刀豆蛋白A条件化培养基对体外培养的兔角膜内皮细胞生长的影响

目的研究刀豆蛋白A(concanavalin A,ConA)条件化培养基对体外培养的兔角膜内皮细胞(rabbit corneal endothelial cells,RCECs)生长的影响。方法采用揭取后弹力层及内皮细胞联合组织块法进行RCECs的体外原代培养,分别用含有体积分数为5%、10%、15%、20%ConA的活化大鼠脾细胞条件上清液的RPMI1640培养基进行RCECs原代培养,并用含10%(体积分数)胎牛血清(fetal bovine serum,FBS)的RPMI1640培养基作为对照。神经烯醇化酶免疫组织化学染色法进行细胞鉴定;噻唑蓝比色法观察各组RCECs生长的状况;SPSS11.0One-way ANOVA及LSD检验进行统计分析。结果成功进行了RCECs的体外培养,培养细胞内神经烯醇化酶阳性表达。ConA条件化培养基各组细胞增殖均高于对照组(P<0.001),且10%、15%ConA条件化培养基组的RCECs细胞数量明显高于其他各实验组(P<0.001)。结论ConA条件化培养基具有促进RCECs生长的作用,可作为培养辅佐剂。     

QoS awared power and admission controls based on non-cooperative game theory in wireless networks

In order to better accommodate heterogeneous quality of service (QoS) in wireless networks, an algorithm called QeS-aware power and admission controls (QAPAC) is proposed. The system is modeled as u non- cooperative game where the users adjust their transmit powers to maximize the utility, thus restraining the interferences. By using adaptive utility functions and tunable pricing parameters according to QoS levels, this algorithm can well meet different QoS reqniremcnts and improve system capacity compared with those that ignore the QoS differ- ences.     

Role of candesartan against cerebral ischemia and oxidative damage in normotensive rats

Objective Angiotensin Ⅱ (Ang Ⅱ ) contributes to modulating blood pressure by stimulation of Ang Ⅱ AT1 receptors. We devised a rat transient middle cerebral artery occlusion (MCAO) model to assess whether oxidative damage is decreased after pretreatment with Angiotensin Ⅱ AT1 receptor blocker (ARB). Methods After 2 weeks pretreatment with ARB 0. 5 and 1 mg/kg, the male Wister rats were subjected to 2 h middle cerebral artery occlusion (MCAO). At 24 h, the lumen diameter of middle cerebral artery, the plasma level of 8-hydroxy-2'-deoxyguanosine (8-OHdG), and HIF-1 a levels were recorded and compared. Results After pretrcatment with ARB 0.5 and 1 mg/kg, blood pressure did not significantly change compared with that of controls. In the group of candesartan at 1 mg/(kg· day), the lumen diameter was significantly increased compared to that in control group [(86.0±5.0) μm vs. (69.0± 2.1) μm; P<0. 01, n = 6- 8]. The plasma 8-OHdG levels of ARB pretreatment groups were decreased. In immunohistochemical findings, 8-OHdG- and HIF-1α-containing cells in ARB pretreatment groups were decreased. Conclusion Brain ischemia and oxidative damage can be reversed by AT1 receptor blockade in normotensive rats after transient cerebral artery occlusion.     

The role of interleukin-8 produced by tumor induced fibroblasts in the development of cutaneous melanoma

Objective To determine the role of interleukin-8 (IL-8) produced by tumor induced fibroblasts in the development of cutaneous melanoma. Methods B16 melanoma cells induced L929 fibroblasts phenotype was transdifferentiated to myofibroblasts (MF) by co-culture in vitro. MF was monitored by morphology and immunophenotype for a-SMA. The level of IL-8 was detected by ELISA. The effect on B16 cell proliferation rate was estimated using MIT method in vitro. Melanoma implanting model was constructed in C57 mice. Results L929 MF phenotype could be modulated by B16 melanoma cells-derived transforming growth factor-β1 (TGF-β1) and elevated the levels of IL-8. L929 MF did not influence the B16 melanoma cells viability in vitro, but shortened the time of tumor formation and increased the incidence rates of tumors in C57 implanting model mice. Conclusion Fibroblasts can be activated by tumor cells and produce IL-8, which acts as an inflammatory cytokine promoting the development of cutaneous melanoma.     

