Institution
University of Tennessee Health Science Center
Education•Memphis, Tennessee, United States•
About: University of Tennessee Health Science Center is a education organization based out in Memphis, Tennessee, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 15716 authors who have published 26884 publications receiving 1176697 citations.
Topics: Population, Medicine, Transplantation, Cancer, Gene
Papers published on a yearly basis
Papers
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TL;DR: Results indicate that Pten regulates neuronal size in vivo in a cell-autonomous manner and provide new insights into the etiology of Lhermitte-Duclos disease.
Abstract: Somatic inactivation of PTEN occurs in different human tumors including glioblastoma, endometrial carcinoma and prostate carcinoma. Germline mutations in PTEN result in a range of phenotypic abnormalities that occur with variable penetrance, including neurological features such as macrocephaly, seizures, ataxia and Lhermitte-Duclos disease (also described as dysplastic gangliocytoma of the cerebellum). Homozygous deletion of Pten causes embryonic lethality in mice. To investigate function in the brain, we used Cre-loxP technology to selectively inactivate Pten in specific mouse neuronal populations. Loss of Pten resulted in progressive macrocephaly and seizures. Neurons lacking Pten expressed high levels of phosphorylated Akt and showed a progressive increase in soma size without evidence of abnormal proliferation. Cerebellar abnormalities closely resembled the histopathology of human Lhermitte-Duclos disease. These results indicate that Pten regulates neuronal size in vivo in a cell-autonomous manner and provide new insights into the etiology of Lhermitte-Duclos disease.
449 citations
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TL;DR: In this paper, a large clinical trial was conducted to evaluate the effect of low-dose aspirin on the frequency of preeclampsia in nulliparous women, and the primary objective of the trial was to identify those clinical characteristics that might be predictive for the development of PPP.
447 citations
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Peninsula College of Medicine and Dentistry1, National Institutes of Health2, University of Florence3, Seconda Università degli Studi di Napoli4, University of Plymouth5, University of Tennessee Health Science Center6, University of Pittsburgh7, California Pacific Medical Center8, University of Bristol9, Wellcome Trust Centre for Human Genetics10, University of Oulu11, Imperial College London12
TL;DR: It is shown that common genetic variation influences levels of clinically relevant proteins in human serum and plasma and the identification of protein quantitative trait loci (pQTLs) may be a powerful complementary method of improving the understanding of disease pathways.
Abstract: There is considerable evidence that human genetic variation influences gene expression. Genome-wide studies have revealed that mRNA levels are associated with genetic variation in or close to the gene coding for those mRNA transcripts – cis effects, and elsewhere in the genome – trans effects. The role of genetic variation in determining protein levels has not been systematically assessed. Using a genome-wide association approach we show that common genetic variation influences levels of clinically relevant proteins in human serum and plasma. We evaluated the role of 496,032 polymorphisms on levels of 42 proteins measured in 1200 fasting individuals from the population based InCHIANTI study. Proteins included insulin, several interleukins, adipokines, chemokines, and liver function markers that are implicated in many common diseases including metabolic, inflammatory, and infectious conditions. We identified eight Cis effects, including variants in or near the IL6R (p = 1.8×10−57), CCL4L1 (p = 3.9×10−21), IL18 (p = 6.8×10−13), LPA (p = 4.4×10−10), GGT1 (p = 1.5×10−7), SHBG (p = 3.1×10−7), CRP (p = 6.4×10−6) and IL1RN (p = 7.3×10−6) genes, all associated with their respective protein products with effect sizes ranging from 0.19 to 0.69 standard deviations per allele. Mechanisms implicated include altered rates of cleavage of bound to unbound soluble receptor (IL6R), altered secretion rates of different sized proteins (LPA), variation in gene copy number (CCL4L1) and altered transcription (GGT1). We identified one novel trans effect that was an association between ABO blood group and tumour necrosis factor alpha (TNF-alpha) levels (p = 6.8×10−40), but this finding was not present when TNF-alpha was measured using a different assay , or in a second study, suggesting an assay-specific association. Our results show that protein levels share some of the features of the genetics of gene expression. These include the presence of strong genetic effects in cis locations. The identification of protein quantitative trait loci (pQTLs) may be a powerful complementary method of improving our understanding of disease pathways.
446 citations
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TL;DR: It is reported that sustained activation by trains of several hundred presynaptic spikes resulted in much stronger depression of synaptic currents at excitatory synapses than at inhibitory ones, suggesting that inhibitory terminals of fast-spiking cells are better equipped to support prolonged transmitter release at a high frequency.
Abstract: The stability of cortical neuron activity in vivo suggests that the firing rates of both excitatory and inhibitory neurons are dynamically adjusted. Using dual recordings from excitatory pyramidal neurons and inhibitory fast-spiking neurons in neocortical slices, we report that sustained activation by trains of several hundred presynaptic spikes resulted in much stronger depression of synaptic currents at excitatory synapses than at inhibitory ones. The steady-state synaptic depression was frequency dependent and reflected presynaptic function. These results suggest that inhibitory terminals of fast-spiking cells are better equipped to support prolonged transmitter release at a high frequency compared with excitatory ones. This difference in frequency-dependent depression could produce a relative increase in the impact of inhibition during periods of high global activity and promote the stability of cortical circuits.
446 citations
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Baylor College of Medicine1, Harvard University2, Kaiser Permanente3, Emory University4, Ochsner Medical Center5, Icahn School of Medicine at Mount Sinai6, Cedars-Sinai Medical Center7, University of California, Los Angeles8, University of Tennessee Health Science Center9, University of Texas Health Science Center at San Antonio10, American Association of Clinical Endocrinologists11, Tulane University12, University of Alabama at Birmingham13, University of Washington14, University of Miami15, Washington University in St. Louis16, Mount Sinai Hospital17, University of California, Irvine18, Grady Memorial Hospital19
TL;DR: The objective of the trial was to establish whether or not the initial treatment strategy improved the patient’s quality of life and/or lowered the risk of adverse events.
445 citations
Authors
Showing all 15827 results
Name | H-index | Papers | Citations |
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George P. Chrousos | 169 | 1612 | 120752 |
Steven N. Blair | 165 | 879 | 132929 |
Bruce L. Miller | 163 | 1153 | 115975 |
Ralph A. DeFronzo | 160 | 759 | 132993 |
Frank J. Gonzalez | 160 | 1144 | 96971 |
Robert G. Webster | 158 | 843 | 90776 |
Anne B. Newman | 150 | 902 | 99255 |
Ching-Hon Pui | 145 | 805 | 72146 |
Barton F. Haynes | 144 | 911 | 79014 |
Yoshihiro Kawaoka | 139 | 883 | 75087 |
Seth M. Steinberg | 137 | 936 | 80148 |
Richard J. Johnson | 137 | 880 | 72201 |
Kristine Yaffe | 136 | 794 | 72250 |
Leslie L. Robison | 131 | 854 | 64373 |
Gerardo Heiss | 128 | 623 | 69393 |