AIM To explore the inhibitory effects of simv astatin on ROS generation and cardiac myocytes hypertrophy induced by ET-1. METHODS The study was performed with primary cultured neonatal rat cardiac myocytes. Intrace llular fluorescence signal was assayed by fluorescence convert microscope. The l evel of intracellular ROS was measured by the ROS-specific probe 2′, 7′-dich lorofluorescin diacetate (DCF-DA). The RNA content was determined by RNA-sensitive fluoresce nce probe propidium iodide (PI) and the total protein of cell was measured by th e methods of coomassie brilliant blue. The cell surface area was measured by ima ge analysis program. RESULTS ①Fluorescence intensity of intracel lular DCF-DA and myocyte hypertrophy increased by ET-1 in dose-dependent mann er. Antioxidant catalase(0 2 U?L -1 ) attenuated the ET-1-induced incre ase of fluorescence intensity of intracellular DCF-DA and myocyte hypertrophy.②Simvastatin inhibited the increase of fluorescence intensity of intracellular DCF-DA and cardiac myocyte hypertrophy induced by ET-1(10 -8 mol?L -1 )in a dose-dependent manner. CONCLUSION ET-1 increases int racellular ROS in the cultured neonatal rat cardiac myocytes. Simvastatin inhibi ted the generation of ET-1-induced ROS and cardiomyocytes hypertrophy.

Aim To investigate the role of physiological concentration of glucocorticoids on the inflammation mediator IL-6 expression in response to LPS in rat alveolar epithelial cells(CCL149).Methods The CCL149 were treated with LPS,H2O2 and glucocorticoid respectively.Flammtory mediator IL-6 protein expression was measured with ELISA,and the activity of histone deacetylase(HDAC) was measured using colorimetric HDAC activity assay kit.Results IL-6 protein levels were increased in cells exposed to 10 mg?L-1 LPS.Hydrocortisone decreased IL-6 protein expression induced by LPS.Such effect of hydrocortisone was blunt by HDAC inhibitor trichostatinA treatment(10 ?g?L-1).LPS decreased HDAC activity.Hydrocortisone increased HDAC activity.The expression of IL-6 protein induced by LPS was further enhanced by H2O2 treatment.Pretreatment with H2O2 resulted in the inhibition of antiflammtion effect of glucocorticoids.Conclusion Physiological concentration of glucocorticoids could suppress inflammatory response,and this effects requires recruitment of HDAC.Oxidants such as H2O2 may cause the failure of glucocorticoids to function effectively,and the reason may be related to the reduction of HDAC activity.This mechanism may contribute to the pathogenesis of pulmonary disorder.

Objective:To summarize and analyze the disease characteristics of the patients in Chinese Level-II Hospital for UN Peacekeepers in Liberia,for offering some references to the pre-mission training of the successive contingents as well as the improvement of medical support to the peacekeeping mission.Methods:A statistical analysis was made of the case history of all the outpatients and inpatients received in Chinese Level-Ⅱ Hospital for UN Peacekeepers in Liberia from May 2004 to December 2005. Results:Out of the total of 7107 outpatients,2539(35.7%) were medical cases,1205(17.0%) surgical,1136(16.0%) dental,787(11.1%) dermatological and 763(10.7%) contagious cases.Malaria was the main type of contagious disease,which accounted for 86.1% of all the contagious cases.There were 39 cases of AIDS/HIV(acquired immunodeficiency syndrome / human immunodeficiency virus).Of the 453 inpatients,233(51.4%) were contagious and 166(36.7%) medical cases,and 185(40.8%) of the total number suffered from malaria.The average hospital stay was 5.2 days.Conclusion:Adequate drugs and equipments should be prepared for both common and special diseases in the peacekeeping mission area.During the pre-mission training at home,special emphasis should be laid on the prevention and treatment of common diseases and frequently occurring diseases,particularly on the diagnosis of and protection against AIDS.

Aim To study the effect of activating Sonic hedgehog( Shh) pathway on the function of endothelial progenitor cells ( EPCs ) in type 1 diabetic mice. Methods EPCs were isolated and cultured by density gradient method from diabetic mice. The effects of Shh N-terminal peptide and agonist SAG on EPCs prolifera-tion were evaluated by using the MTT colorimetric as-say. EPCs migration was measured by Transwell meth-od. EPCs tube formation ability was estimated by Matrigel . EPCs senescence activity was determined by β-galactosidase staining. Results Compared with control mice, the function of EPCs in type 1 diabetic mice was impaired. The proliferation, migration and tube formation of diabetic EPCs could be promoted by Shh peptide and agonist SAG. The senescence of dia-betic EPCs could be decreased by Shh peptide and ag-onist SAG. Conclusion Activating Shh signaling pathway can improve the impared function of diabetic EPCs in type 1 diabetic mice.

AIM:ToinvestigatetheprotectiveeffectofquercetinonangiotensinⅡ(AngⅡ)-inducedcardio-myocyte hypertrophy and its possible mechanism .METHODS: Cardiomyocyte hypertrophy was induced by AngⅡ ( 100 nmol/L) in primary neonatal cardiomyocytes and H 9c2 cells.The cells were treated with different concentration of querce-tin (10 μmol/L, 20 μmol/L and 40 μmol/L) for 48 h and then the cardiomyocyte surface areas were measured by immu-nofluorescence .Proteasome activity was detected by fluorescent peptide substrate .The phosphorylated levels of GSK-3α/βand Akt in H9c2 cells were determined by Western blot .RESULTS:Compared with control group , the cardiomyocyte sur-face areas were both increased in primary cultured neonatal cardiomyocytes and H 9c2 cells, while the surface areas were significantly decreased by quercetin , especially at concentration of 20 μmol/L compared with Ang Ⅱgroup (P<0.05). Compared with control group , the chymotrypsin-like, trypsin-like and caspase-like activities of proteasome were all in-creased in H9c2 cells (P<0.05).The trypsin-like and caspase-like activities of proteasome were inhibited by 20 μmol/L and 40 μmol/L quercetin , while chymotrypsin-like activity was inhibited only at 20 μmol/L of quercetin compared with AngⅡgroup (P<0.05).In addition, phosphorylated levels of GSK-3α-Ser21, GSK-3β-Ser9 and Akt-Ser473 in AngⅡgroup were all increased compared with control group , which were obviously inhibited by in 20 μmol/L and 40 μmol/L quercetin ( P<0.05 ) .CONCLUSION: Quercetin decreases cardiomyocyte hypertrophy through proteasome inhibition , which may be related to the inhibition of Akt and therefore increasing activation of GSK -3α/βin H9c2 cells.

