Chronic high-fat diet induces galectin-3 and TLR4 to activate NLRP3 inflammasome in NASH.

NOD-like receptor protein 3 (NLRP3) inflammasome activation triggers inflammation progression in some metabolism disorders, frequently accompanying the up-regulation of galectin-3 (Gal-3). However, the precise mechanisms of Gal-3 activating NLRP3 inflammasome remain unclear in nonalcoholic steatohepatitis (NASH). Here, male C57BL/6J mice were fed by high-fat diet (HFD) for 32 weeks to induce NASH and then the hepatic damage, cytokines, Gal-3 and TLR4 expression, and NLRP3 inflammasome activation were examined.

Case Report: "Area of Focus" Atypical Trichinellosis and Fascioliasis Coinfection.

Parasitic co-infection is commonly observed in natural populations, yet rare in the laboratory. Multiparasitism can have negative effects on the host, ranging from the atypical manifestations to increased mortality, consequently, it may be misdiagnosed and treated with unsuitable anthelmintic medicines. Therefore, reliable diagnosis is critical for appropriate treatment of parasitic co-infection.

Twelve-Month Systemic Consequences of Coronavirus Disease 2019 (COVID-19) in Patients Discharged From Hospital: A Prospective Cohort Study in Wuhan, China.

Background: Follow-up study of coronavirus disease 2019 (COVID-19) survivors has rarely been reported. We aimed to investigate longitudinal changes in the characteristics of COVID-19 survivors after discharge.

Methods: A total of 594 COVID-19 survivors discharged from Tongji Hospital in Wuhan from February 10 to April 30, 2020 were included and followed up until May 17, 2021.

CAPRL Scoring System for Prediction of 30-day Mortality in 949 Patients with Coronavirus Disease 2019 in Wuhan, China: A Retrospective, Observational Study.

Background: Coronavirus disease 2019 (COVID-19) is a serious and even lethal respiratory illness. The mortality of critically ill patients with COVID-19, especially short term mortality, is considerable. It is crucial and urgent to develop risk models that can predict the mortality risks of patients with COVID-19 at an early stage, which is helpful to guide clinicians in making appropriate decisions and optimizing the allocation of hospital resoureces.

Clinical characteristics and risk factors of liver injury in COVID-19: a retrospective cohort study from Wuhan, China.

Background: Coronavirus disease 2019 (COVID-19) has rapidly become a major international public health concern. This study was designed to evaluate the clinical characteristics and risk factors of COVID-19-associated liver injury.

Methods: A fraction of 657 COVID-19 patients were retrospectively analyzed.

FKBP12 is a predictive biomarker for efficacy of anthracycline-based chemotherapy in breast cancer.

Background: FK506-binding protein 12 (FKBP12) is abundant, ubiquitously expressed cytoplasmic protein with multiple functions in cell signaling transduction. Recently, we reported a novel function for FKBP12 in oncoprotein mouse double minute 2 (MDM2) self-ubiquitination and degradation, which greatly enhanced the sensitivity of cancer cells to chemotherapy. However, the clinical relevance remains unclear.

Salidroside Inhibits Lipopolysaccharide-ethanol-induced Activation of Proinflammatory Macrophages via Notch Signaling Pathway.

Activation of macrophages is a key event for the pathogenesis of various inflammatory diseases. Notch signaling pathway recently has been found to be a critical pathway in the activation of proinflammatory macrophages. Salidroside (Sal), one of main bioactive components in Rhodiola crenulata (Hook.

Quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy.

Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks.

The Relationship between Serum Bilirubin and Elevated Fibrotic Indices among HBV Carriers: A Cross-Sectional Study of a Chinese Population.

The study probed the association between bilirubin and hepatitis B virus (HBV) infection and progression. A cross-sectional analysis of 28,500 middle aged and elderly Chinese participants was performed to analyze the differences of bilirubin in terms of hepatitis B surface antigen (HBsAg) positive or negative and the correlation between bilirubin and severity of hepatic fibrosis estimated by non-invasive indices. Bilirubin was significantly higher in the HBsAg (+) group than the HBsAg (-) group.

Quercetin prevents ethanol-induced iron overload by regulating hepcidin through the BMP6/SMAD4 signaling pathway.

Emerging evidence has demonstrated that chronic ethanol exposure induces iron overload, enhancing ethanol-mediated liver damage. The purpose of this study was to explore the effects of the naturally occurring compound quercetin on ethanol-induced iron overload and liver damage, focusing on the signaling pathway of the iron regulatory hormone hepcidin. Adult male C57BL/6J mice were pair-fed with isocaloric-Lieber De Carli diets containing ethanol (accounting for 30% of total calories) and/or carbonyl iron (0.

