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Charles H. Lang

Researcher at Pennsylvania State University

Publications -  449
Citations -  18744

Charles H. Lang is an academic researcher from Pennsylvania State University. The author has contributed to research in topics: Skeletal muscle & Insulin. The author has an hindex of 71, co-authored 443 publications receiving 16749 citations. Previous affiliations of Charles H. Lang include New York University & University Medical Center New Orleans.

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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Tumor necrosis factor impairs insulin action on peripheral glucose disposal and hepatic glucose output.

TL;DR: It is suggested that sustained elevations of TNF during chronic therapy and prolonged production of T NF by patients and experimental animals with malignancies or infectious diseases may be an important mechanism for the enhanced glucose flux as well as the insulin resistance seen in these conditions.
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Lipopolysaccharide regulates proinflammatory cytokine expression in mouse myoblasts and skeletal muscle

TL;DR: Under in vivo conditions, LPS increased the plasma concentration of TNF-alpha and IL-6 and stimulated the accumulation of their mRNAs in multiple tissues including skeletal muscle from wild-type mice.
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TNF-α impairs heart and skeletal muscle protein synthesis by altering translation initiation

TL;DR: Data suggest that TNF-alpha impairs skeletal muscle and heart protein synthesis, at least in part, by decreasing mRNA translational efficiency resulting from an impairment in translation initiation associated with alterations in eIF-4E availability.
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Regulation of muscle protein synthesis during sepsis and inflammation

TL;DR: Understanding the cellular basis of the sepsis-induced decrease in translational activity will contribute to the rational development of therapeutic interventions and thereby minimize the debilitating affects of the atrophic response that impairs patient recovery.