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Jaehwi Lee

Researcher at Chung-Ang University

Publications -  158
Citations -  4657

Jaehwi Lee is an academic researcher from Chung-Ang University. The author has contributed to research in topics: Kinase & Tumor necrosis factor alpha. The author has an hindex of 31, co-authored 156 publications receiving 3913 citations.

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Preclinical Pharmacokinetic Evaluation of β-Lapachone: Characteristics of Oral Bioavailability and First-Pass Metabolism in Rats

TL;DR: It is suggested that the fairly low oral bioavailability of β-lapachone may be resulted from the first-pass metabolic degradation of α- Lapachone in the liver, small and large intestinal tracts and its low aqueous solubility.
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A pharma-robust design method to investigate the effect of PEG and PEO on matrix tablets.

TL;DR: PEG rate of about 90-150% is suggested for matrix tablet formulations, and the exact ratio could be formulated according to the resulting tablet's properties.
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p38/AP-1 Pathway in Lipopolysaccharide-Induced Inflammatory Responses Is Negatively Modulated by Electrical Stimulation

TL;DR: Results suggest that ACP-induced nanocurrents alter signal transduction pathways that are involved in the inflammatory response and could therefore be utilized in the treatment of various inflammatory diseases such as arthritis and colitis.
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Cell-permeable ceramides act as novel regulators of U937 cell-cell adhesion mediated by CD29, CD98, and CD147.

TL;DR: Novel modulatory effects of ceramides on the functional activation of beta1 integrins (CD29) and their associated molecules are reported, using U937 cell-cell or cell-fibronectin (FN) adhesion events, to suggest a novel possibility that ceramide can be used as a therapeutic drug regarding CD29-mediated pathological events.
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Cafestol, a coffee-specific diterpene, is a novel extracellular signal-regulated kinase inhibitor with AP-1-targeted inhibition of prostaglandin E2 production in lipopolysaccharide-activated macrophages.

TL;DR: The data suggest that cafestol may be a novel ERK inhibitor with AP-1-targeted inhibitory activity against PGE(2) production in LPS-activated RAW264.7 cells.