept Immunol, 369 Fulham Rd, London SW10 9NH, England.
EM a.boasso@imperial.ac.uk
OI Clerici, Mario/0000-0001-5920-6191; Boasso, Adriano/0000-0001-9673-6319
FU Intramural research Program of the CCR, NO; Intramural AIDS Targeted
Antiviral Program (IATAP)
FX This research was supported by the Intramural research Program of the
CCR, NO and by the Intramural AIDS Targeted Antiviral Program (IATAP).
We thank Dr. Jeffrey D. Lifson (AVP, NCI-Frederick, SAIC, Frederick, MD)
for the kind gift of AT-2-treated and non-AT-2 treated HIV.
NR 59
TC 42
Z9 46
U1 0
U2 9
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD OCT
PY 2008
VL 129
IS 1
BP 132
EP 144
DI 10.1016/j.clim.2008.05.009
PG 13
WC Immunology
SC Immunology
GA 351XM
UT WOS:000259459200016
PM 18650129
ER
PT J
AU Yancey, MA
AF Yancey, Mary Ann
TI Oncology Drug Development: What Is Changing?
SO CLINICAL JOURNAL OF ONCOLOGY NURSING
LA English
DT Article
C1 NCI, Bethesda, MD 20892 USA.
RP Yancey, MA (reprint author), NCI, Bethesda, MD 20892 USA.
EM yanceym@mail.nih
NR 11
TC 0
Z9 0
U1 0
U2 1
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 1092-1095
J9 CLIN J ONCOL NURS
JI Clin. J. Oncol. Nurs.
PD OCT
PY 2008
VL 12
IS 5
BP 713
EP 715
DI 10.1188/08.CJON.713-715
PG 3
WC Oncology; Nursing
SC Oncology; Nursing
GA 358XX
UT WOS:000259951900005
PM 18842527
ER
PT J
AU Silva, S
Basser, PJ
Miranda, PC
AF Silva, S.
Basser, P. J.
Miranda, P. C.
TI Elucidating the mechanisms and loci of neuronal excitation by
transcranial magnetic stimulation using a finite element model of a
cortical sulcus
SO CLINICAL NEUROPHYSIOLOGY
LA English
DT Article
DE Transcranial magnetic stimulation; TMS; Model; FEM; Heterogeneity;
Neuronal stimulation; Threshold; Activating function
ID HUMAN MOTOR CORTEX; ELECTROMAGNETIC INDUCTION; ELECTRICAL-STIMULATION;
TISSUE HETEROGENEITY; MYELINATED FIBERS; NERVE-STIMULATION; VOLUME
CONDUCTOR; CEREBRAL-CORTEX; BRAIN; THRESHOLD
AB Objective: This work aims to elucidate by what physical mechanisms and where stimulation occurs in the brain during transcranial magnetic stimulation (TMS), taking into account cortical geometry and tissue heterogeneity.
Methods: An idealized Computer model of TMS was developed, comprising a stimulation coil, a cortical sulcus, and surrounding tissues. The distribution of the induced electric field was computed, and estimates of the relevant parameters were generated to predict the locus and type of neurons stimulated during TMS, assuming three different stimulation mechanisms.
Results: Tissue heterogeneity strongly affects the spatial distribution of the induced electric field and hence which stimulation mechanism is dominant and where it acts. Stimulation of neurons may occur in the gyrus, in the lip of the gyrus, and in the walls of the sulcus. The stimulated cells can be either pyramidal cells having medium to large caliber axons, or intracortical fibers of medium caliber.
Conclusions: The results highlight the influence of cortical folding on the action of magnetic and electric fields on cortical tissue.
Significance: Tissue geometry and heterogeneity in electrical conductivity both must be taken into account to predict accurately stimulation loci and mechanism in TMS. (C) 2008 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
C1 [Silva, S.; Miranda, P. C.] Univ Lisbon, Fac Sci, Dept Phys, Inst Biophys & Biomed Engn, P-1749016 Lisbon, Portugal.
[Basser, P. J.] NIH, NICHD, Sect Tissue Biophys & Biomimet, Bethesda, MD 20892 USA.
RP Silva, S (reprint author), Univ Lisbon, Fac Sci, Dept Phys, Inst Biophys & Biomed Engn, P-1749016 Lisbon, Portugal.
EM ssilva@fc.ul.pt
RI Miranda, Pedro/A-5643-2013; Basser, Peter/H-5477-2011
OI Miranda, Pedro/0000-0002-6793-8111;
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; NIH; Foundation for Science and Technology (FCT); FCT
[SFRH/BD/13815/2003]
FX This work was supported in part by the Intramural Research Program of
the Eunice Kennedy Shriver National Institute of Child Health and Human
Development, NIH and by the Foundation for Science and Technology (FCT),
Portugal. S. Silva was supported by the FCT, under Grant number
SFRH/BD/13815/2003.
NR 43
TC 44
Z9 44
U1 0
U2 13
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 1388-2457
J9 CLIN NEUROPHYSIOL
JI Clin. Neurophysiol.
PD OCT
PY 2008
VL 119
IS 10
BP 2405
EP 2413
DI 10.1016/j.clinph.2008.07.248
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 373LW
UT WOS:000260974400036
PM 18783986
ER
PT J
AU McLennan, G
Clarke, L
Hohl, RJ
AF McLennan, G.
Clarke, L.
Hohl, R. J.
TI Imaging as a biomarker for therapy response: Cancer as a prototype for
the creation of research resources
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Editorial Material
C1 [McLennan, G.] Univ Iowa, Dept Internal Med, Div Pulm & Crit Care, Iowa City, IA 52242 USA.
[Clarke, L.] Natl Canc Inst, Canc Imaging Program, Bethesda, MD USA.
[Hohl, R. J.] Univ Iowa, Div Hematol Oncol & Blood & Marrow Transplantat, Iowa City, IA 52242 USA.
[Hohl, R. J.] Univ Iowa, Div Clin Pharmacol, Dept Internal Med, Iowa City, IA 52242 USA.
[Hohl, R. J.] Univ Iowa, Dept Pharmacol, Iowa City, IA 52242 USA.
RP McLennan, G (reprint author), Univ Iowa, Dept Internal Med, Div Pulm & Crit Care, Iowa City, IA 52242 USA.
EM geoffrey-mclennan@uiowa.edu
NR 13
TC 10
Z9 10
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0009-9236
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD OCT
PY 2008
VL 84
IS 4
BP 433
EP 436
DI 10.1038/clpt.2008.171
PG 4
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 351CS
UT WOS:000259402700001
PM 18802422
ER
PT J
AU Armato, SG
Meyer, CR
McNitt-Gray, MF
McLennan, G
Reeves, AP
Croft, BY
Clarke, LP
AF Armato, S. G., III
Meyer, C. R.
McNitt-Gray, M. F.
McLennan, G.
Reeves, A. P.
Croft, B. Y.
Clarke, L. P.
CA RIDER Res Grp
TI The Reference Image Database to Evaluate Response to therapy in lung
cancer (RIDER) project: A resource for the development of
change-analysis software
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
ID CONSORTIUM LIDC; SOLID TUMORS; SCREENING-PROGRAM; NEW-YORK; CT;
VARIABILITY; ANNOTATION
AB Critical to the clinical evaluation of effective novel therapies for lung cancer is the early and accurate determination of tumor response, which requires an understanding of the sources of uncertainty in tumor measurement and subsequent attempts to minimize their effects on the assessment of the therapeutic agent. The Reference Image Database to Evaluate Response (RIDER) project seeks to develop a consensus approach to the optimization and benchmarking of software tools for the assessment of tumor response to therapy and to provide a publicly available database of serial images acquired during lung cancer drug and radiation therapy trials. Images of phantoms and patient images acquired under situations in which tumor size or biology is known to be unchanged also will be provided. The RIDER project will create standardized methods for benchmarking software tools to reduce sources of uncertainty in vital clinical assessments such as whether a specific tumor is responding to therapy.
C1 [Armato, S. G., III] Univ Chicago, Dept Radiol, Chicago, IL 60637 USA.
[Meyer, C. R.] Univ Michigan, Dept Radiol, Ann Arbor, MI 48109 USA.
[McNitt-Gray, M. F.] Univ Calif Los Angeles, Dept Radiol Sci, Los Angeles, CA 90024 USA.
[McLennan, G.] Univ Iowa, Dept Med, Iowa City, IA 52242 USA.
Univ Iowa, Dept Radiol, Iowa City, IA 52242 USA.
[McLennan, G.] Univ Iowa, Dept Biomed Engn, Iowa City, IA 52242 USA.
[Reeves, A. P.] Cornell Univ, Dept Elect & Comp Engn, Ithaca, NY USA.
[Croft, B. Y.; Clarke, L. P.] Natl Canc Inst, Canc Imaging Program, Bethesda, MD USA.
RP Armato, SG (reprint author), Univ Chicago, Dept Radiol, Chicago, IL 60637 USA.
EM s-armato@uchicago.edu
RI Croft, Barbara/D-1248-2013;
OI Croft, Barbara/0000-0003-2544-150X; Kinahan, Paul/0000-0001-6461-3306;
Bidaut, Luc/0000-0001-8253-2606; Munden, Reginald/0000-0003-3836-5067;
Jackson, Edward/0000-0002-5958-0076; Aberle, Denise/0000-0002-8858-3401;
McNItt-Gray, Michael/0000-0003-3004-4613
FU NCI NIH HHS [U01 CA091090, U01 CA091103]
NR 21
TC 28
Z9 28
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0009-9236
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD OCT
PY 2008
VL 84
IS 4
BP 448
EP 456
DI 10.1038/clpt.2008.161
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 351CS
UT WOS:000259402700009
PM 18754000
ER
PT J
AU Petrick, N
Brown, DG
Suleiman, O
Myers, KJ
AF Petrick, N.
Brown, D. G.
Suleiman, O.
Myers, K. J.
TI Imaging as a tumor biomarker in oncology drug trials for lung cancer:
The FDA perspective
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID CRITICAL PATH; DISCOVERY
AB The US Food and Drug Administration (FDA) is committed to working with the oncology community to expedite the drug evaluation process in view of the many promising new oncology drugs under laboratory development and the time and expense required for such new drugs to reach the patient population. One significant advance would be to enable quantitative imaging as a tumor biomarker. The FDA is working with the pharmaceutical industry, academia, and sister stakeholders in the government, primarily through collaborative educational and research efforts, to identify how imaging can serve this function.
C1 [Petrick, N.; Brown, D. G.; Myers, K. J.] US FDA, Natl Inst Biomed Imaging & Bioengn, Ctr Devices & Radiol Hlth, Lab Assessment Med Imaging Syst, Silver Spring, MD USA.
[Suleiman, O.] US FDA, Off Oncol Drug Prod, Off New Drugs, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
RP Petrick, N (reprint author), US FDA, Natl Inst Biomed Imaging & Bioengn, Ctr Devices & Radiol Hlth, Lab Assessment Med Imaging Syst, Silver Spring, MD USA.
EM nicholas.petrick@fda.hhs.gov
FU National Institute of Biomedical Imaging and Bioengineering; National
Institute of Biomedical Imaging and Bioengineering/Center for Devices
and Radiological Health Laboratory; National Cancer Institute
[224-07-6030]
FX The intramural research program of the National Institute of Biomedical
Imaging and Bioengineering provides partial support for research
conducted in the National Institute of Biomedical Imaging and
Bioengineering/Center for Devices and Radiological Health Laboratory for
the Assessment of Medical Imaging Systems. This work was supported in
part by the National Cancer Institute through IAG no. 224-07-6030.
NR 9
TC 10
Z9 10
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0009-9236
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD OCT
PY 2008
VL 84
IS 4
BP 523
EP 525
DI 10.1038/clpt.2008.155
PG 3
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 351CS
UT WOS:000259402700020
PM 18716616
ER
PT J
AU Figg, WD
AF Figg, W. D.
TI The Pharm.D. Investigator in clinical pharmacology: Supply and demand
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID EDUCATION
AB The field of clinical pharmacology is the discipline engaged in optimal drug discovery, development, and use, based on an in-depth knowledge of human pharmacology and therapeutics. 1 Although many think clinical pharmacology is simply the study of pharmacokinetics, pharmacodynamics, and pharmacogenetics, the role of the clinical pharmacologists covers all avenues of drug discovery, development, therapeutics, optimal drug therapy, and education. 2 This expanded understanding is important as we start to address the overwhelming mandate and the unfortunate shortage of qualified investigators in the field (both physicians and non-physicians).
C1 NCI, NIH, Ctr Canc Res, Med Oncol Branch, Bethesda, MD 20892 USA.
RP Figg, WD (reprint author), NCI, NIH, Ctr Canc Res, Med Oncol Branch, Bethesda, MD 20892 USA.
EM wdfigg@helix.nih.gov
RI Figg Sr, William/M-2411-2016
NR 6
TC 5
Z9 6
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0009-9236
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD OCT
PY 2008
VL 84
IS 4
BP 526
EP 529
DI 10.1038/sj.clpt.6100423
PG 4
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 351CS
UT WOS:000259402700021
PM 19238658
ER
PT J
AU Marini, AM
Popolo, M
Pan, H
Blondeau, N
Lipsky, RH
AF Marini, Ann M.
Popolo, Margherita
Pan, Hongna
Blondeau, Nicolas
Lipsky, Robert H.
TI Brain Adaptation to Stressful Stimuli: A New Perspective on Potential
Therapeutic Approaches Based on BDNF and NMDA Receptors
SO CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS
LA English
DT Review
DE Stress; stroke; brain preconditioning; brain tolerance; NMDA receptors;
BDNF; TrkB receptors; NF-kappa B
ID METHYL-D-ASPARTATE; FOCAL CEREBRAL-ISCHEMIA; CORTICAL SPREADING
DEPRESSION; NERVE GROWTH-FACTOR; FACTOR MESSENGER-RNA; SENSITIVE
POTASSIUM CHANNELS; OXYGEN-GLUCOSE DEPRIVATION;
CUZN-SUPEROXIDE-DISMUTASE; REDUCES INFARCT SIZE; NEUROTROPHIC FACTOR
AB A variety of sublethal or stressful stimuli induce a phenomenon in the brain known as tolerance, an adaptive response that protects the brain against the same stress, or against a different stress (cross-tolerance). Understanding the molecular mechanisms of brain preconditioning holds promise in developing innovative therapies to prevent and treat neurodegenerative disorders, particularly ischemic stroke. Many of the detailed steps involved in tolerance and cross-tolerance are unknown. It is also likely that different stressors differentially regulate sets of genes, transcription factors, and signal transduction pathways that depend upon the molecules that are released in response to the stressor, activation of particular receptors, and the surrounding milieu. The focus of this review is to highlight a few examples of stimuli that induce tolerance: 1) cortical spreading depression; 2) 3-nitropropionic acid; and 3) 2-deoxy-D-glucose. We will summarize by discussing one pathway where intracellular mediators may converge to upregulate intrinsic neuronal survival pathways to promote survival by resisting damage. This mechanism, activation of N-methyl-D-aspartate receptors and its integral relationship with brain-derived neurotrophic factor, may be a critical and general mechanism developed in brain to respond to stressful stimuli.
C1 [Marini, Ann M.; Pan, Hongna] Uniformed Serv Univ Hlth Sci, Dept Neurol, Bethesda, MD 20814 USA.
[Marini, Ann M.; Pan, Hongna] Uniformed Serv Univ Hlth Sci, Program Neurosci, Bethesda, MD 20814 USA.
[Popolo, Margherita] Hop Louis Pasteur, Serv EFSN, F-06000 Nice, France.
[Blondeau, Nicolas] CNRS, Inst Pharmacol Mol & Cellulaire, UMR6097, F-06560 Valbonne, France.
[Blondeau, Nicolas] Univ Nice Sophia Antipolis, Nice 2, France.
[Lipsky, Robert H.] NIAAA, Mol Genet Sect, Neurogenet Lab, NIH, Rockville, MD 20892 USA.
RP Marini, AM (reprint author), Uniformed Serv Univ Hlth Sci, Dept Neurol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM amarini@usuhs.mil
RI Blondeau, Nicolas/M-5002-2016;
OI Blondeau, Nicolas/0000-0001-5954-4094; Lipsky,
Robert/0000-0001-7753-1473
FU Centre National de la Recherche Scientifique (CNRS); NIH [NIAAA
Z01-AA00325]; Defense Brain and Spinal Cord Injury Program (AMM)
[F-192EG-C1]
FX The authors thank Franck Aguila for his technical assistance. N.
Blondeau is supported by the Centre National de la Recherche
Scientifique (CNRS). This study was supported by NIH intramural grant
NIAAA Z01-AA00325 (RHL) and extramural grant F-192EG-C1 from the Defense
Brain and Spinal Cord Injury Program (AMM).
NR 125
TC 10
Z9 13
U1 0
U2 2
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1871-5273
J9 CNS NEUROL DISORD-DR
JI CNS Neurol. Disord.-Drug Targets
PD OCT
PY 2008
VL 7
IS 4
BP 382
EP 390
DI 10.2174/187152708786441849
PG 9
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 397HX
UT WOS:000262654600007
PM 18991667
ER
PT J
AU Dixit, R
Roy, U
Patole, MS
Shouche, YS
AF Dixit, Rajnikant
Roy, Upal
Patole, Millind S.
Shouche, Yogesh S.
TI Molecular and phylogenetic analysis of a novel family of
fibrinogen-related proteins from mosquito Aedes albopictus cell line
SO COMPUTATIONAL BIOLOGY AND CHEMISTRY
LA English
DT Article
DE Mosquito; Pattern recognition receptors; Innate immunity;
Fibrinogen-related proteins
ID VECTOR ANOPHELES-STEPHENSI; INNATE IMMUNITY; IDENTIFICATION;
TRANSCRIPTOMES; INFECTION; LECTINS; GAMBIAE
AB Since lectins have been proposed to function as non-self recognizing molecules, it is important to access the specificity and diversity of lectin molecules that play an important role as pattern recognition receptors (PRRs). Like vertebrates, several lectins containing fibrinogen-like (FBG) domains have been reported as PRRs from different invertebrate species, however, in case of mosquito, very little information is available. In this study, we report identification and characterization of a novel family of fibrinogen-related proteins which exhibits (43-68%) similarities to that of A. gambiae FREPs, isolated from the immune challenged cell line of mosquito Aedes albopictus. Analysis of the longest (790 bp) cDNA (AF-1) appears to encode a 263 deduced amino acid sequence that contains a C-terminal fibrinogen-like domain. Amino acid sequence similarity and phylogenetic analysis showed a high degree of conservation with other known insect fibrinogen-related proteins, suggesting that mosquito A. albopictus FREPs may play a similar role in an innate immunity as pattern recognition receptor molecules; however, further characterization is needed to understand their transcriptional regulation and behavior during microbial infection. (c) 2008 Elsevier Ltd. All rights reserved.
C1 [Dixit, Rajnikant; Roy, Upal; Patole, Millind S.; Shouche, Yogesh S.] Natl Ctr Cell Sci, Mol Biol Unit, Pune 411007, Maharashtra, India.
RP Dixit, R (reprint author), NIAID, NIH, Lab Malaria & Vector Res, Rockville, MD 20852 USA.
EM dixit2k@yahoo.com
RI DIXIT, RAJNIKANT/D-2566-2009; SHOUCHE, YOGESH/C-1231-2009; ROY,
UPAL/C-6126-2012;
OI DIXIT, RAJNIKANT/0000-0002-3536-8329; Roy, Upal/0000-0002-0325-567X
FU Department of Biotechnology, New Delhi, India
FX This work was supported by Department of Biotechnology, New Delhi,
India.
NR 16
TC 5
Z9 6
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1476-9271
J9 COMPUT BIOL CHEM
JI Comput. Biol. Chem.
PD OCT
PY 2008
VL 32
IS 5
BP 382
EP 386
DI 10.1016/j.compbiolchem.2008.07.002
PG 5
WC Biology; Computer Science, Interdisciplinary Applications
SC Life Sciences & Biomedicine - Other Topics; Computer Science
GA 361EQ
UT WOS:000260110700012
PM 18706867
ER
PT J
AU Blithe, D
AF Blithe, Diana
TI Male contraception: what is on the horizon?
SO CONTRACEPTION
LA English
DT Article
DE male contraception; hormonal approach; spermatogenesis; sperm-specific
nonhormonal targets
ID MALE-FERTILITY; SPERM MOTILITY; TESTOSTERONE; ANDROGEN; MEN;
SPERMATOGENESIS; SPERMATOZOA; UNDECANOATE; ANTAGONIST; PROTEINS
AB Male contraception remains an important area of research. Methods can inhibit sperm production or can be targeted to inhibit sperm functions such as motility, orientation or interaction with the egg. Hormonal methods appear to be safe and effective in proof of concept studies but efforts are underway to improve delivery options or lead time until full efficacy is achieved. Nonhormonal methods are based on numerous targets that impact sperm production or function. Several agents that inhibit the sperm-specific or testis-specific targets have been identified and studies in animals have shown promising results. Published by Elsevier Inc.
C1 Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Contracept & Reprod Hlth Branch, Populat Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Blithe, D (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Contracept & Reprod Hlth Branch, Populat Res Ctr, NIH, Bethesda, MD 20892 USA.
EM blithed@mail.nih.gov
NR 35
TC 8
Z9 9
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0010-7824
J9 CONTRACEPTION
JI Contraception
PD OCT
PY 2008
VL 78
IS 4
SU S
BP S23
EP S27
DI 10.1016/j.contraception.2008.03.018
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 357QC
UT WOS:000259860200005
PM 18847595
ER
PT J
AU Yeh, S
Smith, JA
AF Yeh, Steven
Smith, Janine A.
TI Management of acute hydrops with perforation in a patient with
keratoconus and cone dystrophy: Case report and literature review
SO CORNEA
LA English
DT Article
DE keratoconus; cone dystrophy; hydrops; corneal perforation
ID LEBERS CONGENITAL AMAUROSIS; TAPETORETINAL DEGENERATION; GELATINOLYTIC
ACTIVITY; ANTERIOR KERATOCONUS; CANDIDATE GENE; KERATOCONJUNCTIVITIS;
FEATURES; CORNEAS; LOCUS; TWINS
AB Purpose: To describe a patient with colic dystrophy who presented With acute h drops and perforation. leading to the diagnosis of keratoconus.
Methods: Case report and literature review.
Results: A 21-year-old male patient with a history of cone dystrophy presented with a flat anterior chamber, diffuse corneal stromal edema with in intrastomal cleft, and ruptured Descemet membrane, findings consistent with acute hydrops with corneal perforation. After bandage contact lens placement and instillation of a cycloplegic agent, the anterior chamber reformed within 24 hours. Over the next week. conservative management with a bandage lens. pressure patching, topical fluoroquinolone antibiotic, and topical cycloplegic led to the reformation and maintenance of anterior chamber stability. Corneal topography of the unaffected eye showed global corneal thinning and steep still K readings suspicious for early keratoconus.
Conclusions: Although the association between keratoconus and cone dystrophy is extremely rare, our patient's vision-threatening complication of acute hydrops' with cortical perforation highlights the importance of corneal evaluation including topography in colic dystrophy. Conservative management was successful in the restoration of anatomic integrity in this situation.
C1 [Yeh, Steven; Smith, Janine A.] NEI, Div Epidemiol & Clin Res, NIH, Bethesda, MD 20892 USA.
RP Smith, JA (reprint author), NEI, Div Epidemiol & Clin Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM smith@nei.nih.gov
FU National Eye Institute Intramural Funding; Heed Ophthalmic Foundation
FX Supported by National Eye Institute Intramural Funding. S.Y. is
supported by the Heed Ophthalmic Foundation.
NR 35
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-3740
J9 CORNEA
JI Cornea
PD OCT
PY 2008
VL 27
IS 9
BP 1062
EP 1065
DI 10.1097/ICO.0b013e31817618c2
PG 4
WC Ophthalmology
SC Ophthalmology
GA 354TT
UT WOS:000259662600016
PM 18812772
ER
PT J
AU Cobb, JP
Suffredini, AF
Danner, RL
AF Cobb, J. Perren
Suffredini, Anthony F.
Danner, Robert L.
TI The fourth national institutes of health symposium on the functional
genomics of critical injury: Surviving stress from organ systems to
molecules
SO CRITICAL CARE MEDICINE
LA English
DT Review
DE systems biology; septic shock; trauma; organ failure; stress
ID STAPHYLOCOCCAL-ENTEROTOXIN-B; INTENSIVE-CARE-UNIT; GENE-EXPRESSION;
ARGININE METABOLISM; BLOOD; STROKE; DISEASE; NITRITE; SEPSIS; MODEL
AB Recent strides in computational biology and high-throughput technologies have generated considerable interest in understanding complex biological systems. The application of these technologies to critical illness and injury offers the potential to define adaptive and maladaptive programs of gene expression induced by infection, shock, trauma, or other inflammatory triggers, and to detect biomarkers and genetic polymorphisms linked to these responses and outcome. A systems biology approach is timely because despite substantial effort, treatment approaches directed at a single mediator or inflammatory pathway have met with little success in altering outcomes of critically ill or injured patients. Highlights from the Fourth National Institute of Health Functional Genomics of Critical Illness and Injury Symposium are described herein, in addition to deliverables for the field identified during panel discussions. Next steps for the community and suggestions for future research are presented.
C1 [Cobb, J. Perren] Washington Univ, Ctr Crit Illness & Hlth Engn, St Louis, MO 63130 USA.
[Cobb, J. Perren] Washington Univ, Dept Surg, St Louis, MO USA.
[Cobb, J. Perren] Washington Univ, Dept Genet, St Louis, MO USA.
[Suffredini, Anthony F.; Danner, Robert L.] NIH, Dept Crit Care Med, Funct Genom & Prote Facil, Bethesda, MD 20892 USA.
RP Cobb, JP (reprint author), Washington Univ, Ctr Crit Illness & Hlth Engn, St Louis, MO 63130 USA.
EM cobb@wustl.edu
FU NIH [U13 GM73413]
FX Supported in part by NIH U13 GM73413 (to JPC). Information in this
article reflects presentations and discussion at the Fourth Functional
Genomics of Critical Illness and Injury Symposium, held November 13-14,
2006, on the National Institutes of Health campus in Bethesda, Maryland
(http:/hwww.strategicresults. com/fg4/).
NR 50
TC 6
Z9 6
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD OCT
PY 2008
VL 36
IS 10
BP 2905
EP 2911
DI 10.1097/CCM.0b013e318186a720
PG 7
WC Critical Care Medicine
SC General & Internal Medicine
GA 356GF
UT WOS:000259766000026
PM 18828200
ER
PT J
AU Liang, XJ
Chen, CY
Zhao, YL
Jia, L
Wang, PC
AF Liang, Xing-Jie
Chen, Chunying
Zhao, Yuliang
Jia, Lee
Wang, Paul C.
TI Biopharmaceutics and Therapeutic Potential of Engineered Nanomaterials
SO CURRENT DRUG METABOLISM
LA English
DT Review
DE Metabolism; engineered nanomaterials; nanomedicine; fullerenol; carbon
nanotube; titanium dioxide (TiO2); silica dioxide (SiO2); magnetic
nanoparticles
ID WALLED CARBON NANOTUBES; SEMICONDUCTOR QUANTUM DOTS; FLOW LINEAR
DICHROISM; IN-VIVO; ULTRAFINE PARTICLES; TITANIUM-DIOXIDE; GENE
DELIVERY; MANUFACTURED NANOMATERIALS; ELECTRONIC-PROPERTIES; PULMONARY
TOXICITY
AB Engineered nanomaterials are at the leading edge of the rapidly developing nanosciences and are founding an important class of new materials with specific physicochemical properties different from bulk materials with the same compositions. The potential for nanomaterials is rapidly expanding with novel applications constantly being explored in different areas. The unique size-dependent properties of nanomaterials make them very attractive for pharmaceutical applications. Investigations of physical, chemical and biological properties of engineered nanomaterials have yielded valuable information. Cytotoxic effects of certain engineered nanomaterials towards malignant cells form the basis for one aspect of nanomedicine. It is inferred that size, three dimensional shape, hydrophobicity and electronic configurations make them an appealing subject in medicinal chemistry. Their unique structure coupled with immense scope for derivatization forms a base for exciting developments in therapeutics. This review article addresses the fate of absorption, distribution, metabolism and excretion (ADME) of engineered nanoparticles in vitro and in vivo. It updates the distinctive methodology used for studying the biopharmaceutics of nanoparticles. This review addresses the future potential and safety concerns and genotoxicity of nanoparticle formulations in general. It particularly emphasizes the effects of nanoparticles on metabolic enzymes as well as the parenteral or inhalation administration routes of nanoparticle formulations. This paper illustrates the potential of nanomedicine by discussing biopharmaceutics of fullerene derivatives and their suitability for diagnostic and therapeutic purposes. Future direction is discussed as well.
C1 [Liang, Xing-Jie; Chen, Chunying; Zhao, Yuliang] Natl Ctr Nanosci & Technol China, Div Nanomed & Nanobiol, Lab Nanobiomed & Nanosafety, Beijing, Peoples R China.
[Chen, Chunying; Zhao, Yuliang] Chinese Acad Sci, Inst High Energy Phys, Lab Bioenvironm Effects Nanomat & Nanosafety, Beijing 100049, Peoples R China.
[Jia, Lee] NCI, Toxicol & Pharmacol Branch, Div Canc Treatment & Diag, NIH, Rockville, MD 20852 USA.
[Wang, Paul C.] Howard Univ, Dept Radiol, Lab Mol Imaging, Washington, DC 20060 USA.
RP Liang, XJ (reprint author), Natl Ctr Nanosci & Technol China, Div Nanomed & Nanobiol, Lab Nanobiomed & Nanosafety, Beijing, Peoples R China.
EM liangxj@nanoctr.cn; zhaoyuliang@mail.ihep.ac.cn
FU NCI NIH HHS [5U 54CA091431]; NCRR NIH HHS [2G12RR003048, G12 RR003048,
G12 RR003048-190016]
NR 97
TC 64
Z9 64
U1 1
U2 44
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-2002
J9 CURR DRUG METAB
JI Curr. Drug Metab.
PD OCT
PY 2008
VL 9
IS 8
BP 697
EP 709
DI 10.2174/138920008786049230
PG 13
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 359VB
UT WOS:000260015100003
PM 18855608
ER
PT J
AU Isenberg, JS
Frazier, WA
Krishna, MC
Wink, DA
Roberts, DD
AF Isenberg, Jeff S.
Frazier, William A.
Krishna, Murali C.
Wink, David A.
Roberts, David D.
TI Enhancing Cardiovascular Dynamics by Inhibition of Thrombospondin-1/CD47
Signaling
SO CURRENT DRUG TARGETS
LA English
DT Review
DE Ischemic injury; tissue perfusion; angiogenesis; hemostasis; blood flow;
nitric oxide; vascular smooth muscle; platelets
ID VASCULAR SMOOTH-MUSCLE; NITRIC-OXIDE SYNTHASE; ISCHEMIA-REPERFUSION
INJURY; PERIPHERAL ARTERIAL-DISEASE; ENDOTHELIAL GROWTH-FACTOR; SKIN
FLAP SURVIVAL; PROTEIN-KINASE-I; BLOOD-FLOW; PLATELET ACTIVATION; CELL
RESPONSES
AB Activation of soluble guanylate cyclase by nitric oxide (NO) controls signaling pathways that play critical roles in normal vascular physiology and in the pathogenesis of cardiovascular disease. We have identified the secreted protein thrombospondin-1 as a key regulator of NO signaling. Thrombospondin-1 limits the angiogenic activity of NO in endothelial cells, its vasodilator activity in vascular smooth muscle, and its antithrombotic activity in platelets. Loss of either thrombospondin-1 or its receptor CD47 in transgenic mice results in hyperdynamic responses to NO and reveals the importance of this pathway in normal physiology. Thrombospondin-1 and CD47 null mice show improved abilities to respond to ischemic stress, suggesting that therapeutic targeting of this pathway could benefit patients with a variety of ischemic conditions. We review the preclinical development of therapeutics targeting thrombospondin-1 or CD47 for improving survival of fixed ischemia, ischemia due to aging and peripheral vascular disease, and skin grafting.
C1 [Roberts, David D.] NCI, Lab Pathol & Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
Washington Univ, Sch Med, Dept Biochem & Mol Biophys, St Louis, MO 63110 USA.
RP Roberts, DD (reprint author), NCI, Lab Pathol & Radiat Biol Branch, Ctr Canc Res, NIH, Bldg 10,Room 2A33,10 Ctr Dr MSC1500, Bethesda, MD 20892 USA.
EM droberts@helix.nih.gov
RI Roberts, David/A-9699-2008
OI Roberts, David/0000-0002-2481-2981
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute; Center for Cancer Research; NIH [HL54390,
GM57573]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research (D.A.W, M.C.K., D.D.R.) and NIH grants HL54390 and
GM57573 (W. A.F.).
NR 110
TC 15
Z9 15
U1 0
U2 0
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-4501
J9 CURR DRUG TARGETS
JI Curr. Drug Targets
PD OCT
PY 2008
VL 9
IS 10
BP 833
EP 841
DI 10.2174/138945008785909338
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 359VF
UT WOS:000260015500003
PM 18855617
ER
PT J
AU Zustiak, MP
Pollack, JK
Marten, MR
Betenbaugh, MJ
AF Zustiak, Matthew P.
Pollack, Judith K.
Marten, Mark R.
Betenbaugh, Michael J.
TI Feast or famine: autophagy control and engineering in eukaryotic cell
culture
SO CURRENT OPINION IN BIOTECHNOLOGY
LA English
DT Review
ID ENDOPLASMIC-RETICULUM STRESS; ORYZAE FERMENTATION LEADS; COILED-COIL
PROTEIN; ASPERGILLUS-ORYZAE; PENICILLIUM-CHRYSOGENUM; MONITORING
AUTOPHAGY; RECOMBINANT ENZYME; CHEMOSTAT CULTURES; STRUCTURED MODEL;
MAMMALIAN-CELLS
AB Autophagy is a degradative process playing a role in both cell death and cell survival. Its presence is well conserved both in lower and higher eukaryotes. Recent studies have shown that activation or inhibition of autophagy may be possible in biotechnologically important species including mammalian cells and filamentous fungi using both environmental manipulation and genetic engineering. As our understanding of the autophagic biochemical pathways increases and monitoring methods become more user-friendly, the potential exists to obtain an optimum level of autophagy. This may allow for maximum cell survival and production of proteins and other metabolites in these industrially important eukaryotes.
C1 [Pollack, Judith K.; Marten, Mark R.] Univ Maryland Baltimore Cty, Dept Chem & Biochem Engn, Baltimore, MD 21250 USA.
[Zustiak, Matthew P.; Betenbaugh, Michael J.] Johns Hopkins Univ, Dept Chem & Biomol Engn, Baltimore, MD 21218 USA.
[Zustiak, Matthew P.] Natl Canc Inst, Biopharmaceut Dev Program, SAIC Frederick Inc, Ft Detrick, MD 21702 USA.
RP Marten, MR (reprint author), Univ Maryland Baltimore Cty, Dept Chem & Biochem Engn, 1000 Hilltop Circle, Baltimore, MD 21250 USA.
EM zustiakm@mail.nih.gov; Okadar1@umbc.edu; marten@umbc.edu; beten@jhu.edu
RI Betenbaugh, Michael J./A-3252-2010;
OI Betenbaugh, Michael J./0000-0002-6336-4659; Marten,
Mark/0000-0002-1863-8956
NR 58
TC 21
Z9 22
U1 0
U2 5
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0958-1669
J9 CURR OPIN BIOTECH
JI Curr. Opin. Biotechnol.
PD OCT
PY 2008
VL 19
IS 5
BP 518
EP 526
DI 10.1016/j.copbio.2008.07.007
PG 9
WC Biochemical Research Methods; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA 365EE
UT WOS:000260387900016
PM 18725292
ER
PT J
AU Phillips, KR
Biswas, A
Cyr, JL
AF Phillips, Kelli R.
Biswas, Anindita
Cyr, Janet L.
TI How hair cells hear: the molecular basis of hair-cell
mechanotransduction
SO CURRENT OPINION IN OTOLARYNGOLOGY & HEAD AND NECK SURGERY
LA English
DT Article
DE cochlea; hair cell; mechanotransduction; stereocilia
ID MYOSIN-I-BETA; SYNDROME TYPE 1F; TIP LINKS; MECHANOELECTRICAL
TRANSDUCTION; MECHANOSENSORY TRANSDUCTION; MECHANICAL TRANSDUCTION;
PHOSPHATIDYLINOSITOL 4,5-BISPHOSPHATE; SENSORY TRANSDUCTION; BULLFROGS
SACCULUS; ION-CHANNEL
AB Purpose of review
This review aims to summarize our current knowledge regarding mechanotransduction by hair cells and to highlight unresolved questions.
Recent findings
Despite over a quarter of a century of electrophysiological data describing hair-cell mechanotransduction, the molecular basis of this process is just now being revealed. Recent work has begun to identify candidate transduction complex molecules, and current work is aimed at confirming these hypotheses and identifying other proteins important for hair-cell function.
Summary
Our senses of hearing and balance rely on the exquisite sensitivity of the hair cell and its transduction complex. Understanding the molecular basis for hair-cell mechanotransduction may provide us with the foundation for understanding the causes of, and perhaps the treatments for, auditory and vestibular deficits resulting from hair-cell dysfunction.
C1 [Phillips, Kelli R.; Biswas, Anindita; Cyr, Janet L.] W Virginia Univ, Sch Med, Sensory Neurosci Res Ctr, Morgantown, WV 26506 USA.
RP Cyr, JL (reprint author), NIDCD, NIH, 6120 Execut Blvd,EPS 400C, Bethesda, MD 20892 USA.
EM jcyr@hsc.wvu.edu
FU NIH/NIDCD [R01 DC006402]
FX The authors would like to thank David Corey, Peter Gillespie, Jeff Holt,
and Bechara Kachar for use of previously published figures. This work
was supported by NIH/NIDCD grant R01 DC006402 to A.C. 22 23
NR 78
TC 5
Z9 5
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1068-9508
J9 CURR OPIN OTOLARYNGO
JI Curr. Opin. Otolaryngol. Head Neck Surg.
PD OCT
PY 2008
VL 16
IS 5
BP 445
EP 451
DI 10.1097/MOO.0b013e32830f4ac8
PG 7
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 398EV
UT WOS:000262716300009
PM 18797287
ER
PT J
AU Sherwood, P
Brooks, BR
Sansom, MSP
AF Sherwood, Paul
Brooks, Bernard R.
Sansom, Mark S. P.
TI Multiscale methods for macromolecular simulations
SO CURRENT OPINION IN STRUCTURAL BIOLOGY
LA English
DT Article
ID MOLECULAR-DYNAMICS SIMULATIONS; ELASTIC NETWORK MODEL; COARSE-GRAINED
MODELS; MEMBRANE-PROTEINS; AB-INITIO; FORCE-FIELD; FREE-ENERGY;
CRYOELECTRON MICROSCOPY; CONFORMATIONAL DYNAMICS; REDOX PROPERTIES
AB In this article we review the key modeling tools available for simulating biomolecular systems. We consider recent developments and representative applications of mixed quantum mechanics/molecular mechanics (QM/MM), elastic network models (ENMs), coarse-grained molecular dynamics, and grid-based tools for calculating interactions between essentially rigid protein assemblies. We consider how the different length scales can be coupled, both in a sequential fashion (e.g. a coarse-grained or grid model using parameterization from MD simulations), and via concurrent approaches, where the calculations are performed together and together control the progression of the simulation. We suggest how the concurrent coupling approach familiar in the context of QM/MM calculations can be generalized, and describe how this has been done in the CHARMM macromolecular simulation package.
C1 [Sherwood, Paul] STFC Daresbury Lab, Warrington WA4 4AD, Cheshire, England.
[Brooks, Bernard R.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
[Sansom, Mark S. P.] Univ Oxford, Dept Biochem, Oxford OX1 3QU, England.
RP Sherwood, P (reprint author), STFC Daresbury Lab, Warrington WA4 4AD, Cheshire, England.
EM p.sherwood@dl.ac.uk; brb@nih.gov; mark.sansom@bioch.ox.ac.uk
RI Sherwood, Paul/B-9033-2012;
OI Sherwood, Paul/0000-0002-4611-5052; Sansom, Mark/0000-0001-6360-7959
FU BBSRC, EPSRC, MRC; Wellcome Trust; Intramural Research Program; NIH,
NHLBI
FX Work in MSPS's group is supported by grants from the BBSRC, EPSRC, MRC
and the Wellcome Trust. This research was supported in part by the
Intramural Research Program of the NIH, NHLBI. We thank our coworkers
for their contributions to some of the work described.
NR 79
TC 126
Z9 126
U1 3
U2 55
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-440X
EI 1879-033X
J9 CURR OPIN STRUC BIOL
JI Curr. Opin. Struct. Biol.
PD OCT
PY 2008
VL 18
IS 5
BP 630
EP 640
DI 10.1016/j.sbi.2008.07.003
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 371HB
UT WOS:000260821300016
PM 18721882
ER
PT J
AU Jin, T
Xu, XH
Hereld, D
AF Jin, Tian
Xu, Xuehua
Hereld, Dale
TI Chemotaxis, chemokine receptors and human disease
SO CYTOKINE
LA English
DT Review
DE Chemotaxis; Chemokine; GPCR; Inflammation; Human diseases
ID OBSTRUCTIVE PULMONARY-DISEASE; G-BETA-GAMMA; DICTYOSTELIUM-DISCOIDEUM;
CELL POLARITY; LEADING-EDGE; LIVING CELLS; MYOSIN-II; SEVERE
EXACERBATIONS; CANCER METASTASIS; SELF-ORGANIZATION
AB Cell migration is involved in diverse physiological processes including embryogenesis, immunity, and diseases such as cancer and chronic inflammatory disease. The movement of many cell types is directed by extracellular gradients of diffusible chemicals. This phenomenon, referred to as "chemotaxis", was first described in 1888 by Leber who observed the movement of leukocytes toward sites of inflammation. We now know that a large family of small proteins, chemokines, serves as the extracellular signals and a family of G-protein-coupled receptors (GPCRs), chemokine receptors, detects gradients of chemokines and guides cell movement in vivo. Currently, we still know little about the molecular machineries that control chemokine gradient sensing and migration of immune cells. Fortunately, the molecular mechanisms that control these fundamental aspects of chemotaxis appear to be evolutionarily conserved, and studies in lower eukaryotic model systems have allowed us to form concepts, uncover molecular components, develop new techniques, and test models of chemotaxis. These studies have helped our current understanding of this complicated cell behavior. In this review, we wish to mention landmark discoveries in the chemotaxis research field that shaped our current understanding of this fundamental cell behavior and Jay out key questions that remain to be addressed in the future. Published by Elsevier Ltd.
C1 [Jin, Tian] NIAID, Chemotaxis Signal Sect, Immunogenet Lab, NIH,Twinbrook Facil 2, Rockville, MD 20852 USA.
[Xu, Xuehua] Georgetown Univ, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20057 USA.
[Hereld, Dale] NIAAA, Div Metab & Hlth Effects, NIH, Rockville, MD 20852 USA.
RP Jin, T (reprint author), NIAID, Chemotaxis Signal Sect, Immunogenet Lab, NIH,Twinbrook Facil 2, 12441 Parklawn Dr, Rockville, MD 20852 USA.
EM tjin@niaid.nih.gov
OI xu, xuehua/0000-0002-3863-9593
FU NIAID; NIH
FX We thank X. Xiang for helpful comments. T. jin is supported by NIAID,
NIH intramural funding and a grant from NIH intramural AIDS target
antiviral program.
NR 89
TC 100
Z9 107
U1 3
U2 11
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
EI 1096-0023
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2008
VL 44
IS 1
BP 1
EP 8
DI 10.1016/j.cyto.2008.06.017
PG 8
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 369NG
UT WOS:000260700600001
PM 18722135
ER
PT J
AU Hasebe, T
Kajita, M
Shi, YB
Ishizuya-Oka, A
AF Hasebe, Takashi
Kajita, Mitsuko
Shi, Yun-Bo
Ishizuya-Oka, Atsuko
TI Thyroid Hormone-Up-regulated Hedgehog Interacting Protein Is Involved in
Larval-to-Adult Intestinal Remodeling by Regulating Sonic Hedgehog
Signaling Pathway in Xenopus laevis
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE sonic hedgehog (Shh); hedgehog interacting protein (Hip); Xenopus
laevis; metamorphosis; intestinal remodeling
ID TYPE-1 MATRIX-METALLOPROTEINASE; AMPHIBIAN METAMORPHOSIS; EPITHELIAL
DEVELOPMENT; BINDING PROTEIN; EXPRESSION PROFILES; CELL-PROLIFERATION;
GENE-EXPRESSION; GELATINASE-A; INDUCTION; APOPTOSIS
AB Sonic hedgehog (Shh) was previously shown to be involved in the larval-to-adult remodeling of the Xenopus laevis intestine. While Shh is transcriptionally regulated by thyroid hormone (TH), the posttranscriptional regulation of Shh signaling during intestinal remodeling is largely unknown. In the present study, we focused on a role of the pan-hedgehog inhibitor, hedgehog interacting protein (Hip), in the spatiotemporal regulation of Shh signaling. Using real-time reverse transcriptase-polymerase chain reaction and in situ hybridization, we show that Hip expression is transiently up-regulated during both natural and TH-induced metamorphosis and that Hip mRNA is localized in the connective tissue adjacent to the adult epithelial primordia expressing Shh. Interestingly, the expression of bone morphogenetic protein-4, a Shh target gene, is hardly detectable where Hip is strongly expressed. Finally, we demonstrate that Hip binds to the N-terminal fragment of processed Shh in vivo, suggesting that Hip suppresses Shh signaling through sequestering Shh. Developmental Dynamics 237:3006-3015, 2008. (c) 2008 Wiley-Liss, Inc.
C1 [Hasebe, Takashi; Ishizuya-Oka, Atsuko] Nippon Med Sch, Dept Biol, Nakahara Ku, Kanagawa 2110063, Japan.
[Kajita, Mitsuko; Ishizuya-Oka, Atsuko] Nippon Med Sch, Dept Mol Biol, Inst Dev & Aging Sci, Nakahara Ku, Kanagawa 2110063, Japan.
[Shi, Yun-Bo] NICHD, Lab Gene Regulat & Dev, PCRM, NIH, Bethesda, MD USA.
RP Hasebe, T (reprint author), Nippon Med Sch, Dept Biol, Nakahara Ku, 2-297-2 Kosugi Cho, Kanagawa 2110063, Japan.
EM hasebet@nms.ac.jp
FU JSPS [17570051]; NTH
FX Grant sponsor: JSPS Grants-in-Aid for Scientific Research (C); Grant
number: 17570051; Grant sponsor: NTH, Intramural Research Program of
NICHD.
NR 46
TC 14
Z9 14
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1058-8388
J9 DEV DYNAM
JI Dev. Dyn.
PD OCT
PY 2008
VL 237
IS 10
BP 3006
EP 3015
DI 10.1002/dvdy.21698
PG 10
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA 360ZG
UT WOS:000260096700036
PM 18816855
ER
PT J
AU Okano, J
Sakai, Y
Shiota, K
AF Okano, Junko
Sakai, Yasuo
Shiota, Kohei
TI Retinoic Acid Down-Regulates Tbx1 Expression and Induces Abnormal
Differentiation of Tongue Muscles in Fetal Mice
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE retinoic acid; tongue development; tongue muscle development; cleft
palate; CYP26A1; CYP26B1; Tbx1; congenital anomaly
ID INDUCED CLEFT-PALATE; DIGEORGE-SYNDROME; RETINALDEHYDE DEHYDROGENASE;
SYNTHESIZING ENZYME; DELETION SYNDROMES; GENE-EXPRESSION; CANDIDATE
GENE; IN-VIVO; MOUSE; IDENTIFICATION
AB Excess retinoic acid (RA) during pregnancy can cause various developmental anomalies in both humans and rodents. We investigated the mechanisms underlying the aberrant differentiation of tongue muscles in fetal mice exposed to exogenous RA in utero. RA-degrading enzymes (Cyp26a1 and Cyp26b1) were expressed at early stages of normal tongue development, but exogenous RA perturbed their expression in the fetal tongue. RA is normally distributed in the developing tongue muscles but its localization was disrupted by exogenous RA. After RA treatment, myogenic determination factors were reduced and the differentiation was significantly suppressed in tongue muscles. Tbx1, a candidate gene of DiGeorge syndrome, was down-regulated in the fetal tongue in response to excess RA. Moreover, Tbx1 as well as myogenic determination factors were not observed in tongue muscle primordia of Cyp26b1(-/-) fetuses. Our study suggests that RA signaling may play an essential role in tongue muscle differentiation via the regulation of Tbx1. Developmental Dynamics 237:3059-3070, 2008. (c) 2008 Wiley-Liss, Inc.
C1 [Okano, Junko; Shiota, Kohei] Kyoto Univ, Grad Sch Med, Dept Anat & Dev Biol, Kyoto, Japan.
[Sakai, Yasuo] Fujita Hlth Univ, Dept Plast & Reconstruct Surg, Aichi, Japan.
[Shiota, Kohei] Kyoto Univ, Grad Sch Med, Congenital Anomaly Ctr, Kyoto, Japan.
RP Okano, J (reprint author), NIAMS, Dev Skin Biol Unit, NIH, Bethesda, MD 20892 USA.
EM okanoj@mail.gov.nih
FU Japanese Ministry of Education, Culture, Sports, Science and Technology
FX Grant sponsor: Japanese Ministry of Education, Culture, Sports, Science
and Technology.
NR 48
TC 12
Z9 12
U1 1
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1058-8388
J9 DEV DYNAM
JI Dev. Dyn.
PD OCT
PY 2008
VL 237
IS 10
BP 3059
EP 3070
DI 10.1002/dvdy.21715
PG 12
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA 360ZG
UT WOS:000260096700041
PM 18816858
ER
PT J
AU Concannon, P
Onengut-Gumuscu, S
Todd, JA
Smyth, DJ
Pociot, F
Bergholdt, R
Akolkar, B
Erlich, HA
Hilner, JE
Julier, C
Morahan, G
Nerup, J
Nierras, CR
Chen, WM
Rich, SS
AF Concannon, Patrick
Onengut-Gumuscu, Suna
Todd, John A.
Smyth, Deborah J.
Pociot, Flemming
Bergholdt, Regine
Akolkar, Beena
Erlich, Henry A.
Hilner, Joan E.
Julier, Cecile
Morahan, Grant
Nerup, Jorn
Nierras, Concepcion R.
Chen, Wei-Min
Rich, Stephen S.
CA Type 1 Diabet Genetics Consortium
TI A human type 1 diabetes susceptibility locus maps to chromosome 21q22.3
SO DIABETES
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; PROTEIN-TYROSINE-PHOSPHATASE; PEDIGREE
DISEQUILIBRIUM TEST; AUTOIMMUNE-DISEASE; INSULIN GENE; HUMAN THYMUS;
LINKAGE; REGION; PTPN22; POLYMORPHISM
AB OBJECTIVE-The Type 1 Diabetes Genetics Consortium (T1DGC) has assembled and genotyped a large collection of multiplex families for the purpose of mapping genomic regions linked to type 1 diabetes. In the current study, we tested for evidence of loci associated with type 1 diabetes utilizing genome-wide linkage scan data and family-based association methods.
RESEARCH DESIGN AND METHODS-A total of 2,496 multiplex families with type 1 diabetes were genotyped with a panel of 6,090 single nucleotide polymorphisms (SNPs). Evidence of association to disease was evaluated by the pedigree disequilibrium test. Significant results were followed up by genotyping and analyses in two independent sets of samples: 2,214 parent-affected child trio families and a panel of 7,721 case and 9,679 control subjects.
RESULTS-Three of the SNPs most strongly associated with type 1 diabetes localized to previously identified type 1 diabetes risk loci: INS, IFIH1, and KIAA0350. A fourth strongly associated SNP, rs876498 (P = 1.0 x 10(-4)), occurred in the sixth intron of the UBASH3A locus at chromosome 21q22.3. Support for this disease association was obtained in two additional independent sample sets: families with type 1 diabetes (odds ratio [OR] 1.06 [95% CI 1.00-1.11]; P = 0.023) and case and control subjects (1.14 [1.09-1.19]; P = 7.5 x 10(-8)).
CONCLUSIONS-The TIDGC 6K SNP scan and follow-up studies reported here confirm previously reported type 1 diabetes associations at INS, IFIH1, and KIAA0350 and identify an additional disease association on chromosome 21q22.3 in the UBASH3A locus (OR 1.10 [95% CI 1.07-1.13]; P = 4.4 x 10(-12)). This gene and its flanking regions are now validated targets for further resequencing, genotyping, and functional studies in type 1 diabetes.
C1 [Concannon, Patrick] Univ Virginia, Dept Biochem & Mol Genet, Charlottesville, VA 22903 USA.
[Concannon, Patrick; Onengut-Gumuscu, Suna; Chen, Wei-Min; Rich, Stephen S.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA USA.
[Onengut-Gumuscu, Suna] Univ Virginia, Dept Med, Div Endocrinol & Metab, Charlottesville, VA USA.
[Todd, John A.; Smyth, Deborah J.] Univ Cambridge, Cambridge Inst Med Res, Wellcome Trust Diabet & Inflammat Lab, Juvenile Diabet Res Fdn, Cambridge, England.
[Pociot, Flemming; Bergholdt, Regine; Nerup, Jorn] Steno Diabet Ctr, DK-2820 Gentofte, Denmark.
[Akolkar, Beena] NIDDKD, Div Diabet Endocrinol & Metab Dis, NIH, Bethesda, MD 20892 USA.
[Erlich, Henry A.] Roche Mol Syst, Pleasanton, CA USA.
[Hilner, Joan E.] Wake Forest Univ Hlth Sci, Div Publ Hlth Sci, Winston Salem, NC USA.
[Julier, Cecile] INSERM, U730, Evry, France.
[Julier, Cecile] CEA, Inst Genom, Ctr Natl Genotypage, Evry, France.
[Morahan, Grant] Univ Western Australia, Western Australian Inst Med Res, Ctr Diabet Res, Perth, WA 6009, Australia.
[Morahan, Grant] Univ Western Australia, Med Res Ctr, Perth, WA 6009, Australia.
[Nierras, Concepcion R.] Juvenile Diabet Res Fdn, New York, NY USA.
[Chen, Wei-Min] Univ Virginia, Dept Publ Hlth Sci, Div Biostat & Epidemiol, Charlottesville, VA USA.
RP Concannon, P (reprint author), Univ Virginia, Dept Biochem & Mol Genet, Charlottesville, VA 22903 USA.
EM pjc6n@virginia.edu
RI Chen, Wei-Min/A-8469-2009; Todd, John/A-3542-2010; Boehm,
Bernhard/F-8750-2015;
OI smyth, deborah/0000-0002-6330-2669; Concannon,
Patrick/0000-0002-5801-1859; Pociot, Flemming/0000-0003-3274-5448
FU National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK); National Institute of Allergy and Infectious Diseases (NIAID);
National Human Genome Research Institute (NHGRI); National Institute of
Child Health and Human Development (NICHD); Juvenile Diabetes Research
Foundation International (JDRF) [U01 DK062418]; NIDDK [DK46635]; JDRF;
Wellcome Trust; National Institute for Health Research Cambridge
Biomedical Centre
FX This research uses resources provided by the T1DGC, a collaborative
clinical study sponsored by the National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK), National Institute of Allergy and
Infectious Diseases (NIAID), National Human Genome Research Institute
(NHGRI), National Institute of Child Health and Human Development
(NICHD), and Juvenile Diabetes Research Foundation International (JDRF)
and supported by U01 DK062418. Further support was provided by a grant
from the NIDDK (DK46635) to P.C. and a joint JDRF and Wellcome Trust
grant to the Diabetes and Inflammation Laboratory at Cambridge, which
also received support from the National Institute for Health Research
Cambridge Biomedical Centre.
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U2 3
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD OCT
PY 2008
VL 57
IS 10
BP 2858
EP 2861
DI 10.2337/db08-0753
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 360FT
UT WOS:000260043800040
PM 18647951
ER
PT J
AU Pani, LN
Korenda, L
Meigs, JB
Driver, C
Chamany, S
Fox, CS
Sullivan, L
D'Agostino, RB
Nathan, DM
AF Pani, Lydir N.
Korenda, Leslie
Meigs, James B.
Driver, Cynthia
Chamany, Shadi
Fox, Caroline S.
Sullivan, Lisa
D'Agostino, Ralph B.
Nathan, David M.
TI Effect of Aging on A1C Levels in Individuals Without Diabetes
SO DIABETES CARE
LA English
DT Article
ID GLYCATED HEMOGLOBIN; GLYCOSYLATED HEMOGLOBIN; SEVERE HYPOGLYCEMIA;
HBA(1C); AGE; POPULATION; DIAGNOSIS; MELLITUS; GLYCOHEMOGLOBIN; DISEASE
AB OBJECTIVE - Although glycemic levels are known to rise with normal aging, the nondiabetic A1C range is not age specific. We examined whether A1C was associated with age in nondiabetic subjects and in subjects with normal glucose tolerance (NGT) in two population-based cohorts.
RESEARCH DESIGN AND METHODS - We performed cross-sectional analyses 01 A1C across age categories in 2,473 nondiabetic participants of the Framingham Offspring Study (FOS) and in 3,270 nondiabetic participants from the National Health and Nutrition Examination Survey (NHANES) 2001-2004. In FOS, we examined A1C by age in a subset With NGT, i.e., after excluding those With impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT). Multivariate analyses were performed, adjusting for sex, BMI, fasting glucose, and 2-h postload glucose values.
RESULTS- In the FOS and NHANES cohorts, A1C levels were positively associated with age in nondiabetic subjects. Linear regression revealed 0.014- and 0.010-unit increases in A1C per year in the nondiabetic FOS and NHANES populations, respectively. The 97.5th percentiles for A1C were 6.0% and 5.6% for nondiabetic individuals aged < 40 years in FOS and NHANES, respectively, compared With 6.6% and 6.2% for individuals aged >= 70 years (P-trend < 0.001). The association of A1C With age was similar when restricted to the subset of FOS Subjects With NGT and after adjustments for sex, BMI, lasting glucose, and 2-h postload glucose values.
CONCLUSIONS- A1C levels are positively associated with age in nondiabetic populations even after exclusion of subjects With IFG and/or IGT. Further Studies are needed to determine whether age-specific diagnostic and treatment criteria would be appropriate.
C1 [Pani, Lydir N.; Meigs, James B.; Nathan, David M.] Massachusetts Gen Hosp, Ctr Diabet, Boston, MA 02114 USA.
[Pani, Lydir N.; Meigs, James B.; Nathan, David M.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Pani, Lydir N.; Meigs, James B.; Nathan, David M.] Harvard Univ, Sch Med, Boston, MA USA.
[Korenda, Leslie; Driver, Cynthia; Chamany, Shadi] Dept Hlth & Mental Hyg, New York, NY USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Dept Endocrinol Metab & Hypertens, Boston, MA 02115 USA.
[Sullivan, Lisa; D'Agostino, Ralph B.] Boston Univ, Dept Biostat, Boston, MA 02215 USA.
RP Pani, LN (reprint author), Massachusetts Gen Hosp, Ctr Diabet, Boston, MA 02114 USA.
EM lpani@partners.org
FU National Heart, Lung and Blood Institute's Framingham Heart Study
(National Heart, Lung and Blood Institute/National Institutes of Health)
[N01-HC-25195]; Boston University School of Medicine; American Diabetes
Association Career Development Award; National Institute of Diabetes and
Digestive and Kidney Diseases [K24 DK080140]; Earl P. Charlton Fund for
Innovative Diabetes Research; National Research Service Award [T32]
FX This work was supported by the National Heart, Lung and Blood
Institute's Framingham Heart Study (National Heart, Lung and Blood
Institute/National Institutes of Health Contract N01-HC-25195) and
Boston University School of Medicine. J.B.M. is supported by an American
Diabetes Association Career Development Award and National Institute of
Diabetes and Digestive and Kidney Diseases Grant K24 DK080140D.M.N. is
supported in part by the Earl P. Charlton Fund for Innovative Diabetes
Research. L.P. is supported by an institutional National Research
Service Award (T32).; We thank Peter Shrader and Sharon Saydah for
assistance with Statistical analyses. For contribution to the study, we
thank Deborah Wexler, Diana Berger, Randie Little, Eran Bellin, and Curt
Rohlfing.
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U2 9
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2008
VL 31
IS 10
BP 1991
EP 1996
DI 10.2337/dc08-0577
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 360FR
UT WOS:000260043600013
PM 18628569
ER
PT J
AU Shearer, J
Duggan, G
Weljie, A
Hittel, DS
Wasserman, DH
Vogel, HJ
AF Shearer, J.
Duggan, G.
Weljie, A.
Hittel, D. S.
Wasserman, D. H.
Vogel, H. J.
TI Metabolomic profiling of dietary-induced insulin resistance in the high
fat-fed C57BL/6J mouse
SO DIABETES OBESITY & METABOLISM
LA English
DT Article
DE dietary induced; insulin; metabolomics; NMR; obesity
ID INDUCED OBESITY; MICE; PLASMA; ACID; RATS; PREDICTION; EXERCISE;
STRAINS; PATTERN
AB The predictive ability of metabolic profiling to detect obesity-induced perturbations in metabolism has not been clearly established. Complex aetiologies interacting with environmental factors highlight the need to understand how specific manipulations alter metabolite profiles in this state. The aim of this study was to determine if targeted metabolomic profiling could be employed as a reliable tool to detect dietary-induced insulin resistance in a small subset of experimental animals (n = 10/treatment). Following weaning, male C57BL/6J littermates were randomly divided into two dietary groups: chow and high fat. Following 12 weeks of dietary manipulation, mice were fasted for 5 h prior to serum collection. The resultant high fat-fed animals were obese and insulin resistant as shown by a euglycaemic-hyperinsulinaemic clamp. Sera were analysed by proton nuclear magnetic resonance spectroscopy, and 46 known compounds were identified and quantified. Multivariate analysis by orthogonal partial least squares discriminant analysis, a projection method for class separation, was then used to establish models of each treatment. Models were able to predict class separation between diets with 90% accuracy. Variable importance plots revealed the most important metabolites in this discrimination to include lysine, glycine, citrate, leucine, suberate and acetate. These metabolites are involved in energy metabolism and may be representative of the perturbations taking place with insulin resistance. Results show metabolomics to reliably describe the metabolic effects of insulin resistance in a small subset of samples and are an initial step in establishing metabolomics as a tool to understand the biochemical signature of insulin resistance.
C1 [Shearer, J.; Hittel, D. S.] Univ Calgary, Fac Kinesiol, Calgary, AB T2N 1N4, Canada.
[Shearer, J.] Univ Calgary, Fac Med, Dept Biochem & Mol Biol, Calgary, AB T2N 1N4, Canada.
[Duggan, G.; Weljie, A.; Vogel, H. J.] Univ Calgary, Bio NMR Ctr, Dept Biol Sci, Calgary, AB T2N 1N4, Canada.
[Wasserman, D. H.] Vanderbilt Univ, Sch Med, Mouse Metab Phenotyping Ctr, Dept Mol Physiol & Biophys, Nashville, TN 37212 USA.
RP Shearer, J (reprint author), Univ Calgary, Fac Kinesiol, 2500 Univ Dr NW,KIN 306, Calgary, AB T2N 1N4, Canada.
EM jshearer@ucalgary.ca
RI Weljie, Aalim/B-6203-2012
FU Alberta Heritage Foundation for Medical Research; Heart and Stroke
Foundation of Canada; Canadian Institutes for Health Research; National
Science and Engineering Council of Canada; Genome Canada; National
Institutes of Health [U24 DK-59637, RO1 DK-54902]
FX We gratefully acknowledge the technical assistance of Ria Driessen, Lin
Su and Olivia T. Brusslers. The encouragement and guidance of Dr David
Wishart and Dr Christoph Sensen were greatly appreciated. Supported by
the Alberta Heritage Foundation for Medical Research (J. S. and H. J.
V.), the Heart and Stroke Foundation of Canada (J. S.), the Canadian
Institutes for Health Research (J. S. and H. J. V.), the National
Science and Engineering Council of Canada (H. J. V.) and Genome Canada
(J. S.). D. H. W. is supported by National Institutes of Health Grants
U24 DK-59637 and RO1 DK-54902. No other known disclosures or potential
conflicts to declare.
NR 36
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U2 15
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1462-8902
J9 DIABETES OBES METAB
JI Diabetes Obes. Metab.
PD OCT
PY 2008
VL 10
IS 10
BP 950
EP 958
DI 10.1111/j.1463-1326.2007.00837.x
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 348UU
UT WOS:000259236400015
PM 18215169
ER
PT J
AU Yan, SS
Schreckenberger, PC
Zheng, XT
Nelson, NA
Harrington, SM
Tjhio, J
Fedorko, DP
AF Yan, S. Steve
Schreckenberger, Paul C.
Zheng, Xiaotian
Nelson, Nancy A.
Harrington, Susan M.
Tjhio, Joyce
Fedorko, Daniel P.
TI An intrinsic pattern of reduced susceptibility to fluoroquinolones in
pediatric isolates of Streptococcus pyogenes
SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE
LA English
DT Article
DE Sireptococcus pyogenes; pediatric isolates; M/emm type;
fluoroquinolones; resistance; point mutation
ID CLONAL SPREAD; EMM TYPES; RESISTANCE; CIPROFLOXACIN; PNEUMONIAE; PARC;
MUTATIONS; SPAIN; GYRA
AB A total of H 6 clinical isolates collected in 2003 from a tertiary pediatric hospital and a primary pediatric department in Chicago, IL, were screened for reduced susceptibility to selected fluoroquinolones by disc diffusion. Correlation between reduced susceptibility and point Mutations In the quinolone resistance-determining region of parC and gyr4 genes was evaluated, and point mutations were compared with other reports of isolates derived from adult or mixed patient populations. Nine percent of isolates had reduced susceptibility to I or more of these fluoroquinolones by Etest: ciprofloxacin, levofloxacin, and moxifloxacin. A single point mutation (Ser-79) in parC seemed responsible for the reduced susceptibility. Resistant Streptococcus pyogenes isolates were compared using M/emm type, repetitive sequence-based PCR (rep-PCR). and pulsed-field gel electrophoresis (PFGE). Rep-PCR provided no more separation of strains than M/emm typing, and PFGE results with SgrAl were more discriminatory than with Smal. The majority of these isolates were M/emm type 6. PFGE analysis using SgrAl demonstrated 2 different resistant strains among the M/emm type 6 isolates. The findings suggest that a population of S. pyogenes with an intrinsic reduced Susceptibility to fluoroquinolones exists in pediatric clinical isolates. Monitoring of amino acid changes in both parC and gyrA will assist in the prediction of emergence of high-level fluoroquinolone resistance. Published by Elsevier Inc.
C1 [Fedorko, Daniel P.] NIH, Ctr Clin, Dept Lab Med, DHHS, Bethesda, MD 20892 USA.
[Yan, S. Steve] US FDA, DHHS, Rockville, MD 20855 USA.
[Schreckenberger, Paul C.; Tjhio, Joyce] Univ Illinois, Med Ctr, Chicago, IL 60612 USA.
[Zheng, Xiaotian] Childrens Mem Hosp, Chicago, IL 60614 USA.
RP Fedorko, DP (reprint author), NIH, Ctr Clin, Dept Lab Med, DHHS, Bldg 10, Bethesda, MD 20892 USA.
EM dfedorko@mail.cc.nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 15
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U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0732-8893
J9 DIAGN MICR INFEC DIS
JI Diagn. Microbiol. Infect. Dis.
PD OCT
PY 2008
VL 62
IS 2
BP 205
EP 209
DI 10.1016/j.diagmicrobio.2008.04.018
PG 5
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA 356SG
UT WOS:000259797300014
PM 18554840
ER
PT J
AU Peng, XQ
Li, X
Li, J
Ramachandran, PV
Gagare, PD
Pratihar, D
Ashby, CR
Gardner, EL
Xi, ZX
AF Peng, Xiao-Qing
Li, Xia
Li, Jie
Ramachandran, P. Veeraraghavan
Gagare, Pravin D.
Pratihar, Debarshi
Ashby, Charles R., Jr.
Gardner, Eliot L.
Xi, Zheng-Xiong
TI Effects of gabapentin on cocaine self-administration, cocaine-triggered
relapse and cocaine-enhanced nucleus accumbens dopamine in rats
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article; Proceedings Paper
CT 68th Annual Scientific Meeting of the
College-on-Problems-of-Drug-Dependence
CY JUN 17-22, 2006
CL Scottsdale, AZ
SP Problems Drug Dependence
DE gabapentin; cocaine; dopamine; GABA; self-administration; relapse
ID GAMMA-VINYL-GABA; METHADONE-TREATED PATIENTS; PLACEBO-CONTROLLED TRIAL;
ATTENUATES COCAINE; BEHAVIORAL SENSITIZATION; ANTICONVULSANT DRUGS;
LOCOMOTOR-ACTIVITY; AMINOBUTYRIC-ACID; MIMETIC DRUGS; DEPENDENCE
AB Gabapentin is a gamma-aminobutyric acid (GABA) analogue, with GABAmimetic pharmacological properties. Gabapentin is used for the treatment of seizures, anxiety and neuropathic pain. It has been proposed that gabapentin may be useful in the treatment of cocaine dependence. However, clinical trials with gabapentin have shown conflicting results, while preclinical studies are sparse. In the present Study, we investigated the effects of gabapentin on intravenous cocaine self-administration and cocaine-triggered reinstatement of drug-seeking behavior, as well as on cocaine-enhanced dopamine (DA) in the nucleus accumbens (NAc). We found that gabapentin (25-200 mg/kg, i.p., 30 thin or 2 h prior to cocaine) failed to inhibit intravenous cocaine (0.5 mg/kg/infusion) self-administration under a fixed-ratio reinforcement schedule or cocaine-triggered reinstatement of cocaine-seeking behavior. fit vivo microdialysis showed that the same doses of gabapentin produced a modest increase (similar to 50%, p < 0.05) in extracellular NAc GABA levels, but failed to alter either basal or cocaine-enhanced NAc DA. These data suggest that gabapentin is a weak GABA-mimic drug. At the doses tested, it has no effect in the addiction-related animal behavioral models here tested. This is in striking contrast to positive findings in the same animal models shown by another GABAmimetic -gamma-vinyl GABA (see companion piece to present article). Published by Elsevier Ireland Ltd.
C1 [Peng, Xiao-Qing; Li, Xia; Li, Jie; Gardner, Eliot L.; Xi, Zheng-Xiong] Natl Inst Drug Abuse, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Ramachandran, P. Veeraraghavan; Gagare, Pravin D.; Pratihar, Debarshi] Purdue Univ, Herbert C Brown Ctr Borane Res, Dept Chem, W Lafayette, IN 47907 USA.
[Ashby, Charles R., Jr.] St Johns Univ, Dept Pharmaceut Sci, Coll Pharm & Allied Hlth Profess, Jamaica, NY 11439 USA.
RP Xi, ZX (reprint author), 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM zxi@intra.nida.nih.gov
OI PENG, XIAOQING/0000-0002-7272-5428
FU Intramural NIH HHS [Z01 DA000474-03, Z99 DA999999]
NR 60
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U2 5
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0376-8716
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD OCT 1
PY 2008
VL 97
IS 3
BP 207
EP 215
DI 10.1016/j.drugalcdep.2007.09.019
PG 9
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 353IT
UT WOS:000259560600002
PM 18065162
ER
PT J
AU Peng, XQ
Li, X
Gilbert, JG
Pak, AC
Ashby, CR
Brodie, JD
Dewey, SL
Gardner, EL
Xi, ZX
AF Peng, Xiao-Qing
Li, Xia
Gilbert, Jeremy G.
Pak, Arlene C.
Ashby, Charles R., Jr.
Brodie, Jonathan D.
Dewey, Stephen L.
Gardner, Eliot L.
Xi, Zheng-Xiong
TI Gamma-vinyl GABA inhibits cocaine-triggered reinstatement of
drug-seeking behavior in rats by a non-dopaminergic mechanism
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE cocaine; dopamine; GABA; gamma-vinyl GABA; reinstatement; relapse
ID AMINOBUTYRIC-ACID TRANSAMINASE; SELF-ADMINISTRATION BEHAVIOR; VENTRAL
TEGMENTAL AREA; NUCLEUS-ACCUMBENS; DOPAMINE RELEASE; BRAIN REWARD;
SYNAPTIC-TRANSMISSION; MOLECULAR-MECHANISMS; RECEPTORS; ADDICTION
AB Relapse to drug use is a core feature of addiction. Previous studies demonstrate that -gamma-vinyl GABA (GVG), an irreversible GABA transaminase inhibitor, attenuates the acute rewarding effects of cocaine and other addictive drugs. We here report that systemic administration of GVG (25-300 mg/kg) close-dependently inhibits cocaine- or sucrose-induced reinstatement of reward-seeking behavior in rats. In vivo microdialysis data indicated that the same doses of GVG close-dependently elevate extracellular GABA levels in the nucleus accumbens (NAc). However, GVG; when administered systemically or locally into the NAc, failed to inhibit either basal or cocaine-priming enhanced NAc dopamine in either naive rats or cocaine extinction rats. These data suggest that: (1) GVG significantly inhibits cocaine- or sucrose-triggered reinstatement of reward-seeking behavior: and (2) a GABAergic-, but not dopaminergic-, dependent mechanism may underlie the antagonism by GVG of cocaine-triggered reinstatement of drug-seeking behavior, at least with respect to GVG's action on the NAc. Published by Elsevier Ireland Ltd.
C1 [Peng, Xiao-Qing; Li, Xia; Gilbert, Jeremy G.; Pak, Arlene C.; Gardner, Eliot L.; Xi, Zheng-Xiong] Natl Inst Drug Abuse, Neuropsychopharmacol Sect, Intramural Res Program, NIH,DHHS, Baltimore, MD 21224 USA.
[Ashby, Charles R., Jr.] St Johns Univ, Dept Pharmaceut Sci, Jamaica, NY 11439 USA.
[Brodie, Jonathan D.] NYU, Sch Med, Dept Psychiat, New York, NY 10016 USA.
[Dewey, Stephen L.] Brookhaven Natl Lab, Dept Med, Upton, NY 11973 USA.
RP Xi, ZX (reprint author), Natl Inst Drug Abuse, Neuropsychopharmacol Sect, Intramural Res Program, NIH,DHHS, Baltimore, MD 21224 USA.
EM zxi@intra.nida.nih.gov
OI Brodie, Jonathan/0000-0002-2254-8654; PENG, XIAOQING/0000-0002-7272-5428
FU National Institute on Drug Abuse (NIDA); National Institutes of Health
(NIH); U.S. Public Health Service (PHS); U.S. Department of Health and
Human Services (DHHS); Aaron Diamond Foundation of New York City; Old
Stones Foundation of Greenwich, Connecticut; Medical and Chemistry
Departments of the Brookhaven National Laboratory, Upton, New York
FX Funding for this study was provided by funds from the Intramural
Research Program of the National Institute on Drug Abuse (NIDA),
National Institutes of Health (NIH), U.S. Public Health Service (PHS),
U.S. Department of Health and Human Services (DHHS). Preliminary
planning of these experiments was supported by research grants from the
Aaron Diamond Foundation of New York City and from the Old Stones
Foundation of Greenwich, Connecticut, and by funds from the Medical and
Chemistry Departments of the Brookhaven National Laboratory, Upton, New
York. .
NR 48
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U1 0
U2 3
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0376-8716
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD OCT 1
PY 2008
VL 97
IS 3
BP 216
EP 225
DI 10.1016/j.drugalcdep.2007.10.004
PG 10
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 353IT
UT WOS:000259560600003
PM 18063319
ER
PT J
AU Berger, G
Wood, S
Ross, M
Yung, AR
Nelson, B
Hamer, C
Phillips, L
Amminger, P
Jackson, G
Pantelis, C
Husseini, M
McGorry, P
AF Berger, G.
Wood, S.
Ross, M.
Yung, A. R.
Nelson, B.
Hamer, C.
Phillips, L.
Amminger, P.
Jackson, G.
Pantelis, C.
Husseini, M.
McGorry, P.
TI Neuroprotective effects of low dose lithium in individuals at ultra-high
risk for psychosis
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Berger, G.; Wood, S.; Ross, M.; Yung, A. R.; Nelson, B.; Hamer, C.; Phillips, L.; Amminger, P.; Jackson, G.; McGorry, P.] Univ Melbourne, ORYGEN Res Ctr, Melbourne, Vic 3010, Australia.
[Berger, G.] Univ Basel Hosp, Basel, Switzerland.
Sunshine Hosp, Melbourne Neuropsychiat Ctr, Melbourne, Vic, Australia.
[Amminger, P.] Med Univ Vienna, Dept Child & Adolescent Neuropsychiat, Vienna, Austria.
[Husseini, M.] NIMH, Bethesda, MD 20892 USA.
RI Pantelis, Christos/H-7722-2014
OI Pantelis, Christos/0000-0002-9565-0238
NR 0
TC 4
Z9 4
U1 1
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1751-7885
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD OCT
PY 2008
VL 2
BP A28
EP A28
PG 1
WC Psychiatry
SC Psychiatry
GA 449PB
UT WOS:000266341400108
ER
PT J
AU Khanna, C
AF Khanna, C.
TI How naturally occurring cancers in dogs can inform the drug development
path
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Khanna, C.] NCI, Pediat Oncol Branch, Tumor & Metastasis Biol Sect, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 7
EP 7
DI 10.1016/S1359-6349(08)71941-4
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200011
ER
PT J
AU Collins, J
AF Collins, J.
TI Use of phase 0-changes in cancer drug development
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Collins, J.] NCI, Dev Therapeut Programme, Rockville, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 10
EP 11
DI 10.1016/S1359-6349(08)71953-0
PG 2
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200022
ER
PT J
AU Eisenhauer, E
Therasse, P
Bogaerls, J
Schwartz, L
Sargent, D
Ford, R
Dancey, J
Arbuck, S
Gwyther, S
Mooney, M
Rubenstein, L
Shankar, L
Kaplan, R
Lacombe, D
Verweij, J
AF Eisenhauer, E.
Therasse, P.
Bogaerls, J.
Schwartz, L.
Sargent, D.
Ford, R.
Dancey, J.
Arbuck, S.
Gwyther, S.
Mooney, M.
Rubenstein, L.
Shankar, L.
Kaplan, R.
Lacombe, D.
Verweij, J.
TI New response evaluation criteria in solid tumors: revised RECIST
guideline version 1.1
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Eisenhauer, E.] Canc Res Inst, NCIC Clin Trials Grp, Kingston, ON, Canada.
[Therasse, P.] GlaxoSmithKline Inc, Brussels, Belgium.
[Bogaerls, J.; Lacombe, D.] European Org Res Treatment Canc, Ctr Data, Brussels, Belgium.
[Schwartz, L.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Sargent, D.] Mayo Clin, Rochester, MN USA.
[Ford, R.] RadPharm, Princeton, NJ USA.
[Dancey, J.; Mooney, M.; Rubenstein, L.; Shankar, L.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Arbuck, S.] Schering Plough Corp, Kenilworth, NJ 07033 USA.
[Gwyther, S.] E Surrey Hosp, Surrey, England.
[Kaplan, R.] Natl Canc Res Network, Leeds, W Yorkshire, England.
[Verweij, J.] Erasmus Univ, Med Ctr, Rotterdam, Netherlands.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 13
EP 13
DI 10.1016/S1359-6349(08)71964-5
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200030
ER
PT J
AU Chiu, Y
Rudin, CM
Shapiro, GI
Roberts, AW
Brown, JR
Wilson, W
O'Connor, O
Xiong, H
Enschede, S
Krivoshik, A
AF Chiu, Y.
Rudin, C. M.
Shapiro, G. I.
Roberts, A. W.
Brown, J. R.
Wilson, W.
O'Connor, O.
Xiong, H.
Enschede, S.
Krivoshik, A.
TI Advantages of a modified continual reassessment method (CRM) for dose
finding studies: experience in ongoing phase I trials with ABT-263
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Chiu, Y.] Abbott Labs, Clin Pharmacol & Pharmacometr, Abbott Pk, IL 60064 USA.
[Rudin, C. M.] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Shapiro, G. I.; Brown, J. R.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Roberts, A. W.] Royal Melbourne Hosp, Dept Clin Haematol & Med Oncol, Parkville, Vic 3050, Australia.
[Wilson, W.] NCI, Canc Res Ctr, Bethesda, MD 20892 USA.
[O'Connor, O.] Columbia Univ, Herbert Irving Comprehens Canc Ctr, New York, NY USA.
[Xiong, H.; Enschede, S.; Krivoshik, A.] Abbott Labs, Abbott Oncol, Abbott Pk, IL 60064 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 14
EP 14
DI 10.1016/S1359-6349(08)71966-9
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200032
ER
PT J
AU Chen, J
Bai, L
Nikolovska-Coleska, Z
Zhang, J
Gomez, C
Yi, H
Krajewsk, K
Jiang, S
Roller, P
Wang, S
AF Chen, J.
Bai, L.
Nikolovska-Coleska, Z.
Zhang, J.
Gomez, C.
Yi, H.
Krajewsk, K.
Jiang, S.
Roller, P.
Wang, S.
TI Design, synthesis, biochemical and biological evaluations of novel and
potent small-molecule inhibitors of STAT3
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Chen, J.; Bai, L.; Nikolovska-Coleska, Z.; Zhang, J.; Gomez, C.; Yi, H.; Wang, S.] Univ Michigan Hlth Syst, Ann Arbor, MI USA.
[Krajewsk, K.; Jiang, S.; Roller, P.] NIH, Med Chem Lab, Frederick, MD USA.
NR 0
TC 3
Z9 3
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 45
EP 45
DI 10.1016/S1359-6349(08)72070-6
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200136
ER
PT J
AU Sharifi, N
Hurt, EM
Thomas, S
Farrar, WL
AF Sharifi, N.
Hurt, E. M.
Thomas, S.
Farrar, W. L.
TI Effects of SOD2 silencing on androgen receptor function and gene
regulation: implications for castration-resistant prostate cancer
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Sharifi, N.] UT SW Med Ctr, Dallas, TX USA.
[Hurt, E. M.; Farrar, W. L.] Natl Canc Inst, Canc Stem Cell Sect, Frederick, MD USA.
[Thomas, S.] SAIC Frederick, Basic Res Program, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 52
EP 52
DI 10.1016/S1359-6349(08)72094-9
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200160
ER
PT J
AU Monks, A
Turbyville, T
Harris, ED
Kaas, B
Beutler, JA
AF Monks, A.
Turbyville, T.
Harris, E. D.
Kaas, B.
Beutler, J. A.
TI Eph receptor A2 modulation in human glioma cell lines by the natural
product, Schweinfurthin A
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Monks, A.; Turbyville, T.; Harris, E. D.] SAIC Frederick Inc, Natl Canc Inst, Frederick, MD USA.
[Kaas, B.; Beutler, J. A.] NCI, Mol Targets Dev Program, Frederick, MD 21701 USA.
RI Beutler, John/B-1141-2009
OI Beutler, John/0000-0002-4646-1924
NR 0
TC 0
Z9 0
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 57
EP 57
DI 10.1016/S1359-6349(08)72110-4
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200176
ER
PT J
AU Houghton, PJ
Morton, CL
Maris, JM
Keir, ST
Lock, RB
Carol, H
Gorlick, R
Kolb, EA
Kang, MH
Smith, MA
AF Houghton, P. J.
Morton, C. L.
Maris, J. M.
Keir, S. T.
Lock, R. B.
Carol, H.
Gorlick, R.
Kolb, E. A.
Kang, M. H.
Smith, M. A.
TI Pediatric Preclinical Testing Program (PPTP) evaluation of rapamycin
combined with cytotoxic drugs used frequently in treatment of childhood
cancer
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Smith, M. A.] NCI, Canc Treatment Evaluat Program, Bethesda, MD 20892 USA.
[Kang, M. H.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Gorlick, R.; Kolb, E. A.] Albert Einstein Coll, Bronx, NY USA.
[Lock, R. B.; Carol, H.] Childrens Canc Inst, Randwick, NSW, Australia.
[Keir, S. T.] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Maris, J. M.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Houghton, P. J.; Morton, C. L.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
RI Carol, Hernan/F-5750-2013
OI Carol, Hernan/0000-0002-9443-8032
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 60
EP 60
DI 10.1016/S1359-6349(08)72122-0
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200188
ER
PT J
AU Morton, CL
Houghton, PJ
Maris, JM
Gorlick, R
Kolb, EA
Kang, MH
Reynolds, CP
Smith, MA
AF Morton, C. L.
Houghton, P. J.
Maris, J. M.
Gorlick, R.
Kolb, E. A.
Kang, M. H.
Reynolds, C. P.
Smith, M. A.
TI Pediatric Preclinical Testing Program (PPTP) evaluation of the oncolytic
picornavirus, NTX-010 (SVV-001)
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Smith, M. A.] NCI, Canc Therapy & Evaluat Program, Bethesda, MD 20892 USA.
[Kang, M. H.; Reynolds, C. P.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Kolb, E. A.] Alfred I DuPont Hosp Children, Wilmington, DE USA.
[Gorlick, R.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Maris, J. M.] Childrens Hosp Philadelphia, Philadelphia, PA USA.
[Morton, C. L.; Houghton, P. J.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 60
EP 60
DI 10.1016/S1359-6349(08)72123-2
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200189
ER
PT J
AU Lock, R
Carol, H
Houghton, P
Morton, C
Phelps, D
Tucker, C
Payne-Turner, D
Zuany-Amorim, C
Smith, M
AF Lock, R.
Carol, H.
Houghton, P.
Morton, C.
Phelps, D.
Tucker, C.
Payne-Turner, D.
Zuany-Amorim, C.
Smith, M.
TI Pediatric Preclinical Testing Program (PPTP) evaluation of the
anti-CD19-DM4 conjugated antibody SAR3419
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Smith, M.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Zuany-Amorim, C.] Sanofi Aventis, Expt Therapeut & Translat Res, Vitry Sur Seine, France.
[Houghton, P.; Morton, C.; Phelps, D.; Tucker, C.; Payne-Turner, D.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Lock, R.; Carol, H.] Children Canc Inst Australia, Leukaemia Biol Program, Sydney, NSW, Australia.
RI Carol, Hernan/F-5750-2013
OI Carol, Hernan/0000-0002-9443-8032
NR 0
TC 2
Z9 2
U1 0
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 61
EP 61
DI 10.1016/S1359-6349(08)72124-4
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200190
ER
PT J
AU Mackay, H
Tinker, A
Winquist, E
Thomas, G
Sederias, J
Ivy, P
Eisenhauer, EA
AF Mackay, H.
Tinker, A.
Winquist, E.
Thomas, G.
Sederias, J.
Ivy, P.
Eisenhauer, E. A.
TI A phase II study of sunitinib, an oral multi-targeted tyrosine kinase
inhibitor, in patients with unresectable, locally advanced or metastatic
cervical carcinoma: IND184
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Sederias, J.; Eisenhauer, E. A.] Natl Canc Inst Canada CTG, Kingston, ON, Canada.
[Mackay, H.] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Tinker, A.] BC Canc Agcy, Med Oncol, Vancouver, BC, Canada.
[Winquist, E.] London Reg Canc Ctr, London, ON N6A 4L6, Canada.
[Thomas, G.] Sunnybrook Reg Canc Ctr, Toronto, ON, Canada.
[Ivy, P.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 66
EP 66
DI 10.1016/S1359-6349(08)72140-2
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200206
ER
PT J
AU Smith, MA
Houghton, PJ
Morton, CL
Maris, JM
Courtright, J
Carol, H
Lock, RB
Yang, Y
Manfredi, MG
AF Smith, M. A.
Houghton, P. J.
Morton, C. L.
Maris, J. M.
Courtright, J.
Carol, H.
Lock, R. B.
Yang, Y.
Manfredi, M. G.
TI Pediatric Preclinical Testing Program (PPTP) stage 2 testing of the
Aurora A kinase inhibitor MLN8237
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Houghton, P. J.; Morton, C. L.] St Jude Childrens Hosp, Dept Mol Pharmacol, Memphis, TN 38105 USA.
[Smith, M. A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Maris, J. M.; Courtright, J.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Carol, H.; Lock, R. B.] Childrens Canc Inst Australia, Leukaemia Biol Program, Randwick, NSW, Australia.
RI Carol, Hernan/F-5750-2013
OI Carol, Hernan/0000-0002-9443-8032
NR 0
TC 1
Z9 1
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 92
EP 93
DI 10.1016/S1359-6349(08)72220-1
PG 2
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200285
ER
PT J
AU Sei, S
Mussio, J
Borgel, S
Hollingshead, M
AF Sei, S.
Mussio, J.
Borgel, S.
Hollingshead, M.
TI In vivo efficacy and replication dynamics of intravenously administered
oncolytic reovirus in nude mice bearing human melanoma xenografts
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Sei, S.; Mussio, J.; Borgel, S.] SAIC Frederick Inc, NCI Frederick, DTP, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 95
EP 96
DI 10.1016/S1359-6349(08)72231-6
PG 2
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200296
ER
PT J
AU Ho, J
Strevel, E
Chau, N
Pond, GR
Murgo, A
Ivy, P
Siu, LL
AF Ho, J.
Strevel, E.
Chau, N.
Pond, G. R.
Murgo, A.
Ivy, P.
Siu, L. L.
TI Comparison of phase I trial (P1T) abstract quality between the
EORTC-NCI-AACR and ASCO meetings
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Ho, J.; Strevel, E.; Chau, N.; Pond, G. R.; Siu, L. L.] Princess Margaret Hosp, Div Med Oncol & Haematol, Toronto, ON M4X 1K9, Canada.
[Murgo, A.; Ivy, P.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 120
EP 120
DI 10.1016/S1359-6349(08)72316-4
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200381
ER
PT J
AU Phatak, P
Daniels, CM
Shields, AF
Collins, JM
LoRusso, PM
Burger, AM
AF Phatak, P.
Daniels, C. M.
Shields, A. F.
Collins, J. M.
LoRusso, P. M.
Burger, A. M.
TI The role of thymidine kinase and thymidylate synthase in the response of
tumor cells to the suicide prodrug 2 '-F-ara-deoxyuridine
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [LoRusso, P. M.] Wayne State Univ, Karmanos Canc Inst, Internal Med Div Hematol & Oncol, Detroit, MI USA.
[Shields, A. F.; Collins, J. M.] NCI, Dev Therapeut Program, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 150
EP 150
DI 10.1016/S1359-6349(08)72402-9
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200465
ER
PT J
AU Kil, W
Camphausen, K
AF Kil, W.
Camphausen, K.
TI Enhancement of cell motility with radiation-induced VEGF in glioma
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Kil, W.; Camphausen, K.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 172
EP 172
DI 10.1016/S1359-6349(08)72479-0
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200542
ER
PT J
AU Grade, M
Hummon, AB
Camps, J
Emons, G
Spitzner, M
Gaedcke, J
Difilippantonio, MJ
Ghadimi, BM
Caplen, NJ
Ried, T
AF Grade, M.
Hummon, A. B.
Camps, J.
Emons, G.
Spitzner, M.
Gaedcke, J.
Difilippantonio, M. J.
Ghadimi, B. M.
Caplen, N. J.
Ried, T.
TI RNAi-based identification of potential targets in colorectal cancers
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Hummon, A. B.; Camps, J.; Difilippantonio, M. J.; Caplen, N. J.; Ried, T.] NCI, Genet Branch, Bethesda, MD 20892 USA.
[Grade, M.; Emons, G.; Spitzner, M.; Gaedcke, J.; Ghadimi, B. M.] Univ Gottingen, Gottingen, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 174
EP 174
DI 10.1016/S1359-6349(08)72485-6
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200548
ER
PT J
AU Rao, VA
Klein, S
Agama, K
Pommier, Y
Shacter, E
AF Rao, V. A.
Klein, S.
Agama, K.
Pommier, Y.
Shacter, E.
TI The iron chelator di-2-pyridylketone-4,4,-dimethyl-3-thiosemicarbazone
causes DNA damage in breast cancer cells
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT 20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics
CY OCT 21-24, 2008
CL Geneva, SWITZERLAND
SP EORTC, NCI, AACR
C1 [Rao, V. A.; Klein, S.; Shacter, E.] US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA.
[Agama, K.; Pommier, Y.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1359-6349
J9 EJC SUPPL
JI EJC Suppl.
PD OCT
PY 2008
VL 6
IS 12
BP 187
EP 187
DI 10.1016/S1359-6349(08)72533-3
PG 1
WC Oncology
SC Oncology
GA 376ZJ
UT WOS:000261221200596
ER
PT J
AU Sanchez-Lemus, E
Murakami, Y
Larrayoz-Roldan, IM
Moughamian, AJ
Pavel, J
Nishioku, T
Saavedra, JM
AF Sanchez-Lemus, Enrique
Murakami, Yuki
Larrayoz-Roldan, Ignacio M.
Moughamian, Armen J.
Pavel, Jaroslav
Nishioku, Tsuyoshi
Saavedra, Juan M.
TI Angiotensin II AT(1) receptor blockade decreases
lipopolysaccharide-induced inflammation in the rat adrenal gland
SO ENDOCRINOLOGY
LA English
DT Article
ID SPONTANEOUSLY HYPERTENSIVE-RATS; INCREASES INTERLEUKIN-6 RELEASE;
NECROSIS-FACTOR RELEASE; ZONA GLOMERULOSA CELLS; RECEPTOR BLOCKADE;
ALDOSTERONE BIOSYNTHESIS; BRAIN MICROVESSELS; ISOLATION STRESS;
GENE-EXPRESSION; DOWN-REGULATION
AB Peripheral administration of bacterial endotoxin [lipopolysaccharide (LPS)] to rodents produces an innate immune response and hypothalamic-pituitary-adrenal axis stimulation. Renin-angiotensin-aldosterone system inhibition by angiotensin II AT(1) receptor blockade has antiinflammatory effects in the vasculature. We studied whether angiotensin II receptor blockers (ARBs) prevent the LPS response. We focused on the adrenal gland, one organ responsive to LPS and expressing a local renin-angiotensin-aldosterone system. LPS (50 mu g/kg, ip) produced a generalized inflammatory response with increased release of TNF-alpha and IL-6 to the circulation, enhanced adrenal aldosterone synthesis and release, and enhanced adrenal cyclooxygenase-2, IL-6, and TNF-alpha gene expression. ACTH and corticosterone release were also increased by LPS. Pretreatment with the ARB candesartan (1 mg/kg.d, sc for 3 d before the LPS administration) decreased LPS-induced cytokine release to the circulation, adrenal aldosterone synthesis and release, and cyclooxygenase-2 and IL-6 gene expression. Candesartan did not prevent the LPS-induced ACTH and corticosterone release. Our results suggest that AT1 receptors are essential for the development of the full innate immune and stress responses to bacterial endotoxin. The ARB decreased the general peripheral inflammatory response to LPS, partially decreased the inflammatory response in the adrenal gland, prevented the release of the pro-inflammatory hormone aldosterone, and protected the antiinflammatory effects of glucocorticoid release. An unrestricted innate immune response to the bacterial endotoxin may have deleterious effects for the organism and may lead to development of chronic inflammatory disease. We postulate that the ARBs may have therapeutic effects on inflammatory conditions.
C1 [Sanchez-Lemus, Enrique] NIMH, NIH, Div Intramural Res Programs, Dept Hlth & Human Serv,Sect Pharmacol, Bethesda, MD 20892 USA.
RP Sanchez-Lemus, E (reprint author), NIMH, NIH, Div Intramural Res Programs, Dept Hlth & Human Serv,Sect Pharmacol, 10 Ctr Dr,MSC 1514,Bldg 10,Room 2D57, Bethesda, MD 20892 USA.
EM sancheze@mail.nih.gov
RI Larrayoz, Ignacio/I-5613-2012
OI Larrayoz, Ignacio/0000-0003-1629-152X
FU Division of Intramural Research Programs; National Institute of Mental
Health; National Institutes of Health, Department of Health and Human
Services
FX This study was supported by the Division of Intramural Research
Programs, National Institute of Mental Health, National Institutes of
Health, Department of Health and Human Services.
NR 58
TC 31
Z9 35
U1 1
U2 4
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD OCT
PY 2008
VL 149
IS 10
BP 5177
EP 5188
DI 10.1210/en.2008-0242
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351BW
UT WOS:000259400300045
PM 18556352
ER
PT J
AU Manjanatha, MG
Shelton, SD
Dobrovolsky, VN
Shaddock, JG
McGarrity, LG
Doerge, DR
Twaddle, NW
Lin, CJ
Chen, JJ
Mattison, DR
Morrisi, SM
AF Manjanatha, Mugimane G.
Shelton, Sharon D.
Dobrovolsky, Vasily N.
Shaddock, Joseph G.
McGarrity, Lynda G.
Doerge, Daniel R.
Twaddle, Nathan W.
Lin, Chien-Ju
Chen, James J.
Mattison, Donald R.
Morrisi, Suzanne M.
TI Pharmacokinetics, Dose-Range, and Mutagenicity Studies of
Methylphenidate Hydrochloride in B6C3F1 Mice
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE methylphenidate hydrochloride; ritalinic acid; Hprt mutation;
micronucleus assay
ID MICRONUCLEUS TEST; ENANTIOMERS; DISORDER; MONKEY; RAT
AB Methylphenidate hydrochloride (MPH) is one of the most frequently prescribed pediatric drugs for the treatment of attention deficit hyperactivity disorder. In a recent study, increased hepatic adenomas were observed in B6C3F1 mice treated with MPH in their diet. To evaluate the reactive metabolite, ritalinic acid (RA) of MPH and its mode of action in mice, we conducted extensive investigations on the pharmacokinetics (PK) and genotoxicity of the drug in B6C3F1 mice. For the PK study, male B6C3F1 mice were gavaged once with 3 mg/kg body weight (BW) of MPH and groups of mice were sacrificed at various time points (0.25-24 hr) for serum analysis of MPH and RA concentrations. Groups of male B6C3F1 mice were fed diets containing 0, 250, 500, 1,000, 2,000, or 4,000 ppm of MPH for 28 days to determine the appropriate doses for 24-week transgenic mutation studies. Also, the micronucleus frequencies (MN-RETs and MN-NCEs), and the lymphocyte Hart mutants were determined in peripheral blood and splenic lymphocytes, respectively. Mice fed 4,000 ppm of MPH lost significant BW compared to control mice (P < 0.01). There was a significant increase in the average liver weights whereas kidneys, seminal vesicle, testes, thymus, and urinary bladder weights of mice fed higher doses of MPH were significantly lower than the control group (P < 0.05). There was no significant increase in either the Hprt mutant frequency or the micronucleus frequency in the treated animals. These results indicated that although MPH induced liver hypertrophy in mice, no genotoxicity was observed. Environ. Mol. Mutagen. 49:585-593, 2008. Published 2008 Wiley-Liss, Inc.
C1 [Manjanatha, Mugimane G.; Shelton, Sharon D.; Dobrovolsky, Vasily N.; Shaddock, Joseph G.; McGarrity, Lynda G.; Morrisi, Suzanne M.] US FDA, Natl Ctr Toxicol Res, Div Genet & Reprod Toxicol, Jefferson, AR 72079 USA.
[Doerge, Daniel R.; Twaddle, Nathan W.] US FDA, Natl Ctr Toxicol Res, Div Biochem Toxicol, Jefferson, AR 72079 USA.
[Lin, Chien-Ju; Chen, James J.] US FDA, Natl Ctr Toxicol Res, Div Personalized Med & Nutr, Jefferson, AR 72079 USA.
[Mattison, Donald R.] NICHD, NIH, Ctr Res Mothers & Children, Bethesda, MD USA.
RP Manjanatha, MG (reprint author), US FDA, Natl Ctr Toxicol Res, Div Genet & Reprod Toxicol, 3900 NCTR Rd, Jefferson, AR 72079 USA.
EM mugimane.manjanatha@fda.hhs.gov
RI Mattison, Donald/C-2015-2009; Mattison, Donald/L-4661-2013
OI Mattison, Donald/0000-0001-5623-0874
NR 24
TC 19
Z9 19
U1 0
U2 4
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PD OCT
PY 2008
VL 49
IS 8
BP 585
EP 593
DI 10.1002/em.20407
PG 9
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 363OO
UT WOS:000260276800001
PM 18618596
ER
PT J
AU Dellinger, B
D'Alessio, A
D'Anna, A
Ciajolo, A
Gullett, B
Henry, H
Keener, M
Lighty, J
Lomnicki, S
Lucas, D
Oberdorster, G
Pitea, D
Suk, W
Sarofim, A
Smith, KR
Stoeger, T
Tolbert, P
Wyzga, R
Zimmermann, R
AF Dellinger, Barry
D'Alessio, Antonio
D'Anna, Andrea
Ciajolo, Anna
Gullett, Brian
Henry, Heather
Keener, Mel
Lighty, JoAnn
Lomnicki, Slawomir
Lucas, Donald
Oberdorster, Gunter
Pitea, Demetrio
Suk, William
Sarofim, Adel
Smith, Kirk R.
Stoeger, Tobias
Tolbert, Paige
Wyzga, Ron
Zimmermann, Ralf
TI Combustion Byproducts and Their Health Effects: Summary of the 10(th)
International Congress
SO ENVIRONMENTAL ENGINEERING SCIENCE
LA English
DT Article
DE products of incomplete combustion; PICs, biomass combustion; persistent
free radicals; particulate matter; soot; NOC; nanoparticles; ultrafine
particles; dioxins; mercury; tobacco smoke
ID ULTRAFINE CARBON PARTICLES; POLYCYCLIC AROMATIC-HYDROCARBONS;
EMERGENCY-DEPARTMENT VISITS; PARTICULATE AIR-POLLUTION; FLIGHT
MASS-SPECTROMETRY; SMOKE EXPOSURE; ORGANIC-CARBON; SOOT FORMATION;
FLY-ASH; FINE
AB The 10th International Congress on Combustion Byproducts and their Health Effects was held in Ischia, Italy, from June 17-20, 2007. It is sponsored by the US NIEHS, NSF, Coalition for Responsible Waste Incineration (CRWI), and Electric Power Research Institute (EPRI). The congress focused on: the origin, characterization, and health impacts of combustion-generated fine and ultrafine particles; emissions of mercury and dioxins, and the development/ application of novel analytical/diagnostic tools. The consensus of the discussion was that particle-associated organics, metals, and persistent free radicals (PFRs) produced by combustion sources are the likely source of the observed health impacts of airborne PM rather than simple physical irritation of the particles. Ultrafine particle-induced oxidative stress is a likely progenitor of the observed health impacts, but important biological and chemical details and possible catalytic cycles remain unresolved. Other key conclusions were: (1) In urban settings, 70% of airborne fine particles are a result of combustion emissions and 50% are due to primary emissions from combustion sources, (2) In addition to soot, combustion produces one, possibly two, classes of nanoparticles with mean diameters of similar to 10 nm and similar to 1 nm. (3) The most common metrics used to describe particle toxicity, viz. surface area, sulfate concentration, total carbon, and organic carbon, cannot fully explain observed health impacts, (4) Metals contained in combustion-generated ultrafine and fine particles mediate formation of toxic air pollutants such as PCDD/F and PFRs. (5) The combination of metal-containing nanoparticles, organic carbon compounds, and PFRs can lead to a cycle generating oxidative stress in exposed organisms.
C1 [Dellinger, Barry; Lomnicki, Slawomir] Louisiana State Univ, Dept Chem, Baton Rouge, LA 70803 USA.
[D'Alessio, Antonio; D'Anna, Andrea] Univ Naples Federico 2, Dipartimento Ingn Chim, Naples, Italy.
[Ciajolo, Anna] CNR, Ist Ric Combust, I-80125 Naples, Italy.
[Gullett, Brian] US EPA, Off Res & Dev, Res Triangle Pk, NC 27711 USA.
[Henry, Heather; Suk, William] NIEHS, Div Extramural Res & Training, Res Triangle Pk, NC 27709 USA.
[Keener, Mel] CRWI, Washington, DC USA.
[Lighty, JoAnn; Sarofim, Adel] Univ Utah, Dept Chem Engn, Salt Lake City, UT 84112 USA.
[Lucas, Donald] Univ Calif Berkeley, Sch Publ Hlth, Lawrence Berkeley Natl Lab, Environm Hlth & Safety Div, Berkeley, CA 94720 USA.
[Oberdorster, Gunter] Univ Rochester, Dept Environm Med, Rochester, NY USA.
[Pitea, Demetrio] Univ Milano Bicocca, Dipartimento Sci Ambientali, Milan, Italy.
[Stoeger, Tobias; Zimmermann, Ralf] German Res Ctr Environm Hlth, Inst Ecol Chem, Hemholtz Zentrum Munchen, D-85764 Oberschleissheim, Germany.
[Tolbert, Paige] Emory Univ, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA.
[Wyzga, Ron] Elect Power Res Inst, Palo Alto, CA USA.
[Zimmermann, Ralf] Univ Rostock, Inst Chem, Chair Analyt Chem, D-18051 Rostock, Germany.
RP Dellinger, B (reprint author), Louisiana State Univ, Dept Chem, 413 Choppin Hall, Baton Rouge, LA 70803 USA.
EM barryd@lsu.edu
RI Tolbert, Paige/A-5676-2015; Stoger, Tobias/M-9861-2014; ciajolo,
anna/M-7850-2015;
OI Stoger, Tobias/0000-0002-2790-0389; ciajolo, anna/0000-0003-3882-4964;
D'Anna, Andrea/0000-0001-9018-3637
FU Analisi e Monitoraggio del Rischio Ambientale (AMRA); National Research
Council of Italy (CNR); Coalition for Responsible Waste Incineration
(CRWI); Electric Power Research Institute (EPRI); Louisiana State
University (LSU); National Institute of Environmental Health Sciences
(NIEHS); National Science Foundation (NSF); Universita degli Studi di
Napoli Federico II; University of California-Berkeley
FX We would like to acknowledge the sponsors of the conference for their
financial and organizational support: Analisi e Monitoraggio del Rischio
Ambientale (AMRA), National Research Council of Italy (CNR), Coalition
for Responsible Waste Incineration (CRWI), Electric Power Research
Institute (EPRI), Louisiana State University (LSU), National Institute
of Environmental Health Sciences (NIEHS), National Science Foundation
(NSF), Universita degli Studi di Napoli Federico II, and University of
California-Berkeley
NR 52
TC 3
Z9 3
U1 0
U2 21
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1092-8758
J9 ENVIRON ENG SCI
JI Environ. Eng. Sci.
PD OCT
PY 2008
VL 25
IS 8
BP 1107
EP 1114
DI 10.1089/ees.2008.0233
PG 8
WC Engineering, Environmental; Environmental Sciences
SC Engineering; Environmental Sciences & Ecology
GA 359RA
UT WOS:000260004600001
PM 22476005
ER
PT J
AU Ali, R
Olden, K
Xu, SQ
AF Ali, Robbie
Olden, Kenneth
Xu, Shunqing
TI Community-based participatory research: A vehicle to promote public
engagement for environmental health in China
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Editorial Material
DE CBPR; China; China environmental health; community-based participatory
research; environmental justice; international environmental health
ID SCHISTOSOMIASIS CONTROL; EXPOSURE; JUSTICE; WORKERS; HARLEM
AB BACKGROUND: In the past 25 years, China has experienced remarkable economic growth and rapid agricultural-to-industrial and rural-to-urban transitions. As a consequence, China now faces many daunting environmental challenges that are significantly affecting human health and quality of life, including indoor and outdoor air pollution, water pollution, deforestation, loss of agricultural land, and sustainability. Chinese government leaders have recently emphasized the need for better environmental protection practices along with interventions involving strong public participation.
OBJECTIVES: Community-based participatory research (CBPR) is a collaborative approach to research that involves community members, organizational representatives, and researchers as equal participants in all phases of the research process. Over the past 15 years, CBPR has gained recognition and acceptance and is now valued as a means to effect change and provide scientific knowledge relevant to human health and the environment. In this article we highlight the success of CBPR in the United States and suggest that it could be a useful model for addressing environmental health problems in the People's Republic of China.
DISCUSSION: CBPR can reduce the tension between science and society by promoting genuine communication, by enabling scientists and administrators to listen and respond to the public, by allowing communities to help shape the research agenda, and by increasing accountability of researchers and governments to the public.
CONCLUSIONS: CBPR can potentially help improve environmental health in China, but it is likely to take a different form than it has in the West because the government will be leading the way.
C1 [Ali, Robbie] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA 15261 USA.
[Olden, Kenneth] Natl Inst Environm Hlth Sci, Lab Mol Carcinogenesis, Natl Inst Hlth, Dept Hlth & Human Serv, Res Triangle Pk, NC USA.
[Xu, Shunqing] Huazhong Univ Sci & Technol, Tongji Med Coll, Wuhan 430074, Peoples R China.
RP Ali, R (reprint author), Univ Pittsburgh, Grad Sch Publ Hlth, A226A Crabtree Hall,130 Desoto St, Pittsburgh, PA 15261 USA.
EM rali@pitt.edu
NR 29
TC 2
Z9 2
U1 4
U2 16
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2008
VL 116
IS 10
BP 1281
EP 1284
DI 10.1289/ehp.11399
PG 4
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 355TA
UT WOS:000259730100017
PM 18941566
ER
PT J
AU Diwan, BA
Sipowicz, M
Logsdon, D
Gorelick, P
Anver, MR
Kasprzak, KS
Anderson, LM
AF Diwan, Bhalchandra A.
Sipowicz, Marek
Logsdon, Daniel
Gorelick, Peter
Anver, Miriam R.
Kasprzak, Kazimierz S.
Anderson, Lucy M.
TI Marked liver tumorigenesis by Helicobacter hepaticus requires perinatal
exposure
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE adult exposure; Helicobacter hepaticus; hepatocellular tumors; infection
and cancer; perinatal exposure
ID CYTOLETHAL DISTENDING TOXIN; CHRONIC ACTIVE HEPATITIS; A/JCR MICE;
INFECTION; CARCINOGENESIS; COLONIZATION; MAMMARY; CANCER; PYLORI; TUMORS
AB BACKGROUND: Although severe hepatitis and liver tumors occur in a high percentage of A/J male mice naturally infected with Helicobacter hepaticus these effects have not been observed after injection of adult mice with the bacteria.
OBJECTIVES: We tested the hypothesis that perinatal exposure to the bacteria is required for liver tumorigenesis.
METHODS: A/J female mice were infected by intragastric (ig) or intraperitoneal (ip) treatment with 1.5 x 10(8) H. hepaticus before pregnancy. We examined offspring at progressive time intervals, including some kept until natural death in old age. A/J, BALB/c, and C57BL/6 weanling male mice were similarly treated ig with the bacteria and observed for up to 2 years.
RESULTS: After ip bacterial infection of A/J females, 41% of their male offspring developed hepatitis and 33% had hepatocellular tumors, including 18% with hepatocellular carcinoma. Treatment by the ig route resulted in a similar incidence of hepatitis in offspring (35%) but fewer total liver tumors (8%) and carcinomas (4%). By contrast, ig instillation of H. hepaticus in weanling A/J, C57BL/6, or BALB/c mice resulted in low incidence of hepatitis (0-20%) and few liver tumors, despite presence of bacteria confirmed in feces.
CONCLUSIONS: Results indicate that a high incidence of liver tumors in mice infected with H, hepaticus requires perinatal exposure. Contributing perinatal factors could include known high sensitivity of neonatal liver to tumor initiation, and/or modulation of immune response to the bacterium or its toxins. Mechanisms of human perinatal sensitivity to such phenomena can be studied with this model.
C1 [Sipowicz, Marek; Kasprzak, Kazimierz S.; Anderson, Lucy M.] NCI, Comparat Carcinogenesis Lab, Natl Inst Hlth, Dept Hlth & Human Serv, Frederick, MD 21702 USA.
[Diwan, Bhalchandra A.] SAIC Frederick Inc, Basic Res Program, Frederick, MD USA.
[Logsdon, Daniel; Gorelick, Peter] SAIC Frederick Inc, Lab Anim Sci Program, Frederick, MD USA.
[Anver, Miriam R.] SAIC Frederick Inc, Pathol Histotechnol Lab, Frederick, MD USA.
RP Anderson, LM (reprint author), NCI, Comparat Carcinogenesis Lab, Natl Inst Hlth, Dept Hlth & Human Serv, Bldg 538,Room 205B, Frederick, MD 21702 USA.
EM andersol@mail.ncifcrf.gov
FU Intramural NIH HHS; NCI NIH HHS [N01CO12400, N01-CO-12400]
NR 31
TC 4
Z9 4
U1 0
U2 2
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2008
VL 116
IS 10
BP 1352
EP 1356
DI 10.1289/ehp.11493
PG 5
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 355TA
UT WOS:000259730100028
PM 18941577
ER
PT J
AU Lawler, CP
AF Lawler, Cindy P.
TI The "Environment" for autism research: Signs of improvement?
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Editorial Material
C1 [Lawler, Cindy P.] Natl Inst Environm Hlth Sci, Div Extramural Res & Training, InterAgcy Autism Coordinating Comm, Res Triangle Pk, NC USA.
RP Lawler, CP (reprint author), Natl Inst Environm Hlth Sci, Div Extramural Res & Training, InterAgcy Autism Coordinating Comm, Res Triangle Pk, NC USA.
EM lawler@niehs.nih.gov
NR 7
TC 9
Z9 9
U1 0
U2 1
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2008
VL 116
IS 10
BP A416
EP A417
DI 10.1289/ehp.12107
PG 2
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 355TA
UT WOS:000259730100001
PM 18941547
ER
PT J
AU Galperin, MY
AF Galperin, Michael Y.
TI The quest for biofuels fuels genome sequencing
SO ENVIRONMENTAL MICROBIOLOGY
LA English
DT Editorial Material
ID SP NOV.; KOCURIA-RHIZOPHILA; MICROCOCCUS-LUTEUS; GEN. NOV.; BACTERIUM;
PROPOSAL; RECLASSIFICATION; DEGRADATION; EVOLUTION; CLONING
C1 Natl Inst Hlth, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Galperin, MY (reprint author), Natl Inst Hlth, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM galperin@ncbi.nlm.nih.gov
RI Galperin, Michael/B-5859-2013
OI Galperin, Michael/0000-0002-2265-5572
FU Intramural NIH HHS [Z99 LM999999]
NR 37
TC 4
Z9 5
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1462-2912
J9 ENVIRON MICROBIOL
JI Environ. Microbiol.
PD OCT
PY 2008
VL 10
IS 10
BP 2471
EP 2475
DI 10.1111/j.1462-2920.2008.01754.x
PG 5
WC Microbiology
SC Microbiology
GA 347NI
UT WOS:000259147900001
PM 18821974
ER
PT J
AU Ye, XB
Pierik, FH
Hauser, R
Duty, S
Angerer, J
Park, MM
Burdorf, A
Hofman, A
Jaddoe, VWV
Mackenbach, JP
Steegers, EAP
Tiemeier, H
Longnecker, MP
AF Ye, Xibiao
Pierik, Frank H.
Hauser, Russ
Duty, Susan
Angerer, Juergen
Park, Melissa M.
Burdorf, Alex
Hofman, Albert
Jaddoe, Vincent W. V.
Mackenbach, Johan P.
Steegers, Eric A. P.
Tiemeier, Henning
Longnecker, Matthew P.
TI Urinary metabolite concentrations of organophosphorous pesticides,
bisphenol A, and phthalates among pregnant women in Rotterdam, the
Netherlands: The Generation R study
SO ENVIRONMENTAL RESEARCH
LA English
DT Article
DE Organophosphorus (OP) pesticides; Bisphenol A (BPA); Phthalates;
Prenatal exposure; Biological monitoring
ID TANDEM MASS-SPECTROMETRY; DIALKYL PHOSPHATE METABOLITES; HUMAN EXPOSURE;
ANOGENITAL DISTANCE; BIOMONITORING DATA; INTERNAL EXPOSURE; US
POPULATION; MALE INFANTS; HUMAN HEALTH; CHILDREN
AB Concern about potential health impacts of low-level exposures to organ ophosphorus (OP) pesticides, bisphenol A (BPA), and phthalates among the general population is increasing. We measured levels of six dialkyl phosphate (DAP) metabolites of OP pesticides, a chlorpyrifos-specific metabolite (3,5,6-trichloro-2-pyridinol, TCPy), BPA, and 14 phthalate metabolites in urine samples of 100 pregnant women from the Generation R study, the Netherlands. The unadjusted and creatinine-adjusted concentrations were reported, and compared to National Health and Nutrition Examination Survey and other studies. In general, these metabolites were detectable in the urine of the women from the Generation R study and compared with other groups, they had relatively high-level exposures to OP pesticides and several phthalates but similar exposure to BPA. The median concentrations of total dimethyl (DM) metabolites was 264.0 nmol/g creatinine (Cr) and of total DAP was 316.0 nmol/g Cr. The median concentration of mono-ethyl phthalate (MEP) was 222.0 mu g/g Cr: the median concentrations of mono-isobutyl phthalate (MiBP) and mono-n-butyl phthalate (MnBP) were above 50 mu g/g Cr. The median concentrations of the three secondary metabolites of di-2-ethylhexyl phthalate (DEHP) were greater than 20 mu g/g Cr. The data indicate that the Generation R study population provides a wide distribution of selected environmental exposures. Reasons for the relatively high levels and possible health effects need investigation. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Ye, Xibiao; Park, Melissa M.; Longnecker, Matthew P.] NIEHS, Epidemiol Branch, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Pierik, Frank H.] TNO Netherlands Org Appl Sci Res, Dept Environm & Hlth, NL-2600 AA Delft, Netherlands.
[Hauser, Russ] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Duty, Susan] Simmons Coll, Sch Hlth Studies, Dept Nursing, Boston, MA 02115 USA.
[Angerer, Juergen] Univ Erlangen Nurnberg, Inst & Outpatient Clin Occupat Social & Environm, D-8520 Erlangen, Germany.
[Park, Melissa M.] Univ N Carolina, Sch Publ Hlth, Chapel Hill, NC 27599 USA.
[Pierik, Frank H.; Burdorf, Alex; Mackenbach, Johan P.] Univ Med Ctr Rotterdam, Erasmus MC, Dept Publ Hlth, NL-3000 CA Rotterdam, Netherlands.
[Hofman, Albert; Jaddoe, Vincent W. V.] Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, NL-3000 CA Rotterdam, Netherlands.
[Jaddoe, Vincent W. V.] Univ Med Ctr Rotterdam, Erasmus MC, Generat R Study Grp, NL-3000 CA Rotterdam, Netherlands.
[Jaddoe, Vincent W. V.] Univ Med Ctr Rotterdam, Erasmus MC, Dept Pediat, NL-3000 CA Rotterdam, Netherlands.
[Steegers, Eric A. P.] Univ Med Ctr Rotterdam, Erasmus MC, Dept Obstet & Gynecol, NL-3000 CA Rotterdam, Netherlands.
[Tiemeier, Henning] Univ Med Ctr Rotterdam, Erasmus MC, Dept Child & Adolescent Psychiat, NL-3000 CA Rotterdam, Netherlands.
RP Longnecker, MP (reprint author), NIEHS, Epidemiol Branch, NIH, DHHS, MD A3-05,POB 12233, Res Triangle Pk, NC 27709 USA.
EM longnec1@niehs.nih.gov
RI Burdorf, Alex/A-2226-2008;
OI Burdorf, Alex/0000-0003-3129-2862; Tiemeier,
Henning/0000-0002-4395-1397; Longnecker, Matthew/0000-0001-6073-5322
FU Intramural Research Program; NIEHS; Harvard NIEHS Environmental Health
Center [P30ES000002]
FX Funding source: This study was supported by the Intramural Research
Program, NIEHS and the Harvard NIEHS Environmental Health Center Pilot
Project Grant P30ES000002. This study was approved by ethical committees
in National Institutes of Health (NIH) and Erasmus MC.
NR 50
TC 158
Z9 160
U1 5
U2 32
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0013-9351
J9 ENVIRON RES
JI Environ. Res.
PD OCT
PY 2008
VL 108
IS 2
BP 260
EP 267
DI 10.1016/j.envres.2008.07.014
PG 8
WC Environmental Sciences; Public, Environmental & Occupational Health
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health
GA 361MS
UT WOS:000260132400018
PM 18774129
ER
PT J
AU Bottomley, A
Debruyne, C
Felip, E
Millward, M
Thiberville, L
D'Addario, G
Rome, L
Zatloukal, P
Coens, C
Giaccone, G
AF Bottomley, Andrew
Debruyne, Channa
Felip, Enriqueta
Millward, Michael
Thiberville, Luc
D'Addario, Giannicola
Rome, Lisa
Zatloukal, Petr
Coens, Corneel
Giaccone, Giuseppe
TI Symptom and quality of life results of an international randomised phase
III study of adjuvant vaccination with Bec2/BCG in responding patients
with limited disease small-cell lung cancer
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Symptom; Quality of life
ID CLINICAL-TRIALS; QLQ-C30
AB Aims: This study reports the symptom and HRQOL results in which standard treatment was compared to standard therapy plus Bec2, an anti-idiotypic antibody that mimics GD3, a ganglioside antigen.
Methods: Five hundred and fifteen LD SCLC patients were randomised to receive five vaccinations of Bec2 (2.5 mg)/BCG vaccine arm (VA) or an observational arm (OA) administered over a 10-week period. Survival was the primary end-point; HRQOL was a secondary end-point, assessed using the EORTC QLQ-C30/LC 13.
Results: There was no improvement in survival or progression-free survival in the vaccination arm. At baseline patients in both arms demonstrated significantly impaired scores on the global QOL scale, when compared to a normative population. However, HRQOL and symptom scores between the two treatment arms were not statistically different at any time point.
Conclusion: We found no benefits to patient HRQOL by additional vaccination with Bec2/BCG to LD SCLC for patients who have been undergoing standard therapy. (c) 2008 Elsevier Ltd. All rights reserved.
C1 [Bottomley, Andrew; Debruyne, Channa; Coens, Corneel] European Org Res Treatment Canc, EORTC Headquarters, AISBL IVZW, Qual Life Dept, B-1200 Brussels, Belgium.
[Felip, Enriqueta] Vall Hebron Univ Hosp, Barcelona, Spain.
[Millward, Michael] Sir Charles Gairdner Hosp, Nedlands, WA 6009, Australia.
[Thiberville, Luc] Rouen Univ Hosp, Rouen, France.
[D'Addario, Giannicola] Kantonsspital St Gallen, St Gallen, Switzerland.
[Rome, Lisa] VA CT Hlth Care Syst, West Haven, CT USA.
[Zatloukal, Petr] Charles Univ Prague, Postgrad Med Sch, Fac Med 3, Prague, Czech Republic.
[Zatloukal, Petr] Fac Hosp Bulovka, Prague, Czech Republic.
[Giaccone, Giuseppe] NCI, Bethesda, MD 20892 USA.
RP Bottomley, A (reprint author), European Org Res Treatment Canc, EORTC Headquarters, AISBL IVZW, Qual Life Dept, Ave E Mounierlaan 83-11, B-1200 Brussels, Belgium.
EM andrew.bottomley@eortc.be
RI Millward, Michael/H-5456-2014; Giaccone, Giuseppe/E-8297-2017
OI Giaccone, Giuseppe/0000-0002-5023-7562
FU National Cancer Institute [5U10CA11488-30, SU10CA11488-34]; EORTC
Charitable Foundation
FX This study was supported by grants (5U10CA11488-30 through
SU10CA11488-34) from the National Cancer Institute and in part with a
grant from the EORTC Charitable Foundation. We are grateful to Merck
KGaA and Imclone for supporting this independent EORTC study. This was
an intergroup study of the EORTC Lung Cancer Group, Spanish Lung Cancer
Group, Group Francais de pheumo-cancerologie and Schweizerische
Arbeitsgruppe fur Klinische Krebsforschung and the veteran's
administration centers in the United States and centres in New Zealand
and Australia. Other independent centers were also involved and we thank
them all for there participation. All authors had full access to the
data and all authors had full responsibility to submit the publication.
NR 10
TC 14
Z9 16
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
J9 EUR J CANCER
JI Eur. J. Cancer
PD OCT
PY 2008
VL 44
IS 15
BP 2178
EP 2184
DI 10.1016/j.ejca.2008.06.036
PG 7
WC Oncology
SC Oncology
GA 374CU
UT WOS:000261020800015
PM 18676140
ER
PT J
AU Horvath, A
Giatzakis, C
Tsang, K
Greene, E
Osorio, P
Boikos, S
Libe, R
Patronas, Y
Robinson-White, A
Remmers, E
Bertherat, J
Nesterova, M
Stratakis, CA
AF Horvath, Anelia
Giatzakis, Christoforos
Tsang, Kitman
Greene, Elizabeth
Osorio, Paulo
Boikos, Sosipatros
Libe, Rossella
Patronas, Yianna
Robinson-White, Audrey
Remmers, Elaine
Bertherat, Jerome
Nesterova, Maria
Stratakis, Constantine A.
TI A cAMP-specific phosphodiesterase (PDE8B) that is mutated in adrenal
hyperplasia is expressed widely in human and mouse tissues: a novel
PDE8B isoform in human adrenal cortex
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE adrenal gland; Cushing syndrome; protein kinase A; cyclic AMP;
phosphodiesterases
ID NUCLEOTIDE PHOSPHODIESTERASE; ADRENOCORTICAL DISEASE; GENE; MUTATIONS;
CLONING; PDE11A; VARIANTS; 11A; LOCALIZATION; ORGANIZATION
AB Bilateral adrenocortical hyperplasia (BAH) is the second most common cause of corticotropin-independent Cushing syndrome (CS). Genetic forms of BAH have been associated with complex syndromes such as Carney Complex and McCune-Albright syndrome or may present as isolated micronodular adrenocortical disease (iMAD) usually in children and young adults with CS. A genome-wide association study identified inactivating phosphodiesterase (PDE) 11A (PDE11A)-sequencing defects as low-penetrance predisposing factors for iMAD and related abnormalities; we also described a mutation (c.914A>C/H305P) in cyclic AMP (cAMP)-specific PDE8B, in a patient with iMAD. In this study we further characterize this mutation; we also found a novel PDE8B isoform that is highly expressed in the adrenal gland. This mutation is shown to significantly affect the ability of the protein to degrade cAMP in vitro. Tumor tissues from patients with iMAD and no mutations in the coding PDE8B sequence or any other related genes (PRKAR1A, PDE11A) showed downregulated PDE8B expression (compared to normal adrenal cortex). Pde8b is detectable in the adrenal gland of newborn mice and is widely expressed in other mouse tissues. We conclude that PDE8B is another PDE gene linked to iMAD; it is a candidate causative gene for other adrenocortical lesions linked to the cAMP signaling pathway and possibly for tumors in other tissues.
C1 [Horvath, Anelia] NICHD, SEGEN, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
[Libe, Rossella; Bertherat, Jerome] Univ Paris 05, Hop Cochin,Inst Cochin, Serv Endocrinol, Dept Endocrinol Metab & Canc,Inst Natl Sante & Re, Paris, France.
[Libe, Rossella; Bertherat, Jerome] Univ Paris 05, Hop Cochin, Serv Endocrinol, Ctr Natl Rech Sci UMR 8104, Paris, France.
[Libe, Rossella; Bertherat, Jerome] Univ Paris 05, Hop Cochin, Serv Endocrinol, Ctr Reference Maladies Rares Surrenale, Paris, France.
[Remmers, Elaine] NIAMSD, Genet & Genom Branch, NIH, Bethesda, MD 20892 USA.
RP Horvath, A (reprint author), NICHD, SEGEN, Program Dev Endocrinol & Genet, NIH, Bldg 10 Ctr Dr,CRC Room 1E-3216, Bethesda, MD 20892 USA.
EM horvatha@mail.nih.gov
FU US NIH [Z01-HD-000642-04]; Groupement d'Interet Scientifique-Institut
National de la Sante et de la Recherche Medicale Institut des Maladies
Rares; Plan Hospitalier de Recherche Clinique [AOM 02068]
FX It was supported by US NIH intramural project Z01-HD-000642-04 to CAS
and, in part, by Groupement d'Interet Scientifique-Institut National de
la Sante et de la Recherche Medicale Institut des Maladies Rares and the
Plan Hospitalier de Recherche Clinique (AOM 02068) to the Comete
Network.
NR 25
TC 49
Z9 54
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD OCT
PY 2008
VL 16
IS 10
BP 1245
EP 1253
DI 10.1038/ejhg.2008.85
PG 9
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 352MV
UT WOS:000259502200016
PM 18431404
ER
PT J
AU Paisan-Ruiz, C
Nath, P
Wood, NW
Singleton, A
Houlden, H
AF Paisan-Ruiz, C.
Nath, P.
Wood, N. W.
Singleton, A.
Houlden, H.
TI Clinical heterogeneity and genotype-phenotype correlations in hereditary
spastic paraplegia because of Spatacsin mutations (SPG11)
SO EUROPEAN JOURNAL OF NEUROLOGY
LA English
DT Article
DE heredity spastic paraplegia; KIAA1840; Spatacsin; SPG11
ID THIN CORPUS-CALLOSUM; GENETIC-HETEROGENEITY; LOCUS
AB Background: Autosomal recessive hereditary spastic paraplegia (ARHSP) with thin corpus callosum is a distinct and usually severe form of complex hereditary spastic paraplegia classified as SPG11. Recently mutations on SPG11 gene (KIAA1840), which is localized to chromosome 15q13-q15, were shown to cause the majority of SPG11 cases. Methods: We analysed the 40 coding exons of this gene in the probands from eight families with complex ARHSP, four of these families had a thin corpus callosum and two has mild thinning. Results: Three families were identified with novel mutations in the SPG11 gene. One family was of Asian origin with a homozygous nonsense mutation and had a very severe phenotype but only very mild thinning of the corpus callosum. In the other two English families the parents were unrelated and the mutations were compound heterozygotes. In these two families the phenotype was mild and both probands had a thin corpus callosum. Conclusions: Given the probable mechanism of action of the mutations in the Spatacsin gene, we discuss the probable genotype phenotype correlations in these families. This study confirms the frequent occurrence of Spatacsin mutations in complex ARHSP with genotype phenotype effects and exposes the spectrum of clinical heterogeneity in SPG11.
C1 [Paisan-Ruiz, C.; Wood, N. W.; Houlden, H.] Inst Neurol, Dept Mol Neurosci, London WC1N 3BG, England.
[Paisan-Ruiz, C.; Wood, N. W.; Houlden, H.] UCL Natl Hosp Neurol & Neurosurg, London WC1N 3BG, England.
[Nath, P.; Singleton, A.] NIA, Mol Genet Unit, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Paisan-Ruiz, C (reprint author), Inst Neurol, Dept Mol Neurosci, Queen Sq, London WC1N 3BG, England.
EM C.Paisan-Ruiz@ion.ucl.ac.uk; h.houlden@ion.ucl.ac.uk
RI Houlden, Henry/C-1532-2008; Paisan-Ruiz, Coro/C-2912-2009; Singleton,
Andrew/C-3010-2009; Wood, Nicholas/C-2505-2009
OI Houlden, Henry/0000-0002-2866-7777; Wood, Nicholas/0000-0002-9500-3348
FU Medical Research Council; National Institute on Aging; National
Institutes of Health; Department of Health and Human Services, MD, USA;
Department of Health's NIHR Biomedical Research Centres
FX We are grateful to the Medical Research Council for their support. HH
holds an MRC clinician scientist fellowship. This work was supported in
part by the Intramural Program of the National Institute on Aging,
National Institutes of Health, Department of Health and Human Services,
MD, USA. This work was undertaken at UCLH/UCL, which received a
proportion of funding from the Department of Health's NIHR Biomedical
Research Centres funding scheme. We also thank the families involved to
help with our work.
NR 18
TC 18
Z9 18
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1351-5101
J9 EUR J NEUROL
JI Eur. J. Neurol.
