A nomogram of anastomotic stricture after rectal cancer: a retrospective cohort analysis.

BACKGROUND: Anastomotic stricture significantly impacts patients' quality of life and long-term prognosis. However, current clinical practice lacks accurate tools for predicting anastomotic stricture. This study aimed to develop a nomogram to predict anastomotic stricture in patients with rectal cancer who have undergone anterior resection. METHODS: A total of 1542 eligible patients were recruited for the study. Least absolute shrinkage selection operator (Lasso) analysis was used to preliminarily select predictors. A prediction model was constructed using multivariate logistic regression and presented as a nomogram. The performance of the nomogram was evaluated using receiver operating characteristic (ROC) curves, calibration diagrams, and decision curve analysis (DCA). Internal validation was conducted by assessing the model's performance on a validation cohort. RESULTS: 72 (4.7%) patients were diagnosed with anastomotic stricture. Participants were randomly divided into training (n = 1079) and validation (n = 463) sets. Predictors included in this nomogram were radiotherapy, diverting stoma, anastomotic leakage, and anastomotic distance. The area under the ROC curve (AUC) for the training set was 0.889 [95% confidence interval (CI) 0.840-0.937] and for the validation set, it was 0.930 (95%CI 0.879-0.981). The calibration curve demonstrated a strong correlation between predicted and observed outcomes. DCA results showed that the nomogram had clinical value in predicting anastomotic stricture in patients after anterior resection of rectal cancer. CONCLUSION: We developed a predictive model for anastomotic stricture following anterior resection of rectal cancer. This nomogram could assist clinicians in predicting the risk of anastomotic stricture, thus improving patients' quality of life and long-term prognosis.

Development and Characterization of the Shale Stratum Well Wall Stabilized with Nanosomal Sealing Agent.

The development of micro cracks in shale formations can easily lead to wellbore instability caused by liquid phase invasion. In order to effectively seal the shale micropores, the surface treatment of nano-SiO2 particles was developed using the silicane coupling agent A-1891. Then, the temperature-sensitive polypenic acrylamide polymer was modified onto the surface of the nanoprocal particle through reaction to obtain the nanosomal blocking agent ASN. The infrared spectrum shows that there are chemical bonds between the generated polymer chains, rather than simple physical composites, indicating the successful synthesis of the temperature-responsive nanosealing agent ASN. The particle size analysis showed that the synthesized nanoparticles in ASN have a uniform particle size distribution and display no agglomeration phenomenon. Applying ASN as a sealing agent in drilling fluid effectively fills the nanoscale micropores and microcracks in shale, making shale denser and significantly improving the wellbore stability of shale formations. In addition, it has good temperature resistance, can adapt to reservoirs at different temperatures, is non-toxic and environmentally friendly, and has good prospects for stable applications in shale formation wellbore.

PLCD3 inhibits apoptosis and promotes proliferation, invasion and migration in gastric cancer.

Gastric cancer (GC) is a heterogeneous disease whose development is accompanied by alterations in a variety of pathogenic genes. The phospholipase C Delta 3 enzyme is a member of the phospholipase C family, which controls substance transport between cells in the body. However, its role in gastric cancer has not been discovered. The purpose of this study was to investigate the expression and mechanism of action of PLCD3 in connection to gastric cancer. By Western blot analysis and immunohistochemistry, PLCD3 mRNA and protein expression levels were measured, with high PLCD3 expression suggesting poor prognosis. In N87 and HGC-27 cells, the silencing of PLCD3 using small interfering RNA effectively induced apoptosis and inhibited tumor cell proliferation, invasion, and migration. Conversely, overexpression of PLCD3 using overexpressed plasmids inhibited apoptosis in AGS and BGC-823 cells and promoted proliferation, migration, and invasion. In order to investigate the underlying mechanisms, we conducted further analysis of PLCD3, which indicates that this protein is closely related to the cell cycle and EMT. Additionally, we found that overexpression of PLCD3 inhibits apoptosis and promotes the development of GC cells through JAK2/STAT3 signaling. In conclusion, PLCD3 inhibits apoptosis and promotes proliferation, invasion, and migration, which indicated that PLCD3 might serve as a therapeutic target for gastric cancer.

Retinol Binding Protein 4 Serves as a Potential Tumor Biomarker and Promotes Malignant Behavior in Gastric Cancer.

Background: Gastric cancer (GC) is a highly phenotypically heterogeneous disease and is caused by a combination of factors. Retinol binding protein 4 (RBP4) is a member of a family of lipid transport proteins that are involved in the transport of substances between cells and play a crucial role in a variety of cancers. However, the expression and role of RBP4 in GC remain unknown. Methods: In this study, we explored the expression, prognostic significance, immune microenvironment, drug responsiveness and function of associated signaling pathways of RBP4 in GC using web-based bioinformatics tools. Immunohistochemistry and real-time quantitative PCR were utilized to analyze the tissue and cell expression levels of RBP4. CCK-8, colony formation, EDU incorporation, wound healing and transwell assays were applied to demonstrate the effect of RBP4 on GC cell function. Flow cytometric detection of apoptosis after RBP4 knockdown. Nude mice xenograft model elucidates the role of RBP4 for GC in vivo. Related proteins of the RAS signaling pathway were analyzed by employing Western blot assays. Results: RBP4 is highly expressed in GC. RBP4 is closely associated with patient survival and sensitivity to a wide range of antitumor agents. Knockdown of RBP4 promoted apoptosis and inhibited cell proliferation, invasion and migration. RBP4 promotes GC tumorigenesis in vivo. Finally, RBP4 modulates the RAS/RAF/ERK axis. Conclusion: RBP4 may promote gastric carcinogenesis and development through the RAS/RAF/ERK axis and is expected to be a novel target for GC treatment.