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.

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 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.

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.

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.

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 Investigate the effect of substance P and receptor antagonist on the current of NCX in ASMC.Methods Primary rat ASMC cultures were established.Immunofluorescence was used to identify ASMCs.Patch clamp exam was used to assess NCX currents in ASMC before and after intervented by Ach,substance P,NK-1R receptor antagonist and nimodiping,Voltage-current curves were drawn according to variation of voltage and current.PA indicates current amplitude,PF indicates cell area,and PA/PF indicates current density.Results As the voltage increased,the current density increased.When voltage up to-40mV the reverse current appeard.When the voltage is 60mV the current density in the Ach intervention group was highest,but lowest in the nimodipine intervention group;the current density in the substance P intervention group is more than in control group but lower than in Ach interevention group.The current density in the substance P receptor antagonist intervention group higher than nimodipine interevention goup,but lower than the other group (P ＜0.05).Conclusion In asthma airways,Ca2 + overload is related to the appearance of reverse-mode NCX.NK-1R antagonist plays a role in decreasing the Ca2 + concentration,which can relieve the current of reverse-mode NCX,and may benefit alleviating airway inflammation and responsiveness.As a result,NK-1R antagonist may be an attractive target for therapeutic approaches to asthma.