Objective To explore the role of miR-184 in Oxygen-Glucose-Deprivation (OGD) induced SK-N-SH cell ischemic injury and its regulation on AKT2 level. Method We used a combination of oxygen and glucose deprivation to imitate ischemic conditions in vivo. MiR-184 mimic and inhibitor were transfected into SK-N-SH cell to alter miR-184 levels. The expression of miR-184 and AKT2 were determined by using Real-time PCR. The extent of SK-N-SH cell survival rate was assessed by thiazolyl blue tetrazolium bromide (MTT) assay. Result Here, we observed that miR-184 was significantly inhibited in SK-N-SH cell after OGD (P<0.05). The changes of miR-184 level altered the expression of AKT2 mRNA. In addition, alteration of miR-184expressionsignificantly affected cell survival rate after OGD. Conclusion miR-184 plays an important role in ischemic injury through negatively regulating AKT2 level, which may provide a potential therapeutic target for ischemic stroke in miRNA levels.

AIM To explore effects of policosanol on depressing cholesterol in hyperlipidemia rats and the correlated biochemistry mechanism. METHODS The rats were randomly divided into normal control, policosanol 4 mg·kg~(-1) prevention, hyperlipidemia model, policosanol 4, 6 and 8 mg·kg~(-1) and lovastatin positive control groups. The later 5 group rats were fed with high-cholesterol diets for 4 weeks in order to make hyperlipidemia model and beginning from the 5th week, in addition to the normal control and model groups, other groups were ig given policosanol or lovastatin once a day for 6 weeks, respectively, and policosanol protection group rats were ig given with policosanol 4 mg·kg~(-1) once a day for 10 weeks, together with high-cholesterol diets everyday. Total cholesterol(TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) concentrations in the serum and fecal bile acid (FBA) in the exrement were determined by auto-biochemistry analyzer. The activity of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase in hepatocellular microsomes was detected by ultraviolet spectrophotometric analysis and activity of low density lipoprotein receptor (LDL-R) in peripheral blood lymphocyte was detected by fluorescence labelled integrator method. RESULTS Compared with hyperlipemia model group, the levels of TC decreased (39.1%-46.4%), LDL-C decreased (66.6%-80.7%), and FBA increased (9.7%-19.0%), the activity of HMG-CoA reductase decreased （13.8%-23.6%）, and activity of LDL-R increased (27.5%-129.6%) in policosanol prevention, policosanol 4, 6 and 8 mg·kg~(-1) and lovastatin groups, respectively; HDL-C increased （12.2%-16.7%） in policosanol prevention and policosanol 8 mg·kg~(-1) groups; TG decreased in lovastatin group. CONCLUSION Policosanol has significant effects on decreasing cholesterol. The decreasing cholesterol mechanism should include: ① increasing FBA excretion; ② decreasing the activity of HMG-CoA reductase; ③ increasing activity of LDL-R.

OBJECTIVE:To investigate the regulation effects of policosanol on lowering cholesterol and its enzymatic mechanism.METHODS:The rats were randomly assigned into control group,policosanol prevention group (4.0 mg?kg-1?d-1),policosanol low-dose,medium-dose and high-dose groups (4.0 mg?kg-1?d-1,6.0 mg?kg-1?d-1,8.0 mg?kg-1?d-1),lovastatin group (positive control) and hyperlipoidemia model group.The last five groups were induced hyperlipoidemia model for 4 weeks.Blood samples were collected after 6 weeks administration (i.g.).The levels of TC,TG,LDL-C and HDL-C in the serum were determined.Body weight and liver weight were measured and hepatic index was calculated.The activity of lecithin cholesterol acyl transferase (LCAT) in serum,hepatic lipoprotein lipase (LPL) and hepatic lipase (HL) were detected.RESULTS:Policosanol remarkably decreased the levels of TC (ranged from 39.1% to 43.3%) and LDL-C (ranged from 66.6% to 80.7%) in serum and hepatic index (ranged from 11.1% to 11.8%) (P

AIM:To investigate the influence of F10 on the activities of transcription factor NF-?B and AP1 in A549 cells.METHODS:The luciferase report plasmids of NF-?B-Luc,AP1-Luc and F10 gene were introduced into A549 cells and the luciferase activity was detected.The DNA binding activities of AP1 and NF-?B in the cells were measured by the electrophoretic mobility shift assay(EMSA).RESULTS:The luciferase activity in F10+ transfection group decreased 30% and increased 2-fold respectively 48 h after transfected with the luciferase report plasmid of NF-?B-Luc and AP1-Luc in A549 cells.The DNA binding activity decreased 49% and increased 23%,respectively.CONCLUSION:F10 gene up-regulates the transcription activity of AP1 and down-regulates the NF-?B in A549 cells.

