Bile acid homeostasis and intestinal dysbiosis in alcoholic hepatitis

For the prediction of liver ‐ related death the number of events at 10 years was too small (n = 7) for any conclusion. Therefore, the primary aim was to assess the prognostic value

Philippe Boudou, Michel Djibré, Fidaa Ibrahim, Soraya Fellahi, Patrick Gilon, Fabrizio Andreelli, Pascal Ferré, Mathieu Boissand. To cite

To overcome the intrinsic limitations of classical Genome-wide association studies (GWAS) involving univariate tests between statistically dependent markers, we have proposed in

In order to gain insight into the main drivers of gene expression that could result in the devel- opment of hepatocellular failure in AH, we analyzed the predicted activity

19 It has been shown that the IL-33/ST2 pathway attenuates sepsis in the spe- ci fi c setting of infection without liver impairment by enhancing neutrophil in fl ux to the site

Patients: Ninety-three patients with compensated or decompensated cirrhosis (CLF group) but stable liver function and 30 patients with cirrhosis and hospitalized for the management

The ratio between protein expression of laminin and that of fibronectin was extremely high in AH compared with that in alcoholic cirrhosis and normal controls (figure 6B),

TGR5 de fi ciency induced dys- biosis, independently of alcohol intake, and transplantation of the TGR5-KO intestinal microbiota to WT mice was suf fi cient to worsen