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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Scripps Research Institute1, La Jolla Institute for Allergy and Immunology2, Emory University3, Yerkes National Primate Research Center4, Massachusetts Institute of Technology5, Icahn School of Medicine at Mount Sinai6, University of Louisville7, University of California, San Diego8, Wistar Institute9, Karolinska Institutet10
TL;DR: It is found that two independent methods of slow delivery immunization of rhesus monkeys resulted in more robust T follicular helper (TFH) cell responses and GC B cells with improved Env-binding, tracked by longitudinal fine needle aspirates.
258 citations
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TL;DR: In this study, a screening method is used to identify that two miRNAs (miR-25 and miR-30d) directly target the 3′UTR of TP53 to downregulate p53 protein levels and reduce the expression of genes that are transcriptionally activated by p53.
Abstract: The tumor suppressor p53, encoded by the TP53 gene, is recognized as the guardian of the human genome because it regulates many downstream genes to exercise its function in cell cycle and cell death. Recent studies have revealed that several microRNAs (miRNAs) are important components of the p53 tumor suppressor network with miR-125b and miR-504 directly targeting TP53. In this study, we use a screening method to identify that two miRNAs (miR-25 and miR-30d) directly target the 3'UTR of TP53 to downregulate p53 protein levels and reduce the expression of genes that are transcriptionally activated by p53. Correspondingly, both miR-25 and miR-30d adversely affect apoptotic cell death, cell cycle arrest and cellular senescence. Inhibition of either miR-25 or miR-30d expression increases endogenous p53 expression and elevates cellular apoptosis in several cell lines, including one from multiple myeloma that has little TP53 mutations. Thus, beyond miR-125b and miR-504, the human TP53 gene is negatively regulated by two more miRNAs: miR-25 and miR-30d.
258 citations
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Columbia University1, Rutgers University2, Argonne National Laboratory3, University College London4, McGill University5, Harvard University6, Brown University7, University of Manchester8, University of California, Davis9, University of Washington10, Stanford University11, Stony Brook University12, Princeton University13, University of Florida14, SLAC National Accelerator Laboratory15, University of Wisconsin-Madison16, Fermilab17, University of Oregon18, Massachusetts Institute of Technology19, KAIST20, University of Arizona21, Johns Hopkins University22, Heidelberg University23, New York University24, University of Mississippi25, Texas A&M University26, Centre national de la recherche scientifique27, CERN28, University of Göttingen29, Syracuse University30, University of Toronto31, Yale University32, Durham University33, Boston University34, University of California, Berkeley35, University of Louisville36, Spanish National Research Council37, University of Chicago38
TL;DR: In this article, the status of and outlook for calculation and simulation tools for studying jet substructure is reviewed and a new set of benchmark comparisons of substructure techniques, focusing on the set of variables and grooming methods are presented.
Abstract: In this paper, we review recent theoretical progress and the latest experimental results in jet substructure from the Tevatron and the LHC. We review the status of and outlook for calculation and simulation tools for studying jet substructure. Following up on the report of the Boost 2010 workshop, we present a new set of benchmark comparisons of substructure techniques, focusing on the set of variables and grooming methods that are collectively known as ‘top taggers’. To facilitate further exploration, we have attempted to collect, harmonize and publish software implementations of these techniques.
257 citations
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TL;DR: This work presents a series of models in which altruism is a continuously varying trait and individuals are free to choose their associates, based on information that is acquired through experience, observation, or cultural transmission, favoring the evolution of altruism and other group-level adaptations among genealogically unrelated individuals.
Abstract: Natural selection at all levels requires heritable phenotypic variation among units. At the group level, variation is often increased by reproduction coupled with limited dispersal, which forms the basis of kin selection and traditional group selection models. Assortative interactions are another possible mechanism for creating variation among groups that has received less attention. We present a series of models in which altruism is a continuously varying trait and individuals are free to choose their associates, based on information that is acquired through experience, observation, or cultural transmission. Assortative interactions can generate highly nonrandom variation among groups, favoring the evolution of altruism and other group-level adaptations among genealogically unrelated individuals. Altruism can evolve even when the initial phenotypic variation in altruism is not heritable, a form of genetic assimilation. The importance of assortative interactions depends in part on cognitive abilities that...
257 citations
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TL;DR: Tobacco smoke compromises the anti-bacterial function of leukocytes, including neutrophils, monocytes, T cells and B cells, providing a mechanistic explanation for increased infection risk.
Abstract: Active smokers and those exposed to secondhand smoke are at increased risk of bacterial infection. Tobacco smoke exposure increases susceptibility to respiratory tract infections, including tuberculosis, pneumonia and Legionnaires disease; bacterial vaginosis and sexually transmitted diseases, such as chlamydia and gonorrhoea; Helicobacter pylori infection; periodontitis; meningitis; otitis media; and post-surgical and nosocomial infections. Tobacco smoke compromises the anti-bacterial function of leukocytes, including neutrophils, monocytes, T cells and B cells, providing a mechanistic explanation for increased infection risk. Further epidemiological, clinical and mechanistic research into this important area is warranted.
257 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 |