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Articles by L. C Chen
Total Records ( 2 ) for L. C Chen
  L. C Chen , L. Y Kuo , Y. F Tsao , L. S Hong , C. S Wang , C. C Lee , L. J Lin , C. Y Chou and Y. H. Tsieng
 

Ankle-brachial index (ABI) is an important indicator of peripheral arterial disease (PAD) and PAD has a negative impact on quality of life (QOL). However, the correlation between ABI and QOL is unknown among chronic hemodialysis patients. Ankle-brachial index was measured, and WHOQOL-BRIEF (TW) questionnaire was completed. The association between ABI and QOL was analyzed using linear regression. A total of 54 chronic hemodialysis patients (mean age of 56.2 ± 14.6 years) were included. Ankle-brachial index was positively associated with QOL (r = .448, P = .001). The QOL scores were 3.1 ± 2.9 and 2.6 ± 0.4 for 37 patients with an ABI more than 0.9 and 17 patients with an ABI less than 0.9 or more than 1.3 (p < .001). In linear regression, only ABI was significantly associated with QOL scores with a β of .448 (95% CI: 0.443 to 1.55, P = .001). Ankle-brachial index is positively correlated to QOL among chronic hemodialysis patients.

  S Laing , G Wang , T Briazova , C Zhang , A Wang , Z Zheng , A Gow , A. F Chen , S Rajagopalan , L. C Chen , Q Sun and K. Zhang
 

Recent studies have suggested a link between inhaled particulate matter (PM) exposure and increased mortality and morbidity associated with pulmonary and cardiovascular diseases. However, a precise understanding of the biological mechanism underlying PM-associated toxicity and pathogenesis remains elusive. Here, we investigated the impact of PM exposure in intracellular stress signaling pathways with animal models and cultured cells. Inhalation exposure of the mice to environmentally relevant fine particulate matter (aerodynamic diameter < 2.5 µm, PM2.5) induces endoplasmic reticulum (ER) stress and activation of unfolded protein response (UPR) in the lung and liver tissues as well as in the mouse macrophage cell line RAW264.7. Ambient PM2.5 exposure activates double-strand RNA-activated protein kinase-like ER kinase (PERK), leading to phosphorylation of translation initiation factor eIF2 and induction of C/EBP homologous transcription factor CHOP/GADD153. Activation of PERK-mediated UPR pathway relies on the production of reactive oxygen species (ROS) and is critical for PM2.5-induced apoptosis. Furthermore, PM2.5 exposure can activate ER stress sensor IRE1, but it decreases the activity of IRE1 in splicing the mRNA encoding the UPR trans-activator X-box binding protein 1 (XBP1). Together, our study suggests that PM2.5 exposure differentially activates the UPR branches, leading to ER stress-induced apoptosis through the PERK-eIF2-CHOP UPR branch. This work provides novel insights into the cellular and molecular basis by which ambient PM2.5 exposure elicits its cytotoxic effects that may be related to air pollution-associated pathogenesis.

 
 
 
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