Airway remodeling is the result of chronic inflammation, which including airway wall thickening, matrix and collagen deposition, epithelial hyperplasia and fibrosis, smooth proliferation and hypertrophy,fibroblast proliferation, and mucus glands and goblet cell proliferation, micrangium generation and other pathological changes. Airway smooth muscle change is known as the reason of airway hyper - responsiveness and asthma aggravating. There are many factors which can induce airway smooth muscle hypertrophy and proliferation, such as inflammation, cytokines,extracellular matrix and genetic factors. In addition, recent researches reveal the airway smooth muscle is also an important source of inflammation. In this paper the latest opinion of the role of asthma airway smooth muscle in the airway remodeling were elaborated,and inhale hormone earlier was suggested.

The damage of airway epithelial cell in asthma including epithelial cells differentiated into goblet cell, mucous cells metaplasia, which lead to the extracellular matrix increasing, airway walls fibrosis and mucus high secretion. There are many cytokines, growth factors, signal transduction pathways and gene regulating this process.Neuroendocrine cell plays a very important role in the immune adjustment.The repairing process of airway epithelial cells after damaged is a complicated process and affected by many factors.

Asthma is a chronic airway inflammation involved by a variety of cells.Glucocorticoid can relieve most of asthmatic patient's symptom,but cannot treat all patients with asthma.KCa3.1 ion channel expressed in a variety of immune cell surface, participate in a variety of autoimmune disease immune process.Because potassium-calcium ion channels are involved in the immune process mediated by T lymphocytes, the adjustment of the function of KCa3.1ion channels may be a new way for asthma treatment.

Objective To study the effect of the ECV-304 cells modified with LIF gene on the ex vivo culture of HSC/HPC in cord blood.Methods The ECV-304 cells were infected by Eukaryotic Expression plasmid pcDNA3.0LIF,and the positive ECV-304 cells were obtained by selected with G418.These cells were used to co-culture with CD34+ cells of cord blood.The phenotype of CD34+ and CD34+ CD54+、CD34+ CD62L+ primitive progenitors was detected by flow cytometry.Results The LIF gene can express in ECV-304 cells steadily.ECV-304 cells modified with LIF gene can improve expansion of CB CD34+、CD34+CD54+ and CD34+ CD62L+ cells while sustaining the expression of homing-related adhesion molecule.Conclusion The ECV-304 cells modified with LIF gene can not only significantly expand CB hematopoietic progenitor cells ex vivo,but the expanded CD34+ cells may well retain their homing ability.

Objective To investigate the effect of hepatitis B virus X protein (HBx) on the induction of eytochrome P450 (CYP) 3A4 by 1α, 25-(OH)2D3 in HepG2 cells in vitro. Methods HepG2 cells were transiently transfected with plasmid pEGFP-N1 (control) or co-transfected with recombinant HBx eukaryotic expression plasmid pcDNA3-X and pEGFP-N1. All HepG2 cells were divided into four groups: control group (without transfection), plasmid pEGFP-N1 transfection group, plasmid pEGFP-N1 transfection plus 1α ,25-(OH)2D3 group, plasmid pcDNA3-X and pEGFP-N1 co-transfection plus 1α ,25-(OH)2D3 group. The expression of CYP3A4 in HepG2 cell was induced by 0.35 μ mol/L 1α ,25-(OH)2D3 for 72 h, and mRNA levels and protein levels of CYP3A4 in the cells were detected by reverse transcriptase-polymerase chain reaction (RT-PCR) assay and Western-blot assay, respectively. The comparison between groups was done by F test. Results CYP3A4 mRNA level in plasmid pcDNA3-X and pEGFP-N1 co-transfection plus 1α ,25-(OH)2D3 group was 1.52 folds of control group, while that in plasmid pEGFP-N1 transfection plus 1α, 25-(OH)2D3 group was 3.97 folds (F= 4.72, P<0. 05). Similarly, intracellular CYP3A4 protein expression in plasmid pcDNA3-X and pEGFP-N1 co-transfection plus 1α , 25-(OH)2D3 group increased to 2.1 folds of control group, while that in plasmid pEGFP-N1 transfection plus 1α,25-(OH)2D3 group increased to 5.9 folds (F=4.68, P<0.05). Conclusion HBx interferes with the induction of CYP3A4 by 1α , 25-(OH)2D3 in HepG2 cell line, which suggests that HBx has suppressive effect on the expression of CYP3A4.

OBJECTIVE:To investigate release characteristics of sirolimus liposome in vitro.METHODS:The concentration of sirolimus was determined by RP-HPLC.In vitro release rate of sirolimus liposome within 24 h was investigated by the reverse dialysis method with 20% ethanol 500 mL as medium.Release curve of sirolimus was fitted with drug release model equation.RESULTS:The linear range of sirolimus were 0.5～20 ?g.mL-1(r=0.999 8)with an average recovery of 99.42%(RSD=1.23%).At the first 4 hours of release,sirolimus liposome released rapidly with accumulative release rate of 50%.After that release rate of liposome was slowed down with accumulative rate of 80% in 24 h.The in vitro release curve conformed to the first order equation.CONCLUSION:Sirolimus liposome has delayed release capability,and in vitro drug release of sirolimus liposome is in concentration dependant manner.

