Molecular mechanisms in microRNA-mediated TRB3 gene and hypertension left ventricular hypertrophy.

The present study investigated the relationship between microRNA-mediated TRB3 gene and hypertension left ventricular hypertrophy at the molecular level. Polymorphic site in TRB3 gene was identified by direct PCR method, and the correlation between the SNP site and ventricular hypertrophy was determined. MicroRNAs target gene sequence interacting on the TRB3 polymorphic site was screened by bioinformatics, and the effect of microRNAs on the TRB3 polymorphic site was finally verified by luciferase test. Two polymorphic sites rs6186912 and rs6186923 were found in the TRB3 gene, and the direct relationship between rs6186923 polymorphic site and the hypertension left ventricular hypertrophy in patients with myocardial hypertrophy was compared and analyzed. Pictar software was used to analyze the effect of miR-100 on rs6186923, and the argumentation was verified by luciferase test. In conclusion, the study showed that the TRB3 gene polymorphism rs6186923 was able to affect the TRB3 gene by affecting the binding of miR-100, which indirectly caused the formation of hypertension left ventricular hypertrophy.

Expression Changes of Long Noncoding RNA in the Process of Endothelial Cell Activation.

BACKGROUND: Endothelial cells have been shown to be in response to a variety of local and systemic stimuli, and are able to transition between quiescent and activated states. Endothelial cell activation is critical for the pathogenesis of various cardiovascular diseases. However, the expression changes of long non-coding RNAs (lncRNAs) are still unknown in the process of endothelial cell activation. Thus, this study was aimed to investigate expression changes of lncRNA before and after endothelial cell activation. MATERIALS AND METHODS: In an experimental model of peripheral venous congestion, endothelial cells were activated and analyzed with Affymetrix HG-U133 plus2.0 microarray. We analyzed these microarray data and reannotated the microarray probes for lncRNA. RESULTS: According to the definition of absolute fold change>2 and p value <0.05, 27 differentially expressed lncRNAs were identified and only 1 lncRNA transcript, ENST00000509256 was down-regualted. Co-expression network of lncRNA and mRNA were constructed to predict function of the dysregulated lncRNA. Gene set enrichment analyses suggested that these ENST00000509256 was associated with many important functions, such as cell-cell signaling and regulation of cell differentiation. CONCLUSION: Many lncRNAs are dysregulated upon endothelial cell activation and further experiments are needed to identify the potential biological functions of these lncRNAs.

Multiplicative interaction between mean corpuscular volume and red cell distribution width with target organ damage in hypertensive patients.

BACKGROUND: Accumulating evidence suggests that increased red cell distribution width (RDW) and mean corpuscular volume (MCV) were both poor prognostic factors for patients with cardiovascular diseases. Recently, the multiplicative interaction between RDW and MCV has been observed for predicting mortality in elderly patients without anemia; however, the relationship between the product of RDW-MCV and hypertension-induced target organ damage (TOD) has not been evaluated. METHODS: We performed a cross-sectional study in 1115 hypertensive patients. RDW and MCV were determined using automated hematology analyzers. Prevalence of TOD was evaluated by estimated glomerular filtration rate, carotid intima-media thickness, and left ventricular mass index. RESULTS: The prevalence of TOD was observed to be increased with the RDW or product of RDW-MCV quartiles. Moreover, RDW, MCV and product of RDW-MCV were significantly higher in patients with TOD compared to those without TOD. According to two logistic regression models, the associations of RDW and MCV with TOD were lost after adjustment for other factors. However, product of RDW-MCV remains an independent predictor of TOD, with per 0.4 fL increase in the product of RDW-MCV associated with a 16% increased risk of TOD (P=.012). CONCLUSIONS: The inclusion of MCV by calculating the product of RDW-MCV appears to enhance the association of RDW with TOD.

Antibiotic resistance determinants of a group of multidrug-resistant Acinetobacter baumannii in China.

A group of Acinetobacter baumannii confers multidrug resistance, but the molecular epidemiology and multidrug resistance mechanisms are poorly understood. Nineteen isolates were identified, and the antimicrobial susceptibility profile was determined using the disc diffusion method. Then, PCR of 78 kinds of resistance-associated genes were performed. A novel variant of blaADC gene: blaADC-67 gene (Genbank accession No. JX169789) was prevalent in all 19 isolates. Moreover, ISAba1 could also provide strong promoter to upregulate the expression of blaADC67 to confer resistance to beta-lactam. This is the first report of emergence of blaADC-67 in A. baumannii worldwide, which might confer resistance to beta-lactam.

