Explore the vast range of titles available.

YTH Domain Containing 1 (YTHDC1) is one of the m 6 A readers that is essential for oocyte development and tumor progression. The role of YTHDC1 in neuronal survival and ischemic stroke is unknown. Here, we found that YTHDC1 was unregulated in the early phase of ischemic stroke. Knockdown of YTHDC1 exacerbated ischemic brain injury and overexpression of YTHDC1 protected rats against brain injury. Mechanistically, YTHDC1 promoted PTEN mRNA degradation to increase Akt phosphorylation, thus facilitating neuronal survival in particular after ischemia. These data identify YTHDC1 as a novel regulator of neuronal survival and modulating m 6 A reader YTHDC1 may provide a potential therapeutic target for ischemic stroke.

CO is a promising substrate for producing biochemicals and biofuels through mixed microbial cultures, where carboxydotrophs play a crucial role. The previous investigations of mixed microbial cultures focused primarily on overall community structures, but under-characterized taxa and intricate microbial interactions have not yet been precisely explicated. Here, we undertook DNA-SIP based metagenomics to profile the anaerobic CO-driven microbiomes under 95 and 35% CO atmospheres. The time-series analysis of the isotope-labeled amplicon sequencing revealed the essential roles of Firmicutes and Proteobacteria under high and low CO pressure, respectively, and Methanobacterium was the predominant archaeal genus. The functional enrichment analysis based on the isotope-labeled metagenomes suggested that the microbial cultures under high CO pressure had greater potential in expressing carboxylate metabolism and citrate cycle pathway. The genome-centric metagenomics reconstructed 24 discovered and 24 under-characterized metagenome-assembled genomes (MAGs), covering more than 94% of the metagenomic reads. The metabolic reconstruction of the MAGs described their potential functions in the CO-driven microbiomes. Some under-characterized taxa might be versatile in multiple processes; for example, under-characterized Rhodoplanes sp. and Desulfitobacterium_A sp. could encode the complete enzymes in CO oxidation and carboxylate production, improving functional redundancy. Finally, we proposed the putative microbial interactions in the conversion of CO to carboxylates and methane.

Colorectal cancer (CRC) is one of the most common malignancies, and the main cause of death from CRC is tumor metastasis. m1A RNA modification plays critical role in many biological processes. However, the role of m1A modification in CRC remains unclear. Here, we find that the m1A demethylase alkB homolog 1, histone H2A dioxygenase (ALKBH1) is overexpressed in CRC and is associated with metastasis and poor prognosis. Upregulation of ALKBH1 expression promotes CRC metastasis in vitro and in vivo. Mechanistically, knockdown of ALKBH1 results in a decrease in methyltransferase 3, N6‐adenosine‐methyltransferase complex catalytic subunit (METTL3) expression, probably due to m1A modification of METTL3 mRNA, followed by m6A demethylation of SMAD family member 7 (SMAD7) mRNA. In addition, downregulation of SMAD7 establishes an aggressive phenotype. More importantly, the cell migration and invasion defects caused by ALKBH1 depletion or METTL3 depletion are significantly reversed by SMAD7 silencing. Considering these results collectively, we propose that ALKBH1 promotes CRC metastasis by destabilizing SMAD7 through METTL3. Colorectal cancer (CRC) is one of the most common malignancies, and the main cause of death from CRC is tumor metastasis. Here, we identified the important role of ALKBH1‐catalyzed m1A modification in CRC metastasis. ALKBH1‐mediated m1A demethylation of METTL3 mRNA promotes the metastasis of colorectal cancer by downregulating SMAD7 expression.

