Expression of CD68 CD45RO CD20 and proliferating cell nuclear antigen in nasal polyps]

OBJECTIVE: To study the cellular expression of CD45RO, CD20, CD68 and proliferating cell nuclear antigen (PCNA) in nasal polyps. METHODS: Nasal polyp tissues from 50 patients were evaluated for cellular expression of CD45RO, CD20, CD68 and PCNA using immunohistochemistry SP by counting the average number in 5 chosen high-power fields, Histopathological observations were combined with HE. Analyses were performed on SPSS10.0. RESULTS: CD68+ cells were expressed more in nasal polyps dominated by eosinophils than by neutrophils(P < 0.05). There was no difference between CD45RO and CD20, but both of them had negative correlation(P = 0.05). Significant correlation was found between CD68+ cells and eosinophils or PCNA positive cells on epithelium. PCNA positive cells on epithelium had significant correlation on fibroblast (P < 0.05). CONCLUSION: Inflammatory cell infiltration (eosinophilia CD45RO, CD20, CD68) and cell proliferating in epithelium cells, glandular cell and fibroblast are strongly correlated with formation of nasal polyps. The nasal polyps are not only characteristic of eosinophilia but also by lymphocytes dominated by CD45RO and CD68 positive cells. CD68 may be stem cell of nasal polyp.     

Expression of Eph receptor tyrosine kinases and their ligands in human Granulosa lutein cells and human umbilical vein endothelial cells.

Corpus luteum development is regulated by gonadotropins and accompanied by extremely rapid vascularization of the avascular granulosa cell compartiment by endothelial cells (EC). The proliferation of Granulosa cells (GC) and EC is a complex interplay and takes place in a spatially and temporarily coordinated manner. The erythropoietin-producing hepatoma amplified sequence (Eph) receptors and their ligands-the ephrins- are a recently detected family of membrane located protein tyrosine kinases which play a crucial role in the growth and development of nerve and blood vessel network. We report about the mRNA expression pattern of Ephs and their ligands in human GC, in human EC, and in carcinoma cell lines OvCar-3 and Hela. The mRNA of EphA4, EphA7, ephrinA4, ephrinB1 and ephrinB2 was detected in GC and EC, while EphA2 was expressed only in GC. The expression of various Ephs and ephrins did not change in GC after stimulation with human chorion gonadotropin. Our study analyzes for the first time the expression of the complete human Eph/ephriny-system in GC and in EC. The remarkable similarity between these two cell types supports the theory of a functional relationship of EC and GC. In addition, it was shown that hCG is not a major determinant of Eph/ephrin regulation in GC.     

Functional correlates of Doppler flow study of the female urethral vasculature.

OBJECTIVES: To examine the effect of individual patient factors (age, parity, body mass index, menstrual cycle, menopause, hormone replacement therapy, bladder neck position and urethral mobility) on the appearance of Doppler flow in urethral vessels, to investigate the association between the Doppler flow parameters and intrinsic urethral function, storage and voiding, and to explore differences in the urethral vasculature between subjects with and without urodynamic stress incontinence (USI). METHODS: Over a 4-year period we prospectively performed imaging studies in 355 women, including 244 who denied any lower urinary tract symptoms within the previous 3 months (Group A) and 111 who had had lower urinary tract symptoms (Group B). Studies included morphologic assessment and Doppler flow investigation of the lower urinary tract. Vascular flow velocity and vessel density in the urethral vasculature were measured. For women in Group B, multichannel urodynamic studies were also performed. RESULTS: The urethral vasculature has five main branches of vessels. Their appearance was not affected by the menstrual cycle or menopause except for those of the anterior vaginal vessel and anterior branch of the middle urethral vessel. Other than that of the posterior urethral vessel, in which there was a correlation with parity, the resistance index (RI) was not affected by individual patient factors. However, there was a correlation between the vascular index (VI) and individual factors such as age (r = -0.336, P = 0.002), body mass index (r = -0.287, P = 0.028), menopause (r = -0.402, P < 0.001), and hormone replacement therapy (r = 0.392, P = 0.027). Only the VI and RI of the posterior urethral vessel correlated significantly with the urethral pressure profile. In subjects with lower urinary tract symptoms, the appearance of the urethral vasculature on power Doppler imaging and the corresponding RI and VI values were not correlated with objective evidence of USI. CONCLUSION: Patient factors may affect specific Doppler flow parameters of the urethral vasculature, which are related to intrinsic resting urethral closure. There is no difference in the appearance of the urethral vasculature in subjects with or without USI.     

