绝经后女性冠心病患者内源性女性激素分泌异常及其对一氧化氮合成的影响

目的观察绝经后女性冠心病患者内源性女性激素分泌的异常变化及其对一氧化氮合成的影响,探讨造成雌、孕激素联用的性激素替代疗法失败的可能原因。方法筛选绝经后女性冠心病患者100例及年龄、绝经年限和体质指数具可比性的健康绝经后女性100例,采用放射免疫法测定血清雌二醇和孕酮的水平,采用化学比色法测定血清一氧化氮水平及一氧化氮合酶活性,并对雌二醇、孕酮及雌二醇/孕酮与血清一氧化氮及一氧化氮合酶的关系进行相关分析。结果绝经后女性冠心病患者与健康绝经后女性相比,雌二醇水平下降(121±32比156±31 pmol/L),孕酮水平上升(5.67±1.60比3.14±1.10 nmol/L),雌二醇/孕酮明显降低(27.9±26.5比52.4±37.8),相关分析显示雌二醇、雌二醇/孕酮与血清一氧化氮和一氧化氮合酶活性呈正相关关系,血清孕酮水平与一氧化氮和一氧化氮合酶活性呈负相关关系。结论绝经后女性冠心病患者雌激素水平降低,孕激素水平升高,雌激素/孕酮比值降低,这种改变对血管内皮功能有不良影响。性激素替代疗法时雌激素和孕激素剂量搭配不适当孕激素偏高,导致雌/孕激素比偏低可能是其未能有效保护心血管系统的原因之一。     

创伤性脑损伤后孕酮促进神经功能的实验研究

目的观察孕酮对大鼠脑损伤后COX-2和IL-6表达及对神经功能的影响。方法雄性SD大鼠48只随机分为假手术组、脑损伤组和孕酮治疗组,按照改良的Feeney自由落体损伤装置制作大鼠脑损伤模型。孕酮治疗组伤后1、6 h腹腔注射孕酮16 mg/kg。各组于伤后24 h取材。用ELISA法检测COX-2和IL-6含量,用干湿重法测量脑组织含水量,用mNSS评分检测神经功能。结果孕酮治疗组与脑损伤组比较,COX-2和IL-6表达和脑水肿明显减少(P<0.05),神经功能明显改善(P<0.05)。结论孕酮可能通过降低COX-2和IL-6的表达,进而降低脑水肿,改善神经功能,发挥脑损伤保护作用。     

宫腔镜手术联合黄体酮胶囊诊治子宫内膜息肉的临床分析

目的探讨宫腔镜手术联合黄体酮胶囊诊治子宫内膜息肉的临床疗效。方法回顾性的分析我院2009年1月至2013年6月收治的258例子宫内膜息肉患者,所有患者是采用宫腔镜检查发现子宫内膜息肉转行宫腔镜子宫内膜息肉电切术同时予行诊刮术,术中电切出组织及刮出组织全部送病理检查。经病理确诊为子宫内膜息肉者随机分为两组,对照组122例为单纯行子宫内膜息肉电切术组;研究组136例为子宫内膜息肉电切术加服黄体酮胶囊组。比较分析两组的治疗效果。结果对照组复发率13.12%(16/122);异常子宫出血发生率20.49%(25/122);研究组复发率3.68%(5/136);异常子宫出血发生率5.15%(7/136)。两组比较有显著差异性。子宫内膜息肉不孕症患者25例行宫腔镜检查及宫腔镜子宫内膜息肉电切术后联合黄体酮胶囊治疗后19例成功妊娠。宫腔镜诊断与病理诊断比较符合率为91.5%。结论 1宫腔镜诊断和治疗子宫内膜息肉有较高的临床价值;2宫腔镜子宫内膜息肉电切术后应用黄体酮胶囊可以抑制子宫内膜局部过度增生,改善症状和降低子宫内膜息肉的复发;可以提高子宫内膜息肉导致不孕患者的生育能力。值得临床推广应用。     

Interaction between sex hormones and WNT/β-catenin signal transduction in endometrial physiology and disease

Wnt/β-catenin signalling plays a rate-limiting role in early development of many different organs in a broad spectrum of organisms. In the developing Müllerian duct, Wnt/β-catenin signalling is important for initiation, outgrowth, patterning and differentiation into vagina, cervix, uterus and oviducts. In adult life, sex hormones modulate Wnt/β-catenin signalling in the endometrium to maintain the monthly balance between estrogen-induced proliferation and progesterone-induced differentiation, and enhanced Wnt/β-catenin signalling seems to be involved in endometrial carcinogenesis. However, early in pregnancy enhanced Wnt/β-catenin signalling is prerequisite for proper implantation and invasion of trophoblast cells into endometrium and myometrium thus helping to form a placenta. Overall, it seems that tight control of Wnt/β-catenin signalling in time and space is important for initiation, development and normal function of the female reproductive tract. However, if Wnt/β-catenin signalling is not kept in check, it easily seems to initiate or contribute to development of a number of uterine disorders.     

Polycystic ovary syndrome: Understanding the role of the brain

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder and the leading cause of anovulatory infertility. Characterised by hyperandrogenism, menstrual dysfunction and polycystic ovaries, PCOS is a broad-spectrum disorder unlikely to stem from a single common origin. Although commonly considered an ovarian disease, the brain is now a prime suspect in both the ontogeny and pathology of PCOS. We discuss here the neuroendocrine impairments present in PCOS that implicate involvement of the brain and review evidence gained from pre-clinical models of the syndrome about the specific brain circuitry involved. In particular, we focus on the impact that developmental androgen excess and adult hyperandrogenemia have in programming and regulating brain circuits important in the central regulation of fertility. The studies discussed here provide compelling support for the importance of the brain in PCOS ontogeny and pathophysiology and highlight the need for a better understanding of the underlying mechanisms involved.