Vascular progenitor cell senescence in patients with Marfan syndrome

Vascular progenitor cells (VPCs) present in the adventitia of the vessel wall play a critical role in the regulation of vascular repair following injury. This study aimed to assess the function of VPCs isolated from patients with Marfan syndrome (MFS). VPCs were isolated from control and MFS donors and characterized. Compared with control‐VPCs, MFS‐VPCs exhibited cellular senescence as demonstrated by increased cell size, higher SA‐β‐gal activity and elevated levels of p53 and p21. RNA sequencing showed that several cellular process‐related pathways including cell cycle and cellular senescence were significantly enriched in MFP‐VPCs. Notably, the expression level of TGF‐β1 was much higher in MFS‐VPCs than control‐VPCs. Treatment of control‐VPCs with TGF‐β1 significantly enhanced mitochondrial reactive oxidative species (ROS) and induced cellular senescence whereas inhibition of ROS reversed these effects. MFS‐VPCs displayed increased mitochondrial fusion and decreased mitochondrial fission. Treatment of control‐VPCs with TGF‐β1 increased mitochondrial fusion and reduced mitochondrial fission. Nonetheless, treatment of mitofusin2 (Mfn2)‐siRNA inhibited TGF‐β1‐induced mitochondrial fusion and cellular senescence. Furthermore, TGF‐β1‐induced mitochondrial fusion was mediated by the AMPK signalling pathway. Our study shows that TGF‐β1 induces VPC senescence in patients with MFS by mediating mitochondrial dynamics via the AMPK signalling pathway.     

Slot‐Die and Roll‐to‐Roll Processed Single Junction Organic Photovoltaic Cells with the Highest Efficiency

The record efficiency of the state‐of‐the‐art polymer solar cells (PSCs) is rapidly increasing, due to the discovery of high‐performance photoactive donor and acceptor materials. However, strong questions remain as to whether such high‐efficiency PSCs can be produced by scalable processes. This paper reports a high power conversion efficiency (PCE) of 13.5% achieved with single‐junction ternary PSCs based on PTB7‐Th, PC₇₁BM, and COi8DFIC fabricated by slot‐die coating, which shows the highest PCE ever reported in PSCs fabricated by a scalable process. To understand the origin of the high performance of the slot‐die coated device, slot‐die coated photoactive films and devices are systematically investigated. These results indicate that the good performance of the slot‐die PSCs can be due to a favorable molecule‐structure and film‐morphology change by introducing 1,8‐diiodooctane and heat treatment, which can lead to improved charge transport with reduced carrier recombination. The optimized condition is then used for the fabrication of large‐area modules and also for roll‐to‐roll fabrication. The slot‐die coated module with 30 cm² active‐area and roll‐to‐roll produced flexible PSC has shown 8.6% and 9.6%, respectively. These efficiencies are the highest in each category and demonstrate the strong potential of the slot‐die coated ternary system for commercial applications.     

FrzA基因转导干预缺血性心力衰竭小鼠心肌Wnt信号通路的研究

目的:研究重组9型腺相关病毒(recombinant adeno-associated virus serotype 9,rAAV9)携带FrzA基因转导干预缺血性心衰小鼠心肌Wnt信号通路的可行性,为基因治疗心力衰竭提供新的思路.方法:选择3月龄雄性C57BL/6J小鼠共130只,随机分为空白组(n=10),心衰组(n=40),心衰+空病毒(rAAV9-GFP)注射组(n=40),心衰+rAAV9-FrzA组(n=40),采用结扎左冠状动脉定量控制心梗面积,于术后2周行心脏超声评各组心功能变化,再经尾静脉注射已稀释好的病毒,28d后处死小鼠取心脏标本,RT-PCR检测心肌目的基因FrzA以及Dvl-1,β-catenin的表达;Western blot检测心肌Wnt信号通路关键分子Dvl-1,GSK3β,p-GSK3β,β-catenin的表达.结果:与空白组相比,成功建立心衰模型后小鼠心功能均不同程度降低(P＜0.05);FrzA组与心衰组相比,心功能明显改善(P＜0.05);经尾静脉注射可成功将rAAV9-FrzA导入小鼠体内,并且目的基因FrzA在心肌组织中高表达(P＜0.05);心衰小鼠心肌中Wnt信号通路关键分子Dvl-1,p-GSK3β,β-catenin的表达显著升高(P＜0.05),FrzA转导后小鼠心肌中Wnt信号通路中关键分子Dvl-1,p-GSK3β,β-catenin表达均降低(P＜0.05)结论:利用rAAV9-FrzA转导缺血性心衰小鼠可以有效的干预心肌Wnt信号通路,抑制其活性,为基因治疗缺血性心衰提供了新的思路.     

