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 & Transplantation. The organization has 15716 authors who have published 26884 publications receiving 1176697 citations.
Topics: Population, Transplantation, Kidney disease, Cancer, Receptor
Papers published on a yearly basis
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University of Pittsburgh1, University of Tennessee Health Science Center2, University of Alabama3, University of Chicago4, National Institutes of Health5, George Washington University6, Medical University of South Carolina7, Ohio State University8, University of Southern California9, University of Cincinnati10, Wake Forest University11, University of Oklahoma12
TL;DR: A double-blind, randomized, placebo-controlled trial in four groups of pregnant women at high risk for preeclampsia, including 471 women with pregestational insulin-treated diabetes mellitus, 774 women with chronic hypertension, 688 women with multifetal gestations, and 606 women who had had preeClampsia during a previous pregnancy finds aspirin may reduce the incidence of the disease in women athigh risk.
Abstract: Background Whether low-dose aspirin prevents preeclampsia is unclear. It is not recommended as prophylaxis in women at low risk for preeclampsia but may reduce the incidence of the disease in women at high risk. Methods We conducted a double-blind, randomized, placebo-controlled trial in four groups of pregnant women at high risk for preeclampsia, including 471 women with pregestational insulin-treated diabetes mellitus, 774 women with chronic hypertension, 688 women with multifetal gestations, and 606 women who had had preeclampsia during a previous pregnancy. The women were enrolled between gestational weeks 13 and 26 and received either 60 mg of aspirin or placebo daily. Results Outcome data were obtained on all but 36 of the 2539 women who entered the study. The incidence of preeclampsia was similar in the 1254 women in the aspirin group and the 1249 women in the placebo group (aspirin, 18 percent; placebo, 20 percent; P = 0.23). The incidences in the aspirin and placebo groups for each of the four hi...
561 citations
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TL;DR: It is shown that the tumour surveillance pathway mediated by Arf, MDM2, MDMX and p53 is activated after loss of RB1 during retinogenesis, providing evidence that the p53 pathway is inactivated in retinoblastoma and that this cancer does not originate from intrinsically death-resistant cells as previously thought.
Abstract: Most human tumours have genetic mutations in their Rb and p53 pathways, but retinoblastoma is thought to be an exception. Studies suggest that retinoblastomas, which initiate with mutations in the gene retinoblastoma 1 (RB1), bypass the p53 pathway because they arise from intrinsically death-resistant cells during retinal development. In contrast to this prevailing theory, here we show that the tumour surveillance pathway mediated by Arf, MDM2, MDMX and p53 is activated after loss of RB1 during retinogenesis. RB1-deficient retinoblasts undergo p53-mediated apoptosis and exit the cell cycle. Subsequently, amplification of the MDMX gene and increased expression of MDMX protein are strongly selected for during tumour progression as a mechanism to suppress the p53 response in RB1-deficient retinal cells. Our data provide evidence that the p53 pathway is inactivated in retinoblastoma and that this cancer does not originate from intrinsically death-resistant cells as previously thought. In addition, they support the idea that MDMX is a specific chemotherapeutic target for treating retinoblastoma.
560 citations
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TL;DR: The creation of a multifunctional surface can be achieved by co-sputtering the osteoconductive HA with antibacterial Ag with no significant difference in the in vitro cytotoxicty was observed between HA and Ag-HA surfaces.
557 citations
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VU University Medical Center1, Erasmus University Rotterdam2, National Institutes of Health3, Wake Forest University4, University of Pittsburgh5, University of Wisconsin-Madison6, University of Florida7, University of California, San Francisco8, University of Tennessee Health Science Center9, VU University Amsterdam10
TL;DR: TNF-alpha and its soluble receptors showed the most consistent associations with decline in muscle mass and strength, suggesting a weight-associated pathway for inflammation in sarcopenia.
Abstract: Background. There is growing evidence that higher levels of infl ammatory markers are associated with physical decline in older persons, possibly through the catabolic effects of infl ammatory markers on muscle. The aim of this study was to investigate the association between serum levels of infl ammatory markers and loss of muscle mass and strength in older persons. Methods. Using data on 2,177 men and women in the Health, Aging, and Body Composition Study, we examined 5-year change in thigh muscle area estimated by computed tomography and grip and knee extensor strength in relation to serum levels of interleukin-6 (IL-6), C-reactive protein, tumor necrosis factor-alpha (TNF- a ), and soluble receptors (measured in a subsample) at baseline. Results. Higher levels of infl ammatory markers were generally associated with greater 5-year decline in thigh muscle area. Most associations, with the exception of soluble receptors, were attenuated by adjustment for 5-year change in weight. Higher TNF- a and interleukin-6 soluble receptor levels remained associated with greater decline in grip strength in men. Analyses in a subgroup of weight-stable persons showed that higher levels of TNF- a and its soluble receptors were associated with 5-year decline in thigh muscle area and that higher levels of TNF- a were associated with decline in grip strength. Conclusions. TNF- a and its soluble receptors showed the most consistent associations with decline in muscle mass and strength. The results suggest a weight-associated pathway for infl ammation in sarcopenia.
557 citations
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TL;DR: The data demonstrate that molecular diagnostic approaches are invaluable in identifying clinically distinct subgroups, and that the AML1/CBF beta transcription complex is the most frequent target of chromosomal rearrangements in human leukemia.
Abstract: The t(12;21)(p13;q22) is identified by routine cytogenetics in less than 0.05% of pediatric acute lymphoblastic leukemia (ALL) patients. This translocation encodes a TEL/AML-1 chimeric product comprising the helix-loop-helix domain of TEL, a member of the ETS-like family of transcription factors, fused to AML-1, the DNA-binding subunit of the AML-1/CBF beta transcription factor complex. Both TEL and AML-1 are involved in several myeloid leukemia-associated translocations with AML-1/CBF beta being altered in 20-30% of de novo acute myeloid leukemia (AML) cases. We now demonstrate that a TEL/AML1 chimeric transcript encoded by a cryptic t(12;21) is observed in 22% of pediatric ALL, making it the most common genetic lesion in these patients. Moreover, TEL/AML1 expression defined a distinct subgroup of patients characterized by an age between 1 and 10 years, B lineage immunophenotype, non-hyperdiploid DNA content and an excellent prognosis. These data demonstrate that molecular diagnostic approaches are invaluable in identifying clinically distinct subgroups, and that the AML1/CBF beta transcription complex is the most frequent target of chromosomal rearrangements in human leukemia.
556 citations
Authors
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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 |