Kevin J. Tracey
The Feinstein Institute for Medical Research
609 Papers
4.5K Citations
Kevin J. Tracey is an academic researcher from The Feinstein Institute for Medical Research. The author has contributed to research in topics: Inflammation & Medicine. The author has an hindex of 138, co-authored 561 publications. Previous affiliations of Kevin J. Tracey include Memorial Sloan Kettering Cancer Center & Hofstra University.
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Papers
Forebrain Cholinergic Dysfunction and Systemic and Brain Inflammation in Murine Sepsis Survivors.
Nahla Zaghloul,Meghan E. Addorisio,Harold A. Silverman,Harold A. Silverman,Hardik Patel,Sergio I. Valdés-Ferrer,Kamesh Ayasolla,Kurt Lehner,Peder S. Olofsson,Mansoor Nasim,Christine N. Metz,Christine N. Metz,Ping Wang,Ping Wang,Mohamed Ahmed,Sangeeta S. Chavan,Betty Diamond,Betty Diamond,Kevin J. Tracey,Kevin J. Tracey,Valentin A. Pavlov,Valentin A. Pavlov +21 more
TL;DR: The notion of persistent inflammation-immunosuppression and catabolic syndrome in sepsis survivors is reinforced and the relationship between peripheral immunometabolic alterations and brain cholinergic and inflammatory states in mouse survivors of cecal ligation and puncture (CLP)-induced sepsi is studied.
High mobility group box 1 (HMGB1).
Huan Yang,Kevin J. Tracey +1 more
TL;DR: High mobility group box 1 is an extremely abundant protein that is widely distributed in all mammalian tissues; HMGB1like proteins are also found in yeast, bacteria, and plants.
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Renal expression and serum levels of high mobility group box 1 protein in lupus nephritis
Agneta Zickert,Karin Palmblad,Birgitta Sundelin,Sangeeta S. Chavan,Kevin J. Tracey,Annette Bruchfeld,Iva Gunnarsson +6 more
TL;DR: Renal tissue expression and serum levels of HMGB1 were increased in LN and the lack of decrease in serum and tissue after immunosuppressive therapy in the current study may reflect persistent inflammatory activity.
Bioelectronic medicine: technology targeting molecular mechanisms for therapy.
TL;DR: The discipline bioelectronic medicine arose from groundbreaking discoveries of mechanisms for neural control of biological processes that underlie disease, and the development of devices to modulate these specific neural circuits as therapy using electrons instead of drugs.
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Lipopolysaccharide-induced cytokine cascade and lethality in LT alpha/TNF alpha-deficient mice.
TL;DR: The lethality studies simultaneously confirm a role for TNF as a mediator of early lethality and establish that, in the absence of these cytokines, other mediators take over, resulting in the lack of long-term protection from LPS toxicity.