PD OCT
PY 2008
VL 15
IS 10
BP 1065
EP 1070
DI 10.1111/j.1468-1331.2008.02247.x
PG 6
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 353YK
UT WOS:000259605800008
PM 18717728
ER
PT J
AU Zaman, V
Boger, HA
Granholm, AC
Rohrer, B
Moore, A
Buhusi, M
Gerhardt, GA
Hoffer, BJ
Middaugh, LD
AF Zaman, Vandana
Boger, Heather A.
Granholm, Ann-Charlotte
Rohrer, Baerbel
Moore, Alfred
Buhusi, Mona
Gerhardt, Greg A.
Hoffer, Barry J.
Middaugh, Lawrence D.
TI The nigrostriatal dopamine system of aging GFR alpha-1 heterozygous
mice: neurochemistry, morphology and behavior
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE monoamines; neuropharmacology; neurotrophic factors; nigrostriatal
system; growth factor receptors; SKF 82958
ID AGE-RELATED DECLINE; NEUROTROPHIC FACTOR PROTECTS; SUBSTANTIA-NIGRA
NEURONS; FACTOR-RECEPTOR-ALPHA; PARKINSONS-DISEASE; RAT-BRAIN; C-RET;
MESSENGER-RNAS; MOUSE MODEL; DIFFERENTIAL EXPRESSION
AB Given the established importance of glial cell line-derived neurotrophic factor (GDNF) in maintaining dopaminergic neurotransmitter systems, the nigrostriatal system and associated behaviors of mice with genetic reduction of its high-affinity receptor, GDNF receptor (GFR)alpha-1 (GFR alpha-1(+/-)), were compared with wild-type controls. Motor activity and the stimulatory effects of a dopamine (DA) D1 receptor agonist (SKF 82958) were assessed longitudinally at 8 and 18 months of age. Monoamine concentrations and dopaminergic nerve terminals in the striatum and the number of dopaminergic neurons in the substantia nigra (SN) were assessed. The results support the importance of GFR alpha-1 in maintaining normal function of the nigrostriatal dopaminergic system, with deficits being observed for GFR alpha-1(+/-) mice at both ages. Motor activity was lower and the stimulatory effects of the DA agonist were enhanced for the older GFR alpha-1(+/-) mice. DA in the striatum was reduced in the GFR alpha-1(+/-) mice at both ages, and tyrosine hydroxylase-positive cell numbers in the SN were reduced most substantially in the older GFR alpha-1(+/-) mice. The combined behavioral, pharmacological probe, neurochemical and morphological measures provide evidence of abnormalities in GFR alpha-1(+/-) mice that are indicative of an exacerbated aging-related decline in dopaminergic system function. The noted deficiencies, in turn, suggest that GFR alpha-1 is necessary for GDNF to maintain normal function of the nigrostriatal dopaminergic system. Although the precise mechanism(s) for the aging-related changes in the dopaminergic system remain to be established, the present study clearly establishes that genetic reductions in GFR alpha-1 can contribute to the degenerative changes observed in this system during the aging process.
C1 [Zaman, Vandana; Boger, Heather A.; Granholm, Ann-Charlotte; Rohrer, Baerbel; Moore, Alfred; Buhusi, Mona; Middaugh, Lawrence D.] Med Univ S Carolina, Dept Neurosci, Charleston, SC 29425 USA.
[Granholm, Ann-Charlotte; Moore, Alfred] Med Univ S Carolina, Ctr Aging, Charleston, SC 29425 USA.
[Rohrer, Baerbel] Med Univ S Carolina, Dept Ophthalmol, Charleston, SC 29425 USA.
[Gerhardt, Greg A.] Univ Kentucky, Albert B Chandler Med Ctr, Dept Anat & Neurobiol, Lexington, KY 40536 USA.
[Hoffer, Barry J.] NIDA, Intramural Res Program, Baltimore, MD USA.
RP Zaman, V (reprint author), Med Univ S Carolina, Dept Neurosci, Basic Sci Bldg Suite 411,173 Ashley Ave, Charleston, SC 29425 USA.
EM zamanv@musc.edu
FU NIH [AG13494, NS039787, AG013494, AG15239, AG023630]; army
[DAMD17-99-1-9480]
FX The authors would like to thank Ms C. Umphlet and Mr S. Surgener for
excellent technical assistance. We are grateful to Dr J. McGinty for
useful discussions, and critical reading of the manuscript. The work was
supported by grants from the NIH [AG13494, NS039787 (G. Gerhardt),
AG013494 (G. Gerhardt), AG15239 (A.-C. Granholm), and AG023630 (A.-C.
Granholm)] and from the army (DAMD17-99-1-9480).
NR 87
TC 15
Z9 15
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD OCT
PY 2008
VL 28
IS 8
BP 1557
EP 1568
DI 10.1111/j.1460-9568.2008.06456.x
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 360IF
UT WOS:000260050500011
PM 18973577
ER
PT J
AU Perk, LR
Walsum, MSV
Visser, GWM
Kloet, RW
Vosjan, MJWD
Leemans, CR
Giaccone, G
Albano, R
Comoglio, PM
van Dongen, GAMS
AF Perk, Lars R.
Walsum, Marijke Stigter-van
Visser, Gerard W. M.
Kloet, Reina W.
Vosjan, Maria J. W. D.
Leemans, C. Rene
Giaccone, Giuseppe
Albano, Raffaella
Comoglio, Paolo M.
van Dongen, Guus A. M. S.
TI Quantitative PET imaging of Met-expressing human cancer xenografts with
Zr-89-labelled monoclonal antibody DN30
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE Met receptor; immuno-PET; molecular imaging; DN30; zirconium-89
ID POSITRON-EMISSION-TOMOGRAPHY; BEARING NUDE-MICE; ZR-89 IMMUNO-PET;
C-MET; INVASIVE GROWTH; SCATTER-FACTOR; CELL-LINE; BIODISTRIBUTION;
OVEREXPRESSION; AMPLIFICATION
AB Purpose Targeting the c-Met receptor with monoclonal antibodies (MAbs) is an appealing approach for cancer diagnosis and treatment because this receptor plays a prominent role in tumour invasion and metastasis. Positron emission tomography (PET) might be a powerful tool for guidance of therapy with anti-Met MAbs like the recently described MAb DN30 because it allows accurate quantitative imaging of tumour targeting (immuno-PET). We considered the potential of PET with either Zr-89-labelled (residualising radionuclide) or I-124-labelled (non-residualising radionuclide) DN30 for imaging of Met-expressing tumours.
Materials and methods The biodistribution of co-injected Zr-89-DN30 and iodine-labelled DN30 was compared in nude mice bearing either the human gastric cancer line GLT-16 (high Met expression) or the head-and-neck cancer line FaDu (low Met expression). PET images were acquired in both xenograft models up to 4 days post-injection (p.i.) and used for quantification of tumour uptake.
Results Biodistribution studies in GTL-16-tumour-bearing mice revealed that Zr-89-DN30 achieved much higher tumour uptake levels than iodine-labelled DN30 (e.g. 19.6%ID/g vs 5.3%ID/g, 5 days p.i.), while blood levels were similar, indicating internalisation of DN30. Therefore, Zr-89-DN30 was selected for PET imaging of GLT-16-bearing mice. Tumours as small as 11 mg were readily visualised with immuno-PET. A distinctive lower Zr-89 uptake was observed in FaDu compared to GTL-16 xenografts (e.g. 7.8%ID/g vs 18.1%ID/g, 3 days p.i.). Nevertheless, FaDu xenografts were also clearly visualised with Zr-89-DN30 immuno-PET. An excellent correlation was found between PET-image-derived Zr-89 tumour uptake and ex-vivo-assessed Zr-89 tumour uptake (R-2=0.98).
Conclusions The long-lived positron emitter Zr-89 seems attractive for PET-guided development of therapeutic anti-c-Met MAbs.
C1 [Visser, Gerard W. M.; Kloet, Reina W.; van Dongen, Guus A. M. S.] Vrije Univ Amsterdam, Med Ctr, NL-1007 MB Amsterdam, Netherlands.
[Perk, Lars R.; Walsum, Marijke Stigter-van; Vosjan, Maria J. W. D.; Leemans, C. Rene; van Dongen, Guus A. M. S.] Vrije Univ Amsterdam, Med Ctr, Dept Otolaryngol Head & Neck Surg, NL-1007 MB Amsterdam, Netherlands.
[Giaccone, Giuseppe] Natl Canc Inst, Med Oncol Branch CCR, Bethesda, MD USA.
[Albano, Raffaella; Comoglio, Paolo M.] Univ Turin, Sch Med, Div Mol Oncol, Inst Canc Res & Treatment IRCC, Turin, Italy.
RP van Dongen, GAMS (reprint author), Vrije Univ Amsterdam, Med Ctr, NL-1007 MB Amsterdam, Netherlands.
EM gams.vandongen@vumc.nl
RI Giaccone, Giuseppe/E-8297-2017;
OI Giaccone, Giuseppe/0000-0002-5023-7562; Comoglio,
Paolo/0000-0002-7056-5328
FU Dutch Technology Foundation [VBC.6120]; Associazione Italiana per la
Ricerca sul Cancro
FX This project was financially supported by the Dutch Technology
Foundation (grant VBC.6120) and by the Associazione Italiana per la
Ricerca sul Cancro. We thank the technical staff of BV Cyclotron and the
Radionuclide Center for supplying and processing of 89Zr,
Floris van Velden for PET analyses and Otto Hoekstra for providing PET
imaging facilities and for reviewing the manuscript.
NR 35
TC 62
Z9 62
U1 3
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD OCT
PY 2008
VL 35
IS 10
BP 1857
EP 1867
DI 10.1007/s00259-008-0774-5
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 351GV
UT WOS:000259413600013
PM 18491091
ER
PT J
AU De Bruyne, S
Wyffels, L
Rice, K
Boos, T
De Vos, F
AF De Bruyne, S.
Wyffels, L.
Rice, K.
Boos, T.
De Vos, F.
TI Influence of cyclosporin A administration on the biodistribution of
[I-123]-(4-(2-(bis(4-fluorophenyl)methoxy)ethyl)-1-(4-iodobenzyl)piperid
ine
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Meeting Abstract
C1 [De Bruyne, S.; Wyffels, L.; De Vos, F.] Univ Ghent, B-9000 Ghent, Belgium.
[Rice, K.; Boos, T.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD OCT
PY 2008
VL 35
SU 2
BP S163
EP S163
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA V28OS
UT WOS:000208690700164
ER
PT J
AU Finnema, SJ
Donohue, SR
Zoghbi, SS
Brown, AK
Gulyas, B
Innis, B
Halldin, C
Pike, VW
AF Finnema, S. J.
Donohue, S. R.
Zoghbi, S. S.
Brown, A. K.
Gulyas, B.
Innis, B.
Halldin, C.
Pike, V. W.
TI Evaluation in Monkey of [11C]PipISB and [18F]PipISB as Candidate
Radioligands for Imaging Brain Cannabinoid Type 1 (CB1) Receptors In
Vivo
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Meeting Abstract
C1 [Finnema, S. J.; Gulyas, B.; Halldin, C.] Karolinska Inst, Stockholm, Sweden.
[Donohue, S. R.; Zoghbi, S. S.; Brown, A. K.; Innis, B.; Pike, V. W.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD OCT
PY 2008
VL 35
SU 2
BP S172
EP S172
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA V28OS
UT WOS:000208690700209
ER
PT J
AU Panico, M
Lang, L
Del Vecchio, S
Nardelli, A
Castaldi, E
Zaccaro, L
Del Gatto, A
Saviano, M
Zannetti, A
Larobina, M
Gargiulo, S
Pedone, C
Salvatore, M
AF Panico, M.
Lang, L.
Del Vecchio, S.
Nardelli, A.
Castaldi, E.
Zaccaro, L.
Del Gatto, A.
Saviano, M.
Zannetti, A.
Larobina, M.
Gargiulo, S.
Pedone, C.
Salvatore, M.
TI An Improved Radiolabeling Synthesis of RGDECHI with 18F-Fluoride
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Meeting Abstract
C1 [Panico, M.; Castaldi, E.; Zaccaro, L.; Del Gatto, A.; Saviano, M.; Zannetti, A.; Larobina, M.] Univ Naples Federico II, IBB CNR, Naples, Italy.
[Lang, L.] NIH PET Dept, Bethesda, MD USA.
[Del Vecchio, S.; Nardelli, A.; Gargiulo, S.; Salvatore, M.] Univ Naples Federico II, Naples, Italy.
[Pedone, C.] Univ Naples Federico II, Dipartimento Chim, Naples, Italy.
RI Salvatore, Marco/K-8083-2016
OI Salvatore, Marco/0000-0001-9734-7702
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD OCT
PY 2008
VL 35
SU 2
BP S329
EP S330
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA V28OS
UT WOS:000208690701588
ER
PT J
AU Seo, JH
Moon, HS
Kim, IY
Guo, DD
Lee, HG
Choi, YJ
Cho, CS
AF Seo, Ji-Hye
Moon, Hyun-Seuk
Kim, In-Yong
Guo, Ding-Ding
Lee, Hong-Gu
Choi, Yun-Jaie
Cho, Chong-Su
TI PEGylated conjugated linoleic acid stimulation of apoptosis via a
p53-mediated signaling pathway in MCF-7 breast cancer cells
SO EUROPEAN JOURNAL OF PHARMACEUTICS AND BIOPHARMACEUTICS
LA English
DT Article
DE Poly (ethylene glycol) (PEG); PEGylation; Conjugated linoleic acid
(CLA); Nanoparticle; Anti-cancer; Pro-drug
ID POLYETHYLENE-GLYCOL; DRUG-DELIVERY; BCL-2 FAMILY; PROTEIN; GROWTH; PEG;
PROLIFERATION; DERIVATIVES; EXPRESSION; EFFICACY
AB The objective of this study was to investigate whether PEGylated conjugated linoleic acid (PCLA), as compared with conjugated linoleic acid (CLA) alone, displays anti-cancer properties in MCF-7 breast cancer cells. To generate PCLA, CLA was Simply Coupled to poly(ethylene glycol) (PEG) at the melting state of PEG without a solvent or a catalyst. The coupling reaction generated an ester linkage between the carboxyl group of CLA and hydroxyl one of PEG. The half-life of the generated PCLA was 52 h at pH 7.4 at 37 degrees C, indicating that PCLA potentially acts as a pro-drug. Apoptosis of MCF-7 breast cancer cells treated with PCLA showed a dose response to PCLA concentration during treatment. In addition, pro-apoptotic proteins such as Bax were up-regulated, whereas anti-apoptotic proteins, such as Bcl-2, were down-regulated by treatment with both CLA and PCLA. The tumor suppressor gene p53 was significantly up-regulated by treatment with increasing concentrations of PCLA, suggesting that PCLA-induced apoptosis is regulated by a p53-mediated signaling pathway. Overall, the anti-cancer effects of PCLA on MCF-7 breast cancer cells may have therapeutic significance. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Seo, Ji-Hye; Moon, Hyun-Seuk; Kim, In-Yong; Guo, Ding-Ding; Choi, Yun-Jaie; Cho, Chong-Su] Seoul Natl Univ, Sch Agr Biotechnol, Res Inst Agr & Life Sci, Seoul 151921, South Korea.
[Lee, Hong-Gu] Pusan Natl Univ, Sch Bioresources, Miryong 627706, South Korea.
[Lee, Hong-Gu] Pusan Natl Univ, PNU Special Anim Biotechnol Ctr, Miryong 627706, South Korea.
[Moon, Hyun-Seuk] NIAAA, Lab Mol Signaling, NIH, Bethesda, MD 20892 USA.
RP Cho, CS (reprint author), Seoul Natl Univ, Sch Agr Biotechnol, Res Inst Agr & Life Sci, Seoul 151921, South Korea.
EM chocs@plaza.snu.ac.kr
RI Choi, Yunjaie /B-4697-2014; Moon, Hyun-Seuk/G-8576-2015
OI Moon, Hyun-Seuk/0000-0002-5216-2090
FU Agricultural R&D Promotion Center (ARPC) (2006-0053); Brain Korea 21
(BK21)
FX This work was supported by the Agricultural R&D Promotion Center (ARPC)
(2006-0053). We acknowledge the National Instrumentation Center for
Environmental Management (NICEM) for providing measurement opportunities
via NMR, FT-IR, ELS and TEM. J.H. Seo and H.S. Moon were supported by a
Brain Korea 21 (BK21) grant.
NR 41
TC 13
Z9 15
U1 1
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0939-6411
J9 EUR J PHARM BIOPHARM
JI Eur. J. Pharm. Biopharm.
PD OCT
PY 2008
VL 70
IS 2
BP 621
EP 626
DI 10.1016/j.ejpb.2008.05.009
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 369MA
UT WOS:000260697400028
PM 18573337
ER
PT J
AU Lee, SJ
Lattouf, JB
Xanthopoulos, J
Linehan, WM
Bottaro, DP
Vasselli, JR
AF Lee, S. Justin
Lattouf, Jean-Baptiste
Xanthopoulos, Julie
Linehan, W. Marston
Bottaro, Donald P.
Vasselli, James R.
TI Von Hippel-Lindau Tumor Suppressor Gene Loss in Renal Cell Carcinoma
Promotes Oncogenic Epidermal Growth Factor Receptor Signaling via Akt-1
and MEK-1
SO EUROPEAN UROLOGY
LA English
DT Article
DE Akt-1; EGF receptor; MEK-1; Renal cell carcinoma; VHL
ID TYROSINE KINASE INHIBITORS; PHASE-II TRIAL; LUNG-CANCER;
MONOCLONAL-ANTIBODY; GEFITINIB; THERAPY; MUTATIONS; HYPOXIA; PRODUCT;
PATHWAY
AB Objectives: Clear-cell renal cell carcinoma (RCC) is the most prevalent form of kidney cancer and is frequently associated with loss of von Hippel-Lindau (VHL) gene function, resulting in the aberrant transcriptional activation of genes that contribute to tumor growth and metastasis, including transforming growth factor-alpha (TGF-alpha), a ligand of the epidermal growth factor receptor (EGFR) tyrosine kinase. To determine the functional impact of EGFR activation on RCC, we suppressed critical components of this pathway: EGFR, Akt-1, and MEK-1.
Methods: Stable transfection of RCC cells with plasmids bearing shRNA directed against each of these genes was used to individually suppress their expression. Transfectants were characterized for growth and invasiveness in vitro and tumorigenesis in vivo.
Results: RCC cell transfectants displayed significantly reduced growth rate and matrix invasion in vitro and RCC tumor xenograft growth rate in vivo. Analysis of tumor cells that emerged after extended periods in each model showed that significant EGFR suppression was sustained, whereas Akt-1 and MEK-1 knock-down cells had escaped shRNA suppression.
Conclusions: EGFR, Akt-1, and MEK-1 are individually critical for RCC cell invasiveness in vitro and tumorigenicity in vivo, and even partial suppression of each can have a significant impact on tumor progression. The emergence of transfectants that had escaped Akt-1 and MEK-1 suppression during tumorigenicity experiments suggests that these effectors may each be more critical than EGFR for RCC tumorigenesis, consistent with results from clinical trials of EGFR inhibitors for RCC, where durable clinical responses have not been seen. Published by Elsevier B.V. on behalf of European Association of Urology.
C1 [Lee, S. Justin; Lattouf, Jean-Baptiste; Xanthopoulos, Julie; Linehan, W. Marston; Bottaro, Donald P.; Vasselli, James R.] NCI, Urol Oncol Branch, CRC, Bethesda, MD 20892 USA.
RP Bottaro, DP (reprint author), NCI, Urol Oncol Branch, CRC, 10 Ctr Dr MSC 1107,Bldg 10,Rm 1-3961, Bethesda, MD 20892 USA.
EM bottarod@mail.nih.gov
RI Bottaro, Donald/F-8550-2010
OI Bottaro, Donald/0000-0002-5057-5334
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research
FX This research was supported by the intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research.
NR 37
TC 7
Z9 7
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0302-2838
J9 EUR UROL
JI Eur. Urol.
PD OCT
PY 2008
VL 54
IS 4
BP 845
EP 854
DI 10.1016/j.eururo.2008.01.010
PG 10
WC Urology & Nephrology
SC Urology & Nephrology
GA 361LG
UT WOS:000260128600018
PM 18243508
ER
PT J
AU Denisco, RA
Chandler, RK
Compton, WM
AF Denisco, Richard A.
Chandler, Redonna K.
Compton, Wilson M.
TI Addressing the Intersecting Problems of Opioid Misuse and Chronic Pain
Treatment
SO EXPERIMENTAL AND CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Article
DE prescription opioid misuse; drug addiction; chronic pain; prevalence of
opioid abuse; National Institute on Drug Abuse [NIDA]
ID CHRONIC NONMALIGNANT PAIN; ABUSABLE PRESCRIPTION DRUGS; QUALITY-OF-LIFE;
UNITED-STATES; PRIMARY-CARE; BACK-PAIN; MUSCULOSKELETAL PAIN; PATIENTS
PERCEPTIONS; NONCANCER PAIN; NONMEDICAL USE
AB Misuse of prescription opioid medications has continued as a major public health problem in the United States. Review of major epidemiologic databases shows that the prevalence of opioid misuse rose markedly through the 1990s and the early part of the current decade. In this same period of time, the number of prescriptions for chronic noncancer pain increased markedly, and the intersection of these two public health problems remains a concern. Further, despite some leveling off of the overall rate of prescription opioid misuse in the past several years, surveillance data show high and increasing mortality associated with these drugs. Analysis of the 2006 National Survey of Drug Use and Health indicates the increasing prevalence of prescription opioid misuse is associated more with an increase in the general availability of these medications than misuse of the medications by those who were directly prescribed them. National Institute on Drug Abuse initiatives to address the prescription opioid problem include programs to stimulate research in the basic and clinical sciences, and to educate physicians and other health personnel.
C1 [Denisco, Richard A.; Chandler, Redonna K.; Compton, Wilson M.] Natl Inst Drug Abuse, Div Epidemiol Serv & Prevent Res, Bethesda, MD 20892 USA.
RP Compton, WM (reprint author), Natl Inst Drug Abuse, Div Epidemiol Serv & Prevent Res, 6001 Execut Blvd,MSC 9589, Bethesda, MD 20892 USA.
EM wcompton@nida.nih.gov
RI Duncan, Kirsty/H-1911-2011
FU Intramural NIH HHS [Z99 DA999999]
NR 86
TC 53
Z9 53
U1 2
U2 5
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1064-1297
J9 EXP CLIN PSYCHOPHARM
JI Exp. Clin. Psychopharmacol.
PD OCT
PY 2008
VL 16
IS 5
BP 417
EP 428
DI 10.1037/a0013636
PG 12
WC Psychology, Biological; Psychology, Clinical; Pharmacology & Pharmacy;
Psychiatry
SC Psychology; Pharmacology & Pharmacy; Psychiatry
GA 365KB
UT WOS:000260403800007
PM 18837638
ER
PT J
AU Wada, T
Kang, HS
Jetten, AM
Xie, W
AF Wada, Taira
Kang, Hong Soon
Jetten, Anton M.
Xie, Wen
TI The emerging role of nuclear receptor ROR alpha and its crosstalk with
LXR in xeno- and endobiotic gene regulation
SO EXPERIMENTAL BIOLOGY AND MEDICINE
LA English
DT Review
DE nuclear receptor; gene regulation; metabolism
ID PREGNANE-X-RECEPTOR; CONSTITUTIVE ANDROSTANE RECEPTOR; TRANSCRIPTIONAL
ACTIVATION; ORPHAN RECEPTORS; DRUG-METABOLISM; STAGGERER MOUSE;
BILE-ACIDS; CEREBELLAR DEVELOPMENT; OXYSTEROL RECEPTORS; RXR
HETERODIMERS
AB Retinoid-related orphan receptors (RORs), including the alpha, beta and gamma isoforms (NR1F1-3), are orphan nuclear receptors that have been implicated in tissue development, immune responses, and circadian rhythm. Although ROR alpha and ROR gamma have been shown to be expressed in the liver, the hepatic function of these two RORs remains unknown. We have recently shown that loss of ROR alpha and/or ROR gamma can positively or negatively influence the expression of multiple Phase I and Phase II drug metabolizing enzymes and transporters in the liver. Among ROR responsive genes, we identified oxysterol 7 alpha-hydroxylase (Cyp7b1), which plays a critical role in the homeostasis of cholesterol, as a ROR alpha target gene. We showed that ROR alpha is both necessary and sufficient for Cyp7b1 activation. Studies of mice deficient of ROR alpha or liver X receptors (LXRs) revealed an interesting and potentially important functional crosstalk between ROR alpha and LXR. The respective activation of LXR target genes and ROR target genes in ROR alpha null mice and LXR null mice led to our hypothesis that these two receptors are mutually suppressive in vivo. LXRs have been shown to regulate a battery of metabolic genes. We conclude that RORs participate in the xeno- and endobiotic regulatory network by regulating gene expression directly or through crosstalk with LXR, which may have broad implications in metabolic homeostasis.
C1 [Wada, Taira; Xie, Wen] Univ Pittsburgh, Ctr Pharmacogenet, Pittsburgh, PA 15261 USA.
[Wada, Taira; Xie, Wen] Univ Pittsburgh, Dept Pharmaceut Sci, Pittsburgh, PA 15261 USA.
[Kang, Hong Soon; Jetten, Anton M.] NIEHS, Cell Biol Sect, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
RP Xie, W (reprint author), Univ Pittsburgh, Ctr Pharmacogenet, 3501 Terrace St,633 Salk Hall, Pittsburgh, PA 15261 USA.
EM wex6@pitt.edu
RI Xie, Wen/M-1768-2016;
OI Jetten, Anton/0000-0003-0954-4445
FU NIH [CA107011, ES014626]; Intramural Research Program of the NIEHS
FX The original results from our labs described in this article were
generated with the supported of NIH grants CA107011 and ES014626 (W.X.)
and the Intramural Research Program of the NIEHS, NIH (A.M.J.).
NR 87
TC 21
Z9 23
U1 0
U2 5
PU SOC EXPERIMENTAL BIOLOGY MEDICINE
PI MAYWOOD
PA 195 WEST SPRING VALLEY AVE, MAYWOOD, NJ 07607-1727 USA
SN 1535-3702
J9 EXP BIOL MED
JI Exp. Biol. Med.
PD OCT
PY 2008
VL 233
IS 10
BP 1191
EP 1201
DI 10.3181/0802-MR-50
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 355SU
UT WOS:000259729500001
PM 18535165
ER
PT J
AU Chen, JC
Ellison, FA
Keyvanfar, K
Omokaro, SO
Desierto, MJ
Eckhaus, MA
Young, NS
AF Chen, Jichun
Ellison, Felicia A.
Keyvanfar, Keyvan
Omokaro, Stephanie O.
Desierto, Marie J.
Eckhaus, Michael A.
Young, Neal S.
TI Enrichment of hematopoietic stem cells with SLAM and LSK markers for the
detection of hematopoietic stem cell function in normal and Trp53 null
mice
SO EXPERIMENTAL HEMATOLOGY
LA English
DT Article
ID FAMILY RECEPTORS; PROGENITOR CELLS; P21(CIP1/WAF1); PURIFICATION;
EXHAUSTION; SENESCENCE; AGE; P53
AB Objective. To test function of hematopoietic stem cells (HSCs) in vivo in C57BL/6 (136) and Trp53-deficient (Trp53 null) mice by using two HSC enrichment schemes.
Materials and Methods. Bone marrow (BM) Lin(-)CD41(-)CD48(-)CD150(+) (signaling lymphocyte activation molecules [SLAM]), Lin(-)CD41(-)CD48(-)CD150(-) (SLAM(-)) and Lin(-)Scal(+)CD117(+) (LSK) cells were defined by fluorescence-activated cell staining (FACS). Cellular reactive oxygen species (ROS) level was also analyzed by FACS. Sorted SLAM, SLAM(-), and LSK cells were tested in vivo in the competitive repopulation (CR) and serial transplantation assays.
Results. SLAM cell fraction was 0.0078% +/- 0.0010% and 0.0135% +/- 0.0010% of total BM cells in B6 and Trp53 null mice, and was highly correlated (R-2 = 0.7116) with LSK cells. CD150(+) BM cells also contained more ROS cells than did CD150(-) cells. B6 SLAM cells repopulated recipients much better than B6 SLAM- cells, showing high HSC enrichment. B6 SLAM cells also engrafted recipients better than Trp53 null SLAM cells in the CR and the follow-up serial transplantation assays. Similarly, LSK cells from B6 donors also had higher repopulating ability than those from Trp53 null donors. However, whole BM cells from the same B6 and Trp53 null donors showed the opposite functional trend in recipient engraftment.
Conclusion. Both SLAM and LSK marker sets can enrich HSCs from B6 and Trp53 mice. Deficiency of Trp53 upregulates HSC self-renewal but causes no gain of HSC function. (C) 2008 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc.
C1 [Chen, Jichun] NHLBI, Hematol Branch, NIH, Clin Res Ctr, Bethesda, MD 20892 USA.
[Eckhaus, Michael A.] Natl Inst Med, Div Vet Resources, Off Res Serv, Bethesda, MD USA.
RP Chen, JC (reprint author), NHLBI, Hematol Branch, NIH, Clin Res Ctr, Bldg 10,Room 3E-5132,10 Ctr Dr, Bethesda, MD 20892 USA.
EM chenji@nhlbi.nih.gov
FU Intramural NIH HHS [Z99 HL999999]
NR 26
TC 48
Z9 50
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0301-472X
J9 EXP HEMATOL
JI Exp. Hematol.
PD OCT
PY 2008
VL 36
IS 10
BP 1236
EP 1243
DI 10.1016/j.exphem.2008.04.012
PG 8
WC Hematology; Medicine, Research & Experimental
SC Hematology; Research & Experimental Medicine
GA 358DU
UT WOS:000259897700002
PM 18562080
ER
PT J
AU Aravamuthan, BR
Bergstrom, DA
French, RA
Taylor, JJ
Parr-Brownlie, LC
Walters, JR
AF Aravamuthan, Bhooma R.
Bergstrom, Debra A.
French, Robin A.
Taylor, Joseph J.
Parr-Brownlie, Louise C.
Walters, Judith R.
TI Altered neuronal activity relationships between the pedunculopontine
nucleus and motor cortex in a rodent model of Parkinson's disease
SO EXPERIMENTAL NEUROLOGY
LA English
DT Review
DE pedunculopontine nucleus; Parkinson's disease; motor cortex;
oscillations; local field potential; dopamine; deep brain stimulation;
basal ganglia; urethane; ketamine
ID DEEP BRAIN-STIMULATION; LOCAL-FIELD POTENTIALS; PARS RETICULATA NEURONS;
SUBSTANTIA-NIGRA RETICULATA; HIGH-FREQUENCY STIMULATION; BASAL GANGLIA
OUTPUT; SUBTHALAMIC NUCLEUS; TEGMENTAL NUCLEUS; SQUIRREL-MONKEY;
UNILATERAL LESION
AB The pedunculopontine nucleus (PPN) is a new deep brain stimulation (DBS) target for Parkinson's disease (PD), but little is known about PPN firing pattern alterations in PD. The anesthetized rat is a useful model for investigating the effects of dopamine loss oil the transmission of oscillatory cortical activity through basal ganglia Structures. After dopamine loss, synchronous oscillatory activity emerges in the subthalamic nucleus and substantia nigra pars reticulata in phase with cortical slow oscillations. To investigate the impact of dopamine cell lesion-induced changes in basal ganglia output oil activity in the PPN, this study examines PPN spike timing with reference to motor cortex (MCx) local field potential (LFP) activity in urethane- or ketamine-anesthetized rats. Seven to ten days after unilateral 6-hydroxydopamine lesion of the media] forebrain bundle, spectral power in PPN spike trains and coherence between PPN spiking and PPN LFP activity increased in the similar to 1 Hz range in urethane-anesthetized rats. PPN spike timing also changed from firing predominantly in phase with MCx slow oscillations in the intact urethane-anesthetized rat to firing predominantly antiphase to MCx oscillations in the hemi-parkinsonian rat. These changes were not observed in the ketamine-anesthetized preparation. These observations Suggest that dopamine loss alters PPN spike timing by increasing inhibitory oscillatory input to the PPN from basal ganglia output nuclei, a phenomenon that may be relevant to motor dysfunction and PPN DBS efficacy in PD patients. (c) Published by Elsevier Inc.
C1 [Aravamuthan, Bhooma R.; Bergstrom, Debra A.; French, Robin A.; Taylor, Joseph J.; Parr-Brownlie, Louise C.; Walters, Judith R.] Natl Inst Neurol Disorders & Stroke, Neurophysiol Pharmacol Sect, NIH, Bethesda, MD 20892 USA.
[Aravamuthan, Bhooma R.] Univ Oxford, Dept Physiol Anat & Genet, Oxford, England.
RP Walters, JR (reprint author), Natl Inst Neurol Disorders & Stroke, Neurophysiol Pharmacol Sect, NIH, 35 Convent Dr,Bldg 35,Room 1C 905, Bethesda, MD 20892 USA.
EM waltersj@ninds.nih.gov
OI Parr-Brownlie, Louise/0000-0002-3001-7669
FU NINDS; NIH
FX This research was supported by the Intramural Research Program of the
NINDS, NIH. Additional support also came from the George C. Mar-shall
Commission (BRA).
NR 112
TC 26
Z9 28
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4886
J9 EXP NEUROL
JI Exp. Neurol.
PD OCT
PY 2008
VL 213
IS 2
BP 268
EP 280
DI 10.1016/j.expneurol.2008.05.023
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 351ZG
UT WOS:000259464200004
PM 18601924
ER
PT J
AU Khatami, M
AF Khatami, Mahin
TI 'Yin and Yang' in inflammation: duality in innate immune cell function
and tumorigenesis
SO EXPERT OPINION ON BIOLOGICAL THERAPY
LA English
DT Article
DE ageing; Alzheimer's; angiogenesis; apoptosis; atherosclerosis; B cell;
cancer; cardiovascular disease; chemokines; conjunctiva; cytokines;
dendritic cells; dual functions; eosinophils; hyperplasia; hypertention;
inflammatory diseases; innate and adoptive immune cells; interferons;
interleukins; leaky mast cells; lupus; lymphoid hyperplasia;
macrophages; mast cells; natural killers; neoplasia; neutrophils; ocular
inflammation; pleiotropic; resolution of inflammation; T cell;
tumoricidal; tumorigenesis; tumorigenic; wound healing
ID TUMOR-ASSOCIATED MACROPHAGES; TOLL-LIKE RECEPTORS; MAST-CELLS; DENDRITIC
CELLS; T-CELLS; PULMONARY ADENOCARCINOMA; ALLERGIC CONJUNCTIVITIS;
FLUORESCEINYL OVALBUMIN; HUMAN NEUTROPHILS; LANGERHANS CELLS
AB Background: The two stages of the acute inflammatory process are apoptosis ('Yin') and wound healing or resolution ('Yang'). Inflammation defends the host against unwanted elements. Objective/methods: To present a discussion of pleicitropic roles of innate immune cells possessing 'tumoricidal' and/or 'tumorigenic' properties in inflammation-induced dysfunction of the immune system and the genesis of chronic inflammatory diseases, hyperplasia, precancer/neoplasia or tumor and angiogenesis. Results/conclusions: Loss of maintenance of the balance between apoptosis and wound healing and co-existence of death and growth factors in tissues could create 'immunological chaos' with accumulation of 'immune response mismatches'. Unresolved inflammation plays a role in the genesis of chronic inflammatory and autoimmune diseases and cancer. Identification of accumulated 'mismatched' death and growth factors during the developmental phases of immune dysfunction in target tissues or cancer microenvironment presents challenges and opportunities for future studies on diagnosis, prevention and therapy of these diseases.
C1 NCI, NIH, Technol Program Dev, Off Technol & Ind Relat, Bethesda, MD 20892 USA.
RP Khatami, M (reprint author), NCI, NIH, Technol Program Dev, Off Technol & Ind Relat, Bethesda, MD 20892 USA.
EM mkgoodness@aol.com
NR 75
TC 27
Z9 29
U1 1
U2 8
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1471-2598
J9 EXPERT OPIN BIOL TH
JI Expert Opin. Biol. Ther.
PD OCT
PY 2008
VL 8
IS 10
BP 1461
EP 1472
DI 10.1517/14712590802358201
PG 12
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA 357JV
UT WOS:000259843000003
PM 18774915
ER
PT J
AU Harry, GJ
Kraft, AD
AF Harry, Gaylia Jean
Kraft, Andrew D.
TI Neuroinflammation and microglia: considerations and approaches for
neurotoxicity assessment
SO EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY
LA English
DT Review
DE ageing; immunotoxicology; mercury; microglia; neurodegenerative disease;
neuroinflammation; neurotoxicology
ID NECROSIS-FACTOR-ALPHA; HIPPOCAMPAL SLICE CULTURES;
CENTRAL-NERVOUS-SYSTEM; ALZHEIMERS-DISEASE; CELL-DEATH; INFLAMMATORY
RESPONSE; IMMUNE-SYSTEM; DENTATE GYRUS; AMYLOID-BETA; IN-VITRO
AB Background: The impact of an inflammatory response, as well as interactions between the immune and nervous systems, are rapidly assuming major roles in neurodegenerative disease and injury. However, it is now appreciated that the exact nature of such responses can differ with each type of insult and interaction. More recently, neuroinflammation and the associated cellular response of microglia are being considered for their contribution to neurotoxicity of environmental agents; yet, so far, the inclusion of inflammatory end points into neurotoxicity assessment have relied primarily on relatively limited measures or driven by in vitro models of neurotoxicity. Objective: To present background information on relevant biological considerations of neuroinflammation and the microglia response demonstrating the complex integrative nature of these biological processes and raising concern with regards to translation of effects demonstrated in vitro to the in vivo situation. Specific points are addressed that would influence the design and interpretation of neuroinflammation with regards to neurotoxicology assessment. Conclusion: There is a complex and dynamic response in the brain to regulate inflammatory processes and maintain a normal homeostatic level. The classification of such responses as beneficial or detrimental is an oversimplification. Neuroinflammation should be considered as a balanced network of processes in which subtle modifications can shift the cells toward disparate outcomes. The tendency to overinterpret data obtained in an isolated culture system should be discouraged. Rather, the use of cross-disciplinary approaches to evaluate several end points should be incorporated into the assessment of inflammatory contributions to the neurotoxicity of environmental exposures.
C1 [Harry, Gaylia Jean; Kraft, Andrew D.] Natl Inst Environm Hlth Sci, NIH, Neurotoxicol Grp, Neurobiol Lab,Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Harry, GJ (reprint author), Natl Inst Environm Hlth Sci, NIH, Neurotoxicol Grp, Neurobiol Lab,Dept Hlth & Human Serv, POB 12233,MD C1-04, Res Triangle Pk, NC 27709 USA.
EM harry@niehs.nih.gov
FU NIH; National Institute of Environmental Health Sciences
[IZ01ES101623-05]
FX This work was supported by the Intramural Research Program of the NIH,
National Institute of Environmental Health Sciences under Project no.
IZ01ES101623-05.
NR 117
TC 42
Z9 44
U1 0
U2 7
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1742-5255
J9 EXPERT OPIN DRUG MET
JI Expert Opin. Drug Metab. Toxicol.
PD OCT
PY 2008
VL 4
IS 10
BP 1265
EP 1277
DI 10.1517/17425250802384076
PG 13
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 360DL
UT WOS:000260037100002
PM 18798697
ER
PT J
AU Keppler, BR
Archer, TK
AF Keppler, Brian R.
Archer, Trevor K.
TI Chromatin-modifying enzymes as therapeutic targets - Part 1
SO EXPERT OPINION ON THERAPEUTIC TARGETS
LA English
DT Review
DE chromatin; chromatin-modifying enzymes; demethylation; epigenetics;
histone acetylation; histone deacetylation; histories; methylation
ID HISTONE DEACETYLASE INHIBITORS; PROSTATE-CANCER RECURRENCE;
CREB-BINDING-PROTEIN; ANDROGEN-RECEPTOR; GENE-EXPRESSION; BREAST-CANCER;
TRANSCRIPTIONAL COACTIVATOR; MUSCLE DIFFERENTIATION; ARGININE
METHYLATION; PREDICT RISK
AB Background: Disease pathogenesis may result from genetic alterations and/or a more diverse group of epigenetic changes. While events such as DNA methylation are well established, there is significant interest in nucleosome remodeling, RNA interference and histone modifications, as mechanisms that underlie epigenetic effects. While genetic mutations are permanent, epigenetic changes can be transitory. The potential to reverse epigenetic changes has led to the development of therapeutic strategies targeting chromatin-modifying enzymes. Objective: To review the roles of chromatin-modifying enzymes in gene regulation and to highlight their potentials as therapeutic targets. Methods: This review is based on recently published literature and online resources. Results/conclusion: This paper focuses on enzymes responsible for histone acetylation, deacetylation, methylation and demethylation, and their potential as targets for epigenetic therapies. A subsequent paper will do the same for enzymes responsible for histone phosphorylation, ubiquitylation, SUMOylation and poly-ADP-ribosylation as well as ATP-dependent nucleosome remodeling.
C1 [Keppler, Brian R.; Archer, Trevor K.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Archer, TK (reprint author), NIEHS, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM archer1@niehs.nih.gov
NR 100
TC 42
Z9 44
U1 1
U2 7
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1472-8222
J9 EXPERT OPIN THER TAR
JI Expert Opin. Ther. Targets
PD OCT
PY 2008
VL 12
IS 10
BP 1301
EP 1312
DI 10.1517/14728220802384013
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 357JJ
UT WOS:000259841800009
PM 18781828
ER
PT J
AU Csoka, B
Himer, L
Selmeczy, Z
Vizi, ES
Pacher, P
Ledent, C
Deitch, EA
Spolarics, Z
Nemeth, ZH
Hasko, G
AF Csoka, Balazs
Himer, Leondra
Selmeczy, Zsolt
Vizi, E. Sylvester
Pacher, Pal
Ledent, Catherine
Deitch, Edwin A.
Spolarics, Zoltan
Nemeth, Zoltan H.
Hasko, Gyoergy
TI Adenosine A(2A) receptor activation inhibits T helper 1 and T helper 2
cell development and effector function
SO FASEB JOURNAL
LA English
DT Article
DE autoimmunity; allergy; inflammation; rheumatoid arthritis; spleen and
lymph nodes
ID ADENOSINE A(2A) RECEPTORS; HUMAN DENDRITIC CELLS; T-CELLS; EXTRACELLULAR
ADENOSINE; POSTTRANSCRIPTIONAL MECHANISM; HUMAN NEUTROPHILS; HUMAN
EOSINOPHILS; EXPRESSION; INFLAMMATION; MICE
AB Adenosine is an immunosuppressive nucleoside, and adenosine AA receptors inhibit T-cell activation. We investigated the role of A(2A) receptors in regulating T helper (Th)1- and Th2-cell development and effector function. A(2A)-receptor stimulation suppressed the development of Tell receptor (TCR) -stimulated naive T cells into both Th1 and Th2 cells, as indicated by decreased IFN-gamma production by cells developed under Th1-skewing conditions and decreased interleukin (IL)-4, IL-5, and IL-10 production by cells developed under Th2-skewing conditions. Using A(2A) receptor-deficient mice, we demonstrate that A(2A) receptor activation inhibits Th1- and Th2-cell development by decreasing the proliferation and IL,2 production of naive T cells, irrespective of whether the cells are expanded under Th1- or Th2-skewing environment. Using in vivo established Th1 and Th2 cells, we further demonstrate the nonselective nature of A(2A) receptor-mediated immunosuppressive effects, because A(2A) receptor activation decreased IFN-gamma and IL-4 secretion and mRNA level of TCR-stimulated effector Th1 and Th2 cells, respectively. A(2A) receptor mRNA expression in both Th1 and Th2 effector cells increased following TCR stimulation. In summary, these data demonstrate that A(2A) receptor activation has strong inhibitory actions during early developmental, as well as late effector, stages of Th1- and Th2-cell responses.
C1 [Csoka, Balazs; Deitch, Edwin A.; Spolarics, Zoltan; Nemeth, Zoltan H.; Hasko, Gyoergy] Univ Med & Dent New Jersey, Dept Surg, New Jersey Med Sch, Newark, NJ 07103 USA.
[Himer, Leondra; Selmeczy, Zsolt; Vizi, E. Sylvester; Hasko, Gyoergy] Hungarian Acad Sci, Inst Expt Med, Dept Pharmacol, Budapest, Hungary.
[Pacher, Pal] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD USA.
[Ledent, Catherine] Univ Libre Bruxelles, Inst Rech Interdisciplinaire Biol Humaine & Nucl, Brussels, Belgium.
[Nemeth, Zoltan H.] Morristown Mem Hosp, Dept Surg, Morristown, NJ USA.
RP Hasko, G (reprint author), Univ Med & Dent New Jersey, Dept Surg, New Jersey Med Sch, 185 S Orange Ave,Univ Hts, Newark, NJ 07103 USA.
EM haskoge@umdnj.edu
RI Pacher, Pal/B-6378-2008;
OI Pacher, Pal/0000-0001-7036-8108; Csoka, Balazs/0000-0002-7562-1130
FU U.S. National Institutes of Health (NIH) [R01 GM66189]; National
Institute on Alchol Abuse and Alcoholism; Hungarian Research Fund OTKA
[T 049537]; Hungarian National RD Programme [1A/036/2004]
FX This work was supported by U.S. National Institutes of Health (NIH)
grant R01 GM66189 and the Intramural Research Program of NIH, National
Institute on Alchol Abuse and Alcoholism, as well as Hungarian Research
Fund OTKA (T 049537) and Hungarian National R&D Programme 1A/036/2004.
NR 49
TC 57
Z9 57
U1 1
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD OCT
PY 2008
VL 22
IS 10
BP 3491
EP 3499
DI 10.1096/fj.08-107458
PG 9
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 354MB
UT WOS:000259642600011
PM 18625677
ER
PT J
AU Brunk, I
Blex, C
Sanchis-Segura, C
Sternberg, J
Perreau-Lenz, S
Bilbao, A
Hortnagl, H
Baron, J
Juranek, J
Laube, G
Birnbaumer, L
Spanagel, R
Ahnert-Hilger, G
AF Brunk, Irene
Blex, Christian
Sanchis-Segura, Carles
Sternberg, Jan
Perreau-Lenz, Stephanie
Bilbao, Ainhoa
Hoertnagl, Heide
Baron, Jens
Juranek, Judyta
Laube, Gregor
Birnbaumer, Lutz
Spanagel, Rainer
Ahnert-Hilger, Gudrun
TI Deletion of Go2 alpha abolishes cocaine-induced behavioral sensitization
by disturbing the striatal dopamine system
SO FASEB JOURNAL
LA English
DT Article
DE vesicular regulation; VMAT2; locomotor activity; psychostimulants
ID VESICULAR MONOAMINE; PLACE PREFERENCE; TRANSMITTER UPTAKE; LIGHT
RESPONSE; QUANTAL SIZE; PROTEIN; REWARD; MICE; AMPHETAMINE; VMAT2
AB The alpha-subunits of the trimeric Go class of GTPases, comprising the splice variants Go1 alpha and Go2 alpha, are abundantly expressed in brain and reside on both plasma membrane and synaptic vesicles. Go2 alpha is involved in the vesicular storage of monoamines but its physiological relevance is still obscure. We now show that genetic depletion of Go2 alpha reduces motor activity induced by dopamine-enhancing drugs like cocaine, as repeated injections of cocaine fail to provoke behavioral sensitization in Go2 alpha(-/-) mice. In Go2 alpha(-/-) mice, D1 receptor signaling in the striatum is attenuated due to a reduced expression of Golf alpha and Gs alpha. Following cocaine treatment, Go2 alpha(-/-) mice have lower D1 and higher D2 receptor amounts compared to wild-type mice. The lack of behavioral sensitization correlates with reduced dopamine levels in the striatum and decreased expression of tyrosine hydroxylase. One reason for the neurochemical changes may be a reduced uptake of monoamines by synaptic vesicles from Go2 alpha(-/-) mice as a consequence of a lowered set point for filling. We conclude that Go2 alpha optimizes vesicular filling which is instrumental for normal dopamine functioning and for the development of drug-induced behavioral sensitization.
C1 [Sanchis-Segura, Carles; Perreau-Lenz, Stephanie; Bilbao, Ainhoa; Spanagel, Rainer] Cent Inst Mental Hlth, Dept Psychopharmacol, D-68159 Mannheim, Germany.
[Brunk, Irene; Blex, Christian; Sternberg, Jan; Baron, Jens; Juranek, Judyta; Laube, Gregor; Ahnert-Hilger, Gudrun] Charite Univ Med Berlin, Ctr Anat, Inst Integrat Neuroanat, Berlin, Germany.
[Sanchis-Segura, Carles; Perreau-Lenz, Stephanie; Bilbao, Ainhoa; Spanagel, Rainer] Charite Univ Med Berlin, Inst Pharmacol, Berlin, Germany.
[Birnbaumer, Lutz] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
RP Spanagel, R (reprint author), Cent Inst Mental Hlth, Dept Psychopharmacol, J5, D-68159 Mannheim, Germany.
EM gudrun.ahnert@charite.de; rainer.spanagel@zi-mannheim.de
RI Sanchis-Segura, Carla/C-5222-2012; Juranek, Judyta/I-1120-2013;
Perreau-Lenz, Stephanie/D-2309-2014;
OI Sanchis-Segura, Carla/0000-0002-6951-5972; Perreau-Lenz,
Stephanie/0000-0001-9529-6403; Juranek, Judyta /0000-0001-8665-6606
FU Deutsche Forshungsgemeinschaft [AH 67/3-3]; Forschungsforderung der
Charite; German Federal Ministry of Education and Research (BMBF;
Nationales Genomforschungsnetz); Intramural Research Program of the
National Institutes of Health [Z01ES01643]
FX This work was supported by the Deutsche Forshungsgemeinschaft (AH
67/3-3), the Forschungsforderung der Charite to G.A.H., by the German
Federal Ministry of Education and Research (BMBF; Nationales
Genomforschungsnetz) to R.S., and by the Intramural Research Program of
the National Institutes of Health to L.B. (Z01ES01643). Technical
assistance of Marion Mobes and Birgit Metze (both Charite) is gratefully
acknowledged.
NR 35
TC 13
Z9 13
U1 0
U2 8
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD OCT
PY 2008
VL 22
IS 10
BP 3736
EP 3746
DI 10.1096/fj.08-111245
PG 11
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 354MB
UT WOS:000259642600034
PM 18606864
ER
PT J
AU Rohman, MS
Koga, Y
Takano, K
Chon, H
Crouch, RJ
Kanaya, S
AF Rohman, Muhammad S.
Koga, Yuichi
Takano, Kazufumi
Chon, Hyongi
Crouch, Robert J.
Kanaya, Shigenori
TI Effect of the disease-causing mutations identified in human ribonuclease
(RNase) H2 on the activities and stabilities of yeast RNase H2 and
archaeal RNase HII
SO FEBS JOURNAL
LA English
DT Article
DE heterotrimer; Saccharomyces cerevisiae; site-directed mutagenesis;
Thermococcus kodakaraensis; type 2 RNase H
ID HIV-1 REVERSE-TRANSCRIPTASE; AICARDI-GOUTIERES-SYNDROME;
CRYSTAL-STRUCTURE; ESCHERICHIA-COLI; SACCHAROMYCES-CEREVISIAE;
HYPERTHERMOPHILIC ARCHAEON; SUBSTRATE-SPECIFICITY; BACILLUS-SUBTILIS;
DNA-REPLICATION; RNA/DNA HYBRID
AB Eukaryotic ribonuclease (RNase) H2 consists of one catalytic and two accessory subunits. Several single mutations in any one of these subunits of human RNase H2 cause Aicardi-Goutieres syndrome. To examine whether these mutations affect the complex stability and activity of RNase H2, three mutant proteins of His-tagged Saccharomyces cerevisiae RNase H2 (Sc-RNase H2*) were constructed. Sc-G42S*, Sc-L52R*, and Sc-K46W* contain single mutations in Sc-Rnh2Ap*, Sc-Rnh2Bp*, and Sc-Rnh2Cp*, respectively. The genes encoding the three subunits were coexpressed in Escherichia coli, and Sc-RNase H2* and its derivatives were purified in a heterotrimeric form. All of these mutant proteins exhibited enzymatic activity. However, only the enzymatic activity of Sc-G42S* was greatly reduced compared to that of the wild-type protein. Gly42 is conserved as Gly10 in Thermococcus kodakareansis RNase HII. To analyze the role of this residue, four mutant proteins, Tk-G10S, Tk-G10A, Tk-G10L, and Tk-G10P, were constructed. All mutant proteins were less stable than the wild-type protein by 2.9-7.6 degrees C in T-m. A comparison of their enzymatic activities, substrate binding affinities, and CD spectra suggests that the introduction of a bulky side chain into this position induces a local conformational change, which is unfavorable for both activity and substrate binding. These results indicate that Gly10 is required to make the protein fully active and stable.
C1 [Rohman, Muhammad S.; Koga, Yuichi; Takano, Kazufumi; Kanaya, Shigenori] Osaka Univ, Grad Sch Engn, Dept Mat & Life Sci, Osaka 5650871, Japan.
[Takano, Kazufumi] JST, CRESTO, Osaka, Japan.
[Chon, Hyongi; Crouch, Robert J.] NIH, Mol Genet Lab, Bethesda, MD 20892 USA.
RP Kanaya, S (reprint author), Osaka Univ, Grad Sch Engn, Dept Mat & Life Sci, 2-1 Yamadaoka, Osaka 5650871, Japan.
EM kanaya@mls.eng.osaka-u.ac.jp
FU Ministry of Education, Culture, Sports, Science, and Technology of
Japan; New Energy and Industrial Technology Development Organization
(NEDO) of Japan; Eunice Kennedy Shriver National Institutes of Child
Health and Human Development, NIH
FX We thank Drs T. Tadokoro and A. Mukaiyama for helpful discussions. This
work was supported in part by a Grant-in-Aid for Scientific Research on
Priority Areas 'Systems Genomics' from the Ministry of Education,
Culture, Sports, Science, and Technology of Japan, and by an Industrial
Technology Research Grant Program from the New Energy and Industrial
Technology Development Organization (NEDO) of Japan, and also by the
Intramural Research Program of the Eunice Kennedy Shriver National
Institutes of Child Health and Human Development, NIH.
NR 45
TC 18
Z9 18
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1742-464X
EI 1742-4658
J9 FEBS J
JI FEBS J.
PD OCT
PY 2008
VL 275
IS 19
BP 4836
EP 4849
DI 10.1111/j.1742-4658.2008.06622.x
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 348KO
UT WOS:000259209600016
PM 18721139
ER
PT J
AU Gao, S
Peng, DX
Zhang, WH
Muszynski, A
Carlson, RW
Gu, XX
AF Gao, Song
Peng, Daxin
Zhang, Wenhong
Muszynski, Artur
Carlson, Russell W.
Gu, Xin-Xing
TI Identification of two late acyltransferase genes responsible for lipid A
biosynthesis in Moraxella catarrhalis
SO FEBS JOURNAL
LA English
DT Article
DE late acyltransferase; lipo-oligosaccharide; lpxL; lpxX; Moraxella
catarrhalis
ID TEMPERATURE REQUIREMENT GENE; COLI MSBB GENE; BRANHAMELLA-CATARRHALIS;
ESCHERICHIA-COLI; NEISSERIA-MENINGITIDIS; EPITHELIAL-CELLS;
OUTER-MEMBRANE; HAEMOPHILUS-INFLUENZAE; IMMUNE-RESPONSE; SEROTYPE-A
AB Lipid A is a biological component of the lipo-oligosaccharide of a human pathogen, Moraxella catarrhalis. No other acyltransferases except for UDP-GlcNAc acyltransferase, responsible for lipid A biosynthesis in M. catarrhalis, have been identified. By bioinformatics, two late acyltransferase genes, lpxX and lpxL, responsible for lipid A biosynthesis were identified, and knockout mutants of each gene in M. catarrhalis strain O35E were constructed and named O35ElpxX and O35ElpxL. Structural analysis of lipid A from the parental strain and derived mutants showed that O35ElpxX lacked two decanoic acids (C10:0), whereas O35ElpxL lacked one dodecanoic (lauric) acid (C12:0), suggesting that lpxX encoded decanoyl transferase and lpxL encoded dodecanoyl transferase. Phenotypic analysis revealed that both mutants were similar to the parental strain in their toxicity in vitro. However, O35ElpxX was sensitive to the bactericidal activity of normal human serum and hydrophobic reagents. It had a reduced growth rate in broth and an accelerated bacterial clearance at 3 h (P < 0.01) or 6 h (P < 0.05) after an aerosol challenge in a murine model of bacterial pulmonary clearance. O35ElpxL presented similar patterns to those of the parental strain, except that it was slightly sensitive to the hydrophobic reagents. These results indicate that these two genes, particularly lpxX, encoding late acyltransferases responsible for incorporation of the acyloxyacyl-linked secondary acyl chains into lipid A, are important for the biological activities of M. catarrhalis.
C1 [Gao, Song; Peng, Daxin; Zhang, Wenhong; Gu, Xin-Xing] Natl Inst Deafness & Other Commun Disorders, Vaccine Res Sect, Rockville, MD 20850 USA.
[Muszynski, Artur; Carlson, Russell W.] Univ Georgia, Complex Carbohydrate Res Ctr, Athens, GA 30602 USA.
RP Gu, XX (reprint author), Natl Inst Deafness & Other Commun Disorders, Vaccine Res Sect, 5 Res Court, Rockville, MD 20850 USA.
EM guxx@nidcd.nih.gov
OI Muszynski, Artur/0000-0003-3497-9977
FU NIDCD/NIH; Department of Energy [DE-FG09-93-ER20097]
FX We thank E. J. Hansen for providing strain O35E/plasmid pWW115,
Shengqing Yu for advice on the pulmonary clearance assay, R. Morell for
help with DNA sequencing, Yandan Yang for help with Southern blotting,
and Lina Zhu and Yili Chen for help in manuscript preparation. This
research was supported by the Intramural Research Program of the
NIDCD/NIH and a Department of Energy grant (DE-FG09-93-ER20097) to the
CCRC.
NR 54
TC 13
Z9 14
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1742-464X
J9 FEBS J
JI FEBS J.
PD OCT
PY 2008
VL 275
IS 20
BP 5201
EP 5214
DI 10.1111/j.1742-4658.2008.06651.x
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 352QE
UT WOS:000259511300022
PM 18795947
ER
PT J
AU Crain, DA
Janssen, SJ
Edwards, TM
Heindel, J
Ho, SM
Hunt, P
Iguchi, T
Juul, A
McLachlan, JA
Schwartz, J
Skakkebaek, N
Soto, AM
Swan, S
Walker, C
Woodruff, TK
Woodruff, TJ
Giudice, LC
Guillette, LJ
AF Crain, D. Andrew
Janssen, Sarah J.
Edwards, Thea M.
Heindel, Jerrold
Ho, Shuk-mei
Hunt, Patricia
Iguchi, Taisen
Juul, Anders
McLachlan, John A.
Schwartz, Jackie
Skakkebaek, Niels
Soto, Ana M.
Swan, Shanna
Walker, Cheryl
Woodruff, Teresa K.
Woodruff, Tracey J.
Giudice, Linda C.
Guillette, Louis J., Jr.
TI Female reproductive disorders: the roles of endocrine-disrupting
compounds and developmental timing
SO FERTILITY AND STERILITY
LA English
DT Review
DE epigenetic; reproduction; endocrine disruption; aneuploidy; PCOS;
cyclicity; endometriosis; leiomyoma; breast cancer; lactation; puberty
ID POLYCYSTIC-OVARY-SYNDROME; BREAST-CANCER RISK; BISPHENOL-A EXPOSURE;
MENSTRUAL-CYCLE CHARACTERISTICS; MAMMARY-GLAND DEVELOPMENT; BODY-MASS
INDEX; PRENATAL DIETHYLSTILBESTROL EXPOSURE; OVINE UTERINE DEVELOPMENT;
CORONARY HEART-DISEASE; DIOXIN-LIKE COMPOUNDS
AB Objective: To evaluate the possible role of endocrine-disrupting compounds (EDCs) on female reproductive disorders emphasizing developmental plasticity and the complexity of endocrine-dependent ontogeny of reproductive organs. Declining conception rates and the high incidence of female reproductive disruptions warrant evaluation of the impact of EDCs on female reproductive health.
Design: Publications related to the contribution of EDCs to disorders of the ovary (aneuploidy, polycystic ovary syndrome, and altered cyclicity), uterus (endometriosis, uterine fibroids, fetal growth restriction, and pregnancy loss), breast (breast cancer, reduced duration of lactation), and pubertal timing were identified, reviewed, and summarized at a workshop.
Conclusion(S): The data reviewed illustrate that EDCs contribute to numerous human female reproductive disorders and emphasize the sensitivity of early life-stage exposures. Many research gaps are identified that limit full understanding of the contribution of EDCs to female reproductive problems. Moreover, there is an urgent need to reduce the incidence of these reproductive disorders, which can be addressed by correlative studies on early life exposure and adult reproductive dysfunction together with tools to assess the specific exposures and methods to block their effects. This review of the EDC literature as it relates to female health provides an important platform on which women's health can be improved.
C1 [Edwards, Thea M.; Guillette, Louis J., Jr.] Univ Florida, Dept Zool, Gainesville, FL 32611 USA.
[Crain, D. Andrew] Maryville Coll, Maryville, TN USA.
[Janssen, Sarah J.] Natl Resources Def Council, San Francisco, CA USA.
[Heindel, Jerrold] Natl Inst Environm Hlth Sci, Div Extramural Res & Training, Res Triangle Pk, NC USA.
[Ho, Shuk-mei] Univ Cincinnati, Coll Med, Cincinnati, OH USA.
[Hunt, Patricia] Washington State Univ, Pullman, WA 99164 USA.
[Iguchi, Taisen] Natl Inst Basic Biol, Natl Inst Nat Sci, Okazaki, Aichi 444, Japan.
[Juul, Anders; Skakkebaek, Niels] Univ Dept Growth & Reprod, Rigshosp, Copenhagen, Denmark.
[McLachlan, John A.] Tulane Univ, Ctr Bioenvironm Res, New Orleans, LA 70118 USA.
[McLachlan, John A.] Xavier Univ, New Orleans, LA 70125 USA.
[Schwartz, Jackie; Woodruff, Teresa K.] Univ Calif San Francisco, Program Reprod Hlth & Environm, San Francisco, CA 94143 USA.
[Soto, Ana M.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Swan, Shanna] Univ Rochester, Dept Obstet & Gynecol, Rochester, NY USA.
[Walker, Cheryl] Univ Texas MD Anderson Canc Ctr, Smithville, TX USA.
[Woodruff, Teresa K.] Northwestern Univ, Dept Obstet & Gynecol, Inst Womens Hlth Res, Chicago, IL USA.
[Giudice, Linda C.] Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA 94143 USA.
RP Guillette, LJ (reprint author), Univ Florida, Dept Zool, 223 Bartram Hall,Box 118525, Gainesville, FL 32611 USA.
EM ljg@zoology.ufl.edu
RI Juul, Anders /F-5864-2013;
OI Juul, Anders/0000-0002-0534-4350
FU NCRR NIH HHS [UL1 RR024926]; NICHD NIH HHS [U54 HD041857, U54 HD076188];
NIDCR NIH HHS [UL1 DE019587]; NIEHS NIH HHS [P30 ES006096]
NR 308
TC 174
Z9 178
U1 10
U2 78
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2008
VL 90
IS 4
BP 911
EP 940
DI 10.1016/j.fertnstert.2008.08.067
PG 30
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 358UQ
UT WOS:000259943400003
PM 18929049
ER
PT J
AU DeUgarte, CM
Li, M
Surrey, M
Danzer, H
Hill, D
DeCherney, AH
AF DeUgarte, Catherine M.
Li, Man
Surrey, Mark
Danzer, Hal
Hill, David
DeCherney, Alan H.
TI Accuracy of FISH analysis in predicting chromosomal status in patients
undergoing preimplantation genetic diagnosis
SO FERTILITY AND STERILITY
LA English
DT Article
DE PGD; FISH; aneuploidy; confirmation; PPV; NPV
ID IN-SITU HYBRIDIZATION; HUMAN EMBRYOS; MOSAICISM; ABNORMALITIES;
BLASTOMERES; PREEMBRYOS; BIOPSY; VITRO
AB Objective: The purpose of this Study was to determine the positive predictive value (PPV) and negative predictive value (NPV) of FISH analysis and to determine which chromosomal abnormalities are most frequently confirmed.
Design: Prospective observational.
Setting: IVF laboratory.
Patient(s): Two hundred forty-one embryos were analyzed from 98 patients.
Intervention(s): FISH reanalysis.
Main Outcome Measure(s): Embryos that would have been discarded in patients undergoing preimplantation genetic diagnosis (PGD) were fixed and FISH reanalysis was performed. Results of reanalysis were compared with the day 3 diagnosis while PPV and NPV were calculated.
Result(s): Among the 241 embryos, 198 embryos were abnormal and 43 were normal by day 3 FISH analysis. The PPV was 83% and the NPV was 81%. PPV was also determined for specific categories of aneuploidy, and certain abnormalities such as monosomies, trisomies, tetrasomies, and polyploidies were frequently confirmed on reanalysis (PPV >80%), whereas Turner syndrome diagnosis was not (PPV = 17%).
Conclusion(s): FISH analysis offers a PPV of 83% and NPV of 81% when evaluating a single blastomere in conjunction with PGD. FISH errors and mosaicism are primarily responsible for the errors associated with FISH analysis in PGD.
C1 [DeUgarte, Catherine M.] Pacific Fertil Ctr, Los Angeles, CA 90024 USA.
[Li, Man] Fertil & Surg Associates Calif, Thousand Oaks, CA USA.
[Surrey, Mark; Danzer, Hal; Hill, David] So Calif Reprod Ctr, Beverly Hills, CA USA.
[DeCherney, Alan H.] NIH, Bethesda, MD 20892 USA.
RP DeUgarte, CM (reprint author), Pacific Fertil Ctr, 10921 Wilshire Blvd,Suite 700, Los Angeles, CA 90024 USA.
EM cmdeugarte@hotmail.com
NR 20
TC 21
Z9 26
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2008
VL 90
IS 4
BP 1049
EP 1054
DI 10.1016/j.fertnstert.2007.07.1337
PG 6
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 358UQ
UT WOS:000259943400017
PM 18359020
ER
PT J
AU Hammond, CTC
Beckjord, EB
Arora, NK
Bellizzi, KM
Jeffery, DD
Aziz, NM
AF Hammond, Camille T. C.
Beckjord, Ellen B.
Arora, Neeraj K.
Bellizzi, Keith M.
Jeffery, Diana D.
Aziz, Noreen M.
TI Non-Hodgkin's lymphoma survivors' fertility and sexual function-related
information needs
SO FERTILITY AND STERILITY
LA English
DT Editorial Material
ID CASE-MATCHED CONTROLS; CANCER-PATIENTS; BREAST-CANCER; ONCOLOGY; WOMEN
AB This population-based study assessed information needs related to fertility and sexual function in 250 non-Hodgkin's lymphoma survivors from a Los Angeles Surveillance, Epidemiology, and End Results cancer registry 2-5 years after diagnosis. Results suggest that many survivors have persistent fertility and sexual concerns 2-5 years after diagnosis, highlighting the importance of oncologists working collaboratively with reproductive endocrinologists to uniformly inform patients about these issues during routine follow-up cancer care visits.
C1 [Hammond, Camille T. C.] Univ Maryland, Sch Med, Off Policy & Planning, Baltimore, MD 21201 USA.
[Beckjord, Ellen B.] RAND Corp, Behav & Social Sci, Pittsburgh, PA USA.
[Arora, Neeraj K.] NCI, Outcome Res Branch, Appl Res Program, Bethesda, MD 20892 USA.
[Bellizzi, Keith M.; Jeffery, Diana D.; Aziz, Noreen M.] NCI, Div Canc Control & Populat Sci, Off Canc Survivorship, Bethesda, MD 20892 USA.
RP Hammond, CTC (reprint author), Univ Maryland, Sch Med, Off Policy & Planning, 401 W Redwood St, Baltimore, MD 21201 USA.
EM chammond@som.umaryland.edu
FU NCI NIH HHS [N01-PC-35139, N02-PC-15105]; PHS HHS [U55/CCR921930-02]
NR 21
TC 20
Z9 20
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2008
VL 90
IS 4
BP 1256
EP 1258
DI 10.1016/j.fertnstert.2007.08.081
PG 3
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 358UQ
UT WOS:000259943400054
PM 18083170
ER
PT J
AU McGovern, PG
Carson, SA
Barnhart, HX
Myers, ER
Legro, RS
Diamond, MP
Carr, BR
Schlaff, WD
Coutifaris, C
Cataldo, NA
Steinkampf, MP
Nestler, JE
Gosman, G
Leppert, PC
Giudice, LC
AF McGovern, Peter G.
Carson, Sandra A.
Barnhart, Huiman X.
Myers, Evan R.
Legro, Richard S.
Diamond, Michael P.
Carr, Bruce R.
Schlaff, William D.
Coutifaris, Christos
Cataldo, Nicholas A.
Steinkampf, Michael P.
Nestler, John E.
Gosman, Gabey
Leppert, Phyllis C.
Giudice, Linda C.
CA NICHD Reprod Med Network Reprod
TI Medication adherence and treatment success in the National Institute of
Child Health and Human Development-Reproductive Medicine Network's
Pregnancy in Polycystic Ovary Syndrome Trial
SO FERTILITY AND STERILITY
LA English
DT Editorial Material
ID TABLETS; TWICE
AB We investigated whether poor adherence with metformin tablets may have contributed to the poor success rates seen in the metformin-containing arms of the Pregnancy in Polycystic Ovary Syndrome (PPCOS) Trial. Median adherence for both metformin and clomiphene citrate tablets was within acceptable limits and unrelated to ovulation: thus, failure to comply with physician recommendations for metformin dosing was not the reason for low ovulation and pregnancy rates in the PPCOS Trial.
C1 [McGovern, Peter G.] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Obstet Gynecol & Womens Hlth, Newark, NJ 07101 USA.
[Carson, Sandra A.] Brown Univ, Warren Alpert Med Sch, Dept Obstet & Gynecol, Providence, RI 02912 USA.
[Barnhart, Huiman X.; Myers, Evan R.] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC USA.
[Myers, Evan R.] Duke Univ, Med Ctr, Dept Obstet & Gynecol, Durham, NC 27710 USA.
[Legro, Richard S.] Penn State Univ, Dept Obstet & Gynecol, Hershey, PA USA.
[Diamond, Michael P.] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
[Carr, Bruce R.] Univ Texas SW Med Ctr Dallas, Dept Obstet & Gynecol, Dallas, TX 75390 USA.
[Schlaff, William D.] Univ Colorado, Dept Obstet & Gynecol, Denver, CO 80202 USA.
[Coutifaris, Christos] Univ Penn, Sch Med, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
[Cataldo, Nicholas A.] Stanford Univ, Palo Alto, CA 94304 USA.
[Steinkampf, Michael P.] Univ Alabama, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
[Nestler, John E.] Virginia Commonwealth Univ, Sch Med, Dept Med, Richmond, VA USA.
[Gosman, Gabey] Univ Pittsburgh, Dept Obstet & Gynecol, Pittsburgh, PA USA.
[Leppert, Phyllis C.] NICHHD, Reprod Sci Branch, Bethesda, MD 20892 USA.
[Giudice, Linda C.] Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA 94143 USA.
RP McGovern, PG (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Obstet Gynecol & Womens Hlth, 185 S Orange Ave,MSB-E506,POB 1709, Newark, NJ 07101 USA.
EM mcgovepg@umdnj.edu
OI Diamond, Michael/0000-0001-6353-4489
FU NCRR NIH HHS [M01 RR010732, MO1 RR 10732, MO1RR00056, M01 RR000056, C06
RR016499]; NICHD NIH HHS [U10 HD38999, U10 HD38998, U01 HD38997, U10
HD39005, U10 HD27011, U10 HD038988, U10 HD027049, U10 HD27049,
U54-HD29834, U10 HD039005, R01 HD029834, U10 HD38992, U10 HD033172, U10
HD38988, U10 HD33172, U10 HD038992, U10 HD027011, U10 HD038999, U10
HD038998, U01 HD038997]
NR 7
TC 5
Z9 5
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2008
VL 90
IS 4
BP 1283
EP 1286
DI 10.1016/j.fertnstert.2007.09.004
PG 4
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 358UQ
UT WOS:000259943400062
PM 18082737
ER
PT J
AU Yauger, BJ
Feinberg, EC
Levens, ED
Gustofson, RL
Larsen, FW
DeCherney, AH
AF Yauger, Belinda J.
Feinberg, Eve C.
Levens, Eric D.
Gustofson, Robert L.
Larsen, Frederick W.
DeCherney, Alan H.
TI Pre-cycle saline infusion sonography minimizes assisted reproductive
technologies cycle cancellation due to endometrial polyps
SO FERTILITY AND STERILITY
LA English
DT Editorial Material
ID IN-VITRO FERTILIZATION; OFFICE HYSTEROSCOPY; UTERINE; WOMEN;
SONOHYSTEROGRAPHY; INFERTILITY; WORK; IVF
AB Pre-ART cycle screening with saline infusion sonohysterography is effective at limiting cycle cancellation caused by endometrial polyps to 0.5%. Although a thickened lining at the time of baseline ultrasound can be indicative of a uterine polyp, a normal endometrial lining does not eliminate the possibility that a polyp will be discovered during the cycle.
C1 [Yauger, Belinda J.; Feinberg, Eve C.; Levens, Eric D.; Gustofson, Robert L.; Larsen, Frederick W.; DeCherney, Alan H.] NICHHD, Reprod Biol & Branch, NIH, Bethesda, MD 20892 USA.
[Yauger, Belinda J.; Feinberg, Eve C.; Levens, Eric D.; Gustofson, Robert L.; Larsen, Frederick W.; DeCherney, Alan H.] NIH, Walter Reed Army Med Ctr, Natl Naval Med Ctr, Bethesda, MD 20892 USA.
[Yauger, Belinda J.; Feinberg, Eve C.; Levens, Eric D.; Gustofson, Robert L.; Larsen, Frederick W.; DeCherney, Alan H.] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Yauger, Belinda J.; Feinberg, Eve C.; Levens, Eric D.; Gustofson, Robert L.; Larsen, Frederick W.; DeCherney, Alan H.] Walter Reed Army Med Ctr, Assisted Reprod Technol Program, Washington, DC 20307 USA.
RP DeCherney, AH (reprint author), NICHHD, Reprod Biol & Branch, NIH, 10 Ctr Dr MSC 1109,Bldg 10,CRC,1-3140, Bethesda, MD 20892 USA.
EM decherna@mail.nih.gov
NR 18
TC 4
Z9 5
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2008
VL 90
IS 4
BP 1324
EP 1326
DI 10.1016/j.fertnstert.2007.09.050
PG 3
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 358UQ
UT WOS:000259943400073
PM 18155202
ER
PT J
AU McCutchan, TF
AF McCutchan, Thomas F.
TI Malaria control in Africa: a mirage a trois
SO FUTURE MICROBIOLOGY
LA English
DT Editorial Material
ID INFECTION
C1 NIAID, Growth & Dev Sect, NIH, Bethesda, MD 20892 USA.
RP McCutchan, TF (reprint author), NIAID, Growth & Dev Sect, NIH, Bethesda, MD 20892 USA.
EM fmccutchan@niaid.nih.gov
FU Intramural NIH HHS [NIH0010147301]; PHS HHS [NIH0010147301]
NR 9
TC 0
Z9 0
U1 0
U2 1
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1746-0913
J9 FUTURE MICROBIOL
JI Future Microbiol.
PD OCT
PY 2008
VL 3
IS 5
BP 479
EP 483
DI 10.2217/17460913.3.5.479
PG 5
WC Microbiology
SC Microbiology
GA 363AZ
UT WOS:000260239600001
PM 18811229
ER
PT J
AU Zujewski, JA
Kamin, L
AF Zujewski, Jo Anne
Kamin, Leah
TI Trial Assessing Individualized Options for Treatment for breast cancer:
the TAILORx trial
SO FUTURE ONCOLOGY
LA English
DT Article
ID GENE-EXPRESSION; CLINICAL-TRIALS; HORMONAL-THERAPY; ADJUVANT THERAPY;
PROGNOSTIC ROLE; 21-GENE ASSAY; CHEMOTHERAPY; RECURRENCE; SIGNATURE;
TAMOXIFEN
AB Novel genetic profiling tests of breast cancer tissue have been shown to be prognostic for overall survival and predictive of local and distant rates of recurrence in breast cancer patients. One of these tests, Oncotype DX (TM), is a diagnostic test comprised of a 21-gene assay applied to paraffin-em bedded breast cancer tissue, which allows physicians to predict subgroups of hormone-receptor-positive, node-negative patients who may benefit from hormonal therapy alone or require adjuvant chemotherapy to attain the best survival outcome. The results of the assay are converted to a recurrence score (0-100) that has been found to be predictive of 10- and 15-year local and distant recurrence in node-negative, estrogen-receptor-positive breast cancer patients. Previous studies have shown that patients with high recurrence scores benefit from adjuvant chemotherapy, whereas patients with low recurrence scores do not. To evaluate the ability to guide treatment decisions in the group with a mid-range recurrence score, the North American Cooperative Groups developed the Trial Assessing IndiviuaLized Options for Treatment for breast cancer, a randomized trial of chemotherapy followed by hormonal therapy versus hormonal therapy alone on invasive disease-free survival-ductal carcinoma in situ (IDFS-DCIS) survival in women with node-negative, estrogen-receptor-positive breast cancer with a recurrence score of 11-25. The study was initiated in May 2006 and approximately 4500 patients will be randomized. This article describes the rationale, methodology, statistical analysis and implications of the results on clinical practice.
C1 [Zujewski, Jo Anne] NCI, Clin Invest Branch, Canc Therapy Evaluat Program, Div Canc Treatment & Diag, Rockville, MD 20852 USA.
[Kamin, Leah] EMMES Corp, Clin Informat Specialist CTIS, Rockville, MD 20850 USA.
RP Zujewski, JA (reprint author), NCI, Clin Invest Branch, Canc Therapy Evaluat Program, Div Canc Treatment & Diag, 6130 Execut Blvd,EPN Room 7025, Rockville, MD 20852 USA.
EM zujewski@nih.gov; lkamin@emmes.com
NR 57
TC 75
Z9 75
U1 0
U2 11
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1479-6694
J9 FUTURE ONCOL
JI Future Oncol.
PD OCT
PY 2008
VL 4
IS 5
BP 603
EP 610
DI 10.2217/14796694.4.5.603
PG 8
WC Oncology
SC Oncology
GA 384WP
UT WOS:000261775200008
PM 18922117
ER
PT J
AU Schrager, MA
Kelly, VE
Price, R
Ferrucci, L
Shumway-Cook, A
AF Schrager, Matthew A.
Kelly, Valerie E.
Price, Robert
Ferrucci, Luigi
Shumway-Cook, Anne
TI The effects of age on medio-lateral stability during normal and narrow
base walking
SO GAIT & POSTURE
LA English
DT Article
DE mobility; aging; tandem walk; postural controls; frontal plane stability
ID OLDER-ADULTS; FALL RISK; GAIT; BALANCE; MOBILITY; VARIABILITY;
INDICATORS
AB We examined age-related differences in frontal plane stability during performance of narrow base (NB) walking relative to usual gait. A cross-sectional analysis of participants from the Baltimore Longitudinal Study of Aging (BLSA) was performed on data from the BLSA Motion Analysis Laboratory. Participants were 34 adults aged 54-92 without history of falls. We measured step error rates during NB gait and spatial-temporal parameters, frontal plane stability, and gait variability during usual and NB gait. There was a non-significant age-associated linear increase in step error rate (P = 0.12) during NB gait. With increasing age, step width increased (P = 0.002) and step length and stride velocity decreased (P < 0.001). especially during NB gait. Age-associated increases in medio-lateral (M-L) center of mass (COM) peak velocity (P < 0.001) and displacement (P = 0.005) were also greater during NB compared to usual gait. With increasing age there was greater variability in stride velocity (P = 0.001) and step length (P < 0.001) under both conditions. Age-associated differences related to M-L COM stability Suggest that the quantification of COM control during NB gait may improve identification of older persons at increased falls risk. Published by Elsevier B.V.
C1 [Schrager, Matthew A.; Ferrucci, Luigi] NIA, Clin Res Branch, NIH, Harbor Hosp Ctr, Baltimore, MD 21225 USA.
[Kelly, Valerie E.; Price, Robert; Shumway-Cook, Anne] Univ Washington, Dept Rehabil Med, Seattle, WA 98195 USA.
RP Schrager, MA (reprint author), Univ Kansas, Hlth Sports & Exercise Sci Dept, Robinson Ctr, 1301 Sunnyside Ave,Room 101A, Lawrence, KS 66045 USA.
EM schrag17@ku.edu
OI Kelly, Valerie E./0000-0002-0099-9219
FU NIH; National Institute on Aging
FX This research was supported (in part) by the Intramural Research Program
of the NIH, National Institute on Aging. Data for these analyses were
obtained from the Baltimore Longitudinal Study of Aging, a study
performed by the National Institute on Aging.
NR 24
TC 73
Z9 75
U1 2
U2 15
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0966-6362
J9 GAIT POSTURE
JI Gait Posture
PD OCT
PY 2008
VL 28
IS 3
BP 466
EP 471
DI 10.1016/j.gaitpost.2008.02.009
PG 6
WC Neurosciences; Orthopedics; Sport Sciences
SC Neurosciences & Neurology; Orthopedics; Sport Sciences
GA 354GP
UT WOS:000259627200018
PM 18400500
ER
PT J
AU Schatzkin, A
Park, Y
Leitzmann, MF
Hollenbeck, AR
Cross, AJ
AF Schatzkin, Arthur
Park, Yikyung
Leitzmann, Michael F.
Hollenbeck, Albert R.
Cross, Amanda J.
TI Prospective study of dietary fiber, whole grain foods, and small
intestinal cancer
SO GASTROENTEROLOGY
LA English
DT Article
ID HEALTH-AMERICAN-ASSOCIATION; RETIRED-PERSONS DIET; COLORECTAL-CANCER;
RISK-FACTORS; NATIONAL-INSTITUTES; COHORT; ADENOCARCINOMA; CONSUMPTION
AB Background & Aims: Although a number of epidemiologic studies have found dietary fiber and whole grains to be inversely associated with colorectal cancer incidence, studies of dietary and other risk factors for small intestinal cancer have been sparse and all of a case-control design. We conducted a prospective cohort study to determine the relationship between intake of dietary fiber/whole grains and the incidence of small intestinal cancer. Methods: We analyzed dietary data collected in 1995 and 1996 from 293,703 men and 198,618 women in the National Institutes of Health-AARP Diet and Health Study. We used multivariate Cox proportional hazards models to estimate relative risk (RR) and 2-sided 95% confidence intervals (CIs) for quintiles of dietary fiber and whole grain intake. Results: Through 2003, 165 individuals developed small intestinal cancers. Dietary fiber/whole grain intake was generally associated with a lower risk of small intestinal cancer. The multivariate RRs (95% CIs; 5th vs 1st intake quintile) were 0.79 (0.43-1.44; P trend, .41) for total dietary fiber, 0.51 (0.29-0.89; P trend, .01) for fiber from grains, and 0.59 (0.33-1.05; P trend, .06) for whole grain foods. Conclusions: intake of fiber from grains and whole-grain foods was inversely associated with small intestinal cancer incidence; the RR values were consistent with those from the same dietary factors for large bowel cancer in this cohort. In conjunction with the anatomic and physiologic commonalities of the large and small bowel, as well as the mutually increased risks for second cancer for both organs, grain fiber and whole grain foods seem to protect against lower gastrointestinal cancers.
C1 [Schatzkin, Arthur; Park, Yikyung; Leitzmann, Michael F.; Cross, Amanda J.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
RP Schatzkin, A (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd, Rockville, MD 20852 USA.
EM schatzka@mail.nih.gov
OI Park, Yikyung/0000-0002-6281-489X
FU National Cancer Institute; National Institutes of Health; Department of
Health and Human Services
FX Supported by the Intramural Research Program of the National Cancer
Institute, National Institutes of Health, Department of Health and Human
Services.
NR 24
TC 48
Z9 50
U1 0
U2 8
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2008
VL 135
IS 4
BP 1163
EP 1167
DI 10.1053/j.gastro.2008.07.015
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 359JM
UT WOS:000259982800023
PM 18727930
ER
PT J
AU Ladu, S
Calvisi, DF
Conner, EA
Farina, M
Factor, VM
Thorgeirsson, SS
AF Ladu, Sara
Calvisi, Diego F.
Conner, Elizabeth A.
Farina, Miriam
Factor, Valentina M.
Thorgeirsson, Snorri S.
TI E2F1 inhibits c-Myc-driven apoptosis via PIK3CA/Akt/mTOR and COX-2 in a
mouse model of human liver cancer
SO GASTROENTEROLOGY
LA English
DT Article
ID CELL-GROWTH CONTROL; HEPATOCELLULAR-CARCINOMA; RB/E2F PATHWAY; AKT
ACTIVATION; S-PHASE; EXPRESSION; DEATH; GENE; TRANSCRIPTION; PROMOTER
AB Background & Aims: Resistance to apoptosis is essential for cancer growth. We previously reported that hepatic coexpression of c-Myc and E2F1, 2 key regulators of proliferation and apoptosis, enhanced hepatocellular carcinoma (HCC) development in transgenic mice. Here, we investigated the molecular mechanisms underlying oncogenic cooperation between c-Myc and E2F1 in relationship to human liver cancer. Methods: Activation of pro- and antiapoptoric cascades was assessed by immunoblotting in experimental HCC models and in human HCC. Effect of antisense oligodeoxy nucleotides against c-Myc and E2F1 was studied in human HCC cell fines. Suppression of catalytic subunit p110 alpha of phosphatidylinositol 3-kinase (PIK3CA)/Akt, mammalian target of rapamycin (mTOR), and cyclooxygenase (COX)-2 pathways was achieved by pharmacologic inhibitors and small interfering RNA in human and mouse HCC cell lines. Results: Coexpression with E2F1 did not increase proliferation triggered by c-Myc overexpression but conferred a strong resistance to c-Myc-initiated apoptosis via concomitant induction of PIK3CA/Akt/mTOR and c-Myb/COX-2 survival pathways. COX-2 was not induced in c-Myc and rarely in E2F1 tumors. In human HCC, PIK3CA/Akt/mTOR and c-Myb/COX-2 pathways were similarly activated, with levels of PIK3CA/Akt, mTOR, and c-Myb being inversely associated with patients' survival length. Silencing c-Myc and E2F1 reduced PIK3CA/Akt and mTOR and completely abolished c-Myb and COX-2 expression in human HCC cell fines. Finally, simultaneous inhibition of PIK3CA/Akt/mTOR and COX-2 activity in in vitro models caused massive apoptosis of neoplastic hepatocytes. Conclusions: E2F1 may function as a critical antiapoptotic factor both in human and in rodent liver cancer through its ability to counteract c-Myc-driven apoptosis via activation of PIK3CA/Akt/mTOR and c-Myb/COX-2 pathways.
C1 [Ladu, Sara; Calvisi, Diego F.; Conner, Elizabeth A.; Farina, Miriam; Factor, Valentina M.; Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, Natl Inst Hlth, Ctr Canc Res, Bethesda, MD 20892 USA.
[Calvisi, Diego F.] Univ Sassari, Expt Pathol & Oncol Sect, Dept Biomed Sci, I-07100 Sassari, Italy.
RP Thorgeirsson, SS (reprint author), NCI, Expt Carcinogenesis Lab, Natl Inst Hlth, Ctr Canc Res, Bldg 37,Room 4146A,37 Convent Dr, Bethesda, MD 20892 USA.
EM snorri_thorgeirsson@nih.gov
FU National Cancer Institutes of Health; National Cancer Institute; Center
for Cancer Research
FX Supported by funds from the Intramural Research Program of National
Cancer Institutes of Health, National Cancer Institute, and Center for
Cancer Research.
NR 48
TC 60
Z9 63
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2008
VL 135
IS 4
BP 1322
EP 1332
DI 10.1053/j.gastro.2008.07.012
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 359JM
UT WOS:000259982800040
PM 18722373
ER
PT J
AU Moon, KH
Hood, BL
Mukhopadhyay, P
Rajesh, M
Abdelmegeed, MA
Kwon, YI
Conrads, TP
Veenstra, TD
Song, BJ
Pacher, P
AF Moon, Kwan-Hoon
Hood, Brian L.
Mukhopadhyay, Partha
Rajesh, Mohanraj
Abdelmegeed, Mohamed A.
Kwon, Yong-Il
Conrads, Thomas P.
Veenstra, Timothy D.
Song, Byoung-Joon
Pacher, Pal
TI Oxidative inactivation of key mitochondrial proteins leads to
dysfunction and injury in hepatic ischemia reperfusion
SO GASTROENTEROLOGY
LA English
DT Article
ID NITRIC-OXIDE; RAT-LIVER; ISCHEMIA/REPERFUSION INJURY; ALDEHYDE
DEHYDROGENASE; PROTEOMIC ANALYSIS; S-NITROSYLATION; FATTY LIVER;
MOUSE-LIVER; PEROXYNITRITE; TRANSPLANTATION
AB Background & Aims: Ischemia-reperfusion (I/R) is a major mechanism of liver injury following hepatic surgery or transplantation. Despite numerous reports on the role of oxidative/nitrosative stress and mitochondrial dysfunction in hepatic I/R injury, the proteins that are oxidatively modified during I/R damage are poorly characterized. this study was aimed at investigating, the oxidatively modified proteins underlying the mechanism for mitochondrial dysfunction in hepatic I/R injury. We also studied the effects of a superoxide dismutase mimetic/peroxynitrite scavenger metalloporphyrin (MnTMPyP) on oxidatively modified proteins and their functions. Methods: The oxidized and/or S-nitrosylated mitochondrial proteins from I/R-injured mouse livers with or without MnTMPyP pretreatment were labeled with biotin-N-maleimide, purified with streptavidin-agarose, and resolved by 2-dimensional gel electrophoresis. The identities of the oxidatively modified proteins were determined using mass spectrometric analysis. Liver histopathology, serum transaminase levels, nitrosative stress markers, and activities of oxidatively modified mitochondrial proteins were measured. Results: Comparative 2-dimensional gel analysis revealed markedly increased numbers of oxidized and S-nitrosylated mitochondrial proteins following hepatic I/R injury. Many key mitochondrial. enzymes involved in cellular defense, fat metabolism, energy supply, and chaperones were identified as being oxidatively modified proteins. Pre-treatment with MnTMPyP attenuated the I/R-induced increased serum transaminase levels, histologic damage, increased inducible nitric oxide synthase expression, and S-nitrosylation and/or nitration of various key mitochondrial proteins. MnTMPyP pretreatment also restored I/R-induced suppressed activities of mitochondrial aldehyde dehydrogenase, 3-ketoacyl-CoA thiolases, and adenosine triphosphate synthase. Conclusions: These results suggest that increased nitrosative stress is critically important in promoting S-nitrosylation and nitration of various mitochondrial proteins, leading to mitochondrial dysfunction with decreased energy supply and increased hepatic injury.
C1 [Moon, Kwan-Hoon; Abdelmegeed, Mohamed A.; Kwon, Yong-Il; Song, Byoung-Joon] NIAAA, Lab Membrane Biochem & Biophys, Bethesda, MD 20892 USA.
[Hood, Brian L.; Conrads, Thomas P.; Veenstra, Timothy D.] SAIC Frederick Inc, Lab Proteom & Analyt Technol, NCI Frederick, Frederick, MD USA.
[Mukhopadhyay, Partha; Rajesh, Mohanraj; Pacher, Pal] NIAAA, Lab Physiol Studies, Sect Oxidat Stress & Tissue Injury, Bethesda, MD 20892 USA.
RP Song, BJ (reprint author), NIAAA, Lab Membrane Biochem & Biophys, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM bjs@mail.nih.gov
RI MUKHOPADHYAY, PARTHA/G-3890-2010; Pacher, Pal/B-6378-2008
OI MUKHOPADHYAY, PARTHA/0000-0002-1178-1274; Pacher,
Pal/0000-0001-7036-8108
FU National Institute on Alcohol Abuse and Alcoholism; National Cancer
Institute; National Institutes of Health [N01-C0-12400]
FX Supported by the Intramural Research Program of National Institute on
Alcohol Abuse and Alcoholism and National Cancer Institute, National
Institutes of Health, under contract No. N01-C0-12400.
NR 50
TC 65
Z9 66
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2008
VL 135
IS 4
BP 1344
EP 1357
DI 10.1053/j.gastro.2008.06.048
PG 14
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 359JM
UT WOS:000259982800042
PM 18778711
ER
PT J
AU Taylor, GA
Rodriguiz, RM
Greene, RI
Daniell, X
Henry, SC
Crooks, KR
Kotloski, R
Tessarollo, L
Phillips, LE
Wetsel, WC
AF Taylor, Gregory A.
Rodriguiz, Ramona M.
Greene, Robert I.
Daniell, Xiaoju
Henry, Stanley C.
Crooks, Kristy R.
Kotloski, Robert
Tessarollo, Lino
Phillips, Lindsey E.
Wetsel, William C.
TI Behavioral characterization of P311 knockout mice
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE behavior; emotionality; learning; memory; mutant mice; P311
ID FEAR-POTENTIATED STARTLE; CELL-MIGRATION; MUTANT MICE; HIPPOCAMPUS;
MEMORY; EXPRESSION; NEUROGENESIS; PERFORMANCE; INHIBITION; CEREBELLUM
AB P311 is an 8-kDa protein that is expressed in many brain regions, particularly the hippocampus, cerebellum and olfactory lobes, and is under stringent regulation by developmental, mitogenic and other physiological stimuli. P311 is thought to be involved in the transformation and motility of neural cells; however, its role in normal brain physiology is undefined. To address this point, P311-deficient mice were developed through gene targeting and their behaviors were characterized. Mutants displayed no overt abnormalities, bred normally and had normal survival rates. Additionally, no deficiencies were noted in motor co-ordination, balance, hearing or olfactory discrimination. Nevertheless, P311-deficient mice showed altered behavioral responses in learning and memory. These included impaired responses in social transmission of food preference, Morris water maze and contextual fear conditioning. Additionally, mutants displayed altered emotional responses as indicated by decreased freezing in contextual and cued fear conditioning and reduced fear-potentiated startle. Together, these data establish P311 as playing an important role in learning and memory processes and emotional responses.
C1 [Rodriguiz, Ramona M.; Phillips, Lindsey E.; Wetsel, William C.] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC 27710 USA.
[Taylor, Gregory A.; Greene, Robert I.; Henry, Stanley C.] Vet Adm Med Ctr, Ctr Geriatr Res Educ & Clin, Durham, NC 27705 USA.
[Taylor, Gregory A.; Greene, Robert I.; Daniell, Xiaoju; Wetsel, William C.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Taylor, Gregory A.; Daniell, Xiaoju] Duke Univ, Med Ctr, Dept Mol Genet & Microbiol, Durham, NC 27710 USA.
[Taylor, Gregory A.; Greene, Robert I.; Daniell, Xiaoju] Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA.
[Crooks, Kristy R.; Kotloski, Robert; Wetsel, William C.] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA.
[Wetsel, William C.] Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA.
[Taylor, Gregory A.; Greene, Robert I.; Daniell, Xiaoju] Duke Univ, Med Ctr, Div Geriatr, Durham, NC 27710 USA.
[Taylor, Gregory A.; Greene, Robert I.; Daniell, Xiaoju] Duke Univ, Med Ctr, Ctr Study Aging & Human Dev, Durham, NC 27710 USA.
[Rodriguiz, Ramona M.; Phillips, Lindsey E.; Wetsel, William C.] Duke Univ, Med Ctr, Mouse Behav & Neuroendocrine Anal Core Facil, Durham, NC 27710 USA.
[Tessarollo, Lino] Ctr Canc Res, Natl Canc Inst, Mouse Canc Genet Program, Frederick, MD USA.
RP Wetsel, WC (reprint author), Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, 028 CARL Bldg, Durham, NC 27710 USA.
EM wetse001@mc.duke.edu
FU John A. Hartford Foundation; American Psychological Association
postdoctoral diversity fellowship
FX We wish to thank Dr Laura Hale for histological analyses of the P311
mice and Drs Len White and George Vande Woude for many helpful
discussions. We also wish to thank Rosalie Bateson, Sara Jiang, Yuxin
Ma, Lien Nguyen, Natalia Pogorelova, John Wilkins and Sicong Zhou for
their assistance in behavioral testing. This work was supported in part
by a grant from the John A. Hartford Foundation to G. A. T., an American
Psychological Association postdoctoral diversity fellowship to R. M. R.
and unrestricted funds to W. C.W
NR 35
TC 12
Z9 13
U1 5
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD OCT
PY 2008
VL 7
IS 7
BP 786
EP 795
DI 10.1111/j.1601-183X.2008.00420.x
PG 10
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 355AK
UT WOS:000259680800010
PM 18616608
ER
PT J
AU Sourirajan, A
Lichten, M
AF Sourirajan, Anuradha
Lichten, Michael
TI Polo-like kinase Cdc5 drives exit from pachytene during budding yeast
meiosis
SO GENES & DEVELOPMENT
LA English
DT Article
DE Saccharomyces cerevisiae; synaptonemal complex; joint molecules;
crossover; cyclin-dependent kinase; Holliday junction
ID DOUBLE-STRAND BREAKS; MEIOTIC CHROMOSOME SYNAPSIS;
SACCHAROMYCES-CEREVISIAE; SYNAPTONEMAL COMPLEX; RECOMBINATION;
CHECKPOINT; NDT80; PHOSPHORYLATION; DIVISION; LOCALIZATION
AB In budding yeast, exit from the pachytene stage of meiosis requires the mid-meiosis transcription factor Ndt80, which promotes expression of similar to 200 genes. Ndt80 is required for meiotic function of polo-like kinase (PLK, Cdc5) and cyclin-dependent kinase (CDK), two cell cycle kinases previously implicated in pachytene exit. We show that ongoing CDK activity is dispensable for two events that accompany exit from pachytene: crossover formation and synaptonemal complex breakdown. In contrast, CDC5 expression in ndt80 Delta mutants efficiently promotes both events. Thus, Cdc5 is the only member of the Ndt80 transcriptome required for this critical step in meiotic progression.
C1 [Sourirajan, Anuradha; Lichten, Michael] NCI, Lab Biochem & Mol Biol, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Lichten, M (reprint author), NCI, Lab Biochem & Mol Biol, Ctr Canc Res, Bethesda, MD 20892 USA.
EM lichten@helix.nih.gov
RI Lichten, Michael/C-5795-2013
OI Lichten, Michael/0000-0001-9707-2956
FU Intramural NIH HHS
NR 40
TC 73
Z9 73
U1 1
U2 3
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI WOODBURY
PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
SN 0890-9369
J9 GENE DEV
JI Genes Dev.
PD OCT 1
PY 2008
VL 22
IS 19
BP 2627
EP 2632
DI 10.1101/gad.1711408
PG 6
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 355HV
UT WOS:000259700900006
PM 18832066
ER
PT J
AU Kim, SH
Kim, UK
Chae, JJ
Baek, JI
Choi, SY
Bae, JW
Kim, SH
Kim, HS
AF Kim, Sung Han
Kim, Un-Kyung
Chae, Jae Jin
Baek, Jeong-In
Choi, Soo Young
Bae, Jae Woong
Kim, Sang-Hyun
Kim, Hyo-Soo
TI Genetic Variations of the Apolipoprotein B Gene in Korean People and Its
Association with Hypercholesterolemia
SO GENES & GENOMICS
LA English
DT Article
DE apolipoprotein B gene; polymorphisms; hypercholesterolemia; genetics;
coronary artery disease
ID CORONARY-HEART-DISEASE; INSERTION-DELETION POLYMORPHISM;
POLYMERASE-CHAIN-REACTION; LOW-DENSITY LIPOPROTEIN; CHOLESTEROL LEVELS;
LIPID PARAMETERS; LINKAGE DISEQUILIBRIUM; MYOCARDIAL-INFARCTION;
SERUM-CHOLESTEROL; XBAI POLYMORPHISM
AB Genetic polymorphisms at the apolipoprotein B have been associated with elevated plasma concentrations of LDL, atherosclerosis and increased risk of coronary artery disease. 106 individuals composed of 46 hypercholesterolemic patients and 60 controls were analyzed with Ins/Del length polymorphism, four RFLPs (HincII, PvuII, AluI, EcoRI) and 3'-VNTR to clarify the characteristics of the apolipoprotein B gene and to determine their influence on the lipid profile of hypercholesterolemic patients and controls in Korea. A total of 212 apolipoprotein B alleles from six markers were identified in this study. Heterozygosityranges from zero to 0.32, and the genotyope frequencies in the case of 3'-VNTR are significantly different between two groups. Analysis of linkage disequilibrium revealed paired nonrandom associations between four pairs of polymorphic sites of the apolipoprotein B gene (P < 0.05). Moreover, addition of all 4 polymorphic sites provided the highest PIC value. This study also investigated the association of these polymorphisms with the patients and with variation in lipid levels. A significant association between 3'-VNTR genotypes and Lp(a) was observed in hypercholesterolemic patients (p < 0.05). The results suggest that genotypes of six polymorphic markers were not significantly associated with TC, TG or LDL-chol level between the patients and controls in the Koreans.
C1 [Kim, Sang-Hyun; Kim, Hyo-Soo] Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 151, South Korea.
[Kim, Sung Han] Digital Genom, Seoul, South Korea.
[Kim, Un-Kyung; Baek, Jeong-In; Choi, Soo Young; Bae, Jae Woong] Kyungpook Natl Univ, Coll Nat Sci, Dept Biol, Taegu, South Korea.
[Chae, Jae Jin] NIAMSD, Genet & Genom Branch, NIH, Bethesda, MD 20892 USA.
RP Kim, HS (reprint author), Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 151, South Korea.
EM hyosoo@snu.ac.kr
RI Kim, Hyo Soo/J-2753-2012; Kim, Sang-Hyun/J-5402-2012
FU KOREA HEALTH 21 R&D PROJECT, MINISTRY OF HEALTH AND WELFARE, REPUBLIC OF
KOREA [0412-CR02-0704-0001]; Korea Institute of Industrial Technology
Evaluation and Planning [ITEP-10023399]; RIC/NMR; Brain Korea 21
program, Ministry of Education and Human Resources Develpments, Korea
FX This study was supported by a grant of the KOREA HEALTH 21 R&D PROJECT,
MINISTRY OF HEALTH AND WELFARE, REPUBLIC OF KOREA (0412-CR02-0704-0001).
It was also supported by a Korea Institute of Industrial Technology
Evaluation and Planning Grant (No. ITEP-10023399) and the RIC/NMR
program. JIB, SYC and JWB were supported by scholarships from the Brain
Korea 21 program, Ministry of Education and Human Resources Develpments,
Korea.
NR 45
TC 0
Z9 0
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1976-9571
J9 GENES GENOM
JI Genes Genom.
PD OCT
PY 2008
VL 30
IS 5
BP 487
EP 497
PG 11
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 372JD
UT WOS:000260897000007
ER
PT J
AU Dohke, K
Miyazaki, S
Tanaka, K
Urano, T
Grewal, SIS
Murakami, Y
AF Dohke, Kohei
Miyazaki, Shota
Tanaka, Katsunori
Urano, Takeshi
Grewal, Shiv I. S.
Murakami, Yota
TI Fission yeast chromatin assembly factor 1 assists in the
replication-coupled maintenance of heterochromatin
SO GENES TO CELLS
LA English
DT Article
ID HISTONE LYSINE METHYLATION; FACTOR-I; DNA-REPLICATION;
SACCHAROMYCES-CEREVISIAE; SCHIZOSACCHAROMYCES-POMBE; HOMOLOGOUS
RECOMBINATION; CHROMODOMAIN PROTEIN; NEGATIVE REGULATOR; EPIGENETIC
CONTROL; PCNA BINDING
AB Chromatin assembly factor-1 (CAF1) is a well-conserved histone chaperone that loads the histone H3-H4 complex onto newly synthesized DNA in vitro through interaction with the replication factor PCNA. CAF1 is considered to be involved in heterochromatin maintenance in several organisms, but the evidence is circumstantial and functional details have not been established. We identified fission yeast CAF-1 (spCAF1), which interacts with PCNA in S phase. Depletion of spCAF1 caused defects in silencing at centromeric and mating locus heterochromatin, accompanied with a decrease in Swi6, the fission yeast HP1 homologue. Loss of spCAF1 destabilized both the silent and active states of chromatin at the meta-stable heterochromatic region, with a more pronounced effect on the silent state, indicating that spCAF1 is involved in the maintenance of heterochromatin. Swi6 dissociated from heterochromatin during G1/S phase appears to associate with spCAF1. In early S phase, spCAF1 localized to replicating heterochromatin as well as euchromatin and remained associated with Swi6, and Swi6 then bound to heterochromatin. Taken together, we propose that spCAF1 functions in heterochromatin maintenance by recruiting dislocated Swi6 during replication to replicated heterochromatin at the replication fork.
C1 [Dohke, Kohei; Miyazaki, Shota; Murakami, Yota] Kyoto Univ, Inst Virus Res, Dept Cell Biol, Sakyo Ku, Kyoto 6068507, Japan.
[Dohke, Kohei; Miyazaki, Shota] Kyoto Univ, Grad Sch Biostudies, Dept Mammalian Regulatory Network, Sakyo Ku, Kyoto 6068507, Japan.
[Tanaka, Katsunori] Kwansei Gakuin Univ, Sch Sci & Technol, Dept Biosci, Sanda, Hyogo 6691337, Japan.
[Urano, Takeshi] Shimane Med Univ, Sch Med, Lab Biochem 2, Izumo, Shimane 6938501, Japan.
[Grewal, Shiv I. S.] NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Murakami, Y (reprint author), Kyoto Univ, Inst Virus Res, Dept Cell Biol, Sakyo Ku, Kyoto 6068507, Japan.
EM yota@virus.kyoto-u.ac.jp
RI Murakami, Yota/F-8850-2012; Tanaka, Katsunori/F-8086-2010;
OI Urano, Takeshi/0000-0003-3383-3554
FU Japan Society for the Promotion of Science
FX We thank Ms T. Mimuro for assistance in the initial experiments and Dr
J. Nakayama for helpful discussion. We also thank Dr R. Allshire, Dr T.
Tsurimoto, Dr J. Nakayama, Dr J. Kanoh, Dr F. Ishikawa and Dr H.
Masukata for providing yeast strains and antibodies. We thank Dr Tagamai
for kind assistance of some experiments. This work was supported by a
Grant-in-Aid for Scientific Research on Priority Areas from the Japan
Society for the Promotion of Science.
NR 65
TC 27
Z9 27
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1356-9597
EI 1365-2443
J9 GENES CELLS
JI Genes Cells
PD OCT
PY 2008
VL 13
IS 10
BP 1027
EP 1043
DI 10.1111/j.1365-2443.2008.01225.x
PG 17
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 351JG
UT WOS:000259420000004
PM 18761674
ER
PT J
AU Chapman, JAW
AF Chapman, Judith-Anne W.
TI Substantive progress is being made in breast cancer survival
SO GENETIC ENGINEERING & BIOTECHNOLOGY NEWS
LA English
DT Editorial Material
C1 NCI, Canadas Clin Trials Grp, Bethesda, MD 20892 USA.
RP Chapman, JAW (reprint author), NCI, Canadas Clin Trials Grp, Bethesda, MD 20892 USA.
EM jCbapman@ctg.queenssu.ca
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1935-472X
J9 GENET ENG BIOTECHN N
JI Genet. Eng. Biotechnol. News
PD OCT 1
PY 2008
VL 28
IS 17
BP 6
EP +
PG 2
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 356FI
UT WOS:000259763700003
ER
PT J
AU Vazquez, M
Cooper, MT
Zurita, M
Kennison, JA
AF Vazquez, Martha
Cooper, Monica T.
Zurita, Mario
Kennison, James A.
TI gamma Tub23C Interacts Genetically With Brahma Chromatin-Remodeling
Complexes in Drosophila melanogaster
SO GENETICS
LA English
DT Article
ID TUBULIN RING COMPLEX; TRITHORAX GROUP PROTEINS; ACTIN-RELATED PROTEINS;
RNA-POLYMERASE-II; GAMMA-TUBULIN; NUCLEAR ACTIN; MICROTUBULE NUCLEATION;
TRANSCRIPTION; SUBUNIT; TURC
AB The brahma gene encodes the catalytic subunit of the Drosophila melanogaster BRM chromatin-remodeling complexes. Screening for mutations that interact with brahma, we isolated the dominant-negative Pearl-2 allele of gamma Tub23C. gamma Tub23C encodes one of the two gamma-tubulin isoforms in Drosophila and is essential for zygotic viability and normal adult patterning. gamma-Tubulin is a subunit of microtubule organizer complexes. We show that mutations in lethal (1) discs degenerate 4, which encodes the Grip91 subunit of microtubule organizer complexes, suppress the recessive lethality and the imaginal phenotypes caused by gamma Tub23C mutations. The genetic interactions between gamma Tub23C and chromatin-remodeling mutations suggest that gamma-tubulin might have a role in regulating gene expression.
C1 [Vazquez, Martha; Zurita, Mario] Univ Nacl Autonoma Mexico, Inst Biotechnol, Dept Fisiol Mol & Genet Desarrollo, Cuernavaca 62250, Morelos, Mexico.
[Cooper, Monica T.; Kennison, James A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Mol Genet Lab, NIH, Bethesda, MD 20892 USA.
RP Vazquez, M (reprint author), Univ Nacl Autonoma Mexico, Inst Biotechnol, Dept Fisiol Mol & Genet Desarrollo, Av Univ 2001, Cuernavaca 62250, Morelos, Mexico.
EM mvazquez@ibt.unam.mx
FU Consejo Nacional de Ciencia y Technologia; Programa de Apoyo a Proyectos
de Investigacion e Innovacion Tecnologica-Universidad Nacional Autonoma
de Mexico; Howard Hughes Medical Institute; National Institute of Child
Health and Human Development of the National Institutes of Health
FX This work was Supported by grants from the Consejo Nacional de Ciencia y
Technologia (M.V.), the Programa de Apoyo a Proyectos de Investigacion e
Innovacion Tecnologica-Universidad Nacional Autonoma de Mexico (M.V and
M.Z.), and the Howard Hughes Medical Institute (M.Z.). This research was
supported in part by the Intramural Research Program of the National
Institute of Child Health and Human Development of the National
Institutes of Health.
NR 47
TC 2
Z9 2
U1 0
U2 0
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 0016-6731
J9 GENETICS
JI Genetics
PD OCT
PY 2008
VL 180
IS 2
BP 835
EP 843
DI 10.1534/genetics.108.093492
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 363RM
UT WOS:000260284400011
PM 18780727
ER
PT J
AU Bacolla, A
Larson, JE
Collins, JR
Li, J
Milosavljevic, A
Stenson, PD
Cooper, DN
Wells, RD
AF Bacolla, Albino
Larson, Jacquelynn E.
Collins, Jack R.
Li, Jian
Milosavljevic, Aleksandar
Stenson, Peter D.
Cooper, David N.
Wells, Robert D.
TI Abundance and length of simple repeats in vertebrate genomes are
determined by their structural properties
SO GENOME RESEARCH
LA English
DT Article
ID B DNA CONFORMATIONS; BASE-STACKING; ESCHERICHIA-COLI; MICROSATELLITE
INSTABILITY; TRANSCRIPTION FACTORS; GENETIC INSTABILITY; INTRINSIC
DISORDER; HUMAN-DISEASE; SEQUENCES; EXPANSION
AB Microsatellites are abundant in vertebrate genomes, but their sequence representation and length distributions vary greatly within each family of repeats (e. g., tetranucleotides). Biophysical studies of 82 synthetic single-stranded oligonucleotides comprising all tetra-and trinucleotide repeats revealed an inverse correlation between the stability of folded-back hairpin and quadruplex structures and the sequence representation for repeats >= 30 bp in length in nine vertebrate genomes. Alternatively, the predicted energies of base-stacking interactions correlated directly with the longest length distributions in vertebrate genomes. Genome-wide analyses indicated that unstable sequences, such as CAG: CTG and CCG: CGG, were over-represented in coding regions and that micro/ minisatellites were recruited in genes involved in transcription and signaling pathways, particularly in the nervous system. Microsatellite instability (MSI) is a hallmark of cancer, and length polymorphism within genes can confer susceptibility to inherited disease. Sequences that manifest the highest MSI values also displayed the strongest base-stacking interactions; analyses of 62 tri-and tetranucleotide repeat-containing genes associated with human genetic disease revealed enrichments similar to those noted for micro/ minisatellite-containing genes. We conclude that DNA structure and base-stacking determined the number and length distributions of microsatellite repeats in vertebrate genomes over evolutionary time and that micro/ minisatellites have been recruited to participate in both gene and protein function.
C1 [Bacolla, Albino; Larson, Jacquelynn E.; Wells, Robert D.] Texas A&M Univ, Hlth Sci Ctr, Ctr Genome Res, Inst Biosci & Technol, Houston, TX 77030 USA.
[Collins, Jack R.] NCI, Adv Biomed Comp Ctr, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Li, Jian; Milosavljevic, Aleksandar] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Li, Jian; Milosavljevic, Aleksandar] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
[Stenson, Peter D.; Cooper, David N.] Cardiff Univ, Inst Med Genet, Sch Med, Cardiff CF14 4XN, S Glam, Wales.
RP Bacolla, A (reprint author), Texas A&M Univ, Hlth Sci Ctr, Ctr Genome Res, Inst Biosci & Technol, Houston, TX 77030 USA.
EM abacolla@ibt.tamhsc.edu
RI Cooper, David/H-4384-2011; Bacolla, Albino/N-3877-2013
OI Cooper, David/0000-0002-8943-8484; Bacolla, Albino/0000-0003-0206-8423
FU NIH [ES11347, N01-CO-12400]; Friedreich's Ataxia Research Alliance;
Seek-a-Miracle Foundation; Robert A. Welch Foundation; NCI; BIOBASE GmbH
FX This work was supported by the NIH (ES11347), Friedreich's Ataxia
Research Alliance, Seek-a-Miracle Foundation, and the Robert A. Welch
Foundation to R. D. W. and in part by the Intramural Research Program of
the NIH, NCI, and Federal funds from the NCI, NIH to J. R. C. (contract
no. N01-CO-12400), and financial support from BIOBASE GmbH to D. N. C.
We thank J. E. L. for 40 years of research on non-BDNA structures. All
research materials from the R. D. W. laboratory have been transferred to
S. Mirkin (Sergei. Mirkin@ tufts. edu). We thank Xiaolian Gao of the
University of Houston for the use of her facilities and Jin Jen of the
NCI for helpful discussions.
NR 57
TC 65
Z9 66
U1 1
U2 16
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI WOODBURY
PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
SN 1088-9051
J9 GENOME RES
JI Genome Res.
PD OCT
PY 2008
VL 18
IS 10
BP 1545
EP 1553
DI 10.1101/gr.078303.108
PG 9
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 355HU
UT WOS:000259700800001
PM 18687880
ER
PT J
AU Chen, QR
Song, YK
Wei, JS
Bilke, S
Asgharzadeh, S
Seeger, RC
Khan, J
AF Chen, Qing-Rong
Song, Young K.
Wei, Jun S.
Bilke, Sven
Asgharzadeh, Shahab
Seeger, Robert C.
Khan, Javed
TI An integrated cross-platform prognosis study on neuroblastoma patients
SO GENOMICS
LA English
DT Article
DE neuroblastoma; prognosis; microarray; platform
ID GENE-EXPRESSION MEASUREMENTS; MICROARRAY PLATFORMS; OLIGONUCLEOTIDE;
PREDICTION; PROFILES
AB There have been several reports about the potential for predicting prognosis of neuroblastoma patients using microarray gene expression profiling of the tumors. However these studies have revealed an apparent diversity in the identity of the genes in their predictive signatures. To test the contribution of the platform to this discrepancy we applied the z-scoring method to minimize the impact of platform and combine gene expression profiles of neuroblastoma (NB) tumors from two different platforms, cDNA and Affymetrix. A total of 12442 genes were common to both cDNA and Affymetrix arrays in our data set. Two-way ANOVA analysis was applied to the combined data set for assessing the relative effect of prognosis and platform on gene expression. We found that 26.6% (3307) of the genes had significant impact on survival. There was no significant impact of microarray platform on expression after application of z-scoring standardization procedure. Artificial neural network (ANN) analysis of the combined data set in a leave-one-out prediction Strategy correctly predicted the outcome for 90% of the samples. Hierarchical clustering analysis using the top-ranked 160 genes showed the great separation of two clusters, and the majority of matched samples from the different platforms were clustered next to each other. The ANN classifier trained with our combined cross-platform data for these 160 genes could predict the prognosis of 102 independent test samples with 71% accuracy. Furthermore it correctly predicted the outcome for 85/102 (83%) NB patients through the leave-one-out cross-validation approach. Our study showed that gene expression studies performed in different platforms could be integrated for prognosis analysis after removing variation resulting from different platforms. Published by Elsevier Inc.
C1 [Chen, Qing-Rong; Song, Young K.; Wei, Jun S.; Bilke, Sven; Khan, Javed] NCI, Oncogen Sect, Pediat Oncol Branch, Adv Technol Ctr, Gaithersburg, MD 20877 USA.
[Chen, Qing-Rong] NCI, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Asgharzadeh, Shahab; Seeger, Robert C.] Childrens Hosp Los Angeles, Div Hematol Oncol, Dept Pediat, Los Angeles, CA 90027 USA.
RP Khan, J (reprint author), NCI, Oncogen Sect, Pediat Oncol Branch, Adv Technol Ctr, 8717 Grovemont Circle, Gaithersburg, MD 20877 USA.
EM khanjav@mail.nih.gov
RI Khan, Javed/P-9157-2014
OI Khan, Javed/0000-0002-5858-0488
FU National Cancer Institute; National Institutes of Health [N01-CO-12400]
FX We thank Drs. John Maris, Wendy London of the Children's Oncology Group
(COG), Steven Qualman of the Cooperative Human Tissue Network (CHTN),
Daniel Catchpoole at the Children's Hospital at Westmead, Australia,
Frank Westermann, Manfred Schwab of German Cancer Research Center and
Frank Berthold, University of Cologne, Germany, for the tumor samples
and patient demographic information. We thank Drs. Christopher L.
Morton, Malcolm A. Smith, and Peter J. Houghton for providing us the
preclinical pediatric xenograft data generated on Affymetrix platform.
This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. It has been
funded in whole or in part with federal funds from the National Cancer
Institute, National Institutes of Health, under contract N01-CO-12400.
The content of this publication does not necessarily reflect the views
or policies of the Department of Health and Human Services, nor does
mention of trade names, commercial products, or organizations imply
endorsement by the U.S. Government.
NR 18
TC 27
Z9 27
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0888-7543
J9 GENOMICS
JI Genomics
PD OCT
PY 2008
VL 92
IS 4
BP 195
EP 203
DI 10.1016/j.ygeno.2008.05.014
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 354VV
UT WOS:000259668100003
PM 18598751
ER
PT J
AU Melzer, D
Ferrucci, L
Singleton, A
Guralnik, JM
Murray, A
Bandinelli, S
Corsi, A
Frayling, T
Bandinelli, S
AF Melzer, D.
Ferrucci, L.
Singleton, A.
Guralnik, J. M.
Murray, A.
Bandinelli, S.
Corsi, A.
Frayling, T.
Bandinelli, S.
TI GENETIC VARIATION AND RESILIENCE IN HUMAN AGING: THE SAGA STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Melzer, D.; Murray, A.; Frayling, T.] Peninsula Med Sch, Exeter, Devon, England.
[Singleton, A.] NIA, Neurogenet Lab, IRP, NIH, Bethesda, MD 20892 USA.
[Bandinelli, S.; Bandinelli, S.] Azienda Sanit Firenze, Geriatr Unit, Florence, Italy.
[Corsi, A.] Tuscany Reg Hlth Agcy, Florence, Italy.
RI Singleton, Andrew/C-3010-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 1
EP 1
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600002
ER
PT J
AU Tanaka, T
AF Tanaka, T.
TI GENETIC VARIATION AND MUSCLE STRENGTH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Tanaka, T.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 1
EP 1
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600004
ER
PT J
AU Ferrucci, L
AF Ferrucci, L.
TI IS INFLAMMATION CENTRAL TO AGING?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 2
EP 2
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600008
ER
PT J
AU Kim, Y
Rowland, J
Chang, C
Blank, T
AF Kim, Y.
Rowland, J.
Chang, C.
Blank, T.
TI A 360 DEGREE APPROACH TO THE QUALITY OF LIFE AMONG PROSTATE CANCER
SURVIVORS AND THEIR SPOUSES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Kim, Y.] Amer Canc Soc, Atlanta, GA 30329 USA.
[Rowland, J.] NCI, Bethesda, MD 20892 USA.
[Chang, C.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Blank, T.] Univ Connecticut, Sch Family Studies, Storrs, CT 06269 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 3
EP 3
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600012
ER
PT J
AU Niederehe, G
Chavez, M
Evans, J
AF Niederehe, G.
Chavez, M.
Evans, J.
TI UPDATE ON NIMH PROGRAMS IN MENTAL HEALTH AND AGING RESEARCH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Niederehe, G.; Chavez, M.; Evans, J.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 91
EP 91
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600314
ER
PT J
AU Deshpande, N
Metter, E
Ferrucci, L
AF Deshpande, N.
Metter, E.
Ferrucci, L.
TI WALKING SPEED AS A PREDICTOR OF COGNITIVE DECLINE IN ELDERLY. A
PROSPECTIVE STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Deshpande, N.] Univ Kansas, Med Ctr, Kansas City, KS 66103 USA.
[Metter, E.] NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 94
EP 94
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600328
ER
PT J
AU Simonsick, E
Ferrucci, L
AF Simonsick, E.
Ferrucci, L.
TI FOCUS ON MOBILITY: THREATS AND SUPPORTS ACROSS THE LIFESPAN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Simonsick, E.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 98
EP 98
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600339
ER
PT J
AU Simonsick, E
Newman, A
Ferrucci, L
Satterfield, S
Harris, T
Rodondi, N
Bauer, D
AF Simonsick, E.
Newman, A.
Ferrucci, L.
Satterfield, S.
Harris, T.
Rodondi, N.
Bauer, D.
TI SUBCLINICAL HYPOTHYROIDISM: THREAT TO OR PROTECTIVE OF OPTIMAL MOBILITY?
FINDINGS FROM HEALTH ABC
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Simonsick, E.; Ferrucci, L.; Harris, T.] NIA, Baltimore, MD 21224 USA.
[Newman, A.] Univ Pittsburgh, Pittsburgh, PA USA.
[Satterfield, S.] Univ Tennessee Memphis, Memphis, TN USA.
[Rodondi, N.] Univ Lausanne, Lausanne, Switzerland.
[Bauer, D.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 98
EP 98
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600340
ER
PT J
AU Stenholm, S
Alley, D
Bandinelli, S
Griswold, M
Koskinen, S
Rantanen, T
Guralnik, J
Ferrucci, L
AF Stenholm, S.
Alley, D.
Bandinelli, S.
Griswold, M.
Koskinen, S.
Rantanen, T.
Guralnik, J.
Ferrucci, L.
TI SARCOPENIC OBESITY AND LONGITUDINAL CHANGES IN MOBILITY - RESULTS FROM
THE INCHIANTISTUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Stenholm, S.; Guralnik, J.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Alley, D.] Univ Penn, Philadelphia, PA 19104 USA.
[Bandinelli, S.] Azienda Sanit Firenze, Florence, Italy.
[Griswold, M.] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
[Koskinen, S.] Natl Publ Hlth Inst, Helsinki, Finland.
[Rantanen, T.] Univ Jyvaskyla, Jyvaskyla, Finland.
RI Stenholm, Sari/G-6940-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 98
EP 99
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600341
ER
PT J
AU Ko, S
Ling, S
Winters, J
Ferrucci, L
AF Ko, S.
Ling, S.
Winters, J.
Ferrucci, L.
TI AGE-RELATED GAIT CHARACTERISTICS IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ko, S.; Ling, S.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Winters, J.] Medstar Res Inst, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 99
EP 99
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600344
ER
PT J
AU Tolea, M
Paul, C
Terracciano, A
Simonsick, E
Deiana, B
Orru, M
Uda, M
Schlessinger, D
Ferrucci, L
AF Tolea, M.
Paul, C.
Terracciano, A.
Simonsick, E.
Deiana, B.
Orru, M.
Uda, M.
Schlessinger, D.
Ferrucci, L.
TI SEX-SPECIFIC CORRELATES OF USUAL WALKING SPEED ACROSS THE LIFESPAN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Tolea, M.; Paul, C.; Terracciano, A.; Simonsick, E.; Schlessinger, D.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Deiana, B.; Orru, M.; Uda, M.] Gittadella Univ Monserrato, Monserrato, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 99
EP 99
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600342
ER
PT J
AU Ward, R
Simonsick, E
Schrack, J
Deshpande, N
Ferrucci, L
AF Ward, R.
Simonsick, E.
Schrack, J.
Deshpande, N.
Ferrucci, L.
TI SEX DIFFERENCES IN THE RELATIONSHIP BETWEEN RESERVE CAPACITY AND
REPORTED TIREDNESS, ENERGY LEVEL AND FUNCTIONAL MOBILITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ward, R.; Simonsick, E.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Schrack, J.] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
[Deshpande, N.] Univ Kansas, Kansas City, KS USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 99
EP 99
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600343
ER
PT J
AU Schaap, L
Pluijm, S
Deeg, D
Harris, T
Kritchevsky, S
Newman, A
Penninx, B
Yaffe, K
Cauley, J
Visser, M
AF Schaap, L.
Pluijm, S.
Deeg, D.
Harris, T.
Kritchevsky, S.
Newman, A.
Penninx, B.
yaffe, K.
Cauley, J.
Visser, M.
TI LOW TESTOSTERONE LEVELS IN OLDER WOMEN: THE ASSOCIATION WITH DECLINE IN
PHYSICAL PERFORMANCE AND MUSCLE STRENGTH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Schaap, L.; Deeg, D.] Vrije Univ Amsterdam, Med Ctr, EMGO Inst, Amsterdam, Netherlands.
[Pluijm, S.] Erasmus MC, Dept Publ Hlth, Rotterdam, Netherlands.
[Harris, T.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Kritchevsky, S.] Wake Forest Univ, Sch Med, Sticht Ctr Ageing, Winston Salem, NC 27109 USA.
[Newman, A.; Cauley, J.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Penninx, B.] Vrije Univ Amsterdam, Med Ctr, Dept Psychiat, Amsterdam, Netherlands.
[yaffe, K.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
[Visser, M.] Vrije Univ Amsterdam, Inst Hlth Sci, Fac Earth & Life Sci, Amsterdam, Netherlands.
RI Cauley, Jane/N-4836-2015
OI Cauley, Jane/0000-0003-0752-4408
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 101
EP 101
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600350
ER
PT J
AU Bernard, M
Reuben, D
Fulmer, T
Harris, T
Salerno, J
AF Bernard, M.
Reuben, D.
Fulmer, T.
Harris, T.
Salerno, J.
TI PRESIDENTIAL SYMPOSIUM: INSTITUTE OF MEDICINE REPORT: THE FUTURE HEALTH
CARE WORKFORCE FOR OLDER AMERICANS CHAIR
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bernard, M.] Univ Oklahoma, Reynolds Dept Geriatr, Oklahoma City, OK USA.
[Reuben, D.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Fulmer, T.] NYU, New York, NY USA.
[Harris, T.] NIA, Bethesda, MD 20892 USA.
[Salerno, J.] Natl Acad Sci, Inst Med, Washington, DC 20418 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 102
EP 102
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600351
ER
PT J
AU Harden, J
Hodes, R
Barr, R
Sierra, F
Hadley, E
Suzman, R
Morrison-Bogorad, M
Harden, J
AF Harden, J.
Hodes, R.
Barr, R.
Sierra, F.
Hadley, E.
Suzman, R.
Morrison-Bogorad, M.
Harden, J.
TI NIA SYMPOSIUM:RESEARCH ADVANCES, INITIATIVES, FUNDING AND TRAINING
OPPORTUNITIES AT THE NATIONAL INSTITUTE ON AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Harden, J.; Harden, J.] NIA, NIH, Bethesda, MD 20892 USA.
[Barr, R.] NIA, Off Extramural Affairs, Bethesda, MD 20892 USA.
[Hadley, E.] NIA, Geriatr Program, Bethesda, MD 20892 USA.
[Morrison-Bogorad, M.] Neurosci & Neuropsychol Aging Program, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 113
EP 113
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600390
ER
PT J
AU Shardell, M
Hicks, G
Miller, R
Kritchevsky, S
Andersen, D
Bandinelli, S
Cherubini, A
Ferrucci, L
AF Shardell, M.
Hicks, G.
Miller, R.
Kritchevsky, S.
Andersen, D.
Bandinelli, S.
Cherubini, A.
Ferrucci, L.
TI ASSOCIATION OF LOW VITAMIN D LEVELS WITH THE FRAILTY SYNDROME IN MEN AND
WOMEN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Shardell, M.; Miller, R.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Hicks, G.] Univ Delaware, Newark, DE USA.
[Kritchevsky, S.] Wake Forest Univ, Bowman Gray Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Bandinelli, S.] Tuscany Reg Hlth Agcy, Florence, Italy.
[Cherubini, A.] Univ Perugia, Inst Gerontol & Geriatr, I-06100 Perugia, Italy.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 143
EP 143
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600493
ER
PT J
AU Young, H
Harden, J
Beet-Bates, C
AF Young, H.
Harden, J.
Beet-Bates, C.
TI NURSING CARE OF OLDER ADULTS INTEREST GROUP SYMP.: RESILIENCE IN AGING:
STRENGTHENING INDIVIDUALS, CAREGIVERS AND COMMUNITIES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Young, H.] Oregon Hlth & Sci Univ, Sch Nursing, Ashland, OR USA.
[Harden, J.] NIA, NIH, Bethesda, MD 20892 USA.
[Beet-Bates, C.] Grand Valley State Univ, Kirkhof Coll Nursing, Grand Rapids, MI USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 147
EP 147
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600505
ER
PT J
AU Alley, DE
Harris, T
AF Alley, D. E.
Harris, T.
TI WEIGHT AND HEALTH AT OLDER AGES: INSIGHTS FROM STUDIES OF WEIGHT HISTORY
AND WEIGHT CHANGE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Alley, D. E.] Univ Penn, Philadelphia, PA 19104 USA.
[Harris, T.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 150
EP 150
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600516
ER
PT J
AU Koster, A
Visser, M
Simonsick, E
Yu, B
Allison, D
Newman, A
van Eijk, J
Schwartz, A
Satterfield, S
Harris, T
AF Koster, A.
Visser, M.
Simonsick, E.
Yu, B.
Allison, D.
Newman, A.
van Eijk, J.
Schwartz, A.
Satterfield, S.
Harris, T.
TI ASSOCIATION OF FITNESS WITH CHANGES IN WEIGHT, BODY COMPOSITION, AND
MUSCLE STRENGTH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Koster, A.; Simonsick, E.; Yu, B.; Harris, T.] NIA, Bethesda, MD 20892 USA.
[Visser, M.] Vrije Univ Amsterdam Med Ctr, EMGO Inst, Amsterdam, Netherlands.
[Allison, D.] Univ Alabama, Birmingham, AL USA.
[Newman, A.] Univ Pittsburgh, Pittsburgh, PA USA.
[van Eijk, J.] Univ Maastricht, Maastricht, Netherlands.
