ABSTRACT
Objective: To explore the risk factors of recurrence within 1 year after radical resection of non-small cell lung cancer (NSCLC) and construct the nomogram model. Methods: The clinical data of 186 patients with NSCLC treated with radical surgery in Affiliated Hospital of Youjiang Medical University for Nationalities of Baise were retrospectively analyzed. Multivariate logistic regression was applied to analyze the risk factors of recurrence within 1 year after radical resection of NSCLC. The R language (R 4.0.3 software package) was used in constructing the nomogram model, and the predictive value of the model was evaluated. Results: The recurrence rate of 186 patients within 1 year after radical surgery was 29.57%. After multivariate logistic regression analysis, pathological stage, number of lymph node metastasis, chronic obstructive pulmonary disease (COPD), postoperative plasma D-dimer, and carcinoembryonic antigen were independent factors for recurrence within 1 year after radical resection of NSCLC (P < 0.05). Based on the above independent risk factors, a nomogram model was established, with the distinction of AUC = 0.891 (95% CI: 0.819-0.964) and sensitivity and specificity of 70.3% and 97.8%, respectively. The calibration curve was close to the ideal curve. External validation of the model showed AUC = 0.801 (95% CI: 0.674-0.928), and sensitivity and specificity were 66.7% and 84.2%, respectively. Conclusion: The recurrence of NSCLC within 1 year after radical surgery was related to a variety of factors, and the nomogram model constructed based on risk factors had good goodness of fit, calibration, consistency of prediction, and prediction efficiency.
ABSTRACT
Therapy using acellular spinal cord (ASC) scaffolds seeded with bone marrow stromal cells (BMSCs) has previously been shown to restore function of the damaged spinal cord and improve functional recovery in a rat model of acute hemisected spinal cord injury (SCI). The aim of the present study was to determine whether BMSCs and ASC scaffolds promote the functional recovery of the damaged spinal cord in a rat SCI model through regulation of apoptosis and immune responses. Whether this strategy regulates secondary inflammation, which is characterized by the infiltration of immune cells and inflammatory mediators to the lesion site, in SCI repair was investigated. Basso, Beattie, and Bresnahan scores revealed that treatment with BMSCs seeded into an ASC scaffold led to a significant improvement in motor function recovery compared with treatment with an ASC scaffold alone or untreated controls at 2 and 8 weeks after surgery (P<0.05). Two weeks after transplantation, the BMSCs seeded into an ASC scaffold significantly decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells, as compared with the ASC scaffold only and control groups. These results suggested that the use of BMSCs decreased the apoptosis of neural cells and thereby limited tissue damage at the lesion site. Notably, the use of BMSCs with an ASC scaffold also decreased the recruitment of macrophages (microglia; P<0.05) and T lymphocytes (P<0.05) around the SCI site, as indicated by immunofluorescent markers. By contrast, there was no inhibition of the inflammatory response in the control and ASC scaffold only groups. BMSCs regulated inflammatory cell recruitment to promote functional recovery. However, there was no significant difference in IgM-positive expression among the three groups (P>0.05). The results of this study demonstrated that BMSCs seeded into ASC scaffolds for repair of spinal cord hemisection defects promoted functional recovery through the early regulation of inflammatory cell recruitment with inhibition of apoptosis and secondary inflammation.
ABSTRACT
BACKGROUND: Experimental studies showed that 25-hydroxy-vitamin D [25(OH)D] deficiency (defined as 25-hydroxy-vitamin D < 15 ng/ml) has been associated with CKD progression. Patients with IgA nephropathy have an exceptionally high rate of severe 25(OH)D deficiency; however, it is not known whether this deficiency is a risk factor for progression of IgA nephropathy. We conducted this study to investigate the relationship between the plasma level of 25(OH)D and certain clinical parameters and renal histologic lesions in the patients with IgA nephropathy, and to evaluate whether the 25(OH)D level could be a good prognostic marker for IgA nephropathy progression. METHODS: A total of 105 patients with biopsy-proven IgA nephropathy were enrolled between 2012 and 2015. The circulating concentration of 25(OH)D was determined using serum samples collected at the time of biopsy. The primary clinical endpoint was the decline of estimated glomerular filtration rate (eGFR; a 30 % or more decline compared to the baseline). RESULTS: Mean eGFR decreased and proteinuria worsened proportionally as circulating 25(OH)D decreased (P < 0.05). The 25(OH)D deficiency was correlated with a higher tubulointerstitial score by the Oxford classification (P = 0.008). The risk for reaching the primary endpoint was significantly higher in the patients with a 25(OH)D deficiency compared to those with a higher level of 25(OH)D (P = 0.001). As evaluated using the Cox proportional hazards model, 25(OH)D deficiency was found to be an independent risk factor for renal progression [HR 5.99, 95 % confidence intervals (CIs) 1.59-22.54, P = 0.008]. CONCLUSION: A 25(OH)D deficiency at baseline is significantly correlated with poorer clinical outcomes and more sever renal pathological features, and low levels of 25(OH)D at baseline were strongly associated with increased risk of renal progression in IgAN.
