Aims We aimed to assess the eradication efficacy and factors that influencing it of high‐dose dual therapy (HDDT) in Gansu region, Northwest China. Methods A total of 216 treatment‐naive patients with Helicobacter pylori infection were randomly assigned to two groups for the 14‐day eradication treatment: the HDDT group (amoxicillin 750 mg q.i.d. and esomeprazole 40 mg t.i.d.) and the amoxicillin and clarithromycin‐containing bismuth quadruple therapy group (ACBQT: esomeprazole 20 mg, bismuth potassium citrate 2 g, amoxicillin 1 g, and clarithromycin 500 mg; b.i.d.). The eradication rates, adverse effects and patient compliance of these two groups were compared. Eradication efficacy was determined by 13C urea breath test (13C UBT) 4–8 weeks after finishing treatment. Antibiotic resistance was determined by the Epsilometer testing (E‐test) method. Results The eradication rates for the HDDT and ACBQT groups were 71.0% and 74.7% (P = .552) by per‐protocol analysis, and 65.7% and 68.5% (P = .664) by intention‐to‐treat analysis. The overall adverse event rates in the HDDT and ACBQT groups were 2.0% and 43.4% (P < .001), respectively. The resistance rates to amoxicillin, clarithromycin, tetracycline, levofloxacin and metronidazole were 15.2%, 42.0%, 5.4%, 35.7% and 83.0%, respectively. Amoxicillin resistance and delta over baseline (DOB) of 13C UBT ≥ 20 before treatment significantly reduced the eradication rate in 112 participants with H. pylori cultured. Conclusion The HDDT as first‐line treatment for H. pylori was unsatisfactory in Gansu. Amoxicillin resistance and DOB of 13C UBT ≥ 20 before treatment were significantly correlated with H. pylori eradication failure.

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What is known and objective: Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase involved in the pathological processes of several diseases, such as keloid formation, renal fibrosis, atherosclerosis, tumours, and inflammatory processes. The biological barrier is the first line of defence against pathogens, and its disruption is closely related to diseases. In this review, we attempt to elucidate the relationship between DDR1 and the biological barrier, explore the potential biological value of DDR1, and review the current research status and clinical potential of DDR1-selective inhibitors. Methods:We conducted an extensive literature search on PubMed to collect studies on the relevance of DDR1 to biological barriers and DDR1-selective inhibitors. With these studies, we explored the relationship between DDR1 and biological barriers and briefly reviewed representative DDR1-selective inhibitors that have been reported in recent years.Results and discussion: First, the review of the potential mechanisms by which DDR1 regulates biological barriers, including the epithelial, vascular, glomerular filtration, blood-labyrinth, and blood-brain barriers. In the body, DDR1 dysfunction and aberrant expression may be involved in the homeostasis of the biological barrier. Secondly, the review of DDR1 inhibitors reported in recent years shows that DDR1-targeted inhibi-

Ulcerative colitis (UC) is a persistent and diffuse inflammatory disease of the intestine. It is widely prevalent in developed countries. Approximately 30% of patients with UC suffer from widespread and aggressive colitis and are at increased risk of colon cancer. In this study, the genetic features and potential molecular mechanisms shared between UC and colorectal cancer were investigated. The datasets from GEO and TCGA were analyzed to obtain differentially expressed genes, of which there were 116 overlapping genes. A module containing 15 genes was obtained using String and Cytoscape to analyze the module and identify hub genes. Weighted gene co-expression network analysis (WGCNA) was used to identify co-expression modules associated with UC and colon cancer, with 52 overlapping genes. Functional clustering of the two gene cohorts was performed using the Metascape online tool, with three significant functions or pathways associated with both gene cohorts. A total of 19 key genes were included, and CCT2 was identified after expression and survival analyses. CCT2 is highly expressed in colon cancer and lowly expressed in UC, and its low expression is associated with a poor prognostic ratio. This study reveals, for the first time, that CCT2 may be a promoter of UC transformation into colon cancer and identifies new gene candidates that could be used as biomarkers or potential therapeutic targets.