Objective To compare H_p(3) calibration with a homemade (A) thermoluminescent dosimeter (TLD) and an imported (B) TLD in a standard X-ray RQR radiation field, to explore the different responses of A and B, and to provide foundation for the calibration of H_p(3). Methods A column mode was selected. H_p(3) calibration was performed using A and B in a standard X-ray RQR radiation field in the Secondary Standard Dosimetry Laboratory, National Institute for Radiological Protection, China Center for Disease Control and Prevention. Angle response, energy response, and linear response were calibrated with RQR4 (60 kV), RQR7 (90 kV), and RQR9 (120 kV), respectively. Results In terms of angle response, the calibration results of A were relatively high, while the calibration results of B were relatively low. In terms of energy response, the calibration results showed a similar pattern to angle response. In terms of linear response, the calibration results of both A and B were satisfactory. Conclusion Both A and B can be used for normal calibration of H_p(3) in a standard X-ray RQR radiation field. However, in actual monitoring, attention should be paid to the energy and angle response values of TLDs.

In order to study the signal pathway secreting type Ⅰ interferon in porcine alveolar macrophages (PAMs) infected with porcine circovirus type 2 (PCV2), the protein and the mRNA expression levels of cGAS/STING pathways were analyzed by ELISA, Western blotting and quantitative reverse transcriptase PCR in PAMs infected with PCV2. In addition, the roles of cGAS, STING, TBK1 and NF-κB/P65 in the generation of type I interferon (IFN-I) from PAMs were analyzed by using the cGAS and STING specific siRNA, inhibitors BX795 and BAY 11-7082. The results showed that the expression levels of IFN-I increased significantly at 48 h after infection with PCV2 (P<0.05), the mRNA expression levels of cGAS increased significantly at 48 h and 72 h after infection (P<0.01), the mRNA expression levels of STING increased significantly at 72 h after infection (P<0.01), and the mRNA expression levels of TBK1 and IRF3 increased at 48 h after infection (P<0.01). The protein expression levels of STING, TBK1 and IRF3 in PAMs infected with PCV2 were increased, the content of NF-κB/p65 was decreased, and the nuclear entry of NF-κB/p65 and IRF3 was promoted. After knocking down cGAS or STING expression by siRNA, the expression level of IFN-I was significantly decreased after PCV2 infection for 48 h (P<0.01). BX795 and BAY 11-7082 inhibitors were used to inhibit the expression of IRF3 and NF-κB, the concentration of IFN-I in BX795-treated group was significantly reduced than that of the PCV2 group (P<0.01), while no significant difference was observed between the BAY 11-7028 group and the PCV2 group. The results showed that PAMs infected with PCV2 induced IFN-I secretion through the cGAS/STING/TBK1/IRF3 signaling pathway.
Animals ; Cells, Cultured ; Circovirus ; Interferon Type I/genetics* ; Macrophages, Alveolar/virology* ; Membrane Proteins/metabolism* ; Nucleotidyltransferases/metabolism* ; Signal Transduction ; Swine

Objective To compare the clinical characteristics,and outcomes of patients with heart failure with different left ventricular ejection fractions (LVEF).Methods A total of 1 182 hospitalized patients with heart failure (HF) were enrolled and retrospectively studied in the present study.The patients were stratified by LVEF as reduced (HFrEF,LVEF ＜ 40％,n =313),mid-range (HFmrEF,40％ ≤ LVEF ＜50％,n =287) and preserved (HFpEF,LVEF≥50％,n =582) ejection fraction groups.Among the 1 182 cases,941 of them (81.3％,84.9％,and 84.0％ inHFrEF,HFmrEF and HFpEF groups,respectively) were followed up for an median duration of 27.3 months.Results (1) Among the study patients,26.5％ were in HFrEF,24.3％ in HFmrEF,and 49.2％ in HFpEF groups.(2) Ischemic heart disease with HFmrEF was more frequent than that in patients with HFrEF.The average age,percentage of female subjects,systolic blood pressure,uric acid,N terminal B-type natriuretic peptide precursor (NT-proBNP),hemoglobin,and the incidence of hypertensive heart disease,anemia,atrial fibrillation in patients with HFmrEF were higher than those in patients with HFrEF,but lower than those in patients with HFpEF (all P ＜0.01).(3) The all-cause cumulative mortality was 10.8％ at 1 year,20.6％ at 2 years and 35.9％ at 5 years.No difference was observed in the all-cause cumulative mortality at 1 year,2 years,5 years among the three groups (all P ＞ 0.05).Conclusions The HFmrEF patients,as a new and distinct group,were with many intermediate characteristics compared with HFrEF and HFpEF subjects.However,the all-cause mortality was not significantly differeut among HF patients with different LVEF.

