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We study the efficiency of the vector greedy algorithms for simultaneous sparse approximation in a Banach space. We employ a unified way of analyzing the approximation properties of the Vector Weak Chebyshev Greedy Algorithm, the Vector Weak Greedy Algorithm with Free Relaxation and the Vector Rescaled Weak Relaxed Greedy Algorithm. We obtain the necessary and sufficient conditions for the convergence and the optimal convergence rate on the basic sparse class for these algorithms. It shows that these vector greedy algorithms are simple but highly efficient in dealing with multi-target element. [ABSTRACT FROM AUTHOR]

Lithium cobalt oxide (LiCoO2) and graphite-based Li-ion batteries have been widely applied for consumer electronics because of the long cycle life and easy preparation. However, the limited capacity for traditional materials hampers the practical application for high energy-density battery. Conventional electrolyte system could not satisfy the need for high-capacity materials. Here, methylene methanedisulfonate (MMDS) was chosen as electrolyte additive for enhancing the available capacity for LiCoO2 and graphite-based battery. The effect of MMDS on the LiCoO2 cathode and graphite anode was investigated via multi electrochemical methods. It was found that the capacity for cells with MMDS electrolyte additive increases (from 142.6 mAh g−1 for pristine to 193.4 mAh g−1 on LiCoO2/Li battery, from 275.5 mAh g−1 for pristine to 407.0 mAh g−1 on graphite/Li battery). The experimental results indicate that improved capacity by MMDS electrolyte additive can be attributable to the stabilized interface on both cathode and anode sides, leading to superior interfacial Li+ kinetics and mitigated bulk structural degradation, which was further confirmed by the ex-situ electrochemical and structural characterization. [ABSTRACT FROM AUTHOR]

In the pursuit of high-energy density lithium-ion battery, Li-rich Mn-based oxide cathode has gained great attention with unexpectedly high capacity, low cost and excellent thermal stability. However, the cause for the sluggish kinetics remains a mystery, hindering the application of Li-rich cathode material. Here, we reveal the interfacial instability is the driving force for the sluggish kinetics, which severely blocks the interfacial Li-ion transport and triggers fast battery failure. Through rice-husk carbon (RHC) and spinel phase modification on Li-rich Mn-based oxide Li1.2Ni0.16Mn0.56Co0.08O2 (LNMC), the poor lithium ion diffusion and interfacial degradation can be effectively prevented, delivering a high specific capacity of around 300 mAh/g and excellent rate performance. These findings provide a universal method to prepare high electrochemical performance Li-rich oxide materials. Through synergetic modification, the Li-rich Mn-based cathode delivers a high available capacity of 300 mAh/g via accelerated Li+ intercalation kinetics [ABSTRACT FROM AUTHOR]

Laryngeal cancer is a common type of head and neck malignancy. microRNA is implicated in the development and progression of various tumours. The present study aimed to explore the potential roles and mechanisms of miR‐646 in laryngeal carcinoma cells. We detected the expression of miR‐646 and observed that miR‐646 was reduced in laryngeal cell lines. Subsequently, the proliferation, migration and invasion of TU212 and TU686 cells were evaluated using CCK‐8 assays, cell proliferation ELISA BrdU and transwell assays after transfection with miR‐646 mimic. Overexpression of miR‐646 attenuated the proliferative and invasive abilities of TU212 and TU686 cells. Dual luciferase reporter assay confirmed that glutathione peroxidase 1 (GPX1) is a direct target of miR‐646. Interestingly, restoration of GPX1 promoted cell proliferation and migration, and reversed the biological activities of miR‐646 in cell proliferation and migration. It is worth noting that miR‐646 overexpression blocked the activation of PI3K/AKT pathway, and this was partly abrogated by GPX1. 740Y‐P, a PI3K agonist abolished the effects of miR‐646 on cell proliferation and invasion. Taken together, miR‐646 prohibited the proliferation and invasion of laryngeal carcinoma cells through the PI3K/AKT pathway via targeting GPX1. [ABSTRACT FROM AUTHOR]

