特发性无、少精子症病人精浆中性激素水平的测定及意义

目的 :通过测定特发性无、少精子症病人精浆中的性激素水平 ,比较分析精浆性激素与无、少精子症的关系。　方法 :特发性无、少精子症男性各 5 0例 ,正常对照 5 0例。精液常规分析判断精子密度 ,化学发光技术测定精浆性激素水平。　结果 :特发性无、少精子症组黄体生成素 (LH)分别为 (5 .19± 0 .6 7)IU/L和 (4.77± 0 .6 8)IU/L ,与正常组 (2 .19± 0 .2 2 )IU/L相比 ,特发性无精子症组差异有极显著性 (P <0 .0 1) ,特发性少精子症组与正常组相比差异有显著性 (P <0 .0 5 ) ;卵泡刺激素 (FSH)分别为 (1.90± 0 .79)IU/L和 (2 .2 7± 0 .2 5 )IU/L ,与正常组 (1.6 1± 0 .14)IU/L相比 ,差异均有显著性 (P <0 .0 5 ) ;泌乳素 (PRL)分别为 (6 .2 5± 0 .34 )ng/ml和 (6 .33±0 .5 1)ng/ml,与正常组 (6 .36± 0 .32 )ng/ml相比差异均无显著性 (P >0 .0 5 ) ;睾酮 (T)分别为 (1.5 1± 0 .12 )ng/ml和 (1.6 8± 0 .71)ng/ml,与正常组 (1.83± 0 .0 9)ng/ml相比 ,特发性无精子症组差异有显著性 (P <0 .0 5 ) ,特发性少精子症组差异无显著性 (P >0 .0 5 ) ;T/LH的比值分别为 0 .2 9± 0 .0 4和 0 .35± 0 .0 9,与对照组 0 .84± 0 .2 0相比 ,差异均有显著性 (P <0 .0 5 )。　结论 :特发性无、少精子症病人 ,精浆     

思密达联合茵栀黄治疗婴儿肝炎综合征的疗效观察

为了探讨思密达联合茵栀黄治疗婴儿肝炎综合征的疗效 ,将 6 0例婴儿肝炎综合征患儿随机分为观察组和对照组各 30例 ,分别用思密达联合茵栀黄及单用茵栀黄治疗 30 d,观察两组血清总胆红素和丙氨酸转氨酶(AL T)的变化。结果观察组治疗后血清总胆红素从 (10 2 .40± 5 6 .10 ) μm ol/ L 降为 (5 0 .0 0± 40 .2 0 ) μm ol/ L(P<0 .0 1) ,AL T从 (12 0 .40± 110 .0 0 ) IU/ L 降为 (4 0 .10± 42 .0 0 ) IU/ L(P<0 .0 1) ;对照组治疗后血清总胆红素从(110 .10± 5 8.2 0 ) μm ol/ L 降为 (70 .2 2± 5 6 .12 ) μm ol/ L(P<0 .0 5 ) ,AL T从 (130 .2 8± 40 .6 2 ) IU/ L 降为 (6 6 .0 8±46 .0 0 ) IU/ L(P<0 .0 5 )。提示思密达联合茵栀黄治疗婴儿肝炎综合征效果明显优于单一使用茵栀黄。     

睾丸精曲小管精子发生功能量化评价法分析无精子症患者睾丸生精功能

目的 :分析无精子症患者临床和病理资料 ,研究病理学量化评价睾丸精曲小管精子发生功能的方法的临床意义。　方法 :无精子症患者 112例 ,年龄 2 2～ 4 6 (2 9.0± 4 .4 )岁 ,婚龄 2～ 12 (4 .0± 2 .8)年、病程 2～ 6 (2 .70±1.0 2 )年 ,其中原发性无精子症 96例 ,继发性无精子症 16例 ;梗阻性无精子症 7例。不育症患者精液常规检查 3次确认无精子症 ,检测性激素水平 ,常规消毒下睾丸活检病理检查 ,在高倍镜下计数每个精曲小管中各类生精细胞数 ,测定小管直径、生精上皮高度和固有层厚度 ,按制定的精曲小管精子发生功能 10分 5级分度法加以评分 ,进行统计学分析。　结果 :精曲小管生精上皮 10分分度法评分结果 ,1分 5例 (4 .5 % ) ,2分 38例 (33.9% ) ,3分 2例(1.8% ) ,4分 6例 (5 .4 % ) ,5分 2例 (1.8% ) ,6分 17例 (15 .2 % ) ,7分 6例 (5 .4 % ) ,8分 19例 (17% ) ,9分 10例(8.9% ) ,10分 7例 (6 .3% )。精曲小管精子发生功能 5级分度法结果 ,1级 5例 (4 .5 % ) ,2级 38例 (33.9% ) ,3级 33例 (2 9.5 % ) ,4级 2 9例 (2 5 .9% ) ,5级 7例 (6 .3% )。多元回归分析结果 ,精曲小管精子发生功能分级与生精上皮高度、固有层厚度、精曲小管直径和血清卵泡刺激素 (FSH)具有极显著相关性 (P <0 .0 1)。组合     

