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David J. Volsky

Researcher at Icahn School of Medicine at Mount Sinai

Publications -  177
Citations -  9211

David J. Volsky is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Virus & Viral replication. The author has an hindex of 47, co-authored 172 publications receiving 8543 citations. Previous affiliations of David J. Volsky include Columbia University & Mount Sinai St. Luke's and Mount Sinai Roosevelt.

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PAGE: Parametric Analysis of Gene Set Enrichment

TL;DR: PAGE was statistically more sensitive and required much less computational effort than GSEA, it could identify significantly changed biological themes from micro array data irrespective of analysis methods or microarray platforms, and it was useful in comparison of multiple microarray data sets.
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HIV-associated neurocognitive disorder — pathogenesis and prospects for treatment

TL;DR: It is suggested that adjunctive therapies — treatments targeting CNS inflammation and other metabolic processes, including glutamate homeostasis, lipid and energy metabolism — are needed to reverse or improve HAND-related neurological dysfunction.
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Cytokines and arachidonic metabolites produced during human immunodeficiency virus (HIV)-infected macrophage-astroglia interactions: implications for the neuropathogenesis of HIV disease.

TL;DR: The results suggest that the neuronotoxicity associated with HIV central nervous system disorders is mediated, in part, through cytokines and arachidonic acid metabolites, produced during cell-to- cell interactions between HIV-infected brain macrophages and astrocytes.
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Identification and cloning of human astrocyte genes displaying elevated expression after infection with HIV-1 or exposure to HIV-1 envelope glycoprotein by rapid subtraction hybridization, RaSH.

TL;DR: The comparable pattern of regulation of the AEGs following HIV-1 infection or gp120 treatment suggest that HIV- 1 exposure of astrocytes, even in the absence of productive infection, can induce changes in cellular gene expression.
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Mechanism of ceftriaxone induction of excitatory amino acid transporter-2 expression and glutamate uptake in primary human astrocytes

TL;DR: The data indicate that ceftriaxone is a potent modulator of glutamate transport in PHFA through NF-κB-mediated EAAT2 promoter activation, and suggest a mechanism for ceftRIaxone modulation of glutamate Transport and for its potential effects on ameliorating specific neurodegenerative diseases through modulation of extracellular glutamate.