Recent preclinical data have demonstrated that antidiabetic drug metformin can act as an anticancer agent for breast cancer.Epidemiologic evidences show that metformin decreases the incidence of breast cancer and cancer-related mortality in diabetic patients.The metformin treatment also increases complete pathological tumor response rates following neoadjuvant chemotherapy for breast cancer patients.Metformin also displays significant growth inhibitory effects in most types of breast cancer cell lines and tumor xenogra-fts in mice.Preclinical data also shows metformin combined with chemotherapy drugs or HER2-targeted drugs or new anticancer drugs has synergic anti-cancer effect.Reduction of the insulin/insulin-like growth factor signaling pathway in body and activation of LKB1/AMPK and inhibition of downstream mTOR pathway in tumor cells have been found to play the most important role in anti-cancer effect of metformin.Currently,a number of clinical trials are underway in breast cancer patients to evaluate the effective use value of metformin as a cancer therapy

Surgery is the treatment of choice for pancreatic carcinoma.However,only 20％ of patients are eligible for surgery,and local control of disease and survival are not good.Although non-surgical treatments result in poor outcome,chemotherapy has been shown to be an effective treatment.The role of irradiation has not been well-established.Modern irradiation technology has shown promising results but there is still lack of strong prospective research evidence to support its widespread use.Irradiation brings along problems which need to be resolved,including target motion,definition of irradiation target,optimal fractionation,total treatment time and the treatment sequence of surgery,chemotherapy and radiation therapy.

OBJECTIVE:To put forward strategies to evolve the current drug bidding system.METHODS:The objective and efficacy of the drug bidding system was analyzed;and the reasons for the poor efficacy of the system were analyzed using the information asymmetry theory in economics,and the system was compared with its US counterpart.RESULTS & CONCLUSIONS:The drug bidding system in China should adopt such model in which the payers are chosen as agency and charge from the entrusting party.It is a systematic project to standardize drug circulation channels,reduce drug price and reduce the burden of patient,which can't be tackled by drug bidding system only.

Alzheimer's disease (AD) is the most common form of dementia, which affects more than 35 million people worldwide with increasing tendency. AD brings stupendous economic burden for both the society and family. It has become a major global public health issue. Electro-acupuncture (EA) therapy has been widely used in AD treatment with satisfactory results. Based on the basic research, this paper explored the therapeutic effect of EA in AD treatment from the learning ability and morphological changes in AD animal models. From the cholinergic neuronal apoptosis theory, inflammatory response theory, oxidative stress theory and other aspects, the action mechanism of EA in the treatment of AD animal models were reviewed. At last, limitations of EA in AD treatment were analyzed. It proposed the outlook of a new type of EA-music EA in AD treatment. It provided a new idea and method for AD clinical treatment.

Objective: To investigate the role of aldehyde dehydrogenase-2 (ALDH-2) for regulating human endothelial progenitor cells (EPCs) oxidative stress reaction and its mechanism. Methods: Human EPCs were isolated from peripheral blood of healthy adults and the cells were cultured in 4 groups:①Blank control group,②Alda-1 group, the cells were treated by 1μmol/L Alda-1, a speciifc activator of ALDH-2,③tBHP (10μg/ml) group and④Alda-1 pretreatment+tBHP group. EPCs reactive oxygen species (ROS) levels were evaluated by DCFH-DA staining, mitochondrial membrane potentials were detected by JC-1 method, migration capacity was measured by transwell chamber method and the activation of p38 signal pathway was examined by Western blot analysis. Results: Compared with Blank control group, ROS levels in tBHP group and Alda-1 pretreatment+tBHP group were (441.7 ± 24.8) % and (237.4 ± 12.0) %, allP<0.05. In Blank control group, tBHP group and Alda-1 pretreatment+tBHP group, the proportion of EPCs lost their mitochondrial membrane potentials were (5.7 ± 2.1) %, (81.7 ± 3.7) % and (37.4 ± 3.2) % respectively, allP<0.05; the number of EPCs migration were (108 ± 9)/HP, (22 ± 4)/HP and (67 ± 7)/HP respectively, allP<0.05. Compared with Blank control group, the activation of p38 signal pathway increased to (259.1 ± 7.7) % in tBHP group, while it was reduced to (186.4 ± 8.0) % in Alda-1 pretreatment+tBHP group. Conclusion: ALDH-2 could reduce ROS level in human EPCs, it may decrease mitochondrial membrane damage, protect migration which might be related to p38 signal pathway.

