环境内分泌干扰物-双酚A与女性生殖健康关系的研究进展

双酚-A(BPA)等环境内分泌干扰物是一类普遍存在于日常生活中的外源性化学物质,可以结合人体内不同的激素受体,通过多种机制干扰内源激素的功能,导致诸多疾病发生.本文就非持久性环境内分泌干扰物-BPA对女性生殖系统的作用及生殖健康的影响进行了分析和总结,并提出了对今后研究的启示.     

环境内分泌干扰物与儿童性发育异常

环境内分泌干扰物可通过干扰下丘脑-垂体-性腺轴的调节功能,及干扰促性腺激素和性激素的合成、释放、运输、代谢及与受体结合等过程而引起儿童的性发育异常.遗传背景的差异可影响机体对环境内分泌干扰物的敏感性.环境内分泌干扰物与机体易感基因的交互作用可增加儿童性发育异常的发生率.     

环境内分泌干扰物与乳腺癌的关系

环境内分泌干扰物广泛存在于食品包装材料、化妆品等及环境介质中。该文对3种常见环境内分泌干扰物(双酚A、邻苯二甲酸酯、多氯联苯)与乳腺癌关系的相关研究进行综述,包括其在环境中的分布、摄入途径、暴露剂量、在人体内的分布、对乳腺癌发生发展影响的流行病学研究,并列举诱发乳腺癌的相关机制,如基因和表观遗传层面的调节机制、通过雌激素受体(ER)介导的拟雌激素效应、诱导产生活性氧、诱导非ER介导的信号通路激活以及微环境调节等,并对未来相关毒理学和分子机制研究及流行病学研究方向进行展望。     

环境内分泌干扰物与前列腺疾病的研究现况

前列腺疾病是男性泌尿生殖系统的常见病,包括前列腺增生、前列腺癌等,多发生于中老年男性。前列腺是性激素依赖器官,其生长、分化等过程均需要性激素的调控。目前,环境中存在多种内分泌干扰物,可干扰体内正常内分泌激素的合成、释放、结合、代谢等,从而影响机体内环境稳态、生殖、发育及行为。研究表明,某些环境内分泌干扰物可影响前列腺疾病的发生和发展,本文对影响前列腺疾病的常见环境内分泌干扰物进行分类阐述,认为今后应加强相关人群资料的积累和人群流行病学的研究,探讨其发病机制,明确各类内分泌干扰物与前列腺疾病之间的关联。     

036 壬基酚对机体影响的研究进展

调查研究表明,壬基酚作为一种环境内分泌干扰物,具有雌激素样作用,能干扰多种动物的内分泌系统,影响生殖、免疫、神经、心血管等系统的功能.本文从整体和细胞水平介绍了壬基酚对机体不同系统以及对肿瘤发生的影响,重点从与受体作用、激素代谢、生物利用率、细胞信号传导等方面对其作用机制进行讨论.     

环境雌激素和癌症

近年来科学家们将环境中能对机体健康产生不利影响或使其后代内分泌功能发生改变的外源性化学物质称为“环境内分泌干扰物 (environmental endocrinedisruptors,EEDs)”,即这些环境外来化学物质可通过影响体内天然激素的产生、合成、释放、转运、代谢和 /或清除 ,与相应的受体结合并随之在细胞内产生效应 ,干扰血液中激素正常水平的维持 ,模拟或干扰天然激素的生理、生化作用。在“环境内分泌干扰物”中有一类化学物质具有激活或抑制正常内分泌功能 ,或具有雌激素样活性 ,或具有阻断雄激素效应 ,从而破坏其维持机体稳定性和调控作用的物质…     

壬基酚对机体影响的研究进展

调查研究表明 ,壬基酚作为一种环境内分泌干扰物 ,具有雌激素样作用 ,能干扰多种动物的内分泌系统 ,影响生殖、免疫、神经、心血管等系统的功能。本文从整体和细胞水平介绍了壬基酚对机体不同系统以及对肿瘤发生的影响 ,重点从与受体作用、激素代谢、生物利用率、细胞信号传导等方面对其作用机制进行讨论。     

四溴双酚-A及其环境问题

四溴双酚-A是一种在世界范围内被广泛应用的溴代阻燃剂.它是一种类似于持久性有机污染物的潜在环境内分泌干扰物,能在环境和生物体内积累,对环境和生物产生严重的影响,如干扰生物的激素系统,影响骨骼和大脑发育等.该文对四溴双酚-A的环境背景值、人体及生物体中水平、分析方法、毒理学等方面的研究内容进行综述.     

