Objective To discuss the effects of curcuma on different phases of the Hela cell proliferation in order to find the effective medicine in cervix cancer treatment.Methods MTT colorimetry and flow cytometry were used to measure the inhibitory rate of Hela cell proliferation and the changes of cell cycle, and transmission electron microscope(TEM) was used to observe the changes of the Hela subcells treated with the different concentrations of curcuma(0,10,20 and(40 mg?L~(-1))).Results Curcuma(0,10,20 and 40 mg?L~(-1))had obvious inhibitory effects on the Hela cell proliferation in a dose-dependant manner,the inhibitory rates were 3.0%,21.4%,32.8% and 49.2%,respectively.Furthermore,flow cytometry showed that the number of cells in G_1 phase increased and the number of cells in S phase decreased,the number of cells in G_2/M phases relatively increased.The changes of subcell structure could be seen,such as cavernous cells,cytoplasm agglutination,increasing apoptosis.(Conclusion Curcuma) can inhabit the Hela cell proliferation, prevent the cells in G_1 phase from entering into(S phase),and promote Hela cell apoptosis.

Objective:To observe the role of Zhike Qingfei Oral Liquid in treatment of the airway inflammation of chronic obstructive pulmonary diseases(COPD).Methods:50 cases with COPD at stable stage were divided into a treatment group and a control group,25 cases in each.Patients in both groups were treated with conventional therapy,including oxygen therapy,cardiactonic diuresis and relieving cough and asthma,etc.Zhike Qingfei Oral Liquid was added to the patients,of the treatment group,20ml each time,3 times each day,for 6 weeks.Clinical scores,pulmonary function,cell count and classification,interleukin-8(IL-8)and tumor necrosis Factor-?(TNF-?)in the sputum before and after treatment were investigated.Results:In the treatment group.the clinical score,FEV_1 and FEV_1/FVC(%)improved significantly(P

BACKGROUND: Homocysteine(HCY) is emerging as an independent risk factor for atherosclerosis. Its damage to the structure and function of endothelial cell(EC) is seemingly an important mechanism that leads to atherosclerosis.OBJECTIVE: To investigate the effect of HCY on fibrinolysis in elderly patients with coronary heart disease(CHD).DESIGN: A case-controlled study based on CHD patients and normal people as control group.SETTING: Department of general internal medicine and department of cardiology in a university hospital.PARTICIPANTS: The study was completed in the Department of Gerontology Internal Medicine and Department of Cardiology, Beijing Chaoyang Hospital, Capital University of Medical Science. Altogether 177 inpatients and outpatients from this hospital during December 2001 to August 2003 were selected and divided into three groups according to the results of coronary angiography(CAG): CHD group( n = 91 ) with 50 males and 41 females with the mean age of(66 ± 6) years, negative CAG group( n = 86) with 43 males and 43 females with the mean age of(60 ± 6) years, and normal control group( n = 85) with 43 healthy males and 42 healthy females with the mean age of(55± 5) years.METHODS: Peripheral blood samples were collected. ELISA double antibody method was applied to test tissue-type plasminogen activator(t-PA), plasminogen activator inhibitor-1 (PAI-1) and yon Willebrand factor(vWF). HCY was assayed with EIA method and the ratio of PAI-1 to t-PA was calculated.MAIN OUTCOME MEASURES: HCY level, t-PA, PAI-1 and vWF activities, and the ratio of PAI-1 to t-PA.RESULTS: The levels of HCY, PAI-1, PAI-1/t-PA and vWF in CHD group were significantly higher than those in negative CAG group and normal control group( P ＜ 0.01 ); however, the level of t-PA was significantly lower than that in control group( P ＜ 0. 01) . HCY was positively correlated with PAI-1,PAI-1 / t-PA and vWF, while it was negatively correlated with t-PA.CONCLUSION: The increase of serum HCY is accompanied with fibrinolytic dysfunction. HCY is positively correlated with PAI-1 and vWF but negatively correlated with t-PA. Therefore, HCY is a predictor for early coronary lesions,and can provide related laboratory data for the primary prevention and early treatment of CHD.

