Comparison of transjugular intrahepatic portosystemic with endoscopic treatment plus anticoagulation for esophageal variceal bleeding and portal vein thrombosis in liver cirrhosis.

BACKGROUND AND AIM: The optimal management of esophageal variceal bleeding (EVB) and portal vein thrombosis (PVT) in liver cirrhosis has not been well-established. The aim of the present study was to compare the efficacy and safety of transjugular intrahepatic portosystemic shunt (TIPS) and endoscopic treatment (ET) plus anticoagulation in cirrhotic patients with EVB and PVT. PATIENTS AND METHODS: A total of 66 cirrhotic patients with PVT and EVB (31 in the TIPS group and 35 in the ET plus anticoagulation group) were evaluated retrospectively between January 2016 and January 2022. RESULTS: During the follow-up period, 85.5% of patients in the TIPS group achieved complete recanalization of the portal vein, as compared with 19.6% in the ET plus anticoagulation group (p < .001). The cumulative 5-year rate of variceal rebleeding in the TIPS group was significantly lower than that in the ET plus anticoagulation group (31.0 vs. 50.1%; p = .017). The TIPS group exhibited a significantly higher incidence of overt hepatic encephalopathy (HE) than the ET plus anticoagulation group (25.8 vs. 5.7%; p = .037). No difference in the 5-year survival rate (74.1 vs. 85.7%; p = .692) and probability of other complications was observed between the two groups. CONCLUSION: TIPS was superior to ET plus anticoagulation in preventing variceal rebleeding and achieving recanalization of PVT but increased the incidence of overt HE without improving the survival rate.

Sulfite induced degradation of sulfamethoxazole by a silica stabilized ZIF-67(Co) catalyst via non-radical pathways: Formation and role of high-valent Co(IV) and singlet oxygen.

The sulfite (S(IV))-based advanced oxidation process (AOP) has emerged as an appealing alternative to the traditional persulfate-based AOP for the elimination of organic contaminants from diverse water matrices. In this work, a silica reinforced ZIF-67(Co) catalyst (CZS) is fabricated, characterized and tested in the activation of S(IV) for the sulfamethoxazole (SMX) degradation. The prepared CZS demonstrates superior stability and catalytic ability for the degradation of SMX compared to ZIF-67(Co) across a broad pH range. Unlike the conventional radical-dominated oxidation systems, the CZS/S(IV) system for SMX degradation operates through a non-radical mechanism, featuring high-valent Co(IV) and singlet oxygen (1O2) as the predominated reactive species. The hydroxylated Co species exposed on the CZS surface is identified as the pivotal active site, realizing the S(IV) activation through a complexation-electron transfer process, resulting in the production of various reactive intermediates. Co(II) undergoes the conversion to Co(IV) by generated HSO5-, and 1O2 predominantly originates from the intermediate SO4•-. Profiting from the highly selective oxidation capacities of Co(IV) and 1O2, the established oxidative system demonstrates a remarkable interference resistance and exhibits an exceptional decontamination performance under real-world water conditions. In short, this work provides a sustainable S(IV)-based oxidation strategy for environmental remediation via non-radical mechanism.

Dietary fiber alleviates alcoholic liver injury via Bacteroides acidifaciens and subsequent ammonia detoxification.

The gut microbiota and diet-induced changes in microbiome composition have been linked to various liver diseases, although the specific microbes and mechanisms remain understudied. Alcohol-related liver disease (ALD) is one such disease with limited therapeutic options due to its complex pathogenesis. We demonstrate that a diet rich in soluble dietary fiber increases the abundance of Bacteroides acidifaciens (B. acidifaciens) and alleviates alcohol-induced liver injury in mice. B. acidifaciens treatment alone ameliorates liver injury through a bile salt hydrolase that generates unconjugated bile acids to activate intestinal farnesoid X receptor (FXR) and its downstream target, fibroblast growth factor-15 (FGF15). FGF15 promotes hepatocyte expression of ornithine aminotransferase (OAT), which facilitates the metabolism of accumulated ornithine in the liver into glutamate, thereby providing sufficient glutamate for ammonia detoxification via the glutamine synthesis pathway. Collectively, these findings uncover a potential therapeutic strategy for ALD involving dietary fiber supplementation and B. acidifaciens.

Mucosal-Associated Invariant T Cells in the Digestive System: Defender or Destroyer?