雌激素受体在促进生殖系统癌细胞增殖和转化中的作用

环境内分泌干扰物是一类广泛存在于环境中、进入机体后模拟激素作用干扰内分泌系统导致疾病的外源性物质。近年来,生殖系统雌激素依赖性疾病发病率逐年增加,如乳腺癌、卵巢癌、前列腺癌等。研究表明,环境内分泌干扰物暴露可以增加生殖系统癌症的发生率。本文对多种环境内分泌干扰物[壬基酚（nonylphenol,NP）、辛基酚（octylphenol,OP）、双酚A（bisphenol,BPA）等]通过雌激素受体影响类固醇激素的合成、氧化损伤、影响细胞信号传导等途径刺激肿瘤生长,以及诱导/抑制肿瘤细胞上皮-间充质转化的情况进行了综述。     

环境内分泌干扰物对甲状腺功能影响的研究进展

环境内分泌干扰物种类繁多,被广泛应用于杀虫剂、增塑剂、阻燃剂等生产中,能对机体生殖、神经、免疫、内分泌等系统产生影响。笔者综述了烷基酚、邻苯二甲酸酯、多氯联苯等几类常见的环境内分泌干扰物对甲状腺功能的影响,以及这些干扰物可能通过影响甲状腺激素的合成、释放、转运和代谢和核受体介导等机制来影响甲状腺功能,为深入研究环境内分泌干扰物和甲状腺功能的关系及甲状腺疾病的预防提供依据。     

克伦特罗的毒性作用及其中毒机制

克伦特罗是非法的饲料药物添加剂 ,不仅可以造成急性中毒 ,也严重影响运动能力和干扰生殖内分泌活性。本文对其毒性作用和中毒机制进行了介绍     

生长激素诱导的胰岛素抵抗研究进展

生长激素日益广泛地应用于外科临床，但在其使用过程中对机体糖代谢有显著的影响。本文就生长激素导致机体糖代谢异常、胰岛素抵抗的机制及可能采用的纠正进行了综述。     

Contraception--a look forward, Part III: Inhibin and brain-enhanced estrogen delivery

The final installment of this review examines two contraceptive methods, inhibin and brain-enhanced estrogen delivery, which are radically different from any currently available. Inhibin is a gonadal hormone that specifically inhibits pituitary production of follicle-stimulating hormone. Before it was finally isolated in 1985, inhibin was expected to be an ideal contraceptive. Recent research, however, has shown that the inhibin hormonal system is unexpectedly complex, and hopes for clinical use of inhibin must be suspended for the present. Although oral contraception is one of the most effective methods ever devised, use is limited by adverse effects of estrogen (or fears of such effects). A system known as brain-enhanced estrogen delivery specifically delivers estrogen to the brain, including the hypothalamus, there inducing suppression of the gonadotropin-releasing hormone. It has been described and tested in animals, and its successful development could replace current oral contraceptives and extend their availability to many more women.     

环境中内分泌干扰物的作用机制

随着对环境激素问题的关注,对环境中残留化合物的荷尔蒙效应研究已成为一个关系到人类今后生存与繁衍的热点问题.该文从内源性激素的生理学机制出发对当前环境内分泌干扰物的机制研究作了较系统综述.内容不仅阐述了已知的受体介导影响途径,还讨论了环境激素通过破坏内源性激素及其受体的生成和代谢而产生内分泌干扰作用的非受体介导途径,以及污染物对神经系统、免疫系统和内分泌系统的综合效应.同时,该文提出了以环境激素作用机制为基础,为进一步开发和发展新的生物筛选方法提供技术路线.     

药品不良反应损害救济制度探讨

药品不良反应是在正常使用合格药品时产生的有害或意外反应。药品发生不良反应会给患者及其家庭带来严重的伤害,受害者理应得到补偿救济。而我国现行法律对药品不良反应损害的规定缺位。我国应及早建立和完善药品不良反应救济机制,实行药品不良反应救济基金制度。     

