Bromocriptine/SKF38393 ameliorates islet dysfunction in the diabetic (db/db) mouse

Dysfunction of pancreatic islets plays a crucial role in the etiology of type II diabetes. Chronic hyperglycaemia or hyperlipidaemia may impair islet function. Previous studies by our laboratory have demonstrated that dopaminergic agonists ameliorated hyperglycaemia and hyperlipidaemia in obese and diabetic rodents. In the present study, we investigated the effect of a treatment with the dopamine D₂ /D₁ receptor agonists (bromocriptine/SKF38393, BC/SKF) on islet dysfunction in db/db mice. Our results show that a 2-week BC/SKF treatment markedly reduced hyperglycaemia and hyperlipidaemia, and significantly improved islet dysfunction demonstrated by an increase of secretagogue-stimulated insulin release from islets of db/db mice to levels observed in islets from lean mice. There was also a fourfold increase of insulin content in the pancreas of BC/SKF-treated db/db mice compared with that in untreated controls. The effect of BC/SKF on islet function cannot be mimicked in pair-fed animals. BC/SKF had no direct stimulatory effect on islet insulin secretion, suggesting BC/SKF treatment improved islet function via an indirect mechanism. This treatment markedly improved the abnormally elevated daily levels of corticosterone, blood glucose and plasma lipids, supporting the view that BC/SKF may affect the neuroendocrine system that in turn regulates peripheral metabolism and thereby improves islet function. Received 3 April 1998; accepted 27 April 1998     

解聚复肾宁对大鼠肾小球系膜细胞增殖和细胞周期的影响

目的 观察中药复方解聚复肾宁（JJFSN）对高耱环境下大鼠肾小球系膜细胞（mesangial cell,MC）增殖和细胞周期的影响.方法 以高糖诱导MC增殖,采用血清药理学方法制备不同浓度JJFSN舍药血清,加入培养液中,用MTT法检测细胞增殖,流式细胞技术检测细胞周期.结果 MTT显示：JJFSN含药血清可抑制高糖诱导的MC过度增殖（P＜0.05）,并且这种作用具有药物剂量和时间依赖关系.流式细胞技术分析表明：JJFSN可逆转高糖对细胞周期的影响,使G0/G1期细胞比例增加,S期细胞比例下降（P＜0.05） 在高浓度时还能促进MC细胞凋亡.结论 JJFSN可以通过调节细胞周期,促进细胞凋亡,从而抑制高糖诱导的MC过度增殖,这可能是JJFSN防治DN早期的作用杌理.     

Excited-state dynamics in light-harvesting complex of Rhodobacter sphaeroides

Photodynamics of peripheral antenna complexes,light-harvesting complex (LH2) of Rhodobacter (Rb) Sphaeroides 601,was studied using femtosecond pump-probe technique at different laser wavelengths. The obtained results reveal dramatic dynamical evolutions within B800 and B850 absorption bands of antenna complexes LH2. At excitation wavelength around 835 nm,a sharp photobleaching signal was observed which was assigned to the contribution of the two-exciton state,which was further confirmed by the power dependence measurement. Rate equations with eight-level scheme were used to calculate the population evolution in LH2 and the transient dynamics under femtosecond pulse excitation. The research results prove that not only the transition from ground state to one-exciton state but also that from one-exciton state to two-exciton state contribute to the photodynamics of B850.     

车用转子发动机复合进气充气特性研究

提出了车用转子发动机复合进气充气效率模拟计算和试验结果，并分析了充气效率随负荷和转速变化的特性，以及周边气口与端面气口进气气流随转速变化的分配关系，为进一步研究这种进气形式的转子发动机的换气过程、气口与进排气管设计提供了有益的结果。     

弥可保加长龙通治疗糖尿病周围神经病变的临床观察

用弥可保加长龙通治疗40例糖尿病合并周围神经病变的病人,设30例常规采用B族维生素和血管内抗凝药物治疗的病人作对照组.发现弥可保加长龙通可以不同程度地减轻病人的肢体麻木、疼痛、发凉等临床症状,植物神经功能障碍也有所改善,皮肤溃疡愈合的效果较为显著.在治疗过程中,没有明显副作用及不良反应,是安全有效的.     

