OBJECTIVEOver the last few decades, diabetic cardiomyopathy has been identified as a significant contributor in cardiac morbidity. However, the mechanisms of diabetic cardiomyopathy have not been clarified.

METHODSIn the present study, a diabetic rat model was induced by the intraperitoneal injection of streptozotocin. The myocardial CD147 expression and extent of glycosylation, as well as thematrixmetalloproteinases(MMPs) expression and activity, were observed in the diabetic and synchronous rats.

RESULTSThe results showed that CD147 located on sarcolemma of cardiomyocytes. The myocardial CD147 expression and glycosylation were significantly increased in the diabetic rats as compared with the control. Expression of MMP-2 protein, MMP-2 and MMP-9 activity were also increased in left ventricular myocardium in the diabetic rats. Tamoxifen only inhibited the enhanced expression of myocardial CD147 in the diabetic rats, but not in synchronous control rats. Tamoxifen inhibited glycosylation of myocardial CD147 in both diabetic and control rats. The inhibition of tamoxifen on CD147 glycosylation was stronger than on the expression in the myocardium. The extent of myocardial CD147glycosylation was positively related toMMP-2 and MMP-9 activity. Tamoxifen induced an inhibition of myocardial MMP-2 and MMP-9 activity in the control and diabetic rats.

CONCLUSIONThese results indicate that myocardial CD147 expression, especially the extent of glycosylation, regulates MMP-2 and MMP-9 activity, then accelerates cardiac pathological remodeling inducing diabetic cardiomyopathy. Tamoxifen inhibits myocardial CD147 glycosylation and further depress the activity of MMPs. Therefore, tamoxifen may protect the diabetic rats against diabetic myocardium.

Animals ; Basigin ; metabolism ; Diabetes Mellitus, Experimental ; complications ; Diabetic Cardiomyopathies ; drug therapy ; Glycosylation ; Heart ; drug effects ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Myocardium ; metabolism ; Myocytes, Cardiac ; cytology ; Rats ; Sarcolemma ; metabolism ; Tamoxifen ; pharmacology

OBJECTIVETo analyze the impact of depletion of the twin arginine translocation (TAT) system on virulence and physiology of Yersinia enterocolitica for a better understanding of its pathogenicity.

METHODSWe constructed a DeltatatC::SpR mutant of Yersinia enterocolitica by P1 phage mediated transduction using Escherichia coli K-12 DeltatatC::SpR strain as a donor.

RESULTSA P1-mediated genetic material transfer was found between the two species of enterobacteria, indicating a great potential of acquisition of antibiotic resistance in emergency of a new threatening pathogen by genetic material exchanges. Periplasmic trimethylamine N-oxidase reductase activity was detected in the wild type Y. enterocolitica strain and translocation of this enzyme was completely abolished by the DeltatatC::SpR mutation. In addition, the DeltatatC::SpR mutation showed a pleiotropic effect on the metabolism of Y. enterocolitica. However, the tat mutation did not seem to affect the mobility and virulence of Y. enterocolitica under the conditions used.

CONCLUSIONUnlike other pathogenic bacteria studied, the TAT system of Y. enterocolitica might play an important role in the pathogenic process, which is distinct from other pathogens, such as Pseudomonas aeruginosa and enterohemorrhagic E. coli O157:H7.

Drug Resistance, Microbial ; genetics ; Genes, Bacterial ; Mutation ; Oxidoreductases Acting on CH-NH Group Donors ; metabolism ; Transduction, Genetic ; Virulence ; Yersinia enterocolitica ; enzymology ; genetics ; metabolism ; pathogenicity

Cardiac autophagy dramatically increases in heart failure induced by sustained pressure overload. However, it has not yet been addressed if enhanced autophagy plays a role in protecting myocardium or mediating progression from compensative hypertrophy to heart failure. The aim of the present study was to detect autophagic flux of cardiomyocytes from 20-week transverse abdominal aortic constriction (TAC) rats. Fasting rats were used as the positive control for detecting cardiac autophagy. Echocardiography was applied to find the changes of cardiac structure and function. Immunofluorescent histochemistry and Western blot were used to analyze the related biomolecular indexes reflecting cardiac autophagic flux. After the previous methods for detecting cardiac autophagy were confirmed, the autophagic flux in cardiomyocytes of rats subjected to 20-week TAC was examined. The results showed that fasting had no obvious influence on parameters of cardiac structure in rats, including interventricular septal wall thickness and left ventricle posterior wall thickness, but heart rate, diastolic left ventricle internal dimension, fractional shortening of left ventricle dimension, ejection fraction and mitral inflow velocity decreased in rats after fasting for 3 d. Meanwhile, positively stained particles of LC3 and cathepsin D, but not ubiquitin and complement 9, distributed within cardiomyocytes of 3-day fasting rats, indicating augmented autophagic flux. Compared with sham rats, 20-week TAC rats did not show any changes of LC3, cathepsin D, ubiquitin and complement 9 in myocardium detected by immunofluorescent histochemistry. In addition, protein levels of LC3, cathepsin D and p62 in myocardium of TAC rats did not changed. These results reveal the unchanged autophagic flux in cardiomyocytes at middle or late phase of cardiac hypertrophy in TAC rats, implying a balance between inhibition of hypertrophy and activation of pressure load stress on autophagy.
Animals ; Aorta ; pathology ; Autophagy ; Cardiomegaly ; physiopathology ; Constriction ; Heart ; physiopathology ; Myocardium ; pathology ; Myocytes, Cardiac ; cytology ; Rats

Objective To investigate the diagnostic value of CT thin-section target reconstruction technique in patients with pulmonary small size groud glass nodules (sGGN).Methods A total of 109 patients with pulmonary sGGN certified post-operation and/or follow up were analyzed retrospectively,and the clinical and CT images of all patients were completely collected.There were 23 cases of benign group,21 cases of adenocarcinoma in situ group,29 cases of minimally invasive adenocarcinoma group and 36 cases of invasive adenocarcinoma group,respectively.The differential diagnostic value using CT thin-section target reconstruction technique was analyzed between the benign and malignant pulmonary sGGN groups,and the CT feature detection rates were compared between CT thin section target and common reconstruction techniques.Results The CT thin-section target reconstruction technique had improved the diagnostic efficiency of pulmonary sGGN.The diagnostic accuracy,area under curve(AUC),sensitivity and specificity were 85.32 ％,0.679,90.80 ％,63.64 ％ in malignant group and 77.06％,0.764,83.72％,52.17％ in benign pulmonary sGGN group,respectively.The CT features as solid component in whole nodule,"halo sign",speculation sign,pleural retraction sign,lobulation sign were more detected by using the thin-section target reconstruction technique than that by using the common reconstruction among adenocarcinoma in situ group,minimally invasive adenocarcinoma group and invasive adenocarcinoma group (P＜0.05) but not speculation sign in the invasive adenocarcinoma group(P=0.126).Conclusion The CT thin section target reconstruction technique can improve the diagnostic value of pulmonary sGGN.

Brain Mapping ; Cognitive Dysfunction ; Humans ; Magnetic Resonance Imaging ; Schizophrenia/therapy* ; Transcranial Magnetic Stimulation