[Schwartz, A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Satterfield, S.] Univ Tennessee, Coll Med, Memphis, TN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 151
EP 151
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600521
ER
PT J
AU Marsh, A
Rejeski, W
Espeland, M
Miller, M
Church, T
Gill, T
Guralnik, J
Vestergaard, S
Newman, A
Pahor, M
AF Marsh, A.
Rejeski, W.
Espeland, M.
Miller, M.
Church, T.
Gill, T.
Guralnik, J.
Vestergaard, S.
Newman, A.
Pahor, M.
TI PREDICTORS OF RISK FOR MAJOR MOBILITY DISABILITY IN THE LIFESTYLE
INTERVENTIONS AND INDEPENDENCE FOR ELDERS PILOT (LIFE-P)
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Marsh, A.; Rejeski, W.; Espeland, M.; Miller, M.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Church, T.] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Gill, T.] Yale Univ, New Haven, CT USA.
[Guralnik, J.; Vestergaard, S.] NIA, Bethesda, MD 20892 USA.
[Newman, A.] Univ Pittsburgh, Pittsburgh, PA USA.
[Pahor, M.] Univ Florida, Gainesville, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 197
EP 198
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600687
ER
PT J
AU Vestergaard, S
Walkup, M
Pahor, M
Marsh, A
Espeland, M
Studenski, S
Gill, T
Church, T
M, GJ
AF Vestergaard, S.
Walkup, M.
Pahor, M.
Marsh, A.
Espeland, M.
Studenski, S.
Gill, T.
Church, T.
M, G. Jack
TI STOPPING TO REST DURING A 400-METER WALK AND INCIDENT MOBILITY
DISABILITY IN OLDER PERSONS WITH FUNCTIONAL LIMITATIONS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Vestergaard, S.; M, G. Jack] NIA, Bethesda, MD 20892 USA.
[Walkup, M.; Marsh, A.; Espeland, M.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Pahor, M.] Univ Florida, Gainesville, FL USA.
[Studenski, S.] Univ Pittsburgh, Pittsburgh, PA USA.
[Gill, T.] Yale Univ, New Haven, CT USA.
Yale Univ, New Haven, CT USA.
[Church, T.] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 198
EP 198
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600688
ER
PT J
AU Ofstedal, M
Crimmins, E
Guralnik, J
AF Ofstedal, M.
Crimmins, E.
Guralnik, J.
TI EARLY RESULTS ON PHYSICAL MEASURES AND BIOMARKERS FROM THE HEALTH AND
RETIREMENT STUDY (HRS)
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ofstedal, M.] Univ Michigan, Inst Social Res, Ann Arbor, MI USA.
[Crimmins, E.] Univ So Calif, Los Angeles, CA USA.
[Guralnik, J.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 230
EP 230
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600799
ER
PT J
AU Bandeen-Roche, K
Harris, T
AF Bandeen-Roche, K.
Harris, T.
TI DYNAMICS OF SYSTEMIC DYSREGULATION AND FRAILTY:A STATE-OF-THE-ART LOOK
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bandeen-Roche, K.] Bloomberg Sch Publ Hlth, Dept Biostat, Ctr Aging & Hlth, Baltimore, MD USA.
[Harris, T.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 246
EP 247
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600860
ER
PT J
AU Varadhan, R
Metter, E
Windham, B
Ferrucci, L
AF Varadhan, R.
Metter, E.
Windham, B.
Ferrucci, L.
TI EXPLOITING THE DYNAMICS OF GLUCOSE RESPONSE FROM ORAL GLUCOSE TOLERANCE
TESTING (OGTT) IMPROVES PREDICTION OF MORTALITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Varadhan, R.] Johns Hopkins Sch Med, Ctr Aging & Hlth, Baltimore, MD USA.
[Metter, E.; Windham, B.; Ferrucci, L.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 248
EP 248
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600864
ER
PT J
AU Mills, W
Maier, J
Salerno, J
AF Mills, W.
Maier, J.
Salerno, J.
TI MUSIC-BASED INTERVENTIONS AND THE RESILIENCE OF PERSONS WITH DEMENTIA:
PRACTICAL APPLICATIONS, OUTCOMES, AND FUTURE DIRECTIONS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mills, W.] Univ S Florida, Tampa, FL USA.
[Maier, J.] RTI Int, Waltham, MA USA.
[Salerno, J.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 251
EP 252
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810600878
ER
PT J
AU Harris, T
Chen, Z
Visser, M
Koster, A
Marshall, L
AF Harris, T.
Chen, Z.
Visser, M.
Koster, A.
Marshall, L.
TI DEFINING SARCOPENIA -AN EVIDENCE-BASED APPROACH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Chen, Z.] Arizona Geriatr Educ Ctr, Tucson, AZ USA.
[Visser, M.] Vrije Univ Amsterdam, EMGO Inst, Med Ctr, Amsterdam, Netherlands.
[Koster, A.] NIA, LEDB, Bethesda, MD 20892 USA.
[Marshall, L.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 305
EP 305
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601108
ER
PT J
AU Mehrotra, CM
Barr, R
AF Mehrotra, C. M.
Barr, R.
TI EXPANDING THE POOL OF PSYCHOLOGY FACULTY ENGAGED IN AGING RESEARCH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mehrotra, C. M.] Coll St Scholastica, Duluth, MN USA.
[Barr, R.] NIA, Off Extramural Affairs, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 332
EP 332
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601201
ER
PT J
AU Studenski, S
Perera, S
Kwon, S
Guralnik, J
Thibonnier, M
AF Studenski, S.
Perera, S.
Kwon, S.
Guralnik, J.
Thibonnier, M.
TI MEANINGFUL CHANGE IN PHYSICAL PERFORMANCE: WHAT DO WE KNOW? WHAT ELSE DO
WE NEED TO KNOW?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Studenski, S.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Studenski, S.] VA Pittsburgh GRECC, Pittsburgh, PA USA.
[Kwon, S.] Univ Florida, Gainesville, FL USA.
[Guralnik, J.] NIA, Epidemiol Demog & Biometry Program, Bethesda, MD 20892 USA.
[Thibonnier, M.] GlaxoSmith Kline, Res Triangle Pk, NC USA.
RI Perera, Subashan/D-7603-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 364
EP 365
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601312
ER
PT J
AU Perera, S
Harris, T
Simonsick, E
Schwartz, A
Perry, S
Visser, M
Studenski, S
Newman, A
AF Perera, S.
Harris, T.
Simonsick, E.
Schwartz, A.
Perry, S.
Visser, M.
Studenski, S.
Newman, A.
TI CAN PERFORMANCE CHANGE PREDICT FUTURE FUNCTION?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Studenski, S.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Harris, T.] NIA, Lab Epidemiol, Bethesda, MD 20892 USA.
[Simonsick, E.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Schwartz, A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Perry, S.] Univ Tennessee, Memphis, TN USA.
[Visser, M.] Vrije Univ Amsterdam, Amsterdam, Netherlands.
[Studenski, S.] VA Pittsburgh GRECC, Pittsburgh, PA USA.
RI Perera, Subashan/D-7603-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 365
EP 365
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601314
ER
PT J
AU Studenski, S
Perera, S
Harris, T
Schwartz, A
Simonsick, E
Perry, S
Visser, M
Newman, A
AF Studenski, S.
Perera, S.
Harris, T.
Schwartz, A.
Simonsick, E.
Perry, S.
Visser, M.
Newman, A.
TI MEANINGFUL CHANGE: METHODS AND CURRENT BEST ESTIMATES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Studenski, S.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Studenski, S.] VA Pittsburgh GRECC, Pittsburgh, PA USA.
[Harris, T.] NIA, Bethesda, MD 20892 USA.
[Schwartz, A.] UCSF, San Francisco, CA USA.
[Simonsick, E.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Visser, M.] Vrije Univ Amsterdam, EMGO Inst, Amsterdam, Netherlands.
[Perry, S.] Univ Tennessee, Memphis, TN USA.
RI Perera, Subashan/D-7603-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 365
EP 365
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601313
ER
PT J
AU Ram, N
Gerstorf, D
Suzman, R
Austad, S
Gatz, M
Wilson, R
McArdle, J
AF Ram, N.
Gerstorf, D.
Suzman, R.
Austad, S.
Gatz, M.
Wilson, R.
McArdle, J.
TI AGING AND THE LIFESPAN: REVISITING THE ROLE OF "AGE" FROM BIOLOGICAL,
FUNCTIONAL, PSYCHOLOGICAL, AND SOCIAL PERSPECTIVES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ram, N.; Gerstorf, D.] Penn State Univ, University Pk, PA 16802 USA.
[Suzman, R.] NIA, NIH, Bethesda, MD 20892 USA.
[Austad, S.] Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst Longev & Aging Studies, San Antonio, TX 78229 USA.
[Gatz, M.; McArdle, J.] Univ So Calif, Los Angeles, CA USA.
[Wilson, R.] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 384
EP 384
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601377
ER
PT J
AU Nichols, LO
Burns, R
Stahl, S
Sieverding, P
AF Nichols, L. O.
Burns, R.
Stahl, S.
Sieverding, P.
TI TRANSLATION OF DEMENTIA CAREGIVER RESEARCH: EXAMPLES FROM REACH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Nichols, L. O.] VA Med Ctr, Memphis, TN USA.
[Nichols, L. O.; Burns, R.] Univ Tennessee, Memphis, TN USA.
[Burns, R.] Geriatr Grp Memphis, Memphis, TN USA.
[Stahl, S.] NIA, NIH, Bethesda, MD 20892 USA.
[Sieverding, P.] Dept Vet Affairs, Hlth Serv Res & Dev Serv 124P, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 411
EP 412
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601474
ER
PT J
AU Ferrucci, L
Schechter, M
AF Ferrucci, L.
Schechter, M.
TI THE BALTIMORE LONGITUDINAL STUDY OF AGING (BLSA): 50 YEARS OF
GERONTOLOGY AND MORE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ferrucci, L.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 433
EP 433
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601550
ER
PT J
AU Rosano, C
Verghese, J
Guralnik, J
AF Rosano, C.
Verghese, J.
Guralnik, J.
TI THE CENTRAL CONTROL OF MOBILITY IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Rosano, C.] Univ Pittsburgh, Pittsburgh, PA USA.
[Verghese, J.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Guralnik, J.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 434
EP 434
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601552
ER
PT J
AU Strotmeyer, ES
Lauretani, E
Bandinelli, S
Di Iorio, A
Corsi, AM
Abbate, R
Guralnik, JM
Newman, AB
Ferrucci, L
AF Strotmeyer, E. S.
Lauretani, E.
Bandinelli, S.
Di Iorio, A.
Corsi, A. M.
Abbate, R.
Guralnik, J. M.
Newman, A. B.
Ferrucci, L.
TI HOMOCYSTEINE AND VITAMIN B12 LEVELS ARE, RELATED TO PERIPHERAL NERVE
FUNCTION IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Strotmeyer, E. S.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Lauretani, E.] Univ Hosp, Geriatr Unit, Parma, Italy.
[Bandinelli, S.] ASF, Florence, Italy.
[Di Iorio, A.] Univ G dAnnunzio, Chieti, Italy.
[Abbate, R.] Univ Florence, Florence, Italy.
[Guralnik, J. M.; Ferrucci, L.] NIA, Bethesda, MD 20892 USA.
[Corsi, A. M.] Tuscany Reg Agcy Hlth, Florence, Italy.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 435
EP 435
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601559
ER
PT J
AU Volpato, S
Guralnik, JM
Ferrucci, L
AF Volpato, S.
Guralnik, J. M.
Ferrucci, L.
TI TRADITIONAL CARDIOVASCULAR RISK FACTORS AND MOBILITY IMPAIRMENT IN OLDER
PERSONS: IS THE NERVOUS SYSTEM THE LINK?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Volpato, S.] Univ Ferrara, I-44100 Ferrara, Italy.
[Guralnik, J. M.; Ferrucci, L.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 435
EP 436
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601560
ER
PT J
AU de Cabo, R
AF de Cabo, R.
TI RESVERATROL DELAYS AGE-RELATED DETERIORATION AND MIMICS ASPECTS OF
DIETARY RESTRICTION IN MICE ON A STANDARD DIET
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [de Cabo, R.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 436
EP 437
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601565
ER
PT J
AU Iwarsson, S
Rantanen, T
Simonsick, E
AF Iwarsson, S.
Rantanen, T.
Simonsick, E.
TI MOBILITY AND PARTICIPATION IN OLD AGE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Iwarsson, S.] Lund Univ, Dept Hlth Sci, Fac Med, Lund, Sweden.
[Rantanen, T.] Univ Jyvaskyla, Jyvaskyla, Finland.
[Simonsick, E.] NIA, Baltimore, MD 21224 USA.
RI Siming, Pernilla/F-3123-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 454
EP 454
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601627
ER
PT J
AU Newman, A
Harris, T
AF Newman, A.
Harris, T.
TI TRAJECTORIES OF CHANGE INTO LATE LIFE: THE CARDIOVASCULAR HEALTH STUDY
(CHS) ALL STARS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Newman, A.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, T.] NIA, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 462
EP 463
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601655
ER
PT J
AU Hirsch, C
Buzkova, P
Robbins, J
Patel, K
Newman, A
AF Hirsch, C.
Buzkova, P.
Robbins, J.
Patel, K.
Newman, A.
TI TRAJECTORIES OF PHYSICAL PERFORMANCE AND FUTURE DISABILITY OR DEATH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hirsch, C.; Robbins, J.] Univ Calif Davis, Med Ctr, Sacramento, CA 95817 USA.
[Buzkova, P.] Wake Forest Univ, Winston Salem, NC USA.
[Patel, K.] NIA, Bethesda, MD 20892 USA.
[Newman, A.] Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 464
EP 464
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601659
ER
PT J
AU Ferrucci, L
AF Ferrucci, L.
TI FRAILTY, RUNNING OUT OF ENERGY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 471
EP 471
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601683
ER
PT J
AU Yashin, A
Arbeev, K
Kulminski, A
Christensen, K
Borecki, I
Lee, J
Elo, I
Terry, L
Hadley, E
Rossi, W
Cheng, R
AF Yashin, A.
Arbeev, K.
Kulminski, A.
Christensen, K.
Borecki, I.
Lee, J.
Elo, I.
Terry, L.
Hadley, E.
Rossi, W.
Cheng, R.
TI PREDICTING PARENTAL LONGEVITY FROM OFFSPRING ENDOPHENOTYPES USING DATA
FROM THE LONG LIFE FAMILY STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Yashin, A.; Arbeev, K.] Duke Univ, Durham, NC USA.
[Kulminski, A.] Dule Univ, Durham, NC USA.
[Christensen, K.] Univ So Denmark, Odense, Denmark.
[Borecki, I.] Washington Univ, St Louis, MT USA.
[Lee, J.; Cheng, R.] Coll Phys & Surg, New York, NY USA.
[Elo, I.] Univ Penn, Philadelphia, PA 19104 USA.
[Terry, L.] Boston Med Ctr, Boston, MA USA.
[Hadley, E.; Rossi, W.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 492
EP 493
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601755
ER
PT J
AU Bartali, B
Frongillo, E
Laviano, A
Ferrucci, L
Guralnik, J
Bandinelli, S
Gill, T
AF Bartali, B.
Frongillo, E.
Laviano, A.
Ferrucci, L.
Guralnik, J.
Bandinelli, S.
Gill, T.
TI THE EFFECT OF LEPTIN ON CHANGES IN ENERGY INTAKE IN COMMUNITY-LIVING
OLDER PERSONS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bartali, B.; Gill, T.] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA.
[Frongillo, E.] Univ S Carolina, Dept Hlth Promot Educ & Behav, Columbia, SC 29208 USA.
[Laviano, A.] Univ Roma La Sapienza, Dept Clin Med, Rome, Italy.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
[Guralnik, J.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Bandinelli, S.] Tuscany Reg Hlth Agcy, ASF, Geriatr Rehabil Unit, Florence, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 499
EP 499
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810601775
ER
PT J
AU Chang, M
Jonsson, P
Snaedal, J
Bjornsson, S
Saczynski, J
Siggeirsdottir, K
Aspelund, T
Eiriksdottir, G
Gudnason, V
Harris, T
Launer, L
AF Chang, M.
Jonsson, P.
Snaedal, J.
Bjornsson, S.
Saczynski, J.
Siggeirsdottir, K.
Aspelund, T.
Eiriksdottir, G.
Gudnason, V.
Harris, T.
Launer, L.
TI THE EFFECT OF MIDLIFE PHYSICAL ACTIVITY ON PHYSICAL PERFORMANCE AMONG
OLDER ADULTS: AGES -REYKJAVIK STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Chang, M.; Jonsson, P.; Snaedal, J.; Bjornsson, S.] Landspitali Univ Hosp, Reykjavik, Iceland.
[Saczynski, J.] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA USA.
[Saczynski, J.] Meyers Primary Care Inst, Worcester, MA USA.
[Siggeirsdottir, K.; Aspelund, T.; Eiriksdottir, G.; Gudnason, V.] Iceland Heart Assoc, Kopavogur, Iceland.
[Harris, T.; Launer, L.] NIA, Bethesda, MD 20892 USA.
RI Aspelund, Thor/F-4826-2011; Aspelund, Thor/C-5983-2008; Gudnason,
Vilmundur/K-6885-2015
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 529
EP 529
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602100
ER
PT J
AU Patel, K
Ferrucci, L
Ershler, W
Longo, D
Guralnik, J
AF Patel, K.
Ferrucci, L.
Ershler, W.
Longo, D.
Guralnik, J.
TI RED CELL DISTRIBUTION WIDTH AND THE RISK OF DEATH IN MIDDLE-AGED AND
OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Patel, K.; Ferrucci, L.; Ershler, W.; Longo, D.; Guralnik, J.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 530
EP 530
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602103
ER
PT J
AU Robinson, K
Suzman, R
Sykes, K
Weeks, JD
Iams, H
Greenberg, S
AF Robinson, K.
Suzman, R.
Sykes, K.
Weeks, J. Dawson
Iams, H.
Greenberg, S.
TI RECOGNITION OF EXCELLENCE IN AGING RESEARCH AMONG FEDERAL AGENCIES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Robinson, K.; Weeks, J. Dawson] Natl Ctr Hlth Stat, Hyattsville, MD 20782 USA.
[Suzman, R.] NIA, Bethesda, MD 20892 USA.
[Sykes, K.] US EPA, Aging Initiat, Washington, DC 20460 USA.
[Iams, H.] Social Secur Adm, Washington, DC USA.
[Greenberg, S.] Adm Aging, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 541
EP 541
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602142
ER
PT J
AU Vasunilashorn, S
Patel, K
Crimmins, E
Bandinelli, S
Ferrucci, L
Guralnik, J
AF Vasunilashorn, S.
Patel, K.
Crimmins, E.
Bandinelli, S.
Ferrucci, L.
Guralnik, J.
TI INFLAMMATORY MARKERS PREDICT THREE-YEAR INCIDENCE OF THE INABILITY TO
WALK 400 METERS: THE INCHIANTI STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Vasunilashorn, S.; Crimmins, E.] Univ So Calif, Los Angeles, CA USA.
[Patel, K.; Ferrucci, L.; Guralnik, J.] NIA, Bethesda, MD 20892 USA.
[Bandinelli, S.] Inst Geriatr Rehabil Unit, Florence, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 574
EP 575
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602256
ER
PT J
AU Ashida, S
Loscalzo, A
Basen-Engquist, K
Koehly, L
AF Ashida, S.
Loscalzo, A.
Basen-Engquist, K.
Koehly, L.
TI CHANGES IN SOCIAL NETWORKS AND ADAPTATION AFTER BREAST CANCER DIAGNOSIS:
DIFFERENCES BETWEEN OLDER AND YOUNGER PATIENTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ashida, S.; Loscalzo, A.; Koehly, L.] NHGRI, Bethesda, MD 20892 USA.
[Basen-Engquist, K.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 607
EP 607
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602364
ER
PT J
AU Samanez-Larkin, G
Nielsen, L
AF Samanez-Larkin, G.
Nielsen, L.
TI THE AFFECTIVE NEUROSCIENCE OF AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Samanez-Larkin, G.] Stanford Univ, Stanford, CA 94305 USA.
[Nielsen, L.] NIA, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 621
EP 621
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602412
ER
PT J
AU Miller, RR
Orwig, D
Ferrucci, L
Cappola, A
AF Miller, R. R.
Orwig, D.
Ferrucci, L.
Cappola, A.
TI THE ROLE OF INFLAMMATION IN THE YEAR FOLLOWING HIP FRACTURE.
IMPLICATIONS FOR RESILIENCY FROM THE BALTIMORE HIP STUDIES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Miller, R. R.; Orwig, D.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Ferrucci, L.] NIA, Clin Res Branch, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
[Cappola, A.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 633
EP 633
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602455
ER
PT J
AU de Rekeneire, N
Strotmeyer, E
Goodpaster, B
Velasquez, P
Kanaya, A
Gregg, E
Harris, T
AF de Rekeneire, N.
Strotmeyer, E.
Goodpaster, B.
Velasquez, P.
Kanaya, A.
Gregg, E.
Harris, T.
TI THE ASSOCIATION BETWEEN RESISTIN AND INSULIN RESISTANCE IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [de Rekeneire, N.] EPICTR, Paris, France.
[Strotmeyer, E.; Goodpaster, B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Kanaya, A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Velasquez, P.] Univ Memphis, Memphis, TN 38152 USA.
[Gregg, E.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Harris, T.] NIA, Bethesda, MD 20892 USA.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 636
EP 636
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602464
ER
PT J
AU Cooper, R
Hardy, R
Guralnik, J
Richards, M
Kuh, D
AF Cooper, R.
Hardy, R.
Guralnik, J.
Richards, M.
Kuh, D.
TI LIFETIME COGNITIVE PERFORMANCE AND PHYSICAL PERFORMANCE IN MIDLIFE:
FINDINGS FROM A BRITISH BIRTH COHORT STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Cooper, R.; Hardy, R.; Richards, M.; Kuh, D.] Royal Free & Univ Coll Med Sch, London Med Sch, MRC, Unit Lifelong Hlth & Ageing, London, England.
[Guralnik, J.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 693
EP 693
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602660
ER
PT J
AU Guralnik, J
Patel, K
Kuh, D
AF Guralnik, J.
Patel, K.
Kuh, D.
TI EARLY LIFE FACTORS AND PHYSICAL FUNCTION IN MIDLIFE: FINDINGS FROM THE
1946 BRITISH BIRTH COHORT STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Guralnik, J.; Patel, K.] NIA, Bethesda, MD 20892 USA.
[Kuh, D.] Royal Free & Univ Coll Med Sch, London Med Sch, MRC, Unit Lifelong Hlth & Ageing, London, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 693
EP 693
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602661
ER
PT J
AU Devonshire, AL
Windham, B
Ferrucci, L
Ling, S
AF Devonshire, A. L.
Windham, B.
Ferrucci, L.
Ling, S.
TI THE RELATIONSHIP BETWEEN LEPTIN AND BONE MINERAL DENSITY IN THE
BALTIMORE LONGITUDINAL STUDY OF AGING (BLSA)
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Devonshire, A. L.; Windham, B.; Ferrucci, L.; Ling, S.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 696
EP 696
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602670
ER
PT J
AU Wallhagen, MI
Reuben, D
Rymer, Z
Hendrie, H
Gershon, R
Wagster, M
AF Wallhagen, M. I.
Reuben, D.
Rymer, Z.
Hendrie, H.
Gershon, R.
Wagster, M.
TI THE NIH TOOLBOX: CONSISTENT MEASUREMENT OF NEUROLOGICAL AND BEHAVIORAL
FUNCTION
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Wallhagen, M. I.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Reuben, D.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Rymer, Z.] Rehabil Inst Chicago, Chicago, IL 60611 USA.
[Hendrie, H.] Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA.
[Gershon, R.] Evanston NW Healthcare, Evanston, IL USA.
[Wagster, M.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 696
EP 697
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602672
ER
PT J
AU Patel, K
Inzitari, M
Newman, A
AF Patel, K.
Inzitari, M.
Newman, A.
TI VASCULAR DISEASE AND AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Patel, K.] NIA, Bethesda, MD 20892 USA.
[Inzitari, M.; Newman, A.] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Inzitari, M.] Univ Autonoma Barcelona, Inst Aging, E-08193 Barcelona, Spain.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 697
EP 697
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602674
ER
PT J
AU Inzitari, M
Arnold, A
Patel, K
Karlamangla, A
Ding, J
Psaty, B
Williamson, J
Fried, L
Kuller, L
Newman, A
AF Inzitari, M.
Arnold, A.
Patel, K.
Karlamangla, A.
Ding, J.
Psaty, B.
Williamson, J.
Fried, L.
Kuller, L.
Newman, A.
TI VASCULAR DISEASE BURDEN AND RISK OF DEATH IN OLDER COMMUNITY-DWELLERS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Inzitari, M.; Kuller, L.; Newman, A.] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Inzitari, M.] Univ Autonoma Barcelona, Inst Aging, E-08193 Barcelona, Spain.
[Arnold, A.; Psaty, B.] Univ Washington, Seattle, WA 98195 USA.
[Patel, K.] NIA, Bethesda, MD 20892 USA.
[Karlamangla, A.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Ding, J.; Williamson, J.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Fried, L.] Johns Hopkins Univ, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 698
EP 698
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602675
ER
PT J
AU McDermott, M
Guralnik, J
Ferrucci, L
Liu, K
Tian, L
Liao, Y
Criqui, M
AF McDermott, M.
Guralnik, J.
Ferrucci, L.
Liu, K.
Tian, L.
Liao, Y.
Criqui, M.
TI CALF MUSCLE CHARACTERISTICS AND MOBILITY LOSS IN PERSONS WITH PERIPHERAL
ARTERIAL DISEASE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [McDermott, M.; Liu, K.; Tian, L.; Liao, Y.] Northwestern Univ, Chicago, IL 60611 USA.
[Guralnik, J.; Ferrucci, L.] NIA, Bethesda, MD 20892 USA.
[Criqui, M.] Univ Calif San Diego, San Diego, CA 92103 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 698
EP 698
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602677
ER
PT J
AU Najjar, S
Farasat, S
Valdes, C
Shetty, V
Egan, J
Ferrucci, L
Lakatta, E
AF Najjar, S.
Farasat, S.
Valdes, C.
Shetty, V.
Egan, J.
Ferrucci, L.
Lakatta, E.
TI PULSE PRESSURE IS AN INDEPENDENT PREDICTOR OF ALBUMIN EXCRETION IN THE
BALTIMORE LONGITUDINAL STUDY OF AGING (BLSA)
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Najjar, S.; Farasat, S.; Valdes, C.; Shetty, V.; Egan, J.; Ferrucci, L.; Lakatta, E.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 698
EP 699
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602678
ER
PT J
AU Patel, K
Arnold, A
Inzitari, M
Hirsch, C
Chaves, P
Guralnik, J
Newman, A
AF Patel, K.
Arnold, A.
Inzitari, M.
Hirsch, C.
Chaves, P.
Guralnik, J.
Newman, A.
TI SUBCLINICAL VASCULAR DISEASE BURDEN AND DECLINE IN PHYSICAL FUNCTION
OVER TIME AMONG OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Patel, K.; Guralnik, J.] NIA, Bethesda, MD 20892 USA.
[Arnold, A.] Univ Washington, Seattle, WA 98195 USA.
[Inzitari, M.] Univ Pittsburgh, Barcelona, Spain.
[Inzitari, M.] Autonomous Univ Barcelona, Inst Aging, Barcelona, Spain.
[Hirsch, C.] Univ Calif Davis, Sacramento, CA 95817 USA.
[Chaves, P.] Johns Hopkins Univ, Baltimore, MD USA.
[Newman, A.] Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 698
EP 698
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602676
ER
PT J
AU Loeckenhoff, CE
De Fruyt, F
Terracciano, A
McCrae, R
De Boile, M
Costa, P
AF Loeckenhoff, C. E.
De Fruyt, F.
Terracciano, A.
McCrae, R.
De Boile, M.
Costa, P., Jr.
TI INTERNATIONAL DIFFERENCES IN PERCEPTIONS OF AGING AND THEIR
CULTURE-LEVEL CORRELATES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Loeckenhoff, C. E.; Terracciano, A.; McCrae, R.; Costa, P., Jr.] NIA, Baltimore, MD 21224 USA.
[De Fruyt, F.; De Boile, M.] Adolescent Personal Profiles Cultures Project, Ghent, Belgium.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 718
EP 719
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602754
ER
PT J
AU Manini, T
Ferrucci, L
Harris, T
AF Manini, T.
Ferrucci, L.
Harris, T.
TI ENERGY METABOLISM: ASSOCIATIONS WITH AGE, FATIGUE AND ACTIVITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Manini, T.] Univ Florida, Gainesville, FL USA.
[Ferrucci, L.; Harris, T.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 721
EP 721
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602762
ER
PT J
AU Schrack, J
Simonsick, E
Mackey, D
Ferrucci, L
AF Schrack, J.
Simonsick, E.
Mackey, D.
Ferrucci, L.
TI SHORT ON FUEL? MEASURED ENERGY AVAILABILITY AND PERCEIVED FATIGUE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Schrack, J.; Simonsick, E.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Simonsick, E.; Ferrucci, L.] Ctr Aging & Hlth, Baltimore, MD 21224 USA.
[Mackey, D.] San Francisco Coordinating Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 722
EP 722
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602766
ER
PT J
AU Simonsick, E
Schrack, J
Ward, R
Mackey, D
Ferrucci, L
AF Simonsick, E.
Schrack, J.
Ward, R.
Mackey, D.
Ferrucci, L.
TI PACE DECLINE DURING ENDURANCE WALK TESTING: A WINDOW ON FATIGUE?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Simonsick, E.; Ward, R.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Schrack, J.] NIA, Baltimore, MD 21224 USA.
[Schrack, J.] Ctr Aging & Hlth, Baltimore, MD USA.
[Mackey, D.] San Francisco Coordinating Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 722
EP 722
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602765
ER
PT J
AU Khatutsky, G
Callahan, C
Anderson, D
AF Khatutsky, G.
Callahan, C.
Anderson, D.
TI USING DIFFERENT DATA SOURCES FOR ALZHEIMER'S DISEASE AND RELATED
DEMENTIAS STUDIES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Khatutsky, G.] RTI Int, Waltham, MA USA.
[Callahan, C.] Indiana Univ, Ctr Aging Res Regenstrief Inst Inc, Indianapolis, IN 46204 USA.
[Anderson, D.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 754
EP 755
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602876
ER
PT J
AU Tom, S
Power, C
Cooper, R
AF Tom, S.
Power, C.
Cooper, R.
TI FETAL ENVIRONMENT AND EARLY AGE AT MENOPAUSE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Tom, S.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Power, C.] Inst Child Hlth, Dept Paediat Epidemiol & Biostat, London, No, England.
[Cooper, R.] Univ Coll & Royal Free Med Sch, MRC Natl Survey Hlth & Dev, London, No, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 758
EP 758
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602889
ER
PT J
AU Leveille, SG
Bean, J
Shmerling, R
Jones, R
Audette, J
Guralnik, J
Kiel, D
AF Leveille, S. G.
Bean, J.
Shmerling, R.
Jones, R.
Audette, J.
Guralnik, J.
Kiel, D.
TI CHRONIC PAIN CHARACTERISTICS ASSOCIATED WITH RISK FACTORS FOR FALLS IN
THE OLDER POPULATION
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Leveille, S. G.; Shmerling, R.] Beth Israel Deaconess Med Ctr, Brookline, MA USA.
[Bean, J.; Audette, J.] Spaulding Rehabil Ctr, Cambridge, MA USA.
[Jones, R.; Kiel, D.] Hebrew SeniorLife, Inst Aging Res, Boston, MA USA.
[Guralnik, J.] NIA, EDB Lab, Bethesda, MD 20892 USA.
RI Bean, Jonathan/F-5798-2017
OI Bean, Jonathan/0000-0001-8385-8210
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
EI 1758-5341
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2008
VL 48
SI 3
BP 759
EP 759
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 399PA
UT WOS:000262810602891
ER
PT J
AU Gildersleeve, J
Roach, TA
Li, ZT
Gildersleeve, JC
AF Gildersleeve, Jeff
Roach, Timothy A.
Li, Zhitao
Gildersleeve, Jeffrey C.
TI Supplier-dependent antiglycan monoclonal antibody specificities: Comment
on "High-throughput carbohydrate microarray profiling of 27 antibodies
demonstrates widespread specificity problems"
SO GLYCOBIOLOGY
LA English
DT Editorial Material
ID ANTIGEN
C1 [Gildersleeve, Jeff; Roach, Timothy A.; Li, Zhitao; Gildersleeve, Jeffrey C.] NCI, Med Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA.
RP Gildersleeve, J (reprint author), NCI, Med Chem Lab, Ctr Canc Res, 376 Boyles St Bldg 376,Rm 109, Frederick, MD 21702 USA.
EM gildersleevej@ncifcrf.gov
RI Gildersleeve, Jeffrey/N-3392-2014
NR 4
TC 3
Z9 3
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0959-6658
J9 GLYCOBIOLOGY
JI Glycobiology
PD OCT
PY 2008
VL 18
IS 10
BP 746
EP 746
DI 10.1093/glycob/cwn049
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 353QS
UT WOS:000259583900001
PM 18539626
ER
PT J
AU Varki, AP
Baum, LG
Bellis, SL
Cummings, RD
Esko, JD
Hart, GW
Linhardt, RJ
Lowe, JB
McEver, RP
Srivastava, A
Sarkar, R
AF Varki, Ajit P.
Baum, Linda G.
Bellis, Susan L.
Cummings, Richard D.
Esko, Jeffrey D.
Hart, Gerald W.
Linhardt, Robert J.
Lowe, John B.
McEver, Rodger P.
Srivastava, Arun
Sarkar, Rita
TI Working group report: the roles of glycans in hemostasis, inflammation
and vascular biology
SO GLYCOBIOLOGY
LA English
DT Editorial Material
C1 [Varki, Ajit P.] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
[Varki, Ajit P.; Esko, Jeffrey D.] Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA.
[Baum, Linda G.] Univ Calif Los Angeles, Dept Pathol, Los Angeles, CA 90024 USA.
[Bellis, Susan L.] Univ Alabama, Dept Physiol & Biophys, Birmingham, AL 35294 USA.
[Cummings, Richard D.] Emory Univ, Sch Med, Dept Biochem, Atlanta, GA 30322 USA.
[Hart, Gerald W.] Johns Hopkins Univ, Sch Med, Dept Biol Chem, Baltimore, MD 21205 USA.
[Linhardt, Robert J.] Rensselaer Polytech Inst, Dept Chem & Biol Chem, Troy, NY 12180 USA.
[Lowe, John B.] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA.
[McEver, Rodger P.] Oklahoma Med Res Fdn, Cardiovasc Biol Program, Oklahoma City, OK 73104 USA.
[Srivastava, Arun] Univ Florida, Coll Med, Dept Pediat, Div Cellular & Mol Therapy, Gainesville, FL 32610 USA.
[Srivastava, Arun] Univ Florida, Coll Med, Dept Mol Genet & Microbiol, Div Cellular & Mol Therapy, Gainesville, FL 32610 USA.
[Srivastava, Arun] Univ Florida, Coll Med, Powell Gene Therapy Ctr, Gainesville, FL 32610 USA.
[Sarkar, Rita] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Varki, AP (reprint author), Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
EM a1varki@ucsd.edu
RI Baum, Lawrence/B-1005-2013
OI Baum, Lawrence/0000-0002-5345-9355
NR 0
TC 9
Z9 9
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0959-6658
J9 GLYCOBIOLOGY
JI Glycobiology
PD OCT
PY 2008
VL 18
IS 10
BP 747
EP 749
DI 10.1093/glycob/cwn065
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 353QS
UT WOS:000259583900002
PM 18621991
ER
PT J
AU Gouras, P
Ivert, L
Landauer, N
Mattison, JA
Ingram, DK
Neuringer, M
AF Gouras, Peter
Ivert, Lena
Landauer, Noelle
Mattison, Julie A.
Ingram, Donald K.
Neuringer, Martha
TI Drusenoid maculopathy in rhesus monkeys (Macaca mulatta): effects of age
and gender
SO GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the
Association-for-Research-in-Vision-and-Ophthalmology
CY MAY 06-10, 2007
CL Ft Lauderdale, FL
SP Assoc Res Vis & Ophthalmol
DE macula; age-related macular degeneration; drusen; caloric restriction;
diet; monkey
ID SENILE MACULAR DEGENERATION; BRUCHS MEMBRANE; DIETARY RESTRICTION;
ANIMAL-MODEL; PRIMATE; FASCICULARIS; INVOLVEMENT; CELLS
AB Purpose To compare drusenoid maculopathy in monkeys with human age-related macular degeneration, and evaluate the influence of age, gender and caloric restriction.
Methods Examination by indirect ophthalmoscopy, slit-lamp biomicroscopy and fundus photography, including in some cases fluorescein angiography, was performed on 61 male and 60 female rhesus macaques of ages 10-39 years. Fifty-four of the monkeys were maintained on a calorically restricted diet (approximately 30% lower than control levels) and 67 on an approximately ad libitum diet for 2-19 years, with all other environmental factors held constant. Maculopathies were graded on a 5-point scale and the effects of age, sex, and diet on prevalence and severity were examined. The retinas of six monkeys with macular drusen, 19-28 years old, were examined histologically.
Results Rhesus monkeys showed a high prevalence (61%) of drusenoid maculopathy. The prevalence and severity of the maculopathy increased with age (p = 0.012). Fully half of all monkeys aged 10-12 years had some detectable degree of drusen. This high prevalence in young adulthood indicates that drusen develop much earlier in rhesus monkeys than in humans, who develop early maculopathy most rapidly at 50-60 years of age, even when correcting for the 3-fold difference in lifespan. No neovascularization or geographic atrophy was found. Females had a higher prevalence and severity than males (p = 0.019). Calorically restricted monkeys had a slightly lower prevalence and severity at 10-12 years than controls, but the difference was not statistically significant. This is an on-going project, and differences between the caloric restricted and ad-lib groups may emerge as the animals age. Some monkeys developed severe maculopathy in their 20s, with others unaffected in their 30s. The histology of drusen resembled those in human retina.
Conclusions Drusenoid maculopathy is common in rhesus monkeys, even in young adult life. Half of the rhesus monkeys examined have drusen at a much younger age than in humans. Severity of maculopathy was greater in female monkeys, a gender difference not consistently found in humans. No differences were detected due to caloric restriction, but a definitive test of this intervention will require a larger sample, longer period of observation, and/or an earlier institution of caloric restriction. Genetic factors are implied because with similar environments, some monkeys are affected at an early age, while older ones are not.
C1 [Gouras, Peter] Columbia Univ, Dept Ophthalmol, New York, NY 10027 USA.
[Ivert, Lena] Karolinska Inst, St Eriks Eye Hosp, Dept Ophthalmol, S-11282 Stockholm, Sweden.
[Landauer, Noelle; Neuringer, Martha] Oregon Hlth & Sci Univ, Div Neurosci, Oregon Natl Primate Res Ctr, Beaverton, OR 97006 USA.
[Mattison, Julie A.] NIA, Lab Expt Gerontol, Baltimore, MD 21224 USA.
[Ingram, Donald K.] Louisiana State Univ Syst, Nutr Neurosci & Aging Lab, Pennington Biomed Res Ctr, Baton Rouge, LA 70810 USA.
[Neuringer, Martha] Oregon Hlth & Sci Univ, Dept Ophthalmol, Beaverton, OR 97006 USA.
RP Gouras, P (reprint author), Columbia Univ, Dept Ophthalmol, New York, NY 10027 USA.
EM pg10@columbia.edu
FU Intramural NIH HHS [Z01 AG000371-02]; NCRR NIH HHS [P51 RR000163, K01
RR000163]; NEI NIH HHS [R01 EY015293]
NR 32
TC 13
Z9 13
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0721-832X
J9 GRAEF ARCH CLIN EXP
JI Graefes Arch. Clin. Exp. Ophthalmol.
PD OCT
PY 2008
VL 246
IS 10
BP 1395
EP 1402
DI 10.1007/s00417-008-0910-8
PG 8
WC Ophthalmology
SC Ophthalmology
GA 344WX
UT WOS:000258959100006
PM 18709381
ER
PT J
AU Gouras, P
Ivert, L
Mattison, JA
Ingram, DK
Neuringer, M
AF Gouras, Peter
Ivert, Lena
Mattison, Julie A.
Ingram, Donald K.
Neuringer, Martha
TI Drusenoid maculopathy in rhesus monkeys: autofluorescence, lipofuscin
and drusen pathogenesis
SO GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the
Association-for-Research-in-Vision-and-Ophthalmology
CY APR 30-MAY 04, 2006
CL Ft Lauderdale, FL
SP Assoc Res Vis & Ophthalmol
DE macula; age-related macular degeneration; drusen; lipofuscin;
autofluorescence; monkey
ID MACULAR DEGENERATION; BRUCHS MEMBRANE
AB Purpose To examine patterns of retinal pigment epithelial autofluorescence and lipofuscin accumulation in relation to drusen and to explore the pathogenesis of drusen in rhesus monkeys.
Methods The macular areas of six rhesus monkeys, euthanized at 19 to 28 years of age, were studied by bright field and fluorescence light microscopy and transmission electron microscopy.
Result There was strong autofluorescence in the retinal epithelium that tended to diminish over drusen. Electron microscopy revealed that all retinal epithelial cells had large concentrations of lipofuscin bodies. The epithelial cells overlying drusen, however, tended to have less lipofuscin than epithelial cells not associated with drusen. Electron microscopy revealed that the epithelial cells overlying drusen were losing segments of cytoplasm containing lipofuscin bodies. Macrophage-like cells were consistently present in Bruch's membrane microns away from this lipofuscin-containing cytoplasmic material.
Conclusions Retinal epithelial cells overlying drusen have less lipofuscin than neighboring epithelial cells. The loss of lipofuscin seems due to a loss of cytoplasm containing lipofuscin that contributes to drusen formation. Macrophages in Bruch's membrane may be responsible for removing this lipofuscin debris. The results support in vivo studies showing reduced autofluorescence over drusen and support the "budding" of epithelial cytoplasm as a source of drusen material.
C1 [Gouras, Peter] Columbia Univ, Dept Ophthalmol, New York, NY 10027 USA.
[Ivert, Lena] Karolinska Inst, St Eriks Eye Hosp, Dept Ophthalmol, S-11282 Stockholm, Sweden.
[Mattison, Julie A.] NIA, Lab Expt Gerontol, Baltimore, MD 21224 USA.
[Ingram, Donald K.] Louisiana State Univ Syst, Nutr Neurosci & Aging Lab, Pennington Biomed Res Ctr, Baton Rouge, LA 70810 USA.
[Neuringer, Martha] Oregon Hlth & Sci Univ, Div Neurosci, Oregon Natl Primate Res Ctr, Beaverton, OR 97006 USA.
[Neuringer, Martha] Oregon Hlth & Sci Univ, Dept Ophthalmol, Beaverton, OR 97006 USA.
RP Gouras, P (reprint author), Columbia Univ, Dept Ophthalmol, New York, NY 10027 USA.
EM pg10@columbia.edu
FU Intramural NIH HHS [Z01 AG000371-02]; NCRR NIH HHS [K01 RR000163, P51
RR000163]; NEI NIH HHS [R01 EY015293]
NR 14
TC 11
Z9 11
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0721-832X
J9 GRAEF ARCH CLIN EXP
JI Graefes Arch. Clin. Exp. Ophthalmol.
PD OCT
PY 2008
VL 246
IS 10
BP 1403
EP 1411
DI 10.1007/s00417-008-0911-7
PG 9
WC Ophthalmology
SC Ophthalmology
GA 344WX
UT WOS:000258959100007
PM 18696097
ER
PT J
AU Capello, F
Scrimin, S
Pillon, M
Axia, G
Bornstein, MH
Levrero, P
Dufour, C
Carli, M
AF Capello, F.
Scrimin, S.
Pillon, M.
Axia, G.
Bornstein, M. H.
Levrero, P.
Dufour, C.
Carli, M.
TI Onco-hematologic diagnosis in the first three years of life: adaptation
of the family and psychological development of children
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA Italian
DT Meeting Abstract
CT 35th National Congress of the
Associazione-Italiana-Ematologia-Oncologia-Pediatrica
CY OCT 26-28, 2008
CL Ancona, ITALY
SP Assoc Italiana Ematol Oncol Pediat
C1 [Capello, F.; Scrimin, S.; Axia, G.] Univ Padua, Dipartimento Psicol Sviluppo & Socializzaz, I-35100 Padua, Italy.
[Bornstein, M. H.] NICHHD, Bethesda, MD 20892 USA.
[Pillon, M.; Levrero, P.; Carli, M.] Univ Padua, Dipartimento Pediat, I-35100 Padua, Italy.
[Dufour, C.] Osped Pediat Gaslini, Genoa, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOL-HEMATOL J
JI Haematol-Hematol. J.
PD OCT
PY 2008
VL 93
BP S55
EP S55
PG 1
WC Hematology
SC Hematology
GA 368WO
UT WOS:000260653600119
ER
PT J
AU Frank, AC
Zhang, XZ
Kottilil, S
Daucher, M
AF Frank, Astrid C.
Zhang, Xiaozhen
Kottilil, Shyam
Daucher, Marybeth
TI ALTERED REGULATION OF EXTRINSIC AND INTRINSIC APOPTOSIS PATHWAYS IN
HCV-INFECTED HCC CELLS ENHANCES SUSCEPTIBILITY TO APOPTOSIS INDUCED BY
ANTI-TRAIL RECEPTORS AGONISTIC ANTIBODIES
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Frank, Astrid C.; Zhang, Xiaozhen; Kottilil, Shyam; Daucher, Marybeth] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 58
BP 332A
EP 332A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400053
ER
PT J
AU Ishikawa, T
Conner, EA
Hoang, T
Factor, VM
Thorgeirsson, SS
AF Ishikawa, Tsuyoshi
Conner, Elizabeth A.
Hoang, Tanya
Factor, Valentina M.
Thorgeirsson, Snorri S.
TI C-MET SIGNALING IS ESSENTIAL FOR STEM CELL MEDIATED LIVER REGENERATION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Ishikawa, Tsuyoshi; Conner, Elizabeth A.; Hoang, Tanya; Factor, Valentina M.; Thorgeirsson, Snorri S.] NCI, NIH, Expt Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 77
BP 341A
EP 341A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400072
ER
PT J
AU Jensen, GS
Terrault, N
Blei, AT
Merion, RM
Gillespie, BW
Everhart, JE
Brown, RS
Olthoff, KM
Hayashi, PH
Berg, CL
Fisher, RA
Trotter, JF
AF Jensen, Geoffrey S.
Terrault, Norah
Blei, Andres T.
Merion, Robert M.
Gillespie, Brenda W.
Everhart, James E.
Brown, Robert S.
Olthoff, Kim M.
Hayashi, Paul H.
Berg, Carl L.
Fisher, Robert A.
Trotter, James F.
TI LONG-TERM FOLLOW-UP OF LABORATORY VALUES IN RIGHT HEPATIC LOBE LIVER
DONORS FOLLOWING DONATION: THE A2ALL EXPERIENCE
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Jensen, Geoffrey S.] Univ Colorado, Dept Med, Aurora, CO USA.
[Trotter, James F.] Univ Colorado, Dept Surg, Aurora, CO USA.
[Terrault, Norah] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Blei, Andres T.] Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
[Merion, Robert M.] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA.
[Gillespie, Brenda W.] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Brown, Robert S.] Columbia Presbyterian Med Ctr, Dept Med, New York, NY 10032 USA.
[Olthoff, Kim M.] Univ Penn, Dept Surg, Philadelphia, PA 19104 USA.
[Hayashi, Paul H.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Berg, Carl L.] Univ Virginia, Dept Med, Charlottesville, VA USA.
[Fisher, Robert A.] Virginia Commonwealth Univ, Dept Surg, Richmond, VA USA.
[Everhart, James E.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 105
BP 352A
EP 352A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400096
ER
PT J
AU Feld, JJ
Modi, AA
Ahlenstiel, G
El-Diwany, R
Rotman, Y
Koh, C
Titerence, R
Park, Y
Ghany, M
Heller, T
Hoofnagle, JH
Liang, TJ
AF Feld, Jordan J.
Modi, Apurva A.
Ahlenstiel, Golo
El-Diwany, Ramy
Rotman, Yaron
Koh, Christopher
Titerence, Rachel
Park, Yoon
Ghany, Marc
Heller, Theo
Hoofnagle, Jay H.
Liang, T. Joke
TI SAME IMPROVES EARLY VIRAL KINETICS AND INTERFERON STIMULATED GENE
INDUCTION WHEN ADDED TO PEGINTERFERON AND RIBAVIRIN THERAPY FOR PREVIOUS
HEPATITIS C NON-RESPONDERS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Feld, Jordan J.; Modi, Apurva A.; Ahlenstiel, Golo; El-Diwany, Ramy; Rotman, Yaron; Koh, Christopher; Titerence, Rachel; Park, Yoon; Ghany, Marc; Heller, Theo; Hoofnagle, Jay H.; Liang, T. Joke] NIDDK, NIH, Liver Dis Branch, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA LB5
BP 379A
EP 379A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400155
ER
PT J
AU Ahlenstiel, G
Titerence, RH
Koh, C
Feld, JJ
Rotman, Y
Ghany, MG
Kleiner, DE
Hoofnagle, JH
Liang, TJ
Heller, T
Rehermann, B
AF Ahlenstiel, Golo
Titerence, Rachel H.
Koh, Christopher
Feld, Jordan J.
Rotman, Yaron
Ghany, Marc G.
Kleiner, David E.
Hoofnagle, Jay H.
Liang, T. Jake
Heller, Theo
Rehermann, Barbara
TI DISEASE ACTIVITY IN CHRONIC HEPATITIS C CORRELATES TO
IFN-alpha-DEPENDENT POLARIZATION OF NATURAL KILLER CELL FUNCTION TOWARDS
CYTOTOXICITY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Ahlenstiel, Golo; Titerence, Rachel H.; Rehermann, Barbara] NIDDK, Immunol Sect, NIH, DHHS, Bethesda, MD USA.
[Ahlenstiel, Golo; Titerence, Rachel H.; Koh, Christopher; Feld, Jordan J.; Rotman, Yaron; Ghany, Marc G.; Hoofnagle, Jay H.; Liang, T. Jake; Heller, Theo; Rehermann, Barbara] NIDDK, Liver Dis Branch, NIH, DHHS, Bethesda, MD USA.
[Kleiner, David E.] NCI, Pathol Lab, DHHS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 179
BP 389A
EP 389A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400176
ER
PT J
AU Gunay-Aygun, M
Lukose, L
Choyke, P
Turkbey, B
Daryanani, K
Bryant, J
Adams, D
Guay-Woodford, L
Mohan, P
Gahl, WA
Heller, T
AF Gunay-Aygun, Meral
Lukose, Linda
Choyke, Peter
Turkbey, Baris
Daryanani, Kailash
Bryant, Joy
Adams, David
Guay-Woodford, Lisa
Mohan, Parvathi
Gahl, William A.
Heller, Theo
TI NATURAL HISTORY OF CONGENITAL HEPATIC FIBROSIS ASSOCIATED WITH AUTOSOMAL
RECESSIVE POLYCYSTIC KIDNEY DISEASE
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Heller, Theo] NIH, Liver Dis Branch, Bethesda, MD 20892 USA.
[Gunay-Aygun, Meral; Lukose, Linda; Bryant, Joy; Adams, David; Gahl, William A.] NHGRI, NIH, Med Genet Branch, Bethesda, MD 20892 USA.
[Gunay-Aygun, Meral] DHHS, Off Rare Dis, Washington, DC USA.
[Choyke, Peter; Turkbey, Baris; Daryanani, Kailash] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Guay-Woodford, Lisa] Univ Alabama, Birmingham, AL USA.
[Mohan, Parvathi] Childrens Natl Med Ctr, Washington, DC 20010 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 185
BP 391A
EP 392A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400182
ER
PT J
AU Kato, T
Choi, YY
Elmowalid, G
Sapp, RK
Barth, H
Wakita, T
Krawczynski, K
Liang, TJ
AF Kato, Takanobu
Choi, Youkyung
Elmowalid, Gamal
Sapp, Ronda K.
Barth, Heidi
Wakita, Takaji
Krawczynski, K.
Liang, T. Jake
TI HEPATITIS C VIRUS JFH-I STRAIN INFECTION IN CHIMPANZEES IS ASSOCIATED
WITH LOW PATHOGENICITY AND EMERGENCE OF AN ADAPTIVE MUTATION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Kato, Takanobu] Toshiba Gen Hosp, Dept Med Sci, Tokyo, Japan.
[Kato, Takanobu; Elmowalid, Gamal; Sapp, Ronda K.; Barth, Heidi; Liang, T. Jake] NIDDK, NIH, Liver Dis Branch, Bethesda, MD USA.
[Choi, Youkyung; Krawczynski, K.] Ctr Dis Control & Prevent, Div Viral Hepatitis, Atlanta, GA USA.
[Wakita, Takaji] Natl Inst Infect Dis, Dept Virol 2, Tokyo, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 203
BP 399A
EP 399A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400200
ER
PT J
AU Schwarz, KB
Gonzalez-Peralta, RP
Murray, KF
Molleston, JP
Haber, B
Jonas, MM
Mohan, P
Balistreri, WF
Rosenthal, P
Narkewicz, MR
Smith, LJ
Robuck, PR
Barton, B
AF Schwarz, Kathleen B.
Gonzalez-Peralta, Regina P.
Murray, Karen F.
Molleston, Jean P.
Haber, Barbara
Jonas, Maureen M.
Mohan, Parvathi
Balistreri, William F.
Rosenthal, Philip
Narkewicz, Michael R.
Smith, Lesley J.
Robuck, Patricia R.
Barton, Bruce
TI PEGINTERFERON WITH OR WITHOUT RIBAVIRIN FOR CHRONIC HEPATITIS C IN
CHILDREN AND ADOLESCENTS: FINAL RESULTS OF THE PEDS-C TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Schwarz, Kathleen B.] Johns Hopkins Univ, Baltimore, MD USA.
[Gonzalez-Peralta, Regina P.] Univ Florida, Gainesville, FL USA.
[Murray, Karen F.] Univ Washington, Seattle, WA 98195 USA.
[Molleston, Jean P.] Indiana Univ, Indianapolis, IN 46204 USA.
[Haber, Barbara] Univ Penn, Philadelphia, PA 19104 USA.
[Jonas, Maureen M.] Harvard Univ, Boston, MA 02115 USA.
[Mohan, Parvathi] George Washington Univ, Washington, DC USA.
[Balistreri, William F.] Univ Cincinnati, Cincinnati, OH USA.
[Rosenthal, Philip] Univ Calif San Francisco, San Francisco, CA USA.
[Narkewicz, Michael R.] Univ Colorado, Denver, CO 80202 USA.
[Smith, Lesley J.] Univ Miami, Miami, FL USA.
[Robuck, Patricia R.] NIDDK, NIH, Bethesda, MD USA.
[Barton, Bruce] MMRI, Baltimore, MD USA.
NR 0
TC 16
Z9 17
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 242
BP 418A
EP 418A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400239
ER
PT J
AU Snow, KK
Bonkovsky, HL
Fontana, RJ
Hoofnogle, JH
Kim, HY
AF Snow, Kristin K.
Bonkovsky, Herbert L.
Fontana, Robert J.
Hoofnogle, Jay H.
Kim, Hae-Young
TI CHANGES IN HEALTH-RELATED QUALITY OF LIFE ARE ASSOCIATED WITH DISEASE
PROGRESSION AND PEGINTERFERON THERAPY IN PATIENTS WITH ADVANCED
HEPATITIS C IN THE HEPATITIS C ANTIVIRAL LONG-TERM TREATMENT AGAINST
CIRRHOSIS (HALT-C) TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Snow, Kristin K.; Kim, Hae-Young] New England Res Inst, Watertown, MA 02172 USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Dept Med, Farmington, CT 06032 USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Dept Mol & Struct Biol, Farmington, CT 06032 USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Liver Biliary Pancreat Ctr, Farmington, CT 06032 USA.
[Fontana, Robert J.] Univ Michigan, Med Ctr, Div Gastroenterol, Ann Arbor, MI USA.
[Hoofnogle, Jay H.] NIDDKD, Liver Dis Res Branch, Div Digest Dis & Nutr, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 265
BP 428A
EP 429A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400262
ER
PT J
AU Dove, LM
Rosen, RC
Ramcharran, D
Wahed, AS
Belle, SH
Brown, RS
Hoofnagle, JH
AF Dove, Lorna M.
Rosen, Raymond C.
Ramcharran, Darmendra
Wahed, Abdus S.
Belle, Steven H.
Brown, Robert S.
Hoofnagle, Jay H.
TI DECLINE IN SEXUAL DESIRE, FUNCTION AND SATISFACTION IN MEN DURING
PEGINTERFERON AND RIBAVIRIN THERAPY FOR CHRONIC HEPATITIS C
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Dove, Lorna M.; Brown, Robert S.] Columbia Univ Coll Phys & Surg, New York, NY 10032 USA.
[Rosen, Raymond C.] New England Res Inst, Boston, MA USA.
[Ramcharran, Darmendra; Wahed, Abdus S.; Belle, Steven H.] Univ Pittsburgh, Pittsburgh, PA USA.
[Hoofnagle, Jay H.] NIDDKD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 267
BP 430A
EP 430A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400264
ER
PT J
AU Delgado-Borrego, A
Jordan, SH
Negre, B
Healey, D
Lin, WY
Ludwig, DA
Lok, ASF
Everhart, JE
Chung, RT
AF Delgado-Borrego, Aymin
Jordan, Sergio H.
Negre, Betania
Healey, David
Lin, Wenyu
Ludwig, David A.
Lok, Anna S. F.
Everhart, James E.
Chung, Raymond T.
TI REDUCTION OF INSULIN RESISTANCE WITH EFFECTIVE CLEARANCE OF HEPATITIS C
INFECTION: RESULTS FROM THE HALT-C TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Delgado-Borrego, Aymin; Jordan, Sergio H.; Negre, Betania; Ludwig, David A.] Univ Miami, Miami, FL USA.
[Healey, David; Lin, Wenyu; Chung, Raymond T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Lok, Anna S. F.] Univ Michigan, Med Ctr, Div Gastroenterol, Ann Arbor, MI USA.
[Everhart, James E.] NIDDKD, Div Digest Dis & Nutr, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
RI Lok, Anna /B-8292-2009
NR 0
TC 1
Z9 1
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 271
BP 433A
EP 433A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400268
ER
PT J
AU Morishima, C
Shiffman, ML
Lindsay, K
Szabo, G
Dienstag, JL
Wright, EC
AF Morishima, Chihiro
Shiffman, Mitchell L.
Lindsay, Karen
Szabo, Gyongyi
Dienstag, Jules L.
Wright, Elizabeth C.
TI REDUCED HEPATIC INFLAMMATION IS RELATED TO HCV RNA SUPPRESSION AND
CORRELATES WITH LESS FIBROSIS PROGRESSION AND FEWER CIRRHOSIS
COMPLICATIONS IN THE HEPATITIS C ANTIVIRAL LONG-TERM TREATMENT AGAINST
CIRRHOSIS (HALT-C) TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Morishima, Chihiro] Univ Washington, Dept Lab Med, Div Virol, Seattle, WA 98195 USA.
[Shiffman, Mitchell L.] Virginia Commonwealth Univ, Hepatol Sect, Med Ctr, Richmond, VA USA.
[Lindsay, Karen] Univ So Calif, Keck Sch Med, Div Gastrointestinal & Liver Dis, Los Angeles, CA 90033 USA.
[Szabo, Gyongyi] Univ Massachusetts, Sch Med, Dept Med, Hepatol & Liver Ctr,Div Gastroenterol, Worcester, MA USA.
[Dienstag, Jules L.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Wright, Elizabeth C.] NIDDKD, Off Director, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 273
BP 434A
EP 434A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400270
ER
PT J
AU Fu, D
Wakaboyashi, Y
Arias, IM
AF Fu, Dong
Wakaboyashi, Yoshiyuki
Arias, Irwin M.
TI THE METABOLIC SENSOR, AMPK, AND ITS UPSTREAM ACTIVATOR, LKB1,
PARTICIPATE IN FORMATION AND MAINTENANCE OF BILE CANALICULUS AND TIGHT
JUNCTION, AND APICAL CONTENT OF ABCB1
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Fu, Dong; Wakaboyashi, Yoshiyuki; Arias, Irwin M.] NICHD, NIH, Bethesda, MD USA.
RI Fu, Dong /J-1426-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 373
BP 477A
EP 477A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400368
ER
PT J
AU Hikita, H
Takehara, T
Kodama, T
Shimizu, S
Miyagi, T
Ishida, H
Tatsumi, T
Ohkawa, K
Hiromatsu, N
Kanto, T
Henninghausen, L
Yin, XM
Hayashi, N
AF Hikita, Hayato
Takehara, Tetsuo
Kodama, Takahiro
Shimizu, Satoshi
Miyagi, Takuya
Ishida, Hisashi
Tatsumi, Tomohide
Ohkawa, Kazuyoshi
Hiromatsu, Naoki
Kanto, Tatsuya
Henninghausen, Lothar
Yin, Xiao-Ming
Hayashi, Norio
TI BH3-ONLY PROTEIN BID IS REQUIRED FOR HEPATOCYTE APOPTOSIS CAUSED BY
BCL-XL DEFICIENCY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Hikita, Hayato; Takehara, Tetsuo; Kodama, Takahiro; Shimizu, Satoshi; Miyagi, Takuya; Ishida, Hisashi; Tatsumi, Tomohide; Ohkawa, Kazuyoshi; Hiromatsu, Naoki; Kanto, Tatsuya; Hayashi, Norio] Osaka Univ, Grad Sch Med, Suita, Osaka, Japan.
[Henninghausen, Lothar] NIDDK, NIH, Bethesda, MD USA.
[Yin, Xiao-Ming] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 398
BP 487A
EP 487A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400391
ER
PT J
AU Martin, J
Maurhofer, O
Schaller, A
Thorgeirsson, SS
Dufour, JF
AF Martin, Juliette
Maurhofer, Olivier
Schaller, Andre
Thorgeirsson, Snorri S.
Dufour, Jean Francois
TI THE MITOCHONDRIAL HINT2 MODULATES THE EXPRESSION OF PCAF AND HYOU1
PROTEINS UNDER APOPTOTIC CONDITIONS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Martin, Juliette; Maurhofer, Olivier; Dufour, Jean Francois] Univ Bern, Inst Clin Pharmacol, Bern, Switzerland.
[Schaller, Andre] Hosp Bern, Dept Pediat & Genet, Bern, Switzerland.
[Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 414
BP 493A
EP 493A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400406
ER
PT J
AU Caldwell, SH
Lee, VD
Redick, JA
Kleiner, DE
Argo, CK
Al-Osaimi, AM
Lima, VM
Northup, PG
Tetri, BA
AF Caldwell, Stephen H.
Lee, Vanessa D.
Redick, Jan A.
Kleiner, David E.
Argo, Curtis K.
Al-Osaimi, Abdullah M.
Lima, Vicencia M.
Northup, Patrick G.
Tetri, Brent A.
TI APOPTOSIS IN HUMAN NASH: ACTIVATED BUT INCOMPLETE?
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Caldwell, Stephen H.; Lee, Vanessa D.; Argo, Curtis K.; Al-Osaimi, Abdullah M.; Northup, Patrick G.] Univ Virginia, Dept GI Hepatol, Charlottesville, VA USA.
[Kleiner, David E.] Natl Canc Inst, Bathesda, MD USA.
[Lima, Vicencia M.] Univ Sao Paulo, Sao Paulo, Brazil.
[Tetri, Brent A.] St Louis Univ, St Louis, MO 63103 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 480
BP 521A
EP 521A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757400472
ER
PT J
AU Lee, JY
Tuleuova, N
Ramanculov, EM
Jones, CN
Zern, M
Revzin, A
AF Lee, Ji Youn
Tuleuova, Nazgul
Ramanculov, Erlan M.
Jones, Caroline N.
Zern, Mark
Revzin, Alexander
TI MICROPATTERNED CO-CULTURES FOR DIRECTING HEPATIC DIFFERENTIATION OF
EMBRYONIC STEM CELLS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Lee, Ji Youn; Tuleuova, Nazgul; Jones, Caroline N.; Revzin, Alexander] UC Davis, Davis, CA USA.
[Zern, Mark] UC Davis, Med Ctr, Internal Med & Transplant Res Inst, Sacramento, CA USA.
[Ramanculov, Erlan M.] Natl Biotechnol Ctr, Astana, Kazakhstan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 686
BP 613A
EP 613A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401073
ER
PT J
AU Yamashita, T
Ji, JF
Budhu, A
Forgues, M
Jia, HL
Ye, QH
Qin, LX
Wauthier, E
Reid, LM
Minato, H
Honda, M
Kaneko, S
Yang, W
Wang, HY
Tang, ZY
Wang, XW
AF Yamashita, Toro
Ji, Junfang
Budhu, Anuradha
Forgues, Marhonna
Jia, Huliang
Ye, Qinghai
Qin, Lun-Xiu
Wauthier, Eliane
Reid, Lola M.
Minato, Hiroshi
Honda, Masao
Kaneko, Shuichi
Yang, Wen
Wang, Hongyong
Tang, Zhao-You
Wang, Xin W.
TI AUGMENTATION OF HEPATIC CANCER STEM CELLS BY WNT/beta-CATENIN SIGNALING
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Yamashita, Toro; Ji, Junfang; Budhu, Anuradha; Forgues, Marhonna; Wang, Xin W.] NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA.
[Jia, Huliang; Ye, Qinghai; Qin, Lun-Xiu; Tang, Zhao-You] Liver Canc Inst, Shanghai, Peoples R China.
[Jia, Huliang; Ye, Qinghai; Qin, Lun-Xiu; Tang, Zhao-You] Zhongshan Hosp, Shanghai, Peoples R China.
[Wauthier, Eliane; Reid, Lola M.] Univ N Carolina, Sch Med, Dept Cell & Mol Phys, Chapel Hill, NC USA.
[Yamashita, Toro; Minato, Hiroshi; Honda, Masao; Kaneko, Shuichi] Liver Dis Ctr, Kanazawa, Ishikawa, Japan.
[Yamashita, Toro; Minato, Hiroshi; Honda, Masao; Kaneko, Shuichi] Kanazawa Univ Hosp, Kanazawa, Ishikawa, Japan.
[Yang, Wen; Wang, Hongyong] Eastern Hepatobiliary Surg Hosp, Shanghai, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 692
BP 615A
EP 616A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401079
ER
PT J
AU Pati, NT
Kottilil, S
Hissar, SS
Kumari, S
Mishra, SK
Madan, K
Sarin, SK
AF Pati, Nirupmo T.
Kottilil, Shyam
Hissar, Syed S.
Kumari, Shikha
Mishra, Siddharth K.
Madan, Kaushal
Sarin, Shiv K.
TI IMMUNOLOGICAL PROFILE OF PERIPHERAL BLOOD MONONUCLEAR CELLS, NK T CELLS
AND DENDRITIC CELLS IN CHRONIC HBV-INFECTED PATIENTS TREATED WITH
TENOFOVIR DISOPROXIL FUMARATE
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Kottilil, Shyam] NIAID, NIH, LIR, Bethesda, MD 20892 USA.
[Pati, Nirupmo T.; Hissar, Syed S.; Kumari, Shikha; Mishra, Siddharth K.; Sarin, Shiv K.] GB Pant Hosp, Dept Gastroenterol, New Delhi, India.
[Madan, Kaushal; Sarin, Shiv K.] Inst Liver & Biliary Sci, New Delhi, India.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 866
BP 693A
EP 693A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401250
ER
PT J
AU Formentini, E
Neumann, AU
Ghany, MG
Frank, AC
Davey, RT
Kottilil, S
AF Formentini, Elizabeth
Neumann, Avidan U.
Ghany, Marc G.
Frank, Astrid C.
Davey, Richard T.
Kottilil, Shyam
TI BASELINE CD4(+) T CELL COUNT PREDICTS HBV DECLINE IN HIV NEGATIVE AND
POSITIVE AND PATIENTS TREATED WITH ADEFOVIR DIPIVOXIL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Formentini, Elizabeth] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Neumann, Avidan U.] Bar Ilan Univ, Dept Life Sci, Bethesda, MD USA.
[Ghany, Marc G.] NIDDK, LBM, NIH, Bethesda, MD USA.
[Frank, Astrid C.; Davey, Richard T.; Kottilil, Shyam] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 954
BP 735A
EP 735A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401337
ER
PT J
AU Katounas, A
Lempicki, RA
Kottilil, S
Trippler, M
Bein, S
Gerken, G
Schlaak, JF
AF Katounas, Antonios
Lempicki, Richard A.
Kottilil, Shyam
Trippler, Martin
Bein, Sabine
Gerken, Guido
Schlaak, Joerg F.
TI CYTOKINE AND CHEMOKINE EXPRESSION PATTERNS CONNECT VARIOUS HOST AND
VIRAL CHARACTERISTICS WITH CLINICAL OUTCOME IN CHRONIC HCV INFECTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Katounas, Antonios; Trippler, Martin; Bein, Sabine; Gerken, Guido; Schlaak, Joerg F.] Univ Hosp Essen, Dept Gastroenterol & Hepatol, Essen, Germany.
[Katounas, Antonios; Kottilil, Shyam] NIAID, NIH, Bethesda, MD 20892 USA.
[Lempicki, Richard A.] NIAID, SAIC Frederick Inc, Lab Bioinformat & Immunopathogenesis, Frederick, MD USA.
RI Lempicki, Richard/E-1844-2012
OI Lempicki, Richard/0000-0002-7059-409X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1050
BP 776A
EP 777A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401433
ER
PT J
AU Morishima, C
Di Bisceglie, AM
Koziel, MJ
Rothman, AL
Bonkovsky, HL
Lee, WM
Lindsay, K
Wright, EC
AF Morishima, Chihiro
Di Bisceglie, Adrian M.
Koziel, Margaret J.
Rothman, Alan L.
Bonkovsky, Herbert L.
Lee, William M.
Lindsay, Karen
Wright, Elizabeth C.
TI ANTIGEN-SPECIFIC LYMPHOCYTE PROLIFERATION DECREASES OVER TIME IN
ADVANCED CHRONIC HEPATITIS C AND ITS LOSS IS ASSOCIATED WITH THE
PRESENCE OF CIRRHOSIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Morishima, Chihiro] Univ Washington, Div Virol, Dept Lab Med, Seattle, WA 98195 USA.
[Di Bisceglie, Adrian M.] St Louis Univ, Div Gastroenterol & Hepatol, Dept Internal Med, St Louis, MO 63103 USA.
[Koziel, Margaret J.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Infect Dis, Boston, MA 02215 USA.
[Rothman, Alan L.] Univ Massachusetts, Sch Med, Ctr Infect Dis & Vaccine Res, Worcester, MA USA.
[Rothman, Alan L.] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Med, Farmington, CT USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Mol & Struct Biol, Farmington, CT USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Liver Biliary Pancreat Ctr, Farmington, CT USA.
[Lee, William M.] Univ Texas SW Med Ctr Dallas, Div Digest & Liver Dis, Dallas, TX 75390 USA.
[Lindsay, Karen] Univ So Calif, Keck Sch Med, Div Gastroenterol & Liver Dis, Los Angeles, CA 90033 USA.
[Wright, Elizabeth C.] NIDDK, Off Director, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1072
BP 785A
EP 786A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401455
ER
PT J
AU Promrat, K
Kleiner, DE
Niemeier, HM
Jackvony, E
Kearns, M
Wands, JR
Wing, RR
AF Promrat, Kittichai
Kleiner, David E.
Niemeier, Heather M.
Jackvony, Elizabeth
Kearns, Marie
Wands, Jack R.
Wing, Rena R.
TI RANDOMIZED CONTROLLED TRIAL TESTING THE EFFECTS OF WEIGHT LOSS ON
NONALCOHOLIC STEATOHEPATITIS (NASH)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Niemeier, Heather M.; Jackvony, Elizabeth; Kearns, Marie; Wing, Rena R.] Brown Univ, Warren Alpert Med Sch, Weight Control & Diabet Res Ctr, Providence, RI 02912 USA.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1111
BP 802A
EP 802A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401492
ER
PT J
AU Tabesh, A
Duan, ZG
Kleiner, DE
Wright, EC
Loomba, R
Liang, TJ
Hoofnagle, JH
Ghany, MG
AF Tabesh, Alireza
Duan, Zhigang
Kleiner, David E.
Wright, Elizabeth C.
Loomba, Rohit
Liang, T. Jake
Hoofnagle, Jay H.
Ghany, Marc G.
TI SERUM CASPASE-3 GENERATED CYTOKERATIN 18 FRAGMENTS (CK-18) AS A MARKER
FOR NON-ALCOHOLIC STEATOHEPATITIS (NASH) AND RESPONSE TO THERAPY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Tabesh, Alireza; Duan, Zhigang; Wright, Elizabeth C.; Loomba, Rohit; Liang, T. Jake; Hoofnagle, Jay H.; Ghany, Marc G.] Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD USA.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1114
BP 803A
EP 804A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401495
ER
PT J
AU Rotman, Y
Kohl, C
Feld, JJ
Kleiner, DE
Liang, TJ
Hoofnagle, JH
AF Rotman, Yaron
Kohl, Christopher
Feld, Jordan J.
Kleiner, David E.
Liang, T. Jake
Hoofnagle, Jay H.
TI CORRELATION OF BIOCHEMICAL AND HISTOLOGICAL RESPONSES IN THERAPEUTIC
TRIALS OF NONALCOHOLIC STEATOHEAPTITIS (NASH)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Rotman, Yaron; Kohl, Christopher; Feld, Jordan J.; Liang, T. Jake; Hoofnagle, Jay H.] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1122
BP 807A
EP 807A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401503
ER
PT J
AU Gawrieh, S
Wallace, J
Carless, M
Komorowski, R
Nuttleman, P
Andris, D
Makladi, B
Kleiner, DE
Curran, J
Dyer, TD
Charlesworth, J
Blangero, J
Kissebah, A
Olivier, M
AF Gawrieh, Samer
Wallace, James
Carless, Melanie
Komorowski, Richard
Nuttleman, Peter
Andris, Deborah
Makladi, Bassem
Kleiner, David E.
Curran, Joanne
Dyer, Thomas D.
Charlesworth, Jac
Blangero, John
Kissebah, Ahmed
Olivier, Michael
TI DISCOVERY OF GENE NETWORKS INVOLVED IN NON-ALCOHOLIC FATTY LIVER DISEASE
USING GENOME-WIDE TRANSCRIPTIONAL PROFILING
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Gawrieh, Samer; Makladi, Bassem; Kissebah, Ahmed] Med Coll Wisconsin, Dept Med, Milwaukee, WI 53226 USA.
[Wallace, James; Nuttleman, Peter; Andris, Deborah] Med Coll Wisconsin, Dept Surg, Milwaukee, WI 53226 USA.
[Carless, Melanie; Curran, Joanne; Dyer, Thomas D.; Charlesworth, Jac; Blangero, John] SW Fdn Biomed Res, Dept Genet, San Antonio, TX USA.
[Komorowski, Richard] Med Coll Wisconsin, Dept Pathol, Milwaukee, WI 53226 USA.
[Kleiner, David E.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Olivier, Michael] Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA.
[Gawrieh, Samer] Zablocki VA Med Ctr, Div Gastroenterol & Hepatol, Milwaukee, WI USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1131
BP 811A
EP 811A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401512
ER
PT J
AU Kleiner, DE
Yeh, MM
Guy, CD
Ferrell, L
Cummings, O
Contos, MJ
Brunt, EM
Behling, CA
AF Kleiner, David E.
Yeh, Matthew M.
Guy, Cynthia D.
Ferrell, Linda
Cummings, Oscar
Contos, Melissa J.
Brunt, Elizabeth M.
Behling, Cynthia A.
TI CREATION OF A CONTINUOUS VISUAL SCALE OF BALLOONED HEPATOCYTES IN
NON-ALCOHOLIC FATTY LIVER DISEASE
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Kleiner, David E.] NCI, Bethesda, MD 20892 USA.
[Yeh, Matthew M.] Univ Washington, Seattle, WA 98195 USA.
[Guy, Cynthia D.] Duke Univ, Princeton, NJ USA.
[Ferrell, Linda] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Cummings, Oscar] Indiana Univ, Indianapolis, IN 46204 USA.
[Contos, Melissa J.] Virginia Commonwealth Univ, Richmond, VA USA.
[Brunt, Elizabeth M.] Washington Univ, St Louis, MO USA.
[Behling, Cynthia A.] Sharp Mem Hosp & Rehabil Ctr, San Diego, CA USA.
NR 0
TC 7
Z9 7
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1139
BP 815A
EP 815A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401520
ER
PT J
AU Soule, TA
Schrieber, SJ
Zhiming, W
Wahed, AS
Smith, PC
Fried, MW
Reddy, R
Navarro, VJ
Afdhal, NH
Belle, SH
Berman, J
Liu, QY
Doo, E
Hawke, RL
AF Soule, Tedi A.
Schrieber, Sarah J.
Zhiming, Wen
Wahed, Abdus S.
Smith, Philip C.
Fried, Michael W.
Reddy, Raiender
Navarro, Victor J.
Afdhal, Nezam H.
Belle, Steven H.
Berman, Josh
Liu, Qi-Ying
Doo, Edward
Hawke, Roy L.
TI PHASE I STUDY TO EVALUATE THE SAFETY, TOLERABILITY AND PHARMACOKINETICS
(PK) OF SILYMARIN (SM) IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER
DISEASE (NAFLD)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Soule, Tedi A.; Schrieber, Sarah J.; Zhiming, Wen; Smith, Philip C.; Fried, Michael W.; Hawke, Roy L.] Univ N Carolina, Chapel Hill, NC USA.
[Reddy, Raiender] Univ Penn, Philadelphia, PA 19104 USA.
[Navarro, Victor J.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Afdhal, Nezam H.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Wahed, Abdus S.; Belle, Steven H.] Univ Pittsburgh, Pittsburgh, PA USA.
[Berman, Josh; Liu, Qi-Ying] Natl Ctr Complementary & Alternat Med, Bethesda, MD USA.
[Doo, Edward] NIDDKD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1204
BP 844A
EP 845A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401585
ER
PT J
AU Feld, JJ
Ko, MS
Hara, K
Lutchman, GA
Rotman, Y
Heller, T
Ghany, MG
Neumann, AU
Liang, TJ
Hoofnagle, JH
AF Feld, Jordan J.
Ko, Myung S.
Hara, Koji
Lutchman, Glen A.
Rotman, Yaron
Heller, Theo
Ghany, Marc G.
Neumann, Avidan U.
Liang, T. Joke
Hoofnagle, Jay H.
TI RIBAVIRIN IMPROVES SECOND PHASE KINETICS THROUGH ENHANCED INTERFERON
SIGNALING IN GENOTYPE 1 HCV INFECTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Feld, Jordan J.; Ko, Myung S.; Hara, Koji; Rotman, Yaron; Heller, Theo; Ghany, Marc G.; Liang, T. Joke; Hoofnagle, Jay H.] NIDDK, NIH, Liver Dis Branch, Bethesda, MD USA.
[Neumann, Avidan U.] Bar Ilan Univ, Ramat Gan, Israel.
[Lutchman, Glen A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1217
BP 850A
EP 850A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401598
ER
PT J
AU Osinusi, A
Rosimos, JJ
Bishop, R
McLoughlin, M
Polis, MA
Mosur, H
Kottilil, S
AF Osinusi, Anu
Rosimos, Joseph J.
Bishop, Rachel
McLoughlin, Mary
Polis, Michael A.
Mosur, Henry
Kottilil, Shyam
TI HIV/HCV CO-INFECTED VIROLOGIC RESPONDERS TO PEGYLATED IFN AND RIBAVIRIN
THERAPY MORE FREQUENTLY SUFFER IFN-RELATED ADVERSE EVENTS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Osinusi, Anu; McLoughlin, Mary; Polis, Michael A.; Kottilil, Shyam] NIAID, Immunoregulat Lab, Bethesda, MD 20892 USA.
[Bishop, Rachel] NEI, NIH, Bethesda, MD 20892 USA.
[Rosimos, Joseph J.] NIMH, NIH, Bethesda, MD 20892 USA.
[Mosur, Henry] NIH, Crit Care Med Dept, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1291
BP 884A
EP 885A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757401670
ER
PT J
AU Wang, H
Wang, L
Lafdil, F
Park, O
Jeong, WI
Horiguchi, N
Goa, B
AF Wang, Hua
Wang, Lei
Lafdil, Fouad
Park, Ogyi
Jeong, Won-il
Horiguchi, Nario
Goa, Bin
TI HEPATIC STAT3: A DOUBLE-EDGED SWORD IN CHRONIC LIVER INJURY AND FIBROSIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Wang, Hua; Wang, Lei; Lafdil, Fouad; Park, Ogyi; Jeong, Won-il; Horiguchi, Nario; Goa, Bin] NIAAA, LPS, NIH, Bethesda, MD USA.
[Wang, Hua] Anhui Med Univ, Affiliated Prov Hosp, Dept Oncol, Hefei, Peoples R China.
NR 0
TC 1
Z9 1
U1 0
U2 1
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 2008
VL 48
IS 4
SU S
MA 1346
BP 909A
EP 909A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402020
ER
PT J
AU Allison, RD
Katsounas, A
Kleiner, DE
Ater, HJ
Lempicki, RA
Polis, MA
Kottilil, S
AF Allison, Robert D.
Katsounas, Antonios
Kleiner, David E.
Ater, Harvey J.
Lempicki, Richard A.
Polis, Michael A.
Kottilil, Shyam
TI INTERLEUKIN-15 INDUCED PERIPHERAL IMMUNE ACTIVATION CORRELATES WITH HSC
ACTIVATION IN HIV/HCV CO-INFECTED INDIVIDUALS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Allison, Robert D.; Ater, Harvey J.] NIH, Dept Transfus Med, Bethesda, MD 20892 USA.
[Katsounas, Antonios; Polis, Michael A.; Kottilil, Shyam] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Lempicki, Richard A.] SAIC Frederick, Frederick, MD USA.
RI Lempicki, Richard/E-1844-2012
OI Lempicki, Richard/0000-0002-7059-409X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1367
BP 917A
EP 918A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402041
ER
PT J
AU Kastsounas, A
Trippler, M
Wang, B
Bein, S
Gerken, G
Schlaak, JF
AF Kastsounas, Antonios
Trippler, Martin
Wang, Bo
Bein, Sabine
Gerken, Guido
Schlaak, Joerg F.
TI CCL5 IS UP-REGULATED BY TOLL-LIKE RECEPTOR 3/HCV STIMULATION AND ITS
EXPRESSION IN THE PERIPHERAL BLOOD IS INVERSELY CORRELATED WITH THE
STAGE OF FIBROSIS IN PATIENTS WITH CHRONIC HEPATITIS C
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Kastsounas, Antonios; Trippler, Martin; Wang, Bo; Bein, Sabine; Gerken, Guido; Schlaak, Joerg F.] Univ Hosp Essen, Dept Gastroenterol & Hepatol, Essen, Germany.
[Kastsounas, Antonios] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1384
BP 924A
EP 925A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402056
ER
PT J
AU Maass, T
Thieringer, F
Becker, KG
Galle, PR
Kanzler, S
Teufel, A
AF Maass, Thorsten
Thieringer, Florian
Becker, Kevin G.
Galle, Peter R.
Kanzler, Stephan
Teufel, Andreas
TI EVALUATION OF SIGNALING NETWORKS IN PDGF-B MEDIATED LIVER FIBROSIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Maass, Thorsten; Thieringer, Florian; Galle, Peter R.; Teufel, Andreas] Johannes Gutenberg Univ Mainz, Dept Med 1, D-6500 Mainz, Germany.
[Becker, Kevin G.] NIA, Gene Express & Genom Unit, Baltimore, MD 21224 USA.
[Kanzler, Stephan] Leopoldina Hosp, Dept Med 2, Schweinfurt, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1399
BP 931A
EP 931A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402071
ER
PT J
AU Jeong, WI
Park, O
Wang, L
Gao, B
AF Jeong, Won-il
Park, Ogyi
Wang, Lei
Gao, Bin
TI FULLY ACTIVATED HEPATIC STELLATE CELLS ARE RESISTANT TO INTERFERON-gamma
VIA UPREGULATION SOCS1 EXPRESSION: INVOLVEMENT OF RETINOL METABOLISM
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Jeong, Won-il; Park, Ogyi; Wang, Lei; Gao, Bin] NIAAA, LPS, NIH, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1419
BP 939A
EP 939A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402091
ER
PT J
AU Marquardt, JU
Raggi, C
Andersen, JB
Avital, I
Factor, VM
Thorgeirsson, SS
AF Marquardt, Jens U.
Raggi, Chiara
Andersen, Jesper B.
Avital, Itzhak
Factor, Valentina M.
Thorgeirsson, Snorri S.
TI EPIGENETIC MODULATION SELECTS UNIQUE CANCER STEM CELL POPULATION WITHIN
THE SP FRACTION OF HUMAN HCC
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Marquardt, Jens U.; Raggi, Chiara; Andersen, Jesper B.; Factor, Valentina M.; Thorgeirsson, Snorri S.] NCI, LEC, NIH, Bethesda, MD 20892 USA.
[Avital, Itzhak] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1522
BP 983A
EP 983A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402193
ER
PT J
AU Lee, YH
Song, HT
Judge, A
Woo, HG
Andersen, JB
Avital, I
Durkin, M
Ishikawa, T
Toni, A
Lee, JS
Conner, EA
MacLachlon, I
Factor, VM
Thorgeirsson, SS
AF Lee, Yun-Han
Song, Ho-Taek
Judge, Adam
Woo, Hyun Goo
Andersen, Jesper B.
Avital, Itzhak
Durkin, Marian
Ishikawa, Tsuyoshi
Toni, Anita
Lee, Ju-Seog
Conner, Elizabeth A.
MacLachlon, Ian
Factor, Valentina M.
Thorgeirsson, Snorri S.
TI SILENCING OF COP1, A NEGATIVE REGULATOR OF P53, SUPPRESSES GROWTH OF
HUMAN HCC CELLS IN VITRO AND IN VIVO
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Lee, Yun-Han; Woo, Hyun Goo; Andersen, Jesper B.; Avital, Itzhak; Durkin, Marian; Ishikawa, Tsuyoshi; Toni, Anita; Conner, Elizabeth A.; Factor, Valentina M.; Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Song, Ho-Taek] Yonsei Univ, Coll Med, Dept Radiol, Seoul, South Korea.
[Judge, Adam; MacLachlon, Ian] Protiva Biotherapeut Inc, Burnaby, BC, Canada.
[Avital, Itzhak] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Lee, Ju-Seog] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Div Canc Med, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1534
BP 988A
EP 988A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402204
ER
PT J
AU Yoon, JC
Shiina, M
Ahlenstiel, G
Rehermann, B
AF Yoon, Joo Chun
Shiina, Masaaki
Ahlenstiel, Golo
Rehermann, Barbara
TI NATURAL KILLER CELL FUNCTION IS INTACT AFTER DIRECT EXPOSURE TO
INFECTIOUS HEPATITIS C VIRIONS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Yoon, Joo Chun; Shiina, Masaaki; Ahlenstiel, Golo; Rehermann, Barbara] NIDDK, Immunol Sect, LDB, NIH,DHHS, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1576
BP 1006A
EP 1006A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402246
ER
PT J
AU Haber, B
Fredericks, EM
Magee, J
Bezerra, JA
Karpen, SJ
Kerkar, N
Rosenthal, P
Schwarz, KB
Shepherd, RW
Shneider, BL
Whitington, PF
Robuck, PR
Sokol, RJ
AF Haber, Barbara
Fredericks, Emily M.
Magee, John
Bezerra, Jorge A.
Karpen, Saul J.
Kerkar, Nanda
Rosenthal, Philip
Schwarz, Kathleen B.
Shepherd, Ross W.
Shneider, Benjamin L.
Whitington, Peter F.
Robuck, Patricia R.
Sokol, Ronald J.
TI PREDICTORS OF NEURODEVELOPMENTAL OUTCOME IN NON-TRANSPLANTED CHILDREN
WITH BILIARY ATRESIA AT ONE YEAR OF AGE
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Haber, Barbara] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Fredericks, Emily M.; Magee, John] Univ Michigan, Sch Med, Ann Arbor, MI USA.
[Bezerra, Jorge A.] Childrens Hosp, Med Ctr, Cincinnati, OH 45229 USA.
[Karpen, Saul J.] Texas Childrens Liver Ctr, Houston, TX USA.
[Kerkar, Nanda] Mt Sinai Med Ctr, New York, NY 10029 USA.
[Rosenthal, Philip] UCSF, Med Ctr, San Francisco, CA USA.
[Schwarz, Kathleen B.] Johns Hopkins Med Ctr, Baltimore, MD USA.
[Shepherd, Ross W.] Washington Univ, Med Ctr, St Louis, MO USA.
[Shneider, Benjamin L.] Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA.
[Whitington, Peter F.] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Robuck, Patricia R.] NIDDK, Bethesda, MD USA.
[Sokol, Ronald J.] Univ Colorado, Sch Med, Denver, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1616
BP 1028A
EP 1029A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402295
ER
PT J
AU Schwarz, KB
Shepherd, RW
Magee, J
Rosenthal, P
Mack, C
Raghumathan, T
Bezerra, JA
Haber, B
Karpen, SJ
Shneider, BL
Suchy, FJ
Whitington, PF
Robuck, PR
Sokol, RJ
AF Schwarz, Kathleen B.
Shepherd, Ross W.
Magee, John
Rosenthal, Philip
Mack, Cara
Raghumathan, Trivellore
Bezerra, Jorge A.
Haber, Barbara
Karpen, Saul J.
Shneider, Benjamin L.
Suchy, Frederick J.
Whitington, Peter F.
Robuck, Patricia R.
Sokol, Ronald J.
TI CLINICAL AND DEMOGRAPHIC FEATURES OF THREE MAJOR BILIARY ATRESIA
PHENOTYPES IN THE BARC STUDY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Schwarz, Kathleen B.] Johns Hopkins, Baltimore, MD USA.
[Shepherd, Ross W.] Washington Univ, St Louis, MO USA.
[Magee, John; Raghumathan, Trivellore] Univ Michigan, Ann Arbor, MI 48109 USA.
[Rosenthal, Philip] UCSF, San Francisco, CA USA.
[Mack, Cara; Sokol, Ronald J.] Univ Colorado, Denver, CO 80202 USA.
[Bezerra, Jorge A.] Univ Cincinnati, Cincinnati, OH USA.
[Haber, Barbara] Univ Penn, Philadelphia, PA 19104 USA.
[Karpen, Saul J.] Baylor Univ, Houston, TX 77030 USA.
[Shneider, Benjamin L.] Univ Pittsburgh, Pittsburgh, PA USA.
[Whitington, Peter F.] Northwestern Univ, Chicago, IL 60611 USA.
[Robuck, Patricia R.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1615
BP 1028A
EP 1028A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402294
ER
PT J
AU Rosenthal, P
Mohan, P
Barton, B
Robuck, PR
Schwarz, KB
AF Rosenthal, Philip
Mohan, Parvathi
Barton, Bruce
Robuck, Patricia R.
Schwarz, Kathleen B.
TI INCIDENCE OF NEUTROPENIA AND IMPACT ON SUSTAINED VIROLOGICAL RESPONSE
(SVR) IN CHILDREN AND ADOLESCENTS WITH CHRONIC HEPATITIS C TREATED WITH
PEGINTERFERON WITH OR WITHOUT RIBAVIRIN: THE PEDS-C EXPERIENCE
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Rosenthal, Philip] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Mohan, Parvathi] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Barton, Bruce] MMRI, Baltimore, MD USA.
[Robuck, Patricia R.] NIDDK, Div Digest Dis, Bethesda, MD USA.
[Schwarz, Kathleen B.] Johns Hopkins Univ Hosp, Pediat GI, Baltimore, MD 21205 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1623
BP 1031A
EP 1032A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402302
ER
PT J
AU Gaskari, SA
DMello, C
Harvey-White, J
Kunos, G
Lee, SS
AF Gaskari, Seyed Ali
DMello, Charlotte
Harvey-White, Judith
Kunos, George
Lee, Samuel S.
TI PORTAL HYPOTENSIVE ACTION OF TYPE-I CALCIMIMETIC COMPOUNDS IN RATS WITH
CCL4-INDUCED ASCITIC LIVER CIRRHOSIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Gaskari, Seyed Ali; DMello, Charlotte; Lee, Samuel S.] Univ Calgary, Liver Unit, Calgary, AB, Canada.
[Harvey-White, Judith; Kunos, George] NIAAA, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1647
BP 1042A
EP 1042A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402326
ER
PT J
AU Freedman, ND
Everhart, JE
Lindsay, K
Ghany, MG
Curto, TM
Abnet, CC
Sinha, R
AF Freedman, Neal D.
Everhart, James E.
Lindsay, Karen
Ghany, Marc G.
Curto, Teresa M.
Abnet, Christian C.
Sinha, Roshmi
TI COFFEE INTAKE IS ASSOCIATED WITH LOWER RATES OF LIVER DISEASE
PROGRESSION IN CHRONIC HEPATITIS C: FINDINGS FROM THE HEPATITIS C
ANTIVIRAL LONG-TERM TREATMENT AGAINST CIRRHOSIS (HALT-C) TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Freedman, Neal D.; Abnet, Christian C.; Sinha, Roshmi] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
[Everhart, James E.] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD USA.
[Lindsay, Karen] Univ So Calif, Keck Sch Med, Div Gastrointestinal & Liver Dis, Los Angeles, CA 90033 USA.
[Ghany, Marc G.] NIDDK, Liver Dis Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Curto, Teresa M.] New England Res Inst Inc, HALT C Trial, Watertown, MA USA.
RI Sinha, Rashmi/G-7446-2015; Freedman, Neal/B-9741-2015
OI Sinha, Rashmi/0000-0002-2466-7462; Freedman, Neal/0000-0003-0074-1098
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1778
BP 1101A
EP 1102A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402456
ER
PT J
AU Lok, ASF
Everhart, JE
Chung, RT
Kim, HY
Everson, GT
Hoefs, JC
Greenson, JKK
AF Lok, Anna S. F.
Everhart, James E.
Chung, Raymond T.
Kim, Hae-Young
Everson, Gregory T.
Hoefs, John C.
Greenson, Joel K. K.
TI HEPATIC STEATOSIS DECREASES WITH ADVANCING HEPATIC FIBROSIS: FINDINGS
FROM THE HEPATITIS C ANTIVIRAL LONG-TERM TREATMENT AGAINST CIRRHOSIS
TRIAL (HALT-C)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Lok, Anna S. F.] Univ Michigan, Ctr Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Everhart, James E.] NIDDK, Div Digest Dis & Nutr, Bethesda, MD USA.
[Chung, Raymond T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Kim, Hae-Young] New England Res Inst, Watertown, MA 02172 USA.
[Everson, Gregory T.] Univ Colorado, Denver, CO 80202 USA.
[Hoefs, John C.] Univ Calif Irvine, Irvine, CA USA.
[Greenson, Joel K. K.] Univ Michigan, Ann Arbor, MI 48109 USA.
RI Lok, Anna /B-8292-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1777
BP 1101A
EP 1101A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402455
ER
PT J
AU Ghany, MG
Lok, ASF
Everhart, JE
Everson, GT
Lee, WM
Curto, TM
Wright, EC
Stoddard, AM
AF Ghany, Marc G.
Lok, Anna S. F.
Everhart, James E.
Everson, Gregory T.
Lee, William M.
Curto, Teresa M.
Wright, Elizabeth C.
Stoddard, Anne M.
TI PREDICTING CLINICAL OUTCOME USING STANDARD LABORATORY TESTS: ANALYSIS OF
THE HEPATITIS C ANTIVIRAL LONG-TERM TREATMENT AGAINST CIRRHOSIS (HALT-C)
COHORT
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Ghany, Marc G.] NIDDK, NIH, LDB, Bethesda, MD USA.
[Lok, Anna S. F.] Univ Michigan, Ctr Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Everhart, James E.] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD USA.
[Everson, Gregory T.] Univ Colorado, Sect Hepatol, Denver, CO 80202 USA.
[Lee, William M.] Univ Texas SW Med Ctr Dallas, Div Digest & Liver Dis, Dallas, TX 75390 USA.
[Curto, Teresa M.; Stoddard, Anne M.] New England Res Inst, Boston, MA USA.
[Wright, Elizabeth C.] NIDDK, Off Director, NIH, Bethesda, MD USA.
RI Lok, Anna /B-8292-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1785
BP 1105A
EP 1105A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402463
ER
PT J
AU Hara, K
Heller, T
Nagabhyru, PR
Liang, TJ
Hoofnagle, JH
AF Hara, Koji
Heller, Theo
Nagabhyru, Pothu Raju
Liang, T. Jake
Hoofnagle, Joy H.
TI SEQUENCE ANALYSIS OF THE HEPATITIS C VIRUS IN PATIENTS WHO RELAPSE AFTER
SUSTAINED VIROLOGIC RESPONSE: RELAPSE OR REINFECTION?
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Hara, Koji; Heller, Theo; Nagabhyru, Pothu Raju; Liang, T. Jake; Hoofnagle, Joy H.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1786
BP 1105A
EP 1105A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402464
ER
PT J
AU Tuleuova, N
An, CI
Ramanculov, EM
Yokobayashi, Y
Revzin, A
AF Tuleuova, Nazgul
An, Chung-Il
Ramanculov, Erlan M.
Yokobayashi, Yohei
Revzin, Alexander
TI ARTIFICIAL CONTROL OF HEPATIC GENE EXPRESSION USING SHRNA-APTAMER
CONSTRUCT
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Tuleuova, Nazgul; An, Chung-Il; Yokobayashi, Yohei; Revzin, Alexander] Univ Calif Davis, Davis, CA 95616 USA.
[Tuleuova, Nazgul; Ramanculov, Erlan M.] Natl Biotechnol Ctr, Astana, Kazakhstan.
RI Yokobayashi, Yohei/B-5898-2009
OI Yokobayashi, Yohei/0000-0002-2417-1934
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1826
BP 1123A
EP 1123A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402504
ER
PT J
AU Kottilil, S
Frank, AC
Yang, J
Lempicki, RA
Ghany, MG
Sneller, M
AF Kottilil, Shyam
Frank, Astrid C.
Yang, Jun
Lempicki, Richard A.
Ghany, Marc G.
Sneller, Michael
TI WHOLE GENOME TRANSCRIPTIONAL PROFILING IN PERIPHERAL BLOOD MONONUCLEAR
CELLS ILLUSTRATES UNIQUE PATHOGENIC CHARACTERISTICS OF HCV MIXED
CRYOGLOBULINEMIC VASCULITIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 59th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 31-NOV 04, 2008
CL San Francisco, CA
SP Amer Assoc Study Liver Dis, Moscone West Convent Ctr
C1 [Kottilil, Shyam; Frank, Astrid C.; Sneller, Michael] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
[Ghany, Marc G.] NIDDK, LBM, NIH, Bethesda, MD USA.
[Yang, Jun; Lempicki, Richard A.] NCI, SAIC Frederick, Frederick, MD 21701 USA.
RI Lempicki, Richard/E-1844-2012
OI Lempicki, Richard/0000-0002-7059-409X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
SU S
MA 1930
BP 1173A
EP 1174A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CX
UT WOS:000259757402606
ER
PT J
AU Rochon, J
Protiva, P
Seeff, LB
Fontana, RJ
Liangpunsakul, S
Watkins, PB
Davern, T
McHutchison, JG
AF Rochon, James
Protiva, Petr
Seeff, Leonard B.
Fontana, Robert J.
Liangpunsakul, Suthat
Watkins, Patil B.
Davern, Timothy
McHutchison, John G.
CA DILIN
TI Reliability of the Roussel Uclaf Causality Assessment Method for
assessing causality in drug-induced liver injury
SO HEPATOLOGY
LA English
DT Article
ID IDIOPATHIC INFLAMMATORY MYOPATHIES; TERM-FOLLOW-UP; CONSENSUS MEETINGS;
INDUCED HEPATITIS; ADVERSE REACTIONS; CLINICAL-RESEARCH; VALIDATION;
HEPATOTOXICITY; DISEASE; DIAGNOSIS
AB The Roussel Uclaf Causality Assessment Method (RUCAM) was developed to quantify the strength of association between a liver injury and the medication implicated as causing the injury. However, its reliability in a research setting has never been fully explored. The aim of this study was to determine test-retest and interrater reliabilities of RUCAM in retrospectively-identified cases of drug induced liver injury. The Drug-Induced Liver Injury Network is enrolling well-defined cases of hepatotoxicity caused by isoniazid, phenytoin, clavulanate/amoxicillin, or valproate occurring since 1994. Each case was adjudicated by three reviewers working independently; after an interval of at least 5 months, cases were readjudicated by the same reviewers. A total of 40 drug-induced liver injury cases were enrolled including individuals treated with isoniazid (nine), phenytoin (five), clavulanate/amoxicillin (15), and valproate (11). Mean +/- standard deviation age at protocol-defined onset was 44.8 +/- 19.5 years; patients were 68% female and 78% Caucasian. Cases were classified as hepatocellular (44%), mixed (28%), or cholestatic (28%). Test-retest differences ranged from -7 to +8 with complete agreement in only 26% of cases. On average, the maximum absolute difference among the three reviewers was 3.1 on the first adjudication and 2.7 on the second, although much of this variability could be attributed to differences between the enrolling investigator and the external reviewers. The test-retest reliability by the same assessors was 0.54 (upper 95% confidence limit = 0.77); the interrater reliability was 0.45 (upper 95% confidence limit = 0.58). Categorizing the RUCAM to a five-category scale improved these reliabilities but only marginally. Conclusion: The mediocre reliability of the RUCAM is problematic for future studies of drug-induced liver injury. Alternative methods, including modifying the RUCAM, developing drug-specific instruments, or causality assessment based on expert opinion, may be more appropriate.
C1 [Rochon, James; McHutchison, John G.] Duke Univ, Duke Clin Res Inst, Durham, NC 27713 USA.
[Protiva, Petr] Univ Connecticut, Hlth Sci Ctr, Farmington, CT USA.
[Seeff, Leonard B.] NIDDK, Bethesda, MD USA.
[Fontana, Robert J.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Liangpunsakul, Suthat] Indiana Univ, Sch Med, Indianapolis, IN USA.
[Watkins, Patil B.] Univ N Carolina, Chapel Hill, NC USA.
[Davern, Timothy] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Rochon, J (reprint author), Duke Univ, Duke Clin Res Inst, POB 17969, Durham, NC 27713 USA.
EM james.rochon@duke.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[1U01DK065201, 1U01DK065193, 1U01DK065184, 1U01DK065211, 1U01DK065238,
1U01DK065176]
FX Supported by the National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK) under grants 1U01DK065201, 1U01DK065193, 1U01DK065184,
1U01DK065211, 1U01DK065238, and 1U01DK065176.
NR 33
TC 91
Z9 97
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
BP 1175
EP 1183
DI 10.1002/hep.22442
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CT
UT WOS:000259757000019
PM 18798340
ER
PT J
AU Jones, BF
Boyles, RR
Hwang, SY
Bird, GS
Putney, JW
AF Jones, Bertina F.
Boyles, Rebecca R.
Hwang, Sung-Yong
Bird, Gan S.
Putney, James W.
TI Calcium influx mechanisms underlying calcium oscillations in rat
hepatocytes
SO HEPATOLOGY
LA English
DT Article
ID OPERATED CA2+ ENTRY; CA2+-SELECTIVE ARC CHANNELS; EMBRYONIC
KIDNEY-CELLS; PLASMA-MEMBRANE; CRAC CHANNEL; 2-AMINOETHOXYDIPHENYL
BORATE; FURA-2-LOADED HEPATOCYTES; STORE DEPLETION; LIVER-CELLS; ORAI1
AB The process of capacitative or store-operated Ca2+ entry has been extensively investigated, and recently two major molecular players in this process have been described. Stromal interacting molecule (STIM) I acts as a sensor for the level of Ca2+ stored in the endoplasmic reticulum, and Orai proteins constitute pore-forming subunits of the store-operated channels. Store-operated Ca2+ entry is readily demonstrated with protocols that provide extensive Ca2+ store depletion; however, the role of store-operated entry with modest and more physiological cell stimuli is less certain. Recent studies have addressed this question in cell lines; however, the role of store-operated entry during physiological activation of primary cells has not been extensively investigated, and there is little or no information on the roles of STIM and Orai proteins in primary cells. Also, the nature of the Ca2+ influx mechanism with hormone activation of hepatocytes is controversial. Hepatocytes respond to physiological levels of glycogenolytic hormones with well-characterized intracellular Ca2+ oscillations. In the current study, we have used both pharmacological tools and RNA interference (RNAi)-based techniques to investigate the role of store-operated channels in the maintenance of hormone-induced Ca2+ oscillations in rat hepatocytes. Pharmacological inhibitors of store-operated channels blocked thapsigargin-induced Ca2+ entry but only partially reduced the frequency of Ca2+ oscillations. Similarly, RNAi knockdown of STIM1 or Orai I substantially reduced thapsigargin-induced calcium entry, and more modestly diminished the frequency of vasopressin-induced oscillations. Conclusion: Our findings establish that store-operated Ca2+ entry plays a role in the maintenance of agonist-induced oscillations in primary rat hepatocytes but indicate that other agonist-induced entry mechanisms must be involved to a significant extent.
C1 [Jones, Bertina F.; Boyles, Rebecca R.; Hwang, Sung-Yong; Bird, Gan S.; Putney, James W.] NIEHS, Lab Signal Transduct, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Putney, JW (reprint author), NIEHS, Lab Signal Transduct, NIH, Dept Hlth & Human Serv, POB 12233, Res Triangle Pk, NC 27709 USA.
EM putney@niehs.nih.gov
OI Boyles, Rebecca/0000-0003-0073-6854
FU Intramural NIH HHS [Z01 ES090087-11, Z99 ES999999]
NR 49
TC 30
Z9 32
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2008
VL 48
IS 4
BP 1273
EP 1281
DI 10.1002/hep.22461
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 356CT
UT WOS:000259757000029
PM 18802964
ER
PT J
AU Aromando, R
Perez, M
Raimondi, A
Itoiz, M
AF Aromando, R.
Perez, M.
Raimondi, A.
Itoiz, M.
TI Mast cell activation as a collaborative mechanism in the growth of
experimental oral tumors
SO HISTOPATHOLOGY
LA English
DT Meeting Abstract
CT 27th International Congress of the International-Academy-of-Pathology
CY OCT 12-17, 2008
CL Athens, GREECE
SP Int Acad Pathol
C1 [Aromando, R.; Perez, M.; Itoiz, M.] Univ Buenos Aires, Fac Dent, Dept Oral Pathol, RA-1053 Buenos Aires, DF, Argentina.
[Raimondi, A.] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Res Branch, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0309-0167
J9 HISTOPATHOLOGY
JI Histopathology
PD OCT
PY 2008
VL 53
MA 477
BP 209
EP 209
PG 1
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA 352VF
UT WOS:000259524800478
ER
PT J
AU Lugassy, C
Torres-Munoz, J
Kleinman, H
Ghanem, G
Vernon, S
Barnhill, R
AF Lugassy, C.
Torres-Munoz, J.
Kleinman, H.
Ghanem, G.
Vernon, S.
Barnhill, R.
TI Differential gene expression in vascularized angiotropic melanoma areas
versus avascular melanoma areas in a CAM model: implications for
extravascular migratory metastasis
SO HISTOPATHOLOGY
LA English
DT Meeting Abstract
CT 27th International Congress of the International-Academy-of-Pathology
CY OCT 12-17, 2008
CL Athens, GREECE
SP Int Acad Pathol
C1 [Lugassy, C.; Torres-Munoz, J.; Vernon, S.; Barnhill, R.] Univ Miami, Dept Pathol, Coral Gables, FL 33124 USA.
[Kleinman, H.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
[Ghanem, G.] Free Univ Brussels, B-1050 Brussels, Belgium.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0309-0167
J9 HISTOPATHOLOGY
JI Histopathology
PD OCT
PY 2008
VL 53
MA 904
BP 395
EP 395
PG 1
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA 352VF
UT WOS:000259524800904
ER
PT J
AU Adriaansen, J
Perez, P
Goldsmith, CM
Zheng, C
Baum, BJ
AF Adriaansen, J.
Perez, P.
Goldsmith, C. M.
Zheng, C.
Baum, B. J.
TI Differential Sorting of Human Parathyroid Hormone After Transduction of
Mouse and Rat Salivary Glands
SO HUMAN GENE THERAPY
LA English
DT Article
ID MEDIATED GENE-TRANSFER; EPITHELIAL-CELLS; POLARIZED SECRETION;
BASOLATERAL EXOCYTOSIS; SUBMANDIBULAR-GLANDS; ENDOCRINE SECRETION;
GROWTH-HORMONE; PAROTID-GLAND; IN-VIVO; PROTEINS
AB Gene transfer to salivary glands leads to abundant secretion of transgenic protein into either saliva or the bloodstream. This indicates significant clinical potential, depending on the route of sorting. The aim of this study was to probe the sorting characteristics of human parathyroid hormone (hPTH) in two animal models for salivary gland gene transfer. PTH is a key hormone regulating calcium levels in the blood. A recombinant serotype 5 adenoviral vector carrying the hPTH cDNA was administered to the submandibular glands of mice and rats. Two days after delivery, high levels of hPTH were found in the serum of mice, leading to elevated serum calcium levels. Only low amounts of hPTH were found in the saliva. Two days after vector infusion into rats, a massive secretion of hPTH was measured in saliva, with little secretion into serum. Confocal microscopy showed hPTH in the glands, localized basolaterally in mice and apically in rats. Submandibular gland transduction was effective and the produced hPTH was biologically active in vivo. Whereas hPTH sorted toward the basolateral side in mice, in rats hPTH was secreted mainly at the apical side. These results indicate that the interaction between hPTH and the cell sorting machinery is different between mouse and rat salivary glands. Detailed studies in these two species should result in a better understanding of cellular control of transgenic secretory protein sorting in this tissue.
C1 [Adriaansen, J.] Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Adriaansen, J (reprint author), Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, NIH, Dept Hlth & Human Serv, Bldg 10,Room 1N113,MSC-1190,10 Ctr Dr, Bethesda, MD 20892 USA.
EM adriaansenj@mail.nih.gov
FU Division of Intramural Research; National Institute of Dental and
Craniofacial Research; National Institutes of Health
FX This work was supported by the Division of Intramural Research, National
Institute of Dental and Craniofacial Research, National Institutes of
Health. The authors thank A. Voutetakis for help with the initiation of
this study.
NR 40
TC 13
Z9 13
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 2008
VL 19
IS 10
BP 1021
EP 1028
DI 10.1089/hum.2008.079
PG 8
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 368PF
UT WOS:000260633700006
PM 18694295
ER
PT J
AU Ahmed, ZM
Riazuddin, S
Aye, S
Ali, RA
Venselaar, H
Anwar, S
Belyantseva, PP
Qasim, M
Riazuddin, S
Friedman, TB
AF Ahmed, Zubair M.
Riazuddin, Saima
Aye, Sandar
Ali, Rana A.
Venselaar, Hanka
Anwar, Saima
Belyantseva, Polina P.
Qasim, Muhammad
Riazuddin, Sheikh
Friedman, Thomas B.
TI Gene structure and mutant alleles of PCDH15: nonsyndromic deafness
DFNB23 and type 1 Usher syndrome
SO HUMAN GENETICS
LA English
DT Article
ID SENSORY HAIR-CELLS; SYNDROME TYPE 1F; PROTOCADHERIN GENE; MUTATIONS;
CADHERIN-23; CDH23; MICE; COMPLEX; PROTEIN; USH1F
AB Mutations of PCDH15, encoding protocadherin 15, can cause either combined hearing and vision impairment (type 1 Usher syndrome; USH1F) or nonsyndromic deafness (DFNB23). Human PCDH15 is reported to be composed of 35 exons and encodes a variety of isoforms with 3-11 ectodomains (ECs), a transmembrane domain and a carboxy-terminal cytoplasmic domain (CD). Building on these observations, we describe an updated gene structure that has four additional exons of PCDH15 and isoforms that can be subdivided into four classes. Human PCDH15 encodes three alternative, evolutionarily conserved unique cytoplasmic domains (CD1, CD2 or CD3). Families ascertained on the basis of prelingual hearing loss were screened for linkage of this phenotype to markers for PCDH15 on chromosome 10q21.1. In seven of twelve families segregating USH1, we identified homozygous mutant alleles (one missense, one splice site, three nonsense and two deletion mutations) of which six are novel. One family was segregating nonsyndromic deafness DFNB23 due to a homozygous missense mutation. To date, in our cohort of 557 Pakistani families, we have found 11 different PCDH15 mutations that account for deafness in 13 families. Molecular modeling provided mechanistic insight into the phenotypic variation in severity of the PCDH15 missense mutations. We did not find pathogenic mutations in five of the twelve USH1 families linked to markers for USH1F, which suggest either the presence of mutations of yet additional undiscovered exons of PCDH15, mutations in the introns or regulatory elements of PCDH15, or an additional locus for type I USH at chromosome 10q21.1.
C1 [Ahmed, Zubair M.; Riazuddin, Saima; Aye, Sandar; Belyantseva, Polina P.; Friedman, Thomas B.] Natl Inst Deafness & Other Commun Disorders, Sect Human Genet, Mol Genet Lab, Natl Inst Hlth, Rockville, MD 20850 USA.
[Ali, Rana A.; Anwar, Saima; Qasim, Muhammad; Riazuddin, Sheikh] Univ Punjab, Natl Ctr Excellence Mol Biol, Lahore, Pakistan.
[Venselaar, Hanka] Radboud Univ Nijmegen, Ctr Mol & Biomol Informat, NL-6525 ED Nijmegen, Netherlands.
RP Friedman, TB (reprint author), Natl Inst Deafness & Other Commun Disorders, Sect Human Genet, Mol Genet Lab, Natl Inst Hlth, 5 Res Court,Room 2A-19, Rockville, MD 20850 USA.
EM friedman@nidcd.nih.gov
RI Anwar, Saima/C-7477-2016; SHEIKH, RIAZUDDIN/L-2406-2015; Venselaar,
Hanka/D-2009-2016
FU Higher Education Commission, Islamabad, Pakistan; Ministry of Science
and Technology, Islamabad, Pakistan; National Institute on Deafness and
Other Communication Disorders, NIH [1 ZO1 DC000039-11]
FX The authors are grateful to the families who made this research
possible. We thank Barbara Ploplis and Nicholas Kusnezov for their
technical support. We also thank Julie Schultz, Karen Friderici and Anne
Madeo for suggestions regarding this manuscript. This study was
supported by the Higher Education Commission, Islamabad, Pakistan;
Ministry of Science and Technology, Islamabad, Pakistan and by
intramural funds to TBF from the National Institute on Deafness and
Other Communication Disorders, NIH (1 ZO1 DC000039-11).
NR 34
TC 28
Z9 29
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
J9 HUM GENET
JI Hum. Genet.
PD OCT
PY 2008
VL 124
IS 3
BP 215
EP 223
DI 10.1007/s00439-008-0543-3
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 358ID
UT WOS:000259909500003
PM 18719945
ER
PT J
AU Cohen, TV
Klarmann, KD
Sakchaisri, K
Cooper, JP
Kuhns, D
Anver, M
Johnson, PF
Williams, SC
Keller, JR
Stewart, CL
AF Cohen, Tatiana V.
Klarmann, Kimberly D.
Sakchaisri, Krisada
Cooper, Jason P.
Kuhns, Douglas
Anver, Miriam
Johnson, Peter F.
Williams, Simon C.
Keller, Jonathan R.
Stewart, Colin L.
TI The lamin B receptor under transcriptional control of C/EBP epsilon is
required for morphological but not functional maturation of neutrophils
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID BINDING-PROTEIN-EPSILON; 3-BETA-HYDROXYSTEROL DELTA(14)-REDUCTASE
DEFICIENCY; HEM/GREENBERG SKELETAL DYSPLASIA; NUCLEAR-ENVELOPE;
MEMBRANE-PROTEIN; IN-VIVO; EXPRESSION; CHROMATIN; GENE; LAMINOPATHIES
AB The lamin B receptor (LBR) is an integral nuclear envelope protein that interacts with chromatin and has homology to sterol reductases, Mutations in LBR result in Pelger-Huet anomaly and HEM-Greenberg skeletal dysplasia, whereas in mice Lbr mutations result in ichthyosis. To further understand the function of the LBR and its role in disease, we derived a novel mouse model with a gene-trap insertion into the Lbr locus (Lbr(GT/GT)). Phenotypically, the Lbr(GT/GT) mice are similar to ichythyosis mice. The Lbr(GT/GT) granulocytes lack a mature segmented nucleus and have a block in late maturation. Despite these changes in nuclear morphology, the innate granulocyte immune function in the killing of Staphylococcus aureus bacteria appears to be intact. Granulocyte differentiation requires the transcription factor C/EBP epsilon. We identified C/EBP epsilon binding sites within the Lbr promoter and used EMSAs and luciferase assays to show that Lbr is transcriptionally regulated by C/EBP epsilon. Our findings indicate that the Lbr(GT/GT) mice are a model for Pelger-Huet anomaly and that Lbr, under transcriptional regulation of C/EBP epsilon, is necessary for morphological but not necessarily functional granulocyte maturation.
C1 [Cohen, Tatiana V.; Klarmann, Kimberly D.; Keller, Jonathan R.; Stewart, Colin L.] CCR, Canc & Dev Biol Lab, Frederick, MD 21702 USA.
[Klarmann, Kimberly D.; Keller, Jonathan R.] SAIC Frederick Inc, Lab Canc Prevent, Basic Res Program, Frederick, MD 21702 USA.
[Sakchaisri, Krisada; Johnson, Peter F.] CCR, Lab Prot Dynam & Signaling, Frederick, MD 21702 USA.
[Kuhns, Douglas] SAIC Frederick Inc, Clin Serv Program, Frederick, MD 21702 USA.
[Anver, Miriam] NCI, SAIC Frederick, Pathol Histotechnol Lab, Lab Anim Sci Program, Frederick, MD 21702 USA.
[Cooper, Jason P.; Williams, Simon C.] Texas Tech Univ, Hlth Sci Ctr, Dept Biochem & Cell Biol, Lubbock, TX 79430 USA.
RP Stewart, CL (reprint author), Inst Med Biol, 8A Biomed Grove, Immunos 138668, Singapore.
EM colin.stewart@imb.a-star.edu.sg
RI Johnson, Peter/A-1940-2012
OI Johnson, Peter/0000-0002-4145-4725
FU NIH; National Cancer Institute; Center for Cancer Research; National
Institutes of Health [NO1-CO-12400]
FX This research was supported in part by the Intramural Research program
of the NIH, National Cancer Institute, Center for Cancer Research, and
with Federal funds from the National Cancer Institute, National
Institutes of Health, under Contract No. NO1-CO-12400.
NR 56
TC 24
Z9 25
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD OCT 1
PY 2008
VL 17
IS 19
BP 2921
EP 2933
DI 10.1093/hmg/ddn191
PG 13
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 350BK
UT WOS:000259327200001
PM 18621876
ER
PT J
AU Boyle, J
Ueda, T
Oh, KS
Imoto, K
Tamura, D
Jagdeo, J
Khan, SG
Nadem, C
DiGiovanna, JJ
Kraemer, KH
AF Boyle, Jennifer
Ueda, Takahiro
Oh, Kyu-Seon
Imoto, Kyoko
Tamura, Deborah
Jagdeo, Jared
Khan, Sikandar G.
Nadem, Carine
DiGiovanna, John J.
Kraemer, Kenneth H.
TI Persistence of Repair Proteins at Unrepaired DNA Damage Distinguishes
Diseases with ERCC2 (XPD) Mutations: Cancer-Prone Xeroderma Pigmentosum
vs. Non-Cancer-Prone Trichothiodystrophy
SO HUMAN MUTATION
LA English
DT Article
DE DNA repair; skin cancer; ultraviolet radiation; immunofluorescene;
confocal microscopy; ERCC2; XPD; XP; TTD
ID NUCLEOTIDE EXCISION-REPAIR; CYCLOBUTANE PYRIMIDINE DIMERS;
COCKAYNE-SYNDROME CELLS; C-MYC EXPRESSION; TRANSCRIPTION FACTOR; BASAL
TRANSCRIPTION; REPAIR/TRANSCRIPTION GENE; ULTRAVIOLET-RADIATION;
PRENATAL-DIAGNOSIS; POLYMERASE-ETA
AB Patients with xeroderma pigmentosum (XP) have a 1,000-fold increase in ultraviolet (UV)-induced skin cancers while trichothiodystrophy (TTD) patients, despite mutations in the same genes, ERCC2 (XPD) or ERCC3 (XPB), are cancer,free. Unlike XP cells, TTD cells have a nearly normal rate of removal of UV-induced 6-4 photoproducts (6-4PP) in their DNA and low levels of the basal transcription factor, TFIIH. We examined seven XP, TTD, and XP/TTD complex patients and identified mutations in the XPD gene. We discovered large differences in nucleotide excision repair (NER) protein recruitment to sites of localized UV damage in TTD cells compared to XP or normal cells. XPC protein was rapidly localized in all cells. XPC was redistributed in TTD, and normal cells by 3 hr postirradiation, but remained localized in XP cells at 24-hr postirradiation. In XP cells recruitment of other NER proteins (XPB, XPD, XPG, XPA, and XTF) was also delayed and persisted at 24 hr (p < 0.001). In TTD cells with defects in the XPD, XPB, or GTF2H5 (TTDA) genes, in contrast, recruitment of these NER proteins was reduced compared to normals at early time points (p < 0.001) and remained low at 24 hr postirradiation. These data indicate that in XP persistence of NER proteins at sites of unrepaired DNA damage is associated with greatly increased skin cancer risk possibly by blockage of translesion DNA synthesis. In contrast, in TTD, low levels of unstable TFIIH proteins do not accumulate at sites of unrepaired photoproducts and may permit normal translesion DNA synthesis without increased skin cancer.
C1 [Boyle, Jennifer; Ueda, Takahiro; Oh, Kyu-Seon; Imoto, Kyoko; Tamura, Deborah; Jagdeo, Jared; Khan, Sikandar G.; Nadem, Carine; DiGiovanna, John J.; Kraemer, Kenneth H.] NCI, DNA Repair Sect, Basic Res Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[DiGiovanna, John J.] Brown Univ, Dept Dermatol, Warren Alpert Sch Med, Div Dermatopharmacol, Providence, RI 02912 USA.
RP Kraemer, KH (reprint author), NCI, DNA Repair Sect, Basic Res Lab, Ctr Canc Res, Bldg 37,Room 4002,MSC 4258, Bethesda, MD 20892 USA.
EM kraemerk@nih.gov
FU Intramural NIH HHS [Z01 BC004517-31]
NR 77
TC 36
Z9 37
U1 0
U2 4
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1059-7794
J9 HUM MUTAT
JI Hum. Mutat.
PD OCT
PY 2008
VL 29
IS 10
BP 1194
EP 1208
DI 10.1002/humu.20768
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 362QP
UT WOS:000260212500004
PM 18470933
ER
PT J
AU Pacher, P
Mukhopadhyay, P
Mohanraj, R
Godlewski, G
Batkai, S
Kunos, G
AF Pacher, Pal
Mukhopadhyay, Partha
Mohanraj, Rajesh
Godlewski, Grzegorz
Batkai, Sandor
Kunos, George
TI Modulation of the endocannabinoid system in cardiovascular disease -
Therapeutic potential and limitations
SO HYPERTENSION
LA English
DT Review
ID CARDIOMETABOLIC RISK-FACTORS; HEPATIC ISCHEMIA/REPERFUSION INJURY;
SPONTANEOUSLY HYPERTENSIVE-RATS; CANNABINOID-1 RECEPTOR BLOCKER;
ISCHEMIA-REPERFUSION INJURY; RANDOMIZED CONTROLLED-TRIAL; CB1 RECEPTORS;
BLOOD-PRESSURE; OVERWEIGHT PATIENTS; ABDOMINAL OBESITY
C1 [Pacher, Pal; Mukhopadhyay, Partha; Mohanraj, Rajesh] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
[Godlewski, Grzegorz; Batkai, Sandor; Kunos, George] NIAAA, Sect Neuroendocrinol, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
RP Pacher, P (reprint author), NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, 5625 Fishers Lane,MSC 9413, Bethesda, MD 20892 USA.
EM pacher@mail.nih.gov
RI MUKHOPADHYAY, PARTHA/G-3890-2010; Batkai, Sandor/G-3889-2010; Pacher,
Pal/B-6378-2008; Batkai, Sandor/H-7983-2014
OI MUKHOPADHYAY, PARTHA/0000-0002-1178-1274; Pacher,
Pal/0000-0001-7036-8108;
FU NIH
FX This publication was supported by funds from the Intramural Research
Program of NIH (to P. P. and G. K.).
NR 72
TC 59
Z9 62
U1 0
U2 0
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 2008
VL 52
IS 4
BP 601
EP 607
DI 10.1161/HYPERTENSIONAHA.105.063651
PG 7
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 349KF
UT WOS:000259279000002
PM 18779440
ER
PT J
AU de Lange, WJ
Beyer, AM
Halabi, CM
Gonzalez, FJ
Sigmund, CD
AF de lange, Willem J.
Beyer, Andreas M.
Halabi, Carmen M.
Gonzalez, Frank J.
Sigmund, Curt D.
TI Vascular hypercontractility to endothelin-1 in mice lacking endothelial
PPAR gamma
SO HYPERTENSION
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the European-Council-for-Cardiovascular-Research
CY OCT 10-12, 2008
CL Nice, FRANCE
C1 [de lange, Willem J.; Beyer, Andreas M.; Halabi, Carmen M.; Sigmund, Curt D.] Univ Iowa, Iowa City, IA USA.
[Gonzalez, Frank J.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD OCT
PY 2008
VL 52
IS 4
BP E93
EP E93
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 349KF
UT WOS:000259279000452
ER
PT J
AU Gainer, JV
O'Donnell, C
Cupples, LA
Dawson, EP
Capdevila, JH
Waterman, MR
Brown, NJ
AF Gainer, James V., III
O'Donnell, Christopher
Cupples, L. A.
Dawson, Elliot P.
Capdevila, Jorge H.
Waterman, Michael R.
Brown, Nancy J.
TI Association of the loss-of-function CYP4A11 8590C allele with
hypertriglyceridemia in men and HDL-C in women in the Framingham
Offspring Study
SO HYPERTENSION
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the European-Council-for-Cardiovascular-Research
CY OCT 10-12, 2008
CL Nice, FRANCE
C1 [Gainer, James V., III; Dawson, Elliot P.; Capdevila, Jorge H.; Waterman, Michael R.; Brown, Nancy J.] Vanderbilt Univ, Nashville, TN USA.
[Cupples, L. A.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[O'Donnell, Christopher] Natl Inst Hlth, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD OCT
PY 2008
VL 52
IS 4
BP E96
EP E96
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 349KF
UT WOS:000259279000464
ER
PT J
AU Rutherford, S
Voruganti, VS
Goring, HH
Laston, SL
Haack, K
Almasy, L
Comuzzie, A
Lee, ET
Best, LG
Fabsitz, RR
Devereux, RB
Okin, PM
Bella, JN
Howard, BV
MacCluer, JW
Cole, SA
AF Rutherford, Sue
Voruganti, V. S.
Goering, Harald H.
Laston, Sandra L.
Haack, Karin
Almasy, Laura
Comuzzie, Anthony
Lee, Elisa T.
Best, Lyle G.
Fabsitz, Richard R.
Devereux, Richard B.
Okin, Peter M.
Bella, Jonathan N.
Howard, Barbara V.
MacCluer, Jean W.
Cole, Shelley A.
TI A heart rate genetic locus on chromosome 9p21 in the Strong Heart Family
Study
SO HYPERTENSION
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the European-Council-for-Cardiovascular-Research
CY OCT 10-12, 2008
CL Nice, FRANCE
C1 [Rutherford, Sue; Voruganti, V. S.; Goering, Harald H.; Laston, Sandra L.; Haack, Karin; Almasy, Laura; Comuzzie, Anthony; MacCluer, Jean W.; Cole, Shelley A.] SW Fdn Biomed Res, San Antonio, TX 78284 USA.
[Lee, Elisa T.] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA.
[Best, Lyle G.] Breaks Ind Res Inc, Timber Lake, SD USA.
[Fabsitz, Richard R.] NHLBI, Bethesda, MD 20892 USA.
[Devereux, Richard B.; Okin, Peter M.; Bella, Jonathan N.] Cornell Univ, New York Presbyterian Hosp, Weill Med Coll, New York, NY 10021 USA.
[Howard, Barbara V.] Medstar Res Inst, Washington, DC USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
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 2008
VL 52
IS 4
BP E101
EP E102
PG 2
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 349KF
UT WOS:000259279000489
ER
PT J
AU Jeong, J
Berman, P
Przytycka, TM
AF Jeong, Jieun
Berman, Piotr
Przytycka, Teresa M.
TI Improving Strand Pairing Prediction through Exploring Folding
Cooperativity
SO IEEE-ACM TRANSACTIONS ON COMPUTATIONAL BIOLOGY AND BIOINFORMATICS
LA English
DT Article; Proceedings Paper
CT 7th International Workshop on Algorithms in Bioinformatics (WABI 2007)
CY SEP 08-09, 2007
CL Philadelphia, PA
DE Biology and genetics; combinatorial algorithms
ID AB-INITIO PREDICTION; BETA-SHEET TOPOLOGY; GLOBULAR-PROTEINS;
LOCAL-STRUCTURE; RECOGNITION; SEQUENCE; ORGANIZATION; POTENTIALS;
PATHWAYS; DOMAINS
AB The topology of beta-sheets is defined by the pattern of hydrogen-bonded strand pairing. Therefore, predicting hydrogen-bonded strand partners is a fundamental step toward predicting beta-sheet topology. At the same time, finding the correct partners is very difficult due to long-range interactions involved in strand pairing. Additionally, patterns of amino acids observed in beta-sheet formations are very general, and therefore, difficult to use for computational recognition of specific contacts between strands. In this work, we report a new strand pairing algorithm. To address the aforementioned difficulties, our algorithm attempts to mimic elements of the folding process. Namely, in addition to ensuring that the predicted hydrogen-bonded strand pairs satisfy basic global consistency constraints, it takes into account hypothetical folding pathways. Consistently with this view, introducing hydrogen bonds between a pair of strands changes the probabilities of forming hydrogen bonds between other pairs of strand. We demonstrate that this approach provides an improvement over previously proposed algorithms. We also compare the performance of this method to that of a global optimization algorithm that poses the problem as integer linear programming optimization problem and solves it using ILOG CPLEX package.
C1 [Jeong, Jieun; Berman, Piotr] Penn State Univ, Dept Comp Sci & Engn, University Pk, PA 16802 USA.
[Przytycka, Teresa M.] NIH, Computat Biol Branch, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Jeong, J (reprint author), Penn State Univ, Dept Comp Sci & Engn, University Pk, PA 16802 USA.
EM jijeong@cse.psu.edu; berman@cse.psu.edu; przytyck@ncbi.nlm.nih.gov
FU Intramural NIH HHS [Z01 LM779892-05]
NR 35
TC 5
Z9 5
U1 0
U2 2
PU IEEE COMPUTER SOC
PI LOS ALAMITOS
PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1314 USA
SN 1545-5963
J9 IEEE ACM T COMPUT BI
JI IEEE-ACM Trans. Comput. Biol. Bioinform.
