When these studies moved, the heterogeneity was decreased but the pooled results were not influenced, which suggested these data are stable. Thirdly, the methods used for the AbMole 2,3-Dichloroacetophenone assessment of the level of SOX2 expression in NSCLC patients 
differed among these studies. Besides, there were some differences among these studies in cutoff values of defining the specimens as positive SOX2 expression or amplification. The new studies with same cutoff values must be recruited and combined for further evaluation. Moreover, the cutoff value would be obtained by statistic models, such as receiver operator characteristic analysis, the area under thecurve at different cutoff values for survival time was calculated, which has been used in our previous studies. Therefore, additional studies with the larger sample sizes, high quality and different ethnic background are needed to make a more definitive conclusion. In summary, our meta-analysis showed that SOX2 expression was not correlated with clinicopathological parameters except for histology. Simultaneously, SOX2 overexpression predicted a betteroverall survival despite of histology. Therefore, it is appropriate to regard SOX2 expression as a promising prognostic biomarker for NSCLC patients. Prospective studies relating SOX2 expression with surgery, chemotherapy and biologicals in NSCLC are warranted. Mechanical trauma, such as that induced by natural disaster, athletic sports, war, and motor vehicle crashes, represents a major medical and economic problem in modern society. Nowadays, trauma is the leading cause of mortality in the young aged population. A number of studies report that mechanical trauma can cause direct heart damage, such as coronary artery dissection and cardiac contusion. As a result of advanced prehospital care and regional trauma systems development, fewer critically injured patients are dying at the scene of the accident. However, recently published clinical reports have indicated that mechanical trauma may cause cardiac death even in the absence of direct cardiomyocyte injury during the first 24 h. These results suggest that nonlethal mechanical trauma can induce delayed cardiac injury. However, the mechanisms responsible for nonlethal mechanical trauma-induced delayed cardiac injury have not yet been identified. There are two main reasons for delayed cardiac injury, including myocardial cell apoptosis and homeostasis. Studies have shown that apoptosis may contribute to cardiac dysfunction, and the inhibition of apoptosis by a variety of pharmacological inhibitors or genetic strategies results in smaller infarction, improved cardiac function, and attenuated cardiac remodeling. Our previous results revealed that the significant cardiomyocyte apoptosis caused by nonlethal mechanical trauma underlies posttraumatic delayed cardiac dysfunction. However, anti-apoptotic therapy alone cannot completely alleviate the delayed cardiac injury.