Vascular cognitive impairment refers to the learning and memory impairments caused by cerebrovascular lesions.Studies in recent years have shown that oxidative stress plays an important role in vascular cognitive impairment.This article reviews the mechanisms and the prevention and treatment of oxidative stress in vascular cognitive impairment.

In order to do medical educational research better in our country,we analyzed the Department of Medical Education in the University of Illinois and the Center of Medical Education and Ethics in the University of Washington,and besides we suggested some advice for improving our medical educational research level.

Objective: By building database model, to put forward measures to solve the shortage of basic drugs. Methods: There were five factors influencing medicine shortage have been researched, collecting data, using SPSS 18.0 software to build the database model of different parts, and then analyzed the existing problems and inner link, scientifically came up with the basic framework and main solutions of guarantee measures on shortages of essential medicines. Results: The database model of country and six areas in it have been built, and the influence factors of drug shortage in different region have been analyzed, and raised five aspects measures to secure reliable supplies of drugs, including selection, bid and procurement; production and flow; reserve and adjust;pricing and pay;use training. Conclusion: This study extends the application of database, enriches research ideas of drug policy, and the policy put forward to avoid drug shortages to a certain extent.

Chromosome Aberrations ; Environmental Exposure ; adverse effects ; Humans ; Magnetic Fields

Objective To establish a stable model of intraluminal thread approach in making focal cerebral ischemia/reperfusion modelin rabbit.Methods Forty New Zealand white rabbits were randomly divided into three groups:A,B,and C.Angiography of ICA wasperformed in group A(n=5). Control group B(n=5) was sham-operated.In group C(n=30),the focal cerebral ischemia/reperfusionmodel was made by inserting a wire ( d=0.45 mm ) into MCA through ICA and CCA directly and pulling it out 3 hours later . MRI andneurological deficit score were used to evaluate the effectiveness of models.Results Angiography could show the course and bifurcation of ICA clearly.22 models were successful.The pathological changes were shown on MRI.The neurological deficit score (reperfusion 1 h) were 2.8?0.45.Conclusion The focal cerebral ischemia/reperfusion model made by inserting a wire(d=0.45 mm) into MCA through ICA and CCA directly and pulling it out 3 hours later was stable and fit for imaging research.

Objective To explore the anti-inflammatory and anti-angiogenic effect of miR-15a in diabetic retinopathy(DR).Methods High glucose model(HG)was established by treatment with 25 mmol/L glucose in human retinal pigment epithelial cell line HARPE-19,and HARPE-19 cells treated with 5 mmol/L glucose served as control(LG).HG group and LG group were divided into 4 subgroups:miR-15a mimic group,NC-mimic group,miR-15a inhibitor group and NC-inhibitor group.Cell proliferation ability was detected by MTT proliferation assay.Cell migration ability was detected by cell scratch assay.The relationship between miR-15a and ASM was identified by 3′UTR luciferase reporter assay.miR-15a,ASM,VEGF,IL-1β,IL-6,TNF-α mRNA expression was detected by RT-PCR method.Results In NC-mimic cells and NC-inhibitor cells,the expression of miR-15a in HG group was significantly lower than that in LG group(all P<0.05).The expression level of ASM mRNA in miR-15a mimic group was significantly lower than that in NC-mimic group (P<0.05),the expression level of ASM mRNA in miR-15a inhibitor group was significantly higher than that in NC-inhibitor group (P<0.05).The cell scratch width in miR-15a mimic group was significantly higher than that in NC-mimic group(P<0.05).The cell scratch width in miR-15a inhibitor group was significantly lower than that in NC-inhibitor group(P<0.05).The absorbance value in miR-15a mimic group was significantly higher than that in NC-mimic group(P<0.05),the absorbance value in miR-15a inhibitor group was significantly lower than that in NC-inhibitor group(P<0.05).In NC-mimic cells and NC-inhibitor cells,the mRNA expression levels of VEGF,IL-1β,IL-6 and TNF-α in HG group was significantly higher than those in LG group(all P<0.05).Conclusion miR-15a downexpression induces inflammatory reaction and angiogenesis in retinal cells.miR-15a is involved in the pathogenesis of DR by dual regulation of inflammation and angiogenesis.