PD OCT-DEC
PY 2008
VL 5
IS 4
BP 484
EP 491
DI 10.1109/TCBB.2008.88
PG 8
WC Biochemical Research Methods; Computer Science, Interdisciplinary
Applications; Mathematics, Interdisciplinary Applications; Statistics &
Probability
SC Biochemistry & Molecular Biology; Computer Science; Mathematics
GA 365UC
UT WOS:000260433100002
PM 18989036
ER
PT J
AU Caspi, R
AF Caspi, Rachel
TI Autoimmunity in the immune privileged eye: pathogenic and regulatory T
cells
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE T lymphocytes; T regulatory cells; Th1; Th17; Uveitis; Autoimmune
disease
ID OCULAR AUTOIMMUNITY; EFFECTOR RESPONSE; PRODUCE IL-17; IFN-GAMMA;
UVEITIS; DISEASE; INFLAMMATION; IL-23; MICE; INDUCTION
AB Experimental autoimmune uveitis (EAU) in animals serves as a model of human uveitis. EAU can be induced in mice by immunization with the retinal antigen interphotoreceptor retinoid binding protein (IRBP) in complete Freund's adjuvant (CFA) or by IRBP-pulsed mature dendritic cells, and can be driven either by a Th17 or a Th1 effector response, depending on the model. The direction of the response is affected by conditions present during the exposure to antigen, including the quality/quantity of innate receptor stimulation and/or type of APC. IL-17 and IFN-gamma production by innate cells such as NKT may also affect the disease process. If exposure to antigen is via a hydrodynamic DNA vaccination with an IRBP-encoding plasmid, the response is directed to a regulatory phenotype, and disease is ameliorated or prevented. Our data shed light on effector and regulatory responses in autoimmune disease, provide balance to the Th1/Th17 paradigm and help to explain the clinical heterogeneity of human uveitis, which occurs in the face of responses to the same ocular antigen(s).
C1 NEI, UPenn Grad Program, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Caspi, R (reprint author), NEI, UPenn Grad Program, Immunol Lab, NIH, 10 Ctr Dr,Bldg 10,Room 10N222, Bethesda, MD 20892 USA.
EM rcaspi@helix.nih.gov
OI Caspi, Rachel/0000-0002-7140-7671
FU Intramural NIH HHS [Z01 EY000184-25]
NR 40
TC 45
Z9 48
U1 0
U2 2
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
J9 IMMUNOL RES
JI Immunol. Res.
PD OCT
PY 2008
VL 42
IS 1-3
BP 41
EP 50
DI 10.1007/s12026-008-8031-3
PG 10
WC Immunology
SC Immunology
GA 387KW
UT WOS:000261952100005
PM 18629448
ER
PT J
AU Diamond, MS
Pierson, TC
Fremont, DH
AF Diamond, Michael S.
Pierson, Theodore C.
Fremont, Daved H.
TI The structural immunology of antibody protection against West Nile virus
SO IMMUNOLOGICAL REVIEWS
LA English
DT Review
DE infectious diseases; antibodies; emerging infectious disease;
antigens/peptides/epitopes; complement
ID BORNE ENCEPHALITIS-VIRUS; YELLOW-FEVER VIRUS; CD8(+) T-CELLS;
CENTRAL-NERVOUS-SYSTEM; NEUTRALIZING MONOCLONAL-ANTIBODY; FLAVIVIRUS
ENVELOPE GLYCOPROTEIN; CROSS-REACTIVE EPITOPES; DENGUE VIRUS;
DOMAIN-III; MEDIATED NEUTRALIZATION
AB Recent investigations of the interaction between the West Nile virus (WNV) envelope protein (E) and monoclonal antibodies (mAbs) have elucidated fundamental insights into the molecular mechanisms of neutralization. Structural studies have defined an epitope on the lateral ridge of domain III (DIII-lr) of the WNV E protein that is recognized by antibodies with the strongest neutralizing activity in vitro and in vivo. Antibodies that bind this epitope are highly potent because they efficiently block at a post-entry step of viral infection with relatively low virion occupancy requirements. In this review, we discuss the structural, molecular, and immunologic basis for antibody-mediated protection against WNV, and its implications for novel therapeutic or vaccine strategies.
C1 [Diamond, Michael S.] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA.
[Diamond, Michael S.; Fremont, Daved H.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
[Fremont, Daved H.] Washington Univ, Sch Med, Dept Biochem & Mol Biophys, St Louis, MO 63110 USA.
[Pierson, Theodore C.] NIH, Viral Pathogenesis Sect, Viral Dis Lab, Bethesda, MD 20892 USA.
RP Diamond, MS (reprint author), Washington Univ, Sch Med, Dept Med, 660 S Euclid Ave,Box 8051, St Louis, MO 63110 USA.
EM diamond@borcim.wustl.edu
FU Pediatric Dengue Vaccine Initiative; Burroughs Wellcome Fund; NIAID of
the NIH [U01 AI061373, U54 AI057160, R01 AI073755]
FX We thank members of our laboratory for helpful discussions. Work in our
laboratories is supported by the Pediatric Dengue Vaccine Initiative,
the Burroughs Wellcome Fund, and the NIAID of the NIH (grants U01
AI061373, U54 AI057160, R01 AI073755, and NIH intramural funds).
NR 139
TC 70
Z9 74
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0105-2896
J9 IMMUNOL REV
JI Immunol. Rev.
PD OCT
PY 2008
VL 225
BP 212
EP 225
DI 10.1111/j.1600-065X.2008.00676.x
PG 14
WC Immunology
SC Immunology
GA 350IA
UT WOS:000259344700013
PM 18837784
ER
PT J
AU Nadadur, SS
Srirama, K
Mudipalli, A
AF Nadadur, S. S.
Srirama, K.
Mudipalli, Anuradha
TI Iron transport & homeostasis mechanisms: Their role in health & disease
SO INDIAN JOURNAL OF MEDICAL RESEARCH
LA English
DT Review
DE Anaemia; haemochromatosis; hepcidin; homeostasis; iron; trace metal
ID METAL-ION TRANSPORTERS; TRANSCRIPTION FACTORS; MOLECULAR CONTROL; SOLUTE
CARRIERS; GENE-EXPRESSION; HEPCIDIN; METABOLISM; HEMOCHROMATOSIS;
FERRITIN; FAMILY
AB Iron is an essential trace metal required by all living organisms and is toxic in excess. Nature has evolved a delicately balanced network to monitor iron entry, transport it to sites of need, and serve as a unique storage and recycling system, in the absence of an excretory system, to remove excess iron. Due to the unique nature of iron metabolism, iron homeostasis is achieved by integrated specialized mechanisms that operate at the cellular and organism level. The use of positional cloning approaches by multiple researchers has led to the identification and characterization of various proteins and peptides that play a critical role in iron metabolism. These efforts have led to elucidation of the molecular mechanisms involved in the uptake of iron by the enterocytes, transportation across the membrane to circulation, and deliver), to diverse tissues for use and storage and sensor system to co-ordinate and achieve homeostasis. Molecular understanding of these processes and the key regulatory molecules involved in maintaining homeostasis will provide novel insights into understanding human disorders associated with either iron deficiency or overload.
C1 [Nadadur, S. S.] NIEHS, Div Extramural Res & Training, Res Triangle Pk, NC 27709 USA.
[Srirama, K.] Sri Sathya Sai Univ, Dept Biosci, Prasanthinilayam, AP, India.
[Mudipalli, Anuradha] US EPA, Natl Ctr Environm Assessment, Res Triangle Pk, NC 27711 USA.
RP Nadadur, SS (reprint author), NIEHS, Div Extramural Res & Training, POB 12233, Res Triangle Pk, NC 27709 USA.
EM nadadurs@niehs.nih.gov
NR 79
TC 26
Z9 28
U1 2
U2 9
PU INDIAN COUNCIL MEDICAL RES
PI NEW DELHI
PA PO BOX 4911 ANSARI NAGAR, NEW DELHI 110029, INDIA
SN 0971-5916
J9 INDIAN J MED RES
JI Indian J. Med. Res.
PD OCT
PY 2008
VL 128
IS 4
BP 533
EP 544
PG 12
WC Immunology; Medicine, General & Internal; Medicine, Research &
Experimental
SC Immunology; General & Internal Medicine; Research & Experimental
Medicine
GA 390KY
UT WOS:000262164400014
PM 19106445
ER
PT J
AU Oakley, MS
McCutchan, TF
Anantharaman, V
Ward, JM
Faucette, L
Erexson, C
Mahajan, B
Zheng, H
Majam, V
Aravind, L
Kumar, S
AF Oakley, Miranda S.
McCutchan, Thomas F.
Anantharaman, Vivek
Ward, Jerrold M.
Faucette, Laurence
Erexson, Cindy
Mahajan, Babita
Zheng, Hong
Majam, Victoria
Aravind, L.
Kumar, Sanjai
TI Host biomarkers and biological pathways that are associated with the
expression of experimental cerebral malaria in mice
SO INFECTION AND IMMUNITY
LA English
DT Article
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; SEVERE FALCIPARUM-MALARIA;
UNCOUPLING PROTEIN-2; METALLOTHIONEIN EXPRESSION; MICROARRAY ANALYSIS;
MEDIATED APOPTOSIS; SUSCEPTIBLE MICE; AFRICAN CHILDREN; MURINE MALARIA;
RESISTANT MICE
AB Cerebral malaria (CM) is a primary cause of malaria-associated deaths among young African children. Yet no diagnostic tools are available that could be used to predict which of the children infected with Plasmodium falciparum malaria will progress to CM. We used the Plasmodium berghei ANKA murine model of experimental cerebral malaria (ECM) and high-density oligonucleotide microarray analyses to identify host molecules that are strongly associated with the clinical symptoms of ECM. Comparative expression analyses were performed with C57BL/6 mice, which have an ECM-susceptible phenotype, and with mice that have ECM-resistant phenotypes: CD8 knockout and perforin knockout mice on the C57BL/6 background and BALB/c mice. These analyses allowed the identification of more than 200 host molecules (a majority of which had not been identified previously) with altered expression patterns in the brain that are strongly associated with the manifestation of ECM. Among these host molecules, brain samples from mice with ECM expressed significantly higher levels of p21, metallothionein, and hemoglobin alpha 1 proteins by Western blot analysis than mice unaffected by ECM, suggesting the possible utility of these molecules as prognostic biomarkers of CM in humans. We suggest that the higher expression of hemoglobin alpha 1 in the brain may be associated with ECM and could be a source of excess heme, a molecule that is considered to trigger the pathogenesis of CM. Our studies greatly enhance the repertoire of host molecules for use as diagnostics and novel therapeutics in CM.
C1 [Kumar, Sanjai] US FDA, Malaria Res Program, Div Emerging & Transfus Transmitted Dis, Ctr Biol Evaluat & Res, Rockville, MD 20852 USA.
[Mahajan, Babita; Zheng, Hong; Majam, Victoria; Kumar, Sanjai] NIAID, NIH, Rockville, MD USA.
[Oakley, Miranda S.; McCutchan, Thomas F.] Lab Malaria & Vector Res, Rockville, MD USA.
[Ward, Jerrold M.; Faucette, Laurence; Erexson, Cindy] Div Intramural Res, Infect Dis Pathogenesis Sect, Comparat Med Branch, Rockville, MD USA.
[Oakley, Miranda S.] Uniformed Serv Univ Hlth Sci, Emerging Infect Dis Program, Bethesda, MD 20814 USA.
[Anantharaman, Vivek; Aravind, L.] Natl Inst Hlth, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD USA.
RP Kumar, S (reprint author), US FDA, Malaria Res Program, Div Emerging & Transfus Transmitted Dis, Ctr Biol Evaluat & Res, Rockville, MD 20852 USA.
EM Sanjai.kumar@fda.hhs.gov
OI Anantharaman, Vivek/0000-0001-8395-0009
NR 70
TC 15
Z9 15
U1 3
U2 4
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD OCT
PY 2008
VL 76
IS 10
BP 4518
EP 4529
DI 10.1128/IAI.00525-08
PG 12
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 349PM
UT WOS:000259293100018
PM 18644885
ER
PT J
AU Clapper, ML
Gary, MA
Coudry, RA
Litwin, S
Chang, WCL
Devarajan, K
Lubet, RA
Cooper, HS
AF Clapper, Margie L.
Gary, Monique A.
Coudry, Renata A.
Litwin, Samuel
Chang, Wen-Chi L.
Devarajan, Karthik
Lubet, Ronald A.
Cooper, Harry S.
TI 5-Aminosalicylic Acid Inhibits Colitis-Associated Colorectal Dysplasias
in the Mouse Model of Azoxymethane/Dextran Sulfate Sodium-Induced
Colitis
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE ulcerative colitis; colorectal neoplasia; 5-aminosalicylic acid; dextran
sulfate sodium; mouse model
ID INFLAMMATORY-BOWEL-DISEASE; PRIMARY SCLEROSING CHOLANGITIS;
ULCERATIVE-COLITIS; GENE-EXPRESSION; CANCER RISK; SULFASALAZINE;
NEOPLASIA; MESALAZINE; CARCINOMA; ADENOMAS
AB Background: The impact of the antiinflammatory agent 5-aminosalicylic acid (5-ASA) on the risk for colitis-associated colorectal cancer remains controversial. The chemopreventive activity of 5-ASA was evaluated in the Swiss Webster model of azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colitis-associated neoplasia.
Methods: Mice were injected with AOM (7.4 mg/kg i.p.) and randomized to receive either vehicle or 5-ASA (75, 150, and 225 mg/kg) for the remainder of the study. DSS treatment began at 9 weeks of age and continued for 3 cycles. At the time of sacrifice (18 weeks of age), the entire colon and rectum were processed for histopathologic examination.
Results: An inverse trend was observed between dose and Multiplicity of colonic dysplasias in all drug-treated groups (P = 0.03), with animals receiving 75 mg/kg 5-ASA exhibiting 56% of the number of dysplasias of the AOM/DSS controls (mean +/- SEM: 7.6 +/- 1.4 and 13.6 +/- 2.7. respectively). Administration of 75 mg/kg 5-ASA decreased both the mean multiplicity of flat dysplasias (1.8 +/- 0.4 for drug-treated versus 5.6 +/- 1.2 for AOM/DSS control) and the burden of polypoid dysplasias (tumor burden: 6.7 +/- 2.7 for drug-treated versus 14.9 +/- 3.9 units for AOM/DSS controls) significantly (P = 0.002 and 0.04. respectively). Inflammation was least severe in the 75 mg/kg group. which exhibited the fewest number of colorectal tumors.
Conclusions: These data suggest that low-dose 5-ASA may be efficacious in preventing colitis-associated dysplasias and provide strong support for optimizing this therapy for the prevention of colonic neoplasms in patients with ulcerative colitis. (Inflamm Bowel Dis 2008; 14:1341-1347)
C1 [Clapper, Margie L.; Gary, Monique A.; Coudry, Renata A.; Litwin, Samuel; Chang, Wen-Chi L.; Devarajan, Karthik] Fox Chase Canc Ctr, Div Populat Sci, Philadelphia, PA 19111 USA.
[Lubet, Ronald A.] NCI, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Cooper, Harry S.] Fox Chase Canc Ctr, Div Med Sci, Philadelphia, PA 19111 USA.
RP Clapper, ML (reprint author), Fox Chase Canc Ctr, Div Populat Sci, 333 Cottman Ave, Philadelphia, PA 19111 USA.
EM margie.clapper@fccc.edu
FU National Cancer Institute [N01-CN-05121, CA-06927]; Commonwealth of
Pennsylvania
FX Supported by USPHS grants N01-CN-05121 and CA-06927 from the National
Cancer Institute and by an appropriation from the Commonwealth of
Pennsylvania. The contents are solely the responsibility of the authors
and do not necessarily represent the official views of the National
Cancer Institute.
NR 31
TC 35
Z9 37
U1 0
U2 11
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1078-0998
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD OCT
PY 2008
VL 14
IS 10
BP 1341
EP 1347
DI 10.1002/ibd.20489
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 358GG
UT WOS:000259904500003
PM 18452197
ER
PT J
AU Juhn, J
Marinotti, O
Calvo, E
James, AA
AF Juhn, J.
Marinotti, O.
Calvo, E.
James, A. A.
TI Gene structure and expression of nanos (nos) and oskar (osk) orthologues
of the vector mosquito, Culex quinquefasciatus
SO INSECT MOLECULAR BIOLOGY
LA English
DT Article
DE gene expression; osk; nos; mosquito; germline; pole cells; hybridization
in situ
ID MESSENGER-RNA LOCALIZATION; POLE CELL-FORMATION; WEST-NILE-VIRUS;
AEDES-AEGYPTI; INSECTICIDE RESISTANCE; ANOPHELES-GAMBIAE; MALARIA
PARASITE; PIPIENS DIPTERA; DROSOPHILA; SYSTEM
AB The products of the maternal-effect genes, nanos (nos) and oskar (osk), are important for the development of germ cells in insects. Furthermore, these genes have been proposed as candidates for donating functional DNA regulatory sequences for use in gene drive systems to control transmission of mosquito-borne pathogens. The nos and osk genes of the cosmopolitan vector mosquito, Culex quinquefasciatus, encode proteins with domains common to orthologues found in other mosquitoes. Expression analyses support the conclusion that the role of these genes is conserved generally among members of the nematocera. Hybridization in situ analyses reveal differences in mRNA distribution in early embryos in comparison with the cyclorraphan, Drosophila melanogaster, highlighting a possible feature in the divergence of the clades each insect represents.
C1 [Juhn, J.; James, A. A.] Univ Calif Irvine, Dept Microbiol & Mol Genet, Irvine, CA 92697 USA.
[Juhn, J.; Marinotti, O.; Calvo, E.; James, A. A.] Univ Calif Irvine, Dept Mol Biol & Biochem, Irvine, CA 92697 USA.
[Calvo, E.] NIAID, Med Entomol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
RP James, AA (reprint author), Univ Calif Irvine, Dept Microbiol & Mol Genet, 3205 McGaugh Hall, Irvine, CA 92697 USA.
EM aajames@uci.edu
OI Marinotti, Osvaldo/0000-0002-7173-7160
FU National Institutes of Health [AI44238]
FX authors thank Lynn Olson for help in preparing the manuscript. This work
was supported in part by a grant from the National Institutes of Health
(AI44238).
NR 39
TC 16
Z9 16
U1 2
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1075
J9 INSECT MOL BIOL
JI Insect Mol. Biol.
PD OCT
PY 2008
VL 17
IS 5
BP 545
EP 552
DI 10.1111/j.1365-2583.2008.00823.x
PG 8
WC Biochemistry & Molecular Biology; Entomology
SC Biochemistry & Molecular Biology; Entomology
GA 349GX
UT WOS:000259270400011
PM 18828840
ER
PT J
AU Gollob, KJ
Antonelli, LRV
Faria, DR
Keesen, TSL
Dutra, WO
AF Gollob, Kenneth J.
Antonelli, Lis R. V.
Faria, Daniela R.
Keesen, Tatjana S. L.
Dutra, Walderez O.
TI Immunoregulatory mechanisms and CD4-CD8-(double negative) T cell
subpopulations in human cutaneous leishmaniasis: A balancing act between
protection and pathology
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article; Proceedings Paper
CT 13th International Congress of Immunology
CY AUG 21-25, 2007
CL Rio de Janeiro, BRAZIL
DE cutaneous leishmaniasis; Cytokines; T lymphocytes; Th1; NK T cells;
double negative T cells
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; MAJOR INFECTION; MUCOSAL LEISHMANIASIS;
VISCERAL LEISHMANIASIS; NKT CELLS; GAMMA; CD4(-)CD8(-); ANTIGEN; MICE;
INTERLEUKIN-10
AB Cellular immune responses directed against protozoan parasites are key for controlling pathogen replication and disease resolution. However, an uncontrolled, or improperly controlled, response can be deleterious to the host in terms of both allowing for the establishment of pathology, as well as less effective establishment of memory responses. Human cutaneous leishmaniasis is a disease caused by the infection with Leishmania spp. following a bite from the sandfly, the natural vector of this disease. Tens of millions worldwide are currently infected with Leishmania and no effective vaccines have been developed to date. In the face of the complexity presented by the interaction between a host (humans) with the parasite, Leishmania, and the fact that this parasite is inoculated by another complex, biologically active, vector, the sandfly, it is clearly important to study the immunoregutatory mechanisms that are induced in humans naturally infected by this parasite if we hope to develop effective vaccines and immunotherapeutic treatments in the future. Our laboratory has focused over the years on the study of the local and systemic Tcell response during the first episode of cutaneous leishmaniasis suffered by individuals before they undergo antimony treatment. The goal of this review is to briefly outline our findings with hopes of putting our most recent studies concerning the dichotomy between alpha/beta TCR and gamma/deplta TCR expressing, CD4-CD8- (double negative-DN) T cells in the context of a balanced immune response against Leishmania and to discuss the implications of these findings toward our understanding of human leishmaniasis. (c) 2008 Elsevier B.V. All rights reserved.
C1 [Gollob, Kenneth J.; Keesen, Tatjana S. L.] Univ Fed Minas Gerais, Dept Biochem Immunol, Inst Biol Sci, ICB, BR-30161970 Belo Horizonte, MG, Brazil.
[Antonelli, Lis R. V.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Faria, Daniela R.; Dutra, Walderez O.] Univ Fed Minas Gerais, Dept Morphol, Inst Biol Sci, BR-30161970 Belo Horizonte, MG, Brazil.
RP Gollob, KJ (reprint author), Univ Fed Minas Gerais, Dept Biochem Immunol, Inst Biol Sci, ICB, Antonio Carlos 6627, BR-30161970 Belo Horizonte, MG, Brazil.
EM kjgollob@gmail.com
RI Gollob, Kenneth/C-1341-2008; Vacinas, Inct/J-9431-2013; DoenAas
Tropicais, Inct/K-2308-2013; Antonelli, Lis/G-2907-2012
OI Gollob, Kenneth/0000-0003-4184-3867;
FU NIAID NIH HHS [R03 AI066253]
NR 43
TC 23
Z9 23
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD OCT
PY 2008
VL 8
IS 10
SI SI
BP 1338
EP 1343
DI 10.1016/j.intimp.2008.03.016
PG 6
WC Immunology; Pharmacology & Pharmacy
SC Immunology; Pharmacology & Pharmacy
GA 350XC
UT WOS:000259385900006
PM 18687296
ER
PT J
AU Ng, D
Hu, N
Hu, Y
Wang, CY
Giffen, C
Tang, ZZ
Han, XY
Yang, HH
Lee, MP
Goldstein, AM
Taylor, PR
AF Ng, David
Hu, Nan
Hu, Ying
Wang, Chaoyu
Giffen, Carol
Tang, Ze-Zhong
Han, Xiao-You
Yang, Howard H.
Lee, Maxwell P.
Goldstein, Alisa M.
Taylor, Philip R.
TI Replication of a genome-wide case-control study of esophageal squamous
cell carcinoma
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE esophageal cancer; replication study; SNP
ID GASTRIC CANCERS; INCIDENT ESOPHAGEAL; SHANXI-PROVINCE; GROWTH-FACTOR;
FAMILY; EXPRESSION; PATHWAYS; GENES; CHINA
AB In a previous pilot case-control study of individuals diagnosed with esophageal squamous cell carcinoma (ESCC) and matched controls from a high-risk area in China, we identified 38 single nucleotide polymorphisms (SNPs) associated with ESCC located in or near one of 33 genes. In our study, we attempted to replicate the results of these 38 gene-related SNPs in a new sample of 300 ESCC cases and 300 matched controls from the same study conducted in Shanxi Province, China. Among 36 evaluable SNPs, 41,were significant in one or more analyses, including SNPs located in EPHB1, PGLYRP2, PIK30 and SLC9A9, although the odds ratios (ORs) for these genotypes were modest. Associations were found with EPHB1/rs1515366 (OR 0.92, 95% CI 0.86-0.99; p = 0.019), PIK3C3/rs52911 (OR 0.93, 95% CI 0.88-0.99; p = 0.02) and PGLYRP2/rs959117 (OR 0.93, 95% CI, 0.86-1.01; p = 0.061) in general linear models (additive mode); and the genotype distribution differed between cases and controls for SLC9A9/rs956062 (p = 0.024). To examine these 4 genes in more detail, 40 HapMap-based tag SNPs from these 4 genes were evaluated in the same subjects and 7 additional SNPs associated with ESCC were identified. Further confirmation of these findings in other populations and other studies are needed to determine if the signals from these SNPs are indirectly associated due to linkage disequilibrium, or are directly related to biologic function and the development of ESCC.
C1 [Ng, David; Hu, Nan; Wang, Chaoyu; Goldstein, Alisa M.; Taylor, Philip R.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Hu, Ying; Yang, Howard H.; Lee, Maxwell P.] NCI, Ctr Canc Res, NIH, DHHS,Lab Populat Genet, Bethesda, MD 20892 USA.
[Giffen, Carol] Informat Management Serv Inc, Silver Spring, MD USA.
[Tang, Ze-Zhong; Han, Xiao-You] Shanxi Canc Hosp, Taiyuan, Shanxi, Peoples R China.
RP Ng, D (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Execut Blvd,Rm 7112, Bethesda, MD 20892 USA.
EM davidng@mail.nih.gov
FU Intramural Research Program of the NIH; National Cancer Institute;
Division of Cancer Epidemiology and Genetics and Center for Cancer
Research
FX Grant sponsors: Intramural Research Program of the NIH, National Cancer
Institute, Division of Cancer Epidemiology and Genetics and Center for
Cancer Research.
NR 27
TC 8
Z9 9
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD OCT 1
PY 2008
VL 123
IS 7
BP 1610
EP 1615
DI 10.1002/ijc.23682
PG 6
WC Oncology
SC Oncology
GA 343YO
UT WOS:000258892500016
PM 18649358
ER
PT J
AU Silverman, DT
Alguacil, J
Rothman, N
Real, FX
Garcia-Closas, M
Cantor, KP
Malats, N
Tardon, A
Serra, C
Garcia-Closas, R
Carrato, A
Lloreta, J
Samanic, C
Dosemeci, M
Kogevinas, M
AF Silverman, Debra T.
Alguacil, Juan
Rothman, Nathaniel
Real, Francisco X.
Garcia-Closas, Montserrat
Cantor, Kenneth P.
Malats, Nuria
Tardon, Adonina
Serra, Consol
Garcia-Closas, Reina
Carrato, Alfredo
Lloreta, Josep
Samanic, Claudine
Dosemeci, Mustafa
Kogevinas, Manolis
TI Does increased urination frequency protect against bladder cancer?
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE urination frequency; smoking; water intake; bladder neoplasms;
epidemiology
ID URINARY-BLADDER; FLUID INTAKE; RISK; CARCINOGEN; ETIOLOGY; EXPOSURE; MEN
AB Experimental studies suggest that increased urination frequency may reduce bladder cancer risk if carcinogens are present in the urine. Only 2 small studies of the effect of increased urination frequency on bladder cancer risk in humans have been conducted with conflicting results. Our purpose was to evaluate the effect of urination frequency on risk of bladder cancer in a large. multicenter case-control study. We analyzed data based on interviews conducted with 884 patients with newly diagnosed, bladder cancer and 996 controls from 1998 to 2001 in Spain. We observed a consistent, inverse trend in risk with increasing night-time voiding frequency in both men (p = 0.0003) and women (p = 0.07); voiding at least 2 times per night was associated with a significant, 40-50% risk reduction. The protective effect of nocturia,vas apparent among study participants with low, moderate and high water consumption. The risk associated with cigarette smoking was reduced by nocturia. Compared with nonsmokers who did not urinate at night, current smokers who did not urinate at night had an OR of 7.0 (95% CI = 4.7-10.2), whereas those who voided at least twice per night had an OR of 3.3 (95% CI = 1.9-5.8) (p value for trend = 0.0005). Our findings suggest a strong protective effect of nocturia on bladder cancer risk, providing evidence in humans that bladder cancer risk is related to the contact time of the urothelium with carcinogens in urine. Increased urination frequency, coupled with possible dilution of the urine from increased water intake, may diminish the effect of urinary carcinogens on bladder cancer risk. (C) 2008 Wiley-Liss, Inc.
C1 [Silverman, Debra T.; Rothman, Nathaniel; Garcia-Closas, Montserrat; Cantor, Kenneth P.; Samanic, Claudine; Dosemeci, Mustafa] NCI, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Alguacil, Juan] Univ Huelva, Dept Environm Biol & Publ Hlth, Huelva, Spain.
[Real, Francisco X.; Malats, Nuria; Kogevinas, Manolis] Inst Municipal Invest Med, E-08003 Barcelona, Spain.
[Real, Francisco X.; Serra, Consol; Lloreta, Josep] Univ Pompeu Fabra, Unite Recerca Salut Laboral, Barcelona, Spain.
[Tardon, Adonina] Univ Oviedo, Dept Med, Inst Oncol, Oviedo, Spain.
[Serra, Consol] Corp Sanitaria Parc Tauli, Epidemiol Unit, Sabadell, Spain.
[Garcia-Closas, Reina] Hosp Univ Canarias, San Cristobal la Laguna, Spain.
[Carrato, Alfredo] Hosp Gen Univ Elche, Elche, Spain.
[Lloreta, Josep] Hosp Mar, Barcelona, Spain.
[Kogevinas, Manolis] Univ Crete, Sch Med, Dept Social Med, Iraklion, Crete, Greece.
[Kogevinas, Manolis] Ctr Res Environm Epidemiol, Barcelona, Spain.
RP Silverman, DT (reprint author), NCI, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Room 8012, Bethesda, MD 20892 USA.
EM silvermd@mail.nih.gov
RI Serra, C/E-6879-2014; Lloreta, J/I-2112-2014; Garcia-Closas, Montserrat
/F-3871-2015; Malats, Nuria/H-7041-2015; Kogevinas, Manolis/C-3918-2017;
Real, Francisco X/H-5275-2015
OI Serra, C/0000-0001-8337-8356; Lloreta, J/0000-0003-1644-9470;
Garcia-Closas, Montserrat /0000-0003-1033-2650; Malats,
Nuria/0000-0003-2538-3784; Real, Francisco X/0000-0001-9501-498X
FU Intramural Research Program of the NIH; National Cancer Institute.
Division of Cancer Epidemiology and Genetics [N02-CP-11015]
FX Grant sponsor: Intramural Research Program of the NIH. National Cancer
Institute. Division of Cancer Epidemiology and Genetics; Grant number:
N02-CP-11015.
NR 20
TC 18
Z9 19
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD OCT 1
PY 2008
VL 123
IS 7
BP 1644
EP 1648
DI 10.1002/ijc.23572
PG 5
WC Oncology
SC Oncology
GA 343YO
UT WOS:000258892500021
PM 18623081
ER
PT J
AU Erez, A
Chaussepied, M
Castiel, A
Colaizzo-Anas, T
Aplan, PD
Ginsberg, D
Izraeli, S
AF Erez, Ayelet
Chaussepied, Marie
Castiel, Asher
Colaizzo-Anas, Tina
Aplan, Peter D.
Ginsberg, Doron
Izraeli, Shai
TI The mitotic checkpoint gene, SIL is regulated by E2F1
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE SIL; E2F; mitosis
ID DNA-REPLICATION; EXPRESSION; PROLIFERATION; APOPTOSIS; CLONING
AB The SIL gene expression is increased in multiple cancers and correlates with the expression of mitotic spindle checkpoint genes and with increased metastatic potential. SIL regulates mitotic entry, organization of the mitotic spindle and cell survival. The E2F transcription factors regulate cell cycle progression by controlling the expression of genes mediating the G1/S transition. More recently, E2F has been shown to regulate mitotic spindle checkpoint genes as well. As SIL expression correlates with mitotic checkpoint genes, we hypothesized that SIL is regulated by E2F. We mined raw data of published experiments and performed new experiments by modification of E2F expression in cell Ines, reporter assays and chromatin immunoprecipitation. Ectopic expression or endogenous activation of E2F induced the expression of SIL, while knockdown of E2F by shRNA, downregulated SIL expression. E2F activated SIL promoter by reporter assay and bound to SIL promoter in vivo. Taken together these data demonstrate that SIL is regulated by E2F. As SIL is essential for mitotic entry, E2F may regulate G2/M transition through the induction of SIL. Furthermore, as silencing of SIL cause apoptosis in cancer cells, these finding may have therapeutic relevance in tumors with constitutive activation of E2F.
C1 [Izraeli, Shai] Chaim Sheba Med Ctr, Dept Pediat Hematooncol, IL-52621 Tel Hashomer, Israel.
[Erez, Ayelet; Castiel, Asher; Izraeli, Shai] Sheba Canc Res Ctr, Tel Hashomer, Israel.
[Erez, Ayelet; Castiel, Asher; Izraeli, Shai] Tel Aviv Univ, Sackler Fac Med, Tel Aviv, Israel.
[Chaussepied, Marie] Univ Paris 05, Inst Cochin, CNRS, UMR 8104, Paris, France.
[Chaussepied, Marie] INSERM, U567, Paris, France.
[Colaizzo-Anas, Tina] SUNY Buffalo, Dietet & Nutr, Buffalo, NY USA.
[Aplan, Peter D.] NCI, NIH, Genet Branch, Bethesda, MD 20892 USA.
[Ginsberg, Doron] Bar Ilan Univ, Mina & Everard Goodman Fac Life Sci, Ramat Gan, Israel.
RP Izraeli, S (reprint author), Chaim Sheba Med Ctr, Dept Pediat Hematooncol, IL-52621 Tel Hashomer, Israel.
EM sizraeli@sheba.health.gov.il
RI Aplan, Peter/K-9064-2016
FU Israel Science Foundation; Israel Cancer Research Foundation; US-Israel
Binational Science Foundation; NIH; NCI
FX Grant sponsors: Israel Science Foundation; Israel Cancer Research
Foundation; US-Israel Binational Science Foundation; NIH, NCI.
NR 20
TC 11
Z9 11
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD OCT 1
PY 2008
VL 123
IS 7
BP 1721
EP 1725
DI 10.1002/ijc.23665
PG 5
WC Oncology
SC Oncology
GA 343YO
UT WOS:000258892500032
PM 18649360
ER
PT J
AU Wu, GG
Tang, QM
Shen, WD
Liao, Y
Li, HC
Zhao, TM
AF Wu, Guo-guang
Tang, Qiu-ming
Shen, Wei-dong
Liao, Yan
Li, Heng-cong
Zhao, Tong-mao
TI DNA sequencing-based typing of HPA-1 to HPA-17w systems
SO INTERNATIONAL JOURNAL OF HEMATOLOGY
LA English
DT Article
DE human platelet antigens; HPA genotyping; sequencing-based HPA typing
ID ANTIGENS
AB Although several DNA-based human platelet antigens (HPA) typing techniques, such as PCR-SSP and PCR-SSO, have been established, the typing errors and the lack of interlaboratory reproducibility are still the issues of concerns. In the present study, polymerase chain reaction primers were designed for identification of all the phenotypically different HPA-1 to HPA-17w types by sequencing-based typing (SBT) method using genomic DNA samples. No discrepancies were observed between PCR-SSP typing and SBT typing in typing a panel of HPA-typed platelet donors that included all common HPA types and the rare HPA-1b, 2b, 3b, and 6bw homozygous donors.
C1 [Wu, Guo-guang; Tang, Qiu-ming; Shen, Wei-dong; Liao, Yan; Li, Heng-cong] Nan Ning Inst Transfus Med, Nanning 530003, Peoples R China.
[Zhao, Tong-mao] NIH, Bethesda, MD 20892 USA.
RP Wu, GG (reprint author), Nan Ning Inst Transfus Med, 18 Keyuan Ave, Nanning 530003, Peoples R China.
EM guangwu@szonline.net
NR 6
TC 5
Z9 12
U1 0
U2 0
PU SPRINGER TOKYO
PI TOKYO
PA 1-11-11 KUDAN-KITA, CHIYODA-KU, TOKYO, 102-0073, JAPAN
SN 0925-5710
J9 INT J HEMATOL
JI Int. J. Hematol.
PD OCT
PY 2008
VL 88
IS 3
BP 268
EP 271
DI 10.1007/s12185-008-0164-6
PG 4
WC Hematology
SC Hematology
GA 358IK
UT WOS:000259910200004
PM 18802675
ER
PT J
AU Chen, NY
Guimbretiere, F
Lockenhoff, CE
AF Chen, Nicholas Y.
Guimbretiere, Francois
Loeckenhoff, Corinna E.
TI Relative role of merging and two-handed operation on command selection
speed
SO INTERNATIONAL JOURNAL OF HUMAN-COMPUTER STUDIES
LA English
DT Article
DE two-handed input; GUIs; toolglass; palette; marking menu; control menu;
merging; human factors; experimentation
ID MENUS
AB This paper examines the influence of two interface characteristics on command selection speed: the integration of command selection with direct manipulation (merging), and two-handed operation. We compared four interaction techniques representing combinations of these characteristics (Marking Menu, Two-handed Tool Palette, Toolglass, and Control Menu). Results suggest that the one-handed techniques selected for the present study produced a speed advantage over two-handed techniques, whereas the influence of merging was task dependent. A follow-up study examining Bimanual Marking Menu suggests that the performance of two-handed techniques may be reduced due to a split in visual attention required for certain techniques. Taken together, these findings have important implications for the design of command selection mechanisms for pen-based interfaces. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Chen, Nicholas Y.; Guimbretiere, Francois] Univ Maryland, College Pk, MD 20742 USA.
[Loeckenhoff, Corinna E.] NIA, Bethesda, MD 20892 USA.
RP Chen, NY (reprint author), Univ Maryland, 3252 AV Williams Bldg, College Pk, MD 20742 USA.
EM nchen@cs.umd.edu; LoeckenhoffC@grc.nia.nih.gov
OI Loeckenhoff, Corinna/0000-0003-1605-1323
FU NSF [IIS-0414699]; Microsoft Research Center for Interaction Design and
Visualization at the University of Maryland; National Institute on Aging
intramural research program
FX This work was supported in part by NSF Grant IIS-0414699 and by the
Microsoft Research Center for Interaction Design and Visualization at
the University of Maryland. This project was also supported in part by
the National Institute on Aging intramural research program. We would
like to thank Mary Czerwinski for supporting early pilot studies related
to this work and Paul Kabbash for graciously providing us with the
dataset he used in his experiment.
NR 24
TC 1
Z9 1
U1 1
U2 6
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1071-5819
J9 INT J HUM-COMPUT ST
JI Int. J. Hum.-Comput. Stud.
PD OCT
PY 2008
VL 66
IS 10
BP 729
EP 740
DI 10.1016/j.ijhcs.2008.06.003
PG 12
WC Computer Science, Cybernetics; Ergonomics; Psychology, Multidisciplinary
SC Computer Science; Engineering; Psychology
GA 355KF
UT WOS:000259707100003
ER
PT J
AU Yan, Y
Xiong, Z
Zhang, S
Song, J
Huang, Y
Thornton, AM
Wang, H
Yang, XF
AF Yan, Y.
Xiong, Z.
Zhang, S.
Song, J.
Huang, Y.
Thornton, A. M.
Wang, H.
Yang, X-F.
TI CD25(high) T CELLS WITH A PROLONGED SURVIVAL INHIBIT DEVELOPMENT OF
DIABETES
SO INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY
LA English
DT Article
DE regulatory T cells; anti-apoptosis; TCTP; autoimmune diseases; diabetes
ID CD28 COSTIMULATION; FOXP3 EXPRESSION; TRANSGENIC MICE; CUTTING EDGE;
CD4(+)CD25(+); INTERLEUKIN-2; STREPTOZOTOCIN; ACTIVATION; APOPTOSIS;
DEATH
AB The goal of this study is to examine a novel hypothesis that the progression of diabetes is partially due to the weakened survival of CD25(high) T cells, and prolonging survival of CD25(high) T cells inhibits the development of diabetes. Since CD28 co-stimulation is essential for the survival of CD4+CD25(high) T cells, we determined whether CD28-upregulated translationally controlled tumor protein (TCTP) prolongs the survival of CD4+CD25(high) regulatory T cells (Tregs) by a transgenic approach. The TCTP transgene prevents Tregs from undergoing apoptosis induced by interleukin-2 withdrawal-, dexamethasone-, cyclophosphamide-, and anti-Fas treatment in vitro. In addition, transgenic Tregs express higher levels of FOXP3 than wild-type counterparts and maintain suppressive activity, suggesting that TCTP promotes Tregs escape from thymic negative selection, and that prolonged survival does not attenuate Treg suppression. Moreover, TCTP transgenic Tregs inhibit the development of autoimmune diabetes due to increased survival of suppressive Tregs and decreased expression of pancreatic TNF-alpha. Promoting the survival of CD25(high) T cells leads to prolonged survival of Tregs but not activated CD25+ non-Treg T cells. Thus, we propose a new model of "two phase survival" for Tregs. Our results suggest that modulation of Treg survival can be developed as a new therapy for autoimmune diseases.
C1 [Yan, Y.; Xiong, Z.; Zhang, S.; Song, J.; Wang, H.; Yang, X-F.] Temple Univ, Sch Med, Dept Pharmacol, Philadelphia, PA 19140 USA.
[Yan, Y.; Xiong, Z.; Zhang, S.; Song, J.; Wang, H.; Yang, X-F.] Temple Univ, Sch Med, Cardiovasc Res Ctr, Philadelphia, PA 19140 USA.
[Huang, Y.] Temple Univ, Sch Med, Dept Pathol, Philadelphia, PA 19140 USA.
[Thornton, A. M.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Yang, XF (reprint author), Temple Univ, Sch Med, Dept Pharmacol, 3420 N Broad St,MRB 325, Philadelphia, PA 19140 USA.
EM xfyang@temple.edu
FU NIH [1054514]
FX We are grateful to Drs. D. Huston, S.H. Han, and T.H. Tan at Baylor
College of Medicine, P. Relchenbach and M. Nabholz at Swiss Cancer
Center, B. Ashby and N. Dun at Temple University for assistance. This
work was partially supported by NIH grant A 1054514.
NR 35
TC 10
Z9 11
U1 1
U2 2
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0394-6320
J9 INT J IMMUNOPATH PH
JI Int. J. Immunopathol. Pharmacol.
PD OCT-DEC
PY 2008
VL 21
IS 4
BP 767
EP 780
PG 14
WC Immunology; Pathology; Pharmacology & Pharmacy
SC Immunology; Pathology; Pharmacology & Pharmacy
GA 401ST
UT WOS:000262963100001
PM 19144262
ER
PT J
AU Yadav, H
Yadav, M
Jain, S
Bhardwaj, A
Singh, V
Parkash, O
Marotta, F
AF Yadav, H.
Yadav, M.
Jain, S.
Bhardwaj, A.
Singh, V.
Parkash, O.
Marotta, F.
TI ANTIMICROBIAL PROPERTY OF A HERBAL PREPARATION CONTAINING DALBERGIA
SISSOO AND DATURA STRAMONIUM WITH COW URINE AGAINST PATHOGENIC BACTERIA
SO INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY
LA English
DT Article
DE Dalbergia sissoo; Datura stramonium; S. aureus; E. coli; Klebsiela; P.
aeruginosa; Klebsiella pneumoniae; cow urine; antibiotics
ID MEDICINAL-PLANTS; INFECTIONS; RESISTANCE; INDIA
AB In this study, a herbal preparation containing Dalbergia sissoo and Datura stramoium with cow urine (DSDS), was evaluated for its antibacterial potential against pathogenic strains of gram-positive (Staphylococcus aureus and Streptococcus pneumoniae) and gram-negative (Escherichia coli, Pseudomonas aeruginosa and Klebsiella pneumoniae) bacteria. Antibacterial activity was compared to standard antibiotic drugs i.e. Chloramphenicol (30 mcg), Ampicillin (10 mcg), Nalidixic acid (10 mcg) and Rifampicin (30 mcg). Cow urine extract was found to be most active against both gram-positive as well as gram-negative bacteria. Clinical isolate of S. aureus showed higher sensitivity towards cow urine extract of DSDS than standard strains, and inhibited growth on most regulatory levels such as inhibition of protein, DNA, RNA and peptidoglycan synthesis. The results of the present study shows that the cow urine extract of DSDS may be used as a potent antiseptic preparation for prevention and treatment of chronic bacterial infections.
C1 [Yadav, H.] Subhash Chandra Bose Coll Profess Studies, Gwalior, India.
[Yadav, M.] Jiwaji Univ, SOS Chem, Gwalior, India.
[Jain, S.] Univ Illinois, Dept Food Sci & Human Nutr, Urbana, IL USA.
[Bhardwaj, A.] Meerut Inst Engn & Technol, Meerut, UP, India.
[Singh, V.] Barkatullah Univ, Dept Microbiol, Bhopal 462026, MP, India.
[Parkash, O.] Natl JALMA Inst Leprosy & Other Mycobacterial Dis, Agra, UP, India.
[Marotta, F.] GAIA Fdn, Nutraceut Nutragenom Unit, Milan, Italy.
RP Yadav, H (reprint author), NIDDK, Clin Res Ctr, NIH, Bethesda, MD 20892 USA.
EM yadavhariom@gmail.com
NR 29
TC 7
Z9 8
U1 1
U2 2
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0394-6320
J9 INT J IMMUNOPATH PH
JI Int. J. Immunopathol. Pharmacol.
PD OCT-DEC
PY 2008
VL 21
IS 4
BP 1013
EP 1020
PG 8
WC Immunology; Pathology; Pharmacology & Pharmacy
SC Immunology; Pathology; Pharmacology & Pharmacy
GA 401ST
UT WOS:000262963100027
PM 19144288
ER
PT J
AU Venditti, EM
Bray, GA
Carrion-Petersen, ML
Delahanty, LM
Edelstein, SL
Hamman, RF
Hoskin, MA
Knowler, WC
Ma, Y
AF Venditti, E. M.
Bray, G. A.
Carrion-Petersen, M. L.
Delahanty, L. M.
Edelstein, S. L.
Hamman, R. F.
Hoskin, M. A.
Knowler, W. C.
Ma, Y.
CA Diabet Prevention Program Res Grp
TI First versus repeat treatment with a lifestyle intervention program:
attendance and weight loss outcomes
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Article
DE behavior modification; metformin; weight loss; maintenance
ID MAINTENANCE; PREVENTION; REDUCTION
AB Objective: Following unblinding of the Diabetes Prevention Program (DPP) results, a 16-session lifestyle intervention program was offered to all study participants, including those who had initially been randomized to lifestyle treatment. This study compares the effects of the lifestyle program between participants who had previous exposure and those who had not.
Design: A 16-session behavioral intervention was conducted in groups at each of the 27 DPP sites during a transitional (bridge) period from the DPP trial to the DPP Outcomes Study (DPPOS). Session participation for this 6-month behavioral weight loss program was confirmed by originally randomized treatment groups.
Subjects and measurements: Independently assessed weight measurements were available within a 7-month period before and after the program for 2808 ethnically diverse participants.
Results: Participants from the lifestyle group in the DPP were the least likely to attend a repeat offering of a 16-session behavioral weight loss program conducted in groups. Weight loss during the transitional lifestyle program was strongly related to the duration of attendance in the three groups that were participating in the program for the first time (metformin, placebo and troglitazone), but not related to amount of earlier weight loss.
Conclusion: Individuals who were naive to the behavioral program lost a greater amount of weight and this was strongly related to their degree of participation. A second exposure to a behavioral weight loss program resulted in unsatisfactory low attendance rates and weight loss. International Journal of Obesity (2008) 32, 1537-1544; doi: 10.1038/ijo.2008.134; published online 19 August 2008
C1 [Venditti, E. M.] Psychiat Inst & Clin, Pittsburgh, PA USA.
[Bray, G. A.] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Carrion-Petersen, M. L.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Delahanty, L. M.] Massachusetts Gen Hosp, Diabet Res Ctr, Boston, MA 02114 USA.
[Hamman, R. F.] Univ Colorado, Hlth Sci Ctr, Denver, CO USA.
[Hoskin, M. A.; Knowler, W. C.] NIDDK, Phoenix, AZ USA.
RP Venditti, EM (reprint author), George Washington Univ, Diabet Prevent Program Coordinating Ctr, Ctr Biostat, 6110 Execut Blvd,Suite 750, Rockville, MD 20852 USA.
EM dppmail@biostat.bsc.gwu.edu
RI Uwaifo, Gabriel/M-2361-2016
OI Uwaifo, Gabriel/0000-0002-6962-9304
FU NIH [U01DK]
FX Supported by NIH U01DK.
NR 13
TC 35
Z9 35
U1 1
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0307-0565
J9 INT J OBESITY
JI Int. J. Obes.
PD OCT
PY 2008
VL 32
IS 10
BP 1537
EP 1544
DI 10.1038/ijo.2008.134
PG 8
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 358PE
UT WOS:000259929200012
PM 18711387
ER
PT J
AU Rao, CV
Joseph, S
Gao, L
Patlolla, JMR
Choi, CI
Kopelovich, L
Steele, VE
Rigas, B
AF Rao, Chinthalapally V.
Joseph, Stancy
Gao, Li
Patlolla, Jagan M. R.
Choi, Chang-In
Kopelovich, Levy
Steele, Vernon E.
Rigas, Basil
TI Pharmacokinetic and pharmacodynamic study of NO-donating aspirin in F344
rats
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE prostaglandin E-2; thromboxane B-2; nitric oxide-donating aspirin;
cancer; chemoprevention
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; NITRIC-OXIDE RELEASE; IN-VITRO
METABOLISM; COLON-CANCER; NITROASPIRIN NCX-4016; CHEMOPREVENTION;
TARGETS; GROWTH; LC
AB Nitric oxide-donating aspirin (NO-ASA) represents class of promising chernopreventive NO-NSAIDs. NO-ASA combines the beneficial effects of ASA and the gut-sparing effect of the NO moiety. There is, however, limited information on its pharmacokinetic and pharmacodynamic effects in vivo. Herein, experiments were designed to identify the optimal dose, the effective route of administration, and targeted markers in plasma and colonic tissues of male F344 rats. Seven weeks old male F344 rats were randomized into 9 groups (16/group) and fed the control diet. At eight weeks of age, groups 2-5 were each administered one of four different doses of NO-ASA by gavage (33, 66, 132 and 264 mg/kg) and each of groups 6-9 were fed diets containing NO-ASA (35, 700, 1,400 and 2,800 ppm) for two weeks. Rats were sacrificed 2 and 10 h after completion of the two weeks of treatment with NO-ASA and plasma and colonic mucosa were collected and analyzed for NO-ASA, its metabolites, and PGE(2) and TXB2 levels. Our results indicate that NO-ASA is rapidly metabolized, predominantly to salicylic acid; no intact NO-ASA was detected in plasma. Compared to diet-fed NO-ASA. gavaging generated much higher salicylic acid levels over a wide range of doses and a relatively broad time period (10 h). Regardless of its route of administration, NO-ASA lowered the levels of PGE(2) in colonic tissues and plasma, as well as TxB(2) in plasma in a dose- and time-dependent manner. These findings may have practical utility for the administration of NO-ASA to humans.
C1 [Joseph, Stancy; Gao, Li; Rigas, Basil] SUNY Stony Brook, Canc Prevent Div, Stony Brook, NY 11794 USA.
[Rao, Chinthalapally V.; Patlolla, Jagan M. R.; Choi, Chang-In] Univ Oklahoma, Hlth Sci Ctr, Dept Med, Hematol Oncol Sect, Oklahoma City, OK 73104 USA.
[Kopelovich, Levy; Steele, Vernon E.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Rigas, B (reprint author), SUNY Stony Brook, Canc Prevent Div, Stony Brook, NY 11794 USA.
EM basil.rigas@stonybrook.edu
RI Chinthalapally, Rao/B-3633-2010
FU NIH [N01-CN-53300, 2R01 CA92423]
FX Financial support: NIH Contract/Grant: N01-CN-53300; 2R01 CA92423.
NR 15
TC 3
Z9 3
U1 0
U2 5
PU PROFESSOR D A SPANDIDOS
PI ATHENS
PA 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE
SN 1019-6439
J9 INT J ONCOL
JI Int. J. Oncol.
PD OCT
PY 2008
VL 33
IS 4
BP 799
EP 805
DI 10.3892/ijo_00000067
PG 7
WC Oncology
SC Oncology
GA 356HN
UT WOS:000259769400020
PM 18813794
ER
PT J
AU Ngo, TD
Laeyendecker, O
Li, C
Tai, H
Cui, M
Lai, S
Quinn, TC
AF Ngo, T. D.
Laeyendecker, O.
Li, C.
Tai, H.
Cui, M.
Lai, S.
Quinn, T. C.
TI Herpes simplex virus type 2 infection among commercial sex workers in
Kunming, Yunnan Province, China
SO INTERNATIONAL JOURNAL OF STD & AIDS
LA English
DT Article
DE commercial sex workers; herpes simplex virus type 2; human
immunodeficiency virus; hepatitis C virus; China
ID RISK; TRANSMISSION
AB A cross-sectional survey was conducted to determine the sociodemographic correlates of herpes simplex virus type 2 (HSV-2) infection among male and female commercial sex workers in Kunming, Yunnan Province of China. HSV-2 prevalence was 33.0%, human immunodeficiency virus (HIV) infection was 2.4% and hepatitis C virus (HCV) infection was 6.8%. Subjects who were positive for HSV-2 had a significantly higher prevalence of HIV infection (5.5% versus 0.9%, P = 0.002; odds ratio (OR]: 6.4, P = 0.006) and HCV infection (118.7% versus 2.4%, P < 0.001; OR: 7.6, P < 0.001) compared with HSV-2-negative individuals. Risk factors that increased the odds of HSV-2 infection were HIV infection, HCV infection, being female, and having a steady sex partner within the last six months (P <= 0.01). In a multivariate analysis, being female (OR: 6.6, P < 0.001), having HCV infection (OR: 5.9, P < 0.001) and having a sex partner within the last six months (OR: 2.2, P < 0.05) showed greater odds of being infected with HSV-2. A strong relationship was found between HSV-2, HIV and HCV infections.
C1 [Ngo, T. D.; Laeyendecker, O.; Quinn, T. C.] NIH, NIAID, Bethesda, MD 20892 USA.
[Laeyendecker, O.; Quinn, T. C.] Johns Hopkins Univ Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Li, C.] Yunnan Univ, Comprehens Drug Res Ctr, Kunming, Peoples R China.
[Tai, H.] Yunnan Prov Hosp, Dept Lab Med, Kunming, Peoples R China.
[Cui, M.] Kunming Ctr Dis Control, Kunming, Peoples R China.
[Lai, S.] Johns Hopkins Univ Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
RP Quinn, TC (reprint author), Johns Hopkins Univ Sch Med, Dept Infect Dis, 1721 E Madison St,Ross Bldg,Room 1159, Baltimore, MD 21205 USA.
EM tquinn@jhmi.edu
RI Laeyendecker, Oliver/B-9331-2009;
OI Laeyendecker, Oliver/0000-0002-6429-4760
FU Division of Intramural Research; MAID; NIH
FX The authors wish to thank Dr Rhoda Ashley Morrow at the University of
Washington, Dr Andrew Redd at the NIH and Dr Ken Nelson and Dr Anne
Rompalo at file Johns Hopkins University for their critical discussions
and reading of this manuscript.; This research was supported by the
Division of Intramural Research, MAID, NIH.
NR 19
TC 17
Z9 21
U1 0
U2 1
PU ROYAL SOC MEDICINE PRESS LTD
PI LONDON
PA 1 WIMPOLE STREET, LONDON W1G 0AE, ENGLAND
SN 0956-4624
J9 INT J STD AIDS
JI Int. J. STD AIDS
PD OCT
PY 2008
VL 19
IS 10
BP 694
EP 697
DI 10.1258/ijsa.2008.008072
PG 4
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 367VF
UT WOS:000260580000010
PM 18824623
ER
PT J
AU Forooghian, F
Cukras, C
Meyerle, CB
Chew, EY
Wong, WT
AF Forooghian, Farzin
Cukras, Catherine
Meyerle, Catherine B.
Chew, Emily Y.
Wong, Wai T.
TI Evaluation of time domain and spectral domain optical coherence
tomography in the measurement of diabetic macular edema
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID RETINAL THICKNESS; REPRODUCIBILITY; DEGENERATION; REPEATABILITY;
DIAGNOSIS; DISEASE; HOLES
AB PURPOSE. To evaluate macular thickness and volume measurements and their intrasession repeatability in two optical coherence tomography (OCT) systems: the Stratus OCT, a time domain system, and the Cirrus HD-OCT, a spectral domain system (both by Carl Zeiss Meditec, Inc., Dublin, CA), in the context of diabetic macular edema (DME).
METHODS. Thirty-three eyes of 33 diabetic patients with clinically significant macular edema (CSME) were scanned in a single session by a single operator on both OCT systems. Macular thickness measurements of nine standard macular sub-fields and total macular volume were obtained and analyzed. Bland-Altman plots were constructed to assess agreement in macular measurements. Intraclass correlation coefficients (ICCs), coefficients of repeatability (CRW), and coefficients of variation (CVW) were used to assess intrasession repeatability.
RESULTS. Macular thickness in nine retinal subfields and macular volume were significantly higher in the Cirrus HD-OCT system compared with the Stratus OCT system. Subfield thickness and total volume measurements, respectively, were 30 to 55 mu m and 3.2 mm(3) greater for the Cirrus HD-OCT system compared with the Stratus OCT system. Both Stratus OCT and Cirrus HD-OCT systems demonstrated high intrasession repeatability, with overlapping ranges for CRW, CVW, and ICC. Repeatability measures (CRW and CVW) differed significantly between systems in only one of nine subfields (outer temporal subfield).
CONCLUSIONS. Absolute measures of macular thickness and volume in patients with DME differed significantly in magnitude between the Stratus OCT and Cirrus HD-OCT systems. However, both OCT systems demonstrated high intrasessional repeatability. Although the two systems may not be used interchangeably, they appear equally reliable in generating macular measurements for clinical practice and research.
C1 [Wong, Wai T.] NEI, Off Sci Director, NIH, Bethesda, MD 20892 USA.
[Forooghian, Farzin; Cukras, Catherine; Meyerle, Catherine B.; Chew, Emily Y.] NEI, Div Epidemiol & Clin Res, NIH, Bethesda, MD 20892 USA.
RP Wong, WT (reprint author), NEI, Off Sci Director, NIH, 7 Mem Dr,Bldg 7,Room 217, Bethesda, MD 20892 USA.
EM wongw@nei.nih.gov
RI Wong, Wai/B-6118-2017
OI Wong, Wai/0000-0003-0681-4016
FU National Eye Institute Intramural Research Program
FX Supported by the National Eye Institute Intramural Research Program.
NR 17
TC 118
Z9 120
U1 2
U2 3
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
EI 1552-5783
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD OCT
PY 2008
VL 49
IS 10
BP 4290
EP 4296
DI 10.1167/iovs.08-2113
PG 7
WC Ophthalmology
SC Ophthalmology
GA 355IZ
UT WOS:000259703900011
PM 18515567
ER
PT J
AU Cheung, N
Klein, R
Wang, JJ
Cotch, MF
Islam, AFM
Klein, BEK
Cushman, M
Wong, TY
AF Cheung, Ning
Klein, Ronald
Wang, Jie Jin
Cotch, Mary Frances
Islam, Amirul F. M.
Klein, Barbara E. K.
Cushman, Mary
Wong, Tien Yin
TI Traditional and novel cardiovascular risk factors for retinal vein
occlusion: The multiethnic study of atherosclerosis
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID BLUE MOUNTAINS EYE; BEAVER DAM EYE; VENOUS THROMBOSIS; VASCULAR CALIBER;
DISEASE; HOMOCYSTEINE; COMMUNITIES; PREVALENCE; ABNORMALITIES;
INFLAMMATION
AB PURPOSE. To describe the prevalence of retinal vein occlusion (RVO) and its association with cardiovascular, inflammatory, and hematologic risk factors in a multiethnic cohort.
METHODS. This was a population-based, cross-sectional study of 6147 participants (whites, blacks, Hispanics, Chinese) from six U. S. communities. RVO was defined from retinal photographs taken from both eyes according to a standardized protocol. Risk factors were assessed from interviews, examinations, and laboratory and radiologic investigations.
RESULTS. The prevalence of RVO was 1.1% (0.9% for branch RVO and 0.2% for central RVO) and was similar across different ethnic groups: 0.9% in whites, 1.2% in blacks, 1.2% in Hispanics, and 1.1% in Chinese (P = 0.76). Independent risk factors associated with RVO were hypertension (odds ratio [OR], 2.06; 95% confidence interval [CI], 1.18-3.59), older age (OR, 1.34; 95% CI, 1.00-1.81, per decade increase), less education (OR, 4.08; 95% CI, 2.20-7.54), hypertriglyceridemia (OR, 1.98; 95% CI, 1.10-3.56), renal dysfunction (OR, 1.85; 95% CI, 1.01-3.39), and the presence of retinal arteriovenous nicking (OR, 4.01; 95% CI, 2.06-7.81) and focal arteriolar narrowing (OR, 4.38; 95% CI, 1.44-13.34). RVO was not significantly associated with direct measures of subclinical atherosclerosis (e. g., carotid intima media thickness and coronary artery calcium scores) or markers of inflammation (e. g., C reactive protein, interleukin-6) and endothelial dysfunction (e. g., soluble intercellular adhesion molecule-1) or coagulation (e. g., D-dimer).
CONCLUSIONS. The prevalence of RVO is similar across different racial/ethnic groups. In the general population, RVO is associated with hypertension, dyslipidemia, and renal dysfunction, but not with atherosclerotic disease, systemic inflammation, and hematologic abnormalities.
C1 [Cheung, Ning; Wang, Jie Jin; Islam, Amirul F. M.; Wong, Tien Yin] Univ Melbourne, Ctr Eye Res Australia, Royal Victorian Eye & Ear Hosp, Melbourne, Vic 3002, Australia.
[Klein, Ronald; Klein, Barbara E. K.] Univ Wisconsin, Dept Ophthalmol & Visual Sci, Sch Med & Publ Hlth, Madison, WI USA.
[Cotch, Mary Frances] NEI, Div Epidemiol & Clin Res, NIH, Bethesda, MD 20892 USA.
[Cushman, Mary] Univ Vermont, Dept Med, Burlington, VT USA.
[Cushman, Mary] Univ Vermont, Dept Pathol, Burlington, VT 05405 USA.
[Wong, Tien Yin] Natl Univ Singapore, Singapore Eye Res Inst, Yong Loo Lin Sch Med, Singapore 117548, Singapore.
RP Wong, TY (reprint author), Univ Melbourne, Ctr Eye Res Australia, 32 Gisborne St, Melbourne, Vic 3002, Australia.
EM twong@unimelb.edu.au
RI Cheung, Ning Danny/F-2043-2013; Wang, Jie Jin/P-1499-2014;
OI Wang, Jie Jin/0000-0001-9491-4898; Cotch, Mary
Frances/0000-0002-2046-4350; Klein, Ronald/0000-0002-4428-6237
FU Intramural NIH HHS [Z01 EY000403-06, Z01 EY000403-07, Z99 EY999999, ZIA
EY000403-08, ZIA EY000403-09, ZIA EY000403-10]; NEI NIH HHS [Z01
EY000403, Z01EY000403]; NHLBI NIH HHS [R01 HL069979-03, HL69979-03,
N01-HC-95159, N01-HC-95165, N01-HC-95169, N01HC95159, N01HC95165,
N01HC95169, R01 HL069979]
NR 35
TC 66
Z9 66
U1 0
U2 2
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD OCT
PY 2008
VL 49
IS 10
BP 4297
EP 4302
DI 10.1167/iovs.08-1826
PG 6
WC Ophthalmology
SC Ophthalmology
GA 355IZ
UT WOS:000259703900012
PM 18539932
ER
PT J
AU Salomao, SR
Cinoto, RW
Berezovsky, A
Mendieta, L
Nakanami, CR
Lipener, C
Munoz, ED
Ejzenbaum, F
Belfort, R
Pokharel, GP
Ellwein, LB
AF Salomao, Solange R.
Cinoto, Rafael W.
Berezovsky, Adriana
Mendieta, Luana
Nakanami, Celia R.
Lipener, Cesar
Munoz, Emilio de Haro
Ejzenbaum, Fabio
Belfort, Rubens, Jr.
Pokharel, Gopal P.
Ellwein, Leon B.
TI Prevalence and causes of visual impairment in low middle income school
children in Sao Paulo, Brazil
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the
Association-for-Research-in-Vision-and-Ophthalmology
CY MAY 06-10, 2007
CL Ft Lauderdale, FL
SP Assoc Res Vis & Ophthalmol
ID REFRACTIVE ERROR; SOUTHERN CHINA; POPULATION; DISTRICT; MYOPIA
AB PURPOSE. Assess prevalence and causes of vision impairment among low-middle income school children in Sao Paulo.
METHODS. Cluster sampling was used to obtain a random sample of children ages 11 to 14 years from public schools (grades 5-8) in three districts from June to November 2005. The examination included visual acuity testing, ocular motility, and examination of the external eye, anterior segment, and media. Cycloplegic refraction and fundus examination were performed in children with uncorrected visual acuity 20/40 or worse in either eye. A principal cause of visual impairment was determined for eyes with uncorrected visual acuity of 20/40 or worse.
RESULTS. A total of 2825 children were enumerated and 2441 (86.4%) were examined. The prevalence of uncorrected, presenting, and best-corrected visual acuity 20/40 or worse in the better eye was 4.82%, 2.67%, and 0.41%, respectively. Spectacles were used by 144 (5.9%) children. Refractive error was a cause in 76.8% of children with visual impairment in one or both eyes; amblyopia, 11.4%; retinal disorders, 5.9%; other causes, 2.7%; and unexplained causes, 7.7%. Myopic visual impairment (spherical equivalent -0.50 D in one or both eyes) was not associated with age or grade level, but female sex was marginally significant (P = 0.070). Hyperopic visual impairment (+2.00 D or more) was not associated with age, grade level, or sex.
CONCLUSIONS. The prevalence of reduced vision in low-middle income urban Sao Paulo school children was low, most of it because of uncorrected refractive error. Cost-effective strategies are needed to address this easily treated cause of vision impairment.
C1 [Salomao, Solange R.; Cinoto, Rafael W.; Berezovsky, Adriana; Mendieta, Luana; Nakanami, Celia R.; Lipener, Cesar; Munoz, Emilio de Haro; Ejzenbaum, Fabio; Belfort, Rubens, Jr.] Univ Fed Sao Paulo, Dept Ophthalmol, Vis Inst, BR-04023062 Sao Paulo, Brazil.
[Pokharel, Gopal P.] Nepal Netra Jyoti Sangh, Kathmandu, Nepal.
[Ellwein, Leon B.] NEI, NIH, Bethesda, MD 20892 USA.
RP Salomao, SR (reprint author), Univ Fed Sao Paulo, Dept Ophthalmol, Vis Inst, Rua Botucatu 822, BR-04023062 Sao Paulo, Brazil.
EM ssalomao@oftalmo.epm.br
RI Salomao, Solange/G-9500-2012; Belfort Jr, Rubens/E-2252-2012;
Berezovsky, Adriana/F-2341-2013
OI Salomao, Solange/0000-0002-3436-5599; Belfort Jr,
Rubens/0000-0002-8422-3898;
FU NEI NIH HHS [N01-EY2103]
NR 17
TC 21
Z9 22
U1 0
U2 2
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD OCT
PY 2008
VL 49
IS 10
BP 4308
EP 4313
DI 10.1167/iovs.08-2073
PG 6
WC Ophthalmology
SC Ophthalmology
GA 355IZ
UT WOS:000259703900014
PM 18829856
ER
PT J
AU Clemons, TE
Gillies, MC
Chew, EY
Bird, AC
Peto, T
Figueroa, M
Harrington, MW
AF Clemons, Traci E.
Gillies, Mark C.
Chew, Emily Y.
Bird, Alan C.
Peto, Tunde
Figueroa, Maria
Harrington, Molly W.
CA MacTel Res Grp
TI The National Eye Institute Visual Function Questionnaire in the macular
telangiectasia (MacTel) project
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID QUALITY-OF-LIFE; JUXTAFOVEOLAR RETINAL TELANGIECTASIS; NEI-VFQ-25;
DISEASE; CHARTS; TRIAL
AB PURPOSE. To describe vision-targeted health-related quality of life (HR-QOL), measured with the National Eye Institute Visual Functioning Questionnaire (NEI-VFQ-25) in a cohort of patients with macular telangiectasia (MacTel) type 2 and to evaluate the relationship between visual acuity and NEI-VFQ-25 scores.
METHODS. This was an analysis of cross-sectional baseline data from a longitudinal natural history study. Patients with MacTel type 2 were enrolled in the Natural History Study of The Macular Telangiectasia Project (The MacTel Project). NEI-VFQ25 were completed at enrollment. Linear correlation and regression analyses were used to relate baseline NEI-VFQ-25 overall and subscale scores to visual acuity.
RESULTS. Participants reported lower vision-related functioning measured by the NEI-VFQ-25 in most of the domains measured by the NEI VFQ compared with that of a normal reference group (P < 0.001 for all domains except color vision). Visual acuity was found to be associated with the NEI-VFQ-25 in many of the domains measuring degree of difficulty with common visual activities.
CONCLUSIONS. This is the first cross-sectional cohort study to assess vision targeted HR-QOL in patients with MacTel type 2. Patients with MacTel type 2 reported markedly reduced visual functioning compared to reports of a normal reference group. These findings provide support to the use of the NEI-VFQ-25 in patients with MacTel type 2 to measure the effect of disease and potential therapies on vision-targeted HR-QOL.
C1 [Clemons, Traci E.] EMMES Corp, Coordinating Ctr, MacTel Project, Rockville, MD 20850 USA.
[Gillies, Mark C.] Univ Sydney, Dept Clin Ophthalmol, Save Sight Inst, Sydney, NSW 2006, Australia.
[Chew, Emily Y.] NEI, Bethesda, MD 20892 USA.
[Bird, Alan C.; Peto, Tunde] Inst Ophthalmol, London, England.
[Bird, Alan C.; Peto, Tunde] Moorfields Eye Hosp, London, England.
RP Clemons, TE (reprint author), EMMES Corp, Coordinating Ctr, MacTel Project, 401 N Washington St,Suite 700, Rockville, MD 20850 USA.
EM tclemons@emmes.com
RI gillies, mark/B-3242-2012; Sahel, Jose-Alain/F-3172-2017;
OI Finger, Robert P/0000-0003-4253-7597; Charbel Issa,
Peter/0000-0002-0351-6673
FU Lowy Medical Research Institute Limited
FX Supported by The Lowy Medical Research Institute Limited.
NR 26
TC 29
Z9 29
U1 0
U2 1
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD OCT
PY 2008
VL 49
IS 10
BP 4340
EP 4346
DI 10.1167/iovs.08-1749
PG 7
WC Ophthalmology
SC Ophthalmology
GA 355IZ
UT WOS:000259703900019
PM 18586874
ER
PT J
AU Shi, G
Maminishkis, A
Banzon, T
Jalickee, S
Li, R
Hammer, J
Miller, SS
AF Shi, Guangpu
Maminishkis, Arvydas
Banzon, Tina
Jalickee, Stephen
Li, Rong
Hammer, Jeffrey
Miller, Sheldon S.
TI Control of chemokine gradients by the retinal pigment epithelium
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID PROLIFERATIVE DIABETIC-RETINOPATHY; MONOCYTE CHEMOATTRACTANT PROTEIN-1;
NECROSIS-FACTOR-ALPHA; MACULAR DEGENERATION; CHOROIDAL
NEOVASCULARIZATION; GENE-EXPRESSION; DIFFERENTIAL EXPRESSION;
INFLAMMATORY-CYTOKINES; DISTINCT CYTOKINE; FLUID ABSORPTION
AB PURPOSE. Proinflammatory cytokines in degenerative diseases can lead to the loss of normal physiology and the destruction of surrounding tissues. In the present study, the physiological responses of human fetal retinal pigment epithelia (hfRPE) were examined in vitro after polarized activation of proinflammatory cytokine receptors. METHODS. Primary cultures of hfRPE were stimulated with an inflammatory cytokine mixture (ICM): interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. Western blot analysis and immunofluorescence were used to determine the expression/localization of the cytokine receptors on hfRPE. Polarized secretion of cytokines was measured. A capacitance probe technique was used to measure transepithelial fluid flow (J(V)) and resistance (R-T). RESULTS. IL-1R1 was mainly localized to the apical membrane and TNFR1 to the basal membrane, whereas IFN-gamma R1 was detected on both membranes. Activation by apical ICM induced a significant secretion of angiogenic and angiostatic chemokines, mainly across the hfRPE apical membrane. Addition of the ICM to the basal but not the apical bath significantly increased net fluid absorption (J(V)) across the hfRPE within 20 minutes. Similar increases in J(V) were produced by a 24-hour exposure to ICM, which significantly decreased total R-T. CONCLUSIONS. Chemokine gradients across the RPE can be altered (1) through an ICM-induced change in polarized chemokine secretion and (2) through an increase in ICM-induced net fluid absorption. In vivo, both of these factors could contribute to the development of chemokine gradients that help mediate the progression of inflammation/angiogenesis at the retina/RPE/choroid complex.
C1 [Shi, Guangpu; Maminishkis, Arvydas; Banzon, Tina; Jalickee, Stephen; Li, Rong; Hammer, Jeffrey; Miller, Sheldon S.] NEI, NIH, Bethesda, MD 20892 USA.
RP Miller, SS (reprint author), NEI, NIH, 31 Ctr Dr,MSC 2510, Bethesda, MD 20892 USA.
EM millers@nei.nih.gov
FU NEI/NIH
FX Supported by the NEI/NIH Intramural Program.
NR 83
TC 52
Z9 55
U1 1
U2 2
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD OCT
PY 2008
VL 49
IS 10
BP 4620
EP 4630
DI 10.1167/iovs.08-1816
PG 11
WC Ophthalmology
SC Ophthalmology
GA 355IZ
UT WOS:000259703900056
PM 18450597
ER
PT J
AU Prada, N
Davis, B
Jean-Pierre, P
La Roche, M
Duh, FM
Carrington, M
Poles, M
Mehandru, S
Mohri, H
Markowitz, M
AF Prada, Nicole
Davis, Brandi
Jean-Pierre, Patrick
La Roche, Matthew
Duh, Fuh-Mei
Carrington, Mary
Poles, Michael
Mehandru, Saurabh
Mohri, Hiroshi
Markowitz, Martin
TI Drug-susceptible HIV-1 infection despite intermittent fixed-dose
combination tenofovir/emtricitabine as prophylaxis is associated with
low-level viremia, delayed seroconversion, and an attenuated clinical
course
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE prophylaxis; tenofovir; emtricitabine; acute infection
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TENOFOVIR DISOPROXIL FUMARATE; IN-VITRO
SELECTION; ANTIRETROVIRAL ACTIVITY; MACAQUES; TRANSMISSION; PREVENTION;
PHARMACOKINETICS; RESISTANT; MUTATION
AB Background: Continued high rates of HIV-1 transmission have fueled interest in the use of antiretrovirals to prevent infection. Attenuated infection with failure of tenofovir as prophylaxis has been reported in animal models. Here, we report a case of HIV-1 infection despite intermittent use of fixed-dose combination tenofovir and emtricitabine (FTC).
Method: The patient was treated with tenofovir DF/FTC for reported repeated high-risk sexual exposures. After seroconversion, he was subjected to routine laboratory testing, CCR5 and HLA genotyping, and biopsy of gastrointestinal (GI) tissue. Resistance testing was performed both as bulk sequencing of plasma and cloning and sequencing of virus derived from plasma, peripheral blood mononuclear cells, and GI tissue.
Results: In this patient with no readily identifiable modifying host factors, acute HIV-1 infection with tenofovir DF/FTC-susceptible HIV-1 was associated with an attenuated clinical Course, very low postseroconversion HIV-1 RNA levels, slow kinetics of seroconversion, and relative sparing of mucosal CD4+ T cells in the GI tract.
Conclusions: Despite the failure of tenofovir DF/FTC as prophylaxis, selection for drug-resistant transmission did not occur and the blunting of postinfection levels of viremia likely reduced the probability of subsequent forward transmissions during the acute phase. These results support continued investigations of the use of antiretrovirals as a means to reduce HIV-1 transmission.
C1 [Prada, Nicole; Davis, Brandi; Jean-Pierre, Patrick; La Roche, Matthew; Mehandru, Saurabh; Mohri, Hiroshi; Markowitz, Martin] Rockefeller Univ, Aaron Diamond AIDS Res Ctr, New York, NY 10016 USA.
[Duh, Fuh-Mei; Carrington, Mary] NCI, SAIC Frederick, Frederick, MD 21701 USA.
[Poles, Michael] NYU, Sch Med, Dept Med, New York, NY USA.
RP Markowitz, M (reprint author), Rockefeller Univ, Aaron Diamond AIDS Res Ctr, 455 1st Ave,7th Floor, New York, NY 10016 USA.
EM mmarkowitz@adarc.org
FU NCI NIH HHS [N01 CO012400]; NCRR NIH HHS [UL1 RR 024143, UL1 RR024143];
NIAID NIH HHS [AI 41534, R01 AI 47033, R01 AI047033, U01 AI041534]
NR 29
TC 15
Z9 15
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD OCT 1
PY 2008
VL 49
IS 2
BP 117
EP 122
DI 10.1097/QAI.0b013e3181869a9b
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 353SB
UT WOS:000259587400001
PM 18769360
ER
PT J
AU Musoke, PM
Young, AM
Owor, MA
Lubega, IR
Brown, ER
Mmiro, FA
Mofenson, LM
Jackson, JB
Fowler, MG
Guay, LA
AF Musoke, Philippa M.
Young, Alicia M.
Owor, Maxensia A.
Lubega, Irene R.
Brown, Elizabeth R.
Mmiro, Francis A.
Mofenson, Lynne M.
Jackson, J. Brooks
Fowler, Mary Glenn
Guay, Laura A.
TI Total lymphocyte count: Not a surrogate marker for risk of death in
HIV-infected Ugandan children
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE total lymphocyte count; HIV; Africa; children
ID RESOURCE-LIMITED SETTINGS; ACTIVE ANTIRETROVIRAL THERAPY; CD4 CELL
COUNT; DISEASE PROGRESSION; AFRICAN CHILDREN; HIV-1-INFECTED CHILDREN;
LONGITUDINAL DATA; RANDOMIZED-TRIAL; MORTALITY; METAANALYSIS
AB Objectives: To determine the utility of total lymphocyte Count (TLC) in predicting the 12-month mortality in HIV-infected Ugandan children and to correlate TLC and CD4 cell %.
Design: This is a retrospective data analysis of clinical and laboratory data collected prospectively on 128 HIV-infected children in the H I V Network for Prevention Trials 0 12 trial.
Methods: TLC and CD4 cell % measurements were obtained at birth, 14 weeks, and 12, 24, 36, 48, and 60 months of age and assessed with respect to risk of death within 12 months.
Results: Median TLC per microliter (CD4 cell %) was 4150 (41%) at birth, 4900 (24%) at 12 months, 4300 (19%) at 24 months, 4150 (19%) at 36 months, 4100 (18%) at 48 months, and 3800 (20%) at 60 months. The highest risk of mortality within 12 months was 34%-37% at birth and declined to 13%-15% at 24 months regardless of TLC measurement. The correlation between CD4 cell % and TLC was extremely low overall (r = 0.01).
Conclusions: The TLC did not predict a risk of progression to death within 12 months in HIV-infected Ugandan children. Therefore, TLC alone may not be a useful surrogate marker for determining those children at highest risk of death.. who require antiretroviral therapy most urgently.
C1 [Musoke, Philippa M.; Owor, Maxensia A.; Lubega, Irene R.; Mmiro, Francis A.] Makerere Univ, Johns Hopkins Univ Res Collaborat, Kampala, Uganda.
[Musoke, Philippa M.; Lubega, Irene R.] Makerere Univ, Dept Paediat & Child Hlth, Kampala, Uganda.
[Young, Alicia M.; Brown, Elizabeth R.] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98104 USA.
[Brown, Elizabeth R.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
NICHHD, Pediat Adolescent & Maternal AIDS Branch, NIH, Bethesda, MD 20892 USA.
[Jackson, J. Brooks; Fowler, Mary Glenn; Guay, Laura A.] Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21205 USA.
RP Musoke, PM (reprint author), Makerere Univ, Johns Hopkins Univ Res Collaborat, POB 23491, Kampala, Uganda.
EM pmusoke@mujhu.org
RI Brown, Elizabeth/A-8984-2008;
OI Mofenson, Lynne/0000-0002-2818-9808
FU US National Institute of Allergy and Infectious Diseases; National
Institutes of Health (NIH); Department of Health and Human Services
[N01-AI-35173, N01-AI-45200, N01-AI-35173-417]; National Institute of
Allergy and Infectious Diseases; National Institutes of Child Health and
Human Development [U01-AI-068632, U01-AI-069530]; National Institute on
Drug Abuse; National Institute of Mental Health; NIH [U01-AI-46745,
U01-AI-48054, U01-AI-068613]
FX Supported by (1) the HIV Network for Prevention Trials and sponsored by
the US National Institute of Allergy and Infectious Diseases, National
Institutes of Health (NIH), Department of Health and Human Services,
through contract N01-AI-35173 with Family Health International, contract
N01-AI-45200 with Fred Hutchinson Cancer Research Center, and
subcontract (N01-AI-35173-417) with Johns Hopkins University and (2) the
HIV Prevention Trials Network sponsored by the National Institute of
Allergy and Infectious Diseases, National Institutes of Child Health and
Human Development, National Institute on Drug Abuse, National Institute
of Mental Health and Office of AIDS Research, of the NIH, Department of
Health and Human Services (U01-AI-46745, U01-AI-48054, and
U01-AI-068613), and the International Maternal Pediatric Adolescent AIDS
Clinical Trials Group sponsored by the National Institute of Allergy and
Infectious Diseases and National Institutes of Child Health and Human
Development (U01-AI-068632, U01-AI-069530).
NR 32
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD OCT 1
PY 2008
VL 49
IS 2
BP 171
EP 178
DI 10.1097/QAI.0b013e318183a92a
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 353SB
UT WOS:000259587400009
PM 18769352
ER
PT J
AU Bisson, GP
Nthobatsong, R
Thakur, R
Lesetedi, G
Vinekar, K
Tebas, P
Bennett, JE
Gluckman, S
Gaolathe, T
MacGregor, RR
AF Bisson, Gregory P.
Nthobatsong, Rudo
Thakur, Rameshwari
Lesetedi, Gloria
Vinekar, Kavita
Tebas, Pablo
Bennett, John E.
Gluckman, Stephen
Gaolathe, Tendani
MacGregor, Rob R.
TI The use of HAART is associated with decreased risk of death during
initial treatment of cryptococcal meningitis in adults in Botswana
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article; Proceedings Paper
CT 15th Conference on Retroviruses and Opportunistic Infections
CY FEB 03-06, 2008
CL Boston, MA
DE cryptococcal meningitis; HAART; Africa; cohort study
ID RECONSTITUTION INFLAMMATORY SYNDROME; DISEASE
AB Objective: The objective of this study was to evaluate Outcomes among adults with a first episode of cryptococcal meningitis (CM), comparing those on highly active antiretroviral therapy (HAART) with those not on HAART.
Methods: We conducted a prospective cohort Study among HIV-infected adults (aged 18 years and older) with a first episode of CM at the Princess Marina Hospital, in Gaborone, Botswana. The proportions surviving to discharge were compared. Logistic regression was used to evaluate the relationship between HAART use and risk of death in the hospital, adjusting for potential Confounders.
Results: Ninety-two patients [median CD4 41 cells/mm(3) (inter-quartile range 22-85)] were included, 26 of whom were on HAART at the time that they developed CM. The in-hospital mortality was lower among those on HAART (2 of 26 (8%) vs 14 of 66 (21%); odds ratio = 0.36 [95% confidence interval (CI) 0.09 to 1.49]}, and this result was statistically significant after adjustment for male sex and tuberculosis [adjusted odds ratio = 0.19 (95% CI 0.04 to 1.00)].
Conclusions: HAART use at the time of a first admission with CM is associated with decreased risk of death during the acute phase of disease. Reasons for this association should be explored.
C1 [Bisson, Gregory P.; Nthobatsong, Rudo; Thakur, Rameshwari; Lesetedi, Gloria; Vinekar, Kavita; Gluckman, Stephen; MacGregor, Rob R.] Univ Penn, Sch Med, Dept Med, Philadelphia, PA 19104 USA.
[Bennett, John E.] NIAID, Clin Mycol Sect, NIH, Bethesda, MD 20892 USA.
RP Bisson, GP (reprint author), Univ Penn, Sch Med, Dept Med, 832 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM gregbisson@mac.com
FU Intramural NIH HHS [Z99 AI999999]
NR 8
TC 25
Z9 26
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD OCT 1
PY 2008
VL 49
IS 2
BP 227
EP 229
DI 10.1097/QAI.0b013e318183181e
PG 3
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 353SB
UT WOS:000259587400017
PM 18769344
ER
PT J
AU Koch, R
Jaffe, ES
Mensing, C
Zeis, M
Schmitz, N
Sander, CA
AF Koch, R.
Jaffe, E. S.
Mensing, C.
Zeis, M.
Schmitz, N.
Sander, C. A.
TI Cutaneous Gamma/Delta-T-cell-Lymphomas
SO JOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT
LA German
DT Meeting Abstract
C1 [Koch, R.; Sander, C. A.] Eduard Arning Klin Dermatol & Allergol AK St Geor, Hamburg, Germany.
[Jaffe, E. S.] NCI, Hematopathol Sect, Pathol Lab, Bethesda, MD 20892 USA.
[Zeis, M.; Schmitz, N.] Asklepios Klin St Georg, Hamatol Abt, Hamburg, Germany.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1610-0379
J9 J DTSCH DERMATOL GES
JI J. Dtsch. Dermatol. Ges.
PD OCT
PY 2008
VL 6
IS 10
BP 913
EP 913
PG 1
WC Dermatology
SC Dermatology
GA 354AV
UT WOS:000259612200050
ER
PT J
AU Czermak, C
Hauger, R
Drevets, WC
Luckenbaugh, DA
Geraci, M
Charney, DS
Neumeister, A
AF Czermak, Christoph
Hauger, Richard
Drevets, Wayne C.
Luckenbaugh, David A.
Geraci, Marilla
Charney, Dennis S.
Neumeister, Alexander
TI Plasma NPY concentrations during tryptophan and sham depletion in
medication-free patients with remitted depression
SO JOURNAL OF AFFECTIVE DISORDERS
LA English
DT Article
DE major depressive disorder; serotonin; neuropeptide Y; tryptophan
depletion; neurobiology
ID NEUROPEPTIDE-Y NPY; MAJOR DEPRESSION; STRESS; DISORDER; SYSTEM;
PHARMACOLOGY; HUMANS
AB Background: Neuropeptide Y (NPY) and scrotonergic systems have been implicated in the pathophysiology of depression but have not yet been linked together.
Methods: In a randomized, double-blind crossover study, 28 medication-free patients with remitted depression and 26 healthy control subjects underwent tryptophan depletion (TD) and sham depletion. Plasma NPY concentrations were determined at baseline and at +5, +7, and +24 h during TD and sham depletion, respectively. Hamilton Depression Rating Scale (HDRS, 24-item) scores were assessed at baseline and at +7 and +24 h after TD and sham depletion, respectively.
Results: There was no difference between healthy Subjects and patients with remitted depression in baseline plasma NPY concentrations and in plasma NPY concentrations during TD and sham depletion, respectively. Plasma NPY concentrations did not differ between TD and sham depletion. At no time point there was an association between HDRS scores and plasma NPY concentrations in patients with remitted depression. Limitations: Plasma NPY concentrations in rMDD patients were not obtained during the symptomatic phase of the illness. Only peripheral measurements of NPY were used.
Conclusions: Decreased plasma NPY concentrations, as described previously during a spontaneous episode of major depression, appear as state but not as trait marker in depression. No evidence was found for an involvement of plasma NPY in relapse during TD. There appears no direct functional link between serotonergic neurotransmission and plasma NPY concentrations. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Czermak, Christoph; Neumeister, Alexander] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Czermak, Christoph; Neumeister, Alexander] VA Connecticut Healthcare Syst, West Haven, CT USA.
[Hauger, Richard] San Diego VA Healthcare Syst, La Jolla, CA USA.
[Hauger, Richard] Univ Calif San Diego, Sch Med, Dept Psychiat, La Jolla, CA 92093 USA.
[Drevets, Wayne C.; Luckenbaugh, David A.; Geraci, Marilla] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
[Charney, Dennis S.] Mt Sinai Sch Med, New York, NY USA.
RP Neumeister, A (reprint author), Yale Univ, Sch Med, Mol Imaging Program, Clin Neurosci Div, 950 Campbell Ave, West Haven, CT 06516 USA.
EM alexander.neumeister@yale.edu
FU Intramural NIH HHS; NIA NIH HHS [R01 AG022982, AG022982]; NIMH NIH HHS
[R01 MH074697-04A1, MH074697, R01 MH074697]
NR 17
TC 11
Z9 12
U1 0
U2 0
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
PY 2008
VL 110
IS 3
BP 277
EP 281
DI 10.1016/j.jad.2008.01.014
PG 5
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 351IM
UT WOS:000259417900011
PM 18281099
ER
PT J
AU Ashida, S
Heaney, CA
AF Ashida, Sato
Heaney, Catherine A.
TI Differential associations of social support and social connectedness
with structural features of social networks and the health status of
older adults
SO JOURNAL OF AGING AND HEALTH
LA English
DT Article
DE social support; social connectedness; social engagement; companionship;
network characteristics
ID LATER LIFE; LONELINESS; COMMUNITY; COMPANIONSHIP; CONFIDANTS;
DISABILITY; AMERICANS; MORTALITY; SAMPLE
AB Objective: This study explores the extent to which the constructs of social support and social connectedness differ in terms of their associations with the structural characteristics of social networks and the health status of older adults. Method: Trained interviewers conducted 126 face-to-face interviews with community-dwelling older adults aged 65 to 85 years. Results: Having frequent contact with network members was positively associated with social support. Network density and having network members living in close proximity were positively associated with perceived social connectedness. Furthermore, perceived social connectedness had a significant positive association with health status, whereas social support did not. Discussion: Perceived social connectedness may be relatively more important to the health and wellbeing of older adults than the perceived availability of social support. Efforts to enhance older adults' social relationships can be focused on developing friends and companions, allowing them to feel socially engaged in society.
C1 [Ashida, Sato] Ohio State Univ, Columbus, OH 43210 USA.
[Heaney, Catherine A.] Stanford Univ, Stanford, CA 94305 USA.
RP Ashida, S (reprint author), NHGRI, Social & Behav Res Branch, 31 Ctr Dr 31-B1B37C, Bethesda, MD 20892 USA.
EM ashidas@mail.nih.gov
NR 42
TC 40
Z9 40
U1 4
U2 21
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0898-2643
J9 J AGING HEALTH
JI J. Aging Health
PD OCT
PY 2008
VL 20
IS 7
BP 872
EP 893
DI 10.1177/0898264308324626
PG 22
WC Gerontology; Health Policy & Services
SC Geriatrics & Gerontology; Health Care Sciences & Services
GA 355VJ
UT WOS:000259737000007
PM 18815414
ER
PT J
AU Pruitt, LA
Glynn, NW
King, AC
Guralnik, JM
Aiken, EK
Miller, G
Haskell, WL
AF Pruitt, Leslie A.
Glynn, Nancy W.
King, Abby C.
Guralnik, Jack M.
Aiken, Erin K.
Miller, Gary
Haskell, William L.
TI Use of Accelerometry to Measure Physical Activity in Older Adults at
Risk for Mobility Disability
SO JOURNAL OF AGING AND PHYSICAL ACTIVITY
LA English
DT Article
DE assessment; motion sensor; exercise; locomotor activity
ID LOWER-EXTREMITY FUNCTION; AMERICAN-HEART-ASSOCIATION; LIFE-STYLE
INTERVENTIONS; CSA ACTIVITY MONITOR; COMPUTER-SCIENCE; SUBSEQUENT
DISABILITY; PERFORMANCE BATTERY; ENERGY-EXPENDITURE; SPORTS-MEDICINE;
PUBLIC-HEALTH
AB The authors explored using the ActiGraph accelerometer to differentiate activity levels between participants in a physical activity (PA, n = 54) or "successful aging" (SA) program (n = 52). The relationship between a PA questionnaire for older adults (CHAMPS) and accelerometry variables was also determined. Individualized accelerometry-count thresholds (Thresh(IND)) measured during a 400-m walk were used to identify "meaningful activity." Participants then wore the ActiGraph for 7 days. Results indicated more activity bouts/day >= 10 min above Thresh(IND) in the PA group than in the SA group (1.1 +/- 2.0 vs 0.5 +/- 0.8, p = .05) and more activity counts/day above Thresh(IND) for the PA group (28,101 27,52 1) than for the SA group (17,234 15,620, p = .02). Correlations between activity counts/hr and CHAMPS ranged from .27 to .42, p < .01. The ActiGraph and Thresh(IND) might be useful for differentiating PA levels in older adults at risk for mobility disability.
C1 [Pruitt, Leslie A.; King, Abby C.; Haskell, William L.] Stanford Univ, Sch Med, Stanford Prevent Res Ctr, Stanford, CA 94305 USA.
[Glynn, Nancy W.; Aiken, Erin K.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Guralnik, Jack M.] NIA, Bethesda, MD 20892 USA.
[Miller, Gary] Wake Forest Univ, Dept Hlth & Exercise Sci, Winston Salem, NC 27109 USA.
RP Pruitt, LA (reprint author), Stanford Univ, Sch Med, Stanford Prevent Res Ctr, Stanford, CA 94305 USA.
OI Glynn, Nancy/0000-0003-2265-0162
FU National Institutes on Health/National Institute on Aging [U01 AG22376];
Intramural Research Program, National Institute on Aging, NTH
FX The Lifestyle Interventions and Independence for Elders (LIFE-P) Pilot
Study was funded by a National Institutes on Health/National Institute
on Aging Cooperative Agreement (#U01 AG22376) and sponsored in part by
the Intramural Research Program, National Institute on Aging, NTH. This
substudy was supported in part by the Intramural Research Program,
National Institute on Aging, NTH. We would also like to acknowledge Dr.
David K. Ahn for his statistical analysis and programming contributions
to this project and Ann Varady for her programming expertise.
NR 48
TC 68
Z9 68
U1 3
U2 9
PU HUMAN KINETICS PUBL INC
PI CHAMPAIGN
PA 1607 N MARKET ST, PO BOX 5076, CHAMPAIGN, IL 61820-2200 USA
SN 1063-8652
J9 J AGING PHYS ACTIV
JI J. Aging Phys. Act.
PD OCT
PY 2008
VL 16
IS 4
BP 416
EP 434
PG 19
WC Geriatrics & Gerontology; Gerontology; Sport Sciences
SC Geriatrics & Gerontology; Sport Sciences
GA 363MZ
UT WOS:000260272700005
PM 19033603
ER
PT J
AU Goodwin, RS
Darwin, WD
Chiang, CN
Shih, M
Li, SH
Huestis, MA
AF Goodwin, Robert S.
Darwin, William D.
Chiang, C. Nora
Shih, Ming
Li, Shou-Hua
Huestis, Marilyn A.
TI Urinary Elimination of 11-Nor-9-Carboxy-Delta(9)-tetrahydrocannnabinol
in Cannabis Users During Continuously Monitored Abstinence
SO JOURNAL OF ANALYTICAL TOXICOLOGY
LA English
DT Article; Proceedings Paper
CT Meeting of the American-Academy-of-Forensic-Sciences
CY 2008
CL Washington, DC
SP Amer Acad Forens Sci
ID SOLID-PHASE EXTRACTION; MARIJUANA USERS; GAS-CHROMATOGRAPHY; HALF-LIFE;
EXCRETION; TETRAHYDROCANNABINOL; ACID
C1 [Goodwin, Robert S.; Darwin, William D.; Huestis, Marilyn A.] Natl Inst Drug Abuse, Chem & Drug Metab Sect, Intramural Res Program, NIH, Rockville, MD USA.
[Chiang, C. Nora; Shih, Ming; Li, Shou-Hua] Natl Inst Drug Abuse, Div Pharmacotherapies & Med Consequences Drug Abu, NIH, Rockville, MD USA.
RP Huestis, MA (reprint author), NIDA, CDM, IRP, NIH, 251 Bayview Blvd,Suite 05A721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU Intramural NIH HHS [NIH0011996773, Z01 DA000412-10, Z01 DA000413-10]
NR 19
TC 32
Z9 33
U1 1
U2 4
PU PRESTON PUBL INC
PI NILES
PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648 USA
SN 0146-4760
J9 J ANAL TOXICOL
JI J. Anal. Toxicol.
PD OCT
PY 2008
VL 32
IS 8
SI SI
BP 562
EP 569
PG 8
WC Chemistry, Analytical; Toxicology
SC Chemistry; Toxicology
GA 360SO
UT WOS:000260078200005
PM 19007504
ER
PT J
AU Shakleya, DM
Plumley, AE
Kraner, JC
Bell, SC
Callery, PS
AF Shakleya, Diaa M.
Plumley, Anna E.
Kraner, James C.
Bell, Suzanne C.
Callery, Patrick S.
TI Trace Evidence of trans-Phenyl propene as a Marker of Smoked
Methamphetamine
SO JOURNAL OF ANALYTICAL TOXICOLOGY
LA English
DT Article
ID PYROLYSIS PRODUCTS; MASS-SPECTROMETRY; OLD DRUG; SMOKING; TOBACCO;
QUANTIFICATION; HYDROCHLORIDE; URINE; ABUSE; FORM
C1 [Shakleya, Diaa M.] Natl Inst Drug Abuse, Chem & Drug Metab Sect, Baltimore, MD 21224 USA.
[Plumley, Anna E.; Bell, Suzanne C.] W Virginia Univ, Eugene C Bennett Dept Chem, Morgantown, WV 26506 USA.
[Kraner, James C.] Off Chief Med Examiner, Charleston, WV 25302 USA.
[Callery, Patrick S.] W Virginia Univ, Sch Pharm, Dept Basic Pharmaceut Sci, Morgantown, WV 26506 USA.
RP Shakleya, DM (reprint author), Natl Inst Drug Abuse, Chem & Drug Metab Sect, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM shakleyad@intra.nida.nih.gov
FU National Institute of Justice [RC-K013]; Office of Justice Programs;
U.S. Department of Justice; Department of Justice
FX This project was supported by Award RC-K013 through the National
Institute of Justice, Office of Justice Programs, U.S. Department of
Justice. The opinions, findings, and conclusions or recommendations
expressed in this publication are those of the authors and do not
necessarily reflect the views of the Department of Justice.
NR 17
TC 3
Z9 3
U1 0
U2 7
PU PRESTON PUBL INC
PI NILES
PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648 USA
SN 0146-4760
J9 J ANAL TOXICOL
JI J. Anal. Toxicol.
PD OCT
PY 2008
VL 32
IS 8
SI SI
BP 705
EP 708
PG 4
WC Chemistry, Analytical; Toxicology
SC Chemistry; Toxicology
GA 360SO
UT WOS:000260078200026
PM 19007525
ER
PT J
AU Rothney, MP
Apker, GA
Song, YN
Chen, KY
AF Rothney, Megan P.
Apker, Gregory A.
Song, Yanna
Chen, Kong Y.
TI Comparing the performance of three generations of ActiGraph
accelerometers
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE calibration; mechanical testing
ID INTENSITY PHYSICAL-ACTIVITY; CSA ACTIVITY MONITOR; COMPUTER-SCIENCE;
TECHNICAL RELIABILITY; ENERGY-EXPENDITURE; UNITED-STATES; VALIDITY;
CALIBRATION; CHILDREN; FIELD
AB ActiGraph accelerometers are a useful tool for objective assessment of physical activity in clinical and epidemiological studies. Several generations of ActiGraph are being used; however, little work has been done to verify that measurements are consistent across generations. This study employed mechanical oscillations to characterize the dynamic response and intermonitor variability of three generations of ActiGraph monitors, from the oldest 7164 (n = 13), 71256 (n = 12), to the newest GT1M (n = 12). The response due to independent radius (22.1-60.4 mm) and frequency (25-250 rpm) changes were measured, as well as intermonitor variability within each generation. The 7164 and 71256 have similar relationships between activity counts and radius (P = 0.229) but were significantly different from the GT1M (P < 0.001). The frequency responses were nonlinear in all three generations. Although the response curve shapes were similar, the differences between generations at various frequencies were significant (P < 0.017), especially in the extremes of the measurement range. Intermonitor variability was markedly reduced in the GT1M compared with the 7164 and 71256. Other measurement differences between generations include decreased peak counts and decreased sensitivity in low-frequency detection in the GT1M. The results of this study revealed an improvement of the intermonitor variability by the GT1M monitor. However, the reduced sensitivity in low-count ranges in the GT1M may not be well suited for monitoring sedentary or light-intensity movements. Furthermore, the algorithms for energy expenditure predictions developed using older 7164 monitors may need to be modified for the GT1M.
C1 [Rothney, Megan P.; Chen, Kong Y.] NIDDK, CEB, NIH, Bethesda, MD 20892 USA.
[Rothney, Megan P.; Apker, Gregory A.] Vanderbilt Univ, Dept Biomed Engn, Nashville, TN 37235 USA.
[Song, Yanna] Vanderbilt Univ, Med Ctr, Dept Biostat, Nashville, TN USA.
RP Rothney, MP (reprint author), NIDDK, CEB, NIH, 10 Ctr Dr MSC 1613,10 CRC 6-3940, Bethesda, MD 20892 USA.
EM rothneym@niddk.nih.gov
OI Chen, Kong/0000-0002-0306-1904
FU National Institutes of Health [DK02973, DK069465, HL082988]
FX This work was supported by grants from the National Institutes of
Health: DK02973, DK069465, and HL082988.
NR 26
TC 94
Z9 96
U1 0
U2 7
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD OCT
PY 2008
VL 105
IS 4
BP 1091
EP 1097
DI 10.1152/japplphysiol.90641.2008
PG 7
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 357PA
UT WOS:000259857400011
PM 18635874
ER
PT J
AU Lakatta, EG
AF Lakatta, Edward G.
TI Arterial aging is risky
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Editorial Material
C1 NIA, Cardiovasc Sci Lab, Gerontol Res Ctr, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
RP Lakatta, EG (reprint author), NIA, Cardiovasc Sci Lab, Gerontol Res Ctr, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
NR 7
TC 16
Z9 16
U1 0
U2 3
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD OCT
PY 2008
VL 105
IS 4
BP 1321
EP 1322
DI 10.1152/japplphysiol.91145.2008
PG 2
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 357PA
UT WOS:000259857400035
PM 18756003
ER
PT J
AU Csiszar, A
Wang, MY
Lakatta, EG
Ungvari, Z
AF Csiszar, Anna
Wang, Mingyi
Lakatta, Edward G.
Ungvari, Zoltan
TI Inflammation and endothelial dysfunction during aging: role of NF-kappa
B
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Review
DE senescence; resveratrol; caloric restriction; poly(ADP-ribose)
polymerase; renin-angiotensin system; coronary artery disease; stroke;
myocardial infarction
ID NECROSIS-FACTOR-ALPHA; CARDIOVASCULAR-DISEASE ENTERPRISES; ANTIOXIDANT
ENZYME-ACTIVITIES; AGE-ASSOCIATED INCREASES; FLOW-MEDIATED DILATION;
LONGEST-LIVING RODENT; SMOOTH-MUSCLE-CELLS; NAKED MOLE-RAT; OXIDATIVE
STRESS; TNF-ALPHA
AB One of the major conceptual advances in our understanding of the pathogenesis of age-associated cardiovascular diseases has been the insight that age-related oxidative stress may promote vascular inflammation even in the absence of traditional risk factors associated with atherogenesis (e.g., hypertension or metabolic diseases). In the present review we summarize recent experimental data suggesting that mitochondrial production of reactive oxygen species, innate immunity, the local TNF-alpha converting enzyme (TACE)-TNF-alpha, and the renin-angiotensin system may underlie NF-kappa B induction and endothelial activation in aged arteries. The theme that emerges from this review is that multiple proinflammatory pathways converge on NF-kappa B in the aged arterial wall, and that the transcriptional activity of NF-kappa B is regulated by multiple nuclear factors during aging, including nuclear enzymes poly(ADP-ribose) polymerase (PARP-1) and SIRT-1. We also discuss the possibility that nucleophosmin (NPM or nuclear phosphoprotein B23), a known modulator of the cellular oxidative stress response, may also regulate NF-kappa B activity in endothelial cells.
C1 [Csiszar, Anna; Ungvari, Zoltan] New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA.
[Wang, Mingyi; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA.
RP Csiszar, A (reprint author), New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA.
EM anna_csiszar@nymc.edu; zoltan_ungvari@nymc.edu
FU National Institute on Aging; American Heart Association [0430108N,
0435140N]; National Institutes of Health [HL-077256, HL-43023]; American
Diabetes Association, American Federation for Aging Researc; Philip
Morris International
FX This work was funded by the Intramural Research Program of the National
Institute on Aging (M. Wang and E. Lakatta), by grants from the American
Heart Association (0430108N, 0435140N to A. Csiszar and Z. Ungvari) and
the National Institutes of Health (HL-077256 and HL-43023 to Z.
Ungvari), the American Diabetes Association, American Federation for
Aging Research (A. Csiszar), and by Philip Morris and Philip Morris
International (to Z. Ungvari).
NR 115
TC 219
Z9 224
U1 3
U2 19
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD OCT
PY 2008
VL 105
IS 4
BP 1333
EP 1341
DI 10.1152/japplphysiol.90470.2008
PG 9
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 357PA
UT WOS:000259857400037
PM 18599677
ER
PT J
AU Chantler, PD
Lakatta, EG
Najjar, SS
AF Chantler, Paul D.
Lakatta, Edward G.
Najjar, Samer S.
TI Arterial-ventricular coupling: mechanistic insights into cardiovascular
performance at rest and during exercise
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Review
DE left ventricular function; arterial system; exercise; aging; disease
ID PRESERVED EJECTION FRACTION; SYSTEMIC VASCULAR-RESISTANCE;
PRESSURE-VOLUME RELATIONS; HEART-FAILURE; CARDIAC-OUTPUT;
BLOOD-PRESSURE; SYSTOLIC HYPERTENSION; GENDER-DIFFERENCES; AEROBIC
EXERCISE; RISK-FACTOR
AB Understanding the performance of the left ventricle (LV) requires not only examining the properties of the LV itself, but also investigating the modulating effects of the arterial system on left ventricular performance. The interaction of the LV with the arterial system, termed arterial-ventricular coupling (E-A/E-LV), is a central determinant of cardiovascular performance and cardiac energetics. E-A/E-LV can be indexed by the ratio of effective arterial elastance (E-A; a measure of the net arterial load exerted on the left ventricle) to left ventricular end-systolic elastance (E-LV; a load-independent measure of left ventricular chamber performance). At rest, in healthy individuals, E-A/E-LV is maintained within a narrow range, which allows the cardiovascular system to optimize energetic efficiency at the expense of mechanical efficacy. During exercise, an acute mismatch between the arterial and ventricular systems occurs, due to a disproportionate increase in E-LV (from an average of 4.3 to 13.2, and 4.7 to 15.5 mmHg . ml(-1) . m(-2) in men and women, respectively) vs. E-A (from an average of 2.3 to 3.2, and 2.3 to 2.9 mmHg . ml(-1) . m(-2) in men and women, respectively), to ensure that sufficient cardiac performance is achieved to meet the increased energetic requirements of the body. As a result E-A/E-LV decreases from an average of 0.58 to 0.34, and 0.52 to 0.27 in men and women, respectively. In this review, we provide an overview of the concept of E-A/E-LV, and examine the effects of age, hypertension, and heart failure on E-A/E-LV and its components (E-A and E-LV) in men and women. We discuss these effects both at rest and during exercise and highlight the mechanistic insights that can be derived from studying E-A/E-LV.
C1 [Najjar, Samer S.] NIA, Cardiovasc Sci Lab, Intramural Res Program, NIH,Harbor Hosp, Baltimore, MD 21225 USA.
RP Najjar, SS (reprint author), NIA, Cardiovasc Sci Lab, Intramural Res Program, NIH,Harbor Hosp, 5th Floor,3001 S Hanover St, Baltimore, MD 21225 USA.
EM Najjarsa@mail.nih.gov
FU National Institutes of Health; National Institute on Aging
FX This work was supported (in part) by the Intramural Research Program of
the National Institutes of Health, National Institute on Aging.
NR 81
TC 103
Z9 113
U1 1
U2 8
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD OCT
PY 2008
VL 105
IS 4
BP 1342
EP 1351
DI 10.1152/japplphysiol.90600.2008
PG 10
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 357PA
UT WOS:000259857400038
PM 18617626
ER
PT J
AU Vimaleswaran, KS
Luan, JA
Andersen, G
Muller, YL
Wheeler, E
Brito, EC
O'Rahilly, S
Pedersen, O
Baier, LJ
Knowler, WC
Barroso, I
Wareham, NJ
Loos, RJF
Franks, PW
AF Vimaleswaran, Karani Santhanakrishnan
Luan, Jian'an
Andersen, Gitte
Muller, Y. Li
Wheeler, Eleanor
Brito, Ema C.
O'Rahilly, Stephen
Pedersen, Oluf
Baier, Leslie J.
Knowler, William C.
Barroso, Ines
Wareham, Nicholas J.
Loos, Ruth J. F.
Franks, Paul W.
TI The Gly482Ser genotype at the PPARGC1A gene and elevated blood pressure:
a meta-analysis involving 13,949 individuals
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE meta-analysis; gene-environment interaction
ID ACTIVATED-RECEPTOR-GAMMA; TYPE-2 DIABETES-MELLITUS; GENOME-WIDE
ASSOCIATION; COACTIVATOR-1 GENE; METABOLIC SYNDROME; PGC-1-ALPHA GENE;
PHYSICAL-ACTIVITY; PIMA-INDIANS; HYPERTENSION; POLYMORPHISM
AB The protein encoded by the PPARGC1A gene is expressed at high levels in metabolically active tissues and is involved in the control of oxidative stress via reactive oxygen species detoxification. Several recent reports suggest that the PPARGC1A Gly482Ser (rs8192678) missense polymorphism may relate inversely with blood pressure. We used conventional meta-analysis methods to assess the association between Gly482Ser and systolic (SBP) or diastolic blood pressures (DBP) or hypertension in 13,949 individuals from 17 studies, of which 6,042 were previously unpublished observations. The studies comprised cohorts of white European, Asian, and American Indian adults, and adolescents from South America. Stratified analyses were conducted to control for population stratification. Pooled genotype frequencies were 0.47 (Gly482Gly), 0.42 (Gly482Ser), and 0.11 (Ser482Ser). We found no evidence of association between Gly482Ser and SBP [Gly482Gly: mean = 131.0 mmHg, 95% confidence interval (CI) = 130.5-131.5 mmHg; Gly482Ser mean = 133.1 mmHg, 95% CI = 132.6-133.6 mmHg; Ser482Ser: mean = 133.5 mmHg, 95% CI = 132.5-134.5 mmHg; P = 0.409] or DBP (Gly482Gly: mean = 80.3 mmHg, 95% CI = 80.0-80.6 mmHg; Gly482Ser mean = 81.5 mmHg, 95% CI = 81.2-81.8 mmHg; Ser482Ser: mean = 82.1 mmHg, 95% CI = 81.5-82.7 mmHg; P = 0.651). Contrary to previous reports, we did not observe significant effect modification by sex (SBP, P = 0.966; DBP, P = 0.715). We were also unable to confirm the previously reported association between the Ser482 allele and hypertension [odds ratio: 0.97, 95% CI = 0.87-1.08, P = 0.585]. These results were materially unchanged when analyses were focused on whites only. However, statistical evidence of gene-age interaction was apparent for DBP [Gly482Gly: 73.5 (72.8, 74.2), Gly482Ser: 77.0 (76.2, 77.8), Ser482Ser: 79.1 (77.4, 80.9), P = 4.20 x 10(-12)] and SBP [Gly482Gly: 121.4 (120.4, 122.5), Gly482Ser: 125.9 (124.6, 127.1), Ser482Ser: 129.2 (126.5, 131.9), P = 7.20 x 10(-12)] in individuals <50 yr (n = 2,511); these genetic effects were absent in those older than 50 yr (n = 5,088) (SBP, P = 0.41; DBP, P = 0.51). Our findings suggest that the PPARGC1A Ser482 allele may be associated with higher blood pressure, but this is only apparent in younger adults.
C1 [Brito, Ema C.; Franks, Paul W.] Umea Univ Hosp, Dept Publ Hlth & Clin Med, Genet Epidemiol & Clin Res Grp, Div Med, S-90187 Umea, Sweden.
[Vimaleswaran, Karani Santhanakrishnan; Luan, Jian'an; Wareham, Nicholas J.; Loos, Ruth J. F.; Franks, Paul W.] Inst Metab Sci, MRC, Epidemiol Unit, Cambridge, England.
[Andersen, Gitte; Pedersen, Oluf] Steno Diabet Ctr, Copenhagen, Denmark.
[Muller, Y. Li; Baier, Leslie J.; Knowler, William C.] NIDDK, NIH, Phoenix, AZ USA.
[Wheeler, Eleanor; Barroso, Ines] Wellcome Trust Sanger Inst, Metab Dis Grp, Hinxton, Cambs, England.
[O'Rahilly, Stephen] Addenbrookes Hosp, Dept Clin Biochem, Cambridge, England.
[O'Rahilly, Stephen] Addenbrookes Hosp, Dept Med, Cambridge CB2 2QQ, England.
RP Franks, PW (reprint author), Umea Univ Hosp, Dept Publ Hlth & Clin Med, Genet Epidemiol & Clin Res Grp, Div Med, S-90187 Umea, Sweden.
EM paul.franks@medicin.umu.se
OI Karani, Vimal/0000-0002-8485-8930; Franks, Paul/0000-0002-0520-7604
FU National Institute of Diabetes and Digestive and Kidney Diseases; UK
MRC; Wellcome Trust; Vasterbottens ALF Committee; Novo Nordisk
[370579201]; Swedish Heart and Lung Foundation [20070633]; Swedish
Diabetes Association [DIA2006-013]
FX The National Institutes of Health Longitudinal Study of Pima Indians was
supported by the Intramural Program of the National Institute of
Diabetes and Digestive and Kidney Diseases. The Medical Research Council
(MRC) Ely Study and the Cambridgeshire Case Control Study were support
with grants from the UK MRC and the Wellcome Trust (to N. J. Wareham).
Several additional aspects of this study were supported by the Wellcome
Trust, Vasterbottens ALF Committee (Strategic appointment 2006-2009 to
P. W. Franks), Novo Nordisk (370579201 to P. W. Franks), the Swedish
Heart and Lung Foundation (20070633 to P. W. Franks), and the Swedish
Diabetes Association (DIA2006-013 to P. W. Franks).
NR 26
TC 13
Z9 13
U1 0
U2 5
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD OCT
PY 2008
VL 105
IS 4
BP 1352
EP 1358
DI 10.1152/japplphysiol.90423.2008
PG 7
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 357PA
UT WOS:000259857400039
PM 18467552
ER
PT J
AU Scahill, L
Aman, MG
McCracken, JT
McDougle, CJ
Vitiello, B
AF Scahill, Lawrence
Aman, Michael G.
McCracken, James T.
McDougle, Christopher J.
Vitiello, Benedetto
TI Beware of over-interpreting negative trials
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Editorial Material
ID RISPERIDONE
C1 [Scahill, Lawrence] Yale Univ, Ctr Child Study, New Haven, CT 06520 USA.
[Aman, Michael G.] Ohio State Univ, Columbus, OH 43210 USA.
[McCracken, James T.] Univ Calif Los Angeles, Los Angeles, CA USA.
[McDougle, Christopher J.] Indiana Univ, Indianapolis, IN 46204 USA.
[Vitiello, Benedetto] NIMH, Rockville, MD 20857 USA.
RP Scahill, L (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd,POB 207900, New Haven, CT 06520 USA.
EM lawrence.scahill@yale.edu
OI Scahill, Lawrence/0000-0001-5073-1707
FU NIMH NIH HHS [U10MH66768, U10MH66764, U10MH66766]
NR 5
TC 4
Z9 4
U1 1
U2 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2008
VL 38
IS 9
BP 1609
EP 1610
DI 10.1007/s10803-008-0581-7
PG 2
WC Psychology, Developmental
SC Psychology
GA 355TV
UT WOS:000259732500001
PM 18594960
ER
PT J
AU Ben Zakour, NL
Sturdevant, DE
Even, S
Guinane, CM
Barbey, C
Alves, PD
Cochet, MF
Gautier, M
Otto, M
Fitzgerald, JR
Le Loir, Y
AF Ben Zakour, Nouri L.
Sturdevant, Daniel E.
Even, Sergine
Guinane, Caitriona M.
Barbey, Corinne
Alves, Priscila D.
Cochet, Marie-Francoise
Gautier, Michel
Otto, Michael
Fitzgerald, J. Ross
Le Loir, Yves
TI Genome-wide analysis of ruminant Staphylococcus aureus reveals
diversification of the core genome
SO JOURNAL OF BACTERIOLOGY
LA English
DT Article
ID BOVINE MAMMARY-GLAND; METHICILLIN-RESISTANT; ESCHERICHIA-COLI;
GENE-EXPRESSION; INFECTIONS; VIRULENCE; STRAINS; IDENTIFICATION;
SUPERANTIGENS; PREDICTION
AB Staphylococcus aureus causes disease in humans and a wide array of animals. Of note, S. aureus mastitis of ruminants, including cows, sheep, and goats, results in major economic losses worldwide. Extensive variation in genome content exists among S. aureus pathogenic clones. However, the genomic variation among S. aureus strains infecting different animal species has not been well examined. To investigate variation in the genome content of human and ruminant S. aureus, we carried out whole-genome PCR scanning (WGPS), comparative genomic hybridizations (CGH), and the directed DNA sequence analysis of strains of human, bovine, ovine, and caprine origin. Extensive variation in genome content was discovered, including host-and ruminant-specific genetic loci. Ovine and caprine strains were genetically allied, whereas bovine strains were heterogeneous in gene content. As expected, mobile genetic elements such as pathogenicity islands and bacteriophages contributed to the variation in genome content between strains. However, differences specific for ruminant strains were restricted to regions of the conserved core genome, which contained allelic variation in genes encoding proteins of known and unknown function. Many of these proteins are predicted to be exported and could play a role in host-pathogen interactions. The genomic regions of difference identified by the whole-genome approaches adopted in the current study represent excellent targets for studies of the molecular basis of S. aureus host adaptation.
C1 [Ben Zakour, Nouri L.; Even, Sergine; Barbey, Corinne; Alves, Priscila D.; Cochet, Marie-Francoise; Gautier, Michel; Le Loir, Yves] STLO, INRA, UMR1253, F-35000 Rennes, France.
[Ben Zakour, Nouri L.; Even, Sergine; Barbey, Corinne; Alves, Priscila D.; Cochet, Marie-Francoise; Gautier, Michel; Le Loir, Yves] Agrocampus Rennes, UMR1253, F-35000 Rennes, France.
[Ben Zakour, Nouri L.; Guinane, Caitriona M.; Fitzgerald, J. Ross] Univ Edinburgh, Ctr Infect Dis, New Royal Infirm, Edinburgh EH16 4SB, Midlothian, Scotland.
[Sturdevant, Daniel E.] NIAID, Rocky Mt Labs, Res Technol Branch, NIH, Hamilton, MT 59840 USA.
[Otto, Michael] NIAID, Rocky Mt Labs, Lab Human Bacterial Pathogenesis, NIH, Hamilton, MT 59840 USA.
RP Le Loir, Y (reprint author), Agrocampus Rennes, Equipe PSEL, UMR1253, STLO,INRA, 65 Rue St Brieuc,CS 84215, F-35042 Rennes, France.
EM Yves.LeLoir@rennes.inra.fr
RI BEN ZAKOUR, Nouri/B-9338-2011; martel, celine/M-9779-2014;
OI BEN ZAKOUR, Nouri/0000-0002-6949-1755; martel,
celine/0000-0002-1800-4558; Otto, Michael/0000-0002-2222-4115
FU French Ministry of Research and Education; Brazilian government [539/06]
FX N.B.Z. was the recipient of a Ph.D. grant from the French Ministry of
Research and Education. P.D.A. is the recipient of a CAPES grant from
the Brazilian government (CAPES-COFECUB project 539/06).
NR 51
TC 37
Z9 37
U1 1
U2 8
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0021-9193
J9 J BACTERIOL
JI J. Bacteriol.
PD OCT
PY 2008
VL 190
IS 19
BP 6302
EP 6317
DI 10.1128/JB.01984-07
PG 16
WC Microbiology
SC Microbiology
GA 348LP
UT WOS:000259212300003
PM 18567666
ER
PT J
AU Khursigara, CM
Wu, XW
Subramaniam, S
AF Khursigara, Cezar M.
Wu, Xiongwu
Subramaniam, Sriram
TI Chemoreceptors in Caulobacter crescentus: Trimers of receptor dimers in
a partially ordered hexagonally packed array
SO JOURNAL OF BACTERIOLOGY
LA English
DT Article
ID ESCHERICHIA-COLI CHEMOTAXIS; VIVO CROSS-LINKING; BACTERIAL CHEMOTAXIS;
CRYOELECTRON MICROSCOPY; HIGH-SENSITIVITY; VISUALIZATION; ARCHITECTURE;
ORGANIZATION; ADAPTATION; EXPRESSION
AB Chemoreceptor arrays are macromolecular complexes that form extended assemblies primarily at the poles of bacterial cells and mediate chemotaxis signal transduction, ultimately controlling cellular motility. We have used cryo-electron tomography to determine the spatial distribution and molecular architecture of signaling molecules that comprise chemoreceptor arrays in wild-type Caulobacter crescentus cells. We demonstrate that chemoreceptors are organized as trimers of receptor dimers, forming partially ordered hexagonally packed arrays of signaling complexes in the cytoplasmic membrane. This novel organization at the threshold between order and disorder suggests how chemoreceptors and associated molecules are arranged in signaling assemblies to respond dynamically in the activation and adaptation steps of bacterial chemotaxis.
C1 [Khursigara, Cezar M.; Subramaniam, Sriram] NCI, Cell Biol Lab, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
[Wu, Xiongwu] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
RP Subramaniam, S (reprint author), NCI, Cell Biol Lab, Canc Res Ctr, NIH, Bldg 50,Rm 4306, Bethesda, MD 20892 USA.
EM ss1@nih.gov
FU National Cancer Institute
FX We thank Z. Gitai for kindly providing C. crescentus strain CB15N and
helpful advice, E. Sockett for insightful comments, and E. Tyler and A.
Hoofring for expert assistance with preparation of the figures. This
study was supported by funds from the intramural program of the National
Cancer Institute to S. S.
NR 27
TC 53
Z9 53
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0021-9193
EI 1098-5530
J9 J BACTERIOL
JI J. Bacteriol.
PD OCT
PY 2008
VL 190
IS 20
BP 6805
EP 6810
DI 10.1128/JB.00640-08
PG 6
WC Microbiology
SC Microbiology
GA 354IF
UT WOS:000259631900028
PM 18689468
ER
PT J
AU Xia, D
Esser, L
Elberry, M
Zhou, F
Yu, LD
Yu, CA
AF Xia, Di
Esser, Lothar
Elberry, Maria
Zhou, Fei
Yu, Linda
Yu, Chang-An
TI The road to the crystal structure of the cytochrome bc (1) complex from
the anoxigenic, photosynthetic bacterium Rhodobacter sphaeroides
SO JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
LA English
DT Article
ID IRON-SULFUR PROTEIN; BC(1) COMPLEX; PARACOCCUS-DENITRIFICANS; ANGSTROM
RESOLUTION; ELECTRON-TRANSFER; DOMAIN MOVEMENT; BOVINE HEART;
MITOCHONDRIAL; CAPSULATUS; OXIDOREDUCTASE
AB The advantages of using bacterial systems to study the mechanism and function of cytochrome bc (1) complexes do not extend readily to their structural investigations. High quality crystals of bacterial complexes have been difficult to obtain despite the enzymes' smaller sizes and simpler subunit compositions compared to their mitochondrial counterparts. In the course of the structure determination of the bc (1) complex from R. sphaeroides, we observed that the growth of only low quality crystals correlated with low activity and stability of the purified complex, which was mitigated in part by introducing a double mutations to the enzyme. The S287R(cyt b)/V135S(ISP) mutant shows 40% increase in electron transfer activity and displays a 4.3 C increase in thermal stability over wild-type enzyme. The amino acid histidine was found important in maintaining structural integrity of the bacterial complex, while the respiratory inhibitors such as stigmatellin are required for immobilization of the iron-sulfur protein extrinsic domain. Crystal quality of the R. sphaeroides bc (1) complex can be improved further by the presence of strontium ions yielding crystals that diffracted X-rays to better than 2.3 resolution. The improved crystal quality can be understood in terms of participation of strontium ions in molecular packing arrangement in crystal.
C1 [Xia, Di; Esser, Lothar] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Elberry, Maria; Zhou, Fei; Yu, Linda; Yu, Chang-An] Oklahoma State Univ, Dept Biochem & Mol Biol, Stillwater, OK 74078 USA.
RP Xia, D (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM dixia@helix.nih.gov; cayu@okstate.edu
FU Intramural NIH HHS [Z01 BC010319-10]
NR 26
TC 10
Z9 10
U1 1
U2 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0145-479X
J9 J BIOENERG BIOMEMBR
JI J. Bioenerg. Biomembr.
PD OCT
PY 2008
VL 40
IS 5
BP 485
EP 492
DI 10.1007/s10863-008-9180-8
PG 8
WC Biophysics; Cell Biology
SC Biophysics; Cell Biology
GA 376JF
UT WOS:000261179200010
PM 18953640
ER
PT J
AU Chui, DH
Marotta, F
Liu, T
Minelli, E
Yadav, H
Signorelli, P
Lorenzetti, A
Jain, S
AF Chui, D. H.
Marotta, F.
Liu, T.
Minelli, E.
Yadav, H.
Signorelli, P.
Lorenzetti, A.
Jain, S.
TI EFFECT OF MODIFIED ALKALINE SUPPLEMENTATION ON BONE METABOLIC TURNOVER
IN RATS
SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
LA English
DT Article
DE alkaline supplementation; bone metabolism; bone mineral density (BMD);
rats
ID MINERAL DENSITY; EXERCISE; ACIDOSIS; MEN; OSTEOPOROSIS; WOMEN
AB This study aims to determine the effects of a high protein diet and alkaline supplementation on bone metabolic turnover in rats. Eight-week-old male Sprague-Dawley rats were investigated by bone status, including bone mineral density (BMD) and biomechanical markers from blood and urine. Thirty rats were randomly divided into three groups and treated for 8 weeks as follows: baseline control group (n. 10, C), high-protein supplemented diet group (n. 10, chronic acidosis, CA group) and supplemented chronic acidosis (n.10, SCA). Diet-treated rats were fed an acidic high-protein diet and the supplementation consisted in a modified alkaline formula (Basenpulver, Named, Italy). At the end of the experimental period, the rats were sacrificed, blood samples were drawn and femur and tibia were removed for analysis of bone mineral density (BMD) by dual energy X-ray absorptiometry (DEXA). In the CA group, 24-hour urinary calcium (Ca) and phosphorus (P) excretion were increased 2.1-fold (p < 0.05 vs normal diet controls) as well as kidney weight. However, serum Ca and P concentration, as well as urinary Dpd excretion were not significantly changed. Femural and tibial BMD was significantly decreased in the CA group (p < 0.05), but alkaline supplementation prevented such phenomenon (p < 0.05 vs CA). These results suggest that blood Ca and P concentrations in chronic acidosis condition during the 12-week supplementation might be maintained by hypercalciuria and hyperphosphaturia at the expenses of bone structure. However, modified alkaline supplementation is able to prevent such derangements.
C1 [Chui, D. H.; Liu, T.] Peking Univ, Neurosci Res Inst, Beijing 100871, Peoples R China.
[Marotta, F.; Minelli, E.] Univ Milan, WHO Ctr Biotech & Trad Med, I-20122 Milan, Italy.
[Signorelli, P.; Lorenzetti, A.] GAIA Age Management Fdn, Pavia, Italy.
[Yadav, H.] NIDDK, Regenerat Biol Sect, NIH, Bethesda, MD USA.
[Jain, S.] Univ Illinois, Dept Food Sci & Human Nutr, Urbana, IL 61801 USA.
RP Marotta, F (reprint author), Piazza Firenze 12, I-20154 Milan, Italy.
EM fmarchimede@libero.it
NR 25
TC 3
Z9 3
U1 0
U2 4
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0393-974X
EI 1724-6083
J9 J BIOL REG HOMEOS AG
JI J. Biol. Regul. Homeost. Agents
PD OCT-DEC
PY 2008
VL 22
IS 4
BP 225
EP 231
PG 7
WC Endocrinology & Metabolism; Immunology; Medicine, Research &
Experimental; Physiology
SC Endocrinology & Metabolism; Immunology; Research & Experimental
Medicine; Physiology
GA 384XG
UT WOS:000261776900003
PM 19036224
ER
PT J
AU Sahoo, SS
Bodenreider, O
Rutter, JL
Skinner, KJ
Sheth, AP
AF Sahoo, Satya S.
Bodenreider, Olivier
Rutter, Joni L.
Skinner, Karen J.
Sheth, Amit P.
TI An ontology-driven semantic mashup of gene and biological pathway
information: Application to the domain of nicotine dependence
SO JOURNAL OF BIOMEDICAL INFORMATICS
LA English
DT Article
DE Semantic web; Semantic mashup; Nicotine dependence; Information
integration; ontologies
ID E-SCIENCE; WEB; GENOME; ASSOCIATION; ACCESS; MODEL
AB Objectives: This paper illustrates how Semantic Web technologies (especially RDF, OWL, and SPARQL) can support information integration and make it easy to create semantic mashups (semantically integrated resources). In the context Of understanding the genetic basis of nicotine dependence, we integrate gene and pathway information and show how three complex biological queries can be answered by the integrated knowledge base.
Methods: We use an ontology-driven approach to integrate two gene resources (Entrez Gene and Homolo-Gene) and three pathway resources (KEGG, Reactome and BioCyc), for five organisms, including humans. We created the Entrez Knowledge Model (EKoM), an information model in OWL for the gene resources, and integrated it with the extant BioPAX ontology designed for pathway resources. The integrated schema is populated with data from the pathway resources, Publicly available in BioPAX-compatible format, and gene resources for which a Population procedure was created. The SPARQL query language is used to formulate queries over the integrated knowledge base to answer the three biological queries. Results: Simple SPARQL queries could easily identify hub genes, i.e., those genes whose gene products participate in many pathways or interact with many other gene products. The identification of the genes expressed in the brain turned out to be more difficult, due to the lack of a common identification scheme for Proteins.
Conclusion: Semantic Web technologies provide a valid framework for information integration in the life sciences. Ontology-driven integration represents a flexible, Sustainable and extensible solution to the integration of large volumes of information. Additional resources, which enable the creation of mappings between information sources, are required to compensate for heterogeneity across namespaces. Resource pagehttp://knoesis.wright.edu/research/lifesci/integration/structured-data/JBI-2008/ (C) 2008 Elsevier Inc. All rights reserved.
C1 [Sahoo, Satya S.; Bodenreider, Olivier] Natl Lib Med, LHNCBC, Bethesda, MD 20894 USA.
[Sahoo, Satya S.; Sheth, Amit P.] Wright State Univ, Kno E Sis Ctr, Dayton, OH 45435 USA.
[Rutter, Joni L.; Skinner, Karen J.] Natl Inst Drug Abuse, DBNBR, Bethesda, MD USA.
RP Bodenreider, O (reprint author), Natl Lib Med, LHNCBC, 8600 Rockville Pike,MS 3841,Bldg 38A,Room B1N28U, Bethesda, MD 20894 USA.
EM olivier@nlm.nih.gov
OI Rutter, Joni/0000-0002-6502-2361
FU National Institutes of Health (NIH); National Library of Medicine (NI-M)
FX This research Was Supported in part by the Intramural Research Program
of the National Institutes of Health (NIH), National Library of Medicine
(NI-M). The authors want to thank Lee Peters who created the RDF store
in Oracle and helped craft and run the SPARQL queries and Jonathan
Pollock for valuable input on model organism databases. Cytoscape was
used to Visualize the interaction networks.
