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Psychological distress and its association with gender, socioeconomic status, education and health conditions
UHRF2 mediates resistance to DNA methylation reprogramming in primordial germ cells
Abstract In mammals, primordial germ cells (PGCs) undergo global erasure of DNA methylation with delayed demethylation of germline genes and selective retention of DNA methylation at evolutionarily young retrotransposons. However, the molecular mechanisms of persistent DNA methylation in PGCs remain unclear. Here we report that resistance to DNA methylation reprogramming in PGCs requires UHRF2, the paralog of the DNMT1 cofactor UHRF1. PGCs from Uhrf2 knock-out mice show loss of retrotransposon DNA methylation, while DNA methylation is unaffected in somatic cells. This is not associated with changes in the expression of retrotransposons in E13.5 PGCs, indicating that other mechanisms compensate for retrotransposon control at this stage. Furthermore, Uhrf2-deficient PGCs show precocious demethylation of germline genes and overexpress meiotic genes in females. Subsequently, Uhrf2-deficient mice show impaired oocyte development and female-specific reduced fertility, as well as incomplete remethylation of retrotransposons during spermatogenesis. These findings reveal a crucial function for the UHRF1 paralog UHRF2 in controlling DNA methylation in the germline.
Molecular logic gates based on programmable self-assembly of DNA origami triangles for the detection of nucleic acid molecules
Fully printable integrated multifunctional sensor arrays for intelligent lithium-ion batteries
Assessment and nematicidal activity of Cu/Fe and Zn/Fe bimetallic nanoparticles against root-knot nematode in beetroot and cabbage
A covalent organic framework membrane with highly selective and permeable artificial sodium channels via ion recognition
Optimizing agricultural biomass selection for biochar production using multicriteria decision-making
Ligand supplementation restores the cancer therapy efficacy of the antirheumatic drug auranofin from serum inactivation
Administration of heat killed Fructobacillus fructosus OS-1010 attenuates metabolic disease induced by high fat diet in mice
Abstract Heat-killed Fructobacillus fructosus OS-1010 reportedly enhance the number and membrane potential of mitochondria in muscle cell C2C12 in vitro. However, there are no reports on the effects of this strain on mitochondria or the resulting effects on the body in animal models. In this study, we investigated the effects of heat-killed F. fructosus OS-1010 on obesity and other metabolic abnormalities and muscle weakness in mice with high-fat diet (HFD)-induced sarcopenic obesity. C57BL/6 mice were fed HFD supplemented with heat-killed F. fructosus OS-1010 for 13 weeks. The HFD-induced body weight gain was significantly reduced. Additionally, there was a significant decrease in alanine aminotransferase levels, improvement in serum lipid profiles, and a reduction in non-alcoholic fatty liver disease (NAFLD) progression. Skeletal muscle weakness was also mitigated, with changes in gene expression in the quadriceps indicating suppression of intramuscular fat accumulation, and enhancement of mitochondrial density. The findings of this study suggest that heat-killed F. fructosus OS-1010 functions as an anti-obesity postbiotic, potentially benefiting both NAFLD and muscle weakness associated with obesity.
Nanoconfinement promotes CO2 electroreduction to methanol on a molecular catalyst
Application of causal forest double machine learning (DML) approach to assess tuberculosis preventive therapy’s impact on ART adherence
Wood decay under anoxia by the brown-rot fungus Fomitopsis pinicola
Vehicular ad hoc networks verification scheme based on bilinear pairings and networks reverse fuzzy extraction
Lipid-mediated hydrophobic gating in the BK potassium channel
Abstract Structures of the large-conductance, calcium-activated potassium (BK) channel in the Ca2+ −bound and Ca2+ −free states have suggested that K+ conduction is not gated via a steric closure of the pore-lining helices of the channel, in contrast to the gating mechanism of other 6TM channels. This has raised the question of how gating might occur in the absence of apparent steric hindrance by protein residues. To answer this question, we perform molecular simulations and free-energy calculations to develop a microscopic picture of the gating mechanism. Our results highlight an unexpected role for annular lipids, which appear to be an integral part of the gating machinery. In the Ca2+ −free (“closed”) pore, methyl groups from lipid alkyl chains can enter the pore through fenestrations between the pore-lining helices. This dynamic occupancy directly contributes to dewetting of the inner-pore cavity, thus hindering ion conduction. In contrast, Ca2+ binding leads to occlusion of the fenestrations, thus preventing the lipids from entering the pore cavity and permitting pore hydration and ion conduction. This apparent lipid-mediated hydrophobic gating may also explain functional observations that include state-dependent pore accessibility of hydrophobic channel blockers.
