Objective: To investigate the effects of Radix Ginseng and Radix Notoginseng formula on expressions of vascular endothelial growth factor receptor-2 (VEGFR-2) and hypoxia-inducible factor-1alpha (HIF-1alpha) in ischemic myocardium of rats with acute myocardial infarction. Methods: A total of 100 Wistar rats were randomly divided into normal control group, sham-operated group, untreated group, metoprolol (Betaloc) group, and high- and low-dose Radix Ginseng and Radix Notoginseng formula groups. Acute myocardial infarction was induced in the untreated group, Betaloc group, and high- and low-dose Radix Ginseng and Radix Notoginseng formula groups by left anterior descending coronary artery ligation. After 12-day treatment, microvessel density (MVD) in ischemic myocardium was detected by immunohistochemical method, while expressions of VEGFR-2 and HIF-1alpha proteins were detected by Western blotting, and expressions of VEGFR-2 and HIF-1alpha mRNAs were detected by real-time fluorescent quantitative polymerase chain reaction. Results: MVD in the untreated group was increased significantly, higher than those in the normal control group and the sham-operated group (P<0.05) and lower than those in the high- and low-dose Radix Ginseng and Radix Notoginseng formula groups and Betaloc group (P<0.01). VEGFR-2 and HIF-1alpha protein and mRNA expressions in the untreated group were higher than those in the normal control group and the sham-operated group (P<0.05). VEGFR-2 and HIF-1alpha protein and mRNA expressions in the high- and low-dose Radix Ginseng and Radix Notoginseng formula groups and Betaloc group were higher than those in the untreated group (P<0.05). There was a significant difference between the high- and low-dose Radix Ginseng and Radix Notoginseng formula groups (P<0.05). Conclusion: Radix Ginseng and Radix Notoginseng extract can up-regulate the protein and mRNA expressions of VEGFR-2 and HIF-1alpha and increase MVD in ischemic myocardium to improve myocardial ischemia so as to promote the development of collateral circulation.

Objective To investigate the role of Furin in breast cancer cell proliferation and provide a theoretical basis for in￣depth study of breast cancer. Methods Different concentrations of Furin inhibitor were added in MCF￣7 cell culture to test MCF￣7 cell proliferation by MTT essay.Hochest 33342 staining was used to detect the morphological change of apoptosic cells.Western blot analysis was applied to measure the level of cell apoptosis associated proteins,such as Caspase￣3,Caspase￣8 andCaspase￣9.The enzyme￣linked immunosorbent assay was used for detection the CAT and SOD levels in cell culture. ResultsMCF￣7 cell growth was inhibited by Furin inhibitor in a time and dose dependent manner.The results of Western blot and Hochest33342 staining indicated that MCF￣7 cells were apoptosis after Furin inhibitor treatment. The level of CAT was increasedsignificantly,associated with the level of SOD. Conclusion Furin inhibitor could induce MCF cell apoptosis, thereby inhibitcell proliferation by modulating MCF￣7 cell redox state.

Objective To compare the therapeutic effect of Qingre Anchuang Tablets(QAT) processed by new or old technology on rabbit ear acne.Methods Experimental rabbit ear acne was induced by coal tar.After the modeling,the rabbits were administrated with QAT processed by new or old technology.The thickness,weight and PGE2 level of the acne ear were measured,and the pathological changes of the acne ear were also examined.Results QAT processed by new or old technology could decrease the thickness,weight and PGE2 level of the ear significantly,and relieve the pathological changes of the acne ear.The effects of QAT processed by new technology was better than that of QAT processed by old technology.Conclusion QAT processed by new technology has a better therapeutic effect on rabbit ear acne than QAT processed by old technology.