Objective To investigate the influence of benzopyrene on extracellular matrix(ECM) protein deposition of human airway smooth muscle cells(HASMC) and the related pathway mechanism.Methods HASMC were primarily cultured and the 2-6 generations cells were applied in this experiment.The expression amount of ECM gene and protein was detected by real time PCR and Western Blot the phosphorylation level was analyzed by using the Western Blot method.Results Benzopyrene could to increase the expression of HASMC collagen Ⅰ α1 protein (P＜0.01) and ECM protein (including collagen Ⅰ α1,versican,fibronectin,laminin α2) mRNA(P＜0.05).Benzopyrene could induce the rapid increase of ERK1/2 phosphorylation level (P＜0.01).Furthermore,the ERK pathway inhibitor PD98059 could significantly inhibit the increase of benzopyrene-induced collagen Ⅰ α1 (P＜0.01)and ECM protein(including collagen Ⅰ α1,versican,fibronectin,laminin α2) mRNA expression(P＜0.01).Conclusion Benzopyrene induces the ECM protein deposition of HASMC by activating the ERK1/2 pathway,blocking the ERK1/2 signal pathway can inhibit the benzopyrene-induced airway remodeling.

Objective: To explore the relationship between serum levels of immunoglobulin E (IgE) and calciifc aortic valve disease (CAVD) in relevant patients.
Methods: A total of 394 patients were enrolled in our study. Based on echocardiography presentation, the patients were divided into 2 groups: CAVD group,n=169 and Non-CAVD group,n=225. Serum levels of IgE were examined by chemiluminescence method. The IgE levels were compared between 2 groups and the relationship between serum IgE level and CAVD was analyzed.
Results: Serum levels of IgE in CAVD group was significantly higher than Non-CAVD group 113.30 IU/ml vs 63.76 IU/ml (P<0.05); multivariate logistic regression analysis conifrmed above difference (P<0.05) and it also indicated that the alteration of surum IgE level is obviously related to CAVD occurrence.
Conclusion: Serum IgE level is obviously increased in CAVD patients. IgE is an independent biochemical indicator of CAVD, it may play the important role in CAVD pathogenesis.

Objective To investigate of the effect and mechanisman of SERCA2 on the phenotype modulation of HASMCs. Methods HASMCs were starved for 5 days and divided into different groups ,then we observed morphology change of the cells from the microscope and detected a-actin、SERCA2 and p-ERK by Western Blot,cells proliferation was observed by CCK-8 method. Results Compared with the control group,PDGF could reduce a-actin of HASMCs and increased the cells proliferation ability ,TSG could significantly inhibit the effect (P<0.01), PDGF could also significantly inhibit SERCA2 protein and increased the expression p-ERK (P<0.01), while U0126 significantly inhibited the effect (P < 0.01). Conclusion PDGF may induce HASMCs phenotype modulation through the regulation of SERCA2 and p-ERK.

OBJECTIVETo investigate the effect of anti-miR-145 on human airway smooth muscle cell (HASMC) proliferation and osteopontin systhesis in vitro and explore the mechanisms.

METHODSHASMCs were treated with 10-100 nmol/L anti-miR-145, and the cell proliferation and apoptosis were investigated using a CCK-8 assay and flow cytometry, respectively. The changes in osteopontin synthesis after the treatment was quantified with Western blotting.

RESULTSTreatment with 10 and 50 nmol/L anti-miR-145 significantly promoted the proliferation and osteopontin synthesis in HASMCs (P<0.05 or <0.01), and 50 nmol/L anti-miR-145 obviously inhibited the cell apoptosis (P<0.01).

