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James H. Shelhamer

Researcher at National Institutes of Health

Publications -  230
Citations -  23988

James H. Shelhamer is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Mucus & Pneumonia. The author has an hindex of 72, co-authored 230 publications receiving 22498 citations. Previous affiliations of James H. Shelhamer include Walter Reed Army Medical Center & Marshall University.

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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Profound but Reversible Myocardial Depression in Patients with Septic Shock

TL;DR: To characterize the role of cardiac function in septic shock, serial radionuclide cineangiographic and hemodynamic evaluations were done on 20 patients with documented septicShock, finding that nonsurvivors had normal initial ejection fractions and ventricular volumes that did not change during serial studies.
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Pneumocystis carinii Pneumonia: A Comparison Between Patients with the Acquired Immunodeficiency Syndrome and Patients with Other Immunodeficiencies

TL;DR: Survivors with the acquired immunodeficiency syndrome at initial presentation had a significantly lower respiratory rate, and higher room air arterial oxygen tension, lymphocyte count, and serum albumin level compared to nonsurvivors.
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Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells

TL;DR: Recombinant human HMGB1 elicits proinflammatory responses on endothelial cells and may contribute to alterations in endothelial cell function in human inflammation.
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A circulating myocardial depressant substance in humans with septic shock. Septic shock patients with a reduced ejection fraction have a circulating factor that depresses in vitro myocardial cell performance.

TL;DR: The quantitative and temporal correlation between the decreased left ventricular EF and this serum myocardial depressant substance argues for a pathophysiologic role for this depressant substances in producing the reversible cardiomyopathy seen during septic shock in humans.