Objective: To explore the impact of renal function injury on diagnostic value of NT-proBNP in patients with heart failure (HF).
Methods: A total of 420 patients with cardiovascular disease at (50-75) years of age were divided into 2 groups based on left ventricular ejection fraction (LVEF): Control group, the patients with normal cardiac function, LVEF≥40%,n=232 and HF group, LVEF<40%,n=188. According to estimated glomerular ifltration rate (eGFR), each group contained 4 subgroups by Normal renal function (eGFR≥90 ml/min·1.73m2), Mild renal injury (90>eGFR≥60 ml/min·1.73m2), Moderate renal injury (60>eGFR≥30 ml/min·1.73m2) and Severe renal injury (eGFR<30 ml/min·1.73m2). The changes of NT-proBNP level at different subgroups were observed and the optimal cut-off values of NT-proBNP for HF diagnosis were measured.
Results: Compared with Control group, HF group had increased blood level of NT-proBNP,P<0.05; NT-proBNP level was negatively related to eGFR (in all patients:r=-0.664, in Control group:r=-0.686 and in HF group:r=-0.721,P<0.05). Within Control group, NT-proBNP level was similar between Normal renal function and Mild renal injury subgroups,P>0.05, while it was much higher in Moderate and Severe renal injury subgroups than Normal renal function subgroup,P<0.05. Within HF group, Severe renal injury subgroup had increased NT-proBNP level than other subgroups,P<0.05. The best cut-off value of NT-proBNP for HF diagnosis in patients with normal or mild renal injury was 1070 pg/mL (sensitivity: 91.8% and speciifcity 72.6%); with moderate renal injury was 7121 pg/mL (sensitivity: 80.2% and speciifcity: 89.7%); with severe renal injury was 33344 pg/mL (sensitivity: 83.3% and speciifcity: 80%).
Conclusion: Moderate to severe renal function injury could increase circulating level of NT-proBNP and therefore, the cut-off value of NT-proBNP for HF diagnosis should be elevated accordingly in patients of HF combing renal injury.

AIM:The aim of this study is to investigate the relationship between the ratio of transcription factors T-bet/GATA-3 in peripheral blood mononuclear cells(PBMCs)and the imbalance of Th1/Th2 cytokines from patients with asthma,and to examine whether and how CpG ODN intervention would restore the imbalanced Th1/Th2 profile in asthma patients.METHODS:Three groups of subjects with asthma(asthma group),chronic obstructive pulmonary disease(COPD group),and normal controls(control group)were included in this study.T-bet,GATA-3 and TLR9 mRNA levels were measured by reverse transcription-polymerase chain reaction(RT-PCR).Th1 cytokine IFN-? and Th2 cytokines IL-4,IL-5 and IL-13 were measured by enzyme-linked immunoabsorbent assay(ELISA)in asthma group.Cultured PBMCs from asthma patients with CpG ODN incubation were collected for measuring T-bet,GATA-3 mRNA and TLR9 mRNA.RESULTS:The ratio of T-bet/GATA-3 in asthma group was significantly lower than that in the COPD group and control group.The serum levels of IL-4,IL-5 and IL-13 had positive correlation with the ratio of T-bet/GATA-3 in asthmatic patients,and the lower serum level of IFN-? had negative correlation with the ratio.The TLR9 mRNA expression in asthma was significantly attenuated than that in COPD group and control group.Consequently,the ratio of T-bet/GATA-3 in CpG group was significantly enhanced than that in control group.CONCLUSION:These results indicate that the ratio of T-bet/GATA-3 in asthma is decreased and could represent the imbalance of Th1/Th2 cells.CpG ODN influences the ratio of T-bet/GATA-3,upregulating the T-bet mRNA expression and downregulating the GATA-3 mRNA expression,which is able to reverse the imbalance of Th1/Th2 cells.CpG-ODN may be a promising therapeutic target for asthma.

BACKGROUND:To obtain more quantum dot (QD) barcodes,the overlay peaks of fluorescence occur,leading to difficulties in identifying QD barcodes.OBJECTIVE:To identify QD barcodes of two adjacent wave length using wavelet transform technique.METHODS:Through the microscopy,the spectrum of fluorescence induced by 375 nm light was captured by spectroscopy.The spectral signal was split into multi-scale components by wavelet transform.After transformed by spline function,every component constructed a new spectrum with peaks expanded by inverse wavelet transform.RESULTS AND CONCLUSION:Interpolation operation was performed on original data to control the data length to 2n.Following wavelet transform,peak location remained unchanged,so the eigenvalue of spectrum of coding fluorescence was extracted.The spectrum of fluorescence mixed with microspheres was split,and two QD barcodes were identified.The improved barcodes identification of adjacent spectrum increase color of QD barcodes,thereby enhancing code information volume.Results show that following spectrum was processed by wavelet transform,overlay peaks of fluorescence has be expanded,and enhanced the efficiency of recognition,which lays a foundation for detecting tumor markers.

Ischemic stroke has the characteristics of high morbidity, high disability rate, and high fatality rate. There is currently no effective rehabilitation treatment method. With the advancement of basic research and preparation technology of stem cells and the extensive development of animal experiments, stem cell transplantation has shown great potential for application in the treatment of ischemic stroke. This article elaborated on the mechanism, types and sources of stem cell transplantation and transplantation methods. By reviewing the research process of stem cells in ischemic stroke model, we can provide reference for clinical research of stem cell transplantation in the treatment of ischemic stroke.

Objective: Many studies have shown that respiratory syncytial virus persistent infection may be the main cause of chronic respiratory pathology. However, the mechanism is unclear. Cystic fibrosis transmembrane conduction regulator (CFTR) is an apical membrane chloride channel, which is very important for the regulation of epithelial fluid, chloride ion, and bicarbonate transport. CFTR dysfunction will lead to changes in bronchial secretions and impair mucus clearance, which is related to airway inflammation. In our previous study, we observed the down-regulation of CFTR in airway epithelial cells in respiratory syncytial virus (RSV) infected mouse model. In this study, we further investigated the expression and function of CFTR by constructing an airway epithelial cell model of RSV persistent infection. Methods: 16HBE14o- cells were infected with RSV at 0.01 multiplicity of infection (MOI). The expression of CFTR was detected by real-time RT-PCR, immunofluorescence, and Western blotting. The intracellular chloride concentration was measured by N-(ethoxycarbonylmethyl)-6-methoxyquinolium bromide (MQAE) and the chloride current was measured by whole-cell patch clamp recording. Results:16HBE14o-cells infected with RSV were survived to successive passages of the third generation (G3), while the expression and function of CFTR was progressively decreased upon RSV infection from the first generation (G1) to G3. Exposure of 16HBE14o-cells to RSV led to the gradual increase of TGF-β1 as well as phosphorylation of Smad2 following progressive RSV infection. Disruption of TGF-β1 signaling by SB431542 prevented Smad2 phosphorylation and rescued the expression of CFTR. Conclusion:RSV infection can lead to defective CFTR function in airway epithelial cells, which may be mediated via activation of TGF-β1 signaling pathway.