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The misuse of antibiotics has led to the emergence of multidrug-resistant bacteria. There is an urgent need to explore methods to effectively kill bacteria without relying on antibiotics. In this paper, a vanadium carbide-based (V2CTx-Au) nanostructures was successfully synthesized by electrostatic self-assembly for the direct detection and killing of bacteria. The nanostructures could be directly used for label-free surface-enhanced Raman spectroscopy detection of bacteria without tedious processing. Photothermal detection demonstrated that the temperature of the V2CTx-Au nanostructures can increase above 50 °C within just 200 s, and the photothermal conversion efficiency of the material is 37.82%. Reactive oxygen species detection experiments showed that the V2CTx-Au nanostructures can produce the O2·– and 1O2. Combined with SEM images of the bacteria, the results showed that V2CTx-Au nanostructures produced photothermal therapy antibacterial effects under 808 nm laser irradiation and exhibited photodynamic therapy synergistic antibacterial properties. The survival rates of Escherichia coli (E. coli) and extended-spectrum β-lactamase Escherichia coli (ESBL- E. coli) were 6.88 and 1.58%, respectively. In addition, cytotoxicity experiments and hemolytic tests showed that the prepared V2CTx-Au nanostructures exhibited good biocompatibility. This study provides a feasible route for the label-free and rapid detection of bacteria and rapid sterilization without antibiotics, which can help solve the problem of bacterial infection, especially drug-resistant bacteria. [ABSTRACT FROM AUTHOR]

The proliferation of drug-resistant bacteria and infections such as methicillin-resistant Staphylococcus aureus (MRSA) pose a serious challenge to global healthcare. Photothermal therapy (PTT) is becoming a highly effective antimicrobial method. Compared with near infrared I (NIR-I), near infrared II (NIR-II) has deeper penetration depth, less light scattering and higher maximum permissible exposure (MPE). The selection of a photothermal agent (PTA) and laser parameters is important. Three kinds of MXenes, Nb2C, Ti3C2 and V2C, were prepared in this paper, and the extinction coefficient and photothermal conversion efficiency (PCE) of NIR-I and NIR-II were compared. The extinction coefficient of Ti3C2 (26.23 L g−1 cm−1) at 808 nm was greater than those of Nb2C (24.38 L g−1 cm−1) and V2C (19.43 L g−1 cm−1). However, V2C had a higher temperature than Nb2C at 808 nm due to its high PCE (49.26%). Nb2C had a higher extinction coefficient (24.99 L g−1 cm−1) and PCE (45.55%) at 1064 nm, resulting in the highest temperature change. High extinction coefficient and high PCE are the two important factors for an excellent PTA. To reduce laser power used in the treatment, NIR-II laser and a gelation strategy for MXenes were used. The prepared Nb2C/Gel could be rapidly heated to 62 °C at a laser power of 0.112 W (lower than MPE), and the sterilization rate for MRSA was 92.48%. A NIH-3T3 cell activity study showed that the prepared Nb2C had good biocompatibility. Nb2C/Gel has excellent antibacterial properties and it is expected that a rapid, efficient and safe biological antimicrobial strategy against bacterial infections can be established using Nb2C/Gel, especially for drug-resistant bacterial infections. [ABSTRACT FROM AUTHOR]

Dysregulation of hepcidin-iron axis is presumed to account for abnormal iron status in patients with chronic liver disease (CLD). Our aim is to determine the effect of specific etiologies of CLD and of cirrhosis on serum hepcidin levels. PubMed, Embase, Web of Science were searched for studies comparing serum hepcidin levels in patients with CLD to that in controls using enzyme-linked immunosorbent assay. The study was conducted in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis Guidelines. Statistical analysis was carried out with STATA using random effects model to calculate the mean difference (MD) between two groups. Hepcidin levels were significantly lower in subjects with hepatitis C virus (16 studies) [MD −1.6 (95 % CI: −2.66 to −0.54), p<0.01] and alcoholic liver disease (3 studies) [MD −0.84 (95 % CI: −1.6 to −0.07), p=0.03] than controls. Serum hepcidin was significantly higher in subjects with non-alcoholic fatty liver disease (12 studies) [MD 0.62 (95 % CI: 0.21 to 1.03), p<0.01], but did not differ in subjects with hepatitis B and controls (eight studies) [MD −0.65 (95 % CI: −1.47 to 0.16), p=0.12]. Hepcidin levels were significantly lower in patients with cirrhosis of any etiology (four studies) [MD −1.02 (CI: −1.59 to −0.45), p<0.01] vs. controls (CI: confidence interval). Serum hepcidin levels are altered in common forms of CLD albeit not in a consistent direction. Additional study is needed to determine how changes in hepcidin levels are related to dysregulation of iron metabolism in CLD. [ABSTRACT FROM AUTHOR]

