Dengue (DEN) virus is a member of the family flaviviridae which consists of a group of enveloped viruses with a single-stranded positive-sense RNA genome. DEN virus infection is initiated by the binding of envelope protein E to cellular receptor,followed by replication in cytoplasm which associated with a range of induced membrane structures. Further characterization of the DEN replication complex (RC) showed the involvement of NS1, NS2A, NS3, NS4A, and NS5 proteins as the viral replicase. The DEN virion maturation is associated with the cleavage of precursor of protein C by NS2B/NS3 protease and the glucosylase-mediated N-linked oligosaccharide trimming of prM, E protein. This review summarizes recent advance in research on DEN virus life cycle, emphasizing cellular receptor, RNA replication and virion assembly.

ObjectiveTo study the level of temperament and self-esteem of children aged 8～12 in Beijing city,as well as their interaction and influenced factor.Methods203 school children aged 8～12 were assessed with Carey's temperament questionnaire(8～12:MCTQ) and The Self-Esteem Scale(SES).ResultsTemperament and self-esteem of school children aged 8～12 were associated with the parental behavior,especially with work style of their fathers.The rhythmicity was found to be negative correlated to the self-esteem scores,and the intensity of reaction was found to be positive correlated to the self-esteem scores.ConclusionParents' behavior and family environment were important to the temperament and self-esteem of school children.

Allergic rhinitis (AR) is a noninfectious inflammatory response in nasal mucosa caused by allergens, which is contacted by a specific individual. The immune imbalance of Th1/Th2 plays an important role in the pathogenesis of AR. In?terleukin (IL)-33, the novel cytokine of IL-1 family, is an important regulatory factor of allergic diseases, autoimmune diseas?es and various inflammatory diseases. IL-33 is a kind of alarm, which is mainly secreted and released by damaged tissues and cells, especially impaired epithelial cells and endothelial cells. IL-33 binding to its receptor ST2L can activate a variety of immune cells to produce Th2 cytokines, precipitating and maintaining Th2 polarization, increasing AR immune inflamma?tion, which is the new target of AR in research and treatment. In this article, we have done a brief overview for the biological functions of IL-33 and its receptor ST2L and the research progress in the AR.

Aged ; Coal Mining ; Electrocardiography ; Heart Rate ; physiology ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; physiopathology

Aged ; Arrhythmias, Cardiac ; diagnosis ; physiopathology ; Coal Mining ; Electrocardiography ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; complications ; physiopathology

BACKGROUND:Different mechanical stimulations may have an effect on the level of metabolism of chondrocytes, but the effect is not clear.
OBJECTIVE:To investigate expression level changes in metabolic genes that participate in cartilage cel decomposition and synthesis under compressive stress and tensile stress conditions.
METHODS:We obtained articular chondrocytes from 2-week-old Sprague-Dawley rats. Primary cultured chondrocytes were identified. Passage one chondrocytes received cyclic tensile stress and cyclic compressive stress of 3%and 7%, respectively, so as to measure articular changes in chondrocytes-related genes.
RESULTS AND CONCLUSION:When chondrocytes were subjected to cyclic tensile stress of 3%, synthetic metabolic gene col agen types I and II and proteoglycan mRNA expression levels were decreased. If 3%cyclic compressive stress was applied, proteoglycan mRNA expression levels were increased, and type I col agen mRNA expression levels were decreased (P<0.001), and matrix metal oproteinase-13 mRNA expression levels were reduced (P<0.01). When strain reached 7%, cyclic tensile stress and compressive stress could lead to a general decrease in anabolism-related genes. The former could also make matrix metal oproteinase-13 mRNA expression levels increased (P<0.05). 3%cyclic compression ratio and 3%cyclic stretch made cytoskeleton become oval. These results indicated that in vitro, proper cyclic compressive stress is beneficial to maintain the growth characteristics of articular chondrocytes in rats. Smal tensile stress can decrease the synthesis ability of chondrocytes. The effect of stress may be caused by changing the cytoskeleton.

