睾丸：男子性功能晴雨表

睾丸是男性重要的性器官，具有产生精子和分泌雄激素的功能。精子是生育的前提条件，而雄激素在青春期有促进男性性器官的正常发育、维持性功能和体力、精力的重要作用，因此，可以说睾丸是男性生殖和性动力的源泉。关注男性健康和“性福”应该从睾丸开始，重视睾丸的养护对维持男性性功能至关重要。睾丸的大小和质地基本反映了睾丸的功能情况，因此睾丸养护就是要经常关注睾丸的大小和质地。     

睾丸雄激素合成的调节机制及其研究进展

睾丸能产生精子和合成雄激素,前者在生精小管完成,后者由睾丸间质细胞(Leydig cell)完成.雄激素在促进男性性分化、青春期发育、维持第二性征和性成熟、维持男性生育等方面发挥重要作用.间质细胞合成雄激素功能受下丘脑-垂体-睾丸轴调控,经典的分子信号通路是黄体生成激素-黄体生成激素受体-环磷酸腺苷-蛋白激酶A(LH-LHR-cAMP-PKA)途径;实际上,雄激素合成还受睾丸内旁分泌、自分泌甚至细胞内分泌形式的局部调节,如泌乳素、胰岛素、胰岛素样生长因子1(IGF-1)、转化生长因子α(TGF-α)、TGF-β等;除cAMP外,Ca2+也是第二信使,钙调蛋白参与调节雄激素合成.     

少精子症或无精症的不育男性其雄激素受体基因的外显子1(执行区域)的首次分析

正常男性的性分化,睾丸下降和精子形成均要求雄激素以及功能良好的雄激素受体(AR)存在方可完成。AR缺陷将导致完全或部分的雄激素不敏感综合征(AIS),其表现可从46,XY的性逆转女性到具有女性型乳房的雄性不足男性。1979年Aiman等人首次将完全或部分的精子形成障碍病人扩充进     

睾丸也需要养护

睾丸是男性重要的性器官，具有产生精子和分泌雄激素的功能。精子是生育的前提条件，而雄性激素有促进男性性器官的正常发育和维持性功能及体力、精力的重要作用。因此说睾丸是男性生殖和性动力的源泉，关注男性健康和“性福”应该从睾丸开始，日常生活中重视对睾丸的养护。     

壮志凌云 雄风不再——谈谈男性更年期

与女性更年期不同的是，“男性更年期”时，睾丸功能虽有一定程度的下降，但仍然保持相对的完整性，女性更年期发生时，雌激素水平下降，有如坠下山崖般的突然，彻底；而“男性更年期”发生时，雄激素水平下降，则好似在山坡上的平缓下滑，中、老年男性在发生临床症状时，雄激素水下虽有明显的下降，但仍然保持在接近正常低限值的水平。有鉴于此，1994年奥地利男科学会提出了“中、老年男子雄激素部分缺乏症（英文字头缩写为PADAM）的概念。     

神秘无形 统领男性——雄激素的作用

男性的一生，都受到雄激素的统领。男性的雄激素主要来源于睾丸和肾上腺。其中睾丸是最主要的大工厂。雄激素通过血液循环到全身，遇到合适的地方就黏上去发挥作用。雄激素在全身的作用非常广泛，皮肤的细腻粗糙和它有关，头发的茂盛稀少和它有关。精力的充沛萎靡和它有关，心情的晴朗阴霾和它有关。可以说，在不知不觉中，雄激素统治着我们生活的每一部分。     

睾丸扭转早期诊治的体会(附3例报告)

我科自1985年以来,收治了3例睾丸扭转的患者,年龄分别是:15、2 2和2 6岁。因3例患者起病前均无明显的诱因,故在诊治过程中容易出现误诊,错过了保留睾丸的手术时机,本文在总结经验教训使睾丸扭转病例能早期正确诊治。例1:男,15岁,初三学生,无明显诱因,出现右侧睾丸及右下腹疼痛,为持续性疼痛,阵发性加剧,右侧睾丸轻度肿大,但压痛明显,体温正常。到门诊诊治,按急性睾丸炎处理,行抗炎治疗3d后,因症状未见好转而入院,急诊行彩色多普勒B超检查,示右侧睾丸无血流,即行手术探查,发现右侧睾丸已变黑、坏死,睾丸顺时针方向旋转了72 0°,行右侧睾丸切…     

