MicroRNAs are one kind of endogenous noncoding small-molecular RNAs,which play an important role in regulating gene expression,cell proliferation and differentiation and a series of life activity.Hepatocellular carcinoma is a common malignant and life-threatening tumor with a high incidence and low 5-year survival rate.In recent years,the results of researches show that microRNAs in hepatocellular carcinoma have the function of oncogenes or tumor suppressor genes as well as having a close relationship with the occurrence,progression,diagnosis,treatment and prognosis of hepatocellular carcinoma.

Cisplatin has good effects in the treatment of a variety of solid cancers.Studies have shown that cisplatin can make great contributions in treatment of nasopharyngeal carcinoma through DNA,telomeres,cell cycle,apoptosis,apoptotic volume decrease,cell senescence,NK cells and other channels.

The Ⅳ stage esophageal cancer refers to exist regional lymph nodes and distant organs in patients with metastases. Palliative chemotherapy and radiotherapy is the primary treatment. With the deepening of the clinical study,radiotherapy and chemotherapy are no longer single treatment,chemotherapy combined molecular targeted drugs,chemo-radiotherapy and some new treatment methods have been gradually recognized, and especially molecular targeted drugs began to establish its position in the treatment of tumor. Application of various methods individual or combined treatment can effectively prolong survival and improve the quality of life.

Purpose:To study the radiosensitising mechanism of topotecan in cell and molecule level on Nasopharyngeal carcinoma.Methods:To detect cell cycle,apoptosis index and the expression s of apoptosis genes such as p53, bcl2, bax by FCM.Results:The proliferation index of RT20Gy +TPT 12.5mg/kg group was decreased, while the apoptosis index was increased, with statistical signifi cance by comparison with TPT and RT group. Meanwhile, the expressions of apoptos is genes, such as p53,bcl-2,bax had no statistic significance between each grou p and the control group. Conclusions:The mechanisms of radiosensitizion might be its act ion on cell cycle,proliferation index and stimulation of apoptosis.However,the i nduction apoptosis might be independent of P53,bcl-2 and bax genes.

The paper analyzed the needs for care quality management in large general hospitals and progresses made in hospital quality management theories. In respect of care quality management in hospitals, authors hold that the key to care quality is comprehensive scientific management of hospitals, and it is necessary to put in place a long-term management of care quality in line with the development direction of hospital evaluation and by means of total quality management system, as well as enhanced quality management and quality culture building.

AIM: To observe the protective effect of heat stress preconditioning on endothelial cells under anoxia and explore its mechanism. METHODS: The endothelial cells were divided into 4 groups: (1) anoxia; (2) heat stress; (3) heat stress preconditioning + hypoxia; (4) control. LDH activity was measrued by using Automatic Biochemistry Analysis-Meter. Cell death rate was determined by trypan blue, NO production was tested by measuring NO - 2/NO - 3 content in cellular culture medium by using Griess assay. RESULTS: LDH release and cell death rate of the anoxia endothelial cells significantly increased compared with control; 39℃ heat stress preconditioning reduced those increment by 29、47%, 33.67% respectively. 41℃ heat stress preconditioning has no protection against the anoxia-induced injury in endothelial cells. The NO production in anoxic endothelial cells decreased markedly. 39℃ heat stress preconditioning induced the increase in NO production in endothelial cells, but 41℃ heat stress preconditioning made the NOS activity decrease. The NO production was correlated negatively with LDH release and cell death rate in anoxic endothelial cells. CONCLUSION: The heat stress preconditioning within the limits can protect the endothelial cells from anoxia injury. The increase in NO in endothelial cells may play an important role in the mechanism of the protective effect.

Objective To evaluate the clinical toxicity and efficacy of S-1 combined with γ-ray body stereotactic radiation therapy in treatment of locally advanced pancreatic cancer.Methods Forty-five patients with locally advanced pancreatic cancer were randomly divided into two groups.The combination group received γ-ray stereotactic body radiation therapy which was given isodose curve of 50 ％-60 ％,tumor encircling dose of 3.0-4.5 Gy per fraction depended on dimension of tumors,9-12 fractions.Combined with S-1 40 mg/m2,2 times/d,for consecutive twenty-one days for four courses.The control group was given γ-ray stereotactic body radiation therapy only.Toxicities and effects were evaluated according to the criteria of WHO and RTOG.Results The CR rates in combination group and control group were 30.4 ％ (7/23) and 13.6 ％ (3/22),the response rates were 91.3 ％ (21/23) and 63.6 ％ (14/22) (x2 =4.980,P =0.026).The rates of gastrointestinal tract side reaction in combination group and control group were 82.6 ％ and 68.2 ％ (x2 =1.267,P =0.260),myelosuppression in combination group and control group were 78.3 ％ and 63.6 ％ (x2 =1.171,P =0.279).The rate of Ⅲ-Ⅳ grade myelosuppression in combination group were higher than that in control group (x2 =4.874,P =0.027).The median progression-free survival (PFS) rates of two groups were 8 months and 6 months respectively (x2 =1.357,P ＞ 0.05),the median survival period were 17 months and 14 months (x2 =1.017,P ＞ 0.05),1 year survival rates were 60.9 ％ and 54.5 ％ respectively (x2 =0.184,P ＞ 0.05).Conclusions S-1 combined with body gamma system treatment can improve local control rate and effective rate for inoperable patients with local advanced pancreatic carcinoma,and the adverse reactions are well tolerated.This method can be used as locally advanced pancreatic cancer chemoradiation safe and effective choice.

