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Institution

University of Tennessee Health Science Center

EducationMemphis, 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
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Journal ArticleDOI
TL;DR: It is suggested that hypocaloric enteral nutrition support is as least as effective as eucaloric feeding in critically ill, obese patients.

255 citations

Journal ArticleDOI
TL;DR: This work generates HAs with site-specific mutations of a human virus that contain different amino acid residues at these positions of hemagglutinin of the H3 subtype, and shows that the Ser-to-Gly mutation at position 228, in addition to the Leu- to-Gln mutation at location 226, is critical for human virus HA to support virus replication in duck intestine.
Abstract: Influenza A viruses can be isolated from a variety of animals, but their range of hosts is restricted For example, human influenza viruses do not replicate in duck intestine, the major replication site of avian viruses in ducks Although amino acids at positions 226 and 228 of hemagglutinin (HA) of the H3 subtype are known to be important for this host range restriction, the contributions of specific amino acids at these positions to restriction were not known Here, we address this issue by generating HAs with site-specific mutations of a human virus that contain different amino acid residues at these positions We also let ducks select replication-competent viruses from a replication-incompetent virus containing a human virus HA by inoculating animals with 10105 50% egg infectious dose of the latter virus and identified a mutation in the HA Our results showed that the Ser-to-Gly mutation at position 228, in addition to the Leu-to-Gln mutation at position 226 of the HA of the H3 subtype, is critical for human virus HA to support virus replication in duck intestine

255 citations

Journal ArticleDOI
TL;DR: Data from this well-functioning cohort are consistent with a shared pathology underlying cognitive and motor declines but do not suggest that specific executive cognitive deficits account for slowing of usual gait in aging.
Abstract: Background. In community-dwelling older adults, global cognitive function predicts longitudinal gait speed decline. Few prospective studies have evaluated whether specific executive cognitive deficits in aging may account for gait slowing over time.

255 citations

Journal ArticleDOI
TL;DR: The eighth edition of the American Joint Committee on Cancer (AJCC) tumor-nodemetastasis (TNM) staging manual has been updated and improved to ensure the highest degree of clinical relevance and to improve its utility for patient evaluation and clinical research as mentioned in this paper.
Abstract: Answer questions and earn CME/CNE The eighth edition of the American Joint Committee on Cancer (AJCC) tumor-node-metastasis (TNM) Staging Manual has been updated and improved to ensure the highest degree of clinical relevance and to improve its utility for patient evaluation and clinical research. Major changes include: 1) pathologically organ-confined disease is now considered pT2 and is no longer subclassified by extent of involvement or laterality, 2) tumor grading now includes both the Gleason score (as in the seventh edition criteria) and the grade group (introduced in the eighth edition criteria), 3) prognostic stage group III includes select, organ-confined disease based on prostate-specific antigen and Gleason/grade group status, and 4) 2 statistical prediction models are included in the staging manual. The AJCC will continue to critically analyze emerging prostate cancer biomarkers and tools for their ability to prognosticate and guide treatment decision making with the highest level of accuracy and confidence for patients and physicians. CA Cancer J Clin 2017;67:245-253. © 2017 American Cancer Society.

254 citations

Journal ArticleDOI
TL;DR: It is demonstrated that the neonatal mouse cochlea is capable of spontaneous hair cell regeneration after damage in vivo, which might shed light on the competence of supporting cells to regenerate hair cells and on the factors that promote the survival of newly regenerated hair cells.
Abstract: Loss of cochlear hair cells in mammals is currently believed to be permanent, resulting in hearing impairment that affects more than 10% of the population. Here, we developed two genetic strategies to ablate neonatal mouse cochlear hair cells in vivo. Both Pou4f3 DTR/+ and Atoh1-CreER TM ; ROSA26 DTA/+ alleles allowed selective and inducible hair cell ablation. After hair cell loss was induced at birth, we observed spontaneous regeneration of hair cells. Fate-mapping experiments demonstrated that neighboring supporting cells acquired a hair cell fate, which increased in a basal to apical gradient, averaging over 120 regenerated hair cells per cochlea. The normally mitotically quiescent supporting cells proliferated after hair cell ablation. Concurrent fate mapping and labeling with mitotic tracers showed that regenerated hair cells were derived by both mitotic regeneration and direct transdifferentiation. Over time, regenerated hair cells followed a similar pattern of maturation to normal hair cell development, including the expression of prestin, a terminal differentiation marker of outer hair cells, although many new hair cells eventually died. Hair cell regeneration did not occur when ablation was induced at one week of age. Our findings demonstrate that the neonatal mouse cochlea is capable of spontaneous hair cell regeneration after damage in vivo. Thus, future studies on the neonatal cochlea might shed light on the competence of supporting cells to regenerate hair cells and on the factors that promote the survival of newly regenerated hair cells.

254 citations


Authors

Showing all 15827 results

NameH-indexPapersCitations
George P. Chrousos1691612120752
Steven N. Blair165879132929
Bruce L. Miller1631153115975
Ralph A. DeFronzo160759132993
Frank J. Gonzalez160114496971
Robert G. Webster15884390776
Anne B. Newman15090299255
Ching-Hon Pui14580572146
Barton F. Haynes14491179014
Yoshihiro Kawaoka13988375087
Seth M. Steinberg13793680148
Richard J. Johnson13788072201
Kristine Yaffe13679472250
Leslie L. Robison13185464373
Gerardo Heiss12862369393
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202338
2022195
20211,699
20201,503
20191,401
20181,292