Intriguingly, CD133 expression was strongly related with the survival of BA patients (p = 0.0061), but not with age at Kasai procedure (p = 0.36) and the presence of cirrhosis (p = 0.77).
Unbiased genome-wide association study identified variants in/near PNPLA3 and HFE, and candidate variant analysis identified variants in/near TM6SF2, MBOAT7, SERPINA1, HSD17B13, STAT4, and IFNL4 that reproducibly affected cirrhosis.
Routine laboratory markers were determined by standard methods.<b>Results</b>: The Apa1 CC genotype was more frequent (75%) in HCC than in the cirrhosis (35%) and control (20%) groups (<i>P</i><0.0001).
PHB1 located in the nucleus, cytoplasm and the mitochondrial inner membrane has anti-oxidative stress and anti-inflammatory effects in hepatitis and cirrhosis, which can protect liver cells from damage caused by inflammatory factors and reactive oxygen species (ROS) stimulation.
This study aims to investigate the effect of GA in activating PXR and improving associated tight junction integrity and reducing bacterial translocation in gut-liver axis of CCl<sub>4</sub> induced cirrhosis model.
Decreased hepatic FATP5 expression in NAFLD is linked to histological progression, and may be associated with hepatic fat loss during NASH progression to cirrhosis.
Clinical studies on Se or SELENOP in NAFLD are conflicting, apart from those in advanced liver disease (cirrhosis or hepatocellular carcinoma), in which lower circulating Se and SELENOP are constant findings.
PSMP expression was studied in patients with fibrosis/cirrhosis and in 3 murine models of liver fibrosis, including mice treated with carbon tetrachloride (CCl<sub>4</sub>), bile-duct ligation, or a 5-diethoxycarbonyl-1,4-dihydrocollidine diet.
At 24 weeks, HF-CDAA mice developed signs of cirrhosis with 10-fold HYP increase, regenerative nodules, portal hypertension and elevated serum bilirubin and ammonia; 80% of mice (8/10) developed multiple hepatocellular carcinomas (HCC).
Most of these alterations are reversible <i>ex vivo</i> with TLR7/8 agonists (CL097, R848), raising the possibility that these agonists might be used in the future to restore neutrophil antibacterial functions in patients with cirrhosis.
Outcome variables were: a) liver fibrosis (Metavir score) [fibrosis stage (F0, F1, F2, F3 and F4) and advanced fibrosis and cirrhosis (F ≥ 3 and F4, respectively)]; b) non-invasive indexes [FIB-4, APRI, and their cut-offs (FIB-4 ≥ 3.25 and APRI≥1.5)]; c) inflammation-related biomarkers (leptin, HGF, NGF, sFasL, sFas, MIF, HA, Ang-2, TIMP1, MMP1 and MMP2).
Hence, this review summarizes recent progress in studies on TRAIL, including its role in apoptotic signaling, potential therapeutic applications of TRAIL in HCC, hepatitis virus infection, and liver fibrosis and cirrhosis.
Twenty-five HILI cases with pre-existing alcoholic liver disease (ALD) or non-alcoholic fatty liver disease (NAFLD) and 200 ALD or NAFLD controls matched 1:8 for sex, age (±4 years old), body mass index (±2 kg/m<sup>2</sup>), the type of CLD, alcohol intake (±5 g/d) and the presence or absence of cirrhosis.
RT‑PCR demonstrated that the mRNA expression levels of IGF2R were downregulated in HCC compared with in TST samples (P=0.004), which was associated with a worse recurrence‑free survival of patients with HCC (P=0.002) and a lower occurrence of cirrhosis (P=0.05).
When samples were grouped according to the serum level of AKR1B10 (≥232.7pg/ml), serum AKR1B10 positively correlated to serum AFP (χ<sup>2</sup>=6.295, P=0.012), ALT (χ<sup>2</sup>=18.803, P=0.000), AST (χ<sup>2</sup>=33.421, P=0.000), tumor nodule number (χ<sup>2</sup>=6.777, P=0.009), cirrhosis (χ<sup>2</sup>=43.458, P=0.000), and tumor size (χ<sup>2</sup>=6.042, P=0.014) in the Chi-square test.
Outcome variables were: a) liver fibrosis (Metavir score) [fibrosis stage (F0, F1, F2, F3 and F4) and advanced fibrosis and cirrhosis (F ≥ 3 and F4, respectively)]; b) non-invasive indexes [FIB-4, APRI, and their cut-offs (FIB-4 ≥ 3.25 and APRI≥1.5)]; c) inflammation-related biomarkers (leptin, HGF, NGF, sFasL, sFas, MIF, HA, Ang-2, TIMP1, MMP1 and MMP2).