NR 44
TC 33
Z9 33
U1 0
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1532-0464
J9 J BIOMED INFORM
JI J. Biomed. Inform.
PD OCT
PY 2008
VL 41
IS 5
SI SI
BP 752
EP 765
DI 10.1016/j.jbi.2008.02.006
PG 14
WC Computer Science, Interdisciplinary Applications; Medical Informatics
SC Computer Science; Medical Informatics
GA 361OP
UT WOS:000260137300008
PM 18395495
ER
PT J
AU Grishaev, A
Ying, J
Canny, MD
Pardi, A
Bax, A
AF Grishaev, Alexander
Ying, Jinfa
Canny, Marella D.
Pardi, Arthur
Bax, Ad
TI Solution structure of tRNA(Val) from refinement of homology model
against residual dipolar coupling and SAXS data
SO JOURNAL OF BIOMOLECULAR NMR
LA English
DT Article
DE NMR; RDC; refinement; rigid body; SAXS; tRNA
ID X-RAY-SCATTERING; PHOSPHORYL TRANSFER COMPLEX; SMALL-ANGLE SCATTERING;
NUCLEIC-ACIDS; BIOLOGICAL MACROMOLECULES; PROTEIN COMPLEXES; GLOBAL
STRUCTURE; PHOSPHOTRANSFERASE SYSTEM; RELATIVE ORIENTATION; MOLECULAR
ALIGNMENT
AB A procedure is presented for refinement of a homology model of E. coli tRNA(Val), originally based on the X-ray structure of yeast tRNA(Phe), using experimental residual dipolar coupling (RDC) and small angle X-ray scattering (SAXS) data. A spherical sampling algorithm is described for refinement against SAXS data that does not require a globbic approximation, which is particularly important for nucleic acids where such approximations are less appropriate. Substantially higher speed of the algorithm also makes its application favorable for proteins. In addition to the SAXS data, the structure refinement employed a sparse set of NMR data consisting of 24 imino N-H(N) RDCs measured with Pf1 phage alignment, and 20 imino N-H(N) RDCs obtained from magnetic field dependent alignment of tRNA(Val). The refinement strategy aims to largely retain the local geometry of the 58% identical tRNA(Phe) by ensuring that the atomic coordinates for short, overlapping segments of the ribose-phosphate backbone and the conserved base pairs remain close to those of the starting model. Local coordinate restraints are enforced using the non-crystallographic symmetry (NCS) term in the XPLOR-NIH or CNS software package, while still permitting modest movements of adjacent segments. The RDCs mainly drive the relative orientation of the helical arms, whereas the SAXS restraints ensure an overall molecular shape compatible with experimental scattering data. The resulting structure exhibits good cross-validation statistics (jack-knifed Q(free) = 14% for the Pf1 RDCs, compared to 25% for the starting model) and exhibits a larger angle between the two helical arms than observed in the X-ray structure of tRNA(Phe), in agreement with previous NMR-based tRNA(Val) models.
C1 [Grishaev, Alexander; Ying, Jinfa; Bax, Ad] NIDDK, Phys Chem Lab, NIH, Bethesda, MD 20892 USA.
[Canny, Marella D.; Pardi, Arthur] Univ Colorado, Dept Chem & Biochem, Boulder, CO 80309 USA.
RP Pardi, A (reprint author), NIDDK, Phys Chem Lab, NIH, Bethesda, MD 20892 USA.
EM Arthur.Pardi@Colorado.edu; bax@nih.gov
FU NIDDK; NIH [AI33098]
FX This work was supported by the Intramural Research Program of the NIDDK,
NIH, and by the Intramural AIDS-Targeted Antiviral Program of the Office
of the Director, NIH and NIH grant AI33098 (AP).
NR 48
TC 52
Z9 52
U1 0
U2 8
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0925-2738
J9 J BIOMOL NMR
JI J. Biomol. NMR
PD OCT
PY 2008
VL 42
IS 2
BP 99
EP 109
DI 10.1007/s10858-008-9267-x
PG 11
WC Biochemistry & Molecular Biology; Spectroscopy
SC Biochemistry & Molecular Biology; Spectroscopy
GA 357AL
UT WOS:000259818600003
PM 18787959
ER
PT J
AU Fu, YM
Yu, ZX
Lin, HM
Fu, X
Meadows, GG
AF Fu, Ya-Min
Yu, Zu-Xi
Lin, Huimin
Fu, Xing
Meadows, Gary G.
TI Selective amino acid restriction differentially affects the motility and
directionality of DU145 and PC3 prostate cancer cells
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
ID FOCAL ADHESION KINASE; CARCINOMA-CELLS; SIGNAL-TRANSDUCTION; ACTIN
CYTOSKELETON; RHO-GTPASES; IN-VITRO; ALPHA-6-BETA-4 INTEGRINS; NEUTRAL
ENDOPEPTIDASE; ARGININE DEPRIVATION; HUMAN-MELANOMA
AB We previously found that selective restriction of amino acids inhibits invasion of two androgen-independent human prostate cancer cell lines, DU145 and PC3. Here we show that the restriction of tyrosine (Tyr) and phenylalanine (Phe), methionine (Met) or glutamine (Gln) modulates the activity of G proteins and affects the balance between two actin-binding proteins, cofilin and profilin, in these two cell lines. Selective amino acid restriction differentially reduces G protein binding to GTP in DU 145 cells. Tyr/Phe deprivation reduces the amount of Rho-GTP and Rac 1-GTP. Met deprivation reduces the amount of Ras-GTP and Rho-GTP, and GIn deprivation decreases Ras-GTP, 3 Rac-GTP, and Cdc42-GTP. Restriction of these amino acids increases the amount of profilin, cofilin and phosphorylation of cofilin-Ser(3) .Increased PAK 1 expression and phosphorylation of PAK 1-Thr(423), and Ser(199/204) are consistent with the increased phosphorylation of LIMK1-Thr(508). In PC3 cells, Tyr/Phe or GIn deprivation reduces the amount of Ras-GTP, and all of the examined amino acid restrictions reduce the amount of profilin. PAK 1, LIMK I and cofilin are not significantly altered. These data reveal that specific amino acid deprivation differentially affects actin dynamics in DU 145 and PC3. Modulation on Rho, Rac, PAK 1, and LIMK I likely alter the balance between cofilin and profilin in DU 145 cells. In contrast, profilin is inhibited in PC3 cells. These effects modulate directionality and motility to inhibit invasion.
C1 [Fu, Ya-Min; Lin, Huimin; Fu, Xing; Meadows, Gary G.] Washington State Univ, Coll Pharm, Dept Pharmaceut Sci, Canc Prevent & Res Ctr, Pullman, WA 99164 USA.
[Yu, Zu-Xi] NHLBI, Pathol Sect, Bethesda, MD 20892 USA.
RP Meadows, GG (reprint author), Washington State Univ, Coll Pharm, Dept Pharmaceut Sci, Canc Prevent & Res Ctr, Box 646713, Pullman, WA 99164 USA.
EM meadows@wsu.edu
FU National Cancer Institute [R01CA101035]
FX National Cancer Institute R01CA101035
NR 53
TC 11
Z9 12
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0021-9541
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD OCT
PY 2008
VL 217
IS 1
BP 184
EP 193
DI 10.1002/jcp.21490
PG 10
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA 344BJ
UT WOS:000258899900020
PM 18459146
ER
PT J
AU Damjanovic, A
Miller, BT
Wenaus, TJ
Maksimovic, P
Garcia-Moreno, B
Brooks, BR
AF Damjanovic, Ana
Miller, Benjamin T.
Wenaus, Torre J.
Maksimovic, Petar
Garcia-Moreno E, Bertrand
Brooks, Bernard R.
TI Open Science Grid Study of the Coupling between Conformation and Water
Content in the Interior of a Protein
SO JOURNAL OF CHEMICAL INFORMATION AND MODELING
LA English
DT Article
ID MOLECULAR-DYNAMICS; STAPHYLOCOCCAL NUCLEASE; ALL-ATOM; SIMULATION;
PENETRATION; HYDRATION; CAVITIES; POLARITY; AMBER
AB Computational grids are a promising resource for modeling complex biochemical processes such as protein folding, penetration of gases or water into proteins, or protein structural rearrangements coupled to ligand binding. We have enabled the molecular dynamics program CHARMM to run on the Open Science Grid. The implementation is general, flexible, easily modifiable for use with other molecular dynamics programs and other grids and automated in terms of job submission, monitoring, and resubmission. The usefulness of grid computing was demonstrated through the study of hydration of the Glu-66 side chain in the interior of protein staphylococcal nuclease. Multiple simulations started with and without two internal water molecules shown crystallographically to be associated with the side chain of Glu-66 yielded two distinct populations of rotameric states of Glu-66 that differed by as much as 20%. This illustrates how internal water molecules can bias protein conformations. Furthermore, there appeared to be a temporal correlation between dehydration of the side chain and conformational transitions of Glu-66. This example demonstrated how difficult it is to get convergence even in the relatively simple case of a side chain oscillating between two conformations. With grid computing, we also benchmarked the self-guided Langevin dynamics method against the Langevin dynamics method traditionally used for temperature control in molecular dynamics simulations and showed that the two methods yield comparable results.
C1 [Damjanovic, Ana; Garcia-Moreno E, Bertrand] Johns Hopkins Univ, Dept Biophys, Baltimore, MD 21218 USA.
[Damjanovic, Ana; Miller, Benjamin T.; Brooks, Bernard R.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
[Wenaus, Torre J.] Brookhaven Natl Lab, Dept Phys, Upton, NY 11973 USA.
[Maksimovic, Petar] Johns Hopkins Univ, Dept Phys, Baltimore, MD USA.
RP Damjanovic, A (reprint author), Johns Hopkins Univ, Dept Biophys, Baltimore, MD 21218 USA.
EM ad@jhu.edu
OI Miller, Benjamin/0000-0003-1647-0122
FU National Science Foundation; U.S. Department of Energy's Office of
Science; NIH [R01 GM061597]; Intramural Research program at NIH, NHLBI,;
A.P. Sloan foundation [BR-4379]; NSF [PHY-0457374]
FX This research was done using resources provided by the Open Science
Grid, which is supported by the National Science Foundation and the U.S.
Department of Energy's Office of Science. We thank all of the
institutions that have provided computers for this project. We would
like to thank Ruth Pordes, Frank Wurthwein, and Alain Roy for their
assistance with the Open Science Grid, and Rich Pastor for useful
discussions. This work was also supported by NIH grant (R01 GM061597) to
B.G.-M.E., the Intramural Research program at NIH, NHLBI, and the A.P.
Sloan foundation (BR-4379) and NSF grant (PHY-0457374) to P.M.
NR 43
TC 14
Z9 14
U1 2
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1549-9596
J9 J CHEM INF MODEL
JI J. Chem Inf. Model.
PD OCT
PY 2008
VL 48
IS 10
BP 2021
EP 2029
DI 10.1021/ci800263c
PG 9
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Computer Science,
Information Systems; Computer Science, Interdisciplinary Applications
SC Pharmacology & Pharmacy; Chemistry; Computer Science
GA 365ST
UT WOS:000260428800011
PM 18834189
ER
PT J
AU Cerutti, DS
Duke, R
Freddolino, PL
Fan, H
Lybrand, TP
AF Cerutti, David S.
Duke, Robert
Freddolino, Peter L.
Fan, Hao
Lybrand, Terry P.
TI A Vulnerability in Popular Molecular Dynamics Packages Concerning
Langevin and Andersen Dynamics
SO JOURNAL OF CHEMICAL THEORY AND COMPUTATION
LA English
DT Article
ID STOCHASTIC BOUNDARY-CONDITIONS; MONTE-CARLO SIMULATIONS; PROTEIN;
STREPTAVIDIN; WATER; TEMPERATURE; TRANSITION; BEHAVIOR; BINDING; BIOTIN
AB We report a serious problem associated with a number of current implementations of Andersen and Langevin dynamics algorithms. When long simulations are run in many segments, it is sometimes possible to have a repeating sequence of pseudorandom numbers enter the calcuation. We show that, if the sequence repeats rapidly, the resulting artifacts can quickly denature biomolecules and are then easily detectable. However, if the sequence repeats less frequently, the artifacts become subtle and easily overlooked. We derive a formula for the underlying cause of artifacts in the case of the Langevin thermostat, and find it vanishes slowly as the inverse square root of the number of time steps per simulation segment. Numerous examples of simulation artifacts are presented, including dissociation of a tetrameric protein after 110 ns of dynamics, reductions in atomic fluctuations for a small protein in implicit solvent, altered thermodynamic properties of a box of water molecules, and changes in the transition free energies between dihedral angle conformations. Finally, in the case of strong thermocoupling, we link the observed artifacts to previous work in nonlinear dynamics and show that it is possible to drive a 20-residue, implicitly solvated protein into periodic trajectories if the thermostat is not used properly. Our findings should help other investigators re-evaluate simulations that may have been corrupted and obtain more accurate results.
C1 [Cerutti, David S.; Lybrand, Terry P.] Vanderbilt Univ, Struct Biol Ctr, Dept Chem, Nashville, TN 37232 USA.
[Duke, Robert] Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA.
[Duke, Robert] Natl Inst Environm Hlth Sci, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
[Freddolino, Peter L.] Univ Illinois, Ctr Biophys & Computat Biol, Urbana, IL 61801 USA.
[Fan, Hao] Univ Calif San Francisco, Dept Biopharmaceut Sci, San Francisco, CA 94158 USA.
RP Cerutti, DS (reprint author), Vanderbilt Univ, Struct Biol Ctr, Dept Chem, 5140 Med Res Bldg 3,465 21st Ave South, Nashville, TN 37232 USA.
EM david.cerutti@vanderbilt.edu
FU National Institutes of Health [GM080214]
FX This research was supported by National Institutes of Health Grant
GM080214. D.S.C. thanks the GROMACS development team, Dr. Bernard R.
Brooks, Dr. Justin Gullingsrud, and Dr. Ilian Todorov for explanations
about the operation of GROMACS, CHARMM, DESMOND, and DL POLY,
respectively. Dr. Robert Konecny and Dr. Barrett Abel of the Center for
Theoretical Biophysics at the University of California, San Diego,
provided part of the computing resources for this study via National
Science Foundation Grant PHY-0216576.
NR 43
TC 38
Z9 38
U1 1
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1549-9618
J9 J CHEM THEORY COMPUT
JI J. Chem. Theory Comput.
PD OCT
PY 2008
VL 4
IS 10
BP 1669
EP 1680
DI 10.1021/ct8002173
PG 12
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 360HC
UT WOS:000260047600014
PM 19180249
ER
PT J
AU Song, DK
Lonser, RR
AF Song, Debbic K.
Lonser, Russell R.
TI Convection-Enhanced Delivery for the Treatment of Pediatric Neurologic
Disorders
SO JOURNAL OF CHILD NEUROLOGY
LA English
DT Article; Proceedings Paper
CT Annual Neurobiology of Disease in Children Conference
CY OCT 10, 2007
CL Quebec City, CANADA
DE blood-brain barrier; central nervous system; convection-enhanced
delivery; drug delivery
ID PRIMATE BRAIN; COMPUTERIZED-TOMOGRAPHY; MALIGNANT GLIOMA;
GAUCHER-DISEASE; MACROMOLECULES; INFUSION; TIME; STEM; PERFUSION; MODEL
AB Direct perfusion of specific regions of the central nervous system by convection-enhanced delivery is becoming more widely used for the delivery of compounds in the research and treatment of various neural disorders. In contrast to other currently availabe central nervous system delivery techniques, convection- enhanced delivery relies on bulk flow for distribution of solute. This allows for safe, targeted, reliable, and homogeneous delivery of small-molecular-weight and large-molecular-weight substances over clinically releveant volumes in a manner that bypasses the blood-central nervous system barrier. Recent studies have also shown that coinfused imaging surrogate tracers can be used to monitor and control the convective distribution of therapeutic agents in vivo. The unique features of convection-enhanced delivery, including the ability to monitor distribution in realtime, provide an opportunity to develop new research and treatment paradigms for pediatric patients with a variety of intrinsic central nervous system disorders.
C1 [Song, Debbic K.; Lonser, Russell R.] Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Song, Debbic K.] Univ Michigan, Dept Neurol Surg, Ann Arbor, MI 48109 USA.
RP Lonser, RR (reprint author), Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bldg 10,Room 5D37, Bethesda, MD 20892 USA.
EM lonserr@ninds.nih.gov
FU Intramural NIH HHS; NINDS NIH HHS [R13 NS040925, 5R13NS040925-09]
NR 23
TC 21
Z9 21
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0883-0738
J9 J CHILD NEUROL
JI J. Child Neurol.
PD OCT
PY 2008
VL 23
IS 10
BP 1231
EP 1237
DI 10.1177/0883073808321064
PG 7
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 364CG
UT WOS:000260313200015
PM 18952590
ER
PT J
AU Chia, CW
Egan, JM
AF Chia, Chee W.
Egan, Josephine M.
TI Incretin-based therapies in type 2 diabetes mellitus
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Review
ID GLUCAGON-LIKE PEPTIDE-1; DIPEPTIDYL PEPTIDASE-4 INHIBITOR; DEPENDENT
INSULINOTROPIC POLYPEPTIDE; IMPROVES GLYCEMIC CONTROL; DRUG-NAIVE
PATIENTS; BETA-CELL FUNCTION; INITIAL COMBINATION THERAPY; LOWERS
BODY-WEIGHT; DOUBLE-BLIND; HEALTHY-VOLUNTEERS
AB Context: Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide are incretins secreted from enteroendocrine cells postprandially in part to regulate glucose homeostasis. Dysregulation of these hormones is evident in type 2 diabetes mellitus (T2DM). Two new drugs, exenatide (GLP-1 mimetic) and sitagliptin [dipeptidyl peptidase (DPP) 4 inhibitor], have been approved by regulatory agencies for treating T2DM. Liraglutide (GLP-1 mimetic) and vildagliptin (DPP 4 inhibitor) are expected to arrive on the market soon.
Evidence Acquisition: The background of incretin-based therapy and selected clinical trials of these four drugs are reviewed. A MEDLINE search was conducted for published articles using the key words incretin, glucose-dependent insulinotropic polypeptide, GLP-1, exendin-4, exenatide, DPP 4, liraglutide, sitagliptin, and vildagliptin.
Evidence Synthesis: Exenatide and liraglutide are injection based. Three-year follow-up data on exenatide showed a sustained weight loss and glycosylated hemoglobin (HbA(1c)) reduction of 1%. Nausea and vomiting are common. Results from phase 3 studies are pending on liraglutide. Sitagliptin and vildagliptin are orally active. In 24-wk studies, sitagliptin reduces HbA(1c) by 0.6 -0.8% as monotherapy, 1.8% as initial combination therapy with metformin, and 0.7% as add-on therapy to metformin. Vildagliptin monotherapy lowered HbA1c by 1.0 -1.4% after 24 wk. Their major side effects are urinary tract and nasopharyngeal infections and headaches. Exenatide and liraglutide cause weight loss, whereas sitagliptin and vildagliptin do not.
Conclusions: The availability of GLP-1 mimetics and DPP 4 inhibitors has increased our armamentarium for treating T2DM. Unresolved issues such as the effects of GLP-1 mimetics and DPP 4 inhibitors on beta-cell mass, the mechanism by which GLP-1 mimetics lowers glucagon levels, and exactly how DPP 4 inhibitors lead to a decline in plasma glucose levels without an increase in insulin secretion, need further research.
C1 [Chia, Chee W.; Egan, Josephine M.] NIA, Natl Inst Hlth, Baltimore, MD 21224 USA.
RP Egan, JM (reprint author), NIA, Natl Inst Hlth, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM eganj@grc.nia.nih.gov
FU National Institutes of Health (NIH), National Institute on Aging
FX The writing of this special feature was supported by the Intramural
Research Program of the National Institutes of Health (NIH), National
Institute on Aging.
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U2 13
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 2008
VL 93
IS 10
BP 3703
EP 3716
DI 10.1210/jc.2007-2109
PG 14
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 358FY
UT WOS:000259903700007
PM 18628530
ER
PT J
AU Huang, H
Fojo, T
AF Huang, Hui
Fojo, Tito
TI Commentary: Adjuvant Mitotane for adrenocortical cancer - A recurring
controversy
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Editorial Material
ID ADRENAL-CORTICAL CARCINOMA; ORTHO,PARA'-DDD
C1 [Huang, Hui; Fojo, Tito] Natl Canc Inst, Med Oncol Branch, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Huang, H (reprint author), Natl Canc Inst, Med Oncol Branch, Natl Inst Hlth, Bldg 10,Room 12N226,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM huangh@mail.nih.gov
NR 11
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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 2008
VL 93
IS 10
BP 3730
EP 3732
DI 10.1210/jc.2008-0579
PG 3
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 358FY
UT WOS:000259903700010
PM 18842984
ER
PT J
AU Gejman, R
Batista, DL
Zhong, Y
Zhou, YL
Zhang, X
Swearingen, B
Stratakis, CA
Hedley-Whyte, ET
Klibanski, A
AF Gejman, Roger
Batista, Dalia L.
Zhong, Ying
Zhou, Yunli
Zhang, Xun
Swearingen, Brooke
Stratakis, Constantine A.
Hedley-Whyte, E. Tessa
Klibanski, Anne
TI Selective loss of MEG3 expression and intergenic differentially
methylated region hypermethylation in the MEG3/DLK1 locus in human
clinically nonfunctioning pituitary adenomas
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID DLK1-GTL2 IMPRINTED DOMAIN; PROMOTER REGION; GENE-EXPRESSION; TUMORS;
MOUSE-CHROMOSOME-12; TUMORIGENESIS; MECHANISMS; IGF2-H19; CLUSTER;
ORIGIN
AB Context: MEG3 is an imprinted gene encoding a novel noncoding RNA that suppresses tumor cell growth. Although highly expressed in the normal human pituitary, it is unknown which of the normal pituitary cell types and pituitary tumors express MEG3.
Objectives: Our objectives were 1) to investigate cell-type- and tumor-type-specific expression of MEG3 in the human pituitary and 2) to investigate whether methylation in the intergenic differentially methylated region (IG-DMR) at the DLK1/MEG3 locus is involved in the loss of MEG3 expression in tumors.
Design and Methods: RT-PCR, quantitative RT-PCR, Northern blot, and a combination of in situ hybridization and immunofluorescence were used to determine the cell-type- and tumor-type-specific MEG3 expression. Bisulfite treatment and PCR sequencing of genomic DNA were used to measure the CpG methylation status in the normal and tumor tissues. Five normal human pituitaries and 17 clinically nonfunctioning, 11 GH-secreting, seven prolactin-secreting, and six ACTH-secreting pituitary adenomas were used.
Results: All normal human pituitary cell types express MEG3. However, loss of MEG3 expression occurs only in nonfunctioning pituitary adenomas of a gonadotroph origin. All other pituitary tumor phenotypes examined express MEG3. Hypermethylation of the IG-DMR at the DLK1/MEG3 locus is present in nonfunctioning pituitary adenomas.
Conclusions: MEG3 is the first human gene identified expressed in multiple normal human pituitary cell types with loss of expression specifically restricted to clinically nonfunctioning pituitary adenomas. The IG-DMR hypermethylation may be an additional mechanism for MEG3 gene silencing in such tumors.
C1 [Gejman, Roger; Batista, Dalia L.; Zhong, Ying; Zhou, Yunli; Zhang, Xun; Klibanski, Anne] Massachusetts Gen Hosp, Neuroendocrine Unit, Boston, MA 02114 USA.
[Gejman, Roger; Hedley-Whyte, E. Tessa] Massachusetts Gen Hosp, Neuropathol Unit, Boston, MA 02114 USA.
[Swearingen, Brooke] Massachusetts Gen Hosp, Div Neurosurg, Boston, MA 02114 USA.
[Swearingen, Brooke] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Stratakis, Constantine A.] NICHHD, Endocrinol Sect, Bethesda, MD 20892 USA.
[Stratakis, Constantine A.] NICHHD, Genet & Pediat Endocrinol Training Program, Dev Endocrinol Branch, Bethesda, MD 20892 USA.
RP Klibanski, A (reprint author), Massachusetts Gen Hosp, Neuroendocrine Unit, 55 Fruit St,BUL457, Boston, MA 02114 USA.
EM aklibanski@partners.org
FU National Institutes of Health [R01-DK-40947]; The Jarislowsky
Foundation; Pontificia Universidad Catolica de Chile and the Chilean
Government
FX Address all correspondence and requests for reprints to: Anne Klibanski,
M. D., Neuroendocrine Unit, Massachusetts General Hospital, 55 Fruit
Street, BUL457, Boston, Massachusetts 02114. E-mail:
aklibanski@partners.org.; This work was supported by National Institutes
of Health Grant R01-DK-40947, The Jarislowsky Foundation, and
scholarships from Pontificia Universidad Catolica de Chile and the
Chilean Government (R.G.).; Disclosure Statement: B. S. has equity
interests in Pfizer, Roche, and Novartis. E.T.H.-W. has equity interests
in Becton Dickinson. The other authors have nothing to declare.
NR 33
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U2 2
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD OCT
PY 2008
VL 93
IS 10
BP 4119
EP 4125
DI 10.1210/jc.2007-2633
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 358FY
UT WOS:000259903700066
PM 18628527
ER
PT J
AU Morton, LM
AF Morton, Lindsay M.
TI Encouraging participation in medical research: what strategies work?
SO JOURNAL OF CLINICAL EPIDEMIOLOGY
LA English
DT Editorial Material
ID RECRUITMENT STRATEGIES; TRIAL
C1 NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Rockville, MD 20852 USA.
RP Morton, LM (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Execut Blvd,EPS 5100, Rockville, MD 20852 USA.
EM mortonli@mail.nih.gov
RI Morton, Lindsay/B-5234-2015
OI Morton, Lindsay/0000-0001-9767-2310
FU Intramural NIH HHS [Z99 CA999999]
NR 9
TC 6
Z9 6
U1 0
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0895-4356
J9 J CLIN EPIDEMIOL
JI J. Clin. Epidemiol.
PD OCT
PY 2008
VL 61
IS 10
BP 969
EP 970
DI 10.1016/j.jclinepi.2007.09.001
PG 2
WC Health Care Sciences & Services; Public, Environmental & Occupational
Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 350FB
UT WOS:000259336900001
PM 18359193
ER
PT J
AU Cushman, WC
Ford, CE
Einhorn, PT
Wright, JT
Preston, RA
Davis, BR
Basile, JN
Whelton, PK
Weiss, RJ
Bastien, A
Courtney, DL
Hamilton, BP
Kirchner, K
Louis, GT
Retta, TM
Vidt, DG
AF Cushman, William C.
Ford, Charles E.
Einhorn, Paula T.
Wright, Jackson T., Jr.
Preston, Richard A.
Davis, Barry R.
Basile, Jan N.
Whelton, Paul K.
Weiss, Robert J.
Bastien, Arnaud
Courtney, Donald L.
Hamilton, Bruce P.
Kirchner, Kent
Louis, Gail T.
Retta, Tamrat M.
Vidt, Donald G.
CA ALLHAT Collaborat Res Grp
TI Blood Pressure Control by Drug Group in the Antihypertensive and
Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)
SO JOURNAL OF CLINICAL HYPERTENSION
LA English
DT Article
ID JOINT NATIONAL COMMITTEE; HYPERTENSION; OUTCOMES; CHLORTHALIDONE;
MANAGEMENT; RECRUITMENT; POPULATION; CARDIOLOGY; ADULTS
AB Blood pressure (BP) control rates and number of antihypertensive medications were compared (average follow-up, 4.9 years) by randomized groups: chlorthalidone, 12.5-25 mg/d (n=15,255), amlodipine 2.5-10 mg/d (n=9048), or lisinopril 10-40 mg/d (n=9054) in a randomized double-blind hypertension trial. Participants were hypertensives aged 55 or older with additional cardiovascular risk factor(s), recruited from 623 centers. Additional agents from other classes were added as needed to achieve BP control. BP was reduced from 145/83 mm Hg (27% control) to 134/76 mm Hg (chlorthalidone, 68% control), 135/75 mm Hg (amlodipine, 66% control), and 136176 mm Hg (lisinopril, 61% control) by 5 years; the mean number of drugs prescribed was 1.9, 2.0, and 2.1, respectively. Only 28% (chlorthalidone), 24% (amlodipine), and 24% (lisinopril) were controlled on monotherapy. BP control was achieved in the majority of each randomized group-a greater proportion with chlorthalidone. Over time, providers and patients should expect multidrug therapy to achieve BP < 140/90 mm Hg in a majority of patients. J Clin Hypertens (Greenwich). 2008;1.0:751-760. (c) 2008 Le Jacq
C1 [Ford, Charles E.; Davis, Barry R.] Univ Texas Houston, Hlth Sci Ctr, Sch Publ Hlth, Houston, TX 77030 USA.
[Cushman, William C.] Vet Affairs Med Ctr, Memphis, TN USA.
[Einhorn, Paula T.] NHLBI, Bethesda, MD 20892 USA.
[Wright, Jackson T., Jr.] Univ Hosp Cleveland, Gen Clin Res Ctr, Cleveland, OH 44106 USA.
[Preston, Richard A.] Vet Affairs Med Ctr, Miami, FL 33125 USA.
[Basile, Jan N.] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
[Whelton, Paul K.] Loyola Univ, Hlth Syst & Med Ctr, Maywood, IL 60153 USA.
[Weiss, Robert J.] Androscoggin Cardiol Associates, Auburn, ME USA.
[Bastien, Arnaud] Bristol Myers Squibb Co, Princeton, NJ USA.
[Courtney, Donald L.] DD Eisenhower Vet Affairs Med Ctr, Leavenworth, KS USA.
[Hamilton, Bruce P.] Vet Affairs Med Ctr, Baltimore, MD USA.
[Kirchner, Kent] Vet Affairs Med Ctr, Jackson, MS USA.
[Louis, Gail T.] Tulane Univ, Hlth Sci Ctr, New Orleans, LA 70118 USA.
[Retta, Tamrat M.] Howard Univ, Hypertens & Lipid Clin, Washington, DC 20059 USA.
[Vidt, Donald G.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
RP Ford, CE (reprint author), Univ Texas Houston, Hlth Sci Ctr, Sch Publ Hlth, 1200 Hermann Pressler, Houston, TX 77030 USA.
EM charles.e.ford@uth.tmc.edu
FU National Heart, Lung, and Blood Institute [N0.1-HC-35130]; National
Institutes of Health, US Department of Health and Human Services,
Bethesda, MD; AstraZeneca; GlaxoSmithKline; Novartis
FX This research was supported by Health and Human Services contract number
N0.1-HC-35130 from the National Heart, Lung, and Blood Institute,
National Institutes of Health, US Department of Health and Human
Services, Bethesda, MD. The ALLHAT investigators acknowledge
contributions of study medications supplied by Pfizer, Inc (amlodipine),
AstraZeneca (atenolol and lisinopril), and Bristol-Myers Squibb
(pravastatin) and financial support provided by Pfizer, Inc. JNB has
consulted for Novartis and Sankyo and has received honoraria from
AstraZeneca and Pfizer. WCC has consulted for Calpis, King, Myogen,
Novartis, Pfizer, Roche, Sankyo, Sanofi Aventis and Takeda and has
received honoraria from AstraZeneca, Boehringer Ingelheini, Forest
Pharmaceuticals, Novartis, and Sankyo. He has also received research
grants from Abbott 14 Laboratories and Novartis. BRD has consulted for
BioMarin, GlaxoSmithKline, Proctor and Gamble, and Takeda. CEF has
consulted for BioMarin. RAP has received researched grants from Berlex,
Bristol-Myers Squibb, Ferring, Novartis, Schering Plough, Takeda, and
Wyeth and has received honoraria from is Berlex, Ferring, and Pfizer.
DGV has consulted for AstraZeneca, received honoraria from AstraZeneca
and Merck, and has received a research grant from Boehringer Ingelheim.
JTW has consulted for GlaxoSmithKline, Novartis, PfiZer, and
Sanofi-Synthelabo; has received honoraria from GlaxoSmithKline; and has
received research grants from GlaxoSmithKline and Novartis. The rest of
the authors have no financial interests to disclose.
NR 31
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U2 3
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1524-6175
J9 J CLIN HYPERTENS
JI J. Clin. Hypertens.
PD OCT
PY 2008
VL 10
IS 10
BP 751
EP 760
DI 10.1111/j.1751-7176.2008.00015.x
PG 10
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 381XN
UT WOS:000261569300003
PM 19090876
ER
PT J
AU Chun, HJ
Ali, ZA
Kojima, Y
Kundu, RK
Sheikh, AY
Agrawal, R
Zheng, LX
Leeper, NJ
Pearl, NE
Patterson, AJ
Anderson, JP
Tsao, PS
Lenardo, MJ
Ashley, EA
Quertermous, T
AF Chun, Hyung J.
Ali, Ziad A.
Kojima, Yoko
Kundu, Ramendra K.
Sheikh, Ahmad Y.
Agrawal, Rani
Zheng, Lixin
Leeper, Nicholas J.
Pearl, Nathan E.
Patterson, Andrew J.
Anderson, Joshua P.
Tsao, Philip S.
Lenardo, Michael J.
Ashley, Euan A.
Quertermous, Thomas
TI Apelin signaling antagonizes Ang II effects in mouse models of
atherosclerosis
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID ENDOGENOUS PEPTIDE LIGAND; PROTEIN-COUPLED RECEPTORS; VASCULAR
SMOOTH-MUSCLE; APOE-DEFICIENT MICE; ANGIOTENSIN-II; APJ RECEPTOR;
APOLIPOPROTEIN-E; IMMUNOCYTOCHEMICAL LOCALIZATION; CARDIAC
CONTRACTILITY; ENDOTHELIAL-CELLS
AB Apelin and its cognate G protein-coupled receptor APJ constitute a signaling pathway with a positive inotropic effect on cardiac function and a vasodepressor function in the systemic circulation. The apelin-APJ pathway appears to have opposing physiological roles to the renin-angiotensin system. Here we investigated whether the apelin-APJ pathway can directly antagonize vascular disease-related Ang II actions. In ApoE-KO mice, exogenous Ang II induced atherosclerosis and abdominal aortic aneurysm formation; we found that coinfusion of apelin abrogated these effects. Similarly, apelin treatment rescued Ang II-mediated increases in neointimal formation and vascular remodeling in a vein graft model. NO has previously been implicated in the vasodepressor function of apelin; we found that apelin treatment increased NO bioavailability in ApoE-KO mice. Furthermore, infusion of an NO synthase inhibitor blocked the apelin-mediated decrease in atherosclerosis and aneurysm formation. In rat primary aortic smooth muscle cells, apelin inhibited Ang II-mediated transcriptional regulation of multiple targets as measured by reporter assays. In addition, we demonstrated by coimmunoprecipitation and fluorescence resonance energy transfer analysis that the Ang II and apelin receptors interacted physically. Taken together, these findings indicate that apelin signaling can block Ang II actions in vascular disease by increasing NO production and inhibiting Ang II cellular signaling.
C1 [Quertermous, Thomas] Stanford Univ, Sch Med, Div Cardiovasc Med, Dept Med, Stanford, CA 94305 USA.
[Agrawal, Rani; Pearl, Nathan E.; Patterson, Andrew J.] Stanford Univ, Sch Med, Dept Anesthesiol, Stanford, CA 94305 USA.
[Zheng, Lixin; Lenardo, Michael J.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Quertermous, T (reprint author), Stanford Univ, Sch Med, Div Cardiovasc Med, Dept Med, 300 Pasteur Dr, Stanford, CA 94305 USA.
EM tomq1@stanford.edu
RI Chun, Hyung/K-1859-2013
FU NIH [HL077676]; Stanford School of Medicine Dean's Fellowship; Division
of intramural Research; National institute of Allergy and Infectious
Diseases; NIH
FX This work was supported in part by NIH RO1 grant HL077676 (to T.
Quertermous), Stanford School of Medicine Dean's Fellowship (to H.J.
Chun), and Division of intramural Research, National institute of
Allergy and Infectious Diseases, NIH (to M.J. Lenardo and L. Zheng).
NR 55
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U2 5
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 2008
VL 118
IS 10
BP 3343
EP 3354
DI 10.1172/JCI34871
PG 12
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 357EH
UT WOS:000259828600016
PM 18769630
ER
PT J
AU Manches, O
Munn, D
Fallahi, A
Lifson, J
Chaperot, L
Plumas, J
Bhardwaj, N
AF Manches, Olivier
Munn, David
Fallahi, Anahita
Lifson, Jeffrey
Chaperot, Laurence
Plumas, Joel
Bhardwaj, Nina
TI HIV-activated human plasmacytoid DCs induce Tregs through an indoleamine
2,3-dioxygenase-dependent mechanism
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID REGULATORY T-CELLS; IMMUNODEFICIENCY-VIRUS-INFECTION; DRAINING
LYMPH-NODES; DENDRITIC CELLS; TRYPTOPHAN CATABOLISM; TOLL-LIKE;
RETROVIRAL INFECTION; IMMUNE ACTIVATION; VIRAL LOAD; EXPRESSION
AB Plasmacytoid DCs (pDCs) have been implicated as crucial cells in antiviral immune responses. On recognizing HIV, they become activated, secreting large amounts of IFN-alpha and inflammatory cytokines, thereby potentiating innate and adaptive antiviral immune responses. Here, we have shown that HIV-stimulated human pDCs can also induce the differentiation of naive CD4(+)T cells into Tregs with suppressive function. This differentiation was independent of pDC production of IFN-alpha and primarily dependent on pDC expression of indoleamine 2,3-dioxygenase, which was induced through the TLR/MyD88 pathway, following binding of HIV to CD4 and triggering of TLR7 by HIV genomic RNA. Functionally, the Tregs induced by pDCs were shown to inhibit the maturation of bystander conventional DCs. This study therefore reveals what we believe to be a novel mechanism by which pDC may regulate and potentially limit anti-HIV immune responses.
C1 [Manches, Olivier; Fallahi, Anahita; Bhardwaj, Nina] NYU, Inst Canc, New York, NY 10016 USA.
[Munn, David] Med Coll Georgia, Dept Pediat, Inst Mol Med & Genet, Augusta, GA 30912 USA.
[Lifson, Jeffrey] NCI, AIDS Vaccine Program, Sci Applicat Int Corp, Frederick Inc, Frederick, MD 21701 USA.
[Chaperot, Laurence; Plumas, Joel] INSERM, U823, La Tronche, France.
[Chaperot, Laurence; Plumas, Joel] EFS Rhone Alpes, La Tronche, France.
[Chaperot, Laurence; Plumas, Joel] Univ Grenoble 1, Grenoble, France.
RP Bhardwaj, N (reprint author), NYU, Inst Canc, 522 1st Ave, New York, NY 10016 USA.
EM Nina.Bhardwaj@nyumc.org
RI chaperot, laurence/N-2927-2013; Plumas, Joel/N-2516-2013
FU Elizabeth Glaser Pediatric AIDS Foundation; Bill and Melinda Gates
Foundation; Doris Duke Charitable Foundation; Emerald Foundation; Center
for HIV/AIDS Vaccine Initiative [AI067854]; NIH [AI0571278, AI044628,
AI061684]; Cancer Research institute
FX This work was supported by grants from the Elizabeth Glaser Pediatric
AIDS Foundation, the Bill and Melinda Gates Foundation, the Doris Duke
Charitable Foundation, the Emerald Foundation, the Center for HIV/AIDS
Vaccine Initiative (CHAVI; AI067854), and NIH grants AI0571278,
AI044628, and AI061684. O. Manches is a Joan and Robert Arnow Fellow of
the Cancer Research institute. The content of this publication does not
necessarily reflect the views of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organizations imply endorsement by the US government.
NR 49
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U1 2
U2 6
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 2008
VL 118
IS 10
BP 3431
EP 3439
DI 10.1172/JCI34823
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 357EH
UT WOS:000259828600024
PM 18776940
ER
PT J
AU Castle, PE
Porras, C
Quint, WG
Rodriguez, AC
Schiffman, M
Gravitt, PE
Gonzalez, P
Katki, HA
Silva, S
Freer, E
Van Doorn, LJ
Jimenez, S
Herrero, R
Hildesheim, A
AF Castle, Philip E.
Porras, Carolina
Quint, Wim G.
Rodriguez, Ana Cecilia
Schiffman, Mark
Gravitt, Patti E.
Gonzalez, Paula
Katki, Hormuzd A.
Silva, Sandra
Freer, Enrique
Van Doorn, Leen-Jan
Jimenez, Silvia
Herrero, Rolando
Hildesheim, Allan
CA CVT Grp
TI Comparison of two PCR-based human papillomavirus genotyping methods
SO JOURNAL OF CLINICAL MICROBIOLOGY
LA English
DT Article
ID CARCINOGENIC HUMAN-PAPILLOMAVIRUS; INVASIVE CERVICAL-CANCER; HYBRID
CAPTURE 2; LINE BLOT ASSAY; YOUNG-WOMEN; UNDETERMINED SIGNIFICANCE;
QUADRIVALENT VACCINE; UNIVERSITY-STUDENTS; PARTICLE VACCINE;
BROAD-SPECTRUM
AB We compared two consensus primer PCR human papillomavirus (HPV) genotyping methods for the detection of individual HPV genotypes and carcinogenic HPV genotypes as a group, using a stratified sample of enrollment cervical specimens from sexually active women participating in the NCI/Costa Rica HPV16/18 Vaccine Efficacy Trial. For the SPF10 method, DNA was extracted from 0.1% of the cervical specimen by using a MagNA Pure LC instrument, a 65-bp region of the HPV L1 gene was targeted for PCR amplification by using SPF10 primers, and 25 genotypes were detected by reverse-line blot hybridization of the amplicons. For the Linear Array (LA) method, DNA was extracted from 0.5% of the cervical specimen by using an MDx robot, a 450-bp region of the HPV L1 gene was targeted for PCR amplification by using PGMY09/11 L1 primers, and 37 genotypes were detected by reverse-line blot hybridization of the amplicons. Specimens (n = 1,427) for testing by the LA method were randomly selected from strata defined on the basis of enrollment test results from the SPF10 method, cytology, and Hybrid Capture 2. LA results were extrapolated to the trial cohort (n = 5,659). The LA and SPF10 methods detected 21 genotypes in common; HPV16, -18, -31, -33, -35, -39, -45, -51, -52, -56, -58, -59, -66, -68, and -73 were considered the carcinogenic HPV genotypes. There was no difference in the overall results for grouped detection of carcinogenic HPV by the SPF10 and LA methods (35.3% versus 35.9%, respectively; P = 0.5), with a 91.8% overall agreement and a kappa value of 0.82. In comparisons of individual HPV genotypes, the LA method detected significantly more HPV16, HPV18, HPV39, HPV58, HPV59, HPV66, and HPV68/73 and less HPV31 and HPV52 than the SPF10 method; inclusion of genotype-specific testing for HPV16 and HPV18 for those specimens testing positive for HPV by the SPF10 method but for which no individual HPV genotype was detected abrogated any differences between the LA and SPF10 methods. The LA method detected more carcinogenic-HPV-genotype infections per specimen than the SPF10 method (P < 0.001). In conclusion, the LA method and the SPF10 method with HPV16 and HPV18 genotype-specific detection among ungenotyped HPV-positive specimens were comparable for detection of HPV16 and HPV18, the two HPV genotypes targeted by current prophylactic HPV vaccines. Both approaches are suitable for monitoring the impact of HPV16/18 vaccines in clinical trials.
C1 [Castle, Philip E.; Rodriguez, Ana Cecilia; Schiffman, Mark; Katki, Hormuzd A.; Hildesheim, Allan] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Porras, Carolina; Rodriguez, Ana Cecilia; Gonzalez, Paula; Jimenez, Silvia; Herrero, Rolando] Fdn INCIENSA, Proyecto Epidemiol Guanacaste, San Jose, Costa Rica.
[Quint, Wim G.; Van Doorn, Leen-Jan] DDL Diagnost Lab, Voorburg, Netherlands.
[Gravitt, Patti E.] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Gravitt, Patti E.] Johns Hopkins Univ, Dept Mol Microbiol & Immunol, Baltimore, MD USA.
[Silva, Sandra; Freer, Enrique] Univ Costa Rica, San Jose, Costa Rica.
RP Castle, PE (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Room 5004,EPS MSC 7234, Bethesda, MD 20892 USA.
EM castlep@mail.nih.gov
RI Katki, Hormuzd/B-4003-2015; Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU Intramural NIH HHS; NCI NIH HHS [N01CP11005]
NR 37
TC 46
Z9 47
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0095-1137
J9 J CLIN MICROBIOL
JI J. Clin. Microbiol.
PD OCT
PY 2008
VL 46
IS 10
BP 3437
EP 3445
DI 10.1128/JCM.00620-08
PG 9
WC Microbiology
SC Microbiology
GA 356DM
UT WOS:000259758900038
PM 18716224
ER
PT J
AU Gelenberg, AJ
Thase, ME
Meyer, RE
Goodwin, FK
Katz, MM
Kraemer, HC
Potter, WZ
Shelton, RC
Fava, M
Khan, A
Trivedi, MH
Ninan, PT
Mann, JJ
Bergeson, S
Endicott, J
Kocsis, JH
Leon, AC
Manji, HK
Rosenbaum, JF
AF Gelenberg, Alan J.
Thase, Michael E.
Meyer, Roger E.
Goodwin, Frederick K.
Katz, Martin M.
Kraemer, Helena Chmura
Potter, William Z.
Shelton, Richard C.
Fava, Maurizio
Khan, Arif
Trivedi, Madhukar H.
Ninan, Philip T.
Mann, John J.
Bergeson, Susan
Endicott, Jean
Kocsis, James H.
Leon, Andrew C.
Manji, Husseini K.
Rosenbaum, Jerrold F.
TI The History and Current State of Antidepressant Clinical Trial Design: A
Call to Action for Proof-of-Concept Studies
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article; Proceedings Paper
CT Conference on Advancing Signal Strength in Proof of Concept Studies in
Major Depression
CY JUN 21-22, 2007
CL Bethesda, MD
SP Univ Arizona, Dept Psychiat, Best Practice Project Management
ID MAJOR DEPRESSIVE DISORDER; SEROTONIN REUPTAKE INHIBITORS; RESISTANT
RECURRENT DEPRESSION; ANXIOLYTIC-LIKE ACTIVITY; MEASUREMENT-BASED CARE;
HAMILTON RATING-SCALE; ASTERISK-D; ANGER ATTACKS; DRUG RESPONSE;
PLACEBO-RESPONSE
AB Background: The development of new antidepressant drugs has reached a plateau. There is an unmet need for faster, better, and safer medications, but as placebo-response rates rise, effect sizes shrink, and more studies fail or are negative, pharmaceutical companies are increasingly reluctant to invest in new drug development because of the risk of failure. In the absence of an identifiable human pathophysiology that can be modeled in preclinical studies, the principal point of leverage to move beyond the present dilemma may be improving the information gleaned from well-designed proof-of-concept (POC) studies of new antidepressant drugs with novel central nervous system effects. With this in mind, a group of experts was convened under the auspices of the University of Arizona Department of Psychiatry and Best Practice Project Management, Inc.
Participants: Forty-five experts in the study of antidepressant drugs from academia, government (U.S. Food and Drug Administration and National Institute of Mental Health), and industry participated.
Evidence/Consensus Process: In order to define the state of clinical trials methodology in the antidepressant area, and to chart a way forward, a 2-day consensus conference was held June 21-22, 2007, in Bethesda, Md., at which careful reviews of the literature were presented for discussion. Following the presentations, participants were divided into 3 workgroups and asked to address a series of separate questions related to methodology in POC studies. The goals were to review the history of antidepressant drug trials, discuss ways to improve study design and data analysis, and plan more informative POC studies.
Conclusions: The participants concluded that the federal govemment, academic centers, and the pharmaceutical industry need to collaborate on establishing a network of sites at which small, POC studies can be conducted and resulting data can be shared. New technologies to analyze and measure the major affective, cognitive, and behavioral components of depression in relationship to potential biomarkers of response should be incorporated. Standard assessment instruments should be employed across studies to allow for future meta-analyses, but new instruments should be developed to differentiate subtypes and symptom clusters within the disorder that might respond differently to treatment. Better early-stage POC studies are needed and should be able to amplify the signal strength of drug efficacy and enhance the quality of information in clinical trials of new medications with novel pharmacologic profiles. (J Clin Psychiatry 2008;69:1513-1528)
C1 [Gelenberg, Alan J.] Healthcare Technol Syst, Madison, WI 53717 USA.
[Thase, Michael E.] Western Psychiat Inst & Clin, Pittsburgh, PA USA.
[Meyer, Roger E.] Best Practice Project Management Inc, Bethesda, MD USA.
[Goodwin, Frederick K.] George Washington Univ, Med Ctr, Washington, DC 20037 USA.
[Katz, Martin M.] Univ Texas San Antonio, San Antonio, TX USA.
[Kraemer, Helena Chmura] Stanford Univ, Palo Alto, CA 94304 USA.
[Potter, William Z.] Merck & Co Inc, N Wales, PA USA.
[Shelton, Richard C.] Vanderbilt Univ, Med Ctr, Mood Disorders Res Grp, Dept Psychiat, Nashville, TN USA.
[Fava, Maurizio; Rosenbaum, Jerrold F.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Khan, Arif] NW Clin Res Ctr, Bellevue, WA USA.
[Khan, Arif] Duke Univ, Med Ctr, Durham, NC USA.
[Trivedi, Madhukar H.] Univ Texas SW, Sch Med, Dallas, TX USA.
[Ninan, Philip T.] Emory Univ, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA.
[Ninan, Philip T.] Wyeth Pharmaceut, Collegeville, PA USA.
[Mann, John J.] New York State Psychiat Inst & Hosp, Dept Neurosci, New York, NY 10032 USA.
[Bergeson, Susan] Depress & Bipolar Support Alliance, Chicago, IL USA.
[Kocsis, James H.; Leon, Andrew C.] Cornell Univ, Dept Psychiat, Weill Med Coll, New York, NY 10021 USA.
[Manji, Husseini K.] NIMH, Mol Pathophysiol Lab, Bethesda, MD 20892 USA.
RP Gelenberg, AJ (reprint author), Healthcare Technol Syst, 7617 Mineral Point Rd,Suite 300, Madison, WI 53717 USA.
EM agelenberg@Healthtechsys.com
NR 107
TC 55
Z9 56
U1 2
U2 9
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 240008, MEMPHIS, TN 38124 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD OCT
PY 2008
VL 69
IS 10
BP 1513
EP +
PG 16
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 364CD
UT WOS:000260312900001
PM 19192434
ER
PT J
AU Bohl, DL
Brennan, DC
Ryschkewitsch, C
Gaudreault-Keener, M
Major, EO
Storch, GA
AF Bohl, Daniel L.
Brennan, Daniel C.
Ryschkewitsch, Caroline
Gaudreault-Keener, Monique
Major, Eugene O.
Storch, Gregory A.
TI BK virus antibody titers and intensity of infections after renal
transplantation
SO JOURNAL OF CLINICAL VIROLOGY
LA English
DT Article
DE Polyomavirus; BK virus; BK-antibody; BK-viremia; Humoral immunity;
Transplantation; Kidney
ID POLYOMAVIRUS BK; ALLOGRAFT RECIPIENTS; IMMUNE-RESPONSE; JC VIRUS;
NEPHROPATHY; IMMUNOGLOBULIN; REPLICATION; IMPACT
AB Background: The mean urine BK viral load in kidney transplant recipients increases with the intensity of infection as the infection progresses from transient viruria to sustained viremia.
Objectives: This study investigated whether the intensity of infection is associated with the humoral immune response.
Study design: We measured BKV-specific IgG antibody titers in stored samples obtained serially over a 1-year period from 70 kidney transplant recipients with BKV infection and 17 control recipients without active BKV infection.
Results: The mean pre-transplant BKV antibody level was lower in recipients who developed viremia than the mean level in those who never developed viremia (p = 0.004). Mean antibody titers in recipients who never showed evidence of active BKV infection rose slightly after transplant despite immunosuppression. The magnitude of the rise in the mean antibody titers in recipients who developed active BKV infection correlated with the intensity of infection (p < 0.001).
Conclusions: The mean antibody level increased in accordance with the intensity of the infection post-transplant. Pre-transplant seropositivity did not protect against sustained viremia and the antibody response was not associated with clearance of the virus. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Storch, Gregory A.] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA.
[Bohl, Daniel L.; Brennan, Daniel C.; Storch, Gregory A.] Washington Univ, Sch Med, Dept Internal Med, St Louis, MO 63110 USA.
[Ryschkewitsch, Caroline; Major, Eugene O.] NINDS, Lab Mol Med & Neurosci, Bethesda, MD 20892 USA.
[Gaudreault-Keener, Monique] St Louis Childrens Hosp, Virol Lab, St Louis, MO 63110 USA.
RP Storch, GA (reprint author), Washington Univ, Sch Med, Dept Pediat, 660 S Euclid Ave, St Louis, MO 63110 USA.
EM storch@kids.wustl.edu
FU NIH [1 K24-02886]; NKF [22 3062 38053]; 2004 Amgen Renal Fellowship
Award
FX This work was supported in part by NIH 1 K24-02886 (D.C.B.) and NKF 22
3062 38053 (D.L.B.). D.L.B. is a recipient of the 2004 Amgen Renal
Fellowship Award.
NR 22
TC 45
Z9 46
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1386-6532
J9 J CLIN VIROL
JI J. Clin. Virol.
PD OCT
PY 2008
VL 43
IS 2
BP 184
EP 189
DI 10.1016/j.jcv.2008.06.009
PG 6
WC Virology
SC Virology
GA 360QF
UT WOS:000260071700010
PM 18676176
ER
PT J
AU Landry, ML
Eid, T
Bannykh, S
Major, E
AF Landry, Marie L.
Eid, Tore
Bannykh, Serguei
Major, Eugene
TI False negative PCR despite high levels of JC virus DNA in spinal fluid:
Implications for diagnostic testing
SO JOURNAL OF CLINICAL VIROLOGY
LA English
DT Article
DE JC virus; PML; Job's syndrome; Hyper IgE; PCR; Polyomavirus
ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; CEREBROSPINAL-FLUID
AB Genome amplification methods such as polymerase chain reaction (PCR) have revolutionized our ability to detect viruses in spinal fluids of patients with neurologic diseases. It is not as well appreciated among clinicians that PCR protocols, quality assurance, and technical expertise vary significantly among laboratories. In a multi-laboratory blinded study of herpes simplex virus PCR, the most widely used and best validated CSF PCR assay, low-level positives were often missed and false positives were not uncommon [Schloss L, van Loon AM, Cinque P, Cleator G, Echevarria JM, Falk KI, et al. An international external quality assessment of nucleic acid amplification of herpes simplex virus. J Clin Virol 2003;28(2):175-85]. In addition, genome variability and mutations, which are increasingly recognized for a number of different viruses, can lead to falsely low or negative results. Both clinicians and laboratories must recognize the limitations of PCR, since misleading results may have serious consequences.
We present here a case of a rapidly progressive, fatal neurologic illness in a young mother, whose CSFJCV DNA PCR at a reference laboratory was falsely negative. Ultimately, brain biopsy established the diagnosis of progressive multifocal leukoencephalopathy (PML). Repeat PCR testing of the same CSF targeting a different region of the genome yielded a high positive result. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Landry, Marie L.; Eid, Tore] Yale Univ, Sch Med, Dept Lab Med, New Haven, CT 06520 USA.
[Bannykh, Serguei] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA.
[Major, Eugene] NINDS, Bethesda, MD 20892 USA.
RP Landry, ML (reprint author), Yale Univ, Sch Med, Dept Lab Med, POB 208035,333 Cedar St, New Haven, CT 06520 USA.
EM marie.landry@yale.edu
FU Intramural NIH HHS [Z01 NS003049-01]
NR 10
TC 21
Z9 23
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1386-6532
J9 J CLIN VIROL
JI J. Clin. Virol.
PD OCT
PY 2008
VL 43
IS 2
BP 247
EP 249
DI 10.1016/j.jcv.2008.07.003
PG 3
WC Virology
SC Virology
GA 360QF
UT WOS:000260071700025
PM 18701345
ER
PT J
AU Ferrari, V
Codispoti, M
Cardinale, R
Bradley, MM
AF Ferrari, Vera
Codispoti, Maurizio
Cardinale, Rossella
Bradley, Margaret M.
TI Directed and motivated attention during processing of natural scenes
SO JOURNAL OF COGNITIVE NEUROSCIENCE
LA English
DT Article
ID HUMAN VISUAL-SYSTEM; BRAIN POTENTIALS; COGNITIVE MODULATION; SELECTIVE
ATTENTION; DECISION-MAKING; ERP ANALYSIS; CATEGORIZATION; PERCEPTION;
STIMULI; EMOTION
AB Visual attention can be voluntarily oriented to detect target stimuli in order to facilitate goal-directed behaviors. Other visual stimuli capture attention because of motivational significance. The aim of the present study was to investigate the relationship between directed and motivated attention using event-related potentials. Affectively engaging pictures were presented either as target stimuli or as nontargets in a categorization task. Results indicated that both task relevance and emotional significance modulated the late positive potential (LPP) over centro-parietal sensors. Effects of directed and motivated attention on the LPP were additive, with the largest centro-parietal positivity found for emotional pictures that were targets of directed attention, and the least for neutral pictures that were nontargets. Taken together, the data provide new information regarding the relationship between motivated and directed attention, and suggest that the LPP reflects the operation of attentional neural circuits that are utilized by both top down and bottom-up processes.
C1 [Ferrari, Vera] Univ Florida, NIMH, Ctr Study Emot & Attent, Gainesville, FL 32610 USA.
[Codispoti, Maurizio; Cardinale, Rossella] Univ Bologna, I-40126 Bologna, Italy.
RP Ferrari, V (reprint author), Univ Florida, NIMH, Ctr Study Emot & Attent, 2800 SW Archer Rd, Gainesville, FL 32610 USA.
EM vera.ferrari2@unibo.it
RI Codispoti, Maurizio/B-7672-2008
OI Codispoti, Maurizio/0000-0002-7285-4342
NR 59
TC 88
Z9 89
U1 1
U2 19
PU M I T PRESS
PI CAMBRIDGE
PA 238 MAIN STREET, STE 500, CAMBRIDGE, MA 02142-1046 USA
SN 0898-929X
J9 J COGNITIVE NEUROSCI
JI J. Cogn. Neurosci.
PD OCT
PY 2008
VL 20
IS 10
BP 1753
EP 1761
DI 10.1162/jocn.2008.20121
PG 9
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 349RC
UT WOS:000259298100002
PM 18370595
ER
PT J
AU Peercy, BE
AF Peercy, Bradford E.
TI Initiation and propagation of a neuronal intracellular calcium wave
SO JOURNAL OF COMPUTATIONAL NEUROSCIENCE
LA English
DT Article
DE evanescent calcium wave; calcium signaling; mathematical model;
hippocampal CA1 pyramidal cell
ID CA1 PYRAMIDAL NEURONS; BACKPROPAGATING ACTION-POTENTIALS; CA2+ RELEASE;
INOSITOL 1,4,5-TRISPHOSPHATE; SPATIAL SEGREGATION; GENE-REGULATION;
MODEL; DENDRITES; CELLS; ACTIVATION
AB The ability to image calcium movement within individual neurons inspires questions of functionality including whether calcium entry into the nucleus is related to genetic regulation for phenomena such as long term potentiation. Calcium waves have been initiated in hippocampal pyramidal cells with glutmatergic signals both in the presence and absence of back propagating action potentials (BPAPs). The dendritic sites of initiation of these calcium waves within about 100 mu m of the soma are thought to be localized near oblique junctions. Stimulation of synapses on oblique dendrites leads to production of inositol 1,4,5-trisphosphate (IP(3)) which diffuses to the apical dendrite igniting awaiting IP(3) receptors (IP(3)Rs) and initiating and propagating catalytic calcium release from the endoplasmic reticulum. We construct a reduced mathematical system which accounts for calcium wave initiation and propagation due to elevated IP(3). Inhomogeneity in IP(3) distribution is responsible for calcium wave initiation versus subthreshold or spatially uniform suprathreshold activation. However, the likelihood that a calcium wave is initiated does not necessarily increase with more calcium entering from BPAPs. For low transient synaptic stimuli, timing between IP(3) generation and BPAPs is critical for calcium wave initiation. We also show that inhomogeneity in IP(3)R density can account for calcium wave directionality. Simulating somatic muscarinic receptor production of IP(3), we can account for the critical difference between calcium wave entry into the soma and failure to do so.
C1 NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA.
RP Peercy, BE (reprint author), NIDDK, Lab Biol Modeling, NIH, Bldg 12A,Rm 4007,MSC 5621,South Dr, Bethesda, MD 20892 USA.
EM peercyb@mail.nih.gov
FU Intramural NIH HHS
NR 39
TC 6
Z9 6
U1 0
U2 9
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0929-5313
J9 J COMPUT NEUROSCI
JI J. Comput. Neurosci.
PD OCT
PY 2008
VL 25
IS 2
BP 334
EP 348
DI 10.1007/s10827-008-0082-x
PG 15
WC Mathematical & Computational Biology; Neurosciences
SC Mathematical & Computational Biology; Neurosciences & Neurology
GA 343GP
UT WOS:000258841600009
PM 18320300
ER
PT J
AU Kahler, CW
Metrik, J
LaChance, HR
Ramsey, SE
Abrams, DB
Monti, PM
Brown, RA
AF Kahler, Christopher W.
Metrik, Jane
LaChance, Heather R.
Ramsey, Susan E.
Abrams, David B.
Monti, Peter M.
Brown, Richard A.
TI Addressing Heavy Drinking in Smoking Cessation Treatment: A Randomized
Clinical Trial
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
DE smoking; alcohol; brief alcohol intervention; smoking cessation
treatment
ID ALCOHOL-CONSUMPTION; CIGARETTE-SMOKING; QUITTING SMOKING; TOBACCO USE;
TREATMENT-SEEKING; LUNG HEALTH; RELAPSE; SUCCESS; INTERVENTIONS;
CONSEQUENCES
AB Heavy alcohol use frequently co-occurs with cigarette smoking and may impede smoking cessation. This clinical trial examined whether smoking cessation treatment that incorporates brief alcohol intervention can improve smoking cessation outcomes (7-day verified point prevalence abstinence) and reduce drinks consumed per week. Heavy drinkers seeking smoking cessation treatment were assigned by urn randomization to receive, along with 8 weeks of nicotine replacement therapy, either a 4-session standard smoking cessation treatment (ST, n = 119) or standard treatment of equal intensity that incorporated brief alcohol intervention (ST-BI, n = 117). Across follow-ups over 26 weeks, participants in ST-BI reported approximately 20% fewer drinks per week (p < .027) and greater smoking abstinence (adjusted odds ratio = 1.56; 95% confidence interval = 1.01, 2.43) than did those in ST; however, effects on smoking were primarily evident at 2 weeks after quit date and were essentially absent by 16 weeks. The effect of ST-BI on smoking outcome was most robust among moderately heavy drinkers compared with that on very heavy drinkers. Integrating brief alcohol intervention into smoking cessation treatment appears feasible, but further development is needed to yield lasting effects on smoking.
C1 [Kahler, Christopher W.; Metrik, Jane; Monti, Peter M.] Brown Univ, Ctr Alcohol & Addict Studies, Providence, RI 02912 USA.
[LaChance, Heather R.] Natl Jewish Med & Res Ctr, Denver, CO USA.
[Ramsey, Susan E.; Brown, Richard A.] Brown Univ, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Ramsey, Susan E.] Rhode Isl Hosp, Providence, RI 02903 USA.
[Abrams, David B.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Monti, Peter M.] Brown Univ, Providence VA Med Ctr, Providence, RI 02912 USA.
[Brown, Richard A.] Butler Hosp, Providence, RI 02906 USA.
RP Kahler, CW (reprint author), Brown Univ, Ctr Alcohol & Addict Studies, Box G-S121-5, Providence, RI 02912 USA.
EM Christopher_Kahler@brown.edu
FU NIDA NIH HHS [R01 DA15534, R01 DA015534, R01 DA015534-01A1, R01
DA015534-02, R01 DA015534-03, R01 DA015534-04]
NR 56
TC 35
Z9 35
U1 2
U2 5
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD OCT
PY 2008
VL 76
IS 5
BP 852
EP 862
DI 10.1037/a0012717
PG 11
WC Psychology, Clinical
SC Psychology
GA 360PR
UT WOS:000260070300014
PM 18837602
ER
PT J
AU Putnick, DL
Bornstein, MH
Hendricks, C
Painter, KM
Suwalsky, JTD
Collins, WA
AF Putnick, Diane L.
Bornstein, Marc H.
Hendricks, Charlene
Painter, Kathleen M.
Suwalsky, Joan T. D.
Collins, W. Andrew
TI Parenting Stress, Perceived Parenting Behaviors, and Adolescent
Self-Concept in European American Families
SO JOURNAL OF FAMILY PSYCHOLOGY
LA English
DT Article
DE parenting stress; parenting behavior; self-concept; adolescence
ID ACADEMIC-ACHIEVEMENT; SOCIOECONOMIC-STATUS; MIDDLE CHILDHOOD; ESTEEM;
PERCEPTIONS; COMPETENCE; ATTACHMENT; GENDER; RISKS
AB This study assesses whether the stresses associated with parenting a child are indirectly related to adolescent self-concept through parenting behaviors. We examined longitudinal associations among mothers' and fathers' parenting stress at age 10, children's perceptions of parenting at age 10, and adolescents' self-concept at age 14 in 120 European American families. Mothers' and fathers' parenting stress was related to children's perceptions of acceptance and psychologically controlling behavior, and psychologically controlling behavior (and lax control for fathers) was related to adolescent self-concept. We further examined which domains of parenting stress and perceived parenting behaviors were associated with adolescents' scholastic competence, social acceptance, physical appearance, and behavioral conduct. Parenting stress was related to specific parenting behaviors, which were, in turn, related to specific domains of self-concept in adolescence. Parenting stress appears to exert its effects on early adolescent self-concept indirectly through perceived parenting behavior.
C1 [Putnick, Diane L.; Bornstein, Marc H.; Hendricks, Charlene; Painter, Kathleen M.; Suwalsky, Joan T. D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Collins, W. Andrew] Univ Minnesota, Inst Child Dev, Minneapolis, MN 55455 USA.
RP Putnick, DL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv, Suite 8030,6705 Rockledge Dr, Bethesda, MD 20892 USA.
EM putnickd@mail.nih.gov
RI Putnick, Diane/B-1707-2009;
OI Putnick, Diane/0000-0002-6323-749X
FU Intramural NIH HHS [Z99 HD999999]
NR 44
TC 19
Z9 20
U1 3
U2 16
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0893-3200
J9 J FAM PSYCHOL
JI J. Fam. Psychol.
PD OCT
PY 2008
VL 22
IS 5
BP 752
EP 762
DI 10.1037/a0013177
PG 11
WC Psychology, Clinical; Family Studies
SC Psychology; Family Studies
GA 359ZC
UT WOS:000260025800010
PM 18855511
ER
PT J
AU Katon, W
Fan, MY
Unutzer, J
Taylor, J
Pincus, H
Schoenbaum, M
AF Katon, Wayne
Fan, Ming-Yu
Unuetzer, Juergen
Taylor, Jennifer
Pincus, Harold
Schoenbaum, Michael
TI Depression and diabetes: A potentially lethal combination
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE depression; diabetes; mortality
ID CORONARY-HEART-DISEASE; CARDIOVASCULAR-DISEASE; MAJOR DEPRESSION;
RATE-VARIABILITY; MORTALITY; TYPE-2; INFLAMMATION; MEDICATION;
INFARCTION; SYMPTOMS
AB OBJECTIVE: To assess whether Medicare fee-for-service beneficiaries with depression and diabetes had a higher mortality rate over a 2-year period compared with beneficiaries with diabetes alone.
DESIGN: Evidence of depression was based on a physician diagnosis or self-reported prescription of an antidepressant in the year prior to screening, or a score of >= 3 on the Patient Health Questionnaire two-item questionnaire. Mortality was assessed bi-monthly by checking Medicare claims and eligibility files or from information from telephone contact with the participant's family. Cox proportional hazard regression models were used to calculate adjusted hazard ratios of death in depressed versus nondepressed beneficiaries with diabetes.
PARTICIPANTS: A total of 10,704 beneficiaries with diabetes enrolled in a disease management program were surveyed with a health assessment questionnaire and followed over a two-year period.
MAIN RESULTS: Comorbid depression in Medicare beneficiaries with diabetes participating in a disease management program was associated with an increased risk for all-cause mortality over a two-year period of approximately 36% to 38%, depending on the definition of depression that was used. No significant increase in rates of cause-specific mortality from macrovascular disease were found in depressed versus nondepressed beneficiaries.
CONCLUSION: Among a large Medicare cohort of fee-for-service beneficiaries with diabetes, comorbid depression was associated with an increase in all-cause mortality over a two-year period. Future research will be required to determine whether the increase in mortality associated with depression is due to potential behavioral mediators (i.e., smoking, poor adherence to diet) or physiologic abnormalities (i.e., hypothalamic-pituitary axis dysregulation) associated with depression.
C1 [Katon, Wayne; Fan, Ming-Yu; Unuetzer, Juergen] Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Taylor, Jennifer] Green Ribbon Hlth LLC, Tampa, FL USA.
[Pincus, Harold] Columbia Univ, Dept Psychiat, New York, NY USA.
[Pincus, Harold] Columbia Univ, Irving Inst Clin & Translat Res, New York, NY USA.
[Pincus, Harold] RAND Corp, Pittsburgh, PA USA.
[Schoenbaum, Michael] Natl Inst Mental Hlth Epidemiol & Econ, Div Serv & Intervent Res, Bethesda, MD USA.
RP Katon, W (reprint author), Univ Washington, Sch Med, Dept Psychiat & Behav Sci, 1959 NE Pacific St,POB 356560, Seattle, WA 98195 USA.
EM wkaton@u.washington.edu
FU NIMH [MH 0751590, K24 MH 069741]
FX This research has been supported by NIMH grants MH 0751590 (Unutzer,
Principal Investigator), and K24 MH 069741 (Katon, Principal
Investigator).
NR 22
TC 105
Z9 106
U1 4
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD OCT
PY 2008
VL 23
IS 10
BP 1571
EP 1575
DI 10.1007/s11606-008-0731-9
PG 5
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 347LD
UT WOS:000259142200005
PM 18649108
ER
PT J
AU Kirklin, JK
Naftel, DC
Stevenson, LW
Kormos, RL
Pagani, FD
Miller, MA
Ulisney, K
Young, JB
AF Kirklin, James K.
Naftel, David C.
Stevenson, Lynne Warner
Kormos, Robert L.
Pagani, Francis D.
Miller, Marissa A.
Ulisney, Karen
Young, James B.
TI INTERMACS database for durable devices for circulatory support: First
annual report
SO JOURNAL OF HEART AND LUNG TRANSPLANTATION
LA English
DT Article
AB The Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) database, funded by the United States National Heart, Lung and Blood Institute (NHLBI), is a registry for patients who receive durable United States Food and Drug Administration (FDA)-approved mechanical circulatory Support devices (see the Appendix for the list of approved devices) for the treatment of advanced heart failure. This first report will briefly review the background of INTERMACS and report the data analysis for the first 18 months of data collection.
C1 [Kirklin, James K.; Naftel, David C.] Univ Alabama, Birmingham, AL 35294 USA.
[Stevenson, Lynne Warner] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Kormos, Robert L.] Univ Pittsburgh, Pittsburgh, PA USA.
[Pagani, Francis D.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Miller, Marissa A.; Ulisney, Karen] NHLBI, Bethesda, MD 20892 USA.
[Young, James B.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
RP Kirklin, JK (reprint author), Univ Alabama, 1900 Univ Blvd,760 THT, Birmingham, AL 35294 USA.
EM jkirklin@uab.edu
FU National Institutes of Health [HHSN268200548198C]
FX This work was supported by National Institutes of Health Contract No.
HHSN268200548198C.
NR 0
TC 146
Z9 149
U1 1
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1053-2498
J9 J HEART LUNG TRANSPL
JI J. Heart Lung Transplant.
PD OCT
PY 2008
VL 27
IS 10
BP 1065
EP 1072
DI 10.1016/j.healun.2008.07.021
PG 8
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery;
Transplantation
SC Cardiovascular System & Cardiology; Respiratory System; Surgery;
Transplantation
GA 358WI
UT WOS:000259947800001
PM 18926395
ER
PT J
AU Morgan, TR
Lambrecht, RW
Bonkovsky, HL
Chung, RT
Naishadham, D
Sterling, RK
Fontana, RJ
Lee, WM
Ghany, MG
Wright, EC
O'Brien, TR
AF Morgan, Timothy R.
Lambrecht, Richard W.
Bonkovsky, Herbert L.
Chung, Raymond T.
Naishadham, Deepa
Sterling, Richard K.
Fontana, Robert J.
Lee, William M.
Ghany, Marc G.
Wright, Elizabeth C.
O'Brien, Thomas R.
CA HALT C Trial Grp
TI DNA polymorphisms and response to treatment in patients with chronic
hepatitis C: Results from the HALT-C trial
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE hepatitis C; chronic/genetics; polymorphism; genetic;
interferon-alfa/therapeutic use; gene frequency
ID TUMOR-NECROSIS-FACTOR; INTERLEUKIN-10 GENE PROMOTER; VIRUS-INFECTION;
FACTOR-ALPHA; COMBINATION THERAPY; TNF-ALPHA; PEGINTERFERON ALPHA-2A;
INTERFERON-ALPHA; PLUS RIBAVIRIN; LIVER-DISEASE
AB Background/Aims: Certain host genetic polymorphisms reportedly affect the likelihood of a sustained virological response (SVR) to interferon treatment in subjects infected with hepatitis C virus (HCV). As part of the HALT-C trial we evaluated genetic associations among patients infected with HCV genotype 1 who had failed previous interferon treatment.
Methods: SVR was determined 24 weeks after completing treatment with pegylated interferon alfa-2a and ribavirin. Eight single nucleotide polymorphisms (SNPs) were selected on the basis of previously reported associations with treatment response. Genotypes were assessed by polymerase chain reaction-based assays. The percentage of patients who achieved SVR was determined for each genotype and for an IL10 promoter diplotype.
Results: Among 637 non-Hispanic Caucasian patients there were no significant associations between genotype for any individual SNP (IL10-1082, IL10-592, TNF-308, TNF-238, TGFB1 codon 25, CCL2-2518, EPHX1 codon 113 and AGT-6) and SVR, but SVR was more common among the patients who were homozygous for the ACC IL10 promoter diplotype (adjusted odds ratio, 3.24; 95% confidence interval, 1.33-7.78; p = 0.001).
Conclusions: Among non-Hispanic Caucasian patients treated with peginterferon and ribavirin after failing previous treatment with interferon, homozygosity for the ACC IL10 promoter diplotype was associated with SVR. (C) 2008 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Morgan, Timothy R.] Univ Calif Irvine, Div Gastroenterol, Irvine, CA 92717 USA.
[Morgan, Timothy R.] VA Long Beach Healthcare Syst, Gastroenterol Serv, Long Beach, CA USA.
[Lambrecht, Richard W.; Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Med, Farmington, CT USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Med, Farmington, CT USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Mol & Struct Biol, Farmington, CT USA.
[Bonkovsky, Herbert L.] Carolinas Med Ctr, Charlotte, NC 28203 USA.
[Chung, Raymond T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Med Serv, Boston, MA 02114 USA.
[Chung, Raymond T.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Naishadham, Deepa] New England Res Inst, Watertown, MA 02172 USA.
[Sterling, Richard K.] Virginia Commonwealth Univ, Hepatol Sect, Med Ctr, Richmond, VA USA.
[Fontana, Robert J.] Univ Michigan, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Lee, William M.] Univ Texas SW Med Ctr Dallas, Div Digest & Liver Dis, Dallas, TX 75390 USA.
[Ghany, Marc G.] NIDDK, Liver Dis Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Wright, Elizabeth C.] NIDDK, Off Director, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[O'Brien, Thomas R.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
RP Morgan, TR (reprint author), Univ Calif Irvine, Div Gastroenterol, Irvine, CA 92717 USA.
EM timothy.morgan@va.gov
FU Intramural NIH HHS [Z99 CA999999, Z99 DK999999]; NCRR NIH HHS [M01
RR-00043, M01 RR000827, M01 RR001066, M01 RR-00042, M01 RR-00827, M01
RR-00633, M01 RR-06192, M01 RR000065, M01 RR000043, M01 RR-00051, M01
RR-01066, M01 RR006192, M01 RR-00065, M01 RR000051, M01 RR000042, M01
RR000633]; NIDDK NIH HHS [N01-DK-9-2326, N01-DK-9-2324, N01 DK092327,
N01-DK-9-2323, N01DK92327, N01 DK092318, N01-DK-9-2322, N01-DK-9-2327,
N01 DK092326, N01 DK092320, N01-DK-9-2328, N01-DK-9-2320, N01-DK-9-2321,
N01-DK-9-2318, N01-DK-9-2319, N01 DK092319, N01 DK092323, N01 DK092328,
N01 DK092325, N01 DK092324, N01 DK092321, N01-DK-9-2325]
NR 40
TC 34
Z9 35
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD OCT
PY 2008
VL 49
IS 4
BP 548
EP 556
DI 10.1016/j.jhep.2008.05.011
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 358YO
UT WOS:000259953600010
PM 18619701
ER
PT J
AU Paul, WE
AF Paul, William E.
TI Th1 fate determination in CD4(+) T cells: Notice is served of the
importance of IL-12!
SO JOURNAL OF IMMUNOLOGY
LA English
DT Editorial Material
ID INTERFERON-GAMMA; B-CELLS; INTERLEUKIN-4; BET; LEISHMANIASIS;
PURIFICATION; EXPRESSION; DIRECTS
C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20891 USA.
RP Paul, WE (reprint author), NIAID, Immunol Lab, NIH, Bethesda, MD 20891 USA.
EM wpaul@niaid.nih.gov
FU Intramural NIH HHS [Z01 AI000493-21]
NR 16
TC 2
Z9 3
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 OCT 1
PY 2008
VL 181
IS 7
BP 4435
EP 4436
PG 2
WC Immunology
SC Immunology
GA 356CG
UT WOS:000259755700003
PM 18802043
ER
PT J
AU Shimamura, T
Fujisawa, T
Husain, SR
Kioi, M
Nakajima, A
Puri, RK
AF Shimamura, Takeshi
Fujisawa, Toshio
Husain, Syed R.
Kioi, Mitomu
Nakajima, Atsushi
Puri, Rai K.
TI Novel role of IL-13 in fibrosis induced by nonalcoholic steatohepatitis
and its amelioration by IL-13R-directed cytotoxin in a rat model
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID RECEPTOR ALPHA-2 CHAIN; INTERLEUKIN-13 FUSION CYTOTOXIN; FATTY
LIVER-DISEASE; SIGNAL-TRANSDUCTION; HEPATIC-FIBROSIS; MALIGNANT GLIOMA;
TISSUE FIBROSIS; UNITED-STATES; CANCER-CELLS; EXPRESSION
AB Nonalcoholic steatohepatitis (NASH), the most common cause of chronic liver fibrosis, progresses to cirrhosis in up to 20% of patients. We report that hepatic stellate cells (HSC) in sinusoidal lesions of liver of patients with NASH express high levels of high-affinity IL-13R (IL-13R alpha 2), which is colocalized with smooth muscle actin, whereas fatty liver and normal liver specimens do not express IL-13R alpha 2. HSCs engineered to overexpress IL-13R alpha 2 respond to IL-13 and induce TGFBI promoter activity and TGF-beta 1 production. We also developed NASH in rats by feeding a choline-deficient L-amino acid diet. These rats developed liver fibrosis as assessed by H&E staining, Masson's trichrome and Sirius red staining, and hydroxyproline assays. Treatment of these rats with IL-13R-directed cytotoxin caused a substantial decline in fibrosis and liver enzymes without organ toxicity. These studies demonstrate that functional IL-13R alpha 2 are overexpressed in activated HSCs involved in NASH and that IL-13 cytotoxin ameliorates pathological features of NASH in rat liver, indicating a novel role of this cytotoxin in potential therapy.
C1 [Shimamura, Takeshi; Fujisawa, Toshio; Husain, Syed R.; Kioi, Mitomu; Puri, Rai K.] US FDA, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res,NIH, Bethesda, MD 20892 USA.
[Nakajima, Atsushi] Yokohama City Univ, Grad Sch Med, Div Gastroenterol, Yokohama, Kanagawa 232, Japan.
RP Puri, RK (reprint author), US FDA, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res,NIH, Bldg 29B,Room 2NN20 HFM-735,29 Lincoln Dr, Bethesda, MD 20892 USA.
EM raj.puri@fda.hhs.gov
OI Kioi, Mitomu/0000-0002-7981-3340
NR 49
TC 32
Z9 34
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2008
VL 181
IS 7
BP 4656
EP 4665
PG 10
WC Immunology
SC Immunology
GA 356CG
UT WOS:000259755700028
PM 18802068
ER
PT J
AU Grajewski, RS
Hansen, AM
Agarwal, RK
Kronenberg, M
Sidobre, S
Su, SB
Silver, PB
Tsuji, M
Franck, RW
Lawton, AP
Chan, CC
Caspi, RR
AF Grajewski, Rafael S.
Hansen, Anna M.
Agarwal, Rajeev K.
Kronenberg, Mitchell
Sidobre, Stephane
Su, Shao Bo
Silver, Phyllis B.
Tsuji, Moriya
Franck, Richard W.
Lawton, Anne P.
Chan, Chi-Chao
Caspi, Rachel R.
TI Activation of invariant NKT cells ameliorates experimental ocular
autoimmunity by a mechanism involving innate IFN-gamma production and
dampening of the adaptive Th1 and Th17 responses
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID KILLER T-CELLS; RETINOID-BINDING PROTEIN; IMMUNE-PRIVILEGED SITE;
INTERFERON-GAMMA; EFFECTOR RESPONSE; CUTTING EDGE; MICE; UVEITIS;
ENCEPHALOMYELITIS; DISEASE
AB Invariant NKT cells (iNKT cells) have been reported to play a role not only in innate immunity but also to regulate several models of autoimmunity. Furthermore, iNKT cells are necessary for the generation of the prototypic eye-related immune regulatory phenomenon, anterior chamber associated immune deviation (ACAID). In this study, we explore the role of iNKT cells in regulation of autoimmunity to retina, using a model of experimental autoimmune uveitis (EAU) in mice immunized with a uveitogenic regimen of the retinal Ag, interphotoreceptor retinoid-binding protein. Natural strain-specific variation in iNKT number or induced genetic deficiencies in iNKT did not alter baseline susceptibility to EAU. However, iNKT function seemed to correlate with susceptibility and its pharmacological enhancement in vivo by treatment with iNKT TCR ligands at the time of uveitogenic immunization reproducibly ameliorated disease scores. Use of different iNKT TCR ligands revealed dependence on the elicited cytokine profile. Surprisingly, superior protection against EAU was achieved with a-C-GalCer, which induces a strong IFN-gamma but only a weak IL-4 production by iNKT cells, in contrast to the ligands alpha-GalCer (both IFN-gamma and IL-4) and OCH (primarily IL-4). The protective effect of alpha-C-GalCer was associated with a reduction of adaptive Ag-specific IFN-gamma and IL-17 production and was negated by systemic neutralization of IFN-gamma. These data suggest that pharmacological activation of iNKT cells protects from EAU at least in part by a mechanism involving innate production of IFN-gamma and a consequent dampening of the Th1 as well as the Th17 effector responses.
C1 [Grajewski, Rafael S.; Hansen, Anna M.; Agarwal, Rajeev K.; Su, Shao Bo; Silver, Phyllis B.; Chan, Chi-Chao; Caspi, Rachel R.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Kronenberg, Mitchell; Sidobre, Stephane; Lawton, Anne P.] La Jolla Inst Allergy & Immunol, La Jolla, CA 92037 USA.
[Tsuji, Moriya] Rockefeller Univ, Aaron Diamond AIDS Res Ctr, New York, NY 10016 USA.
[Franck, Richard W.] CUNY Hunter Coll, New York, NY 10021 USA.
RP Caspi, RR (reprint author), NEI, Immunol Lab, NIH, 10 Ctr Dr,10-10N222, Bethesda, MD 20892 USA.
EM rcaspi@helix.nih.gov
FU National Institutes of Health
FX This work was supported by National Institutes of Health Intramural
funding.
NR 37
TC 39
Z9 43
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 OCT 1
PY 2008
VL 181
IS 7
BP 4791
EP 4797
PG 7
WC Immunology
SC Immunology
GA 356CG
UT WOS:000259755700042
PM 18802082
ER
PT J
AU Rada, B
Lekstrom, K
Damian, S
Dupuy, C
Leto, TL
AF Rada, Balazs
Lekstrom, Kristen
Damian, Sorin
Dupuy, Corinne
Leto, Thomas L.
TI The Pseudomonas toxin pyocyanin inhibits the dual oxidase-based
antimicrobial system as it imposes oxidative stress on airway epithelial
cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID NEUTROPHIL MYELOPEROXIDASE SYSTEM; CYSTIC-FIBROSIS; HYDROGEN-PEROXIDE;
HOST-DEFENSE; NADPH OXIDASE; AERUGINOSA; LACTOPEROXIDASE;
HYPOTHIOCYANITE; INACTIVATION; TRANSPORT
AB The dual oxidase-thiocyanate-lactoperoxidase (Duox/SCN-/LPO) system generates the microbicidal oxidant hypothiocyanite in the airway surface liquid by using LPO, thiocyanate, and Duox-derived hydrogen peroxide released from the apical surface of the airway epithelium. This system is effective against several microorganisms that infect airways of cystic fibrosis and other immunocompromised patients. We show herein that exposure of airway epithelial cells to Pseudomonas aeruginosa obtained from long-term cultures inhibits Duox1-dependent hydrogen peroxide release, suggesting that some microbial factor suppresses Duox activity. These inhibitory effects are not seen with the pyocyanin-deficient P. aeruginosa strain PA14 Phz1/2. We show that purified pyocyanin, a redox-active virulence factor produced by P. aeruginosa, inhibits human airway cell Duox activity by depleting intracellular stores of NADPH, as it generates intracellular superoxide. Long-term exposure of human airway (primary normal human bronchial and NCI-H292) cells to pyocyanin also blocks induction of Duox1 by Th2 cytokines (IL-4, IL-13), which was prevented by the antioxidants glutathione and N-acetyleysteine. Furthermore, we showed that low concentrations of pyocyanin blocked killing of wild-type P. aeruginosa by the Duox/SCN-/LPO system on primary normal human bronchial epithelia] cells. Thus, pyocyanin can subvert Pseudomonas killing by the Duox-based system as it imposes oxidative stress on the host. We also show that lactoperoxidase can oxidize pyocyanin, thereby diminishing its cytotoxicity. These data establish a novel role for pyocyanin in the survival of P. aeruginosa in human airways through competitive redox-based reactions between the pathogen and host.
C1 [Rada, Balazs; Lekstrom, Kristen; Leto, Thomas L.] NIAID, NIH, Host Def Lab, Rockville, MD 20852 USA.
[Damian, Sorin] Lonza Walkersville, Walkersville, MD 21793 USA.
[Dupuy, Corinne] Univ Paris 11, Orsay, France.
[Dupuy, Corinne] CNRS, FRE 2939, Villejuif, France.
[Dupuy, Corinne] Inst Gustave Roussy, Villejuif, France.
RP Leto, TL (reprint author), NIAID, NIH, 12441 Parklawn Dr, Bethesda, MD 20892 USA.
EM tleto@nih.gov
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases
FX This work was supported by funding through the Intramural Research
Program of the National Institutes of Health, National Institute of
Allergy and Infectious Diseases.
NR 42
TC 56
Z9 58
U1 2
U2 11
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2008
VL 181
IS 7
BP 4883
EP 4893
PG 11
WC Immunology
SC Immunology
GA 356CG
UT WOS:000259755700052
PM 18802092
ER
PT J
AU Li, ZQ
Liu, BY
Maminishkis, A
Mahesh, SP
Yeh, S
Lew, J
Lim, WK
Sen, HN
Clarke, G
Buggage, R
Miller, SS
Nussenblatt, RB
AF Li, Zhuqing
Liu, Baoying
Maminishkis, Arvydas
Mahesh, Sankaranarayana P.
Yeh, Steven
Lew, Julie
Lim, Wee Kiak
Sen, H. Nida
Clarke, Grace
Buggage, Ronald
Miller, Sheldon S.
Nussenblatt, Robert B.
TI Gene expression profiling in autoimmune noninfectious uveitis disease
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID B-CELL LYMPHOMA; T-CELLS; TH17 CELLS; S-ANTIGEN; INFLAMMATION; DISTINCT;
MODEL; SUSCEPTIBILITY; CYCLOSPORINE; MECHANISMS
AB Noninfectious uveitis is a predominantly T cell-mediated autoimmune, intraocular inflammatory disease. To characterize the gene expression profile from patients with noninfectious uveitis, PBMCs were isolated from 50 patients with clinically characterized noninfectious uveitis syndrome. A pathway-specific cDNA microarray was used for gene expression profiling and real-time PCR array for further confirmation. Sixty-seven inflammation- and autoimmune-associated genes were found differentially expressed in uveitis patients, with 28 of those genes being validated by real-time PCR. Several genes previously unknown for autoimmune uveitis, including IL-22, IL-19, 11,20, and IL-25/IL-17E, were found to be highly expressed among uveitis patients compared with the normal subjects with IL-22 expression highly variable among the patients. Furthermore, we show that IL-22 can affect primary human retinal pigment epithelial cells by decreasing total tissue resistance and inducing apoptosis possibly by decreasing phospho-Bad level. In addition, the microarray data identified a possible uveitis-associated gene expression pattern, showed distinct gene expression profiles in patients during periods of clinical activity and quiescence, and demonstrated similar expression patterns in related patients with similar clinical phenotypes. Our data provide the first evidence that a subset of IL-10 family genes are implicated in noninfectious uveitis and that IL-22 can affect human retinal pigment epithelial cells. The results may facilitate further understanding of the molecular mechanisms of autoimmune uveitis and other autoimmune originated inflammatory diseases.
C1 [Li, Zhuqing; Liu, Baoying; Mahesh, Sankaranarayana P.; Yeh, Steven; Lew, Julie; Lim, Wee Kiak; Sen, H. Nida; Clarke, Grace; Buggage, Ronald; Nussenblatt, Robert B.] NEI, Immunol Lab, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Maminishkis, Arvydas; Miller, Sheldon S.] NEI, Sect Epithelial & Retinal Physiol & Dis, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Lim, Wee Kiak] Singapore Natl Eye Ctr, Singapore, Singapore.
RP Nussenblatt, RB (reprint author), NEI, Immunol Lab, Natl Inst Hlth, Bldg 10,Room 10N112,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM DrBob@nei.nih.gov
FU Intramural NIH HHS [Z99 AI999999, Z01 EY000376-07, Z01 EY000356-07, Z01
EY000393-06]
NR 43
TC 40
Z9 46
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2008
VL 181
IS 7
BP 5147
EP 5157
PG 11
WC Immunology
SC Immunology
GA 356CG
UT WOS:000259755700079
PM 18802119
ER
PT J
AU Tran, KQ
Zhou, JH
Durflinger, KH
Langhan, MM
Shelton, TE
Wunderlich, JR
Robbins, PF
Rosenberg, SA
Dudley, ME
AF Tran, Khoi Q.
Zhou, Juhua
Durflinger, Katherine H.
Langhan, Michelle M.
Shelton, Thomas E.
Wunderlich, John R.
Robbins, Paul F.
Rosenberg, Steven A.
Dudley, Mark E.
TI Minimally cultured tumor-infiltrating lymphocytes display optimal
characteristics for adoptive cell therapy
SO JOURNAL OF IMMUNOTHERAPY
LA English
DT Article
DE tumor-infiltrating lymphocyte; adoptive cell therapy; melanoma;
telomere; interleukin-2
ID CD8(+) T-CELLS; IN-VIVO PERSISTENCE; METASTATIC MELANOMA; CANCER
REGRESSION; CD8-T-CELL MEMORY; TELOMERE LENGTH; CD4-T-CELL HELP;
PHASE-I; INTERLEUKIN-2; IMMUNOTHERAPY
AB Adoptive cell therapy (ACT) with tumor-reactive lymphocytes in patients with refractory melanoma can result in tumor regression and prolonged survival. Generating tumor-reactive lymphocyte cultures is technically difficult and resource intensive; these limitations have restricted the widespread application of ACT. Tumor-infiltrating lymphocytes (TIL) from melanoma contain tumor antigen-reactive cells. The "standard" method for producing TIL cultures for clinical administration requires extended in vitro expansion in interleukin-2, then identification of tumor-reactive cells by immunologic assays. We show here that limitations in reagents and methods during screening underrepresent the actual reactivity of TIL cultures. Furthermore, the extended culture times necessitated by the screening assays resulted in telomere shortening and reduced expression of CD27 and CD28 in the TIL cultures, properties that our prior studies showed are correlated with in vivo persistence and clinical response. We have thus developed an alternative "young" TIL method that demonstrated superior in vitro attributes compared with standard TIL. This approach uses the entire resected tumor to rapidly expand TIL for administration without in vitro testing for tumor recognition. Our observations suggest that Younger TIL can have an undetermined but high level of antigen reactivity, and other advantageous attributes such as long telomeres and high levels of CD27 and CD28. We suggest that minimally cultured, unselected lymphocytes represent an alternative strategy for generating TIL cultures Suitable for use in ACT that, if effective in vivo, may facilitate the widespread application of this approach to a broader population of patients with melanoma.
C1 [Tran, Khoi Q.; Durflinger, Katherine H.; Langhan, Michelle M.; Wunderlich, John R.; Robbins, Paul F.; Rosenberg, Steven A.; Dudley, Mark E.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Zhou, Juhua] Univ S Carolina, Sch Med, Dept Pathol, Columbia, SC 29208 USA.
RP Dudley, ME (reprint author), NCI, Surg Branch, NIH, CRC 3W-5752,10 Ctr Dr, Bethesda, MD 20892 USA.
EM Mark_Dudley@nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 30
TC 113
Z9 116
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1524-9557
J9 J IMMUNOTHER
JI J. Immunother.
PD OCT
PY 2008
VL 31
IS 8
BP 742
EP 751
DI 10.1097/CJI.0b013e31818403d5
PG 10
WC Oncology; Immunology; Medicine, Research & Experimental
SC Oncology; Immunology; Research & Experimental Medicine
GA 352ND
UT WOS:000259503000007
PM 18779745
ER
PT J
AU Morens, DM
Taubenberger, JK
Fauci, AS
AF Morens, David M.
Taubenberger, Jeffery K.
Fauci, Anthony S.
TI Predominant role of bacterial pneumonia as a cause of death in pandemic
influenza: Implications for pandemic influenza preparedness
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the American-Epidemiological-Society
CY MAR 26, 2007
CL Boston, MA
SP Amer Epidemiol Soc
ID ASIAN INFLUENZA; RESPIRATORY-TRACT; A VIRUS; X-RAY; EPIDEMIC; INFECTION;
PATHOLOGY; COMPLICATIONS; PNEUMOCOCCUS; EXPRESSION
AB Background. Despite the availability of published data on 4 pandemics that have occurred over the past 120 years, there is little modern information on the causes of death associated with influenza pandemics.
Methods. We examined relevant information from the most recent influenza pandemic that occurred during the era prior to the use of antibiotics, the 1918 - 1919 "Spanish flu" pandemic. We examined lung tissue sections obtained during 58 autopsies and reviewed pathologic and bacteriologic data from 109 published autopsy series that described 8398 individual autopsy investigations.
Results. The postmortem samples we examined from people who died of influenza during 1918 - 1919 uniformly exhibited severe changes indicative of bacterial pneumonia. Bacteriologic and histopathologic results from published autopsy series clearly and consistently implicated secondary bacterial pneumonia caused by common upper respiratory - tract bacteria in most influenza fatalities.
Conclusions. The majority of deaths in the 1918 - 1919 influenza pandemic likely resulted directly from secondary bacterial pneumonia caused by common upper respiratory - tract bacteria. Less substantial data from the subsequent 1957 and 1968 pandemics are consistent with these findings. If severe pandemic influenza is largely a problem of viral-bacterial copathogenesis, pandemic planning needs to go beyond addressing the viral cause alone (e. g., influenza vaccines and antiviral drugs). Prevention, diagnosis, prophylaxis, and treatment of secondary bacterial pneumonia, as well as stockpiling of antibiotics and bacterial vaccines, should also be high priorities for pandemic planning.
C1 [Morens, David M.; Taubenberger, Jeffery K.; Fauci, Anthony S.] NIAID, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Morens, DM (reprint author), NIAID, Natl Inst Hlth, Bldg 31,Room 7A-10,31 Ctr Dr,MSC 2520, Bethesda, MD 20892 USA.
EM dmorens@niaid.nih.gov
FU Intramural NIH HHS [Z99 AI999999]
NR 102
TC 534
Z9 570
U1 11
U2 48
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD OCT 1
PY 2008
VL 198
IS 7
BP 962
EP 970
DI 10.1086/591708
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 345EO
UT WOS:000258979100003
PM 18710327
ER
PT J
AU Ibrahim, AS
Gebremariam, T
Liu, MF
Chamilos, G
Kontoyiannis, DP
Mink, R
Kwon-Chung, KJ
Fu, Y
Skory, CD
Edwards, JE
Spellberg, B
AF Ibrahim, Ashraf S.
Gebremariam, Teclegiorgis
Liu, Mingfu
Chamilos, Georgios
Kontoyiannis, Dimitrios P.
Mink, Richard
Kwon-Chung, Kyung J.
Fu, Yue
Skory, Christopher D.
Edwards, John E., Jr.
Spellberg, Brad
TI Bacterial endosymbiosis is widely present among Zygomycetes but does not
contribute to the pathogenesis of mucormycosis
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article; Proceedings Paper
CT 47th Interscience Conference on Antimicrobial Agents and Chemotherapy
CY SEP 17-20, 2007
CL Chicago, IL
ID MACROCYCLIC LACTONE ANTIBIOTICS; TRANSPLANT RECIPIENTS;
RHIZOPUS-MICROSPORUS; RHIZOXIN; ZYGOMYCOSIS; CELLS; EPIDEMIOLOGY;
INFECTIONS; METABOLITE; ORYZAE
AB Environmental isolates of the fungus Rhizopus have been shown to harbor a bacterial endosymbiont (Burkholderia) that produces rhixozin, a plant mycotoxin. We sought to define the role of rhizoxin production by endosym-bionts in the pathogenesis of mucormycosis. Endosymbiotic bacteria were identified by polymerase chain reaction in 15 (54%) of 28 clinical isolates of Zygomycetes, with 33% of the bacterial strains showing >= 87% identity to Burkholderia 16S rDNA. The presence of rhizoxin in myclial extracts from fungi harboring bacteria was confirmed by high-performance liquid chromatography analysis. However, fungal strains with or without endosym-bionts did not differ in their ability to cause endothelial cell injury in vitro, nor did antibiotic-mediated eradication of endosymbionts and rhizoxin production decrease the virulence of fungal strains in mice or flies. In summary, although bacterial endosymbiosis is widely detected in clinical isolates of Zygomycetes, including Rhizopus oryzae strains, we found no evidence that bacterial endosymbionts and rhizoxin contribute to the pathogenesis of mucormycosis in the models studied.
C1 [Ibrahim, Ashraf S.; Gebremariam, Teclegiorgis; Liu, Mingfu; Fu, Yue; Edwards, John E., Jr.; Spellberg, Brad] Univ Calif Los Angeles, Med Ctr, Div Infect Dis, Los Angeles Biomed Res Inst Harbor, Torrance, CA 90502 USA.
[Mink, Richard] Univ Calif Los Angeles, Med Ctr, Div Pediat Crit Care Med, Los Angeles Biomed Res Inst Harbor, Torrance, CA 90502 USA.
[Ibrahim, Ashraf S.; Mink, Richard; Fu, Yue; Edwards, John E., Jr.; Spellberg, Brad] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Chamilos, Georgios; Kontoyiannis, Dimitrios P.] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Kwon-Chung, Kyung J.] Natl Inst Hlth, Bethesda, MD USA.
[Skory, Christopher D.] USDA, Peoria, IL USA.
RP Ibrahim, AS (reprint author), Univ Calif Los Angeles, Med Ctr, Div Infect Dis, Los Angeles Biomed Res Inst Harbor, 1124 W Carson St, Torrance, CA 90502 USA.
EM ibrahim@labiomed.org
RI a, a/M-9467-2013
FU Intramural NIH HHS [Z01 AI000657-16]; NIAID NIH HHS [R21 AI064716, R01
AI063503, K08 AI060641]
NR 30
TC 17
Z9 17
U1 0
U2 10
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD OCT 1
PY 2008
VL 198
IS 7
BP 1083
EP 1090
DI 10.1086/591461
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 345EO
UT WOS:000258979100019
PM 18694335
ER
PT J
AU Gahl, WA
AF Gahl, W. A.
TI Chemical individuality: Concept and outlook
SO JOURNAL OF INHERITED METABOLIC DISEASE
LA English
DT Article; Proceedings Paper
CT Annual Symposium of the
Society-for-the-Study-of-Inborn-Errors-of-Metabolism
CY SEP 02-05, 2008
CL Lisbon, PORTUGAL
SP Soc Study Inborn Errors Metabolism
ID ACETYLGLUCOSAMINE 2-EPIMERASE/N-ACETYLMANNOSAMINE KINASE;
CHEDIAK-HIGASHI-SYNDROME; NEPHROPATHIC CYSTINOSIS; NATURAL-HISTORY;
CYSTEAMINE THERAPY; ACID BIOSYNTHESIS; CORNEAL CRYSTALS; CTNS MUTATIONS;
ALKAPTONURIA; TRANSPORT
AB Sir Archibald Garrod's concept of chemical individuality introduced a century ago provided the basis for the entire discipline of inborn errors of metabolism. Human disorders are defined by variation in disease-causing mutations, environmental influences, genetic factors other than the primary genetic defect, and evolution itself. Myriad examples support the prescience of Garrod with respect to these issues, each of which has therapeutic implications. Just as Garrod predicted that the future of biochemical genetics would be intertwined with the concept of chemical variability, we might forecast that variation will influence emotions, dreams, and the human thinking process itself.
C1 NHGRI, Sect Human Biochem Genet, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
RP Gahl, WA (reprint author), NHGRI, Sect Human Biochem Genet, Med Genet Branch, NIH, 10 Ctr Dr,MSC 1851,Bldg 10,Room 10C-103, Bethesda, MD 20892 USA.
EM bgahl@helix.nih.gov
FU Intramural NIH HHS
NR 38
TC 2
Z9 2
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0141-8955
J9 J INHERIT METAB DIS
JI J. Inherit. Metab. Dis.
PD OCT
PY 2008
VL 31
IS 5
BP 630
EP 640
DI 10.1007/s10545-008-0995-6
PG 11
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 369AD
UT WOS:000260664000008
PM 18836888
ER
PT J
AU Zaidi, MR
Day, CP
Merlino, G
AF Zaidi, M. Raza
Day, Chi-Ping
Merlino, Glenn
TI From UVs to metastases: Modeling melanoma initiation and progression in
the mouse
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Article
ID STEM-CELL FACTOR; CUTANEOUS MELANOMA; MALIGNANT-MELANOMA;
ULTRAVIOLET-RADIATION; GENE-EXPRESSION; HUMAN SKIN; PROMOTER
HYPERMETHYLATION; MOLECULAR-MECHANISMS; ANTITUMOR IMMUNITY; DNA
METHYLATION
AB Cutaneous malignant melanoma is highly invasive and capable of metastasizing to distant sites where it is typically resistant to available therapy. While striving to prevent or eradicate melanoma, researchers have two significant advantages not shared by those working on many other cancers. The main environmental etiological agent, UV radiation, is known and melanocytic lesions are excisable for molecular analysis from most stages. Yet knowledge about how UV initiates melanoma has been insufficient to achieve prevention, and the understanding of metastatic mechanisms has been inadequate to reduce mortality. Here, we review the value of melanoma mouse models, focusing on these critical early and late stages.
C1 [Zaidi, M. Raza; Day, Chi-Ping; Merlino, Glenn] NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Merlino, G (reprint author), NCI, Chief Lab Canc Biol & Genet, NIH, 9000 Rockville Pike,Bldg 37,Room 5002, Bethesda, MD 20892 USA.
EM gmerlino@helix.nih.gov
RI Zaidi, M. Raza/H-1386-2016
OI Zaidi, M. Raza/0000-0003-0480-3188
NR 78
TC 25
Z9 26
U1 0
U2 11
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD OCT
PY 2008
VL 128
IS 10
BP 2381
EP 2391
DI 10.1038/jid.2008.177
PG 11
WC Dermatology
SC Dermatology
GA 348RW
UT WOS:000259228600006
PM 18787547
ER
PT J
AU Fargnoli, MC
Pike, K
Pfeiffer, RM
Tsang, S
Rozenblum, E
Munroe, DJ
Golubeva, Y
Calista, D
Seidenari, S
Massi, D
Carli, P
Bauer, J
Elder, DE
Bastian, BC
Peris, K
Landi, MT
AF Fargnoli, Maria Concetta
Pike, Kris
Pfeiffer, Ruth M.
Tsang, Shirley
Rozenblum, Ester
Munroe, David J.
Golubeva, Yelena
Calista, Donato
Seidenari, Stefania
Massi, Daniela
Carli, Paolo
Bauer, Juergen
Elder, David E.
Bastian, Boris C.
Peris, Ketty
Landi, Maria T.
TI MC1R variants increase risk of melanomas harboring BRAF mutations
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Article
ID MELANOCORTIN-1 RECEPTOR MC1R; CUTANEOUS MELANOMA; GENE VARIANTS;
MEDITERRANEAN POPULATION; FAMILIAL MELANOMA; DNA-REPAIR; PHENOTYPE;
POLYMORPHISMS; ASSOCIATION; CANCER
AB Melanocortin-1 receptor (MC1R) variants have been associated with BRAF(v-raf murine sarcoma viral oncogene homolog B1) mutations in non-CSD (chronic solar-damaged) melanomas in an Italian and an American population. We studied an independent Italian population of 330 subjects (165 melanoma patients and 165 controls) to verify and estimate the magnitude of this association and to explore possible effect modifiers. We sequenced MC1R in all subjects and exon 15 of BRAF in 92/165 melanoma patients. Patients with MC1R variants had a high risk of carrying BRAF mutations in melanomas (odds ratio (OR) = 7.0, 95% confidence interval (CI) = 2.1-23.8) that increased with the number of MC1R variants and variants associated with red hair color. Combining these subjects with the originally reported Italian population (513 subjects overall), MC1R variant carriers had a 5- to 15-fold increased risk of BRAF-mutant melanomas based on carrying one or two variants (P < 0.0001, test for trend), and regardless of signs of chronic solar damage. In contrast, no association with BRAF-negative melanomas was found (OR = 1.0, 95% CI = 0.6-1.6). No characteristics of subjects or melanomas, including age, nevus count, pigmentation, and melanoma thickness or location on chronically or intermittently sun-exposed body sites, substantially modified this association, although results could be affected by the small numbers in some categories. This study confirms that the known MC1R-melanoma risk association is confined to subjects whose melanomas harbor BRAF mutations.
C1 [Landi, Maria T.] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Fargnoli, Maria Concetta; Peris, Ketty] Univ Aquila, Dept Dermatol, I-67100 Laquila, Italy.
[Pike, Kris; Tsang, Shirley; Rozenblum, Ester; Munroe, David J.] SAIC Frederick Inc, NCI Frederick, Adv Technol Program, Lab Mol Technol, Frederick, MD USA.
[Golubeva, Yelena] SAIC Frederick Inc, NCI Frederick, Pathol Histotechnol Lab, Frederick, MD USA.
[Calista, Donato] Bufalini Hosp, Dept Dermatol, Cesena, Italy.
[Seidenari, Stefania] Univ Modena & Reggio Emilia, Dept Dermatol, Modena, Italy.
[Massi, Daniela] Univ Florence, Dept Human Pathol & Oncol, Florence, Italy.
[Carli, Paolo] Univ Florence, Dept Dermatol, Florence, Italy.
[Bauer, Juergen; Bastian, Boris C.] Univ Calif San Francisco, Dept Pathol, San Francisco, CA USA.
[Elder, David E.] Univ Penn, Dept Pathol, Philadelphia, PA 19104 USA.
RP Landi, MT (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS 7114, Bethesda, MD 20892 USA.
EM landim@mail.nih.gov
RI Pfeiffer, Ruth /F-4748-2011; Bauer, Jurgen/B-4656-2008;
OI Bauer, Jurgen/0000-0001-8789-1536; Peris, Ketty/0000-0002-5237-0463;
Fargnoli, Maria Concetta/0000-0002-7249-2556
FU talian Ministry of University and Scientific Research [2001068929_004];
National Institutes of Health, National Cancer Institute, Division of
Cancer Epidemiology and Genetics [01-CO-12400]
FX This study was supported by the Italian Ministry of University and
Scientific Research (2001068929_004); the Intramural Research Program of
National Institutes of Health, National Cancer Institute, Division of
Cancer Epidemiology and Genetics; and the National Cancer Institute,
National Institutes of Health (contract no. 01-CO-12400).
NR 19
TC 50
Z9 50
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD OCT
PY 2008
VL 128
IS 10
BP 2485
EP 2490
DI 10.1038/jid.2008.67
PG 6
WC Dermatology
SC Dermatology
GA 348RW
UT WOS:000259228600017
PM 18368129
ER
PT J
AU Tait, AS
Butts, CL
Sternberg, EM
AF Tait, A. Sasha
Butts, Cherie L.
Sternberg, Esther M.
TI The role of glucocorticoids and progestins in inflammatory, autoimmune,
and infectious disease
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article; Proceedings Paper
CT Pennington Scientific Symposium on Neuro-Immune Signaling and
Inflammation
CY DEC 02-05, 2007
CL Baton Rouge, LA
DE progesterone; polymorphism; inflammation
ID RECEPTOR-BETA-ISOFORM; PITUITARY-ADRENAL AXIS;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; ANTHRAX LETHAL TOXIN; BODY-MASS INDEX;
PROGESTERONE-RECEPTOR; IN-VIVO; RHEUMATOID-ARTHRITIS; DENDRITIC CELLS;
CLOSTRIDIUM-SORDELLII
AB A bidirectional communication exists between the CNS and the immune system. The autonomic nervous system, through neurotransmitters and neuropeptides, works in parallel with the hypothalamic-pituitary-adrenal axis through the actions of glucocorticoids to modulate inflammatory events. The immune system, through the action of cytokines and other factors, in turn, activates the CNS to orchestrate negative-feedback mechanisms that keep the immune response in check. Disruption of these interactions has been associated with a number of syndromes including inflammatory, autoimmune, and cardiovascular diseases, metabolic and psychiatric disorders, and the development of shock. The hypothalamic-pituitary-gonadal axis also plays an important part in regulating immunity through the secretion of sex hormones. Although numerous studies have established a role for immunomodulation by estrogen and testosterone, the role of progesterone is less well understood. Progesterone is crucial for reproductive organ development and maintenance of pregnancy, and more recent studies have clearly shown its role as an important immune regulator. The main focus of this review will be about the role of steroid hormones, specifically glucocorticoids and progesterone, in inflammatory responses and infectious diseases and how dysregulation of their actions may contribute to development of autoimmune and inflammatory disease.
C1 [Tait, A. Sasha; Butts, Cherie L.; Sternberg, Esther M.] NIMH, Sect Neuroendocrine Immunol & Behav, NIH, Rockville, MD 20852 USA.
RP Sternberg, EM (reprint author), NIMH, Sect Neuroendocrine Immunol & Behav, NIH, 5625 Fishers Lane,MSC 9401, Rockville, MD 20852 USA.
EM sternbee@mail.nih.gov
NR 122
TC 51
Z9 52
U1 1
U2 7
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD OCT 1
PY 2008
VL 84
IS 4
BP 924
EP 931
DI 10.1189/jlb.0208104
PG 8
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 354KW
UT WOS:000259639500006
PM 18664528
ER
PT J
AU Klinman, D
Shirota, H
Tross, D
Sato, T
Klaschik, S
AF Klinman, Dennis
Shirota, Hidekazu
Tross, Debra
Sato, Takashi
Klaschik, Sven
TI Synthetic oligonucleotides as modulators of inflammation
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article; Proceedings Paper
CT Pennington Scientific Symposium on Neuro-Immune Signaling and
Inflammation
CY DEC 02-05, 2007
CL Baton Rouge, LA
DE CpG; suppressive; ODN; cancer; therapy
ID PLASMACYTOID DENDRITIC CELLS; INDUCED IMMUNE ACTIVATION; CPG-CONTAINING
OLIGODEOXYNUCLEOTIDES; SYSTEMIC-LUPUS-ERYTHEMATOSUS; ALLERGIC LUNG
INFLAMMATION; 4TH INTERNATIONAL WORKSHOP; COLLAGEN-INDUCED ARTHRITIS;
LICENSED ANTHRAX VACCINE; BACTERIAL-DNA; SUPPRESSIVE
OLIGODEOXYNUCLEOTIDES
AB Synthetic oligodeoxynucleotides (ODN) containing unmethylated CpG motifs mimic the immunostimulatory activity of bacterial DNA. CpG ODN directly stimulate human B cells and plasmacytoid dendritic cells, promote the production of Th1 and proinflammatory cytokines, and trigger the maturation/activation of professional APC. CpG ODN are finding use in the treatment of cancer, allergy, and infection. In contrast, ODN containing multiple TTAGGG motifs mimic the immunosuppressive activity of self-DNA, down-regulating the production of proinflammatory and Th1 cytokines. Preclinical studies suggest that "suppressive" ODN may slow or prevent diseases characterized by pathologic immune stimulation, including autoimmunity and septic shock. Extensive studies in animal models suggest that the therapeutic value of CpG and TTAGGG ODN may be optimized by early administration.
C1 [Klinman, Dennis; Shirota, Hidekazu; Tross, Debra; Sato, Takashi; Klaschik, Sven] NCI, Canc & Inflammat Program, Frederick, MD 21702 USA.
RP Klinman, D (reprint author), NCI, Canc & Inflammat Program, Bldg 567,Rm 205, Frederick, MD 21702 USA.
EM klinmand@mail.nih.gov
NR 87
TC 27
Z9 29
U1 0
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD OCT 1
PY 2008
VL 84
IS 4
BP 958
EP 964
DI 10.1189/jlb.1107775
PG 7
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 354KW
UT WOS:000259639500010
PM 18430787
ER
PT J
AU Fang, L
Lee, VC
Cha, E
Zhang, H
Hwang, ST
AF Fang, Lei
Lee, Vivian C.
Cha, Emily
Zhang, Hong
Hwang, Sam T.
TI CCR7 regulates B16 murine melanoma cell tumorigenesis in skin
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article; Proceedings Paper
CT Pennington Scientific Symposium on Neuro-Immune Signaling and
Inflammation
CY DEC 02-05, 2007
CL Baton Rouge, LA
DE chemokine; tumor immunology
ID LYMPH-NODE METASTASIS; TUMOR-INFILTRATING LYMPHOCYTES; BREAST-CANCER
METASTASIS; MATURE DENDRITIC CELLS; INDUCIBLE PROTEIN-10; CHEMOKINE
RECEPTORS; CERVICAL-CANCER; T-LYMPHOCYTES; EXPRESSION; INDUCTION
AB Tumor cell-associated chemokine receptors play distinct roles in cancer biology, including enhancement of lymph node (LN) metastasis. To determine if CCR7 influences tumor formation in skin, we inoculated B16 cells transduced with CCR7 and luciferase (CCR7-luc-B16) or with retroviral vector and luciferase (pLNCX2-luc-B16) into ear skin and footpads of wild-type (WT) mice. In contrast to pLNCX2-luc-B16 cells, 97% of CCR7-luc-B16 cell-inoculated mice formed skin tumors as well as cervical LN metastases by Day 21 following ear inoculation. CCR7-expressing and control B16 cells, however, formed tumors of similar size and with high-efficiency in SCID-beige mice. Cells from both lines accumulated in the skin of WT mice in similar numbers until Day 7. By Day 11, however, control cells decreased tenfold, whereas CCR7-luc-B16 cells formed small tumor nodules. Tumor cells were infrequently detected in draining cervical LNs up to 11 days after injection of both cell lines, but stable nodal metastases were only observed after CCR7-lucB16 ear tumors had been established (similar to Day 21). ELISPOT assays revealed that IFN-gamma-producing cells in draining LNs from CCR7-luc-B16-injected ears were reduced through Day 7. After footpad injection, tumor formation by CCR7-expressing B16 cells was enhanced only with small, initial tumor cell inocula. With larger inocula, tumor formation was equivalent, but the numbers of tumor-infiltrating leukocytes were reduced by approximately sixfold in CCR7-B16 tumors compared with pLNCX2-B16 tumors of equal size. IFN-gamma and CXCL10 were reduced 35- and sixfold, respectively, in CCR7-B16 cell tumors (vs. control tumors). Thus, CCR7 expression enhances tumorigenesis in addition to facilitating LN metastasis.
C1 [Fang, Lei; Lee, Vivian C.; Cha, Emily; Zhang, Hong; Hwang, Sam T.] NCI, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Hwang, ST (reprint author), NCI, Dermatol Branch, Ctr Canc Res, 10 Ctr Dr,Bldg 10,Rm 12N238, Bethesda, MD 20892 USA.
EM hwangs@mail.nih.gov
NR 28
TC 17
Z9 18
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD OCT 1
PY 2008
VL 84
IS 4
BP 965
EP 972
DI 10.1189/jlb.1107776
PG 8
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 354KW
UT WOS:000259639500011
PM 18519742
ER
PT J
AU Wuest, TY
Willette-Brown, J
Durum, SK
Hurwitz, AA
AF Wuest, Thomas Y.
Willette-Brown, Jami
Durum, Scott K.
Hurwitz, Arthur A.
TI The influence of IL-2 family cytokines on activation and function of
naturally occurring regulatory T cells
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article; Proceedings Paper
CT Pennington Scientific Symposium on Neuro-Immune Signaling and
Inflammation
CY DEC 02-05, 2007
CL Baton Rouge, LA
DE FoxP3; IL-7; IL-15; CD25; IL-21; gamma c cytokines
ID IMMUNOLOGICAL SELF-TOLERANCE; IN-VITRO; CUTTING EDGE; SUPPRESSOR
FUNCTION; AUTOIMMUNE-DISEASE; DENDRITIC CELLS; RECEPTOR-ALPHA;
GROWTH-FACTOR; ANTIGEN; EXPANSION
AB IL-2 is essential for CD4+ CD25+ forkhead box P3+ (FoxP3+) naturally occurring regulatory T cell (Treg) homeostasis and activation. Binding of IL-2 to its receptor leads to phosphorylation of STAT5, and binding of phosphorylated STAT5 to the foxp3 promoter increases foxp3 transcription, resulting in elevated levels of FoxP3 protein in Tregs. Transcriptional regulation by the elevated levels of FoxP3 is thought to be essential for the strong suppressor function seen in activated Tregs. IL-2 belongs to a family cytokines, which all depend on the common gamma-receptor chain (gamma c). Given the well-documented effects of IL-2 on Treg function, the effect of other IL-2 family cytokines (IL-7, -15, and -21) on Tregs was examined. We observed that IL-7 and IL-15 induce STAT5 phosphorylation and up-regulation of FoxP3 in Tregs. STAT5 activation correlated with enhanced viability. However, only in the presence of IL-2 did Tregs acquire potent suppressor function. This finding is surprising, as IL-15 as well as IL-2 use the same IL-2R beta c and gamma c for signaling. In contrast, IL-21 activated STAT3 but did not activate STAT5 and had no effect on Treg viability, activation, or function. We therefore conclude that phosphorylation of STAT5, mediated through the IL-2R gamma, promotes Treg survival in a resting and activated state. However, activation of STAT5 alone in conjunction with TCR signaling is not sufficient for the induction of potent suppressor function in Tregs, as IL-7 and IL-15 are not capable of inducing potent Treg suppressor function.
C1 [Wuest, Thomas Y.; Willette-Brown, Jami; Hurwitz, Arthur A.] NCI, Tumor Immun & Tolerance Sect, Canc & Inflammat Program, Mol Immunoregulat Lab, Frederick, MD 21701 USA.
[Durum, Scott K.] NCI, Immunol Cytokine Res Grp, Canc & Inflammat Program, Mol Immunoregulat Lab, Frederick, MD 21701 USA.
RP Hurwitz, AA (reprint author), NCI, Tumor Immun & Tolerance Sect, Canc & Inflammat Program, Mol Immunoregulat Lab, POB B, Frederick, MD 21701 USA.
EM hurwitza@ncifcrf.gov
FU Intramural NIH HHS
NR 50
TC 61
Z9 67
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD OCT 1
PY 2008
VL 84
IS 4
BP 973
EP 980
DI 10.1189/jlb.1107778
PG 8
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 354KW
UT WOS:000259639500012
PM 18653463
ER
PT J
AU Gasperini, P
Sakakibara, S
Tosato, G
AF Gasperini, Paola
Sakakibara, Shuhei
Tosato, Giovanna
TI Contribution of viral and cellular cytokines to Kaposi's
sarcoma-associated herpesvirus pathogenesis
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article; Proceedings Paper
CT Pennington Scientific Symposium on Neuro-Immune Signaling and
Inflammation
CY DEC 02-05, 2007
CL Baton Rouge, LA
DE primary effusion lymphoma; multicentric Castleman's disease;
angiogenesis; cell migration
ID PRIMARY EFFUSION LYMPHOMA; MULTICENTRIC CASTLEMANS-DISEASE; ENDOTHELIAL
GROWTH-FACTOR; EPSTEIN-BARR-VIRUS; HIV-INFECTED PATIENTS; PERMEABILITY
FACTOR; DNA-SEQUENCES; ENCODED INTERLEUKIN-6; VASCULAR ENDOTHELIUM;
IN-VIVO
AB Kaposi's sarcoma (KS)-associated herpesvirus is associated with the proliferative/malignant disorders KS, primary effusion lymphoma (PEL), and multicentric Castleman's disease (MCD) in patients with AIDS. In spite of recent advances in the treatment of KS, PEL and MCD represent therapeutic challenges. Recent advances in dissecting the pathogenesis of these diseases have indicated that the viral cytokine IL-6 and the cellular cytokines/growth factors IL-10, IL-6, stromal cell-derived factor 1, and vascular endothelial growth factor are important contributors to the growth, survival, and spread of PEL and MCD and are therefore potential targets for drug development.
C1 [Gasperini, Paola; Sakakibara, Shuhei; Tosato, Giovanna] NCI, Cellular Oncol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Tosato, G (reprint author), NCI, Cellular Oncol Lab, Ctr Canc Res, NIH, Bldg 37,Room 4124, Bethesda, MD 20892 USA.
EM tosatog@mail.nih.gov
NR 57
TC 20
Z9 20
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD OCT 1
PY 2008
VL 84
IS 4
BP 994
EP 1000
DI 10.1189/jlb.1107777
PG 7
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 354KW
UT WOS:000259639500015
PM 18319288
ER
PT J
AU Bar-Shir, A
Avram, L
Ozarslan, E
Basser, PJ
Cohen, Y
AF Bar-Shir, Amnon
Avram, Liat
Ozarslan, Evren
Basser, Peter J.
Cohen, Yoram
TI The effect of the diffusion time and pulse gradient duration ratio on
the diffraction pattern and the structural information estimated from
q-space diffusion MR: Experiments and simulations
SO JOURNAL OF MAGNETIC RESONANCE
LA English
DT Article
DE Diffusion; NMR; q-Space; QSI; Diffraction; Diffusion time; Pulse
duration
ID NUCLEAR-MAGNETIC-RESONANCE; STUDYING TRANSLATIONAL DIFFUSION;
CENTRAL-NERVOUS-SYSTEM; SPIN-ECHO ANALYSIS; FIELD-GRADIENT; RESTRICTED
DIFFUSION; NMR-DIFFUSION; WEIGHTED MRI; MULTIPLE-SCLEROSIS; STIMULATED
ECHO
AB q-Space diffusion MRI (QSI) provides a means of obtaining microstructural information about porous materials and neuronal tissues from diffusion data. However, the accuracy of this structural information depends on experimental parameters used to collect the MR data. q-Space diffusion MR performed on clinical scanners is generally collected with relatively long diffusion gradient pulses, in which the gradient pulse duration, delta, is Comparable to the diffusion time, Delta. In this study, we used phantoms, consisting of ensembles Of MiCFOtubes, and mathematical models to assess the effect of the ratio of the diffusion time and the duration of the diffusion pulse gradient, i.e., Delta/delta, on the MR signal attenuation vs. q, and on the measured structural information extracted therefrom. We found that for Delta/delta similar to 1, the diffraction pattern obtained from q-space MR data are shallower than when the short gradient pulse (SGP) approximation is satisfied. For long delta the estimated compartment size is, as expected, smaller than the real size. Interestingly, for Delta/delta similar to 1 the diffraction peaks are shifted to even higher q-values, even when delta is kept constant, giving the impression that the restricted compartments are even smaller than they are. When phantoms composed of microtubes of different diameters are used, it is more difficult to estimate the diameter distribution in this regime. Excellent agreement is found between the experimental results and simulations that explicitly account for the use of long duration gradient pulses. Using such experimental data and this mathematical framework, one can estimate the true compartment dimensions when long and finite gradient pulses are used even when Delta/delta similar to 1. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Bar-Shir, Amnon; Avram, Liat; Cohen, Yoram] Tel Aviv Univ, Raymond & Beverly Sackler Fac Exact Sci, Sch Chem, IL-69978 Tel Aviv, Israel.
[Ozarslan, Evren; Basser, Peter J.] NICHD, Sect Tissue Biophys & Biomimet, NIH, Bethesda, MD USA.
RP Cohen, Y (reprint author), Tel Aviv Univ, Raymond & Beverly Sackler Fac Exact Sci, Sch Chem, IL-69978 Tel Aviv, Israel.
EM ycohen@post.tau.ac.il
RI Ozarslan, Evren/B-4858-2013; Basser, Peter/H-5477-2011
OI Ozarslan, Evren/0000-0003-0859-1311;
FU US-Israel Binational Foundation [353/03]; Intramural Research Program;
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, NIH
FX This research was supported by a grant from the US-Israel Binational
Foundation (BSF, Grant Number 353/03). This work was also supported in
part by the Intramural Research Program of the Eunice Kennedy Shriver
National Institute of Child Health and Human Development, NIH.
NR 51
TC 43
Z9 43
U1 4
U2 14
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1090-7807
J9 J MAGN RESON
JI J. Magn. Reson.
PD OCT
PY 2008
VL 194
IS 2
BP 230
EP 236
DI 10.1016/j.jmr.2008.07.009
PG 7
WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical;
Spectroscopy
SC Biochemistry & Molecular Biology; Physics; Spectroscopy
GA 358XY
UT WOS:000259952000009
PM 18667345
ER
PT J
AU Faghri, S
Tamura, D
Kraemer, KH
DiGiovanna, JJ
AF Faghri, S.
Tamura, D.
Kraemer, K. H.
DiGiovanna, J. J.
TI Trichothiodystrophy: a systematic review of 112 published cases
characterises a wide spectrum of clinical manifestations
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article; Proceedings Paper
CT 68th Annual Meeting of the Society-for-Investigative-Dermatology
CY MAY 09-12, 2007
CL Los Angeles, CA
SP Soc Investigat Dermatol
ID HAIR-SHAFT ABNORMALITIES; PIGMENTOSUM GROUP-D; DEFICIENT BRITTLE HAIR;
CENTRAL-NERVOUS-SYSTEM; SYNDROME CONGENITAL ICHTHYOSIS; GROUP-D
MUTATION; XERODERMA-PIGMENTOSUM; DNA-REPAIR; MENTAL-RETARDATION; TAY
SYNDROME
AB Trichothiodystrophy (TTD) is a rare, autosomal recessive disease, characterised by brittle, sulfur deficient hair and multisystem abnormalities. A systematic literature review identified 112 patients ranging from 12 weeks to 47 years of age (median 6 years). In addition to hair abnormalities, common features reported were developmental delay/intellectual impairment (86%), short stature (73%), ichthyosis (65%), abnormal characteristics at birth (55%), ocular abnormalities (51%), infections (46%), photosensitivity (42%), maternal pregnancy complications (28%) and defective DNA repair (37%). There was high mortality, with 19 deaths under the age of 10 years (13 infection related), which is 20-fold higher compared to the US population. The spectrum of clinical features varied from mild disease with only hair involvement to severe disease with profound developmental defects, recurrent infections and a high mortality at a young age. Abnormal characteristics at birth and pregnancy complications, unrecognised but common features of TTD, suggest a role for DNA repair genes in normal fetal development.
C1 [Faghri, S.; Tamura, D.; Kraemer, K. H.; DiGiovanna, J. J.] NCI, DNA Repair Sect, Basic Res Lab, Clin Res Ctr, Bethesda, MD 20892 USA.
[Faghri, S.; DiGiovanna, J. J.] Brown Univ, Warren Alpert Med Sch, Dept Dermatol, Div Dermatopharmacol, Providence, RI 02912 USA.
RP Kraemer, KH (reprint author), NCI, DNA Repair Sect, Basic Res Lab, Clin Res Ctr, Bldg 37,Room 4002,MSC 4258, Bethesda, MD 20892 USA.
EM kraemerk@nih.gov
FU Intramural NIH HHS [Z01 BC004517-31]
NR 124
TC 71
Z9 71
U1 0
U2 2
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
J9 J MED GENET
JI J. Med. Genet.
PD OCT
PY 2008
VL 45
IS 10
BP 609
EP 621
DI 10.1136/jmg.2008.058743
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 355LJ
UT WOS:000259710100001
PM 18603627
ER
PT J
AU Perino, MG
Yamanaka, S
Li, JL
Wobus, AM
Boheler, KR
AF Perino, Maria Grazia
Yamanaka, Satoshi
Li, Jinliang
Wobus, Anna M.
Boheler, Kenneth R.
TI Cardiomyogenic stem and progenitor cell plasticity and the dissection of
cardiopoiesis
SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
LA English
DT Review
DE Embryonic stem cells; Adult stem cells; Cardiomyocytes;
Cardiomyogenesis; Plasticity
ID REGENERATE INFARCTED MYOCARDIUM; BONE MORPHOGENETIC PROTEINS; WNT
SIGNALING PATHWAY; MARROW-DERIVED CELLS; HEMATOPOIETIC STEM;
GROWTH-FACTOR; IN-VITRO; SMOOTH-MUSCLE; CARDIAC MYOCYTES;
SKELETAL-MUSCLE
AB Cell-based therapies hold promise of repairing an injured heart, and the description of stem and progenitor cells with cardiomyogenic potential is critical to its realization. At the vanguard of these efforts are analyses of embryonic stem cells, which clearly have the capacity to generate large numbers of cardiomyocytes in vitro. Through the use of this model system, a number of signaling mechanisms have been worked out that describes at least partially the process of cardiopoiesis. Studies on adult stem and on progenitor cells with cardiomyogenic potential are still in their infancy, and much less is known about the molecular signals that are required to induce the differentiation to cardiomyocytes. It is also unclear whether the pathways are similar or different between embryonic and adult cell-induced cardiomyogenesis, partly because of the continued controversies that surround the stem cell theory of cardiac self-renewal. Irrespective of any perceived or actual limitations, the study of stem and progenitor cells has provided important insights into the process of cardiomyogenesis, and it is likely that future research in this area will turn the promise of repairing an injured heart into a reality. Published by Elsevier Inc.
C1 [Boheler, Kenneth R.] NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA.
Leibniz Inst Plant Genet & Crop Plant Res IPK, Vitro Differentiat Grp, Gatersleben, Germany.
