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Simon C. Watkins

Researcher at University of Pittsburgh

Publications -  999
Citations -  75771

Simon C. Watkins is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Apoptosis & Immune system. The author has an hindex of 135, co-authored 950 publications receiving 68358 citations. Previous affiliations of Simon C. Watkins include Harvard University & Children's National Medical Center.

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Accelerated aging of intervertebral discs in a mouse model of progeria

TL;DR: Progression of disc aging is examined in a murine model of a human progeroid syndrome caused by deficiency of the DNA repair endonuclease, ERCC1–XPF (Ercc1−/Δ mice) and novel evidence that DNA damage negatively impacts PG synthesis is provided.
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Nitric oxide inhibits lipopolysaccharide-induced apoptosis in pulmonary artery endothelial cells

TL;DR: It is confirmed that cultured sheep pulmonary artery endothelial cells (SPAECs) became resistant to lipopolysaccharide (LPS)-induced apoptosis several days after constitutive synthesis of nitric oxide (NO) after adenoviral transfer of inducible NO synthase (iNOS) or exposure to the NO donor S-nitroso- N-acetylpenicillamine (SNAP) and used all three approaches to determine underlying mechanisms of this phenomenon.
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Diversity in the Strength and Structure of Unruptured Cerebral Aneurysms

TL;DR: There is a need to refine the end-point of risk assessment studies that currently do not distinguish risk levels among unruptured aneurysms, and it is proposed that a measure of wall integrity that identifies this vulnerable wall subpopulation will be useful for interpreting future biological and structural data.
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The Murine P84 Neural Adhesion Molecule Is SHPS-1, a Member of the Phosphatase-Binding Protein Family

TL;DR: By cloning the cDNA encoding murine P84, it is discovered that this molecule is a member of a family of phosphatase-binding proteins and is identical to the murine SHPS-1 cDNA.
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Bid activates multiple mitochondrial apoptotic mechanisms in primary hepatocytes after death receptor engagement

TL;DR: In vivo studies in intact hepatocytes provide novel findings not previously disclosed by in vitro studies, and indicates the importance of several mechanisms in contributing Bid-mediated mitochondria dysfunction that could be potential cellular targets of intervention.