Objective: To investigate the mechanism by which icariin ( ICA) inhibits the invasion and metastasis of human triple-negative breast cancer ( TNBC) cells via downregulation of the transforming growth factor-β/ Smad ( TGF-β/ Smad) signaling pathway． Methods: TNBC cells ( MDA-MB-231 and MDA-MB-468) were cultured in vitro and divided into four groups: an experimental group treated with 15 μmol / L ICA; a model group treated with 10 μmol / L TGF-β receptor inhibitor LY2109761; a combination group ( LY2109761 + ICA) treated with both 15 μmol / L ICA and 10 μmol / L LY2109761; and a control group．Cell proliferation，migration，and invasion were as- sessed using CCK-8，colony formation，5-ethynyl-2 '-deoxyuridine ( EdU) ，wound healing，and Transwell assays． The expression levels of epithelial-mesenchymal transition ( EMT) -related proteins，as well as TGF-β1，Smad2， and phosphorylated Smad2 ( P-Smad2) were detected by immunofluorescence and Western blot． Results: CCK-8 results showed that cell proliferation decreased gradually with increasing concentrations of ICA ( P＜0. 05) ．Colony formation and EdU assays indicated significantly inhibited proliferation in the ICA-treated group compared to the control ( P＜0. 05) ．Wound healing and Transwell assays demonstrated reduced migration and invasion capabilities in the experimental group relative to the control ( P＜0. 05) ．Compared to the model group，the LY2109761 + ICA group exhibited further suppression of invasion ( P＜0. 05) ．Immunofluorescence revealed decreased Vimentin ex- pression in the experimental group ( P＜0. 05) ，with an even more pronounced reduction in the LY2109761 + ICA group ( P＜0. 01) ．Western blot analysis showed that the protein levels of N-cadherin，matrix metalloproteinase-9( MMP9) ，Vimentin，TGF-β1，Smad2，and P-Smad2 were downregulated in the experimental group compared to the control ( P＜0. 05) ．These proteins were further suppressed in the LY2109761 + ICA group compared to the model group ( P＜0. 05) ． Conclusion ICA inhibits TNBC cells proliferation，invasion，metastasis，and EMT by downregulating the TGF-β/ Smad signaling pathway．

Objective:To explore the correlation between cerebrovascular hemodynamic index (CVHI) accumulative score and subclinical arteriosclerosis indicators.Methods:A total of 27 184 cases were collected from the Health Management Center,the Third Xiangya Hospital,Central South University.Linear regression analysis was carried out to confirm the correlations between CVHI accumulative score and the modified Framingham stroke profile (FSP),as well as between CVHI accumulative score and cerebrovascular diseases (ICVD) scale.The correlation between CVHI accumulative score and brachial-ankle pulse wave velocity (baPWV),carotid plaque orcarotid intima-media thickness (CIMT) was analyzed by multifactor logistic regression model in 11 580 cases.Moreover,the correlation between CVHI accumulative score and microalbuminuria or serum cystatin C was performed by multifactor logistic regression model in 9 860 cases.Results:In this study,the people whose CVHI accumulative score was less than 75 accounted for 12.98％.The CVHI accumulative score was negatively related with the modified FSP score (r=-0.484,P＜0.01) or ICVD score (r=-0.455,P＜0.01).The multifactor logistic regression model found that the baPWV,carotid plaque,microalbuminuria and serum cystatin C were independent predictors for CVHI accumulative score.Conclusion:The CVHI accumulative score is correlated with the modified FSP score,ICVD score and indexes of subclinical arteriosclerosis (baPWV,carotid plaque,microalbuminuria and serum cystatin C).The CVHI accumulative score could be used as a tool for zero-level and primary prevention of cerebral stroke.

Objective To evaluate the utility of serum thymidine kinase 1(STK1)in health screening.Methods A total of 8896 adults who participated in health check-up during November 2009 and November 2010 were tested for STK1 by using sensitive chemiluminescence's dot blot assay.Results The level of STK1 of group A(STK1 ＞ 2 pmol/L)was much higher than that of the group B(STK1 ＜ 2 pmol/L)[(5.47 ±4.23)vs(0.62 ±0.48)pmol/L;t =11.90,P =0.00].The STK1 level was not correlated with gender.However,the mean age of individuals in the group A was higher than that in the group B[(48.2 ± 12.0)vs(41.8 ± 12.3)years; t =5.37,P =0.00].The positive detection rate of STK1 was 1.2％(108/ 8896).In the group A,there were 1.9％ pre-or post-treatment malignancy,27.8％ pre-malignant tumor or benign disease,36.0％ nontumorous proliferation disease,14.8％ hepatitis B virus/HP infection,10.2％fatty liver,and 9.3％ other diseases.No pre-treatment malignancy and pre-malignancy were found in the group B.Conclusion STK1 measurement could reflect the situation of cell proliferation and predict the risk of any type of malignancy.

Objective To approach the effect of blocking the JAK-STAT signal pathway in the treatment of rat's rheumatoid arthritis.Methods Thirty-six arthritis rat models,which had arthritis index more than 2 scores,were built successfully by Department of Rheumatology and Immunology,the First Affiliated Hospital of China Medical University,and they were divided into model group one and two,low dose of AG490 group,middle dose of AG490 group,high dose of AG490 group and leflunomide group.Besides,6 rats were treated as normal control group.And they were given normal sodium 1 mL,AG490 1、5、10 mg/(kg?d)and leflunomide 10 mg/(kg?d) by intraperitoneal injection or intragastric administration,then all the rats were sacrificed after 44 days.After that,compared the weight,arthritis index,the volume of toe,pathological score,and the change of p-STAT1,p-STAT3.Results The arthritis of model group developed rapidly,and the arthritis index,the volume of toe increased obviously,and the expression of p-STAT1 and p-STAT3 increased and the body weight decreased,all of which had significant meaning compared with that of control group.The body weights of rats in low dose group of AG490 were heavier than that of control group,the symptom of arthrocele in low dose group of AG490 was lighter than that of control group,and could inhibited the activation of JAK-STAT signal pathway in some degree,but the arthritis index numbers and the pathological score had no significant difference from that of model group.The body weights,arthritis index,the volume of toe and pathological score in middle dose group of AG490 improved obviously(P