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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Journal ArticleDOI
Lipid-Mediated Delivery of Oligonucleotide to Pulmonary Endothelium
Zheng Ma,Junlan Zhang,Sean Alber,John Dileo,Yoichi Negishi,Donna B. Stolz,Simon C. Watkins,Leaf Huang,Bruce R. Pitt,Song Li +9 more
TL;DR: A lipidic vector that is composed of 1,2-dioleoyl-3-trimethylammonium-propane (DOTAP) liposomes, protamine, and ODN is developed that is highly efficient in delivering ODN to the lung via the vascular route and associated with minimal proinflammatory cytokine response and other hematologic toxicities when the ODN lack a potent unmethylated CpG motif.
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Redox (phospho)lipidomics of signaling in inflammation and programmed cell death.
Yulia Y. Tyurina,Claudette M. St. Croix,Simon C. Watkins,Alan M. Watson,Michael W. Epperly,Tamil S. Anthonymuthu,Elena R. Kisin,Irina I. Vlasova,Olga Krysko,Dmitri V. Krysko,Alexandr A. Kapralov,Haider H. Dar,Vladimir A. Tyurin,Andrew A. Amoscato,Popova En,Sergey Bolevich,Peter S. Timashev,John A. Kellum,Sally E. Wenzel,Rama K. Mallampalli,Joel S. Greenberger,Hülya Bayır,Anna A. Shvedova,Valerian E. Kagan,Valerian E. Kagan +24 more
TL;DR: Technological developments promise to make redox lipidomics a powerful approach in the arsenal of diagnostic and therapeutic instruments for personalized medicine of inflammatory diseases and conditions.
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Deficiency in the c-Jun NH2-terminal kinase signaling pathway confers susceptibility to hyperoxic lung injury in mice.
Danielle Morse,Leo E. Otterbein,Simon C. Watkins,Sean Alber,Zhihong Zhou,Richard A. Flavell,Roger J. Davis,Augustine M.K. Choi +7 more
TL;DR: Results indicate that JNK pathways participate in adaptive responses to hyperoxia in mice, which generates an oxidative stress in the mouse lung, which activates the major stress-inducible kinase pathways, including c-Jun NH2-terminal kinase (JNK).
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α-Actinin-4 is required for amoeboid-type invasiveness of melanoma cells.
TL;DR: Down-regulation of ACTN4 significantly reduced invasion of WM1158 cells into the three-dimensional collagen I gel, a representative of the dermis, suggesting that ACTn4 plays an important role in maintaining the amoeboidal morphology of invasive melanoma and thus promoting dissemination through collagen-rich matrices.
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Breast milk protects the neonate from bacterial translocation.
TL;DR: Using bacterial translocation (BT) as a measure of gut barrier function, a series of experiments was designed to explore the relationship between the neonatal gut barrier and breast milk as well as the factors associated with the feeding of breast milk.