Objective:To explore the radioprotective effect of TFA on the 60Co?-rayirradiated mice and provide an experimental basis for the clinical use of TFA.Methods:Normal female Kunming mice were intragastrically administered with TFA for 3days before exposure to lethal dose of 60Co?-ray radiation and then continuously administered with TFA for 11days.The 30-days survival rate and average life span of irradiated mice were estimated.Meanwhile the body weight,peripheral blood parameters,spleen indexes and the pathological changes of spleen were also observed in the sublethal dose irradiated mice.Results:TFA could not only increase the 30-days survival rate and the average survival days of dead mice(P

Objective To investigate the effect of budesonide atomization on tracheal extubation in children.Methods A total of 85 patients with tracheal intubation in Tianjin Children's Hospital from May 2013 to September 2016 were selected in this study.Patients were randomly divided into budesonide group (n=44) and dexamethasone group (n=41).The budesonide group was given 1 mg of budesonide for inhalation 30 min before extubation,and 1 mg of budesonide inhalation immediately after extubation.Then every 8 hours for 0.5-1.0 mg budesonide inhalation for 4 days.The dexamethasone group was given dexamethasone 0.2-0.3 mg/kg intravenously 30 min before extubation,and dexamethasone 2.5-5.0 mg inhalation immediately after extubation.Then dexamethasone 2.5-5.0 mg inhalation was given every 8 hours for 4 days.The incidence of laryngeal edema (stridor,hoarseness),the time of extinction,the expression of hypoxia,reintubation rate within 24 hours and secondary infection rate after extubation were compared between the two groups.Results There were no significant differences in the mission success rate,the incidence of laryngeal edema,the time of extinction,the incidence of hypoxia and re-intubation rate between the two groups (P ＞ 0.05).Two patients were found secondary infection after extubation in dexamethasone group.Conclusion Both budesonide and dexamethasone show curative effects on the prevention and treatment of laryngeal edema after extubation.Budesonide atomization can replace systemic corticosteroids,thus reducing the adverse reactions of glucocorticoids.We recommend the use of budesonide in treating adverse events after extubation.

Objective To investigate the effect of interleukin-17 (IL-17) in the gastric cancer cell migration and invasion via regulating epithelial-mesenchymal transition (EMT) and its potential function.Methods (1) Human gastric cancer cell MGC-803 lines in the logarithmic growth phase were stimulated by 0, 1 ng/mL, 10 ng/mL,100 ng/mL and 1μg/mL of IL-17 for 48 hours, and the phenotypic changes were observed.The concentration of IL-17 was selected for follow-on experiments based on the most obvious phenotypic changes.Gastric cancer cell MGC-803 which were stimulated by 100 ng/mL of IL-17 and PBS for 48 hours were allocated into the experimental group and control group, respectively.(2) The expressions of E-cadherin and Vimentin mRNA in gastric cancer cells were assayed through real-time PCR (RT-PCR).(3) The relative expressions of E-cadherin and Vimentin proteins in gastric cancer cells were assayed by the Western blot.(4) The scratch test and Transwell detection were also utilized to study the migration and invasion of gastric cancer cell MGC-803 in vitro.Measurement data with normal distribution were presented as-x ± s and comparison between groups was analyzed using the t test.Results (1) There were significant phenotypic changes in the gastric cancer cell after the different concentration of IL-17 stimulated gastric cancer cell MGC-803 for 48 hours.Cells were changed from polygonal and tight junction to spindle and loosely junction with a deterioration of cell adhesion.Cell phenotypes were gradually changed as the concentration of IL-17 was changed from 0 to 100 ng/mL.Phenotypic changes were the most obvious when 100 ng/mL of IL-17 was used, but these were non-significant as the concentration of IL-17 increased to 1 μg/mL with the death and floating of some cells.(2) The relative expressions of E-cadherin mRNA and Vimentin mRNA in RT-PCR were 0.45 ±0.13 and 1.06 ±0.23 in the experimental group and 2.39 ±0.55 and 1.23±0.41 in the control group, respectively, with significant differences (t =3.811, 2.923, P ＜0.05).(3) The results of Western blot showed the relative expressions of E-cadherin and Vimentin proteins were 0.86 ± 0.17 and 1.56 ± 0.29 in the experimental group and 1.01 ± 0.12 and 0.56 ± 0.17 in the control group, respectively, with significant differences (t =3.551, 3.601, P ＜ 0.05).(4) Cell migration in the 2 groups were detected by the scratch test at 36 hours after scratch test, and the width of scratch in the experimental and control groups were (0.76 ± 0.13) mm and (0.40 ± 0.15) mm, showing a significant difference (t =3.095, P ＜ 0.05).Transwell detection showed number of transmembrane cell in the experimental and control groups were 159 ±28 and 94 ± 18, respectively, with a significant difference (t =3.307, P ＜ 0.05).Conclusion IL-17 can promote the migration and invasion of gastric cancer cells via stimulating alteration of EMT.