RP Boheler, KR (reprint author), NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM bohelerk@grc.nia.nih.gov
FU NIH; National Institute on Aging
FX This research was supported by the Intramural Research Program of the
NIH, National Institute on Aging.
NR 184
TC 23
Z9 23
U1 1
U2 14
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2828
EI 1095-8584
J9 J MOL CELL CARDIOL
JI J. Mol. Cell. Cardiol.
PD OCT
PY 2008
VL 45
IS 4
BP 475
EP 494
DI 10.1016/j.yjmcc.2008.05.002
PG 20
WC Cardiac & Cardiovascular Systems; Cell Biology
SC Cardiovascular System & Cardiology; Cell Biology
GA 371PX
UT WOS:000260844500003
PM 18565538
ER
PT J
AU Bindewald, E
Grunewald, C
Boyle, B
O'Connor, M
Shapiro, BA
AF Bindewald, Eckart
Grunewald, Calvin
Boyle, Brett
O'Connor, Mary
Shapiro, Bruce A.
TI Computational strategies for the automated design of RNA nanoscale
structures from building blocks using NanoTiler
SO JOURNAL OF MOLECULAR GRAPHICS & MODELLING
LA English
DT Article
DE RNA; Design; Nanotechnology; Building block; Topology; Ring closure
ID NUCLEIC-ACID STRUCTURES; SECONDARY STRUCTURES; INFO-RNA; PREDICTION;
SEQUENCE; ARCHITECTURE; CONSTRAINTS; APTAMER; PROTEIN; MOTIFS
AB one approach to designing RNA nanoscale structures is to use known RNA structural motifs such as junctions, kissing loops or bulges and to construct a molecular model by connecting these building blocks with helical struts. We previously developed an algorithm for detecting internal loops, junctions and kissing loops in RNA structures.
Here we present algorithms for automating or assisting many of the steps that are involved in creating RNA structures from building blocks: (I) assembling building blocks into nanostructures using either a combinatorial search or constraint satisfaction; (2) optimizing RNA 3D ring structures to improve ring closure; (3) sequence optimisation; (4) creating a unique non-degenerate RNA topology descriptor. This effectively creates a computational pipeline for generating molecular models of RNA nanostructures and more specifically RNA ring structures with optimized sequences from RNA building blocks. We show several examples of how the algorithms can be utilized to generate RNA tecto-shapes. Published by Elsevier B.V.
C1 [Bindewald, Eckart] NCI, SAIC Frederick Inc, Basic Res Program, Frederick, MD 21702 USA.
[Grunewald, Calvin; Boyle, Brett; O'Connor, Mary; Shapiro, Bruce A.] NCI, Ctr Canc Res Nanobiol Program, Frederick, MD 21702 USA.
RP Shapiro, BA (reprint author), NCI, SAIC Frederick Inc, Basic Res Program, Bldg 469,Room 150, Frederick, MD 21702 USA.
EM bshapiro@ncifcrf.gov
FU Federal funds from the National Cancer Institute; National Institutes of
Health [N01-CO-12400]; Intramural Research Program of the NIH; National
Cancer Institute; Center for Cancer Research
FX We thank Luc Jaeger for helpful discussions. We wish to thank the
Advanced Biomedical Computing Center (ABCC) at the NCI for their
computing support. This work has been funded in whole or in part with
Federal funds from the National Cancer Institute, National Institutes of
Health, under Contract No. N01-CO-12400. This research was supported by
the Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research.
NR 41
TC 36
Z9 36
U1 1
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1093-3263
J9 J MOL GRAPH MODEL
JI J. Mol. Graph.
PD OCT
PY 2008
VL 27
IS 3
BP 299
EP 308
DI 10.1016/j.jmgm.2008.05.004
PG 10
WC Biochemical Research Methods; Biochemistry & Molecular Biology; Computer
Science, Interdisciplinary Applications; Crystallography; Mathematical &
Computational Biology
SC Biochemistry & Molecular Biology; Computer Science; Crystallography;
Mathematical & Computational Biology
GA 374AA
UT WOS:000261013400007
PM 18838281
ER
PT J
AU Schmitt, AG
Hall, FS
Perona, MTG
Ortega, G
Hofmann, M
Gagel, C
Sora, I
Uhl, GR
Riederer, P
Lesch, KP
Gerlach, M
Grunblatt, E
AF Schmitt, Angelika G.
Hall, F. Scott
Perona, Maria T. G.
Ortega, Gabriela
Hofmann, Miryame
Gagel, Carola
Sora, I.
Uhl, G. R.
Riederer, Peter
Lesch, Klaus-Peter
Gerlach, Manfred
Gruenblatt, Edna
TI Methylphenidate treatment and stress differentially modify gene
expression of immediate early genes in the DAT knockout mouse, a mouse
model for ADHD
SO JOURNAL OF NEURAL TRANSMISSION
LA English
DT Meeting Abstract
CT Joint Meeting of the
Israel-Academy-of-Sciences-and-Humanities/German-Academy-of-Sciences-Leo
poldina
CY NOV 02-05, 2008
CL Jerusalem, ISRAEL
SP Israel Acad Sci & Humanities, German Acad Sci Leopoldina
C1 [Schmitt, Angelika G.; Ortega, Gabriela; Hofmann, Miryame; Gagel, Carola; Riederer, Peter; Lesch, Klaus-Peter; Gruenblatt, Edna] Univ Wurzburg, Neurochem Lab, Clin Psychiat Psychosomat & Psychotherapy, D-97080 Wurzburg, Germany.
[Hall, F. Scott; Perona, Maria T. G.; Uhl, G. R.] Natl Inst Drug Abuse, Mol Neurobiol Branch, Intramural Res Program, NIH DHHS, Baltimore, MD USA.
[Gerlach, Manfred] Univ Wurzburg, Clin Child & Adolescence Psychiat, D-97080 Wurzburg, Germany.
[Sora, I.] Tohoku Univ, Grad Sch Med, Dept Neurosci, Sendai, Miyagi 980, Japan.
RI Grunblatt, Edna/A-6762-2016; Hall, Frank/C-3036-2013
OI Grunblatt, Edna/0000-0001-8505-7265; Hall, Frank/0000-0002-0822-4063
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0300-9564
J9 J NEURAL TRANSM
JI J. Neural Transm.
PD OCT
PY 2008
VL 115
IS 10
BP 1483
EP 1483
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 350RW
UT WOS:000259371800071
ER
PT J
AU Hayward, RM
Patronas, N
Baker, EH
Vezina, G
Albert, PS
Warren, KE
AF Hayward, Robert M.
Patronas, Nicolas
Baker, Eva H.
Vezina, Gilbert
Albert, Paul S.
Warren, Katherine E.
TI Inter-observer variability in the measurement of diffuse intrinsic
pontine gliomas
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Article
DE brainstem; chemotherapy; childhood malignant gliomas; diffuse intrinsic
pontine gliomas; magnetic resonance imaging; tumor measurements
ID CLINICAL-TRIALS; BRAIN-TUMORS; CHILDHOOD; CHILDREN
AB Diffuse intrinsic pontine glioma (DIPG) is an invasive pediatric brainstem tumor with a poor prognosis. Patients commonly enter investigational trials, many of which use radiographic response as an endpoint for assessing drug efficacy. However, DIPGs are difficult to measure on magnetic resonance imaging (MRI). In this study, we characterized the reproducibility of these commonly performed measurements. Each of four readers measured 50 MRI scans from DIPG patients and inter-observer variability was estimated with descriptive statistics. Results confirmed that there is wide variability in DIPG tumor measurements between readers for all image types. Measurements on FLAIR imaging were most consistent. For patients on clinical trials, measurement of DIPG should be performed by a single reader while comparing prior images side-by-side. Endpoints for clinical trials determining efficacy in this population should also include more objective measures, such as survival, and additional endpoints need to be investigated.
C1 [Hayward, Robert M.; Warren, Katherine E.] Natl Canc Inst, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Patronas, Nicolas; Baker, Eva H.] NIH, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD 20892 USA.
[Vezina, Gilbert] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Albert, Paul S.] NIH, Biometr Res Branch, Bethesda, MD 20892 USA.
RP Warren, KE (reprint author), Natl Canc Inst, Pediat Oncol Branch, NIH, 9000 Rockville Pike,Bldg 10 CRC,Rm 1-3940, Bethesda, MD 20892 USA.
EM warrenk@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute, Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research. The views expressed do not necessarily represent the
views of the National Institutes of Health or the United States
Government.
NR 10
TC 20
Z9 20
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD OCT
PY 2008
VL 90
IS 1
BP 57
EP 61
DI 10.1007/s11060-008-9631-4
PG 5
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 341HN
UT WOS:000258704900010
PM 18587536
ER
PT J
AU Veeranna
Lee, JH
Pareek, TK
Jaffee, H
Boland, B
Vinod, KY
Amin, N
Kulkarni, AB
Pant, HC
Nixon, RA
AF Veeranna
Lee, Ju-Hyun
Pareek, Tej K.
Jaffee, Howard
Boland, Barry
Vinod, K. Yaragudri
Amin, Niranjana
Kulkarni, Ashok B.
Pant, Harish C.
Nixon, Ralph A.
TI Neurofilament tail phosphorylation: identity of the RT-97 phosphoepitope
and regulation in neurons by cross-talk among proline-directed kinases
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE cytoskeleton; neurodegenerative disease; cdk5; JNK; ERK; GSK3-beta
ID CYCLIN-DEPENDENT KINASE-5; SHARE ANTIGENIC DETERMINANTS;
GLYCOGEN-SYNTHASE KINASE-3; MONOCLONAL-ANTIBODIES SHOW; TANDEM
MASS-SPECTROMETRY; GANGLION-CELL NEURONS; N-TERMINAL KINASE; RAT
SPINAL-CORD; NEUROFIBRILLARY TANGLES; INTERMEDIATE-FILAMENTS
AB As axons myelinate, establish a stable neurofilament network, and expand in caliber, neurofilament proteins are extensively phosphorylated along their C-terminal tails, which is recognized by the monoclonal antibody, RT-97. Here, we demonstrate in vivo that RT-97 immunoreactivity (IR) is generated by phosphorylation at KSPXK or KSPXXXK motifs and requires flanking lysines at specific positions. extracellular signal regulated kinase 1,2 (ERK1,2) and pERK1,2 levels increase in parallel with phosphorylation at the RT-97 epitope during early postnatal brain development. Purified ERK1,2 generated RT-97 on both KSP motifs on recombinant NF-H tail domain proteins, while cdk5 phosphorylated only KSPXK motifs. RT-97 epitope generation in primary hippocampal neurons was regulated by extensive cross-talk among ERK1,2, c-Jun N-terminal kinase 1,2 (JNK1,2) and cdk5. Inhibition of both ERK1,2 and JNK1,2 completely blocked RT-97 generation. Cdk5 influenced RT-97 generation indirectly by modulating JNK activation. In mice, cdk5 gene deletion did not significantly alter RT-97 IR or ERK1,2 and JNK activation. In mice lacking the cdk5 activator P35, the partial suppression of cdk5 activity increased RT-97 IR by activating ERK1,2. Thus, cdk5 influences RT-97 epitope generation partly by modulating ERKs and JNKs, which are the two principal kinases regulating neurofilament phosphorylation. The regulation of a single target by multiple protein kinases underscores the importance of monitoring other relevant kinases when the activity of a particular one is blocked.
C1 [Veeranna; Lee, Ju-Hyun; Boland, Barry; Nixon, Ralph A.] Nathan S Kline Inst Psychiat Res, Ctr Dementia Res, Orangeburg, NY 10962 USA.
[Veeranna; Lee, Ju-Hyun; Nixon, Ralph A.] NYU, Sch Med, Dept Psychiat, New York, NY USA.
[Pareek, Tej K.; Kulkarni, Ashok B.] NIDCR, Lab Cell & Dev Biol, NIH, Bethesda, MD USA.
[Jaffee, Howard] NINDS, Mass Spectrometry Facil, Funct Genom Sect, NIH, Bethesda, MD 20892 USA.
[Boland, Barry] Univ Coll Dublin, Conway Inst, UCD Sch Biomol & Biomed Sci, Lab Neurodegenerat Res, Dublin 2, Ireland.
[Amin, Niranjana; Pant, Harish C.] NINDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA.
[Nixon, Ralph A.] NYU, Dept Cell Biol, Sch Med, New York, NY 10016 USA.
RP Veeranna (reprint author), Nathan S Kline Inst Psychiat Res, Ctr Dementia Res, Orangeburg, NY 10962 USA.
RI Boland, Barry/D-1235-2010;
OI Lee, Ju-hyun/0000-0002-0280-8375; Pareek, Tej/0000-0001-5134-1647
FU NIA [AG05604, P01A02219]; NIH intramural program
FX The authors thank Ramaswamy Neelakantan for useful discussions, Corrinne
Peterhoff for assistance with figures, and Nicole Piorkowski for
assistance with manuscript preparation. This work was supported by NIA
AG05604, NIA P01A02219 and NIH intramural program.
NR 71
TC 9
Z9 9
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
EI 1471-4159
J9 J NEUROCHEM
JI J. Neurochem.
PD OCT
PY 2008
VL 107
IS 1
BP 35
EP 49
DI 10.1111/j.1471-4159.2008.05547.x
PG 15
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 349HA
UT WOS:000259270700003
PM 18715269
ER
PT J
AU Londono, D
Carvajal, J
Arguelles-Grande, C
Marques, A
Cadavid, D
AF Londono, Diana
Carvajal, Jenny
Arguelles-Grande, Carolina
Marques, Adriana
Cadavid, Diego
TI Interleukin 10 protects the brain microcirculation from spirochetal
injury
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE apoptosis; Borrelia; endothelial cell; interleukin 10; neuroprotection;
spirochete intfection; tumor necrosis factor
ID BORNE RELAPSING FEVER; NONHUMAN PRIMATE MODEL; NECROSIS-FACTOR-ALPHA;
BORRELIA-TURICATAE; LYME BORRELIOSIS; PERSISTENT INFECTION;
PLASMODIUM-CHABAUDI; NEUROTROPIC STRAIN; ENDOTHELIAL-CELLS; CEREBRAL
MALARIA
AB Spirochetal infections are an important cause of neurological disease. In previous studies of the pathogenesis of spirochetal brain infection, mice inoculated with Borrelia turicatae, an agent of tick-borne relapsing fever in North America, developed mild meningitis and parenchymal activation/infiltration by interleukin 10 (IL-10)producing microglia/macrophages. Here, we investigated the neuroprotective effects of IL-10 during spirochetal infection by comparing the Outcomes of B. turicatae infection in wild-type and IL-10-deficient RAG2-deficient mice. Mice were infected with either serotype 1 (130), which causes more brain infection but lower bacteremia, or Bt2, which causes less brain infection but higher bacteremia. Interleukin 10 deficiency resulted in early death from subarachnoid/intraparenchymal brain hemorrhage in Bt2-infected mice. These mice had marked apoptosis of brain microvascular endothelial cells as assessed by terminal transferase-mediated DNA nick end-labeling, staining. In contrast, Bt1 infection caused milder subarachnoid hemorrhage. Neuronal apoptosis was observed in mice infected with both serotypes and was prominent in the cerebellum. Neutralization of tumor necrosis factor prevented death and reduced morbidity and brain injury in mice infected by both serotypes. We conclude that IL-10 plays a critical role protecting the cerebral microcirculation from spirochetal injury possibly by inhibition effects of tumor necrosis factor.
C1 [Londono, Diana; Carvajal, Jenny; Arguelles-Grande, Carolina; Cadavid, Diego] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurol & Neurosci, Newark, NJ 07103 USA.
[Londono, Diana; Carvajal, Jenny; Arguelles-Grande, Carolina; Cadavid, Diego] Univ Med & Dent New Jersey, New Jersey Med Sch, Ctr Emerging Pathogens, Newark, NJ 07103 USA.
[Marques, Adriana] NIAID, Clin Studies Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Cadavid, D (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurol & Neurosci, 185 S Orange Ave, Newark, NJ 07103 USA.
EM cadavidi@umdnj.edu
FU National Institutes of Health [IR21NS053997-01]; UMDNJ Foundation;
National Institutes of Health-National Institute of Allergy and
Infectious Diseases
FX This study was supported by Grant No. IR21NS053997-01 from the National
Institutes of Health and 6 the UMDNJ Foundation to Diego Cadavid. This
research was also supported by the intramural research program of the
National Institutes of Health-National Institute of Allergy and
Infectious Diseases. The Content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services. nor does mention of trade names. commercial
products, or organizations imply endorsement by the US Government.
NR 52
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Z9 10
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD OCT
PY 2008
VL 67
IS 10
BP 976
EP 983
DI 10.1097/NEN.0b013e318187a279
PG 8
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 356QQ
UT WOS:000259793100006
PM 18800010
ER
PT J
AU Kim, J
Nadal, MS
Clemens, AM
Baron, M
Jung, SC
Misumi, Y
Rudy, B
Hoffman, DA
AF Kim, Jinhyun
Nadal, Marcela S.
Clemens, Ann M.
Baron, Matthew
Jung, Sung-Cherl
Misumi, Yoshio
Rudy, Bernardo
Hoffman, Dax A.
TI Kv4 accessory protein DPPX (DPP6) is a critical regulator of membrane
excitability in hippocampal CA1 pyramidal neurons
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
ID LONG-TERM POTENTIATION; DENDRITIC K+ CHANNELS; POTASSIUM CHANNELS;
EXPRESSION; INACTIVATION; MODULATION; SUBUNITS; BRAIN; REPOLARIZATION;
INTEGRATION
AB A-type K+ currents have unique kinetic and voltage-dependent properties that allow them to finely tune synaptic integration, action potential (AP) shape and firing patterns. In hippocampal CA1 pyramidal neurons, Kv4 channels make up the majority of the somatodendritic A-type current. Studies in heterologous expression systems have shown that Kv4 channels interact with transmembrane dipeptidyl-peptidase-like proteins (DPPLs) to regulate the surface trafficking and biophysical properties of Kv4 channels. To investigate the influence of DPPLs in a native system, we conducted voltage-clamp experiments in patches from CA1 pyramidal neurons expressing short-interfering RNA (siRNA) targeting the DPPL variant known to be expressed in hippocampal pyramidal neurons, DPPX (siDPPX). In accordance with heterologous studies, we found that DPPX downregulation in neurons resulted in depolarizing shifts of the steady-state inactivation and activation curves, a shallower conductance-voltage slope, slowed inactivation, and a delayed recovery from inactivation for A-type currents. We carried out current-clamp experiments to determine the physiological effect of the A-type current modifications by DPPX. Neurons expressing siDPPX exhibited a surprisingly large reduction in subthreshold excitability as measured by a decrease in input resistance, delayed time to AP onset, and an increased AP threshold. Suprathreshold DPPX downregulation resulted in slower AP rise and weaker repolarization. Computer simulations supported our experimental results and demonstrated how DPPX remodeling of A-channel properties can result in opposing sub- and suprathreshold effects on excitability. The Kv4 auxiliary subunit DPPX thus acts to increase neuronal responsiveness and enhance signal precision by advancing AP initiation and accelerating both the rise and repolarization of APs.
C1 [Kim, Jinhyun; Clemens, Ann M.; Baron, Matthew; Jung, Sung-Cherl; Hoffman, Dax A.] NICHHD, NIH, Lab Cellular & Synapt Neurophysiol, Mol Neurophysiol & Biophys Unit, Bethesda, MD 20892 USA.
[Nadal, Marcela S.; Rudy, Bernardo] NYU, Sch Med, Dept Physiol & Neurosci, Smilow Neurosci Program, New York, NY USA.
[Misumi, Yoshio] Fukuoka Univ, Sch Med, Dept Cell Biol, Fukuoka 81401, Japan.
RP Hoffman, DA (reprint author), NICHHD, NIH, Lab Cellular & Synapt Neurophysiol, Mol Neurophysiol & Biophys Unit, 35 Lincoln Dr,Rm 3C-905, Bethesda, MD 20892 USA.
EM hoffmand@mail.nih.gov
RI Hoffman, Dax/E-5155-2011;
OI Hoffman, Dax/0000-0001-6999-2157; Rudy, Bernardo/0000-0001-5748-6900
FU National Institute of Child Health; Human Development Intramural
Research Program; National Institute of Neurological Disorders and
Stroke [NS-30989, NS-045217]; National Science Foundation [IBN-0314645]
FX This work was supported by the National Institute of Child Health and
Human Development Intramural Research Program and by National Institute
of Neurological Disorders and Stroke Grants NS-30989 and NS-045217 and
National Science Foundation Grant IBN-0314645 to B. Rudy.
NR 50
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Z9 41
U1 1
U2 3
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD OCT
PY 2008
VL 100
IS 4
BP 1835
EP 1847
DI 10.1152/jn.90261.2008
PG 13
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 359DQ
UT WOS:000259967000013
PM 18667548
ER
PT J
AU Zhou, ZS
Belluscio, L
AF Zhou, Zhishang
Belluscio, Leonardo
TI Intrabulbar projecting external tufted cells mediate a timing-based
mechanism that dynamically gates olfactory bulb output
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE olfactory bulb; intrabulbar; glomerulus; external tufted cells;
chemosensory; mice
ID CENTER-SURROUND INHIBITION; MITRAL CELLS; LATERAL INHIBITION; CORTEX;
GLOMERULI; SYNCHRONIZATION; EXCITATION; INPUT; MAPS; INTERNEURONS
AB In the mammalian olfactory system, intrabulbar projections (IBPs) mediated by a class of external tufted cells (ET cells) specifically link isofunctional odor columns within the same olfactory bulb. To study the function of these ET cells within the glomerular network, we developed a "hemibulb" preparation that maintains IBPs intact enabling the select activation of ET cells associated with specific glomeruli. Using P2-GFP mice, a line in which the P2 glomeruli are labeled with green fluorescent protein, we recorded from P2 mitral cells (MT cells) while selectively stimulating P2 ET cells. Here, we show that ET-cell activity evokes a slow modulatory (SM) potential within MT cells, which is mediated by the glomerular network and consists of both excitatory and inhibitory components. Interestingly, the timing of the SM potential with respect to olfactory nerve (ON) stimulation can produce converse effects on MT-cell output. When ET-cell activity precedes ON stimulation, the MT-cell response is potentiated; however, when ET-cell activity follows ON stimulation, the MT-cell response is inhibited. Thus, intrabulbar projecting ET cells can shape olfactory bulb output through intraglomerular modulation of MT cells.
C1 [Zhou, Zhishang; Belluscio, Leonardo] NINDS, Dev Neural Plast Unit, NIH, Bethesda, MD 20892 USA.
RP Belluscio, L (reprint author), NINDS, Dev Neural Plast Unit, NIH, Bethesda, MD 20892 USA.
EM belluscl@ninds.nih.gov
FU National Institute of Neurological Disorders; Stroke-National Institutes
of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke-National
Institutes of Health. We thank Beth Belluscio, Rory McQuiston, and John
Isaac as well as the members of the Belluscio laboratory for helpful
discussions and critical review of this manuscript.
NR 36
TC 11
Z9 12
U1 0
U2 2
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD OCT 1
PY 2008
VL 28
IS 40
BP 9920
EP 9928
DI 10.1523/JNEUROSCI.3082-08.2008
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 355IJ
UT WOS:000259702300004
PM 18829950
ER
PT J
AU Sarabi, AS
Shen, H
Wang, Y
Hoffer, BJ
Backman, CM
AF Sarabi, Arezou S.
Shen, Hui
Wang, Yun
Hoffer, Barry J.
Backman, Cristina. M.
TI Gene expression patterns in mouse cortical penumbra after focal ischemic
brain injury and reperfusion
SO JOURNAL OF NEUROSCIENCE RESEARCH
LA English
DT Article
DE stroke; penumbra; LCM; microarray
ID HEAT-SHOCK PROTEINS; CEREBRAL-ISCHEMIA; CELL RESPONSES; STROKE; FAMILY;
MICROARRAY; HYPOXIA; DEATH; MODEL; RAT
AB Ischemic stress in the brain causes acute and massive cell death in the targeted core area followed by a second phase of damage in the neighboring penumbra. The purpose of this study was to examine the global gene expression patterns in the penumbra, because the ischemic lesion in this region could be rescued by restoration of blood flow and other protective therapies. Adult C57BI/6 mice were subjected to a 90-min middle cerebral artery occlusion (MCAO). Laser capture microdissection (LCM) was used for tissue dissection at 4 and 24 hr after reperfusion. Sham-operated animals were used as controls. Gene expression in the penumbra was examined by using microarray analysis and quantitative RT-PCR. In agreement with previous reports, most genes were down-regulated at 4 hr after the onset of reperfusion in the ischemic penumbra compared with controls. In contrast, at 24 hr after reperfusion, most genes were up-regulated in the ischemic penumbra. Several genes not previously reported to be associated with ischemia were found. The gene lists generated in this study will help us to understand better the spatial and temporal distribution of molecules involved in the ischemic cascade. Published 2008 Wiley-Liss, Inc.
C1 [Sarabi, Arezou S.; Shen, Hui; Wang, Yun; Hoffer, Barry J.; Backman, Cristina. M.] Natl Inst Drug Abuse, Cellular Neurobiol Sect, NIH, Baltimore, MD 21224 USA.
RP Sarabi, AS (reprint author), Natl Inst Drug Abuse, Cellular Neurobiol Sect, NIH, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM sarabis@mail.nih.gov
RI backman, cristina/C-1276-2013
NR 40
TC 15
Z9 17
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0360-4012
J9 J NEUROSCI RES
JI J. Neurosci. Res.
PD OCT
PY 2008
VL 86
IS 13
BP 2912
EP 2924
DI 10.1002/jnr.21734
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 356PU
UT WOS:000259790900012
PM 18506852
ER
PT J
AU Ilias, I
Chen, CC
Carrasquillo, JA
Whatley, M
Ling, A
Lazurova, I
Adams, KT
Perera, S
Pacak, K
AF Ilias, Ioannis
Chen, Clara C.
Carrasquillo, Jorge A.
Whatley, Millie
Ling, Alexander
Lazurova, Ivica
Adams, Karen T.
Perera, Shiromi
Pacak, Karel
TI Comparison of 6-(18) F-Fluorodopamine PET with
(123)I-Metaiodobenzylguanidine and (111)In-Pentetreotide Scintigraphy in
Localization of Nonmetastatic and Metastatic Pheochromocytoma
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE radionuclide imaging; (18)F-fluorodopamine;
(123)I-metaiodobenzylguanidine; (111)In-pentetreotide; pheochromocytoma
ID POSITRON-EMISSION-TOMOGRAPHY; SOMATOSTATIN RECEPTOR SCINTIGRAPHY;
MALIGNANT PHEOCHROMOCYTOMA; DIAGNOSTIC LOCALIZATION; OCTREOTIDE
SCINTIGRAPHY; MAGNETIC-RESONANCE; MIBG SCINTIGRAPHY; ADRENAL-TUMORS;
METAIODOBENZYLGUANIDINE; HEAD
AB We compared functional imaging modalities including PET with 6-(18)F-fluorodopamine ((18)F-DA) with (123)I-metaiodobenzylguanidine ((123)I-MIBG) and somatostatin receptor scintigraphy (SRS) with (111)In-pentetreotide in nonmetastatic and metastatic pheochromocytoma (PHEO). Methods: We studied 25 men and 28 women (mean age +/- SD, 44.2 +/- 14.2 y) with biochemically proven nonmetastatic (n = 17) or metastatic (n = 36) PHEO. Evaluation included anatomic imaging with CT or MRI and functional imaging that included at least 2 nuclear medicine modalities: (18)FDA PET, (123)I-MIBG scintigraphy, or SRS. Sensitivity of functional imaging versus anatomic imaging was assessed on a per-patient and a per-region basis. Results: For this available cohort, on a per-patient basis overall sensitivity (combined for nonmetastatic and metastatic PHEO) was 90.2% for (18)F-DA PET, 76.0% for (123)I-MIBG scintigraphy, and 22.0% for SRS. On a per-region basis, overall sensitivity was 75.4% for (18)F-DA PET, 63.4% for (123)I-MIBG scintigraphy, and 64.0% for SRS. Conclusion: If available, (18)F-DA PET should be used in the evaluation of PHEO, because it is more sensitive than (123)I-MIBG scintigraphy or SRS. If (18)F-DA PET is not available, (123)I-MIBG scintigraphy (for nonmetastatic or adrenal PHEO) and SRS (for metastatic PHEO) should be the first alternative imaging methods to be used.
C1 [Pacak, Karel] NICHHD, Sect Med Neuroendocrinol, Reprod Biol & Adult Endocrinol Program, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Chen, Clara C.; Carrasquillo, Jorge A.; Whatley, Millie] Natl Inst Hlth, Dept Nucl Med, Ctr Clin, Bethesda, MD USA.
[Ling, Alexander] Natl Inst Hlth, Dept Radiol, Ctr Clin, Bethesda, MD USA.
[Lazurova, Ivica] Safarik Univ, Dept Med, Fac Med, Kosice, Slovakia.
RP Pacak, K (reprint author), NICHHD, Sect Med Neuroendocrinol, Reprod Biol & Adult Endocrinol Program, Natl Inst Hlth, Bldg 10,CRC,1 E,Room 1-3140,10 Ctr Dr,MSC-1109, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
RI Carrasquillo, Jorge/E-7120-2010;
OI Carrasquillo, Jorge/0000-0002-8513-5734
FU National Institute of Child Health and Human Development
FX This work was supported in part by the Intramural Research Program of
the National Institute of Child Health and Human Development.
NR 50
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Z9 77
U1 0
U2 2
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD OCT
PY 2008
VL 49
IS 10
BP 1613
EP 1619
DI 10.2967/jnumed.108.052373
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 362XG
UT WOS:000260229900039
PM 18794260
ER
PT J
AU Mukhin, AG
Kimes, AS
Chefer, SI
Matochikl, JA
Contoreggi, CS
Horti, AG
Vaupel, DB
Pavlova, O
Stein, EA
AF Mukhin, Alexey G.
Kimes, Alane S.
Chefer, Svetlana I.
Matochikl, John A.
Contoreggi, Carlo S.
Horti, Andrew G.
Vaupel, D. Bruce
Pavlova, Olga
Stein, Elliot A.
TI Greater Nicotinic Acetylcholine Receptor Density in Smokers Than in
Nonsmokers: A PET Study with 2-F-18-FA-85380
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE molecular imaging; PET; radiotracer tissue kinetics; neuroimaging;
nicotinic acetylcholine receptors; smoking
ID HUMAN BRAIN; CIGARETTE-SMOKING; UP-REGULATION; BINDING; BIODISTRIBUTION;
QUANTIFICATION; TOLERANCE; INFUSION; TRACER; MOUSE
AB Assays of human postmortem brain tissue have revealed that smokers have greater densities of high-affinity nicotinic acetylcholine receptors (nAChRs) in several brain regions than do nonsmokers or exsmokers. Quantitative PET imaging of nAChRs in humans has recently been reported using the alpha 4 beta 2* subtypespecific radioligand 2-F-18-FA-85380 (2FA). Methods: We used PET and 2FA to measure total volumes of distribution corrected for the free fraction of 2FA in plasma (V-T/f(p)) in 10 nonsmokers and 6 heavy smokers (>14 cigarettes/d; abstinent for >36 h). Dynamic PET scans were performed over 8 h, commencing immediately after a bolus injection of 2FA. Anatomic sampling was performed on PET images that were coregistered to MR images acquired from each volunteer. Data were analyzed by Logan plots and by 1- and 2-tissue-compartment models using unbound, unmetabolized arterial 2FA concentration as the input function. Results: All modeling methods yielded similar results. V-T/f(p) was significantly higher in smokers than in nonsmokers in all brain regions tested, except the thalamus. We used measures of V-T/f(p) and estimates of nondisplaceable volume of distribution and found 25%-200% higher values in smokers than in nonsmokers for the volume of distribution for the specific binding compartment in the frontal cortex, midbrain, putamen, pons, cerebellum, and corpus callosum. These findings were consistent with voxel-based analysis using statistical parametric mapping. Conclusion: Our findings suggest that PET with 2FA can be used to study the role of nicotine-induced upregulation of nAChRs in active smokers and during smoking cessation.
C1 [Mukhin, Alexey G.; Kimes, Alane S.; Chefer, Svetlana I.; Matochikl, John A.; Vaupel, D. Bruce; Pavlova, Olga; Stein, Elliot A.] Natl Inst Drug Abuse Intramural Res Program, Neuroimaging Res Branch, Dept Hlth & Human Serv, Natl Inst Hlth, Baltimore, MD 21224 USA.
[Contoreggi, Carlo S.] Natl Inst Drug Abuse Intramural Res Program, Off Clin Director, Dept Hlth & Human Serv, Natl Inst Hlth, Baltimore, MD 21224 USA.
[Horti, Andrew G.] Johns Hopkins Univ, Dept Radiol, Baltimore, MD USA.
RP Kimes, AS (reprint author), Natl Inst Drug Abuse Intramural Res Program, Neuroimaging Res Branch, Dept Hlth & Human Serv, Natl Inst Hlth, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM akimes@intra.nida.nih.gov
FU NIDA
FX A preliminary report of this study was presented at the 2006
NeuroReceptor Mapping Meeting in Copenhagen, Denmark. We acknowledge
Peter Willis, Andrew Hall, and Larry Koenig for radiosynthesis of the
radioligand; Varughese Kurian and Amy Kunce for maintaining the PET
camera and acquiring the PET scans; Dean Shumway for analyzing the blood
samples; Betty Jo Salmeron for her medical expertise; and Joyce Lutz,
Kathy Demuth, and the rest of the National Institute on Drug Abuse
(NIDA) nursing staff for their medical assistance with the study. This
study was supported by the Intramural Research Program of the NIDA.
NR 40
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Z9 73
U1 0
U2 3
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD OCT
PY 2008
VL 49
IS 10
BP 1628
EP 1635
DI 10.2967/jnumed.108.050716
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 362XG
UT WOS:000260229900041
PM 18794265
ER
PT J
AU Taylor, CL
Yetley, EA
AF Taylor, Christine L.
Yetley, Elizabeth A.
TI Nutrient risk assessment as a tool for providing scientific assessments
to regulators
SO JOURNAL OF NUTRITION
LA English
DT Article; Proceedings Paper
CT 7th Amino Acid Assessment Workshop
CY NOV 02-03, 2007
CL Japan, JAPAN
SP Int Council Amino Acid Sci
AB Regulatory officials world-wide are paying attention to the process for establishing the upper level of intake for nutrient substances. The rapidly expanding use of dietary supplements, fortified foods, and functional foods, coupled with increased trade in these products, has focused attention on ensuring their safety and on harmonizing standards internationally. The more traditional approaches, in which the regulators either provided no standards for upper levels of intake or developed standards based on some arbitrary multiple of the intake level known to provide an adequate amount of the nutrient, are recognized as outdated or inappropriate for the emerging issues. Preferred approaches are those that rely on the systematic scientific assessment of risk to determine the levels of intake below which no harm may occur. The scientific study of risk is playing an increased role in establishing the regulatory upper levels of "safe" nutrient intake. Risk assessment, as a component of risk analysis, offers a scientific basis for regulatory decision-making regarding the regulators' task associated with specifying safe upper levels of intake for nutrient substances. This article describes the key components of risk assessment as they are applied within the nutrition field. Although regulatory frameworks vary from country to country and all countries retain their right to determine their own level of protection, regulatory systems operate most effectively and are more likely to converge toward harmonization if they are informed by independent, organized, and scientific reviews that are conducted systematically in a transparent manner.
C1 [Taylor, Christine L.] Natl Acad, Inst Med, Washington, DC 20001 USA.
[Yetley, Elizabeth A.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
RP Taylor, CL (reprint author), Natl Acad, Inst Med, Washington, DC 20001 USA.
EM cltaylor@nas.edu
NR 21
TC 2
Z9 3
U1 0
U2 1
PU AMER SOC NUTRITIONAL SCIENCE
PI BETHESDA
PA 9650 ROCKVILLE PIKE, RM L-2407A, BETHESDA, MD 20814 USA
SN 0022-3166
J9 J NUTR
JI J. Nutr.
PD OCT
PY 2008
VL 138
IS 10
BP 1987S
EP 1991S
PG 5
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 353GQ
UT WOS:000259554500025
PM 18806112
ER
PT J
AU Phang, JM
Pandhare, J
Liu, YM
AF Phang, James M.
Pandhare, Jui
Liu, Yongmin
TI The metabolism of proline as microenvironmental stress substrate
SO JOURNAL OF NUTRITION
LA English
DT Article; Proceedings Paper
CT 7th Amino Acid Assessment Workshop
CY NOV 02-03, 2007
CL Japan, JAPAN
SP Int Council Amino Acid Sci
ID ACTIVATED-RECEPTOR-GAMMA; MATRIX METALLOPROTEINASES; PPAR-GAMMA;
COLORECTAL-CANCER; INDUCED APOPTOSIS; GENE-EXPRESSION; LUNG-CANCER;
COLLAGEN; OXIDASE; MODEL
AB Proline, a unique proteogenic secondary amino acid, has its own metabolic system with special features. Recent findings defining the regulation of this system led us to propose that proline is a stress substrate in the microenvironment of inflammation and tumorigenesis. The criteria for proline as a stress substrate are: 1) the enzymes utilizing proline respond to stress signaling; 2) there is a large, mobilizable pool of proline, and 3) the metabolism of proline serves special stress functions. Studies show that the proline-utilizing enzyme, proline oxidase (POX)/proline dehydrogenase (PRODH), responds to genotoxic, inflammatory, and nutrient stress. Proline as substrate is stored as collagen in extracellular matrix, connective tissue, and bone and it is rapidly released from this reservoir by the sequential action of matrix metalloproteinases, peptidases, and prolidase. Special functions include the use of proline by POX/PRODH to generate superoxide radicals that initiate apoptosis by intrinsic and extrinsic pathways. Under conditions of nutrient stress, proline is an energy source. It provides carbons for the tricarboxylic acid cycle and also participates in the proline cycle. The latter, catalyzed by mitochondrial POX and cytosolic pyrroline-5-carboxylate reductase, shuttles reducing potential from the pentose phosphate pathway into mitochondria to generate ATP and oxidizing potential to activate the cytosolic pentose phosphate pathway.
C1 [Phang, James M.; Pandhare, Jui] NCI, Comparat Carcinogenesis Lab, Ctr Canc Res, Frederick, MD 21702 USA.
[Liu, Yongmin] NCI, Basic Res Program, Sci Applicat Int Corp, Frederick, MD 21702 USA.
RP Phang, JM (reprint author), NCI, Comparat Carcinogenesis Lab, Ctr Canc Res, Frederick, MD 21702 USA.
EM phang@mail.ncifcrf.gov
FU Intramural NIH HHS [Z01 BC010744-02]; NCI NIH HHS [N01-CO-12400,
N01CO12400]
NR 73
TC 24
Z9 25
U1 2
U2 8
PU AMER SOC NUTRITIONAL SCIENCE
PI BETHESDA
PA 9650 ROCKVILLE PIKE, RM L-2407A, BETHESDA, MD 20814 USA
SN 0022-3166
J9 J NUTR
JI J. Nutr.
PD OCT
PY 2008
VL 138
IS 10
BP 2008S
EP 2015S
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 353GQ
UT WOS:000259554500029
PM 18806116
ER
PT J
AU Amr, S
Wolpert, B
Loffredo, CA
Zheng, YL
Shields, PG
Jones, R
Harris, CC
AF Amr, Sania
Wolpert, Beverly
Loffredo, Christopher A.
Zheng, Yun-Ling
Shields, Peter G.
Jones, Raymond
Harris, Curtis C.
TI Occupation, Gender, Race, and Lung Cancer
SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID MULTICENTER CASE-CONTROL; RISK-FACTORS; RESIDENTIAL RADON; HISTOLOGIC
TYPE; WOMEN; SMOKING; DISEASE; NONSMOKERS; SMOKERS; GERMANY
AB Objective: To examine associations between occupation and lung cancer by gender and race. Methods: We used data from the Maryland Lung Cancer Study of nonsmall cell lung carcinoma (NSCLC), a multicenter case control study, to estimate odds ratios (ORs) of NSCLC in different occupations. Results: After adjusting or smoking, environmental tobacco smoke, and other covariates, NSCLC ORs among women but not men were elevated in clerical-sales, service, and transportation-material handling occupations; ORs were significantly increased in all three categories (OR [95% confidence interval]: 4.07 [1.44 to 11.48]; 5.15 [1.62 to 16.34]; 7.82 [1.08 to 56.25], respectively), among black women, but only in transportation-material handling occupations (OR [95% confidence interval[: 3.43 [1.02 to 11.50]) among white women. Conclusions: Women, especially black women, in certain occupations had increased NSCLC ORs. (J Occup Environ Med. 2008;50:1167-1175)
C1 [Amr, Sania; Wolpert, Beverly] Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA.
[Jones, Raymond] Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA.
[Loffredo, Christopher A.; Zheng, Yun-Ling; Shields, Peter G.] Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, Washington, DC 20007 USA.
[Harris, Curtis C.] NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA.
RP Amr, S (reprint author), Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, 660 W Redwood St,Suite 133C,Howard Hall, Baltimore, MD 21201 USA.
EM samr@epi.umaryland.edu
RI Shields, Peter/I-1644-2012
FU NCI [N02BC71006]
FX This Study was supported by NCI contract N02BC71006.
NR 52
TC 6
Z9 6
U1 3
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1076-2752
J9 J OCCUP ENVIRON MED
JI J. Occup. Environ. Med.
PD OCT
PY 2008
VL 50
IS 10
BP 1167
EP 1175
DI 10.1097/JOM.0b013e31817d3639
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 361JR
UT WOS:000260124400012
PM 18849762
ER
PT J
AU Shanti, RM
Torres-Cabala, CA
Jaffe, ES
Wilson, WH
Brahim, JS
AF Shanti, Rabie M.
Torres-Cabala, Carlos A.
Jaffe, Elaine S.
Wilson, Wyndham H.
Brahim, Jaime S.
TI Lymphomatoid granulomatosis with involvement of the hard palate: A case
report
SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
ID POLYMORPHIC RETICULOSIS; B-LYMPHOCYTES; CELL; PROLIFERATION; NASAL
AB Lymphomatoid granulomatosis (ING) is a rare angiocentric-destructive process with Epstein-Barr virus (EBV)-positive B cells and reactive T cells. Lymphomatoid granulomatosis at grades I and II shows rare to moderate numbers of EBV-positive B Cells (usually polyclonal or oligoclonal), whereas grade III shows numerous, large EBV-positive B cells (usually monoclonal), likely reflecting the progressive transformation of infected B cells.(1,2) Clinically, LYG nearly always presents in the lung, but commonly involves the skin, kidney, and central nervous system(4,3); lymph nodes are rarely enlarged. We report on an unusual active erosive lesion of the hard palate in a 32-year-old woman with a history of LYG involving the lungs.
C1 [Brahim, Jaime S.] Natl Inst Dent & Craniofacial Res, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Shanti, Rabie M.] Univ Med & Dent New Jersey, Dept Oral & Maxillofacial Surg, Newark, NJ 07103 USA.
[Torres-Cabala, Carlos A.] NCI, Pathol Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Brahim, JS (reprint author), Natl Inst Dent & Craniofacial Res, NIH, Dept Hlth & Human Serv, Bldg 10,Room 1N-117,10 Ctr Dr,MSC 1191, Bethesda, MD 20892 USA.
EM jbrahim@dir.nidcr.nih.gov
FU Intramural NIH HHS [Z99 DE999999]
NR 13
TC 5
Z9 5
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0278-2391
J9 J ORAL MAXIL SURG
JI J. Oral Maxillofac. Surg.
PD OCT
PY 2008
VL 66
IS 10
BP 2161
EP 2163
DI 10.1016/j.joms.2008.06.026
PG 3
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 355QL
UT WOS:000259723300029
PM 18848119
ER
PT J
AU Ebersole, JL
Steffen, MJ
Reynolds, MA
Branch-Mays, GL
Dawson, DR
Novak, KF
Gunsolley, JC
Mattison, JA
Ingram, DK
Novak, MJ
AF Ebersole, J. L.
Steffen, M. J.
Reynolds, M. A.
Branch-Mays, G. L.
Dawson, D. R.
Novak, K. F.
Gunsolley, J. C.
Mattison, J. A.
Ingram, D. K.
Novak, M. J.
TI Differential gender effects of a reduced-calorie diet on systemic
inflammatory and immune parameters in nonhuman primates
SO JOURNAL OF PERIODONTAL RESEARCH
LA English
DT Article
DE nonhuman primates; calorie restriction; oral infections; host responses
ID MONKEYS MACACA-MULATTA; FEMALE RHESUS-MONKEYS; ACUTE-PHASE REACTANTS;
PERIODONTAL-DISEASE; ANTIBODY-RESPONSES; LIFE-SPAN;
PORPHYROMONAS-GINGIVALIS; ORAL MICROORGANISMS; ENERGY RESTRICTION;
VASCULAR-RESPONSES
AB Background and Objective: Dietary manipulation, including caloric restriction, has been shown to impact host response capabilities significantly, particularly in association with aging. This investigation compared systemic inflammatory and immune-response molecules in rhesus monkeys (Macaca mulatta).
Material and Methods: Monkeys on continuous long-term calorie-restricted diets and a matched group of animals on a control ad libitum diet, were examined for systemic response profiles including the effects of both gender and aging.
Results: The results demonstrated that haptoglobin and alpha 1-antiglycoprotein levels were elevated in the serum of male monkeys. Serum IgG responses to Campylobacter rectus, Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis were significantly elevated in female monkeys. While only the antibody to Fusobacterium nucleatum was significantly affected by the calorie-restricted diet in female monkeys, antibody levels to Prevotella intermedia, C. rectus and Treponema denticola demonstrated a similar trend.
Conclusion: In this investigation, only certain serum antibody levels were influenced by the age of male animals, which was seemingly related to increasing clinical disease in this gender. More generally, analytes were modulated by gender and/or diet in this oral model system of mucosal microbial challenge.
C1 [Ebersole, J. L.; Steffen, M. J.; Dawson, D. R.; Novak, K. F.; Novak, M. J.] Univ Kentucky, Coll Dent, Ctr Oral Hlth Res, Lexington, KY 40506 USA.
[Reynolds, M. A.; Branch-Mays, G. L.; Gunsolley, J. C.] Univ Maryland, Sch Dent, Baltimore, MD 21201 USA.
[Mattison, J. A.; Ingram, D. K.] NIA, Lab Expt Gerontol, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Ebersole, JL (reprint author), Univ Kentucky, Coll Dent, Ctr Oral Hlth Res, Lexington, KY 40506 USA.
EM jleber2@pop.uky.edu
FU USPHS [U01 AG-021406]; National Institute on Aging; Division of Research
Resources of the National Institutes of Health
FX This work was supported by USPHS grant U01 AG-021406 from the National
Institute of Aging and by funds from the Intramural Research Program of
the National Institute on Aging and the Veterinary Research Program of
the Division of Research Resources of the National Institutes of Health.
We extend our gratitude to the entire technical support group from the
NIH Animal Research Center, especially April Hobbs, Edward Tilmont,
Tommy Thompson and Suzanne Pazzi, for managing the sample collection and
shipment for analyses, and to Rick Herbert (DVM) and Doug Powell (DVM)
for their outstanding clinical assistance that assured the good health
of the monkeys in this study. The contributions of Dr George Roth and Dr
Mark Lane in facilitating this research program are also greatly
appreciated.
NR 94
TC 18
Z9 18
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3484
J9 J PERIODONTAL RES
JI J. Periodont. Res.
PD OCT
PY 2008
VL 43
IS 5
BP 500
EP 507
DI 10.1111/j.1600-0765.2008.01051.x
PG 8
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 342KX
UT WOS:000258784100003
PM 18565132
ER
PT J
AU McCrae, RR
Martin, TA
Hrebickova, M
Urbanek, T
Boomsma, DI
Willemsen, G
Costa, PT
AF McCrae, Robert R.
Martin, Thomas A.
Hrebickova, Martina
Urbanek, Tomas
Boomsma, Dorret I.
Willemsen, Gonneke
Costa, Paul T., Jr.
TI Personality Trait Similarity Between Spouses in Four Cultures
SO JOURNAL OF PERSONALITY
LA English
DT Article
ID NETHERLANDS TWIN REGISTER; AGE-DIFFERENCES; MARITAL SATISFACTION; MATE
PREFERENCES; MARRIED-COUPLES; FAMILY; ABILITIES; SELECTION; STYLE
AB We examined patterns of trait similarity (assortative mating) in married couples in four cultures, using both self-reports and spouse ratings on versions of the Revised NEO personality Inventory. There was evidence of a subtle but pervasive perceived contrast bias in the spouse-rating data. However, there was strong agreement across methods of assessment and moderate agreement across cultures in the pattern of results. Most assortment agreement across cultures in the pattern of results. Most assortment effects were small, but correlations exceeding .40 were seen for a subset of traits, chiefly from the Openness and Agreeableness domains. Except in Russia, where more positive assortment was seen for younger couples, comparisons of younger and older cohorts showed little systematic difference. This suggested that mate selection, rather than convergence over time, accounted for similarity. Future research on personality similarity in dyads can utilize different designs but should assess personality at both domain and the facet levels.
C1 [McCrae, Robert R.; Costa, Paul T., Jr.] NIA, NIH, DHHS, Biomed Res Ctr, Baltimore, MD 21224 USA.
[Martin, Thomas A.] Susquehanna Univ, Selinsgrove, PA USA.
[Boomsma, Dorret I.; Willemsen, Gonneke] Vrije Univ Amsterdam, Amsterdam, Netherlands.
RP McCrae, RR (reprint author), NIA, NIH, DHHS, Biomed Res Ctr, 251 Bayview Blvd,Suite 100,Room 04B329, Baltimore, MD 21224 USA.
EM mccraej@grc.nia.nih.gov
RI Urbanek, Tomas/G-9427-2014; Hrebickova, Martina/H-4410-2014;
OI Urbanek, Tomas/0000-0002-8807-4869; Hrebickova,
Martina/0000-0003-4356-567X; Costa, Paul/0000-0003-4375-1712
FU Intramural NIH HHS [Z01 AG000183-19]
NR 45
TC 30
Z9 30
U1 2
U2 20
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND
SN 0022-3506
J9 J PERS
JI J. Pers.
PD OCT
PY 2008
VL 76
IS 5
BP 1137
EP 1163
DI 10.1111/j.1467-6494.2008.00517.x
PG 27
WC Psychology, Social
SC Psychology
GA 358OH
UT WOS:000259926900005
PM 18665894
ER
PT J
AU Dai, SJ
Jia, YF
Wu, SL
Isenberg, JS
Ridnour, LA
Bandle, RW
Wink, DA
Roberts, DD
Karger, BL
AF Dai, Shujia
Jia, Yifeng
Wu, Shiaw-Lin
Isenberg, Jeff S.
Ridnour, Lisa A.
Bandle, Russell W.
Wink, David A.
Roberts, David D.
Karger, Barry L.
TI Comprehensive characterization of heat shock protein 27 phosphorylation
in human endothelial cells stimulated by the microbial dithiole
thiolutin
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE Hsp27; acetylation; phosphorylation; N-terminal cleavage; recovery of
large peptides; label-free quantitation of PTMs; immunoprecipitation;
LC-MS
ID RANGE PROTEOMIC ANALYSIS; P38 MAP KINASE; HEAT-SHOCK PROTEINS;
POSTTRANSLATIONAL MODIFICATIONS; HSP27 PHOSPHORYLATION; MAMMALIAN HSP27;
AKT ACTIVATION; SIGNAL COMPLEX; SMOOTH-MUSCLE; ANALYSIS ERPA
AB Thiolutin is a sulfur-based microbial compound with known activity as an angiogenesis inhibitor. Relative to previously studied angiogenesis inhibitors, thiolutin is a remarkably potent inducer of heat shock protein 27 (Hsp27) phosphorylation. This phosphorylation requires p38 kinase but is independent of increased p38 phosphorylation. To elucidate how thiolutin regulates Hsp27 phosphorylation and ultimately angiogenesis, Hsp27 was immunoprecipitated using nonphosphorylated and phospho-Ser78 specific antibodies from lysates of thiolutin treated and untreated human umbilical vein endothelial cells and analyzed by LC-MS. Separate LC-MS analyses of Lys-C, Lys-C plus trypsin, and Lys-C plus Glu-C digests provided 100% sequence coverage, including the identification of a very large 13 kDa Lys-C fragment using a special sample handling procedure (4 M guanidine HCl) prior to the LC-MS analysis to improve the large peptide recovery. The analysis revealed a novel post-translational modification of Hsp27 involving truncation of the N-terminal Met and acetylation of the penultimate Thr. Analysis of a Glu-C fragment containing two phosphorylation sites, Ser78 and Ser82, and a tryptic fragment containing the other phosphorylation site, Ser15, enabled quantitative stoichiometry of Hsp27 phosphorylation by LC-MS. The strategy revealed details of Hsp27 phosphorylation, including significant di-phosphorylation at both Ser78 and Ser82, that would be difficult to obtain by traditional approaches because oligomerization of the hydrophobic N-terminal region of the molecule prevents efficient enzymatic cleavage. The combination of Western blotting, immunoprecipation, and LC-MS provides a quantitative analysis of thiolutin-stimulated Hsp27 phosphorylation and further defines the role of Hsp27 in the antiangiogenic activities of thiolutin and related dithiolethiones.
C1 [Dai, Shujia; Wu, Shiaw-Lin; Karger, Barry L.] Northeastern Univ, Barnett Inst, Boston, MA 02115 USA.
[Jia, Yifeng; Isenberg, Jeff S.; Bandle, Russell W.; Roberts, David D.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Ridnour, Lisa A.; Wink, David A.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Karger, BL (reprint author), Northeastern Univ, Barnett Inst, Boston, MA 02115 USA.
EM b.karger@neu.edu
RI Roberts, David/A-9699-2008
OI Roberts, David/0000-0002-2481-2981
FU NIH [GM 15847]; Intramural Research Program of the NIH; NCI; Center for
Cancer Research
FX We acknowledge support from NIH grant GM 15847 (BLK) and the Intramural
Research Program of the NIH, NCI, Center for Cancer Research (D.D.R.,
D.A.W.). Contribution Number 925 from the Barnett Institute.
NR 42
TC 16
Z9 18
U1 1
U2 2
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
J9 J PROTEOME RES
JI J. Proteome Res.
PD OCT
PY 2008
VL 7
IS 10
BP 4384
EP 4395
DI 10.1021/pr800376w
PG 12
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 356NG
UT WOS:000259784300017
PM 18720982
ER
PT J
AU Lockenhoff, CE
Sutin, AR
Ferrucci, L
Costa, PT
AF Loeckenhoff, Corinna E.
Sutin, Angelina R.
Ferrucci, Luigi
Costa, Paul T., Jr.
TI Personality traits and subjective health in the later years: The
association between NEO-PI-R and SF-36 in advanced age is influenced by
health status
SO JOURNAL OF RESEARCH IN PERSONALITY
LA English
DT Article
DE Personality; Subjective health; Self-rated health; Five-Factor Model;
NEO-PI-R; SF-36; Older adults; Aging
ID PRIMARY-CARE PATIENTS; SELF-RATED HEALTH; ALL-CAUSE MORTALITY;
QUALITY-OF-LIFE; 5-FACTOR MODEL; PERCEIVED HEALTH; FUNCTIONAL STATUS;
PHYSICAL HEALTH; REPORTED HEALTH; OLDER PERSONS
AB This study examined the association between personality traits (as measured by the NEO-PI-R) and subjective ratings of mental and physical health (as measured by the SF-36) in two samples of older adults differing in health status (Baltimore Longitudinal Study of Aging, BLSA, n = 393, vs. Medicare Primary and Consumer-Directed Care Demonstration, Medicare PCC, n = 648). The association between personality traits and subjective mental health did not differ significantly across samples. The association between personality and subjective physical health, however, was significantly stronger in the healthy BLSA sample than in the medically challenged Medicare PCC sample. Differences in health conditions and recent hospitalizations partially accounted for this effect. Lifespan developmental considerations and implications for the use of subjective health ratings as outcome measures in clinical studies are discussed. Published by Elsevier Inc.
C1 [Loeckenhoff, Corinna E.; Sutin, Angelina R.; Ferrucci, Luigi; Costa, Paul T., Jr.] NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA.
RP Lockenhoff, CE (reprint author), NIA, Gerontol Res Ctr, NIH, Box 03,5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM LoeckenhoffC@grc.nia.nih.gov
OI Loeckenhoff, Corinna/0000-0003-1605-1323; Costa,
Paul/0000-0003-4375-1712
NR 66
TC 17
Z9 17
U1 2
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0092-6566
J9 J RES PERS
JI J. Res. Pers.
PD OCT
PY 2008
VL 42
IS 5
BP 1334
EP 1346
DI 10.1016/j.jrp.2008.05.006
PG 13
WC Psychology, Social
SC Psychology
GA 363XU
UT WOS:000260301600015
ER
PT J
AU Elder, JP
Shuler, L
Moe, SG
Grieser, M
Pratt, C
Cameron, S
Hingle, M
Pickrel, JL
Saksvig, BI
Schachter, K
Greer, S
Bothwell, EKG
AF Elder, John P.
Shuler, LaVerne
Moe, Stacey G.
Grieser, Mira
Pratt, Charlotte
Cameron, Sandra
Hingle, Melanie
Pickrel, Julie L.
Saksvig, Brit I.
Schachter, Kenneth
Greer, Susan
Bothwell, Elizabeth K. Guth
TI Recruiting a diverse group of middle school girls into the trial of
activity for adolescent girls
SO JOURNAL OF SCHOOL HEALTH
LA English
DT Article
DE recruitment; TAAG; adolescent girls; school-based research; physical
activity
ID PARTICIPANTS; RETENTION; EXPERIENCES; INCENTIVES; STRATEGIES; SUBJECT;
PROJECT
AB BACKGROUND: School-based study recruitment efforts are both time consuming and challenging. This paper highlights the recruitment strategies employed by the national, multisite Trial of Activity for Adolescent Girls (TAAG), a study designed to measure the effectiveness of an intervention to reduce the decline of physical activity levels among middle school-aged girls. TAAG provided a unique opportunity to recruit large cohorts of randomly sampled girls within 36 diverse middle schools across the United States.
METHODS: Key elements of the formative planning, coordination, and design of TAAG's recruitment efforts included flexibility, tailoring, and the use of incentives. Various barriers, including a natural disaster, political tension, and district regulations, were encountered throughout the recruitment process, but coordinated strategies and frequent communication between the 6 TAAG sites were helpful in tailoring the recruitment process at the 36 intervention and control schools.
RESULTS: Progressively refined recruitment strategies and specific attention to the target audience of middle school girls resulted in overall study recruitment rates of 80%, 85%, and 89%, for the baseline, posttest, and follow-up period, respectively.
DISCUSSION: The steady increase in recruitment rates over time is attributed to an emphasis on successful strategies and a willingness to modify less successful methods. Open and consistent communication, an increasingly coordinated recruitment strategy, interactive recruitment presentations, and participant incentives resulted in an effective recruitment campaign.
C1 [Elder, John P.] San Diego State Univ, Grad Sch Publ Hlth, Div Hlth Promot, San Diego, CA 92182 USA.
[Shuler, LaVerne] Hlth Sci S Carolina, Columbia, SC 29201 USA.
[Moe, Stacey G.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN 55454 USA.
[Grieser, Mira] Univ Maryland, Coll Hlth & Human Performance, Dept Kinesiol, College Pk, MD 20742 USA.
[Pratt, Charlotte] NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
[Cameron, Sandra] Tulane Univ, Sch Publ Hlth & Trop Med, Dept Biostat, New Orleans, LA 70112 USA.
[Hingle, Melanie] Univ Arizona, Dept Nutr Sci, Tucson, AZ 85721 USA.
[Elder, John P.; Pickrel, Julie L.; Bothwell, Elizabeth K. Guth] San Diego State Univ, Grad Sch Publ Hlth, Ctr Behav & Community Hlth Studies, San Diego, CA 92123 USA.
[Saksvig, Brit I.] Univ Maryland, Sch Publ Hlth, Dept Epidemiol & Biostat, College Pk, MD 20742 USA.
[Schachter, Kenneth] Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Div Community Environm & Policy, Tucson, AZ 85724 USA.
[Greer, Susan] Univ N Carolina, Sch Publ Hlth, Dept Biostat, Chapel Hill, NC 27514 USA.
RP Elder, JP (reprint author), San Diego State Univ, Grad Sch Publ Hlth, Ctr Behav & Community Hlth Studies, 9245 Sky Pk Court,Suite 221, San Diego, CA 92123 USA.
EM jelder@mail.sdsu.edu
FU NHLBI NIH HHS [U01HL066858, U01 HL066845, U01 HL066852, U01 HL066855,
U01 HL066856, U01 HL066856-01, U01 HL066858, U01HL066845, U01HL066852,
U01HL066853, U01HL066855, U01HL066856, U01HL066857]
NR 17
TC 18
Z9 18
U1 1
U2 2
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND
SN 0022-4391
J9 J SCHOOL HEALTH
JI J. Sch. Health
PD OCT
PY 2008
VL 78
IS 10
BP 523
EP 531
DI 10.1111/j.1746-1561.2008.00339.x
PG 9
WC Education & Educational Research; Education, Scientific Disciplines;
Health Care Sciences & Services; Public, Environmental & Occupational
Health
SC Education & Educational Research; Health Care Sciences & Services;
Public, Environmental & Occupational Health
GA 350IX
UT WOS:000259347100002
PM 18808471
ER
PT J
AU Guo, WG
Rao, MB
AF Guo, Wenge
Rao, M. Bhaskara
TI On control of the false discovery rate under no assumption of dependency
SO JOURNAL OF STATISTICAL PLANNING AND INFERENCE
LA English
DT Article
DE critical constants; false discovery rate; knapsack problem; multiple
testing; positive regression dependence; p-value; step-up procedure;
step-down procedure
ID TESTS
AB Most false discovery rate (FDR) controlling procedures require certain assumptions on the joint distribution of p-values. Benjamini and Hochberg [1995. Controlling the false discovery rate: a practical and powerful approach to multiple testing. J. Roy. Statist. Soc. Ser. B 57, 289-300] proposed a step-up procedure with critical constants alpha(i) = (i/m)alpha, 1 <= i <= m, for a given level 0 < alpha < 1 and showed that FDR <= (m(0)/m)alpha under the assumption of independence of p-values, where m is the total number of null hypotheses and m(0) the number of true null hypotheses. Benjamini and Yekutieli [2001. The control of the false discovery rate in multiple testing under dependency. Ann. Statist. 29, 1165-1188] showed that for the same procedure FDR <= (m(0)/m)alpha Sigma(m)(j=1) 1/j, whatever may be the joint distribution of p-values. In one of the results in this paper, we show that this upper bound for FDR cannot be improved in the sense that there exists a joint distribution of p-values for which the upper bound is attained. A major thrust of this paper is to work in the realm of step-down procedures without imposing any condition on the joint distribution of the underlying p-values. As a starting point, we give an explicit expression for FDR specially tailored for step-down procedures. Using the same critical constants as those of the Benjamini-Hochberg procedure, we present a new step-down procedure for which the upper bound for FDR is much lower than what is given by Benjamini and Yekutieli. The explicit expression given for FDR and some optimization techniques stemming from the knapsack problem are instrumental in getting the main result. We also present some general results on stepwise procedures built on non-decreasing sequences of critical constants. (C) 2008 Elsevier B.V. All fights reserved.
C1 [Guo, Wenge] Natl Inst Environm Hlth Sci, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Rao, M. Bhaskara] Univ Cincinnati, Dept Environm Hlth, Cincinnati, OH 45267 USA.
RP Guo, WG (reprint author), Natl Inst Environm Hlth Sci, Biostat Branch, MD A3-03,POB 12233, Res Triangle Pk, NC 27709 USA.
EM wenge.guo@gmail.com
OI Guo, Wenge/0000-0003-3777-2058
NR 13
TC 14
Z9 16
U1 1
U2 18
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-3758
J9 J STAT PLAN INFER
JI J. Stat. Plan. Infer.
PD OCT 1
PY 2008
VL 138
IS 10
BP 3176
EP 3188
DI 10.1016/j.jspi.2008.01.003
PG 13
WC Statistics & Probability
SC Mathematics
GA 334BE
UT WOS:000258196500025
ER
PT J
AU Narasimha, R
Aganj, I
Bennett, AE
Borgnia, MJ
Zabransky, D
Sapiro, G
McLaughlin, SW
Milne, JLS
Subramaniam, S
AF Narasimha, Rajesh
Aganj, Iman
Bennett, Adam E.
Borgnia, Mario J.
Zabransky, Daniel
Sapiro, Guillermo
McLaughlin, Steven W.
Milne, Jacqueline L. S.
Subramaniam, Sriram
TI Evaluation of denoising algorithms for biological electron tomography
SO JOURNAL OF STRUCTURAL BIOLOGY
LA English
DT Article
DE automated techniques; denoising; diffusion; electron tomography; feature
extraction; template matching
ID AUTOMATIC PARTICLE-DETECTION; CRYOELECTRON TOMOGRAPHY; ANISOTROPIC
DIFFUSION; MICROSCOPY; RECONSTRUCTION; SEGMENTATION; FILTER; FEATURES
AB Tomograms of biological specimens derived using transmission electron microscopy can be intrinsically noisy due to the use of low electron doses, the presence of a "missing wedge" in most data collection schemes, and inaccuracies arising during 3D volume reconstruction. Before tomograms can be interpreted reliably, for example, by 3D segmentation, it is essential that the data be suitably denoised using procedures that can be individually optimized for specific data sets. Here, we implement a systematic procedure to compare various nonlinear denoising techniques on tomograms recorded at room temperature and at cryogenic temperatures, and establish quantitative criteria to select a denoising approach that is most relevant for a given tomogram. We demonstrate that using an appropriate denoising algorithm facilitates robust segmentation of tomograms of HIV-infected macrophages and Bdellovibrio bacteria obtained from specimens at room and cryogenic temperatures, respectively. We validate this strategy of automated segmentation of optimally denoised tomograms by comparing its performance with manual extraction of key features from the same tomograms. Published by Elsevier Inc.
C1 [Narasimha, Rajesh; Bennett, Adam E.; Borgnia, Mario J.; Milne, Jacqueline L. S.; Subramaniam, Sriram] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
[Narasimha, Rajesh; McLaughlin, Steven W.] Georgia Inst Technol, Sch Elect & Comp Engn, Atlanta, GA 30332 USA.
[Aganj, Iman; Sapiro, Guillermo] Univ Minnesota, Dept Elect & Comp Engn, Minneapolis, MN 55455 USA.
RP Subramaniam, S (reprint author), NCI, Cell Biol Lab, NIH, Bldg 50 S Dr,Room 4306, Bethesda, MD 20892 USA.
EM ss1@nih.gov
FU National Cancer Institute; NIH, Bethesda
FX This work was supported by funds from the intramural program of the
National Cancer Institute, NIH, Bethesda, MD. We thank Dr. Alexander
Shapiro of the ISYE department and Muhammad Mukarram Bin Tariq of the
College of Computing: Georgia Institute of Technology for useful
discussion on the GOF tests.
NR 32
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Z9 20
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1047-8477
J9 J STRUCT BIOL
JI J. Struct. Biol.
PD OCT
PY 2008
VL 164
IS 1
BP 7
EP 17
DI 10.1016/j.jsb.2008.04.006
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 354SX
UT WOS:000259660400002
PM 18585059
ER
PT J
AU Gorbach, AM
Wang, HL
Dhanani, NN
Gage, FA
Pinto, PA
Smith, PD
Kirk, AD
Elster, EA
AF Gorbach, Alexander M.
Wang, Hengliang
Dhanani, Nadeem N.
Gage, Fred A.
Pinto, Peter A.
Smith, Paul D.
Kirk, Allan D.
Elster, Eric A.
TI Assessment of critical renal ischemia with real-time infrared Imaging
SO JOURNAL OF SURGICAL RESEARCH
LA English
DT Article
DE infrared imaging; kidney vasculature; blood flow regulation; ischemia
ID BLOOD-FLOW REGULATION; INTESTINAL VIABILITY; PERFUSION SIGNAL;
OSCILLATIONS; BRAIN; REPERFUSION; PRESSURE; DYNAMICS; SURGERY; MODEL
AB Background. Currently visual and tactile clues such as color, mottling, and tissue turgor are used in the operating room for subjective assessments of organ ischemia. Studies have demonstrated that infrared (IR) imaging is a reliable tool to identify perfusion of brain tumors and kidneys during human surgery. Intraoperative IR imaging has the potential for more objective real-time detection and quantitative assessment of organ viability including early ischemia. We hypothesize, by detecting variations of the IR signal, we can assess the degree to which renal surface temperature reflects underlying renal ischemia. To address this hypothesis, IR imaging-derived temperature fluctuations were evaluated during laparotomy in a porcine model (n = 15). These temperature profiles then underwent spectral (frequency) analysis to assess their relationship to well-described oscillations of the microcirculation. Materials and methods. An IR camera was positioned 30-60 cm above the exposed kidneys. Images (3-5 mu m wavelength) were collected (1.0/s) at baseline, during warm renal ischemia, and during reperfusion. Dominant frequency (DF) of the tissue temperature fluctuations were determined by a Fourier transformation (spectral) analysis. Results. I:R images immediately showed which segments of the kidney were ischemic. DF at similar to 0.008 Hz that corresponds to blood flow oscillations was observed in thermal profiles. The oscillations were diminished or disappeared after 25 min of warm ischemia and were recovered with reperfusion in a time-dependent fashion. Oscillations were attenuated substantially in ischemic segments, but not in perfused segments of the kidney. Conclusions. The described oscillations can be measured noninvasively using IR imaging in the operating room, as represented by the DF, and may be an early marker of critical renal ischemia. (c) 2008 Elsevier Inc. All rights reserved.
C1 [Wang, Hengliang; Gage, Fred A.; Elster, Eric A.] USN, Med Res Ctr, Silver Spring, MD 20910 USA.
[Gorbach, Alexander M.; Smith, Paul D.] Natl Inst Biomed Imaging & Bioengn, Lab Bioengn & Phys Sci, NIH, Bethesda, MD USA.
[Dhanani, Nadeem N.; Pinto, Peter A.] NCI, Urol Oncol Branch, Bethesda, MD 20892 USA.
[Kirk, Allan D.] NIDDKD, Transplant Branch, Bethesda, MD 20892 USA.
[Elster, Eric A.] Natl Naval Med Ctr, Dept Surg, Bethesda, MD USA.
[Elster, Eric A.] Uniformed Serv Univ Hlth Sci, Dept Surg, Bethesda, MD 20814 USA.
RP Elster, EA (reprint author), USN, Med Res Ctr, 503 Robert Grant Ave,Suite 2W123, Silver Spring, MD 20910 USA.
EM elstere@nmrc.navy.mil
RI Kirk, Allan/B-6905-2012
FU National Institutes of Health and Department of Defense
[602227D.0483.01.A0518]
FX The authors would like to acknowledge the significant contributions of
Mehrdad Alemozaffar, B.S., Neil Kansal, M.D., Doug K. Tadaki, Ph.D. to
the implementation and support of this study. The authors would like to
thank Henry Eden, M.D., Ph.D., for his invaluable critique and
insightful comments during preparation of this manuscript. This work was
supported by the intramural research funds of National Institutes of
Health and Department of Defense (work unit number:
602227D.0483.01.A0518, Medical Free Electron Laser program). The views
expressed in this article are those of the author and do not necessarily
reflect the official policy or position of the Department of the Navy,
Department of Defense, nor the U.S. Government. I am a military service
member (or employee of the U.S. Government). This work was prepared as
part of my official duties. Title 17 U.S.C. 105 provides that "Copyright
protection under this title is not available for any work of the United
States Government." Title 17 U.S.C. 101 defines a U.S. Government work
as a work prepared by a military service member or employee of the U.S.
Government as part of that person's official duties.
NR 26
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Z9 6
U1 2
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4804
J9 J SURG RES
JI J. Surg. Res.
PD OCT
PY 2008
VL 149
IS 2
BP 310
EP 318
DI 10.1016/j.jss.2008.02.007
PG 9
WC Surgery
SC Surgery
GA 350DG
UT WOS:000259332200020
PM 18468641
ER
PT J
AU Gogtay, N
Rapoport, JL
AF Gogtay, Nitin
Rapoport, Judith L.
TI Childhood-onset schizophrenia: Insights from neuroimaging studies
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
ID CORTICAL GRAY-MATTER; BRAIN-DEVELOPMENT; SPECTRUM DISORDER; TWINS
DISCORDANT; WHITE-MATTER; ABNORMALITIES; SIBLINGS; MRI; ADOLESCENCE;
HIPPOCAMPUS
C1 [Gogtay, Nitin; Rapoport, Judith L.] NIMH, Child Psychiat Branch, US Dept HHS, NIH, Bethesda, MD 20892 USA.
RP Gogtay, N (reprint author), NIMH, Child Psychiat Branch, US Dept HHS, NIH, Bldg 10,Room 3N202,10 Ctr Dr,MSC-1600, Bethesda, MD 20892 USA.
EM gogtayn@mail.nih.gov
NR 47
TC 10
Z9 10
U1 3
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD OCT
PY 2008
VL 47
IS 10
BP 1120
EP 1124
DI 10.1097/CHI.0b013e31817eed7a
PG 5
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 352PT
UT WOS:000259510100005
PM 20566189
ER
PT J
AU Greenstein, DK
Wolfe, S
Gochman, P
Rapoport, JL
Gogtay, N
AF Greenstein, Deanna K.
Wolfe, Sarah
Gochman, Peter
Rapoport, Judith L.
Gogtay, Nitin
TI Remission status and cortical thickness in childhood-onset schizophrenia
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE childhood-onset schizophrenia; magnetic resonance imaging; remission;
cortical thickness
ID 1ST-EPISODE SCHIZOPHRENIA; DOUBLE-BLIND; MRI DATA; BRAIN; VALIDATION;
MORPHOLOGY; CRITERIA; CORTEX; ADOLESCENCE; PREDICTORS
AB Objective: Few studies have examined prediction of schizophrenia outcome in relation to brain magnetic resonance imaging measures. In this study, remission status at the time of discharge was examined in relation to admission cortical thickness for childhood-onset schizophrenia probands. We hypothesized that total, frontal, temporal, and parietal gray matter thickness would be greater in patients who subsequently remit. Method: The relation between admission cortical brain thickness on magnetic resonance imaging and remission status at the time of discharge an average of 3 months later was examined for 56 individuals (32 males) ages 6 to 19 diagnosed with childhood-onset schizophrenia. Cortical thickness was measured across the cerebral hemispheres at admission. Discharge remission criteria were adapted from the 2005 Remission in Schizophrenia Working Group criteria. Results: Patients remitted at discharge (n = 16 [29%]) had thicker regional cortex in left orbitofrontal, left superior, and middle temporal gyri and bilateral postcentral and angular gyri (p <= .008). Conclusions: Our results provide neuroanatomic correlates of clinical remission in schizophrenia and evidence that response to treatment may be mediated by these cortical brain regions.
C1 [Greenstein, Deanna K.; Wolfe, Sarah; Gochman, Peter; Rapoport, Judith L.; Gogtay, Nitin] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
RP Greenstein, DK (reprint author), NIMH, Child Psychiat Branch, NIH, Bldg 10,Room 3N 202, Bethesda, MD 20892 USA.
EM greenstd@mail.nih.gov
FU Intramural NIH HHS [Z99 MH999999]
NR 51
TC 10
Z9 10
U1 4
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD OCT
PY 2008
VL 47
IS 10
BP 1133
EP 1140
DI 10.1097/CHI.0b013e3181825b0c
PG 8
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 352PT
UT WOS:000259510100007
PM 18724254
ER
PT J
AU Roy, AK
Vasa, RA
Bruck, M
Mogg, K
Bradley, BP
Sweeney, M
Bergman, RL
McClure-Tone, EB
Pine, DS
AF Roy, Amy Krain
Vasa, Roma A.
Bruck, Maggie
Mogg, Karin
Bradley, Brendan P.
Sweeney, Michael
Bergman, R. Lindsey
McClure-Tone, Erin B.
Pine, Daniel S.
CA Cams Team
TI Attention bias toward threat in pediatric anxiety disorders
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE anxiety disorders; attentional bias; threat
ID POSTTRAUMATIC-STRESS-DISORDER; GENERALIZED-ANXIETY; EMOTIONAL
INFORMATION; SOCIAL PHOBIA; PANIC DISORDER; ANGRY FACES; CHILDREN;
ADOLESCENTS; AMYGDALA; DEPRESSION
AB Objective: To examine attention bias toward threat faces in a large sample of anxiety-disordered youths using a well-established visual probe task. Method: Study participants included 101 children and adolescents (ages 7-18 years) with generalized anxiety disorder, social phobia, and/or separation anxiety disorder enrolled in a multisite anxiety treatment study. Nonanxious youths (n = 51; ages 9-18 years) were recruited separately. Participants were administered a computerized visual probe task that presents pairs of faces portraying threat (angry), positive (happy), and neutral expressions. They pressed a response key to indicate the spatial location of a probe that replaced one of the faces on each trial. Attention bias scores were calculated from response times to probes for each emotional face type. Results: Compared to healthy youths, anxious participants demonstrated a greater attention bias toward threat faces. This threat bias in anxious patients did not significantly vary across the anxiety disorders. There was no group difference in attention bias toward happy faces. Conclusions: These results suggest that pediatric anxiety disorders are associated with an attention bias toward threat. Future research may examine the manner in which cognitive bias in anxious youths changes with treatment.
C1 [Roy, Amy Krain] NYU, Sch Med, Ctr Child Study, New York, NY 10016 USA.
[Mogg, Karin; Bradley, Brendan P.] Univ Southampton, Sch Psychol, Southampton SO9 5NH, Hants, England.
[Sweeney, Michael] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Bergman, R. Lindsey] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
[McClure-Tone, Erin B.] Georgia State Univ, Dept Psychol, Atlanta, GA 30303 USA.
[Pine, Daniel S.] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
RP Roy, AK (reprint author), NYU, Sch Med, Ctr Child Study, 215 Lexington Ave,Suite 1307, New York, NY 10016 USA.
EM amy.roy@nyumc.org
RI Mogg, Karin/C-1181-2008; Bradley, Brendan/B-9724-2008; Roy,
Amy/J-7613-2013;
OI Mogg, Karin/0000-0002-2738-7378; Bradley, Brendan/0000-0003-2801-4271
FU NIMH NIH HHS [U01 MH064089, U01 MH063747, U01 MH063747-01A1, U01
MH064003, U01 MH064003-01A1, U01 MH064088, U01 MH064088-01A1, U01
MH064089-01A1, U01 MH064092, U01 MH064092-01A1, U01 MH064107, U01
MH064107-01A1, U01 MH63747-04, U01 MH64003, U01 MH64088, U01 MH64092,
U01 MH64107]
NR 47
TC 100
Z9 102
U1 10
U2 29
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD OCT
PY 2008
VL 47
IS 10
BP 1189
EP 1196
DI 10.1097/CHI.0b013e3181825ace
PG 8
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 352PT
UT WOS:000259510100014
PM 18698266
ER
PT J
AU Jackson, SN
Moyer, SC
Woods, AS
AF Jackson, Shelley N.
Moyer, Susanne C.
Woods, Amina S.
TI The Role of Phosphorylated Residues in Peptide-Peptide Noncovalent
Complexes Formation
SO JOURNAL OF THE AMERICAN SOCIETY FOR MASS SPECTROMETRY
LA English
DT Article
ID MASS-SPECTROMETRY; GAS-PHASE; PHOSPHATE; ARGININE; DNA
AB Electrospray mass spectrometry (ESI-MS) has become the tool of choice for the study of noncovalent complexes. Our previous work has highlighted the role of phosphorylated amino acid residues in the formation Of noncovalent complexes through electrostatic interaction with arginine residues' guanidinium groups. In this study, we employ tandem mass spectrometry to investigate the gas-phase stability and dissociation pathways of these noncovalent complexes. The only difference in the three phosphopeptides tested is the nature of the phosphorylated amino acid residue. In addition the absence of acidic residues and an amidated carboxyl terminus insured that the only negative charge came from the phosphate, which allowed for the comparison of the noncovalent bond between arginine residues and each of the different phosphorylated residues. Dissociation Curves were generated by plotting noncovalent complex ion intensities as a function of the nominal energy given to the noncovalent complex ion before entering the collision cell. These results showed that noncovalent complexes formed with phosphorylated tyrosine were the most stable, followed by serine and threonine, which had similar stability. (J Am Soc Mass Spectrom 2008, 19, 1535-1541) Published by Elsevier Inc. On behalf of American Society for Mass Spectrometry
C1 [Jackson, Shelley N.; Moyer, Susanne C.; Woods, Amina S.] NIDA, IRP, NIH, Baltimore, MD 21224 USA.
RP Woods, AS (reprint author), NIDA, IRP, NIH, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM awoods@intra.nida.nih.gov
FU Intramural Research Program of the National Institute Oil Drug Abuse;
NIH; Office of National Drug Control Policy (ONDCP)
FX The authors acknowledge support for this research by the Intramural
Research Program of the National Institute Oil Drug Abuse, NIH The
authors thank the Office of National Drug Control Policy (ONDCP) for
instrumentation funding, Without Which thiS and Other project, could
riot have been accomplished.
NR 16
TC 11
Z9 11
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1044-0305
J9 J AM SOC MASS SPECTR
JI J. Am. Soc. Mass Spectrom.
PD OCT
PY 2008
VL 19
IS 10
BP 1535
EP 1541
DI 10.1016/j.jasms.2008.06.023
PG 7
WC Chemistry, Analytical; Chemistry, Physical; Spectroscopy
SC Chemistry; Spectroscopy
GA 363LJ
UT WOS:000260268500019
PM 18657435
ER
PT J
AU Kottgen, A
Hwang, SJ
Rampersaud, E
Coresh, J
North, KE
Pankow, JS
Meigs, JB
Florez, JC
Parsa, A
Levy, D
Boerwinkle, E
Shuldiner, AR
Fox, CS
Kao, WHL
AF Kottgen, Anna
Hwang, Shih-Jen
Rampersaud, Evadnie
Coresh, Josef
North, Kari E.
Pankow, James S.
Meigs, James B.
Florez, Jose C.
Parsa, Afshin
Levy, Daniel
Boerwinkle, Eric
Shuldiner, Alan R.
Fox, Caroline S.
Kao, W. H. Linda
TI TCF7L2 variants associate with CKD progression and renal function in
population-based cohorts
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID GLOMERULAR-FILTRATION-RATE; GENOME-WIDE ASSOCIATION; POLYCYSTIC
KIDNEY-DISEASE; OLD ORDER AMISH; ATHEROSCLEROSIS RISK;
INSULIN-RESISTANCE; DIABETES-MELLITUS; SERUM CREATININE; LINKAGE
ANALYSIS; SHORT-TERM
AB Genetic variants may increase susceptibility to both diabetes and kidney disease. Whether known diabetes-associated variants in the transcription factor 7-like 2 (TCF7L2) gene are associated with chronic kidney disease (CKD) progression and markers of kidney function is unknown. Participants of the Atherosclerosis Risk in Communities Study (ARIC; n = 11,061 self-identified white and n = 4014 black), Framingham Heart Offspring Cohort (FHS; n = 2468), and Heredity and Phenotype Intervention Heart Study (HAPI; n = 861) were genotyped at five (ARIC) and two (FHS) common TCF7L2 variants. The diabetes-conferring risk alleles at rs7903146 and rs7901695 were significantly associated with CKD progression among ARIC participants overall and among those without baseline diabetes. The overall adjusted hazard ratios per rs7903146 T allele were 1.17 (95% confidence interval [CI] 1.04 to 1.32) for white individuals and 1.20 (95% Cl 1.03 to 1.41) for black individuals. Similarly, the overall hazard ratios per rs7901695 C allele were 1.19 (95% Cl 1.06to 1.34) for white individuals and 1.27 (95% CI 1.09to 1.48) for black individuals. The FHS cohort supported these results: The rs7903146 T allele was significantly associated with lower estimated GFR (P = 0.01) and higher cystatin C (P = 0.004) in adjusted analyses overall and among those without diabetes. In the HAPI cohort, the rs7901695 C allele was significantly associated with lower estimated GFR in adjusted analyses (P = 0.049), as were several variants upstream and downstream of TCF7L2 (P < 0.003). No identified variant in the ARIC or FHS cohorts was associated with albuminuria. In conclusion, several population-based samples suggest that variants in the TCF7L2 gene are associated with reduced kidney function or CKD progression, overall and specifically among participants without diabetes.
C1 [Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA 01702 USA.
[Hwang, Shih-Jen; Levy, Daniel; Fox, Caroline S.] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
[Kottgen, Anna; Coresh, Josef; Kao, W. H. Linda] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
Johns Hopkins Univ, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
[Rampersaud, Evadnie; Parsa, Afshin; Shuldiner, Alan R.] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
[North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
[Pankow, James S.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Meigs, James B.; Florez, Jose C.; Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
[Florez, Jose C.] Massachusetts Gen Hosp, Dept Med, Diabet Unit, Boston, MA 02114 USA.
[Florez, Jose C.] Massachusetts Gen Hosp, Dept Med, Ctr Human Genet Res, Boston, MA 02114 USA.
Broad Inst Harvard, Program Med & Populat Genet, Cambridge, MA USA.
MIT, Cambridge, MA 02139 USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr, Ctr Human Genet, Houston, TX USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr, Inst Mol Med, Houston, TX USA.
[Shuldiner, Alan R.] Vet Adm Med Ctr, Geriatr Res & Educ Clin Ctr, Baltimore, MD 21218 USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol Hypertens & Metab, Boston, MA 02115 USA.
RP Fox, CS (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM foxca@nhlbi.nih.gov; wkao@jhsph.edu
RI Kottgen, Anna/D-2920-2012;
OI Pankow, James/0000-0001-7076-483X
FU National Heart, Lung, and Blood Institute (NHLBI) [N01-HC-55015,
N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021,
N01-HC-55022, N01-HC-25195]; National Institutes of Health
(NIH)/NHLBI-sponsored National Research Service Award Institutional
Training Grant in Cardiac and Vascular Cell Biology [T32HL072751]; NIH
[U01 HL72515, K24 DK080140]; University of Maryland General Clinical
Research Center [M01 RR 16500]; Johns Hopkins University General
Clinical Research Center [M01 RR 000052]; Clinical Nutrition Research
Unit of Maryland [P30 DK072488]; American Diabetes Association Research
Award; ADA Career Development Award; NIH Research Career Award [K23
DK65978-03]; [1K12RR023250-01]; [K01DK067207]
FX The ARIC Study was Supported by contracts N01-HC-55015, N01-HC-55016,
N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, and N01-HC-55022
with the National Heart, Lung, and Blood Institute (NHLBI). The FHS is
Supported by the National Heart, Lung, and Blood Institute
(N01-HC-25195). The HAN Heart Study is Supported by the National
Institutes of Health (NIH)/NHLBI-sponsored National Research Service
Award Institutional Training Grant in Cardiac and Vascular Cell Biology
T32HL072751, NIH research grant U01 HL72515, the University of Maryland
General Clinical Research Center grant M01 RR 16500, the Johns Hopkins
University General Clinical Research Center grant M01 RR 000052, and the
Clinical Nutrition Research Unit of Maryland (P30 DK072488). A.K. is
supported by an Get-man Research Foundation Fellowship. LB.M. is
supported by an American Diabetes Association Research Award, an ADA
Career Development Award, and NIH grant K24 DK080140. LCT. is supported
by an NIH Research Career Award K23 DK65978-03. A.P. is supported by
1K12RR023250-01. W.H.K. is Supported by K01DK067207.
NR 47
TC 24
Z9 24
U1 0
U2 2
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD OCT
PY 2008
VL 19
IS 10
BP 1989
EP 1999
DI 10.1681/ASN.2007121291
PG 11
WC Urology & Nephrology
SC Urology & Nephrology
GA 357FE
UT WOS:000259830900020
PM 18650481
ER
PT J
AU Featherstone, RM
Lyon, BJ
Ruffin, AB
AF Featherstone, Robin M.
Lyon, Becky J.
Ruffin, Angela B.
TI Library roles in disaster response: an oral history project by the
National Library of Medicine
SO JOURNAL OF THE MEDICAL LIBRARY ASSOCIATION
LA English
DT Article; Proceedings Paper
CT 108th Annual Meeting of the Medical-Library-Association
CY MAY 18, 2008
CL Chicago, IL
SP Med Lib Assoc
AB Objectives: To develop a knowledgebase of stories illustrating the variety of roles that librarians can assume in emergency and disaster planning, preparedness, response, and recovery, the National Library of Medicine conducted an oral history project during the summer of 2007. The history aimed to describe clearly and compellingly the activities-both expected and unusual-that librarians performed during and in the aftermath of the disasters. While various types of libraries were included in interviews, the overall focus of the project was on elucidating roles for medical libraries.
Methods: Using four broad questions as the basis for telephone and email interviews, the investigators recorded the stories of twenty-three North American librarians who responded to bombings and other acts of terrorism, earthquakes, epidemics, fires, floods, hurricanes, and tornados.
Results: Through the process of conducting the oral history, an understanding of multiple roles for libraries in disaster response emerged. The roles fit into eight categories: institutional supporters, collection managers, information disseminators, internal planners, community supporters, government partners, educators and trainers, and information community builders.
Conclusions: Librarians-particularly health sciences librarians-made significant contributions to preparedness and recovery activities surrounding recent disasters. Lessons learned from the oral history project increased understanding of and underscored the value of collaborative relationships between libraries and local, state, and federal disaster management agencies and organizations.
C1 [Featherstone, Robin M.] Yale Univ, Natl Lib Med, New Haven, CT 06520 USA.
[Lyon, Becky J.; Ruffin, Angela B.] Natl Lib Med, Natl Network Lib Med, Bethesda, MD 20894 USA.
RP Featherstone, RM (reprint author), Yale Univ, Natl Lib Med, 333 Cedar St,POB 208014, New Haven, CT 06520 USA.
EM robin.featherstone@yale.edu; blyon@nlm.nih.gov;
angela_ruffin@nlm.nih.gov
RI Featherstone, Robin/J-5165-2014
OI Featherstone, Robin/0000-0003-2517-2258
NR 12
TC 10
Z9 11
U1 2
U2 17
PU MEDICAL LIBRARY ASSOC
PI CHICAGO
PA 65 EAST WACKER PLACE, STE 1900, CHICAGO, IL 60601-7298 USA
SN 1536-5050
J9 J MED LIBR ASSOC
JI J. Med. Libr. Assoc.
PD OCT
PY 2008
VL 96
IS 4
BP 343
EP 350
DI 10.3163/1536-5050.96.4.009
PG 8
WC Information Science & Library Science
SC Information Science & Library Science
GA 360GF
UT WOS:000260045300009
PM 18974811
ER
PT J
AU Ziegler, RG
Anderson, WF
Gail, MH
AF Ziegler, Regina G.
Anderson, William F.
Gail, Mitchell H.
TI Increasing breast cancer incidence in china: The numbers add up
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID NURSES HEALTH; POPULATION; SHANGHAI; TRENDS; WOMEN; RISK
C1 [Ziegler, Regina G.] NCI, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Ziegler, RG (reprint author), NCI, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, EPS 8098, Bethesda, MD 20892 USA.
EM zieglerr@mail.nih.gov
NR 19
TC 38
Z9 48
U1 1
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD OCT 1
PY 2008
VL 100
IS 19
BP 1339
EP U33
DI 10.1093/jnci/djn330
PG 3
WC Oncology
SC Oncology
GA 356HO
UT WOS:000259769500001
PM 18812546
ER
PT J
AU Ellison, GL
Weinrich, SP
Lou, M
Xu, H
Powell, IJ
Baquet, CR
AF Ellison, Gary L.
Weinrich, Sally P.
Lou, Mimi
Xu, Hongyan
Powell, Isaac J.
Baquet, Claudia R.
TI A Randomized Trial Comparing Web-Based Decision Aids on Prostate Cancer
Knowledge for African-American Men
SO JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
LA English
DT Article
DE African Americans; prostate cancer; screening
ID HEALTH INFORMATION; ANTIGEN TEST; PATIENT EDUCATION; SCREENING DILEMMA;
INTERNET; IMPACT; TESTS; VIDEO
AB Objectives: Few decision aids are tailored for African-American men. We sought to determine if web-based decision aids increased knowledge of prostate cancer screening among African men.
Methods: This postintervention, quasiexperimental research measured knowledge of prostate cancer screening among African-American men following receipt of I of 2 web-based decision aids: enhanced or usual care. Men ages 40-65 were recruited at the annual convention of the Prince Hall Masons in the summer of 2007, which was attended by 1, 1 70,masons. The primary outcome was knowledge of prostate cancer screening.
Results: There were 87 participants in the sample with a mean age of 52 years (standard deviation=6.9). Forty-six masons were randomized to the enhanced decision aid, and 41 masons were randomized to the usual care decision aid, Knowledge scores were statistically significantly higher among the men receiving the enhanced decision aid compared to the usual care decision aid after simultaneously adjusting for age, educational level, marital status, family history, previous prostate specific antigen test and digital rectal exam (p=0.01).
Conclusion: We found evidence that the enhanced web decision aid was significantly more effective than the usual care decision aid in promoting knowledge of the benefits, limitations and risks of prostate cancer screening. Web-based sites may be effective in facilitating discussions about screening between patients and health care providers.
C1 [Ellison, Gary L.] Univ Maryland, Sch Med, Dept Family & Community Med, Baltimore, MD 21201 USA.
[Baquet, Claudia R.] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
[Weinrich, Sally P.] Med Coll Georgia, Sch Nursing, Augusta, GA 30912 USA.
[Lou, Mimi; Xu, Hongyan] Med Coll Georgia, Dept Biostat, Augusta, GA 30912 USA.
[Powell, Isaac J.] Wayne State Univ, Dept Urol, Detroit, MI USA.
[Powell, Isaac J.] Karmanos Canc Inst, Detroit, MI USA.
RP Ellison, GL (reprint author), NCI, Epidemiol & Genet Res Program, Div Canc Control & Populat Sci, 6130 Execut Blvd,Execut Plaza, Bethesda, MD 20892 USA.
EM gellison@som.umaryland.edu
FU Georgia Cancer Coalition Distinguished Cancer Scholar Award; National
Cancer Institute (NCI) [U01 CA114650]
FX This work was supported by the Georgia Cancer Coalition Distinguished
Cancer Scholar Award (to SPW) and the National Cancer Institute (NCI)
through a Research Supplement to Promote Diversity in Health-Related
Research (to GLE, NCI U01 CA114650).
NR 49
TC 14
Z9 14
U1 2
U2 4
PU NATL MED ASSOC
PI WASHINGON
PA 1012 10TH ST, N W, WASHINGON, DC 20001 USA
SN 0027-9684
J9 J NATL MED ASSOC
JI J. Natl. Med. Assoc.
PD OCT
PY 2008
VL 100
IS 10
BP 1139
EP 1145
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 361NU
UT WOS:000260135200003
PM 18942274
ER
PT J
AU Ohye, RG
Gaynor, JW
Ghanayem, NS
Goldberg, CS
Laussen, PC
Frommelt, PC
Newburger, JW
Pearson, GD
Tabbutt, S
Wernovsky, G
Wruck, LM
Atz, AM
Colan, SD
Jaggers, J
McCrindle, BW
Prakash, A
Puchalski, MD
Sleeper, LA
Stylianou, MP
Mahony, L
AF Ohye, Richard G.
Gaynor, J. William
Ghanayem, Nancy S.
Goldberg, Caren S.
Laussen, Peter C.
Frommelt, Peter C.
Newburger, Jane W.
Pearson, Gail D.
Tabbutt, Sarah
Wernovsky, Gil
Wruck, Lisa M.
Atz, Andrew M.
Colan, Steve D.
Jaggers, James
McCrindle, Brian W.
Prakash, Ashwin
Puchalski, Michael D.
Sleeper, Lynn A.
Stylianou, Mario P.
Mahony, Lynn
CA Pediat Heart Network
TI Design and rationale of a randomized trial comparing the Blalock-Taussig
and right ventricle-pulmonary artery shunts in the Norwood procedure
SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
LA English
DT Article
ID LEFT-HEART SYNDROME; STAGE-I NORWOOD; FONTAN PROCEDURE; RISK-FACTORS;
CONDUIT; OPERATION; PALLIATION; CHILDREN; OUTCOMES; SURGERY
AB Objective: The initial palliative procedure for patients born with hypoplastic left heart syndrome and related single right ventricle anomalies, the Norwood procedure, remains among the highest risk procedures in congenital heart surgery. The classic Norwood procedure provides pulmonary blood flow with a modified Blalock-Taussig shunt. Improved outcomes have been reported in a few small, nonrandomized studies of a modification of the Norwood procedure that uses a right ventricle-pulmonary artery shunt to provide pulmonary blood flow. Other nonrandomized studies have shown no differences between the two techniques.
Methods: The Pediatric Heart Network designed a randomized clinical trial to compare outcomes for subjects undergoing a Norwood procedure with either the right ventricle -pulmonary artery or modified Blalock-Taussig shunt. Infants with a diagnosis of single, morphologically right ventricle anomaly who are undergoing a Norwood procedure are eligible for inclusion in this study. The primary outcome is death or cardiac transplant 12 months after random assignment. Secondary outcomes include postoperative morbidity after Norwood and stage II palliation procedures, right ventricular function and pulmonary arterial growth at stage II palliation, and neurodevelopmental outcomes at 14 months old. Incidence of adverse events will also be compared between treatment groups.
Conclusion: This study will make an important contribution to the care of patients with hypoplastic left heart syndrome and related forms of single, morphologically right ventricle. It also establishes a model with which other operative interventions for patients with congenital cardiovascular malformations can be evaluated in the future.
C1 [Ohye, Richard G.; Goldberg, Caren S.] Univ Michigan, Sch Med, Ann Arbor, MI USA.
[Gaynor, J. William; Tabbutt, Sarah; Wernovsky, Gil] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Ghanayem, Nancy S.; Frommelt, Peter C.] Childrens Hosp Wisconsin, Herma Heart Ctr, Milwaukee, WI 53201 USA.
[Laussen, Peter C.; Newburger, Jane W.; Colan, Steve D.] Childrens Hosp, Boston, MA 02115 USA.
[Laussen, Peter C.; Newburger, Jane W.; Colan, Steve D.] Harvard Univ, Sch Med, Boston, MA USA.
[Pearson, Gail D.; Stylianou, Mario P.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Wruck, Lisa M.; Sleeper, Lynn A.] New England Res Inst, Watertown, MA 02172 USA.
[Atz, Andrew M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Jaggers, James] Duke Univ, Med Ctr, Durham, NC USA.
[McCrindle, Brian W.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Prakash, Ashwin] Columbia Univ, Med Ctr, New York, NY USA.
[Puchalski, Michael D.] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Mahony, Lynn] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
RP Ohye, RG (reprint author), 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM ohye@umich.edu
RI gaynor, James william/E-5194-2013
OI gaynor, James william/0000-0001-7955-5604
FU National Heart, Lung, and Blood Institute, National Institutes of
Health, Department of Health and Human Services [U01 HL068285, U01
HL068270, U01 HL068269, U01 HL068292, U01 HL068290, U01 HL068288, U01
HL068281, U01 HL068279]
FX Supported by U01 HL068285 (J.W.N., P.C.L.); U01 HL068270 (S.D.C., L.M.,
L.A.S., L.M.W.), U01 HL068269 (J.J.), U01 HL068292 (M.D.P.), U01
HL068290 (A.P.), U01 HL068288 (B.W.M.), U01 HL068281 (A.M.A.), and U01
HL068279 (W.P, S.T., G.W.) from the National Heart, Lung, and Blood
Institute, National Institutes of Health, Department of Health and Human
Services.
NR 30
TC 52
Z9 53
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5223
J9 J THORAC CARDIOV SUR
JI J. Thorac. Cardiovasc. Surg.
PD OCT
PY 2008
VL 136
IS 4
BP 968
EP 975
DI 10.1016/j.jtcvs.2008.01.013
PG 8
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 364CW
UT WOS:000260314800025
PM 18954638
ER
PT J
AU Liu, PY
Lin, CC
Tsai, WC
Li, YH
Lin, LJ
Shi, GY
Hong, JS
Chen, JH
Wu, HL
AF Liu, P. -Y.
Lin, C. -C.
Tsai, W. -C.
Li, Y. -H.
Lin, L. -J.
Shi, G. -Y
Hong, J. -S.
Chen, J. -H.
Wu, H. -L.
TI Treatment with dextromethorphan improves endothelial function,
inflammation and oxidative stress in male heavy smokers
SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
DE dextromethorphan; endothelial function; inflammation; oxidative stress;
smoking
ID CORONARY-ARTERY-DISEASE; NITRIC-OXIDE BIOSYNTHESIS; HEALTHY-YOUNG
ADULTS; VITAMIN-C; NADPH OXIDASE; UP-REGULATION; IN-VITRO; SMOKING;
ATHEROSCLEROSIS; ACTIVATION
AB Background: Dextromethorphan (DM) is reported to reduce the inflammation-mediated degeneration of dopaminergic neurons. Objective: The goal of this study was to test if DM can improve the endothelial dysfunction and inflammatory markers in heavy smokers. Patients and methods: Forty habitual smoking healthy male volunteers (mean age, 31.5 +/- 1.4 years) were randomly given either DM (120 mg day(-1)) or a placebo for 6 months. We determined endothelial function using the brachial artery diameter changes in flow-mediated dilatation (FMD) and measured their inflammatory and oxidative markers. A sex-and-age matched non-smoking group (n = 20) was compared as normal parameters. Results: Habitual smokers showed impaired baseline endothelial function in FMD (smoking vs. non-smoking: 6.3 +/- 1.8 vs. 10.2 +/- 2.3% respectively, P < 0.01). Without change in smoking behavior, lipid and metabolic parameters, a significant increase in FMD was found in the DM-treated group (32%), accompanied by a decrease in high-sensitivity C-reactive protein (hs-CRP), phospholipase A(2), matrix metalloproteinase-3, interleukin 6 (IL-6) and tumor necrosis factor-alpha receptor II (TNF-alpha RII) (all P < 0.05), but unchanged in von Willebrand factor (VWF)and plasminogen activator inhibitor-1 (PAI-1). An increase in plasma glutathione peroxidase and a decrease in spot urinary excretion of 8-epi-prostaglandin F(2a) were found in DM-treated smokers. Conclusions: Our study suggests that a 6-month treatment with DM can improve endothelial function and attenuate vascular oxidative stress and inflammation markers in habitual smokers.
C1 [Shi, G. -Y; Wu, H. -L.] Natl Cheng Kung Univ, Coll Med, Dept Biochem & Mol Biol, Tainan 701, Taiwan.
[Liu, P. -Y.; Lin, C. -C.; Tsai, W. -C.; Li, Y. -H.; Lin, L. -J.; Chen, J. -H.] Natl Cheng Kung Univ, Dept Internal Med, Div Cardiol, Tainan 701, Taiwan.
[Liu, P. -Y.; Tsai, W. -C.; Li, Y. -H.; Lin, L. -J.; Shi, G. -Y; Chen, J. -H.; Wu, H. -L.] Natl Cheng Kung Univ, Cardiol Res Ctr, Tainan 701, Taiwan.
[Hong, J. -S.] Natl Inst Environm Hlth Sci, Neuropharmacol Sect, Lab Pharmacol & Chem, Res Triangle Pk, NC USA.
RP Wu, HL (reprint author), Natl Cheng Kung Univ, Coll Med, Dept Biochem & Mol Biol, 1 Univ Rd, Tainan 701, Taiwan.
EM halnwu@mail.ncku.edu.tw
FU Ministry of Education Program for Promoting Academic Excellence in
Universities [91-B-FA09-2-4]; National Science Council [NSC
952752-B-006-003-PAE, NSC 95-2752-B-006-004-PAE, NSC
95-2752-B-006-005-PAE]; National Health Research Institute from Taiwan;
National Cheng Kung University Hospital in 2008 [NCKUH-9702028]
FX This study was supported in part by the Ministry of Education Program
for Promoting Academic Excellence in Universities under grant number
91-B-FA09-2-4, and by grants NSC 952752-B-006-003-PAE, NSC
95-2752-B-006-004-PAE and NSC 95-2752-B-006-005-PAE from the National
Science Council, Executive Yuan, Taipei, Taiwan. P.-Y. Liu is a
recipient of Scientist Physician Award Grant from National Health
Research Institute from Taiwan. This study was also support by the
Research Grant NCKUH-9702028 from National Cheng Kung University
Hospital in 2008.
NR 36
TC 7
Z9 7
U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1538-7933
J9 J THROMB HAEMOST
JI J. Thromb. Haemost.
PD OCT
PY 2008
VL 6
IS 10
BP 1685
EP 1692
DI 10.1111/j.1538-7836.2008.03082.x
PG 8
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 350OK
UT WOS:000259361900012
PM 18647232
ER
PT J
AU Minami, K
Nakajima, M
Fujiki, Y
Katoh, M
Gonzalez, FJ
Yokoi, T
AF Minami, Keiichi
Nakajima, Miki
Fujiki, Yuto
Katoh, Miki
Gonzalez, Frank J.
Yokoi, Tsuyoshi
TI Regulation of insulin-like growth factor binding protein-1 and
lipoprotein lipase by the aryl hydrocarbon receptor
SO JOURNAL OF TOXICOLOGICAL SCIENCES
LA English
DT Article
DE aryl hydrocarbon receptor; knockout mice; Igfbp-1; Lpl
ID AH RECEPTOR; GENE-EXPRESSION; KNOCKOUT MICE;
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN; INVOLVEMENT; FIBROSIS; LACKING;
LIGAND; BETA
AB The aryl hydrocarbon receptor (Ahr), a ligand-activated transcriptional factor, mediates the transcriptional activation of a battery of genes encoding drug metabolism enzymes. In the present study, we investigated the hepatic mRNA expression profile in Ahr-null (Ahr KO) mice compared to wildtype mice by microarray analysis to find new Ahr target genes. Pooled total RNA samples of liver extracted from 7- and 60-week-old Ahr KO or wild-type mice were studied by DNA microarray representing 19,867 genes. It was demonstrated that 23 genes were up-regulated and 20 genes were down-regulated over 2 fold in Ahr KO mice compared with wild-type mice commonly within the different age groups. We focused on insulin-like growth factor binding protein-1 (Igfbp-1) and lipoprotein lipase (Lpl) that were Up-regulated in Ahr KO mice. The higher expression in Ahr KO mice compared to wild-type mice were confirmed by real-time RT-PCR analysis. In the wild-type mice but not in the Ahr KO mice, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment increased the Igfbp-1 and Lpl mRNA levels. The expression profile of Igfbp-1 protein was consistent with that of Igfbp-1 mRNA. Since Lpl is the primary enzyme responsible for hydrolysis of lipids in lipoproteins, the serum triglyceride levels were determined. Indeed, the serum triglyceride levels in Ahr KO mice was lower than that in wild-type mice in accordance with the Lpl mRNA levels. Contrary to our expectation, TCDD treatment significantly increased the serum triglyceride levels in wild-type, but did not in Ahr KO mice. These results suggest that serum triglyceride levels are not correlated with hepatic Lpl expression levels. In the present study, we found that Ahr paradoxically regulates Igfbp-1 and Lpl expressions in the liver.
C1 [Minami, Keiichi; Nakajima, Miki; Fujiki, Yuto; Katoh, Miki; Yokoi, Tsuyoshi] Kanazawa Univ, Div Pharmaceut Sci, Grad Sch Med Sci, Kanazawa, Ishikawa 9201192, Japan.
[Gonzalez, Frank J.] NCI, Lab Metab, Bethesda, MD 20892 USA.
RP Yokoi, T (reprint author), Kanazawa Univ, Div Pharmaceut Sci, Grad Sch Med Sci, Kanazawa, Ishikawa 9201192, Japan.
EM tyokoi@kenroku.kanazawa-u.ac.jp
RI Nakajima, Miki/C-3990-2015; yokoi, tsuyoshi/I-7115-2014
NR 20
TC 8
Z9 8
U1 0
U2 1
PU JAPANESE SOC TOXICOLOGICAL SCIENCES
PI TOKYO
PA INTERNATIONAL MEDICAL INFORMATION CENTER, SHINANOMACHI RENGAKAN, 35
SHINANO-MACHI, SHINJUKU-KU, TOKYO, 160-0016, JAPAN
SN 0388-1350
EI 1880-3989
J9 J TOXICOL SCI
JI J. Toxicol. Sci.
PD OCT
PY 2008
VL 33
IS 4
BP 405
EP 413
DI 10.2131/jts.33.405
PG 9
WC Toxicology
SC Toxicology
GA 356CI
UT WOS:000259755900002
PM 18827440
ER
PT J
AU Schley, MT
Wilms, P
Toepfner, S
Schaller, HP
Schmelz, M
Konrad, CJ
Birbaumer, N
AF Schley, Marcus T.
Wilms, Petra
Toepfner, Stephanie
Schaller, Hanns-Peter
Schmelz, Martin
Konrad, Christoph J.
Birbaumer, Niels
TI Painful and Nonpainful Phantom and Stump Sensations in Acute Traumatic
Amputees
SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE
LA English
DT Article
DE Phantom pain; Phantom sensations; Stump pain; Stump sensation; Acute
amputees; Incidence; Prevalence; Dynamic of pain
ID UPPER-EXTREMITY AMPUTEES; PERIPHERAL-NERVE INJURY; UPPER-LIMB AMPUTEES;
RAT DORSAL-HORN; CORTICAL REORGANIZATION; CLINICAL CHARACTERISTICS;
SOMATOSENSORY CORTEX; ADOLESCENT AMPUTEES; RECEPTOR ANTAGONIST; RAPID
MODULATION
AB Background: The formation, prevalence, intensity, course, and predisposing factors of phantom limb pain were investigated to determine possible mechanisms of the origin of phantom limb pain in traumatic upper limb amputees.
Methods: Ninety-six upper limb amputees participated in the study. A questionnaire assessed the following question: side, date, extension, and cause of amputation; preamputation pain; and presence or absence of phantom pain, phantom and stump sensations or stump pain or both.
Results: The response rate was 84%. Sixty-five (81%) participants returned the questionnaire. In 64 (98.5%) participants a traumatic injury led to amputation; the amputation was necessary because of in-fection in one patient (1.5%). The median follow-up time (from amputation to evaluation) was 3.2 years (range, 0.9-3.8 years) The prevalence of phantom pain was 44.6%, phantom sensation 53.8%, stump pain 61.5%, and stump sensation 78.5%. After its first appearance, phantom pain had a decreasing course in 14 (48.2%) of 29 amputees, was stable in 11 (37.9%) amputees, and worsened in 2 (6.9%) of 29 amputees. Stump pain had a decreasing course in 19 (47.5%) of 40 amputees but was stable in 12 (30%) amputees. Phantom pain occurred immediately after amputation in 8 (28%) of 29 amputees between I month and 12 months in 3 (10%) amputees and after 12 or more months in 12 (41 %) amputees.
Conclusion: stump pain and stump sensation predominate traumatic amputees' somatosensory experience immediately after amputation; phantom pain and phantom sensations are often long-term consequences of amputation. Amputees experience phantom sensations and phantom pain within 1 month after amputation, a second peak occurs 12 months after amputation. Revised diagnostic criteria for phantom pain are proposed on the basis of these data.
C1 [Schley, Marcus T.; Schmelz, Martin; Konrad, Christoph J.] Univ Heidelberg, Dept Anesthesiol & Intens Care, D-68135 Mannheim, Germany.
[Wilms, Petra; Toepfner, Stephanie; Birbaumer, Niels] Univ Tubingen, Inst Med Psychol & Behav Neurobiol, Tubingen, Germany.
[Birbaumer, Niels] NINDS, NIH, Human Cort Physiol Unit, Bethesda, MD USA.
[Schaller, Hanns-Peter] Univ Tubingen, Dept Hand Surg & Plast Surg, Tubingen, Germany.
RP Schley, MT (reprint author), Univ Heidelberg, Dept Anesthesiol & Intens Care, Theodeor Kutzer Ufer 1-3, D-68135 Mannheim, Germany.
EM marcus.schley@medma.uni-heidelberg.de
OI Schmelz, Martin/0000-0002-9736-7241
FU Bundesministerium fur Forschung and Technologie (BMFT); Deutsche
ForschUngsgerneinschaft (DFG).
FX Supported by the Bundesministerium fur Forschung and Technologie (BMFT)
and the Deutsche ForschUngsgerneinschaft (DFG).
NR 56
TC 28
Z9 33
U1 2
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-5282
J9 J TRAUMA
JI J. Trauma-Injury Infect. Crit. Care
PD OCT
PY 2008
VL 65
IS 4
BP 858
EP 864
DI 10.1097/TA.0b013e31812eed9e
PG 7
WC Critical Care Medicine; Surgery
SC General & Internal Medicine; Surgery
GA 361JS
UT WOS:000260124500023
PM 18849803
ER
PT J
AU Loeb, S
Kettermann, A
Carter, HB
Ferrucci, L
Metter, EJ
Walsh, PC
AF Loeb, Stacy
Kettermann, Anna
Carter, H. Ballentine
Ferrucci, Luigi
Metter, E. Jeffrey
Walsh, Patrick C.
TI Does prostate growth confound prostate specific antigen velocity? Data
from the Baltimore Longitudinal Study of Aging
SO JOURNAL OF UROLOGY
LA English
DT Article
DE prostate; organ size; prostatic neoplasms; prostate-specific antigen;
mass screening
ID PSA VELOCITY; CANCER; VOLUME; MEN; AGE; HYPERPLASIA; DEATH; RISK; MRI
AB Purpose: Although prostate specific antigen velocity was proposed to increase the specificity of prostate specific antigen-based screening, there are little published data on the effect of differential prostate growth on prostate specific antigen velocity. If a patient presents with rising prostate specific antigen over a year or more, it would be useful to know whether such a change in prostate specific antigen could be explained by prostate growth. Thus, we investigated the relationship between changes in prostate size and prostate specific antigen changes in a large cohort of men without prostate cancer.
Materials and Methods: We identified 242 men without prostate cancer from the Baltimore Longitudinal Study of Aging who had 2 or greater serial pelvic magnetic resonance imaging studies and contemporaneous prostate specific antigen measurements. In this population we used the t test, correlation coefficients, and regression analysis to examine the relationship between prostate specific antigen changes and prostate volume changes, as assessed by magnetic resonance imaging.
Results: The mean age was 55 years. During 4.2 years of median followup, the median rate of volume change was 0.6 cc per year (range -9.9 to 11.8), and the median prostate specific antigen change was 0.03 ng/ml per year. There was no correlation between prostate specific antigen changes and prostate growth, as measured in cc per year (r = -0.01, p = - 0.9) or the percent change per year (r = 0.07, p = 0.3). On multivariate analysis, there was no significant relationship between changes in prostate volume and prostate specific antigen changes.
Conclusions: Our data suggest that volume increases alone do not cause a high prostate specific antigen velocity. Despite growth rates as high as 10 cc per year, prostate specific antigen velocity was less than 0. 1 ng/ml per year in most men without prostate cancer. Thus, differential rates of prostatic growth should not confound the use of prostate specific antigen velocity for prostate cancer detection and prognostication.
C1 [Loeb, Stacy] Johns Hopkins Med Inst, James Buchanan Brady Urol Inst, Baltimore, MD 21205 USA.
[Ferrucci, Luigi; Metter, E. Jeffrey] Natl Inst Hlth Clin Res Branch, Natl Inst Aging, Baltimore, MD 21205 USA.
RP Loeb, S (reprint author), Johns Hopkins Med Inst, James Buchanan Brady Urol Inst, Baltimore, MD 21205 USA.
OI Loeb, Stacy/0000-0003-3933-9207
FU National Institutes of Health; National Institute on Aging Intramural
Research Program
FX Supported by the National Institutes of Health, National Institute on
Aging Intramural Research Program.
NR 16
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
J9 J UROLOGY
JI J. Urol.
PD OCT
PY 2008
VL 180
IS 4
BP 1314
EP 1317
DI 10.1016/j.juro.2008.06.033
PN 1
PG 4
WC Urology & Nephrology
SC Urology & Nephrology
GA 350VS
UT WOS:000259382300050
PM 18707733
ER
PT J
AU Gulley, JL
Aragon-Ching, JB
Steinberg, SM
Hussain, MH
Sartor, O
Higano, CS
Petrylak, DP
Chatta, GS
Arlen, PM
Figg, WD
Dahut, WL
AF Gulley, James L.
Aragon-Ching, Jeanny B.
Steinberg, Seth M.
Hussain, Maha H.
Sartor, Oliver
Higano, Celestia S.
Petrylak, Daniel P.
Chatta, Gurkamal S.
Arlen, Philip M.
Figg, William D.
Dahut, William L.
TI Kinetics of serum androgen normalization and factors associated with
testosterone reserve after limited androgen deprivation therapy for
nonmetastatic prostate cancer
SO JOURNAL OF UROLOGY
LA English
DT Article
DE prostate; prostatic neoplasms; androgen antagonists; testosterone;
gonadotropin-releasing hormone
ID HORMONE AGONIST TREATMENT; WHITE MEN; RADIATION; TRIAL; TIME; CARCINOMA;
BLACK
AB Purpose: Groups have investigated time to testosterone recovery in patients who have undergone androgen deprivation therapy, usually by measuring androgen every 3 months, with varying results. To our knowledge this represents the largest study using monthly testosterone and dihydroxytestosterone measurement to evaluate the kinetics of androgen recovery following limited androgen deprivation therapy.
Materials and Methods: Monthly serum androgen levels were analyzed following 2, 6-month cycles of gonadotropin-releasing hormone agonist therapy as part of a randomized, placebo controlled study of the role of thalidomide in delaying time to prostate specific androgen progression.
Results: By the Kaplan-Meier method the median time to testosterone normalization in cycles 1 vs 2 was 15.4 vs 18.3 weeks with similar dihydroxytestosterone recovery times. Neither on-study prostate specific antigen, Gleason score nor thalidomide treatment had a significant impact on time to testosterone normalization. However, in cycle 1 men with low baseline dihydroxytestosterone and those who were more than 67 years old had significantly longer time to T normalization on Cox model analysis. Additionally, in cycle 2 patients with prior local radiation therapy had longer time to testosterone normalization, although this was no longer significant on Cox model analysis. Cox model analysis in cycle 2 showed that low baseline dihydroxytestosterone and testosterone, low testosterone nadir and white race were associated with longer time to testosterone normalization.
Conclusions: Findings of delayed testosterone recovery may be useful for designing and analyzing clinical trials of limited androgen deprivation therapy and for estimating the duration of treatment associated side effects in patients undergoing limited androgen deprivation therapy.
C1 [Gulley, James L.; Arlen, Philip M.] Natl Canc Inst, Lab Tumor Immunol & Biol, Ctr Canc Res, Bethesda, MD 20892 USA.
[Aragon-Ching, Jeanny B.; Figg, William D.; Dahut, William L.] Natl Canc Inst, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] Natl Canc Inst, Biostat & Data Management Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
[Figg, William D.] Natl Canc Inst, Mol Pharmacol Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
[Chatta, Gurkamal S.] Univ Pittsburgh, Dept Med, Inst Canc, Pittsburgh, PA USA.
[Petrylak, Daniel P.] Columbia Univ, New York Presbyterian Hosp, Med Ctr, Dept Med, New York, NY USA.
[Higano, Celestia S.] Univ Washington, Dept Med, Seattle, WA USA.
[Higano, Celestia S.] Univ Washington, Dept Urol, Seattle, WA 98195 USA.
[Sartor, Oliver] Tulane Med Sch, New Orleans, LA USA.
[Hussain, Maha H.] Wayne State Univ, Barbara Ann Karmanos Canc Inst, Dept Med Oncol, Detroit, MI USA.
[Hussain, Maha H.] Univ Michigan, Med Ctr, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Hussain, Maha H.] Univ Michigan, Med Ctr, Dept Urol, Ann Arbor, MI 48109 USA.
RP Gulley, JL (reprint author), Natl Canc Inst, Lab Tumor Immunol & Biol, Ctr Canc Res, 10 Ctr Dr,Room 8B09,MSC 1750, Bethesda, MD 20892 USA.
EM gulleyj@mail.nih.gov
RI Gulley, James/K-4139-2016; Figg Sr, William/M-2411-2016;
OI Gulley, James/0000-0002-6569-2912; Aragon-Ching,
Jeanny/0000-0002-6714-141X
FU Intramural NIH HHS [NIH0011802535, Z99 CA999999]
NR 20
TC 23
Z9 24
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
J9 J UROLOGY
JI J. Urol.
PD OCT
PY 2008
VL 180
IS 4
BP 1432
EP 1437
DI 10.1016/j.juro.2008.06.017
PN 1
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 350VS
UT WOS:000259382300079
PM 18710748
ER
PT J
AU Giacovelli, JK
Egorova, N
Nowygrod, R
Gelijns, A
Kent, KC
Morrissey, NJ
AF Giacovelli, Jeannine K.
Egorova, Natalia
Nowygrod, Roman
Gelijns, Annetine
Kent, K. Craig
Morrissey, Nicholas J.
TI Insurance status predicts access to care and outcomes of vascular
disease
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Article; Proceedings Paper
CT Vascular Annual Meeting
CY MAR 21-24, 2007
CL Baltimore, MD
ID ABDOMINAL AORTIC-ANEURYSM; HEALTH-INSURANCE; UNITED-STATES; MORTALITY;
RACE; SURGERY; PATIENT; CANCER; REPAIR; RISK
AB Objective: To determine if insurance status predicts severity of vascular disease at the time of treatment or outcomes following intervention.
Methods. Hospital discharge databases from Florida and New York from 2000-2005 were analyzed for lower extremity revascularization (LEF, n = 73,532), carotid revascularization (CR, n = 116,578), or abdominal aortic aneurysm repair (AAA, n = 35,593), using ICD-9 codes for diagnosis and procedure. The indications for intervention as well as the post-operative outcomes were examined assigning insurance status as the independent variable. Patients covered under a variety of commercial insurers, as well as Medicare, were compared to those who either had no insurance or were covered by Medicaid.
Results: Patients without insurance or with Medicaid were at significantly greater risk of presenting with a ruptured AAA compared to insured (non-Medicaid) patients; while insurance status did not seem to impact post-operative mortality rates for elective and ruptured AAA repair. The uninsured or Medicaid recipients presented with symptomatic carotid disease nearly twice as often as the insured, but stroke rates after CR did not differ significantly based on insurance status. Patients with Medicaid or without insurance were more likely to present with limb threatening ischemia than claudication. In contrast to AAA repair and CR, the outcomes of LER were worse in the uninsured and Medicaid beneficiaries who had higher rates of post-revascularization amputation compared to the insured (non-Medicaid) group.
Conclusion: Insurance status predicts disease severity at the time of treatment, but once treated, the outcomes are similar among insurance categories, with the exception of lower extremity revascularization. This data suggests inferior access to preventative vascular care in the Medicaid and the uninsured populations.
C1 [Giacovelli, Jeannine K.; Nowygrod, Roman; Kent, K. Craig; Morrissey, Nicholas J.] Cornell Univ, Weill Med Coll, Columbia Coll Phys & Surg, New York Presbyterian Hosp,Div Vasc Surg, New York, NY 10021 USA.
[Giacovelli, Jeannine K.; Egorova, Natalia; Gelijns, Annetine] Columbia Univ Hlth Sci, Int Ctr Hlth Outcomes & Innovat Res, New York, NY USA.
[Giacovelli, Jeannine K.] NIH T32HL007854 Post Doctoral Training Cardiovasc, New York, NY USA.
RP Giacovelli, JK (reprint author), 600 W 168th St, New York, NY 10032 USA.
EM jg2671@columbia.edu
FU NIMHD NIH HHS [L60 MD002558-01]
NR 29
TC 39
Z9 39
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD OCT
PY 2008
VL 48
IS 4
BP 905
EP 911
DI 10.1016/j.jvs.2008.05.010
PG 7
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 353NR
UT WOS:000259575200022
PM 18586449
ER
PT J
AU Schmitz, A
Portier, CJ
Thormann, W
Theurillat, R
Mevissen, M
AF Schmitz, A.
Portier, C. J.
Thormann, W.
Theurillat, R.
Mevissen, M.
TI Stereoselective biotransformation of ketamine in equine liver and lung
microsomes
SO JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS
LA English
DT Article
ID ADMINISTERED KETAMINE; PHARMACOKINETICS; METABOLISM; HORSE;
PHARMACODYNAMICS; PHARMACOLOGY; NORKETAMINE; ENANTIOMERS; VOLUNTEERS;
PERCEPTION
AB Stereoselectivity has to be considered for pharmacodynamic and pharmacokinetic features of ketamine. Stereoselective biotransformation of ketamine was investigated in equine microsomes in vitro. Concentration curves were constructed over time, and enzyme activity was determined for different substrate concentrations using equine liver and lung microsomes. The concentrations of R/S-ketamine and R/S-norketamine were determined by enantioselective capillary electrophoresis. A two-phase model based on Hill kinetics was used to analyze the biotransformation of R/S-ketamine into R/S-norketamine and, in a second step, into R/S-downstream metabolites.
In liver and lung microsomes, levels of R-ketamine exceeded those of S-ketamine at all time points and S-norketamine exceeded R-norketamine at time points below the maximum concentration. In liver and lung microsomes, significant differences in the enzyme velocity (V(max)) were observed between Sand R-norketamine formation and between Vmax of S-norketamine formation when S-ketamine was compared to S-ketamine of the racemate. Our investigations in microsomal reactions in vitro suggest that stereoselective ketamine biotransformation in horses occurs in the liver and the lung with a slower elimination of S-ketamine in the presence of R-ketamine. Scaling of the in vitro parameters to liver and lung organ clearances provided an excellent fit with previously published in vivo data and confirmed a lung first-pass effect.
C1 [Schmitz, A.; Mevissen, M.] Univ Bern, Vetsuisse Fac, Div Vet Pharmacol & Toxicol, CH-3012 Bern, Switzerland.
[Portier, C. J.] NIEHS, Res Triangle Pk, NC 27709 USA.
[Thormann, W.; Theurillat, R.] Univ Bern, Dept Clin Pharmacol, Bern, Switzerland.
RP Mevissen, M (reprint author), Univ Bern, Vetsuisse Fac, Div Vet Pharmacol & Toxicol, Langgassstr 124, CH-3012 Bern, Switzerland.
EM meike.mevissen@vpi.unibe.ch
RI Portier, Christopher/A-3160-2010
OI Portier, Christopher/0000-0002-0954-0279
FU Vetsuisse; Swiss National Science Foundation; NIH; NIEHS
FX S-ketamine was kindly supplied by Dr E. Graeub (Bern, Switzerland). This
work was funded by Vetsuisse. The analytical part was partly funded by
the Swiss National Science Foundation. This research was supported (in
part) by the Intramural Research Program of the NIH, and NIEHS.
NR 35
TC 19
Z9 19
U1 3
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0140-7783
J9 J VET PHARMACOL THER
JI J. Vet. Pharmacol. Ther.
PD OCT
PY 2008
VL 31
IS 5
BP 446
EP 455
DI 10.1111/j.1365-2885.2008.00972.x
PG 10
WC Pharmacology & Pharmacy; Veterinary Sciences
SC Pharmacology & Pharmacy; Veterinary Sciences
GA 355AZ
UT WOS:000259682300008
PM 19000264
ER
PT J
AU Chang, KO
George, DW
Patton, JB
Green, KY
Sosnovtsev, SV
AF Chang, Kyeong-Ok
George, David W.
Patton, John B.
Green, Kim Y.
Sosnovtsev, Stanislav V.
TI Leader of the capsid protein in feline calicivirus promotes replication
of Norwalk virus in cell culture
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MAMMALIAN-CELLS; UNITED-STATES; RNA; NOROVIRUSES; INTERFERONS; GENOME;
GASTROENTERITIS; ORGANIZATION; INFECTIVITY; EXPRESSION
AB The inability to grow human noroviruses in cell culture has greatly impeded the studies of their pathogenesis and immunity. Vesiviruses, in the family Caliciviridae, grow efficiently in cell culture and encode a unique protein in the subgenomic region designated as leader of the capsid protein (LC). We hypothesized that LC might be associated with the efficient replication of vesiviruses in cell culture and promote the replication of human norovirus in cells. To test this hypothesis, a recombinant plasmid was engineered in which the LC region of feline calicivirus (FCV) was placed under the control of the cytomegalovirus promoter (pCI-LC) so that the LC protein could be provided in trans to replicating calicivirus genomes bearing a reporter gene. We constructed pNV-GFP, a recombinant plasmid containing a full-length NV genome with a green fluorescent protein (GFP) in the place of VP1. The transfection of pNV-GFP in MVA-T7-infected cells produced few GFP-positive cells detected by fluorescence microscopy and flow cytometry analysis. When pNV-GFP was cotransfected with pCI-LC in MVA-T7-infected cells, we observed an increase in the number of GFP-positive cells (ca. 3% of the whole-cell population). Using this cotransfection method with mutagenesis study, we identified potential cis-acting elements at the start of subgenomic RNA and the 3' end of NV genome for the virus replication. We conclude that LC may be a viral factor which promotes the replication of NV in cells, which could provide a clue to growing the fastidious human noroviruses in cell culture.
C1 [Chang, Kyeong-Ok] Kansas State Univ, Dept Diagnost Med & Pathobiol, Coll Vet Med, Manhattan, KS 66506 USA.
[Green, Kim Y.; Sosnovtsev, Stanislav V.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Chang, KO (reprint author), Kansas State Univ, Dept Diagnost Med & Pathobiol, Coll Vet Med, 1800 Denison Ave, Manhattan, KS 66506 USA.
EM kchang@vet.ksu.edu
FU NIH COBRE [2 P20 RR016443-07]
FX This study was partly supported by NIH COBRE grant 2 P20 RR016443-07.;
This paper is contribution no. 08-208-J from the Kansas Agricultural
Experiment Station.
NR 34
TC 8
Z9 10
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9306
EP 9317
DI 10.1128/JVI.00301-08
PG 12
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700001
PM 18632864
ER
PT J
AU Thomas, JA
Bosche, WJ
Shatzer, TL
Johnson, DG
Gorelick, RJ
AF Thomas, James A.
Bosche, William J.
Shatzer, Teresa L.
Johnson, Donald G.
Gorelick, Robert J.
TI Mutations in human immunodeficiency virus type 1 nucleocapsid protein
zinc fingers cause premature reverse transcription
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID ROUS-SARCOMA-VIRUS; MURINE LEUKEMIA-VIRUS; PRIMER ACTIVATION SIGNAL;
ACID-CHAPERONE ACTIVITY; PROVIRAL DNA-SYNTHESIS; INTEGRATION IN-VITRO;
INFECTION PROCESSES; GENOMIC RNA; VIRAL REPLICATION; CELLULAR-PROTEINS
AB Human immunodeficiency virus type 1 (HIV-1) requires that its genome be reverse transcribed into double-stranded DNA for productive infection of cells. This process requires not only reverse transcriptase but also the nucleocapsid protein (NC), which functions as a nucleic acid chaperone. Reverse transcription generally begins once the core of the virion enters the cytoplasm of a newly infected cell. However, some groups have reported the presence of low levels of viral DNA (vDNA) within particles prior to infection, the significance and function of which is controversial. We report here that several HIV-1 NC mutants, which we previously identified as being replication defective, contain abnormally high levels of intravirion DNA. These findings were further reinforced by the inability of these NC mutants to perform endogenous reverse transcription (ERT), in contrast to the readily measurable ERT activity in wild-type HIV-1. When either of the NC mutations is combined with a mutation that inactivates the viral protease, we observed a significant reduction in the amount of intravirion DNA. Interestingly, we also observed high levels of intravirion DNA in the context of wild-type NC when we delayed budding by means of a PTAP((-)) (Pro-Thr-Ala-Pro) mutation. Premature reverse transcription is most probably occurring before these mutant virions bud from producer cells, but we fail to see any evidence that the NC mutations alter the timing of Pr55(Gag) processing. Critically, our results also suggest that the presence of intravirion vDNA could serve as a diagnostic for identifying replication-defective HIV-1.
