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作者能较准确地使用学术词汇，但文章中拼写错误稍多；句式变化多样，句法方面做的很棒；上下文衔接稍显不流畅。
The present study demonstrated that both HOXA10 mRNA and protein expression levels in endometrial stromal cells were significantly lower in infertile patients with endometriosis, in those with myoma uteri and in UI patients compared with that in healthy fertile controls. In addition, the percentage of patients in the studied population with altered HOXA-10 protein expression was significantly higher in patients with only superficial peritoneal endometriosis compared with that of infertile patients with other types of endometriosis, those with UF, and UI patients. Tubal adhesions in patients with severe endometriosis can clearly cause infertility. However, the reason for infertility is less obvious in patients with only superficial per-itoneal endometriosis that does not mechanically compromise tubal patency or function. The present findings as well as those by Lessey et al . (1994) suggested that one of the major underlying causes of infertility in patients with only superficial endometriosis might be implantation failure. However, HOXA-10 is not the sole molecule responsible for successful implantation (Giudice and Kao, 2004). Many different molecules could be involved in implantation failure and different underlying molecular defects might be involved in the molecular mechanisms of endometriosis-associated infertility (Giudice and Kao, 2004). Further studies to investigate other endo-metrial molecular defects during the window of implantation in infer-tile patients with endometriosis, particularly those who do not have altered expression levels of HOXA-10 protein, might shed light on the underlying mechanisms of endometriosis-associated infertility. To date, it remains unknown why some patients with endometriosis are infertile, whereas others are not. Endometriosis is detected in 4 – 8% of cases during laparoscopic tubal ligation in women of proven fertility (D’Hooghe et al ., 2003). If endometrial molecular defects are a consequence of the disease in women with endometrio-sis as demonstrated by baboon studies (Gashaw et al ., 2006; Kim et al ., 2007), the biological effect of each endometriotic lesion on eutopic endometrium might be different, and consequently only some women with endometriosis might have endometrial molecular defects which alter embryo implantation. Further studies are needed, both in vivo and in vitro , to investigate interactions between endometriotic tissues and eutopic endometrium and to confirm the baboon studies. One mechanism by which HOXA10 levels are decreased in endo-metriosis is by the methylation of this gene. Wuet al . (2005) demon-strated that methylation of HOXA10 in the endometrium of women with stage III and IV endometriosis is aberrant compared with those without endometriosis. Baboon and mouse studies have demon-strated that the presence of peritoneal endometriotic lesions could induce aberrant methylation of HOXA10 in the eutopic endometrium (Kim et al ., 2007; Lee et al ., 2009). These studies have suggested that superficial peritoneal endometriotic lesions might induce aberrant methylation of the HOXA10 in eutopic endometrium, resulting in decreased HOXA10 protein expression in endometrial stromal cells
