0.05).Conclusion BNP and hsCRP may be involved in the occurrence and sustainment of atrial fibrillation.The serum levels of BNP and hsCRP may serve as independent indexes of atrial fibrillation.CK-MB may be not involved in the incidence and development of atrial fibrillation.

With the understanding of the immune inflammatory response in the pathogenesis of dry eyes, and the limitations of widely used artificial tears and numerous pharmaceuticals and methods to promote tear secretion, clinicians pay more attention to the therapies that can promote tear secretion actively. Acupuncture treatment for dry eye may meet this requirement.

OBJECTIVE:To establish an HPLC method for determining nicardipine hydrochloride(NCD) microspheres in cerebrospinal fluid(CSF) of rabbits by HPLC.METHODS:NCD microspheres were injected into the cistern of rabbits.Cerebrospinal fluid was sampled at different time points and NCD was separated on Agilent-Zorbax column at a flow rate of 1.0 mL?min-1 with column temperature of 30 ℃.The mobile phase consisted of methanol-water(75 :25,pH=6.0) and detection wavelength was set at 236 nm.RESULTS:The linear range of NCD was 2～128 ng?mL-1(r=0.999 8) with recovery of 98.07%.The RSD of intra-day and inter-day were both below 1.47%.The LOD was about 0.5 ng?mL-1.On 3～11 day after medication,the concentration of NCD fluctuated within(14.15?0.37) ng?mL-1.CONCLUSION:The method is simple,rapid and accurate for determination of NCD in cerebrospinal fluid of rabbits.

8-hydroxydeoxyguanosine (8-OHdG) in human urine is a marker reflecting oxidative stress and DNA oxidative damage. People spend 80%-90% of their life indoors; therefore, indoor air quality is directly related to human health. In this paper, the urinary 8-OHdG levels were presented in populations grouped by different demographic characteristics, lifestyle, occupational exposure, and health status, and elucidated indoor pollutants affecting human urinary 8-OHdG level, such as pollutants from outdoor sources, smoking, indoor combustion and cooking fumes, the chemicals in interior decoration materials, and building foundation soils. The article aims to provide a theoretical basis for predicting the impact of indoor air pollution on human health (DNA oxidative damage and related diseases) by measuring the concentration of 8-OHdG in human urine.

Objective To observe the effect of cytokine-induced killer (CIK) cells on the apoptosis of human leukemia cells,and explore the role of miR-155 in this process.Methods The cytotoxicity of CIK cells against a variety of leukemic cell lines (NALM-6,Jurkat) was investigated by MTT technique,miR-155 was determined by real time quantitative PCR,and the apoptosis was detected by flow cytometry in NALM-6 and Jurkat cells induced by CIK cells.Psi CHECK2-CEBP/β 3'-UTR containing the binding site of miR-155 was constructed,and then it was transfected into NALM-6 and Jurkat cells.Luciferase activity of CEBP/β (CCAAT/enhancer binding protein beta) was determined with the assistance of dual luciferase report system.Results CIK cells possessed strong cytotoxicity against NALM-6 and Jurkat cells,which was time-dependent and dose-dependent (P ＜ 0.05).CIK cells could increase the expression of miR-155 in NALM-6 cells by (2.87±0.19) fold (t =2.787,P ＜ 0.05),and in Jurkat cells by (1.98±0.25) fold (t =3.513,P ＜ 0.05).Moreover,miR-155 mimics could promote the apoptosis of NALM-6 and Jurkat cells induced by CIK cells (t =4.239,P ＜ 0.05;t =3.565,P ＜ 0.05).However,miR-155 inhibitor might block this process (t =3.772,P ＜ 0.05;t =4.017,P ＜ 0.05).MiR-155 targeted at the site of CEBP/β3'-UTR,and CIK cells could decrease the luciferase activity of NALM-6 cells by (42.89±2.07) ％ (t =3.578,P ＜ 0.05),meanwhile,in Jurkat cells by (37.02±1.95) ％ (t =4.393,P ＜ 0.05).Conclusion CIK cells could enhance human leukemia NALM-6 and Jurkat cells apoptosis by upregulating miR-155,which may provide a new database to elucidate leukemia cell therapy using CIK cells.

Objective To investigate the effect of Atorvastatin on the proliferation and apoptosis of leukemic HL-60-cell line,and to explore the possible role of phosphatidylinositol 3-kinase/serine/threonine protein kinase /mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway in this process.Methods HL-60 cells were incubated with different concentrations of Atorvastatin (1,5,10 μmol/L),and HL-60 cells without any treatment were used as controls.The proliferation of HL-60 which was investigated by four methyl thiazolyl tetrazolium assay when cells were cultured for 12,24,48 hours.The apoptosis was detected by flow cytometry after cells were incubated for 48 hours.The mRNA and protein expressions of AKT,PI3K and mTOR were detected by reverse transcription-polymerase chain reaction and Western blot methods,respectively.Results The results indicated that Atorvastatin could inhibit the proliferation and induce the apoptosis of HL-60 cells.When treated with 10 μmol/L Atorvastatin after 48 h,the proliferation inhibition of HL-60 was observed most obviously,with a high rate of (39.77 ± 3.01) ％,compared with the control group,it had statistical significance (t =4.016,P ＜ 0.01),meanwhile,the apoptosis of HL-60 was most notable,at a rate of (43.29 ±3.91)％,compared with the control group,it had statistical significance (t =3.625,P ＜ 0.05).There were basal expression of AKT,PI3K and mTOR in the control group.When treated with 10 μmol/L Atorvastatin after 48 h,the mRNA expression of PI3K,AKT and mTOR were down-regulated most obviously,at a decrease of (37.05 ± 4.11) ％,(53.79 ± 3.27) ％,(40.63 ± 2.42) ％ (t =4.805,3.799,4.312,all P ＜ 0.05),respectively,in comparison with the control group.At the same condition,the protein expression of PI3K,AKT and mTOR were decreased most visibly,with a decline of (41.09 ± 3.17) ％,(45.67 ± 2.92) ％,(63.41 ± 3.59) ％ (t =3.576,4.727,4.902,all P ＜ 0.05) respectively in comparison with the control group.Conclusions Atorvastatin can inhibit the proliferation and induce the apoptosis of leukemic cell HL-60,and the mechanism may be associated with the PI3K/ AKT/mTOR signal pathway.

