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Between P14 and P21,CIAPIN1 immunoreaction in the brain,heart and liverbecame much lower. However,between P21 and P28,CIAPIN1 immunoreactionin the heart,brain,liver and skeletal muscle became much lower,while with thekidney development,CIAPIN1 immunoreaction in the kidney became higher. Invarious tissues from adult mouse,CIAPIN1 immunoreaction could be seen incardiac muscle cell,brain,hepatocyte,epithelium of renal tubule,skeletal muscle,lung tissue,gastric mucosa and gland,acinus lienalis.2. Distribution of CIAPIN1 in normal fetal and adult human tissuesTo reveal the possible physiological role of CIAPIN1,we examined theexpression and distribution of CIAPIN1 in fetal and adult human tissues usingimmunohistochemistry. We found that CIAPIN1 was ubiquitously distributed infetal and adult tissues,and was localized in both the cytoplasm and the nucleus.

然而,在3个月大的成年鼠中,CIAPIN1阳性反应物在心、脑、肝和肾小管中的表达强度要低于P28小鼠;但CIAPIN1阳性反应物在成年鼠骨骼肌中较P28小鼠高。2、CIAPIN1蛋白在人5个月胚胎及成人多器官组织内的表达在人5月胚胎多器官组织中,CIAPIN1阳性反应物见于心脏、胆囊单层柱状上皮和粘膜、结肠粘膜、小肠粘膜和绒毛、肝脏、直肠腺体、胃粘膜、肾上腺束状带、甲状腺滤泡、脾索、胸腺小叶间隔、皮肤真皮层和汗腺、睾丸白膜和间质、脑组织内神经元和神经胶质、肺小支气管和肺泡、骨骼肌、肾脏皮髓质和肾小管、子宫内膜、胰腺腺泡和胰岛、卵巢、输卵管粘膜等绝大多数组织细胞。

Results showed that TDI induced toxic action on spermatogenic cell,while the chondriosome was its target within the length and concentrations.

结果表明:在本实验染毒时间和染毒剂量范围内,TD I对雄性的生殖毒性主要表现为对各级生精细胞均有一定的毒性作用,作用的靶点是细胞内的线粒体;TD I通过影响各种酶的活性,干扰了睾丸组织的有氧代谢和无氧供能,抑制了细胞对能量的利用,损伤了各级生精细胞,导致生精上皮不可逆的损害,从而造成了其对雄性生殖系统的损伤;TD I对雄性生殖细胞的核酸代谢以及DNA合成有一定影响。

Sertoli cell, Leydig cell and germ cell are major cells in mammal testis and they have close relations.

Sertoli细胞、Leydig细胞和精细胞是哺乳动物睾丸内的三种主要的细胞,它们之间关系密切。

Methods Male infertility couples from October 2006 to July 2008 were chosen and divided into ICSI group and TESA+ICSI group. ICSI group were 584 oligozoospermia cases with alive normal sperm in spermatic fluid. TESA+ICSI group were 54 obstructive azoospermia cases with alive normal sperm in testicle. Two groups were treated with ICSI after wives obtained oocytes by ovarian stimulation.

选择2006年10月~2008年7月因男性不孕症夫妇行ICSI治疗的患者638例分成两组,ICSI组和TESA+ICSI组,ICSI组为自行排精后精液内可以找到正常形态活精子的少精症患者行ICSI治疗584例,TESA+ICSI组为梗阻性无精子症患者经睾丸穿刺找到睾丸内形态正常活精子行ICSI治疗共54例,两组女方均给予超促排卵用药获取卵母细胞。

It is unclear whether the cells have this capacity under natural conditions inside the testes.

尚不清楚这些细胞在睾丸内的自然条件下是否具有这种能力。

Objective: To observe the change of Leydig cell and extra-cellular matrix of testis in mice during experimental orchiditis.

目的:研究小鼠睾丸间质细胞和睾丸内细胞外基质在实验性睾丸炎期间的变化。

The decreased function of Leydig cells and damage of ECM in testis during experimental orchiditis might be the factors associated with the poor fertile ability.

发生睾丸炎期间,睾丸间质细胞功能下降,睾丸内细胞外基质受损,这可能是导致生育力下降的原因之一。

At postnatal 1st week immunopositive reaction of NGF was detected mainly in sustentacular cells and the spermatogonia also showed positive staining. NGF positive staining in the testes was observed in interstitial cells, spermatogenetic cells, sustentacular cells and Leydig cells at 3rd week. After the postnatal 5th week, NGF-positive immunostaining was also detected in intersitial cells and spermatogenetic cells, but the intensity of reaction was weaker than that at 1st and 3rd weeks.

免疫组化定位分析显示:睾丸组织的神经生长因子蛋白表达于小鼠出生后的各个时期内,1周龄睾丸组织免疫阳性反应主要位于支持细胞,精原细胞也有着色;3周龄睾丸组织的间质细胞、各级生精细胞、支持细胞、管周肌样细胞表达均呈现阳性;5周后的睾丸组织内神经生长因子呈低水平表达,主要表达于间质细胞和生精细胞内。

In other words, the embryonic period and the infancy of testicular tubules is solid thin tube, did not occur and mature sperm.

也就是说,胚胎期和婴儿期睾丸内的曲细精管是实心的细管,并没有精子的发生和成熟。

The results showed that (1) COX-2 mRNA and protein existed in the mature male rat testis. COX-2 was localized in spermatocytes by immunohistochemistry.(2) COX-2 also existed in adult man testis. COX-2 protein was positively stained in spermatocytes and Leydig cells.(3) 2 weeks after administration of rofecoxib, the level of testosterone in the whole testis reached its lower values, being only 50% of control values. However, testosterone level recovered during 4 weeks. After such treatment, histologic examination of these testes showed atrophy of the seminiferous tubules and maturation arrest of spermatogenesis.(4) 2 weeks post-EDS, expression of COX-2 decreased significantly (P.005), in comparison with vehicle-treatment control. 4 weeks after treatment, a new generation of fetal like Leydig cells repopulated in the testicular interstitium resulting in COX-2 expression partially recovered. Although the expression of COX-2 mRNA and protein are enhanced at 8th week after using external testosterone, it wasn't significant higher than control group.

实验研究证明:(1)正常成年雄性大鼠睾丸组织中COX-2在mRNA和蛋白质水平均存在表达,免疫组织化学结果显示COX-2定位于曲细精管内的生精细胞;正常成年男性睾丸组织中同样存在COX-2表达,免疫组织化学结果显示COX-2定位于曲细精管内的生精细胞和Leydig细胞;(2)服用特异性COX-2酶抑制剂rofecoxib 2周后,实验组大鼠睾丸组织内睾酮的含量减少,为正常对照组的50%;持续用药4周后睾丸组织内睾酮浓度逐渐恢复至正常水平;COX-2酶活性降低后病理组织切片显示睾丸内曲细精管萎缩,生精紊乱,持续用药4周时影响最明显;(3)注射特异性Leydig细胞杀灭剂EDS 2周后,实验组大鼠睾丸组织内睾酮浓度降至极低水平时,COX-2的蛋白和基因表达水平也显著低于正常空白对照组(P.005);使用EDS后第4周,睾丸组织中的睾酮浓度逐渐回升,同样组织中COX-2蛋白表达和mRNA表达水平也相应提高接近正常水平;使用EDS后4周开始给予外源性睾酮,6周和8周时COX-2表达水平的绝对值虽有提高,但与正常大鼠空白对照组比较并无显著性差异,说明外源性雄激素刺激睾丸合成COX-2的作用并不明显。

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