Successful withdrawal of thyroid hormone therapy in nursing home patients

BACKGROUND: Studies of community-dwelling patients have indicated that substantial numbers of patients might have had thyroid hormone therapy prescribed inappropriately and that thyroid hormone therapy in some can be discontinued without adverse effects or evidence of clinical hypothyroidism. We wanted to find out whether thyroid hormone therapy in selected nursing home patients could be withdrawn without adverse effect. METHODS: Participants for the study were drawn from four skilled nursing facilities in Connecticut. All patients on thyroid hormone therapy who resided in one of the four facilities at the time the study began were eligible if they met the inclusion criteria and gave consent to participate in the study. We measured baseline thyrotropin (TSH) levels and reduced thyroid hormone therapy by approximately onehalf if baseline TSH levels were 7 mU/L or less. If at a 1-month follow-up measurement a patient's TSH level was 7 mU/L or less, we discontinued thyroid hormone therapy. If TSH levels remained 7 mU/L or less at the next follow-up measurement 1 month later, we measured the free thyroxine (T4) level. If the free T4 level was normal, the patient remained off thyroid hormone therapy, and a final TSH value was measured after a further 2 months. RESULTS: There were 915 patients residing at the four homes at the time the study began. One hundred fifteen were on thyroid hormone therapy; 40 had elevated TSH levels in their nursing home records; and 31 refused to participate in the study. Twenty-two patients were excluded because they died or were discharged before completion of the study, had an elevated baseline TSH reading, or were taking medications that could complicate the accurate measurement of TSH. Twenty-two patients began hormone withdrawal. One patient had an increase in psychiatric symptoms during the withdrawal phase. No other adverse effects were noted. Eleven patients (50%) had the thyroid hormone therapy withdrawn successfully. CONCLUSION: Thyroid hormone therapy was successfully withdrawn from one half of the nursing home residents studied. Previous studies conducted in community-dwelling patients have shown similar findings. Many older patients began taking thyroid hormone therapy when younger either for inappropriate reasons or for what turned out to be transient hypothyroidism. If the findings of this study are generalizable for other nursing home residents, there are important implications for health and health care costs.     

杀虫剂对女性生殖系统激素功能的影响

女性生殖系统受多种因素的影响,其中激素是影响女性生殖系统(尤其对卵巢)的一个重要因素,如果激素功能受到影响,患低生殖力的危险将增加.杀虫剂被广泛应用于农业及公共卫生来控制蚊虫等带菌媒介,这对人类是有益的,但某些杀虫剂可通过多种机制干扰女性的激素功能,进而对生殖系统产生负面影响.杀虫剂对女性生殖系统的危害,包括月经周期紊乱、不孕、自然流产/死胎、TTP延长及发育缺陷等,这些已经从流行病学角度得到证实.     

妊娠期母体低甲状腺素血症与后代神经精神发育

低甲状腺素（T4）血症即低T4血症,是指游离甲状腺素（FT4）降低而促甲状腺激素（TSH）水平在正常范围内,是亚临床甲状腺激素缺乏的一种现象。妊娠期母体低T4血症可以影响后代脑发育,包括对学习、认知、记忆、运动的影响,以及对精神疾病发生的影响。本文就妊娠期母体低T4血症对后代脑发育的人群研究和可能的机制进行综述,旨在为相关研究提供新思路。     

左炔诺孕酮宫内节育系统的疗效分析

目的探究对子宫腺肌症患者实施左炔诺孕酮宫内节育系统治疗的效果。方法随机将2017年1月-2018年9月我院66例子宫腺肌症患者分为对照组(33例,应用孕三烯酮胶囊治疗)、试验组(33例,应用左炔诺孕酮宫内节育系统治疗)。对比两组月经量、子宫内膜厚度、子宫体积、痛经评分、血清性激素水平及不良反应发生率。结果试验组治疗后半年月经量、痛经评分较对照组更少,P<0.05;试验组治疗后半年子宫内膜厚度、子宫体积较对照组更小,P<0.05;试验组治疗后半年雌二醇、促卵泡激素、促黄体生成素水平较对照组更高,P<0.05;两组不良反应发生率无明显差异,P>0.05。结论对子宫腺肌症患者实施左炔诺孕酮宫内节育系统治疗具有较显著的效果,且安全性较高。     

Retinoic Acid: Sexually Dimorphic,Anti-Insulin and Concentration-Dependent Effects on Energy

This review addresses the fasting vs. re-feeding effects of retinoic acid (RA) biosynthesis and functions, and sexually dimorphic RA actions. It also discusses other understudied topics essential for understanding RA activities—especially interactions with energy-balance-regulating hormones, including insulin and glucagon, and sex hormones. This report will introduce RA homeostasis and hormesis to provide context. Essential context also will encompass RA effects on adiposity, muscle function and pancreatic islet development and maintenance. These comments provide background for explaining interactions among insulin, glucagon and cortisol with RA homeostasis and function. One aim would clarify the often apparent RA contradictions related to pancreagenesis vs. pancreas hormone functions. The discussion also will explore the adverse effects of RA on estrogen action, in contrast to the enhancing effects of estrogen on RA action, the adverse effects of androgens on RA receptors, and the RA induction of androgen biosynthesis.