Objective: To observe the influence of sot alol on the QT dispersion in patients with atrioventricular accessory pathways u nderwent radiofrequency catheter ablation (RFCA). Methods: Thirt y-six patients were divided into 2 groups by random. One was the drug group(18 cases) treated by RFCA， and sotalol 160 mg was orally administered and intracar diac electrophysiological study was performed every 30 min for 5 times. Th e other group(control group, 18 cases) only treated by RFCA.QTd,QTcd and QTLcd w ere measured before and after RFCA. Results: There was no signif icant difference with QT dispersion before and after RFCA in control group. When compared with before RFCA, QTd in patients administered sotalol was (30.9 ±14.3) ms vs (24.7±9.6) ms; QTcd(33.7±17.1) ms vs (25.2±10.1) ms; QT Lcd(30.8±14.1)ms vs (25.6±19.4) ms (P<0.05). Conclusion: Sotalol can slightly lower QT dispersion, which is beneficial for preventing malignant ventricular arrthythmia. It is safe in RFCA in pateints with accessory pathway.

Objective To investigate the risk factors of delirium in elderly patients with intertrochanteric fracture after internal fixation.Methods The data of 160 patients with intertrochanteric fractures who received internal fixation in our hospital from January 2012 to July 2014 were analyzed retrospectively.The risk factors such as age,sex,preoperative complications,preoperative cognitive function,fracture location,operation mode,operation time,anesthesia method,hospital-to-operation time and intraoperative blood loss were summarized.Results The incidence of postoperative delirium was 28.15％ in postoperative elderly patients with intertrochanteric fractures.Univariate analysis showed that delirium had correlated with preoperative cognitive impairment,preoperative preparation time,serum sodium,fentanyl,atrial fibrillation,anesthesia method,operation time and perioperative blood loss (P ＜ 0.05).The multivariate Logistic regression analysis showed that the independent risk factors of postoperative delirium were preoperative cognitive dysfunction,operative time more than 2 hours and preoperative preparation time more than 4 days.Conclusion The occurrence of postoperative delirium was associated with anesthesia method,cognitive deficits,preoperative preparation time and perioperative blood loss.The anesthesia method which had less effect on the whole body condition and less time of operation preparation can decrease the occurrence of postoperative delirium in a certain extent,which is conducive to improving the prognosis.

Objective: To observe the influence of sotalol on the QT dispersion in patients with atrioventricular accessory pathways underwent radiofrequency catheter ablation (RFCA). Methods: Thirty six patients were divided into 2 groups by random. One was the drug group(18 cases) treated by RFCA, and sotalol 160 mg was orally administered and intracardiac electrophysiological study was performed every 30 min for 5 times. The other group(control group, 18 cases) only treated by RFCA.QTd,QTcd and QTLcd were measured before and after RFCA. Results: There was no significant difference with QT dispersion before and after RFCA in control group. When compared with before RFCA, QTd in patients administered sotalol was (30.9?14.3) ms vs (24.7?9.6) ms; QTcd(33.7?17.1) ms vs (25.2?10.1) ms; QTLcd(30.8?14.1)ms vs (25.6?19.4) ms ( P

Objective:To investigate the effect of transforming growth factor (TGF- β) signal in muscle fiber itself during inflammation/immunity response on intramuscular inflammation. Methods:Sixteen wild C57BL/6 mice (wild group) and sixteen mice with skeletal muscle-specific deficiency of T βRⅡ (knock-out group) between 4-8 weeks of age were selected for this study. Acute muscle injury in mice was induced by injection of myotoxin cardiotoxin (CTX) into gastrocnemius. The differences in intramuscular inflammation were compared between the wild and knock-out groups on 0, 4, 7 and 10 d after CTX injection by observing exudation of mononuclear phagocytes, macrophages, M1 type macrophages, CD4 +T cells and helpers T cells (Th1, 2&17). Two newborn C57BL/6 wild mice and 2 SM TGF- βr2-/- knock-out mice were selected to culture primary myoblasts in vitro which were divided into 2 groups: an interferon group subjected to interferon simulation and a control group subjected to addition of an equal amount of solvent. The differences in expression of IL-6, IL-10, MCP-1, MIP-1α, H-2K b, H2-Ea, Toll-like receptor (TLR)3 and TLR7 were compared between the interferon and control groups, as well as between the wild and knock-out groups. Results:On 4&7 d after CTX injection, the ratios of mononuclear/macrophage (75.73%±3.62%, 45.27%± 2.32%), macrophages (38.67%±2.76%, 24.87%±2.19%), M1 macrophages (43.21%±0.11%, 30.43%±2.19%), CD4 +T cells (20.13%±1.62%, 5.67%±0.32%) in the muscle tissue from the knock-out mice were significantly higher than those from the wild mice (58.52%±2.43%, 29.21%±2.45%; 20.63%±2.32%, 16.23%±1.25%; 24.98%±0.35%, 14.23%±1.69%; 10.70%±0.43%, 2.50%±0.45%), with a majority of Th1&Th17 ( P<0.05). In vitro results showed that the levels of IL-6, MCP-1, MIP-1α, H-2K b, H2-Ea and TLR3 were significantly upregulated in the interferon group compared with the control group and that such upregulation in the nock-out mice was more significant than in the wild mice ( P<0.05). Conclusions:Endogenous TGF- β signal activation plays a role in the functional recovery after muscle trauma, because it is involved in the regulation of immune behavior of muscle fibers, thus affecting intramuscular inflammation and muscle regeneration.

