Sodium‐Ion Batteries: From Academic Research to Practical Commercialization

Sodium‐ion batteries (SIBs) have been considered as the most promising candidate for large‐scale energy storage system owing to the economic efficiency resulting from abundant sodium resources, superior safety, and similar chemical properties to the commercial lithium‐ion battery. Despite the long period of academic research, how to realize sodium‐ion battery commercialization for market applications is still a great challenge. Thus, from the perspective of future practical application, this review will identify the factors that are restricting commercialization, and evaluate the existing active materials and sodium‐ion‐based full‐cell system. The design and development trends that are needed for SIBs to meet the requirements of practical applications in large‐scale energy storage will also be discussed in detail.     

A Comprehensive Review on Controlling Surface Composition of Pt‐Based Bimetallic Electrocatalysts

With increasing energy demands worldwide, significant efforts have been made to develop superior electrocatalysts for efficient energy conversion systems. Among all the electrocatalysts exploited, Pt‐based bimetallic nanomaterials stand out by virtue of their high catalytic activity and relatively low cost due to the introduction of a nonprecious metal component. It should be noted that electrocatalytic reactions only take place on the surface of catalysts, so investigations of the surface composition of Pt‐based bimetallic nanomaterials are necessary for practical electrocatalysts. In this review, recent studies on controlling the surface composition of Pt‐based bimetallic catalysts for the oxygen reduction reaction, formic acid electrooxidation, and ethanol electrooxidation are summarized. The controlling strategies, including the chemical method and the electrochemical method, are discussed. The impacts of surface composition compositions on the electrocatalytic performance are also discussed. Finally, the challenges and future directions for controlling the surface composition of Pt‐based bimetallic nanomaterials are addressed.     

Species of family <Emphasis Type="Italic">Promicromonosporaceae</Emphasis> and family <Emphasis Type="Italic">Cellulomonadeceae</Emphasis> that produce cellulosome-like multiprotein complexes

Objectives

To screen the phylogenetically-nearest members of Cellulosimicrobium cellulans for the production of cellulosome-like multienzyme complexes and extracellular β-xylosidase activity against 7-xylosyltaxanes and to get corresponding molecular insights.

Results

Cellulosimicrobium (family Promicromonosporaceae) and all genera of the family Cellulomonadeceaec produced both cellulosome-like multienzyme complexes and extracellular β-xylosidase activity, while the other genera of the family Promicromonosporaceae did not. Multiple sequence alignments further indicated that hypothetic protein M768_06655 might be a possible key subunit.

Conclusion

This is the first report that many actinobacteria species can produce cellulosome-like multienzyme complexes. The production of cellulosome-like complexes and the extracellular β-xylosidase activity against 7-xylosyltaxanes might be used to differentiate the genus Cellulosimicrobium from other genera of the family Promicromonosporaceae.

     

In vitro and in vivo pharmacokinetic and pharmacodynamic study of MBRI-001, a deuterium-substituted plinabulin derivative as a potent anti-cancer agent

MBRI-001 was demonstrated preliminary better pharmacokinetics and antitumor effects than that of plinabulin in vivo. In this approach, we further carried out systematic pharmacokinetic and pharmacodynamic study of MBRI-001 in vitro and in vivo. MBRI-001 was tested stable in rat plasma and more stable in liver microsomes than plinabulin in vitro. In vivo, MBRI-001 could be distributed rapidly and widely in various tissues, especially the concentration of MBRI-001 in lung was remarkably higher than other tissues. Excretion study indicated that MBRI-001 might been decomposed and excreted as metabolites. Additionally, the combination treatment of MBRI-001 and gefitinib revealed better antitumor inhibition rate than monotherapy in vivo. Therefore, we suggest that MBRI-001 could be developed as a promising anti-cancer agent in near future.     

