Objective To study the effect of 17?-estradial(E-2) on apoptosis of cardiomyocytes induced by norepinephrine(NE) in vitro and its mechanism. Methods The cultured neonatal rat cardiomyocytes were treated with NE(50??mol/L),E-2(10?nmol/L) or NE(50??mol/L)+E-2(10?nmol/L) respectively in serum-free DMEM for 48?h.The morphological changes of myocytes were studied by phase-microscopy and transmission electron microscopy;apoptosis was identified by DNA laddering and apoptotic rate was assayed by flow cytometer;cfos protein in cardiomyocytes was detected using semiquantitative immunofluorescence cytochemistry technique. Results 17?-estradiol inhibited the morphological changes of apoptotic cardiomyocytes induced by norepinephine such as cell atrophy,condensed chromatin clumps against the nuclear envelope associated with swelling of mitochondria and presentation of apoptotic body,DNA laddering disappeared,the apoptotic rate decreased and the expression of c-fos protein inhibited in cardiomyocytes.Conclusion 17?-estradiol can protect cultured cardiomyocytes from apoptosis induced by norepinephrine,its mechanism might associate with suppression of c-fos protein expression.

Objective:This study aimed to investigate the relationship between estrogen receptor (ER) and Bcl-2 in cervical can-cer and precancerous lesions. Methods:ER and Bcl-2 were evaluated by immunohistochemistry in 20 non-tumor tissues, 30 low-grade cervical intraepithelial neoplasias, 70 high-grade cervical intraepithelial neoplasias, and 80 cervical cancers. Results:The positive rate of ER was 75%in non-tumor tissues;this rate decreased with disease severity (χ2=24.266, P<0.01). The overexpression of ER protein was remarkably lower in cervical intraepithelial neoplasias (CIN) Ⅱ-Ⅲ and carcinomas than in non-tumorous cervices. Differences were not significant between CINⅠand non-tumorous cervices (χ2=0.751, P=0.386). Furthermore, ER expression was not correlated with histological type and tumor grade. The positive rate of Bcl-2 was 75.38%in squamous cell carcinoma. This rate increased with dis-ease severity (χ2=27.715, P<0.01). The Bcl-2 protein overexpression was remarkably higher in CINⅠ, CINⅡ-Ⅲ, and carcinomas than in non-tumorous cervices. Bcl-2 expression was also not correlated with histological type (P=0.500);by comparison, Bcl-2 expression was correlated with tumor pathological grade (χ2=4.862, P=0.027). The co-expression of ER and Bcl-2 was 38.57%and 15.38%in CINⅡ-Ⅲand squamous cell carcinoma, respectively;the differences between these two values were significant (χ2=9.108, P=0.003). A cor-relation between ER and Bcl-2 was observed in CINⅡ-Ⅲ(r=0.506, P<0.01);no correlation was observed between other groups. Con-clusion: ER expression was inversely correlated with Bcl-2 in cervical cancer progression. The co-expression of these markers may have an important function in the course of high-grade cervical intraepithelial neoplasia.

Objective To investigate the characteristics of frequently cited papers in Chinese Journal of Nuclear Medicine and Molecular Imaging (CJNMMI) during year 1998-2013.Methods Based on Wan Fang database,the citation number of each paper published in CJNMMI during year 1998-2013 was recorded.Percentage method was used to determine the number of frequently cited paper.The published year,regional distribution,number of authors,columns,key words and funding of the frequently cited paper were analyzed.Results There was 5.43％ (140/2 580) of the papers published in CJNMMI from year 1998-2013 were considered frequently cited.These 140 frequently cited papers accounted for 37.49％ (2 533/6 757) of the total number of citations,with an average citation number of 18.09.A total of 77.86％ (109/140) of these frequently cited papers were published during year 2000-2005,and 65.00％ (91/140)of them had 3-6 authors.Seven authors published 3 or more of these frequently cited papers.Most papers were from Beijing,Guangdong and Shanghai.The top 3 columns with frequently cited papers were nuclear oncology,endocrinology and neurology (16.43％,10.00％,9.29％).Conclusion Analysis of the frequently cited papers in CJNMMI with regard to characteristics,such as published year,research field and district distribution,may provide useful reference for topic selection in the future.

