Objective To observe the hemodynamic changes on right ventricular hypertrophy induced by monocrotaline in rats . Methods Male SD rats were given monocrotaline 60 mg/kg by a single intraperitoneal injection ,the mRNA expression of RV/BW , RVHI and ANF were took as the indicators .Intraperitoneal injection with 10% chloral hydrate was performed ,the artery cannulae and right ventricular catheter were inserted ,and the right ventricle pressure was measured .Results The RVHI and RV/BW were significantly increased in M2W and M4W groups ,compared with vehicle control (P<0 .01) ,and the ANF mRNA expression was significantly increased in both groups .Bp and HR did not change in model groups .RVEDP markedly decreased (P< 0 .01) and RVP ,± dp/dtmax ,t dp/dtmax and Vpm increased (P<0 .001) in M2W groups ;and all parameters increased significantly in M4W groups (P<0 .01) .Conclusion Monocrotaline can induce RVH ,which accompany hemodynamic changes and the systolic and dias‐tolic dysfunction in right ventricle may eventually cause right heart failure .

Brain Ischemia ; etiology ; Child ; Humans ; Male ; Metabolic Syndrome ; complications ; Stroke ; etiology

DNA methylation is part of the epigenetic modification process,which can lead to aberrant gene expression. Cytochrome P450 enzyme,cyclooxygenase,lipoxygenase and monoamine oxidase are a class of enzymes produced by human tissues,which are involved in the oxidization pro?cess of endogenous and exogenous chemicals. The methylation patterns of these enzyme genes are dif?ferent between normal tissues and pathological ones. Abnormal methylation patterns will change en?zymes′expression and function,and affect the occurrence and development of diseases. This paper re?viewed the characteristic changes of four oxidative metabolic enzyme genes in certain diseased tis?sues,the impact on methylation status of the metabolic activity of chemicals and on human health. It is hoped that this review can provide a new theoretical basis for the study on the toxic mechanism of chemicals and for diagnosis of diseases.

Objective: To investigate the regulatory effect of C-Jun N-terminal kinase (JNK) signal transduction pathway on multi-resistance in the human hepatic cancer Bel-7402/5-fluorouracil (FU) cells, and provide a possible novel target for study on the mechanism of multidrug-resistance in human hepatic cancer cells. Methods: The protein expression levels of JNK and phospho-JNK (p-JNK) in parental human hepatic cancer Bel-7402 cells and the drug-resistant Bel-7402/FU cells were detected by Western blotting. After the inhibition of JNK pathway induced by specific inhibitior SP600125, the expressions of multi-drug resistance 1 (MDR1) mRNA and P-glycoprotein (P-gp) in Bel-7402/FU cells were detected by RT-PCR and immunocytochemistry, respectively. The accumulation and efflux of rhodanmine 123 (Rh123) in the cells were examined by flow cytometry, and the sensitivity to 5-FU of Bel-7402/FU cells was detected by MTT method. Results: The expression of JNK protein was not significantly different between the Bel-7402/FU cells and the parental Bel-7402 cells, but the expression of p-JNK protein in the Bel-7402/FU cells was significantly increased. After inhibition of JNK pathway, the expressions of MDR1 mRNA and P-gp protein were obviously decreased, with a markedly increased accumulation and decreased efflux of Rh123, leading to enhhanced sensitivity to 5-FU of Bel-7402/FU cells. Conclusion: JNK signal transduction pathway is involved in the expressions of MDR1 gene and P-gp in drug-resistant human hepatic cancer Bel-7402/FU cells, and it can regulate the sensitivity to 5-FU of Bel-7402/FU cells.