小问答：性功能有没有减退

睾丸是男性主要的生殖器官．其相对应的女性生殖器官为卵巢。睾丸主要作用为产生精子、分泌雄激素（即睾酮）等：卵巢的主要作用为产生卵子．分泌雌激素等。与女性的性器官卵巢相比．男性性器官睾丸潜力比较大,不像卵巢那样容易发生萎缩、退化和功能衰退。历史上有记载：一位瑞典男性在85岁结婚后还生了8个孩子。     

leptin对男性生殖的调节作用

主要由白色脂肪组织产生的瘦素(1eptin)可通过对下丘脑神经元的作用来调节摄食行为,能量代谢和生殖内分泌功能.其不仅对女性营养和生殖平衡有重要作用,而且在男性生殖中也具有重要作用.leptin能作用于下丘脑ARC-VMN调节生殖,但其刺激GnRH分泌效应具有两重性:长期高leptin血症可引起中枢对leptin信号传递的敏感性下调.leptin对ARC的调节主要通过神经肽Y(NPY)、可卡因-安非他明-调节转录物(CART)和Galanin样多肽(GALP)等多肽发挥.睾丸中也存在leptin受体,leptin对hCG诱导的睾丸培养组织睾酮分泌具有明显的抑制作用且存在剂量相关性,其对雄激素合成的影响位点在孕激素下游.睾酮可能是调节leptin水平的重要因子,它与血清leptin呈负相关,而这种负相关依赖于IGF结合蛋白-1(IGFBP-1)的作用.     

慢性前列腺炎会引起前列腺增生吗?

这是一个常被患者误解的问题,很多患者认为慢性前列腺炎久治不愈会导致前列腺增生,其实从现代研究看,二者并不存在必然联系。前列腺增生症是男性老年人的常见疾病,对其发病机制研究颇多,病因至今仍未能阐明。但前列腺增生必须具备两个条件,即睾丸存在及年龄增长。睾丸存在说明有正常的男性激素分泌,研究表明雄激素和雌激素的协同作用在前列腺增     

完全型雄激素不敏感综合征2例临床特点及处理

雄激素不敏感综合征(androgen insensitivity syndrome,AIS)又称为睾丸女性化综合征(testicular feminization syndrome,TFS),是一种X连锁遗传病,是男性假两性畸形中较常见的类型,可分为完全型AIS和不完全型AIS,其原因主要是雄激素受体(androgen receptor,AR)基因的突变导致其对雄激素产生抵抗和不应答。本文回顾南京医科大学附属妇产医院2例CAIS患者的临床资料及诊疗过程,以期能进一步提高对该病的认知及诊治水平。     

Estrogen receptor-α mediates diethylstilbestrol-induced feminization of the seminal vesicle in male mice

Background: Studies have shown that perinatal exposure to the synthetic estrogen diethylstilbestrol (DES) leads to feminization of the seminal vesicle (SV) in male mice, as illustrated by tissue hyperplasia, ectopic expression of the major estrogen-inducible uterine secretory protein lactoferrin (LF), and reduced expression of SV secretory protein IV (SVS IV).Objectives: The present study was designed to evaluate the role of the estrogen receptor (ER) in this action by using ER-knockout (ERKO) mice.Methods: Wild-type (WT), ERα-null (αERKO), and ERβ-null (βERKO) male mice were treated with either vehicle or DES (2 μg/day) on neonatal days 1–5. These mice were divided into two groups: In the first group, intact mice were sacrificed at 10 weeks of age; in the second group, mice were castrated at 10 weeks of age, allowed to recover for 10 days, treated with dihydrotestosterone (DHT) or placebo, and sacrificed 2 weeks later. Body weights and SV weights were recorded, and mRNA expression levels of Ltf (lactoferrin), Svs4, and androgen receptor (Ar) were assessed.Results: In DES-treated intact mice, SV weights were reduced in WT and βERKO mice but not in αERKO mice. DES-treated WT and βERKO males, but not αERKO males, exhibited ectopic expression of LF in the SV. DES treatment resulted in decreased SVS IV protein and mRNA expression in WT males, but no effect was seen in αERKO mice. In addition, DES-treated βERKO mice exhibited reduced Svs4 mRNA expression but maintained control levels of SVS IV protein. In DES-treated castrated mice, DHT implants restored SV weights to normal levels in αERKO mice but not in WT mice, suggesting full androgen responsiveness in αERKO mice.Conclusions: These data suggest that DES-induced SV toxicity and feminization are primarily mediated by ERα; however, some aspects of androgen response may require the action of ERβ.     

