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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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Endocytic adaptor molecules reveal an endosomal population of clathrin by total internal reflection fluorescence microscopy.

TL;DR: Highly motile clathrin structures are apparently distinct from the plasma membrane, accompany transferrin, and contain AP-1, revealing an endosomal population of clathin structures.
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Microtubules and desmin filaments during onset of heart hypertrophy in rat: a double immunoelectron microscope study.

TL;DR: The distribution of tubulin and desmin, the constituent proteins of microtubules and intermediate filaments, respectively, were studied in normal and hypertrophied rat myocardium by high-resolution immunofluorescence and immunoelectron microscopy to suggest that, during the development of cardiac hypertrophy, desmin filaments are mainly involved in maintaining the myofibrils in register.
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Subcellular and cell-cycle expression profiles of CDK-inhibitors in normal differentiating myeloid cells.

TL;DR: This report studied the expression of the cell-cycle inhibitors p21 and p27 during the in vitro differentiation of normal CD34 + blast cells along the myeloid lineage to further understand what genetic regulators might couple proliferation status to differentiation.
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Immunoglobulin A supplementation abrogates bacterial translocation and preserves the architecture of the intestinal epithelium

TL;DR: In contrast to the normal-appearing distal ileum of neonates fed breast milk, intestinal epithelium from neonates that received formula or formula with IgG or IgA demonstrated prominent vacuoles by light microscopy.
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A novel nitric oxide scavenger decreases liver injury and improves survival after hemorrhagic shock

TL;DR: It is suggested that excess NO mediates shock-induced tissue injury and that suppression of NO availability with NO scavengers may reduce the pathophysiological sequelae of severe hemorrhage.