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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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Evidence for the presence of multilineage chimerism and progenitors of donor dendritic cells in the peripheral blood of bone marrow-augmented organ transplant recipients

TL;DR: Phenotypic analysis of cultured DCs from BM-augmented patients, unlike that of controls, exhibited a marked down-regulation of B7-1 (CD80) while retaining normal levels of expression of B 7-2 (CD86) cell surface molecules, suggesting that the chimerism in BM-AUgmented Patients is multilineage.
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The flow field of automobile add-ons — with particular reference to the vibration of external mirrors

TL;DR: In this paper, the flowfield of externally mounted car mirrors is discussed and a wind-tunnel study of the local flowfield is presented, where mean velocities, pitch and yaw angles and turbulence intensities and spectra were measured using hot-wire anemometers.
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Epinephrine promotes COX-2-dependent immune suppression in myeloid cells and cancer tissues.

TL;DR: The current demonstration of the interplay between inflammation and the induction of immunosuppressive factors by catecholamines suggest a contextual impact of stress, helping to explain variable results of epidemiologic studies of the link between sympathetic activity and cancer progression, and implicating COX-2 blockade as a potential means to mitigate stress-related immune suppression.
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Gliotoxin causes apoptosis and necrosis of rat Kupffer cells in vitro and in vivo in the absence of oxidative stress: exacerbation by caspase and serine protease inhibition.

TL;DR: In the fibrotic liver, gliotoxin nonspecifically causes death of hepatic cell types and modification of gliot toxin molecule may be necessary for selective targeting and elimination of activated stellate cells.
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Highly efficient expression of transgenic proteins by naked DNA-transfected dendritic cells through terminal differentiation.

TL;DR: CD40 signaling of DCs results in the highly efficient expression and presentation of transgenic antigens and the induction of "in vivo" cytotoxic T-cell responses specific for transgenic antigen peptides, demonstrating the functional potential of genetically engineered DCs.