Objective : To investigate the dynamic changes of the expression of GLUT1 mRNA and GLUT4 mRNA in rats myocardium with transient ischemia and reperfusion, and the relationship between the dynamic changes and the time during reperfusion. Methods : In rats, the left anterior descending coronary artery was occluded for 20 min followed by reperfusion for 4 hours, 1, 3 or 7 days as ischemia reperfusion model. The relative content of GLUT1 mRNA and GLUT4 mRNA in myocardium was detected by RT-PCR and gel electrophoresis imaging. Results: During myocardial post-ischemia and reperfusion, the levels of GLUT1 mRNA got up to the peak at 4th hour[ (0.666?0. 003 ) vs (0. 509?0.002) controls , P 0.05). Conclusion; Transient ischemia and reperfusion induce the expression of glucose transporters GLUT1 and GLUT4 genes in rat myocardi- um, which contribute to promote glucose utilization during ischemia, protect ischemic myocardium and improve functional recovery on reperfusion.

Objective To investigate the effects of methamphetamine (Meth) on the outward K+ currents and elucidate the role of outward K+ channels in Meth induced hippocampal neuron damage.Methods Hippocampal neurons were harvest from 18-day-old embryonic rats and were divided into two groups:the control group and the Meth treated group.Both of 4-AP and TEA sensitive K+ currents were recorded after the treatment of Meth by performing the whole cell patch clamp.Furthermore,the MTT and TUNEL assays were performed to evaluate the effects of K+ channel on hippocampal neuron damage mediated by Meth.For statistical comparison,One-way ANOVA and LSD multiple comparison test or t-test was used.P-value ＜ 0.05 was considered to be statistically significant.Results The density of 4-AP sensitive K+ channel currents in Meth treated group [(120.1 ± 19.6) pA/pF,n =7] were significantly increased when compared with control group [(87.4 ± 12.5) pA/pF,n =10,P ＜0.01] and the increments of the currents induced by Meth was dose dependent.The MTT data showed that the cell viability was obviously decreased in Meth treated group (48.72 ± 4.38) ％ relative to the control group (100.07 ± 3.36) ％.Moreover,application of K+ channel antagonist,4-AP (61.39 ± 3.15)％,and the high K+ solution (78.25 ± 9.42) ％ substantially enhanced the cell viability.The TUNEL assay showed there were protective effects of 4-AP and the high K+ solution against neuron damage observed during cells exposed to Meth.Conclusions The increments of 4-AP sensitive K+ channel currents induced by Meth might be involved in hippocampal neuron damage.

Adolescent ; Adult ; Cytarabine ; administration & dosage ; blood ; pharmacology ; Drug Interactions ; Female ; Humans ; Instillation, Drug ; Leukemia ; blood ; drug therapy ; Male ; Methotrexate ; administration & dosage ; blood ; pharmacology ; Middle Aged ; Young Adult

Aim To study effects of loganin and morro-niside on aging astrocytes induced by D-galactose. Methods Cortex astrocytes of newly born rats were cultured in vivo and indentified by immunofluorescence method.Firstly,appropriate D-galactose concentration was selected and effects of loganin and morroniside on proliferation activity of aging astrocytes induced by D-galactose were determined by MTT test.Then SOD, MDA were taken as indicators to study the effects of loganin and morroniside on aging astrocytes induced by D-galactose.Thirdly,growth factors like gliar cell line-derived neurotrophic factor (GDNF),basic fibro-blast growth factor (bFGF)tested by ELISA method and expression of Bax,caspase-3,phospho-extracellu-lar signal-regulated kinese (p-ERK1 /2),phospho-mi-togen-actived protein kinase /extracellular signal-regu-lated kinase kinase (p-MEK1 /2)were taken as indi-cators to discuss the potential protection mechanism. Results Loganin and morroniside exerted certain effects on proliferation of aging astrocytes induced by D-galactose,improving SOD,GDNF,bFGF release and lowering MDA release significantly (P <0.05 ). The expressions of Bax and caspase-3 proteins had no difference between model group and loganin group, morroniside group.While the expressions of p-ERK1 /2,p-MEK1 /2 of loganin group,morroniside group were improved significantly compared with model group.Conclusion Loganin and morroniside have protective effects on aging astrocytes induced by D-ga-lactose,and increase the proliferation ability.Protec-ting their antioxidant systems and improving the expres-sion of p-ERK1 /2,p-MEK1 /2 proteins are possible mechanisms.