Aim To identify the effect of policosanol on LDL-R activity.Methods In vitro cell culture experiments conventional methods were used to observe the direct effect of policosanol on mononuclear cells LDL-R.In vivo experiments self-control and negative-control group design methods were used to observe the effect of policosanol on LDL-R activity in the patients with hypercholesterolemia.LDL-R activity was analysed by fluorescence flow cytometry and labeled by the fluorescent reagent DiI.Results Policosanol 5~20 mg?L-1 obviously activated the activity of LDL-R in human mononuclear cells,policosanol levels and the activity of LDL-R in human mononuclear cells showed significantly dose-effect relationship in vitro study.These tendency could also be seen in the patients with hypercholesterolemia after policosanol treatment for four weeks in vivo study.As the increasing of policosanol dose,the activity of LDL-R in human mononuclear cells remarkably increased in the patients with hypercholesterolemia Conclusions Policosanol up-regulates the activity of the LDL-R in the mononuclear cells and reduce cholesterol level in the body.Policosanol reduce lipids through multiple ways including LDL-R.

This study examined the effect of nicotine on the expression of mutant p53 (mt-p53) in bladder cancer rats. The rat models of bladder cancer were established by infusing N-methyl-nitroso-urea (MNU, 10 mg/kg every 2 weeks for 8 weeks) into the bladder. Pathological examination on the bladder was conducted to confirm the establishment of the model. All the bladder cancer rats were randomly divided into an MNU group and 3 nicotine groups. In the nicotine groups, the rats were intragastrically administered nicotine at different concentrations (25, 15, 5 mg/kg respectively) 3 times per week for 8 weeks. The mt-p53 expression was detected by the immunohistochemical method. The results showed that rat bladder cancer models developed histopathological changes of bladder transitional cell carcinoma. The positive rate of mt-p53 expression in the 3 nicotine groups (25, 15, 5 mg/kg) was 75.00%, 58.33% and 41.67% by the 14th week, respectively, significantly higher than that in the MNU group (33.33%) (all P<0.05). The mt-p53 expression rate was positively correlated with the medication dose and time (P<0.05). It is concluded that nicotine may play an important role in the development of bladder cancer partially by increasing the expression of mt-p53.

Objective: To systematically review the safety and efifciency for dual antiplatelet therapy (DAPT) ≤ 6 months and DAPT ≥ 12 months in patients after drug eluting stent (DES) implantation. Methods: We collected the data for randomized clinical trials for DAPT ≤ 6 months and DAPT ≥ 12 months in patients after DES implantation up to 2015-01 by searching the literatures of PubMed, EMBASE, Cochrane Library, Scopus and Chinese literature database, and meanwhile collected the relevant reporting cases from both domestic and international cardiovascular conferences for this study. There were 2 investigators independently conducted the literature screening, data extraction and quality evaluation, Meta analysis was performed with STATA 12.0 software. Results: A total of 15,378 patients from 7 eligible studies were enrolled and the patients were divided into 2 groups: DAPT ≤ 6 months group,n=7672 and DAPT ≥ 12 months group,n=7706. Meta analysis indicated that DAPT ≤ 6 months could effectively reduce the major bleeding (OR=0.58, 95% CI 0.37-0.91,P=0.017). While the other incidences between 2 groups were similar as all cause death (OR=0.90, 95% CI 0.73-1.11,P=0.314), cardiac death (OR=0.93, 95% CI 0.70-1.24,P=0.617), myocardial infarction (OR=1.13, 95% CI 0.91-1.41,P=0.275), in stent thrombosis (OR=1.21, 95% CI 0.79-1.85,P=0.382) and cerebrovascular accidents (OR=1.00, 95% CI 0.66-1.51,P=1.000). Conclusion: The incidence rates of cardiovascular and cerebrovascular events are similar in patients with DAPT ≤ 6 months and DAPT ≥ 12 months after DES implantation. DAPT ≤ 6 month had the lower risk of bleeding, which is rather suitable for the patients received new generation of DES, with higher risk of bleeding, lower risk of thrombosis and with poor compliance to medication; however, the large and randomized clinical trials are needed to make ifnal conclusion.

