特发性无精子症和严重少精子症患者无精子因子检测的临床意义

20 0 1年10月至2 0 0 3年1月,我们采用PCR方法对5 0例正常生育男性和5 0例特发性无精子症和严重少精子症患者进行无精子因子(AZF)检测,现报告如下。材料与方法　5 0例正常生育男性。年龄2 8～38岁,平均33岁。精液常规检查精子数均>4 0×10 6/ml。5 0例特发性不育男性患者年龄2 8～4 2岁,平均34岁。临床检查排除相关的泌尿生殖系疾患。精子计数(2～5×10 6/ml) ,符合WHO诊断标准。患者均有正常4 6XY核型,外周血性激素指标正常。38例无精子症患者睾丸病理检查符合精子发生不完全的诊断。取抗凝血1ml,加入5倍体积重蒸馏水溶解红细胞,离心…     

特发性无精子症和严重少精子症患者无精子因子的检测及其意义

目的：探讨引起特发性无精子和严重少精子造成男性不育的遗传学原因和检测无精子因子(AZF)的临床意义。方法：对50例特发性男性不育患者(不育组)和50例正常生育者(对照组)的外周血标本．提取基因组DNA,通过多重聚合酶链反应检测Y染色体AZt?微缺失。结果：对照组均可见SRY、SY84、SY86、YRRM1(RBM1)和SY254(DAZ)扩增带。不育组6例(无精子症4例．严重少精子症2例)可见SRY扩增带．但未见SY254扩增带,其中2例同时未见YRRM。扩增带;1例仅未见YRRM。扩增带。结论：Y染色体AZF微缺失是引起无精子和严重少精子并造成男性不育的重要原因之一;AZF微缺失检测对男性不育症患者进行遗传学诊断与筛查有一定意义。     

特发性无精子症和严重少精子症患者Y染色体基因微缺失研究

目的:研究Y染色体基因微缺失与特发性无精子症和严重少精子症的关系,及探讨Y染色体基因微缺失的位点、缺失率有无民族间的差异性.方法:应用多重实时荧光定量聚合酶链反应(PCR)法,对40例汉族及维吾尔族特发性无精子和严重少精子症患者进行Y染色体Azoospermia Factor(AZF)因子多位点的微缺失检测.结果:23例特发性无精子患者中,3例发生AZF因子缺失,缺失率为13.04%;17例严重少精子症患者中,2例发生AZF因子缺失,缺失率为11.76%.结论:Y染色体AZF因子微缺失的范围和位置对于胞质内体外受精治疗男性不育具有重要意义,但Y染色体AZF因子的缺失的位点及缺失率有无民族间的差异性,值得进一步研究.     

中国特发性无精子症和少精子症患者雄激素受体基因CAG重复多态性研究

目的分析中国特发性无精子症和少精子症患者雄激素受体(AR)基因(CAG)n微卫星多态性并探讨该多态性与精子生成障碍发生的关系。方法应用PCR和变性聚丙烯酰胺凝胶电泳分析技术对52例少精子症患者和31例无精子症患者的外周血标本进行CAG重复数测定,分析该微卫星多态性和精子生成障碍发生的关系。结果少精子症患者组和无精子症患者组CAG重复数均数分别为22.19和22.13,CAG重复数≥28的百分率分别为1.9%和3.2%,比例逐渐升高。结论AR基因(CAG)n微卫星的CAG重复数在中国男性不育患者中呈现多态性,与精子生成障碍发生的关系有待进一步研究。     

特发性无精子症与精索静脉曲张无精子症的生殖内分泌及睾丸病理学研究

对特发性无精子症50例、精索静脉曲张无精子症16例及对照57例分别从血FSH、LH和T,睾丸体积,曲细精管直径、管壁厚度、管内上皮及间质病变情况进行了比较。二类无精子症的FSH、LH及T水平无显著差异,但特发性的FSH、精索静脉曲张的LH有较对方升高更多的趋势。二类无精子症的睾丸体积、曲细精管直径及管壁厚度无明显差异,但精索静脉曲张无精子症曲细精管内细胞脱落严重并伴有间质水肿及小血管病变,而特发性无精子症则曲细精管内生精阻滞明显。提示间质病变及有可能继发于之的曲细精管内细胞脱落是精索静脉曲线无精子症有别于特发性无精子症的重要特征。     