丹参对大鼠肝脏低温保存损伤的保护作用

目的　研究丹参对大鼠肝脏低温保存损伤的保护作用。方法　采用大鼠肝脏离体非循环灌注模型 ,观察乳酸林格液 (LR液 )中加入不同剂量丹参后保存大鼠肝脏 1 2h的效果。结果　丹参组 ( 60 0mg/g)肝组织ATP含量 ( 6.0 8± 0 .67) μmol/g及分泌胆汁量 ( 1 0 5.6± 1 2 .4) μl/h明显高于对照组 ( 2 .52± 0 .31 ) μmol/g及 ( 57.4± 8.2 ) μl/h(P <0 .0 5) ,丹参组 ( 60 0mg/g)肝组织 2 ,3 二羟苯甲酸 ( 2 ,3 DHBA) ( 0 .1 54± 0 .0 1 3)nmol/g、2 ,5 DHBA( 1 .354± 0 .0 68)nmol/g及流出液天门冬氨酸转氨酶 (AST) ( 38.4± 3.7)U/L明显低于对照组 ( 0 .2 4 5± 0 .0 2 1 )nmol/g、( 2 .1 0 5± 0 .0 97)nmol/g及( 76.4± 9.2 )U/L ,差异有显著性 (P <0 .0 5)。结论　丹参可明显提高供体肝脏的保存效果 ,其作用机理可能主要与改善低温保存肝脏的能量代谢及抗氧自由基的作用有关     

缺血预处理对大鼠移植肝脏保存再灌注损伤的保护及机制探讨

目的探讨缺血预处理 (ischemicpreconditioning ,IP)对大鼠移植肝脏保存再灌注损伤的保护作用及机理。方法采用SD大鼠原位肝移植动物模型 ,12 8只大鼠随机分成A(对照组 )、B(IP组 )、C(腺苷 ,Ado组 )、D(NO合成抑制剂 ,NAME组 )组 ,每组 32只。其中各组的半数用于观察存活率 ,另一半用于移植肝脏再灌注 2h后取血及肝脏检测。结果IP组和Ado组的 1周存活率、血清NO水平及肝组织腺苷含量分别为 88% (7/ 8)和 88% (7/ 8) ,(33 0± 6 1) μmol/l和 (2 9 1± 6 5 ) μmol/l,(7 2± 1 8) μmol/g和 (5 7± 1 3) μmol/g ,均高于对照组的 38% (3/ 8) ,(15 4± 3 0 )mol/L和 (3 6 9±0 5 4 ) μmol/g (P <0 0 5 ) ,血清ALT及TNF含量分别为 (2 87± 82 )IU/L和 (35 7± 93)IU/L ,(1 15± 0 2 3)ng/ml和 (1 14± 0 2 7)ng/ml,均低于对照组的 (5 88± 5 8)IU/L及 (1 5 9± 0 35 )ng/ml(P <0 0 5 ) ,组织的病理学改变也轻于对照组 ;NAME组的 1周存活率、血清NO及ALT含量等分别为 2 5 % (2 / 8)、(13 74± 3 11) μmol/l及 (6 34± 6 5 )IU/L ,与对照组相近 (P >0 0 5 ) ,而肝组织腺苷含量为 (5 5 6± 1 19)μmol/g ,与对照组差异有显著意义 (P <0 0 5 )。 结论IP对大鼠移植肝脏的保存再灌注损伤具有保护     

