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Tien‐Yao Tsai Iat‐Lon Leong Ka‐Shun Cheng Lian‐Ru Shiao Tzu‐Hui Su Kar‐Lok Wong Paul Chan Yuk‐Man Leung 《Fundamental & clinical pharmacology》2019,33(1):52-62
A pathological feature in atherosclerosis is the dysfunction and death of vascular endothelial cells (EC). Oxidized low‐density lipoprotein (LDL), known to accumulate in the atherosclerotic arterial walls, impairs endothelium‐dependent relaxation and causes EC apoptosis. A major bioactive ingredient of the oxidized LDL is lysophosphatidylcholine (LPC), which at higher concentrations causes apoptosis and necrosis in various EC. There is hitherto no report on LPC‐induced cytotoxicity in brain EC. In this work, we found that LPC caused cytosolic Ca2+ overload, mitochondrial membrane potential decrease, p38 activation, caspase 3 activation and eventually apoptotic death in mouse cerebral bEND.3 EC. In contrast to reported reactive oxygen species (ROS) generation by LPC in other EC, LPC did not trigger ROS formation in bEND.3 cells. Pharmacological inhibition of p38 alleviated LPC‐inflicted cell death. We examined whether heparin could be cytoprotective: although it could not suppress LPC‐triggered Ca2+ signal, p38 activation and mitochondrial membrane potential drop, it did suppress LPC‐induced caspase 3 activation and alleviate LPC‐inflicted cytotoxicity. Our data suggest LPC apoptotic death mechanisms in bEND.3 might involve mitochondrial membrane potential decrease and p38 activation. Heparin is protective against LPC cytotoxicity and might intervene steps between mitochondrial membrane potential drop/p38 activation and caspase 3 activation. 相似文献
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Recognizing and managing a deteriorating patient: a randomized controlled trial investigating the effectiveness of clinical simulation in improving clinical performance in undergraduate nursing students
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Fluid role boundaries: exploring the contribution of the advanced nurse practitioner to multi‐professional palliative care
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Anne-Marie Selzler Veronica Moore Razanne Habash Lauren Ellerton Erica Lenton Roger Goldstein 《COPD》2020,17(4):452-461
Abstract The purpose of this study was to investigate the strength of the relationships between self-efficacy and (i) functional exercise capacity and (ii) physical activity in chronic obstructive pulmonary disease (COPD), and whether self-efficacy assessment type (i.e., COPD symptoms, exercise-task, exercise-barrier, general, falls) and physical activity assessment type (i.e., self-report vs. objective) are moderators. A systematic search of COPD and self-efficacy concepts was conducted using eight databases from inception to 23 January 2019. Studies were included if they provided correlation coefficients of the relationship between self-efficacy and functional exercise capacity or physical activity, were conducted in adults diagnosed with COPD, and were published in English-language journals. A total of 14 correlation coefficients were included in the self-efficacy and functional exercise capacity meta-analysis, and 16 in the self-efficacy and physical activity meta-analysis. Data were screened, reviewed, and extracted independently by two reviewers, with discrepancies resolved by a third reviewer. Stronger self-efficacy was associated with better functional exercise capacity (weighted r?=?0.38, 95%CI [0.25, 0.50]), and greater physical activity (weighted r?=?0.25, 95%CI [0.17, 0.34]). Exercise-task self-efficacy had the strongest relationship to functional exercise capacity (weighted r?=?0.64, 95% CI [0.51, 0.73]). For physical activity, the type of self-efficacy most strongly related was inconclusive. In COPD, self-efficacy has a relationship to functional exercise capacity and physical activity, the strength of which is influenced by the choice of self-efficacy measure. An understanding of these relationships will assist clinicians in selecting the self-efficacy measure most closely related to the outcome of interest. 相似文献