OBJECTIVE: To recognize the research status on the mechanism of reactive oxygen species (ROS) and NADPH oxidases in cell growth and death,and explore the effects of ROS and NADPH oxidases on cardiomyocyte differentiation.DATA SOURCES: A computer-based online search of Medline was undertaken for the articles about the action mechanism of reactive oxygen and NADPH oxidases in cell growth and death published in English between January 1997 and December 2003 with the key words of "Reactive oxygen species, NADPH oxidase, Cardiomyocytes, Differentiation, Signal transduction".STUDY SELECTION: Inclusive criteria: ①Articles on ROS production and structure and activation of NADPH oxidase and their action mechanism in cell growth and death; ②Research about the molecule mechanism of cardiomyocytes differentiation. The repetitive research and review articles were excluded.DATA EXTRACTION: Totally 132 articles about the action mechanism of ROS and NADPH oxidase and cardiomyocytes differentiation were collected, and 78 ones met the inclusive criteria.DATA SYNTHESIS: ①ROS involved in pathogenesis of many diseases were mainly from intramitochondrial electron transport chains, and NADPH oxidase was closely related with ROS production; NADPH oxidase firstly found in phagocyte was a kind of multienzyme complex, and its activity was regulated by the concentration of Ca2+ in cells and mRNA expression of its subunits. ②At present, many researchers presumed that oxidative stress was a double-edged sword, and it two-ways regulated the cell proliferation and death, in which ROS served as the second messenger in the signal transduction. Recent data showed that ROS and NADPH oxidase played important roles in cardiomyocytes differentiation; however, it was not identified which subunit of NADPH oxidase expressed in myocardial cells and its detail regulative pathway. Those problems were important for further study in the molecule mechanism of cardiomyocytes differentiation.CONCLUSION: ROS including superoxide anion (O2-), hydrogen peroxide (H2O2) and hydroxyl radical (OH-), are generated in cardiomyocytes mainly by a membrane-bound NADPH oxidase (NOX). The NOX-derived ROS, as the second passenger, play important roles in various intracellular signaling pathways. In cardiomyocytes, ROS have the potential to alter the balance between cell growth and death through these signaling pathways. Recently,ROS have been demonstrated to play a critical role in regulation of cardiomyocyte differentiation from embryonic stem cells. Research in the regulation mechanisms of ROS will contribute to our better understanding of he role of ROS and NADPH oxidase in cardicomyocyte differentiation and will lead to the identification of factors able to promote cardiac differentiation.

The incidence of hyperuricemia and relevant diseases has been increasing recently since the living improvement and dietary changing. Both patients and doctors do not pay enough attention to this disease, due to the lack of obvious clinical presentations in early stage. This paper comments on the relationship between hyperuricemia and gout, gouty nephropathy, impaired glucose metabolism,and atherosclerotic diseases in order to arouse enough attention to this disease.

Epidemiological studies indicate that obesity is associated with metabolic disorders, such as type 2 diabetes hyperlipidemia and hypertension. Early nutrition, especially during pregnancy and lactation can lead to the permanent programming of system by some adaptive effects in physiological, cellular and molecular levels. These adaptive effects persistently changed the metabolic throughout life, hence resulted in increased risk of obesity and metabolic related disease.This review focuses upon the influence of nutrition in early life on adulthood obesity and researches on their pathophysiological mechanism .

Objective To investigate the effect of budesonide on NK-1 receptor expression in airway smooth muscle cell (ASMC). Methods According to the random method,45 wistar rats were divided into three groups: asthmatic group, budesonide treatment group and control group. Aerosolize ovalbumin was used to make asthmatic rat model. Budesonide treatment group were given budesonide after inhaled ovalbumin. On day 21 .primary rat ASMC culture was conducted. The fourth cell passage and purified ASMC was collected for RT-PCR. The content of NK-1R was determined by real-time quantitative PCR. Data were expressed as mean±standard error (SE). The ANOVE Tukey test was carried out by using SPSS17.0 software and P＜0. 05 was considered significant. Results As compared with that of asthmatic group(1.1687±0.1356),NK-1R mRNA in therapy group( 1.0820 ±0. 1146) decreased significantly (P ＜0.05) ,but remained still higher than that of control group(1.034 7±0.2503) (P＜0. 05). Conclusion NK-1R may be involved in the pathogenesis of asthma. Budesonide may down-regulate the expression of the NK-1R mRNA in the airway smooth muscle cell, which may inhibit inflammation in asthmatic attacks.