胎儿睾丸组织异种移植后生精细胞发育初探

目的 :以人胎儿睾丸组织为供体 ,免疫缺陷小鼠为受体 ,研究人类睾丸生精细胞异种移植后的继续发育情况。　方法 :将 2 6周胎儿的睾丸组织植入去势裸鼠背部 ,于移植后 1 35d取出移植物 ,进行组织形态学观察 ,分析原始生精细胞在异种异位的发育情况。　结果 :移植 1 35d后取出的移植物显示 ,其生长幅度已由移植前直径约 1mm和湿重约 5mg ,分别增加到移植后大于 3mm和 2 0mg。组织形态学观察发现 ,移植前的睾丸主要是由直径为(6 0± 1 5 ) μm的精曲小管索构成 ,其中包含的细胞主要是原始Sertoli细胞和少量原始生精细胞 ,细胞排列呈弥散无规则状态 ;而移植后 1 35d的精曲小管索已发育成具有管腔的精曲小管 ,出现由Sertoli细胞和生精细胞组成的完整生精上皮 ,直径增大到 (80± 2 5 ) μm。原本呈不规则分布的原始Sertoli细胞和生精细胞大部分已迁移到基膜处 ,其中有少数生精细胞发育成为精原细胞。　结论 :人胎儿睾丸组织移植到去势裸鼠背部后 ,可以继续存活并进一步生长发育。     

腺苷预处理对心脏直视手术心肌保护作用的临床研究

目的　探讨腺苷预处理对心脏直视手术的心肌保护效果。方法　将 30例择期心脏瓣膜置换术患者随机分成治疗组和对照组 ,治疗组在开心术前实施腺苷预处理。观察血清心肌肌钙蛋白T(cTnT)、磷酸肌酸激酶同工酶 (CK MB)、血浆丙二醛 (MDA)、心肌三磷酸腺苷 (ATP)、能量储备(EC)及心肌超微结构 (线粒体计分 )的变化。结果　主动脉开放后 30min ,治疗组cTnT为 ( 0 .42±0 .1 8) μg/L、CK MB为 ( 35.42± 1 5.87)U/L、MDA为 ( 4 .2 8± 0 .35)mmol/L升高值均明显低于对照组 [( 1 .1 6± 0 .32 ) μg/L、( 56.2 6± 1 6.36)U//L、( 6.37± 2 .46)nmol/L(P <0 .0 5) ];治疗组ATP含量( 1 5.86± 3.51 ) μmol/g干重和EC值 0 .4857± 0 .0 578均明显高于对照组 [( 6.2 5± 2 .79) μmol/g干重、0 .2 992± 0 .0 4 1 9(P <0 .0 1 ) ];治疗组线粒体计分 0 .860 2± 0 .2 381明显低于对照组 2 .740 6±0 .9792 ,(P <0 .0 1 )。结论　腺苷预处理对心脏具有明显的保护作用     

单侧隐睾大鼠生殖股神经在对侧睾丸损害中的作用机制研究

目的 :探讨单侧隐睾大鼠模型生殖股神经在对侧睾丸损害中的作用机制。　方法 :建立单侧隐睾大鼠模型 (2 1d龄 ) ,切断该侧生殖股神经 ,12 0d后观察对侧睾丸的生精细胞凋亡变化及组织乳酸含量变化。　结果 :切断生殖股神经后 ,对侧睾丸生精细胞凋亡为 (5 .76± 0 .76 ) % ,与对照组 (17.2 8± 1.36 ) %相比明显减少 (P <0 .0 5 ) ;乳酸含量也由 (2 .19± 0 .2 4 )mmol/L下降为 (1.70± 0 .31)mmol/L(P <0 .0 5 ) ,且乳酸含量与细胞凋亡呈正相关(P <0 .0 5 )。　结论 :单侧隐睾症对侧睾丸损伤可能与其神经传导反射性血流减少引起生精细胞凋亡有关     

