Recent Research Articles from UNTHSC

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NCBI: db=pubmed; Term="University of North Texas Health Science Center"[All Fields] OR "Univ. of North Texas Health Science Center"[All Fields] OR "UNT Health Science Center"[All Fields] OR "Osteopathic Research Center"[All Fields] OR "University of North Texas System College of Pharmacy"[All Fields] OR "UNT System College of Pharmacy"[All Fields] OR "College of Pharmacy, University of North Texas System"[All Fields]
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HIV-1 and alcohol abuse promote astrocyte inflammation: A mechanistic synergy via the cytosolic phospholipase A2 pathway.

Fri, 06/10/2016 - 06:36
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HIV-1 and alcohol abuse promote astrocyte inflammation: A mechanistic synergy via the cytosolic phospholipase A2 pathway.

Cell Death Dis. 2015;6:e2017

Authors: Pandey R, Ghorpade A

PMID: 26658191 [PubMed - indexed for MEDLINE]

Interaction of astrocytes and T cells in physiological and pathological conditions.

Fri, 06/10/2016 - 06:36
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Interaction of astrocytes and T cells in physiological and pathological conditions.

Brain Res. 2015 Oct 14;1623:63-73

Authors: Xie L, Yang SH

Abstract
The central nervous system (CNS) has long been recognized as a site of 'immune privilege' because of the existence of the blood brain barrier (BBB) which presumably isolates CNS from the peripheral immunosurveillance. Different from the peripheral organs, CNS is unique in response to all forms of CNS injury and disease which is mainly mediated by resident microglia and astrocyte. There is increasing evidence that immune cells are not only involved in neuroinflammation process but also the maintenance of CNS homeostasis. T cells, an important immune cell population, are involved in the pathogenesis of some neurological diseases by inducing either innate or adaptive immune responses. Astrocytes, which are the most abundant cell type in the CNS, maintain the integrity of BBB and actively participate in the initiation and progression of neurological diseases. Surprisingly, how astrocytes and T cells interact and the consequences of their interaction are not clear. In this review we briefly summarized T cells diversity and astrocyte function. Then, we examined the evidence for the astrocytes and T cells interaction under physiological and pathological conditions including ischemic stroke, multiple sclerosis, viral infection, and Alzheimer's disease. This article is part of a Special Issue entitled SI: Cell Interactions In Stroke.

PMID: 25813828 [PubMed - indexed for MEDLINE]

Coupling of neurogenesis and angiogenesis after ischemic stroke.

Fri, 06/10/2016 - 06:36
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Coupling of neurogenesis and angiogenesis after ischemic stroke.

Brain Res. 2015 Oct 14;1623:166-73

Authors: Ruan L, Wang B, ZhuGe Q, Jin K

Abstract
Stroke is a leading cause of mortality and severe long-term disability worldwide. Development of effective treatment or new therapeutic strategies for ischemic stroke patients is therefore crucial. Ischemic stroke promotes neurogenesis by several growth factors including FGF-2, IGF-1, BDNF, VEGF and chemokines including SDF-1, MCP-1. Stroke-induced angiogenesis is similarly regulated by many factors most notably, eNOS and CSE, VEGF/VEGFR2, and Ang-1/Tie2. Important findings in the last decade have revealed that neurogenesis is not the stand-alone consideration in the fight for full functional recovery from stroke. Angiogenesis has been also shown to be critical in improving post-stroke neurological functional recovery. More than that, recent evidence has shown a highly possible interplay or dependence between stroke-induced neurogenesis and angiogenesis. Moving forward, elucidating the underlying mechanisms of this coupling between stroke-induced neurogenesis and angiogenesis will be of great importance, which will provide the basis for neurorestorative therapy. This article is part of a Special Issue entitled SI: Cell Interactions In Stroke.

PMID: 25736182 [PubMed - indexed for MEDLINE]

Postmortem medicolegal genetic diagnostics also require reporting guidance.

Fri, 06/10/2016 - 06:36
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Postmortem medicolegal genetic diagnostics also require reporting guidance.

Eur J Hum Genet. 2016 Mar;24(3):329-30

Authors: Sajantila A, Budowle B

PMID: 25469540 [PubMed - indexed for MEDLINE]

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