The present study investigated the changes of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8) and sleep ability in patients with obstructive sleep apnea hypopnea syndrome (OSAHS). A total of 684 patients who were admitted to Xuzhou Central Hospital between June 2012 and June 2016 were enrolled to serve as the experimental group and 192 healthy subjects were selected as the control group. Polysomnography was performed on both groups, and serum TNF-α and IL-8 levels were measured by ELISA. Pearson's correlation analysis was used to analyze correlations between factors. Compared with control group, the levels of TNF-α and IL-8, the morning systolic and diastolic pressure in OSAHS group were significantly higher (P<0.01). Furthermore, the mean oxygen saturation (MSaO2) and lowest oxygen saturation (LSaO2) of the OSAHS group were significantly lower compared with those in control group (P<0.01). Results also indicated that TNF-α was positively correlated with apnea-hypopnea index (AHI), morning systolic and diastolic pressure (r=0.621, 0.464, 0.539; P<0.05), and negatively correlated with MSaO2 and LSaO2 (r=−0.526, −0.466; P<0.05). Notably, IL-8 was positively correlated with AHI, morning systolic and diastolic pressure (r=0.337, 0.413 and 0.629; P<0.05), and negatively correlated with MSaO2 and LSaO2 (r=−0.329 and −0.417; P<0.05). Therefore, it was concluded that TNF-α and IL-8 may be involved in the occurrence and development of OSAHS, are closely related to OSAHS and may be important risk factors for cardiovascular disease in patients with OSAHS. The present findings suggest that TNF-α and IL-8 can be used to assess the degree of OSAHS.

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We have explored the role of Chondromodulin-I (ChM-I) in chondrogenesis of bone marrow-derived mesenchymal stem cells (BMSCs) in 3-dimensional (3D) scaffold for cartilage tissue engineering. BMSCs of Sprague Dawley (SD) rats were cultured on poly-(L-lactic acid) [PLLA] scaffolds with different pore sizes (80-200 μm, 200-450 μm) with or without surface modification by chitosan. Cell viability, proliferation, and morphology were measured using confocal microscope and the CCK-8 method. Untransfected BMSCs, BMSCs expressing pcDNA3.1(+), BMSCs expressing plasmid pcDNA3.1 (+)/ChM-I were cultured on 3D scaffolds in standard growth medium or transforming growth factor-β1 (TGF-β1) supplemented chondrogenic induction medium in vitro for 3 weeks and the expression of collagen type II was determined. Cell-scaffolds constructs were implanted subcutaneously for 3 months in vivo. BMSCs had a higher viability and proliferation in PLLA scaffolds of pore size 200-450 μm than that of 80-200 μm, and surface modification with chitosan did not enhance cell attachment. The ChM-I gene enhanced chondrogenesis and increased collagen type II synthesis. Immunohistochemistry from in vivo study showed enhanced cartilage regeneration in BMSCs expressing pcDNA3.1 (+)/ChM-I on 3D PLLA scaffolds. It also demonstrated that TGF-β1 might promote chondrogenesis of rat BMSCs by synergizing with the ChM-I gene. ChM-I could be beneficial to future applications in cartilage repair.

Background: Infections after acute ischemic stroke are common and likely to complicate the clinical course and negatively affect patient outcomes. Despite the development of various risk factors and predictive models for infectious and inflammatory disorders (IAID) after stroke, more objective and easily obtainable predictors remain necessary. This study involves the development and validation of an accessible, accurate nomogram for predicting in-hospital IAID in patients with acute ischemic stroke (AIS).Methods: A retrospective cohort of 2,257 patients with AIS confirmed by neurological examination and radiography was assessed. The International Statistical Classification of Diseases and Health related Problem's definition was used for IAID. Data was obtained from two hospitals between January 2016 and March 2020.Results: The incidence of IAID was 19.8 and 20.8% in the derivation and validation cohorts, respectively. Using an absolute shrinkage and selection operator (LASSO) algorithm, four biochemical blood predictors and four clinical indicators were optimized from fifty-five features. Using a multivariable analysis, four predictors, namely age (adjusted odds ratio, 1.05; 95% confidence interval [CI], 1.038–1.062; p &lt; 0.001), comatose state (28.033[4.706–536.403], p = 0.002), diabetes (0.417[0.27–0.649], p &lt; 0.001), and congestive heart failure (CHF) (5.488[2.451–12.912], p &lt; 0.001) were found to be risk factors for IAID. Furthermore, neutrophil, monocyte, hemoglobin, and high-sensitivity C-reactive protein were also found to be independently associated with IAID. Consequently, a reliable clinical-lab nomogram was constructed to predict IAID in our study (C-index value = 0.83). The results of the ROC analysis were consistent with the calibration curve analysis. The decision curve demonstrated that the clinical-lab model added more net benefit than either the lab-score or clinical models in differentiating IAID from AIS patients.Conclusions: The clinical-lab nomogram predicted IAID in patients with acute ischemic stroke. As a result, this nomogram can be used for identification of high-risk patients and to further guide clinical decisions.

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