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
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Mayo Clinic1, Yale University2, Johns Hopkins University3, Rhode Island Hospital4, University of North Carolina at Chapel Hill5, Medical College of Wisconsin6, Cleveland Clinic7, Beaumont Health8, Dartmouth College9, University of Louisville10, Tufts University11, NorthShore University HealthSystem12, Rutgers University13
TL;DR: This document, developed by experts in laboratory and adult and pediatric clinical medicine, provides information on which tests are valuable and in which contexts, and on tests that add little or no value for diagnostic decisions.
Abstract: The critical nature of the microbiology laboratory in infectious disease diagnosis calls for a close, positive working relationship between the physician/advanced practice provider and the microbiologists who provide enormous value to the healthcare team. This document, developed by experts in laboratory and adult and pediatric clinical medicine, provides information on which tests are valuable and in which contexts, and on tests that add little or no value for diagnostic decisions. This document presents a system-based approach rather than specimen-based approach, and includes bloodstream and cardiovascular system infections, central nervous system infections, ocular infections, soft tissue infections of the head and neck, upper and lower respiratory infections, infections of the gastrointestinal tract, intra-abdominal infections, bone and joint infections, urinary tract infections, genital infections, and other skin and soft tissue infections; or into etiologic agent groups, including arthropod-borne infections, viral syndromes, and blood and tissue parasite infections. Each section contains introductory concepts, a summary of key points, and detailed tables that list suspected agents; the most reliable tests to order; the samples (and volumes) to collect in order of preference; specimen transport devices, procedures, times, and temperatures; and detailed notes on specific issues regarding the test methods, such as when tests are likely to require a specialized laboratory or have prolonged turnaround times. In addition, the pediatric needs of specimen management are also emphasized. There is intentional redundancy among the tables and sections, as many agents and assay choices overlap. The document is intended to serve as a guidance for physicians in choosing tests that will aid them to quickly and accurately diagnose infectious diseases in their patients.
345 citations
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Université de Montréal1, University of Texas MD Anderson Cancer Center2, Wayne State University3, University of Louisville4, Christiana Care Health System5, Fox Chase Cancer Center6, Medical College of Wisconsin7, Johns Hopkins University8, University of California, San Francisco9, Ohio State University10, University of Chicago11, Stanford University12
TL;DR: Long-term high survival rates in p16-positive patients with oropharyngeal cancer support the ongoing efforts to explore deintensification and neither improved outcome nor increased late toxicity in patients with LA-HNC when combined with cisplatin.
Abstract: Purpose We tested the efficacy and toxicity of cisplatin plus accelerated fractionation with a concomitant boost (AFX-C) versus standard fractionation (SFX) in locally advanced head and neck carcinoma (LA-HNC). Patients and Methods Patients had stage III to IV carcinoma of the oral cavity, oropharynx, hypopharynx, or larynx. Radiation therapy schedules were 70 Gy in 35 fractions over 7 weeks (SFX) or 72 Gy in 42 fractions over 6 weeks (AFX-C). Cisplatin doses were 100 mg/m 2 once every 3 weeks for two (AFX-C) or three (SFX) cycles. Toxicities were scored by using National Cancer Institute Common Toxicity Criteria 2.0 and the Radiation Therapy Oncology Group/European Organisation for Research and Treatment of Cancer criteria. Overall survival (OS) and progression-free survival (PFS) rates were estimated by using the Kaplan-Meier method and were compared by using the one-sided log-rank test. Locoregional failure (LRF) and distant metastasis (DM) rates were estimated by using the cumulative incidence method and Gray’s test. Results In all, 721 of 743 patients were analyzable (361, SFX; 360, AFX-C). At a median follow-up of 7.9 years (range, 0.3 to 10.1 years) for 355 surviving patients, no differences were observed in OS (hazard ratio [HR], 0.96; 95% CI, 0.79 to 1.18; P .37; 8-year survival, 48% v 48%), PFS (HR, 1.02; 95% CI, 0.84 to 1.24; P .52; 8-year estimate, 42% v 41%), LRF (HR, 1.08; 95% CI, 0.84 to 1.38; P .78; 8-year estimate, 37% v 39%), or DM (HR, 0.83; 95% CI, 0.56 to 1.24; P .16; 8-year estimate, 15% v 13%). For oropharyngeal cancer, p16-positive patients had better OS than p16-negative patients (HR, 0.30; 95% CI, 0.21 to 0.42; P .001; 8-year survival, 70.9% v 30.2%). There were no statistically significant differences in the grade 3 to 5 acute or late toxicities between the two arms and p-16 status. Conclusion When combined with cisplatin, AFX-C neither improved outcome nor increased late toxicity in patients with LA-HNC. Long-term high survival rates in p16-positive patients with oropharyngeal cancer support the ongoing efforts to explore deintensification. J Clin Oncol 32:3858-3867. © 2014 by American Society of Clinical Oncology
345 citations
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TL;DR: There is evidence to suggest that continuously high levels of exercise (e.g., marathon running) could have detrimental effects on cardiovascular health and further studies are needed to identify the mechanisms that impart cardiovascular benefits of exercise in order to develop more effective exercise regimens.
