Publications by authors named "Kun-Wu Yu"

Atherosclerosis is an inflammatory disease involving activation of adaptive and innate immune responses to antigens, including oxidized low-density lipoprotein (oxLDL) and phosphorylcholine (PC). Dendritic cells (DCs), which are antigen-presenting cells that activate T cells, are present in atherosclerotic lesions and are activated in immune organs. However, the mechanism by which PC promotes atherosclerosis is unclear.

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Oxidative stress and subsequent cardiac myocyte apoptosis play central roles in the initiation and progression of myocardial ischemia-reperfusion (I/R) injury. Homeobox transcript antisense intergenic RNA () was previously implicated in various heart diseases, yet its role in myocardial I/R injury has not been clearly demonstrated. Mice with cardiac-restricted knockdown or overexpression of were exposed to I/R surgery.

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Article Synopsis
  • - The study investigates the role of CD4(+) latency-associated peptide (LAP)(+) regulatory T cells (Tregs) in patients with acute coronary syndrome (ACS), a condition not previously explored in this context.
  • - In the research involving 111 ACS patients and 117 control patients, findings showed that ACS patients had significantly lower levels and functionality of CD4(+)LAP(+) Tregs, indicating potential immune system dysfunction.
  • - The researchers concluded that this novel Treg subset is defective in ACS patients, as evidenced by reduced expression of GARP and lower levels of TGF-β in their blood, while IL-10 levels remained similar between the two groups.
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Imatinib mesylate (IM), a widely prescribed powerful tyrosine kinase inhibitor, has been associated with increased risk of heart failure and is known to induce cell apoptosis and death in isolated cardiomyocytes. In addition to acquired long QT syndrome, pharmacological inhibition of human ether-à-go-go-related gene (HERG) channel has been reported to involve in apoptosis. The present study was undertaken to characterize the biophysical properties of IM on HERG and the molecular determinants of HERG blockade using mutant channels (Y652A and F656A).

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