Objective To determine the impact of dental nurses′knowledge sharing behavior and self-efficiency on professional identity. Methods A total of 88 dental nurses in Xiangyang were tested by Professional Identity Inventory for Nurse,Knowledge Sharing Behavior Scale and General Self-efficacy Scale. Results The mean score of professional identity was (5.60 ± 0.56) points, the mean score of knowledge sharing behavior was (2.59 ± 0.77) points, the mean score of general self-efficacy was (2.66 ± 0.46) points. Knowledge sharing behavior and self-efficiency were positively correlated with professional identity(r=0.626, 0.342, P<0.01). Regression analysis showed that the organizational communications, communities of practice, written contributions and general self-efficacy could explain 54.3% of the variance for dental nurses′professional identity. Conclusions Nursing managers should focus on the shortcomings of dental nurses′ knowledge sharing behavior and general self-efficacy, and promote interventions to enhance dental nurses′knowledge sharing behavior and general self-efficacy and improve the level of professional identity.

Objective:To investigate impacts of usnic acid(UA)on malignant behavior of gastric cancer cells by regulating the chemokine(C-C motif)ligand 2(CCL2)-CCL2 receptor(CCR2)signal axis.Methods:SGC-7901 cells,a well growing human gastric cancer cell line,were treated with different concentrations of UA,which were grouped into low concentration(UA-L)group(62.5 μmol/L UA),medium concentration(UA-M)group(125 μmol/L UA)and high concentration(UA-H)group(250 μmol/L UA);meantime,the cells were transfected with CCL2 overexpression vector(pc DNA3.1 CCL2),empty vector(pc DNA3.1),silenced CCL2(si CCL2)and negative control(si control),and SGC-7901 cells were treated with 250 μmol/L UA,labeled as UA-H+pc DNA3.1 CCL2 group,UA-H+pc DNA3.1 group,UA-H+si control group and UA-H+si CCL2 group,another untreated SGC-7901 cells were taken as the control group.Flow cytometry,MTT and qRT-PCR were applied to detect cell apoptosis,proliferation,and expres-sion levels of CCL2 and CCR2 mRNA;Western blot was applied to detect expression levels of PD-L1,apoptotic protein(Bax),proli-ferative protein(CyclinD1,CCL2,CCR2)and immune escape related protein(B7H1);after co-culturing with CD8+T cells isolated and cultured in vitro,ELISA was applied to detect levels of IL-4,IFN-γ and IL-10 in the supernatant.Gastric cancer cells in each group were co-cultured with activated peripheral blood mononuclear cell(PBMC)1∶1 for 72 hours,and the sensitivity of gastric can-cer cells in each group to T-cell-mediated killing was compared.Results:Compared with control group,cell proliferation rate,IL-10 level,CyclinD1,PD-L1,CCL2,CCR2 and B7H1 protein and mRNA expressions,cell counts after co-culturing with activated PBMC 1∶1 for 72 hours in UA-L group,UA-M group and UA-H group were obviously reduced,while apoptosis rate,IL-4 and IFN-γ levels,Bax protein expression were obviously increased(P<0.05);compared with UA-H+pc DNA3.1 group,cell proliferation rate,IL-10 level,CyclinD1,PD-L1,CCL2,CCR2 protein and mRNA expressions,cell counts after co-culturing with activated PBMC 1∶1 for 72 hours in UA-H+pc DNA3.1 CCL2 group were obviously increased,while apoptosis rate,IL-4 and IFN-γ levels,and Bax protein ex-pression were obviously reduced(P<0.05);compared with UA-H+si control group,cell proliferation rate,IL-10 level,CyclinD1,PD-L1,CCL2,CCR2 and B7H1 protein and mRNA expressions,cell counts after co-culturing with activated PBMC 1∶1 for 72 hours in UA-H+si CCL2 group were obviously reduced,while apoptosis rate,IL-4 and IFN-γ levels and Bax protein expression were obviously increased(P<0.05).Conclusion:UA can inhibit gastric cancer cells proliferation,immune escape,and induce apoptosis,which may be related to the inhibition of the CCL2-CCR2 signaling axis.