The changes of neuronal activity of the zone incerta in a rodent model of Parkinson＇s disease

Objective To study the changes in neuronal activity of the zone incerta (ZI) following the unilateral lesion of the nigrostriatal pathway. Methods Eiectrophysiological recordings of ZI neurons were made in normal rats and in two groups of rats at different time intervals after injection of 6-hydrodopamine (6-OHDA) into the pars compacta of snbstantia nigra by extracellular recording in vivo. Results The results showed a significant increase in the mean firing rate of ZI during the second and fourth weeks after 6-OHDA lesion [-n=32, (3.6±2. 2)Hz, P<0.001; n=35, (9.3±6.6)Hz, P<0. 001, respectively] compared to that of normal rats [n=39, (9.2±5.2)Hz]. However, no significant change was observed between two groups of 6-OHDA-lesioned rats. With regard to firing pattern, 7.7%(3/39) of ZI neurons discharged regularly, 82.1% (32/39) irregularly and 10. 3% (4/39) in bursts in normal rats. During the second week after 6-OHDA lesion, the regular, irregular and bursting firing neurons recorded in the ZI were 9.4% (3/32), 59. 4% (19/32) and 31.3% (10/32), and during fourth week, the regular, irregular and bursting firing neurons were 14.3% (5/35), 57.1% (20/35) and 28. 6% (10/35), respectively. The firing pattern of the neurons in the three different groups did not change significantly. Conclusion These results suggest that the firing rate of ZI neurons in 6-OHDA-lesioned rats is increased significantly, which may contribute to the pathophysiology of Parkinson's disease.     

Effect of ABCA1-V771M polymorphism on plasma lipid levels and its relationship with coronary atherosclerotic heart disease

Objective To explore the risk association of ABCA1-V771M polymorphism with coronary heart disease (CHD) in Hart nationality in Northwest of China. Methods With case-control study, ABCA1-V771M polymorphism was detected in 204 unrelated Hart nationality people in Northwest of China, and all the subjects by coronary angiography were grouped into 106 cases and 98 controls. The genotypes and alleles frequency distribution of ABCA1-V771M polymorphisms were analyzed by PCR-RFLP analysis, and the clinical statistics of serum lipids were compared and its effects of ABCA1-V771M polymorphism on the plasma lipid levels and coronary atherosclerotic heart disease were analyzed. Results The genotypic frequencies of ABCA1-V771M polymorphism matched well under Hardy-Weinberg equilibrium (P>0.05), V and M allelic frequencies were 33.3% and 66.7%. In comparison with VV VM genotype carriers, MM genotypes carriers had much lower plasma levels of HDL-C (P<0. 001) and much higher plasma levels of TG (P<0. 05). M allelic frequency in CHD group was significantly higher than V allelic frequency (P<0. 05). M allele was related with more severity of atherosclerosis in the coronary artery than V allele (P<0.05). However, there was no obvious difference in the incidence of AMI among carriers with three genotypes of ABCA1-V771M polymorphism (P>0.05). Conclusion ABCA1-V771M polymorphism was not only associated with the plasma levels of HDL-C and TG, but also related to the susceptibility and severity of coronary atheroselerotic heart disease. Moreover, M771 allele appeared to be atherogenie among Han population in Northwest of China.     

正常绒毛和葡萄胎中Mel-CAM标记中间型滋养细胞的增殖情况

目的探讨葡萄胎中Mel-CAM与滋养细胞黏附、浸润之间的关系以及Mel-CAM标记中间型滋养细胞(IT)的增殖情况。方法采用双重免疫组化法,检测Mel-CAM标记IT的Ki-67表达情况。结果葡萄胎中Mel-CAM表达较正常绒毛明显增高,差异有统计学意义(P<0.05);葡萄胎绒毛表面有Mel-CAM标记IT出现,而正常绒毛表面则无;葡萄胎组织中IT的Ki-67指数较正常绒毛明显增高,差异有统计学意义(P<0.05)。结论葡萄胎绒毛表面有Mel-CAM表达,表现出双重分化方向,这可能与葡萄胎的发病机制有关;检测葡萄胎组织中IT的Ki-67指数对于预测葡萄胎的转归有潜在的价值。     