Syndromes of Androgen Resistance

Probably more common than all other forms of primary hormone resistance combined, androgen resistance is now known to cause many disorders. Their phenotypic spectrum ranges from complete testicular feminization in genotypic males to infertility in men who are otherwise normal. These syndromes have helped elucidate mechanisms of sexual development.     

Androgen insensitivity syndrome: clinical features and molecular defects

The end-organ resistance to androgens has been designated as androgen insensitivity syndrome (AIS), an X-linked disorder caused by mutations in the androgen receptor (AR) gene. It is generally accepted that defects in the AR gene prevent the normal development of both internal and external genital structures in 46,XY individuals, causing a variety of phenotypes ranging from male infertility to completely normal female external genitalia. Precise diagnosis requires clinical, hormonal and molecular investigation and is of great importance for appropriate gender assignment and management in general. The complexity of phenotypic presentation of AIS with genotype-phenotype variability of identical mutations complicates both the diagnostic procedure and genetic counseling of the affected families. More than 400 different AR gene mutations have thus far been reported but the receptor structure-function relationship and its phenotypic outcome is not yet fully understood. This review focuses on the clinical features and molecular pathophysiology of AIS and explores the relationship of the molecular defects in the AR gene to their clinical expression.     

From gene to disease; androgen receptor gene, androgen insensitivity syndrome, and spinal and bulbar muscle atrophy]

Androgen insensitivity is an X-linked disorder of male sexual differentiation resulting from a defective androgen receptor. Spinal and bulbar muscular atrophy (Kennedy's disease) is an X-linked disease, resulting from expansion of the polyglutamine stretch in the N-terminal part of the androgen receptor. Mutation analysis confirms the clinical diagnosis of androgen insensitivity and enables carrier detection and prenatal diagnosis. Kennedy's disease, with its diagnostic problem of clinical variability, is diagnosed or excluded when an expanded CAG-repeat is present or absent in exon 1 of the androgen receptor. Molecular testing can be used for carrier detection and genetic counselling.     

Characterization of atrazine-induced gonadal malformations in African clawed frogs (Xenopus laevis) and comparisons with effects of an androgen antagonist (cyproterone acetate) and exogenous estrogen (17beta-estradiol): Support for the demasculinization/feminization hypothesis

Atrazine is a potent endocrine disruptor that both chemically castrates and feminizes male amphibians. It depletes androgens in adult frogs and reduces androgen-dependent growth of the larynx in developing male larvae. It also disrupts normal gonadal development and feminizes the gonads of developing males. Gonadal malformations induced by atrazine include hermaphrodites and males with multiple testes [single sex polygonadism (SSP)], and effects occur at concentrations as low as 0.1 ppb (microg/L). Here, we describe the frequencies at which these malformations occur and compare them with morphologies induced by the estrogen, 17beta-estradiol (E2) , and the antiandrogen cyproterone acetate, as a first step in testing the hypothesis that the effects of atrazine are a combination of demasculinization and feminization. The various forms of hermaphroditism did not occur in controls. Nonpigmented ovaries, which occurred at relatively high frequencies in atrazine-treated larvae, were found in four individuals out of more than 400 controls examined (1%). Further, we show that several types of gonadal malformations (SSP and three forms of hermaphroditism) are produced by E2 exposure during gonadal differentiation, whereas a final morphology (nonpigmented ovaries) appears to be the result of chemical castration (disruption of androgen synthesis and/or activity) by atrazine. These experimental findings suggest that atrazine-induced gonadal malformations result from the depletion of androgens and production of estrogens, perhaps subsequent to the induction of aromatase by atrazine, a mechanism established in fish, amphibians, reptiles, and mammals (rodents and humans).     

