Institution
University of North Texas Health Science Center
Education•Fort Worth, Texas, United States•
About: University of North Texas Health Science Center is a education organization based out in Fort Worth, Texas, United States. It is known for research contribution in the topics: Population & Receptor. The organization has 2972 authors who have published 5401 publications receiving 153180 citations. The organization is also known as: UNT Health Science Center & UNTHSC.
Topics: Population, Receptor, Health care, Neuroprotection, Cancer
Papers published on a yearly basis
Papers
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TL;DR: Aerobic exercise training augments the intermediary metabolic capacity of canine myocardium by selectively increasing the concentrations of regulatory enzymes of glycolysis and oxidative metabolism.
56 citations
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TL;DR: The data suggest that post-exercise hypotension may be the mechanism for a gain of intravascular albumin via the lymph return, which enhances plasma water retention and PV restoration during recovery from exercise induced hypovolaemia, even without rehydration.
Abstract: The aim of this study was to test the hypothesis that post-exercise hypotension was the mechanism for the plasma volume and albumin gain during recovery. Seven healthy young men completed two experiments (> or =1 week apart) to exercise continuously at 65% of peak aerobic capacity for 60 min followed by the recovery without (experiment 1) or with phenylephrine infusion (experiment 2) to counteract post-exercise hypotension. Heart rate, arterial pressure (Finapres), plasma volume (PV, Evans blue dye dilution), haematocrit, haemoglobin, plasma total solutes (refractometer), albumin, total proteins (colorimetric method), [Na+] and [K+] were not different prior to the experiments. Exercise decreased PV -13.7% (-521 mL) and -14.2% (-566 mL) at the end of 60 min in experiments 1 and 2, respectively, associated with increases in the concentrations of plasma albumin, total protein and solutes. These changes were similar between the two experiments. Following 30 min recovery in experiment 1 the decreased PV was not significantly different from the baseline. Although the volume restoration was complete at the end of 90 min recovery, the change in the albumin concentration was still above zero, indicating a gain of 11 g albumin (P < 0.05). When phenylephrine was infused during recovery, there was no gain in intravascular albumin associated with a sustained decrease in PV (-7% or -280 mL, P < 0.05) observed at the end of experiment 2. These data suggest that post-exercise hypotension may be the mechanism for a gain of intravascular albumin via the lymph return, which enhances plasma water retention and PV restoration during recovery from exercise induced hypovolaemia, even without rehydration.
56 citations
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TL;DR: It is found that the emission of BSA Au clusters can be enhanced by a magnitude of two-fold by resonance energy transfer (RET) from the high extinction donor PB, and BSA au clusters can act as an acceptor to nanosecond lifetime organic dyes.
Abstract: Bovine serum albumin (BSA) protected nanoclusters (Au and Ag) represent a group of nanomaterials that holds great promise in biophysical applications due to their unique fluorescence properties and lack of toxicity. These metal nanoclusters have utility in a variety of disciplines including catalysis, biosensing, photonics, imaging and molecular electronics. However, they suffer from several disadvantages such as low fluorescence quantum efficiency (typically near 6%) and broad emission spectrum (540 nm to 800 nm). We describe an approach to enhance the apparent brightness of BSA Au clusters by linking them with a high extinction donor organic dye pacific blue (PB). In this conjugate PB acts as a donor to BSA Au clusters and enhances its brightness by resonance energy transfer (RET). We found that the emission of BSA Au clusters can be enhanced by a magnitude of two-fold by resonance energy transfer (RET) from the high extinction donor PB, and BSA Au clusters can act as an acceptor to nanosecond lifetime organic dyes. By pumping the BSA Au clusters using a high extinction donor, one can increase the effective brightness of less bright fluorophores like BSA Au clusters. Moreover, we prepared another conjugate of BSA Au clusters with the near infrared (NIR) dye Dylight 750 (Dy750), where BSA Au clusters act as a donor to Dy750. We observed that BSA Au clusters can function as a donor, showing 46% transfer efficiency to the NIR dye Dy750 with a long lifetime component in the acceptor decay through RET. Such RET-based probes can be used to prevent the problems of a broad emission spectrum associated with the BSA Au clusters. Moreover, transferring energy from BSA Au clusters to Dy750 will result in a RET probe with a narrow emission spectrum and long lifetime component which can be utilized in imaging applications.
56 citations
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TL;DR: While oligomeric Aβ directly down-regulates MMP2 expression and activation in astrocytes, it induces production of proinflammatory cytokines which could serve as strong stimulators for M MP2.
56 citations
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31 Dec 2012TL;DR: Finding the remaining genetic factors that contribute to the development of late onset Alzheimer's disease holds the potential to provide novel targets for treatment and prevention, leading to thedevelopment of effective strategies to combat this devastating disease.
Abstract: Alzheimer's disease is a progressive, neurodegenerative disease that represents a growing global health crisis. Two major forms of the disease exist: early onset (familial) and late onset (sporadic). Early onset Alzheimer's is rare, accounting for less than 5% of disease burden. It is inherited in Mendelian dominant fashion and is caused by mutations in three genes (APP, PSEN1, and PSEN2). Late onset Alzheimer's is common among individuals over 65 years of age. Heritability of this form of the disease is high (79%), but the etiology is driven by a combination of genetic and environmental factors. A large number of genes have been implicated in the development of late onset Alzheimer's. Examples that have been confirmed by multiple studies include ABCA7, APOE, BIN1, CD2AP, CD33, CLU, CR1, EPHA1, MS4A4A/MS4A4E/MS4A6E, PICALM, and SORL1. Despite tremendous progress over the past three decades, roughly half of the heritability for the late onset of the disease remains unidentified. Finding the remaining genetic factors that contribute to the development of late onset Alzheimer's disease holds the potential to provide novel targets for treatment and prevention, leading to the development of effective strategies to combat this devastating disease.
56 citations
Authors
Showing all 3001 results
Name | H-index | Papers | Citations |
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John T. Potts | 90 | 359 | 29359 |
Evan A. Stein | 80 | 340 | 36392 |
James W. Simpkins | 79 | 431 | 20574 |
Robert J. Gatchel | 79 | 494 | 25583 |
Douglas B. Cines | 79 | 397 | 27792 |
Ranajit Chakraborty | 77 | 407 | 25474 |
Kunlin Jin | 75 | 258 | 23282 |
Bruce Budowle | 70 | 613 | 20227 |
Lisa L. Barnes | 69 | 280 | 20190 |
Abbot F. Clark | 65 | 297 | 13938 |
Yong Fang Kuo | 65 | 447 | 14938 |
Alexander C. Wagenaar | 63 | 241 | 13661 |
David P. Siderovski | 62 | 180 | 19698 |
Yogesh C. Awasthi | 61 | 254 | 12304 |
Ignacy Gryczynski | 61 | 545 | 16705 |