Objective To detect the proliferation and the expression levels of downstream target genes of Notch pathway of T-ALL CCRF-CEM(CEM)cell line treated with exogenous DLK1 protein,in order to investigatethe effects of DLK1 protein on the Notch pathway in CEM cells.Methods CCK-8 assay was performed to examine the proliferation of CCRF-CEM cells,which were treated with various concentration(0.5,1.0,1.5 μg/ml)DLK1 for various time(24,48,72 h).RFQ-PCR was applied to assess the mRNA expression level of Notch1 receptor and downstream target genes of Notch pathway in CEM cells,which were treated for various time(24,48,72 h).Results DLK1 protein stimulated the proliferation of CCRF-CEM cells,and the proliferation rates with different concentrations of DLK1 were 0.14±0.03,0.17±0.04,0.55±0.01 in 72 hours,respectively,there were statistic differences between that in the experimental group and that in the control group(P＜0.05).DLK1 protein up-regulated the Notch1 receptor and its downstream target genes HES1,c-myc and NF-κB.The relative transcript levels of target genes HES1 in 72 hours,c-myc in 48 hours and NF-κB in 72 hours were 3.2551±0.3100,1.6086±0.0941,2.0515±0.3453 respectively,and there were statistic differences between that in the experimental group and that in the control group(P＜0.05).Conclusion DLK1 protein stimulates the proliferation of T-ALL CCRF-CEM cells by up-regulating Notch1 receptor and downstream target genes HES1,c-myc and NF-κB of Notch pathway.

Objective To investigate the serum level of visfatin, C-reactive protein (CRP) and monocyte chemoattractant protein-1 (MCP-1) in patients with polycystic ovarian syndrome (PCOS), and provide the basis for understanding the pathogenesis of PCOS. Meth-ods 94 patients with PCOS and 100 healthy subjects were divided into 4 subgroups according to their body mass index(BMI), including obese PCOS subgroup(n = 52), non - obese PCOS subgroup (n = 42), obese healthy subject subgroup (n = 43) and non - obese healthy subject (n = 57). Serum visfatin, CRP, MCP-1, sex hormone levels and metabolic parameters were measured by enzyme-linked immu-nosorbent assay (ELISA), automatic chemistry analyzer or chemiluminescent immunoassay. Results Serum levels of testosterone (T), lu-teiizing hormone (LH) and prolactin (PRL) in the PCOS group were significantly higher than those in healthy subjects group(P <0.05～0.01), and follicle-stimulating hormone (FSH) levels were significantly decreased in PCOS group(P<0.01). Serum levels of Visfatin, CRP, MCP-1,fasting insulin(Fins) and insulin resistance homa model (HOMA-IR) in the obese or non - obese PCOS subgroup were signif-icantly increased than that in the obese or non - obese healthy subjects subgroup respectively (P<0.01). Pearson correlation analysis showed that the visfatin, CRP and MCP-1 levels were positively related to BMI, FINS and HOMA-IR(r=0.323～0.675, P<0.01). Par-tial correlation showed that serum visfatin levels were correlated with HOMA-IR(r=0.491, P<0.01), and serum MCP-1 levels were cor-related with LH (r=0.267, P<0.05) in the PCOS group. Conclusion The patients with PCOS had higher visfatin, CRP and MCP-1 lev-els, and visfatin levels were positively correlated with insulin resistance. Obesity were involved in the chronic inflammation course in patients with PCOS.

Objective To investigate the effect of rosiglitazone on the CD4+regulatory T cells in the patients with latent autoimmune diabetes in adults(LADA).Methods The CIM+T cells from IADA patients were isolated with anti-CD4-dynal magnetic beads.The expression of Foxp3 mRNA,along with peroxisome proliferators activator receptors gamma(PPARγ)mRNA and TGF-131 mRNA was determined.The effect of rosiglitazone on CD4+T cells was measured,after treated with rosiglitazone for 48 h.Cell viability was assessed by Mtit assay.The proliferation was assayed with 3 H-TdR.Two-color staining(anti-CD4,anti-CD25)flow cytometric analysis was employed to measure the percentage of CD4+CD25+T cells of Deriph eral blood.Resuits PPARγmRNA was expressed in peripheral CD4+T lymphocytes.RosiglitazoBe inhibited phytohemagglutinin(PHA)-induced human CD4+T cell proliferation in dose dependence.The percentage of CD4+CD25+T cells showed no significant change after the peripheral blood culture with 1 μmol/Land 10μmot/L rosiglitazone.10 μmol/L of rosiglitazone induced Foxp3 mRNA expression in vitro (3.27fold,P<0.05),whereas TGF-β1 mRNA expression did not change.Furthermore,only 1 μmol/L of rosiglitazone could promote Foxp3 mRNA expression if adding IL-2(10 U/m1)in cultures(3.48 fold.P

Objective To study the drug resistance of neonatal sepsis caused by Klebsiella pneumoniae and provide evidence for drug treatment. Method Retrospectively analysis was conducted on the clinical data and antibiotic resistance of Klebsiella pneumoniae in 50 neonates with sepsis. Results The majority of the 50 cases were infected in hospital. There were 13 ESBLs strains in 50 Klebsiella pneumoniae strains (26%), and the others were negative ESBLs starins (74%). All the strains were multidrug-resistance to the β-lactam antibiotics and only sensitive to few antibiotics such as Imipenem and Amikacin. The sensitive rate was 100%. Conclusions The first selected antibiotic for the treatment of neonatal sepsis caused by Klebsiella pnemoniae was Imipenem or Amikacin.

