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

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.

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 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 standardize the operation processes of neonatal instrument,ensure the standards effectiveness and safety of equipment use.Methods A retrospective study had been taken on after the developments and implementations of all neonatal instruments standard operation procedure (SOP).The equipment maintenance data were collected and analyzed one year before and after the implementation of SOP.Results After the effective implementation of the SOP,the incidence of instrument repair due to misoperation,improper maintenance reduad by 59％(19/32),9/14,4/7,the instrument management efficiency was enhanced,and the safety of nurses and patients was guaranteed,and the patients satisfaction was improved,and also the quality of care was enhanced.Conclusions SOP procedure plays a very important role in improving neonatal care management and overall efficiency.It makes a continuous improvement of nursing care which is worth widely being implemented.

0.05);the therapeutic effect on slight syncope-collapse syndrome and septic shock is superior to the control group(P

Objective To observe the efficiency of clopidogrel combined with emergency corona interventional therapy for non-ST segment elevation myocardial infarction.Methods A total of 112 patients with non-ST segment elevation myocardial infarction who were admitted in our hospital from February 2004 to November 2007 were divided into 2 groups at random with 56 patients in each,the experimental group and the control group.All patients were treated with emergency corona interventional therapy and the other routine standard therapies.The experimental group was treated with clopidogrel(75 mg,once per day for 8 weeks),and the control group administered ticlopidine(250 mg,twice per day for 8 weeks).The two group were followed up for a time of half a year.Results The TIMI(thrombolysis in myocardial infarction) myocardial-perfusion grade 3 angiographic flow was achieved in 91.1% of the experimental group,higher than that of the control group(87.5%),but there was no significant difference between them.What's more,there was no obvious difference between the 2 group in cardiac functional grading and life-threatening bleeding.The experimental group had significantly lesser hyporrhea,and lower platelet degradation and total white blood cells counts in comparison to the control group.After the followed-up of half a year,there was significant difference between them in combination-end point.Conclusion Addition of clopidogrel is effective in emergency corona interventional therapy for non-ST segment elevation myocardial infarction,which can degrade the risk of emergency corona interventional therapy.

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

Atrial fibrillation ( AF) is an abnormal heart rhythm characterised by rapid and irregular beating.It is caused by multiple factors and can lead to ischemia-associated thrombosis, heart failure and other complex symptoms. Based on the etiology and characteristics of AF, animal models have 3 main categories including electrical, neurohormonal or vessel-related, and structural remodeling models.New technologies such as microRNA knock-down/overexpression or CRISPR-Cas9 gene editing provide tools for constructing animal AF models and directions in the development of AF thera-peutic strategies.Currently these strategies have largely focused on the cellular and molecular therapeutics rather than tradi-tional invasive electrophysiological methods or antiarrhythmic drugs.With the aid of new tools, progress has been greatly made in a broad range of therapeutic research areas including molecular mechanisms, drug targeting and screening.This re-view summarizes the animal models of atrial fibrillation currently used in studies of the molecular and cellular therapeutics and notes their contributions to this research area.