FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Trimble, EL
Abrams, JS
Meyer, RM
Calvo, F
Cazap, E
Deye, J
Eisenhauer, E
Fitzgerald, TJ
Lacombe, D
Parmar, M
Seibel, N
Shankar, L
Swart, AM
Therasse, P
Vikram, B
von Frenckell, R
Friedlander, M
Fujiwara, K
Kaplan, RS
Meunier, F
AF Trimble, Edward L.
Abrams, Jeffrey S.
Meyer, Ralph M.
Calvo, Fabien
Cazap, Eduardo
Deye, James
Eisenhauer, Elizabeth
Fitzgerald, Thomas J.
Lacombe, Denis
Parmar, Max
Seibel, Nita
Shankar, Lalitha
Swart, Ann Marie
Therasse, Patrick
Vikram, Bhadrasain
von Frenckell, Remy
Friedlander, Michael
Fujiwara, Keiichi
Kaplan, Richard S.
Meunier, Francoise
TI Improving Cancer Outcomes Through International Collaboration in
Academic Cancer Treatment Trials
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
ID MINIMAL RESIDUAL DISEASE; BREAST-CANCER; CLINICAL-TRIALS; RESPONSE
CRITERIA; SOLID TUMORS; BCR-ABL; RECOMMENDATIONS; LEUKEMIA; PCR;
STANDARDIZATION
AB Purpose
The need for international collaboration in cancer clinical trials has grown stronger as we have made progress both in cancer treatment and screening. We sought to identify those efforts already underway which facilitate such collaboration, as well as barriers to greater collaboration.
Methods
We reviewed the collective experiences of many cooperative groups, governmental organizations, nongovernmental organizations, and academic investigators in their work to build international collaboration in cancer clinical trials across multiple disease sites.
Results
More than a decade of work has led to effective global harmonization for many of the elements critical to cancer clinical trials. Many barriers remain, but effective international collaboration in academic cancer treatment trials should become the norm, rather than the exception.
Conclusion
Our ability to strengthen international collaborations will result in maximization of our resources and patients, permitting us to change practice by establishing more effective therapeutic strategies. Regulatory, logistical, and financial hurdles, however, often hamper the conduct of joint trials. We must work together as a global community to overcome these barriers so that we may continue to improve cancer treatment for patients around the world.
C1 NCI, Bethesda, MD 20892 USA.
Univ Massachusetts, Worcester, MA 01605 USA.
Natl Canc Inst, Canada Clin Trials Grp, Kingston, ON, Canada.
Natl Canc Inst, Paris, France.
Latin Amer & Caribbean Soc Med Oncol, Buenos Aires, DF, Argentina.
European Org Res Treatment Canc, Brussels, Belgium.
GlaxoSmithKline Biol, Rixensart, Belgium.
MRC, Clin Trials Unit, London, England.
Natl Canc Res Network, Leeds, W Yorkshire, England.
Univ New S Wales, Sydney, NSW, Australia.
Saitama Med Univ, Hidaka City, Saitama, Japan.
RP Trimble, EL (reprint author), 6130 Execut Blvd,Suite 7025, Bethesda, MD 20892 USA.
EM tt6m@nih.gov
RI friedlander, michael/G-3490-2013
OI friedlander, michael/0000-0002-6488-0604
FU Medical Research Council [MC_U122861379]
NR 28
TC 22
Z9 22
U1 0
U2 5
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD OCT 20
PY 2009
VL 27
IS 30
BP 5109
EP U194
DI 10.1200/JCO.2009.22.5771
PG 6
WC Oncology
SC Oncology
GA 507SN
UT WOS:000270875100030
PM 19720905
ER
PT J
AU Kramer, BS
Hagerty, KL
Somerfield, MR
Schellhammer, P
AF Kramer, Barnett S.
Hagerty, Karen L.
Somerfield, Mark R.
Schellhammer, Paul
TI Guideline for 5-alpha-Reductase Inhibitors in the Prevention of Prostate
Cancer Is Premature Reply
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
C1 [Kramer, Barnett S.] NIH, Bethesda, MD 20892 USA.
[Hagerty, Karen L.; Somerfield, Mark R.] Amer Soc Clin Oncol, Alexandria, VA USA.
[Schellhammer, Paul] Eastern Virginia Med Sch, Sentara Med Grp, Norfolk, VA 23501 USA.
RP Kramer, BS (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD OCT 20
PY 2009
VL 27
IS 30
BP E165
EP E165
DI 10.1200/JCO.2009.25.0886
PG 1
WC Oncology
SC Oncology
GA 507SN
UT WOS:000270875100041
ER
PT J
AU Song, HT
Jordan, EK
Lewis, BK
Liu, W
Ganjei, J
Klaunberg, B
Despres, D
Palmieri, D
Frank, JA
AF Song, Ho-Taek
Jordan, Elaine K.
Lewis, Bobbi K.
Liu, Wei
Ganjei, Justin
Klaunberg, Brenda
Despres, Daryl
Palmieri, Diane
Frank, Joseph A.
TI Rat model of metastatic breast cancer monitored by MRI at 3 tesla and
bioluminescence imaging with histological correlation
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
ID IN-VIVO; BRAIN METASTASES; CELL-LINES; TRANSFECTION AGENT; CONTRAST
AGENTS; CNS METASTASIS; MOUSE MODEL; STEM-CELLS; NANOPARTICLES;
FERUMOXIDES
AB Background: Establishing a large rodent model of brain metastasis that can be monitored using clinically relevant magnetic resonance imaging (MRI) techniques is challenging. Non-invasive imaging of brain metastasis in mice usually requires high field strength MR units and long imaging acquisition times. Using the brain seeking MDA-MB-231BR transfected with luciferase gene, a metastatic breast cancer brain tumor model was investigated in the nude rat. Serial MRI and bioluminescence imaging (BLI) was performed and findings were correlated with histology. Results demonstrated the utility of multimodality imaging in identifying unexpected sights of metastasis and monitoring the progression of disease in the nude rat.
Methods: Brain seeking breast cancer cells MDA-MB-231BR transfected with firefly luciferase (231BRL) were labeled with ferumoxides-protamine sulfate (FEPro) and 1-3 x 10(6) cells were intracardiac (IC) injected. MRI and BLI were performed up to 4 weeks to monitor the early breast cancer cell infiltration into the brain and formation of metastases. Rats were euthanized at different time points and the imaging findings were correlated with histological analysis to validate the presence of metastases in tissues.
Results: Early metastasis of the FEPro labeled 231BRL were demonstrated on T2*-weighted MRI and BLI within 1 week post IC injection of cells. Micro-metastatic tumors were detected in the brain on T2-weighted MRI as early as 2 weeks post-injection in greater than 85% of rats. Unexpected skeletal metastases from the 231BRL cells were demonstrated and validated by multimodal imaging. Brain metastases were clearly visible on T2 weighted MRI by 3-4 weeks post infusion of 231BRL cells, however BLI did not demonstrate photon flux activity originating from the brain in all animals due to scattering of the photons from tumors.
Conclusion: A model of metastatic breast cancer in the nude rat was successfully developed and evaluated using multimodal imaging including MRI and BLI providing the ability to study the temporal and spatial distribution of metastases in the brain and skeleton.
C1 [Song, Ho-Taek; Jordan, Elaine K.; Lewis, Bobbi K.; Liu, Wei; Ganjei, Justin; Frank, Joseph A.] NIH, Frank Lab, Radiol & Imaging Sci Clin Ctr, Bethesda, MD 20892 USA.
[Song, Ho-Taek] Yonsei Univ, Coll Med, Dept Radiol, Seoul, South Korea.
[Liu, Wei] Philips Res N Amer, Briarcliff Manor, NY USA.
[Klaunberg, Brenda; Despres, Daryl] NINDS, Mouse Imaging Facil, NIH, Bethesda, MD 20892 USA.
[Palmieri, Diane] NCI, Womens Canc Sect, Mol Pharmacol Lab, NIH, Bethesda, MD 20892 USA.
[Frank, Joseph A.] Natl Inst Biomed Imaging & Bioengn, Intramural Res Program, Bethesda, MD 20892 USA.
RP Song, HT (reprint author), NIH, Frank Lab, Radiol & Imaging Sci Clin Ctr, Bldg 10, Bethesda, MD 20892 USA.
EM hotsong@yuhs.ac; ekj@helix.nih.gov; blewis@cc.nih.gov;
wei.liu_1@philips.com; ganjeijb@cc.nih.gov; klaunbeb@mail.nih.gov;
despres@mail.nih.gov; palmierd@mail.nih.gov; jafrank@helix.nih.gov
RI Palmieri, Diane/B-4258-2015
FU National Institutes of Health
FX This work was supported by the Intramural Research Program of the
Clinical Center at the National Institutes of Health. We would also like
to acknowledge Philips Medical Systems as part of a cooperative research
and development agreement for providing the radiofrequency coil.
NR 36
TC 31
Z9 32
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD OCT 20
PY 2009
VL 7
AR 88
DI 10.1186/1479-5876-7-88
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 516HB
UT WOS:000271531700001
PM 19840404
ER
PT J
AU Kim, A
Gillespie, A
Dombi, E
Goodwin, A
Goodspeed, W
Fox, E
Balis, FM
Widemann, BC
AF Kim, A.
Gillespie, A.
Dombi, E.
Goodwin, A.
Goodspeed, W.
Fox, E.
Balis, F. M.
Widemann, B. C.
TI Characteristics of children enrolled in treatment trials for NF1-related
plexiform neurofibromas
SO NEUROLOGY
LA English
DT Article
ID PHASE-I TRIAL; REFRACTORY SOLID TUMORS; PEDIATRIC-PATIENTS;
ANGIOGENESIS; ONCOLOGY; HYPERTENSION; GROWTH; TYPE-1; NF1
AB Objective: To describe the characteristics of children enrolled in treatment trials for neurofibromatosis type 1 (NF1)-related plexiform neurofibroma (PN), PN tumor burden, PN-related complications, and treatment outcomes and to highlight the differences between characteristics of children with NF1 vs children with cancers entered on early phase drug trials.
Methods: Pre-enrollment characteristics and complications of PN were retrospectively analyzed in a cohort of 59 children with NF1-related PN treated on 1 of 7 clinical trials at the NIH between 1996 and 2007. Outcome was analyzed in a subset of 19 patients enrolled in phase I trials. Comparisons to children with cancer were made from a similar analysis performed recently.
Results: The median age at enrollment was 8 years. The median PN volume was 555 mL. Most patients had no prior chemotherapy or radiation, but nearly half had previous surgery for PN. PN-associated complications and NF1 manifestations were common, including pain (53%), other tumors (18%), and hypertension (8%). Investigational drug therapy was well tolerated. A median of 10 treatment cycles was administered. Patients with NF1-related PN were younger, had better performance score, had less prior therapy, and remained on study longer than cancer patients.
Conclusions: Children with NF1-related plexiform neurofibroma (PN) enrolled in clinical trials had large tumors with substantial morbidity. Clinical trials in these children provide information about drug tolerance, cumulative toxicity, and pharmacokinetics in a younger population than early phase pediatric cancer trials. This report may aid in the evaluation of the applicability of traditional pediatric cancer trial designs and endpoints for NF1-related PN. Neurology (R) 2009;73:1273-1279
C1 [Kim, A.; Gillespie, A.; Dombi, E.; Goodwin, A.; Goodspeed, W.; Fox, E.; Balis, F. M.; Widemann, B. C.] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Kim, A (reprint author), NCI, Pediat Oncol Branch, Ctr Canc Res, 10 Ctr Dr,Bldg 10 CRC,Room 1-3872, Bethesda, MD 20892 USA.
EM kimaer@mail.nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research
FX Supported by the Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research. The views expressed do not
necessarily represent the views of the NIH or the US government.
NR 25
TC 29
Z9 29
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD OCT 20
PY 2009
VL 73
IS 16
BP 1273
EP 1279
DI 10.1212/WNL.0b013e3181bd1326
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 508GU
UT WOS:000270918800005
PM 19841379
ER
PT J
AU Chen, G
Henter, ID
Manji, HK
AF Chen, Guang
Henter, Ioline D.
Manji, Husseini K.
TI A role for PKC in mediating stress-induced prefrontal cortical
structural plasticity and cognitive function
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Editorial Material
ID GENOME-WIDE ASSOCIATION; BIPOLAR-DISORDER; WORKING-MEMORY; LITHIUM
TREATMENT; SCHIZOPHRENIA; MORPHOLOGY; CORTEX
C1 [Manji, Husseini K.] Johnson & Johnson Pharmaceut Res & Dev, Titusville, NJ 08560 USA.
[Chen, Guang; Henter, Ioline D.] NIMH, Mood & Anxiety Disorders Program, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Manji, HK (reprint author), Johnson & Johnson Pharmaceut Res & Dev, Titusville, NJ 08560 USA.
EM hmanji@its.jnj.com
RI Chen, Guang/A-2570-2017
NR 20
TC 6
Z9 6
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 20
PY 2009
VL 106
IS 42
BP 17613
EP 17614
DI 10.1073/pnas.0909771106
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 508UR
UT WOS:000270963100004
PM 19828441
ER
PT J
AU Matsumoto, S
Yasui, H
Batra, S
Kinoshita, Y
Bernardo, M
Munasinghe, JP
Utsumi, H
Choudhuri, R
Devasahayam, N
Subramanian, S
Mitchell, JB
Krishna, MC
AF Matsumoto, Shingo
Yasui, Hironobu
Batra, Sonny
Kinoshita, Yuichi
Bernardo, Marcelino
Munasinghe, Jeeva P.
Utsumi, Hideo
Choudhuri, Rajani
Devasahayam, Nallathamby
Subramanian, Sankaran
Mitchell, James B.
Krishna, Murali C.
TI Simultaneous imaging of tumor oxygenation and microvascular permeability
using Overhauser enhanced MRI
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE angiogenesis; dynamic nuclear polarization; hyperpolarized MRI; tumor
hypoxia; DCE-MRI
ID ANTI-ANGIOGENIC THERAPY; CONTRAST AGENTS; MOLECULAR-WEIGHTS; RESONANCE;
HYPOXIA; CANCER; VASCULATURE; MATURATION; RADIATION
AB Architectural and functional abnormalities of blood vessels are a common feature in tumors. A consequence of increased vascular permeability and concomitant aberrant blood flow is poor delivery of oxygen and drugs, which is associated with treatment resistance. In the present study, we describe a strategy to simultaneously visualize tissue oxygen concentration and microvascular permeability by using a hyperpolarized (1)H-MRI, known as Over-hauser enhanced MRI (OMRI), and an oxygen-sensitive contrast agent OX63. Substantial MRI signal enhancement was induced by dynamic nuclear polarization (DNP). The DNP achieved up to a 7,000% increase in MRI signal at an OX63 concentration of 1.5 mM compared with that under thermal equilibrium state. The extent of hyperpolarization is influenced mainly by the local concentration of OX63 and inversely by the tissue oxygen level. By collecting dynamic OMRI images at different hyperpolarization levels, local oxygen concentration and microvascular permeability of OX63 can be simultaneously determined. Application of this modality to murine tumors revealed that tumor regions with high vascular permeability were spatio- temporally coincident with hypoxia. Quantitative analysis of image data from individual animals showed an inverse correlation between tumor vascular leakage and median oxygen concentration. Immunohistochemical analyses of tumor tissues obtained from the same animals after OMRI experiments demonstrated that lack of integrity in tumor blood vessels was associated with increased tumor microvascular permeability. This dual imaging technique may be useful for the longitudinal assessment of changes in tumor vascular function and oxygenation in response to chemotherapy, radiotherapy, or anti-angiogenic treatment.
C1 [Matsumoto, Shingo; Yasui, Hironobu; Batra, Sonny; Choudhuri, Rajani; Devasahayam, Nallathamby; Subramanian, Sankaran; Mitchell, James B.; Krishna, Murali C.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Bernardo, Marcelino] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Batra, Sonny] Natl Inst Hlth Res Scholar Program, Howard Hughes Med Inst, NIH, Bethesda, MD USA.
[Munasinghe, Jeeva P.] NINDS, NIH, Bethesda, MD 20892 USA.
[Kinoshita, Yuichi; Utsumi, Hideo] Kyushu Univ, Fac Pharmaceut Sci, Fukuoka 8128581, Japan.
[Bernardo, Marcelino] NCI, SAIC Frederick, Frederick, MD 21702 USA.
RP Krishna, MC (reprint author), NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM murali@helix.nih.gov
RI Yasui, Hironobu/E-3794-2010; U-ID, Kyushu/C-5291-2016
FU Intramural Research Program; Center for Cancer Research; National Cancer
Institute; National Institutes of Health
FX We thank the National Institutes of Health Fellows Editorial Board for
editing this manuscript. This work was supported by the Intramural
Research Program, Center for Cancer Research, National Cancer Institute,
National Institutes of Health.
NR 32
TC 48
Z9 48
U1 1
U2 17
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 20
PY 2009
VL 106
IS 42
BP 17898
EP 17903
DI 10.1073/pnas.0908447106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 508UR
UT WOS:000270963100054
PM 19815528
ER
PT J
AU Senkevich, TG
Koonin, EV
Moss, B
AF Senkevich, Tatiana G.
Koonin, Eugene V.
Moss, Bernard
TI Predicted poxvirus FEN1-like nuclease required for homologous
recombination, double-strand break repair and full-size genome formation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE DNA processing; poxvirus genome replication
ID VACCINIA VIRUS TELOMERES; DNA POLYMERASE; INFECTED CELLS; REPLICATION;
PROTEIN; RESOLVASE; RNA; SUBSTITUTIONS; REPRESSION; CLEAVAGE
AB Poxviruses encode many if not all of the proteins required for viral genome replication in the cytoplasm of the host cell. In this context, we investigated the function of the vaccinia virus G5 protein because it belongs to the FEN1-like family of nucleases and is conserved in all poxviruses. A vaccinia virus G5 deletion mutant was severely impaired, as the yield of infectious virus was reduced by approximately two orders of magnitude. The mutant virions contained an apparently normal complement of proteins but appeared spherical rather than brick-shaped and contained no detectable DNA. The inability of G5 with substitutions of the predicted catalytic aspartates to complement the deletion mutant suggested that G5 functions as a nuclease during viral DNA replication. Although the amount of viral DNA produced in the absence of G5 was similar to that made by wild-type virus, the mean size was approximately one-fourth of the genome length. Experiments with transfected plasmids showed that G5 was required for double-strand break repair by homologous recombination, suggesting a similar role during vaccinia virus genome replication.
C1 [Senkevich, Tatiana G.; Moss, Bernard] NIAID, Viral Dis Lab, Bethesda, MD 20892 USA.
[Koonin, Eugene V.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, 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 David Evans (University of Alberta, Edmonton, Canada) for
plasmids, Jerry Weirfortheloan ofapulsed- field gel apparatus, Andrea
Weisberg for electron microscopy, Catherine Cotter for preparation of
cell cultures, and David Evans and Paula Traktman for critical comments
and suggestions. The work was supported by funds from the Division of
Intramural Research, National Institute of Allergy and Infectious
Diseases, National Institutes of Health.
NR 30
TC 21
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U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 20
PY 2009
VL 106
IS 42
BP 17921
EP 17926
DI 10.1073/pnas.0909529106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 508UR
UT WOS:000270963100058
PM 19805122
ER
PT J
AU Zhou, P
Zhao, YT
Guo, YB
Xu, SM
Bai, SH
Lakatta, EG
Cheng, HP
Hao, XM
Wang, SQ
AF Zhou, Peng
Zhao, Yan-Ting
Guo, Yun-Bo
Xu, Shi-Ming
Bai, Shu-Hua
Lakatta, Edward G.
Cheng, Heping
Hao, Xue-Mei
Wang, Shi-Qiang
TI beta-Adrenergic signaling accelerates and synchronizes cardiac ryanodine
receptor response to a single L-type Ca2+ channel
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE beta-adrenergic receptor; calcium signaling; excitation-contraction
coupling; isoproterenol; protein kinase A
ID KINASE-A PHOSPHORYLATION; PROTEIN-KINASE; SARCOPLASMIC-RETICULUM;
HEART-FAILURE; VENTRICULAR MYOCYTES; CALCIUM CHANNELS; SR CA2+; RELEASE;
MODULATION; CELLS
AB As the most prototypical G protein-coupled receptor, beta-adrenergic receptor (beta AR) regulates the pace and strength of heart beating by enhancing and synchronizing L-type channel (LCC) Ca2+ influx, which in turn elicits greater sarcoplasmic reticulum (SR) Ca2+ release flux via ryanodine receptors (RyRs). However, whether and how beta AR-protein kinase A (PKA) signaling directly modulates RyR function remains elusive and highly controversial. By using unique single-channel Ca2+ imaging technology, we measured the response of a single RyR Ca2+ release unit, in the form of a Ca2+ spark, to its native trigger, the Ca2+ sparklet from a single LCC. We found that acute application of the selective beta AR agonist isoproterenol (1 mu M, <= 20 min) increased triggered spark amplitude in an LCC unitary current-independent manner. The increased ratio of Ca2+ release flux underlying a Ca2+ spark to SR Ca2+ content indicated that beta AR stimulation helps to recruit additional RyRs in synchrony. Quantification of sparklet-spark kinetics showed that beta AR stimulation synchronized the stochastic latency and increased the fidelity (i.e., chance of hit) of LCC-RyR intermolecular signaling. The RyR modulation was independent of the increased SR Ca2+ content. The PKA antagonists Rp-8-CPT-cAMP (100 mu M) and H89 (10 mu M) both eliminated these effects, indicating that beta AR acutely modulates RyR activation via the PKA pathway. These results demonstrate unequivocally that RyR activation by a single LCC is accelerated and synchronized during beta AR stimulation. This molecular mechanism of sympathetic regulation will permit more fundamental studies of altered beta AR effects in cardiovascular diseases.
C1 [Zhou, Peng; Zhao, Yan-Ting; Guo, Yun-Bo; Xu, Shi-Ming; Bai, Shu-Hua; Hao, Xue-Mei; Wang, Shi-Qiang] Peking Univ, Coll Life Sci, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China.
[Cheng, Heping] Peking Univ, Inst Mol Med, Beijing 100871, Peoples R China.
[Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA.
RP Wang, SQ (reprint author), Peking Univ, Coll Life Sci, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China.
EM wsq@pku.edu.cn
RI Zhou, Peng/M-3917-2013; Zhao, Yan-Ting/K-5096-2015
OI Zhao, Yan-Ting/0000-0001-8541-893X
FU 973 Major State Basic Research Development Program of China
[2004CB720007, 2007CB512100]; 863 Program [2007AA02Z457]; National
Natural Science Foundation of China [30730013, 30721064, 30728012,
30630021]; National Institutes of Health [R01 TW007269]; National
Institute on Aging of the National Institutes of Health
FX This work was funded by 973 Major State Basic Research Development
Program of China Grants 2004CB720007 (to S.-Q. W.) and 2007CB512100 (to
H. C.), 863 Program Grant 2007AA02Z457, National Natural Science
Foundation of China Grants 30730013, 30721064, 30728012 (to S.Q. W.),
and 30630021 (to H. C.), National Institutes of Health Grant R01
TW007269 (to S.-Q. W.), and the Intramural Research Program of the
National Institute on Aging of the National Institutes of Health.
NR 39
TC 30
Z9 32
U1 1
U2 10
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 20
PY 2009
VL 106
IS 42
BP 18028
EP 18033
DI 10.1073/pnas.0906560106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 508UR
UT WOS:000270963100076
PM 19815510
ER
PT J
AU Philosof-Mazor, L
Volinsky, R
Jopp, J
Blumberg, P
Rapaport, H
Marquez, VE
Jelinek, R
AF Philosof-Mazor, Liron
Volinsky, Roman
Jopp, Jurgen
Blumberg, Peter
Rapaport, Hanna
Marquez, Victor E.
Jelinek, Raz
TI Lipid-Modulated Pharmacophore Nanorods Assembled at the Air/Water
Interface
SO CHEMPHYSCHEM
LA English
DT Article
DE biomimetic chemistry; DAG lactones; Langmuir-Blodgett films; monolayers;
nanostructures
ID PROTEIN-KINASE-C; WHITE-LIGHT INTERFEROMETRY; PEPTIDE NANOSTRUCTURES;
DAG-LACTONES; NANOFIBERS; DERIVATIVES; MONOLAYERS; MECHANISM; FIBRILS;
FILMS
C1 [Marquez, Victor E.] NCI, Med Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
[Philosof-Mazor, Liron; Volinsky, Roman; Jopp, Jurgen; Jelinek, Raz] Ben Gurion Univ Negev, Dept Chem, IL-84105 Beer Sheva, Israel.
[Philosof-Mazor, Liron; Volinsky, Roman; Jopp, Jurgen; Jelinek, Raz] Ben Gurion Univ Negev, Ilse Katz Inst Nanotechnol, IL-84105 Beer Sheva, Israel.
[Blumberg, Peter] NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bethesda, MD 20992 USA.
[Rapaport, Hanna] Ben Gurion Univ Negev, Dept Biotechnol Engn, IL-84105 Beer Sheva, Israel.
RP Marquez, VE (reprint author), NCI, Med Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
EM marquezv@mail.nih.gov; razj@bgu.ac.il
RI Volinsky, Roman/B-8443-2011; JELINEK, RAZ/F-2023-2012;
OI jelinek, raz/0000-0002-0336-1384
FU National Cancer Institute; Center of Cancer Research; National
Institutes of Health
FX This work was supported in part by the intramural research program of
the National Cancer Institute, Center of Cancer Research, the National
Institutes of Health.
NR 23
TC 3
Z9 3
U1 0
U2 5
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY
SN 1439-4235
J9 CHEMPHYSCHEM
JI ChemPhysChem
PD OCT 19
PY 2009
VL 10
IS 15
BP 2615
EP 2619
DI 10.1002/cphc.200900539
PG 5
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 515RN
UT WOS:000271490600008
PM 19672915
ER
PT J
AU Bogen, K
Biener, L
Garrett, CA
Allen, J
Cummings, KM
Hartman, A
Marcus, S
McNeill, A
O'Connor, RJ
Parascandola, M
Pederson, L
AF Bogen, Karen
Biener, Lois
Garrett, Catherine A.
Allen, Jane
Cummings, K. Michael
Hartman, Anne
Marcus, Stephen
McNeill, Ann
O'Connor, Richard J.
Parascandola, Mark
Pederson, Linda
TI Surveillance indicators for potential reduced exposure products (PREPs):
developing survey items to measure awareness
SO HARM REDUCTION JOURNAL
LA English
DT Article
ID TOBACCO PRODUCTS; SMOKELESS TOBACCO; HARM REDUCTION; CONSUMER AWARENESS;
CIGARETTES; ATTITUDES; BELIEFS; SMOKING; PERCEPTIONS; EXPERTS
AB Background: Over the past decade, tobacco companies have introduced cigarettes and smokeless tobacco products (known as Potential Reduced Exposure Products, PREPs) with purportedly lower levels of some toxins than conventional cigarettes and smokeless products. It is essential that public health agencies monitor awareness, interest, use, and perceptions of these products so that their impact on population health can be detected at the earliest stages.
Methods: This paper reviews and critiques existing strategies for measuring awareness of PREPs from 16 published and unpublished studies. From these measures, we developed new surveillance items and subjected them to two rounds of cognitive testing, a common and accepted method for evaluating questionnaire wording.
Results: Our review suggests that high levels of awareness of PREPs reported in some studies are likely to be inaccurate. Two likely sources of inaccuracy in awareness measures were identified: 1) the tendency of respondents to misclassify "no additive" and "natural" cigarettes as PREPs and 2) the tendency of respondents to mistakenly report awareness as a result of confusion between PREPs brands and similarly named familiar products, for example, Eclipse chewing gum and Accord automobiles.
Conclusion: After evaluating new measures with cognitive interviews, we conclude that as of winter 2006, awareness of reduced exposure products among U. S. smokers was likely to be between 1% and 8%, with the higher estimates for some products occurring in test markets. Recommended measurement strategies for future surveys are presented.
C1 [Bogen, Karen] Math Policy Res, Cambridge, MA USA.
[Biener, Lois; Garrett, Catherine A.] Univ Massachusetts, Survey Res Ctr, Boston, MA 02125 USA.
[Allen, Jane] Amer Legacy Fdn, Washington, DC USA.
[Cummings, K. Michael; O'Connor, Richard J.] Roswell Pk Canc Inst, Dept Hlth Behav, Buffalo, NY 14263 USA.
[Hartman, Anne; Marcus, Stephen; Parascandola, Mark] NCI, NIH, Washington, DC USA.
[McNeill, Ann] Univ Nottingham, Div Epidemiol & Publ Hlth, Nottingham NG7 2RD, England.
[Pederson, Linda] Univ Colorado, Beth El Coll Nursing & Hlth Sci, Colorado Springs, CO 80907 USA.
RP Bogen, K (reprint author), Math Policy Res, Cambridge, MA USA.
EM kbogen@mathematica-mpr.com; lois.biener@umb.edu;
catherine.garrett@comcast.net; JAllen@americanlegacy.org;
Michael.Cummings@roswellpark.org; Anne_Hartman@nih.gov;
marcusst@mail.nih.gov; Ann.Mcneill@nottingham.ac.uk;
Richard.Oconnor@roswellpark.org; mark.parascandola@nih.hhs.gov;
lindap@mindspring.com
RI O'Connor, Richard/A-6961-2009;
OI Biener, Lois/0000-0002-4130-8138
FU NCI NIH HHS [R01 CA086257]
NR 28
TC 5
Z9 5
U1 1
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1477-7517
J9 HARM REDUCT J
JI Harm Reduct. J.
PD OCT 19
PY 2009
VL 6
AR 27
DI 10.1186/1477-7517-6-27
PG 8
WC Substance Abuse
SC Substance Abuse
GA 542YA
UT WOS:000273534000001
PM 19840394
ER
PT J
AU Lim, PJ
Danner, R
Liang, J
Doong, H
Harman, C
Srinivasan, D
Rothenberg, C
Wang, HM
Ye, YH
Fang, SY
Monteiro, MJ
AF Lim, Precious J.
Danner, Rebecca
Liang, Jing
Doong, Howard
Harman, Christine
Srinivasan, Deepa
Rothenberg, Cara
Wang, Hongmin
Ye, Yihong
Fang, Shengyun
Monteiro, Mervyn J.
TI Ubiquilin and p97/VCP bind erasin, forming a complex involved in ERAD
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID RETICULUM-ASSOCIATED DEGRADATION; UNFOLDED PROTEIN RESPONSE;
ENDOPLASMIC-RETICULUM; CAENORHABDITIS-ELEGANS; QUALITY-CONTROL;
AAA-ATPASE; ALZHEIMERS-DISEASE; PROTEASOME; MEMBRANE; PATHWAYS
AB Unwanted proteins in the endoplasmic reticulum (ER) are exported into the cytoplasm and degraded by the proteasome through the ER-associated protein degradation pathway (ERAD). Disturbances in ERAD are linked to ER stress, which has been implicated in the pathogenesis of several human diseases. However, the composition and organization of ERAD complexes in human cells is still poorly understood. In this paper, we describe a trimeric complex that we propose functions in ERAD. Knockdown of erasin, a platform for p97/VCP and ubiquilin binding, or knockdown of ubiquilin in human cells slowed degradation of two classical ERAD substrates. In Caenorhabditis elegans, ubiquilin and erasin are ER stress-response genes that are regulated by the ire-1 branch of the unfolded protein response pathway. Loss of ubiquilin or erasin resulted in activation of ER stress, increased accumulation of polyubiquitinated proteins, and shortened lifespan in worms. Our results strongly support a role for this complex in ERAD and in the regulation of ER stress.
C1 [Lim, Precious J.; Danner, Rebecca; Liang, Jing; Doong, Howard; Harman, Christine; Srinivasan, Deepa; Rothenberg, Cara; Wang, Hongmin; Fang, Shengyun; Monteiro, Mervyn J.] Univ Maryland, Inst Biotechnol, Ctr Med Biotechnol, Baltimore, MD 21201 USA.
[Ye, Yihong] NIDDKD, NIH, Bethesda, MD 20892 USA.
RP Monteiro, MJ (reprint author), Univ Maryland, Inst Biotechnol, Ctr Med Biotechnol, Baltimore, MD 21201 USA.
EM monteiro@umbi.umd.edu
RI Monteiro, Mervyn/H-3813-2011; Fang, Shengyun/H-3802-2011
FU National Institutes of Health [GM066287, AG016839, GM06696]
FX This work was supported by National Institutes of Health grants GM066287
and AG016839 to M. J. Monteiro, and GM06696 to S. Fang.
NR 60
TC 63
Z9 76
U1 1
U2 6
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 950 THIRD AVE, 2ND FLR, NEW YORK, NY 10022 USA
SN 0021-9525
EI 1540-8140
J9 J CELL BIOL
JI J. Cell Biol.
PD OCT 19
PY 2009
VL 187
IS 2
BP 201
EP 217
DI 10.1083/jcb.200903024
PG 17
WC Cell Biology
SC Cell Biology
GA 508FN
UT WOS:000270914600009
PM 19822669
ER
PT J
AU Shiao, YH
Lupascu, ST
Gu, YD
Kasprzak, W
Hwang, CJ
Fields, JR
Leighty, RM
Quinones, O
Shapiro, BA
Alvord, WG
Anderson, LM
AF Shiao, Yih-Horng
Lupascu, Sorin T.
Gu, Yuhan D.
Kasprzak, Wojciech
Hwang, Christopher J.
Fields, Janet R.
Leighty, Robert M.
Quinones, Octavio
Shapiro, Bruce A.
Alvord, W. Gregory
Anderson, Lucy M.
TI An Intergenic Non-Coding rRNA Correlated with Expression of the rRNA and
Frequency of an rRNA Single Nucleotide Polymorphism in Lung Cancer Cells
SO PLOS ONE
LA English
DT Article
ID PARALLEL GENETIC ALGORITHM; EXTERNAL TRANSCRIBED SPACER; SECONDARY
STRUCTURE; IN-VIVO; PREDICTION; PROMOTER; SEQUENCE; DNA; METHYLATION;
BIOGENESIS
AB Background: Ribosomal RNA (rRNA) is a central regulator of cell growth and may control cancer development. A cis noncoding rRNA (nc-rRNA) upstream from the 45S rRNA transcription start site has recently been implicated in control of rRNA transcription in mouse fibroblasts. We investigated whether a similar nc-rRNA might be expressed in human cancer epithelial cells, and related to any genomic characteristics.
Methodology/Principal Findings: Using quantitative rRNA measurement, we demonstrated that a nc-rRNA is transcribed in human lung epithelial and lung cancer cells, starting from approximately -1000 nucleotides upstream of the rRNA transcription start site (+1) and extending at least to +203. This nc-rRNA was significantly more abundant in the majority of lung cancer cell lines, relative to a nontransformed lung epithelial cell line. Its abundance correlated negatively with total 45S rRNA in 12 of 13 cell lines (P = 0.014). During sequence analysis from -388 to +306, we observed diverse, frequent intercopy single nucleotide polymorphisms (SNPs) in rRNA, with a frequency greater than predicted by chance at 12 sites. A SNP at +139 (U/C) in the 59 leader sequence varied among the cell lines and correlated negatively with level of the nc-rRNA (P = 0.014). Modelling of the secondary structure of the rRNA 5'-leader sequence indicated a small increase in structural stability due to the +139 U/C SNP and a minor shift in local configuration occurrences.
Conclusions/Significance: The results demonstrate occurrence of a sense nc-rRNA in human lung epithelial and cancer cells, and imply a role in regulation of the rRNA gene, which may be affected by a +139 SNP in the 5' leader sequence of the primary rRNA transcript.
RP Shiao, YH (reprint author), Natl Canc Inst Frederick, Comparat Carcinogenesis Lab, Frederick, MD USA.
EM shiaoy@mail.nih.gov
FU CCR NIH HHS [HHSN261200800001C]; Intramural NIH HHS; NCI NIH HHS
[HHSN261200800001E]; PHS HHS [HHSN261200800001E]
NR 61
TC 7
Z9 8
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 19
PY 2009
VL 4
IS 10
AR e7505
DI 10.1371/journal.pone.0007505
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 507UP
UT WOS:000270880900009
PM 19838300
ER
PT J
AU Biesova, Z
Miller, MA
Schneerson, R
Shiloach, J
Green, KY
Robbins, JB
Keith, JM
AF Biesova, Zuzana
Miller, Mark A.
Schneerson, Rachel
Shiloach, Joseph
Green, Kim Y.
Robbins, John B.
Keith, Jerry M.
TI Preparation, characterization, and immunogenicity in mice of a
recombinant influenza H5 hemagglutinin vaccine against the avian H5N1
A/Vietnam/1203/2004 influenza virus
SO VACCINE
LA English
DT Article
DE Influenza; Hemagglutinin; Rapid production
ID A VIRUSES; ANTIBODY; PROTECTION; INFECTION; PROTEINS; EFFICACY; TOXOIDS;
HUMANS
AB Production of influenza vaccines requires a minimum of 6 months after the circulating strain is isolated and the use of infectious viruses. The hemagglutinin (protective antigen) of circulating influenza viruses mutates rapidly requiring reformulation of the vaccines. Our goal is to eliminate the risk of working with infectious virus and reduce significantly the production time.
A cDNA fragment encoding the influenza virus A/Vietnam/1203/2004 (H5N1) HA gene was prepared using RT-PCR with viral RNA as a template. Recombinant HA (rHA) protein was produced in Escherichia coli and purified from isolated inclusion bodies by urea solubilization and Ni(+)-ion column chromatography. Vaccine candidates were prepared by treating the rHA with formalin, adsorption onto alum or with both. Mice were injected subcutaneously with candidate vaccines two or three times 2 weeks apart. Sera were collected 1 week after the last injection and antibody measured by ELISA and hemagglutination inhibition (HI). The highest antibody response (GM 449 EU) was elicited by three injections of 15 mu g alum-adsorbed rHA. Dosages of 5 p,g of rHA formulated with formalin and alum, and 5 mu g alum-adsorbed rHA elicited IgG anti-HA of GM 212 and 177 EU, respectively. HI titers, >= 40 were obtained in >= 80% of mice with three doses of all formulations.
We developed a method to produce rHA in a time-frame suitable for annual and pandemic influenza vaccination. Using this method, rHA vaccine can be produced in 3-4 weeks and when formulated with alum, induces HA antibody levels in young outbred mice consistent with the FDA guidelines for vaccines against epidemic and pandemic influenza. Published by Elsevier Ltd.
C1 [Biesova, Zuzana; Schneerson, Rachel; Robbins, John B.; Keith, Jerry M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev & Mol Immun, NIH, Bethesda, MD 20892 USA.
[Miller, Mark A.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Shiloach, Joseph] NIDDK, Biotechnol Unit, NIH, Bethesda, MD 20892 USA.
[Green, Kim Y.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Keith, JM (reprint author), NICHD, NIH, 31 Ctr Dr,Room 2A29,MSC 2423, Bethesda, MD 20892 USA.
EM keithjer@mail.nih.gov
FU Intramural NIH HHS [Z99 AI999999, Z99 HD999999]
NR 34
TC 35
Z9 37
U1 0
U2 5
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD OCT 19
PY 2009
VL 27
IS 44
BP 6234
EP 6238
DI 10.1016/j.vaccine.2009.07.107
PG 5
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 515QB
UT WOS:000271486100020
PM 19686692
ER
PT J
AU Ben-Efraim, I
Frosst, PD
Gerace, L
AF Ben-Efraim, Iris
Frosst, Phyllis D.
Gerace, Larry
TI Karyopherin binding interactions and nuclear import mechanism of nuclear
pore complex protein Tpr
SO BMC CELL BIOLOGY
LA English
DT Article
ID MESSENGER-RNA EXPORT; ATTACHED INTRANUCLEAR FILAMENTS; MYOSIN-LIKE
PROTEIN-1; NUCLEOCYTOPLASMIC TRANSPORT; CELL-CYCLE; NUCLEOPORINS; YEAST;
IDENTIFICATION; RAN; ASSOCIATION
AB Background: Tpr is a large protein with an extended coiled-coil domain that is localized within the nuclear basket of the nuclear pore complex. Previous studies [1] involving antibody microinjection into mammalian cells suggested a role for Tpr in nuclear export of proteins via the CRM1 export receptor. In addition, Tpr was found to co-immunoprecipitate with importins alpha and beta from Xenopus laevis egg extracts [2], although the function of this is unresolved. Yeast Mlp1p and Mlp2p, which are homologous to vertebrate Tpr, have been implicated in mRNA surveillance to retain unspliced mRNAs in the nucleus[3,4]. To augment an understanding of the role of Tpr in nucleocytoplasmic trafficking, we explored the interactions of recombinant Tpr with the karyopherins CRM1, importin beta and importin alpha by solid phase binding assays. We also investigated the conditions required for nuclear import of Tpr using an in vitro assay.
Results: We found that Tpr binds strongly and specifically to importin alpha, importin beta, and a CRM1 containing trimeric export complex, and that the binding sites for importins alpha and beta are distinct. We also determined that the nuclear import of Tpr is dependent on cytosolic factors and energy and is efficiently mediated by the importin alpha/beta import pathway.
Conclusion: Based on the binding and nuclear import assays, we propose that Tpr is imported into the nucleus by the importin alpha/beta heterodimer. In addition, we suggest that Tpr can serve as a nucleoporin binding site for importin beta during import of importin beta cargo complexes and/or importin beta recycling. Our finding that Tpr bound preferentially to CRM1 in an export complex strengthens the notion that Tpr is involved in protein export.
C1 [Ben-Efraim, Iris; Frosst, Phyllis D.; Gerace, Larry] Scripps Res Inst, Dept Cell Biol, La Jolla, CA 92037 USA.
[Frosst, Phyllis D.] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Gerace, L (reprint author), Scripps Res Inst, Dept Cell Biol, La Jolla, CA 92037 USA.
EM ibenefra@gmail.com; Frosst@mail.nih.gov; lgerace@scripps.edu
FU [GM41955]
FX We thank Dr. Ralph H. Kehlenbach for preparing the polyclonal antibodies
against the C-terminus of CRM1. This work was supported by grant GM41955
to L. G.
NR 52
TC 16
Z9 17
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2121
J9 BMC CELL BIOL
JI BMC Cell Biol.
PD OCT 16
PY 2009
VL 10
AR 74
DI 10.1186/1471-2121-10-74
PG 9
WC Cell Biology
SC Cell Biology
GA 520PV
UT WOS:000271858500001
PM 19835572
ER
PT J
AU Yarmolinsky, DA
Zuker, CS
Ryba, NJP
AF Yarmolinsky, David A.
Zuker, Charles S.
Ryba, Nicholas J. P.
TI Common Sense about Taste: From Mammals to Insects
SO CELL
LA English
DT Article
ID DROSOPHILA GUSTATORY SYSTEM; TO-CELL COMMUNICATION; BITTER TASTE;
RECEPTOR-CELLS; OLFACTORY RECEPTORS; UMAMI TASTE; SALT TASTE; CAFFEINE
RESPONSE; ION CHANNELS; SWEET
C1 [Yarmolinsky, David A.; Zuker, Charles S.] Columbia Univ, Columbia Coll Phys & Surg, Howard Hughes Med Inst, Dept Biochem & Mol Biophys, New York, NY 10032 USA.
[Yarmolinsky, David A.; Zuker, Charles S.] Columbia Univ, Columbia Coll Phys & Surg, Howard Hughes Med Inst, Dept Neurosci, New York, NY 10032 USA.
[Ryba, Nicholas J. P.] NIDCR, Bethesda, MD 20892 USA.
RP Zuker, CS (reprint author), Columbia Univ, Columbia Coll Phys & Surg, Howard Hughes Med Inst, Dept Biochem & Mol Biophys, New York, NY 10032 USA.
EM cz2195@columbia.edu
RI Marion-Poll, Frederic/D-8882-2011
OI Marion-Poll, Frederic/0000-0001-6824-0180
FU Howard Hughes Medical Institute; Intramural NIH HHS
NR 89
TC 248
Z9 253
U1 9
U2 103
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD OCT 16
PY 2009
VL 139
IS 2
BP 234
EP 244
DI 10.1016/j.cell.2009.10.001
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 507MI
UT WOS:000270857500010
PM 19837029
ER
PT J
AU Krashes, MJ
DasGupta, S
Vreede, A
White, B
Armstrong, JD
Waddell, S
AF Krashes, Michael J.
DasGupta, Shamik
Vreede, Andrew
White, Benjamin
Armstrong, J. Douglas
Waddell, Scott
TI A Neural Circuit Mechanism Integrating Motivational State with Memory
Expression in Drosophila
SO CELL
LA English
DT Article
ID LONG-TERM-MEMORY; RAT HIPPOCAMPAL SLICE; NEUROPEPTIDE Y-LIKE;
FEEDING-BEHAVIOR; MUSHROOM BODY; PRESYNAPTIC INHIBITION;
PANCREATIC-POLYPEPTIDE; SYNAPTIC-TRANSMISSION; TARGETED EXPRESSION;
LOCOMOTOR-ACTIVITY
AB Behavioral expression of food-associated memory in fruit flies is constrained by satiety and promoted by hunger, suggesting an influence of motivational state. Here, we identify a neural mechanism that integrates the internal state of hunger and appetitive memory. We show that stimulation of neurons that express neuropeptide F(dNPF), an ortholog of mammalian NPY, mimics food deprivation and promotes memory performance in satiated flies. Robust appetitive memory performance requires the dNPF receptor in six dopaminergic neurons that innervate a distinct region of the mushroom bodies. Blocking these dopaminergic neurons releases memory performance in satiated flies, whereas stimulation suppresses memory performance in hungry flies. Therefore, dNPF and dopamine provide a motivational switch in the mushroom body that controls the output of appetitive memory.
C1 [Krashes, Michael J.; DasGupta, Shamik; Waddell, Scott] Univ Massachusetts, Sch Med, Dept Neurobiol, Worcester, MA 01605 USA.
[Vreede, Andrew; White, Benjamin] NIMH, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Armstrong, J. Douglas] Univ Edinburgh, Sch Informat, Inst Adapt & Neural Computat, Edinburgh EH1 2QL, Midlothian, Scotland.
[Krashes, Michael J.] Harvard Univ, Sch Med, Div Endocrinol Diabet & Metab, Dept Med, Boston, MA 02215 USA.
RP Waddell, S (reprint author), Univ Massachusetts, Sch Med, Dept Neurobiol, 364 Plantat St, Worcester, MA 01605 USA.
EM scott.waddell@umassmed.edu
RI Marion-Poll, Frederic/D-8882-2011
OI Marion-Poll, Frederic/0000-0001-6824-0180
FU National Institutes of Health [MH09883, MH081982]; National Research
Service Award [DA024499]
FX We thank Andre Fiala, Paul Garrity, Julie Simpson, Ping Shen, Tim Tully,
and Troy Zars for flies. We also thank Geraldine Wright, Hans Hoffman,
Tzumin Lee, and Stanley Heinze for their input. This work was supported
by National Institutes of Health grants MH09883 and MH081982 to S. W.
and National Research Service Award DA024499 to M. J. K.
NR 82
TC 216
Z9 223
U1 4
U2 32
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD OCT 16
PY 2009
VL 139
IS 2
BP 416
EP 427
DI 10.1016/j.cell.2009.08.035
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 507MI
UT WOS:000270857500023
PM 19837040
ER
PT J
AU Gomez-Rodriguez, J
Sahu, N
Handon, R
Davidson, TS
Anderson, SM
Kirby, MR
August, A
Schwartzberg, PL
AF Gomez-Rodriguez, Julio
Sahu, Nisebita
Handon, Robin
Davidson, Todd S.
Anderson, Stacie M.
Kirby, Martha R.
August, Avery
Schwartzberg, Pamela L.
TI Differential Expression of Interleukin-17A and-17F Is Coupled to T Cell
Receptor Signaling via Inducible T Cell Kinase
SO IMMUNITY
LA English
DT Article
ID ARYL-HYDROCARBON RECEPTOR; TEC-FAMILY KINASES; ROR-GAMMA-T; MICE
LACKING; TGF-BETA; IL-17 PRODUCTION; TYROSINE KINASE; GENE-EXPRESSION;
ALLERGIC-ASTHMA; TH2 DEVELOPMENT
AB T helper 17 (Th17) cells play major roles in autoimmunity and bacterial infections, yet how T cell receptor (TCR) signaling affects Th17 cell differentiation is relatively unknown. We demonstrate that CD4(+) T cells lacking ltk, a tyrosine kinase required for full TCR-induced phospholipase C-gamma (PLC-gamma 1) activation, exhibit decreased interleukin-17A (IL-17A) expression in vitro and in vivo, despite relatively normal expression of retinoic acid receptor-related orphan receptor-gamma T (ROR-gamma T) and IL-17F. IL-17A expression was rescued by pharmacologically induced Ca(2+) influx or constitutively activated nuclear factor of activated T cells (NFAT). Conversely, decreased TCR stimulation or calcineurin inhibition preferentially reduced IL-17A expression. We further found that the promoter of Il17a but not Il17f has a conserved NFAT binding site that bound NFATc1 in wild-type but not ltk-deficient cells, even though both exhibited open chromatin conformations. Finally, ltk(-/-) mice also showed differential regulation of IL-17A and IL-17F in vivo. Our results suggest that ltk specifically couples TCR signaling to Il17a expression and the differential regulation of Th17 cell cytokines through NFATc1.
C1 [Gomez-Rodriguez, Julio; Handon, Robin; Anderson, Stacie M.; Kirby, Martha R.; Schwartzberg, Pamela L.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Sahu, Nisebita] Penn State Univ, Dept Biochem & Mol Biol, University Pk, PA 16802 USA.
[Davidson, Todd S.] NIAID, NIH, Bethesda, MD 20892 USA.
[Sahu, Nisebita; August, Avery] Penn State Univ, Dept Vet & Biomed Sci, Ctr Mol Immunol & Infect Dis, University Pk, PA 16802 USA.
RP Schwartzberg, PL (reprint author), NHGRI, NIH, Bethesda, MD 20892 USA.
EM pams@mail.nih.gov
FU NHGRI, NIH; NIH [A1051626]
FX We would like to thank the Schwartzberg laboratory, J. Zhu, H. Yamane
and J. Cote-Sierra for advice and helpful discussions; D. Littman, N.
Clipstone, and L. Berg for retroviral constructs and mice, J. Fekecs and
D. Leja for graphics assistance, and J. O'Shea, J. Zhu, J. Cannons and
W. Paul for critical reading of the manuscript. This work was supported
by funding from the intramural research program of the NHGRI, NIH (to
PLS) and NIH grant A1051626 (to AA).
NR 51
TC 92
Z9 95
U1 1
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD OCT 16
PY 2009
VL 31
IS 4
BP 587
EP 597
DI 10.1016/j.immuni.2009.07.009
PG 11
WC Immunology
SC Immunology
GA 514OI
UT WOS:000271403900010
PM 19818650
ER
PT J
AU Crawford, NPS
Yang, HL
Mattaini, KR
Hunter, KW
AF Crawford, Nigel P. S.
Yang, Hailiu
Mattaini, Katherine R.
Hunter, Kent W.
TI The Metastasis Efficiency Modifier Ribosomal RNA Processing 1 Homolog B
(RRP1B) Is a Chromatin-associated Factor
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BROMODOMAIN PROTEIN BRD4; TRANSGENIC MOUSE MODEL; BREAST-CANCER
SURVIVAL; EXPRESSION SIGNATURE; IDENTIFICATION; NUCLEOPHOSMIN;
POLYMORPHISMS; TRANSCRIPTION; LOCALIZATION; PROGRESSION
AB There is accumulating evidence for a role of germ line variation in breast cancer metastasis. We have recently identified a novel metastasis susceptibility gene, Rrp1b (ribosomal RNA processing 1 homolog B). Overexpression of Rrp1b in a mouse mammary tumor cell line induces a gene expression signature that predicts survival in breast cancer. Here we extend the analysis of RRP1B function by demonstrating that the Rrp1b activation gene expression signature accurately predicted the outcome in three of four publicly available breast carcinoma gene expression data sets. In addition, we provide insights into the mechanism of RRP1B. Tandem affinity purification demonstrated that RRP1B physically interacts with many nucleosome binding factors, including histone H1X, poly(ADP-ribose) polymerase 1, TRIM28 (tripartite motif-containing 28), and CSDA (cold shock domain protein A). Co-immunofluorescence and co-immunoprecipitation confirmed these interactions and also interactions with heterochromatin protein-1 alpha and acetyl-histone H4 lysine 5. Finally, we investigated the effects of ectopic expression of an RRP1B allelic variant previously associated with improved survival in breast cancer. Gene expression analyses demonstrate that, compared with ectopic expression of wild type RRP1B in HeLa cells, the variant RRP1B differentially modulates various transcription factors controlled by TRIM28 and CSDA. These data suggest that RRP1B, a tumor progression and metastasis susceptibility candidate gene, is potentially a dynamic modulator of transcription and chromatin structure.
C1 [Hunter, Kent W.] NCI, Lab Canc Biol & Genet, CCR, NIH, Bethesda, MD 20892 USA.
RP Hunter, KW (reprint author), NCI, Lab Canc Biol & Genet, CCR, NIH, Bldg 37,Rm 5046,37 Convent Dr, Bethesda, MD 20892 USA.
EM hunter@mail.nih.gov
FU National Institutes of Health; NCI; Center for Cancer Research;
Intramural Research Program
FX This work was supported, in whole or in part, by the National Institutes
of Health, NCI, Center for Cancer Research, Intramural Research Program.
NR 45
TC 18
Z9 19
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 16
PY 2009
VL 284
IS 42
BP 28660
EP 28673
DI 10.1074/jbc.M109.023457
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 505GD
UT WOS:000270678900021
PM 19710015
ER
PT J
AU O'Connell, MP
Fiori, JL
Kershner, EK
Frank, BP
Indig, FE
Taub, DD
Hoek, KS
Weeraratna, AT
AF O'Connell, Michael P.
Fiori, Jennifer L.
Kershner, Emily K.
Frank, Brittany P.
Indig, Fred E.
Taub, Dennis D.
Hoek, Keith S.
Weeraratna, Ashani T.
TI Heparan Sulfate Proteoglycan Modulation of Wnt5A Signal Transduction in
Metastatic Melanoma Cells
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID EXPRESSION; GROWTH; DOMAIN; MIGRATION; SYNDECAN-1; PERLECAN; PATHWAY;
QSULF1; GENE; PHOSPHORYLATION
AB Heparan sulfate proteoglycans (HSPGs) are important modulators for optimizing signal transduction of many pathways, including the Wnt pathways. We demonstrate that HSPG glycosaminoglycan levels increased with increasing metastatic potential of melanoma cells. Previous studies have demonstrated that Wnt5A increases the invasiveness of melanoma cells. We further demonstrate that HSPGs potentiate Wnt5A signaling, since enzymatic removal of the HSPG backbone resulted in a decrease in cellular Wnt5A levels, an increase in secreted Wnt5A in cell media, a decrease in downstream signaling, and ultimately, a decrease in invasiveness. Specifically, syndecan 1 and syndecan 4 expression correlated to Wnt5A expression and melanoma malignancy. Knockdown of syndecan 1 or 4 caused decreases in cell invasion, which could be restored by treating the cells with recombinant Wnt5A. These data indicate that syndecan 1 and 4 correlate to increased metastatic potential in melanoma patients and are an important component of the Wnt5A autocrine signaling loop, the activation of which leads to increased metastasis of melanoma.
C1 [Weeraratna, Ashani T.] NIA, Immunol Lab, Res Resources Branch, NIH, Baltimore, MD 21224 USA.
[Fiori, Jennifer L.] NIA, Clin Invest Lab, Res Resources Branch, NIH, Baltimore, MD 21224 USA.
[Indig, Fred E.] NIA, Confocal Imaging Unit, Res Resources Branch, NIH, Baltimore, MD 21224 USA.
[Hoek, Keith S.] Univ Zurich Hosp, Dept Dermatol, CH-8091 Zurich, Switzerland.
RP Weeraratna, AT (reprint author), 251 Bayview Blvd,Suite 100,Rm08C226, Baltimore, MD 21224 USA.
EM weerarat@mail.nih.gov
FU National Institutes of Health Intramural Research Program of the NIA
FX This work was supported, in whole or in part, by the National Institutes
of Health Intramural Research Program of the NIA (Baltimore, MD).
NR 47
TC 39
Z9 40
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 16
PY 2009
VL 284
IS 42
BP 28704
EP 28712
DI 10.1074/jbc.M109.028498
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 505GD
UT WOS:000270678900026
PM 19696445
ER
PT J
AU Aleman, C
Jimenez, AI
Cativiela, C
Nussinov, R
Casanovas, J
AF Aleman, Carlos
Jimenez, Ana I.
Cativiela, Carlos
Nussinov, Ruth
Casanovas, Jordi
TI Conformational Preferences of 1-Amino-2-phenylcyclohexanecarboxylic
Acid, a Phenylalanine Cyclohexane Analogue
SO JOURNAL OF ORGANIC CHEMISTRY
LA English
DT Article
ID BACKBONE AMIDE INTERACTIONS; SIDE-CHAIN; AMINO-ACIDS; SOLVATION MODEL;
PEPTIDES; PROTEINS; DIPEPTIDES; DENSITY; ENERGY; DERIVATIVES
AB The intrinsic conformational preferences of the restricted phenylalanine analogue generated by including the alpha and beta carbon atoms into a cyclohexane ring (1-amino-2-phenylcyclohexanecarboxylic acid, c(6)Phe) have been determined using quantum mechanical calculations. Specifically, the conformational profile of the N-acetyl-N'-methylamide derivative Of the c(6)Phe stereoisomers exhibiting either a cis or a trans relative orientation between the amino and phenyl substituents has been analyzed in different environments (gas phase, chloroform, and aqueous solutions). Calculations were performed using B3LYP, MP2, and HF methods combined with the 6-31 + G(d,p) and 6-311 + + G(d,p) basis sets, and a self-consistent reaction-field (SCRF) method was applied to analyze the influence of the solvent. The amino acids investigated can be viewed as constrained phenylalanine analogues with a rigidly oriented aromatic side chain that may interact with the peptide backbone not only sterically but also electronically through the aromatic pi orbitals. Their conformational propensities have been found to be strongly influenced by the specific orientation of the aromatic substituent in each stercoisomer and the conformation adopted by the cyclohexane ring, as well as by the environment.
C1 [Aleman, Carlos] Univ Politecn Cataluna, Dept Engn Quim, ETS Engn Ind Barcelona, E-08028 Barcelona, Spain.
[Aleman, Carlos] Univ Politecn Cataluna, Ctr Res Nanoengn, E-08028 Barcelona, Spain.
[Jimenez, Ana I.; Cativiela, Carlos] Univ Zaragoza, CSIC, Dept Quim Organ, Inst Ciencia Mat Aragon, E-50009 Zaragoza, Spain.
[Nussinov, Ruth] NCI, Basic Res Program, SAIC Frederick Inc, Ctr Canc Res Nanobiol Program, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Fac Med, Dept Human Genet, IL-69978 Tel Aviv, Israel.
[Casanovas, Jordi] Univ Lleida, Escola Politecn Super, Dept Quim, E-25001 Lleida, Spain.
RP Aleman, C (reprint author), Univ Politecn Cataluna, Dept Engn Quim, ETS Engn Ind Barcelona, Diagonal 647, E-08028 Barcelona, Spain.
EM carlos.aleman@upc.edu; jcasanovas@quimica.udl.cat
RI Casanovas, Jordi/B-5435-2013
OI Casanovas, Jordi/0000-0002-4914-9194
FU Ministerio de Educacion y Ciencia - FEDER [CTQ2007-62245]; Gobierno de
Aragon [E40]; Generalitat de Catalunya [SGR 925]; National Cancer
Institute, National Institutes of Health [N01-CO-12400]; NIH, National
Cancer Institute, Center for Cancer Research
FX Gratitude is expressed to the Centre de Supercomputacio de Catalunya
(CESCA) for computational facilities. Financial support from the
Ministerio de Educacion y Ciencia - FEDER (project CTQ2007-62245),
Gobierno de Aragon (research group E40), and Generalitat de Catalunya
(research group 2009 SGR 925) is gratefully acknowledged. Support for
the research of C.A. was received through the prize "ICREA Academia" for
excellence in research funded by the Generalitat de Catalunya. This
project 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. The content of this publication does not necessarily
reflect the view of the policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organization imply endorsement by the U.S. Government. This research was
supported (in part) by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research.
NR 49
TC 7
Z9 7
U1 0
U2 2
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-3263
J9 J ORG CHEM
JI J. Org. Chem.
PD OCT 16
PY 2009
VL 74
IS 20
BP 7834
EP 7843
DI 10.1021/jo901594e
PG 10
WC Chemistry, Organic
SC Chemistry
GA 503AZ
UT WOS:000270504900029
PM 19772338
ER
PT J
AU Chandrashekar, J
Yarmolinsky, D
von Buchholtz, L
Oka, Y
Sly, W
Ryba, NJP
Zuker, CS
AF Chandrashekar, Jayaram
Yarmolinsky, David
von Buchholtz, Lars
Oka, Yuki
Sly, William
Ryba, Nicholas J. P.
Zuker, Charles S.
TI The Taste of Carbonation
SO SCIENCE
LA English
DT Article
ID CARBONIC-ANHYDRASE; MAMMALIAN SWEET; RECEPTOR-CELLS; ORAL SENSATION;
BITTER TASTE; UMAMI TASTE; FAMILY; RAT; ACETAZOLAMIDE; DROSOPHILA
AB Carbonated beverages are commonly available and immensely popular, but little is known about the cellular and molecular mechanisms underlying the perception of carbonation in the mouth. In mammals, carbonation elicits both somatosensory and chemosensory responses, including activation of taste neurons. We have identified the cellular and molecular substrates for the taste of carbonation. By targeted genetic ablation and the silencing of synapses in defined populations of taste receptor cells, we demonstrated that the sour-sensing cells act as the taste sensors for carbonation, and showed that carbonic anhydrase 4, a glycosylphosphatidylinositol-anchored enzyme, functions as the principal CO(2) taste sensor. Together, these studies reveal the basis of the taste of carbonation as well as the contribution of taste cells in the orosensory response to CO(2).
C1 [Chandrashekar, Jayaram; Yarmolinsky, David; Oka, Yuki; Zuker, Charles S.] Univ Calif San Diego, Howard Hughes Med Inst, La Jolla, CA 92093 USA.
[Chandrashekar, Jayaram; Yarmolinsky, David; Oka, Yuki; Zuker, Charles S.] Univ Calif San Diego, Dept Neurobiol, La Jolla, CA 92093 USA.
[Chandrashekar, Jayaram; Yarmolinsky, David; Oka, Yuki; Zuker, Charles S.] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA.
[von Buchholtz, Lars; Ryba, Nicholas J. P.] NIDCR, Bethesda, MD 20892 USA.
[Sly, William] St Louis Univ, Sch Med, Dept Biochem & Mol Biol, St Louis, MO 63104 USA.
RP Zuker, CS (reprint author), Columbia Univ, Dept Biochem & Mol Biophys, 630 W 168th St, New York, NY 10032 USA.
EM cz2195@columbia.edu
RI Marion-Poll, Frederic/D-8882-2011
OI Marion-Poll, Frederic/0000-0001-6824-0180
FU NIH; NIDCR; Howard Hughes Medical Institute
FX We thank W. Guo and A. Becker for generation and maintenance of mouse
lines, M. Hoon for help in the initial phase of this work, E. R. Swenson
for a generous gift of benzolamide, M. Goulding for
Rosa26-flox-STOP-TeNT mice, A. Waheed for Car4 antibodies, and members
of the Zuker laboratory for valuable comments. Supported in part by the
intramural research program of the NIH, NIDCR (N.J.P.R.). C.S.Z. is an
investigator of the Howard Hughes Medical Institute.
NR 38
TC 130
Z9 133
U1 10
U2 59
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD OCT 16
PY 2009
VL 326
IS 5951
BP 443
EP 445
DI 10.1126/science.1174601
PG 3
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 506ZM
UT WOS:000270818600058
PM 19833970
ER
PT J
AU Lubin, JH
Purdue, M
Kelsey, K
Zhang, ZF
Winn, D
Wei, QY
Talamini, R
Szeszenia-Dabrowska, N
Sturgis, EM
Smith, E
Shangina, O
Schwartz, SM
Rudnai, P
Neto, JE
Muscat, J
Morgenstern, H
Menezes, A
Matos, E
Mates, IN
Lissowska, J
Levi, F
Lazarus, P
La Vecchia, C
Koifman, S
Herrero, R
Franceschi, S
Wunsch, V
Fernandez, L
Fabianova, E
Daudt, AW
Dal Maso, L
Curado, MP
Chen, C
Castellsague, X
Brennan, P
Boffetta, P
Hashibe, M
Hayes, RB
AF Lubin, Jay H.
Purdue, Mark
Kelsey, Karl
Zhang, Zuo-Feng
Winn, Debbie
Wei, Qingyi
Talamini, Renato
Szeszenia-Dabrowska, Neonilia
Sturgis, Erich M.
Smith, Elaine
Shangina, Oxana
Schwartz, Stephen M.
Rudnai, Peter
Neto, Jose Eluf
Muscat, Joshua
Morgenstern, Hal
Menezes, Ana
Matos, Elena
Mates, Ioan Nicolae
Lissowska, Jolanta
Levi, Fabio
Lazarus, Philip
La Vecchia, Carlo
Koifman, Sergio
Herrero, Rolando
Franceschi, Silvia
Wuensch-Filho, Victor
Fernandez, Leticia
Fabianova, Eleonora
Daudt, Alexander W.
Dal Maso, Luigino
Curado, Maria Paula
Chen, Chu
Castellsague, Xavier
Brennan, Paul
Boffetta, Paolo
Hashibe, Mia
Hayes, Richard B.
TI Total Exposure and Exposure Rate Effects for Alcohol and Smoking and
Risk of Head and Neck Cancer: A Pooled Analysis of Case-Control Studies
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE alcohol drinking; risk model; smoking
ID UPPER AERODIGESTIVE TRACT; SQUAMOUS-CELL CARCINOMAS; MODELING TOTAL
EXPOSURE; LUNG-CANCER; CIGARETTE-SMOKING; ORAL-CANCER; BLADDER-CANCER;
TOBACCO; DNA; REPAIR
AB Although cigarette smoking and alcohol consumption increase risk for head and neck cancers, there have been few attempts to model risks quantitatively and to formally evaluate cancer site-specific risks. The authors pooled data from 15 case-control studies and modeled the excess odds ratio (EOR) to assess risk by total exposure (pack-years and drink-years) and its modification by exposure rate (cigarettes/day and drinks/day). The smoking analysis included 1,761 laryngeal, 2,453 pharyngeal, and 1,990 oral cavity cancers, and the alcohol analysis included 2,551 laryngeal, 3,693 pharyngeal, and 3,116 oval cavity cancers, with over 8,000 controls. Above 15 cigarettes/day, the EOR/pack-year decreased with increasing cigarettes/day, suggesting that greater cigarettes/day for a shorter duration was less deleterious than fewer cigarettes/day for a longer duration. Estimates of EOR/pack-year were homogeneous across sites, while the effects of cigarettes/day varied, indicating that the greater laryngeal cancer risk derived from differential cigarettes/day effects and not pack-years. EOR/drink-year estimates increased through 10 drinks/day, suggesting that greater drinks/day for a shorter duration was more deleterious than fewer drinks/day for a longer duration. Above 10 drinks/day, data were limited. EOR/drink-year estimates varied by site, while drinks/day effects were homogeneous, indicating that the greater pharyngeal/oral cavity cancer risk with alcohol consumption derived from the differential effects of drink-years and not drinks/day.
C1 [Lubin, Jay H.; Purdue, Mark; Winn, Debbie; Hayes, Richard B.] NCI, Bethesda, MD 20892 USA.
[Kelsey, Karl] Brown Univ, Ctr Environm Hlth & Technol, Providence, RI 02912 USA.
[Zhang, Zuo-Feng] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90024 USA.
[Wei, Qingyi; Sturgis, Erich M.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Talamini, Renato; Dal Maso, Luigino] Aviano Canc Ctr, I-33081 Aviano, Italy.
[Szeszenia-Dabrowska, Neonilia] Inst Occupat Med, Lodz, Poland.
[Smith, Elaine] Univ Iowa, Coll Publ Hlth, Iowa City, IA USA.
[Shangina, Oxana] Russian Acad Med Sci, Canc Res Ctr, Moscow, Russia.
[Schwartz, Stephen M.; Chen, Chu] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Rudnai, Peter] Natl Inst Environm Hlth, Budapest, Hungary.
[Neto, Jose Eluf; Wuensch-Filho, Victor] Univ Sao Paulo, Sao Paulo, Brazil.
[Muscat, Joshua; Lazarus, Philip] Penn State Univ, Coll Med, Hershey, PA USA.
[Morgenstern, Hal] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Morgenstern, Hal] Univ Michigan, Sch Publ Hlth, Dept Environm Hlth Sci, Ann Arbor, MI 48109 USA.
[Morgenstern, Hal] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Menezes, Ana] Univ Fed Pelotas, Pelotas, Brazil.
[Matos, Elena] Univ Buenos Aires, Inst Oncol Angel H Roffo, Buenos Aires, DF, Argentina.
[Mates, Ioan Nicolae] Univ Med & Pharm Carol Davila, Bucharest, Romania.
[Lissowska, Jolanta] M Sklodowska Curie Mem Can Ctr, Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Levi, Fabio] Univ Lausanne, Inst Med Sociale & Prevent, Lausanne, Switzerland.
[La Vecchia, Carlo] Univ Milan, Milan, Italy.
[La Vecchia, Carlo] Ist Ric Farmacol Mario Negri, Milan, Italy.
[Koifman, Sergio] Fundacao Oswaldo Cruz, Escola Nacl Saude Publ, Rio De Janeiro, Brazil.
[Herrero, Rolando] Inst Invest Epidemiol, San Jose, Costa Rica.
[Franceschi, Silvia; Curado, Maria Paula; Brennan, Paul; Boffetta, Paolo; Hashibe, Mia] Int Agcy Res Canc, F-69372 Lyon, France.
[Fernandez, Leticia] Inst Oncol & Radiobiol, Havana, Cuba.
[Fabianova, Eleonora] Specialized State Hlth Inst, Banska Bystrica, Slovakia.
[Daudt, Alexander W.] Hosp Clin Porto Alegre, Porto Alegre, RS, Brazil.
[Castellsague, Xavier] CIBER ESP, ICO, IDIBELL, Barcelona, Spain.
RP Lubin, JH (reprint author), NCI, Biostat Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd, Rockville, MD 20852 USA.
EM lubinj@mail.nih.gov
RI Wunsch Filho, Victor/C-4475-2012; Inca, Inct/K-2204-2013;
Epidemiologicas, Centro de pesquisas /D-4561-2013; Menezes,
Ana/G-7266-2012; Szeszenia-Dabrowska, Neonila/F-7190-2010; Castellsague
Pique, Xavier/N-5795-2014; Eluf-Neto, Jose/B-2522-2009; Curado, Maria
Paula/M-6200-2013; Mates, Ioan Nicolae/E-9255-2017
OI dal maso, luigino/0000-0001-6163-200X; La Vecchia,
Carlo/0000-0003-1441-897X; Hayes, Richard/0000-0002-0918-661X; Ioan
Nicoale, Mates/0000-0001-7210-0615; Lissowska,
Jolanta/0000-0003-2695-5799; Castellsague Pique,
Xavier/0000-0002-0802-3595; Eluf-Neto, Jose/0000-0001-7504-2115; Curado,
Maria Paula/0000-0001-8172-2483;
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute; Department of Health and Human Services
FX This research was supported by the Intramural Research Program of the
National Institutes of Health and the National Cancer Institute,
Department of Health and Human Services.
NR 51
TC 47
Z9 47
U1 1
U2 14
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD OCT 15
PY 2009
VL 170
IS 8
BP 937
EP 947
DI 10.1093/aje/kwp222
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 502GT
UT WOS:000270445300001
PM 19745021
ER
PT J
AU Jorgensen, TJ
Ruczinski, I
Kessing, B
Smith, MW
Shugart, YY
Alberg, AJ
AF Jorgensen, Timothy J.
Ruczinski, Ingo
Kessing, Bailey
Smith, Michael W.
Shugart, Yin Yao
Alberg, Anthony J.
TI Hypothesis-Driven Candidate Gene Association Studies: Practical Design
and Analytical Considerations
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE cancer; data analysis; DNA repair; genetic epidemiology; genome-wide
association study; haplotypes; polymorphism; single nucleotide; research
design
ID GENOME-WIDE ASSOCIATION; SINGLE-NUCLEOTIDE POLYMORPHISMS; TAGGING SNP
SELECTION; MULTIPLE SNPS; DISEASE; POWER; LINKAGE; PRIORITIZATION;
PREDICTION; SEQUENCE
AB Candidate gene association studies (CGAS) are a useful epidemiologic approach to drawing inferences about relations between genes and disease, especially when experimental data support the involvement of specific biochemical pathways. The value of CGAS is apparent when allele frequencies are low, effect sizes are small, or the study population is limited or unique. CGAS is also valuable for validating previous reports of genetic associations with disease in different populations. Despite the many advantages, the information generated from CGAS is sometimes compromised because of either inefficient study design or suboptimal analytical approaches. Here the authors discuss issues related to the study design and statistical analyses of CGAS that can help to optimize their usefulness and information content. These issues include judicious hypothesis-driven selection of biochemical pathways, genes, and single nucleotide polymorphisms, as well as appropriate quality control and analytical procedures for measuring main effects and for evaluating environmental exposure modifications and interactions. A study design algorithm using the example of DNA repair genes and cancer is presented for purposes of illustration.
C1 [Jorgensen, Timothy J.] Georgetown Univ, Dept Radiat Med, Med Ctr, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
[Ruczinski, Ingo] Johns Hopkins Univ, Dept Biostat, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
[Kessing, Bailey; Smith, Michael W.] NCI, Lab Genom Divers, Frederick, MD 21701 USA.
[Shugart, Yin Yao] NIMH, Genom Res Branch, Div Neurosci, Rockville, MD 20857 USA.
[Alberg, Anthony J.] Med Univ S Carolina, Hollings Canc Ctr, Charleston, SC 29425 USA.
[Alberg, Anthony J.] Med Univ S Carolina, Dept Biostat Bioinformat & Epidemiol, Charleston, SC 29425 USA.
RP Jorgensen, TJ (reprint author), Georgetown Univ, Dept Radiat Med, Med Ctr, Lombardi Comprehens Canc Ctr, 3970 Reservoir Rd NW, Washington, DC 20057 USA.
EM tjorge01@georgetown.edu
RI Smith, Michael/B-5341-2012
FU National Cancer Institute [CA105069, N01-CO-12400]; National Heart,
Lung, and Blood Institute [HL090577]; Intramural Research Program of the
National Institutes of Health; National Cancer Institute; Center for
Cancer Research
FX This work was supported in part by the National Cancer Institute (grant
CA105069) and the National Heart, Lung, and Blood Institute (grant
HL090577). Additionally, this project was supported in part with federal
funds from the National Cancer Institute, under contract N01-CO-12400.;
This research was also supported in part by the Intramural Research
Program of the National Institutes of Health, National Cancer Institute,
Center for Cancer Research.
NR 56
TC 35
Z9 35
U1 0
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD OCT 15
PY 2009
VL 170
IS 8
BP 986
EP 993
DI 10.1093/aje/kwp242
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 502GT
UT WOS:000270445300008
PM 19762372
ER
PT J
AU Wilson, RH
Whitehead, GS
Nakano, H
Free, ME
Kolls, JK
Cook, DN
AF Wilson, Rhonda H.
Whitehead, Gregory S.
Nakano, Hideki
Free, Meghan E.
Kolls, Jay K.
Cook, Donald N.
TI Allergic Sensitization through the Airway Primes Th17-dependent
Neutrophilia and Airway Hyperresponsiveness
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE asthma; lung; immunity
ID T-CELLS; EOSINOPHILIC INFLAMMATION; LUNG INFLAMMATION; TH2 RESPONSES;
SEVERE ASTHMA; ANTIGEN; INTERLEUKIN-17; DISSOCIATION; CHEMOKINE; MICE
AB Rationale: In humans, immune responses to inhaled aeroallergens develop in the lung and draining lymph nodes. Many animal models of asthma bypass this route and instead use intraperitoneal injections of allergen using aluminum hydroxide as an adjuvant. Objectives: We investigated whether allergic sensitization through the airway elicits immune responses qualitatively different than those arising in the peritoneum.
Methods: Mice were sensitized to allergen through the airway using low-dose LIPS as an adjuvant, or through the peritoneum using aluminum hydroxide as an adjuvant. After a single allergen challenge, ELISA and flow cytometry were used to measure cytokines and leukocyte subsets. Invasive measurements of airway resistance were used to measure allergen-induced airway hyperreactivity (AHR).
Measurements and Main Results: Sensitization through the peritoneum primed strong Th2 responses and eosinophilia, but not AHR, after a single allergen challenge. By contrast, allergic sensitization through the airway primed only modest Th2 responses, but strong Th17 responses. Th17 cells homed to the lung and released IL-17 into the airway on subsequent encounter with inhaled allergen. As a result, these mice developed IL-17-dependent airway neutrophilia and AHR. This AHR was neutrophil-dependent because it was abrogated in CXCR2-deficient mice and also in wild-type mice receiving a neutrophil-depleting antibody. Individually, neither IL-17 nor ongoing Th2 responses were sufficient to confer AHR, but together they acted synergistically to promote neutrophil recruitment, eosinophil recruitment and AHR.
Conclusions: Allergic sensitization through the airway primes modest Th2 responses but strong Th17 responses that promote airway neutrophilia and acute AHR. These findings support a causal role for neutrophils in severe asthma.
C1 [Cook, Donald N.] Natl Inst Environm Hlth Sci, Div Intramural Res, NIH, Lab Resp Biol, Res Triangle Pk, NC 27709 USA.
[Kolls, Jay K.] Childrens Hosp Pittsburgh, Dept Pediat & Immunol, Pittsburgh, PA 15213 USA.
RP Cook, DN (reprint author), Natl Inst Environm Hlth Sci, Div Intramural Res, NIH, Lab Resp Biol, 111 TW Alexander Dr,Bldg 101,Rm E244, Res Triangle Pk, NC 27709 USA.
EM usa.cookd@niehs.nih.gov
FU Intramural NIH HHS
NR 35
TC 181
Z9 203
U1 0
U2 12
PU AMER THORACIC SOC
PI NEW YORK
PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD OCT 15
PY 2009
VL 180
IS 8
BP 720
EP 730
DI 10.1164/rccm.200904-0573OC
PG 11
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 506AB
UT WOS:000270743100006
PM 19661246
ER
PT J
AU Oz, M
Lorke, DE
Petroianu, GA
AF Oz, Murat
Lorke, Dietrich E.
Petroianu, George A.
TI Methylene blue and Alzheimer's disease
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Methylene blue; Alzheimer disease; Neurodegenerative diseases;
Phenothiazines
ID MANIC-DEPRESSIVE PSYCHOSIS; PHENOTHIAZINE-DERIVATIVES; SEROTONIN
TOXICITY; IFOSFAMIDE ENCEPHALOPATHY; BETA OLIGOMERIZATION; CHOLINERGIC
SYSTEM; FILAMENT FORMATION; OXIDASE ACTIVITY; INHIBITION; BRAIN
AB The relationship between methylene blue (MB) and Alzheimer's disease (AD) has recently attracted increasing scientific attention since it has been suggested that MB may slow down the progression of this disease. In fact, MO, in addition to its well characterized inhibitory actions on the cGMP pathway, affects numerous cellular and molecular events closely related to the progression of AD. Currently, MB has been shown to attenuate the formations of amyloid plaques and neurofibrillary tangles, and to partially repair impairments in mitochondrial function and cellular metabolism. Furthermore, various neurotransmitter systems (cholinergic, serotonergic and glutamatergic), believed to play important roles in the pathogenesis of AD and other cognitive disorders, are also influenced by MB. Recent studies suggest that the combination of diverse actions of MB on these cellular functions is likely to mediate potential beneficial effects of MB. This has lead to attempts to develop novel MB-based treatment modalities for AD. In this review article, actions of MB on neurotransmitter systems and multiple cellular and molecular targets are summarized with regard to their relevance to AD. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Oz, Murat] Natl Inst Drug Abuse, Integrat Neurosci Sect, Intramural Res Program, NIH,DHHS, Baltimore, MD 21224 USA.
[Oz, Murat; Petroianu, George A.] UAE Univ, Dept Pharmacol, Fac Med & Hlth Sci, Al Ain, U Arab Emirates.
[Lorke, Dietrich E.] UAE Univ, Dept Anat, Fac Med & Hlth Sci, Al Ain, U Arab Emirates.
RP Oz, M (reprint author), Natl Inst Drug Abuse, Integrat Neurosci Sect, Intramural Res Program, NIH,DHHS, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM moz@intra.nida.nih.gov
RI Oz, Murat/E-2148-2012
NR 83
TC 94
Z9 94
U1 4
U2 36
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD OCT 15
PY 2009
VL 78
IS 8
BP 927
EP 932
DI 10.1016/j.bcp.2009.04.034
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 501KL
UT WOS:000270380500001
PM 19433072
ER
PT J
AU Helyar, SG
Patel, B
Headington, K
El Assal, M
Chatterjee, PK
Pacher, P
Mabley, JG
AF Helyar, Simon G.
Patel, Bella
Headington, Kevin
El Assal, Mary
Chatterjee, Prabal K.
Pacher, Pal
Mabley, Jon G.
TI PCB-induced endothelial cell dysfunction: Role of poly(ADP-ribose)
polymerase
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Polychlorinated biphenyl; Oxidative stress; PARP; Cardiovascular;
Atherosclerosis
ID E-DEFICIENT MICE; IN-VIVO EVIDENCE; NITRIC-OXIDE; PHARMACOLOGICAL
INHIBITION; POLYCHLORINATED-BIPHENYLS; PLAQUE STABILITY; ACTIVATION;
EXPRESSION; HYPERTENSION; SYNTHETASE
AB Polychlorinated biphenyls (PCBs) are persistent environmental pollutants implicated in the development of pro-inflammatory events critical in the pathology of atherosclerosis and cardiovascular disease. PCB exposure of endothelial cells results in increased cellular oxidative stress, activation of stress and inflammatory pathways leading to increased expression of cytokines and adhesion molecules and ultimately cell death, all of which can lead to development of atherosclerosis. To date no studies have been performed to examine the direct effects of PCB exposure on the vasculature relaxant response which if impaired may predispose individuals to hypertension, an additional risk factor for atherosclerosis. Overactivation of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP) following oxidative/nitrosative stress in endothelial cells and subsequent depletion of NADPH has been identified as a central mediator of cellular dysfunction. The aim therefore was to investigate whether 2,2',4,6,6'-pentachlorobiphenyl (PCB 104) directly causes endothelial cell dysfunction via increased oxidative stress and subsequent overactivation of PARP. Exposure of ex vivo rat aortic rings to PCB 104 impaired the acetylcholine-mediated relaxant response, an effect that was dependent on both concentration and exposure time. In vitro exposure of mouse endothelial cells to PCB 104 resulted in increased cellular oxidative stress through activation of the cytochrome p450 enzyme CYP1A1 with subsequent overactivation of PARP and NADPH depletion. Pharmacological inhibition of CYP1A1 or PARP protected against the PCB 104-mediated endothelial cell dysfunction. In conclusion, the environmental contaminants, PCBs, can activate PARP directly impairing endothelial cell function that may predispose exposed individuals to development of hypertension and cardiovascular disease. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Patel, Bella; Headington, Kevin; El Assal, Mary; Chatterjee, Prabal K.; Mabley, Jon G.] Univ Brighton, Sch Pharm & Biomol Sci, Brighton BN2 4GJ, E Sussex, England.
[Helyar, Simon G.] Brighton & Sussex Med Sch, Brighton BN1 9PH, E Sussex, England.
[Pacher, Pal] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
RP Mabley, JG (reprint author), Univ Brighton, Sch Pharm & Biomol Sci, Cockcroft Bldg,Lewes Rd, Brighton BN2 4GJ, E Sussex, England.
EM j.g.mabley@brighton.ac.uk
RI Mabley, Jon/D-2296-2010; Pacher, Pal/B-6378-2008
OI Pacher, Pal/0000-0001-7036-8108
FU Heart Research UK [RG2550/07/08]
FX SGH was supported by a Heart Research UK intercalated B.Sc. scholarship
(RG2550/07/08).
NR 51
TC 16
Z9 16
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD OCT 15
PY 2009
VL 78
IS 8
BP 959
EP 965
DI 10.1016/j.bcp.2009.06.019
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 501KL
UT WOS:000270380500005
PM 19549508
ER
PT J
AU Neveol, A
Mork, JG
Aronson, AR
AF Neveol, Aurelie
Mork, James G.
Aronson, Alan R.
TI Comment on 'MeSH-up: effective MeSH text classification for improved
document retrieval'
SO BIOINFORMATICS
LA English
DT Editorial Material
C1 [Neveol, Aurelie; Mork, James G.; Aronson, Alan R.] US Natl Lib Med, Bethesda, MD 20894 USA.
RP Neveol, A (reprint author), US Natl Lib Med, Bethesda, MD 20894 USA.
EM neveola@ncbi.nlm.nih.gov
FU Intramural NIH HHS
NR 7
TC 1
Z9 1
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
J9 BIOINFORMATICS
JI Bioinformatics
PD OCT 15
PY 2009
VL 25
IS 20
BP 2770
EP 2771
DI 10.1093/bioinformatics/btp483
PG 2
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA 505ID
UT WOS:000270685200032
PM 19671694
ER
PT J
AU Salvadore, G
Nugent, AC
Chen, G
Akula, N
Yuan, PX
Cannon, DM
Zarate, CA
McMahon, FJ
Manji, HK
Drevets, WC
AF Salvadore, Giacomo
Nugent, Allison C.
Chen, Guang
Akula, Nirmala
Yuan, Peixiong
Cannon, Dara M.
Zarate, Carlos A.
McMahon, Francis J.
Manji, Husseini K.
Drevets, Wayne C.
TI Bcl-2 Polymorphism Influences Gray Matter Volume in the Ventral Striatum
in Healthy Humans
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Accumbens; magnetic resonance imaging; neurogenetics; neuroplasticity;
voxel-based morphometry (VBM)
ID MOOD DISORDERS; HUMAN BRAIN; DEPRESSION; RESILIENCE; EXPRESSION;
LITHIUM; GENE
AB Background: Bcl-2 is a major regulator of neural plasticity and cellular resilience. A single nucleotide polymorphism (SNP) in the Bcl-2 gene, Bcl-2 rs956572, significantly modulates the expression of Bcl-2 protein and cellular vulnerability to apoptosis. We tested the hypothesis that this SNP would modulate gray matter (GM) volume in the limbic-cortical-striatal-pallidal-thalamic circuitry that plays major roles in mood regulation.
Methods: Forty-seven healthy subjects participated in this study (30 A carriers, 17 G homozygotes). Neuromorphometric differences between G homozygotes and A carriers were investigated using optimized voxel-based morphometry (VBM). Statistical significance was set at p<.05, corrected for multiple comparisons.
Results: A carriers showed less GM volume than G homozygotes in the left ventral striatum (p(corrected)<.05).
Conclusions: Genetic variation in the Bcl-2 gene modulates GM volume in areas known to play key roles in the neurobiology of reward processes and emotion regulation and in the pathophysiology of mood disorders. Thus, the findings from the current study are noteworthy insofar as they converge with preclinical findings that Bcl-2 functions to enhance neuronal viability and might indirectly extend this evidence to humans.
C1 [Salvadore, Giacomo; Nugent, Allison C.; Chen, Guang; Akula, Nirmala; Yuan, Peixiong; Zarate, Carlos A.; McMahon, Francis J.; Manji, Husseini K.; Drevets, Wayne C.] NIMH, Mood & Anxiety Disorders Program, US Dept HHS, Bethesda, MD 20892 USA.
[Cannon, Dara M.] Natl Univ Ireland Galway, Dept Psychiat, Galway, Ireland.
RP Salvadore, G (reprint author), NIMH, Mood & Anxiety Disorders Program, US Dept HHS, 15K N Dr,Room 300 F, Bethesda, MD 20892 USA.
EM salvadoreg@mail.nih.gov
RI Cannon, Dara/C-1323-2009; Chen, Guang/A-2570-2017;
OI Cannon, Dara/0000-0001-7378-3411; Nugent, Allison/0000-0003-2569-2480;
McMahon, Francis/0000-0002-9469-305X
FU National Institute of Mental Health, National Institutes of Health
FX This study was supported by the Intramural Research Program at the
National Institute of Mental Health, National Institutes of Health.
NR 20
TC 18
Z9 18
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD OCT 15
PY 2009
VL 66
IS 8
BP 804
EP 807
DI 10.1016/j.biopsych.2009.05.025
PG 4
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 502ZA
UT WOS:000270498500014
PM 19589501
ER
PT J
AU Cinelli, MA
Cordero, B
Dexheimer, TS
Pommier, Y
Cushman, M
AF Cinelli, Maris A.
Cordero, Brenda
Dexheimer, Thomas S.
Pommier, Yves
Cushman, Mark
TI Synthesis and biological evaluation of
14-(aminoalkyl-aminomethyl)aromathecins as topoisomerase I inhibitors:
Investigating the hypothesis of shared structure-activity relationships
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE Topoisomerase I; Aromathecins; Anticancer; Polyamine
ID DNA COVALENT COMPLEX; CAMPTOTHECIN ANALOGS; CLEAVAGE COMPLEXES;
ANTITUMOR-ACTIVITY; ORGANIC-SYNTHESIS; CHAIN-LENGTH; DERIVATIVES;
CANCER; CYTOTOXICITY; RESISTANCE
AB The aromathecin topoisomerase I (top1) inhibitors offer promising scaffolds for the development of novel cancer chemotherapeutics. They are 'composites' of the camptothecin and indenoisoquinoline top1 inhibitors. Interestingly, some structure-activity relationship (SAR) overlap between the aromathecins and the indenoisoquinolines has been observed. For both classes, placement of certain polar groups in similar regions of the heteroaromatic system improves top1 inhibitory and antiproliferative activities. A series of water-soluble aromathecins substituted at position 14 with diaminoalkanes of various lengths has been prepared. These compounds all possess similar antiproliferative potency, but a general trend is observed: aromathecins with longer diaminoalkane substituents (>6 carbons) possess lower anti-top1 activity than their smaller counterparts (2-4 carbons), presumably as a result of unfavorable hydrophobic interactions. This trend is also noted with the indenoisoquinolines, revealing additional SAR overlap that supports the hypothesis that there is a 'universal' top1 inhibitor SAR. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Cinelli, Maris A.; Cordero, Brenda; Cushman, Mark] Purdue Univ, Sch Pharm & Pharmaceut Sci, Dept Med Chem & Mol Pharmacol, W Lafayette, IN 47907 USA.
[Cinelli, Maris A.; Cordero, Brenda; Cushman, Mark] Purdue Univ, Purdue Canc Ctr, W Lafayette, IN 47907 USA.
[Dexheimer, Thomas S.; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Cushman, M (reprint author), Purdue Univ, Sch Pharm & Pharmaceut Sci, Dept Med Chem & Mol Pharmacol, W Lafayette, IN 47907 USA.
EM cushman@pharmacy.purdue.edu
FU National Institutes of Health (NIH) [UO1 CA89566]; Purdue University;
NIH, National Cancer Institute, Center for Cancer Research
FX This work was made possible by the National Institutes of Health (NIH)
through support with Research Grant UO1 CA89566. This work was also made
possible by the Lynn and McKeehan Fellowships (Purdue University,
MA.C.), and by the CIC/SROP program (Purdue University, B C.). This
research was supported in part by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. M.A.C.
wishes to thank Drs. Andrew Morrell, Karl Wood, and Huaping Mo for their
assistance and insight.
NR 57
TC 28
Z9 28
U1 0
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD OCT 15
PY 2009
VL 17
IS 20
BP 7145
EP 7155
DI 10.1016/j.bmc.2009.08.066
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 502DD
UT WOS:000270434000009
PM 19783447
ER
PT J
AU Germeshausen, M
Kratz, CP
Ballmaier, M
Welte, K
AF Germeshausen, Manuela
Kratz, Christian P.
Ballmaier, Matthias
Welte, Karl
TI RAS and CSF3R mutations in severe congenital neutropenia
SO BLOOD
LA English
DT Letter
ID ACUTE MYELOID-LEUKEMIA; RECEPTOR; CELLS
C1 [Germeshausen, Manuela; Ballmaier, Matthias; Welte, Karl] Hannover Med Sch, D-30625 Hannover, Germany.
[Kratz, Christian P.] NCI, Clin Genet Branch, Rockville, MD USA.
RP Germeshausen, M (reprint author), Hannover Med Sch, Carl Neuberg Str 1, D-30625 Hannover, Germany.
EM Germeshausen.Manuela@mh-hannover.de
FU NIAID NIH HHS [R24 AI049393]
NR 10
TC 1
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD OCT 15
PY 2009
VL 114
IS 16
BP 3504
EP 3505
DI 10.1182/blood-2009-07-232512
PG 2
WC Hematology
SC Hematology
GA 507EO
UT WOS:000270834500027
PM 19833857
ER
PT J
AU Warren, KE
AF Warren, Katherine E.
TI Noninvasive assessment of pediatric brain tumors
SO CANCER BIOLOGY & THERAPY
LA English
DT Review
DE imaging; pediatric; glioma; tumor measurement; spectroscopy; perfusion;
diffusion
ID MAGNETIC-RESONANCE-SPECTROSCOPY; PROTON MR SPECTROSCOPY;
POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL BLOOD-VOLUME; APPARENT
DIFFUSION-COEFFICIENT; INTRACRANIAL MASS LESIONS; LOW-GRADE GLIOMAS;
IN-VIVO; CLINICAL-APPLICATIONS; RADIATION-THERAPY
AB The use of imaging techniques to noninvasively characterize pediatric CNS tumors and assess response to therapy has advanced in recent years. Newer techniques, such as perfusion, diffusion and proton spectroscopy allow for evaluation of different tumor and tissue characteristics. The clinical utility of these techniques in the diagnosis, treatment, prognosis and assessment of pediatric patients is currently being assessed. This article reviews these techniques and their potential application to children with brain tumors.
C1 NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
RP Warren, KE (reprint author), NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
EM warrenk@mail.nih.gov
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research
FX This work 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 81
TC 2
Z9 2
U1 0
U2 1
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD OCT 15
PY 2009
VL 8
IS 20
BP 1881
EP 1888
PG 8
WC Oncology
SC Oncology
GA 533BB
UT WOS:000272795800001
PM 19738439
ER
PT J
AU Akbari, MR
Malekzadeh, R
Shakeri, R
Nasrollahzadeh, D
Foumani, M
Sun, YL
Pourshams, A
Sadjadi, A
Jafari, E
Sotoudeh, M
Kamangar, F
Boffetta, P
Dawsey, SM
Ghadirian, P
Narod, SA
AF Akbari, Mohammad R.
Malekzadeh, Reza
Shakeri, Ramin
Nasrollahzadeh, Dariush
Foumani, Maryam
Sun, Yulong
Pourshams, Akram
Sadjadi, Alireza
Jafari, Elham
Sotoudeh, Masoud
Kamangar, Farin
Boffetta, Paolo
Dawsey, Sanford M.
Ghadirian, Parviz
Narod, Steven A.
TI Candidate Gene Association Study of Esophageal Squamous Cell Carcinoma
in a High-Risk Region in Iran
SO CANCER RESEARCH
LA English
DT Article
ID ALCOHOL-DEHYDROGENASE; AROMATIC-HYDROCARBONS; CANCER-RISK;
POLYMORPHISMS; DNA; POPULATION; CHINA; 1-HYDROXYMETHYLPYRENE;
O-6-METHYLGUANINE; 1-METHYLPYRENE
AB There is a region with a high risk for esophageal squamous cell carcinoma (ESCC) in the northeast of Iran. Previous studies suggest that hereditary factors play a role in the high incidence of cancer in the region. We selected 22 functional variants (and 130 related tagSNPs) from 15 genes that have been associated previously with the risk of ESCC. We genotyped a primary set of samples from 451 Turkmens (197 cases and 254 controls). Seven of 152 variants were associated with ESCC at the P = 0.05 level; these single nucleotide polymorphisms were then studied in a validation set of 549 cases and 1,119 controls, which included both Turkmens and non-Turkmens. The association observed for a functional variant in ADH1B was confirmed in the validation set, and that of a tagSNP in MGMT, the association was borderline significant in the validation set, after correcting for multiple testing. The other 5 variants that were associated in the primary set were not significantly associated in the validation set. The histidine allele at codon 48 of ADH1B gene was associated with a significantly decreased risk of ESCC in the joint data set (primary and validation set) under a recessive model (odds ratio, 0.41; 95% confidence interval, 0.29-0.76; P = 4 x 10(-4)). The A allele of the rs7087131 variant of MGMT gene was associated with a decreased risk of ESCC under a dominant model (odds ratio, 0.79; 95% confidence interval, 0.64-0.96; P = 0.02). These results support the hypothesis that genetic predisposition plays a role in the high incidence of ESSC in Iran. [Cancer Res 2009;69(20):7994-8000]
C1 [Akbari, Mohammad R.; Foumani, Maryam; Sun, Yulong; Narod, Steven A.] Univ Toronto, Fac Med, Womens Coll, Res Inst, Toronto, ON M5G 1N8, Canada.
[Akbari, Mohammad R.; Malekzadeh, Reza; Shakeri, Ramin; Nasrollahzadeh, Dariush; Pourshams, Akram; Sadjadi, Alireza; Jafari, Elham; Sotoudeh, Masoud] Univ Tehran Med Sci, Digest Dis Res Ctr, Tehran, Iran.
[Akbari, Mohammad R.] Univ Toronto, Fac Med, Inst Med Sci, Toronto, ON M5G 1N8, Canada.
[Kamangar, Farin; Dawsey, Sanford M.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Boffetta, Paolo] IARC, Lyon, France.
[Ghadirian, Parviz] Univ Montreal, CHUM Hotel Dieu, Epidemiol Res Unit, Res Ctr, Montreal, PQ, Canada.
RP Narod, SA (reprint author), Univ Toronto, Fac Med, Womens Coll, Res Inst, 7th Floor,790 Bay St, Toronto, ON M5G 1N8, Canada.
EM steven.narod@wchospital.ca
OI Sun, Yulong/0000-0002-6665-677X; , Ramin/0000-0003-0487-3629;
Malekzadeh, Reza/0000-0003-1043-3814
FU Tehran University of Medical Sciences
FX Grant support: Canadian Institutes of Health Research and Digestive
Disease Research Center of the Tehran University of Medical Sciences.
NR 42
TC 20
Z9 22
U1 1
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 15
PY 2009
VL 69
IS 20
BP 7994
EP 8000
DI 10.1158/0008-5472.CAN-09-1149
PG 7
WC Oncology
SC Oncology
GA 508MM
UT WOS:000270935500014
PM 19826048
ER
PT J
AU Moore, LE
Brennan, P
Karami, S
Menashe, I
Berndt, SI
Dong, LM
Meisner, A
Yeager, M
Chanock, S
Colt, J
Schwartz, K
Davis, F
Zaridze, D
Mattveev, V
Janout, V
Kollarova, H
Bencko, V
Navratilova, M
Szeszenia-Dabrowska, N
Mates, D
Holcatova, I
Boffetta, P
Chow, WH
Rosenberg, PS
Rothman, N
AF Moore, Lee E.
Brennan, Paul
Karami, Sara
Menashe, Idan
Berndt, Sonja I.
Dong, Linda M.
Meisner, Allison
Yeager, Meredith
Chanock, Stephen
Colt, Joanne
Schwartz, Kendra
Davis, Faith
Zaridze, David
Mattveev, Vsevolod
Janout, Vladimir
Kollarova, Hellena
Bencko, Vladimir
Navratilova, Marie
Szeszenia-Dabrowska, Neonilia
Mates, Dana
Holcatova, Ivana
Boffetta, Paolo
Chow, Wong-Ho
Rosenberg, Philip S.
Rothman, Nathaniel
TI Apolipoprotein E/C1 Locus Variants Modify Renal Cell Carcinoma Risk
SO CANCER RESEARCH
LA English
DT Article
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; CASE-CONTROL ASSOCIATION; KIDNEY
CANCER; EASTERN-EUROPE; UNITED-STATES; LUNG-CANCER; E GENE; DISEASE;
SUSCEPTIBILITY; HYPERTENSION
AB Lipid peroxidation is considered a unifying mechanistic pathway through which known risk factors induce renal cell carcinoma (RCC). We hypothesized that genes selected a priori for their role in lipid peroxidation would modify cancer risk. We genotyped 635 single nucleotide polymorphisms (SNP) in 38 candidate genes in 777 Caucasian RCC cases and 1,035 controls enrolled in a large European case-control study. Top candidate SNPs were confirmed among 718 Caucasian cases and 615 controls in a second study in the United States. Two of the three SNPs (rs8106822 and rs405509) that replicated in the U.S. study were within a regulatory region of the APOE promoter. The OR for rs8106822 A>G variant was 1.22(AG) an 1.41(GG) (P(trend) = 0.01) in the European study, 1.05(AG) and 1.51(GG) (P(trend) = 0.03) in the U.S. study, and 1.15(AG) and 1.44(GG) (P(trend) = 0.001) among 1,485 cases and 1,639 controls combine. T e rs405509 G>T variant was associated with risk in the European (OR, 0.87(TG); OR, 0.71(TT); P(trend) = 0.02), the U.S. (OR, 0.68(TG); OR, 0.71(TT); P(trend) = 0.02), and both studies combined (OR(TG), 0.79; OR(TT), 0.71; P(trend) = 0.001), as was the G-G haplotype (r(2) = 0.64; P = 4.7 x 10(-4)). This association is biologically plausible as SNP rs405509 was shown to modify protein binding and transcriptional activity of the APOE protein in vitro and is in linkage disequilibrium with key known variants defining the e2, e3, and e4 alleles that modify risk of atherosclerosis, Alzheimer's disease risk, and progression to AIDS. In two large case-control studies, our findings further define a functional region of interest at the APOE locus that increases RCC susceptibility. [Cancer Res 2009;69(20):8001-8]
C1 [Moore, Lee E.; Karami, Sara; Menashe, Idan; Berndt, Sonja I.; Dong, Linda M.; Meisner, Allison; Colt, Joanne; Chow, Wong-Ho; Rosenberg, Philip S.; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Brennan, Paul; Boffetta, Paolo] IARC, Lyon, France.
[Yeager, Meredith; Chanock, Stephen] NCI, Core Genotyping Facil, Gaithersburg, MD USA.
[Schwartz, Kendra] Wayne State Univ, Dept Family Med & Publ Hlth Sci, Detroit, MI USA.
[Schwartz, Kendra] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
[Davis, Faith] Univ Illinois, Dept Biostat & Epidemiol, Chicago, IL USA.
[Zaridze, David; Mattveev, Vsevolod] Russian Acad Med Sci, Canc Res Ctr, Inst Carcinogenesis, Moscow, Russia.
[Janout, Vladimir; Kollarova, Hellena] Palacky Univ, Fac Med, Dept Prevent Med, CR-77147 Olomouc, Czech Republic.
[Bencko, Vladimir; Holcatova, Ivana] Inst Hyg & Epidemiol, CR-10042 Prague, Czech Republic.
[Navratilova, Marie] Masaryk Mem Canc Inst, Brno, Czech Republic.
[Szeszenia-Dabrowska, Neonilia] Inst Occupat Med, Lodz, Poland.
[Mates, Dana] Inst Publ Hlth, Bucharest, Romania.
RP Moore, LE (reprint author), NCI, 6120 Execut Blvd EPS, Rockville, MD 20852 USA.
EM moorele@mail.nih.gov
RI Liao, Linda/B-3960-2011; Zaridze, David/K-5605-2013; Janout,
Vladimir/M-5133-2014; Szeszenia-Dabrowska, Neonila/F-7190-2010;
OI mates, dana/0000-0002-6219-9807
FU NIH; NCI; Division of Cancer Epidemiology and Genetics (Bethesda, MD)
FX Grant support: Intramural Research Program of the NIH, NCI, Division of
Cancer Epidemiology and Genetics (Bethesda, MD).
NR 33
TC 17
Z9 17
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 15
PY 2009
VL 69
IS 20
BP 8001
EP 8008
DI 10.1158/0008-5472.CAN-09-1734
PG 8
WC Oncology
SC Oncology
GA 508MM
UT WOS:000270935500015
PM 19808960
ER
PT J
AU Rao, CV
Steele, VE
Swamy, MV
Patlolla, JMR
Guruswamy, S
Kopelovich, L
AF Rao, Chinthalapatty V.
Steele, Vernon E.
Swamy, Malisetty V.
Patlolla, Jagan M. R.
Guruswamy, Suresh
Kopelovich, Levy
TI Inhibition of Azoxymethane-Induced Colorectal Cancer by CP-31398, a TP53
Modulator, Alone or in Combination with Low Doses of Celecoxib in Male
F344 Rats
SO CANCER RESEARCH
LA English
DT Article
ID P53 TUMOR-SUPPRESSOR; WILD-TYPE P53; FAMILIAL ADENOMATOUS POLYPOSIS;
COLON CARCINOGENESIS; MUTANT P53; CYCLOOXYGENASE-2 INHIBITOR;
DNA-BINDING; IN-VIVO; CHEMOPREVENTION; RESTORATION
AB Tumor suppressor p53 plays a major role in colorectal cancer development. The present study explores the effects of p53-modulating agent CP-31398 alone and combined with celecoxib on azoxymethane-induced aberrant crypt foci (ACF) and colon adenocarcinomas in F344 rats. Maximum tolerated doses were 400 and 3,000 ppm for CP-31398 and celecoxib, respectively. ACF and tumor efficacy endpoints were carried out on azoxymethane-treated 7-week-old rats (48 per group) fed the control AIN-76A diet. Two weeks after carcinogen treatment, rats were fed the diets containing 0, 150, or 300 ppm CP-31398, 3 ppm celecoxib, or 150 ppm CP-31398 plus 300 ppm celecoxib ACF and colon adenocarcinomas were determined at 8 and 48 weeks after azoxymethane treatment, respectively. Dietary CP-31398 was shown to suppress mean colonic total ACF by 43% an multicrypt ACF by 63%; dietary CP-31398 at 150 and 300 ppm suppressed adenocarcinoma incidence by 30.4% (P < 0.02) and 44% (P < 0.005), respectively, and adenocarcinoma multiplicity by 51% (P < 0.005) and 65% (P < 0.0001), respectively. Dietary celecoxib suppressed colon adenocarcinoma incidence (60%; P < 0.0003) and multiplicity (70%; P < 0.0001). Importantly, combination of low-dose CP-31398 and celecoxib suppressed colon adenocarcinoma incidence by 78% and multiplicity by 90%. Rats that were fed the high-dose CP-31398 or a combination of low-dose CP-31398 and celecoxib showed considerable enhancement of p53 and p21(WAF1/CIP) expression, apoptosis, and reduced tumor cell proliferation in colonic tumors. These observations show, for the first time, that CP-31398 possesses significant dose-dependent chemopreventive activity in a well-established colon cancer model and that a combination of low-dose CP-31398 and celecoxib significantly enhanced colon cancer chemopreventive efficacy. [Cancer Res 2009;69(20):8175-82]
C1 [Rao, Chinthalapatty V.; Swamy, Malisetty V.; Patlolla, Jagan M. R.; Guruswamy, Suresh] Univ Oklahoma, Hlth Sci Ctr, Inst Canc, Hem Onc Sect,Dept Med, Oklahoma City, OK 73104 USA.
[Steele, Vernon E.; Kopelovich, Levy] NCI, Chemoprevent Agent Dev Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Rao, CV (reprint author), Univ Oklahoma, Hlth Sci Ctr, Inst Canc, Hem Onc Sect,Dept Med, 975 NE 10th St,BRC 1203, Oklahoma City, OK 73104 USA.
EM cv-rao@ouhsc.edu
FU National Cancer Institute [CA-94962, NO1-CN-25114, N01-CN-53300]
FX Grant support: National Cancer Institute grants CA-94962 and
NO1-CN-25114 and N01-CN-53300.
NR 50
TC 21
Z9 21
U1 0
U2 3
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 15
PY 2009
VL 69
IS 20
BP 8175
EP 8182
DI 10.1158/0008-5472.CAN-09-1377
PG 8
WC Oncology
SC Oncology
GA 508MM
UT WOS:000270935500036
PM 19826045
ER
PT J
AU Zhuang, ZP
Lu, J
Lonser, R
Kovach, JS
AF Zhuang, Zhengping
Lu, Jie
Lonser, Russell
Kovach, John S.
TI Enhancement of cancer chemotherapy by simultaneously altering cell cycle
progression and DNA-damage defenses through global modification of the
serine/threonine phospho-proteome
SO CELL CYCLE
LA English
DT Article
DE PP2A; phospho-proteome; DNA-damage; cancer chemotherapy; cell cycle
modulation
ID MITOTIC CATASTROPHE; SOLID TUMORS; PHASE-I; TCTP; DEATH; INHIBITION;
SENESCENCE; PROTECTS; KINASES; MANNER
AB Despite improvements in the therapeutic efficacy of rationally designed cancer treatment regimens, most cancers remain incurable once spread beyond their sites of origin. Failure to achieve sustained control or eradication of cancers arises in large part because a sub-population of quiescent "cancer stem cells" is insensitive to drugs targeting cell growth and replication and because defense mechanisms critical to survival of the normal cell also protect the cancer cell from cytotoxic injury. Global alteration of signal transduction by inhibition of serine/threonine dephosphorylation has recently been shown to markedly potentiate cancer cell killing by the DNA-methylating drug, temozolomide. Inhibition of the multifunctional protein phosphatase 2A appears to drive quiescent cancer cells into cycle and simultaneously inhibits cycle arrest, permitting cancer cell entry into mitosis despite the presence of chemotherapy induced DNA-damage. Absence of toxicity in animal models suggests that multi-site mutations in pathways regulating cell cycle in cancer cells make them more vulnerable than normal cells to large changes in the balance of phosphorylation-regulated signaling. Global modulation of the serine-threonine phospho-proteome may be a general method for enhancing the effectiveness of cytotoxic cancer therapy.
C1 [Zhuang, Zhengping; Lu, Jie; Lonser, Russell] Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bethesda, MD USA.
[Kovach, John S.] Lixte Biotechnol Holdings Inc, E Setauket, NY USA.
RP Zhuang, ZP (reprint author), Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bethesda, MD USA.
EM zhuangp@ninds.nih.gov; jkovach@lixte.com
FU National Institute of Neurological Disorders and Stroke at the National
Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke at the National
Institutes of Health and a cooperative research and development
agreement between the National Institute of Neurological Disorders and
Stroke at the National Institutes of Health and Lixte Biotechnology
Holdings, Inc.
NR 37
TC 12
Z9 15
U1 0
U2 5
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 15
PY 2009
VL 8
IS 20
BP 3303
EP 3306
PG 4
WC Cell Biology
SC Cell Biology
GA 514DK
UT WOS:000271374300018
PM 19806030
ER
PT J
AU Zhang, DP
AF Zhang, Dapeng
TI Homology between DUF784, DUF1278 domains and the plant prolamin
superfamily typifies evolutionary changes of disulfide bonding patterns
SO CELL CYCLE
LA English
DT Letter
DE DUF784; DUF1278; prolamin superfamily; fold recognition; disulfide bond;
plant allergen; evolution
ID PROTEIN; DATABASE
C1 [Zhang, Dapeng] Univ Ottawa, Dept Biol, CAREG, Ottawa, ON, Canada.
RP Zhang, DP (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
EM zhangd3@ncbi.nlm.nih.gov
NR 17
TC 2
Z9 2
U1 0
U2 1
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 15
PY 2009
VL 8
IS 20
BP 3428
EP 3430
PG 3
WC Cell Biology
SC Cell Biology
GA 514DK
UT WOS:000271374300034
PM 19806031
ER
PT J
AU Jackson, MI
Han, TH
Serbulea, L
Dutton, A
Ford, E
Miranda, KM
Houk, KN
Wink, DA
Fukuto, JM
AF Jackson, Matthew I.
Han, Tae H.
Serbulea, Laura
Dutton, Andrew
Ford, Eleonora
Miranda, Katrina M.
Houk, K. N.
Wink, David A.
Fukuto, Jon M.
TI Kinetic feasibility of nitroxyl reduction by physiological reductants
and biological implications
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Nitroxyl; Kinetics; Nitric oxide; Reduction; Nitrogen oxides; Thiols;
Free radicals
ID DENSITY-FUNCTIONAL THEORY; NITRIC-OXIDE; ANGELIS SALT;
SUPEROXIDE-DISMUTASE; AQUEOUS-SOLUTION; GLYCERALDEHYDE-3-PHOSPHATE
DEHYDROGENASE; ALDEHYDE DEHYDROGENASE; SODIUM TRIOXODINITRATE;
METABOLIC-ACTIVATION; HYDROGEN-PEROXIDE
AB Nitroxyl (HNO), the one-electron reduced and protonated congener of nitric oxide (NO), is a chemically unique species with potentially important biological activity. Although HNO-based pharmaceuticals are currently being considered for the treatment of chronic heart failure or stroke/transplant-derived ischemia, the chemical events leading to therapeutic responses are not established. The interaction of HNO with oxidants results in the well-documented conversion to NO, but HNO is expected to be readily reduced as well. Recent thermodynamic calculations predict that reduction of HNO is biologically accessible. Herein, kinetic analysis suggests that the reactions of HNO with several mechanistically distinct reductants are also biologically feasible. Product analysis verified that the reductants had in fact been oxidized and that in several instances HNO had been converted to hydroxylamine. Moreover, a theoretical analysis suggests that in the reaction of HNO with thiol reductants, the pathway producing sulfinamide is significantly more favorable than that leading to disulfide. Additionally, simultaneous production of HNO and NO yielded a biphasic oxidative capacity. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Fukuto, Jon M.] Sonoma State Univ, Dept Chem, Rohnert Pk, CA 94928 USA.
[Wink, David A.] Natl Canc Inst, Radiat Biol Branch, Bethesda, MD 20892 USA.
[Miranda, Katrina M.] Univ Arizona, Dept Chem, Tucson, AZ 85721 USA.
[Ford, Eleonora] Univ Calif Los Angeles, Dept Mol & Med Pharmacol, Los Angeles, CA 90095 USA.
[Serbulea, Laura; Dutton, Andrew; Houk, K. N.] Univ Calif Los Angeles, Dept Chem & Biochem, Los Angeles, CA 90095 USA.
[Han, Tae H.] Univ Calif Los Angeles, Dept Chem Engn, Los Angeles, CA 90095 USA.
[Jackson, Matthew I.] Univ Calif Los Angeles, Sch Publ Hlth, Interdepartmental Program Mol Toxicol, Los Angeles, CA 90095 USA.
RP Fukuto, JM (reprint author), Sonoma State Univ, Dept Chem, Rohnert Pk, CA 94928 USA.
EM jon.fukuto@somoma.edu
RI Miranda, Katrina/B-7823-2009; Liu, Peng/D-1233-2013
FU National Science Foundation [0096380]; USPHS National Research Service
Awar [GM08496]; National Institute of General Medical Sciences, National
Institutes of Health [GM 59446]
FX This work was funded by grants from the National Science Foundation
(0096380; J.M.F.), the USPHS National Research Service Award (GM08496;
A. D.), and the National Institute of General Medical Sciences, National
Institutes of Health (GM 59446; K.N.H.).
NR 84
TC 23
Z9 23
U1 0
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD OCT 15
PY 2009
VL 47
IS 8
BP 1130
EP 1139
DI 10.1016/j.freeradbiomed.2009.06.034
PG 10
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 542LJ
UT WOS:000273494500004
PM 19577638
ER
PT J
AU Yamaji, D
Na, RS
Feuermann, Y
Pechhold, S
Chen, WP
Robinson, GW
Hennighausen, L
AF Yamaji, Daisuke
Na, Risu
Feuermann, Yonatan
Pechhold, Susanne
Chen, Weiping
Robinson, Gertraud W.
Hennighausen, Lothar
TI Development of mammary luminal progenitor cells is controlled by the
transcription factor STAT5A
SO GENES & DEVELOPMENT
LA English
DT Article
DE STAT5; alveologenesis; mammary gland; progenitor; CD61; tetracycline
ID STEM-CELLS; LYMPHOID DEVELOPMENT; GLAND DEVELOPMENT; DIFFERENTIATION;
EPITHELIUM; GENE; PROLIFERATION; MORPHOGENESIS; ACTIVATION; EXPRESSION
AB Mammary alveologenesis is abrogated in the absence of the transcription factors STAT5A/5B, which mediate cytokine signaling. To reveal the underlying causes for this developmental block, we studied mammary stem and progenitor cells. While loss of STAT5A/5B did not affect the stem cell population and its ability to form mammary ducts, luminal progenitors were greatly reduced and unable to form alveoli during pregnancy. Temporally controlled expression of transgenic STAT5A in mammary epithelium lacking STAT5A/5B restored the luminal progenitor population and rescued alveologenesis in a reversible fashion in vivo. Thus, STAT5A is necessary and sufficient for the establishment of luminal progenitor cells.
C1 [Yamaji, Daisuke; Na, Risu; Feuermann, Yonatan; Robinson, Gertraud W.; Hennighausen, Lothar] NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA.
[Pechhold, Susanne] NIDDK, Diabet Branch, NIH, Bethesda, MD 20892 USA.
[Chen, Weiping] NIDDK, Genom Core Lab, NIH, Bethesda, MD 20892 USA.
RP Robinson, GW (reprint author), NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA.
EM traudl@nih.gov; lotharh@mail.nih.gov
RI Robinson, Gertraud/I-2136-2012;
OI Feuermann, Yonatan/0000-0002-6561-6397
FU National Institute of Diabetes and Digesitve and Kidney Diseases, NIH
FX We are grateful to Dr. Lewis Chodosh for MMTV-rtTA transgenic mice, Dr.
Priscilla Furth for plasmid p43, and all the members of the Laboratory
of Genetics and Physiology for helpful discussions. This research was
supported by the Intramural Research Program of the National Institute
of Diabetes and Digesitve and Kidney Diseases, NIH.
NR 27
TC 78
Z9 79
U1 0
U2 1
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 15
PY 2009
VL 23
IS 20
BP 2382
EP 2387
DI 10.1101/gad.1840109
PG 6
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 507JP
UT WOS:000270849700005
PM 19833766
ER
PT J
AU Prokunina-Olsson, L
Welch, C
Hansson, O
Adhikari, N
Scott, LJ
Usher, N
Tong, M
Sprau, A
Swift, A
Bonnycastle, LL
Erdos, MR
He, Z
Saxena, R
Harmon, B
Kotova, O
Hoffman, EP
Altshuler, D
Groop, L
Boehnke, M
Collins, FS
Hall, JL
AF Prokunina-Olsson, Ludmila
Welch, Cullan
Hansson, Ola
Adhikari, Neeta
Scott, Laura J.
Usher, Nicolle
Tong, Maurine
Sprau, Andrew
Swift, Amy
Bonnycastle, Lori L.
Erdos, Michael R.
He, Zhi
Saxena, Richa
Harmon, Brennan
Kotova, Olga
Hoffman, Eric P.
Altshuler, David
Groop, Leif
Boehnke, Michael
Collins, Francis S.
Hall, Jennifer L.
TI Tissue-specific alternative splicing of TCF7L2
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; TRANSCRIPTION-FACTOR-7-LIKE-2 GENE TCF7L2;
HUMAN PANCREATIC-ISLETS; INSULIN-SECRETION; BETA-CATENIN; TRANSCRIPTION
FACTOR; SUSCEPTIBILITY GENE; DIABETES-MELLITUS; MEXICAN-AMERICANS;
ADIPOSE-TISSUE
AB Common variants in the transcription factor 7-like 2 (TCF7L2) gene have been identified as the strongest genetic risk factors for type 2 diabetes (T2D). However, the mechanisms by which these non-coding variants increase risk for T2D are not well-established. We used 13 expression assays to survey mRNA expression of multiple TCF7L2 splicing forms in up to 380 samples from eight types of human tissue (pancreas, pancreatic islets, colon, liver, monocytes, skeletal muscle, subcutaneous adipose tissue and lymphoblastoid cell lines) and observed a tissue-specific pattern of alternative splicing. We tested whether the expression of TCF7L2 splicing forms was associated with single nucleotide polymorphisms (SNPs), rs7903146 and rs12255372, located within introns 3 and 4 of the gene and most strongly associated with T2D. Expression of two splicing forms was lower in pancreatic islets with increasing counts of T2D-associated alleles of the SNPs: a ubiquitous splicing form (P = 0.018 for rs7903146 and P = 0.020 for rs12255372) and a splicing form found in pancreatic islets, pancreas and colon but not in other tissues tested here (P = 0.009 for rs12255372 and P = 0.053 for rs7903146). Expression of this form in glucose-stimulated pancreatic islets correlated with expression of proinsulin (r(2) = 0.84-0.90, P < 0.00063). In summary, we identified a tissue-specific pattern of alternative splicing of TCF7L2. After adjustment for multiple tests, no association between expression of TCF7L2 in eight types of human tissue samples and T2D-associated genetic variants remained significant. Alternative splicing of TCF7L2 in pancreatic islets warrants future studies. GenBank Accession Numbers: FJ010164-FJ010174.
C1 [Prokunina-Olsson, Ludmila; Tong, Maurine; Sprau, Andrew; Swift, Amy; Bonnycastle, Lori L.; Erdos, Michael R.; Collins, Francis S.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
[Prokunina-Olsson, Ludmila] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Welch, Cullan; Usher, Nicolle; Hall, Jennifer L.] Univ Minnesota, Lillehei Heart Inst, Dept Med, Minneapolis, MN 55455 USA.
[Hall, Jennifer L.] Univ Minnesota, Ctr Dev Biol, Minneapolis, MN 55455 USA.
[Hansson, Ola; Kotova, Olga; Groop, Leif] Lund Univ, Ctr Diabet, Dept Clin Sci, S-20502 Malmo, Sweden.
[Adhikari, Neeta; Scott, Laura J.; He, Zhi; Boehnke, Michael] Univ Michigan, Ctr Stat Genet, Dept Biostat, Ann Arbor, MI 48109 USA.
[Saxena, Richa; Altshuler, David] Broad Inst Harvard & MIT, Cambridge, MA 02142 USA.
[Harmon, Brennan; Hoffman, Eric P.] Med Genet Res Ctr, Childrens Natl Med Ctr, Washington, DC 20010 USA.
RP Prokunina-Olsson, L (reprint author), NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
EM prokuninal@mail.nih.gov
RI Altshuler, David/A-4476-2009; Hansson, Ola/F-1793-2011;
OI Altshuler, David/0000-0002-7250-4107; Hansson, Ola/0000-0002-7394-7639;
Prokunina-Olsson, Ludmila/0000-0002-9622-2091
FU NIH [1R21DK078029-01]; NCI; Swedish Research Council; Wallenberg
Foundation; Novo Nordisk Foundation
FX The project was supported by NIH grant 1R21DK078029-01 (JH), Intramural
Research Programs of NHGRI and NCI of NIH. Work at LUDC was funded by
grants from the Swedish Research Council, the Wallenberg Foundation and
the Novo Nordisk Foundation. Funding to pay the Open Access publication
charges for this article was provided by the intramural research program
of NCI/NIH.
NR 59
TC 60
Z9 62
U1 0
U2 6
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 15
PY 2009
VL 18
IS 20
BP 3795
EP 3804
DI 10.1093/hmg/ddp321
PG 10
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 499KF
UT WOS:000270218300003
PM 19602480
ER
PT J
AU Jewett, MW
Lawrence, KA
Bestor, A
Byram, R
Gherardini, F
Rosa, PA
AF Jewett, Mollie W.
Lawrence, Kevin A.
Bestor, Aaron
Byram, Rebecca
Gherardini, Frank
Rosa, Patricia A.
TI GuaA and GuaB Are Essential for Borrelia burgdorferi Survival in the
Tick-Mouse Infection Cycle
SO JOURNAL OF BACTERIOLOGY
LA English
DT Article
ID LYME-DISEASE SPIROCHETE; LINEAR PLASMIDS 1P25; SURFACE PROTEIN-C; PURINE
SALVAGE; VIRULENCE DETERMINANTS; SALMONELLA-TYPHIMURIUM; CIRCULAR
PLASMIDS; MAMMALIAN HOST; OSPC OPERATOR; IN-VITRO
AB Pathogens lacking the enzymatic pathways for de novo purine biosynthesis are required to salvage purines and pyrimidines from the host environment for synthesis of DNA and RNA. Two key enzymes in purine salvage pathways are IMP dehydrogenase (GuaB) and GMP synthase (GuaA), encoded by the guaB and guaA genes, respectively. While these genes are typically found on the chromosome in most bacterial pathogens, the guaAB operon of Borrelia burgdorferi is present on plasmid cp26, which also harbors a number of genes critical for B. burgdorferi viability. Using molecular genetics and an experimental model of the tick-mouse infection cycle, we demonstrate that the enzymatic activities encoded by the guaAB operon are essential for B. burgdorferi mouse infectivity and provide a growth advantage to spirochetes in the tick. These data indicate that the GuaA and GuaB proteins are critical for the survival of B. burgdorferi in the infection cycle and highlight a potential difference in the requirements for purine salvage in the disparate mammalian and tick environments.
C1 [Jewett, Mollie W.; Lawrence, Kevin A.; Bestor, Aaron; Byram, Rebecca; Gherardini, Frank; Rosa, Patricia A.] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Byram, Rebecca] Univ Wyoming, Dept Mol Biol, Laramie, WY 82701 USA.
RP Jewett, MW (reprint author), 903 S 4th St, Hamilton, MT 59840 USA.
EM jewettm@niaid.nih.gov
FU NIH NIAID
FX This research was supported by the Intramural Research Program of the
NIH NIAID.
NR 67
TC 41
Z9 42
U1 1
U2 5
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 15
PY 2009
VL 191
IS 20
BP 6231
EP 6241
DI 10.1128/JB.00450-09
PG 11
WC Microbiology
SC Microbiology
GA 499NG
UT WOS:000270227500005
PM 19666713
ER
PT J
AU Pricola, KL
Kuhn, NZ
Haleem-Smith, H
Song, YJ
Tuan, RS
AF Pricola, Katie L.
Kuhn, Nastaran Z.
Haleem-Smith, Hana
Song, Yingjie
Tuan, Rocky S.
TI Interleukin-6 Maintains Bone Marrow-Derived Mesenchymal Stem Cell
Stemness by an ERK1/2-Dependent Mechanism
SO JOURNAL OF CELLULAR BIOCHEMISTRY
LA English
DT Article
DE MESENCHYMAL STEM CELLS; DIFFERENTIATION; STEMNESS; INTERLEUKIN-6
ID HUMAN ADIPOSE-TISSUE; STROMAL CELLS; PROGENITOR CELLS; IL-6; PROTEIN;
DIFFERENTIATION; PROLIFERATION; PLURIPOTENCY; ACTIVATION; CYTOKINES
AB Adult human mesenchymal stem cells (MSCs) hold promise for an increasing list of therapeutic uses due to their ease of isolation, expansion, and multi-lineage differentiation potential. To maximize the clinical potential of MSCs, the underlying mechanisms by which MSC functionality is controlled must be understood. We have taken a deconstructive approach to understand the individual components in vitro, namely the role of candidate "stemness" genes. Our recent microarray gene expression profiling data suggest that interleukin-6 (IL-6) may contribute to the maintenance of MSCs in their undifferentiated state. In this study, we showed that IL-6 gene expression is significantly higher in undifferentiated MSCs as compared to their chondrogenic, osteogenic, and adipogenic derivatives. Moreover, we found that MSCs secrete copious amounts of IL-6 protein, which decreases dramatically during osteogenic differentiation. We further evaluated the role of IL-6 for maintenance of MSC "stemness," using a series of functional assays. The data showed that IL-6 is both necessary and sufficient for enhanced MSC proliferation, protects MSCs from apoptosis, inhibits adipogenic and chondrogenic differentiation of MSCs, and increases the rate of in vitro wound healing of MSCs. We further identified ERK1/2 activation as the key pathway through which IL-6 regulates both MSC proliferation and inhibition of differentiation. Taken together, these findings show for the first time that IL-6 maintains the proliferative and undifferentiated state of bone marrow-derived MSCs, an important parameter for the optimization of both in vitro and in vivo manipulation of MSCs. J. Cell. Biochem. 108: 577-588, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Pricola, Katie L.; Kuhn, Nastaran Z.; Haleem-Smith, Hana; Song, Yingjie; Tuan, Rocky S.] NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Tuan, RS (reprint author), NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, Dept Hlth & Human Serv, 50 S Dr,Room 1140,MSC 8022, Bethesda, MD 20892 USA.
EM tuanr@mail.nih.gov
FU Intramural Research Program of NIAMS, NIH [Z01 AR41131]
FX Grant sponsor: Intramural Research Program of NIAMS, NIH; Grant number:
Z01 AR41131.
NR 45
TC 82
Z9 87
U1 3
U2 19
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0730-2312
J9 J CELL BIOCHEM
JI J. Cell. Biochem.
PD OCT 15
PY 2009
VL 108
IS 3
BP 577
EP 588
DI 10.1002/jcb.22289
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 503UU
UT WOS:000270567100005
PM 19650110
ER
PT J
AU Shafer-Weaver, KA
Anderson, MJ
Stagliano, K
Malyguine, A
Greenberg, NM
Hurwitz, AA
AF Shafer-Weaver, Kimberly A.
Anderson, Michael J.
Stagliano, Katherine
Malyguine, Anatoli
Greenberg, Norman M.
Hurwitz, Arthur A.
TI Cutting Edge: Tumor-Specific CD8(+) T Cells Infiltrating Prostatic
Tumors Are Induced to Become Suppressor Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TGF-BETA; REGULATORY CELLS; ANTITUMOR IMMUNITY; DENDRITIC CELLS; CANCER;
TOLERANCE; CD4(+); FOXP3; GENERATION; INDUCTION
AB We previously reported that naive, tumor-specific CD8(+) (TcR-I) T cells transferred into prostate tumor-bearing mice traffic to the prostate where they become tolerized. We now report that TcR-I cells suppress the proliferation of naive T cells. This suppression is mediated at least in part by secreted factors, and the suppressive activity can be blocked by Abs directed against TGF-beta. We further report that TcR-I cells must infiltrate the prostate to acquire suppressive activity. Delivery of tumor-specific CD4(+) T cells prevents the conversion of TcR-I cells into suppressor cells. Taken together, our findings may have critical implications for sustaining T cell responsiveness during immunotherapy, as the development of suppressor cells in the tumor microenvironment may eliminate the potency of T cells primed in the periphery or delivered during adoptive immunotherapy. The Journal of Immunology, 2009, 183: 4848-4852.
C1 [Shafer-Weaver, Kimberly A.; Anderson, Michael J.; Stagliano, Katherine; Hurwitz, Arthur A.] NCI, Tumor Immun & Tolerance Sect, Mol Immunoregulat Lab, Canc & Inflammat Program, Frederick, MD 21702 USA.
[Shafer-Weaver, Kimberly A.; Malyguine, Anatoli] SAIC Frederick Inc, Lab Cell Mediated Immun, Frederick, MD 21702 USA.
[Greenberg, Norman M.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98109 USA.
RP Hurwitz, AA (reprint author), NCI, NIH, Frederick Canc Res Facil, Bldg 567,Room 209, Frederick, MD 21701 USA.
EM hurwitza@mail.nih.gov
FU National Cancer Institute, National Institutes of Health; Department of
Defense Prostate Cancer Research Program [N01-CO-12400]
FX This work was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health and the
Department of Defense Prostate Cancer Research Program and has been
funded in part with federal funds under contract N01-CO-12400 (to
K.A.S.-W. and A.M.). K.A.S.-W. was a predoctoral student in the
Immunology Program of the Institute for Biomedical Sciences at George
Washington University, Washington DC, and this work is from a
dissertation in partial fulfillment of the requirements for the Ph.D.
degree.
NR 30
TC 40
Z9 42
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 15
PY 2009
VL 183
IS 8
BP 4848
EP 4852
DI 10.4049/jimmunol.0900848
PG 5
WC Immunology
SC Immunology
GA 507DC
UT WOS:000270830300007
PM 19801511
ER
PT J
AU Lisboa, FA
Peng, Z
Combs, CA
Beaven, MA
AF Lisboa, Felipe A.
Peng, Ze
Combs, Christian A.
Beaven, Michael A.
TI Phospholipase D Promotes Lipid Microdomain-Associated Signaling Events
in Mast Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID FC-EPSILON-RI; AFFINITY IGE RECEPTOR; PROTEIN-KINASE-C; PLASMA-MEMBRANE;
TYROSINE PHOSPHORYLATION; PHOSPHATIDIC-ACID; RBL-2H3 CELLS; LYN KINASE;
ACTIVATION; RAFTS
AB Initial IgE-dependent signaling events are associated with detergent-resistant membrane microdomains. Following Ag stimulation, the IgE-receptor (Fc epsilon RI) accumulates within these domains. This facilitates the phosphorylation of Fc epsilon RI subunits by the Sire kinase, Lyn, and the interaction with adaptor proteins, such as the linker for activation of T cells. Among the phospholipases (PL) subsequently activated, PLD is of interest because of its presence in lipid microdomains and the possibility that its product, phosphatidic acid, may regulate signal transduction and membrane trafficking. We find that in Ag-stimulated RBL-2H3 mast cells, the association of Fc epsilon RI with detergent-resistant membrane fractions is inhibited by 1-butanol, which subverts production of phosphatidic acid to the biologically inert phosphatidylbutanol. Furthermore, the knockdown of PLD2, and to a lesser extent PLD1 with small inhibitory RNAs, also suppressed the accumulation of Fc epsilon RI and Lyn in these fractions as well as the phosphorylation of Src kinases, Fc epsilon RI, linker for activation of T cells, and degranulation. These effects were accompanied by changes in distribution of the lipid microdomain component, ganglioside 1, in the plasma membrane as determined by binding of fluorescent-tagged cholera toxin B subunit and confocal microscopy in live cells. Collectively, these findings suggest that PLD activity plays an important role in promoting IgE-dependent signaling events within lipid microdomains in mast cells. The Journal of Immunology, 2009, 183: 5104-5112.
C1 [Lisboa, Felipe A.; Peng, Ze; Beaven, Michael A.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Combs, Christian A.] NHLBI, Light Microscopy Core Facil, NIH, Bethesda, MD 20892 USA.
RP Beaven, MA (reprint author), NHLBI, Lab Mol Immunol, NIH, Room 8N109,Bldg 10, Bethesda, MD 20892 USA.
EM beavenm@nhlbi.nih.gov
FU National Heart, Lung, and Blood Institute at the National Institutes of
Health
FX This work was supported by the intramural program of the National Heart,
Lung, and Blood Institute at the National Institutes of Health.
NR 55
TC 5
Z9 5
U1 1
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 15
PY 2009
VL 183
IS 8
BP 5104
EP 5112
DI 10.4049/jimmunol.0802728
PG 9
WC Immunology
SC Immunology
GA 507DC
UT WOS:000270830300036
PM 19794068
ER
PT J
AU Memoli, MJ
Jagger, BW
Dugan, VG
Qi, L
Jackson, JP
Taubenberger, JK
AF Memoli, Matthew J.
Jagger, Brett W.
Dugan, Vivien G.
Qi, Li
Jackson, Jadon P.
Taubenberger, Jeffery K.
TI Recent Human Influenza A/H3N2 Virus Evolution Driven by Novel Selection
Factors in Addition to Antigenic Drift
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article; Proceedings Paper
CT 48th Annual Interscience Conference on Antimicrobial Agents and
Chemotherapy/46th Annual Meeting of the
Infectious-Diseases-Society-of-America
CY OCT 25, 2008
CL Washington, DC
SP Infect Dis Soc Amer
ID A VIRUSES; H3N2 VIRUSES; GENOME; REVEALS
AB Background. Examination of the evolutionary dynamics of complete influenza viral genomes reveals that other processes, in conjunction with antigenic drift, play important roles in viral evolution and selection, but there is little biological evidence to support these genomic data. Previous work demonstrated that after the A/Fujian/411/2002-like H3N2 influenza A epidemic during 2003-2004, a preexisting nondominant Fujian-like viral clade gained a small number of changes in genes encoding the viral polymerase complex, along with several changes in the antigenic regions of hemagglutinin, and in a genome-wide selective sweep, it replaced other co-circulating H3N2 clades.
Methods. Representative strains of these virus clades were evaluated in vitro and in vivo.
Results. The newly dominant 2004-2005 A/California/7/2004-like H3N2 clade, which featured 2 key amino acid changes in the polymerase PA segment, grew to higher titers in MDCK cells and ferret tissues and caused more-severe disease in ferrets. The polymerase complex of this virus demonstrated enhanced activity in vitro, correlating directly to the enhanced replicative fitness and virulence in vivo.
Conclusion. These data suggest that influenza strains can be selected in humans through mutations that increase replicative fitness and virulence, in addition to the well-characterized antigenic changes in the surface glycoproteins.
C1 [Memoli, Matthew J.; Jagger, Brett W.; Dugan, Vivien G.; Qi, Li; Jackson, Jadon P.; Taubenberger, Jeffery K.] NIAID, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Taubenberger, JK (reprint author), NIAID, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, NIH, 33 North Dr,Rm 3E19A-2, Bethesda, MD 20892 USA.
EM taubenbergerj@niaid.nih.gov
FU Intramural NIH HHS [Z99 AI999999, ZIA AI000986-03]
NR 33
TC 25
Z9 25
U1 0
U2 3
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 15
PY 2009
VL 200
IS 8
BP 1232
EP 1241
DI 10.1086/605893
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 497UV
UT WOS:000270089400009
PM 19743921
ER
PT J
AU Cuenco, KT
Ottesen, EA
Williams, SA
Nutman, TB
Steel, C
AF Cuenco, Karen T.
Ottesen, Eric A.
Williams, Steven A.
Nutman, Thomas B.
Steel, Cathy
TI Heritable Factors Play a Major Role in Determining Host Responses to
Wuchereria bancrofti Infection in an Isolated South Pacific Island
Population
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article; Proceedings Paper
CT 55th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 11-16, 2006
CL Atlanta, GA
SP Amer Soc Trop Med & Hyg
ID HUMAN LYMPHATIC FILARIASIS; ENDEMIC FILARIASIS; PARASITE ANTIGEN;
BRUGIA-MALAYI; HLA; IMMUNITY; SUSCEPTIBILITY; RESPONSIVENESS; IGE;
PEDIGREES
AB Background. It is increasingly recognized that host genetic factors may play an important role in determining the outcome of filarial infections. To test this hypothesis in bancroftian lymphatic filariasis, pedigree data were collected twice during an 18-year period from an isolated Polynesian population living on a Pacific island where lymphatic filariasis is endemic.
Methods. Using variance-component analysis, we examined the contribution of shared genetic and environmental effects on host clinical and immune responses to filarial infection, along with potential confounding determinants.
Results. Sex was found to have a negligible influence on heritability estimates, but shared-household effects accounted for up to 32% of host variability. After accounting for these shared-household effects, heritability estimates suggested that levels of microfilariae and circulating adult worm antigen, as well as host eosinophil and immunoglobulin G antibody responses to larval and adult worm antigens, were highly heritable (range of heritability estimates, 0.15-0.84).
Conclusions. These data provide evidence of a key role for genetic factors in determining the host response to filarial infections in humans and emphasize the complexity of the relationships among the host, parasite, and environment.
C1 [Nutman, Thomas B.; Steel, Cathy] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Cuenco, Karen T.] Univ Pittsburgh, Sch Med & Dent, Dept Oral Biol, Ctr Craniofacial & Dent Genet, Pittsburgh, PA 15260 USA.
[Cuenco, Karen T.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Human Genet, Pittsburgh, PA 15260 USA.
[Ottesen, Eric A.] Lymphat Filariasis Support Ctr, Decatur, GA USA.
[Williams, Steven A.] Smith Coll, Dept Biol Sci, Northampton, MA 01063 USA.
RP Steel, C (reprint author), NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
EM csteel@niaid.nih.gov
FU Intramural NIH HHS
NR 44
TC 12
Z9 13
U1 0
U2 3
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 15
PY 2009
VL 200
IS 8
BP 1271
EP 1278
DI 10.1086/605844
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 497UV
UT WOS:000270089400014
PM 19754310
ER
PT J
AU Tweedie, D
Luo, WM
Short, RG
Brossi, A
Holloway, HW
Li, YZ
Yu, QS
Greig, NH
AF Tweedie, David
Luo, Weiming
Short, Ryan G.
Brossi, Arnold
Holloway, Harold W.
Li, Yazhou
Yu, Qian-sheng
Greig, Nigel H.
TI A cellular model of inflammation for identifying TNF-alpha synthesis
inhibitors
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE Neuroinflammation; TNF-alpha; RAW 264.7; Thalidomide; Lenalidomide;
Lipopolysaccharide (LPS); Neurodegeneration; Alzheimer's disease
ID NECROSIS-FACTOR-ALPHA; ALZHEIMERS-DISEASE; MULTIPLE-MYELOMA;
THALIDOMIDE; CELLS; MICROGLIA; TARGETS
AB Neuroinflammation is a common facet of both acute and chronic neurodegenerative conditions, exemplified by stroke and by Alzheimer's and Parkinson's disease, and the presence of elevated levels of the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), has been documented in each. Although initial TNF-alpha generation is associated with a protective compensatory response, its unregulated chronic elevation is generally detrimental and can drive the disease process. In such circumstances, therapeutic strategies that can both gain access to the brain and target the production of TNF-alpha are predicted to be of clinical benefit. An in vitro mouse macrophage-like cellular screen, utilizing RAW 264.7 cells, was hence developed to identify novel TNF-alpha lowering agents incorporating lipophilic physicochemical characteristics predicted to allow penetration of the blood-brain barrier. Cultured RAW 264.7 cells exposed to lipopolysaccharide (LPS) induced a rapid, marked and concentration-dependent cellular release of TNF-alpha into the cell culture media, which was readily detected by enzyme linked immunosorbent assay (ELISA). The effects of four characterized thalidomide-based TNF-alpha lowering agents were assessed alongside 10 novel uncharacterized compounds synthesized on the same backbone. One of these new analogs possessed activity of sufficient magnitude to warrant further investigation. Activity determined in the cellular model translated to an in vivo rodent model of acute LPS-induced TNF-alpha elevation. The utility of the TNF-alpha cellularassay lies in its simplicity and robust nature, providing a tool for initial pharmacological screening to allow for the rapid identification novel TNF-alpha lowering agents. Published by Elsevier B.V.
C1 [Tweedie, David] NIA, Drug Design & Dev Sect, Neurosci Lab, Intramural Res Program,Biomed Res Ctr, Baltimore, MD 21224 USA.
[Brossi, Arnold] Univ N Carolina, Sch Pharm, Chapel Hill, NC 27599 USA.
RP Tweedie, D (reprint author), NIA, Drug Design & Dev Sect, Neurosci Lab, Intramural Res Program,Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM tweedieda@grc.nia.nih.gov
FU Intramural Research Program; National Institute on Aging; NIH
FX The described research was supported by the Intramural Research Program,
National Institute on Aging, NIH. Animal studies were undertaken on an
approved protocol in accord with the Animal Care and Use Committee of
the Intramural Research Program, NIA, NIH. Dr. David Tweedie is
supported by the Medstar Research Institute.
NR 20
TC 18
Z9 19
U1 3
U2 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0270
J9 J NEUROSCI METH
JI J. Neurosci. Methods
PD OCT 15
PY 2009
VL 183
IS 2
BP 182
EP 187
DI 10.1016/j.jneumeth.2009.06.034
PG 6
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 502SD
UT WOS:000270479500011
PM 19583982
ER
PT J
AU Larkin, JD
Markham, GD
Milkevitch, M
Brooks, BR
Bock, CW
AF Larkin, Joseph D.
Markham, George D.
Milkevitch, Matt
Brooks, Bernard R.
Bock, Charles W.
TI Computational Investigation of the Oxidative Deboronation of
Boroglycine, H2N-CH2-B(OH)(2), Using H2O and H2O2
SO JOURNAL OF PHYSICAL CHEMISTRY A
LA English
DT Review
ID BORONATE AFFINITY-CHROMATOGRAPHY; POLARIZABLE CONTINUUM MODEL;
CORRELATED MOLECULAR CALCULATIONS; PROTEASOME INHIBITOR BORTEZOMIB;
METHYL TRANSFER-REACTIONS; ALPHA-AMINOBORONIC ACIDS; CROSS-COUPLING
REACTIONS; PANCREATIC-CANCER CELLS; NEUTRON-CAPTURE THERAPY;
GAUSSIAN-BASIS SETS
AB We report results from a computational investigation of the oxidative deboronation of boroglycine, H2N-CH2-B(OH)(2), using H2O and H2O2 as the reactive oxygen species (ROS) to yield aminomethanol, H2N-CH2-OH; these results complement Our study on the protodeboronation of boroglycine to produce methylamine, H2N-CH3 (Larkin et al. J. Phys. Chem. A 2007, 111, 6489-6500). Second-order Moller-Plesset (MP2) perturbation theory with Dunning-Woon correlation-consistent (cc) basis sets were used for the calculations with comparisons made to results from density functional theory (DFT) at the PBE1PBE/6-311++G(d,p)(cc-pVDZ) levels. The effects of a bulk aqueous environment were also incorporated into the calculations employing PCM and CPCM methodology. Using H2O as the ROS, the reaction H2O + H2N-CH2-B(OH)(2) -> H2N-CH2-OH + H-B(OH)(2) was calculated to be endothermic; the value of Delta H-298(0) was + 12.0 kcal/mol at the MP2(FC)/cc-pVTZ computational level in vacuo and + 13.7 kcal/mol in PCM aqueous media; the corresponding value for the activation barrier, Delta H double dagger, was +94.3 kcal/mol relative to the separated reactants in vacuo and +89.9 kcal/mol in PCM aqueous media. In contrast, the reaction H2O2 + H2N-CH2-B(OH)(2) -> H2N-CH2-OH + B(OH)(3) was calculated to be highly exothermic with an Delta H-298(0) value of -100.9 kcal/mol at the MP2(FC)/cc-pVTZ computational level in vacuo and -99.6 kcal/mol in CPCM aqueous media; the highest-energy transition state for the multistep process associated with this reaction involved the rearrangement of H2N-CH2-B(OH)(OOH) to H2N-CH2-O-B(OH)(2) with a Delta H double dagger value of +23.2 kcal/mol in vacuo relative to the separated reactants. These computational results for boroglycine are in accord with the experimental observations for the deboronation of the FDA approved anticancer drug bortezomib (Velcade, PS-341), where it was found to be the principle deactivation pathway (Labutti et al. Chem. Res. Toxicol. 2006, 19, 539-546).
C1 [Milkevitch, Matt; Bock, Charles W.] Philadelphia Univ, Dept Chem & Biochem, Sch Sci & Hlth, Philadelphia, PA 19144 USA.
[Larkin, Joseph D.; Brooks, Bernard R.] NHLBI, NIH, Rockville, MD 20852 USA.
[Markham, George D.; Bock, Charles W.] Fox Chase Canc Ctr, Inst Canc Res, Philadelphia, PA 19111 USA.
RP Bock, CW (reprint author), Philadelphia Univ, Dept Chem & Biochem, Sch Sci & Hlth, Sch House Lane & Henry Ave, Philadelphia, PA 19144 USA.
EM bock@philau.com
FU NIH [GM31186]; NHLBI; NCI [CA06927]; Commonwealth of Pennsylvania
FX This research was partially supported (J.D.L. and B.R.B.) by the
Intramural Research Program of the NIH, NHLBI. G.D.M. would like to
thank the NIH (GM31186) and NCI (CA06927) for financial support of this
work, which was also supported by an appropriation from the Commonwealth
of Pennsylvania. The High Performance Computing Facility at the Fox
Chase Cancer Center and the PQS Cluster Facility at Philadelphia
University were used for the calculations described in this manuscript.
This study also utilized the high-performance computational capabilities
of the Biowulf Linux cluster at the National Institutes of Health,
Bethesda, MD (http://biowulf.nih.gov).
NR 100
TC 9
Z9 9
U1 1
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1089-5639
J9 J PHYS CHEM A
JI J. Phys. Chem. A
PD OCT 15
PY 2009
VL 113
IS 41
BP 11028
EP 11034
DI 10.1021/jp904149w
PG 7
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 503MO
UT WOS:000270538800020
PM 19810757
ER
PT J
AU Anez, G
Men, RH
Eckels, KH
Lai, CJ
AF Anez, German
Men, Ruhe
Eckels, Kenneth H.
Lai, Ching-Juh
TI Passage of Dengue Virus Type 4 Vaccine Candidates in Fetal Rhesus Lung
Cells Selects Heparin-Sensitive Variants That Result in Loss of
Infectivity and Immunogenicity in Rhesus Macaques
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID GLYCOSAMINOGLYCAN-BINDING VARIANTS; JAPANESE ENCEPHALITIS-VIRUS; HUMAN
DENDRITIC CELLS; PROTEIN DOMAIN-III; WEST-NILE-VIRUS; ENVELOPE PROTEIN;
VIRULENCE ATTENUATION; PUTATIVE RECEPTOR; E2 GLYCOPROTEIN; SULFATE
BINDING
AB Three dengue virus type 4 (DENV-4) vaccine candidates containing deletions in the 3' noncoding region were prepared by passage in DBS-FRhL-2 (FRhL) cells. Unexpectedly, these vaccine candidates and parental DENV-4 similarly passaged in the same cells failed to elicit either viremia or a virus-neutralizing antibody response. Consensus sequence analysis revealed that each of the three viruses, as well as the parental DENV-4 when passaged in FRhL cells, rapidly acquired a single Glu(327)-Gly substitution in domain III (DIII) of the envelope protein (E). These variants appear to have accumulated in response to growth adaptation to FRhL cells as shown by growth analysis, and the mutation was not detected in the virus following passage in C6/36 cells, primary African green monkey kidney cells, or Vero cells. The Glu(327)-Gly substitution was predicted by molecular modeling to increase the net positive charge on the surface of E. The Glu(327)-Gly variant of the full-length DENV-4 selected after three passages in FRhL cells showed increased affinity for heparan sulfate compared to the unpassaged DENV-4, as measured by heparin binding and infectivity inhibition assays. Evidence indicates that the Glu(327)-Gly mutation in DIII of the DENV-4 E protein was responsible for reduced infectivity and immunogenicity in rhesus monkeys. Our results point out the importance of cell substrates for vaccine preparation since the virus may change during passages in certain cells through adaptive selection, and such mutations may affect cell tropism, virulence, and vaccine efficacy.
C1 [Anez, German; Men, Ruhe; Lai, Ching-Juh] NIAID, Mol Viral Biol Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Eckels, Kenneth H.] Walter Reed Army Inst Res, Silver Spring, MD 20910 USA.
RP Lai, CJ (reprint author), NIAID, Mol Viral Biol Sect, Infect Dis Lab, NIH, 50 South Dr, Bethesda, MD 20892 USA.
EM clai@niaid.nih.gov
RI Anez, German/B-3643-2008
OI Anez, German/0000-0001-5361-3001
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases; National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health. This research project received partial financial
support from the WHO Global Programme for Vaccines.
NR 57
TC 31
Z9 32
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 15
PY 2009
VL 83
IS 20
BP 10384
EP 10394
DI 10.1128/JVI.01083-09
PG 11
WC Virology
SC Virology
GA 498FC
UT WOS:000270121600007
PM 19656873
ER
PT J
AU Sun, Y
Bailer, RT
Rao, SS
Mascola, JR
Nabel, GJ
Koup, RA
Letvin, NL
AF Sun, Yue
Bailer, Robert T.
Rao, Srinivas S.
Mascola, John R.
Nabel, Gary J.
Koup, Richard A.
Letvin, Norman L.
TI Systemic and Mucosal T-Lymphocyte Activation Induced by Recombinant
Adenovirus Vaccines in Rhesus Monkeys
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HIV-1 VACCINE; CELL RESPONSES; IMMUNITY; REPLICATION; VECTORS; SURVIVAL;
STEP
AB The administration of vectors designed to elicited cell-mediated immune responses may have other consequences that are clinically significant. To explore this possibility, we evaluated T-cell activation during the first 2 months after recombinant adenovirus serotype 5 (rAd5) prime or boost immunizations in rhesus monkeys. We also evaluated the kinetics of T-lymphocyte activation in both the systemic and the mucosal compartments after rAd5 administration in monkeys with preexisting immunity to Ad5. The rAd5 immunization induced lower-frequency Gag epitope-specific CD8(+) T cells in the colonic mucosa than in the peripheral blood. There was evidence of an expansion of the simian immunodeficiency virus Gag-specific CD8(+) T-cell responses, but not the Ad5 hexon-specific T-cell responses, following a homologous rAd5 boost. A striking but transient T-lymphocyte activation in both the systemic and the mucosal compartments of rhesus monkeys was observed after rAd5 immunization. These findings indicate that the administration of a vaccine vector such as Ad5 can induce a global activation of T cells.
C1 [Letvin, Norman L.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr,Dept Med, Div Viral Pathogenesis,Ctr Life Sci, Boston, MA 02115 USA.
[Bailer, Robert T.; Rao, Srinivas S.; Mascola, John R.; Nabel, Gary J.; Koup, Richard A.; Letvin, Norman L.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Letvin, NL (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr,Dept Med, Div Viral Pathogenesis,Ctr Life Sci, 330 Brookline Ave, Boston, MA 02115 USA.
EM nletvin@bidmc.harvard.edu
FU Vaccine Research Center, National Institute of Allergy and Infectious
Diseases, National Institutes of Health; Harvard Medical School CFAR
[AI060354]; CAVD CTC-VIMC, Bill and Melinda Gates Foundation [38650]
FX This study was supported in part by funds from the intramural research
program of the Vaccine Research Center, National Institute of Allergy
and Infectious Diseases, National Institutes of Health; Harvard Medical
School CFAR grant AI060354; and CAVD CTC-VIMC grant 38650 from the Bill
and Melinda Gates Foundation.
NR 16
TC 14
Z9 14
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 15
PY 2009
VL 83
IS 20
BP 10596
EP 10604
DI 10.1128/JVI.01170-09
PG 9
WC Virology
SC Virology
GA 498FC
UT WOS:000270121600026
PM 19656883
ER
PT J
AU Whitney, JB
Luedemann, C
Hraber, P
Rao, SS
Mascola, JR
Nabel, GJ
Letvin, NL
AF Whitney, James B.
Luedemann, Corinne
Hraber, Peter
Rao, Srinivas S.
Mascola, John R.
Nabel, Gary J.
Letvin, Norman L.
TI T-Cell Vaccination Reduces Simian Immunodeficiency Virus Levels in Semen
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID SEXUAL TRANSMISSION; HETEROSEXUAL TRANSMISSION; HIV-INFECTION; VIRAL
LOAD; URETHRITIS; VACCINES; IMPACT; MODEL
AB Recent findings suggest that most sexual transmission of human immunodeficiency virus type 1 (HIV-1) occurs during the acute phase of infection when viral replication is most intense. Here, we show that vaccine-elicited cellular immune responses can significantly reduce simian immunodeficiency virus levels in the semen during the period of primary infection in monkeys. A vaccine that decreases the quantity of HIV-1 in the semen of males during primary infection might decrease HIV-1 transmission in human populations and therefore affect the spread of AIDS.
C1 [Whitney, James B.; Luedemann, Corinne; Letvin, Norman L.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Viral Pathogenesis,Dept Med, Boston, MA 02215 USA.
[Hraber, Peter] Los Alamos Natl Lab, Los Alamos, NM 87545 USA.
[Rao, Srinivas S.; Mascola, John R.; Nabel, Gary J.; Letvin, Norman L.] NIAID, Vaccine Res Ctr, Bethesda, MD 20892 USA.
RP Letvin, NL (reprint author), Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Viral Pathogenesis,Dept Med, CLS 1043,3 Blackfan Circle, Boston, MA 02215 USA.
EM nletvin@bidmc.harvard.edu
OI Hraber, Peter/0000-0002-2920-4897
FU Intramural Research Program of the Vaccine Research Center, NIAID
FX This work was supported by the Intramural Research Program of the
Vaccine Research Center, NIAID.
NR 22
TC 13
Z9 13
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 15
PY 2009
VL 83
IS 20
BP 10840
EP 10843
DI 10.1128/JVI.01202-09
PG 4
WC Virology
SC Virology
GA 498FC
UT WOS:000270121600050
PM 19640980
ER
PT J
AU Thomas, AG
Marrett, S
Saad, ZS
Ruff, DA
Martin, A
Bandettini, PA
AF Thomas, Adam G.
Marrett, Sean
Saad, Ziad S.
Ruff, Douglas A.
Martin, Alex
Bandettini, Peter A.