Objective To evaluate the effects of dexmedetomidine on the expression of neuronal nitric oxide synthase (nNOS) and c-fos in the lcuos cruleus (LC) in a rat model of endotoxic shock.Methods Twentyeight male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly divided into 4 groups (n =7 each):control group (group C),endotoxic shock induced by lipopolysaccharide (LPS) group (group L),lowdose dexmedetomidine group (groupLD) and high-dose dexmedetomidine group (group HD).Normal saline 0.5 ml/kg was injected via the tail vein in C and L groups.Dexmedetomidine 0.5 and 4.5μg/kg were injected via the tail vein in group LD and group HD,respectively.Normal saline 0.5 ml/kg was injected via the tail vein 10 min later in C,while LPS 5 mg/kg was injected intravenously 10 min later in the other groups.The rats were sacrificed and their brains were removed for determination of brain water content,the number of nNOS and c-fos positive cells and expression of nNOS and c-fos in the LC by immuno-histochemistry.Results Compared with group C,the brain water content was significantly increased,the number of nNOS and c-fos positive cells in the LC was enlarged,and the expression of nNOS and c-fos in the LC was up-regulated in group L (P ＜ 0.05).The brain water content was significantly lower,the number of nNOS and c-fos positive cells in the LC was smaller,and the expression of nNOS and c-fos in the LC was lower in LD and HD groups than in group L (P ＜ 0.05).The number of nNOS and c-fos positive cells in the LC was significantly smaller,and the expression of nNOS and c-fos in the LC was lower in HD group than in group LD (P ＜ 0.05).Conclusion Dexmedetomidine can down-regulate the expression of nNOS and c-fos in the LC,which may be one of brain-protective mechanisms of dexmedetomidine in a rat model of endotoxic shock.

To explore the effects of dietary conjugated linoleic acid(CLA) on body fat accumulation in male Wistar rats. The obese rat model was established by feeding high lipid forage. The rats were fed a semi-purified diet containing 0.5,1.0,3.0g?kg -1 CLA for 36 days. Low dose group, middle dose group and high dose group all could remarkably reduce the gain of body weight. Low dose group could reduce the body adipose, middle and high dose group could remarkably decrease the body adipose. There were significant differences in the fat and protein contents in the rats thigh between the control group and the group fed high dose CLA. These results suggested that CLA can reduce the body fat in obese Wistar rats.

[Objective]To analyze the clinical effect of intertrochanteric fractures treated with percutaneous proximal femoral nails(PFN).[Method]From January 2004 to May 2009,PFN using percutaneous technique was performed in 180 elderly patients of femoral intertrochanteric fractures(180 hips,80 males and 98 females),with mean age of 76 years(range from 57-99 years).According to Evans classification,12 cases were type Ⅰ,28 were type Ⅱ,62 were Ⅲa,20 were Ⅲb,49 were Ⅳ,9 were Ⅴ.Traction table and C-arm fluroscopic intensifier were used with close reduction and interlocking during the course of operation.[Result]One hundred and seventy two cases in 180 patients were followed up for 8 to 21 months with a mean of 13.5 months.Other 8 patients were lost to follow up after discharge.Of 172 patients followed up,166 cases' radiographs showed the callus during 6-8 weeks postoperatively,while they had a full range of hip motion as the original level.Partial weight bearing exercises were carried out since the 8th postoperative week.The time of clinical fracture healing was from 12 to 16 weeks,the rate of healing was 98.8%.In the function assessment of 172 patients the satisfactory rate reached to 87.8 percents.[Conclusion]Percutaneous proximal femoral nails is an ideal way for the treatment of intertrochanteric fractures in aged because of its simple procedure,minimal invasion,less fluoroscopy exposures,less complications,stable fixation,early fracture healing and satisfied functional outcomes.

Objective To explore the clinical experience of endovascular treatment for arteriosclerosis obliterans (ASO) of lower extremities.Methods Endovascular treatment were performed on 22 patients (26 limbs) suffering from ASO which were diagnosed by magnetic resonance angiography (MRA).The clinical efficacy after operation was analyzed.Results Twenty-two lower extremities of 18 patients successfully accepted endovascular treatment with 12 stents planted without major complications.Four cases failed to endovascular treatment and 2 of them converted to bypass surgery.The clinical symptoms of limb ischemia vanished or significantly improved after treatment.The ankle brachial index (ABI) of affected extremities increased from 0.35?0.13 (before operation) to 0.70?0.15 (after operation),P