Aim To develop a modified model of subarachnoid hemorrhage in rats. Motheds The SAH model was induced by injecting autologous blood into the cisterna magna without exposing the occipitoaxial ligament.The main modified point was a hole bored by a dental drill at the middle point of the boundary between the parietal bone and the occipital bone,then a catheter was inserted 8 mm to cisterna magna and the autologous blood was injected . Hemorrheological parameters were measured after the model was created.The intrinsic oversxidase method was used to show the microvessel of CA_1 region. The diameter, density ,and the aera of microvessel were measured and ananlyzed by Image-Pro Plus image analysis system. Results The total blood viscosity(?b) and erythroagglutation index(AL) in SAH model group increased significantly,however,the microvesse area and microvesse density in SAH model group decreased obviously. Conclusion The modified model of subarachnoid hemorrhage in rats is reliable and easy to operate on.

Objective:To observe influence of simvastatin on p 27 protein (cyclin‐dependent kinase inhibitor ) expres‐sions of vascular smooth muscle cells (SMC) and endothelial cells (EC) in rats for screening new generation coating drugs of eluting stents .Methods :Primary aortic SMC and EC of rat were isolated and cultured by methods of adher‐ent and enzymatic digestion respectively .Which were inoculated on fibronectin -coated culture plates .α smooth muscle actin immunofluorescence staining was used to identify SMC ,and von Willebrand factor (vWF) immunofluo‐rescence staining was used to identify EC .SMC and EC were cultured for 24h with different concentrations of simv‐astatin (0.01 ,0.1 ,1 and 10 μmol/L) ,then Western blot was used to measure p27 protein expression .Results:Compared with blank control group ,0.01μmol/L simvastatin had no significant influence on p 27 protein expression of SMC ,but 0.1 ,1 and 10 μmol/L simvastatin significantly raised p27 protein expression of SMC [ (0.53 ± 0.08) vs .(0.86 ± 0.05) ,(1.20 ± 0.05) ,(1.60 ± 0.04)] , P< 0.01 all .Besides ,different concentrations of simvastatin had no significant influence on p27 protein expression of EC , P> 0.05 ,indicating that simvastatin only dose‐de‐pendently promoted p27 protein expression of SMC .Conclusion:Simvastatin dose -dependently promotes p27 pro‐tein expression of vascular smooth muscle cells without affecting p 27 protein expression of endothelial cells .So local application of simvastatin may inhibit restenosis and promote reendothelialization of injured vessels .

Aim To investigate the effects of Astragalus Mongholicus Bunge Lectin (AMML) on tumor cells proliferation,cell cycle and apoptosis by using human leukemia cell line (K562 cells).Methods The antiproliferation effect of AMML on K562 cells was detected by the colorimetric MTT assay.The apoptosis induced by AMML on K562 cells was explored by means of cell morphological and flow cytometry.Results AMML showed strong inhibiton of the growth of K562 cells in a time-and concentration-dependence. After incubation of K562 cells with AMML at a concentration of 60 mg?L-1 for 72 h,the inhibition ratio was 89%.Morphological observation showed that AMML-treated K562 cells displayed outstanding apoptosis characteristics,such as nuclear fragmentation,chromatin condensation. AMML induced significant cell cycle arrest at S phase in K562 cells,and the apoptosis of K562 cells was confirmed by flow cytometry.Conclusion AMML can inhibit the growth of K562 cells through S arrest and induce the apoptosis of K562 cells. Thus,AMML may be valuable for the treatment of cancer.

Objective To investigate the serum of soluble CD40 ligand(sCD40L) in coronary heart disease and its relationship with serum lipid levels and the extent of coronary stenosis,whether upregulation of CD40L system is related to stability of atherosclerotic plaque in patients with acute coronary syndrome.Methods Enzyme-linked immunosorbent assay(ELISA) was used to measure the level of sCD40L in 64 patients with coronary heart disease(18 with acute myocardial infarction,19 with unstable angina pectoris and the other 27 with stable angina pectoris) and 20 matched healthy controls.Coronary stenosis of 29 patients were assessed by angiographic coronary stenosis morphology.Results sCD40L level was significantly higher in patients with acute coronary syndrome(ACS)((19.8?3.0)、(19.6?4.3)ng/mL in acute myocardial infarction and unstable angina pectoris group,respectively)than that of those with stable coronary heart disease and that of controls((8.3?3.2)ng/mL and(2.6?1.9)ng/mL,respectively P

