Autophagy during Mycobacterium tuberculosis infection and implications for future tuberculosis medications

Autophagy is a cellular homeostasis mechanism to eliminate unwanted or excessive organelles, or for the turnover of long-life cytosolic macromolecules. During Mycobacterium tuberculosis infection, autophagy represents not only an antimicrobial mechanism for the clearance of the intracellular pathogen, but also prevents excessive inflammation, avoiding the adverse effects on host. Here we focus on the anti-tuberculosis autophagy and signal pathways involved, and attempt to depict an integrative map of the interaction between autophagy and cytokine, ROS production, vitamin D, and inflammatory response. Novel autophagy-based therapy is also summarized. This integrative insight might add some novel thoughts for better tuberculosis medications.     

水稻二化螟内共生菌杀雄菌属和沃尔巴克氏体的检测与分析

应用杀雄菌属(Arsenophonus)23S rDNA基因和沃尔巴克氏体(Wolbachia) wsp基因的特异引物,通过PCR扩增的方法对我国20个水稻二化螟地理种群感染两类内共生菌的情况进行了检测.结果表明: 我国水稻二化螟不同地理种群的Arsenophonus和Wolbachia感染率不一致,哈尔滨、惠水、吉林、南阳和扬州5个地理种群的Arsenophonus感染率为5.0%～50.0%;汉中、南宁和扬州3个地理种群的Wolbachia感染率为25.0%～40.0%,其他地理种群中没有检测到这两种共生菌的存在.水稻二化螟不同地理种群感染的Arsenophonus 23S rDNA基因序列完全一致,将该基因株型命名为csArs.但所检测到的Wolbachia wsp基因序列不一致,分别为wChisup1、wChisup5和wChisup6,其中wChisup1属于A群,其他属于B群.这说明水稻二化螟感染的Arsenophonus为同一株型,而感染的Wolbachia株型较为复杂.通过构建系统发育树发现,水稻二化螟体内的Arsenophonus23S rDNA基因和Wolbachia wsp基因与其他物种体内相关序列完全一致或高度相似.     

云南美味牛肝菌ITS 区域结构特点

利用ITS 的通用引物(ITS5-ITS4) 对云南的美味牛肝菌( Boletus edulis) 子实体的DNA 进行PCR 扩增, 扩增产物回收后直接测序。序列的聚类分析表明, 在ITS1-5 . 8S rDNA-ITS2 区域, 云南的美味牛肝菌与欧洲的夏牛肝菌( B. aestivalis) 和铜色牛肝菌( B . aereus) 同源性较高, 但在ITS2 区域夏牛肝菌和铜色牛肝菌分别有一段美味牛肝菌没有的大小分别为73 bp 和26 bp 的特征序列。     

Weitere Hinweise zur Prüfung der Additivität bei Streuungszerlegungen (Varianzanalysen)

Zusammenfassung Für die Ermittlung nicht-additiver Effekte bei einfachen und doppelten Streuungszerlegungen reicht das vonTukey (1949) angegebene Verfahren nicht aus, da es, wieMandel (1961) nachgewiesen hat, nur einen Teil der nichtadditiven Effekte berücksichtigt. Es wird eine Möglichkeit aufgezeigt, wie die nicht-additiven Effekte nachMandel auf möglichst einfache Weise, und zwar unter weitgehender Anwendung der bei der Streuungszerlegung ohnehin anfallenden Rechengrößen ermittelt werden können. Ferner wird angegeben, in welchen Fällen die Prüfung auf nicht-additive Effekte sinnvoll ist.     

Nitrotyrosine proteome survey in asthma identifies oxidative mechanism of catalase inactivation

Reactive oxygen species and reactive nitrogen species produced by epithelial and inflammatory cells are key mediators of the chronic airway inflammation of asthma. Detection of 3-nitrotyrosine in the asthmatic lung confirms the presence of increased reactive oxygen and nitrogen species, but the lack of identification of modified proteins has hindered an understanding of the potential mechanistic contributions of nitration/oxidation to airway inflammation. In this study, we applied a proteomic approach, using nitrotyrosine as a marker, to evaluate the oxidation of proteins in the allergen-induced murine model of asthma. Over 30 different proteins were targets of nitration following allergen challenge, including the antioxidant enzyme catalase. Oxidative modification and loss of catalase enzyme function were seen in this model. Subsequent investigation of human bronchoalveolar lavage fluid revealed that catalase activity was reduced in asthma by up to 50% relative to healthy controls. Analysis of catalase isolated from asthmatic airway epithelial cells revealed increased amounts of several protein oxidation markers, including chloro- and nitrotyrosine, linking oxidative modification to the reduced activity in vivo. Parallel in vitro studies using reactive chlorinating species revealed that catalase inactivation is accompanied by the oxidation of a specific cysteine (Cys(377)). Taken together, these studies provide evidence of multiple ongoing and profound oxidative reactions in asthmatic airways, with one early downstream consequence being catalase inactivation. Loss of catalase activity likely amplifies oxidative stress, contributing to the chronic inflammatory state of the asthmatic airway.     

慢性缺氧模型与病证相关性的研究进展

长期或反复处于缺氧状态,可以影响机体组织器官的正常供氧,使心血管、呼吸和神经等系统功能紊乱,从而诱导机体多系统损伤,严重危害人体健康.随着现代人生活方式以及饮食结构的改变,生活中有氧运动不足再加上地球污染与破坏逐年加剧,人类不知不觉地处在一个慢性缺氧的环境中.因此,了解并重视慢性缺氧对生理功能的影响造成的危害,从而采取相应的防治措施具有重要的意义.国内外学者根据宏观指征与生理生化指标等微观指征变化的不同,采用不同缺氧周期与缺氧强度制备模拟不同疾病与证候的慢性缺氧模型,对慢性缺氧诱导的生理病理演变过程进行了大量的探索研究.本文综述了近5年来慢性缺氧模型与阻塞性睡眠呼吸暂停综合征、肺动脉高压、心血管疾病、神经退行性病变等疾病以及气阴两虚、气滞血瘀等证候相关性的研究进展,为遴选体现与缺氧相关病证临床特点的动物模型,并用以合理评价药物的作用特点提供参考.