Mucosal-associated invariant T (MAIT) cells are a subset of innate T lymphocytes that express the semi-invariant T cell receptor and recognize riboflavin metabolites via the major histocompatibility complex class I-related protein. Given the abundance of MAIT cells in the human body, their role in human diseases has been increasingly studied in recent years. MAIT cells may serve as targets for clinical therapy. Specifically, this review discusses how MAIT cells are altered in gastric, esophageal, intestinal, and hepatobiliary diseases and describes their protective or pathogenic roles. A greater understanding of MAIT cells will provide a more favorable therapeutic approach for digestive diseases in the clinical field.

Interplay Between Liver Type 1 Innate Lymphoid Cells and NK Cells Drives the Development of Alcoholic Steatohepatitis.

BACKGROUND & AIMS: Liver contains high frequency of group 1 innate lymphoid cells (ILC), which are composed of comparable number of type 1 ILC (ILC1) and natural killer (NK) cells in steady state. Little is known about whether and how the interaction between ILC1 and NK cells affects the development of alcoholic liver disease. METHODS: A mouse model of chronic alcohol abuse plus single-binge (Gao-Binge model) was established. The levels of alanine aminotransferase/aspartate aminotransferase, hepatic lipid, and inflammatory cytokines or neutrophils were measured to evaluate the degree of liver injury, steatosis, and inflammation. Flow cytometric analysis, cell depletion, or adoptive transfer were used to interrogate the interaction between ILC1 and NK cells. RESULTS: Upon chronic alcohol consumption, NK cells, but not ILC1, underwent apoptosis, resulting in ILC1 dominance among group 1 ILC. Interleukin (IL) 17A expression was up-regulated, and increased IL17A was mainly derived from liver ILC1 after chronic alcohol feeding. Either depletion of ILC1 or neutralization of IL17A could significantly attenuate liver steatosis, inflammation, and injury in alcohol-fed mice. In contrast, normalization of the ILC1/NK cells ratio through NK cells transfer or expanding NK cells had a significant hepatoprotection against alcohol-induced steatohepatitis. Furthermore, NK cell-derived interferon gamma exerted a protective function via inhibiting IL17A production by liver ILC1 during alcoholic steatohepatitis. CONCLUSIONS: This is the first study showing that the interplay between liver ILC1 and NK cells occurs and drives the development of alcoholic steatohepatitis. Our findings support further exploration of liver ILC1 or NK cells as a therapeutic target for the treatment of alcohol-associated liver disease.

[Effect of Electroacupuncture Stimulation of "Guanyuan" (CV 4) and "Zusanli" (ST 36) on Spleen Lymphocytes Treg/Th 17 Immune Balance in Ulcerative Colitis Mice].

OBJECTIVE: To observe the effect of electroacupuncture (EA) intervention on spleen T-helper 17 (Th 17) and regulatory T (Treg) cell levels in mice with ulcerative colitis (UC), so as to reveal its mechanisms underlying improvement of UC. METHODS Kunming mice were randomized into control, UC model and EA groups, with 8 mice in each group. The UC model was established by giving the mice with 3% Dextran Sulfate Sodium (DSS) for 5 days. EA (15 Hz/25 Hz, 0.1-0.2 mA) was applied at "Guanyuan" (CV 4) and bilateral "Zusanli" (ST 36, used alternatively) for 10 min, once a day for 5 days. The animals' disease activity index [DAl, = (body weight index score + stool score + bleeding score)/3; 0-4 points] were calculated. The pathological changes of colon tissues were observed by light microscopy after H. E. stain, and spleen Treg (CD4⁺ CD²5⁺ Foxp³âº Treg) and Th 17 (CD³âº CD8⁺ IL-17⁺ Th 17) lymphocyte levels were determined by flow cytometry. RESULTS: Compared to the control group, the DAl score and the ratio of Th 17/CD8⁺ T cells were significantly increased, while the ratio of Treg/CD4⁺ T cells obviously decreased in the model group (P < 0.05). After EA intervention, the increased DAI score and the ratio of Th 17/CD8⁺ T cells and the decreased Treg/CD4⁺ T cells were reversed (P < 0.05), and the inflammatory cell infiltration degree of the colon tissue was attenuated. CONCLUSION: EA intervention can improve the, UC rats' symptoms of activity state, bloody or viscidity stool and colonic inflammation, probably by regulating the balance between the spleenic Treg and Th 17 lymphocytes.