Abstract: Aspects of the present technology comprise a positioning and stabilising structure to hold a seal-forming structure in a therapeutically effective position on a head of a patient. The seal-forming structure may be constructed and arranged to form a seal with a region of the patient's face surrounding an entrance to the patient's airways for sealed delivery of a flow of air at a therapeutic pressure of at least 4 cmH2O with respect to ambient air pressure throughout the patient's respiratory cycle in use. The positioning and stabilising structure may comprise at least one gas delivery tube to deliver the flow of air to the entrance of a patient's airways via the seal-forming structure. The positioning and stabilising structure may comprise an adjustment mechanism for adjustment of a length of the at least one gas delivery tube to enable the positioning and stabilising structure to fit different size heads.

Abstract: Sustained hepatic and systemic inflammation, in particular originating from monocyte/macrophages, is a driving force for chronic liver disease progression to cirrhosis and underlies the development of multiorgan failure. Therefore, reprogramming mono-cyte/macrophage phenotype has emerged as an interesting strategy to limit inflammation during chronic liver injury. The inventors report here that a non-canonical form of autophagy, LC3-associated phagocytosis (LAP), is endogenously enhanced in blood and liver monocytes from cirrhotic patients and is negatively correlated to the levels of inflammatory markers in these patients. Pharmacological inhibition of LAP components or genetic disruption of LAP (Rubicon-deficient mice in myeloid cells), exacerbates the inflammatory signature in isolated human cirrhotic monocytes and the hepatic inflammatory profile in mice with chronic liver injury, resulting in enhanced liver fibrosis.

Abstract: Persistent inflammation is a driving force of fibrosis progression. Mucosal-Associated Invariant T (MAIT) cells are non-conventional T cells that display altered functions during chronic inflammatory diseases. Here, the inventors report a loss of circulating MAIT cells in cirrhotic patients and their hepatic accumulation in an activated phenotype within the fibrotic septa. Using two models of chronic liver injury, the inventors demonstrate that mice enriched in MAIT cells (V?19TCRTg) show exacerbated liver fibrosis and higher number of hepatic fibrogenic cells than wild type counterparts, whereas MAIT cell-deficient mice (MR1?/?mice) are resistant. The results highlight the profibrogenic functions of MAIT cells and suggest that 1 targeting MAIT cells may constitute an attractive antifibrogenic strategy during chronic liver injury.

Abstract: The present invention relates to methods for predicting the survival time of patients with decompensated alcoholic cirrhosis. In particular, the present invention relates to a method for predicting the survival time of a patient with decompensated alcoholic cirrhosis comprising i) determining the expression level of OAS2 or MX2 in a sample of peripheral blood mononuclear cells obtained from the patient, ii) comparing the level determined at step i) with a predetermined reference value and iii) and concluding that the patient will have a short survival time when the level determined at step i) is higher than its predetermined reference value or concluding that the patient will have a long survival time when the level determined at step i) is lower than the predetermined reference value.

Abstract: The present invention relates to methods for predicting the survival time of patients with decompensated alcoholic cirrhosis. In particular, the present invention relates to a method for predicting the survival time of a patient with decompensated alcoholic cirrhosis comprising i) determining the expression level of OAS2 or MX2 in a sample of peripheral blood mononuclear cells obtained from the patient, ii) comparing the level determined at step i) with a predetermined reference value and iii) and concluding that the patient will have a short survival time when the level determined at step i) is higher than its predetermined reference value or concluding that the patient will have a long survival time when the level determined at step i) is lower than the predetermined reference value.