Identifying and evaluating a disulfidptosis-related gene signature to predict prognosis in colorectal adenocarcinoma patients.

Disulfidptosis, a regulated form of cell death, has been recently reported in cancers characterized by high SLC7A11 expression, including invasive breast carcinoma, lung adenocarcinoma, and hepatocellular carcinoma. However, its role in colon adenocarcinoma (COAD) has been infrequently discussed. In this study, we developed and validated a prognostic model based on 20 disulfidptosis-related genes (DRGs) using LASSO and Cox regression analyses. The robustness and practicality of this model were assessed via a nomogram. Subsequent correlation and enrichment analysis revealed a relationship between the risk score, several critical cancer-related biological processes, immune cell infiltration, and the expression of oncogenes and cell senescence-related genes. POU4F1, a significant component of our model, might function as an oncogene due to its upregulation in COAD tumors and its positive correlation with oncogene expression. In vitro assays demonstrated that POU4F1 knockdown noticeably decreased cell proliferation and migration but increased cell senescence in COAD cells. We further investigated the regulatory role of the DRG in disulfidptosis by culturing cells in a glucose-deprived medium. In summary, our research revealed and confirmed a DRG-based risk prediction model for COAD patients and verified the role of POU4F1 in promoting cell proliferation, migration, and disulfidptosis.

Hybrid Approaches for Complex Parastomal Hernia Repair.

Parastomal hernia is one of the major complications of colostomy with high occurrence. From October 2011 to November 2014, a retrospective study was conducted by analyzing and following up data of 16 patients suffering from parastomal hernia who underwent a hybrid technique repair. The safety and efficacy of the hybrid technique for parastomal hernia repair was investigated in terms of complications. All cases were operated successfully and had no major immediate postoperative complications other than mild abdominal pain in 5 cases. No long-term postoperative complications were reported in the follow-up. The authors found hybrid technique to be safe and effective for parastomal hernia repair with fewer complications.

Predictive value of serum caspase-cleaved cytokeratin-18 concentrations after acute intracerebral hemorrhage.

BACKGROUND: Caspase-cleaved Cytokeratin-18 (CCCK-18) is released during apoptosis. Serum CCCK-18 concentrations are associated with prognosis of some critical illness. We investigated the potential relationships between serum CCCK-18 concentrations and disease severity and long-term clinical outcomes after intracerebral hemorrhage. METHODS: Serum CCCK-18 concentrations were determined in a total of 102 patients and 102 controls. Multivariate models were used to predict high concentration of CCCK-18 and 6-month clinical outcomes. The predictive values were evaluated based on areas under receiver operating curve. RESULTS: Compared with controls, serum CCCK-18 concentrations were increased in patients (245.8±108.3U/l vs. 23.6±18.1U/l, P<0.001). National Institute of Health Stroke Scale scores [odds ratio (OR), 1.164; 95% confidence interval (CI), 1.027-1.320; P=0.003] and hematoma volumes (OR, 1.079; 95% CI, 1.018-1.205; P=0.008) were independent predictors of high concentration of CCCK-18. CCCK-18 was identified as an independent predictor of 6-month mortality (OR, 1.019; 95% CI, 1.010-1.038; P=0.013) and 6-month unfavorable outcome (OR, 1.017; 95% CI, 1.008-1.029; P=0.032) and possessed high predictive values. CONCLUSION: Increased serum CCCK-18 concentrations are associated with disease severity and clinical outcomes, suggesting that CCCK represent a novel prognostic predictive biomarker after intracerebral hemorrhage.

Admission plasma visfatin level strongly correlates with hematoma growth and early neurologic deterioration in patients with acute spontaneous basal ganglia hemorrhage.

BACKGROUND: Visfatin, a proinflammatory mediator, has been associated with poor clinical outcomes after acute brain injury. The present study is designed to investigate the potential association between plasma visfatin levels and the risk of hematoma growth (HG) and early neurologic deterioration (END) after intracerebral hemorrhage. METHODS: There were 85 patients as cases who presented with first-time hemorrhagic stroke that were assessed within 6h after the incident. The control group consisted of 85 healthy volunteers. HG was defined as hematoma enlargement >33% at 24h. END was defined as an increase of ≥ 4 points in National Institute of Health Stroke Scale score at 24h from symptoms onset. Plasma visfatin levels were determined using enzyme immunoassay. RESULTS: Plasma visfatin levels were significantly higher in patients compared to controls. Plasma visfatin level emerged as an independent predictor of HG [odds ratio (OR), 1.154; 95% confidence interval (CI), 1.046-3.108; P=0.009] and END (OR, 1.195; 95% CI, 1.073-3.516; P=0.005). For predicting HG, area under curve (AUC) of plasma visfatin level (0.814; 95% CI: 0.715-0.890) was similar to that of hematoma volume (0.839; 95% CI, 0.743-0.909) (P=0.703). For predicting END, AUC of plasma visfatin level (0.828; 95% CI: 0.730-0.901) was similar to that of hematoma volume (0.863; 95% CI, 0.771-0.928) (P=0.605). Visfatin did not improve AUC of hematoma volume for predicting HG and END (both P>0.05). CONCLUSION: Plasma visfatin level represents a novel biomarker for predicting HG and END.