兔视网膜方向选择性神经节细胞树突的独特分枝模式及其生理意义

本实验研究了兔视网膜中的方向选择性神经节细胞 (direction selective retinal ganglion cells,DS cells)树突野的分枝模式。测量了视网膜中方向选择性神经节细胞和作为经典分枝模式神经元代表的α神经节细胞的树突直径。发现 ,方向选择性神经节细胞的树突在分枝后直径达到 0 .5 μm,进一步分枝树突直径仍保持在 0 .5 μm左右 ,这样 ,在方向选择性神经节细胞树突野中大多数树突直径在 0 .5μm左右。而作为经典分枝模式神经元代表的α神经元的树突每次分枝后都逐级变细 ,最终直径达到 0 .5μm左右 ,这样 ,α神经节细胞的树突直径大部分都大于 0 .5μm。我们应用程序“NEU RON”对在两种神经元模型中 ,抑制点落于兴奋点与胞体之间 (proximal)和抑制点不落于兴奋点与胞体之间 (distal)这两种情况进行模拟。我们发现 ,当抑制点不落于兴奋点与胞体之间时 ,在方向选择性神经节细胞的树突分枝模型中 ,抑制效果更强。那么 ,将使得方向选择性神经节细胞对抑制点落于兴奋点和胞体之间的要求变得不是那么迫切。所以 ,方向选择性神经节细胞的这种独特分枝模式 ,也许可以避免或至少减轻其在发育中可能会产生的连线的复杂性。并且 ,我们对得出的结论进行了电路分析 ,对方向选择性神经节细胞这种独特的分枝模式具有的?     

急性胆囊炎腹腔镜手术时机探讨及操作技巧

目的 探讨急性胆囊炎行腹腔镜胆囊切除术的手术时机，并总结操作技巧。方法 回顾性分析2000年6月～2005年6月265例腹腔镜胆囊切除术治疗急性胆囊炎的临床资料。结果 265例中手术成功244例，成功率92．1％。中转开腹21例，其中小于72小时（Ⅰ组），超过72小时（Ⅱ组）的中转率分别为3．1％（4／129），12．5％（17／136）。Ⅰ组与Ⅱ组比较成功率无明显差别（P〉0．05）。全组无死亡病例，也无严重并发症发生。结论 急性胆囊炎行腹腔镜胆囊切除术安全可行，只要无内科禁忌证，应积极开展腹腔镜手术。     

自体腹白线片修补十二指肠溃疡穿孔(附13例报告)

目的探讨用游离自体腹白线片修补急性十二指肠溃疡穿孔的应用价值。方法从2006年1月至2006年7月对13例用自体腹白线片修补急性十二指肠溃疡穿孔的病人的临床资料和随访情况进行回顾性分析,其中2例穿孔大于2cm2,平均手术时间60分钟,平均失血量20ml,平均住院天数9±1天。结果游离自体腹白线片修补急性十二指肠溃疡穿孔13例均痊愈出院。随访15天至6个月,无手术并发症。结论本方法操作较简单、安全、效果好,其适应症广,是一种可行的新方法。     

Angiopoietin1/Tie2 and VEGF/Flk1 induced by MSC treatment amplifies angiogenesis and vascular stabilization after stroke.

Bone marrow stromal cells (MSCs) increase vascular endothelial growth factor (VEGF) expression and promote angiogenesis after stroke. Angiopoietin-1 (Ang1) and its receptor Tie2 mediate vascular integrity and angiogenesis as does VEGF and its receptors. In this study, we tested whether MSC treatment of stroke increases Ang1/Tie2 expression, and whether Ang1/Tie2 with VEGF/ vascular endothelial growth factor receptor 2 (VEGFR2) (Flk1), in combination, induced by MSCs enhances angiogenesis and vascular integrity. Male Wistar rats were subjected to middle cerebral artery occlusion (MCAo) and treated with or without MSCs. Marrow stromal cell treatment significantly decreased blood-brain barrier (BBB) leakage and increased Ang1, Tie2, and occludin (a tight junction protein) expression in the ischemic border compared with MCAo control. To further test the mechanisms of MSC-induced angiogenesis and vascular stabilization, cocultures of MSCs with mouse brain endothelial cells (MBECs) or astrocytes were performed. Supernatant derived from MSCs cocultured with MBECs significantly increased MBEC expression of Ang1/Tie2 and Flk1 compared with MBEC alone. Marrow stromal cells cocultured with astrocytes also significantly increased astrocyte VEGF and Ang1/Tie2 expression compared with astrocyte culture alone. Conditioned media from MSCs alone, and media from cocultures of MSCs with astrocytes or MBECs, all significantly increased capillary tube-like formation of MBEC compared with control Dulbecco's modified Eagle's medium media. Inhibition of Flk1 and/or Ang1 significantly decreased MSC-induced MBEC tube formation. Knockdown of Tie2 expression in MBECs significantly inhibited MSC-induced tube formation. Our data indicate MSC treatment of stroke promotes angiogenesis and vascular stabilization, which is at least partially mediated by VEGF/Flk1 and Ang1/Tie2.