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Wei Chao,Long Gongwei,Zhang Yucong,Wang Tao,Wang Shaogang,Liu Jihong,Ma Delin,Liu Xiaming 대한남성과학회 2021 The World Journal of Men's Health Vol.39 No.4
Purpose: Pulsatile gonadotropin-releasing hormone (GnRH) therapy and gonadotropin therapy (GT) were widely used for male patients with congenital hypogonadotropic hypogonadism (CHH), but their efficacy was not well compared before. We conducted this meta-analysis to compare the efficacy of restoring fertility using these two therapies. Materials and Methods: PubMed, Web of Science, and Scopus were systematically searched for comparative studies evaluating the efficiency of GnRH therapy and GT for male patients with CHH. For continuous outcomes, the weighted mean difference (WMD) was used to measure the difference, whereas the risk ratio with 95% confidence interval was calculated for binary variables. Results: Overall, eight articles from seven studies with 420 patients enrolled were included in the analysis. Patients from the two different groups were determined to be comparable in age, proportion with Kallmann syndrome, percentage of cryptorchidism and pretreatment hormones (follicular-stimulating hormone, luteinizing hormone, and testosterone). GnRH therapy was related to a larger testicular volume (standardized mean difference=-1.43; p=0.01) and earlier spermatogenesis (WMD=- 5.30 months; p=0.004) compared to GT. However, the difference in the rate of positive sperm detection (p=0.08), sperm concentration (p=0.37), and pregnancy rate (p=0.11) were not significant. Allergic reactions mostly occurred during GnRH therapy, while GT was related to a higher incidence of gynecomastia and acne. Conclusions: Compared to GT, GnRH was related to earlier spermatogenesis and less estradiol-related adverse reactions, although there were no significant differences in spermatogenesis rate, sperm concentration, and pregnancy rate. High-quality randomized controlled trials are needed for future research.
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Tang Zhe,Song Jingyu,Yu Zhe,Cui Kai,Ruan Yajun,Liu Yang,Wang Tao,Wang Shaogang,Liu Jihong,Yang Jun 대한남성과학회 2023 The World Journal of Men's Health Vol.41 No.1
Purpose: To determine whether microRNA could be a therapy target of erectile dysfunction (ED) and the underlying mecha-nisms. Materials and Methods: Eight-week-old fasting male SD rats were intraperitoneally injected with streptozotocin to construct diabetic rat models. Diabetic ED rats were treated with miRNA-92a inhibitor. The cavernous nerves were electrically stimu-lated to measure the intracavernous pressure and mean arterial pressure of rats in each group. After the detection, the penile cavernous tissues are properly stored for subsequent experiments. Rat aortic endothelial cells were used in in vitro studies. Results: The expression of miR-92a was significantly increased in the corpus cavernosum of Streptozocin (STZ)-induced di- abetic rats and injection of miR-92a antagomir into the corpus cavernosum of diabetic rats significantly increased eNOS/NO/ cGMP signaling pathway activities, cavernous endothelial cell proliferation, endothelial cell-cell junction protein expression and decreased the levels of oxidative stress. These changes restored erectile function in STZ-induced diabetic rats. Moreover, in vitro study demonstrated that the miR-92a expression increased significantly in endothelial cells treated with high glucose, inhibiting AMPK/eNOS and AMPK/Nrf2/HO-1 signaling pathways in rat aortic endothelial cells via targeting Prkaa2, causing endothelial dysfunction and overactive oxidative stress, miR-92a inhibitor can improve the above parameters. Conclusions: miRNA-92a inhibitor could exert an inhibition role on oxidative stress and endothelial dysfunction to improve diabetic ED effectively.
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Yang, Kun,Park, Chae G,Cheong, Cheolho,Bulgheresi, Silvia,Zhang, Shusheng,Zhang, Pei,He, Yingxia,Jiang, Lingyu,Huang, Hongping,Ding, Honghui,Wu, Yiping,Wang, Shaogang,Zhang, Lin,Li, Anyi,Xia, Lianxu,B Nature Publishing Group 2015 Immunology and Cell Biology Vol. No.
<P><I>Yersinia pestis</I> is a Gram‐negative bacterium that causes plague. After <I>Y. pestis</I> overcomes the skin barrier, it encounters antigen‐presenting cells (APCs), such as Langerhans and dendritic cells. They transport the bacteria from the skin to the lymph nodes. However, the molecular mechanisms involved in bacterial transmission are unclear. Langerhans cells (LCs) express Langerin (CD207), a calcium‐dependent (C‐type) lectin. Furthermore, <I>Y. pestis</I> possesses exposed core oligosaccharides. In this study, we show that <I>Y. pestis</I> invades LCs and Langerin‐expressing transfectants. However, when the bacterial core oligosaccharides are shielded or truncated, <I>Y. pestis</I> propensity to invade Langerhans and Langerin‐expressing cells decreases. Moreover, the interaction of <I>Y. pestis</I> with Langerin‐expressing transfectants is inhibited by purified Langerin, a DC‐SIGN (DC‐specific intercellular adhesion molecule 3 grabbing nonintegrin)‐like molecule, an anti‐CD207 antibody, purified core oligosaccharides and several oligosaccharides. Furthermore, covering core oligosaccharides reduces the mortality associated with murine infection by adversely affecting the transmission of <I>Y. pestis</I> to lymph nodes. These results demonstrate that direct interaction of core oligosaccharides with Langerin facilitates the invasion of LCs by <I>Y. pestis</I>. Therefore, Langerin‐mediated binding of <I>Y. pestis</I> to APCs may promote its dissemination and infection.</P>
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