Establishment of a nomogram for predicting prolonged mechanical ventilation in cardiovascular surgery patients.

AIMS: This study aimed to develop a nomogram model for predicting prolonged mechanical ventilation (PMV) in patients undergoing cardiovascular surgery. METHODS AND RESULTS: In total, 693 patients undergoing cardiovascular surgery at an Affiliated Hospital of Nantong University between January 2018 and June 2020 were studied. Postoperative PMV was required in 147 patients (21.2%). Logistic regression analysis showed that delirium [odds ratio (OR), 3.063; 95% confidence interval (CI), 1.991-4.713; P < 0.001], intraoperative blood transfusion (OR, 2.489; 95% CI, 1.565-3.960; P < 0.001), obesity (OR, 2.789; 95% CI, 1.543-5.040; P = 0.001), postoperative serum creatinine level (mmol/L; OR, 1.012; 95% CI, 1.007-1.017; P < 0.001), postoperative serum albumin level (g/L; OR, 0.937; 95% CI, 0.902-0.973; P = 0.001), and postoperative total bilirubin level (µmol/L; OR, 1.020; 95% CI, 1.005-1.034; P = 0.008) were independent risk factors for PMV. The area under the receiver operating characteristic curve for our nomogram was found to be 0.770 (95% CI, 0.727-0.813). The goodness-of-fit test indicated that the model fitted the data well (χ2 = 12.480, P = 0.131). After the model was internally validated, the calibration plot demonstrated good performance of the nomogram, as supported by the Harrell concordance index of 0.760. Decision curve analysis demonstrated that the nomogram was clinically useful in identifying patients at risk for PMV. CONCLUSION: We established a new nomogram model that may provide an individual prediction of PMV. This model may provide nurses, social workers, physicians, and administrators with an accurate and objective assessment tool to identify patients at high risk for PMV after cardiovascular surgery.

Endoplasmic reticulum stress participates in the progress of senescence and apoptosis of osteoarthritis chondrocytes.

Endoplasmic reticulum stress (ERS) has been shown to participate in many disease pathologies. Recent reports have reported that ERS exists in human osteoarthritis (OA) chondrocytes. During OA, chondrocytes exhibit increased level of some senescence marker, such as senescence-associated ß-galactosidase (SA ß-gal) activity. However, the persistence and accumulation of senescent cells in various tissues can also impair function and have been involved in the pathogenesis of many age-related diseases, including OA. In this present study, we used IL-1ß (10 ng/ml) to mimic OA chondrocytes and we found that IL-1ß stimulated chondrocytes caused the increasing expression of ADAMTS5 and MMP13, decreasing COL2A1 expression, which were in accord with OA chondrocytes changes. Our data also showed that ERS is involved in the OA chondrocytes, SA ß-gal activity significantly increases and inhibition of ERS can decrease the SA ß-gal activity, apoptosis of OA chondrocytes and increase cell viability. These results help us to open new perspectives for the development of molecular-targeted treatment approaches and thus present an effective novel therapeutic approach for OA.