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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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Morphogenetic events in mixed cultures of rat hepatocytes and nonparenchymal cells maintained in biological matrices in the presence of hepatocyte growth factor and epidermal growth factor.

TL;DR: The results show that the mixed cultures of proliferating hepatocytes and nonparenchymal cells can reproduce the hallmark structures of hepatic histological architecture while maintaining differentiation and the capacity to proliferate.
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DC-SIGN on B lymphocytes is required for transmission of HIV-1 to T lymphocytes.

TL;DR: It is shown that a subset of B cells in the blood and tonsils of normal donors expressed DC-SIGN, and that this increased after stimulation in vitro with interleukin 4 and CD40 ligand, with enhanced expression of activation and co-stimulatory molecules CD23, CD58, CD80, and CD86, andCD22.
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Differential effects of nonselective nitric oxide synthase (NOS) and selective inducible NOS inhibition on hepatic necrosis, apoptosis, ICAM-1 expression, and neutrophil accumulation during endotoxemia.

TL;DR: No produced by eNOS may be adequate to prevent necrosis by a mechanism independent of PMN, while induced NO appears to prevent apoptosis in LPS-treated rats receiving infusions of either NAME or NIL.
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Widespread and Stable Pancreatic Gene Transfer by Adeno-Associated Virus Vectors via Different Routes

TL;DR: It is shown that, for the first time, appropriate serotypes of adeno-associated virus, coupled with a double-stranded vector DNA cassette, enable extensive and long-term in vivo gene transfer in the adult mouse pancreas by three different delivery methods.
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Conjugated Linoleic Acid Is a Preferential Substrate for Fatty Acid Nitration

TL;DR: Conjugated linoleic acid (CLA) is identified as the primary endogenous substrate for fatty acid nitration in vitro and in vivo, yielding up to 105 greater extent of nitration products as compared with bis-allylic linolesic acid, affirm that metabolic and inflammatory reactions yield electrophilic products that can modulate adaptive cell signaling mechanisms.