肾移植术后肝功能异常患者用他克莫司替换环孢素A疗效的初步观察

目的　观察他克莫司 (FK5 0 6 )替换环孢素A(CsA)并联合应用霉酚酸酯 (MMF)及泼尼松 (Pred)防治肾移植术后肝功能异常患者的有效性及安全性。方法　肾移植术后 8例肝功能异常患者 (男性 5例 ,女性 3例 ,平均 38.2 3岁 ) ,用FK5 0 6替换CsA治疗 ,停用CsA 2 4h后 ,开始给予FK5 0 6。FK5 0 6初始剂量根据患者体重、肝功能损害程度及术后时间确定 ,服药 1周后 ,根据全血FK5 0 6谷值浓度调整剂量 ,使其谷值浓度维持于 5～ 15 μg/L。结果　用FK5 0 6替换CsA ,1个月后患者血中直接胆红素从替换前的 (2 2 .6 6± 17.19) μmol/L下降至 (7.0 5± 2 .32 ) μmol/L ,P <0 .0 5 ;间接胆红素从替换前的 (4 2 .15± 34.15 ) μmol/L下降至 (14.5 4± 2 .5 9) μmol/L ,P <0 .0 5 ;血清丙氨酸转氨酶从替换前的 (83 .0 0± 93 .14)IU/L下降至 1个月后的 (2 9.5 0± 15 .41)IU/L ,P >0 .0 5 ;血清肌酐从 (177.91±86 .41) μmol/L下降至 (135 .92± 34.0 5 ) μmol/L ,P >0 .0 5。 3例腹水的患者均于药物替换 1个月后完全消失。仅有 1例患者出现便秘、食欲下降伴上肢颤抖。结论　用FK5 0 6替换CsA并联合应用MMF及Pred对防治肾移植术后肝功能异常是安全和有效的措施     

钝性胸部创伤后体内部分激素含量与血流动力学变化的关系

目的　探讨钝性胸部创伤 (BCT)后体内部分激素含量和血流动力学变化及意义。方法　随机选取兔 1 2只 ,采用BIM Ⅱ型生物撞击机致成BCT模型 ,分别在伤前、伤后 2、4、8、2 4h测定甲状腺素 (T3、T4 )、促甲状腺激素 (TSH)、肾素 血管紧张素 AⅠ、AⅡ、胰岛素及C 肽含量 ,并监测血流动力学改变。结果　BCT后 2 4hT3、T4 、TSH分别由伤前的 (1 .43± 0 .62 )nmol/L、(55 .2 0± 1 4 .60 )nmol/L、(8.34± 4 .30 )mU/L降为 (0 .54± 0 .2 8)nmol/L(P <0 .0 1 )、(32 .50± 2 .70 )nmol/L(P <0 .0 1 )、(2 .2 4± 0 .79)mU/L(P <0 .0 1 ) ;AⅠ、AⅡ、胰岛素和C肽分别由伤前的(0 .44± 0 .2 5) μg·L- 1 ·h- 1 、(48.0± 1 0 .9)ng/L、(5 .96± 2 .66)mIU/L、(0 .2 3± 0 .1 6)nmol/L增高至 (1 .38± 0 .88) μg·L- 1 ·h- 1 (P <0 .0 5)、(70 .0± 9.9)ng/L(P <0 .0 5)、(7.92± 3 .2 2 )mIU/L(P <0 .0 5)、(0 .52± 0 .0 9)nmol/L(P <0 .0 5) ;左室舒张末压 (LVEDP)和左室内压最大下降速率( dp/dtmax)增高 ;相关分析表明血清甲状腺激素、肾素 血管紧张素、胰岛素及C肽含量改变与血流动力学变化呈明显相关 (P <0 .0 5、P <0 .0 1 )。结论　BCT后体内部分激素明显改变是引起心功能障碍的原因之一。     

Testicular pathology in 46,XY dysgenetic male pseudohermaphroditism: an approach to pathogenesis of testis cancer.

