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Byung-Hyun Park

Researcher at Chonbuk National University

Publications -  245
Citations -  7649

Byung-Hyun Park is an academic researcher from Chonbuk National University. The author has contributed to research in topics: Proinflammatory cytokine & Apoptosis. The author has an hindex of 42, co-authored 227 publications receiving 6430 citations. Previous affiliations of Byung-Hyun Park include University of Texas Southwestern Medical Center.

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Overexpression of SIRT1 Protects Pancreatic β-Cells Against Cytokine Toxicity by Suppressing the Nuclear Factor-κB Signaling Pathway

TL;DR: This study will provide valuable information not only into the mechanisms underlying β-cell destruction but also into the regulation of SIRT1 as a possible target to attenuate cytokine-inducedβ-cell damage.
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Rapid transformation of white adipocytes into fat-oxidizing machines

TL;DR: Phosphorylation of both acetyl CoA carboxylase and AMP-activated protein kinase was increased, thus explaining the increase in fatty acid oxidation and the ability to transform adipocytes into unique fat-burning cells may suggest novel therapeutic strategies for obesity.
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Making insulin-deficient type 1 diabetic rodents thrive without insulin

TL;DR: It is suggested that leptin reverses the catabolic consequences of total lack of insulin, potentially by suppressing glucagon action on liver and enhancing the insulinomimetic actions of IGF-1 on skeletal muscle, and suggest strategies for making type 1 diabetes insulin-independent.
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Expression of DBC1 and SIRT1 is associated with poor prognosis of gastric carcinoma.

TL;DR: This study shows that expression of DBC1 and SIRT1 is a significant prognostic indicator for gastric carcinoma patients and were independent prognostic factors significantly associated with overall survival and relapse-free survival.
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Induction of apoptosis by diallyl disulfide through activation of caspase-3 in human leukemia HL-60 cells.

TL;DR: Results indicate that DADS-induced apoptosis is triggered by the generation of hydrogen peroxide, activation of caspase-3, degradation of PARP, and fragmentation of DNA.