Tks5 recruits AFAP-110, p190RhoGAP, and cortactin for podosome formation

Podosome formation in vascular smooth muscle cells is characterized by the recruitment of AFAP-110, p190RhoGAP, and cortactin, which have specific roles in Src activation, local down-regulation of RhoA activity, and actin polymerization, respectively. However, the molecular mechanism that underlies their specific recruitment to podosomes remains unknown. The scaffold protein Tks5 is localized to podosomes in Src-transformed fibroblasts and in smooth muscle cells, and may serve as a specific recruiting adapter for various components during podosome formation. We show here that induced mislocalization of Tks5 to the surface of mitochondria leads to a major subcellular redistribution of AFAP-110, p190RhoGAP, and cortactin, and to inhibition of podosome formation. Analysis of a series of similarly mistargeted deletion mutants of Tks5 indicates that the fifth SH3 domain is essential for this recruitment. A Tks5 mutant lacking the PX domain also inhibits podosome formation and induces the redistribution of AFAP-110, p190RhoGAP, and cortactin to the perinuclear area. By expressing a catalytically inactive point mutant and by siRNA-mediated expression knock-down we also provide evidence that p190RhoGAP is required for podosome formation. Together our findings demonstrate that Tks5 plays a central role in the recruitment of AFAP-110, p190RhoGAP, and cortactin to drive podosome formation.     

血管内皮生长因子特异性鼠源单链抗体的人源化

以抗体阻断血管生成信号来治疗实体肿瘤显示了很好的前景,但鼠源抗体首先必须经人源化改造以降低其免疫原性才能应用于人体。本研究以同源模建预测了一体人血管内皮生长因子（VEGF）特异性鼠源单链抗体E11的三维结构,以结构数据为基础并采取单个最相似框架区替代法对其进行人源化设计;合成并组装了人源化单链抗体基因并在大肠杆菌中表达,包含体形式的产物以凝胶柱色谱法复性,经ELISA检测表明,人源化后的单链抗体保持了与天然VEGF结合的活性,表明采取的人源化路线具有可行性。     

Active interfacial dynamic transport of fluid in a network of fibrous connective tissues throughout the whole body

Fluid in interstitial spaces accounts for ~20% of an adult body weight and flows diffusively for a short range. Does it circulate around the body like vascular circulations? This bold conjecture has been debated for decades. As a conventional physiological concept, interstitial space is a micron‐sized space between cells and vasculature. Fluid in interstitial spaces is thought to be entrapped within interstitial matrix. However, our serial data have further defined a second space in interstitium that is a nanosized interfacial transport zone on a solid surface. Within this fine space, fluid along a solid fibre can be transported under a driving power and identically, interstitial fluid transport can be visualized by tracking the oriented fibres. Since 2006, our data from volunteers and cadavers have revealed a long‐distance extravascular pathway for interstitial fluid flow, comprising at least four types of anatomic distributions. The framework of each extravascular pathway contains the longitudinally assembled and oriented fibres, working as a fibrorail for fluid flow. Interestingly, our data showed that the movement of fluid in a fibrous pathway is in response to a dynamic driving source and named as dynamotaxis. By analysis of previous studies and our experimental results, a hypothesis of interstitial fluid circulatory system is proposed.     

The life cycle of Hymenoscyphus fraxineus on Manchurian ash,Fraxinus mandshurica,in Japan

Hymenoscyphus fraxineus causes a lethal disease known as “ash dieback” in the common ash, Fraxinus excelsior, in Europe. It is hypothesized that the fungus originated from East Asia. This fungus is found on the leaf litter of the Manchurian ash, Fraxinus mandshurica, in Japan and is reported to produce apothecia on pseudosclerotial plates formed mainly on decomposing rachises. However, dieback disease has not been reported in Japan, and little is known about the life cycle of H. fraxineus. This study was conducted to explore the behavior and life cycle of this fungus. It was revealed that, after infection by ascospores, H. fraxineus endophytically inhabits the living leaves of F. mandshurica. On fallen leaves, the fungus behaves saprophytically, producing apothecia on pseudosclerotial plates formed mainly on the decomposing rachises. Analysis by real-time quantitative polymerase chain reaction (qPCR) revealed that the amount of H. fraxineus DNA sharply increased in rachises, while such sharp increase of DNA was not found in leaflets.     

重庆维管植物1个新记录属和5个新记录种

通过野外调查、资料查阅及馆藏标本比对,确定了重庆维管植物1个新记录属——水东哥属（Saurauia Willd.）及其新记录种——水东哥（Saurauia tristyla DC.）,另4个维管植物新记录种分别是二褶羊耳蒜（Liparis cathcartii Hook. f.）、莸状黄芩（Scutellaria caryopteroides Hand.-Mazz.）、白鳞酢浆草（Oxalis leucolepis Diels）、包氏凤仙花（Impatiens bodinieri Hook. f.）。文中描述了物种识别特征、标本引证和地理分布,提供了原生境照片。引证标本均收藏于西南大学自然博物馆植物标本室（SWNTU）。     

USP10 exacerbates neointima formation by stabilizing Skp2 protein in vascular smooth muscle cells

