Kaifu Zheng

To investigate the influence of health education based on the precede-proceed model (PPM) on the eradication rate and experience of Helicobacter pylori (H. pylori) infection. 200 patients with asymptomatic H. pylori infections were randomly assigned to a PPM group (n = 100) or a control group (n = 100) using the random number table method based on the time of their medical records. The control group received modified bismuth quadruple therapy (BQT), while the PPM group received modified BQT and health education based on the PPM. Completion rate, eradication rate, drug-related adverse events (AEs), discontinuation rate due to AEs, reexamination rate, recurrence rate, H. pylori knowledge scores, and satisfaction with medical experience were evaluated. The treatment completion rate was 96% vs. 84% (P0.05); the drug-related AEs were 14% vs. 16%(P>0.05), the discontinuation rate due to AEs was 14.3% vs. 37.5%(P>0.05) in the PPM and control groups, respectively. After treatment, the mean H. pylori knowledge scores were significantly higher in the PPM than in the control groups; the mean knowledge scores of the recurrent patients were significantly lower than those of the non-recurrent patients (P<0.001). Satisfaction with the medical experience was significantly higher in the PPM group than in the control group (P<0.001). Health education based on the PPM can effectively improve the completion rate of H. pylori eradication treatment, the eradication rate of the ITT analysis, the reexamination rate, and patient compliance, significantly improving patients’ knowledge of H. pylori and their experience.

Purpose This narrative review evaluates the clinical value of key globally marketed potassium-competitive acid blockers (P-CABs) for acid-related diseases (ARDs) based on current evidence-based medical research to inform clinical practice. Methods We compare P-CABs and proton pump inhibitors (PPIs) in terms of their mechanisms of acid suppression, speed of onset, metabolic pathways, and long-term safety. We present a detailed comparison of the clinical efficacy of individual P-CABs and PPIs for gastroesophageal reflux disease (GERD), peptic ulcers, and Helicobacter pylori (H. pylori) eradication, synthesizing findings from recent clinical trials and meta-analyses. Results This highlights the advantages of P-CABs, such as rapid acid control and the achievement of maximal efficacy with the first dose, as well as their reduced susceptibility to CYP2C19 polymorphisms. Evidence suggests that P-CABs have potential advantages in the initial and maintenance treatment of erosive esophagitis (EE). P-CABs demonstrate non-inferiority to PPIs in ulcer healing. For H. pylori eradication, P-CABs are comparable to PPIs in standard regimens; however, P-CAB-based dual therapy (e.g., P-CAB + high-dose amoxicillin) is emerging as a promising first-line treatment option. Conclusion This review emphasizes the evolving role of P-CABs in optimizing management strategies for ARDs.

Background: Esophageal cancer is still a leading cause of death among all tumors in males, with unsatisfactory responses to novel immunotherapies such as anti-PD-1 agents. Herein, we explored the role of CD155 in esophageal squamous cell cancer (ESCA) and its underlying molecular mechanisms. Methods: Publicly available datasets were used for differential gene expression and immune infiltration analyses, and their correlation with patient survival. A total of 322 ESCA and 161 paracancer samples were collected and evaluated by performing immunohistochemistry and the H score was obtained by performing semiquantitative analysis. In vitro transfection of ESCA cell lines with lentivirus vectors targeting CD155 was performed to knockdown the protein. These cells were analyzed by conducting RNA sequencing, and the effects of CD155 knockdown on cell cycle and apoptosis were verified with flow cytometry and Western blotting. In addition, in vivo experiments using these engineered cell lines were performed to determine the role of CD155 in tumor formation. A small interfering RNA-mediated knockdown of Nectin3 was used to determine whether it phenocopied the profile of CD155 knockdown. Results: CD155 is highly expressed in ESCA tissues and is positively associated with PD1, PDL1, CD4, IL2RA, and S100A9 expression. Furthermore, CD155 knockdown inhibited ESCA cells’ proliferation by impairing the cell cycle and inducing cell apoptosis. Bioinformatics analysis of the gene expression profile of these engineered cells showed that CD155 mainly contributed to the regulation of PI3K/Akt and MAPK signals. The downregulation of Nectin3 expression phenocopied the profile of CD155 knockdown. Discussion: CD155 may cooperate with PD-1/PD-L1 to support ESCA proliferation in ways other than regulating its underlying immune mechanisms. Indeed, CD155 downregulation can impair ESCA cell pro-cancerous behavior via the inhibition of the PI3K/Akt and MAPK signaling pathways. Moreover, Nectin3 may be a ligand of CD155 and participate in the regulation of ESCA cells’ proliferation. Hence, the inhibition of CD155 may enhance the therapeutic effect of anti-PD-1 immunotherapies in ESCA.

Cancer remains a serious social health problem, and immunotherapy has become the major treatments in tumor treatment. Additionally, improving the efficiency and safety of treatment is necessary. Further, more therapy targets are warranted for future tumor treatments. In this review, in addition to examining the currently recognized role of immune regulation, we focus on the proliferative role of 15 immune checkpoints in various tumors, including PD1, PD-L1, FGL1, CD155, CD47, SIRPα, CD276, IDO1, SIGLEC-15, TIM3, Galectin-9, CD70, CD27, 4-1BBL, and HVEM. We managed to conclude that various immune checkpoints such as PD1/PD-L1, FGL1, CD155, CD47/SIRPα, CD276, and SIGLEC-15 all regulate the cell cycle, and specifically through Cyclin D1 regulation. Furthermore, a variety of signal pathways engage in proliferation regulation, such as P13K, AKT, mTOR, and NK-κB, which are also the most common pathways involved in the regulation of immune checkpoint proliferation. Currently, only PD1/PD-L1, CD47/SIRPα, TIM3/Galectin-9, and CD70/CD27 checkpoints have been shown to interact with each other to regulate tumor proliferation in pairs. However, for other immune checkpoints, the role of their receptors or ligands in tumor proliferation regulation is still unknown, and we consider the enormous potential in this area. An increasing number of studies have validated the various role of immune checkpoints in tumors, and based on this literature review, we found that most of the immune checkpoints play a dual regulatory role in immunity and proliferation. Therefore, the related pathways in proliferation regulation can served the role of therapy targets in tumor therapy. Further, great potential is displayed by IDO1, SIGLEC-15, 4-1BBL, and HVEM in tumor proliferation regulation, which may become novel therapy targets in tumor treatment.