C1 [Thomas, James A.; Bosche, William J.; Shatzer, Teresa L.; Johnson, Donald G.; Gorelick, Robert J.] NCI Frederick, SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick, MD 21702 USA.
RP Gorelick, RJ (reprint author), NCI Frederick, SAIC Frederick Inc, AIDS & Canc Virus Program, POB B, Frederick, MD 21702 USA.
EM gorelick@ncifcrf.gov
OI Thomas, James/0000-0002-2509-490X
FU National Cancer Institute; National Institutes of Health [N01-CO-12400]
FX We thank David Ott of the AIDS Vaccine Program, SAIC-Frederick, Inc.,
Alan Rein of the HIV-Drug Resistance Program, NCI-Frederick, and
Christopher Aiken of Vanderbilt University School of Medicine,
Nashville, TN, for critical comments and helpful suggestions. We also
thank Gilead Sciences, Inc., Foster City, CA, for the PMPA.; This
project has been funded in whole or in part with federal funds from the
National Cancer Institute, National Institutes of Health, under contract
N01-CO-12400.; The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organizations imply endorsement by the U. S. government.
NR 75
TC 33
Z9 34
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9318
EP 9328
DI 10.1128/JVI.00583-08
PG 11
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700002
PM 18667500
ER
PT J
AU Baas, T
Roberts, A
Teal, TH
Vogel, L
Chen, J
Tumpey, TM
Katze, MG
Subbarao, K
AF Baas, Tracey
Roberts, Anjeanette
Teal, Thomas H.
Vogel, Leatrice
Chen, Jun
Tumpey, Terrence M.
Katze, Michael G.
Subbarao, Kanta
TI Genomic analysis reveals age-dependent innate immune responses to severe
acute respiratory syndrome coronavirus
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PLASMACYTOID DENDRITIC CELLS; MICROARRAY DATA; SARS-CORONAVIRUS; LUNG
PATHOLOGY; I INTERFERON; HOST IMMUNE; BALB/C MICE; MOUSE MODEL;
HONG-KONG; T-CELLS
AB The relationship between immunosenescence and the host response to virus infection is poorly understood at the molecular level. Two different patterns of pulmonary host responses to virus were observed when gene expression profiles from severe acute respiratory syndrome coronavirus (SARS-CoV)-infected young mice that show minimal disease were compared to those from SARS-CoV-infected aged mice that develop pneumonitis. In young mice, genes related to cellular development, cell growth, and cell cycle were downregulated during peak viral replication, and these transcripts returned to basal levels as virus was cleared. In contrast, aged mice had a greater number of upregulated immune response and cell-to-cell signaling genes, and the expression of many genes was sustained even after viral clearance, suggesting an exacerbated host response to virus. Interestingly, in SARS-CoV-infected aged mice, a subset of genes, including Tnfa, Il6, Ccl2, Ccl3, Cxcl10, and Ifng, was induced in a biphasic pattern that correlated with peak viral replication and a subsequent influx of lymphocytes and severe histopathologic changes in the lungs. We provide insight into gene expression profiles and molecular signatures underlying immunosenescence in the context of the host response to viral infection.
C1 [Baas, Tracey; Teal, Thomas H.; Katze, Michael G.] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA.
[Roberts, Anjeanette; Vogel, Leatrice; Chen, Jun; Subbarao, Kanta] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Tumpey, Terrence M.] Ctr Dis Control & Prevent, Influenza Div, Natl Ctr Immunizat & Resp Dis, Atlanta, GA USA.
RP Baas, T (reprint author), Univ Washington, Dept Microbiol, Box 358070, Seattle, WA 98195 USA.
EM traceybaas@gmail.com
FU NIAID; NIH
FX This study was supported in part by the Intramural Research Program of
NIAID, NIH (K.S.); P51 RR00166-45, NCRR, NIH, Regional Primate Research
Center (Core Grant), Division of Functional Genomics and Infectious
Disease (M. G. K., Division Head); and R01 HL080621-01, NHLBI, NIH,
Macaque Model and Gene Expression Profiling of SARS (M. G. K.).
NR 43
TC 23
Z9 23
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9465
EP 9476
DI 10.1128/JVI.00489-08
PG 12
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700017
PM 18632870
ER
PT J
AU Inagaki, K
Piao, CC
Kotchey, NM
Wu, XL
Nakai, H
AF Inagaki, Katsuya
Piao, Chuncheng
Kotchey, Nicole M.
Wu, Xiaolin
Nakai, Hiroyuki
TI Frequency and spectrum of genomic integration of recombinant
adeno-associated virus serotype 8 vector in neonatal mouse liver
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID TRANSDUCTION IN-VIVO; GENE-THERAPY; HEPATOCELLULAR-CARCINOMA;
INTRAMUSCULAR INJECTION; TRANSGENE EXPRESSION; RNA INTERFERENCE;
MAMMALIAN-CELLS; TANDEM REPEATS; VIRAL VECTORS; VII MICE
AB Neonatal injection of recombinant adeno-associated virus serotype 8 (rAAV8) vectors results in widespread transduction in multiple organs and therefore holds promise in neonatal gene therapy. On the other hand, insertional mutagenesis causing liver cancer has been implicated in rAAV- mediated neonatal gene transfer. Here, to better understand rAAV integration in neonatal livers, we investigated the frequency and spectrum of genomic integration of rAAV8 vectors in the liver following intraperitoneal injection of 2.0 x 10(11) vector genomes at birth. This dose was sufficient to transduce a majority of hepatocytes in the neonatal period. In the first approach, we injected mice with a beta-galactosidase-expressing vector at birth and quantified rAAV integration events by taking advantage of liver regeneration in a chronic hepatitis animal model and following partial hepatectomy. In the second approach, we performed a new, quantitative rAAV vector genome rescue assay by which we identified rAAV integration sites and quantified integrations. As a result, we find that at least similar to 0.05% of hepatocytes contained rAAV integration, while the average copy number of integrated double-stranded vector genome per cell in the liver was similar to 0.2, suggesting concatemer integration. Twenty-three of 34 integrations (68%) occurred in genes, but none of them were near the mir-341 locus, the common rAAV integration site found in mouse hepatocellular carcinoma. Thus, rAAV8 vector integration occurs preferentially in genes at a frequency of 1 in approximately 103 hepatocytes when a majority of hepatocytes are once transduced in the neonatal period. Further studies are warranted to elucidate the relationship between vector dose and integration frequency or spectrum.
C1 [Inagaki, Katsuya; Piao, Chuncheng; Kotchey, Nicole M.; Nakai, Hiroyuki] Univ Pittsburgh, Dept Microbiol & Mol Genet, Sch Med, Pittsburgh, PA 15261 USA.
[Wu, Xiaolin] NCI Frederick, SAIC Frederick Inc, Lab Mol Technol, Frederick, MD 21702 USA.
RP Nakai, H (reprint author), Univ Pittsburgh, Dept Microbiol & Mol Genet, Sch Med, W1244 BSTWR,200 Lothrop St, Pittsburgh, PA 15261 USA.
EM nakaih@pitt.edu
FU National Institutes of Health [DK68636, DK78388, HL64274]; National
Hemophilia Foundation; National Cancer Institute, DHHS [N01-CO-12400]
FX This work was supported by Public Health Service grants DK68636 and
DK78388 from the National Institutes of Health (to H.N.), a career
development award from the National Hemophilia Foundation (to H.N.),
and, at least in part, the National Cancer Institute, DHHS, under
contract number N01-CO-12400 with SAIC-Frederick, Inc., and Public
Health Service grant HL64274 from the National Institutes of Health.
NR 45
TC 21
Z9 22
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9513
EP 9524
DI 10.1128/JVI.01001-08
PG 12
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700021
PM 18614641
ER
PT J
AU Kolb, G
Kristie, TM
AF Kolb, Gaelle
Kristie, Thomas M.
TI Association of the cellular coactivator HCF-1 with the Golgi apparatus
in sensory neurons
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HERPES-SIMPLEX-VIRUS; UNFOLDED PROTEIN RESPONSE; GENE-EXPRESSION;
TRANSCRIPTION FACTOR; FACTOR-I; EARLY TIMES; ER STRESS; C1 FACTOR; VP16;
LATENCY
AB HCF-1 is a cellular transcriptional coactivator that is critical for mediating the regulated expression of the immediate-early genes of the alphaherpesviruses herpes simplex virus type 1 and varicella-zoster virus. HCF-1 functions, at least in part, by modulating the modification of nucleosomes at these viral promoters to reverse cell-mediated repressive marks and promote activating marks. Strikingly, HCF-1 is specifically sequestered in the cytoplasm of sensory neurons where these viruses establish latency and is rapidly relocalized to the nucleus upon stimuli that result in viral reactivation. However, the analysis of HCF-1 in latently infected neurons and the protein's specific subcellular location have not been determined. Therefore, in this study, the localization of HCF-1 in unstimulated and induced latently infected sensory neurons was investigated and was found to be similar to that observed in uninfected mice, with a time course of induced nuclear accumulation that correlated with viral reactivation. Using a primary neuronal cell culture system, HCF-1 was localized to the Golgi apparatus in unstimulated neurons, a unique location for a transcriptional coactivator. Upon disruption of the Golgi body, HCF-1 was rapidly relocalized to the nucleus in contrast to other Golgi apparatus-associated proteins. The location of HCF-1 is distinct from that of CREB3, an endoplasmic reticulum-resident HCF-1 interaction partner that has been proposed to sequester HCF-1. The results support the model that HCF-1 is an important component of the viral latency-reactivation cycle and that it is regulated by association with a component that is distinct from the identified HCF-1 interaction factors.
C1 [Kolb, Gaelle; Kristie, Thomas M.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Kristie, TM (reprint author), NIAID, Viral Dis Lab, NIH, 4-129,4 Ctr Dr, Bethesda, MD 20892 USA.
EM thomas_kristie@nih.gov
FU Laboratory of Viral Diseases; Division of Intramural Research; National
Institute of Allergy and Infectious Diseases; National Institutes of
Health
FX These studies were supported by the Laboratory of Viral Diseases,
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health.
NR 45
TC 17
Z9 17
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9555
EP 9563
DI 10.1128/JVI.01174-08
PG 9
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700025
PM 18667495
ER
PT J
AU Vaccari, M
Mattapallil, J
Song, K
Tsai, WP
Hryniewicz, A
Venzon, D
Zanetti, M
Reimann, KA
Roederer, M
Franchini, G
AF Vaccari, Monica
Mattapallil, Joseph
Song, Kaimei
Tsai, Wen-Po
Hryniewicz, Anna
Venzon, David
Zanetti, Maurizio
Reimann, Keith A.
Roederer, Mario
Franchini, Genoveffa
TI Reduced protection from simian immunodeficiency virus SIVmac251
infection afforded by memory CD8(+) T cells induced by vaccination
during CD4(+) T-cell deficiency
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RHESUS MACAQUES; ANTIRETROVIRAL THERAPY; GASTROINTESTINAL-TRACT; TYPE-1
INFECTION; SMALLPOX VACCINE; MONKEYPOX VIRUS; FLOW-CYTOMETRY; SIV
INFECTION; DEPLETION; RESPONSES
AB Adaptive CD4(+) and CD8(+) T-cell responses have been associated with control of human immunodeficiency virus/simian immunodeficiency virus (HIV/SIV) replication. Here, we have designed a study with Indian rhesus macaques to more directly assess the role of CD8 SIV-specific responses in control of viral replication. Macaques were immunized with a DNA prime-modified vaccinia virus Ankara (MVA)-SIV boost regimen under normal conditions or under conditions of antibody-induced CD4(+) T-cell deficiency. Depletion of CD4(+) cells was performed in the immunized macaques at the peak of SIV-specific CD4(+) T-cell responses following the ;DNA prime dose. A group of naive macaques was also treated with the anti-CD4 depleting antibody as a control, and an additional group of macaques immunized under normal conditions was depleted of CD8(+) T cells prior to challenge exposure to SIVmac251. Analysis of the quality and quantity of vaccine-induced CD8(+) T cells demonstrated that SIV-specific CD8(+) T cells generated under conditions of CD4(+) T-cell deficiency expressed low levels of Bcl-2 and interleukin-2 (IL-2), and plasma virus levels increased over time. Depletion of CD8(+) T cells prior to challenge exposure abrogated vaccine-induced protection as previously shown. These data support the notion that adaptive CD4(+) T cells are critical for the generation of effective CD8(+) T-cell responses to SIV that, in turn, contribute to protection from AIDS. Importantly, they also suggest that long-term protection from disease will be afforded only by T-cell vaccines for HIV that provide a balanced induction of CD4(+) and CD8(+) T-cell responses and protect against early depletion of CD4(+) T cells postinfection.
C1 [Vaccari, Monica; Tsai, Wen-Po; Hryniewicz, Anna; Franchini, Genoveffa] NCI, Anim Models & Retroviral Vaccines Sect, Bethesda, MD 20892 USA.
[Venzon, David] NCI, Biostat & Data Management Sect, Bethesda, MD 20892 USA.
[Mattapallil, Joseph] Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Bethesda, MD 20814 USA.
[Song, Kaimei; Roederer, Mario] NIAID, ImmunoTechnol Sect, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Zanetti, Maurizio] Univ Calif San Diego, Immunol Lab, Dept Med, La Jolla, CA 92093 USA.
[Zanetti, Maurizio] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
[Reimann, Keith A.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Viral Pathogenesis, Boston, MA 02215 USA.
RP Franchini, G (reprint author), NCI, Anim Models & Retroviral Vaccines Sect, Bldg 41,Room D804, Bethesda, MD 20892 USA.
EM franchig@mail.nih.gov
FU Intramural Research Program of the NIH; National Cancer Institute;
Center for Cancer Research; National Institute of Allergy and Infectious
Diseases
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research, and the
National Institute of Allergy and Infectious Diseases.; We thank V. S.
Kalyanaraman for the detection of anti-SIVmac251 antibodies
and P. D. Markham, S. Orndorff, D. Weiss, and J. Treece of Advanced
BioScience Laboratories, Inc., Kensington, MD. We thank also Barbara
Felber and George Pavlakis for providing the Gag, Pol, and Env DNA
plasmids and Steven Snodgrass and Ryan Kelly for editorial assistance.;
Author contributions were as follows: M.V. and G.F. designed the study,
performed experiments, and wrote the paper; J.M., K.S., W.-P.T., and
A.H. performed research; D.V., M. R., J.J.M., and K.S. performed
analysis; and K.A.R. and M.R. contributed vital reagents and software
for analysis, respectively. M.Z. helped with the study design and
editing.
NR 50
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PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9629
EP 9638
DI 10.1128/JVI.00893-08
PG 10
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700031
PM 18667509
ER
PT J
AU Meunier, JC
Russell, RS
Engle, RE
Faulk, KN
Purcell, RH
Emerson, SU
AF Meunier, Jean-Christophe
Russell, Rodney S.
Engle, Ronald E.
Faulk, Kristina N.
Purcell, Robert H.
Emerson, Suzanne U.
TI Apolipoprotein C1 association with hepatitis C virus
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID DENSITY-LIPOPROTEIN RECEPTOR; NEUTRALIZING ANTIBODIES; CELL-CULTURE;
ENTER CELLS; HUMAN SERA; ENTRY; PARTICLES; PSEUDOPARTICLES; ENHANCEMENT;
INFECTIVITY
AB Accumulating evidence suggests that cellular lipoprotein components are involved in hepatitis C virus (HCV) morphogenesis, but the precise contribution of these components remains unclear. We investigated the involvement of apolipoprotein C1 (ApoC1) in HCV infection in the HCV pseudotyped particle system (HCVpp), in the recently developed cell culture infection model (HCVcc), and in authentic HCV isolated from viremic chimpanzees. Viral genomes associated with HCVcc or authentic HCV were efficiently immunoprecipitated by anti-ApoC1, demonstrating that ApoC1 was a normal component of HCV. The infectivities of HCVpp that had been mixed with ApoC1 and, more importantly, untreated HCVcc collected from lysates or media of infected Huh7.5 cells were directly neutralized by anti-ApoC1. Indeed, convalescent anti-HCV immunoglobulin G and anti-ApoC1 each neutralized over 75% of infectious HCVcc particles, indicating that many, if not all, infectious particles were recognized by both antibodies. Moreover, peptides corresponding to the C-terminal region of ApoC1 blocked infectivity of both HCVpp and HCVcc. Altogether, these results suggest that ApoC1 associates intracellularly via its C-terminal region with surface components of virions during viral morphogenesis and may play a major role in the replication cycle of HCV.
C1 [Meunier, Jean-Christophe; Russell, Rodney S.; Engle, Ronald E.; Faulk, Kristina N.; Purcell, Robert H.; Emerson, Suzanne U.] NIAID, Hepatitis Viruses & Mol Hepatitis Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Meunier, JC (reprint author), Ecole Normale Super Lyon, INSERM, U758, Human Virol Dept, 46 Allee Italie, Lyon 07, France.
EM jean-christophe.meunier@ens-lyon.fr
FU Intramural Research Program of the National Institutes of Health;
National Institute of Allergy and Infectious Diseases
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases.; Tokyo, Japan) for kindly providing the infectious
molecular clone of JFH1, Stanley Lemon (University of Texas Medical
Branch, Galveston, TX) for kindly providing the H77/JFH1 HCVcc chimera,
and Harry Greenberg (Stanford University, Stanford, CA) for providing
the A4 monoclonal Ab.
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PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9647
EP 9656
DI 10.1128/JVI.00914-08
PG 10
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700033
PM 18667498
ER
PT J
AU Sato, S
Yuste, E
Lauer, WA
Chang, EH
Morgan, JS
Bixby, JG
Lifson, JD
Desrosiers, RC
Johnson, WE
AF Sato, Shuji
Yuste, Eloisa
Lauer, William A.
Chang, Eun Hyuk
Morgan, Jennifer S.
Bixby, Jacqueline G.
Lifson, Jeffrey D.
Desrosiers, Ronald C.
Johnson, Welkin E.
TI Potent antibody-mediated neutralization and evolution of antigenic
escape variants of simian immunodeficiency virus strain SIVmac239 in
vivo
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID AMINO-ACID SITES; GP120 ENVELOPE GLYCOPROTEIN; MONOCLONAL-ANTIBODIES;
RECEPTOR-BINDING; POINT MUTATION; TRANSMEMBRANE PROTEIN; MACROPHAGE
TROPISM; SEQUENCE VARIATION; CRYSTAL-STRUCTURE; RHESUS-MONKEYS
AB Here, we describe the evolution of antigenic escape variants in a rhesus macaque that developed unusually high neutralizing antibody titers to SIVmac239. By 42 weeks postinfection, 50% neutralization of SIVmac239 was achieved with plasma dilutions of 1:1,000. Testing of purified immunoglobulin confirmed that the neutralizing activity was antibody mediated. Despite the potency of the neutralizing antibody response, the animal displayed a typical viral load profile and progressed to terminal AIDS with a normal time course. Viral envelope sequences from week 16 and week 42 plasma contained an excess of nonsynonymous substitutions, predominantly in V1 and V4, including individual sites with ratios of nonsynonymous to synonymous substitution rates (dN/dS) highly suggestive of strong positive selection. Recombinant viruses encoding envelope sequences isolated from these time points remained resistant to neutralization by all longitudinal plasma samples, revealing the failure of the animal to mount secondary responses to the escaped variants. Substitutions at two sites with significant dN/dS values, one in V1 and one in V4, were independently sufficient to confer nearly complete resistance to neutralization. Substitutions at three additional sites, one in V4 and two in gp41, conferred moderate to high levels of resistance when tested individually. All the amino acid changes leading to escape resulted from single nucleotide substitutions. The observation that antigenic escape resulted from individual, single amino acid replacements at sites well separated in current structural models of Env indicates that the virus can utilize multiple independent pathways to rapidly achieve similar levels of resistance.
C1 [Sato, Shuji; Yuste, Eloisa; Lauer, William A.; Chang, Eun Hyuk; Morgan, Jennifer S.; Bixby, Jacqueline G.; Desrosiers, Ronald C.; Johnson, Welkin E.] Harvard Univ, Sch Med, New England Primate Res Ctr, Dept Microbiol & Mol Genet, Southborough, MA 01772 USA.
[Lifson, Jeffrey D.] SAIC Frederick Inc, NCI, AIDS & Canc Virus Program, Frederick, MD 21702 USA.
RP Johnson, WE (reprint author), Harvard Univ, Sch Med, New England Primate Res Ctr, Dept Microbiol & Mol Genet, Southborough, MA 01772 USA.
EM welkin_johnson@hms.harvard.edu
FU NIH [AI057039, RR00168, AI25328]; International AIDS Vaccine Initiative
Neutralizing Antibody Consortium; National Cancer Institute
[NO1-CO-124000]
FX We especially thank M. P. Cummings and the MBL Workshop on Molecular
Evolution. We also thank L. A. Pozzi, S. P. O'Neil, and members of the
Division of Comparative Pathology, NEPRC, for advice and assistance with
sample procurement; H. B. Sanford of the Division of Microbiology,
NEPRC, for technical assistance; and M. Piatak, Jr., of the AIDS and
Cancer Virus Program, SAIC Frederick, Inc., for plasma viral load
analyses. SIVsmmPGm5.3 expression vector was kindly donated by F. J.
Novembre of the Yerkes Regional Primate Research Center, Emory
University.; This study was supported in part by grants from the NIH,
including AI057039 (to W.E.J.), RR00168 (NEPRC), and AI25328 (to
R.C.D.); the International AIDS Vaccine Initiative Neutralizing Antibody
Consortium; and federal funds from the National Cancer Institute and the
NIH under contract NO1-CO-124000 (J.D.L.). An equipment purchase was
made possible by a gift from the James B. Pendleton Charitable Trust.
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PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9739
EP 9752
DI 10.1128/JVI.00871-08
PG 14
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700041
PM 18667507
ER
PT J
AU Waheed, AA
Ablan, SD
Soheilian, F
Nagashima, K
Ono, A
Schaffner, CP
Freed, EO
AF Waheed, Abdul A.
Ablan, Sherimay D.
Soheilian, Ferri
Nagashima, Kunio
Ono, Akira
Schaffner, Carl P.
Freed, Eric O.
TI Inhibition of human immunodeficiency virus type 1 assembly and release
by the cholesterol-binding compound amphotericin B methyl ester:
Evidence for Vpu dependence
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PLASMA-MEMBRANE; LIPID RAFTS; GAG MULTIMERIZATION; PARTICLE-PRODUCTION;
MOLECULAR CLONE; PROTEIN; MATRIX; REPLICATION; ENVELOPE; RETROVIRUS
AB We investigated the mechanism by which the cholesterol- binding compound amphotericin B methyl ester (AME) inhibits human immunodeficiency virus type 1 (HIV-1) particle production. We observed no significant effect of AME on Gag binding to the plasma membrane, Gag association with lipid rafts, or Gag multimerization, indicating that the mechanism of inhibition by AME is distinct from that by cholesterol depletion. Electron microscopy analysis indicated that AME significantly disrupts virion morphology. Interestingly, we found that AME does not inhibit the release of Vpu-defective HIV-1 or Vpu(-) retroviruses such as murine leukemia virus and simian immunodeficiency virus. We demonstrated that the ability of Vpu to counter the activity of CD317/BST-2/tetherin is markedly reduced by AME. These results indicate that AME interferes with the anti-CD317/BST-2/tetherin function of Vpu.
C1 [Waheed, Abdul A.; Ono, Akira; Freed, Eric O.] NCI, HIV Drug Resistance Program, Virus Cell Interact Sect, Frederick, MD 21702 USA.
[Soheilian, Ferri; Nagashima, Kunio] NCI, SAIC Frederick, Res Technol Program, Image Anal Lab, Frederick, MD 21702 USA.
[Schaffner, Carl P.] Rutgers State Univ, Waksman Inst, Dept Microbiol & Biochem, New Brunswick, NJ 08903 USA.
RP Waheed, AA (reprint author), NCI, HIV Drug Resistance Program, Virus Cell Interact Sect, Bldg 535,Rm 108, Frederick, MD 21702 USA.
EM awaheed@ncifcrf.gov
OI Ono, Akira/0000-0001-7841-851X
FU Intramural Research Program of the Center for Cancer Research; National
Cancer Institute; NIH [N01-CO-12400]; NIH Intramural AIDS Targeted
Antiviral Program (IATAP)
FX We thank members of the Freed laboratory for helpful discussions and
critical review of the manuscript. AME was generously supplied by
Karykion Corporation, Princeton, NJ. We thank K. Strebel, K.-T. Jeang,
B. Crise, Y. Li, and P. Bieniasz for generously providing plasmids. The
following reagents were obtained from the NIH AIDS Research and
Reference Reagent Program: HIV immunoglobulin (Ig), anti-SIVmac239
antiserum, and plasmid pSV psi- MLV-env-; This
research was supported by the Intramural Research Program of the Center
for Cancer Research, National Cancer Institute, NIH, and the NIH
Intramural AIDS Targeted Antiviral Program (IATAP) and was funded in
part by federal funds from the National Cancer Institute, NIH, under
contract N01-CO-12400.; The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does the mention of trade names, commercial
products, or organizations imply endorsement by the U. S. government.
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PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9776
EP 9781
DI 10.1128/JVI.00917-08
PG 6
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700045
PM 18653459
ER
PT J
AU Shin, EC
Capone, S
Cortese, R
Colloca, S
Nicosia, A
Folgori, A
Rehermann, B
AF Shin, Eui-Cheol
Capone, Stefania
Cortese, Riccardo
Colloca, Stefano
Nicosia, Alfredo
Folgori, Antonella
Rehermann, Barbara
TI The kinetics of hepatitis C virus-specific CD8 T-cell responses in the
blood mirror those in the liver in acute hepatitis C virus infection
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID IMMUNE-RESPONSES; VIRAL CLEARANCE; PERSISTENCE; CHIMPANZEES;
DETERMINANTS; RECOVERY
AB Peripheral blood T-cell responses are used as biomarkers in hepatitis C virus (HCV) vaccine trials. However, it is not clear how T-cell responses in the blood correlate with those in the liver, the infection site. By studying serial liver and blood samples of five vaccinated and five mock-vaccinated control chimpanzees during acute HCV infection, we demonstrate a correlation between HCV-specific CD8 T-cell responses in the blood and molecular and functional markers of T-cell responses in the liver. Thus, HCV-specific CD8 T-cell responses in the blood are valid markers for intrahepatic T-cell activity.
C1 [Shin, Eui-Cheol; Rehermann, Barbara] NIDDK, Immunol Sect, LDB, NIH,DHHS, Bethesda, MD 20892 USA.
[Capone, Stefania; Cortese, Riccardo; Colloca, Stefano; Nicosia, Alfredo; Folgori, Antonella] Okairos, Naples, Italy.
RP Rehermann, B (reprint author), NIDDK, Immunol Sect, LDB, NIH,DHHS, Bethesda, MD 20892 USA.
EM Rehermann@nih.gov
RI Shin, Eui-Cheol/C-1690-2011;
OI Capone, Stefania/0000-0002-2272-120X
FU NIDDK; NIH
FX We thank M.-H. Sung (National Cancer Institute, NIH) for helpful advice
on statistical analysis.; This work was supported in part by the NIDDK,
NIH intramural research program.
NR 20
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PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9782
EP 9788
DI 10.1128/JVI.00475-08
PG 7
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700046
PM 18667501
ER
PT J
AU Collins, PL
Bukreyev, A
Murphy, BR
AF Collins, Peter L.
Bukreyev, Alexander
Murphy, Brian R.
TI What are the risks - Hypothetical and observed - of recombination
involving live vaccines and vaccine vectors based on nonsegmented
negative-strain RNA viruses?
SO JOURNAL OF VIROLOGY
LA English
DT Letter
ID NEWCASTLE-DISEASE VIRUS; RESPIRATORY SYNCYTIAL VIRUS; AVIAN INFLUENZA;
HEMAGGLUTININ GENE; ATTENUATED VACCINE; PROTECTS CHICKENS; IMMUNIZATION;
PRIMATES
C1 [Collins, Peter L.; Bukreyev, Alexander; Murphy, Brian R.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Collins, PL (reprint author), NIAID, NIH, 50 South Dr,Room 6503, Bethesda, MD 20892 USA.
EM pcollins@niaid.nih.giv
FU Intramural NIH HHS
NR 20
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U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 19
BP 9805
EP 9806
DI 10.1128/JVI.01336-08
PG 2
WC Virology
SC Virology
GA 349DT
UT WOS:000259259700050
PM 18796655
ER
PT J
AU Watashi, K
Khan, M
Yedavalli, VRK
Yeung, ML
Strebel, K
Jeang, KT
AF Watashi, Koichi
Khan, Mohammad
Yedavalli, Venkat R. K.
Yeung, Man Lung
Strebel, Klaus
Jeang, Kuan-Teh
TI Human Immunodeficiency Virus Type 1 Replication and Regulation of
APOBEC3G by Peptidyl Prolyl Isomerase Pin1
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PROTEIN-KINASE-C; EDITING ENZYME APOBEC3G; FACTOR MESSENGER-RNA; VIF
PROTEIN; HIV-1 VIF; ANTIVIRAL ACTIVITY; ANTIRETROVIRAL DEFENSE; VIRION
INCORPORATION; CYTIDINE DEAMINASES; STRESS GRANULES
AB APOBEC3G (A3G) is a cytidine deaminase that restricts human immunodeficiency virus type 1 (HIV-1) replication. HIV-1 synthesizes a viral infectivity factor (Vif) to counter A3G restriction. Currently, it is poorly understood how A3G expression/activity is regulated by cellular factors. Here, we show that the prolyl isomerase Pin1 protein modulates A3G expression. Pin1 was found to be an A3G-interacting protein that reduces A3G expression and its incorporation into HIV-1 virion, thereby limiting A3G-mediated restriction of HIV-1. Intriguingly, HIV-1 infection modulates the phosphorylation state of Pin1, enhancing its ability to moderate A3G activity. These new findings suggest a potential Vif-independent way for HIV-1 to moderate the cellular action of A3G.
C1 [Watashi, Koichi; Yedavalli, Venkat R. K.; Yeung, Man Lung; Jeang, Kuan-Teh] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Khan, Mohammad; Strebel, Klaus] NIAID, Viral Biochem Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
RP Jeang, KT (reprint author), 9000 Rockville Pike,Bldg 4,Room 306, Bethesda, MD 20892 USA.
EM kj7e@nih.gov
RI Jeang, Kuan-Teh/A-2424-2008
FU NIAID; NIH; Intramural AIDS Targeted Antiviral Program (IATAP)
FX We are grateful to Alicia Buckler-White and Ronald Plishka for sequence
analysis. We also thank the members of K.-T.J.' s laboratory for
critical readings of the manuscript.; Work in the laboratory of K.-T.J.
and K.S. is supported through intramural funds from NIAID, NIH, and from
the Intramural AIDS Targeted Antiviral Program ( IATAP) from the office
of the Director, NIH.
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PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 20
BP 9928
EP 9936
DI 10.1128/JVI.01017-08
PG 9
WC Virology
SC Virology
GA 361EA
UT WOS:000260109100012
PM 18684817
ER
PT J
AU Guan, WX
Cheng, F
Yoto, YK
Kleiboeker, S
Wong, SS
Zhi, N
Pintel, DJ
Qiu, JM
AF Guan, Wuxiang
Cheng, Fang
Yoto, Yuko
Kleiboeker, Steve
Wong, Susan
Zhi, Ning
Pintel, David J.
Qiu, Jianming
TI Block to the Production of Full-Length B19 Virus Transcripts by Internal
Polyadenylation Is Overcome by Replication of the Viral Genome
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN PARVOVIRUS B19; HUMAN-BONE MARROW; ADENOASSOCIATED-VIRUS; TYPE-5
RNA; ALTERNATIVE POLYADENYLATION; ADENOVIRUS REPLICATION; ERYTHROID
PROGENITORS; CELLULAR CORECEPTOR; INFECTIOUS CLONE; GENE-PRODUCTS
AB The pre-mRNA processing strategy of the B19 virus is unique among parvoviruses. B19 virus-generated pre-mRNAs are transcribed from a single promoter and are extensively processed by alternative splicing and alternative polyadenylation to generate 12 transcripts. Blockage of the production of full-length B19 virus transcripts at the internal polyadenylation site [(pA)p] was previously reported to be a limiting step in B19 virus permissiveness. We show here that in the absence of genome replication, internal polyadenylation of B19 virus RNAs at (pA) p is favored in cells which are both permissive and nonpermissive for B19 viral replication. Replication of the B19 virus genome, however, introduced either by viral infection or by transfection of an infectious clone into permissive cells or forced by heterologous replication systems in nonpermissive cells, enhanced readthrough of (pA)p and the polyadenylation of B19 virus transcripts at the distal site [(pA)d]. Therefore, replication of the genome facilitates the generation of sufficient full-length transcripts that encode the viral capsid proteins and the essential 11-kDa nonstructural protein. Furthermore, we show that polyadenylation of B19 viral RNA at (pA) p likely competes with splicing at the second intron. Thus, we conclude that replication of the B19 virus genome is the primary limiting step governing B19 virus tropism.
C1 [Guan, Wuxiang; Cheng, Fang; Qiu, Jianming] Univ Kansas, Med Ctr, Dept Microbiol Mol Genet & Immunol, Kansas City, KS 66103 USA.
[Yoto, Yuko; Pintel, David J.] Univ Missouri, Dept Mol Microbiol & Immunol, Columbia, MO USA.
[Kleiboeker, Steve] ViraCor Labs, Lees Summit, MO 64086 USA.
[Wong, Susan; Zhi, Ning] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
RP Qiu, JM (reprint author), Univ Kansas, Med Ctr, Dept Microbiol Mol Genet & Immunol, MS3029,3901 Rainbow Blvd, Kansas City, KS 66103 USA.
EM jqiu@kumc.edu
FU NIAID [RO1 AI070723, RO1 AI46458, RO1 AI56310, RO1 AI21302]; NCRR COBRE
[P20 RR016443]
FX This work was supported by PHS grant RO1 AI070723 from NIAID and grant
P20 RR016443 from the NCRR COBRE program to J. Q. and by PHS grants RO1
AI46458, RO1 AI56310, and RO1 AI21302 from NIAID to D. J. P.; We thank
John Brunstein at University of British Columbia, Vancouver, for
providing the pSVOdB19 plasmids.
NR 49
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PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 20
BP 9951
EP 9963
DI 10.1128/JVI.01162-08
PG 13
WC Virology
SC Virology
GA 361EA
UT WOS:000260109100014
PM 18684834
ER
PT J
AU Gustchina, E
Bewley, CA
Clore, GM
AF Gustchina, Elena
Bewley, Carole A.
Clore, G. Marius
TI Sequestering of the Prehairpin Intermediate of gp41 by Peptide
N36(Mut(e,g)) Potentiates the Human Immunodeficiency Virus Type 1
Neutralizing Activity of Monoclonal Antibodies Directed against the
N-Terminal Helical Repeat of gp41
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID GLYCOPROTEIN-MEDIATED FUSION; PROXIMAL EXTERNAL REGION; TRIMERIC
COILED-COIL; HIV-1 GP41; ENVELOPE GLYCOPROTEIN; MEMBRANE-FUSION; VACCINE
DEVELOPMENT; ENTRY INHIBITION; ATOMIC-STRUCTURE; SOLUBLE CD4
AB Human immunodeficiency virus type 1 (HIV-1) neutralization can be effected by several classes of inhibitors that target distinct regions of gp41 that are accessible in the prehairpin intermediate (PHI) state and block the formation of the six-helix bundle (6-HB) conformation of gp41. The N-heptad repeat (N-HR) of gp41 is the site of action of two classes of inhibitors. One class binds to the trimeric N-HR coiled coil, while the other, exemplified by the peptide N-36Mut(e,N-g), disrupts the trimer and sequesters the PHI through the formation of heterotrimers. We recently reported a neutralizing Fab (Fab 3674), selected from a nonimmune phage library, that binds to the trimeric N-HR coiled coil through an epitope that remains exposed in the 6-HB and is also present in heterotrimers of the N-HR and N36(Mut(e,g)) peptide. Here we show that N36(Mut(e,g)) prolongs the temporal window during which the virus is susceptible to neutralization by the bivalent Fab 3674 and that bivalent Fab 3674 and N36(Mut(e,g)) neutralize HXB2 and SF162 strains of HIV-1, as well as isolates of diverse primary B and C HIV-1 strains, synergistically in a Env-pseudotyped virus neutralization assay. N36(Mut(e,g)) also rescues neutralizing activity of Fab 3674 against resistant virus strains and renders a series of related nonneutralizing Fabs neutralizing. Moreover, N36(Mut(e,g)) exhibits the same effects on the broadly neutralizing 2F5 and 4E10 monoclonal antibodies directed against the membrane-proximal extended region of gp41. The mechanistic implications of these findings are discussed.
C1 [Gustchina, Elena; Clore, G. Marius] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Bewley, Carole A.] NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
RP Clore, GM (reprint author), NIDDKD, Chem Phys Lab, NIH, Bldg 5, Bethesda, MD 20892 USA.
EM mariusc@mail.nih.gov
RI Clore, G. Marius/A-3511-2008
OI Clore, G. Marius/0000-0003-3809-1027
FU NIH
FX We thank Michael Zwick for providing us with a sample of the 8K8 MAb,
Shibo Jiang for a sample of NC-1, and John Louis for useful
discussions.; This work was supported by the AIDS Targeted Antiviral
Program of the Office of the Director of the NIH and by the Intramural
Program of NIDDK, NIH (to G.M.C. and C.A.B.).
NR 55
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U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 20
BP 10032
EP 10041
DI 10.1128/JVI.01050-08
PG 10
WC Virology
SC Virology
GA 361EA
UT WOS:000260109100020
PM 18667502
ER
PT J
AU Sood, CL
Ward, JM
Moss, B
AF Sood, Cindy L.
Ward, Jerrold M.
Moss, Bernard
TI Vaccinia Virus Encodes I5, a Small Hydrophobic Virion Membrane Protein
That Enhances Replication and Virulence in Mice
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MATURE VIRION; IDENTIFICATION; POXVIRUSES; PARTICLES; GENOME
AB The vaccinia virus I5L open reading frame encodes a 79-amino-acid protein, with two predicted transmembrane domains, that is conserved among all sequenced members of the chordopoxvirus subfamily. No nonpoxvirus homologs or functional motifs have been recognized, and the role of the I5 protein remains unknown. We found that synthesis of I5 was dependent on viral DNA replication and occurred exclusively at late times, consistent with a consensus late promoter motif adjacent to the start of the open reading frame. I5 was present in preparations of purified virions and could be extracted with nonionic detergent, suggesting membrane insertion. Transmission electron microscopy of immunogold-labeled thawed cryosections of infected cells revealed the association of an epitope-tagged I5 with the membranes of immature and mature virions. Viable I5L deletion and frameshift mutants were constructed and found to replicate like wild-type virus in a variety of cell lines and primary human epidermal keratinocytes, indicating that the protein was dispensable for in vitro cultivation. However, mouse intranasal challenge experiments indicated that a mutant virus with a frameshift resulting in a stop codon near the N terminus of I5 was attenuated compared to control virus. The attenuation was correlated with clearance of mutant viruses from the respiratory tract and with less progression and earlier resolution of pathological changes. We suggest that I5 is involved in an aspect of host defense that is evolutionarily conserved although a role in cell tropism should also be considered.
C1 [Sood, Cindy L.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20814 USA.
[Ward, Jerrold M.] NIAID, Comparat Med Branch, NIH, Bethesda, MD 20814 USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, 33 N Dr,MSC 3210, Bethesda, MD 20892 USA.
EM bmoss@nih.gov
FU Division of Intramural Research; National Institute of Allergy and
Infectious Diseases; National Institutes of Health
FX We thank Norman Cooper and Catherine Cotter for providing cells, Andrea
S. Weisberg for electron microscopy, Lacey Cashell and Felix J. Santiago
for mouse surgery, and Heather Hickman and Scott Hensley for advice on
titration of virus from mouse lung tissue.; The work was supported by
funds from the Division of Intramural Research, National Institute of
Allergy and Infectious Diseases, National Institutes of Health.
NR 26
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U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 20
BP 10071
EP 10078
DI 10.1128/JVI.01355-08
PG 8
WC Virology
SC Virology
GA 361EA
UT WOS:000260109100024
PM 18701595
ER
PT J
AU Stewart-Maynard, KM
Cruceanu, M
Wang, F
Vo, MN
Gorelick, RJ
Williams, MC
Rouzina, I
Musier-Forsyth, K
AF Stewart-Maynard, Kristen M.
Cruceanu, Margareta
Wang, Fei
Vo, My-Nuong
Gorelick, Robert J.
Williams, Mark C.
Rouzina, Ioulia
Musier-Forsyth, Karin
TI Retroviral Nucleocapsid Proteins Display Nonequivalent Levels of Nucleic
Acid Chaperone Activity
SO JOURNAL OF VIROLOGY
LA English
DT Review
ID MURINE LEUKEMIA-VIRUS; RNA PACKAGING SIGNAL; MINUS-STRAND TRANSFER;
PRIMER BINDING-SITE; T4 GENE-32 PROTEIN; HIV-1 REVERSE TRANSCRIPTION;
MOLECULE FORCE SPECTROSCOPY; SEQUENCE-DEPENDENT BINDING; ZINC-FINGER
STRUCTURES; ROUS-SARCOMA-VIRUS
AB Human immunodeficiency virus type 1 (HIV-1) nucleocapsid protein (NC) is a nucleic acid chaperone that facilitates the remodeling of nucleic acids during various steps of the viral life cycle. Two main features of NC's chaperone activity are its abilities to aggregate and to destabilize nucleic acids. These functions are associated with NC's highly basic character and with its zinc finger domains, respectively. While the chaperone activity of HIV-1 NC has been extensively studied, less is known about the chaperone activities of other retroviral NCs. In this work, complementary experimental approaches were used to characterize and compare the chaperone activities of NC proteins from four different retroviruses: HIV-1, Moloney murine leukemia virus (MLV), Rous sarcoma virus (RSV), and human T-cell lymphotropic virus type 1 (HTLV-1). The different NCs exhibited significant differences in their overall chaperone activities, as demonstrated by gel shift annealing assays, decreasing in the order HIV-1 similar to RSV > MLV >> HTLV-1. In addition, whereas HIV-1, RSV, and MLV NCs are effective aggregating agents, HTLV-1 NC, which exhibits poor overall chaperone activity, is unable to aggregate nucleic acids. Measurements of equilibrium binding to single- and double-stranded oligonucleotides suggested that all four NC proteins have moderate duplex destabilization capabilities. Single-molecule DNA-stretching studies revealed striking differences in the kinetics of nucleic acid dissociation between the NC proteins, showing excellent correlation between nucleic acid dissociation kinetics and overall chaperone activity.
C1 [Stewart-Maynard, Kristen M.; Vo, My-Nuong] Univ Minnesota, Dept Mol Biol Biochem & Biophys, Minneapolis, MN 55455 USA.
[Musier-Forsyth, Karin] Ohio State Univ, Dept Chem, Columbus, OH 43210 USA.
[Musier-Forsyth, Karin] Ohio State Univ, Dept Biochem, Columbus, OH 43210 USA.
[Stewart-Maynard, Kristen M.; Vo, My-Nuong] Univ Minnesota, Dept Chem, Minneapolis, MN 55455 USA.
[Stewart-Maynard, Kristen M.; Vo, My-Nuong] Univ Minnesota, Inst Mol Virol, Minneapolis, MN 55455 USA.
[Cruceanu, Margareta; Wang, Fei; Williams, Mark C.] Northeastern Univ, Dept Phys, Boston, MA 02115 USA.
[Gorelick, Robert J.] NCI, AIDS Vaccine Program, Basic Res Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Rouzina, I (reprint author), Univ Minnesota, Dept Mol Biol Biochem & Biophys, Minneapolis, MN 55455 USA.
EM rouzi002@umn.edu; musier@chemistry.ohio-state.edu
OI Williams, Mark C./0000-0003-3219-376X
FU NIH [GM065056, GM073462, GM072396, N01-CO-12400]; NSF [MCB-0744456];
National Cancer Institute
FX We thank Cathy V. Hixson and Donald G. Johnson for their assistance in
preparing the recombinant NC proteins. This work was supported by NIH
grants GM065056 (to K. M.- F.) and GM073462 ( to M. C. W.), by NSF grant
MCB-0744456 ( to M. C. W.), and by an NIH Ruth L. Kirschstein National
Service Award GM072396 ( to K. M. S.-M.). This publication was funded in
part with federal funds from the National Cancer Institute, National
Institutes of Health, under contract N01-CO-12400. The content of this
publication does not necessarily reflect the views or policies of the
Department of Health and Human Services, nor does mention of trade
names, commercial products, or organizations imply endorsement by the U.
S. government.
NR 114
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U1 1
U2 9
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2008
VL 82
IS 20
BP 10129
EP 10142
DI 10.1128/JVI.01169-08
PG 14
WC Virology
SC Virology
GA 361EA
UT WOS:000260109100030
PM 18684831
ER
PT J
AU Pinn, VW
AF Pinn, Vivian W.
TI Fifth Annual NIH Interdisciplinary Women's Health Research Symposium
November 19, 2008 Introduction
SO JOURNAL OF WOMENS HEALTH
LA English
DT Editorial Material
C1 NIH, Off Res Womens Hlth, Bethesda, MD 20892 USA.
RP Pinn, VW (reprint author), NIH, Off Res Womens Hlth, 6707 Democracy Blvd,Suite 400, Bethesda, MD 20892 USA.
EM ORWH-Research@od.nih.gov
NR 0
TC 1
Z9 1
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT
PY 2008
VL 17
IS 8
BP 1227
EP 1228
DI 10.1089/jwh.2008.AC02
PG 2
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 378OE
UT WOS:000261331200001
PM 18816198
ER
PT J
AU Park, AN
Buist, DSM
Tiro, JA
Taplin, SH
AF Park, Alice N.
Buist, Diana S. M.
Tiro, Jasmin A.
Taplin, Stephen H.
TI Mediating Factors in the Relationship between Income and Mammography Use
in Low-Income Insured Women
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID BREAST-CANCER; SCREENING MAMMOGRAPHY; PARTICIPATION; PROGRAM; COST
AB Aim: We used secondary data from a prospective randomized mammography recruitment trial to examine whether attitudinal and facilitating characteristics mediate the observed relationship between annual household income and mammogram receipt among women in an integrated health plan.
Methods: We compared 1419 women due for a screening mammogram based on the 1995 annual household income poverty definition for a family of four (<$15,000 vs. >$15,000). A telephone survey was used to collect information on household income, demographics, health behavior, attitudinal and facilitating variables. Administrative databases were used to document mammography receipt. We used Cox proportional hazards models to estimate the hazards ratio (HR) and 95% confidence interval (CI) of subsequent mammography use separately for women with and without a prior mammogram.
Results: Several variables, including employment, living alone, believing that mammograms are unnecessary, having friends supportive of mammography, and ease of arranging transportation, completely mediated the effect of income on mammography use. In multivariable models, the direct predictive effect of income on mammography was reduced to nonsignificance (HR 1.13, 95% CI 0.82-1.54 in women with previous mammogram and HR 0.91, 95% CI 0.41-2.00 in women without previous mammogram).
Conclusions: Providing insurance does not ensure low-income populations will seek screening mammography. Efficacious interventions that address attitudes and facilitating conditions may motivate mammography use among low-income women with insurance.
C1 [Buist, Diana S. M.] Ctr Hlth Studies, Grp Hlth, Seattle, WA 98101 USA.
[Park, Alice N.] Seattle Indian Hlth Board, Urban Indian Hlth Inst, Seattle, WA USA.
[Tiro, Jasmin A.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Bethesda, MD 20892 USA.
[Taplin, Stephen H.] NCI, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Buist, DSM (reprint author), Ctr Hlth Studies, Grp Hlth, 1730 Minor Ave,Suite 1600, Seattle, WA 98101 USA.
EM buist.d@ghc.org
OI Tiro, Jasmin/0000-0001-8300-0441
FU National Cancer Institute cooperative agreement [U01CA63731, CA63188];
American Cancer Society [CRTG-03-024-01-CCE]
FX This research was supported by National Cancer Institute cooperative
agreement, grants U01CA63731 and CA63188. D. S. M. B. was supported in
part by American Cancer Society grant CRTG-03-024-01-CCE.
NR 26
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U1 0
U2 9
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT
PY 2008
VL 17
IS 8
BP 1371
EP 1378
DI 10.1089/jwh.2007.0625
PG 8
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 378OE
UT WOS:000261331200098
PM 18788984
ER
PT J
AU Goldman, SE
Ancoli-Israel, S
Boudredu, R
Cauley, JA
Hall, M
Stone, KL
Rubin, SM
Sattertield, S
Simonsick, EM
Newman, AB
AF Goldman, Suzanne E.
Ancoli-Israel, Sonia
Boudredu, Robert
Cauley, Jane A.
Hall, Martica
Stone, Katie L.
Rubin, Susan M.
Sattertield, Suzanne
Simonsick, Eleanor M.
Newman, Anne B.
CA Hlth Aging
TI Sleep Problems and Associated Daytime Fatigue in Community-Dwelling
Older Individuals
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Sleep; Fatigue; Aging
ID SUBJECTIVE FATIGUE; CANCER-PATIENTS; HEART HEALTH; LONG-SLEEP;
FOLLOW-UP; MORTALITY; APNEA; EPIDEMIOLOGY; TIREDNESS; INSOMNIA
AB Background. Reported fatigue has been identified as a component of frailty. The contribution of nighttime sleep quality (duration and complaints) to fatigue symptoms in community-dwelling older adults has not been evaluated.
Methods. We studied 2264 men and women, aged 75-84 years (mean 77.5 years; standard deviation [SD] 2.9). participating in the Year 5 (2001-2002) clinic visit of the Health, Aging, and Body Composition (Health ABC) study. Fatigue was determined using a subscale of the Modified Piper Fatigue Scale (0-50; higher score indicating higher fatigue). Hours of sleep per night, trouble falling asleep, waking up during the night, and waking up too early in the morning were assessed using interviewer-administered questionnaires.
Results. The average fatigue score was 17.7 (SD 8.4). In multivariate models, women had a 3.8% higher fatigue score than men did. Individuals who slept <= 6 hours/night had a 4.3% higher fatigue score than did those who slept 7 hours/ night. Individuals with complaints of awakening too early in the morning had a 5.5% higher fatigue score than did those without these complaints. These associations remained significant after multivariate adjustment for multiple medical conditions.
Conclusion. The association between self-reported short sleep duration (<= 6 hours), and waking up too early and fatigue symptoms suggests that better and more effective management of sleep behaviors may help reduce fatigue in older adults.
C1 [Goldman, Suzanne E.] Vanderbilt Univ, Med Ctr, Dept Neurol, Sleep Disorders Program, Nashville, TN 37232 USA.
[Ancoli-Israel, Sonia] Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA.
[Boudredu, Robert; Cauley, Jane A.; Newman, Anne B.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15260 USA.
[Hall, Martica] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
[Stone, Katie L.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Stone, Katie L.] San Francisco Coordinating Ctr, San Francisco, CA USA.
[Rubin, Susan M.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Sattertield, Suzanne] Univ Tennessee, Dept Prevent Med, Memphis, TN USA.
[Simonsick, Eleanor M.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
RP Goldman, SE (reprint author), Vanderbilt Univ, Med Ctr, Dept Neurol, Sleep Disorders Program, 1301 Med Ctr Dr,Room B-727, Nashville, TN 37232 USA.
EM suzanne.goldman@vanderbilt.edu
RI Hall, Martica/D-2809-2012; Newman, Anne/C-6408-2013; Cauley,
Jane/N-4836-2015;
OI Hall, Martica/0000-0003-0642-2098; Newman, Anne/0000-0002-0106-1150;
Cauley, Jane/0000-0003-0752-4408; Boudreau, Robert/0000-0003-0162-5187
FU National Institutes of Health (NIH) [N01-AG-6-2101, 2103, 2106,
AG000181-16, T32]; National Institute on Aging (NIA) [AG08415]; National
Cancer Institute [CA85264, CA112035]; University of California
[111B-0034]
FX This work was supported by National Institutes of Health (NIH) contracts
N01-AG-6-2101, 2103, and 2106; National Institute on Aging (NIA) grant
AG08415; and National Cancer Institute grants CA85264 and CA112035. This
research was also supported in part by the Intramural Research program
of the NIH, NIA (Aging Training Grant 2, T32, AG000181-16) and by funds
from the California Breast Cancer Research Program of the University of
California (Grant 111B-0034).
NR 43
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U1 3
U2 7
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD OCT
PY 2008
VL 63
IS 10
BP 1069
EP 1075
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 366LS
UT WOS:000260483600007
PM 18948557
ER
PT J
AU Lamb, SE
McCabe, C
Becker, C
Fried, LP
Guralnik, JM
AF Lamb, Sarah E.
McCabe, Chris
Becker, Clemens
Fried, Linda P.
Guralnik, Jack M.
TI The Optimal Sequence and Selection of Screening Test Items to Predict
Fall Risk in Older Disabled Women: The Women's Health and Aging Study
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Accidental falls; Multiphasic screening; Aged
ID FUNCTIONAL MOBILITY; COMMUNITY; PEOPLE; METAANALYSIS; PREVENTION;
ADULTS; IMPAIRMENT; DISABILITY; DEPRESSION; INJURY
AB Background. Falls are a major cause of disability, dependence, and death in older people. Brief screening algorithms may he helpful in identifying risk and leading to more detailed assessment. Our aim was to determine the most effective sequence of falls screening test items from a wide selection of recommended items including self-report and performance tests, and to compare performance with other published guidelines.
Methods. Data were from a prospective, age-stratified, cohort study. Participants were 1002 community-dwelling women aged 65 years old or older, experiencing at least some mild disability. Assessments of fall risk factors were conducted in participants' homes. Fall outcomes were collected at 6 monthly intervals. Algorithms were built for prediction of any fall over a 12-month period using tree classification with cross-set validation.
Results. Algorithms using performance tests provided the best prediction of fall events, and achieved moderate to strong performance when compared to commonly accepted benchmarks. The items selected by the best performing algorithm were the number of falls in the last year and, in selected subpopulations, frequency of difficulty balancing while walking, a 4 m walking speed test, body mass index, and a test of knee extensor strength. The algorithm performed better than that from the American Geriatric Society/British Geriatric Society/American Academy of Orthopaedic Surgeons and other guidance, although these findings should be treated with caution.
Conclusions. Suggestions are made on the type, number, and sequence of tests that could be used to maximize estimation of the probability of falling in older disabled women.
C1 [Lamb, Sarah E.] Univ Warwick, Warwick Med Sch, Warwick Clin Trials Unit, Coventry CV4 7AL, W Midlands, England.
[McCabe, Chris] Univ Warwick, Warwick Med Sch, Hlth Sci Res Inst, Coventry CV4 7AL, W Midlands, England.
[Becker, Clemens] Robert Bosch Krankenhaus, Klin Geriatr Rehabil, Stuttgart, Germany.
[Fried, Linda P.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Guralnik, Jack M.] NIA, Epidemiol Demog & Biometry Program, Bethesda, MD 20892 USA.
RP Lamb, SE (reprint author), Univ Warwick, Warwick Med Sch, Warwick Clin Trials Unit, Coventry CV4 7AL, W Midlands, England.
EM S.Lamb@warwick.ac.uk
FU National Institute on Aging (NIA) [NO1-AG12112]; NIA Intramural Research
Program
FX This work was supported by the National Institute on Aging (NIA:
contract NO1-AG12112 and the NIA Intramural Research Program.; We
acknowledge with thanks the assistance of Angeliki Chorti and Christelle
Evaert in the preparation of the manuscript.
NR 34
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U1 4
U2 8
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD OCT
PY 2008
VL 63
IS 10
BP 1082
EP 1088
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 366LS
UT WOS:000260483600009
PM 18948559
ER
PT J
AU Briggs, JP
AF Briggs, Josephine P.
TI The hunt for the perfect biomarker for acute kidney injury: back to
gamma-trace?
SO KIDNEY INTERNATIONAL
LA English
DT Editorial Material
ID TUBULAR PROTEINURIA; DIAGNOSIS
AB The hunt for a good biomarker for acute kidney injury (AKI) is currently hot. It has recently been the subject of several excellent reviews(1-3) and a useful meta-analysis,(4) and we are hearing exhortations that this hunt should get high priority.(3,5) The ideal marker (or set of markers) should facilitate early identification, stratify risk, and contribute to informative diagnostic classification. Perhaps most importantly, a good marker should aid the testing of interventions to prevent development of AKI and improve management. So, there are very good reasons to get on with it!.
C1 NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
RP Briggs, JP (reprint author), NIH, Natl Ctr Complementary & Alternat Med, 9000 Rockville Pike,Bldg 31,Room 2B11, Bethesda, MD 20892 USA.
EM Briggsj@mail.nih.gov
RI Briggs, Josephine/B-9394-2009
OI Briggs, Josephine/0000-0003-0798-1190
FU Intramural NIH HHS
NR 15
TC 7
Z9 7
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
J9 KIDNEY INT
JI Kidney Int.
PD OCT
PY 2008
VL 74
IS 8
BP 987
EP 989
DI 10.1038/ki.2008.426
PG 4
WC Urology & Nephrology
SC Urology & Nephrology
GA 355AP
UT WOS:000259681300003
PM 18827797
ER
PT J
AU Doi, K
Leelahavanichkul, A
Hu, XZ
Sidransky, L
Zhou, H
Qin, Y
Eisner, C
Schnermann, J
Yuen, PST
Star, RA
AF Doi, Kent
Leelahavanichkul, Asada
Hu, Xuzhen
Sidransky, L.
Zhou, Hua
Qin, Yan
Eisner, Christoph
Schnermann, Juegen
Yuen, Peter S. T.
Star, Robert A.
TI Pre-existing renal disease promotes sepsis-induced acute kidney injury
and worsens outcome
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE acute-on-chronic; cecal ligation puncture; VEBGF; SFlt-1; chloroquine
ID ENDOTHELIAL GROWTH-FACTOR; MODULATES CYTOKINE EXPRESSION; HUMAN SEPTIC
SHOCK; VASCULAR-PERMEABILITY; HEMODIALYSIS-PATIENTS; ORGAN DYSFUNCTION;
IMPROVES SURVIVAL; HUMAN MONOCYTES; UNITED-STATES; BURN INJURY
AB While it is known that risk of death from sepsis is higher in patients with pre-existing chronic kidney disease its mechanism is unknown. To study this we established a two-stage mouse model where renal disease was first induced by folic acid injection followed by sub-lethal cecal ligation and puncture to induce sepsis. Septic mice with pre-existing renal disease had significantly higher mortality, serum creatinine, vascular permeability, plasma vascular endothelial growth factor (VEGF) levels, bacteremia, serum IL-10, splenocyte apoptosis and more severe septic shock when compared to septic mice without pre-existing disease. To evaluate the contribution of vascular and immunological dysfunction, we treated the folate-septic mice with soluble Flt-1 to bind VEGF and chloroquine to reduce splenocyte apoptosis. These treatments together resulted in a significant improvement in kidney injury, hemodynamics and survival. Our study shows that the sequential mouse model mimics human sepsis frequently complicated by pre-existing renal disease and might be useful in evaluating preventive and therapeutic strategies.
C1 [Doi, Kent; Leelahavanichkul, Asada; Hu, Xuzhen; Sidransky, L.; Zhou, Hua; Qin, Yan; Eisner, Christoph; Schnermann, Juegen; Yuen, Peter S. T.; Star, Robert A.] NIDDKD, NIH, Bethesda, MD 20892 USA.
RP Star, RA (reprint author), NIDDK, Renal Diagnost & Therapeut Unit, NIH, 10 Ctr Dr,Room 3N108, Bethesda, MD 20892 USA.
EM robert_star@nih.gov
RI Yuen, Peter/B-1954-2008
OI Yuen, Peter/0000-0001-9557-3909
FU Intramural Research Program of the NIH, NIDDK
FX This research was supported by the Intramural Research Program of the
NIH, NIDDK.
NR 54
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U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
J9 KIDNEY INT
JI Kidney Int.
PD OCT
PY 2008
VL 74
IS 8
BP 1017
EP 1025
DI 10.1038/ki.2008.346
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 355AP
UT WOS:000259681300010
PM 18633340
ER
PT J
AU Tansey, G
AF Tansey, Ginger
TI Approval spot-check
SO LAB ANIMAL
LA English
DT Editorial Material
C1 NEI, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Tansey, G (reprint author), NEI, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 0093-7355
J9 LAB ANIMAL
JI Lab Anim.
PD OCT
PY 2008
VL 37
IS 10
BP 446
EP 446
DI 10.1038/laban1008-446a
PG 1
WC Veterinary Sciences
SC Veterinary Sciences
GA 356YO
UT WOS:000259813700005
PM 18810260
ER
PT J
AU Thomas, LA
Labar, KS
AF Thomas, Laura A.
LaBar, Kevin S.
TI Fear relevancy, strategy use, and probabilistic learning of cue-outcome
associations
SO LEARNING & MEMORY
LA English
DT Article
ID MULTIPLE MEMORY-SYSTEMS; AMYGDALA MODULATION; EMOTIONAL AROUSAL; TASK;
DISTRACTION; AWARENESS; FEEDBACK; BRAIN; RISK
AB The goal of this study was to determine how the fear relevancy of outcomes during probabilistic classification learning affects behavior and strategy use. Novel variants of the "weather prediction" task were created, in which cue cards predicted either looming fearful or neutral outcomes in a between-groups design. Strategy use was examined by goodness-of-fit estimates of response patterns across trial blocks to mathematical models of simple, complex, and nonidentifiable strategies. Participants in the emotional condition who were fearful of the outcomes had greater skin conductance responses compared with controls and performed worse, used suboptimal strategies, and had less insight into the predictive cue features during initial learning. In contrast, nonfearful participants in the emotional condition used more optimal strategies than the other groups by the end of the two training days. Results have implications for understanding how individual differences in fear relevancy alter the impact of emotion on feedback-based learning.
C1 [Thomas, Laura A.; LaBar, Kevin S.] Duke Univ, Ctr Cognit Neurosci, Durham, NC 27708 USA.
[Thomas, Laura A.; LaBar, Kevin S.] Duke Univ, Dept Psychol & Neurosci, Durham, NC 27708 USA.
[Thomas, Laura A.] NIMH, Mood & Anxiety Program, Bethesda, MD 20892 USA.
RP Labar, KS (reprint author), Duke Univ, Ctr Cognit Neurosci, Durham, NC 27708 USA.
EM klabar@duke.edu
OI Thomas, Laura/0000-0002-4106-1358
FU NSF [0239614]; NIH [2 P01 NS041328]; NRSA [F31MH75327]
FX We thank Russ Poldrack, Adam Aron, Martijn Meeter, and David Lagnado for
assistance with experimental setup, design, and analysis. This work was
supported by NSF Career Award 0239614 (K. S. L.), NIH 2 P01 NS041328,
and an individual Predoctoral NRSA F31MH75327 (L. A. T.).
NR 38
TC 12
Z9 12
U1 0
U2 4
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1072-0502
J9 LEARN MEMORY
JI Learn. Mem.
PD OCT
PY 2008
VL 15
IS 10
BP 777
EP 784
DI 10.1101/lm.1048808
PG 8
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 366CT
UT WOS:000260458900006
PM 18832564
ER
PT J
AU Reynolds, HY
Rothgeb, A
Colombini-Hatch, S
Gail, DB
Kiley, JP
AF Reynolds, Herbert Y.
Rothgeb, Ann
Colombini-Hatch, Sandra
Gail, Dorothy B.
Kiley, James P.
TI The pipeline: Preparing and training pulmonary scientists for research
careers
SO LUNG
LA English
DT Editorial Material
DE physician-scientist; fellowship training; research support
ID INVESTIGATORS
AB New technologies have made this an opportune time to prepare and embark on an academic career in respiratory disease research. The pulmonary physician-scientist has a special advantage to take basic research findings to the patient's illness and impact medical care. But is there a sufficient work force emerging to capitalize on current research opportunities? The aim of this study was to analyze the present workforce of potential clinical investigators available by reviewing the mechanisms of training support as provided by the National Heart Lung and Blood Institute (NHLBI) and by the professional pulmonary societies, including their patient advocacy groups and pharmaceutical partners, and by discussing how support for research training might be improved for advanced clinical fellows. Of the approximately 500 fellows/year in a final training year in Pulmonary/Critical Care Medicine and related programs, about one third are involved mainly in supervised research and of whom about two thirds plan to continue fellowship training for an additional year or more (approximately 100-120 trainees). It seems especially important to encourage his particular group who are planning to extend fellowship for research training. Both the NHLBI and the professional pulmonary societies and their partners provide support for advanced fellowship trainees, but resources are limited. To insure that enough well-trained new clinical investigators will be available to conduct future pulmonary research, funding support and other career inducements should be discussed collectively by the NHLBI and the professional pulmonary societies for the purpose of optimizing support for advanced fellowship trainees.
C1 [Reynolds, Herbert Y.; Rothgeb, Ann; Colombini-Hatch, Sandra; Gail, Dorothy B.; Kiley, James P.] NHLBI, Div Lung Dis, Rockledge Ctr 2, Bethesda, MD 20892 USA.
[Reynolds, Herbert Y.; Rothgeb, Ann; Colombini-Hatch, Sandra; Gail, Dorothy B.; Kiley, James P.] NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Reynolds, HY (reprint author), NHLBI, Div Lung Dis, Rockledge Ctr 2, 6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM Reynoldh@nhlbi.nih.gov
NR 12
TC 7
Z9 7
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0341-2040
J9 LUNG
JI Lung
PD OCT
PY 2008
VL 186
IS 5
BP 279
EP 291
DI 10.1007/s00408-008-9100-z
PG 13
WC Respiratory System
SC Respiratory System
GA 350SB
UT WOS:000259372300001
PM 18633568
ER
PT J
AU Novozhilov, AS
AF Novozhilov, Artem S.
TI On the spread of epidemics in a closed heterogeneous population
SO MATHEMATICAL BIOSCIENCES
LA English
DT Article
DE SIR model; Heterogeneous populations; Transmission function; Distributed
susceptibility
ID NONLINEAR INCIDENCE RATES; TRANSMISSION DYNAMICS; EPIDEMIOLOGIC MODELS;
INFECTIOUS-DISEASE; HOST HETEROGENEITY; PATHOGEN; SUSCEPTIBILITY;
BEHAVIOR
AB Heterogeneity is an important property of any population experiencing a disease. Here we apply general methods of the theory of heterogeneous populations to the simplest mathematical models in epidemiology. In particular, an SIR (susceptible-infective-removed) model is formulated and analyzed when susceptibility to or infectivity of a particular disease is distributed. It is shown that a heterogeneous model can be reduced to a homogeneous model with a nonlinear transmission function, which is given in explicit form. The widely used power transmission function is deduced from the model with distributed susceptibility and infectivity with the initial gamma-distribution of the disease parameters. Therefore, a mechanistic derivation of the phenomenological model, which is believed to mimic reality with high accuracy, is provided. The equation for the final size of an epidemic for an arbitrary initial distribution of susceptibility is found. The implications of population heterogeneity are discussed, in particular, it is pointed out that usual moment-closure methods can lead to erroneous conclusions if applied for the study of the long-term behavior of the models. Published by Elsevier Inc.
C1 NCBI, NIH, Bethesda, MD 20894 USA.
RP Novozhilov, AS (reprint author), NCBI, NIH, 8600 Rockville Pike,Bldg 38A Room 8N811H, Bethesda, MD 20894 USA.
EM novozhil@ncbi.nlm.nih.gov
RI Novozhilov, Artem/D-7544-2012; Novozhilov, Artem/C-9248-2013
OI Novozhilov, Artem/0000-0001-5469-2557
FU NIH, National Library of Medicine
FX The author thanks Dr. A. Bratus' and Dr. G. Karev for insightful
discussions and helpful suggestions. The constructive comments from the
two anonymous reviewers are appreciated. The author's research is
supported by the Department of Health and Human Services intramural
program (NIH, National Library of Medicine).
NR 39
TC 17
Z9 17
U1 0
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0025-5564
EI 1879-3134
J9 MATH BIOSCI
JI Math. Biosci.
PD OCT
PY 2008
VL 215
IS 2
BP 177
EP 185
DI 10.1016/j.mbs.2008.07.010
PG 9
WC Biology; Mathematical & Computational Biology
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology
GA 368HI
UT WOS:000260611800007
PM 18722386
ER
PT J
AU Sander, M
Avlund, K
Lauritzen, M
Gottlieb, T
Halliwell, B
Stevnsner, T
Wewer, U
Bohr, VA
AF Sander, Miriam
Avlund, Kirsten
Lauritzen, Martin
Gottlieb, Tina
Halliwell, Barry
Stevnsner, Tinna
Wewer, Ulla
Bohr, Vilhelm A.
TI Aging-From molecules to populations
SO MECHANISMS OF AGEING AND DEVELOPMENT
LA English
DT Article; Proceedings Paper
CT Workshop on Aging-From Molecules to Populations 2008
CY MAY 12-14, 2008
CL Elsinore, DENMARK
SP Univ Copenhagen Fac Hlth Sci, Univ Aarhus, Danish Aging Res Ctr
DE Lifespan; Life course; Proteosome; Cognitive decline; Elite aging;
Alzheimer's disease
ID COGNITIVE DECLINE; OLDER WOMEN; RISK-FACTOR; METAANALYSIS; EXERCISE;
DEMENTIA
AB The mean age of the human population is steadily increasing in many areas around the globe, a phenomenon with large social, political, economic and biological/medical implications. Inevitably, this phenomenon is stimulating great interest in understanding and potentially modulating the process of human aging. To foster interactions and collaboration between diverse scientists interested in the biochemical, physiological, epidemiological and psychosocial aspects of aging, The University of Copenhagen Faculty of Health Sciences recently organized and co-sponsored a workshop entitled Aging-From Molecules to Populations. The following questions about human aging were discussed at the workshop: What is the limit of human life expectancy? What are the key indicators of human aging? What are the key drivers of human aging? Which genes have the greatest impact on human aging? How similar is aging-related cognitive decline to pathological cognitive decline associated with neurological disease? Are human progeriod diseases, characterized by premature aging, good models for "normal" human aging? Is delayed or "elite" aging informative about "normal" human aging? To what extent and by what mechanisms do early life environmental factors influence aging-associated physical and cognitive decline? To what extent and by what mechanism does the social environment influence life course outcomes? What physiological factors underlie the timing and extent of aging-associated physical and cognitive decline? How do cultural stereotypes and perceptions of aging influence the process and experience of aging? One of the primary outcomes of the workshop was a recognition that cross-disciplinary studies and "out-of-the-box" approaches, especially those that adopt an integrated life course perspective on human health status, are needed to expedite advances in aging research. This and other outcomes of the workshop are summarized and discussed in this report.
C1 [Bohr, Vilhelm A.] NIA, Dept Mol Gerontol, NIH, Bethesda, MD 20892 USA.
[Sander, Miriam] Page One Editorial Serv, Boulder, CO USA.
[Avlund, Kirsten] Univ Copenhagen, Dept Publ Hlth, Sect Social Med, DK-1168 Copenhagen, Denmark.
[Lauritzen, Martin] Univ Copenhagen, Fac Hlth Sci, Dept Neurosci & Pharmacol, DK-1168 Copenhagen, Denmark.
[Halliwell, Barry] Natl Univ Singapore, Singapore 117548, Singapore.
[Stevnsner, Tinna] Univ Aarhus, Danish Aging Res Ctr, DK-8000 Aarhus C, Denmark.
[Stevnsner, Tinna] Univ Aarhus, Danish Ctr Mol Gerontol, DK-8000 Aarhus C, Denmark.
RP Bohr, VA (reprint author), NIA, Dept Mol Gerontol, NIH, Bethesda, MD 20892 USA.
EM vbohr@nih.gov
RI Halliwell, Barry/C-8318-2009
FU Intramural NIH HHS [Z01 AG000727-16]
NR 16
TC 9
Z9 10
U1 0
U2 10
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0047-6374
J9 MECH AGEING DEV
JI Mech. Ageing Dev.
PD OCT
PY 2008
VL 129
IS 10
BP 614
EP 623
DI 10.1016/j.mad.2008.08.002
PG 10
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 379BF
UT WOS:000261368800007
PM 18789959
ER
PT J
AU Riey, GF
Warren, JL
Potosky, AL
Klabunde, CN
Harlan, LC
Osswald, MB
AF Riey, Gerald F.
Warren, Joan L.
Potosky, Arnold L.
Klabunde, Carrie N.
Harlan, Linda C.
Osswald, Michael B.
TI Comparison of Cancer Diagnosis and Treatment in Medicare Fee-for-Service
and Managed Care Plans
SO MEDICAL CARE
LA English
DT Article
DE managed care; cancer diagnosis; cancer treatment; Medicare
ID STAGE BREAST-CANCER; ACUTE MYOCARDIAL-INFARCTION; LOCALIZED
PROSTATE-CANCER; QUALITY-OF-LIFE; RADICAL PROSTATECTOMY;
COLORECTAL-CANCER; RADIATION-THERAPY; COLON-CANCER; HEALTH-CARE; HMO
SETTINGS
AB Objective: To compare the Medicare managed care(MC) and fee-for-service (FFS) sectors on stage at diagnosis and treatment patterns for prostate, female breast, and colorectal cancers, and no examine patterns across MC plans.
Data: Surveillance, Epidemiology, and End Results-Medicare linked data.
Methods: Among cases diagnosed at ages 65-79 between 1998 and 2002, we selected all MC enrollees (n = 42,467) and beneficiaries in FFS (n = 82,998) who resided in the same counties. MC and FFS samples were compared using logistic regression, adjusting for demographic, geographic and clinical covariates.
Results: The percentage of late stage cases was similar in MC and FFS for prostate and colorectal cancers; there were slightly fewer late stage breast cancer cases in MC after adjustment (7.3% vs. 8.5%, P < 0.001). Within MC, radical prostatectomy was performed less frequently for clinically localized prostate cancer (18.3% vs 22.4%, P < 0.0001), and 12 or more lymph nodes were examined less often for resected colon cancer cases (40.9% vs 43.0%, P < 0.05). Treatment patterns for early stage breast cancer were similar in MC and FFS. Analyses of treatment patterns at the individual plan level revealed significant variation among plans, as well as within the FFS sector, for all 3 types of cancer.
Conclusions: On average, there are few significant differences in cancer diagnosis and treatment MC and FFS. Such comparisons, however mask the wide variability among MC plans, as well as FFS providers. Observed variation in patterns of care may be related to patient selection, but can potentially lead to outcome differences. These findings support the need for quality measures toe evaluate plan practices and performance.
C1 [Riey, Gerald F.] Ctr Medicare, Off Res Dev & Informat, Baltimore, MD 21244 USA.
[Riey, Gerald F.] Ctr Medicaid Serv, Baltimore, MD 21244 USA.
[Warren, Joan L.; Potosky, Arnold L.; Klabunde, Carrie N.; Harlan, Linda C.] NCI, Appl Res Program, Bethesda, MD 20892 USA.
[Osswald, Michael B.] USAF, San Antonio Mil Med Ctr, Dept Med, Lackland AFB, TX USA.
RP Riey, GF (reprint author), Ctr Medicare, Off Res Dev & Informat, 7500 Secur Blvd,Mail Stop C3-21-27, Baltimore, MD 21244 USA.
EM Gerald.riley@cms.hhs.gov
NR 50
TC 0
Z9 0
U1 2
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD OCT
PY 2008
VL 46
IS 10
BP 1108
EP 1115
PG 8
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 358IF
UT WOS:000259909700018
ER
PT J
AU Lenfant, C
AF Lenfant, Claude
TI Low birth weight and blood pressure
SO METABOLISM-CLINICAL AND EXPERIMENTAL
LA English
DT Article
ID ACTIVATED RECEPTOR-GAMMA-2 GENE; ADULT HYPERTENSION; FETAL ORIGINS;
ANTIHYPERTENSIVE MEDICATION; SIZE; DISEASE; LIFE; CHILDHOOD;
ASSOCIATION; HYPOTHESIS
AB Evidence supporting the association of normal and pathologically elevated blood pressure with low birth weight is presented and discussed in this article because of the overwhelming global prevalence of hypertension and its impact on individuals and nations. The findings provide strong impetus for the medical and public health communities to consider the concept of the "developmental origins of health and disease" in developing approaches to address the growing burden of hypertension worldwide. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Lenfant, Claude] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Lenfant, C (reprint author), POB 65278, Vancouver, WA 98665 USA.
EM lenfantc@prodigy.net
NR 29
TC 14
Z9 16
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0026-0495
EI 1532-8600
J9 METABOLISM
JI Metab.-Clin. Exp.
PD OCT
PY 2008
VL 57
IS 10
SU 2
BP S32
EP S35
DI 10.1016/j.metabol.2008.07.013
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 364ZI
UT WOS:000260374200008
PM 18803963
ER
PT J
AU Card, DAG
Hebbar, PB
Li, LP
Trotter, KW
Komatsu, Y
Mishina, Y
Archer, TK
AF Card, Deborah A. Greer
Hebbar, Pratibha B.
Li, Leping
Trotter, Kevin W.
Komatsu, Yoshihiro
Mishina, Yuji
Archer, Trevor K.
TI Oct4/Sox2-regulated miR-302 targets cyclin D1 in human embryonic stem
cells
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID RNA-POLYMERASE-II; TRANSCRIPTIONAL REGULATION; PROTEIN EXPRESSION;
MICRORNA TARGETS; MESSENGER-RNAS; OCT4; SOX2; GENE; ZEBRAFISH; COMPLEX
AB Oct4 and Sox2 are transcription factors required for pluripotency during early embryogenesis and for the maintenance of embryonic stem cell (ESC) identity. Functional mechanisms contributing to pluripotency are expected to be associated with genes transcriptionally activated by these factors. Here, we show that Oct4 and Sox2 bind to a conserved promoter region of miR-302, a cluster of eight microRNAs expressed specifically in ESCs and pluripotent cells. The expression of miR-302a is dependent on Oct4/Sox2 in human ESCs (hESCs), and miR-302a is expressed at the same developmental stages and in the same tissues as Oct4 during embryogenesis. miR-302a is predicted to target many cell cycle regulators, and the expression of miR-302a in primary and transformed cell lines promotes an increase in S-phase and a decrease in G(1)-phase cells, reminiscent of an ESC-like cell cycle profile. Correspondingly, the inhibition of miR-302 causes hESCs to accumulate in G(1) phase. Moreover, we show that miR-302a represses the productive translation of an important G(1) regulator, cyclin D1, in hESCs. The transcriptional activation of miR-302 and the translational repression of its targets, such as cyclin D1, may provide a link between Oct4/Sox2 and cell cycle regulation in pluripotent cells.
C1 [Card, Deborah A. Greer; Hebbar, Pratibha B.; Trotter, Kevin W.; Archer, Trevor K.] Natl Inst Environm Hlth Sci, Mol Carcinogenesis Lab, Chromatin & Gene Express Sect, Res Triangle Pk, NC 27709 USA.
[Li, Leping] Natl Inst Environm Hlth Sci, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Komatsu, Yoshihiro; Mishina, Yuji] Natl Inst Environm Hlth Sci, Mol Dev Biol Grp, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC 27709 USA.
RP Archer, TK (reprint author), Natl Inst Environm Hlth Sci, Mol Carcinogenesis Lab, Chromatin & Gene Express Sect, 111 Alexander Dr,MD D4-01,POB 12233, Res Triangle Pk, NC 27709 USA.
EM archer1@niehs.nih.gov
FU National Institute of Environmental Health Sciences, NIH [Z01
ES071006-09]
FX We thank Lois Annab for maintenance of MEFs; Paul Wade, Sayura Aoyagi,
and Jeff Card for helpful discussion; Gina Goulding and Trisha Castriano
for assistance with mouse embryology; Ajeet Singh for mouse embryonic
samples; Julie Foley for assistance with immunohistochemistry; Grace
Kissling for assistance with statistical analysis; and Carl Bortner and
Maria Sifre for assistance with flow cytometry.; This research was
supported by the Intramural Research Program of the National Institute
of Environmental Health Sciences, NIH, project number Z01 ES071006-09.
NR 42
TC 286
Z9 314
U1 6
U2 28
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD OCT
PY 2008
VL 28
IS 20
BP 6426
EP 6438
DI 10.1128/MCB.00359-08
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 354JB
UT WOS:000259634800022
PM 18710938
ER
PT J
AU Garcia-Regalado, A
Guzman-Hernandez, ML
Ramirez-Rangel, I
Robles-Molina, E
Balla, T
Vazquez-Prado, J
Reyes-Cruz, G
AF Garcia-Regalado, Alejandro
Luisa Guzman-Hernandez, Maria
Ramirez-Rangel, Iliana
Robles-Molina, Evelyn
Balla, Tamas
Vazquez-Prado, Jose
Reyes-Cruz, Guadalupe
TI G Protein-coupled Receptor-promoted Trafficking of G beta(1)gamma(2)
Leads to AKT Activation at Endosomes via a Mechanism Mediated by G
beta(1)gamma(2)-Rab11a Interaction
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID BETA-GAMMA-SUBUNITS; HETEROTRIMERIC G-PROTEINS; PLASMA-MEMBRANE; RAB
GTPASES; BETA(2)-ADRENERGIC RECEPTOR; INTRACELLULAR TRAFFICKING;
PHOSPHOINOSITIDE 3-KINASE; 7-TRANSMEMBRANE RECEPTORS;
SIGNAL-TRANSDUCTION; ENDOCYTIC PATHWAY
AB G-protein coupled receptors activate heterotrimeric G proteins at the plasma membrane in which most of their effectors are intrinsically located or transiently associated as the external signal is being transduced. This paradigm has been extended to the intracellular compartments by studies in yeast showing that trafficking of G alpha activates phosphatidylinositol 3-kinase (PI3K) at endosomal compartments, suggesting that vesicle trafficking regulates potential actions of G alpha and possibly G beta gamma at the level of endosomes. Here, we show that G beta gamma interacts with Rab11a and that the two proteins colocalize at early and recycling endosomes in response to activation of lysophosphatidic acid (LPA) receptors. This agonist-dependent association of G beta gamma to Rab11a-positive endosomes contributes to the recruitment of PI3K and phosphorylation of AKT at this intracellular compartment. These events are sensitive to the expression of a dominant-negative Rab11a mutant or treatment with wortmannin, suggesting that Rab11a-dependent G beta gamma trafficking promotes the activation of the PI3K/AKT signaling pathway associated with endosomal compartments. In addition, RNA interference-mediated Rab11a depletion, or expression of a dominant-negative Rab11a mutant attenuated LPA-dependent cell survival and proliferation, suggesting that endosomal activation of the PI3K/AKT signaling pathway in response to G beta gamma trafficking, via its interaction with Rab11, is a relevant step in the mechanism controlling these fundamental events.
C1 [Garcia-Regalado, Alejandro; Reyes-Cruz, Guadalupe] Inst Politecn Nacl, Ctr Invest & Estudios Avanzados, Dept Cell Biol, Mexico City 07000, DF, Mexico.
[Luisa Guzman-Hernandez, Maria; Ramirez-Rangel, Iliana; Robles-Molina, Evelyn; Vazquez-Prado, Jose] Inst Politecn Nacl, Ctr Invest & Estudios Avanzados, Dept Pharmacol, Mexico City 07000, DF, Mexico.
[Balla, Tamas] NICHHD, Sect Mol Signal Transduct, NIH, Bethesda, MD 20892 USA.
RP Reyes-Cruz, G (reprint author), Inst Politecn Nacl, Ctr Invest & Estudios Avanzados, Dept Cell Biol, Mexico City 07000, DF, Mexico.
EM guadaluper@cell.cinvestav.mx
RI VAZQUEZ-PRADO, JOSE/C-1630-2017;
OI Balla, Tamas/0000-0002-9077-3335
FU Consejo Nacional de Ciencia y Tecnologia (CONACyT) [45957, 61127];
Eunice Kennedy Shriver National Institute of Child Health; Human
Development, National Institutes of Health
FX We thank Margarita Valadez Sanchez for expert technical assistance, Omar
Hernandez Garcia and Jaime Estrada Trejo for assistance, and Blanca E.
Reyes for confocal microscopy assistance. This work was supported by
Consejo Nacional de Ciencia y Tecnologia (CONACyT) grants 45957 (to G.
R. C.) and 61127 (to J. V. P.) and National Institutes of Health grant
R01-TW006664 ( to J. V. P). A. G.- R., M. L. G.- H., I. R.- R., and E.
R.- M. are graduate students supported by fellowships from CONACyT. The
research of T. B. was supported in part by the Intramural Research
Program of the Eunice Kennedy Shriver National Institute of Child Health
and Human Development, National Institutes of Health.
NR 76
TC 36
Z9 37
U1 1
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD OCT
PY 2008
VL 19
IS 10
BP 4188
EP 4200
DI 10.1091/mbc.E07-10-1089
PG 13
WC Cell Biology
SC Cell Biology
GA 366HU
UT WOS:000260472200016
PM 18701709
ER
PT J
AU Inoue, H
Ha, VL
Prekeris, R
Randazzo, PA
AF Inoue, Hiroki
Ha, Vi Luan
Prekeris, Rytis
Randazzo, Paul A.
TI Arf GTPase-activating Protein ASAP1 Interacts with Rab11 Effector FIP3
and Regulates Pericentrosomal Localization of Transferrin
Receptor-positive Recycling Endosome
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID CLATHRIN-MEDIATED ENDOCYTOSIS; ADP-RIBOSYLATION FACTORS; ACTIN
CYTOSKELETON; STRUCTURAL BASIS; NUCLEAR-FALLOUT; CELL-MIGRATION;
BAR-DOMAIN; MEMBRANE CURVATURE; CLEAVAGE FURROW; FOCAL ADHESIONS
AB ADP-ribosylation factors (Arfs) and Arf GTPase-activating proteins (GAPs) are key regulators of membrane trafficking and the actin cytoskeleton. The Arf GAP ASAP1 contains an N-terminal BAR domain, which can induce membrane tubulation. Here, we report that the BAR domain of ASAP1 can also function as a protein binding site. Two-hybrid screening identified FIP3, which is a putative Arf6- and Rab11-effector, as a candidate ASAP1 BAR domain-binding protein. Both coimmunoprecipitation and in vitro pulldown assays confirmed that ASAP1 directly binds to FIP3 through its BAR domain. ASAP1 formed a ternary complex with Rab11 through FIP3. FIP3 binding to the BAR domain stimulated ASAP1 GAP activity against Arf1, but not Arf6. ASAP1 colocalized with FIP3 in the pericentrosomal endocytic recycling compartment. Depletion of ASAP1 or FIP3 by small interfering RNA changed the localization of transferrin receptor, which is a marker of the recycling endosome, in HeLa cells. The depletion also altered the trafficking of endocytosed transferrin. These results support the conclusion that ASAP1, like FIP3, functions as a component of the endocytic recycling compartment.
C1 [Inoue, Hiroki; Ha, Vi Luan; Randazzo, Paul A.] NCI, Cellular & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Prekeris, Rytis] Univ Colorado, Hlth Sci Ctr, Sch Med, Dept Cellular & Dev Biol, Denver, CO 80262 USA.
RP Randazzo, PA (reprint author), NCI, Cellular & Mol Biol Lab, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM Randazzo@helix.nih.gov
FU National Cancer Institute, Department of Health and Human Services
FX We thank Drs. Gwyn W. Gould (University of Glasgow, Scotland), Julie G.
Donaldson (National Heart, Lung, and Blood Institute, Bethesda, MD),
Roberto Weigert (National Institute of Dental and Craniofacial Research,
Bethesda, MD), and Yoshiyuki Wakabayashi (National Institute of Child
Health and Human Development, Bethesda, MD) for reagents. We also thank
Drs. Susan Garfield and Valarie Barr (National Cancer Institute,
Bethesda, MD) for technical assistance with confocal microscopy. This
work was supported by the Intramural Research Program of the National
Cancer Institute, Department of Health and Human Services.
NR 62
TC 35
Z9 37
U1 1
U2 4
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD OCT
PY 2008
VL 19
IS 10
BP 4224
EP 4237
DI 10.1091/mbc.E08-03-0290
PG 14
WC Cell Biology
SC Cell Biology
GA 366HU
UT WOS:000260472200019
PM 18685082
ER
PT J
AU Federovitch, CM
Jones, YZ
Tong, AH
Boone, C
Prinz, WA
Hampton, RY
AF Federovitch, Christine M.
Jones, Ying Z.
Tong, Amy H.
Boone, Charles
Prinz, William A.
Hampton, Randolph Y.
TI Genetic and Structural Analysis of Hmg2p-induced Endoplasmic Reticulum
Remodeling in Saccharomyces cerevisiae
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID HMG-COA REDUCTASE; 3-HYDROXY-3-METHYLGLUTARYL-COENZYME-A REDUCTASE;
PHOSPHATIDYLSERINE DECARBOXYLASE; STEROL-METABOLISM; DELETION MUTANTS;
YEAST; ER; DEGRADATION; PROTEIN; CELLS
AB The endoplasmic reticulum (ER) is highly plastic, and increased expression of distinct single ER-resident membrane proteins, such as HMG-CoA reductase (HMGR), can induce a dramatic restructuring of ER membranes into highly organized arrays. Studies on the ER-remodeling behavior of the two yeast HMGR isozymes, Hmg1p and Hmg2p, suggest that they could be mechanistically distinct. We examined the features of Hmg2p required to generate its characteristic structures, and we found that the molecular requirements are similar to those of Hmg1p. However, the structures generated by Hmg1p and Hmg2p have distinct cell biological features determined by the transmembrane regions of the proteins. In parallel, we conducted a genetic screen to identify HER genes (required for Hmg2p-induced ER Remodeling), further confirming that the mechanisms of membrane reorganization by these two proteins are distinct because most of the HER genes were required for Hmg2p but not Hmg1p-induced ER remodeling. One of the HER genes identified was PSD1, which encodes the phospholipid biosynthetic enzyme phosphatidylserine decarboxylase. This direct connection to phospholipid biosynthesis prompted a more detailed examination of the effects of Hmg2p on phospholipid mutants and composition. Our analysis revealed that overexpression of Hmg2p caused significant and specific growth defects in nulls of the methylation pathway for phosphatidylcholine biosynthesis that includes the Psd1p enzyme. Furthermore, increased expression of Hmg2p altered the composition of cellular phospholipids in a manner that implied a role for PSD1. These phospholipid effects, unlike Hmg2p-induced ER remodeling, required the enzymatic activity of Hmg2p. Together, our results indicate that, although related, Hmg2p- and Hmg1p-induced ER remodeling are mechanistically distinct.
C1 [Federovitch, Christine M.; Hampton, Randolph Y.] Univ Calif San Diego, UCSD Div Biol Sci, Sect Cell & Dev Biol, La Jolla, CA 92093 USA.
[Jones, Ying Z.] Univ Calif San Diego, Dept Neurosci, Natl Ctr Microscopy & Imaging Res, La Jolla, CA 92093 USA.
[Tong, Amy H.; Boone, Charles] Univ Toronto, Banting & Best Dept Med Res, Toronto, ON M5G 1L6, Canada.
[Prinz, William A.] NIDDK, Lab Cell Biochem & Biol, NIH, US Dept HHS, Bethesda, MD 20892 USA.
RP Hampton, RY (reprint author), Univ Calif San Diego, UCSD Div Biol Sci, Sect Cell & Dev Biol, La Jolla, CA 92093 USA.
EM rhampton@ucsd.edu
FU National Institutes of Health [5 R01 DK051996-15, 5T32GM008666]
FX We thank Scott Emr for use of the DeltaVision microscope, Gentry Patrick
for use of the Leica DM6000 microscope, and National Center for
Microscopy and Imaging Research at UCSD for use of the JEOL 1200
microscope. Plasmid pIU2589 was a kind gift from Martin Bard (Indiana
University-Purdue University Indianapolis, Indianapolis, IN). Mark Rose
(Princeton University, Princeton, NJ) provided anti-Kar2p antibody. We
thank Dennis Voelker (University of Colorado Health Sciences Center,
Denver, CO) for insightful discussions and the rescue plasmid
YCp50-PSD1. CMF wishes to thank Matthew Kinseth, Alicia Bicknell,
Danielle Huffman, and Renee Garza for many scientific discussions
regarding this work. RYH wishes to thank the Hampton laboratory for
patience, flexibility, and independent spirit during the past
(sabbatical) year. These studies were supported by National Institutes
of Health grant 5 R01 DK051996-15 (to R.Y.H.). C. M. F. was a trainee
under the National Institutes of Health genetic training grant
5T32GM008666.
NR 50
TC 11
Z9 13
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD OCT
PY 2008
VL 19
IS 10
BP 4506
EP 4520
DI 10.1091/mbc.E07-11-1188
PG 15
WC Cell Biology
SC Cell Biology
GA 366HU
UT WOS:000260472200043
PM 18667535
ER
PT J
AU Lorenzi, PL
Llamas, J
Gunsior, M
Ozbun, L
Reinhold, WC
Varma, S
Ji, H
Kim, H
Hutchinson, AA
Kohn, EC
Goldsmith, PK
Birrer, MJ
Weinstein, JN
AF Lorenzi, Philip L.
Llamas, Jenny
Gunsior, Michele
Ozbun, Laurent
Reinhold, William C.
Varma, Sudhir
Ji, Helen
Kim, Hijoo
Hutchinson, Amy A.
Kohn, Elise C.
Goldsmith, Paul K.
Birrer, Michael J.
Weinstein, John N.
TI Asparagine synthetase is a predictive biomarker of L-asparaginase
activity in ovarian cancer cell lines
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID GENE-EXPRESSION; LUNG-CANCER; RESISTANCE; LEUKEMIA
AB We recently used RNA interference to show that a negative correlation Of L-asparaginase (L-ASP) chemotherapeutic activity with asparagine synthetase (ASNS) expression in the ovarian subset of the NCI-60 cell line panel is causal. To determine whether that relationship would be sustained in a larger, more diverse set of ovarian cell lines, we have now measured ASNS mRNA expression using microarrays and a branched-DNA RNA assay, ASNS protein expression using an electrochemiluminescent immunoassay, and L-ASP activity using an MTS assay on 19 human ovarian cancer cell lines. Contrary to our previous findings, L-ASP activity was only weakly correlated with ASNS mRNA expression; Pearson's correlation coefficients were r = -0.21 for microarray data and r = -0.39 for the branched-DNA RNA assay, with just the latter being marginally statistically significant (P = 0.047, one-tailed). ASNS protein expression measured by liquid-phase immunoassay exhibited a much stronger correlation (r = -0.65; P = 0.0014, one-tailed). We conclude that ASNS protein expression measured by immunoassay is a strong univariate predictor Of L-ASP activity in ovarian cancer cell lines. These findings provide rationale for evaluation of ASNS protein expression as a predictive biomarker of clinical L-ASP activity in ovarian cancer. [Mol Cancer Ther 2008;7(10):3123-8]
C1 [Lorenzi, Philip L.; Llamas, Jenny; Reinhold, William C.; Varma, Sudhir; Ji, Helen; Kim, Hijoo; Weinstein, John N.] NCI, Genom & Bioinformat Grp, Mol Pharmacol Lab, NIH, Bethesda, MD 20892 USA.
[Gunsior, Michele; Goldsmith, Paul K.] NCI, Antibody & Prot Purificat Unit, NIH, Bethesda, MD 20892 USA.
[Ozbun, Laurent; Birrer, Michael J.] NCI, Cell & Canc Biol Branch, NIH, Bethesda, MD 20892 USA.
[Kohn, Elise C.] NCI, Mol Signalling Sect, Med Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Hutchinson, Amy A.] NCI, Core Genotyping Facil, Div Canc Epidemiol & Genet, Adv Technol Program,SAIC Frederick, Frederick, MD 21701 USA.
RP Weinstein, JN (reprint author), MD Anderson Canc Ctr, Dept Bioinformat & Computat Biol, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM jweinste@mdanderson.org
RI Varma, Sudhir/N-8763-2014; Mendez, Pedro /J-8955-2016
OI Varma, Sudhir/0000-0002-4096-4782; Mendez, Pedro /0000-0001-6713-7907
FU NIH; National Cancer Institute; Center for Cancer Research
[N01-CO-12400]; National Institute of General Medical Sciences; NIH
Pharmacology Research Associate Fellowship
FX Grant support: Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research under contract N01-CO-12400.
National Institute of General Medical Sciences, NIH Pharmacology
Research Associate Fellowship (P.L. Lorenzi).
NR 12
TC 44
Z9 45
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD OCT
PY 2008
VL 7
IS 10
BP 3123
EP 3128
DI 10.1158/1535-7163.MCT-08-0589
PG 6
WC Oncology
SC Oncology
GA 362MO
UT WOS:000260202000001
PM 18852115
ER
PT J
AU Saunders, LP
Ouellette, A
Bandle, R
Chang, WC
Zhou, HW
Misra, RN
De La Cruz, EM
Braddock, DT
AF Saunders, Lauren P.
Ouellette, Amy
Bandle, Russ
Chang, William Chozen
Zhou, Hongwen
Misra, Raj N.
De La Cruz, Enrique M.
Braddock, Demetrios T.
TI Identification of small-molecule inhibitors of autotaxin that inhibit
melanoma cell migration and invasion
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID OVARIAN-CANCER PATIENTS; SECRETED LYSOPHOSPHOLIPASE-D; LYSOPHOSPHATIDIC
ACID; NUCLEOTIDE PHOSPHODIESTERASE; GLIOBLASTOMA-MULTIFORME; ASCITIC
FLUID; EXPRESSION; MOTILITY; GROWTH; PROTEIN
AB Autotaxin (ATX) is a prometastatic enzyme initially isolated from the conditioned medium of human melanoma cells that stimulates a myriad of biological activities, including angiogenesis and the promotion of cell growth, survival, and differentiation through the production of lysophosphatidic acid (LPA). ATX increases the aggressiveness and invasiveness of transformed cells, and ATX levels directly correlate with tumor stage and grade in several human malignancies. To study the role of ATX in the pathogenesis of malignant melanoma, we developed antibodies and small-molecule inhibitors against recombinant human protein. Immunohistochemistry of paraffin-embedded human tissue shows that ATX levels are markedly increased in human primary and metastatic melanoma relative to benign nevi. Chemical screens identified several small-molecule inhibitors with binding constants ranging from nanomolar to low micromolar. Cell migration and invasion assays with melanoma cell lines show that ATX markedly stimulates melanoma cell migration and invasion, an effect suppressed by ATX inhibitors. The migratory phenotype can be rescued by the addition of the enzymatic product of ATX, LPA, confirming that the observed inhibition is linked to suppression of LPA production by ATX. Chemical analogues of the inhibitors show structure-activity relationships important for ATX inhibition and indicate pathways for their optimization. These studies suggest that ATX is an approachable molecular target for the rational design of chemotherapeutic agents directed against malignant melanoma. [Mol Cancer Ther 2008;7(10):3352-62]
C1 [Saunders, Lauren P.; De La Cruz, Enrique M.] Yale Univ, Dept Mol Biophys & Biochem, New Haven, CT 06520 USA.
[Ouellette, Amy; Chang, William Chozen; Zhou, Hongwen; Braddock, Demetrios T.] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA.
[Bandle, Russ] NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Misra, Raj N.] NCI, Dev Therapeut Program, Bethesda, MD 20892 USA.
RP De La Cruz, EM (reprint author), Yale Univ, Dept Mol Biophys & Biochem, POB 208114, New Haven, CT 06520 USA.
EM enrique.delacruz@yale.edu; demetrios.braddock@yale.edu
FU American Cancer Society [RSG-0-222-01]; Argall and Anna Hull Cancer
Research; NIH [GM071688, GM 07223]; National Science Foundation
[MCB-0546353]; American Heart Association [0655849T]
FX Grant support: American Cancer Society grant RSG-0-222-01 and Argall and
Anna Hull Cancer Research fund (D.T. Braddock); NIH grant GM071688,
National Science Foundation grant MCB-0546353, and American Heart
Association grant 0655849T (E.M. De La Cruz); and NIH Predoctoral
Training Program grant GM 07223 (L.P. Saunders).
NR 46
TC 49
Z9 49
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD OCT
PY 2008
VL 7
IS 10
BP 3352
EP 3362
DI 10.1158/1535-7163.MCT-08-0463
PG 11
WC Oncology
SC Oncology
GA 362MO
UT WOS:000260202000024
PM 18852138
ER
PT J
AU VanMeter, AJ
Rodriguez, AS
Bowman, ED
Jen, J
Harris, CC
Deng, J
Calvert, VS
Silvestri, A
Fredolini, C
Chandhoke, V
Petricoin, EF
Liotta, LA
Espina, V
AF VanMeter, Amy J.
Rodriguez, Adrianna S.
Bowman, Elise D.
Jen, Jin
Harris, Curtis C.
Deng, Jianghong
Calvert, Valerie S.
Silvestri, Alessandra
Fredolini, Claudia
Chandhoke, Vikas
Petricoin, Emanuel F.
Liotta, Lance A.
Espina, Virginia
TI Laser Capture Microdissection and Protein Microarray Analysis of Human
Non-small Cell Lung Cancer DIFFERENTIAL EPIDERMAL GROWTH FACTOR RECEPTOR
(EGFR) PHOSPHORYLATION EVENTS ASSOCIATED WITH MUTATED EGFR COMPARED WITH
WILD TYPE
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID TYROSINE KINASE DOMAIN; DOWN-REGULATION; GENE-MUTATIONS;
GEFITINIB-RESISTANCE; APOPTOTIC PATHWAYS; PROTEOMIC ANALYSIS; CBL
ASSOCIATION; ACTIVATION; SURVIVAL; EXPRESSION
AB Little is known about lung carcinoma epidermal growth factor (EGF) kinase pathway signaling within the context of the tissue microenvironment. We quantitatively profiled the phosphorylation and abundance of signal pathway proteins relevant to the EGF receptor within laser capture microdissected untreated, human non-small cell lung cancer (NSCLC) (n = 25) of known epidermal growth factor receptor ( EGFR) tyrosine kinase domain mutation status. We measured six phosphorylation sites on EGFR to evaluate whether EGFR mutation status in vivo was associated with the coordinated phosphorylation of specific multiple phosphorylation sites on the EGFR and downstream proteins. Reverse phase protein array quantitation of NSCLC revealed simultaneous increased phosphorylation of EGFR residues Tyr-1148 (p < 0.044) and Tyr-1068 (p < 0.026) and decreased phosphorylation of EGFR Tyr-1045 (p < 0.002), HER2 Tyr-1248 (p < 0.015), IRS-1 Ser-612 (p < 0.001), and SMAD Ser-465/467 (p < 0.011) across all classes of mutated EGFR patient samples compared with wild type. To explore which subset of correlations was influenced by ligand induction versus an intrinsic phenotype of the EGFR mutants, we profiled the time course of 115 cellular signal proteins for EGF ligand-stimulated ( three dosages) NSCLC mutant and wild type cultured cell lines. EGFR mutant cell lines (H1975 L858R) displayed a pattern of EGFR Tyr-1045 and HER2 Tyr-1248 phosphorylation similar to that found in tissue. Persistence of phosphorylation for AKT Ser-473 following ligand stimulation was found for the mutant. These data suggest that a higher proportion of the EGFR mutant carcinoma cells may exhibit activation of the phosphatidylinositol 3-kinase/protein kinase B (AKT)/mammalian target of rapamycin (MTOR) pathway through Tyr-1148 and Tyr- 1068 and suppression of IRS-1 Ser-612, altered heterodimerization with ERBB2, reduced response to transforming growth factor beta suppression, and reduced ubiquitination/degradation of the EGFR through EGFR Tyr-1045, thus providing a survival advantage. This is the first comparison of multiple, site-specific phosphoproteins with the EGFR tyrosine kinase domain mutation status in vivo. Molecular & Cellular Proteomics 7: 1902-1924, 2008.
C1 [VanMeter, Amy J.; Deng, Jianghong; Calvert, Valerie S.; Silvestri, Alessandra; Fredolini, Claudia; Chandhoke, Vikas; Petricoin, Emanuel F.; Liotta, Lance A.; Espina, Virginia] George Mason Univ, Ctr Appl Prote & Mol Med, Manassas, VA 20110 USA.
[Rodriguez, Adrianna S.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Bowman, Elise D.; Harris, Curtis C.] NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Jen, Jin] NCI, Lab Populat Genet, NIH, Bethesda, MD 20892 USA.
[Silvestri, Alessandra] NCI, Ctr Riferimento Oncol, Ist Ricovero & Cura Carattere Sci, Pordenone Aviano, Italy.
[Fredolini, Claudia] Univ Turin, San Giovanni Battista Hosp, Ctr Expt Res & Med Studies, Turin, Italy.
RP Espina, V (reprint author), George Mason Univ, Ctr Appl Prote & Mol Med, 10900 Univ Blvd,MS 1A9, Manassas, VA 20110 USA.
EM vespina@gmu.edu
FU National Institutes of Health; George Mason University
FX This work was supported, in whole or in part, by a National Institutes
of Health Grant from the intramural program of the NCI. This work was
also supported in part by George Mason University. The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked "advertisement" in
accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
NR 87
TC 77
Z9 79
U1 0
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD OCT
PY 2008
VL 7
IS 10
BP 1902
EP 1924
DI 10.1074/mcp.M800204-MCP200
PG 23
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 365RE
UT WOS:000260424700011
PM 18687633
ER
PT J
AU Schrohl, AS
Wurtz, S
Kohn, E
Banks, RE
Nielsen, HJ
Sweep, FCGJ
Brunner, N
AF Schrohl, Anne-Sofie
Wurtz, Sidse
Kohn, Elise
Banks, Rosamonde E.
Nielsen, Hans Jorgen
Sweep, Fred C. G. J.
Brunner, Nils
TI Banking of Biological Fluids for Studies of Disease-associated Protein
Biomarkers
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Review
ID BLOOD-TRANSFUSION COMPONENTS; PLASMA TISSUE INHIBITOR; PRIMARY
COLORECTAL-CANCER; ENDOTHELIAL GROWTH-FACTOR; C-REACTIVE PROTEIN;
METALLOPROTEINASES-1; STORAGE; MARKER; VEGF; VARIABILITY
AB With the increasing demand of providing personalized medicine the need for biobanking of biological material from individual patients has increased. Such samples are essential for molecular research aimed at characterizing diseases at several levels ranging from epidemiology and diagnostic and prognostic classification to prediction of response to therapy. Clinically validated biomarkers may provide information to be used for diagnosis, screening, evaluation of risk/predisposition, assessment of prognosis, monitoring (recurrence of disease), and prediction of response to treatment and as a surrogate response marker. Many types of biological fluids or tissues can be collected and stored in biorepositories. Samples of blood can be further processed into plasma and serum, and tissue pieces can be either frozen or fixed in formalin and then embedded into paraffin. The present review focuses on biological fluids, especially serum and plasma, intended for study of protein biomarkers. In biomarker studies the process from the decision to take a sample from an individual to the moment the sample is safely placed in the biobank consists of several phases including collection of samples, transport of the samples, and handling and storage of samples. Critical points in each step important for high quality biomarker studies are described in this review. Failure to develop and adhere to robust standardized protocols may have significant consequences as the quality of the material stored in the biobank as well as conclusions and clinical recommendations based on analysis of such material may be severely affected. Molecular & Cellular Proteomics 7: 2061-2066, 2008.
C1 [Schrohl, Anne-Sofie; Wurtz, Sidse; Brunner, Nils] Univ Copenhagen, Fac Life Sci, Dept Vet Pathobiol, DK-1870 Frederiksberg C, Denmark.
[Kohn, Elise] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Banks, Rosamonde E.] St James Univ Hosp, Canc Res UK Clin Ctr, Leeds YO23 2QJE, W Yorkshire, England.
[Nielsen, Hans Jorgen] Hvidovre Univ Hosp, Dept Surg Gastroenterol, DK-2650 Hvidovre, Denmark.
[Sweep, Fred C. G. J.] Radboud Univ Nijmegen, Med Ctr, Dept Chem Endocrinol, NL-6500 Nijmegen, Netherlands.
RP Brunner, N (reprint author), Univ Copenhagen, Fac Life Sci, Dept Vet Pathobiol, Ridebanevej 9, DK-1870 Frederiksberg C, Denmark.
EM nbr@life.ku.dk
RI Sweep, C.G.J./H-8096-2014;
OI Banks, Rosamonde/0000-0002-0042-8715
NR 26
TC 60
Z9 62
U1 0
U2 8
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD OCT
PY 2008
VL 7
IS 10
BP 2061
EP 2066
DI 10.1074/mcp.R800010-MCP200
PG 6
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 365RE
UT WOS:000260424700022
PM 18676364
ER
PT J
AU Trigo, TC
Freitas, TRO
Kunzler, G
Cardoso, L
Silva, JCR
Johnson, WE
O'Brien, SJ
Bonatto, SL
Eizirik, E
AF Trigo, T. C.
Freitas, T. R. O.
Kunzler, G.
Cardoso, L.
Silva, J. C. R.
Johnson, W. E.
O'Brien, S. J.
Bonatto, S. L.
Eizirik, E.
TI Inter-species hybridization among Neotropical cats of the genus
Leopardus, and evidence for an introgressive hybrid zone between
L-geoffroyi and L-tigrinus in southern Brazil
SO MOLECULAR ECOLOGY
LA English
DT Article
DE carnivora; hybridization; introgression; Leopardus geoffroyi; Leopardus
tigrinus; South America
ID MULTILOCUS GENOTYPE DATA; ENDANGERED RED WOLF; MICROSATELLITE LOCI;
POPULATION-STRUCTURE; MITOCHONDRIAL-DNA; FELIS-SILVESTRIS; PHYLOGENETIC
TREES; CANIS-RUFUS; WILD; CONSERVATION
AB Natural hybrid zones between distinct species have been reported for many taxa, but so far, few examples involve carnivores or Neotropical mammals in general. In this study, we employed mitochondrial DNA (mtDNA) sequences and nine microsatellite loci to identify and characterize a hybrid zone between two Neotropical felids, Leopardus geoffroyi and L. tigrinus, both of which are well-established species having diverged from each other c. 1 million years ago. These two felids are mostly allopatric throughout their ranges in South America, with a narrow contact zone that includes southern Brazil. We present strong evidence for the occurrence of hybridization between these species and identify at least 14 individuals (most of them originating from the geographical contact zone) exhibiting signs of interspecific genomic introgression. The genetic structure of Brazilian L. tigrinus populations seems to be affected by this introgression process, showing a gradient of differentiation from L. geoffroyi correlated with distance from the contact zone. We also corroborate and extend previous findings of hybridization between L. tigrinus and a third related felid, L. colocolo, leading to an unusual situation for a mammal, in which the former species contains introgressed mtDNA lineages from two distinct taxa in addition to its own.
C1 [Trigo, T. C.; Freitas, T. R. O.] Univ Fed Rio Grande do Sul, Dept Genet, Porto Alegre, RS, Brazil.
[Kunzler, G.; Cardoso, L.; Bonatto, S. L.; Eizirik, E.] Pontificia Univ Catolica Rio Grand do Sul, Fac Biociencias, BR-90619900 Porto Alegre, RS, Brazil.
[Silva, J. C. R.; Eizirik, E.] Assoc Mata Ciliar, Ctr Brasileiro Conservacao Felinos Neotropicais, Jundiai, SP, Brazil.
[Silva, J. C. R.] Univ Fed Rural Pernambuco, Dept Vet Med, Recife, PE, Brazil.
[Silva, J. C. R.] Inst Brasileiro Med Conservacao Triade, Sao Paulo, Brazil.
[Johnson, W. E.; O'Brien, S. J.; Eizirik, E.] NCI, Lab Genom Div, NIH, Bethesda, MD USA.
RP Trigo, TC (reprint author), Univ Fed Rio Grande do Sul, Dept Genet, Porto Alegre, RS, Brazil.
EM tatiane.trigo@gmail.com; eduardo.eizirik@pucrs.br
RI Bonatto, Sandro/A-1240-2010; Eizirik, Eduardo/K-8034-2012; Freitas,
Thales/G-1160-2012; Johnson, Warren/D-4149-2016
OI Bonatto, Sandro/0000-0002-0064-467X; Eizirik,
Eduardo/0000-0002-9658-0999; Freitas, Thales/0000-0002-1019-9303;
Johnson, Warren/0000-0002-5954-186X
NR 79
TC 37
Z9 40
U1 1
U2 23
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1083
J9 MOL ECOL
JI Mol. Ecol.
PD OCT
PY 2008
VL 17
IS 19
BP 4317
EP 4333
DI 10.1111/j.1365-294X.2008.03919.x
PG 17
WC Biochemistry & Molecular Biology; Ecology; Evolutionary Biology
SC Biochemistry & Molecular Biology; Environmental Sciences & Ecology;
Evolutionary Biology
GA 352VQ
UT WOS:000259525900013
PM 18785898
ER
PT J
AU Hu, L
Gustofson, RL
Feng, H
Leung, PK
Mores, N
Krsmanovic, LZ
Catt, KJ
AF Hu, Lian
Gustofson, Robert L.
Feng, Hao
Leung, Po Ki
Mores, Nadia
Krsmanovic, Lazar Z.
Catt, Kevin J.
TI Converse regulatory functions of estrogen receptor-alpha and -beta
subtypes expressed in hypothalamic gonadotropin-releasing hormone
neurons
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID MESSENGER-RIBONUCLEIC-ACID; GNRH NEURONS; PULSATILE NEUROSECRETION;
INTRACELLULAR CALCIUM; POSITIVE FEEDBACK; PLASMA-MEMBRANE;
BINDING-SITES; PREOPTIC AREA; LHRH NEURONS; FEMALE RAT
AB Estradiol (E(2)) acts as a potent feedback molecule between the ovary and hypothalamic GnRH neurons, and exerts both positive and negative regulatory actions on GnRH synthesis and secretion. However, the extent to which these actions are mediated by estrogen receptors (ERs) expressed in GnRH neurons has been controversial. In this study, Single-cell RT-PCR revealed the expression of both ER alpha and ER beta isoforms in cultured fetal and adult rat hypothalamic GnRH neurons. Both ER alpha and ER beta or individual ERs were expressed in 94% of cultured fetal GnRH neurons. In adult female rats at diestrus, 68% of GnRH neurons expressed ERs, followed by 54% in estrus and 19% in proestrus. Expression of individual ERs was found in 24% of adult male GnRH neurons. ER alpha exerted marked G(i)-mediated inhibitory effects on spontaneous action potential (AP) firing, cAMP production, and pulsatile GnRH secretion, indicating its capacity for negative regulation of GnRH neuronal function. In contrast, increased E(2) concentration and ER beta agonists increase the rate of AP firing, GnRH secretion, and cAMP production, consistent with ER beta-dependent positive regulation of GnRH secretion. Consonant with the coupling of ER alpha to pertussis toxin-sensitive G(i/o) proteins, E(2) also activates G protein-activated inwardly rectifying potassium channels, decreasing membrane excitability and slowing the firing of spontaneous APs in hypothalamic GnRH neurons. These findings demonstrate that the dual actions of E(2) on GnRH neuronal membrane excitability, cAMP production, and GnRH secretion are mediated by the dose-dependent activation of ER alpha and ER beta expressed in hypothalamic GnRH neurons.
C1 [Hu, Lian; Gustofson, Robert L.; Feng, Hao; Leung, Po Ki; Mores, Nadia; Krsmanovic, Lazar Z.; Catt, Kevin J.] NICHHD, Endocrinol & Reprod Res Branch, PDEGEN, NIH, Bethesda, MD 20892 USA.
RP Krsmanovic, LZ (reprint author), NICHHD, Endocrinol & Reprod Res Branch, PDEGEN, NIH, Bldg 49,Room 6A-36, Bethesda, MD 20892 USA.
EM lazar@mail.nih.gov
OI MORES, Nadia/0000-0002-4197-0914
NR 44
TC 30
Z9 30
U1 0
U2 1
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 2008
VL 22
IS 10
BP 2250
EP 2259
DI 10.1210/me.2008-0192
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 353RK
UT WOS:000259585700005
PM 18701637
ER
PT J
AU Basta, M
AF Basta, Milan
TI Ambivalent effect of immunoglobulins on the complement system:
Activation versus inhibition
SO MOLECULAR IMMUNOLOGY
LA English
DT Article; Proceedings Paper
CT 22nd International Complement Workshop
CY SEP 28-OCT 02, 2008
CL Basel, SWITZERLAND
DE Complement activation pathways; Immunoglobulins; Complement fragments;
Scavenging; High-dose intravenous immunoglobulins (IVIG)
ID DOSE INTRAVENOUS IMMUNOGLOBULIN; MANNAN-BINDING LECTIN; IN-VITRO;
SENSITIZED ERYTHROCYTES; IMMUNE DAMAGE; IGG; COMPLEXES; PATHWAY;
DISEASE; FRAGMENTS
AB Pathogen and self-specific antibodies are known for their ability to trigger generation of active complement fragments that then serve as effectors of cell damage. The remainder of the immunoglobulin pool of the host has the capacity to quench harmful effects of activated complement cascade by preventing active complement fragments from binding to their specific receptors. This scavenging function is mediated by different acceptor sites within the immunoglobulin molecule. Large fragments, such as C3b and C4b are preferentially bound to the Fc region, while biologically potent C3a and C5a anaphylatoxins get neutralized by low-affinity interaction with the constant domain of the F(ab)'(2). The ambivalent effect of immunoglobulins on the complement system implies their role in homeostasis as well as expansion of use of high-dose intravenous immunoglobulins in diseases and states mediated by inappropriate complement activation. (C) 2008 Elsevier Ltd. All rights reserved.
C1 NINDS, NIH, Bethesda, MD 20892 USA.
RP Basta, M (reprint author), NINDS, NIH, Bethesda, MD 20892 USA.
EM basta.milan@gmail.com
OI Basta, Milan/0000-0001-5958-9241
NR 43
TC 37
Z9 37
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD OCT
PY 2008
VL 45
IS 16
SI SI
BP 4073
EP 4079
DI 10.1016/j.molimm.2008.07.012
PG 7
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 363DB
UT WOS:000260245000005
PM 18706699
ER
PT J
AU Lynch, A
Murphy, J
Levine, R
Gibbs, R
Giclas, P
Byers, T
Parish, M
Salmon, J
Holers, VM
AF Lynch, Anne
Murphy, James
Levine, Richard
Gibbs, Ronald
Giclas, Patricia
Byers, Tim
Parish, Mark
Salmon, Jane
Holers, V. Michael
TI Complement activation fragment Bb, angiogenic factors and pre-eclampsia
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 22nd International Complement Workshop
CY SEP 28-OCT 02, 2008
CL Basel, SWITZERLAND
C1 [Lynch, Anne; Gibbs, Ronald; Parish, Mark; Holers, V. Michael] Univ Colorado, Denver, CO 80202 USA.
[Giclas, Patricia] Natl Jewish Med & Res Ctr, Dept Pediat, Denver, CO USA.
[Levine, Richard] Natl Inst Child Hlth & Dev, NIH, Bethesda, MD USA.
[Byers, Tim] Colorado Sch Publ Hlth, Dept Epidemiol, Aurora, CO USA.
[Salmon, Jane] Cornell Univ, Weill Med Coll, Hosp Special Surg, Ithaca, NY 14853 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD OCT
PY 2008
VL 45
IS 16
SI SI
MA 064
BP 4117
EP 4117
DI 10.1016/j.molimm.2008.08.065
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 363DB
UT WOS:000260245000072
ER
PT J
AU Ninkovic, M
Colic, M
Basta, M
AF Ninkovic, Milica
Colic, Miodrag
Basta, Milan
TI The effect of IVIG in the rat model of free-fall haemorrhage
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 22nd International Complement Workshop
CY SEP 28-OCT 02, 2008
CL Basel, SWITZERLAND
C1 [Ninkovic, Milica; Colic, Miodrag] Mil Med Acad, Inst Med Res, Belgrade, Serbia.
[Basta, Milan] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD OCT
PY 2008
VL 45
IS 16
SI SI
MA P198
BP 4161
EP 4161
DI 10.1016/j.molimm.2008.08.197
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 363DB
UT WOS:000260245000204
ER
PT J
AU Huber, G
Banki, Z
Ammann, C
Dierich, M
Stoiber, H
AF Huber, Georg
Banki, Zoltan
Ammann, Christoph
Dierich, Manfred
Stoiber, Heribert
TI Enhancement of complement-mediated lysis by blocking factor H as an
antiretroviral treatment option?
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 22nd International Complement Workshop
CY SEP 28-OCT 02, 2008
CL Basel, SWITZERLAND
C1 [Huber, Georg; Banki, Zoltan; Dierich, Manfred; Stoiber, Heribert] Med Univ Innsbruck, Innsbruck, Austria.
[Ammann, Christoph] NIH, Hamilton, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD OCT
PY 2008
VL 45
IS 16
SI SI
MA P260
BP 4181
EP 4182
DI 10.1016/j.molimm.2008.08.259
PG 2
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 363DB
UT WOS:000260245000266
ER
PT J
AU Brett, PJ
Burtnick, MN
Fenno, JC
Gherardini, FC
AF Brett, Paul J.
Burtnick, Mary N.
Fenno, J. Christopher
Gherardini, Frank C.
TI Treponema denticola TroR is a manganese- and iron-dependent
transcriptional repressor
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID DIPHTHERIA-TOXIN REPRESSOR; GRAM-NEGATIVE BACTERIA; METAL
ION-ACTIVATION; CORYNEBACTERIUM-DIPHTHERIAE; SUBGINGIVAL PLAQUE;
ESCHERICHIA-COLI; DNA-BINDING; PROTEIN; IDENTIFICATION; ACQUISITION
AB Treponema denticola harbours a genetic locus with significant homology to most of the previously characterized Treponema pallidum tro operon. Within this locus are five genes (troABCDR) encoding for the components of an ATP-binding cassette cation-transport system (troABCD) and a DtxR-like transcriptional regulator (troR). In addition, a sigma(70)-like promoter and an 18 bp region of dyad symmetry were identified upstream of the troA start codon. This putative operator sequence demonstrated similarity to the T. pallidum TroR (TroR(Tp)) binding sequence; however, the position of this motif with respect to the predicted tro promoters differed. Interestingly, unlike the T. pallidum orthologue, T. denticola TroR (TroR(Td)) possesses a C-terminal Src homology 3-like domain commonly associated with DtxR family members. In the present study, we show that TroR(Td) is a manganese- and iron-dependent transcriptional repressor using Escherichia coli reporter constructs and in T. denticola. In addition, we demonstrate that although TroR(Td) possessing various C-terminal deletions maintain metal-sensing capacities, these truncated proteins exhibit reduced repressor activities in comparison with full-length TroR(Td). Based upon these findings, we propose that TroR(Td) represents a novel member of the DtxR family of transcriptional regulators and is likely to play an important role in regulating both manganese and iron homeostases in this spirochaete.
C1 [Brett, Paul J.; Burtnick, Mary N.; Gherardini, Frank C.] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Fenno, J. Christopher] Univ Michigan, Sch Dent, Ann Arbor, MI 48109 USA.
RP Gherardini, FC (reprint author), NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
EM fgherardini@niaid.nih.gov
FU NIH; National Institute of Allergy and Infectious Diseases
FX We would like to thank Patricia Rosa and Mollie Jewett for critical
review of this manuscript. We would like to thank Dan Sturdevant for
Taqman primer and probe design and Brandon Kramer for help with NOS-E
media. We are grateful to Gary Hettrick and Anita Mora for graphics
support. This research was supported by the Intramural Research Program
of the NIH, National Institute of Allergy and Infectious Diseases.
NR 53
TC 10
Z9 10
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD OCT
PY 2008
VL 70
IS 2
BP 396
EP 409
DI 10.1111/j.1365-2958.2008.06418.x
PG 14
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 352VS
UT WOS:000259526100010
PM 18761626
ER
PT J
AU Eckstrand, K
Addington, AM
Stromberg, T
Merriman, B
Miller, R
Gochman, P
Long, R
Dutra, A
Chen, Z
Meltzer, P
Nelson, SF
Rapoport, JL
AF Eckstrand, K.
Addington, A. M.
Stromberg, T.
Merriman, B.
Miller, R.
Gochman, P.
Long, R.
Dutra, A.
Chen, Z.
Meltzer, P.
Nelson, S. F.
Rapoport, J. L.
TI Sex chromosome anomalies in childhood onset schizophrenia: an update
SO MOLECULAR PSYCHIATRY
LA English
DT Letter
ID TURNER-SYNDROME; ABNORMALITIES; RARE
C1 [Eckstrand, K.; Addington, A. M.; Stromberg, T.; Miller, R.; Gochman, P.; Long, R.; Rapoport, J. L.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Merriman, B.; Chen, Z.; Nelson, S. F.] Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA.
[Dutra, A.] NHGRI, NIH, Genet Dis Res Branch, Bethesda, MD 20892 USA.
[Meltzer, P.] Natl Canc Inst, NIH, Canc Genet Branch, Bethesda, MD USA.
RP Eckstrand, K (reprint author), NIMH, Child Psychiat Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM addingta@mail.nih.gov
RI Nelson, Stanley/D-4771-2009
FU Intramural NIH HHS [Z01 MH002581-17, Z01 MH002240-21]; NCRR NIH HHS [P41
RR013642-070069]
NR 18
TC 8
Z9 8
U1 2
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD OCT
PY 2008
VL 13
IS 10
BP 910
EP 911
DI 10.1038/mp.2008.67
PG 3
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 349MM
UT WOS:000259284900001
PM 18800051
ER
PT J
AU Prokhorenko, OA
Vasconcelos, OM
Lupu, VD
Campbell, WW
Jabbari, B
AF Prokhorenko, Olga A.
Vasconcelos, Olavo M.
Lupu, Vitalie D.
Campbell, William W.
Jabbari, Bahman
TI Sensory physiology assessed by evoked potentials in survivors of
poliomyelitis
SO MUSCLE & NERVE
LA English
DT Article
DE magnetic resonance imaging; polio; poliomyelitis; post-polio syndrome;
somatosensory evoked potentials
ID POSTPOLIO SYNDROME; POLIO SURVIVORS; PATHOGENESIS; PATHOLOGY; NERVE
AB Evidence suggests that sensory loss may occur in a proportion of patients affected by poliomyelitis. We hypothesize that sensory problems may be a lasting sequela in some polio survivors. Sensory pathways in polio survivors were evaluated clinically and electrophysiologically using sensory evoked potentials (SEPs). Patients with sensory deficits or abnormal SEPs were further evaluated by magnetic resonance imaging (MRI). Twenty-two patients were studied. The mean age was 64.7 years (age range: 56-81 years). Clinically, sensory impairments were found in 4 patients. Upper limb SEPs were normal. Lower limb SEPs were abnormal in 10 patients. In 1 patient, clinical and electrographic findings correlated with a patch of atrophy in the spinal cord, as shown by MRI. Sensory derangements may be found in a proportion of aging polio survivors. SEP studies may add sensitivity when evaluating sensory function in this cohort. It remains unclear whether these sensory abnormalities are related to remote poliomyelitis. Further studies are necessary.
C1 [Prokhorenko, Olga A.; Vasconcelos, Olavo M.] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Jabbari, Bahman] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06510 USA.
[Lupu, Vitalie D.; Campbell, William W.] NINDS, EMG Lab, NINOS, NIH, Bethesda, MD 20892 USA.
RP Vasconcelos, OM (reprint author), Uniformed Serv Univ Hlth Sci, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM ovasconcelos@usuhs.edu
FU Department of Defense [MDA 905-01-007]
FX This study was sponsored by a grant from the Department of Defense
(Health Affairs, Grant MDA 905-01-007), administered by the Henry
Jackson Foundation (HJF), Rockville, MD, and by the Intramural Program
of the National Institutes of Health, Bethesda, MD. The study is
registered with ClinicalTrials.gov, identifier no. NCT00080600. The
present findings were presented in abstract form at the 131st meeting of
the American Neurological Association, October 2006, Chicago, IL. The
authors thank Dr. Mary Kay Floeter, Deputy Clinical Director, NINDS,
NIH, for her insightful revision Of the manuscript.
NR 25
TC 4
Z9 4
U1 2
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0148-639X
J9 MUSCLE NERVE
JI Muscle Nerve
PD OCT
PY 2008
VL 38
IS 4
BP 1266
EP 1271
DI 10.1002/mus.21093
PG 6
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 357KC
UT WOS:000259843700007
PM 18816600
ER
PT J
AU Longmire, M
Choyke, PL
Kobayashi, H
AF Longmire, Michelle
Choyke, Peter L.
Kobayashi, Hisataka
TI Clearance properties of nano-sized particles and molecules as imaging
agents: considerations and caveats
SO NANOMEDICINE
LA English
DT Review
DE clearance; excretion; kidney; liver; macromolecules; molecular imaging;
nano-materials; nanoparticles; nanotechnology; toxicity
ID MRI CONTRAST AGENTS; ENHANCED HEPATIC-UPTAKE; IN-VIVO; QUANTUM DOTS;
GOLD NANOPARTICLES; PHYSICOCHEMICAL CHARACTERISTICS; SUPERPARAMAGNETIC
AGENTS; COMPLEMENT ACTIVATION; MONOCLONAL-ANTIBODY; CARBON NANOTUBES
AB Nanoparticles possess enormous potential as diagnostic imaging agents and hold promise for the development of multimodality agents with both imaging and therapeutic capabilities. Yet, some of the most promising nanoparticles demonstrate prolonged tissue retention and contain heavy metals. This presents serious concerns for toxicity. The creation of nanoparticles with optimal clearance characteristics will minimize toxicity risks by reducing the duration of exposure to these agents. Given that many nanoparticles possess easily modifiable surface and interior chemistry, if nanoparticle characteristics associated with optimal clearance from the body were well established, it would be feasible to design and create agents with more favorable clearance properties. This article presents a thorough discussion of the physiologic aspects of nanoparticle clearance, focusing on renal mechanisms, and provides an overview of current research investigating clearance of specific types of nanoparticles and nano-sized macromolecules, including dendrimers, quantum dots, liposomes and carbon, gold and silica-based nanoparticles.
C1 [Longmire, Michelle; Choyke, Peter L.; Kobayashi, Hisataka] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
RP Kobayashi, H (reprint author), NCI, Mol Imaging Program, NIH, Bldg 10,Room 1 B40,MSC 1088, Bethesda, MD 20892 USA.
EM kobayash@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999, ZIA BC010657-05]
NR 77
TC 546
Z9 552
U1 30
U2 206
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1743-5889
J9 NANOMEDICINE-UK
JI Nanomedicine
PD OCT
PY 2008
VL 3
IS 5
BP 703
EP 717
DI 10.2217/17435889.3.5.703
PG 15
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
SC Biotechnology & Applied Microbiology; Science & Technology - Other
Topics
GA 363UC
UT WOS:000260291400016
PM 18817471
ER
PT J
AU Schloss, JA
AF Schloss, Jeffery A.
TI How to get genomes at one ten-thousandth the cost
SO NATURE BIOTECHNOLOGY
LA English
DT Letter
ID SINGLE MOLECULES; DNA; SEQUENCE
C1 NHGRI, US Natl Inst Hlth, Div Extramural Res, Bethesda, MD 20892 USA.
RP Schloss, JA (reprint author), NHGRI, US Natl Inst Hlth, Div Extramural Res, Bethesda, MD 20892 USA.
EM jeff_schloss@nih.gov
NR 21
TC 50
Z9 52
U1 1
U2 15
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1087-0156
J9 NAT BIOTECHNOL
JI Nat. Biotechnol.
