Objective To explore the effect and molecular mechanism of miR-34c in cell proliferation and invasion of human prostate cancer PC3 cells.Methods miR-34c was synthesized and transfected into prostate cancer PC3 cells.The ability of cell pro liferation was examined with methyl thiazolyl tetrazolium (MTT),and invasion with Transwell assay.The level of c-met mRNA was analyzed by real-time reversing transcription polymerase chain reaction (RT-PCR).Western blot was used to detect the expressions of cmet,cyclin D1,and EMT-associated markers.Results Over-expression of miR-34c reduced PC3 cell proliferation,and inhibited the abilities of invasion.Bioinformatics analysis showed that 3'-UTR of c-met had two miR-34c matched sites,and miR-34c inhibited the expressions of c-met mRNA and protein.Meantime,miR-34c obviously decreased the expressions of cyclin D1 and N-cadherin,but increased the expression of E-cadherin in PC3 cells.Conclusions miR-34c may suppress cell proliferation and invasion in prostate cancer PC3 cells,by which mechanism is related to reduction of the expressions of c-met,cyclin D1,N-cadherin,and upregulation of E-cadherin.

The self-microemulsion formulation of potassium dehydroandrographolidi succinas (PDS) has been optimized and the performance in vitro has been evaluated preliminary. Kinds of prescription accessories were screened by solubility based on the emulsifying result and efficiency, particle size of emulsions. The optimal formulation composition and compatibility proportion were determined by orthogonal design and pseudo-ternary phase diagrams. The appearance, particle size, Zeta potential and stability of this formulation were also investigated. The optimized prescription of PDS was 10% MCT, 40% Tween-20 and 50% glycerol. It can spontaneously form a transparent pale blue opalescent emulsion with emulsification time 31.27 s, particle size 37.1 nm, Zata potential -17.4 mV and good stability.

Objective To investigate the relationship of glycoprotein serglycin (SRGN) expression with invasion and metastasis of breast cancer cells,and the role of microRNA in the regulation of SRGN expression.Methods Real-time quantitative polymer ase chain reaction (PCR) and Western blot were used to detect the differences in SRGN expression between higher metastasis Michigan cancer foundation-7 (MCF-7)/5-Fu breast cancer cell lines and weaker metastasis MCF-7 cell line.The siRNA interference experiment and in vitro Transwell experiment were used to detect effect of SRGN on the ability of invasion and metastasis of breast cancer cells.Bioinformatics software was used to predict miRNAs targeting SRGN,and integrated microRNA differentially expressed chip data between breast cancer cell MCF-7 versus MCF-7/5-Fu.The miRNA quantitative PCR was used to determine the differences of candi date miRNA expression.After transfection of microRNA minics,Western blot was used to test candidate microRNA target SRGN.Transwell experiment was used to test the effects of candidate microRNAs on tumor cell invasion and metastasis.Results SRGN was increased significantly in MCF-7/5-Fu cells,and the invasion and metastasis of tumor cells were inhibited when SRGN was interfered.In addition,miR181 b/c expressed in MCF-7/5-Fu cells was reduced significantly,negatively correlated with SRGN expression,and targeted SRGN expression.It inhibited invasion and metastasis of tumor cells.Conclusions MicroRNA181b/c inhibits metastasis of breast cancer by targeting SRGN.

Objective To study the changes of insulin-like growth factor-1(IGF-1) in serum of patients with obstructive jaundice.Methods The clinical data of 20 patients with obstructive jaundice were collected and the measurement of serum TNF-?,ALT, ALP, endotoxin and IGF-1 were performed. Results The serum IGF-1 in obstructive jaundice was significantly lower than that in gallbladder stone(P

Objective To investigate the effect of histone deacetylase inhibitor on Her2 positive breast cancer cell line BT474 and SKBR3 in apoptosis and metastasis.Methods Histone deacetylase inhibitor MS-275,suberoylanilide hydroxamic acid (SAHA)(4 μmol/L,and 50 μmol/iL,respectively) treated the cell lines BT474 and SKBR3 cells.Flow cytometer examined the apoptosis ratio.Transwell tested their metastatic activity.Western blot assay was performed to detect the associated proteins.Results SAHA and MS-275 inhibited the cell survival.The BT474 cell survival was (39 ± 11) ％,(54 ± 8) ％,and the SKBR3 survival was (62 ± 6) ％,(71 ± 9) ％,according to the fluorescence-activated cell sorting (FACS) result.SAHA and MS-275 induced the BT474 cell apoptosis 8.46± 0.28 (P ＜0.01),4.15 ± 0.71 (P ＜0.01) fold change,respectively;and upregulated the SKBR3 cell apoptosis ratio 5.51 ± 1.24 (P ＜0.01),4.04 ±0.69 (P ＜0.01) fold.The Transwell result showed that SAHA,MS-275 inhibited the Transwell ability of BT474 from the control 184.7 ± 18.8 to 104.3 ± 7.1,131.3 ±9.1 per view,and the SKBR3 from control 60 ± 16.7 per view to 14.3 ± 6.5,34.3 ± 8.7 per view.The Western blot result showed that SAHA,MS-275 inhibited the protein level of vimentin,Her2,β-catenin,histone deacetylase inhibitor (HDACi),and upregulated the acetylation level of histone 3.The E-caherin protein was regulated in BT474 and SKBR3 cells.Conclusions MS-275,SAHA can induce BT474 and SKBR3 apoptosis significantly,also inhibit their metastatic activity.