Promoting the coverage and ownership of health insurance constitutes a key strategy to achieving universal healthcare, thereby meeting the Sustainable Development Goal (SDG 3.8) of safeguarding the vulnerable population from financial risk resulting from catastrophic health expenditures. In sub-Saharan Africa, accessing medical services is particularly challenging among women due to inadequate opportunities for socio-economic empowerment and meeting their unique healthcare needs. The present study aimed to explore the sociodemographic factors associated with health insurance ownership among women in selected countries in sub-Saharan Africa. We extracted cross-sectional data on health insurance ownership and conceptually relevant sociodemographic variables on women aged 15-49 years from Demographic and Health Surveys on five selected countries in sub-Saharan Africa (n = 55,438), including Burkina Faso, DR Congo, Cameroon, Gabon and Kenya. Data were analyzed using descriptive and multivariate regression analysis, and the associations were reported in terms of average marginal effects. Data revealed considerable cross-country variation in health insurance ownership: Gabon (57.9%), Kenya (6.1%), DR Congo (2.8%), Cameroon (1.1%), Burkina Faso (0.4%). In the multivariate regression analysis, women's age, marital status, place of residency, educational level, household wealth status, employment, and media access were significant predictors of insurance ownership. The associations were generally similar across the five countries, with higher age, better educational level and wealth status showing a consistently positive relationship with insurance ownership. Our findings revealed striking inequality in health insurance ownership among the studied countries, which should be given due attention to achieving universal healthcare-related goals. There also exist considerable sociodemographic disparities in health insurance ownership among women that should be addressed using context-specific programmatic interventions. Our findings revealed striking inequality in health insurance ownership among the studied countries, which should be given due attention to achieving universal healthcare-related goals. There also exist considerable sociodemographic disparities in health insurance ownership among women that should be addressed using context-specific programmatic interventions.

The effects of humic acid (HA) and fulvic acid (FA) on Cu 2+ adsorption on biochar were investigated, with mechanisms confirmed by excitation-emission matrix spectroscopy, Fourier transform infrared spectroscopy, and scanning electron microscopy. HA loading enhanced Cu 2+ adsorption on biochar, with the maximum enhancement of 55.0% occurring at an HA loading of 100 mg-C/L. The adsorbed HA introduced many additional functional groups to biochar, thus enhancing Cu 2+ adsorption, which decreased at HA concentrations >100 mg-C/L due to self-association of HA at high loading concentrations. In contrast, FA loading caused no enhancement on Cu 2+ adsorption on biochar. FA was adsorbed through H-bonding with the functional groups of biochar, which set up a competition with Cu 2+ for adsorption on biochar. The functional groups occupied by adsorbed FA were offset by the newly introduced functional groups of FA, thus there was no net increase in the amount of Cu 2+ adsorption upon FA loading. These findings imply that, because of the enhanced adsorption of HA-loaded biochar, the amount of Cu 2+ immobilized would increase by 28.2% for mature compost and 31.9% for fresh compost if there exist interaction between biochar and HA compared with the amounts immobilized by non-interactive HA and biochar.

Background Cancer stem cells (CSCs) play a critical role in tumor development and progression and are involved in cancer metastasis. The role of reactive oxygen species (ROS) in CSCs and cancer metastasis remains controversial. The aim of the present study was to investigate the correlation between ROS level of CSCs and cancer metastasis and to explore the possible underlying molecular mechanisms. Methods Four different cell lines were used to isolate tumor spheres and to analyze intrinsic properties of tumor sphere cells including proliferation, self-renewal potential, differentiation, drug-resistance and cancer metastasis in vitro and in vivo. ROS assays were used to detect the intracellular ROS level of tumor spheres cells. Gene expression analysis and western blot were used to investigate the underlying mechanisms of ROS in regulating cancer metastasis. Results Tumor spheres possessed the characteristic features of CSCs, and ROS-high tumor spheres (RH-TS) displayed elevated mitochondrial ROS level exclusively drove metastasis formation. The gene expression analysis showed elevated fatty acid β-oxidation, downregulation of epithelial marker upregulation of mesenchymal markers, and the activation of MAP kinase cascades. Furthermore, 14 up-regulated genes in RH-TS cells were associated with reduced overall survival of different cancer patients. Conclusions Our findings demonstrate that CSCs characterized by elevated mitochondrial ROS level potentiate cancer metastasis. Mechanistically, elevated mitochondrial ROS via fatty acid β-oxidation, activates the MAPK cascades, resulting in the epithelial-mesenchymal transition (EMT) process of RH-TS cells, thereby potentiating caner invasion and metastasis. Therefore, targeting mitochondrial ROS might provide a promising approach to prevent and alleviate cancer metastasis induced by RH-TS cells.