It presented in detail the acquisition of Qingdao Wan Jie Hospital by the Affiliated Hospital of Medical College Qingdao University, describing the operational mechanisms in organizational setup, specialty setup, personnel management, logistic management, hospital culture and branding of the newly acquired section. It also summarized the achievements in medical resources reorganization and advantages complementary without government investment in a fast and low-cost manner. It is demonstrated that hospital acquisitions are in line with the medical reform, as they expand the service coverage of public hospitals, and extend medical service to the communities and lower levels, thus enhancing hospitals' impact and reach to integrate medical resources in a short timeframe.

Aim To investigate the anti-proliferative effect of salinomycin on doxorubicin-resistant human breast cancer MCF-7 /DOX cells.Methods MCF-7 and MCF-7 /DOX cells were treated or untreated with salinomycin.Cell viability was detected by MTS assay. Cell apoptosis was detected by Annexin V-FITC /PI as-say.Reactive oxygen species (ROS)was measured by DCFH-DA staining.Mitochondrial membrane potential was measured by JC-1 assay.The expression of apopto-sis related proteins BAX, BCL-2, caspase-3, and caspase-9 were evaluated by Western blot analysis. Results The cell viability was significantly reduced by salinomycin treatment in a dose-dependent manner. The flow cytometry results showed that salinomycin in-duced MCF-7 /DOX cell apoptosis,increased ROS pro-duction,and decreased mitochondrial membrane poten-tial.Furthermore,salinomycin decreased the expres-sion of BCL-2,and increased the expression of BAX, cleaved caspase-3,and cleaved caspase-9.Moreover, the antioxidant N-acetylcysteine (NAC ) markedly blocked the above effects.Conclusions Our results suggest that salinomycin-induced apoptosis in MCF-7 /DOX is associated with induction of ROS production, and activation of mitochondria apoptosis pathway, which may become a potential chemotherapeutic agent for the therapy of doxorubicin resistant breast cancer.

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.

Background Implantable contact lens (ICL) surgery is a primary intraocular refractive corrective surgery for high myopia.However,whether there will be enough distance between ICL and anterior face of lens to avoid the occurrence of anterior capsular cataract in non-accommodated and the largest physiological accommodated state after ICL implantation is worthy of investigation.Objective The purpose of this study was to investigate the alteration of lens vault after ICL implantation and explore the relationship between accommodation and change of lens vault.Methods A observational study was carried out.Sixty-six eyes of 33 patients with high myopia who received ICL implantation were enrolled in Affiliated First Hospital of Guiyang Medical College from May to November,2012.Best corrected visual acuity (BCVA),uncorrected visual acuity (UCVA),refractive diopter were regularly examined using synthetical optometry,and crystalline lens rise (CLR) and lens vault in non-accommodative or accommodative condition were observed by the anterior segment OCT (Visante OCT) and ultrasound biomicoscopy (UBM) before operation and 1 day,1 week,l month and 3 months after operation.Data were analyzed with SPSS version 16.0.Repeated measurement one-way analysis of variance was used to compare the differences of vision and refractive diopter among various time points.The relationship between accommodation and CLR was assessed using Pearson linear correlation.The alteration of CLR with accommodation change was analyzed by linear regression equation.Lens vault was measured and compared between non-accommodation and maximal physical accommodation status by paired t test.Results The postoperative UCVA was improved in comparison with preoperative BCVA,and the postoperative diopter was significantly lower than that of preoperation,with significant differences among various time points (F =16.904,P =0.000 ; F =1.498,P =0.000),and the diopter was stable after operation.A positive correlation was found between the alteration of CLR and accommodation under the physical accommodative stimulation in high myopic eyes (R2 =0.49,P =0.00).Under physiological accommodation,CLR elevated 20 μm for per 1.0 D accommodation.In addition,the difference of lens vault values within postoperative 3 months was statistically significant (F=16.025,P=0.000).The lens vault values lowed with the enlargement of accommodation in 48.5％ eyes,and the lens vault values increased with the enlargement of accommodation in 50.0％ eyes.However,1.5％ of the lens vault were in a stable state under the maximal physiological accommodated condition 3 months after operation.Lens vault were greater than zero in 97.0％ eyes (64/66),and only 3.0％ eyes (2/66) were zero under the maximalphysiological accommodated condition.Significant differences were seen in the lens vault between nonaccommodated and the maximal physiological accommodated state 1 day or 1 week after operation (t =4.755,P =0.000 ;t =3.327,P =0.001) ; but there was no statistical significance in 1 month or 3 months after operation (t =1.544,P=0.127,t=0.621,P=0.537).Conclusions During physiological accommodation,the alteration of CLR with accommodation in high myopic eyes.The location of ICL in the eyes is unstable within 3 months after operation.Majority of operative eyes remain enough vault in the maximal physiological accommodated state,but minority of operative eyes occur contact of ICL with the anterior surface of lens.Whether this contact causes anterior capsular cataract still needs to study.

Objective To determine pharmacokinetics profiles of sodium alginate dexamethasone in perilymph after trans-round window administration of the sodium alginate dexamethasone gel in vivo.Methods 30 healthy guinea pig were randomly divided into 6 groups.Alg-Dex gel was placed into the niche of the round window of the guinea pig on the right ear.The perilymphetic samples were harvested on day 1,2,3,4 and 5 after administration of Alg-Dex gel respectively.The concentrations of dexamethasone in perilymph were assayed with high performance liquid chromatograph(HPLC).Results Concentrations of dexamethasone in perilymph on day 1,2,3,4 and 5 after administration of Alg-Dex gel were 0.49?0.06,1.32?0.28,0.65?0.08,0.66?0.05,0.53?0.17 mg/L respectively.Concentrations of dexamethasone in perilymph reached a peak on the second day and maintained 0.61?0.07 mg/L steadily on following days after administration.Conclusion Dexamethasone can be released from the sodium alginate dexamethasone gel persisitently and steadily in vivo.