特发性无精子症和严重少精子症患者Y染色体基因微缺失分析

目的：研究Y染色体基因微缺失与特发性无精子症和严重少精子症的关系，并建立一个灵敏、操作简便的分子检测方法。方法：应用实时荧光定量聚合酶链反应(PCR)法对65例特发性无精子症患者、27例严重少精子症患者进行Y染色体YRRM1、DAZ、DYS1基因微缺失的检测。结果：65例特发性无精子症患者中，3例发生YRRM1基因微缺失，发生率为4．6％；5例发生DAZ基因微缺失，发生率为7．7％。27例严重少精子症患者中，1例发生YRRM1基因微缺失，发生率为3．7％；2例发生DAZ基因微缺失，发生率为7．4％。92例患者中均未发现DYS1基因微缺失。结论：YRRM1和DAZ基因位点的微缺失与特发性无精子症和严重少精子症有一定的相关性，DYS1基因缺失与男性生精障碍的相关性仍需进一步研究明确。应用荧光定量PCR法检测Y染色体微缺失具有灵敏、快速、操作简便的特点。     

无精子症患者Y染色体基因异常的意义

目的 研究特发性无精子症患与Y染色体基因微缺失的关系。方法 应用PCR技术对65例无精子症患进行Y染色体YRRM1和DYS240基因位点检测。结果 65例中无精症患YRRM1缺失6例，DYS 240缺失6例，其中1例双重缺失。结论 YRRM1和DYS240是无精子因子的重要候选成份，其缺失可造成精子发生障碍。     

无精子症患者的精子获取方法

随着辅助生育技术的极大进展，卵泡浆内精子显微主射已忧为当今治疗男性不良中无精子症的首要方法。从附睾或睾丸获取精子是这一技术中的首要步骤。本文概述了目前常用的几种精子获取方法及其临床应用现状。     

无精子症患者的精子获取方法

随着辅助生育技术的极大进展,卵泡浆内精子显微注射已成为当今治疗男性不育中无精子症的首要方法。从附睾或睾丸获取精子是这一技术中的首要步骤。本文概述了目前常用的几种精子获取方法及其临床应用现状。     

SERUM ESTRADIOL LEVELS IN NORMAL MEN AND MEN WITH IDIOPATHIC INFERTILITY

Serum estradiol levels were measured in 360 men attending an infertility clinic and 68 proven fertile men to determine whether estradiol measurements are clinically useful. The normal range of estradiol levels found in fertile men was 10–82 pg/ml. Serum concentrations of estradiol in azoospermic or oligozoospermic patients were significantly lower than those in normozoospermic men (p < 0.021). Serum concentrations of testosterone were also significantly decreased in infertile patients (p < 0.025). This decrease in serum estradiol may be partly due to reduced testosterone levels in these men because estradiol is mainly formed by peripheral aromatization of testosterone in fatty and muscle tissues. However, the exact mechanism for the decrease in the serum estradiol levels remains undetermined. It is concluded that serum estradiol levels are significantly low in the men with various testicular disorders.     

微波照射雄兔阴囊对睾丸间质细胞及附性腺的影响

本实验观察经微波照射阴囊后雄兔睾丸间质细胞的形态、结构和功能的变化情况,及其间质细胞分泌的睾酮的靶器官——前列腺、精囊腺的结构和功能的变化情况,发现经照射后,睾酮浓度一度上升(从127.1→220.50g/dl),随后很快呈下降趋势(从220.5→89.87ng/dl)。精囊腺,前列腺的形态及功能性指标(果糖、酸性磷酸酶)于微波照射前后均无明显改变(P>0.05,P>0.05)。     