As2O3诱导人卵巢癌细胞株HO8910凋亡和端粒酶活性的关系

目的探讨As2O3诱导HO8910细胞凋亡和端粒酶活性变化的关系。方法用不同浓度的As2O3溶液作用卵巢癌细胞株HO8910,于不同时间点收集细胞,MTT法检测细胞生长抑制率;FCM检测细胞凋亡率;TRAP-银染法观察端粒酶活性的变化。结果As2O3溶液对HO8910有生长抑制和诱导凋亡的作用,与药物浓度和作用时间相关。不同浓度As2O3作用HO8910细胞,其端粒酶活性在24h无明显改变,随着作用时间的延长,端粒酶活性逐渐下降,随着药物浓度的升高端粒酶活性也呈不断下降趋势,以致消失。结论As2O3可以诱导卵巢癌细胞株HO8910发生凋亡,其机制可能不是通过端粒酶活性下降直接调控的,但端粒酶调控与凋亡调控有一定相关性。     

2型糖尿病患者一级亲属正常糖代谢人群胰岛素抵抗分析

目的探讨2型糖尿病(T2DM)患者糖耐量正常的一级亲属胰岛β细胞功能及胰岛素抵抗情况,并分析胰岛素抵抗的相关因素。方法选取T2DM患者糖耐量正常的一级亲属63例,根据胰岛素抵抗指数分为胰岛素抵抗组及非抵抗组;选取30例健康体检者作为正常对照组。对所选的93例对象进行血压、血糖、胰岛素、血脂的测定,并计算稳态模型胰岛素抵抗指数(HOMA-IR)及胰岛β细胞功能指数(HOMA-β)。结果①糖尿病患者一级亲属组与对照组相比,胰岛素水平、HOMA-IR、HOMA-β明显升高(P<0.05);②胰岛素抵抗组体质指数、舒张压、甘油三酯、餐后血糖、HOMA-β明显高于胰岛素非抵抗组(P<0.05);③相关分析示胰岛素抵抗与体质指数、舒张压、甘油三酯、餐后胰岛素呈正相关(P<0.01,P<0.05),与空腹血糖、餐后血糖、空腹胰岛素、收缩压、胆固醇无显著相关性(P>0.05)。结论T2DM患者一级亲属存在胰岛β细胞代偿性的高分泌,早期已经出现胰岛素敏感性的下降和胰岛素抵抗。胰岛素抵抗与体重增加、舒张压升高及甘油三酯的升高有关。提示对糖尿病患者一级亲属应严格控制体重、血压及血脂,对减少T2DM具有积极意义。     

脑弥漫性轴索损伤实验装置的研制及动物模型的建立

目的 自制一种脑弥漫性轴索损伤(DAI)装置并成功建立DAI动物模型.方法 自制头颅瞬间旋转损伤装置,使大鼠头颅在瞬间(<3ms)旋转90°造成剪切损伤.观察损伤后大鼠的生命体征及行为学改变;于伤后2、6、12、24、36、72h及10d分别处死损伤组动物,制备脑石蜡切片,行镀银及HE染色,光镜下观察神经轴索变化.结果 伤后大鼠均即刻出现原发昏迷,其中2只于损伤后20min内死亡,余持续时间1-30min不等;伤后大鼠呼吸节律紊乱,瞳孔对光反射减弱或消失,醒后均有程度不等的反应性下降,肢体活动迟缓;肉眼可见广泛蛛网膜下腔出血或脑室出血;光镜下可见皮髓交界区、胼胝体区、脑干、小脑白质等部位的神经轴索有不同程度的肿胀、断裂、轴索球形成,后期有小胶质细胞增生,局部呈巢样聚集.结论 本装置能造成大鼠脑DAI,且具有简便、可控、确切的特点,适合进行中、小型动物DAI模型的实验研究.