Objective To evaluate the efficacy of using dual laser system in off clamp nephronsparing surgery.Methods We used dual laser system in the patients who underwent off-clamp NSS between Jan 2016 and Apr 2016 in our institution.There were 16 males and 8 females with average age of 49 years.Mean tumor size was 1.9 cm (range 0.8-3.2 cm).The mean R.E.N.A.L.score was 3.8 (range 3-6).The mean Zhongshan score was 3.5(range 3-5).The mean ZⅡ(zero ischemia index)was 1.6(range 1-4).The Evolve Dual (980 nm/1 470 nm) laser system set at 60 W in continuous mode was used.Results Offclamp NSS was successfully performed in 22 patients except for renal artery occlusion in 2 case.Mean operative time was 74 min(range 50-100 min);The average estimated blood loss was 52.9 ml(range 10-200 ml);Mean postoperative drainage was 65.4 ml(range 20-150ml);Mean postoperative hospital stay was 5.2 days (range:4-7days).No severe post-operative complication was found.The mean pre-and postoperative serum creatinine levels were 76.2 μmol/L(range:48-112μ mol/L) and 81.5μ mol/L(range:54-122 μ mol/L) with no significant difference(P ＞0.05).The postoperative pathology indicated that 20 cases of clear cell carcinomas,3 cases of chromophobe renal cell carcinomas,one case of papillary carcinoma.Conclusions Dual laser system can be used in off clamp nephron-sparing surgery safely and effectively.

Objective:To investigate the effects of ursolic acid (UA) on the proliferation and differentiation of osteoclasts (OC), and to explore its role in orthodontic force-induced root resorption and its relationship with OC.Methods:The mononuclear / macrophage cells RAW264.7 were induced to the OC.Tacrolimus acid phosphatase (TRAP) staining and bone resorption lacunae observation were used to identify the induction.CCK-8 method was used to select the appropriate concentration of UA for RAW264.7 cell-free biotoxicity and to observe its effect on the proliferation and differentiation of RAW264.7.In experimental groups, UA with gradient concentrations (1.0,2.5,5.0,10.0,20.0and 40.0 μmol·L-1)were added.UA was not added in control group.Results:The TRAP staining and bone resorption lacunae observation showed that after the RAW264.7 cells were induced for 5 d, the TRAP staining positive cells were found;the resorption lacunae were rounded,and oval, etc,the bottom wall was coarser,and the boundary was clear,which indicated that the RAW264.7 cells were successfully differentiated into the osteoclasts.The CCK-8 detection results showed that high concentration of UA (> 10.0 μmol·L-1) significantly inhibited the proliferation of OC;the appropriate concentration of UA (5.0 μmol·L-1) was in the biological safety concentration range and could inhibit the OC proliferation;low concentration of UA (<2.5 μmol·L-1) had no effect.Conclusion:RANKL can induce the differentiation and maturation of RAW264.7 cells.UA is correlated with the proliferation and differentiation of OC;UA has inhibitory effect on OC at the appropriate concentration (5.0 μmol·L-1) in a time-dependent manner.

Objective To explore the neural damage induced by acute exposure to methamphetamine (METH).Methods The mice were administrated with METH,then the stereotyped behavior of mice was evaluated,and spatial recognition memory was analyzed by Y-maze test.In addition,nitric oxide synthase (NOS) activity was detected by kit,and the apoptotic proteins including Bax,Bcl-2,Caspase-3 were assayed by using Western blot.The DNA injury induced by METH was observed by using the comet assay.Moreover,mitochondrial membrane potential was detected to assess the toxic effects of METH on mitochondria by JC-1.With the Western blot assay,the phosphorylation of MAPK signaling pathways were also investigated.Results Acute METH exposure significantly increased the stereotyped behavior in mice,and spatial recognition ability of mice was obviously decreased.On the molecular level,total nitric oxide synthase (TNOS) and induced nitric oxide synthase (iNOS) were increased,and the apoptotic proteins,such as Bax and cleaved caspase-3 were markedly enhanced.With the comet assay,it showed that METH exposure resulted in DNA damage.In parallel,mitochondrial membrane was damaged which manifested as mitochondrial membrane potential decreased.With the western blot,It was further found that METH enhanced the activation of MAPKs.However,p38 MAPK signahng pathway was demonstrated to be the only one factor involved in METH-induced neural damage.Conclusion METH induced neural damage,and MAPK signaling pathways might be involved in this process,since inhibition of p38 MAPK signaling pathway significantly ameliorated METH-induced neural damage.