Androgens, well-being and libido in women

Women with an androgen deficiency complain about a loss of libido and a lack of well-being. It is difficult to link these symptoms to low circulating androgen levels in blood. This is because these complaints often arise during a period of life characterized by major psychosocial changes. Furthermore, coinciding oestrogen deficiency may give rise to similar symptoms. Another problem is the assessment of androgen deficiency. The androgen assay used is designed for men presenting with levels much higher than normal. Finally, concentrations in the peripheral blood are a poor reflection of intracellular androgen receptor stimulation. Patients with complaints suggestive of a relative androgen deficiency (based on the pattern of complaints and low serum androgen concentrations) should first of all be counselled for psychosocial problems. Oestrogen deficiency should subsequently be ruled out or substituted. If the complaints still persist then androgen substitution can be considered.     

Fortune-telling and women--contemporary characteristics of fortune-telling in Japanese society

It is a well-known fact that women almost monopolize the field of fortune-telling in the present Japanese society--fortune-tellers and their customers (or clients) are mostly women. But once we view the relationship between women and fortune-telling in a general way, we can understand that fortune-telling is not necessarily monopolized by women. In other words, if we take for granted only the relationship between the two, we will overlook some sociological questions. Close observation of the relationship in question reveals several phenomena. One of them is 'the feminization of fortune-telling'. The feminization of fortune-telling is the process by which women's interests are channeled into fortune-telling and their monopolization of it. The purpose of this paper is to focus on this phenomenon--the feminization of fortune-telling'. By focusing on this phenomenon and analyzing its process, we can understand not only some aspects of the relationship between women and fortune-telling, but also bring up other questions regarding the image of Japanese women in the modern era.     

Increased serum estrogenic bioactivity in three male newborns with ambiguous genitalia: a potential consequence of prenatal exposure to environmental endocrine disruptors

In the past 15 years, anomalies of male sexual differentiation have greatly increased in both wildlife and humans in different parts of the world. Environmental endocrine disruptors have been implicated in the dramatic rise in neonatal ambiguous genitalia with variable rates of severity, such as micropenis, cryptorchidism, and isolated or associated hypospadias. Because most environmental pollutants, such as organochlorine pesticides, polychlorinated biphenyls, dioxins and furans, alkylphenol polyetholyethoxylates, and phytoestrogens and phtalates, have estrogenic and antiandrogenic activity, they are able to interfere with normal fetal male sexual differentiation. In a neonatal screening program of ambiguous genitalia, we had the opportunity to evaluate three newborns with male pseudohermaphroditism (MPH) whose mothers were exposed to endocrine disruptors during pregnancy. All had normal testosterone production after human chorionic gonadotrophin stimulation testing, suggesting androgen resistance or so-called idiopathic MPH. Sequences of the 5alpha reductase and androgen receptor genes were normal. Since environmental pollutants are known for their estrogenic activity and can be released progressively from the adipose tissue where they accumulate, we detected their presence by measuring the estrogenic bioactivity of the newborns' serum with a recently developed ultrasensitive bioassay. We found higher estrogenic bioactivity in these newborns than in controls. In conclusion, the maternal exposure to environmental pollutants during pregnancy and high estrogenic bioactivity in the newborns' serum highly suggest that ambiguous genitalia are related to fetal exposure to endocrine disruptors.     

雄激素受体基因突变与无精症、少精症关系的临床研究

目的：探讨雄激素受体基因外显子A突变与无精症、少精症的关系,为辅助生殖技术的遗传咨询提供依据。方法：选择60例正常男性（对照组）和65例无精症、少精症患者（病例组）,采用聚合酶链反应-单链构象多态性分析方法（PCR-SSCP）检测雄激素受体基因外显子A点突变,采用琼脂糖凝胶电泳方法检测插入和缺失突变。结果：对照组中未发现基因突变,突变率为0;病例组中有5例发生基因突变,均为点突变,未发现基因插入和缺失突变,突变率为7.69%;两组比较差异有统计学意义（P〈0.05）。结论：雄激素受体基因外显子A突变是引起无精症、少精症的重要原因之一。