Objective To explore the effect of metformin on hepatoma cells senescence and the underlying mechanism.Methods Cell proliferation,cycle and apoptosis were examined by MTS and flow cytometry assay in response to different concentrations of metformin(0,0.01,0.1,1,10 and 50mmol/L).Senescence-associated β-galactosidase (SA-β-ga1) staining and senescence marker Dec1 protein levels were used to evaluate the effect of metformin on hepatoma cells senescence.In addition,protein expression of p-AMPK,p-ACC and AMPK was detected by Western blot analysis.Results Metformin suppressed proliferation of HepG2 cells in a dose-dependent manner.High concentrations of metformin (10 and 50mmol/L) promoted cell apoptosis,while lower doses of metformin (0.01,0.1 and 1mmol/L) led to enlarged and flatten senescent morphology and increased SA-β-ga1 positive cells.Moreover,cell cycle was blocked in G0/G1 phase and protein levels of senescent marker Dec1,p-AMPK and p-ACC were significantly enhanced,whereas AMPK protein expression was almost unchanged.Conclusion We showed here that high dose of metformin promotes HepG2 cells apoptosis,but low doses of metformin induce cellular senescence,which may be related to the activation of AMPK signaling.These data will provide vital evidence for improving the outcome of comprehensive treatment in HCC patients by driving hepatoma cells to undergo senescence.

Objective To investigate the correlation between corneal neovascularization (CNV) in rat after cautery with acid and the defect in epithelium, the infiltrating of leucocytes. Methods The model of mild, moderate and severe acid burn in rat cornea was established. Corneal angiogenesis and the diameter of the epithelial defect were observed with a slit lamp microscope. The ratio of neovascularization area to that of cornea was calculated. The specimens were taken to stain with hematoxylin and eosin (HE) at different time points after cautery and the number of the leucocytes in cornea was calculated with light microscope. The relation between CNV and the diameter of epithelial defect and the infiltrating leucocytes in cornea was analyzed with Pearson's correlation. Results The healing of epithelium differed with different degree of acid burn. The more damage the eye suffered, the more time it would take to heal. Leucocytes infiltrated in cornea after cautery. The more damage the eye suffer, the more leucocytes can be observed, and the statistical difference was significant (P

3.0 cm in diameters.Contrast-enhancement CT showed tumors with abundant blood vessel,1 case appeared as uniform enhancement and was difficult to distinguish between tumor body and internal carotid and external carotid because of the iso-density of them.On MRI,the flow void blood vessels inside the tumors could be identified and internal carotid and external carotid separated.MRA displayed all the relation between the tumors and carotid and its branches.DSA could demonstrate the supply arteries of the tumors.Conclusion Ultrasonics,CT,MRI and DSA have own definitely characteristic value in diagnosing carotid body tumor.

Objective To explore the effect and molecular mechanism of HDAC inhibitor SNDX-275 inhibiting cell proliferation in ErbB2-overexpressing breast cancer BT474 cells.Methods Breast cancer BT474 cells were treated with HDAC inhibitor SNDX-275,setting as test group,and the cell line treated with phosphate buffered saline (PBS)as control.The concentration of SNDX-275 were 0,0.5,1 .0,2.0,3.0,4.0 μmol/L respectively.Cell proliferation was analyzed by MTS assay and colony formation assay,the expressions of ErbB2, ErbB3,p-Akt were analyzed by Western blotting,and the expressions of miR-125a,miR-125b were analyzed by RT-PCR.After transfecting miRNA125 inhibitor into BT474 cells,the inhibition rate of SNDX-275 was tested by MTS assay .Results MTS result showed that SNDX-275 inhibited cell proliferation in BT474 cells in a dose-dependent manner.The inhibition rate of 4.0 μmol/L SNDX-275 was about (68.00 ±4.45)%.Clone assay indicated SNDX-275 could inhibit the proliferation of BT474 cells.Western blotting result indicated that SNDX-275 significantly inhibited the protein expressions of ErbB2,ErbB3 and p-Akt,RT-PCR result illustrated 2 μmol/L SNDX-275 could increase the expressions of miR-125a and miR-125b about 3.22 ±1 .17,5.42 ±0.38 times compared with the PBS control respectively,the difference has a statistical significance (t =4.338,P =0.049;t =21 .805,P =0.002).MTS result indicated that compared with the PBS control,the inhibition rate of SNDX-275 group was (56.97 ±3.56)%,while the inhibition rate of SNDX-275 and miRNA125 inhibitor group
was (10.67 ±2.21 )%,with a statistical significance(t =-10.993,P =0.008).Conclusion SNDX-275 could inhibit cell proliferation of ErbB2-overexpressing breast cancer BT474 cells,by inhibiting ErbB2-ErbB3-Akt sig-nal pathway through up-regulating miR-125a and miR-125b.

Objective To observe the clinical efficieney and safety of Rosiglitazone(Avandia)Monotherapy or combi- nation with oral hypoglycemic agents in treating type 2 diabetes mellitus with Metabolic syndrome.Methods 68 type 2 diabetic patients with Metabolic syndrome were assigned to receive Avandia treatment at doses of 4mg for 12 weeks.Re,. sults Avandia used alone or in combination with oral hypoglycemic agents significantly reduced fasting plasma glucose (FBG)and fasting plasma insulin(FINS).Mean glycosylated hemoglobin values were significantly deereaseel.Home- ostasis model assessmen indicate that RSG reduced insulin resistance.There were statistically significiant decrease in systolic blood pressure(SBP)and diastolic blood pressure(DBP).No significant side-effects on kidney and liver function were found.Conclusion Avandia is an insulin sensitizer that is effective and safe on the treatment of Type 2 Diabetes with Metabolic syndrome by decreasing blood glucose and blood lipid,improving insulin resistance,and main- taining the function of pancreatic island cells.