Eleven children with dysgenic male pseudohermaphroditism (DMP) and 18 boys with isolated penile hypospadias, all with 46,XY karyotype, were studied. Testicular dysgenesis was associated with significantly lower testosterone response to human chorionic gonadotropin (0.9 +/- 0.2 ng/mL) than it was in hypospadias (3.3 +/- 0.1 ng/mL), and with significantly higher mean serum follicle-stimulating hormone (FSH) levels (8.4 +/- 2.3 IU/L vs 1.5 +/- 0.3 IU/L). Gonadoblastoma, a tumor that arises from the sex cords, was found in more than 1/4 of patients with DMP, whereas testicular carcinoma in situ (CIS) cells were present in all of these patients. Forty-two percent to 98% of CIS cells revealed an aneuploid pattern of nuclear DNA, indicating that most of them are neoplastic cells. In patients with hypospadias, CIS was not seen, and no other abnormalities were detected. In children with DMP, the percentage of tubules populated with germ cells was significantly lower than it was in those with hypospadias (48.3% +/- 10.6% vs 92.4% +/- 4.0%). The total number of germ cells (CIS cells + spermatogonia) did not differ significantly between the 2 groups, but the number of spermatogonia was significantly reduced in children with DMP (0.08 +/- 0.05 vs 3.65 +/- 0.2), suggesting impaired differentiation of gonocytes to spermatogonia. The following significant correlations were present with DMP: 1) the higher the seminiferous tubule cross-section area, the higher the number of CIS cells (r = 0.78); and 2) the higher the serum gonadotropin levels, the higher were tubular diameter (r = 0.93 for FSH and r = 0.75 for luteinizing hormone [LH]), area (r = 0.79 for FSH and r = 0.82 for LH), percentage of tubules populated with germ cells (r = 0.86 for FSH and r = 0.81 for LH), and number of CIS cells (r = 0.87 for FSH and r = 0.79 for LH). The results indicate that in intersex children with 46,XY karyotype, CIS occurs in dysgenetic testes in all cases and is frequently associated with gonadoblastoma. Impaired organogenesis of sex cords, relative inhibition of testosterone secretion, and the associated increased secretion of gonadotropins may create a milieu that induces or is favorable for the formation or maintenance of neoplastic lesions in dysgenetic testes early in childhood.     

Androgens in various fluid compartments of the rat testis and epididymis after hypophysectomy and gonadotropin supplementation

Hypophysectomized male rats were administered LH or LH + FSH for 14 days and subjected to in vivo micropuncture collection of reproductive tract fluids to determine if FSH alters the compartmentalization of testosterone in the rat testis or of 5 alpha-dihydrotestosterone (DHT) in the epididymis. Testosterone and DHT concentrations were determined in cardiac blood serum, testicular venous serum, testicular interstitial fluid, and seminiferous tubule fluid, and in intraluminal fluid and tissue extracts from the caput and cauda epididymidis. Testosterone is the predominant androgen in the testis, and compared with control values, concentrations in venous sera, interstitial fluid, and tubule fluid were returned to values indistinguishable from controls by supplementation with 24 micrograms LH/day. 24 micrograms LH + 24 micrograms FSH/day did not augment the intratubular partition of testosterone. Epididymal DHT values were returned to control levels by LH alone, but additional supplementation with FSH significantly increased DHT from the caput epididymidis even further. It is speculated that FSH does not alter the compartmentalization of androgens in the rat testis, but may play a role in retaining androgens in the epididymis.     

精液中性激素水平与生殖细胞凋亡的关系

目的:探讨人精液中性激素水平与生殖细胞凋亡的关系。方法:随机选择66例不育患者及30例生育男性,采用ELISA法进行卵泡刺激素(FSH)、黄体生成素(LH)、泌乳素(PRL)和睾酮(T)水平分析,并用脱氧核苷酸末端转移酶(TdT)介导的缺口末端标记(TUNEL)法检测生殖细胞的凋亡。结果:精液中FSH、LH、PRL和T水平30例生育者分别为(1.63±0.15)U/L、(2.18±0.21)U/L、(6.34±0.30)nmol/L、(1.85±0.11)nmol/L,生殖细胞凋亡率为(4.61±1.23)%,而66例不育者4种性激素水平分别为(1.25±0.18)U/L、(1.76±0.32)U/L、(5.86±0.31)nmol/L、(1.45±0.13)nmol/L,生殖细胞凋亡率为(18.36±2.04)%。两者相比各参数差异均有显著性(P<0.01)。不育组FSH、LH、PRL、T水平与生殖细胞的凋亡率呈负相关(r分别为-0.88、-0.93、-0.90、-0.98,P均<0.01)。凋亡的生殖细胞体积缩小,核染色质致密,凝聚在核周形成新月形,或核裂解形成凋亡小体。结论:精液性激素水平与生殖细胞的凋亡有着密切关系,低水平的性激素可能导致睾丸生殖细胞凋亡率增加。     

