Genome-wide identification and functional analysis of dysregulated alternative splicing profiles in sepsis.

Background: An increasing body of evidence now shows that the long-term mortality of patients with sepsis are associated with various sepsis-related immune cell defects. Alternative splicing (AS), as a sepsis-related immune cell defect, is considered as a potential immunomodulatory therapy target to improve patient outcomes. However, our understanding of the role AS plays in sepsis is currently insufficient.

[Research progress of T cell immunoglobulin mucin molecule 1 in the pathogenesis of sepsis].

Sepsis 3.0 is defined as a life-threatening organ dysfunction caused by the host' uncontrol response to infection, with poor prognosis, high morbidity and fatality. Sepsis is one of the main causes of death in severe patients.

Downregulation of miR-155 attenuates sepsis-induced acute lung injury by targeting SIRT1.

Sepsis-induced acute lung injury (ALI) characterized by devastating hyperinflammatory response in the lungs is the ultimate cause of high mortality and mobility in septic patients. miR-155 was reported to be significantly upregulated in sepsis-induced ALI cases and alleviated inflammation in septic lung injury in mouse and cell models. However, the detailed role of miR-155 and its underlying mechanism in sepsis-associated ALI remain to be further explored.

[The initial CT findings in patients suffering from invasive pulmonary aspergillosis].

Objective: To approach the initial CT findings of invasive pulmonary aspergillosis (IPA) in patients with immunosuppression.

Methods: All consecutive adult patients who met the diagnostic criteria of the 2008 European Organization for Research and Treatment of Cancer/ Mycoses Study Group (EORTC/MSG) for proven or probable IPA were included as of January 2005 to June 2011. The patients were divided into two groups according to patients with or without hematological malignancy.