Effects of age and size on critical swimming speed of juvenile Chinese sturgeon Acipenser sinensis at seasonal temperatures

Changes in the critical swimming speed (U_crit, cm s^?1) with ontogeny of 2·5–12·5 month‐old juvenile anadromous Chinese sturgeon Acipenser sinesis were measured in a modified Blazka‐type swimming tunnel. The absolute U_crit increased with length, mass and age; the relative U^′_crit (body lengths, s^?1), however, decreased. Juvenile A. sinesis did not display a parr–smolt transformation at the length or age threshold to tolerate full‐strength seawater.     

四川地区幼儿和学龄前儿童的鼻部测量

本文报告１１１６例四川地区幼儿和学龄前儿童（２－７岁）鼻部９项指标的测量均数,性差及年龄发育特点。性差：仅鼻凹鼻底距４－６．５岁等少数指标部分年龄段男女性间出现显著性划异（男＞女）。此外各项指标的绝大多数年龄段男女性间无显著性差异。年龄发育：９项测量指标中７项的生长曲线随年产长而上升,数值随年龄增大,并有１－２个发育高峰;提示鼻部发育具有阶段性;２项指标的曲线随年龄增长变化较小。４项指标男女性的曲     

p47phox participates in activation of RelA in endothelial cells

Activation of endothelial cell NF-kappaB by interleukin (IL)-1 constitutes an event critical to the progression of the innate immune response. In this context, oxidants have been associated with NF-kappaB activation, although the molecular source and mechanism of targeting have remained obscure. We found that RelA, essential for NF-kappaB activation by IL-1, was associated with the NADPH oxidase adapter protein p47(phox) in yeast two-hybrid, coprecipitation, and in vitro binding studies. RelA and p47-GFP also colocalized in endothelial cells in focal submembranous dorsoventral protrusions. Overexpression of p47(phox) synergized with IL-1beta in the activation of an artificial kappaB-luciferase reporter and specifically augmented IL-1beta-induced RelA transactivation activity. p47(phox) overexpression also greatly increased IL-1beta-stimulated RelA phosphorylation, whereas it had no effect on I-kappaB degradation or on RelA nuclear translocation or kappaB binding. The tandem SH3 domains of p47(phox) were found to associate with a proline-rich mid-region of RelA (RelA-PR) located between the Rel homology and transactivation domains. The RelA-PR peptide blocked interaction of p47(phox) and RelA, and ectopic expression of RelA-PR abrogated IL-1beta-induced transactivation of the NF-kappaB-dependent E-selectin promoter. Further, suppression of NADPH oxidase function through the inhibitor diphenylene iodonium, the superoxide dismutase mimetic Mn(III) tetrakis(4-benzoic acid)porphyrin (MnTBAP), or expression of a dominant interfering mutant of a separate NADPH oxidase subunit (p67(V204A)) decreased IL-1beta-induced E-selectin promoter activation, suggesting that p47(phox) facilitates NF-kappaB activation through linkage with the NADPH oxidase. IL-1beta rapidly increased tyrosine phosphorylation of IL-1 type I receptor-associated proteins, suggesting that oxidants may operate through inactivation of local protein-tyrosine phosphatases in the proximal IL-1beta signaling pathway leading to RelA activation.