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.

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.

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.

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.

Objective To investigate the clinical significance of the changes of hypersensitive C-reactive protein (hs-CRP) and myocardial enzyme spectrum,cardiac troponin Ⅰ (cTn Ⅰ) in patients with Henoch-Schnlein purpura.Methods 100 patients with Henoch-Schnlein purpura were selected.50 patients only skin involved were selected as the simple group,50 patients accompanied by other organs involved were selected as mixed group.50 healthy people in the same period were selected as the control group.The serum hs-CRP,myocardial enzyme spectrum and cTn Ⅰ were tested and compared.Results The hs-CRP,serum myocardial enzyme spectrum and cTn Ⅰ levels of mixed and simple group were significantly higher than the control group(all P ＜ 0.05) ; Serum CK-MB,cTn Ⅰ and hs-CRP levels of the mixed group were significantly higher than those of simple group (all P ＜ 0.05).The abnormalities number of CK-MB and cTn Ⅰ respectively accounted for 33％ (33/100) and 32％ (32/100) ;The constituent ratio of the number of abnormal serum CK-MB and cTn Ⅰ of the mixed group was significantly higher than the simple group (x2 =4.047,3.908,all P ＜ 0.05) ;The Pearson correlation analysis showed that the relationship between the serum hs-CRP and CK-MB,cTn Ⅰ levels was linear,which were positively correlated (r =0.872,0.801,all P ＜ 0.05).Conclusion Patients with allergic purpura should early detect the serum levels of hs-CRP,myocardial enzyme spectrum and cTn Ⅰ,and treat the myocardial injury in time.

Objective To evaluate the efficiency and safety of non- nasogastric tube on fast-track surgery patients with colorectal cancer. Methods We searched PubMed, CBM, Cochrane Library, CNKI, Wanfang and Vip data. Controlled trials that met the criteria were selected. All reports were collected and analyzed by RevMan5.3. Results 8 reports were enrolled. The non-nasogastric tube group had a shorter anus exhausting time and lower morbidity of pulmonary and throat complications , and it also had a shorter postoperative length of hospital stays. Significant differences were found between the non-nasogastric tube group and the control group (P< 0.01). There are no significant difference in the morbidity of gastrointestinal complications (P > 0.05). Conclusion Current evidence shows that non-nasgastric tubes are recommended for the patients with colorectal cancer surgery.

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.

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 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.