TI Functional but not structural changes associated with learning: An
exploration of longitudinal Voxel-Based Morphometry (VBM)
SO NEUROIMAGE
LA English
DT Article
ID BRAIN STRUCTURE CHANGES; CEREBELLAR CORTEX; RANDOM-FIELD; MR-IMAGES;
FMRI; NEUROPLASTICITY; VISUALIZATION; SEGMENTATION; ANGIOGENESIS;
REGISTRATION
AB Voxel-Based Morphometry (VBM) has been used for several years to study differences in brain structure between populations. Recently, a longitudinal version of VBM has been used to show changes in gray matter associated with relatively short periods of training. In the present study we use fMRI and three different standard implementations of longitudinal VBM: SPM2, FSL, and SPM5 to assess functional and structural changes associated with a simple learning task. Behavioral and fMRI data clearly showed a significant learning effect. However, initially positive VBM results were found to be inconsistent across minor perturbations of the analysis technique and ultimately proved to be artifactual. When alignment biases were controlled for and recommended statistical procedures were used, no significant changes in grey matter density were found. This work, initially intended to show structural and functional changes with learning, rather demonstrates some of the potential pitfalls of existing longitudinal VBM methods and prescribes that these tools be applied and interpreted with extreme caution. Published by Elsevier Inc.
C1 [Thomas, Adam G.; Marrett, Sean; Bandettini, Peter A.] NIMH, Funct MRI Facil, Bethesda, MD 20892 USA.
[Saad, Ziad S.] NIMH, Sci & Stat Comp Unit, Bethesda, MD 20892 USA.
[Ruff, Douglas A.] Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA.
[Martin, Alex] NIMH, Cognit Neuropsychol Sect, Bethesda, MD 20892 USA.
[Bandettini, Peter A.] NIMH, Funct Imaging Methods Sect, Bethesda, MD 20892 USA.
RP Thomas, AG (reprint author), Bldg 10,Rm 1D80,10 Ctr Dr, Bethesda, MD 20815 USA.
EM adamt@nih.gov
RI martin, alex/B-6176-2009;
OI Marrett, Sean/0000-0001-8179-6511; Thomas, Adam/0000-0002-2850-1419;
Ruff, Douglas/0000-0001-7228-8822
FU NIMH Intramural Research Program
FX This work was supported by the NIMH Intramural Research Program. This
study utilized the high-performance computational capabilities of the
Biowulf Linux cluster at the National Institutes of Health, Bethesda, MD
(http://biowulf.nih.gov). The authors would like to acknowledge comments
and assistance from Rasmus Birn, Gang Chen, Dan Handwerker, David
McMahon, Kevin Murphy, Allison Nugent, and Regina Nuzzo.
NR 49
TC 52
Z9 52
U1 1
U2 5
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 15
PY 2009
VL 48
IS 1
BP 117
EP 125
DI 10.1016/j.neuroimage.2009.05.097
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 488AO
UT WOS:000269321100015
PM 19520171
ER
PT J
AU Bright, MG
Bulte, DP
Jezzard, P
Duyn, JH
AF Bright, Molly G.
Bulte, Daniel P.
Jezzard, Peter
Duyn, Jeff H.
TI Characterization of regional heterogeneity in cerebrovascular reactivity
dynamics using novel hypocapnia task and BOLD fMRI
SO NEUROIMAGE
LA English
DT Article
DE fMRI; Reactivity; BOLD; Dynamics; Breath-holding; Hypocapnia;
Hypercapnia; Deep breathing
ID BLOOD OXYGENATION; HUMAN BRAIN; SIGNAL; TOMOGRAPHY; MRI
AB We offer a new method for characterizing the magnitude and dynamics of the vascular response to changes in arterial gas tensions using non-invasive blood oxygenation level-dependent functional magnetic resonance imaging (BOLD fMRI) and paradigms appropriate for clinical settings. A novel respiratory task, "Cued Deep Breathing" (CDB), consisting of two consecutive cycles of cued breaths, has been developed to cause transient hypocapnia, and consequently a strong, short-lived BOLD signal decrease. Data from CDB hypocapnia paradigms and traditional breath-holding hypercapnia paradigms were analyzed on a voxel-wise basis to map regional heterogeneity in magnitude and timing parameters. The tasks caused comparable absolute BOLD percent signal changes (similar to 0.5-3.0% in gray matter) and both datasets suggested consistent regional heterogeneity in the response timing: parts of the basal ganglia, particularly the putamen, and bilateral areas of medial cortex reached their maximum signal change several seconds earlier than remaining cortical gray matter voxels. This phenomenon and a slightly delayed response in posterior cortical regions were present in group-maps often healthy subjects. An auxiliary experiment in different subjects measured end-tidal CO2 changes associated with the new CDB task and quantitatively compared the resulting reactivity maps with those acquired using a traditional hypercapnia challenge of 4% CO2 gas inspiration. The CDB task caused average end-tidal CO2 decreases between 6.0 +/- 1.1 and 10.5 +/- 2.6 mm Hg, with levels returning to baseline after approximately three breaths, giving evidence that the task indeed causes transient mild hypocapnia. Similarity between resulting reactivity maps suggest CDB offers an alternative method for mapping cerebrovascular reactivity. Published by Elsevier Inc.
C1 [Bright, Molly G.; Duyn, Jeff H.] Natl Inst Neurol Disorders & Stroke, Lab Adv MRI, Lab Funct & Mol Imaging, NIH, Bethesda, MD USA.
[Bright, Molly G.; Bulte, Daniel P.; Jezzard, Peter] Univ Oxford, Oxford Ctr Funct MRI Brain, Dept Clin Neurol, Oxford OX3 9DU, England.
RP Bright, MG (reprint author), Univ Oxford, John Radcliffe Hosp, Dept Clin Neurol, FMRIB Ctr, Oxford OX3 9DU, England.
EM molly.bright@clneuro.ox.ac.uk
RI Duyn, Jozef/F-2483-2010; Bright, Molly/F-6394-2010; Bulte,
Daniel/F-8679-2011;
OI Bright, Molly/0000-0001-7257-9646; Jezzard, Peter/0000-0001-7912-2251
FU NIH; NINDS; EPSRC; UK MRC
FX We thank Silvina G. Horovitz and Susan C. Fulton at the National
Institutes of Health for their assistance with experiment planning and
data collection. This research was supported by the Intramural Research
Program of the NIH, NINDS, EPSRC, and the UK MRC.
NR 29
TC 36
Z9 37
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 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD OCT 15
PY 2009
VL 48
IS 1
BP 166
EP 175
DI 10.1016/j.neuroimage.2009.05.026
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 488AO
UT WOS:000269321100019
PM 19450694
ER
PT J
AU Hardin, MG
Pine, DS
Ernst, M
AF Hardin, Michael G.
Pine, Daniel S.
Ernst, Monique
TI The influence of context valence in the neural coding of monetary
outcomes
SO NEUROIMAGE
LA English
DT Article
ID EVENT-RELATED FMRI; MEDIAL PREFRONTAL CORTEX; DECISION-MAKING;
ORBITOFRONTAL CORTEX; NUCLEUS-ACCUMBENS; CHOICE SELECTION; ADOLESCENT
BRAIN; FINANCIAL REWARD; RISK-TAKING; RESPONSES
AB The emotional significance of objects and events depends on the context in which they occur. Using functional magnetic resonance imaging, we examined the modulation of neural responses to monetary outcomes while subjects performed a decision-making task in a positive and a negative economic context. Neural responses indicated a relative regional specialization in the neural coding of outcome valence and followed three distinct patterns. The nucleus accumbens (NAc) and orbital frontal cortex (OFC) appeared to code the most extreme outcome in each context, with a potentiated response for favorable outcomes by a positive context. The amygdala and insula appeared to also code highly salient outcomes, but showed a potentiated response to unfavorable outcomes occurring in a negative context. The medial prefrontal cortex (medPFC), on the other hand, only coded favorable responses occurring in a positive context. Moreover, the medPFC showed large inter-individual variability when responding to outcomes in a negative context, Suggesting that its role in a negative context may depend on a number of individual factors. The results of this work provide evidence of complex valence-based regional dissociations that are influenced by contextual factors. Published by Elsevier Inc.
C1 [Ernst, Monique] NIMH, Mood & Anxiety Disorders Program, NIH, DHHS,Emot Dev & Affect Neurosci Branch, Bethesda, MD 20892 USA.
RP Ernst, M (reprint author), NIMH, Mood & Anxiety Disorders Program, NIH, DHHS,Emot Dev & Affect Neurosci Branch, 15K N Dr, Bethesda, MD 20892 USA.
EM ernstm@mail.nih.gov
FU Intramural NIH HHS [Z99 MH999999]
NR 48
TC 15
Z9 16
U1 2
U2 4
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 15
PY 2009
VL 48
IS 1
BP 249
EP 257
DI 10.1016/j.neuroimage.2009.06.050
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 488AO
UT WOS:000269321100028
PM 19560546
ER
PT J
AU Abrams, D
Levy, Y
Losso, MH
Babilker, A
Collins, G
Cooper, DA
Darbyshire, J
Emery, S
Fox, L
Gordin, F
Lane, HC
Lundgren, JD
Mitsuyasu, R
Neaton, JD
Phillips, A
Routy, JP
Tambussi, G
Wentworth, D
AF Abrams, D.
Levy, Y.
Losso, M. H.
Babilker, A.
Collins, G.
Cooper, D. A.
Darbyshire, J.
Emery, S.
Fox, L.
Gordin, F.
Lane, H. C.
Lundgren, J. D.
Mitsuyasu, R.
Neaton, J. D.
Phillips, A.
Routy, J. P.
Tambussi, G.
Wentworth, D.
CA INSIGHT-ESPRIT Study Grp
SILCAAT Sci Comm
TI Interleukin-2 Therapy in Patients with HIV Infection
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; RANDOMIZED CONTROLLED-TRIAL; CD4(+) CELL
COUNTS; SUBCUTANEOUS INTERLEUKIN-2; ANTIRETROVIRAL THERAPY;
CLINICAL-TRIALS; INTRAVENOUS INTERLEUKIN-2; T-LYMPHOCYTES; AIDS;
METAANALYSIS
AB BACKGROUND
Used in combination with antiretroviral therapy, subcutaneous recombinant interleukin-2 raises CD4+ cell counts more than does antiretroviral therapy alone. The clinical implication of these increases is not known.
METHODS
We conducted two trials: the Subcutaneous Recombinant, Human Interleukin-2 in HIV-Infected Patients with Low CD4+ Counts under Active Antiretrovial Therapy (SILCAAT) study and the Evaluation of Subcutaneous Proleukin in a Randomized International Trial (ESPRIT). In each, patients infected with the human immunodeficiency virus (HIV) who had CD4+ cell counts of either 50 to 299 per cubic millimeter (SILCAAT) or 300 or more per cubic millimeter (ESPRIT) were randomly assigned to receive Interleukin-2 plus antiretrovial therapy or antiretrovial therapy alone. The Interleukin-2 regimen consisted of cycles of 5 consecutive days each, administered at 8-week intervals. The SILCAAT study involved six cycles and a dose or 4.5 million IU of interleukin-2 twice daily; ESPRIT involved three cycles and a dose of 7.5 million IU twice daily. Additional cycles were recommended to maintain the CD4+ cell count above predefined target levels. The primary end point of both studies was opportunistic disease or death from any cause.
RESULTS
In the SILCAAT study, 1695 patients (849 receiving interleukin-2 plus antiretroviral therapy and 846 receiving antiretroviral therapy alone) who had a median CD4+ cell count of 202 cells per cubic millimeter were enrolled; in ESPRIT, 4111 patients (2071 receiving interleukin 2 plus antiretroviral therapy and 2040 receiving antiretroviral therapy alone) who had a median CD4+ cell count of 457 cells per cubic millimeter were enrolled. Over a median follow-up period of 7 to 8 years, the CD4+ cell count was higher in the interleukin 2 group than in the group receiving antiretroviral therapy alone - by 53 and 159 cells per cubic millimeter, on average, in the SILCAAT study and ESPRIT, respectively. Hazard ratios for opportunistic disease or death from any cause with interleukin-2 plus antiretroviral therapy (vs. antiretroviral therapy alone) were 0.91 (95% confidence interval [CI], 0.70 to 1.18; P=0.47) in the SILCAAT study and 0.94 (95 h CI, 0.75 to 1.16; P=0.55) in ESPRIT. The hazard ratios for death from any cause and for grade 4 clinical events were 1.06 (P=0.73) and 1.10 (P=0.35), respectively; in the SILCAAT study and 0.90 (P=0.42) and 1.23 (P=0.003), respectively, in ESPRIT.
CONCLUSIONS
Despite a substantial and sustained increase in the CD4+ cell count, as compared with antiretroviral therapy alone, interleukin-2 plus antiretroviral therapy yielded no clinical benefit in either study. (ClinicalTrials.gov numbers, NCT00004978 [ESPRIT] and NCT00013611 [SILCAAT study].)
C1 [Abrams, D.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Levy, Y.] Univ Paris 12, INSERM, U955, Paris, France.
[Levy, Y.] Grp Henri Mondor Albert Chenevier, AP HP, Paris, France.
[Losso, M. H.] Hosp Gen Agudos JM Ramos Mejia, Buenos Aires, DF, Argentina.
[Babilker, A.; Darbyshire, J.] MRC, London, England.
[Phillips, A.] UCL, Sch Med, London WC1E 6BT, England.
[Neaton, J. D.] Univ Minnesota, Sch Publ Hlth, Div Biostat, Minneapolis, MN 55414 USA.
[Cooper, D. A.; Emery, S.] Natl Ctr HIV Epidemiol & Clin Res, Sydney, NSW, Australia.
[Fox, L.; Lane, H. C.] NIAID, Bethesda, MD 20892 USA.
[Gordin, F.] Washington Vet Med Ctr, Washington, DC USA.
[Lundgren, J. D.] Rigshosp, DK-2100 Copenhagen, Denmark.
[Lundgren, J. D.] Univ Copenhagen, Copenhagen, Denmark.
[Mitsuyasu, R.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Routy, J. P.] McGill Univ, Royal Victoria Hosp, Ctr Hlth, Montreal, PQ H3A 1A1, Canada.
[Tambussi, G.] Fdn San Raffaele Monte Tabor, Milan, Italy.
RP Neaton, JD (reprint author), Univ Minnesota, Sch Publ Hlth, Div Biostat, 221 Univ Ave SE,Suite 200, Minneapolis, MN 55414 USA.
EM jim@ccbr.umn.edu
RI Phillips, Andrew/B-4427-2008; Yee, Thynn Thynn/H-5862-2012
OI Phillips, Andrew/0000-0003-2384-4807;
FU MAID [U01 AI46957, U01 AI068641]; Chiron and Novartis; SILCAAT
FX Supported by grants from the MAID for ESPRIT (U01 AI46957 and U01
AI068641) and from Chiron and Novartis for ESPRIT and the SILCAAT study
(to Dr. Neaton). For both studies, interleukin-2 was provided by
Chiron-Novartis.
NR 27
TC 216
Z9 220
U1 2
U2 16
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD OCT 15
PY 2009
VL 361
IS 16
BP 1548
EP 1559
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 506LT
UT WOS:000270777000008
ER
PT J
AU Williams, DJ
Puhl, HL
Ikeda, SR
AF Williams, Damian J.
Puhl, Henry L., III
Ikeda, Stephen R.
TI Rapid Modification of Proteins Using a Rapamycin-Inducible Tobacco Etch
Virus Protease System
SO PLOS ONE
LA English
DT Article
ID POTASSIUM CHANNEL INACTIVATION; TEV PROTEASE; SUBSTRATE-SPECIFICITY;
FLUORESCENT PROTEIN; FRET EFFICIENCY; LIVING CELLS; IN-VIVO;
COMPLEMENTATION; STRATEGIES; SITE
AB Background: The ability to disrupt the function of a specific protein on a rapid time scale provides a powerful tool for biomedical research. Specific proteases provide a potential method to selectively cleave a chosen protein, but rapid control of protease activity is difficult.
Methodology/Principal Findings: A heterologous expression system for rapid target-directed proteolysis in mammalian cells was developed. The system consists of an inducible NIa protease from the tobacco etch virus (TEVp) and a chosen protein into which a TEVp substrate recognition sequence (TRS) has been inserted. Inducible activity was conferred to the TEVp using rapamycin-controlled TEVp fragment complementation. TEVp activity was assayed using a FRET-based reporter construct. TEVp expression was well tolerated by mammalian cells and complete cleavage of the substrate was possible. Cleavage at 37 degrees C proceeded exponentially with a time constant of approximately 150 minutes. Attempts to improve cleavage efficiency were hampered by substantial background activity, which was attributed to inherent affinity between the TEVp fragments. A second TEVp assay, based on changes in inactivation of a modified K(V)3.4 channel, showed that functional properties of a channel can be using altered using an inducible TEVp system. Similar levels of background activity and variability were observed in both electrophysiological and FRET assays.
Conclusions/Significance: The results suggested that an optimum level of TEVp expression leading to sufficient inducible activity (with minimal background activity) exists but the variability in expression levels between cells makes the present system rather impractical for single cell experiments. The system is likely to be more suitable for experiments in which the cell-to-cell variability is less of an issue; for example, in experiments involving large populations of cells.
RP Williams, DJ (reprint author), NIAAA, Lab Mol Physiol, NIH, Bethesda, MD USA.
EM sikeda@mail.nih.gov
OI Puhl, Henry/0000-0003-3095-7201; Ikeda, Stephen/0000-0002-4088-9508
FU Intramural NIH HHS
NR 47
TC 15
Z9 16
U1 0
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 15
PY 2009
VL 4
IS 10
AR e7474
DI 10.1371/journal.pone.0007474
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 507JB
UT WOS:000270847800012
PM 19830250
ER
PT J
AU Nam, JM
AF Nam, Jun-Mo
TI Efficient interval estimation of a ratio of marginal probabilities in
matched-pair data: Non-iterative method
SO STATISTICS IN MEDICINE
LA English
DT Article
DE constrained maximum likelihood estimators; Fieller-type method; interval
estimation of a ratio of marginal probabilities; matched-pair data;
Wald-type log method; Wilson interval
ID CONFIDENCE-INTERVALS; RISK RATIO; PROPORTIONS; LIMITS
AB Matched-pair designs have been commonly employed in diagnostic, epidemiologic and laboratory studies. For estimation of a ratio of two marginal probabilities in matched-pair data, a Wald-type logarithmic method is computationally simple, but an actual coverage rate is known to be smaller than a nominal one and a length of the confidence interval is shorter than it should be. The Fieller-type method based on constrained maximum likelihood (CML) estimators possesses asymptotically optimum statistical properties and a coverage rate is close to a nominal one. However, hitherto the limits have been obtained by numerical iterations. In this paper, we derive the efficient confidence lit-nits based on CML as analytical solutions of a quartic equation and present the confidence limits in a closed form. Published in 2009 by John Wiley & Sons, Ltd.
C1 NCI, DCEG, Biostat Branch, Rockville, MD 20852 USA.
RP Nam, JM (reprint author), NCI, DCEG, Biostat Branch, EPS Room 8028,6120 Execut Blvd, Rockville, MD 20852 USA.
EM namj@mail.nih.gov
FU NIH National Cancer Institute
FX Contract/grant sponsor: NIH National Cancer Institute
NR 18
TC 6
Z9 6
U1 0
U2 2
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD OCT 15
PY 2009
VL 28
IS 23
BP 2929
EP 2935
DI 10.1002/sim.3685
PG 7
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA 507EB
UT WOS:000270833000006
PM 19691020
ER
PT J
AU Blombach, F
Makarova, KS
Marrero, J
Siebers, B
Koonin, EV
van der Oost, J
AF Blombach, Fabian
Makarova, Kira S.
Marrero, Jeannette
Siebers, Bettina
Koonin, Eugene V.
van der Oost, John
TI Identification of an ortholog of the eukaryotic RNA polymerase III
subunit RPC34 in Crenarchaeota and Thaumarchaeota suggests
specialization of RNA polymerases for coding and non-coding RNAs in
Archaea
SO BIOLOGY DIRECT
LA English
DT Article
ID TRANSCRIPTION INITIATION; STRUCTURE PREDICTION; EVOLUTION; SEQUENCES;
COMPLEXES; PROTEINS; DATABASE; SEARCH; ORIGIN; SERVER
AB One of the hallmarks of eukaryotic information processing is the co-existence of 3 distinct, multi-subunit RNA polymerase complexes that are dedicated to the transcription of specific classes of coding or non-coding RNAs. Archaea encode only one RNA polymerase that resembles the eukaryotic RNA polymerase II with respect to the subunit composition. Here we identify archaeal orthologs of the eukaryotic RNA polymerase III subunit RPC34. Genome context analysis supports a function of this archaeal protein in the transcription of non-coding RNAs. These findings suggest that functional separation of RNA polymerases for protein-coding genes and non-coding RNAs might predate the origin of the Eukaryotes.
C1 [Blombach, Fabian; van der Oost, John] Wageningen Univ, Microbiol Lab, Wageningen, Netherlands.
[Makarova, Kira S.; Koonin, Eugene V.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
[Marrero, Jeannette; Siebers, Bettina] Univ Duisburg Essen, Fac Chem, Biofilm Ctr, Duisburg, Germany.
RP Blombach, F (reprint author), Wageningen Univ, Microbiol Lab, Wageningen, Netherlands.
EM fabian.blombach@wur.nl; makarova@ncbi.nlm.nih.gov;
jeanette.marrero@uni-due.de; bettina.siebers@uni-due.de;
koonin@ncbi.nlm.nih.gov; John.vanderOost@wur.nl
OI Blombach, Fabian/0000-0001-5337-8662
FU NWO [865.05.001]; DFG [GRK 1431/1]; DHHS
FX This work was supported by NWO (ALW-Vici project 865.05.001 to JO. JM is
supported by the DFG program "GRK 1431/1, Transcription, Chromatin
Structure and DNA Repair in Development and Differentiation". KM and EK
are supported by intramural funds of the DHHS (NIH, National Library of
Medicine). FB and JO would like to thank Finn Werner for helpful
comments on the manuscript.
NR 26
TC 21
Z9 21
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1745-6150
J9 BIOL DIRECT
JI Biol. Direct
PD OCT 14
PY 2009
VL 4
AR 39
DI 10.1186/1745-6150-4-39
PG 7
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 519LK
UT WOS:000271767900001
PM 19828044
ER
PT J
AU Dieffenbach, CW
Fauci, AS
AF Dieffenbach, Carl W.
Fauci, Anthony S.
TI Strategies for Preventing HIV Transmission Reply
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
C1 [Dieffenbach, Carl W.; Fauci, Anthony S.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Dieffenbach, CW (reprint author), NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM cdieffenba@niaid.nih.gov
NR 1
TC 1
Z9 1
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD OCT 14
PY 2009
VL 302
IS 14
BP 1531
EP 1532
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 505UA
UT WOS:000270721800018
ER
PT J
AU Greenberg, ME
Xu, BJ
Lu, B
Hempstead, BL
AF Greenberg, Michael E.
Xu, Baoji
Lu, Bai
Hempstead, Barbara L.
TI New Insights in the Biology of BDNF Synthesis and Release: Implications
in CNS Function
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID ACTIVITY-DEPENDENT SECRETION; NEUROTROPHIC FACTOR; NEURONAL-ACTIVITY;
HIPPOCAMPAL-NEURONS; PROTEIN-SYNTHESIS; PROBDNF; BRAIN; PLASTICITY;
EXPRESSION; TRANSCRIPTION
AB BDNF has pleiotropic effects on neuronal development and synaptic plasticity that underlie circuit formation and cognitive function. Recent breakthroughs reveal that neuronal activity regulates BDNF cell biology, including Bdnf transcription, dendritic targeting and trafficking of BDNF mRNA and protein, and secretion and extracellular conversion of proBDNF to mature BDNF. Defects in these mechanisms contribute differentially to cognitive dysfunction and anxiety-like behaviors. Here we review recent studies, presented at a symposium at Neuroscience 2009, that describe regulatory mechanisms that permit rapid and dynamic refinement of BDNF actions in neurons.
C1 [Hempstead, Barbara L.] Weill Cornell Med Coll, New York, NY 10065 USA.
[Greenberg, Michael E.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Xu, Baoji] Georgetown Univ, Washington, DC 20057 USA.
[Lu, Bai] Natl Inst Child Hlth & Dev, NIH, Bethesda, MD 20847 USA.
RP Hempstead, BL (reprint author), Weill Cornell Med Coll, New York, NY 10065 USA.
EM blhempst@med.cornell.edu
FU National Institute of Neurological Disorders and Stroke (NINDS); Kirby
Foundation; NINDS; National Institutes of Health Intramural Research
Program
FX The studies described above were supported by funds from the National
Institute of Neurological Disorders and Stroke (NINDS) and the Kirby
Foundation to M. E. G., from NINDS to B. X. and B. L. H., and from the
National Institutes of Health Intramural Research Program to B. L.
NR 28
TC 226
Z9 234
U1 0
U2 20
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 14
PY 2009
VL 29
IS 41
BP 12764
EP 12767
DI 10.1523/JNEUROSCI.3566-09.2009
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA 507IF
UT WOS:000270845000008
PM 19828787
ER
PT J
AU Ma, H
Cai, Q
Lu, WB
Sheng, ZH
Mochida, S
AF Ma, Huan
Cai, Qian
Lu, Wenbo
Sheng, Zu-Hang
Mochida, Sumiko
TI KIF5B Motor Adaptor Syntabulin Maintains Synaptic Transmission in
Sympathetic Neurons
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID READILY RELEASABLE POOL; CULTURED HIPPOCAMPAL-NEURONS; KINESIN
HEAVY-CHAIN; AXONAL-TRANSPORT; TRANSMITTER RELEASE; NEUROTRANSMITTER
RELEASE; NEUROMUSCULAR-JUNCTION; CALCIUM-CHANNELS; MYOSIN-II;
MITOCHONDRIA
AB Newly synthesized synaptic proteins and mitochondria are transported along lengthy neuronal processes to assist in the proper assembly of developing synapses and activity-dependent remodeling of mature synapses. Neuronal transport is mediated by motor proteins that associate with their cargoes via adaptors and travel along the cytoskeleton within neuronal processes. Our previous studies in developing hippocampal neurons revealed that syntabulin acts as a KIF5B motor adaptor and mediates anterograde transport of presynaptic cargoes and mitochondria, presynaptic assembly, and activity-induced plasticity. Here, using cultured superior cervical ganglion neurons combined with manipulation of syntabulin expression or interference with its interaction with KIF5B, we uncover a crucial role for syntabulin in the maintenance of presynaptic function. Syntabulin loss-of-function delayed the appearance of synaptic activity in developing neurons and impaired synaptic transmission in mature neurons, including reduced basal activity, accelerated synaptic depression under high-frequency firing, slowed recovery rates after synaptic vesicle depletion, and impaired presynaptic short-term plasticity. These defects correlated with reduced mitochondrial distribution along neuronal processes and were rescued by the application of ATP within presynaptic neurons. These results suggest that syntabulin supports the axonal transport of mitochondria and concomitant ATP production at presynaptic terminals. ATP supply from locally stationed mitochondria is in turn necessary for the efficient mobilization of synaptic vesicles into the readily releasable pool. These findings emphasize the critical role of KIF5B-syntabulin-mediated axonal transport in the maintenance of presynaptic function and regulation of synaptic plasticity.
C1 [Ma, Huan; Lu, Wenbo; Mochida, Sumiko] Tokyo Med Univ, Dept Physiol, Tokyo 1608402, Japan.
[Ma, Huan; Lu, Wenbo; Mochida, Sumiko] Shanghai Jiao Tong Univ, Neurobiol Lab, Sch Med, Shanghai 200025, Peoples R China.
[Cai, Qian; Sheng, Zu-Hang] Natl Inst Neurol Disorders & Stroke, Synapt Funct Sect, NIH, Bethesda, MD 20892 USA.
RP Mochida, S (reprint author), Tokyo Med Univ, Dept Physiol, Tokyo 1608402, Japan.
EM Shengz@ninds.nih.gov; mochida@tokyo-med.ac.jp
RI Ma, Huan/A-1379-2012
FU grants-in-aid for Scientific Research B; National Institute of
Neurological Disorders and Stroke-National Institutes of Health
FX This work was supported by grants-in-aid for Scientific Research B (S.
M.) and the Intramural Research Program of the National Institute of
Neurological Disorders and Stroke-National Institutes of Health
(Z-H.S.).
NR 68
TC 39
Z9 39
U1 0
U2 3
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 14
PY 2009
VL 29
IS 41
BP 13019
EP 13029
DI 10.1523/JNEUROSCI.2517-09.2009
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 507IF
UT WOS:000270845000036
PM 19828815
ER
PT J
AU Lowery, CA
Park, J
Gloeckner, C
Meijler, MM
Mueller, RS
Boshoff, HI
Ulrich, RL
Barry, CE
Bartlett, DH
Kravchenko, VV
Kaufmann, GF
Janda, KD
AF Lowery, Colin A.
Park, Junguk
Gloeckner, Christian
Meijler, Michael M.
Mueller, Ryan S.
Boshoff, Helena I.
Ulrich, Ricky L.
Barry, Clifton E., III
Bartlett, Douglas H.
Kravchenko, Vladimir V.
Kaufmann, Gunnar F.
Janda, Kim D.
TI Defining the Mode of Action of Tetramic Acid Antibacterials Derived from
Pseudomonas aeruginosa Quorum Sensing Signals
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID GRAM-NEGATIVE BACTERIA; ESCHERICHIA-COLI; NATURAL-PRODUCTS;
VIBRIO-CHOLERAE; OUTER-MEMBRANE; SMALL-MOLECULE; CELL-DIVISION;
IDENTIFICATION; GENE; REUTERICYCLIN
AB In nature, bacteria rarely exist as single, isolated entities, but rather as communities comprised of many other species including higher host organisms. To survive in these competitive environments, microorganisms have developed elaborate tactics such as the formation of biofilms and the production of antimicrobial toxins. Recently, it was discovered that the Gram-negative bacterium Pseudomonas aeruginosa, an opportunistic human pathogen, produces an antibiotic, 3-(1-hydroxydecylidene)-5-(2-hydroxyethyl)pyrrolidine-2,4-dione (C(12)-TA), derived from one of its quorum sensing molecules. Here, we present a comprehensive study of the expanded spectrum Of C(12)-TA antibacterial activity against microbial competitors encountered by P. aeruginosa in nature as well as significant human pathogens. The mechanism of action Of C(12)-TA was also elucidated, and C(12)-TA was found to dissipate both the membrane potential and the pH gradient of Gram-positive bacteria, correlating well with cell death. Notably, in stark contrast to its parent molecule 3-oxo-dodecanoyl homoserine lactone (3-oxo-C(12)-HSL), neither activation of cellular stress pathways nor cytotoxicity was observed in human cells treated with C(12)-TA. Our results suggest that the QS machinery of P. aeruginosa has evolved for a dual-function, both to signal others of the same species and also to defend against host immunity and competing bacteria. Because of the broad-spectrum antibacterial activity, established mode of action, lack of rapid resistance development, and tolerance by human cells, the C(12)-TA scaffold may also serve as a new lead compound for the development of antimicrobial therapeutics.
C1 [Lowery, Colin A.; Park, Junguk; Gloeckner, Christian; Meijler, Michael M.; Kaufmann, Gunnar F.; Janda, Kim D.] Scripps Res Inst, Skaggs Inst Chem Biol, La Jolla, CA 92037 USA.
[Lowery, Colin A.; Park, Junguk; Gloeckner, Christian; Meijler, Michael M.; Kaufmann, Gunnar F.; Janda, Kim D.] Scripps Res Inst, Dept Chem, La Jolla, CA 92037 USA.
[Lowery, Colin A.; Park, Junguk; Gloeckner, Christian; Meijler, Michael M.; Kravchenko, Vladimir V.; Kaufmann, Gunnar F.; Janda, Kim D.] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
[Mueller, Ryan S.; Bartlett, Douglas H.] Univ Calif San Diego, Scripps Inst Oceanog, Div Marine Biol Res, Ctr Marine Biotechnol & Biomed, La Jolla, CA 92037 USA.
[Boshoff, Helena I.; Barry, Clifton E., III] NIAID, TB Res Sect, Bethesda, MD 20892 USA.
[Ulrich, Ricky L.] USA, Med Res Inst Infect Dis, Bacteriol Div, Ft Detrick, MD 21704 USA.
[Janda, Kim D.] Scripps Res Inst, WIRM, La Jolla, CA 92037 USA.
RP Kaufmann, GF (reprint author), Scripps Res Inst, Skaggs Inst Chem Biol, 10550 N Torrey Pines Rd, La Jolla, CA 92037 USA.
EM kaufmann@scripps.edu; kdjanda@scripps.edu
RI Barry, III, Clifton/H-3839-2012
FU NIAID/NIH [HHSN272200700055C]; National Institutes of Health [AI079503,
AI080715, AI079436]; Skaggs Institute for Chemical Biology;
Sanofi-Aventis; NIAID, NIH
FX We thank Professor Michael Ganzle of the University of Alberta,
Edmonton, AB, Canada, for generously providing us with reutericyclin,
and 'Prof. Floyd Romesberg for providing the mutant E. coli strains. The
following isolate was obtained through the Network on Antimicrobial
Resistance in Staphylococcus aureus (NARSA) Program: Staphylococcus
aureus USA300 (NRS384), supported under NIAID/NIH contract no.
HHSN272200700055C. We would also like to thank Prof. Bastiaan P. Krom of
the University of Groningen for critical reading of the manuscript. This
work was supported by the National Institutes of Health (AI079503 to
K.D.J., AI080715 to G.F.K., AI079436 to V.V.K.), the Skaggs Institute
for Chemical Biology, and a Sanofi-Aventis Graduate Fellowship (C.A.L.),
and in part by the Intramural Research program of the NIAID, NIH.
NR 44
TC 51
Z9 52
U1 4
U2 22
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD OCT 14
PY 2009
VL 131
IS 40
BP 14473
EP 14479
DI 10.1021/ja9056079
PG 7
WC Chemistry, Multidisciplinary
SC Chemistry
GA 512SS
UT WOS:000271271500087
PM 19807189
ER
PT J
AU Palmieri, G
Capone, M
Ascierto, ML
Gentilcore, G
Stroncek, DF
Casula, M
Sini, MC
Palla, M
Mozzillo, N
Ascierto, PA
AF Palmieri, Giuseppe
Capone, Mariaelena
Ascierto, Maria Libera
Gentilcore, Giusy
Stroncek, David F.
Casula, Milena
Sini, Maria Cristina
Palla, Marco
Mozzillo, Nicola
Ascierto, Paolo A.
TI Main roads to melanoma
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Review
ID NITRIC-OXIDE-SYNTHASE; MICROPHTHALMIA TRANSCRIPTION FACTOR; CELL-CYCLE
ARREST; NF-KAPPA-B; CUTANEOUS MALIGNANT-MELANOMA; TUMOR-SUPPRESSOR GENE;
DNA-DAMAGE RESPONSE; MULTIPLE PRIMARY MELANOMAS; AKT/PROTEIN KINASE-B;
SIGNALING PATHWAY
AB The characterization of the molecular mechanisms involved in development and progression of melanoma could be helpful to identify the molecular profiles underlying aggressiveness, clinical behavior, and response to therapy as well as to better classify the subsets of melanoma patients with different prognosis and/or clinical outcome. Actually, some aspects regarding the main molecular changes responsible for the onset as well as the progression of melanoma toward a more aggressive phenotype have been described. Genes and molecules which control either cell proliferation, apoptosis, or cell senescence have been implicated. Here we provided an overview of the main molecular changes underlying the pathogenesis of melanoma. All evidence clearly indicates the existence of a complex molecular machinery that provides checks and balances in normal melanocytes. Progression from normal melanocytes to malignant metastatic cells in melanoma patients is the result of a combination of down- or up-regulation of various effectors acting on different molecular pathways.
C1 [Capone, Mariaelena; Ascierto, Maria Libera; Gentilcore, Giusy; Palla, Marco; Mozzillo, Nicola; Ascierto, Paolo A.] Fdn Pascale, Ist Nazl Tumori, Naples, Italy.
[Palmieri, Giuseppe; Casula, Milena; Sini, Maria Cristina] CNR, Ist Chim Biomol, Sassari, Italy.
[Stroncek, David F.] NIH, Cell Proc Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Ascierto, PA (reprint author), Fdn Pascale, Ist Nazl Tumori, Naples, Italy.
EM gpalmieri@yahoo.com; marilenacapone@virgilio.it; asciertoml@cc.nih.gov;
giusy.gentilcore@libero.it; pasciert@tin.it; casulam@yahoo.it;
mc.sini@tiscali.it; pallamarco@hotmail.com; nimozzi@tin.it;
paolo.ascierto@gmail.com
RI Ascierto, Maria Libera/A-9239-2012;
OI Palmieri, Giuseppe/0000-0002-4350-2276
NR 216
TC 67
Z9 67
U1 3
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD OCT 14
PY 2009
VL 7
AR 86
DI 10.1186/1479-5876-7-86
PG 17
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 516GZ
UT WOS:000271531500001
PM 19828018
ER
PT J
AU Dauter, Z
Wlodawer, A
AF Dauter, Zbigniew
Wlodawer, Alexander
TI Proteins Do Not Have Strong Spines After All
SO STRUCTURE
LA English
DT Editorial Material
ID REFINEMENT
AB In this issue of Structure, Berkholz et al. show that the detailed backbone geometry of proteins depends on the local conformation and suggest how this information can be practically used in modeling and refining protein structures.
C1 [Dauter, Zbigniew] Argonne Natl Lab, NCI, Macromol Crystallog Lab, Synchrotron Radiat Res Sect, Argonne, IL 60439 USA.
[Wlodawer, Alexander] FCRDC, NCI, Macromol Crystallog Lab, Prot Struct Sect, Ft Detrick, MD 21702 USA.
RP Dauter, Z (reprint author), Argonne Natl Lab, NCI, Macromol Crystallog Lab, Synchrotron Radiat Res Sect, 9700 S Cass Ave, Argonne, IL 60439 USA.
EM zdauter@anl.gov
NR 9
TC 5
Z9 5
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0969-2126
J9 STRUCTURE
JI Structure
PD OCT 14
PY 2009
VL 17
IS 10
BP 1278
EP 1279
DI 10.1016/j.str.2009.09.002
PG 2
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 509VS
UT WOS:000271047700002
PM 19836327
ER
PT J
AU Dolinska, MB
Sergeev, YV
Chan, MP
Palmer, I
Wingfield, PT
AF Dolinska, Monika. B.
Sergeev, Yuri V.
Chan, May P.
Palmer, Ira
Wingfield, Paul T.
TI N-Terminal Extension of beta B1-Crystallin: Identification of a Critical
Region That Modulates Protein Interaction with beta A3-Crystallin
SO BIOCHEMISTRY
LA English
DT Article
ID LENS BETA-B1 CRYSTALLIN; AGE-RELATED-CHANGES; SEQUENCE EXTENSIONS;
MASS-SPECTROMETRY; ASSOCIATION PROPERTIES; CIRCULAR-DICHROISM;
STABILITY; DEAMIDATION; CATARACT; CLEAVAGE
AB The human lens proteins beta-crystalline are subdivided into acidic (beta A1-beta A4) and basic (beta B1-beta B3) subunit groups. These structural proteins exist at extremely high concentrations and associate into oligomers under physiological conditions. Crystallin acidic-basic pairs tend to form strong heteromolecular associations. The long N-terminal extensions of beta-crystallins may influence both homo- and heteromolecular interactions. However, identification of the critical regions of the extensions mediating protein associations has not been previously addressed. This was studied by comparing the self-association and heteromolecular associations of wild-type recombinant beta A3- and beta B1-crystalline and their N-terminally truncated counterparts (beta A3 Delta N30 and beta B1 Delta N56) using several biophysical techniques, including analytical ultracentrifugation and fluorescence spectroscopy. Removal of the N-terminal extension of beta A3 had no effect on dimerization or heteromolecular tetramer formation with beta B1. In contrast, the level of self-association of beta B1 Delta N56 increased, resulting in homotetramer formation, and heteromolecular association with beta A3 was blocked. Limited proteolysis of beta B1 produced beta B1 Delta N47, which is similar to intact protein formed dimers but in contrast showed enhanced heteromolecular tetramer formation with beta A3. The cryptic. digestion was physiologically significant, corresponding to protease processing sites observed in vivo. Molecular modeling of the N-terminal beta B1 extension indicates structural features that position a mobile loop in the vicinity of these processing sites. The loop is derived from residues 48-56 which appear to be critical for mediating protein interactions with beta A3-crystallin.
C1 [Sergeev, Yuri V.] NEI, OGVFB, NIH, Bethesda, MD 20892 USA.
[Palmer, Ira; Wingfield, Paul T.] NIAMSD, NIH, Bethesda, MD 20892 USA.
RP Sergeev, YV (reprint author), NEI, OGVFB, NIH, 10B10 10 Ctr Dr, Bethesda, MD 20892 USA.
EM sergeevy@nei.nih.gov
FU Howard Hughes Medical Institute Research Scholars Program
FX We thank Dr. Oleg Voloshin (National Institute of Diabetes and Digestive
and Kidney Diseases, National Institutes of Health) for assistance with
circular dichroism and Dr. Fielding Hejtmancik (National Eye Institute,
National Institutes of Health) for useful discussions and criticism.
M.P.C. was supported by the Howard Hughes Medical Institute Research
Scholars Program.
NR 56
TC 12
Z9 12
U1 3
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD OCT 13
PY 2009
VL 48
IS 40
BP 9684
EP 9695
DI 10.1021/bi9013984
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 502KU
UT WOS:000270459100038
PM 19746987
ER
PT J
AU Sinilnikova, OM
Antoniou, AC
Simard, J
Healey, S
Leone, M
Sinnett, D
Spurdle, AB
Beesley, J
Chen, X
Greene, MH
Loud, JT
Lejbkowicz, F
Rennert, G
Dishon, S
Andrulis, IL
Domchek, SM
Nathanson, KL
Manoukian, S
Radice, P
Konstantopoulou, I
Blanco, I
Laborde, AL
Duran, M
Osorio, A
Benitez, J
Hamann, U
Hogervorst, FBL
van Os, TAM
Gille, HJP
Peock, S
Cook, M
Luccarini, C
Evans, DG
Lalloo, F
Eeles, R
Pichert, G
Davidson, R
Cole, T
Cook, J
Paterson, J
Brewer, C
Hughes, DJ
Coupier, I
Giraud, S
Coulet, F
Colas, C
Soubrier, F
Rouleau, E
Bieche, I
Lidereau, R
Demange, L
Nogues, C
Lynch, HT
Schmutzler, RK
Versmold, B
Engel, C
Meindl, A
Arnold, N
Sutter, C
Deissler, H
Schaefer, D
Froster, UG
Aittomaki, K
Nevanlinna, H
McGuffog, L
Easton, DF
Chenevix-Trench, G
Stoppa-Lyonnet, D
AF Sinilnikova, O. M.
Antoniou, A. C.
Simard, J.
Healey, S.
Leone, M.
Sinnett, D.
Spurdle, A. B.
Beesley, J.
Chen, X.
Greene, M. H.
Loud, J. T.
Lejbkowicz, F.
Rennert, G.
Dishon, S.
Andrulis, I. L.
Domchek, S. M.
Nathanson, K. L.
Manoukian, S.
Radice, P.
Konstantopoulou, I.
Blanco, I.
Laborde, A. L.
Duran, M.
Osorio, A.
Benitez, J.
Hamann, U.
Hogervorst, F. B. L.
van Os, T. A. M.
Gille, H. J. P.
Peock, S.
Cook, M.
Luccarini, C.
Evans, D. G.
Lalloo, F.
Eeles, R.
Pichert, G.
Davidson, R.
Cole, T.
Cook, J.
Paterson, J.
Brewer, C.
Hughes, D. J.
Coupier, I.
Giraud, S.
Coulet, F.
Colas, C.
Soubrier, F.
Rouleau, E.
Bieche, I.
Lidereau, R.
Demange, L.
Nogues, C.
Lynch, H. T.
Schmutzler, R. K.
Versmold, B.
Engel, C.
Meindl, A.
Arnold, N.
Sutter, C.
Deissler, H.
Schaefer, D.
Froster, U. G.
Aittomaki, K.
Nevanlinna, H.
McGuffog, L.
Easton, D. F.
Chenevix-Trench, G.
Stoppa-Lyonnet, D.
CA kConFab
OCGN
HEBON
EMBRACE
GEMO
GC-HBOC
Consortium Investigators Modifiers
TI The TP53 Arg72Pro and MDM2 309G > T polymorphisms are not associated
with breast cancer risk in BRCA1 and BRCA2 mutation carriers
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE TP53; MDM2; BRCA1/2; breast cancer; polymorphism; risk
ID SINGLE NUCLEOTIDE POLYMORPHISM; LI-FRAUMENI-SYNDROME; P53; SNP309;
CARCINOGENESIS; CONSORTIUM; MODIFIERS; INS16BP; PATHWAY
AB BACKGROUND: The TP53 pathway, in which TP53 and its negative regulator MDM2 are the central elements, has an important role in carcinogenesis, particularly in BRCA1- and BRCA2-mediated carcinogenesis. A single nucleotide polymorphism (SNP) in the promoter region of MDM2 (309T > G, rs2279744) and a coding SNP of TP53 (Arg72Pro, rs1042522) have been shown to be of functional significance.
METHODS: To investigate whether these SNPs modify breast cancer risk for BRCA1 and BRCA2 mutation carriers, we pooled genotype data on the TP53 Arg72Pro SNP in 7011 mutation carriers and on the MDM2 309T > G SNP in 2222 mutation carriers from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). Data were analysed using a Cox proportional hazards model within a retrospective likelihood framework.
RESULTS: No association was found between these SNPs and breast cancer risk for BRCA1 (TP53: per-allele hazard ratio (HR) = 1.01, 95% confidence interval (CI): 0.93-1.10, P(trend) = 0.77; MDM2: HR = 0.96, 95% CI: 0.84-1.09, P(trend) = 0.54) or for BRCA2 mutation carriers (TP53: HR = 0.99, 95% CI: 0.87-1.12, P(trend) = 0.83; MDM2: HR = 0.98, 95% CI: 0.80-1.21, P(trend) = 0.88). We also evaluated the potential combined effects of both SNPs on breast cancer risk, however, none of their combined genotypes showed any evidence of association.
CONCLUSION: There was no evidence that TP53 Arg72Pro or MDM2 309T > G, either singly or in combination, influence breast cancer risk in BRCA1 or BRCA2 mutation carriers. British Journal of Cancer (2009) 101, 1456-1460. doi: 10.1038/sj.bjc.6605279 www.bjcancer.com Published online 25 August 2009 (C) 2009 Cancer Research UK
C1 [Sinilnikova, O. M.; Leone, M.; Giraud, S.] Hosp Civils Lyon Ctr Leon Berard, Unite Mixte Genet Constitut Canc Frequents, F-69373 Lyon, France.
[Sinilnikova, O. M.] Univ Lyon, CNRS, Lab Genet Mol Signalisat & Canc, UMR5201, F-69373 Lyon, France.
[Antoniou, A. C.; Peock, S.; Cook, M.; Easton, D. F.; EMBRACE] Univ Cambridge, Dept Publ Hlth & Primary Care, Genet Epidemiol Unit, Canc Res UK, Cambridge CB1 8RN, England.
[Simard, J.] CHU Laval, Canc Genom Lab, Canada Res Chair Oncogenet, Quebec City, PQ G1V 4G2, Canada.
[Simard, J.] Univ Laval, Quebec City, PQ G1V 4G2, Canada.
[Healey, S.; Spurdle, A. B.; Beesley, J.; Chen, X.; Chenevix-Trench, G.] Queensland Inst Med Res, Brisbane, Qld 4029, Australia.
[Sinnett, D.] Univ Montreal, Dept Pediat, Montreal, PQ H3T 1C5, Canada.
[Sinnett, D.] CHU St Justine, Res Ctr, Div Hematol Oncol, Montreal, PQ H3T 1C5, Canada.
[kConFab] Peter MacCallum Canc Ctr, Melbourne, Vic 3002, Australia.
[Greene, M. H.; Loud, J. T.] NCI, Div Canc Epidemiol & Genet, Clin Genet Branch, Rockville, MD 20852 USA.
[Lejbkowicz, F.; Rennert, G.; Dishon, S.] CHS Natl Canc Control Ctr, IL-34362 Haifa, Israel.
[Lejbkowicz, F.; Rennert, G.; Dishon, S.] Carmel Hosp, Dept Community Med & Epidemiol, IL-34362 Haifa, Israel.
[Lejbkowicz, F.; Rennert, G.; Dishon, S.] Technion Israel Inst Technol, Fac Med, IL-34362 Haifa, Israel.
[Andrulis, I. L.; OCGN] Univ Toronto, Dept Mol Genet, Ontario Canc Genet Network, Toronto, ON M5G 1X5, Canada.
[Andrulis, I. L.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
[Domchek, S. M.; Nathanson, K. L.] Univ Penn, Sch Med, Dept Med, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Manoukian, S.] Fdn IRCCS Ist Nazl Tumori, Unit Med Genet, Milan, Italy.
[Radice, P.] Fdn IRCCS Ist Nazl Tumori, Dept Expt Oncol, I-20133 Milan, Italy.
[Radice, P.] Fdn Ist FIRC Oncol Mol, IFOM, I-20139 Milan, Italy.
[Konstantopoulou, I.] NCSR Demokritos, Mol Diagnost Lab, IRRP, Athens 15310, Greece.
[Blanco, I.] Inst Catala Oncol, Canc Genet Counseling Program, Barcelona 08907, Spain.
[Laborde, A. L.] Hosp Santa Creu i Sant Pau, Serv Genet, Barcelona 08025, Spain.
[Duran, M.] Univ Valladolid, Inst Mol Biol & Genet, Canc Genet Lab, E-47002 Valladolid, Spain.
[Osorio, A.; Benitez, J.] Spanish Natl Canc Res Ctr CNIO, Human Canc Genet Programme, Madrid 28029, Spain.
[Hamann, U.] Deutsch Krebsforschungszentrum, Mol Genet Breast Canc, D-69120 Heidelberg, Germany.
[Hogervorst, F. B. L.] Netherlands Canc Inst, Dept Pathol, NL-1066 CX Amsterdam, Netherlands.
[Hogervorst, F. B. L.; HEBON] Netherlands Canc Inst, Family Canc Clin, NL-1066 CX Amsterdam, Netherlands.
[van Os, T. A. M.] Univ Amsterdam, Med Ctr, Dept Clin Genet, NL-1105 AZ Amsterdam, Netherlands.
[Gille, H. J. P.] Free Univ Amsterdam, Med Ctr, Dept Clin Mol Genet, NL-1081 HV Amsterdam, Netherlands.
[Luccarini, C.] Univ Cambridge, Dept Oncol, Cambridge CB1 8RN, England.
[Evans, D. G.; Lalloo, F.] Cent Manchester Univ Hosp NHS Fdn Trust, Manchester Acad Hlth Sci Ctr, Manchester M13 OJH, Lancs, England.
[Eeles, R.] Inst Canc Res, Translat Canc Genet Team, Sutton SM2 5NG, Surrey, England.
[Eeles, R.] Royal Marsden NHS Fdn Trust, Sutton SM2 5NG, Surrey, England.
[Pichert, G.] Guys Hosp, London SE1 9RT, England.
[Davidson, R.] Ferguson Smith Ctr Clin Genet, Glasgow G3 8SJ, Lanark, Scotland.
[Cole, T.] Birmingham Womens Hosp Healthcare NHS Trust, W Midlands Reg Genet Serv, Birmingham B15 2TG, W Midlands, England.
[Cook, J.] Sheffield Childrens Hosp, Sheffield Clin Genet Serv, Sheffield S10 2TH, S Yorkshire, England.
[Paterson, J.] Addenbrookes Hosp, E Anglian Reg Genet Serv, Dept Clin Genet, Cambridge CB2 8QE, England.
[Brewer, C.] Royal Devon & Exeter Hosp, Dept Clin Genet, Exeter EX2 5DW, Devon, England.
[Hughes, D. J.] Adelaide & Meath Hosp, Trinity Coll, Ctr Hlth Sci, Dept Clin Med, Dublin 24, Ireland.
[Coupier, I.] CHU Arnaud Villeneuve, Unite Oncogenet, Serv Genet Med, F-34295 Montpellier, France.
[Coupier, I.] CRLCC Val Aurelle, Unite Oncogenet, F-34295 Montpellier, France.
[Rouleau, E.; Bieche, I.; Lidereau, R.] Ctr Rene Huguenin, INSERM, Oncogenet U735, F-92210 St Cloud, France.
[Coulet, F.; Colas, C.; Soubrier, F.] Univ Paris 06, Grp Hosp Pitie Salpetriere, AP HP, Lab Oncogenet & Angiogenet Mol, F-75651 Paris, France.
[Demange, L.; Nogues, C.] Ctr Rene Huguenin, Epidemiol Clin, F-92210 St Cloud, France.
[Lynch, H. T.] Creighton Univ, Dept Prevent Med, Omaha, NE 68178 USA.
[Stoppa-Lyonnet, D.; GEMO] Univ Paris 05, Inst Curie, Serv Genet Oncol, INSERM,U508, F-75248 Paris, France.
[Schmutzler, R. K.; Versmold, B.] Univ Cologne, Dept Obstet & Gynaecol, Ctr Hereditary Breast & Ovarian Canc, D-50924 Cologne, Germany.
[Engel, C.] Univ Leipzig, Inst Med Informat Stat & Epidemiol, D-04103 Leipzig, Germany.
[Meindl, A.] Tech Univ Munich, Dept Obstet & Gynaecol, D-80333 Munich, Germany.
[Arnold, N.] Univ Schleswig Holstein, Dept Obstet & Gynaecol, D-24105 Kiel, Germany.
[Sutter, C.] Univ Heidelberg, Inst Human Genet, D-69117 Heidelberg, Germany.
[Deissler, H.] Univ Ulm, Dept Obstet & Gynaecol, D-89069 Ulm, Germany.
[Schaefer, D.; GC-HBOC] Goethe Univ Frankfurt, Inst Human Genet, D-60325 Frankfurt, Germany.
[Froster, U. G.] Univ Leipzig, Inst Human Genet, D-04103 Leipzig, Germany.
[Aittomaki, K.] Univ Helsinki, Cent Hosp, Dept Clin Genet, Helsinki 00029, Finland.
[Nevanlinna, H.] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, Helsinki 00029, Finland.
RP Sinilnikova, OM (reprint author), Hosp Civils Lyon Ctr Leon Berard, Unite Mixte Genet Constitut Canc Frequents, F-69373 Lyon, France.
EM sinilnik@lyon.fnclcc.fr
RI Spurdle, Amanda/A-4978-2011; Arnold, Norbert/E-3012-2010; Blanco,
Ignacio/D-2565-2013; Andrulis, Irene/E-7267-2013; Radice,
Paolo/O-3119-2013; Osorio, Ana/I-4324-2014; manoukian,
siranoush/E-7132-2017;
OI Nevanlinna, Heli/0000-0002-0916-2976; Evans, Gareth/0000-0002-8482-5784;
Nathanson, Katherine/0000-0002-6740-0901; Eeles,
Rosalind/0000-0002-3698-6241; Spurdle, Amanda/0000-0003-1337-7897;
Arnold, Norbert/0000-0003-4523-8808; Blanco,
Ignacio/0000-0002-7414-7481; Osorio, Ana/0000-0001-8124-3984; manoukian,
siranoush/0000-0002-6034-7562; Konstantopoulou,
Irene/0000-0002-0470-0309
FU German Cancer Aid [107054]; Center for Molecular Medicine Cologne
[TV93]; Helsinki University Central Hospital Research Fund; Academy of
Finland [110663]; Finnish Cancer Society; Sigrid Juselius Foundation
FX We thank Juliane Koehler for her excellent technical assistance and the
12 centers of the GC-HBOC (German Consortium of Hereditary Breast and
Ovarian Cancer) for providing samples and clinical data. GC-HBOC is
supported by a grant of the German Cancer Aid (grant 107054) and the
Center for Molecular Medicine Cologne (grant TV93) to Rita K Schmutzler.
We thank Drs Kirsimari Aaltonen, Carl Blomqvist and RN Hanna Jantti for
their help with the patient data and Dr Johanna Tommiska for her kind
help with the genetic analyses. The Finnish Cancer registry is
gratefully acknowledged for the cancer data. The HEBCS study has been
financially supported by the Helsinki University Central Hospital
Research Fund, Academy of Finland (110663), Finnish Cancer Society and
the Sigrid Juselius Foundation.
NR 22
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U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD OCT 13
PY 2009
VL 101
IS 8
BP 1456
EP 1460
DI 10.1038/sj.bjc.6605279
PG 5
WC Oncology
SC Oncology
GA 506HZ
UT WOS:000270767200031
PM 19707196
ER
PT J
AU Mutskov, V
Felsenfeld, G
AF Mutskov, Vesco
Felsenfeld, Gary
TI The human insulin gene is part of a large open chromatin domain specific
for human islets
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE histone modifications; intergenic transcription; pancreatic islets
ID PANCREATIC BETA-CELLS; HISTONE MODIFICATIONS; TRANSCRIPTION INITIATION;
TYROSINE-HYDROXYLASE; CONTROL REGION; GROWTH-FACTORS; PROMOTER DNA;
HUMAN GENOME; EXPRESSION; METHYLATION
AB Knowledge of how insulin (INS) gene expression is regulated will lead to better understanding of normal and abnormal pancreatic beta cell function. We have mapped histone modifications over the INS region, coupled with an expression profile, in freshly isolated islets from multiple human donors. Unlike many other human genes, in which active modifications tend to be concentrated within 1 kb around the transcription start site, these marks are distributed over the entire coding region of INS as well. Moreover, a region of approximate to 80 kb around the INS gene, which contains the {tyrosine hydroxylase (TH)-(INS)-insulin-like growth factor 2 antisense (IGF2AS)-insulin-like growth factor 2 (IGF2)} gene cluster, unusually is marked by almost uniformly elevated levels of histone acetylation and H3K4 dimethylation, extending both downstream into IGF2 and upstream beyond the TH gene. This is accompanied by islet specific coordinate expression with INS of the neighboring TH and IGF2 genes. The presence of islet specific intergenic transcripts suggests their possible function in the maintenance of this unusual large open chromatin domain.
C1 [Mutskov, Vesco; Felsenfeld, Gary] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Felsenfeld, G (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM gary.felsenfeld@nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health
FX We thank the Islet Cell Resource Basic Science Islet Distribution
Program; Drs. David Harlan (NIDDK, National Institutes of Health) and
Eric Liu (National Institute of Diabetes and Digestive and Kidney
Diseases) for providing human islets; Dr. Gaelle Lefevre for stimulating
discussions; Dr. Sandeep Dayal (NIDDK, National Institutes of Health)
for the primary human fibroblasts, and members of the Felsenfeld
laboratory for critical reading of this manuscript. This work was
supported by the Intramural Research Program of the National Institute
of Diabetes and Digestive and Kidney Diseases, National Institutes of
Health.
NR 35
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U1 0
U2 5
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 13
PY 2009
VL 106
IS 41
BP 17419
EP 17424
DI 10.1073/pnas.0909288106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 506DS
UT WOS:000270754400037
PM 19805079
ER
PT J
AU Hinrichs, CS
Borman, ZA
Cassard, L
Gattinoni, L
Spolski, R
Yu, ZY
Sanchez-Perez, L
Muranski, P
Kern, SJ
Logun, C
Palmer, DC
Ji, Y
Reger, RN
Leonard, WJ
Danner, RL
Rosenberg, SA
Restifo, NP
AF Hinrichs, Christian S.
Borman, Zachary A.
Cassard, Lydie
Gattinoni, Luca
Spolski, Rosanne
Yu, Zhiya
Sanchez-Perez, Luis
Muranski, Pawel
Kern, Steven J.
Logun, Carol
Palmer, Douglas C.
Ji, Yun
Reger, Robert N.
Leonard, Warren J.
Danner, Robert L.
Rosenberg, Steven A.
Restifo, Nicholas P.
TI Adoptively transferred effector cells derived from naive rather than
central memory CD8(+) T cells mediate superior antitumor immunity
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID TUMOR-REGRESSION; VIRAL-INFECTION; DIFFERENTIATION; CANCER;
IMMUNOTHERAPY; THERAPY; ANTIGEN; LYMPHOCYTES; AUTOIMMUNITY; PROTECTION
AB Effector cells derived from central memory CD8(+) T cells were reported to engraft and survive better than those derived from effector memory populations, suggesting that they are superior for use in adoptive immunotherapy studies. However, previous studies did not evaluate the relative efficacy of effector cells derived from naive T cells. We sought to investigate the efficacy of tumor-specific effector cells derived from naive or central memory T-cell subsets using transgenic or retrovirally transduced T cells engineered to express a tumor-specific T-cell receptor. We found that naive, rather than central memory T cells, gave rise to an effector population that mediated superior antitumor immunity upon adoptive transfer. Effector cells developed from naive T cells lost the expression of CD62L more rapidly than those derived from central memory T cells, but did not acquire the expression of KLRG-1, a marker for terminal differentiation and replicative senescence. Consistent with this KLRG-1(-) phenotype, naive-derived cells were capable of a greater proliferative burst and had enhanced cytokine production after adoptive transfer. These results indicate that insertion of genes that confer antitumor specificity into naive rather than central memory CD8(+) T cells may allow superior efficacy upon adoptive transfer.
C1 [Hinrichs, Christian S.; Borman, Zachary A.; Cassard, Lydie; Gattinoni, Luca; Yu, Zhiya; Sanchez-Perez, Luis; Muranski, Pawel; Palmer, Douglas C.; Ji, Yun; Reger, Robert N.; Rosenberg, Steven A.; Restifo, Nicholas P.] NCI, Bethesda, MD 20892 USA.
[Spolski, Rosanne; Leonard, Warren J.] NHLBI, Bethesda, MD 20824 USA.
[Kern, Steven J.; Logun, Carol; Danner, Robert L.] NIH, Funct Genom & Prote Facil, Dept Crit Care Med, Bethesda, MD 20892 USA.
RP Restifo, NP (reprint author), NCI, Bethesda, MD 20892 USA.
EM restifo@nih.gov
RI Gattinoni, Luca/A-2281-2008; Ji, Yun/B-7245-2009; Restifo,
Nicholas/A-5713-2008; Muranski, Pawel/E-5572-2010; Palmer,
Douglas/B-9454-2008;
OI Gattinoni, Luca/0000-0003-2239-3282; Ji, Yun/0000-0001-6340-7009;
Palmer, Douglas/0000-0001-5018-5734; Restifo, Nicholas
P./0000-0003-4229-4580
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research; National Heart Lung and Blood Institute
FX The authors thank Lindsay Garvin, Arnold Mixon, Shawn Farid, and W.
David Jones for their assistance with this project. We also thank
Christopher A. Klebanoff for critically reading the paper and making
numerous helpful suggestions. This research was supported by the
Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research and the National
Heart Lung and Blood Institute. This study was performed in partial
fulfillment of a Ph.D. in Biochemistry (to D. C. P.) at the George
Washington University, Washington, DC.
NR 42
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U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 13
PY 2009
VL 106
IS 41
BP 17469
EP 17474
DI 10.1073/pnas.0907448106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 506DS
UT WOS:000270754400046
PM 19805141
ER
PT J
AU Laliberte, JP
Moss, B
AF Laliberte, Jason P.
Moss, Bernard
TI Appraising the apoptotic mimicry model and the role of phospholipids for
poxvirus entry
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE blebbing; endocytosis; macropinocytosis; phosphatidylserine; vaccinia
virus
ID CELL-CELL FUSION; INTRACELLULAR MATURE VIRION; ENVELOPED VACCINIA VIRUS;
SURFACE HEPARAN-SULFATE; MEMBRANE-PROTEIN; L1 PROTEIN;
PHOSPHATIDYLSERINE RECEPTOR; PLASMA-MEMBRANE; VIRAL MEMBRANE; HOST-CELLS
AB Entry of vaccinia virus (VACV) into cells occurs by fusion with the plasma membrane and via a low pH-dependent endosomal pathway, presumably involving unidentified cellular receptors. In addition to approximate to 25 viral proteins, the membrane of VACV mature virions contains several phospholipids including phosphatidylserine (PS). A recent model posits that PS flags virions as apoptotic debris to activate a common cellular uptake pathway to gain cell entry, perhaps through an interaction with a PS-specific cell surface receptor. To evaluate the apoptotic mimicry model, we reconstituted the membrane of detergent-extracted virions with several different phospholipids. Although the ability of the L-stereoisomer of PS to reconstitute infectivity was confirmed, the nonbiologically relevant D-stereoisomer of PS, and phosphatidylglycerol, which are not normally present in the virion membrane, functioned as well. Regardless of which phospholipid reconstituted infectivity, virus entry was inhibited by a neutralizing monoclonal antibody to a virion surface protein and by the drugs blebbistatin and bafilomycin A1, suggesting that in each case virus uptake was specific and occurred by a similar mechanism involving macropinocytosis and a low-pH endocytic pathway. Lipid-reconstituted and nonreconstituted, membrane-extracted virions were equally capable of binding to cells. However, the physical association of phospholipids with virus particles during membrane reconstitution correlated directly with rescue of particle infectivity and cell entry capability. Our results support a role for PS in poxvirus entry, but demonstrate that other phospholipids, not known to signal uptake of apoptotic debris, can function similarly.
C1 [Laliberte, Jason P.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM bmoss@mail.nih.gov
FU Division of Intramural Research; National Institute of Allergy and
Infectious Diseases; National Institutes of Health
FX We thank Catherine Cotter (National Institutes of Health, Bethesda, MD)
for cells; George Katsafanas (National Institutes of Health, Bethesda,
MD) for theWRA4-YFP recombinant virus; Zain Benglai, Panayampalli
Subbian Satheshkumar, Amanda Howard, and Nir Paran for helpful
discussions; Jason Mercer for details regarding methods of lipid
reconstitution; and Robert Doms and Richard Condit for useful comments
on the manuscript. This work was supported by the Division of Intramural
Research, National Institute of Allergy and Infectious Diseases,
National Institutes of Health.
NR 49
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U1 0
U2 3
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 13
PY 2009
VL 106
IS 41
BP 17517
EP 17521
DI 10.1073/pnas.0909376106
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 506DS
UT WOS:000270754400054
PM 19805093
ER
PT J
AU Jia, L
Oh, ECT
Ng, L
Srinivas, M
Brooks, M
Swaroop, A
Forrest, D
AF Jia, Li
Oh, Edwin C. T.
Ng, Lily
Srinivas, Maya
Brooks, Matthew
Swaroop, Anand
Forrest, Douglas
TI Retinoid-related orphan nuclear receptor ROR beta is an early-acting
factor in rod photoreceptor development
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE cone; differentiation
ID TRANSCRIPTION FACTOR NRL; MOUSE RETINA; CONE PHOTORECEPTORS; CELL-FATE;
RD7 MOUSE; EXPRESSION; NR2E3; GENES; MICE; CRX
AB Rods and cones are morphologically and developmentally distinct photoreceptor types with different functions in vision. Cones mediate daylight and color vision and in most mammals express M and S opsin photopigments for sensitivity to medium-long and short light wavelengths, respectively. Rods mediate dim light vision and express rhodopsin photopigment. The transcription factor networks that direct differentiation of each photoreceptor type are incompletely defined. Here, we report that Rorb(-/-) mice lacking retinoid-related orphan nuclear receptor beta lose rods but overproduce primitive S cones that lack outer segments. The phenotype reflects pronounced plasticity between rod and cone lineages and resembles that described for Nrl(-/-) mice lacking neural retina leucine zipper factor. Rorb(-/-) mice lack Nrl expression and reexpression of Nrl in Rorb(-/-) mice converts cones to rod-like cells. Thus, Rorb directs rod development and does so at least in part by inducing the Nrl-mediated pathway of rod differentiation.
C1 [Jia, Li; Ng, Lily; Forrest, Douglas] NIDDK, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
[Brooks, Matthew; Swaroop, Anand] NEI, Neurodegenerat & Repair Lab, NIH, Bethesda, MD 20892 USA.
[Oh, Edwin C. T.; Swaroop, Anand] Univ Michigan, Dept Ophthalmol & Human Genet, Ann Arbor, MI 48105 USA.
[Srinivas, Maya] Mt Sinai Sch Med, Dept Human Genet, New York, NY 10029 USA.
RP Forrest, D (reprint author), NIDDK, Clin Endocrinol Branch, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM forrestd@niddk.nih.gov
FU Hirschl Award; National Institutes of Health [EY11115]; Kidney Diseases;
National Eye Institute
FX We thank H. Stunnenberg for antiserum, R. J. Desnick and Mount Sinai
School of Medicine for initial support, M. Becker-Andre, M. Dubocovich,
Northwestern University and GlaxoSmithKline for Rorb-/- mice,
R. Khanna, D. Sharlin, M. Ma, S. Kjellstro r m, and R. Bush for
assistance and advice. Supported by a Hirschl Award, National Institutes
of Health grant EY11115, and intramural programs at National Institute
of Diabetes and Digestive and Kidney Diseases and National Eye
Institute.
NR 35
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PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 13
PY 2009
VL 106
IS 41
BP 17534
EP 17539
DI 10.1073/pnas.0902425106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 506DS
UT WOS:000270754400057
PM 19805139
ER
PT J
AU Hoque, M
Hanauske-Abel, HM
Palumbo, P
Saxena, D
Gandolfi, DD
Park, MH
Pe'ery, T
Mathews, MB
AF Hoque, Mainul
Hanauske-Abel, Hartmut M.
Palumbo, Paul
Saxena, Deepti
Gandolfi, Darlene D'Alliessi
Park, Myung Hee
Pe'ery, Tsafi
Mathews, Michael B.
TI Inhibition of HIV-1 gene expression by Ciclopirox and Deferiprone, drugs
that prevent hypusination of eukaryotic initiation factor 5A
SO RETROVIROLOGY
LA English
DT Article
ID LONG-TERMINAL REPEAT; TEFB-DEPENDENT TRANSCRIPTION; ENDOTHELIAL-CELL
GROWTH; AMINO-ACID-RESIDUES; NF-KAPPA-B; IRON CHELATORS; DEOXYHYPUSINE
SYNTHASE; CONTAINING PROTEIN; SACCHAROMYCES-CEREVISIAE; NUCLEAR EXPORT
AB Background: Eukaryotic translation initiation factor eIF5A has been implicated in HIV-1 replication. This protein contains the apparently unique amino acid hypusine that is formed by the post-translational modification of a lysine residue catalyzed by deoxyhypusine synthase and deoxyhypusine hydroxylase (DOHH). DOHH activity is inhibited by two clinically used drugs, the topical fungicide ciclopirox and the systemic medicinal iron chelator deferiprone. Deferiprone has been reported to inhibit HIV-1 replication in tissue culture.
Results: Ciclopirox and deferiprone blocked HIV-1 replication in PBMCs. To examine the underlying mechanisms, we investigated the action of the drugs on eIF5A modification and HIV-1 gene expression in model systems. At early times after drug exposure, both drugs inhibited substrate binding to DOHH and prevented the formation of mature eIF5A. Viral gene expression from HIV-1 molecular clones was suppressed at the RNA level independently of all viral genes. The inhibition was specific for the viral promoter and occurred at the level of HIV-1 transcription initiation. Partial knockdown of eIF5A-1 by siRNA led to inhibition of HIV-1 gene expression that was non-additive with drug action. These data support the importance of eIF5A and hypusine formation in HIV-1 gene expression.
Conclusion: At clinically relevant concentrations, two widely used drugs blocked HIV-1 replication ex vivo. They specifically inhibited expression from the HIV-1 promoter at the level of transcription initiation. Both drugs interfered with the hydroxylation step in the hypusine modification of eIF5A. These results have profound implications for the potential therapeutic use of these drugs as antiretrovirals and for the development of optimized analogs.
C1 [Hoque, Mainul; Pe'ery, Tsafi; Mathews, Michael B.] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Biochem & Mol Biol, Newark, NJ 07103 USA.
[Hanauske-Abel, Hartmut M.] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Obstet Gynecol & Womens Hlth, Newark, NJ 07103 USA.
[Hanauske-Abel, Hartmut M.; Palumbo, Paul; Saxena, Deepti] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Pediat, Newark, NJ 07103 USA.
[Gandolfi, Darlene D'Alliessi] Manhattanville Coll, Dept Chem, Purchase, NY 10577 USA.
[Park, Myung Hee] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA.
[Pe'ery, Tsafi] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Med, Newark, NJ 07103 USA.
RP Pe'ery, T (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Biochem & Mol Biol, Newark, NJ 07103 USA.
EM hoquema@umdnj.edu; hanaushm@mac.com; Paul.E.Palumbo@Dartmouth.edu;
Deepti.Saxena@Dartmouth.edu; gandolfid@mville.edu; parkm@mail.nih.gov;
peeryts@umdnj.edu; mathews@umdnj.edu
FU NIH; BIRCWH Scholar [HD-1457]
FX We thank Drs. Benjamin Chen, Matija Peterlin and David Price and the NIH
AIDS Research and Reference Reagent Program for reagents. We are
grateful to Anita Antes for technical assistance. This work was
supported by grants from NIH to Tsafi Pe'ery and Michael B. Mathews, and
to Hartmut M. Hanauske-Abel as a BIRCWH Scholar (HD-1457).
NR 96
TC 37
Z9 37
U1 0
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD OCT 13
PY 2009
VL 6
AR 90
DI 10.1186/1742-4690-6-90
PG 17
WC Virology
SC Virology
GA 518EV
UT WOS:000271674200002
PM 19825182
ER
PT J
AU Shepard, JD
Chambers, CO
Busch, C
Mount, A
Schulkin, J
AF Shepard, Jack D.
Chambers, Charles O.
Busch, Chris
Mount, Alexander
Schulkin, Jay
TI Chronically elevated corticosterone in the dorsolateral bed nuclei of
stria terminalis increases anxiety-like behavior
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Bed nuclei of stria terminalis; BNST; BST; Fear; Anxiety;
Corticosterone; Glucocorticoids; Extended amygdala
ID FACTOR MESSENGER-RNA; PLUS-MAZE; COLONIC SENSITIVITY; PARAVENTRICULAR
NUCLEUS; EXTENDED AMYGDALA; RAT BEHAVIOR; FEAR; STRESS; RESPONSES;
NEUROENDOCRINE
AB We previously discovered that corticosterone administration into the amygdala increases anxiety-like behaviors in rats tested on an elevated plus maze. However the behavioral effects of elevated corticosterone in a functionally related structure, the bed nuclei of stria terminalis (BNST) are unknown. The current study examined the effects of corticosterone administration into the dorsolateral BNST on exploratory behavior on an elevated plus maze. Corticosterone reduced open arm exploration on the plus maze indicating an increase in anxiety-like behavior. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Shepard, Jack D.; Chambers, Charles O.; Busch, Chris; Mount, Alexander] Towson Univ, Dept Biol Sci, Towson, MD 21252 USA.
[Schulkin, Jay] Georgetown Univ, Dept Physiol & Biophys, Washington, DC USA.
[Schulkin, Jay] Amer Coll Obstetricians & Gynecologists, Res Dept, Washington, DC 20024 USA.
[Schulkin, Jay] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
RP Shepard, JD (reprint author), Towson Univ, Dept Biol Sci, 8000 York Rd, Towson, MD 21252 USA.
EM jshepard@towson.edu
FU Towson University Faculty Development Grant
FX This study was supported by a Towson University Faculty Development
Grant.
NR 33
TC 9
Z9 9
U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD OCT 12
PY 2009
VL 203
IS 1
BP 146
EP 149
DI 10.1016/j.bbr.2009.04.029
PG 4
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 470FU
UT WOS:000267961400021
PM 19409934
ER
PT J
AU Jackson, MC
Huang, L
Luo, J
Hachey, M
Feuer, E
AF Jackson, Monica C.
Huang, Lan
Luo, Jun
Hachey, Mark
Feuer, Eric
TI Comparison of tests for spatial heterogeneity on data with global
clustering patterns and outliers
SO INTERNATIONAL JOURNAL OF HEALTH GEOGRAPHICS
LA English
DT Article
ID POWER
AB Background: The ability to evaluate geographic heterogeneity of cancer incidence and mortality is important in cancer surveillance. Many statistical methods for evaluating global clustering and local cluster patterns are developed and have been examined by many simulation studies. However, the performance of these methods on two extreme cases (global clustering evaluation and local anomaly (outlier) detection) has not been thoroughly investigated.
Methods: We compare methods for global clustering evaluation including Tango's Index, Moran's I, and Oden's I(pop)*; and cluster detection methods such as local Moran's I and SaTScan elliptic version on simulated count data that mimic global clustering patterns and outliers for cancer cases in the continental United States. We examine the power and precision of the selected methods in the purely spatial analysis. We illustrate Tango's MEET and SaTScan elliptic version on a 1987-2004 HIV and a 1950-1969 lung cancer mortality data in the United States.
Results: For simulated data with outlier patterns, Tango's MEET, Moran's I and I(pop)* had powers less than 0.2, and SaTScan had powers around 0.97. For simulated data with global clustering patterns, Tango's MEET and I(pop)* (with 50% of total population as the maximum search window) had powers close to I. SaTScan had powers around 0.7-0.8 and Moran's I has powers around 0.2-0.3. In the real data example, Tango's MEET indicated the existence of global clustering patterns in both the HIV and lung cancer mortality data. SaTScan found a large cluster for HIV mortality rates, which is consistent with the finding from Tango's MEET. SaTScan also found clusters and outliers in the lung cancer mortality data.
Conclusion: SaTScan elliptic version is more efficient for outlier detection compared with the other methods evaluated in this article. Tango's MEET and Oden's I(pop)* perform best in global clustering scenarios among the selected methods. The use of SaTScan for data with global clustering patterns should be used with caution since SatScan may reveal an incorrect spatial pattern even though it has enough power to reject a null hypothesis of homogeneous relative risk. Tango's method should be used for global clustering evaluation instead of SaTScan.
C1 [Jackson, Monica C.] American Univ, Dept Math & Stat, Washington, DC 20016 USA.
[Huang, Lan; Feuer, Eric] NCI, NIH, Rockville, MD 20852 USA.
[Luo, Jun; Hachey, Mark] Informat Management Serv Inc, Silver Spring, MD 20904 USA.
RP Jackson, MC (reprint author), American Univ, Dept Math & Stat, Washington, DC 20016 USA.
EM monica@american.edu; huangla@mail.nih.gov; LuoJ@imsweb.com;
HacheyM@imsweb.com; feuerr@mail.nih.gov
FU PHS HHS [263-MQ-706620]
NR 24
TC 13
Z9 15
U1 0
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-072X
J9 INT J HEALTH GEOGR
JI Int. J. Health Geogr.
PD OCT 12
PY 2009
VL 8
AR 55
DI 10.1186/1476-072X-8-55
PG 14
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 515GC
UT WOS:000271454800001
PM 19822013
ER
PT J
AU De Giorgi, V
Monaco, A
Worchech, A
Tornesello, M
Izzo, F
Buonaguro, L
Marincola, FM
Wang, E
Buonaguro, FM
AF De Giorgi, Valeria
Monaco, Alessandro
Worchech, Andrea
Tornesello, MariaLina
Izzo, Francesco
Buonaguro, Luigi
Marincola, Francesco M.
Wang, Ena
Buonaguro, Franco M.
TI Gene profiling, biomarkers and pathways characterizing HCV-related
hepatocellular carcinoma
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
ID CHRONIC HEPATITIS-C; SPINDLE ASSEMBLY CHECKPOINT; UNITED-STATES;
EXPRESSION PATTERNS; CDNA MICROARRAYS; VIRAL-HEPATITIS; LIVER-CANCER; AH
RECEPTOR; VIRUS; MAD2
AB Background: Hepatitis C virus (HCV) infection is a major cause of hepatocellular carcinoma (HCC) worldwide. The molecular mechanisms of HCV-induced hepatocarcinogenesis are not yet fully elucidated. Besides indirect effects as tissue inflammation and regeneration, a more direct oncogenic activity of HCV can be postulated leading to an altered expression of cellular genes by early HCV viral proteins. In the present study, a comparison of gene expression patterns has been performed by microarray analysis on liver biopsies from HCV-positive HCC patients and HCV-negative controls.
Methods: Gene expression profiling of liver tissues has been performed using a high-density microarray containing 36'000 oligos, representing 90% of the human genes. Samples were obtained from 14 patients affected by HCV-related HCC and 7 HCV-negative non-liver-cancer patients, enrolled at INT in Naples. Transcriptional profiles identified in liver biopsies from HCC nodules and paired non-adjacent non-HCC liver tissue of the same HCV-positive patients were compared to those from HCV-negative controls by the Cluster program. The pathway analysis was performed using the BRB-Array- Tools based on the "Ingenuity System Database". Significance threshold of t-test was set at 0.001.
Results: Significant differences were found between the expression patterns of several genes falling into different metabolic and inflammation/immunity pathways in HCV-related HCC tissues as well as the non-HCC counterpart compared to normal liver tissues. Only few genes were found differentially expressed between HCV-related HCC tissues and paired non-HCC counterpart.
Conclusion: In this study, informative data on the global gene expression pattern of HCV-related HCC and non-HCC counterpart, as well as on their difference with the one observed in normal liver tissues have been obtained. These results may lead to the identification of specific biomarkers relevant to develop tools for detection, diagnosis, and classification of HCV-related HCC.
C1 [De Giorgi, Valeria; Tornesello, MariaLina; Buonaguro, Luigi; Buonaguro, Franco M.] Ist Naz Tumori Fond G Pascale, Mol Biol & Viral Oncogenesis & AIDS Refer, Naples, Italy.
[De Giorgi, Valeria] Univ Naples Federico 2, Dept Chem, Naples, Italy.
[Monaco, Alessandro; Worchech, Andrea; Marincola, Francesco M.; Wang, Ena] NIH, IDIS, Dept Transfus Med, Clin Ctr & Trans NIH,CHI, Bethesda, MD USA.
[Worchech, Andrea] Genelux Corp, Res & Dev, San Diego Sci Ctr, San Diego, CA USA.
[Worchech, Andrea] Univ Wurzburg, Bioctr, Dept Biochem, Wurzburg, Germany.
[Izzo, Francesco] Ist Naz Tumori Fond G Pascale, Div Surg D, Naples, Italy.
RP Buonaguro, FM (reprint author), Ist Naz Tumori Fond G Pascale, Mol Biol & Viral Oncogenesis & AIDS Refer, Naples, Italy.
EM valeriadegiorgi@tin.it; monacoal@cc.nih.gov; worschecha@cc.nih.gov;
mltornesello@alice.it; izzo@connect.it; lbuonaguro@tin.it;
FMarincola@mail.cc.nih.gov; ewang@mail.cc.nih.gov; irccsvir@unina.it
RI Tornesello, Maria Lina/A-1564-2009; Worschech, Andrea/I-3919-2012;
Monaco, Alessandro/O-5338-2015; De Giorgi, Valeria/D-4582-2017; Izzo,
Francesco/K-5261-2016;
OI Tornesello, Maria Lina/0000-0002-3523-3264; Worschech,
Andrea/0000-0002-4303-8653; Monaco, Alessandro/0000-0002-9941-7003;
Izzo, Francesco/0000-0003-3093-5408; Buonaguro,
Luigi/0000-0002-6380-7114
FU Italian Ministry of Health - Ministero Italiano Salute
FX We are indebted to Dr. Marianna Sabatino for her invaluable technical
support and fruitful discussions. This study was supported by grants
from the Italian Ministry of Health - Ministero Italiano Salute (Ricerca
Corrente 2008-9 and FSN 2005 Cnv 89).
NR 40
TC 19
Z9 20
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD OCT 12
PY 2009
VL 7
AR 85
DI 10.1186/1479-5876-7-85
PG 14
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 516GY
UT WOS:000271531400001
PM 19821982
ER
PT J
AU Solomon, D
Castle, P
Hildesheim, A
Katki, HA
Schiffman, M
Wacholder, S
AF Solomon, Diane
Castle, Phil
Hildesheim, Allan
Katki, Hormuzd A.
Schiffman, Mark
Wacholder, Sholom
TI HPV vaccination in women aged 24-45 years
SO LANCET
LA English
DT Letter
C1 [Castle, Phil; Hildesheim, Allan; Katki, Hormuzd A.; Schiffman, Mark; Wacholder, Sholom] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20892 USA.
[Solomon, Diane] NCI, Canc Prevent Div, NIH, Dept Hlth & Human Serv, Rockville, MD 20892 USA.
RP Castle, P (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, 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 [Z01 CP010177-07]
NR 3
TC 3
Z9 3
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
J9 LANCET
JI Lancet
PD OCT 10
PY 2009
VL 374
IS 9697
BP 1239
EP 1239
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 507KQ
UT WOS:000270852500023
PM 19819386
ER
PT J
AU Ludek, OR
Marquez, VE
AF Ludek, Olaf R.
Marquez, Victor E.
TI A greener enantioselective synthesis of the antiviral agent
North-methanocarbathymidine (N-MCT) from 2-deoxy-D-ribose
SO TETRAHEDRON
LA English
DT Article
DE Conformationally locked carbocyclic nucleosides;
North-methanocarbathymidine; Antiviral; Enantioselective synthesis
ID RING-CLOSING METATHESIS; CARBOCYCLIC NUCLEOSIDES; ORTHOPOXVIRUS
INFECTIONS; ERYTHRULOSE DERIVATIVES; CONFORMATIONAL-ANALYSIS;
ASYMMETRIC-SYNTHESIS; ADENOSINE-DEAMINASE; BIOLOGICAL-ACTIVITY;
EFFICIENT SYNTHESIS; SUGAR RING
AB An enantioselective synthesis of suitably protected (1R,2S,4S,5S)-4-amino-1-(hydroxymetllyl)bicyclo[3,1,0]hexan-2-ol, a key starting material for the synthesis of conformationally locked carbocyclic nucleosides, including the antiviral active North-methanocarbathymidine, is reported. Starting from 2-deoxyribose the target Boc-protected amine was prepared in 33% overall yield under conditions that are ecologically friendlier than previous methods. Published by Elsevier Ltd.
C1 [Ludek, Olaf R.; Marquez, Victor E.] NCI, Med Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
RP Marquez, VE (reprint author), NCI, Med Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
EM marquezv@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. The
authors wish to thank Dr. James A. Kelley for the HRMS analysis.
NR 41
TC 15
Z9 15
U1 0
U2 9
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0040-4020
J9 TETRAHEDRON
JI Tetrahedron
PD OCT 10
PY 2009
VL 65
IS 41
BP 8461
EP 8467
DI 10.1016/j.tet.2009.08.035
PG 7
WC Chemistry, Organic
SC Chemistry
GA 500ZN
UT WOS:000270345900002
PM 20625519
ER
PT J
AU Heeregrave, EJ
Geels, MJ
Brenchley, JM
Laan, E
Ambrozak, DR
van der Sluis, RM
Bennemeer, R
Douek, DC
Goudsmit, J
Pollakis, G
Koup, RA
Paxton, WA
AF Heeregrave, Edwin J.
Geels, Mark J.
Brenchley, Jason M.
Laan, Elly
Ambrozak, David R.
van der Sluis, Renee M.
Bennemeer, Rune
Douek, Daniel C.
Goudsmit, Jaap
Pollakis, Georgios
Koup, Richard A.
Paxton, William A.
TI Lack of in vivo compartmentalization among HIV-1 infected naive and
memory CD4(+) T cell subsets
SO VIROLOGY
LA English
DT Article
DE HIV-1; CD4 subsets; Compartmentalization
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HUMAN LYMPHOID-TISSUE; HIV-1 INFECTION;
BLOOD MONOCYTES; SIV INFECTION; ANTIRETROVIRAL THERAPY;
GASTROINTESTINAL-TRACT; ENVELOPE GLYCOPROTEIN; DISEASE PROGRESSION;
CORECEPTOR USAGE
AB Viral compartmentalization between naive and memory CD4(+) T cell subsets has been described, but only for individuals who were receiving antiretroviral therapy (ART). We present here an extensive analysis of the viral quasispecies residing in the naive, central and effector memory CD4(+) T cell Subsets in a number of therapy naive individuals and representing an array of HIV-1 subtypes. We longitudinally analyzed subset-specific infection and evolution in a subtype B infected individual who switches from CCR5 to dual CCR5/CXCR4 coreceptor usage. We show that the central memory subset, the predominantly infected subset, harbors a more diverse viral population compared to the others. Through sequence analysis of the env C2V3 region we demonstrate a lack of viral compartmentalization among all subsets. Upon coreceptor switch we observe a pronounced increase in the infection level of the naive population. Our findings emphasize the importance of all CD4(+) T cell subsets to viral evolution. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Heeregrave, Edwin J.; Geels, Mark J.; Laan, Elly; van der Sluis, Renee M.; Bennemeer, Rune; Pollakis, Georgios; Paxton, William A.] Univ Amsterdam, Acad Med Ctr, Lab Expt Virol, Dept Med Microbiol,CINIMA, NL-1105 AZ Amsterdam, Netherlands.
[Brenchley, Jason M.; Douek, Daniel C.; Koup, Richard A.] NIAID, Human Immunol Sect, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Ambrozak, David R.] NIAID, Immunol Lab, NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Goudsmit, Jaap] Crucell Holland BV, Leiden, Netherlands.
RP Paxton, WA (reprint author), Univ Amsterdam, Acad Med Ctr, Lab Expt Virol, Dept Med Microbiol,CINIMA, Meibergdreef 15, NL-1105 AZ Amsterdam, Netherlands.
EM w.a.paxton@amc.uva.nl
OI van der Sluis, Renee/0000-0002-7668-2517; Pollakis,
Georgios/0000-0002-9659-5461
FU NWO-Wotro (EJH) [01.53.2004.025]; Dutch AIDS fonds (MJG and EB) [6002];
Netherlands Organization of Scientific Research; The Royal Netherlands
Academy of Arts and Sciences
FX This work was financially supported by NWO-Wotro (EJH; project number
01.53.2004.025) and Dutch AIDS fonds (MJG and EB: grant 6002). Travel
grants from the Netherlands Organization of Scientific Research and The
Royal Netherlands Academy of Arts and Sciences (Van Walree Fund) were
allocated to MG. The authors would like to thank the participants of the
Amsterdam Cohort Studies on HIV-1 infection and AIDS, which is a
collaboration of the Municipal Health Service, the Academic Medical
Center and Sanquin Research. The authors thank M. Bakker, L. Dekker and
co-workers for processing of patient material and Brenna J. Hill for the
excellent technical assistance.
NR 61
TC 17
Z9 18
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD OCT 10
PY 2009
VL 393
IS 1
BP 24
EP 32
DI 10.1016/j.virol.2009.07.011
PG 9
WC Virology
SC Virology
GA 502JA
UT WOS:000270453600005
PM 19698967
ER
PT J
AU Gustchina, E
Louis, JM
Frisch, C
Ylera, F
Lechner, A
Bewley, CA
Clore, GM
AF Gustchina, Elena
Louis, John M.
Frisch, Christian
Ylera, Francisco
Lechner, Annette
Bewley, Carole A.
Clore, G. Marius
TI Affinity maturation by targeted diversification of the CDR-H2 loop of a
monoclonal Fab derived from a synthetic naive human antibody library and
directed against the internal trimeric coiled-coil of gp41 yields a set
of Fabs with improved HIV-1 neutralization potency and breadth
SO VIROLOGY
LA English
DT Article
DE gp41 envelope; HIV-1; Broadly neutralizing antibodies; Naive phage
library; Affinity maturation
ID TYPE-1 ENVELOPE GLYCOPROTEIN; PHAGE LIBRARY; PEPTIDE INHIBITOR; ENTRY
INHIBITION; ATOMIC-STRUCTURE; MEMBRANE-FUSION; VIRAL ENTRY; DESIGN;
ECTODOMAIN; DIVERSE
AB Previously we reported a broadly HIV-1 neutralizing mini-antibody (Fab 3674) of modest potency that was derived from a human non-immune phage library by panning against the chimeric gp41-derived construct N(CCG)-gp41. This construct presents the N-heptad repeat of the gp41 ectodomain as a stable, helical, disulfide-linked trimer that extends in helical phase from the six-helix bundle of gp41. In this paper, Fab 3674 was subjected to affinity maturation against the N(CCG)-gp41 antigen by targeted diversification of the CDR-H2 loop to generate a panel of Fabs with diverse neutralization activity. Three affinity-matured Fabs selected for further study, Fabs 8060, 8066 and 8068, showed significant increases in both potency and breadth of neutralization against HIV-1 pseudotyped with envelopes of primary isolates from the standard subtype B and C HIV-1 reference panels. The parental Fab 3674 is 10-20-fold less potent in monovalent than bivalent format over the entire B and C panels of HIV-1 pseudotypes. Of note is that the improved neutralization activity of the affinity-matured Fabs relative to the parental Fab 3674 was, on average, significantly greater for the Fabs in monovalent than bivalent format. This suggests that the increased avidity of the Fabs for the target antigen in bivalent format can be partially offset by kinetic and/or steric advantages afforded by the smaller monovalent Fabs. Indeed, the best affinity-matured Fab (8066) in monovalent format (similar to 50 kDa) was comparable in HIV-1 neutralization potency to the parental Fab 3674 in bivalent format (similar to 120 kDa) across the subtype B and C reference panels. Published by Elsevier Inc.
C1 [Gustchina, Elena; Louis, John M.; Clore, G. Marius] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Frisch, Christian; Ylera, Francisco; Lechner, Annette] MorphoSys, AbD Serotec, D-82152 Martinsried, Germany.
[Bewley, Carole A.] NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
RP Clore, GM (reprint author), NIDDKD, Chem Phys Lab, NIH, Bldg 2, 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 National Institute of Diabetes and Digestive and Kidney Diseases; NIH;
AIDS Targeted Antiviral Program of the Office of the Director of the
National Institutes of Health
FX We thank Annie Aniana for technical assistance. This work was supported
by the Intramural program of the National Institute of Diabetes and
Digestive and Kidney Diseases, NIH, and by the AIDS Targeted Antiviral
Program of the Office of the Director of the National Institutes of
Health (to G.M.C. and C.A.B.).
NR 57
TC 13
Z9 13
U1 1
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD OCT 10
PY 2009
VL 393
IS 1
BP 112
EP 119
DI 10.1016/j.virol.2009.07.019
PG 8
WC Virology
SC Virology
GA 502JA
UT WOS:000270453600014
PM 19695655
ER
PT J
AU Parrish, S
Hurchalla, M
Liu, SW
Moss, B
AF Parrish, Susan
Hurchalla, Megan
Liu, Shin-Wu
Moss, Bernard
TI The African swine fever virus g5R protein possesses mRNA decapping
activity
SO VIROLOGY
LA English
DT Article
DE mRNA decapping; Nudix enzyme; African swine fever virus; g5R protein
ID GENE-EXPRESSION; VERO CELLS; INDUCED POLYPEPTIDES; NUDIX HYDROLASES; D10
PROTEIN; HUMAN DCP2; ENZYME; IDENTIFICATION; TRANSCRIPTION; SEQUENCE
AB The African Swine Fever Virus (ASFV) encodes a single NUdix enzyme in its genome, termed the g5R protein (g5Rp). Nudix phosphohydrolases cleave a variety of substrates, Such as nucleotides and diphosphoinositol polyphosphates. Previously, ASFV g5Rp was shown to hydrolyze diphosphoinositol polyphosphates and GTP, but was unable to cleave methylated mRNA cap analogues. In vaccinia virus (VACV), a distant relative of ASFV, the D9 and D10 Nudix enzymes were shown to cleave the mRNA cap, but only when the cap was attached to an RNA body. Here, we show that recombinant ASFV g5Rp hydrolyzes the mRNA cap when tethered to an RNA moiety, liberating m(7)GDP as a product. Mutations in the Nudix motif abolished mRNA decapping activity, confirming that g5Rp was responsible for cap cleavage. The decapping activity of g5Rp was potently inhibited by excess uncapped RNA but not by methylated cap analogues, suggesting that Substrate recognition occurs by RNA binding. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Parrish, Susan; Hurchalla, Megan] McDaniel Coll, Westminster, MD 21157 USA.
[Liu, Shin-Wu; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Parrish, S (reprint author), McDaniel Coll, 2 Coll Hill,Eaton Hall,Room 212, Westminster, MD 21157 USA.
EM sparrish@mcdaniel.edu
FU National Institute of Allergy and Infectious Diseases/National
Institutes of Health; McDaniel College Faculty Development Grant
FX We thank Wolfgang Resch, George Katsafanas, and Teri Shors for helpful
discussions. This research was supported by the Intramural Research
Program of the National Institute of Allergy and Infectious
Diseases/National Institutes of Health and a McDaniel College Faculty
Development Grant.
NR 31
TC 9
Z9 10
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD OCT 10
PY 2009
VL 393
IS 1
BP 177
EP 182
DI 10.1016/j.virol.2009.07.026
PG 6
WC Virology
SC Virology
GA 502JA
UT WOS:000270453600022
PM 19695654
ER
PT J
AU Muniandy, PA
Thapa, D
Thazhathveetil, AK
Liu, ST
Seidman, MM
AF Muniandy, Parameswary A.
Thapa, Dennis
Thazhathveetil, Arun Kalliat
Liu, Su-ting
Seidman, Michael M.
TI Repair of Laser-localized DNA Interstrand Cross-links in G(1) Phase
Mammalian Cells
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NUCLEOTIDE EXCISION-REPAIR; DOUBLE-STRAND BREAKS; UV-DAMAGED DNA;
CYCLOBUTANE PYRIMIDINE DIMERS; COMPLEMENTATION GROUP-E; PIGMENTOSUM
GROUP-E; IN-VIVO; ESCHERICHIA-COLI; BINDING PROTEIN; MITOMYCIN-C
AB Interstrand cross-links (ICLs) are absolute blocks to transcription and replication and can provoke genomic instability and cell death. Studies in bacteria define a two-stage repair scheme, the first involving recognition and incision on either side of the cross-link on one strand (unhooking), followed by recombinational repair or lesion bypass synthesis. The resultant monoadduct is removed in a second stage by nucleotide excision repair. In mammalian cells, there are multiple, but poorly defined, pathways, with much current attention on repair in S phase. However, many questions remain, including the efficiency of repair in the absence of replication, the factors involved in cross-link recognition, and the timing and demarcation of the first and second repair cycles. We have followed the repair of laser-localized lesions formed by psoralen (cross-links/monoadducts) and angelicin (only monoadducts) in mammalian cells. Both were repaired in G, phase by nucleotide excision repair-dependent pathways. Removal of psoralen adducts was blocked in XPC-deficient cells but occurred with wild type kinetics in cells deficient in DDB2 protein (XPE). XPC protein was rapidly recruited to psoralen adducts. However, accumulation of DDB2 was slow and XPC-dependent. Inhibition of repair DNA synthesis did not interfere with DDB2 recruitment to angelicin but eliminated recruitment to psoralen. Our results demonstrate an efficient ICL repair pathway in G, phase cells dependent on XPC, with entry of DDB2 only after repair synthesis that completes the first repair cycle. DDB2 accumulation at sites of cross-link repair is a marker for the start of the second repair cycle.
C1 [Muniandy, Parameswary A.; Thapa, Dennis; Seidman, Michael M.] NIA, LMG, NIH, Baltimore, MD 21224 USA.
[Thazhathveetil, Arun Kalliat] Northwestern Univ, Dept Chem, Evanston, IL 60208 USA.
[Liu, Su-ting] BASF Co, Hong Kong, Hong Kong, Peoples R China.
RP Seidman, MM (reprint author), NIA, LMG, NIH, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM seidmanm@grc.nia.nih.gov
FU National Institutes of Health, NIA; Fanconi Anemia Research Fund
FX This work was supported, in whole or in part, by the National Institutes
of Health, NIA, Intramural Research Program. This work was also
supported by the Fanconi Anemia Research Fund.
NR 88
TC 53
Z9 53
U1 2
U2 9
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 9
PY 2009
VL 284
IS 41
BP 27908
EP 27917
DI 10.1074/jbc.M109.029025
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 505FP
UT WOS:000270676300018
PM 19684342
ER
PT J
AU Navarro, G
Aymerich, MS
Marcellino, D
Cortes, A
Casado, V
Mallol, J
Canela, EI
Agnati, L
Woods, AS
Fuxe, K
Lluis, C
Lanciego, JL
Ferre, S
Franco, R
AF Navarro, Gemma
Aymerich, Marisol S.
Marcellino, Daniel
Cortes, Antoni
Casado, Vicent
Mallol, Josefa
Canela, Enric I.
Agnati, Luigi
Woods, Amina S.
Fuxe, Kjell
Lluis, Carmen
Luis Lanciego, Jose
Ferre, Sergi
Franco, Rafael
TI Interactions between Calmodulin, Adenosine A(2A), and Dopamine D-2
Receptors
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PROTEIN-COUPLED RECEPTORS; ENERGY-TRANSFER BRET; ELECTROSTATIC
INTERACTION; HETEROMERIZATION; ACTIVATION; BINDING; LOOP;
OLIGOMERIZATION; PHARMACOLOGY; RECOGNITION
AB The Ca2+-binding protein calmodulin (CaM) has been shown to bind directly to cytoplasmic domains of some G protein-coupled receptors, including the dopamine D-2 receptor. CaM binds to the N-terminal portion of the long third intracellular loop of the D-2 receptor, within an Arg-rich epitope that is also involved in the binding to G(i/o) proteins and to the adenosine A(2A) receptor, with the formation of A(2A)-D-2 receptor heteromers. In the present work, by using proteomics and bioluminescence resonance energy transfer (BRET) techniques, we provide evidence for the binding of CaM to the A(2A) receptor. By using BRET and sequential resonance energy transfer techniques, evidence was obtained for CaM-A(2A)-D-2 receptor oligomerization. BRET competition experiments indicated that, in the A(2A)-D-2 receptor heteromer, CaM binds preferentially to a proximal C terminus epitope of the A(2A) receptor. Furthermore, Ca2+ was found to induce conformational changes in the CaM-A(2A)-D-2 receptor oligomer and to selectively modulate A(2A) and D-2 receptor-mediated MAPK signaling in the A(2A)-D-2 receptor heteromer. These results may have implications for basal ganglia disorders, since A(2A)-D-2 receptor heteromers are being considered as a target for anti-parkinsonian agents.
C1 [Aymerich, Marisol S.; Luis Lanciego, Jose; Franco, Rafael] Univ Navarra, CIMA Neurociencias, Pamplona 31008, Spain.
[Navarro, Gemma; Cortes, Antoni; Casado, Vicent; Mallol, Josefa; Canela, Enric I.; Lluis, Carmen; Franco, Rafael] Univ Barcelona, Fac Biol, Dept Biochem & Mol Biol, E-08028 Barcelona, Spain.
[Navarro, Gemma; Cortes, Antoni; Casado, Vicent; Mallol, Josefa; Canela, Enric I.; Lluis, Carmen; Franco, Rafael] Univ Barcelona, Fac Biol, Ctr Invest Biomed Red Enfermedades Neurodegenerat, Inst Invest Biomed August Pi & Sunyer, E-08028 Barcelona, Spain.
[Marcellino, Daniel; Agnati, Luigi; Fuxe, Kjell] Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden.
[Woods, Amina S.; Ferre, Sergi] Natl Inst Drug Abuse, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Franco, R (reprint author), Univ Navarra, CIMA Neurociencias, Avda Pio XII 55, Pamplona 31008, Spain.
EM rfranco@unav.es
RI Canela, Enric I./M-8726-2013; Ferre, Sergi/K-6115-2014; Franco,
Rafael/C-3694-2015; Casado, Vicent/K-1660-2014;
OI Canela, Enric I./0000-0003-4992-7440; Ferre, Sergi/0000-0002-1747-1779;
Franco, Rafael/0000-0003-2549-4919; Marcellino,
Daniel/0000-0002-4618-7267; Casado, Vicent/0000-0002-1764-3825;
Lanciego, Jose/0000-0003-2301-5419
FU National Institutes of Health; NIDA; Spanish Ministry of Education and
Science [SAF2008-00146, SAF2006-05481]; Fundacio La Marato de [060110]
FX This work was supported, in whole or in part, by the National Institutes
of Health, NIDA, Intramural Research Program (to S. F. and A. S. W.).
This work was also supported by Spanish Ministry of Education and
Science Grants SAF2008-00146 (to E. I. C) and SAF2006-05481 (to R. F.)
and Fundacio La Marato de TV3 Grant 060110 (to E. I. Q. The Proteomics
Laboratory at CIMA belongs to the network of the Spanish National
Institute of Proteomics Facilities, ProteoRed.
NR 37
TC 37
Z9 39
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 9
PY 2009
VL 284
IS 41
BP 28058
EP 28068
DI 10.1074/jbc.M109.034231
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 505FP
UT WOS:000270676300033
PM 19632986
ER
PT J
AU Campa, F
Yoon, HY
Ha, VL
Szentpetery, Z
Balla, T
Randazzo, PA
AF Campa, Fanny
Yoon, Hye-Young
Ha, Vi Luan
Szentpetery, Zsofia
Balla, Tamas
Randazzo, Paul A.
TI A PH Domain in the Arf GTPase-activating Protein (GAP) ARAP1 Binds
Phosphatidylinositiol 3,4,5-Trisphosphate and Regulates Arf GAP Activity
Independently of Recruitment to the Plasma Membranes
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ADP-RIBOSYLATION FACTOR; PLECKSTRIN HOMOLOGY DOMAINS;
INOSITOL-LIPID-BINDING; ACTIN CYTOSKELETON; MYRISTOYLATED ARF1;
STRUCTURAL BASIS; ASAP1; ADAPTER; COMPLEX; FAMILY
AB ARAP1 is a phosphatidylinositol 3,4,5-trisphosphate (PtdIns-(3,4,5)P(3))-dependent Arf GTPase-activating protein (GAP) with five PH domains that regulates endocytic trafficking of the epidermal growth factor receptor (EGFR). Two tandem PH domains are immediately N-terminal of the Arf GAP domain, and one of these fits the consensus sequence for PtdIns(3,4,5)P(3) binding. Here, we tested the hypothesis that PtdIns(3,4,5)P(3)-dependent recruitment mediated by the first PH domain of ARAP1 regulates the in vivo and in vitro function of ARAP1. We found that PHI of ARAP1 specifically bound to PtdIns(3,4,5)P(3), but with relatively low affinity (approximate to 1.6 mu M), and the PH domains did not mediate PtdIns(3,4,5)P(3)-dependent recruitment to membranes in cells. However, PtdIns(3,4,5)P(3) binding to the PH domain stimulated GAP activity and was required for in vivo function of ARAP1 as a regulator of endocytic trafficking of the EGFR. Based on these results, we propose a variation on the model for the function of phosphoinositide-binding PH domains. In our model, ARAP1 is recruited to membranes independently of PtdIns(3,4,5)P(3), the subsequent production of which triggers enzymatic activity.
C1 [Campa, Fanny; Yoon, Hye-Young; Ha, Vi Luan; Randazzo, Paul A.] NCI, Lab Cellular & Mol Biol, NIH, Bethesda, MD 20892 USA.
[Szentpetery, Zsofia; Balla, Tamas] NICHD, Program Dev Neurosci, NIH, Bethesda, MD 20892 USA.
RP Randazzo, PA (reprint author), NCI, Lab Cellular & Mol Biol, NIH, Bldg 37,Rm 2042, Bethesda, MD 20892 USA.
EM randazzo@helix.nih.gov
FU National Institutes of Health; NICHID
FX This work was supported, in whole or in part, by National Institutes of
Health grants from the NCI Intramural Program and NICHID.
NR 60
TC 14
Z9 14
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 9
PY 2009
VL 284
IS 41
BP 28069
EP 28083
DI 10.1074/jbc.M109.028266
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 505FP
UT WOS:000270676300034
PM 19666464
ER
PT J
AU Liu, Y
Prasad, R
Beard, WA
Hou, EW
Horton, JK
McMurray, CT
Wilson, SH
AF Liu, Yuan
Prasad, Rajendra
Beard, William A.
Hou, Esther W.
Horton, Julie K.
McMurray, Cynthia T.
Wilson, Samuel H.
TI Coordination between Polymerase beta and FEN1 Can Modulate CAG Repeat
Expansion
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BASE-EXCISION-REPAIR; HUMAN FLAP ENDONUCLEASE-1; DNA SECONDARY
STRUCTURE; TRANSGENIC MOUSE MODEL; PROTEIN CROSS-LINKS; HUMAN-DISEASE;
TRINUCLEOTIDE REPEATS; MYOTONIC-DYSTROPHY; TRIPLET REPEATS; IN-VITRO
AB The oxidized DNA base 8-oxoguanine (8-oxoG) is implicated in neuronal CAG repeat expansion associated with Huntington disease, yet it is unclear how such a DNA base lesion and its repair might cause the expansion. Here, we discovered size-limited expansion of CAG repeats during repair of 8-oxoG in a wildtype mouse cell extract. This expansion was deficient in extracts from cells lacking pol beta and HMGB1. We demonstrate that expansion is mediated through pol beta multinucleotide gap-filling DNA synthesis during long-patch base excision repair. Unexpectedly, FEN1 promotes expansion by facilitating ligation of hairpins formed by strand slippage. This alternate role of FEN1 and the polymerase beta (pol beta) multinucleotide gap-filling synthesis is the result of uncoupling of the usual coordination between pol beta and FEN1. HMGB1 probably promotes expansion by stimulating APEI and FEN1 in forming single strand breaks and ligatable nicks, respectively. This is the first report illustrating that disruption of pol beta and FEN1 coordination during long-patch BER results in CAG repeat expansion.
C1 [Liu, Yuan; Prasad, Rajendra; Beard, William A.; Hou, Esther W.; Horton, Julie K.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[McMurray, Cynthia T.] Mayo Clin & Mayo Fdn, Dept Pharmacol & Expt Therapeut, Rochester, MN 55905 USA.
RP Wilson, SH (reprint author), 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
FU NIEHS Intramural Research Program [Z01-ES050158, Z01-ES050159];
[GM066359]; [CA092584]
FX This work was supported, in whole or in part, by National Institutes of
Health Research Projects Z01-ES050158 and Z01-ES050159 from the NIEHS
Intramural Research Program and Grants GM066359 and CA092584 (to C. T.
M.).
NR 68
TC 59
Z9 60
U1 0
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 9
PY 2009
VL 284
IS 41
BP 28352
EP 28366
DI 10.1074/jbc.M109.050286
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 505FP
UT WOS:000270676300061
PM 19674974
ER
PT J
AU Juan, AH
Kumar, RM
Marx, JG
Young, RA
Sartorelli, V
AF Juan, Aster H.
Kumar, Roshan M.
Marx, Joseph G.
Young, Richard A.
Sartorelli, Vittorio
TI Mir-214-Dependent Regulation of the Polycomb Protein Ezh2 in Skeletal
Muscle and Embryonic Stem Cells
SO MOLECULAR CELL
LA English
DT Article
ID HISTONE H3 METHYLATION; GENE-EXPRESSION; NONCODING RNA; ES CELLS;
DEVELOPMENTAL REGULATORS; MOUSE DEVELOPMENT; NETWORK MOTIFS; RETINOIC
ACID; SELF-RENEWAL; IN-VITRO
AB Polycomb group (PcG) proteins exert essential functions in the most disparate biological processes. The contribution of PcG proteins to cell commitment and differentiation relates to their ability to repress transcription of developmental regulators in embryonic stem (ES) cells and in committed cell lineages, including skeletal muscle cells (SMC). PcG proteins are preferentially removed from transcribed regions, but the underlying mechanisms remain unclear. Here, PcG proteins are found to occupy and repress transcription from an intronic region containing the microRNA miR-214 in undifferentiated SMC. Differentiation coincides with PcG disengagement, recruitment of the developmental regulators MyoD and myogenin, and activation of miR-214 transcription. Once transcribed, miR-214 negatively feeds back on PcG by targeting the Ezh2 3'UTR the catalytic subunit of the PRC2 complex. miR-214-mediated Ezh2 protein reduction accelerates SMC differentiation and promotes unscheduled transcription of developmental regulators in ES cells. Thus, miR-214 and Ezh2 establish a regulatory loop controlling PcG-dependent gene expression during differentiation.
C1 [Juan, Aster H.; Marx, Joseph G.; Sartorelli, Vittorio] NIAMSD, Lab Muscle Stem Cells & Gene Regulat, NIH, Bethesda, MD 20892 USA.
[Kumar, Roshan M.; Young, Richard A.] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA.
[Young, Richard A.] MIT, Dept Biol, Cambridge, MA 02139 USA.
RP Sartorelli, V (reprint author), NIAMSD, Lab Muscle Stem Cells & Gene Regulat, NIH, 50 S Dr, Bethesda, MD 20892 USA.
EM sartorev@mail.nih.gov
RI Young, Richard/F-6495-2012
OI Young, Richard/0000-0001-8855-8647
FU National Institute of Arthritis, Musculoskeletal, and Skin Diseases of
the National Institutes of Health
FX We would like to thank I.-h. Su and A. Taralkhovsky for providing the
Ezh2floxed mice; Kambiz Mousavi for assistance with myofiber isolation
and culture; and Rafael Casellas for sharing lentiviral constructs. This
work was supported, in part, by the Intramural Research Program of the
National Institute of Arthritis, Musculoskeletal, and Skin Diseases of
the National Institutes of Health.
NR 59
TC 182
Z9 192
U1 0
U2 18
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD OCT 9
PY 2009
VL 36
IS 1
BP 61
EP 74
DI 10.1016/j.molcel.2009.08.008
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 510AN
UT WOS:000271060500007
PM 19818710
ER
PT J
AU Sha, Z
Brill, LM
Cabrera, R
Kleifeld, O
Scheliga, JS
Glickman, MH
Chang, EC
Wolf, DA
AF Sha, Zhe
Brill, Laurence M.
Cabrera, Rodrigo
Kleifeld, Oded
Scheliga, Judith S.
Glickman, Michael H.
Chang, Eric C.
Wolf, Dieter A.
TI The elF3 Interactome Reveals the Translasome, a Supercomplex Linking
Protein Synthesis and Degradation Machineries
SO MOLECULAR CELL
LA English
DT Article
ID INITIATION-FACTOR 3; YEAST SCHIZOSACCHAROMYCES-POMBE; GLOBAL TRANSLATION
INITIATION; PROPER SPINDLE FORMATION; AFFECTS SPORE FORMATION;
MAMMARY-TUMOR VIRUS; FISSION YEAST; NUCLEAR IMPORT;
SACCHAROMYCES-CEREVISIAE; 26S PROTEASOME
AB elF3 promotes translation initiation, but relatively little is known about its full range of activities in the cell. Here, we employed affinity purification and highly sensitive LC-MS/MS to decipher the fission yeast elF3 interactome, which was found to contain 230 proteins. elF3 assembles into a large supercomplex, the translasome, which contains elongation factors, tRNA synthetases, 40S and 60S ribosomal proteins, chaperones, and the proteasome. elF3 also associates with ribosome biogenesis factors and the importins-beta Kap123p and Sal3p. Our genetic data indicated that the binding to both importins-beta is essential for cell growth, and photobleaching experiments revealed a critical role for Sal3p in the nuclear import of one of the translasome constituents, the proteasome. Our data reveal the breadth of the elF3 interactome and suggest that factors involved in translation initiation, ribosome biogenesis, translation elongation, quality control, and transport are physically linked to facilitate efficient protein synthesis.
C1 [Sha, Zhe; Cabrera, Rodrigo; Chang, Eric C.] Baylor Coll Med, Dept Mol & Cellular Biol, Lester & Sue Smith Breast Ctr, Houston, TX 77030 USA.
[Brill, Laurence M.; Scheliga, Judith S.; Wolf, Dieter A.] NCI, Burnham Inst Med Res, Signal Transduct Program, Canc Ctr Prote Facil, La Jolla, CA 92037 USA.
[Kleifeld, Oded; Glickman, Michael H.] Technion Israel Inst Technol, Dept Biol, IL-32000 Haifa, Israel.
RP Chang, EC (reprint author), Baylor Coll Med, Dept Mol & Cellular Biol, Lester & Sue Smith Breast Ctr, Houston, TX 77030 USA.
EM echang1@bcm.edu; dwolf@burnham.org
RI Kleifeld, Oded/G-7304-2012
FU NSF [0920229]; NIH [GM059780, CA90464, CA107187, 5 P30 CA30199-28, 5
P30NS057096]; DOD [BC030443]
FX We thank D. Balasunclararn (Singapore University) for providing
materials, M. Petroski for reviewing the manuscript, and K.
Motamedchaboki and A. Iranli for bioinformatics support. We also thank
Mike Mancini and his staff at the Integrated Microscopy Core at the Dan
Duncan Cancer Center for technical assistance. This work was funded by
NSF grant 0920229 and NIH grant GM059780 to D.A.W. and by NIH grants
CA90464 and CA107187 to E.C.C.; Z.S. was supported by a predoctoral
fellowship from the DOD (BC030443). L.M.B. is funded through the NIH
Center Grants 5 P30 CA30199-28 and 5 P30NS057096. We also thank Glen and
Judy Smith for their generous support.
NR 76
TC 60
Z9 61
U1 2
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD OCT 9
PY 2009
VL 36
IS 1
BP 141
EP 152
DI 10.1016/j.molcel.2009.09.026
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 510AN
UT WOS:000271060500014
PM 19818717
ER
PT J
AU Zhu, DM
Saul, A
Huang, SH
Martin, LB
Miller, LH
Rausch, KM
AF Zhu, Daming
Saul, Allan
Huang, Shuhui
Martin, Laura B.
Miller, Louis H.
Rausch, Kelly M.
TI Use of o-phthalaldehyde assay to determine protein contents of
Alhydrogel-based vaccines
SO VACCINE
LA English
DT Article
DE OPA; o-Phthalaidehyde; Aluminum hydroxide; Alum; Vaccine; Protein assay
ID AMINO-ACIDS; ADJUVANTS
AB Aluminum based adjuvants (alum), including aluminum hydroxide (Alhydrogel (R)) and aluminum phosphate are the most commonly used adjuvant in the US. In order to ensure quality of vaccines, regulatory authorities require evaluation of antigen content in final vaccine products. Currently, there are no generic methods available for the determination of protein content in alum-based vaccines. Aluminum hydroxide gets exist as particles in solution, which interfere with direct quantitation of protein content in formulations using assays such as Lowry, BCA or Bradford protein assay. The present study adapts a simple fluorescent assay to directly (without the need for antigen extraction) determine antigen content on Alhydrogel (R) with accuracy and sensitivity using the o-phthalaldehyde (CPA) reagent. Malaria vaccine candidates AMA1-C1/Alhydrogel, AMA1-C2/Alhydrogel, MSP1(42)-3D7/Alhydrogel, MSP1(42)-Cl/Alhydrogel or BSAM-2/Alhydrogel were used as model formulations. The results of the present study show that the OPA assay is highly accurate (87-100%), reproducible, and simple with a linear detection range of 25-400 mu g/mL for Athydrogel (R) vaccines (except for MSP1(42)-C1, which has a linear detection range of 31.25-500 mu g/mL). This assay has proven to be highly useful in our laboratory and been used in routine vaccine quality control processes. Published by Elsevier Ltd.
C1 [Zhu, Daming; Saul, Allan; Huang, Shuhui; Martin, Laura B.; Miller, Louis H.; Rausch, Kelly M.] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD 20852 USA.
RP Zhu, DM (reprint author), NIAID, Malaria Vaccine Dev Branch, NIH, 5640 Fishers Lane, Rockville, MD 20852 USA.
EM dzhu@niaid.nih.gov
RI Saul, Allan/I-6968-2013; Martin, Laura/N-1789-2013
OI Saul, Allan/0000-0003-0665-4091; Martin, Laura/0000-0002-4431-4381
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases; National Institutes of Health
FX We thank David Narum and Richard Shimp,jr. for providing antigens. This
work was supported in part by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 23
TC 13
Z9 14
U1 1
U2 6
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD OCT 9
PY 2009
VL 27
IS 43
BP 6054
EP 6059
DI 10.1016/j.vaccine.2009.07.067
PG 6
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 511MW
UT WOS:000271170500020
PM 19660590
ER
PT J
AU Gandhi, RT
O'Neill, D
Bosch, RJ
Chan, ES
Bucy, RP
Shopis, J
Baglyos, L
Adams, E
Fox, L
Purdue, L
Marshak, A
Flynn, T
Masih, R
Schock, B
Mildvan, D
Schlesinger, SJ
Marovich, MA
Bhardwaj, N
Jacobson, JM
AF Gandhi, Rajesh T.
O'Neill, David
Bosch, Ronald J.
Chan, Ellen S.
Bucy, R. Pat
Shopis, Janet
Baglyos, Lynn
Adams, Elizabeth
Fox, Lawrence
Purdue, Lynette
Marshak, Ann
Flynn, Theresa
Masih, Reena
Schock, Barbara
Mildvan, Donna
Schlesinger, Sarah J.
Marovich, Mary A.
Bhardwaj, Nina
Jacobson, Jeffrey M.
CA AIDS Clinical Trials Grp A5130 Tea
TI A randomized therapeutic vaccine trial of canarypox-HIV-pulsed dendritic
cells vs. canarypox-HIV alone in HIV-1-infected patients on
antiretroviral therapy
SO VACCINE
LA English
DT Article
DE HIV-1; Dendritic cells; Canarypox; Therapeutic vaccine; Clinical trial
ID CD8(+) T-CELL; VIRUS TYPE-1 HIV-1; LYMPHOCYTE RESPONSES; RECOMBINANT
GP160; IMMUNIZATION; INFECTION; CD4(+); VCP1452; PROTEIN; IMMUNOGENICITY
AB Targeting canarypox (CP)-HIV vaccine to dendritic cells (DCs) elicits anti-HIV-1 immune responses in vitro. We conducted a phase I/II clinical trial to evaluate whether adding DC to a CP-HIV vaccine improved virologic control during analytic treatment interruption (ATI) in HIV-1-infected subjects. Twenty-nine subjects on suppressive antiretroviral therapy were randomized to vaccination with autologous DCs infected with CP-HIV + keyhole limpet hemocyanin (KLH) (arm A, n = 14) or CP-HIV + KLH alone (arm B, n = 15). The mean viral load (VL) setpoint during ATI did not differ between subjects in arms A and B. A higher percentage of subjects in the DC group had a VL setpoint <5000 c/mL during ATI (4/13 or 31% in arm A compared with 0/13 in arm B, p = 0.096), but virologic control was transient. Subjects in arm A had a greater increase in KLH lymphoproliferative response than subjects in arm B; however. summed ELISPOT responses to HIV-1 antigens did not differ by treatment arm. We conclude that a DC-CP-HIV vaccine is well-tolerated in HIV-1-infected patients, but does not lower VL setpoint during ATI compared with CP-HIV alone. New methods to enhance the immunogenicity and antiviral efficacy of DC-based vaccines for HIV-1 infection are needed. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Gandhi, Rajesh T.; Shopis, Janet; Flynn, Theresa] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[O'Neill, David; Bhardwaj, Nina] NYU, Sch Med, New York, NY 10003 USA.
[Bosch, Ronald J.; Chan, Ellen S.] Harvard Univ, Sch Publ Hlth, Cambridge, MA 02138 USA.
[Bucy, R. Pat] Univ Alabama, Birmingham, AL USA.
[Adams, Elizabeth; Fox, Lawrence; Purdue, Lynette; Masih, Reena] NIH, Bethesda, MD 20892 USA.
[Marshak, Ann; Mildvan, Donna] Beth Israel Deaconess Med Ctr, New York, NY 10003 USA.
[Schlesinger, Sarah J.] Rockefeller Univ, New York, NY USA.
[Marovich, Mary A.] Walter Reed Army Inst, Silver Spring, MD 20910 USA.
[Jacobson, Jeffrey M.] Drexel Univ, Coll Med, Philadelphia, PA USA.
RP Gandhi, RT (reprint author), Massachusetts Gen Hosp, 55 Fruit St,GRJ 504, Boston, MA 02114 USA.
EM rgandhi@partners.org
FU NIAID NIH HHS [AI38855, AI38858, AI68634, AI68636, R01 AI066992, R01
AI066992-04, R37 AI044628, R37 AI044628-08, U01 AI038855, U01 AI038858,
U01 AI068634, U01 AI068634-01, U01 AI068636, U01 AI068636-01, U01
AI069472, U01 AI069472-01, UM1 AI068634, UM1 AI068636]; PHS HHS
[A146370, AIO69472]
NR 34
TC 48
Z9 52
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD OCT 9
PY 2009
VL 27
IS 43
BP 6088
EP 6094
DI 10.1016/j.vaccine.2009.05.016
PG 7
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 511MW
UT WOS:000271170500023
PM 19450647
ER
PT J
AU Castle, PE
Scarinci, I
AF Castle, Philip E.
Scarinci, Isabel
TI Should HPV vaccine be given to men?
SO BRITISH MEDICAL JOURNAL
LA English
DT Editorial Material
ID PREVENT CERVICAL-CANCER; AGED 13-17 YEARS; HUMAN-PAPILLOMAVIRUS;
UNITED-STATES; COVERAGE; MODEL
C1 [Castle, Philip E.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Scarinci, Isabel] Univ Alabama, Div Prevent Med, Birmingham, AL 35205 USA.
RP Castle, PE (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM castlep@mail.nih.gov
NR 12
TC 12
Z9 12
U1 0
U2 0
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0959-8146
J9 BRIT MED J
JI Br. Med. J.
PD OCT 8
PY 2009
VL 339
AR b4127
DI 10.1136/bmj.b4127
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 505TH
UT WOS:000270719300006
PM 19815585
ER
PT J
AU Lee, H
de Vries, AH
Marrink, SJ
Pastor, RW
AF Lee, Hwankyu
de Vries, Alex H.
Marrink, Siewert-Jan
Pastor, Richard W.
TI A Coarse-Grained Model for Polyethylene Oxide and Polyethylene Glycol:
Conformation and Hydrodynamics
SO JOURNAL OF PHYSICAL CHEMISTRY B
LA English
DT Article
ID MOLECULAR-DYNAMICS SIMULATIONS; ATTACHED POLY(ETHYLENE GLYCOL); PARTICLE
MESH EWALD; PHASE-BEHAVIOR; POLYAMIDOAMINE DENDRIMERS;
NEUTRON-SCATTERING; AQUEOUS-SOLUTIONS; SHAPE ANISOTROPY; ACTION
MECHANISM; SIZE DEPENDENCE
AB A coarse-grained (CG) model for polyethylene oxide (PEO) and polyethylene glycol (PEG) developed within the framework of the MARTINI CG force field (FF) using the distributions of bonds, angles, and dihedrals from the CHARMM all-atom FF is presented. Densities of neat low molecular weight PEO agree with experiment, and the radius of gyration R-g = 19.1 angstrom +/- 0.7 for 76-mers of PEO (M-w approximate to 3400), in excellent agreement with neutron scattering results for an equal sized PEG. Simulations of 9, 18, 27, 36, 44, 67, 76, 90, 112, 135, and 158-mers of the CG PEO (442 < M-w < 6998) at low concentration in water show the experimentally observed transition from ideal chain to real chain behavior at 1600 < M-w < 2000, in excellent agreement with the dependence of experimentally observed hydrodynamic radii of PEG. Hydrodynamic radii of PEO calculated from diffusion coefficients of the higher M-w PEO also agree well with experiment. R-g calculated from both all-atom and CG simulations of PEO76 at 21 and 148 mg/cm(3) are found to be nearly equal. This lack of concentration dependence implies that apparent R-g from scattering experiments at high concentration should not be taken to be the chain dimension. Simulations of PEO grafted to a nonadsorbing surface yield a mushroom to brush transition that is well described by the Alexander-de Gennes formalism.
C1 [Lee, Hwankyu; Pastor, Richard W.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
[de Vries, Alex H.; Marrink, Siewert-Jan] Univ Groningen, Groningen Biomol Sci & Biotechnol Inst, NL-9747 AG Groningen, Netherlands.
[de Vries, Alex H.; Marrink, Siewert-Jan] Univ Groningen, Zernike Inst Adv Mat, NL-9747 AG Groningen, Netherlands.
RP Pastor, RW (reprint author), NHLBI, Lab Computat Biol, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM pastorr@nhlbi.nih.gov
RI Marrink, Siewert /G-3706-2014
FU Intramural Research Program of the NIH; National Heart, Lung and Blood
Institute
FX We thank Richard Venable, Edward O'Brien, Monica Pate, and P.
Thiyagarajan for helpful discussions. This research was supported by the
Intramural Research Program of the NIH, National Heart, Lung and Blood
Institute. This study utilized the high-performance computational
capabilities of the CIT Biowulf/LoBoS3 and NHLBI LOBOS clusters at the
National Institutes of Health, Bethesda, MD.
NR 72
TC 162
Z9 163
U1 6
U2 113
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1520-6106
J9 J PHYS CHEM B
JI J. Phys. Chem. B
PD OCT 8
PY 2009
VL 113
IS 40
BP 13186
EP 13194
DI 10.1021/jp9058966
PG 9
WC Chemistry, Physical
SC Chemistry
GA 501EX
UT WOS:000270363500009
PM 19754083
ER
PT J
AU Lee, H
Larson, RG
AF Lee, Hwankyu
Larson, Ronald G.
TI Molecular Dynamics Study of the Structure and Interparticle Interactions
of Polyethylene Glycol-Conjugated PAMAM Dendrimers
SO JOURNAL OF PHYSICAL CHEMISTRY B
LA English
DT Article
ID SUPPORTED LIPID-BILAYERS; NONVIRAL GENE DELIVERY; COARSE-GRAINED MODEL;
POLY(AMIDOAMINE) DENDRIMERS; POLYAMIDOAMINE DENDRIMERS; LINEAR
POLYELECTROLYTES; POLY(ETHYLENE GLYCOL); PORE FORMATION; POLYCATIONIC
POLYMERS; SIZE DEPENDENCE
AB We performed molecular dynamics (MD) simulations of one or two copies of polyethylene glycol of molecular weight 550 (PEG550) and 5000 (PEG5000) daltons, conjugated to generation 3 (G3) to 5 (G5) polyamidoamine (PAMAM) dendrimers with explicit water using a coarse-grained model. We found the radii of gyration of these dendrimer-PEG molecules to be close to those measured in experiments by Hedden and Bauer (Hedden, R. C.; Bauer, B. J. Macromolecules 2003, 36, 1829.), Densely grafted PEG ligands (>50% of the dendrimer Surface) extend like brushes, with layer thickness in agreement with theory for starlike polymers. Two dendrimer-PEG complexes in the box drift away from each other, indicating that no aggregation is induced by either short or long PEG chains. conflicting with a recent view that the cytotoxicity of some PEGylated particles might be due to particle aggregation for long PEG lengths.
C1 [Lee, Hwankyu] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
[Larson, Ronald G.] Univ Michigan, Dept Chem Engn, Biomed Engn Mech Engn & Macromol Sci & Engn Progr, Ann Arbor, MI 48109 USA.
RP Lee, H (reprint author), NHLBI, Lab Computat Biol, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM leeh3@nhlbi.nih.gov
FU Intramural NIH HHS [NIH0013263008]; PHS HHS [NIH0013263008]
NR 60
TC 38
Z9 38
U1 3
U2 36
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1520-6106
J9 J PHYS CHEM B
JI J. Phys. Chem. B
PD OCT 8
PY 2009
VL 113
IS 40
BP 13202
EP 13207
DI 10.1021/jp906497e
PG 6
WC Chemistry, Physical
SC Chemistry
GA 501EX
UT WOS:000270363500011
PM 19754139
ER
PT J
AU Manolio, TA
Collins, FS
Cox, NJ
Goldstein, DB
Hindorff, LA
Hunter, DJ
McCarthy, MI
Ramos, EM
Cardon, LR
Chakravarti, A
Cho, JH
Guttmacher, AE
Kong, A
Kruglyak, L
Mardis, E
Rotimi, CN
Slatkin, M
Valle, D
Whittemore, AS
Boehnke, M
Clark, AG
Eichler, EE
Gibson, G
Haines, JL
Mackay, TFC
McCarroll, SA
Visscher, PM
AF Manolio, Teri A.
Collins, Francis S.
Cox, Nancy J.
Goldstein, David B.
Hindorff, Lucia A.
Hunter, David J.
McCarthy, Mark I.
Ramos, Erin M.
Cardon, Lon R.
Chakravarti, Aravinda
Cho, Judy H.
Guttmacher, Alan E.
Kong, Augustine
Kruglyak, Leonid
Mardis, Elaine
Rotimi, Charles N.
Slatkin, Montgomery
Valle, David
Whittemore, Alice S.
Boehnke, Michael
Clark, Andrew G.
Eichler, Evan E.
Gibson, Greg
Haines, Jonathan L.
Mackay, Trudy F. C.
McCarroll, Steven A.
Visscher, Peter M.
TI Finding the missing heritability of complex diseases
SO NATURE
LA English
DT Review
ID GENOME-WIDE ASSOCIATION; DENSITY-LIPOPROTEIN CHOLESTEROL; COPY-NUMBER
VARIATION; RARE VARIANTS; SUSCEPTIBILITY LOCI; BREAST-CANCER; STRUCTURAL
VARIATION; MENTAL-RETARDATION; CROHNS-DISEASE; INCREASE RISK
AB Genome-wide association studies have identified hundreds of genetic variants associated with complex human diseases and traits, and have provided valuable insights into their genetic architecture. Most variants identified so far confer relatively small increments in risk, and explain only a small proportion of familial clustering, leading many to question how the remaining, 'missing' heritability can be explained. Here we examine potential sources of missing heritability and propose research strategies, including and extending beyond current genome-wide association approaches, to illuminate the genetics of complex diseases and enhance its potential to enable effective disease prevention or treatment.
C1 [Collins, Francis S.] NIH, Bethesda, MD 20892 USA.
[Cox, Nancy J.] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Cox, Nancy J.] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA.
[Goldstein, David B.] Duke Univ, IGSP, Durham, NC 27708 USA.
[Hindorff, Lucia A.; Ramos, Erin M.] NHGRI, Off Populat Genom, Rockville, MD 20892 USA.
[Hunter, David J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[McCarthy, Mark I.] Univ Oxford, Churchill Hosp, Oxford Ctr Diabet Endocrinol & Metab, Oxford OX3 7LJ, England.
[McCarthy, Mark I.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England.
[Cardon, Lon R.] GlaxoSmithKline Inc, King Of Prussia, PA 19406 USA.
[Chakravarti, Aravinda; Valle, David] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD 21205 USA.
[Cho, Judy H.] Yale Univ, Dept Med, Div Digest Dis, New Haven, CT 06520 USA.
[Kong, Augustine] DeCODE Genet, IS-101 Reykjavik, Iceland.
[Kruglyak, Leonid] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Kruglyak, Leonid] Princeton Univ, Howard Hughes Med Inst, Lewis Sigler Inst Integrat Genom, Princeton, NJ 08544 USA.
[Mardis, Elaine] Washington Univ, Sch Med, Genome Ctr, St Louis, MO 63108 USA.
[Manolio, Teri A.; Rotimi, Charles N.] NHGRI, Ctr Res Genom & Global Hlth, Bethesda, MD 20892 USA.
[Slatkin, Montgomery] Univ Calif Berkeley, Dept Integrat Biol, Berkeley, CA 94720 USA.
[Whittemore, Alice S.] Stanford Univ, Stanford, CA 94305 USA.
[Boehnke, Michael] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Clark, Andrew G.] Cornell Univ, Dept Mol Biol & Genet, Ithaca, NY 14853 USA.
[Eichler, Evan E.] Univ Washington, Howard Hughes Med Inst, Seattle, WA 98195 USA.
[Eichler, Evan E.] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA.
[Gibson, Greg] Univ Queensland, Sch Biol Sci, Brisbane, Qld 4072, Australia.
[Haines, Jonathan L.] Vanderbilt Univ, Ctr Human Genet Res, Nashville, TN 37232 USA.
[Mackay, Trudy F. C.] N Carolina State Univ, Dept Genet, Raleigh, NC 27695 USA.
[McCarroll, Steven A.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Visscher, Peter M.] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
RP Manolio, TA (reprint author), NHGRI, Ctr Res Genom & Global Hlth, Bldg 31,Room 4B09,31 Ctr Dr,MSC 2152, Bethesda, MD 20892 USA.
EM manoliot@mail.nih.gov
RI Haines, Jonathan/C-3374-2012;
OI McCarroll, Steven/0000-0002-6954-8184; Visscher,
Peter/0000-0002-2143-8760
FU NCRR NIH HHS [UL1 RR024992]; NHGRI NIH HHS [R01 HG003229]; NHLBI NIH HHS
[R01 HL072904, R01 HL072904-07, U01 HL084706]; NIGMS NIH HHS [P50
GM065509, P50 GM065509-080006]; NIMH NIH HHS [R01 MH084695]
NR 83
TC 3310
Z9 3410
U1 60
U2 524
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD OCT 8
PY 2009
VL 461
IS 7265
BP 747
EP 753
DI 10.1038/nature08494
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 503OR
UT WOS:000270547500027
PM 19812666
ER
PT J
AU Thomas, DL
Thio, CL
Martin, MP
Qi, Y
Ge, D
O'hUigin, C
Kidd, J
Kidd, K
Khakoo, SI
Alexander, G
Goedert, JJ
Kirk, GD
Donfield, SM
Rosen, HR
Tobler, LH
Busch, MP
McHutchison, JG
Goldstein, DB
Carrington, M
AF Thomas, David L.
Thio, Chloe L.
Martin, Maureen P.
Qi, Ying
Ge, Dongliang
O'hUigin, Colm
Kidd, Judith
Kidd, Kenneth
Khakoo, Salim I.
Alexander, Graeme
Goedert, James J.
Kirk, Gregory D.
Donfield, Sharyne M.
Rosen, Hugo R.
Tobler, Leslie H.
Busch, Michael P.
McHutchison, John G.
Goldstein, David B.
Carrington, Mary
TI Genetic variation in IL28B and spontaneous clearance of hepatitis C
virus
SO NATURE
LA English
DT Article
ID NATURAL-HISTORY; INFECTION; HEMOPHILIA; ALPHA-2A; FAMILY; HOST
AB Hepatitis C virus (HCV) infection is the most common bloodborne infection in the United States, with estimates of 4 million HCV-infected individuals in the United States and 170 million worldwide(1). Most (70-80%) HCV infections persist and about 30% of individuals with persistent infection develop chronic liver disease, including cirrhosis and hepatocellular carcinoma(2). Epidemiological, viral and host factors have been associated with the differences in HCV clearance or persistence, and studies have demonstrated that a strong host immune response against HCV favours viral clearance(3,4). Thus, variation in genes involved in the immune response may contribute to the ability to clear the virus. In a recent genome-wide association study, a single nucleotide polymorphism (rs12979860) 3 kilobases upstream of the IL28B gene, which encodes the type III interferon IFN-lambda 3, was shown to associate strongly with more than a twofold difference in response to HCV drug treatment(5). To determine the potential effect of rs12979860 variation on outcome to HCV infection in a natural history setting, we genotyped this variant in HCV cohorts comprised of individuals who spontaneously cleared the virus (n = 388) or had persistent infection (n = 620). We show that the C/C genotype strongly enhances resolution of HCV infection among individuals of both European and African ancestry. To our knowledge, this is the strongest and most significant genetic effect associated with natural clearance of HCV, and these results implicate a primary role for IL28B in resolution of HCV infection.
C1 [Martin, Maureen P.; Qi, Ying; O'hUigin, Colm; Carrington, Mary] NCI Frederick, SAIC Frederick Inc, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MD 21702 USA.
[Thomas, David L.; Thio, Chloe L.] Johns Hopkins Univ, Div Infect Dis, Baltimore, MD 21205 USA.
[Martin, Maureen P.; Qi, Ying; O'hUigin, Colm; Carrington, Mary] MIT, Massachusetts Gen Hosp, Ragon Inst, Boston, MA 02114 USA.
[Martin, Maureen P.; Qi, Ying; O'hUigin, Colm; Carrington, Mary] Harvard Univ, Boston, MA 02114 USA.
[Ge, Dongliang; Goldstein, David B.] Duke Univ, Inst Genome Sci & Policy, Ctr Human Genome Variat, Durham, NC 27708 USA.
[Kidd, Judith; Kidd, Kenneth] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06520 USA.
[Alexander, Graeme] Univ Cambridge, Dept Med, Cambridge CB2 2QQ, England.
[Khakoo, Salim I.] Univ London Imperial Coll Sci Technol & Med, Div Med, London W2 1NY, England.
[Goedert, James J.] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Kirk, Gregory D.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
[Donfield, Sharyne M.] Rho Inc, Chapel Hill, NC 27517 USA.
[Rosen, Hugo R.] Univ Colorado, Hlth Sci Ctr, Div Gastroenterol & Hepatol, Aurora, CO 80045 USA.
[Tobler, Leslie H.] Blood Syst Res Inst, San Francisco, CA 94118 USA.
[Busch, Michael P.] Duke Univ, Duke Clin Res Inst, Durham, NC 27705 USA.
[McHutchison, John G.] Duke Univ, Sch Med, Div Gastroenterol, Durham, NC 27705 USA.
RP Carrington, M (reprint author), NCI Frederick, SAIC Frederick Inc, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MD 21702 USA.
EM carringm@mail.nih.gov
RI Ge, Dongliang/A-2073-2010;
OI Khakoo, Salim/0000-0002-4057-9091
FU National Cancer Institute; National Institutes of Health
[HHSN261200800001E, R01DA013324, R01DA004334, R01HL076902, R01DK60590,
R01HD41224]; Wellcome Trust Senior Clinical Fellow
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
Contract number HHSN261200800001E. 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. This
Research was supported in part by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. This
research was supported by NIH grants R01DA013324 ( D. L. T.),
R01DA004334 ( G. D. K.), R01HL076902 ( M. P. B.), R01DK60590 ( H. R. R.)
and R01HD41224 ( S. M. D.). S. I. K. is a Wellcome Trust Senior Clinical
Fellow.
NR 24
TC 1275
Z9 1331
U1 4
U2 52
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD OCT 8
PY 2009
VL 461
IS 7265
BP 798
EP U52
DI 10.1038/nature08463
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 503OR
UT WOS:000270547500037
PM 19759533
ER
PT J
AU Nalley, K
Johnston, SA
Kodadek, T
AF Nalley, Kip
Johnston, Stephen Albert
Kodadek, Thomas
TI Gal4 turnover and transcription activation reply
SO NATURE
LA English
DT Letter
ID DYNAMICS
C1 [Nalley, Kip; Johnston, Stephen Albert; Kodadek, Thomas] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA.
RP Nalley, K (reprint author), NCI, Lab Receptor Biol & Gene Express, Bldg 41,Room B602,41 Lib Dr,MSC 5055, Bethesda, MD 20892 USA.
EM kodadek@scripps.edu
NR 6
TC 4
Z9 4
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD OCT 8
PY 2009
VL 461
IS 7265
BP E8
EP E8
DI 10.1038/nature08407
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 503OR
UT WOS:000270547500048
ER
PT J
AU Ji, JF
Shi, J
Budhu, A
Yu, ZP
Forgues, M
Roessler, S
Ambs, S
Chen, YD
Meltzer, PS
Croce, CM
Qin, LX
Man, K
Lo, CM
Lee, J
Ng, IOL
Fan, J
Tang, ZY
Sun, HC
Wang, XW
AF Ji, Junfang
Shi, Jiong
Budhu, Anuradha
Yu, Zhipeng
Forgues, Marshonna
Roessler, Stephanie
Ambs, Stefan
Chen, Yidong
Meltzer, Paul S.
Croce, Carlo M.
Qin, Lun-Xiu
Man, Kwan
Lo, Chung-Mau
Lee, Joyce
Ng, Irene O. L.
Fan, Jia
Tang, Zhao-You
Sun, Hui-Chuan
Wang, Xin Wei
TI MicroRNA Expression, Survival, and Response to Interferon in Liver
Cancer
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; PROGNOSIS; RESECTION; PROFILES; GENDER; MICE;
SEX; INTERLEUKIN-6; RECURRENCE; SIGNATURE
AB Background
Hepatocellular carcinoma is a common and aggressive cancer that occurs mainly in men. We examined microRNA expression patterns, survival, and response to interferon alfa in both men and women with the disease.
Methods
We analyzed three independent cohorts that included a total of 455 patients with hepatocellular carcinoma who had undergone radical tumor resection between 1999 and 2003. MicroRNA-expression profiling was performed in a cohort of 241 patients with hepatocellular carcinoma to identify tumor-related microRNAs and determine their association with survival in men and women. In addition, to validate our findings, we used quantitative reverse-transcriptase-polymerase-chain-reaction assays to measure microRNAs and assess their association with survival and response to therapy with interferon alfa in 214 patients from two independent, prospective, randomized, controlled trials of adjuvant interferon therapy.
Results
In patients with hepatocellular carcinoma, the expression of miR-26a and miR-26b in nontumor liver tissue was higher in women than in men. Tumors had reduced levels of miR-26 expression, as compared with paired noncancerous tissues, which indicated that the level of miR-26 expression was also associated with hepatocellular carcinoma. Moreover, tumors with reduced miR-26 expression had a distinct transcriptomic pattern, and analyses of gene networks revealed that activation of signaling pathways between nuclear factor kappa B and interleukin-6 might play a role in tumor development. Patients whose tumors had low miR-26 expression had shorter overall survival but a better response to interferon therapy than did patients whose tumors had high expression of the microRNA.
Conclusions
The expression patterns of microRNAs in liver tissue differ between men and women with hepatocellular carcinoma. The miR-26 expression status of such patients is associated with survival and response to adjuvant therapy with interferon alfa.
C1 [Ji, Junfang; Shi, Jiong; Budhu, Anuradha; Yu, Zhipeng; Forgues, Marshonna; Roessler, Stephanie; Wang, Xin Wei] NCI, Liver Carcinogenesis Sect, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Ambs, Stefan] NCI, Breast & Prostate Unit, Human Carcinogenesis Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Chen, Yidong; Meltzer, Paul S.] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Shi, Jiong; Qin, Lun-Xiu; Fan, Jia; Tang, Zhao-You; Sun, Hui-Chuan] Fudan Univ, Zhongshan Hosp, Shanghai 200433, Peoples R China.
[Shi, Jiong; Qin, Lun-Xiu; Fan, Jia; Tang, Zhao-You; Sun, Hui-Chuan] Fudan Univ, Liver Canc Inst, Shanghai 200433, Peoples R China.
[Croce, Carlo M.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Man, Kwan; Lo, Chung-Mau] Univ Hong Kong, Dept Surg, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China.
[Lee, Joyce; Ng, Irene O. L.] Univ Hong Kong, Dept Pathol, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China.
RP Wang, XW (reprint author), NCI, Liver Carcinogenesis Sect, Ctr Canc Res, NIH, 37 Convent Dr,Bldg 37,Rm 3044A, Bethesda, MD 20892 USA.
EM sun.huichuan@zs-hospital.sh.cn; xw3u@nih.gov
RI Wang, Xin/B-6162-2009; Fan, Jia/C-6689-2017
FU Intramural Research Program of the Center for Cancer Research of the
National Cancer Institute [Z01-BC 010313, Z01-BC 010876]
FX Supported in part by grants (Z01-BC 010313 and Z01-BC 010876) from the
Intramural Research Program of the Center for Cancer Research of the
National Cancer Institute.
NR 25
TC 447
Z9 491
U1 8
U2 51
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD OCT 8
PY 2009
VL 361
IS 15
BP 1437
EP 1447
DI 10.1056/NEJMoa0901282
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 503MU
UT WOS:000270540000005
PM 19812400
ER
PT J
AU Coulibaly, YI
Dembele, B
Diallo, AA
Lipner, EM
Doumbia, SS
Coulibaly, SY
Konate, S
Diallo, DA
Yalcouye, D
Kubofcik, J
Doumbo, OK
Traore, AK
Keita, AD
Fay, MP
Traore, SF
Nutman, TB
Klion, AD
AF Coulibaly, Yaya I.
Dembele, Benoit
Diallo, Abdallah A.
Lipner, Ettie M.
Doumbia, Salif S.
Coulibaly, Siaka Y.
Konate, Siaka
Diallo, Dapa A.
Yalcouye, Daniel
Kubofcik, Joseph
Doumbo, Ogobara K.
Traore, Abdel K.
Keita, Adama D.
Fay, Michael P.
Traore, Sekou F.
Nutman, Thomas B.
Klion, Amy D.
TI A Randomized Trial of Doxycycline for Mansonella perstans Infection
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID WUCHERERIA-BANCROFTI; LOA-LOA; MACROFILARICIDAL ACTIVITY;
MOLECULAR-IDENTIFICATION; WOLBACHIA; IVERMECTIN; ONCHOCERCIASIS;
MICROFILAREMIA; FILARIASIS; EFFICACY
AB Background
Mansonella perstans infection is common in areas of Africa where Wuchereria bancrofti, a causative agent of lymphatic filariasis, is endemic. M. perstans is refractory to standard antifilarial therapies. The recent discovery of bacterial endosymbionts ( e. g., wolbachia) in most filarial species, including M. perstans, provides new therapeutic options for reducing microfilaremia.
Methods
In an open-label, randomized trial, we recruited subjects with M. perstans microfilaremia, with or without concomitant W. bancrofti infection, from four villages in Mali and randomly assigned them to receive doxycycline, at a dose of 200 mg daily for 6 weeks ( 106 subjects), or no treatment ( 110). At 6 months, subjects who were co-infected with W. bancrofti underwent a second random assignment, to treatment with a single dose of albendazole ( 400 mg) and ivermectin ( 150 mu g per kilogram of body weight) or no treatment. Subjects were monitored daily during the first 6-week study period for adverse events. M. perstans and W. bancrofti microfilarial levels were assessed at 6, 12, and 36 months.
Results
At 12 months, 67 of 69 subjects who had received treatment with doxycycline only (97%) had no detectable M. perstans microfilariae per 60 mu l of blood, as compared with 10 of 63 subjects who had received no treatment (16%) ( relative risk, 6.18; 95% confidence interval, 3.63 to 11.89; P<0.001). At 36 months, M. perstans microfilaremia remained suppressed in 48 of 64 subjects who had received treatment with doxycycline only (75%), a finding that was consistent with a macrofilaricidal effect of doxycycline. Vomiting was more frequent in the doxycycline-treated group than in the untreated group (17% vs. 4%).
Conclusions
These results are consistent with previous findings that M. perstans harbors the intracellular endosymbiont, wolbachia, and suggest that doxycycline is an effective therapy for M. perstans infection. (ClinicalTrials.gov number, NCT00340691.)
C1 [Kubofcik, Joseph; Nutman, Thomas B.; Klion, Amy D.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Coulibaly, Yaya I.; Dembele, Benoit; Diallo, Abdallah A.; Doumbia, Salif S.; Coulibaly, Siaka Y.; Konate, Siaka; Diallo, Dapa A.; Yalcouye, Daniel; Doumbo, Ogobara K.; Traore, Sekou F.] Univ Bamako, Fac Med Pharm & Odontostomatol, Bamako, Mali.
[Traore, Abdel K.] Ctr Dis Control, Bamako, Mali.
[Keita, Adama D.] Hosp Point G, Dept Radiol, Bamako, Mali.
[Lipner, Ettie M.; Fay, Michael P.] NIAID, Biostat & Res Branch, NIH, Bethesda, MD 20892 USA.
RP Klion, AD (reprint author), NIAID, Parasit Dis Lab, NIH, Bldg 50,Rm 6351, Bethesda, MD 20892 USA.
EM aklion@nih.gov
OI Klion, Amy/0000-0002-4986-5326; Fay, Michael P./0000-0002-8643-9625
FU Division of Intramural Research of the National Institutes of Health;
National Institute of Allergy and Infectious Diseases, Bethesda, MD
FX Supported by the Division of Intramural Research of the National
Institutes of Health, National Institute of Allergy and Infectious
Diseases, Bethesda, MD.
NR 25
TC 35
Z9 36
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD OCT 8
PY 2009
VL 361
IS 15
BP 1448
EP 1458
DI 10.1056/NEJMoa0900863
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 503MU
UT WOS:000270540000006
PM 19812401
ER
PT J
AU Coulouarn, C
Factor, VM
Andersen, JB
Durkin, ME
Thorgeirsson, SS
AF Coulouarn, C.
Factor, V. M.
Andersen, J. B.
Durkin, M. E.
Thorgeirsson, S. S.
TI Loss of miR-122 expression in liver cancer correlates with suppression
of the hepatic phenotype and gain of metastatic properties
SO ONCOGENE
LA English
DT Article
DE hepatocellular carcinoma; microRNA; differentiation; metastasis;
microarray
ID HUMAN HEPATOCELLULAR-CARCINOMA; C VIRUS-RNA; GENE-EXPRESSION; MICRORNA
EXPRESSION; FUNCTIONAL GENOMICS; TUMOR-SUPPRESSOR; CELL-LINES; IN-VIVO;
MOUSE; IDENTIFICATION
AB Growing evidence indicates that microRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. In this study, we evaluated the clinical and functional relevance of microRNA-122 (miR-122) expression in human hepatocellular carcinoma (HCC). We report that miR-122 is specifically repressed in a subset of primary tumors that are characterized by poor prognosis. We further show that the loss of miR-122 expression in tumor cells segregates with specific gene expression profiles linked to cancer progression, namely the suppression of hepatic phenotype and the acquisition of invasive properties. We identify liver-enriched transcription factors as central regulatory molecules in the gene networks associated with loss of miR-122, and provide evidence suggesting that miR-122 is under the transcriptional control of HNF1A, HNF3A and HNF3B. We further show that loss of miR-122 results in an increase of cell migration and invasion and that restoration of miR-122 reverses this phenotype. In conclusion, miR-122 is a marker of hepatocyte-specific differentiation and an important determinant in the control of cell migration and invasion. From a clinical point of view, our study emphasizes miR-122 as a diagnostic and prognostic marker for HCC progression. Oncogene (2009) 28, 3526-3536; doi: 10.1038/onc.2009.211; published online 20 July 2009
C1 [Coulouarn, C.; Factor, V. M.; Andersen, J. B.; Durkin, M. E.; Thorgeirsson, S. S.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Thorgeirsson, SS (reprint author), NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, 37 Convent Dr,Bldg 37,Room 4146A, Bethesda, MD 20892 USA.
EM snorri_s_thorgeirsson@nih.gov
RI Coulouarn, Cedric/E-5472-2011;
OI Andersen , Jesper B/0000-0003-1760-5244
FU Intramural Research Program of the Center for Cancer Research
FX This project was supported in part by the Intramural Research Program of
the Center for Cancer Research.
NR 46
TC 323
Z9 348
U1 7
U2 32
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD OCT 8
PY 2009
VL 28
IS 40
BP 3526
EP 3536
DI 10.1038/onc.2009.211
PG 11
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 507KI
UT WOS:000270851700002
PM 19617899
ER
PT J
AU Koshiol, J
Rotunno, M
Consonni, D
Pesatori, AC
De Matteis, S
Goldstein, AM
Chaturvedi, AK
Wacholder, S
Landi, MT
Lubin, JH
Caporaso, NE
AF Koshiol, Jill
Rotunno, Melissa
Consonni, Dario
Pesatori, Angela Cecilia
De Matteis, Sara
Goldstein, Alisa M.
Chaturvedi, Anil K.
Wacholder, Sholom
Landi, Maria Teresa
Lubin, Jay H.
Caporaso, Neil E.
TI Chronic Obstructive Pulmonary Disease and Altered Risk of Lung Cancer in
a Population-Based Case-Control Study
SO PLOS ONE
LA English
DT Article
AB Background: Chronic obstructive pulmonary disease ( COPD) has been consistently associated with increased risk of lung cancer. However, previous studies have had limited ability to determine whether the association is due to smoking.
Methodology/Principal Findings: The Environment And Genetics in Lung cancer Etiology ( EAGLE) population-based case-control study recruited 2100 cases and 2120 controls, of whom 1934 cases and 2108 controls reported about diagnosis of chronic bronchitis, emphysema, COPD (chronic bronchitis and/or emphysema), or asthma more than 1 year before enrollment. We estimated odds ratios (OR) and 95% confidence intervals (CI) using logistic regression. After adjustment for smoking, other previous lung diseases, and study design variables, lung cancer risk was elevated among individuals with a history of chronic bronchitis (OR = 2.0, 95% CI = 1.5-2.5), emphysema (OR = 1.9, 95% CI = 1.4-2.8), or COPD (OR = 2.5, 95% CI = 2.0-3.1). Among current smokers, association between chronic bronchitis and lung cancer was strongest among lighter smokers. Asthma was associated with a decreased risk of lung cancer in males (OR = 0.48, 95% CI = 0.30-0.78).
Conclusions/Significance: These results suggest that the associations of personal history of chronic bronchitis, emphysema, and COPD with increased risk of lung cancer are not entirely due to smoking. Inflammatory processes may both contribute to COPD and be important for lung carcinogenesis.
RP Koshiol, J (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM koshiolj@mail.nih.gov
OI pesatori, angela/0000-0002-0261-3252
FU Intramural NIH HHS
NR 49
TC 69
Z9 71
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 8
PY 2009
VL 4
IS 10
AR e7380
DI 10.1371/journal.pone.0007380
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 504DL
UT WOS:000270594200006
PM 19812684
ER
PT J
AU Frewen, TA
Hummer, G
Kevrekidis, IG
AF Frewen, Thomas A.
Hummer, Gerhard
Kevrekidis, Ioannis G.