逐步判别分析在无精子症分类和病理类型间鉴别诊断中的应用

本文采用逐步判别分析的多因素分析法对６２例无精子症病人的睾丸活检、睾丸大小、血清生殖激素水平（ＦＳＨ、ＬＨ、Ｔ及Ｔ／ＬＨ）等资料进行计算机统计处理，以建立无精子症临床分类和病理类型间鉴别诊断的函数模型，结果得出了临床两类间和病理五类间的判别函数式。对方程作判别显著性检验证明方程成立（Ｐ＜０．０１），利用原观察资料分别回代判别函数式，判别总符合率分别为９５．１６％、７７．４２％，说明判别效果较可靠。因此认为这些数学模型有一定的临床应用前景。     

男性海洛因依赖者性功能研究

对５６名男性海洛因依赖者进行体检、吸毒史与性生活史调查，其中３０名检测了血清Ｔ、ＦＴ、ＰＲＬ、ＦＳＨ、ＬＨ及血ＳＨＢＧ等浓度水平。以３０名健康男性为对照组。结果表明，吸毒前性功能基本正常，吸毒后８３．９％出现性欲低下，性交频率明显低于吸毒前（Ｐ＜０．０１），９４．６％存在阴茎勃起障碍，２１．４％有射精延迟；血清Ｔ、ＦＴ、ＦＴ／Ｔ及ＬＨ浓度明显低于对照组；血清ＰＲＬ浓度则高于对照组。本结果证实了海洛因依赖可导致男性下丘脑－垂体－睾丸轴功能紊乱及男性性功能异常，并阐明了两者之间的内在联系。     

CO-ADMINISTRATION OF FUROSEMIDE AUGMENTS TACROLIMUS-INDUCED IMPAIRMENT IN KIDNEY FUNCTION IN RATS

Sodium-depletion in rats reproduces functional and morphological tacrolimus nephrotoxicity observed in man. Potent diuretics induce sodium-depletion. Our objective was to determine the effect of a loop diuretic furosemide on tacrolimus-mediated functional and pathological impairment of the kidney in rats. Sprague-Dawley rats were divided into four groups; group 1, rats received vehicle (saline) only; group 2, rats were treated with tacrolimus (1mg/kg body weight) and furosemide (5mg/kg body weight); group 3, rats were treated with tacrolimus alone; and group 4, rats were treated with furosemide (5mg/kg body weight) alone. On day 28, tail blood pressure was measured and the rats were placed in metabolic cages for urine collection. After 24 hr the rats were sacrificed. Tacrolimus alone tended to cause growth retardation, hypotension, hypomagnesemia and a rise in blood urea nitrogen. Furosemide co-administration enhanced the effects of tacrolimus on hypotension, hypomagnesemia and a rise in blood urea nitrogen. The renal histology characterized by cytoplasmic vacuolization of the proximal tubules was not different between the rats treated with both tacrolimus and furosemide and the rats treated with tacrolimus alone. A strong immunostaining for FKBP-12, a tacrolimus-binding protein, was observed in the medulla of the kidneys of rats treated with tacrolimus either with or without furosemide.These results indicate that furosemide further augments tacrolimus induced impairment in kidney function, and that furosemide should be used with discretion in patients on tacrolimus therapy.     

正常生育男子和精索静脉曲张不育男子精子形态学分析

本文报道用改良巴氏染色法对144例生育男子和64例精索脉曲张不育者的精子形态学进行分析的结果。生育男子组和精索静脉曲张患者组正常形态精子的范围(均值±标准差)分别为:53-99％(79.7±12.5),5-90％(54.5±20.5)。后者显著低于前者。并随精索静脉曲张的严重程度而降低。精索静脉曲张者中精液内含有小头畸形精子的例数比例显著高于生育者,同时精子中大头、小头,尖头和不定型精子的比例也显著高于生育者。     

