戊酸雌二醇配伍药物流产在早中期妊娠引产中的疗效观察

目的探讨戊酸雌二醇联合米非司酮和米索前列醇终止10～20周早中期妊娠的临床疗效。方法对146例妊娠10～20周要求终止妊娠的孕妇以戊酸雌二醇联合米非司酮和米索前列醇引产。观察胚胎排出时间、胚胎流产情况、产后出血量及药物不良反应。结果 146例孕妇用药24h后,妊娠物排出者144例(98.6%),仅2例(1.4%)无任何妊娠物排出。完全流产124例(84.9%),不全流产20例(13.7%),失败2例(1.4%)。出血量为5～20ml,无大出血发生。不良反应均轻微,无需处理。结论戊酸雌二醇联合米非司酮和米索前列醇终止10～20周妊娠简便、安全、有效,具有胃肠道不良反应轻、引产时间短、出血量少、组织残留率低、并发症少、成功率高等优点,值得临床推广应用。     

产后抑郁与分娩前后血清同型半胱氨酸、雌二醇水平变化的相关性分析

目的分析产后抑郁与分娩前后血清同型半胱氨酸(Hcy)、雌二醇(E2)水平变化的相关性。方法选取我院2018年7月至2019年7月收治的120例初产妇,在分娩后7天时采用爱丁堡产后抑郁量表(EPDS)评估产妇的抑郁状态,根据评估结果分为产后抑郁组(n=15)和非抑郁组(n=105)。比较两组产妇的一般资料及分娩前、分娩后7天的血清Hcy、 E2水平,分析EPDS评分与血清Hcy、 E2水平的相关性。结果 120例产妇中,有15例(12.5%)发生产后抑郁。产后抑郁组的受教育程度显著低于非抑郁组(P <0.05)。分娩前,两组的血清Hcy、 E2水平比较无统计学差异(P>0.05);分娩后7天,产后抑郁组的血清Hcy水平显著高于非抑郁组,血清E2水平显著低于非抑郁组(P均<0.05)。EPDS评分与分娩后血清Hcy水平呈正相关(r=0.233, P <0.05),与分娩后血清E2水平呈负相关(r=-0.691, P <0.05)。结论分娩后血清Hcy水平升高、 E2水平降低可能是产后抑郁的危险因素,检测分娩后Hcy、 E2水平有助于产后抑郁症的预测。     

Irreversible Changes in Rat Erythrocyte Na+ Transport Systems with Progesterone and Estradiol Administration

In order to test whether alterations in Na⁺ transport systems occurring in women when the hormonal status is disturbed such as in pregnancy, under contraceptive or estradiol therapy are a direct result of hormonal action on these transport systems, Na⁺, K⁺-pump Na⁺, K⁺ outward cotransport and passive Na⁺ permeability were measured in erythrocytes of ovariectomized rats receiving estradiol or progesterone. No significant changes in Na⁺, K⁺-pump were observed in either conditions. Conversely, progesterone was found to decrease Na⁺, K⁺-cotransport and estradiol to increase this system, whereas both steroids increased passive Na⁺ permeability.     

女性不同性激素水平下脑源性神经营养因子的变化

目的:观察女性不同性激素水平下脑源性神经营养因子(brain-derived neurotrophic factor,BD-NF)的变化.方法:临床纳入62例围绝经期及绝经后妇女,根据STRAW分期以及绝经年限长短进行分组,同时纳入16例健康育龄妇女作为对照组.分别采集所有入组者的血液标本,检测血清雌二醇(E2)、睾酮(T)、卵泡刺激素(FSH)以及BDNF的水平.结果:围绝经期组以及绝经后的妇女,血清BD-NF水平明显低于健康育龄妇女,BDNF水平与E2水平有明显相关性(r=0.302,P=0.016).结论:血清BDNF水平与脑源性雌激素水平有着密切的联系.     

17β雌二醇对大鼠创伤性脑损伤的保护作用

目的 探讨大鼠创伤性脑损伤后17β雌二醇对脑组织的保护作用。方法 选择雄性成年 SD大鼠 45 只, 按随机数字表法分为三组, 每组15只: 对照组仅开骨窗, 不损伤脑组织;致伤组制大鼠自由落体脑撞击伤模型;处理组在致伤组的基础上, 伤前1周腹腔注射17β雌二醇溶液(1 mg/kg), 1次/d。余两组仅注射同体积的蓖麻油。在伤后 6 h、 24 h 及48 h 测量各组脑组织含水量、 丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果 致伤组和处理组在伤后 6 h、24 h、48 h 三个时间点脑组织含水量均高于对照组(P<0.05)。在伤后 6 h, 致伤组和处理组脑组织含水量比较差异无统计学意义[(58.39±0.29)%比(57.03±0.27)%] (P> 0.05), 而在伤后24 h、48 h 致伤组脑组织含水量明显高于处理组,差异有统计学意义 [(67.41±0.37)%比(64.77±0.33)%, (81.95±0.47)%比(75.26±0.41)%](P<0.05)。在伤后 6 h 致伤组、处理组 MDA含量明显增加, 并且一直维持在较高水平, 而 SOD活性则明显下降, 与对照组比较差异有统计学意义 (P<0.05)。处理组在伤后6 h MDA含量和 SOD活性与致伤组比较差异无统计学意义(P>0.05), 而在伤后24 h、48 h MDA 含量显著降低[(130.39±7.02) μmol/g 比(149.41±8.25) μmol/g, (125.41±6.59) μmol/g 比(157.72±8.93) μmol/g], SOD活性则明显增高[(88.46±7.17)U/g比(80.10±4.87)U/g, (97.31±7.89)U/g 比(84.29±6.13) U/g], 差异均有统计学意义 (P<0.05)。结论 17β雌二醇对创伤性脑损伤有保护作用。     