Objective To obtain the lung adenocarcinoma initiating cells from the A 549 cell line based on paclitaxel treatment combination with serum-free cultivation and to validate spared cells can represent tumor initiating cells (TICs) .Methods After dis-sociated by trypsogen ,about 106 /mL cells were suspended in serum-free medium supplemented with 0 .4% bovine serum albumin (BSA) ,insulin ,basic fibroblast growth factor (bFGF) ,human recombinant epidermal growth factor (EGF) and obtained spheroid cells .At the second passage ,paclitaxel was added at a concentration of 100 nmol/L for 48 h and then replaced with completely fresh medium once or twice per week until new spheroids emerged .Results The subpopulation of cells that survived serum-free cultiva-tion and paclitaxel treatment could highly express the cluster of differentiation 133/cluster of differentiation (CD133/CD326) mo-lecular markers and have features of stemness including differentiation ,high expression of cancer stem cells (CSCs)-associated genes and stronger capability of tumorigenesis .Conclusion The survived subpopulation that highly express the CD 133/CD326 molecu-lar markers presenting the characteristics of stemness in vitro and in vivo ,and could be used in future researches of biological functions .

Objective To identify the effect of arsenic trioxide (As2O3) on the differentiation and apoptosis of different types of neuroblastoma(NB) cell lines.Methods The cell lines [SK-N-SH,SK-N-BE2,SH-SY5 Y] were induced with different concentrations (0 μmol/L,1 μmol/L,3 μmol/L,5 μ mol/L and 7 μ mol/L) of arsenic trioxide for 24 h,48 h,72 h under the same conditions.The expression of MYCN gene was examined by fluorescence in situ hybridization assay in SK-N-BE2,cell proliferation,cell cycle and cell apoptosis were detected with cell counting kit-8 (CCK-8) assay and flow cytometry.Results 5 μmol/L of As2O3 inhibited the expression of MYCN gene in SK-N-BE2;CCK-8 assay indicated that As2O3 inhibited the proliferation of NB cell in a dose-and time-dependent manner,the cell proliferation was significantly suppressed compared with the low concentration (1 μ mol/L) after treated with As2O3 by 1 μmol/L,3 μmol/L,5 μmol/L and 7 μmol/L in 24 h,48 h and 72 h,SH-SY5Y:24 h(chisq =9.666 7,P ＜ 0.05),48 h (chisq =9.666 7,P ＜ O.05),72 h (chisq =9.512 8,P ＜ 0.05);SK-N-SH,24 h (chisq =10.38,P＜0.054 6),48 h(chisq=8.641 0,P＜0.05),72 h(chisq=9.461 5,P＜0.05);SK-N-BE2:24 h (chisq =8.435 9,P ＜0.05),48 h(chisq =8.641 O,P ＜0.05),72 h(chisq =9.545 5,P ＜0.05);compared with the control group,the As2O3-treated cells showed increased apoptosis percentage,with the percentage of 1.6％ (0 μmol/L),3.8％ (1 μmol/L),6.1％ (3 μmol/L),10.4％ (5 μmol/L),40.2％ (7 μ mol/L);the cell cycle was arrested at G2/M phase,which prevented cell division.Conclusions (1) As2O3 play an important role on the NB cells proliferation,apoptosis which were dose-and time-dependent manner.(2)As2O3 can inhibit the expression of MYCN gene.(3)As2O3 also could block NB cell cycle at S and G2/M,and inhibit the cell nucleus replication and the As2O3 had different induced effect between different types of NB cell.

Objective To investigate the effects of 13-cis retinoic acid (13-cis RA) in inducing differentiation of 3 types of human neuroblastoma (NB) cells in vitro.Methods The status of MYCN gene amplification of cultured SH-SY5Y,SK-N-SH and SK-N-BE2 cells was detected by fluorescence in situ hybridization.After treatment with different concentrations of 13-cis RA,morphological changes were observed by phase-contrast microscope,and neuron-specific enolase (NSE) concentrations were determined by enzyme linked immunosorbent assay.The cell viability was measured through cell counting kit-8 assay,and the cell apoptosis was assayed with flow cytometry (FCM).Results The morphological changes in differentiation were observed in all 3 types of NB cells after 13-cis RA treatment.MYCN amplification was detected in SK-N-BE2 cells even after 13-cis RA treatment,while the other 2 cell lines were amplification-null.After different concentrations of 13-cis RA treatment,NSE concentration increased with prolonged time,especially for SK-N-BE2 cell(F =27.00,P ＜ 0.000 1).13-cis RA stimulated cell proliferation within 48 hours of treatment,and then inhibited cell growth.FCM indicated that the degree of apoptosis in SH-SY5Y cell was significantly higher after 13-cis RA treatment of 10 μmol/L concentration for continuous 96 h and 120 h as compared to the control group (F =16.21,P =0.011;F =16.04,P =0.016).Cell apoptosis of SK-N-SH cell after 13-cis RA treatment of 1 μ mol/L and 10 μ mol/L concentration for 48 h,were significantly higher than those of the control group (F =15.05,P =0.012;F =31.18,P =0.005);while SK-N-BE2 cell with different concentrations of 13-cis RA(1 μmol/L,5 μmol/L,10 μ mol/L) for 120 h were significantly higher than those of the control group(F =9.05,P =0.030;F =11.38,P =0.028;F =7.88,P =0.041).Conclusions The present study showed that 13-cis RA could induce differentiation of human NB ceils in vitro.It induces cell proliferation within 48 hours of 13-cis RA,and thereafter suppresses cell growth.No improvement was found in MYCN amplification cells with the detection of DNA level after 13-cis RA treatment,which suggests that combined treatment is possibly needed.