[Retracted] Resveratrol reduces acute lung injury in a LPS­induced sepsis mouse model via activation of Sirt1.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the ß­actin control western blotting data shown in Fig. 3D on p. 1893 were very similar to the contol data shown in Fig. 4A on p. 1894; furthermore, the data shown for the MMP­9 and the INOS protein bands in Fig. 4C were remarkably similar to the data shown for the IL­1ß and IL­6 proteins, respectively, albeit the backgrounds surrounding the bands were different. Moreover, various of the western blotting data shown in these figures were strikingly similar to data that had already been published in different form in other articles written by (largely) different authors at different research institutes. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, and due to the number of apparent duplications of strikingly similar data between Figs. 3 and 4, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 7: 1889­1895, 2013; DOI: 10.3892/mmr.2013.1444].

Outcomes of surgical repair of anterior or posterior ventricular septal rupture after myocardial infarction.

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.

Development and Validation of a Novel Nomogram for Preoperative Prediction of In-Hospital Mortality After Coronary Artery Bypass Grafting Surgery in Heart Failure With Reduced Ejection Fraction.

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.

Preparation of Nano Zinc Particles and Evaluation of Its Application in Mouse Myocardial Infarction Model.

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.

[Distribution and antibiotics resistance related to nosocomial pathogenic bacteria infection in patients after cardiac surgery].

OBJECTIVE: To investigate the clinical distribution and antibiotics resistance of nosocomial infection caused pathogenic bacteria in patients after cardiac surgery. METHODS: Clinical data from 612 patients after cardiac surgery under microbiologically documented nosocomial infection was retrospectively analyzed from January 2007 to December 2012. Identification on related bacterial was performed in an automatic ATB Expression system while antimicrobial susceptibility was tested by Kirby-Bauer method. RESULTS: were analyzed by WHONET5.4. RESULTS: There were 697 strains of clinical pathogenic bacilli isolates identified and 421 (60.4%) of them were isolated from sputum while 185 (26.5%) were from blood. Acinetobacter spp. (124 strains, 17.8%), Pseudomonas aeruginosa (85 strains, 12.2%) and Klebsiella pneumoniae (50 strains, 7.2%) were the predominant Gram-negative bacilli while S. epidermidis (75 strains, 10.8%) was the predominant Gram-positive cocci. The predominant eumycete was Candida albicans (43 strains, 6.2%). RESULTS: from the susceptibility test showed that carbapenems, cefoperazone/sulbactam and piperacillin/tazobactam were the most active antibiotics. The detection of meticillin-resistant Staphylococcus (MRS) were 82.9% in S aureus and 95.9% in coagulase negative Staphylococcus. There was no Staphylococcus strains resistant to vancomycin found. CONCLUSION: Non-fermenting Gram-negative bacilli and Staphylococcus appeared the important pathogens in patients after cardiac surgery. Drug resistance to antibiotics was quite common. Prevention on nosocomial infection and rational use of antibiotics remained very important in reducing the amount of drug resistant strains.

Resveratrol reduces acute lung injury in a LPS­induced sepsis mouse model via activation of Sirt1.

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 anti­inflammatory properties. However, the role of resveratrol for the treatment of ALI during sepsis is not fully understood. In the present study, the anti­inflammatory role of Sirt1 in the lipopolysaccharide (LPS)­induced TC­1 cell line and its therapeutic role in ALI was investigated in a mouse model of sepsis. The upregulation of matrix metalloproteinase-9, interleukin (IL)­1ß, IL­6 and inducible nitric oxide synthase was induced by LPS in the mouse model of sepsis and the TC­1 cell line, and resveratrol suppressed the overexpression of these proinflammatory molecules in a dose­dependent 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 TC­1 cells to LPS stimulation and diminished the anti­inflammatory effect of resveratrol. These results demonstrated that resveratrol inhibits LPS­induced ALI and inflammation via Sirt1, and indicated that Sirt1 is an efficient target for the regulation of LPS­induced ALI and inflammation. The present study provides insights into the treatment of ALI during sepsis.

Myocardial autophagy variation during acute myocardial infarction in rats: the effects of carvedilol.

BACKGROUND: The loss of cardiac myocytes is one of the mechanisms involved in acute myocardial infarction (AMI)-related heart failure. Autophagy is a common biological process in eukaryote cells. The relationship between cardiac myocyte loss and autophagy after AMI is still unclear. Carvedilol, a non-selective alpha1- and beta-receptor blocker, also suppresses cardiac myocyte necrosis and apoptosis induced by ischemia. However, the association between the therapeutic effects of carvedilol and autophagy is still not well understood. The aim of the present study was to establish a rat model of AMI and observe changes in autophagy in different zones of the myocardium and the effects of carvedilol on autophagy in AMI rats. METHODS: The animals were randomly assigned to a sham group, an AMI group, a chloroquine intervention group and a carvedilol group. The AMI rat model was established by ligating the left anterior descending coronary artery. The hearts were harvested at 40 minutes, 2 hours, 24 hours and 2 weeks after ligation in the AMI group, at 40 minutes in the chloroquine intervention group and at 2 weeks in other groups. Presence of autophagic vacuoles (AV) in the myocytes was observed by electron microscopy. The expression of autophagy-, anti-apoptotic- and apoptotic-related proteins, MAPLC-3, Beclin-1, Bcl-xl and Bax, were detected by immunohistochemical staining and Western blotting. RESULTS: AVs were not observed in necrotic regions of the myocardium 40 minutes after ligation of the coronary artery. A large number of AVs were found in the region bordering the infarction. Compared with the infarction region and the normal region, the formation of AV was significantly increased in the region bordering the infarction (P < 0.05). The expression of autophagy- and anti-apoptotic-related proteins was significantly increased in the region bordering the infarction. Meanwhile, the expression of apoptotic-related proteins was significantly increased in the infarction region. In the chloroquine intervention group, a large number of initiated AVs (AVis) were found in the necrotic myocardial region. At 2 weeks after AMI, AVs were frequently observed in myocardial cells in the AMI group, the carvedilol group and the sham group, and the number of AVs was significantly increased in the carvedilol group compared with both the AMI group and the sham group (P < 0.05). The expression of autophagy- and anti-apoptotic-related proteins was significantly increased in the carvedilol group compared with that in the AMI group, and the positive expression located in the infarction region and the region bordering the infarction. CONCLUSIONS: AMI induces the formation of AV in the myocardium. The expression of anti-apoptosis-related proteins increases in response to upregulation of autophagy. Carvedilol increases the formation of AVs and upregulates autophagy and anti-apoptosis of the cardiac myocytes after AMI.