AngⅡ受体拮抗剂联合复方活血散治疗糖尿病肾病的疗效分析

目的观察血管紧张素（Ang）受体拮抗剂联合复方活血散（三七、红花、水蛭、川芎、生地、赤芍、甘草）治疗糖尿病肾病的疗效和对肾功能的保护作用。方法47例糖尿病肾病患者进入该项研究,其血糖均控制在理想水平,血压基本恒定。随机分为治疗组24例,对照组23例,两组降压、降糖等治疗相仿,治疗组加用Ang受体拮抗剂替米沙坦80 mg,每天1次。结果治疗8周后,治疗组尿蛋白为（1.97±0.60）g/d,与治疗前的（3.12±1.20）g/d相比明显下降（P〈0.01）与对照组的（3.11±1.35）g/d比较,差异有显著性（P〈0.01）;对照组血肌酐为（225.5±26.6）μmol.L^-1,与治疗前的（177.3±22.8）μmol.L^-1相比明显上升（P〈0.01）,与治疗组的（115.6±34.2）μmol.L^-1比较,差异有显著性（P〈0.01）。结论Ang受体拮抗剂联合复方活血散治疗糖尿病肾病具有降低尿蛋白、保护肾功能的作用。     

计算机及其外部设备的防信息泄漏技术

计算机中的电磁泄漏严重威胁系统的安全,必须采取有效的防泄漏措施.介绍了计算机中信息的泄漏方式,分析了TEMPEST技术研究的内容,探讨了利用噪声干扰源,采用屏蔽技术、"红"/"黑"隔离技术、滤波技术和布线与元器件选择等计算机防泄漏技术,以及键盘、软盘驱动器、CRT显示器和打印机等外部设备的防泄漏技术,探讨了发展我国TEMPEST技术的5项措施.     

松花粉对糖尿病肾病小鼠肾脏损伤的保护作用

 探讨松花粉对链脲霉素（streptozotocin,STZ）诱导糖尿病肾病小鼠肾脏损伤的保护作用及可能机制。成年雄性C57BL/6J（Wild Type）小鼠50 只,采用STZ 诱导糖尿病肾病小鼠动物模型。实验小鼠随机分为正常对照组（10 只）、STZ 模型组（40只）;STZ 模型组按150 mg/kg 腹腔注射STZ 一次,复制小鼠糖尿病肾病模型,对照组小鼠则腹腔注射柠檬酸钠缓冲液。在造模1周后,小鼠空腹血糖值大于11.1 mmol/L 视为糖尿病诱导成功,此后定期每周监测血糖和24 h 尿蛋白,持续出现蛋白尿的小鼠视为成模小鼠。成模糖尿病肾病小鼠28 只,将其随机分为STZ 模型组和松花粉治疗组各14 只;松花粉治疗组每天给予750 mg/kg体重的松花粉灌胃,正常对照组与STZ 模型组以等体积的0.9%氯化钠注射液灌胃。连续7 周后,检测小鼠血糖、24 h 尿微量白蛋白、尿肌酐、血肌酐、血浆尿素氮水平;计算肾重/体重比、肾脏组织丙二醛（MDA）含量等指标,并对肾脏组织切片行Masson 和Jones 六胺银染色;Western Blot 的方法观察p38 和ERK 信号分子的磷酸化激活情况。与模型组相比,松花粉治疗组肾重/体重比、肾小球细胞外基质增生程度和肾功能损害程度均明显减轻;松花粉能够降低糖尿病肾脏的MDA 含量并抑制p38 和ERK 信号分子的激活。由此可以看出,松花粉能通过抑制p38 和ERK 信号分子的磷酸化激活,减轻肾脏的氧化损伤和肾小球细胞外基质增生。