TI Exploration of effective potential landscapes using coarse reverse
integration
SO JOURNAL OF CHEMICAL PHYSICS
LA English
DT Article
ID FINDING SADDLE-POINTS; NUDGED ELASTIC BAND; CHEMICALLY REACTING SYSTEMS;
MINIMUM ENERGY PATHS; MOLECULAR-DYNAMICS; TRANSITION-STATES; STOCHASTIC
SIMULATION; INVARIANT-MANIFOLDS; DIFFUSION MAPS; STRING METHOD
AB We describe a reverse integration approach for the exploration of low-dimensional effective potential landscapes. Coarse reverse integration initialized on a ring of coarse states enables efficient navigation on the landscape terrain: Escape from local effective potential wells, detection of saddle points, and identification of significant transition paths between wells. We consider several distinct ring evolution modes: Backward stepping in time, solution arc length, and effective potential. The performance of these approaches is illustrated for a deterministic problem where the energy landscape is known explicitly. Reverse ring integration is then applied to noisy problems where the ring integration routine serves as an outer wrapper around a forward-in-time inner simulator. Two versions of such inner simulators are considered: A Gillespie-type stochastic simulator and a molecular dynamics simulator. In these "equation-free" computational illustrations, estimation techniques are applied to the results of short bursts of inner simulation to obtain the unavailable (in closed-form) quantities (local drift and diffusion coefficient estimates) required for reverse ring integration; this naturally leads to approximations of the effective landscape. (C) 2009 American Institute of Physics. [doi:10.1063/1.3207882]
C1 [Frewen, Thomas A.; Kevrekidis, Ioannis G.] Princeton Univ, Dept Chem Engn, Princeton, NJ 08544 USA.
[Hummer, Gerhard] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Kevrekidis, Ioannis G.] Princeton Univ, Dept Math, Princeton, NJ 08544 USA.
[Kevrekidis, Ioannis G.] Princeton Univ, PACM, Princeton, NJ 08544 USA.
RP Frewen, TA (reprint author), Princeton Univ, Dept Chem Engn, Olden St, Princeton, NJ 08544 USA.
EM tfrewen@princeton.edu; gerhard.hummer@nih.gov; yannis@princeton.edu
RI Hummer, Gerhard/A-2546-2013
OI Hummer, Gerhard/0000-0001-7768-746X
FU Intramural NIH HHS
NR 69
TC 3
Z9 3
U1 1
U2 7
PU AMER INST PHYSICS
PI MELVILLE
PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1,
MELVILLE, NY 11747-4501 USA
SN 0021-9606
J9 J CHEM PHYS
JI J. Chem. Phys.
PD OCT 7
PY 2009
VL 131
IS 13
AR 134104
DI 10.1063/1.3207882
PG 15
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 507BR
UT WOS:000270825500005
PM 19814540
ER
PT J
AU Minh, DDL
Chodera, JD
AF Minh, David D. L.
Chodera, John D.
TI Optimal estimators and asymptotic variances for nonequilibrium
path-ensemble averages
SO JOURNAL OF CHEMICAL PHYSICS
LA English
DT Article
ID FREE-ENERGY DIFFERENCES; HISTOGRAM ANALYSIS METHOD; MOLECULE PULLING
EXPERIMENTS; MONTE-CARLO INTEGRATION; EMPIRICAL DISTRIBUTIONS;
COMPUTER-SIMULATIONS; FLUCTUATION THEOREM; EQUILIBRIUM; MODELS; BOUNDS
AB Existing optimal estimators of nonequilibrium path-ensemble averages are shown to fall within the framework of extended bridge sampling. Using this framework, we derive a general minimal-variance estimator that can combine nonequilibrium trajectory data sampled from multiple path-ensembles to estimate arbitrary functions of nonequilibrium expectations. The framework is also applied to obtain asymptotic variance estimates, which are a useful measure of statistical uncertainty. In particular, we develop asymptotic variance estimates pertaining to Jarzynski's equality for free energies and the Hummer-Szabo expressions for the potential of mean force, calculated from uni- or bidirectional path samples. These estimators are demonstrated on a model single-molecule pulling experiment. In these simulations, the asymptotic variance expression is found to accurately characterize the confidence intervals around estimators when the bias is small. Hence, the confidence intervals are inaccurately described for unidirectional estimates with large bias, but for this model it largely reflects the true error in a bidirectional estimator derived by Minh and Adib. (C) 2009 American Institute of Physics. [doi:10.1063/1.3242285]
C1 [Minh, David D. L.] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Chodera, John D.] Univ Calif Berkeley, Calif Inst Quantitat Biosci QB3, Berkeley, CA 94720 USA.
RP Minh, DDL (reprint author), Argonne Natl Lab, Biosci Div, 9700 S Cass Ave, Argonne, IL 60439 USA.
EM daveminh@gmail.com; jchodera@berkeley.edu
RI Minh, David/A-4655-2009;
OI Minh, David/0000-0002-4802-2618; Chodera, John/0000-0003-0542-119X
FU Intramural NIH HHS
NR 61
TC 29
Z9 29
U1 1
U2 13
PU AMER INST PHYSICS
PI MELVILLE
PA 1305 WALT WHITMAN RD, STE 300, MELVILLE, NY 11747-4501 USA
SN 0021-9606
EI 1089-7690
J9 J CHEM PHYS
JI J. Chem. Phys.
PD OCT 7
PY 2009
VL 131
IS 13
AR 134110
DI 10.1063/1.3242285
PG 9
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 507BR
UT WOS:000270825500011
PM 19814546
ER
PT J
AU Krag, DN
Ashikaga, T
Harlow, SP
Skelly, JM
Julian, TB
Brown, AM
Weaver, DL
Wolmark, N
AF Krag, David N.
Ashikaga, Takamaru
Harlow, Seth P.
Skelly, Joan M.
Julian, Thomas B.
Brown, Ann M.
Weaver, Donald L.
Wolmark, Norman
CA Natl Surgical Adjuvant Breast Bowe
TI Surgeon Training, Protocol Compliance, and Technical Outcomes From
Breast Cancer Sentinel Lymph Node Randomized Trial
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID DISSECTION; RESECTION; QUALITY
AB The National Surgical Adjuvant Breast and Bowel Project B-32 trial was designed to determine whether sentinel lymph node resection can achieve the same therapeutic outcomes as axillary lymph node resection but with fewer side effects and is one of the most carefully controlled and monitored randomized trials in the field of surgical oncology. We evaluated the relationship of surgeon trial preparation, protocol compliance audit, and technical outcomes.
Preparation for this trial included a protocol manual, a site visit with key participants, an intraoperative session with the surgeon, and prerandomization documentation of protocol compliance. Training categories included surgeons who submitted material on five prerandomization surgeries and were trained by a core trainer (category 1) or by a site trainer (category 2). An expedited group (category 3) included surgeons with extensive experience who submitted material on one prerandomization surgery. At completion of training, surgeons could accrue patients. Two hundred twenty-four surgeons enrolled 4994 patients with breast cancer and were audited for 94 specific items in the following four categories: procedural, operative note, pathology report, and data entry. The relationship of training method; protocol compliance performance audit; and the technical outcomes of the sentinel lymph node resection rate, false-negative rate, and number of sentinel lymph nodes removed was determined. All statistical tests were two-sided.
The overall sentinel lymph node resection success rate was 96.9% (95% confidence interval [CI] = 96.4% to 97.4%), and the overall false-negative rate was 9.5% (95% CI = 7.4% to 12.0%), with no statistical differences between training methods. Overall audit outcomes were excellent in all four categories. For all three training groups combined, a statistically significant positive association was observed between surgeons' average number of procedural errors and their false-negative rate ( = +0.188, P = .021).
All three training methods resulted in uniform and high overall sentinel lymph node resection rates. Subgroup analyses identified some variation in false-negative rates that were related to audited outcome performance measures.
C1 [Krag, David N.] Univ Vermont, Dept Surg, Coll Med, Burlington, VT 05405 USA.
[Julian, Thomas B.; Wolmark, Norman] Natl Surg Adjuvant Breast & Bowel Project, Pittsburgh, PA USA.
[Brown, Ann M.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15261 USA.
[Julian, Thomas B.; Wolmark, Norman] Allegheny Gen Hosp, Dept Human Oncol, Pittsburgh, PA 15212 USA.
RP Krag, DN (reprint author), Univ Vermont, Dept Surg, Coll Med, Given Bldg,Rm E309,89 Beaumont Ave, Burlington, VT 05405 USA.
EM david.krag@uvm.edu
FU National Cancer Institute, Department of Health and Human Services,
Public Health Service [P30 CA022435, 5RO1CA74137-9, U10-CA-12027,
U10-CA-69651, U10-CA-37377, U10-CA-69974]
FX National Cancer Institute, Department of Health and Human Services,
Public Health Service Grants (P30 CA022435 Vermont Cancer Center,
5RO1CA74137-9 D.N.K., U10-CA-12027, U10-CA-69651, U10-CA-37377, and
U10-CA-69974 to National Surgical Adjuvant Breast and Bowel Project).
NR 11
TC 12
Z9 12
U1 0
U2 0
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 7
PY 2009
VL 101
IS 19
BP 1356
EP 1362
DI 10.1093/jnci/djp281
PG 7
WC Oncology
SC Oncology
GA 505QR
UT WOS:000270709900014
PM 19704072
ER
PT J
AU Yan, YH
Liu, QP
Kozak, CA
AF Yan, Yuhe
Liu, Qingping
Kozak, Christine A.
TI Six host range variants of the xenotropic/polytropic gammaretroviruses
define determinants for entry in the XPR1 cell surface receptor
SO RETROVIROLOGY
LA English
DT Article
ID MURINE LEUKEMIA VIRUSES; SPECIES MUS-CASTANEUS; MOUSE GAMMARETROVIRUSES;
ENDOGENOUS PROVIRUSES; BINDING DOMAIN; RESISTANCE; MICE; RETROVIRUS;
SEQUENCE; GENE
AB Background: The evolutionary interactions between retroviruses and their receptors result in adaptive selection of restriction variants that can allow natural populations to evade retrovirus infection. The mouse xenotropic/polytropic (X/PMV) gammaretroviruses rely on the XPR1 cell surface receptor for entry into host cells, and polymorphic variants of this receptor have been identified in different rodent species.
Results: We screened a panel of X/PMVs for infectivity on rodent cells carrying 6 different XPR1 receptor variants. The X/PMVs included 5 well-characterized laboratory and wild mouse virus isolates as well as a novel cytopathic XMV-related virus, termed Cz524, isolated from an Eastern European wild mouse-derived strain, and XMRV, a xenotropic-like virus isolated from human prostate cancer. The 7 viruses define 6 distinct tropisms. Cz524 and another wild mouse isolate, CasE#1, have unique species tropisms. Among the PMVs, one Friend isolate is restricted by rat cells. Among the XMVs, two isolates, XMRV and AKR6, differ from other XMVs in their PMV-like restriction in hamster cells. We generated a set of Xpr1 mutants and chimeras, and identified critical amino acids in two extracellular loops (ECLs) that mediate entry of these different viruses, including 3 residues in ECL3 that are involved in PMV entry (E500, T507, and V508) and can also influence infectivity by AKR6 and Cz524.
Conclusion: We used a set of natural variants and mutants of Xpr1 to define 6 distinct host range variants among naturally occurring X/PMVs (2 XMV variants, 2 PMVs, 2 different wild mouse variants). We identified critical amino acids in XPR1 that mediate entry of these viruses. These gammaretroviruses and their XPR1 receptor are thus highly functionally polymorphic, a consequence of the evolutionary pressures that favor both host resistance and virus escape mutants. This variation accounts for multiple naturally occurring virus resistance phenotypes and perhaps contributes to the widespread distribution of these viruses in rodent and non-rodent species.
C1 [Yan, Yuhe; Liu, Qingping; Kozak, Christine A.] NIAID, Mol Microbiol Lab, Bethesda, MD 20892 USA.
RP Kozak, CA (reprint author), NIAID, Mol Microbiol Lab, Bethesda, MD 20892 USA.
EM yyan@niaid.nih.gov; liuqing@niaid.nih.gov; ckozak@niaid.nih.gov
FU Intramural Research Program of the NIH, NIAID
FX This research was supported by the Intramural Research Program of the
NIH, NIAID.
NR 42
TC 33
Z9 33
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD OCT 7
PY 2009
VL 6
AR 87
DI 10.1186/1742-4690-6-87
PG 11
WC Virology
SC Virology
GA 518ES
UT WOS:000271673900001
PM 19811656
ER
PT J
AU Sanghvi, M
Hamouda, AK
Davis, MI
Morton, RA
Srivastava, S
Pandhare, A
Duddempudi, PK
Machu, TK
Lovinger, DM
Cohen, JB
Blanton, MP
AF Sanghvi, Mitesh
Hamouda, Ayman K.
Davis, Margaret I.
Morton, Russell A.
Srivastava, Shouryadeep
Pandhare, Akash
Duddempudi, Phaneendra K.
Machu, Tina K.
Lovinger, David M.
Cohen, Jonathan B.
Blanton, Michael P.
TI Hydrophobic Photolabeling Studies Identify the Lipid-Protein Interface
of the 5-HT3A Receptor
SO BIOCHEMISTRY
LA English
DT Article
ID NICOTINIC ACETYLCHOLINE-RECEPTOR; NEURO-BLASTOMA CELLS; GATED
ION-CHANNEL; 5-HYDROXYTRYPTAMINE(3) RECEPTORS; FUNCTIONAL EXPRESSION;
ALLOSTERIC MODULATION; RADIOLIGAND BINDING; RECOGNITION SITES;
NERVOUS-SYSTEM; SUBUNIT
AB A HEK-293 cell line that stably expresses mouse 5-HT(3A)Rs containing a C-terminal extension that confers high-affinity binding of alpha-bungarotoxin (alpha BgTx) was established (alpha BgTx-5-HT(3A)Rs) and used to purify alpha BgTx-5-HT(3A)Rs in a lipid environment for use in structural studies using photoaffinity labeling. alpha BgTx-5-HT(3A)Rs were expressed robustly (60 pmol of [H-3]BRL-43694 binding sites (similar to 3 mu g of receptor) per milligram of protein) and displayed the same functional properties as wild-type receptors (serotonin EC50 = 5.3 +/- 0.04 mu M). While [I-125]alpha BgTx bound to the alpha BgTx-5-HT(3A)Rs with high affinity (K-d = 11 nM), application of nonradioactive alpha B-Tx (up to 300 mu M) had no effect on serotonin-induced current responses. alpha BgTx-5-HT(3A)Rs were purified on an alpha BgTx-derivatized affinity column from detergent extracts in milligram quantities and at similar to 25% purity. The hydrophobic photolabel 3-trinuoromethyl-3-(m-[I-125]iodophenyl)diazirine ([I-125]TID) was used to identify the amino acids at the lipid-protein interface of purified and lipid-reconstituted alpha BgTx-5-HT(3A)Rs. [I-125]TID photoincorporation into the alpha BgTx-5-HT3AR subunit was initially mapped to subunit proteolytic fragments of 8 kDa, containing the M4 transmembrane segment and similar to 60% of incorporated I-125, and 17 kDa, containing the M1-M3 transmembrane segments. Within the M4 segment, [I-125]TID labeled Ser(451), equivalent to the [I-125]TID-labeled residue Thr(422) at the lipid-exposed face of the Torpedo nicotinic acetylcholine receptor (nAChR) alpha 1M4 alpha-helix. These results provide a first definition of the surface of the 5-HT3AR M4 helix that is exposed to lipid and establish that this surface is equivalent to the surface exposed to lipid in the Torpedo nAChR.
C1 [Sanghvi, Mitesh; Hamouda, Ayman K.; Srivastava, Shouryadeep; Pandhare, Akash; Duddempudi, Phaneendra K.; Blanton, Michael P.] Texas Tech Univ, Hlth Sci Ctr, Sch Med, Dept Pharmacol & Neurosci, Lubbock, TX 79430 USA.
[Sanghvi, Mitesh; Hamouda, Ayman K.; Srivastava, Shouryadeep; Pandhare, Akash; Duddempudi, Phaneendra K.; Blanton, Michael P.] Texas Tech Univ, Hlth Sci Ctr, Sch Med, Ctr Membrane Prot Res, Lubbock, TX 79430 USA.
[Davis, Margaret I.; Morton, Russell A.; Lovinger, David M.] NIAAA, Sect Synapt Pharmacol, Lab Integrat Neurosci, NIH, Bethesda, MD 20892 USA.
[Machu, Tina K.] Univ N Texas, Hlth Sci Ctr, Dept Pharmacol & Neurosci, Ft Worth, TX 76107 USA.
[Hamouda, Ayman K.; Cohen, Jonathan B.] Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA.
RP Blanton, MP (reprint author), Texas Tech Univ, Hlth Sci Ctr, Sch Med, Dept Pharmacol & Neurosci, Lubbock, TX 79430 USA.
EM michael.blanton@ttuhsc.edu
RI Davis, Margaret/F-4165-2010; Sanghvi, Mitesh/C-6740-2013; Pandhare,
Akash/M-1827-2016;
OI Davis, Margaret/0000-0002-0489-8351; Hamouda, Ayman/0000-0001-7819-3074
FU American Heart Association South Central Affiliate [0755029Y]; South
Plains Foundation; National Institute of General Medical Sciences
[GM-58448]; National Institute for Neurological Disorders and Stroke
[NS-43438]
FX This research was supported in part by American Heart Association South
Central Affiliate Grant-In-Aid 0755029Y (M.P.B.), by the South Plains
Foundation (M.P.B), by Grant GM-58448 from the National Institute of
General Medical Sciences (J.B.C.), and by NS-43438 from the National
Institute for Neurological Disorders and Stroke (T.K.M.).
NR 45
TC 7
Z9 7
U1 1
U2 7
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD OCT 6
PY 2009
VL 48
IS 39
BP 9278
EP 9286
DI 10.1021/bi901208j
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 498JU
UT WOS:000270136600013
PM 19715355
ER
PT J
AU Guttmacher, AE
Nabel, EG
Collins, FS
AF Guttmacher, Alan E.
Nabel, Elizabeth G.
Collins, Francis S.
TI Why data-sharing policies matter
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Editorial Material
C1 [Guttmacher, Alan E.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Nabel, Elizabeth G.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Guttmacher, AE (reprint author), NHGRI, NIH, Bethesda, MD 20892 USA.
EM guttmach@mail.nih.gov
NR 2
TC 13
Z9 14
U1 1
U2 5
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 6
PY 2009
VL 106
IS 40
BP 16894
EP 16894
DI 10.1073/pnas.0910378106
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 503MD
UT WOS:000270537500002
PM 19805161
ER
PT J
AU Sacks, D
AF Sacks, David
TI BAC talk about cell type-specific regulation of human IL-10
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Editorial Material
ID HUMAN VISCERAL LEISHMANIASIS; INTERLEUKIN-10 GENE; MICE; PATHOGENESIS;
DISTINCT
C1 NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Sacks, D (reprint author), NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
EM dsacks@nih.gov
NR 20
TC 1
Z9 1
U1 0
U2 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 6
PY 2009
VL 106
IS 40
BP 16895
EP 16896
DI 10.1073/pnas.0909138106
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 503MD
UT WOS:000270537500003
PM 19805024
ER
PT J
AU Zhang, ZB
Shen, XN
Gude, DR
Wilkinson, BM
Justice, MJ
Flickinger, CJ
Herr, JC
Eddy, EM
Strauss, JF
AF Zhang, Zhibing
Shen, Xuening
Gude, David R.
Wilkinson, Bonney M.
Justice, Monica J.
Flickinger, Charles J.
Herr, John C.
Eddy, Edward M.
Strauss, Jerome F., III
TI MEIG1 is essential for spermiogenesis in mice
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID COREGULATED GENE-PRODUCT; EARLY-ONSET PARKINSONISM; MOUSE
SPERMIOGENESIS; SERTOLI-CELLS; PACRG; EXPRESSION; IDENTIFICATION;
CENTROSOME; DELETION; MEIOSIS
AB Spermatogenesis can be divided into three stages: spermatogonial mitosis, meiosis of spermatocytes, and spermiogenesis. During spermiogenesis, spermatids undergo dramatic morphological changes including formation of a flagellum and chromosomal packaging and condensation of the nucleus into the sperm head. The genes regulating the latter processes are largely unknown. We previously discovered that a bi-functional gene, Spag16, is essential for spermatogenesis. SPAG16S, the 35 kDa, testis-specific isoform derived from the Spag16 gene, was found to bind to meiosis expressed gene 1 product (MEIG1), a protein originally thought to play a role in meiosis. We inactivated the Meig1 gene and, unexpectedly, found that Meig1 mutant male mice had no obvious defect in meiosis, but were sterile as a result of impaired spermatogenesis at the stage of elongation and condensation. Transmission electron microscopy revealed that the manchette, a microtubular organelle essential for sperm head and flagellar formation was disrupted in spermatids of MEIG1-deficient mice. We also found that MEIG1 associates with the Parkin co-regulated gene (PACRG) protein, and that testicular PACRG protein is reduced in MEIG1-deficient mice. PACRG is thought to play a key role in assembly of the axonemes/flagella and the reproductive phenotype of Pacrg-deficient mice mirrors that of the Meig1 mutant mice. Our findings reveal a critical role for the MEIG1/PARCG partnership in manchette structure and function and the control of spermiogenesis.
C1 [Zhang, Zhibing; Shen, Xuening; Gude, David R.; Strauss, Jerome F., III] Virginia Commonwealth Univ, Dept Obstet & Gynecol, Richmond, VA 23298 USA.
[Zhang, Zhibing; Gude, David R.; Strauss, Jerome F., III] Virginia Commonwealth Univ, Dept Biochem, Richmond, VA 23298 USA.
[Wilkinson, Bonney M.; Justice, Monica J.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Flickinger, Charles J.; Herr, John C.] Univ Virginia, Dept Cell Biol, Ctr Res Contracept & Reprod Hlth, Charlottesville, VA 22908 USA.
[Eddy, Edward M.] NIEHS, Labs Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
RP Zhang, ZB (reprint author), Virginia Commonwealth Univ, Dept Obstet & Gynecol, Richmond, VA 23298 USA.
EM zzhang4@vcu.edu
FU National Institutes of Health [HD37416, HD045783, CA115503]; National
Institutes of Health, National Institute of Environmental Health
Sciences [ZO1-ES070076]; National Institute of Child Health and Human
Development F31 [IF3IHD0G2314-01]; Virginia Commonwealth University
[5P30NS047463]
FX We thank Glenn L. Radice and Igor Kostetskii for their suggestions of
making Meig1 conditional knockout construct; Dr. Rita Shiang (Virginia
Commonwealth University) for providing CMV-Cretransgenic mice; and Emily
Jumet and Sonya Washington for assistance in photographing light
microscopic histology preparations. This work was supported by National
Institutes of Health Grants HD37416(to J.F.S.), HD045783 (to J.C.H.),
CA115503 (to M.J.J.), and in part by the Intramural Research Program of
the National Institutes of Health, National Institute of Environmental
Health Sciences Grant ZO1-ES070076 (to E.M.E.) and National Institute of
Child Health and Human Development F31 Predoctoral Fellowship
IF3IHD0G2314-01 (to D.R.G.). Tissue processing and staining were
performed in Histology Core Facility of Virginia Commonwealth
University. Transmission electron microscopy was performed in the
Imaging Core of Virginia Commonwealth University (5P30NS047463).
NR 43
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Z9 32
U1 3
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 6
PY 2009
VL 106
IS 40
BP 17055
EP 17060
DI 10.1073/pnas.0906414106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 503MD
UT WOS:000270537500036
PM 19805151
ER
PT J
AU Papper, Z
Jameson, NM
Romero, R
Weckle, AL
Mittal, P
Benirschke, K
Santolaya-Forgas, J
Uddin, M
Haig, D
Goodman, M
Wildman, DE
AF Papper, Zack
Jameson, Natalie M.
Romero, Roberto
Weckle, Amy L.
Mittal, Pooja
Benirschke, Kurt
Santolaya-Forgas, Joaquin
Uddin, Monica
Haig, David
Goodman, Morris
Wildman, Derek E.
TI Ancient origin of placental expression in the growth hormone genes of
anthropoid primates
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE adaptive evolution; gene duplication; placental lactogen; Platyrrhini;
pregnancy
ID MARMOSET CALLITHRIX-JACCHUS; PROLACTIN RECEPTOR; FETAL-GROWTH;
MESSENGER-RNA; EVOLUTION; GH; PREGNANCY; LACTOGEN; VARIANT; PROTEIN
AB In anthropoid primates, growth hormone (GH) genes have undergone at least 2 independent locus expansions, one in platyrrhines (New World monkeys) and another in catarrhines (Old World monkeys and apes). In catarrhines, the GH cluster has a pituitary-expressed gene called GH1; the remaining GH genes include placental GHs and placental lactogens. Here, we provide cDNA sequence evidence that the platyrrhine GH cluster also includes at least 3 placenta expressed genes and phylogenetic evidence that placenta expressed anthropoid GH genes have undergone strong adaptive evolution, whereas pituitary-expressed GH genes have faced strict functional constraint. Our phylogenetic evidence also points to lineage-specific gene gain and loss in early placental mammalian evolution, with at least three copies of the GH gene present at the time of the last common ancestor (LCA) of primates, rodents, and laurasiatherians. Anthropoid primates and laurasiatherians share gene descendants of one of these three copies, whereas rodents and strepsirrhine primates each maintain a separate copy. Eight of the amino-acid replacements that occurred on the lineage leading to the LCA of extant anthropoids have been implicated in GH signaling at the maternal-fetal interface. Thus, placental expression of GH may have preceded the separate series of GH gene duplications that occurred in catarrhines and platyrrhines (i.e., the roles played by placenta-expressed GHs in human pregnancy may have a longer evolutionary history than previously appreciated).
C1 [Papper, Zack; Jameson, Natalie M.; Romero, Roberto; Weckle, Amy L.; Goodman, Morris; Wildman, Derek E.] Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI 48201 USA.
[Mittal, Pooja; Wildman, Derek E.] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Goodman, Morris] Wayne State Univ, Sch Med, Dept Anat & Cell Biol, Detroit, MI 48201 USA.
[Romero, Roberto; Weckle, Amy L.; Mittal, Pooja; Wildman, Derek E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Detroit, MI 48201 USA.
[Benirschke, Kurt] Univ Calif San Diego, Dept Pathol, San Diego, CA 92103 USA.
[Santolaya-Forgas, Joaquin] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Obstet & Gynecol, Boston, MA 02115 USA.
[Uddin, Monica] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Haig, David] Harvard Univ, Dept Organism & Evolutionary Biol, Cambridge, MA 02138 USA.
RP Romero, R (reprint author), Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI 48201 USA.
EM prbchiefstaff@med.wayne.edu; mgoodwayne@aol.com; dwildman@med.wayne.edu
FU Perinatology Research Branch; Division of Intramural Research; Eunice
Kennedy Shriver National Institute of Child Health and Human
Development; National Institutes of Health; Department of Health and
Human Services; National Science Foundation [BCS-0751508]
FX Dr. Offer Erez (Wayne State University, Detroit, MI) critically read the
manuscript. This research was supported in part by the Perinatology
Research Branch, Division of Intramural Research, Eunice Kennedy Shriver
National Institute of Child Health and Human Development, National
Institutes of Health, Department of Health and Human Services, and by
National Science Foundation grant BCS-0751508 (to D.E.W.).
NR 51
TC 14
Z9 14
U1 0
U2 8
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 6
PY 2009
VL 106
IS 40
BP 17083
EP 17088
DI 10.1073/pnas.0908377106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 503MD
UT WOS:000270537500041
PM 19805162
ER
PT J
AU Jiao, XD
Yang, ZL
Yang, X
Chen, YH
Tong, ZZ
Zhao, C
Zeng, JX
Chen, HY
Gibbs, D
Sun, XF
Li, B
Wakins, WS
Meyer, C
Wang, XL
Kasuga, D
Bedell, M
Pearson, E
Weinreb, RN
Leske, MC
Hennis, A
Dewan, A
Nemesure, B
Jorde, LB
Hoh, J
Hejtmancik, JF
Zhang, K
AF Jiao, Xiaodong
Yang, Zhenglin
Yang, Xian
Chen, Yuhong
Tong, Zongzhong
Zhao, Chao
Zeng, Jiexi
Chen, Haoyu
Gibbs, Daniel
Sun, Xufang
Li, Bei
Wakins, W. Scott
Meyer, Cynthia
Wang, Xiaolei
Kasuga, Daniel
Bedell, Matthew
Pearson, Erik
Weinreb, Robert N.
Leske, M. Cristina
Hennis, Anselm
DeWan, Andrew
Nemesure, Barbara
Jorde, Lynn B.
Hoh, Josephine
Hejtmancik, J. Fielding
Zhang, Kang
TI Common variants on chromosome 2 and risk of primary open-angle glaucoma
in the Afro-Caribbean population of Barbados
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE association study; linkage analysis; SNP; eye; intraocular pressure
ID GENOME-WIDE SCAN; GENETIC-LINKAGE; FAMILY; LOCUS; MAPS; IDENTIFICATION;
REGION; POAG; CLASSIFICATION; ASSOCIATION
AB Primary open-angle glaucoma (POAG) is the second leading cause of blindness worldwide. Although a number of genetic loci have shown association or genetic linkage to monogenic forms of POAG, the identified genes and loci do not appear to have a major role in the common POAG phenotype. We seek to identify genetic loci that appear to be major risk factors for POAG in the Afro-Caribbean population of Barbados, West Indies. We performed linkage analyses in 146 multiplex families ascertained through the Barbados Family Study of Glaucoma (BFSG) and identified a strong linkage signal on chromosome 2p (logarithm of odds score = 6.64 at theta = 0 with marker D2S2156). We subsequently performed case-control analyses using unrelated affected individuals and unaffected controls. A set of SNPs on chromosome 2p was evaluated in two independent groups of BFSG participants, a discovery group (130 POAG cases, 65 controls) and a replication group (122 POAG cases, 65 controls), and a strong association was identified with POAG and rs12994401 in both groups (P < 3.34 E-09 and P < 1.21E-12, respectively). The associated SNPs form a common disease haplotype. In summary, we have identified a locus with a major impact on susceptibility to the common POAG phenotype in an Afro-Caribbean population in Barbados. Our approach illustrates the merit of using an isolated population enriched with common disease variants as an efficient method to identify genetic underpinning of POAG.
C1 [Leske, M. Cristina; Nemesure, Barbara] SUNY Stony Brook, Sch Med, Dept Prevent Med, Stony Brook, NY 11794 USA.
[Leske, M. Cristina; Nemesure, Barbara] SUNY Stony Brook, Barbados Family Study Grp, Stony Brook, NY 11794 USA.
[Jiao, Xiaodong; Hejtmancik, J. Fielding] NEI, Ophthalm Genet & Visual Funct Branch, Bethesda, MD 20892 USA.
[Jiao, Xiaodong; Hejtmancik, J. Fielding] NIH, Barbados Family Study Grp, Bethesda, MD 20892 USA.
[Yang, Zhenglin; Yang, Xian; Chen, Yuhong; Zhao, Chao; Zeng, Jiexi; Sun, Xufang; Li, Bei; Meyer, Cynthia; Wang, Xiaolei; Kasuga, Daniel; Bedell, Matthew; Weinreb, Robert N.; Zhang, Kang] Univ Calif San Diego, Inst Genom Med, La Jolla, CA 92093 USA.
[Yang, Zhenglin; Yang, Xian; Chen, Yuhong; Zhao, Chao; Zeng, Jiexi; Sun, Xufang; Li, Bei; Meyer, Cynthia; Wang, Xiaolei; Kasuga, Daniel; Bedell, Matthew; Weinreb, Robert N.; Zhang, Kang] Univ Calif San Diego, Shiley Eye Ctr, La Jolla, CA 92093 USA.
[Yang, Zhenglin; Yang, Xian; Chen, Yuhong; Tong, Zongzhong; Zhao, Chao; Zeng, Jiexi; Chen, Haoyu; Gibbs, Daniel; Pearson, Erik; Zhang, Kang] Univ Utah, Sch Med, Moran Eye Ctr, Salt Lake City, UT 84132 USA.
[Wakins, W. Scott; Jorde, Lynn B.] Univ Utah, Sch Med, Dept Human Genet, Salt Lake City, UT 84132 USA.
[DeWan, Andrew; Hoh, Josephine] Yale Univ, Dept Epidemiol & Publ Hlth, Sch Med, New Haven, CT 06520 USA.
[Yang, Xian] Qingdao Univ, Sch Med, Dept Ophthalmol, Qingdao 266021, Peoples R China.
[Yang, Zhenglin] Sichuan Prov Peoples Hosp, Ctr Human Biol & Genet, Sichuan 610072, Peoples R China.
[Chen, Yuhong] Fudan Univ, Dept Ophthalmol & Vis Sci, Eye & ENT Hosp, Shanghai 200031, Peoples R China.
[Zhang, Kang] W China Hosp, Dept Ophthalmol & Ophthalm Labs, Sichuan 610041, Peoples R China.
[Hennis, Anselm] Univ W Indies, Chron Dis Res Ctr, Res Inst Trop Med, Cave Hill, Barbados.
[Hennis, Anselm] Univ W Indies, Barbados Family Study Grp, Cave Hill, Barbados.
RP Nemesure, B (reprint author), SUNY Stony Brook, Sch Med, Dept Prevent Med, Stony Brook, NY 11794 USA.
EM bnemesure@notes.cc.sunysb.edu; josephine.hoh@yale.edu; f3h@nei.nih.gov;
kang.zhang@gmail.com
RI Chen, Haoyu/A-7432-2013; Chu, Kai On/E-2325-2016
OI Chen, Haoyu/0000-0003-0676-4610;
FU National Institutes of Health; Foundation Fighting Blindness; Research
to Prevent Blindness; Burroughs Wellcome Fund
FX We thank the BFSG (the names of investigators are listed below) and
other POAG participants and the staff of the F.H. and K.Z. laboratories.
This work was supported by grants from the National Institutes of Health
(to M.C.L., J.H., J.F.H., and K.Z.), the Foundation Fighting Blindness
(to K.Z.), Research to Prevent Blindness (to K. Z.), and the Burroughs
Wellcome Fund Clinical Scientist Award in Translational Research (to K.
H.). Members of the BFSG are: M. C. L. (Principal Investigator), B.N.,
Qimei He, Suh-Yuh Wu, Nancy Mendell, Lixin Jiang, and Koumudi Manthani
(Coordinating Center, Stony Brook University); A. H., M. Ann Bannister,
Muthu Thangaraj, Rajiv Luthra, Coreen Barrow, and Anthanette Holder
(Data Collection Center, Ministry of Health, Bridgetown, Barbados, West
Indies; Andrew P. Schachat, Judith A. Alexander, Deborah Phillips, and
Reva Ward-Strozykowski (Fundus Photography Reading Center, The Johns
Hopkins University, Baltimore, MD); J.F.H. and X.J. (Laboratory Center,
National Eye Institute); Trevor Hassell, and Henry Fraser (Faculty of
Medicine Sciences, University of the West Indies, Bridgetown, Barbados);
and Clive Gibbons (Queen Elizabeth Hospital, Bridgetown, Barbados)
(Advisory Group).
NR 37
TC 31
Z9 35
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 6
PY 2009
VL 106
IS 40
BP 17105
EP 17110
DI 10.1073/pnas.0907564106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 503MD
UT WOS:000270537500045
PM 19805132
ER
PT J
AU Ranatunga, D
Hedrich, CM
Wang, FY
McVicar, DW
Nowak, N
Joshi, T
Feigenbaum, L
Grant, LR
Stager, S
Bream, JH
AF Ranatunga, Dilini
Hedrich, Christian M.
Wang, Fengying
McVicar, Daniel W.
Nowak, Nathan
Joshi, Trupti
Feigenbaum, Lionel
Grant, Lindsay R.
Staeger, Simona
Bream, Jay H.
TI A human IL10 BAC transgene reveals tissue-specific control of IL-10
expression and alters disease outcome
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE leishmania; LPS; T cell; transgenic; IL-27
ID REGULATORY T-CELLS; HUMAN VISCERAL LEISHMANIASIS; INTERLEUKIN-10
PRODUCTION; IMMUNE CELLS; MICE; GENE; DONOVANI; DISTINCT; LOCUS;
SUSCEPTIBILITY
AB Interleukin (IL)-10 is an immunoregulatory cytokine that is produced by diverse cell populations. Studies in mice suggest that the cellular source of IL-10 is a key determinant in various disease pathologies, yet little is known regarding the control of tissue-specific human IL-10 expression. To assess cell type-specific human IL-10 regulation, we created a human IL-10 transgenic mouse with a bacterial artificial chromosome (hIL10BAC) in which the IL10 gene is positioned centrally. Since human IL-10 is biologically active in the mouse, we could examine the in vivo capacity of tissue-specific human IL-10 expression to recapitulate IL-10-dependent phenotypes by reconstituting Il10(-/-) mice (Il10(-/-)/hIL10BAC). In response to LPS, Il10(-/-)/hIL10BAC mice proficiently regulate IL-10-target genes and normalize sensitivity to LPS toxicity via faithful human IL- 10 expression from macrophages and dendritic cells. However, in the Leishmania donovani model of pathogen persistence, Il10(-/-)/hIL10BAC mice did not develop the characteristic IL-10(+)IFN-gamma(+)CD4 T cell subset thought to mediate persistence and, like Il10(-/-) mice, cleared the parasites. Furthermore, the IL-10-promoting cytokine IL-27 failed to regulate transgenic human IL-10 production in CD4(+) T cells in vitro which together suggests that the hIL10BAC encodes for weak T cell-specific IL-10 expression. Thus, the hIL10BAC mouse is a model of human gene structure and function revealing tissue-specific regulatory requirements for IL-10 expression which impacts disease outcomes.
C1 [Ranatunga, Dilini; Hedrich, Christian M.; Wang, Fengying; Grant, Lindsay R.; Bream, Jay H.] Johns Hopkins Bloomberg Sch Publ Hlth, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA.
[McVicar, Daniel W.] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Nowak, Nathan] Transnetyx Inc, Cordova, TN 38016 USA.
[Joshi, Trupti; Staeger, Simona] Johns Hopkins Sch Med, Baltimore, MD 21205 USA.
[Feigenbaum, Lionel] NCI, SAIC Frederick, Frederick, MD 21702 USA.
RP Bream, JH (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA.
EM jbream@jhsph.edu
RI McVicar, Daniel/G-1970-2015
FU Deutsche Forschungsgemeinschaft (DFG) [HE 5507/1-1]; National Institutes
of Health [5R01AI070594-02]
FX We thank Dr. John O'Shea for his support and careful review of this
manuscript, Dr. Fidel Zavala and Bob Bean for helpful discussions, and
Dr. Mark Kaplan for providing Stat4-/- mice; Paul Fallon and
the Becton Dickinson Immune Function Laboratory for flow cytometry
assistance; and Anitha Moorthy for technical assistance. This work was
supported by Deutsche Forschungsgemeinschaft (DFG) Research Fellowship
HE 5507/1-1 (to C.M.H.) and National Institutes of Health Grant
5R01AI070594-02 to (to J.H.B.).
NR 40
TC 19
Z9 19
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 6
PY 2009
VL 106
IS 40
BP 17123
EP 17128
DI 10.1073/pnas.0904955106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 503MD
UT WOS:000270537500048
PM 19805095
ER
PT J
AU Maheshwari, M
Shi, JJ
Badner, JA
Skol, A
Willour, VL
Muzny, DM
Wheeler, DA
Gerald, FR
Detera-Wadleigh, S
McMahon, FJ
Potash, JB
Gershon, ES
Liu, CY
Gibbs, RA
AF Maheshwari, Manjula
Shi, Jiajun
Badner, Judith A.
Skol, Andrew
Willour, Virginia L.
Muzny, Donna M.
Wheeler, David A.
Gerald, Fowler R.
Detera-Wadleigh, Sevilla
McMahon, Francis J.
Potash, James B.
Gershon, Elliot S.
Liu, Chunyu
Gibbs, Richard A.
TI Common and Rare Variants of DAOA in Bipolar Disorder
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
LA English
DT Article
DE G72; DAOA; bipolar disorder; resequencing; single nucleotide
polymorphism; genetic association
ID GENOME-WIDE ASSOCIATION; AMINO-ACID OXIDASE; SUSCEPTIBILITY LOCUS; MAJOR
DEPRESSION; LINKAGE ANALYSES; HUMAN-DISEASE; SCHIZOPHRENIA; G72/G30;
GENES; METAANALYSIS
AB The D-amino acid oxidase activator (DAOA, previously known as G72) gene, mapped on 13q33, has been reported to be genetically associated with bipolar disorder (BP) in several populations. The consistency of associated variants is unclear and rare variants in exons of the DAOA gene have not been investigated in psychiatric diseases. We employed a conditional linkage method-STatistical Explanation for Positional Cloning (STEPC) to evaluate whether any associated single nucleotide polymorphisms (SNPs) account for the evidence of linkage in a pedigree series that previously has been linked to marker D13S779 at 13q33. We also performed an association study in a sample of 376 Caucasian BP parent-proband trios by genotyping 38 common SNPs in the gene region. Besides, we resequenced coding regions and flanking intronic sequences of DAOA in 555 Caucasian unrelated BP patients and 564 mentally healthy controls, to identify putative functional rare variants that may contribute to disease. One SNP rs1935058 cotdd "explain" the linkage signal in the family sample set (P = 0.055) using STEPC analysis. No significant allelic association was detected in an association study by genotyping 38 common SNPs in 376 Caucasian BP trios. Resequencing identified 53 SNPs, of which 46 were novel SNPs. There was no significant excess of rare variants in cases relative to controls. Our results suggest that DAOA does not have a major effect on BP susceptibility. However, DAOA may contribute to bipolar susceptibility in some specific families as evidenced by the STEPC analysis. (C) 2009 Wiley-Liss, Inc.
C1 [Liu, Chunyu] Univ Chicago, Dept Psychiat, Knapp Ctr, Chicago, IL 60637 USA.
[Maheshwari, Manjula; Muzny, Donna M.; Wheeler, David A.; Gerald, Fowler R.; Gibbs, Richard A.] Baylor Coll Med, Human Genome Sequencing Ctr, Dept Mol, Houston, TX 77030 USA.
[Maheshwari, Manjula; Muzny, Donna M.; Wheeler, David A.; Gerald, Fowler R.; Gibbs, Richard A.] Baylor Coll Med, Dept Human Genet, Houston, TX 77030 USA.
[Skol, Andrew] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Willour, Virginia L.; Potash, James B.] Johns Hopkins Sch Med, Dept Psychiat, Baltimore, MD USA.
[Detera-Wadleigh, Sevilla; McMahon, Francis J.] NIMH, Genet Basis Mood & Anxiety Disorders Unit, Mood & Anxiety Program, NIH,US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Gershon, Elliot S.] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA.
RP Liu, CY (reprint author), Univ Chicago, Dept Psychiat, Knapp Ctr, 924 E 57th St,R012, Chicago, IL 60637 USA.
EM cliu@yoda.bsd.uchicago.edu
RI Liu, Chunyu/G-7561-2012;
OI Liu, Chunyu/0000-0002-5986-4415; McMahon, Francis/0000-0002-9469-305X
FU National Institute of Mentat Health (NIMH) [R01MH061613, R01 MH042243,
1R21MH083521]; National Alliance for Research on Schizophrenia and
Depression (NARSAD); Brain Research Foundation, University of Chicago;
Geraldi Norton Foundation
FX Grant sponsor: National Institute of Mentat Health (NIMH); Grant
numbers: R01MH061613, R01 MH042243, 1R21MH083521; Grant sponsor:
National Alliance for Research on Schizophrenia and Depression (NARSAD);
Grant sponsor: Brain Research Foundation at the University of Chicago;
Grant sponsor: Geraldi Norton Foundation.
NR 49
TC 9
Z9 10
U1 2
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4841
J9 AM J MED GENET B
JI Am. J. Med. Genet. B
PD OCT 5
PY 2009
VL 150B
IS 7
BP 960
EP 966
DI 10.1002/ajmg.b.30925
PG 7
WC Genetics & Heredity; Psychiatry
SC Genetics & Heredity; Psychiatry
GA 502FN
UT WOS:000270441100009
PM 19194963
ER
PT J
AU Grover, D
Verma, R
Goes, FS
Mahon, PLB
Gershon, ES
McMahon, FJ
Potash, JB
AF Grover, Deepak
Verma, Ranjana
Goes, Fernando S.
Mahon, Pamela L. Belmonte
Gershon, Elliot S.
McMahon, Francis J.
Potash, James B.
CA NIMH Genetics Initiative Bipolar C
Bipolar Disorder Phenome Grp
TI Family-Based Association of YWHAH in Psychotic Bipolar Disorder
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
LA English
DT Article
DE YWHAH; bipolar disorder; schizophrenia; psychosis; 14-3-3
ID GENOME SCAN METAANALYSIS; ETA CHAIN GENE; SUSCEPTIBILITY LOCUS;
CANDIDATE GENES; 14-3-3 PROTEIN; DIAGNOSTIC INTERVIEW; SUGGESTIVE
LINKAGE; WIDE ASSOCIATION; SCHIZOPHRENIA; PEDIGREES
AB YWHAH is a positional and functional candidate gene for both schizophrenia and bipolar disorder (BP). This gene has been previously shown to be associated with both disorders, and the chromosome location (22q12.3) has been repeatedly implicated in linkage studies for these disorders. It codes for the eta subtype of the 14-3-3 protein family, is expressed mainly in brain, and is involved in HPA axis regulation. We investigated the association of YWMAH with BP in a large sample, consisting of 1211 subjects from 318 nuclear families including 554 affected offspring. We tested for association with the standard BP phenotype as well as subtypes defined by psychotic and mood-incongruent features. We genotyped five tag SNPs and the (GCCTGCA)(n) polymorphic locus present in this gene. Using a family-based association test, we found that rs2246704 was associated with BP (OR 1.31, P = 0.03) and psychotic BP (OR = 1.66, P = 0.002). The polymorphic repeat and two other SNPs were also modestly associated with psychotic BP. We have provided additional evidence for association of variants in YWHAH with major mental illness. Additional association analyses of larger sample sets will be required to clarify the role of YWHAH in schizophrenia and BP. The use of clinical sub-phenotypes such as psychotic features or other potential schizophrenia/BP overlap variables including cognitive abnormalities and poor functioning might shed further light on the potential subtypes of illness most closely associated with genetic variation in YWHAH. (C) 2009 Wiley-Liss, Inc.
C1 [Grover, Deepak; Verma, Ranjana; Goes, Fernando S.; Mahon, Pamela L. Belmonte; Potash, James B.] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21287 USA.
[Gershon, Elliot S.] Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA.
[McMahon, Francis J.] NIMH, Genet Basis Mood & Anxiety Disorders Unit, Mood & Anxiety Program, NIH,US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Potash, JB (reprint author), Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Meyer 4-119,600 N Wolfe St, Baltimore, MD 21287 USA.
EM jpotash@jhmi.edu
RI Meyer, Eric/C-1029-2011;
OI Meyer, Eric/0000-0002-1998-7162; Nurnberger, John/0000-0002-7674-1767;
McMahon, Francis/0000-0002-9469-305X; Edenberg,
Howard/0000-0003-0344-9690
FU NIMH [R01 MH-042243, R01 MH-061613]; National Alliance for Research on
Schizophrenia and Depression; Stanley Medical Research Institute; NIMH
Intramural Research Program
FX Grant sponsor: NIMH; Grant number: R01 MH-042243; Grant number: R01
MH-061613; Grant sponsor: National Alliance for Research on
Schizophrenia and Depression; Grant sponsor: Stanley Medical Research
Institute; Funder: NIMH Intramural Research Program.
NR 36
TC 27
Z9 27
U1 0
U2 4
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4841
J9 AM J MED GENET B
JI Am. J. Med. Genet. B
PD OCT 5
PY 2009
VL 150B
IS 7
BP 977
EP 983
DI 10.1002/ajmg.b.30927
PG 7
WC Genetics & Heredity; Psychiatry
SC Genetics & Heredity; Psychiatry
GA 502FN
UT WOS:000270441100011
PM 19160447
ER
PT J
AU Jackson, MS
Lee, JC
AF Jackson, Mark S.
Lee, Jennifer C.
TI Identification of the Minimal Copper(II)-Binding alpha-Synuclein
Sequence
SO INORGANIC CHEMISTRY
LA English
DT Article
ID AMYOTROPHIC-LATERAL-SCLEROSIS; AMYLOID-BETA PEPTIDE; HUMAN PRION
PROTEIN; COPPER-BINDING SITES; PARKINSONS-DISEASE; ALZHEIMERS-DISEASE;
METAL-BINDING; NEURODEGENERATIVE DISORDERS; PHYSIOLOGICAL PH; CU(II)
AB Parkinson's disease has been long linked to environmental factors, such as transition metals and recently to alpha-synuclein, a presynaptic protein. Using tryptophan-containing peptides, we identified the minimal Cu(II)-binding sequence to be within the first four residues, MDV(F/W), anchored by the alpha-amino terminus. In addition, mutant peptide 1 - 10 (Lys -> Arg) verified that neither Lys6 nor Lys10 are necessary for Cu(II) binding. Interestingly, Trp4 excited-state decay kinetics measured for peptides and proteins reveal two quenching modes, possibly arising from two distinct Cu(II)-polypeptide structures.
C1 [Jackson, Mark S.; Lee, Jennifer C.] NHLBI, Lab Mol Biophys, NIH, Bethesda, MD 20892 USA.
RP Lee, JC (reprint author), NHLBI, Lab Mol Biophys, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM leej4@mail.nih.gov
RI Lee, Jennifer/E-9658-2015
OI Lee, Jennifer/0000-0003-0506-8349
FU National Institutes of Health, National Heart, Lung, and Blood Institute
FX This work is supported by the Intramural Research Program of the
National Institutes of Health, National Heart, Lung, and Blood
Institute. We thank Hank Fales (Laboratory of Applied Mass Spectrometry,
NHLBI) for technical assistance with ESI-MS, Candace Pfefferkorn for
purifying the F4W protein, and Heather Lucas for helpful discussions.
NR 46
TC 36
Z9 37
U1 0
U2 7
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0020-1669
J9 INORG CHEM
JI Inorg. Chem.
PD OCT 5
PY 2009
VL 48
IS 19
BP 9303
EP 9307
DI 10.1021/ic901157w
PG 5
WC Chemistry, Inorganic & Nuclear
SC Chemistry
GA 497VJ
UT WOS:000270091000035
PM 19780617
ER
PT J
AU O'Connell, CB
Loncarek, J
Kalab, P
Khodjakov, A
AF O'Connell, Christopher B.
Loncarek, Jadranka
Kalab, Petr
Khodjakov, Alexey
TI Relative contributions of chromatin and kinetochores to mitotic spindle
assembly
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID XENOPUS EGG EXTRACTS; CELL-CYCLE PROGRESSION; MICROTUBULE DYNAMICS;
FIBERS CONTRIBUTES; SELF-ORGANIZATION; VERTEBRATE CELLS;
MAMMALIAN-CELLS; RANGTP GRADIENT; HELA-CELLS; MITOSIS
AB During mitosis and meiosis in animal cells, chromosomes actively participate in spindle assembly by generating a gradient of Ran guanosine triphosphate (RanGTP). A high concentration of RanGTP promotes microtubule nucleation and stabilization in the vicinity of chromatin. However, the relative contributions of chromosome arms and centromeres/kinetochores in this process are not known. In this study, we address this issue using cells undergoing mitosis with unreplicated genomes (MUG). During MUG, chromatin is rapidly separated from the forming spindle, and both centrosomal and noncentrosomal spindle assembly pathways are active. MUG chromatin is coated with RCC1 and establishes a RanGTP gradient. However, a robust spindle forms around kinetochores/centromeres outside of the gradient peak. When stable kinetochore microtubule attachment is prevented by Nuf2 depletion in both MUG and normal mitosis, chromatin attracts astral microtubules but cannot induce spindle assembly. These results support a model in which kinetochores play the dominant role in the chromosomemediated pathway of mitotic spindle assembly.
C1 [O'Connell, Christopher B.; Loncarek, Jadranka; Khodjakov, Alexey] New York State Dept Hlth, Wadsworth Ctr, Div Translat Med, Albany, NY 12201 USA.
[Kalab, Petr] NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA.
RP O'Connell, CB (reprint author), New York State Dept Hlth, Wadsworth Ctr, Div Translat Med, Albany, NY 12201 USA.
EM oconnell@wadsworth.org
RI Kalab, Petr/B-2478-2009
FU National Institutes of Health [59363]; Kirschstein National Research
Service Award [GM077911]; National Institutes of Health Program Z01 [BC
011084]
FX This work was supported by a grant from the National Institutes of
Health (GMS 59363) to A. Khodjakov, a Kirschstein National Research
Service Award postdoctoral fellowship (GM077911) to C. B. O'Connell, and
National Institutes of Health Program Z01 (BC 011084) to P. Kalab.
NR 37
TC 37
Z9 37
U1 0
U2 1
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
J9 J CELL BIOL
JI J. Cell Biol.
PD OCT 5
PY 2009
VL 187
IS 1
BP 43
EP 51
DI 10.1083/jcb.200903076
PG 9
WC Cell Biology
SC Cell Biology
GA 502IU
UT WOS:000270452800007
PM 19805628
ER
PT J
AU Nicolescu, AC
Holt, A
Kandasamy, AD
Pacher, P
Schulz, R
AF Nicolescu, Adrian C.
Holt, Andrew
Kandasamy, Arulmozhi D.
Pacher, Pal
Schulz, Richard
TI Inhibition of matrix metalloproteinase-2 by PARP inhibitors
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Matrix metalloproteinase-2; Oxidative stress; Peroxynitrite;
Poly(ADP-ribosyl)polymerase
ID ISCHEMIA-REPERFUSION INJURY; ISOLATED RAT HEARTS; PHARMACOLOGICAL
INHIBITION; CARDIOVASCULAR-DISEASES; PEROXYNITRITE; FAILURE; ZINC;
POLY(ADP-RIBOSE); POLYMERASE; CONTRIBUTES
AB Matrix metalloproteinase-2 (MMP-2), a ubiquitously expressed zinc-dependent endopeptidase, and poly(ADP-ribosyl) polymerase (PARP), a nuclear enzyme regulating DNA repair, are activated by nitroxidative stress associated with various pathologies. As MMP-2 plays a detrimental role in heart injuries resulting from enhanced nitroxidative stress, where PARP and MMP inhibitors are beneficial, we hypothesized that PARP inhibitors may affect MMP-2 activity. Using substrate degradation assays to determine MMP-2 activity we found that four PARP inhibitors (3-AB, PJ-34, 5-AIQ, and EB-47) inhibited 64 kDa MMP-2 in a concentration-dependent manner. The IC(50) values of PJ-34 and 5-AIQ were in the high micromolar range and comparable to those of known MMP-2 inhibitors doxycycline, minocycline or o-phenanthroline, whereas those for 3-AB and EB-47 were in the millimolar range. Co-incubation of PARP inhibitors with doxycycline showed an additive inhibition of MMP-2 that was significant for 3-AB alone. These data demonstrate that the protective effects of some PARP inhibitors may include inhibition of MMP-2 activity. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Nicolescu, Adrian C.; Holt, Andrew; Kandasamy, Arulmozhi D.; Schulz, Richard] Univ Alberta, Dept Pharmacol, Cardiovasc Res Ctr, Edmonton, AB T6G 2S2, Canada.
[Nicolescu, Adrian C.; Holt, Andrew; Kandasamy, Arulmozhi D.; Schulz, Richard] Univ Alberta, Dept Pediat, Cardiovasc Res Ctr, Edmonton, AB T6G 2S2, Canada.
[Pacher, Pal] NIAAA, NIH, Lab Physiol Studies, Bethesda, MD USA.
RP Schulz, R (reprint author), Univ Alberta, Dept Pharmacol, Cardiovasc Res Ctr, Edmonton, AB T6G 2S2, Canada.
EM richard.schulz@ualberta.ca
RI Nicolescu, Adrian/B-9735-2011; Schulz, Richard/A-8739-2012; Pacher,
Pal/B-6378-2008;
OI Schulz, Richard/0000-0002-5045-3193; Pacher, Pal/0000-0001-7036-8108;
Nicolescu, Adrian/0000-0002-1721-4684
FU Canadian Institute of Health Research [MOP-77526, MOP-77529]; NIH/NIAAA;
Alberta Heritage Foundation; Heart and Stroke Foundation of Canada
FX This project was supported by Canadian Institute of Health Research
operating grants MOP-77526 to R. S. and MOP-77529 to A. H., and by the
Intramural Program of NIH/NIAAA to P. P. R. S. is a Senior Scientist of
the Alberta Heritage Foundation for Medical Research. A. C. N. is a
recipient of Alberta Heritage Foundation for Medical Research and Heart
and Stroke Foundation of Canada Fellowships. We thank Owen Degenhardt
for technical assistance.
NR 38
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 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD OCT 2
PY 2009
VL 387
IS 4
BP 646
EP 650
DI 10.1016/j.bbrc.2009.07.080
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 555SF
UT WOS:000274534000005
PM 19619515
ER
PT J
AU Xiao, Y
Gao, XG
Taratula, O
Treado, S
Urbas, A
Holbrook, RD
Cavicchi, RE
Avedisian, CT
Mitra, S
Savla, R
Wagner, PD
Srivastava, S
He, HX
AF Xiao, Yan
Gao, Xiugong
Taratula, Oleh
Treado, Stephen
Urbas, Aaron
Holbrook, R. David
Cavicchi, Richard E.
Avedisian, C. Thomas
Mitra, Somenath
Savla, Ronak
Wagner, Paul D.
Srivastava, Sudhir
He, Huixin
TI Anti-HER2 IgY antibody-functionalized single-walled carbon nanotubes for
detection and selective destruction of breast cancer cells
SO BMC CANCER
LA English
DT Article
ID RAMAN-SPECTROSCOPY; YOLK ANTIBODIES; MEDICAL APPLICATIONS; DELIVERY;
GENE; DRUG; NANOPARTICLES; TRANSPORTERS; FLUORESCENCE; INFECTIONS
AB Background: Nanocarrier-based antibody targeting is a promising modality in therapeutic and diagnostic oncology. Single-walled carbon nanotubes (SWNTs) exhibit two unique optical properties that can be exploited for these applications, strong Raman signal for cancer cell detection and near-infrared (NIR) absorbance for selective photothermal ablation of tumors. In the present study, we constructed a HER2 IgY-SWNT complex and demonstrated its dual functionality for both detection and selective destruction of cancer cells in an in vitro model consisting of HER2-expressing SK-BR-3 cells and HER2-negative MCF-7 cells.
Methods: The complex was constructed by covalently conjugating carboxylated SWNTs with anti-HER2 chicken IgY antibody, which is more specific and sensitive than mammalian IgGs. Raman signals were recorded on Raman spectrometers with a laser excitation at 785 nm. NIR irradiation was performed using a diode laser system, and cells with or without nanotube treatment were irradiated by 808 nm laser at 5 W/cm(2) for 2 min. Cell viability was examined by the calcein AM/ethidium homodimer-1 (EthD-1) staining.
Results: Using a Raman optical microscope, we found the Raman signal collected at single-cell level from the complex-treated SK-BR-3 cells was significantly greater than that from various control cells. NIR irradiation selectively destroyed the complex-targeted breast cancer cells without harming receptor-free cells. The cell death was effectuated without the need of internalization of SWNTs by the cancer cells, a finding that has not been reported previously.
Conclusion: We have demonstrated that the HER2 IgY-SWNT complex specifically targeted HER2-expressing SK-BR-3 cells but not receptor-negative MCF-7 cells. The complex can be potentially used for both detection and selective photothermal ablation of receptor-positive breast cancer cells without the need of internalization by the cells. Thus, the unique intrinsic properties of SWNTs combined with high specificity and sensitivity of IgY antibodies can lead to new strategies for cancer detection and therapy.
C1 [Xiao, Yan; Urbas, Aaron; Holbrook, R. David; Cavicchi, Richard E.] NIST, Chem Sci & Technol Lab, Gaithersburg, MD 20899 USA.
[Gao, Xiugong] Translabion, Res & Dev, Clarksburg, MD USA.
[Taratula, Oleh; Savla, Ronak; He, Huixin] Rutgers State Univ, Dept Chem, Newark, NJ 07102 USA.
[Treado, Stephen] NIST, Bldg Environm Div, Gaithersburg, MD 20899 USA.
[Avedisian, C. Thomas; Srivastava, Sudhir] Cornell Univ, Sibley Sch Mech & Aerosp Engn, Ithaca, NY 14853 USA.
New Jersey Inst Technol, Dept Chem & Environm Sci, Newark, NJ 07102 USA.
[Wagner, Paul D.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Xiao, Y (reprint author), NIST, Chem Sci & Technol Lab, Gaithersburg, MD 20899 USA.
EM yan.xiao@nist.gov; xiugong.gao@translabion.com; olehtaratula@gmail.com;
stephen.treado@nist.gov; aaron.urbas@nist.gov; dave.holbrook@nist.gov;
richard.cavicchi@nist.gov; cta2@cornell.edu; somenath.mitra@njit.edu;
rsavla@eden.rutgers.edu; wagnerp@mail.nih.gov; srivasts@mail.nih.gov;
huixinhe@newark.rutgers.edu
FU NCI-Early Detection Research Network joint NIST-Biochemical Science
Division Interagency Agreement [Y1 CN5001]; National Science Foundation
(NSF) [CHE-0750201]; New York State Office of Science, Technology, and
Academic Research
FX We thank Joseph Hodges and Kristen Steffens of NIST for their help with
the laser radiation apparatus. This work was supported by NCI-Early
Detection Research Network joint NIST-Biochemical Science Division
Interagency Agreement # Y1 CN5001 and in part by National Science
Foundation (NSF) Grant # CHE-0750201. The contribution of CTA was
supported partly by the New York State Office of Science, Technology,
and Academic Research. Certain commercial equipment or materials are
identified in this paper in order to specify adequately the experimental
procedures. Such identification does not imply recommendation or
endorsement by the National Institute of Standards and Technology, nor
does it imply that the materials or equipment identified are necessarily
the best available for the purpose.
NR 51
TC 68
Z9 71
U1 1
U2 40
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD OCT 2
PY 2009
VL 9
AR 351
DI 10.1186/1471-2407-9-351
PG 11
WC Oncology
SC Oncology
GA 510WZ
UT WOS:000271125500002
PM 19799784
ER
PT J
AU Nishiyama, A
Xin, L
Sharov, AA
Thomas, M
Mowrer, G
Meyers, E
Piao, YL
Mehta, S
Yee, S
Nakatake, Y
Stagg, C
Sharova, L
Correa-Cerro, LS
Bassey, U
Hoang, H
Kim, E
Tapnio, R
Qian, Y
Dudekula, D
Zalzman, M
Li, MX
Falco, G
Yang, HT
Lee, SL
Monti, M
Stanghellini, I
Islam, MN
Nagaraja, R
Goldberg, I
Wang, WD
Longo, DL
Schlessinger, D
Ko, MSH
AF Nishiyama, Akira
Xin, Li
Sharov, Alexei A.
Thomas, Marshall
Mowrer, Gregory
Meyers, Emily
Piao, Yulan
Mehta, Samir
Yee, Sarah
Nakatake, Yuhki
Stagg, Carole
Sharova, Lioudmila
Correa-Cerro, Lina S.
Bassey, Uwem
Hoang, Hien
Kim, Eugene
Tapnio, Richard
Qian, Yong
Dudekula, Dawood
Zalzman, Michal
Li, Manxiang
Falco, Geppino
Yang, Hsih-Te
Lee, Sung-Lim
Monti, Manuela
Stanghellini, Ilaria
Islam, Md. Nurul
Nagaraja, Ramaiah
Goldberg, Ilya
Wang, Weidong
Longo, Dan L.
Schlessinger, David
Ko, Minoru S. H.
TI Uncovering Early Response of Gene Regulatory Networks in ESCs by
Systematic Induction of Transcription Factors
SO CELL STEM CELL
LA English
DT Article
ID EMBRYONIC STEM-CELLS; GENOME-WIDE; DEVELOPMENTAL REGULATORS; SIGNALING
PATHWAYS; MOUSE EMBRYOS; SELF-RENEWAL; PLURIPOTENCY; EXPRESSION;
DIFFERENTIATION; CHROMATIN
AB To examine transcription factor (TF) network(s), we created mouse ESC lines, in each of which 1 of 50 TFs tagged with a FLAG moiety is inserted into a ubiquitously controllable tetracycline-repressible locus. Of the 50 TFs, Cdx2 provoked the most extensive transcriptome perturbation in ESCs, followed by Esx1, Sox9, Tcf3, KIN, and Gata3. ChIP-Seq revealed that CDX2 binds to promoters of upregulated target genes. By contrast, genes downregulated by CDX2 did not show CDX2 binding but were enriched with binding sites for POU5F1, SOX2, and NANOG. Genes with binding sites for these core TFs were also downregulated by the induction of at least 15 other TFs, suggesting a common initial step for ESC differentiation mediated by interference with the binding of core TFs to their target genes. These ESC lines provide a fundamental resource to study biological networks in ESCs and mice.
C1 [Nishiyama, Akira; Xin, Li; Sharov, Alexei A.; Thomas, Marshall; Mowrer, Gregory; Meyers, Emily; Piao, Yulan; Mehta, Samir; Yee, Sarah; Nakatake, Yuhki; Stagg, Carole; Sharova, Lioudmila; Correa-Cerro, Lina S.; Bassey, Uwem; Hoang, Hien; Kim, Eugene; Tapnio, Richard; Qian, Yong; Dudekula, Dawood; Zalzman, Michal; Li, Manxiang; Falco, Geppino; Yang, Hsih-Te; Lee, Sung-Lim; Monti, Manuela; Stanghellini, Ilaria; Islam, Md. Nurul; Nagaraja, Ramaiah; Goldberg, Ilya; Wang, Weidong; Longo, Dan L.; Schlessinger, David; Ko, Minoru S. H.] NIA, NIH, Baltimore, MD 21224 USA.
RP Ko, MSH (reprint author), NIA, NIH, Baltimore, MD 21224 USA.
EM kom@mail.nih.gov
RI Goldberg, Ilya/H-5307-2011; Ko, Minoru/B-7969-2009; Nakatake,
Yuhki/K-5405-2013;
OI Goldberg, Ilya/0000-0001-8514-6110; Ko, Minoru/0000-0002-3530-3015;
Dudekula, Dawood/0000-0002-4054-1827
FU Intramural Research Program of the NIH, National Institute on Aging
FX We thank Dr. Hitoshi Niwa for providing the Tet-inducible vector system
and some cDNA clones and for discussion. This research was supported
entirely by the Intramural Research Program of the NIH, National
Institute on Aging.
NR 59
TC 105
Z9 107
U1 1
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1934-5909
EI 1875-9777
J9 CELL STEM CELL
JI Cell Stem Cell
PD OCT 2
PY 2009
VL 5
IS 4
BP 420
EP 433
DI 10.1016/j.stem.2009.07.012
PG 14
WC Cell & Tissue Engineering; Cell Biology
SC Cell Biology
GA 514NP
UT WOS:000271401900013
PM 19796622
ER
PT J
AU Nakano, T
Katafuchi, A
Matsubara, M
Terato, H
Tsuboi, T
Masuda, T
Tatsumoto, T
Pack, SP
Makino, K
Croteau, DL
Van Houten, B
Iijima, K
Tauchi, H
Ide, H
AF Nakano, Toshiaki
Katafuchi, Atsushi
Matsubara, Mayumi
Terato, Hiroaki
Tsuboi, Tomohiro
Masuda, Tasuku
Tatsumoto, Takahiro
Pack, Seung Pil
Makino, Keisuke
Croteau, Deborah L.
Van Houten, Bennett
Iijima, Kenta
Tauchi, Hiroshi
Ide, Hiroshi
TI Homologous Recombination but Not Nucleotide Excision Repair Plays a
Pivotal Role in Tolerance of DNA-Protein Cross-links in Mammalian Cells
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID GUANINE LESIONS; UVRABC NUCLEASE; IN-VIVO; DAMAGE; METHYLTRANSFERASE;
PATHWAY; 5-AZA-2'-DEOXYCYTIDINE; FORMALDEHYDE; INHIBITION; ACTIVATION
AB DNA-protein cross-links (DPCs) are unique among DNA lesions in their unusually bulky nature. The steric hindrance imposed by cross-linked proteins (CLPs) will hamper DNA transactions, such as replication and transcription, posing an enormous threat to cells. In bacteria, DPCs with small CLPs are eliminated by nucleotide excision repair (NER), whereas oversized DPCs are processed exclusively by RecBCD-dependent homologous recombination (HR). Here we have assessed the roles of NER and HR for DPCs in mammalian cells. We show that the upper size limit of CLPs amenable to mammalian NER is relatively small (8-10 kDa) so that NER cannot participate in the repair of chromosomal DPCs in mammalian cells. Moreover, CLPs are not polyubiquitinated and hence are not subjected to proteasomal degradation prior to NER. In contrast, HR constitutes the major pathway in tolerance of DPCs as judged from cell survival and RAD51 and gamma-H2AX nuclear foci formation. Induction of DPCs results in the accumulation of DNA double strand breaks in HR-deficient but not HR-proficient cells, suggesting that fork breakage at the DPC site initiates HR and reactivates the stalled fork. DPCs activate both ATR and ATM damage response pathways, but there is a time lag between two responses. These results highlight the differential involvement of NER in the repair of DPCs in bacterial and mammalian cells and demonstrate the versatile and conserved role of HR in tolerance of DPCs among species.
C1 [Nakano, Toshiaki; Katafuchi, Atsushi; Matsubara, Mayumi; Terato, Hiroaki; Tsuboi, Tomohiro; Masuda, Tasuku; Tatsumoto, Takahiro; Ide, Hiroshi] Hiroshima Univ, Grad Sch Sci, Dept Math & Life Sci, Higashihiroshima 7398526, Japan.
[Pack, Seung Pil] Korea Univ, Dept Biotechnol & Bioinformat, Jochiwon 339700, Chungnam, South Korea.
[Makino, Keisuke] Kyoto Univ, Inst Adv Energy, Uji 6110011, Japan.
[Croteau, Deborah L.; Van Houten, Bennett] NIEHS, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Iijima, Kenta; Tauchi, Hiroshi] Ibaraki Univ, Fac Sci, Dept Environm Sci, Mito, Ibaraki 3108512, Japan.
RP Ide, H (reprint author), Hiroshima Univ, Grad Sch Sci, Dept Math & Life Sci, Higashihiroshima 7398526, Japan.
EM ideh@hiroshima-u.ac.jp
FU Japan Society for the Promotion of Science; Ministry of Education,
Culture, Sports, Science and Technology
FX This work was supported in part by Grants-in-aid for Scientific Research
from the Japan Society for the Promotion of Science (to T. N., H. T.,
and H. I.) and by a Grant-in-aid for the Scientific Research on Priority
Areas from the Ministry of Education, Culture, Sports, Science and
Technology (to H. I.).
NR 41
TC 46
Z9 47
U1 0
U2 6
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 2
PY 2009
VL 284
IS 40
BP 27065
EP 27076
DI 10.1074/jbc.M109.019174
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 499OJ
UT WOS:000270232300008
PM 19674975
ER
PT J
AU Sonoda, A
Iwamoto, T
Nakamura, T
Fukumoto, E
Yoshizaki, K
Yamada, A
Arakaki, M
Harada, H
Nonaka, K
Nakamura, S
Yamada, Y
Fukumoto, S
AF Sonoda, Akira
Iwamoto, Tsutomu
Nakamura, Takashi
Fukumoto, Emiko
Yoshizaki, Keigo
Yamada, Aya
Arakaki, Makiko
Harada, Hidemitsu
Nonaka, Kazuaki
Nakamura, Seiji
Yamada, Yoshihiko
Fukumoto, Satoshi
TI Critical Role of Heparin Binding Domains of Ameloblastin for Dental
Epithelium Cell Adhesion and Ameloblastoma Proliferation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID LAMININ ALPHA-1 CHAIN; ODONTOGENIC-TUMORS; ENAMEL PROTEINS;
IMMUNOHISTOCHEMICAL-DEMONSTRATION; TOOTH DEVELOPMENT; CALCIUM-BINDING;
ROOT SHEATH; GENE; DIFFERENTIATION; EXPRESSION
AB AMBN (ameloblastin) is an enamel matrix protein that regulates cell adhesion, proliferation, and differentiation of ameloblasts. In AMBN-deficient mice, ameloblasts are detached from the enamel matrix, continue to proliferate, and form a multiple cell layer; often, odontogenic tumors develop in the maxilla with age. However, the mechanism of AMBN functions in these biological processes remains unclear. By using recombinant AMBN proteins, we found that AMBN had heparin binding domains at the C-terminal half and that these domains were critical for AMBN binding to dental epithelial cells. Overexpression of full-length AMBN protein inhibited proliferation of human ameloblastoma AM-1 cells, but overexpression of heparin binding domain-deficient AMBN protein had no inhibitory effect. In full-length AMBN-overexpressing AM-1 cells, the expression of Msx2, which is involved in the dental epithelial progenitor phenotype, was decreased, whereas the expression of cell proliferation inhibitors p21 and p27 was increased. We also found that the expression of enamelin, a marker of differentiated ameloblasts, was induced, suggesting that AMBN promotes odontogenic tumor differentiation. Thus, our results suggest that AMBN promotes cell binding through the heparin binding sites and plays an important role in preventing odontogenic tumor development by suppressing cell proliferation and maintaining differentiation phenotype through Msx2, p21, and p27.
C1 [Sonoda, Akira; Yoshizaki, Keigo; Nonaka, Kazuaki; Fukumoto, Satoshi] Kyushu Univ, Sect Pediat Dent, Div Oral Hlth Growth & Dev, Fukuoka 8128582, Japan.
[Sonoda, Akira; Nakamura, Seiji] Kyushu Univ, Dept Oral & Maxillofacial Surg 1, Fac Dent Sci, Fukuoka 8128582, Japan.
[Iwamoto, Tsutomu; Nakamura, Takashi; Fukumoto, Emiko; Yamada, Aya; Arakaki, Makiko; Fukumoto, Satoshi] Tohoku Univ, Grad Sch Dent, Dept Oral Hlth & Dev Sci, Div Pediat Dent, Sendai, Miyagi 9808575, Japan.
[Nakamura, Takashi; Yamada, Yoshihiko] NIDCR, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA.
[Harada, Hidemitsu] Iwate Med Coll, Sch Dent, Dept Oral Anat 2, Morioka, Iwate 0208505, Japan.
RP Fukumoto, S (reprint author), Kyushu Univ, Sect Pediat Dent, Div Oral Hlth Growth & Dev, Fukuoka 8128582, Japan.
EM fukumoto@mail.tains.tohoku.ac.jp
RI Nakamura, Takashi/P-7796-2016
OI Nakamura, Takashi/0000-0001-9904-1037
FU Intramural Program of the National Institutes of Health, NIDCR; Ministry
of Education, Science and Culture of Japan [17689058]; Japan Society for
the Promotion of Science [20679006]
FX This work was supported, in whole or in part, by the Intramural Program
of the National Institutes of Health, NIDCR (to Y.Y.). This work was
also supported in part by Ministry of Education, Science and Culture of
Japan Grants-in-aid for Research Fellows of the Japan Society for the
Promotion of Science 17689058 and 20679006 (to S. F.).
NR 47
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Z9 29
U1 1
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 2
PY 2009
VL 284
IS 40
BP 27176
EP 27184
DI 10.1074/jbc.M109.033464
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 499OJ
UT WOS:000270232300018
PM 19648121
ER
PT J
AU Hu, KN
Havlin, RH
Yau, WM
Tycko, R
AF Hu, Kan-Nian
Havlin, Robert H.
Yau, Wai-Ming
Tycko, Robert
TI Quantitative Determination of Site-Specific Conformational Distributions
in an Unfolded Protein by Solid-State Nuclear Magnetic Resonance
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE solid-state NMR; protein folding; villin; HP35; polyproline II
ID VILLIN HEADPIECE SUBDOMAIN; RESIDUAL DIPOLAR COUPLINGS; C-13
CHEMICAL-SHIFT; ULTRAFAST FOLDING PROTEIN; POLYPROLINE-II HELIX;
ANGLE-SPINNING NMR; MOLECULAR-DYNAMICS SIMULATIONS; FREE-ENERGY
LANDSCAPE; LONG-RANGE STRUCTURE; 8 M UREA
AB Solid-state nuclear magnetic resonance (NMR) techniques are used to investigate the structure of the 35-residue villin headpiece subdomain (HP35) in folded, partially denatured, and fully denatured states. Experiments are carried out in frozen glycerol/water solutions, with chemical denaturation by guanidine hydrochloride (GdnHCl). Without GdnHCl, two-dimensional solid-state (13)C NMR spectra of samples prepared with uniform (13)C labeling of selected residues show relatively sharp cross-peaks at chemical shifts that are consistent with the known three-helix bundle structure of folded HP35. At high GdnHCl concentrations, most cross-peaks broaden and shift, qualitatively indicating disruption of the folded structure and development of static conformational disorder in the frozen denatured state. Conformational distributions at one residue in each helical segment are probed quantitatively with three solid-state NMR techniques that provide independent constraints on backbone phi and psi torsion angles in samples with sequential pairs of carbonyl (13)C labels. Without GdnHCl, the combined data are well fit by alpha-helical conformations. At [GdnHCl] = 4.5 M, corresponding to the approximate denaturation midpoint, the combined data are well fit by a combination of alpha-helical and partially extended conformations at each site, but with a site-dependent population ratio. At [GdnHCl] = 7.0 M, corresponding to the fully denatured state, the combined data are well fit by a combination of partially extended and polyproline 11 conformations, again with a site-dependent population ratio. Two entirely different models for conformational distributions lead to nearly the same best-fit distributions, demonstrating the robustness of these conclusions. This work represents the first quantitative investigation of site-specific conformational distributions in partially folded and unfolded states of a protein by solid-state NMR. Published by Elsevier Ltd.
C1 [Hu, Kan-Nian; Havlin, Robert H.; Yau, Wai-Ming; Tycko, Robert] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Tycko, R (reprint author), NIDDK, Chem Phys Lab, NIH, Bldg 5,Room 112, Bethesda, MD 20892 USA.
EM robertty@mail.nih.gov
FU Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases of the National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases of the
National Institutes of Health.
NR 93
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 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD OCT 2
PY 2009
VL 392
IS 4
BP 1055
EP 1073
DI 10.1016/j.jmb.2009.07.073
PG 19
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 504FM
UT WOS:000270601200018
PM 19647001
ER
PT J
AU Rappuoli, R
Del Giudice, G
Nabel, GJ
Osterhaus, ADME
Robinson, R
Salisbury, D
Stohr, K
Treanor, JJ
AF Rappuoli, Rino
Del Giudice, Giuseppe
Nabel, Gary J.
Osterhaus, Albert D. M. E.
Robinson, Robin
Salisbury, David
Stoehr, Klaus
Treanor, John J.
TI Rethinking Influenza
SO SCIENCE
LA English
DT Editorial Material
ID H5N1 VACCINE; TRIAL
C1 [Rappuoli, Rino; Del Giudice, Giuseppe] Novartis Vaccines & Diagnost Srl, I-53100 Siena, Italy.
[Nabel, Gary J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Osterhaus, Albert D. M. E.] Erasmus Univ, NL-3015E Rotterdam, Netherlands.
[Robinson, Robin] US Dept Hlth & Human Serv HHS, Washington, DC 20201 USA.
[Salisbury, David] WHO, SAGE, CH-1211 Geneva 27, Switzerland.
[Stoehr, Klaus] Novartis Vaccines & Diagnost Inc, Cambridge, MA 02139 USA.
[Treanor, John J.] Univ Rochester, Rochester, NY 14642 USA.
RP Rappuoli, R (reprint author), Novartis Vaccines & Diagnost Srl, I-53100 Siena, Italy.
EM rino.rappuoli@novartis.com
NR 10
TC 11
Z9 11
U1 0
U2 4
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD OCT 2
PY 2009
VL 326
IS 5949
BP 50
EP 50
DI 10.1126/science.1179475
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 501CA
UT WOS:000270355600025
PM 19797644
ER
PT J
AU Nabel, GJ
AF Nabel, Gary J.
TI The Coordinates of Truth
SO SCIENCE
LA English
DT Editorial Material
ID DEPENDENT DNA POLYMERASE; RNA; VIRIONS; SCIENCE
C1 NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Nabel, GJ (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM gnabel@nih.gov
NR 8
TC 16
Z9 16
U1 0
U2 8
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD OCT 2
PY 2009
VL 326
IS 5949
BP 53
EP 54
DI 10.1126/science.1177637
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 501CA
UT WOS:000270355600028
PM 19797647
ER
PT J
AU Cadieu, E
Neff, MW
Quignon, P
Walsh, K
Chase, K
Parker, HG
VonHoldt, BM
Rhue, A
Boyko, A
Byers, A
Wong, A
Mosher, DS
Elkahloun, AG
Spady, TC
Andre, C
Lark, KG
Cargill, M
Bustamante, CD
Wayne, RK
Ostrander, EA
AF Cadieu, Edouard
Neff, Mark W.
Quignon, Pascale
Walsh, Kari
Chase, Kevin
Parker, Heidi G.
VonHoldt, Bridgett M.
Rhue, Alison
Boyko, Adam
Byers, Alexandra
Wong, Aaron
Mosher, Dana S.
Elkahloun, Abdel G.
Spady, Tyrone C.
Andre, Catherine
Lark, K. Gordon
Cargill, Michelle
Bustamante, Carlos D.
Wayne, Robert K.
Ostrander, Elaine A.
TI Coat Variation in the Domestic Dog Is Governed by Variants in Three
Genes
SO SCIENCE
LA English
DT Article
ID MAJOR DETERMINANT; HAIR FOLLICLE; MUTATIONS; GENOME; FGF5; MULTIPLE;
SEQUENCE; CATENIN; TRAITS; CYCLE
AB Coat color and type are essential characteristics of domestic dog breeds. Although the genetic basis of coat color has been well characterized, relatively little is known about the genes influencing coat growth pattern, length, and curl. We performed genome-wide association studies of more than 1000 dogs from 80 domestic breeds to identify genes associated with canine fur phenotypes. Taking advantage of both inter- and intrabreed variability, we identified distinct mutations in three genes, RSPO2, FGF5, and KRT71 (encoding R-spondin-2, fibroblast growth factor-5, and keratin-71, respectively), that together account for most coat phenotypes in purebred dogs in the United States. Thus, an array of varied and seemingly complex phenotypes can be reduced to the combinatorial effects of only a few genes.
C1 [Cadieu, Edouard; Quignon, Pascale; Parker, Heidi G.; Byers, Alexandra; Mosher, Dana S.; Elkahloun, Abdel G.; Spady, Tyrone C.; Ostrander, Elaine A.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Neff, Mark W.; Walsh, Kari; Rhue, Alison; Wong, Aaron] Univ Calif Davis, Vet Genet Lab, Davis, CA 95616 USA.
[Chase, Kevin; Lark, K. Gordon] Univ Utah, Dept Biol, Salt Lake City, UT 84112 USA.
[VonHoldt, Bridgett M.; Wayne, Robert K.] Univ Calif Los Angeles, Dept Ecol & Evolutionary Biol, Los Angeles, CA 90095 USA.
[Boyko, Adam; Bustamante, Carlos D.] Cornell Univ, Dept Biol Stat & Computat Biol, Ithaca, NY 14853 USA.
[Cargill, Michelle] Affymetrix Corp, Santa Clara, CA 95051 USA.
[Andre, Catherine] Univ Rennes 1, CNRS, Fac Med, UMR 6061, Rennes, France.
RP Ostrander, EA (reprint author), NHGRI, NIH, Bethesda, MD 20892 USA.
EM eostrand@mail.nih.gov
OI Ostrander, Elaine/0000-0001-6075-9738
FU NSF [0733033, 516310]; NIH [1RO1GM83606, GM063056]; Nestle Purina
company; AKC Canine Health Foundation; University of California-Davis
Veterinary Genetics Laboratory; Intramural Program of the National Human
Genome Research Institute
FX We gratefully acknowledge support from NSF grants 0733033 ( R. K. W.)
and 516310 ( C. D. B.), NIH grants 1RO1GM83606 ( C. D. B.) and GM063056
( K. G. L. and K. C.), the Nestle Purina company, the AKC Canine Health
Foundation, the University of California-Davis Veterinary Genetics
Laboratory, and the Intramural Program of the National Human Genome
Research Institute. We thank L. Warren and S. Stafford for providing
pictures. Finally, we thank the many dog owners who generously provided
us with samples from their pets.
NR 25
TC 132
Z9 138
U1 6
U2 67
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD OCT 2
PY 2009
VL 326
IS 5949
BP 150
EP 153
DI 10.1126/science.1177808
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 501CA
UT WOS:000270355600058
PM 19713490
ER
PT J
AU Reynolds, HY
AF Reynolds, Herbert Y.
TI Free Medical Clinics: Helping Indigent Patients and Dealing With
Emerging Health Care Needs
SO ACADEMIC MEDICINE
LA English
DT Article
AB An innovative movement of free medical clinics, which began in the 1960s, has helped indigent people without access to traditional health care. In this article, the author relates his experiences at three free clinics. Aside from the delivery of good care to deserving people, these clinics also had an impact on other relevant issues in medicine: The first of these clinics became involved with a chronic illness that affected medical research, the second provided another venue for medical teaching, and the third increased volunteerism, especially among senior clinicians. These secondary features are the focus of this article. The first clinic, created in a time of troubling social change, cared for many young people with infections, probably including some who were part of an evolving epidemic that was only later recognized as HIV/AIDS. The second clinic began when the traditional hospital and outpatient clinic settings for teaching medical students-both in their preclinical years and during clerkship rotations-were not conducive to learning the skills of interviewing and physical examination of cooperative patients. The more informal, less frenetic pace of a free clinic appealed to students and some residents as a place to build clinical skills. The new Liaison Committee on Medical Education standard to provide student service learning may formalize the use of free clinics in medical schools. The third clinic, like any of the 1,200 or more free clinics in the United States, cares for indigent people who have no access to established health care. The free clinic movement, which can provide some of the needed care, relies on volunteer physicians, many of whom are older and retired clinicians, who find that their contribution to free clinic care can be both useful to the patients and most rewarding to themselves. Acad Med. 2009; 84:1434-1439.
C1 [Reynolds, Herbert Y.] NHLBI, DLD, Rockledge Ctr 2, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Reynolds, Herbert Y.] Penn State Coll Med, Milton S Hershey Med Ctr, Hershey, PA USA.
RP Reynolds, HY (reprint author), NHLBI, DLD, Rockledge Ctr 2, NIH,Dept Hlth & Human Serv, 6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM reynoldh@nhlbi.nih.gov
NR 25
TC 6
Z9 6
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD OCT
PY 2009
VL 84
IS 10
BP 1434
EP 1439
DI 10.1097/ACM.0b013e3181b6c3eb
PG 6
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA V15EU
UT WOS:000207786100031
PM 19881438
ER
PT J
AU Lountos, GT
Tropea, JE
Cherry, S
Waugh, DS
AF Lountos, George T.
Tropea, Joseph E.
Cherry, Scott
Waugh, David S.
TI Overproduction, purification and structure determination of human
dual-specificity phosphatase 14
SO ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY
LA English
DT Article
ID PROTEIN-TYROSINE PHOSPHATASES; MAP KINASE PHOSPHATASES;
CRYSTAL-STRUCTURE; PHYSIOLOGICAL FUNCTIONS; SIGNAL-TRANSDUCTION;
MOLECULAR-GRAPHICS; CATALYTIC DOMAIN; TARGETS; DISEASE; FAMILY
AB Dual-specificity phosphatases (DUSPs) are enzymes that participate in the regulation of biological processes such as cell growth, differentiation, transcription and metabolism. A number of DUSPs are able to dephosphorylate phosphorylated serine, threonine and tyrosine residues on mitogen-activated protein kinases (MAPKs) and thus are also classified as MAPK phosphatases (MKPs). As an increasing number of DUSPs are being identified and characterized, there is a growing need to understand their biological activities at the molecular level. There is also significant interest in identifying DUSPs that could be potential targets for drugs that modulate MAPK-dependent signaling and immune responses, which have been implicated in a variety of maladies including cancer, infectious diseases and inflammatory disorders. Here, the overproduction, purification and crystal structure at 1.88 angstrom resolution of human dual-specificity phosphatase 14, DUSP14 (MKP6), are reported. This structural information should accelerate the study of DUSP14 at the molecular level and may also accelerate the discovery and development of novel therapeutic agents.
C1 [Lountos, George T.; Tropea, Joseph E.; Cherry, Scott; Waugh, David S.] NCI, Macromol Crystallog Lab, Frederick, MD 21702 USA.
RP Waugh, DS (reprint author), NCI, Macromol Crystallog Lab, POB B, Frederick, MD 21702 USA.
EM waughd@ncifcrf.gov
RI Lountos, George/B-3983-2015
FU Intramural Research Program of the NIH; National Cancer Institute;
Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. Electrospray
mass-spectrometry experiments were conducted on the LC/ESMS instrument
maintained by the Biophysics Resource in the Structural Biophysics
Laboratory, Center for Cancer Research, National Cancer Institute at
Frederick.
NR 59
TC 11
Z9 12
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0907-4449
J9 ACTA CRYSTALLOGR D
JI Acta Crystallogr. Sect. D-Biol. Crystallogr.
PD OCT
PY 2009
VL 65
BP 1013
EP 1020
DI 10.1107/S0907444909023762
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Crystallography
SC Biochemistry & Molecular Biology; Biophysics; Crystallography
GA 494UY
UT WOS:000269845500001
PM 19770498
ER
PT J
AU Strunk, T
Currie, A
Philbin, V
Richmond, P
Simmer, K
Doherty, D
Otto, M
Levy, O
Burgner, D
AF Strunk, T.
Currie, A.
Philbin, V.
Richmond, P.
Simmer, K.
Doherty, D.
Otto, M.
Levy, O.
Burgner, D.
TI INNATE IMMUNE RESPONSES TO STAPHYLOCOCCUS EPIDERMIDIS ARE GESTATIONAL
AGE-DEPENDENT
SO ACTA PAEDIATRICA
LA English
DT Meeting Abstract
C1 [Strunk, T.; Simmer, K.] King Edward Mem Hosp, Dept Neonatal Paediat, Perth, WA, Australia.
[Strunk, T.; Currie, A.; Richmond, P.; Simmer, K.; Burgner, D.] Univ Western Australia, Sch Paediat & Child Hlth, Perth, WA 6009, Australia.
[Philbin, V.; Levy, O.] Childrens Hosp Boston, Div Infect Dis, Boston, MA USA.
[Philbin, V.; Levy, O.] Harvard Univ, Harvard Med Sch, Boston, MA 02115 USA.
[Simmer, K.; Doherty, D.] Univ Western Australia, Sch Womens & Infants Hlth, Perth, WA 6009, Australia.
[Otto, M.] NIAID, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Strunk, T.; Simmer, K.] Princess Margaret Hosp, Dept Neonatal Paediat, Perth, WA, Australia.
RI Richmond, Peter/G-3379-2012; Simmer, Karen/H-5834-2014; Currie,
Andrew/C-2778-2015
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 0803-5253
J9 ACTA PAEDIATR
JI Acta Paediatr.
PD OCT
PY 2009
VL 98
SU 460
BP 56
EP 56
PG 1
WC Pediatrics
SC Pediatrics
GA 495AR
UT WOS:000269862100142
ER
PT J
AU Bornstein, M
AF Bornstein, M.
TI DIFFERENTIATED BRAIN ACTIVITY FOR FAMILIAR AND UNFAMILIAR FACES IN 3-AND
6-MONTH-OLD INFANTS AND THEIR MOTHERS
SO ACTA PAEDIATRICA
LA English
DT Meeting Abstract
C1 [Bornstein, M.] NICHHD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0803-5253
J9 ACTA PAEDIATR
JI Acta Paediatr.
PD OCT
PY 2009
VL 98
BP 92
EP 92
PG 1
WC Pediatrics
SC Pediatrics
GA 495AR
UT WOS:000269862100238
ER
PT J
AU Nguyen, R
Dombi, E
Widemann, B
Fuensterer, C
Friedman, JM
Mautner, VF
AF Nguyen, R.
Dombi, E.
Widemann, B.
Fuensterer, C.
Friedman, J. M.
Mautner, V-F
TI FOLLOW UP OF INTERNAL PLEXIFORM TUMORS IN PEDIATRIC PATIENTS WITH NF1 BY
WHOLE BODY MRI AND VOLUMETRIC ANALYSIS
SO ACTA PAEDIATRICA
LA English
DT Meeting Abstract
C1 [Nguyen, R.; Mautner, V-F] Univ Hamburg, Dept Maxillofacial Surg, Hamburg, Germany.
[Dombi, E.; Widemann, B.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Fuensterer, C.] MRI Inst, Hamburg, Germany.
[Friedman, J. M.] Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada.
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 0803-5253
J9 ACTA PAEDIATR
JI Acta Paediatr.
PD OCT
PY 2009
VL 98
BP 200
EP 200
PG 1
WC Pediatrics
SC Pediatrics
GA 495AR
UT WOS:000269862100513
ER
PT J
AU Cox, LS
Mattison, JA
AF Cox, Lynne S.
Mattison, Julie A.
TI Increasing longevity through caloric restriction or rapamycin feeding in
mammals: common mechanisms for common outcomes?
SO AGING CELL
LA English
DT Editorial Material
DE aging; caloric restriction; lifespan; primates; rapamycin; TOR
ID INDUCED WEIGHT-LOSS; T-CELL SENESCENCE; LIFE-SPAN; RHESUS-MONKEYS;
DIETARY RESTRICTION; C-ELEGANS; GASTRIC DILATATION; SIGNALING PATHWAY;
CANCER-THERAPY; PRIMATE MODEL
AB Significant extension of lifespan in important mammalian species is bound to attract the attention not only of the aging research community, but also the media and the wider public. Two recent papers published byHarrison et al. (2009) in Nature and by Colman et al. (2009) in Science report increased longevity of mice fed with rapamycin and of rhesus monkeys undergoing caloric restriction, respectively. These papers have generated considerable debate in the aging community. Here we assess what is new about these findings, how they fit with our knowledge of lifespan extension from other studies and what prospects this new work holds out for improvements in human longevity and human health span.
C1 [Cox, Lynne S.] Univ Oxford, Dept Biochem, Oxford OX1 3QU, England.
[Mattison, Julie A.] NIA Primate Aging Studies, Lab Expt Gerontol, Baltimore, MD USA.
RP Cox, LS (reprint author), Univ Oxford, Dept Biochem, S Parks Rd, Oxford OX1 3QU, England.
EM lynne.cox@bioch.ox.ac.uk; mattisonj@mail.nih.gov
FU Biotechnology and Biological Sciences Research Council [BB/E000924/1];
Intramural NIH HHS [, Z01 AG000371-03]
NR 59
TC 28
Z9 29
U1 2
U2 9
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1474-9718
J9 AGING CELL
JI Aging Cell
PD OCT
PY 2009
VL 8
IS 5
BP 607
EP 613
DI 10.1111/j.1474-9726.2009.00509.x
PG 7
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 498FU
UT WOS:000270123400011
PM 19678809
ER
PT J
AU Schug, TT
AF Schug, Thaddeus T.
TI Awakening p53 in senescent cells using nutlin-3
SO AGING-US
LA English
DT Article
DE Senescence; p53; tumor suppression; nutlin-3
ID CELLULAR SENESCENCE; DNA-DAMAGE; ACETYLATION; FIBROBLASTS; ACTIVATION;
PATHWAY; DEATH; MDM2
C1 NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
RP Schug, TT (reprint author), NIEHS, Lab Signal Transduct, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM schugt@niehs.nih.gov
NR 16
TC 1
Z9 1
U1 0
U2 2
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD OCT
PY 2009
VL 1
IS 10
BP 842
EP 844
PG 3
WC Cell Biology
SC Cell Biology
GA 579UV
UT WOS:000276402500003
PM 20157556
ER
PT J
AU Reitano, KN
Kottilil, S
Gille, CM
Zhang, X
Yan, M
O'Shea, MA
Roby, G
Hallahan, CW
Yang, J
Lempicki, RA
Arthos, J
Fauci, AS
AF Reitano, K. N.
Kottilil, S.
Gille, C. M.
Zhang, X.
Yan, M.
O'Shea, M. A.
Roby, G.
Hallahan, C. W.
Yang, J.
Lempicki, R. A.
Arthos, J.
Fauci, A. S.
TI Defective Plasmacytoid Dendritic Cell-NK Cell Cross-Talk in HIV
Infection
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
ID NATURAL-KILLER-CELLS; CPG OLIGODEOXYNUCLEOTIDE; ANTIRETROVIRAL THERAPY;
ACTIVATING RECEPTORS; T-CELLS; IN-VIVO; VIREMIA; ALPHA; DNA;
IMMUNOTHERAPY
AB HIV viremia is associated with a wide range of immune dysfunctions that contribute to the immunocompromised state. HIV viremia has been shown to have a broad effect on several immune cell types and/or their interactions that are vital for mounting an effective immune response. In this study, we investigated the integrity of plasmacytoid dendritic cell (pDC)-NK cell interactions among HIV viremic, aviremic, and seronegative individuals. We describe a critical defect in the ability of pDCs from HIV-infected individuals to secrete IFN-alpha and TNF and subsequently activate NK cells. We also describe an inherent defect on NK cells from HIV-infected individuals to respond to pDC-secreted cytokines. Furthermore, we were able to demonstrate a direct effect of HIV trimeric gp120 on NK cells in vitro similar to that described ex vivo. Finally, we were able to establish that the HIV gp120-mediated suppressive effect on NK cells was a result of its binding to the integrin alpha(4)beta(7) expressed on NK cells. These findings suggest a novel mechanism by which HIV is capable of suppressing an innate immune function in infected individuals.
C1 [Reitano, K. N.; Kottilil, S.; Gille, C. M.; Zhang, X.; Yan, M.; Yang, J.; Lempicki, R. A.; Arthos, J.; Fauci, A. S.] NIAID, Immunoregulat Lab, NIH, Dept Hlth & Human Serv, Frederick, MD 21702 USA.
[O'Shea, M. A.; Roby, G.] NIH, Dept Crit Care Med, Ctr Clin, Dept Hlth & Human Serv, Frederick, MD 21702 USA.
[Hallahan, C. W.] NCI, Biostat Res Branch, NIAID, NIH,Dept Hlth & Human Serv,SAIC Frederick, Frederick, MD 21702 USA.
RP Kottilil, S (reprint author), NIAID, Immunopathogenesis Sect, Immunoregulat Lab, NIH, Bldg 10,Rm 11N204, Bethesda, MD 20892 USA.
EM skottilil@niaid.nih.gov
RI Lempicki, Richard/E-1844-2012
OI Lempicki, Richard/0000-0002-7059-409X
FU NIH [National Institute of Allergy and Infectious Diseases]
FX This research was supported in whole by the Intramural Research Program
of the NIH [National Institute of Allergy and Infectious Diseases]. The
content of this publication does not necessarily reflect the views or
the 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. K.N. Reitano and S. Kottilil
contributed equally to this article.
NR 37
TC 21
Z9 21
U1 0
U2 1
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2009
VL 25
IS 10
BP 1029
EP 1037
DI 10.1089/aid.2008.0311
PG 9
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 508SQ
UT WOS:000270956200012
PM 19795986
ER
PT J
AU Collinson-Streng, AN
Redd, AD
Sewankambo, NK
Serwadda, D
Rezapour, M
Lamers, SL
Gray, RH
Wawer, MJ
Quinn, TC
Laeyendecker, O
AF Collinson-Streng, Aleisha N.
Redd, Andrew D.
Sewankambo, Nelson K.
Serwadda, David
Rezapour, Mona
Lamers, Susanna L.
Gray, Ronald H.
Wawer, Maria J.
Quinn, Thomas C.
Laeyendecker, Oliver
TI Geographic HIV Type 1 Subtype Distribution in Rakai District, Uganda
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
ID DISEASE PROGRESSION; GENETIC DIVERSITY; PREDOMINANCE; INFECTION;
VARIANTS; WOMEN
AB To analyze HIV-1 subtype distribution, sequence analysis was performed on serum specimens obtained in 1994 from the Rakai Health Sciences community cohort in Uganda. Portions of gag-p24 and env-gp41 were sequenced and HIV subtype was determined for 773 subjects residing in 10 community clusters in rural Uganda. Subtypes A (17%) and D (70%) were the most common strains in the population. Subtype distribution varied by geographic region with significantly more subtype A in northern community clusters compared with southern clusters (21% vs. 8%, p < 0.001) and more subtype D in southern clusters compared with northern clusters (78% vs. 65%, p < 0.008). These data illustrate the geographic complexity of subtype variation, which has important implications for HIV-1 vaccine design.
C1 [Collinson-Streng, Aleisha N.; Redd, Andrew D.; Rezapour, Mona; Quinn, Thomas C.; Laeyendecker, Oliver] NIAID, Immunoregulat Lab, Div Intramural Res, NIH, Baltimore, MD 21205 USA.
[Sewankambo, Nelson K.] Makerere Univ, Sch Med, Kampala, Uganda.
[Serwadda, David] Makerere Univ, Sch Publ Hlth, Kampala, Uganda.
[Lamers, Susanna L.] BioInfoExperts, Thibodaux, LA 70301 USA.
[Gray, Ronald H.; Wawer, Maria J.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
[Quinn, Thomas C.; Laeyendecker, Oliver] Johns Hopkins Univ, Sch Med, Baltimore, MD 21205 USA.
RP Laeyendecker, O (reprint author), John Rangos Sr Bldg,Room 538A,855 N Wolfe St, Baltimore, MD 21205 USA.
EM olaeyen@jhmi.edu
RI Laeyendecker, Oliver/B-9331-2009; Redd, Andrew/D-1802-2010;
OI Sewankambo, Nelson/0000-0001-9362-053X; Laeyendecker,
Oliver/0000-0002-6429-4760
FU NIAID; NIH
FX The authors would like to thank all the participants of the Rakai
community cohort and the staff of the Rakai Health Sciences Group for
their tireless work. Funding for this project was provided by the
Laboratory of Immuno-regulation, Division of Intramural Research, NIAID,
NIH. GenBank accession numbers for these sequences are
GQ332766-GQ334183, GQ253866-GQ253897, and GQ252692-GQ252793.
NR 14
TC 13
Z9 13
U1 0
U2 1
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2009
VL 25
IS 10
BP 1045
EP 1048
DI 10.1089/aid.2009.0127
PG 4
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 508SQ
UT WOS:000270956200014
PM 19803713
ER
PT J
AU Guerreiro, RJ
Vaskov, T
Crews, C
Singleton, A
Hardy, J
AF Guerreiro, Rita J.
Vaskov, Tina
Crews, Cynthia
Singleton, Andrew
Hardy, John
TI A Case of Dementia With PRNP D178Ncis-129M and No Insomnia
SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS
LA English
DT Article
DE dementia; prion gene; familial fatal insomnia
ID CREUTZFELDT-JAKOB-DISEASE; FATAL FAMILIAL INSOMNIA; ALZHEIMERS-DISEASE;
PHENOTYPIC VARIABILITY; MUTATION; VARIANT; GENE
AB Objective: To describe a dementia case clinically diagnosed as Alzheimer disease with a PRNP genotype usually associated with familial fatal insomnia.
Methods: Polymerase chain reaction amplification and subsequent direct sequencing of PGRN, MAPT PSEN1, PSEN2, APP, and PRNP genes.
Results: A point mutation (D178N) was found in the PRNP gene.
Conclusions: The mutation D178N in the PRNP gene associated with the M129 genotype is usually associated with Familial fatal insomnia. However, a few cases have been reported with different clinical phenotypes. Here, we describe one of these cases and stress the importance of genetic screening of PRNP in early onset dementia cases.
C1 [Guerreiro, Rita J.] NIA, Mol Genet Sect, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Guerreiro, Rita J.] Univ Coimbra, Ctr Neurosci & Cell Biol, Coimbra, Portugal.
[Vaskov, Tina] Ctr Clin, Neurol Clin, Skopje, Macedonia.
[Hardy, John] UCL, Queen Sq Brain Bank, London, England.
[Hardy, John] UCL, Inst Neurol, Dept Mol Neurosci, London, England.
RP Guerreiro, RJ (reprint author), NIA, Mol Genet Sect, Neurogenet Lab, NIH, Room 1A-1010,Bldg 35,35 Lincoln Dr, Bethesda, MD 20892 USA.
EM portalegrer@nia.nih.gov
RI Singleton, Andrew/C-3010-2009; Hardy, John/C-2451-2009; Guerreiro,
Rita/A-1327-2011
FU Intramural Research Program of the National Institute on Aging; National
Institutes of Health; Department of Health and Human Services [Z01
AG000957-05]; Fundacao para a Ciencia e Teclinologia, Portugal
[SFRH/BD/27442/2006]
FX Supported in part by the Intramural Research Program of the National
Institute on Aging, National Institutes of Health, Department of Health
and Human Services; project number Z01 AG000957-05 and grant
SFRH/BD/27442/2006 from Fundacao para a Ciencia e Teclinologia,
Portugal.
NR 25
TC 8
Z9 8
U1 2
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0893-0341
J9 ALZ DIS ASSOC DIS
JI Alzheimer Dis. Assoc. Dis.
PD OCT-DEC
PY 2009
VL 23
IS 4
BP 415
EP 417
PG 3
WC Clinical Neurology; Pathology
SC Neurosciences & Neurology; Pathology
GA 527XE
UT WOS:000272403700020
PM 19571725
ER
PT J
AU Flynn, KE
Lin, L
Ellis, SJ
Russell, SD
Spertus, JA
Whellan, DJ
Pina, IL
Fine, LJ
Schulman, KA
Weinfurt, KP
AF Flynn, Kathryn E.
Lin, Li
Ellis, Stephen J.
Russell, Stuart D.
Spertus, John A.
Whellan, David J.
Pina, Ileana L.
Fine, Lawrence J.
Schulman, Kevin A.
Weinfurt, Kevin P.
CA HF-ACTION Investigators
TI Outcomes, health policy, and managed care: Relationships between
patient-reported outcome measures and clinical measures in outpatients
with heart failure
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID QUALITY-OF-LIFE; CARDIAC RESYNCHRONIZATION; QUESTIONNAIRE; MORBIDITY;
MORTALITY; SURVIVAL; TRIAL
AB Background Patient-reported outcomes are increasingly used to assess the efficacy of new treatments. Understanding relationships between these and clinical measures can facilitate their interpretation. We examined associations between patient-reported measures of health-related quality of life and clinical indicators of disease severity in a large, heterogeneous sample of patients with heart failure.
Methods Patient-reported measures, including the Kansas City Cardiomyopathy Questionnaire (KCCQ) and the EuroQol Visual Analog Scale (VAS), and clinical measures, including peak VO(2), 6-minute walk distance, and New York Heart Association (NYHA) class, were assessed at baseline in 233 1 patients with heart failure. We used general linear models to regress patient-reported measures on each clinical measure. Final models included for significant sociodemographic variables and 2-way interactions.
Results The KCCQ was correlated with peak VO(2) (r=.21) and 6-minute walk distance (r=.27). The VAS was correlated with peak VO(2) (r=.09) and 6-minute walk distance (r=.11). Using the KCCQ as the response variable, a 1-SD difference in peak VO(2) (4.7 mL/kg/min) was associated with a 2.86-point difference in the VAS (95% Cl, 1.98-3.74) and a 4.75-point difference in the KCCQ (95% Cl, 3.78-5.72). A 1-SD difference in 6-minute walk distance (105 m) was associated with a 2.78-point difference in the VAS (95% Cl, 1.92-3.64) and a 5.92-point difference in the KCCQ (95% Cl, 4.98-6.87); NYHA class III was associated with an 8.26-point lower VAS (95% Cl, 6.59-9.93) and a 12.73-point lower KCCQ (95% Cl, 10.92-14.53) than NYHA class II.
Conclusions These data may inform deliberations about how to best measure benefits of heart failure interventions, and they generally support the practice of considering a 5-point difference on the KCCQ and a 3-point difference on the VAS to be clinically meaningful. (Am Heart J 2009;158:S64-S71.)
C1 [Flynn, Kathryn E.; Lin, Li] Duke Univ, Ctr Clin & Genet Econ, Duke Clin Res Inst, Sch Med, Durham, NC 27715 USA.
[Flynn, Kathryn E.; Weinfurt, Kevin P.] Duke Univ, Sch Med, Dept Psychiat & Behav Sci, Durham, NC 27715 USA.
[Schulman, Kevin A.] Duke Univ, Sch Med, Dept Med, Durham, NC 27715 USA.
[Russell, Stuart D.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Spertus, John A.] Univ Missouri Kansas City, Mid Amer Heart Inst, Kansas City, MO USA.
[Whellan, David J.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Med, Philadelphia, PA 19107 USA.
[Pina, Ileana L.] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
[Fine, Lawrence J.] NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
RP Flynn, KE (reprint author), Duke Univ, Ctr Clin & Genet Econ, Duke Clin Res Inst, Sch Med, POB 17969, Durham, NC 27715 USA.
EM kathryn.flynn@duke.edu
RI Flynn, Kathryn/M-5346-2013
OI Flynn, Kathryn/0000-0002-4427-3583
FU National Institutes of Health [5U01HL063747, 5U01HL068973, U01HL066501,
5U01HL066482, 5U01HL064250, 5U01HL066494, 5U01HL064257, 5U01HL066497,
U01HL068980, 5U01HL064265, 5U01HL066491, 5U01HL064264, 5U01HL066461,
R37AG18915, P60AG10484]
FX This research was supported by National Institutes of Health grants:
5U01HL063747, 5U01HL068973, U01HL066501, 5U01HL066482, 5U01HL064250,
5U01HL066494, 5U01HL064257, 5U01HL066497, U01HL068980, 5U01HL064265,
5U01HL066491, 5U01HL064264, 5U01HL066461, R37AG18915, and P60AG10484.
NR 24
TC 23
Z9 23
U1 0
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD OCT
PY 2009
VL 158
IS 4
BP S64
EP S71
DI 10.1016/j.ahj.2009.07.010
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 505PG
UT WOS:000270705800009
PM 19782791
ER
PT J
AU Forman, DE
Clare, R
Kitzman, DW
Ellis, SJ
Fleg, JL
Chiara, T
Fletcher, G
Kraus, WE
AF Forman, Daniel E.
Clare, Robert
Kitzman, Dalane W.
Ellis, Stephen J.
Fleg, Jerome L.
Chiara, Toni
Fletcher, Gerald
Kraus, William E.
CA HF-ACTION Investigators
TI Relationship of age and exercise performance in patients with heart
failure: The HF-ACTION study
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID TRIAL INVESTIGATING OUTCOMES; BODY-MASS INDEX; CHRONOTROPIC
INCOMPETENCE; VENTILATORY EFFICIENCY; AEROBIC CAPACITY; EJECTION
FRACTION; VE/VCO2 SLOPE; ADVANCING AGE; HEALTHY-MEN; ARTERIAL
AB Background More than three fourths of patients with heart failure (HF) are 65 years and older, and older age is associated with worse symptoms and prognoses than is younger age. Reduced exercise capacity is a chief HF complaint and indicates poorer prognosis, especially among elderly persons, but the mechanisms underlying functional decline in older patients with HF are largely unknown.
Methods Baseline cardiopulmonary exercise testing data from the HF-ACTION trial were assessed to clarify age effects on peak oxygen consumption (VO(2)) and ventilation-carbon dioxide production (VE/VCO(2)) slope.
Results Among 2,331 New York Heart Association class II-IV patients with HF, increased age corresponded to decreased peak VO(2) (-0.14 mL kg(-1) min(-1) per year >40 years; P<.0001) and increased VE/VCO(2) slope (0.30 U/y>70years; P<.0001). In a multivariable model with 34 other potential determinants, age was the strongest independent predictor of peak VO(2) (partial R(2) 0.130, total R(2) 0.392; P<.001) and a significant but relatively weaker predictor of VE/VCO(2) slope (partial R(2) 0.037, total R(2) 0.199; P<.001). Blunted peak heart rate was also a strong predictor of peak VO(2). Although peak heart rate and age were strongly correlated, both were significant independent predictors of peak VO(2) when analyzed simultaneously in a model. Aggregate comorbidity increased significantly with age but did not account for age effects on peak VO(2).
Conclusions Age is the strongest predictor of peak VO(2) and a significant predictor of VE/VCO(2) slope in the HF-ACTION population. Age-dependent comorbidities do not explain changes in peak VO(2). Age-related changes in cardiovascular physiology, potentially magnified by the HF disease state, should be considered a contributor to the pathophysiology and a target for more effective therapy in older patients with HF. (Am Heart J 2009; 1 58:S6-S15.)
C1 [Kraus, William E.] Duke Univ, Med Ctr, Dept Med, Div Cardiol, Durham, NC 27710 USA.
[Forman, Daniel E.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
[Forman, Daniel E.] VA Boston Healthcare Syst, Ctr Geriatr Res Educ & Clin, Boston, MA USA.
[Clare, Robert; Ellis, Stephen J.] Duke Clin Res Inst, Durham, NC USA.
[Kitzman, Dalane W.] Wake Forest Univ Hlth Sci, Dept Internal Med, Cardiol Sect, Winston Salem, NC USA.
[Kitzman, Dalane W.] Wake Forest Univ Hlth Sci, Dept Internal Med, Sect Geriatr, Winston Salem, NC USA.
[Fleg, Jerome L.] NHLBI, Div Cardiovasc Dis, Bethesda, MD 20892 USA.
[Chiara, Toni] Univ Florida, Coll Publ Hlth & Hlth Profess, Dept Phys Therapy, Malcom Randall VA Med Ctr, Gainesville, FL USA.
[Fletcher, Gerald] Mayo Clin Jacksonville, Jacksonville, FL 32224 USA.
RP Kraus, WE (reprint author), Duke Univ, Med Ctr, Dept Med, Div Cardiol, POB 3327, Durham, NC 27710 USA.
EM william.kraus@duke.edu
OI Kraus, William E/0000-0003-1930-9684
FU National Institutes of Health [5U01HL063747, 5U01HL068973, 5UO1HL066501,
5U01HL066482, 5U01HL064250, 5U01HL066494, 5U01HL064257, 5U01HL066497,
5U01HL068980, 5U01HL064265, 5U01HL066491, 5U01HL064264, R37AG18915,
P60AG10484]
FX A complete list of the HF-ACTION investigators is available as on
appendix in the introduction of this supplement. This study was
supported by National Institutes of Health grants 5U01HL063747,
5U01HL068973, 5UO1HL066501, 5U01HL066482, 5U01HL064250, 5U01HL066494,
5U01HL064257, 5U01HL066497, 5U01HL068980, 5U01HL064265, 5U01HL066491,
5U01HL064264, R37AG18915, and P60AG10484.
NR 40
TC 17
Z9 18
U1 0
U2 8
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD OCT
PY 2009
VL 158
IS 4
BP S6
EP S15
DI 10.1016/j.ahj.2009.07.018
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 505PG
UT WOS:000270705800002
PM 19782790
ER
PT J
AU Gardin, JM
Leifer, ES
Fleg, JL
Whellan, D
Kokkinos, P
LeBlanc, MH
Wolfel, E
Kitzman, DW
AF Gardin, Julius M.
Leifer, Eric S.
Fleg, Jerome L.
Whellan, David
Kokkinos, Peter
LeBlanc, Marie-Helene
Wolfel, Eugene
Kitzman, Dalane W.
CA HF-ACTION Investigators
TI Relationship of Doppler-Echocardiographic left ventricular diastolic
function to exercise performance in systolic heart failure: The
HF-ACTION study
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID TRIAL INVESTIGATING OUTCOMES; SOCIETY-OF-ECHOCARDIOGRAPHY; TISSUE
DOPPLER; FILLING PRESSURES; STANDARDS COMMITTEE; TASK-FORCE;
RECOMMENDATIONS; CAPACITY; PARAMETERS
AB Introduction Patients with systolic heart failure often have concomitant left ventricular (LV) diastolic dysfunction. Although in animal models diastolic dysfunction is associated with worsening exercise capacity and prognosis, information regarding these relationships in patients with established systolic heart failure (HF) is sparse.
Methods HF-ACTION was a large, multicenter National Institutes of Health-funded trial of exercise training in systolic HF JLV ejection fraction [LVEF] <= 35%) and included detailed Doppler-echocardiographic (echo) and cardiopulmonary exercise testing at baseline. We tested the hypothesis that echo measures of LV diastolic function predict key cardiopulmonary exercise outcomes, including aerobic exercise capacity (peak exercise oxygen consumption, VO(2)), distance in the 6-minute walk test (6MWD), and ventilatory efficiency (VE/VCO(2) slope) in patients with systolic HE
Results Overall, 2,331 patients (28% women, median age 59 years, median LVEF 25%) were enrolled. There were significant bivariate correlations between echo diastolic function variables and peak VO(2) (inverse) and VE/VCO(2) slope (direct) that were strongest for ratio of early diastolic peak transmitral (MV) to myocardial tissue velocity (E/E(1)), peak MV early-to-late diastolic velocity ratio (E/A), and left atrial dimension (range of absolute r = 0.16-0.28). Both MV E/A and E/E' were more strongly related to all 3 exercise variables than was LVEF. The relationships of E/A and E/E' with 6MWD were weaker than with peak VO(2) or VE/VCO(2) slope. A multivariable model with peak VO(2) as the dependent variable, which included MV E/A and 9 demographic predictors including age, sex, race, body mass index, and New York Heart Association class, explained 40% of the variation in peak VO(2), with MV E/A explaining 6% of the variation. Including LVEF in the model explained less than an additional 1% of the variance in peak VO(2). In a multivariable model for VE/VCO(2) slope, MV E/A was the strongest independent echo predictor, explaining 10% of the variance. The relationship of LV diastolic function variables with 6MWD was weaker than with peak VO(2) or VE/VCO(2) slope.
Conclusion In patients with systolic HF, LV early diastolic function is a modest independent predictor of aerobic exercise capacity and appears to be a better predictor than LVEF (Am Heart J 2009; 158:S45-S52.)
C1 [Gardin, Julius M.] Hackensack Univ, Med Ctr, Hackensack, NJ 07601 USA.
[Gardin, Julius M.] St John Hosp & Med Ctr, Detroit, MI USA.
[Leifer, Eric S.; Fleg, Jerome L.] NHLBI, Bethesda, MD 20892 USA.
[Whellan, David] Duke Clin Res Inst, Durham, NC USA.
[Whellan, David] Temple Univ, Sch Med, Philadelphia, PA 19122 USA.
[Kokkinos, Peter] VA Med Ctr, Washington, DC USA.
[LeBlanc, Marie-Helene] Laval Hosp, Ste Foy, PQ, Canada.
[Wolfel, Eugene] Univ Colorado, Hlth Sci Ctr, Aurora, CO USA.
[Kitzman, Dalane W.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
RP Gardin, JM (reprint author), Hackensack Univ, Med Ctr, 30 Prospect Ave, Hackensack, NJ 07601 USA.
EM JGardin@humed.com
FU National Institutes of Health [5U01HL063747, 5U01HL068973, 5U01HL066501,
5U01HL066482, 5U01HL064250, 5U01HL066494, 5U01HL064257, 5U01HL066497,
5U01HL068980, 5U01HL064265, 5U01HL066491, 5U01HL064264, R37AG18915,
P60AG10484]
FX This research was supported by National Institutes of Health grants:
5U01HL063747, 5U01HL068973, 5U01HL066501, 5U01HL066482, 5U01HL064250,
5U01HL066494, 5U01HL064257, 5U01HL066497, 5U01HL068980, 5U01HL064265,
5U01HL066491, 5U01HL064264, R37AG18915, P60AG10484.
NR 26
TC 33
Z9 35
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD OCT
PY 2009
VL 158
IS 4
BP S45
EP S52
DI 10.1016/j.ahj.2009.07.015
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 505PG
UT WOS:000270705800007
PM 19782788
ER
PT J
AU Horwich, TB
Leifer, ES
Brawner, CA
Fitz-Gerald, MB
Fonarow, GC
AF Horwich, Tamara B.
Leifer, Eric S.
Brawner, Clinton A.
Fitz-Gerald, Meredith B.
Fonarow, Gregg C.
CA HF-ACTION Investigators
TI The relationship between body mass index and cardiopulmonary exercise
testing in chronic systolic heart failure
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID PEAK OXYGEN-CONSUMPTION; LEFT-VENTRICULAR DYSFUNCTION; PROGNOSTIC VALUE;
OBESITY PARADOX; CARDIAC TRANSPLANTATION; MORTALITY; RECOMMENDATIONS;
CARDIOMYOPATHY; PERFORMANCE; STATEMENT
AB Background Cardiopulmonary exercise testing (CPX) in patients with systolic heart failure (HF) is important for determining HF prognosis and helping guide timing of heart transplantation. Although approximately 20% to 30% of patients with HF are obese (body mass index [BMI] >30 kg/m(2)), the impact of BMI on CPX results is not well established. The objective of this study was to assess the relationship between BMI and CPX variables, including peak oxygen uptake (VO(2)) at ventilatory threshold, oxygen pulse, and ventilation-carbon dioxide production ratio.
Methods Consecutive patients with systolic HF (n = 2,324) enrolled in the Heart Failure and A Controlled Trial Investigating Outcomes of Exercise Training trial who had baseline BMI recorded were included in this study. Subjects were divided into strata based on BMI: underweight (BMI <18.5 kg/m(2)), normal weight (BMI 18.5-24.9 kg/m(2)), overweight (BMI 25.0-29.9 kg/m(2)), obese I (BMI 30-34.9 kg/m(2)), obese II (BMI 35-39.9 kg/m(2)), and obese III (BMI >= 40 kg/m(2)).
Results Obese III, but not overweight; obese I; or obese II was associated with decreased peak VO(2) (mL kg(-1) min(-1)) compared to normal weight status. Increasing BMI category was inversely related to ventilation/carbon dioxide production (V(E)/V(CO2)) ratio (P<.0001). On multivariable analysis, BMI was a significant independent predictor of peak VO(2) (partial R(2) = 0.07, P<.0001) and V(E)/V(CO2) slope (partial R(2) = 0.03, P<.0001) in patients with chronic systolic HF.
Conclusions Body mass index is significantly associated with key CPX fitness variables in patients with HF. The influence of BMI on the prognostic value of CPX in HF requires further evaluation in longitudinal studies. (Am HeartJ 2009J 58:S31-S36.)
C1 [Fonarow, Gregg C.] Ronald Reagan UCLA Med Ctr, Ahmanson UCLA Cardiomyopathy Ctr, Los Angeles, CA 90095 USA.
[Leifer, Eric S.] NHLBI, Bethesda, MD 20892 USA.
[Brawner, Clinton A.] Henry Ford Hosp, Detroit, MI 48202 USA.
[Fitz-Gerald, Meredith B.] Univ Alabama, Birmingham, AL USA.
RP Fonarow, GC (reprint author), Ronald Reagan UCLA Med Ctr, Ahmanson UCLA Cardiomyopathy Ctr, 10833 LeConte Ave,Room 47-123 CHS, Los Angeles, CA 90095 USA.
EM gfonarow@mednet.ucla.edu
RI Sriwisit, Sukhumaphorn/G-1405-2011;
OI Brawner, Clinton A./0000-0002-1705-6620
FU National Heart Lung and Blood Institute [5U01HL063747, 5U01HL066461,
HL068973, HL066501, HL066482, HL064250, HL066494, HL064257, HL066497,
HL068980, HL064265, HL066491, HL064264]
FX HF-ACTION is funded by the National Heart Lung and Blood Institute
(grants 5U01HL063747,5U01-HL066461, HL068973, HL06650 1, HL066482,
HL064250, HL066494, HL064257, HL066497 HL068980, HL064265, HL066491, and
HL064264. HF-ACTION is registered:.clinicoltriols.gov, study number
NCT00047437.
NR 29
TC 11
Z9 14
U1 1
U2 9
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD OCT
PY 2009
VL 158
IS 4
BP S31
EP S36
DI 10.1016/j.ahj.2009.07.016
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 505PG
UT WOS:000270705800005
PM 19782786
ER
PT J
AU Pina, IL
Kokkinos, P
Kao, A
Bittner, V
Saval, M
Clare, B
Goldberg, L
Johnson, M
Swank, A
Ventura, H
Moe, G
Fitz-Gerald, M
Ellis, SJ
Vest, M
Cooper, L
Whellan, D
AF Pina, Ileana L.
Kokkinos, Peter
Kao, Andrew
Bittner, Vera
Saval, Matt
Clare, Bob
Goldberg, Lee
Johnson, Maryl
Swank, Ann
Ventura, Hector
Moe, Gordon
Fitz-Gerald, Meredith
Ellis, Stephen J.
Vest, Marianne
Cooper, Lawton
Whellan, David
CA HF-ACTION Investigators
TI Baseline differences in the HF-ACTION trial by sex
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID CHRONIC HEART-FAILURE; NATIONAL REGISTRY ADHERE; PEAK
OXYGEN-CONSUMPTION; GENDER-DIFFERENCES; CARDIAC-RESYNCHRONIZATION;
UNITED-STATES; WOMEN; EXERCISE; TRANSPLANTATION; OUTCOMES
AB Background In patients with heart failure (HF), assessment of functional capacity plays an important prognostic role. Both 6-minute walk and cardiopulmonary exercise testing have been used to determine physical function and to determine prognosis and even listing for transplantation. However, as in HF trials, the number of women reported has been small, and the cutoffs for transplantation have been representative of male populations and extrapolated to women. It is also well known that peak VO(2) as a determinant of fitness is inherently lower in women than in men and potentially much lower in the presence of HF. Values for a female population from which to draw for this important determination are lacking.
Methods The HF-ACTION trial randomized 2,331 patients (28% women) with New York Heart Association class II-IV HF due to systolic dysfunction to either a formal exercise program in addition to optimal medical therapy or to optimal medical therapy alone without any formal exercise training. To characterize differences between men and women in the interpretation of final cardiopulmonary exercise testing models, the interaction of individual covariates with sex was investigated in the models of (1) VE/VCO(2), (2) VO(2) at ventilatory threshold (VT), (3) distance on the 6-minute walk, and (4) peak VO(2).
Results The women were younger than the men and more likely to have a nonischemic etiology and a higher ejection fraction. Dose of angiotensin converting enzyme inhibitor (ACEI) was lower in the women, on average. The lower ACEI dose may reflect the higher use of angiotensin II receptor blocker (ARB) in women. Both the peak VO(2) and the 6-minute walk distance were significantly lower in the women than in the men. Perhaps the most significant finding in this dataset of baseline characteristics is that the peak VO(2) for women was significantly lower than that for men with similar ventricular function and health status.
Conclusion Therefore, in a well-medicated, stable, class II-IV HF cohort of patients who are able to exercise, women have statistically significantly lower peak VO(2) and 6-minute walk distance than men with similar health status and ventricular function. These data should prompt careful thought when considering prognostic markers for women and listing for cardiac transplant. (Am Heart J 20091-158:S16-S23.)
C1 [Pina, Ileana L.; Vest, Marianne] Case Western Reserve Univ, Cleveland VA Med Ctr, Dept Educ, Cleveland, OH 44106 USA.
[Kokkinos, Peter] Washington VA Med Ctr, Washington, DC USA.
[Kao, Andrew] St Lukes Mid Amer Heart Inst, Kansas City, MO USA.
[Bittner, Vera; Fitz-Gerald, Meredith] Univ Alabama, Tuscaloosa, AL USA.
[Saval, Matt] Henry Ford Hosp, Detroit, MI 48202 USA.
[Clare, Bob; Ellis, Stephen J.] Duke Univ, Durham, NC USA.
[Goldberg, Lee] Univ Penn, Philadelphia, PA 19104 USA.
[Johnson, Maryl] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Swank, Ann] Univ Louisville, Louisville, KY 40292 USA.
[Ventura, Hector] Ochsner Med Ctr, Baton Rouge, LA USA.
[Moe, Gordon] Univ Toronto, Toronto, ON, Canada.
[Cooper, Lawton] NHLBI, Bethesda, MD 20892 USA.
[Whellan, David] Thomas Jefferson Univ, Jefferson Med Coll, Philadelphia, PA 19107 USA.
RP Pina, IL (reprint author), Case Western Reserve Univ, Cleveland VA Med Ctr, Dept Educ, Wade Pk, Cleveland, OH 44106 USA.
RI Ventura, Hector/A-7691-2011;
OI Bittner, Vera/0000-0001-9456-850X; Goldberg, Lee/0000-0002-7906-9638
FU National Institutes of Health [5U01HL063747, 5U01HL068973, 5U01HL066501,
5U01HL066482, 5U01HL064250, 5U01HL066494, 5U01HL064257, 5U01HL066497,
5U01HL068980, 5U01HL064265, 5U01HL066491, 5U01HL064264, 5U01HL066461,
R37AG18915, P60AG10484]
FX This research was supported by grants from the National Institutes of
Health: 5U01HL063747, 5U01HL068973, 5U01HL066501, 5U01HL066482,
5U01HL064250, 5U01HL066494, 5U01HL064257, 5U01HL066497, 5U01HL068980,
5U01HL064265, 5U01HL066491, 5U01HL064264, 5U01HL066461, R37AG18915, and
P60AG10484.
NR 29
TC 16
Z9 17
U1 1
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD OCT
PY 2009
VL 158
IS 4
BP S16
EP S23
DI 10.1016/j.ahj.2009.07.012
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 505PG
UT WOS:000270705800003
PM 19782784
ER
PT J
AU Savastano, DM
Tanofsky-Kraff, M
Han, JC
Ning, C
Sorg, RA
Roza, CA
Wolkoff, LE
Anandalingam, K
Jefferson-George, KS
Figueroa, RE
Sanford, EL
Brady, S
Kozlosky, M
Schoeller, DA
Yanovski, JA
AF Savastano, David M.
Tanofsky-Kraff, Marian
Han, Joan C.
Ning, Cong
Sorg, Rachael A.
Roza, Caroline A.
Wolkoff, Laura E.
Anandalingam, Kavitha
Jefferson-George, Kyra S.
Figueroa, Roberto E.
Sanford, Ethan L.
Brady, Sheila
Kozlosky, Merel
Schoeller, Dale A.
Yanovski, Jack A.
TI Energy intake and energy expenditure among children with polymorphisms
of the melanocortin-3 receptor
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID LABELED WATER METHOD; GENE VARIANTS; CHILDHOOD OBESITY;
AFRICAN-AMERICAN; BODY-FAT; MC3R; OVERWEIGHT; INSULIN; LINKAGE; MOUSE
AB Background: Homozygosity for 2 protein-altering polymorphisms in the melanocortin-3 receptor gene (MC3R) coding sequence, C17A and G241A, has been reported to be associated with an obesity phenotype in children, yet how these polymorphisms affect energy homeostasis is unknown. Association between adult body weight and +2138InsCAGACC, another variant in the 3' untranslated region of MC3R, has also been described.
Objective: The objective of this study was to examine associations of C17A + G241A and + 2138InsCAGACC MC3R variants with children's energy balance.
Design: Children aged 6-19 y were genotyped for MC3R C17A, G241A, and + 2138InsCAGACC. Subjects underwent studies of energy intake from a 9835-kcal food array (n = 185), resting energy expenditure (REE) by using indirect calorimetry (n = 302), or total daily energy expenditure (TEE) by using doubly labeled water (n = 120). Linear regression was used to examine the associations between MC3R polymorphisms and the measures of energy balance.
Results: Body mass index and fat mass were greater in those with double homozygosity for C17A + G241A (P = 0.001). After accounting for covariates (including body composition), the number of minor C17A + G241A alleles was associated with significantly greater energy intake (beta = +0.15, P = 0.02) but not altered REE or TEE. No significant associations were observed between + 2138InsCAGACC and measures of either fat mass or energy balance.
Conclusions: C17A + G241A polymorphisms may be associated with pediatric obesity because of greater energy intake rather than because of diminished energy expenditure. + 2138InsCAGACC does not appear to be associated with obesity or measures of energy balance in children. Am J Clin Nutr 2009; 90: 912-20.
C1 [Savastano, David M.; Tanofsky-Kraff, Marian; Han, Joan C.; Ning, Cong; Sorg, Rachael A.; Roza, Caroline A.; Wolkoff, Laura E.; Anandalingam, Kavitha; Jefferson-George, Kyra S.; Figueroa, Roberto E.; Sanford, Ethan L.; Brady, Sheila; Yanovski, Jack A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Growth & Obes, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
[Tanofsky-Kraff, Marian; Wolkoff, Laura E.] Uniformed Serv Univ Hlth Sci, Dept Med & Clin Psychol, Bethesda, MD 20814 USA.
[Kozlosky, Merel] NIH, Ctr Clin, Dept Nutr, Bethesda, MD 20892 USA.
[Schoeller, Dale A.] Univ Wisconsin, Dept Nutr Sci, Madison, WI 53706 USA.
RP Yanovski, JA (reprint author), NICHHD, Unit Growth & Obes, Program Dev Endocrinol & Genet, NIH,Hatfield Clin Res Ctr, 10 Ctr Dr,Room 1-3330,, Bethesda, MD 20892 USA.
EM jy15i@nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institutes of Health; National Center on Minority
Health and Health Disparities
FX Supported by the Intramural Research Program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
National Institutes of Health ( JAY), and by supplemental funding from
the National Center on Minority Health and Health Disparities ( JAY).
NR 38
TC 24
Z9 24
U1 0
U2 2
PU AMER SOC CLINICAL NUTRITION
PI BETHESDA
PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998
USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD OCT 1
PY 2009
VL 90
IS 4
BP 912
EP 920
DI 10.3945/ajcn.2009.27537
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 496GC
UT WOS:000269956700005
PM 19656839
ER
PT J
AU Gaskins, AJ
Mumford, SL
Zhang, CL
Wactawski-Wende, J
Hovey, KM
Whitcomb, BW
Howards, PP
Perkins, NJ
Yeung, E
Schisterman, EF
AF Gaskins, Audrey J.
Mumford, Sunni L.
Zhang, Cuilin
Wactawski-Wende, Jean
Hovey, Kathleen M.
Whitcomb, Brian W.
Howards, Penelope P.
Perkins, Neil J.
Yeung, Edwina
Schisterman, Enrique F.
CA BioCycle Study Grp
TI Effect of daily fiber intake on reproductive function: the BioCycle
Study
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID SERUM ESTROGEN CONCENTRATIONS; PREMENOPAUSAL WOMEN; BREAST-CANCER;
MENSTRUAL-CYCLE; DIETARY FIBER; GLYCEMIC INDEX; HORMONE-LEVELS;
SEX-HORMONES; RISK; FAT
AB Background: High-fiber diets have been associated with decreased breast cancer risk, likely mediated by the effect of fiber on lowering circulating estrogen concentrations. The influence of fiber on aspects of reproduction, which include ovulation, has not been well studied in premenopausal women.
Objective: The objective was to determine if fiber consumption is associated with hormone concentrations and incident anovulation in healthy, regularly menstruating women.
Design: The BioCycle Study was a prospective cohort study conducted from 2004 to 2006 that followed 250 women aged 18-44 y for 2 cycles. Dietary fiber consumption was assessed <= 4 times/cycle by using 24-h recall. Outcomes included concentrations of estradiol, progesterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH), which were measured <= 8 times/cycle, and incident anovulation.
Results: Dietary fiber consumption was inversely associated with hormone concentrations (estradiol, progesterone, LH, and FSH; P, 0.05) and positively associated with the risk of anovulation (P = 0.003) by using random-effects models with adjustment for total calories, age, race, and vitamin E intake. Each 5-g/d increase in total fiber intake was associated with a 1.78-fold increased risk (95% CI: 1.11, 2.84) of an anovulatory cycle. The adjusted odds ratio of 5 g fruit fiber/d was 3.05 (95% CI: 1.07, 8.71).
Conclusions: These findings suggest that a diet high in fiber is significantly associated with decreased hormone concentrations and a higher probability of anovulation. Further study of the effect of fiber on reproductive health and of the effect of these intakes in reproductive-aged women is warranted. Am J Clin Nutr 2009;90:1061-9.
C1 [Gaskins, Audrey J.; Mumford, Sunni L.; Zhang, Cuilin; Perkins, Neil J.; Yeung, Edwina; Schisterman, Enrique F.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Bethesda, MD USA.
[Wactawski-Wende, Jean; Hovey, Kathleen M.] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
[Whitcomb, Brian W.] Univ Massachusetts, Div Biostat & Epidemiol, Amherst, MA 01003 USA.
[Howards, Penelope P.] Emory Univ, Dept Epidemiol, Atlanta, GA 30322 USA.
RP Schisterman, EF (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, 6100 Execut Blvd,7B03M, Rockville, MD 20852 USA.
EM schistee@mail.nih.gov
RI Yeung, Edwina/F-5992-2015;
OI Yeung, Edwina/0000-0002-3851-2613; Perkins, Neil/0000-0002-6802-4733;
Schisterman, Enrique/0000-0003-3757-641X
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institutes of Health
FX Supported by the Intramural Research Program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
National Institutes of Health.
NR 44
TC 46
Z9 46
U1 1
U2 5
PU AMER SOC CLINICAL NUTRITION
PI BETHESDA
PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998
USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD OCT 1
PY 2009
VL 90
IS 4
BP 1061
EP 1069
DI 10.3945/ajcn.2009.27990
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 496GC
UT WOS:000269956700023
PM 19692496
ER
PT J
AU Beydoun, MA
Kuczmarski, MTF
Mason, MA
Ling, SM
Evans, MK
Zonderman, AB
AF Beydoun, May A.
Kuczmarski, Marie T. Fanelli
Mason, Marc A.
Ling, Shari M.
Evans, Michele K.
Zonderman, Alan B.
TI Role of depressive symptoms in explaining socioeconomic status
disparities in dietary quality and central adiposity among US adults: a
structural equation modeling approach
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID BODY-MASS INDEX; JOLLY FAT HYPOTHESIS; MULTIPLE-PASS METHOD; MIDDLE-AGED
WOMEN; WAIST-HIP RATIO; GENERAL-POPULATION; UNITED-STATES; OLDER-ADULTS;
HYPERCORTISOLEMIC DEPRESSION; ADOLESCENT DEPRESSION
AB Background: The link between socioeconomic status (SES), depression, dietary quality, and central adiposity remains unclear.
Objective: Pathways linking SES to dietary quality and central adiposity through depressive symptoms were examined across sex-ethnicity groups.
Design: Extensive data on US adults aged 30-64 y from the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study were used in multiple linear logistic regression models and structural equation models to test pathway associations. Measures included Center for Epidemiologic Studies-Depression (CES-D) scores, 2005 Healthy Eating Index (HEI) values, and dual-energy X-ray absorptiometry. Sample sizes for most analyses ranged between 1789 for anthropometric outcomes and 1227 for trunk fat outcomes.
Results: The CES-D score was associated with lower HEI scores in all sex-ethnicity groups, except in African American men, and with higher waist-to-hip ratios (WHRs) among African American women. A CES-D score >= 16 was positively associated with waist circumference (WC) and with trunk fat among white women and men, respectively. SES was positively related to central adiposity among African American men (central obesity and WC) and African American women (central obesity and percentage trunk fat) but was inversely related to central adiposity among white women. Among whites only, the total positive effect of SES on HEI was significantly mediated by CES-D score. Among white women, the total inverse effect of SES on WC and WHR was significantly explained by the CES-D score and HEI, whereas the CES-D score was positively associated with WHR among African American women, independently of SES.
Conclusion: Future mental health interventions targeted at reducing SES disparities in dietary quality and central adiposity may have different effects across sex-ethnicity groups. Am J Clin Nutr 2009;90:1084-95.
C1 [Beydoun, May A.] NIA, NIH, Biomed Res Ctr, Lab Personal & Cognit,Intramural Res Program, Baltimore, MD 21224 USA.
[Ling, Shari M.; Evans, Michele K.] NIA, Clin Res Branch, NIH, Intramural Res Program, Baltimore, MD 21224 USA.
[Kuczmarski, Marie T. Fanelli] Univ Delaware, Dept Hlth Nutr & Exercise Sci, Newark, DE USA.
[Mason, Marc A.] MedStar Res Inst, Baltimore, MD USA.
RP Beydoun, MA (reprint author), NIA, NIH, Biomed Res Ctr, Lab Personal & Cognit,Intramural Res Program, IRP 251,Bayview Blvd,Suite 100,Room 04B118, Baltimore, MD 21224 USA.
EM baydounm@mail.nih.gov
OI Zonderman, Alan B/0000-0002-6523-4778
FU Intramural Research Program of the NIH; National Institute on Aging
FX Supported entirely by the Intramural Research Program of the NIH,
National Institute on Aging.
NR 97
TC 26
Z9 26
U1 5
U2 11
PU AMER SOC CLINICAL NUTRITION
PI BETHESDA
PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998
USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD OCT 1
PY 2009
VL 90
IS 4
BP 1084
EP 1095
DI 10.3945/ajcn.2009.27782
PG 12
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 496GC
UT WOS:000269956700026
PM 19710191
ER
PT J
AU Mills, KT
Blair, A
Freeman, LEB
Sandler, DP
Hoppin, JA
AF Mills, Katherine T.
Blair, Aaron
Freeman, Laura E. Beane
Sandler, Dale P.
Hoppin, Jane A.
TI Pesticides and Myocardial Infarction Incidence and Mortality Among Male
Pesticide Applicators in the Agricultural Health Study
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE agriculture; cardiovascular diseases; myocardial infarction;
occupational exposure; pesticides
ID ISCHEMIC-HEART-DISEASE; PARTICULATE AIR-POLLUTION; CARDIAC
MANIFESTATIONS; OCCUPATIONAL-EXPOSURE; RISK-FACTORS; LIFE-STYLE;
FARMERS; ORGANOPHOSPHATES; PARTICIPANTS; INFORMATION
AB Acute organophosphate and carbamate pesticide poisonings result in adverse cardiac outcomes. The cardiac effects of chronic low-level pesticide exposure have not been studied. The authors analyzed self-reported lifetime use of pesticides reported at enrollment (1993-1997) and myocardial infarction mortality through 2006 and self-reported nonfatal myocardial infarction through 2003 among male pesticide applicators in the Agricultural Health Study. Using proportional hazard models, the authors estimated the association between lifetime use of 49 pesticides and fatal and nonfatal myocardial infarction. There were 476 deaths from myocardial infarction among 54,069 men enrolled in the study and 839 nonfatal myocardial infarctions among the 32,024 participants who completed the follow-up interview. Fatal and nonfatal myocardial infarctions were associated with commonly reported risk factors, including age and smoking. There was little evidence of an association between having used pesticides, individually or by class, and myocardial infarction mortality (e.g., insecticide hazard ratio (HR) = 0.91, 95% confidence interval (CI): 0.67, 1.24; herbicide HR = 0.74, 95% CI: 0.49, 1.10) or nonfatal myocardial infarction incidence (e.g., insecticide HR = 0.85, 95% CI: 0.66, 1.09; herbicide HR = 0.91, 95% CI: 0.61, 1.36). There was no evidence of a dose response with any pesticide measure. In a population with low risk for myocardial infarction, the authors observed little evidence of increased risk of myocardial infarction mortality or nonfatal myocardial infarction associated with the occupational use of pesticides.
C1 [Sandler, Dale P.; Hoppin, Jane A.] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Mills, Katherine T.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Blair, Aaron; Freeman, Laura E. Beane] NCI, Occupat & Environm Epidemiol Branch, NIH, Dept Hlth & Human Serv, Rockville, MD USA.
RP Hoppin, JA (reprint author), Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Dept Hlth & Human Serv, MD A3-05,POB 12233, Res Triangle Pk, NC 27709 USA.
EM hoppin1@niehs.nih.gov
OI Sandler, Dale/0000-0002-6776-0018
FU National Institutes of Health; National Institute of Environmental
Health Sciences [Z01-ES049030]; National Cancer Institute [Z01-CP010119]
FX Author affiliations: Department of Epidemiology, University of North
Carolina, Chapel Hill, North Carolina (Katherine T. Mills); Occupational
and Environmental Epidemiology Branch, National Cancer Institute,
National Institutes of Health, Department of Health and Human Services,
Rockville, Maryland (Aaron Blair, Laura E. Beane Freeman); and
Epidemiology Branch, National Institute of Environmental Health
Sciences, National Institutes of Health, Department of Health and Human
Services, Research Triangle Park, North Carolina (Dale P. Sandler, Jane
A. Hoppin).; This work was supported by the Intramural Research Program
of the National Institutes of Health, National Institute of
Environmental Health Sciences (Z01-ES049030) and National Cancer
Institute (Z01-CP010119).; The authors greatly appreciate the hard work
of Stuart Long for data analysis, as well as the Agricultural Health
Study Iowa and North Carolina field stations and coordinating center.;
Conflict of interest: none declared.
NR 22
TC 13
Z9 13
U1 1
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD OCT 1
PY 2009
VL 170
IS 7
BP 892
EP 900
DI 10.1093/aje/kwp214
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 499JY
UT WOS:000270217600012
PM 19700503
ER
PT J
AU Koh, C
Kleiner, DE
Sherry, RM
Fowler, DH
Heller, T
AF Koh, Christopher
Kleiner, David E.
Sherry, Richard M.
Fowler, Daniel H.
Heller, Theo
TI When the Left Got Left Behind
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Letter
ID OF-THE-LITERATURE; ECTOPIC LIVER; HEPATOCARCINOGENESIS
C1 [Koh, Christopher; Heller, Theo] NIDDK, NIH, Liver Dis Branch, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Sherry, Richard M.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Fowler, Daniel H.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
RP Koh, C (reprint author), NIDDK, NIH, Liver Dis Branch, 10 Ctr Dr,Bldg 10,Room 9B16, Bethesda, MD 20892 USA.
EM Kohchris@mail.nih.gov
OI Kleiner, David/0000-0003-3442-4453
FU Intramural NIH HHS [ZIA DK075008-04]
NR 3
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD OCT
PY 2009
VL 104
IS 10
BP 2644
EP 2645
DI 10.1038/ajg.2009.376
PG 3
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 507KY
UT WOS:000270853300049
PM 19806108
ER
PT J
AU Islami, F
Kamangar, F
Boffetta, P
AF Islami, Farhad
Kamangar, Farin
Boffetta, Paolo
TI Use of Proton Pump Inhibitors and Risk of Progression of Barrett's
Esophagus to Neoplastic Lesions
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Letter
ID ADENOCARCINOMA; DYSPLASIA
C1 [Islami, Farhad] Univ Tehran Med Sci, Shariati Hosp, Digest Dis Res Ctr, Tehran, Iran.
[Islami, Farhad; Boffetta, Paolo] Int Agcy Res Canc, F-69372 Lyon, France.
[Islami, Farhad] Kings Coll London, Thames Canc Registry, London WC2R 2LS, England.
[Kamangar, Farin] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Islami, F (reprint author), Univ Tehran Med Sci, Shariati Hosp, Digest Dis Res Ctr, Tehran, Iran.
EM islamif@fellows.iarc.fr
FU Intramural NIH HHS
NR 6
TC 11
Z9 11
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD OCT
PY 2009
VL 104
IS 10
BP 2646
EP 2648
DI 10.1038/ajg.2009.369
PG 3
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 507KY
UT WOS:000270853300050
PM 19806109
ER
PT J
AU Parkman, H
Yates, K
Koch, K
Snape, W
Abell, T
Hasler, W
Lee, L
Nguyen, L
McCallum, R
Farrugia, G
Pasricha, P
Tonascia, J
Hamilton, F
AF Parkman, Henry
Yates, Kathryn
Koch, Kenneth
Snape, William
Abell, Thomas
Hasler, William
Lee, Linda
Nguyen, Linda
McCallum, Richard
Farrugia, Gianrico
Pasricha, Pankaj
Tonascia, James
Hamilton, Frank
TI Dietary Intake and Nutritional Deficiencies in Patients with
Gastroparesis
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Meeting Abstract
CT 74th Annual Scientific Meeting and Postgraduate Course of the
American-College-of-Gastroenterology
CY OCT 23-28, 2009
CL San Diego, CA
SP Amer Coll Gastroenterol
C1 [Parkman, Henry; Yates, Kathryn; Koch, Kenneth; Snape, William; Abell, Thomas; Hasler, William; Lee, Linda; Nguyen, Linda; McCallum, Richard; Farrugia, Gianrico; Pasricha, Pankaj; Tonascia, James; Hamilton, Frank] NIH Gastroparesis Consortium, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD OCT
PY 2009
VL 104
SU 3
MA 138
BP S55
EP S55
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 507LA
UT WOS:000270853600138
ER
PT J
AU Simonaitis, L
McDonald, CJ
AF Simonaitis, Linas
McDonald, Clement J.
TI Using National Drug Codes and drug knowledge bases to organize
prescription records from multiple sources
SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY
LA English
DT Article
DE Codes; Databases; Hospitals; National Drug Code; Pharmacy,
institutional, hospital; Records
ID HEALTH-CARE; NETWORK
AB Purpose. The utility of National Drug Codes (NDCs) and drug knowledge bases (DKBs) in the organization of prescription records from multiple sources was studied.
Methods. The master files of most pharmacy systems include NDCs and local codes to identify the products they dispense. We obtained a large sample of prescription records from seven different sources. These records carried a national product code or a local code that could be translated into a national product code via their formulary master. We obtained mapping tables from five DKBs. We measured the degree to which the DKB mapping tables covered the national product codes carried in or associated with the sample of prescription records.
Results. Considering the total prescription volume, DKBs covered 93.0-99.8% of the product codes from three outpatient sources and 77.4-97.0% of the product codes from four inpatient sources. Among the inpatient sources, invented codes explained 36-94% of the noncoverage. Outpatient pharmacy sources rarely invented codes, which comprised only 0.11-0.21% of their total prescription volume, compared with inpatient pharmacy sources for which Invented codes comprised 1.7-7.4% of their prescription volume. The distribution of prescribed products was highly skewed, with 1.4-4.4% of codes accounting for 50% of the message volume and 10.7-34.5% accounting for 90% of the message volume.
Conclusion. DKBs cover the product codes used by outpatient sources sufficiently well to permit automatic mapping. Changes in policies and standards could increase coverage of product codes used by inpatient sources.
C1 [Simonaitis, Linas; McDonald, Clement J.] Regenstrief Inst Hlth Care, Indianapolis, IN 46202 USA.
[Simonaitis, Linas; McDonald, Clement J.] Indiana Univ, Sch Med, Indianapolis, IN USA.
[McDonald, Clement J.] Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD USA.
RP Simonaitis, L (reprint author), Regenstrief Inst Hlth Care, 410 W 10th St,Suite 2000, Indianapolis, IN 46202 USA.
EM lsimonaitis@regenstrief.org
FU Regenstrief Institute; National Library of Medicine [T15 LM07117];
National Cancer Institute [U01 CA91343]; Cooperative Agreement for the
Shared Pathology Informatics Network; National Institutes of Health [P20
GM66402]; Indiana TWenty-First Century Research and Technology Fund
FX This work was performed at the Regenstrief Institute and supported by
grant T15 LM07117 from the National Library of Medicine; by National
Cancer Institute grant U01 CA91343, a Cooperative Agreement for the
Shared Pathology Informatics Network; by Biomedical Information Science
and Technology Initiative grant P20 GM66402 from the National Institutes
of Health; and by a grant from the Indiana TWenty-First Century Research
and Technology Fund for proposal ID 510040784.
NR 17
TC 2
Z9 3
U1 0
U2 1
PU AMER SOC HEALTH-SYSTEM PHARMACISTS
PI BETHESDA
PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 USA
SN 1079-2082
J9 AM J HEALTH-SYST PH
JI Am. J. Health-Syst. Pharm.
PD OCT 1
PY 2009
VL 66
IS 19
BP 1743
EP 1753
DI 10.2146/ajhp080221
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 496EJ
UT WOS:000269951900014
PM 19767382
ER
PT J
AU Mei, H
Gu, DF
Rice, TK
Hixson, JE
Chen, J
Jaquish, CE
Zhao, Q
Chen, CS
Chen, JC
Gu, CC
Kelly, TN
He, J
AF Mei, Hao
Gu, Dongfeng
Rice, Treva K.
Hixson, James E.
Chen, Jing
Jaquish, Cashell E.
Zhao, Qi
Chen, Chung-Shiuan
Chen, Ji-Chun
Gu, C. Charles
Kelly, Tanika N.
He, Jiang
TI Heritability of Blood Pressure Responses to Cold Pressor Test in a
Chinese Population
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Article
ID CARDIOVASCULAR RISK-FACTORS; TRAIT LINKAGE ANALYSIS; FAMILIAL
RESEMBLANCE; GENETIC INFLUENCES; HYPERTENSION; PREDICTOR; PAIRS; TWIN
AB BACKGROUND
Genetic determinants of blood pressure (BP) responses to the cold pressor test (CPT), a phenotype associated with risk of hypertension and cardiovascular disease has not been well studied.
METHODS
We examined the heritability of BP response to CPT in 1,994 subjects from 627 families in rural north China. BP was measured before and at 0, 1, 2, and 4 min after the participants immersed their hand in ice water for I min. Heritabilities of baseline BP and responses at 0 min, maximum response, and area-under-the-curve (AUC) during CPT were computed using a variance components method. Additionally, bivariate heritabilities were calculated to test the existence of shared genetic determinants between baseline BP and responses to CPT.
RESULTS
Heritabilities of baseline BP and responses to CPT were estimated from 14 to 35%, which all significantly differed from 0 (P <= 0.002). Genetic correlations (s.e.) due to the same genes between baseline BP and responses to CPT ranged from -0.07 (0.14) to 0.21 (0.15), which were not significantly different from 0. Genetic correlations between reactivity and recovery were 0.67 (0.10) and 0.59 (0.10) for systolic (SBP) and diastolic BP (DBP), respectively, which were significantly different from 0.
CONCLUSIONS
We concluded that (i) baseline BP and BP responses to CPT had strong genetic determinants; (ii) baseline BP and BP response to CPT did not share the same genetic components; and (iii) BP reactivity and recovery shared the same genetic components. These findings may lead to a better understanding of the genetic mechanism of BP responses to CPT.
C1 [Mei, Hao; Zhao, Qi; Chen, Chung-Shiuan; Kelly, Tanika N.; He, Jiang] Tulane Univ, Sch Publ Hlth & Trop Med, Dept Epidemiol, New Orleans, LA 70118 USA.
[Gu, Dongfeng; Chen, Ji-Chun] Chinese Acad Med Sci, Div Populat Genet & Prevent, Cardiovasc Inst, Beijing 100037, Peoples R China.
[Gu, Dongfeng; Chen, Ji-Chun] Chinese Acad Med Sci, Fu Wai Hosp, Beijing 100037, Peoples R China.
[Rice, Treva K.; Gu, C. Charles] Washington Univ, Div Biostat, Sch Med, St Louis, MO USA.
[Hixson, James E.] Univ Texas Houston, Sch Publ Hlth, Ctr Human Genet, Houston, TX USA.
[Chen, Jing; He, Jiang] Tulane Univ, Sch Med, Dept Med, New Orleans, LA 70112 USA.
[Jaquish, Cashell E.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Mei, H (reprint author), Tulane Univ, Sch Publ Hlth & Trop Med, Dept Epidemiol, New Orleans, LA 70118 USA.
EM hmei@tulane.edu
RI Rice, Treva/D-1385-2009; Gu, Charles/A-7934-2010
OI Gu, Charles/0000-0002-8527-8145
FU National Heart, Lung, and Blood Institute [U01HL072507, R01HL087263,
R01HL090682]; National Institutes of Health, Bethesda, Maryland
FX We express our sincere appreciation to the Genetic Epidemiology Network
of Salt Sensitivity Study participants for their participation and
cooperation in this project. The Genetic Epidemiology Network of Salt
Sensitivity (GenSalt) is supported by research grants (U01HL072507,
R01HL087263, and R01HL090682) from the National Heart, Lung, and Blood
Institute, National Institutes of Health, Bethesda, Maryland.
NR 22
TC 7
Z9 7
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0895-7061
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD OCT
PY 2009
VL 22
IS 10
BP 1096
EP 1100
DI 10.1038/ajh.2009.139
PG 5
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 504YD
UT WOS:000270653300013
PM 19661924
ER
PT J
AU Brody, R
Peleg, E
Grossman, E
Sharabi, Y
AF Brody, Raphaelle
Peleg, Edna
Grossman, Ehud
Sharabi, Yehonatan
TI Production and Secretion of Adiponectin from 3T3-L1 Adipocytes:
Comparison of Antihypertensive Drugs
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Article
ID ANGIOTENSIN-RECEPTOR BLOCKER; HYPERTENSIVE PATIENTS; PLASMA ADIPONECTIN;
INSULIN-RESISTANCE; METABOLIC SYNDROME; GAMMA ACTIVATION; IN-VITRO;
TELMISARTAN; ANTAGONIST; EXPRESSION
AB BACKGROUND
Adiponectin is an important vascular protective adipocytokine that possesses antidiabetic, antiatherogenic, and anti-inflammatory properties. The aim of this study was to evaluate the effect of various antihypertensive drugs on the production and secretion of adiponectin from adipocytes.
METHODS
3T3-L1 adipocytes were incubated for 6 h with increased doses of the following drugs: hydrochlorothiazide, atenolol, losartan, telmisartan, captopril, and nifedipine. Adiponectin levels, as well as adiponectin-mRNA expression, were measured in the medium and cells.
RESULTS
Significant increases of adiponectin were induced by telmisartan: 56% with a dose of 0.1 mu mol/l (P < 0.05),131% with 10 pmol/l (P < 0.05), and 125% with 100 pmol/l (P < 0.01). Losartan (100 mu mol/l) also increased adiponectin by 65% (P < 0.05). Conversely, hydrochlorothiazide, 0.1 pmol/l, reduced adiponectin by 37% (P < 0.01). Captopril, atenolol, and nifedipine had no effect on adiponectin. Gene expression of adiponectin correlated with these results: with telmisartan, it increased by 27%, and with hydrochlorothiazide it decreased by 38% (P < 0.05 for both compared to the control).
