Sepsis is a life-threatening syndrome driven by a dysregulated host response to infection, with endothelial dysfunction and glycocalyx disruption playing central roles in vascular failure. Despite growing recognition of the glycocalyx as a therapeutic target, its temporal dynamics and potential pharmacological modulation remain poorly understood. We performed a translational study combining longitudinal clinical observations in septic patients with mechanistic investigations in a murine cecal...

CONCLUSION: Primary candidemia accounts for a substantial proportion of cases and is associated with high 7-day mortality. The predominance of C. albicans and N. glabratus, common gut colonisers, supports gastrointestinal translocation as a potential source. Delayed diagnosis, particularly of N. glabratus, highlights the need for appropriate empirical therapy and rapid diagnostic tools.

CONCLUSION: Lower baseline CD(4) ^(+) T lymphocyte count, HIV infection through homosexual transmission, use of DTG + 3TC + TDF as a second-line regimen, hepatitis B co-infection or HCV seropositivity, and the presence of specific resistance-associated mutations were associated with a higher hazard of LLV and VF. Therefore, enhanced monitoring of resistance markers and immunological indicators is warranted among patients receiving second-line ART to facilitate timely clinical evaluation and...

Sepsis is accompanied by extensive expansion and remodeling of the myeloid compartment, yet a dysfunctional circulating phenotype does not by itself reveal where that dysfunction arose. Immature markers, low-density fractions, HLA-DR-low phenotypes, transcriptional clusters, and direct T-cell suppression describe different biological levels and carry different mechanistic implications. This review examines sepsis-associated myeloid dysfunction as a source-attribution problem across a...