AE-BPNN: autoencoder and backpropagation neural network-based model for lithium-ion battery state of health estimation
Non-coding genetic elements of lung cancer identified using whole genome sequencing in 13,722 Chinese
The chain mediating role of emotion regulation and stress perception in physical activity alleviating college students’ health anxiety
Changes in susceptibility of Plasmodium falciparum to antimalarial drugs in Uganda over time: 2019–2024
Abstract The treatment and control of malaria in Africa is challenged by drug resistance. We characterized ex vivo susceptibilities to nine drugs of isolates collected from individuals presenting with uncomplicated falciparum malaria in eastern (2019-2024) and northern (2021-2024) Uganda and performed deep sequencing, with analysis of 80 Plasmodium falciparum genes, to evaluate associations between susceptibilities and potential resistance markers for samples studied since 2016. For 1114 evaluated isolates, median half-maximal inhibitory concentrations (IC50s) were low-nanomolar for chloroquine, monodesethylamodiaquine, piperaquine, pyronaridine, lumefantrine, mefloquine, and DHA, but higher for quinine and pyrimethamine. Over time, susceptibilities improved for chloroquine, decreased for lumefantrine, mefloquine, and DHA, and were unchanged for other drugs. Changes in prevalences of known markers of altered drug susceptibility followed the same patterns. Genotypes associated with drug susceptibility were those previously identified for aminoquinolines and pyrimethamine. For lumefantrine, susceptibility was decreased with wild-type PfCRT K76T or PfMDR1 N86Y, mutant PfK13 C469Y or A675V, mutant PfCARL D611N, and other polymorphisms. For DHA, susceptibility was decreased with the PfK13 C469Y or A675V and PfMDR1 Y500N mutations. Decreasing activities of lumefantrine and DHA suggest potential loss of efficacies of leading regimens, although the clinical consequences of these changes are, to date, uncertain.
Carbon footprint awareness scale (CFAS): validity and reliability study on university students
Abstract This study was designed with a mixed model to develop a valid and reliable measurement tool to measure university students’ carbon footprint awareness. A total of 1053 university students, 454 female and 599 male, were included in the study voluntarily. To provide evidence for the scale’s validity, exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) were applied to the measurement tool within the scope of construct validity. In the Exploratory Factor Analysis (EFA) conducted in the first stage of the study, and the Confirmatory Factor Analysis (CFA) in the second stage, scale questions consisting of 50 items (n = 500) were applied to the participants. The higher the variance from exploratory factor analysis, the stronger the scale’s factor structure. Our item loadings vary between 0.40 and 0.70. These ratios show that the items in our scale are significant. No item was removed from the scale due to the item analysis. One modification process was made. It was proven that the Cronbach’s Alpha coefficient, tested in line with the reliability of the measurement tool, was high. As a result of the analyzes performed, Cronbach’s Alpha reliability coefficients; For “Buildings factor” it was found as 0.783, for “Fossil Fuel Transportation and Transportation factor” it was found as 0.873, for “Oil Refinery factor” it was found as 0.857, for “Industry factor” it was found as 0.826, for “Electricity and Heat Production factor” it was found as 0.807, for “Land Use and Forestry factor” it was found as 0.790, for “Agricultural Activity factor” it was found as 0.858, for “Waste factor” it was found as 0.781, for “Other Energy Production factor” it was found as 0.864, for “Sports Organizations factor” it was found as 0.910 and for “Carbon Footprint Awareness Scale” it was found as 0.966. As a result of confirmatory factor analysis, the χ2/sd value, one of the fit indexes of the model, was determined as 2.79. Accordingly, it was determined that the χ2/sd ratio was the perfect fit for the analysis. In the second stage of the study, scale questions consisting of 50 items (n = 553) were applied to the participants. In the CFA applied to the obtained data, the value of χ2/sd, one of the fit indexes of the model, was determined as 2.75. In CFA, the Chi-Square/degrees of freedom (df) ratio being below three corresponds to a perfect fit, and below five corresponds to a moderate fit. In this direction, it was determined that the χ2/sd ratio was perfect for the analysis. RMSEA value showed a good fit at a 0.056 level. Thus, it was determined that the 50-item and 10-factor structure of the scale was confirmed as a model. In this context, it can be said that the Carbon Footprint Awareness Scale is a valid and reliable data collection tool that can measure carbon footprint awareness to create awareness and a conscious society among university students and the society in general.