CONCLUSION
In this comparative model, telmisartan, and to a lesser extent, losartan, increased production and secretion of adiponectin from 3T3-L1 adipocytes compared to the other anti hypertensive drugs.
C1 [Brody, Raphaelle; Peleg, Edna; Grossman, Ehud; Sharabi, Yehonatan] Chaim Sheba Med Ctr, Hypertens Unit, IL-52621 Tel Hashomer, Israel.
[Brody, Raphaelle; Peleg, Edna; Grossman, Ehud; Sharabi, Yehonatan] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel.
[Sharabi, Yehonatan] NINDS, NIH, Bethesda, MD 20892 USA.
RP Sharabi, Y (reprint author), Chaim Sheba Med Ctr, Hypertens Unit, IL-52621 Tel Hashomer, Israel.
EM sharabiy@sheba.health.gov.il
OI Grossman, Ehud/0000-0001-8353-0661
NR 20
TC 9
Z9 9
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0895-7061
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD OCT
PY 2009
VL 22
IS 10
BP 1126
EP 1129
DI 10.1038/ajh.2009.171
PG 4
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 504YD
UT WOS:000270653300018
PM 19730415
ER
PT J
AU Gyamfi, C
Horton, AL
Momirova, V
Rouse, DJ
Caritis, SN
Peaceman, AM
Sciscione, A
Meis, PJ
Spong, CY
Dombrowski, M
Sibai, B
Varner, MW
Iams, JD
Mercer, BM
Carpenter, MW
Lo, J
Ramin, SM
O'Sullivan, MJ
Miodovnik, M
Conway, D
AF Gyamfi, Cynthia
Horton, Amanda L.
Momirova, Valerija
Rouse, Dwight J.
Caritis, Steve N.
Peaceman, Alan M.
Sciscione, Anthony
Meis, Paul J.
Spong, Catherine Y.
Dombrowski, Mitchell
Sibai, Baha
Varner, Michael W.
Iams, Jay D.
Mercer, Brian M.
Carpenter, Marshall W.
Lo, Julie
Ramin, Susan M.
O'Sullivan, Mary Jo
Miodovnik, Menachem
Conway, Deborah
CA Eunice Kennedy Shriver Natl Inst C
TI The effect of 17-alpha hydroxyprogesterone caproate on the risk of
gestational diabetes in singleton or twin pregnancies
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article; Proceedings Paper
CT 29th Annual Meeting of the Society-for-Maternal-Fetal-Medicine
CY JAN 26-31, 2009
CL San Diego, CA
SP Soc Mat Fetal Med
DE 17-alpha hydroxy progesterone caproate; gestational diabetes;
singletons; twins
ID RECURRENT PRETERM DELIVERY; 17-ALPHA-HYDROXYPROGESTERONE CAPROATE; SHORT
CERVIX; DOUBLE-BLIND; PROGESTERONE; BIRTH; WOMEN; PREVENTION; TRIAL;
SECONDARY
AB OBJECTIVE: To compare the rates of gestational diabetes among women who received serial doses of 17-alpha hydroxyprogesterone caproate vs placebo.
STUDY DESIGN: Secondary analysis of 2 double-blind randomized placebo-controlled trials of 17-alpha hydroxyprogesterone caproate given to women at risk for preterm delivery. The incidence of gestational diabetes was compared between women who received 17-alpha hydroxyprogesterone caproate or placebo.
RESULTS: We included 1094 women; 441 had singleton and 653 had twin gestations. Combining the 2 studies, 616 received 17-alpha hydroxyprogesterone caproate and 478 received placebo. Among single-ton and twin pregnancies, rates of gestational diabetes were similar in women receiving 17-alpha hydroxyprogesterone caproate vs placebo (5.8% vs 4.7%; P = .64 and 7.4% vs 7.6%; P = .94, respectively). In the multivariable model, progesterone was not associated with gestational diabetes (adjusted odds ratio, 1.04; 95% confidence interval, 0.62-1.73).
CONCLUSION: Weekly administration of 17-alpha hydroxyprogesterone caproate is not associated with higher rates of gestational diabetes in either singleton or twin pregnancies.
C1 [Gyamfi, Cynthia] Columbia Univ, Coll Phys & Surg, Dept Obstet, New York, NY 10027 USA.
Columbia Univ, Coll Phys & Surg, Dept Gynecol, New York, NY USA.
Univ N Carolina, Sch Med, Chapel Hill, NC USA.
Univ Alabama, Sch Med, Birmingham, AL USA.
Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
Drexel Univ, Coll Med, Philadelphia, PA 19104 USA.
Univ Utah, Sch Med, Salt Lake City, UT USA.
Ohio State Univ, Coll Med, Columbus, OH 43210 USA.
Case Western Reserve Univ, Sch Med, Cleveland, OH USA.
Wayne State Univ, Sch Med, Detroit, MI USA.
Brown Univ, Sch Med, Providence, RI 02912 USA.
Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
Univ Tennessee, Memphis, TN USA.
Univ Miami, Leonard M Miller Sch Med, Miami, FL USA.
Univ Cincinnati, Coll Med, Cincinnati, OH USA.
Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
George Washington Univ, Ctr Biostat, Washington, DC USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Gyamfi, C (reprint author), Columbia Univ, Coll Phys & Surg, Dept Obstet, New York, NY 10027 USA.
RI Varner, Michael/K-9890-2013;
OI caritis, steve/0000-0002-2169-0712; Varner, Michael/0000-0001-9455-3973;
Peaceman, Alan/0000-0002-4515-4850
FU NICHD NIH HHS [HD27860, HD21410, HD21414, HD27861, HD27869, HD27915,
HD27917, HD34116, HD34136, HD34208, HD34210, HD36801, HD40485, HD40500,
HD40512, HD40544, HD40545, HD40560, U01 HD036801, U10 HD021410, U10
HD027860, U10 HD027869, U10 HD027905, U10 HD027915, U10 HD027917, U10
HD034116, U10 HD034122, U10 HD034136, U10 HD034208, U10 HD036801, U10
HD040485, U10 HD040485-09, U10 HD040500, U10 HD040512, U10 HD040544, U10
HD040545, U10 HD040560, UG1 HD027869, UG1 HD027915, UG1 HD034116, UG1
HD034208, UG1 HD040485, UG1 HD040500, UG1 HD040512, UG1 HD040544, UG1
HD040545, UG1 HD040560]
NR 17
TC 9
Z9 9
U1 0
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD OCT
PY 2009
VL 201
IS 4
AR 392.e1
DI 10.1016/j.ajog.2009.06.036
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 502LP
UT WOS:000270461800021
PM 19716543
ER
PT J
AU Laughon, SK
Catov, J
Provins, T
Roberts, JM
Gandley, RE
AF Laughon, S. Katherine
Catov, Janet
Provins, Traci
Roberts, James M.
Gandley, Robin E.
TI Elevated first-trimester uric acid concentrations are associated with
the development of gestational diabetes
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article; Proceedings Paper
CT 29th Annual Meeting of the Society-for-Maternal-Fetal-Medicine
CY JAN 26-31, 2009
CL San Diego, CA
SP Soc Mat Fetal Med
DE gestational diabetes; hyperuricemia; uric acid
ID METABOLIC SYNDROME; CARDIOVASCULAR RISK; INSULIN-RESISTANCE;
HYPERURICEMIA; WOMEN; HYPERTENSION; PREVALENCE; PREGNANCY; MELLITUS;
GLUCOSE
AB OBJECTIVE: We sought to demonstrate that elevated first-trimester uric acid is associated with development of gestational diabetes mellitus (GDM).
STUDY DESIGN: Uric acid was measured in 1570 plasma samples collected at mean gestational age of 8.9 +/- 2.5 weeks. The primary outcome was GDM, diagnosed by 3-hour glucose tolerance test using Carpenter and Coustan criteria or by a 1-hour value of >= 200 mg/dL. Logistic regression was performed, adjusting for relevant covariates.
RESULTS: Almost half (46.6%) of the women with GDM had first-trimester uric acid concentrations in the highest quartile (> 3.57-8.30 mg/dL). Women with uric acid in the highest quartile had a 3.25-fold increased risk (95% confidence interval, 1.35-7.83) of developing GDM after adjustment for body mass index and age. This effect was concentration dependent as risk increased with increasing uric acid quartiles (P = .003).
CONCLUSION: First-trimester hyperuricemia is associated with an increased risk of developing GDM, independent of body mass index.
C1 [Laughon, S. Katherine; Catov, Janet; Roberts, James M.; Gandley, Robin E.] Univ Pittsburgh, Sch Med, Dept Obstet, Pittsburgh, PA USA.
[Laughon, S. Katherine; Catov, Janet; Roberts, James M.; Gandley, Robin E.] Univ Pittsburgh, Sch Med, Dept Gynecol & Reprod Serv, Pittsburgh, PA USA.
[Catov, Janet; Roberts, James M.] Univ Pittsburgh, Dept Epidemiol, Sch Med, Pittsburgh, PA 15261 USA.
[Gandley, Robin E.] Univ Pittsburgh, Dept Environm & Occupat Hlth, Sch Med, Pittsburgh, PA USA.
[Catov, Janet; Provins, Traci; Roberts, James M.; Gandley, Robin E.] Univ Pittsburgh, Magee Womens Res Inst, Pittsburgh, PA USA.
RP Laughon, SK (reprint author), NICHD, NIH, Div Epidemiol Stat & Prevent Res, Bldg 6100,Room 7B03, Bethesda, MD 20892 USA.
EM laughonsk@mail.nih.gov
OI Grantz, Katherine/0000-0003-0276-8534
FU NCATS NIH HHS [UL1 TR000005]; NCRR NIH HHS [UL1 RR024153, UL1
RR024153-01]; NICHD NIH HHS [P01 HD030367, P01 HD030367-07]
NR 21
TC 3
Z9 3
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD OCT
PY 2009
VL 201
IS 4
AR 402.e1
DI 10.1016/j.ajog.2009.06.065
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 502LP
UT WOS:000270461800026
PM 19788971
ER
PT J
AU Rouse, DJ
Weiner, SJ
Bloom, SL
Varner, MW
Spong, CY
Ramin, SM
Caritis, SN
Peaceman, AM
Sorokin, Y
Sciscione, A
Carpenter, MW
Mercer, BM
Thorp, JM
Malone, FD
Harper, M
Iams, JD
Anderson, GD
AF Rouse, Dwight J.
Weiner, Steven J.
Bloom, Steven L.
Varner, Michael W.
Spong, Catherine Y.
Ramin, Susan M.
Caritis, Steve N.
Peaceman, Alan M.
Sorokin, Yoram
Sciscione, Anthony
Carpenter, Marshall W.
Mercer, Brian M.
Thorp, John M., Jr.
Malone, Fergal D.
Harper, Margaret
Iams, Jay D.
Anderson, Garland D.
CA Eunice Kennedy Shriver Natl Inst C
TI Second-stage labor duration in nulliparous women: relationship to
maternal and perinatal outcomes
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE duration; nulliparous women; second stage of labor
ID PROLONGED 2ND-STAGE; 2ND STAGE; NEONATAL OUTCOMES; CESAREAN DELIVERY;
MORBIDITY
AB OBJECTIVE: The purpose of this study was to assess maternal and perinatal outcomes as a function of second-stage labor duration.
STUDY DESIGN: We assessed outcomes in nulliparous laboring women who were enrolled in a trial of fetal pulse oximetry.
RESULTS: Of 5341 participants, 4126 women reached the second stage of labor. As the duration of the second stage increased, spontaneous vaginal delivery rates declined, from 85% when the duration was < 1 hour to 9% when it was >= 5 hours. Adverse maternal outcomes that were associated significantly with the duration of the second stage of labor included chorioamnionitis (overall rate, 3.9%), third-or fourth-degree perineal laceration (overall rate, 8.7%), and uterine atony (overall rate, 3.9%). Odds ratios for each additional hour of the second stage of labor ranged from 1.3-1.8. Among individual adverse neonatal outcomes, only admission to a neonatal intensive care unit was associated significantly with second stage duration (odds ratio, 1.4).
CONCLUSION: The second stage of labor does not need to be terminated for duration alone.
C1 [Rouse, Dwight J.] Univ Alabama, Dept Obstet, Birmingham, AL 35294 USA.
[Rouse, Dwight J.] Univ Alabama, Dept Gynecol, Birmingham, AL USA.
[Weiner, Steven J.] George Washington Univ, Ctr Biostat, Washington, DC USA.
[Bloom, Steven L.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Varner, Michael W.] Univ Utah, Salt Lake City, UT USA.
[Spong, Catherine Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Ramin, Susan M.] Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
[Caritis, Steve N.] Univ Pittsburgh, Pittsburgh, PA USA.
[Peaceman, Alan M.] Northwestern Univ, Chicago, IL 60611 USA.
[Sorokin, Yoram] Wayne State Univ, Detroit, MI USA.
[Sciscione, Anthony] Drexel Univ, Philadelphia, PA 19104 USA.
[Carpenter, Marshall W.] Brown Univ, Providence, RI 02912 USA.
[Mercer, Brian M.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Thorp, John M., Jr.] Univ N Carolina, Chapel Hill, NC USA.
[Malone, Fergal D.] Columbia Univ, New York, NY USA.
[Harper, Margaret] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Iams, Jay D.] Ohio State Univ, Columbus, OH 43210 USA.
[Anderson, Garland D.] Univ Texas Med Branch, Galveston, TX USA.
RP Rouse, DJ (reprint author), Univ Alabama, Dept Obstet, Birmingham, AL 35294 USA.
RI Malone, Fergal/D-6233-2012; Varner, Michael/K-9890-2013;
OI caritis, steve/0000-0002-2169-0712; Varner, Michael/0000-0001-9455-3973;
Peaceman, Alan/0000-0002-4515-4850
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [HD21410, HD27860, HD27869, HD27915, HD27917, HD34116,
HD34136, HD34208, HD40485, HD40500, HD40512, HD40544, HD40545, HD40560,
HD36801]
FX Supported by Grants from the Eunice Kennedy Shriver National Institute
of Child Health and Human Development (HD21410, HD27860, HD27869,
HD27915, HD27917, HD34116, HD34136, HD34208, HD40485, HD40500, HD40512,
HD40544, HD40545, HD40560, and HD36801).
NR 11
TC 20
Z9 22
U1 0
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD OCT
PY 2009
VL 201
IS 4
AR 357.e1
DI 10.1016/j.ajog.2009.08.003
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 502LP
UT WOS:000270461800008
PM 19788967
ER
PT J
AU Pasadhika, S
Kempen, JH
Newcomb, CW
Liesegang, TL
Pujari, SS
Rosenbaum, JT
Thorne, JE
Foster, CS
Jabs, DA
Levy-Clarke, GA
Nussenblatt, RB
Suhler, EB
AF Pasadhika, Sirichai
Kempen, John H.
Newcomb, Craig W.
Liesegang, Teresa L.
Pujari, Siddharth S.
Rosenbaum, James T.
Thorne, Jennifer E.
Foster, C. Stephen
Jabs, Douglas A.
Levy-Clarke, Grace A.
Nussenblatt, Robert B.
Suhler, Eric B.
TI Azathioprine for Ocular Inflammatory Diseases
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID LONG-TERM; IMMUNOSUPPRESSIVE THERAPY; BEHCETS-SYNDROME; CONTROLLED
TRIAL; DRUGS; MANAGEMENT; PREGNANCY; ARTHRITIS; UVEITIS; AGENTS
AB PURPOSE: To evaluate treatment outcomes of azathioprine for noninfectious ocular inflammatory diseases.
DESIGN: Retrospective cohort study.
METHODS: Medical records of 145 patients starting azathioprine as a sole noncorticosteroid immunosuppressant at 4 tertiary uveitis services were reviewed. Main outcome measures included control of ocular inflammation, sustained control after tapering prednisone to <= 10 mg/day, and discontinuation of treatment because of side effects.
RESULTS: Among 145 patients (255 eyes) treated with azathioprine, 63% had uveitis, 23% had mucous membrane pemphigoid, 11% bad scleritis, and 3% had other inflammatory diseases. By Kaplan-Meier analysis, 62% (95% confidence interval [CI], 50% to 74%) of patients with active disease initially gained complete inactivity of inflammation sustained over at least 28 days within 1 year of therapy, and 47% (95% CI, 37% to 58%) tapered systemic corticosteroids to <= 10 mg daily while maintaining control of inflammation within 1 year of therapy. Treatment success was most common for intermediate uveitis (90% with sustained inactivity within 1 year; 95% CI, 64% to 99%). Over the median follow-up of 230 days (interquartile range, 62 to 679 days), azathioprine was discontinued at a rate of 0.45 per person,years (/PY): 0.16/PY because of side effects, 0.10/PY because of ineffectiveness, 0.09/PY because of disease remission, and 0.10/PY because of unspecified causes.
CONCLUSIONS: Azathioprine was moderately effective as a single corticosteroid-sparing immunosuppressive agent in terms of control of inflammation and corticosteroid-sparing benefits, but required several months to achieve treatment goals; it seems especially useful for patients with intermediate uveitis. Treatment-limiting side effects occurred in approximately one-fourth of patients within 1 year, but typically were reversible. (Am J Ophthalmol 2009;148:500-509. (C) 2009 by Elsevier Inc. All rights reserved.)
C1 [Kempen, John H.] Univ Penn, Dept Ophthalmol, Ctr Prevent Ophthalmol & Biostat, Philadelphia, PA 19104 USA.
[Pasadhika, Sirichai; Liesegang, Teresa L.; Rosenbaum, James T.; Suhler, Eric B.] Oregon Hlth & Sci Univ, Dept Ophthalmol, Portland, OR 97201 USA.
[Rosenbaum, James T.] Oregon Hlth & Sci Univ, Dept Internal Med, Portland, OR 97201 USA.
[Kempen, John H.] Univ Penn, Scheie Eye Inst, Ocular Inflammat Serv, Philadelphia, PA 19104 USA.
[Kempen, John H.; Newcomb, Craig W.] Univ Penn, Ctr Clin Epidemiol & Biostat, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Pujari, Siddharth S.; Foster, C. Stephen] Massachusetts Eye Res & Surg Inst, Cambridge, MA USA.
[Thorne, Jennifer E.; Jabs, Douglas A.] Johns Hopkins Univ, Dept Ophthalmol, Baltimore, MD USA.
[Thorne, Jennifer E.; Jabs, Douglas A.] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Foster, C. Stephen] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA.
[Jabs, Douglas A.] Mt Sinai Sch Med, Dept Ophthalmol, New York, NY USA.
[Jabs, Douglas A.] Mt Sinai Sch Med, Dept Med, New York, NY USA.
[Levy-Clarke, Grace A.; Nussenblatt, Robert B.] NEI, Immunol Lab, Bethesda, MD 20892 USA.
[Levy-Clarke, Grace A.] St Lukes Cataract & Laser Inst, Tarpon Springs, FL USA.
[Suhler, Eric B.] Portland VA Med Ctr, Portland, OR USA.
RP Kempen, JH (reprint author), Univ Penn, Dept Ophthalmol, Ctr Prevent Ophthalmol & Biostat, 3535 Market St,Suite 700, Philadelphia, PA 19104 USA.
EM john.kempen@uphs.upenn.edu
FU NATIONAL EYE INSTITUTE, BETHESDA, MARYLAND [EY-014943]; Research to
Prevent Blindness; Veterans' Administration; Genentech; Eyegate; Lux
Biosciences; Abbott
FX THIS STUDY WAS SUPPORTED BY THE NATIONAL EYE INSTITUTE, BETHESDA,
MARYLAND, GRANT NO. EY-014943 (DR KEMPEN); the Paul and Evanina Mackall
Foundation, New York, New York; and Research to Prevent Blindness Inc,
New York, New York. Dr Kempen is a Research to Prevent Blindness James
S. Adams Special Scholar Award recipient. Drs Jabs and Rosenbaum are
recipients of Research to Prevent Blindness Senior Scientific
Investigator Awards. Dr Levy-Clarke previously was supported by and Dr
Nussenblatt is supported by intramural funds of the National Eye
Institute, Bethesda, Maryland. Dr Sublet also received support from the
Veterans' Administration. Dr Foster has served as a consultant to
Allergan, Bausch & Lomb, and Sirion; owns equity or stock options in
Eyegate; and h is received speaking fees from Alcon, Allergan, Inspire,
Ista, Bausch & Lomb, and Centocor. Dr Jabs has served as a consultant to
Abbott, Genzyme Corporation, Novartis, Allergan, the Emmes Corporation
(DSMC member), and the Johns Hopkins University Dana Center for
Preventive Ophthalmology. Dr Kempen has served as a Consultant to Lux
Biosciences and has participated in clinical trials funded by Allergan
and Eyegate. Dr Rosenbaum has served as a Consultant to Abbott, Amgen,
Allergan, Lux Biosciences, and Novartis; holds equity ownership/stock
options in Amgen; and has received research Support from Genentech, Lux
Biosciences, and Abbott. Dr Suhler has received research support from
Eyegate, Genentech, Lux Biosciences, and Abbott. Involved in design of
study (S.P., J.H.K., C.W.N.); conduct of study (S.P., J.H.K., E.B.S.);
collection of data (S.P., J.H.K., CW.N., T.L.L., S.S.P., J.T.R., J.E.T.,
C.S.F., D.A.J., G.A.L.-C., R.B.N., E.B.S.); management (S.P., J.H.K.,
JT.R., J.E.T., C.S.F., D.A.]., G.A.L.-C., R.B.N., E.B.S.), analysis, and
interpretation of data (S.P., J.H.K., CW.N., E.B.S.); and preparation
(S.P., J.H.K., E.B.S.), review, and approval of the manuscript (S.P.,
J.H.K., C.W.N., T.L.L., S.S.P., J.T.R., J.E.T., C.S.F., D.A.J.,
G.A.L.-C., R.B.N., E.B.S.). The protocol was approved by Institutional
Review Boards of all participating institutions and was conducted in
accordance with the principles of the Declaration of Helsinki and the
Health Insurance Portability and Accountability Act.
NR 26
TC 68
Z9 71
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD OCT
PY 2009
VL 148
IS 4
BP 500
EP 509
DI 10.1016/j.ajo.2009.05.008
PG 10
WC Ophthalmology
SC Ophthalmology
GA 503MI
UT WOS:000270538000006
PM 19570522
ER
PT J
AU Wong, WT
Forooghian, F
Majumdar, Z
Bonner, RF
Cunningham, D
Chew, EY
AF Wong, Wai T.
Forooghian, Farzin
Majumdar, Zigurts
Bonner, Robert F.
Cunningham, Denise
Chew, Emily Y.
TI Fundus Autofluorescence in Type 2 Idiopathic Macular Telangiectasia:
Correlation with Optical Coherence Tomography and Microperimetry
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID JUXTAFOVEOLAR RETINAL TELANGIECTASIS; CLASSIFICATION; FLUORESCENCE;
DISEASE
AB PURPOSE: To use multiple imaging methods to investigate patients with type 2 idiopathic macular telangiectasia (IMT) at different disease severity stages so as to characterize and categorize disease progression through the full spectrum of disease phenotypes.
DESIGN: Observational case series.
METHODS: Twelve patients with type 2 IMT (22 eyes) examined with fundus photography, angiography, optical coherence tomography imaging, fundus autofluorescence (FAF), and microperimetry testing in an institutional setting.
RESULTS: Eyes examined by multiple imaging methods were classified into 5 proposed categories (0 through 4): category 0 (fellow) eyes had normal results on all imaging methods. Category 1 eyes had increased foveal autofluorescence on FAF imaging as the only imaging abnormality. Category 2 eyes had increased foveal autofluorescence together with fun, duscopic and angiographic features typical of type 2 IMT. Category 3 eyes had additional evidence of foveal atrophy on optical coherence tomography, and category 4 eyes had all the above features plus clinically evident pigment clumping. FAF signal increased in intensity in the foveal region from category 0 through category 3, whereas category 4 eyes demonstrated a mixed pattern of increased and decreased FAF signal.
CONCLUSIONS: The findings here outline a sequence of progressive changes seen with multiple imaging methods in advancing stages of disease. Increase in foveal autofluorescence is an early anatomic change in type 2 IMT that may precede typical clinical and angiographic changes. Loss of macular pigment density in the fovea and a changing composition of fluorophores in the retinal pigment epithelium may underlie these changes on FAF in the fundus. (Am J Ophthalmol 2009;148:573-583. Published by Elsevier Inc.)
C1 [Chew, Emily Y.] NEI, Div Epidemiol & Clin Res, NIH, NICHHD, Bethesda, MD 20892 USA.
[Majumdar, Zigurts; Bonner, Robert F.] NICHHD, Sect Med Biophys, NIH, Bethesda, MD 20892 USA.
[Wong, Wai T.] NICHHD, Off Sci Director, NIH, Bethesda, MD 20892 USA.
RP Chew, EY (reprint author), NEI, Div Epidemiol & Clin Res, NIH, NICHHD, 10 Ctr Dr,MSC 120410 CRC,Room 3-2531, Bethesda, MD 20892 USA.
EM echew@nei.nih.gov
RI Bonner, Robert/C-6783-2015; Wong, Wai/B-6118-2017
OI Wong, Wai/0000-0003-0681-4016
FU NATIONAL EYE INSTITUTE; National Institutes of Health, Bethesda,
Maryland
FX THIS STUDY WAS SUPPORTED BY THE INTRAMURAL DIVISION OF THE NATIONAL EYE
INSTITUTE INTRAMURAL RESEARCH Program, National Institutes of Health,
Bethesda, Maryland. The authors indicate no financial conflict of
interest. Involved in design of study (W.T.W., F.F., E.Y.C., Z.M.,
R.F.B., D.C.); conduct of study (W.T.W., F.F., Z.M., R.F.B., D.C.);
collection of data (W.T.W., F.F., D.C., E.Y.C.); writing of article
(W.T.W., F.F., Z.M., E.Y.C.); management, analysis, and interpretation
of data (W.T.W., F.F., D.C., Z.M., R.F.B., E.Y.C.); and preparation,
review, and approval of manuscript (W.T.W., F.F., D.C., Z.M., R.F.B.,
E.Y.C.). This Study was approved by an Institutional Review Board at the
National Institutes of Health. Clinical research in this study followed
the tenets of the Declaration of Helsinki.
NR 24
TC 35
Z9 35
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD OCT
PY 2009
VL 148
IS 4
BP 573
EP 583
DI 10.1016/j.ajo.2009.04.030
PG 11
WC Ophthalmology
SC Ophthalmology
GA 503MI
UT WOS:000270538000017
PM 19573860
ER
PT J
AU List, K
Kosa, P
Szabo, R
Bey, AL
Wang, CB
Molinolo, A
Bugge, TH
AF List, Karin
Kosa, Peter
Szabo, Roman
Bey, Alexandra L.
Wang, Chao Becky
Molinolo, Alfredo
Bugge, Thomas H.
TI Epithelial Integrity Is Maintained by a Matriptase-Dependent Proteolytic
Pathway
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID HEPATOCYTE GROWTH-FACTOR; MACROPHAGE-STIMULATING PROTEIN; AUTOSOMAL
RECESSIVE ICHTHYOSIS; EPIDERMAL BARRIER FUNCTION; SERINE-PROTEASE;
HYPOTRICHOSIS SYNDROME; FACTOR ACTIVATOR; TIGHT JUNCTIONS;
SODIUM-CHANNEL; CELL-SURFACE
AB A pericellular proteolytic pathway initiated by the transmembrane serine protease matriptase plays a critical role in the terminal differentiation of epidermal tissues. Matriptase is constitutively expressed in multiple other epithelia, suggesting a putative role of this membrane serine protease in general epithelial homeostasis. Here we generated mice with conditional deletion of the St14 gene, encoding matriptase, and show that matriptase indeed is essential for the maintenance of multiple types of epithelia in the mouse. Thus, embryonic or postnatal ablation of St14 in epithelial tissues of diverse origin and function caused severe organ dysfunction, which was often associated with increased permeability, loss of tight junction function, mislocation of tight junction-associated proteins, and generalized epithelial demise. The study reveals that the homeostasis of multiple simple and stratified epithelia is matriptase-dependent, and provides an important animal model for the exploration of this membrane serine protease in a range of physiological and pathological processes. (Am J Pathol 2009, 175:1453-1463; DOI: 10.2353/ajpath.2009.090240)
C1 [Bugge, Thomas H.] Natl Inst Dent & Craniofacial Res, Proteases & Tissue Remodeling Sect, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
[List, Karin; Wang, Chao Becky] Wayne State Univ, Sch Med, Dept Pharmacol, Barbara Ann Karmanos Canc Inst, Detroit, MI 48201 USA.
RP Bugge, TH (reprint author), Natl Inst Dent & Craniofacial Res, Proteases & Tissue Remodeling Sect, Oral & Pharyngeal Canc Branch, NIH, 30 Convent Dr,Room 211, Bethesda, MD 20892 USA.
EM thomas.bugge@nih.gov
FU National Institute of Dental and Craniofacial Research; Wayne State
University; Barbara Ann Karmanos Institute
FX Supported by the National Institute of Dental and Craniofacial Research
Intramural Research Program (T.H.B.) and by startup funds from Wayne
State University and the Barbara Ann Karmanos Institute (K.L.).
NR 44
TC 71
Z9 71
U1 0
U2 0
PU AMER SOC INVESTIGATIVE PATHOLOGY, INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3993 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD OCT
PY 2009
VL 175
IS 4
BP 1453
EP 1463
DI 10.2353/ajpath.2009.090240
PG 11
WC Pathology
SC Pathology
GA 503AM
UT WOS:000270503100012
PM 19717635
ER
PT J
AU McGuinness, OP
Ayala, JE
Laughlin, MR
Wasserman, DH
AF McGuinness, Owen P.
Ayala, Julio E.
Laughlin, Maren R.
Wasserman, David H.
TI NIH experiment in centralized mouse phenotyping: the Vanderbilt
experience and recommendations for evaluating glucose homeostasis in the
mouse
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Review
DE insulin resistance; insulin clamp; diabetes
ID CONSCIOUS MICE; IN-VIVO; INSULIN; OVEREXPRESSION; THERMOGENESIS;
METABOLISM; RESISTANCE; TOLERANCE; STRAINS; TORPOR
AB McGuinness OP, Ayala JE, Laughlin MR, Wasserman DH. NIH experiment in centralized mouse phenotyping: the Vanderbilt experience and recommendations for evaluating glucose homeostasis in the mouse. Am J Physiol Endocrinol Metab 297: E849-E855, 2009. First published July 28, 2009; doi:10.1152/ajpendo.90996.2008.-This article addresses two topics. We provide an overview of the National Institutes of Health Mouse Metabolic Phenotyping Center (MMPC) Program. We then discuss some observations we have made during the first eight years of the Vanderbilt MMPC regarding common phenotyping practices. We include specific recommendations to improve phenotyping practices for tests of glucose tolerance and insulin action. We recommend that methods for experiments in vivo be described in manuscripts. We make specific recommendations for data presentation, interpretation, and experimental design for each test. To facilitate and maximize the exchange of scientific information, we suggest that guidelines be developed for methods used to assess glucose tolerance and insulin action in vivo.
C1 [McGuinness, Owen P.; Ayala, Julio E.; Wasserman, David H.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Sch Med, Vanderbilt NIH Mouse Metab Phenotyping Ctr, Nashville, TN 37232 USA.
[Laughlin, Maren R.] NIDDKD, NIH, Bethesda, MD 20892 USA.
RP McGuinness, OP (reprint author), Vanderbilt Univ, Dept Mol Physiol & Biophys, Sch Med, Vanderbilt NIH Mouse Metab Phenotyping Ctr, Nashville, TN 37232 USA.
EM owen.mcguinness@vanderbilt.edu
FU NIDDK [DK-59637]
FX The Vanderbilt Mouse Metabolic Phenotyping Center is supported by NIDDK
Grant DK-59637.
NR 27
TC 57
Z9 57
U1 1
U2 12
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1849
J9 AM J PHYSIOL-ENDOC M
JI Am. J. Physiol.-Endocrinol. Metab.
PD OCT
PY 2009
VL 297
IS 4
BP E849
EP E855
DI 10.1152/ajpendo.90996.2008
PG 7
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 498KR
UT WOS:000270139400003
PM 19638507
ER
PT J
AU Cao, ZL
Bell, JB
Mohanty, JG
Nagababu, E
Rifkind, JM
AF Cao, Zeling
Bell, Jeffrey B.
Mohanty, Joy G.
Nagababu, Enika
Rifkind, Joseph M.
TI Nitrite enhances RBC hypoxic ATP synthesis and the release of ATP into
the vasculature: a new mechanism for nitrite-induced vasodilation
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE nitrite reduction; nitric oxide; anerobic glycolysis; hypoxia; red blood
cell; adenosine 5 '-triphosphate
ID SIGNAL-TRANSDUCTION PATHWAY; HUMAN-ERYTHROCYTE-MEMBRANE;
RED-BLOOD-CELLS; G-PROTEIN G(I); S-NITROSOHEMOGLOBIN; CYTOPLASMIC
DOMAIN; ENDOTHELIAL-CELLS; PLASMA NITRITE; OXIDE; HEMOGLOBIN
AB Cao Z, Bell JB, Mohanty JG, Nagababu E, Rifkind JM. Nitrite enhances RBC hypoxic ATP synthesis and the release of ATP into the vasculature: a new mechanism for nitrite-induced vasodilation. Am J Physiol Heart Circ Physiol 297: H1494-H1503, 2009. First published August 21, 2009; doi: 10.1152/ajpheart.01233.2008.-A role for nitric oxide (NO) produced during the reduction of nitrite by deoxygenated red blood cells (RBCs) in regulating vascular dilation has been proposed. It has not, however, been satisfactorily explained how this NO is released from the RBC without first reacting with the large pools of oxyhemoglobin and deoxyhemoglobin in the cell. In this study, we have delineated a mechanism for nitrite-induced RBC vasodilation that does not require that NO be released from the cell. Instead, we show that nitrite enhances the ATP release from RBCs, which is known to produce vasodilation by several different methods including the interaction with purinergic receptors on the endothelium that stimulate the synthesis of NO by endothelial NO synthase. This mechanism was established in vivo by measuring the decrease in blood pressure when injecting nitrite-reacted RBCs into rats. The observed decrease in blood pressure was not observed if endothelial NO synthase was inhibited by N(omega)-nitro-L-arginine methyl ester (L-NAME) or when any released ATP was degraded by apyrase. The nitrite-enhanced ATP release was shown to involve an increased binding of nitrite-modified hemoglobin to the RBC membrane that displaces glycolytic enzymes from the membrane, resulting in the formation of a pool of ATP that is released from the RBC. These results thus provide a new mechanism to explain nitrite-induced vasodilation.
C1 [Cao, Zeling; Mohanty, Joy G.; Nagababu, Enika; Rifkind, Joseph M.] NIA, Mol Dynam Sect, NIH, Baltimore, MD 21224 USA.
[Bell, Jeffrey B.] NIA, Comparat Med Sect, NIH, Baltimore, MD 21224 USA.
RP Rifkind, JM (reprint author), NIA, Mol Dynam Sect, NIH, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM rifkindj@mail.nih.gov
FU Intramural Research Program of the National Institute on Aging
FX This research was supported by the Intramural Research Program of the
National Institute on Aging.
NR 53
TC 38
Z9 40
U1 1
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD OCT
PY 2009
VL 297
IS 4
BP H1494
EP H1503
DI 10.1152/ajpheart.01233.2008
PG 10
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 498KC
UT WOS:000270137700039
PM 19700624
ER
PT J
AU March, JS
Vitiello, B
AF March, John S.
Vitiello, Benedetto
TI Clinical Messages From the Treatment for Adolescents With Depression
Study (TADS)
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Review
ID COGNITIVE-BEHAVIORAL THERAPY; RANDOMIZED CONTROLLED-TRIALS; PEDIATRIC
DEPRESSION; COST-EFFECTIVENESS; SUICIDAL IDEATION; MAJOR DEPRESSION;
RESEARCH FORUM; CHILDREN; DISORDERS; PLACEBO
AB Objective: The purpose of this report was to summarize the key clinical messages from the Treatment for Adolescents with Depression Study (TADS).
Methods: TADS is a National Institute of Mental Health (NIMH)-funded randomized controlled trial designed to evaluate the relative effectiveness of fluoxetine, cognitive-behavioral therapy (CBT), and the combination of fluoxetine plus CBT across acute treatment, maintenance treatment, and naturalistic follow-up periods among adolescents with major depressive disorder.
Results: Findings revealed that 6 to 9 months of combined fluoxetine plus CBT should be the modal treatment from a public health perspective as well as to maximize benefits and minimize harms for individual patients.
Conclusion: The combination of fluoxetine and CBT appears to be superior to both CBT monotherapy and fluoxetine monotherapy as a treatment for moderate to severe major depressive disorder in adolescents.
C1 [March, John S.] Duke Univ, Med Ctr, Duke Clin Res Inst, Div Neurosci Med, Durham, NC 27705 USA.
[Vitiello, Benedetto] NIMH, Bethesda, MD 20892 USA.
RP March, JS (reprint author), Duke Univ, Med Ctr, Duke Clin Res Inst, Div Neurosci Med, 2400 Pratt St,Rm 0311, Durham, NC 27705 USA.
EM john.march@duke.edu; bvitiell@mail.nih.gov
FU NIMH to Duke University Medical Center [RFP-NIH-NIMH 98-DS-0008]
FX TADS was supported by contract RFP-NIH-NIMH 98-DS-0008 from NIMH to Duke
University Medical Center. The cited research meets all applicable Duke
University and federal guidelines for research.
NR 45
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U1 2
U2 6
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD OCT
PY 2009
VL 166
IS 10
BP 1118
EP 1123
DI 10.1176/appi.ajp.2009.08101606
PG 6
WC Psychiatry
SC Psychiatry
GA 501NU
UT WOS:000270389400011
PM 19723786
ER
PT J
AU White, AM
Philogene, GS
Fine, L
Sinha, S
AF White, Ann Marie
Philogene, G. Stephane
Fine, Lawrence
Sinha, Sarbajit
TI Social Support and Self-Reported Health Status of Older Adults in the
United States
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID RATED HEALTH; MORTALITY; NETWORKS; DISEASE; INTEGRATION; COMMUNITY; MEN;
AGE; ASSOCIATION; SURVIVAL
AB Objectives. We determined whether a representative national probability sample of US community-dwelling older adults who reported less social support also reported poorer general health status, which is a robust predictor of prospective mortality among elders.
Methods. We analyzed 2 subsamples generated via random sampling with replacement from the full analytic sample of adults aged 60 years and older in the 1999-2002 National Health and Nutrition Examination Survey (n=3476). We built multinomial logit models with the first analytic subsample (n=1732). Then we tested the final models on the second subsample (n=1744) to assess the differences in odds of reporting poor, fair, or good versus very good or excellent health. We fit the cross-validated final models to the full analytic sample.
Results. After we controlled for age, race, gender, and educational attainment, older persons across all analytic samples who reported that they needed more support also reported having poorer health compared with better health 2 times more often than did older persons who were satisfied with the support available to them (odds ratio [OR]=2.4; 95% confidence interval [CI]=1.7, 3.4; P<.001).
Conclusions. In the United States, older persons' satisfaction with the emotional support available to them is associated with better self-reported health status. (Am J Public Health. 2009;99:1872-1878. doi:10.2105/AJPH.2008.146894)
C1 [White, Ann Marie; Philogene, G. Stephane; Fine, Lawrence; Sinha, Sarbajit] NIH, Off Behav & Social Sci Res, Off Director, Bethesda, MD 20892 USA.
RP White, AM (reprint author), Univ Rochester, Med Ctr, Dept Psychiat, Box PSYCH,300 Crittenden Blvd, Rochester, NY 14642 USA.
EM annmarie_white@urmc.rochester.edu
FU Office of Behavioral and Social Sciences Research; National Institutes
of Health; University of Rochester
FX The Office of Behavioral and Social Sciences Research and the National
Institutes of Health supported the work described in this article.
Institutional support via staff time to conduct and write up secondary
analyses was also funded in part by the University of Rochester.
NR 42
TC 52
Z9 52
U1 1
U2 13
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD OCT
PY 2009
VL 99
IS 10
BP 1872
EP 1878
DI 10.2105/AJPH.2008.146894
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 507IS
UT WOS:000270846500025
PM 19696390
ER
PT J
AU El Khouli, RH
Macura, KJ
Jacobs, MA
Khalil, TH
Kamel, IR
Dwyer, A
Bluemke, DA
AF El Khouli, Riham H.
Macura, Katarzyna J.
Jacobs, Michael A.
Khalil, Tarek H.
Kamel, Ihab R.
Dwyer, Andrew
Bluemke, David A.
TI Dynamic Contrast-Enhanced MRI of the Breast: Quantitative Method for
Kinetic Curve Type Assessment
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE breast cancer; breast imaging; contrast-enhanced MRI; dynamic MRI;
kinetic curve; washout
ID LESIONS; VARIABILITY; RESOLUTION; IMAGES
AB OBJECTIVE. The type of contrast enhancement kinetic curve (i.e., persistently enhancing, plateau, or washout) seen on dynamic contrast-enhanced MRI (DCE-MRI) of the breast is predictive of malignancy. Qualitative estimates of the type of curve are most commonly used for interpretation of DCE-MRI. The purpose of this study was to compare qualitative and quantitative methods for determining the type of contrast enhancement kinetic curve on DCE-MRI.
MATERIALS AND METHODS. Ninety-six patients underwent breast DCE-MRI. The type of DCE-MRI kinetic curve was assessed qualitatively by three radiologists on two occasions. For quantitative assessment, the slope of the washout curve was calculated. Kappa statistics were used to determine inter- and intraobserver agreement for the qualitative method. Matched sample tables, the McNemar test, and receiver operating characteristic (ROC) curve statistics were used to compare quantitative versus qualitative methods for establishing or excluding malignancy.
RESULTS. Seventy-eight lesions (77.2%) were malignant and 23 (22.8%) were benign. For the qualitative assessment, the intra- and interobserver agreement was good (kappa = 0.76-0.88), with an area under the ROC curve (AUC) of 0.73-0.77. For the quantitative method, the highest AUC was 0.87, reflecting significantly higher diagnostic accuracies compared with qualitative assessment (p < 0.01 for the difference between the two methods).
CONCLUSION. Quantitative assessment of the type of contrast enhancement kinetic curve on breast DCE-MRI resulted in significantly higher diagnostic performance for establishing or excluding malignancy compared with assessment based on the standard qualitative method.
C1 [El Khouli, Riham H.; Macura, Katarzyna J.; Jacobs, Michael A.; Kamel, Ihab R.] Johns Hopkins Univ, Sch Med, Dept Radiol & Radiol Sci, Baltimore, MD 21287 USA.
[El Khouli, Riham H.; Dwyer, Andrew; Bluemke, David A.] NIH, Dept Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[El Khouli, Riham H.; Khalil, Tarek H.] Suez Canal Univ, Sch Med, Dept Diagnost Radiol, Ismailia, Egypt.
[Jacobs, Michael A.] Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21287 USA.
RP Bluemke, DA (reprint author), Johns Hopkins Univ, Sch Med, Dept Radiol & Radiol Sci, 600 N Wolfe St, Baltimore, MD 21287 USA.
EM dbluemke@jhmi.edu
RI Jacobs, Michael/G-2901-2010;
OI Bluemke, David/0000-0002-8323-8086
FU National Institutes of Health (NIH) [1R01CA100184, P50CA103175]
FX This research was supported by the National Institutes of Health (NIH
grants 1R01CA100184 and P50CA103175) and by the intramural research
program of the NIH Clinical Center.
NR 12
TC 46
Z9 46
U1 0
U2 2
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD OCT
PY 2009
VL 193
IS 4
BP W295
EP W300
DI 10.2214/AJR.09.2483
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 497CZ
UT WOS:000270033300045
PM 19770298
ER
PT J
AU Zhu, H
Stybayeva, G
Silangcruz, J
Yan, J
Ramanculov, E
Dandekar, S
George, MD
Revzin, A
AF Zhu, He
Stybayeva, Gulnaz
Silangcruz, Jaime
Yan, Jun
Ramanculov, Erlan
Dandekar, Satya
George, Michael D.
Revzin, Alexander
TI Detecting Cytokine Release from Single T-cells
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID CYTOMETRY PLATFORM; INFECTION; SUBSETS; BLOOD; PHOTOLITHOGRAPHY;
MICROSTRUCTURES; LYMPHOCYTES; FABRICATION; ANTIBODIES; LEUKOCYTES
AB The cytokine production by leukocytes correlates with body's ability to mount an immune response and therefore has high diagnostic value. In the present study we employed microfabricated surfaces to capture T-cells from minimally processed human blood, arrange these cells into a single cell array, and then detect interferon (IFN)-gamma released from individual cells. The fabrication of cell capture surfaces started with coating a silane-modified glass slide with a uniform layer of poly(ethylene glycol) (PEG) hydrogel. The hydrogel-coated slide was lyophilized and then incubated with a mixture of monoclonal anti-IFN-gamma and anti-CD4 antibodies (Abs). To define sites for single cell attachment, PEG hydrogel microwells (20 mu m diameter) were photolithographically patterned on top of the Ab-containing hydrogel layer. This micropatterning process resulted in fabrication of PEG hydrogel microwells with Ab-decorated bottom and nonfouling walls. To minimize the blood volume requirement and to precisely define shear stress conditions, the engineered surface was enclosed inside a PDMS-based microfluidic device. Introduction of red blood cell (RBC) depleted whole human blood followed by controlled washing led to the isolation of individual CD4 T-cells within PEG microwells. Mitogenic activation and immunofluorescent staining performed inside the microfluidic chamber revealed IFN-gamma cytokine signal colocalized with specific T-cells. The device and process presented here will be expanded in the future to enable multiparametric functional analysis of immune cells organized into high density single cell arrays.
C1 [Zhu, He; Stybayeva, Gulnaz; Silangcruz, Jaime; Yan, Jun; Dandekar, Satya; George, Michael D.; Revzin, Alexander] Univ Calif Davis, Davis, CA 95616 USA.
[Stybayeva, Gulnaz; Ramanculov, Erlan] Natl Biotechnol Ctr, Astana, Kazakhstan.
RP Revzin, A (reprint author), Univ Calif Davis, Davis, CA 95616 USA.
EM arevzin@ucdavis.edu
RI Yan, Jun/E-8783-2012; Ramanculov, Erlan/E-2823-2013
FU California Research Center for the Biology of HIV in Minorities;
California HIV/AIDS Research [CH05-D-606]; NSF [EFRI 0937997]; NIH
[EB003827, AI43267, DK43183]; National Center for Biotechnology,
Republic of Kazakhstan
FX We thank Prof. Louie's lab in the Department of Biomedical Engineering
at UC Davis for providing assistance with confocal microscopy. Financial
support for this work was provided in part by the California Research
Center for the Biology of HIV in Minorities, California HIV/AIDS
Research Program no. CH05-D-606. Additional support was provided by NSF
Grant (EFRI 0937997). H.Z. was supported through an NIH Training Grant
(EB003827). G.S. was supported in part through a Biotechnology
Fellowship from National Center for Biotechnology, Republic of
Kazakhstan. S.D. acknowledges support from NIH Grants AI43267 and
DK43183. The first two authors contributed equally to this work.
NR 29
TC 53
Z9 53
U1 1
U2 31
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
J9 ANAL CHEM
JI Anal. Chem.
PD OCT 1
PY 2009
VL 81
IS 19
BP 8150
EP 8156
DI 10.1021/ac901390j
PG 7
WC Chemistry, Analytical
SC Chemistry
GA 501EA
UT WOS:000270361100042
PM 19739655
ER
PT J
AU Lytle, LA
Murray, DM
Evenson, KR
Moody, J
Pratt, CA
Metcalfe, L
Parra-Medina, D
AF Lytle, Leslie A.
Murray, David M.
Evenson, Kelly R.
Moody, Jamie
Pratt, Charlotte A.
Metcalfe, Lauve
Parra-Medina, Deborah
TI Mediators Affecting Girls' Levels of Physical Activity Outside of
School: Findings from the Trial of Activity in Adolescent Girls
SO ANNALS OF BEHAVIORAL MEDICINE
LA English
DT Article
DE After school physical activity; Mediators of physical activity;
Adolescent girls
ID RANDOMIZED CONTROLLED-TRIAL; MIDDLE SCHOOLS; SELF-EFFICACY; CHILDREN;
INTERVENTION; TAAG; YOUTH; BEHAVIORS; NUTRITION; PROMOTION
AB Providing after school activities is a community level approach for reducing the decline in physical activity of girls as they reach early adolescence.
The purpose of this study was to examine psychosocial, environmental, and behavioral factors as potential mediators of after school physical activity in adolescent girls.
We assessed objectively measured levels of physical activity occurring outside of school and potential predictors and mediators of activity in girls participating in the Trial of Activity in Adolescent Girls (TAAG).
We found that the TAAG intervention had a statistically significant and positive effect on out of school activity in the 2006 cohort. Self-efficacy, friends' social support, total social support, and difficulty getting to and from community activities mediated the level of moderate to vigorous physical activity in girls.
Parents, communities, and schools should provide and enhance opportunities outside of the school day for adolescents to be active. Reducing transportation barriers and enlisting social support appear to be key.
C1 [Lytle, Leslie A.] Univ Minnesota, Div Epidemiol & Community Hlth, Sch Publ Hlth, Minneapolis, MN 55454 USA.
[Murray, David M.] Ohio State Univ, Div Epidemiol, Div Biostat, Coll Publ Hlth, Columbus, OH 43210 USA.
[Evenson, Kelly R.] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Bank Amer Ctr, Chapel Hill, NC 27514 USA.
[Moody, Jamie] SDSU Res Fdn, MOVE Me Muevo, Obes Prevent & Control Community Rec Ctr, San Diego, CA 92123 USA.
[Pratt, Charlotte A.] Natl Heart Lung & Blood Inst, Div Prevent & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Metcalfe, Lauve] Univ Arizona, Ctr Phys Act & Nutr, Tucson, AZ 85750 USA.
[Parra-Medina, Deborah] Univ Texas Hlth Sci Ctr San Antonio, Sch Med, Dept Epidemiol & Biostat, Inst Hlth Promot Res, San Antonio, TX 78230 USA.
RP Lytle, LA (reprint author), Univ Minnesota, Div Epidemiol & Community Hlth, Sch Publ Hlth, 1300 S 2nd St,Suite 300, Minneapolis, MN 55454 USA.
EM lalytle@umn.edu; dmurray@cph.osu.edu; kelly_evenson@unc.edu;
prattc@nhlbi.nih.gov; Lauve@u.arizona.edu; parramedina@uthscsa.edu
FU NHLBI NIH HHS [U01 HL066845, U01 HL066845-01]
NR 51
TC 34
Z9 34
U1 7
U2 15
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0883-6612
J9 ANN BEHAV MED
JI Ann. Behav. Med.
PD OCT
PY 2009
VL 38
IS 2
BP 124
EP 136
DI 10.1007/s12160-009-9127-2
PG 13
WC Psychology, Multidisciplinary
SC Psychology
GA 532WH
UT WOS:000272780500006
PM 20012810
ER
PT J
AU Espeland, MA
Bray, GA
Neiberg, R
Rejeski, WJ
Knowler, WC
Lang, W
Cheskin, LJ
Williamson, D
Lewis, CB
Wing, R
AF Espeland, Mark A.
Bray, George A.
Neiberg, Rebecca
Rejeski, W. Jack
Knowler, William C.
Lang, Wei
Cheskin, Lawrence J.
Williamson, Don
Lewis, C. Beth
Wing, Rena
CA Look Ahead Study Grp
TI Describing Patterns of Weight Changes Using Principal Components
Analysis: Results from the Action for Health in Diabetes (Look AHEAD)
Research Group
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Principal Components Analysis; Intervention Studies; Weight Loss
ID PREVENTION-PROGRAM; BODY-COMPOSITION; LOSS MAINTENANCE; WOMEN; TRIAL;
INTERVENTION; ADHERENCE; PHASE
AB PURPOSE: To demonstrate how principal components analysis can be used to describe patterns of weight changes in response to an intensive lifestyle intervention.
METHODS: Principal components analysis was applied to monthly percent weight changes measured on 2,485 individuals enrolled in the lifestyle arm of the Action for Health in Diabetes (Look AHEAD) clinical trial. These individuals were 45 to 75 years of age, with type 2 diabetes and body mass indices greater than 25 kg/m(2). Associations between baseline characteristics and weight loss patterns were described using analyses of variance.
RESULTS: Three components collectively accounted for 97.0% of total intrasubject variance: a gradually decelerating weight loss (88.8%), early versus late weight loss (6.6%), and a mid-year trough (1.6%). In agreement with previous reports, each of the baseline characteristics we examined had statistically significant relationships with weight loss patterns. As examples, males tended to have a steeper trajectory of percent weight loss and to lose weight more quickly than women. Individuals with higher hemoglobin A(1c) (glycosylated hernoglobin; HbA(1c)) tended to have a flatter trajectory of percent weight loss and to have mid-year troughs in weight loss compared to those with lower HbA(1c).
CONCLUSIONS: Principal components analysis provided a coherent description of characteristic patterns of weight changes and is a useful vehicle for identifying their correlates and potentially for predicting weight control outcomes. Ann Epidemiol 2009;19:701-710. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Espeland, Mark A.; Neiberg, Rebecca; Lang, Wei] Wake Forest Univ, Bowman Gray Sch Med, Dept Biostat Sci, Winston Salem, NC 27157 USA.
[Rejeski, W. Jack] Wake Forest Univ, Bowman Gray Sch Med, Dept Hlth & Exercise Sci, Winston Salem, NC 27157 USA.
[Bray, George A.; Williamson, Don] Pennington Biomed Res Ctr, Div Clin Obes & Metab, Baton Rouge, LA USA.
[Knowler, William C.] NIDDKD, Diabet Epidemiol & Clin Res Sect, Phoenix, AZ USA.
[Cheskin, Lawrence J.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Hlth Behav & Soc, Baltimore, MD USA.
[Lewis, C. Beth] Univ Alabama Birmingham, Div Prevent Med, Birmingham, AL USA.
[Wing, Rena] Miriam Hosp, Sch Med, Ctr Behav Med, Providence, RI 02906 USA.
[Wing, Rena] Miriam Hosp, Sch Med, Ctr Prevent Med, Providence, RI 02906 USA.
RP Espeland, MA (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Dept Biostat Sci, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM mespelan@wfubmc.edu
FU National Institutes of Health (NIH) [DK57136, DK57149, DK56990, DK57177,
DK57171, DK57151, DK57182, DK57131, DK57002, DK57078, DK57154, DK57178,
DK57219, DK57008, DK57135, DK56992]; National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK); National Heart, Lung, and Blood
Institute; National Institute of Nursing Research; National Center on
Minority Health and Health Disparities; Office of Research on Women's
Health; Centers for Disease Control and Prevention; The Johns Hopkins
Medical Institutions Bayview General Clinical Research Service;
Department of Veterans Affairs; Frederic C. Bartter General Clinical
Research Center [M01RR01346]
FX This Study is supported by the Department of Health and Human Services
through the following cooperative agreements from the National
Institutes of Health (NIH): DK57136, DK57149, DK56990, DK57177, DK57171,
DK57151, DK57182, DK57131, DK57002, DK57078, DK57154, DK57178, DK57219,
DK57008, DK57135, and DK56992. The following federal agencies have
contributed support: National Institute of Diabetes and Digestive and
Kidney Diseases (NIDDK); National Heart, Lung, and Blood Institute;
National Institute of Nursing Research; National Center on Minority
Health and Health Disparities; Office of Research on Women's Health; and
the Centers for Disease Control and Prevention. This research was
supported in part by the Intramural Research Program of the NIDDK.;
Additional support was received from The Johns Hopkins Medical
Institutions Bayview General Clinical Research Service, Department of
Veterans Affairs; Frederic C. Bartter General Clinical Research Center
(M01RR01346).; The following organizations have committed to make major
contributions to Look AHEAD: FedEx Corporation; Health Management
Resources; LifeScan, Inc., a Johnson & Johnson Company; Optifast (R) of
Nestle HealthCare Nutrition, Inc.; Hoffmann-La Roche Inc.; Abbott
Nutrition; and Slim-Fast Brand of Unilever North America.
NR 24
TC 19
Z9 19
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1047-2797
EI 1873-2585
J9 ANN EPIDEMIOL
JI Ann. Epidemiol.
PD OCT
PY 2009
VL 19
IS 10
BP 701
EP 710
DI 10.1016/j.annepidem.2009.06.001
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 499BR
UT WOS:000270192000003
PM 19628410
ER
PT J
AU Caldwell, SH
Lee, VD
Kleiner, DE
Al-Osaimi, AMS
Argo, CK
Northup, PG
Berg, CL
AF Caldwell, Stephen H.
Lee, Vanessa D.
Kleiner, David E.
Al-Osaimi, Abdullah M. S.
Argo, Curtis K.
Northup, Patrick G.
Berg, Carl L.
TI NASH and cryptogenic cirrhosis: A histological analysis
SO ANNALS OF HEPATOLOGY
LA English
DT Article
DE Cryptogenic cirrhosis; Non-alcoholic steatohepatitis (NASH);
Non-alcoholic fatty liver disease (NAFLD); Macrosteatosis; Acidophil
bodies
ID FATTY LIVER-DISEASE; NONALCOHOLIC STEATOHEPATITIS; NATURAL-HISTORY;
RISK-FACTORS; FOLLOW-UP; TRANSPLANTATION; PREVALENCE; NAFLD;
PROGRESSION; POPULATION
AB Introduction. Epidemiological studies indicate that nonalcoholic steatohepatitis (NASH) is a common cause of cirrhosis described as 'cryptogenic'. To address this from a histological perspective and to examine the significance of residual histological findings as an indication of prior NASH, we looked back at biopsies in patients who presented with cirrhosis without sufficient histological features to diagnose NASH but who had prior histologically confirmed non-cirrhotic NASH. Methods. Seven patients were identified with biopsy pairs showing non-specific (cryptogenic) cirrhosis in the latest specimen and a prior biopsy showing non-cirrhotic NASH. Using an expanded NASH-CRN system scored blindly by tight microscopy, we compared the early and late biopsies to each other and to a cohort of 13 patients with cirrhosis due to hepatitis C without co-existing metabolic syndrome. Results. Macrosteatosis, although uniformly present in the non0cirrhotic NASH specimens, declined in the late stage cirrhotic NASH specimens and was not useful in the distinction of late cirrhotic NASH from cirrhotic viral hepatitis. However, the presence of ballooned cells, Mallory-Denk bodies, and megamitochondria and the absence of apoptotic bodies were significantly different in late stage cirrhotic NASH compared to cirrhosis due to hepatitis C. Conclusions. Histologically advanced NASH presenting as non-specific or cryptogenic cirrhosis has residual changes which are consistent with prior steatohepatitis but which differ from cirrhosis due to hepatitis C. These results provide histological support for the more established epidemiological associations of NASH with cryptogenic cirrhosis and for criteria used in several proposed classifications of cryptogenic cirrhosis.
C1 [Caldwell, Stephen H.] Univ Virginia, GI Hepatol, Digest Hlth Ctr, Div Gastroenterol & Hepatol, Charlottesville, VA 22908 USA.
[Kleiner, David E.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
RP Caldwell, SH (reprint author), Univ Virginia, GI Hepatol, Digest Hlth Ctr, Div Gastroenterol & Hepatol, Box 800708, Charlottesville, VA 22908 USA.
EM shc5c@virginia.edu
OI Kleiner, David/0000-0003-3442-4453
FU Intramural NIH HHS
NR 27
TC 31
Z9 32
U1 0
U2 0
PU MEXICAN ASSOC HEPATOLOGY
PI MEXICO
PA PUNTE DE PIEDRA 150, COLONIA TORIELLO GUERRA, MEXICO, DF CP 14040,
MEXICO
SN 1665-2681
J9 ANN HEPATOL
JI Ann. Hepatol.
PD OCT-DEC
PY 2009
VL 8
IS 4
BP 346
EP 352
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 530JN
UT WOS:000272586100009
PM 20009134
ER
PT J
AU McFarland, HF
AF McFarland, Henry F.
TI Examination of the role of magnetic resonance imaging in multiple
sclerosis: A problem-orientated approach
SO ANNALS OF INDIAN ACADEMY OF NEUROLOGY
LA English
DT Review
DE Magnetic resonance imaging; multiple sclerosis; problem-oriented
clinical approach
ID APPEARING WHITE-MATTER; LONG-TERM DISABILITY; DISEASE-ACTIVITY;
CORTICAL-LESIONS; GADOLINIUM ENHANCEMENT; DIAGNOSTIC-CRITERIA; PREDICT
CONVERSION; INTERFERON BETA-1B; CLINICAL-TRIALS; BLACK-HOLES
AB Magnetic Resonance Imaging (MRI) has brought in several benefits to the study of Multiple Sclerosis (MS). It provides accurate measurement of disease activity, facilitates precise diagnosis, and aid in the assessment of newer therapies. The imaging guidelines for MS are broadly divided in to approaches for imaging patients with suspected MS or clinically isolated syndromes (CIS) or for monitoring patients with established MS. In this review, the technical aspects of MR imaging for MS are briefly discussed. The imaging process need to capture the twin aspects of acute MS viz. the autoimmune acute inflammatory process and the neurodegenerative process. Gadolinium enhanced MRI can identify acute inflammatory lesions precisely. The commonly applied MRI marker of disease progression is brain atrophy. Whole brain magnetization Transfer Ratio (MTR) and Magnetic Resonance Spectroscopy (MRS) are two other techniques use to monitor disease progression. A variety of imaging techniques such as Double Inversion Recovery (DIR), Spoiled Gradient Recalled (SPGR) acquisition, and Fluid Attenuated Inversion Recovery (FLAIR) have been utilized to study the cortical changes in MS. MRI is now extensively used in the Phase I, II and III clinical trials of new therapies. As the technical aspects of MRI advance rapidly, and higher field strengths become available, it is hoped that the impact of MRI on our understanding of MS will be even more profound in the next decade.
C1 NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
RP McFarland, HF (reprint author), NINDS, Neuroimmunol Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM henrymcf@gmail.com
NR 65
TC 8
Z9 8
U1 0
U2 1
PU MEDKNOW PUBLICATIONS
PI MUMBAI
PA A-108-109 KANARA BUSINESS CENTRE, GHAKTOPAR, MUMBAI, 400075, INDIA
SN 0972-2327
J9 ANN INDIAN ACAD NEUR
JI Ann. Indian Acad. Neurol.
PD OCT-DEC
PY 2009
VL 12
IS 4
BP 254
EP 263
DI 10.4103/0972-2327.58284
PG 10
WC Clinical Neurology
SC Neurosciences & Neurology
GA 531NU
UT WOS:000272675100010
PM 20182573
ER
PT J
AU Palm, WM
Saczynski, JS
van der Grond, J
Sigurdsson, S
Kjartansson, O
Jonsson, PV
Eiriksdottir, G
Gudnason, V
Admiraal-Behloul, F
Launer, LJ
van Buchem, MA
AF Palm, Walter M.
Saczynski, Jane S.
van der Grond, J.
Sigurdsson, Sigurdur
Kjartansson, Olafur
Jonsson, Palmi V.
Eiriksdottir, Gudny
Gudnason, Vilmundur
Admiraal-Behloul, Faiza
Launer, Lenore J.
van Buchem, Mark A.
CA Age Gene Environm Susceptibil Reyk
TI Ventricular Dilation Association With Gait and Cognition
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID NORMAL-PRESSURE HYDROCEPHALUS; CORONARY-HEART-DISEASE; BINSWANGERS
DISEASE; APOLIPOPROTEIN-E; NURSING-HOME; RISK-FACTORS; DIAGNOSIS;
DEMENTIA; IMPAIRMENT; HEALTH
AB Objective: Normal pressure hydrocephalus is characterized by gait impairment, cognitive impairment, and urinary incontinence, and is associated with disproportionate ventricular dilation. Here we report the distribution of ventricular volume relative to sulcal cerebrospinal fluid (CSF) volume, and the association of increasing ventricular volume relative to sulcal CSF volume with a cluster of gait impairment, cognitive impairment, and urinary incontinence in a stroke-free cohort of elderly persons from the general population.
Methods: Data are based on 858 persons (35.4% men; age range, 66-92 years) who participated in the Age, Gene/Environment Susceptibility-Reykjavik Study. Gait was evaluated with an assessment of gait speed. Composite scores representing speed of processing, memory, and executive function were constructed from a neuropsychological battery. Bladder function was assessed with a questionnaire. Magnetic resonance brain imaging was followed by semiaucomated segmentation of intracranial CSF volume. White matter hyperintensity (WMH) volume was assessed with a semiquantitative scale. For the analysis of ventricular dilation relative to the sulcal spaces, ventricular volume was divided by sulcal CSF volume (VV/SV).
Results: Disproportion between ventricular and sulcal CSF volume, defined as the highest quartile of the VV/SV z score, was associated with gait impairment (odds ratio [OR], 1.9; 95% confidence interval [CI], 1.1-3.3) and cognitive impairment (OR, 1.8; 95% CI, 1.1-3.0). We did not find an association between the VV/SV z score and bladder dysfunction.
Interpretation: The prevalence and severity of gait impairment and cognitive impairment increases with ventricular dilation in persons without stroke from the general population, independent of WMH volume.
C1 [Palm, Walter M.; van der Grond, J.; Admiraal-Behloul, Faiza; van Buchem, Mark A.] Leiden Univ, Dept Radiol, Med Ctr, Leiden, Netherlands.
[Saczynski, Jane S.] Univ Massachusetts, Sch Med, Div Geriatr Med, Worcester, MA USA.
[Saczynski, Jane S.] Univ Massachusetts, Sch Med, Meyers Primary Care Inst, Worcester, MA USA.
[Sigurdsson, Sigurdur; Kjartansson, Olafur; Jonsson, Palmi V.; Eiriksdottir, Gudny; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Jonsson, Palmi V.; Gudnason, Vilmundur] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
RP Launer, LJ (reprint author), NIA, EDB, NIH, 7201 Wisconsin Ave,Suite 3C-309, Bethesda, MD 20892 USA.
EM launerl@nia.nih.gov
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
FU National Institutes of Health [N01-AG-12100]; National Institute on
Aging Intramural Research Program; Hjartavernd (the Icelandic Heart
Association); Althingi (the Icelandic Parliament)
FX This study has been funded by National Institutes of Health contract
N01-AG-12100, the National Institute on Aging Intramural Research
Program, Hjartavernd (the Icelandic Heart Association), and the Althingi
(the Icelandic Parliament).
NR 45
TC 17
Z9 18
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2009
VL 66
IS 4
BP 485
EP 493
DI 10.1002/ana.21739
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 507SJ
UT WOS:000270874700008
PM 19847895
ER
PT J
AU Ponti, G
Losi, L
Pellacani, G
Cesinaro, A
Boni, E
Pepe, P
Landi, MT
Luppi, G
Conte, PF
Seidenari, S
AF Ponti, Giovanni
Losi, Lorena
Pellacani, Giovanni
Cesinaro, Annamaria
Boni, Elisa
Pepe, Patrizia
Landi, Maria Teresa
Luppi, Gabriele
Conte, Pier Franco
Seidenari, Stefania
TI CLINICAL AND IMMUNOHISTOCHEMICAL CHARACTERIZATION OF MULTIPLE PRIMARY
MELANOMAS TO IDENTIFY FAMILIAL MELANOMA SYNDROME
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
C1 [Ponti, Giovanni; Luppi, Gabriele; Conte, Pier Franco] Univ Modena & Reggio Emilia, Dept Haematol & Oncol, Modena, Italy.
[Losi, Lorena; Cesinaro, Annamaria] Univ Modena & Reggio Emilia, Dept Pathol, Modena, Italy.
[Pellacani, Giovanni; Boni, Elisa; Pepe, Patrizia; Seidenari, Stefania] Univ Modena & Reggio Emilia, Div Dermatol, Dept Internal Med, Modena, Italy.
[Landi, Maria Teresa] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
RI pellacani, giovanni/E-8573-2011; Ponti, Giovanni/A-5565-2012; Losi,
Lorena/B-2583-2012; Conte, PierFranco/F-7418-2014
OI pellacani, giovanni/0000-0002-7222-2951; Ponti,
Giovanni/0000-0002-1971-7306; Losi, Lorena/0000-0002-8483-3936; Conte,
PierFranco/0000-0002-5210-5344
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD OCT
PY 2009
VL 20
SU 8
PG 1
WC Oncology
SC Oncology
GA V15CV
UT WOS:000207781000272
ER
PT J
AU Remondo, C
Tagliaferri, P
Del Vecchio, MT
Migali, C
Tsang, KY
Rotundo, MS
Tassone, P
Francini, G
Correale, P
AF Remondo, Cinzia
Tagliaferri, Pierosandro
Del Vecchio, Maria Teresa
Migali, Cristina
Tsang, Kwong Y.
Rotundo, Maria Saveria
Tassone, Pierfrancesco
Francini, Guido
Correale, Pierpaolo
TI IMMUNE-REGULATORY (FOXP3(+))-T-CELL TUMOR INFILTRATION STATUS IS
PREDICTIVE OF BENEFIT FROM CHEMOIMMUNOTHERAPY WITH GEMCITABINE,
OXALIPLATIN, 5-FU/FA PLUS GM-CSF AND ALDESLEUKINE (GOLFIG) IN METASTATIC
COLON CANCER PATIENTS
SO ANNALS OF ONCOLOGY
LA English
DT Meeting Abstract
C1 [Remondo, Cinzia; Migali, Cristina; Francini, Guido; Correale, Pierpaolo] Univ Siena, Sch Med, Sect Med Oncol, Dept Giorgio Segre Pharmacol, I-53100 Siena, Italy.
[Del Vecchio, Maria Teresa] Univ Siena, Sch Med, Pathol Sect, I-53100 Siena, Italy.
[Tagliaferri, Pierosandro; Tassone, Pierfrancesco] Magna Graecia Univ Catanzaro, Sch Med Catanzaro, Med Oncol Unit, Catanzaro, Italy.
[Tassone, Pierfrancesco] Magna Graecia Univ Catanzaro, Sch Med Catanzaro, Referral Ctr Genet Counseling, Catanzaro, Italy.
[Rotundo, Maria Saveria] NCI, Lab Tumor Immunol & Biol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD OCT
PY 2009
VL 20
SU 8
PG 1
WC Oncology
SC Oncology
GA V15CV
UT WOS:000207781000467
ER
PT J
AU Cobb, JP
Moore, EE
Hayden, DL
Minei, JP
Cuschieri, J
Yang, JY
Li, Q
Lin, N
Brownstein, BH
Hennessy, L
Mason, PH
Schierding, WS
Dixon, DJ
Tompkins, RG
Warren, HS
Schoenfeld, DA
Maier, RV
AF Cobb, J. Perren
Moore, Ernest E.
Hayden, Doug L.
Minei, Joseph P.
Cuschieri, Joseph
Yang, Jingyun
Li, Qing
Lin, Nan
Brownstein, Bernard H.
Hennessy, Laura
Mason, Philip H.
Schierding, William S.
Dixon, David J.
Tompkins, Ronald G.
Warren, H. Shaw
Schoenfeld, David A.
Maier, Ronald V.
TI Validation of the Riboleukogram to Detect Ventilator-Associated
Pneumonia After Severe Injury
SO ANNALS OF SURGERY
LA English
DT Article
DE trauma; sepsis; micro array; genechip; diagnosis; RNA; glue grant
ID GENE-EXPRESSION PROFILES; INTENSIVE-CARE-UNIT; SEPSIS; BLOOD;
MICROARRAYS; DIAGNOSIS; RESPONSES; INFLAMMATION; ACTIVATION; PREDICTION
AB Objective: We hypothesized that circulating leukocyte RNA profiles or 'riboleukograrns" detect ventulator-associaied pneumonia after blunt trauma
Summary Background Data: A pilot microarray Study of 11 ventilator-associated pneumonia (VAP) patients suggested that 85 leukocyte genes can be used to diagnose VAII. Validation of this gene set to detect VAP was tested using data from an independent patient cohort
Methods: A total of 158 intubated blunt trauma patients were enrolled at 5 centers. where 57 (36%) developed VAP. Patient age was 34.2 +/- 11.1 years. 65% were male Circulating leukocyte GeneChip U 133 2 0 expression values were measured at time 0.5. 1, 4, 7, 14, 21 and 28 days after injury DChip normalized leukocyte transcriptional profiles were analyzed using repeated measures logistic regression A compound covariate model based on leukocyte gene transcriptional profiles in a training subset of patients was tested to determine predictive accuracy for VAII 4 days prior to (clinical diagnosis in the test subset.
Results: Using gene expression values measured on each study (lay at all FDR <0.05, 27 (32%) of the 85 genes were associated with Lhe diagnosis of VAP 1 to 4 days before diagnosis However, the compound covariate model based on these 85-genes did not predict VAP in the test cohort better than chance (P = 027) 111 contrast, a compound covariate model based upon de novo transcriptional analysis of the 158 patients predicted VAP better than chance 4 days before diagnosis with a sensitivity of 57% and a specificity of 69%.
Conclusion: Our results validate those described in I pilot study, confirming that riboleukograms are associated with the development of VAP days prior to clinical diagnosis Similarly. a riboleukogram predictive model tested oil a larger cohort of 158 patients was better than chance at predicting VAP (lays prior to clinical diagnosis
C1 Washington Univ, Ctr Crit Illness & Hlth Engn, St Louis, MO USA.
Massachusetts Gen Hosp, NIGMS Inflammat & Host Response Injury Program, Boston, MA 02114 USA.
RP Cobb, JP (reprint author), Campus Box 8109,660 S Euclid Ave, St Louis, MO 63110 USA.
FU NIGMS NIH HHS [U54 GM062119, R01 GM081524, R01GM081524, R01 GM081524-04,
R21 GM075023, R21GM075023, U54GM6211906]
NR 53
TC 15
Z9 16
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-4932
J9 ANN SURG
JI Ann. Surg.
PD OCT
PY 2009
VL 250
IS 4
BP 531
EP 539
DI 10.1097/SLA.0b013e3181b81bd5
PG 9
WC Surgery
SC Surgery
GA 504FA
UT WOS:000270599800004
PM 19730236
ER
PT J
AU Di Mascio, M
Srinivasula, S
Bhattacharjee, A
Cheng, L
Martiniova, L
Herscovitch, P
Lertora, J
Kiesewetter, D
AF Di Mascio, Michele
Srinivasula, Sharat
Bhattacharjee, Abesh
Cheng, Lily
Martiniova, Lucia
Herscovitch, Peter
Lertora, Juan
Kiesewetter, Dale
TI Antiretroviral Tissue Kinetics: In Vivo Imaging Using Positron Emission
Tomography
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HIV-INFECTED PATIENTS; LATENT RESERVOIR;
DRUG-RESISTANCE; RADIATION-DOSIMETRY; IMPROVED SURVIVAL; CELLULAR
FACTORS; THERAPY; PET; TENOFOVIR
AB Our current knowledge on the antiviral efficacy, dosing, and toxicity of available highly active antiretroviral therapy regimens is mostly derived from plasma or blood kinetics of anti-human immunodeficiency virus (anti-HIV) drugs. However, the blood comprises only 2% of the total target cells in the body. Tissue drug levels may differ substantially from corresponding plasma levels, and drug distribution processes may be characterized by high intertissue variability, leading to suboptimal target site concentrations and the potential risk for therapeutic failures. Positron emission tomography has greatly expanded the scope of the pharmacokinetic measurements that can be performed noninvasively in animal models or humans. We have prepared [(18)F]FPMPA, a fluorine-18-radiolabeled analogue of tenofovir, to study antiretroviral tissue kinetics in vivo noninvasively and tested the imaging probe in rats. The biodistribution of the fluorine-18 analogue closely follows that of nonfluorinated tenofovir. Compared to that in the blood, the levels of penetration of the antiretroviral drug were found to be significantly reduced in the spleen and submandibular lymph nodes (similar to 2-fold), in the mesenteric lymph nodes and the testes (similar to 4-fold), and in the brain compartment (similar to 25-fold). Intersubject variability of the trough drug concentration ( measured at 120 min) in certain tissues, like the colon ( coefficient of variation, > 100%), is not reflected by the intersubject variability in the blood compartment ( coefficient of variation, 24%). Positron emission tomography imaging of the fluorine-18 analogue revealed the accumulation of the antiretroviral drug in the cortex of the kidneys, a potential correlate of tenofovir-induced nephrotoxicity observed in HIV-1-infected treated patients. Thus, [(18)F]FPMPA is a promising radiotracer for evaluation of tenofovir biodistribution under carefully controlled drug administration protocols.
C1 [Di Mascio, Michele] NIAID, Div Clin Res, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Srinivasula, Sharat] NCI Frederick, SAIC Frederick Inc, Biostat Res Branch, Frederick, MD 21702 USA.
[Bhattacharjee, Abesh; Kiesewetter, Dale] Natl Inst Biomed Imaging & Bioengn, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Cheng, Lily] NIAID, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Martiniova, Lucia] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Reprod & Adult Endocrinol Program, NIH, Bethesda, MD 20892 USA.
[Herscovitch, Peter] NIH, Warren G Magnuson Clin Ctr, Positron Emiss Tomog Dept, Bethesda, MD 20892 USA.
[Lertora, Juan] NIH, Warren G Magnuson Clin Ctr, Clin Pharmacol Program, Bethesda, MD 20892 USA.
RP Di Mascio, M (reprint author), NIAID, Div Clin Res, Biostat Res Branch, NIH, 6700B Rockledge Dr MSC 7609, Bethesda, MD 20892 USA.
EM mdimascio@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases; National
Institute of Biomedical Imaging and Bioengineering; National Cancer
Institute; NIH [HHSN261200800001E]
FX This work was supported in part by the Intramural Research Programs of
the National Institute of Allergy and Infectious Diseases and the
National Institute of Biomedical Imaging and Bioengineering. Additional
funding has been provided by the National Cancer Institute, NIH, under
contract no. HHSN261200800001E.
NR 54
TC 22
Z9 22
U1 0
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2009
VL 53
IS 10
BP 4086
EP 4095
DI 10.1128/AAC.00419-09
PG 10
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 496ZS
UT WOS:000270020600005
PM 19667288
ER
PT J
AU Kuehl, R
Al-Bataineh, S
Gordon, O
Luginbuehl, R
Otto, M
Textor, M
Landmann, R
AF Kuehl, Richard
Al-Bataineh, Sameer
Gordon, Oliver
Luginbuehl, Reto
Otto, Michael
Textor, Marcus
Landmann, Regine
TI Furanone at Subinhibitory Concentrations Enhances Staphylococcal Biofilm
Formation by luxS Repression
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID POLYSACCHARIDE INTERCELLULAR ADHESIN; QUORUM-SENSING SYSTEM;
DEVICE-ASSOCIATED INFECTIONS; GENE-EXPRESSION; DELISEA-PULCHRA;
EPIDERMIDIS; AUREUS; INHIBITION; VIRULENCE; TITANIUM
AB Brominated furanones from marine algae inhibit multicellular behaviors of gram-negative bacteria such as biofilm formation and quorum sensing (QS) without affecting their growth. The interaction of furanone with QS in gram-positive bacteria is unknown. Staphylococci have two QS systems, agr and luxS, which lower biofilm formation by two different pathways, RNAIII upregulation and bacterial detachment, and polysaccharide intercellular adhesin ( PIA) reduction, respectively. We synthesized natural furanone compound 2 [(5Z)-4-bromo-5-(bromomethylene)-3-butyl-2(5H)-furanone] from Delisea pulchra and three analogues to investigate their effect on biofilm formation in gram-positive bacteria. Compound 2, but not the analogues, enhanced the biofilms of Staphylococcus epidermidis 1457 and 047 and of S. aureus Newman at concentrations between 1.25 and 20 mu M. We show the growth inhibition of S. epidermidis and S. aureus by free furanone and demonstrate bactericidal activity. An induction of biofilm occurred at concentrations of 10 to 20% of the MIC and correlated with an increase in PIA. The biofilm effect was agr independent. It was due to interference with luxS, as shown by reduced luxS expression in the presence of compound 2 and independence of the strong biofilm formation in a luxS mutant upon furanone addition. Poly(L-lysine)-grafted/poly(ethylene glycol)-grafted furanone was ineffective on biofilm and not bactericidal, indicating the necessity for free furanone. Free furanone was similarly toxic for murine fibroblasts as for staphylococci, excluding a therapeutic application of this compound. In summary, we observed a biofilm enhancement by furanone in staphylococci at subinhibitory concentrations, which was manifested by an increase in PIA and dependent on luxS.
C1 [Kuehl, Richard; Gordon, Oliver; Landmann, Regine] Univ Basel Hosp, Dept Biomed, Div Infect Biol, CH-4031 Basel, Switzerland.
[Al-Bataineh, Sameer; Textor, Marcus] Swiss Fed Inst Technol, Dept Mat, Lab Surface Sci & Technol, BioInterfaceGrp, Zurich, Switzerland.
[Luginbuehl, Reto] RMS Fdn, Bettlach, Switzerland.
[Otto, Michael] NIAID, NIH, Bethesda, MD 20892 USA.
RP Landmann, R (reprint author), Univ Basel Hosp, Dept Biomed, Div Infect Biol, Hebelstr 20, CH-4031 Basel, Switzerland.
EM regine.landmann@unibas.ch
RI Al-Bataineh, Sameer/D-4604-2009; Textor, Marcus/A-6200-2012;
OI Al-Bataineh, Sameer/0000-0003-1711-8032; Textor,
Marcus/0000-0002-0178-1801; Otto, Michael/0000-0002-2222-4115
FU RMS Foundation
FX We thank the RMS Foundation for supporting R. Kuehl. We are grateful for
the advice of M. Schmaler, N. Jann, and W. Zimmerli and for the
technical help of F. Ferracin and Z. Rajacic. We thank D. Mack and L.
Harris, Swansea, Great Britain, for providing the anti-PIA antibody.
NR 46
TC 34
Z9 37
U1 1
U2 22
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2009
VL 53
IS 10
BP 4159
EP 4166
DI 10.1128/AAC.01704-08
PG 8
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 496ZS
UT WOS:000270020600014
PM 19620329
ER
PT J
AU Li, M
Rigby, K
Lai, YP
Nair, V
Peschel, A
Schittek, B
Otto, M
AF Li, Min
Rigby, Kevin
Lai, Yuping
Nair, Vinod
Peschel, Andreas
Schittek, Birgit
Otto, Michael
TI Staphylococcus aureus Mutant Screen Reveals Interaction of the Human
Antimicrobial Peptide Dermcidin with Membrane Phospholipids
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID HOST-DEFENSE PEPTIDES; BACTERIAL-MEMBRANES; SWEAT GLANDS; RESISTANCE;
INFECTIONS; EXPRESSION; REPLACEMENT; TRANSPOSON; CARNOSUS; BILAYERS
AB Antimicrobial peptides (AMPs) form an important part of the innate host defense. In contrast to most AMPs, human dermcidin has an anionic net charge. To investigate whether bacteria have developed specific mechanisms of resistance to dermcidin, we screened for mutants of the leading human pathogen, Staphylococcus aureus, with altered resistance to dermcidin. To that end, we constructed a plasmid for use in mariner-based transposon mutagenesis and developed a high-throughput cell viability screening method based on luminescence. In a large screen, we did not find mutants with strongly increased susceptibility to dermcidin, indicating that S. aureus has no specific mechanism of resistance to this AMP. Furthermore, we detected a mutation in a gene of unknown function that resulted in significantly increased resistance to dermcidin. The mutant strain had an altered membrane phospholipid pattern and showed decreased binding of dermcidin to the bacterial surface, indicating that dermcidin interacts with membrane phospholipids. The mode of this interaction was direct, as shown by assays of dermcidin binding to phospholipid preparations, and specific, as the resistance to other AMPs was not affected. Our findings indicate that dermcidin has an exceptional value for the human innate host defense and lend support to the idea that it evolved to evade bacterial resistance mechanisms targeted at the cationic character of most AMPs. Moreover, they suggest that the antimicrobial activity of dermcidin is dependent on the interaction with the bacterial membrane and might thus assist with the determination of the yet unknown mode of action of this important human AMP.
C1 [Li, Min; Rigby, Kevin; Lai, Yuping; Otto, Michael] NIAID, Lab Human Bacterial Pathogenesis, NIH, Bethesda, MD 20892 USA.
[Nair, Vinod] NIAID, Res Technol Sect, Microscopy Unit, NIH, Hamilton, MT USA.
[Peschel, Andreas] Univ Tubingen, Med Microbiol & Hyg Dept, Cellular & Mol Microbiol Unit, Tubingen, Germany.
[Schittek, Birgit] Univ Tubingen, Dept Dermatol, Tubingen, Germany.
RP Otto, M (reprint author), NIAID, Lab Human Bacterial Pathogenesis, NIH, Bldg 33 1W10,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM motto@niaid.nih.gov
OI Otto, Michael/0000-0002-2222-4115
FU NIAID; National Institutes of Health; German Research Council [510/3-3,
SFB 766]
FX This work was supported by the Intramural Research Program of the NIAID,
National Institutes of Health ( to M.O.) and the German Research Council
( grant Schi 510/3-3 to B. S. and grant SFB 766 to B. S. and A. P.).
NR 32
TC 32
Z9 33
U1 3
U2 10
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2009
VL 53
IS 10
BP 4200
EP 4210
DI 10.1128/AAC.00428-09
PG 11
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 496ZS
UT WOS:000270020600020
PM 19596877
ER
PT J
AU Panchal, RG
Ulrich, RL
Lane, D
Butler, MM
Houseweart, C
Opperman, T
Williams, JD
Peet, NP
Moir, DT
Nguyen, T
Gussio, R
Bowlin, T
Bavari, S
AF Panchal, Rekha G.
Ulrich, Ricky L.
Lane, Douglas
Butler, Michelle M.
Houseweart, Chad
Opperman, Timothy
Williams, John D.
Peet, Norton P.
Moir, Donald T.
Nguyen, Tam
Gussio, Rick
Bowlin, Terry
Bavari, Sina
TI Novel Broad-Spectrum Bis-(Imidazolinylindole) Derivatives with Potent
Antibacterial Activities against Antibiotic-Resistant Strains
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID DNA-BINDING LIGANDS; STAPHYLOCOCCUS-AUREUS; DIARYLAMIDINE DERIVATIVES;
BACILLUS-ANTHRACIS; IN-VITRO; SUSCEPTIBILITY; LETHAL
AB Given the limited number of structural classes of clinically available antimicrobial drugs, the discovery of antibacterials with novel chemical scaffolds is an important strategy in the development of effective therapeutics for both naturally occurring and engineered resistant strains of pathogenic bacteria. In this study, several diarylamidine derivatives were evaluated for their ability to protect macrophages from cell death following infection with Bacillus anthracis, a gram-positive spore-forming bacterium. Four bis-(imidazolinylindole) compounds were identified with potent antibacterial activity as measured by the protection of macrophages and by the inhibition of bacterial growth in vitro. These compounds were effective against a broad range of gram-positive and gram-negative bacterial species, including several antibiotic-resistant strains. Minor structural variations among the four compounds correlated with differences in their effects on bacterial macromolecular synthesis and mechanisms of resistance. In vivo studies revealed protection by two of the compounds of mice lethally infected with B. anthracis, Staphylococcus aureus, or Yersinia pestis. Taken together, these results indicate that the bis-(imidazolinylindole) compounds represent a new chemotype for the development of therapeutics for both gram-positive and gram-negative bacterial species as well as against antibiotic-resistant infections.
C1 [Panchal, Rekha G.; Ulrich, Ricky L.; Bavari, Sina] USA, Med Res Inst Infect Dis, Ft Detrick, MD 21702 USA.
[Lane, Douglas; Nguyen, Tam] NCI, Target Struct Based Drug Discovery Grp, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Butler, Michelle M.; Houseweart, Chad; Opperman, Timothy; Williams, John D.; Peet, Norton P.; Moir, Donald T.; Bowlin, Terry] Microbiotix Inc, Worcester, MA 01605 USA.
[Gussio, Rick] NCI, Target Struct Based Drug Discovery Grp, Informat Technol Branch, Dev Therapeut Program, Frederick, MD 21702 USA.
RP Panchal, RG (reprint author), USA, Med Res Inst Infect Dis, 1425 Porter St, Ft Detrick, MD 21702 USA.
EM rekha.panchal@amedd.army.mil; sina.bavari@amedd.army.mil
FU NCI NIH HHS [N01-CO-12400, N01CO12400]
NR 25
TC 26
Z9 27
U1 1
U2 9
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2009
VL 53
IS 10
BP 4283
EP 4291
DI 10.1128/AAC.01709-08
PG 9
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 496ZS
UT WOS:000270020600032
PM 19635954
ER
PT J
AU Sarkar, A
Tilly, K
Stewart, P
Bestor, A
Battisti, JM
Rosa, PA
AF Sarkar, Amit
Tilly, Kit
Stewart, Philip
Bestor, Aaron
Battisti, James M.
Rosa, Patricia A.
TI Borrelia burgdorferi Resistance to a Major Skin Antimicrobial Peptide Is
Independent of Outer Surface Lipoprotein Content
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID LYME-DISEASE SPIROCHETE; INVASIVE BACTERIAL-INFECTION;
CRYSTAL-STRUCTURE; CIRCULAR PLASMID; PROTEIN-C; MONOCLONAL-ANTIBODY;
TREPONEMA-PALLIDUM; OSPC GENE; HOST; LEPTOSPIRA
AB We hypothesize a potential role for Borrelia burgdorferi OspC in innate immune evasion at the initial stage of mammalian infection. We demonstrate that B. burgdorferi is resistant to high levels (> 200 mu g/ml) of cathelicidin and that this antimicrobial peptide exhibits limited binding to the spirochetal outer membrane, irrespective of OspC or other abundant surface lipoproteins. We conclude that the essential role of OspC is unrelated to resistance to this component of innate immunity.
C1 [Sarkar, Amit; Tilly, Kit; Stewart, Philip; Bestor, Aaron; Battisti, James M.; Rosa, Patricia A.] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Sarkar, A (reprint author), NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, 903 S 4th St, Hamilton, MT 59840 USA.
EM sarkara@niaid.nih.gov
FU NIAID; NIH
FX This research work was supported by the Intramural Research Program of
the NIAID, NIH.
NR 50
TC 5
Z9 5
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2009
VL 53
IS 10
BP 4490
EP 4494
DI 10.1128/AAC.00558-09
PG 5
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 496ZS
UT WOS:000270020600060
PM 19651916
ER
PT J
AU Pongas, GN
Ben-Ami, R
Lewis, RE
Walsh, TJ
Kontoyiannis, DP
AF Pongas, Georgios N.
Ben-Ami, Ronen
Lewis, Russell E.
Walsh, Thomas J.
Kontoyiannis, Dimitrios P.
TI Culture Medium Composition Affects the Lethality of Cunninghamella
bertholletiae in a Fly Model of Mucormycosis
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Letter
ID ZYGOMYCOSIS
C1 [Kontoyiannis, Dimitrios P.] Univ Texas MD Anderson Canc Ctr, Dept Infect Dis Infect Control & Employee Hlth, Unit 1406, Houston, TX 77030 USA.
[Walsh, Thomas J.] NCI, Bethesda, MD 20892 USA.
RP Kontoyiannis, DP (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Infect Dis Infect Control & Employee Hlth, Unit 1406, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM dkontoyi@mdanderson.org
OI Lewis, Russell/0000-0002-2002-4339
NR 5
TC 4
Z9 4
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD OCT
PY 2009
VL 53
IS 10
BP 4569
EP 4569
DI 10.1128/AAC.00994-09
PG 1
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 496ZS
UT WOS:000270020600083
PM 19635953
ER
PT J
AU Leto, TL
Morand, S
Hurt, D
Ueyama, T
AF Leto, Thomas L.
Morand, Stanislas
Hurt, Darrell
Ueyama, Takehiko
TI Targeting and Regulation of Reactive Oxygen Species Generation by Nox
Family NADPH Oxidases
SO ANTIOXIDANTS & REDOX SIGNALING
LA English
DT Review
ID CHRONIC GRANULOMATOUS-DISEASE; AIRWAY EPITHELIAL-CELLS;
PHOSPHORYLATION-INDUCED ACTIVATION; DEPENDENT H2O2 GENERATION; THYROID
PLASMA-MEMBRANES; R-MEDIATED PHAGOCYTOSIS; SRC HOMOLOGY-3 DOMAINS;
PROTEIN-KINASE-C; SUPEROXIDE-PRODUCTION; HYDROGEN-PEROXIDE
AB Nox family NADPH oxidases serve a variety of functions requiring reactive oxygen species (ROS) generation, including antimicrobial defense, biosynthetic processes, oxygen sensing, and redox-based cellular signaling. We explored targeting, assembly, and activation of several Nox family oxidases, since ROS production appears to be regulated both spatially and temporally. Nox1 and Nox3 are similar to the phagocytic (Nox2-based) oxidase, functioning as multicomponent superoxide-generating enzymes. Factors regulating their activities include cytosolic activator and organizer proteins and GTP-Rac. Their regulation varies, with the following rank order: Nox2>Nox1>Nox3. Determinants of subcellular targeting include: (a) formation of Nox-p22(phox) heterodimeric complexes allowing plasma membrane translocation, (b) phospholipids-binding specificities of PX domain-containing organizer proteins (p47(phox) or Nox organizer 1 (Noxo1 and p40(phox)), and (c) variably splicing of Noxo1 PX domains directing them to nuclear or plasma membranes. Dual oxidases (Duox1 and Duox2) are targeted by different mechanisms. Plasma membrane targeting results in H2O2 release, not superoxide, to support extracellular peroxidases. Human Duox1 and Duox2 have no demonstrable peroxidase activity, despite their extensive homology with heme peroxidases. The dual oxidases were reconstituted by Duox activator 2 (Duoxa2) or two Duoxa1 variants, which dictate maturation, subcellular localization, and the type of ROS generated by forming stable complexes with Duox. Antioxid Redox Signal. 11, 2607-2619.
C1 [Leto, Thomas L.; Morand, Stanislas] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
[Hurt, Darrell] NIAID, Bioinformat & Computat Biosci Branch, NIH, Bethesda, MD 20892 USA.
[Ueyama, Takehiko] Kobe Univ, Biosignal Res Ctr, Mol Pharmacol Lab, Kobe, Hyogo 657, Japan.
RP Leto, TL (reprint author), NIAID, NIH, Twinbrook Facil 2, 12441 Parklawn Dr, Rockville, MD 20852 USA.
EM tleto@nih.gov
RI Hurt, Darrell/B-5076-2013
OI Hurt, Darrell/0000-0002-9829-8567
FU National Institutes of Health; National Institute of Allergy and
Infectious Diseases
FX This work was supported by the National Institutes of Health Intramural
Research Program, National Institute of Allergy and Infectious Diseases,
and Grant-in-Aid for Scientific Research on ( C), on Priority Areas, and
on the Global-COE Program in Japan. We thank to Dr. Corinne Dupuy,
Institut Gustave Roussy,
NR 113
TC 162
Z9 165
U1 0
U2 6
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1523-0864
EI 1557-7716
J9 ANTIOXID REDOX SIGN
JI Antioxid. Redox Signal.
PD OCT
PY 2009
VL 11
IS 10
BP 2607
EP 2619
DI 10.1089/ars.2009.2637
PG 13
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 496NC
UT WOS:000269980200019
PM 19438290
ER
PT J
AU Liu, XF
Bera, TK
Liu, LJ
Pastan, I
AF Liu, Xiu Fen
Bera, Tapan K.
Liu, Lisa J.
Pastan, Ira
TI A primate-specific POTE-actin fusion protein plays a role in apoptosis
SO APOPTOSIS
LA English
DT Article
DE POTE paralogs; Ankrd26; Bax/Bak; Death receptor
ID CELL-DEATH; FAMILY PROTEINS; BAX; EXPRESSION; PARALOGS; PROSTATE;
CANCER; TESTIS; GENES
AB The primate-specific gene family, POTE, is expressed in many cancers but only in a limited number of normal tissues (testis, ovary, prostate). The 13 POTE paralogs are dispersed among 8 human chromosomes. They evolved by gene duplication and remodeling from an ancestral gene, Ankrd26, recently implicated in controlling body size and obesity. In addition, several POTE paralogs are fused to an actin retrogene producing POTE-actin fusion proteins. The biological function of the POTE genes is unknown, but their high expression in primary spermatocytes, some of which are undergoing apoptosis, suggests a role in inducing programmed cell death. We have chosen Hela cells as a model to study POTE function in human cancer, and have identified POTE-2 alpha-actin as the major transcript and the protein it encodes in Hela cells. Transfection experiments show that both POTE-2 alpha-actin and POTE-2 gamma C are localized to actin filaments close to the inner plasma membrane. Transient expression of POTE-2 alpha-actin or POTE-2 gamma C induces apoptosis in Hela cells. Using wild-type and mutant mouse embryo cells, we find apoptosis induced by over-expression of POTE-2 gamma C is decreased in Bak (-/-) or Bak (-/-) Bax (-/-) cells indicating POTE is acting through a mitochondrial pathway. Endogenous POTE-actin protein levels but not RNA levels increased in a time dependent manner by stimulation of death receptors with their cognate ligands. Our data indicates that the POTE gene family encodes a new family of proapoptotic proteins.
C1 [Liu, Xiu Fen; Bera, Tapan K.; Liu, Lisa J.; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Pastan, I (reprint author), NCI, Mol Biol Lab, Ctr Canc Res, NIH, 37 Convent Dr,Room 5106, Bethesda, MD 20892 USA.
EM pastani@mail.nih.gov
FU NIH
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. We thank Dr.
Susan Garfield, Poonam Mannan and Lim Langston of the Center for Cancer
Research Confocal Core Facility for technical assistance.
NR 21
TC 15
Z9 17
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1360-8185
J9 APOPTOSIS
JI Apoptosis
PD OCT
PY 2009
VL 14
IS 10
BP 1237
EP 1244
DI 10.1007/s10495-009-0392-0
PG 8
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 494TH
UT WOS:000269839300010
PM 19669888
ER
PT J
AU Singh, A
Kapur, S
Chattopadhyay, I
Purkayastha, J
Sharma, J
Mishra, A
Hewitt, SM
Saxena, S
AF Singh, Avninder
Kapur, Sujala
Chattopadhyay, Indranil
Purkayastha, Joydeep
Sharma, Jagannath
Mishra, Ashwani
Hewitt, Stephen M.
Saxena, Sunita
TI Cytokeratin Immunoexpression in Esophageal Squamous Cell Carcinoma of
High-risk Population in Northeast India
SO APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY
LA English
DT Article
DE cytokeratins; esophageal cancer; high risk; immunohistochemistry;
squamous cell carcinoma; tissue microarray
ID MICROARRAY ANALYSIS; KERATIN PROTEINS; EXPRESSION; EPITHELIUM; PATTERNS;
CANCER; PROGRESSION
AB Esophageal cancer is a frequently fatal malignancy, and is described in certain regions in Northeast India with an incidence of esophageal squamous cell carcinoma many fold higher than the rest of the population. The population in Northeast India is at higher risk due to poor nutritional status, consumption of fermented betel quid and other oral tobacco products besides smoking and alcohol intake. Cytokeratins (CKs) are the major constituents of the esophageal epithelium and may show gain or loss of CKs as the cancer progresses from normal epithelium to invasive phenotype. In this study, we studied the immunohistochemical expression of 5 CKs (CK4, CK5, CK8, CK14, and CK17) in the normal esophageal epithelium and esophageal squamous cell carcinoma from both the general population and the high-risk population of Assam in Northeast India. The CK expression profile was similar to other published data in general. Further analysis demonstrated differences in CK expression between the general and the high-risk tumor samples. CK5 and CK8 expression was altered in the high-risk population. The significance of these differences is unclear, but suggests a connection to the etiologic factors.
C1 [Singh, Avninder; Kapur, Sujala; Chattopadhyay, Indranil; Mishra, Ashwani; Saxena, Sunita] Indian Council Med Res, Inst Pathol, New Delhi, India.
[Purkayastha, Joydeep; Sharma, Jagannath] B Borooah Canc Inst, Gauhati, Assam, India.
[Hewitt, Stephen M.] NCI, Tissue Array Res Lab, NIH, Bethesda, MD 20892 USA.
RP Hewitt, SM (reprint author), NCI, Tissue Array Res Lab, NIH, Bethesda, MD 20892 USA.
EM hewitts@mail.nih.gov
OI Hewitt, Stephen/0000-0001-8283-1788
FU UICC (International Union against Cancer); NIH, National Cancer
Institute, Center for Cancer Research
FX Source of support: Financial support to Avninder Singh for the ICRETT
technology transfer fellowship UICC (International Union against
Cancer). This research was supported in part by the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research.
NR 22
TC 8
Z9 8
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1062-3345
J9 APPL IMMUNOHISTO M M
JI Appl. Immunohistochem.
PD OCT
PY 2009
VL 17
IS 5
BP 419
EP 424
PG 6
WC Anatomy & Morphology; Medical Laboratory Technology; Pathology
SC Anatomy & Morphology; Medical Laboratory Technology; Pathology
GA 500GP
UT WOS:000270287100009
PM 19417629
ER
PT J
AU Huey, ED
Pardini, M
Cavanagh, A
Wassermann, EM
Kapogiannis, D
Spina, S
Ghetti, B
Grafman, J
AF Huey, Edward D.
Pardini, Matteo
Cavanagh, Alyson
Wassermann, Eric M.
Kapogiannis, Dimitrios
Spina, Salvatore
Ghetti, Bernardino
Grafman, Jordan
TI Association of Ideomotor Apraxia With Frontal Gray Matter Volume Loss in
Corticobasal Syndrome
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID PROGRESSIVE SUPRANUCLEAR PALSY; VOXEL-BASED MORPHOMETRY; SUPPLEMENTARY
MOTOR AREA; LIMB APRAXIA; DEGENERATION SYNDROME; ALZHEIMERS-DISEASE;
BRAIN-LESIONS; DISORDERS; REPRESENTATIONS; PERFORMANCE
AB Objective: To determine the brain areas associated with specific components of ideomotor apraxia (IMA) in corticobasal syndrome (CBS).
Design: Case-control and cross-sectional study.
Participants: Forty-eight patients with CBS and 14 control subjects.
Intervention: Administration of the Test of Oral and Limb Apraxia.
Main Outcome Measures: Differences between patients with CBS and healthy controls and associations between areas of gray matter volume and IMA determined by voxel-based morphometry in patients with CBS.
Results: Overall, IMA was associated with decreased gray matter volume in the left supplemental motor area, premotor cortex, and caudate nucleus of patients with CBS. The overall degree of apraxia was independent of the side of motor impairment. Praxis to imitation (vs command) was particularly impaired in the patients with CBS. Patients demonstrated equal impairment in transitive and intransitive praxis.
Conclusions: In patients with CBS, IMA is associated with left posterior frontal cortical and subcortical volume loss. Despite showing left frontal volume loss associated with IMA, patients with CBS have particularly impaired imitation of gestures. These findings suggest either that the IMA of CBS affects a route of praxis that bypasses motor engrams or that motor engrams are affected but that they exist in areas other than the inferior parietal cortex.
C1 [Huey, Edward D.; Pardini, Matteo; Cavanagh, Alyson; Wassermann, Eric M.; Kapogiannis, Dimitrios; Grafman, Jordan] NINDS, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA.
[Wassermann, Eric M.; Kapogiannis, Dimitrios] NINDS, Brain Stimulat Unit, NIH, Bethesda, MD 20892 USA.
[Huey, Edward D.] Feinstein Inst Med Res, Litwin Zucker Res Ctr Study Alzheimers Dis & Memo, Manhasset, NY USA.
[Pardini, Matteo] Univ Genoa, Magnet Resonance Res Ctr Nervous Syst Dis, Genoa, Italy.
[Pardini, Matteo] Univ Genoa, Dept Neurosci, Genoa, Italy.
[Pardini, Matteo] Univ Genoa, Dept Ophthalmol, Genoa, Italy.
[Pardini, Matteo] Univ Genoa, Dept Genet, Genoa, Italy.
[Spina, Salvatore] Univ Siena, Dept Neurol Neurosurg & Behav Sci, I-53100 Siena, Italy.
[Spina, Salvatore; Ghetti, Bernardino] Indiana Univ, Sch Med, Dept Pathol & Lab Med, Indiana Alzheimer Dis Ctr, Indianapolis, IN USA.
RP Grafman, J (reprint author), NINDS, Cognit Neurosci Sect, NIH, Bldg 10,Room 7D43,MSC 1440, Bethesda, MD 20892 USA.
EM grafmanj@ninds.nih.gov
RI Pardini, Matteo/F-8414-2010;
OI Pardini, Matteo/0000-0002-4740-1982; Grafman, Jordan
H./0000-0001-8645-4457
FU National Institutes of Health/National Institute of Neurological
Disorders and Stroke (NIH/NINDS); NINDS [5R00NS060766]; National
Institute on Aging [5P30AG010133]; Litwin-Zucker Center for Research on
Alzheimer's Disease and Memory Disorders
FX This study was supported by the intramural program of the National
Institutes of Health/National Institute of Neurological Disorders and
Stroke (NIH/NINDS), grant 5R00NS060766 from the NINDS (Dr Huey), grant
5P30AG010133 from the National Institute on Aging (Dr Ghetti), and the
Litwin-Zucker Center for Research on Alzheimer's Disease and Memory
Disorders (Dr Huey).
NR 45
TC 14
Z9 14
U1 1
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD OCT
PY 2009
VL 66
IS 10
BP 1274
EP 1280
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 504LA
UT WOS:000270617000014
PM 19822784
ER
PT J
AU Kreisl, WC
Mbeo, G
Fujita, M
Zoghbi, SS
Pike, VW
Innis, RB
McArthur, JC
AF Kreisl, William C.
Mbeo, Gilbert
Fujita, Masahiro
Zoghbi, Sami S.
Pike, Victor W.
Innis, Robert B.
McArthur, Justin C.
TI Stroke Incidentally Identified Using Improved Positron Emission
Tomography for Microglial Activation
SO ARCHIVES OF NEUROLOGY
LA English
DT Editorial Material
ID PERIPHERAL BENZODIAZEPINE-RECEPTORS; ISCHEMIA; RAT
C1 [Innis, Robert B.] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
RP Innis, RB (reprint author), NIMH, Mol Imaging Branch, 31 Ctr Dr,Room B2B37, Bethesda, MD 20892 USA.
EM innisr@mail.nih.gov
FU Intramural NIH HHS [Z99 MH999999]; NIMH NIH HHS [P30 MH075673,
Z01-MH-002793-04, Z01-MH-002795-04, Z01 MH002793, 1P030MH075673, Z01
MH002795]
NR 3
TC 9
Z9 9
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD OCT
PY 2009
VL 66
IS 10
BP 1288
EP 1289
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 504LA
UT WOS:000270617000017
PM 19822787
ER
PT J
AU Washington, MK
Berlin, J
Branton, P
Burgart, LJ
Carter, DK
Fitzgibbons, PL
Halling, K
Frankel, W
Jessup, J
Kakar, S
Minsky, B
Nakhleh, R
Compton, CC
AF Washington, Mary Kay
Berlin, Jordan
Branton, Philip
Burgart, Lawrence J.
Carter, David K.
Fitzgibbons, Patrick L.
Halling, Kevin
Frankel, Wendy
Jessup, John
Kakar, Sanjay
Minsky, Bruce
Nakhleh, Raouf
Compton, Carolyn C.
CA Coll Amer Pathologists
TI Protocol for the Examination of Specimens From Patients With Primary
Carcinoma of the Colon and Rectum
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID NONPOLYPOSIS COLORECTAL-CANCER; TOTAL MESORECTAL EXCISION;
MICROSATELLITE-INSTABILITY; PROGNOSTIC-SIGNIFICANCE; PATHOLOGICAL
ASSESSMENT; RESECTION SPECIMENS; CURATIVE RESECTION; MINIMUM NUMBER;
LYMPH-NODES; TUMOR
C1 [Washington, Mary Kay] Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA.
[Berlin, Jordan] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN 37232 USA.
[Branton, Philip] Inova Fairfax Hosp, Dept Pathol, Falls Church, VA USA.
[Burgart, Lawrence J.] Abbott NW Hosp, Allina Labs, Minneapolis, MN 55407 USA.
[Carter, David K.] St Marys Duluth Clin Hlth Syst, Dept Pathol, Duluth, MN USA.
[Fitzgibbons, Patrick L.] St Jude Med Ctr, Dept Pathol, Fullerton, CA USA.
[Halling, Kevin] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
[Frankel, Wendy] Ohio State Univ, Med Ctr, Dept Pathol, Columbus, OH 43210 USA.
[Jessup, John] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Compton, Carolyn C.] NCI, Off Biorepositories & Biospecimen Res, Bethesda, MD 20892 USA.
[Kakar, Sanjay] Univ Calif San Francisco, Dept Pathol, San Francisco, CA USA.
[Kakar, Sanjay] Vet Affairs Med Ctr, San Francisco, CA 94121 USA.
[Minsky, Bruce] Univ Chicago, Dept Radiat Oncol, Chicago, IL 60637 USA.
[Nakhleh, Raouf] St Lukes Hosp, Dept Pathol, Jacksonville, FL USA.
RP Washington, MK (reprint author), Vanderbilt Univ, Med Ctr, Dept Pathol, C-3321 MCN, Nashville, TN 37232 USA.
EM kay.washington@vanderbilt.edu
OI Fitzgibbons, Patrick/0000-0002-2998-6913
FU NCI NIH HHS [P50 CA095103, P50 CA095103-06, P50 CA095103-099001]
NR 46
TC 117
Z9 129
U1 0
U2 1
PU COLL AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
EI 1543-2165
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD OCT
PY 2009
VL 133
IS 10
BP 1539
EP 1551
PG 13
WC Medical Laboratory Technology; Medicine, Research & Experimental;
Pathology
SC Medical Laboratory Technology; Research & Experimental Medicine;
Pathology
GA 506ZU
UT WOS:000270819500002
PM 19792043
ER
PT J
AU Taneja, G
Brenner, RA
AF Taneja, Gitanjali
Brenner, Ruth A.
TI Formal Swimming Lessons Must Be Defined Reply
SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE
LA English
DT Editorial Material
C1 [Taneja, Gitanjali] NICHHD, Natl Childrens Study, Bethesda, MD 20892 USA.
RP Taneja, G (reprint author), NICHHD, Natl Childrens Study, 6100 Execut Blvd,Room 3A01, Bethesda, MD 20892 USA.
EM tanejagi@mail.nih.gov
NR 3
TC 0
Z9 0
U1 1
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 1072-4710
J9 ARCH PEDIAT ADOL MED
JI Arch. Pediatr. Adolesc. Med.
PD OCT
PY 2009
VL 163
IS 10
BP 962
EP 962
PG 1
WC Pediatrics
SC Pediatrics
GA 502YG
UT WOS:000270496300019
ER
PT J
AU Li, L
Wu, ZY
Rotheram-Borus, MJ
Guan, JH
Yin, YP
Detels, R
Wu, S
Lee, SJ
Cao, HJ
Lin, CQ
Rou, KM
Liu, ZD
AF Li, Li
Wu, Zunyou
Rotheram-Borus, Mary Jane
Guan, Jihui
Yin, Yueping
Detels, Roger
Wu, Sheng
Lee, Sung-Jae
Cao, Haijun
Lin, Chunqing
Rou, Keming
Liu, Zhendong
CA NIMH Collaborative HIV STD Prevent
TI Visiting Entertainment Venues and Sexual Health in China
SO ARCHIVES OF SEXUAL BEHAVIOR
LA English
DT Article
DE China; Behavioral intervention; HIV; STD; Entertainment venues
ID TRANSMITTED-DISEASES; COMMERCIAL SEX; WORKERS; RISK; BEHAVIOR;
POPULATION; INFECTION; YUNNAN
AB Entertainment venues in China are associated with risky sexual behavior. Most previous studies related to entertainment venues in China have focused on sex workers and commercial sex, but this study addressed sexual health in a sample of the general urban population. A randomly selected sample of market vendors (n = 4,510) from an eastern city was recruited and assessed to examine relationships between entertainment venue visits and sexual risk. Both behavioral (self-reports of unprotected sex) and biomedical (STD test results) measures were used. About 18% of the sample (26.8% of men and 9% of women) reported visiting entertainment venues in the past 30 days. Those who visited entertainment venues were more likely to be male, younger, single, with higher education, and to have more discretionary income. For both men and women, visiting entertainment venues was a significant predictor for unprotected sex and STD infection. Gender differences were observed in predicting unprotected sex and STD infections. Entertainment venues could be potential sites for place-based intervention programs and outreach for the general population.
C1 [Li, Li] Univ Calif Los Angeles, Semel Inst, Ctr Community Hlth, Los Angeles, CA 90024 USA.
[Li, Li; Rotheram-Borus, Mary Jane; Wu, Sheng; Lee, Sung-Jae] Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Ctr Community Hlth, Los Angeles, CA 90024 USA.
[Wu, Zunyou; Rou, Keming; Liu, Zhendong] Chinese Centers Dis Control & Prevent, Natl Ctr AIDS STD Control & Prevent, Beijing, Peoples R China.
[Guan, Jihui] Fujian Ctr Dis Control & Prevent, Fuzhou, Peoples R China.
[Detels, Roger; Cao, Haijun; Lin, Chunqing] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90024 USA.
[Yin, Yueping] Natl STD Reference Lab, Nanjing, Peoples R China.
NIMH Collaborat HIV STD Prevent Trial Grp, Rockville, MD USA.
RP Li, L (reprint author), Univ Calif Los Angeles, Semel Inst, Ctr Community Hlth, 10920 Wilshire Blvd,Suite 350, Los Angeles, CA 90024 USA.
EM lililili@ucla.edu
RI Li, Li/D-3776-2009
FU NIMH NIH HHS [U10 MH061513, U10 MH061513-05, U10MH61513]
NR 36
TC 13
Z9 14
U1 0
U2 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0004-0002
J9 ARCH SEX BEHAV
JI Arch. Sex. Behav.
PD OCT
PY 2009
VL 38
IS 5
BP 814
EP 820
DI 10.1007/s10508-008-9311-7
PG 7
WC Psychology, Clinical; Social Sciences, Interdisciplinary
SC Psychology; Social Sciences - Other Topics
GA 495HX
UT WOS:000269882800022
PM 18256918
ER
PT J
AU Krejnusova, I
Gocnikova, H
Bystricka, M
Blaskovicova, H
Polakova, K
Yewdell, J
Bennink, J
Russ, G
AF Krejnusova, Ingrid
Gocnikova, Hana
Bystricka, Magdalena
Blaskovicova, Hana
Polakova, Katarina
Yewdell, Jonathan
Bennink, Jack
Russ, Gustav
TI Antibodies to PB1-F2 protein are induced in response to influenza A
virus infection
SO ARCHIVES OF VIROLOGY
LA English
DT Article
ID NONSTRUCTURAL PROTEIN; CELL-DEATH; EXPRESSION; PATHOGENESIS; NS1
AB PB1-F2 is a small influenza A virus (IAV) protein encoded by an alternative (+1) reading frame of the PB1 gene. While dispensable for IAV replication in cultured cells, PB1-F2 has been implicated in IAV pathogenicity. To better understand PB1-F2 expression in vivo and its immunogenicity, we analyzed anti-PB1-F2 antibodies (Abs) in sera of mice infected intranasally (i.n.) with A/PR/8/34 (H1N1) virus and human acute and convalescent sera collected from the influenza H3N2 winter 2003-2004 epidemic. We explored a number of methods for detecting anti-PB1-F2 Abs, finding that PB1-F2-specific Abs could clearly be detected via immunoprecipitation or immunofluorescence assays using both immune mouse and human convalescent sera. Importantly, paired human sera exhibited similar increases in HI titers and PB1-F2-specific Abs. This study indicates that PB1-F2 is expressed in sufficient quantities in mice and humans infected with IAV to elicit an Ab response, supporting the biological relevance of this intriguing accessory protein.
C1 [Krejnusova, Ingrid; Gocnikova, Hana; Bystricka, Magdalena; Russ, Gustav] Slovak Acad Sci, Inst Virol, Bratislava, Slovakia.
[Blaskovicova, Hana] Off Publ Hlth, Bratislava, Slovakia.
[Polakova, Katarina] Slovak Acad Sci, Canc Res Inst, Bratislava, Slovakia.
[Yewdell, Jonathan; Bennink, Jack] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Russ, G (reprint author), Slovak Acad Sci, Inst Virol, Bratislava, Slovakia.
EM virugrus@savba.sk
RI yewdell, jyewdell@nih.gov/A-1702-2012
FU Scientific Grant Agency of the Ministry of Education of the Slovak
Republic [2/6022/6]; Slovak Academy of Sciences; Research and
Development Support Agency of the Slovak Republic [1605/06]; Division of
Intramural Research, NIAID, Bethesda, MD
FX We thank Margita Misovicova for excellent technical assistance. The
authors are indebted to Dr. Paul Calvo for providing the plasmid
producing PB1-F2-MBP fusion protein. This work was supported by grant
No. 2/6022/6 from the Scientific Grant Agency of the Ministry of
Education of the Slovak Republic and Slovak Academy of Sciences, by
grant no. 1605/06 from the Research and Development Support Agency of
the Slovak Republic and by the Division of Intramural Research, NIAID,
Bethesda, MD.
NR 25
TC 15
Z9 15
U1 0
U2 0
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0304-8608
J9 ARCH VIROL
JI Arch. Virol.
PD OCT
PY 2009
VL 154
IS 10
BP 1599
EP 1604
DI 10.1007/s00705-009-0479-5
PG 6
WC Virology
SC Virology
GA 504TS
UT WOS:000270641200003
PM 19672555
ER
PT J
AU Sovershaev, MA
Egorina, EM
Hansen, JB
Osterud, B
Pacher, P
Stasch, JP
Evgenov, OV
AF Sovershaev, Mikhail A.
Egorina, Elena M.
Hansen, John-Bjarne
Osterud, Bjarne
Pacher, Pal
Stasch, Johannes-Peter
Evgenov, Oleg V.
TI Soluble Guanylate Cyclase Agonists Inhibit Expression and Procoagulant
Activity of Tissue Factor
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE tissue factor; procoagulant activity; soluble guanylate cyclase; BAY
41-2272; BAY 58-2667
ID THP-1 MONOCYTIC CELLS; TUMOR-NECROSIS-FACTOR; FACTOR-KAPPA-B;
PULMONARY-HYPERTENSION; ENDOTHELIAL-CELLS; HEART-FAILURE; NITRIC-OXIDE;
CD40 LIGAND; P-SELECTIN; PLATELETS
AB Objective-Tissue factor (TF), a major initiator of blood coagulation, contributes to inflammation, atherosclerosis, angiogenesis, and vascular remodeling. Pharmacological agonists of soluble guanylate cyclase (sGC) attenuate systemic and pulmonary hypertension, vascular remodeling, and platelet aggregation. However, the influence of these novel pharmacophores on TF is unknown.
Methods and Results-We evaluated effects of BAY 41-2272 and BAY 58-2667 on expression and activity of TF in human monocytes and umbilical vein endothelial cells (HUVECs). Both compounds reduced expression of active TF protein in monocytes stimulated with lipopolysaccharide, as demonstrated by immunoblotting and a TF procoagulant activity assay. In-cell Western assay revealed that this effect was associated with a marked reduction of total and surface TF presentation. Furthermore, BAY 41-2272 and BAY 58-2667 decreased TF protein expression and the TF-dependent procoagulant activity in HUVECs stimulated with TNF-alpha. The sGC agonists also suppressed transcriptional activity of NF-kappa B. A siRNA-mediated knockdown of the alpha 1-subunit of sGC in monocytes and HUVECs confirmed that the inhibitory effect of BAY 41-2272 and BAY 58-2667 on TF expression is mediated through the sGC-dependent mechanisms.
Conclusions-Inhibition of TF expression and activity by sGC agonists might provide therapeutic benefits in cardiovascular diseases associated with enhanced procoagulant and inflammatory response. (Arterioscler Thromb Vasc Biol. 2009;29:1578-1586.)
C1 [Sovershaev, Mikhail A.; Egorina, Elena M.; Evgenov, Oleg V.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Sovershaev, Mikhail A.; Egorina, Elena M.; Osterud, Bjarne] Univ Tromso, Dept Biochem, Inst Med Biol, N-9001 Tromso, Norway.
[Hansen, John-Bjarne] Univ Tromso, Ctr Atherothrombot Res, Inst Clin Med, N-9001 Tromso, Norway.
[Sovershaev, Mikhail A.; Hansen, John-Bjarne] Univ Hosp No Norway, Dept Med, Tromso, Norway.
[Pacher, Pal] NIAAA, Lab Physiol Studies, NIH, Bethesda, MD USA.
[Stasch, Johannes-Peter] Bayer Schering Pharma AG, Inst Cardiovasc Res, Wuppertal, Germany.
RP Evgenov, OV (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, 55 Fruit St,Gray Bigelow 444, Boston, MA 02114 USA.
EM oevgenov@partners.org
RI Pacher, Pal/B-6378-2008
OI Pacher, Pal/0000-0001-7036-8108
FU Northern Norway Regional Health Authority; NIH/NIAAA
FX This work was supported in part by departmental funds, the Northern
Norway Regional Health Authority ( to M. A. S. and J.B.H.), and the
Intramural Research Program of NIH/NIAAA ( to P. P.).
NR 39
TC 7
Z9 7
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1079-5642
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD OCT
PY 2009
VL 29
IS 10
BP 1578
EP U446
DI 10.1161/ATVBAHA.109.192690
PG 27
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 494VY
UT WOS:000269848600029
PM 19592462
ER
PT J
AU Okada, S
Kamb, ML
Pandey, JP
Philen, RM
Love, LA
Miller, FW
AF Okada, Satoshi
Kamb, Mary L.
Pandey, Janardan P.
Philen, Rossanne M.
Love, Lori A.
Miller, Frederick W.
TI Immunogenetic Risk and Protective Factors for the Development of
L-Tryptophan-Associated Eosinophilia-Myalgia Syndrome and Associated
Symptoms
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
AB Objective. To assess L-tryptophan (LT) dose, age, sex, and immunogenetic markers as possible risk or protective factors for the development of LT-associated eosinophilia-myalgia syndrome (EMS) and related clinical findings.
Methods. HLA-DRB1 and DQA1 allele typing and Gm/Km phenotyping were performed on a cohort of 94 white subjects with documented LT ingestion and standardized evaluations. Multivariate analyses compared LT dose, age, sex, and alleles among groups of subjects who ingested LT and subsequently developed surveillance criteria for EMS, developed EMS or characteristic features of EMS (EMS spectrum disorder), or developed no features of EMS (unaffected).
Results. Considering all sources of LT, higher LT dose (odds ratio [OR] 1.4, 95% confidence interval [95% CI] 1.1-1.8), age > 45 years (OR 3.0, 95% CI 1.0-8.8), and HLA-DRB1* 03 (OR 3.9, 95% CI 1.2-15.2), DRB1* 04 (OR 3.9, 95% CI 1.1-16.4), and DQA1* 0601 (OR 13.7, 95% CI 1.3-1.8) were risk factors for the development of EMS, whereas DRB1* 07 (OR 0.12, 95% CI 0.02-0.48) and DQA1* 0501 (OR 0.23, 95% CI 0.05-0.85) were protective. Similar risk and protective factors were seen for developing EMS following ingestion of implicated LT, except that DRB1* 03 was not a risk factor and DQA1* 0201 was an additional protective factor. EMS spectrum disorder also showed similar findings, but with DRB1* 04 being a risk factor and DRB1* 07 and DQA1* 0201 being protective. There were no differences in sex distribution, Gm/Km allotypes, or Gm/Km phenotypes among any groups.
Conclusion. In addition to the xenobiotic dose and subject age, polymorphisms in immune response genes may underlie the development of certain xenobiotic-induced immune-mediated disorders, and these findings may have implications for future related epidemics.
C1 [Okada, Satoshi] Ichikawa Gen Hosp, Tokyo Dent Coll, Ichikawa, Japan.
[Kamb, Mary L.; Philen, Rossanne M.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Pandey, Janardan P.] Univ S Carolina, Charleston, SC USA.
[Love, Lori A.; Miller, Frederick W.] NIEHS, NIH, Bethesda, MD 20892 USA.
[Love, Lori A.; Miller, Frederick W.] US Dept HHS, Bethesda, MD USA.
RP Miller, FW (reprint author), NIEHS, Environm Autoimmun Grp, NIH 10, Room 4-2352,10 Ctr Dr,MSC 1301, Bethesda, MD 20892 USA.
EM millerf@mail.nih.gov
OI Miller, Frederick/0000-0003-2831-9593
FU Intramural NIH HHS [Z01 ES101074-06]
NR 23
TC 8
Z9 9
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2151-464X
EI 2151-4658
J9 ARTHRIT CARE RES
JI Arthritis Care Res.
PD OCT
PY 2009
VL 61
IS 10
BP 1305
EP 1311
DI 10.1002/art.24460
PG 7
WC Rheumatology
SC Rheumatology
GA V26IA
UT WOS:000208538100005
PM 19790128
ER
PT J
AU Rizza, S
Tesauro, M
Cardillo, C
Galli, A
Iantorno, M
Gigli, F
Sbraccia, P
Federici, M
Quon, MJ
Lauro, D
AF Rizza, Stefano
Tesauro, Manfredi
Cardillo, Carmine
Galli, Angelica
Iantorno, Micaela
Gigli, Fabrizio
Sbraccia, Paolo
Federici, Massimo
Quon, Michael J.
Lauro, Davide
TI Fish oil supplementation improves endothelial function in normoglycemic
offspring of patients with type 2 diabetes
SO ATHEROSCLEROSIS
LA English
DT Article
DE Fish oil; Type 2 diabetes; Endothelial function; TNF-alpha; Inflammation
ID CARDIOVASCULAR RISK-FACTORS; INSULIN SENSITIVITY; 1ST-DEGREE RELATIVES;
DYSLIPIDEMIC PATIENTS; METABOLIC SYNDROME; OLDER-ADULTS; DOUBLE-BLIND;
FATTY-ACIDS; INFLAMMATION; ALPHA
AB Objective: Offspring of patients with type 2 diabetes (OPDs) exhibits endothelial dysfunction (ED) associated with a chronic inflammatory state. N-3 polyunsaturated fatty acids (n-3 PUFA) may have antioxidant and anti-inflammatory properties that are beneficial for cardiovascular and metabolic health. Therefore, in the present study, we tested the hypothesis that dietary supplementation with fish oil rich in n-3 PUFA may improve ED in otherwise healthy OPDs.
Methods and design: A double-blind, placebo-controlled trial was conducted with 50 OPDs. Participants were randomized to treatment with either placebo or n-3 PUFA (2 g/day) for 12 weeks. Before and after treatment we evaluated endothelial function (using flow-mediated dilation (FMD) of the brachial artery), circulating inflammatory markers (adiponectin, TNF-alpha, and high sensitivity-CRP), and insulin resistance (QUICKI).
Results: No significant changes were observed in study outcomes in subjects treated with placebo. By contrast, when compared with baseline values, subjects treated with n-3 PUFA had significant improvement in FMD (9.1 +/- 5.8% vs. 11.7 +/- 4.4%, p = 0.02) that was accompanied by decreased plasma triglycerides (117 +/- 73 mg/dl vs. 86 +/- 44 mg/dl, p = 0.001) and TNF-alpha levels (8.9 +/- 2.3 pg/ml vs. 6.8 +/- 2.7 pg/ml, p = 0.001), and a trend towards increased plasma adiponectin levels (7.8 +/- 4.5 mu g/ml vs. 9.5 +/- 5.1 mu g/ml, p = 0.09). When data were analyzed by multiple regression analysis, decreased TNF-alpha after treatment with n-3 PUFA predicted increased FMD.
Conclusion: Dietary supplementation with n-3 PUFA significantly improved endothelial function and reduced pro-inflammatory markers in OPDs. Thus, fish oil consumption may have beneficial cardiovascular and metabolic health effects in otherwise healthy subjects predisposed to diabetes and its vascular complications. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
C1 [Rizza, Stefano; Tesauro, Manfredi; Galli, Angelica; Gigli, Fabrizio; Sbraccia, Paolo; Federici, Massimo; Lauro, Davide] Policlin Tor Vergata Univ Hosp, Ctr Atherosclerosis, Dept Internal Med, Rome, Italy.
[Cardillo, Carmine] Univ Cattolica Sacro Cuore, Div Terapia Med, Rome, Italy.
[Iantorno, Micaela; Quon, Michael J.] NIH, Diabet Unit, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
RP Rizza, S (reprint author), Univ Roma Tor Vergata, Dept Internal Med, Via Montpellier 1, I-00133 Rome, Italy.
EM stefano.rizza@tin.it
RI Federici, Massimo/G-9940-2012;
OI Federici, Massimo/0000-0003-4989-5194; Quon,
Michael/0000-0002-9601-9915; Lauro, Davide/0000-0002-8597-4415; Quon ,
Michael /0000-0002-5289-3707
FU Italian Ministero della Salute RS; Italian Ministero dell'Universita e
della Ricerca Scientifica/Tecnologica
FX Funding: This manuscript was funded in part by research grants: Italian
Ministero della Salute RS 2003 (to Drs. Tremoli and D. Lauro) and
Italian Ministero dell'Universita e della Ricerca
Scientifica/Tecnologica (to Drs. Mannarino and D. Lauro).
NR 36
TC 57
Z9 59
U1 2
U2 12
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0021-9150
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD OCT
PY 2009
VL 206
IS 2
BP 569
EP 574
DI 10.1016/j.atherosclerosis.2009.03.006
PG 6
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 512XY
UT WOS:000271287000044
PM 19394939
ER
PT J
AU Woo, P
Colbert, RA
AF Woo, Patricia
Colbert, Robert A.
TI An overview of genetics of paediatric rheumatic diseases
SO BEST PRACTICE & RESEARCH IN CLINICAL RHEUMATOLOGY
LA English
DT Article
DE juvenile idiopathic arthritis; candidate gene association study;
genome-wide association study; microarray; epigenetics
ID JUVENILE IDIOPATHIC ARTHRITIS; GENOME-WIDE ASSOCIATION; MACROPHAGE
ACTIVATION SYNDROME; UNFOLDED PROTEIN RESPONSE; CELL DNA METHYLATION;
PERIPHERAL-BLOOD; TRANSGENIC RATS; EXPRESSION PROFILES; T-CELLS; ONSET
AB The evidence so far suggests that the paediatric inflammatory diseases encountered in rheumatology practice may be largely genetic in origin, where common single nucleotide polymorphisms (SNPs) in multiple genes contribute to risk, with real but variable environmental components. As far as genetic susceptibility to common paediatric rheumatic diseases is concerned, only juvenile idiopathic arthritis (JIA) has been investigated in any substantial way so fir. This article discusses susceptibility for different types of JIA, the different methods used and their advantages and disadvantages. The genetic code is also modifiable by epigenetic mechanisms and examples of these in immunity and rheumatoid arthritis are given to indicate another area of research in the elucidation of the genetics of paediatric rheumatic diseases. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Woo, Patricia] UCL, London W1T 4JF, England.
[Colbert, Robert A.] NIH, Bethesda, MD 20892 USA.
RP Woo, P (reprint author), UCL, Windeyer Bldg,46 Cleveland St, London W1T 4JF, England.
EM Patricia.woo@ucl.ac.uk; colbertr@mail.nih.gov
FU Arthritis Research UK [17287]; Intramural NIH HHS [ZIA AR041184-01]
NR 49
TC 6
Z9 6
U1 0
U2 0
PU BAILLIERE TINDALL
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1521-6942
J9 BEST PRACT RES CL RH
JI Best Pract. Res. Clin. Rheumatol.
PD OCT
PY 2009
VL 23
IS 5
BP 589
EP 597
DI 10.1016/j.berh.2009.08.001
PG 9
WC Rheumatology
SC Rheumatology
GA 521IZ
UT WOS:000271915600002
PM 19853825
ER
PT J
AU Wedderburn, LR
Rider, LG
AF Wedderburn, Lucy R.
Rider, Lisa G.
TI Juvenile dermatomyositis: new developments in pathogenesis, assessment
and treatment
SO BEST PRACTICE & RESEARCH IN CLINICAL RHEUMATOLOGY
LA English
DT Review
DE juvenile dermatomyositis (JDM); idiopathic inflammatory myopathy (IIM);
immunogenetics; myositis autoantibodies; outcome measures; therapy
ID IDIOPATHIC INFLAMMATORY MYOPATHIES; CUTANEOUS ASSESSMENT-TOOL;
NECROSIS-FACTOR-ALPHA; MHC CLASS-I; MYOSITIS-SPECIFIC AUTOANTIBODIES;
DISEASE-ACTIVITY; INTERNATIONAL CONSENSUS; MUSCLE BIOPSY; CORE SET;
CLINICAL CHARACTERISTICS
AB Juvenile dermatomyositis (JDM) is a rare, potentially life-threatening systemic autoimmune disease primarily affecting muscle and skin. Recent advances in the recognition, standardised assessment and treatment of JDM have been greatly facilitated by large collaborative research networks. Through these networks, a number of immunogenetic risk factors have now been defined, as well as a number of potential pathways identified in the aetiopathogenesis of JDM. Myositis-associated and myositis-specific autoantibodies are helping to sub-phenotype JDM, defined by clinical features, outcomes and immunogenetic risk factors. Partially validated tools to assess disease activity and damage have assisted in standardising outcomes. Aggressive treatment approaches, including multiple initial therapies, as well as new drugs and biological therapies for refractory disease, offer promise of improved outcomes and less corticosteroid-related toxicity. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Wedderburn, Lucy R.] UCL, Inst Child Hlth, Rheumatol Unit, London WC1N 1EH, England.
[Rider, Lisa G.] NIEHS, Environm Autoimmun Grp, Off Clin Res, NIH,US Dept HHS, Bethesda, MD USA.
RP Wedderburn, LR (reprint author), UCL, Inst Child Hlth, Rheumatol Unit, 30 Guilford St, London WC1N 1EH, England.
EM l.wedderburn@ich.ucl.ac.uk
OI Rider, Lisa/0000-0002-6912-2458
FU Wellcome Trust UK, Action Medical Research UK; National Institute of
Environmental Health Sciences, National Institutes of Health. USA
FX Acknowledgements of grant funding: This work was supported in part by
grants from the Wellcome Trust UK, Action Medical Research UK, the UK
Myositis Support Group and the intramural research program of the
National Institute of Environmental Health Sciences, National Institutes
of Health. USA.
NR 102
TC 31
Z9 33
U1 0
U2 1
PU BAILLIERE TINDALL
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1521-6942
J9 BEST PRACT RES CL RH
JI Best Pract. Res. Clin. Rheumatol.
PD OCT
PY 2009
VL 23
IS 5
BP 665
EP 678
DI 10.1016/j.berh.2009.07.007
PG 14
WC Rheumatology
SC Rheumatology
GA 521IZ
UT WOS:000271915600008
PM 19853831
ER
PT J
AU Kaila, VRI
Verkhovsky, MI
Hummer, G
Wikstrom, M
AF Kaila, Ville R. I.
Verkhovsky, Michael I.
Hummer, Gerhard
Wikstrom, Marten
TI Mechanism and energetics by which glutamic acid 242 prevents leaks in
cytochrome c oxidase
SO BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
LA English
DT Article
DE Cell respiration; Gating mechanism; Proton leak; Proton translocation;
Coupled proton and electron transfer
ID PROTON-PUMPING MECHANISM; HEME-COPPER OXIDASES; ELECTRON-TRANSFER;
PARACOCCUS-DENITRIFICANS; RHODOBACTER-SPHAEROIDES; BINUCLEAR CENTER;
BOUND HISTIDINE; RESPIRATORY OXIDASES; MOLECULAR-DYNAMICS; CATALYTIC
CYCLE
AB Cytochrome c oxidase (CcO) is the terminal enzyme of aerobic respiration. The energy released from the reduction of molecular oxygen to water is used to pump protons across the mitochondrial or bacteria[ membrane. The pump function introduces a mechanistic requirement of a valve that prevents protons from flowing backwards during the process. It was recently found that Glu-242, a key amino acid in transferring protons to be pumped across the membrane and to the site of oxygen reduction, fulfils the function of such a valve by preventing simultaneous contact to the pump site and to the proton-conducting D-channel (Kaila V. M. et al. Proc. Natl. Acad. Sci. USA 105,2008). Here we have incorporated the valve model into the framework of the reaction mechanism. The function of the Glu valve is studied by exploring how the redox state of the surrounding metal centers, dielectric effects, and membrane potential, affects the energetics and leaks of this valve. Parallels are drawn between the dynamics of Glu-242 and the long-standing obscure difference between the metastable O(H) and stable O states of the binuclear center. Our model provides a suggestion for why reduction of the former state is coupled to proton translocation while reduction of the latter is not (C) 2009 Elsevier B.V. All rights reserved.
C1 [Kaila, Ville R. I.; Verkhovsky, Michael I.; Wikstrom, Marten] Univ Helsinki, Inst Biotechnol, Helsinki Bioenerget Grp, Struct Biol & Biophys Program, Helsinki 00014, Finland.
[Hummer, Gerhard] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Kaila, VRI (reprint author), Univ Helsinki, Inst Biotechnol, Helsinki Bioenerget Grp, Struct Biol & Biophys Program, PB 65,Viikinkaari 1, Helsinki 00014, Finland.
EM ville.kaila@helsinki.fl; marten.wikstrom@helsinki.fl
RI Hummer, Gerhard/A-2546-2013
OI Hummer, Gerhard/0000-0001-7768-746X
FU Sigrid Juselius Foundation, Biocentrum Helsinki; Academy of Finland;
Graduate School of Biotechnology and Molecular Biology; Finnish Cultural
Foundation; NIDDK, NIH
FX This work was supported by the grants from the Sigrid Juselius
Foundation, Biocentrum Helsinki, and the Academy of Finland. CSC, The
Finnish IT Center for Science is acknowledged for computational
resources. V.R.I.K. is supported by the Graduate School of Biotechnology
and Molecular Biology, and the Finnish Cultural Foundation. G.H. is
supported by the Intramural Research program of the NIDDK, . MW
acknowledges helpful discussions with Margareta Blomberg and Per
Siegbahn.
NR 63
TC 37
Z9 37
U1 2
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0005-2728
J9 BBA-BIOENERGETICS
JI Biochim. Biophys. Acta-Bioenerg.
PD OCT
PY 2009
VL 1787
IS 10
BP 1205
EP 1214
DI 10.1016/j.bbabio.2009.04.008
PG 10
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 476EV
UT WOS:000268422200007
PM 19406098
ER
PT J
AU Jacobson, KA
AF Jacobson, Kenneth A.
TI Functionalized Congener Approach to the Design of Ligands for G
Protein-Coupled Receptors (GPCRs)
SO BIOCONJUGATE CHEMISTRY
LA English
DT Review
ID A(3) ADENOSINE RECEPTOR; PHOTOAFFINITY CROSS-LINKING; HUMAN P2Y(1)
RECEPTOR; A1-ADENOSINE RECEPTORS; BIVALENT LIGANDS; HIGH-AFFINITY;
MOLECULAR PROBES; RAT-BRAIN; PHARMACOLOGICAL EVALUATION; A(1)-ADENOSINE
RECEPTOR
AB Functionalized congeners, in which a chemically functionalized chain is incorporated at an insensitive site on a pharmacophore, have been designed from the agonist and antagonist ligands of various G protein-coupled receptors (GPCRs). These chain extensions enable a conjugation strategy for detecting and characterizing GPCR structure and function and pharmacological modulation. The focus in many studies of functionalized congeners has been on two families of GPCRs: those responding to extracellular purines and pyrimidines-i.e., adenosine receptors (ARs) and P2Y nucleotide receptors. Functionalized congeners of small molecule as ligands for other GPCRs and non-G protein coupled receptors have also been design:W. For example, among biogenic amine neurotransmitter receptors, muscarinic acetylcholine receptor antagonists and adrenergic receptor ligands have been studied with a functionalized congener approach. Adenosine A(1), A(2A), and A(3) receptor functionalized congeners have yielded macromolecular conjugates, irreversibly binding AR ligands for receptor inactivation and cross-linking, radioactive probes that use prosthetic groups, immobilized ligands for affinity chromatography, and dual-acting ligands that function as binary drugs. Poly (amidoamine) dendrimers have served as nanocarriers for covalently conjugated AR functionalized congeners. Rational methods of ligand design derived from molecular modeling and templates have been included in these studies. Thus, the design of novel ligands, both small molecules and macromolecular conjugates, for studying the chemical and biological properties of GPCRs have been developed with this approach, has provided researchers with a strategy that is more versatile than the classical medicinal chemical approaches.
C1 NIDDKD, Bioorgan Chem Lab, Mol Recognit Sect, NIH, Bethesda, MD 20892 USA.
RP Jacobson, KA (reprint author), NIDDKD, Bioorgan Chem Lab, Mol Recognit Sect, NIH, Bethesda, MD 20892 USA.
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
FU NIDDK/NIH Intramural Research
FX This work was supported by the NIDDK/NIH Intramural Research Program. We
also thank Can-Fite Biopharma for funding. We thank Dr. Andrei A. Ivanov
(NIDDK) for providing.. Figure 1C.
NR 134
TC 29
Z9 30
U1 1
U2 7
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD OCT
PY 2009
VL 20
IS 10
BP 1816
EP 1835
DI 10.1021/bc9000596
PG 20
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 507MM
UT WOS:000270858300002
PM 19405524
ER
PT J
AU Kim, Y
Hechler, B
Gao, ZG
Gachet, C
Jacobson, KA
AF Kim, Yoonkyung
Hechler, Beatrice
Gao, Zhan-Guo
Gachet, Christian
Jacobson, Kenneth A.
TI PEGylated Dendritic Unimolecular Micelles as Versatile Carriers for
Ligands of G Protein-Coupled Receptors
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID A(3) ADENOSINE RECEPTOR; DRUG-DELIVERY; RAT-BRAIN; DENDRIMERS;
NANOCARRIERS; DERIVATIVES; AFFINITY
AB Despite its widespread application in nanomedicine, poly(ethylene glycol) (PEG) is seldom used for covalent modification of ligands for G protein-coupled receptors (GPCRs) due to potential steric complications. In order to study the influence of PEG chains on the biological activity of GPCR ligands bound to a common macromolecular carrier, we prepared a series of G3 polyamidoamine (PAMAM) dendrimers derivatized with Alexa Fluor 488, varying numbers of PEG(550)/PEG(750)/PEG(2000), and nucleoside moieties derived from the A(2A) adenosine receptor (AR) agonist CGS21680 (2-[4-(2-carboxylethyl)phenylethylamino]-5'-N-ethylcarboxamidoadenosine). These dendrimer conjugates were purified by size exclusion chromatography and characterized by H-1 NMR and MALDI MS. In radioligand binding assays, some PAMAM-PEG conjugates showed enhanced subtype-selectivity at the human A(2A) AR compared to monomeric ligands of comparable affinity. The functional potency was measured in the A(2A) AR-mediated activation of adenylate cyclase. and inhibition of ADP-induced platelet aggregation. Interestingly, the dendrimer conjugate 10c bearing 11 PEG(750) chains (out of theoretical 32 amino end groups) and 14 nucleoside moieties was 5-fold more potent in A(2A) AR-mediated stimulation of cyclic AMP formation than 10d with 4 PEG(2000) chains and 21 nucleosides although the binding affinities of these 2 compounds were similar. Thus, a relatively small (<= 10 nm) multivalent ligand 10c modified for water solubility maintained high potency and displayed increased A2A AR binding selectivity over the monomeric nucleosides. The current study demonstrates the feasibility of using short PEG chains in the design of carriers that target ligand-receptor interactions.
C1 [Kim, Yoonkyung; Gao, Zhan-Guo; Jacobson, Kenneth A.] NIDDKD, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Hechler, Beatrice; Gachet, Christian] Univ Strasbourg, INSERM, UMR 5949, Etab Francais Sang Alsace, Strasbourg, France.
RP Kim, Y (reprint author), Korea Res Inst Biosci & Biotechnol, BioNanotechnol Res Ctr, Taejon 305806, South Korea.
EM kajacobs@helix.nih.gov
RI Jacobson, Kenneth/A-1530-2009; Hechler, Beatrice/D-4227-2017; Gachet,
Christian/H-9156-2016
OI Jacobson, Kenneth/0000-0001-8104-1493;
FU NIH; NIDDK; Can-Fite Biopharma
FX This research was supported in part by the Intramural Research Program
of the NIH, NIDDK. We thank Dr. Haijun Yao at the Mass Spectrometry
Laboratory of the University of Illinois for collecting MALDI spectra of
our dendrimer samples, and Dr. Herman Yeh at the NIDDK for the helpful
advice on the NMR experiments. Y.K. thanks the Can-Fite Biopharma for
financial support.
NR 35
TC 15
Z9 16
U1 1
U2 18
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD OCT
PY 2009
VL 20
IS 10
BP 1888
EP 1898
DI 10.1021/bc9001689
PG 11
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 507MM
UT WOS:000270858300010
PM 19785401
ER
PT J
AU Liu, M
Chen, XW
Jothi, R
AF Liu, Mei
Chen, Xue-wen
Jothi, Raja
TI Knowledge-guided inference of domain-domain interactions from incomplete
protein-protein interaction networks
SO BIOINFORMATICS
LA English
DT Article
ID INTERACTION DATASETS; SYSTEMS BIOLOGY; INTERACTION MAP; DATABASE;
PREDICTION; SEQUENCE; YEAST; CONSERVATION; COEVOLUTION; RELIABILITY
AB Motivation: Protein-protein interactions (PPIs), though extremely valuable towards a better understanding of protein functions and cellular processes, do not provide any direct information about the regions/domains within the proteins that mediate the interaction. Most often, it is only a fraction of a protein that directly interacts with its biological partners. Thus, understanding interaction at the domain level is a critical step towards (i) thorough understanding of PPI networks; (ii) precise identification of binding sites; (iii) acquisition of insights into the causes of deleterious mutations at interaction sites; and (iv) most importantly, development of drugs to inhibit pathological protein interactions. In addition, knowledge derived from known domain-domain interactions (DDIs) can be used to understand binding interfaces, which in turn can help discover unknown PPIs.
Results: Here, we describe a novel method called K-GIDDI (knowledge-guided inference of DDIs) to narrow down the PPI sites to smaller regions/domains. K-GIDDI constructs an initial DDI network from cross-species PPI networks, and then expands the DDI network by inferring additional DDIs using a divide-and-conquer biclustering algorithm guided by Gene Ontology (GO) information, which identifies partial-complete bipartite sub-networks in the DDI network and makes them complete bipartite sub-networks by adding edges. Our results indicate that K-GIDDI can reliably predict DDIs. Most importantly, K-GIDDI's novel network expansion procedure allows prediction of DDIs that are otherwise not identifiable by methods that rely only on PPI data.
C1 [Liu, Mei; Chen, Xue-wen] Univ Kansas, Bioinformat & Computat Life Sci Lab, ITTC, Dept Elect Engn & Comp Sci, Lawrence, KS 66045 USA.
[Jothi, Raja] NIEHS, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
RP Chen, XW (reprint author), Univ Kansas, Bioinformat & Computat Life Sci Lab, ITTC, Dept Elect Engn & Comp Sci, 1520 W 15th St, Lawrence, KS 66045 USA.
EM xwchen@ku.edu
RI Jothi, Raja/G-3780-2015
FU National Science Foundation [IIS-0644366]; National Institutes of
Health, NIEHS
FX National Science Foundation (Award IIS-0644366 to X-W. C.); Intramural
Research Program of the National Institutes of Health, NIEHS ( to R.
J.).
NR 54
TC 13
Z9 14
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
J9 BIOINFORMATICS
JI Bioinformatics
PD OCT 1
PY 2009
VL 25
IS 19
BP 2492
EP 2499
DI 10.1093/bioinformatics/btp480
PG 8
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA 502HB
UT WOS:000270446400006
PM 19667081
ER
PT J
AU Grillon, C
AF Grillon, Christian
TI D-Cycloserine Facilitation of Fear Extinction and Exposure-Based Therapy
Might Rely on Lower-Level, Automatic Mechanisms
SO BIOLOGICAL PSYCHIATRY
LA English
DT Review
DE Anxiety disorders; D-cycloserine; DCS; extinction; exposure-based
therapy; fear conditioning; phobia
ID OBSESSIVE-COMPULSIVE DISORDER; RANDOMIZED CONTROLLED-TRIAL; SOCIAL
ANXIETY DISORDER; CONDITIONED FEAR; POTENTIATED STARTLE; LEARNED FEAR;
PANIC DISORDER; AMYGDALA; HUMANS; ACQUISITION
AB Exposure-based therapy, a leading technique in the treatment of a range of anxiety disorders, is facilitated by D-cycloserine (DCS), a partial N-methyl-D-aspartate receptor agonist. This review discusses the potential mechanisms involved in this facilitation and its implications for developing theories of fear conditioning in humans. Basic research in rodents suggests that DCS acts by speeding up extinction. However, several laboratory-based investigations found that DCS had no effect on extinction in humans. This report proposes that these observations can be accounted for by a dual-model theory of fear conditioning in humans that engages two complementary defensive systems: a reflexive lower-order system independent of conscious awareness and a higher-order cognitive system associated with conscious awareness of danger and expectation. The DCS studies in animals seem to have explored lower-order conditioning mechanisms, whereas human studies have explored higher-order cognitive processes. These observations suggest that DCS might act preferentially on lower-rather than higher-order learning. This report presents evidence suggesting that, in humans, DCS might similarly affect lower-order learning during exposure-based therapy and, consequently, might be less effective during cognitive therapy (e.g., cognitive restructuring). Finally, it is recommended that extinction studies using DCS in humans be conducted with fear-relevant stimuli (e.g., snakes), short conditional stimulus-unconditioned stimulus intervals and intense unconditioned stimulus to promote lower-order conditioning processes.
C1 NIMH, Mood & Anxiety Disorders Program, NIH, MAP, Bethesda, MD 20892 USA.
RP Grillon, C (reprint author), NIMH, Mood & Anxiety Disorders Program, NIH, MAP, 15K North Dr,Bldg 15K,Room 113,MSC 2670, Bethesda, MD 20892 USA.
EM Christian.grillon@nih.gov
FU National Institute of Mental Health
FX Financial support for his study was provided by the Intramural Research
Program of the National Institute of Mental Health. I would like to
thank Monique Ernst, Schmuel Lissek, Brian Cornwell, and Ruben Alvarez
for comments on earlier versions of this manuscript and Ioline Henter
for her editorial assistance.
NR 81
TC 45
Z9 46
U1 5
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD OCT 1
PY 2009
VL 66
IS 7
BP 636
EP 641
DI 10.1016/j.biopsych.2009.04.017
PG 6
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 496NQ
UT WOS:000269981700003
PM 19520359
ER
PT J
AU Nelson, EE
Herman, KN
Barrett, CE
Noble, PL
Wojteczko, K
Chisholm, K
Delaney, D
Ernst, M
Fox, NA
Suomi, SJ
Winslow, JT
Pine, DS
AF Nelson, Eric E.
Herman, Khalisa N.
Barrett, Catherine E.
Noble, Pamela L.
Wojteczko, Kimberly
Chisholm, Kelli
Delaney, Deborah
Ernst, Monique
Fox, Nathan A.
Suomi, Stephen J.
Winslow, James T.
Pine, Daniel S.
TI Adverse Rearing Experiences Enhance Responding to Both Aversive and
Rewarding Stimuli in Juvenile Rhesus Monkeys
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Anxiety; depression; development; fear; hedonic
ID FEAR-POTENTIATED STARTLE; EARLY DEPRIVATION; PRIMATE AMYGDALA; NONHUMAN
PRIMATE; RESPONSES; RATS; INHIBITION; SUCROSE; STRESS; ABUSE
AB Background: While adverse rearing is thought to alter threat responding, the effects on appetitive behavior remains minimally explored. This study examines the effects that early life emotional adversity has on response to both threatening and appetitive stimuli in juvenile rhesus monkeys.
Methods: Twenty-four, 2-year-old monkeys with differential rearing histories were tested for fear-potentiated startle responding and consumption of an artificially sweetened solution.
Results: Relative to monkeys reared under typical conditions, monkeys removed from their mothers at birth and reared with peers demonstrated both increases in reward responding, as evidenced by greater consumption of a palatable solution in a free choice test, and increased threat responding, as evidenced by enhanced fear-potentiated startle responding.
Conclusions: Findings suggest that early rearing impacts juvenile manifestations of both appetitive and aversive emotional systems. Results are discussed in the context of development, anxiety, depression, and substance abuse.
C1 [Nelson, Eric E.; Ernst, Monique; Fox, Nathan A.; Winslow, James T.; Pine, Daniel S.] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
[Herman, Khalisa N.; Barrett, Catherine E.; Noble, Pamela L.; Wojteczko, Kimberly; Chisholm, Kelli; Delaney, Deborah; Winslow, James T.] NIMH, Primate Core Facil, Bethesda, MD 20892 USA.
[Fox, Nathan A.] Univ Maryland, Dept Human Dev, College Pk, MD 20742 USA.
[Herman, Khalisa N.; Suomi, Stephen J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Comparat Ethol Lab, Bethesda, MD USA.
RP Nelson, EE (reprint author), NIMH, Mood & Anxiety Disorders Program, Bldg 106-C,MSC 2606,5413 W Cedar Lane, Bethesda, MD 20892 USA.
EM nelsone@mail.nih.gov
RI Nelson, Eric/B-8980-2008
OI Nelson, Eric/0000-0002-3376-2453
FU National Institutes of Health (NIH); National Institute of Mental Health
(NIMR)
FX This research was supported entirely by the Intramural Research Program
of the National Institutes of Health (NIH), National Institute of Mental
Health (NIMR).
NR 20
TC 24
Z9 24
U1 2
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD OCT 1
PY 2009
VL 66
IS 7
BP 702
EP 704
DI 10.1016/j.biopsych.2009.04.007
PG 3
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 496NQ
UT WOS:000269981700013
PM 19450795
ER
PT J
AU Zeng, HW
Uthus, EO
Ross, SA
Davis, CD
AF Zeng, Huawei
Uthus, Eric O.
Ross, Sharon A.
Davis, Cindy D.
TI High Dietary Intake of Sodium Selenite Does Not Affect Gene Mutation
Frequency in Rat Colon and Liver
SO BIOLOGICAL TRACE ELEMENT RESEARCH
LA English
DT Article
DE Selenium; Colon; Cancer; Glutathione peroxidase; Gene mutation
ID ABERRANT CRYPT FOCI; THIOREDOXIN REDUCTASE-ACTIVITY; DNA-DAMAGE; CANCER
PREVENTION; PROSTATE-CANCER; OXIDATIVE STRESS; ANTIOXIDANT
SUPPLEMENTATION; CELL-PROLIFERATION; GROWTH ARREST; CARCINOGENESIS
AB Our previous studies have shown that selenium (Se) is protective against dimethylhydrazine (DMH)-induced preneoplastic colon cancer lesions, and protection against DNA damage has been hypothesized to be one mechanism for the anticancer effect of Se. The present study was designed to determine whether dietary selenite affects somatic mutation frequency in vivo. We used the Big Blue transgenic model to evaluate the in vivo mutation frequency of the cII gene in rats fed either a Se-deficient (0 mu g Se/g diet) or Se-supplemented diet (0.2 or 2 mu g Se/g diet; n = 3 rats/diet in experiment 1 and n = 5 rats/group in experiment 2) and injected with DMH (25 mg/kg body weight, i.p.). There were no significant differences in body weight between the Se-deficient and Se-supplemented (0.2 or 2 mu g Se/g diet) rats, but the activities of liver glutathione peroxidase and thioredoxin reductase and concentration of liver Se were significantly lower (p < 0.0001) in Se-deficient rats compared to rats supplemented with Se. We found no effect of dietary Se on liver 8-hydroxy-2'-deoxyguanosine. Gene mutation frequency was significantly lower in liver (p < 0.001) than that of colon regardless of dietary Se. However, there were no differences in gene mutation frequency in DNA from colon mucosa or liver from rats fed the Se-deficient diet compared to those fed the Se-supplemented (0.2 or 2 mu g Se/g diet) diet. Although gene mutations have been implicated in the etiology of cancer, our data suggest that decreasing gene mutation is not likely a key mechanism through which dietary selenite exerts its anticancer action against DMH-induced preneoplastic colon cancer lesions in a Big Blue transgenic rat model.
C1 [Zeng, Huawei; Uthus, Eric O.] ARS, USDA, Grand Forks Human Nutr Res Ctr, Grand Forks, ND 58202 USA.
[Ross, Sharon A.; Davis, Cindy D.] NCI, NIH, Nutr Grp, Rockville, MD 20892 USA.
RP Uthus, EO (reprint author), ARS, USDA, Grand Forks Human Nutr Res Ctr, POB 9034, Grand Forks, ND 58202 USA.
EM eric.uthus@ars.usda.gov
NR 62
TC 2
Z9 2
U1 0
U2 1
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0163-4984
J9 BIOL TRACE ELEM RES
JI Biol. Trace Elem. Res.