Objective Mechanisms of pulmonary vein isolation (PVI) for atrial fibrillation remain controversy.This study aimed to investigate the impact of PVI on vagal modulation to atria.Methods Eighteen adult mongrel dogs under general anesthesia were randomly divided into two groups.Bilateral cervical sympathovagal trunks were decentralized and sympathetic effects was blocked by metoprolol administration.Atrial electrical remodeling (AER) was established by rapid right atrial pacing at the rate of 600 bpm for 30 minutes.PVI was performed in group A.Atrial effective refractory period (ERP),vulnerability window (VW) of atrial fibrillation,and sinus rhythm cycle length (SCL) were measured at baseline and during vagal stimulation before and after atrial rapid pacing with and without PVI at fight atrial appendage (RAA),left atrial appendage (LAA),distal coronary sinus (CSd) and proximal coronary sinus (CSp).Results (1) Effects of PVI on vagal modulation:Shortening of SCL during vagal stimulation decreased significantly after PVI compared with that before PVI in group A (P＜0.001).Shortening of ERP during vagal stimulation decreaseed significantly after PVI compared with that before PVI (P＜0.05).VW of atrial fibrillation during vagal stimulation decreased significantly after PVI compared with that before PVI (P＜0.05).(2) Effects of PVI on AER:shortening of ERP before and after atrial rapid pacing increased significantly at baseline and vagal stimulation in group B compared with that in group A (P＜0.05).VW during vagal stimulation increased significantly after atrial rapid pacing in group B (P＜0.05).Conclusion PVI attenuates the vagal modulation to the atria,thereby decreases the susceptibility to atrial fibrillation mediated by vagal activity.PVI releases AER,which maybe contributes to the vagal denervation.Our study indicates that PVI not only can eradicate triggered foci but also modify substrates for AF.(J Geriatr Cardiol 2008;5:28-32)

Objective To investigate the effect of arginase (Arg) inhibitor N-ω-Hydroxy-L norArginine (nor-NOHA) on high glucose cultured rhesus macaque retinal vascular endothelial cell line (RF/6A) in vitro.Methods The RF/6A cells were divided into the following 4 groups:normal control group (5.0 mmol/L of glucose,group A),high glucose group (25.0 mmol/L,group B),high glucose with 125 mg/L nor-NOHA group (group C),and high glucose with 1％ DMSO group (group D).The proliferation,migration ability and angiogenic ability of RF/6A cells were measured by Methyl thiazolyl tetrazolium (MTT),transwell chamber and tube assay respectively.The express of Arg Ⅰ,eNOS,iNOS mRNA of RF/6A cells were measured by real-time polymerase chain reaction (RT-PCR),Enzyme-linked immuno sorbent assay (ELISA) was used to detect the expression of NO and interleukine (IL)-1b of RF/6A cells.Results The proliferation,migration,and tube formation ability of group A (t=2.367,5.633,7.045;P＜0.05) and group C (t=5.260,6.952,8.875;P＜0.05)were significantly higher than group B.RT-PCR results showed the Arg Ⅰ and iNOS expression in group B was higher than that in group A (t=6.836,3.342;P＜0.05) and group C (t=4.904,7.192;P＜0.05).The eNOS expression in group B was lower than that in group A and group C (t=4.165,6.594;P＜0.05).ELISA results showed NO expression in group B was lower than that in group A and group C (t=4.925,5.368;P＜0.05).IL-1b expression in group B was higher than that in group A and group C (t=5.032,7.792;P＜0.05).Conclusions Nor-NOHA has a protective effect on cultured RF/6A cells in vitro and can enhance its proliferation,migration and tube formation.The mechanism may be inhibiting the oxidative stress by balancing the expression of Arg/NOS.

