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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TL;DR: In this study, in vivo evidence for a late phase of Olig gene expression independent of Nkx6 and Shh gene activities is provided and a brief second wave of oligodendrogenesis in the dorsal spinal cord is revealed.
333 citations
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TL;DR: It is demonstrated that a piRNA-induced silencing complex (pi-RISC) containing murine PIWI and deadenylase CAF1 is selectively assembled in ES, which is responsible for inducing mRNAdeadenylation and decay via a mechanism that resembles the action of miRNAs in somatic cells.
Abstract: Spermatogenesis in mammals is characterized by two waves of piRNA expression: one corresponds to classic piRNAs responsible for silencing retrotransponsons and the second wave is predominantly derived from nontransposon intergenic regions in pachytene spermatocytes, but the function of these pachytene piRNAs is largely unknown. Here, we report the involvement of pachytene piRNAs in instructing massive mRNA elimination in mouse elongating spermatids (ES). We demonstrate that a piRNA-induced silencing complex (pi-RISC) containing murine PIWI (MIWI) and deadenylase CAF1 is selectively assembled in ES, which is responsible for inducing mRNA deadenylation and decay via a mechanism that resembles the action of miRNAs in somatic cells. Such a highly orchestrated program appears to take full advantage of the enormous repertoire of diversified targeting capacity of pachytene piRNAs derived from nontransposon intergenic regions. These findings suggest that pachytene piRNAs are responsible for inactivating vast cellular programs in preparation for sperm production from ES.
333 citations
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TL;DR: Recent developments in the understanding of the immediate traumatic and subsequent secondary degeneration of local tissue and long projecting pathways in animal models and the still limited understanding ofThe neuropathology in humans is discussed, including the reduced glial scarring, inflammation and demyelination, the increased Schwannosis and the protracted Wallerian degeneration in humans.
Abstract: Spinal cord injury results in acute as well as progressive secondary destruction of local and distant nervous tissue through a number of degenerative mechanisms. Spinal cord injury also initiates a number of endogenous neuroprotective and regenerative responses. Understanding of these mechanisms might identify potential targets for treatments after spinal cord injury in humans. Here, we first discuss recent developments in our understanding of the immediate traumatic and subsequent secondary degeneration of local tissue and long projecting pathways in animal models. These include the inflammatory and vascular responses during the acute phase, as well as cell death, demyelination and scar formation in the subacute and chronic phases. Secondly, we discuss the spontaneous axonal regeneration of injured and plasticity of uninjured systems, and other repair-related responses in animals, including the upregulation of regeneration-associated genes in some neurons, increases in neurotrophic factors in the spinal cord and remyelination by oligodendrocyte precursors and invading Schwann cells. Lastly, we comment on the still limited understanding of the neuropathology in humans, which is largely similar to that in rodents. However, there also are potentially important differences, including the reduced glial scarring, inflammation and demyelination, the increased Schwannosis and the protracted Wallerian degeneration in humans. The validity of current rodent models for human spinal cord injury is also discussed. The emphasis of this review is on the literature from 2002 to early 2005.
332 citations
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TL;DR: Clinicians should use timely epidemiologic data to ascertain if influenza is circulating in their communities, then either treat patients with influenza-like illness empirically or obtain a rapid influenza test to assist with management decisions.
Abstract: ContextInfluenza vaccination lowers, but does not eliminate, the risk of influenza.
Making a reliable, rapid clinical diagnosis is essential to appropriate patient
management that may be especially important during shortages of antiviral
agents caused by high demand.ObjectivesTo systematically review the precision and accuracy of symptoms and
signs of influenza. A secondary objective was to review the operating characteristics
of rapid diagnostic tests for influenza (results available in <30 min).Data SourcesStructured search strategy using MEDLINE (January 1966-September 2004)
and subsequent searches of bibliographies of retrieved articles to identify
articles describing primary studies dealing with the diagnosis of influenza
based on clinical signs and symptoms. The MEDLINE search used the Medical
Subject Headings EXP influenza or EXP influenza A virus or EXP influenza A virus human or EXP influenza B virus and the Medical
Subject Headings or terms EXP sensitivity and specificity or EXP medical history taking or EXP physical examination or EXP reproducibility of
results or EXP observer variation or symptoms.mp or clinical signs.mp or sensitivity.mp or specificity.mp.Study SelectionOf 915 identified articles on clinical assessment of influenza-related
illness, 17 contained data on the operating characteristics of symptoms and
signs using an independent criterion standard. Of these, 11 were eliminated
based on 4 inclusion criteria and availability of nonduplicative primary data.Data ExtractionTwo authors independently reviewed and abstracted data for estimating
the likelihood ratios (LRs) of clinical diagnostic findings. Differences were
resolved by discussion and consensus.Data SynthesisNo symptom or sign had a summary LR greater than 2 in studies that enrolled
patients without regard to age. For decreasing the likelihood of influenza,
the absence of fever (LR, 0.40; 95% confidence interval [CI], 0.25-0.66),
cough (LR, 0.42; 95% CI, 0.31-0.57), or nasal congestion (LR, 0.49; 95% CI,
0.42-0.59) were the only findings that had summary LRs less than 0.5. In studies
limited to patients aged 60 years or older, the combination of fever, cough,
and acute onset (LR, 5.4; 95% CI, 3.8-7.7), fever and cough (LR, 5.0; 95%
CI, 3.5-6.9), fever alone (LR, 3.8; 95% CI, 2.8-5.0), malaise (LR, 2.6; 95%
CI, 2.2-3.1), and chills (LR, 2.6; 95% CI, 2.0-3.2) increased the likelihood
of influenza to the greatest degree. The presence of sneezing among older
patients made influenza less likely (LR, 0.47; 95% CI, 0.24-0.92).ConclusionsClinical findings identify patients with influenza-like illness but
are not particularly useful for confirming or excluding the diagnosis of influenza.
Clinicians should use timely epidemiologic data to ascertain if influenza
is circulating in their communities, then either treat patients with influenza-like
illness empirically or obtain a rapid influenza test to assist with management
decisions.
332 citations
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TL;DR: The effect of the environment on inbreeding depression scales linearly with the magnitude of stress; a population suffers one additional lethal equivalent, on average, for each 30% reduction in fitness induced by the stressful environment.
Abstract: Inbreeding–environment interactions occur when inbreeding leads to differential fitness loss in different environments. Inbred individuals are often more sensitive to environmental stress than are outbred individuals, presumably because stress increases the expression of deleterious recessive alleles or cellular safeguards against stress are pushed beyond the organism's physiological limits. We examined inbreeding–environment interactions, along two environmental axes (temperature and rearing host) that differ in the amount of developmental stress they impose, in the seed-feeding beetle Callosobruchus maculatus. We found that inbreeding depression (inbreeding load, L) increased with the stressfulness of the environment, with the magnitude of stress explaining as much as 66% of the variation in inbreeding depression. This relationship between L and developmental stress was not explainable by an increase in phenotypic variation in more stressful environments. To examine the generality of this experimental result, we conducted a meta-analysis of the available data from published studies looking at stress and inbreeding depression. The meta-analysis confirmed that the effect of the environment on inbreeding depression scales linearly with the magnitude of stress; a population suffers one additional lethal equivalent, on average, for each 30% reduction in fitness induced by the stressful environment. Studies using less-stressful environments may lack statistical power to detect the small changes in inbreeding depression. That the magnitude of inbreeding depression scales with the magnitude of the stress applied has numerous repercussions for evolutionary and conservation genetics and may invigorate research aimed at finding the causal mechanism involved in such a relationship.
331 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 |