PD OCT
PY 2009
VL 131
IS 1
BP 71
EP 80
DI 10.1007/s12011-009-8348-3
PG 10
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 487WG
UT WOS:000269307800008
PM 19263001
ER
PT J
AU Adewale, HB
Jefferson, WN
Newbold, RR
Patisaul, HB
AF Adewale, Heather B.
Jefferson, Wendy N.
Newbold, Retha R.
Patisaul, Heather B.
TI Neonatal Bisphenol-A Exposure Alters Rat Reproductive Development and
Ovarian Morphology Without Impairing Activation of
Gonadotropin-Releasing Hormone Neurons
SO BIOLOGY OF REPRODUCTION
LA English
DT Article
DE AVPV; corpora lutea; development; disruption; endocrine disruptors; ER
alpha; ESR1; estradiol; estradiol receptor; estrogen; estrogen receptor;
GnRH; gonad; hypothalamus; lordosis; neuroendocrinology; ovary; PPT;
puberty
ID ESTROGEN-RECEPTOR-ALPHA; ENDOCRINE-DISRUPTING COMPOUNDS; ORPHAN NUCLEAR
RECEPTORS; IN-UTERO EXPOSURE; SEXUAL-DIFFERENTIATION; FEMALE RATS;
GENE-EXPRESSION; ERR-GAMMA; ESTRADIOL BENZOATE; PERINATAL EXPOSURE
AB Developmental exposure to endocrine-disrupting compounds is hypothesized to adversely affect female reproductive physiology by interfering with the organization of the hypothalamic-pituitary-gonadal axis. Here, we compared the effects of neonatal exposure to two environmentally relevant doses of the plastics component bisphenol-A (BPA; 50 mu g/kg and 50 mg/kg) with the ESR1 (formerly known as ERalpha)-selective agonist 4,4',4 ''-(4-propyl-[H-1] pyrazole-1,3,5-triyl)trisphenol (PPT; 1 mg/kg) on the development of the female rat hypothalamus and ovary. An oil vehicle and estradiol benzoate (EB; 25 mu g) were used as negative and positive controls. Exposure to EB, PPT, or the low dose of BPA advanced pubertal onset. A total of 67% of females exposed to the high BPA dose were acyclic by 15 wk after vaginal opening compared with 14% of those exposed to the low BPA dose, all of the EB- and PPT-treated females, and none of the control animals. Ovaries from the EB-treated females were undersized and showed no evidence of folliculogenesis, whereas ovaries from the PPT-treated females were characterized by large antral-like follicles, which did not appear to support ovulation. Severity of deficits within the BPA-treated groups increased with dose and included large antral-like follicles and lower numbers of corpora lutea. Sexual receptivity, examined after ovariectomy and hormone replacement, was normal in all groups except those neonatally exposed to EB. FOS induction in hypothalamic gonadotropic (GnRH) neurons after hormone priming was impaired in the EB- and PPT-treated groups but neither of the BPA-treated groups. Our data suggest that BPA disrupts ovarian development but not the ability of GnRH neurons to respond to steroid-positive feedback.
C1 [Adewale, Heather B.; Patisaul, Heather B.] N Carolina State Univ, Dept Biol, Raleigh, NC 27695 USA.
[Jefferson, Wendy N.; Newbold, Retha R.] Natl Inst Environm Hlth Sci, Mol Toxicol Lab, Dev Endocrinol Sect, Res Triangle Pk, NC USA.
RP Patisaul, HB (reprint author), N Carolina State Univ, Dept Biol, Raleigh, NC 27695 USA.
EM Heather_Patisaul@ncsu.edu
FU National Institute of Environmental Health Sciences [R01 ES016001]
FX Supported by National Institute of Environmental Health Sciences grant
R01 ES016001 to H. B. P.
NR 98
TC 86
Z9 92
U1 2
U2 11
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1691 MONROE ST,SUITE # 3, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PD OCT
PY 2009
VL 81
IS 4
BP 690
EP 699
DI 10.1095/biolreprod.109.078261
PG 10
WC Reproductive Biology
SC Reproductive Biology
GA 498XE
UT WOS:000270178400010
PM 19535786
ER
PT J
AU Bencherif, SA
Siegwart, DJ
Srinivasan, A
Horkay, F
Hollinger, JO
Washburn, NR
Matyjaszewski, K
AF Bencherif, Sidi A.
Siegwart, Daniel J.
Srinivasan, Abiraman
Horkay, Ferenc
Hollinger, Jeffrey O.
Washburn, Newell R.
Matyjaszewski, Krzysztof
TI Nanostructured hybrid hydrogels prepared by a combination of atom
transfer radical polymerization and free radical polymerization
SO BIOMATERIALS
LA English
DT Article
DE Hydrogels; Nanogels; Hyaluronic acid; Hybrid; Atom transfer radical
polymerization (ATRP); Free radical photopolymerization (FRP)
ID HYALURONIC-ACID HYDROGELS; DRUG-DELIVERY; RATIONAL DESIGN; NANOGELS;
ATRP; CHEMISTRY; POLYMERS; BEHAVIOR; CELLS
AB A new method to prepare nanostructured hybrid hydrogels by incorporating well-defined poly(oligo (ethylene oxide) monomethyl ether methacrylate) (POEO(300)MA) nanogels of sizes 110-120 nm into a larger three-dimensional (3D) matrix was developed for drug delivery scaffolds for tissue engineering applications. Rhodamine B isothiocyanate-labeled dextran (RITC-Dx) or fluorescein isothiocyanate-labeled dextran (FITC-Dx)-loaded POEO(300)MA nanogels with pendant hydroxyl groups were prepared by activators generated electron transfer atom transfer radical polymerization (AGET ATRP) in cyclohexane inverse miniemulsion. Hydroxyl-containing nanogels were functionalized with methacrylated groups to generate photoreactive nanospheres.
(1)H NMR spectroscopy confirmed that polymerizable nanogels were successfully incorporated covalently into 3D hyaluronic acid-glycidyl methacrylate (HAGM) hydrogels after free radical photopolymerization (FRP). The introduction of disulfide moieties into the polymerizable groups resulted in a controlled release of nanogels from cross-linked HAGM hydrogels under a reducing environment. The effect of gel hybridization on the macroscopic proper-ties (swelling and mechanics) was studied. It is shown that swelling and nanogel content are independent of scaffold mechanics. In-vitro assays showed the nanostructured hybrid hydrogels were cytocompatible and the GRGDS (Gly-Arg-Gly-Asp-Ser) contained in the nanogel structure promoted cell-substrate interactions within 4 days of incubation. These nanostructured hydrogels have potential as an artificial extracellular matrix (ECM) impermeable to low molecular weight biomolecules and with controlled pharmaceutical release capability. Moreover, the nanogels can control drug or biomolecule delivery, while hyaluronic acid based-hydrogels can act as a macroscopic scaffold for tissue regeneration and regulator for nanogel release. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Bencherif, Sidi A.; Washburn, Newell R.; Matyjaszewski, Krzysztof] Carnegie Mellon Univ, Dept Chem, Pittsburgh, PA 15213 USA.
[Siegwart, Daniel J.] MIT, Dept Chem Engn, Cambridge, MA 02139 USA.
[Srinivasan, Abiraman; Hollinger, Jeffrey O.] Carnegie Mellon Univ, Bone Tissue Engn Ctr, Pittsburgh, PA 15219 USA.
[Horkay, Ferenc] NICHD, Sect Tissue Biophys & Biomimet, Lab Integrat & Med Biophys, NIH, Bethesda, MD 20892 USA.
RP Matyjaszewski, K (reprint author), 4400 5th Ave, Pittsburgh, PA 15213 USA.
EM km3b@andrew.cmu.edu
RI Matyjaszewski, Krzysztof/A-2508-2008;
OI Matyjaszewski, Krzysztof/0000-0003-1960-3402; BENCHERIF,
SIDI/0000-0002-7704-5608
FU NIDCR DE [R01-15392-4]; NSF DMR [05-43953]; U.S. Army DAMD
[17-02-1-0717]
FX The authors gratefully acknowledge Professor Simon Watkins (Center for
Biologic Imaging, University of Pittsburgh School of Medicine) for
access to the confocal microscope and Glenn Papworth operating the
confocal microscope. Financial support was provided from NIDCR DE
R01-15392-4 UOH), NSF DMR 05-43953, and from U.S. Army DAMD 17-02-1-0717
(NRW).
NR 35
TC 48
Z9 51
U1 4
U2 71
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0142-9612
J9 BIOMATERIALS
JI Biomaterials
PD OCT
PY 2009
VL 30
IS 29
BP 5270
EP 5278
DI 10.1016/j.biomaterials.2009.06.011
PG 9
WC Engineering, Biomedical; Materials Science, Biomaterials
SC Engineering; Materials Science
GA 498CW
UT WOS:000270115200003
PM 19592087
ER
PT J
AU Lin, DC
Shreiber, DI
Dimitriadis, EK
Horkay, F
AF Lin, David C.
Shreiber, David I.
Dimitriadis, Emilios K.
Horkay, Ferenc
TI Spherical indentation of soft matter beyond the Hertzian regime:
numerical and experimental validation of hyperelastic models
SO BIOMECHANICS AND MODELING IN MECHANOBIOLOGY
LA English
DT Article
DE Indentation; Elasticity; Hyperelasticity; Mechanical properties
ID ATOMIC-FORCE MICROSCOPY; STRESS-STRAIN CURVES; MODERATELY LARGE
DEFORMATIONS; BOVINE ARTICULAR-CARTILAGE; MECHANICAL-PROPERTIES;
VISCOELASTIC MATERIALS; PERICELLULAR MATRIX; ELASTOMER NETWORKS;
CONSTITUTIVE MODEL; RUBBER ELASTICITY
AB The lack of practicable nonlinear elastic contact models frequently compels the inappropriate use of Hertzian models in analyzing indentation data and likely contributes to inconsistencies associated with the results of biological atomic force microscopy measurements. We derived and validated with the aid of the finite element method force-indentation relations based on a number of hyperelastic strain energy functions. The models were applied to existing data from indentation, using microspheres as indenters, of synthetic rubber-like gels, native mouse cartilage tissue, and engineered cartilage. For the biological tissues, the Fung and single-term Ogden models achieved the best fits of the data while all tested hyperelastic models produced good fits for the synthetic gels. The Hertz model proved to be acceptable for the synthetic gels at small deformations (strain < 0.05 for the samples tested), but not for the biological tissues. Although this finding supports the generally accepted view that many soft materials can be assumed to be linear elastic at small deformations, the nonlinear models facilitate analysis of intrinsically nonlinear tissues and large-strain indentation behavior.
C1 [Lin, David C.; Horkay, Ferenc] NICHD, Sect Tissue Biophys & Biomimet, NIH, Bethesda, MD 20892 USA.
[Shreiber, David I.] Rutgers State Univ, Dept Biomed Engn, Piscataway, NJ 08854 USA.
[Dimitriadis, Emilios K.] NIBIB, Lab Bioengn & Phys Sci, NIH, Bethesda, MD 20892 USA.
RP Lin, DC (reprint author), NICHD, Sect Tissue Biophys & Biomimet, NIH, 9 Mem Dr, Bethesda, MD 20892 USA.
EM lindavid@mail.nih.gov
OI Shreiber, David/0000-0001-8248-419X
FU NIH, NICHD
FX This work was supported by the Intramural Research Program of the NIH,
NICHD. The authors are grateful to Dr. Edward Mertz of NICHD for
providing the mouse cartilage samples and assisting in their
preparation.
NR 64
TC 64
Z9 64
U1 8
U2 50
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1617-7959
J9 BIOMECH MODEL MECHAN
JI Biomech. Model. Mechanobiol.
PD OCT
PY 2009
VL 8
IS 5
BP 345
EP 358
DI 10.1007/s10237-008-0139-9
PG 14
WC Biophysics; Engineering, Biomedical
SC Biophysics; Engineering
GA 486QM
UT WOS:000269212700001
PM 18979205
ER
PT J
AU Li, ZM
Kulakova, L
Li, L
Galkin, A
Zhao, ZM
Nash, TE
Mariano, PS
Herzberg, O
Dunaway-Mariano, D
AF Li, Zhimin
Kulakova, Liudmila
Li, Ling
Galkin, Andrey
Zhao, Zhiming
Nash, Theodore E.
Mariano, Patrick S.
Herzberg, Osnat
Dunaway-Mariano, Debra
TI Mechanisms of catalysis and inhibition operative in the arginine
deiminase from the human pathogen Giardia lamblia
SO BIOORGANIC CHEMISTRY
LA English
DT Article
DE L-Arginine deiminase; Nucleophilic catalysis; L-Arginine dehydrolase
pathway; Mechanism-based inhibition; Giardia lamblia
AB Giardia lamblia arginine deiminase (GlAD), the topic of this paper, belongs to the hydrolase branch of the guanidine-modifying enzyme superfamily, whose members employ Cys-mediated nucleophilic catalysis to promote deimination of L-arginine and its naturally occurring derivatives. G. lamblia is the causative agent in the human disease giardiasis. The results of RNAi/antisense RNA gene-silencing studies reported herein indicate that GlAD is essential for G. lamblia trophozoite survival and thus, a potential target for the development of therapeutic agents for the treatment of giardiasis. The homodimeric recombinant protein was prepared in Escherichia coli for in-depth biochemical characterization. The 2-domain GlAD monomer consists of a N-terminal domain that shares an active site structure (depicted by an in silico model) and kinetic properties (determined by steady-state and transient state kinetic analysis) with its bacterial AD counterparts, and a C-terminal domain of unknown fold and function. GlAD was found to be active over a wide pH range and to accept L-arginine, L-arginine ethyl ester, N(alpha)-benzoyl-L-arginine, and N(omega)-amino-L-arginine as substrates but not agmatine, L-homoarginine, N(alpha)-benzoyl- L-arginine ethyl ester or a variety of arginine-containing peptides. The intermediacy of a Cys424-alkylthiouronium ion covalent enzyme adduct was demonstrated and the rate constants for formation (k(1) = 80 s(-1)) and hydrolysis (k(2) = 35 s(-1)) of the intermediate were determined. The comparatively lower value of the steady-state rate constant (k(cat) = 2.6 s(-1)), suggests that a step following citrulline formation is rate-limiting. Inhibition of GlAD using Cys directed agents was briefly explored. S-Nitroso-L-homocysteine was shown to be an active site directed, irreversible inhibitor whereas N omega-cyano-L-arginine did not inhibit GlAD but instead proved to be an active site directed, irreversible inhibitor of the Bacillus cereus AD. (C) 2009 Published by Elsevier Inc.
C1 [Li, Zhimin; Li, Ling; Zhao, Zhiming; Mariano, Patrick S.; Dunaway-Mariano, Debra] Univ New Mexico, Dept Chem & Chem Biol, Albuquerque, NM 87131 USA.
[Kulakova, Liudmila; Galkin, Andrey; Herzberg, Osnat] Univ Maryland, Inst Biotechnol, Ctr Adv Res Biotechnol, Rockville, MD 20850 USA.
[Nash, Theodore E.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Dunaway-Mariano, D (reprint author), 1 Univ New Mexico, Dept Chem & Chem Biol, MSC03 2060, Albuquerque, NM 87131 USA.
EM dd39@unm.edu
RI Li, Zhimin/A-9671-2011
OI Li, Zhimin/0000-0001-7036-9282
FU NIH [AI059733]
FX Supported by NIH Grant AI059733 to O.H., P.S.M and D. D.-M.
NR 42
TC 17
Z9 19
U1 1
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0045-2068
J9 BIOORG CHEM
JI Bioorganic Chem.
PD OCT
PY 2009
VL 37
IS 5
BP 149
EP 161
DI 10.1016/j.bioorg.2009.06.001
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA V15EL
UT WOS:000207785200002
PM 19640561
ER
PT J
AU Romagnoli, R
Baraldi, PG
Carrion, MD
Cara, CL
Cruz-Lopez, O
Tolomeo, M
Grimaudo, S
Di Cristina, A
Pipitone, MR
Balzarini, J
Zonta, N
Brancale, A
Hamel, E
AF Romagnoli, Romeo
Baraldi, Pier Giovanni
Carrion, Maria Dora
Cara, Carlota Lopez
Cruz-Lopez, Olga
Tolomeo, Manlio
Grimaudo, Stefania
Di Cristina, Antonietta
Pipitone, Maria Rosaria
Balzarini, Jan
Zonta, Nicola
Brancale, Andrea
Hamel, Ernest
TI Design, synthesis and structure-activity relationship of 2-(3 ',4 ',5
'-trimethoxybenzoyl)-benzo[b]furan derivatives as a novel class of
inhibitors of tubulin polymerization
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE Benzo[b]furan derivatives; Antitubulin agents; Combretastatin-A4;
Colchicine; Antiproliferative agents
ID BIOLOGICAL EVALUATION; ANTIMITOTIC AGENTS; ANTINEOPLASTIC AGENTS;
COLCHICINE; CANCER; COMBRETASTATIN-A-4; PHOSPHATE; DISCOVERY; GROWTH
AB The biological importance of microtubules in mitosis and cell division makes them an interesting target for the development of anticancer agents. Small molecules such as benzo[b]furans are attractive as inhibitors of tubulin polymerization. Thus, a new class of inhibitors of tubulin polymerization based on the 2-(3',4',5'-trimethoxybenzoyl)-benzo[b]furan molecular skeleton, with electron-donating (Me, OMe or OH) or electron-withdrawing (F, Cl and Br) substituents on the benzene ring, was synthesized and evaluated for antiproliferative activity, inhibition of tubulin polymerization and cell cycle effects. Adding a methyl group at the C-3 position resulted in increased activity. The most promising compound in this series was 2-(3',4',5'-trimethoxybenzoyl)-3-methyl-6-ethoxy-benzo[b]furan, which inhibits cancer cell growth at nanomolar concentrations and interacts strongly with tubulin by binding to the colchicine site. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Romagnoli, Romeo; Baraldi, Pier Giovanni; Carrion, Maria Dora; Cara, Carlota Lopez; Cruz-Lopez, Olga] Univ Ferrara, Dipartimento Sci Farmaceut, I-44100 Ferrara, Italy.
[Tolomeo, Manlio; Grimaudo, Stefania; Di Cristina, Antonietta; Pipitone, Maria Rosaria] Univ Palermo, Dipartimento Biomed Med Interna & Specialist, Palermo, Italy.
[Balzarini, Jan] Katholieke Univ Leuven, Rega Inst Med Res, Lab Virol & Chemotherapy, B-3000 Louvain, Belgium.
[Zonta, Nicola; Brancale, Andrea] Cardiff Univ, Welsh Sch Pharm, Cardiff CF10 3XF, S Glam, Wales.
[Hamel, Ernest] NCI, Toxicol & Pharmacol Branch, Dev Therapeut Program, Div Canc Treatment & Diag,NIH, Frederick, MD 21702 USA.
RP Romagnoli, R (reprint author), Univ Ferrara, Dipartimento Sci Farmaceut, Via Fossato Mortara 17-19, I-44100 Ferrara, Italy.
EM rmr@unife.it; baraldi@unife.it
RI antonietta, di cristina/I-9251-2012; Brancale, Andrea/N-9445-2014;
LOPEZ-CARA, LUISA CARLOTA/F-9686-2014; Carrion, M. Dora/G-8638-2015;
Romagnoli, Romeo/G-9887-2015; Baraldi, Pier Giovanni/B-7933-2017;
Cruz-Lopez, Olga /F-3060-2017;
OI Brancale, Andrea/0000-0002-9728-3419; LOPEZ-CARA, LUISA
CARLOTA/0000-0003-1142-6448; Carrion, M. Dora/0000-0002-6794-3949;
PIPITONE, Rosaria Maria/0000-0002-6721-3962; Grimaudo,
Stefania/0000-0003-3225-4112
FU Intramural NIH HHS [Z99 CA999999]
NR 31
TC 45
Z9 48
U1 2
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD OCT 1
PY 2009
VL 17
IS 19
BP 6862
EP 6871
DI 10.1016/j.bmc.2009.08.027
PG 10
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 493GU
UT WOS:000269724600009
PM 19736015
ER
PT J
AU Tanpure, RP
Harkrider, AR
Strecker, TE
Hamel, E
Trawick, ML
Pinney, KG
AF Tanpure, Rajendra P.
Harkrider, Amanda R.
Strecker, Tracy E.
Hamel, Ernest
Trawick, Mary Lynn
Pinney, Kevin G.
TI Application of the McMurry coupling reaction in the synthesis of tri-
and tetra-arylethylene analogues as potential cancer chemotherapeutic
agents
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE Combretastatin analogues; Tamoxifen analogues; Triarylethylene
analogues; Tetraarylethylene analogues; Anti-cancer agents; Inhibition
of tubulin assembly
ID ENDOGENOUS MAMMALIAN METABOLITE; INHIBITS TUBULIN POLYMERIZATION;
LOW-VALENT TITANIUM; ANTINEOPLASTIC AGENTS; ESTROGEN ANTAGONIST;
ANTIMITOTIC AGENT; COLCHICINE SITE; TAMOXIFEN; TUMOR; 2-METHOXYESTRADIOL
AB Structural redesign of selected non-steroidal estrogen receptor binding compounds has previously been successful in the discovery of new inhibitors of tubulin assembly. Accordingly, tetra-substituted alkene analogues (21-30) were designed based in part on combinations of the structural and electronic components of tamoxifen and combretastatin A-4 (CA4). The McMurry coupling reaction was used as the key synthetic step in the preparation of these tri- and tetra-arylethylene analogues. The structural assignment of E, Z isomers was determined on the basis of 2D-NOESY experiments. The ability of these compounds to inhibit tubulin polymerization and cell growth in selected human cancer cell lines was evaluated. Although the compounds were found to be less potent than CA4, these analogues significantly advance the known structure-activity relationship associated with the colchicine binding site on beta-tubulin. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Tanpure, Rajendra P.; Harkrider, Amanda R.; Strecker, Tracy E.; Trawick, Mary Lynn; Pinney, Kevin G.] Baylor Univ, Dept Chem & Biochem, Waco, TX 76798 USA.
[Hamel, Ernest] NCI, Toxicol & Pharmacol Branch, Dev Therapeut Program, Div Canc Treatment & Diag,NIH, Frederick, MD 21702 USA.
RP Pinney, KG (reprint author), Baylor Univ, Dept Chem & Biochem, 1 Bear Pl,97348, Waco, TX 76798 USA.
EM Kevin_Pinney@baylor.edu
OI Pinney, Kevin/0000-0003-1262-8631
FU Welch Foundation [AA-1278]; Department of Chemistry and Biochemistry at
Baylor University; National Science Foundation [CHE-0420802,
CHE-0321214]
FX The authors are grateful to the Welch Foundation (Grant No. AA-1278 to
K. G. P.), and the Department of Chemistry and Biochemistry at Baylor
University for their generous financial support of this project, and to
the National Science Foundation for funding both the Varian 500 MHz NMR
spectrometer (Award CHE-0420802), and the Bruker X8 APEX diffractometer
(Grant CHE-0321214). The authors express their appreciation to Dr. Kevin
Klausmeyer and Mr. Cody Carson, Department of Chemistry and
Biochemistry, Baylor University, for assisting with structural analysis
of selected compounds. The authors would also like to thank Dr. James
Karban and Dr. Alejandro Ramirez (Mass Spectrometry Core Facility,
Baylor University) for mass spectra analyses and Dr. James Karban and
Dr. Michelle Nemec (Director) of the Molecular Biosciences Center at
Baylor University for use of these facilities. The authors are also
grateful to Professor George R. Pettit (Arizona State University) for
providing initial cell line data for some of the described compounds
(data not included in this manuscript).
NR 54
TC 11
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U1 0
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
EI 1464-3391
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD OCT 1
PY 2009
VL 17
IS 19
BP 6993
EP 7001
DI 10.1016/j.bmc.2009.08.011
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 493GU
UT WOS:000269724600023
PM 19733085
ER
PT J
AU Burnett, JC
Wang, C
Nuss, JE
Nguyen, TL
Hermone, AR
Schmidt, JJ
Gussio, R
Wipf, P
Bavari, S
AF Burnett, J. C.
Wang, C.
Nuss, J. E.
Nguyen, T. L.
Hermone, A. R.
Schmidt, J. J.
Gussio, R.
Wipf, P.
Bavari, S.
TI Pharmacophore-guided lead optimization: The rational design of a
non-zinc coordinating, sub-micromolar inhibitor of the botulinum
neurotoxin serotype a metalloprotease
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE Inhibitor design; Inhibitor synthesis; Botulinum neurotoxin;
Metalloprotease; Biothreat agent; Pharmacophore; Drug design
ID SMALL-MOLECULE INHIBITORS; NEUROTRANSMITTER RELEASE; PROTEASE
INHIBITORS; IDENTIFICATION; ENDOPEPTIDASE; TOXIN; VAMP/SYNAPTOBREVIN;
PROTEOLYSIS; TETANUS; SNAP-25
AB Botulinum neurotoxins, responsible for the neuroparalytic syndrome botulism, are the deadliest of known biological toxins. The work described in this study was based on a three-zone pharmacophore model for botulinum neurotoxin serotype A light chain inhibition. Specifically, the pharmacophore defined a separation between the overlaps of several different, non-zinc(II)-coordinating small molecule chemotypes, enabling the design and synthesis of a new structural hybrid possessing a K(i) = 600 nM (+/- 100 nM). (C) 2009 Published by Elsevier Ltd.
C1 [Burnett, J. C.; Nguyen, T. L.; Hermone, A. R.] NCI, SAIC Frederick Inc, Target Struct Based Drug Discovery Grp, Frederick, MD 21702 USA.
[Wang, C.; Wipf, P.] Univ Pittsburgh, Combinatorial Chem Ctr, Pittsburgh, PA 15260 USA.
[Nuss, J. E.; Bavari, S.] USA, Med Res Inst Infect Dis, Dept Immunol Target Identificat & Translat Res, Div Bacteriol, Frederick, MD 21702 USA.
[Schmidt, J. J.] USA, Med Res Inst Infect Dis, Dept Cell Biol & Biochem, Div Biochem, Frederick, MD 21702 USA.
[Gussio, R.] NCI, Informat Technol Branch, Dev Therapeut Program, Frederick, MD 21702 USA.
RP Burnett, JC (reprint author), NCI, SAIC Frederick Inc, Target Struct Based Drug Discovery Grp, POB B, Frederick, MD 21702 USA.
EM burnett.james@mail.nih.gov; pwipf@pitt.edu; sina.bavari@us.army.mil
FU Defense Threat Reduction Agency [3.10024_06_RD_B]; MRMC and NCI,
National Institutes of Health [Y3CM 100505, N01-CO-12400]; Developmental
Therapeutics Program in the Division of Cancer Treatment and Diagnosis
of the National Cancer Institute
FX This research was funded by Defense Threat Reduction Agency project
3.10024_06_RD_B and Agreement Y3CM 100505 ( MRMC and NCI, National
Institutes of Health). Additionally, 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 that views or policies
of the Department of Health and Human Services or the U. S. Army, nor
does mention of trade names, commercial products, or organizations imply
endorsement by the U. S. Army or the U. S. Government. This research was
supported [ in part] by the Developmental Therapeutics Program in the
Division of Cancer Treatment and Diagnosis of the National Cancer
Institute.
NR 34
TC 32
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U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD OCT 1
PY 2009
VL 19
IS 19
BP 5811
EP 5813
DI 10.1016/j.bmcl.2009.01.111
PG 3
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA 498AH
UT WOS:000270106700065
PM 19703771
ER
PT J
AU Fowler, D
AF Fowler, Daniel
TI T cells helping GVHD: take-away lessons
SO BLOOD
LA English
DT Editorial Material
ID VERSUS-HOST-DISEASE; BONE-MARROW-TRANSPLANTATION; LETHALITY; ABSENCE;
GAMMA; IL-4
C1 NIH, Bethesda, MD 20892 USA.
RP Fowler, D (reprint author), NIH, Bethesda, MD 20892 USA.
NR 10
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD OCT 1
PY 2009
VL 114
IS 14
BP 2858
EP 2859
DI 10.1182/blood-2009-07-234179
PG 4
WC Hematology
SC Hematology
GA 501MX
UT WOS:000270387100006
PM 19797532
ER
PT J
AU Burns, WR
Zheng, ZL
Rosenberg, SA
Morgan, RA
AF Burns, William R.
Zheng, Zhili
Rosenberg, Steven A.
Morgan, Richard A.
TI Lack of specific gamma-retroviral vector long terminal repeat promoter
silencing in patients receiving genetically engineered lymphocytes and
activation upon lymphocyte restimulation
SO BLOOD
LA English
DT Article
ID DNA METHYLTRANSFERASE INHIBITION; HIV-INFECTED INDIVIDUALS; TRANSDUCED
T-LYMPHOCYTES; ADOPTIVE CELL TRANSFER; DIRECTED GENE-THERAPY; METASTATIC
MELANOMA; TRANSGENE EXPRESSION; CANCER REGRESSION; STEM-CELLS; IN-VIVO
AB Retroviral transduction of tumor antigen-specific T-cell receptor (TCR) genes into lymphocytes redirects T cells to lyse tumors. Furthermore, adoptive transfer of these lymphocytes has mediated objective responses in patients with metastatic cancer. From 2004 to 2006, more than 40 patients were treated with autologous gene-modified lymphocytes expressing a melanoma antigen-specific TCR at the National Cancer Institute. Eighteen such patients were analyzed for persistence and gene expression in vivo. In addition, the impact of epigenetic silencing and of lymphocyte restimulation was studied. Although gene-modified lymphocytes persisted in vivo, the shutdown of TCR transgene expression was observed. Bisulfite sequencing analysis and ex vivo DNA methyltransferase inhibition demonstrated that the decrease in gene expression did not result from DNA methylation. Surprisingly, down-regulation of vector-driven transgene transcriptional activity was not vector specific but mimicked that of endogenous genes. The decrease in TCR transgene expression, however, was reversed upon lymphocyte stimulation. These data demonstrate a lack of gamma-retroviral promoter-specific gene silencing in adoptively transferred human lymphocytes and support that transgene expression is largely affected by global cellular mechanisms. The use of immunomodulatory adjuvants, eg, vaccination or cytokine therapy, for in vivo T-cell activation may help overcome this metabolic quiescence and thus augment cellular immunotherapy-based cancer therapy. (Blood. 2009; 114: 2888-2899)
C1 [Burns, William R.; Zheng, Zhili; Rosenberg, Steven A.; Morgan, Richard A.] NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Morgan, RA (reprint author), NCI, Surg Branch, Ctr Canc Res, NIH, Bldg 10-CRC,Rm 3W-3-5940,10 Ctr Dr, Bethesda, MD 20892 USA.
EM rmorgan@mail.nih.gov
FU Intramural Research Program of the Center for Cancer Research, National
Cancer Institute, National Institutes of Health
FX This work was supported by the Intramural Research Program of the Center
for Cancer Research, National Cancer Institute, National Institutes of
Health.
NR 50
TC 40
Z9 41
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD OCT 1
PY 2009
VL 114
IS 14
BP 2888
EP 2899
DI 10.1182/blood-2009-01-199216
PG 12
WC Hematology
SC Hematology
GA 501MX
UT WOS:000270387100012
PM 19589923
ER
PT J
AU Zhang, K
Kagan, D
DuBois, W
Robinson, R
Bliskovsky, V
Vass, WC
Zhang, SL
Mock, BA
AF Zhang, Ke
Kagan, Daniel
DuBois, Wendy
Robinson, Richard
Bliskovsky, Valery
Vass, William C.
Zhang, Shuling
Mock, Beverly A.
TI Mndal, a new interferon-inducible family member, is highly polymorphic,
suppresses cell growth, and may modify plasmacytoma susceptibility
SO BLOOD
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; TUMOR-SUPPRESSOR; SPONTANEOUS
AUTOIMMUNITY; NEGATIVE REGULATOR; MULTIPLE-MYELOMA; CYCLE REGULATION;
HIN-200 FAMILY; C57BL/6 MICE; I INTERFERON; GENE
AB The human HIN-200 gene cluster and its mouse counterpart, the interferon inducible-200 (Ifi200) family, both on Chr 1, are associated with several diseases, including solid tumors and lupus. Our study was initiated to identify the modifier gene(s) encoded by the Pctm locus, in which mouse B-cell plasmacytomas induced by pristane are associated with heterozygosity of Chr 1 genes near the Ifi200 cluster. A screen for differentially expressed genes in granulomatous tissues induced by pristane in resistant and susceptible strains identified a new Ifi200 member whose expression was 1000-fold higher in the strain carrying the resistant allele of Pctm and was the most highly expressed Ifi200 gene. The gene, designated Mndal (for MNDA-like, myeloid nuclear differentiation antigen-like), was absent in the susceptible genome, as were genomic sequences upstream of Ifi203, the gene adjacent to Mndal. Ectopic expression of MNDAL suppressed cell growth, which, together with the disease susceptibility of heterozygotes at the Pctm locus, suggests that Mndal, perhaps with Ifi203, acts as a tumor suppressor and display(s) haploinsufficiency. Mndal is highly polymorphic among inbred mouse strains, because it is absent in 10 of 24 strains. This polymorphism may have implications for other disease modifiers mapping to the same region. (Blood. 2009; 114: 2952-2960)
C1 [Zhang, Ke; Kagan, Daniel; DuBois, Wendy; Robinson, Richard; Bliskovsky, Valery; Zhang, Shuling; Mock, Beverly A.] NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Vass, William C.] NCI, Cellular Oncol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Mock, BA (reprint author), NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bldg 37,Rm 3146,37 Convent Dr,MSC 4258, Bethesda, MD 20892 USA.
EM bev@helix.nih.gov
RI Kagan, Daniel/B-1485-2012; Mock, Beverly/B-3110-2015
OI Mock, Beverly/0000-0003-2479-4549
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research
FX 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 40
TC 14
Z9 16
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD OCT 1
PY 2009
VL 114
IS 14
BP 2952
EP 2960
DI 10.1182/blood-2009-01-198812
PG 9
WC Hematology
SC Hematology
GA 501MX
UT WOS:000270387100019
PM 19654412
ER
PT J
AU Cidlowski, JA
Lu, NZ
Jewell, CM
Beckley, A
Ren, R
Revollo, J
Lannan, E
Duma, D
Gross, K
Oakley, RH
AF Cidlowski, J. A.
Lu, N. Z.
Jewell, C. M.
Beckley, A.
Ren, R.
Revollo, J.
Lannan, E.
Duma, D.
Gross, K.
Oakley, R. H.
TI The glucocorticoid receptor: One gene, many proteins - New mechanisms
for tissue specific anti-inflammatory actions of glucocorticoids in
health and disease
SO BONE
LA English
DT Meeting Abstract
CT 6th International Conference on Glucocorticoid Induced Osteoporosis
CY OCT 08-10, 2009
CL Siena, ITALY
C1 [Cidlowski, J. A.; Lu, N. Z.; Jewell, C. M.; Beckley, A.; Ren, R.; Revollo, J.; Lannan, E.; Duma, D.; Gross, K.; Oakley, R. H.] NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 8756-3282
J9 BONE
JI Bone
PD OCT
PY 2009
VL 45
BP S120
EP S120
DI 10.1016/j.bone.2009.07.020
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 499GB
UT WOS:000270204800003
ER
PT J
AU Pulanic, D
Lozier, JN
Pavletic, SZ
AF Pulanic, D.
Lozier, J. N.
Pavletic, S. Z.
TI Thrombocytopenia and hemostatic disorders in chronic graft versus host
disease
SO BONE MARROW TRANSPLANTATION
LA English
DT Review
DE thrombocytopenia; chronic graft versus host disease; hemostatic
disorders; megakaryocytes
ID STEM-CELL TRANSPLANTATION; BONE-MARROW-TRANSPLANTATION;
COLONY-STIMULATING FACTOR; CONSENSUS DEVELOPMENT PROJECT; CHRONIC
MYELOGENOUS LEUKEMIA; HEMOLYTIC-UREMIC SYNDROME;
CYTOMEGALOVIRUS-INFECTION; IN-VITRO; GANCICLOVIR PROPHYLAXIS;
RETROSPECTIVE ANALYSIS
AB Chronic graft versus host disease (cGVHD) is a major and frequent late complication in allogeneic stem cell transplantation recipients. Although thrombocytopenia in cGVHD patients is among the most consistent and strongest predictors of poor survival across many cGVHD studies, such correlation is still neither clearly explained nor well understood. Low platelet counts in the setting of cGVHD are associated with an increase in complications and treatment-related mortality, but usually not with higher relapse rate or engraftment failure rate. Bleeding might be occasionally increased along with, paradoxically, thrombosis. Hemostatic disorders in the context of cGVHD are significant complications with multifactorial etiology, including tissue injury with releasing microparticles, cytokine release, macrophage/monocyte clearance, CMV infection, production of transforming growth factor-beta, and low levels of thrombopoietin. Future clinical trials with agents that stimulate megakaryocytopoiesis or influence underlying impaired hemostasis mechanisms should investigate whether such interventions may improve outcomes in patients with cGVHD. Bone Marrow Transplantation (2009) 44, 393-403; doi: 10.1038/bmt.2009.196; published online 17 August 2009
C1 [Pulanic, D.; Pavletic, S. Z.] NCI, Graft Versus Host & Autoimmun Unit, Expt Transplantat & Immunol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Lozier, J. N.] NIH, Dept Lab Med, Hematol Lab, Ctr Clin, Bethesda, MD 20892 USA.
[Pulanic, D.] Univ Zagreb, Clin Hosp Ctr Zagreb, Univ Dept Internal Med, Div Hematol, Zagreb, Croatia.
RP Pavletic, SZ (reprint author), NCI, Graft Versus Host & Autoimmun Unit, Expt Transplantat & Immunol Branch, Ctr Canc Res,NIH, 9000 Rockville Pike,10 Ctr Dr,Room CRC 3-3330, Bethesda, MD 20892 USA.
EM pavletis@mail.nih.gov
FU National Cancer Institute, Center for Cancer Research
FX We thank Drs Georgia Vogelsang and Ronald Gress for their valuable
comments and the critical review of the manuscript. This work is
supported in part by the intramural program of the National Cancer
Institute, Center for Cancer Research.; Disclaimer: The opinions
expressed here are those of the authors and do not represent the
official position of the National Institutes of Health or the US
Government.
NR 113
TC 13
Z9 13
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2009
VL 44
IS 7
BP 393
EP 403
DI 10.1038/bmt.2009.196
PG 11
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 508LN
UT WOS:000270933000001
PM 19684626
ER
PT J
AU Tomblyn, M
Chiller, T
Einsele, H
Gress, R
Sepkowitz, K
Storek, J
Wingard, JR
Young, JAH
Boeckh, MJ
AF Tomblyn, M.
Chiller, T.
Einsele, H.
Gress, R.
Sepkowitz, K.
Storek, J.
Wingard, J. R.
Young, J-A H.
Boeckh, M. J.
TI Guidelines for preventing infectious complications among hematopoietic
cell transplant recipients: a global perspective PREFACE
SO BONE MARROW TRANSPLANTATION
LA English
DT Editorial Material
DE infection; prevention; guidelines
ID BONE-MARROW-TRANSPLANTATION; BLOOD STEM-CELL; RESPIRATORY SYNCYTIAL
VIRUS; HERPES-SIMPLEX-VIRUS; VERSUS-HOST-DISEASE;
PNEUMOCYSTIS-CARINII-PNEUMONIA; HUMAN-IMMUNODEFICIENCY-VIRUS;
INTENSIVE-CARE-UNIT; HEPATITIS-B-VIRUS; RESISTANT STAPHYLOCOCCUS-AUREUS
C1 [Tomblyn, M.] Univ Minnesota, Dept Hematol Oncol & Transplantat, Minneapolis, MN USA.
[Chiller, T.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Einsele, H.] Univ Klin Wurzburg, Med Klin & Poliklin 2, Wurzburg, Germany.
[Gress, R.] NIH, Bethesda, MD 20892 USA.
[Sepkowitz, K.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Storek, J.] Univ Calgary, Dept Med Oncol Microbiol & Infect Dis, Calgary, AB, Canada.
[Wingard, J. R.] Univ Florida, Dept Hematol & Oncol, Gainesville, FL USA.
[Young, J-A H.] Univ Minnesota, Div Infect Dis, Minneapolis, MN USA.
[Boeckh, M. J.] Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
RP Tomblyn, M (reprint author), H Lee Moffitt Canc Ctr & Res Inst, 12902 Magnolia Dr FOB 3, Tampa, FL 33612 USA.
EM marcie.tomblyn@moffitt.org
RI Young, Jo-Anne/G-2617-2013
OI Young, Jo-Anne/0000-0003-4182-341X
NR 774
TC 96
Z9 98
U1 2
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2009
VL 44
IS 8
BP 453
EP +
DI 10.1038/bmt.2009.254
PG 34
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 512KJ
UT WOS:000271247300001
PM 19861977
ER
PT J
AU Mackall, C
Fry, T
Gress, R
Peggs, K
Storek, J
Toubert, A
AF Mackall, C.
Fry, T.
Gress, R.
Peggs, K.
Storek, J.
Toubert, A.
TI Background to hematopoietic cell transplantation, including post
transplant immune recovery
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE immune recovery; hematopoietic cell transplantation
C1 [Mackall, C.; Fry, T.; Gress, R.] NCI, NIH, Bethesda, MD 20892 USA.
[Peggs, K.] Univ Coll London Hosp, Dept Haematol, London, England.
[Storek, J.] Univ Calgary, Dept Med Oncol Microbiol & Infect Dis, Calgary, AB, Canada.
[Toubert, A.] Univ Paris Diderot, Lab Immunol & Histocompatibilite, Hop St Louis, Paris, France.
RP Mackall, C (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM mackallc@mail.nih.gov
RI PEGGS, Karl/B-3869-2009
NR 0
TC 40
Z9 40
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2009
VL 44
IS 8
BP 457
EP 462
DI 10.1038/bmt.2009.255
PG 6
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 512KJ
UT WOS:000271247300002
PM 19861978
ER
PT J
AU Confer, D
Gress, R
Tomblyn, M
Ehninger, G
AF Confer, D.
Gress, R.
Tomblyn, M.
Ehninger, G.
TI Hematopoietic cell graft safety
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE regulations; graft safety
C1 [Confer, D.] Natl Marrow Donor Program, Minneapolis, MN 55413 USA.
[Gress, R.] NIH, Bethesda, MD 20892 USA.
[Tomblyn, M.] Univ Minnesota, Dept Hematol Oncol & Transplantat, Minneapolis, MN USA.
[Ehninger, G.] Univ Klinikum Dresden, Med Klin & Poliklin 1, Dresden, Germany.
RP Confer, D (reprint author), Natl Marrow Donor Program, Suite 500,3001 Broadway St NE, Minneapolis, MN 55413 USA.
EM dconfer@nmdp.org; marcie.tomblyn@moffitt.org
NR 0
TC 2
Z9 2
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2009
VL 44
IS 8
BP 463
EP 465
DI 10.1038/bmt.2009.256
PG 3
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 512KJ
UT WOS:000271247300003
PM 19861979
ER
PT J
AU Gea-Banacloche, J
Masur, H
da Cuhna, CA
Chiller, T
Kirchoff, L
Shaw, P
Tomblyn, M
Cordonnier, C
AF Gea-Banacloche, J.
Masur, H.
da Cuhna, C. Arns
Chiller, T.
Kirchoff, L.
Shaw, P.
Tomblyn, M.
Cordonnier, C.
TI Regionally limited or rare infections: prevention after hematopoietic
cell transplantation
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE Tb; PCP; hematopoietic cell transplantation
C1 [Gea-Banacloche, J.; Masur, H.] NCI, NIH, Bethesda, MD 20892 USA.
[da Cuhna, C. Arns] Univ Fed Parana, BR-80060000 Curitiba, Parana, Brazil.
[Chiller, T.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Kirchoff, L.] Univ Iowa, Dept Med, Iowa City, IA 52242 USA.
[Shaw, P.] Childrens Hosp Westmead, Sydney, NSW, Australia.
[Tomblyn, M.] Univ Minnesota, Dept Hematol Oncol & Transplantat, Minneapolis, MN USA.
[Cordonnier, C.] Hop Henri Mondor, Dept Hematol, F-94010 Creteil, France.
RP Gea-Banacloche, J (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM banacloj@mail.nih.gov; marcie.tomblyn@moffitt.org
NR 0
TC 14
Z9 15
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2009
VL 44
IS 8
BP 489
EP 494
DI 10.1038/bmt.2009.260
PG 6
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 512KJ
UT WOS:000271247300007
PM 19861983
ER
PT J
AU Yokoe, D
Casper, C
Dubberke, E
Lee, G
Munoz, P
Palmore, T
Sepkowitz, K
Young, JAH
Donnelly, JP
AF Yokoe, D.
Casper, C.
Dubberke, E.
Lee, G.
Munoz, P.
Palmore, T.
Sepkowitz, K.
Young, J-A H.
Donnelly, J. P.
TI Infection prevention and control in health-care facilities in which
hematopoietic cell transplant recipients are treated
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE infection control; hematopoietic cell transplantation
C1 [Yokoe, D.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Yokoe, D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Casper, C.] Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
[Dubberke, E.] Washington Univ, Sch Med, Div Infect Dis, St Louis, MO 63110 USA.
[Lee, G.] Childrens Hosp, Boston, MA 02115 USA.
[Munoz, P.] Univ Madrid, Hosp Gen Gregorio Maranon, Madrid 3, Spain.
[Palmore, T.] NIH, Bethesda, MD 20892 USA.
[Sepkowitz, K.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Young, J-A H.] Univ Minnesota, Div Infect Dis, Minneapolis, MN USA.
[Donnelly, J. P.] Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
RP Yokoe, D (reprint author), Brigham & Womens Hosp, 181 Longwood Ave, Boston, MA 02115 USA.
EM deborah.yokoe@channing.harvard.edu
RI Young, Jo-Anne/G-2617-2013;
OI Young, Jo-Anne/0000-0003-4182-341X; Munoz Garcia, Patricia
Carmen/0000-0001-5706-5583; Donnelly, J Peter/0000-0002-8521-335X
NR 0
TC 25
Z9 25
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2009
VL 44
IS 8
BP 495
EP 507
DI 10.1038/bmt.2009.261
PG 13
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 512KJ
UT WOS:000271247300008
PM 19861984
ER
PT J
AU Yokoe, D
Casper, C
Dubberke, E
Lee, G
Munoz, P
Palmore, T
Sepkowitz, K
Young, JAH
Donnelly, JP
AF Yokoe, D.
Casper, C.
Dubberke, E.
Lee, G.
Munoz, P.
Palmore, T.
Sepkowitz, K.
Young, J-A H.
Donnelly, J. P.
TI Safe living after hematopoietic cell transplantation
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE foods; activities; hematopoietic cell transplantation
C1 [Yokoe, D.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Yokoe, D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Casper, C.] Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
[Dubberke, E.] Washington Univ, Sch Med, Div Infect Dis, St Louis, MO 63110 USA.
[Lee, G.] Childrens Hosp, Boston, MA 02115 USA.
[Munoz, P.] Univ Madrid, Hosp Gen Gregorio Maranon, Madrid 3, Spain.
[Palmore, T.] NIH, Bethesda, MD 20892 USA.
[Sepkowitz, K.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Young, J-A H.] Univ Minnesota, Div Infect Dis, Minneapolis, MN USA.
[Donnelly, J. P.] Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
RP Yokoe, D (reprint author), Brigham & Womens Hosp, 181 Longwood Ave, Boston, MA 02115 USA.
EM deborah.yokoe@channing.harvard.edu
RI Young, Jo-Anne/G-2617-2013;
OI Young, Jo-Anne/0000-0003-4182-341X; Munoz Garcia, Patricia
Carmen/0000-0001-5706-5583; Donnelly, J Peter/0000-0002-8521-335X
NR 0
TC 11
Z9 11
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2009
VL 44
IS 8
BP 509
EP 519
DI 10.1038/bmt.2009.262
PG 11
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 512KJ
UT WOS:000271247300009
PM 19861985
ER
PT J
AU Voon, V
Krack, P
Lang, AE
Lozano, AM
Dujardin, K
Schupbach, M
Thobois, S
Tamma, F
Herzog, J
Samanta, J
Kubu, C
Rossignol, H
Poon, YY
Saint-Cyr, JA
Ardouin, C
Moro, E
AF Voon, Valerie
Krack, Paul
Lang, Anthony E.
Lozano, Andres M.
Dujardin, Kathy
Schuepbach, Michael
Thobois, Stephane
Tamma, Filippo
Herzog, Jan
Samanta, Johan
Kubu, Cynthia
Rossignol, Helene
Poon, Yu-Yan
Saint-Cyr, Jean A.
Ardouin, Claire
Moro, Elena
TI Reply: Parkinson's disease, DBS and suicide: a role for serotonin ?
SO BRAIN
LA English
DT Letter
ID DEEP BRAIN-STIMULATION; SUBTHALAMIC NUCLEUS STIMULATION; 5-HT DEPLETION;
ANTIDEPRESSANTS; DEPRESSION; BEHAVIOR; MULTICENTER; IMPULSIVITY;
INHIBITION; DOPAMINE
C1 [Voon, Valerie] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD 20892 USA.
[Voon, Valerie; Lang, Anthony E.; Lozano, Andres M.; Poon, Yu-Yan; Saint-Cyr, Jean A.; Moro, Elena] Univ Toronto, Dept Med, Div Neurol, UHN, Toronto, ON, Canada.
[Krack, Paul; Rossignol, Helene; Ardouin, Claire] Univ Grenoble 1, Dept Neurol, Grenoble, France.
[Dujardin, Kathy] Lille Univ Hosp, Neurol Clin, Lille, France.
[Schuepbach, Michael] Hop La Pitie Salpetriere, INSERM, Natl Inst Hlth & Med Res, Paris, France.
[Thobois, Stephane] Univ Lyon 1, Dept Neurol, Hosp Neurol Pierre Wertheimer, F-69365 Lyon, France.
[Tamma, Filippo] Univ Milan, Dept Neurol, I-20122 Milan, Italy.
[Herzog, Jan] Univ Kiel, Dept Neurol, D-2300 Kiel, Germany.
[Samanta, Johan] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands.
[Kubu, Cynthia] Univ Arizona, Dept Psychiat & Psychol, Phoenix, AZ USA.
Cleveland Clin Fdn, Cleveland, OH USA.
RP Voon, V (reprint author), Natl Inst Neurol Disorders & Stroke, NIH, 10 Ctr Dr,Bldg 10,Room 5S213, Bethesda, MD 20892 USA.
EM voonv@ninds.nih.gov
NR 24
TC 1
Z9 1
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
J9 BRAIN
JI Brain
PD OCT
PY 2009
VL 132
AR e127
DI 10.1093/brain/awp151
PG 3
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 505IG
UT WOS:000270685600007
ER
PT J
AU Sanchez-Lemus, E
Benicky, J
Pavel, J
Saavedra, JM
AF Sanchez-Lemus, Enrique
Benicky, Julius
Pavel, Jaroslav
Saavedra, Juan M.
TI In vivo Angiotensin II AT(1) receptor blockade selectively inhibits
LPS-induced innate immune response and ACTH release in rat pituitary
gland
SO BRAIN BEHAVIOR AND IMMUNITY
LA English
DT Article
DE Renin-angiotensin system; Inflammation; IL-6; LIF; NF-kappa B; COX-2;
iNOS; NOS activity; HPA axis; Paraventricular nucleus
ID NITRIC-OXIDE SYNTHASE; ANTERIOR-PITUITARY; GENE-EXPRESSION;
PARAVENTRICULAR NUCLEUS; MESSENGER-RNA; SUBFORNICAL ORGAN; ISOLATION
STRESS; PERIPHERAL LIPOPOLYSACCHARIDE; INTERLEUKIN-6 RELEASE; DEPENDENT
MECHANISM
AB Systemic lipopolysaccharide (LPS) administration induces an innate immune response and stimulates the hypothalamic-pituitary-adrenal axis. We studied Angiotensin II AT(1) receptor participation in the LPS effects with focus on the pituitary gland. LPS (50 mu g/kg, i.p.) enhanced, 3 h after administration, gene expression of pituitary CD14 and that of Angiotensin II AT(1A) receptors in pituitary and hypothalamic paraventricular nucleus (PVN); stimulated ACTH and corticosterone release; decreased pituitary CRF1 receptor mRNA and increased all plasma and pituitary pro-inflammatory factors studied.
The AT(1) receptor blocker (ARB) candesartan (1 mg/kg/day, s.c. daily for 3 days before LPS) blocked pituitary and PVN AT(1) receptors, inhibited LPS-induced ACTH but not corticosterone secretion and decreased LPS-induced release of TNF-alpha, IL-1 beta and IL-6 to the circulation. The ARB reduced LPS-induced pituitary gene expression of IL-6, LIF, iNOS, COX-2 and I kappa B-alpha; and prevented LPS-induced increase of nNOS/eNOS activity. The ARB did not affect LPS-induced TNF-alpha and IL-1 beta gene expression, IL-6 or IL-1 beta protein content or LPS-induced decrease of CRF1 receptors. When administered alone, the ARB increased basal plasma corticosterone levels and basal PGE(2) mRNA in pituitary.
Our results demonstrate that the pituitary gland is a target for systemically administered LPS. AT(1) receptor activity is necessary for the complete pituitary response to LPS and is limited to specific proinflammatory pathways. There is a complementary and complex influence of the PVN and circulating cytokines on the initial pituitary response to LPS. Our findings support the proposal that ARBs may be considered for the treatment of inflammatory conditions. Published by Elsevier Inc.
C1 [Sanchez-Lemus, Enrique; Benicky, Julius; Pavel, Jaroslav; Saavedra, Juan M.] NIMH, Pharmacol Sect, Div Intramural Res Programs, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Sanchez-Lemus, E (reprint author), NIMH, Pharmacol Sect, Div Intramural Res Programs, NIH,Dept Hlth & Human Serv, 10 Ctr Dr,MSC 1514,Bldg 10,Room 2D-57, Bethesda, MD 20892 USA.
EM sancheze@mail.nih.gov
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 82
TC 20
Z9 21
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0889-1591
J9 BRAIN BEHAV IMMUN
JI Brain Behav. Immun.
PD OCT
PY 2009
VL 23
IS 7
BP 945
EP 957
DI 10.1016/j.bbi.2009.04.012
PG 13
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 540PV
UT WOS:000273348600010
PM 19427376
ER
PT J
AU Baatar, D
Olkhanud, PB
Wells, V
Indig, FE
Mallucci, L
Biragyn, A
AF Baatar, Dolgor
Olkhanud, Purevdorj B.
Wells, Valerie
Indig, Fred E.
Mallucci, Livio
Biragyn, Arya
TI Tregs utilize beta-galactoside-binding protein to transiently inhibit
PI3K/p21(ras) activity of human CD8(+) T cells to block their
TCR-mediated ERK activity and proliferation
SO BRAIN BEHAVIOR AND IMMUNITY
LA English
DT Article
DE beta GBP; Galectin-1; Regulatory T cells; TCR signaling; MAPK; ERK;
Anergy
ID IMMUNOLOGICAL SELF-TOLERANCE; NEGATIVE GROWTH-FACTOR; REGULATORY CELLS;
RECOMBINANT GALECTIN-1; AUTOIMMUNE-DISEASES; PERIPHERAL-BLOOD; CUTTING
EDGE; ACTIVATION; RECEPTOR; PHOSPHORYLATION
AB Regulatory T cells (Tregs) and beta-galactoside-binding protein (beta GBP), a regulatory protein often found expressed at sites of immunological privilege, have similar functions. Their presence affects the outcome of harmful autoimmunity and cancers, including experimental autoimmune encephalomyelitis and malignant gliomas. Here we report a novel pathway by which Tregs express and utilize beta GBP to control CD8(+) T cell responses partially activating TCR signaling but blocking PI3K activity. As a result, this leads to a loss of p21(ras), ERK and Akt activities despite activation of TCR proximal signals, such as phosphorylation of CD3 zeta, Zap70, Lat and PKC theta. Although non-processive TCR signaling often leads to cell anergy, Tregs/beta GBP did not affect cell viability. Instead, beta GBP/Tregs transiently prevented activation of CD8(+) T cells with self-antigens, while keeping their responses to xenogeneic antigens unaffected. Published by Elsevier Inc.
C1 [Baatar, Dolgor; Olkhanud, Purevdorj B.; Biragyn, Arya] NIA, Immunotherapeut Unit, Immunol Lab, Baltimore, MD 21224 USA.
[Indig, Fred E.] NIA, Res Resources Branch, NIH, Baltimore, MD 21224 USA.
[Wells, Valerie; Mallucci, Livio] Kings Coll London, Sch Biomed & Hlth Sci, Cell Signaling & Growth Lab, London WC2R 2LS, England.
RP Biragyn, A (reprint author), NIA, Immunotherapeut Unit, Immunol Lab, 251 Bayview Blvd,Suite 100,Room 08C220, Baltimore, MD 21224 USA.
EM biragyna@mail.nih.gov
FU National Institute on Aging, NIH
FX We are grateful to Karen Madara (Apheresis Unit and the Clinical Core
Laboratory, NIA) for providing human blood samples; Gary Collins (NIA)
and Dr. Giovanni Almanzar (NIA), for help with processing human blood
samples; Brittany Frank (NIA) for help with confocal microscopy imaging;
Dr. Dan L. Longo, Dr. Paritosh Gosh, and Ana Lustig (NIA) for critical
reading of the manuscript and helpful comments and suggestions. This
research was supported by the Intramural Research Program of the
National Institute on Aging, NIH.
NR 53
TC 10
Z9 10
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0889-1591
J9 BRAIN BEHAV IMMUN
JI Brain Behav. Immun.
PD OCT
PY 2009
VL 23
IS 7
BP 1028
EP 1037
DI 10.1016/j.bbi.2009.06.003
PG 10
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 540PV
UT WOS:000273348600019
PM 19520156
ER
PT J
AU Tuysuz, B
Goldin, E
Metin, B
Korkmaz, B
Yalcinkaya, C
AF Tuysuz, Beyhan
Goldin, Ehud
Metin, Baris
Korkmaz, Baris
Yalcinkaya, Cengiz
TI Mucolipidosis type IV in a Turkish boy associated with a novel MCOLN1
mutation
SO BRAIN & DEVELOPMENT
LA English
DT Article
DE Mucolipidosis type IV; Turkish boy; MCOLN1
ID GENE; IDENTIFICATION
AB Mucolipidosis type IV is a rare neurodegenerative lysosomal storage disorder that usually presents during the first year of life with severe mental retardation, delayed motor milestones and corneal opacities. Mucolipidosis IV is caused by mutations in MCOLN1, a gene encoding mucolipin-1 which is responsible for maintaining lysosomal function. The majority of known patients with this disorders are Ashkenazi Jews, and most have a splice IVS3-2 A>G, or a 6.4 kb deletion mutation in MCOLN1. Here, we present a Turkish patient who, in addition to the typical neurological and visceral characteristics of mucolipidosis type IV, also demonstrates defects in the posterior limb of internal capsule by MRI, micrognathia and clinodactyly of the fifth fingers. Direct sequencing of his DNA revealed a homozygous c. 1364C>T (S456L) mutation in MCOLN1, which was heterozygous in both consanguineous parents. This mutation, like several previously described, changes the protein sequence in the channel pore domain of the protein. Serine 456 is conserved in mucolipin proteins throughout evolution, therefore the mutation is considered as causative for the severe phenotype of this patient. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Tuysuz, Beyhan] Istanbul Univ, Cerrahpasa Med Fac, Dept Pediat Genet, Istanbul, Turkey.
[Goldin, Ehud] NHGRI, NIH, Med Genet Branch, Bethesda, MA USA.
[Metin, Baris; Korkmaz, Baris; Yalcinkaya, Cengiz] Istanbul Univ, Cerrahpasa Med Fac, Dept Pediat Neurol, Istanbul, Turkey.
RP Tuysuz, B (reprint author), Istanbul Univ, Cerrahpasa Tip Fak, Cocuk Klinigi, Cerrahpasa Istanbul, Turkey.
EM beyhan@istanbul.edu.tr
RI Yalcinkaya, Cengiz/B-6288-2012
OI Yalcinkaya, Cengiz/0000-0002-3443-8524
NR 10
TC 7
Z9 7
U1 3
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0387-7604
J9 BRAIN DEV-JPN
JI Brain Dev.
PD OCT
PY 2009
VL 31
IS 9
BP 702
EP 705
DI 10.1016/j.braindev.2008.10.001
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA 499WO
UT WOS:000270257700008
PM 19006653
ER
PT J
AU Hunsberger, JG
Austin, DR
Chen, G
Manji, HK
AF Hunsberger, Joshua G.
Austin, Daniel R.
Chen, Guang
Manji, Husseini K.
TI Cellular mechanisms underlying affective resiliency: The role of
glucocorticoid receptor- and mitochondrially-mediated plasticity
SO BRAIN RESEARCH
LA English
DT Review
DE Resiliency; Bipolar disorder; Bcl-2; BAG-1; FKBP5; Glucocorticoid
receptor
ID CHRONIC LITHIUM TREATMENT; HIGH FAMILIAL RISK; BIPOLAR DISORDER; MAJOR
DEPRESSION; MOOD DISORDERS; ANTIDEPRESSANT TREATMENT; NEUROTROPHIC
FACTOR; DOWN-REGULATION; PROTEIN BCL-2; IN-VIVO
AB Bipolar disorder (BPD) is a devastating psychiatric illness marked by recurrent episodes of mania and depression. While the underlying pathophysiology of BPD remains elusive, an abnormal hypothalamic-pituitary-adrenal (HPA) axis and dysfunctional glucocorticoid receptor (GR) signaling are considered hallmarks. This review will examine how targeting resiliency signaling cascades at the cellular level may serve as a mechanism to treat BPD. Here, cellular resiliency is defined as the ability of a cell to adapt to an insult or stressor. Such resiliency at the cellular level could confer resiliency at the systems level and, ultimately, help individuals to cope with stressors or recover from depressive or manic states. This review will focus on four molecular targets of mood stabilizers that are known to play integral roles in these cellular resiliency signaling pathways: (1) B-cell CLL/lymphoma 2 (Bcl-2), (2) Bcl-2-associated athanogene (BAG-1), (3) glucocorticoid receptors (GRs), and (4) 51 kDa FK506-binding protein (FKBP5). These targets have emerged from neurobiological and human genetic studies and employ mechanisms that modulate GR function or promote anti-apoptotic processes critical to affective resilience. Future research should focus on elucidating sustainable treatments that target resiliency factors-such as BAG-1 or FKBP5-which could ultimately be used to treat individuals suffering from BPD and prevent relapses in afflicted individuals. Further identification of resiliency and susceptibility factors will also be vital. Ultimately, these developments would allow for the treatment of susceptible individuals prior to the development of BPD. (C) 2009 Published by Elsevier B.V.
C1 [Hunsberger, Joshua G.; Austin, Daniel R.; Chen, Guang; Manji, Husseini K.] NIMH, Mol Pathophysiol Lab, Mood & Anxiety Disorders Program, NIH, Bethesda, MD 20892 USA.
RP Manji, HK (reprint author), NIMH, Mol Pathophysiol Lab, Mood & Anxiety Disorders Program, NIH, 9000 Rockville Pike,Bldg 35,1C912, Bethesda, MD 20892 USA.
EM manji@nih.gov
RI Chen, Guang/A-2570-2017
FU National Institute of Mental Health
FX We would like to acknowledge the support of the Intramural Research
Program of the National Institute of Mental Health. We would also like
to acknowledge the superb editorial services of Ioline Henter.
NR 70
TC 33
Z9 35
U1 1
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD OCT 1
PY 2009
VL 1293
BP 76
EP 84
DI 10.1016/j.brainres.2009.06.103
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 507PB
UT WOS:000270865600008
PM 19595676
ER
PT J
AU Rapoport, SI
Basselin, M
Kim, HW
Rao, JS
AF Rapoport, Stanley I.
Basselin, Mireille
Kim, Hyung-Wook
Rao, Jagadeesh S.
TI Bipolar disorder and mechanisms of action of mood stabilizers
SO BRAIN RESEARCH REVIEWS
LA English
DT Review
DE Bipolar disorder; Brain; Lithium; Valproic; Carbamazepine; Lamotrigine;
Arachidonic acid; Phospholipase A(2); Mood stabilizer; Antidepressant;
Antipsychotic; Mania; Depression; Rat; Kinetic
ID CYTOSOLIC PHOSPHOLIPASE A(2); RAT FRONTAL-CORTEX; ARACHIDONIC-ACID
METABOLISM; DNA-BINDING ACTIVITY; D-ASPARTATE RECEPTOR; POLYUNSATURATED
FATTY-ACIDS; GLYCOGEN-SYNTHASE KINASE-3; TRANSCRIPTION FACTOR-BINDING;
PLACEBO-CONTROLLED TRIALS; GENOME-WIDE ASSOCIATION
AB Bipolar disorder (BD) is a major medical and social burden, whose cause, pathophysiology and treatment are not agreed on. it is characterized by recurrent periods of mania and depression (Bipolar I) or of hypomania and depression (Bipolar II). Its inheritance is polygenic, with evidence of a neurotransmission imbalance and disease progression. Patients often take multiple agents concurrently, with incomplete therapeutic success, particularly with regard to depression. Suicide is common. Of the hypotheses regarding the action of mood stabilizers in BD, the "arachidonic acid (AA) cascade" hypothesis is presented in detail in this review. It is based on evidence that chronic administration of lithium, carbamazepine, sodium valproate, or lamotrigine to rats downregulated AA turnover in brain phospholipids, formation of prostaglandin E-2, and/or expression of AA cascade enzymes, including cytosolic phospholipase A(2), cyclooxygenase-2 and/or acyl-CoA synthetase. The changes were selective for AA, since brain docosahexaenoic or palmitic acid metabolism, when measured, was unaffected, and topiramate, ineffective in BD, did not modify the rat brain AA cascade. Downregulation of the cascade by the mood stabilizers corresponded to inhibition of AA neurotransmission via dopaminergic D-2-like and glutamatergic NMDA receptors. Unlike the mood stabilizers, antidepressants that increase switching of bipolar depression to mania upregulated the rat brain AA cascade. These observations suggest that the brain AA cascade is a common target of mood stabilizers, and that bipolar symptoms, particularly mania, are associated with an upregulated cascade and excess AA signaling via D-2-like and NMDA receptors. This review presents ways to test these suggestions. Published by Elsevier B.V.
C1 [Rapoport, Stanley I.; Basselin, Mireille; Kim, Hyung-Wook; Rao, Jagadeesh S.] NIA, Brain Physiol & Metab Sect, NIH, Bethesda, MD 20892 USA.
RP Rapoport, SI (reprint author), NIA, Brain Physiol & Metab Sect, NIH, Bldg 9,Rm 1S128,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM sir@helix.nih.gov
FU National Institute on Aging, National Institutes of Health
FX This work was entirely supported by the Intramural Research Program of
the National Institute on Aging, National Institutes of Health. We thank
Professor Donald S. Klein and Dr. Jakob Shimshoni for their helpful
comments on this paper.
NR 297
TC 72
Z9 73
U1 1
U2 16
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0173
EI 1872-6321
J9 BRAIN RES REV
JI Brain Res. Rev.
PD OCT
PY 2009
VL 61
IS 2
BP 185
EP 209
DI 10.1016/j.brainresrev.2009.06.003
PG 25
WC Neurosciences
SC Neurosciences & Neurology
GA 511MI
UT WOS:000271169000011
PM 19555719
ER
PT J
AU Beck, S
Houdayer, E
Richardson, SP
Hallett, M
AF Beck, Sandra
Houdayer, Elise
Richardson, Sarah Pirio
Hallett, Mark
TI The role of inhibition from the left dorsal premotor cortex in
right-sided focal hand dystonia
SO BRAIN STIMULATION
LA English
DT Article
DE transcranial magnetic stimulation; human; motor cortex; inhibition;
dystonia
ID TRANSCRANIAL MAGNETIC STIMULATION; HUMAN MOTOR CORTEX; WRITERS CRAMP;
FUNCTIONAL CONNECTIVITY; INTERHEMISPHERIC INHIBITION; SURROUND
INHIBITION; SELECTION; ACTIVATION; DOMINANCE; AREAS
AB Background
The left dorsal premotor cortex (PMd) plays an important role in movement selection and is abnormally activated in imaging studies in patients with right-sided focal hand dystonia (FHD).
Objective
The aims of this study were to assess the role of left PMd in patients with FHD and in the genesis of surround inhibition, which is deficient in FHD.
Methods
Single- and paired-pulse transcranial magnetic stimulation (TMS) was applied during different phases of an index finger movement using the abductor pollicis brevis muscle (APB). a surrounding, nonsynergistic muscle, as target muscle. To look at the effect of PMd on the primary motor cortex (M1), a subthreshold conditioning pulse was applied to PMd 6 milliseconds before stimulation over M1.
Results
There was surround inhibition during movement initiation in controls, but not in FHD patients. In contrast, FHD patients, but not controls, showed premotor-motor inhibition (PMI) at rest. During movement, PMI was absent in both groups.
Conclusions
We conclude that PMI does not appear to play a key role in the formation of surround inhibition in normal subjects, because it was not enhanced during movement initiation. However, in FHD, inhibition from PMd on M1 was abnormally increased at rest and declined during movement initiation. The behavior of PMd can therefore partly explain the loss of surround inhibition in the FHD patients. The functional significance of increased PMI at rest is not clear, but might be an attempt of compensation for losses of inhibition from other brain areas. (C) 2009 Elsevier Inc.
C1 [Beck, Sandra; Houdayer, Elise; Richardson, Sarah Pirio; Hallett, Mark] NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
[Beck, Sandra] Univ Freiburg, Dept Clin Neurol & Neurophysiol, D-7800 Freiburg, Germany.
[Richardson, Sarah Pirio] Univ New Mexico, Dept Neurol, Albuquerque, NM 87131 USA.
RP Hallett, M (reprint author), NINDS, Human Motor Control Sect, NIH, Bldg 10-7D37,10 Ctr Dr, Bethesda, MD 20892 USA.
EM hallettm@ninds.nih.gov
FU Deutsche Forschungsgemeinschaft (DFG) [BE-3792/1]; NINDS, National
Institutes of Health
FX This work was supported by the Deutsche Forschungsgemeinschaft (DFG;
BE-3792/1) and by the Intramural Research Program of the NINDS, National
Institutes of Health.
NR 33
TC 25
Z9 25
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1935-861X
J9 BRAIN STIMUL
JI Brain Stimul.
PD OCT
PY 2009
VL 2
IS 4
BP 208
EP 214
DI 10.1016/j.brs.2009.03.004
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 513AX
UT WOS:000271295300004
PM 20633420
ER
PT J
AU Priori, A
Hallett, M
Rothwell, JC
AF Priori, Aberto
Hallett, Mark
Rothwell, John C.
TI Repetitive transcranial magnetic stimulation or transcranial direct
current stimulation?
SO BRAIN STIMULATION
LA English
DT Article
DE rTMS; tDCS; brain stimulation; neuromodulation
ID MOTOR CORTEX; DC STIMULATION; SAFETY ASPECTS; HUMANS; MECHANISMS; BRAIN;
INHIBITION; RECOVERY; STROKE
AB In recent years two techniques have become available to stimulate the human brain noninvasively through the scalp: repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS). Prolonged application of either method (eg, several hundred TMS pulses [rTMS] or several minutes of tDCS) leads to changes in excitability of the cortex that outlast the period of stimulation. Because of this, besides the implications for experimental neuroscientists, there is increasing interest in the potential for applying either method as a therapy in neurology, psychiatry, rehabilitation, and pain. Given that both techniques lead to the same final result, this article discusses in theory several issues that can help an investigator to decide whether rTMS or tDCS would be more suitable for the scope of the planned work. (C) 2009 Elsevier Inc.
C1 [Priori, Aberto] Univ Milan, Osped Maggiore Policlin Mangiagalli & Regina Elen, Ctr Clin Neuronanotecnol & Neurostimolaz, Dipartimento Sci Neurol,Fdn IRCCS, I-20122 Milan, Italy.
[Hallett, Mark] NINDS, Human Motor Control Sect, Bethesda, MD 20892 USA.
[Rothwell, John C.] ULC, Inst Neurol, Sobell Dept, London, England.
RP Priori, A (reprint author), Univ Milan, Osped Maggiore, Policlin Milano, Dipartimento Sci Neurol, Via Francesco Sforza 35, I-20122 Milan, Italy.
EM alberto.priori@unimi.it
OI Rothwell, John/0000-0003-1367-6467
FU Medical Research Council, UK; NINDS, NIH
FX MH is supported by the Intramural Program of NINDS, NIH.
NR 25
TC 89
Z9 91
U1 4
U2 18
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1935-861X
J9 BRAIN STIMUL
JI Brain Stimul.
PD OCT
PY 2009
VL 2
IS 4
BP 241
EP 245
DI 10.1016/j.brs.2009.02.004
PG 5
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 513AX
UT WOS:000271295300009
PM 20633424
ER
PT J
AU Albain, KS
Paik, S
van't Veer, L
AF Albain, Kathy S.
Paik, Soonmyung
van't Veer, Laura
TI Prediction of adjuvant chemotherapy benefit in endocrine responsive,
early breast cancer using multigene assays
SO BREAST
LA English
DT Article
DE Early breast cancer; Multigene assays; Adjuvant therapy; Chemotherapy
prediction
AB Background: Multigene assays performed on the primary tumors from women with nonmetastatic breast cancer provide useful prognostic information and discriminate excellent versus poor outcome potential in diverse clinical scenarios. Recently, analyses were conducted to determine if these assays predict who benefits from adjuvant chemotherapy added to endocrine therapy and conversely, who might avoid chemotherapy because of lack of substantial benefit. This literature-based review summarizes these data and provides a perspective on the limitations and clinical utility of these assays.
Methods: The literature regarding multigene assays and signatures in early breast cancer was surveyed. Only two assays - the 21-gene recurrence score (RS) assay (Oncotype DX) and the 70-gene signature (MammaPrint) - were analyzed in randomized or non-randomized clinical populations in order to determine the predictive utility of the test in the adjuvant chemotherapy setting in patients whose tumors were estrogen-receptor positive. These data are summarized by type of clinical analysis, with information on clinical utility and comparative studies with standard clinical-pathologic factors.
Results: From 2 independent analyses in phase III clinical trial settings with tamoxifen-alone control arms, the 21-gene RS assay defines a group of patients with low scores who do not appear to benefit from chemotherapy, and a second group with very high scores who derive major benefit from CMF or CAF chemotherapy. One study was conducted in node-negative disease, and the second in a node-positive population. Interaction terms were significant in both studies, and the effect of the assay remained upon adjustment for other standard factors. Utilizing a non-randomized clinical setting, the 70-gene signature could also predict chemotherapy benefit in the high risk group, versus no apparent benefit in the low risk group, an effect that remained after adjustment for standard factors. For both assays, the discordance rate between the assay prediction and clinical-pathologic risk category was approximately 30%. Clinical utility studies showed use of the assay results in a change in treatment decision in 25-30% of cases, most commonly from chemoendocrine therapy to endocrine therapy alone.
Summary: The prediction of adjuvant chemotherapy benefit over and above endocrine therapy using multigene assay-determined risk category differs greatly across risk level and challenges the previous adjuvant therapy paradigm that degree of benefit is the same regardless of risk. These data justify current clinical use of these assays, while ongoing prospective studies will refine their role in practice settings. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Albain, Kathy S.] Loyola Univ Chicago, Stritch Sch Med, Div Hematol Oncol, Maywood, IL 60153 USA.
[Albain, Kathy S.] Cardinal Bernardin Canc Ctr, Dept Med, Breast Clin Res Program, Maywood, IL 60153 USA.
[Albain, Kathy S.] Cardinal Bernardin Canc Ctr, Dept Med, Thorac Oncol Program, Maywood, IL 60153 USA.
[Paik, Soonmyung] Natl Surg Adjuvant Breast & Bowel Project, Div Pathol, Pittsburgh, PA 15212 USA.
[van't Veer, Laura] Netherlands Canc Inst, Dept Pathol, NL-1066 CX Amsterdam, Netherlands.
RP Albain, KS (reprint author), Loyola Univ Chicago, Stritch Sch Med, Div Hematol Oncol, 2160 S 1st Ave, Maywood, IL 60153 USA.
EM kalbain@lumc.edu; Soon.paik@nsabp.org; l.vt.veer@nki.nl
NR 38
TC 56
Z9 61
U1 0
U2 3
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0960-9776
J9 BREAST
JI Breast
PD OCT
PY 2009
VL 18
SU 3
BP S141
EP S145
PG 5
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA V26HG
UT WOS:000208536100026
PM 19914534
ER
PT J
AU Faumont, N
Durand-Panteix, S
Schlee, M
Gromminger, S
Schuhmacher, M
Holzel, M
Laux, G
Mailhammer, R
Rosenwald, A
Staudt, LM
Bornkamm, GW
Feuillard, J
AF Faumont, N.
Durand-Panteix, S.
Schlee, M.
Groemminger, S.
Schuhmacher, M.
Holzel, M.
Laux, G.
Mailhammer, R.
Rosenwald, A.
Staudt, L. M.
Bornkamm, G. W.
Feuillard, J.
TI c-Myc and NF-kappa B are two transcriptional systems activated during
the immortalization of B cells after an infection by EBV
SO BULLETIN DU CANCER
LA French
DT Meeting Abstract
C1 [Faumont, N.; Durand-Panteix, S.; Feuillard, J.] Univ Limoges, CHU Dupuytren, CNRS, UMR 6101, Limoges, France.
[Schlee, M.; Groemminger, S.; Holzel, M.; Laux, G.; Mailhammer, R.; Bornkamm, G. W.] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Clin Mol Biol & Tumor Genet, Munich, Germany.
[Schuhmacher, M.] GPC Biotech AG, Martinsried, Germany.
[Rosenwald, A.] Univ Wurzburg, Inst Pathol, D-97070 Wurzburg, Germany.
[Staudt, L. M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU JOHN LIBBEY EUROTEXT LTD
PI MONTROUGE
PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE
SN 0007-4551
J9 B CANCER
JI Bull. Cancer
PD OCT
PY 2009
VL 96
BP S21
EP S22
PG 2
WC Oncology
SC Oncology
GA 511TG
UT WOS:000271191000014
ER
PT J
AU Stein, EV
Price, DK
Figg, WD
AF Stein, Erica V.
Price, Douglas K.
Figg, William D.
TI shRNA technology Investigating Ras-dependent cancer
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE cancer; antisense; shRNA; KRAS; Ras-dependent cancer; synthetic
lethality; STK33; PLK1
ID THERAPY; STK33
C1 [Stein, Erica V.; Price, Douglas K.; Figg, William D.] NCI, Mol Pharmacol Sect, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Figg, WD (reprint author), NCI, Mol Pharmacol Sect, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
EM figgw@mail.nih.gov
RI Figg Sr, William/M-2411-2016;
OI Stein, Erica/0000-0001-8778-8846
NR 8
TC 3
Z9 3
U1 0
U2 0
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD OCT 1
PY 2009
VL 8
IS 19
BP 1798
EP 1799
PG 2
WC Oncology
SC Oncology
GA 533AV
UT WOS:000272795200011
PM 19713764
ER
PT J
AU Azad, N
Perroy, A
Gardner, E
Imamura, CK
Graves, C
Sarosy, GA
Minasian, L
Kotz, H
Raggio, M
Figg, WD
Kohn, EC
AF Azad, Nilofer
Perroy, Alyssa
Gardner, Erin
Imamura, Chiyo K.
Graves, Cynthia
Sarosy, Gisele A.
Minasian, Lori
Kotz, Herbert
Raggio, Miranda
Figg, William D.
Kohn, Elise C.
TI A Phase I study of paclitaxel and continuous daily CAI in patients with
refractory solid tumors
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE carboxyamidotriazole; clinical trial; ovarian cancer; paclitaxel;
pharmacokinetics
ID MEDIATED SIGNAL-TRANSDUCTION; CALCIUM INFLUX; CARBOXYAMIDO-TRIAZOLE;
GROWTH-INHIBITION; OVARIAN-CANCER; TRIAL; CELLS; PHARMACOKINETICS;
EXPRESSION; EFFICACY
AB Background: Carboxyamido-triazole (CAI) is a calcium influx inhibitor with anti-angiogenic and anti-invasive properties and stabilizes tumor progression in patients. We hypothesized daily oral micronized CAI with q3 week paclitaxel would be well-tolerated and active.
Results: Twenty-nine heavily pretreated patients [median 3 (0-7)] were enrolled on five dose levels. No additive or cumulative toxicity was observed, and grade III nonhematological toxicity was rare. Neutropenia was the most common hematologic toxicity, seen in 79% of patients, with a trend towards increasing grade with higher paclitaxel doses. The recommended phase II dose defined by the maximum tolerated dose (MTD) was CAI 250 mg daily and paclitaxel 200 mg/m(2) q3weeks. Pharmacokinetic analysis revealed paclitaxel increases CAI trough concentration at all dose levels by over 100% (p < 0.0001). a trend towards higher steady-state CAI trough concentrations was found in patients with a partial response (PR; p = 0.09). six patients had confirmed PR (24%; 4-67 cycles, median 10); two patients had minor responses.
Patients and methods: eligible patients with solid tumors received micronized CAI daily (150-250 mg PO) and paclitaxel intravenously q3weeks (175-250 mg/m(2)), sequentially escalating each drug. CAI preceded paclitaxel by one week to permit pharmacokinetic analysis. patients were assessed for toxicity, pharmacokinetics and disease outcome.
Conclusions: The MTD of the combination of CAI and paclitaxel is 250 mg daily and 200 mg/m(2) q3weeks, respectively. The combination is tolerable and has potential antitumor activity.
C1 [Azad, Nilofer; Perroy, Alyssa; Imamura, Chiyo K.; Graves, Cynthia; Sarosy, Gisele A.; Minasian, Lori; Kotz, Herbert; Raggio, Miranda; Figg, William D.; Kohn, Elise C.] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Gardner, Erin] NCI Frederick, Clin Pharmacol Program, SAIC Frederick, Frederick, MD USA.
RP Azad, N (reprint author), NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
EM nazad2@jhmi.edu
RI Figg Sr, William/M-2411-2016
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research; National Cancer Institute, National
Institutes of Health [N01-CO-12400]
FX The authors thank the patients who participated in this study. This
research was supported by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research. This project has
been also 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 28
TC 5
Z9 5
U1 0
U2 1
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD OCT 1
PY 2009
VL 8
IS 19
BP 1800
EP 1805
PG 6
WC Oncology
SC Oncology
GA 533AV
UT WOS:000272795200012
PM 19738417
ER
PT J
AU Li, JH
Chigurupati, S
Agarwal, R
Mughal, MR
Mattson, MP
Becker, KG
Wood, WH
Zhang, YQ
Morin, PJ
AF Li, Jianghong
Chigurupati, Srinivasulu
Agarwal, Rachana
Mughal, Mohamed R.
Mattson, Mark P.
Becker, Kevin G.
Wood, William H., III
Zhang, Yongqing
Morin, Patrice J.
TI Possible angiogenic roles for claudin-4 in ovarian cancer
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE ovarian cancer; expression profiling; claudin; interleukin; interferon;
angiogenesis
ID SURFACE EPITHELIAL-CELLS; DIFFERENTIAL GENE-EXPRESSION; ENDOTHELIAL
GROWTH-FACTOR; TIGHT JUNCTION PROTEINS; HUMAN-MELANOMA; MATRIX
METALLOPROTEINASES; INHIBIT ANGIOGENESIS; REDUCED EXPRESSION; SEROUS
PAPILLARY; TUMOR-GROWTH
AB Claudin proteins are frequently overexpressed in various tumors such as breast, prostate and ovarian cancer. While their functions in cancer have not been completely elucidated, roles in survival, adhesion and invasion have been suggested. In order to clarify the roles of claudins in ovarian cancer, we have performed gene expression profiling of ovarian surface epithelial cells overexpressing claudin-4 and compared the expression patterns to the parental, non-expressing cells. Claudin-4 expression leads to the differential expression of several genes, including many that have previously been implicated in angiogenesis. In particular, angiogenic cytokines, such as IL-8, were found elevated while genes of the angiostatic interferon pathway were found downregulated. In vitro assays show that claudin-4-expressing cells produce factors that can stimulate angiogenesis as measured by tube formation and migration in HUVEC cells. In addition, an in vivo mouse dorsal skinfold assay confirms that cells expressing claudin-4 secrete factors that can mediate angiogenesis in the dorsal skin of mice. Our data suggest a novel function for claudin-4 in cancer and provide an additional rationale for its common overexpression in human tumors.
C1 [Li, Jianghong; Agarwal, Rachana; Morin, Patrice J.] NIA, Cellular & Mol Biol Lab, Baltimore, MD 21224 USA.
[Becker, Kevin G.; Wood, William H., III; Zhang, Yongqing] NIA, Res Resources Branch, Baltimore, MD 21224 USA.
[Chigurupati, Srinivasulu] UCF Coll Med, Burnett Sch Biomed Sci, Orlando, FL USA.
[Agarwal, Rachana] Johns Hopkins Sch Med, Dept Med, Baltimore, MD USA.
RP Morin, PJ (reprint author), NIA, Cellular & Mol Biol Lab, Baltimore, MD 21224 USA.
EM morinp@mail.nih.gov
RI Mattson, Mark/F-6038-2012;
OI Becker, Kevin/0000-0002-6794-6656
FU National institutes of Health, National Institute on Aging
FX We thank members of our laboratory for helpful comments on the
manuscript. This research was supported entirely by the Intramural
Research Program of the National institutes of Health, National
Institute on Aging.
NR 58
TC 15
Z9 16
U1 0
U2 1
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD OCT 1
PY 2009
VL 8
IS 19
BP 1806
EP 1814
PG 9
WC Oncology
SC Oncology
GA 533AV
UT WOS:000272795200013
PM 19657234
ER
PT J
AU Gathany, AH
Hartge, P
Davis, S
Cerhan, JR
Severson, RK
Cozen, W
Rothman, N
Chanock, SJ
Wang, SS
AF Gathany, Allison H.
Hartge, Patricia
Davis, Scott
Cerhan, James R.
Severson, Richard K.
Cozen, Wendy
Rothman, Nathaniel
Chanock, Stephen J.
Wang, Sophia S.
TI Relationship between interferon regulatory factor 4 genetic
polymorphisms, measures of sun sensitivity and risk for non-Hodgkin
lymphoma
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Non-Hodgkin lymphoma; Interferon regulatory factor-4; Single nucleotide
polymorphism; Sunlight; Pigmentation
ID INTERLYMPH-CONSORTIUM; TRANSCRIPTION FACTOR; POOLED ANALYSIS;
FAMILY-HISTORY; EXPRESSION; CLONING; MEMBER; IRF4
AB Objective Sun exposure and sensitivity, including pigmentation, are associated with risk for non-Hodgkin lymphoma (NHL). One variant in the immune regulatory factor 4 (IRF4) gene (rs12203592) is associated with pigmentation, and a different IRF4 variant (rs12211228) is associated with NHL risk. We evaluated the independent roles of these IRF4 polymorphisms and sun sensitivity in mediating NHL risk and explored whether they are confounded or modified by each other.
Methods Genotyping of tag single nucleotide polymorphisms (SNPs) in the IRF4 gene was conducted in 990 NHL cases and 828 controls from a multi-center US study. Measures of sun sensitivity and exposure were ascertained from computer-assisted personal interviews. We used logistic regression to compute odds ratios (OR) and 95% confidence intervals (CI) for NHL in relation to sun exposures, sun exposures in relation to IRF4 genotypes, and NHL in relation to sun exposures. We further assessed the effects of sun exposures in relation to IRF4 genotypes.
Results As previously reported, we found significant associations between IRF4 rs12211228 and NHL and between hair and eye color and NHL. The IRF4 rs12203592 polymorphism (CT/TT genotype) was statistically significantly associated with eye color and particularly with hair color (OR(Light Blonde) = 0.24, 95% CI = 0.11-0.50, overall Chi square p = 0.0002). Analysis of joint effects between eye and hair color with the IRF4 rs12203592 SNP did not reveal statistically significant p-interactions although NHL risk did decline with lighter hair color and presence of the variant IRF4 rs12203592 allele, compared to those without a variant allele and with black/brown hair color.
Conclusions Our data do not statistically support a joint effect between IRF4 and sun sensitivity in mediating risk for NHL. Further evaluation of joint effects in other and larger populations is warranted.
C1 [Gathany, Allison H.; Hartge, Patricia; Rothman, Nathaniel; Chanock, Stephen J.; Wang, Sophia S.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Rockville, MD 20852 USA.
[Cozen, Wendy] Univ So Calif, Los Angeles, CA USA.
[Severson, Richard K.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
[Severson, Richard K.] Wayne State Univ, Dept Family Med, Detroit, MI USA.
[Cerhan, James R.] Mayo Clin, Coll Med, Rochester, MN USA.
[Davis, Scott] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Davis, Scott] Univ Washington, Seattle, WA 98195 USA.
[Gathany, Allison H.] Yale Univ, Sch Publ Hlth, New Haven, CT USA.
RP Wang, SS (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Executive Blvd,EPS 7070, Rockville, MD 20852 USA.
EM wangso@mail.nih.gov
OI Cerhan, James/0000-0002-7482-178X
FU Intramural Research Program (IRP) of the NIH; National Cancer Institute;
Public Health Service (PHS) [N01-PC-65064, N01-PC-67008, N01-PC-67009,
N01-PC-67010, N01-OC-71105]
FX We gratefully acknowledge the staff and scientists at the SEER centers
in Iowa, Los Angeles, Detroit, and Seattle for conducting the study's
fieldwork and collection of biological specimens. We also thank Peter
Hui of Information Management Services, Inc. for his programming
support. This research was supported by the Intramural Research Program
(IRP) of the NIH, National Cancer Institute. Financial support was
provided by Public Health Service (PHS) contracts: N01-PC-65064,
N01-PC-67008, N01-PC-67009, N01-PC-67010, N01-OC-71105.
NR 24
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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 2009
VL 20
IS 8
BP 1291
EP 1302
DI 10.1007/s10552-009-9348-5
PG 12
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505YJ
UT WOS:000270737900006
PM 19396635
ER
PT J
AU Saydah, S
Ballard-Barbash, R
Potischman, N
AF Saydah, Sharon
Ballard-Barbash, Rachel
Potischman, Nancy
TI Association of metabolic syndrome with insulin-like growth factors among
adults in the US
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Insulin-like growth factors; Metabolic syndrome; NHANES
ID FACTOR BINDING PROTEIN-1; ISCHEMIC-HEART-DISEASE; FACTOR-I;
SERUM-LEVELS; IGF-I; GLUCOSE-TOLERANCE; COLORECTAL-CANCER;
PROSTATE-CANCER; BREAST-CANCER; BODY-MASS
AB Objective To examine the association of insulin-like growth factors (IGFs) with metabolic syndrome in a nationally representative sample.
Methods We used data from the Third National Health and Nutrition Examination Survey. Analysis is based on participants who provided a fasting blood sample and were aged 20 years and older (n = 5,903). Participants were classified by a number of risk factors for metabolic syndrome and stratified by diabetes status.
Results Each of the components of metabolic syndrome (increased waist circumference, higher triglycerides, lower HDL cholesterol, higher blood pressure, higher fasting glucose and diabetes) was each associated with lower levels of IGF-I, IGF-BP3 and the Ratio IGF-I/IGF-BP3. Each of the metabolic syndrome components was also associated with higher levels of insulin. Participants with 3-5 components of metabolic syndrome had significantly lower IGF-I and higher IGF-BP3 levels compared to adults with 1-2 components or 0 components, after adjustment for potential confounders. Participants with diabetes had lower levels of IGF-I and IGF-BP3, and higher levels of insulin, regardless of the number of metabolic syndrome components.
Conclusion These findings may prove useful to an understanding of the role of IGF-I in human disease, in
C1 [Saydah, Sharon] Ctr Dis Control & Prevent, Div Diabet Translat, Hyattsville, MD 20782 USA.
[Ballard-Barbash, Rachel; Potischman, Nancy] NCI, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Saydah, S (reprint author), Ctr Dis Control & Prevent, Div Diabet Translat, 3311 Toledo Rd, Hyattsville, MD 20782 USA.
EM ssaydah@cdc.gov
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PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2009
VL 20
IS 8
BP 1309
EP 1316
DI 10.1007/s10552-009-9351-x
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505YJ
UT WOS:000270737900008
PM 19415508
ER
PT J
AU Jackson, MC
Davis, WW
Waldron, W
McNeel, TS
Pfeiffer, R
Breen, N
AF Jackson, Monica C.
Davis, William W.
Waldron, William
McNeel, Timothy S.
Pfeiffer, Ruth
Breen, Nancy
TI Impact of geography on mammography use in California
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Mammogram; Health care; Rural; Spatial distribution
ID CANCER SCREENING PRACTICES; HEALTH INTERVIEW SURVEYS; UNITED-STATES
WOMEN; BREAST-CANCER; CERVICAL-CANCER; TRAVEL; DISTANCE; PARTICIPATION;
NEIGHBORHOOD; NONRESPONSE
AB Objective Despite its benefit, about 30% of women report that they did not have a recent mammogram. We examine impact of distance, rural-urban residence, and other characteristics on mammography screening rates.
Methods We linked data on 33,938 women aged 40-84 years from the 2003 and 2005 California Health Interview Survey with FDA data on the location of mammography facilities in California, and with socioeconomic and geographic variables from the 2000 Census. We use logistic regression models to estimate the impact of selected variables on a woman's probability of having had a recent mammogram and developed a new mapping scheme to help visualize differences in mammography use across California.
Results Though distance to a facility did not impact a woman's probability of having had a recent mammogram, women who resided in urban areas had somewhat higher screening rates than those living in more rural areas, as displayed on our map.
Conclusions Our findings suggest that more research is needed on possible disparities in access to mammography between rural and non-rural areas in California. Therefore, data adequately powered to examine rural populations and to compare them with urban populations are needed.
C1 [Jackson, Monica C.] American Univ, Dept Math & Stat, Washington, DC 20016 USA.
[Davis, William W.; Pfeiffer, Ruth; Breen, Nancy] NCI, Bethesda, MD 20892 USA.
[Waldron, William; McNeel, Timothy S.] Informat Management Serv Inc, Silver Spring, MD USA.
RP Jackson, MC (reprint author), American Univ, Dept Math & Stat, 4400 Massachusetts Ave NW, Washington, DC 20016 USA.
EM monica@american.edu
RI Pfeiffer, Ruth /F-4748-2011
FU Statistical Research and Applications Branch of the National Cancer
Institute [263-MQ-706620]; Intergovernmental Personnel Act (IPA)
FX We thank Dr. Eric "Rocky'' Feuer and Dr. Martin Brown for their review
during the preparation of this manuscript. We are grateful to Brandon
Traudt and Dr. David Grant for linking the CHIS data to socioeconomic
and geographic variables from the 2000 Census data. We thank the
anonymous reviewers for their helpful comments. Financial support was
provided to Dr. Monica Jackson by the Statistical Research and
Applications Branch of the National Cancer Institute as part of contract
number 263-MQ-706620 and the Intergovernmental Personnel Act (IPA).
NR 54
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PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2009
VL 20
IS 8
BP 1339
EP 1353
DI 10.1007/s10552-009-9355-6
PG 15
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505YJ
UT WOS:000270737900011
PM 19449107
ER
PT J
AU Pfeiffer, RM
Mitani, A
Landgren, O
Ekbom, A
Kristinsson, SY
Bjorkholm, M
Biggar, RJ
Brinton, LA
AF Pfeiffer, Ruth M.
Mitani, Aya
Landgren, Ola
Ekbom, Anders
Kristinsson, Sigurdur Y.
Bjorkholm, Magnus
Biggar, Robert J.
Brinton, Louise A.
TI Timing of births and endometrial cancer risk in Swedish women
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Endometrial carcinoma; Parity; Registry; Reproductive factors
ID REPRODUCTIVE FACTORS; BREAST-CANCER; OVARIAN-CANCER; AGE; HYSTERECTOMY;
PREGNANCY; CORPUS; PARITY; SWEDEN; HEALTH
AB While a protective long-term effect of parity on endometrial cancer risk is well established, the impact of timing of births is not fully understood. We examined the relationship between endometrial cancer risk and reproductive characteristics in a population-based cohort of 2,674,465 Swedish women, 20-72 years of age. During follow-up from 1973 to 2004, 7,386 endometrial cancers were observed. Compared to uniparous women, nulliparous women had a significantly elevated endometrial cancer risk (hazard ratio [HR] = 1.32, 95% confidence interval [CI], 1.22-1.42). Endometrial cancer risk decreased with increasing parity; compared to uniparous women, women with >= 4 births had a HR = 0.66 (95% CI, 0.59-0.74); p-trend <0.001. Among multiparous women, we observed no relationship of risk with age at first birth after adjustment for other reproductive factors. While we initially observed a decreased risk with later ages at last birth, this appeared to reflect a stronger relationship with time since last birth, with women with shorter times being at lowest risk. In models for multiparous women that included number of births, age at first and last birth, and time since last birth, age at last birth was not associated with endometrial cancer risk, while shorter time since last birth and increased parity were associated with statistically significantly reduced endometrial cancer risks. The HR was 3.95 (95% CI; 2.17-7.20; p-trend = <0.0001) for women with >= 25 years since a last birth compared to women having given birth within 4 years. Our findings support that clearance of initiated cells during delivery may be important in endometrial carcinogenesis.
C1 [Pfeiffer, Ruth M.; Landgren, Ola; Brinton, Louise A.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Landgren, Ola] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Mitani, Aya] Brigham & Womens Hosp, Dept Anesthesiol Perioperat & Pain Med, Boston, MA 02115 USA.
[Ekbom, Anders; Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Univ Hosp & Inst, Dept Med, Div Hematol, Stockholm, Sweden.
[Biggar, Robert J.] Statens Serum Inst, Dept Epidemiol Res, DK-2300 Copenhagen, Denmark.
RP Pfeiffer, RM (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS RM 8030, Bethesda, MD 20892 USA.
EM pfeiffer@mail.nih.gov
RI Pfeiffer, Ruth /F-4748-2011; Brinton, Louise/G-7486-2015; Kristinsson,
Sigurdur /M-2910-2015
OI Brinton, Louise/0000-0003-3853-8562; Kristinsson, Sigurdur
/0000-0002-4964-7476
FU Intramural NIH HHS [Z01 CP010182-05]
NR 27
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U2 1
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 2009
VL 20
IS 8
BP 1441
EP 1449
DI 10.1007/s10552-009-9370-7
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505YJ
UT WOS:000270737900021
PM 19565342
ER
PT J
AU Meersman, SC
Breen, N
Pickle, LW
Meissner, HI
Simon, P
AF Meersman, Stephen C.
Breen, Nancy
Pickle, Linda W.
Meissner, Helen I.
Simon, Paul
TI Access to mammography screening in a large urban population: a
multi-level analysis
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Breast neoplasms; Mammography; Healthcare disparities; Inequalities;
GIS; Logistic models; Socioeconomic factors; Multi-level spatial models
ID BREAST-CANCER; UNITED-STATES; CERVICAL-CANCER; PUBLIC-HEALTH; OLDER
WOMEN; SOCIOECONOMIC-STATUS; PREVENTIVE CARE; LOS-ANGELES; SELF-REPORT;
PHYSICIAN
AB Objective To understand area-based sociodemographics, physician and medical practice characteristics, and community indicators associated with mammography use in Los Angeles County. An earlier multi-level analysis by Gumpertz et al. found that distance to the nearest mammography facility helped explain the higher proportion of Latinas diagnosed with late stage breast cancer compared with non-Latina Whites in Los Angeles County. Our study examined whether Latinas also have lower rates of mammography use.
Methods We used a multi-level spatial modeling approach to examine individual and community level associations with mammography use among a diverse group of women aged 40-84 years in Los Angeles County. To build our multi-level spatial data set, we integrated five data sources: (1) 2001 California Health Interview Survey (CHIS) data, (2) 2001 Food and Drug Administration (FDA) certified mammography facility data, (3) 2003 LA Transit Authority data, (4) 2000 US Decennial Census data, and (5) 2001 Community Tracking Study (CTS) Physician's Survey data.
Results Our study confirmed for Los Angeles County many associations for mammography use found in other locations. An unexpected finding was that women with limited English proficiency (predominantly Latina) were significantly more likely to have had a recent mammogram than English-proficient women. We also found that, after controlling for other factors, mammography use was higher in neighborhoods with a greater density of mammography facilities.
Conclusion Women with limited English proficiency were especially likely to report recent mammography in Los Angeles. This unexpected finding suggests that the intensive Spanish-language outreach program conducted by the Every Woman Counts (EWC) Program in low-income Latina communities in Los Angeles has been effective. Our study highlights the success of this targeted community-based outreach conducted between 1999 and 2001. These are the same populations that Gumpertz et al. identified as needing intervention. It would be useful to conduct another study of late-stage diagnosis in Los Angeles County to ascertain whether increased rates of mammography have also led to less late-stage diagnosis among Latinas in the neighborhoods where they are concentrated in Los Angeles.
C1 [Meersman, Stephen C.] NCI, Surveillance Res Program, Div Canc Control & Populat Sci, Rockville, MD 20892 USA.
[Breen, Nancy] NCI, Appl Res Program, Div Canc Control & Populat Sci, Rockville, MD 20892 USA.
[Pickle, Linda W.] StatNet Consulting LLC, Laytonville, MD USA.
[Pickle, Linda W.] Penn State Univ, University Pk, PA 16802 USA.
[Meissner, Helen I.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Simon, Paul] Los Angeles Cty Dept Publ Hlth, Los Angeles, CA USA.
RP Meersman, SC (reprint author), NCI, Surveillance Res Program, Div Canc Control & Populat Sci, 6116 Execut Blvd,Suite 504, Rockville, MD 20892 USA.
EM meersmas@mail.nih.gov
NR 58
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U1 2
U2 8
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 2009
VL 20
IS 8
BP 1469
EP 1482
DI 10.1007/s10552-009-9373-4
PG 14
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505YJ
UT WOS:000270737900024
PM 19543987
ER
PT J
AU Leitzmann, MF
Flood, A
Ferrucci, LM
Schoenfeld, P
Cash, B
Schatzkin, A
Cross, AJ
AF Leitzmann, Michael F.
Flood, Andrew
Ferrucci, Leah M.
Schoenfeld, Philip
Cash, Brooks
Schatzkin, Arthur
Cross, Amanda J.
TI Adiposity in relation to colorectal adenomas and hyperplastic polyps in
women
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Adiposity; Obesity; Colorectal adenoma; Hyperplastic polyps; Women
ID BODY-MASS INDEX; PHYSICAL-ACTIVITY; RISK-FACTORS; SIGMOID COLON;
LARGE-BOWEL; LIFE-STYLE; ASYMPTOMATIC INDIVIDUALS; CARCINOMA SEQUENCE;
INSULIN-RESISTANCE; CIGARETTE-SMOKING
AB Objective To examine whether BMI is independently related to colorectal adenomas and hyperplastic polyps. Methods We conducted a cross-sectional study among 1,420 asymptomatic women aged 40-79 years who had undergone complete colonoscopy. Logistic regression was used to estimate the odds ratios (OR) and the corresponding 95% confidence intervals (CI) of adenomas and hyperplastic polyps.
Results We identified 953 women (67.1%) with no polyps, 292 (20.6%) with adenomas, and 175 (12.3%) with hyperplastic polyps. Among those with polyps, 75 women (5.3% of total women) were classified as having both adenomas and hyperplastic polyps. After adjusting for potential risk factors for colorectal cancer, BMI was related to increased risk of adenomas (OR comparing obese to normal weight women = 1.57; 95% CI = 1.07-2.29). Further, BMI was associated with enhanced risk of hyperplastic polyps (OR = 3.76; 95% CI = 2.35-6.01) and the combination of adenomas and hyperplastic polyps (OR = 2.84; 95% CI = 1.41-5.72).
Conclusions Excess body mass is positively related to colorectal adenomas and hyperplastic polyps, particularly when both kinds of polyps are present in combination. Future studies should continue to delineate the possible differences in potential risk factors between colorectal adenomas and hyperplastic polyps. Such work should help further elucidate the possible causes of colorectal cancer.
C1 [Leitzmann, Michael F.] Univ Regensburg, Med Ctr, Dept Epidemiol & Prevent Med, D-93053 Regensburg, Germany.
[Leitzmann, Michael F.; Ferrucci, Leah M.; Schatzkin, Arthur; Cross, Amanda J.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv,NIH, Bethesda, MD 20892 USA.
[Ferrucci, Leah M.] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[Schoenfeld, Philip] Univ Michigan, Sch Med, Div Gastroenterol, Ann Arbor, MI 48105 USA.
[Schoenfeld, Philip] Vet Affairs Ctr Excellence Hlth Serv Res, Ann Arbor, MI 48105 USA.
[Schoenfeld, Philip; Cash, Brooks] Uniformed Serv Univ Hlth Sci, Div Gastroenterol, Bethesda, MD 20889 USA.
[Flood, Andrew] Univ Minnesota, Mason Canc Ctr, Minneapolis, MN 55454 USA.
[Flood, Andrew] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN 55454 USA.
RP Leitzmann, MF (reprint author), Univ Regensburg, Med Ctr, Dept Epidemiol & Prevent Med, Franz Josef Strauss Allee 11, D-93053 Regensburg, Germany.
EM michael.leitzmann@klinik.uni-regensburg.de
FU NIH; National Cancer Institute
FX Financial support: This research was supported by the Intramural
Research Program of the NIH, National Cancer Institute.
NR 56
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U2 1
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PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2009
VL 20
IS 8
BP 1497
EP 1507
DI 10.1007/s10552-009-9346-7
PG 11
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505YJ
UT WOS:000270737900026
PM 19387851
ER
PT J
AU Murphy, G
Shu, XO
Gao, YT
Ji, BT
Cook, MB
Yang, G
Li, HL
Rothman, N
Zheng, W
Chow, WH
AF Murphy, Gwen
Shu, Xiao-Ou
Gao, Yu-Tang
Ji, Bu-Tian
Cook, Michael Blaise
Yang, Gong
Li, Hong Lan
Rothman, Nathaniel
Zheng, Wei
Chow, Wong-Ho
TI Family cancer history affecting risk of colorectal cancer in a
prospective cohort of Chinese women
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Colorectal cancer; Cohort studies; Family history
ID GENOME-WIDE ASSOCIATION; SHANGHAI; HEALTH
AB An elevated risk of colorectal cancer has been associated with sporadic colorectal cancer in first-degree relatives, mostly in Western populations. Limited data exist from traditionally low-risk areas, such as Asia, where the prevalence of risk factors may differ. We examined the association of family history of cancer and subsequent colorectal cancer risk in a cohort of traditionally low-risk Chinese women. We followed 73,358 women in the Shanghai Women's Health Study for cancer incidence until December 2005. After an average of 7 years of follow-up, 391 women were diagnosed with colorectal cancer. We calculated hazard ratios and 95% confidence intervals using Cox proportional hazards models adjusted for age, smoking, family income, education, body mass index, physical activity, and history of diabetes. We observed a significant association between colorectal cancer risk and history of a parent being diagnosed with colorectal cancer (hazard ratio: 3.34; 95% confidence interval: 1.58, 7.06). No association was observed for colorectal cancer diagnosed among siblings. Colorectal cancer risk was not influenced by a positive family history of cancer generally or any of the other cancers investigated (lung, breast, prostate, gastric, esophageal, endometrial, ovarian, urinary tract, central nervous system, and small bowel). Our cohort results suggest that consistent with findings from Western populations, having a family history of colorectal cancer may influence colorectal cancer risk to a similar extent in a low-risk population.
C1 [Murphy, Gwen] NCI, Infect & Immunoepidemiol Branch, DCEG, NIH,Dept Hlth & Human Serv, Rockville, MD 20892 USA.
[Murphy, Gwen] NCI, Canc Prevent Fellowship Program, Off Prevent Oncol, NIH,Dept Hlth & Human Serv, Rockville, MD 20892 USA.
[Murphy, Gwen; Ji, Bu-Tian; Cook, Michael Blaise; Rothman, Nathaniel; Chow, Wong-Ho] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20892 USA.
[Shu, Xiao-Ou; Yang, Gong; Zheng, Wei] Vanderbilt Univ, Dept Med, Vanderbilt Epidemiol Ctr, Nashville, TN USA.
[Shu, Xiao-Ou; Yang, Gong; Zheng, Wei] Vanderbilt Univ, Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Gao, Yu-Tang; Li, Hong Lan] Shanghai Canc Inst, Shanghai, Peoples R China.
RP Murphy, G (reprint author), NCI, Infect & Immunoepidemiol Branch, DCEG, NIH,Dept Hlth & Human Serv, 6120 Executive Blvd,EPS 7076, Rockville, MD 20892 USA.
EM murphygw@mail.nih.gov
RI Cook, Michael/A-5641-2009; Murphy, Gwen/G-7443-2015
OI Cook, Michael/0000-0002-0533-7302;
FU National Institute of Health [R01 CA70867]; Intramural Research Program
[N02 CP1101066]; Health Research Board of Ireland
FX The authors thank the participants and research staff of the Shanghai
Women's Health Study. This study was supported by National Institute of
Health research grant R01 CA70867 and the Intramural Research Program
contract N02 CP1101066. Dr Murphy is supported by the Ireland-Northern
Ireland-National Cancer Institute Cancer Consortium and the Health
Research Board of Ireland.
NR 18
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U1 0
U2 0
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 2009
VL 20
IS 8
BP 1517
EP 1521
DI 10.1007/s10552-009-9353-8
PG 5
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505YJ
UT WOS:000270737900028
PM 19418234
ER
PT J
AU Clauser, SB
AF Clauser, Steven B.
TI National Cancer Institute Partnerships in Quality-of-Care Research
SO CANCER CONTROL
LA English
DT Article
AB Background: Improving the quality of cancer care delivery is a research priority for the National Cancer Institute (NCI). The NCI addresses this priority in part through a variety of research partnerships with public and private organizations designed to measure, monitor, and improve the quality of cancer care delivery.
Methods: NCI-sponsored quality-of-care initiatives are reviewed in three areas: improving process and outcome measures, building strong data infrastructures to monitor the quality of cancer care, and developing practice-based quality-of-care research partnerships for privately sponsored and government-sponsored delivery programs.
Results: Research partnerships strengthen the overall portfolio of NCI-sponsored research into understanding and improving cancer care delivery. These partnerships have made significant contributions in standardizing metrics of clinical effectiveness and health-related quality of life, in developing monitoring systems to track disparities in cancer care and identify opportunities for improvement, and in understanding ways to intervene in cancer care delivery to improve adherence to evidence-based practice. These partnerships also contribute to the productivity of investigator-initiated quality-of-care studies and often provide leverage for rapid adoption of this science by organizations that participate in these projects.
Conclusions: Research partnerships in measurement, data infrastructure, and service delivery are an essential part of the NCI's research program to advance the science of quality of cancer care. Collectively, these projects inform participating organizations on gaps in quality and opportunities for improving cancer care delivery. They also foster the development of tools for changing care processes that can lead to better outcomes for cancer patients and survivors.
C1 NCI, Outcomes Res Branch, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Clauser, SB (reprint author), NCI, Outcomes Res Branch, Appl Res Program, Div Canc Control & Populat Sci, EPN 4086,Mail Stop 7344,6301 Execut Blvd, Bethesda, MD 20892 USA.
EM clausers@mail.nih.gov
NR 61
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Z9 3
U1 3
U2 5
PU H LEE MOFFITT CANCER CENTER & RESEARCH INST
PI TAMPA
PA 12902 MAGNOLIA DR, TAMPA, FL 33612 USA
SN 1073-2748
J9 CANCER CONTROL
JI Cancer Control
PD OCT
PY 2009
VL 16
IS 4
BP 283
EP 292
PG 10
WC Oncology
SC Oncology
GA V24TU
UT WOS:000208433500002
PM 19910914
ER
PT J
AU Gold, LS
De Roos, AJ
Brown, EE
Lan, Q
Milliken, K
Davis, S
Chanock, SJ
Zhang, YW
Severson, R
Zahm, SH
Zheng, TZ
Rothman, N
Baris, D
AF Gold, Laura S.
De Roos, Anneclaire J.
Brown, Elizabeth E.
Lan, Qing
Milliken, Kevin
Davis, Scott
Chanock, Stephen J.
Zhang, Yawei
Severson, Richard
Zahm, Sheila H.
Zheng, Tongzhang
Rothman, Nat
Baris, Dalsu
TI Associations of common variants in genes involved in metabolism and
response to exogenous chemicals with risk of multiple myeloma
SO CANCER EPIDEMIOLOGY
LA English
DT Article
DE Arylhydrocarbon hydroxylase receptor (AHR); Cytochrome P450 enzymes
(CYP1B1, CYP2C9); Epoxide hydrolase (EPHX1); Multiple myeloma; NAD (P)
H: quinone oxidoreductase (NQO1); Paraoxonase 1 (PON1)
ID NON-HODGKINS-LYMPHOMA; CANCER INCIDENCE; PESTICIDE APPLICATORS;
AGRICULTURAL HEALTH; CONNECTICUT WOMEN; ORGANIC-SOLVENTS; BENZENE
EXPOSURE; BREAST-CANCER; UNITED-STATES; WORKERS
AB Background: We examined risk of multiple myeloma (MM) associated with variants in genes involved in metabolism and response to exogenous chemicals [cytochrome P450 enzymes (CYP1B1, CYP20), epoxide hydrolase (EPHX1), paraoxonase 1 (PON1), arylhydrocarbon hydroxylase receptor (AHR), and NAD(P)H:quinone oxidoreductase (NQO1)]. Methods: This study included 279 MM cases and 782 controls in a pooled analysis of two population-based case-control studies. One common variant from each candidate gene was genotyped using DNA from blood or buccal cells. We estimated risk of MM associated with each genotype, controlling for race, gender, study site, and age, using odds ratios (OR) and 95% confidence intervals (CI). Results: Evaluations of the CYP1B1 V432L variant (rs1056836) suggested increased risk of MM among persons with the CG and GG genotypes compared to the CC genotype [OR (95% Cl) = 1.4 (1.0-2.0)]. Similar results were seen in analyses stratified by race and gender. We did not find any associations between MM and the CYP2C9, EPHX1, NQO1, or PON1 genes. Conclusions: CYP1B1 activates chemicals such as polycyclic aromatic hydrocarbons and dioxins to create oxidized, reactive intermediates, and higher gene activity has been shown for the G allele. We conducted the largest analysis to date on MM and these genetic variants and our results provide preliminary evidence that variation in CYP1B1 may influence susceptibility to MM. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Gold, Laura S.; De Roos, Anneclaire J.; Milliken, Kevin; Davis, Scott] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA.
[Gold, Laura S.; De Roos, Anneclaire J.; Milliken, Kevin; Davis, Scott] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Brown, Elizabeth E.] Univ Alabama, Dept Epidemiol, Birmingham, AL USA.
[Brown, Elizabeth E.] Univ Alabama, Dept Med, Birmingham, AL 35294 USA.
[Brown, Elizabeth E.] Univ Alabama, Dept Microbiol, Birmingham, AL 35294 USA.
[Lan, Qing; Chanock, Stephen J.; Zahm, Sheila H.; Rothman, Nat; Baris, Dalsu] Natl Canc Inst, Div Canc Epidemiol & Genet, Bethesda, MD USA.
[Zhang, Yawei; Zheng, Tongzhang] Yale Univ, Div Environm Hlth Sci, New Haven, CT USA.
[Severson, Richard] Wayne State Univ, Dept Family Med & Publ Hlth Sci, Karmanos Canc Inst, Detroit, MI USA.
RP Gold, LS (reprint author), 1100 Fairview Ave N,POB 19024, Seattle, WA USA.
EM lgold@fhcrc.org
RI Zahm, Shelia/B-5025-2015
FU National Institutes of Health, National Institute of Environmental
Health Sciences [T32ES07262]; Intramural Research Program of the
National Institutes of Health
FX This work was partially supported by training grant T32ES07262 from
National Institutes of Health, National Institute of Environmental
Health Sciences and by the Intramural Research Program of the National
Institutes of Health.
NR 58
TC 11
Z9 11
U1 1
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1877-7821
J9 CANCER EPIDEMIOL
JI Cancer Epidemiol.
PD OCT
PY 2009
VL 33
IS 3-4
BP 276
EP 280
DI 10.1016/j.canep.2009.08.005
PG 5
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 519RD
UT WOS:000271784200019
PM 19736056
ER
PT J
AU Weinstein, SJ
Mackrain, K
Stolzenberg-Solomon, RZ
Selhub, J
Virtamo, J
Albanes, D
AF Weinstein, Stephanie J.
Mackrain, Katrina
Stolzenberg-Solomon, Rachael Z.
Selhub, Jacob
Virtamo, Jarmo
Albanes, Demetrius
TI Serum Creatinine and Prostate Cancer Risk in a Prospective Study
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID NUTRITION EXAMINATION SURVEY; 3RD NATIONAL-HEALTH; PROGNOSTIC-FACTORS;
RENAL-FUNCTION; ANTIGEN LEVELS; HOMOCYSTEINE; DETERMINANTS; POPULATION;
PREVALENCE; MORTALITY
AB Background: Several studies have examined serum creatinine as a marker for prostate cancer stage, recurrence, and prognosis. We evaluated whether serum creatinine concentration was associated with risk of developing prostate cancer in a prospective cohort of male smokers.
Methods: A nested case-control study within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study of 50- to 69-year-old Finnish men was conducted. Two controls (n = 464) were matched to each case (n = 232) on study center, intervention group, date of baseline blood draw (+/- 45 days), and age (+/- 5 years). Conditional logistic regression was used to calculate odds ratios and 95% confidence intervals. All P values were two-sided.
Results: Cases had significantly higher prediagnostic serum creatinine concentrations compared with controls (medians of 1.13 versus 1.10 mg/dL, respectively; P = 0.004). Serum creatinine was associated with a significantly greater risk of prostate cancer (multivariate odds ratio, 2.23; 95% confidence interval, 1.33-3.75 for highest versus lowest quartile), with a significant trend (P trend = 0.0008). Exclusion of subjects with a reported history of diabetes, benign prostatic hyperplasia, or hypertension, or whose cancer was diagnosed within the first 5 years of follow-up, did not alter the association. Risk did not differ by disease stage or time from blood draw to diagnosis.
Conclusion: Prospectively measured serum creatinine, within normal ranges, is positively related to prostate cancer risk. Future research should reexamine the association in other populations, including any interrelationship with serum prostate-specific antigen. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2643-9)
C1 [Selhub, Jacob] Tufts Univ, Jean Mayer USDA, Human Nutr Res Ctr Aging, Boston, MA 02111 USA.
[Weinstein, Stephanie J.] NCI, Nutr Epidemiol Branch, DCEG, NIH,DHHS, Bethesda, MD 20892 USA.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
RP Weinstein, SJ (reprint author), NCI, Nutr Epidemiol Branch, DCEG, NIH,DHHS, 6120 Execut Blvd,Suite 320, Bethesda, MD 20892 USA.
EM weinstes@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015
FU NIH; National Cancer Institute [N01-CN-45165, N01-RC-45035,
N01-RC-37004]
FX Intramural Research Program of the NIH and the National Cancer
Institute. Additionally, this research was supported by Public Health
Service contracts N01-CN-45165, N01-RC-45035, and N01-RC-37004 from the
National Cancer Institute, Department of Health and Human Services.
NR 33
TC 11
Z9 11
U1 0
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 2009
VL 18
IS 10
BP 2643
EP 2649
DI 10.1158/1055-9965.EPI-09-0322
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505NZ
UT WOS:000270702100009
PM 19755655
ER
PT J
AU Safaeian, M
Kemp, T
Falk, RT
Rodriguez, AC
Hildesheim, A
Williams, M
Porras, C
Herrero, R
Pinto, LA
AF Safaeian, Mahboobeh
Kemp, Troy
Falk, Roni T.
Rodriguez, Ana Cecilia
Hildesheim, Allan
Williams, Marcus
Porras, Carolina
Herrero, Rolando
Pinto, Ligia A.
TI Determinants and Correlation of Systemic and Cervical Concentrations of
Total IgA and IgG
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS TYPE-16; PARTICLE VACCINE; MENSTRUAL-CYCLE; WOMEN;
EFFICACY; HORMONES; TRIAL; MUCUS; SERA
AB We compared systemic and cervical total IgA and IgG during the menstrual cycle among 154 women who attended clinic visits at follicular/early, periovulatory/mid, and luteal/late phases of menstrual cycle. Paired serum and cervical secretions were tested at each visit for total IgA and IgG using ELISA. Geometric mean titers for systemic IgA and IgG were 1.92 and 8.25 mg/mL, respectively. There were no differences in titers by menstrual cycle phase, neither were they correlated to cervical titers (rho = 0.17 and 0.16, respectively). The lack of correlation between systemic and cervical total IgA and IgG suggests that systemic concentrations are not reflective of cervical levels. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2672-6)
C1 [Safaeian, Mahboobeh] NCI, Div Canc Epidemiol & Genet, Infect & Immunoepidemiol Branch, NIH, Rockville, MD 20852 USA.
[Kemp, Troy; Williams, Marcus; Pinto, Ligia A.] NCI, HPV Immunol Lab, Sci Applicat Int Corp Frederick Inc, Frederick, MD 21701 USA.
[Rodriguez, Ana Cecilia; Porras, Carolina; Herrero, Rolando] Fdn INCIENSA, San Jose, Costa Rica.
RP Safaeian, M (reprint author), NCI, Div Canc Epidemiol & Genet, Infect & Immunoepidemiol Branch, NIH, 6120 Execut Blvd,Suite 550, Rockville, MD 20852 USA.
EM safaeianm@mail.nih.gov
RI Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU National Cancer Institute; NIH [N01-CO-12400]
FX Intramural Research Program of the National Cancer Institute, NIH This
project has been funded in whole or in part with 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
mention of trade names, commercial products, or organizations imply
endorsement by the U.S. Government.
NR 15
TC 2
Z9 2
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 2009
VL 18
IS 10
BP 2672
EP 2676
DI 10.1158/1055-9965.EPI-09-0348
PG 5
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505NZ
UT WOS:000270702100014
PM 19815637
ER
PT J
AU Barry, EL
Sansbury, LB
Grau, MV
Ali, IU
Tsang, S
Munroe, DJ
Ahnen, DJ
Sandler, RS
Saibil, F
Gui, J
Bresalier, RS
McKeown-Eyssen, GE
Burke, C
Baron, JA
AF Barry, Elizabeth L.
Sansbury, Leah B.
Grau, Maria V.
Ali, Iqbal U.
Tsang, Shirley
Munroe, David J.
Ahnen, Dennis J.
Sandler, Robert S.
Saibil, Fred
Gui, Jiang
Bresalier, Robert S.
McKeown-Eyssen, Gail E.
Burke, Carol
Baron, John A.
TI Cyclooxygenase-2 Polymorphisms, Aspirin Treatment, and Risk for
Colorectal Adenoma Recurrence-Data from a Randomized Clinical Trial
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; SERVICES-TASK-FORCE; COLON-CANCER
RISK; AFRICAN-AMERICANS; GENETIC POLYMORPHISMS; PRIMARY PREVENTION;
MOLECULAR TARGET; EXPRESSION; COX-2; INFLAMMATION
AB Cyclooxygenase-2 (COX-2) catalyzes the rate-limiting step in the production of prostaglandins, potent mediators of inflammation. Chronic inflammation plays an important role in the development and progression of colorectal cancer. Aspirin inhibits COX-2 activity and lowers the risk for colorectal adenomas and cancer. We investigated whether common genetic variation in COX-2 influenced risk for colorectal adenoma recurrence among 979 participants in the Aspirin/Folate Polyp Prevention Study who were randomly assigned to placebo or aspirin and followed for 3 years for the occurrence of new adenomas. Of these participants, 44.20% developed at least one new adenoma during follow-up. Adjusted relative risks and 95% confidence intervals (95% CI) were calculated to test the association between genetic variation at six COX-2 single-nucleotide polymorphisms and adenoma occurrence and interaction with aspirin treatment. Two single-nucleotide polymorphisms were significantly associated with increased adenoma recurrence: for rs5277, homozygous carriers of the minor C allele had a 51% increased risk compared with GG homozygotes (relative risk, 1.51; 95% CI, 1.01-2.25), and for rs4648310, heterozygous carriers of the minor G allele had a 37% increased risk compared with AA homozygotes (relative risk, 1.37; 95% CI, 1.05-1.79). (There were no minor allele homozygotes.) In stratified analyses, there was suggestive evidence that rs4648319 modified the effect of aspirin. These results support the hypothesis that COX-2 plays a role in the etiology of colon cancer and may be a target for aspirin chemoprevention and warrant further investigation in other colorectal adenoma and cancer populations. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2726-33)
C1 [Barry, Elizabeth L.] Dartmouth Med Sch, Dept Community & Family Med, Evergreen Ctr, Lebanon, NH 03756 USA.
[Baron, John A.] Dartmouth Med Sch, Dept Med, Lebanon, NH 03756 USA.
[Sansbury, Leah B.] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Ali, Iqbal U.] NCI, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Tsang, Shirley; Munroe, David J.] Sci Applicat Int Corp Inc, Lab Mol Technol, Frederick, MD USA.
[Ahnen, Dennis J.] Univ Colorado, Dept Med, Denver, CO USA.
[Sandler, Robert S.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Saibil, Fred] Univ Toronto, Sunnybrook Hlth Sci Ctr, Div Gastroenterol, Toronto, ON, Canada.
[McKeown-Eyssen, Gail E.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[Sandler, Robert S.] Univ Texas MD Anderson Canc Ctr, Dept Gastroenterol Hepatol & Nutr, Houston, TX 77030 USA.
[Burke, Carol] Cleveland Clin Fdn, Dept Gastroenterol, Cleveland, OH 44195 USA.
RP Barry, EL (reprint author), Dartmouth Med Sch, Dept Community & Family Med, Evergreen Ctr, Suite 300,46 Centerra Pkwy, Lebanon, NH 03756 USA.
EM Elizabeth.L.Barry@Dartmouth.edu
OI Ali, Imran/0000-0001-6511-8374
FU National Cancer Institute; NIH [CA-059005, HHSN261200800001E]
FX This project has been funded in whole or in part with federal foods from
the National Cancer Institute, NIH, under grant CA-059005 and contract
HHSN261200800001E.
NR 56
TC 31
Z9 34
U1 0
U2 2
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 2009
VL 18
IS 10
BP 2726
EP 2733
DI 10.1158/1055-9965.EPI-09-0363
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505NZ
UT WOS:000270702100022
PM 19755647
ER
PT J
AU Travis, RC
Schumacher, F
Hirschhorn, JN
Kraft, P
Allen, NE
Albanes, D
Berglund, G
Berndt, SI
Boeing, H
Bueno-de-Mesquita, HB
Calle, EE
Chanock, S
Dunning, AM
Hayes, R
Feigelson, HS
Gaziano, JM
Giovannucci, E
Haiman, CA
Henderson, BE
Kaaks, R
Kolonel, LN
Ma, J
Rodriguez, L
Riboli, E
Stampfer, M
Stram, DO
Thun, MJ
Tjonneland, A
Trichopoulos, D
Vineis, P
Virtamo, J
Le Marchand, L
Hunter, DJ
AF Travis, Ruth C.
Schumacher, Fredrick
Hirschhorn, Joel N.
Kraft, Peter
Allen, Naomi E.
Albanes, Demetrius
Berglund, Goran
Berndt, Sonja I.
Boeing, Heiner
Bueno-de-Mesquita, H. Bas
Calle, Eugenia E.
Chanock, Stephen
Dunning, Alison M.
Hayes, Richard
Feigelson, Heather Spencer
Gaziano, J. Michael
Giovannucci, Edward
Haiman, Christopher A.
Henderson, Brian E.
Kaaks, Rudolf
Kolonel, Laurence N.
Ma, Jing
Rodriguez, Laudina
Riboli, Elio
Stampfer, Meir
Stram, Daniel O.
Thun, Michael J.
Tjonneland, Anne
Trichopoulos, Dimitrios
Vineis, Paolo
Virtamo, Jarmo
Le Marchand, Loic
Hunter, David J.
TI CYP19A1 Genetic Variation in Relation to Prostate Cancer Risk and
Circulating Sex Hormone Concentrations in Men from the Breast and
Prostate Cancer Cohort Consortium
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GROWTH-FACTOR-I; POSTMENOPAUSAL WOMEN; ESTROGEN-LEVELS; UNRELATED
INDIVIDUALS; ANDROGEN BIOSYNTHESIS; JAPANESE POPULATION; MULTIETHNIC
COHORT; ALLELIC VARIANTS; STEROID-HORMONES; SERUM ANDROGENS
AB Sex hormones, particularly the androgens, are important for the growth of the prostate gland and have been implicated in prostate cancer carcinogenesis, yet the determinants of endogenous steroid hormone levels remain poorly understood. Twin studies suggest a heritable component for circulating concentrations of sex hormones, although epidemiologic evidence linking steroid hormone gene variants to prostate cancer is limited. Here we report on findings from a comprehensive study of genetic variation at the CYP19A1 locus in relation to prostate cancer risk and to circulating steroid hormone concentrations in men by the Breast and Prostate Cancer Cohort Consortium (BPC3), a large collaborative prospective study. The BPC3 systematically characterized variation in CYP19A1 by targeted resequencing and dense genotyping; selected haplotype-tagging single nuclecitide polymorphisms (htSNP) that efficiently predict common variants in U.S. and Europe-an whites, Latinos, Japanese Americans, and Native Hawaiians; and genotyped these htSNPs; in 8,166 prostate cancer cases and 9,079 study-, age-, and ethnicity-matched controls. CYP19A1 htSNPs, two common missense variants and common haplotypes were not significantly associated with risk of prostate cancer. However, several htSNPs in linkage disequilibrium blocks 3 and 4 were significantly associated with a 5% to 10% difference in estradiol concentrations in men [association per copy of the two-SNP haplotype rs749292-rs727479 (A-A) versus noncarriers; P = 1 x 10(-5)], and with inverse, although less marked changes, in free testosterone concentrations. These results suggest that although germline variation in CYP19A1 characterized by the htSNPs produces measurable differences in sex hormone concentrations in men, they do not substantially influence risk of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2734-44)
C1 [Travis, Ruth C.; Allen, Naomi E.] Univ Oxford, Nuffield Dept Clin Med, Canc Epidemiol Unit, Oxford, England.
[Schumacher, Fredrick; Haiman, Christopher A.; Henderson, Brian E.; Stram, Daniel O.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Hirschhorn, Joel N.] Harvard Univ, Sch Med, Broad Inst Harvard & MIT, Div Genet, Boston, MA USA.
[Hirschhorn, Joel N.] Harvard Univ, Sch Med, Broad Inst Harvard & MIT, Div Endocrinol, Boston, MA USA.
[Hirschhorn, Joel N.] Harvard Univ, Sch Med, Program Genom, Dept Genet,Childrens Hosp, Boston, MA USA.
[Giovannucci, Edward; Ma, Jing; Stampfer, Meir; Hunter, David J.] Harvard Univ, Sch Med, Channing Lab, Boston, MA 02115 USA.
[Kraft, Peter; Giovannucci, Edward; Stampfer, Meir; Trichopoulos, Dimitrios; Hunter, David J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Gaziano, J. Michael; Giovannucci, Edward; Ma, Jing; Stampfer, Meir; Hunter, David J.] Brigham & Womens Hosp, Dept Med, VA Boston, Boston, MA 02115 USA.
[Albanes, Demetrius; Berndt, Sonja I.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Berglund, Goran; Le Marchand, Loic] Lund Univ, Malmo Univ Hosp, Dept Clin Sci, Malmo, Sweden.
[Boeing, Heiner] German Inst Human Nutr, Dept Epidemiol, Potsdam, Germany.
[Bueno-de-Mesquita, H. Bas] Natl Inst Publ Hlth & Environm, RIVM, NL-3720 BA Bilthoven, Netherlands.
[Calle, Eugenia E.; Thun, Michael J.] Amer Canc Soc, Dept Epidemiol, Atlanta, GA 30329 USA.
[Chanock, Stephen] NCI, Core Genotyping Facil, Gaithersburg, MD USA.
[Dunning, Alison M.] Univ Cambridge, Dept Oncol, Cambridge, England.
[Hayes, Richard] NYU, Langone Med Ctr, Div Epidemiol, New York, NY USA.
[Feigelson, Heather Spencer] Kaiser Permanente Colorado, Inst Hlth Res, Denver, CO USA.
[Kaaks, Rudolf] DKFZ, German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Kolonel, Laurence N.] Univ Hawaii, Canc Res Ctr, Program Epidemiol, Honolulu, HI 96813 USA.
[Rodriguez, Laudina] Hlth & Hlth Care Serv Council, Publ Hlth & Participat Directorate, Asturias, Spain.
[Riboli, Elio; Vineis, Paolo] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Publ Hlth, London, England.
[Tjonneland, Anne] Danish Canc Soc, Inst Canc Epidemiol, Copenhagen, Denmark.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
RP Travis, RC (reprint author), Univ Oxford, Nuffield Dept Clin Med, Canc Epidemiol Unit, Richard Doll Bldg, Oxford, England.
EM ruth.travis@ceu.ox.ac.uk
RI Albanes, Demetrius/B-9749-2015;
OI Dunning, Alison Margaret/0000-0001-6651-7166; Hayes,
Richard/0000-0002-0918-661X
FU National Cancer Institute [U01-CA98233, UO1-CA98710, UO1-CA98216,
UO1-CA98758]; Cancer Research UK
FX National Cancer Institute cooperative agreements U01-CA98233,
UO1-CA98710, UO1-CA98216, and UO1-CA98758 and Cancer Research UK (R.C.
Travis).
NR 58
TC 17
Z9 18
U1 0
U2 4
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 2009
VL 18
IS 10
BP 2734
EP 2744
DI 10.1158/1055-9965.EPI-09-0496
PG 11
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505NZ
UT WOS:000270702100023
PM 19789370
ER
PT J
AU Fuhrman, BJ
Pfeiffer, R
Xu, X
Wu, AH
Korde, L
Gail, MH
Keefer, LK
Veenstra, TD
Hoover, RN
Ziegler, RG
AF Fuhrman, Barbara J.
Pfeiffer, Ruth
Xu, Xia
Wu, Anna H.
Korde, Larissa
Gail, Mitchell H.
Keefer, Larry K.
Veenstra, Timothy D.
Hoover, Robert N.
Ziegler, Regina G.
TI Soy Intake is Associated with Increased 2-Hydroxylation and Decreased 16
alpha-Hydroxylation of Estrogens in Asian-American Women
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID BREAST-CANCER RISK; POSTMENOPAUSAL CHINESE WOMEN; PREMENOPAUSAL WOMEN;
MENSTRUAL-CYCLE; ISOFLAVONES; METABOLITES; DIET; EXCRETION; HORMONES;
DISEASE
AB Introduction: In Asian and Asian-American women, soy consumption is associated with reduced breast cancer risk, perhaps due to its effects on estrogen production or metabolism. In a sample of Asian-American women, we investigated the associations of usual adult soy intake with the urinary concentrations of 15 estrogens and estrogen metabolites (EM) measured using liquid chromatography-tandem mass spectrometry.
Methods: Participants included 430 Chinese-American, Japanese-American, and Filipino-American women, ages 20 to 55 years, and living in San Francisco-Oakland (California), Los Angeles (California), or Oahu (Hawaii). They were postmenopausal (n = 167) or premenopausal in luteal phase (n = 263) when 12-hour urine samples were collected. Robust linear regression was used to assess soy tertiles as predictors of log-transformed EM measures. Individual and grouped EM were considered as concentrations (pmol/mg creatinine) and as percentages of total EM (%EM).
Results: Factor analysis confirmed that EM groups defined by metabolic pathways appropriately captured covariation in EM profiles. Total EM concentrations were not significantly associated with soy in premenopausal or postmenopausal women. Among all women, %2-hydroxylated EM and %4-hydroxylation pathway EM were 16% higher (P(trend) = 0.02) and 19% higher (P(trend) = 0.03) in the highest versus lowest soy tertiles, respectively. In contrast, 16% hydroxylated EM were 11% lower (P(trend) < 0.01). Results were consistent across ethnic and menopausal groups and after adjustment for westernization measured by birthplace (Asia or United States).
Discussion: Findings suggest that regular soy intake is associated with increased ratios of 2:16-pathway EM and with higher relative levels of 4-hydroxylated EM. The observed variations in estrogen metabolism might modify breast cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2751-60)
C1 [Fuhrman, Barbara J.] NCI, Div Canc Epidemiol & Genet, Epidemiol & Biostat Program, Rockville, MD 20852 USA.
[Pfeiffer, Ruth; Gail, Mitchell H.; Hoover, Robert N.] NCI, Biostat Branch, Rockville, MD 20852 USA.
[Korde, Larissa] NCI, Clin Genet Branch, Human Genet Program, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Xu, Xia; Veenstra, Timothy D.] Sci Applicat Int Corp Inc, Lab Prote & Analyt Technol, Adv Technol Program, Frederick, MD USA.
[Keefer, Larry K.] NCI, Comparat Carcinogenesis Lab, Frederick, MD 21701 USA.
[Wu, Anna H.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
RP Fuhrman, BJ (reprint author), NCI, Div Canc Epidemiol & Genet, Epidemiol & Biostat Program, 6120 Execut Blvd,Room 5003, Rockville, MD 20852 USA.
EM fuhrmanb@mail.nih.gov
RI Keefer, Larry/N-3247-2014;
OI Keefer, Larry/0000-0001-7489-9555; Fuhrman, Barbara/0000-0002-1777-9888
FU NIH [N01-CO-12400]; National Cancer Institute; Center for Cancer
Research and Division of Cancer Epidemiology and Genetics
FX Intramural Research Programs of the NIH, National Cancer Institute,
Center for Cancer Research and Division of Cancer Epidemiology and
Genetics, and federal funds from the National Cancer Institute, NIH,
under contract N01-CO-12400. The contents 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 organization imply endorsement by the U.S. Government.
NR 55
TC 9
Z9 9
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 2009
VL 18
IS 10
BP 2751
EP 2760
DI 10.1158/1055-9965.EPI-09-0388
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505NZ
UT WOS:000270702100025
PM 19789363
ER
PT J
AU D'Aloisio, AA
Baird, DD
Poole, C
North, KE
AF D'Aloisio, Aimee A.
Baird, Donna D.
Poole, Charles
North, Kari E.
TI IGF1 and IGFBP3 Polymorphisms and Plasma Levels in Women Response
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Letter
C1 [D'Aloisio, Aimee A.; Baird, Donna D.] Natl Inst Environm Hlth Sci, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Poole, Charles; North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
RP D'Aloisio, AA (reprint author), Natl Inst Environm Hlth Sci, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
NR 4
TC 0
Z9 0
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 2009
VL 18
IS 10
BP 2795
EP 2795
DI 10.1158/1055-9965.EPI-09-0796
PG 1
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 505NZ
UT WOS:000270702100034
ER
PT J
AU Reuschenbach, M
Doeberitz, MV
Wentzensen, N
AF Reuschenbach, Miriam
Doeberitz, Magnus von Knebel
Wentzensen, Nicolas
TI A systematic review of humoral immune responses against tumor antigens
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Review
DE Humoral immune response; Autoantibodies; Cancer; Tumor antigens
ID SQUAMOUS-CELL CARCINOMA; SERUM P53 ANTIBODIES; LUNG-CANCER PATIENTS;
BREAST-CANCER; OVARIAN-CANCER; HEPATOCELLULAR-CARCINOMA;
COLORECTAL-CANCER; ANTI-P53 ANTIBODIES; PROSTATE-CANCER; MUC1 MUCIN
AB This review summarizes studies on humoral immune responses against tumor-associated antigens (TAAs) with a focus on antibody frequencies and the potential diagnostic, prognostic, and etiologic relevance of antibodies against TAAs. We performed a systematic literature search in Medline and identified 3,619 articles on humoral immune responses and TAAs. In 145 studies, meeting the inclusion criteria, humoral immune responses in cancer patients have been analyzed against over 100 different TAAs. The most frequently analyzed antigens were p53, MUC1, NY-ESO-1, c-myc, survivin, p62, cyclin B1, and Her2/neu. Antibodies against these TAAs were detected in 0-69% (median 14%) of analyzed tumor patients. Antibody frequencies were generally very low in healthy individuals, with the exception of few TAAs, especially MUC1. For several TAAs, including p53, Her2/neu, and NY-ESO-1, higher antibody frequencies were reported when tumors expressed the respective TAA. Antibodies against MUC1 were associated with a favorable prognosis while antibodies against p53 were associated with poor disease outcome. These data suggest different functional roles of endogenous antibodies against TAAs. Although data on prediagnostic antibody levels are scarce and antibody frequencies for most TAAs are at levels precluding use in diagnostic assays for cancer early detection, there is some promising data on achieving higher sensitivity for cancer detection using panels of TAAs.
C1 [Reuschenbach, Miriam; Doeberitz, Magnus von Knebel] Univ Heidelberg, Dept Appl Tumor Biol, Inst Pathol, D-69120 Heidelberg, Germany.
[Wentzensen, Nicolas] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Reuschenbach, M (reprint author), Univ Heidelberg, Dept Appl Tumor Biol, Inst Pathol, Im Neuenheimer Feld 220, D-69120 Heidelberg, Germany.
EM miriam.reuschenbach@med.uni-heidelberg.de
FU Intramural NIH HHS [Z99 CA999999]
NR 120
TC 116
Z9 119
U1 2
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD OCT
PY 2009
VL 58
IS 10
BP 1535
EP 1544
DI 10.1007/s00262-009-0733-4
PG 10
WC Oncology; Immunology
SC Oncology; Immunology
GA 474OS
UT WOS:000268294400001
PM 19562338
ER
PT J
AU Elkord, E
Dangoor, A
Burt, DJ
Southgate, TD
Daayana, S
Harrop, R
Drijfhout, JW
Sherlock, D
Hawkins, RE
Stern, PL
AF Elkord, Eyad
Dangoor, Adam
Burt, Deborah J.
Southgate, Thomas D.
Daayana, Sai
Harrop, Richard
Drijfhout, Jan W.
Sherlock, David
Hawkins, Robert E.
Stern, Peter L.
TI Immune evasion mechanisms in colorectal cancer liver metastasis patients
vaccinated with TroVax (MVA-5T4)
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Colorecta cancer; 5T4; TroVax; Immune evasion; T regulatory cell
ID 5T4 ONCOFETAL ANTIGEN; REGULATORY T-CELLS; TUMOR-INFILTRATING
LYMPHOCYTES; PROSTATE-CANCER; CARCINOMA; EXPRESSION; RESPONSES;
DIFFERENTIATION; IMMUNOTHERAPY; STRATEGIES
AB We have recently reported the results of a phase II trial in which two TroVax [modified vaccinia ankara (MVA) encoding the tumour antigen 5T4] vaccinations were given to patients both pre- and post-surgical resection of liver metastases secondary to colorectal cancer (CRC). 5T4-specific cellular responses were assessed at the entry and 2 weeks after each vaccination by proliferation of fresh lymphocytes and ELISA for antibody responses; 18 from the 19 CRC patients mounted a 5T4-specific cellular and/or humoral response. Here, we present a comparison of individual and between patient responses over the course of the treatments using cryopreserved peripheral blood mononuclear cells (PBMC) samples from the baseline until after the fourth vaccination at 14 weeks. Assays used were proliferation assay with 5T4-Fc fusion protein, overlapping 32mer 5T4 peptides, MVA-LacZ and MVA-5T4 infected autologous monocytes. Responses to 5T4 protein or one or more peptide pools were pre-existing in 12/20 patients and subsequently 10 and 12 patients showed boosted and/or de novo responses, respectively. Cumulatively, 13/20 patients showed proliferative responses by week 14. We also assessed the levels of systemic T regulatory cells, plasma cytokine levels, phenotype of tumour-infiltrating lymphocytes including T regulatory cells and tumour HLA class I loss of expression. More than half of the patients showed phenotypes consistent with relative immune suppression and/or escape highlighting the complexity of positive and negative factors challenging any simple correlation with clinical outcome.
C1 [Elkord, Eyad; Dangoor, Adam; Burt, Deborah J.; Southgate, Thomas D.; Daayana, Sai; Stern, Peter L.] Univ Manchester, Christie Hosp NHS Trust, Paterson Inst Canc Res, CR UK Immunol Grp, Manchester M20 4BX, Lancs, England.
[Elkord, Eyad; Dangoor, Adam; Hawkins, Robert E.] Univ Manchester, Christie Hosp NHS Trust, Dept Med Oncol, Manchester M20 4BX, Lancs, England.
[Drijfhout, Jan W.] Leiden Univ, Med Ctr, Dept Immunohematol & Blood Transfus, Leiden, Netherlands.
[Harrop, Richard] Oxford BioMed, Medawar Ctr, Oxford OX4 4GA, England.
[Sherlock, David] N Manchester Healthcare NHS Trust, Dept Surg, Manchester, Lancs, England.
RP Elkord, E (reprint author), NIH, Cellular Immunol Sect, Immunol Lab, Bldg 10, Bethesda, MD 20892 USA.
EM eelkord@picr.man.ac.uk; pstern@picr.man.ac.uk
OI Sherlock, David/0000-0001-7630-0833; Elkord, Eyad/0000-0002-3868-0318
FU Cancer Research UK; Cancer Research UK Drug Development Office; CR UK;
Wigan Cancer Research Fund
FX This trial was sponsored by Cancer Research UK and monitored by the
Cancer Research UK Drug Development Office. EE, AD, DB, TS and PLS were
supported by CR UK; SD by Wigan Cancer Research Fund as a Joseph Starkey
Fellow. We thank Ester Martin for her contribution to the HLA expression
studies. We are very grateful for all patients who participated in this
trial.
NR 31
TC 20
Z9 20
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD OCT
PY 2009
VL 58
IS 10
BP 1657
EP 1667
DI 10.1007/s00262-009-0674-y
PG 11
WC Oncology; Immunology
SC Oncology; Immunology
GA 474OS
UT WOS:000268294400012
PM 19221742
ER
PT J
AU Rao, CV
Steele, VE
Stoner, GD
Conney, AH
AF Rao, Chinthalapally V.
Steele, Vernon E.
Stoner, Gary D.
Conney, Allan H.
TI Bandaru S. Reddy: In Memoriam (1930-2009) Obituary
SO CANCER PREVENTION RESEARCH
LA English
DT Biographical-Item
C1 [Rao, Chinthalapally V.] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK 73190 USA.
[Steele, Vernon E.] NCI, Bethesda, MD 20892 USA.
[Stoner, Gary D.] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
[Conney, Allan H.] Rutgers State Univ, Piscataway, NJ USA.
RP Rao, CV (reprint author), Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK 73190 USA.
NR 0
TC 0
Z9 0
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 2009
VL 2
IS 10
BP 912
EP 913
DI 10.1158/1940-6207.CAPR-09-0180
PG 2
WC Oncology
SC Oncology
GA 506ZS
UT WOS:000270819300010
PM 19805402
ER
PT J
AU Liu, JL
Kaur, G
Zhawar, VK
Zimonjic, DB
Popescu, NC
Kandpal, RP
Athwal, RS
AF Liu, Jinglan
Kaur, Gurpreet
Zhawar, Vikramjit K.
Zimonjic, Drazen B.
Popescu, Nicholas C.
Kandpal, Raj P.
Athwal, Raghbir S.
TI Role of SV40 Integration Site at Chromosomal Interval 1q21.1 in
Immortalized CRL2504 Cells
SO CANCER RESEARCH
LA English
DT Article
ID EPIDERMAL DIFFERENTIATION COMPLEX; CELLULAR SENESCENCE; VIRUS
INTEGRATION; FIBROBLAST CELLS; TUMOR-SUPPRESSOR; EPITHELIAL-CELLS;
FRAGILE SITES; HUMAN GENOME; GENE; EXPRESSION
AB We have applied a functional gene transfer strategy to show the importance of viral integration site in cellular immortalization. The large tumor antigen of SV40 is capable of extending the cellular life span by sequestering tumor suppressor proteins pRB and p53 in virus-transformed human cells. Although SV40 large T antigen is essential, it is not sufficient for cellular immortalization, suggesting that additional alterations in cellular genes are required to attain infinite proliferation. We show here that the disruption of human chromosomal interval at 1q21.1 by SV40 integration can be an essential step for cellular immortalization. The transfer of a 150-kb bacterial artificial chromosome (BAC) clone, RP364B14, corresponding to viral integration site in CRL2504 cells, reverted their immortal phenotype. Interestingly, the BAC transfer clones of CRL2504 cells displayed characteristics of either senescence as shown by beta-galactosidase activity or apoptosis as revealed by positive staining with M30 CytoDEATH antibody. The SV40 integration at 1q21.1, in the vicinity of epidermal differentiation complex (EDC) genes, resulted in the down-regulation of the filaggrin (FLG) gene that is part of the EDC. FLG gene expression was increased in BAC transfer senescent and apoptotic clones. Our results suggest that the disruption of native genomic sequence by SV40 may alter expression of genes involved in senescence and apoptosis by modulating chromatin structure. These studies imply that identification of genes located in the vicinity of viral integration sites in human cancers may be helpful in developing new diagnostic and therapeutic strategies. [Cancer Res 2009;69(19):7819-25]
C1 [Liu, Jinglan; Kaur, Gurpreet; Zhawar, Vikramjit K.; Athwal, Raghbir S.] Temple Univ, Sch Med, Fels Inst Canc Res & Mol Biol, Philadelphia, PA 19140 USA.
[Zimonjic, Drazen B.; Popescu, Nicholas C.] NCI, Expt Carcinogenesis Lab, Bethesda, MD 20892 USA.
[Kandpal, Raj P.] Western Univ Hlth Sci, Dept Basic Med Sci, Pomona, CA USA.
RP Athwal, RS (reprint author), Temple Univ, Sch Med, Fels Inst Canc Res & Mol Biol, AHB 202,3307 N Broad St, Philadelphia, PA 19140 USA.
EM rathwal@temple.edu
FU NIH [CA74983]; U.S. Army Breast Cancer Research Program
[DAMD17-99-1-9393, DAMD17-02-1-0574]; Susan G. Kamen Breast Cancer
Foundation [BCTR9830, BCTR1092]
FX NIH grant CA74983, U.S. Army Breast Cancer Research Program grants
DAMD17-99-1-9393 and DAMD17-02-1-0574, and Susan G. Kamen Breast Cancer
Foundation grants; BCTR9830 and BCTR1092.
NR 44
TC 2
Z9 2
U1 1
U2 3
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 2009
VL 69
IS 19
BP 7819
EP 7825
DI 10.1158/0008-5472.CAN-09-1003
PG 7
WC Oncology
SC Oncology
GA 502VE
UT WOS:000270487600042
PM 19789346
ER
PT J
AU Liu, Y
Liu, PY
Wen, WD
James, MA
Wang, Y
Bailey-Wilson, JE
Amos, CI
Pinney, SM
Yang, P
de Andrade, M
Petersen, GM
Wiest, JS
Fain, PR
Schwartz, AG
Gazdar, A
Gaba, C
Rothschild, H
Mandal, D
Kupert, E
Lee, J
Seminara, D
Minna, J
Anderson, MW
You, M
AF Liu, Yan
Liu, Pengyuan
Wen, Weidong
James, Michael A.
Wang, Yian
Bailey-Wilson, Joan E.
Amos, Christopher I.
Pinney, Susan M.
Yang, Ping
de Andrade, Mariza
Petersen, Gloria M.
Wiest, Jonathan S.
Fain, Pamela R.
Schwartz, Ann G.
Gazdar, Adi
Gaba, Colette
Rothschild, Henry
Mandal, Diptasri
Kupert, Elena
Lee, Juwon
Seminara, Daniela
Minna, John
Anderson, Marshall W.
You, Ming
TI Haplotype and Cell Proliferation Analyses of Candidate Lung Cancer
Susceptibility Genes on Chromosome 15q24-25.1
SO CANCER RESEARCH
LA English
DT Article
ID NICOTINIC ACETYLCHOLINE-RECEPTORS; HEAVY SMOKING; DEPENDENCE; VARIANTS;
DISEASE; ASSOCIATION; LOCUS; RISK; SNPS
AB Recent genome-wide association studies have linked the chromosome 15q24-25.1 locus to nicotine addiction and lung cancer susceptibility. To refine the 15q24-25.1 locus' we performed a haplotype-based association analysis of 194 familial lung cases and 219 cancer-free controls from the Genetic Epidemiology of Lung Cancer Consortium (GELCC) collection, and used proliferation and apoptosis analyses to determine which gene(s) in the 15q24-25.1 locus mediates effects on lung cancer cell growth in vitro. We identified two distinct subregions, hapL (P = 3.20 x 10(-6)) and hapN (P = 1.51 x 10(-6)), which were significantly associated with familial lung cancer. hapL encompasses IREB2, LOC123688, and PSAM4, and hapN encompasses the three nicotinic acetylcholine receptor subunit genes CHRNA5, CHRNA3, and CHRNB4. Examination of the genes around hapL revealed that PSAM4 plays a role in promoting cancer cell proliferation. PSAM4 mRNA levels were increased in lung tumors compared with normal lung tissues. Down-regulation of PSMA4 expression decreased proteasome activity and induced apoptosis. Proteasome dysfunction leads to many diseases including cancer, and drugs that inhibit proteasome activity show promise as a form of cancer treatment. Genes around hapN were also investigated, but did not show any direct effect on lung cancer cell proliferation. We concluded that PSMA4 is a strong candidate mediator of lung cancer cell growth, and may directly affect lung cancer susceptibility through its modulation of cell proliferation and apoptosis. [Cancer Res 2009;69(19):7844-50]
C1 [You, Ming] Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA.
[Bailey-Wilson, Joan E.] NHGRI, Bethesda, MD 20892 USA.
[Amos, Christopher I.] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Yang, Ping; de Andrade, Mariza; Petersen, Gloria M.] Mayo Clin, Coll Med, Rochester, MN USA.
[Wiest, Jonathan S.; Seminara, Daniela] NCI, Rockville, MD USA.
[Pinney, Susan M.; Kupert, Elena; Lee, Juwon; Anderson, Marshall W.] Univ Cincinnati, Cincinnati, OH USA.
[Schwartz, Ann G.] Karmanos Canc Inst, Detroit, MI USA.
[Fain, Pamela R.] Univ Colorado, Denver, CO 80202 USA.
[Gazdar, Adi; Minna, John] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Gaba, Colette] Univ Toledo, Coll Med, Toledo, OH 43606 USA.
[Rothschild, Henry; Mandal, Diptasri] Louisiana State Univ, Hlth Sci Ctr, New Orleans, LA USA.
RP You, M (reprint author), Washington Univ, Sch Med, Dept Surg, 660 Euclid Ave,Box 8109, St Louis, MO 63110 USA.
EM youm@wustl.edu
OI Bailey-Wilson, Joan/0000-0002-9153-2920
FU NIH [U01CA76293, R01CA058554, R01CA0936A3, R01CA099147, R01CA099187,
R01ES012063, R01ES013340, R03CA77118, R01CA80127, P30ES06096,
P50CA70907, N01HG65404, N01-PC35145, P30CA22453, R01CA63700,
FGB-95ER62060]; NIH, the Intramural Research Programs; National Cancer
Institute; National Human Genome Research Institute
FX NIH grants U01CA76293 (Genetic Epidemiology of Lung Cancer Consortium),
R01CA058554, R01CA0936A3, R01CA099147, R01CA099187, R01ES012063,
R01ES013340, R03CA77118, R01CA80127, P30ES06096, P50CA70907 (Specialized
Program of Research Excellence), N01HG65404, N01-PC35145, P30CA22453,
R01CA63700, DE-FGB-95ER62060, Mayo Clinic intramural research funds, and
Department of Defense VITAL grant. This study was also supported in part
by NIH, the Intramural Research Programs of the National Cancer
Institute, and the National Human Genome Research Institute.
NR 21
TC 25
Z9 26
U1 1
U2 5
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 2009
VL 69
IS 19
BP 7844
EP 7850
DI 10.1158/0008-5472.CAN-09-1833
PG 7
WC Oncology
SC Oncology
GA 502VE
UT WOS:000270487600045
PM 19789337
ER
PT J
AU Goto, K
Watashi, K
Inoue, D
Hijikata, M
Shimotohno, K
AF Goto, Kaku
Watashi, Koichi
Inoue, Daisuke
Hijikata, Makoto
Shimotohno, Kunitada
TI Identification of cellular and viral factors related to anti-hepatitis C
virus activity of cyclophilin inhibitor
SO CANCER SCIENCE
LA English
DT Article
ID RNA REPLICATION; CYCLOSPORINE-A; PROTEASE INHIBITOR; SANGLIFEHRIN-A;
PLUS RIBAVIRIN; IN-VITRO; RESISTANCE; MUTATIONS; INFECTION; NS5B
AB We have so far reported that an immunosuppressant cyclosporin A (CsA), a well-known cyclophilin (CyP) inhibitor (CPI), strongly suppressed hepatitis C virus (HCV) replication in cell culture, and that CyPB was a cellular cofactor for viral replication. To further investigate antiviral mechanisms of CPI, we here developed cells carrying CsA-resistant HCV replicons, by culturing the HCV subgenomic replicon cells for 4 weeks in the presence of CsA with G418. Transfection of total RNA from the isolated CsA-resistant cells to naive Huh7 cells conferred CsA resistance, suggesting that the replicon RNA itself was responsible for the resistant phenotype. Of the identified amino acid mutations, D320E in NS5A conferred the CsA resistance. The replicon carrying the D320E mutation was sensitive to interferon-alpha, but was resistant to CsA and other CPIs including NIM811 and sanglifehrin A. Knockdown of individual CyP subtypes revealed CyP40, in addition to CyPA and CyPB, contributed to viral replication, and CsA-resistant replicons acquired independence from CyPA for efficient replication. These data provide important evidence on the mechanisms underlying the regulation of HCV replication by CyP and for designing novel and specific anti-HCV strategies with CPIs. (Cancer Sci 2009; 100: 1943-1950).