Objective To investigate the effect of E2 signaling in myofibers on muscular macrophage efferocytosis in mice with cardiotoxin-induced acute skeletal muscle injury.Methods Female wild-type C57BL/6 mice with and without ovariectomy and male C57BL/6 mice were given a CTX injection into the anterior tibial muscle to induce acute muscle injury,followed by intramuscular injection of β-estradiol(E2)or 4-hydroxytamoxifen(4-OHT).The changes in serum E2 of the mice were detected using ELISA,and the number,phenotypes,and efferocytosis of the macrophages in the inflammatory exudates and myofiber regeneration and repair were evaluated using immunofluorescence staining and flow cytometry.C2C12 cells were induced to differentiate into mature myotubes,which were treated with IFN-γ for 24 before treatment with β-Estradiol or 4-OHT.The treated myotubes were co-cultured with mouse peritoneal macrophages in a 1:2 ratio,followed by addition of PKH67-labeled apoptotic mouse mononuclear spleen cells induced by UV irradiation,and macrophage efferocytosis was observed using immunofluorescence staining and flow cytometry.Results Compared with the control mice,the female mice with ovariectomy showed significantly increased mononuclear macrophages in the inflammatory exudates,with increased M1 cell percentage,reduced M2 cell percentage and macrophage efferocytosis in the injured muscle,and obviously delayed myofiber regeneration and repair.In the cell co-culture systems,treatment of the myotubes with β-estradiol significantly increased the number and proportion of M2 macrophages and macrophage efferocytosis,while 4-OHT treatment resulted in the opposite changes.Conclusion In injured mouse skeletal muscles,myofiber E2 signaling promotes M1 to M2 transition to increase macrophage efferocytosis,thereby relieving inflammation and promoting muscle regeneration and repair.

Objective To investigate the effect of E2 signaling in myofibers on muscular macrophage efferocytosis in mice with cardiotoxin-induced acute skeletal muscle injury.Methods Female wild-type C57BL/6 mice with and without ovariectomy and male C57BL/6 mice were given a CTX injection into the anterior tibial muscle to induce acute muscle injury,followed by intramuscular injection of β-estradiol(E2)or 4-hydroxytamoxifen(4-OHT).The changes in serum E2 of the mice were detected using ELISA,and the number,phenotypes,and efferocytosis of the macrophages in the inflammatory exudates and myofiber regeneration and repair were evaluated using immunofluorescence staining and flow cytometry.C2C12 cells were induced to differentiate into mature myotubes,which were treated with IFN-γ for 24 before treatment with β-Estradiol or 4-OHT.The treated myotubes were co-cultured with mouse peritoneal macrophages in a 1:2 ratio,followed by addition of PKH67-labeled apoptotic mouse mononuclear spleen cells induced by UV irradiation,and macrophage efferocytosis was observed using immunofluorescence staining and flow cytometry.Results Compared with the control mice,the female mice with ovariectomy showed significantly increased mononuclear macrophages in the inflammatory exudates,with increased M1 cell percentage,reduced M2 cell percentage and macrophage efferocytosis in the injured muscle,and obviously delayed myofiber regeneration and repair.In the cell co-culture systems,treatment of the myotubes with β-estradiol significantly increased the number and proportion of M2 macrophages and macrophage efferocytosis,while 4-OHT treatment resulted in the opposite changes.Conclusion In injured mouse skeletal muscles,myofiber E2 signaling promotes M1 to M2 transition to increase macrophage efferocytosis,thereby relieving inflammation and promoting muscle regeneration and repair.