Lexington, KY, United States
Lexington, KY, United States

The University of Kentucky is a public co-educational university in Lexington, Kentucky. Founded in 1865 by John Bowman as the Agricultural and Mechanical College of Kentucky, the university is one of the state's two land-grant universities, the largest college or university in the state, with 28,928 students as of Fall 2012, and the highest ranked research university in the state according to U.S. News and World Report.The institution comprises 16 colleges, a graduate school, 93 undergraduate programs, 99 master programs, 66 doctoral programs, and four professional programs. The University of Kentucky has fifteen libraries on campus. The largest is William T. Young Library, a federal depository, hosting subjects related to social science, humanities and life science collections. In recent years, the university has focused expenditures increasingly on research, following a compact formed by the Kentucky General Assembly in 1997. The directive mandated that the university become a Top 20 public research institution, in terms of an overall ranking to be determined by the university itself, by the year 2020. Wikipedia.


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Patent
University of Kentucky | Date: 2016-11-09

A proppant for use in hydraulic fracturing to stimulate a well is provided. The proppant is fly ash particles having a mean particle size (d50) of between 45 m and 150 m and a size distribution defined by (d10)5 m and (d98)250 m.


Patent
Vermillion and University of Kentucky | Date: 2016-11-30

The present invention provides protein-based biomarkers and biomarker combinations that am useful in qualifying ovarian cancer status in a patient. In particular, the biomarkers of this invention are useful to classify a subject sample as ovarian cancer, ovarian cancer of low malignant potential, benign ovarian disease or other malignant condition. The biomarkers can be detected by SELDI mass spectrometry.


Horbinski C.,University of Kentucky
Acta Neuropathologica | Year: 2013

Whole genome analyses have facilitated the discovery of clinically relevant genetic alterations in a variety of diseases, most notably cancer. A prominent example of this was the discovery of mutations in isocitrate dehydrogenases 1 and 2 (IDH1/2) in a sizeable proportion of gliomas and some other neoplasms. Herein the normal functions of these enzymes, how the mutations alter their catalytic properties, the effects of their D-2-hydroxyglutarate metabolite, technical considerations in diagnostic neuropathology, implications about prognosis and therapeutic considerations, and practical applications and controversies regarding IDH1/2 mutation testing are discussed. © Springer-Verlag Berlin Heidelberg 2013.


Mid-life obesity and type 2 diabetes mellitus (T2DM) confer a modest, increased risk for Alzheimer's disease (AD), though the underlying mechanisms are unknown. We have created a novel mouse model that recapitulates features of T2DM and AD by crossing morbidly obese and diabetic db/db mice with APPΔNL/ΔNLx PS1P264L/P264L knock-in mice. These mice (db/AD) retain many features of the parental lines (e.g. extreme obesity, diabetes, and parenchymal deposition of β-amyloid (Aβ)). The combination of the two diseases led to additional pathologies-perhaps most striking of which was the presence of severe cerebrovascular pathology, including aneurysms and small strokes. Cortical Aβ deposition was not significantly increased in the diabetic mice, though overall expression of presenilin was elevated. Surprisingly, Aβ was not deposited in the vasculature or removed to the plasma, and there was no stimulation of activity or expression of major Aβ-clearing enzymes (neprilysin, insulin degrading enzyme, or endothelin-converting enzyme). The db/AD mice displayed marked cognitive impairment in the Morris Water Maze, compared to either db/db or APPΔNLx PS1P264L mice. We conclude that the diabetes and/or obesity in these mice leads to a destabilization of the vasculature, leading to strokes and that this, in turn, leads to a profound cognitive impairment and that this is unlikely to be directly dependent on Aβ deposition. This model of mixed or vascular dementia provides an exciting new avenue of research into the mechanisms underlying the obesity-related risk for age-related dementia, and will provide a useful tool for the future development of therapeutics.


Anthony J.E.,University of Kentucky
Chemistry of Materials | Year: 2011

In the field of polymer bulk-heterojunction organic photovoltaics, fullerenes and fullerene derivatives clearly play the dominant role as acceptor materials. Recently, a number of research efforts have focused on the development of new small-molecule acceptors for this device configuration. Although few materials prepared to-date have demonstrated power conversion efficiencies close to those achieved with fullerenes, numerous design rules and some interesting new materials classes have been explored. This short review will highlight the progress toward higher efficiency in nonfullerene small-molecule acceptors for organic solar cells. © 2010 American Chemical Society.


Calmodulin (CaM) is a key mediator of calcium-dependent signalling and is subject to regulatory post-translational modifications, including trimethylation of Lys-115. In this paper, we identify a class I, non-SET domain protein methyltransferase, calmodulin-lysine N-methyltransferase (EC 2.1.1.60). A polypeptide chosen from a fraction enriched in calmodulin methyltransferase activity was trypsinized and analysed by tandem mass spectrometry. The amino-acid sequence obtained identified conserved, homologous proteins of unknown function across a wide range of species, thus implicating a broad role for lysine methylation in calcium-dependent signalling. Encoded by c2orf34, the human homologue is a component of two related multigene deletion syndromes in humans. Human, rat, frog, insect and plant homologues were cloned and Escherichia coli-recombinant proteins catalysed the formation of a trimethyllysyl residue at position 115 in CaM, as verified by product analyses and mass spectrometry.


