BACKGROUND & AIMS: :Varicocele is considered a predominantly unilateral left-sided disease. However, since male fertility is preserved with only one healthy testis, infertility perforce represents bilateral testicular dysfunction. It was hypothesized that: (i) right varicocele cannot be diagnosed by palpation and therefore has not been treated in the past by the traditional treatment, and (ii) right varicocele causes impaired oxygen supply in the right testicular microcirculation, leading to germ cell degeneration. This study performed venographies of both right and left internal spermatic veins during the treatment of 840 infertile men with varicocele and analysed the results using tools of fluid mechanics. Histopathology of the right testis revealed stagnation of blood flow and degenerative changes attributed to lack of adequate oxygenation in all testicular cell types. Right varicocele was found in the vast majority of the patients. We found that due to the destruction of one-way valves, pathologic hydrostatic pressure is produced in the testicular venous microcirculatory system about five times higher than normal, exceeding arteriolar pressure. The pressure gradient between the arterioles and venules in the testicular tissue is therefore reversed, leading to persistent hypoxia. Right varicocele, although undetected, is prevalent in infertile men with varicocele, hence only bilateral occlusion of the internal spermatic veins, including the associated bypasses, eliminating the pathologic hydrostatic pressure will lead to resumption of arterial blood flow in the testicular microcirculation.

背景与目标： ：精索静脉曲张被认为是主要的单侧左侧疾病。但是，由于只有一个健康的睾丸才能维持男性的生育能力，因此不育症的强迫表现为双侧睾丸功能障碍。假设：（i）右精索静脉曲张不能通过触诊诊断，因此过去没有用传统疗法治疗；（ii）右精索静脉曲张导致右睾丸微循环中的氧气供应受损，导致生殖细胞变性。这项研究在治疗840名不育男性精索静脉曲张的过程中对左右两侧的精索静脉进行了静脉造影，并使用流体力学工具对结果进行了分析。右睾丸的组织病理学显示血流停滞和变性变化归因于所有睾丸细胞类型缺乏足够的氧合。在绝大多数患者中发现了右精索静脉曲张。我们发现由于单向阀的破坏，睾丸静脉微循环系统中产生的病理性静水压力比正常高约五倍，超过了小动脉压力。因此，睾丸组织中小动脉和小静脉之间的压力梯度会反向，从而导致持续的缺氧。右精索静脉曲张虽然未被发现，但在精索静脉曲张的不育男性中很普遍，因此，只有双侧内精子静脉闭塞，包括相关的旁路，消除病理性静水压会导致睾丸微循环中动脉血流的恢复。

BACKGROUND & AIMS: PURPOSE:Peptide growth factors are known accelerators of corneal wound healing, probably mediated through increased proliferation of the cells; however, information about their effect on keratocyte motility is lacking. The influence of peptide growth factors on keratocyte migratory activity was investigated, using the following growth factors: platelet derived growth factor (PDGF-BB), epidermal growth factor (EGF), acidic fibroblast growth factor (aFGF), basic fibroblast growth factor (bFGF), insulin-like growth factor-I (IGF-I) and transforming growth factor-beta-1 (TGF-beta 1).

METHODS:Keratocytes were seeded on gels of type 1 collagen, growth factor added, and the cells left to migrate for 72 hours. Subsequently, the number of keratocytes at the different levels in the collagen gel was evaluated by optically sectioning the gel at 20 microns, intervals, with an inverted phase contrast microscope.

RESULTS:PDGF, EGF and bFGF at 10 ng/ml, all increased the number of keratocytes at the different levels of the gel as compared to a non-stimulated control (p < 0.05 or p < 0.01, students t-test). TGF-beta proved to be a strong inhibitor of keratocyte migration, decreasing the number of keratocytes observed at every level in the gel (p < 0.05 and p < 0.01, students t-test), whereas no effect of IGF-I and aFGF was found. During the 72 hours of migration, no contraction of the collagen gels was observed. Autoradiography of histological sections of the gels showed that during the 72-hour period only TGF-beta and 10% fetal bovine serum induced an increase in keratocyte proliferation.

CONCLUSION:PDGF, EGF and bFGF increase keratocyte migration, independent of proliferation in a collagen gel invasion assay and might promote corneal wound healing, not only by increasing cell proliferation, but also through increased motility.

背景与目标： 目的：肽生长因子是已知的角膜伤口愈合促进剂，可能是通过细胞增殖的增加来介导的。然而，缺乏有关它们对角膜细胞运动性影响的信息。使用以下生长因子研究了肽生长因子对角膜细胞迁移活性的影响：血小板衍生生长因子（PDGF-BB），表皮生长因子（EGF），酸性成纤维细胞生长因子（aFGF），碱性成纤维细胞生长因子（bFGF） ），胰岛素样生长因子I（IGF-I）和转化生长因子β-1（TGF-beta 1）。

方法：将角质形成细胞接种在1型胶原蛋白，添加了生长因子，细胞迁移了72小时。随后，通过倒置相差显微镜以20微米的间隔对凝胶进行光学切片，评估胶原蛋白凝胶中不同水平的角质形成细胞的数量。

结果：PDGF ，与未刺激的对照组相比，在10 ng / ml的EGF和bFGF均增加了凝胶水平不同时的角化细胞数量（p <0.05或p <0.01，学生t检验）。 TGF-β被证明是一种强烈的角膜细胞迁移抑制剂，可减少凝胶中各个水平上观察到的角膜细胞数量（p <0.05和p <0.01，学生t检验），而IGF-I和aFGF没有作用成立。在迁移的72小时内，未观察到胶原凝胶的收缩。凝胶组织学切片的放射自显影显示，在72小时内，只有TGF-β和10％的胎牛血清诱导了角膜细胞增殖的增加。

结论：PDGF，EGF bFGF和bFGF可以增加角膜细胞的迁移，而不受胶原凝胶入侵试验中的增殖的影响，不仅可以通过增加细胞增殖，而且可以通过增加运动性来促进角膜伤口愈合。