C1 [Goto, Kaku; Watashi, Koichi; Inoue, Daisuke; Hijikata, Makoto; Shimotohno, Kunitada] Kyoto Univ, Inst Virus Res, Dept Viral Oncol, Lab Human Tumor Viruses, Kyoto 606, Japan.
[Watashi, Koichi] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Shimotohno, Kunitada] Chiba Inst Technol, Res Ctr, Chiba, Japan.
RP Shimotohno, K (reprint author), Kyoto Univ, Inst Virus Res, Dept Viral Oncol, Lab Human Tumor Viruses, Kyoto 606, Japan.
EM kunitada.shimotono@it-chiba.ac.jp
FU Ministry of Health, Labor and Welfare of Japan; Ministry of Education,
Culture, Sports, Science and Technology of Japan
FX We thank Novartis (Basel, Switzerland) for providing the CsA derivative,
NIM811, and SFA. This work was supported by Grants-in-Aid from the
Ministry of Health, Labor and Welfare of Japan. This work was also
supported by Grants-in-Aid for Cancer Research from the Ministry of
Education, Culture, Sports, Science and Technology of Japan, by
Grants-in-Aid for the Research for the Future Program from the Japan
Society for the Promotion of Science (JSPS), and by Grants-in-Aid for
the Program for Promotion of Fundamental Studies in Health Science from
the Organization for Pharmaceutical Safety of Japan. K.W. is a recipient
of a JSPS Postdoctoral Fellowship for Research Abroad, and K.G. is a
recipient of a JSPS Research Fellowship for Young Scientists.
NR 31
TC 44
Z9 45
U1 0
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1347-9032
J9 CANCER SCI
JI Cancer Sci.
PD OCT
PY 2009
VL 100
IS 10
BP 1943
EP 1950
DI 10.1111/j.1349-7006.2009.01263.x
PG 8
WC Oncology
SC Oncology
GA 494HH
UT WOS:000269802000024
PM 19659609
ER
PT J
AU Dickey, JS
Baird, BJ
Redon, CE
Sokolov, MV
Sedelnikova, OA
Bonner, WM
AF Dickey, Jennifer S.
Baird, Brandon J.
Redon, Christophe E.
Sokolov, Mykyta V.
Sedelnikova, Olga A.
Bonner, William M.
TI Intercellular communication of cellular stress monitored by gamma-H2AX
induction
SO CARCINOGENESIS
LA English
DT Article
ID DOUBLE-STRAND BREAKS; PRIMARY HUMAN FIBROBLASTS; BYSTANDER CELLS;
DNA-DAMAGE; NITRIC-OXIDE; CHO-CELLS; OXIDATIVE-METABOLISM; SIGNALING
MOLECULE; ALPHA-PARTICLES; GLIOMA-CELLS
AB When cells are exposed to ionizing radiation (IR), unexposed cells that share media with damaged cells exhibit similar effects to irradiated cells including increased levels of DNA double-strand breaks (DSBs). Hypothesizing that this effect, known as the radiation-induced bystander effect, may be a specific instance of communication between damaged and undamaged cells regardless of damage source, we demonstrated that exposure of target cells to non-IR induces bystander damage in non-targeted cells as measured by gamma-H2AX and 53BP1 focal formation. Initially, bystander damage was found primarily in S-phase cells, but at later times, non-S-phase cells were also affected. In addition, media from undamaged malignant and senescent cells also was found to induce DSBs in primary cultures. Media conditioned on cells targeted with either ionizing or non-IR as well as on undamaged malignant and senescent cells contained elevated levels of several cytokines. One of these, transforming growth factor beta (TGF-beta), and nitric oxide (NO) were found to elevate numbers of gamma-H2AX/53BP1 foci in normal cell cultures similar to levels found in bystander cells, and this elevation was abrogated by NO synthase inhibitors, TGF-beta blocking antibody and antioxidants. These findings support the hypothesis that damage in bystander cells results from their exposure to cytokines or reactive compounds released from stressed cells, regardless of damage source. These results have implications for oncogenesis in that they indicate that damaged normal cells or undamaged tumor cells may induce genomic instability, leading to an increased risk of oncogenic transformation in other cells with which they share media or contact directly.
C1 [Dickey, Jennifer S.; Baird, Brandon J.; Redon, Christophe E.; Sokolov, Mykyta V.; Sedelnikova, Olga A.; Bonner, William M.] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20952 USA.
RP Dickey, JS (reprint author), NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20952 USA.
EM dickeyj@mail.nih.gov; bonnerw@mail.nih.gov
FU National Cancer Institute
FX Intramural research program of the National Cancer Institute.
NR 51
TC 67
Z9 70
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 2009
VL 30
IS 10
BP 1686
EP 1695
DI 10.1093/carcin/bgp192
PG 10
WC Oncology
SC Oncology
GA 505II
UT WOS:000270685800005
PM 19651821
ER
PT J
AU Yan, B
Wang, HL
Xie, DH
Wakamatsu, N
Anscher, MS
Dewhirst, MW
Mitchel, REJ
Chen, BJ
Li, CY
AF Yan, Bin
Wang, Huili
Xie, Donghua
Wakamatsu, Nobuko
Anscher, Mitchell S.
Dewhirst, Mark W.
Mitchel, Ron E. J.
Chen, Benny J.
Li, Chuan-Yuan
TI Increased skin carcinogenesis in caspase-activated DNase knockout mice
SO CARCINOGENESIS
LA English
DT Article
ID FRAGMENTATION FACTOR; NEUROBLASTOMA TUMORS; APOPTOSIS; DEGRADATION;
INHIBITOR; MUTATIONS; STABILITY; CARCINOMA
AB Caspase-activated DNase (CAD), also called DNA fragmentation factor (DFF), is the enzyme responsible for DNA fragmentation during apoptosis, a hallmark of programmed cell death. CAD/DFF has been shown to suppress radiation-induced carcinogenesis by preventing genomic instability in cells. In this study, we have investigated the role of CAD in chemical carcinogenesis using CAD-null mice and two-stage model of skin carcinogenesis. After topical treatment of mouse skin with dimethylbenz[a]anthracene (DMBA) as an initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as a promoting agent, there was a 4-fold increase in the number of papillomas per mouse and 50.8% increase in the incidence of papilloma formation in the CAD knockout mice compared with wild-type littermates. The papillomas in CAD-null mice grew faster and reached larger sizes. These data indicate that loss of CAD function enhances tumorigenesis induced by a chemical carcinogen in the DMBA/TPA two-stage model of skin carcinogenesis in mice.
C1 [Yan, Bin; Dewhirst, Mark W.; Li, Chuan-Yuan] Duke Univ, Med Ctr, Dept Radiat Oncol, Durham, NC 27710 USA.
[Wang, Huili; Xie, Donghua; Chen, Benny J.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Yan, Bin; Anscher, Mitchell S.] Virginia Commonwealth Univ, Dept Radiat Oncol, Med Ctr, Richmond, VA 23298 USA.
[Wakamatsu, Nobuko] Natl Inst Environm Hlth Sci, Lab Expt Pathol, Res Triangle Pk, NC 27709 USA.
[Mitchel, Ron E. J.] Atom Energy Canada Ltd, Chalk River Labs, Radiat Biol & Hlth Phys Branch, Chalk River, ON K0J 1J0, Canada.
[Li, Chuan-Yuan] Univ Colorado, Dept Radiat Oncol, Hlth Sci Ctr, Aurora, CO 80045 USA.
RP Li, CY (reprint author), Duke Univ, Med Ctr, Dept Radiat Oncol, Durham, NC 27710 USA.
EM chuan.li@uchsc.edu
RI Li, Chuan-Yuan/H-4148-2013;
OI Anscher, Mitchell/0000-0003-4480-111X
FU US Department of Defense Prostate Cancer Research Program
[DAMD17-02-1-0052]; US Department of Energy Low Dose Research Program
[DE-FG02-03ER63635]; National Aeronautics and Space Administration
[NAG2-1629]
FX US Department of Defense Prostate Cancer Research Program
(DAMD17-02-1-0052); US Department of Energy Low Dose Research Program
(DE-FG02-03ER63635); National Aeronautics and Space Administration
(NAG2-1629).
NR 17
TC 5
Z9 5
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD OCT
PY 2009
VL 30
IS 10
BP 1776
EP 1780
DI 10.1093/carcin/bgp146
PG 5
WC Oncology
SC Oncology
GA 505II
UT WOS:000270685800017
PM 19541853
ER
PT J
AU Peng, W
Zhang, Y
Zhu, WZ
Cao, CM
Xiao, RP
AF Peng, Wei
Zhang, Yan
Zhu, Weizhong
Cao, Chun-Mei
Xiao, Rui-Ping
TI AMPK and TNF-alpha at the crossroad of cell survival and death in
ischaemic heart
SO CARDIOVASCULAR RESEARCH
LA English
DT Editorial Material
ID ACTIVATED PROTEIN-KINASE; TUMOR-NECROSIS-FACTOR; EXPRESSION; FAILURE;
INJURY; MICE; REPERFUSION; RATS
C1 [Zhu, Weizhong; Xiao, Rui-Ping] NIA, Cardiovasc Sci Lab, NIH, Gerontol Res Ctr, Baltimore, MD 21224 USA.
[Peng, Wei; Zhang, Yan; Cao, Chun-Mei] Peking Univ, Inst Mol Med, Beijing 100871, Peoples R China.
RP Xiao, RP (reprint author), NIA, Cardiovasc Sci Lab, NIH, Gerontol Res Ctr, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM xiaor@grc.nia.nih.gov
RI Zhang, Yan/B-2831-2012
FU Intramural NIH HHS
NR 18
TC 4
Z9 6
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0008-6363
J9 CARDIOVASC RES
JI Cardiovasc. Res.
PD OCT 1
PY 2009
VL 84
IS 1
BP 1
EP 3
DI 10.1093/cvr/cvp272
PG 3
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 493KN
UT WOS:000269735600001
PM 19671584
ER
PT J
AU Li, XR
Lee, C
Tang, ZS
Zhang, F
Arjunan, P
Li, Y
Hou, X
Kumar, A
Dong, LJ
AF Li, Xuri
Lee, Chunsik
Tang, Zhongshu
Zhang, Fan
Arjunan, Pachiappan
Li, Yang
Hou, Xu
Kumar, Anil
Dong, Lijin
TI VEGF-B A survival, or an angiogenic factor?
SO CELL ADHESION & MIGRATION
LA English
DT Review
DE VEGF-B; survival factor; angiogenesis; apoptosis; vascular biology
AB Despite its early discovery and high sequence homology to the other VEGF family members, the biological function of VEGF-B remained debatable for a long time, and VEGF-B has received little attention from the field thus far. Recently, we and others have found that (1) VEGF-B is a potent survival factor for different types of cells by inhibiting apoptosis via suppressing the expression of BH3-only protein and other apoptotic/cell death-related genes. (2) VEGF-B has a negligible role in inducing blood vessel growth in most organs. Instead, it is critically required for blood vessel survival. VEGF-B targeting inhibited pathological angiogenesis by abolishing blood vessel survival in different animal models. (3) Using different types of neuro-injury and neurodegenerative disease models, VEGF-B treatment protected endangered neurons from apoptosis without inducing undesired blood vessel growth or permeability. Thus, VEGF-B is the first member of the VEGF family that has a potent survival/antiapoptotic effect, while lacking a general angiogenic activity. Our work thus advocates that the major function of VEGF-B is to act as a "survival," rather than an "angiogenic" factor and implicates a therapeutic potential of VEGF-B in treating different types of vascular and neurodegenerative diseases.
C1 [Li, Xuri; Lee, Chunsik; Tang, Zhongshu; Zhang, Fan; Arjunan, Pachiappan; Li, Yang; Hou, Xu; Kumar, Anil; Dong, Lijin] NEI, NIH, Bethesda, MD 20892 USA.
RP Li, XR (reprint author), NEI, NIH, Bethesda, MD 20892 USA.
EM lixur@nei.nih.gov
RI Kumar, Anil/K-8504-2012
NR 62
TC 31
Z9 32
U1 0
U2 5
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 2009
VL 3
IS 4
BP 322
EP 327
DI 10.4161/cam.3.4.9459
PG 6
WC Cell Biology
SC Cell Biology
GA V22OZ
UT WOS:000208285800004
PM 19684473
ER
PT J
AU Kennedy, CH
Catallo, WJ
Wilson, VL
Mitchell, JB
AF Kennedy, Christopher H.
Catallo, W. James
Wilson, Vincent L.
Mitchell, James B.
TI Combustion products of 1,3-butadiene inhibit catalase activity and
induce expression of oxidative DNA damage repair enzymes in human
bronchial epithelial cells
SO CELL BIOLOGY AND TOXICOLOGY
LA English
DT Article
DE APE-1; Butadiene soot; Catalase; OGG1; Oxidative DNA damage; Oxidative
stress
ID DIESEL EXHAUST PARTICLES; HMTH1 MESSENGER-RNA; LUNG-CANCER; STRESS;
PROTEIN; 8-HYDROXYGUANINE; 8-OXOGUANINE; GLYCOSYLASE; HOMOLOG; HOGG1
AB 1,3-Butadiene, an important petrochemical, is commonly burned off when excess amounts need to be destroyed. This combustion process produces butadiene soot (BDS), which is composed of a complex mixture of polycyclic aromatic hydrocarbons in particulates ranging in size from < 1 mu m to 1 mm. An organic extract of BDS is both cytotoxic and genotoxic to normal human bronchial epithelial (NHBE) cells. Based on the oxidizing potential of BDS, we hypothesized that an organic extract of this particulate matter would (1) cause enzyme inactivation due to protein amino acid oxidation and (2) induce oxidative DNA damage in NHBE cells. Thus, our aims were to determine the effect of butadiene soot ethanol extract (BSEE) on both enzyme activity and the expression of proteins involved in the repair of oxidative DNA damage. Catalase was found to be sensitive to BDS as catalase activity was potently diminished in the presence of BSEE. Using Western analysis, both the alpha isoform of human 8-oxoguanine DNA glycosylase (alpha-hOGG1) and human apurinic/apyrimidinic endonuclease (APE-1) were shown to be significantly overexpressed as compared to untreated controls after exposure of NHBE cells to BSEE. Our results indicate that BSEE is capable of effectively inactivating the antioxidant enzyme catalase, presumably via oxidation of protein amino acids. The presence of oxidized biomolecules may partially explain the extranuclear fluorescence that is detected when NHBE cells are treated with an organic extract of BDS. Overexpression of both alpha-hOGG1 and APE-1 proteins following treatment of NHBE cells with BSEE suggests that this mixture causes oxidative DNA damage.
C1 [Kennedy, Christopher H.] Lake Erie Coll Osteopath Med, Dept Biochem, Erie, PA 16509 USA.
[Catallo, W. James] Louisiana State Univ, Sch Vet Med, Dept Comparat Biomed Sci, Baton Rouge, LA 70803 USA.
[Wilson, Vincent L.] Louisiana State Univ, Sch Coast & Environm, Baton Rouge, LA 70803 USA.
[Mitchell, James B.] NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
RP Kennedy, CH (reprint author), Lake Erie Coll Osteopath Med, Dept Biochem, 1858 W Grandview Blvd, Erie, PA 16509 USA.
EM ckennedy@lecom.edu
FU Intramural NIH HHS [ZIA SC006387-25]
NR 46
TC 1
Z9 1
U1 0
U2 1
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 2009
VL 25
IS 5
BP 457
EP 470
DI 10.1007/s10565-008-9100-z
PG 14
WC Cell Biology; Toxicology
SC Cell Biology; Toxicology
GA 487ZX
UT WOS:000269319400004
PM 18685817
ER
PT J
AU Stefanova, N
Staneva, G
Petkova, D
Lupanova, T
Pankov, R
Momchilova, A
AF Stefanova, Nadezhda
Staneva, Galya
Petkova, Diana
Lupanova, Teodora
Pankov, Roumen
Momchilova, Albena
TI Cell culturing in a three-dimensional matrix affects the localization
and properties of plasma membrane cholesterol
SO CELL BIOLOGY INTERNATIONAL
LA English
DT Article
DE Cholesterol; Sphingomyelin; Phospholipids; Cholesterol oxidase; 3D
matrix
ID THIN-LAYER CHROMATOGRAPHY; PHOSPHOLIPIDS; FIBROBLASTS; HOMEOSTASIS;
ACTIVATION; PATHWAY; OXIDASE; BIOLOGY; RAFTS; MODEL
AB Most in vitro studies use 2-dimensional (2D) monolayer cultures, where cells are forced to adjust to unnatural substrates that differ significantly from the natural 3-dimensional (3D) extracellular matrix that surrounds cells in living organisms. Our analysis demonstrates significant differences in the cholesterol and sphingomyelin content, structural organization and cholesterol susceptibility to oxidation of plasma membranes isolated from cells cultured in 3D cultures compared with conventional 2D cultures. Differences occurred in the asymmetry of cholesterol molecules and the physico-chemical properties of the 2 separate leaflets of plasma membranes in 2D and 3D cultured fibroblasts. Transmembrane distribution of other membrane phospholipids was not different, implying that the cholesterol asymmetry could not be attributed to alterations in the scramblase transport system. Differences were also established in the chemical activity of cholesterol, assessed by its susceptibility to cholesterol oxidase in conventional and "matrix" cell cultures. The influence of plasma membrane sphingomyelin and phospholipid content on cholesterol susceptibility to oxidation in 2D and 3D cells was investigated with exogenous sphingomyelinase (SMase) and phospholipase C (PLC) treatment. Sphingomyelin was more effective than membrane phospholipids in protecting cholesterol from oxidation. We presume that the higher cholesterol/sphingomyelin molar ratio is the reason for the higher rate of cholesterol oxidation in plasma membranes of 3D cells. (C) 2009 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.
C1 [Stefanova, Nadezhda; Staneva, Galya; Petkova, Diana; Lupanova, Teodora; Momchilova, Albena] Bulgarian Acad Sci, Inst Biophys, BU-1113 Sofia, Bulgaria.
[Stefanova, Nadezhda; Pankov, Roumen] Univ Sofia, Fac Biol, Dept Cytol Histol & Embryol, Sofia 1164, Bulgaria.
[Pankov, Roumen] Natl Inst Dent & Craniofacial Res, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA.
RP Momchilova, A (reprint author), Bulgarian Acad Sci, Inst Biophys, BU-1113 Sofia, Bulgaria.
EM albena@obzor.bio21.bas.bg
RI Pankov, Roumen/B-3284-2014
OI Pankov, Roumen/0000-0002-3157-3659
FU Bulgarian Fund for Scientific Research [D002-212/08, BY-B-1/05]
FX This work was financially supported by the Bulgarian Fund for Scientific
Research (Grants D002-212/08 and BY-B-1/05).
NR 28
TC 8
Z9 8
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1065-6995
J9 CELL BIOL INT
JI Cell Biol. Int.
PD OCT
PY 2009
VL 33
IS 10
BP 1079
EP 1086
DI 10.1016/j.cellbi.2009.06.024
PG 8
WC Cell Biology
SC Cell Biology
GA 491JA
UT WOS:000269573500006
PM 19589391
ER
PT J
AU Sikdar, N
Banerjee, S
Lee, KY
Wincovitch, S
Pak, E
Nakanishi, K
Jasin, M
Dutra, A
Myung, K
AF Sikdar, Nilabja
Banerjee, Soma
Lee, Kyoo-young
Wincovitch, Stephen
Pak, Evgenia
Nakanishi, Koji
Jasin, Maria
Dutra, Amalia
Myung, Kyungjae
TI DNA damage responses by human ELG1 in S phase are important to maintain
genomic integrity
SO CELL CYCLE
LA English
DT Article
DE ELG1; genome stability; RFC; DNA replication
ID REPLICATION-FACTOR-C; GROSS CHROMOSOMAL REARRANGEMENTS; DOUBLE-STRAND
BREAKS; SACCHAROMYCES-CEREVISIAE; NUCLEAR FOCI; COMPLEX; INSTABILITY;
CANCER; REPAIR; CHECKPOINT
AB Genomic integrity depends on DNA replication, recombination and repair, particularly in S phase. We demonstrate that a human homologue of yeast Elg1 plays an important role in S phase to preserve genomic stability. The level of ELG1 is induced during recovery from a variety of DNA damage. In response to DNA damage, ELG1 forms distinct foci at stalled DNA replication forks that are different from DNA double strand break foci. Targeted gene knockdown of ELG1 resulted in spontaneous foci formation of gamma-H2AX, 53BP1 and phosphorylated-ATM that mark chromosomal breaks. Abnormal chromosomes including fusions, inversions and hypersensitivity to DNA damaging agents were also observed in cells expressing low level of ELG1 by targeted gene knockdown. Knockdown of ELG1 by siRNA reduced homologous recombination frequency in the I-SceI induced double strand break-dependent assay. In contrast, spontaneous homologous recombination frequency and sister chromatin exchange rate were upregulated when ELG1 was silenced by shRNA. Taken together, we propose that ELG1 would be a new member of proteins involved in maintenance of genomic integrity.
C1 [Sikdar, Nilabja; Banerjee, Soma; Lee, Kyoo-young; Myung, Kyungjae] NHGRI, Genome Instabil Sect, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Nakanishi, Koji; Jasin, Maria] Mem Sloan Kettering Canc Ctr, Dev Biol Program, New York, NY 10021 USA.
RP Myung, K (reprint author), NHGRI, Genome Instabil Sect, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
EM kmyung@mail.nih.gov
FU NIH [RO154688]; NHGRI, NIH [HG012003-06]
FX We thank D. Bodine (NHGRI), A. D'Andrea (DFCI), P. Liu (NHGRI), M.
Lichten (NCI), P. Meltzer (NCI) and Y. Shiloh (Tel Aviv U., Israel) for
helpful discussions; J. Taylor (NIEHS) for plasmids; T. Wolfsberg
(NHGRI) for helping sequence analysis, S. Anderson (NHGRI) and M. Kirby
(NHGRI) for FACS analysis; and D. Bodine, S. Burgess (NHGRI), A.
D'Andrea, D. Lim (KAIST, Korea), P. Liu, A. Nussenzweig (NCI), Y.
Shiloh, and members in Myung laboratory for comments on the manuscript;
J. Fekecs (NHGRI) for figure preparation. K. M. especially thanks E.
Cho. This research was supported by an NIH grant (RO154688 to M. J.),
and the intramural research program of the NHGRI, NIH (HG012003-06 to K.
M.).
NR 31
TC 27
Z9 27
U1 0
U2 1
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 2009
VL 8
IS 19
BP 3199
EP 3207
DI 10.4161/cc.8.19.9752
PG 9
WC Cell Biology
SC Cell Biology
GA 502XZ
UT WOS:000270495500028
PM 19755857
ER
PT J
AU Franco, R
Cidlowski, JA
AF Franco, R.
Cidlowski, J. A.
TI Apoptosis and glutathione: beyond an antioxidant
SO CELL DEATH AND DIFFERENTIATION
LA English
DT Review
DE GSH; redox regulation; oxidative stress; thiols; glutathionylation;
glutathione transport
ID INDUCED CELL-DEATH; MITOCHONDRIAL PERMEABILITY TRANSITION;
GLUTAMATE-CYSTEINE LIGASE; STRESS-INDUCED APOPTOSIS;
TUMOR-NECROSIS-FACTOR; ENDOPLASMIC-RETICULUM STRESS; BETA-MEDIATED
NEUROTOXICITY; SUBUNIT GENE-EXPRESSION; PROTEIN S-NITROSYLATION;
CYTOCHROME-C RELEASE
AB Apoptosis is a conserved homeostatic process critical for organ and tissue morphogenesis, development, and senescence. This form of programmed cell death also participates in the etiology of several human diseases including cancer, neurodegenerative, and autoimmune disorders. Although the signaling pathways leading to the progression of apoptosis have been extensively characterized, recent studies highlight the regulatory role of changes in the intracellular milieu (permissive apoptotic environment) in the efficient activation of the cell death machinery. In particular, glutathione (GSH) depletion is a common feature of apoptotic cell death triggered by a wide variety of stimuli including activation of death receptors, stress, environmental agents, and cytotoxic drugs. Although initial studies suggested that GSH depletion was only a byproduct of oxidative stress generated during cell death, recent discoveries suggest that GSH depletion and post-translational modifications of proteins through glutathionylation are critical regulators of apoptosis. Here, we reformulate these emerging paradigms into our current understanding of cell death mechanisms.
C1 [Franco, R.; Cidlowski, J. A.] Natl Inst Environm Hlth Sci, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
RP Cidlowski, JA (reprint author), Natl Inst Environm Hlth Sci, Lab Signal Transduct, NIH, POB 12233,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM cidlows1@mail.nih.gov
RI Franco, Rodrigo/D-9470-2013
OI Franco, Rodrigo/0000-0003-3241-8615
FU Intramural Research Program of the NIH/National Institute of
Environmental Health Oakley
FX This work was supported by the Intramural Research Program of the
NIH/National Institute of Environmental Health Oakley, and Dr. John B
Pritchard critical comments of this manuscript. Owing to space
considerations we apologize for not citing many important contributions
to this field. The supplemental data contain a list of these important
works. Color figures are included in the HTML version of this manuscript
NR 150
TC 254
Z9 261
U1 3
U2 25
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1350-9047
J9 CELL DEATH DIFFER
JI Cell Death Differ.
PD OCT
PY 2009
VL 16
IS 10
BP 1303
EP 1314
DI 10.1038/cdd.2009.107
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 494BU
UT WOS:000269785100001
PM 19662025
ER
PT J
AU Lee, SE
Myung, K
AF Lee, Sang Eun
Myung, Kyungjae
TI Faithful after break-up: suppression of chromosomal translocations
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Review
DE Chromosomal translocation; Double strand break; DNA repair; Homologous
recombination; End joining
ID DOUBLE-STRAND-BREAK; SISTER-CHROMATID RECOMBINATION;
SACCHAROMYCES-CEREVISIAE HOMOLOG; HOLLIDAY JUNCTION RESOLUTION;
MAINTAINS GENOMIC STABILITY; DNA-DAMAGE CHECKPOINT; V(D)J RECOMBINATION;
MITOTIC RECOMBINATION; SGS1 HELICASE; HISTONE H2AX
AB Chromosome integrity in response to chemically or radiation-induced chromosome breaks and the perturbation of ongoing replication forks relies on multiple DNA repair mechanisms. However, repair of these lesions may lead to unwanted chromosome rearrangement if not properly executed or regulated. As these types of chromosomal alterations threaten the cell's and the organism's very own survival, multiple systems are developed to avoid or at least limit break-induced chromosomal rearrangements. In this review, we highlight cellular strategies for repressing DNA break-induced chromosomal translocations in multiple model systems including yeast, mouse, and human. These pathways select proper homologous templates or broken DNA ends for the faithful repair of DNA breaks to avoid undesirable chromosomal translocations.
C1 [Lee, Sang Eun] Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, Inst Biotechnol, San Antonio, TX 78245 USA.
[Myung, Kyungjae] NHGRI, Genome Instabil Sect, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
RP Lee, SE (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, Inst Biotechnol, 15355 Lambda Dr, San Antonio, TX 78245 USA.
EM lees4@uthscsa.edu; kmyung@mail.nih.gov
FU National Institutes of Health [083010]; National Human Genome Research
Institute, NIH; Leukemia and Lymphoma Society Scholar
FX We are grateful to members of the S. Lee and K. Myung's laboratories for
helpful discussions. We also thank to D. Walther and D. Daee for
editorial help and J. Fekecs (NHGRI) for figure preparation. This work
was supported by grants in the National Institutes of Health GM 083010
and the CTRC CDP pilot grants to S. E. L. and the intramural research
program of the National Human Genome Research Institute, NIH to K. M. S.
E. L. is a Leukemia and Lymphoma Society Scholar.
NR 127
TC 10
Z9 10
U1 0
U2 4
PU BIRKHAUSER VERLAG AG
PI BASEL
PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
SN 1420-682X
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD OCT
PY 2009
VL 66
IS 19
BP 3149
EP 3160
DI 10.1007/s00018-009-0068-5
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 496DN
UT WOS:000269949400006
PM 19547915
ER
PT J
AU Gudmundsson, LS
Aspelund, T
Scher, AI
Eliasson, JH
Johannsson, M
Thorgeirsson, G
Launer, LJ
Gudnason, V
AF Gudmundsson, L. S.
Aspelund, T.
Scher, A., I
Eliasson, J. H.
Johannsson, M.
Thorgeirsson, G.
Launer, L. J.
Gudnason, V
TI Migraine, headache and survival in the Reykjavik study
SO CEPHALALGIA
LA English
DT Meeting Abstract
CT 14th Congress of the International-Headache-Society
CY SEP 10-13, 2009
CL Philadelphia, PA
SP Int Headache Soc
C1 [Gudmundsson, L. S.; Johannsson, M.] Univ Iceland, Dept Pharmacol & Toxicol, Reykjavik, Iceland.
[Aspelund, T.; Gudnason, V] Iceland Heart Assoc, Kopavogur, Iceland.
[Scher, A., I] Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, Bethesda, MD USA.
[Thorgeirsson, G.] Univ Iceland, Dept Med, Reykjavik, Iceland.
[Launer, L. J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
Univ Iceland, Fac Med, Reykjavik, Iceland.
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 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0333-1024
J9 CEPHALALGIA
JI Cephalalgia
PD OCT
PY 2009
VL 29
BP 59
EP 59
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 493MW
UT WOS:000269742100144
ER
PT J
AU Zielinski, DS
AF Zielinski, David S.
TI Child maltreatment and adult socioeconomic well-being
SO CHILD ABUSE & NEGLECT
LA English
DT Editorial Material
DE Child maltreatment; Socioeconomic status; Employment; Education;
Long-term outcomes
ID NATIONAL-COMORBIDITY-SURVEY; SEXUAL-ABUSE; PHYSICAL ABUSE;
UNITED-STATES; LABOR-MARKET; GASTROINTESTINAL DISORDERS; ADOLESCENT
VICTIMIZATION; PSYCHIATRIC-DISORDERS; HEALTH CONSEQUENCES; SCHOOL
PERFORMANCE
AB Objective: Little empirical research has examined the impact that child maltreatment may have on victims' long-term socioeconomic well-being. The current study Sought to address this gap by exploring the relationship between childhood experiences of abuse and neglect and several indicators of socioeconomic well-being in adulthood.
Method: Data front the nationally representative National Comorbidity Survey (NCS) (n = 5004) were analyzed using logistic regression models to examine whether maltreatment in childhood (any maltreatment, physical abuse, sexual abuse, severe neglect, and multiple types of maltreatment) affected employment status, income, and health care coverage in adulthood. Several potential confounds of this relationship were Included as covariates in the models, including race, sex, age. and several indicators of childhood socioeconomic status (SES)
Results: The results show that adults who had experienced maltreatment differed significantly from non-maltreated adults across each of the socioeconomic domains examined. Effects were additionally found to differ depending on the number of types of maltreatment experienced
Conclusions: Increased rates Of unemployment, poverty, and Medicaid usage indicate the significant long-term personal impact of early victimization. They also suggest a substantial societal cost from this problem through lost economic productivity and Lax revenue, and increased social spending. Low socioeconomic status among parents has also been identified as a salient risk factor for the perpetration of maltreatment, and, as Such, these results indicate a potential mechanism in the intergenerational transmission of violence.
Practice implications: The findings from this Study suggest that victims of child maltreatment are at increased risk for financial and employment-related difficulties in adulthood. Approximately one million children are identified each year by state agencies as victims of maltreatment in the United States. Many maltreated children, furthermore, go undetected by protective service agencies. indicating the high prevalence of this problem, and under scoring its large economic costs to society By highlighting the long-term socioeconomic costs of maltreatment, this research should encourage policy makers to focus on improving prevention, intervention, and treatment efforts for Victims of abuse and neglect Published by Elsevier Ltd.
C1 NIMH, Off Director, Bethesda, MD 20852 USA.
RP Zielinski, DS (reprint author), NIMH, Off Director, 6001 Execut Bld,Rm 8206, Bethesda, MD 20852 USA.
NR 80
TC 79
Z9 81
U1 11
U2 54
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2134
J9 CHILD ABUSE NEGLECT
JI Child Abuse Negl.
PD OCT
PY 2009
VL 33
IS 10
BP 666
EP 678
DI 10.1016/j.chiabu.2009.09.001
PG 13
WC Family Studies; Psychology, Social; Social Work
SC Family Studies; Psychology; Social Work
GA 512EN
UT WOS:000271227100002
PM 19811826
ER
PT J
AU Johnson, AD
AF Johnson, Andrew D.
TI Single-Nucleotide Polymorphism Bioinformatics A Comprehensive Review of
Resources
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Review
ID GENOME-WIDE ASSOCIATION; SUPPORT VECTOR MACHINES; ALLELIC EXPRESSION
IMBALANCE; GENOTYPE CALLING ALGORITHM; RNA SECONDARY STRUCTURE;
NON-SYNONYMOUS SNPS; WEB-BASED TOOL; COMPLEX TRAITS; MISSENSE
SUBSTITUTIONS; PROTEIN STRUCTURES
C1 NHLBI Framingham Heart Study, Framingham, MA 01702 USA.
RP Johnson, AD (reprint author), NHLBI Framingham Heart Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM johnsonad2@nhlbi.nih.gov
RI Johnson, Andrew/G-6520-2013
FU National Institutes of Health Intramural Research
FX Dr Johnson is supported by a National Institutes of Health Intramural
Research Training Award position within the National Heart, Lung and
Blood Institute.
NR 180
TC 13
Z9 16
U1 1
U2 6
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 2009
VL 2
IS 5
BP 530
EP U289
DI 10.1161/CIRCGENETICS.109.872010
PG 43
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 574HH
UT WOS:000275979500016
PM 20031630
ER
PT J
AU Hunsberger, S
Zhao, YD
Simon, R
AF Hunsberger, Sally
Zhao, Yingdong
Simon, Richard
TI A Comparison of Phase II Study Strategies
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID ADVANCED PANCREATIC-CANCER; SAMPLE-SIZE CONSIDERATIONS; CLINICAL-TRIAL
DESIGNS; GEMCITABINE; OXALIPLATIN; COMBINATION; CARCINOMA; CISPLATIN;
GERCOR; AGENTS
AB The traditional oncology drug development paradigm of single arm phase II studies followed by a randomized phase III study has limitations for modern oncology drug development. Interpretation of single arm phase II study results is difficult when a new drug is used in combination with other agents or when progression-free survival is used as the endpoint rather than tumor shrinkage. Randomized phase II studies are more informative for these objectives but increase both the number of patients and time required to determine the value of a new experimental agent. In this article, we compare different phase II study strategies to determine the most efficient drug development path in terms of number of patients and length of time to conclusion of drug efficacy on overall survival. (Clin Cancer Res 2009;15(19):5950-5)
C1 [Hunsberger, Sally; Zhao, Yingdong; Simon, Richard] NCI, Biometr Res Branch, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
RP Hunsberger, S (reprint author), NCI, Biometr Res Branch, Div Canc Treatment & Diag, 6130 Execut Blvd,EPN 8120,MSC 7434, Bethesda, MD 20892 USA.
EM sallyh@ctep.nci.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 20
TC 21
Z9 21
U1 0
U2 6
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 2009
VL 15
IS 19
BP 5950
EP 5955
DI 10.1158/1078-0432.CCR-08-3205
PG 6
WC Oncology
SC Oncology
GA 502ZC
UT WOS:000270498700003
PM 19789306
ER
PT J
AU Thiele, CJ
Li, ZJ
Mckee, AE
AF Thiele, Carol J.
Li, Zhijie
McKee, Amy E.
TI On Trk-The TrkB Signal Transduction Pathway Is an Increasingly Important
Target in Cancer Biology
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID TYROSINE-KINASE INHIBITOR; CELLS IN-VITRO; NEUROTROPHIC FACTOR
ACTIVATION; PROTECTS NEUROBLASTOMA-CELLS; GROWTH-FACTOR RECEPTOR;
GENE-EXPRESSION; UP-REGULATION; NEURONAL DEVELOPMENT; NTRK1/NGF
RECEPTOR; ANTITUMOR-ACTIVITY
AB In the beginning, Trk was an oncogene. Yet Neurotrophin-Trk signaling came to preeminence in the field of neurobiology. Now it is appreciated that Trks regulate important processes in nonneuronal cells and, in addition to their impact on tumors of neural origin, may contribute to the pathogenesis of carcinomas, myelomas, and prostate and lymphoid tumors. Although mutations and rearrangements of Trk are seen only sporadically in human cancers, such as medullary thyroid carcinoma, a number of recent studies indicate that expression of TrkB contributes to tumor pathology. In neuroblastoma, TrkA expression marks good prognosis which TrkB and Brain-derived neurotrophic factor (BDNF) expression marks poor prognosis. Activation of the BDNF/TrkB signal transduction pathway also stimulates tumor cell survival and angiogenesis and contributes to resistance to cytotoxic drugs and anoikis, enabling cells to acquire many of the characteristic features required for tumorigenesis. Small molecule inhibitors, such as Cephalon's CEP-701, are in phase 1 and 2 clinical trials, and a series of AstraZeneca Trk inhibitors are poised to enter the clinic. As monotherapy, inhibitors may be effective only in tumors with activating Trk mutations. Important clinical follow-up will be the assessment of Trk inhibitors in combination with standard chemo-or radiotherapy or other signal transduction pathway inhibitors. (Clin Cancer Res 2009;15(19):5962-7)
C1 [Thiele, Carol J.; Li, Zhijie; McKee, Amy E.] NCI, Cell & Mol Biol Sect, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Thiele, CJ (reprint author), NCI, Cell & Mol Biol Sect, Pediat Oncol Branch, Ctr Canc Res, 1-3940,10 Ctr Dr MSC 1105, Bethesda, MD 20892 USA.
EM ct47a@nih.gov
FU Intramural NIH HHS [Z01 BC010789-01, Z99 CA999999]
NR 76
TC 101
Z9 107
U1 3
U2 17
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 2009
VL 15
IS 19
BP 5962
EP 5967
DI 10.1158/1078-0432.CCR-08-0651
PG 6
WC Oncology
SC Oncology
GA 502ZC
UT WOS:000270498700005
PM 19755385
ER
PT J
AU Arun, P
Brown, MS
Ehsanian, R
Chen, Z
Van Waes, C
AF Arun, Pattatheyil
Brown, Matthew S.
Ehsanian, Reza
Chen, Zhong
Van Waes, Carter
TI Nuclear NF-kappa B p65 Phosphorylation at Serine 276 by Protein Kinase A
Contributes to the Malignant Phenotype of Head and Neck Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; RI-ALPHA-SUBUNIT; TRANSCRIPTIONAL ACTIVITY;
GENE-EXPRESSION; IKK-BETA; CYCLOOXYGENASE-2 EXPRESSION; SER(276)
PHOSPHORYLATION; RELA PHOSPHORYLATION; ANTITUMOR-ACTIVITY; SIGNALING
PATHWAY
AB Purpose: Aberrant nuclear activation and phosphorylation of the canonical NF-kappa B subunit RELA/p65 at Serine-536 by inhibitor kappa B kinase is prevalent in head and neck squamous cell carcinoma (HNSCC), but the role of other kinases in NF-kappa B activation has not been well defined. Here, we investigated the prevalence and function of p65-Ser276 phosphorylation by protein kinase A (PKA) in the malignant phenotype and gene transactivation, and studied p65-Ser276 as a potential target for therapy.
Experimental Design: Phospho and total p65 protein expression and localization were determined in HNSCC tissue array and in cell lines. The effects of the PKA inhibitor H-89 on NF-kappa B activation, downstream gene expression, cell proliferation and cell cycle were examined. Knockdown of PKA by specific siRNA confirmed the specificity.
Results: NF-kappa B p65 phosphorylated at Ser276 was prevalent in HNSCC and adjacent dysplastic mucosa, but localized to the cytoplasm in normal mucosa. In HNSCC lines, tumor necrosis factor-alpha (TNF-alpha) significantly increased, whereas H-89 inhibited constitutive and TNF-alpha-induced nuclear p65 (Ser276) phosphorylation, and significantly suppressed NF-kappa B and target gene IL-8 reporter activity. Knockdown of PKA by small interfering RNA inhibited NF-kappa B, IL-8, and BCL-XL reporter gene activities. H-89 suppressed cell proliferation, induced cell death, and blocked the cell cycle in G(1)-S phase. Consistent with its biological effects, H-89 down-modulated expression of NF-kappa B-related genes Cyclin D1, BCL2, BCL-XL, COX2, IL-8, and VEGF, as well as induced cell cycle inhibitor p21(CIP1/WAF1), while suppressing proliferative marker Ki67
Conclusions: NF-kappa B p65 (Ser276) phosphorylation by PKA promotes the malignant phenotype and holds potential as a therapeutic target in HNSCC. (Clin Cancer Res 2009;15(19): 5974-84)
C1 [Arun, Pattatheyil; Brown, Matthew S.; Ehsanian, Reza; Chen, Zhong; Van Waes, Carter] Natl Inst Deafness & Other Commun Disorders, Tumor Biol Sect, Head & Neck Surg Branch, NIH, Bethesda, MD USA.
[Ehsanian, Reza] NIH, Howard Hughes Med Inst, Res Scholars Program, Chevy Chase, MD 20815 USA.
RP Van Waes, C (reprint author), NIDCD, NIH, Bldg 10 CRC Rm 4-2732,10 Ctr DR,MSC 1419, Bethesda, MD 20892 USA.
EM chenz@nidcd.nih.gov; vanwaesc@nidcd.nih.gov
FU Howard Hughes Medical Institute; Intramural NIH HHS [Z01 DC000016-14];
NIDCD NIH HHS [Z01 DC000016, Z01 DC000073]
NR 50
TC 37
Z9 38
U1 1
U2 4
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 2009
VL 15
IS 19
BP 5974
EP 5984
DI 10.1158/1078-0432.CCR-09-1352
PG 11
WC Oncology
SC Oncology
GA 502ZC
UT WOS:000270498700007
PM 19789307
ER
PT J
AU Palmieri, D
Lockman, PR
Thomas, FC
Hua, E
Herring, J
Hargrave, E
Johnson, M
Flores, N
Qian, YZ
Vega-Valle, E
Taskar, KS
Rudraraju, V
Mittapalli, RK
Gaasch, JA
Bohn, KA
Thorsheim, HR
Liewehr, DJ
Davis, S
Reilly, JF
Walker, R
Bronder, JL
Feigenbaum, L
Steinberg, SM
Camphausen, K
Meltzer, PS
Richon, VM
Smith, QR
Steeg, PS
AF Palmieri, Diane
Lockman, Paul R.
Thomas, Fancy C.
Hua, Emily
Herring, Jeanne
Hargrave, Elizabeth
Johnson, Matthew
Flores, Natasha
Qian, Yongzhen
Vega-Valle, Eleazar
Taskar, Kunal S.
Rudraraju, Vinay
Mittapalli, Rajendar K.
Gaasch, Julie A.
Bohn, Kaci A.
Thorsheim, Helen R.
Liewehr, David J.
Davis, Sean
Reilly, John F.
Walker, Robert
Bronder, Julie L.
Feigenbaum, Lionel
Steinberg, Seth M.
Camphausen, Kevin
Meltzer, Paul S.
Richon, Victoria M.
Smith, Quentin R.
Steeg, Patricia S.
TI Vorinostat Inhibits Brain Metastatic Colonization in a Model of
Triple-Negative Breast Cancer and Induces DNA Double-Strand Breaks
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID SUBEROYLANILIDE HYDROXAMIC ACID; HISTONE DEACETYLASE INHIBITOR;
REPLICATION PROTEIN-A; CENTRAL-NERVOUS-SYSTEM; IN-VITRO; RAD51
RECOMBINASE; CELLS; BARRIER; DRUGS; SAHA
AB Purpose: As chemotherapy and molecular therapy improve the systemic survival of breast cancer patients, the incidence of brain metastases increases. Few therapeutic strategies exist for the treatment of brain metastases because the blood-brain barrier severely limits drug access. We report the pharmacokinetic, efficacy, and mechanism of action studies for the histone deactylase inhibitor vorinostat (suberoylanilide hydroxamic acid) in a preclinical model of brain metastasis of triple-negative breast cancer.
Experimental Design: The 231-BR brain trophic subline of the MDA-MB-231 human breast cancer cell line was injected into immunocompromised mice for pharmacokinetic and metastasis studies. Pharmacodynamic studies compared histone acetylation, apoptosis, proliferation, and DNA damage in vitro and in vivo.
Results: Following systemic administration, uptake of [(14)C]vorinostat was significant into normal rodent brain and accumulation was up to 3-fold higher in a proportion of metastases formed by 231-BR cells. Vorinostat prevented the development of 231-BR micrometastases by 28% (P = 0.017) and large metastases by 62% (P < 0.0001) compared with vehicle-treated mice when treatment was initiated on day 3 post-injection. The inhibitory activity of vorinostat as a single agent was linked to a novel function in vivo: induction of DNA double-strand breaks associated with the down-regulation of the DNA repair gene Rad52.
Conclusions: We report the first preclinical data for the prevention of brain metastasis of triple-negative breast cancer. Vorinostat is brain permeable and can prevent the formation of brain metastases by 62%. Its mechanism of action involves the induction of DNA double-strand breaks, suggesting rational combinations with DNA active drugs or radiation. (Clin Cancer Res 2009;15(19):6148-57)
C1 [Palmieri, Diane; Hua, Emily; Hargrave, Elizabeth; Johnson, Matthew; Flores, Natasha; Bronder, Julie L.; Steeg, Patricia S.] NCI, Womens Canc Sect, Mol Pharmacol Lab, NIH, Bethesda, MD 20892 USA.
[Liewehr, David J.; Steinberg, Seth M.] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Davis, Sean; Walker, Robert; Meltzer, Paul S.] NCI, Mol Genet Sect, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Camphausen, Kevin] NCI, Imaging & Mol Therapeut Sect, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Lockman, Paul R.; Thomas, Fancy C.; Taskar, Kunal S.; Rudraraju, Vinay; Mittapalli, Rajendar K.; Gaasch, Julie A.; Bohn, Kaci A.; Thorsheim, Helen R.; Smith, Quentin R.] Texas Tech Univ, Hlth Sci Ctr, Sch Pharm, Dept Pharmaceut Sci, Amarillo, TX USA.
[Herring, Jeanne; Qian, Yongzhen; Vega-Valle, Eleazar; Feigenbaum, Lionel] NCI, Lab Anim Sci Program, Sci Applicat Int Corp Frederick, NIH, Frederick, MD 21701 USA.
[Reilly, John F.; Richon, Victoria M.] Merck Res Labs, Boston, MA USA.
RP Palmieri, D (reprint author), 37 Convent Dr,Bldg 37,Room 1122,MSC 4254, Bethesda, MD 20892 USA.
EM palmierd@mail.nih.gov
RI Palmieri, Diane/B-4258-2015;
OI Mason, Julie/0000-0002-5144-175X; Davis, Sean/0000-0002-8991-6458
FU National Cancer Institute; Department of Defense Breast Cancer Research
Program [W81XWH-062-0033]
FX Grant support: Intramural Program of the National Cancer Institute and
Department of Defense Breast Cancer Research Program grant
W81XWH-062-0033.
NR 38
TC 84
Z9 84
U1 2
U2 10
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 2009
VL 15
IS 19
BP 6148
EP 6157
DI 10.1158/1078-0432.CCR-09-1039
PG 10
WC Oncology
SC Oncology
GA 502ZC
UT WOS:000270498700026
PM 19789319
ER
PT J
AU Mathe, EA
Nguyen, GH
Bowman, ED
Zhao, YQ
Budhu, A
Schetter, AJ
Braun, R
Reimers, M
Kumamoto, K
Hughes, D
Altorki, NK
Casson, AG
Liu, CG
Wang, XW
Yanaihara, N
Hagiwara, N
Dannenberg, AJ
Miyashita, M
Croce, CM
Harris, CC
AF Mathe, Ewy A.
Nguyen, Giang Huong
Bowman, Elise D.
Zhao, Yiqiang
Budhu, Anuradha
Schetter, Aaron J.
Braun, Rosemary
Reimers, Mark
Kumamoto, Kensuke
Hughes, Duncan
Altorki, Nasser K.
Casson, Alan G.
Liu, Chang-Gong
Wang, Xin Wei
Yanaihara, Nozomu
Hagiwara, Nobutoshi
Dannenberg, Andrew J.
Miyashita, Masao
Croce, Carlo M.
Harris, Curtis C.
TI MicroRNA Expression in Squamous Cell Carcinoma and Adenocarcinoma of the
Esophagus: Associations with Survival
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID TUMOR-SUPPRESSOR GENE; CANCER; PROFILES; TARGETS; PROLIFERATION;
SIGNATURE; METASTASIS; ACTIVATION; DIAGNOSIS; PROGNOSIS
AB Purpose: The dismal outcome of esophageal cancer patients highlights the need for novel prognostic biomarkers, such as microRNAs (miRNA). Although recent studies have established the role of miRNAs in esophageal carcinoma, a comprehensive multicenter study investigating different histologic types, including squamous cell carcinoma (SCC) and adenocarcinoma with or without Barrett's, is still lacking.
Experimental Design: miRNA expression was measured in cancerous and adjacent noncancerous tissue pairs collected from 100 adenocarcinoma and 70 SCC patients enrolled at four clinical centers from the United States, Canada, and Japan. Microarray-based expression was measured in a subset of samples in two cohorts and was validated in all available samples.
Results: In adenocarcinoma patients, miR-21, miR-223, miR-192, and miR-194 expression was elevated, whereas miR-203 expression was reduced in cancerous compared with noncancerous tissue. In SCC patients, we found elevated miR-21 and reduced miR-375 expression levels in cancerous compared with noncancerous tissue. When comparing cancerous tissue expression between adenocarcinoma and SCC patients, miR-194 and miR-375 were elevated in adenocarcinoma patients. Significantly, elevated miR-21 expression in noncancerous tissue of SCC patients and reduced levels of miR-375 in cancerous tissue of adenocarcinoma patients with Barrett's were strongly associated with worse prognosis. Associations with prognosis were independent of tumor stage or nodal status, cohort type, and chemoradiation therapy.
Conclusions: Our multicenter-based results highlight miRNAs involved in major histologic types of esophageal carcinoma and uncover significant associations with prognosis. Elucidating miRNAs relevant to esophageal carcinogenesis is potentially clinically useful for developing prognostic biomarkers and identifying novel drug targets and therapies. (Clin Cancer Res 2009;15(19):6192-200)
C1 [Mathe, Ewy A.; Nguyen, Giang Huong; Bowman, Elise D.; Zhao, Yiqiang; Budhu, Anuradha; Schetter, Aaron J.; Braun, Rosemary; Kumamoto, Kensuke; Wang, Xin Wei; Yanaihara, Nozomu; Harris, Curtis C.] NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Nguyen, Giang Huong] Howard Hughes Med Inst, NIH, Bethesda, MD 20817 USA.
[Zhao, Yiqiang] Peking Univ, Beijing 100871, Peoples R China.
[Reimers, Mark] Virginia Commonwealth Univ, Dept Biostat, Richmond, VA USA.
[Hughes, Duncan; Altorki, Nasser K.; Dannenberg, Andrew J.] Weill Cornell Med Coll, New York, NY USA.
[Casson, Alan G.] Univ Saskatchewan, Dept Surg, Saskatoon, SK, Canada.
[Liu, Chang-Gong; Croce, Carlo M.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Hagiwara, Nobutoshi; Miyashita, Masao] Nippon Med Sch, Tokyo 113, Japan.
RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, NIH, Bldg 37,Room 3068, Bethesda, MD 20892 USA.
EM harrisc@mail.nih.gov
RI Wang, Xin/B-6162-2009;
OI Braun, Rosemary/0000-0001-9668-9866
FU Intramural Research Program of the National Cancer Institute/NIH, Center
for Cancer Research; Howard Hughes Medical Institute Grant for Graduate
Medical Education; Cancer Prevention Fellowship Program, National Cancer
Institute/NIH; Nova Scotia Health Research Foundation; Canadian Cancer
Society
FX Grant support: Intramural Research Program of the National Cancer
Institute/NIH, Center for Cancer Research; Howard Hughes Medical
Institute Grant for Graduate Medical Education (G.H. Nguyen); Cancer
Prevention Fellowship Program, National Cancer Institute/NIH (R. Braun);
and Nova Scotia Health Research Foundation and National Cancer Institute
of Canada with funds from the Canadian Cancer Society (A.G. Casson).
This study used the high-performance computational capabilities of the
Biowulf Linux cluster at the NIH (http://biowulf.nih.gov).
NR 50
TC 235
Z9 254
U1 3
U2 23
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 2009
VL 15
IS 19
BP 6192
EP 6200
DI 10.1158/1078-0432.CCR-09-1467
PG 9
WC Oncology
SC Oncology
GA 502ZC
UT WOS:000270498700031
PM 19789312
ER
PT J
AU Lin, JQ
Gilbert, J
Rudek, MA
Zwiebel, JA
Gore, S
Jiemjit, A
Zhao, M
Baker, SD
Ambinder, RF
Herman, JG
Donehower, RC
Carducci, MA
AF Lin, Jianqing
Gilbert, Jill
Rudek, Michelle A.
Zwiebel, James A.
Gore, Steve
Jiemjit, Anchalee
Zhao, Ming
Baker, Sharyn D.
Ambinder, Richard F.
Herman, James G.
Donehower, Ross C.
Carducci, Michael A.
TI A Phase I Dose-Finding Study of 5-Azacytidine in Combination with Sodium
Phenylbutyrate in Patients with Refractory Solid Tumors
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID HISTONE DEACETYLASE INHIBITORS; BARR-VIRUS GENOME; DNA METHYLATION;
LEUKEMIA-CELLS; CANCER-THERAPY; DEMETHYLATION; METHYLTRANSFERASE;
INDUCTION; DIFFERENTIATION; MALIGNANCIES
AB Purpose: This was a phase I trial to determine the minimal effective dose and optimal dose schedule for 5-azacytidine (5-AC) in combination with sodium phenylbutyrate in patients with refractory solid tumors. The pharmacokinetics, pharmacodynamics, and antineoplastic effects were also studied.
Experimental Design: Three dosing regimens were studied in 27 patients with advanced solid tumors, and toxicity was recorded. The pharmacokinetics of the combination of drugs was evaluated. Repeat tumor biopsies and peripheral blood mononuclear cells (PBMC) were analyzed to evaluate epigenetic changes in response to therapy. EBV titers were evaluated as a surrogate measure for gene re-expression of epigenetic modulation in PBMC.
Results: The three dose regimens of 5-AC and phenylbutyrate were generally well tolerated and safe. A total of 48 cycles was administrated to 27 patients. The most common toxicities were bone marrow suppression-related neutropenia and anemia, which were minor. The clinical response rate was disappointing for the combination of agents. One patient showed stable disease for 5 months whereas 26 patients showed progressive disease as the best tumor response. The administration of phenylbutyrate and 5-AC did not seem to alter the pharmacokinetics of either drug. Although there were individual cases of targeted DNA methyltransferase activity and histone H3/4 acetylation changes from paired biopsy or PBMC, no conclusive statement can be made based on these limited correlative studies.
Conclusion: The combination of 5-AC and phenylbutyrate across three dose schedules was generally well tolerated and safe, yet lacked any real evidence for clinical benefit. (Clin Cancer Res 2009;15(19):6241-9)
C1 [Lin, Jianqing; Rudek, Michelle A.; Jiemjit, Anchalee; Zhao, Ming; Donehower, Ross C.; Carducci, Michael A.] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Chem Therapeut Program, Baltimore, MD 21231 USA.
[Gilbert, Jill] Vanderbilt Univ, Dept Med Oncol, Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Baker, Sharyn D.] St Jude Childrens Res Hosp, Memphis, TN USA.
[Zwiebel, James A.] NCI, Canc Therapy & Evaluat Program, NIH, Bethesda, MD 20892 USA.
RP Carducci, MA (reprint author), Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Chem Therapeut Program, CRBI 1M59,1650 Orleans St, Baltimore, MD 21231 USA.
EM Carducci@jhmi.edu
FU NCI [UO1-CA70095, P50-CA58236, P30-CA08973]; Prostate Cancer Foundation;
AEGON International Fellowship; National Cancer Institute; NCI CA
Specialized Programs of Research Excellence; AEGON
FX Grant support: NCI UO1-CA70095 (R.C. Donehower and M.A. Carducci), NCI
P50-CA58236 (J.G. Herman and M.A. Carducci), NCI P30-CA08973 (M.A.
Rudek, M.A. Carducci, and R.F. Ambinder), Prostate Cancer Foundation
(M.A. Carducci), AEGON International Fellowship in Oncology (J.
Gilbert), and NCI T32 (J. Lin). This study was sponsored by the Cancer
Therapy Evaluation Program of the National Cancer Institute, NCI CA
Specialized Programs of Research Excellence, and AEGON.
NR 39
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U1 0
U2 4
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 2009
VL 15
IS 19
BP 6241
EP 6249
DI 10.1158/1078-0432.CCR-09-0567
PG 9
WC Oncology
SC Oncology
GA 502ZC
UT WOS:000270498700037
PM 19789320
ER
PT J
AU Ribas, A
Comin-Anduix, B
Chmielowski, B
Jalil, J
de la Rocha, P
McCannel, TA
Ochoa, MT
Seja, E
Villanueva, A
Oseguera, DK
Straatsma, BR
Cochran, AJ
Glaspy, JA
Hui, L
Marincola, FM
Wang, E
Economou, JS
Gomez-Navarro, J
AF Ribas, Antoni
Comin-Anduix, Begona
Chmielowski, Bartosz
Jalil, Jason
de la Rocha, Pilar
McCannel, Tara A.
Ochoa, Maria Teresa
Seja, Elizabeth
Villanueva, Arturo
Oseguera, Denise K.
Straatsma, Bradley R.
Cochran, Alistair J.
Glaspy, John A.
Hui, Liu
Marincola, Francesco M.
Wang, Ena
Economou, James S.
Gomez-Navarro, Jesus
TI Dendritic Cell Vaccination Combined with CTLA4 Blockade in Patients with
Metastatic Melanoma
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID T-CELLS; MONOCLONAL-ANTIBODY; ANTITUMOR IMMUNITY; PEPTIDE VACCINE; TUMOR
LYSATE; IMMUNOTHERAPY; RESPONSES; TRIAL; TREMELIMUMAB; CP-675,206
AB Purpose: Tumor antigen-loaded dendritic cells (DC) are believed to activate antitumor immunity by stimulating T cells, and CTL-associated antigen 4 (CTLA4)-blocking antibodies should release a key negative regulatory pathway on T cells. The combination was tested in a phase I clinical trial in patients with advanced melanoma.
Experimental Design: Autologous DC were pulsed with MART-1(26-35) peptide and administered with a dose escalation of the CTLA4-blocking antibody tremelimumab. Sixteen patients were accrued to five dose levels. Primary end points were safety and immune effects; clinical efficacy was a secondary end point.
Results: Dose-limiting toxicities of grade 3 diarrhea and grade 2 hypophysitis developed in two of three patients receiving tremelimumab at 10 mg/kg monthly. Four patients had an objective tumor response, two partial responses and two complete responses, all melanoma free between 2 and 4 years after study initiation. There was no difference in immune monitoring results between patients with an objective tumor response and those without a response. Exploratory gene expression analysis suggested that immune-related gene signatures, in particular for B-cell function, may be important in predicting response.
Conclusion: The combination of MART-1 peptide-pulsed DC and tremelimumab results in objective and durable tumor responses at the higher range of the expected response rate with either agent alone. (Clin Cancer Res 2009;15(19):6267-76)
C1 [Ribas, Antoni] Univ Calif Los Angeles, Med Ctr, Div Hematol Oncol, Dept Med, Los Angeles, CA 90095 USA.
[Ribas, Antoni; Comin-Anduix, Begona; Jalil, Jason; de la Rocha, Pilar; Cochran, Alistair J.; Economou, James S.] Univ Calif Los Angeles, Dept Surg, Div Surg Oncol, Los Angeles, CA 90095 USA.
[Ribas, Antoni; Cochran, Alistair J.; Glaspy, John A.; Economou, James S.] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA.
[McCannel, Tara A.; Straatsma, Bradley R.] Univ Calif Los Angeles, Dept Ophthalmol, Los Angeles, CA 90095 USA.
[McCannel, Tara A.; Straatsma, Bradley R.] Univ Calif Los Angeles, Jules Stein Eye Inst, Los Angeles, CA 90095 USA.
[Ochoa, Maria Teresa] Univ Calif Los Angeles, Div Dermatol, Dept Med, Los Angeles, CA 90095 USA.
[Cochran, Alistair J.] Univ Calif Los Angeles, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
[Hui, Liu; Marincola, Francesco M.; Wang, Ena] NIH, Infect Dis & Immunogenet Sect, Bethesda, MD 20892 USA.
[Hui, Liu; Marincola, Francesco M.; Wang, Ena] NIH, Ctr Human Immunol, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Gomez-Navarro, Jesus] Pfizer Global Res & Dev, New London, CT USA.
RP Ribas, A (reprint author), Univ Calif Los Angeles, Med Ctr, Div Hematol Oncol, Dept Med, 11-934 Factor Bldg,10833 Conte Ave, Los Angeles, CA 90095 USA.
EM aribas@mednet.ucla.edu
OI Chmielowski, Bartosz/0000-0002-2374-3320
FU Pfizer, Inc; Melanoma Research Foundation; Harry J. Lloyd Charitable
Trust; California Institute for Regenerative Medicine [P50 CA086306, U54
CA119347, RN2-00902-1]; USPHS [M01-RR-0865]; NIH [CA-16042, AI-28697]
FX Grant support: The clinical trial was conducted under a research grant
from Pfizer, Inc. This work was additionally supported by the Melanoma
Research Foundation, the Harry J. Lloyd Charitable Trust, P50 CA086306,
U54 CA119347, and RN2-00902-1 New Faculty Award 2 from the California
Institute for Regenerative Medicine (A. Ribas). The University of
California at Los Angeles General Clinical Research Center is supported
by USPHS grant M01-RR-0865. The University of California at Los Angeles
Flow Cytometry Core Facility is supported by the NIH awards CA-16042 and
AI-28697. 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 46
TC 103
Z9 112
U1 0
U2 4
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 2009
VL 15
IS 19
BP 6267
EP 6276
DI 10.1158/1078-0432.CCR-09-1254
PG 10
WC Oncology
SC Oncology
GA 502ZC
UT WOS:000270498700040
PM 19789309
ER
PT J
AU Rini, BI
Garcia, JA
Cooney, MM
Elson, P
Tyler, A
Beatty, K
Bokar, J
Mekhail, T
Bukowski, RM
Budd, GT
Triozzi, P
Borden, E
Ivy, P
Chen, HX
Dolwati, A
Dreicer, R
AF Rini, Brian I.
Garcia, Jorge A.
Cooney, Matthew M.
Elson, Paul
Tyler, Allison
Beatty, Kristi
Bokar, Joseph
Mekhail, Tarek
Bukowski, R. M.
Budd, G. Thomas
Triozzi, Pierre
Borden, Ernest
Ivy, Percy
Chen, Helen X.
Dolwati, Afshin
Dreicer, Robert
TI A Phase I Study of Sunitinib plus Bevacizumab in Advanced Solid Tumors
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID RENAL-CELL CARCINOMA; ENDOTHELIAL GROWTH-FACTOR; THROMBOTIC
MICROANGIOPATHY; INTERFERON-ALPHA; CANCER; VEGF; ANTIBODY; THERAPY;
TRIAL; PACLITAXEL
AB Purpose: Bevacizumab is an antibody against vascular endothelial growth factor; sunitinib is an inhibitor of vascular endothelial growth factor and related receptors. The safety and maximum tolerated dose of sunitinib plus bevacizumab was assessed in this phase I trial.
Experimental Design: Patients with advanced solid tumors were treated on a 3+3 trial design. Patients received sunitinib daily (starting dose level, 25 mg) for 4 weeks on followed by 2 weeks off and bevacizumab (starting dose level, 5 mg/kg) on days 1, 15, and 29 of a 42-day cycle. Dose-limiting toxicities during the first 6-week cycle were used to determine the maximum tolerated dose.
Results: Thirty-eight patients were enrolled. Patients received a median of 3 cycles of treatment (range, 1-17(+)). There was one dose-limiting toxicity (grade 4 hypertension) at 37.5 mg sunitinib and 5 mg/kg bevacizumab. Grade 3 or greater toxicity was observed in 87% of patients including hypertension (47%), fatigue (24%), thrombocytopenia (18%), proteinuria (13%), and hand-foot syndrome (13%). Dose modifications and delays were common at higher dose levels. No clinical or laboratory evidence of microangiopathic hemolytic anemia was observed. Seven patients had a confirmed Response Evaluation Criteria in Solid Tumors-defined partial response (18%; 95% confidence interval, 8-34%). Nineteen of the 32 patients with a postbaseline scan (59%) had at least some reduction in overall tumor burden (median, 32%; range, 3-73%).
Conclusions: The combination of sunitinib and bevacizumab in patients with advanced solid tumors is feasible, albeit with toxicity at higher dose levels and requiring dose modification with continued therapy. Antitumor activity was observed across multiple solid tumors. (Clin Cancer Res 2009;15(19):6277-83)
C1 [Rini, Brian I.; Garcia, Jorge A.; Elson, Paul; Tyler, Allison; Mekhail, Tarek; Bukowski, R. M.; Budd, G. Thomas; Triozzi, Pierre; Borden, Ernest; Dreicer, Robert] Cleveland Clin, Taussig Canc Inst, Dept Solid Tumor Oncol, Cleveland, OH 44195 USA.
[Cooney, Matthew M.; Beatty, Kristi; Bokar, Joseph; Dolwati, Afshin] Univ Hosp, Ireland Canc Ctr, Case Med Ctr, Cleveland, OH USA.
[Ivy, Percy; Chen, Helen X.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Rini, BI (reprint author), Cleveland Clin, Taussig Canc Inst, Dept Solid Tumor Oncol, 9500 Euclid Ave Desk R35, Cleveland, OH 44195 USA.
EM rinib2@ccf.org
FU Cancer Therapy Evaluation Program [U01CA062502]
FX Grant support: Cancer Therapy Evaluation Program (U01CA062502) through
the Case Comprehensive Cancer Center and Pfizer, Inc.
NR 23
TC 57
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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 2009
VL 15
IS 19
BP 6277
EP 6283
DI 10.1158/1078-0432.CCR-09-0717
PG 7
WC Oncology
SC Oncology
GA 502ZC
UT WOS:000270498700041
PM 19773375
ER
PT J
AU Hancock, H
Dreher, MR
Crawford, N
Pollock, CB
Shih, J
Wood, BJ
Hunter, K
Frenkel, V
AF Hancock, Hilary
Dreher, Matthew R.
Crawford, Nigel
Pollock, Claire B.
Shih, Jennifer
Wood, Bradford J.
Hunter, Kent
Frenkel, Victor
TI Evaluation of pulsed high intensity focused ultrasound exposures on
metastasis in a murine model
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Article
DE Pulsed-high intensity focused ultrasound; Mvt-1; Metastasis; Image
processing; Metastatic burden
ID SOLID TUMORS; LUNG METASTASIS; GROWTH; EXPERIENCE; DELIVERY; CELLS;
MECHANOTRANSDUCTION; ENHANCEMENT; PROGRESSION; EXPRESSION
AB High intensity focused ultrasound (HIFU) may be employed in two ways: continuous exposures for thermal ablation of tissue (> 60A degrees C), and pulsed-exposures for non-ablative effects, including low temperature hyperthermia (37-45A degrees C), and non thermal effects (e.g. acoustic cavitation and radiation forces). Pulsed-HIFU effects may enhance the tissue's permeability for improved delivery of drugs and genes, for example, by opening up gaps between cells in the vasculature and parenchyma. Inducing these effects may improve local targeting of therapeutic agents, however; concerns exist that pulsed exposures could theoretically also facilitate dissemination of tumor cells and exacerbate metastases. In the present study, the influence of pulsed-HIFU exposures on increasing metastatic burden was evaluated in a murine model with metastatic breast cancer. A preliminary study was carried out to validate the model and determine optimal timing for treatment and growth of lung metastases. Next, the effect of pulsed-HIFU on the metastatic burden was evaluated using quantitative image processing of whole-lung histological sections. Compared to untreated controls (2/15), a greater number of mice treated with pulsed-HIFU were found to have lungs "overgrown" with metastases (7/15), where individual metastases grew together such that they could not accurately be counted. Furthermore, area fraction of lung metastases (area of metastases/area of lungs) was similar to 30% greater in mice treated with pulsed-HIFU; however, these differences were not statistically significant. The present study details the development of an animal model for investigating the influence of interventional techniques or exposures (such as pulsed HIFU) on metastatic burden.
C1 [Frenkel, Victor] Natl Inst Hlth, Mol Imaging Lab, Ctr Clin, Dept Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[Crawford, Nigel; Pollock, Claire B.; Hunter, Kent] NCI, Lab Canc Biol & Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Frenkel, V (reprint author), Natl Inst Hlth, Mol Imaging Lab, Ctr Clin, Dept Radiol & Imaging Sci, Bldg 10,Room 1N306A,10 Ctr Dr, Bethesda, MD 20892 USA.
EM vfrenkel@cc.nih.gov
FU Howard Hughes Medical Institute NIH Research Scholars Program; NIH
Clinical Center
FX We would like to thank Dr Arnulfo Mendoza and Ms. Mary Angstadt for
their technical assistance, and Dr Marius Linguraru for helpful
consultations on image processing. This study was supported in part by
Howard Hughes Medical Institute NIH Research Scholars Program (J.S.),
and by the intramural research program of the NIH Clinical Center.
NR 37
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U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 729
EP 738
DI 10.1007/s10585-009-9272-9
PG 10
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300014
PM 19517258
ER
PT J
AU Takahashi, M
Miyazaki, H
Furihata, M
Sakai, H
Konakahara, T
Watanabe, M
Okada, T
AF Takahashi, Munehisa
Miyazaki, Hiroshi
Furihata, Mutsuo
Sakai, Hirofumi
Konakahara, Takeo
Watanabe, Morihiro
Okada, Tomoko
TI Chemokine CCL2/MCP-1 negatively regulates metastasis in a highly bone
marrow-metastatic mouse breast cancer model
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Article
DE CCL2/MCP-1; Breast cancer; Metastasis; ICAM-1
ID MONOCYTE CHEMOATTRACTANT PROTEIN-1; TUMOR-ASSOCIATED MACROPHAGES;
COMPLEX CLASS-II; MELANOMA-CELLS; IN-VIVO; EXPRESSION; GROWTH; INVASION;
INFILTRATION; CARCINOMA
AB Bone is the most frequent site of breast cancer metastasis, and once such metastasis occurs, complete remission is extremely difficult to achieve. In an effort to define the mechanisms underlying metastatic spread of breast cancer to bone, we previously developed and characterized the highly bone metastatic 4T1E/M3 mouse breast cancer cells. We found that following injection into mice, 4T1E/M3 cells exhibited greater bone metastasis and greater in vitro anchorage-independent growth and cell migration than their parental cells (4T1E). We also found that expression of intracellular adhesion molecule-1 (ICAM-1) is crucially involved in these metastatic activities of 4T1E/M3 cells. In the present study, our analysis of gene and protein expression revealed that production of chemokine CCL2 (MCP-1) is dramatically reduced in 4T1E/M3 cells, and that restoration of CCL2 expression in 4T1E/M3 cells diminishes their metastasis to bone and lung. Overexpression of CCL2 in 4T1E/M3 cells significantly reduced not only in vitro anchorage-independent cell growth and cell migration, but also mRNA and cell surface expression of ICAM-1. Conversely, knocking down CCL2 in 4T1E parental cells augmented their metastatic spread to spine and lung. The expression of ICAM-1 was also upregulated in 4T1E-derived CCL2 knockdown cells. Taken together, these results suggest that CCL2 expression may negatively regulate breast cancer metastasis to bone marrow and lung in our model and that expression of ICAM-1 plays a crucial role in that process.
C1 [Takahashi, Munehisa; Sakai, Hirofumi; Okada, Tomoko] Natl Inst Adv Ind Sci & Technol, Neurosci Res Inst, Tsukuba, Ibaraki 3058566, Japan.
[Miyazaki, Hiroshi] Virginia Commonwealth Univ, Philips Inst, Richmond, VA 23298 USA.
[Furihata, Mutsuo] Kochi Med Sch, Dept Pathol, Nanko Ku, Kochi 7838505, Japan.
[Sakai, Hirofumi; Konakahara, Takeo] Tokyo Univ Sci, Fac Sci & Technol, Chiba 2788510, Japan.
[Watanabe, Morihiro] NCI, Expt Immunol Lab, Frederick, MD 21702 USA.
RP Okada, T (reprint author), Natl Inst Adv Ind Sci & Technol, Neurosci Res Inst, 1-1-1 Higashi, Tsukuba, Ibaraki 3058566, Japan.
EM t.okada@aist.go.jp
FU Japan Science and Technology Agency (JST)
FX We thank Dr. Joost J. Oppenheim and Dr. Teizo Yoshimura for critical
reading and comments on the manuscript; Dr. Toru Imamura for access to
equipment used for taking photographs of the tissue sections; and Ms.
Yoko Ezaki for her technical assistance. This work was financially
supported by Japan Science and Technology Agency (JST).
NR 58
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Z9 29
U1 0
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 817
EP 828
DI 10.1007/s10585-009-9281-8
PG 12
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300023
PM 19629725
ER
PT J
AU Lee, JH
Horak, CE
Khanna, C
Meng, ZJ
Yu, LR
Veenstra, TD
Steeg, PS
AF Lee, Jong Heun
Horak, Christine E.
Khanna, Chand
Meng, Zhaojing
Yu, Li Rong
Veenstra, Timothy D.
Steeg, Patricia S.
TI Alterations in Gemin5 expression contribute to alternative mRNA splicing
patterns and tumor cell motility
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Lee, Jong Heun; Horak, Christine E.; Steeg, Patricia S.] NCI, Lab Molecularpharmacol, Bethesda, MD 20892 USA.
[Khanna, Chand] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Meng, Zhaojing; Yu, Li Rong; Veenstra, Timothy D.] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 855
EP 855
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300043
ER
PT J
AU Casey, O
Yin, JJ
Tracy, K
Kelly, K
AF Casey, Orla
Yin, Juan Juan
Tracy, Kirsten
Kelly, Kathleen
TI Gene expression analysis of prostate cancer metastasis to bone
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Casey, Orla; Yin, Juan Juan; Tracy, Kirsten; Kelly, Kathleen] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 857
EP 857
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300049
ER
PT J
AU Barkan, D
Kleinman, H
Simmons, JL
Asmussen, H
Kamaraju, AK
Hoenorhoff, MJ
Liu, ZY
Costes, SV
Cho, EH
Lockett, S
Khanna, C
Chambers, AF
Green, JE
AF Barkan, Dalit
Kleinman, Hynda
Simmons, Justin L.
Asmussen, Holly
Kamaraju, Anil K.
Hoenorhoff, Mark J.
Liu, Zi-yao
Costes, Sylvain V.
Cho, Edward H.
Lockett, Stephen
Khanna, Chand
Chambers, Ann F.
Green, Jeffrey E.
TI Inhibition of metastatic outgrowth from single dormant tumor cells by
targeting the cytoskeleton
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Barkan, Dalit; Simmons, Justin L.; Asmussen, Holly; Kamaraju, Anil K.; Hoenorhoff, Mark J.; Liu, Zi-yao; Khanna, Chand; Green, Jeffrey E.] NCI, Bethesda, MD 20892 USA.
[Kleinman, Hynda] Natl Inst Dent & Craniofacial Res, Bethesda, MD USA.
[Costes, Sylvain V.] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA.
[Cho, Edward H.; Lockett, Stephen] NCI, SAIC Frederick, Frederick, MD 21701 USA.
[Chambers, Ann F.] London Reg Canc Program, London, ON, Canada.
RI Costes, Sylvain/D-2522-2013; Chambers, Ann/L-6285-2015; Cho,
Edward/B-3727-2012
OI Costes, Sylvain/0000-0002-8542-2389; Chambers, Ann/0000-0002-9509-5123;
Cho, Edward/0000-0002-0278-334X
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 867
EP 867
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300075
ER
PT J
AU Olkhanud, P
Damdinsuren, B
Bodogai, M
Baatar, D
Anderson, R
Sen, R
Biragyn, A
AF Olkhanud, Purevdorj
Damdinsuren, Bazarragcha
Bodogai, Monica
Baatar, Dolgor
Anderson, Robin
Sen, Ranjan
Biragyn, Arya
TI Lung metastasis of breast cancer cells is mediated by chemokine receptor
CCR4 but regulated by immune cells
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Olkhanud, Purevdorj; Damdinsuren, Bazarragcha; Bodogai, Monica; Baatar, Dolgor; Sen, Ranjan; Biragyn, Arya] NIA, Baltimore, MD 21224 USA.
[Anderson, Robin] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 867
EP 868
PG 2
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300077
ER
PT J
AU Buquo, L
Khan, MA
Mendoza, A
Hong, SH
Ren, L
Hunter, K
Wakefield, L
Khanna, C
AF Buquo, Lauren
Khan, M. Ali
Mendoza, Arnulfo
Hong, Sung-Hyeok
Ren, Ling
Hunter, Kent
Wakefield, Lalage
Khanna, Chand
TI An ex vivo lung organ culture assay to evaluate therapeutic strategies
directed against pulmonary metastases
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Buquo, Lauren; Khan, M. Ali; Mendoza, Arnulfo; Hong, Sung-Hyeok; Ren, Ling; Hunter, Kent; Wakefield, Lalage; Khanna, Chand] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 869
EP 869
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300081
ER
PT J
AU Fitzgerald, DP
Palmieri, D
Gril, B
Qian, YZ
Vega-Valle, E
Davis, S
Meltzer, PS
Herring, J
Steeg, PS
AF Fitzgerald, Daniel P.
Palmieri, Diane
Gril, Brunilde
Qian, Yongzhen
Vega-Valle, Eleazar
Davis, Sean
Meltzer, Paul S.
Herring, Jeanne
Steeg, Patricia S.
TI Interactions between metastases and the brain microenvironment reveal
potential therapeutic targets for intervention of brain metastasis of
breast cancer
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Fitzgerald, Daniel P.; Palmieri, Diane; Gril, Brunilde; Davis, Sean; Meltzer, Paul S.; Steeg, Patricia S.] NCI, Bethesda, MD 20892 USA.
[Qian, Yongzhen; Vega-Valle, Eleazar; Herring, Jeanne] SAIC Frederick, Frederick, MD USA.
RI Palmieri, Diane/B-4258-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 873
EP 873
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300092
ER
PT J
AU Mendoza, M
Ren, L
Davicioni, E
Wai, D
Triche, T
Khanna, C
AF Mendoza, Martin
Ren, Ling
Davicioni, Elai
Wai, Daniel
Triche, Tim
Khanna, Chand
TI Characterization of the ezrin: CLIC4 interaction in osteosarcoma
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Mendoza, Martin; Ren, Ling; Khanna, Chand] NCI, Bethesda, MD 20892 USA.
[Davicioni, Elai; Wai, Daniel; Triche, Tim] Univ So Calif, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 877
EP 877
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300103
ER
PT J
AU Gril, B
Palmieri, D
Hua, EK
Vega-Valle, E
Herring, J
Feigenbaum, L
Liewehr, DJ
Steinberg, SM
Rubin, SD
Steeg, PS
AF Gril, Brunilde
Palmieri, Diane
Hua, Emily K.
Vega-Valle, Eleazar
Herring, Jeanne
Feigenbaum, Lionel
Liewehr, David J.
Steinberg, Seth M.
Rubin, Stephen D.
Steeg, Patricia S.
TI Lapatinib prevents metastatic colonization of EGFR and Her-2
overexpressing breast cancer cells in the brain
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Gril, Brunilde; Palmieri, Diane; Hua, Emily K.; Liewehr, David J.; Steinberg, Seth M.; Steeg, Patricia S.] NCI, Bethesda, MD 20892 USA.
[Vega-Valle, Eleazar; Herring, Jeanne; Feigenbaum, Lionel] NCI, SAIC, Frederick, MD 21701 USA.
[Rubin, Stephen D.] GlaxoSmithKline Inc, Philadelphia, PA USA.
RI Palmieri, Diane/B-4258-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 880
EP 880
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300111
ER
PT J
AU Sivendran, R
Li, HM
Seo, DW
Stetler-Stevenson, W
AF Sivendran, Renuka
Li, Hongmei
Seo, Dong-wan
Stetler-Stevenson, William
TI A novel cytoplasmic mechanism for the regulation of receptor tyrosine
kinase, VEGFR-2, dimerization
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Sivendran, Renuka; Li, Hongmei; Seo, Dong-wan; Stetler-Stevenson, William] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RI Stetler-Stevenson, William/H-6956-2012
OI Stetler-Stevenson, William/0000-0002-5500-5808
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 884
EP 884
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300122
ER
PT J
AU Kohn, EA
Du, ZJ
Ju, WJ
Bottinger, E
Hooke, CM
Wakefield, LM
AF Kohn, Ethan A.
Du, Zhijun
Ju, Wenjun
Bottinger, Erwin
Hooke, Catherine M.
Wakefield, Lalage M.
TI Smad3 gene dosage differentially impacts multiple TGF-betamediated
biological responses in the mammary epithelium, and influences
metastasis
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Kohn, Ethan A.; Du, Zhijun; Hooke, Catherine M.; Wakefield, Lalage M.] NCI, Bethesda, MD 20892 USA.
[Ju, Wenjun; Bottinger, Erwin] Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 886
EP 887
PG 2
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300129
ER
PT J
AU Moon, HS
Park, JM
Kleinman, HK
AF Moon, Hye-Sung
Park, Jung Min
Kleinman, Hynda K.
TI CXCR4 Expression is regulated by thymosin beta 4 through Akt signal
pathway
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Moon, Hye-Sung; Park, Jung Min] Ewha Womans Univ, Sch Med, Seoul, South Korea.
[Kleinman, Hynda K.] NIDCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 889
EP 889
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300136
ER
PT J
AU Ren, L
Hong, SH
Briggs, J
Xia, A
Cassavaugh, J
Khanna, C
AF Ren, Ling
Hong, Sung-Hyeok
Briggs, Joseph
Xia, Ashley
Cassavaugh, Jessica
Khanna, Chand
TI The regulation of phosphorylation of ezrin at T567 in tumor progression
and metastasis in osteosarcoma
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Ren, Ling; Hong, Sung-Hyeok; Briggs, Joseph; Cassavaugh, Jessica; Khanna, Chand] NCI, Tumor & Metastasis Biol Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Xia, Ashley] NIAID, Off Biomed Informat, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 889
EP 889
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300138
ER
PT J
AU Edwards, C
Finkelstein, D
VanOsdol, S
Kaplan-Singer, B
Belani, K
Hozumi, K
Nomizu, M
Koblinski, JE
AF Edwards, Chevaunne
Finkelstein, David
VanOsdol, Sherlyn
Kaplan-Singer, Benjamin
Belani, Kiran
Hozumi, Kentaro
Nomizu, Motoyoshi
Koblinski, Jennifer E.
TI The laminin-alpha-1 chain derived peptide, AG73, increases breast cancer
metastasis to bone and brain
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Edwards, Chevaunne; Finkelstein, David; Koblinski, Jennifer E.] Northwestern Univ, Chicago, IL 60611 USA.
[VanOsdol, Sherlyn; Kaplan-Singer, Benjamin; Belani, Kiran] NIDCR, Bethesda, MD USA.
[Hozumi, Kentaro; Nomizu, Motoyoshi] Tokyo Univ Pharm & Life Sci, Tokyo, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 895
EP 896
PG 2
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300154
ER
PT J
AU Palmieri, D
Hua, EK
Johnson, MM
Bronder, JL
Qian, YZ
Vega-Valle, E
Herring, J
Liewehr, DJ
Steinberg, SM
Davis, S
Meltzer, PS
Steeg, PS
AF Palmieri, Diane
Hua, Emily K.
Johnson, Matthew M.
Bronder, Julie L.
Qian, Yongzhen
Vega-Valle, Eleazar
Herring, Jeanne
Liewehr, David J.
Steinberg, Seth M.
Davis, Sean
Meltzer, Paul S.
Steeg, Patricia S.
TI Preclinical studies in support of the use of vorinostat (SAHA) for the
treatment of brain metastases of breast cancer
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Palmieri, Diane; Hua, Emily K.; Johnson, Matthew M.; Bronder, Julie L.; Liewehr, David J.; Steinberg, Seth M.; Davis, Sean; Meltzer, Paul S.; Steeg, Patricia S.] NCI, Bethesda, MD 20892 USA.
[Qian, Yongzhen; Vega-Valle, Eleazar; Herring, Jeanne] NCI, SAIC, Frederick, MD USA.
RI Palmieri, Diane/B-4258-2015
NR 0
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 905
EP 906
PG 2
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300181
ER
PT J
AU Yang, YA
Nam, JS
Terabe, M
Kang, MJ
Chae, H
Voong, N
Laurence, A
Michalowska, A
Mamura, M
Lonning, S
Berzofsky, JA
Wakefield, LM
AF Yang, Yu-an
Nam, Jeong-Seok
Terabe, Masaki
Kang, Mi-Jin
Chae, Helen
Voong, Nga
Laurence, Arian
Michalowska, Aleksandra
Mamura, Mizuko
Lonning, Scott
Berzofsky, Jay A.
Wakefield, Lalage M.
TI TGF-beta promotes metastasis number and metastasis size through two
distinct immune-mediated mechanisms
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Yang, Yu-an; Nam, Jeong-Seok; Kang, Mi-Jin; Chae, Helen; Voong, Nga; Michalowska, Aleksandra; Mamura, Mizuko; Wakefield, Lalage M.] NCI, LCBG, CCR, Bethesda, MD 20892 USA.
[Terabe, Masaki; Berzofsky, Jay A.] NCI, Vaccine Branch, Bethesda, MD 20892 USA.
[Laurence, Arian] NCI, Mol Immunol & Inflammat Branch, Bethesda, MD 20892 USA.
[Lonning, Scott] Genzyme Corp, Framingham, MA 01701 USA.
RI Laurence, Arian/A-8770-2009
OI Laurence, Arian/0000-0003-0942-8292
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 908
EP 908
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300188
ER
PT J
AU Yu, YL
Merlino, G
AF Yu, Yanlin
Merlino, Glenn
TI Inhibition of metastasis through a combination of ezrin shRNA and HDAC
inhibitors
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Yu, Yanlin; Merlino, Glenn] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 908
EP 909
PG 2
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300189
ER
PT J
AU Sato, M
Kadota, M
Maxwell, L
Zhang, HE
Clifford, R
Wakefield, L
AF Sato, Misako
Kadota, Mitsutaka
Maxwell, Lee
Zhang, Hongen
Clifford, Robert
Wakefield, Lalage
TI Identification of direct Smad3 target genes mediating the
TGF-beta-dependent metastatic switch
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Sato, Misako; Kadota, Mitsutaka; Maxwell, Lee; Zhang, Hongen; Clifford, Robert; Wakefield, Lalage] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 912
EP 913
PG 2
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300201
ER
PT J
AU Roberts, JD
George, MD
Garcia, MC
Akiyama, SK
Olden, K
AF Roberts, John D.
George, Margaret D.
Garcia, Melissa C.
Akiyama, Steven K.
Olden, Kenneth
TI p38 MAPK regulates multiple pathways during arachidonic acid modulation
of human carcinoma cell adhesion
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Roberts, John D.; George, Margaret D.; Garcia, Melissa C.; Akiyama, Steven K.; Olden, Kenneth] NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 915
EP 915
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300207
ER
PT J
AU Wan, XL
Kim, SY
Choh, Y
Mendoza, A
Currier, D
Li, WJ
Tuan, RS
Khanna, C
Helman, LJ
AF Wan, Xiaolin
Kim, Su Young
Choh, Yeung
Mendoza, Arnulfo
Currier, Duane
Li, Wan-Ju
Tuan, Rocky S.
Khanna, Chand
Helman, Lee J.
TI Beta4 integrin is required for the metastatic phenotype in a murine
model of human osteosarcoma
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Wan, Xiaolin; Kim, Su Young; Choh, Yeung; Mendoza, Arnulfo; Currier, Duane; Khanna, Chand; Helman, Lee J.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Li, Wan-Ju; Tuan, Rocky S.] NIAMSD, Cartilage Biol & Orthoped Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2009
VL 26
IS 7
BP 927
EP 927
PG 1
WC Oncology
SC Oncology
GA 518VE
UT WOS:000271722300239
ER
PT J
AU Palmore, TN
Shah, NL
Loomba, R
Borg, BB
Lopatin, U
Feld, JJ
Khokhar, F
Lutchman, G
Kleiner, DE
Young, NS
Childs, R
Barrett, AJ
Liang, TJ
Hoofnagle, JH
Heller, T
AF Palmore, Tara N.
Shah, Neeral L.
Loomba, Rohit
Borg, Brian B.
Lopatin, Uri
Feld, Jordan J.
Khokhar, Farooq
Lutchman, Glen
Kleiner, David E.
Young, Neal S.
Childs, Richard
Barrett, A. John
Liang, T. Jake
Hoofnagle, Jay H.
Heller, Theo
TI Reactivation of Hepatitis B With Reappearance of Hepatitis B Surface
Antigen After Chemotherapy and Immunosuppression
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION;
OF-THE-LITERATURE; ANTIBODY-POSITIVE DONORS; LOW-DOSE METHOTREXATE;
VERSUS-HOST-DISEASE; VIRUS REACTIVATION; REVERSE SEROCONVERSION;
LIVER-TRANSPLANTATION; LAMIVUDINE THERAPY
AB BACKGROUND & AIMS: HBV infection may reactivate in the setting of immunosuppression, although the frequency and consequences of HBV reactivation are not well known. We report 6 patients who experienced loss of serologic markers of hepatitis B immunity and reappearance of HBsAg in the serum as a result of a variety of acquired immune deficiencies. METHODS: Between 2000 and 2005, six patients with reactivation of hepatitis B were seen in consultation by the Liver Diseases Branch at the Clinical Center, National Institutes of Health. The course and outcome of these 6 patients were reviewed. RESULTS: All 6 patients developed reappearance of HBsAg and evidence of active liver disease after stem cell transplantation (n = 4), immunosuppressive therapy (n = 1), or change in human immunodeficiency virus antiretroviral regimen (n = 1), despite having antibody to HBsAg (anti-HBs) or antibody to hepatitis B core antigen (anti-HBc) without HBsAg before. All 6 patients developed chronic hepatitis B, 2 patients transmitted hepatitis B to their spouses, and 1 patient developed cirrhosis. The diagnosis of hepatitis B reactivation was frequently missed or delayed and often required interruption of the therapy for the underlying condition. None of the patients received antiviral prophylaxis against HBV reactivation. CONCLUSIONS: Serologic evidence of recovery from hepatitis B infection does not preclude its reactivation after immunosuppression. Screening for serologic evidence of hepatitis B and prophylaxis of those with positive results by using nucleoside analogue antiviral therapy should be provided to individuals in whom immunosuppressive therapy is planned.
C1 [Palmore, Tara N.] NIAID, NIH, Bethesda, MD 20892 USA.
[Shah, Neeral L.] Univ Virginia Hlth Syst, Charlottesville, VA USA.
[Loomba, Rohit] Univ Calif San Diego, San Diego, CA 92103 USA.
[Borg, Brian B.] Washington Univ, St Louis, MO USA.
[Lopatin, Uri] Roche Pharmaceut, Nutley, NJ USA.
[Feld, Jordan J.] Univ Toronto, Toronto, ON, Canada.
[Khokhar, Farooq] Chambersburg Gastroenterol Associates LTD, Chambersburg, PA USA.
[Lutchman, Glen] Stanford Univ, Palo Alto, CA 94304 USA.
[Kleiner, David E.] NCI, NIH, Bethesda, MD 20892 USA.
[Young, Neal S.; Childs, Richard; Barrett, A. John] NHLBI, NIH, Bethesda, MD 20892 USA.
[Liang, T. Jake; Hoofnagle, Jay H.; Heller, Theo] NIDDK, NIH, Bethesda, MD USA.
RP Palmore, TN (reprint author), NIAID, NIH, 10 Ctr Dr,MSC 1888, Bethesda, MD 20892 USA.
EM tpalmore@niaid.nih.gov
OI Kleiner, David/0000-0003-3442-4453
FU Intramural Research Programs of the NIDDK [Z01 DK054514-02]; MAID;
NHLBI; NCI; NIH
FX This research was supported by the Intramural Research Programs of the
NIDDK (Z01 DK054514-02), MAID, NHLBI, and NCI, NIH.
NR 66
TC 29
Z9 31
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD OCT
PY 2009
VL 7
IS 10
BP 1130
EP 1137
DI 10.1016/j.cgh.2009.06.027
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 509TR
UT WOS:000271041800022
PM 19577007
ER
PT J
AU Fleg, JL
Howard, BV
Howard, WJ
AF Fleg, Jerome L.
Howard, Barbara V.
Howard, Wm James
TI Lessons in lipid lowering from the Stop Atherosclerosis in Native
Diabetics Study (SANDS)
SO CLINICAL LIPIDOLOGY
LA English
DT Editorial Material
ID CARDIOVASCULAR-DISEASE; LDL CHOLESTEROL; MEDIA THICKNESS; EZETIMIBE;
SURROGATE; PREDICTOR; TRIALS
C1 [Fleg, Jerome L.] NHLBI, Div Cardiovasc Dis, Bethesda, MD 20892 USA.
[Howard, Barbara V.] Medstar Res Inst, Hyattsville, MD USA.
[Howard, Wm James] Washington Hosp Ctr, Washington, DC 20010 USA.
RP Fleg, JL (reprint author), NHLBI, Div Cardiovasc Dis, 6701 Rockledge Dr,Room 8150, Bethesda, MD 20892 USA.
EM flegj@nhlbi.nih.gov
NR 9
TC 0
Z9 0
U1 0
U2 0
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1758-4299
J9 CLIN LIPIDOL
JI Clin. Lipidol.
PD OCT
PY 2009
VL 4
IS 5
BP 523
EP 525
DI 10.2217/CLP.09.17
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 507RI
UT WOS:000270871900001
ER
PT J
AU Roilides, E
Zaoutis, TE
Walsh, TJ
AF Roilides, E.
Zaoutis, T. E.
Walsh, T. J.
TI Invasive zygomycosis in neonates and children
SO CLINICAL MICROBIOLOGY AND INFECTION
LA English
DT Article
CT 1st International Forum on Zygomycosis
CY MAY 30-JUN 01, 2008
CL Athens, GREECE
SP Hellen Soc Med Mycol
DE Cutaneus zygomycosis; gastrointestinal zygomycosis; Mucormycosis;
Rhizopus spp
ID SALVAGE THERAPY; FUNGAL-INFECTIONS; POSACONAZOLE; INFANTS; DISEASE
AB P>Invasive zygomycosis in neonates and children has both similarities to and differences from that in adults. We searched PubMed and individual references for English-language reports of single cases or case series of neonatal (< 1 month) and paediatric (< 18 years) zygomycosis and compared the results with published results in adults. Cases were included if they fulfilled pre-specified criteria. A total of 59 cases of neonatal zygomycosis were reported to July 2007; 157 paediatric cases were published up to 2004 and an additional 30 paediatric cases were reported more recently. Prematurity was a major underlying factor among neonatal cases. The most common manifestations of zygomycosis were gastrointestinal (54%) and cutaneous (36%). This pattern differs from the sinopulmonary and rhinocerebral patterns typical in older children and adults. Overall mortality was 64% in neonates, 56% in children and 53% in adults. A tendency for dissemination was higher in neonates than adults. Dissemination and young age (< 1 year) were independent risk factors for death in children. Most patients who survived received antifungal therapy. Surgery combined with antifungal therapy was a protective factor against death. Most neonates and children who survived had received an amphotericin B formulation. Zygomycosis is a life-threatening infection in children and neonates with differing patterns of involvement in individuals of different ages. The most common management strategy in survivors involved a combination of amphotericin B and surgery.
C1 [Roilides, E.] Aristotle Univ Thessaloniki, Dept Paediat 3, GR-54642 Thessaloniki, Greece.
[Roilides, E.; Walsh, T. J.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Zaoutis, T. E.] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.
[Zaoutis, T. E.] Univ Penn, Ctr Clin Epidemiol & Biostat, Sch Med, Philadelphia, PA 19104 USA.
[Zaoutis, T. E.] Childrens Hosp Philadelphia, Div Infect Dis, Philadelphia, PA 19104 USA.
RP Roilides, E (reprint author), Aristotle Univ Thessaloniki, Dept Paediat 3, Sch Med, Hippokrat Hosp, Konstantinoupoleos 49, GR-54642 Thessaloniki, Greece.
EM roilides@med.auth.gr
NR 23
TC 29
Z9 29
U1 1
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1198-743X
J9 CLIN MICROBIOL INFEC
JI Clin. Microbiol. Infect.
PD OCT
PY 2009
VL 15
BP 50
EP 54
DI 10.1111/j.1469-0691.2009.02981.x
PG 5
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA 493KM
UT WOS:000269735500011
PM 19754758
ER
PT J
AU Bozi, M
Matarin, M
Theocharis, I
Potagas, C
Stefanis, L
AF Bozi, Maria
Matarin, Mar
Theocharis, Ioannis
Potagas, Costas
Stefanis, Leonidas
TI A patient with pantothenate kinase-associated neurodegeneration and
supranuclear gaze palsy
SO CLINICAL NEUROLOGY AND NEUROSURGERY
LA English
DT Article
DE PKAN; PANK2 mutation; Phenotype; Retinopathy; Eye movement
abnormalities; Supranuclear gaze palsy
ID HALLERVORDEN-SPATZ-SYNDROME; BRAIN IRON ACCUMULATION; PANK2 MUTATIONS;
DISEASE; ABNORMALITIES; PARKINSONISM
AB Pantothenate kinase-associated neurodegeneration (PKAN) is a genetic disease with childhood onset characterized clinically by dystonia, parkinsonism, pyramidal signs, visual failure and mental retardation. Progression is usually relentless culminating in severe disability and death within 15 years of onset. Eye movement abnormalities have been described in patients with PKAN including slowed vertical saccades and saccadic vertical pursuit. We here report a patient with PKAN and supranuclear gaze palsy broadening the phenotypic spectrum of the disease. (C) 2009 Published by Elsevier B.V.
C1 [Bozi, Maria; Stefanis, Leonidas] Univ Athens, Sch Med, Dept Neurol 2, GR-11527 Athens, Greece.
[Bozi, Maria] Gen Hosp Syros, Syros, Greece.
[Matarin, Mar] NIA, Mol Genet Unit, NIH, Bethesda, MD 20892 USA.
[Theocharis, Ioannis] Iasso Gen Hosp, Dept Ophthalmol, Athens, Greece.
[Potagas, Costas] Univ Athens, Sch Med, Dept Neurol 1, GR-11527 Athens, Greece.
RP Bozi, M (reprint author), POB 232, GR-84100 Ermoupolis, Syros, Greece.
EM mbozigr@yahoo.gr
RI Matarin, Mar/F-1771-2016
OI Matarin, Mar/0000-0002-4717-5735
NR 16
TC 4
Z9 4
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0303-8467
J9 CLIN NEUROL NEUROSUR
JI Clin. Neurol. Neurosurg.
PD OCT
PY 2009
VL 111
IS 8
BP 688
EP 690
DI 10.1016/j.clineuro.2009.04.007
PG 3
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 496VI
UT WOS:000270007100009
PM 19570605
ER
PT J
AU Camus, M
Ragert, P
Vandermeeren, Y
Cohen, LG
AF Camus, Mickael
Ragert, Patrick
Vandermeeren, Yves
Cohen, Leonardo G.
TI Mechanisms controlling motor output to a transfer hand after learning a
sequential pinch force skill with the opposite hand
SO CLINICAL NEUROPHYSIOLOGY
LA English
DT Article
DE Motor cortex; Intermanual transfer; Interhemispheric inhibition; Pinch
force control
ID TRANSCRANIAL MAGNETIC STIMULATION; REACTION-TIME-TASK; INTERMANUAL
TRANSFER; INTERHEMISPHERIC INHIBITION; INTRACORTICAL INHIBITION;
VISUOMOTOR INFORMATION; CORTICAL PLASTICITY; SPINAL-CORD; CORTEX;
IMPLICIT
AB Objective: Training to perform a serial reaction-time task (procedural motor learning) with one hand results in performance improvements in the untrained as well as in the trained hand, a phenomenon referred to as intermanual transfer. The aim of this study was to investigate the neurophysiological changes associated with intermanual transfer associated with learning to perform an eminently different task involving fine force control within the primary motor cortex (M1). We hypothesized that intermanual transfer of learning Such a task would reveal intracortical changes within M1.
Methods: Speed (time to complete each sequence) and accuracy (% of accuracy errors) of motor performance were measured in both hands before and after right (dominant) hand practice. Transcranial magnetic stimulation (TMS) was used to characterize recruitment curves (RC), short intracortical inhibition (SICI), intracortical facilitation (ICF) and interhemispheric inhibition (IHI) from the left to the right M1.
Results: Practice resulted in significant improvements in both speed and accuracy in the right trained hand and in the left untrained hand. RC increased in the left M1, SICI decreased in both M1s, and IHI from the left to the right M1 decreased. No changes were identified in ICF nor in RC in the right M1.
Conclusions: Our results suggest that some neurophysiological mechanisms operating in the M1 controlling performance of an untrained hand may contribute to optimize the procedure for selecting and implementing correct pinch force levels.
Significance: These results raise the hypothesis of a contribution of modulation of SICI and IHI, or an interaction between both to intermanual transfer after learning a sequential pinch force task. (C) 2009 Published by Elsevier Ireland Ltd. on behalf of International Federation of Clinical Neurophysiology.
C1 [Camus, Mickael; Ragert, Patrick; Vandermeeren, Yves; Cohen, Leonardo G.] NINDS, Human Cort Physiol & Stroke Neurorehabil Sect, NIH, Bethesda, MD 20817 USA.
[Ragert, Patrick] Max Planck Inst Human Cognit & Brain Sci, Dept Cognit Neurol, D-04103 Leipzig, Germany.
[Vandermeeren, Yves] Univ Catholique Louvain, Dept Neurol, Clin Univ UCL Mt Godinne, Louvain, Belgium.
RP Cohen, LG (reprint author), NINDS, Human Cort Physiol & Stroke Neurorehabil Sect, 10 Ctr Dr,MSC 1428,Bldg 10,Rm 5N226, Bethesda, MD 20892 USA.
EM cohenl@ninds.nih.gov
FU National Institutes of Health (NIH); National Institute of Neurological
Disorders and Stroke (NINDS)
FX This research was supported by the Intramural Research Program of the
National Institutes of Health (NIH), National Institute of Neurological
Disorders and Stroke (NINDS).
NR 50
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U2 8
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 2009
VL 120
IS 10
BP 1859
EP 1865
DI 10.1016/j.clinph.2009.08.013
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 522SL
UT WOS:000272018900017
PM 19766535
ER
PT J
AU March, JS
Vitiello, B
AF March, J. S.
Vitiello, B.
TI Benefits Exceed Risks of Newer Antidepressant Medications in Youth-Maybe
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Editorial Material
ID COGNITIVE-BEHAVIORAL THERAPY; RANDOMIZED CONTROLLED-TRIAL; ADOLESCENT
PSYCHOPHARMACOLOGY; DEPRESSION; CHILDREN; COMBINATION; FLUOXETINE;
SUICIDALITY; PSYCHIATRY; SERTRALINE
C1 [March, J. S.] Duke Univ, Med Ctr, Duke Clin Res Inst, Div Neurosci Med, Durham, NC 27710 USA.
[Vitiello, B.] NIMH, NIH, Bethesda, MD 20892 USA.
RP March, JS (reprint author), Duke Univ, Med Ctr, Duke Clin Res Inst, Div Neurosci Med, Durham, NC 27710 USA.
EM john.march@duke.edu
FU NIMH NIH HHS [1R01MH079154, 1 P30 MH66386, 1 U01 MH64107, 1 N01 MH80008,
2R01 MH55121, 1 K24 MH01557]
NR 18
TC 3
Z9 3
U1 3
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 2009
VL 86
IS 4
BP 355
EP 357
DI 10.1038/clpt.2009.172
PG 3
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 500LO
UT WOS:000270303500008
PM 19763113
ER
PT J
AU Miller, FG
Wendler, D
AF Miller, Franklin G.
Wendler, David
TI The ethics of sham invasive intervention trials
SO CLINICAL TRIALS
LA English
DT Editorial Material
C1 [Miller, Franklin G.; Wendler, David] NIH Clin Ctr, Dept Bioeth, Bethesda, MD USA.
RP Miller, FG (reprint author), NIH Clin Ctr, Dept Bioeth, Bethesda, MD USA.
EM dwendler@nih.gov
NR 6
TC 6
Z9 6
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
J9 CLIN TRIALS
JI Clin. Trials
PD OCT
PY 2009
VL 6
IS 5
BP 401
EP 402
DI 10.1177/1740774509344146
PG 2
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 510KD
UT WOS:000271086500001
PM 19846893
ER
PT J
AU Mount, DL
Feeney, P
Fabricatore, AN
Coday, M
Bahnson, J
Byington, R
Phelan, S
Wilmoth, S
Knowler, WC
Hramiak, I
Osei, K
Sweeney, ME
Espeland, MA
AF Mount, David L.
Feeney, Patricia
Fabricatore, Anthony N.
Coday, Mace
Bahnson, Judy
Byington, Robert
Phelan, Suzanne
Wilmoth, Sharon
Knowler, William C.
Hramiak, Irene
Osei, Kwame
Sweeney, Mary Ellen
Espeland, Mark A.
CA Look AHEAD & ACCORD Res Grp
TI Constructing common cohorts from trials with overlapping eligibility
criteria: implications for comparing effect sizes between trials
SO CLINICAL TRIALS
LA English
DT Article
ID HEALTHY RESEARCH VOLUNTEERS; LIFE-STYLE INTERVENTION;
COST-EFFECTIVENESS; CLINICAL-TRIALS; PARTICIPATION; ADULTS; DRUG;
PREVENTION; EXERCISE; BIAS
AB Background Comparing findings from separate trials is necessary to choose among treatment options, however differences among study cohorts may impede these comparisons.
Purpose As a case study, to examine the overlap of study cohorts in two large randomized controlled clinical trials that assess interventions to reduce risk of major cardiovascular disease events in adults with type 2 diabetes in order to explore the feasibility of cross-trial comparisons
Methods The Action for Health in Diabetes (Look AHEAD) and The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trials enrolled 5145 and 10,251 adults with type 2 diabetes, respectively. Look AHEAD assesses the efficacy of an intensive lifestyle intervention designed to produce weight loss; ACCORD tests pharmacological therapies for control of glycemia, hyperlipidemia, and hypertension. Incidence of major cardiovascular disease events is the primary outcome for both trials. A sample was constructed to include participants from each trial who appeared to meet eligibility criteria and be appropriate candidates for the other trial's interventions. Demographic characteristics, health status, and outcomes of members and nonmembers of this constructed sample were compared.
Results Nearly 80% of Look AHEAD participants were projected to be ineligible for ACCORD; ineligibility was primarily due to better glycemic control or no early history of cardiovascular disease. Approximately 30% of ACCORD participants were projected to be ineligible for Look AHEAD, often for reasons linked to poorer health. The characteristics of participants projected to be jointly eligible for both trials continued to reflect differences between trials according to factors likely linked to retention, adherence, and study outcomes.
Limitations Accurate ascertainment of cross-trial eligibility was hampered by differences between protocols.
Conclusions Despite several similarities, the Look AHEAD and ACCORD cohorts represent distinct populations. Even within the subsets of participants who appear to be eligible and appropriate candidates for trials of both modes of intervention,differences remained. Direct comparisons of results from separate trials of lifestyle and pharmacologic interventions are compromised by marked differences in enrolled cohorts. Clinical Trials 2009; 6: 416-429. http://ctj.sagepub.com
C1 [Espeland, Mark A.] Wake Forest Univ, Sch Med, Dept Biostat Sci, Winston Salem, NC 27157 USA.
[Fabricatore, Anthony N.] Univ Penn, Philadelphia, PA 19104 USA.
[Coday, Mace] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Phelan, Suzanne] Miriam Hosp, Providence, RI 02906 USA.
[Knowler, William C.] NIDDK, Diabet Epidemiol & Clin Res Sect, Phoenix, AZ USA.
[Hramiak, Irene] St Josephs Hlth Care, London, ON, Canada.
[Osei, Kwame] Ohio State Univ, Sch Med, Columbus, OH 43210 USA.
[Sweeney, Mary Ellen] Emory Univ, Sch Med Atlanta VAMC, Atlanta, GA 30322 USA.
RP Espeland, MA (reprint author), Wake Forest Univ, Sch Med, Dept Biostat Sci, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM mespelan@wfubmc.edu
FU National Institutes of Health [DK57136, DK57149, DK56990, DK57177,
DK57171, DK57151, DK57182, DK57131, DK57002, DK57078, DK57154, DK57178,
DK57219, DK57008, DK57135, DK56992]; National Institute of Diabetes and
Digestive and Kidney Diseases; National Heart, Lung and Blood Institute
[IAA Y-HC-1010]; National Institute of Nursing Research; National Center
on Minority Health and Health Disparities; Office of Research on Women's
Health; Centers for Disease Control and Prevention; National, Heart,
Lung, and Blood Institute [N01-HC-95178, N01-HC-957179, N01-HC-95181,
N01-HC-95182, N01-HC-95183, N01-HC-95184, IAA Y1-HC-9035]; National Eye
Institute; National Institute on Aging; National Institutes of Diabetes
and Digestive and Kidney Diseases [U01-DK057136-08S1]
FX Look AHEAD is supported by the following cooperative agreements from the
National Institutes of Health; DK57136, DK57149, DK56990, DK57177,
DK57171, DK57151, DK57182, DK57131, DK57002, DK57078, DK57154, DK57178,
DK57219, DK57008, DK57135, and DK56992. The following federal agencies
contributed to its support; National Institute of Diabetes and Digestive
and Kidney Diseases; National Heart, Lung and Blood Institute; National
Institute of Nursing Research, National Center on Minority Health and
Health Disparities, Office of Research on Women's Health, the Intramural
Research Program of the National Institute of Diabetes and Digestive and
Kidney Diseases and the Centers for Disease Control and Prevention. The
following organizations have committed to make major contributions to
Look AHEAD: FedEx Corporation; Health Management Resources; LifeScan,
Inc., a Johnson & Johnson Company, Optifast of Nestle HealthCare
Nutrition, Inc., Hoffmann-La Roche Inc., Abbott Nutrition, and Slim-Fast
Brand of Unilever North America. ACCORD is supported by contract nos.
N01-HC-95178, N01-HC-957179, N01-HC-95181, N01-HC-95182, N01-HC-95183,
N01-HC-95184, IAA # Y1-HC-9035, and IAA # Y-HC-1010 from the National,
Heart, Lung, and Blood Institute, with additional support from the
National Institute of Diabetes and Digestive and Kidney Diseases, the
National Eye Institute, and the National Institute on Aging, the Centers
for Disease Control and Prevention. General Clinical Research Centers
provide support at many sites. Dr. Mount has been supported by
U01-DK057136-08S1 from the National Institutes of Diabetes and Digestive
and Kidney Diseases.
NR 27
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U2 14
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
J9 CLIN TRIALS
JI Clin. Trials
PD OCT
PY 2009
VL 6
IS 5
BP 416
EP 429
DI 10.1177/1740774509344440
PG 14
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 510KD
UT WOS:000271086500003
PM 19737845
ER
PT J
AU Wan, FY
Lenardo, MJ
AF Wan, Fengyi
Lenardo, Michael J.
TI Specification of DNA Binding Activity of NF-kappa B Proteins
SO COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
LA English
DT Article
ID CASEIN KINASE-II; INDUCIBLE NUCLEAR-PROTEIN; OXIDE SYNTHASE EXPRESSION;
NECROSIS-FACTOR-ALPHA; TERMINAL PEST DOMAIN; TRANSCRIPTION FACTOR;
MEDIATED PHOSPHORYLATION; TRANSACTIVATION DOMAIN; NEGATIVE REGULATION;
NITRIC-OXIDE
AB Nuclear factor-kappa B (NF-kappa B) is a pleiotropic mediator of inducible and specific gene regulation involving diverse biological activities including immune response, inflammation, cell proliferation, and death. The fine-tuning of the NF-kappa B DNA binding activity is essential for its fundamental function as a transcription factor. An increasing body of literature illustrates that this process can be elegantly and specifically controlled at multiple levels by different protein subsets. In particular, the recent identification of a non-Rel subunit of NF-kappa B itself provides a new way to understand the selective high-affinity DNA binding specificity of NF-kappa B conferred by a synergistic interaction within the whole complex. Here, we review the mechanism of the specification of DNA binding activity of NF-kappa B complexes, one of the most important aspects of NF-kappa B transcriptional control.
C1 [Wan, Fengyi; Lenardo, Michael J.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Lenardo, MJ (reprint author), NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
EM lenardo@nih.gov
FU National Institutes of Health (NIH), NIAID [K99CA137171]
FX We thank Andrew Snow and Amanda Weaver for critical reading of the
manuscript. The work in the authors' laboratory is supported by the
Intramural Research Program of the National Institutes of Health (NIH),
NIAID. F. W. is a recipient of NIH grant K99CA137171. We apologize to
those who made also important contributions to the issues discussed and
who could not be cited because of space limits.
NR 99
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U1 0
U2 3
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI WOODBURY
PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
SN 1943-0264
J9 CSH PERSPECT BIOL
JI Cold Spring Harbor Perspect. Biol.
PD OCT
PY 2009
VL 1
IS 4
AR a000067
DI 10.1101/cshperspect.a000067
PG 16
WC Cell Biology
SC Cell Biology
GA 625FG
UT WOS:000279879500002
PM 20066093
ER
PT J
AU Ramanathan, M
Luckarift, HR
Sarsenova, A
Wild, JR
Ramanculov, EK
Olsen, EV
Simonian, AL
AF Ramanathan, Madhumati
Luckarift, Heather R.
Sarsenova, Ainur
Wild, James R.
Ramanculov, Erlan K.
Olsen, Eric V.
Simonian, Aleksandr L.
TI Lysozyme-mediated formation of protein-silica nano-composites for
biosensing applications
SO COLLOIDS AND SURFACES B-BIOINTERFACES
LA English
DT Article
DE Lysozyme; Silicification; Silica; OPH; Array biosensor; Paraoxon
ID TIO2 THIN-FILMS; ARRAY BIOSENSOR; ENZYME; FLUORESCENCE; BIOSILICA;
PEPTIDES; TITANIA; SURFACE
AB We demonstrate a rapid method for enzyme immobilization directly on a waveguide surface by encapsulation in a silica matrix. Organophosphate hydrolase (OPH). an enzyme that catalytically hydrolyzes organophosphates, was used as a model enzyme to demonstrate the utility of lysozyme-mediated silica formation for enzyme stabilization. Silica morphology and the efficiency of OPH encapsulation were directly influenced by the precursor choice used in silica formation. Covalent attachment of the lysozyme template directly to the waveguide surface provided a stable basis for silica formation and significantly increased the surface area for OPH encapsulation. OPH conjugated to a pH-responsive fluorophore was encapsulated in silica and patterned to a waveguide surface to demonstrate the immobilization strategy for the development of an organophosphate array biodetector. Silica-encapsulated OPH retained its catalytic activity for nearly 60 days with a detection limit of paraoxon of similar to 35 mu M. The encapsulation technique provides a potentially versatile tool with specific application to biosensor development. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Simonian, Aleksandr L.] Auburn Univ, Samuel Ginn Coll Engn, Mat Res & Educ Ctr, Wilmore Labs 274, Auburn, AL 36849 USA.
[Luckarift, Heather R.] USAF, Res Lab, Tyndall AFB, FL 32403 USA.
[Luckarift, Heather R.] Universal Technol Corp, Dayton, OH 45432 USA.
[Sarsenova, Ainur; Ramanculov, Erlan K.] Natl Ctr Biotechnol Republ Kazakhstan, Astana 010000, Kazakhstan.
[Wild, James R.] Texas A&M Univ, Dept Biochem & Biophys, College Stn, TX 77843 USA.
[Olsen, Eric V.] 81st Med Grp, Clin Res Facil, Keesler AFB, MS 39534 USA.
RP Simonian, AL (reprint author), Auburn Univ, Samuel Ginn Coll Engn, Mat Res & Educ Ctr, Wilmore Labs 274, Auburn, AL 36849 USA.
EM simonal@auburn.edu
RI Ramanculov, Erlan/E-2823-2013
FU NSF [CTS-0330189]
FX The authors would like to acknowledge Glenn R. Johnson (Airforce
Research Laboratory)for his useful suggestions. This work was supported
by NSF under the Grant CTS-0330189, by NC13 of Republic of Kazakhstan
Grant #65, by USAF SG approved Clinical Investigation FDG20060049N and
USAF CRADA 08-272-60MDG-CRADA01, and by the USDA-CSREES under grant
2006-34394-16953. Additionally, this material was based on work which
supported A ' L ' S ' by the National Science Foundation, while working
at the Foundation. Any opinion, finding, and conclusions or
recommendations expressed in this material are those of the authors and
do not necessarily reflect the views of the National Science Foundation,
the United States Air Force, Department of Defense, or the U.S.
Government.
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U1 2
U2 30
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0927-7765
J9 COLLOID SURFACE B
JI Colloid Surf. B-Biointerfaces
PD OCT 1
PY 2009
VL 73
IS 1
BP 58
EP 64
DI 10.1016/j.colsurfb.2009.04.024
PG 7
WC Biophysics; Chemistry, Physical; Materials Science, Biomaterials
SC Biophysics; Chemistry; Materials Science
GA 479KF
UT WOS:000268657500009
PM 19481427
ER
PT J
AU Ghosh, P
Huang, L
Yu, BB
Tiwari, RC
AF Ghosh, Pulak
Huang, Lan
Yu, Binbing
Tiwari, Ram C.
TI Semiparametric Bayesian approaches to joinpoint regression for
population-based cancer survival data
SO COMPUTATIONAL STATISTICS & DATA ANALYSIS
LA English
DT Article
ID DIRICHLET PROCESS PRIOR; NONPARAMETRIC PROBLEMS; MODELS; RATES;
BREAKTHROUGH; SELECTION; MIXTURES; PRIORS; POINT
AB According to the American Cancer Society report (1999), cancer surpasses heart disease as the leading cause of death in the United States of America (USA) for people of age less than 85. Thus, medical research in cancer is an important public health interest. Understanding how medical improvements are affecting cancer incidence, mortality and survival is critical for effective cancer control. In this paper, we study the cancer survival trend on the population level cancer data. In particular, we develop a parametric Bayesian joinpoint regression model based on a Poisson distribution for the relative survival. To avoid identifying the cause of death, we only conduct analysis based on the relative survival. The method is further extended to the semiparametric Bayesian joinpoint regression models wherein the parametric distributional assumptions of the joinpoint regression models are relaxed by modeling the distribution of regression slopes using Dirichlet process mixtures. We also consider the effect of adding covariates of interest in the joinpoint model. Three model selection criteria, namely, the conditional predictive ordinate (CPO), the expected predictive deviance (EPD), and the deviance information criteria (DIC), are used to select the number of joinpoints. We analyze the grouped survival data for distant testicular cancer from the Surveillance, Epidemiology, and End Results (SEER) Program using these Bayesian models. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Ghosh, Pulak] Georgia State Univ, Dept Math & Stat, Atlanta, GA 30303 USA.
[Huang, Lan] NCI, Stat Res & Applicat Branch, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Yu, Binbing] NIA, Bethesda, MD 20892 USA.
[Tiwari, Ram C.] US FDA, Off Biostat, Silver Spring, MD USA.
RP Ghosh, P (reprint author), Georgia State Univ, Dept Math & Stat, Atlanta, GA 30303 USA.
EM pulakghosh@gmail.com
FU National Institutes of Health (NIH) [263-MQ-610994]; Intramural Research
Program of the National Institute on Aging
FX The views expressed by the last author do not necessarily reflect those
of the FDA and NCL The research of Dr. Ghosh was supported in part by
National Institutes of Health (NIH) contract 263-MQ-610994. Dr. Yu was
supported in part by the Intramural Research Program of the National
Institute on Aging.
NR 43
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U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-9473
J9 COMPUT STAT DATA AN
JI Comput. Stat. Data Anal.
PD OCT 1
PY 2009
VL 53
IS 12
BP 4073
EP 4082
DI 10.1016/j.csda.2009.04.011
PG 10
WC Computer Science, Interdisciplinary Applications; Statistics &
Probability
SC Computer Science; Mathematics
GA 504NV
UT WOS:000270624600014
PM 22210971
ER
PT J
AU Richmond, JQ
Reid, DT
Ashton, KG
Zamudio, KR
AF Richmond, Jonathan Q.
Reid, Duncan T.
Ashton, Kyle G.
Zamudio, Kelly R.
TI Delayed genetic effects of habitat fragmentation on the ecologically
specialized Florida sand skink (Plestiodon reynoldsi)
SO CONSERVATION GENETICS
LA English
DT Article
DE Habitat fragmentation; Skink; Ecological specialization; Genetic
inertia; Plestiodon reynoldsi
ID POPULATION-STRUCTURE; EXTINCTION DEBT; MICROSATELLITE LOCI;
NEOSEPS-REYNOLDSI; SPECIES RESPONSES; COMPUTER-PROGRAM; SCRUB HABITAT;
LIFE-HISTORY; MANTEL TEST; PINE SCRUB
AB Populations rarely show immediate genetic responses to habitat fragmentation, even in taxa that possess suites of traits known to increase their vulnerability to extinction. Thus conservation geneticists must consider the time scale over which contemporary evolutionary processes operate to accurately portray the effects of habitat isolation. Here, we examine the genetic impacts of fragmentation on the Florida sand skink Plestiodon reynoldsi, a sand swimming lizard that is highly adapted to the upland scrub habitat of central Florida. We studied fragments located on the southern Lake Wales Ridge, where human activity in the latter half of the 20th century has modified the natural patchiness of the landscape. Based on a relaxed molecular clock method, we estimate that sand skinks have persisted in this region for approximately 1.5 million years and that the time frame of human disturbance is equivalent to fewer than 30 skink generations. Using genotypes from eight microsatellite loci, we screened for molecular signatures of this disturbance by assessing congruence between population structure, as inferred from spatially-informed Bayesian assignment tests, and the current geography of scrub fragments. We also tested for potential intrapopulation genetic effects of inbreeding in isolated populations by comparing the average pairwise relatedness of individuals within fragments of different areas and isolation. Our results indicate that although some patches show a higher degree of relatedness than expected under random mating, the genetic effects of recent isolation are not evident in this part of the species' range. We argue that this result is an artefact of a time-lag in the response to disturbance, and that species-typical demographic features may explain the genetic inertia observed in these populations.
C1 [Richmond, Jonathan Q.; Reid, Duncan T.; Zamudio, Kelly R.] Cornell Univ, Dept Ecol & Evolutionary Biol, Ithaca, NY 14850 USA.
[Reid, Duncan T.] NIH, Bethesda, MD 20892 USA.
[Ashton, Kyle G.] Archbold Biol Stn, Lake Placid, FL 33862 USA.
RP Richmond, JQ (reprint author), Cornell Univ, Dept Ecol & Evolutionary Biol, Ithaca, NY 14850 USA.
EM jqr2@cornell.edu
RI Zamudio, Kelly/R-3533-2016
OI Zamudio, Kelly/0000-0001-5107-6206
FU National Science Foundation [DEB 9907798]; Cornell College of Arts and
Sciences (KZ)
FX We thank A. Knipps, B. Branciforte, B. Meneken, J. Zipser, and
volunteers from the Earthwatch Institute for help with fieldwork, S.
Bogdanowicz for help with microsatellite development, and R. Pickert for
assistance with GIS landscape modelling. H. Mushinsky provided
constructive comments on the manuscript. We also thank H. Swain for
providing support with field efforts and landscape modelling at the
Archbold Biological Station. O. Franc, ois provided valuable advice
concerning the HMRF models. R. Bukowski facilitated the use of computer
resources at the Computational Biology Service Unit (Cornell University)
that receives partial funding from Microsoft. This study was funded by
research grants from: Archbold Biological Station, the Florida Fish and
Wildlife Conservation Commission, and the Earthwatch Institute (KGA);
the Cornell Hughes Scholars Program, Sigma Xi Grants in Aid of Research,
Einhorn Discovery Grant, and the Cornell Undergraduate Board (DTR); and
the National Science Foundation (DEB 9907798) and Cornell College of
Arts and Sciences (KZ).
NR 98
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PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1566-0621
J9 CONSERV GENET
JI Conserv. Genet.
PD OCT
PY 2009
VL 10
IS 5
BP 1281
EP 1297
DI 10.1007/s10592-008-9707-x
PG 17
WC Biodiversity Conservation; Genetics & Heredity
SC Biodiversity & Conservation; Genetics & Heredity
GA 505YF
UT WOS:000270737400009
ER
PT J
AU Perez, MA
Cohen, LG
AF Perez, Monica A.
Cohen, Leonardo G.
TI Scaling of motor cortical excitability during unimanual force generation
SO CORTEX
LA English
DT Article
DE Primary motor cortex; Transcranial magnet stimulation; Voluntary
movement; Force; Bilateral movements
ID TRANSCRANIAL MAGNETIC STIMULATION; FUNCTIONAL MRI; CORTEX; HUMANS;
MUSCLE; AREAS; HAND; FACILITATION; CONTRACTION; OUTPUT
AB During performance of a unimanual force generation task primary motor cortices (M1s) experience clear functional changes. Here, we evaluated the way in which M1s interact during parametric increases in right wrist flexion force in healthy volunteers. We measured the amplitude and the slope of motor evoked potentials (MEP) recruitment curves to transcranial magnetic stimulation (TMS) in the left and right flexor carpi radialis (FCR) muscles at rest and during 10%, 30% and 70% of maximal wrist flexion force. At rest, no differences were observed in the amplitude and slope of MEP recruitment curves in the left and right FCR muscles. With increasing right wrist flexion force, MEP amplitudes increased in both FCR muscles, with larger amplitudes in the right FCR. We found a significant correlation between the left and right MEP amplitudes across conditions. The slope of right and left FCR MEP recruitment curve was significantly steeper at 70% of force compared to rest and 10% of force. A significant correlation between the slope of left and right FCR MEP amplitudes was found at 70% of force only. our results indicate a differential scaling of excitability in the corticospinal system controlling right and left FCR muscles at increasing levels of unimanual force generation. Specifically, these data highlights that at strong levels of unimanual force the increases in motor cortical excitability with increasing TMS stimulus intensities follow a similar pattern in both M1s, while at low levels of force they do not. (C) 2009 Elsevier Srl. All rights reserved.
C1 [Perez, Monica A.] Natl Inst Neurol Disorders & Stroke, Human Cort Physiol Sect, Natl Inst Hlth, Bethesda, MD USA.
Natl Inst Neurol Disorders & Stroke, Stroke Neurorehabil Clin, Natl Inst Hlth, Bethesda, MD USA.
RP Perez, MA (reprint author), Natl Inst Neurol Disorders & Stroke, Human Cort Physiol Sect, Natl Inst Hlth, 10 Ctr Dr, Bethesda, MD USA.
EM perezmo@pitt.edu
FU NIH; NINDS
FX This research was supported (in part) by the Intramural Research Program
of the NIH, NINDS.
NR 28
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U1 1
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PU ELSEVIER MASSON
PI MILANO
PA VIA PALEOCAPA 7, 20121 MILANO, ITALY
SN 0010-9452
J9 CORTEX
JI Cortex
PD OCT
PY 2009
VL 45
IS 9
BP 1065
EP 1071
DI 10.1016/j.cortex.2008.12.006
PG 7
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 489YD
UT WOS:000269461800007
PM 19243741
ER
PT J
AU Prinz, WA
Hinshaw, JE
AF Prinz, William A.
Hinshaw, Jenny E.
TI Membrane-bending proteins
SO CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Review
DE Membrane; bending; curvature; bilayer; binding
ID CLATHRIN-MEDIATED ENDOCYTOSIS; MITOCHONDRIAL CRISTAE MORPHOLOGY;
CORTICAL ENDOPLASMIC-RETICULUM; GUANINE-NUCLEOTIDE EXCHANGE; PLECKSTRIN
HOMOLOGY DOMAIN; DIMERIC ATP SYNTHASE; ESCRT-III COMPLEX; STRUCTURAL
BASIS; PLASMA-MEMBRANE; COPII VESICLE
AB Cellular membranes can assume a number of highly dynamic shapes. Many cellular processes also require transient membrane deformations. Membrane shape is determined by the complex interactions of proteins and lipids. A number of families of proteins that directly bend membranes have been identified. Most associate transiently with membranes and deform them. These proteins work by one or more of three types of mechanisms. First, some bend membranes by inserting amphipathic domains into one of the leaflets of the bilayer; increasing the area of only one leaflet causes the membrane to bend. Second, some proteins form a rigid scaffold that deforms the underlying membrane or stabilizes an already bent membrane. Third, some proteins may deform membranes by clustering lipids or by affecting lipid ordering in membranes. Still other proteins may use novel but poorly understood mechanisms. In this review, we summarize what is known about how different families of proteins bend membranes.
C1 [Prinz, William A.; Hinshaw, Jenny E.] NIDDK, Lab Cell Biochem & Biol, NIH, Bethesda, MD 20892 USA.
RP Prinz, WA (reprint author), NIDDK, Lab Cell Biochem & Biol, NIH, 8 Ctr Dr, Bethesda, MD 20892 USA.
EM wprinz@helix.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases
FX This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases.
NR 147
TC 21
Z9 21
U1 1
U2 7
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 1040-9238
J9 CRIT REV BIOCHEM MOL
JI Crit. Rev. Biochem. Mol. Biol.
PD OCT
PY 2009
VL 44
IS 5
BP 278
EP 291
DI 10.1080/10409230903183472
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 614KK
UT WOS:000279057100003
PM 19780639
ER
PT J
AU Drazen, JM
Van Der Weyden, MB
Sahni, P
Rosenberg, J
Marusic, A
Laine, C
Kotzin, S
Horton, R
Hebert, PC
Haug, C
Godlee, F
Frizelle, FA
de Leeuw, PW
DeAngelis, CD
AF Drazen, Jeffrey M.
Van Der Weyden, Martin B.
Sahni, Peush
Rosenberg, Jacob
Marusic, Ana
Laine, Christine
Kotzin, Sheldon
Horton, Richard
Hebert, Paul C.
Haug, Charlotte
Godlee, Fiona
Frizelle, Frank A.
de Leeuw, Peter W.
DeAngelis, Catherine D.
TI Uniform Format for Disclosure of Competing Interests in ICMJE Journals
SO CROATIAN MEDICAL JOURNAL
LA English
DT Editorial Material
C1 [Kotzin, Sheldon] Natl Lib Med, Bethesda, MD 20894 USA.
RI Marusic, Ana/E-7683-2013;
OI Marusic, Ana/0000-0001-6272-0917; Sahni, Peush/0000-0002-6910-062X
NR 0
TC 4
Z9 4
U1 0
U2 1
PU MEDICINSKA NAKLADA
PI ZAGREB
PA VLASKA 69, HR-10000 ZAGREB, CROATIA
SN 0353-9504
J9 CROAT MED J
JI Croat. Med. J.
PD OCT
PY 2009
VL 50
IS 5
BP 427
EP 428
DI 10.3325/cmj.2009.50.427
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 516WT
UT WOS:000271574700002
PM 19839065
ER
PT J
AU Holliday, BG
AF Holliday, Bertha Garrett
TI The History and Visions of African American Psychology: Multiple
Pathways to Place, Space, and Authority
SO CULTURAL DIVERSITY & ETHNIC MINORITY PSYCHOLOGY
LA English
DT Review
DE African American/Black history; psychology; professional associations;
intellectual history
ID MULTICULTURAL COUNSELING COMPETENCES; ASSOCIATION; EDUCATION; BOARD; APA
AB The author describes the multiple pathways of events and strategies that served to nurture African American psychology in the United States. Special attention is given to strategies for inclusion and empowerment used in 4 psychological professional and scholarly associations: the American Counseling Association, the American Psychological Association, the Association of Black Psychologists, and the Society for Research in Child Development. In addition, the author describes 4 major intellectual traditions that informed not only the strategic,, of inclusion but also the theoretical, research, and intervention perspectives and other professional and academic efforts of African American psychologists. Those perspectives are the Afrocentric/African-centered tradition derived front longstanding nationalist/Pan-African and culturally centered traditions within African American communities: the social contextual/multidisciplinary research tradition of the University of Chicago School of Social Science: the empirical social science research tradition of the University of Michigan; and the Black scholar/activist tradition of Howard University. This article also presents a chronological timeline of major events in the history of African American psychology.
C1 [Holliday, Bertha Garrett] Amer Psychol Assoc, Off Ethn Minor Affairs, Washington, DC 20002 USA.
[Holliday, Bertha Garrett] NIGMS, NIH, Bethesda, MD 20892 USA.
RP Holliday, BG (reprint author), Amer Psychol Assoc, Off Ethn Minor Affairs, 750 1st St NE, Washington, DC 20002 USA.
EM bholliday@apa.org
NR 111
TC 6
Z9 6
U1 1
U2 8
PU EDUCATIONAL PUBLISHING FOUNDATION
PI WASHINGTON
PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA
SN 1099-9809
J9 CULT DIVERS ETHN MIN
JI Cult. Divers. Ethn. Minor. Psychol.
PD OCT
PY 2009
VL 15
IS 4
BP 317
EP 337
DI 10.1037/a0016971
PG 21
WC Ethnic Studies; Psychology, Social
SC Ethnic Studies; Psychology
GA 520DF
UT WOS:000271819500002
PM 19916668
ER
PT J
AU Myslobodsky, M
AF Myslobodsky, Michael
TI The Paradox of Caffeine-Zolpidem Interaction: A Network Analysis
SO CURRENT DRUG TARGETS
LA English
DT Review
DE Antioxidants; oxidative stress; sleep disorders; melatonin; GABA(A)beta
3 receptor; networks; polypharmacology
ID EXTRACELLULAR ADENOSINE LEVELS; POSSIBLE GABAERGIC MODULATION;
LITHIUM-PILOCARPINE MODEL; ACUTE ISCHEMIC-STROKE; NITRIC-OXIDE; GABA(A)
RECEPTORS; ANTIOXIDANT ACTIVITY; COFFEE CONSUMPTION; PARKINSONS-DISEASE;
SLEEP-DEPRIVATION
AB A widely prescribed and potent short-acting hypnotic, zolpidem has become the mainstay for the treatment of middle-of-the-night sleeplessness. It is expected to be antagonized by caffeine. Paradoxically, in some cases caffeine appears to slightly enhance zolpidem sedation. The pharmacokinetic and pharmacodynamic nature of this odd effect remains unexplored. The purpose of this study is to reproduce a hypothetical molecular network recruited by caffeine when co-administered with zolpidem using Ingenuity Pathway Analysis. Thus generated, network drew attention to several possible contributors to caffeine sedation, such as tachykinin precursor 1, cannabinoid, and GABA receptors. The present overview is centered on the possibility that caffeine potentiation of zolpidem sedation does not involve a centralized interaction of specific neurotransmitters, but rather is contributed by its antioxidant capacity. It is proposed that by modifying the cellular redox state, caffeine ultimately reduces the pool of reactive oxygen species, thereby increasing the bioavailability of endogenous melatonin for interaction with zolpidem. This side effect of caffeine encourages further studies of multiple antioxidants as an attractive way to potentially increasing somnolence.
C1 [Myslobodsky, Michael] NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA.
[Myslobodsky, Michael] Howard Univ, Grad Sch, Washington, DC 20059 USA.
RP Myslobodsky, M (reprint author), NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA.
EM myslobom@mail.nih.gov
NR 121
TC 2
Z9 2
U1 1
U2 5
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 2009
VL 10
IS 10
BP 1009
EP 1020
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 514FU
UT WOS:000271380500008
PM 19860644
ER
PT J
AU Oyelaran, O
Gildersleeve, JC
AF Oyelaran, Oyindasola
Gildersleeve, Jeffrey C.
TI Glycan arrays: recent advances and future challenges
SO CURRENT OPINION IN CHEMICAL BIOLOGY
LA English
DT Review
ID POLYSACCHARIDE MICROARRAY TECHNOLOGY; CARBOHYDRATE MICROARRAYS;
BURKHOLDERIA-PSEUDOMALLEI; PROTEIN INTERACTIONS; QUANTITATIVE-ANALYSIS;
FUNCTIONAL GLYCOMICS; BACILLUS-ANTHRACIS; PHASE SYNTHESIS; ONE-STEP;
SURFACE
AB Carbohydrate arrays, also referred to as glycan arrays, are composed of various oligosaccharides and/or polysaccharides immobilized on a solid support in a spatially defined arrangement. This technology provides a powerful, high-throughput approach to examining carbohydrate-macromolecule interactions, and glycan arrays have had a significant impact on the field of glycobiology. This review focuses on recent advances in glycan array technology, limitations, and opportunities for improvement. In particular, new methods for the production of natural glycan arrays and chemoenzymatic approaches are greatly expanding the diversity of structures on arrays. Since multivalent complex formation is generally required to achieve tight binding, methods to evaluate and modulate presentation are vital for enhancing the capabilities of this technology.
C1 [Oyelaran, Oyindasola; Gildersleeve, Jeffrey C.] NCI, Med Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA.
RP Gildersleeve, JC (reprint author), NCI, Med Chem Lab, Ctr Canc Res, 376 Boyles St, Frederick, MD 21702 USA.
EM gildersleevej@ncifcrf.gov
RI Gildersleeve, Jeffrey/N-3392-2014
FU NIH, National Cancer Institute, Center for Cancer Research
FX OO and JCG are supported by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research.
NR 60
TC 126
Z9 127
U1 4
U2 57
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1367-5931
J9 CURR OPIN CHEM BIOL
JI Curr. Opin. Chem. Biol.
PD OCT
PY 2009
VL 13
IS 4
BP 406
EP 413
DI 10.1016/j.cbpa.2009.06.021
PG 8
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 516SU
UT WOS:000271563800006
PM 19625207
ER
PT J
AU Fessler, MB
Rudel, LL
Brown, JM
AF Fessler, Michael B.
Rudel, Lawrence L.
Brown, J. Mark
TI Toll-like receptor signaling links dietary fatty acids to the metabolic
syndrome
SO CURRENT OPINION IN LIPIDOLOGY
LA English
DT Review
DE atherosclerosis; insulin resistance; obesity; polyunsaturated fatty
acids; saturated fatty acids; Toll-like receptor 4
ID INDUCED INSULIN-RESISTANCE; INNATE IMMUNITY; ADIPOSE-TISSUE; MEMBRANE
RAFTS; LIPID-COMPOSITION; APOLIPOPROTEIN-E; CELL ACTIVATION; INDUCED
OBESITY; ATHEROSCLEROSIS; MICE
AB Purpose of review
Dietary saturated fatty acids (SFAs) have been implicated in promoting the metabolic syndrome and atherosclerotic cardiovascular disease. Recent evidence suggests that SFAs promote the metabolic syndrome by activating Toll-like receptor 4 (TLR4). Here we examine emerging molecular evidence that SFAs directly engage pathways of innate immunity, thereby promoting inflammatory aspects of the metabolic syndrome.
Recent findings
Accumulation of SFA in the body is tightly regulated by stearoyl-CoA desaturase 1, an enzyme that converts endogenous SFA to monounsaturated fatty acids. Recent studies have demonstrated that the accumulation of SFA seen with genetic deletion or inhibition of stearoyl-CoA desaturase 1 promotes inflammation, TLR4 hypersensitivity, and accelerated atherosclerosis, Therefore, stearoyl-CoA desaturase 1 may play an unexpected role in suppressing inflammation by preventing excessive accumulation of endogenous SFA-derived TLR4 agonists. In parallel, several independent laboratories have demonstrated that TLR4 is necessary for dietary SFAs to induce obesity, insulin resistance, and vascular inflammation in rodent models.
Summary
The metabolic syndrome and atherosclerotic cardiovascular disease have long been linked to dietary SFA intake and inflammation. Recent mechanistic insights into how SFAs and downstream metabolites can potentiate inflammation-driven metabolic disease are discussed here.
C1 [Rudel, Lawrence L.; Brown, J. Mark] Wake Forest Univ, Bowman Gray Sch Med, Sect Liod Sci, Dept Pathol, Winston Salem, NC 27157 USA.
[Fessler, Michael B.] NIEHS, Lab Resp Biol, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
RP Brown, JM (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Sect Liod Sci, Dept Pathol, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM mabrown@wfubmc.edu
FU National Institutes of Health [NIH-1K99HL096166-01, NIH-P01-HL49373];
National Center for Complimentary and Alternative Medicine
[NCCAM-P50AT002782]; Intramural Research Program of the National
Institutes of Health; National Institute of Environmental Health
Sciences
FX The present work was supported by grants from the National Institutes of
Health (NIH-1K99HL096166-01 to J.M.B. and NIH-P01-HL49373 to L.L.R), the
National Center for Complimentary and Alternative Medicine
(NCCAM-P50AT002782 to L.L.R.), and by the Intramural Research Program of
the National Institutes of Health, National Institute of Environmental
Health Sciences (M.B.F.). The authors thank Rosanne Crooke, Mark Graham,
and Richard Lee (ISIS Pharmaceuticals, Inc. Carlsbad, CA USA) for
providing the SCD1 antisense oligonucleotides described here. We also
thank Lois Wyrick for assistance with figure production.
NR 82
TC 97
Z9 116
U1 0
U2 16
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0957-9672
J9 CURR OPIN LIPIDOL
JI Curr. Opin. Lipidology
PD OCT
PY 2009
VL 20
IS 5
BP 379
EP 385
DI 10.1097/MOL.0b013e32832fa5c4
PG 7
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Peripheral
Vascular Disease
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Cardiovascular System & Cardiology
GA 497MB
UT WOS:000270062500004
PM 19625959
ER
PT J
AU Kelley, MW
Driver, EC
Puligilla, C
AF Kelley, Matthew W.
Driver, Elizabeth C.
Puligilla, Chandrakala
TI Regulation of cell fate and patterning in the developing mammalian
cochlea
SO CURRENT OPINION IN OTOLARYNGOLOGY & HEAD AND NECK SURGERY
LA English
DT Article
DE atoh1; hair cell; organ of Corti; pillar cell; Sox2
ID FIBROBLAST-GROWTH-FACTOR; INNER-EAR DEVELOPMENT; SENSORY ORGAN
DEVELOPMENT; MATH1 GENE-TRANSFER; HEARING-LOSS; HAIR-CELLS; POLARITY
REGULATION; RECEPTOR-3 GENE; NOTCH LIGANDS; MOUSE MODEL
AB Purpose of review
A significant proportion of hearing loss and deafness is caused by defects in the structure or function of cells within the organ of Corti. Identification of the molecular factors that regulate the development of this structure should provide valuable insights regarding inner ear formation and the signaling pathways that underlie congenital auditory deficits. In addition, targeted modulation of these same factors could be developed as therapies for hair cell regeneration.
Recent findings
Results from experiments using transgenic and mutant mice, as well as in-vitro techniques, have identified genes and signaling pathways that are required to either specify unique auditory cell types, such as hair cells or supporting cells, or to generate the highly ordered cellular pattern that is characteristic for the organ of Corti. In particular, the hedgehog and fibroblast growth factor signaling pathways modulate the formation of the progenitor cells that will give rise to the organ of Corti. SRY-box containing gene 2, a transcription factor that is required for the formation of the cochlear progenitor cell population, has paradoxically been shown to also act as an inhibitor of hair cell development. Finally, the motor protein myosin II regulates extension of the organ of Corti and the alignment of hair cells and supporting cells into ordered rows.
Summary
A better understanding of the signaling pathways that direct different aspects of cochlear development, such as specific of cell fates or cellular patterning, offers the potential to identify new pathways or molecules that could be targeted for therapeutic interventions.
C1 [Kelley, Matthew W.; Driver, Elizabeth C.; Puligilla, Chandrakala] Natl Inst Deafness & Commun Disorders, Sect Dev Neurosci, NIH, Bethesda, MD USA.
RP Kelley, MW (reprint author), Porter Neurosci Res Ctr, 35 Convent Dr,Room 2A-100, Bethesda, MD 20892 USA.
EM kelleymt@nidcd.nih.gov
OI Driver, Elizabeth/0000-0002-5618-1053
FU National Institute on Deafness and other Communication Disorders at the
National Institutes of Health
FX This study was supported by the Intramural Program of the National
Institute on Deafness and other Communication Disorders at the National
Institutes of Health. The authors wish to apologize to any of their
colleagues whose study was unavoidably excluded from this review due to
space constraints.
NR 63
TC 23
Z9 24
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 2009
VL 17
IS 5
BP 381
EP 387
DI 10.1097/MOO.0b013e3283303347
PG 7
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 504AJ
UT WOS:000270584500009
PM 19623076
ER
PT J
AU Sakaguchi, H
Tokita, J
Muller, U
Kachar, B
AF Sakaguchi, Hirofumi
Tokita, Joshua
Mueller, Ulrich
Kachar, Bechara
TI Tip links in hair cells: molecular composition and role in hearing loss
SO CURRENT OPINION IN OTOLARYNGOLOGY & HEAD AND NECK SURGERY
LA English
DT Article
DE cadherins; deafness; hair cells; hearing; inherited deafness;
mechanoelectrical transduction; tip links
ID ALTERNATIVE SPLICE FORMS; SYNDROME TYPE 1D; SYNDROME TYPE 1F;
USHER-SYNDROME; MYOSIN VIIA; NONSYNDROMIC DEAFNESS; PROTOCADHERIN GENE;
CADHERIN-23 CDH23; CALCIUM CHELATION; GENOMIC STRUCTURE
AB Purpose of review
Tip links are thought to be an essential element of the mechanoelectrical transduction (MET) apparatus in sensory hair cells of the inner ear. The molecules that form tip links have recently been identified, and the analysis of their properties has not only changed our view of MET but also suggests that tip-link defects can cause hearing loss.
Recent findings
Structural, histological and biochemical studies show that the extracellular domains of two deafness-associated cadherins, cadherin 23 (CDH23) and protocadherin 15 (PCDH15), interact in trans to form the upper and lower part of each tip link, respectively. High-speed Ca(2+) imaging suggests that MET channels are localized exclusively at the lower end of each tip link. Biochemical and genetic studies provide evidence that defects in tip links cause hearing impairment in humans.
Summary
The identification of the proteins that form tip links have shed new light on the molecular basis of MET and the mechanisms causing hereditary deafness, noise-induced hearing loss and presbycusis.
C1 [Kachar, Bechara] NIDCD, Sect Struct Cell Biol, Lab Cell Struct & Dynam, NIH, Bethesda, MD 20892 USA.
[Sakaguchi, Hirofumi] Kyoto Prefectural Univ Med, Dept Otolaryngol Head & Neck Surg, Kyoto, Japan.
[Tokita, Joshua] Univ Illinois, Coll Med, Chicago, IL USA.
[Mueller, Ulrich] Scripps Res Inst, Dept Cell Biol, La Jolla, CA 92037 USA.
[Mueller, Ulrich] Scripps Res Inst, Inst Childhood & Neglected Dis, La Jolla, CA 92037 USA.
RP Kachar, B (reprint author), NIDCD, Sect Struct Cell Biol, Lab Cell Struct & Dynam, NIH, Bldg 50,Room 4249,50 South Dr, Bethesda, MD 20892 USA.
EM kacharb@nidcd.nih.gov
FU NIDCD, NIH
FX The work was supported by the Intramural Program of NIDCD, NIH.
NR 61
TC 25
Z9 26
U1 1
U2 10
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 2009
VL 17
IS 5
BP 388
EP 393
DI 10.1097/MOO.0b013e3283303472
PG 6
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 504AJ
UT WOS:000270584500010
PM 19633555
ER
PT J
AU Horowitz, LM
Ballard, ED
Pao, M
AF Horowitz, Lisa M.
Ballard, Elizabeth D.
Pao, Maryland
TI Suicide screening in schools, primary care and emergency departments
SO CURRENT OPINION IN PEDIATRICS
LA English
DT Review
DE emergency department; pediatric; primary care; schools; screening;
suicide
ID MENTAL-HEALTH PROBLEMS; PEDIATRIC EMERGENCY; ADOLESCENT SUICIDE; MAJOR
DEPRESSION; YOUTH SUICIDE; EARLY IDENTIFICATION; PREVENTION PROGRAM;
MEDICAL-SERVICES; RISK-FACTORS; BEHAVIOR
AB Purpose of review
Every year, suicide claims the lives of tens of thousands of young people worldwide. Despite its high prevalence and known risk factors, suicidality is often undetected. Early identification of suicide risk may be an important method of mitigating this public health crisis. Screening youth for suicide may be a critical step in suicide prevention. This paper reviews suicide screening in three different settings: schools, primary care clinics and emergency departments (EDs).
Recent findings
Unrecognized and thus untreated suicidality leads to substantial morbidity and mortality. With the onus of detection falling on nonmental health professionals, brief screening tools can be used to initiate more in-depth evaluations. Nonetheless, there are serious complexities and implications of screening all children and adolescents for suicide. Recent studies show that managing positive screens is a monumental challenge, including the problem of false positives and the burden subsequently posed on systems of care. Furthermore, nearly 60% of youth in need of mental health services do not receive the care they need, even after suicide attempt. Schools, primary care clinics and EDs are logical settings where screening that leads to intervention can be initiated.
Summary
Valid, brief and easy-to-administer screening tools can be utilized to detect risk of suicide in children and adolescents. Targeted suicide screening in schools, and universal suicide screening in primary care clinics and EDs may be the most effective way to recognize and prevent self-harm. These settings must be equipped to manage youth who screen positive with effective and timely interventions. Most importantly, the impact of suicide screening in various settings needs to be further assessed.
C1 [Horowitz, Lisa M.] NIMH, Off Clin Director, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Ballard, Elizabeth D.] Catholic Univ Amer, Dept Psychol, Washington, DC 20064 USA.
RP Horowitz, LM (reprint author), NIMH, Off Clin Director, Natl Inst Hlth, 10 CRC,Room 6-5340,10 Ctr Dr, Bethesda, MD 20892 USA.
EM horowitzl@mail.nih.gov
FU NIH; National Institute of Mental Health
FX This research was supported by the Intramural Research Program of the
NIH and the National Institute of Mental Health. The authors are
grateful to Janet Heekin and Anne Bowles for their help with the
literature search, retrieving articles and managing the references. The
views expressed in this paper are the authors views and do not
necessarily represent the views of the NIH, DHHS or any other government
agency or official.
NR 82
TC 40
Z9 43
U1 3
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8703
J9 CURR OPIN PEDIATR
JI CURR. OPIN. PEDIATR.
PD OCT
PY 2009
VL 21
IS 5
BP 620
EP 627
DI 10.1097/MOP.0b013e3283307a89
PG 8
WC Pediatrics
SC Pediatrics
GA 502UV
UT WOS:000270486700012
PM 19617829
ER
PT J
AU Kobayashi, SD
Deleo, FR
AF Kobayashi, Scott D.
DeLeo, Frank R.
TI An update on community-associated MRSA virulence
SO CURRENT OPINION IN PHARMACOLOGY
LA English
DT Article
ID RESISTANT STAPHYLOCOCCUS-AUREUS; PANTON-VALENTINE LEUKOCIDIN; CASSETTE
CHROMOSOME MEC; ALPHA-TOXIN; NECROTIZING PNEUMONIA; HUMAN NEUTROPHILS;
SKIN INFECTIONS; IMMUNE EVASION; EMERGENCE; CLONE
AB Staphylococcus aureus is a major health problem worldwide and the leading cause of bacterial infections in the United States. Historically, the success of S. aureus as a human pathogen has been facilitated by a strong propensity to develop antibiotic resistance and multidrug resistant strains are endemic in hospitals. However, one of the most striking developments in recent bacterial infectious disease history was the rapid emergence of community-associated methicillin-resistant S. aureus (CA-MRSA). First reported in the 1990s, CA-MRSA has since emerged worldwide and is epidemic in the United States. The pathogen is characterized by its ability to spread rapidly and cause infections in otherwise healthy individuals. This review focuses on current progress toward understanding the enhanced virulence properties of CA-MRSA, with an emphasis on Panton-Valentine leukocidin, alpha-hemolysin, and the recently discovered a-type phenol-soluble modulins.
C1 [Kobayashi, Scott D.; DeLeo, Frank R.] NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Deleo, FR (reprint author), NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
EM fdeleo@niaid.nih.gov
OI DeLeo, Frank/0000-0003-3150-2516
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This article was supported by the Intramural Research program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health. We thank Anita Mora (graphics, NIAID) and David W
Dorward (transmission electron microscopy, NIAID) for their help in
generating the figures, and Michael Otto (NIAID) for critical review of
the manuscript.
NR 65
TC 49
Z9 50
U1 1
U2 10
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4892
J9 CURR OPIN PHARMACOL
JI Curr. Opin. Pharmacol.
PD OCT
PY 2009
VL 9
IS 5
BP 545
EP 551
DI 10.1016/j.coph.2009.07.009
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 507YA
UT WOS:000270890700003
PM 19726228
ER
PT J
AU Schulden, JD
Thomas, YF
Compton, WM
AF Schulden, Jeffrey D.
Thomas, Yonette F.
Compton, Wilson M.
TI Substance Abuse in the United States: Findings From Recent Epidemiologic
Studies
SO CURRENT PSYCHIATRY REPORTS
LA English
DT Article
ID DRUG-USE DISORDERS; ANXIETY DISORDERS; MENTAL-DISORDERS; ALCOHOL;
COMORBIDITY; PREVALENCE; DEPENDENCE; RISK; HEALTH; MOOD
AB Recent research on the epidemiology of substance use disorders (SUDs) has provided important insights into these conditions and their impact on public health. In the United States, annual surveys of drug use in household and school populations serve as one of the primary sources of information about the distribution of illicit drug use. This research has demonstrated continued shifts in trends in illicit drug use in the United States and called attention to rising rates of prescription drug misuse and abuse. Findings have also continued to highlight the substantial comorbidity of SUDs with other psychiatric disorders and with the ongoing HIV epidemic. Building on these foundations, future challenges for research in substance abuse epidemiology will include using novel methodologic approaches to further unravel the complex interrelationships that link individual vulnerabilities for SUDs, including genetic factors, with social and environmental risk factors.
C1 [Schulden, Jeffrey D.] NIDA, Epidemiol Res Branch, Div Epidemiol Serv & Prevent Res, NIH, Bethesda, MD 20892 USA.
RP Schulden, JD (reprint author), NIDA, Epidemiol Res Branch, Div Epidemiol Serv & Prevent Res, NIH, 6001 Execut Blvd,MSC 9589, Bethesda, MD 20892 USA.
EM schuldenj@nida.nih.gov
FU Intramural NIH HHS [Z99 DA999999]
NR 50
TC 32
Z9 33
U1 3
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3812
EI 1535-1645
J9 CURR PSYCHIAT REP
JI Curr. Psychiatry Rep.
PD OCT
PY 2009
VL 11
IS 5
BP 353
EP 359
PG 7
WC Psychiatry
SC Psychiatry
GA V16XQ
UT WOS:000207902700004
PM 19785975
ER
PT J
AU Shaw, P
Rabin, C
AF Shaw, Philip
Rabin, Cara
TI New Insights Into Attention-Deficit/Hyperactivity Disorder Using
Structural Neuroimaging
SO CURRENT PSYCHIATRY REPORTS
LA English
DT Article
AB This article reviews recent advances in structural neuroimaging in attention-deficit/hyperactivity disorder (ADHD). Observational studies have found treatment with psychostimulants to be associated more closely with dimensions of some brain structures in typically developing children than in those found in treatment-nave children with ADHD. Novel analytic approaches allow for greater precision in the definition of brain regions that are most compromised in ADHD, with meta-analyses highlighting compromise of the basal ganglia. Cortical changes, particularly in the lateral prefrontal and parietal cortex, are also commonly reported, but with less consensus on the exact location of structural change. Anomalies in the shape of subcortical structures, specifically of the basal ganglia, hippocampus, and amygdala, implicate frontostriatal loops and the limbic system in the disorder. Finally, longitudinal data suggest that ADHD in childhood may be characterized by a delay in cortical maturation and that different clinical outcomes may be associated with different developmental trajectories in adolescence and beyond.
C1 [Shaw, Philip] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
RP Shaw, P (reprint author), NIMH, Child Psychiat Branch, Room 3N202,Bldg 10,Ctr Dr, Bethesda, MD 20892 USA.
EM shawp@mail.nih.gov
NR 37
TC 46
Z9 46
U1 4
U2 18
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3812
J9 CURR PSYCHIAT REP
JI Curr. Psychiatry Rep.
