An unbiased transcriptomic analysis enhances understanding of inflammatory pathways and genes linked to TBM pathogenesis and mortality, identifying potential markers for poor prognosis or therapeutic targets.

Staphylococcus aureus NAD kinase promotes infection by protecting bacteria from host antimicrobial defenses and by supporting production of major virulence factors.

Immature hematopoietic cells from mice with a large segmental deletion found in human myeloid malignancies exhibit cardinal features of myelodysplastic syndrome.

The bacterial pathogen Listeria monocytogenes requires respiration for the maintenance of cellular redox homeostasis.

Cannabinoid receptors CNR1 and CNR2 play distinct roles in endometriosis pathogenesis, potentially contributing to disease initiation and progression through differential modulation of T cell function and the lesion microenvironment.

ESRP1 is central to intestinal barrier integrity in mice and humans and alterations in ESRP1 function or expression contribute to intestinal pathology, partly through modified expression of ESRP1-specific GPR137 isoforms.

Cross-species transcriptomic analysis and high-throughput behavioral assays in a Drosophila model of Huntington's disease show that downregulation of glial genes involved in synaptic function compensates for disease-related excitotoxicity.

The sickle cell trait strongly protects against not only retinopathy-positive cerebral malaria but also retinopathy-negative cerebral malaria, providing evidence that malarial parasites also contribute to retinopathy-negative cerebral malaria and are not innocent bystanders.

Structural and biophysical studies detail how Neisseria LbpB interacts with human lactoferrin for iron piracy and provides insight for how LbpB interacts with the antimicrobial peptide lactoferricin.

The interplay of the host metabolic reprogramming, its negative association with antiviral biological signaling pathways and the IFN-mediated host antiviral mechanism during Crimean–Congo hemorrhagic fever orthonairovirus (CCHFV) infection could provide attractive options for therapeutic intervention of CCHF.