Objective To analyze the clinical characteristics and the endocrine changes in children with craniopharyngioma,and to improve the pediatrician understanding of the disease.Methods The study subjects consisted of 14 children with craniopharyngioma admitted to the Department of Endocrinology,Beijing Children's Hospital Affiliated to Capital Medical University from Jan.2004 to Dec.2012.All the patients were followed up to analyze the clinical symptoms improvement,endocrine test results and medication,et al.Results The main clinical manifestations were headache (7/14 cases,50.0％),growth retardation(4/14 cases,28.6％),vomiting (4/14 cases,28.6％),polydipsia/ polyuria (3/14 cases,21.4％) and vision diminution (3/14 cases,21.4％).Three patients didn' t undergo the surgery,and 3 cases with diabetes insipidus and 2 cases with growth hormone deficiency,and 1 case with central hypothyroidism by laboratory test.The rest 11 children received surgery and all patients had changes in endocrine after it.Five cases got polydipsia and polyuria,other 5 cases had electrolyte disturbances,and 2 cases had epilepsy.Nine patients were followed up,and the follow-up duration ranged from 5 months to 10 years [(3.29 ± 3.52) years] after surgery.Seven patients got better and 2 patients got worse.Conclusions For clinical symptoms of increased intracranial pressure,changes in endocrine,the vision and visual field,the possibility of craniopharyngioma should be taken into account.Surgery is the main treatment,but it can lead to the damage of hypothalamus and pituitary gland.Changes in endocrine,electrolyte disturbances and epilepsy are the common complications.According to the level of endocrine,longterm hormone replacement therapy for some postoperative patients should be continued.

Objective To study the hemoprotective effects of a rotary magnetic field (RMF) to radiation-injured mice. Methods 132 male BALB/c mice were randomly divided into four groups: a normal group (N), a magnetic treatment group (M), an irradiation group(R) and an irradiation combining magnetic treatment group (R + M). Mice in the N group received no treatment. Mice in the R and R + M groups received total body irradiation with 6.0 Gy 60Co γ/rays. Mice in the M and R + M groups were treated with a RMF for one and half an hour at a time, twice a day, totally for 30 days. The survival rate was observed for 30 days. On days 0, 5, 9, 15, 21, 30, the subjects' peripheral blood cells were counted. On day 9, 23 and 30, the number of bone marrow nucleated cells (BMNCs), colony forming unit-spleen (CFU-S), spleen-body ratio, the cell cycle and apoptosis of bone marrow cells were measured. The pathological sectioning of the femur was performed and the expression level of bone morphogenetic proteins (BMP2/4) in the bone marrow was evaluated. Results ①No mice died in the N and M group. The RMF treatment increased the survival rate and survival days among the irradiated mice (P < 0.01). ②The RMF treatment increased the number of blood cells in their peripheral blood of the R + M group. ③The number of BMNCs, CFU-S and the proportation of G2 + M stage in the R + M were markedly higher than that of the R group, but the proportation of the apoptosis was lower than that of the R group on the 9th day (P < 0.05). Furthermore, the spleen index in the R + M group was also higher than that of the R group on the 23rd day (P < 0.05). ④RMF could improve the expression level of BMP2/4 in the radiation-injued mice. Conclusion The RMF treatment had an obvious protective effect against the effects of irradiation and it accelerated the recovery of hematopeiesis and the hematopoietic microenvironment in mouse bone marrow.