CONCLUSIONAnti-miR-145 promotes HASMC proliferation and osteopontin synthesis and inhibits HASMC apoptosis in vitro, indicating the important role of anti-miR-145 in the pathogenesis of airway remodeling.

Airway Remodeling ; Apoptosis ; Cell Proliferation ; Cells, Cultured ; Humans ; MicroRNAs ; antagonists & inhibitors ; Myocytes, Smooth Muscle ; drug effects ; Osteopontin ; biosynthesis ; Respiratory System ; cytology

Objective To investigate the effect of anti-miR-145 on human airway smooth muscle cell (HASMC) proliferation and osteopontin systhesis in vitro and explore the mechanisms. Methods HASMCs were treated with 10-100 nmol/L anti-miR-145, and the cell proliferation and apoptosis were investigated using a CCK-8 assay and flow cytometry, respectively. The changes in osteopontin synthesis after the treatment was quantified with Western blotting. Results Treatment with 10 and 50 nmol/L anti-miR-145 significantly promoted the proliferation and osteopontin synthesis in HASMCs (P<0.05 or<0.01), and 50 nmol/L anti-miR-145 obviously inhibited the cell apoptosis (P<0.01). Conclusion Anti-miR-145 promotes HASMC proliferation and osteopontin synthesis and inhibits HASMC apoptosis in vitro, indicating the important role of anti-miR-145 in the pathogenesis of airway remodeling.

Objective To investigate the effect of anti-miR-145 on human airway smooth muscle cell (HASMC) proliferation and osteopontin systhesis in vitro and explore the mechanisms. Methods HASMCs were treated with 10-100 nmol/L anti-miR-145, and the cell proliferation and apoptosis were investigated using a CCK-8 assay and flow cytometry, respectively. The changes in osteopontin synthesis after the treatment was quantified with Western blotting. Results Treatment with 10 and 50 nmol/L anti-miR-145 significantly promoted the proliferation and osteopontin synthesis in HASMCs (P<0.05 or<0.01), and 50 nmol/L anti-miR-145 obviously inhibited the cell apoptosis (P<0.01). Conclusion Anti-miR-145 promotes HASMC proliferation and osteopontin synthesis and inhibits HASMC apoptosis in vitro, indicating the important role of anti-miR-145 in the pathogenesis of airway remodeling.

OBJECTIVETo investigate the effects of curcumin on the expression of syndecan-4 protein and p44/42 mitogen- activated protein kinase(MAPK) phosphorylation in rat vascular smooth muscle cells (VSMCs) induced by tumor necrosis factor-α (TNF-α) in vitro.

METHODSRat VSMCs cultured in vitro were stimulated for 24 h by 20 ng/ml TNF-α, 20 µmol/L curcumin, or 20 ng/ml TNF-α plus 20 µmol/lL curcumin. /assay was adopted to evaluate the proliferation of the VSMCs, and the expression of syndecan-4 protein and phosphorylated p44/42 MAPK were determined by Western blotting.

RESULTSCompared with the normal control cells, VSMCs exposed to TNF-α showed significantly enhanced proliferation (P/0.01). Curcumin treatment did not obviously affect the growth of otherwise untreated VSMCs(P>0.05), but could significantly suppress TNF-α-induced proliferation of VSMCs (P/0.01). TNF-α treatment also significantly increased the expression of syndecan-4 protein and phosphorylated p44/42 MAPK (P<0.01), which was markedly lowered by treatment with curcumin (P/0.01). Curcumin alone did not produce any obvious effects on the expression of syndecan-4 protein or phosphorylated p44/42 MAPK (P>0.05).

CONCLUSIONCurcumin can suppress the proliferation of rat VSMCs and lower the expression of syndecan-4 protein and phosphorylated p44/42 MAPK in TNF-α-induced VSMCs.

Animals ; Cells, Cultured ; Curcumin ; pharmacology ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Muscle, Smooth, Vascular ; drug effects ; metabolism ; Phosphorylation ; drug effects ; Rats ; Rats, Sprague-Dawley ; Syndecan-4 ; metabolism ; Tumor Necrosis Factor-alpha ; pharmacology