PD OCT
PY 2009
VL 11
IS 5
BP 393
EP 398
PG 6
WC Psychiatry
SC Psychiatry
GA V16XQ
UT WOS:000207902700010
PM 19785981
ER
PT J
AU Chen, WJ
AF Chen, Wanjun
TI A critical function of TGF-beta in the generation of adaptive and
natural CD4(+)Foxp3(+) regulatory T cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokines Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Chen, Wanjun] NIDCR, Mucosal Immunol Unit, OIIB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
SI SI
BP 5
EP 6
DI 10.1016/j.cyto.2009.07.026
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100017
ER
PT J
AU Zhou, R
Caspi, RR
AF Zhou, Ru
Caspi, Rachel R.
TI Dual function for a vision-related molecule: Retinoic acid in the eye
may contribute to ocular immune privilege by inducing T regulatory cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Zhou, Ru; Caspi, Rachel R.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 6
EP 6
DI 10.1016/j.cyto.2009.07.027
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100018
ER
PT J
AU Rani, A
Kelly, A
Berhan, LT
Jurevic, S
Ragheb, J
Lavender, P
John, S
AF Rani, Aradhana
Kelly, Audrey
Berhan, Lemlem Tewolde
Jurevic, Stipo
Ragheb, Jack
Lavender, Paul
John, Susan
TI Regulation of c-maf by IL-2
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Rani, Aradhana; Berhan, Lemlem Tewolde; John, Susan] Kings Coll London, Dept Immunobiol, London SE1 9RT, England.
[Kelly, Audrey; Lavender, Paul] Kings Coll London, Dept Asthma Allergy & Resp Dis, London SE1 9RT, England.
[Jurevic, Stipo] Kings Coll London, Dept Nephrol & Transplantat, London SE1 9RT, England.
[Ragheb, Jack] NIH, US FDA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 11
EP 11
DI 10.1016/j.cyto.2009.07.049
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100034
ER
PT J
AU Ozato, K
Chang, TH
Kubota, T
Matsuoka, M
Bray, M
Jones, S
AF Ozato, Keiko
Chang, Tsung-Hsien
Kubota, Toru
Matsuoka, Mayumi
Bray, Mike
Jones, Steven
TI Inhibition of type I interferon transcription by IRF3/7 SUMOylation the
process hijacked by the Ebola virus VP35
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Ozato, Keiko; Chang, Tsung-Hsien; Kubota, Toru; Matsuoka, Mayumi] NICHD, Program Genom Differentiat, NIH, Bethesda, MD USA.
[Kubota, Toru; Matsuoka, Mayumi] Natl Inst Infect Dis, Tokyo, Japan.
[Bray, Mike] NIAID, IRF, Bethesda, MD 20892 USA.
[Jones, Steven] Natl Microbiol Lab, Winnipeg, MB, Canada.
NR 2
TC 0
Z9 0
U1 4
U2 6
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 15
EP 15
DI 10.1016/j.cyto.2009.07.064
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100047
ER
PT J
AU Hodge, DL
Berthet, C
Subleski, J
Coppola, V
Buschman, M
Razook, C
Young, HA
AF Hodge, Deborah L.
Berthet, Cyril
Subleski, Jeff
Coppola, Vincenzo
Buschman, Matthew
Razook, Catherine
Young, Howard A.
TI Novel gene expression patterns in IFN-gamma 3 ' untranslated region
AU-rich element-deleted mice
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Hodge, Deborah L.; Berthet, Cyril; Subleski, Jeff; Coppola, Vincenzo; Buschman, Matthew; Razook, Catherine; Young, Howard A.] NCI, CCR, Bethesda, MD 20892 USA.
RI Coppola, Vincenzo/E-2917-2011
OI Coppola, Vincenzo/0000-0001-6163-1779
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 25
EP 25
DI 10.1016/j.cyto.2009.07.099
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100077
ER
PT J
AU Kennedy, M
Nechaev, S
Gilchrist, DA
Muse, GW
Chinenov, Y
Adelman, K
Rogatsky, I
AF Kennedy, Megan
Nechaev, Sergei
Gilchrist, Daniel A.
Muse, Ginger W.
Chinenov, Yurii
Adelman, Karen
Rogatsky, Inez
TI Immediate mediators of the inflammatory response are poised for rapid
gene activation through RNA polymerase stalling
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Kennedy, Megan; Chinenov, Yurii; Rogatsky, Inez] Cornell Univ, Hosp Special Surg, Weill Med Coll, Dept Microbiol & Immunol, New York, NY 10021 USA.
[Nechaev, Sergei; Gilchrist, Daniel A.; Muse, Ginger W.; Adelman, Karen] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 25
EP 25
DI 10.1016/j.cyto.2009.07.097
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100075
ER
PT J
AU Wynn, TA
Ramalingam, T
Wilson, M
Thompson, R
Mentink-Kane, M
Urban, J
Cheever, A
Murray, P
Pesce, J
AF Wynn, Thomas A.
Ramalingam, Thirumalai
Wilson, Mark
Thompson, Robert
Mentink-Kane, Margaret
Urban, Joe
Cheever, Allen
Murray, Peter
Pesce, John
TI Dissecting "Alternative Macrophage Activation": The role of L-arginine
metabolism in chronic inflammation and fibrosis
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Wynn, Thomas A.; Ramalingam, Thirumalai; Wilson, Mark; Thompson, Robert; Mentink-Kane, Margaret; Cheever, Allen; Pesce, John] NIAID, Immunopathogenesis Sect, LPD, NIH, Bethesda, MD 20892 USA.
[Urban, Joe; Pesce, John] USDA, Beltsville, MD 20705 USA.
[Murray, Peter; Pesce, John] St Jude Childrens Hosp, Memphis, TN 38105 USA.
RI Wynn, Thomas/C-2797-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 32
EP 32
DI 10.1016/j.cyto.2009.07.122
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100098
ER
PT J
AU Gordon, S
AF Gordon, Siamon
TI Role of pattern recognition receptors and Th2 cytokines in macrophage
functions
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Gordon, Siamon] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 33
EP 33
DI 10.1016/j.cyto.2009.07.327
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100099
ER
PT J
AU Hall, JA
Sun, CM
Oldenhove, G
Wohlfert, E
Kastenmeyer, R
Belkaid, Y
AF Hall, Jason A.
Sun, Cheng-Ming
Oldenhove, Guillaume
Wohlfert, Elizabeth
Kastenmeyer, Robin
Belkaid, Yasmine
CA B50 Breeder Techs
TI Vitamin A derived retinoic acid signaling mediates intestinal immune
homeostasis and immunity
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Hall, Jason A.; Sun, Cheng-Ming; Oldenhove, Guillaume; Wohlfert, Elizabeth; Kastenmeyer, Robin; Belkaid, Yasmine; B50 Breeder Techs] NIAID, LPD, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 42
EP 42
DI 10.1016/j.cyto.2009.07.359
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100126
ER
PT J
AU Baron, S
Horowitz, J
Poast, J
Morrow, A
Fey, S
Finbloom, J
Schmeisser, H
Bekisz, J
Zoon, K
AF Baron, Samuel
Horowitz, Julie
Poast, Joyce
Morrow, Angel
Fey, Samuel
Finbloom, Joel
Schmeisser, Hana
Bekisz, Joseph
Zoon, Kathryn
TI Role of interferon-activated macrophages in eradication of human tumor
cells by innate immunity
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Baron, Samuel; Horowitz, Julie; Morrow, Angel; Fey, Samuel; Finbloom, Joel; Schmeisser, Hana; Bekisz, Joseph; Zoon, Kathryn] NIAID, NIH, Bethesda, MD 20892 USA.
[Baron, Samuel; Poast, Joyce] Univ Texas Med Branch, Dept Microbiol & Immunol, Galveston, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 48
EP 48
DI 10.1016/j.cyto.2009.07.134
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100145
ER
PT J
AU Zaidi, MR
De Fabo, E
Davis, S
Graff-Cherry, C
Hawley, T
Feigenbaum, L
Fuchs, E
Hornyak, T
Arnheiter, H
Trinchieri, G
Noonan, F
Meltzer, P
Merlino, G
AF Zaidi, M. Raza
De Fabo, Edward
Davis, Sean
Graff-Cherry, Cari
Hawley, Teresa
Feigenbaum, Lionel
Fuchs, Elaine
Hornyak, Thomas
Arnheiter, Heinz
Trinchieri, Giorgio
Noonan, Frances
Meltzer, Paul
Merlino, Glenn
TI Ultraviolet B-induced activation of melanocytes is mediated through
interferon-gamma secreted by macrophages
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Zaidi, M. Raza; Merlino, Glenn] NIH, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
[Davis, Sean; Meltzer, Paul] NIH, Genet Branch, Bethesda, MD 20892 USA.
[Hornyak, Thomas; Noonan, Frances] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[De Fabo, Edward; Hawley, Teresa] George Washington Univ, Med Ctr, Washington, DC 20037 USA.
[Graff-Cherry, Cari; Feigenbaum, Lionel; Trinchieri, Giorgio] NCI, Lab Anim Sci Program, Frederick, MD 21701 USA.
[Arnheiter, Heinz] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Fuchs, Elaine] Rockefeller Univ, New York, NY 10021 USA.
RI Zaidi, M. Raza/H-1386-2016
OI Zaidi, M. Raza/0000-0003-0480-3188
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 52
EP 52
DI 10.1016/j.cyto.2009.07.151
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100161
ER
PT J
AU Wilhelm, C
Proschan, M
Travis, F
Hague, B
Roby, G
Rehm, C
Lane, C
Catalfamo, M
AF Wilhelm, Christopher
Proschan, Michael
Travis, Friesen
Hague, Bishop
Roby, Gregg
Rehm, Catherine
Lane, Clifford
Catalfamo, Marta
TI Increased IL-7 availability could overcome the anti-proliferative
capacity of type-I IFN in Naive CD8 T cells during HIV infection
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Wilhelm, Christopher; Proschan, Michael; Travis, Friesen; Hague, Bishop; Roby, Gregg; Rehm, Catherine; Lane, Clifford; Catalfamo, Marta] NIAID, NIH, CMRS Lab Immunoregulat, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 63
EP 63
DI 10.1016/j.cyto.2009.07.200
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100206
ER
PT J
AU Mikovits, JA
Hagen, KS
Peterson, DL
Dean, M
Lombardi, VC
AF Mikovits, Judy A.
Hagen, Kathryn S.
Peterson, Daniel L.
Dean, Michael
Lombardi, Vincent C.
TI Aberrant type I IFN pathway response to viral infection in chronic
fatigue syndrome (CFS)
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Mikovits, Judy A.; Hagen, Kathryn S.; Peterson, Daniel L.; Lombardi, Vincent C.] Whittemore Peterson Inst, Reno, NV USA.
[Dean, Michael] NCI, Expt Immunol Lab, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 64
EP 65
DI 10.1016/j.cyto.2009.07.206
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100212
ER
PT J
AU Balinsky, CA
Schmeisser, H
Zoon, KC
AF Balinsky, Corey A.
Schmeisser, Hana
Zoon, Kathryn C.
TI Dengue virus core protein mediates reduction of antiviral activity in
Huh7 cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Balinsky, Corey A.; Schmeisser, Hana; Zoon, Kathryn C.] NIAID, Div Intramural Res, Bethesda, MD 20892 USA.
[Balinsky, Corey A.; Schmeisser, Hana; Zoon, Kathryn C.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 68
EP 68
DI 10.1016/j.cyto.2009.07.220
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100225
ER
PT J
AU Kottilil, S
Kim, C
Schmeisser, H
Lempicki, RA
Yang, J
Zoon, K
Young, H
Polis, MA
Fauci, AS
AF Kottilil, S.
Kim, C.
Schmeisser, H.
Lempicki, R. A.
Yang, J.
Zoon, K.
Young, H.
Polis, M. A.
Fauci, A. S.
TI Connecting the dots on interferon responsiveness in HCV/HIV
co-infection: The virus, the cytokine, the receptor and the gene
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Kottilil, S.; Kim, C.; Schmeisser, H.; Lempicki, R. A.; Yang, J.; Zoon, K.; Young, H.; Polis, M. A.; Fauci, A. S.] NIAID, AID, NIH, Bethesda, MD 20892 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 ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 84
EP 84
DI 10.1016/j.cyto.2009.07.301
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100292
ER
PT J
AU Thomas, E
Li, QS
Clark, SA
Feld, JJ
Liang, TJ
AF Thomas, Emmanuel
Li, Qisheng
Clark, Shauna A.
Feld, Jordan J.
Liang, T. Jake
TI Characterization of gene induction and antiviral effects on HCVcc
following ribavirin, interferon and polyIC stimulation
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Thomas, Emmanuel; Li, Qisheng; Clark, Shauna A.; Feld, Jordan J.; Liang, T. Jake] NIDDK, NIH, Bethesda, MD USA.
RI Li, Qisheng/K-1909-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 85
EP 85
DI 10.1016/j.cyto.2009.07.305
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100296
ER
PT J
AU Ezelle, HJ
Andersen, JB
Hao, I
Hassel, BA
AF Ezelle, Heather J.
Andersen, Jesper B.
Hao, Irene
Hassel, Bret A.
TI LNX is a novel protein interactor for the antiviral endoribonuclease,
RNase-L
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Ezelle, Heather J.; Hassel, Bret A.] Univ Maryland, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Ezelle, Heather J.; Hassel, Bret A.] Univ Maryland, Dept Microbiol & Immunol, Baltimore, MD 21201 USA.
[Andersen, Jesper B.] NCI, Expt Carcinogenesis Lab, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
[Hao, Irene] Univ Med & Dent New Jersey, Dept Med, Newark, NJ 07101 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 86
EP 87
DI 10.1016/j.cyto.2009.07.313
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100302
ER
PT J
AU Schmeisser, H
Mejido, JA
Balinsky, C
Zoon, KC
AF Schmeisser, Hana
Mejido, Josef A.
Balinsky, Corey
Zoon, Kathryn C.
TI Identification of IFN-alpha-induced genes and proteins associated with
antiviral activity in daudi cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Schmeisser, Hana; Mejido, Josef A.; Balinsky, Corey; Zoon, Kathryn C.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 87
EP 87
DI 10.1016/j.cyto.2009.07.314
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100303
ER
PT J
AU Bekisz, J
Schmeisser, H
Stephany, D
Zoon, K
AF Bekisz, Joseph
Schmeisser, Hana
Stephany, David
Zoon, Kathryn
TI Using luminex (xMAP) technology to assay for inflammatory cytokines in
cell culture supernatants from daudi and ovcar-3 cells treated with
interferon
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Bekisz, Joseph; Schmeisser, Hana; Stephany, David; Zoon, Kathryn] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 115
EP 115
DI 10.1016/j.cyto.2009.07.487
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100416
ER
PT J
AU Zarember, KA
De Ravin, SS
Long-Priel, D
Gallin, I
Kuhns, D
Malech, HL
AF Zarember, Kol A.
De Ravin, Suk See
Long-Priel, Debra
Gallin, John I.
Kuhns, Douglas
Malech, Harry L.
TI Superoxide-independent kynurenine synthesis in human chronic
granulomatous disease: A 'radical' difference between mice and humans
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Zarember, Kol A.; De Ravin, Suk See; Gallin, John I.; Malech, Harry L.] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA.
[Long-Priel, Debra; Kuhns, Douglas] SAIC Frederick, Clin Serv Program, Neutrophil Monitoring Lab, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 119
EP 119
DI 10.1016/j.cyto.2009.07.502
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100431
ER
PT J
AU Magracheva, E
Li, W
Kotenko, S
Wlodawer, A
Zdanov, A
AF Magracheva, Eugenia
Li, Wei
Kotenko, Sergei
Wlodawer, Alex
Zdanov, Alexander
TI High resolution structure of the complex of interferon-lambda 1 with its
receptor interferon-lambda R1
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Magracheva, Eugenia] SAIC Frederick, Basic Res Program, Frederick, MD 21702 USA.
[Li, Wei; Kotenko, Sergei] UMDNJ New Jersey Med Sch, Dept Biochem & Mol Biol, Newark, NJ USA.
[Wlodawer, Alex; Zdanov, Alexander] NCI, Macromol Crystallog Lab, Frederick, MD 21702 USA.
RI Li, Wei/I-8060-2014
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 121
EP 121
DI 10.1016/j.cyto.2009.07.512
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100441
ER
PT J
AU Carter, SL
Kanno, T
Ozato, K
Campbell, IL
AF Carter, Sally L.
Kanno, Tomohiko
Ozato, Keiko
Campbell, Iain L.
TI IRF8 is present in microglia in the CNS and modulates the response of
these cells to IFN-gamma
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Carter, Sally L.; Campbell, Iain L.] Univ Sydney, Sch Mol & Microbial Biosci, Sydney, NSW 2006, Australia.
[Carter, Sally L.; Campbell, Iain L.] Univ Sydney, Bosch Inst, Sydney, NSW 2006, Australia.
[Kanno, Tomohiko; Ozato, Keiko] NICHHD, Lab Mol Growth Regulat, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 122
EP 122
DI 10.1016/j.cyto.2009.07.516
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100444
ER
PT J
AU Szelag, M
Potla, R
Sisler, J
Hamed, H
Dent, P
Larner, AC
AF Szelag, Magdalena
Potla, Ramesh
Sisler, Jennifer
Hamed, Hossein
Dent, Paul
Larner, Andrew C.
TI STAT1 Expression represses the expression of mitochondrial encoded RNAS
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
ID INTERFERON
C1 [Szelag, Magdalena; Sisler, Jennifer; Hamed, Hossein; Dent, Paul; Larner, Andrew C.] Virginia Commonwealth Univ, Dept Biochem & Mol Biol, Richmond, VA USA.
[Potla, Ramesh] NINDS, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 123
EP 124
DI 10.1016/j.cyto.2009.07.522
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100450
ER
PT J
AU Kruth, HS
Anzinger, JJ
Chang, J
Leyva, FJ
Park, BC
Greene, LE
AF Kruth, Howard S.
Anzinger, Joshua J.
Chang, Janet
Leyva, Francisco J.
Park, Bum-Chan
Greene, Lois E.
TI Native low-density lipoprotein uptake by macrophage colony-stimulating
factor differentiated macrophages is mediated by macropinocytosis and
micropinocytosis
SO CYTOKINE
LA English
DT Meeting Abstract
CT Tri-Society Annual Conference of the
International-Cytokine-Society/International-Society-of-Interferon-and-C
ytokine-Research/Society-of-Leukocyte-Biology
CY OCT 17-21, 2009
CL Lisbon, PORTUGAL
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res, Soc Leukocyte Biol
C1 [Kruth, Howard S.; Anzinger, Joshua J.; Chang, Janet; Leyva, Francisco J.; Park, Bum-Chan; Greene, Lois E.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT-NOV
PY 2009
VL 48
IS 1-2
BP 135
EP 135
DI 10.1016/j.cyto.2009.07.572
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 507LN
UT WOS:000270855100498
ER
PT J
AU Hwang, YS
Luo, T
Xu, YH
Sargent, TD
AF Hwang, Yoo-Seok
Luo, Ting
Xu, Yanhua
Sargent, Thomas D.
TI Myosin-X Is Required for Cranial Neural Crest Cell Migration in Xenopus
laevis
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE MyoX; Myo10; Myosin-X; filopodia
ID TRANSCRIPTION FACTOR AP-2; MOLECULAR MOTOR; IN-VIVO; INDUCTION; EMBRYOS;
FILOPODIA; ACTIN; EXPRESSION; INITIATION; RECEPTORS
AB Myosin-X (MyoX) belongs to a large family of unconventional, nonmuscle, actin-dependent motor proteins. We show that MyoX is predominantly expressed in cranial neural crest (CNC) cells in embryos of Xenopus laevis and is required for head and jaw cartilage development. Knockdown of MyoX expression using antisense morpholino oligonucleotides resulted in retarded migration of CNC cells into the pharyngeal arches, leading to subsequent hypoplasia of cartilage and inhibited outgrowth of the CNC-derived trigeminal nerve. In vitro migration assays on fibronectin using explanted CNC cells showed significant inhibition of filopodia formation, cell attachment, spreading and migration, accompanied by disruption of the actin cytoskeleton. These data support the conclusion that MyoX has an essential function in CNC migration in the vertebrate embryo. Developmental Dynamics 238:2522-2529, 2009. Published 2009 Wiley-Liss, Inc.
C1 [Hwang, Yoo-Seok; Luo, Ting; Xu, Yanhua; Sargent, Thomas D.] NICHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA.
RP Sargent, TD (reprint author), NICHD, Mol Genet Lab, NIH, Bldg 6B,Room 412,6 Ctr Dr, Bethesda, MD 20892 USA.
EM tsargent@nih.gov
FU National Institute of Child Health and Human Development, NIH
FX Grant sponsor: the Intramural Research Program of the National Institute
of Child Health and Human Development, NIH.
NR 52
TC 18
Z9 20
U1 0
U2 6
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 2009
VL 238
IS 10
BP 2522
EP 2529
DI 10.1002/dvdy.22077
PG 8
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA 506IU
UT WOS:000270769300007
PM 19718754
ER
PT J
AU Jia, SJ
Nakaya, N
Piatigorsky, J
AF Jia, Sujuan
Nakaya, Naoki
Piatigorsky, Joram
TI Differential Expression Patterns and Developmental Roles of Duplicated
Scinderin-Like Genes in Zebrafish
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE gene duplication; crystallin scinderin-like proteins; expression
pattern; transgenic zebrafish; gene regulation
ID EYE LENS TRANSPARENCY; CORNEAL CRYSTALLIN; TRANSGENIC MICE; PROTEINS;
GELSOLIN; RECRUITMENT; PROMOTER; DISTINCT
AB Scinderin, the closest homologue of the actin-severing protein, gelsolin, has two similar paralogs (Scinla and Scinlb) in zebrafish. Scinla is abundant in the adult cornea; Scinlb comprises considerably less corneal protein. Here, we show that scinla is expressed in the nose, tens, brain, cornea and annular ligament of the iridocorneal angle; by contrast, scinlb is expressed in the hatching gland, floor plate, notochord, otic vesicle, brain, pharynx, cartilage, swim bladder and cornea. Activity of scinla and scinlb promoter fragments driving the EGFP reporter gene in transgenic zebrafish resembled scinla or scinlb expression. Previously, we showed that reduction of scinla by injection of antisense morpholino oligonucleotides ventralized embryos; here, specific reduction of scinlb expression led to subtle brain abnormalities associated with increased cell death, decreased shhb expression in the floor plate, and slightly reduced eye distance. Thus, scinla and scinlb have different expression patterns and developmental roles during zebrafish development. Developmental Dynamics 238.2633-2640, 2009. Published 2009 Wiley-Liss, Inc.
C1 [Jia, Sujuan; Nakaya, Naoki; Piatigorsky, Joram] NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Piatigorsky, J (reprint author), NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
EM sujuan.jia@stjude.org; joramp@nei.nih.gov
FU National Eye Institute [EY11490]
FX Grant sponsor: National Eye Institute, NIH Intramural Program; Grant
number: EY11490.
NR 35
TC 4
Z9 5
U1 2
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 2009
VL 238
IS 10
BP 2633
EP 2640
DI 10.1002/dvdy.22064
PG 8
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA 506IU
UT WOS:000270769300017
PM 19681161
ER
PT J
AU Nelson, KB
AF Nelson, Karin B.
TI Preventing cerebral palsy: paths not (yet) taken
SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY
LA English
DT Editorial Material
ID NEONATAL ENCEPHALOPATHY; NEWBORN ENCEPHALOPATHY; RISK-FACTORS;
MAGNESIUM-SULFATE; ANTECEDENTS; HYPOTHERMIA; POPULATION; TRIAL
C1 [Nelson, Karin B.] Natl Inst Neurol Disorders & Stroke, NIH, Washington, DC USA.
[Nelson, Karin B.] Childrens Natl Med Ctr, Dept Neurol, Washington, DC 20010 USA.
RP Nelson, KB (reprint author), Natl Inst Neurol Disorders & Stroke, NIH, Washington, DC USA.
NR 17
TC 4
Z9 4
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0012-1622
J9 DEV MED CHILD NEUROL
JI Dev. Med. Child Neurol.
PD OCT
PY 2009
VL 51
IS 10
BP 765
EP 766
PG 2
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 491PE
UT WOS:000269590500001
PM 19747279
ER
PT J
AU Moreau, NG
Teefey, SA
Damiano, DL
AF Moreau, Noelle G.
Teefey, Sharlene A.
Damiano, Diane L.
TI In vivo muscle architecture and size of the rectus femoris and vastus
lateralis in children and adolescents with cerebral palsy
SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY
LA English
DT Article
ID MEDIAL GASTROCNEMIUS; FUNCTIONAL STATUS; SPASTIC DIPLEGIA; FASCICLE
LENGTH; LOWER-LIMB; ADULTS; IMMOBILIZATION; ADAPTATIONS; THICKNESS;
STRENGTH
AB AIM Our aim was to investigate muscle architecture and size of the rectus femoris (RF) and vastus lateralis (VL) in children and adolescents with cerebral palsy (CP) compared with age-matched typically developing participants.
METHOD Muscle architecture and size were measured with ultrasound imaging in 18 participants with spastic CP (9 females, 9 males; age range 7.5-19y; mean age 12y [SD 3y 2mo]) within Gross Motor Function Classification System levels 1 (n=4), II (n=2), III (n=9), and IV (n=3) and 12 typically developing participants (10 females, 2 males; age range 7-20y; mean age 12y 4mo [SD 3y 11mo]). Exclusion criteria were orthopedic surgery or neurosurgery within 6 months before testing or botulinum toxin injections to the quadriceps within 3 months before testing.
RESULTS RF cross-sectional area was significantly lower (48%), RF and VL muscle thickness 30% lower, RF fascicle length 27% lower, and VL fascicle angle 3 degrees less in participants with CP compared to the typically developing participants (p<0.05). Intraclass correlation coefficients were >= 0.93 (CP) and >= 0.88 (typical development), indicating excellent reliability.
INTERPRETATION These results provide the first evidence of altered muscle architecture and size of the RF and VL in CP, similar to patterns observed with disuse and aging. These alterations may play a significant role in the decreased capacity for force generation as well as decreased shortening velocity and range of motion over which the quadriceps can act.
C1 [Moreau, Noelle G.] Med Univ S Carolina, Dept Hlth Profess, Charleston, SC 29425 USA.
[Teefey, Sharlene A.] Washington Univ, Sch Med, Dept Radiol, St Louis, MO 63110 USA.
[Damiano, Diane L.] NIH, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Moreau, NG (reprint author), Med Univ S Carolina, Dept Hlth Profess, 151 B Rutledge Ave,MSC965, Charleston, SC 29425 USA.
EM moreau@musc.edu
RI Damiano, Diane/B-3338-2010
OI Damiano, Diane/0000-0002-2770-5356
FU National Center for Medical Rehabilitation Research/National Institutes
of Health [T32HD007434-16]; Section on Pediatrics of the American
Physical Therapy Association
FX Dr Noelle Moreau was a postdoctoral fellow in the Movement Science
Program at Washington University in St Louis, MO, USA, when this study
was conducted and was supported by a National Center for Medical
Rehabilitation Research/National Institutes of Health grant
(T32HD007434-16). This project was also supported by a clinical research
grant from the Section on Pediatrics of the American Physical Therapy
Association to Dr Moreau. The authors would like to thank Chris Stanley
for assistance with data collection and processing, and Dr Janice
Brunstrom and Jennifer Miros PT, for their support and assistance with
recruitment. We would also like to thank GE Healthcare and Tania
Gordley, Applications Specialist for GE Healthcare Ultrasound, for their
support and technical assistance with this project.
NR 28
TC 45
Z9 51
U1 3
U2 12
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0012-1622
J9 DEV MED CHILD NEUROL
JI Dev. Med. Child Neurol.
PD OCT
PY 2009
VL 51
IS 10
BP 800
EP 806
DI 10.1111/j.1469-8749.2009.03307.x
PG 7
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 491PE
UT WOS:000269590500009
PM 19459913
ER
PT J
AU Harlan, DM
Kenyon, NS
Korsgren, O
Roep, BO
AF Harlan, David M.
Kenyon, Norma Sue
Korsgren, Olle
Roep, Bart O.
CA Diabet Soc
TI Current Advances and Travails in Islet Transplantation
SO DIABETES
LA English
DT Article
ID TYPE-1 DIABETES-MELLITUS; EMBRYONIC STEM-CELLS; LONG-TERM SURVIVAL; CD8
T-CELLS; BETA-CELL; TISSUE FACTOR; IN-VIVO; INSULIN-INDEPENDENCE;
PERIPHERAL-BLOOD; FOLLOW-UP
C1 [Harlan, David M.] NIDDKD, NIH, Diabet Branch, Bethesda, MD 20892 USA.
[Kenyon, Norma Sue] Diabet Res Inst, Miami, FL USA.
[Korsgren, Olle] Rudbeck Lab, Dept Clin Immunol, Uppsala, Sweden.
[Roep, Bart O.] Leiden Univ, Med Ctr IHB, Leiden, Netherlands.
RP Harlan, DM (reprint author), NIDDKD, NIH, Diabet Branch, Bethesda, MD 20892 USA.
EM davidmh@intra.niddk.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases;
National Institutes of Health of the Department of Health and Human
Services
FX D.M.H. is supported by the Intramural Research Program of the National
Institute of Diabetes and Digestive and Kidney Diseases/National
Institutes of Health of the Department of Health and Human Services.
NR 98
TC 94
Z9 96
U1 0
U2 12
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 2009
VL 58
IS 10
BP 2175
EP 2184
DI 10.2337/db09-0476
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 506LL
UT WOS:000270776200003
PM 19794074
ER
PT J
AU Liu, SH
Le May, C
Wong, WPS
Ward, RD
Clegg, DJ
Marcelli, M
Korach, KS
Mauvais-Jarvis, F
AF Liu, Suhuan
Le May, Cedric
Wong, Winifred P. S.
Ward, Robert D.
Clegg, Deborah J.
Marcelli, Marco
Korach, Kenneth S.
Mauvais-Jarvis, Franck
TI Importance of Extranuclear Estrogen Receptor-alpha and Membrane G
Protein-Coupled Estrogen Receptor in Pancreatic Islet Survival
SO DIABETES
LA English
DT Article
ID BETA-CELL APOPTOSIS; PLASMA-MEMBRANE; DIABETES-MELLITUS; SELECTIVE
LIGANDS; GPR30; 17-BETA-ESTRADIOL; MICE; BINDING; ACTIVATION; EXPRESSION
AB OBJECTIVE-We showed that 17 beta-estradiol (E(2)) favors pancreatic beta-cell survival via the estrogen receptor-alpha (ER alpha) in mice. E(2) activates nuclear estrogen receptors via an estrogen response element (ERE). E(2) also activates nongenomic signals via an extranuclear form of ER alpha and the G protein-coupled estrogen receptor (GPER). We studied the contribution of estrogen receptors to islet survival.
RESEARCH DESIGN AND METHODS-We used mice and islets deficient in estrogen receptor-alpha (alpha ERKO(-/-)), estrogen receptor-beta (beta ERKO(-/-)), estrogen receptor-alpha and estrogen receptor-beta (alpha beta ERKO(-/-)), and GPER (GPERKO(-/-)); a mouse lacking ER alpha binding to the ERE; and human islets. These mice and islets were studied in combination with receptor-specific pharmacological probes.
RESULTS-We show that ER alpha protection of islet survival is ERE independent and that E(2) favors islet survival through extranuclear and membrane estrogen receptor signaling. We show that ER beta plays a minor cytoprotective role compared to ER alpha. Accordingly, beta ERKO(-/-) mice are mildly predisposed to streptozotocin-induced islet apoptosis. However, combined elimination of ER alpha and ER beta in mice does not synergize to provoke islet apoptosis. In alpha beta ERKO(-/-) mice and their islets, E(2) partially prevents apoptosis suggesting that an alternative pathway compensates for ER alpha/ER beta deficiency. We find that E(2) protection of islet survival is reproduced by a membrane-impermeant E(2) formulation and a selective GPER agonist. Accordingly, GPERKO(-/-) mice are susceptible to streptozotocin-induced insulin deficiency.
CONCLUSIONS-E(2) protects beta-cell survival through ER alpha and ER beta via ERE-independent, extra-nuclear mechanisms, as well as GPER-dependent mechanisms. The present study adds a novel dimension to estrogen biology in beta-cells and identifies GPER as a target to protect islet survival. Diabetes 58:2292-2302, 2009
C1 [Liu, Suhuan; Le May, Cedric; Wong, Winifred P. S.; Mauvais-Jarvis, Franck] Northwestern Univ, Sch Med, Dept Med, Div Endocrinol Metab & Mol Med, Chicago, IL 60611 USA.
[Ward, Robert D.; Marcelli, Marco] Baylor Coll Med, Dept Med, Div Endocrinol Diabet & Metab, Houston, TX 77030 USA.
[Clegg, Deborah J.] Univ Texas SW Med Ctr Dallas, Touchstone Diabet Ctr, Dept Internal Med, Dallas, TX 75390 USA.
[Korach, Kenneth S.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Mauvais-Jarvis, F (reprint author), Northwestern Univ, Sch Med, Dept Med, Div Endocrinol Metab & Mol Med, Chicago, IL 60611 USA.
EM f-mauvais-jarvis@northwestern.edu
RI Le May, cedric/D-2691-2009;
OI Korach, Kenneth/0000-0002-7765-418X
FU National Institutes of Health (NIH) [R01 DK074970, P50 HD044405];
Juvenile Diabetes Research Foundation; Juvenile Diabetes Research
Foundation Post-Doctoral
FX This work was supported by National Institutes of Health (NIH) Grants
R01 DK074970 and P50 HD044405, the Juvenile Diabetes Research
Foundation, and the March of Dimes to F.M.-J. C.L.M. was the recipient
of a Juvenile Diabetes Research Foundation Post-Doctoral Fellowship.
NR 39
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U1 1
U2 5
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 2009
VL 58
IS 10
BP 2292
EP 2302
DI 10.2337/db09-0257
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 506LL
UT WOS:000270776200017
PM 19587358
ER
PT J
AU de Boer, IH
Katz, R
Cao, JJ
Fried, LF
Kestenbaum, B
Mukamal, K
Rifkin, DE
Sarnak, MJ
Shlipak, MG
Siscovick, DS
AF de Boer, Ian H.
Katz, Ronit
Cao, Jie J.
Fried, Linda F.
Kestenbaum, Bryan
Mukamal, Ken
Rifkin, Dena E.
Sarnak, Mark J.
Shlipak, Michael G.
Siscovick, David S.
TI Cystatin C, Albuminuria, and Mortality Among Older Adults With Diabetes
SO DIABETES CARE
LA English
DT Article
ID GLOMERULAR-FILTRATION-RATE; ALL-CAUSE MORTALITY; KIDNEY-FUNCTION;
CARDIOVASCULAR MORTALITY; SERUM CREATININE; FUNCTION DECLINE; ELDERLY
PERSONS; RISK-FACTORS; DISEASE; PROTEINURIA
AB OBJECTIVE - Albuminuria and impaired glomerular filtration rate (GFR) are each associated with poor health Outcomes among individuals with diabetes. joint associations of albuminuria and impaired GFR with mortality have not been comprehensively evaluated in this population.
RESEARCH DESIGN AND METHODS - This is a cohort study among Cardiovascular Health Study participants with diabetes, mean age 78 years. GFR was estimated using serum cystatin C and serum creatinine. Albumin-to-creatinine ratio (ACR) was measured in single-voided urine samples.
RESULTS - Of 691 participants, 378 died over 1.0 years of follow-up. Cystatin C-estimated GFR <60 ml/min per 1.73 m(2), creatinine-based estimated GFR <60 ml/min per 1.73 m(2), and urine ACR >= 30 mg/g were each associated with increased mortality risk with hazard ratios of 1.73 (95% CI 1.37-2.18), 1.54 (1.21-1.97), and 1.73 (1.39-2.17), respectively, adjusting for age, sex, race, diabetes duration, hypoglycemic medications, hypertension, BMI, smoking, cholesterol, lipid-lowering medications, prevalent cardiovascular disease (CVD), and prevalent heart failure. Cystatin C-estimated GFR and urine ACR were additive in terms of mortality risk. Cystatin C-estimated GFR predicted mortality more strongly than creatinine-based estimated GFR.
CONCLUSIONS - Albuminuria and impaired GFR were independent, additive risk factors for mortality among older adults with diabetes. These Findings support current recommendations to regularly assess both albuminuria and GFR in the clinical care of patients with diabetes a focus on interventions to prevent or treat CVD in the presence of albuminuria, impaired GFR, or both; and further consideration of cystatin C use in clinical care.
C1 [de Boer, Ian H.; Katz, Ronit; Kestenbaum, Bryan; Siscovick, David S.] Univ Washington, Seattle, WA 98195 USA.
[Cao, Jie J.] NHLBI, Bethesda, MD 20892 USA.
[Fried, Linda F.] Vet Affairs Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Mukamal, Ken] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Rifkin, Dena E.; Sarnak, Mark J.] Tufts Med Ctr, Boston, MA USA.
[Shlipak, Michael G.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP de Boer, IH (reprint author), Univ Washington, Seattle, WA 98195 USA.
EM deboer@u.washington.edu
FU National Heart, Lung, and Blood Institute [N01-HC-85079, N01-HC-85086,
N01-HC-35129, N01 HC-15103, N01 HC-55222, N01-HC-75150, N01-HC-45133,
U01-HL-080295]; National Institute of Neurological Disorders and Stroke;
National Institutes of Health [R01-AG-027002, 1KL2-RR-025015-01]
FX The research reported in this article was supported by the National
Heart, Lung, and Blood Institute (contracts N01-HC-85079 through
N01-HC-85086, N01-HC-35129, N01 HC-15103, N01 HC-55222, N01-HC-75150,
and N01-HC-45133 and Grant U01-HL-080295), with additional contribution
from the National Institute of Neurological Disorders and Stroke.
Additional support came from National Institutes of Health grants
R01-AG-027002 and 1KL2-RR-025015-01.
NR 25
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U1 0
U2 1
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2009
VL 32
IS 10
BP 1833
EP 1838
DI 10.2337/dc09-0191
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 509HE
UT WOS:000271004900013
PM 19587367
ER
PT J
AU Pavkov, ME
Curtis, JM
Mason, CC
Knowler, WC
Bennett, PH
Nelson, RG
AF Pavkov, Meda E.
Curtis, Jeffrey M.
Mason, Clinton C.
Knowler, William C.
Bennett, Peter H.
Nelson, Robert G.
TI Change in the Distribution of Albuminuria According to Estimated
Glomerular Filtration Rate in Pima Indians With Type 2 Diabetes
SO DIABETES CARE
LA English
DT Article
ID RENAL-DISEASE; MELLITUS; NEPHROPATHY; INSUFFICIENCY; PROTEINURIA;
PROGRESSION; POPULATION; PRESSURE; EQUATION; DIET
AB OBJECTIVE - We examined secular trends in the frequency distribution of albuminuria and estimated glomerular filtration rate (eGFR) in subjects with type 2 diabetes in 1982-1988 and 2001-2006, two periods associated with major changes in the management of diabetes.
RESEARCH DESIGN AND METHODS - The cross-sectional study included Pima Indians >= 15 years old with type 2 diabetes and measures of serum creatinine and urinary albumin-to-creatinine ratios (ACR). The continuous probability density distributions of ACR and eGFR were compared for the two time periods. eGFR was calculated using the Modification of Diet in Renal Disease Study equation.
RESULTS - The overall standardized distribution of ACR shifted toward lower values between time periods (P = 0.001), whereas the standardized distribution of eGFR did not (P = 0.45). In the first period, eGFR was <60 ml/min per 1.73 m(2) in 6.5% of the 837 subjects. Of these, 9.3% had normal ACR, 7.4% had microalbuminuria, and 83.3% had macroalbuminuria. in the second period, the prevalence of low eGFR was similar (6.6% of the 1,310 subjects). Among those with low eGFR, normal ACR prevalence doubled to 17.2%, microalbuminuria prevalence nearly tripled to 19.5%, and macroalbuminuria prevalence declined to 63.2%. Twice as man), subjects in the second period received antihypertensive medicines and 30% more received hypoglycemic medicines than in the first period.
CONCLUSIONS - The distribution of albuminuria changed significantly among diabetic Pima Indians over the past 20 years, as treatment with medicines to control hyperglycemia and hypertension increased. The distribution of eGFR, however, remained unchanged. Consequently, the frequency of chronic kidney disease characterized by normoalbuminuria and low eGFR doubled.
C1 [Pavkov, Meda E.; Curtis, Jeffrey M.; Mason, Clinton C.; Knowler, William C.; Bennett, Peter H.; Nelson, Robert G.] NIDDKD, Diabet Epidemiol & Clin Res Sect, NIH, Phoenix, AZ USA.
[Pavkov, Meda E.] Ctr Dis Control & Prevent, Natl Ctr Chron Dis Prevent & Hlth Promot, Div Diabet Translat, Atlanta, GA USA.
RP Pavkov, ME (reprint author), NIDDKD, Diabet Epidemiol & Clin Res Sect, NIH, Phoenix, AZ USA.
EM mpavkov@cdc.gov
RI Nelson, Robert/B-1470-2012
FU National Institute of Diabetes and Digestive and Kidney Diseases;
American Diabetes Association
FX This research was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases. M.E.P.
was supported by a Mentor-Based Fellowship award from the American
Diabetes Association.
NR 24
TC 8
Z9 8
U1 0
U2 1
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD OCT
PY 2009
VL 32
IS 10
BP 1845
EP 1850
DI 10.2337/dc08-2325
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 509HE
UT WOS:000271004900015
PM 19592626
ER
PT J
AU Perry, JRB
Ferrucci, L
Bandinelli, S
Guralnik, J
Semba, RD
Rice, N
Melzer, D
Saxena, R
Scott, LJ
McCarthy, MI
Hattersley, AT
Zeggini, E
Weedon, MN
Frayling, TM
AF Perry, J. R. B.
Ferrucci, L.
Bandinelli, S.
Guralnik, J.
Semba, R. D.
Rice, N.
Melzer, D.
Saxena, R.
Scott, L. J.
McCarthy, M. I.
Hattersley, A. T.
Zeggini, E.
Weedon, M. N.
Frayling, T. M.
CA DIAGRAM Consortium
TI Circulating beta-carotene levels and type 2 diabetes-cause or effect?
SO DIABETOLOGIA
LA English
DT Article
DE beta-Carotene; Mendelian randomisation; Type 2 diabetes
ID MENDELIAN RANDOMIZATION; RISK; MELLITUS; SUPPLEMENTATION; EPIDEMIOLOGY;
DIETARY; LOCI
AB Circulating beta-carotene levels are inversely associated with risk of type 2 diabetes, but the causal direction of this association is not certain. In this study we used a Mendelian randomisation approach to provide evidence for or against the causal role of the antioxidant vitamin beta-carotene in type 2 diabetes.
We used a common polymorphism (rs6564851) near the BCMO1 gene, which is strongly associated with circulating beta-carotene levels (p = 2 x 10(-24)), with each G allele associated with a 0.27 standard deviation increase in levels. We used data from the InCHIANTI and Uppsala Longitudinal Study of Adult Men (ULSAM) studies to estimate the association between beta-carotene levels and type 2 diabetes. We next used a triangulation approach to estimate the expected effect of rs6564851 on type 2 diabetes risk and compared this with the observed effect using data from 4549 type 2 diabetes patients and 5579 controls from the Diabetes Genetics Replication And Meta-analysis (DIAGRAM) Consortium.
A 0.27 standard deviation increase in beta-carotene levels was associated with an OR of 0.90 (95% CI 0.86-0.95) for type 2 diabetes in the InCHIANTI study. This association was similar to that of the ULSAM study (OR 0.90 [0.84-0.97]). In contrast, there was no association between rs6564851 and type 2 diabetes (OR 0.98 [0.93-1.04], p = 0.58); this effect size was also smaller than that expected, given the known associations between rs6564851 and beta-carotene levels, and the associations between beta-carotene levels and type 2 diabetes.
Our findings in this Mendelian randomisation study are in keeping with randomised controlled trials suggesting that beta-carotene is not causally protective against type 2 diabetes.
C1 [Perry, J. R. B.; Rice, N.; Melzer, D.; Hattersley, A. T.; Weedon, M. N.; Frayling, T. M.] Peninsula Med Sch, Exeter EX1 2LU, Devon, England.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Bethesda, MD 20892 USA.
[Bandinelli, S.] Geriatr Unit, Florence, Italy.
[Guralnik, J.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Semba, R. D.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Saxena, R.] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Scott, L. J.] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Scott, L. J.] Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[McCarthy, M. I.] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford, England.
[McCarthy, M. I.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
[Zeggini, E.] Wellcome Trust Sanger Inst, Cambridge, England.
RP Frayling, TM (reprint author), Peninsula Med Sch, Genet Complex Traits,Magdalen Rd, Exeter EX1 2LU, Devon, England.
EM tim.frayling@pms.ac.uk
OI Zeggini, Eleftheria/0000-0003-4238-659X; Melzer,
David/0000-0002-0170-3838
FU Intramural Research Program of the National Institutes of Health (NIH);
National Institute on Aging (NIA) [N01-AG-6-2101, N01-AG-6-2103,
N01-AG-6- 2106]; NIH/NIA [R01 AG24233-01]
FX We thank the DIAGRAM consortium for their collaboration. This work was
supported in part by the Intramural Research Program of the National
Institutes of Health (NIH), National Institute on Aging (NIA). This work
is supported in part by NIH/NIA; grant R01 AG24233-01; D. Melzer is
supported by a NHS Executive National Public Health Career Scientist
Awards, Ref: PHCSA/00/002. The NIA contract numbers of the Health ABC
participating centers are: N01-AG-6-2101; N01-AG-6-2103; N01-AG-6- 2106.
NR 19
TC 12
Z9 12
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
EI 1432-0428
J9 DIABETOLOGIA
JI Diabetologia
PD OCT
PY 2009
VL 52
IS 10
BP 2117
EP 2121
DI 10.1007/s00125-009-1475-8
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 494VT
UT WOS:000269848100018
PM 19662379
ER
PT J
AU Ashktorab, H
Belgrave, K
Hosseinkhah, F
Brim, H
Nouraie, M
Takkikto, M
Hewitt, S
Lee, EL
Dashwood, RH
Smoot, D
AF Ashktorab, Hassan
Belgrave, Kevin
Hosseinkhah, Fatemeh
Brim, Hassan
Nouraie, Mehdi
Takkikto, Mikiko
Hewitt, Steve
Lee, Edward L.
Dashwood, R. H.
Smoot, Duane
TI Global Histone H4 Acetylation and HDAC2 Expression in Colon Adenoma and
Carcinoma
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Global histone acetylation; HDAC2; Colon cancer
ID CELL LUNG-CANCER; DEACETYLASE INHIBITORS; COLORECTAL-CANCER;
GENE-EXPRESSION; MICROSATELLITE INSTABILITY; AFRICAN-AMERICANS; DNA
METHYLATION; CHROMATIN; HYPERMETHYLATION; CLASSIFICATION
AB Chromatin remodeling and activation of transcription are important aspects of gene regulation, but these often go awry in disease progression, including during colon cancer development. We investigated the status of global histone acetylation (by measuring H3, H4 acetylation of lysine residues, which also occur over large regions of chromatin including coding regions and non-promoter sequences) and expression of histone deacetylase 2 (HDAC2) in colorectal cancer (CRC) tissue microarrays using immunohistochemical staining. Specifically, HDAC2 and the acetylation of histones H4K12 and H3K18 were evaluated in 134 colonic adenomas, 55 moderate to well differentiated carcinomas, and 4 poorly differentiated carcinomas compared to matched normal tissue. In addition, the correlation between expression of these epigenetic biomarkers and various clinicopathological factors including, age, location, and stage of the disease were analyzed. HDAC2 nuclear expression was detected at high levels in 81.9%, 62.1%, and 53.1% of CRC, adenomas, and normal tissue, respectively (P = 0.002). The corresponding nuclear global expression levels in moderate to well differentiated tumors for H4K12 and H3K18 acetylation were increased while these levels were decreased in poorly differentiated tumors (P = 0.02). HDAC2 expression was correlated significantly with progression of adenoma to carcinoma (P = 0.002), with a discriminative power of 0.74, when comparing cancer and non-cancer cases. These results suggest HDAC2 expression is significantly associated with CRC progression.
C1 [Ashktorab, Hassan; Belgrave, Kevin; Hosseinkhah, Fatemeh; Brim, Hassan; Nouraie, Mehdi; Lee, Edward L.; Smoot, Duane] Howard Univ, Coll Med, Dept Med, Washington, DC 20059 USA.
[Ashktorab, Hassan; Belgrave, Kevin; Hosseinkhah, Fatemeh; Brim, Hassan; Nouraie, Mehdi; Lee, Edward L.; Smoot, Duane] Howard Univ, Ctr Canc, Coll Med, Washington, DC 20059 USA.
[Brim, Hassan; Lee, Edward L.] Howard Univ, Coll Med, Dept Pathol, Washington, DC 20059 USA.
[Takkikto, Mikiko; Hewitt, Steve] NCI, Tissue Array Res Program, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Dashwood, R. H.] Oregon State Univ, Linus Pauling Inst, Corvallis, OR 97331 USA.
RP Ashktorab, H (reprint author), Howard Univ, Coll Med, Dept Med, 2041 Georgia Ave NW, Washington, DC 20059 USA.
EM hashktorab@howard.edu
RI Dashwood, Roderick/E-9090-2011;
OI Hewitt, Stephen/0000-0001-8283-1788
FU National Cancer Institute [A102681, CA122959]
FX This work was supported in part by grants A102681 and CA122959 from the
National Cancer Institute.
NR 41
TC 37
Z9 37
U1 1
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD OCT
PY 2009
VL 54
IS 10
BP 2109
EP 2117
DI 10.1007/s10620-008-0601-7
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 490UK
UT WOS:000269531900008
PM 19057998
ER
PT J
AU Henderson, DK
Malanoski, MP
Corapi, G
Passamani, E
Notobartolo, C
Gillette, C
Hawes, P
Lee, LM
AF Henderson, David K.
Malanoski, Michael P.
Corapi, Gene
Passamani, Eugene
Notobartolo, Cynthia
Gillette, Chris
Hawes, Patricia
Lee, Laura M.
TI Bethesda Hospitals' Emergency Preparedness Partnership: A Model for
Transinstitutional Collaboration of Emergency Responses
SO DISASTER MEDICINE AND PUBLIC HEALTH PREPAREDNESS
LA English
DT Article
ID PUBLIC-HEALTH EMERGENCIES; SURGE CAPACITY; DISASTER RESPONSE; CARE;
AGENCIES; CASUALTY
AB The events of September 11, 2001 identified a need for health care institutions to develop flexible, creative, and adaptive response mechanisms in the event of a local, regional, or national disaster. The 3 major health care institutions in Bethesda, MD-the National Naval Medical Center (NNMC), the Suburban Hospital Healthcare System (SHHS), and the National Institutes of Health Clinical Center (NIHCC)-have created a preparedness partnership that outstrips what any of the institutions could provide independently by pooling complementary resources. The creation of the partnership initially was driven by geographic proximity and by remarkably complementary resources. This article describes the creation of the partnership, the drivers and obstacles to creation, and the functioning and initial accomplishments of the partnership. The article argues that similar proximity and resource relationships exist among institutions at academic centers throughout the United States and suggests that this partnership may serve as a template for other similarly situated institutions. (Disaster Med Public Health Preparedness. 2009;3:168-173)
C1 [Henderson, David K.; Lee, Laura M.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Henderson, DK (reprint author), NIH, Ctr Clin, Bldg 10,Room 6-1480,10 Ctr Dr, Bethesda, MD 20892 USA.
EM dkh@nih.gov
NR 26
TC 0
Z9 0
U1 0
U2 0
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1935-7893
EI 1938-744X
J9 DISASTER MED PUBLIC
JI Dis. Med. Public Health Prep.
PD OCT
PY 2009
VL 3
IS 1
BP 168
EP 173
DI 10.1097/DMP.0b013e3181aa2719
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 553MA
UT WOS:000274369700012
ER
PT J
AU Henderson, DK
Malanoski, MP
Corapi, G
Passamani, E
Notobartolo, C
Gillette, C
Hawes, P
Lee, LM
AF Henderson, David K.
Malanoski, Michael P.
Corapi, Gene
Passamani, Eugene
Notobartolo, Cynthia
Gillette, Chris
Hawes, Patricia
Lee, Laura M.
TI Bethesda Hospitals' Emergency Preparedness Partnership: A Model for
Transinstitutional Collaboration of Emergency Responses
SO DISASTER MEDICINE AND PUBLIC HEALTH PREPAREDNESS
LA English
DT Article
ID PUBLIC-HEALTH EMERGENCIES; SURGE CAPACITY; DISASTER RESPONSE; CARE;
AGENCIES; CASUALTY
AB The events of September 11, 2001 identified a need for health care institutions to develop flexible, creative, and adaptive response mechanisms in the event of a local, regional, or national disaster. The 3 major health care institutions in Bethesda, MD-the National Naval Medical Center (NNMC), the Suburban Hospital Healthcare System (SHHS), and the National Institutes of Health Clinical Center (NIHCC)-have created a preparedness partnership that outstrips what any of the institutions could provide independently by pooling complementary resources. The creation of the partnership initially was driven by geographic proximity and by remarkably complementary resources. This article describes the creation of the partnership, the drivers and obstacles to creation, and the functioning and initial accomplishments of the partnership. The article argues that similar proximity and resource relationships exist among institutions at academic centers throughout the United States and suggests that this partnership may serve as a template for other similarly situated institutions. (Disaster Med Public Health Preparedness. 2009; 3: 168-173)
C1 [Henderson, David K.; Lee, Laura M.] NIH Clin Ctr, Bethesda, MD 20892 USA.
RP Henderson, DK (reprint author), NIH Clin Ctr, Bldg 10,Room 6-1480,10 Ctr Dr, Bethesda, MD 20892 USA.
EM dkh@nih.gov
NR 26
TC 0
Z9 0
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 1935-7893
J9 DISASTER MED PUBLIC
JI Dis. Med. Public Health Prep.
PD OCT
PY 2009
VL 3
IS 3
BP 168
EP 173
DI 10.1097/DMP.0b013e3181aa2719
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 583QD
UT WOS:000276692500011
ER
PT J
AU Sharov, AA
Ko, MSH
AF Sharov, Alexei A.
Ko, Minoru S. H.
TI Exhaustive Search for Over-represented DNA Sequence Motifs with
CisFinder
SO DNA RESEARCH
LA English
DT Article
DE algorithm; software; transcription factor binding site; ChIP-seq;
embryonic stem cells
ID EMBRYONIC STEM-CELLS; FACTOR-BINDING SITES; POU DIMER CONFIGURATION;
CIS-REGULATORY MODULES; CHROMATIN-IMMUNOPRECIPITATION; SYSTEMATIC
DISCOVERY; ENHANCER BLOCKING; HUMAN GENOME; CTCF; ALGORITHM
AB We present CisFinder software, which generates a comprehensive list of motifs enriched in a set of DNA sequences and describes them with position frequency matrices (PFMs). A new algorithm was designed to estimate PFMs directly from counts of n-mer words with and without gaps; then PFMs are extended over gaps and flanking regions and clustered to generate non-redundant sets of motifs. The algorithm successfully identified binding motifs for 12 transcription factors (TFs) in embryonic stem cells based on published chromatin immunoprecipitation sequencing data. Furthermore, CisFinder successfully identified alternative binding motifs of TFs (e.g. POU5F1, ESRRB, and CTCF) and motifs for known and unknown co-factors of genes associated with the pluripotent state of ES cells. CisFinder also showed robust performance in the identification of motifs that were only slightly enriched in a set of DNA sequences.
C1 [Sharov, Alexei A.; Ko, Minoru S. H.] NIA, Dev Genom & Aging Sect, Genet Lab, NIH, Baltimore, MD 21224 USA.
RP Ko, MSH (reprint author), NIA, Dev Genom & Aging Sect, Genet Lab, NIH, Baltimore, MD 21224 USA.
EM kom@mail.nih.gov
RI Ko, Minoru/B-7969-2009
OI Ko, Minoru/0000-0002-3530-3015
FU NIH, National institute on Aging
FX This research was supported entirely by the Intramural Research Program
of the NIH, National institute on Aging.
NR 53
TC 64
Z9 64
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1340-2838
J9 DNA RES
JI DNA Res.
PD OCT
PY 2009
VL 16
IS 5
BP 261
EP 273
DI 10.1093/dnares/dsp014
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 517JV
UT WOS:000271610400002
PM 19740934
ER
PT J
AU Uhl, GR
Drgon, T
Li, CY
Johnson, C
Liu, QR
AF Uhl, George R.
Drgon, Tomas
Li, Chuan-Yun
Johnson, Catherine
Liu, Qing-Rong
TI Smoking and smoking cessation in disadvantaged women: Assessing genetic
contributions
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Review
DE Genetics; Genome wide association; Tobacco; Dependence
ID GENOME-WIDE ASSOCIATION; FAGERSTROM TOLERANCE QUESTIONNAIRE;
POPULATION-BASED SAMPLE; TWINS REARED APART; NICOTINE DEPENDENCE;
MOLECULAR-GENETICS; SUBSTANCE USE; ENVIRONMENTAL-INFLUENCES;
LUNG-CANCER; ADULT TWINS
AB Abundant evidence from family, adoption and twin studies points to large genetic contributions to individual differences in vulnerability to develop dependence on one or more addictive substances, including tobacco. Twin data suggests that much of this genetic vulnerability is shared by individuals who are dependent on a variety of addictive substances. Interestingly, some twin data also supports Substantial differences in the apparent heritability of nicotine dependence in women as environmental conditions become more permissive for their smoking. In addition, twin studies also support the idea that ability to quit smoking displays substantial heritability, and that this heritable influence overlaps partially with genetic influences on nicotine dependence. Candidate gene molecular genetic studies and genome wide association studies of substance dependence and ability to quit smoking each document apparent polygenic influences that identify lists of genes that display partial overlap, as expected from classical genetic studies. More of these genes are expressed in the brain than would be anticipated by chance. These lists of genes overlap significantly with those identified in molecular genetic studies of individual differences in cognitive abilities, frontal lobe brain volumes as well as personality and psychiatric phenotypes. Though most available genome wide association data do not separate results by gender, it may be notable that few of these genes lie on sex chromosomes. These data provide a substrate to improve understanding of nicotine dependence, the ability to quit smoking, the potential for less permissive environments to restrict the expression of genetic influences on smoking and the possibility that brain features that underlie phenotypes such as individual differences in cognitive abilities might interact with environmental features that are especially prominent for disadvantaged women to provide special circumstances that should be considered in prevention and treatment efforts to reduce smoking. Published by Elsevier Ireland Ltd.
C1 [Uhl, George R.; Drgon, Tomas; Li, Chuan-Yun; Johnson, Catherine; Liu, Qing-Rong] NIDA, Mol Neurobiol Branch, NIH IRP, Baltimore, MD USA.
[Li, Chuan-Yun] Peking Univ, Coll Life Sci, Natl Lab Prot Engn & Plant Genet Engn, Beijing 100871, Peoples R China.
RP Uhl, GR (reprint author), Box 5180, Baltimore, MD 21224 USA.
EM guhl@intra.nida.nih.gov
RI Liu, Qing-Rong/A-3059-2012
OI Liu, Qing-Rong/0000-0001-8477-6452
FU NIH, NIDA; Peking University
FX Funding for this study was provided by NIH, NIDA Intrarnural Research
Program and Peking University (CYL). NIDA-IRP and Peking University had
no further role in study design; in the collection, analysis and
interpretation of data; in the writing of the report; or in the decision
to submit the paper for publication.
NR 45
TC 8
Z9 8
U1 0
U2 4
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 2009
VL 104
BP S58
EP S63
DI 10.1016/j.drugalcdep.2009.03.012
PG 6
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 496PW
UT WOS:000269988400009
PM 19442458
ER
PT J
AU Borland, MG
Perdew, GH
Gonzalez, FJ
Peters, JM
AF Borland, Michael G.
Perdew, Gary H.
Gonzalez, Frank J.
Peters, Jeffrey M.
TI Regulation of AhR signaling by PPAR beta/delta in skin
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 16th North American Regional ISSX Meeting
CY OCT 18-22, 2009
CL Baltimore, MD
C1 [Borland, Michael G.; Peters, Jeffrey M.] Penn State Univ, Ctr Mol Toxicol & Carcinogenesis, University Pk, PA 16802 USA.
[Perdew, Gary H.] Penn State Univ, Ctr Molec Toxicol, University Pk, PA 16802 USA.
[Gonzalez, Frank J.] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD OCT
PY 2009
VL 41
SU 3
MA 35
BP 19
EP 19
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 629AB
UT WOS:000280165300026
ER
PT J
AU Stern, ST
Myer, L
Paciotti, GF
Tamarkin, L
McNeil, SE
AF Stern, Stephan T.
Myer, Lonnie
Paciotti, Giulio F.
Tamarkin, Lawrence
McNeil, Scott E.
TI Pharmacokinetics and allometric scaling of a TNF nanoformulation
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 16th North American Regional ISSX Meeting
CY OCT 18-22, 2009
CL Baltimore, MD
C1 [Stern, Stephan T.; McNeil, Scott E.] SAIC Frederick Inc, NCI Frederick, Nanotechnol Characterizat Lab, Adv Technol Program, Frederick, MD 21702 USA.
[Myer, Lonnie; Paciotti, Giulio F.; Tamarkin, Lawrence] CytImmune Sci Inc, College Pk, MD 20740 USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD OCT
PY 2009
VL 41
SU 3
MA 75
BP 38
EP 38
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 629AB
UT WOS:000280165300064
ER
PT J
AU Bourdi, M
Davies, JS
Sendide, K
Pohl, LR
AF Bourdi, Mohammed
Davies, John S.
Sendide, Khalid
Pohl, Lance R.
TI Not all C57BL/6 mice are created equal
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 16th North American Regional ISSX Meeting
CY OCT 18-22, 2009
CL Baltimore, MD
C1 [Bourdi, Mohammed; Davies, John S.; Sendide, Khalid; Pohl, Lance R.] NHLBI, Lab Mol Immunol, Natl Inst Hlth, DHHS, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD OCT
PY 2009
VL 41
SU 3
MA 220
BP 108
EP 108
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 629AB
UT WOS:000280165300207
ER
PT J
AU Osabe, M
AF Osabe, Makoto
TI The molecular mechanism by which ERK1/2 regulates CAR activation
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 16th North American Regional ISSX Meeting
CY OCT 18-22, 2009
CL Baltimore, MD
ID RECEPTOR CAR
C1 [Osabe, Makoto] NIEHS, Lrdt, NIH, Durham, NC 27709 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD OCT
PY 2009
VL 41
SU 3
MA 340
BP 169
EP 169
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 629AB
UT WOS:000280165300327
ER
PT J
AU Yamazaki, Y
Moore, R
Negishi, M
AF Yamazaki, Yuichi
Moore, Rick
Negishi, Masahiko
TI The roles of nuclear xenobiotic receptor CAR in DDC-induced Oval cell
proliferation in mouse liver
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 16th North American Regional ISSX Meeting
CY OCT 18-22, 2009
CL Baltimore, MD
C1 [Yamazaki, Yuichi; Moore, Rick; Negishi, Masahiko] NIEHS, Pharmacogenet Sect, LRDT, NIH, Res Triangle Pk, NC 27709 USA.
NR 1
TC 0
Z9 0
U1 0
U2 1
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD OCT
PY 2009
VL 41
SU 3
MA 343
BP 170
EP 171
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 629AB
UT WOS:000280165300330
ER
PT J
AU Kodama, S
Negishi, M
AF Kodama, Susumu
Negishi, Masahiko
TI Nuclear receptor PXR Elicits p38 MAPK signal via activation of the
GADD45 beta gene
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 16th North American Regional ISSX Meeting
CY OCT 18-22, 2009
CL Baltimore, MD
C1 [Kodama, Susumu; Negishi, Masahiko] NIEHS, Pharmacogenet Sect, LRDT, NIH, Res Triangle Pk, NC 27709 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD OCT
PY 2009
VL 41
SU 3
MA 344
BP 171
EP 171
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 629AB
UT WOS:000280165300331
ER
PT J
AU Osabe, M
Mutoh, S
Moore, R
Sueyoshi, T
Negishi, M
AF Osabe, Makoto
Mutoh, Shingo
Moore, Rick
Sueyoshi, Tatsuya
Negishi, Masahiko
TI The molecular mechanism by which ERK 1/2 regulates CAR activation
SO DRUG METABOLISM REVIEWS
LA English
DT Meeting Abstract
CT 16th North American Regional ISSX Meeting
CY OCT 18-22, 2009
CL Baltimore, MD
ID RECEPTOR CAR
C1 [Osabe, Makoto; Mutoh, Shingo; Moore, Rick; Sueyoshi, Tatsuya; Negishi, Masahiko] NIEHS, Pharmacogenet Sect, LRDT, NIH, Res Triangle Pk, NC 27709 USA.
NR 2
TC 0
Z9 0
U1 0
U2 3
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD OCT
PY 2009
VL 41
SU 3
MA 345
BP 171
EP 172
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 629AB
UT WOS:000280165300332
ER
PT J
AU Cara, LCL
Romagnoli, R
Baraldi, PG
Carrion, MD
Cruz-Lopez, O
Balzarini, J
Hamel, E
Canella, A
Fabbri, E
Gambari, R
Basso, G
Viola, G
AF Cara, L. C. Lopez
Romagnoli, R.
Baraldi, P. G.
Carrion, M. D.
Cruz-Lopez, O.
Balzarini, Jan
Hamel, Ernest
Canella, Alessandro
Fabbri, Enrica
Gambari, Roberto
Basso, Giuseppe
Viola, Giampietro
TI HYBRID alpha-BROMOACRYLOYLAMIDO CHALCONES. DESIGN, SYNTHESIS AND
BIOLOGICAL EVALUATION
SO DRUGS OF THE FUTURE
LA English
DT Meeting Abstract
C1 [Cara, L. C. Lopez; Romagnoli, R.; Baraldi, P. G.; Carrion, M. D.; Cruz-Lopez, O.] Univ Ferrara, Dipartimento Sci Farmaceut, I-44100 Ferrara, Italy.
[Balzarini, Jan] Rega Inst, Lab Virol & Chemotherapy, B-3000 Louvain, Belgium.
[Hamel, Ernest] NCI, Toxicol & Pharmacol Branch, Dev Therapeut Program, Div Canc Treatment & Diag,NIH, Frederick, MD 21702 USA.
[Canella, Alessandro; Fabbri, Enrica; Gambari, Roberto] Univ Ferrara, Dipartmento Biochim & Biol Mol, BioPharmaNet, I-44100 Ferrara, Italy.
[Basso, Giuseppe; Viola, Giampietro] Univ Padua, Dipartimento Pediat, Lab Oncoematol, I-35131 Padua, Italy.
RI Gambari, Roberto/F-9555-2015; Romagnoli, Romeo/G-9887-2015; LOPEZ-CARA,
LUISA CARLOTA/F-9686-2014; Baraldi, Pier Giovanni/B-7933-2017;
Cruz-Lopez, Olga /F-3060-2017
OI Gambari, Roberto/0000-0001-9205-6033; LOPEZ-CARA, LUISA
CARLOTA/0000-0003-1142-6448;
NR 4
TC 0
Z9 0
U1 0
U2 2
PU PROUS SCIENCE, SA-THOMSON REUTERS
PI BARCELONA
PA PO BOX 540, PROVENZA 388, 08025 BARCELONA, SPAIN
SN 0377-8282
J9 DRUG FUTURE
JI Drug Future
PD OCT
PY 2009
VL 34
SU A
BP 64
EP 64
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 561NG
UT WOS:000274983700035
ER
PT J
AU Higgins, RD
Shankaran, S
AF Higgins, Rosemary D.
Shankaran, Seetha
TI Hypothermia for hypoxic ischemic encephalopathy in infants >= 36 weeks
SO EARLY HUMAN DEVELOPMENT
LA English
DT Article; Proceedings Paper
CT 1st International Conference on Clinical Neonatology
CY NOV, 2009
CL Torino, ITALY
ID WHOLE-BODY HYPOTHERMIA; MILD SYSTEMIC HYPOTHERMIA; NEONATAL
ENCEPHALOPATHY; PERINATAL ASPHYXIA; SELECTIVE HEAD; MODERATE
HYPOTHERMIA; FETAL SHEEP; NEUROPROTECTIVE THERAPY; POSTISCHEMIC
SEIZURES; CEREBRAL HYPOTHERMIA
AB Hypoxic ischemic encephalopathy is a serious condition affecting infants which can result in death and disability. This is a summary of pathogenesis of HIE, animal studies of cooling for hypoxic and ischemic models, human hypothermia trials, and the American Academy of Pediatrics publication on hypothermia for HIE. Hypothermia for neonatal HIE is continuing to evolve as a therapy. Studies, gaps in knowledge and opportunities for research are presented herein. Published by Elsevier Ltd.
C1 Wayne State Univ, Sch Med, Dept Pediat, Div Neonatal Perinatal Med, Detroit, MI 48201 USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, Ctr Dev Biol & Perinatal Med, NIH, Bethesda, MD USA.
RP Higgins, RD (reprint author), NICHD, Pregnancy & Perinatol Branch, Ctr Dev Biol & Perinatal Med, NIH 6100 Execut Blvd,Room 4B03B,MSC 7510, Bethesda, MD 20892 USA.
EM higginsr@mail.nih.gov
FU Intramural NIH HHS [Z99 HD999999]
NR 41
TC 8
Z9 8
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0378-3782
J9 EARLY HUM DEV
JI Early Hum. Dev.
PD OCT
PY 2009
VL 85
IS 10
BP S49
EP S52
DI 10.1016/j.earlhumdev.2009.08.015
PG 4
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 523WK
UT WOS:000272105200014
PM 19762176
ER
PT J
AU Kohn, E
AF Kohn, E.
TI Clinical application of biomarkers: discovery, validation, and
application
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT Annual Meeting of the EORTC/NCI/ASCO on Molecular Markers in Cancer
CY OCT 15-17, 2009
CL Brussels, BELGIUM
SP EORTC, NCI, ASCO
C1 [Kohn, E.] 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 2009
VL 7
IS 4
BP 5
EP 5
PG 1
WC Oncology
SC Oncology
GA 536CC
UT WOS:000273018800019
ER
PT J
AU Rubinstein, L
AF Rubinstein, L.
TI Methodology and design of phase 0 and phase 2 trials with biomarker
variables and endpoints
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT Annual Meeting of the EORTC/NCI/ASCO on Molecular Markers in Cancer
CY OCT 15-17, 2009
CL Brussels, BELGIUM
SP EORTC, NCI, ASCO
C1 [Rubinstein, L.] 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 2009
VL 7
IS 4
BP 7
EP 7
PG 1
WC Oncology
SC Oncology
GA 536CC
UT WOS:000273018800029
ER
PT J
AU Giovannetti, E
Zucali, P
Tibaldi, C
Smit, E
Falcone, A
Santoro, A
Leon, L
Giaccone, G
Danesi, R
Peters, G
AF Giovannetti, E.
Zucali, P.
Tibaldi, C.
Smit, E.
Falcone, A.
Santoro, A.
Leon, L.
Giaccone, G.
Danesi, R.
Peters, G.
TI Polymorphisms in AKT1 and EGFR as possible new biomarkers of clinical
outcome and toxicity in non-small-cell lung cancer patients treated with
gefitinib
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT Annual Meeting of the EORTC/NCI/ASCO on Molecular Markers in Cancer
CY OCT 15-17, 2009
CL Brussels, BELGIUM
SP EORTC, NCI, ASCO
C1 [Giovannetti, E.; Smit, E.; Leon, L.; Peters, G.] Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands.
[Zucali, P.; Santoro, A.] Ist Clin Humanitas, Dept Med Oncol & Hematol, Milan, Italy.
[Tibaldi, C.] Azienda USL 6 Livorno, Dept Oncol, Div Oncol, Livorno, Italy.
[Falcone, A.; Danesi, R.] Univ Pisa, I-56100 Pisa, Italy.
[Giaccone, G.] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 2009
VL 7
IS 4
BP 9
EP 9
PG 1
WC Oncology
SC Oncology
GA 536CC
UT WOS:000273018800034
ER
PT J
AU Hsiao, YH
Deng, C
Su, YA
Tsai, HD
Wang, X
Mason, JT
Chou, MC
Man, YG
AF Hsiao, Y-H.
Deng, C.
Su, Y. A.
Tsai, H. -D.
Wang, X.
Mason, J. T.
Chou, M. -C.
Man, Y-g.
TI Reduced p63 expression in myoepithelium correlating with increased
invasiveness in epithelium
SO EJC SUPPLEMENTS
LA English
DT Meeting Abstract
CT Annual Meeting of the EORTC/NCI/ASCO on Molecular Markers in Cancer
CY OCT 15-17, 2009
CL Brussels, BELGIUM
SP EORTC, NCI, ASCO
C1 [Hsiao, Y-H.; Chou, M. -C.] Chung Shan Med Univ, Inst Med, Taichung, Taiwan.
[Deng, C.] NIDDK, Mammalian Genet Sect, GDDB, NIH, Bethesda, MD 20892 USA.
[Su, Y. A.; Wang, X.] George Washington Univ, Sch Med & Hlth Sci, Washington, DC 20052 USA.
[Mason, J. T.] Armed Forces Inst Pathol, Dept Biophys, Washington, DC 20306 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 2009
VL 7
IS 4
BP 35
EP 36
PG 2
WC Oncology
SC Oncology
GA 536CC
UT WOS:000273018800127
ER
PT J
AU Scroggins, BT
Neckers, L
AF Scroggins, Bradley T.
Neckers, Len
TI Just say NO: nitric oxide regulation of Hsp90
SO EMBO REPORTS
LA English
DT Article
DE Hsp90; molecular chaperone; S-nitrosylation
ID MOLECULAR CHAPERONE; S-NITROSYLATION; SYNTHASE
C1 [Scroggins, Bradley T.; Neckers, Len] NCI, Urol Oncol Branch, Ctr Canc Res, Hatfield Clin Res Ctr, Bethesda, MD 20892 USA.
RP Neckers, L (reprint author), NCI, Urol Oncol Branch, Ctr Canc Res, Hatfield Clin Res Ctr, 9000 Rockville Pike,Room 1-5940, Bethesda, MD 20892 USA.
EM len@helix.nih.gov
NR 13
TC 6
Z9 6
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1469-221X
J9 EMBO REP
JI EMBO Rep.
PD OCT
PY 2009
VL 10
IS 10
BP 1093
EP 1094
DI 10.1038/embor.2009.212
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 501BU
UT WOS:000270354800008
PM 19763143
ER
PT J
AU Chakraborty, P
Seemann, J
Mishra, RK
Wei, JH
Weil, L
Nussenzveig, DR
Heiber, J
Barber, GN
Dasso, M
Fontoura, BMA
AF Chakraborty, Papia
Seemann, Joachim
Mishra, Ram K.
Wei, Jen-Hsuan
Weil, Lauren
Nussenzveig, Daniel R.
Heiber, Joshua
Barber, Glen N.
Dasso, Mary
Fontoura, Beatriz M. A.
TI Vesicular stomatitis virus inhibits mitotic progression and triggers
cell death
SO EMBO REPORTS
LA English
DT Article
DE nuclear pore complex; nucleoporins; mRNA export; mitosis; spindle
assembly
ID GENE-EXPRESSION; MATRIX PROTEIN; COMPLEX; REPLICATION; TRANSLATION;
TRANSPORT; ONCOLYSIS; DEFECTS
AB Vesicular stomatitis virus (VSV) infects and kills a wide range of cell types; however, the mechanisms involved in VSV-mediated cell death are not fully understood. Here we show that VSV infection interferes with mitotic progression, resulting in cell death. This effect requires the interaction of VSV matrix (M) protein with the Rae1-Nup98 complex in mitosis, which is associated with a subset of ribonucleoproteins (RNPs). VSV displaced Rae1 from spindle poles, caused spindle abnormalities and triggered substantial cell death during metaphase. These effects were attenuated in cells infected with VSV expressing a mutant M protein that does not bind efficiently to the Rae1-Nup98-RNP complex. In cells that progressed to late mitosis, M protein prevented proper nuclear formation and chromatin decondensation. VSV is an oncolytic (anti-tumour) agent as it preferentially replicates and kills tumour cells. As tumour cells have a high mitotic index, VSV-mediated mitotic cell death probably contributes to its oncolytic activity.
C1 [Chakraborty, Papia; Seemann, Joachim; Wei, Jen-Hsuan; Weil, Lauren; Fontoura, Beatriz M. A.] Univ Texas SW Med Ctr Dallas, Dept Cell Biol, Dallas, TX 75390 USA.
[Mishra, Ram K.; Dasso, Mary] NICHHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
[Nussenzveig, Daniel R.] Univ Texas SW Med Ctr Dallas, Dept Pathol, Dallas, TX 75390 USA.
[Nussenzveig, Daniel R.] Vet Affairs N Texas Hlth Care Syst, Pathol & Lab Med Serv, Dallas, TX 75216 USA.
[Barber, Glen N.] Univ Miami, Sch Med, Dept Med, Miami, FL 33136 USA.
[Barber, Glen N.] Univ Miami, Sch Med, Sylvester Canc Ctr, Miami, FL 33136 USA.
RP Fontoura, BMA (reprint author), Univ Texas SW Med Ctr Dallas, Dept Cell Biol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM beatriz.fontoura@utsouthwestern.edu
OI Dasso, Mary/0000-0002-5410-1371
FU National Institutes of Health [R01 GM07159]; Texas HEB (Higher Education
Board) [010019-0022-2006]
FX We thank M. Blower for Rae1 antibodies and K. Phelps for imaging studies
carried out at University of Texas Southwestern Imaging Facility. This
study was supported by National Institutes of Health R01 GM07159 and
Texas HEB (Higher Education Board) 010019-0022-2006 to BMAF.
NR 18
TC 15
Z9 16
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1469-221X
J9 EMBO REP
JI EMBO Rep.
PD OCT
PY 2009
VL 10
IS 10
BP 1154
EP 1160
DI 10.1038/embor.2009.179
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 501BU
UT WOS:000270354800017
PM 19745842
ER
PT J
AU Billinger, ME
Olivier, KN
Viboud, C
de Oca, RM
Steiner, C
Holland, SM
Prevots, DR
AF Billinger, Megan E.
Olivier, Kenneth N.
Viboud, Cecile
de Oca, Ruben Montes
Steiner, Claudia
Holland, Steven M.
Prevots, D. Rebecca
TI Nontuberculous Mycobacteria-associated Lung Disease in Hospitalized
Persons, United States, 1998-2005
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID AVIUM COMPLEX; PULMONARY-DISEASE; ENVIRONMENTAL MYCOBACTERIA;
CYSTIC-FIBROSIS; INFECTION; INTRACELLULARE; EPIDEMIOLOGY; PREVALENCE;
SPECIMENS; DIAGNOSIS
AB The prevalence and trends of pulmonary nontuberculous mycobacteria (NTM)-associated hospitalizations in the United States were estimated using national hospital discharge data. Records were extracted for all persons with a pulmonary NTM International Classification of Diseases code (031.0) hospitalized in the 11 states with continuous data available from 1998 through 2005. Prevalence was calculated using US census data. Pulmonary NTM hospitalizations (031.0) increased significantly with age among both sexes: relative prevalence for persons 70-79 years of age compared with those 40-49 years of age was 15/100,000 for women (9.4 vs. 0.6) and 9/100,000 for men (7.6 vs. 0.83). Annual prevalence increased significantly among men and women in Florida (3.2%/year and 6.5%/year, respectively) and among women in New York (4.6%/year) with no significant changes in California. The prevalence of pulmonary NTM-associated hospitalizations is increasing in selected geographic areas of the United States.
C1 [Prevots, D. Rebecca] NIAID, NIH, Bethesda, MD 20892 USA.
[Billinger, Megan E.] George Washington Univ, Washington, DC USA.
[Steiner, Claudia] Agcy Healthcare Res & Qual, Rockville, MD USA.
RP Prevots, DR (reprint author), NIAID, NIH, 8 West Dr,MSC 2665, Bethesda, MD 20892 USA.
EM rprevots@niaid.nih.gov
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases
FX This work was supported by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases.
NR 37
TC 66
Z9 74
U1 0
U2 5
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD OCT
PY 2009
VL 15
IS 10
BP 1562
EP 1569
DI 10.3201/eid1510.090196
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 503ZD
UT WOS:000270580600003
PM 19861046
ER
PT J
AU Dorji, T
Yoon, IK
Holmes, EC
Wangchuk, S
Tobgay, T
Nisalak, A
Chinnawirotpisan, P
Sangkachantaranon, K
Gibbons, RV
Jarman, RG
AF Dorji, Tandin
Yoon, In-Kyu
Holmes, Edward C.
Wangchuk, Sonam
Tobgay, Tashi
Nisalak, Ananda
Chinnawirotpisan, Piyawan
Sangkachantaranon, Kanittha
Gibbons, Robert V.
Jarman, Richard G.
TI Diversity and Origin of Dengue Virus Serotypes 1, 2, and 3, Bhutan
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID NEPAL
AB To determine the serotype and genotype of dengue virus (DENV) in Bhutan, we conducted phylogenetic analyses of complete envelope gene sequences. DENV-2 (Cosmopolitan genotype) predominated in 2004, and DENV-3 (genotype III) predominated in 2005-2006; these viruses were imported from India. Primary dengue infections outnumbered secondary infections, suggesting recent emergence.
C1 [Dorji, Tandin] Minist Hlth, Thimphu, Bhutan.
[Yoon, In-Kyu; Nisalak, Ananda; Chinnawirotpisan, Piyawan; Sangkachantaranon, Kanittha; Gibbons, Robert V.; Jarman, Richard G.] US Army Med Command, Armed Forces Res Inst Med Sci, Bangkok, Thailand.
[Holmes, Edward C.] Penn State Univ, University Pk, PA 16802 USA.
[Holmes, Edward C.] NIH, Bethesda, MD 20892 USA.
[Tobgay, Tashi] Minist Hlth, Gelephu, Bhutan.
EM richard.jarman@afrims.org
RI Valle, Ruben/A-7512-2013;
OI Holmes, Edward/0000-0001-9596-3552
NR 9
TC 23
Z9 23
U1 0
U2 1
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD OCT
PY 2009
VL 15
IS 10
BP 1630
EP 1632
DI 10.3201/eid1510.090123
PG 3
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 503ZD
UT WOS:000270580600015
PM 19861059
ER
PT J
AU He, J
Makey, D
Fojo, T
Adams, KT
Havekes, B
Eisenhofer, G
Sullivan, P
Lai, EW
Pacak, K
AF He, J.
Makey, D.
Fojo, T.
Adams, K. T.
Havekes, B.
Eisenhofer, G.
Sullivan, P.
Lai, E. W.
Pacak, K.
TI Successful chemotherapy of hepatic metastases in a case of succinate
dehydrogenase subunit B-related paraganglioma
SO ENDOCRINE
LA English
DT Article
DE Paraganglioma; Chemotherapy; Succinate dehydrogenase
ID PHEOCHROMOCYTOMA; SDHB; MUTATIONS
AB Compared to other familial pheochromocytoma/paragangliomas (PHEO/PGLs), the succinate dehydrogenase subunit B (SDHB)-related PHEO/PGLs often present with aggressive and rapidly growing metastatic lesions. Currently, there is no proven effective treatment for malignant PHEO/PGLs. Here, we present a 35-year-old white man with primary malignant abdominal extra-adrenal 11 cm paraganglioma underwent surgical successful resection. But 6 months later, he developed extensive bone, liver, and lymph nodes metastasis, which were demonstrated by computed tomography scan and the (18)F-fluorodeoxyglucose positron emission tomography. However, his (123)I-metaiodobenzylguanidine scintigraphy was negative; therefore, the cyclophosphamide, vincristine, and dacarbazine (CVD) combination chemotherapy was initiated. The combination chemotherapy was very effective showing 80% overall reduction in the liver lesions and 75% overall reduction in the retroperitoneal mass and adenopathy, and normalization of plasma catecholamine and metanephrine levels. However, plasma levels of dopamine (DA) and methoxytyramine (MTY) were only partially affected and remained consistently elevated throughout the remaining period of follow-up evaluation. Genetic testing revealed an SDHB gene mutation. Here, we present an SDHB-related PHEO/PGL patient with extensive tumor burden, numerous organ lesions, and rapidly growing tumors, which responded extremely well to CVD therapy. We conclude patients with SDHB-related PHEO/PGLs can be particularly sensitive to CVD chemotherapy and may have an excellent outcome if this therapy is used and continued on periodic basis. The data in this patient also illustrate the importance of measuring plasma levels of DA and MTY to provide a more complete and accurate assessment of the biochemical response to therapy than provided by measurements restricted to other catecholamines and O-methylated metabolites.
C1 [He, J.; Makey, D.; Adams, K. T.; Havekes, B.; Lai, E. W.; Pacak, K.] NICHHD, Sect Med Neuroendocrinol, Reprod & Adult Endocrinol Program, NIH, Bethesda, MD 20892 USA.
[Fojo, T.] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Havekes, B.] Univ Hosp Maastricht, Div Endocrinol, Dept Internal Med, Maastricht, Netherlands.
[Eisenhofer, G.] Univ Dresden, Div Clin Neurochem, Inst Clin Chem & Lab Med, Dresden, Germany.
[Eisenhofer, G.] Univ Dresden, Dept Med, Dresden, Germany.
[Sullivan, P.] NIH, Dept Lab Med, Bethesda, MD 20892 USA.
RP Pacak, K (reprint author), NICHHD, Sect Med Neuroendocrinol, Reprod & Adult Endocrinol Program, NIH, 10 Ctr Dr,Bldg 10,CRC,RM 1-E 3140,MSC 1109, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
FU NICHD/NIH
FX This research was supported in part by the Intramural Research Program
of the NICHD/NIH.
NR 10
TC 4
Z9 4
U1 0
U2 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0969-711X
J9 ENDOCRINE
JI Endocrine
PD OCT
PY 2009
VL 36
IS 2
BP 189
EP 193
DI 10.1007/s12020-009-9219-6
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 498UO
UT WOS:000270169800002
PM 19618298
ER
PT J
AU Hoffler, U
Hobbie, K
Wilson, R
Bai, R
Rahman, A
Malarkey, D
Travlos, G
Ghanayem, BI
AF Hoffler, Undi
Hobbie, Kristen
Wilson, Ralph
Bai, Re
Rahman, Akef
Malarkey, David
Travlos, Greg
Ghanayem, Burhan I.
TI Diet-induced obesity is associated with hyperleptinemia,
hyperinsulinemia, hepatic steatosis, and glomerulopathy in C57Bl/6J mice
SO ENDOCRINE
LA English
DT Article
DE Diet-induced obesity; Hyperinsulinemia; Hyperleptinemia; Diabetes;
Hepatic steatosis; Glomerulopathy; Mice
ID PLASMINOGEN-ACTIVATOR INHIBITOR-1; HIGH-FAT DIET; TYPE-2
DIABETES-MELLITUS; IGF-BINDING PROTEIN-1; BLOOD-BRAIN-BARRIER;
C-REACTIVE PROTEIN; INSULIN-RESISTANCE; ADIPOSE-TISSUE; LEPTIN
RESISTANCE; GENE-EXPRESSION
AB Obesity and obesity-related illnesses are global epidemics impacting the health of adults and children. The purpose of the present work is to evaluate a genetically intact obese mouse model that more accurately reflects the impact of aging on diet-induced obesity and type 2 diabetes in humans. Male C57Bl/6J mice consumed either a control diet or one in which 60% kcal were due to lard beginning at 5-6 weeks of age. Body weight and fat measurements were obtained and necropsy performed at 15, 20, 30, and 40 weeks of age. Serum chemistry, histopathology, gene expression of the liver, and renal and hepatic function were also evaluated. In concert with significant increases in percent body fat and weight, mice fed the high-fat versus control diet had significantly increased levels of serum cholesterol. At ages 20 and 30 weeks, serum glucose was significantly higher in obese versus controls, while serum insulin levels were a parts per thousand yen4-fold higher in obese mice at ages 30 and 40 weeks. The effect of age exacerbated the effects of consuming a high-fat diet. In addition to being hyperinsulinemic and leptin resistant, older obese mice exhibited elevated hepatic PAI-1 and downregulation of GLUT4, G6PC, IGFBP-1, and leptin receptor mRNA in the liver, steatosis with subsequent inflammation, glomerular mesangial proliferation, elevated serum ALT, AST, and BUN, and increased numbers of pancreatic islets.
C1 [Hoffler, Undi; Wilson, Ralph; Rahman, Akef; Ghanayem, Burhan I.] NIEHS, Pharmacol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Wilson, Ralph; Malarkey, David; Travlos, Greg] NIEHS, Cellular & Mol Pathol Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Hobbie, Kristen] Integrated Syst Lab, Res Triangle Pk, NC USA.
RP Ghanayem, BI (reprint author), NIEHS, Pharmacol Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM ghanayem@niehs.nih.gov
FU NIH; National Institute of Environmental Health Sciences
FX We extend our thanks to Drs. Retha Newbold and Susan Elmore for their
commentary and careful review of this manuscript. We also sincerely
appreciate Dr. Grace Kissling for her assistance with the statistical
analyses. This research was supported by the Intramural Research Program
of the NIH, National Institute of Environmental Health Sciences.
NR 71
TC 35
Z9 37
U1 0
U2 5
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1355-008X
EI 1559-0100
J9 ENDOCRINE
JI Endocrine
PD OCT
PY 2009
VL 36
IS 2
BP 311
EP 325
DI 10.1007/s12020-009-9224-9
PG 15
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 498UO
UT WOS:000270169800020
PM 19669948
ER
PT J
AU Sackett, DL
Olivero, O
AF Sackett, Dan L.
Olivero, Ofelia
TI Centrosome Structure and Function Under Normal and Pathological
Conditions
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Editorial Material
C1 [Sackett, Dan L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Lab Integrat & Med Biophys, Program Phys Biol, Bethesda, MD USA.
[Olivero, Ofelia] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
RP Sackett, DL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Lab Integrat & Med Biophys, Program Phys Biol, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
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 2009
VL 50
IS 8
BP 591
EP 592
DI 10.1002/em.20535
PG 2
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 511HF
UT WOS:000271153900001
PM 19774609
ER
PT J
AU Ried, T
AF Ried, Thomas
TI Homage to Theodor Boveri (1862-1915): Boveri's Theory of Cancer as a
Disease of the Chromosomes, and the Landscape of Genomic Imbalances in
Human Carcinomas
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Editorial Material
ID CENTROSOME AMPLIFICATION; CELL-LINES; CYTOGENETIC ANALYSIS; GENETIC
INSTABILITY; BURKITT LYMPHOMAS; COPY NUMBER; HYBRIDIZATION; ANEUPLOIDY;
TUMORS; ABERRATIONS
C1 NCI, NIH, Ctr Canc Res, Gent Branch, Bethesda, MD 20892 USA.
RP Ried, T (reprint author), NCI, NIH, Ctr Canc Res, Gent Branch, Bethesda, MD 20892 USA.
FU Intramural NIH HHS
NR 55
TC 19
Z9 20
U1 0
U2 2
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 2009
VL 50
IS 8
BP 593
EP 601
DI 10.1002/em.20526
PG 9
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 511HF
UT WOS:000271153900002
PM 19739242
ER
PT J
AU Lukasiewicz, KB
Lingle, WL
AF Lukasiewicz, Kara B.
Lingle, Wilma L.
TI Aurora A, Centrosome Structure, and the Centrosome Cycle
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Review
DE phosphorlyation; cell cycle; centrosome cycle; aurora kinases;
centrosome amplification
ID CENTROMERE PROTEIN INCENP; COMPARATIVE GENOMIC HYBRIDIZATION;
KINETOCHORE-MICROTUBULE ATTACHMENT; CHROMOSOME SEGREGATION REGULATORS;
HISTONE H3 PHOSPHORYLATION; INVASIVE DUCTAL CARCINOMA; BIPOLAR MITOTIC
SPINDLE; HUMAN PANCREATIC-CANCER; XENOPUS EGG EXTRACTS; HAMSTER OVARY
CELLS
AB The centrosome, also known as the microtubule organizing center of the cell, is a membrane-less organelle composed of a pair of barrel-shaped centrioles surrounded by electron-dense pericentriolar material. The centrosome progresses through the centrosome cycle in step with the cell cycle such that centrosomes are duplicated in time to serve as the spindle poles during mitosis and that each resultant daughter cell contains a single centrosome. Regulation of the centrosome cycle with relation to the cell cycle is an essential process to maintain the ratio of one centrosome per new daughter cell. Numerous mitosis-specific kinases have been implicated in this regulation, and phosphorlyation plays on important role in coordinating the centrosome and cell cycles. Centrosome amplification can occur when the cycles are uncoupled, and this amplification is associated with cancer and with an increase in the levels of chromosomal instability. The aurora kinases A, B, and C are serine/threonine kinases that are active during mitosis. Aurora A is associated with centrosomes, being localized at the centrosome just prior to the onset of mitosis and for the duration of mitosis. Overexpression of aurora A leads to centrosome amplification and cellular transformation. The activity of aurora A is regulated by phosphorlyation and proteasomal degradation. Environ. Mal. Mutagen. 50:602-619, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Lingle, Wilma L.] Mayo Clin, Dept Lab Med & Pathol, Div Expt Pathol, Rochester, MN 55905 USA.
[Lukasiewicz, Kara B.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Cell Cycle Regulat, Program Cellular Regulat & Metab, NIH, Bethesda, MD USA.
RP Lingle, WL (reprint author), Mayo Clin, Dept Lab Med & Pathol, Div Expt Pathol, Rochester, MN 55905 USA.
EM lingle.wilma@mayo.edu
NR 214
TC 31
Z9 33
U1 0
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0893-6692
EI 1098-2280
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PD OCT
PY 2009
VL 50
IS 8
SI SI
BP 602
EP 619
DI 10.1002/em.20533
PG 18
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 511HF
UT WOS:000271153900003
PM 19774610
ER
PT J
AU Moore, A
Golden, A
AF Moore, Akilah
Golden, Andy
TI Hypothesis: Bifunctional Mitochondrial Proteins Have Centrosomal
Functions
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Editorial Material
DE centrosome; bifunctional; mitochondria
ID CAENORHABDITIS-ELEGANS EMBRYOS; CYTOPLASMIC DYNEIN; CELL-CYCLE; EARLY
EMBRYOGENESIS; DYNACTIN COMPLEX; DROSOPHILA; MUTATIONS; ORGANIZATION;
REQUIREMENT; MECHANISMS
AB Mitochondria are dynamic organelles that are involved in a number of diverse processes. Most often the mitochondrion is associated with energy generation, but other important processes occur in this organelle such as fatty acid synthesis and amino acid metabolism. Although mitochondria encode less than 40 genes, all of the other similar to 1,000 genes required for their function are nuclear encoded. The protein products from these nuclear encoded genes are subsequently translocated to the mitochondria and utilized in the variety of processes within the organelle. Is it possible then that any of these nuclear encoded proteins could be translocated to other areas of the cell to participate in functions not normally attributed to the mitochondria? There is growing evidence that mitochondrial proteins not only localize to sites outside of the organelle, but also have functionality at these other locales. We suggest that a subset of nuclear encoded mitochondrial proteins are bifunctional and are involved in processes outside of the mitochondria. In this perspective, we will discuss published data demonstrating mitochondrial proteins that influence progression of the cell cycle, alter chromosome morphology, localize to centrosomes, and affect centrosome number in the cell. Overall, the mitochondrion is an interesting organelle that participates in a variety of vital functions. We suggest that these essential functions are not solely due to the ability of the mitochondria to produce high amounts of energy. Throughout this discussion we attempt to demonstrate that a cell cannot live without mitochondria and study this issue from a nonenergetic perspective. Environ. Mol. Mutagen. 50:637-648, 2009. Published 2009 Wiley-Liss, Inc.
C1 [Moore, Akilah; Golden, Andy] NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Golden, A (reprint author), NIDDK, Lab Biochem & Genet, NIH, 8 Ctr Dr, Bethesda, MD 20892 USA.
EM andyg@mail.nih.gov
FU Intramural NIH HHS [Z01 DK024947-08]
NR 34
TC 1
Z9 1
U1 0
U2 1
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 2009
VL 50
IS 8
BP 637
EP 648
DI 10.1002/em.20508
PG 12
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 511HF
UT WOS:000271153900005
PM 19565650
ER
PT J
AU Difilippantonio, MJ
Ghadimi, BM
Howard, T
Camps, J
Nguyen, QT
Ferris, DK
Sackett, DL
Ried, T
AF Difilippantonio, Michael J.
Ghadimi, B. Michael
Howard, Tamara
Camps, Jordi
Nguyen, Quang Tri
Ferris, Douglas K.
Sackett, Dan L.
Ried, Thomas
TI Nucleation Capacity and Presence of Centrioles Define a Distinct
Category of Centrosome Abnormalities that Induces Multipolar Mitoses in
Cancer Cells
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE centrosome; aneuploidy; chromosome instability; gene expression
ID POLO-LIKE KINASE; GROUP-C PROTEIN; GAMMA-TUBULIN; GENETIC INSTABILITY;
COLORECTAL CANCERS; CYCLE PROGRESSION; MITOTIC SPINDLE; AMPLIFICATION;
TUMORS; ORGANIZATION
AB Analysis of centrosome number and structure has become one means of assessing the potential for aberrant chromosome segregation and aneuploidy in tumor cells. Centrosome amplification directly causes multipolar catastrophic mitoses in mouse embryonic fibroblasts (MEFs) deficient for the tumor suppressor genes Brca1 or Trp53. We observed super-numerary centrosomes in cell lines established from aneuploid, but not from diploid, colorectal carcinomas; however, multipolar mitoses were never observed. This discrepancy prompted us to thoroughly characterize the centrosome abnormalities in these and other cancer cell lines with respect to both structure and function. The most striking result was that supernumerary centrosomes in aneuploid colorectal cancer cell lines were unable to nucleate microtubules, despite the presence of gamma-tubulin, pericentrin, PLK1, and AURKA. Analysis by scanning electron microscopy revealed that these supernumerary structures are devoid of centrioles, a result significantly different from observations in aneuploid pancreatic cancer cell lines and in Trp53 or Brca1 deficient MEFs. Thus, multipolar mitoses are dependent upon the ability of extra gamma-tubulin containing structures to nucleate microtubules, and this correlated with the presence of centrioles. The assessment of centrosome function with respect to chromosome segregation must therefore take into consideration the presence of centrioles and the capacity to nucleate microtubules. The patterns and mechanisms of chromosomal aberrations in hematologic malignancies and solid tumors are fundamentally different. The former is characterized by specific chromosome translocations, whose consequence is the activation of oncogenes. Most carcinomas, however, reveal variations in the nuclear DNA content. The observed genomic imbalances and gross variations in chromosome number can result from unequal chromosome segregation during mitotic cell division. It is therefore fundamental to elucidate mechanisms involved in distribution of the genome to daughter cells. Prior to cell division, the centrosome organizes microtubules and the mitotic spindle. Deciphering the consequences of alterations in centrosome number, structure, and important step towards understanding how a diploid genome is maintained. Although extra centrosomes have now been observed in carcinomas and were correlated with aneuploidy, a careful functional investigation of these structures and their role in generating chromosome imbalances may lead to the identification of distinct mechanistic pathways of genomic instability. Understanding these pathways will also be important in determining whether they are potential molecular targets of therapeutic intervention. Environ. Mal. Mutagen. 50:672-696, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Difilippantonio, Michael J.; Ghadimi, B. Michael; Camps, Jordi; Nguyen, Quang Tri; Ried, Thomas] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Howard, Tamara] Univ New Mexico, Dept Cell Biol & Physiol, Hlth Sci Ctr, Albuquerque, NM 87131 USA.
[Ferris, Douglas K.] NCI, SAIC, Basic Res Lab, FCRDC,NIH, Bethesda, MD 20892 USA.
[Sackett, Dan L.] NICHD, Lab Integrat & Med Biophys, Program Phys Biol, NIH, Bethesda, MD USA.
RP Difilippantonio, MJ (reprint author), 50 S Dr,Rm 1408, Bethesda, MD 20892 USA.
EM difilipm@mail.nih.gov
FU NIH, National Cancer Institute; Eunice Kennedy Shriver National
Institute of Child Health and Human Development, NIH
FX Grant sponsor: This work was supported in part by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research and by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, NIH.
NR 53
TC 6
Z9 6
U1 0
U2 5
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 2009
VL 50
IS 8
BP 672
EP 696
DI 10.1002/em.20532
PG 25
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 511HF
UT WOS:000271153900009
PM 19768832
ER
PT J
AU Yu, M
Ward, Y
Poirier, MC
Olivero, OA
AF Yu, Mia
Ward, Yvona
Poirier, Miriam C.
Olivero, Ofelia A.
TI Centrosome Amplification Induced by the Antiretroviral Nucleoside
Reverse Transcriptase Inhibitors Lamivudine, Stavudine, and Didanosine
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE centrosomes; nucleoside analogs; aneuploidy
ID CANCER PROGRESSION; CELLS; ABERRATIONS; INSTABILITY; DEFECTS; TUMORS
AB in cultured cells, exposure to the nucleoside reverse transcriptase inhibitor (NRTI) zidovudine (AZT) induces genomic instability, cell cycle arrest, micronuclei, sister chromatid exchanges, and shortened telomeres. In previous studies, we demonstrated AZT-induced centrosome amplification (>2 centrosomes/cell). Here, we investigate centrosome amplification in cells exposed to other commonly used NRTIs. Experiments were performed using Chinese Hamster ovary (CHO) cells, and two normal human mammary epithelial cell (NHMEC) strains: M99005 and M98040, which are high and low incorporators of AZT into DNA, respectively. Cells were exposed for 24 hr to lamivudine (3TC), stavudine (d4T), didanosine (ddl), and thymidine, and stained with anti-pericentrin antibody. Dose response curves were performed to determine cytotoxicity and a lower concentration at near plasma levels and a 10 fold higher concentration were chosen for the experiments. In CHO cells, there was a concentration-dependent, significant (P < 0.05) increase in centrosome amplification for each of the NRTIs. In NHMEC strain M99005, an NRTI-induced increase (P < 0.05) in centrosome amplification was observed for the high concentrations of each NRTI and the low doses of 3TC and ddl. In NHMEC strain M98040, the high doses of ddl and d4T showed significant increases in centrosome amplification. Functional viability of amplified centrosomes was assessed by arresting microtubule nucleation with nocodazole. In cells with more than two centrosomes, the ability to recover microtubule nucleation was similar to that of unexposed cells. We conclude that centrosome amplification is a consequence of exposure to NRTIs and that cells with centrosome amplification are able to accomplish cell division. Environ. Mal. Mutagen. 50:718-724, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Yu, Mia; Poirier, Miriam C.; Olivero, Ofelia A.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
[Ward, Yvona] NCI, Cell & Canc Biol Branch, CCR, NIH, Bethesda, MD 20892 USA.
RP Olivero, OA (reprint author), NCI, Lab Canc Biol & Genet, NIH, 37 Convent Dr MSC 4255,Bldg 37 Rm 4032, Bethesda, MD 20892 USA.
EM oliveroo@exchange.nih.gov
FU NIH, National Cancer Institute, Center for Cancer Research
FX Grant sponsors: Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research.
NR 18
TC 8
Z9 8
U1 0
U2 1
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 2009
VL 50
IS 8
BP 718
EP 724
DI 10.1002/em.20509
PG 7
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 511HF
UT WOS:000271153900012
PM 19562754
ER
PT J
AU Yasunaga, J
Jeang, KT
AF Yasunaga, Junichiro
Jeang, Kuan-Teh
TI Viral Transformation and Aneuploidy
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Review
DE spindle assembly checkpoint; centrosome; aneuploidy; human T-cell
leukemia virus type I (HTLV-I); tax
ID T-CELL LEUKEMIA; SPINDLE ASSEMBLY CHECKPOINT; VIRUS TYPE-1 TAX;
TRANSGENIC MOUSE MODEL; DNA-DAMAGE-RESPONSE; EPSTEIN-BARR-VIRUS; HTLV-I
TAX; CENTROSOME AMPLIFICATION; CHROMOSOME INSTABILITY; TUMOR-SUPPRESSOR
AB Human tumor viruses are associated with a variety of human malignancies, and it is estimated that 15% of all human cancers have a viral etiology. An abnormality in chromosomal ploidy or aneuploidy is a hallmark of cancers. In normal cells, euploidy is governed by several factors including an intact spindle assembly checkpoint, accurate centrosome duplication, and proper cytokinesis. Viral oncoproteins are suggested to perturb the cellular machineries for chromosomal segregation creating aneuploidy which can lead to the malignant transformation of infected cells. Here, we review in brief some of the mechanisms used by viruses that can cause cellular aneuploidy. Environ. Mol. Mutagen. 50:733-740, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Yasunaga, Junichiro; Jeang, Kuan-Teh] NIAID, Mol Virol Sect, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
RP Jeang, KT (reprint author), Bldg 4,Room 303A,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kj7e@nih.gov
RI Jeang, Kuan-Teh/A-2424-2008;
OI Yasunaga, Jun-ichirou/0000-0002-7939-2080
FU National Institute of Allergy and Infectious Diseases, NIH
FX Grant sponsor: The National Institute of Allergy and Infectious
Diseases, NIH.
NR 85
TC 10
Z9 11
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 2009
VL 50
IS 8
BP 733
EP 740
DI 10.1002/em.20480
PG 8
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 511HF
UT WOS:000271153900014
PM 19326462
ER
PT J
AU Lioy, PJ
Isukapalli, SS
Trasande, L
Thorpe, L
Dellarco, M
Weisel, C
Georgopoulos, PG
Yung, C
Brown, M
Landrigan, PJ
AF Lioy, Paul J.
Isukapalli, Sastry S.
Trasande, Leonardo
Thorpe, Lorna
Dellarco, Michael
Weisel, Clifford
Georgopoulos, Panos G.
Yung, Christopher
Brown, Margot
Landrigan, Philip J.
TI Using National and Local Extant Data to Characterize Environmental
Exposures in the National Children's Study: Queens County, New York
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Review
DE children; environmental measurements; EXIS; exposure index; exposure
information system; microinventories; National Children's Study;
national databases; NCS
ID IMPLEMENTATION
AB OBJECTIVE: The National Children's Study is a long-term epidemiologic study of 100,000 children from 105 locations across the United States. It will require information on a large number of environmental variables to address its core hypotheses. The resources available to collect actual home and personal exposure samples are limited, with most of the home sampling completed on periodic visits and the personal sampling generally limited to biomonitoring. To fill major data gaps, extant data will be required for each study location. The Queens Vanguard Center has examined the extent of those needs and the types of data that are generally and possibly locally available.
DATA: In this review we identify three levels of data-national, state and county-and local data and information sets (levels 1-3, respectively), each with different degrees of availability and completeness, that can be used as a starting point for the extant data collection in each study location over time. We present an example on the use of this tiered approach, to tailor the data needs for Queens County and to provide general guidance for application to other NCS locations.
CONCLUSIONS: Preexisting and continually evolving databases are available for use in the NCS to characterize exposure. The three levels of data we identified will be used to test a method for developing exposure indices for segments and homes during the pilot phase of NCS, as outlined in this article.
C1 [Lioy, Paul J.; Isukapalli, Sastry S.; Weisel, Clifford; Georgopoulos, Panos G.; Yung, Christopher] Univ Med & Dent New Jersey, EOHSI, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA.
[Lioy, Paul J.; Isukapalli, Sastry S.; Weisel, Clifford; Georgopoulos, Panos G.; Yung, Christopher] Rutgers State Univ, Piscataway, NJ USA.
[Trasande, Leonardo; Landrigan, Philip J.] Mt Sinai Sch Med, New York, NY USA.
[Thorpe, Lorna] New York City Dept Hlth & Mental Hyg, New York, NY USA.
[Dellarco, Michael; Brown, Margot] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Natl Childrens Study, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
RP Lioy, PJ (reprint author), Univ Med & Dent New Jersey, EOHSI, Robert Wood Johnson Med Sch, 170 Frelinghuysen Rd, Piscataway, NJ 08854 USA.
EM plioy@eohsi.rutgers.edu
OI Trasande, Leonardo/0000-0002-1928-597X
FU NICHD NIH HHS [N01-HD-5-3411]; NIEHS NIH HHS [P30 ES005022,
P30ES005022]; PHS HHS [HHSN275200503411C]
NR 46
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 2009
VL 117
IS 10
BP 1494
EP 1504
DI 10.1289/ehp.0900623
PG 11
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 503JI
UT WOS:000270529800022
PM 20019897
ER
PT J
AU Purdue, MP
Engel, LS
Langseth, H
Needham, LL
Andersen, A
Barr, DB
Blair, A
Rothman, N
McGlynn, KA
AF Purdue, Mark P.
Engel, Lawrence S.
Langseth, Hilde
Needham, Larry L.
Andersen, Aage
Barr, Dana B.
Blair, Aaron
Rothman, Nathaniel
McGlynn, Katherine A.
TI Prediagnostic Serum Concentrations of Organochlorine Compounds and Risk
of Testicular Germ Cell Tumors
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE chlordanes; organochlorine compounds; polychlorinated biphenyls; p,p
'-dichlorodiphenyldichloroethylene; testicular germ cell tumors
ID POLYCHLORINATED BIPHENYL CONGENERS; ANDROGEN RECEPTOR ACTIVITIES;
PERSISTENT PESTICIDES; SWISS MICE; IN-VITRO; ESTROGEN; ACTIVATION;
CHLORDANE; CANCER; BLOOD
AB BACKGROUND: Recent findings suggest that exposure to organochlorine (OC) compounds, chlordanes and p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) in particular, may increase the risk of developing testicular germ cell tumors (TGCTs).
OBJECTIVE: To further investigate this question, we conducted a nested case-control study of TGCTs within the Norwegian Janus Serum Bank cohort.
METHODS: The study was conducted among individuals with serum collected between 1972 and 1978. TGCT cases diagnosed through 1999 (n = 49; 27-62 years of age at diagnosis) were identified through linkage to the Norwegian Cancer Registry. Controls (n = 5 1) were matched to cases on region, blood draw year, and age at blood draw. Measurements of 11 OC insecticide compounds and 34 polychlorinated biphenyl (PCB) congeners were performed using gas chromatography/high-resolution mass spectrometry. Case-control comparisons of lipid-adjusted analyte concentrations were performed using the Wilcoxon signed-rank test. Odds ratios (ORs) and 95% confidence intervals (CIs) for tertiles of analyte concentration were calculated using conditional logistic regression.
RESULTS: TGCT cases had elevated concentrations of p,p'-DDE (tertile 3 vs. tertile 1. OR (ORT3) 2.2; 95% CI, 0.7-6.5; p(Wilcoxon) = 0.07), oxychlordane (ORT3 3.2; 95% CI, 0.6-16.8; p(Wilcoxon) = 0.05), trans-nonachlor (ORT3 2.6; 95% CI, 0.7-8.9; p(Wilcoxon) = 0.07), and total chlordanes (ORT3 2.0; 95% CI, 0.6-7.2; p(Wilcoxon) = 0.048) compared with controls, although no ORs were statistically significant. Seminoma cases had significantly lower concentrations of PCB congeners 44, 49, and 52 and significantly higher concentrations of PCBs 99, 138, 153, 167, 183, and 195.
CONCLUSIONS: Our study provides additional but qualified evidence supporting an association between exposures to p,p'-DDE and chlordane compounds, and possibly some PCB congeners, and TGCT risk.
C1 [Purdue, Mark P.; Blair, Aaron; Rothman, Nathaniel; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Rockville, MD 20852 USA.
[Engel, Lawrence S.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Langseth, Hilde; Andersen, Aage] Norwegian Canc Registry, Oslo, Norway.
[Needham, Larry L.; Barr, Dana B.] Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Atlanta, GA USA.
RP Purdue, MP (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, EPS Room 8009,6120 Execut Blvd, Rockville, MD 20852 USA.
EM purduem@mail.nih.gov
RI Needham, Larry/E-4930-2011; Barr, Dana/E-6369-2011; Barr,
Dana/E-2276-2013; Purdue, Mark/C-9228-2016;
OI Purdue, Mark/0000-0003-1177-3108; Engel, Lawrence/0000-0001-9268-4830
FU Intramural NIH HHS
NR 40
TC 32
Z9 32
U1 0
U2 3
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
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2009
VL 117
IS 10
BP 1514
EP 1519
DI 10.1289/ehp.0800359
PG 6
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 503JI
UT WOS:000270529800024
PM 20019899
ER
PT J
AU Cao, Y
Chen, AM
Radcliffe, J
Dietrich, KN
Jones, RL
Caldwell, K
Rogan, WJ
AF Cao, Yang
Chen, Aimin
Radcliffe, Jerilynn
Dietrich, Kim N.
Jones, Robert L.
Caldwell, Kathleen
Rogan, Walter J.
TI Postnatal Cadmium Exposure, Neurodevelopment, and Blood Pressure in
Children at 2, 5, and 7 Years of Age
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE behavior; blood pressure; cadmium; children; clinical trial;
intelligence; neurodevelopment
ID CHELATION-THERAPY; URINARY CADMIUM; LEAD; HAIR; HYPERTENSION;
POPULATION; MAIN; POLLUTANTS; BEHAVIOR; ALCOHOL
AB BACKGROUND: Adverse health effects of cadmium in adults are well documented, but little is known about the neuropsychological effects of cadmium in children, and no studies of cadmium and blood pressure in children have been conducted.
OBJECTIVE: We examined the potential effects of low-level cadmium exposure on intelligence quotient, neuropsychological functions, behavior, and blood pressure among children, using blood cadmium as a measure of exposure.
METHODS: We used the data from a multicenter randomized clinical trial of lead-exposed children and analyzed blood cadmium concentrations using the whole blood samples collected when children were 2 years of age. We compared neuropsychological and behavioral scores at 2, 5, and 7 years of age by cadmium level and analyzed the relationship between blood cadmium levels at 2 years of age and systolic and diastolic blood pressure at 2, 5, and 7 years of age.
RESULTS: The average cadmium concentration of these children was 0.21 mu g/L, lower than for adults in the National Health and Nutrition Examination Survey (NHANES), but comparable to concentrations in children < 3 years of age in NHANES. Except for the California Verbal Learning Test for Children, there were no differences in test scores among children in different cadmium categories. For children with detectable pretreatment blood cadmium, after adjusting for a variety of covariates, general linear model analyses showed that at none of the three age points was the coefficient of cadmium on Mental Development Index or IQ statistically significant. Spline regression analysis suggested that behavioral problem scores at 5 and 7 years of age tended to increase with increasing blood cadmium, but the trend was not significant. We found no significant associations between blood cadmium levels and blood pressure.
CONCLUSION: We found no significant associations between background blood cadmium levels at 2 years of age and neurodevelopmental end points and blood pressure at 2, 5, and 7 years of age. The neuropsychological or hypertensive effects from longer background exposures to cadmium need further study.
C1 [Cao, Yang] Second Mil Med Univ, Fac Hlth Serv, Dept Hlth Stat, Shanghai 200433, Peoples R China.
[Cao, Yang; Rogan, Walter J.] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC USA.
[Chen, Aimin] Creighton Univ, Sch Med, Dept Prevent Med & Publ Hlth, Omaha, NE USA.
[Radcliffe, Jerilynn] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Radcliffe, Jerilynn] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Dietrich, Kim N.] Univ Cincinnati, Coll Med, Dept Environm Hlth, Div Epidemiol & Biostat, Cincinnati, OH 45267 USA.
[Jones, Robert L.; Caldwell, Kathleen] Ctr Dis Control & Prevent, Inorgan & Radiat Analyt Toxicol Branch, Atlanta, GA USA.
RP Cao, Y (reprint author), Second Mil Med Univ, Fac Hlth Serv, Dept Hlth Stat, Shanghai 200433, Peoples R China.
EM caoy2@niehs.nih.gov
RI Rogan, Walter/I-6034-2012
OI Rogan, Walter/0000-0002-9302-0160
FU National Institute of Health; National Institute of Environmental Health
Sciences
FX This research was supported by the Intramural Research Program of the
National Institute of Health, National Institute of Environmental Health
Sciences.
NR 66
TC 33
Z9 36
U1 3
U2 9
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
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2009
VL 117
IS 10
BP 1580
EP 1586
DI 10.1289/ehp.0900765
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 503JI
UT WOS:000270529800034
PM 20019909
ER
PT J
AU Lynch, SM
Mahajan, R
Freeman, LEB
Hoppin, JA
Alavanja, MCR
AF Lynch, Shannon M.
Mahajan, Rajeev
Freeman, Laura E. Beane
Hoppin, Jane A.
Alavanja, Michael C. R.
TI Cancer incidence among pesticide applicators exposed to butylate in the
Agricultural Health Study (AHS)
SO ENVIRONMENTAL RESEARCH
LA English
DT Article
DE Butylate; Pesticide; Cancer; Agricultural Health Study
ID NON-HODGKINS-LYMPHOMA; PROSTATE-CANCER; OCCUPATIONAL-EXPOSURE;
UNITED-STATES; PHYSICAL-ACTIVITY; RISK-FACTORS; COHORT; METAANALYSIS;
SOLVENTS; BENZENE
AB Although limited, epidemiologic studies suggest possible associations between butylate use and cancer risk, specifically prostate cancer and non-Hodgkin lymphoma (NHL). We examined butylate use and cancer risk more broadly in the AHS, a cohort of licensed pesticide applicators in Iowa and North Carolina. Pesticide use information was collected using self-administered questionnaires. Poisson regression was used to calculate rate ratios (RR) and 95% confidence intervals (CI). Two exposure metrics were used: lifetime exposure days (LD) and intensity-weighted lifetime exposure days (IWLD). We used two referent groups: unexposed to butylate and the lowest butylate usage category. This analysis included 19,655 applicators with complete butylate use information; 5297 applicators were exposed to butylate, making this the largest study of butylate to date. The mean follow-up time since enrollment was 9 years. Prostate cancer risk was significantly elevated among applicators in the highest LD category in both referent groups (low-exposed referent: RR(LD) = 2.09, 95% CI = 1.27-3.44). We observed a significantly elevated joint effect of prostate cancer family history and high butylate usage across both exposure metrics and both referent groups (low-exposed referent: RR(LD) = 2.00, 95% CI = 1.07-3.74), and a non-significant, elevated interaction between butylate use and prostate cancer family history, similar to a previous AHS finding. Statistically significant increased risks and exposure-response trends were seen for all lymphohematopoietic cancers (AL) and NHL for both exposure metrics and referent groups (low-exposed referent: AL:RR(LD) = 2.27, 95% Cl = 1.18-4.37; NHL: RR(LD) = 3.44, 95% Cl = 1.29-9.21). Our analysis did not find meaningful associations for other cancers analyzed. Further study is warranted for AL, NHL and prostate cancers. Published by Elsevier Inc.
C1 [Mahajan, Rajeev; Freeman, Laura E. Beane; Alavanja, Michael C. R.] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Lynch, Shannon M.] NCI, Epidemiol & Genet Res Program, Div Canc Control & Populat Sci, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Hoppin, Jane A.] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC USA.
RP Alavanja, MCR (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, 6120 Execut Blvd,EPS 8000, Rockville, MD 20852 USA.
EM Alavanjm@mail.nih.gov
RI Beane Freeman, Laura/C-4468-2015
OI Beane Freeman, Laura/0000-0003-1294-4124
FU Intramural Research Program of the National Cancer Institute; National
Institute of Environmental Health Sciences, National Institutes of
Health
FX This research was supported by the Intramural Research Program of the
National Cancer Institute and National Institute of Environmental Health
Sciences, National Institutes of Health.
NR 47
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U1 1
U2 4
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 2009
VL 109
IS 7
BP 860
EP 868
DI 10.1016/j.envres.2009.06.006
PG 9
WC Environmental Sciences; Public, Environmental & Occupational Health
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health
GA 499UV
UT WOS:000270252600009
PM 19615679
ER
PT J
AU Groisman, P
Soja, AJ
AF Groisman, Pavel
Soja, Amber J.
TI Ongoing climatic change in Northern Eurasia: justification for expedient
research
SO ENVIRONMENTAL RESEARCH LETTERS
LA English
DT Editorial Material
ID FOREST-FIRE; 20TH-CENTURY
C1 [Groisman, Pavel] NOAA, Natl Climat Data Ctr, Asheville, NC 28801 USA.
[Soja, Amber J.] NIA, Hampton, VA 23681 USA.
RP Groisman, P (reprint author), NOAA, Natl Climat Data Ctr, Asheville, NC 28801 USA.
EM pasha.groisman@noaa.gov; amber.j.soja@nasa.gov
NR 41
TC 25
Z9 26
U1 0
U2 8
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 1748-9326
J9 ENVIRON RES LETT
JI Environ. Res. Lett.
PD OCT-DEC
PY 2009
VL 4
IS 4
AR 045002
DI 10.1088/1748-9326/4/4/045002
PG 7
WC Environmental Sciences; Meteorology & Atmospheric Sciences
SC Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences
GA 534ME
UT WOS:000272900500019
ER
PT J
AU Tchebakova, NM
Parfenova, E
Soja, AJ
AF Tchebakova, N. M.
Parfenova, E.
Soja, A. J.
TI The effects of climate, permafrost and fire on vegetation change in
Siberia in a changing climate
SO ENVIRONMENTAL RESEARCH LETTERS
LA English
DT Article
DE climate change; forest fire; permafrost; vegetation; Siberia
ID NORTHERN EURASIA; BOREAL FOREST; MODEL; PARAMETERS
AB Observations and general circulation model projections suggest significant temperature increases in Siberia this century that are expected to have profound effects on Siberian vegetation. Potential vegetation change across Siberia was modeled, coupling our Siberian BioClimatic Model with several Hadley Centre climate change scenarios for 2020, 2050 and 2080, with explicit consideration of permafrost and fire activity. In the warmer and drier climate projected by these scenarios, Siberian forests are predicted to decrease and shift northwards and forest-steppe and steppe ecosystems are predicted to dominate over half of Siberia due to the dryer climate by 2080. Despite the large predicted increases in warming, permafrost is not predicted to thaw deep enough to sustain dark (Pinus sibirica, Abies sibirica, and Picea obovata) taiga. Over eastern Siberia, larch (Larix dahurica) taiga is predicted to continue to be the dominant zonobiome because of its ability to withstand continuous permafrost. The model also predicts new temperate broadleaf forest and forest-steppe habitats by 2080. Potential fire danger evaluated with the annual number of high fire danger days (Nesterov index is 4000-10 000) is predicted to increase by 2080, especially in southern Siberia and central Yakutia. In a warming climate, fuel load accumulated due to replacement of forest by steppe together with frequent fire weather promotes high risks of large fires in southern Siberia and central Yakutia, where wild fires would create habitats for grasslands because the drier climate would no longer be suitable for forests.
C1 [Tchebakova, N. M.; Parfenova, E.] Russian Acad Sci, Siberian Branch, VN Sukachev Inst Forest, Krasnoyarsk 660036, Russia.
[Soja, A. J.] NASA Langley Res Ctr, NIA, Hampton, VA 23681 USA.
RP Tchebakova, NM (reprint author), Russian Acad Sci, Siberian Branch, VN Sukachev Inst Forest, Krasnoyarsk 660036, Russia.
EM ncheby@forest.akadem.ru; Amber.J.Soja@nasa.gov
NR 49
TC 65
Z9 68
U1 6
U2 58
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 1748-9326
J9 ENVIRON RES LETT
JI Environ. Res. Lett.
PD OCT-DEC
PY 2009
VL 4
IS 4
AR 045013
DI 10.1088/1748-9326/4/4/045013
PG 9
WC Environmental Sciences; Meteorology & Atmospheric Sciences
SC Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences
GA 534ME
UT WOS:000272900500030
ER
PT J
AU So, EL
Hirsch, JL
Donner, JE
Noebels, LJ
Jacobs, PM
Buchhalter, RJ
AF So, E. L.
Hirsch, J. L.
Donner, J. E.
Noebels, L. J.
Jacobs, P. M.
Buchhalter, R. J.
TI SUMMARY OF THE US NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND
STROKE (NINDS) WORKSHOP ON SUDEP
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 28th International Epilespy Congress
CY 2009
CL Budapest, HUNGARY
C1 [So, E. L.] Mayo Clin, Rochester, MN USA.
[Hirsch, J. L.] Columbia Univ, New York, NY USA.
[Donner, J. E.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Noebels, L. J.] Baylor Univ, Houston, TX 77030 USA.
[Jacobs, P. M.] NINDS, Washington, DC USA.
[Buchhalter, R. J.] Phoenix Childrens Hosp, Phoenix, AZ 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 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD OCT
PY 2009
VL 50
BP 10
EP 10
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 502DB
UT WOS:000270433800035
ER
PT J
AU Theodore, W
Fingerish, A
Cannon, D
Lim, Y
Dustin, I
Reeves-Tyer, P
Herscovitch, P
AF Theodore, W.
Fingerish, A.
Cannon, D.
Lim, Y.
Dustin, I.
Reeves-Tyer, P.
Herscovitch, P.
TI REDUCED SEROTONIN TRANSPORT IN EPILEPSY MEASURED BY POSITRON EMISSION
TOMOGRAPHY
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 28th International Epilespy Congress
CY 2009
CL Budapest, HUNGARY
C1 [Theodore, W.; Fingerish, A.; Cannon, D.; Lim, Y.; Dustin, I.; Reeves-Tyer, P.] NIH, Clin Epilepsy Sect, Bethesda, MD 20892 USA.
[Cannon, D.] Natl Univ Ireland, Clin Neuroimaging Lab, Galway, Ireland.
[Herscovitch, P.] NIH, PET Dept, Bethesda, MD 20892 USA.
RI Cannon, Dara/C-1323-2009
OI Cannon, Dara/0000-0001-7378-3411
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 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD OCT
PY 2009
VL 50
BP 134
EP 134
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 502DB
UT WOS:000270433800485
ER
PT J
AU Fasano, R
Shamim, S
Liew, C
Wlker, J
Theodore, W
Gaillard, W
Sato, S
AF Fasano, R.
Shamim, S.
Liew, C.
Wlker, J.
Theodore, W.
Gaillard, W.
Sato, S.
TI MEG IN PEDIATRIC EPILEPSY: DIPOLE ANALYSIS VS. SAM
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 28th International Epilespy Congress
CY 2009
CL Budapest, HUNGARY
C1 [Fasano, R.; Shamim, S.; Liew, C.; Theodore, W.; Sato, S.] NINDS, NIH, Bethesda, MD 20892 USA.
[Wlker, J.; Gaillard, W.] Childrens Natl Med Ctr, Washington, DC 20010 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 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD OCT
PY 2009
VL 50
BP 154
EP 154
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 502DB
UT WOS:000270433800559
ER
PT J
AU Burneo, JG
Jette, N
Theodore, W
Begley, C
Parko, K
Thurman, DJ
Wiebe, S
AF Burneo, Jorge G.
Jette, Nathalie
Theodore, William
Begley, Charles
Parko, Karen
Thurman, David J.
Wiebe, Samuel
CA Task Force Disparties Epilepsy
N Amer Commission Int League
TI Disparities in epilepsy: Report of a systematic review by the North
American Commission of the International League Against Epilepsy
SO EPILEPSIA
LA English
DT Editorial Material
DE Epilepsy; Disparity; North America
ID TEMPORAL-LOBE EPILEPSY; PUBLIC ATTITUDES; SOCIAL-SKILLS; SELF-EFFICACY;
UNITED-STATES; CHILDREN; HEALTH; SEIZURES; RACE/ETHNICITY; PREVALENCE
AB P>Purpose:
We undertook a systematic review of the evidence on disparities in epilepsy with a focus on North American data (Canada, United States, and the English-speaking Caribbean).
Methods:
We identified and evaluated: access to and outcomes following medical and surgical treatment, disability, incidence and prevalence, and knowledge and attitudes. An exhaustive search (1965-2007) was done, including: (1) disparities by socioeconomic status (SES), race/ethnicity, age, or education of subgroups of the epilepsy population; or (2) disparities between people with epilepsy (PWE) and healthy people or with other chronic illnesses.
Results:
From 1,455 citations, 278 eligible abstracts were identified and 44 articles were reviewed. Comparative research data were scarce in all areas. PWE have been shown to have lower education and employment status; among PWE, differences in access to surgery have been shown by racial/ethnic groups. Aboriginals, women, and children have been shown to differ in use of health resources. Poor compliance has been shown to be associated with lower SES, insufficient insurance, poor relationship with treating clinicians, and not having regular responsibilities.
Discussion:
Comprehensive, comparative research on all aspects of disparities in epilepsy is needed to understand the causes of disparities and the development of any policies aimed at addressing health disparities and minimizing their impact.
C1 [Burneo, Jorge G.] Univ Western Ontario, Epilepsy Programme, London, ON N6A 5A5, Canada.
[Jette, Nathalie; Wiebe, Samuel] Univ Calgary, Dept Clin Neurosci, Calgary, AB, Canada.
[Theodore, William] NIH, Epilepsy Sect, Bethesda, MD 20892 USA.
[Begley, Charles] Univ Texas Hlth Sci Ctr, Sch Publ Hlth, Houston, TX USA.
[Parko, Karen] Univ Calif San Francisco, US Publ Hlth Serv, San Francisco, CA 94143 USA.
[Thurman, David J.] Ctr Dis Control & Prevent, Atlanta, GA USA.
RP Burneo, JG (reprint author), Univ Western Ontario, Epilepsy Programme, 339 Windermere Rd, London, ON N6A 5A5, Canada.
EM jburneo2@uwo.ca
RI shengkun, yu/B-8440-2012
FU Intramural NIH HHS [Z01 NS002236-32]
NR 56
TC 41
Z9 41
U1 2
U2 3
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD OCT
PY 2009
VL 50
IS 10
BP 2285
EP 2295
DI 10.1111/j.1528-1167.2009.02282.x
PG 11
WC Clinical Neurology
SC Neurosciences & Neurology
GA 498GW
UT WOS:000270126300014
PM 19732134
ER
PT J
AU Shamim, S
Wiggs, E
Heiss, J
Sato, S
Liew, C
Solomon, J
Theodore, WH
AF Shamim, Sadat
Wiggs, Edythe
Heiss, John
Sato, Susumu
Liew, Clarissa
Solomon, Jeffrey
Theodore, William H.
TI Temporal lobectomy: Resection volume, neuropsychological effects, and
seizure outcome
SO EPILEPSY & BEHAVIOR
LA English
DT Article
DE Epilepsy; Cognition; Neuropsychology; Temporal lobe; Resection;
Mesiotemporal sclerosis
ID MATERIAL-SPECIFIC MEMORY; LOBE EPILEPSY; FOLLOW-UP; SURGERY; EXTENT
AB Objective: The goal of the work described here was to evaluate relationships among resection volume, seizure outcome, and cognitive morbidity after temporal lobectomy for intractable epilepsy.
Methods: Thirty patients with mesial temporal sclerosis were evaluated pre- and postoperatively with the Wechsler Adult Intelligence Scale III, Wechsler Memory Scale III, and three-dimensional coronal spoiled gradient recall acquisition MRI. Preoperative whole-brain volumes were calculated with Statistical Parametric Mapping. Resection volume was calculated by manual tracing. Systat was used for statistical analysis.
Results: All resections included the temporal tip, at least 1 cm of the superior temporal gyrus, and 3 to 5 cm of the middle and inferior temporal gyri. Left were significantly smaller than right temporal resections. Seizure-free patients had significantly larger resections. Immediate verbal memory was significantly worse after left temporal lobectomy. Surgical outcome and resection volume did not affect postoperative neuropsychological results.
Conclusions: Dominant temporal lobe resections are associated with immediate verbal memory deficits Larger resection volume was associated with improved seizure control but not worse cognitive outcome (C) 2009 Published by Elsevier Inc.
C1 [Shamim, Sadat; Liew, Clarissa; Theodore, William H.] NINDS, Clin Epilepsy Sect, NIH, Bethesda, MD 20892 USA.
[Wiggs, Edythe] NINDS, Off Clin Director, NIH, Bethesda, MD 20892 USA.
[Heiss, John] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Sato, Susumu; Liew, Clarissa] NINDS, EEG Sect, OCD, NIH, Bethesda, MD 20892 USA.
RP Theodore, WH (reprint author), 10 Ctr Dr,Room 5N-250, Bethesda, MD 20892 USA.
EM theodorw@ninds.nih.gov
OI Heiss, John/0000-0002-3890-0165
FU Intramural NIH HHS [Z01 NS002858-16]
NR 13
TC 13
Z9 13
U1 0
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1525-5050
J9 EPILEPSY BEHAV
JI Epilepsy Behav.
PD OCT
PY 2009
VL 16
IS 2
BP 311
EP 314
DI 10.1016/j.yebeh.2009.07.040
PG 4
WC Behavioral Sciences; Clinical Neurology; Psychiatry
SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry
GA 510JG
UT WOS:000271083800017
PM 19703792
ER
PT J
AU Brown, PH
Balbo, A
Schuck, P
AF Brown, Patrick H.
Balbo, Andrea
Schuck, Peter
TI On the analysis of sedimentation velocity in the study of protein
complexes
SO EUROPEAN BIOPHYSICS JOURNAL WITH BIOPHYSICS LETTERS
LA English
DT Article
DE Analytical ultracentrifugation; Hydrodynamics; Direct boundary modeling;
Lamm equation
ID SIZE-DISTRIBUTION ANALYSIS; FIELD-FLOW FRACTIONATION; ANALYTICAL
ULTRACENTRIFUGATION; LAMM EQUATION; CONFORMATIONAL-CHANGE; ANTI-TRAP;
DISTRIBUTIONS; QUANTITATION; MODEL; COEFFICIENTS
AB Sedimentation velocity analytical ultracentrifugation has experienced a significant transformation, precipitated by the possibility of efficiently fitting Lamm equation solutions to the experimental data. The precision of this approach depends on the ability to account for the imperfections of the experiment, both regarding the sample and the instrument. In the present work, we explore in more detail the relationship between the sedimentation process, its detection, and the model used in the mathematical data analysis. We focus on configurations that produce steep and fast-moving sedimentation boundaries, such as frequently encountered when studying large multi-protein complexes. First, as a computational tool facilitating the analysis of heterogeneous samples, we introduce the strategy of partial boundary modeling. It can simplify the modeling by restricting the direct boundary analysis to species with sedimentation coefficients in a predefined range. Next, we examine factors related to the experimental detection, including the magnitude of optical aberrations generated by out-of-focus solution columns at high protein concentrations, the relationship between the experimentally recorded signature of the meniscus and the meniscus parameter in the data analysis, and the consequences of the limited radial and temporal resolution of the absorbance optical scanning system. Surprisingly, we find that large errors can be caused by the finite scanning speed of the commercial absorbance optics, exceeding the statistical errors in the measured sedimentation coefficients by more than an order of magnitude. We describe how these effects can be computationally accounted for in SEDFIT and SEDPHAT.
C1 [Brown, Patrick H.; Balbo, Andrea; Schuck, Peter] Natl Inst Biomed Imaging & Bioengn, Lab Bioengn & Phys Sci, NIH, Bethesda, MD 20892 USA.
RP Schuck, P (reprint author), Natl Inst Biomed Imaging & Bioengn, Lab Bioengn & Phys Sci, NIH, Bldg 13,Rm 3N17,13 S Dr, Bethesda, MD 20892 USA.
EM pschuck@helix.nih.gov
OI Schuck, Peter/0000-0002-8859-6966
FU National Institute of Bioimaging and Bioengineering, NIH
FX We thank Dr. Cole for allowing us to use his data on the TRAP system,
and thank Dr. Philo for providing us with a copy of his analysis (Philo
2006). This work was supported by the Intramural Research Program of the
National Institute of Bioimaging and Bioengineering, NIH.
NR 54
TC 39
Z9 39
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0175-7571
J9 EUR BIOPHYS J BIOPHY
JI Eur. Biophys. J. Biophys. Lett.
PD OCT
PY 2009
VL 38
IS 8
BP 1079
EP 1099
DI 10.1007/s00249-009-0514-1
PG 21
WC Biophysics
SC Biophysics
GA 502BT
UT WOS:000270429800006
PM 19644686
ER
PT J
AU Hilton, E
Johnston, J
Whalen, S
Okamoto, N
Hatsukawa, Y
Nishio, J
Kohara, H
Hirano, Y
Mizuno, S
Torii, C
Kosaki, K
Manouvrier, S
Boute, O
Perveen, R
Law, C
Moore, A
Fitzpatrick, D
Lemke, J
Fellmann, F
Debray, FG
Dastot-Le-Moal, F
Gerard, M
Martin, J
Bitoun, P
Goossens, M
Verloes, A
Schinzel, A
Bartholdi, D
Bardakjian, T
Hay, B
Jenny, K
Johnston, K
Lyons, M
Belmont, JW
Biesecker, LG
Giurgea, I
Black, G
AF Hilton, Emma
Johnston, Jennifer
Whalen, Sandra
Okamoto, Nobuhiko
Hatsukawa, Yoshikazu
Nishio, Juntaro
Kohara, Hiroshi
Hirano, Yoshiko
Mizuno, Seiji
Torii, Chiharu
Kosaki, Kenjiro
Manouvrier, Sylvie
Boute, Odile
Perveen, Rahat
Law, Caroline
Moore, Anthony
Fitzpatrick, David
Lemke, Johannes
Fellmann, Florence
Debray, Francois-Guillaume
Dastot-Le-Moal, Florence
Gerard, Marion
Martin, Josiane
Bitoun, Pierre
Goossens, Michel
Verloes, Alain
Schinzel, Albert
Bartholdi, Deborah
Bardakjian, Tanya
Hay, Beverly
Jenny, Kim
Johnston, Kathreen
Lyons, Michael
Belmont, John W.
Biesecker, Leslie G.
Giurgea, Irina
Black, Graeme
TI BCOR analysis in patients with OFCD and Lenz microphthalmia syndromes,
mental retardation with ocular anomalies, and cardiac laterality defects
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE BCL-6 corepressor; oculofaciocardiodental syndrome; Lenz microphthalmia
syndrome; mental retardation; ocular defects
ID DENTAL SYNDROME; CONGENITAL-ANOMALIES; HEART-DEFECTS; ANOPHTHALMIA;
MUTATIONS; CATARACTS; CONFIRMATION; HETEROTAXY; EXPRESSION; DISORDER
AB Oculofaciocardiodental (OFCD) and Lenz microphthalmia syndromes form part of a spectrum of X-linked microphthalmia disorders characterized by ocular, dental, cardiac and skeletal anomalies and mental retardation. The two syndromes are allelic, caused by mutations in the BCL-6 corepressor gene (BCOR). To extend the series of phenotypes associated with pathogenic mutations in BCOR, we sequenced the BCOR gene in patients with (1) OFCD syndrome, (2) putative X-linked ('Lenz') microphthalmia syndrome, (3) isolated ocular defects and (4) laterality phenotypes. We present a new cohort of females with OFCD syndrome and null mutations in BCOR, supporting the hypothesis that BCOR is the sole molecular cause of this syndrome. We identify for the first time mosaic BCOR mutations in two females with OFCD syndrome and one apparently asymptomatic female. We present a female diagnosed with isolated ocular defects and identify minor features of OFCD syndrome, suggesting that OFCD syndrome may be mild and underdiagnosed. We have sequenced a cohort of males diagnosedwith putative X-linked microphthalmia and found a mutation, p. P85L, in a single case, suggesting that BCOR mutations are not a major cause of X-linked microphthalmia in males. The absence of BCOR mutations in a panel of patients with non-specific laterality defects suggests that mutations in BCOR are not a major cause of isolated heart and laterality defects. Phenotypic analysis of OFCD and Lenz microphthalmia syndromes shows that in addition to the standard diagnostic criteria of congenital cataract, microphthalmia and radiculomegaly, patients should be examined for skeletal defects, particularly radioulnar synostosis, and cardiac/laterality defects. European Journal of Human Genetics (2009) 17, 1325-1335; doi: 10.1038/ejhg.2009.52; published online 15 April 2009
C1 [Johnston, Jennifer; Biesecker, Leslie G.] NHGRI, NIH, Genet Dis Res Branch, Bethesda, MD 20892 USA.
[Hilton, Emma; Perveen, Rahat; Black, Graeme] St Marys Hosp, Acad Unit Med Genet, Manchester M13 0JH, Lancs, England.
[Hilton, Emma] Univ Manchester, Ctr Mol Med, Manchester, Lancs, England.
[Whalen, Sandra; Dastot-Le-Moal, Florence; Martin, Josiane; Goossens, Michel; Giurgea, Irina] Hop Henri Mondor, INSERM, U841, Dept Genet,Inst Mondor Rech Biomed, F-94010 Creteil, France.
[Whalen, Sandra; Dastot-Le-Moal, Florence; Martin, Josiane; Goossens, Michel; Giurgea, Irina] Univ Paris 12, Fac Med, Creteil, France.
[Whalen, Sandra; Dastot-Le-Moal, Florence; Martin, Josiane; Goossens, Michel; Giurgea, Irina] APHP, Serv Biochem & Genet, Grp Henri Mondor Albert Chenevier, Creteil, France.
[Okamoto, Nobuhiko; Hatsukawa, Yoshikazu; Nishio, Juntaro; Kohara, Hiroshi; Hirano, Yoshiko] Osaka Med Ctr & Res Inst, Osaka, Japan.
[Mizuno, Seiji] Cent Hosp Kasugai, Aichi Human Serv Ctr, Dept Pediat, Kasugai, Aichi, Japan.
[Torii, Chiharu; Kosaki, Kenjiro] Keio Univ, Sch Med, Dept Pediat, Tokyo, Japan.
[Manouvrier, Sylvie; Boute, Odile] CHRU, Serv Genet Clin, Lille, France.
[Law, Caroline] Princess Anne Hosp, Wessex Clin Genet Serv, Southampton, Hants, England.
[Moore, Anthony] Moorfields Eye Hosp, London, England.
[Fitzpatrick, David] Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland.
[Lemke, Johannes; Schinzel, Albert; Bartholdi, Deborah] Univ Zurich, Inst Med Genet, Zurich, Switzerland.
[Fellmann, Florence] CHU Vaudois, Serv Genet Med, CH-1011 Lausanne, Switzerland.
[Debray, Francois-Guillaume] CHU Sart Tilman, Ctr Genet Humaine, B-4000 Liege, Belgium.
[Gerard, Marion; Verloes, Alain] Hop Robert Debre, Dept Med Genet, F-75019 Paris, France.
[Bitoun, Pierre] Hop Jean Verdier, Dept Genet, Bondy, France.
[Bardakjian, Tanya] Albert Einstein Med Ctr, Div Genet, Philadelphia, PA 19141 USA.
[Hay, Beverly] UMass Mem Med Ctr, Dept Genet, Worcester, MA USA.
[Jenny, Kim] Alfred I DuPont Hosp Children, Div Med Genet, Wilmington, DE USA.
[Johnston, Kathreen] Permanente Med Grp Inc, Dept Genet, San Francisco, CA USA.
[Lyons, Michael] Stanford Univ, Dept Pediat, Div Med Genet, Sch Med, Stanford, CA 94305 USA.
[Lyons, Michael] Greenwood Genet Ctr, Greenwood, SC 29646 USA.
[Belmont, John W.] Baylor Coll Med, Dept Mol Genet, Houston, TX 77030 USA.
[Black, Graeme] Cent Manchester & Manchester Childrens Univ Hosp, Manchester Royal Eye Hosp, Manchester, Lancs, England.
RP Biesecker, LG (reprint author), NHGRI, NIH, Genet Dis Res Branch, 49 Convent Dr,MSC 4472, Bethesda, MD 20892 USA.
EM leslieb@helix.nih.gov
RI FitzPatrick, David/C-7301-2013; Kosaki, Kenjiro/K-5350-2013;
OI Belmont, John/0000-0001-7409-3578; Hilton, Emma/0000-0002-3750-577X; ,
Alain/0000-0003-4819-0264; Black, Graeme/0000-0001-8727-6592;
FitzPatrick, David R./0000-0003-4861-969X
FU Intramural NIH HHS [Z01 HG200328-04]; Medical Research Council
[MC_U127561093]; Wellcome Trust
NR 42
TC 25
Z9 26
U1 0
U2 1
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 2009
VL 17
IS 10
BP 1325
EP 1335
DI 10.1038/ejhg.2009.52
PG 11
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 497YP
UT WOS:000270101600015
PM 19367324
ER
PT J
AU Ahlers, JD
Belyakov, IM
AF Ahlers, Jeffrey D.
Belyakov, Igor M.
TI Strategies for optimizing targeting and delivery of mucosal HIV vaccines
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Review
DE Adjuvants; CD8(+)CTL; HIV; Mucosa; Vaccine
ID CD8(+) T-CELLS; HUMAN-IMMUNODEFICIENCY-VIRUS; HUMAN DENDRITIC CELLS;
ESCHERICHIA-COLI ENTEROTOXIN; PRIME-BOOST IMMUNIZATION; HEAT-LABILE
ENTEROTOXIN; MENINGITIDIS-ADHESIN-A; TLR5 LIGAND FLAGELLIN;
IMMUNE-RESPONSES; CHOLERA-TOXIN
AB Effective frontline defenses against HIV-1 will require targeting vaccines to mucosal tissue in order to induce alpha beta CD8(+) lymphocytes in mucosal effector sites (lamina propria and intraepithelial compartment) as well as antibody secreting plasma cells that can neutralize and limit free virus. A concerted second wave of assault against the virus will require the activation and recruitment of antigen specific memory CD4(+) and CD8(+) T cells in mesenteric lymph nodes and distal secondary lymphoid organs. New delivery strategies targeting the "right" DC subsets in combination with delivery of mucosal adjuvants and innate signals for activating DC will be essential for mucosal vaccines in order to circumvent the naturally tolerogenic environment and the induction of Tregs. Mucosal delivery of antigen in combination with inflammatory signals has been shown to empower systemic immunization by directing responses to mucosal sites for imprinting optimum mucosal memory. Here, we discuss novel vaccine strategies and adjuvants for optimizing mucosal delivery of HIV vaccines.
C1 [Ahlers, Jeffrey D.] NIAID, Div Aids, NIH, Vaccine Discovery Branch, Rockville, MD 20817 USA.
[Belyakov, Igor M.] Midwest Res Inst, Frederick, MD 21072 USA.
RP Ahlers, JD (reprint author), NIAID, Div Aids, NIH, Vaccine Discovery Branch, 67008 Rocledge Dr, Rockville, MD 20817 USA.
EM jahlers@niaid.nih.gov; igorbelyakov@yahoo.com
NR 133
TC 21
Z9 21
U1 2
U2 6
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY
SN 0014-2980
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD OCT
PY 2009
VL 39
IS 10
BP 2657
EP 2669
DI 10.1002/eji.200939269
PG 13
WC Immunology
SC Immunology
GA 511GD
UT WOS:000271151000004
PM 19609978
ER
PT J
AU Liepinsh, DJ
Kruglov, AA
Galimov, AR
Shakhov, AN
Shebzukhov, YV
Kuchmiy, AA
Grivennikov, SI
Tumanov, AV
Drutskaya, MS
Feigenbaum, L
Kuprash, DV
Nedospasov, SA
AF Liepinsh, Dmitry J.
Kruglov, Andrei A.
Galimov, Arthur R.
Shakhov, Alexander N.
Shebzukhov, Yuriy V.
Kuchmiy, Anna A.
Grivennikov, Sergei I.
Tumanov, Alexei V.
Drutskaya, Marina S.
Feigenbaum, Lionel
Kuprash, Dmitry V.
Nedospasov, Sergei A.
TI Accelerated thymic atrophy as a result of elevated homeostatic
expression of the genes encoded by the TNF/lymphotoxin cytokine locus
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE Cytokine receptors; Cytokines; T cells; Thymus
ID TUMOR-NECROSIS-FACTOR; MAJOR HISTOCOMPATIBILITY COMPLEX; T-CELL
DEVELOPMENT; FACTOR-ALPHA; RHEUMATOID-ARTHRITIS; LYMPHOTOXIN-ALPHA;
LYMPHOID-TISSUES; ENTRY MEDIATOR; FACTOR-BETA; TNF-ALPHA
AB TNF, lymphotoxin (LT)-alpha, LT-beta and LIGHT are members of a larger superfamily of TNF-related cytokines that can cross-utilize several receptors. Although LIGHT has been implicated in thymic development and function, the role of TNF and LT remains incompletely defined. To address this, we created a model of modest homeostatic overexpression of TNF/LT cytokines; using the genomic human TNF/LT locus as a low copy number Tg. Strikingly, expression of Tg TNF/LT gene products led to profound early thymic atrophy characterized by decreased numbers of thymocytes and cortical thymic epithelial cells, partial block of thymocyte proliferation at double negative (DN) 1 stage, increased apoptosis of DN2 thymocytes and severe decline of T-cell numbers in the periphery. Results of backcrossing to TNFR1-, LT beta R- or TNF/LT-deficient backgrounds and of reciprocal bone marrow transfers implicated both LT-alpha/LT-beta to LT beta R and TNF/LT-alpha to TNFR1 signaling in accelerated thymus degeneration. We hypothesize that chronic infections can promote thymic atrophy by upregulating LT and TNF production.
C1 [Liepinsh, Dmitry J.; Kruglov, Andrei A.; Galimov, Arthur R.; Kuchmiy, Anna A.; Grivennikov, Sergei I.; Tumanov, Alexei V.; Drutskaya, Marina S.; Kuprash, Dmitry V.; Nedospasov, Sergei A.] Russian Acad Sci, Lab Mol Immunol, VA Engelhardt Mol Biol Inst, Moscow 119991, Russia.
[Liepinsh, Dmitry J.; Shakhov, Alexander N.; Shebzukhov, Yuriy V.; Grivennikov, Sergei I.; Nedospasov, Sergei A.] SAIC Frederick Inc, Basic Res Program, Frederick, MD USA.
[Liepinsh, Dmitry J.; Shakhov, Alexander N.; Shebzukhov, Yuriy V.; Grivennikov, Sergei I.; Nedospasov, Sergei A.] NCI, Mol Immunoregulat Lab, Ctr Canc Res, Frederick, MD 21701 USA.
[Kruglov, Andrei A.; Galimov, Arthur R.; Shebzukhov, Yuriy V.; Nedospasov, Sergei A.] German Rheumatism Res Ctr DRFZ, Berlin, Germany.
[Feigenbaum, Lionel] NCI, Lab Anim Sci Program, Ctr Canc Res, Frederick, MD 21701 USA.
RP Nedospasov, SA (reprint author), Russian Acad Sci, Lab Mol Immunol, VA Engelhardt Mol Biol Inst, 32 Vavilov Str, Moscow 119991, Russia.
EM sergei.nedospasov@gmail.com
RI Nedospasov, Sergei/J-5936-2013; Nedospasov, Sergei/L-1990-2015; Kuprash,
Dmitry/O-4899-2015; Nedospasov, Sergei/Q-7319-2016; Kuchmiy,
Anna/S-2275-2016;
OI Kuprash, Dmitry/0000-0002-1488-4148; Kuchmiy, Anna/0000-0001-7277-736X;
kruglov, andrey/0000-0002-4597-2087
FU Russian Academy of Sciences; NIH; National Cancer Institute
[N01-CO-12400]; Deutsches Forschungsgemeinschaft; European Commission
FX The authors thank T. Spies for providing cosmid 031A and L. Drutskaya,
S. Stull, T. Stull and 1. Mufazalov for technical assistance. They also
thank A. Hovsepyan, G. Telegin and the personnel of Laboratory Animal
Breeding Center, Branch of Schemyakin and Ovchinnikov Institute of
Bioorganic Chemistry for expert help with mouse breeding and production.
Finally, they are grateful to Drs. M. Heikenwalder, A. Rudensky, A.
Hurwitz, A. Hamann, S. Fillatreau and A. A.Yarilin for valuable comments
on the manuscript. This research was supported by MCB grants from the
Russian Academy of Sciences, by Intramural Research Program of the NIH,
by contract N01-CO-12400 from the National Cancer Institute, TR52 from
Deutsches Forschungsgemeinschaft and by TB REACT grant from European
Commission FP6. S.A.N. is an International Research Scholar of the
Howard Hughes Medical 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 52
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Z9 22
U1 0
U2 3
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY
SN 0014-2980
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD OCT
PY 2009
VL 39
IS 10
BP 2906
EP 2915
DI 10.1002/eji.200839191
PG 10
WC Immunology
SC Immunology
GA 511GD
UT WOS:000271151000028
PM 19735075
ER
PT J
AU Conforto, AB
Ferreiro, KN
Tomasi, C
dos Santos, RL
Moreira, VL
Marie, SKN
Baltieri, SC
Cohen, LG
AF Conforto, A. B.
Ferreiro, K. N.
Tomasi, C.
dos Santos, R. L.
Moreira, V. L.
Marie, S. K. N.
Baltieri, S. C.
Cohen, L. G.
TI Effects of somatosensory stimulation on motor function after subacute
stroke
SO EUROPEAN JOURNAL OF NEUROLOGY
LA English
DT Meeting Abstract
CT 13th Congress of the European-Federation-of-Neurological-Societies
CY SEP 12-15, 2009
CL Florence, ITALY
SP European Federat Neurol Soc
C1 [Conforto, A. B.; Ferreiro, K. N.; Tomasi, C.; dos Santos, R. L.; Moreira, V. L.; Marie, S. K. N.; Baltieri, S. C.] Univ Sao Paulo, Hosp Clin, Dept Neurol, Sao Paulo, Brazil.
[Conforto, A. B.] Hosp Israelita Albert Einstein, Inst Israelita Ensino & Pesquisa Albert Einstein, Sao Paulo, Brazil.
[Cohen, L. G.] NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20892 USA.
RI Marie, Suely/D-1870-2012
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
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 2009
VL 16
BP 41
EP 41
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 494IC
UT WOS:000269804100090
ER
PT J
AU Stevanin, G
Forlani, S
Cazeneuve, C
Cagnoli, C
Figueroa, K
Lorenzo, D
Johnson, J
van de Leemput, J
Viemont, M
Camuzat, A
Singleton, A
Ranum, L
Pulst, S
Brusco, A
Leguern, E
Brice, A
Durr, A
AF Stevanin, G.
Forlani, S.
Cazeneuve, C.
Cagnoli, C.
Figueroa, K.
Lorenzo, D.
Johnson, J.
van de Leemput, J.
Viemont, M.
Camuzat, A.
Singleton, A.
Ranum, L.
Pulst, S.
Brusco, A.
Leguern, E.
Brice, A.
Durr, A.
TI Conventional mutations are associated with a different phenotype than
polyglutamine expansions in spinocerebellar ataxias
SO EUROPEAN JOURNAL OF NEUROLOGY
LA English
DT Meeting Abstract
CT 13th Congress of the European-Federation-of-Neurological-Societies
CY SEP 12-15, 2009
CL Florence, ITALY
SP European Federat Neurol Soc
C1 [Stevanin, G.; Forlani, S.; Camuzat, A.; Leguern, E.; Brice, A.; Durr, A.] CRim NEB, U975, INSERM, Paris, France.
[Stevanin, G.; Cazeneuve, C.; Viemont, M.; Leguern, E.; Brice, A.; Durr, A.] Hop La Pitie Salpetriere, AP HP, Dept Genet, Paris, France.
[Cagnoli, C.; Brusco, A.] Univ Turin, Dept Genet Biol & Biochem, Turin, Italy.
[Figueroa, K.; Pulst, S.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Lorenzo, D.; Ranum, L.] Univ Minnesota, Minneapolis, MN USA.
[Johnson, J.; van de Leemput, J.; Singleton, A.] NIA, NIH, Bethesda, MD 20892 USA.
RI Singleton, Andrew/C-3010-2009; Stevanin, Giovanni/E-5038-2016
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 1351-5101
J9 EUR J NEUROL
JI Eur. J. Neurol.
PD OCT
PY 2009
VL 16
BP 284
EP 284
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 494IC
UT WOS:000269804100590
ER
PT J
AU Conforto, AB
Melo, EDS
dos Reis, FI
Tomasi, C
Scaff, M
Cohen, LG
AF Conforto, A. B.
Melo, E. D. S.
dos Reis, F. I.
Tomasi, C.
Scaff, M.
Cohen, L. G.
TI Safety of repetitive transcranial magnetic stimulation of the unaffected
hemisphere in subacute stroke patients
SO EUROPEAN JOURNAL OF NEUROLOGY
LA English
DT Meeting Abstract
CT 13th Congress of the European-Federation-of-Neurological-Societies
CY SEP 12-15, 2009
CL Florence, ITALY
SP European Federat Neurol Soc
C1 [Conforto, A. B.; Melo, E. D. S.; dos Reis, F. I.; Tomasi, C.; Scaff, M.] Univ Sao Paulo, Dept Neurol, Hosp Clin, Sao Paulo, Brazil.
[Conforto, A. B.] Hosp Israelita Albert Einstein, Inst Israelita Ensino & Pesquisa Albert Einstein, Sao Paulo, Brazil.
[Cohen, L. G.] NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
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 2009
VL 16
BP 309
EP 309
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 494IC
UT WOS:000269804100643
ER
PT J
AU Du, CW
Tully, M
Volkow, ND
Schiffer, WK
Yu, M
Luo, ZC
Koretsky, AP
Benveniste, H
AF Du, Congwu
Tully, Melissa
Volkow, Nora D.