Objective To quantitatively study right ventricular function in the normal second and third trimester fetuses by M-mode tricuspid annular displacement(TAD).Methods TAD was measured using conventional M-mode echocardiography on 161 normal second and third trimester fetuses with gestation age (GA) between 19-38 weeks,meanwhile multiple parameters for evaluating right ventricular function were obtained using pulsed Doppler echocardiography (PW) and myocardial Dopple tissue imaging (DTI).The correlation between TAD and other parameters were analyzed using SPSS 17.0.Results In normal second and third trimester fetuses,the TAD was (9.38 ± 1.71)mm with a range of 5.79-13.90 mm,and was increased with the growth of GA.TAD was correlated with GA,E,A,Em,Am and Sm significantly (r =0.759,0.547,0.320,0.497,0.483 and 0.598 respectively,all P ＜0.001).TAD was not correlated with HR(P ＞0.05).TAD showed differences between the second trimester fetuses and the third trimester fetuses (P ＜ 0.05).Conclusions In normal second and third trimester fetuses,the TAD is increased with the growth of GA,and has good correlation with GA,E,A,Em,Am and Sm respectively,and may become a new promising modality to evaluate function of RV simply and accurately.The technique will be propitious to use in hospitals (without DTI) because of simplicity of operator and lower requirement on the technology and equipment precision.

Objective To establish the ischemic precondition ([PC) model of PC12 cell line in vitro, and to explore the effect of nitric oxide (NO) on the IPC cerebral protection. Method PC12 cells were cultured and used for producing the model of ischemie precondition by the way of oxygen-glucose deprivation. Twenty dishes of cells were randomly divided into four groups (5 dishes for each group): control group, ischemic precondition group (IPC),non-ischemic precondition group (NIPC) and L-NAME treatment group (L-NAME). In control group, the cells were in-cubated with low glucose (<1 g/L) and2% FBS medium in normal oxygen; in IPC group, the cells were administrated with oxygen-glucose deprivation (OGD) for 6 hours, and then subjected with reperfuaion before OGD 15 hours; in NIPC group, the cells were treated the same as control group for 6 hours, and then subjected with reperfusion before OGD 15 hours; in L-NAME group, the cells received L-NAME (1 mmol/L) and cocultured for 30 minutes before OGD 6 hours, and then received the same treatment as the IPC group. To test whether the model was established, metabolic rate of MIT, LDH release were measured and the apoptosis rate was detected by flow cytometry following oxygen-glucose deprivation 15 hours. The activity of nitric oxide synthases (NOS) was as-sessed by biochemical assay. One-way ANOVA and LSD multiple comparison test were used to analyze differences among different groups, and P<0.05 was considered different. Results Compared with NIPC group, the metabolic rate of MTT increased (94.9%±35.1%, P<0.05), while LDH release and the cell apoptotic rate decreased significantly in IPC group (279.1%±28.1%, P<0.03). Compared with control group(100.0%± 13.5%),the activities of NOS increased both in NIPC and IPC groups (390.0%±14.6%, P<0.01;126.3% ±10.6%, P<0.01). Moreover, the apoptosis rates in each group (control group, IPC group, NIPC group and L-NAME group) were 5.90, 8.73, 38.62 and 11.73%,respectively. Conclusions IPC reduces the death and apoptosis rate of PC12 cell after oxygen-glucose deprivation injury. NO might be involved, but it is not the only factor.

Objective To explore the effectiveness,safety and influencing factors of arterial infusion of oxaliplatin for the treatment of colorectal l1iver metastases after surgery.Methods Totally 68 colorectal liver metastases after surgery patients pathologically confirmed received at least two course of arterial infusion of oxaliplatin combined with TACE.According to postoperative intravenous chemotherapy,the patients were divided into group A (no chemotherapy) and group B (chemotherapy).Survival time of patients were followed up.According to the efficacy of solid tumor evaluation criteria the objective effect was evaluated,the adverse reactions were compared between two groups.Cox regression analysis was performed to assess the possible factors influencing survival time.Results The median overall survival (OS) of all the 68 patients was 18 months,with complete remission 16 cases,partial remission 26 cases,stable diseasse 21 cases,stable diseasse 5 cases,the response rate (RR) was 61.76％ (42/68).The median progression-free survival (PFS) was 10 months.The RR,OS and PFS had no statistical difference (all P＞0.05).The variables that eventually entered the Cox regression model were tumor differentiation (P=0.003,hazard ratio 2.202).Conclusion Arterial infusion of oxaliplatin and TACE is effective in treating colorectal liver metastases after surgery,with high objective response rate.