Putative roles of retinoblastoma protein in apoptosis

Cell numbers are regulated by a balance between processes of proliferation and apoptosis (programmed cell death). Proper regulation in a cell requires an accurate co-ordination between these two processes. Indeed, it has recently been found that dysregulation of cell cycle progression is essential for the initiation of apoptosis. Retinoblastoma protein (RB) is an important tumour suppressor and a cell cycle regulator. Most recent studies suggest that RB also plays a regulatory role in the process of apoptosis. During the onset of apoptosis, the hyperphosphorylated form of RB (p120/hyper) is converted to a hypophosphorylated form (p115/hypo), which is mediated by a specific protein-serine/ threonine phosphatase activity. The p115/hypo/RB may play an active role in the regulation of apoptosis. Accompanied by the endonucleosomal fragmentation of DNA, the newly formed p115/hypo/RB is immediately cleaved by a protease that has properties of the interleukin-1beta-converting enzyme family. By contrast, the unphosphorylated form of RB (p110/unphos) remains uncleaved during apoptosis. Further studies suggest that p110/unphos/RB functions as an inhibitor of apoptosis. Therefore, a balance between RB phosphatases and kinases and consequent RB phosphorylation status may be important for the determination of cellular fate.     

Rational Improvement of Peptide Affinity to Human Pregnancy-Related Serine Protease HtrA3 PDZ Domain by Introducing a Halogen Bond to the Domain–Peptide Complex Interface

The pregnancy-related serine protease HtrA3 plays an important role in human placental development and has recently been recognized as a potential therapeutic target in the treatment of cancer. Previously, a C-terminal pentapeptide FGRWV^–COOH was identified to bind at the PDZ domain of HtrA3 with a moderate affinity. Here, based on the high-resolution complex crystal structure of HtrA3 PDZ domain with the pentapeptide ligand we successfully introduced a rationally designed halogen bond to the complex interface by substituting R₄-hydrogen atom of the indole moiety of peptide Trp_-1 residue with a halogen atom. High-level theoretical calculations suggested that bromine is the best choice that can render strong interaction energy for the halogen bond and can confer high affinity to the PDZ–peptide complex. Fluorescence spectroscopy characterizations revealed that the resulting R₄-brominated peptide (K _d = 0.15 ± 0.03 μM) exhibited 12-fold affinity improvement relative to its nonhalogenated counterpart (K _d = 1.8 ± 0.4 μM). In contrast, the PDZ-binding affinity of R₆-brominated peptide (K _d = 1.2 ± 0.1 μM), a negative control that was unable to form the halogen bond according to theoretical investigations, did not change substantially as compared to the nonhalogenated peptide.     

MicroRNA‐20a‐5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression

Recently, it is implicated that aberrant expression of microRNAs (miRs) is associated with insulin resistance. However, the role of miR‐17 family in hepatic insulin resistance and its underlying mechanisms remain unknown. In this study, we provided mechanistic insight into the effects of miR‐20a‐5p, a member of miR‐17 family, on the regulation of AKT/GSK pathway and glycogenesis in hepatocytes. MiR‐20a‐5p was down‐regulated in the liver of db/db mice, and NCTC1469 cells and Hep1‐6 cells treated with high glucose, accompanied by reduced glycogen content and impaired insulin signalling. Notably, inhibition of miR‐20a‐5p significantly reduced glycogen synthesis and AKT/GSK activation, whereas overexpression of miR‐20a‐5p led to elevated glycogenesis and activated AKT/GSK signalling pathway. In addition, miR‐20a‐5p mimic could reverse high glucose‐induced impaired glycogenesis and AKT/GSK activation in NCTC1469 and Hep1‐6 cells. P63 was identified as a target of miR‐20a‐5p by bioinformatics analysis and luciferase reporter assay. Knockdown of p63 in the NCTC1469 cells and the Hep1‐6 cells by transfecting with siRNA targeting p63 could increase glycogen content and reverse miR‐20a‐5p inhibition‐induced reduced glycogenesis and activation of AKT and GSK, suggesting that p63 participated in miR‐20a‐5p‐mediated glycogenesis in hepatocytes. Moreover, our results indicate that p63 might directly bind to p53, thereby regulating PTEN expression and in turn participating in glycogenesis. In conclusion, we found novel evidence suggesting that as a member of miR‐17 family, miR‐20a‐5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression.