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Colorectal cancer (CRC) is one of the most common gastrointestinal malignancies. Vasorin (VASN) has been reported to be critical in tumor development and angiogenesis. However, VASN has not been reported in CRC, and its role is unclear. In this study, VASN expression is upregulated in CRC compared with the normal tissues, and VASN expression positively correlates with N stage and poor overall survival by analysis of different datasets and 32 CRC clinicopathologic samples. Overexpression of VASN significantly promotes CRC cell progression, including proliferation, migration, invasion, and epithelial‐mesenchymal transition (EMT), while knockdown of VASN inhibits CRC progression. We found that VASN was associated with the YAP/TAZ and PI3K/AKT pathways by gene set enrichment analysis (GSEA) and gene ontology (GO) analysis. Notably, western blotting, immunofluorescence staining and co‐immunofluorescence (co‐IP) confirmed that VASN could interact with YAP and activate the YAP/TAZ and PTEN/PI3K/AKT pathways, and knockdown of YAP reversed this effect. Importantly, our findings indicate that VASN interacts with YAP to inhibit YAP phosphorylation and stimulates CRC proliferation, migration, and invasion through activation of the YAP/TAZ‐TEAD target gene CTGF and PTEN/PI3K/AKT pathways. Our results also show that knockdown of YAP reverses the cellular phenotype induced by increased VASN. In conclusion, our study reveals that VASN acts as an oncogene to stimulate tumor progression in CRC, providing new insights into the molecular mechanisms of CRC development and representing a possible novel biomarker for CRC.

Repairment and replacement of organs and tissues are part of the history of struggle against human diseases, in addition to the research and development (R&D) of drugs. Acquisition and processing of specific substances and physiological signals are very important to understand the effects of pathology and treatment. These depend on the available biomedical materials. The family of diamond-like carbon coatings (DLCs) has been extensively applied in many industrial fields. DLCs have also been demonstrated to be biocompatible, both in vivo and in vitro. In many cases, the performance of biomedical devices can be effectively enhanced by coating them with DLCs, such as vascular stents, prosthetic heart valves and surgical instruments. However, the feasibility of the application of DLC in biomedicine remains under discussion. This review introduces the current state of research and application of DLCs in biomedical devices, their potential application in biosensors and urgent problems to be solved. It will be useful to build a bridge between DLC R&D workers and biomedical workers in order to develop high-performance DLC films/coatings, promote their practical use and develop their potential applications in the biomedical field.

Aim: Investigate the prevalence of irritable bowel syndrome (IBS) after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and assess the association between IBS and SARS-CoV-2 infection. Methods: A systematic literature search for PubMed, Web of Science, Embase, Scopus, and the Cochrane Library was performed to identify all reports published before 31 December 2022. The confidence interval (CI), estimation effect (ES) of prevalence, and risk ratios (RR) were calculated to evaluate the prevalence of IBS after SARS-CoV-2 infection and their association. Individual results were pooled by the random-effects (RE) model. Subgroup analyses conducted a further investigation of the results. We employed funnel plots, Egger’s test, and Begg’s test to evaluate publication bias. Sensitivity analysis was performed for the assessment of the robustness of the result. Results: The data on IBS prevalence after SARS-CoV-2 infection were extracted from two cross-sectional studies and ten longitudinal studies from nineteen countries with 3950 individuals. The IBS prevalence after SARS-CoV-2 infection ranges from 3% to 91% in different countries, and the overall pooled prevalence of IBS following SARS-CoV-2 infection is 15% (ES: 0.15; 95% CI, 0.11–0.20; p = 0.000). The data on the association between IBS and SARS-CoV-2 infection were extracted from six cohort studies from fifteen countries with 3595 individuals. The risk of IBS increased following SARS-CoV-2 infection but was not significant (RR: 1.82; 95% CI, 0.90–3.69; p = 0.096). Conclusions: In conclusion, the overall pooled prevalence of IBS following SARS-CoV-2 infection was 15%, and SARS-CoV-2 infection increased the overall risk of IBS but was not statistically significant. Further extra high-quality epidemiological evidence and studies to clarify the underlying mechanism of IBS following SARS-CoV-2 infection are needed.

Nowadays, the relationship between Helicobacter pylori infection (HPI) and irritable bowel syndrome (IBS) remains controversial. Objective: The aim of this study is to investigate the relationship between HPI and IBS through a systematic review and meta-analysis based on the current evidence. Methods: We performed a systematic literature search in electronic databases (PubMed, EMBASE, and the Cochrane library) by computer to identify all reports published before 8 August 2021. The odds ratio (OR) and confidence interval (CI) were calculated to evaluate the association between HPI and IBS. Subgroup analyses were conducted for further assessment and exploration of heterogeneity sources. In addition, we assessed publication bias through funnel plots, Egger’s test, and Begg’s test. Finally, we conducted a sensitivity analysis to evaluate the robustness of the results. Results: Thirteen studies with 13,173 participants were included in the meta-analysis. The pooled OR of the association between HPI and IBS was 1.03 (95% CI [0.80,1.31]; p = 0.84). The adjusted OR of the association between HPI and IBS after excluding the studies with confounding factors defined by our team was 1.29 (95% CI [1.03,1.62]; p = 0.03). We found a positive association between HPI and IBS-D (diarrhea subtype) (OR: 1.54; 95% CI [1.22,1.95]; p = 0.0003). The OR of the relationship between cytotoxin-associated gene A (Cag A) positive HPI and IBS was 4.3 (95% CI [0.51,36.17]; p = 0.18). Conclusions: The likelihood of HPI in IBS patients is relatively higher than that of non-IBS participants but not statistically significant, implying that HPI is not significantly associated with IBS, albeit we may underestimate this association. Moreover, we found a positive association between HPI and IBS-D. We also observed an increased likelihood of Cag-A positive HPI in IBS patients than that of non-IBS participants but not statistically significant.