Objective To study the value of three dimensional dynamic contrast and digital subtraction MRI in diagnosing breast cancer.Methods 52 patients with breast diseases were enrolled in this study,including 27 malignant lesions and 36 benign lesions verified by histopathology.the morphologic features and enhancement kinetics of breast lesion on MRI were observed.The morphologic manifestation,early-phase enhancement rate,peak enhancement rate,peak time and time-signal intensity curve were evaluated.Results The benign lesions were mainly characterized by regular mass,well-defined border,internal septation,homogeneous enhancement,and the malignant lesions by irregular shape,speculated margin,rim enhancement,inhomogeneous enhancement.The early-phase enhancement rate,peak time and curve type were significantly different between breast benign and malignant lesions(P

AIM To examine whether pretreatment with simvastatin protects the heart against free radical injury. METHODS 1 1 diphenyl 2 picryl hydrazyl (DPPH) was used for triggering free radical injury in cardiac tissue. Simvastatin against free radical injury was investigated in a Langendorff fused rat heart. Left ventricular developed pressure (LVDP), maximal velocity of increase of LVP (+d p /d t max ), heart rate (HR) coronary flow (CF) and malondialdehyde (MDA) formation in cardiac tissue were measured. RESULT In the DPPH free radical group, DPPH signficantly decreased LVDP, +d p /d t max , HR was slowed and CF was reduced. The formation of MDA was significantly enhanced. ( P

OBJECTIVE: Discussion of expression and its significance of CD44 in SP cells of nasopnaryngeal carcinoma. METHOD: Flow cytometry was used to sort cultured CNE-2 cells of nasopharyngeal carcinoma for obtaining CD44-SP and CD44+SP cells. Biological differences of CNE-2, CNE-2 SP, CNE-2 NSP, CNE-2 CD44+SP and CNE-2 CD44-SP cells were statistically analyzed by experiments such as cell migration experiments, plate clone formation assay, cell cycle analysis and sensitivity tests to chemotherapeutics. RESULT: Two point 3 perent of SP cells were extracted from CNE-2 cells of nasopharyngeal carcinoma, among which 36.5% was CD44+SP cells. Abilities of proliferation, cell migration and plate clone of CD44+SP cells were significantly higher than other cells (P < 0.01), and its tolerance to chemotherapeutics was significantly higher too (P < 0.01). CONCLUSION The proportion of SP cells in nasopharyngeal carcinoma cells was small, but SP cells had strong activeness in the aspect of cell proliferation with a "seed" characteristic of tumor cells. As CD44+SP cells played an important role in proliferation and chemotherapy resistance of nasopharyngeal carcinoma, it indicated that CD44 can be one of the surface markers of SP cells of nasopharyngeal carcinoma.
Biomarkers, Tumor ; metabolism ; Carcinoma ; Cell Cycle ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Flow Cytometry ; Humans ; Hyaluronan Receptors ; metabolism ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms ; metabolism

Objective To investigate the expression of nucleotide-binding oligomerization domain protein 2 (NOD2)in serum of patients with hepatocellular carcinoma (HCC),and to analyse the roles of NOD2 in HCC development and its clinical diagnostic value.Methods This study including 66 patients with HCC in the hospi-tal from March 1,2013 to December 31,2014 and 61 healthy controls.Serum NOD2 levels were determined by enzyme-linked immunosorbent assay (ELISA).Analysis of significance was performed with rank sum test using SPSS statistical 16.0 software.Results Serum levels of NOD2 in HCC patients were 171 pg/ml,significantly higher than that of healthy controls(95 pg/ml,Z =-5.00,P =0.00),and the serum NOD2 levels were correla-ted with clinical stage of HCC (H=56.26,P =0.00).Compared with the serum NOD2 levels in stageⅠ,Ⅱpatients (106 pg/ml)and healthy controls (95 pg/ml),the serum NOD2 level in stage Ⅲ and Ⅳ (220 pg/ml) were significantly increased (χ2 =31.24,P =0.00;χ2 =47.23,P =0.00),but the expression of NOD2 in stageⅠandⅡwere nearly equal to that of the healthy controls (χ2 =0.36,P =0.83).The ROC analysis revealed that the best diagnostic cutoff-point of serum NOD2 levels for predicting the Ⅲ and Ⅳ stages of HCC was 148.78 pg/ml,meanwhile corresponding sensitivity was 89.1% and specificity was 77.0%.Additionally,corre-lation analysis demonstrated that there was no significant correlation between NOD2 and alpha-fetal protein (r =0.44,P =0.14).Survival curves obtained that the survival time of HCC patients with NOD2 serum concentrations≥ 200 pg/ml was significantly less than that <200 pg/ml (χ2 =15.32,P <0.05).Conclusion NOD2 is highly expressed in the serum of HCC patients,especially in advanced patients,which is possibly involved in the development of HCC and has the potential to become an effective marker used for HCC diagnosis.