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Mitchell P. Fink

Researcher at University of California, Los Angeles

Publications -  270
Citations -  30828

Mitchell P. Fink is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Sepsis & Intensive care. The author has an hindex of 78, co-authored 270 publications receiving 29464 citations. Previous affiliations of Mitchell P. Fink include University of Massachusetts Amherst & Beth Israel Deaconess Medical Center.

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2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference

TL;DR: This document reflects a process whereby a group of experts and opinion leaders revisited the 1992 sepsis guidelines and found that apart from expanding the list of signs and symptoms of sepsi to reflect clinical bedside experience, no evidence exists to support a change to the definitions.
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2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference

TL;DR: A hypothetical model for staging sepsis is presented, which, in the future, may better characterize the syndrome on the basis of predisposing factors and premorbid conditions, the nature of the underlying infection, the characteristics of the host response, and the extent of the resultant organ dysfunction.
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The CRIT Study: Anemia and blood transfusion in the critically ill--current clinical practice in the United States.

TL;DR: The number of RBC transfusions a patient received during the study was independently associated with longer ICU and hospital lengths of stay and an increase in mortality and a nadir hemoglobin level of <9 g/dL was a predictor of increased mortality and length of stay.
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Reversing established sepsis with antagonists of endogenous high-mobility group box 1

TL;DR: Observations demonstrate that specific inhibition of endogenous HMGB1 therapeutically reverses lethality of established sepsis indicating thatHMGB1 inhibitors can be administered in a clinically relevant time frame.
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The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion

TL;DR: It is demonstrated that HMGB1 is an early mediator of injury and inflammation in liver I/R and implicates TLR4 as one of the receptors that is involved in the process.