Myeloid-derived suppressor cells (MDSCs) are a group of heterogeneous and immature myeloid-derived cells,which accumulate largely in blood,lymphoid organs,spleen and tumor tissue and so on under the different pathogenic conditions such as infection,trauma,hematosepsis,especially tumor and so on.MDSCs can suppress tumor immune through many mechanisms.The number of MDSCs in periphery blood of patients is closely related with tumor stage,tumor burden,remote metastasis and prognosis.The major results are from laboratory mice.Because of the complexity of MDSCs in patients with tumor,there are many difficulties and debate on the research of them,and the researches of human MDSCs progress slowly.

Objective To investigate the effects of different anesthesia methods on immunity in patients underwent radical resection of rectal carcinoma.Methods 82 patients underwent radical resection of rectal carcinoma were divided into two groups,each group had 41 cases.A group received total intravenous anesthesia while B group received total intravenous anesthesia combined with eqidural anesthesia.CD3+,CD4+,CD4+/CD8+,CD3+HLA-DR+and NK cells were inspected before induction of anesthesia(T0),2 h after skin incision(T1),2 h(T2) and 24 h(T3) after the end of operation.The T-lymphocyte subsets,activated T cells and NK cells were measured by flow cytometry. Visual analogue scale(VAS) was observed at T2 and T3.Results The VAS score of T2,T3 in A group[(3.86 ± 0.46)points,(3.62 ±0.26)points]were higher than those in B group[(1.67 ±0.57)points,(1.94 ±0.42)points] (all P<0.05).The percentages of CD3+,CD4+,CD4+/CD8+,CD3+HLA-DR+and NK cells of T1,T2,T3 were lower than those of T0 in A group(all P<0.05);The percentages of CD3+,CD4+,CD4+/CD8+,CD3+HLA-DR+and NK cells of T1, T2 were lower than those of T0 in B group ( all P <0.05 );The percentages of CD3+, CD4+, CD4+/CD8+, CD3+HLA-DR+ and NK cells of T1, T2, T3 in A group were lower than those in B group ( all P <0.05 ). Conclusion Total intravenous anesthesia combined with eqidural anesthesia produces less immune suppression than total intravenous anesthesia.

Objective:To establish a method for isolating tumor infiltrating dendritic cells(TIDC)from mice models of Lewis lung cancer by positive selection using anti-CD11c magnetic beads.Methods:A total of 1.0?10~6 Lewis lung cancer cells were subcutaneously injected into a C57BL/6 mice at the lateral abdominal wall to establish the mouse model of lung cancer.TIDC were isolated positively using anti-mouse CD11c magnetic beads;they were labeled by anti-mouse CD11c,and then the purity of the isolated cells was tested by FACScan flow cytometer.The cells were also double labeled by PE-conjugated MHC-ⅡmAb and FITC-conjugated CD83 mAb or FITC-conjugated CD86 mAb to analyze the phenotype of cells by FACScan flow cytometer.Results:The positive selection using anti-CD11 c magnetic beads isolated(1.73?0.31)?10~6 TIDC from each gram of Lewis lung cancer tissue,which accounted for(2.18?0.29)%of the cells in the tumor tissues.The purity of TIDC was 96.49%.Electron microscope showed that the isolated TIDC had the typical character of DC cells.The positive rates of MHC-Ⅱ,CD83 and CD86 molecules in TIDC surface were(51.25?4.21)%, (3.48?0.34)%and(3.07?0.65)%,respectively.Conclusion:The positive selection using anti-CD11c magnetic beads is highly effective,simple,and economic,and is worth popularizing.

Objective:Investigate the relation between the phosphorylation of FOXO1 and the apoptosis and the proliferation of lymphoma cells and to clarify its specific mechanism.Methods:The lymphoma cells Namalwa and Jurkat were treated with PI3K inhibitor wort mannin or etoposide or Wortmannin plus etoposide for different times-pan and at different concentration.The inhibition rates for cell growth of lymphoma cells were examined by XTT assay.Apoptosis were detected by flow cytometry.The expressions of p-Akt,p-FOXO1,FOXO1 and Bim were determined by Western blot analysis.Results:Wortmannin induced apoptosis of Jurkat cells and Namalwa cells and inhibited their survival effectively.The growth inhibition rate and the apoptosis rate of lymphoma cells induced by Wortmannin plus etoposide were higher than those induced by etoposide alone.After treated with Wortmannin,phosphorylation of FOXO1 remarkably reduced and bim markedly increased.Conclusion:The dephosphorylation of FOXO1 inhibits proliferation of Jurkat cells and Namalwa cells,promotes their apoptosis and enhanced the sensitivity of Non-Hodgkin lymphoma cells to etoposide.Bim activated by FOXO1 promotes cell apoptosis.