Objective: To explore the characteristics of Auditory Brainstem Response (ABR) in children with ASD, and analyze their relation with the core symptoms of ASD. Methods: Ninty children aged 2-6 with ASD were recruited from Harbin in this study. The data of ABR was collected by using BAEP, and the association among children’s absolute latency and interpeak latency of ABR, core symptoms of ASD children’s behavior and clinical manifestation was analyzed. Results: Compared with the normal average value, children with ASD had longer the absolute latency of wave Ⅰ,Ⅲ,Ⅴ in bilateral ears, which were (1.51±0.20)(3.83±0.34)(5.63±0.23)ms, (1.54±0.16) (3.78±0.23) (5.63±0.22)ms, respectively(P<0.05). Some children’s interpeak latency of Ⅰ-Ⅲ, Ⅲ-Ⅴ, Ⅰ-Ⅴ were longer than normal values. Children younger than 3 years old showed prolonged peak intervals of Ⅰ-Ⅲ and Ⅰ-Ⅴ than children in 3-7 years old. The study has also showed that there was positive correlation between the absolute latency of waveⅠin left ear and the social function defect(r=0.45, P<0.05); there was positive correlation between the latency of wave Ⅴin right ear or the latency of waveⅠin left ear or the Ⅰ-Ⅲ peakinterval and nonverbal communication ability dysfunction(r=0.35, 0.39, 0.34, P<0.05); there was positive correlation between the Ⅰ-Ⅲ peak interval and the repeated stereotyped symptoms(r=0.39, 0.35, P<0.05). Conclusion Children with ASD have abnormal auditory behavior. The absolute latency and interpeak latency of ABR is correlated to some parts of core symptoms of ASD.

Guillain-Barré syndrome (GBS) is a rare, but potentially fatal, immune-mediated disease of the peripheral nerves and nerve roots, which is usually triggered by infections. It is characterized by rapidly progressive, symmetrical weakness of the extremities. Some patients develop respiratory insufficiency and many show signs of autonomic dysfunction. Diagnosis can usually be made on clinical grounds, but lumbar puncture and electrophysiological studies can help to substantiate the diagnosis and to differentiate demyelinating from axonal subtypes of GBS. Molecular mimicry of pathogen-borne antigens, leading to generation of crossreactive antibodies that also target gangliosides, is generally accepted pathogenesis of GBS. The treatment of GBS is intravenous immunoglobulin or plasma exchange with general clinical treatment. Most patients have a good prognosis and basically recover within weeks to months. A few patients have persistent neurological dysfunction or even death.

This study examined the effect of nicotine on the expression of mutant p53 (mt-p53) in bladder cancer rats.The rat models of bladder cancer were established by infusing N-methyl-nitroso-urea (MNU,10 mg/kg every 2 weeks for 8 weeks) into the bladder.Pathological examination on the bladder was conducted to confirm the establishment of the model.All the bladder cancer rats were randomly divided into an MNU group and 3 nicotine groups.In the nicotine groups,the rats were intragastrically administered nicotine at different concentrations (25,15,5 mg/kg respectively)3 times per week for 8 weeks.The mt-p53 expression was detected by the immunohistochemical method.The results showed that rat bladder cancer models developed histopathological changes of bladder transitional cell carcinoma.The positive rate of mt-p53 expression in the 3 nicotine groups (25,15,5 mg/kg) was 75.00％,58.33％ and 41.67％ by the 14th week,respectively,significantly higher than that in the MNU group (33.33％) (all P＜0.05).The mt-p53 expression rate was positively correlated with the medication dose and time (P＜0.05).It is concluded that nicotine may play an important role in the development of bladder cancer partially by increasing the expression of mt-p53.