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Elissa J. Schwartz

Researcher at Washington State University

Publications -  35
Citations -  1176

Elissa J. Schwartz is an academic researcher from Washington State University. The author has contributed to research in topics: Equine infectious anemia & Vaccination. The author has an hindex of 14, co-authored 35 publications receiving 1101 citations. Previous affiliations of Elissa J. Schwartz include Mount Sinai Hospital & Icahn School of Medicine at Mount Sinai.

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The human blood‐brain barrier glucose transporter (GLUT1) is a glucose transporter of gray matter astrocytes

TL;DR: The GLUT1 isoform of glucose transporter is present both in endothelium of the blood‐brain barrier and in astrocytes surrounding gray matter blood vessels and synapses, and is likely to have a lower molecular weight than the form found in cerebral endothelia.
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Highly Active Antiretroviral Therapy and the Epidemic of HIV+ End-Stage Renal Disease

TL;DR: Prevention of progression to ESRD should focus on early antiretroviral treatment of HIV-infected patients who have evidence ofAIDS-associated nephropathy, and an increase in HIV+ E SRD prevalence in the future is projected as a result of the increase in the AIDS population among black individuals.
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HIV-1 Nef Induces Proliferation and Anchorage-Independent Growth in Podocytes

TL;DR: Data indicate that Nef induces multiple proliferative effects in podocytes in culture and that nef may therefore be an important gene in the pathogenesis of HIVAN in vivo.
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32 bp CCR-5 gene deletion and resistance to fast progression in HIV-1 infected heterozygotes

TL;DR: The data in the table suggest that 348 (70·6%) individuals have PM phenotype, which may have major implications for the efficacy of proguanil in this population, which is also involved in the metabolism of other drugs such as imipramine, omeprazole, and diazepam.
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Human Immunodeficiency Virus-1 Induces Loss of Contact Inhibition in Podocytes

TL;DR: It was demonstrated that HIV-1 mRNA is expressed in renal epithelium of the transgenic mouse and in patients with HIVAN, suggesting a direct role for HIV- 1 in disease pathogenesis in both humans and the murine model.