PD OCT
PY 2008
VL 26
IS 10
BP 1113
EP 1115
DI 10.1038/nbt1008-1113
PG 3
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 358NY
UT WOS:000259926000025
PM 18846084
ER
PT J
AU Branton, D
Deamer, DW
Marziali, A
Bayley, H
Benner, SA
Butler, T
Di Ventra, M
Garaj, S
Hibbs, A
Huang, XH
Jovanovich, SB
Krstic, PS
Lindsay, S
Ling, XSS
Mastrangelo, CH
Meller, A
Oliver, JS
Pershin, YV
Ramsey, JM
Riehn, R
Soni, GV
Tabard-Cossa, V
Wanunu, M
Wiggin, M
Schloss, JA
AF Branton, Daniel
Deamer, David W.
Marziali, Andre
Bayley, Hagan
Benner, Steven A.
Butler, Thomas
Di Ventra, Massimiliano
Garaj, Slaven
Hibbs, Andrew
Huang, Xiaohua
Jovanovich, Stevan B.
Krstic, Predrag S.
Lindsay, Stuart
Ling, Xinsheng Sean
Mastrangelo, Carlos H.
Meller, Amit
Oliver, John S.
Pershin, Yuriy V.
Ramsey, J. Michael
Riehn, Robert
Soni, Gautam V.
Tabard-Cossa, Vincent
Wanunu, Meni
Wiggin, Matthew
Schloss, Jeffery A.
TI The potential and challenges of nanopore sequencing
SO NATURE BIOTECHNOLOGY
LA English
DT Review
ID SOLID-STATE NANOPORE; SINGLE-STRANDED-DNA; TRANSVERSE ELECTRONIC
TRANSPORT; POLYNUCLEOTIDE MOLECULES; POLYMER TRANSLOCATION; FABRICATED
NANOPORES; PROTEIN NANOPORE; MEMBRANE CHANNEL; ALPHA-HEMOLYSIN; PORES
AB A nanopore-based device provides single-molecule detection and analytical capabilities that are achieved by electrophoretically driving molecules in solution through a nano-scale pore. The nanopore provides a highly confined space within which single nucleic acid polymers can be analyzed at high throughput by one of a variety of means, and the perfect processivity that can be enforced in a narrow pore ensures that the native order of the nucleobases in a polynucleotide is reflected in the sequence of signals that is detected. Kilobase length polymers (single-stranded genomic DNA or RNA) or small molecules (e.g., nucleosides) can be identified and characterized without amplification or labeling, a unique analytical capability that makes inexpensive, rapid DNA sequencing a possibility. Further research and development to overcome current challenges to nanopore identification of each successive nucleotide in a DNA strand offers the prospect of 'third generation' instruments that will sequence a diploid mammalian genome for similar to$1,000 in similar to 24 h.
C1 [Branton, Daniel] Harvard Univ, Dept Mol & Cell Biol, Cambridge, MA 02138 USA.
[Deamer, David W.] Univ Calif Santa Cruz, Dept Chem & Biochem, Santa Cruz, CA 95064 USA.
[Marziali, Andre; Tabard-Cossa, Vincent] Univ British Columbia, Dept Phys & Astron, Vancouver, BC V6T 1Z1, Canada.
[Bayley, Hagan] Univ Oxford, Dept Biol Chem, Oxford OX1 3TA, England.
[Benner, Steven A.] Fdn Appl Mol Evolut, Gainesville, FL 32604 USA.
[Butler, Thomas] Univ Washington, Dept Phys, Seattle, WA 98195 USA.
[Di Ventra, Massimiliano; Pershin, Yuriy V.] Univ Calif San Diego, Dept Phys, La Jolla, CA 92093 USA.
[Garaj, Slaven] Harvard Univ, Dept Phys, Cambridge, MA 02138 USA.
[Hibbs, Andrew] Elect BioSci, San Diego, CA 92121 USA.
[Huang, Xiaohua] Univ Calif San Diego, Dept Bioengn, San Diego, CA 92093 USA.
[Jovanovich, Stevan B.] Microchip Biotechnol Inc, Dublin, CA 94568 USA.
[Krstic, Predrag S.] Oak Ridge Natl Lab, Oak Ridge, TN 37831 USA.
[Lindsay, Stuart] Arizona State Univ, Dept Phys, Tempe, AZ 85287 USA.
[Lindsay, Stuart] Arizona State Univ, Dept Chem, Tempe, AZ 85287 USA.
[Lindsay, Stuart] Arizona State Univ, Biodesign Inst, Tempe, AZ 85287 USA.
[Ling, Xinsheng Sean] Brown Univ, Dept Phys, Providence, RI 02912 USA.
[Mastrangelo, Carlos H.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Meller, Amit; Soni, Gautam V.] Boston Univ, Boston, MA 02215 USA.
[Oliver, John S.] NABsys Inc, Providence, RI 02906 USA.
[Ramsey, J. Michael] Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA.
[Riehn, Robert] N Carolina State Univ, Dept Phys, Raleigh, NC 27695 USA.
[Wiggin, Matthew] Univ British Columbia, Dept Biochem, Vancouver, BC V6T 1Z3, Canada.
[Schloss, Jeffery A.] Natl Human Genome Res Inst, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Branton, D (reprint author), Harvard Univ, Dept Mol & Cell Biol, Cambridge, MA 02138 USA.
EM dbranton@harvard.edu
RI Wanunu, Meni/A-3627-2011; Riehn, Robert/A-7195-2011; Di Ventra,
Massimiliano/E-1667-2011; Ling, Xinsheng/A-9219-2008; Pershin,
Yuriy/F-4453-2012; Garaj, Slaven/B-9782-2013; Tabard-Cossa,
Vincent/M-5202-2013
OI Riehn, Robert/0000-0002-4408-3560; Di Ventra,
Massimiliano/0000-0001-9416-189X; Soni, Gautam/0000-0002-0134-5583;
Meller, Amit/0000-0001-7082-0985; Garaj, Slaven/0000-0001-5529-4040;
Tabard-Cossa, Vincent/0000-0003-4375-717X
FU NHGRI NIH HHS [R01 HG003583, R01 HG003703, R01 HG003703-03, R01
HG003703-04, R21 HG004383, R21 HG004764-01]
NR 88
TC 1143
Z9 1157
U1 87
U2 631
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1087-0156
J9 NAT BIOTECHNOL
JI Nat. Biotechnol.
PD OCT
PY 2008
VL 26
IS 10
BP 1146
EP 1153
DI 10.1038/nbt.1495
PG 8
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 358NY
UT WOS:000259926000029
PM 18846088
ER
PT J
AU Diks, SH
da Silva, MAS
Hillebrands, JL
Bink, RJ
Versteeg, HH
van Rooijen, C
Brouwers, A
Chitnis, AB
Peppelenbosch, MP
Zivkovic, D
AF Diks, Sander H.
da Silva, Maria A. Sartori
Hillebrands, Jan-Luuk
Bink, Robert J.
Versteeg, Henri H.
van Rooijen, Carina
Brouwers, Anke
Chitnis, Ajay B.
Peppelenbosch, Maikel P.
Zivkovic, Danica
TI d-Asb11 is an essential mediator of canonical Delta-Notch signalling
SO NATURE CELL BIOLOGY
LA English
DT Article
ID UBIQUITIN LIGASE; CELL FATE; MIND BOMB; ZEBRAFISH; DROSOPHILA;
ENDOCYTOSIS; PATHWAY; PROTEIN; GENE; NRARP
AB In canonical Delta-Notch signalling, expression of Delta activates Notch in neighbouring cells, leading to of Delta in these cells(1). This process of lateral inhibition results in selection of either Delta-signalling cells or Notch-signalling cells. Here we show that d-Asb11 is an important mediator of this lateral inhibition. In zebrafish embryos, morpholino oligonucleotide (MO)-mediated knockdown of d-Asb11 caused repression of specific Delta-Notch elements and their transcriptional targets, whereas these were induced when d-Asb11 was misexpressed. d-Asb11 also activated legitimate Notch reporters cell-non-autonomously in vitro and in vivo when co-expressed with a Notch reporter. However, it repressed Notch reporters when expressed in Delta-expressing cells. Consistent with these results, d-Asb11 was able to specifically ubiquitylate and degrade DeltaA both in vitro and in vivo. We conclude that d-Asb11 is a component in the regulation of Delta-Notch signalling, important in fine-tuning the lateral inhibition gradients between DeltaA and Notch through a cell non-autonomous mechanism.
C1 [Diks, Sander H.; da Silva, Maria A. Sartori; Hillebrands, Jan-Luuk; Versteeg, Henri H.; Peppelenbosch, Maikel P.] Univ Groningen, Univ Med Ctr Groningen, Dept Cell Biol, NL-9713 AV Groningen, Netherlands.
[da Silva, Maria A. Sartori; Bink, Robert J.; van Rooijen, Carina; Brouwers, Anke; Zivkovic, Danica] Hubrecht Inst, NL-3584 CT Utrecht, Netherlands.
[Chitnis, Ajay B.] NICHD, Sect Neural Dev Dynam, Mol Genet Lab, NIH, Bethesda, MD 20892 USA.
RP Peppelenbosch, MP (reprint author), Univ Groningen, Univ Med Ctr Groningen, Dept Cell Biol, Deusinglaan 1, NL-9713 AV Groningen, Netherlands.
EM M.P.Peppelenbosch@med.umcg.nl
RI Sartori, Maria/R-9317-2016;
OI Sartori, Maria/0000-0002-6474-280X; Versteeg, Henri/0000-0003-4294-175X
NR 34
TC 14
Z9 14
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD OCT
PY 2008
VL 10
IS 10
BP 1190
EP 1198
DI 10.1038/ncb1779
PG 9
WC Cell Biology
SC Cell Biology
GA 355BF
UT WOS:000259682900013
PM 18776899
ER
PT J
AU Cravedi, P
Mannon, RB
Remuzzi, G
AF Cravedi, Paolo
Mannon, Roslyn B.
Remuzzi, Giuseppe
TI Lymphocyte depletion for kidney transplantation: back to the past?
SO NATURE CLINICAL PRACTICE NEPHROLOGY
LA English
DT Editorial Material
ID REGULATORY T-CELLS; THYMOCYTE GLOBULIN; INDUCTION THERAPY; BASILIXIMAB
C1 [Cravedi, Paolo; Remuzzi, Giuseppe] Mario Negri Inst Pharmacol Res, Clin Res Ctr Rare Dis Aldo & Cele Dacco, I-24125 Bergamo, Italy.
[Mannon, Roslyn B.] NIDDK, Transplantat Branch, NIH, Bethesda, MD USA.
RP Cravedi, P (reprint author), Mario Negri Inst Pharmacol Res, Clin Res Ctr Rare Dis Aldo & Cele Dacco, Via Gavazzeni 11, I-24125 Bergamo, Italy.
EM p.cravedi@gmail.com
NR 13
TC 2
Z9 2
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1745-8323
J9 NAT CLIN PRACT NEPHR
JI Nat. Clin. Pract. Nephrol.
PD OCT
PY 2008
VL 4
IS 10
BP 534
EP 535
DI 10.1038/ncpneph0914
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA 349TC
UT WOS:000259305200006
PM 18725917
ER
PT J
AU Hazra, A
Kraft, P
Selhub, J
Giovannucci, EL
Thomas, G
Hoover, RN
Chanock, SJ
Hunter, DJ
AF Hazra, Aditi
Kraft, Peter
Selhub, Jacob
Giovannucci, Edward L.
Thomas, Gilles
Hoover, Robert N.
Chanock, Stephen J.
Hunter, David J.
TI Common variants of FUT2 are associated with plasma vitamin B-12 levels
SO NATURE GENETICS
LA English
DT Article
ID HELICOBACTER-PYLORI INFECTION; SECRETOR PHENOTYPE; HUMAN-POPULATIONS;
GENE FUT2; MALABSORPTION; HOMOCYSTEINE; CANCER; RISK
AB We identified a strong association (P = 5.36 x 10(-17)) between rs492602 in FUT2 and plasma vitamin B-12 levels in a genome-wide scan (n = 1,658) and an independent replication sample (n = 1,059) from the Nurses' Health Study. Women homozygous for the rs492602[G] allele had higher B12 levels. This allele is in strong linkage disequilibrium with the FUT2 nonsecretor variant encoding W143X, suggesting a plausible mechanism for altered B12 absorption and plasma levels.
C1 [Hazra, Aditi; Kraft, Peter; Hunter, David J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol, Boston, MA 02115 USA.
[Hazra, Aditi; Giovannucci, Edward L.; Hunter, David J.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Hazra, Aditi; Giovannucci, Edward L.; Hunter, David J.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Selhub, Jacob] Tufts Univ, Jean Mayer US Dept Agr, Human Nutr Res Ctr Aging, Vitamin Metab & Aging Lab, Boston, MA 02111 USA.
[Giovannucci, Edward L.; Hunter, David J.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Thomas, Gilles; Hoover, Robert N.; Chanock, Stephen J.; Hunter, David J.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Hunter, David J.] MIT, Broad Inst, Program Med & Populat Genet, Cambridge, MA 02142 USA.
[Hunter, David J.] Harvard Univ, Cambridge, MA 02142 USA.
RP Hunter, DJ (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol, 677 Huntington Ave, Boston, MA 02115 USA.
EM dhunter@hsph.harvard.edu
FU National Institutes of Health Research [U54 CA100971, P01 CA87969, P01
CA55075, U01 CA098233, R01 CA 065725, CA070817]; NIH [T-32 CA 09001-30]
FX We thank H. Ranu, C. Chen and the staff at the Core Genotyping Facility
at the National Cancer Institute for their expertise. This research is
supported by the National Institutes of Health Research Grants U54
CA100971, P01 CA87969, P01 CA55075, U01 CA098233, R01 CA 065725 and
CA070817. A. H. is supported in part by training grant NIH T-32 CA
09001-30.
NR 15
TC 63
Z9 67
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2008
VL 40
IS 10
BP 1160
EP 1162
DI 10.1038/ng.210
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 354PH
UT WOS:000259651000013
PM 18776911
ER
PT J
AU Kopp, JB
Smith, MW
Nelson, GW
Johnson, RC
Freedman, BI
Bowden, DW
Oleksyk, T
McKenzie, LM
Kajiyama, H
Ahuja, TS
Berns, JS
Briggs, W
Cho, ME
Dart, RA
Kimmel, PL
Korbet, SM
Michel, DM
Mokrzycki, MH
Schelling, JR
Simon, E
Trachtman, H
Vlahov, D
Winkler, CA
AF Kopp, Jeffrey B.
Smith, Michael W.
Nelson, George W.
Johnson, Randall C.
Freedman, Barry I.
Bowden, Donald W.
Oleksyk, Taras
McKenzie, Louise M.
Kajiyama, Hiroshi
Ahuja, Tejinder S.
Berns, Jeffrey S.
Briggs, William
Cho, Monique E.
Dart, Richard A.
Kimmel, Paul L.
Korbet, Stephen M.
Michel, Donna M.
Mokrzycki, Michele H.
Schelling, Jeffrey R.
Simon, Eric
Trachtman, Howard
Vlahov, David
Winkler, Cheryl A.
TI MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis
SO NATURE GENETICS
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; STAGE RENAL-DISEASE; AFRICAN-AMERICANS;
HYPERTENSIVE NEPHROSCLEROSIS; GENOME-SCAN; HAPLOTYPE MAP; UNITED-STATES;
ADMIXTURE; LOCUS; NEPHROPATHY
AB The increased burden of chronic kidney and end-stage kidney diseases (ESKD) in populations of African ancestry has been largely unexplained. To identify genetic variants predisposing to idiopathic and HIV-1-associated focal segmental glomerulosclerosis (FSGS), we carried out an admixture-mapping linkage-disequilibrium genome scan on 190 African American individuals with FSGS and 222 controls. We identified a chromosome 22 region with a genome-wide logarithm of the odds (lod) score of 9.2 and a peak lod of 12.4 centered on MYH9, a functional candidate gene expressed in kidney podocytes. Multiple MYH9 SNPs and haplotypes were recessively associated with FSGS, most strongly a haplotype spanning exons 14 through 23 (OR = 5.0, 95% CI 3.5-7.1; P = 4 x 10(-23), n = 852). This association extended to hypertensive ESKD (OR = 2.2, 95% CI = 1.5-3.4; n = 433), but not type 2 diabetic ESKD (n 476). Genetic variation at the MYH9 locus substantially explains the increased burden of FSGS and hypertensive ESKD among African Americans.
C1 [Smith, Michael W.; Nelson, George W.; Johnson, Randall C.; Oleksyk, Taras; McKenzie, Louise M.; Winkler, Cheryl A.] NCI, Lab Genom Divers, SAIC Frederick, Frederick, MD 21702 USA.
[Kopp, Jeffrey B.; Kajiyama, Hiroshi; Cho, Monique E.] NIDDK, Kidney Dis Sect, NIH, Bethesda, MD 20892 USA.
[Freedman, Barry I.; Bowden, Donald W.] Wake Forest Univ, Bowman Gray Sch Med, Nephrol Sect, Winston Salem, NC 27157 USA.
[Ahuja, Tejinder S.] Univ Texas Galveston, Med Branch, Galveston, TX 77555 USA.
[Berns, Jeffrey S.] Univ Penn, Sch Med, Renal Electrolyte & Hypertens Div, Philadelphia, PA 19104 USA.
[Briggs, William] William Beaumont Hosp, Royal Oak, MI 48073 USA.
[Dart, Richard A.] Marshfield Clin Fdn Med Res & Educ, Dept Hypertens & Nephrol, Marshfield, WI 54449 USA.
[Kimmel, Paul L.] George Washington Univ, Med Ctr, Div Renal Dis & Hypertens, Dept Med, Washington, DC 20037 USA.
[Korbet, Stephen M.] Rush Univ, Med Ctr, Dept Med, Chicago, IL 60612 USA.
[Michel, Donna M.] Hypertens & Kidney Specialists, Lancaster, PA 17601 USA.
[Mokrzycki, Michele H.] Albert Einstein Coll Med, Div Nephrol, Bronx, NY 10461 USA.
[Schelling, Jeffrey R.] Case Western Reserve Univ, Dept Med, Cleveland, OH 44109 USA.
[Simon, Eric] Tulane Univ, Sch Med, Nephrol Sect, New Orleans, LA 70112 USA.
[Trachtman, Howard] Schneider Childrens Hosp Syst, Div Nephrol, Dept Pediat, New Hyde Pk, NY 11040 USA.
[Vlahov, David] New York Acad Med, New York, NY 10029 USA.
RP Winkler, CA (reprint author), NCI, Lab Genom Divers, SAIC Frederick, Frederick, MD 21702 USA.
EM winkler@ncifcrf.gov
RI Smith, Michael/B-5341-2012; Taras, Oleksyk/J-8805-2013; Johnson,
Randall/B-1517-2014;
OI Taras, Oleksyk/0000-0002-8148-3918; Johnson,
Randall/0000-0001-7754-0847; Trachtman, Howard/0000-0001-7447-9489;
Kopp, Jeffrey/0000-0001-9052-186X
FU Intramural NIH HHS [Z01 DK043308-12]; NCI NIH HHS [N01-CO-12400,
N01CO12400]; NIDDK NIH HHS [R01 DK059997-04, R01 DK059997, R01 DK067528,
R01 DK067528-05, R01 DK070941, R01 DK072348, R01 DK072348-04, Z01
DK043308, ZO-1 DK043308]
NR 50
TC 393
Z9 410
U1 2
U2 10
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2008
VL 40
IS 10
BP 1175
EP 1184
DI 10.1038/ng.226
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 354PH
UT WOS:000259651000016
PM 18794856
ER
PT J
AU Kao, WHL
Klag, MJ
Meoni, LA
Reich, D
Berthier-Schaad, Y
Li, M
Coresh, J
Patterson, N
Tandon, A
Powe, NR
Fink, NE
Sadler, JH
Weir, MR
Abboud, HE
Adler, SG
Divers, J
Iyengar, SK
Freedman, BI
Kimmel, PL
Knowler, WC
Kohn, OF
Kramp, K
Leehey, DJ
Nicholas, SB
Pahl, MV
Schelling, JR
Sedor, JR
Thornley-Brown, D
Winkler, CA
Smith, MW
Parekh, RS
AF Kao, W. H. Linda
Klag, Michael J.
Meoni, Lucy A.
Reich, David
Berthier-Schaad, Yvette
Li, Man
Coresh, Josef
Patterson, Nick
Tandon, Arti
Powe, Neil R.
Fink, Nancy E.
Sadler, John H.
Weir, Matthew R.
Abboud, Hanna E.
Adler, Sharon G.
Divers, Jasmin
Iyengar, Sudha K.
Freedman, Barry I.
Kimmel, Paul L.
Knowler, William C.
Kohn, Orly F.
Kramp, Kristopher
Leehey, David J.
Nicholas, Susanne B.
Pahl, Madeleine V.
Schelling, Jeffrey R.
Sedor, John R.
Thornley-Brown, Denyse
Winkler, Cheryl A.
Smith, Michael W.
Parekh, Rulan S.
CA FIND Res Grp
TI MYH9 is associated with nondiabetic end-stage renal disease in African
Americans
SO NATURE GENETICS
LA English
DT Article
ID MYOSIN HEAVY-CHAIN; ADMIXTURE LINKAGE DISEQUILIBRIUM; MAY-HEGGLIN;
ADMIXED POPULATIONS; KIDNEY-DISEASE; GENE; GENOME; RISK; NEPHROPATHY;
PROGRESSION
AB As end-stage renal disease (ESRD) has a four times higher incidence in African Americans compared to European Americans, we hypothesized that susceptibility alleles for ESRD have a higher frequency in the West African than the European gene pool. We carried out a genome-wide admixture scan in 1,372 ESRD cases and 806 controls and found a highly significant association between excess African ancestry and nondiabetic ESRD (lod score = 5.70) but not diabetic ESRD (lod = 0.47) on chromosome 22q12. Each copy of the European ancestral allele conferred a relative risk of 0.50 (95% CI = 0.39-0.63) compared to African ancestry. Multiple common SNPs (allele frequencies ranging from 0.2 to 0.6) in the gene encoding nonmuscle myosin heavy chain type II isoform A (MYH9) were associated with two to four times greater risk of nondiabetic ESRD and accounted for a large proportion of the excess risk of ESRD observed in African compared to European Americans.
C1 [Kao, W. H. Linda; Klag, Michael J.; Berthier-Schaad, Yvette; Li, Man; Coresh, Josef; Powe, Neil R.; Fink, Nancy E.; Parekh, Rulan S.] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD 21287 USA.
[Kao, W. H. Linda; Klag, Michael J.; Meoni, Lucy A.; Powe, Neil R.; Fink, Nancy E.; Parekh, Rulan S.] Johns Hopkins Univ, Dept Med, Baltimore, MD 21287 USA.
[Kao, W. H. Linda; Klag, Michael J.; Meoni, Lucy A.; Coresh, Josef; Powe, Neil R.; Fink, Nancy E.; Parekh, Rulan S.] Johns Hopkins Univ, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD 21287 USA.
[Meoni, Lucy A.; Coresh, Josef] Johns Hopkins Univ, Dept Biostat, Sch Med, Baltimore, MD 21287 USA.
[Meoni, Lucy A.; Coresh, Josef] Johns Hopkins Univ, Dept Biostat, Bloomberg Sch Publ Hlth, Baltimore, MD 21287 USA.
[Reich, David; Tandon, Arti] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Reich, David; Patterson, Nick; Tandon, Arti] Harvard Univ, Broad Inst, Cambridge, MA 02142 USA.
[Reich, David; Patterson, Nick; Tandon, Arti] MIT, Cambridge, MA 02142 USA.
[Sadler, John H.; Weir, Matthew R.] Univ Maryland, Dept Med, Baltimore, MD 21201 USA.
[Abboud, Hanna E.] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, San Antonio, TX 78229 USA.
[Adler, Sharon G.] Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Dept Med, Los Angeles, CA 90502 USA.
[Divers, Jasmin; Freedman, Barry I.] Wake Forest Univ, Bowman Gray Sch Med, Dept Med, Winston Salem, NC 27157 USA.
[Iyengar, Sudha K.; Kramp, Kristopher] Case Western Reserve Univ, Sch Med, Dept Epidemiol & Biostat, Cleveland, OH 44109 USA.
[Kimmel, Paul L.] NIDDK, NIH, Bethesda, MD 20892 USA.
[Knowler, William C.] NIDDK, Diabet Epidemiol & Clin Res Sect, NIH, Phoenix, AZ 85014 USA.
[Kohn, Orly F.] Loyola Univ, Dept Med, Chicago, IL 60153 USA.
[Leehey, David J.] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Nicholas, Susanne B.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90024 USA.
[Pahl, Madeleine V.] Univ Calif Irvine, Dept Med, Irvine, CA 92868 USA.
[Schelling, Jeffrey R.; Sedor, John R.] Case Western Reserve Univ, Sch Med, Dept Med, Cleveland, OH 44109 USA.
[Sedor, John R.] Case Western Reserve Univ, Sch Med, Dept Biophysiol & Biophys, Cleveland, OH 44109 USA.
[Thornley-Brown, Denyse] Univ Alabama, Dept Med, Birmingham, AL 35294 USA.
[Winkler, Cheryl A.; Smith, Michael W.] NCI, Lab Genom Divers, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Parekh, Rulan S.] Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21287 USA.
RP Kao, WHL (reprint author), Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD 21287 USA.
EM wkao@jhsph.edu
RI Nelson, Robert/B-1470-2012; Smith, Michael/B-5341-2012;
OI Jun, Gyungah/0000-0002-3230-8697
FU AHRQ HHS [R01 HS008365, HS08365]; Intramural NIH HHS; NCI NIH HHS
[N01-CO-12400, N01CO12400]; NCRR NIH HHS [M01 RR000080, M01 RR000425,
M01 RR000827, M01 RR001346, M01 RR007122, M01-RR-000080, M01-RR-00425,
M01-RR-00827-29, M01-RR-01346, M01-RR-07122]; NHLBI NIH HHS [HL62985,
R01 HL062985]; NIDDK NIH HHS [DK07024, K01 DK067207, K01DK067207, R01
DK059997, R01 DK059997-04, R01 DK067528, R01 DK067528-05, R01 DK072348,
R01 DK072348-04, U01 DK057292, U01 DK057304, U01 DK070657, U01
DK070657-01, U01 DK070657-02, U01 DK070657-03, U01DK070657, U01DK57292,
U01DK57304]
NR 35
TC 365
Z9 381
U1 2
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2008
VL 40
IS 10
BP 1185
EP 1192
DI 10.1038/ng.232
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 354PH
UT WOS:000259651000017
PM 18794854
ER
PT J
AU Raychaudhuri, S
Remmers, EF
Lee, AT
Hackett, R
Guiducci, C
Burtt, NP
Gianniny, L
Korman, BD
Padyukov, L
Kurreeman, FAS
Chang, M
Catanese, JJ
Ding, B
Wong, S
Mil, AHMV
Neale, BM
Coblyn, J
Cui, J
Tak, PP
Wolbink, GJ
Crusius, JBA
van der Horst-Bruinsma, IE
Criswell, LA
Amos, CI
Seldin, MF
Kastner, DL
Ardlie, KG
Alfredsson, L
Costenbader, KH
Altshuler, D
Huizinga, TWJ
Shadick, NA
Weinblatt, ME
de Vries, N
Worthington, J
Seielstad, M
Toes, REM
Karlson, EW
Begovich, AB
Klareskog, L
Gregersen, PK
Daly, MJ
Plenge, RM
AF Raychaudhuri, Soumya
Remmers, Elaine F.
Lee, Annette T.
Hackett, Rachel
Guiducci, Candace
Burtt, Noel P.
Gianniny, Lauren
Korman, Benjamin D.
Padyukov, Leonid
Kurreeman, Fina A. S.
Chang, Monica
Catanese, Joseph J.
Ding, Bo
Wong, Sandra
Mil, Annette H. M. van der Helm-van
Neale, Benjamin M.
Coblyn, Jonathan
Cui, Jing
Tak, Paul P.
Wolbink, Gert Jan
Crusius, J. Bart A.
van der Horst-Bruinsma, Irene E.
Criswell, Lindsey A.
Amos, Christopher I.
Seldin, Michael F.
Kastner, Daniel L.
Ardlie, Kristin G.
Alfredsson, Lars
Costenbader, Karen H.
Altshuler, David
Huizinga, Tom W. J.
Shadick, Nancy A.
Weinblatt, Michael E.
de Vries, Niek
Worthington, Jane
Seielstad, Mark
Toes, Rene E. M.
Karlson, Elizabeth W.
Begovich, Ann B.
Klareskog, Lars
Gregersen, Peter K.
Daly, Mark J.
Plenge, Robert M.
TI Common variants at CD40 and other loci confer risk of rheumatoid
arthritis
SO NATURE GENETICS
LA English
DT Article
ID NF-KAPPA-B; SINGLE-NUCLEOTIDE POLYMORPHISM; GENOME-WIDE ASSOCIATION;
GRAVES-DISEASE; SUSCEPTIBILITY; GENE; COOPERATION; EXPRESSION;
INTERACTS; ANTIBODY
AB To identify rheumatoid arthritis risk loci in European populations, we conducted a meta-analysis of two published genome-wide association (GWA) studies totaling 3,393 cases and 12,462 controls(1,2). We genotyped 31 top-ranked SNPs not previously associated with rheumatoid arthritis in an independent replication of 3,929 autoantibody-positive rheumatoid arthritis cases and 5,807 matched controls from eight separate collections. We identified a common variant at the CD40 gene locus (rs4810485, P = 0.0032 replication, P = 8.2 x 10(-9) overall, OR = 0.87). Along with other associations near TRAF1 (refs. 2,3) and TNFAIP3 (refs. 4,5), this implies a central role for the CD40 signaling pathway in rheumatoid arthritis pathogenesis. We also identified association at the CCL21 gene locus (rs2812378, P = 0.00097 replication, P = 2.8 x 10(-7) overall), a gene involved in lymphocyte trafficking. Finally, we identified evidence of association at four additional gene loci: MMEL1-TNFRSF14 (rs3890745, P = 0.0035 replication, P = 1.1 x 10(-7) overall), CDK6 (rs42041, P = 0.010 replication, P = 4.0 x 10(-6) overall), PRKCQ (rs4750316, P = 0.0078 replication, P = 4.4 x 10(-6) overall), and KIF5A-PIP4K2C (rs1678542, P = 0.0026 replication, P = 8.8 x 10(-8) overall).
C1 [Raychaudhuri, Soumya; Hackett, Rachel; Guiducci, Candace; Burtt, Noel P.; Gianniny, Lauren; Wong, Sandra; Neale, Benjamin M.; Ardlie, Kristin G.; Altshuler, David; Daly, Mark J.; Plenge, Robert M.] Harvard Univ, Broad Inst, Program Med & Populat Genet, Cambridge, MA 02142 USA.
[Raychaudhuri, Soumya; Hackett, Rachel; Guiducci, Candace; Burtt, Noel P.; Gianniny, Lauren; Wong, Sandra; Neale, Benjamin M.; Ardlie, Kristin G.; Altshuler, David; Daly, Mark J.; Plenge, Robert M.] MIT, Cambridge, MA 02142 USA.
[Raychaudhuri, Soumya; Coblyn, Jonathan; Cui, Jing; Costenbader, Karen H.; Shadick, Nancy A.; Weinblatt, Michael E.; Karlson, Elizabeth W.; Plenge, Robert M.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA.
[Raychaudhuri, Soumya; Neale, Benjamin M.; Altshuler, David; Daly, Mark J.; Plenge, Robert M.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Remmers, Elaine F.; Korman, Benjamin D.; Kastner, Daniel L.] NIAMSD, Genet & Genom Branch, NIH, Bethesda, MD 20892 USA.
[Lee, Annette T.; Gregersen, Peter K.] N Shore Long Isl Jewish Hlth Syst, Feinstein Inst Med Res, Manhasset, NY 11030 USA.
[Padyukov, Leonid; Klareskog, Lars] Karolinska Univ Hosp Solna, Karolinska Inst, Dept Med, Rheumatol Unit, S-17176 Stockholm, Sweden.
[Kurreeman, Fina A. S.; Mil, Annette H. M. van der Helm-van; Huizinga, Tom W. J.; Toes, Rene E. M.] Leiden Univ, Med Ctr, Dept Rheumatol, NL-2333 ZA Leiden, Netherlands.
[Chang, Monica; Catanese, Joseph J.; Begovich, Ann B.] Celera, Alameda, CA 94502 USA.
[Ding, Bo; Alfredsson, Lars] Karolinska Inst, Inst Environm Med, S-17177 Stockholm, Sweden.
[Neale, Benjamin M.] Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Ctr, London SE5 8AF, England.
[Tak, Paul P.] Univ Amsterdam, Acad Med Ctr, NL-326 Amsterdam, Netherlands.
[Wolbink, Gert Jan] Jan van Breemen Inst, NL-1056 AB Amsterdam, Netherlands.
[Wolbink, Gert Jan] Univ Amsterdam, Acad Med Ctr, Sanquin Res Landsteiner Lab, NL-1006 AD Amsterdam, Netherlands.
[van der Horst-Bruinsma, Irene E.] Vrije Univ Amsterdam, Med Ctr, Dept Rheumatol, NL-1007 MB Amsterdam, Netherlands.
[Crusius, J. Bart A.] Vrije Univ Amsterdam, Med Ctr, Immunogenet Lab, Dept Pathol, NL-1007 MB Amsterdam, Netherlands.
[Criswell, Lindsey A.] Univ Calif San Francisco, Dept Med, Rosalind Russell Med Res Ctr Arthrit, San Francisco, CA 94143 USA.
[Amos, Christopher I.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Seldin, Michael F.] Univ Calif Davis, Rowe Program Genet, Davis, CA 95616 USA.
[Ardlie, Kristin G.] SeraCare Life Sci, Cambridge, MA 02139 USA.
[Worthington, Jane] Univ Manchester, Arthrit Res Campaign Epidemiol Unit, Manchester M13 9PT, Lancs, England.
[Seielstad, Mark] Genome Inst Singapore, Singapore 138672, Singapore.
RP Plenge, RM (reprint author), Harvard Univ, Broad Inst, Program Med & Populat Genet, Cambridge, MA 02142 USA.
EM rplenge@partners.org
RI Padyukov, Leonid/A-4890-2009; Altshuler, David/A-4476-2009; de Vries,
Niek/J-9348-2013; Worthington, Jane/M-9770-2014;
OI Padyukov, Leonid/0000-0003-2950-5670; Altshuler,
David/0000-0002-7250-4107; de Vries, Niek/0000-0002-6257-8604;
Worthington, Jane/0000-0003-0544-042X; Seielstad,
Mark/0000-0001-5783-1401; Alfredsson, Lars/0000-0003-1688-6697;
Klareskog, Lars/0000-0001-9601-6186
FU T32 NIH training grant [AR007530-23]; NIH [KAR055688A, AI55314-3,
RO1-AR44422, NO1-AR-2-2263, R01 AR49880, CA87969, P60 AR047782, K24
AR0524-01, BIRCWH K12 HD051959]; Fox Trot Fund; William Randolph Hearst
Fund of Harvard University; Burroughs Wellcome Fund; UO1 NIH [UO1
HG004171]; Millennium Pharmaceuticals and Biogen-Idec; National Center
for Research Resources [U54 RR020278]; National Institutes of Health;
Swedish Medical Research Council; Swedish Council for Working Life and
Social Research; King Gustaf V's 80-year Foundation; Swedish Rheumatic
Foundation; Stockholm County Council; Arbetsmarknadens
Forrsarkringsaktiebolag; lCounty of Sormland Research and Development
Center; Agency for Science Technology and Research (Singapore); Doris
Duke Charitable Foundation; US National Institute of Mental Health;
National Institute of Allergy and Infectious Diseases; National
Institute of Child Health and Human Development; American College of
Rheumatology Arthritis Investigator Award; Katherine Swan Ginsburg
Memorial Award; Kirkland Scholar Awardee [K24 AR02175, R01 AI065841, 5
M01 RR-00079]; European Community's FP6 funding
FX We thank the WTCCC for making access to genotype data available online,
and for providing autoantibody status of the WTCCC rheumatoid arthritis
cases. We thank S. Myers and J. Marchini for help with IMPUTE. S. R. is
supported by a T32 NIH training grant (AR007530-23), a K08 grant from
the NIH (KAR055688A), and through the BWH Rheumatology Fellowship
program, directed by S. Helfgott. R. M. P. is supported by a K08 grant
from the NIH (AI55314-3), a private donation from the Fox Trot Fund, the
William Randolph Hearst Fund of Harvard University, and holds a Career
Award for Medical Scientists from the Burroughs Wellcome Fund. M. J. D.
is supported by a UO1 NIH grant (UO1 HG004171). The BRASS Registry is
supported by a grant from Millennium Pharmaceuticals and Biogen-Idec.
The Broad Institute Center for Genotyping and Analysis is supported by
grant U54 RR020278 from the National Center for Research Resources. The
NARAC is supported by NIH grants RO1-AR44422 and NO1-AR-2-2263 (P. K.
G.). This work was also supported in part by the Intramural Research
Program of the National Institute of Arthritis and Musculoskeletal and
Skin Diseases of the National Institutes of Health. The EIRA study is
supported by grants from the Swedish Medical Research Council, the
Swedish Council for Working Life and Social Research, King Gustaf V's
80-year Foundation, the Swedish Rheumatic Foundation, the Stockholm
County Council, the insurance company Arbetsmarknadens
Forrsarkringsaktiebolag, and the County of Sormland Research and
Development Center. Genotyping of the EIRA cohort was supported by the
Agency for Science Technology and Research (Singapore). Genotyping of
the GCI and LUMC samples was funded by Celera. D. A. is a Burroughs
Wellcome Fund Clinical Scholar in Translational Research, and a
Distinguished Clinical Scholar of the Doris Duke Charitable Foundation.
B. D. K. was supported by the NIH Clinical Research Training Program, a
public-private partnership between the Foundation for the National
Institutes of Health and Pfizer Inc. E. W. K. is supported by NIH grants
R01 AR49880, CA87969, P60 AR047782, K24 AR0524-01 and BIRCWH K12
HD051959 (supported by US National Institute of Mental Health, National
Institute of Allergy and Infectious Diseases, National Institute of
Child Health and Human Development and the Office of the Director). K.
H. C. is the recipient of an Arthritis Foundation/American College of
Rheumatology Arthritis Investigator Award and a Katherine Swan Ginsburg
Memorial Award. L. A. C. is a Kirkland Scholar Awardee and her work on
this project was supported by K24 AR02175, R01 AI065841 and 5 M01
RR-00079. P. P. T. and N. d. V. were supported by European Community's
FP6 funding (Autocure). We acknowledge the help of C. Ellen van der
Schoot for healthy control samples for GENRA and the help of B. A. C.
Dijkmans, D. van Schaardenburg, A. S. Pena, P.L. Klarenbeek, Z. Zhang,
M. T. Nurmohammed, W. F. Lems, R. R. J. van de Stadt, W. H. Bos, J.
Ursum, M. G. M. Bartelds, D. M. Gerlag, M. G. H. van der Sande, C. A.
Wijbrandts and M. M. J. Herenius in gathering GENRA subject samples and
data. We thank Y. Li, S. Schrodi, and J. Sninsky (Celera); and B. Voight
and C. Cotsapas (Broad Institute) for comments on the manuscript.
NR 30
TC 337
Z9 342
U1 2
U2 18
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2008
VL 40
IS 10
BP 1216
EP 1223
DI 10.1038/ng.233
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 354PH
UT WOS:000259651000022
PM 18794853
ER
PT J
AU Wang, L
Wildt, KF
Zhu, JF
Zhang, XY
Feigenbaum, L
Tessarollo, L
Paul, WE
Fowlkes, BJ
Bosselut, R
AF Wang, Lie
Wildt, Kathryn F.
Zhu, Jinfang
Zhang, Xianyu
Feigenbaum, Lionel
Tessarollo, Lino
Paul, William E.
Fowlkes, B. J.
Bosselut, Remy
TI Distinct functions for the transcription factors GATA-3 and ThPOK during
intrathymic differentiation of CD4(+) T cells
SO NATURE IMMUNOLOGY
LA English
DT Article
ID CD4-CD8 LINEAGE DIFFERENTIATION; ZINC-FINGER PROTEINS; TRANSGENIC MICE;
THYMOCYTE DEVELOPMENT; POSITIVE SELECTION; ANTIGEN RECEPTOR; TH2 CELLS;
C-MYB; EXPRESSION; CD8
AB The transcription factors GATA-3 and ThPOK are required for intrathymic differentiation of CD4(+) T cells, but their precise functions in this process remain unclear. Here we show that, contrary to previous findings, Gata3 disruption blocked differentiation into the CD4(+) T cell lineage before commitment to the CD4(+) lineage and in some contexts permitted the 'redirection' of major histocompatibility complex class II-restricted thymocytes into the CD8(+) lineage. GATA-3 promoted ThPOK expression and bound to a region of the locus encoding ThPOK established as being critical for ThPOK expression. Finally, ThPOK promoted differentiation into the CD4(+) lineage in a way dependent on GATA-3 but inhibited differentiation into the CD8(+) lineage independently of GATA-3. We propose that GATA-3 acts as a specification factor for the CD4(+) lineage 'upstream' of the ThPOK-controlled CD4(+) commitment checkpoint.
C1 [Wang, Lie; Wildt, Kathryn F.; Bosselut, Remy] NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Zhu, Jinfang; Paul, William E.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Zhang, Xianyu; Fowlkes, B. J.] NIAID, Cellular & Mol Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Feigenbaum, Lionel] NCI, Sci Applicat Int Corp, Frederick, MD 21702 USA.
[Tessarollo, Lino] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
RP Bosselut, R (reprint author), NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM remy@helix.nih.gov
RI Zhu, Jinfang/B-7574-2012
FU Intramural Research Programs of the National Cancer Institute, Center
for Cancer Research; National Institute of Allergy and Infectious
Diseases, National Institutes of Health
FX We thank Y. Xiong, R. Jenkinson and J. Rozenberg for assistance with
ChIP assays; E. Southon for embryonic stem cell recombination; M.
Pellegrini and A. Nussenzweig for assistance with recombination-mediated
genetic engineering; E. Castro and G. Sanchez for mouse technical
assistance; B. Taylor and S. Banerjee for cell sorting; and A. Ge gonne
and A. Singer for reading the manuscript. Supported by the Intramural
Research Programs of the National Cancer Institute, Center for Cancer
Research, and of the National Institute of Allergy and Infectious
Diseases, National Institutes of Health.
NR 50
TC 99
Z9 103
U1 2
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD OCT
PY 2008
VL 9
IS 10
BP 1122
EP 1130
DI 10.1038/ni.1647
PG 9
WC Immunology
SC Immunology
GA 349XC
UT WOS:000259315600010
PM 18776904
ER
PT J
AU Cammarata, M
Levantino, M
Schotte, F
Anfinrud, PA
Ewald, F
Choi, J
Cupane, A
Wulff, M
Ihee, H
AF Cammarata, Marco
Levantino, Matteo
Schotte, Friedrich
Anfinrud, Philip A.
Ewald, Friederike
Choi, Jungkweon
Cupane, Antonio
Wulff, Michael
Ihee, Hyotcherl
TI Tracking the structural dynamics of proteins in solution using
time-resolved wide-angle X-ray scattering
SO NATURE METHODS
LA English
DT Article
ID QUATERNARY STRUCTURE; BIOLOGICAL MACROMOLECULES; CONFORMATIONAL-CHANGES;
LASER PHOTOLYSIS; CYTOCHROME-C; HEMOGLOBIN; ABSORPTION; CRYSTALLOGRAPHY;
SPECTROSCOPY; RESOLUTION
AB We demonstrate tracking of protein structural changes with time-resolved wide-angle X-ray scattering (TR-WAXS) with nanosecond time resolution. We investigated the tertiary and quaternary conformational changes of human hemoglobin under nearly physiological conditions triggered by laser-induced ligand photolysis. We also report data on optically induced tertiary relaxations of myoglobin and refolding of cytochrome c to illustrate the wide applicability of the technique. By providing insights into the structural dynamics of proteins functioning in their natural environment, TR-WAXS complements and extends results obtained with time-resolved optical spectroscopy and X-ray crystallography.
C1 [Cammarata, Marco; Ewald, Friederike; Wulff, Michael] European Synchrotron Radiat Facil, F-38043 Grenoble, France.
[Cammarata, Marco] Univ Copenhagen, Niels Bohr Inst, Ctr Mol Movies, DK-2100 Copenhagen, Denmark.
[Levantino, Matteo; Cupane, Antonio] Univ Palermo, Dept Phys & Astron Sci, I-90123 Palermo, Italy.
[Schotte, Friedrich; Anfinrud, Philip A.] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Choi, Jungkweon; Ihee, Hyotcherl] Korea Adv Inst Sci & Technol, Dept Chem BK21, Ctr Time Resolved Diffract, Taejon 305701, South Korea.
RP Cammarata, M (reprint author), European Synchrotron Radiat Facil, BP 220, F-38043 Grenoble, France.
EM marco.cammarata@esrf.eu; hyotcherl.ihee@kaist.ac.kr
RI Cammarata, Marco/C-2322-2008; Ihee, Hyotcherl/C-1614-2011; Cupane,
Antonio/B-7293-2012; Levantino, Matteo/C-2433-2008
OI Cammarata, Marco/0000-0003-3013-1186; Levantino,
Matteo/0000-0002-1224-4809
FU National Institutes of Health; EU [FP6-503641]; Ministry of Education,
Science and Technology; Korea Science and Engineering Foundation
FX We thank W. A. Eaton and E. Henry for helpful comments, H.-S. Cho and S.
Ahn for helpful discussions about the data analysis, and Y.O. Jung, K.H.
Kim and J.H. Lee for their assistance with sample preparation and
experiments. This research was supported in part by the Intramural
Research Program of the National Institutes of Health to P.A.A., by EU
grant FLASH: FP6-503641 to M.W., and a grant from the Creative Research
Initiatives (Center for Time-Resolved Diffraction) of the Ministry of
Education, Science and Technology, Korea Science and Engineering
Foundation to H.I.
NR 31
TC 132
Z9 133
U1 4
U2 47
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
J9 NAT METHODS
JI Nat. Methods
PD OCT
PY 2008
VL 5
IS 10
BP 881
EP 886
DI 10.1038/NMETH.1255
PG 6
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 354OY
UT WOS:000259650100014
PM 18806790
ER
PT J
AU Ito, I
Ong, RCY
Raman, B
Stopfer, M
AF Ito, Iori
Ong, Rose Chik-ying
Raman, Baranidharan
Stopfer, Mark
TI Sparse odor representation and olfactory learning
SO NATURE NEUROSCIENCE
LA English
DT Article
ID HONEYBEES APIS-MELLIFERA; DROSOPHILA ANTENNAL LOBE; MOTH MANDUCA-SEXTA;
MUSHROOM BODY; PROJECTION NEURONS; MEMORY; BODIES; OCTOPAMINE; REWARD;
BRAIN
AB Sensory systems create neural representations of environmental stimuli and these representations can be associated with other stimuli through learning. Are spike patterns the neural representations that get directly associated with reinforcement during conditioning? In the moth Manduca sexta, we found that odor presentations that support associative conditioning elicited only one or two spikes on the odor's onset (and sometimes offset) in each of a small fraction of Kenyon cells. Using associative conditioning procedures that effectively induced learning and varying the timing of reinforcement relative to spiking in Kenyon cells, we found that odor-elicited spiking in these cells ended well before the reinforcement was delivered. Furthermore, increasing the temporal overlap between spiking in Kenyon cells and reinforcement presentation actually reduced the efficacy of learning. Thus, spikes in Kenyon cells do not constitute the odor representation that coincides with reinforcement, and Hebbian spike timing-dependent plasticity in Kenyon cells alone cannot underlie this learning.
C1 [Ito, Iori; Ong, Rose Chik-ying; Raman, Baranidharan; Stopfer, Mark] NICHHD, US Natl Inst Hlth, Bethesda, MD 20982 USA.
[Ong, Rose Chik-ying] Chinese Univ Hong Kong, Dept Biochem, Shatin, Hong Kong, Peoples R China.
[Raman, Baranidharan] NIST, Chem Sci & Technol Lab, Gaithersburg, MD 20899 USA.
RP Stopfer, M (reprint author), NICHHD, US Natl Inst Hlth, Bldg 35,Room 3A-102, Bethesda, MD 20982 USA.
EM stopferm@mail.nih.gov
RI NAMEKAWA, IORI/A-3172-2009; Marion-Poll, Frederic/D-8882-2011
OI Marion-Poll, Frederic/0000-0001-6824-0180
FU Japan Society for the Promotion of Science [00169, 70510]; NIH-National
Institutes of Standards and Technology; National Research Council;
NIH-NICHD
FX We are grateful to members of the Stopfer laboratory for helpful
discussions. We especially thank K. Sun for her excellent animal care.
Micrographs were made at the Microscopy and Imaging Core (US National
Institute of Child Health and Development, NICHD) with the assistance of
V. Schram. We thank C. Wu in the Biometry and Mathematical Statistics
Branch, US National Institutes of Health (NIH)/NICHD for his advice on
the statistical analysis of the behavioral experiments. This work was
supported by grants from the Japan Society for the Promotion of Science
(00169, 70510) to I.I., a joint NIH-National Institutes of Standards and
Technology postdoctoral fellowship award by the National Research
Council to B. R. and an intramural grant from NIH-NICHD to M. S.
NR 43
TC 61
Z9 61
U1 1
U2 17
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD OCT
PY 2008
VL 11
IS 10
BP 1177
EP 1184
DI 10.1038/nn.2192
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 352WQ
UT WOS:000259528500015
PM 18794840
ER
PT J
AU Maier, A
Wilke, M
Aura, C
Zhu, C
Ye, FQ
Leopold, DA
AF Maier, Alexander
Wilke, Melanie
Aura, Christopher
Zhu, Charles
Ye, Frank Q.
Leopold, David A.
TI Divergence of fMRI and neural signals in V1 during perceptual
suppression in the awake monkey
SO NATURE NEUROSCIENCE
LA English
DT Article
ID PRIMARY VISUAL-CORTEX; LATERAL GENICULATE-NUCLEUS; RESONANCE-IMAGING
SIGNAL; BINOCULAR-RIVALRY; FLUCTUATIONS; MODULATION; ATTENTION;
AWARENESS; BRAIN; FLASH
AB The role of primary visual cortex (V1) in determining the contents of perception is controversial. Human functional magnetic resonance imaging (fMRI) studies of perceptual suppression have revealed a robust drop in V1 activity when a stimulus is subjectively invisible. In contrast, monkey single-unit recordings have failed to demonstrate such perception-locked changes in V1. To investigate the basis of this discrepancy, we measured both the blood oxygen level-dependent (BOLD) response and several electrophysiological signals in two behaving monkeys. We found that all signals were in good agreement during conventional stimulus presentation, showing strong visual modulation to presentation and removal of a stimulus. During perceptual suppression, however, only the BOLD response and the low-frequency local field potential (LFP) power showed decreases, whereas the spiking and high-frequency LFP power were unaffected. These results demonstrate that the coupling between the BOLD and electrophysiological signals in V1 is context dependent, with a marked dissociation occurring during perceptual suppression.
C1 [Maier, Alexander; Wilke, Melanie; Aura, Christopher; Leopold, David A.] NIMH, Unit Cognit Neurophysiol & Imaging, Neuropsychol Lab, Bethesda, MD 20892 USA.
NEI, Neurophysiol Imaging Facil, NIMH, NINDS,US Natl Inst Hlth,US Dept HHS, Bethesda, MD 20892 USA.
RP Maier, A (reprint author), NIMH, Unit Cognit Neurophysiol & Imaging, Neuropsychol Lab, 49 Convent Dr,B2J-45,MSC 4400, Bethesda, MD 20892 USA.
EM maiera@mail.nih.gov
RI Maier, Alexander/B-7489-2009;
OI Maier, Alexander/0000-0002-7250-502X; Leopold, David/0000-0002-1345-6360
FU National Institute of Mental Health; National Institute of Neurological
Disorders and Stroke; National Eye Institute
FX We would like to thank G. Dold, D. Ide, N. Nichols and T. Talbot, as
well as K. Smith, N. Phipps and J. Yu for technical assistance. We also
thank H. Merkle for extensive guidance on the design and fabrication of
radio frequency coils, R. Cox for assistance with magnetic resonance
image alignment, D. Sheinberg for help with the stimulus software, K.
King and C. Brewer for auditory testing and ear plug manufacture, W.
Vinje for help with the multi- contact electrodes, K. Tanji, A.H. Bell
and Z. Saad for help with the fMRI analysis, and S. Guderian, M. Schmid
and K.- M. Mueller for discussions. This work was supported by the
Intramural Research Programs of the National Institute of Mental Health,
the National Institute of Neurological Disorders and Stroke and the
National Eye Institute.
NR 40
TC 155
Z9 156
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD OCT
PY 2008
VL 11
IS 10
BP 1193
EP 1200
DI 10.1038/nn.2173
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 352WQ
UT WOS:000259528500017
PM 18711393
ER
PT J
AU Rivera, J
Proia, RL
Olivera, A
AF Rivera, Juan
Proia, Richard L.
Olivera, Ana
TI The alliance of sphingosine-1-phosphate and its receptors in immunity
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Review
ID PROTEIN-COUPLED RECEPTOR; SPHINGOSINE 1-PHOSPHATE RECEPTOR; NONOBESE
DIABETIC MICE; T-CELL PROLIFERATION; TRAFFICKING IN-VIVO; ZONE B-CELLS;
MAST-CELL; LYMPHOCYTE EGRESS; DENDRITIC CELLS; IMMUNOMODULATOR FTY720
AB Sphingosine-1-phosphate (S1P) is a biologically active metabolite of plasma-membrane sphingolipids that is essential for immune-cell trafficking. Its concentration is increased in many inflammatory conditions, such as asthma and autoimmunity. Much of the immune function of S1P results from the engagement of a family of G-protein-coupled receptors (S1PR1-S1PR5). Recent findings on the role of S1P in immunosurveillance, the discovery of regulatory mechanisms in S1P-mediated immune-cell trafficking and new advances in understanding the mechanism by which S1P affects immune-cell function indicate that the alliance between S1P and its receptors has a fundamental role in immunity.
C1 [Rivera, Juan; Olivera, Ana] NIAMSD, Lab Immune Cell Signaling, Bethesda, MD 20892 USA.
[Proia, Richard L.] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Rivera, J (reprint author), NIAMSD, Lab Immune Cell Signaling, Bethesda, MD 20892 USA.
EM juan.rivera@nih.gov
RI Proia, Richard/A-7908-2012
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases
(NIAMS); National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK); National Institutes of Health, USA
FX Our work is supported by the intramural research programmes of the
National Institute of Arthritis and Musculoskeletal and Skin Diseases
(NIAMS) and the National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK), National Institutes of Health, USA. We apologize to
those authors whose work we could not cite owing to space constraints.
NR 105
TC 297
Z9 302
U1 2
U2 21
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1733
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD OCT
PY 2008
VL 8
IS 10
BP 753
EP 763
DI 10.1038/nri2400
PG 11
WC Immunology
SC Immunology
GA 352WR
UT WOS:000259528600009
PM 18787560
ER
PT J
AU Singer, A
Adoro, S
Park, JH
AF Singer, Alfred
Adoro, Stanley
Park, Jung-Hyun
TI Lineage fate and intense debate: myths, models and mechanisms of
CD4-versus CD8-lineage choice
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Review
ID T-CELL DEVELOPMENT; CD4 GENE-EXPRESSION; POSITIVELY SELECTED THYMOCYTES;
CHROMATIN REMODELER MI-2-BETA; TRANSCRIPTION FACTOR GATA-3; NEGATIVE
SELECTION; TRANSGENIC MICE; TYROSINE KINASE; HMG-BOX; DIFFERENTIAL
REQUIREMENTS
AB Following successful gene rearrangement at alpha beta T-cell receptor (TCR) loci, developing thymocytes express both CD4 and CD8 co-receptors and undergo a life-or-death selection event, which is known as positive selection, to identify cells that express TCRs with potentially useful ligand specificities. Positively selected thymocytes must then differentiate into either CD4(+) helper T cells or CD8(+) cytotoxic T cells, a crucial decision known as CD4/CD8-lineage choice. In this Review, we summarize recent advances in our understanding of the cellular and molecular events involved in lineage-fate decision and discuss them in the context of the major models of CD4/CD8-lineage choice.
C1 [Singer, Alfred; Adoro, Stanley; Park, Jung-Hyun] NCI, Expt Immunol Branch, Bethesda, MD 20892 USA.
RP Singer, A (reprint author), NCI, Expt Immunol Branch, Bldg 10, Bethesda, MD 20892 USA.
EM singera@mail.nih.gov
FU US National Institutes of Health; National Cancer Institute; Center for
Cancer Research, USA
FX We thank our many colleagues who contributed to our current
understanding of CD4/CD8 lineage-fate decisions in the thymus that we
were unable to adequately acknowledge and reference in this Review. We
are grateful to B. Erman, S. Sarafova, R. Bosselut and N. Taylor for
many discussions and for their critical reading of the manuscript. This
research was supported by the Intramural Research Program of the US
National Institutes of Health, National Cancer Institute, Center for
Cancer Research, USA.
NR 117
TC 202
Z9 203
U1 2
U2 18
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1733
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD OCT
PY 2008
VL 8
IS 10
BP 788
EP 801
DI 10.1038/nri2416
PG 14
WC Immunology
SC Immunology
GA 352WR
UT WOS:000259528600012
PM 18802443
ER
PT J
AU Mehta, GU
Shively, SB
Duong, H
Tran, M
Moncrief, TJ
Smith, JH
Li, J
Edwards, NA
Lonser, RL
Zhuang, Z
Merrill, MJ
Raffeld, M
Maxwell, P
Oldfield, EH
Vortmeyer, AO
AF Mehta, Gautam U.
Shively, Sharon B.
Duong, Heng
tran, maxine
Moncrief, Travis J.
Smith, Jonathan H.
Li, Jie
Edwards, Nancy A.
Lonser, Russell L.
Zhuang, Zhengping
Merrill, Marsha J.
Raffeld, Mark
Maxwell, Patrick
Oldfield, Edward H.
Vortmeyer, Alexander O.
TI Progression of epididymal maldevelopment into hamartoma-like neoplasia
in VHL disease
SO NEOPLASIA
LA English
DT Article
ID TUMOR-SUPPRESSOR PROTEIN; HYPOXIA-INDUCIBLE FACTORS; HIPPEL-LINDAU
PROTEIN; FACTORS HIF-1-ALPHA; GENE; EXPRESSION; DEFICIENCY; BINDING;
HIF-2-ALPHA; CARCINOMA
AB Inactivation of the von Hippel-Lindau (VHL) gene and activation of the hypoxia-inducible factor (HIF) in susceptible cells precedes formation of tumorlets and frank tumor in the epididymis of male VHL patients. We performed detailed histologic and molecular pathologic analysis of tumor-free epididymal tissues from VHL patients to obtain further insight into early epididymal tumorigenesis. Four epididymides from two VHL patients were serially sectioned to allow for three-dimensional visualization of morphologic changes. Areas of interest were genetically analyzed by tissue microdissection, immunohistochemistry for HIF and markers for mesonephric differentiation, and in situ hybridization for HIF downstream target vascular endothelial growth factor. Structural analysis of the epididymides revealed marked deviations from the regular anatomic structure resulting from impaired organogenesis. Selected efferent ductules were represented by disorganized mesonephric cells, and the maldeveloped mesonephric material was VHL-deficient by allelic deletion analysis. Furthermore, we observed maldeveloped mesonephric material near cystic structures, which were also VHL-deficient and were apparent derivatives of maldeveloped material. Finally, a subset of VHL-deficient cells was structurally integrated in regular efferent ductules; proliferation of intraductular VHL-deficient cells manifests itself as papillary growth into the ductular lumen. Furthermore, we clarify that that there is a pathogenetic continuum between microscopic tumorlets and formation of tumor. In multiple locations, three-dimensional reconstruction revealed papillary growth to extend deeply into ductular lumina, indicative of progression into early hamartoma-like neoplasia. We conclude epididymal tumorigenesis in VHL disease to occur in two distinct sequential steps: maldevelopment of VHL-deficient mesonephric cells, followed by neoplastic papillary proliferation.
C1 [Vortmeyer, Alexander O.] Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Vortmeyer, AO (reprint author), Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, 10 Ctr Dr,Room 5D37, Bethesda, MD 20892 USA.
EM alexander.vortmeyer@yale.edu
RI Maxwell, Patrick/C-5557-2008;
OI Maxwell, Patrick/0000-0002-0338-2679; Mehta, Gautam/0000-0002-8009-6430
FU National Institute of Neurological Disorders and Stroke; National
Institutes of Health; Cancer Research, UK; Medical Research Council;
Charitable foundation of Guy's and St Thomas' Hospitals, London
FX This work was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke, National
Institutes of Health; by Cancer Research, UK; the Medical Research
Council; and by the Charitable foundation of Guy's and St Thomas'
Hospitals, London. Sharon B. Shively is a doctoral student in the
Molecular and Cellular Oncology Program of the Institute for Biomedical
Sciences at George Washington University. This work is from a
dissertation to be presented at George Washington University in partial
fulfillment of the requirements for the Ph.D. degree.
NR 31
TC 12
Z9 14
U1 0
U2 1
PU NEOPLASIA PRESS
PI ANN ARBOR
PA 1150 W MEDICAL CENTER DR, MSRB III, RM 9303, ANN ARBOR, MI 48109-0648
USA
SN 1522-8002
J9 NEOPLASIA
JI Neoplasia
PD OCT
PY 2008
VL 10
IS 10
BP 1146
EP 1153
DI 10.1593/neo.08476
PG 8
WC Oncology
SC Oncology
GA 348AY
UT WOS:000259184400013
PM 18813354
ER
PT J
AU Rajaraman, P
Hutchinson, A
Rothman, N
Black, PM
Fine, HA
Loeffler, JS
Selker, RG
Shapiro, WR
Linet, MS
Inskip, PD
AF Rajaraman, Preetha
Hutchinson, Amy
Rothman, Nathaniel
Black, Peter M.
Fine, Howard A.
Loeffler, Jay S.
Selker, Robert G.
Shapiro, William R.
Linet, Martha S.
Inskip, Peter D.
TI Oxidative response gene polymorphisms and risk of adult brain tumors
SO NEURO-ONCOLOGY
LA English
DT Article
DE acoustic neuroma; brain; case-control; glioma; meningioma; neoplasm;
oxidative response; polymorphism; tumor
ID MANGANESE SUPEROXIDE-DISMUTASE; BREAST-CANCER RISK; PROSTATE-CANCER;
GLUTATHIONE-PEROXIDASE; ANTIOXIDANT ENZYMES; OVARIAN-CANCER; STRESS
GENES; MNSOD; CATALASE; ASSOCIATIONS
AB Oxidative stress is believed to play a key role in tumor formation. Although this mechanism could be especially pertinent for brain tumors given the high oxygen consumption of the brain, very little has been published regarding brain tumor risk with respect to genes mediating oxidative stress. Using data from non-Hispanic whites in a hospital-based case-control study conducted by the National Cancer Institute between 1994 and 1998, we evaluated risk of glioma (n = 362), meningioma (n = 134), and acoustic neuroma (n = 69) compared to noncancer controls (n = 494) with respect to nine single nucleotide polymorphisms from seven genes involved in oxidative stress response (CAT, GPX1, NOS3, PON1, SOD1, SOD2, and SOD3). We observed increased risk of glioma (odds ratio [OR](CT/CC) = 1.3; 95% confidence interval [95% CI], 1.0-1.7) and meningioma (OR(CT/CC) = 1.7; 95% CI, 1.1-2.7) with the C variant of SOD3 rs699473. There was also indication of increased acoustic neuroma risk with the SOD2 rs4880 Ala variant (OR(CT/CC) = 2.0; 95% CI, 1.0-4.2) and decreased acoustic neuroma risk with the CAT rs1001179 T allele variant (OR(CT/TT) = 0.6; 95% CI, 0.3-1.0). These relationships persisted when major groups of disease controls were excluded from the analysis. Our results suggest that common variants in the SOD2, SOD3, and CAT genes may influence brain tumor risk. Neuro-Oncology 10, 709-715, 2008 (Posted to Neuro-Oncology [serial online], Doc. 08-00008, August 4, 2008. URL http://neuro-oncology.dukejournals.org; DOI: 10.1215/15228517-2008-037)
C1 [Rajaraman, Preetha; Rothman, Nathaniel; Linet, Martha S.; Inskip, Peter D.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Fine, Howard A.] NCI, Neurooncol Branch, NIH, DHHS, Bethesda, MD 20892 USA.
[Hutchinson, Amy] NCI, Core Genotyping Facil, Div Canc Epidemiol & Genet, Adv Technol Program,SAIC Frederick Inc, Frederick, MD USA.
[Black, Peter M.] Brigham & Womens Hosp, Dept Neurosurg, Boston, MA 02115 USA.
[Loeffler, Jay S.] Massachusetts Gen Hosp, Ctr Canc, Dept Radiat Oncol, Boston, MA USA.
[Selker, Robert G.] Western Penn Hosp, Div Neurosurg, Pittsburgh, PA 15224 USA.
[Shapiro, William R.] St Josef Hosp & Med Ctr, Barrow Neurol Inst, Phoenix, AZ USA.
RP Rajaraman, P (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Execut Blvd,EPS Room 7085, Bethesda, MD 20892 USA.
EM rajarama@mail.nih.gov
FU National Cancer Institute; National Institutes of Health [N01-CO-12400];
Department of Health and Human Services
FX This research was supported by Intramural funds from the National Cancer
Institute, National Institutes of Health, Department of Health and Human
Services. This project has been funded in whole or in part with federal
fund from the National Cancer Institute, National Institutes of Health,
under contract N01-CO-12400. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. government.
NR 34
TC 48
Z9 49
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 709
EP 715
DI 10.1215/15228517-2008-037
PG 7
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500007
PM 18682580
ER
PT J
AU Bradley, KA
Pollack, IF
Reid, JM
Adamson, PC
Ames, MM
Vezina, G
Blaney, S
Ivy, P
Zhou, T
Krallo, M
Reaman, G
Mehta, MP
AF Bradley, Kristin A.
Pollack, Ian F.
Reid, Joel M.
Adamson, Peter C.
Ames, Matthew M.
Vezina, Gilbert
Blaney, Susan
Ivy, Percy
Zhou, Tianni
Krallo, Mark
Reaman, Gregory
Mehta, Minesh P.
TI Motexafin gadolinium and involved field radiation therapy for intrinsic
pontine glioma of childhood: A Children's Oncology Group phase I study
SO NEURO-ONCOLOGY
LA English
DT Article
DE motexafin gadolinium; pontine glioma; radiation therapy
ID BRAIN-STEM GLIOMAS; HYPERFRACTIONATED RADIOTHERAPY;
GLIOBLASTOMA-MULTIFORME; RANDOMIZED-TRIAL; I/II TRIAL; METASTASES;
TUMORS; RADIOSENSITIZER; CARBOPLATIN; TOPOTECAN
AB The purpose of this study was to determine the dose-limiting toxicities, maximum tolerated dose, pharmacokinetics, and intratumor and brain distribution of motexafin gadolinium (MGd) with involved field radiation therapy in children with newly diagnosed intrinsic pontine gliomas. MGd was administered as a 5-min intravenous bolus 2-5 h prior to standard radiation. The starting dose was 1.7 mg/kg. After first establishing that 5 doses/week for 6 weeks was tolerable, the dose of MGd was escalated until dose-limiting toxicity was reached. Radiation therapy was administered to 54 Gy in 30 once-daily fractions. Forty-four children received MGd at doses of 1.7 to 9.2 mg/kg daily prior to radiation therapy for 6 weeks. The maximum tolerated dose was 4.4 mg/kg. The primary dose-limiting toxicities were grade 3 and 4 hypertension and elevations in serum transaminases. Median elimination half-life and clearance values were 6.6 h and 25.4 ml/kg/h, respectively. The estimated median survival was 313 days (95% confidence interval, 248-389 days). The maximum tolerated dose of MGd and the recommended phase II dose was 4.4 mg/kg when administered as a daily intravenous bolus in conjunction with 6 weeks of involved field radiation therapy for pediatric intrinsic pontine gliomas. Neuro-Oncology 10, 752-758, 2008 (Posted to Neuro-Oncology [serial online], Doc. D07-00206, August 20, 2008. URL http://neuro-oncology.dukejournals.org; DOI: 10.1215/15228517-2008-043)
C1 [Bradley, Kristin A.; Mehta, Minesh P.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
[Pollack, Ian F.] Univ Pittsburgh, Pittsburgh, PA USA.
[Reid, Joel M.; Ames, Matthew M.] Mayo Clin, Rochester, MN USA.
[Adamson, Peter C.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Vezina, Gilbert] Childrens Natl Med Ctr DC, Washington, DC USA.
[Blaney, Susan] Baylor Coll Med, Texas Childrens Canc Ctr, Houston, TX 77030 USA.
[Ivy, Percy] NCI, Investigat Drug Branch, CTEP, Bethesda, MD USA.
[Zhou, Tianni] Operat Ctr, Childrens Oncol Grp, Arcadia, CA USA.
[Krallo, Mark] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Reaman, Gregory] Chairs Off, Childrens Oncol Grp, Bethesda, MD USA.
RP Mehta, MP (reprint author), Univ Wisconsin, Sch Med & Publ Hlth, Dept Human Oncol, Univ Hosp & Clin, 600 Highland Ave,K4 B100 Radiotherapy, Madison, WI 53792 USA.
EM mehta@humonc.wisc.edu
OI mehta, minesh/0000-0002-4812-5713
FU COG [CA 98543, CA 97452]
FX This research was supported by COG grant CA 98543 and COG Phase I CA
97452. A complete listing of grant support for research conducted by the
Children's Cancer Group and Pediatric Oncology Group before initiation
of the COG grant in 2003 is available online at:
http://www.Childrensoncologygroup.org/admin/grantinfo.htm.
NR 30
TC 24
Z9 24
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 752
EP 758
DI 10.1215/15228517-2008-043
PG 7
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500012
PM 18715950
ER
PT J
AU Joy, A
Smirnov, I
Nakada, M
Rennert, J
Yeh, RF
Beaudry, C
Zenklusen, J
Fine, H
Berens, M
Feuerstein, B
AF Joy, Anna
Smirnov, Ivan
Nakada, Mitsitoshi
Rennert, Jessica
Yeh, Ru-Fang
Beaudry, Christian
Zenklusen, Jean
Fine, Howard
Berens, Michael
Feuerstein, Burt
TI AKT1 AND AKT2 MEDIATE MALIGNANT FUNCTION IN GBM
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Joy, Anna; Feuerstein, Burt] St Josephs Hosp, Phoenix, AZ USA.
[Nakada, Mitsitoshi; Rennert, Jessica; Beaudry, Christian; Berens, Michael] Translat Genom Res Inst, Phoenix, AZ USA.
[Yeh, Ru-Fang] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Zenklusen, Jean; Fine, Howard] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 775
EP 775
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500071
ER
PT J
AU Mccarthy, B
Aldape, K
Bondy, M
Butler, M
Inskip, P
Ruder, A
Wrensch, M
Davis, F
AF Mccarthy, Bridget
Aldape, Kenneth
Bondy, Melissa
Butler, Maryann
Inskip, Peter
Ruder, Avima
Wrensch, Margaret
Davis, Faith
TI A COLLABORATIVE STUDY OF THE EPIDEMIOLOGY OF OLIGODENDROGLIAL TUMORS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Mccarthy, Bridget; Davis, Faith] Univ Illinois, Chicago, IL USA.
[Aldape, Kenneth; Bondy, Melissa] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Butler, Maryann; Ruder, Avima] NIOSH, Cincinnati, OH 45226 USA.
[Inskip, Peter] NCI, NIH, Bethesda, MD 20892 USA.
[Wrensch, Margaret] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RI Ruder, Avima/I-4155-2012
OI Ruder, Avima/0000-0003-0419-6664
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 779
EP 779
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500086
ER
PT J
AU Kuhn, J
Robins, I
Mehta, M
Fine, H
Cloughesy, T
Wen, P
Chang, S
Deangelis, L
Lieberman, F
Reardon, D
Abrey, L
Lassman, A
Aldape, K
Yung, WKA
Dancey, J
Lamborn, K
Prados, M
AF Kuhn, John
Robins, Ian
Mehta, Minesh
Fine, Howard
Cloughesy, Timothy
Wen, Patrick
Chang, Susan
Deangelis, Lisa
Lieberman, Frank
Reardon, David
Abrey, Lauren
Lassman, Andrew
Aldape, Kenneth
Yung, W. K. Alfred
Dancey, Janet
Lamborn, Kathleen
Prados, Michael
TI TUMOR SEQUESTRATION OF LAPATINIB (NABTC 04-01)
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Kuhn, John] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Robins, Ian; Mehta, Minesh] Univ Wisconsin, Madison, WI USA.
[Fine, Howard] NIH, Bethesda, MD 20892 USA.
[Cloughesy, Timothy] Univ Calif Los Angeles, Los Angeles, CA USA.
[Chang, Susan] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Deangelis, Lisa] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Lieberman, Frank] Univ Pittsburgh, Pittsburgh, PA USA.
[Aldape, Kenneth; Yung, W. K. Alfred] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Dancey, Janet] NCI, Bethesda, MD 20892 USA.
NR 0
TC 8
Z9 8
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 783
EP 783
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500099
ER
PT J
AU Kreisl, T
Kim, L
Heinrich, E
Royce, C
Stroud, I
Nancy, G
Albert, P
Musily, L
Thornton, DE
Fine, H
AF Kreisl, Teri
Kim, Lyndon
Heinrich, Elinzano
Royce, Cheryl
Stroud, Irene
Nancy, Garren
Albert, Paul
Musily, Luna
Thornton, Donald E.
Fine, Howard
TI A PHASE I TRIAL OF ENZASTAURIN (LY317615) IN PATIENTS WITH RECURRENT
GLIOMAS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Kreisl, Teri; Kim, Lyndon; Albert, Paul] NIH, Bethesda, MD 20892 USA.
[Musily, Luna] Eli Lilly & Co, Biopharm, Indianapolis, IN 46285 USA.
[Thornton, Donald E.] Eli Lilly & Co, Oncol, Indianapolis, IN 46285 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 786
EP 786
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500110
ER
PT J
AU Duncan, C
Leary, R
Cummins, J
Di, CH
Wang, TL
Bigner, D
Kopelovich, L
Vogelstein, B
Velculescu, V
Yan, H
AF Duncan, Chris
Leary, Rebecca
Cummins, Jordan
Di, Chunhui
Wang, Tian-Li
Bigner, Darell
Kopelovich, Levy
Vogelstein, Bert
Velculescu, Victor
Yan, Hai
TI IDENTIFICATION OF MICROBIAL DNAS IN BRAIN TUMORS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Duncan, Chris; Di, Chunhui; Bigner, Darell; Yan, Hai] Duke Univ, Durham, NC USA.
[Leary, Rebecca; Cummins, Jordan; Wang, Tian-Li; Vogelstein, Bert; Velculescu, Victor] Johns Hopkins Univ, Baltimore, MD USA.
[Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 800
EP 800
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500159
ER
PT J
AU Gaur, A
Colburn, N
Israel, M
AF Gaur, Arti
Colburn, Nancy
Israel, Mark
TI MICRORNA-21 INHIBITION OF PROGRAMMED CELL DEATH4 (PDCD4) ENABLES
GLIOBLASTOMA MULTIFORME PROGRESSION
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Gaur, Arti; Israel, Mark] Norris Cotton Canc Ctr, Dartmouth Med Sch, Lebanon, NH USA.
[Colburn, Nancy] NCI, Lab Canc Prevent, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 806
EP 807
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500183
ER
PT J
AU Lassman, A
Wang, M
Gilbert, M
Aldape, K
Wright, J
Wagner, H
Brachman, D
Malkin, M
Mehta, M
AF Lassman, Andrew
Wang, Meihua
Gilbert, Mark
Aldape, Kenneth
Wright, John
Wagner, Henry
Brachman, David
Malkin, Mark
Mehta, Minesh
TI PHASE II TRIAL OF DASATINIB FOR RECURRENT GLIOBLASTOMA (RTOG 0627)
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Lassman, Andrew] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Aldape, Kenneth] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Wright, John] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Wagner, Henry] Penn State Univ, Hershey, PA USA.
[Malkin, Mark] Med Coll Wisconsin, Milwaukee, WI USA.
[Mehta, Minesh] Univ Wisconsin, Madison, WI USA.
NR 0
TC 3
Z9 3
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 824
EP 824
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500246
ER
PT J
AU Wen, P
Kuhn, J
Chang, S
Lamborn, K
Robbins, H
Cloughesy, T
Lieberman, F
Mehra, M
Gilbert, M
Cooper, J
Drappatz, J
Kesari, S
Norden, A
Groves, M
Aldape, K
Yung, WKA
Dancey, J
Prados, M
AF Wen, Patrick
Kuhn, John
Chang, Susan
Lamborn, Kathleen
Robbins, Hi
Cloughesy, Timothy
Lieberman, Frank
Mehra, Minesh
Gilbert, Mark
Cooper, Josh
Drappatz, Jan
Kesari, Santosh
Norden, Andrew
Groves, Morris
Aldape, Kenneth
Yung, W. K. Alfred
Dancey, Janet
Prados, Michael
TI PHASE I/II STUDY OF ERLOTINIB AND TEMSIROLIMUS (CCI-779) FOR PATIENTS
WITH RECURRENT MALIGNANT GLIOMAS (NABTC 04-02)
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Wen, Patrick] Ctr Neurooncol, Boston, MA USA.
[Kuhn, John] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Chang, Susan; Lamborn, Kathleen; Prados, Michael] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Robbins, Hi] Univ Wisconsin, Madison, WI 53706 USA.
[Cloughesy, Timothy] Univ Calif Los Angeles, Los Angeles, CA USA.
[Lieberman, Frank] Univ Pittsburgh, Pittsburgh, PA USA.
[Mehra, Minesh] Univ Wisconsin, Madison, WI USA.
[Drappatz, Jan] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Groves, Morris; Aldape, Kenneth; Yung, W. K. Alfred] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Dancey, Janet] NCI, Bethesda, MD 20892 USA.
RI Kesari, Santosh/E-8461-2013
NR 0
TC 2
Z9 2
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 824
EP 824
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500245
ER
PT J
AU Puduvalli, VK
Wick, W
Chamberlain, M
Carpentier, A
Cher, L
Mason, W
Van Den Bent, M
Hong, S
Thornton, DE
Fine, H
AF Puduvalli, Vinay K.
Wick, Wolfgang
Chamberlain, Marc
Carpentier, Antoine
Cher, Lawrence
Mason, Warren
Van Den Bent, Martin
Hong, Sam
Thornton, Donald E.
Fine, Howard
TI ENZASTAURIN VERSUS LOMUSTINE IN THE TREATMENT OF RECURRENT, INTRACRANIAL
GLIOBLASTOMA: A PHASE III STUDY
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Puduvalli, Vinay K.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Wick, Wolfgang] Univ Heidelberg, Heidelberg, Germany.
[Chamberlain, Marc] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Carpentier, Antoine] Hop La Pitie Salpetriere, Serv Neurol Mazarin, Paris, France.
[Mason, Warren] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Van Den Bent, Martin] Erasmus Canc Ctr, Rotterdam, Netherlands.
[Thornton, Donald E.] Eli Lilly & Co, Oncol, Indianapolis, IN 46285 USA.
[Fine, Howard] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 825
EP 825
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500251
ER
PT J
AU Kreisl, T
Burman, JA
Albert, P
Kim, L
Moore, K
Fine, H
AF Kreisl, Teri
Burman, John A.
Albert, Paul
Kim, Lyndon
Moore, Kraig
Fine, Howard
TI A PHASE II TRIAL OF VANDETANIB FOR PATIENTS WITH RECURRENT GLIOBLASTOMA
MULTIFORME
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Kreisl, Teri; Burman, John A.; Albert, Paul; Kim, Lyndon] NIH, Bethesda, MD 20892 USA.
[Fine, Howard] NCI, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 827
EP 827
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500256
ER
PT J
AU Warren, K
Goldman, S
Stewart, C
Jakacki, R
Fangusaro, J
Schaiquevich, P
Boyett, J
Kun, L
AF Warren, Katherine
Goldman, Stewart
Stewart, Clinton
Jakacki, Regina
Fangusaro, Jason
Schaiquevich, Paula
Boyett, James
Kun, Larry
TI PHASE I TRIAL OF CC-5013 (LENALIDOMIDE) IN PEDIATRIC PATIENTS WITH
RECURRENT OR REFRACTORY PRIMARY CNS TUMORS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Warren, Katherine] NIH, Bethesda, MD 20892 USA.
[Jakacki, Regina] Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA.
[Fangusaro, Jason] Northwestern Univ, Chicago, IL 60611 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 835
EP 836
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500286
ER
PT J
AU Grossman, S
Ye, XB
Chamberlain, M
Mikkelsen, T
Batchelor, T
Desideri, S
Piantadosi, S
Fine, H
AF Grossman, Stuart
Ye, Xiaobu
Chamberlain, Marc
Mikkelsen, Tom
Batchelor, Tracy
Desideri, Serena
Piantadosi, Steven
Fine, Howard
TI EIGHTEEN-MONTH SURVIVAL RESULTS FROM A MULTICENTER PHASE II TRIAL OF
TALAMPANEL IN CONJUNCTION WITH STANDARD RADIATION AND TEMOZOLOMIDE IN
PATIENTS WITH NEWLY DIAGNOSED GLIOBLASTOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Grossman, Stuart; Ye, Xiaobu; Desideri, Serena; Piantadosi, Steven] Johns Hopkins Univ, Baltimore, MD USA.
[Fine, Howard] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 837
EP 837
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500292
ER
PT J
AU Rahrmann, E
Keng, V
Dupuy, A
Tessarollo, L
Jenkins, N
Copeland, N
Largaespada, D
AF Rahrmann, Eric
Keng, Vincent
Dupuy, Adam
Tessarollo, Lino
Jenkins, Nancy
Copeland, Neal
Largaespada, David
TI A MURINE INSERTIONAL MUTAGENESIS SCREEN TO IDENTIFY ONCOGENES AND TUMOR
SUPPRESSOR GENES INVOLVED IN GLIAL TUMOR INITIATION AND PROGRESSION
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Rahrmann, Eric; Keng, Vincent; Largaespada, David] Univ Minnesota, Minneapolis, MN USA.
[Dupuy, Adam] Univ Iowa, Iowa City, IA USA.
[Tessarollo, Lino] Natl Canc Inst, Frederick, MD USA.
[Copeland, Neal] Inst Mol & Cellular Biol, Singapore, Singapore.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 846
EP 847
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500325
ER
PT J
AU Lai, JS
Gershon, R
Blitz, D
Magasi, S
Nowinski, C
Reuben, D
Rymer, W
Weintraub, S
Wagster, M
AF Lai, Jin-Shei
Gershon, Richard
Blitz, David
Magasi, Susan
Nowinski, Cindy
Reuben, David
Rymer, William
Weintraub, Sandra
Wagster, Molly
TI THE NIH TOOLBOX: A NEW ASSESSMENT TOOL FOR MEASURING NEUROLOGICAL AND
BEHAVIORAL FUNCTION
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Lai, Jin-Shei] Evanston NW Healthcare, Ctr Outcomes Res & Educ, Evanston, IL USA.
[Lai, Jin-Shei] Northwestern Univ, Evanston, IL USA.
[Reuben, David] Univ Calif Los Angeles, Los Angeles, CA USA.
[Rymer, William; Weintraub, Sandra] Northwestern Univ, Chicago, IL 60611 USA.
[Wagster, Molly] NIA, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 874
EP 875
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500427
ER
PT J
AU Zach, L
Ning, H
Ondos, J
Arora, B
Smith, S
Miller, RW
Citrin, D
Camphausen, K
AF Zach, Leor
Ning, Holly
Ondos, John
Arora, Barbara
Smith, Sharon
Miller, Robert William
Citrin, Deborah
Camphausen, Kevin
TI A DOSIMETRIC COMPARISON OF FOUR TREATMENT PLANNING METHODS FOR
HIGH-GRADE GLIOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Zach, Leor] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 883
EP 884
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500458
ER
PT J
AU Neuwelt, E
Raslan, A
Gahramanov, S
Jacobs, P
Haluska, M
Njus, J
Rooney, W
Hamilton, B
Nesbit, G
AF Neuwelt, Edward
Raslan, Ahmed
Gahramanov, Seymur
Jacobs, Paula
Haluska, Marianne
Njus, Jeff
Rooney, William
Hamilton, Bronwyn
Nesbit, Gary
TI DSC-MRI USING FERUMOXYTOL MAY HELP DIFFERENTIATE PSEUDOPROGRESSION FROM
TRUE PROGRESSION IN PATIENTS WITH GLIOBLASTOMA. A PRELIMINARY REPORT
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)
CY NOV 20-23, 2008
CL Las Vegas, NV
SP Soc Neuro Oncol
C1 [Neuwelt, Edward; Raslan, Ahmed; Gahramanov, Seymur; Haluska, Marianne; Njus, Jeff; Rooney, William; Hamilton, Bronwyn; Nesbit, Gary] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Jacobs, Paula] NCI, Canc Imaging Program, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 2
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2008
VL 10
IS 5
BP 894
EP 894
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 357NX
UT WOS:000259854500494
ER
PT J
AU Petrovitch, H
Ross, GW
He, QM
Uyehara-Lock, J
Markesbery, W
Davis, D
Nelson, J
Masaki, K
Launer, L
White, LR
AF Petrovitch, Helen
Ross, G. Webster
He, Qimei
Uyehara-Lock, Jane
Markesbery, William
Davis, Daron
Nelson, James
Masaki, Kamal
Launer, Lenore
White, Lon R.
TI Characterization of Japanese-American men with a single neocortical AD
lesion type
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Alzheimer's disease; neocortical neuritic plaques; neocortical
neurofibrillary tangles; braak stage; apolipoprolein epsilon E4;
cerebral amyloid angiopathy
ID CEREBRAL AMYLOID ANGIOPATHY; MILD COGNITIVE IMPAIRMENT;
ALZHEIMERS-DISEASE; NEUROFIBRILLARY TANGLES; APOLIPOPROTEIN-E;
SENILE-DEMENTIA; RISK-FACTORS; NEURITIC PLAQUES; EDUCATION; PATHOLOGY
AB Neocortical neuritic plaques (NP) and neurofibrillary tangles (NFT) are hallmarks of Alzheimer's disease (AD) and usually, both are present. could represent in early phase of the AD process. If so, such individuals with only one neocortical AD lesion type. These AD. We compared frequency of apolipoprotein epsilon E4 (APOE4) allele, average Braak stage, and burden of'cerebral ainyloid angiopathy (CAA) among the two single lesion type groups, a group without AD lesions, and groups with high and low frequencies of both AD lesions. Single AD lesion groups shared only the characteristics associated with their unique lesion type with the combined AD lesion group and did not have higher prevalence of dementia than the no AD lesion group. Only the NP + NFT group showed a "close-response-relationship with greater probability of dementia with higher neocortical of either AD lesion. The single neocortical AD lesion groups do not appear to represent early AD. (C) 2007 Elsevier Inc. All rights reserved.
C1 [Petrovitch, Helen; Ross, G. Webster; He, Qimei; Uyehara-Lock, Jane; Nelson, James; Masaki, Kamal; White, Lon R.] Pacific Hlth Res Inst, Honolulu, HI 96813 USA.
[Petrovitch, Helen; Ross, G. Webster; He, Qimei; White, Lon R.] Spark M Matsunaga Med & Reg Off Ctr, Honolulu Dept Vet Affairs, Honolulu, HI 96819 USA.
[Petrovitch, Helen; Ross, G. Webster; He, Qimei; Uyehara-Lock, Jane; Nelson, James; Masaki, Kamal; White, Lon R.] Kuakini Med Ctr, Honolulu Asia Aging Study, Honolulu, HI 96817 USA.
[Petrovitch, Helen; Ross, G. Webster] Univ Hawaii, John A Burns Sch Med, Dept Med, Honolulu, HI 96822 USA.
[Petrovitch, Helen; Ross, G. Webster; Masaki, Kamal; White, Lon R.] Univ Hawaii, John A Burns Sch Med, Dept Geriatr, Honolulu, HI 96822 USA.
[Uyehara-Lock, Jane] Univ Hawaii, John A Burns Sch Med, Dept Pathol, Honolulu, HI 96822 USA.
[Markesbery, William] Univ Kentucky, Sanders Brown Ctr Aging, Med Ctr, Lexington, KY 40536 USA.
[Markesbery, William] Univ Kentucky, Dept Pathol, Med Ctr, Lexington, KY 40536 USA.
[Markesbery, William] Univ Kentucky, Dept Neurol, Med Ctr, Lexington, KY 40536 USA.
[Davis, Daron] Pathol & Cytol Labs, Lexington, KY 40503 USA.
[Launer, Lenore] NIA, Div Epidemiol Demog & Biostat, NIH, Bethesda, MD 20892 USA.
RP Petrovitch, H (reprint author), 846 S Hotel St,Suite 307, Honolulu, HI 96813 USA.
EM hpetrovitch@phrihawaii.org
FU National Institutes Of Health: National Institute on Aging [1 U01
AG19349, 5 R01 AG017155]
FX This work was supported by the National Institutes Of Health: National
Institute on Aging, Grant Numbers: 1 U01 AG19349 and 5 R01 AG017155 and
with resources from the Spark M. Matsunaoa Veterans Affairs Medical
Center, Honolulu, Hawaii. The authors would like to thank the
Honolulu-Asia Aging Study/Honolulu Heart Program cohort members for
their important and long-term participation in the study and the
Honolutu-Asia Aging Study staff who make the study possible.
NR 47
TC 10
Z9 10
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD OCT
PY 2008
VL 29
IS 10
BP 1448
EP 1455
DI 10.1016/j.neurobiolaging.2007.03.026
PG 8
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 342XU
UT WOS:000258817700001
PM 17499884
ER
PT J
AU Launer, LJ
Petrovitch, H
Ross, GW
Markesbery, W
White, LR
AF Launer, Lenore J.
Petrovitch, Helen
Ross, G. Webster
Markesbery, William
White, Lon R.
TI AD brain pathology: Vascular origins? Results from the HAAS autopsy
study
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Alzheimer's disease; vascular disease; neuropathology; community sample
ID ALZHEIMERS-DISEASE
AB An increasing number of studies suggest a vascular contribution to Alzheimer's disease (AD). One major question these findings raise is whether vascular disease enhances the formation of AD-like lesions, or whether vascular disease just adds to clinical severity. We examined this question in a fully characterized autopsy sample based oil the Honolulu Asia Aging Study. We found that AD markers of neurodegeneration (amyloid plaques, cerebral amyloid angiopathy and neurofibrillary tangles) were no more prevalent in those with neuropathologically defined vascular lesions compared to those without lesions. Our study suggests the burden of vascular and AD type lesions are independent of each other, and are consistent with an additive effect of the two types of lesions oil cognitive impairment. (C) 2007 Elsevier Inc. All rights reserved.
C1 [Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Petrovitch, Helen; Ross, G. Webster; White, Lon R.] Pacific Hlth Res Inst, Honolulu, HI USA.
[Ross, G. Webster] Kuakini Med Ctr, Honolulu Dept Vet Affairs, Honolulu, HI USA.
[Markesbery, William] Univ Kentucky, Med Ctr, Dept Pathol, Lexington, KY 40536 USA.
[Markesbery, William] Univ Kentucky, Med Ctr, Sanders Brown Ctr Aging, Lexington, KY 40536 USA.
RP Launer, LJ (reprint author), NIA, Lab Epidemiol Demog & Biometry, 7201 Wisconsin Ave,3C-309, Bethesda, MD 20892 USA.
EM launer1@nia.nih.gov
FU National Institute on Aging; National Institutes of Health [NIA U01 AG
19349-01, 5 RO1 AG017155-04]; Sparks M. Matsunaga Veterans Affairs
Medical Center; NIA
FX Funding is provided through grants and contracts from the National
Institute on Aging, National Institutes of Health, (NIA U01 AG 19349-01;
5 RO1 AG017155-04), the Sparks M. Matsunaga Veterans Affairs Medical
Center and the NIA Intramural Research Program.
NR 7
TC 67
Z9 67
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD OCT
PY 2008
VL 29
IS 10
BP 1587
EP 1590
DI 10.1016/j.neurobiolaging.2007.03.008
PG 4
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 342XU
UT WOS:000258817700015
PM 17466414
ER
PT J
AU Yang, SF
Zhang, D
Yang, ZQ
Hu, XM
Qian, S
Liu, J
Wilson, B
Block, M
Hong, JS
AF Yang, Sufen
Zhang, Dan
Yang, Zhengqin
Hu, Xiaoming
Qian, Steven
Liu, Jie
Wilson, Belinda
Block, Michelle
Hong, Jau-Shyong
TI Curcumin protects dopaminergic neuron against LPS induced neurotoxicity
in primary rat neuron/glia culture
SO NEUROCHEMICAL RESEARCH
LA English
DT Article
DE curcumin; microglia; dopaminergic neuron; neuroprotection
ID NF-KAPPA-B; PARKINSONS-DISEASE; CELL-DEATH; INFLAMMATORY DAMAGE;
PRION-DISEASE; NADPH OXIDASE; NITRIC-OXIDE; INFLAMMOGEN
LIPOPOLYSACCHARIDE; FEMTOMOLAR CONCENTRATIONS; MICROGLIAL ACTIVATION
AB Using primary rat mesencephalic neuron-glia cultures as an in vitro model of Parkinson's disease (PD), we tested the effect of curcumin, a natural dietary pigment with well-known anti-inflammation effects, on dopaminergic (DA) degeneration. Curcumin pretreatment mitigated LPS-induced DA neurotoxicity in a concentration-dependent manner and curcumin post-treatment also showed protective effect. Microglia depletion abolished this protective effect of curcumin, indicating that microglia play an important role in this effect. Supportively, observation by immunocytochemistry staining using OX-42 antibody showed that curcumin treatment inhibited LPS-induced morphological change of microglia. Besides, LPS-induced production of many proinflammatory factors and their gene expressions decreased dramatically after curcumin treatment. Results also revealed that curcumin treatment decreased LPS-induced activation of two transcription factors-nuclear factors kappa B (NF-kappa B) and activator protein-1 (AP-1). Taken together, our study implicated that curcumin might be a potential preventive and therapeutic strategy for inflammation-related neurodegenerative diseases.
C1 [Yang, Sufen; Zhang, Dan; Hu, Xiaoming; Qian, Steven; Wilson, Belinda; Block, Michelle; Hong, Jau-Shyong] NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA.
[Yang, Zhengqin] Zhengzhou Univ, Sch Pharmaceut Sci, NIH, NIEHS,Natl Ctr Toxicogenom, Zhengzhou 450001, Peoples R China.
[Liu, Jie] NIEHS, Comparat Carcinogenesis Lab, NCI, Res Triangle Pk, NC 27709 USA.
RP Hong, JS (reprint author), NIEHS, Lab Pharmacol & Chem, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM hong3@niehs.nih.gov
NR 53
TC 38
Z9 40
U1 1
U2 10
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0364-3190
J9 NEUROCHEM RES
JI Neurochem. Res.
PD OCT
PY 2008
VL 33
IS 10
BP 2044
EP 2053
DI 10.1007/s11064-008-9675-z
PG 10
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 348DJ
UT WOS:000259190900018
PM 18368483
ER
PT J
AU Blair, RJR
AF Blair, R. J. R.
TI The Cognitive Neuroscience of Psychopathy and Implications for Judgments
of Responsibility
SO NEUROETHICS
LA English
DT Review
DE Psychopathy; Emotion; Amygdala; Responsibility
ID VENTROMEDIAL PREFRONTAL CORTEX; CALLOUS-UNEMOTIONAL TRAITS; RESPONSE
REVERSAL; ORBITOFRONTAL CORTEX; FEARFUL EXPRESSIONS; ANTERIOR CINGULATE;
DECISION-MAKING; AMYGDALA RESPONSE; ANXIETY DISORDERS; VIOLENT BEHAVIOR
AB Psychopathy is a developmental disorder associated with specific forms of emotional dysfunction and an increased risk for both frustration-based reactive aggression and goal-directed instrumental antisocial behavior. While the full behavioral manifestation of the disorder is under considerable social influence, the basis of this disorder appears to be genetic. At the neural level, individuals with psychopathy show atypical responding within the amygdala and ventromedial prefrontal cortex (vmPFC). Moreover, the roles of the amygdala in stimulus-reinforcement learning and responding to emotional expressions and vmPFC in the representation of reinforcement expectancies are compromised. The implications of these functional impairments for responsibility are discussed.
C1 NIMH, Mood & Anxiety Program, NIH, Bethesda, MD 20892 USA.
RP Blair, RJR (reprint author), NIMH, Mood & Anxiety Program, NIH, 15K North Dr, Bethesda, MD 20892 USA.
EM blairj@intra.nimh.nih.gov
FU NIH: NIMH
FX This research was supported by the Intramural Research Program of the
NIH: NIMH.
NR 82
TC 20
Z9 21
U1 6
U2 31
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1874-5490
J9 NEUROETHICS-NETH
JI Neuroethics
PD OCT
PY 2008
VL 1
IS 3
BP 149
EP 157
DI 10.1007/s12152-008-9016-6
PG 9
WC Ethics; Medical Ethics; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Biomedical Social
Sciences
GA V14OG
UT WOS:000207743100001
ER
PT J
AU Lee, HS
Goldfarb, LG
AF Lee, H. -S.
Goldfarb, L. G.
TI Global distribution of Fatal familial insomnia: founder or recurrent
mutations
SO NEUROGENETICS
LA English
DT Letter
C1 [Lee, H. -S.; Goldfarb, L. G.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Goldfarb, LG (reprint author), NINDS, NIH, Bethesda, MD 20892 USA.
EM goldfarbl@ninds.nih.gov
FU Intramural NIH HHS [Z01 NS002973-09]
NR 3
TC 2
Z9 3
U1 2
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1364-6745
J9 NEUROGENETICS
JI Neurogenetics
PD OCT
PY 2008
VL 9
IS 4
BP 301
EP 302
DI 10.1007/s10048-008-0135-3
PG 2
WC Genetics & Heredity; Clinical Neurology
SC Genetics & Heredity; Neurosciences & Neurology
GA 353NY
UT WOS:000259575900009
PM 18568368
ER
PT J
AU Volkow, ND
Wang, GJ
Telang, F
Fowler, JS
Thanos, PK
Logan, J
Alexoff, D
Ding, YS
Wong, C
Ma, Y
Pradhan, K
AF Volkow, Nora D.
Wang, Gene-Jack
Telang, Frank
Fowler, Joanna S.
Thanos, Panayotis K.
Logan, Jean
Alexoff, David
Ding, Yu-Shin
Wong, Christopher
Ma, Yeming
Pradhan, Kith
TI Low dopamine striatal D2 receptors are associated with prefrontal
metabolism in obese subjects: Possible contributing factors
SO NEUROIMAGE
LA English
DT Article
DE orbitofrontal cortex; cingulate gyrus; dorsolateral prefrontal; dopamine
transporters; raclopride; PET
ID POSITRON-EMISSION-TOMOGRAPHY; HUMAN BRAIN; ORBITOFRONTAL CORTEX; C-11
RACLOPRIDE; EXECUTIVE DYSFUNCTION; MOLECULAR-MECHANISMS;
PARKINSONS-DISEASE; HEALTHY-VOLUNTEERS; COGNITIVE FUNCTION;
FRONTAL-CORTEX
AB Dopamine's role in inhibitory control is well recognized and its disruption may contribute to behavioral disorders of discontrol such as obesity. However, the mechanism by which impaired dopamine neurotransmission interferes with inhibitory control is poorly understood. We had previously documented a reduction in dopamine D2 receptors in morbidly obese subjects. To assess if the reductions in dopamine D2 receptors were associated with activity in prefrontal brain regions implicated in inhibitory control we assessed the relationship between dopamine D2 receptor availability in striatum with brain glucose metabolism (marker of brain function) in ten morbidly obese subjects (BMl>40 kg/m(2)) and compared it to that in twelve non-obese controls. PET Was used with [C-11]raclopride to assess D2 receptors and with [F-18] FDG to assess regional brain glucose metabolism. In obese Subjects striatal D2 receptor availability was lower than controls and was positively correlated with metabolism in dorsolateral prefrontal, medial orbitofrontal, anterior cingulate gyrus and somatosensory cortices. In controls cot-relations with prefrontal metabolism were not significant but comparisons with those in obese subjects were not significant, which does not permit to ascribe the associations as unique to obesity. The associations between striatal D2 receptors and prefrontal metabolism in obese subjects suggest that decreases in striatal D2 receptors could contribute to overeating via their modulation of striatal prefrontal pathways, which participate in inhibitory control and salience attribution. The association between striatal D2 receptors and metabolism in somatosensory cortices (regions that process palatability) Could underlie one of the mechanisms through which dopamine regulates the reinforcing properties of food.
C1 [Volkow, Nora D.] Natl Inst Drug Abuse, Bethesda, MD 20892 USA.
[Volkow, Nora D.; Telang, Frank; Ma, Yeming] NIAAA, Bethesda, MD 20892 USA.
[Wang, Gene-Jack; Fowler, Joanna S.; Logan, Jean; Alexoff, David; Wong, Christopher; Pradhan, Kith] Brookhaven Natl Lab, Dept Med, Upton, NY 11973 USA.
[Ding, Yu-Shin] Yale Univ, Sch Med, Dept Diagnost Radiol, New Haven, CT 06520 USA.
RP Volkow, ND (reprint author), Natl Inst Drug Abuse, 6001 Execut Blvd,Room 5274, Bethesda, MD 20892 USA.
EM nvolkow@nida.nih.gov
OI Logan, Jean/0000-0002-6993-9994
FU NIH's Intramural Research Program (NIAAA); DOE [DE-AC01-76CH00016]
FX We thank David Schlyer, David Alexoff, Paul Vaska, Colleen Shea, Youwen
XU, Pauline Carter, Karen Apelskog, and Linda Thomas for their
contributions. This research was supported by NIH's Intramural Research
Program (NIAAA) and by DOE (DE-AC01-76CH00016).
NR 80
TC 222
Z9 223
U1 9
U2 27
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD OCT 1
PY 2008
VL 42
IS 4
BP 1537
EP 1543
DI 10.1016/j.neuroimage.2008.06.002
PG 7
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 351CB
UT WOS:000259401000026
PM 18598772
ER
PT J
AU Bjork, JM
Smith, AR
Hommer, DW
AF Bjork, James M.
Smith, Ashley R.
Hommer, Daniel W.
TI Striatal sensitivity to reward deliveries and omissions in substance
dependent patients
SO NEUROIMAGE
LA English
DT Article
DE reward; active avoidance; loss; nucleus accumbens; insula; ventral
striatum; persistence; cocaine dependence; alcohol dependence; fMRI;
impulsivity
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DECISION-MAKING;
NUCLEUS-ACCUMBENS; PREFRONTAL CORTEX; BRAIN ACTIVATION; RISK-TAKING;
DISCOUNTING PROCESSES; ABSTINENT ALCOHOLICS; NEURAL RESPONSES;
CAUDATE-NUCLEUS
AB Some motivational theories of substance dependence (SD) posit either pathologically increased or decreased ventral striatum (VS) recruitment by cues for nondrug rewards. The incentive-sensitization hypothesis, alternatively, attributes SD to enhanced incentive salience of drug-predictive cues specifically, with no requirement for altered nondrug incentive processing. We assessed whether individuals undergoing inpatient therapy for SD are characterized by altered recruitment of mesolimbic incentive neurocircuitry by cues and deliveries of nondrug rewards. During functional magnetic resonance imaging, substance-dependent patients (SDP) and controls performed a modified monetary incentive delay task featuring: a) anticipatory cues that signaled opportunities to respond to a target to either win money or avoid losing money, b) notifications of wins and losses, and c) unexpected replacement of reward trial outcomes with a demand to repeat the trial. Both anticipatory reward cues and loss cues elicited similar mood responses and VS activation between SDP and controls. However, in SDP (but not controls), reward notifications also activated VS and mesial frontal cortex, and loss notifications activated anterior insula. Finally, substitution of expected outcomes in reward trials with notifications to repeat the trial deactivated the VS in SDP but not in controls. These data do not suggest that SD is characterized by altered recruitment of VS circuitry by cues for nondrug incentives. Rather, SDP may instead have increased limbic system sensitivity to reward and loss delivery, consistent with the role of impulsivity in SD.
C1 [Bjork, James M.] NIDA DCNBR, Bethesda, MD 20892 USA.
[Smith, Ashley R.; Hommer, Daniel W.] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
RP Bjork, JM (reprint author), NIDA DCNBR, 6001 Execut Blvd,Room 3151, Bethesda, MD 20892 USA.
EM jbjork@mail.nih.gov
OI Bjork, James/0000-0003-0593-3291
FU National Institute on Alcohol Abuse and Alcoholism
FX This research was sponsored by intramural research funds of the National
Institute on Alcohol Abuse and Alcoholism. The authors thank Christopher
Geyer, Cinnamon Danube and Swati Murthy for assistance in subject
recruitment and data collection. The authors also thank Debbie Hill for
classification of the substance-related symptomatology of SDP.
NR 80
TC 87
Z9 89
U1 4
U2 17
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD OCT 1
PY 2008
VL 42
IS 4
BP 1609
EP 1621
DI 10.1016/j.neuroimage.2008.06.035
PG 13
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 351CB
UT WOS:000259401000034
PM 18672069
ER
PT J
AU Schmidt, J
Barthel, K
Wrede, A
Salajegheh, M
Baehr, M
Dalakas, MC
AF Schmidt, J.
Barthel, K.
Wrede, A.
Salajegheh, M.
Baehr, M.
Dalakas, M. C.
TI Inflammatory diseases of muscle and nerve; Poster presentations
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 13th International Congress of the World-Muscle-Society
CY SEP 29-OCT 02, 2008
CL Newcastle upon Tyne, ENGLAND
SP World Muscle Soc
C1 [Schmidt, J.; Barthel, K.; Baehr, M.] Univ Goettingen, Dept Neurol & Neuroimmunol, Gottingen, Germany.
[Wrede, A.] Univ Goettingen, Dept Neuropathol, Gottingen, Germany.
[Salajegheh, M.] Natl Inst Hlth, Bethesda, MD USA.
[Dalakas, M. C.] Thomas Jefferson Univ Hosp, Neuromuscular Div, Philadelphia, PA 19107 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2008
VL 18
IS 9-10
BP 769
EP 769
DI 10.1016/j.nmd.2008.06.157
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 356JQ
UT WOS:000259774900152
ER
PT J
AU Olive, M
Shatunov, A
Carmona, O
Martinez-Matos, JA
Goldfarb, LG
Ferrer, I
AF Olive, M.
Shatunov, A.
Carmona, O.
Martinez-Matos, J. A.
Goldfarb, L. G.
Ferrer, I.
TI Novel mutation in telethonin causing autosomal recessive muscular
dystrophy type 2G in a Moldavian patient
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 13th International Congress of the World-Muscle-Society
CY SEP 29-OCT 02, 2008
CL Newcastle upon Tyne, ENGLAND
SP World Muscle Soc
C1 [Olive, M.; Martinez-Matos, J. A.; Ferrer, I.] Hosp Llobregat, Inst Neuropatol, IDIBELL Hosp Bellvitge, Barcelona, Spain.
[Shatunov, A.; Goldfarb, L. G.] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD USA.
[Carmona, O.] Hosp Figueres, Serv Neurol, Figueres, Girona, Spain.
RI Shatunov, Aleksey/E-6946-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2008
VL 18
IS 9-10
BP 817
EP 817
DI 10.1016/j.nmd.2008.06.321
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 356JQ
UT WOS:000259774900311
ER
PT J
AU Boyce-Rustay, JM
Palachick, B
Hefner, K
Chen, YC
Karlsson, RM
Millstein, RA
Harvey-White, J
Holmes, A
AF Boyce-Rustay, Janel M.
Palachick, Benjamin
Hefner, Kathryn
Chen, Yi-Chyan
Karlsson, Rose-Marie
Millstein, Rachel A.
Harvey-White, Judith
Holmes, Andrew
TI Desipramine potentiation of the acute depressant effects of ethanol:
Modulation by alpha 2-adrenoreceptors and stress
SO NEUROPHARMACOLOGY
LA English
DT Article
DE Ethanol; Norepinephrine; Norepinephrine transporter; Sedation; Stress;
Serotonin
ID LOCUS COERULEUS NEURONS; SELECTIVE NORADRENERGIC NEUROTOXIN; MECHANISMS
MEDIATING DIFFERENCES; SEROTONIN REUPTAKE INHIBITORS; DORSAL RAPHE
NUCLEUS; CHRONIC SWIM STRESS; SHORT-SLEEP MICE; IN-VIVO;
ALPHA(2)-ADRENOCEPTOR ANTAGONIST; FRONTAL-CORTEX
AB Ethanol exerts effects on the brain noradrenergic system, and these are thought to contribute to the sedative/hypnotic (depressant) effects of ethanol. Recent studies suggest that the norepinephrine transporter (NET) plays an important role in modulating ethanol's depressant effects. The aim of the present study was to further characterize this role. Transporter blockers with varying affinity for NET versus the serotonin transporter (desipramine > fluoxetine > citalopram) were tested for their ability to alter ethanol's depressant effects, and for comparison, hypothermic effects. Effects of desipramine on another depressant, pentobarbital, were examined. Desipramine potentiation of ethanol's depressant effects was assessed following depletion of brain norepinephrine via N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSPA) treatment, or depletion of brain 5-HT via para-chlorophenylalanine methyl ester hydrochloride (PCPA) treatment. The effects of co-administration of either the selective alpha 2-adrenoreceptor agonist (dexmedetomidine) or the selective alpha 2-adrenoreceptor antagonist (atipamezole) on desipramine's effect on ethanol's depressant effects were examined. Given the close link between stress, ethanol and norepinephrine, desipramine potentiation of ethanol's depressant effects was tested following repeated forced swim stress. Results showed that desipramine, but not SERT-selective doses of citalopram or fluoxetine, strongly potentiated the depressant (not hypothermic) effects of ethanol. These effects were mimicked by dexmedetomidine and blocked by atipamezole, but not by depletion of either norepinephrine or 5-HT. Desipramine potentiation of ethanol's depressant effects was abolished following repeated stress. Present findings further support a major role for NET and the alpha 2-adrenoreceptor in modulating the depressant effects of ethanol, with possible implications for understanding the role of noradrenergic dysfunction in stress-related alcoholism. Published by Elsevier Ltd.
C1 [Boyce-Rustay, Janel M.; Palachick, Benjamin; Hefner, Kathryn; Millstein, Rachel A.; Holmes, Andrew] NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA.
[Chen, Yi-Chyan] TriServ Gen Hosp, Natl Def Med Ctr, Dept Psychiat, Taipei, Taiwan.
[Karlsson, Rose-Marie] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Karlsson, Rose-Marie] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
[Harvey-White, Judith] NIAAA, Lab Physiol Studies, NIH, Rockville, MD 20852 USA.
RP Boyce-Rustay, JM (reprint author), Abbott Labs, R4N5 AP9A L018,100 Abbott Pk Rd, Abbott Pk, IL 60064 USA.
EM janel.boyce-rustay@abbott.com
OI Hefner, Kathryn/0000-0002-5208-7860
FU National Institute of Alcohol Abuse and Alcoholism [Z01-AA000411]
FX Research supported by the Intramural Research Program of the National
Institute of Alcohol Abuse and Alcoholism (Z01-AA000411).
NR 99
TC 15
Z9 16
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD OCT
PY 2008
VL 55
IS 5
BP 803
EP 811
DI 10.1016/j.neuropharm.2008.06.032
PG 9
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 361VF
UT WOS:000260154600022
PM 18625256
ER
PT J
AU Leandri, M
Leandri, S
Lunardi, G
AF Leandri, M.
Leandri, S.
Lunardi, G.
TI Effect of temperature on sensory and motor conduction of the rat tail
nerves
SO NEUROPHYSIOLOGIE CLINIQUE-CLINICAL NEUROPHYSIOLOGY
LA English
DT Article
DE Rat tail; Compound action potential; Temperature; Conduction vetocity;
Amplitude
AB Aims of the study. -To assess the effect of temperature upon conduction velocity, amplitude and signal energy of the sensory and motor rat tail nerves.
Materials and methods. -Sensory and motor responses were recorded from the tail nerves in 10 adult rats at different temperatures, starting from 40 degrees C and cooling down to 16 degrees C in steps of 2 degrees C.
Results. -The conduction velocity of the various components of the orthodromic sensory response was directly and linearly related to temperature (fastest fibres ranged from 47.7 down to 19.7 m/s), with Q(10) values of approximately 1.30, suggesting that all fibres, regardless of their diameter, were equally sensitive to changes in temperature. The motor conduction was similarly affected with a Q(10) value of 1.28 and a velocity range from 24.2 down to 9.6 m/s. Amplitude and energy of the sensory responses were inversely related to temperature, reaching their maximum at 16 degrees C. Energy was by far the most temperature sensitive parameter, with a Q(10) of approximately 3 both for fast or stow conducting fibres. Amplitude and energy of the motor responses also showed an inverse correlation with temperature, but were influenced by a more complex set of factors (neuromuscular synapse, muscle membrane) than the simple neural conduction.
Conclusions. -Besides providing new normative data upon conduction in the rat tail nerves at different temperatures, our results suggest that this method may represent an excellent toot to study models of peripheral-nerve conduction in vivo under various physiological and pathological conditions. (c) 2008 Elsevier Masson SAS. All rights reserved.
C1 [Leandri, M.; Leandri, S.] Interuniv Ctr Pain Neurophysiol, I-16146 Genoa, Italy.
[Lunardi, G.] Natl Canc Inst, I-16132 Genoa, Italy.
RP Leandri, M (reprint author), Interuniv Ctr Pain Neurophysiol, Via Dodecaneso 35, I-16146 Genoa, Italy.
EM massimo.leandri@unige.it
OI Leandri, Massimo/0000-0002-5197-7431
NR 7
TC 6
Z9 6
U1 2
U2 15
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0987-7053
J9 NEUROPHYSIOL CLIN
JI Neurophysiol. Clin.-Clin. Neurophysiol.
PD OCT
PY 2008
VL 38
IS 5
BP 297
EP 304
DI 10.1016/j.neucli.2008.08.002
PG 8
WC Clinical Neurology; Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 377DL
UT WOS:000261231800004
PM 18940617
ER
PT J
AU Quiroz, JA
Gray, NA
Kato, T
Manji, HK
AF Quiroz, Jorge A.
Gray, Neil A.
Kato, Tadafumi
Manji, Husseini K.
TI Mitochondrially mediated plasticity in the pathophysiology and treatment
of bipolar disorder
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Review
DE bipolar disorder; mitochondria; synaptic plasticity; bcl-2; lithium;
calcium regulation
ID MAGNETIC-RESONANCE-SPECTROSCOPY; PLATELET INTRACELLULAR CALCIUM;
GLYCOGEN-SYNTHASE KINASE-3-BETA; EMERGING EXPERIMENTAL THERAPEUTICS;
PERMEABILITY TRANSITION PORE; MAJOR DEPRESSIVE DISORDER;
N-ACETYL-ASPARTATE; COMPLEX-I ACTIVITY; GENE-EXPRESSION; MOOD
STABILIZERS
AB Bipolar disorder (BPD) has traditionally been conceptualized as a neurochemical disorder, but there is mounting evidence for impairments of cellular plasticity and resilience. Here, we review and synthesize the evidence that critical aspects of mitochondrial function may play an integral role in the pathophysiology and treatment of BPD. Retrospective database searches were performed, including MEDLINE, abstract booklets, and conference proceedings. Articles were also obtained from references therein and personal communications, including original scientific work, reviews, and meta-analyses of the literature. Material regarding the potential role of mitochondrial function included genetic studies, microarray studies, studies of intracellular calcium regulation, neuroimaging studies, postmortem brain studies, and preclinical and clinical studies of cellular plasticity and resilience. We review these data and discuss their implications not only in the context of changing existing conceptualizations regarding the pathophysiology of BPD, but also for the strategic development of improved therapeutics. We have focused on specific aspects of mitochondrial dysfunction that may have major relevance for the pathophysiology and treatment of BPD. Notably, we discuss calcium dysregulation, oxidative phosphorylation abnormalities, and abnormalities in cellular resilience and synaptic plasticity. Accumulating evidence from microarray studies, biochemical studies, neuroimaging, and postmortem brain studies all support the role of mitochondrial dysfunction in the pathophysiology of BPD. We propose that although BPD is not a classic mitochondrial disease, subtle deficits in mitochondrial function likely play an important role in various facets of BPD, and that enhancing mitochondrial function may represent a critical component for the optimal long-term treatment of the disorder.
C1 [Manji, Husseini K.] NIMH, Mol Pathophysiol Lab, Dept Hlth & Human Serv, Mood & Anxiety Disorders Program,NIH, Bethesda, MD 20892 USA.
[Gray, Neil A.; Manji, Husseini K.] Columbia Univ, Coll Phys & Surg, New York, NY USA.
[Kato, Tadafumi] RIKEN Brain Sci Inst, Lab Mol Dynam Mental Disorders, Saitama, Japan.
RP Manji, HK (reprint author), NIMH, Mol Pathophysiol Lab, Dept Hlth & Human Serv, Mood & Anxiety Disorders Program,NIH, Bldg 35,IC-912,35 Convent Dr, Bethesda, MD 20892 USA.
EM manji@nih.gov
RI Kato, Tadafumi/J-3583-2014
OI Kato, Tadafumi/0000-0001-7856-3952
FU National Institute of Mental Heath; NARSAD; Stanley Medical Research
Institute
FX We acknowledge the support of the Intramural Research Program of the
National Institute of Mental Heath, NARSAD, and the Stanley Medical
Research Institute. We thank Alex Noury, Lisa Catapano, and Ioline
Henter for outstanding editorial assistance and critical review. Due to
space limitations, we often cited review papers and apologize to those
authors whose original data could not be included.
NR 135
TC 85
Z9 86
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD OCT
PY 2008
VL 33
IS 11
BP 2551
EP 2565
DI 10.1038/sj.npp.1301671
PG 15
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 348EE
UT WOS:000259193000001
PM 18235426
ER
PT J
AU Yang, RJ
Mozhui, K
Karlsson, RM
Cameron, HA
Williams, RW
Holmes, A
AF Yang, Rebecca J.
Mozhui, Khyobeni
Karlsson, Rose-Marie
Cameron, Heather A.
Williams, Robert W.
Holmes, Andrew
TI Variation in mouse basolateral amygdala volume is associated with
differences in stress reactivity and fear learning
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE amygdala; gene; fear; memory; PTSD; stress
ID MEDIAL PREFRONTAL CORTEX; QUANTITATIVE TRAIT LOCI; SMALLER HIPPOCAMPAL
VOLUME; RECOMBINANT INBRED STRAINS; ELEVATED PLUS-MAZE;
ELECTRICAL-STIMULATION; SEROTONIN TRANSPORTER; GENETIC-CONTROL;
RAT-BRAIN; MICE
AB A wealth of research identifies the amygdala as a key brain region mediating negative affect, and implicates amygdala dysfunction in the pathophysiology of anxiety disorders. Although there is a strong genetic component to anxiety disorders such as posttraumatic stress disorder (PTSD) there remains debate about whether abnormalities in amygdala function predispose to these disorders. In the present study, groups of C57BL/6 x DBA/2 (B x D) recombinant inbred strains of mice were selected for differences in volume of the basolateral amygdala complex (BLA). Strains with relatively small, medium, or large BLA volumes were compared for Pavlovian fear learning and memory, anxiety-related behaviors, depression-related behavior, and glucocorticoid responses to stress. Strains with relatively small BLA exhibited stronger conditioned fear responses to both auditory tone and contextual stimuli, as compared to groups with larger BLA. The small BLA group also showed significantly greater corticosterone responses to stress than the larger BLA groups. BLA volume did not predict clear differences in measures of anxiety-like behavior or depression-related behavior, other than greater locomotor inhibition to novelty in strains with smaller BLA. Neither striatal, hippocampal nor cerebellar volumes correlated significantly with any behavioral measure. The present data demonstrate a phenotype of enhanced fear conditioning and exaggerated glucocorticoid responses to stress associated with small BLA volume. This profile is reminiscent of the increased fear processing and stress reactivity that is associated with amygdala excitability and reduced amygdala volume in humans carrying loss of function polymorphisms in the serotonin transporter and monoamine oxidase A genes. Our study provides a unique example of how natural variation in amygdala volume associates with specific fear-and stress-related phenotypes in rodents, and further supports the role of amygdala dysfunction in anxiety disorders such as PTSD.
C1 [Yang, Rebecca J.; Karlsson, Rose-Marie; Holmes, Andrew] NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA.
[Mozhui, Khyobeni; Williams, Robert W.] Univ Tennessee, Ctr Hlth Sci, Dept Anat & Neurobiol, Memphis, TN 38163 USA.
[Cameron, Heather A.] NIMH, Unit Neuroplast, Mood & Anxiety Disorders Program, NIH, Bethesda, MD 20892 USA.
RP Holmes, A (reprint author), NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIH, 5625 Fishers Lane,Room 2N09, Rockville, MD 20852 USA.
EM holmesan@mail.nih.gov
RI Cameron, Heather/E-6221-2011;
OI Cameron, Heather/0000-0002-3245-5777; Williams,
Robert/0000-0001-8924-4447
FU NIAAA [Z01-AA000411]; NIMH [Z01-MH002784]; NIDA; NIMH; NIAAA HPG [P20-DA
21131]; NCRR BIRN [U24 RR021760]; NIAAA INIA [U01AA13499, U24AA13513]
FX We thank Dr. Glenn D. Rosen for access to a new striatal volume data set
on the BXD strains available in GeneNetwork (BXD Phenotype GNID 10710).
This research was supported by the NIAAA (Z01-AA000411) and NIMH
(Z01-MH002784) intramural research programs, and by NIDA, NIMH, and
NIAAA HPG grant P20-DA 21131, NCRR BIRN grant U24 RR021760 (BIRN), and
NIAAA INIA grants U01AA13499 and U24AA13513.
NR 86
TC 59
Z9 60
U1 2
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD OCT
PY 2008
VL 33
IS 11
BP 2595
EP 2604
DI 10.1038/sj.npp.1301665
PG 10
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 348EE
UT WOS:000259193000005
PM 18185497
ER
PT J
AU Sartorius, LJ
Weinberger, DR
Hyde, TM
Harrison, PJ
Kleinman, JE
Lipska, BK
AF Sartorius, Leah J.
Weinberger, Daniel R.
Hyde, Thomas M.
Harrison, Paul J.
Kleinman, Joel E.
Lipska, Barbara K.
TI Expression of a GRM3 splice variant is increased in the dorsolateral
prefrontal cortex of individuals carrying a schizophrenia risk SNP
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE post mortem; metabotropic; glutamate; mGluR3; neuroleptic; bipolar
disorder
ID METABOTROPIC GLUTAMATE RECEPTORS; GLUTAMATE-RECEPTOR-3; GENE; AGONIST;
IDENTIFICATION; POPULATION; ACTIVATION; ENHANCERS; DISORDER; MEMORY
AB Genetic variation in the metabotropic glutamate receptor 3 (GRM3, mGluR3) has been associated with schizophrenia, but the mechanism by which it confers risk is unknown. Previously, we reported the existence of a splice variant, GRM3 Delta 4, which has an exon 4 deletion and encodes a truncated form of the receptor that is expressed in brain. The aim of the present study was to determine whether expression of this splice variant is altered in individuals with schizophrenia and is affected by a risk genotype. We measured GRM3 and GRM3 Delta 4 transcripts in human dorsolateral prefrontal cortex (DLPFC) and hippocampus of the CBDB/NIMH collection (similar to 70 controls, similar to 30 schizophrenia patients) and in the DLPFC of the Stanley Array Collection. Expression data of GRM3 mRNA in the DLPFC were inconsistent: GRM3 was increased in schizophrenia patients in the CBDB/NIMH collection, but not in the Stanley Array Collection. GRM3 expression did not change in the frontal cortex of rats treated chronically with haloperidol or clozapine. An exon 3 SNP previously associated with schizophrenia (rs2228595) predicted increased expression of the GRM3 Delta 4 splice variant. Our results suggest that rs2228595, or a neighboring SNP in linkage disequilibrium with it, may contribute to risk for schizophrenia by modulating GRM3 splicing.
C1 [Sartorius, Leah J.; Weinberger, Daniel R.; Hyde, Thomas M.; Kleinman, Joel E.; Lipska, Barbara K.] NIMH, Genes Cognit & Psychosis Program, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA.
[Sartorius, Leah J.; Harrison, Paul J.] Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford, England.
RP Lipska, BK (reprint author), NIMH, Genes Cognit & Psychosis Program, Clin Brain Disorders Branch, NIH, 10 Ctr Dr,Rm 4N306, Bethesda, MD 20892 USA.
EM lipskab@intra.nimh.nih.gov
FU NIH/Oxford Graduate Partnership; NIH; NIMH
FX LJS is a student in the NIH/Oxford Graduate Partnership Program. This
research was supported by the Intramural Research Program of the NIH,
NIMH. Post-mortem brain tissue was donated by the Stanley Medical
Research Institute, courtesy of Drs Michael B Knable, E Fuller Torrey,
Maree J Webster, Serge Weis, and Robert H Yolken. We thank Ms Cara
Horowitz, Ms Tricia Peters, and Mr Krishna Vakkalanka for their
excellent technical assistance, Dr Mary M Herman for her
neuropathological assessments, and Amy Deep-Soboslay for her work on the
demographic and clinical data. We thank the staff of the Offices of the
Chief Medical Examiner of District of Columbia and of Northern Virginia
for their assistance. We also thank the families of the deceased, who
generously donated brain tissue as well as their time and effort to make
this study possible.
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD OCT
PY 2008
VL 33
IS 11
BP 2626
EP 2634
DI 10.1038/sj.npp.1301669
PG 9
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 348EE
UT WOS:000259193000009
PM 18256595
ER
PT J
AU Schoser, B
Hill, V
Raben, N
AF Schoser, Benedikt
Hill, Victoria
Raben, Nina
TI Therapeutic approaches in glycogen storage disease type II/Pompe disease
SO NEUROTHERAPEUTICS
LA English
DT Review
DE enzyme replacement therapy; gene therapy; glycogen storage disease type
II; Pompe disease; lysosome
ID ACID-ALPHA-GLUCOSIDASE; ENZYME REPLACEMENT THERAPY; ONSET POMPE-DISEASE;
ADENOVIRUS-MEDIATED TRANSFER; VIRUS SEROTYPE-1 VECTORS; GSD-II MICE;
GENE-THERAPY; MALTASE DEFICIENCY; MUSCLE-FIBERS; KNOCKOUT MICE
AB Glycogen storage disease type II (GSDII)/Pompe disease is an autosomal recessive multi-system disorder due to a deficiency of the glycogen-degrading lysosomal enzyme, acid alpha-glucosidase. Without adequate levels of alpha-glucosidase, there is a progressive accumulation of glycogen inside the lysosome, resulting in lysosomal expansion in many tissues, although the major clinical manifestations are seen in cardiac and skeletal muscle. Pompe disease presents as a continuum of clinical phenotypes. In the most severe cases, disease onset occurs in infancy and death results from cardiac and respiratory failure within the first 1 or 2 years of life. In the milder late-onset forms, cardiac muscle is spared and muscle weakness is the primary symptom. Weakness of respiratory muscles is the major cause of mortality in these cases. Enzyme replacement therapy (ERT) with alglucosidase alfa (Myozyme; Genzyme Corp., Framingham, MA) is now available for all forms of glycogen storage disease type II. ERT has shown remarkable success in reversing pathology in cardiac muscle and extending life expectancy in infantile patients. However, skeletal muscle has proven to be a more challenging target for ERT. Although ERT is less effective in skeletal muscle than was hoped for, the lessons learned from both clinical and pre-clinical ERT studies have greatly expanded our understanding of the pathogenesis of the disease. A combination of fundamental studies and clinical follow-up, as well as exploration of other therapies, is necessary to take treatment for glycogen storage disease type II to the next level.
C1 [Hill, Victoria; Raben, Nina] NIAMS, NIH, Arthritis & Rheumatism Branch, Bethesda, MD 20892 USA.
[Schoser, Benedikt] Univ Munich, Dept Neurol, Friedrich Baur Inst, D-8000 Munich, Germany.
RP Raben, N (reprint author), NIAMS, NIH, Arthritis & Rheumatism Branch, 50 S Dr,Room 1345, Bethesda, MD 20892 USA.
EM rabenn@arb.niams.nih.gov
FU German ministry of education and research (Bundes Ministerium fur
Bildung und Forschung [German Ministry of Education and Research], Bonn,
Germany)
FX Benedikt Schoser is member of the German network on muscular dystrophies
(MD- NET, 01GM0601) funded by the German ministry of education and
research (Bundes Ministerium fur Bildung und Forschung [German Ministry
of Education and Research], Bonn, Germany).
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1933-7213
J9 NEUROTHERAPEUTICS
JI Neurotherapeutics
PD OCT
PY 2008
VL 5
IS 4
BP 569
EP 578
DI 10.1016/j.nurt.2008.08.009
PG 10
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 355SE
UT WOS:000259727800010
PM 19019308
ER
PT J
AU Wise, RA
AF Wise, Roy A.
TI Dopamine and Reward: The Anhedonia Hypothesis 30 years on
SO NEUROTOXICITY RESEARCH
LA English
DT Review
DE Dopamine; Reward; Reinforcement; Motivation; Anhedondia
ID INTRACRANIAL SELF-STIMULATION; VENTRAL TEGMENTAL AREA; NUCLEUS-ACCUMBENS
DOPAMINE; PIMOZIDE-INDUCED EXTINCTION; MEDIAL FOREBRAIN-BUNDLE;
FOOD-SEEKING BEHAVIOR; BRAIN-STIMULATION; TASTE-REACTIVITY; MOTIVATIONAL
PROCESSES; MOVEABLE ELECTRODE
AB The anhedonia hypothesis - that brain dopamine plays a critical role in the subjective pleasure associated with positive rewards - was intended to draw the attention of psychiatrists to the growing evidence that dopamine plays a critical role in the objective reinforcement and incentive motivation associated with food and water, brain stimulation reward, and psychomotor stimulant and opiate reward. The hypothesis called to attention the apparent paradox that neuroleptics, drugs used to treat a condition involving anhedonia (schizophrenia), attenuated in laboratory animals the positive reinforcement that we normally associate with pleasure. The hypothesis held only brief interest for psychiatrists, who pointed out that the animal studies reflected acute actions of neuroleptics whereas the treatment of schizophrenia appears to result from neuroadaptations to chronic neuroleptic administration, and that it is the positive symptoms of schizophrenia that neuroleptics alleviate, rather than the negative symptoms that include anhedonia. Perhaps for these reasons, the hypothesis has had minimal impact in the psychiatric literature. Despite its limited heuristic value for the understanding of schizophrenia, however, the anhedonia hypothesis has had major impact on biological theories of reinforcement, motivation, and addiction. Brain dopamine plays a very important role in reinforcement of response habits, conditioned preferences, and synaptic plasticity in cellular models of learning and memory. The notion that dopamine plays a dominant role in reinforcement is fundamental to the psychomotor stimulant theory of addiction, to most neuroadaptation theories of addiction, and to current theories of conditioned reinforcement and reward prediction. Properly understood, it is also fundamental to recent theories of incentive motivation.
C1 Natl Inst Drug Abuse, Behav Neurosc Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Wise, RA (reprint author), Natl Inst Drug Abuse, Behav Neurosc Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM rwise@intra.nida.nih.gov
RI Wise, Roy/A-6465-2012
FU Intramural NIH HHS [ZIA DA000471-07]
NR 150
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U1 4
U2 45
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1029-8428
J9 NEUROTOX RES
JI Neurotox. Res.
PD OCT
PY 2008
VL 14
IS 2-3
BP 169
EP 183
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 399KH
UT WOS:000262798300009
PM 19073424
ER
EF