Objective: To establish the method of dissolution determination for evaluating and improving the quality of Xindakang sugar coated Tablets. Xindakang Sugar coated Tablets from three enterprises were investigated. Methods: To adopt 900mL0.5% Tween80 H 2O as dissolvent and rotating basket method at 100r?min -1 , the cumulative dissolution percentage was determined by UV. The dissolution parameters was obtained by Weibull distribution model and dealed with one way ANOVA. Results: The significant differences in dissolution parameters(T d, T 50 ,m)( P

AIM:To investigate the proliferation property of stable chemerin gene knockdown vascular smooth muscle cells ( VSMCs) and to explore its mechanism .METHODS:The normal VSMCs , chemerin gene interfering control VSMCs and stable chemerin gene knockdown VSMCs were divided into normal group , PDGF group, control group and knockdown group .The VSMCs in PDGF group were given platelet-derived growth factor-BB ( PDGF-BB) to initiate proli-feration.The cell counting and BrdU assay were employed to investigate the proliferation property of VSMCs .The mitogen-activated protein kinase ( MAPK) signal pathway was determined by Western blot .RESULTS:The cell number and BrdU A value in PDGF-BB-treated VSMCs significantly increased as compared with the normal VSMCs ( P<0.05 ) .Compared with the normal VSMCs , the chemerin knockdown VSMCs showed obviously decreased cell number and BrdU A value ( P<0.05).Simultaneously, no significant difference in the proliferation of VSMCs between the normal VSMCs and the control VSMCs was observed.No significant difference of the protein levels of p-ERK1/2, ERK1/2, p-p38 MAPK and p38 MAPK among 4 kinds of VSMCs was found .The protein level of p-JNK in PDGF-BB-treated VSMCs was up-regulated, while it was down-regulated in chemerin knockdown VSMCs compared with the normal VSMCs .CONCLUSION: Chemerin pro-motes the proliferation of mouse vascular smooth muscle cells by up-regulating p-JNK production .

ObjectiveTo investigate the cell toxicity of a novel macropores calcium phosphate cement (CPC) scaffold and its influence on cell adhesion,growth and proliferation.MethodsA novel CPC material was synthesized by means of adding mannitol porogens and applying sodium solution as the cement liquid.The cell growth and proliferation in the novel CPC material extraction was observed by CCK8 assay.Scanning electron microscopy was used to observe hole diameter of the material,cell adhesion and growth in the material.The experiment of three point bending was used to test the biomechanic performance of the CPC material.ResultsThe novel CPC material reached hole diameter value of (267.43±118.01)μm,microporosity of (66.15±6.91)％.Maximum load,flexural strength and toughness of the novel CPC material was increased about one time compared to the traditional CPC(P＜0.05).CCK8 assay showed there were no significant difference of the light absorption value of cells in the CPC extraction in the 4th,6th,8th day compare to the control group (P＞0.05).ConclusionThe novel CPC material has the strong biomechanics performance,macropores,high microporosity and excellent biocompatibility,which is promising for ideal bone tissue engineering scaffold.

Objective To explore the influence of lamotrigine(LTG)and valproate(VAP)on cognitive function in children with epilepsy.Methods Seventy-six epileptic children firstly diagnosed were chosen,36 cases received LTG monotherapy and 40 cases undwent the treatment of VPA.The intelligence quotient(IQ)value was measured before and after 6 months treatment respectively,and 20 healthy children were selected as healthy control.Results 1.The epileptic children had poor verbal intelligence quotient(VIQ),performance intelligence quotient(PIQ)and full intelligence quotient(FIQ)compared to the control subjects(Pa0.05).But among the subtestings,the know-ledge,wood-graph,coded score of the VPA groups had significant difference(Pa

ObjectiveTo construct one recombinant adenovirus AdE7E6 expressing HPV16 E6 and E7 fusion protein as candidate for HPV16 therapeutic vaccine.MethodsThe codon-optimized E6 and E7 gene,were fused to create one open reading frame,then inserted into adenovirus vector pCD316.A strain of recombinant adenovirus was constructed through homologous recombinant in 293 cells,and identified by PCR and Western blot.Finally,it was employed to study it's immunogenicity and the activity of the tumor growth regression.ResultsThe PCR result showed that E6E7 fusion gene had been integrated in recombinant Ad5 DNA.Western blot test confirmed that the E6E7 fusion protein was highly expressed in 293 cells infected with Ad5E7E6 recombinant adenovirus.The recombinant adenovirus elicited significant E7 specific CD8+ T lymphocyte response in vaccinated mice.These responses could completely prevent the TG-1 tumor cell bearing mice treated with AdE7E6 from developing into tumor.ConclusionThese results suggested that rAd5E7E6 could be a potent vaccine candidate for the treatment of HPV16-associated tumors and their precancerous transformations.

