Cations-Pillared and Polyaniline-Encapsulated Vanadate Cathode for High-Performance Aqueous Zinc-Ion Batteries.

Layered vanadium-based oxides have emerged as highly promising candidates for aqueous zinc-ion batteries (AZIBs) due to their open-framework layer structure and high theoretical capacity among the diverse cathode materials investigated. However, the susceptibility to structural collapse during charge-discharge cycling severely hampers their advancement. Herein, we propose an effective strategy to enhance the cycling stability of vanadium oxides. Initially, the structural integrity of the host material is significantly reinforced by incorporating bi-cations Na+ and NH4 + as "pillars" between the V2O5 layers (NaNVO). Subsequently, surface coating with polyaniline (PA) is employed to further improve the conductivity of the active material. As anticipated, the assembled Zn//NaNVO@PA cell exhibits a remarkable discharge capacity of 492 mAh g-1 at 0.1 A g-1 and exceptional capacity retention up to 89.2 % after 1000 cycles at a current density of 5 A g-1. Moreover, a series of in-situ and ex-situ characterization techniques were utilized to investigate both Zn ions insertion/extraction storage mechanism and the contribution of polyaniline protonation process towards enhancing capacity.

miR-31-5p Regulates 14-3-3 ɛ to Inhibit Prostate Cancer 22RV1 Cell Survival and Proliferation via PI3K/AKT/Bcl-2 Signaling Pathway.

INTRODUCTION: Prostate cancer (PCa) is one of the most common malignancies, and almost all patients with advanced PCa will develop castration-resistant prostate cancer (CRPC) after receiving endocrine therapy. Effective treatment for patients with CRPC has not been established. Novel approaches are needed to identify therapeutic targets for CRPC. PURPOSE: Recent research studies have found that members of the 14-3-3 family play an important role in the development and progression of PCa. Previous results have shown that 14-3-3 ɛ is significantly upregulated in several cancers. This study aimed to identify novel miRNAs that regulate 14-3-3 ɛ expression and therapeutic targets for CRPC. METHODS: In this study, we used computation and experimental approaches for the prediction and verification of the miRNAs targeting 14-3-3 ɛ, and investigated the potential roles of 14-3-3 ɛ in the survival and proliferation of 22RV1 cells. RESULTS: We confirm that mir-31-5p is downregulated in 22RV1 cells and acts as a tumor suppressor by regulating 14-3-3 ɛ. Ectopic expression of miR-31-5p or 14-3-3 ɛ interference significantly inhibits cell proliferation, invasion, and migration in 22RV1 cells, as well as promotes cell apoptosis via the PI3K/AKT/Bcl-2 signaling pathway. Moreover, 14-3-3 ɛ is required for the miR-31-5p-mediated upregulation of the PI3K/AKT/Bcl-2 signaling pathway. CONCLUSION: Our findings provide information on the underlying mechanisms of miR-31-5p/14-3-3 ɛ in 22RV1 cell proliferation and apoptosis through the PI3K/AKT/Bcl-2 signaling pathway. These results suggest that miR-31-5p and 14-3-3 ɛ may potentially be utilized as novel prognostic markers and therapeutic targets for PCa treatment.

TMT-based quantitative proteomics analysis reveals the attenuated replication mechanism of Newcastle disease virus caused by nuclear localization signal mutation in viral matrix protein.

Nuclear localization of cytoplasmic RNA virus proteins mediated by intrinsic nuclear localization signal (NLS) plays essential roles in successful virus replication. We previously reported that NLS mutation in the matrix (M) protein obviously attenuates the replication and pathogenicity of Newcastle disease virus (NDV), but the attenuated replication mechanism remains unclear. In this study, we showed that M/NLS mutation not only disrupted M's nucleocytoplasmic trafficking characteristic but also impaired viral RNA synthesis and transcription. Using TMT-based quantitative proteomics analysis of BSR-T7/5 cells infected with the parental NDV rSS1GFP and the mutant NDV rSS1GFP-M/NLSm harboring M/NLS mutation, we found that rSS1GFP infection stimulated much greater quantities and more expression changes of differentially expressed proteins involved in host cell transcription, ribosomal structure, posttranslational modification, and intracellular trafficking than rSS1GFP-M/NLSm infection. Further in-depth analysis revealed that the dominant nuclear accumulation of M protein inhibited host cell transcription, RNA processing and modification, protein synthesis, posttranscriptional modification and transport; and this kind of inhibition could be weakened when most of M protein was confined outside the nucleus. More importantly, we found that the function of M protein in the cytoplasm effected the inhibition of TIFA expression in a dose-dependent manner, and promoted NDV replication by down-regulating TIFA/TRAF6/NF-κB-mediated production of cytokines. It was the first report about the involvement of M protein in NDV immune evasion. Taken together, our findings demonstrate that NDV replication is closely related to the nucleocytoplasmic trafficking of M protein, which accelerates our understanding of the molecular functions of NDV M protein.

Association between serum tumor markers and metabolic tumor volume or total lesion glycolysis in patients with recurrent small cell lung cancer.

The aim of the present study was to investigate the association between serum tumor markers and the metabolic tumor volume (MTV) or total lesion glycolysis (TLG), as determined by fluorine-18 fluorodeoxyglucose (18F-FDG) positron emission tomography-computed tomography (PET/CT) in patients with recurrent small cell lung cancer (SCLC). Data from 21 patients with recurrent SCLC were collected. The levels of neuron-specific enolase (NSE), carcinoembryonic antigen (CEA) and cytokeratin 19 fragment 21-1 were measured at the time of the 18F-FDG PET/CT examination. The MTV and TLG of all lesions were calculated. Pearson correlation analyses were used to estimate the correlations between NSE level and PET findings. Pearson correlation analyses showed that NSE was the only tumor marker to have a strong correlation with MTV or TLG (r=0.787, P<0.001; r=0.866, P<0.001, respectively). In patients with a normal NSE level, no correlation was found between NSE and MTV or TLG (r=0.018, P=0.958; r=-0.003, P=0.92, respectively), but a significant correlation was found in patients with an abnormal NSE level (r=0.789, P<0.01; r=0.872, P=0.01, respectively). Therefore, TLG and MTV may serve as sensitive markers of tumor burden in patients with recurrent SCLC, with TLG showing greater sensitivity. In patients with an abnormal NSE level, a higher NSE level indicates greater MTV and TLG.