Objective:To evaluate the clinical effects of topical administration of phenytoin ( PHT) on wound healing. Methods:The clinical trials on PHT topically used for wound healing were collected from Cocharne Library and PubMed ( from database establish-ment to May, 2016. Meta-analysis was performed using RevMan 5. 0 software and Stata 12. 0 software. Results:A total of 15 stud-ies involving 1 048 patients were included. Topical PHT treatment was significantly associated with complete healing rate (OR=3. 28, 95%CI:1. 23-8. 75, P=0. 02), production rate of health granulation tissue (OR=2. 18,95%CI:1. 33-3. 59, P=0. 002) and aver-age percentage reduction of wound surface size (SMD=1. 77, 95%CI:0. 53-3. 02, P<0. 000 01). However, heterogeneity existed in complete healing rate and average percentage reduction of wound surface size among the studies. Meta-regression analysis showed that wound types (P=0. 02) and treatment periods(P=0. 08) were associated with the heterogeneity of complete healing rate outcomes, and mean age was associated with the heterogeneity of average percentage reduction of wound surface size(P=0. 07). Conclusion:Meta-analysis suggests that topical PHT treatment has significant positive clinical effect on wound healing. There is heterogeneity among the studies, so topical PHT treatment still should be applied in clinical practice prudently.

Approximately 15% of couples suffer from infertility worldwide, and male factors contribute to about 30% of total sterility cases. However, there is little progress in treatments due to the obscured understanding of underlying mechanisms. Recently microRNAs have emerged as a key player in the process of spermatogenesis. Expression profiling of miR-181a was carried out in murine testes and spermatocyte culture system. In vitro cellular and biochemical assays were used to examine the effect of miR-181a and identify its target S6K1, as well as elucidate the function with chemical inhibitor of S6K1. Human testis samples analysis was employed to validate the findings. miR-181a level was upregulated during mouse spermatogenesis and knockdown of miR-181a attenuated the cell proliferation and G1/S arrest and increased the level of S6K1, which was identified as a downstream target of miR-181a. Overexpression of S6K1 also led to growth arrest of spermatocytes while inhibitor of S6K1 rescued the miR-181a knockdown-mediated cell proliferation defect. In human testis samples of azoospermia patients, low level of miR-181a was correlated with defects in the spermatogenic process. miR-181a is identified as a new regulator and high level of miR-181a contributes to spermatogenesis via targeting S6K1.

Approximately 15% of couples suffer from infertility worldwide, and male factors contribute to about 30% of total sterility cases. However, there is little progress in treatments due to the obscured understanding of underlying mechanisms. Recently microRNAs have emerged as a key player in the process of spermatogenesis. Expression profiling of miR-181a was carried out in murine testes and spermatocyte culture system. In vitro cellular and biochemical assays were used to examine the effect of miR-181a and identify its target S6K1, as well as elucidate the function with chemical inhibitor of S6K1. Human testis samples analysis was employed to validate the findings. miR-181a level was upregulated during mouse spermatogenesis and knockdown of miR-181a attenuated the cell proliferation and G1/S arrest and increased the level of S6K1, which was identified as a downstream target of miR-181a. Overexpression of S6K1 also led to growth arrest of spermatocytes while inhibitor of S6K1 rescued the miR-181a knockdown-mediated cell proliferation defect. In human testis samples of azoospermia patients, low level of miR-181a was correlated with defects in the spermatogenic process. miR-181a is identified as a new regulator and high level of miR-181a contributes to spermatogenesis via targeting S6K1.