The underlying mechanism of neointima formation remains unclear. Ubiquitin-specific peptidase 10 (USP10) is a deubiquitinase that plays a major role in cancer development and progression. However, the function of USP10 in arterial restenosis is unknown. Herein, USP10 expression was detected in mouse arteries and increased after carotid ligation. The inhibition of USP10 exhibited thinner neointima in the model of mouse carotid ligation. In vitro data showed that USP10 deficiency reduced proliferation and migration of rat thoracic aorta smooth muscle cells (A7r5) and human aortic smooth muscle cells (HASMCs). Mechanically, USP10 can bind to Skp2 and stabilize its protein level by removing polyubiquitin on Skp2 in the cytoplasm. The overexpression of Skp2 abrogated cell cycle arrest induced by USP10 inhibition. Overall, the current study demonstrated that USP10 is involved in vascular remodeling by directly promoting VSMC proliferation and migration via stabilization of Skp2 protein expression.     

补镁对大鼠血管钙化的影响

目的:在大鼠血管钙化模型上,观察外源性补充硫酸镁对大鼠血管钙化的影响,以探讨硫酸镁在血管钙化中作用及机制。方法:用维生素D3加尼古丁诱导大鼠血管钙化,von Kossa染色、钙含量测定及碱性磷酸酶活性测定判断血管钙化程度;用半定量RT-PCR方法测定血管钙化标志分子骨桥蛋白mRNA水平;用生物化学方法测定血管一氧化氮(NO)、超氧化物歧化酶(SOD)和丙二醛(MDA)含量。结果:钙化组大鼠血压升高,收缩压较对照组高27%(P<0.05);血管von Kossa染色见血管中膜弹性纤维间可见大量棕黑色颗粒沉积,主动脉钙含量及碱性磷酸酶活性分别较对照高3.9倍和3.4倍(P<0.01),钙化血管组织骨桥蛋白mRNA表达上调40%(P<0.01),血管钙化后可加重血管组织过氧化损伤;而诱导钙化后外源性补充硫酸镁可减轻血管钙化程度,与钙化组比较,低、高剂量硫酸镁组均明显缓解上述指标的变化。结论:诱导血管钙化后外源性补充硫酸镁可以减轻大鼠血管钙化和血管损伤程度。     

Xylem pathways in liana stems with variant secondary growth

FISHER, J. B. & EWERS, F. W., 1992. Xylem pathways in liana stems with variant secondary growth. The three-dimensional construction of stem xylem in tropical lianas (woody vines) was studied using several approaches: 1. observations of the xylem surface in stems with bark removed after NaOH treatment or natural retting; 2. reconstructions from serial transverse sections; 3. movement of dye solutions up isolated xylem sectors in intact plants, and 4. flow of dye solutions down branches and xylem sectors in isolated stem segments. Long distance (up to several metres) xylem pathways in unbranched stems and connections between lateral branches and main stems are described for !5 species in eight families which represented seven differnt patterns of secondary growth. The xylem in even the most complex stems is integrated by three-dimensional interconnections of xylem regions which may appear isolated in transverse section. Interconnections are most common at leaf and branch nodes. Some old stems have peripheral xylem that remains isolated over long distances in unbranched stems, but even these had structural and physiological interconnections between xylem regions at branch nodes.     

水稻穗颈维管束及穗部性状的QTL分析

以籼稻 (OryzasativaL .ssp .indicaZYQ8)和粳稻 (O .sativassp .japonicaJX17)的杂交F1代花培加倍的DH群体为材料考察了该群体的穗颈节大小维管束数、一次枝梗数、每穗颖花数、穗颈节顶部直径和穗长 ,并用该群体构建的分子图谱进行数量性状座位 (QTL)分析。检测到控制大维管束的 3个QTL (qLVB_1、qLVB_6和qLVB_7)分别位于第 1、第 6和第 7染色体 ;控制小维管束的 2个QTL (qSVB_4和qSVB_6 )分别位于第 4和第 6染色体 ;控制一次枝梗的 4个QTL (qPRB_4a、qPRB_4b、qPRB_6和qPRB_7)分别位于第 4(2个 )、第 6和第 7染色体 ;每穗颖花数的 3个QTL (qSPN_4a、qSPN_4b和qSPN_6 )分别位于第 4(2个 )和第 6染色体上 ;穗颈节顶部直径的 5个QTL (qPTD_2、qPTD_5、qPTD_6、qPTD_8和qPTD_12 )分别位于第 2、第 5、第 6、第 8和第 12染色体 ;穗长的 3个QTL (qPL_4、qPL_6和qPL_8)分别位于第 4、第 6、第 8染色体上。其中qLVB_6、qSVB_6、qSPN_6、qPTD_6和qPL_6均位于第 6染色体的G12 2_G1314b之间 ;qPL_8和qPTD_8位于第 8染色体的GA40 8_BP12 7a之间 ;qPRB_4a和qSPN_4a位于第 4染色体的G177_CT2 0 6之间 ;qPL_4和qSPN_4b位于第 4染色体CT40 4_CT5 0 0之间 ;qSVB_4所在的区间与qPL_4、qSPN_4b和qPRB_4b所在的区间相邻。