Background: The close relationship between colorectal cancer and inflammation has been widely reported. However, the relationship between colorectal cancer and inflammation at the genetic level is not fully understood. Method: From a genetic perspective, this study explored the relationship between inflammation-related genes and the immune microenvironment in colorectal cancer. We identified prognostic genes, namely CX3CL1 , CCL22 , SERPINE1 , LTB4R , XCL1 , GAL, TIMP1 , ADIPOQ , and CRH , by using univariate and multivariate regression analyses. A risk scoring model for inflammatory response was established, and patients in The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database were divided into two groups: high risk group and low risk group. Results: The analysis showed that the prognosis of the two groups was significantly different, and the low-risk group had a higher survival rate and longer survival time. Pathways related to apoptosis, inflammatory response, and hypoxia were significantly enriched as shown via Gene Set Enrichment Analysis (GSEA). Activated dendritic cell infiltration was found in both the TCGA and GEO databases, and the CCL21 gene played a significant role in the process of activated dendritic cell infiltration. CCL21 gene was also positively correlated with inflammatory response, and the gene expression and risk score were significantly different between the two groups. Conclusion: In summary, inflammatory response has a direct impact on patients with colorectal cancer in the prognosis and immune infiltration and further research studies on the inflammatory response can help in advancing the development of immunotherapy for colorectal cancer. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori (H. pylori) is a type I biological carcinogen, which may cause about 75% of the total incidence of gastric cancer worldwide. H. pylori infection can induce and activate the cancer-promoting signaling pathway and affect the occurrence and outcome of gastric cancer through controlling the regulatory functions of long non-coding RNAs (lncRNAs). However, we have no understanding of the prognostic worth of lncRNAs for gastric cancer patients infected with H. pylori. Method: We screened differentially expressed lncRNAs using DESeq2 method among TCGA database. And we built the H. pylori infection-related lncRNAs regulatory patterns. Then, we constructed H. pylori infection-based lncRNAs prognostic signatures for gastric cancer patients together with H. pylori infection, via uni-variable and multi-variable COX regression analyses. Based on receiver operator characteristic curve (ROC) analysis, we evaluated the prediction effectiveness for this model. Results: We identified 115 H. pylori infection–related genes were differentially expressed among H. pylori –infected gastric cancer tissues versus gastric cancer tissues. Functional enrichment analysis implies that H. pylori infection might interfere with the immune-related pathways among gastric cancer tissues. Then, we built H. pylori infection–related dys-regulated lncRNA regulatory networks. We also identified 13 differentially expressed lncRNAs were associated with prognosis for gastric cancer patients together with H. pylori infection. Kaplan-Meier analysis demonstrated that the lncRNA signatures were correlated with the poor prognosis. What is more, the AUC of the lncRNA signatures was 0.712. Also, this prognostic prediction model was superior to the traditional clinical characters. Conclusion: We successfully constructed a H. pylori –related lncRNA risk signature and nomogram associated with H. pylori –infected gastric cancer patients prognosis, and the signature and nomogram can predict the prognosis of these patients. [ABSTRACT FROM AUTHOR]

Background: Chronic inflammation and immune cell dysfunction in the tumor microenvironment are key factors in the development and progression of gastric tumors. However, inflammation-related genes associated with gastric cancer prognosis and their relationship with the expression of immune genes are not fully understood. Method: In this study, we established an inflammatory response model score called "Riskscore", based on differentially expressed genes in gastric cancer. We used Survival and Survminer packages in R to analyze patient survival and prognosis in risk groups. The survival curve was plotted using the Kaplan–Meier method, and the log-rank test was used to assess statistical significance, and we performed the ROC analysis using the R language package to analyze the 1-, 3-, and 5-year survival of patients in the GEO and TCGA databases. Single-factor and multi-factor prognostic analyses were carried out for age, sex, T, N, M, and risk score. Pathway enrichment analysis indicated immune factor-related pathway enrichment in both patient groups. Next, we screened for important genes that are involved in immune cell regulation. Finally, we created a correlation curve to explore the correlation between Riskscore and the expression of these genes. Results: The prognosis was significantly different between high- and low-risk groups, and the survival rate and survival time of the high-risk group were lower than those of the low-risk group. we found that the pathways related to apoptosis, hypoxia, and immunity were most enriched in the risk groups. we found two common tumor-infiltrating immune cell types (i.e., follicular helper T cells and resting dendritic cells) between the two risk groups and identified 10 genes that regulate these cells. Additionally, we found that these 10 genes are positively associated with the two risk groups. Conclusion: Finally, a risk model of the inflammatory response in gastric cancer was established, and the inflammation-related genes used to construct the model were found to be directly related to immune infiltration. This model can improve the gastric cancer prognosis prediction. Our findings contribute to the development of immunotherapy for the treatment of gastric cancer patients. [ABSTRACT FROM AUTHOR]

Background: Imbalanced nutritional supply and demand in the tumor microenvironment often leads to hypoxia. The subtle interaction between hypoxia and immune cell behavior plays an important role in tumor occurrence and development. However, the functional relationship between hypoxia and the tumor microenvironment remains unclear. Therefore, we aimed to investigate the effect of hypoxia on the intestinal tumor microenvironment. Method: We extracted the names of hypoxia-related genes from the Gene Set Enrichment Analysis (GSEA) database and screened them for those associated with colorectal cancer prognosis, with the final list including ALDOB , GPC1 , ALDOC , and SLC2A3. Using the sum of the expression levels of these four genes, provided by The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, and the expression coefficients, we developed a hypoxia risk score model. Using the median risk score value, we divided the patients in the two databases into high- and low-risk groups. GSEA was used to compare the enrichment differences between the two groups. We used the CIBERSORT computational method to analyze immune cell infiltration. Finally, the correlation between these five genes and hypoxia was analyzed. Result: The prognosis of the two groups differed significantly, with a higher survival rate in the low-risk group than in the high-risk group. We found that the different risk groups were enriched by immune-related and inflammatory pathways. We identified activated M0 macrophages in TCGA and GEO databases and found that CCL2/4/5 , and CSF1 contributed toward the increased infiltration rate of this immune cell type. Finally, we observed a positive correlation between the five candidate genes' expression and the risk of hypoxia, with significant differences in the level of expression of each of these genes between patient risk groups. Conclusion: Overall, our data suggest that hypoxia is associated with the prognosis and rate of immune cell infiltration in patients with colorectal cancer. This finding may improve immunotherapy for colorectal cancer. [ABSTRACT FROM AUTHOR]