Objective To investigate whether thalidomide inhibits the over expression of type I collagen in pulmonary fibrosis rats via inhibiting the JNK signaling pathway,thereby reducing bleomycin induced pulmonary interstitial fibrosis in rats.Methods 90 healthy male SD rats were randomly divided into normal control group (group N),model group (group M),thalidomide group (group T),SP600125 group (group SP) and thalidomide+SP600125 group (group T+SP).The pulmonary fibrosis models were prepared via intratracheal injection of 5mg/kg bleomycin,and rats in groups were given corresponding drugs from the first day after preparing model.Rats were randomly sacrificed at 7,14 and 28 days after treatment.The degree of pulmonary alveolitis and fibrosis was evaluated by H&E and trichrome masson stainings.The level of hydroxyproline in the lung tissue was detected by applying alkaline hydrolysis technique,and expression levels of p-JNK and type I collagen were tested by Western bloting for protein expression and real-time polymerase chain reaction (RT-PCR) for mRNA expression.Results In group M,alveolitis was the most serious on day 7; a marked pulmonary fibrosis formed on day 28; the level of hydroxyproline also peaked on day 28,and the contents of p-JNK and type I collagen were higher than in group N(F=277.87,472.51,both P＜ 0.01).Group T,SP and T+SP showed mild alveolitis and fibrosis at all time points,and their levels of hydroxyproline,p-JNK and type I collagen were remarkably decreased as compared with group M (F=14.77,61.59,101.73,all P＜0.01;F=10.33、79.12、57.48,all P＜0.01).No significant difference in p JNK was found between group SP and group T+SP.Conclusions Thalidomide may inhibit the over expression of type I collagen in pulmonary fibrosis rats via inhibiting the JNK signaling pathway,thereby reducing bleomycin induced pulmonary interstitial fibrosis in rats.

Objective To establish an ideal focal cerebral ischemia reperfusion model in monkeys.Methods Adult healthy rhesus monkeys(Macaca mulatta) 12 cases(male 6 and female 6),aged 4-7 years and weighted 4.8-7.5kg.were used in this study.The middle cerebral artery occlusion/reperfusion(MCAO/R) model was established by inserting a standard micro-balloon catheter intraluminally from the carotid common artery or femoral artery into the proximal segment of the middle cerebral artery(MCA).The regional cerebral blood flow of MCA was occluded by expanding the micro-balloon to cause ischemia,and withdrawing the micro-ballon catheter to reperfuse the MCA.The MCAO/R model was evaluated by angiography,magnetic resonance angiography(MRA),magnetic resonance imaging(MRI),tetrazolium chloride(TTC) staining and neurological behavoral function scores.Results By inserting a micro-balloon catheter intraluminally from the carotid common artery or femoral artery into the MCA,the micro-balloon catheter could be inserted into the MCA to occlude blood flow,and no image of MCA shown on TV screen.In MCA blood flow supplied area,magnetic resonance T1,T2 and DWI showed high signals,TTC staining showed cerebral ischemic infarction,and correspondly the monkeys showed neurological function disorders.This method used a simple operatire procedure had a high successful rate,and could be repeated.Conclusion We showed ideal method to establish the MCAO/R model in monkeys by inserting intraluminally a micro-balloon catheter into the MCA.

Objective To explore the effect and mechanism of TGF beta1/smad3 signaling pathways on apoptosis in mouse pulmonary fibrosis.Methods Fifty-four healthy male C57BL/6 mice were randomly divided into three groups:normal control (n=18),pulmonary fibrosis model (n =18) and TGF-β1/smad3 inhibitor group (n=18).Six mice in each group were randomly killed on days 7,14 and 28.Hematoxyli~eosin and Masson staining were adopted to evaluate the severity of pulmonary inflammation and fibrosis.The content of hydroxyproline (Hyp) in the lung tissues was detected by alkaline hydrolysis technique.The apoptosis was observed by tunnel apoptosis assay kit.P-smad3 and caspase3 protein expressions were assessed via Western blot.Results Lung in model mice versus normal control showed alveolar inflammatory change in 7 days and significant pulmonary fibrosis in 28 days(P＜0.05).Meanwhile,apoptosis index,hydroxyproline content,caspase3,and phosphorylated Smad3 were obviously higher in model mice than in control group (P ＜ 0.05).Compared with model group,TGF-β1/smad3 inhibitor group showed that alveolitis and pulmonary fibrosis degree,hydroxyproline content,cell apoptosis index,the expressions of p-smad3 and caspase3 were decreased at same time point (P ＜ 0.05).Conclusions TGF beta1/smad3 signaling pathways may participate the abnormal apoptosis during the development of pulmonary fibrosis,and TGF-β1/smad3 inhibitor SB431542 could inhibit this process.

