Evaluation of charge storage ability of chrome doped Mn2O3 nanostructures derived by cathodic electrodeposition

A facile synthetic route has been proposed to prepare cauliflower-like nanostructures of Cr doped Mn2O3. The synthesis was carried out by constant current cathodic electrodeposition from Mn2+ nitrate solutions containing minor amounts of dichromate. It was found that the presence of Cr mediates the formation of cathodic MnO2 which then reacts with the excess Mn2+ species to form Mn2O3 nanostructures. X-Ray Diffraction (XRD), Scanning Electron Microscopy (SEM) and Differential Thermal Analysis (DTA) were used to characterize the nanostructures. The storage ability of the obtained nanostructures was investigated by cyclic voltammetry (CV) in 0.5 M Na2SO4 solution. The results indicated that the Cr doped manganese oxide material shows better performance than the non-doped one, and the charge capacity (SC) of doped manganese oxide (218 F/g) was higher than pure manganese oxide (208 F/g).     

Pathogenic mutation in the ALS/FTD gene, <Emphasis Type="Italic">CCNF,</Emphasis> causes elevated Lys48-linked ubiquitylation and defective autophagy

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are fatal neurodegenerative disorders that have common molecular and pathogenic characteristics, such as aberrant accumulation and ubiquitylation of TDP-43; however, the mechanisms that drive this process remain poorly understood. We have recently identified CCNF mutations in familial and sporadic ALS and FTD patients. CCNF encodes cyclin F, a component of an E3 ubiquitin–protein ligase (SCF^{cyclin F}) complex that is responsible for ubiquitylating proteins for degradation by the ubiquitin–proteasome system. In this study, we examined the ALS/FTD-causing p.Ser621Gly (p.S621G) mutation in cyclin F and its effect upon downstream Lys48-specific ubiquitylation in transfected Neuro-2A and SH-SY5Y cells. Expression of mutant cyclin F^S621G caused increased Lys48-specific ubiquitylation of proteins in neuronal cells compared to cyclin F^WT. Proteomic analysis of immunoprecipitated Lys48-ubiquitylated proteins from mutant cyclin F^S621G-expressing cells identified proteins that clustered within the autophagy pathway, including sequestosome-1 (p62/SQSTM1), heat shock proteins, and chaperonin complex components. Examination of autophagy markers p62, LC3, and lysosome-associated membrane protein 2 (Lamp2) in cells expressing mutant cyclin F^S621G revealed defects in the autophagy pathway specifically resulting in impairment in autophagosomal–lysosome fusion. This finding highlights a potential mechanism by which cyclin F interacts with p62, the receptor responsible for transporting ubiquitylated substrates for autophagic degradation. These findings demonstrate that ALS/FTD-causing mutant cyclin F^S621G disrupts Lys48-specific ubiquitylation, leading to accumulation of substrates and defects in the autophagic machinery. This study also demonstrates that a single missense mutation in cyclin F causes hyper-ubiquitylation of proteins that can indirectly impair the autophagy degradation pathway, which is implicated in ALS pathogenesis.     

协同网络组织——新型商业模式的研究议程

最近涌现出的协同网络组织（CNO）或者称为简单协同网络的概念正在根本性地改变着商业、工业、文化和社会行为的组织形式，它代表着一个动态、多学科的研究和开发领域。本书从包含在协同网络组织中的各个学科里总结出了一些建议，目的在于为悄然兴起的协同网络建立起一系列的研究议程。本书罗列的建议和结论都得自于“THINK创新”计划，该计划涉及到了跨越学术、研究和工业领域250余位专家和预言家。     

特细砂替代率对自密实砂浆流变性的影响

为解决在中砂资源匮乏地区配制自密实砂浆时原材料短缺的问题,同时提高特细砂的资源利用率,使用特细砂替代中砂配制自密实砂浆,并研究了不同替代率(0～50％)对自密实砂浆流变性能的影响.结果 表明:特细砂替代率对自密实砂浆流变性能的影响存在临界点,这是由于特细砂高的吸水率会使砂浆基体中自由水的含量降低,进而导致自密实砂浆的流变性能变差.然而,特细砂的颗粒效应会改善自密实砂浆的级配,使更多的自由水在拌和时被释放,改善砂浆的流变性能.随着特细砂替代率增大,砂浆的黏度和屈服应力也随之增大;当特细砂替代率大于30％后,替代率增加会使浆体稠度急剧增加,因此从自密实砂浆流变学性能稳定性考虑,特细砂替代率应在30％内.