Objective The aim of this study is to evaluate the effects of drug,electric cardiovertion,radiofrepuency ablation and implantable anti-atrial-fibrillation pacemaker on patients with persistent idiopathic atrial fibrillation.Methods 58 patients with persistent idiopathic atrial fibrillation were treated with drug or electric cardjovertion,radiofrequence ablation and anti-atrial-fibrillation pacemaker.Results There were 30 patients successfully converted to sinus rhythm by drug.The mean conversion time of drug was 8?5 days.22 patients were converted by electric cardioversion.10% of cases(6 of 58)failed to convert by both methods.In follow-up period,12 cases of patients were healed,19 cases got significant improvement,14 cases got moderate improvement,8 cases had no improvement.The total efficiency rate was 76%.18 cases in successful cardioversion patients were healed,5 cases got significant improvement,5 cases got moderate improvement,4 cases had no improvement.The total efficiency rate was 75%(14 of 18).2 cases got improvement by anti-atrial-fibrillation pacemaker.Conclusion Combined treatment of drug,electric cardioversion,radiofreqency ablation and anti-atrial-fibrillation pacemaker can imrove cure rate of persistent idiopathic atrial fibrillation.

Objective: To study the effects of deguelin on proliferation and apoptosis of human breast cancer cell line MCF-7 and on phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Methods: After treatment with 0, 1, 5, 10, 15 and 20 μmol/L of deguelin for 6, 24, 48 and 72 hours, the proliferation inhibition rate of MCF-7 cells was measured by cell counting kit-8 assay. Apoptosis rate of MCF-7 cells was detected with Annexin V-fluorescein isothiocyanate/propidium iodide double staining by flow cytometry and the apoptotic morphology was observed under a transmission electron microscope. After treatment with 0, 1 and 5 μmol/L of deguelin for 6 hours, 5 proteins involved in the PI3K/Akt signaling pathway were examined by Western blot analysis. Results: Deguelin at doses of 5, 10, 15 and 20 μmol/L inhibited the proliferation of MCF-7 cells at 6, 24, 48 and 72 hours. There was a significant difference in each group compared with the control group (P<0.01). The inhibitory effect was more marked with increasing concentration and duration of treatment. There were statistical differences (P<0.05) among 5, 10, 15 and 20 μmol/L groups. However, 1 μmol/L of deguelin had no obvious effects on the proliferation of MCF-7 cells at 6, 24, 48 and 72 hours, showing no significant difference compared with control group (P>0.05). Deguelin at doses of 5, 10, 15 and 20 μmol/L induced apoptosis of MCF-7 cells at 6 hours. There were significant differences (P<0.01) in the early and late apoptosis rate between the treated groups and the control group. The typical apoptotic MCF-7 cells were observed under the transmission electron microscopy. However, 1 μmol/L of deguelin had no apparent effect in inducing apoptosis of MCF-7 cells at 6 hours. After treatment with 5 μmol/L of deguelin for 6 hours the expression of phosphorylated phosphatase and tensin homologue deleted on chromosome 10 (PTEN) (Ser380), phosphorylated 3-phosphoinositide-dependent protein kinase 1 (PDK1) (Ser241), phosphorylated Akt (Thr308) and phosphorylated glycogen synthase kinase-3β (GSK-3β) (Ser9) proteins were significantly reduced in MCF-7 cells, while there was no significant change in the expression of total Akt protein. However, after treatment with 1 μmol/L of deguelin for 6 hours, there was no apparent change in the expression of these 5 proteins. Conclusion: Deguelin can inhibit the phosphorylation of GSK-3β (Ser9) via inhibition of the phosphorylation of PTEN (Ser380) and PDK1 (Ser241) pathway, thus inducing apoptosis and inhibiting proliferation of MCF-7 cells.

Objective To investigate the effects of intrathecal different doses of dexmedetomidine hydrochloride in spinal block by ropivacaine hydrochloride . Methods Forty lower limb surgery scheduled for elective under spinal anesthesia, were randomly divided into 2 groups (n = 20 each): the control and the treatment groups.The control and the treatment group were intrathecally injected with 4,12 μg dexmedetomidine hydrochloride respectively.The 0.75% ropivacaine hydrochloride 1.5 mL was injected for spinal anesthesia.SBP,DBP,HR,SpO2 and Ramsay Sedation Score were recorded before the spinal anesthesia conduct and thereafter every five minutes. And the onset and duration of block were recorded,adverse reaction like nausea, vomiting and respiratory depression were also observed. Results Compared with the control group,the onset of sensory block was shorter [(6.9±2.6) min vs (8.7±2.9) min] (P<0.05),and the duration of sensory and motor block was longer in the treatment group[(130.8±30.1) min vs (115.9±23.9) min] (P<0.05) and [(145.9±29.0) min vs (130.0±30.1) min] (P<0.05). Conclusion Intrathecal dexmedetomidine hydrochloride at 12 μg improves anesthesia via shortening the sensory block onset and prolonging sensory and motor block,which maintains hemodynamically stable,and does not generate adverse reactions as nausea,vomiting,bradycardia and respiratory depression.