• Chinese1 genotype Wh6 strain (TgCtwh6) infection not only leads to phosphorylation of tau via activating GSK3 β but also promotes hippocampal neuron apoptosis. • The signaling of p -GSK3 β - p -tau might be involved in the hippocampal neuron injury infected by an avirulent cyst-forming TgCtwh6. • These results are helpful for better understanding of mental disorders caused by T. gondii infection. • Prevention TgCtWh6 from infection may be an effective method to reduce the occurrence and delay the development of neurodegenerative diseases. Toxoplasma gondii (T. gondii) is a neurophilic and intracellular parasite that can affect plenty of vertebrate animals, including humans. Recent researches indicate that T. gondii infection is associated with neurodegenerative diseases such as Alzheimer's disease(AD). In addition, tau hyper-phosphorylation is a crucial event leading to the formation of nerve fiber tangles in AD. Despite the efforts to understand the interactions between T. gondii and AD, there are no clear results available so far. Here, we infected mice with the T. gondii of the Chinese 1 genotype Wh6 strain (TgCtwh6) for 60 days. Then we observed the formation of tissue cysts in the brain, the damage of neuron and the increased expression of phosphorylated tau (p -tau) in the hippocampal tissue of the mice. Similarly, we also found that p -tau, glycogen synthase kinase 3 beta (GSK3 β), and phosphorylated GSK3 β (p -GSK3 β) were upregulated in vitro in TgCtwh6 challenged hippocampal neuron cell strain, HT22 cells. We noted a down-regulated expression of GSK3 β , p -GSK3 β , and p -tau in HT22 cells, which were pretreated with LiCl, an inhibitor of GSK3 β. These data suggested that p -GSK3 β may mediate tau phosphorylation after TgCtwh6 infection. Furthermore, TgCtwh6 infection also caused the increased expression of Bax and Caspase3, the decreased expression of Bcl-XL in HT22 cells, which had both early and late apoptosis. In all, our results indicated that TgCtwh6 infection not only led to phosphorylation of tau via activating GSK3 β but also promoted hippocampal neuron apoptosis. Our research may partially reveal the mechanism with which TgCtwh6 induce neurofibrillary pathology. [ABSTRACT FROM AUTHOR]

• Lipid rafts are required for activation of PI3K/Akt signaling both at early and late stages of CA16 infection. • Lipid raft-associated PI3K/Akt plays critical roles in mediating SREBP1 maturation during late stage of CA16 infection. • This finding of lipid raft-associated PI3K/Akt/SREBP1 will deepen our understanding mechanism of CA16 infection. Coxsackievirus A16 (CA16) is one of predominant Enterovirus that possesses high pathogenicity. Lipid rafts, as cholesterol - and sphingolipid - enriched membrane nanodomains, are involved into many aspects of the virus life cycle. Our previous study found that lipid rafts integrity was essential for CA16 replication, but how lipid rafts regulate CA16 replication through activating downstream signaling remains largely unknown. Thus, in this study, we revealed that lipid rafts were required for activation of PI3K/Akt signaling at early stage of CA16 infection. Treatment with wortmannin significantly reduced the expression of virus protein, indicating PI3K/Akt signaling was beneficial for early stage of virus infection. In addition, lipid rafts integrity was also indispensable for PI3K/Akt activation during the late stage of CA16 infection, which played critical functions in mediating sterol regulatory element-binding proteins 1 (SREBP1) maturation. Whereas, over-expression of SREBP1 exhibited inhibition on virus replication, suggesting that PI3K/Akt signaling and SREBP1 might positively and negatively influence virus replication in two different stages of infection, respectively. Taken together, our study demonstrates an important role of the lipid raft-associated PI3K/Akt/SREBP1 signaling in modulating CA16 replication, which will deepen our understanding mechanism of CA16 infection. [ABSTRACT FROM AUTHOR]

