S
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
Marla T. Rugeles,A Aitouche,Adriana Zeevi,John J. Fung,Simon C. Watkins,Thomas E. Starzl,Abdul S. Rao +6 more
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
Simon C. Watkins,Greg Oswald +1 more
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.
Ravikumar Muthuswamy,Nana J. Okada,Frank J. Jenkins,Kandace P. McGuire,Priscilla F. McAuliffe,Herbert J. Zeh,David L. Bartlett,Callen T. Wallace,Simon C. Watkins,Jill D. Henning,Dana H. Bovbjerg,Pawel Kalinski +11 more
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.
Kristin Anselmi,Donna B. Stolz,Michael A. Nalesnik,Simon C. Watkins,Ravindra Kamath,Chandrashekhar R. Gandhi +5 more
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.
Adriana T. Larregina,Adrian E. Morelli,Olga A. Tkacheva,Geza Erdos,Cara Donahue,Simon C. Watkins,Angus W. Thomson,Louis D. Falo +7 more
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.