Objective To explore the mechanism of Exenatide-induced rat pancreatic tissue lesion.Methods Thirty SD male rats were divided into three groups according to complete random design,and each group had 10 rats,namely Exenatide group,diabetes-model group and control group.Diabetes-model rats were induced by streptozotocin (STZ,35mg/kg) and high-sugar and high-fat diet.The Exenatide group and diabetes group were subcutaneously administered with Exenatide at a dose of 5 μg/kg twice a day.The control group was treated with same amount of saline.Ten weeks later,all the rats were sacrificed and the pancreatic tissues were harvested for routine pathological examination.Immunohistochemical method was used to detect the expression of α-smooth muscle actin (α-SMA) and type Ⅲ collagen protein in pancreatic tissue,and ELISA was applied to measure the expression of matrix metalloprotei-nase-2 (MMP-2) and MMP-9 in pancreatic tissue.Results In control group,there was no pathological change in pancreatic tissue.In Exenatide group,chronic inflammatory changes were observed; and the degree of inflammatory changes were much severe in diabetes group,and the pathological scores were gradually increased in the 3 groups (P ＜0.05).The expressions of MMP 2 in pancreatic tissue in control group,Exenatide group,diabetes group were (186.98 ± 23.24),(306.07 ± 59.82),(365.08 ± 89.55) μg/L,and the expressions of MMP-9 were (49.37 ± 7.08),(67.24 ±14.73),(87.37 ±13.39)μg/L.The values were significantly higher in Exenatide group and diabetes group than those in control group (P ＜ 0.05),but the difference between the two groups was not statistically significant.The numbers of α-SMA positive cells per high power field were (13.4 ± 5.97),(29.5 ± 8.80),(79.3 ± 27.23) in control group,Exenatide group,diabetes group,and the numbers of type Ⅲ collagen positive cells were (10.6 ± 4.93),(29.3 ± 12.95),(56.0 ± 27.21).The values were significantly higher in Exenatide group than those in control group,and the values were significantly higher in diabetes group than those in Exenatide group (P ＜ 0.05).Conclusions Long-term subcutaneous injection of Exenatide may activate pancreatic stellate cells and cause expression of α-SMA,Ⅲ collagen protein,and MMP-2,MMP-9,then induce chronic inflammatory changes.

Objective:To explore the antipyretic effect on rabbit fever induced by endotoxin and the anti-inflammatory effect on the increase of mouse abdominal cavity capillary permeability caused by 0. 6% glacial acetic acid of Bazhong gardenia. Methods:The rab-bit fever model was made by ear margin vein injection of endotoxin in physiological saline solution, and the mouse inflammation model of abdominal cavity capillary permeability increase was established by 0. 6% glacial acetic acid solution. The animals were respectively intragastrically administrated with gardenia water-soluble effective parts and 70% alcohol-soluble effective parts. The rabbit body tem-perature and mouse celiac fluid absorbance values were detected. The effects of gardenia from different habitats were studied and com-pared. Results:The antipyretic effect of water-soluble effective parts from Bazhong gardenia extract was better than that of gardenia ex-tract from Jiangxi, Hubei and Jiangjin (P<0. 01), and that of alcohol-soluble effective parts from Bazhong gardenia extract was better than that of gardenia extract from Jiangjin and Jiangxi (P<0. 05 or 0. 01). Although compared with that of Hubei gardenia, the anti-pyretic effect of alcohol-soluble effective parts from Bazhong gardenia extract was weaker than that of gardenia extract from Hubei, the difference was not significant (P>0. 05). Bazhong gardenia could inhibit the increase of abdominal blood capillary permeability in mouse inflammation model, and the effect was better than the other gardenia, however without significant difference (P>0. 05). Con-clusion:Bazhong gardenia shows better antipyretic effect compared with that from other habitats.