Objective:To observe influence of simvastatin on differentiation ,proliferation ,migration and adhesion of marrow-derived smooth muscle progenitor cells (SPCs) and screen coated eluting stent drugs of new generation . Methods :The mononuclear cells (MNCs) were isolated from rat marrow by density gradient centrifugation method , and then plated on fibronectin-coated culture dishes ,after culture 8d ,marrow-derived SPCs were identified by α-smooth muscle actin (α-SMA) immunofluorescent staining and counted under inverted fluorescence microscope .The MNCs and adhesion cells were treated with simvastatin (0.01~10 μmol/L) respectively for 8 d and 24h .SPCs pro-liferation ,migration and adhesion were observed by Tritium thymidine (3 H-TdR) intake method ,modified Boyden chamber assay and adhesion assay .Results:Compared with control group (no simvastatin intervention ) ,0.01μmol/L simvastatin significantly inhibited the MNCs differentiation towards SPCs [ (85 ± 4) vs .(79 ± 5)] ,proliferation [ (4070 ± 184) vs .(3833 ± 126)] ,migration [ (44 ± 3) vs .(39 ± 3)] and adhesion of SPCs [ (59 ± 5) vs .(52 ± 4)] , P<0.05 all ,and number of SPCs significantly reduced along with simvastatin concentration increased (P<0.01) . Conclusion:Simvastatin could inhibit the differentiation ,proliferation ,migration and adhesion of marrow-derived smooth muscle progenitor cells .

AIM:To explore the effect of peptidyl-prolyl cis/trans isomerase (Pin1) inhibitor juglone on apop-tosis of human cervical cancer SiHa cells.METHODS:Cultured SiHa cells were incubated with juglone at concentrations of 10, 20, 50, 80 and 100 μmol/L for 24 h.The SiHa cell activity was detected by methyl thiazolyl tetrazolium ( MTT) assay.The cell apoptosis was analyzed by flow cytometry with Hoechst 33258 staining.The protein levels of cleaved caspase-3,8,9 and PTEN was determined by Western blotting.RESULTS:In different doses of juglone groups, the SiHa cell growth was greatly inhibited ( P<0.05) in a dose-dependent manner as compared with control group.The IC50 of ju-glone was 20.4 μmol/L.After treatment with juglone at concentration of 20 μmol/L for 12 h, the apoptosis of SiHa cells was induced, and the typical morphological changes of cell apoptosis such as karyopyknotic pyknic hyperfluorescence bolus, nuclear fragmentation and apoptotic body were observed by Hoechst 33258 staining.The early apoptotic rate was increased significantly as compared with the control.The protein levels of cleaved caspase-3, 8, 9 and PTEN were also increased sig-nificantly as compared with control group.CONCLUSION:Juglone significantly inhibits the cell activity and induces the apoptosis of SiHa cells in vitro by inhibiting the caspase pathway and increasing the expression of anti-oncogene.

Objective To investigate the effects of different concentrations of isoflurane on viability in rat primary cortical neurons. Methods Primary cortical neurons were isolated from neonatal Wistar rats (less than 24 h after birth) and exposed to 0.6 %, 1.2 % and 2.4 % isoflurane for 1, 2, 4, 8, 12 or 24 h, cell viability was evaluated by MTT reduction and LDH release assays. Changes in intracellular [Ca2+]i were detected by real-time confocal microscopy after the neurons were exposed to different concentrations of isoflurane. Results Exposure to 0.6% isoflurane for 24 h significantly increased viability of the primary rat cortical neurons as shown by decrease in LDH release and increase in MTT and elevation of peak [Ca2+]i. Exposure to 1.2% isoflurane for 12 or 24 h and to 2.4% isoflurane for 8, 12 or 24 h significantly reduced viability of cortical neurons associated with high and fast elevation of peak [Ca2 +] i. Conclusion Exposure to 0.6 % isoflurane increases viability of the primary rat cortical neurons. Exposure to 1.2% isoflurane and to 2.4% isoflurane decreases cell viability and the mechanism may be related to the changes in calcium concentrations in the neurons.