0.05). Minor hematoma occurred in four patients with transradial approach and in 59 with transfemoral approach (1.46% vs 17.78%, P0.05), and two patients required blood transfusion in group F. None of the patients suffered from pseudoaneurysm, arteriovenous fistula, and ischemia of the hand. Conclusion Coronary angioplasty can be performed safely using the transradial approach with relatively few vascular complications and with better patient′s comfort.

Objective To investigate the effects of first external fixator and second locking plate fixation in treating open tibiofibular fractures. Methods We retrospectively analyzed the 36 patients with Gustilo'sⅢtype tibia and fibula fractures from Jan. 2009 to Dec. 2010. All the patients were treated with first external fixator and second locking plate fixation,and the curative effect and the extremity function were evaluated.Results All patients were followed-up for 18 months (6 to 24 months) in average,and all the fractures were healed in 5.5 months averagely. According the Johner-Wruhs evaluation standard, excellent was in 24 cases, good was 10 cases,and bad was in 2 cases. The excellent and good rate was 94%. According the Merchant evaluation standard, excellent was in 26 cases,good was in 5 cases,fair was in 4 cases,bad was in 2 cases. The excellent and good rate was 86.1%.The outcome was satisfactory. Conclusion The first external Fixator and second locking plate fixation in treating open tibiofibular fractures can improve the healing rate and the functional recovery.

To improve the clinical skills of medical students and to train qualified and profes-sional ophthalmologist,the school of optometry and ophthalmology in Wenzhou Medical College car-ried out reforms and innovations in clinical practice and training. In order to strengthen and train clin-ical thinking and clinical skills,and to cultivate the humanistic qualities of medical students,the di-verse-training mode were applied in clinical practice and training. In this paper explored the design goal, objective and actual effect of diverse-training mode for clinical practice and training.

Objective To observe the release of inflammation-related factors after angiotensin Ⅱ (Ang Ⅱ ) stimulation in rat tubular epithelial cells (NRK-52E), to analyze whether these effects were mediated by TLR4-MyD88 pathway, and to reveal the novel mechanism of injury by Ang Ⅱ on NRK-52E cells. Methods After synchronization, cells incubated with AngⅡ (10-7 mmol/L) were used as the stimulation group, cells without stimulation were as normal control. To determine the role of TLR4 and the adaptor MyD88, equal number of NRK-52E cells was added with 10-5 mmol/L candesartan or 20 mg/L TLR4 blocking peptide for 1 h and then incubated with Ang Ⅱ (10-7 mmol/L) respectively. RT-PCR was used to analyze TLR4 mRNA and MyD88 mRNA expression. Immunofluorescence and confocal microscopy were used to observe TLR4 protein expression. ELISA was used to detect the concentration of tumor necrosis factor-alpha (TNF-α) and heat shock protein 47(HSP47) in cell supernatant respectively. Results TLR4 and MyD88 were highly expressed in Ang Ⅱ-induced NRK-52E cells (P＜0.01), and the TNF-α and HSP47 levels were also increased markedly compared with control group (P＜0.01). In NRK-52E cells that were pre-incubated with candesartan, TLR4 and MyD88 expression were obviously inhibited,subsequently, HSP47 and TNF-α production decreased remarkably compared with Ang Ⅱ group (P＜0.01). TLR4 blocking peptide had the similar effect in a dose-dependent manner, in which its effect was dependent on inhibiting TLR4-MyD88 expression. Conclusion The mechanism of Ang Ⅱ -induced injury effect on NRK-52E cells is related to the increase of TLR4-MyD88 activity,which is followed by the enhance of TNF-α and HSP47 expression. This process is inhibited by candesartan via modulation of innate immune pathway.