The Src family kinases (SFKs) c-Src and Yes mediate vascular leakage in response to various stimuli including lipopolysaccharide (LPS) and vascular endothelial growth factor (VEGF). Here, we define an opposing function of another SFK, Lyn, which in contrast to other SFKs, strengthens endothelial junctions and thereby restrains the increase in vascular permeability. Mice lacking Lyn displayed increased mortality in LPS-induced endotoxemia and increased vascular permeability in response to LPS or VEGF challenge compared with wild-type littermates. Lyn knockout mice repopulated with wild-type bone marrow-derived cells have higher vascular permeability than wild-type mice, suggesting a role of endothelial Lyn in the maintenance of the vascular barrier. Small interfering RNA-mediated down-regulation of Lyn disrupted endothelial barrier integrity, whereas expression of a constitutively active mutant of Lyn enhanced the barrier. However, down-regulation of Lyn did not affect LPS-induced endothelial permeability. We demonstrate that Lyn association with focal adhesion kinase (FAK) and phosphorylation of FAK at tyrosine residues 576/577 and 925 were required for Lyn-dependent stabilization of endothelial adherens junctions. Thus, in contrast to c-Src and Yes, which increase vascular permeability in response to stimuli, Lyn stabilizes endothelial junctions through phosphorylation of FAK. Therefore, therapeutics activating Lyn kinase may strengthen the endothelial barrier junction and hence have anti-inflammatory potential.


Karim Z.A.,University of Kentucky
Blood | Year: 2013

Platelet secretion plays a key role in thrombosis, thus the platelet secretory machinery offers a unique target to modulate hemostasis. We report the regulation of platelet secretion via phosphorylation of SNAP-23 at Ser95. Phosphorylation of this t-soluble N-ethylmaleimide sensitive factor attachment protein receptor (SNARE) occurs upon activation of known elements of the platelet signaling cascades (ie, phospholipase C, [Ca(2+)]i, protein kinase C) and requires IκB kinase (IKK)-β. Other elements of the nuclear factor κB/IκB cascade (ie, IKK-α,-β,-γ/NEMO and CARMA/MALT1/Bcl10 complex) are present in anucleate platelets and IκB is phosphorylated upon activation, suggesting that this pathway is active in platelets and implying a nongenomic role for IKK. Inhibition of IKK-β, either pharmacologically (with BMS-345541, BAY11-7082, or TPCA-1) or by genetic manipulation (platelet factor 4 Cre:IKK-β(flox/flox)), blocked SNAP-23 phosphorylation, platelet secretion, and SNARE complex formation; but, had no effect on platelet morphology or other metrics of platelet activation. Consistently, SNAP-23 phosphorylation enhanced membrane fusion of SNARE-containing proteoliposomes. In vivo studies with IKK inhibitors or platelet-specific IKK-β knockout mice showed that blocking IKK-β activity significantly prolonged tail bleeding times, suggesting that currently available IKK inhibitors may affect hemostasis.


Wang K.,University of Kentucky
Nucleic acids research | Year: 2010

The accurate mapping of reads that span splice junctions is a critical component of all analytic techniques that work with RNA-seq data. We introduce a second generation splice detection algorithm, MapSplice, whose focus is high sensitivity and specificity in the detection of splices as well as CPU and memory efficiency. MapSplice can be applied to both short (<75 bp) and long reads (≥ 75 bp). MapSplice is not dependent on splice site features or intron length, consequently it can detect novel canonical as well as non-canonical splices. MapSplice leverages the quality and diversity of read alignments of a given splice to increase accuracy. We demonstrate that MapSplice achieves higher sensitivity and specificity than TopHat and SpliceMap on a set of simulated RNA-seq data. Experimental studies also support the accuracy of the algorithm. Splice junctions derived from eight breast cancer RNA-seq datasets recapitulated the extensiveness of alternative splicing on a global level as well as the differences between molecular subtypes of breast cancer. These combined results indicate that MapSplice is a highly accurate algorithm for the alignment of RNA-seq reads to splice junctions. Software download URL: http://www.netlab.uky.edu/p/bioinfo/MapSplice.


Robertson M.,University of Kentucky
Transactions of the Institute of British Geographers | Year: 2012

The development of markets in water quality, biodiversity and carbon sequestration signals a new intensification and financialisation in the encounter between nature and late capitalism. Following Neil Smith's observations on this transformation, I argue that the commodification of such 'ecosystem services' is not merely an expansion of capital toward the acquisition or industrialisation of new resources, but the making of a new social world comparable to the transformation by which individual human labours became social labour under capitalism. Technologies of measurement developed by ecosystem scientists describe nature as exchange values, as something always already encountered in the commodity form. Examining these developments through specific cases in US water policy, I propose that examining this transformation can provide political ecology and the study of 'neoliberal natures' with a thematic unity that has been absent. I understand capital's encounter with nature as a process of creating socially-necessary abstractions that are adequate to bear value in capitalist circulation. Such an argument supersedes the issue of nature's materiality and points toward a common language for the analysis of both humans and nature as two participants in the labour process. Political ecologists struggling with the commodification of nature have tended to overlook the social constitution of nature's value in favour of explicit or implicit physical theories of value, often as more-or-less latent realisms. I suggest that critical approaches to nature must retain and elaborate a critical value theory, to understand both the imperatives and the silences in the current campaign to define the world as an immense collection of service commodities. © 2011 Royal Geographical Society.

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