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.

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.

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.

Sleep apnea includes obstructive sleep apnea,central sleep apnea and mixed sleep apnea.Ob-structive sleep apnoea syndrome(OSAS)is affecting up to 5.7% of children,which hss adverse impact on growth,development cognitive and behavioral outcomes,and untreated OSAS increases cardiovascular risk,so paying closer attention to childhood OSAS early diagnosis and treatment seems more important.First-line treat-ment in OSAS children is adenotonsillectomy,although other treatment options available include continuous posi-tive airways pressure,anti-inflammatory therapies,airway adjuncts and orthodontic appliances.Central sleep ap-nea may be related to respiratory regulation center immaturity or dysplasia.Central sleep apnea may be hereditary or acquired.Therefore,the treatment of central sleep apnea should be focused on primariy etiology.

Objective To investigate the effect of neuropeptide substance P on airway smooth muscle cell contraction amplitude.Methods According to random method, 10 Wistar rats were divided into normal group and asthmatic group.By inhaled OVA to make asthmatic rat model;primary culture ASMC;confocal microscopy were used to observe the morphological changes and measure the length before and after different intervention.The percent of contraction length come from different group ASMC were used for statistical analysis.Results The ASMCs volume in acetylcholine intervented group and substance P intervented group decreased significantly,cell diameters shorten, cytoplasm reduction and cell arranged densely.The ASMCs volume in substance P receptor antagonist intervented group and nimodipine intervented group are about the same size as the ones in normal control group, were spindle-shaped, abundant cytoplasm and arrangement regularly.The contraction length percent of Ach intervened group is the biggest(19.60 ± 3.47) ％, contraction length percent of nimodiping intervented group is the shortest(3.25 ± 1.14)％ ,the contraction length percent in substance Precepter antagonist intervented group is bigger than the one in control group (3.54 ± 1.26) ％, but less than the one in Ach intervented group, asthmatic (14.36 ± 2.37) ％ and substance P intervened group (17.79 ± 3.19) ％.Conclusion Substance P can increase the amplitude of airway smooth muscle cell contraction, but the effect less than Ach;substance P receptor antagonists can inhibit smooth muscle cell contractility, but the effect less than nimodipine.Substance P participates in acute attack of asthma, increases airway reactivity by increasing airway smooth muscle contraction intensity.

Induced pluripotent stem cells can differentiate into a variety of cell types,which promote the development of human disease model,drug toxicity screening and sources of autologous cells.However,there have been many problems in the induced pluripotent stem cells reprogramming,such as safety and low efficiency.Small molecules are considered as a promising method to improve the reprogramming processes of induced pluripotent stem cell,and more and more small molecules have been identified to maintain stem cell self-renewal,providing a new approach to produce the desired reprogramming cells.