Objective:To evaluate the relationship between preoperative malnutrition and postoperative pulmonary complications (PPCs) in elderly patients undergoing thoracoscopic and laparoscopic radical esophagectomy.Methods:The elderly patients who underwent elective thoracoscopic and laparoscopic radical esophagectomy in the Affiliated Hospital of Jiangnan University were enrolled.The general clinical data and nutritional status, Assess Respiratory Risk in Surgical Patients in Catalonia (ARISCAT) score, tumor pathological stage and operation-related variables based on the Gobal Leader Initiative on Malnutrition criteria were recorded.The patients were divided into 2 groups according to whether PPCs occurred during hospitalization, and the differences between the variables were compared.Logistic regression analysis was used to identify the risk factors for PPCs in elderly patients undergoing thoracoscopic and laparoscopic radical esophagectomy.The accuracy of the ARISCAT score and ARISCAT score combined with malnutrition in predicting the occurrence of PPCs was evaluated by receiver operating characteristic curve.Results:A total of 256 elderly patients undergoing thoracoscopic and laparoscopic radical esophagectomy were included, and the incidence of PPCs was 23.8%.There were no significant differences between patients with and without PPCs in FEV 1/FVC, age, American Society of Anesthesiologists physical status, chronic obstructive pulmonary disease ratio, malnutrition ratio and ratio of patients with high ARISCAT score ( P<0.05). The results of logistic regression analysis showed that increasing age, chronic obstructive pulmonary disease, malnutrition and high ARISCAT score were independent risk factors for PPCs.The area under the receiver operating characteristic curve of ARISCAT score and malnutrition combined with ARISCAT score in predicting the occurrence of PPCs was 0.722 and 0.777, respectively, and the difference was statistically significant ( P<0.05). Conclusions:Preoperative malnutrition is an independent risk factor for the occurrence of PPCs in elderly patients undergoing thoracoscopic and laparoscopic radical esophagectomy, which is helpful in improving the accuracy of ARISCAT score in predicting the occurrence of PPCs.

Objective:To evaluate the role of ubiquitin-specific peptidase 22 (USP22) in myocardial ischemia-reperfusion (I/R) injury in diabetic mice.Methods:Seventy-eight SPF male C57BL/6 mice, aged 6-8 weeks, were divided into 6 groups using a random number table method: sham operation group (Sham group, n=12), type 1 diabetes mellitus + sham operation group (T1D+ Sham group, n=12), myocardial I/R injury group (I/R group, n=12), type 1 diabetes mellitus + myocardial I/R injury group (DI/R group, n=12), type 1 diabetes mellitus + myocardial I/R injury + empty vector group (DI/R+ V group, n=15), and type 1 diabetes mellitus + myocardial I/R injury + USP22 overexpression group (DI/R+ U group, n=15). Type 1 diabetes mellitus was induced by intraperitoneal injection of streptozotocin-citrate buffer. Myocardial I/R was induced by ligation of the left coronary artery. At 1 day before developing the myocardial I/R injury model, DI/R+ U group and DI/R+ V group received an intramyocardial injection of USP22 overexpression plasmid or empty vector plasmid, respectively. At 24 h of reperfusion, cardiac function was assessed using the echocardiography to measure the left ventricular ejection fraction and left ventricular fractional shortening. The mice were then sacrificed, and their hearts were harvested for measurement of the myocardial infarct size, for microscopic examination of pathological changes (using HE staining) and for determination of the apoptosis rate (TUNEL staining), reactive oxygen species(ROS) activity (DHE staining), and USP22 expression (by Western blot, immunofluorescence, and immunohistochemistry). Proteomic analysis was performed to identify downstream proteins regulated by USP22, and protein-protein interactions were investigated using co-immunoprecipitation. Results:Compared with Sham group, the cardiac function indices were significantly decreased, the apoptosis rate of myocardial cells and ROS activity were increased, and USP22 expression in myocardial tissues was down-regulated in I/R group ( P<0.05). Compared with I/R group, the percentage of myocardial infarct size was significantly increased, the cardiac function indices were decreased, the apoptosis rate of myocardial cells and ROS activity were increased, and USP22 expression in myocardial tissues was up-regulated ( P<0.05), and the pathological damage to myocardial tissues was aggravated in DI/R group. Compared with DI/R+ V group, the percentage of myocardial infarct size was significantly decreased, the cardiac function indices were increased, the apoptosis rate of myocardial cells and ROS activity were decreased, and USP22 expression in myocardial tissues was up-regulated ( P<0.05), and the pathological damage to myocardial tissues was alleviated in DI/R+ U group. The results of proteomics combined with co-immunoprecipitation experiments showed an interaction between calponin 1 and USP22. Conclusions:During myocardial I/R injury in diabetic mice, USP22 may act as an endogenous protective mechanism, and calponin 1 might be a downstream mechanism through which USP22 exerts its protective effects.