Schiffer, Wynne K.
Yu, Mei
Luo, Zhongchi
Koretsky, Alan P.
Benveniste, Helene
TI Differential effects of anesthetics on cocaine's pharmacokinetic and
pharmacodynamic effects in brain
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE brain imaging; cerebral blood flow; cerebral blood volume and hemoglobin
oxygenation of tissue; cocaine and anesthesia; pharmacodynamic;
pharmacokinetics of cocaine
ID CEREBRAL-BLOOD-FLOW; RAT SOMATOSENSORY CORTEX; OPTICAL COHERENCE
TOMOGRAPHY; FUNCTIONAL ACTIVATION; DOPAMINE TRANSPORTER;
HEMODYNAMIC-CHANGES; OXYGEN-CONSUMPTION; ALPHA-CHLORALOSE; BARREL
CORTEX; BINDING-SITES
AB Most studies of the effect of cocaine on brain activity in laboratory animals are preformed under anesthesia, which could potentially affect the physiological responses to cocaine. Here we assessed the effects of two commonly used anesthetics [alpha-chloralose (alpha-CHLOR) and isofluorane (ISO)] on the effects of acute cocaine (1 mg/kg i.v.) on cerebral blood flow (CBF), cerebral blood volume (CBV), and tissue hemoglobin oxygenation (S(t)O(2)) using optical techniques and cocaine's pharmacokinetics (PK) and binding in the rat brain using (PET) and [11C]cocaine. We showed that acute cocaine at a dose abused by cocaine abusers decreased CBF, CBV and S(t)O(2) in rats anesthetized with ISO, whereas it increased these parameters in rats anesthetized with alpha-CHLOR. Importantly, in ISO-anesthetized animals cocaine-induced changes in CBF and S(t)O(2) were coupled, whereas for alpha-CHLOR these measures were uncoupled. Moreover, the clearance of [11C]cocaine from the brain was faster for ISO (peak half-clearance 15.8 +/- 2.8 min) than for alpha-CHLOR (27.5 +/- 0.6 min), and the ratio of specific to non-specific binding of [11C]cocaine in the brain was higher for ISO- (3.37 +/- 0.32) than for alpha-CHLOR-anesthetized rats (2.24 +/- 0.4). For both anesthetics, cocaine-induced changes in CBF followed the fast uptake of [11C]cocaine in the brain (peaking at similar to 2.5-4 min), but only for ISO did the duration of the CBV and S(t)O(2) changes correspond to the rate of [11C]cocaine's clearance from the brain. These results demonstrate that anesthetics influence cocaine's hemodynamic and metabolic changes in the brain, and its binding and PK, which highlights the need to better understand the interactions between anesthetics and pharmacological challenges in brain functional imaging studies.
C1 [Du, Congwu; Benveniste, Helene] SUNY Stony Brook, Dept Anesthesiol, Stony Brook, NY 11794 USA.
[Du, Congwu; Schiffer, Wynne K.; Yu, Mei; Luo, Zhongchi; Benveniste, Helene] Brookhaven Natl Lab, Dept Med, Upton, NY 11973 USA.
[Tully, Melissa; Luo, Zhongchi] SUNY Stony Brook, Dept Biomed Engn, Stony Brook, NY 11794 USA.
[Volkow, Nora D.] Natl Inst Drug Abuse, NIH, Bethesda, MD USA.
[Koretsky, Alan P.] NIH, Lab Funct & Mol Imaging, Bethesda, MD 20892 USA.
RP Du, CW (reprint author), SUNY Stony Brook, Dept Anesthesiol, Stony Brook, NY 11794 USA.
EM congwu@bnl.gov
RI Koretsky, Alan/C-7940-2015
OI Koretsky, Alan/0000-0002-8085-4756
FU NIH [1K25DA021200]; NYSTAR; Department of Energy [DE-AC02-98CH10886]
FX This work was supported in part by NIH (1K25DA021200) and NYSTAR. The
experiments were conducted in Brookhaven National Laboratory supported
by Department of Energy (Contract DE-AC02-98CH10886). The authors thank
Yingtain Pan, Jim Ma and Mario Rebecchi for valuable discussions, and
David Smith for assistance on the physiological monitoring.
NR 46
TC 17
Z9 17
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
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 2009
VL 30
IS 8
BP 1565
EP 1575
DI 10.1111/j.1460-9568.2009.06931.x
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 508TH
UT WOS:000270958700015
PM 19821842
ER
PT J
AU Mattson, MP
AF Mattson, Mark P.
TI Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the
metabolic syndrome, and associated vascular and neurodegenerative
disorders
SO EXPERIMENTAL GERONTOLOGY
LA English
DT Review
DE Alzheimer's disease; Atherosclerosis; Diabetes; Insulin resistance;
Lipid peroxidation; Metabolic syndrome
ID AMYLOID BETA-PEPTIDE; LOW-DENSITY-LIPOPROTEIN; TRANSGENIC MOUSE MODEL;
AMYOTROPHIC-LATERAL-SCLEROSIS; ALPHA-LIPOIC ACID; OXIDATIVE STRESS;
ALZHEIMERS-DISEASE; INSULIN-RESISTANCE; CALORIE RESTRICTION; DIETARY
RESTRICTION
AB A rising tide of obesity and type 2 diabetes has resulted from the development of technologies that have made inexpensive high calorie foods readily available and exercise unnecessary for many people. Obesity and the metabolic syndrome (insulin resistance, visceral adiposity and dyslipidemia) wreak havoc on cells throughout the body thereby promoting cardiovascular and kidney disease, and degenerative diseases of the brain and body. Obesity and insulin resistance promote disease by increasing oxidative damage to proteins, lipids and DNA as the result of a combination of increased free radical production and an impaired ability of cells to detoxify the radicals and repair damaged molecules. By covalently modifying membrane-associated proteins, the membrane lipid peroxidation product 4-hydroxynonenal (HNE) may play particularly sinister roles in the metabolic syndrome and associated disease processes. HNE can damage pancreatic beta cells and can impair the ability of muscle and liver cells to respond to insulin. HNE may promote atherosclerosis by modifying lipoproteins and can cause cardiac cell damage by impairing metabolic enzymes. An adverse role for HNE in the brain in obesity and the metabolic syndrome is suggested by studies showing that HNE levels are increased in brain cells with aging and Alzheimer's disease. HNE can cause the dysfunction and degeneration of neurons by modifying membrane-associated glucose and glutamate transporters, ion-motive ATPases, enzymes involved in amyloid metabolism, and cytoskeletal proteins. Exercise and dietary energy restriction reduce HNE production and may also increase cellular systems for HNE detoxification including glutathione and oxidoreductases. The recent development of low molecular weight molecules that scavenge HNE suggests that HNE can be targeted in the design of drugs for the treatment of obesity, the metabolic syndrome, and associated disorders. (C) 2009 Published by Elsevier Inc.
C1 NIA, Intramural Res Program, Neurosci Lab, Baltimore, MD 21224 USA.
RP Mattson, MP (reprint author), NIA, Intramural Res Program, Neurosci Lab, BRC 5C214,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM mattsonm@grc.nia.nih.gov
RI Mattson, Mark/F-6038-2012
FU National Institute on Aging
FX I thank KC Alexander for editorial assistance. This work was supported
by the Intramural Research Program of the National Institute on Aging.
NR 134
TC 121
Z9 125
U1 1
U2 20
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0531-5565
EI 1873-6815
J9 EXP GERONTOL
JI Exp. Gerontol.
PD OCT
PY 2009
VL 44
IS 10
BP 625
EP 633
DI 10.1016/j.exger.2009.07.003
PG 9
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 513ZL
UT WOS:000271362700001
PM 19622391
ER
PT J
AU Cokic, VP
Beleslin-Cokic, BB
Smith, RD
Economou, AP
Wahl, LM
Noguchi, CT
Schechter, AN
AF Cokic, Vladan P.
Beleslin-Cokic, Bojana B.
Smith, Reginald D.
Economou, Antaeus P.
Wahl, Larry M.
Noguchi, Constance T.
Schechter, Alan N.
TI Stimulated stromal cells induce gamma-globin gene expression in
erythroid cells via nitric oxide production
SO EXPERIMENTAL HEMATOLOGY
LA English
DT Article
ID SOLUBLE GUANYLYL CYCLASE; ENDOTHELIAL-CELLS; BONE-MARROW; PROGENITOR
CELLS; MACROPHAGES; PROTEIN; GROWTH; HEMATOPOIESIS; ERYTHROBLASTS;
HEMOGLOBIN
AB Objective. We have previously shown that nitric oxide (NO) is involved in the hydroxyurea-induced increase of gamma-globin gene expression in cultured human erythroid progenitor cells and that hydroxyurea increases NO production in endothelial cells via endothelial NO synthase (NOS). We have now expanded those studies to demonstrate that stimulation of gamma-globin gene expression is also mediated by NOS induction in stromal cells within the bone marrow microenvironment.
Materials and Methods. Using NO analyzer, we measured NO production in endothelial and macrophage cell cultures. In coculture studies of erythroid and stromal cells, we measured globin gene expression during stimulation by NO induers.
Results. Hydroxyurea (30 - 100 mu M) induced NOS-dependent production of NO in human macrophages (up to 1.2 mu M). Coculture studies of human macrophages with erythroid progenitor cells also resulted in induction of gamma-globin mRNA expression (up to threefold) in the presence of hydroxyurea. NOS-dependent stimulation of NO by lipopolysaccharide (up to 0.6 mu M) has been observed in human macrophages. We found that lipopolysaccharide and interferon-gamma together increased gamma-globin gene expression (up to twofold) in human macrophage/erythroid cell cocultures. Coculture of human bone marrow endothelial cells with erythroid progenitor cells also induced gamma-globin mRNA expression (2.4-fold) in the presence of hydroxyurea (40 mu M).
Conclusion. These results demonstrate an arrangement by which NO and fetal hemoglobin inducers may stimulate globin genes in erythroid cells via the common paracrine effect of bone marrow stromal cells. (C) 2009 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc.
C1 [Cokic, Vladan P.] Univ Belgrade, Inst Med Res, Lab Expt Hematol, Belgrade 11129, Serbia.
[Beleslin-Cokic, Bojana B.] Univ Clin Ctr, Inst Endocrinol Diabet & Metab Dis, Belgrade, Serbia.
[Smith, Reginald D.] GE Global Res Ctr, Niskayuna, NY USA.
[Economou, Antaeus P.] Radboud Univ Nijmegen, Med Ctr, Dept Periodontol & Biomat, NL-6525 ED Nijmegen, Netherlands.
[Wahl, Larry M.] Natl Inst Dent & Craniofacial Res, Immunopathol Sect, NIH, Bethesda, MD USA.
[Noguchi, Constance T.; Schechter, Alan N.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
RP Cokic, VP (reprint author), Univ Belgrade, Inst Med Res, Lab Expt Hematol, Dr Subotica 4,POB 102, Belgrade 11129, Serbia.
EM vl@imi.bg.ac.rs
OI Schechter, Alan N/0000-0002-5235-9408
FU National Institutes of Health (Bethesda, MD, USA); National Institute of
Diabetes and Digestive and Kidney Diseases (Bethesda, MD, USA); Serbian
Ministry of Science and Technological Development (Belgrade, Serbia)
[145048B]
FX This research was supported by the Intramural Research Program of the
National Institutes of Health (Bethesda, MD, USA) and National Institute
of Diabetes and Digestive and Kidney Diseases (Bethesda, MD, USA) and by
grant from the Serbian Ministry of Science and Technological Development
(Belgrade, Serbia) (145048B).
NR 24
TC 2
Z9 3
U1 0
U2 1
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 2009
VL 37
IS 10
BP 1230
EP 1237
DI 10.1016/j.exphem.2009.06.009
PG 8
WC Hematology; Medicine, Research & Experimental
SC Hematology; Research & Experimental Medicine
GA 502XK
UT WOS:000270493600010
PM 19576950
ER
PT J
AU Cui, LW
Su, XZ
AF Cui, Liwang
Su, Xin-zhuan
TI Discovery, mechanisms of action and combination therapy of artemisinin
SO EXPERT REVIEW OF ANTI-INFECTIVE THERAPY
LA English
DT Review
DE antimalarial drugs; artemisinin-based combinatory therapy;
drug-resistant malaria; Plasmodium
ID UNCOMPLICATED FALCIPARUM-MALARIA; ANTIMALARIAL-DRUG RESISTANCE;
ARTESUNATE-MEFLOQUINE COMBINATION; PARASITE PLASMODIUM-FALCIPARUM;
CONTROLLED TUMOR PROTEIN; HUMAN LIVER-MICROSOMES; PFMDR1 COPY NUMBER; L.
ANNUAL WORMWOOD; IN-VIVO SELECTION; ARTEMETHER-LUMEFANTRINE
AB Despite great international efforts, malaria still inflicts an enormous toll on human lives, especially in Africa. Throughout history, antimalarial medicines have been one of the most powerful tools in malaria control. However, the acquisition and spread of parasite strains that are resistant to multiple antimalarial drugs have become one of the greatest challenges to malaria treatment, and are associated with the increase in morbidity and mortality in many malaria-endemic countries. To deal with this grave situation, artemisinin-based combinatory therapies (ACTS) have been introduced and widely deployed in malarious regions. Artemisinin is a new class of antimalarial compounds discovered by Chinese scientists from the sweet wormwood Artemisia annua. The potential development of resistance to artemisinins by Plasmodium falciparum threatens the usable lifespan of ACTS, and therefore is a subject of close surveillance and extensive research. Studies at the Thai-Cambodian border, a historical epicenter of multidrug resistance, have detected reduced susceptibility to artemisinins as manifested by prolonged parasite-clearance times, raising considerable concerns on resistance development. Despite this significance, there is still controversy on the mode of action of artemisinins. Although a number of potential cellular targets of artemisinins have been proposed, they remain to be verified experimentally. Here, we review the history of artemisinin discovery, discuss the mode of action and potential drug targets, and present strategies to elucidate resistance mechanisms.
C1 [Cui, Liwang] Penn State Univ, Dept Entomol, University Pk, PA 16802 USA.
[Su, Xin-zhuan] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
RP Cui, LW (reprint author), Penn State Univ, Dept Entomol, 537 ASI Bldg, University Pk, PA 16802 USA.
EM luc2@psu.edu; xsu@niaid.nih.gov
OI Su, Xinzhuan/0000-0003-3246-3248
FU National Institute of Allergy and Infectious Diseases, NIH [R01
AI064553]
FX This work was supported by grant R01 AI064553 to Liwang Cui and by
Intramural Research Program of the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases, NIH to Xin-zhuan
Su. The authors have no other relevant affiliations or financial
involvement with any organization or entity with a financial interest in
or financial conflict with the subject matter or materials discussed in
the manuscript apart from those disclosed.
NR 199
TC 80
Z9 85
U1 5
U2 48
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1478-7210
J9 EXPERT REV ANTI-INFE
JI Expert Rev. Anti-Infect. Ther.
PD OCT
PY 2009
VL 7
IS 8
BP 999
EP 1013
DI 10.1586/ERI.09.68
PG 15
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 506KA
UT WOS:000270772500013
PM 19803708
ER
PT J
AU Tocchini-Valentini, GP
Tocchini-Valentini, MA
Schlessinger, D
AF Tocchini-Valentini, Glauco P.
Tocchini-Valentini, Marta A.
Schlessinger, David
TI How to build a kangaroo the way a kangaroo builds itself
SO FASEB JOURNAL
LA English
DT Editorial Material
C1 [Tocchini-Valentini, Glauco P.] CNR, Ist Biol Cellulare, I-00015 Rome, Italy.
[Schlessinger, David] NIA, Genet Lab, Baltimore, MD 21224 USA.
RP Tocchini-Valentini, GP (reprint author), CNR, Ist Biol Cellulare, I-00015 Rome, Italy.
NR 10
TC 0
Z9 0
U1 0
U2 1
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 2009
VL 23
IS 10
BP 3257
EP 3259
DI 10.1096/fj.09-1002
PG 3
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 501BQ
UT WOS:000270354300002
PM 19797299
ER
PT J
AU Hong, S
Derfoul, A
Pereira-Mouries, L
Hall, DJ
AF Hong, Sohee
Derfoul, Assia
Pereira-Mouries, Lucilia
Hall, David J.
TI A novel domain in histone deacetylase 1 and 2 mediates repression of
cartilage-specific genes in human chondrocytes
SO FASEB JOURNAL
LA English
DT Article
DE osteoarthritis; transcription; collagen 2(alpha 1); chromatin
ID II COLLAGEN; ARTICULAR-CARTILAGE; TRANSCRIPTIONAL CONTROL;
EXTRACELLULAR-MATRIX; INDUCED ARTHRITIS; HDAC INHIBITORS;
TRICHOSTATIN-A; MOUSE MODEL; EXPRESSION; CELLS
AB The role of histone deacetylase 1 and 2 (HDAC1 and HDAC2) in regulating cartilage-specific gene expression was explored in primary human chondrocytes. HDAC1 and HDAC2 protein levels were elevated in chondrocytes from osteoarthritic patients, consistent with a down-regulation of some cartilage marker genes. When expressed in these cells, HDAC1 and HDAC2 repressed aggrecan and collagen 2(alpha 1) expression but differed in their repression of collagen 9(alpha 1), collagen 11(alpha 1), dermatopontin, and cartilage oligomeric matrix protein (COMP). To identify the basis of these differences between HDAC1 and HDAC2, their carboxy-terminal domains (CTDs) were deleted, which led to proteins that retained enzymatic activity but were unable to repress cartilage gene expression. Further, exchange of the CTDs between HDAC1 and HDAC2 led to proteins that were enzymatically active but displayed altered target gene specificity, indicating that these CTDs can function independently of HDAC enzymatic activity, to target the HDACs to specific genes. The Snail transcription factor was identified as a mediator of HDAC1 and HDAC2 repression of the collagen 2(alpha 1) gene, via its interaction with the HDAC1 and 2 CTDs. The data indicate that the CTD serves a novel function within HDAC1 and HDAC2, to mediate repression of cartilage-specific gene expression in human chondrocytes.-Hong, S., Derfoul, A., Pereira-Mouries, L., Hall, D. J. A novel domain in histone deacetylase 1 and 2 mediates repression of cartilage-specific genes in human chondrocytes. FASEB J. 23, 3539-3552 (2009). www.fasebj.org
C1 [Hong, Sohee; Derfoul, Assia; Pereira-Mouries, Lucilia; Hall, David J.] NIAMSD, Cartilage Mol Genet Grp, Cartilage Biol & Orthopaed Branch, NIH, Bethesda, MD 20892 USA.
RP Hall, DJ (reprint author), 50 S Dr,Rm 1524, Bethesda, MD 20892 USA.
EM halld@mail.nih.gov
FU National Institutes of Arthritis and Musculoskeletal and Skin Diseases
within the National Institutes of Health
FX We thank the National Disease Research Interchange (Philadelphia, PA,
USA) for providing the human cartilage tissue samples. We also thank Dr.
Ed Seto (Moffitt Cancer Center, Tampa, FL, USA) for the gift of the
HDAC2 expression plasmid. The HDAC1 expression plasmid was provided by
Origene Technologies (Rockville, MD, USA). This work was supported by
the Intramural Research Program of the National Institutes of Arthritis
and Musculoskeletal and Skin Diseases within the National Institutes of
Health (Bethesda, MD, USA).
NR 42
TC 37
Z9 39
U1 1
U2 4
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 2009
VL 23
IS 10
BP 3539
EP 3552
DI 10.1096/fj.09-133215
PG 14
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 501BQ
UT WOS:000270354300030
PM 19561124
ER
PT J
AU Salmon, AB
Perez, VI
Bokov, A
Jernigan, A
Kim, G
Zhao, H
Levine, RL
Richardson, A
AF Salmon, Adam B.
Perez, Viviana I.
Bokov, Alex
Jernigan, Amanda
Kim, Geumsoo
Zhao, Hang
Levine, Rodney L.
Richardson, Arlan
TI Lack of methionine sulfoxide reductase A in mice increases sensitivity
to oxidative stress but does not diminish life span
SO FASEB JOURNAL
LA English
DT Article
DE longevity; free radical; stress resistance; aging; antioxidant
ID FIBROBLAST CELL-LINES; ANTIOXIDANT ENZYMES; MULTIPLE FORMS; KNOCKOUT
MOUSE; DWARF MICE; RESISTANCE; MSRA; DAMAGE; GENE; OVEREXPRESSION
AB Methionine sulfoxide reductase A (MsrA) repairs oxidized methionine residues within proteins and may also function as a general antioxidant. Previous reports have suggested that modulation of MsrA in mice and mammalian cell culture can affect the accumulation of oxidized proteins and may regulate resistance to oxidative stress. Thus, under the oxidative stress theory of aging, these results would predict that MsrA regulates the aging process in mammals. We show here that MsrA(-/-) mice are more susceptible to oxidative stress induced by paraquat. Skin-derived fibroblasts do not express MsrA, but fibroblasts cultured from MsrA(-/-) mice were, nevertheless, also more susceptible to killing by various oxidative stresses. In contrast to previous reports, we find no evidence for neuromuscular dysfunction in MsrA(-/-) mice in either young adult or in older animals. Most important, we found no difference between MsrA(-/-) and control mice in either their median or maximum life span. Thus, our results show that MsrA regulates sensitivity to oxidative stress in mice but has no effect on aging, as determined by life span.-Salmon, A. B., Perez, V. I., Bokov, A., Jernigan, A., Kim, G., Zhao, H., Levine, R. L., Richardson, A. Lack of methionine sulfoxide reductase A in mice increases sensitivity to oxidative stress but does not diminish life span. FASEB J. 23, 3601-3608 (2009). www.fasebj.org
C1 [Richardson, Arlan] Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, Sam & Ann Barshop Inst Longev & Aging Studies, San Antonio, TX 78245 USA.
[Kim, Geumsoo; Zhao, Hang; Levine, Rodney L.] NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA.
[Richardson, Arlan] S Texas Vet Hlth Care Syst, Ctr Geriatr Res Educ & Clin, San Antonio, TX USA.
RP Richardson, A (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, Sam & Ann Barshop Inst Longev & Aging Studies, 15355 Lambda Dr, San Antonio, TX 78245 USA.
EM richardsona@uthscsa.edu
RI Zhao, Hang/A-2558-2012; Levine, Rodney/D-9885-2011
FU National Institutes of Health (NIH) [T32 AG021890-05, R37AG026557]; San
Antonio Nathan Shock Center for Excellence in the Basic Biology of
Aging; National Heart, Lung, and Blood Institute
FX We thank Jay Cox, Marian Sabia, and Quy Fung for assistance in animal
care. We also thank Dr. James Harper for statistical analysis assistance
and intellectual discourse. This study was supported by National
Institutes of Health (NIH) training grant T32 AG021890-05 (A. B. S.),
NIH MERIT grant R37AG026557 (A. R.), the San Antonio Nathan Shock Center
for Excellence in the Basic Biology of Aging (A.R.), and the Intramural
Research Program of the National Heart, Lung, and Blood Institute (G.K.,
H.Z., and R.L.L.).
NR 44
TC 63
Z9 65
U1 0
U2 4
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 2009
VL 23
IS 10
BP 3601
EP 3608
DI 10.1096/fj.08-127415
PG 8
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 501BQ
UT WOS:000270354300036
PM 19487311
ER
PT J
AU Appella, E
Anderson, CW
AF Appella, Ettore
Anderson, Carl W.
TI Dynamic interactions of proteins in complex networks
SO FEBS JOURNAL
LA English
DT Editorial Material
C1 [Appella, Ettore] NCI, Chem Immunol Sect, Cell Biol Lab, Bethesda, MD 20892 USA.
[Anderson, Carl W.] Brookhaven Natl Lab, Dept Biol, Upton, NY 11973 USA.
RP Appella, E (reprint author), NCI, Chem Immunol Sect, Cell Biol Lab, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1742-464X
J9 FEBS J
JI FEBS J.
PD OCT
PY 2009
VL 276
IS 19
BP 5380
EP 5380
DI 10.1111/j.1742-4658.2009.07252.x
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 499AC
UT WOS:000270187500006
PM 19712105
ER
PT J
AU Ambudkar, IS
AF Ambudkar, Indu S.
TI Unraveling Smooth Muscle Contraction: The TRP Link
SO GASTROENTEROLOGY
LA English
DT Editorial Material
ID NONSELECTIVE CATION CHANNELS; SIGNAL-TRANSDUCTION; ESSENTIAL COMPONENT;
G-PROTEIN; CELLS; MICE
C1 [Ambudkar, Indu S.] NIDCR, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
[Ambudkar, Indu S.] NIDCR, Secretory Physiol Sect, NIH, Bethesda, MD 20892 USA.
RP Ambudkar, IS (reprint author), NIDCR, Mol Physiol & Therapeut Branch, NIH, Bldg 10,Room 1N-113, Bethesda, MD 20892 USA.
EM indu.ambudkar@nih.gov
FU Intramural NIH HHS [Z01 DE000438-22]
NR 20
TC 4
Z9 4
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 2009
VL 137
IS 4
BP 1211
EP 1214
DI 10.1053/j.gastro.2009.08.025
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 499VT
UT WOS:000270255200009
PM 19717126
ER
PT J
AU von Rosenvinge, EC
Wank, SA
Lim, RM
AF von Rosenvinge, Erik C.
Wank, Stephen A.
Lim, Ramona M.
TI Gastric Masses in Multiple Endocrine Neoplasia Type I-Associated
Zollinger-Ellison Syndrome
SO GASTROENTEROLOGY
LA English
DT Editorial Material
C1 [von Rosenvinge, Erik C.; Wank, Stephen A.; Lim, Ramona M.] NIDDK, Digest Dis Branch, NIH, Bethesda, MD 20892 USA.
RP von Rosenvinge, EC (reprint author), NIDDK, Digest Dis Branch, NIH, Bethesda, MD 20892 USA.
FU Intramural NIH HHS
NR 3
TC 3
Z9 3
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2009
VL 137
IS 4
BP 1222
EP +
DI 10.1053/j.gastro.2009.03.050
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 499VT
UT WOS:000270255200012
PM 19723598
ER
PT J
AU Tsvilovskyy, VV
Zholos, AV
Aberle, T
Philipp, SE
Dietrich, A
Zhu, MX
Birnbaumer, L
Freichel, M
Flockerzi, V
AF Tsvilovskyy, Volodymyr V.
Zholos, Alexander V.
Aberle, Thomas
Philipp, Stephan E.
Dietrich, Alexander
Zhu, Michael X.
Birnbaumer, Lutz
Freichel, Marc
Flockerzi, Veit
TI Deletion of TRPC4 and TRPC6 in Mice Impairs Smooth Muscle Contraction
and Intestinal Motility In Vivo
SO GASTROENTEROLOGY
LA English
DT Article
ID NONSELECTIVE CATION CHANNELS; OPERATED CA2+ ENTRY; GUINEA-PIG ILEUM;
G-PROTEIN; MUSCARINIC RECEPTORS; ESSENTIAL COMPONENT; PHOSPHOLIPASE-C;
CELLS; ACTIVATION; CARBACHOL
AB BACKGROUND & AIMS: Downstream effects of muscarinic receptor stimulation in intestinal smooth muscle include contraction and intestinal transit. We thought to determine whether classic transient receptor potential (TRPC) channels integrate the intracellular signaling cascades evoked by the stimulated receptors and thereby contribute to the control of the membrane potential, Ca-influx, and cell responses. METHODS: We created trpc4-, trpc6-, and trpc4/trpc6-gene- deficient mice and analyzed them for intestinal smooth muscle function in vitro and in vivo. RESULTS: In intestinal smooth Muscle cells TRPC4 forms a 55 pS cation channel and underlies more than 80% of the muscarinic receptor-induced cation current (mI(CAT)). The residual mI(CAT) depends on the expression of TRPC6, indicating that TRPC6 and TP-PC4 determine mI(CAT) channel activity independent of other channel subunits. In TRPC4-deficient ileal myocytes the carbachol-induced membrane depolarizations are diminished greatly and the atropine-sensitive contraction elicited. by acetylcholine release from excitatory motor neurons is reduced greatly. Additional deletion of TRPC6 aggravates these effects. Intestinal transit is slowed down in mice lacking TRPC4 and TRPC6. CONCLUSIONS: In intestinal smooth muscle cells TRPC4 and TRPC6 channels are gated by muscarinic receptors and are responsible for MICAT. They couple muscarinic receptors to depolarization of intestinal smooth muscle cells and voltage-activated Ca2+-influx and contraction, and thereby accelerate small intestinal motility in vivo.
C1 [Tsvilovskyy, Volodymyr V.; Aberle, Thomas; Philipp, Stephan E.; Freichel, Marc; Flockerzi, Veit] Univ Saarland, D-66421 Homburg, Germany.
[Zholos, Alexander V.] Queens Univ Belfast, Ctr Vis & Vasc Sci, Sch Med Dent & Biomed Sci, Belfast, Antrim, North Ireland.
[Dietrich, Alexander] Univ Marburg, Inst Pharmakol & Toxikol, Fak Med, D-3550 Marburg, Germany.
[Zhu, Michael X.] Ohio State Univ, Dept Neurosci, Columbus, OH 43210 USA.
[Zhu, Michael X.] Ohio State Univ, Ctr Mol Neurobiol, Columbus, OH 43210 USA.
[Birnbaumer, Lutz] Natl Inst Environm Hlth Sci, Signal Transduct Lab, Div Intramural Res, NIH, Res Triangle Pk, NC USA.
[Birnbaumer, Lutz] Natl Inst Environm Hlth Sci, Neurobiol Lab, Div Intramural Res, NIH, Res Triangle Pk, NC USA.
RP Freichel, M (reprint author), Univ Saarland, Kirrberger Str,Gebaude 46, D-66421 Homburg, Germany.
EM marc.freichel@uks.eu
RI Zholos, Alexander/A-7017-2011; Dietrich, Alexander/G-8619-2013;
OI Zholos, Alexander/0000-0002-4320-149X; Dietrich,
Alexander/0000-0002-1168-8707
FU Intramural Research Programs of the National Institutes of Health;
National Institute of Environmental Health Sciences [Z01-ES-101684];
National Institutes of Health [DK081654]; Homburger Forschungsforderung
sprogramm; Deutsche Forschungsgemelnschaft; Forschungskommisslon der
UdS; Fonds der Chemischen Industrie
FX Supported in part by the Intramural Research Programs of the National
Institutes of Health, National Institute of Environmental Health
Sciences (Z01-ES-101684) to (L.B.), by National Institutes of Health
grant DK081654 (MXZ. and A.V.Z.), by Homburger Forschungsforderung
sprogramm (HOMFOR) (M.F., V.V.T., S.E.P., and V.F.), by Deutsche
Forschungsgemenschaft and Forschungskommisslon der UdS (M.F. and V.F.),
and by Fonds der Chemischen Industrie (V.F.).
NR 50
TC 79
Z9 80
U1 0
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2009
VL 137
IS 4
BP 1415
EP 1424
DI 10.1053/j.gastro.2009.06.046
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 499VT
UT WOS:000270255200033
PM 19549525
ER
PT J
AU Kim, MS
Hong, JH
Li, Q
Shin, DM
Abramowitz, J
Birnbaumer, L
Muallem, S
AF Kim, Min Seuk
Hong, Jeong Hee
Li, Qin
Shin, Dong Min
Abramowitz, Joel
Birnbaumer, Lutz
Muallem, Shmuel
TI Deletion of TRPC3 in Mice Reduces Store-Operated Ca2+ Influx and the
Severity of Acute Pancreatitis
SO GASTROENTEROLOGY
LA English
DT Article
ID INOSITOL TRISPHOSPHATE; CHANNEL FUNCTION; CATION CHANNELS; EXOCRINE
CELLS; ACINAR-CELLS; STIM1; CALCIUM; ORAI1; RELEASE; CRAC
AB BACKGROUND & AIMS: Receptor-stimulated Ca2+ influx is a critical component of the Ca2+ signal and mediates all cellular functions regulated by Ca2+. However, excessive Ca2+ influx is highly toxic, resulting in cell death, which is the nodal point in all forms of pancreatitis. Ca2+ influx is mediated by store-operated channels (SOCs). The identity and function of the native SOCs in most cells is unknown. METHODS: Here, we determined the role of deletion of Trpc3 in mice on Ca2+ signaling, exocytosis, intracellular trypsin activation, and pancreatitis. RESULTS: Deletion of TRPC3 reduced the receptor-stimulated and SOC-mediated Ca2+ influx by about 50%, indicating that TRPC3 functions as an SOC in vivo. The reduced Ca2+ influx in TRPC3(-/-) acini resulted in reduced frequency of the physiologic Ca2+ oscillations and of the pathologic sustained increase in cytosolic Ca2+ levels caused by supramaximal stimulation and by the toxins bile acids and palmitoleic acid ethyl ester. Consequently, deletion of TRPC3 shifted the dose response for receptor-stimulated exocytosis and prevented the pathologic inhibition of digestive enzyme secretion at supramaximal agonist concentrations. Accordingly, deletion of TRPC3 markedly reduced intracellular trypsin activation and excessive actin depolymerization in vitro and the severity of pancreatitis in vivo. CONCLUSIONS: These findings establish the native TRPC3 as an SOC in vivo and a role for TRPC3-mediated Ca2+ influx in the pathogenesis of acute pancreatitis and suggest that TRPC3 should be considered a target for prevention of pancreatic damage in acute pancreatitis.
C1 [Kim, Min Seuk; Hong, Jeong Hee; Li, Qin; Muallem, Shmuel] Univ Texas SW Med Ctr Dallas, Dept Physiol, Dallas, TX 75390 USA.
[Shin, Dong Min] Yonsei Univ, Coll Dent, Dept Oral Biol, Brain Korea Project 21, Seoul 120749, South Korea.
[Abramowitz, Joel; Birnbaumer, Lutz] Natl Inst Environm Hlth Sci, Neurobiol Lab, Res Triangle Pk, NC USA.
RP Muallem, S (reprint author), Univ Texas SW Med Ctr Dallas, Dept Physiol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM birnbau1@niehs.nih.gov; shmuel.muallem@utsouthwestern.edu
RI Abramowitz, Joel/A-2620-2015
FU National Institutes of Health [DE12309, DK38938, ZOI-ES-101684]; Ruth S.
Harrell Professorship in Medical Research
FX Supported by National Institutes of Health grants DE12309 and DK38938,
the Ruth S. Harrell Professorship in Medical Research (to S.M.), and the
Intramural Research Program of the National Institutes of Health
(ZOI-ES-101684 to L.B.).
NR 39
TC 66
Z9 67
U1 1
U2 6
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 2009
VL 137
IS 4
BP 1509
EP 1517
DI 10.1053/j.gastro.2009.07.042
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 499VT
UT WOS:000270255200042
PM 19622358
ER
PT J
AU Sloane, E
Langer, S
Jekich, B
Mahoney, J
Hughes, T
Frank, M
Seibert, W
Huberty, G
Coats, B
Harrison, J
Klinman, D
Poole, S
Maier, S
Johnson, K
Chavez, R
Watkins, LR
Leinwand, L
Milligan, E
AF Sloane, E.
Langer, S.
Jekich, B.
Mahoney, J.
Hughes, T.
Frank, M.
Seibert, W.
Huberty, G.
Coats, B.
Harrison, J.
Klinman, D.
Poole, S.
Maier, S.
Johnson, K.
Chavez, R.
Watkins, L. R.
Leinwand, L.
Milligan, E.
TI Immunological priming potentiates non-viral anti-inflammatory gene
therapy treatment of neuropathic pain
SO GENE THERAPY
LA English
DT Article
DE non-viral; interleukin-10; neuropathic pain; CNS
ID CHRONIC CONSTRICTION INJURY; NECROSIS-FACTOR-ALPHA; DORSAL-ROOT GANGLIA;
RAT SCIATIC-NERVE; SPINAL-CORD; PROINFLAMMATORY CYTOKINES;
PERITONEAL-MACROPHAGES; INFLAMMATORY PAIN; CLINICAL PAIN; PLASMID DNA
AB We recently described a non-viral gene therapy paradigm offering long-term resolution of established neuropathic pain in several animal models. Here, the requirements for long-term therapeutic effects are described, and evidence is provided for a mechanism of action based on immunological priming of the intrathecal (i.t.) space. Long-term pain reversal was achieved when two i.t. injections of various naked plasmid DNA doses were separated by 5 h to 3 days. We show that an initial DNA injection, regardless of whether a transgene is included, leads to an accumulation of phagocytic innate immune cells. This accumulation coincides with the time in which subsequent DNA injection efficacy is potentiated. We show the ability of non-coding DNA to induce short-term pain reversal that is dependent on endogenous interleukin-10 (IL-10) signaling. Long-term efficacy requires the inclusion of an IL-10(F129S) transgene in the second injection. Blockade of IL-10, by a neutralizing antibody, either between the two injections or after the second injection induces therapeutic failure. These results show that this gene therapy paradigm uses an initial 'priming' injection of DNA to induce accumulation of phagocytic immune cells, allowing for potentiated efficacy of a subsequent 'therapeutic' DNA injection in a time- and dose-dependent manner. Gene Therapy (2009) 16, 1210-1222; doi: 10.1038/gt.2009.79; published online 2 July 2009
C1 [Sloane, E.; Jekich, B.; Mahoney, J.; Frank, M.; Seibert, W.; Huberty, G.; Coats, B.; Harrison, J.; Maier, S.; Watkins, L. R.] Univ Colorado, Dept Psychol & Neurosci, Boulder, CO 80309 USA.
[Sloane, E.; Jekich, B.; Mahoney, J.; Frank, M.; Seibert, W.; Huberty, G.; Coats, B.; Harrison, J.; Maier, S.; Watkins, L. R.] Univ Colorado, Ctr Neurosci, Boulder, CO 80309 USA.
[Langer, S.; Hughes, T.; Leinwand, L.] Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USA.
[Klinman, D.] NCI, Frederick, MD 21701 USA.
[Poole, S.] Natl Inst Biol Stand & Controls, Potters Bar, Herts, England.
[Johnson, K.; Chavez, R.] Avigen Inc, Alameda, CA USA.
[Milligan, E.] Univ New Mexico, Hlth Sci Ctr, Dept Neurosci, Albuquerque, NM 87131 USA.
RP Watkins, LR (reprint author), Univ Colorado, Dept Psychol & Neurosci, Campus Box 345, Boulder, CO 80309 USA.
EM linda.watkins@colorado.edu
OI LEINWAND, LESLIE/0000-0003-1470-4810
FU Avigen; NIH [DA018156, DA015642, DA015656, HL5510]
FX Financial support to this work is provided by Avigen and the NIH grants
DA018156, DA015642, DA015656 and HL5510.
NR 52
TC 12
Z9 12
U1 1
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0969-7128
J9 GENE THER
JI Gene Ther.
PD OCT
PY 2009
VL 16
IS 10
BP 1210
EP 1222
DI 10.1038/gt.2009.79
PG 13
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity; Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity; Research & Experimental Medicine
GA 508LW
UT WOS:000270933900006
PM 19571887
ER
PT J
AU Choi, BY
Stewart, AK
Nishimura, KK
Cha, WJ
Seong, MW
Park, SS
Kim, SW
Chun, YS
Chung, JW
Park, SN
Chang, SO
Kim, CS
Alper, SL
Griffith, AJ
Oh, SH
AF Choi, Byung Yoon
Stewart, Andrew K.
Nishimura, Katherine K.
Cha, Won Jae
Seong, Moon-Woo
Park, Sung Sup
Kim, Seung Won
Chun, Yang Sook
Chung, Jong Woo
Park, Shi-Nae
Chang, Sun O.
Kim, Chong-Sun
Alper, Seth L.
Griffith, Andrew J.
Oh, Seung-Ha
TI Efficient Molecular Genetic Diagnosis of Enlarged Vestibular Aqueducts
in East Asians
SO GENETIC TESTING AND MOLECULAR BIOMARKERS
LA English
DT Article
ID GENOTYPE-PHENOTYPE CORRELATION; NONSYNDROMIC HEARING-LOSS; TRANSPORTER
DTDST GENE; PENDRED-SYNDROME GENE; SLC26A4 MUTATIONS;
ENDOPLASMIC-RETICULUM; FOUNDER MUTATION; UNIQUE SPECTRUM; IODIDE EFFLUX;
PDS MUTATIONS
AB Context: Enlargement of the vestibular aqueduct (EVA) is a commonly detected inner ear anomaly related to hearing loss and often associated with mutations of SLC26A4 encoding pendrin, a transmembrane exchanger of Cl(-), I(-), and HCO(3)(-). Here we describe the phenotypes of 27 Korean EVA subjects and their SLC26A4 genotypes determined by bidirectional nucleotide sequencing. Results: The detected variants include two novel missense substitutions (p. V138L and p. P542R). We characterized the ability of p. V138L and p. P542R pendrin products to traffic to the plasma membrane in COS-7 cells and to transport Cl(-), I(-), and HCO3- in Xenopus oocytes. The results indicate that p. P542R is a benign polymorphic variant, whereas p. V138L is a pathogenic mutation. Since this and other studies of East Asian EVA cohorts show that the majority of SLC26A4 mutations affect either or both of two amplicons (exons 7-8 and 19), we developed a hierarchical protocol that integrates direct sequencing with denaturing high-performance liquid chromatography analyses for detection of SLC26A4 mutations in these populations. We validated the cost efficiency of the integrated protocol by a simulated screen of published East Asian EVA cohorts with known SLC26A4 genotypes. Conclusions: Our study further defines the spectrum of SLC26A4 mutations among East Asians and demonstrates a rapid and efficient protocol for their detection.
C1 [Choi, Byung Yoon; Cha, Won Jae; Chang, Sun O.; Kim, Chong-Sun; Oh, Seung-Ha] Seoul Natl Univ, Coll Med, Dept Otolaryngol Head & Neck Surg, Seoul 110744, South Korea.
[Choi, Byung Yoon] Natl Inst Deafness & Other Commun Disorders, Mol Genet Lab, NIH, Rockville, MD USA.
[Stewart, Andrew K.; Nishimura, Katherine K.; Alper, Seth L.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
[Seong, Moon-Woo; Park, Sung Sup] Seoul Natl Univ, Coll Med, Dept Lab Med, Seoul 110744, South Korea.
[Kim, Seung Won; Chun, Yang Sook] Seoul Natl Univ, Coll Med, Human Genome Res Inst, Seoul 110744, South Korea.
[Chung, Jong Woo] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Otolaryngol, Seoul, South Korea.
[Park, Shi-Nae] Catholic Univ Korea, Kangnam St Marys Hosp, Coll Med, Dept Otolaryngol HNS, Seoul, South Korea.
[Griffith, Andrew J.] Natl Inst Deafness & Other Commun Disorders, Otolaryngol Branch, NIH, Rockville, MD USA.
[Oh, Seung-Ha] Seoul Natl Univ, Med Res Ctr, Sensory Organ Res Inst, Seoul 110744, South Korea.
RP Oh, SH (reprint author), Seoul Natl Univ, Coll Med, Dept Otolaryngol Head & Neck Surg, 28 Yongon Dong, Seoul 110744, South Korea.
EM shaoh@snu.ac.kr
RI Chun, Yang Sook/J-2789-2012; Park, Sung Sup/J-2756-2012; Chung, Jong
Woo/A-4287-2013; Oh, Seung Ha/J-5540-2012; Chang, Sun O/J-5627-2012;
OI Cha, Wonjae/0000-0001-7292-9474
FU Korea Healthcare Technology RD Project; Ministry for Health; Welfare and
Family Affairs; Republic of Korea [A080588]; Seoul National University
Hospital research fund [21-2005-016]; NIDCD; NIH intramural research
funds [Z01-DC-00060-07, Z01DC00039-10, DK43495, DK34854]; NIH Fellows
Editorial Board
FX This work was supported by a grant from the Korea Healthcare Technology
R&D Project, Ministry for Health, Welfare and Family Affairs, Republic
of Korea (Project No. A080588) and also by Grant No. 21-2005-016 from
the Seoul National University Hospital research fund, NIDCD/NIH
intramural research funds Z01-DC-00060-07 (A.J.G.), Z01DC00039-10 (T. B.
F.), and NIH grants DK43495 (S. L. A.) and DK34854 (Harvard Digestive
Diseases Center support to S. L. A.). We thank Dr. Thomas Friedman for
support and critical review of the manuscript and the NIH Fellows
Editorial Board for editorial assistance.
NR 41
TC 12
Z9 14
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1945-0265
J9 GENET TEST MOL BIOMA
JI Genet. Test. Mol. Biomark.
PD OCT
PY 2009
VL 13
IS 5
BP 679
EP 687
DI 10.1089/gtmb.2009.0054
PG 9
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 504FO
UT WOS:000270601500021
PM 19645628
ER
PT J
AU Bauer, GL
Praetorius, C
Bergsteinsdottir, K
Hallsson, JH
Gisladottir, BK
Schepsky, A
Swing, DA
O'Sullivan, TN
Arnheiter, H
Bismuth, K
Debbache, J
Fletcher, C
Warming, S
Copeland, NG
Jenkins, NA
Steingrimsson, E
AF Bauer, Georg L.
Praetorius, Christian
Bergsteinsdottir, Kristin
Hallsson, Jon H.
Gisladottir, Bryndis K.
Schepsky, Alexander
Swing, Deborah A.
O'Sullivan, T. Norene
Arnheiter, Heinz
Bismuth, Keren
Debbache, Julien
Fletcher, Colin
Warming, Soren
Copeland, Neal G.
Jenkins, Nancy A.
Steingrimsson, Eirikur
TI The Role of MITF Phosphorylation Sites During Coat Color and Eye
Development in Mice Analyzed by Bacterial Artificial Chromosome
Transgene Rescue
SO GENETICS
LA English
DT Article
ID MICROPHTHALMIA TRANSCRIPTION FACTOR; MELANOCYTE DEVELOPMENT; GENE;
MUTATIONS; PROTEIN; FAMILY; LOCUS
AB The microphthalmia-associated transcription factor (Mitf) has emerged as an important model for gene regulation in eukaryotic organisms. In vertebrates, it regulates the development of several cell types including melanocytes and has also been shown to play all important role in melanoma. In vitro, the activity of MITE is regulated by multiple signaling pathways, including the KITL/KIT/B-Raf pathway, which results in phosphorylation of MITE on serine residues 73 and 409. However, the precise role of signaling to MITE in. vivo remains largely unknown. Here, we use a BAC transgene rescue approach to introduce specific mutations in MITF to study the importance of specific phospho-acceptor sites and protein domains. We show that mice that carry a BAC transgene where single-amino-acid substitutions have been made in the Mitf gene rescue the phenotype of the loss-of-function mutations in Mitf. This may indicate that. signaling from KIT to MITF affects other phospho-acceptor sites in MITF or that alternative sites can be phosphorylated when Set73 and Ser409 have been mutated. Our results have implications for understanding signaling to transcription factors. Furthermore, as MITF and signaling mechanisms have been shown to play all important. role in melanomas, our findings may lead to novel insights into this resilient disease.
C1 [Bauer, Georg L.; Praetorius, Christian; Bergsteinsdottir, Kristin; Hallsson, Jon H.; Gisladottir, Bryndis K.; Schepsky, Alexander; Steingrimsson, Eirikur] Univ Iceland, Dept Biochem & Mol Biol, Fac Med, IS-101 Reykjavik, Iceland.
[Bauer, Georg L.; Praetorius, Christian; Bergsteinsdottir, Kristin; Hallsson, Jon H.; Gisladottir, Bryndis K.; Schepsky, Alexander; Steingrimsson, Eirikur] Univ Iceland, Biomed Ctr, Fac Med, IS-101 Reykjavik, Iceland.
[Swing, Deborah A.; O'Sullivan, T. Norene; Warming, Soren] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Arnheiter, Heinz; Bismuth, Keren; Debbache, Julien] Natl Inst Neurol Disorders & Stroke, Lab Dev Neurogenet, Porter Neurosci Res Ctr, Bethesda, MD 20892 USA.
[Fletcher, Colin] NHGRI, Knock Out Mouse Program, NIH, Bethesda, MD 20892 USA.
[Copeland, Neal G.; Jenkins, Nancy A.] Inst Mol & Cell Biol, Singapore 138673, Singapore.
RP Steingrimsson, E (reprint author), Univ Iceland, Dept Biochem & Mol Biol, Fac Med, Vatnsmyrarvegur 16, IS-101 Reykjavik, Iceland.
EM eirikurs@hi.is
RI ASTAR, IMCB/E-2320-2012;
OI Praetorius, Christian/0000-0001-7514-5333
FU Icelandic Research Fund; Science Fund of the University of Iceland;
Sigurdur Jonsson and Helga Sigurdardottir Memorial Fund; National
Institutes of Health; National Institute of Neurological Disorders and
Stroke
FX We thank Petur Henry Petersen, Benedikta St. Haflidadottir, Merle
Fleischer, Helga Eyja Hrafnkelsdottir, Gunnhildur A. Traustadottir,
Helgi Mar Jonsson, and Gudrun Valdimarsdottir for expert assistance. We
also thank Gudmundur Ingolfsson for assistance with photography. This
work Was supported by grants from The Icelandic Research Fund and from
the Science Fund of the University of Iceland and by all award from the
Sigurdur Jonsson and Helga Sigurdardottir Memorial Fund (E.S.). This
work was supported in part by the intramural research program of the
National Institutes of Health, National Institute of Neurological
Disorders and Stroke.
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U1 0
U2 4
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 0016-6731
J9 GENETICS
JI Genetics
PD OCT
PY 2009
VL 183
IS 2
BP 581
EP 594
DI 10.1534/genetics.109.103945
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 516QU
UT WOS:000271558300014
PM 19635938
ER
PT J
AU Khoury, MJ
Rich, EC
Randhawa, G
Teutsch, SM
Niederhuber, J
AF Khoury, Muin J.
Rich, Eugene C.
Randhawa, Gurvaneet
Teutsch, Steven M.
Niederhuber, John
TI Comparative effectiveness research and genomic medicine: An evolving
partnership for 21st century medicine
SO GENETICS IN MEDICINE
LA English
DT Editorial Material
DE genomics; medicine; comparative effectiveness; evidence-based medicine
ID EGAPP WORKING GROUP; PERSONALIZED MEDICINE; WARFARIN; POLICY;
RECOMMENDATIONS; ANTICOAGULATION; PREDICTION; GENETICS; CANCER; HEALTH
AB The American Recovery and Reinvestment Act has provided resources for comparative effectiveness research that will lead to evidence-based decisions about health and health care choices. Some have voiced concerns that evidence-based comparative effectiveness research principles are only relevant to "average" patients and not as much to individuals with unique combinations of genes, exposures and disease outcomes, intrinsic to genomic medicine. In this commentary, we argue that comparative effectiveness research and genomic medicine not only can and should coexist but also they will increasingly benefit front each other. The promise and success of genomic medicine will depend on rigorous comparative effectiveness research to compare outcomes for genome-based applications in practice to traditional non-genome-based approaches. In addition, the success of comparative effectiveness research will depend on developing new methods and clinical research infrastructures to integrate genome-based personalized perspectives into point of care decisions by patients and providers. There is a need to heal the apparent schism between genomic medicine and comparative effectiveness research to enhance knowledge-driven practice of medicine in the 21st century. Genet Aled 2009:11(10):707-711.
C1 [Khoury, Muin J.] Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA 30333 USA.
[Khoury, Muin J.; Niederhuber, John] NCI, Bethesda, MD 20892 USA.
[Rich, Eugene C.] Assoc Amer Med Coll, Washington, DC USA.
[Randhawa, Gurvaneet] Agcy Healthcare Res & Qual, Rockville, MD USA.
[Teutsch, Steven M.] Los Angeles Cty Dept Publ Hlth, Los Angeles, CA USA.
RP Khoury, MJ (reprint author), Ctr Dis Control & Prevent, Off Publ Hlth Genom, 1600 Clifton Rd, Atlanta, GA 30333 USA.
EM mkhoury@cdc.gov
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1098-3600
J9 GENET MED
JI Genet. Med.
PD OCT
PY 2009
VL 11
IS 10
BP 707
EP 711
DI 10.1097/GIM.0b013e3181b99b90
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 515EK
UT WOS:000271449800003
PM 19752739
ER
PT J
AU Ersig, AL
Williams, JK
Hadley, DW
Koehly, LM
AF Ersig, Anne L.
Williams, Janet K.
Hadley, Donald W.
Koehly, Laura M.
TI Communication, encouragement, and cancer screening in families with and
without mutations for hereditary nonpolyposis colorectal cancer: A pilot
study
SO GENETICS IN MEDICINE
LA English
DT Article
DE hereditary nonpolyposis colorectal cancer; cancer screening;
communication; encouragement; indeterminate genetic test results
ID LYNCH-SYNDROME; INHERITED PREDISPOSITION; ENDOMETRIAL CANCER;
COLON-CANCER; INDIVIDUALS; HEALTH; RISK; RECOMMENDATIONS; KNOWLEDGE;
ONSET
AB Purpose: Known and suspected mutation carriers for hereditary non-polyposis colorectal cancer are advised to have colonoscopies every 1 to 2 years to detect colorectal cancer. Little is known about colonoscopy completion in families Suspected of having hereditary nonpolyposis colorectal cancer but without identified mutations. Methods: This study examined the effect of communication and encouragement on colonoscopy in families with and without known mutations. Twenty-three respondents from 11 families with indeterminate genetic test results were matched with 23 respondents from 11 families with Mutation-positive results. Hierarchical modeling examined the effects of relational characteristics on time since last colonoscopy in index cases and their first-degree relatives. Results: Nearly one fifth of respondents were not screening appropriately. Time since last screening did not differ according to family mutation status. However, respondents who communicated about risk and received encouragement to screen from a greater proportion of named family members, and those who had a greater proportion of named family members involved in both communication and encouragement were significantly more likely to have a shorter time interval since last colonoscopy. Conclusion: Identifying patterns of interaction within at-risk families, regardless of gene mutation status, may be one avenue for promoting screening adherence. Genet Med 2009:11(10):728-734.
C1 [Ersig, Anne L.; Williams, Janet K.] Univ Iowa, Parent Child & Family Area, Coll Nursing, Iowa City, IA 52242 USA.
[Ersig, Anne L.; Hadley, Donald W.; Koehly, Laura M.] NHGRI, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA.
[Ersig, Anne L.] NINR, Grad Partnerships Program, NIH, Bethesda, MD 20892 USA.
RP Ersig, AL (reprint author), Univ Iowa, Parent Child & Family Area, Coll Nursing, 50 Newton Rd,340NB, Iowa City, IA 52242 USA.
EM anne-ersig@uiowa.edu
FU National Human Genome Research Institute [Z01HG200335-01]; National
Cancer Institute at the National Institutes of Health, Bethesda,
Maryland; National Institute of Nursing Research, National Institutes of
Health
FX This research was supported by the Intramural Research Programs of the
National Human Genome Research Institute (Z01HG200335-01, Laura Koehly,
PI) and the National Cancer Institute at the National Institutes of
Health, Bethesda, Maryland. The data presented in this manuscript were
collected through a protocol monitored by the Institutional Review
Boards at the National Human Genome Research Institute (Protocol
#95-HG-0165; Donald Hadley, PI) and the National Naval Medical Center
(NNMC. 1995.0045; Ismail Jatoi, PI). Dr. Ersig was supported by a
Graduate Partnerships Program fellowship from the National Institute of
Nursing Research, National Institutes of Health.
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1098-3600
J9 GENET MED
JI Genet. Med.
PD OCT
PY 2009
VL 11
IS 10
BP 728
EP 734
DI 10.1097/GIM.0b013e3181b3f42d
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 515EK
UT WOS:000271449800007
PM 19707152
ER
PT J
AU Barski, A
Jothi, R
Cuddapah, S
Cui, KR
Roh, TY
Schones, DE
Zhao, K
AF Barski, Artem
Jothi, Raja
Cuddapah, Suresh
Cui, Kairong
Roh, Tae-Young
Schones, Dustin E.
Zhao, Keji
TI Chromatin poises miRNA- and protein-coding genes for expression
SO GENOME RESEARCH
LA English
DT Article
ID RNA-POLYMERASE-II; HUMAN GENOME; HISTONE MODIFICATIONS; ACTIVE
CHROMATIN; MICRORNA GENES; STEM-CELLS; T-CELLS; TRANSCRIPTION;
METHYLATION; PROMOTERS
AB Chromatin modifications have been implicated in the regulation of gene expression. While association of certain modifications with expressed or silent genes has been established, it remains unclear how changes in chromatin environment relate to changes in gene expression. In this article, we used ChIP-seq (chromatin immunoprecipitation with massively parallel sequencing) to analyze the genome-wide changes in chromatin modifications during activation of total human CD4(+) T cells by T-cell receptor (TCR) signaling. Surprisingly, we found that the chromatin modification patterns at many induced and silenced genes are relatively stable during the short-term activation of resting T cells. Active chromatin modifications were already in place for a majority of inducible protein-coding genes, even while the genes were silent in resting cells. Similarly, genes that were silenced upon T-cell activation retained positive chromatin modifications even after being silenced. To investigate if these observations are also valid for miRNA-coding genes, we systematically identified promoters for known miRNA genes using epigenetic marks and profiled their expression patterns using deep sequencing. We found that chromatin modifications can poise miRNA-coding genes as well. Our data suggest that miRNA-and protein-coding genes share similar mechanisms of regulation by chromatin modifications, which poise inducible genes for activation in response to environmental stimuli.
C1 [Barski, Artem; Jothi, Raja; Cuddapah, Suresh; Cui, Kairong; Roh, Tae-Young; Schones, Dustin E.; Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Zhao, K (reprint author), NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
EM zhaok@nhlbi.nih.gov
RI Jothi, Raja/G-3780-2015;
OI Barski, Artem/0000-0002-1861-5316
FU National Heart, Lung and Blood Institute (NHLBI); National Institutes of
Health
FX This work was supported by the Intramural Research Program of the
National Heart, Lung and Blood Institute (NHLBI), National Institutes of
Health. The gene expression analysis using the Affy-metrix microarrays
was performed by the Genomics Core Facility at NHLBI.
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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 2009
VL 19
IS 10
BP 1742
EP 1751
DI 10.1101/gr.090951.109
PG 10
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 501NX
UT WOS:000270389700006
PM 19713549
ER
PT J
AU Xie, B
Pearson, G
AF Xie, B.
Pearson, G.
TI PROTOTYPE GOOGLE MAPS WEB SITE TO SELECT NURSING HOMES: USABILITY
TESTING BY OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Xie, B.] Univ Maryland, Coll Informat Studies, College Pk, MD 20742 USA.
[Pearson, G.] Natl Lib Med, Bethesda, MD USA.
NR 0
TC 0
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U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 1
EP 1
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900002
ER
PT J
AU Visser, M
Brychta, R
Kong, C
Deeg, DJ
AF Visser, M.
Brychta, R.
Kong, C.
Deeg, D. J.
TI MISPERCEPTION OF MEETING THE PHYSICAL ACTIVITY RECOMMENDATION IN OLDER
PERSONS USING ACCELEROMETRY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Visser, M.] Vrije Univ Amsterdam, Dept Hlth Sci, Amsterdam, Netherlands.
[Visser, M.; Deeg, D. J.] Vrije Univ Amsterdam, Dept Epidemiol & Biostat, Med Ctr, Amsterdam, Netherlands.
[Brychta, R.; Kong, C.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
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U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 18
EP 18
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900075
ER
PT J
AU Vogelzangs, N
Beekman, A
Milaneschi, Y
Ferrucci, L
Penninx, B
AF Vogelzangs, N.
Beekman, A.
Milaneschi, Y.
Ferrucci, L.
Penninx, B.
TI CORTISOL AND 6-YEAR CARDIOVASCULAR MORTALITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Vogelzangs, N.; Beekman, A.; Penninx, B.] Vrije Univ Amsterdam, Med Ctr, Psychiat & EMGO Inst Hlth & Care Res, Amsterdam, Netherlands.
[Milaneschi, Y.] Tuscany Hlth Reg Agcy, Florence, Italy.
[Ferrucci, L.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
NR 0
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U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 24
EP 24
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900107
ER
PT J
AU Simonsick, E
Yaffe, K
Carlson, M
Newman, AB
AF Simonsick, E.
Yaffe, K.
Carlson, M.
Newman, A. B.
TI ACTIVITY AND COGNITIVE PERFORMANCE: IS IT JUST FITNESS? INSIGHT FROM THE
COGNITIVE VITALITY SUBSTUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Simonsick, E.] NIA, Baltimore, MD 21224 USA.
[Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Carlson, M.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
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U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 47
EP 47
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900219
ER
PT J
AU Strotmeyer, ES
Newman, AB
Harris, T
Satterfield, S
Atkinson, H
Yaffe, K
Rosano, C
AF Strotmeyer, E. S.
Newman, A. B.
Harris, T.
Satterfield, S.
Atkinson, H.
Yaffe, K.
Rosano, C.
TI GREATER CUMULATIVE FUNCTION IN BRAIN, PERIPHERAL NERVES AND MUSCLES IS
ASSOCIATED WITH FASTER GAIT: THE HEALTH, AGING AND BODY COMPOSITION
(HEALTH ABC) STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Strotmeyer, E. S.; Newman, A. B.; Rosano, C.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
[Harris, T.] NIA, Bethesda, MD 20892 USA.
[Satterfield, S.] Univ Tennessee, Memphis, TN USA.
[Atkinson, H.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Newman, A. B.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
RI Strotmeyer, Elsa/F-3015-2014
NR 0
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U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 47
EP 47
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900220
ER
PT J
AU Watson, N
Youk, A
Sutton-Tyrrell, K
Boudreau, R
Simonsick, E
Bauer, DC
Johnson, KC
Newman, AB
AF Watson, N.
Youk, A.
Sutton-Tyrrell, K.
Boudreau, R.
Simonsick, E.
Bauer, D. C.
Johnson, K. C.
Newman, A. B.
TI LOWER LEVELS OF SUBCLINICAL CARDIOVASCULAR DISEASE ARE ASSOCIATED WITH
FASTER GAIT
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Watson, N.; Youk, A.; Sutton-Tyrrell, K.; Boudreau, R.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Johnson, K. C.] Univ Tennessee, Memphis, TN USA.
[Bauer, D. C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Simonsick, E.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 47
EP 47
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900221
ER
PT J
AU Chang, M
Snaedal, J
Saczynski, J
Aspelund, T
Harris, T
Gudnason, V
Launer, LJ
Jonsson, PV
AF Chang, M.
Snaedal, J.
Saczynski, J.
Aspelund, T.
Harris, T.
Gudnason, V.
Launer, L. J.
Jonsson, P. V.
TI THE ASSOCIATION BETWEEN MIDLIFE PHYSICAL ACTIVITY AND DEPRESSIVE
SYMPTOMS IN LATE LIFE: AGE GENE/ENVIRONMENT SUSCEPTIBILITY - REYKJAVIK
STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Chang, M.; Snaedal, J.; Jonsson, P. V.] Landspitali Univ Hosp, Reykjavik, Iceland.
[Snaedal, J.; Aspelund, T.; Gudnason, V.; Jonsson, P. V.] Univ Iceland, Reykjavik, Iceland.
[Saczynski, J.] Univ Massachusetts, Worcester, MA 01605 USA.
[Aspelund, T.; Gudnason, V.] Iceland Heart Assoc, Kopavogur, Iceland.
[Harris, T.; Launer, L. J.] Natl Inst Aging, Bethesda, MD 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
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U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 51
EP 52
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900238
ER
PT J
AU Yu, B
Boudreau, R
Thomas, F
Garcia, M
Harris, T
AF Yu, B.
Boudreau, R.
Thomas, F.
Garcia, M.
Harris, T.
TI MAKING SENSE OF LONGITUDINAL TRAJECTORIES IN AGING COHORTS: WHAT ABOUT
BIAS DUE TO INFORMATIVE DROPOUT AND DEATH?: IMPUTATION METHODS TO THE
RESCUE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Yu, B.; Garcia, M.; Harris, T.] NIA, Bethesda, MD 20892 USA.
[Boudreau, R.] Univ Pittsburgh, Pittsburgh, PA USA.
[Thomas, F.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 55
EP 55
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900259
ER
PT J
AU Barr, R
AF Barr, R.
TI THE CHANGING LANDSCAPE AT NIA: NAVIGATION AIDS FOR GRANT APPLICANTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Barr, R.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 64
EP 64
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900303
ER
PT J
AU Hodes, RJ
Harden, J
Sierra, F
Hadley, E
Suzman, R
Morrison-Bogorad, M
Hunter, C
Barr, R
AF Hodes, R. J.
Harden, J.
Sierra, F.
Hadley, E.
Suzman, R.
Morrison-Bogorad, M.
Hunter, C.
Barr, R.
TI NIA SYMPOSIUM: CREATIVE & INTERACTIVE ROUNDTABLE DISCUSSIONS ON AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hodes, R. J.; Harden, J.; Sierra, F.; Hadley, E.; Suzman, R.; Morrison-Bogorad, M.; Hunter, C.; Barr, R.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 64
EP 64
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900302
ER
PT J
AU Shieh, C
AF Shieh, C.
TI ASSESSING ELDER'S HEALTH AND INSURANCE STATUS: THE EFFECTS OF RACE AND
MARRIAGE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Shieh, C.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 85
EP 85
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900399
ER
PT J
AU Weston, AL
Costa, P
Simonsick, E
Ayonayon, HN
Harris, T
Rosano, C
Satterfield, S
Yaffe, K
AF Weston, A. L.
Costa, P.
Simonsick, E.
Ayonayon, H. N.
Harris, T.
Rosano, C.
Satterfield, S.
Yaffe, K.
TI THE ASSOCIATION OF PERSONALITY DOMAINS AND COGNITIVE FUNCTION: FINDINGS
FROM THE HEALTH ABC STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Weston, A. L.; Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Costa, P.; Simonsick, E.; Harris, T.] NIA, Baltimore, MD 21224 USA.
[Rosano, C.] Univ Pittsburgh, Sch Publ Hlth, Pittsburgh, PA 15260 USA.
[Satterfield, S.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Weston, A. L.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Ayonayon, H. N.; Yaffe, K.] Univ Calif San Francisco Epidemiol & Biostat, San Francisco, CA USA.
[Yaffe, K.] Univ Calif San Francisco Neurol, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 92
EP 92
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900433
ER
PT J
AU Insel, K
Vidrine, AN
Hsiao, C
Montgomery, DW
AF Insel, K.
Vidrine, A. N.
Hsiao, C.
Montgomery, D. W.
TI OXIDATIVE STRESS, COGNITIVE FUNCTION AND MEDICATION ADHERENCE AMONG
INDIVIDUALS WITH HYPERTENSION
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Insel, K.; Vidrine, A. N.; Montgomery, D. W.] Univ Arizona, Tucson, AZ USA.
[Hsiao, C.] Natl Inst Nursing Res, Washington, DC USA.
[Montgomery, D. W.] So Arizona Vet Adm Hlth Care Syst, Tucson, AZ USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 108
EP 108
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900507
ER
PT J
AU Watson, N
Sutton-Tyrrell, K
Rosano, C
Boudreau, R
Simonsick, E
Yaffe, K
Satterfield, S
Newman, AB
AF Watson, N.
Sutton-Tyrrell, K.
Rosano, C.
Boudreau, R.
Simonsick, E.
Yaffe, K.
Satterfield, S.
Newman, A. B.
TI ARTERIAL STIFFNESS AND DOMAIN-SPECIFIC COGNITIVE DECLINE IN
WELL-FUNCTIONING OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Watson, N.; Sutton-Tyrrell, K.; Rosano, C.; Boudreau, R.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Simonsick, E.] NIA, Baltimore, MD 21224 USA.
[Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Satterfield, S.] Univ Tennessee, Memphis, TN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 126
EP 126
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900592
ER
PT J
AU Milaneschi, Y
Bandinelli, S
Corsi, A
Vazzana, R
Penninx, B
Ferrucci, L
Guralnik, J
AF Milaneschi, Y.
Bandinelli, S.
Corsi, A.
Vazzana, R.
Penninx, B.
Ferrucci, L.
Guralnik, J.
TI PERSONAL MASTERY AND INCIDENT DISABILITY OVER SIX YEARS IN OLDER
PERSONS: THE INCHIANTI STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Milaneschi, Y.; Corsi, A.] InCHIANTI Study Grp, Florence, 21224, Italy.
[Milaneschi, Y.] Univ Bologna, Hlth Psychol Sch, Dept Psychol, Bologna, 20892, Italy.
[Bandinelli, S.] ASF, Geriatr Unit, Florence, Italy.
[Vazzana, R.] Univ G dAnnunzio, Chieti, Italy.
[Penninx, B.] Vrije Univ Amsterdam, Psychiat & EMGO Inst Hlth & Care Res, Med Ctr, Amsterdam, Netherlands.
[Ferrucci, L.] NIA, Clin Res Branch, Baltimore, MD USA.
[Guralnik, J.] NIA, Lab Epidemiol Demog & Biometry, 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
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 129
EP 129
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900603
ER
PT J
AU Ashida, S
Wilkinson, AV
Koehly, L
AF Ashida, S.
Wilkinson, A. V.
Koehly, L.
TI INTENTION TO SCREEN AND ENCOURAGEMENT FROM SOCIAL NETWORK MEMBERS: A
CROSS-GENERATIONAL PERSPECTIVE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ashida, S.; Koehly, L.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Wilkinson, A. V.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 165
EP 165
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900777
ER
PT J
AU Leveille, SG
Jones, R
Kiely, DK
Shmerling, R
Hausdorff, J
Guralnik, J
Lipsitz, L
Bean, J
AF Leveille, S. G.
Jones, R.
Kiely, D. K.
Shmerling, R.
Hausdorff, J.
Guralnik, J.
Lipsitz, L.
Bean, J.
TI CHRONIC MUSCULOSKELETAL PAIN AND THE INCIDENCE OF FALLS IN AN OLDER
POPULATION: THE MOBILIZE BOSTON STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Leveille, S. G.; Shmerling, R.; Lipsitz, L.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Leveille, S. G.; Jones, R.; Shmerling, R.; Hausdorff, J.; Lipsitz, L.; Bean, J.] Harvard Univ, Sch Med, Boston, MA USA.
[Jones, R.; Kiely, D. K.; Lipsitz, L.] Hebrew SeniorLife, Boston, MA USA.
[Hausdorff, J.] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, IL-69978 Tel Aviv, Israel.
[Guralnik, J.] NIA, Bethesda, MD 20892 USA.
[Bean, J.] Spaulding Rehabil Hosp, Boston, MA 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 GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 169
EP 169
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900794
ER
PT J
AU Newman, AB
Glynn, NW
Sebastiani, P
Perls, TT
Mayeux, R
Christensen, K
Simonsick, E
Hadley, E
AF Newman, A. B.
Glynn, N. W.
Sebastiani, P.
Perls, T. T.
Mayeux, R.
Christensen, K.
Simonsick, E.
Hadley, E.
TI HEALTH AND FUNCTION OF PARTICIPANTS IN THE LONG LIFE FAMILY STUDY: A
COMPARISON WITH OTHER COHORTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Newman, A. B.; Glynn, N. W.] Univ Pittsburgh, Pittsburgh, PA USA.
[Perls, T. T.] Boston Univ, Med Ctr, Boston, MA USA.
[Mayeux, R.] Columbia Univ, New York, NY USA.
[Christensen, K.] Univ So Denmark, Odense, Denmark.
[Simonsick, E.; Hadley, E.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 171
EP 172
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900806
ER
PT J
AU Province, MA
Hadley, E
Barmada, M
Schupf, N
Sebastiani, P
Costa, R
Christensen, K
Daw, EW
AF Province, M. A.
Hadley, E.
Barmada, M.
Schupf, N.
Sebastiani, P.
Costa, R.
Christensen, K.
Daw, E. W.
TI FAMILIAL CLUSTERING OF LONGEVITY PATHWAY PHENOTYPES IN THE LONG LIFE
FAMILY STUDY (LLFS)
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Province, M. A.; Barmada, M.; Daw, E. W.] Washington Univ, St Louis, MO USA.
[Schupf, N.; Costa, R.] Columbia Univ, New York, NY USA.
[Christensen, K.] Univ So Denmark, Odense, Denmark.
[Hadley, E.] NIA, Bethesda, MD 20892 USA.
[Sebastiani, P.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
RI Christensen, Kaare/C-2360-2009
OI Christensen, Kaare/0000-0002-5429-5292
NR 0
TC 0
Z9 0
U1 0
U2 2
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 171
EP 171
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900805
ER
PT J
AU Zeng, Y
Zhang, Z
Xu, T
Ma, E
Gu, D
Zhang, F
Corless, J
AF Zeng, Y.
Zhang, Z.
Xu, T.
Ma, E.
Gu, D.
Zhang, F.
Corless, J.
TI ASSOCIATION OF BIRTH OUTCOME WITH LONG-TERM SURVIVAL AND GENERAL HEALTH
AT OLDER AGES IN CHINA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Zeng, Y.; Corless, J.] Duke Univ, Durham, NC USA.
[Zhang, Z.; Xu, T.; Ma, E.] Beijing Union Med Coll Hosp, Beijing, Peoples R China.
[Zeng, Y.] Peking Univ, Beijing 100871, Peoples R China.
[Gu, D.] Portland State Univ, Portland, OR 97207 USA.
[Zhang, F.] NIMH, Genes Cognit & Psychosis Program, IRP, NIH, Bethesda, MD 20892 USA.
RI Zeng, Yi/B-1638-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 171
EP 171
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900802
ER
PT J
AU Newman, AB
Glynn, NW
Sebastiani, P
Perls, TT
Mayeux, R
Christensen, K
Simonsick, E
Hadley, E
AF Newman, A. B.
Glynn, N. W.
Sebastiani, P.
Perls, T. T.
Mayeux, R.
Christensen, K.
Simonsick, E.
Hadley, E.
TI HEALTH AND FUNCTION OF PARTICIPANTS IN THE LONG LIFE FAMILY STUDY: A
COMPARISON WITH OTHER COHORTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Newman, A. B.; Glynn, N. W.] Univ Pittsburgh, Grad Sch Publ Hlth, Epidemiol & Div Geriatr Med, Pittsburgh, PA USA.
[Newman, A. B.; Glynn, N. W.] Univ Pittsburgh, Sch Med, Epidemiol & Div Geriatr Med, Pittsburgh, PA USA.
[Sebastiani, P.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Perls, T. T.] Boston Univ, Med Ctr, Boston, MA USA.
[Simonsick, E.; Hadley, E.] NIA, Bethesda, MD 20892 USA.
[Mayeux, R.] Columbia Univ, New York, NY USA.
[Christensen, K.] Univ So Denmark, Odense, Denmark.
RI Christensen, Kaare/C-2360-2009
OI Christensen, Kaare/0000-0002-5429-5292
NR 0
TC 0
Z9 0
U1 0
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 172
EP 172
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900808
ER
PT J
AU Sebastiani, P
Hadley, E
Province, MA
Christensen, K
Rossi, W
Perls, TT
Ash, A
AF Sebastiani, P.
Hadley, E.
Province, M. A.
Christensen, K.
Rossi, W.
Perls, T. T.
Ash, A.
TI A FAMILY LONGEVITY SELECTION SCORE (FLOSS): RANKING SIBSHIPS BY THEIR
LONGEVITY AND AVAILABILITY FOR STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Sebastiani, P.; Ash, A.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Hadley, E.; Rossi, W.] NIA, Bethesda, MD 20892 USA.
[Christensen, K.] Univ So Denmark, Odense, Denmark.
[Province, M. A.] Washington Univ, St Louis, MO USA.
[Perls, T. T.] Boston Med Ctr, Boston, MA USA.
RI Christensen, Kaare/C-2360-2009
OI Christensen, Kaare/0000-0002-5429-5292
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 172
EP 172
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900807
ER
PT J
AU Haaga, JG
AF Haaga, J. G.
TI DIVERGENT PATHS FOR AMERICA'S DEPENDENTS-25 YEARS LATER
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Haaga, J. G.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 178
EP 178
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900836
ER
PT J
AU Vogelzangs, N
Boelhouwer, I
Beekman, A
Milaneschi, Y
Ferrucci, L
Penninx, B
AF Vogelzangs, N.
Boelhouwer, I.
Beekman, A.
Milaneschi, Y.
Ferrucci, L.
Penninx, B.
TI THE METABOLIC SYNDROME AND THE ONSET AND PERSISTENCE OF DEPRESSIVE
SYMPTOMS IN LATER LIFE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Vogelzangs, N.; Boelhouwer, I.; Beekman, A.; Penninx, B.] Vrije Univ Amsterdam, Med Ctr, EMGO Inst Hlth & Care Res, Amsterdam, Netherlands.
[Milaneschi, Y.] Tuscany Hlth Reg Agcy, Florence, Italy.
[Ferrucci, L.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 183
EP 183
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UI
UT WOS:000271793900864
ER
PT J
AU Caserotti, P
Aagaard, P
Harris, T
AF Caserotti, P.
Aagaard, P.
Harris, T.
TI ASSESSMENT OF MUSCLE POWER IN OLDER ADULTS AND ASSOCIATION WITH
FUNCTIONAL PERFORMANCES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Caserotti, P.; Harris, T.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Aagaard, P.] Univ So Denmark, Inst Sport Sci & Clin Biomech, Odense, Denmark.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 210
EP 210
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100025
ER
PT J
AU D'Adamo, C
Shardell, M
Miller, RR
Hicks, G
Orwig, D
Hochberg, M
Ferrucci, L
Magaziner, J
AF D'Adamo, C.
Shardell, M.
Miller, R. R.
Hicks, G.
Orwig, D.
Hochberg, M.
Ferrucci, L.
Magaziner, J.
TI THE ASSOCIATIONS BETWEEN BASELINE SERUM VITAMIN E CONCENTRATIONS AND
RECOVERY OF PHYSICAL FUNCTION DURING THE YEAR AFTER HIP FRACTURE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [D'Adamo, C.; Shardell, M.; Miller, R. R.; Orwig, D.; Hochberg, M.; Magaziner, J.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Hicks, G.] Univ Delaware, Newark, DE USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 211
EP 211
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100028
ER
PT J
AU Hicks, G
Shardell, M
Miller, RR
Alley, D
Cherubini, A
Bandinelli, S
Ferrucci, L
AF Hicks, G.
Shardell, M.
Miller, R. R.
Alley, D.
Cherubini, A.
Bandinelli, S.
Ferrucci, L.
TI LONGITUDINAL ASSOCIATIONS OF VITAMIN D WITH MUSCLE COMPOSITION AND
STRENGTH: THE INCHIANTI STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hicks, G.] Univ Delaware, Newark, DE USA.
[Shardell, M.; Miller, R. R.; Alley, D.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Cherubini, A.] Univ Perugia, Sch Med, Inst Gerontol & Geriatr, I-06100 Perugia, Italy.
[Bandinelli, S.] INRCA Geriatr Dept, Lab Clin Epidemiol, Florence, Italy.
[Ferrucci, L.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 215
EP 215
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100049
ER
PT J
AU Shardell, M
Hicks, G
Miller, RR
Alley, D
Cherubini, A
Bandinelli, S
Ferrucci, L
AF Shardell, M.
Hicks, G.
Miller, R. R.
Alley, D.
Cherubini, A.
Bandinelli, S.
Ferrucci, L.
TI ASSOCIATION OF 25(OH)D LEVELS WITH DECLINE AND RECOVERY FROM THE
PREFRAIL STATE: THE INCHIANTI STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Shardell, M.; Miller, R. R.; Alley, D.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Hicks, G.] Univ Delaware, Newark, DE USA.
[Cherubini, A.] Univ Perugia, Inst Gerontol & Geriatr, I-06100 Perugia, Italy.
[Bandinelli, S.] Tuscany Reg Hlth Agcy, Florence, Italy.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 215
EP 215
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100051
ER
PT J
AU Shea, K
Houston, DK
Tooze, J
Hausman, DB
Johnson, M
Bauer, DC
Harris, T
Kritchevsky, S
AF Shea, K.
Houston, D. K.
Tooze, J.
Hausman, D. B.
Johnson, M.
Bauer, D. C.
Harris, T.
Kritchevsky, S.
TI 25-HYDROXYVITAMIN-D, INFLAMMATION, AND RACE IN HEALTH ABC
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Shea, K.; Houston, D. K.; Tooze, J.; Kritchevsky, S.] Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA.
[Hausman, D. B.; Johnson, M.] Univ Georgia, Athens, GA 30602 USA.
[Bauer, D. C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Harris, T.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 215
EP 216
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100053
ER
PT J
AU Tom, SE
Patel, KV
Wallace, R
Guralnik, J
AF Tom, S. E.
Patel, K. V.
Wallace, R.
Guralnik, J.
TI SLEEP DIFFICULTY AND MORTALITY IN A COHORT OF OLDER ADULTS WITH 27 YEARS
OF FOLLOW-UP
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Tom, S. E.; Patel, K. V.; Guralnik, J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Wallace, R.] Univ Iowa, Iowa City, IA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 243
EP 243
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100185
ER
PT J
AU Faulkner, K
Studenski, S
Scheier, M
Morse, J
Coday, M
Simonsick, E
Yaffe, K
Cauley, JA
AF Faulkner, K.
Studenski, S.
Scheier, M.
Morse, J.
Coday, M.
Simonsick, E.
Yaffe, K.
Cauley, J. A.
TI DOES CONSCIENTIOUSNESS PROTECT AGAINST RECURRING FALLS IN OLDER MEN?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Faulkner, K.; Studenski, S.; Morse, J.; Cauley, J. A.] Univ Pittsburgh, Pittsburgh, PA USA.
[Scheier, M.] Carnegie Mellon Univ, Pittsburgh, PA 15213 USA.
[Coday, M.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Simonsick, E.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Yaffe, K.] San Francisco VA Med Ctr, San Francisco, CA USA.
RI Cauley, Jane/N-4836-2015
OI Cauley, Jane/0000-0003-0752-4408
NR 0
TC 0
Z9 0
U1 1
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 244
EP 244
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100188
ER
PT J
AU Sheu, Y
Harris, T
Koster, A
Mackey, D
Womack, CR
Newman, AB
Cauley, JA
AF Sheu, Y.
Harris, T.
Koster, A.
Mackey, D.
Womack, C. R.
Newman, A. B.
Cauley, J. A.
TI ASSOCIATION BETWEEN PULMONARY FUNCTION AND RISK OF RECURRENT FALLS WAS
MEDIATED BY MUSCLE STRENGTH
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Sheu, Y.; Newman, A. B.; Cauley, J. A.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, T.; Koster, A.] NIA, Bethesda, MD 20892 USA.
[Mackey, D.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Womack, C. R.] Univ Tennessee, Memphis, TN USA.
RI Cauley, Jane/N-4836-2015
OI Cauley, Jane/0000-0003-0752-4408
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 245
EP 246
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100193
ER
PT J
AU Koster, A
Stenholm, S
Alley, D
Visser, M
Simonsick, E
Nicklas, B
Kanaya, A
Harris, T
AF Koster, A.
Stenholm, S.
Alley, D.
Visser, M.
Simonsick, E.
Nicklas, B.
Kanaya, A.
Harris, T.
TI BODY COMPOSITION DIFFERENCES AMONG OBESE OLDER PERSONS WITH AND WITHOUT
METABOLIC SYNDROME
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Koster, A.; Harris, T.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Stenholm, S.; Simonsick, E.] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
[Alley, D.] Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA.
[Visser, M.] Vrije Univ Amsterdam, Fac Earth & Life Sci, Inst Hlth Sci, Amsterdam, Netherlands.
[Nicklas, B.] Wake Forest Univ, Sch Med, Ctr Aging, Winston Salem, NC 27109 USA.
[Kanaya, A.] Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA.
RI Stenholm, Sari/G-6940-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 293
EP 293
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100420
ER
PT J
AU Stenholm, S
Koster, A
Visser, M
Newman, AB
Satterfield, S
Kanaya, A
Harris, T
Ferrucci, L
AF Stenholm, S.
Koster, A.
Visser, M.
Newman, A. B.
Satterfield, S.
Kanaya, A.
Harris, T.
Ferrucci, L.
TI OBESITY STATUS AND METABOLIC ALTERATIONS AS PREDICTORS OF INCIDENT
MOBILITY LIMITATION IN WELL-FUNCTIONING OLDER PERSONS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Stenholm, S.; Ferrucci, L.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Stenholm, S.] Natl Inst Hlth & Welf, Helsinki, Finland.
[Koster, A.; Harris, T.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Visser, M.] Vrije Univ Amsterdam, Amsterdam, Netherlands.
[Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Satterfield, S.] Univ Tennessee, Memphis, TN USA.
[Kanaya, A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RI Stenholm, Sari/G-6940-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 294
EP 294
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100421
ER
PT J
AU Bartali, B
Kritchevsky, S
Newman, AB
Harris, T
Cesari, MKA
Sellmeyer, DTF
De Rekeneire, NLJS
Gill, TAH
AF Bartali, B.
Kritchevsky, S.
Newman, A. B.
Harris, T.
Cesari, M. Koster A.
Sellmeyer, D. Tylavsky F.
De Rekeneire, N. Lee J. S.
Gill, T. Allore H.
TI DOES DIETARY INTAKE OF ANTIOXIDANTS CONTRIBUTE TO CHANGE IN MUSCLE
STRENGTH AMONG OLDER PERSONS?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bartali, B.; De Rekeneire, N. Lee J. S.; Gill, T. Allore H.] Yale Univ, New Haven, CT USA.
[Kritchevsky, S.] Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA.
[Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, T.] NIA, NIH, Bethesda, MD 20892 USA.
[Cesari, M. Koster A.] Univ Cattolica Sacro Cuore, Rome, Italy.
[De Rekeneire, N. Lee J. S.] Univ Georgia, Athens, GA 30602 USA.
[Sellmeyer, D. Tylavsky F.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Cesari, M. Koster A.] Univ Maastricht, Maastricht, Netherlands.
[Sellmeyer, D. Tylavsky F.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
RI Cesari, Matteo/A-4649-2008
OI Cesari, Matteo/0000-0002-0348-3664
NR 0
TC 0
Z9 0
U1 0
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 306
EP 306
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100484
ER
PT J
AU Milner, JA
AF Milner, J. A.
TI OPPORTUNITIES AND CHALLENGES IN NUTRIGENOMICS, CANCER PREVENTION AND
AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Milner, J. A.] NCI, Nutr Sci Res Grp, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 309
EP 309
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100494
ER
PT J
AU Deshpande, N
Metter, E
Ferrucci, L
AF Deshpande, N.
Metter, E.
Ferrucci, L.
TI CUMULATIVE SOMATOSENSORY IMPAIRMENT INDEX PREDICTS GLOBAL POSTURAL
CONTROL OVER THREE YEARS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Deshpande, N.] Univ Kansas, Med Ctr, Lenexa, KS USA.
[Metter, E.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 331
EP 331
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100604
ER
PT J
AU Bernard, M
AF Bernard, M.
TI ELDERLY WOMEN IN CLINICAL TRIALS WITHIN NIH/NIA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bernard, M.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 345
EP 345
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100674
ER
PT J
AU Maggio, M
Ceda, G
Lauretani, F
Bandinelli, S
Basaria, S
Guralnik, J
Valenti, G
Ferrucci, L
AF Maggio, M.
Ceda, G.
Lauretani, F.
Bandinelli, S.
Basaria, S.
Guralnik, J.
Valenti, G.
Ferrucci, L.
TI GONADAL STATUS AND PHYSICAL PERFORMANCE IN OLDER MEN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Maggio, M.; Ceda, G.; Lauretani, F.; Valenti, G.] Univ Parma, Dept Internal Med, Sect Geriatr, I-43100 Parma, Italy.
[Bandinelli, S.] Azienda Sanitaria Firenze, Rehabil Unit, Florence, Italy.
[Basaria, S.] Boston Univ, Sch Med, Div Endocrinol & Metab, Boston, MA 02118 USA.
[Guralnik, J.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 377
EP 377
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100833
ER
PT J
AU Pate, KV
Ahmed, M
Salter, M
Mehta, S
Guralnik, J
Kirk, G
AF Pate, K. V.
Ahmed, M.
Salter, M.
Mehta, S.
Guralnik, J.
Kirk, G.
TI HIV INFECTION, IMMUNE FUNCTION, AND PHYSICAL PERFORMANCE AMONG INJECTION
DRUG USERS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Pate, K. V.; Guralnik, J.] NIA, Bethesda, MD 20892 USA.
[Ahmed, M.; Salter, M.; Mehta, S.; Kirk, G.] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 377
EP 377
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100832
ER
PT J
AU Studenski, S
Perera, S
Patel, KV
Chandler, J
Guralnik, J
AF Studenski, S.
Perera, S.
Patel, K. V.
Chandler, J.
Guralnik, J.
TI GAIT SPEED PREDICTSLONG TERM SURVIVAL: A META-ANALYSIS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Studenski, S.; Perera, S.] Univ Pittsburgh, Pittsburgh, PA USA.
[Patel, K. V.; Guralnik, J.] NIA, Bethesda, MD 20892 USA.
[Chandler, J.] Merck Co, Blue Bell, NJ USA.
RI Perera, Subashan/D-7603-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 377
EP 377
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100830
ER
PT J
AU Vestergaard, S
Patel, KV
Bandinelli, S
Ferrucci, L
Guralnik, J
AF Vestergaard, S.
Patel, K. V.
Bandinelli, S.
Ferrucci, L.
Guralnik, J.
TI WALKING PERFORMANCE AND SUBSEQUENT MORTALITY RISK IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Vestergaard, S.; Patel, K. V.; Guralnik, J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Patel, K. V.] MedStar Res Inst, Hyattsville, MD USA.
[Bandinelli, S.] ASF, Geriatr Unit, Florence, Italy.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 377
EP 377
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100831
ER
PT J
AU Volpato, S
Sioulis, F
Cavalieri, M
Guerra, G
Fellin, R
Guralnik, J
AF Volpato, S.
Sioulis, F.
Cavalieri, M.
Guerra, G.
Fellin, R.
Guralnik, J.
TI PREDICTIVE VALUE OF PERFORMANCE-BASED FUNCTIONAL ASSESSMENT IN OLDER
HOSPITALIZED PATIENTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Volpato, S.; Sioulis, F.; Cavalieri, M.; Guerra, G.; Fellin, R.] Univ Ferrara, I-44100 Ferrara, Italy.
[Guralnik, J.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
RI Cavalieri, Margherita/G-8053-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 377
EP 377
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100834
ER
PT J
AU Loeckenhoff, CE
Terracciano, A
Ferrucci, L
Costa, P
AF Loeckenhoff, C. E.
Terracciano, A.
Ferrucci, L.
Costa, P.
TI LONGITUDINAL TRAJECTORIES OF SUBJECTIVE HEALTH DIFFER BY FRAME OF
COMPARISON
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Loeckenhoff, C. E.] Cornell Univ, Ithaca, NY USA.
[Terracciano, A.; Ferrucci, L.; Costa, P.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
SU 2
BP 403
EP 403
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UK
UT WOS:000271794100957
ER
PT J
AU Carr, A
Caskie, GI
Evans, MK
Zonderman, AB
AF Carr, A.
Caskie, G. I.
Evans, M. K.
Zonderman, A. B.
TI FACTORIAL INVARIANCE OF THE BRIEF COPE ACROSS POVERTY LEVEL
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Carr, A.; Caskie, G. I.] Lehigh Univ, Bethlehem, PA 18015 USA.
[Evans, M. K.; Zonderman, A. B.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 406
EP 406
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200002
ER
PT J
AU Alley, D
Koster, A
Ferrucci, L
Mackey, D
Tylavsky, F
Cawthon, P
Newman, AB
Harris, T
AF Alley, D.
Koster, A.
Ferrucci, L.
Mackey, D.
Tylavsky, F.
Cawthon, P.
Newman, A. B.
Harris, T.
TI HOSPITALIZATION AND CHANGES IN BODY COMPOSITION IN A POPULATION-BASED
COHORT OF OLDER PERSONS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Alley, D.] Univ Maryland, Baltimore, MD 21201 USA.
[Koster, A.; Harris, T.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
[Tylavsky, F.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Mackey, D.; Cawthon, P.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 411
EP 411
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200030
ER
PT J
AU Simonsick, E
Windham, B
Metter, E
Ferrucci, L
AF Simonsick, E.
Windham, B.
Metter, E.
Ferrucci, L.
TI MOBILITY IMPLICATIONS OF "NOT QUITE NORMAL" GLUCOSE TOLERANCE IN OLDER
BLSA PARTICIPANTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Simonsick, E.; Metter, E.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
[Simonsick, E.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Windham, B.] Univ Mississippi, Jackson, MS 39216 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 413
EP 413
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200039
ER
PT J
AU Ko, S
Hausdorff, J
Ferrucci, L
AF Ko, S.
Hausdorff, J.
Ferrucci, L.
TI AGE-RELATED DIFFERENCES IN GAIT PATTERN RESPONSE TO INCREASED SPEED AND
FATIGUE - RESULTS FROM THE BLSA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ko, S.; Ferrucci, L.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Hausdorff, J.] Harvard Univ, Sch Med, Boston, MA USA.
[Hausdorff, J.] Tel Aviv Sourasky Med Ctr, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 414
EP 414
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200041
ER
PT J
AU Schreiber, C
Devonshire, A
Penmetsa, A
Nesbitt, M
Metter, E
Simonsick, E
Ferrucci, L
Ling, SM
AF Schreiber, C.
Devonshire, A.
Penmetsa, A.
Nesbitt, M.
Metter, E.
Simonsick, E.
Ferrucci, L.
Ling, S. M.
TI INDEPENDENT AND JOINT ASSOCIATIONS OF MUSCLE QUALITY, ADIPOSITY AND KNEE
OSTEOARTHRITIS ON WALKING SPEED IN THE BLSA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Schreiber, C.; Devonshire, A.; Penmetsa, A.; Nesbitt, M.; Metter, E.; Simonsick, E.; Ferrucci, L.; Ling, S. M.] NIH NIA, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 414
EP 414
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200040
ER
PT J
AU Tanaka, T
Roy, CN
Yao, W
Matteini, A
Semba, R
Walston, JD
Bandinelli, S
AF Tanaka, T.
Roy, C. N.
Yao, W.
Matteini, A.
Semba, R.
Walston, J. D.
Bandinelli, S.
TI GENETIC BASIS FOR VARIATION IN PLASMA IRON CONCENTRATION AND
ANEMIA-RELATED TRAITS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Tanaka, T.] NIA, Baltimore, MD 21224 USA.
[Tanaka, T.] Medstar Res Inst, Baltimore, MD USA.
[Roy, C. N.; Yao, W.; Matteini, A.; Semba, R.; Walston, J. D.] Johns Hopkins Univ, Baltimore, MD USA.
[Bandinelli, S.] ASF, Florence, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 414
EP 414
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200042
ER
PT J
AU Tolea, MI
Costa, P
Terracciano, A
Metter, EJ
Ferrucci, L
AF Tolea, M. I.
Costa, P.
Terracciano, A.
Metter, E. J.
Ferrucci, L.
TI CHANGING ROLE OF PERSONALITY ON STRENGTH DECLINE ACROSS THE AGE
SPECTRUM: FINDINGS FROM THE BLSA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Tolea, M. I.; Costa, P.; Terracciano, A.; Metter, E. J.; Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 414
EP 414
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200043
ER
PT J
AU Semba, R
Houston, DK
Sun, K
Shardell, M
Bandinelli, S
Cherubini, A
Guralnik, J
Ferrucci, L
AF Semba, R.
Houston, D. K.
Sun, K.
Shardell, M.
Bandinelli, S.
Cherubini, A.
Guralnik, J.
Ferrucci, L.
TI SERUM 25-HYDROXYVITAMIN D LEVELS PREDICT WALKING SPEED IN OLDER
COMMUNITY-DWELLING ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Semba, R.; Sun, K.] Johns Hopkins Univ, Baltimore, MD USA.
[Houston, D. K.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Shardell, M.] Univ Maryland, Baltimore, MD 21201 USA.
[Bandinelli, S.] Azienda Sanit Firenze, Florence, Italy.
[Cherubini, A.] Univ Perugia, I-06100 Perugia, Italy.
[Guralnik, J.] NIA, Bethesda, MD 20892 USA.
[Ferrucci, L.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 419
EP 419
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200064
ER
PT J
AU Masi, C
Hawkley, L
Xu, X
Veenstra, T
Cacioppo, JT
AF Masi, C.
Hawkley, L.
Xu, X.
Veenstra, T.
Cacioppo, J. T.
TI SERUM ESTROGEN METABOLITES AND SYSTOLIC BLOOD PRESSURE IN A
POPULATION-BASED SAMPLE OF POSTMENOPAUSAL WOMEN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Masi, C.; Hawkley, L.; Cacioppo, J. T.] Univ Chicago, Chicago, IL 60637 USA.
[Xu, X.; Veenstra, T.] NCI Adv Technol Program, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 420
EP 420
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200068
ER
PT J
AU Rice, M
Waldstein, SR
Evans, MK
Zonderman, AB
AF Rice, M.
Waldstein, S. R.
Evans, M. K.
Zonderman, A. B.
TI DIABETES AND PHYSICAL FUNCTION IN THE HANDLS STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Rice, M.] Univ Maryland Baltimore Cty, Gerontol Program, Baltimore, MD 21228 USA.
[Rice, M.; Evans, M. K.; Zonderman, A. B.] NIA, Intramural Res Program, Baltimore, MD 21224 USA.
[Waldstein, S. R.] Univ Maryland Baltimore Cty, Dept Psychol, Baltimore, MD 21228 USA.
[Waldstein, S. R.] Geriatr Res Educ & Clin Ctr, Baltimore VA Med Ctr, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 475
EP 475
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200332
ER
PT J
AU Lemelin, ET
Hardy, R
Ben-Shlomo, Y
Southall, H
Aucott, P
Kuh, D
Guralnik, J
AF Lemelin, E. T.
Hardy, R.
Ben-Shlomo, Y.
Southall, H.
Aucott, P.
Kuh, D.
Guralnik, J.
TI LIFE COURSE INDIVIDUAL AND NEIGHBORHOOD SOCIOECONOMIC POSITIONS AND
PHYSICAL FUNCTIONING AT AGE 53: A MULTILEVEL PROSPECTIVE ANALYSIS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Lemelin, E. T.; Hardy, R.; Kuh, D.] Royal Free & Univ Coll Med Sch, MRC, Unit Lifelong Hlth & Ageing, London WC1E 6BT, England.
[Ben-Shlomo, Y.] Univ Bristol, Dept Social Med, Bristol, Avon, England.
[Southall, H.; Aucott, P.] Great Britain Hist GIS Project, Dept Geog, Portsmouth, Hants, England.
[Lemelin, E. T.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 501
EP 501
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200450
ER
PT J
AU Wadley, VG
Unverzagt, FW
McGuire, LC
Moy, CS
Kissela, B
McClure, LA
Crowe, M
Howard, VJ
AF Wadley, V. G.
Unverzagt, F. W.
McGuire, L. C.
Moy, C. S.
Kissela, B.
McClure, L. A.
Crowe, M.
Howard, V. J.
TI REGIONAL DISPARITIES IN INCIDENT COGNITIVE DECLINE: THE REGARDS STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Wadley, V. G.; McClure, L. A.; Crowe, M.; Howard, V. J.] Univ Alabama, Birmingham, AL USA.
[Unverzagt, F. W.] Indiana Univ, Sch Med, Indianapolis, IN USA.
[McGuire, L. C.] Ctr Dis Control & Prevent, Healthy Aging Program, Atlanta, GA USA.
[Moy, C. S.] NINDS, NIH, Bethesda, MD 20892 USA.
[Kissela, B.] Univ Cincinnati, Cincinnati, OH USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 524
EP 524
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200565
ER
PT J
AU Matteini, A
Fallin, D
Kammerer, CM
Schupf, N
Mayeux, R
Newman, AB
Hadley, E
Walston, JD
AF Matteini, A.
Fallin, D.
Kammerer, C. M.
Schupf, N.
Mayeux, R.
Newman, A. B.
Hadley, E.
Walston, J. D.
TI ENDOPHENOTYPES ACROSS PHYSIOLOGIC DOMAINS HAVE HIGH HERITABILITY IN THE
LONG LIFE FAMILY STUDY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Matteini, A.; Fallin, D.; Walston, J. D.] Johns Hopkins Univ, Baltimore, MD USA.
[Kammerer, C. M.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Schupf, N.; Mayeux, R.] Columbia Univ, New York, NY USA.
[Hadley, E.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD OCT
PY 2009
VL 49
BP 526
EP 526
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 519UL
UT WOS:000271794200573
ER
PT J
AU Caillava, C
Vandenbosch, R
Jablonska, B
Kaldis, P
Berthet, C
Gallo, V
Malgrange, B
Belachew, S
Van Evercooren, AB
AF Caillava, C.
Vandenbosch, R.
Jablonska, B.
Kaldis, P.
Berthet, C.
Gallo, V
Malgrange, B.
Belachew, S.
Van Evercooren, Baron A.
TI EXPLORING THE REQUIREMENT OF CDK2 FOR NORMAL WHITE MATTER DEVELOPMENT
AND MYELIN REPAIR
SO GLIA
LA English
DT Meeting Abstract
CT 9th European Meeting on Glial Cells in Health and Disease
CY SEP 08-12, 2009
CL Paris, FRANCE
C1 [Caillava, C.; Van Evercooren, Baron A.] UPMC, INSERM, Paris, France.
[Vandenbosch, R.; Malgrange, B.; Belachew, S.] Dev Neurobiol Unit, Liege, Belgium.
[Jablonska, B.; Gallo, V] Neurosci Res Ctr, Washington, DC USA.
[Kaldis, P.; Berthet, C.] NCI, Frederick, MD 21701 USA.
RI Kaldis, Philipp/G-2714-2010
OI Kaldis, Philipp/0000-0002-7247-7591
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-1491
J9 GLIA
JI Glia
PD OCT
PY 2009
VL 57
IS 13
BP S157
EP S157
PG 1
WC Neurosciences
SC Neurosciences & Neurology
GA 497QK
UT WOS:000270075500646
ER
PT J
AU Fields, D
AF Fields, D.
TI REGULATION OF OLIGODENDROCYTE DEVELOPMENT AND MYELINATION BY
NON-VESICULAR, ACTIVITY-DEPENDENT RELEASE OF NEUROTRANSMITTER FROM AXONS
SO GLIA
LA English
DT Meeting Abstract
CT 9th European Meeting on Glial Cells in Health and Disease
CY SEP 08-12, 2009
CL Paris, FRANCE
C1 [Fields, D.] NICHHD, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-1491
J9 GLIA
JI Glia
PD OCT
PY 2009
VL 57
IS 13
BP S20
EP S20
PG 1
WC Neurosciences
SC Neurosciences & Neurology
GA 497QK
UT WOS:000270075500085
ER
PT J
AU Kazanis, I
Lathia, JD
Vadakkan, TJ
Mattson, MP
Dickinon, ME
Ffrench-Constant, C
AF Kazanis, I
Lathia, J. D.
Vadakkan, T. J.
Mattson, M. P.
Dickinon, M. E.
Ffrench-Constant, C.
TI ACTIVATED ADULT NEURAL STEM CELLS GENERATE DISTINCT LAMININ/INTEGRIN
INTERACTIONS DURING REGENERATION OF THE SUBEPENDYMAL ZONE NEUROGENIC
NICHE
SO GLIA
LA English
DT Meeting Abstract
CT 9th European Meeting on Glial Cells in Health and Disease
CY SEP 08-12, 2009
CL Paris, FRANCE
C1 [Kazanis, I] Univ Cambridge, Cambridge, England.
[Lathia, J. D.] Lerner Res Inst, Cleveland, OH USA.
[Vadakkan, T. J.; Dickinon, M. E.] Baylor Coll Med, Houston, TX 77030 USA.
[Mattson, M. P.] NIA, Baltimore, MD 21224 USA.
[Ffrench-Constant, C.] MRC Ctr Regenerat Med, Edinburgh, Midlothian, Scotland.
RI Mattson, Mark/F-6038-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-1491
J9 GLIA
JI Glia
PD OCT
PY 2009
VL 57
IS 13
BP S76
EP S76
PG 1
WC Neurosciences
SC Neurosciences & Neurology
GA 497QK
UT WOS:000270075500313
ER
PT J
AU Marshall, L
Jensen, P
Ryschkewitsch, C
Major, E
AF Marshall, L.
Jensen, P.
Ryschkewitsch, C.
Major, E.
TI BINDING OF THE LYMPHOCYTE-SPECIFIC TRANSCRIPTION FACTOR SPI-B TO UNIQUE
TARGET SITES ON THE JC VIRUS PROMOTER IN PROGENITOR DERIVED ASTROCYTES
SO GLIA
LA English
DT Meeting Abstract
CT 9th European Meeting on Glial Cells in Health and Disease
CY SEP 08-12, 2009
CL Paris, FRANCE
C1 [Marshall, L.; Jensen, P.; Ryschkewitsch, C.; Major, E.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-1491
J9 GLIA
JI Glia
PD OCT
PY 2009
VL 57
IS 13
BP S90
EP S91
PG 2
WC Neurosciences
SC Neurosciences & Neurology
GA 497QK
UT WOS:000270075500374
ER
PT J
AU Monaco, MC
Maric, D
Major, EO
AF Monaco, M. C.
Maric, D.
Major, E. O.
TI ESTABLISHMENT OF A HUMAN FETAL BRAIN PROGENITOR-DERIVED OLIGODENDROCYTE
CULTURE SYSTEM AND ITS USE TO STUDY JC VIRUS INFECTION
SO GLIA
LA English
DT Meeting Abstract
CT 9th European Meeting on Glial Cells in Health and Disease
CY SEP 08-12, 2009
CL Paris, FRANCE
C1 [Monaco, M. C.; Major, E. O.] NINDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
[Maric, D.] NINDS, Neurophysiol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-1491
J9 GLIA
JI Glia
PD OCT
PY 2009
VL 57
IS 13
BP S87
EP S87
PG 1
WC Neurosciences
SC Neurosciences & Neurology
GA 497QK
UT WOS:000270075500360
ER
PT J
AU Van den Elsen, PJ
Van Eggermond, M
Benard, A
Van Leeuwen, JC
Marquez, VE
Wierda, RJ
Kuipers, HF
AF Van den Elsen, P. J.
Van Eggermond, M.
Benard, A.
Van Leeuwen, J. C.
Marquez, V. E.
Wierda, R. J.
Kuipers, H. F.
TI EPIGENETIC CONTROL OF CCR5 TRANSCRIPTION
SO GLIA
LA English
DT Meeting Abstract
CT 9th European Meeting on Glial Cells in Health and Disease
CY SEP 08-12, 2009
CL Paris, FRANCE
C1 [Van den Elsen, P. J.] Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands.
[Van Eggermond, M.; Benard, A.; Van Leeuwen, J. C.; Wierda, R. J.; Kuipers, H. F.] Leiden Univ, Med Ctr, Leiden, Netherlands.
[Marquez, V. E.] NCI, Ctr Canc Res, Frederick, MD 21701 USA.
RI Wierda, Rutger/C-1031-2009
NR 0
TC 0
Z9 0
U1 1
U2 3
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-1491
J9 GLIA
JI Glia
PD OCT
PY 2009
VL 57
IS 13
BP S49
EP S49
PG 1
WC Neurosciences
SC Neurosciences & Neurology
GA 497QK
UT WOS:000270075500205
ER
PT J
AU Yuen, TJ
Mcfarland, HF
Quandt, J
Johnson, KR
Franklin, RJM
Ffrench-Constant, C
AF Yuen, T. J.
Mcfarland, H. F.
Quandt, J.
Johnson, K. R.
Franklin, R. J. M.
Ffrench-Constant, C.
TI IDENTIFICATION OF INFLAMMATORY FACTORS THAT PROMOTE MYELINATION
SO GLIA
LA English
DT Meeting Abstract
CT 9th European Meeting on Glial Cells in Health and Disease
CY SEP 08-12, 2009
CL Paris, FRANCE
C1 [Yuen, T. J.; Franklin, R. J. M.] Univ Cambridge, Ctr Brain Repair, Cambridge, England.
[Yuen, T. J.; Franklin, R. J. M.] Univ Cambridge, Dept Vet Med, Cambridge, England.
[Mcfarland, H. F.; Quandt, J.] NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
[Johnson, K. R.] NINDS, Bioinformat Neurosci Grp, NIH, Bethesda, MD 20892 USA.
[Ffrench-Constant, C.] Univ Edinburgh, MRC Ctr Regenerat Med, Ctr MS, Edinburgh, Midlothian, Scotland.
[Ffrench-Constant, C.] Univ Edinburgh, MRC Ctr Regenerat Med, Ctr Inflammat Res, Edinburgh, Midlothian, Scotland.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-1491
J9 GLIA
JI Glia
PD OCT
PY 2009
VL 57
IS 13
BP S143
EP S144
PG 2
WC Neurosciences
SC Neurosciences & Neurology
GA 497QK
UT WOS:000270075500592
ER
PT J
AU Schetter, AJ
Harris, CC
AF Schetter, Aaron J.
Harris, Curtis C.
TI Plasma microRNAs: a potential biomarker for colorectal cancer?
SO GUT
LA English
DT Editorial Material
ID MARKERS; SERUM
C1 [Schetter, Aaron J.; Harris, Curtis C.] NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20852 USA.
RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20852 USA.
EM curtis_harris@nih.gov
NR 11
TC 33
Z9 35
U1 1
U2 2
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
J9 GUT
JI Gut
PD OCT
PY 2009
VL 58
IS 10
BP 1318
EP 1319
DI 10.1136/gut.2009.176875
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 494BY
UT WOS:000269785500004
PM 19749133
ER
PT J
AU Maggioni, A
Minig, L
Zanagnolo, V
Peiretti, M
Sanguineti, F
Bocciolone, L
Colombo, N
Landoni, F
Roviglione, G
Velez, JI
AF Maggioni, Angelo
Minig, Lucas
Zanagnolo, Vanna
Peiretti, Michele
Sanguineti, Fabio
Bocciolone, Luca
Colombo, Nicoletta
Landoni, Fabio
Roviglione, Giovanni
Velez, Jorge Ivan
TI Robotic approach for cervical cancer: Comparison with laparotomy A case
control study
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE Robotic surgery; Robotic radical hysterectomy; Cervical cancer;
Laparotomic radical hysterectomy
ID LAPAROSCOPIC RADICAL HYSTERECTOMY; PELVIC LYMPHADENECTOMY; VAGINAL
HYSTERECTOMY; ENDOMETRIAL CANCER; ABDOMINAL HYSTERECTOMY; MORBIDITY;
DISSECTION; EXPERIENCE; CARCINOMA; OUTCOMES
AB Objective. To compare the surgical outcome of robotic radical hysterectomy (RRH) versus abdominal radical hysterectomy (ARH) for the treatment of early stage cervical cancer.
Methods. A prospective collection of data of all RRH for stages IA2-IIA cervical cancer was done. The procedures were performed at the European Institute of Oncology, Milan, Italy, between November 1, 2006 and February 1, 2009.
Results. A total of 40 RRH were analyzed, and compared with 40 historic ARH cases. The groups did not differ significantly in body mass index, stage, histology, or intraoperative complications, but in age (p = 0.035). The mean (SD) operative time was significantly shorter for ARH than RRH, 199.6 (65.6) minutes and 272.27 (42.3) minutes respectively (p = 0.0001). The mean (SD) estimated blood loss (EBL) was 78 ml (94.8) in RRH group and 221.8 ml (132.4) in ARK This difference was statistically significant in favor of RRH group (p<0.0001). Statistically significantly higher number of pelvic lymph nodes was removed by ARH than by RRH, mean (SD) 26.2 (11.7) versus 20.4 (6.9), p<0.05. Mean length of stay was significantly shorter for the RRH group (3.7 versus 5.0 days, p<0.01). There was no significant difference in terms of postoperative complications between groups.
Conclusion. This study shows that RRH is safe and feasible. However, a comparison of oncologic outcomes and cost-benefit analysis is still needed and it has to be carefully evaluated in the future. (C) 2009 Published by Elsevier Inc.
C1 [Minig, Lucas] NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
[Maggioni, Angelo; Minig, Lucas; Zanagnolo, Vanna; Peiretti, Michele; Sanguineti, Fabio; Bocciolone, Luca; Colombo, Nicoletta; Landoni, Fabio; Roviglione, Giovanni] European Inst Oncol, Dept Gynecol, Milan, Italy.
[Velez, Jorge Ivan] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
RP Minig, L (reprint author), NCI, Div Canc Treatment & Diag, NIH, Bldg 10 B3B69C, Bethesda, MD 20892 USA.
EM lucasminig@yahoo.com
FU Intramural Research Program of the National Human Genome Research
Institute; National Institutes of Health
FX This research was supported, in part, by the Intramural Research Program
of the National Human Genome Research Institute, National Institutes of
Health.
NR 36
TC 53
Z9 54
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0090-8258
J9 GYNECOL ONCOL
JI Gynecol. Oncol.
PD OCT
PY 2009
VL 115
IS 1
BP 60
EP 64
DI 10.1016/j.ygyno.2009.06.039
PG 5
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 496IZ
UT WOS:000269965700012
PM 19638333
ER
PT J
AU Schaefer, EW
Loaiza-Bonilla, A
Juckett, M
DiPers, JF
Roy, V
Slack, J
Wu, WT
Laumann, K
Espinoza-Delgado, I
Gore, SD
AF Schaefer, Eric W.
Loaiza-Bonilla, Arturo
Juckett, Mark
DiPers, John F.
Roy, Vivek
Slack, James
Wu, Wenting
Laumann, Kristina
Espinoza-Delgado, Igor
Gore, Steven D.
CA Mayo P2C Phase II Consortium
TI A phase 2 study of vorinostat in acute myeloid leukemia
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Article
DE acute myeloid leukemia; acute myeloid leukemia; HDAC; histone
deacetylase inhibitor; phase 2; SAHA; suberoylanilide hydroxamic acid;
vorinostat
ID HISTONE DEACETYLASE INHIBITORS; SUBEROYLANILIDE HYDROXAMIC ACID;
TRANSFORMED-CELL DIFFERENTIATION; BONE-MARROW-TRANSPLANTATION; MALIGNANT
B-CELLS; MYELODYSPLASTIC SYNDROMES; SODIUM PHENYLBUTYRATE;
CYTOSINE-ARABINOSIDE; CANCER CELLS; APOPTOSIS
AB Background
This two-stage; multi-institutional, randomized phase 2 trial assessed the toxicity and response rate associated with two treatment schedules of the histone deacetylase inhibitor, vonnostat (suberoylanilide hydroxamic acid SAHA) in patients with relapsed acute myeloid leukemia and in selected untreated patients with high-risk acute myeloid leukemia
Design and Methods
Patients with relapsed or untreated acute myeloid leukemia who were not candidates for chemotherapy entered one of the two treatment arms In both arms a total dose of 8400 mg of vorinostat was delivered in each 21-day cycle of treatment in arm A the dose regimen was 400 mg daily whereas in arm B the dose regimen was 200 mg three times daily for 14 days followed by 1 week rest
Results
Data from all 37 patients were used for the analyses In arm A (n=15), the confirmed complete remission rate was 0% (95% CI; 0% to 23%), this arm was closed at the planned interim analysis. In arm B (n=22), the confirmed complete remission rate was 4.5% (1 response, 95% CI, 0.4% to 24%), with a duration of response exceeding 398 days The median time to treatment failure in arm A was 42 days (95% Cl, 26 to 57), although a minimum of four cycles of treatment were planned, 11 patients (79%) received no more than two cycles The median time to treatment failure in arm B was 46 days (95% CI, 20 to 71); 13 patients (59%) received no more than two cycles of treatment
Conclusions
Vorinostat monotherapy demonstrated minimal activity in this group of patients with acute myeloid leukemia. Therapy was discontinued in many patients before the planned four cycles had been administered, either because of failure of vorinostat to control the leukocyte count or patients" and physicians' preference. Future studies of vonnostat in acute myeloid leukemia should focus on combinations with other drugs with which it might interact pharmacodynamically Clinical Trials gov Identifier. NCT00305773
C1 [Schaefer, Eric W.; Wu, Wenting; Laumann, Kristina] Mayo Clin, Ctr Canc, Rochester, MN USA.
[Loaiza-Bonilla, Arturo] Harbor Hosp Ctr, Dept Med, Baltimore, MD USA.
[Juckett, Mark] Univ Wisconsin, Ctr Comprehens Canc, Madison, WI USA.
[DiPers, John F.] Washington Univ, Sch Med, St Louis, MO USA.
[Roy, Vivek] Mayo Clin, Jacksonville, FL 32224 USA.
[Slack, James] Mayo Clin, Scottsdale, AZ USA.
[Espinoza-Delgado, Igor] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Gore, SD (reprint author), Comprehens Canc Ctr Johns Hopkins, 1650 Orleans St,Room 288, Baltimore, MD 21231 USA.
EM gorest@jhmi.edu
OI Loaiza-Bonilla, Arturo/0000-0002-3655-9602
FU NCI NIH HHS [K24 CA111717, N01 CM17104, K24 CA111717-05]
NR 45
TC 58
Z9 60
U1 0
U2 2
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 2009
VL 94
IS 10
BP 1375
EP 1382
DI 10.3324/haematol.2009.009217
PG 8
WC Hematology
SC Hematology
GA 510ML
UT WOS:000271092500009
PM 19794082
ER
PT J
AU Toro, JR
Blake, PW
Bjorkholm, M
Kristinsson, SY
Wang, ZQ
Landgren, O
AF Toro, Jorge R.
Blake, Patrick W.
Bjoerkholm, Magnus
Kristinsson, Sigurdur Y.
Wang, Zhuoqiao
Landgren, Ola
TI Prior history of non-melanoma skin cancer is associated with increased
mortality in patients with chronic lymphocytic leukemia
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Article
DE chronic lymphocytic leukemia; non-melanoma skin cancer; squamous cell
carcinoma; susceptibility; pathogenesis; immune disruption;
immunosuppression; survival; prognosis
ID SQUAMOUS-CELL CARCINOMA; NON-HODGKINS-LYMPHOMA; POOR-PROGNOSIS;
POPULATION; SURVIVAL; FINLAND; SWEDEN; MARKER; RISK
AB We investigated whether a previous diagnosis of non-melanoma skin cancer among chronic lymphocytic leukemia patients is a predictor of poor outcome Using the Swedish Cancer Registry, we conducted a population-based study to evaluate the survival patterns among chronic lymphocytic leukemia patients with and without non-melanoma skin cancer. Cox proportional hazards regression models were used and Kaplan-Meier curves were constructed. Of a total of 12,041 chronic lymphocytic leukemia cases identified, 236 cases, including 111 squamous cell cancer, had a prior history of non-melanoma skin cancer Chronic lymphocytic leukemia patients with a prior history of non-melanoma skin cancer had a 1 29-fold (95% CI 1.10-1.52, p=0.0024) increased risk of dying, and those with a history of squamous cell cancer had a further elevated 1.86-fold (95% CI 1.46-2.36; p<0.0001) risk of dying Kaplan-Meier plots showed that patients with a history of non-melanoma skin cancer, particularly those with squamous Cell cancer, had significantly poorer survival than chronic lymphocytic leukemia patients without non-melanoma skin cancer (p<0.0001, log-rank test) Non-melanoma skin cancer may be a novel clinical predictor of worse chronic lymphocytic leukemia outcome
C1 [Toro, Jorge R.] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Blake, Patrick W.] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Bjoerkholm, Magnus; Kristinsson, Sigurdur Y.] Karolinska Univ Hosp Solna, Dept Med, Div Hematol, Stockholm, Sweden.
[Bjoerkholm, Magnus; Kristinsson, Sigurdur Y.] Karolinska Inst, Stockholm, Sweden.
[Wang, Zhuoqiao] Informat Management Serv Inc, Rockville, MD USA.
RP Toro, JR (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,Bldg EPS Room 7012, Bethesda, MD 20892 USA.
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
FU Howard Hughes Medical Institute; Intramural NIH HHS
NR 28
TC 4
Z9 4
U1 0
U2 1
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 2009
VL 94
IS 10
BP 1460
EP 1464
DI 10.3324/haematol.2008.004721
PG 5
WC Hematology
SC Hematology
GA 510ML
UT WOS:000271092500022
PM 19794092
ER
PT J
AU Kristinsson, SY
Landgren, O
Sjoberg, J
Turesson, I
Bjorkholm, M
Goldin, LR
AF Kristinsson, Sigurdur Y.
Landgren, Ola
Sjoberg, Jan
Turesson, Ingemar
Bjorkholm, Magnus
Goldin, Lynn R.
TI Autoimmunity and risk for Hodgkin's lymphoma by subtype
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Letter
ID RHEUMATOID-ARTHRITIS; SUSCEPTIBILITY; DISEASE
C1 [Kristinsson, Sigurdur Y.; Landgren, Ola; Sjoberg, Jan; Bjorkholm, Magnus] Karolinska Univ, Hosp Solna, Dept Med, Div Hematol, SE-17176 Stockholm, Sweden.
[Kristinsson, Sigurdur Y.; Landgren, Ola; Sjoberg, Jan; Bjorkholm, Magnus] Karolinska Inst, Stockholm, Sweden.
[Landgren, Ola; Goldin, Lynn R.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Landgren, Ola] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Turesson, Ingemar] Malmo Univ Hosp, Dept Med, Sect Hematol, Malmo, Sweden.
RP Kristinsson, SY (reprint author), Karolinska Univ, Hosp Solna, Dept Med, Div Hematol, SE-17176 Stockholm, Sweden.
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
FU Intramural NIH HHS
NR 11
TC 13
Z9 13
U1 0
U2 3
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 2009
VL 94
IS 10
BP 1468
EP 1469
DI 10.3324/haematol.2009.010512
PG 2
WC Hematology
SC Hematology
GA 510ML
UT WOS:000271092500026
PM 19794095
ER
PT J
AU Kobrin, S
Hall, KL
Croyle, RT
AF Kobrin, Sarah
Hall, Kara L.
Croyle, Robert T.
TI Advancing Theory in Cancer Screening and Beyond: A Conversation Across
Fields
SO HEALTH EDUCATION & BEHAVIOR
LA English
DT Editorial Material
DE cancer; culture, measurement; theory; transdisciplinary
C1 [Kobrin, Sarah] NCI, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Kobrin, S (reprint author), NCI, Behav Res Program, Div Canc Control & Populat Sci, 6130 Execut Blvd,Room 4096, Bethesda, MD 20892 USA.
EM kobrins@mail.nih.gov
FU PHS HHS [HHSN261200900383P]
NR 10
TC 0
Z9 0
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1090-1981
J9 HEALTH EDUC BEHAV
JI Health Educ. Behav.
PD OCT
PY 2009
VL 36
BP 7S
EP 10S
DI 10.1177/1090198109340518
PG 4
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 516ZJ
UT WOS:000271581900002
PM 19830880
ER
PT J
AU Kryuchkov, V
Chumak, V
Maceika, E
Anspaugh, LR
Cardis, E
Bakhanova, E
Golovanov, I
Drozdovitch, V
Luckyanov, N
Kesminiene, A
Voilleque, P
Bouville, A
AF Kryuchkov, Victor
Chumak, Vadim
Maceika, Evaldas
Anspaugh, Lynn R.
Cardis, Elisabeth
Bakhanova, Elena
Golovanov, Ivan
Drozdovitch, Vladimir
Luckyanov, Nickolas
Kesminiene, Ausrele
Voilleque, Paul
Bouville, Andre
TI RADRUE METHOD FOR RECONSTRUCTION OF EXTERNAL PHOTON DOSES FOR CHERNOBYL
LIQUIDATORS IN EPIDEMIOLOGICAL STUDIES
SO HEALTH PHYSICS
LA English
DT Article
DE bone marrow; Chernobyl; dosimetry, external; thyroid
ID PRECISION EPR DOSIMETRY; CLEANUP WORKERS; UKRAINIAN-AMERICAN; DISORDERS;
LEUKEMIA; RISK
AB Between 1986 and 1990, several hundred thousand workers, called "liquidators" or "clean-up workers," took part in decontamination and recovery activities within the 30-km zone around the Chernobyl nuclear power plant in Ukraine, where a major accident occurred in April 1986. The Chernobyl liquidators were mainly exposed to external ionizing radiation levels that depended primarily on their work locations and the time after the accident when the work was performed. Because individual doses were often monitored inadequately or were not monitored at all for the majority of liquidators, a new method of photon (i.e., gamma and x rays) dose assessment, called "RADRUE" (Realistic Analytical Dose Reconstruction with Uncertainty Estimation), was developed to obtain unbiased and reasonably accurate estimates for use in three epidemiologic studies of hematological malignancies and thyroid cancer among liquidators. The RADRUE program implements a time-and-motion dose-reconstruction method that is flexible and conceptually easy to understand. It includes a large exposure rate database and interpolation and extrapolation techniques to calculate exposure rates at places where liquidators lived and worked within similar to 70 km of the destroyed reactor. The RADRUE technique relies on data collected from subjects' interviews conducted by trained interviewers, and on expert dosimetrists to interpret the information and provide supplementary information, when necessary, based upon their own Chernobyl experience. The RADRUE technique was used to estimate doses from external irradiation, as well as uncertainties, to the bone marrow for 929 subjects and to the thyroid gland for 530 subjects enrolled in epidemiologic studies. Individual bone marrow dose estimates were found to range from less than one mu Gy to 3,300 mGy, with an arithmetic mean of 71 mGy. Individual thyroid dose estimates were lower and ranged from 20 mu Gy to 507 mGy, with an arithmetic mean of 29 mGy. The uncertainties, expressed in terms of geometric standard deviations, ranged from 1.1 to 5.8, with an arithmetic mean of 1.9. Health Phys. 97(4):275-298; 2009
C1 [Drozdovitch, Vladimir; Luckyanov, Nickolas; Bouville, Andre] NCI, DHHS, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Kryuchkov, Victor; Golovanov, Ivan] Burnasyan Fed Med Biophys Ctr, Moscow 123182, Russia.
[Chumak, Vadim; Bakhanova, Elena] AMS Ukraine, Res Ctr Radiat Med, UA-04050 Kiev, Ukraine.
[Maceika, Evaldas] Inst Phys, LT-02300 Vilnius, Lithuania.
[Anspaugh, Lynn R.] Univ Utah, Div Radiobiol, Salt Lake City, UT 84108 USA.
[Cardis, Elisabeth] Ctr Res Environm Epidemiol CREAL, Barcelona, Spain.
[Cardis, Elisabeth] Hosp del Mar, IMIM, Municipal Inst Med Res, Barcelona, Spain.
[Cardis, Elisabeth] CIBERESP, Barcelona, Spain.
[Kesminiene, Ausrele] Int Agcy Res Canc, F-69008 Lyon, France.
[Voilleque, Paul] MJP Risk Assessment Inc, Denver, CO 80220 USA.
RP Bouville, A (reprint author), NCI, DHHS, NIH, Div Canc Epidemiol & Genet, Execut Plaza S,EPS 7094, Bethesda, MD 20892 USA.
EM bouvilla@mail.nih.gov
RI Chumak, Vadim/N-6960-2015; Cardis, Elisabeth/C-3904-2017;
OI Chumak, Vadim/0000-0001-6045-9356; Maceika, Evaldas/0000-0002-9251-6789
FU U.S. National Cancer Institute, National Institutes of Health;
Department of Health and Human Services; International Agency for
Research on Cancer; U.S. Centers for Disease Control and Prevention
[1R01CCR015763-02]; European Union [F14C-CT96-0011, ERBIC15-CT96-0317];
U.S. Department of Energy; National Institute of Allergy and Infectious
Diseases (U.S.); National Cancer Institute [Y2-Al-5077]; NCI
[Y3-CO-5117]
FX This research was supported by the Intramural Research Program of the
U.S. National Cancer Institute, National Institutes of Health, the
Department of Health and Human Services, and the International Agency
for Research on Cancer; by the U.S. Centers for Disease Control and
Prevention (Grant number 1R01CCR015763-02); the European Union (Nuclear
Fission Safety Programme contract F14C-CT96-0011 and INCO-Copernicus
Programme contract ERBIC15-CT96-0317); the U.S. Department of Energy;
and the Intra-Agency Agreement between the National Institute of Allergy
and Infectious Diseases (U.S.) and the National Cancer Institute, NIAID
agreement #Y2-Al-5077 and NCI agreement #Y3-CO-5117. The U.S. Nuclear
Regulatory Commission and the French Institute for Radiological
Protection and Nuclear Safety provided the initial funds for purchase of
equipment.
NR 27
TC 14
Z9 21
U1 1
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0017-9078
EI 1538-5159
J9 HEALTH PHYS
JI Health Phys.
PD OCT
PY 2009
VL 97
IS 4
BP 275
EP 298
PG 24
WC Environmental Sciences; Public, Environmental & Occupational Health;
Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical
Imaging
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Nuclear Science & Technology; Radiology, Nuclear Medicine &
Medical Imaging
GA 493KO
UT WOS:000269735700001
PM 19741357
ER
PT J
AU Zheng, ZL
Jia, YB
Hou, LF
Persson, C
Yeager, M
Lissowska, J
Chanock, SJ
Blaser, M
Chow, WH
Ye, WM
AF Zheng, Zongli
Jia, Yanbin
Hou, Lifang
Persson, Christina
Yeager, Meredith
Lissowska, Jolanta
Chanock, Stephen J.
Blaser, Martin
Chow, Wong-Ho
Ye, Weimin
TI Genetic Variation in a4GnT in Relation to Helicobacter pylori Serology
and Gastric Cancer Risk
SO HELICOBACTER
LA English
DT Article
DE Helicobacter pylori; genetic susceptibility; gastric cancer
ID CHOLESTEROL ALPHA-GLUCOSYLTRANSFERASE; EXPRESSION CLONING; INFECTION;
MUCIN; CELL; ALPHA-1,4-N-ACETYLGLUCOSAMINYLTRANSFERASE; POLYMORPHISMS;
MUCOSA; FORMS; TIME
AB Background:
Helicobacter pylori, a known risk factor of gastric cancer, rarely colonize the deeper portion of normal gastric glands, where the mucus is rich in alpha-1,4-linked N-acetylglucosamine capped O-glycans, that strongly inhibit H. pylori growth in vitro.
Materials and methods:
We investigated the association between genetic variation in the O-glycan transferase encoding gene (a4GnT) and H. pylori infection and gastric cancer risk using a Polish population-based case-control study (273 gastric cancer patients and 377 controls).
Results:
A haplotype at the rs2622694-rs397266 locus was associated with H. pylori infection, with the A-A haplotype associated with a higher risk compared with the most frequent G-G haplotype (odds ratio 2.30; 95% confidence interval 1.35-3.92). The association remained significant after correction for multiple tests (global p value: nominal 0.002, empirical 0.045). Neither this haplotype nor the tagSNPs were associated with overall gastric cancer risk.
Conclusion:
a4GnT genetic variation may be relevant to H. pylori infection, but not to gastric cancer risk.
C1 [Zheng, Zongli; Jia, Yanbin; Persson, Christina; Ye, Weimin] Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.
[Jia, Yanbin] Baotou Med Coll, Dept Basic Med, Baotou, Peoples R China.
[Hou, Lifang; Chow, Wong-Ho] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Yeager, Meredith; Chanock, Stephen J.] NCI, Adv Technol Ctr, Gaithersburg, MD USA.
[Lissowska, Jolanta] M Sklodowska Curie Mem Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
[Blaser, Martin] NYU, Sch Med, Dept Med, New York, NY USA.
RP Ye, WM (reprint author), Karolinska Inst, Dept Med Epidemiol & Biostat, Box 281, SE-17177 Stockholm, Sweden.
EM weimin.ye@ki.se
RI Ye, Weimin/A-5939-2008; zheng, zongli/B-2917-2011;
OI zheng, zongli/0000-0003-4849-4903; Lissowska,
Jolanta/0000-0003-2695-5799
FU NIH [R01 GM 63270]; Swedish Research Council [K009-69x-15372-05-2]
FX This study was supported in part by the Intramural Research Program of
NIH, Division of Cancer Epidemiology and Genetics, a grant from the
Swedish Research Council (K009-69x-15372-05-2), and R01 GM 63270 from
the National Institutes of Health. We thank Dr. Chuen Seng Tan for
statistical consultancy.
NR 24
TC 5
Z9 5
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1083-4389
J9 HELICOBACTER
JI Helicobacter
PD OCT
PY 2009
VL 14
IS 5
BP 120
EP 125
PG 6
WC Gastroenterology & Hepatology; Microbiology
SC Gastroenterology & Hepatology; Microbiology
GA 492ZG
UT WOS:000269701400007
PM 19751437
ER
PT J
AU Mrozek, K
Harper, DP
Aplan, PD
AF Mrozek, Krzysztof
Harper, David P.
Aplan, Peter D.
TI Cytogenetics and Molecular Genetics of Acute Lymphoblastic Leukemia
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Review
DE Acute lymphoblastic leukemia; Gene mutations; Chromosome aberrations;
Human; Prognosis
ID CHILDRENS-CANCER-GROUP; ACUTE MYELOID-LEUKEMIA; IN-SITU HYBRIDIZATION;
CRYPTIC CHROMOSOMAL REARRANGEMENTS; COMPARATIVE GENOMIC HYBRIDIZATION;
ACUTE LYMPHOCYTIC-LEUKEMIA; ONCOLOGY-GROUP POG; GROUP-B EXPERIENCE;
PROGNOSTIC-SIGNIFICANCE; CLINICAL-SIGNIFICANCE
AB Acute lymphoblastic leukemia (ALL) is a malignant disease that often features nonrandom numerical or structural chromosome aberrations that can be detected microscopically. The application of contemporary genome-wide molecular analyses is revealing additional genetic alterations that are not detectable cytogenetically. This article describes the cytogenetic methodology and summarizes major cytogenetic findings and their clinical relevance in ALL. The article provides a review of modern molecular techniques and their application in the research on the genetics and epigenetics of ALL.
C1 [Mrozek, Krzysztof] Ohio State Univ, Dept Internal Med, James Canc Hosp, Div Hematol & Oncol,Comprehens Canc Ctr, Columbus, OH 43210 USA.
[Harper, David P.; Aplan, Peter D.] NCI, Genet Branch, Ctr Canc Res, Bethesda, MD 20889 USA.
[Harper, David P.] Uniformed Serv Univ Hlth Sci, Dept Pediat, Bethesda, MD 20814 USA.
RP Mrozek, K (reprint author), Ohio State Univ, Dept Internal Med, James Canc Hosp, Div Hematol & Oncol,Comprehens Canc Ctr, Room 1248B,300 W 10th Ave, Columbus, OH 43210 USA.
EM krzysztof.mrozek@osumc.edu
RI Mrozek, Krzysztof/A-3142-2008; Aplan, Peter/K-9064-2016
FU NIH; NCI [CA101140, CA16058]; Coleman Leukemia Research Foundation
FX K Mrozek and DP Harper contributed equally to this work. The authors
have no conflicting financial interests to disclose. This research was
supported in part by the Intramural Research Program of the NIH, NCI,
and NCI grants CA101140 and CA16058, and The Coleman Leukemia Research
Foundation.
NR 105
TC 25
Z9 30
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8588
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD OCT
PY 2009
VL 23
IS 5
BP 991
EP +
DI 10.1016/j.hoc.2009.07.001
PG 21
WC Oncology; Hematology
SC Oncology; Hematology
GA 513KK
UT WOS:000271321000004
PM 19825449
ER
PT J
AU Everson, GT
Terrault, N
Lok, AS
Brown, RS
Saab, S
Shiffman, ML
Al-Osaimi, AM
Kulik, LM
Gillespie, BW
Everhart, JE
AF Everson, Gregory T.
Terrault, Norah
Lok, Anna S.
Brown, Robert S.
Saab, Sammy
Shiffman, Mitchell L.
Al-Osaimi, Abdullah M.
Kulik, Laura M.
Gillespie, Brenda W.
Everhart, James E.
TI INTERIM ANALYSIS OF A CONTROLLED TRIAL OF PRE-TRANSPLANT PEGINTERFERON
ALFA-2B/RIBAVIRIN (PEG/RBV) TO PREVENT RECURRENT HEPATITIS C VIRUS (HCV)
INFECTION AFTER LIVER TRANSPLANTATION (LT) IN THE ADULT-TO-ADULT LIVER
TRANSPLANTATION (A2ALL) STUDY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Everson, Gregory T.] Univ Colorado, Dept Med, Aurora, CO USA.
[Terrault, Norah] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Lok, Anna S.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Brown, Robert S.] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
[Saab, Sammy] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Shiffman, Mitchell L.] Virginia Commonwealth Univ, Dept Med, Med Coll Virginia Hosp, Richmond, VA 23298 USA.
[Al-Osaimi, Abdullah M.] Univ Virginia, Dept Med, Charlottesville, VA USA.
[Kulik, Laura M.] Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
[Everhart, James E.] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD 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 2009
VL 50
IS 4
MA 1
BP 302A
EP 302A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000002
ER
PT J
AU Choi, D
Park, KY
Heo, J
Cho, CH
Durkin, M
Holczbauer, A
Marquardt, JU
Factor, VM
Si-Tayeb, K
Duncan, SA
Thorgeirsson, SS
AF Choi, Dongho
Park, Kye-Yoon
Heo, Jeonghoon
Cho, Cheul Hyung
Durkin, Marian
Holczbauer, Agnes
Marquardt, Jens U.
Factor, Valentina M.
Si-Tayeb, Karim
Duncan, Stephen A.
Thorgeirsson, Snorri S.
TI COMPARISON OF HEPATIC DIFFERENTIATION POTENTIAL BETWEEN HUMAN ES AND IPS
CELLS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Choi, Dongho; Durkin, Marian; Holczbauer, Agnes; Marquardt, Jens U.; Factor, Valentina M.; Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Park, Kye-Yoon] NINDS, Stem Cell Unit, NIH, Bethesda, MD 20892 USA.
[Heo, Jeonghoon] Kosin Univ, Dept Mol Biol, Coll Med, Pusan, South Korea.
[Cho, Cheul Hyung] New Jersey Inst Technol, Dept Biomed Engn, Newark, NJ 07102 USA.
[Si-Tayeb, Karim; Duncan, Stephen A.] Med Coll Wisconsin, Dept Cell Biol Neurobiol & Anat, Milwaukee, WI 53226 USA.
RI Si-Tayeb, Karim/D-3543-2015
OI Si-Tayeb, Karim/0000-0003-4599-7441
NR 0
TC 0
Z9 0
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 2009
VL 50
IS 4
MA 48
BP 325A
EP 325A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000049
ER
PT J
AU Berg, CL
Merion, RM
Shearon, TH
Olthoff, KM
Brown, RS
Baker, TB
Everson, GT
Hong, JC
Terrault, N
Hayashi, PH
Fisher, RA
Everhart, JE
AF Berg, Carl L.
Merion, Robert M.
Shearon, Tempie H.
Olthoff, Kim M.
Brown, Robert S.
Baker, Talia B.
Everson, Gregory T.
Hong, Johnny C.
Terrault, Norah
Hayashi, Paul H.
Fisher, Robert A.
Everhart, James E.
TI BENEFIT OF LIVING DONOR LIVER TRANSPLANTATION ACCORDING TO MELD SCORE
AND DIAGNOSIS OF HEPATOCELLULAR CARCINOMA
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Berg, Carl L.] Univ Virginia, Dept Med, Charlottesville, VA USA.
[Merion, Robert M.] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA.
[Shearon, Tempie H.] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Olthoff, Kim M.] Univ Penn, Dept Surg, Philadelphia, PA 19104 USA.
[Brown, Robert S.] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
[Baker, Talia B.] Northwestern Univ, Dept Surg, Chicago, IL 60611 USA.
[Everson, Gregory T.] Univ Colorado, Dept Med, Aurora, CO USA.
[Hong, Johnny C.] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA.
[Terrault, Norah] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Hayashi, Paul H.] Univ N Carolina, Dept Surg, Chapel Hill, NC USA.
[Fisher, Robert A.] Virginia Commonwealth Univ, Dept Surg, Coll Med, Virginia Hosp, Richmond, VA USA.
[Everhart, James E.] NIDDKD, Div Digest Dis & Nutr, 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 2009
VL 50
IS 4
MA 75
BP 339A
EP 339A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000076
ER
PT J
AU Morgan, TR
Ghany, MG
Kim, HY
Snow, KK
Lindsay, K
Lok, AS
AF Morgan, Timothy R.
Ghany, Marc G.
Kim, Hae-Young
Snow, Kristin K.
Lindsay, Karen
Lok, Anna S.
TI OUTCOME OF SUSTAINED VIROLOGICAL RESPONDERS (SVR) AND NON-RESPONDERS IN
THE HEPATITIS C ANTIVIRAL LONG-TERM TREATMENT AGAINST CIRRHOSIS (HALT-C)
TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Morgan, Timothy R.] VA Med Ctr, Long Beach, CA USA.
[Morgan, Timothy R.] Univ Calif Irvine, Irvine, CA USA.
[Kim, Hae-Young; Snow, Kristin K.] New England Res Inst, Boston, MA USA.
[Lok, Anna S.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Lindsay, Karen] Univ So Calif, Los Angeles, CA USA.
[Ghany, Marc G.] NIDDK, NIH, Bethesda, MD 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 2009
VL 50
IS 4
MA 115
BP 357A
EP 358A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000116
ER
PT J
AU Thomas, E
Feld, JJ
Fried, MW
Liang, TJ
AF Thomas, Emmanuel
Feld, Jordan J.
Fried, Michael W.
Liang, T. Jake
TI A NOVEL INNATE IMMUNE MECHANISM OF ACTION OF RIBAVIRIN IN ANTIVIRAL
THERAPY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Thomas, Emmanuel; Liang, T. Jake] NIDDK, NIH, LDB, Bethesda, MD USA.
[Fried, Michael W.] Univ N Carolina, Chapel Hill, NC USA.
[Feld, Jordan J.] Univ Toronto, Div Gastroenterol, Toronto, ON, Canada.
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 2009
VL 50
IS 4
MA 124
BP 362A
EP 362A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000125
ER
PT J
AU Wakabayashi, Y
Fu, D
Lippincott-Schwartz, J
Arias, IM
AF Wakabayashi, Yoshiyuki
Fu, Dong
Lippincott-Schwartz, Jennifer
Arias, Irwin M.
TI RAB11A AND MYOSIN VB ARE REQUIRED FOR CANALICULAR NETWORK FORMATION AND
ABC TRANSPORTER CYCLING IN PRIMARY RAT HEPATOCYTES
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Wakabayashi, Yoshiyuki; Fu, Dong; Lippincott-Schwartz, Jennifer; Arias, Irwin M.] NICHD, CBMP, 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 2009
VL 50
IS 4
MA 160
BP 378A
EP 379A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000161
ER
PT J
AU Davern, TJ
Chalasani, NP
Fontana, RJ
Hayashi, PH
Kleiner, DE
Engle, RE
Purcell, RH
Rochon, J
Serrano, J
Hoofnagle, JH
AF Davern, Timothy J.
Chalasani, Naga P.
Fontana, Robert J.
Hayashi, Paul H.
Kleiner, David E.
Engle, Ronald E.
Purcell, Robert H.
Rochon, James
Serrano, Jose
Hoofnagle, Jay H.
TI ANTIBODY TO HEPATITIS E IN PATIENTS WITH SUSPECTED DRUG-INDUCED LIVER
INJURY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Davern, Timothy J.] Calif Pacific Med Ctr, Liver Transplant Program, San Francisco, CA USA.
[Chalasani, Naga P.] Indiana Univ, Dept Med, Indianapolis, IN USA.
[Fontana, Robert J.] Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA.
[Hayashi, Paul H.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Kleiner, David E.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Engle, Ronald E.; Purcell, Robert H.] NIAID, Hepatitis Virus Sect, Bethesda, MD 20892 USA.
[Rochon, James] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC USA.
[Serrano, Jose; Hoofnagle, Jay H.] NIDDKD, Liver Dis Res Branch, 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 2009
VL 50
IS 4
MA 163
BP 380A
EP 380A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000164
ER
PT J
AU Ryan, JC
Lehil, M
Kim, MS
Duh, FM
Martin, M
George, S
Kennedy, AE
Yee, RM
Tracy, D
Cozen, M
Carrington, M
Monto, A
AF Ryan, James C.
Lehil, Mandeep
Kim, Michael S.
Duh, Fuh-Mei
Martin, Maureen
George, Sally
Kennedy, Alan E.
Yee, Russell M.
Tracy, Daniel
Cozen, Myrna
Carrington, Mary
Monto, Alexander
TI NK CELL KIR CONTROL DIVERGENT OUTCOMES IN HEPATITIS C VIRUS INFECTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Ryan, James C.; Lehil, Mandeep; Kim, Michael S.; George, Sally; Kennedy, Alan E.; Yee, Russell M.; Tracy, Daniel; Cozen, Myrna; Monto, Alexander] San Francisco VA Med Ctr, San Francisco, CA USA.
[Ryan, James C.; Kim, Michael S.; Cozen, Myrna; Monto, Alexander] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Duh, Fuh-Mei; Martin, Maureen; Carrington, Mary] NCI, Frederick, MD 21701 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 2009
VL 50
IS 4
MA 176
BP 386A
EP 386A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000177
ER
PT J
AU Shin, EC
Nascimbeni, M
Mihalik, K
Feinstone, SM
Rice, CM
Rehermann, B
AF Shin, Eui-Cheol
Nascimbeni, Michelina
Mihalik, Kathleen
Feinstone, Stephen M.
Rice, Charles M.
Rehermann, Barbara
TI DELAYED INDUCTION NOT IMPAIRED RECRUITMENT OF HEPATITIS C VIRUS-SPECIFIC
CD8 T CELLS IS RESPONSIBLE FOR THE LATE ONSET OF ACUTE HEPATITIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Shin, Eui-Cheol; Nascimbeni, Michelina; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH, Bethesda, MD USA.
[Mihalik, Kathleen; Feinstone, Stephen M.] US FDA, Lab Hepatitis Viruses, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA.
[Rice, Charles M.] Rockefeller Univ, Ctr Study Hepatitis C, New York, NY 10021 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 2009
VL 50
IS 4
MA 179
BP 387A
EP 387A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000180
ER
PT J
AU Katsounas, A
Rasimas, JJ
Lempicki, RA
McLaughlin, M
Masur, H
Polis, MA
Kottilil, S
AF Katsounas, Antonios
Rasimas, Joseph J.
Lempicki, Richard A.
McLaughlin, Mary
Masur, Henry
Polis, Michael A.
Kottilil, Shyam
TI REGULATION OF PROTEIN KINASE C SUBSTRATE, AS A MECHANISM FOR
INTERFERON-alpha-INDUCED NEUROPSYCHIATIRIC ADVERSE EFFECTS OBSERVED IN
HIV/HCV-CO-INFECTED PATIENTS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Katsounas, Antonios; Lempicki, Richard A.] NCI Frederick, SAIC, Bethesda, MD USA.
[McLaughlin, Mary; Polis, Michael A.; Kottilil, Shyam] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
[Rasimas, Joseph J.] NIMH, NIH, Bethesda, MD 20892 USA.
[Masur, Henry] NIH, CCMD, Bethesda, MD 20892 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 2009
VL 50
IS 4
MA 196
BP 396A
EP 397A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000197
ER
PT J
AU Rodrigue, JR
Balistreri, WF
Haber, B
Jonas, MM
Mohan, P
Molleston, JP
Murray, KF
Narkewicz, M
Rosenthal, P
Smith, LL
Schwarz, KB
Robuck, PR
Barton, B
Gonzalez-Peralta, RP
AF Rodrigue, James R.
Balistreri, William F.
Haber, Barbara
Jonas, Maureen M.
Mohan, Parvathi
Molleston, Jean P.
Murray, Karen F.
Narkewicz, Michael
Rosenthal, Philip
Smith, Lesley. L.
Schwarz, Kathleen B.
Robuck, Patricia R.
Barton, Bruce
Gonzalez-Peralta, Regino P.
TI PEGINTERFERON ALFA-2A WITH OR WITHOUT RIBAVIRIN RESULTS IN MINIMAL
EFFECT ON QUALITY OF LIFE, EMOTIONAL, AND COGNITIVE OUTCOMES: RESULTS OF
THE PEDS-C TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Rodrigue, James R.] Beth Israel Deaconess Med Ctr, Transplant Ctr, Boston, MA 02215 USA.
[Balistreri, William F.] Univ Cincinnati, Cincinnati, OH USA.
[Haber, Barbara] Univ Penn, Philadelphia, PA 19104 USA.
[Jonas, Maureen M.] Harvard Univ, Sch Med, Boston, MA USA.
[Mohan, Parvathi] George Washington Univ, Washington, DC USA.
[Molleston, Jean P.] Indiana Univ, Indianapolis, IN 46204 USA.
[Murray, Karen F.] Univ Washington, Seattle, WA 98195 USA.
[Narkewicz, Michael] Univ Colorado, Denver, CO 80202 USA.
[Rosenthal, Philip] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Smith, Lesley. L.] Univ Miami, Miami, FL USA.
[Schwarz, Kathleen B.] Johns Hopkins Univ, Baltimore, MD USA.
[Robuck, Patricia R.] NIH, Bethesda, MD 20892 USA.
[Barton, Bruce] Maryland Med Res Inst, Baltimore, MD USA.
[Gonzalez-Peralta, Regino P.] Univ Florida, Gainesville, FL 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 2009
VL 50
IS 4
MA 238
BP 418A
EP 418A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000239
ER
PT J
AU Schwarz, KB
Valsamakis, A
Balistreri, WF
Gonzalez-Peralta, RP
Haber, B
Jonas, MM
Mohan, P
Molleston, JP
Murray, KF
Narkewicz, M
Rosenthal, P
Smith, LJ
Rossi, SJ
Robuck, PR
Barton, B
AF Schwarz, Kathleen B.
Valsamakis, Alexandra
Balistreri, William F.
Gonzalez-Peralta, Regina P.
Haber, Barbara
Jonas, Maureen M.
Mohan, Parvathi
Molleston, Jean P.
Murray, Karen F.
Narkewicz, Michael
Rosenthal, Philip
Smith, Lesley J.
Rossi, Stephen J.
Robuck, Patricia R.
Barton, Bruce
TI EARLY CHANGES IN VIRAL LOAD PREDICT SUSTAINED VIRAL RESPONSE (SVR) IN
THE PEDS C TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Schwarz, Kathleen B.; Valsamakis, Alexandra] Johns Hopkins, Pediat, Baltimore, MD USA.
[Balistreri, William F.] Univ Cincinnati, Cincinnati, OH USA.
[Gonzalez-Peralta, Regina P.] Univ Florida, Gainesville, FL 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.
[Molleston, Jean P.] Indiana Univ, Indianapolis, IN 46204 USA.
[Murray, Karen F.] Univ Washington, Seattle, WA 98195 USA.
[Narkewicz, Michael] Univ Colorado, Denver, CO 80202 USA.
[Rosenthal, Philip] UCSF, San Francisco, CA USA.
[Smith, Lesley J.] Univ Miami, Miami, FL USA.
[Rossi, Stephen J.] Roche Mol Diagnost, Nutley, NJ USA.
[Robuck, Patricia R.] NIDDK, Bethesda, MD USA.
[Barton, Bruce] Maryland Med Res Inst, Baltimore, 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 2009
VL 50
IS 4
MA 240
BP 419A
EP 419A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000241
ER
PT J
AU Pati, NT
Kottilil, S
Shrivastava, S
Hissar, S
Sarin, SK
AF Pati, Nirupma Trehan
Kottilil, Shyam
Shrivastava, Shikha
Hissar, Syed
Sarin, Shiv K.
TI HBV REPLICATION MODULATES HBV SPECIFIC ADAPTIVE IMMUNE RESPONSES BY
INDUCING AND MAINTAINING T REGULATORY CELL ACTIVITY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Pati, Nirupma Trehan; Sarin, Shiv K.] Inst Liver & Biliary Sci, New Delhi, India.
[Kottilil, Shyam] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
[Shrivastava, Shikha; Hissar, Syed; Sarin, Shiv K.] GB Pant Hosp, Dept Gastroenterol, 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 2009
VL 50
IS 4
MA 385
BP 486A
EP 486A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000386
ER
PT J
AU Martino, AC
Henderson, WA
Rivera, E
Liang, JT
Hoofnagle, JH
Ghany, MG
AF Martino, Angela C.
Henderson, Wendy A.
Rivera, Elenita
Liang, Jake T.
Hoofnagle, Jay H.
Ghany, Marc G.
TI PATIENT-RELATED SYMPTOMS IN INDIVIDUALS WITH CHRONIC HEPATITIS B VIRUS
TREATED WITH LAMIVUDINE AND ADEFOVIR OR ADEFOVIR MONOTHERAPY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Martino, Angela C.; Henderson, Wendy A.] NINR, Symptom Management Branch, Biobehav Unit, NIH, Bethesda, MD 20892 USA.
[Rivera, Elenita; Liang, Jake T.; Hoofnagle, Jay H.; Ghany, Marc G.] NIDDK, LDB, 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 2009
VL 50
IS 4
MA 473
BP 528A
EP 529A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000474
ER
PT J
AU Fu, D
Wakabayashi, Y
Lippincott-Schwartz, J
Arias, IM
AF Fu, Dong
Wakabayashi, Yoshiyuki
Lippincott-Schwartz, Jennifer
Arias, Irwin M.
TI BILE ACIDS REGULATE BILE CANALICULAR FORMATION IN PRIMARY HEPATOCYTES
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Fu, Dong; Wakabayashi, Yoshiyuki; Lippincott-Schwartz, Jennifer; 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 2009
VL 50
IS 4
MA 678
BP 623A
EP 623A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000678
ER
PT J
AU Shneider, BL
Abel, RB
Raghumathan, T
Magee, JC
Bezerra, JA
Haber, B
Karpen, SJ
Rosenthal, P
Schwarz, KB
Shepherd, RW
Suchy, FJ
Whitington, PF
Robuck, PR
Sokol, RJ
AF Shneider, Benjamin L.
Abel, Robert B.
Raghumathan, Trivellore
Magee, John C.
Bezerra, Jorge A.
Haber, Barbara
Karpen, Saul J.
Rosenthal, Philip
Schwarz, Kathleen B.
Shepherd, Ross W.
Suchy, Frederick J.
Whitington, Peter F.
Robuck, Patricia R.
Sokol, Ronald J.
TI A PROSPECTIVE MULTI-CENTERED INVESTIGATION OF VITAMIN SUPPLEMENTATION IN
INFANTS WITH BILIARY ATRESIA: INTERIM ANALYSIS FROM THE BILIARY ATRESIA
RESEARCH CONSORTIUM (BARC)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Shneider, Benjamin L.] Childrens Hosp Pittsburgh, Div Gastroenterol Hepatol & Nutr, Pittsburgh, PA 15213 USA.
[Abel, Robert B.; Raghumathan, Trivellore; Magee, John C.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Bezerra, Jorge A.] Childrens Hosp, Med Ctr, Cincinnati, OH 45229 USA.
[Haber, Barbara] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Karpen, Saul J.] Texas Childrens Hosp, Houston, TX 77030 USA.
[Rosenthal, Philip] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Schwarz, Kathleen B.] Johns Hopkins Univ, Baltimore, MD USA.
[Shepherd, Ross W.] Washington Univ, St Louis, MO USA.
[Whitington, Peter F.] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Robuck, Patricia R.] NIH, Bethesda, MD 20892 USA.
[Sokol, Ronald J.] Childrens Hosp Denver, Denver, CO USA.
[Suchy, Frederick J.] Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
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 2009
VL 50
IS 4
MA 698
BP 631A
EP 632A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000697
ER
PT J
AU Sundaram, SS
Fredericks, EM
Kamath, BM
Haber, B
Raghumathan, T
Magee, JC
Bezerra, JA
Karpen, SJ
Kerkar, N
Rosenthal, P
Schwarz, KB
Shepherd, RW
Shneider, BL
Whitington, PF
Robuck, PR
Sokol, RJ
AF Sundaram, Shikha S.
Fredericks, Emily M.
Kamath, Binita M.
Haber, Barbara
Raghumathan, Trivellore
Magee, John C.
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 A MULTICENTER CROSS SECTIONAL ASSESSMENT OF QUALITY OF LIFE IN BILIARY
ATRESIA PATIENTS AGED 2-25 YEARS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases
CY OCT 30-NOV 03, 2009
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Sundaram, Shikha S.; Sokol, Ronald J.] Univ Colorado, Sch Med, Childrens Hosp, Aurora, CO USA.
[Fredericks, Emily M.; Raghumathan, Trivellore; Magee, John C.] Univ Michigan, Sch Med, Ann Arbor, MI USA.
[Kamath, Binita M.; Haber, Barbara] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Robuck, Patricia R.] NIDDK, Bethesda, MD USA.
[Whitington, Peter F.] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Bezerra, Jorge A.] Cincinnati Childrens Hosp, Med Ctr, Cincinnati, OH USA.
[Kerkar, Nanda] Mt Sinai Med Ctr, New York, NY 10029 USA.
[Schwarz, Kathleen B.] Johns Hopkins Univ, Baltimore, MD USA.
[Shneider, Benjamin L.] Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA.
[Karpen, Saul J.] Texas Childrens Liver Ctr, Houston, TX USA.
[Rosenthal, Philip] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Shepherd, Ross W.] Washington Univ, St Louis, MO 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 2009
VL 50
IS 4
MA 699
BP 632A
EP 633A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 502JV
UT WOS:000270456000698
ER
EF