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BackgroundPrevious studies revealed that vitamin K might help maintain muscle homeostasis, but this association has received little attention. We aimed to explore the associations of vitamin K intake with skeletal muscle mass and strength.MethodsWe included cross-sectional data from the U.S. National Health and Nutrition Examination Survey (NHANES, 2011–2018). Vitamin K intake was assessed via 24-h recall. Covariate-adjusted multiple linear regression and restricted cubic splines were used to evaluate the associations of dietary vitamin K intake with skeletal muscle mass and strength, measured by dual-energy X-ray absorptiometry and handgrip dynamometer, respectively.ResultsDietary vitamin K intake was positively associated with skeletal muscle mass in males (β = 0.05747, p = 0.0204) but not in females. We also revealed a positive association between dietary vitamin K intake and handgrip strength within the range of 0–59.871 μg/d (Pnonlinear = 0.049). However, beyond this threshold, increasing vitamin K intake did not cause additional handgrip strength improvements.ConclusionWe provided evidence for a positive relationship between dietary vitamin K intake and skeletal muscle mass in males. Moreover, our study revealed a nonlinear relationship between dietary vitamin K intake and handgrip strength, highlighting an optimal intake range.

Abstract Objectives The risk of intracranial aneurysms (IAs) development and rupture is significantly higher in patients with periodontitis (PD), suggesting an association between the two. However, the specific mechanisms of association between these two diseases have not been fully investigated. Materials and methods In this study, we downloaded IAs and PD data from the Gene Expression Omnibus. Differentially expressed genes (DEGs) were identified, and functional enrichment analysis was performed. The protein-protein interaction (PPI) network and weighted gene co-expression network analysis (WGCNA) was performed to identified key modules and key crosstalk genes. In addition, the immune cell landscape was assessed and the correlation of key crosstalk genes with each immune cell was calculated. Finally, transcription factors (TFs) regulating key crosstalk genes were explored. Results 127 overlapping DEGs were identified and functional enrichment analysis highlighted the important role of immune reflection in the pathogenesis of IAs and PD. We identified ITGAX and COL4A2 as key crosstalk genes. In addition, the expression of multiple immune cells was significantly elevated in PDs and IAs compared to controls, and both key crosstalk genes were significantly negatively associated with Macrophages M2. Finally, GATA2 was identified as a potential key transcription factor (TF), which regulates two key crosstalk gene. Conclusions The present study identifies key crosstalk genes and TF in PD and IAs, providing new insights for further study of the co-pathogenesis of PD and IAs from an immune and inflammatory perspective. Also, this is the first study to report the above findings.

Abstract Despite clinical and epidemiological evidence suggestive of a link between glioblastoma (GBM) and periodontitis (PD), the shared mechanisms of gene regulation remain elusive. In this study, we identify differentially expressed genes (DEGs) that overlap between the GEO datasets GSE4290 [GBM] and GSE10334 [PD]. Functional enrichment analysis was conducted, and key modules were identified using protein–protein interaction (PPI) network and weighted gene co-expression network analysis (WGCNA). The expression levels of CXCR4, LY96, and C3 were found to be significantly elevated in both the test dataset and external validation dataset, making them key crosstalk genes. Additionally, immune cell landscape analysis revealed elevated expression levels of multiple immune cells in GBM and PD compared to controls, with the key crosstalk genes negatively associated with Macrophages M2. FLI1 was identified as a potential key transcription factor (TF) regulating the three key crosstalk genes, with increased expression in the full dataset. These findings contribute to our understanding of the immune and inflammatory aspects of the comorbidity mechanism between GBM and PD.

[This corrects the article DOI: 10.1371/journal.ppat.1008437.].

Abstract The dynamic assembly of the actin cytoskeleton is vital for Magnaporthe oryzae development and host infection. The actin-related protein MoFim1 is a key factor for organizing the M. oryzae actin cytoskeleton. Currently, how MoFim1 is regulated in M. oryzae to precisely rearrange the actin cytoskeleton is unclear. In this study, we found that MoFim1 associates with the M. oryzae mitogen-activated protein (MAP) kinase Pmk1 to regulate actin assembly. MoFim1 directly interacted with Pmk1, and the phosphorylation level of MoFim1 was decreased in Δpmk1, which led to a change in the subcellular distribution of MoFim1 in the hyphae of Δpmk1. Moreover, the actin cytoskeleton was aberrantly organized at the hyphal tip in the Δpmk1, which was similar to what was observed in the Δmofim1 during hyphal growth. Furthermore, phosphorylation analysis revealed that Pmk1 could phosphorylate MoFim1 at serine 94. Loss of phosphorylation of MoFim1 at serine 94 decreased actin bundling activity. Additionally, the expression of the site mutant of MoFim1 S94D (in which serine 94 was replaced with aspartate to mimic phosphorylation) in Δpmk1 could reverse the defects in actin organization and hyphal growth in Δpmk1. It also partially rescues the formation of appressorium failure in Δpmk1. Taken together, these findings suggest a regulatory mechanism in which Pmk1 phosphorylates MoFim1 to regulate the assembly of the actin cytoskeleton during hyphal development and pathogenesis.

Microbially enhanced coalbed methane (MECBM) production has drawn significant interest worldwide in recent years since the direct combustion of fossil energy sources including oil and coal, would cause global environmental pollution and have detrimental effects on human health. MECBM shows great potential in producing biomethane and thus reducing fossil fuel related pollution. Although much progress has been achieved in understanding the mechanism of how coal is converted into biomethane, studies have shown that the biodegradation efficiency is still low. The present review mainly focuses on discussing recent advances in enhancing the biomethane yield and affecting key factors. Strategies aimed at improving coal solubility or coal bioavailability, stimulating bacterial growth, changing bacterial communities, and altering metabolic pathways or activity of functional genes of microbacteria exert a significantly positive effect on the yield of biomethane production. Coal rank, coal maceral, coal structure, microbial community, culture condition and culture nutrient are key factors that determine the coal degradation efficiency. Expanded investigations on determining key microorganisms that play decisive roles in the conversion of coal to biomethane and what components of coal are consumed by these bacteria will help to clarify the mechanism underlying the MECBM and provide guidance for future in-situ biostimulation of coalbed-methane production from coal seam.