射线损伤对睾丸Claudin-11 mRNA表达的影响

目的:Claudin-11为支持细胞紧密连接的组分,在构建血睾屏障及维持生精上皮空间构象中呈现重要作用。本研究拟通过射线局部照射致睾丸氧化应激,观察Claudin-11转录水平变化,探讨氧化应激损伤精子发生的作用机制。方法:48只雄性昆明小鼠随机分配至A、B、C、D 4组,每组12只,A组空白对照,B、C、D 3组分别以2、6、10 Gy剂量60Co-γ射线局部照射实验动物下腹部1次,于4周后处死,测定实验小鼠体重及双睾丸重量;HE染色观察睾丸组织学变化;酶联免疫法检测血清性激素水平;实时荧光PCR监测睾丸组织内抑制素βB及Claudin-11转录水平变化。结果:不同剂量射线致睾丸氧化应激损伤后睾丸重量,A组为(182.9±8.43)mg,B组为(129.4±10.81)mg,C组为(87.5±16.83)mg,D组为(56.1±12.36)mg,呈下降趋势,与A组相比,差异有显著性(P<0.05);睾丸指数A组为(4.28±0.31)mg/g,B组为(3.39±0.57)mg/g,C组为(2.46±0.46)mg/g,D组为(1.63±0.44)mg/g,下降更为明显,与A组相比,差异有显著性(P<0.01);组织学分析示,与A组相比,受射线照射3组生精小管分化指数(TDI)下降明显(P<0.01),生精小管直径减小,生精上皮高度显著降低并层次紊乱。血清FSH,A组为(5.77±1.62)IU/L,B组为(6.74±1.95)IU/L,C组为(8.41±2.44)IU/L,D组为(10.93±3.16)IU/L,逐渐升高,D组较A组升高1.9倍。伴随照射睾丸射线剂量增加,组织内抑制素βB mRNA含量下降,Clau-din11转录水平呈现增高趋势,C、D两组Claudin-11 mRNA水平高于正常对照A组(P均<0.01)。结论:射线局部照射致睾丸氧化应激,组织内抑制素βB mRNA降低、血清FSH升高,支持细胞合成及分泌功能受损;同时,睾丸组织Claudin-11表达量则增加。增加的紧密连接组分同升高的FSH致使血睾屏障重建周期延长,生精上皮内处于减数分裂的精母细胞数量减少,导致不育发生。     

抗FSH自身抗体对大鼠睾丸生精功能影响的初步研究

目的:建立抗FSH自身抗体大鼠模型,同时研究抗FSH自身抗体对雄性大鼠生精功能的影响。方法:30只SD大鼠(21d龄),随机分为实验组、对照组,各15只。合成大鼠FSHβ亚基上一段特异性氨基酸序列(18肽),将合成多肽与钥孔戚血蓝素(keyholelimpethemocyanin,KLH)偶联,免疫SD大鼠,作为实验组。对照组大鼠用KLH免疫。初次免疫之后,每隔2周加强免疫1次,共7次,于第3次加强免疫后1周(即,免疫第49d)眼眶取血测定血清抗体效价,之后每隔两周测一次抗体效价,至实验结束。并于免疫第77d、91d和105d时,分别处死实验组和对照组大鼠各5只,用光镜和电镜观察大鼠睾丸生精小管结构和附睾精子结构的变化,计数附睾尾精子数量及肿胀精子百分率,并用ELISA法检测大鼠血清T水平。结果:免疫第49d后,实验组大鼠血清抗18肽-KLH抗体效价为1∶200,免疫第63d后,抗体效价达到1∶400,之后抗体效价一直维持在1∶400。免疫第91d后,实验组大鼠附睾尾肿胀精子百分率显著低于对照组(60.4±6.23vs50.60±3.05,P<0.05);免疫第105d后,实验组大鼠生精小管内生精细胞数量及管腔内精子数量均减少,且附睾尾精子数量(46.08±6.56vs32.53±3.41)和肿胀精子百分率(60.60±5.86vs48.60±3.85)均显著低于对照组(P<0.05),而血清T水平显著高于对照组(P<0.05)。结论:抗FSH自身抗体可能会引起睾丸生精障碍。     

