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Objective: To investigate the clinical potential and safety of Moluodan to reverse gastric precancerous lesions. Methods: Patients aged 18–70 years diagnosed with moderate‐to‐severe atrophy and/or moderate‐to‐severe intestinal metaplasia, with or without low‐grade dysplasia, and negative for Helicobacter pylori were recruited in this randomized, double‐blind, parallel‐controlled trial. The primary outcome was the improvement of global histological diagnosis at 1‐year follow‐up endoscopy using the operative link for gastritis assessment, the operative link for gastric intestinal metaplasia assessment, and the disappearance rate of dysplasia. Results: Between November 3, 2017 and January 27, 2021, 166 subjects were randomly assigned to the Moluodan group, 168 to the folic acid group, 84 to the combination group, and 84 to the high‐dose Moluodan group. The improvement in global histological diagnosis was achieved in 60 (39.5%) subjects receiving Moluodan, 59 (37.8%) receiving folic acid, 26 (32.1%) receiving the combined drugs, and 36 (47.4%) receiving high‐dose Moluodan. Moluodan was non‐inferior to folic acid (95% confidence interval: −9.2 to 12.5; P = 0.02). High‐dose Moluodan had a trend for better protective efficacy, though there was no statistical significance. The disappearance rate of dysplasia was 82.8% in the Moluodan group, which was superior to folic acid (53.9%; P = 0.006). No drug‐related serious adverse events were observed. Conclusions: One pack of Moluodan three times daily for 1 year was safe and effective in reversing gastric precancerous lesions, especially dysplasia. Doubling its dose showed a better efficacy trend. [ABSTRACT FROM AUTHOR]

Understanding the zoonotic origin and evolution history of SARS-CoV-2 will provide critical insights for alerting and preventing future outbreaks. A significant gap remains for the possible role of pangolins as a reservoir of SARS-CoV-2 related coronaviruses (SC2r-CoVs). Here, we screened SC2r-CoVs in 172 samples from 163 pangolin individuals of four species, and detected positive signals in muscles of four Manis javanica and, for the first time, one M. pentadactyla . Phylogeographic analysis of pangolin mitochondrial DNA traced their origins from Southeast Asia. Using in-solution hybridization capture sequencing, we assembled a partial pangolin SC2r-CoV (pangolin-CoV) genome sequence of 22 895 bp (MP20) from the M. pentadactyla sample. Phylogenetic analyses revealed MP20 was very closely related to pangolin-CoVs that were identified in M. javanica seized by Guangxi Customs. A genetic contribution of bat coronavirus to pangolin-CoVs via recombination was indicated. Our analysis revealed that the genetic diversity of pangolin-CoVs is substantially higher than previously anticipated. Given the potential infectivity of pangolin-CoVs, the high genetic diversity of pangolin-CoVs alerts the ecological risk of zoonotic evolution and transmission of pathogenic SC2r-CoVs.

Aim: To investigate the role of calmodulin-dependent protein kinase II (CaMKII) in colon cancer growth, migration and invasion., Methods: CaMKII expression in colon cancer and paracancerous tissues was evaluated via immunochemistry. Transcriptional and posttranscriptional levels of CaMKIIin tissue samples and MMP2, MMP9 and TIMP-1 expression in the human colon cancer cell line HCT116 were assessed by qRT-PCR and western blot. Cell proliferation was detected with the MTT assay. Cancer cell migration and invasion were investigated with the Transwell culture system and wound-healing assay., Results: We first demonstrated that CaMKII was over-expressed in human colon cancers and was associated with cancer differentiation. In the human colon cancer cell line HCT116, the CaMKII-specific inhibitor KN93, but not its inactive analogue KN92, decreased cancer cell proliferation. Furthermore, KN93 also significantly prohibited HCT116 cell migration and invasion. The specific inhibition of ERK1/2 or p38 decreased the proliferation and migration of colon cancer cells., Conclusion: Our findings highlight CaMKII as a potential critical mediator in human colon tumor development and metastasis., Competing Interests: Conflict-of-interest statement: The authors have no relevant conflicts of interest to disclose.

The aim of the present study was to investigate the effects of 2,3,4',5-tetrahydroxystilbene-2-O-beta-D-glucoside, an active component extracted from Polygonum multiflorum, on pressure overload-induced cardiac remodeling in rats. A rat model with cardiac remodeling was induced by abdominal aortic banding. 2,3,4',5-Tetrahydroxystilbene-2-O-beta-D-glucoside (30, 60, 120 mg/kg/day) was administered 3 days after abdominal aortic banding and continued for 30 days. The abdominal aortic banding-treated rats had significantly elevated blood pressure, left ventricular hypertrophy, and myocardial fibrosis. Left ventricular hypertrophy was characterized by an increase in the ratios of the heart and left ventricular weights to body weight, and increased myocyte cross-sectional areas, hypertrophic ventricular septum, and left ventricular posterior wall. The accumulation of myocardial interstitial perivascular collagen and elevated cardiac hydroxyproline content indicated myocardial fibrosis. The pathological changes above were attenuated by 2,3,4',5-tetrahydroxystilbene-2-O-beta-D-glucoside. Additionally, it markedly reduced collagen I and III expressions and regulated matrix metalloproteinase-2,9 and inhibitors of metalloproteinase expressions, as markers of myocardial fibrosis. Furthermore, we explored the underlying mechanisms for such effects of 2,3,4',5-tetrahydroxystilbene-2-O-beta-D-glucoside. The results showed that it significantly reduced myocardium angiotensin II, enhanced the activities of superoxide dismutase and glutathione peroxidase in serum and myocardial tissue, as well as inhibited protein expression of transforming growth factor-β1 and phosphorylation of extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase in the myocardial tissue. Our results suggest that 2,3,4',5-tetrahydroxystilbene-2-O-beta-D-glucoside could prevent cardiac remodeling induced by pressure overload in rats. The underlying mechanisms may be related to a decreasing angiotensin II level, an antioxidant effect of the tested compound, suppression of transforming growth factor-β1 expression, and inhibition of extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase activation., (Georg Thieme Verlag KG Stuttgart · New York.)

Objective: To evaluate the therapeutic effect and mechanism of extract of ginkgo biloba (EGB) in treatment of diet-induced non-alcoholic steatohepatitis (NASH) in rats., Methods: The experiment was conducted in the Laboratory, Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China from June 2009 to December 2009. In this study, the rat model of NASH was produced by feeding high-fat diet. Sixty rats were randomly divided into 3 groups: Normal group: normal diet, drinking water; Model group: high-fat diet, single-distilled water 10 ml/kg gavage once a day for 12 weeks; and Treated group: high-fat diet, EGB 6 mg/kg gavage once a day for 12 weeks. At the end of 12 weeks, all rats were killed. The serum biochemical, fibrosis markers, superoxide dismutase (SOD), malondialdehyde (MDA), the pathological changes, and the expression levels of nuclear factor KB (NF-κB)p65 protein in the liver were observed., Results: The contents of serum alanine transaminase aspartate aminotransferase, fibrosis markers, and pathological grading of liver fibrosis and the staining intensity of NF-κBp65 protein in the liver of rats in treated group were significantly lower than those in the model group. Activities of superoxide dismutase were elevated, but levels of malondialdehyde were decreased in the treated group as compared with the model group., Conclusion: Extract of ginkgo biloba has antioxidant and hepatoprotective effects and can inhibit liver fibrosis in rat of NAHS.