Institution
University of Kentucky
Education•Lexington, Kentucky, United States•
About: University of Kentucky is a education organization based out in Lexington, Kentucky, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 43933 authors who have published 92195 publications receiving 3256087 citations. The organization is also known as: UK.
Topics: Population, Poison control, Health care, Gene, Cancer
Papers published on a yearly basis
Papers
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B. I. Abelev1, Madan M. Aggarwal2, Zubayer Ahammed3, A. V. Alakhverdyants4 +345 more•Institutions (49)
1,696 citations
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Massachusetts Institute of Technology1, University of California, Riverside2, University of Oregon3, University of Edinburgh4, Celera Corporation5, Texas A&M University6, University of New Mexico7, University of Colorado Denver8, University of Kansas9, University of Florida10, Hebrew University of Jerusalem11, University of Düsseldorf12, Rockefeller University13, Technische Universität München14, University of Kentucky15, University of Texas at Austin16, J. Craig Venter Institute17, University of California, Berkeley18, University of California, Los Angeles19, Sapienza University of Rome20, Flinders University21, Ohio State University22, University of Arizona23, University of Missouri–Kansas City24, Dartmouth College25, University of Leeds26, California State Polytechnic University, Pomona27, Oregon Health & Science University28
TL;DR: A high-quality draft sequence of the N. crassa genome is reported, suggesting that RIP has had a profound impact on genome evolution, greatly slowing the creation of new genes through genomic duplication and resulting in a genome with an unusually low proportion of closely related genes.
Abstract: Neurospora crassa is a central organism in the history of twentieth-century genetics, biochemistry and molecular biology. Here, we
report a high-quality draft sequence of the N. crassa genome. The approximately 40-megabase genome encodes about 10,000
protein-coding genes—more than twice as many as in the fission yeast Schizosaccharomyces pombe and only about 25% fewer
than in the fruitfly Drosophila melanogaster. Analysis of the gene set yields insights into unexpected aspects of Neurospora biology
including the identification of genes potentially associated with red light photobiology, genes implicated in secondary metabolism,
and important differences in Ca21 signalling as compared with plants and animals. Neurospora possesses the widest array of
genome defence mechanisms known for any eukaryotic organism, including a process unique to fungi called repeat-induced
point mutation (RIP). Genome analysis suggests that RIP has had a profound impact on genome evolution, greatly slowing the
creation of new genes through genomic duplication and resulting in a genome with an unusually low proportion of closely related
genes.
1,659 citations
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TL;DR: The Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway is one of a handful of pleiotropic cascades used to transduce a multitude of signals for development and homeostasis in animals, from humans to flies.
Abstract: The Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway is one of a handful of pleiotropic cascades used to transduce a multitude of signals for development and homeostasis in animals, from humans to flies. In mammals, the JAK/STAT pathway is the principal signaling
1,658 citations
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TL;DR: The hypothesis that beta-amyloid can destabilize neuronal calcium regulation and render neurons more vulnerable to environmental stimuli that elevate intracellular calcium levels is tested.
Abstract: In Alzheimer's disease (AD), abnormal accumulations of beta-amyloid are present in the brain and degenerating neurons exhibit cytoskeletal aberrations (neurofibrillary tangles). Roles for beta-amyloid in the neuronal degeneration of AD have been suggested based on recent data obtained in rodent studies demonstrating neurotoxic actions of beta- amyloid. However, the cellular mechanism of action of beta-amyloid is unknown, and there is no direct information concerning the biological activity of beta-amyloid in human neurons. We now report on experiments in human cerebral cortical cell cultures that tested the hypothesis that beta-amyloid can destabilize neuronal calcium regulation and render neurons more vulnerable to environmental stimuli that elevate intracellular calcium levels. Synthetic beta-amyloid peptides (beta APs) corresponding to amino acids 1–38 or 25–35 of the beta-amyloid protein enhanced glutamate neurotoxicity in cortical cultures, while a peptide with a scrambled sequence was without effect. beta APs alone had no effect on neuronal survival during a 4 d exposure period. beta APs enhanced both kainate and NMDA neurotoxicity, indicating that the effect was not specific for a particular subtype of glutamate receptor. The effects of beta APs on excitatory amino acid (EAA)-induced neuronal degeneration were concentration dependent and required prolonged (days) exposures. The beta APs also rendered neurons more vulnerable to calcium ionophore neurotoxicity, indicating that beta APs compromised the ability of the neurons to reduce intracellular calcium levels to normal limits. Direct measurements of intracellular calcium levels demonstrated that beta APs elevated rest levels of calcium and enhanced calcium responses to EAAs and calcium ionophore. The neurotoxicity caused by EAAs and potentiated by beta APs was dependent upon calcium influx since it did not occur in calcium-deficient culture medium. Finally, the beta APs made neurons more vulnerable to neurofibrillary tangle-like antigenic changes induced by EAAs or calcium ionophore (i.e., increased staining with tau and ubiquitin antibodies). Taken together, these data suggest that beta-amyloid destabilizes neuronal calcium homeostasis and thereby renders neurons more vulnerable to environmental insults.
1,647 citations
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TL;DR: It is suggested that a modified version of the scheme of the Russian seed physiologist Marianna G. Nikolaeva be adopted and includes three hierarchical layers – class, level and type; thus, a class may contain levels and types, and a level may contain only types.
Abstract: The proposal is made that seed scientists need an internationally acceptable hierarchical system of classification for seed dormancy. Further, we suggest that a modified version of the scheme of the Russian seed physiologist Marianna G. Nikolaeva be adopted. The modified system includes three hierarchical layers – class, level and type; thus, a class may contain levels and types, and a level may contain only types. The system includes five classes of dormancy: physiological dormancy (PD), morphological dormancy (MD), morphophysiological dormancy (MPD), physical dormancy (PY) and combinational dormancy (PY + PD). The most extensive classification schemes are for PD, which contains three levels and five types (in the non-deep level), and MPD, which contains eight levels but no types. PY is not subdivided at all but probably should be, for reasons given. Justifications are presented for not including mechanical dormancy or chemical dormancy in the modified scheme. PD (non-deep level) is the most common kind of dormancy, and occurs in gymnosperms (Coniferales, Gnetales) and in all major clades of angiosperms. Since, first, this is the class and level of dormancy in seeds of wild populations of Arabidopsis thaliana and, secondly, Type 1 (to which seeds of A. thaliana belong) is also common, and geographically and phylogenetically widespread, it seems that biochemical, molecular and genetic studies on seed dormancy in this model species might have rather broad application in explaining the basic mechanism(s) of physiological dormancy in seeds.
1,644 citations
Authors
Showing all 44305 results
Name | H-index | Papers | Citations |
---|---|---|---|
Mark P. Mattson | 200 | 980 | 138033 |
Carlo M. Croce | 198 | 1135 | 189007 |
Charles A. Dinarello | 190 | 1058 | 139668 |
Richard A. Gibbs | 172 | 889 | 249708 |
Gang Chen | 167 | 3372 | 149819 |
David A. Bennett | 167 | 1142 | 109844 |
Carl W. Cotman | 165 | 809 | 105323 |
Rodney S. Ruoff | 164 | 666 | 194902 |
David Tilman | 158 | 340 | 149473 |
David Cella | 156 | 1258 | 106402 |
Richard E. Smalley | 153 | 494 | 111117 |
Deepak L. Bhatt | 149 | 1973 | 114652 |
Kevin Murphy | 146 | 728 | 120475 |
Jian Yang | 142 | 1818 | 111166 |
Thomas J. Smith | 140 | 1775 | 113919 |