actively inhibits the production of extracellular vesicles by human neutrophils.

is the etiologic agent of the plague. A hallmark of plague is subversion of the host immune response by disrupting host signaling pathways required for inflammation. This non-inflammatory environment permits bacterial colonization and has been shown to be essential for disease manifestation.

Multi-conflict islands are a widespread trend within Serratia spp.

Bacteria carry numerous anti-phage systems in "defense islands" or hotspots. Recent studies have delineated the content and boundaries of these islands in various species, revealing instances of islands that encode additional factors, including antibiotic resistance genes, stress genes, type VI secretion system (T6SS)-dependent effectors, and virulence factors. Our study identifies three defense islands in the Serratia genus with a mixed cargo of anti-phage systems, virulence factors, and different types of anti-bacterial modules, revealing a widespread trend of co-accumulation that extends beyond T6SS-dependent effectors to colicins and contact-dependent inhibition systems.

Molecular determinants of resurgent sodium currents mediated by Navβ4 peptide and A-type FHFs.

Introduction: Resurgent current ( ) generated by voltage-gated sodium channels (VGSCs) plays an essential role in maintaining high-frequency firing of many neurons and contributes to disease pathophysiology such as epilepsy and painful disorders. Targeting may present a highly promising strategy in the treatment of these diseases. Navβ4 and A-type fibroblast growth factor homologous factors (FHFs) have been identified as two classes of important mediators; however, their receptor sites in VGSCs remain unknown, which hinders the development of novel agents to effectively target .

The threat from ozone to vegetation in Ireland.

Ozone is the most damaging air pollutant to vegetation globally. Metrics of accumulated ozone above a concentration threshold (e.g.

Induction of astrocyte reactivity promotes neurodegeneration in human pluripotent stem cell models.

Reactive astrocytes are known to exert detrimental effects upon neurons in several neurodegenerative diseases, yet our understanding of how astrocytes promote neurotoxicity remains incomplete, especially in human systems. In this study, we leveraged human pluripotent stem cell (hPSC) models to examine how reactivity alters astrocyte function and mediates neurodegeneration. hPSC-derived astrocytes were induced to a reactive phenotype, at which point they exhibited a hypertrophic profile and increased complement C3 expression.