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that the oncolytic activity of NDV/HK84 was dependent on the activation of type I interferon signaling.The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide, reflecting the current epidemics of obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome. NAFLD is characterized by the accumulation of fat in the liver, and is known to be a cause of cirrhosis. Although many pathways have been proposed, the cause of NAFLD-linked fibrosis progression is still unclear, which posed challenges for the development of new therapies to prevent NASH-related cirrhosis and hepatocellular carcinoma. Cirrhosis is associated with activation of hepatic stellate cells (HSC) and accumulation of excess extracellular matrix proteins, and inhibiting the activation of HSCs would be expected to slow the progression of NAFLD-cirrhosis. Multiple molecular signals and pathways such as oxidative stress and glutaminolysis have been reported to promote HSC activation. Crenigacestat Both mechanisms are plausible antifibrotic targets in NASH, as the activation of HSCs the proliferation of myofibroblasts depend on those processes. This review summarizes the role of the glutaminolysis-ammonia-urea cycle axis in the context of NAFLD progression, and shows how the axis could be a novel therapeutic target.
Although activation of hepatic stellate cells (HSCs) plays a central role in the development of liver fibrosis, the mechanism underlying the activation of HSCs remains unclear. Keratin 17 (KRT17), a member of the intermediate filament family, can regulate tumor cell proliferation and migration. The current study aimed to elucidate the role of KRT17 in the activation of HSCs and the mechanisms underlying liver fibrosis.

The expression of KRT17 was determined using immunohistochemistry in tissue microarray. Western blotting and qRT-PCR assays were used to determine the KRT17 expression in fibrotic liver tissues obtained from human subjects and mice. LX-2 cells were treated with TGF-β1 recombinant protein and adipocyte differentiation mixture (MDI) mix to induce and reverse LX-2 cell activation, respectively, in order to explore the correlation between KRT17 and HSC activation. Additionally, cell proliferation and migration abilities of LX-2 cells transfected with KRT17-overexpressing plasmid or small interfreatment of liver fibrosis.Non-alcoholic fatty liver disease (NAFLD) is closely related to insulin resistance, type 2 diabetes mellitus and obesity. It is considered a multisystem disease and there is a strong association with cardiovascular disease and arterial hypertension, which interfere with changes in the coagulation system. Coagulation disorders are common in patients with hepatic impairment and are dependent on the degree of liver damage. Through a review of the literature, we consider and discuss possible disorders in the coagulation cascade and fibrinolysis, endothelial dysfunction and platelet abnormalities in patients with NAFLD.
Long non-coding RNA small nucleolar RNA host genes (SNHGs) play a critical role in the occurrence and development of tumors. In this study, we aimed to investigate the role of
in hepatocellular carcinoma (HCC) and its underlining mechanism.

Datasets were acquired from The Cancer Genome Atlas (TCGA) database. lncLocator 2.0 was used to identify the distribution of
in HCC cells. Gene expression, Kaplan-Meier survival, microRNA and transcription factor target analyses were performed with the University of Alabama Cancer (UALCAN) Database, Kaplan-Meier Plotter, LinkedOmics, WebGestalt and gene set enrichment analysis, respectively. Gene Ontology and pathway enrichment analyses and assessment of RNA binding proteins were performed by R software, circlncRNAnet and Encyclopedia of RNA Interactomes (ENCORI). In addition, CirclncRNAnet and ENCORI were used to find the correlation between
and important proteins, while the prognostic value was assessed with the Human Protein Atlas database and Kaplan-Meier Plotter.

Expression of
in HCC is higher in HCC tissue than in normal healthy liver tissues and is mainly distributed in the nucleus.
positively correlated with poor prognosis (
<0.01 for overall survival and recurrence-free survival). Functional enrichment analysis revealed
involvement with regulation of ribosomal RNA synthesis and the RNA processing and surveillance pathway.
is closely associated with miR-154 and miR-206, transcription factor target E2F family and the signaling pathway for MAPK/ERK and mTOR. U2 auxiliary factor 2 (U2AF2) showed strong correlation with
, while low-expression of U2AF2 showed good prognosis.

Based on our findings, we infer
may play a role in the formation of HCC via regulation of tumor-related pathways.
Based on our findings, we infer SNHG4 may play a role in the formation of HCC via regulation of tumor-related pathways.
Irreversible electroporation (IRE) is an emerging local ablation therapy which may be effective for unresectable tumors. This study aimed to evaluate the safety and efficacy of percutaneous IRE in the treatment of hepatocellular carcinoma (HCC) abutting the diaphragm.

A total of 26 participants with 39 tumors abutting the diaphragm were prospectively evaluated between July 2015 and September 2018. Complications associated with IRE were recorded, and the survival benefit of IRE was analyzed. The factors associated with time to local tumor progression (LTP) were analyzed using univariate and multivariate Cox regression models.

No major complications or treatment-related deaths occurred. The technical success rate was 96.2% (25/26) and complete ablation rate was 92.3% (36/39). The median follow-up period was 16.7 months (range 3.0-43.0 months), the LTP occurred in 15.2% of tumors and median time to LTP was 20.4 months. Overall, tumor size (hazard ratio 1.24 [95% confidence interval 0.38, 3.81],
=0.03) was the only factor associated with time to LTP.

