Clinical endpoint committee (CEC) plays an important role in the process of the endpoint events adjudication in clinical trials. It greatly influences quality control of clinical trials, the importance of which increases especially after the emergency of the definition of clinical endpoint events by Academic Research Consortium (ARC). In this paper, we briefly introduce the role of CEC in the process of the quality control of clinical trials, application of CEC in China and abroad, and its influence to the primary endpoints. We also investigate the application and development of CEC in the field of cardiovascular diseases, and discuss how to reasonably apply CEC and maximize its role in the process of the endpoint events adjudication of clinical trials.
【Abstract】 Objective To investigate the effect of verapamil on apoptosis, calcium and expressions of bcl-2 and c-myc of pancreatic cells in ischemia-reperfusion rat model. Methods Wistar rats were randomly divided into three groups: control group （n=10）; ischemia-reperfusion group （n=10）; verapamil treatment group （n=10）. The anterior mesenteric artery and the celiac artery of rats in both ischemia-reperfusion group and verapamil treatment group were occluded for 15 min followed by 12-hour reperfusion. Verapamil （1 mg／kg） was injected via caudal vein to the rats in verapamil treatment group 15 min before occlusion and 1 hour after the initiation of reperfusion, respectively; and ischemia-reperfusion group was given the same volume of salient twice intravenously. Pancreatic tissues were collected from the dead rats after twelve hours since the reperfusion. The pathologic characters of pancreatic tissue were observed under light microscope; The level of calcium in the tissue was measured by atomic absorption spectrometer; TUNEL was used to detect apoptosis of pancreatic cells; and the expressions of c-myc and bcl-2 in the cells were also analyzed by immunohistochemistry technique and flow cytometry. Results The pathologic change in verapamil treatment group was less conspicuous than that of ischemia-reperfusion group. Both the calcium level and the number of apoptotic cells in verapamil treatment group were less than those of ischemia-reperfusion group 〔（411.1±55.8） μg/g dry weight vs （470.9±31.9） μg/g dry weight, P＜0.05 and （9.5±2.9）% vs （18.4±3.1）% 〕, P＜0.05. After taking verapamil, the number of apoptotic cells decreased, whereas the expressions of bcl-2 and c-myc increased. The fluorescent indexes of bcl-2 and c-myc in verapamil treatment group were significantly higher than those of ischemia-reperfusion group (1.72±0.11 vs 1.41±0.07, P＜0.05; 1.76±0.19 vs 1.55±0.13, P＜0.05. Conclusion Ischemia-reperfusion injury can induce apoptosis of pancreatic cells. Verapamil could protect the injured pancreatic tissue by reducing the level of calcium, stimulating the expressions of bcl-2 and c-myc and inhibiting apoptosis of pancreatic cells.