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The inflammasome is a cytoplasmic multiprotein complex that induces the maturation of the proinflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18) or pyroptosis by activating caspases, which play critical roles in regulating inflammation, cell death, and various cellular processes. Multiple studies have shown that the inflammasome is a key regulator of the host defence response against pathogen infections. During the process of pathogenic microbe invasion into host cells, the host's innate immune system recognizes these microbes by activating inflammasomes, triggering inflammatory responses to clear the microbes and initiate immune responses. Moreover, microbial pathogens have evolved various mechanisms to inhibit or evade the activation of inflammasomes. Therefore, we review the interactions between viruses and microbes with inflammasomes during the invasion process, highlight the molecular mechanisms of inflammasome activation induced by microbial pathogen infection, and highlight the corresponding strategies that pathogens employ to evade inflammasome activity. Finally, we also discuss potential therapeutic strategies for the treatment of pathogenic microbial infections via the targeting of inflammasomes and their products. [ABSTRACT FROM AUTHOR]

To provide a systematic and quantitative summary of dietary factors and rheumatoid arthritis (RA) risk. A systematic review and meta-analysis included prospective cohort studies from 2000 to 2024 reporting relative risks (RRs) with 95% confidence intervals (CIs) for RA incidence relating to 32 different dietary exposures. Linear and non-linear dose–response analyses were conducted. Thirty studies were included, involving 2,986,747 participants with 9,677 RA cases. Linear dose–response analysis suggested that each 2-unit per week increase in total alcohol intake was linked to 4% risk reduction (RR (95%-CI), heterogeneity (I2), NutriGrade score: 0.96 (0.94, 0.98), 58%, moderate certainty), and beer consumption was associated with a 10% reduction per 2 units/week increase (0.90 (0.84, 0.97), 0%, very low certainty). Each 2-unit/week increase in total alcohol intake was associated with a 3% decrease in seropositive RA risk (0.97 (0.96, 0.99), 28%, moderate certainty). Increased intakes of fruit (per 80 g/day) and cereals (per 30 g/day) were associated with 5% (0.95 (0.92, 0.99), 57%, moderate certainty) and 3% (0.97 (0.96, 0.99), 20%, moderate certainty) reduced risk, respectively. Conversely, tea consumption showed a 4% increased risk per additional cup/day (1.04 (1.02, 1.05), 0%, moderate certainty). Non-linear associations were observed for total coffee, vegetables, oily fish, and vitamin D supplementation. Data on dietary patterns and specific micronutrients were limited. The findings suggest that moderate alcohol consumption and a higher intake of fruits, oily fish, and cereals are associated with a reduced risk of RA, while tea and coffee may be linked to an increased risk. Optimising dietary intake of certain food components may reduce RA risk, despite moderate-quality evidence. [ABSTRACT FROM AUTHOR]

The editorial discusses the urgent need to address sustainability challenges and climate change, highlighting the importance of materials like CaCO3 in mitigating these issues. Researchers explore the potential of CaCO3 in various applications, from carbon capture to construction materials, and even consider its use in extraterrestrial environments. The article emphasizes the incremental methodological improvements in materials science that are crucial for advancing scientific and technological achievements in the face of pressing global challenges. [Extracted from the article]

In calcified tissues such as bones and teeth, mineralization is regulated by an extracellular matrix, which includes non-collagenous proteins (NCP). This natural process has been adapted or mimicked to restore tissues following physical damage or demineralization by using polyanionic acids in place of NCPs, but the remineralized tissues fail to fully recover their mechanical properties. Here we show that pre-treatment with certain amphiphilic peptoids, a class of peptide-like polymers consisting of N-substituted glycines that have defined monomer sequences, enhances ordering and mineralization of collagen and induces functional remineralization of dentin lesions in vitro. In the vicinity of dentin tubules, the newly formed apatite nano-crystals are co-aligned with the c-axis parallel to the tubular periphery and recovery of tissue ultrastructure is accompanied by development of high mechanical strength. The observed effects are highly sequence-dependent with alternating polar and non-polar groups leading to positive outcomes while diblock sequences have no effect. The observations suggest aromatic groups interact with the collagen while the hydrophilic side chains bind the mineralizing constituents and highlight the potential of synthetic sequence-defined biomimetic polymers to serve as NCP mimics in tissue remineralization.

Objective DM with positive anti-melanoma differentiation-related gene 5 (MDA5) antibody is an autoimmune disease with multiple complications. Interstitial lung diseases (ILDs) are significantly associated with DM and are particularly related to MDA5+ DM. This article aims to explore potential molecular mechanisms and develop new diagnostic biomarkers for MDA5+ DM-ILD. Methods The series matrix files of DM and non-specific interstitial pneumonia (NSIP) were downloaded from the Gene Expression Omnibus (GEO) database to identify the differentially expressed genes (DEGs). Gene set enrichment analysis (GSEA) was used to screen the common enriched pathways related to DM and NSIP. Next, the co-expressed differential expressed genes (co-DEGs) between MDA5+, MDA5− and NSIP groups were identified by Venn plots, and then selected for different enrichment analyses and protein–protein interaction (PPI) network construction. The mRNA expression levels of IFN-beta and EIF2AK2 were measured by RT-qPCR. The protein expression levels of IFN-beta were measured by ELISA. Results Using GSEA, the enriched pathway 'herpes simplex virus 1 infection' was both up-regulated in DM and NSIP. Enrichment analysis in MDA5+ DM, MDA5− DM and NSIP reported that the IFN-beta signalling pathway was an important influencing factor in the MDA5+ DM-ILD. We also identified that eukaryotic translation initiation factor 2 alpha kinase 2 (EIF2AK2) was an important gene signature in the MDA5+ DM-ILD by PPI analysis. The expression levels of IFN-beta and EIF2AK2 were significantly increased in MDA5+ DM-ILD patients. Conclusions IFN-beta and EIF2AK2 contributed to the pathogenesis of MDA5+ DM-ILD, which could be used as potential therapeutic targets. [ABSTRACT FROM AUTHOR]