Objective To observe the activation of anti-viral innate immune response of type Ⅰinterferon and inhibition of hepatitis B virus (HBV)genome replication in mice by HBV-3p-siRNA. Methods HBV-3p-siRNA was designed by targeting specific sequence of HBV S/P mRNA and was generated by in vitro transcription.Negative control siRNA (NC-siRNA)and non-modified HBV-siRNA were used as control groups.Blood samples were collected from tail vein of mice and the model of HBV-infected mice were established by hydrodynamic injection.Forty mice were divided into 4 groups with 10 in each group.The model group was only injected with pGL3.0-HBV1 .2 copy plasmid.The negative control group received peritoneal injection of NC-siRNA.HBV-siRNA group received peritoneal injection of HBV-siRNA and HBV-3p-siRNA group received peritoneal injection of HBV-3p-siRNA.The interferon-β(IFN-β)and hepatitis B surface antigen (HBsAg)in serum were detected by enzyme linked immunosorbent assay (ELISA).The copies of HBV DNA were assessed by fluore scence quantitative polymerase chain reaction (PCR ).The statistical difference between groups was determined using One way-ANOVA analysis by LSD or Dunnett T3.Results Serum level of IFN-β was (12.37±5 .32)pg/mL in model group,(22.61 ±6.29 )pg/mL in negative control group,(26.40±5 .39)pg/mL in HBV-siRNA group and (68.37± 21 .00 ) pg/mL in HBV-3p-siRNA group.The secretions of IFN-β into serum were significantly enhanced by HBV-siRNA and HBV-3p-siRNA compared with model group (F =23.988 and 46.523,respectively,both P <0.01).Serum level of HBsAg was (2 864.86±907.11 )ng/mL in model group,(2 198.86±456.89 )ng/mL in negative control group,(1 049.71 ± 396.28 )ng/mL in HBV-siRNA group and (640.86±383.08)ng/mL in HBV-3p-siRNA group.The expressions of HBsAg were inhibited by HBV-3p-siRNA and HBV-siRNA compared with model group (F = 23.537 and 39.144, respectively;P =0.025 and 0.010,respectively).Serum level of HBV DNA was (2.54 ×104 ±1 .46 × 104 )copy/mL in model group,(2.22×104 ±2.62×103 )copy/mL in negative control group,(3.59×103 ±2.88×103 )copy/mL in HBV-siRNA group and (2.65 ×103 ±1 .46×103 )copy/mL in HBV-3p-siRNA group.Serum level of HBV DNA were inhibited by HBV-3p-siRNA and HBV-siRNA compared with model group (F =15 .013 and 16.741 ,respectively,both P <0.05 ).All of the indicated siRNA used in the experiments showed no apparent effects on the body mass index of the mice models.Conclusion HBV-3p-siRNA,which induces the production of IFN-β and inhibits HBV replication through gene silencing in vivo ,may be a powerful bifunctional antiviral molecule.

Objective To report a three-generation Chinese family with freckle and to make a genetic linkage analysis in this family.MethodsGenetic linkage analysis was carried out in this family using microsatellite markers distributed over chromosome 4q and 1.Two-point logarithm of odds(LOD)scores were calculated using the Linkage program package(version 5.1),and haplotype was analyzed with Cyrillic version 2.01 software.Results Freckle was inherited in an autosomal dominant pattern with a penetrance of99.9% in this family;linkage to chromosome 4q was ruled out however,supportive evidence was obtained for linkage to microsatellite markers D1S2635 and D1S2844 in chromosome 1q with a maximum LOD score of 1.50.Haplotype analysis in this family localized the locus of freckle to a 12 Mb region flanked by D1S2624 and D1S2799.Conclusions Freckle is a genetically heterogeneous disorder.The causative gene may be located in a 21.2 cM region on chromosome 1q22-24.