Objective To explore the effect and molecular mechanism of N-myc downstream regulated gene 1 (NDRG1) on transforming growth factor-beta (TGF-β)-induced epithelial-mesenchymal transition (EMT) in human lung cancer cells.Methods Lung cancer A549 cells were transfected with NDRG1 overexpressed vector,and then treated with 5 μg/L TGF-β1.The abilities of invasion were detected by Transwell assay.The expressions of NDRG1 mRNA and protein were analyzed by teal-time reverse transcription polymerase chain reaction (RT-PCR) were examined with Western blot.The expressions of EMT-associated markers E-cadherin and Vimentin,and EMT-associated signaling molecules Snail,AKT and Smad were detected with Western blot.Results We found that TGF-β1 treatment could induce morphological alteration of A549 cells from epithelial morphology to mesenchymal morphology.TGF-β1 significantly increased the migration of A549 cells,and increased the expression of mesenchymal maker vimentin and decreased epithelial marker E-cadherin.More importantly,overexpression of NDRG1 significandy reversed the effects of TGF-β1 on A549 cells.Moreover,NDRG1 significandy decreased the levels of phospho-AKT,and suppressed the expression of EMT-related transcription factor Snail.Conclusions NDRG1 could reverse the effects of TGF-β1 on EMT in A549 cells,by which mechanism is related to reduction of the expressions of phospho-AKT and Snail.

Objective To investigate the effect of percutaneous eoronary intervention (PCI) on the prognosis of acute ST-segment elevation myocardial infarction (ASTEMI) in the elderly.Methods The 1318 ASTEMI patients in our hospital from June 1998 to June 2008 were retrospectively analyzed. Among them, 338 (25.6%) elderly patients were over 60 years old, and 316patients consistent with inclusion and exclusion criteria were consecutively enrolled in our research.Then they were divided into two groups: PCI group (136 cases, 43.0%) and conservative drug treatment group (180 cases, 57. 0%). The clinical data of study objects were collected. Then they were followed up regularly for two years. Results There were no statistically significant differences between the two groups in mean age, gender, hypertension, diabetes, dyslipidemia, excess smoking,wine and family history (all P＞ 0.05). And there were no statistically significant differences in anterior wall STEMI, Killip Ⅲ-Ⅳ class, thrombolysis therapy and malignant ventricular arrhythmia (all P＞0. 05). Most of the objects proceeded therapeutic lifestyle improvements, such as giving up smoking, restricting wine, regulating diet, losing weight and insisting on exercises, and so on.Secondary prevention drugs of acute myocardial infarction including angiotensin converting enzyme inhibitor, angiotensin receptors blockers, beta receptor, aspirin and statins were regularly administrated in the two follow-up years. In the retrospective research, incidence rates of reinfarction, NYHA (New York Heart Association) Ⅲ-Ⅳ class heart function and one-month mortality were much higher in conservative treatment group than in PCI group (17.2% vs. 2. 2%, OR=9. 224,95% CI: 2. 756-30. 857; 31.1% vs. 8.1%,OR=5.132, 95%CI: 2. 568-10. 257; 8. 3% vs. 1.5%,OR= 6. 091, 95% CI: 1. 369-27. 105, respectively; all P ＜ 0. 01). Above all, one and two-year mortalities were much higher in conservative treatment group than in PCI group (21.1% vs. 2. 2 %,OR=11.864, 95%CI: 3.577-39.349; 32.2% vs. 4.4%, OR=10.301, 95%CI: 4.289-24.736,respectively; all P＜0. 01). Conclusions PCI may reduce the re-infarction, NYHA Ⅲ-Ⅳ class heart function and one-month mortality, especially so in view of the one and two-year mortality. PCIcan significantly improve the prognosis of ASTEMI in the elderly.

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 role of forkhead box protein O3a (FOXO3a) in inhibiting the proliferation and metastasis of breast cancer cells by downregulation of vascular endothelial growth factorA (VEGF-A).Methods Cell proliferation bioassay and plate clone formation assay were used to compare the changes of proliferation after siRNA interference.Wound healing and Transwell were used to compare the changes of invasion metastasis after interference.Meanwhile,the changes of VEGF-A expression in the cells before and after interference were compared by real time polymerase chain reaction (RT-PCR) and Western blot.Furthermore,the expressions of mRNA FOXO3a and VEGF-A were detected in 20 cases of breast cancer patients in breast cancer tissues and adjacent normal breast tissues.Results The MCF-7 and MDA-MB-231 cells were increased in cell proliferation and invasion after interference.Further studies found that mRNA and protein expression of VEGF-A were up-regulated in MCF-7 and MDA-MB-231cells after interference.In vivo the expression of FOXO3a was lower in 15 cases of cancer compared to normal tissues,and the expression of VEGF-A was high in 15 cases of cancer (75％).FOXO3a and VEGF-A expression was highly negatively correlated.Conclusions This study showed that FOXO3a could inhibit the proliferation and invasion of breast cancer cells,which might be regulated by VEGF-A.It provides an important theoretical evidence for targeted inhibition of breast cancer metastasis.

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.