Objective To investigate the effects of exosomes from cultured human retinal pigment epithelium (ARPE-19) cells affected by oxidative stress on the proliferation and expression of vascular endothelial growth factor-A (VEGF-A) and Akt of ARPE-19 cells. Methods Culture ARPE-19 cells. The concentration of 2.5μmol/L rotenone was selected to simulate oxidative stress and isolated ARPE-19-exosome. Exosomes were isolated by ExoQuick exosome precipitation solution. Transmission electron microscopy was used to identify the morphology of exosomes. Western blot was used to detect exosomes’ surface-specific maker protein CD63. ARPE-19 cells affected by oxidative stress were cultured with exosome as experimental group, normal ARPE-19 cells were cultured with exosome as control group. The cell proliferation was examined by methyl thiazolyl tetrazolium assay. Western blot and immunofluorescence assay were used to detect the expression levels of VEGF-A and Akt protein. Real-time quantitative polymerase chain reaction (RT-PCR) was used to detect the levels of VEGF-A mRNA and Akt mRNA. Results The diameter of normal ARPE-19-exosomes ranged from 50 to 150 nm. The isolated exosomes expressed CD63. AREP-19 cells were cultured with ARPE-19 (affected by rotenone)-exosome, the cell viability in experimental group was significantly reduced than in the control group. Green fluorescence was observed in the cytoplasm under fluorescence microscope. Compared with the control group, VEGF-A was up-regulated expressed and Akt was down-regulated expressed. Western blot results showed that, VEGF-A protein expression in the experimental group were higher than the control group. Akt protein expression in the experimental group were less than the control group. The difference was statically significant (t=3.822, 6.527;P<0.05). RT-PCR results showed that VEGF-A mRNA expression levels was higher in the experimental group than the control group. Akt mRNA expression levels was lower in the experimental group than the control group. The difference was statically significant (t=8.805,?7.823;P<0.05). Conclusions Exosomes from ARPE-19 cells affected by oxidative stress inhibit the proliferation of normal ARPE-19 cells, increase the expression of VEGF-A and reduce the expression of Akt.

ObjectiveTo investigate the effects of moxa smoke versus tobaccosmoke on autonomous behaviors and hippocampal expression of glial fibrillary acidic protein (GFAP) in apolipoprotein E gene knockout (ApoE-/-) mice.Method Thirteen 8-week-old C57BL/6 mice constituted a blank control group. Twenty-seven ApoE-/-mice of the same age were randomized into ApoE-/-model, moxa smoke and tobacco smoke groups. The tobacco smoke and moxa smoke groups of mice were exposed to smoke 5-15 mg/m3circumstances. Every group of mice was intervened in 20 min. daily, six days a week, for atotal of 12 weeks. A behavioral test was conducted in week 13. The animals were then sacrificed to take the materials. Hippocampal GFAP in the brain was measured by an immunohistochemical method.ResultAutonomous activities were significantly more in theblank group than in the model group (P<0.05) and significantly fewer in the tobacco smoke group than in the blank group (P<0.05). There was no statistically significant difference in autonomous activities between the tobacco smoke group and the model or moxa smoke group (P>0.05). Moving distance was longer in the moxa smoke group than in the model group (P<0.05). Standing-up number was smaller in the moxa smoke group than in the blank group (P<0.05). Integral optical density of GFAP immune reaction products in the hippocampus was significantlyhigher in the model group of mice than in the blank and moxa smoke groups (P<0.05). Hippocampal GFAP expression was significantly higher in the group of mice than in the moxa smoke and blank groups (P<0.05).Conclusion Moxa smoke can increase the excitability of central nervous system in mice and reduce hippocampal GFAP expression in a mice model of Alzheimer disease.