Abstract: It is widely accepted that regular physical activity is beneficial for cardiovascular health. Frequent exercise is robustly associated with a decrease in cardiovascular mortality as well as the risk of developing cardiovascular disease. Physically active individuals have lower blood pressure, higher insulin sensitivity, and a more favorable plasma lipoprotein profile. Animal models of exercise show that repeated physical activity suppresses atherogenesis and increases the availability of vasodilatory mediators such as nitric oxide. Exercise has also been found to have beneficial effects on the heart. Acutely, exercise increases cardiac output and blood pressure, but individuals adapted to exercise show lower resting heart rate and cardiac hypertrophy. Both cardiac and vascular changes have been linked to a variety of changes in tissue metabolism and signaling, although our understanding of the contribution of the underlying mechanisms remains incomplete. Even though moderate levels of exercise have been found to be consistently associated with a reduction in cardiovascular disease risk, there is evidence to suggest that continuously high levels of exercise (e.g., marathon running) could have detrimental effects on cardiovascular health. Nevertheless, a specific dose response relationship between the extent and duration of exercise and the reduction in cardiovascular disease risk and mortality remains unclear. Further studies are needed to identify the mechanisms that impart cardiovascular benefits of exercise in order to develop more effective exercise regimens, test the interaction of exercise with diet, and develop pharmacological interventions for those unwilling or unable to exercise.
345 citations
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TL;DR: The results provide strong support for the hypothesis that Abeta is neurotoxic in vivo and that such toxicity is mediated by free radicals and validate the transgenic approach for the study of oxidative stress in AD and for the evaluation of antioxidant therapies in vivo.
Abstract: Increased expression of antioxidant enzymes and heat-shock proteins are key markers of oxidative stress Such proteins are abnormally present within the neuropathological lesions of Alzheimer's disease (AD), suggesting that oxidative stress may play significant but yet undefined roles in this disorder To gain further insight into the role of oxidative stress in AD, we studied the expression of CuZn superoxide dismutase (SOD) and hemoxygenase-1 (HO-1), two established markers of oxidative stress, in a transgenic mouse model of AD Immunohistochemistry with anti-SOD and anti-HO-1 antibodies revealed a very pronounced increase of these proteins only in aged transgene-positive mice Interestingly, the distribution of the oxidative burden was largely overlapping with dystrophic neuritic elements in the mice as highlighted with anti-ubiquitin antibodies Because the most conspicuous alterations were identified around amyloid (Abeta) deposits, our results provide strong support for the hypothesis that Abeta is neurotoxic in vivo and that such toxicity is mediated by free radicals To obtain additional experimental evidence for such an interpretation (ie, a cause-effect relationship between Abeta and oxidative neurotoxicity), PC12 cells were exposed to increasing concentrations of Abeta or to oxidative stress In agreement with the in vivo findings, either treatment caused marked induction of SOD or HO-1 in a dose-dependent fashion These results validate the transgenic approach for the study of oxidative stress in AD and for the evaluation of antioxidant therapies in vivo
345 citations
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TL;DR: In this paper, the role of aP2 in macrophage biology and the molecular mechanisms underlying its actions was investigated, and it was shown that aP 2-deficient macrophages display defects in cholesterol accumulation and alterations in pro-inflammatory responsiveness, leading to elevated CD36 expression and enhanced uptake of modified low denwsity lipoprotein.
345 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 |