Objective To investigate the role of polymorphisms of scavenger receptor class B gene CD36 in affecting the progress of subclinical atherosclerosis (AS) and the associated factors affecting the expression of CD36 on the surface of peripheral blood monouclear cells (PBMC) and the association between CD36 expression and progress of subclinical AS in type 2 diabetic patients.Methods CD36 polymorphisms (CD36-rs1984112, CD36-T620C) were typed by PCR-RFLP in 470 cases of type 2 diabetes mellitus and 220 non-diabetic controls of Hans in Hunan area.The genotypes and allele frequencies were compared between cases and controls.Fluorescence intensity of CD36 on the surface of PBMC was analyzed in 102 cases of type 2 diabetes mellitus by flow cytometry and was compared between the patients without AS and the patients with subclinical AS.Multiple linear regression was applied to evaluate the relevant factors contributing to CD36 expression.Results The genotypes and allele frequencies of CD36-rs1984112 in type 2 diabetes mellitus were not significantly different between cases and controls (P＞0.05), either did CD36-T620C (P＞0.05).The mean florescence intensity (MFI) of CD36 in type 2 diabetics with subclinical AS was higher than that without AS (1 382±659 vs 1 173±340, P＜0.05).Factors affecting the CD36 expression were: age (P=0.005), gender (P=0.021), systolic blood pressure (SBP) (P=0.027), standardized coefficients Beta was 0.28, 0.31 and -0.21, respectively.Age contributed to the CD36 expression level in males (P=0.002) and diastolic blood pressure in females (P=0.001) respectively.Conclusion CD36-rs1984112 and T620C seem not to be a functional polymorphism sites in Hans of Hunan, southern China.CD36 expression level is higher in type 2 diabetics with subclinical AS in contrast with those without AS.CD36 expression on PBMC surface is higher in aged males with lower SBP.

OBJECTIVEIn this study, we aimed to investigate the expressions of adhesion molecules on human bronchial epithelial cells and neutrophils in co-culture system, assess the effects of puerarin on suppressing these adhesion molecules expressions, and explore the roles of two crucial signal-transduction elements p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor kappa B (NF-κB) in modulating adhesion molecules expressions.

METHODSNeutrophils and BEAS-2B cells (one human bronchial epithelial cell line) were co-cultured, and adhesion molecules expressions on cell surface were detected using flow cytometry. The mRNA levels of adhesion molecules were assessed by real-time quantitative polymerase chain reaction (real-time qPCR). Phosphorylated p38 MAPK and inhibitor κB were analyzed by Western blot.

RESULTSIn co-culture system, adhesion molecules expressions on BEAS-2B cells and neutrophils were enhanced significantly (P<0.05). Correspondingly, the mRNA levels of adhesion molecules were also increased greatly. Moreover, the pretreatment of peurarin obviously suppressed adhesion molecules expressions on cell surface. Furthermore, phosphorylated p38 MAPK and inhibitor κB in BEAS-2B cells and neutrophils were elevated in co-culture system, but decreased significantly after upon the treatment of peurarin (P<0.05).

CONCLUSIONSCoculture boosted the interactions between human bronchial epithelial cells and neutrophils mimicking airway inflflammation, whereas peurarin decreased the expression of adhesion molecules on cell surface by suppressing the activities of p38 MAPK and NF-κB pathways, and exhibiting its anti-inflflammation activity.

Animals ; Base Sequence ; Bronchi ; cytology ; enzymology ; metabolism ; Cattle ; Cell Adhesion Molecules ; metabolism ; Cell Line ; Coculture Techniques ; DNA Primers ; Down-Regulation ; drug effects ; Epithelial Cells ; enzymology ; metabolism ; Isoflavones ; pharmacology ; NF-kappa B ; metabolism ; Neutrophils ; enzymology ; metabolism ; Phosphorylation ; Real-Time Polymerase Chain Reaction ; p38 Mitogen-Activated Protein Kinases ; metabolism