This study shows for the first time that percutaneous IRE is a safe and effective ablation technology for HCC abutting the diaphragm.
This study shows for the first time that percutaneous IRE is a safe and effective ablation technology for HCC abutting the diaphragm.
Chronic kidney disease (CKD) usually occurs during the chronic infection of hepatitis B virus (HBV). However, the risk factors of CKD in an HBV population have not been completely demonstrated. Our present study aimed to investigate the risk factors of CKD in chronic HBV infection using a hospital based cross-sectional study in the northern area of China.

During January 2013 to December 2017, a total of 94 patients with CKD complicated by chronic HBV infection were consecutively enrolled in the study, as well as 548 age- and sex-matched hepatitis B patients without CKD who were enrolled as controls. Univariate and multivariate regression analyses were used to determine the effects of each variable after adjusting for cofounding factors.

Multivariate analysis showed that HBeAg-positive status (odds ratio [OR]=2.099, 95% CI 1.128-3.907), dyslipidemia (OR 3.025, 95% CI 1.747-5.239), and hypertension (OR 12.523, 95% CI 6.283-24.958) were independently associated with the incidence of CKD, while duration of HBV infection (≥240 months) (OR 0.401, 95% CI 0.179-0.894), Log
HBsAg (OR 0.514, 95% CI 0.336-0.786), and coronary heart disease (OR 0.078, 95% CI 0.008-0.768) were protective factors for the incidence of CKD. Duration of HBV infection, Log
HBsAg, HBeAg-positive status and dyslipidemia remained the risk factors for CKD after adjusting for diabetes mellitus, hypertension, and coronary heart disease.

Duration of HBV infection, Log
HBsAg, HBeAg-positive status and dyslipidemia contributed to the incidence of CKD during chronic HBV infection in a Chinese population.
Duration of HBV infection, Log10 HBsAg, HBeAg-positive status and dyslipidemia contributed to the incidence of CKD during chronic HBV infection in a Chinese population.
Previous studies have reported that the single nucleotide polymorphisms (SNPs) of
and
are associated with nonalcoholic fatty liver disease (NAFLD). However, no studies have examined the effect of interactions between these three genotypes to affect liver disease severity. We assessed the effect of these three SNPs on nonalcoholic steatohepatitis (NASH) and also examined the gene-gene interactions in a Chinese population with biopsy-confirmed NAFLD.

We enrolled 415 consecutive adult individuals with biopsy-proven NAFLD. Multivariable logistic regression analysis was undertaken to test associations between NASH and SNPs in
and
. Gene-gene interactions were analyzed by performing a generalized multifactor dimensionality reduction (GMDR) analysis.

The mean ± standard deviation age of these 415 patients was 41.3±12.5 years, and 75.9% were men. Patients with
TT,
AA or
GG genotypes had a higher risk of NASH, even after adjustment for age, sex and body mass index. GMDR analysis showed that the combination of all three SNPs was the best model for predicting NASH. Additionally, the odds ratio of the haplotype T-A-G for predicting the risk of NASH was nearly three times higher than that of the haplotype G-C-C.

NAFLD patients carrying the
TT,
AA or
GG genotypes are at greater risk of NASH. These three SNPs may synergistically interact to increase susceptibility to NASH.
NAFLD patients carrying the SAMM50-rs738491 TT, PARVB-rs5764455 AA or PNPLA3-rs738409 GG genotypes are at greater risk of NASH. These three SNPs may synergistically interact to increase susceptibility to NASH.
Gallbladder polyp (GBP) assessment aims to identify the early stages of gallbladder carcinoma. Many studies have analyzed the risk factors for malignant GBPs. In this retrospective study, we aimed to establish a more accurate predictive model for potential neoplastic polyps in patients with GBPs.

We developed a nomogram-based model in a training cohort of 233 GBP patients. Clinical information, ultrasonographic findings, and blood test findings were analyzed. Mann-Whitney U test and multivariate logistic regression analyses were used to identify independent predictors and establish the nomogram model. An internal validation was conducted in 225 consecutive patients. Performance and clinical benefit of the model were evaluated using receiver operating characteristic curves and decision curve analysis (DCA), respectively.

Age, cholelithiasis, carcinoembryonic antigen, polyp size, and sessile shape were confirmed as independent predictors of GBP neoplastic potential in the training group. Compared with five other proposed prediction methods, the established nomogram model presented better discrimination of neoplastic GBPs in the training cohort (area under the curve [AUC] 0.846) and the validation cohort (AUC 0.835). DCA demonstrated that the greatest clinical benefit was provided by the nomogram compared with the other five methods.

Our developed preoperative nomogram model can successfully be used to evaluate the neoplastic potential of GBPs based on simple clinical variables that maybe useful for clinical decision-making.
Our developed preoperative nomogram model can successfully be used to evaluate the neoplastic potential of GBPs based on simple clinical variables that maybe useful for clinical decision-making.
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