Objective To investigate the effect of norepinephrine (NE) on the proliferation and migration capacity of endo‐thelial progenitor cells (EPCs) ,and bone marrow mobilization and to analyze its molecular mechanism .Methods The 8‐week old C57 mice were taken and randomly divided into 3 groups ,5 cases in each group :the blank control group(subcutaneous injection of normal saline without operaion) ,model group(subcutaneous injection of normal saline and ischemia in left lower extremity ) and NE group(subcutaneous injection of NE 100μmol/100 μL and ischemia in left lower extremity) .The limb ischemia model was prepared by adopting the femoral arterial ligation in mouse left lower extremity ,then NE was continuously pumped by the micro‐osmotic pump .The EPCs contents from bone marrow ,peripheral blood and spleen were assayed with the flow cytometric analyzer ;human peripheral blood EPCs were cultured and stimulated by NE .The proliferation and migration capacity ,and the activation situation of Akt and eNOS signal pathway were detected .Results NE could promote the mobilization of bone marrow EPCs in limb ischemia mice ,increased the EPCs quantity of peripheral blood and spleen ,comparing the NE group with the model group ,the EPCs quantity was increased for bone marrow [(3 .271 ± 0 .772)% vs .(1 .320 ± 0 .256)% ] ,peripheral circulation[(0 .261 ± 0 .041)% vs .(0 .110 ± 0 .028)% ] and spleen[(4 .671 ± 0 .345)% vs .(1 .880 ± 0 .0 .381)% ] ,the differences were statistically significant (P<0 .01) .NE could promote the proliferation and migration capacity ,moreover could activate the Akt‐eNOS signal pathway in EPCs with a dose dependent manner .Conclusion NE could promote the proliferation and migration of EPCs and mouse bone marrow mobilization via the Akt‐eNOS signal pathway .

Objective: To evaluate the effectiveness that gelatin lines the injured vasuclar wall to prevent from restenosis.Methods: The animal model of restenosis was established by balloon dilation in femoral artery,and 30% gelatin was lined on injured vascular wall in experimental group.The samples were collected at the 2nd week and 4th week after operation.The neointimal area(NEA),neointimal area/media area(NEA/MA)and cell apoptosis were observed by image analysis system and TUNEL technique. Results: The intima of the control group was thicker than that of the experimental group,and more cells appeared in the control group.Compared with the control group,the NEA was reduced significantly in the experimental group at the 2nd and 4th week (0.67?0.25cm 2 vs 1.02?0.41cm 2,and 1.18?0.36cm 2 vs 1.46?0.15cm 2).The NEA/MA ratio in the experimental group was lower than the control group at the 2nd and 4th week(0.35?0.05% vs 0.54?0.14%,and 0.62?0.25% vs 0.75?0.10%).The apoptosis rate of vascular smooth muscle in the experimental group was higher than the control group at the 2nd and 4th week(18.2?5.8% vs 13.6?2.4%,and 15.1?2.1% vs 13.0?1.5%).These diffences were all significant (P

Objective To study the immunosuppression mechanism induced by ultraviolet (UV) and cis urocanic acid. Method The auto lymphocyte proliferation test with Langerhans′ cell (LC) in guinea-pig was performed. Results In exposure to low dose of UVB (25 J/m2) radiation, the inhibition rate of lymphocyte proliferation stimulated by LC was 10.5％ , the inhibition rates of UVB radiation in doses of 50 J/m2 and 100 J/m2 were 22.4％ or 50％ , respectively. The lymphocyte proliferation was almost completely suppressed by 200 J/m2 UVB radiation, while the inhibition of LC function by cis urocanic acid was weak. Conclusion UVB significantly inhibits LC auto-stimulation in dose-dependent way, which may play an important role in UVB induced immunosuppression.

Objective To study the clinical significance of neuron specific enolase (NSE),carcinoembryonic antigen(CEA) and carcinoma associated antigen(CA125) in diagnosis,evaluation of therapy and monitoring metastasis and recurrence of lung cancer.Methods The levels of NSE,CEA and CA125 were detected in the sera from 30 healthy controls,48 patients with benign diseases,50 patients with non-small cell lung cancer(NSCLC) and 14 patients with small cell lung cancer(SCLC) by using microparticle enzyme linked immunoassay and bioantibodies sandwich one step assay by using streptavidin technique,respectively.Results The levels of NSE and CEA in the sera of patients with NSCLC and SCLC were significantly higher than those of healthy controls and patients with benign diseases (both P0 05).The levels of NSE CEA and CA125 decreased after the treatment and increased greatly with the metastasis and recurrence of the cancer.After the combination of NSE and CEA and CA125,the sensitivity significantly increased,but no difference was found in the specifity.Conclusion Measuring serum levels of NSE,CEA and CA125 are very useful in diagnosis,evaluation of therapy and monitoring of metastasis and recurrence of lung cancer.

Objective To study the immunosuppression mechanism induced by ultraviolet (UV) and cis-urocanic acid. Method The auto lymphocyte proliferation test with Langerhans＇ cell (LC) in guinea -pig was performed. Results In exposure to low dose of UVB (25 J/m2) radiation, the inhibition rate of lymphocyte proliferation stimulated by LC was 10. 5%, the inhibition rates of UVB radiation in doses of 50 J/m2 and 100 J/m2 were 22.4% or 50%, respectively. The lymphocyte proliferation was almost completely suppressed by200J/m2 UVB radiation, while the inhibition of LC function by cis-urocanic acid was weak. Conclusion UVB significantly inhibits LC auto -stimulation in dose -dependent way, which may play an important role in UVB induced immunosuppression.