[Role of liver X receptors on cardiomyocyte hypertrophy].

OBJECTIVE: To investigate the expression of liver X receptors (LXR) in hypertrophic myocardium and the effect of LXR agonist T0901317 on angiotensin II (AngII) induced cardiomyocyte hypertrophy. METHODS: Transverse aortic coarctation (TAC) or sham operation were performed in 2-month-old wide type mice (C57/B6). Two weeks later, the expression of LXR in myocardium was detected by quantitative real-time PCR analysis and Western blot analysis. The effect of LXR agonist T0901317 on AngII-induced hypertrophy in cultured neonatal rat cardiomyocytes was also assessed. RESULTS: Quantitative real-time PCR analysis and Western blot analysis showed that LXRalpha but not LXRbeta expression was upregulated post TAC both at mRNA and protein levels (All P < 0.05). AngII induced increased [(3)H] leucine incorporation and cardiomyocyte hypertrophy were significantly reduced by T0901317 in a dose-dependent manner (P < 0.05). T0901317 also dose-dependently inhibited atrial natriuretic peptide (ANP) gene expression in cardiomyocytes (P < 0.05). CONCLUSION: Our findings strongly suggest that LXR is a potent mediator of cardiomyocyte hypertrophy and LXR activation could attenuate AngII induced cardiomyocyte hypertrophy in vitro.

Relationship between drug resistance of Pseudomonas aeruginosa isolated from burn wounds and its mobile genetic elements / 中华烧伤杂志

<p><b>OBJECTIVE</b>To investigate the relationship between the drug resistance of Pseudomonas aeruginosa (PA) isolated from burn patients wounds and its mobile genetic elements, including plasmid, transposon, and integron.</p><p><b>METHODS</b>Thirty-two strains of PA were isolated from wounds exudate of hospitalized burn patients in Ningbo No. 2 Hospital. PA drug sensitivity was determined using GNS-448 drug sensitivity card and K-B tests. The genetic markers of plasmid, transposon and integron including traA, traF, tnpA, tnpU, merA, int I 1 were amplified by PCR and verified by gene sequencing.</p><p><b>RESULTS</b>Drug resistant rate of 32 PA strains to gentamicin, amikacin, cefoperazone/sulbactam, ciprofloxacin was 43.7%, 32.0%, 46.8%, 49.9%, respectively. PA drug resistant rates to piperacillin, cefotaxime, ceftazidime, cefepime, aztreonam, piperacillin/tazobactam, levofloxacin, imipenem and meropenem were all above 56.0%. Seventeen out of 32 PA strains were found to carry transposon and (or) integron genetic markers. One strain was positive for both tnpA and merA, 8 strains were positive for both merA and int I 1, 1 strain was only positive for tnpA, 2 strains were only positive for merA, and 5 strains were positive for int I 1 only.</p><p><b>CONCLUSIONS</b>PA isolated from burn wounds of hospitalized patients in Ningbo No. 2 Hospital is seriously drug resistant, which may relate with its high positive rate of mobile genetic elements of transposon and (or) integron.</p>

Interaction between polysaccharides and interferon-gamma using an improved ELISA approach / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To establish an ELISA approach to study the interaction of polysaccharides with cytokine in vitro.</p><p><b>METHODS</b>The heparin BSA complexes (HBC) were synthesized with a chemistry method and separated using a 1 X 90 cm column of Separose 4B. After identification of the complex via SDS-PAGE,the wells of ELISA plates were coated with HBC and the interaction of HBC with interferon-gamma (IFN-gamma) was detected. The effects of heparin, low molecular weight heparin (LMW heparin), chondroitin sulfate (CS), hyaluronic acid (HA) and carrageenans on the binding of HBC to IFN-gamma were tested in this system.</p><p><b>RESULT</b>Human recombinant IFN-gamma bound to heparin in a concentration dependent manner, the binding of IFN-gamma to HBC was detected at the concentration of 0.25 ng, and saturated at around 2 ng. Free heparin, LMW heparin, CS,HA and carrageenans competed for the binding of IFN-gamma to HBC with significant different ability. The IC(50)concentrations of heparin and LMW heparin were 2.40 microg/ml and 18.60 microg/ml respectively.</p><p><b>CONCLUSION</b>IFN-gamma is a cytokine with high binding affinity to heparin and carrageenans family but poor to CS-A and CS-C. ELISA is a simple, sensitive approach to detect the interaction of polysaccharides with cytokine in vitro.</p>