正常促性腺激素妇女垂体降调节后晚卵泡期黄体生成素浓度对体外受精结局的影响

目的 :探讨正常促性腺激素妇女超促排卵时晚卵泡期黄体生成素 (LH)水平对体外受精 (IVF)结局的影响。　方法 :正常促性腺激素妇女 4 32个周期 ,于黄体中期开始采用促性腺激素释放激素激动剂 (GnRHa)行垂体降调节后 ,应用卵泡刺激素 (FSH)刺激卵巢的促排卵方案。当卵泡直径达 1 4mm时 ,添加hMG(FSH +hMG组 ) ,对照组不添加hMG(FSH组 )。hCG注射日测定血LH和雌二醇 (E2 )浓度。按照LH浓度 ,将FSH +hMG组分为 4个亚组。　结果 :FSH +hMG组的hCG注射日E2 浓度高于FSH组 [(3435 .5 1± 2 0 2 9.0 1 )pg/ml和 2 6 2 0 .6 2± 1 6 0 4 .80 )pg/ml,P<0 .0 5 ],胚胎移植数少于后者 [(2 .77± 0 .4 5 )个和 (2 .2 2± 0 .4 6 )个 ,P <0 .0 0 1 ]。两组受精率、胚胎种植率和临床妊娠率无统计学差异 (77.5 2 %和 78.31 %,4 1 .4 2 %和 4 1 .6 8%,6 4 .5 6 %和 6 2 .6 4 %,P均 >0 .0 5 ) ;FSH +hMG组的 4个亚组的受精率、胚胎种植率和临床妊娠率也无统计学差异 (P >0 .0 5 )。　结论 :正常促性腺激素妇女超促排卵时 ,晚卵泡期血清LH在生理范围内以及在晚卵泡期适量添加LH ,不会对IVF结局产生负面影响。     

Post-transplant erythrocytosis: role of erythropoietin and male sex hormones.

Seventeen patients with post-renal transplant erythrocytosis and 17 non-erythrocytotic controls, matched in age, sex, serum creatinine and source of donor kidney, were studied to determine the role of erythropoietin, male sex hormones (testosterone, FSH, LH), and various patient risk factors in post-transplant erythrocytosis. Serum erythropoietin was significantly greater in erythrocytotic patients (35.6 +/- 5.7 mU/ml) than non-erythrocytotic patients (18.8 +/- 2.6 mU/ml) (P less than 0.05) and normal subjects (22.5 +/- 0.95 mU/ml) P less than 0.05). Serum testosterone was similar between the male study (13.2 +/- 6.2 nmol/l) and control (13.1 +/- 6.0 nmol/l) patients. This might be due to the greater basal LH in the male control subjects (13.9 +/- 11.7 IU/l versus 8.0 +/- 3.3 IU/l in erythrocytotic males, P = 0.084). Basal FSH in the male controls was greater than that in the study group (13.7 +/- 14 IU/l versus 6.8 +/- 2.9 IU/l, P = 0.067). Among the demographic risk factors, only the smoking history was important. There were more smokers among the erythrocytotic patients than controls (P = 0.051).     

Luteinizing hormone pulsatility in men with damage to the germinal epithelium

Bioactive-LH (B-LH) was measured in plasma by in-vitro bioassay and immunoactive-LH (I-LH) by immunoassay at 10 min intervals for 6 h in five men after standard chemotherapy for Hodgkin's disease. Eleven normal men acted as controls. Follicle-stimulating hormone (FSH) was markedly raised in the treated patients (mean +/- SEM; 12.8 +/- 2.8 vs. 2.7 +/- 0.4 IU l-1, P less than 0.006) reflecting damage to the germinal epithelium. Bioactive (27.4 +/- 2.8 vs. 12.9 +/- 1.3 IU l-1) and I-LH (9.6 +/- 2.0 vs. 4.9 +/- 0.4 IU l-1) were elevated (P less than 0.006) in the patient group whilst testosterone levels (24.0 +/- 3.8 vs. 19.6 +/- 2.4 nmol l-1) were normal. The testosterone I-LH ratio, a putative index of Leydig cell dysfunction, was negatively correlated with FSH levels (r = -0.85, P less than 0.02). Bioactive and I-LH pulse peak amplitude were elevated, as were pulse maxima (P less than 0.05). In contrast, B-LH pulse frequency was similar between the patients (2 pulses per 6 h) and controls (median 2, range 1-3 pulses per 6 h) as was the I-LH pulse frequency (median 2, 1-2 pulses per 6 h in both groups). The mean B:I LH ratios were similar (2.94 +/- 0.09 vs. 2.63 +/- 0.14) in both groups, although the inter-pulse B:I ratio was increased (P less than 0.007) in the patient group.(ABSTRACT TRUNCATED AT 250 WORDS)