Objective:To analyze the expression of E-cadherin in the epithelial-mesenchymal transition (EMT) induced by transforming growth factor-β1 (TGF-β1) in neuroblastoma.Methods:TGF-β1(1 μg/L, 5 μg/L, 10 μg/L), was applied to SK-N-SH cells in vitro compared with the blank control group.EMT-related genes mRNA and protein expression were detected by carrying out real-time PCR assays and Western blot.A scratch test and migration assay were performed to verify the alteration of SK-N-SH cell migration capacity.Data collected from 18 cases of neuroblastoma patients were selected from the Department of Hematology Oncology, Shanghai Children′s Hospital from January 2008 to December 2012.The expression of E-cadherin in the tumor tissue of the neuroblastoma patients after operation was detected by immunohistochemistry.The clinical features and survival prognosis of these patients were analyzed. Results:Compared with the control group, after SK-N-SH cells were treated with TGF-β1(1 μg/L, 5 μg/L, 10 μg/L), real-time PCR assays and Western blot revealed that the mRNA(0.603±0.081, 0.606±0.008, 0.716±0.166 vs.1.000) and protein expression levels(0.855±0.026, 0.600±0.017, 0.495±0.011 vs.1.000) of E-cadherin were significantly decreased ( F=8.144, P=0.040; F=74.810, P<0.001), while the mRNA(2.132±0.167, 3.494±0.017, 4.184±0.021 vs.1.000) and protein expression levels (1.175±0.053, 1.189±0.058, 1.225±0.106 vs.1.000)of α - smooth muscle actin were significantly increased ( F=547.300, P<0.001; F=68.810, P=0.007), suggesting that EMT changes occur in cells.Scratch test and Transwell migration assay revealed that the number of migrating cells increased obvious with the treatment of TGF-β1 (5 μg/L) ( t=16.070, P=0.040). The 10-year overall survival(OS) rates of neuroblastoma patients with E-cadherin strong positive expression, positive expression, weak positive expression and negative expression in the pathology were (77.78±13.86)%, (75.00±21.66)%, (25.00±21.65)% and 0, respectively ( F=8.160, P=0.040). Conclusions:TGF-β1 can induce the EMT in SK-N-SH cells and increase cell migration.The decrease expression of E-cadherin in neuroblastoma patients is closely associated with clinical progress and recurrence or metastasis of the disease.

Objective To analyze the clinical data of children with Langerhans cell histiocytosis (LCH),to discuss the therapeutic effect,and to analyze the factors related to prognosis.Methods A total of 45 children diagnosed as LCH were divided into group A (18 cases with bone lesion only),group B(6 cases with soft tissue lesion),and group C (21 cases with viscera lesion) according to Shanghai Children's Hospital-LCH-2007 scheme [SCH-LCH-2007 (modified DAL-HX83/90) scheme].(1) Initial treatment:group A was treated with Prednisone (Pred) + Vincristine (VCR) for 28 weeks,and group B was treated with Pred + VCR + Etoposide (VP16) + Mercaptopurine (6MP) for 43 weeks,and group C was treated with Pred + VCR + VP16 + Methotrexate (MTX) +6MP for 52 weeks.(2) Re-treatment scheme after relapse included:①upgrading treatment,group A to group B,group B to group C.②Individual treatment for group C included VP16 modification,and maintained Thymosin and/or Ciclosporin etc.Results The total survival rate was 93.3％ (42/45 cases) and recurrence rate was 26.7％ (12/45 cases).Children in group A and B were all effective,while 2 patients in group C died,and 1 case missed follow-up.Multi-factor analysis showed that the factors like age,sex,group,skeleton,soft tissue,erythra,lymph gland,lung,mouth,ears,hypophysis pituitary had no statistical significance,but liver,spleen and blood involvement had statistical significance in disease relapse:liver (P=0.007 1),spleen (P=0.016 9),and blood (P=0.011 1).Conclusion LCH can affect several organs of children and relapse,and modified DAL-HX83/90 scheme is very effective.The liver,spleen and hematopoiesis system involvement is correlates with the relapse.

AIM To study the effects of polydatin on free radical induced rat cortex mitochondria injury. METHODS Fe 2++VitC system was used to produce ?OH. The mitochondria was isolated. Mitochondria membrane fluidity, swelling and contents of phospholipid were determined to measure the function of mitochondria membrane. The activities of ATPase and Cytochrome C oxidase were determined to measure the ability of mitochondria energy metabolism. The activity of superoxide dismutase (SOD) and content of malondial dehyde (MDA) were determined to measure the ability of anti oxygenation. RESULTS ?OH resulted in severe neuronal mitochondria injuries and the injuries and the injuries was alleviated by Polydatin (content of 100,200,400 mg?L -1). The swelling of mitochondria was ameliorated, the decomposability of mitochondrion membrane phospholipid was decreased, the membrane fluidity of mitochondria was increased. Polydatin also significantly inhibited the decrease in SOD, Cytochrome C oxidase and ATPase activity and the increase in MDA levels caused by free radical. CONCLUSION Polydatin has a protective action against the rat neuronal mitochondria injuries induced by oxygen free radical. The mechanisms may be derived from scavenging free radicals, reducing lipid peroxides, and improving the energy metabolism.