THE EFFECT OF LOSARTAN ON INSULIN RESISTANCE AND BETA CELL FUNCTION IN CHRONIC HEMODIALYSIS PATIENTS

Insulin resistance (IR) is prevalent in hemodialysis patients. IR and hyperinsulinemia have an important role in the development of atherosclerosis, which is the most common cause of morbidity and mortality in hemodialysis patients. Thus, antihypertensive drugs that lower IR, may have an additional beneficial effect in the treatment of cardiovascular diseases in these patients. In this preliminary study we examined the effect of Losartan (an angiotensin II receptor antagonist) treatment on IR and beta cell function in five hypertensive non-diabetic chronic hemodialysis patients. All other known causes of IR in end stage renal failure were excluded. After a washout period of two weeks, Losartan 50 mg, was administered for 6 weeks. Fasting blood glucose (FBG) and insulin levels were measured before and after the treatment IR and beta cell function were calculated using the “homeostasis model assessment”-HOMA. Systolic and diastolic blood pressure (BP) have not changed significantly throughout the study. FBG increased significantly from 76 mg/dL ± 1 to 89 mg/dL ±4 (p < 0.01), however, insulin levels have not changed significantly. Calculated IR values did not show a difference, but calculated beta cell function decreased significantly after Losartan treatment from 291% ± 50 to 146% ± 10, (p < 0.016). These preliminary results suggest that in chronic hemodialysis hypertensive non-diabetic patients short treatment with Losartan has deleterious effect on glucose homeostasis mediated via a decrease in beta cell function     

瘢痕Bcl-2基因与细胞增殖和凋亡的关系

目的:探讨增生性瘢痕成纤维细胞Bcl-2基因表达水平与细胞增殖活性及凋亡程度的关系。方法:用原位杂交、免疫组化染色ABC法,对79例增生性瘢痕组织分别检测Bcl-2mRNA、Bcl-2蛋白和增殖细胞核抗原的表达,并用TUNEL法作原位细胞凋亡检测。结果:75例（94.9％）表达Bcl-2mRNA,70例（88.6％）表达Bcl-2蛋白,两者表达水平呈正相关（rs=0.989,P<0.01）;随成纤维细胞Bcl-2蛋白表达水平升高其增殖活性相应增加,而凋亡相应减少,Bcl-2蛋白+++组与++组（P<0.05）及前两组分别与-组和+组间（P<0.01）两项指标差异均有显著性。结论:增生性瘢痕中成纤维细胞Bcl-2基因高表达可抑制其凋亡,可能由此引起的细胞凋亡减少与其他基因异常所致的细胞过度增殖共同导致瘢痕的形成。     

瘢痕疙瘩中皮肤附件结构破坏与瘢痕增生的关系

目的　探讨瘢痕疙瘩 (keloid K)形成过程中皮肤附件 (skin appendages,SAs)结构破坏与瘢痕增生的关系。　方法　将来自 17例 K患者的活检标本按浸润生长 (K- I,n=9)、瘢痕增生 (K- P,n=17)、瘢痕萎缩 (K- A,n=10 )和边缘正常皮肤 (K- N,n=6 )进行分组 ,另以非 K患者胸部正常皮肤 (NS,n=6 )为对照 ,采用免疫组织化学方法观察SAs密度与广谱细胞角蛋白 (pan- fytokeratin,CKp)、CK19、腺上皮分泌成分 (secretory component,SC)和增殖细胞核抗原 (proliferating cell nuclearantigen,PCNA) ,以及凋亡相关蛋白 Bcl- 2和 Bax之间的变化规律 ,同时用组织学、解剖显微镜及扫描电镜观察 K胶原纤维和 SAs结构的组织形态学改变。　结果　与 K- N和 NS组相比 ,K组织中 CKp和 SC阳性的 SAs密度迅速减少 ,可见 SAs结构消失后残留 CKp阳性蛋白痕迹 ;多数 SAs上皮细胞 Bax表达增强 ,但 Bcl- 2、PC-NA和 CK19阳性的 SAs则呈现复层 (鳞状 )上皮化和形态结构异常。 K组织形态学大致经历浸润、增殖和成熟的过程 ,SAs也相应地发生增生 ,细胞迁移、炎性反应和血管闭塞等引起的形态结构破坏和几乎被纤维结缔组织完全取代的变化过程。直线相关分析显示 ,K的瘢痕厚度与 SAs密度之间呈显著的负相关 (r=- 0 .341,P<0 .0 1)。　结论