Ethanol induces hyperprolactinemia by increasing prolactin release and lactotrope growth in female rats

BACKGROUND: Alcohol drinking is known to cause hyperprolactinemia in both humans and laboratory animals. The mechanism by which alcoholism causes hyperprolactinemia is not known. This study investigated whether increased pituitary production of prolactin, which leads to alcohol-induced hyperprolactinemia, results from an increase in cell number and/or cell production of prolactin in the pituitary. METHODS: The effects of ethanol on lactotropes were determined in vivo using female rats as an animal model and in vitro using primary cultures of mixed rat anterior pituitary cells and enriched lactotropes. In vivo experiments involved administration of ethanol for 2 and 4 weeks using a liquid diet containing 8.7% ethanol (v/v), which provides 37% of the calories in cyclic, ovariectomized, and estradiol-17beta-treated ovariectomized Fischer-344 rats. The control group was pair-fed an isocaloric diet minus the ethanol or fed a normal diet ad libitum. These animals were used to determine ethanol's effects on plasma prolactin levels, pituitary wet weights, pituitary total protein levels, and the number of mitotic lactotropes. In vitro studies determined ethanol's effects in the presence and absence of estradiol on prolactin release and lactotropic cell proliferation. Prolactin levels in plasma and media samples were measured using radioimmunoassay. Mitotic lactotropes were determined using bromodeoxyuridine incorporation assay. RESULTS: Ethanol treatment increased in a time-dependent manner the plasma levels of prolactin in cyclic, ovariectomized, and estradiol-treated ovariectomized rats. Ethanol treatment also increased pituitary wet weight and/or pituitary total protein levels and DNA synthesis in lactotropes. Determination of ethanol's action on lactotropic cell proliferation and hormone secretion in vitro using primary cultures of mixed pituitary cells revealed that ethanol stimulated both basal and estradiol-induced prolactin secretion and lactotropic cell proliferation. When ethanol's actions were studied in isolated lactotropes, ethanol alone or in combination with estradiol stimulated prolactin secretion but failed to increase lactotropic cell proliferation. CONCLUSIONS: These results suggest that ethanol causes hyperprolactinemia by elevating prolactin release from lactotropes and by increasing the number of lactotropes in the anterior pituitary gland. The mitotic action of ethanol requires cell-cell communication between lactotropes and other pituitary cells. Furthermore, ethanol's mode of action on prolactin release and lactotrope growth is similar to that observed for estradiol.     

Age at menopause,body mass index,and risk of type 2 diabetes mellitus in postmenopausal Chinese women: The Henan Rural Cohort study

Background and aimThe present study was conducted to explore the stratified and joint effects of age at menopause and body mass index (BMI) with the risk of type 2 diabetes mellitus (T2DM) in Chinese rural adults.Methods and resultsA total of 15,406 postmenopausal Chinese women were included in this study. Multivariable logistic regression analysis was used to quantify the stratified and joint effects of age at menopause and BMI on T2DM. Overall, the mean age at menopause and BMI was 48.8 ± 4.7 years and 25.1 ± 3.6 kg/m², respectively. In general, data suggest that: 1) women with BMI ≥ 24 had a higher risk of T2DM, irrespective of age at menopause; 2) in women with BMI < 24, later menopause had a higher risk of T2DM (OR, 1.52; 95% CI, 1.16–2.01); 3) the risk of T2DM was higher only in patients with early or normal age at menopause and BMI ≥ 24, with 0R (95% CI) of (1.58, 1.28–1.94) and (1.48, 1.31–1.67), respectively.ConclusionOur findings suggest that: 1) women with BMI ≥ 24 had a higher risk of T2DM, irrespective of age at menopause; 2) in women with BMI < 24, a higher risk of T2DM was found only in those with later menopause; 3) women with later menopause had a higher risk of T2DM, irrespective of BMI; 4) in patients with early or normal age at menopause, a higher risk of T2DM was found only in patients with BMI ≥ 24.The Chinese Clinical Trial RegistrationChiCTR–OOC–1500669(URL:http://www.chictr.org.cn/showproj.aspx?proj=11375)