Objective To observe the effect of PM10 (inhalable particles) in moxa smoke on apoptosis of human lung adenocarcinoma cell line-A549 cells, and explore the possible mechanisms of inducing apoptosisMethods The A549 cells were studied in vitro experiment method, which were stained by Hoechest33258 staining method. Their morphological changes of apoptosis were observed by the fluorescence microscopy. The levels of intracellular Ca2+ and reactive oxygen species (ROS), and expression of NF-κB p65 were also measured.Results Some apoptotic cells were observed after treated with moxa smoke PM10 in the concerntration of 400μg/mL. After 4 hours intervention by moxa smoke PM10 in A549 cells, the intracellular Ca2+ level increased significantly (P<0.01). Compared with the blank control group, the expression of NF-κB p65 decreased significantly (P<0.05) after intervention of moxa smoke PM10 with different concerntrations for 4 hours. When the A549 cells were cultured with moxa smoke PM10 for 20 hours, the expression of p65 decreased significantly (P<0.05) in the concerntrations of 70, 280μg/mL, while there was no significant change in the concerntration of 140μg/mL (P>0.05). Compared with the blank control group, ROS level was significantly lower (P<0.05) in A549 cells after intervention of moxa smoke PM10.Conclusion PM10 in moxa smoke could induce apoptosis of A549 cells, could increase cytosolic Ca2+ level.

Background Atrial electrical remodeling(AER)plays an important role in the pathogenesis and maintenance of atrialfibrillation.However,little is known about modulation of vagal activilty to AER.This study aimed to investigate the relationshipbetween vagal moduation and AER. Methods Twenty four adult mongrel dogs under general anesthesia were randomized into 3groups.Sympathetic activity was blocked by administration of metoprolol in 3 groups.The changes in vagal modulation to atria afterAER were observed in 10 dogs without vagal interruption in group A.The effects of vagal intervention on AER were investigated in 8dogs with administration of atropine in group B.The impact of aggressively vagal activity on AER was studied in 6 dogs with bilateralcervical vag sympathetic trunLks stimulation during AER in group C.Bilateral cervicall vagosympathetic trunks were decentralized.Multipolar catheters wereplaced into high right atria(RA),coronary sinus(CS)and rightventricle(RV).AER was induced by 600 bpmpacing through RA catheter for 30 minutes.Attial effective refractory period(ERP)and vulnerability window (VW)of atrial fibrillationwere measured with and without vagal stimulation before and after AER.Results In group A,ERP decreased significantly at baselineand during vagal stimulation after AER compared with that beforeAER(all P＜0.05).In group B,ERP remaind unchanged at baselineand vagal stimulation after AER compared with tbat before AER (all P＞0.05).In group C,ERP shortened significantly at baseline andvagal stimulation after AER compared with that before AER(all P＜0.05).ERP shortening after AER in Groups A and C increasedsignificantly than that in group B (all P＜0.05).Atrial fibrillation could not be induced at baseline(VW close to 0) before and after AERin three groups.VW became widen significantly during vagal stimulation after AER compared with that before AER in Groups A and C(all P＜0.05),while VW remained unchanged in group B (VW close to 0).Conclusions Short-term AER results in the decrease inERP.AER is accompanied by the increases in atrial vagal modulation.The increased vagal activity and vagal stimulation promote AER,thereby increase the susceptibility to atrial fibrillation.The interrupted vagal activity attenuates AER.thereby suppresses the atriaIfibrillation mediated by vagal stimutlation.

Astract:Objective To investigate the ultrastructural changes and HSP70 expression in liver of mice after microwave irradiation with lethal dose and to explore the application of these indexes as the basis of medical identification in microwave irradiation induced death. Methods The mice were divided into the control group and the irradiation group. Mice of the irradiation group were induced death by whole body exposure to 129 W/cm2 microwave irradiation for 30 minutes. The ultrastructure of liver was observed by transmission electron micro-scope;changes of the HSP70 mRNA and protein expression in liver were detected by reverse transcription polymerase chain reaction ( RT-PCR) and Western blotting respectively. Results Liver cytoplasm was observed dissolved with points and sheets and there were mitochondri-al crest and membrane solution in the irradiation group. And the HSP70 mRNA and protein expression level increases significantly compared with the control group with statistically significant difference (P<0. 01). Conclusion Death induced by microwave irradiation could lead to liver cytoplasm dissolution, mitochondria damage, mRNA and protein expression of HSP70 up-regulation, which may be used as important diagnostic indicators of microwave irradiation induced death.