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Shreveport, LA, United States

Wang B.,Health Science Center | Wang B.,Center for Cardiovascular Diseases and Science | Wang B.,Huazhong University of Science and Technology | Aw T.Y.,Health Science Center | And 4 more authors.
Free Radical Biology and Medicine | Year: 2016

Diabetes, a risk factor for stroke, leads to elevated blood methylglyoxal (MG) levels. This is due to increased MG generation from the high glucose levels, and because diabetes impairs the glutathione (GSH)-glyoxalase system for MG elimination. MG glycates proteins and causes dicarbonyl stress. We investigated the contribution of MG and GSH to stroke outcome. Cerebral ischemia/reperfusion was performed in chemical-induced (streptozotocin) and genetic Akita mouse models of Type 1 diabetes. Brain infarction and functions of the GSH-dependent MG elimination pathway were determined. Diabetes increased post-ischemia-reperfusion cerebral infarct area in association with elevated MG and diminished GSH levels. Infarct size correlated with brain MG-to-GSH ratio. Expression of glutamate-cysteine ligase catalytic subunit (GCLc) was increased in diabetic brain. GCL activity was unchanged. MG-adducts were elevated in the diabetic brain and, using immunoprecipitation, we identified one of the bands as glycated occludin. This was accompanied by increased blood-brain barrier permeability. Total protein carbonyls were elevated, indicative of oxidative/carbonyl stress. N-acetylcysteine (NAC) corrected MG-to-GSH ratio, and reduced diabetic brain infarct area, occludin glycation and permeability. In addition, protein carbonyls were decreased by NAC. We showed that the diabetic brain exhibited a lower GSH-dependent potential for MG elimination, which contributed to increased protein glycation, and oxidative/carbonyl stress. The consequence of these changes was aggravated post-stroke brain injury. NAC administration protected against the exacerbated brain damage via restored GSH generation and normalization of the MG-to-GSH ratio and possibly by attenuating oxidative/carbonyl stress. This treatment could contribute to the successful management of stroke risk/outcome in diabetes. © 2016 Elsevier Inc. All rights reserved.


Brunson J.L.,Health Science Center | Brunson J.L.,Center for Molecular and Tumor Virology | Brunson J.L.,Center for Cardiovascular Disease and science | Becker F.,Health Science Center | And 4 more authors.
Pathophysiology | Year: 2015

Cytomegalovirus (CMV) infects 60-100% of the population worldwide. CMV has been implicated in many diseases through the induction of inflammation. Inflammatory bowel disease (IBD) affects over 1 million Americans annually. IBD, in particular ulcerative colitis, has been associated with CMV infection. Here we use a murine model to test if both primary and persistent CMV infections exacerbate colitis. C57Bl/6J mice were injected with Mock inoculum or murine CMV (mCMV) 4. d (primary infection) or 6. wks (persistent infection) before inducing colitis. Colitis was induced by administering 3% DSS (dextran sodium sulfate) in the drinking water for 6 days. Distilled water was given to controls. Disease activity index (DAI), derived from scores for stool consistency, body weight loss, occult blood, and rectal bleeding, was recorded daily. DAI increased early with DSS treatment in Mocks when compared with water-treated controls. This was accelerated by both primary and persistent mCMV and appeared to be primarily due to the earlier appearance of gross bleeding vs. their Mock controls. Mocks reached similar DAI values by day 6. Myeloperoxidase was modestly elevated in the mCMV 4. d-DSS over the Mock 4. d-DSS, however there was no such synergism in the 6. wk groups. Histology was comparable in Mock and mCMV groups. Taken together our findings show that mCMV accelerated the development of acute colitis although a milder model of colitis may be needed to better delineate the impact of the virus on disease progression. Further work focusing on disruption of barrier function and bleeding may help determine the underlying mechanisms. © 2014 Elsevier B.V.


Trutschl M.,LSU | Trutschl M.,Laboratory for Advanced Biomedical Informatics | Trutschl M.,Center for Molecular and Tumor Virology | Kilgore P.C.S.R.,LSU | And 4 more authors.
Proceedings of the 2012 3rd International Conference on Networking and Computing, ICNC 2012 | Year: 2012

Previous application of Kohonen's self organizing map to common visualizations has yielded promising results. In this research, we extend the classic two-dimensional scatter plot visualization algorithm into the third dimension by permitting competition to occur within a three-dimensional search space. This approach takes advantage of spatial memory and increases the intrinsic dimensionality of a widely used visualization technique. We also present a method of parallelizing this novel algorithm as a method of overcoming the runtime complexity associated with it using MPI. We note that this algorithm responds extremely well to parallelization and that it leads to an effective method for knowledge discovery in complex multidimensional datasets. © 2012 IEEE.


Doss J.,LSU | Holloway R.,LSU | Slack J.,LSU | Smith J.,LSU | And 7 more authors.
Proceedings of the International Conference on Information Visualisation | Year: 2010

Intravital microscopy permits observation of live events in intact tissues to study a variety of issues, including quantifying cell-vessel wall interactions. The analysis of the parameters is labor-intensive, subjective and limited to broad categories of blood cell-vessel wall interactions. We are developing an algorithmic approach that aids in analysis, automatically and objectively detects and tracks platelets, and expands information derived from such videos. We integrate computer vision and break the identification, tracking, and visualization into steps. We enable simple and computationally efficient means of eliminating movement within a video based on positional shifting of an identified feature and visualize platelet paths. © 2010 IEEE.


Chan G.,Center for Molecular and Tumor Virology | Chan G.,SUNY Upstate Medical University | Nogalski M.T.,Center for Molecular and Tumor Virology | Stevenson E.V.,Center for Molecular and Tumor Virology | And 2 more authors.
Journal of Leukocyte Biology | Year: 2012

HCMV pathogenesis is a direct consequence of the hematogenous dissemination of the virus to multiple host organ sites. The presence of infected monocytes in the peripheral blood and organs of individuals exhibiting primary HCMV infection have long suggested that these blood sentinels are responsible for mediating viral spread. Despite monocytes being "at the right place at the right time", their short lifespan and the lack of productive viral infection in these cells complicate this scenario of a monocyte-driven approach to viral dissemination by HCMV. However, our laboratory has provided evidence that HCMV infection is able to induce a highly controlled polarization of monocytes toward a unique and long-lived proinflammatory macrophage, which we have demonstrated to be permissive for viral replication. These observations suggest that HCMV has evolved as a distinct mechanism to induce select proinflammatory characteristics that provide infected monocytes with the necessary tools to mediate viral spread following a primary infection. In the absence of viral gene products during the early stages of infection, the process by which HCMV "tunes" the inflammatory response in infected monocytes to promote viral spread and subsequently, viral persistence remains unclear. In this current review, we focus on the viral entry process of HCMV and the potential role of receptor-ligand interactions in modulating monocyte biology. Specifically, we examine the signaling pathways initiated by the distinct combination of cellular receptors simultaneously engaged and activated by HCMV during viral entry and how the acquisition of this distinct signalsome results in a nontraditional activation of monocytes leading to the induction of the unique, functional attributes observed in monocytes following HCMV infection. © Society for Leukocyte Biology.

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