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941.
    
Perivalvular leaks are usually caused by suture interruption in prosthetic valves or infective endocarditis. Traumatic mitral annular dehiscence is a very uncommon event. We present a rare case of severe mitral regurgitation secondary to perivalvular abnormal communication in a 35‐year‐old man with a history of blunt chest trauma. He presented with symptoms of cough and chest tightness for 3 months. Preoperative two‐dimensional and real time three‐dimensional transesophageal echocardiography clearly showed the position and size of the perivalvular abnormal communication and the incident damage of the left ventricular wall. The patient finally underwent successful surgical repair.  相似文献   
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The effect of adjuvant chemotherapy on survival of patients with thoracic esophageal squamous cell carcinomas is still controversial, and the subgroup of patients who will most likely benefit from the adjuvant chemotherapy on long‐term survival has not yet been identified clearly. Studies published from 1995 to May 2012 were searched in Medline, Embase, PubMed, Cancerlit, the Cochrane Library, CNKI and major scientific meetings. Randomized controlled trials and nonrandomized studies comparing surgery plus adjuvant chemotherapy with surgery alone in patients with resectable thoracic esophageal squamous cell carcinomas were included. Eleven studies with a total of 2047 patients were identified, consisting of the adjuvant chemotherapy arm (n = 887) and surgery‐alone arm (n = 1160). There was not statistically significant benefit on 3‐year overall survival for adjuvant chemotherapy (risk ratio [RR] = 0.89, 95% confidence interval [CI], 0.72 to 1.09; P = 0.25). Adjuvant chemotherapy could significantly prolong the 1‐year disease‐free survival (DFS) (RR = 0.68, 95%CI, 0.51 to 0.89; P = 0.006), but not 3‐year DFS (RR = 0.97, 95%CI, 0.73 to 1.29; P = 0.84). Further analysis showed that patients with stage III‐IV diseases could benefit from adjuvant chemotherapy on 3‐year overall survival (RR = 0.43, 95%CI, 0.31 to 0.61; P = 0.00001), but not in the case of patients with stageI‐IIdiseases (RR = 1.12, 95%CI, 0.65 to 1.93; P = 0.68). Additionally, patients with positive lymph node could benefit on 5‐year DFS from adjuvant chemotherapy (RR = 0.79, 95%CI, 0.64 to 0.99; P = 0.04). The modality treatment with adjuvant chemotherapy for patients with squamous cell carcinoma of thoracic esophagus might be determined according to pathological stage or the status of lymph node metastasis.  相似文献   
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Objective

Regulation of the conversion of plasminogen to plasmin by tissue plasminogen activator (tPA) is critical in the control of fibrin deposition. While several plasminogen activators have been described, soluble plasma cofactors that stimulate fibrinolysis have not been characterized. The purpose of this study was to investigate the effects of β2‐glycoprotein I (β2GPI), an abundant plasma glycoprotein, on tPA‐mediated plasminogen activation.

Methods

The effect of β2GPI on tPA‐mediated activation of plasminogen was assessed using amidolytic assays, a fibrin gel, and plasma clots. Binding of β2GPI to tPA and plasminogen was determined in parallel. The effects of IgG fractions and anti‐β2GPI antibodies from patients with antiphospholipid syndrome (APS) on tPA‐mediated plasminogen activation were also measured.

Results

Beta2‐glycoprotein I stimulated tPA‐dependent plasminogen activation in the fluid phase and within a fibrin gel. The β2GPI region responsible for stimulating tPA activity was shown to be at least partly contained within β2GPI domain V. In addition, β2GPI bound tPA with high affinity (Kd ∼20 nM), stimulated tPA amidolytic activity, and caused an overall 20‐fold increase in the catalytic efficiency (Kcat/Km) of tPA‐mediated conversion of Glu‐plasminogen to plasmin. Moreover, depletion of β2GPI from plasma led to diminished rates of clot lysis, with restoration of normal lysis rates following β2GPI repletion. Stimulation of tPA‐mediated plasminogen activity by β2GPI was inhibited by monoclonal anti‐β2GPI antibodies as well as by anti‐β2GPI antibodies from patients with APS.

Conclusion

These findings suggest that β2GPI may be an endogenous regulator of fibrinolysis. Impairment of β2GPI‐stimulated fibrinolysis by anti‐β2GPI antibodies may contribute to the development of thrombosis in patients with APS.
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