The development of acute lung injury (ALI) during sepsis almost doubles the mortality rate of patients. The efficacy of current treatment strategies is low as treatment is usually initiated following the onset of symptoms. Inflammation is one of the main mechanisms of autoimmune disorders and is a common feature of sepsis. The suppression of inflammation is therefore an important mechanism for the treatment of sepsis. Sirtuin 1 (Sirt1) has been demonstrated to play a role in the regulation of inflammation. Resveratrol, a potent Sirt1 activator, exhibits anti‑inflammatory properties. However, the role of resveratrol for the treatment of ALI during sepsis is not fully understood. In the present study, the anti‑inflammatory role of Sirt1 in the lipopolysaccharide (LPS)‑induced TC‑1 cell line and its therapeutic role in ALI was investigated in a mouse model of sepsis. The upregulation of matrix metalloproteinase-9, interleukin (IL)‑1β, IL‑6 and inducible nitric oxide synthase was induced by LPS in the mouse model of sepsis and the TC‑1 cell line, and resveratrol suppressed the overexpression of these proinflammatory molecules in a dose‑dependent manner. Resveratrol decreased pulmonary edema in the mouse model of sepsis induced by LPS. In addition, resveratrol improved lung function and reduced pathological alterations in the mouse model of sepsis. Knockdown of Sirt1 by RNA interference resulted in an increased susceptibility of TC‑1 cells to LPS stimulation and diminished the anti‑inflammatory effect of resveratrol. These results demonstrated that resveratrol inhibits LPS‑induced ALI and inflammation via Sirt1, and indicated that Sirt1 is an efficient target for the regulation of LPS‑induced ALI and inflammation. The present study provides insights into the treatment of ALI during sepsis.

Background and Aims: Patients with heart failure with reduced ejection fraction (HFrEF) are among the most challenging patients undergoing coronary artery bypass grafting surgery (CABG). Several surgical risk scores are commonly used to predict the risk in patients undergoing CABG. However, these risk scores do not specifically target HFrEF patients. We aim to develop and validate a new nomogram score to predict the risk of in-hospital mortality among HFrEF patients after CABG.Methods: The study retrospectively enrolled 489 patients who had HFrEF and underwent CABG. The outcome was postoperative in-hospital death. About 70% (n = 342) of the patients were randomly constituted a training cohort and the rest (n = 147) made a validation cohort. A multivariable logistic regression model was derived from the training cohort and presented as a nomogram to predict postoperative mortality in patients with HFrEF. The model performance was assessed in terms of discrimination and calibration. Besides, we compared the model with EuroSCORE-2 in terms of discrimination and calibration.Results: Postoperative death occurred in 26 (7.6%) out of 342 patients in the training cohort, and in 10 (6.8%) out of 147 patients in the validation cohort. Eight preoperative factors were associated with postoperative death, including age, critical state, recent myocardial infarction, stroke, left ventricular ejection fraction (LVEF) ≤35%, LV dilatation, increased serum creatinine, and combined surgery. The nomogram achieved good discrimination with C-indexes of 0.889 (95%CI, 0.839–0.938) and 0.899 (95%CI, 0.835–0.963) in predicting the risk of mortality after CABG in the training and validation cohorts, respectively, and showed well-fitted calibration curves in the patients whose predicted mortality probabilities were below 40%. Compared with EuroSCORE-2, the nomogram had significantly higher C-indexes in the training cohort (0.889 vs. 0.762, p = 0.005) as well as the validation cohort (0.899 vs. 0.816, p = 0.039). Besides, the nomogram had better calibration and reclassification than EuroSCORE-2 both in the training and validation cohort. The EuroSCORE-2 underestimated postoperative mortality risk, especially in high-risk patients.Conclusions: The nomogram provides an optimal preoperative estimation of mortality risk after CABG in patients with HFrEF and has the potential to facilitate identifying HFrEF patients at high risk of in-hospital mortality.

Background: Ventricular septal rupture (VSR) is a rare and fatal complication of myocardial infarction.Surgery is the main treatment for the condition. It is currently believed that surgery is less effective for posterior VSR than for anterior VSR. The objective of this study was to investigate the clinical outcomes of surgical treatment for myocardial infarction combined with an anterior or posterior VSR.Methods: This was a single-center, retrospective, observational, cohort study. Clinical data of 68 patients with myocardial infarction combined with VSR were retrospectively analyzed. According to the site of the VSR, patients were divided into the anterior (43 cases) and posterior (25 cases) VSR groups, and the general clinical data, preoperative examination results, surgery, and follow-up results were compared between the two groups.Results: Compared with the anterior VSR group, the operative time in the posterior VSR group was longer {300 [240, 360] vs. 360 [300, 400] min; P=0.003}, and the cardiopulmonary bypass time was longer (142.0±52.2 vs. 180.2±52.3 min; P=0.005), and the aortic clamp time was longer (84.0±32.5 vs. 115.9±39.8 min; P=0.001).There were no significant differences in the incidence of perioperative complications, including bleeding, low cardiac output, pulmonary, and cerebrovascular complications, and the incidence of perioperative death between the two groups (P>0.05). The patients were followed up for 1.0-10.5 (median, 4.2) years. There were no significant differences in the survival rate and the incidence of major adverse cardiovascular and cerebrovascular events (MACCEs) including myocardial infarction, heart failure, revascularization, and cerebrovascular events between the two groups (P>0.05). Conclusions:The perioperative risks and medium-and long-term outcomes of the surgical repair of anterior or posterior VSR after myocardial infarction were similar.

Nanometer zinc particles were synthesized by orthogonal test with manganese chloride, iron chloride and zinc sulfate as raw materials and NaOH as coprecipitating agent. The optimum synthesis conditions of coprecipitation method were obtained and the samples were characterized by various means. In this experiment, the SV, EF, FS, lvaws, lvawd, lvpws and lvpwd of left ventricle in mice with myocardial infarction were decreased, while the LVEDd, lveds and lvevs were increased in the environment exposed to ultrafine zinc nanoparticles, which proved that exposure to ultrafine zinc nanoparticles could lead to the enlargement of left ventricle, the thinning of ventricular wall, and the decrease of cardiac systolic and diastolic function. Further study on the heart tissue sections showed that the normal left ventricular myocardium of mice exposed to ultrafine zinc nanoparticles decreased, apoptotic cells increased, collagen content increased significantly, and myocardial fibrosis intensified. At the same time, WGA staining results of myocardial cell membrane showed that inhalation of ultra-fine nano zinc particles increased the size of myocardial infarction cells and disordered cell arrangement, which further proved that inhalation of ultra-fine nano zinc particles accelerated left ventricular pathological remodeling. The results of this study prove that the ultra-fine zinc nanoparticles in the air play an important role in the structural remodeling of myocardial infarction heart, and provide a theoretical basis for formulating targeted policies to control air pollution.