Institution
University of Louisville
Education•Louisville, Kentucky, United States•
About: University of Louisville is a education organization based out in Louisville, Kentucky, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 24600 authors who have published 49248 publications receiving 1573346 citations. The organization is also known as: UofL.
Topics: Population, Poison control, Transplantation, Stem cell, Breast cancer
Papers published on a yearly basis
Papers
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Columbia University1, University of Miami2, University of Florida3, Washington University in St. Louis4, University of California, Los Angeles5, Harvard University6, NewYork–Presbyterian Hospital7, University of Louisville8, Cleveland Clinic9, Hospital of the University of Pennsylvania10, University of Arizona11, University of Pittsburgh12, Hackensack University Medical Center13, Schering-Plough14, University of York15
TL;DR: These four histological lesions are useful pathological parameters in the diagnosis of liver disease caused by HCV and are likely to be seen in HCV than in HBV infection.
362 citations
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TL;DR: This report presents a simple and generic concept involving metal nanoclusters supported on metal oxide nanowires as stable and high capacity anode materials for Li-ion batteries, which exhibited an exceptional capacity over hundred cycles with a low capacity fading of less than 1% per cycle.
Abstract: In this report, we present a simple and generic concept involving metal nanoclusters supported on metal oxide nanowires as stable and high capacity anode materials for Li-ion batteries. Specifically, SnO(2) nanowires covered with Sn nanoclusters exhibited an exceptional capacity of >800 mAhg(-1) over hundred cycles with a low capacity fading of less than 1% per cycle. Post lithiation analyses after 100 cycles show little morphological degradation of the hybrid nanowires. The observed, enhanced stability with high capacity retention is explained with the following: (a) the spacing between Sn nanoclusters on SnO(2) nanowires allowed the volume expansion during Li alloying and dealloying; (b) high available surface area of Sn nanoclusters for Li alloying and dealloying; and (c) the presence of Sn nanoclusters on SnO(2) allowed reversible reaction between Sn and Li(2)O to produce both Sn and SnO phases.
361 citations
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TL;DR: It appears that adrenergic and renin-angiotensin system overactivity contributes to the early chronic elevated blood pressure in rat intermittent hypoxia and perhaps to human hypertension associated with obstructive sleep apnea.
Abstract: One of the major manifestations of obstructive sleep apnea is profound and repeated hypoxia during sleep. Acute hypoxia leads to stimulation of the peripheral chemoreceptors, which in turn increases sympathetic outflow, acutely increasing blood pressure. The chronic effect of these repeated episodic or intermittent periods of hypoxia in humans is difficult to study because chronic cardiovascular changes may take many years to manifest. Rodents have been a tremendous source of information in short- and long-term studies of hypertension and other cardiovascular diseases. Recurrent short cycles of normoxia-hypoxia, when administered to rats for 35 days, allows examination of the chronic cardiovascular response to intermittent hypoxia patterned after the episodic desaturation seen in humans with sleep apnea. The result of this type of intermittent hypoxia in rats is a 10- to 14-mmHg increase in resting (unstimulated) mean blood pressure that lasts for several weeks after cessation of the daily cyclic hypoxia. Carotid body denervation, sympathetic nerve ablation, renal sympathectomy, adrenal medullectomy, and angiotensin II receptor blockade block the blood pressure increase. It appears that adrenergic and renin-angiotensin system overactivity contributes to the early chronic elevated blood pressure in rat intermittent hypoxia and perhaps to human hypertension associated with obstructive sleep apnea.
361 citations
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TL;DR: This review focuses on cellular and molecular aspects of lung inflammation during acute and chronic inflammatory states, which include infection, trauma, and hypersensitivity.
Abstract: Inflammation is the body's response to insults, which include infection, trauma, and hypersensitivity. The inflammatory response is complex and involves a variety of mechanisms to defend against pathogens and repair tissue. In the lung, inflammation is usually caused by pathogens or by exposure to toxins, pollutants, irritants, and allergens. During inflammation, numerous types of inflammatory cells are activated. Each releases cytokines and mediators to modify activities of other inflammatory cells. Orchestration of these cells and molecules leads to progression of inflammation. Clinically, acute inflammation is seen in pneumonia and acute respiratory distress syndrome (ARDS), whereas chronic inflammation is represented by asthma and chronic obstructive pulmonary disease (COPD). Because the lung is a vital organ for gas exchange, excessive inflammation can be life threatening. Because the lung is constantly exposed to harmful pathogens, an immediate and intense defense action (mainly inflammation) is required to eliminate the invaders as early as possible. A delicate balance between inflammation and anti-inflammation is essential for lung homeostasis. A full understanding of the underlying mechanisms is vital in the treatment of patients with lung inflammation. This review focuses on cellular and molecular aspects of lung inflammation during acute and chronic inflammatory states.
360 citations
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TL;DR: Evidence is reviewed that the failure of resolution programs contributes to metabolic diseases and that SPMs may play pivotal roles in their resolution, and specialized proresolving lipid mediators (SPMs) are novel autacoids that resolve inflammation, protect organs, and stimulate tissue regeneration.
360 citations
Authors
Showing all 24802 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert M. Califf | 196 | 1561 | 167961 |
Aaron R. Folsom | 181 | 1118 | 134044 |
Yang Gao | 168 | 2047 | 146301 |
Stephen J. O'Brien | 153 | 1062 | 93025 |
James J. Collins | 151 | 669 | 89476 |
Anthony E. Lang | 149 | 1028 | 95630 |
Sw. Banerjee | 146 | 1906 | 124364 |
Hermann Kolanoski | 145 | 1279 | 96152 |
Ferenc A. Jolesz | 143 | 631 | 66198 |
Daniel S. Berman | 141 | 1363 | 86136 |
Aaron T. Beck | 139 | 536 | 170816 |
Kevin J. Tracey | 138 | 561 | 82791 |
C. Dallapiccola | 136 | 1717 | 101947 |
Michael I. Posner | 134 | 414 | 104201 |
Alan Sher | 132 | 486 | 68128 |