Background: Type 1 Diabetes Mellitus (T1DM) is one of the most common endocrine disorders of childhood and adolescence, showing a rapidly increasing prevalence worldwide. A study indicated that the composition of the oropharyngeal and gut microbiota changed in T1DM. However, no studies have yet associated the changes between the microbiomes of the oropharyngeal and intestinal sites, nor between the flora and clinical indicators. In this study, we examined the composition and characteristics of oropharyngeal and intestinal flora in patients with T1DM in compared to healthy children. We identified correlations between oropharyngeal and intestinal flora and evaluated their association with clinical laboratory tests in patients with T1DM., Methods: The oropharyngeal and fecal samples from 13 T1DM and 20 healthy children were analyzed by high-throughput sequencing of the V3-V4 region of 16S rRNA. The associations between microbes and microorganisms in oropharyngeal and fecal ecological niches, as well as the correlation between these and clinical indicators were further analyzed., Results: It was revealed that T1DM children had distinct microbiological characteristics, and the dominant oropharyngeal microbiota genus included Streptococcus, Prevotella, Leptotrichia, and Neisseria; that of intestinal microbiota included Blautia, Fusicatenibacter, Bacteroides, and Eubacterium_hallii_group. Furthermore, oropharyngeal Staphylococcus was significantly positively correlated with intestinal norank_f__Ruminococcaceae and Ruminococcus_torques_group in TIDM children. Moreover, in these children, differential genes in oropharyngeal and intestinal samples were enriched in metabolic pathways such as amino acid generation, fatty acid metabolism, and nucleotide sugar biosynthesis. Additionally, correlation analysis between the oropharyngeal/intestinal microbiome with laboratory tests showed significant correlations between several bacterial taxa in the oropharynx and intestines and glycated hemoglobin and C-peptide., Conclusion: Unique microbial characteristics were found in the oropharynx and intestine in children with T1DM compared to healthy children. Positive correlations were found between changes in the relative abundance of oropharyngeal and gut microbiota in children with T1DM. Associations between the oropharyngeal/intestinal microbiota and laboratory investigations in children with T1DM suggest that the composition of the oropharyngeal and intestinal flora in children with T1DM may have some impact on glycemic control., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Wang, Gong, Wang, Wang, Yang and Wang.)

Objectives: Interleukin-10 (IL-10) polymorphisms have been reported to be associated with systemic lupus erythematosus (SLE), however, the results are controversial. Therefore, we conducted a meta-analysis with trial sequential analysis to evaluate a more accurate estimation of the associations., Methods: Eligible studies were retrieved by searching PubMed, Embase, Google Scholar, VIP, Wan Fang and China National Knowledge Infrastructure databases. Hardy-Weinberg equilibrium (HWE) was evaluated. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. Heterogeneity was evaluated by Q statistic and I2 statistic. Sensitivity analysis and subgroup analysis (stratified by HWE, region, event sample size, source of controls, genotyping method) were conducted and the potential for publication bias was assessed. Trial sequential analysis was introduced to assess the information size and the positive results., Results: Twenty case-control studies were included. Overall results from IL10-1082A/G polymorphism showed increased risk of systemic lupus erythematosus, but no significant associations were observed in both IL10-819C/T and IL10-592C/A polymorphism. Increased risk of SLE was also observed in IL10A/G polymorphism in Asian population, hospital-based and PCR-RFLP (polymerase chain reaction restriction fragment length polymorphism) subgroups. In addition, decreased risk of SLE was widely detected in IL10-819C/T and IL10-592C/A polymorphisms in subgroup analysis., Conclusions: Our study suggests that the IL10-1082A/G polymorphism is a risk factor in systemic lupus erythematosus. A decreased risk of SLE in the IL10-819C/T and IL10-592C/A polymorphisms in subgroups was also observed, but further rigorously studies are needed to confirm these results.