Quercetin attenuates chronic ethanol hepatotoxicity: implication of "free" iron uptake and release.

Emerging evidence has displayed that oxygen free radicals especially ones promoted by "free" iron play an important role in the development of alcoholic liver disease (ALD). Naturally-occurring quercetin has been reported to prevent ALD and iron overload-induced damage aside from the "free" iron. The purpose was to explore the potential mechanisms by which quercetin arrests alcohol-induced "free" iron disorder.

Carbon monoxide alleviates ethanol-induced oxidative damage and inflammatory stress through activating p38 MAPK pathway.

Stress-inducible protein heme oxygenase-1(HO-1) is well-appreciative to counteract oxidative damage and inflammatory stress involving the pathogenesis of alcoholic liver diseases (ALD). The potential role and signaling pathways of HO-1 metabolite carbon monoxide (CO), however, still remained unclear. To explore the precise mechanisms, ethanol-dosed adult male Balb/c mice (5.

Bilirubin participates in protecting of heme oxygenase-1 induction by quercetin against ethanol hepatotoxicity in cultured rat hepatocytes.

To attenuate alcohol liver disease (ALD) is extremely urgent since ALD has been emerged as a major liver disease. The aim of the present study is to investigate the hepatoprotective effect against ethanol-induced injury of bilirubin, a product of heme metabolism degradation via HO and biliverdin reductase catalysis. Ethanol-incubated primary rat hepatocytes (100 mmol/L) were treated by quercetin, bilirubin, inflammatory factors, and/or HO-1 inducer/inhibitor for 24 h, and the cellular damage was assayed.

Role of MexA-MexB-OprM efflux pump system in chronic Pseudomonas aeruginosa pulmonary infection in mice.

In order to investigate the role of the MexA-MexB-OprM efflux pump system in the pathogenesis of Pseudomonas aeruginosa (PA)-induced pulmonary infection, pulmonary infection models were established by intratracheal injection of K767 (wild type), nalB (MexA-MexB-OprM up-regulated mutant), and ΔmexB (knockout) strains, separately. All mice were treated with Meropenem (intraper Δ itoneal injection, 100 mg/kg body weight, twice every day), and strain-related pathology, bacteria count, cytokine level, myeloperoxidase (MPO, indicator of neutrophil recruitment) activity, and macrophage inflammatory protein-2 (MIP-2) expression were evaluated at early (3rd day post-infection) and late (7th and 14th day post-infection) stages of infection. E-test showed that ΔmexB was more significantly Δ sensitive to panipenan (ETP), meropenem (MP) and imipenem (IP) than K767 and nalB strains.

Quercetin prevents ethanol-induced dyslipidemia and mitochondrial oxidative damage.

Lipid metabolism disorder and oxidative stress play an important role on the development and progression of alcoholic liver disease (ALD), and mitochondria compartment is presumed as the main source and susceptible target of intracellular ROS. The objective of this study was to evaluate the protective effect of quercetin, a naturally occurring flavonoids possessing both antioxidant and hypolipidemic effect, on ethanol-induced dyslipidemia and oxidative damage focused on mitochondria. Chronic alcohol administration for adult male rats (4.

Immunostaining of PD-1/PD-Ls in liver tissues of patients with hepatitis and hepatocellular carcinoma.

Aim: To investigate the expression of programmed death (PD)-1, PD ligand 1 (PD-L1) and PD-L2 in liver tissues in the context of chronic hepatitis and hepatocellular carcinoma (HCC).

Methods: Liver biopsies and HCC specimens from patients were collected and histologically examined. The expression of PD-1, PD-L1, and PD-L2 in biopsy specimens of chronic hepatitis and HCC specimens was evaluated by immunohistochemical staining.

Glycogen synthase kinase 3beta induces apoptosis in cancer cells through increase of survivin nuclear localization.

Glycogen synthase kinase 3beta (GSK3beta) regulates numerous signaling pathways that control a wide range of cellular processes, including cell proliferation, differentiation, apoptosis and metabolism. We report a novel function of GSK3beta: It interacts with the inhibitor-of-apoptosis protein (IAP) survivin to modulate its expression, thus regulating apoptosis in human lung cancer cells. A co-immunoprecipitation assay revealed that GSK3beta can bind survivin.