Objective To study the effects of TGFβ-activated kinase-1 (TAK1)mediated cell autophagy after global cerebral ischemia-reperfusion (IR ) in rats.Methods Seventy-two male Kunming rats were randomly divided into six groups:control group (group C),sham operation group (group S),ischemia-reperfusion group (group IR),TAK1 shRNA lentivirus group (group T),nega-tive lentivirus group (group Y)and normal saline group (group NS)(n = 12 each).The rats in groups T,Y and NS received cerebral ventricles injection of TAK1 shRNA lentivirus,negative lenti-virus and normal saline 10 μl two weeks before preparing animal model.Using thread embolism of the right middle cerebral artery occlusion (MCAO)to cause focal ischemia for 2 h and released for 24 h for reperfusion in groups IR,T,Y and NS.The common carotid arteries were separated but not liga-ted in group S,the rest of the procedure as the same as group IR.The rats of each group were evalua-ted by neurological severity scores (NSS)24 h after reperfusion,the cerebral infarct volume was measured with the method of TTC and the expression of TAK1,LC3Ⅱ/LC3Ⅰ,Beclin1 and p62 pro-tein in rat hippocampus were determined by using Western blot.Results The infarct volume and NSS in groups IR,T,Y and NS were significantly higher than those in group C (P <0.05).The infarct volume and NSS in group T were significantly lower than those in group IR (P <0.05).TAK1 pro-tein of hippocampus in groups IR,Y and NS was significantly higher than that in group C (P <0.05).TAK1 protein of hippocampus in group T were significantly lower than that in group IR (P <0.05).LC3Ⅱ/LC3 Ⅰand Beclin1 protein of hippocampus in groups IR,T,Y and NS were signifi-cantly higher than those in group C,and the p62 protein of hippocampus in groups IR,T,Y and NS was significantly lower than that in group C (P <0.05).The LC3 Ⅱ/LC3 Ⅰand Beclin1 in group T were significantly lower than those in group IR,and the p62 protein of hippocampus in group T was significantly higher than that in group C (P < 0.05 ).Conclusion TAK1 mediated cell autophagy takes part in the mechanism of brain ischemia-reperfusion injury in rats.

Kawasaki disease (KD) is an acute systemic vasculitis that primarily affects young children aged from 6 months to 4 years.KD may lead to coronary artery abnormalities in 25％-30％ of the children.The timely use of high dose intravenous immunoglobulin (IVIG) can significantly reduce the incidence of coronary artery aneurysms.Most clinicians use IVIG combined with aspirin as conventional therapy.But how to deal with those IVIG-resistant patients is a dilemma.With the deepening of research,many researchers have found that some second-line or third-line drugs such as corticosteroids,tumor necrosis factor-α inhibitors,and calcineurin inhibitors work better,and can effectively reduce the complication rate.The recent advances of the treatment of KD were summarized in this paper.

Objective To investigate the effect of dexmedetomidine postconditioning on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rats.Methods Fifty male Spragne-Dawley rats,aged 7-8 weeks,weighing 200-250 g,were randomly divided into 5 groups (n =10 each) using a random number table:control group (group C),LPS group and postconditioning with 3 different doses of dexmedetomidine groups (LD,MD and HD groups).ALI was induced with LPS 8 mg/kg injected via the caudal vein in LPS,LD,MD and HD groups.Dexmedetomidine 5,10 and 15 μg/kg were injected intraperitoneally in LD,MD and HD groups,respectively,at 1 h after LPS injection.The equal volume of normal saline was injected intraperitoneally in C and L groups.Blood samples were taken from the left ventricle at 6 h after dexmedetomidine administration,then the animals were sacrificed and broncheoalveolar lavage fluid (BALF) was collected.The concentrations of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in plasma and BALF were detected by ELISA.The lungs were removed for microscopic examination of pathological changes and for determination of wet/dry lung weight (W/D) ratio and expression of Toll-like receptor 4 (TLR4) mRNA (by RT-PCR) in lung tissues.Results Compared with group C,W/D ratio,pathological scores,and the concentrations of IL-6 and TNF-α in plasma and BALF were significantly increased,and the expression of TLR4 mRNA was up-regulated in LPS,LD,MD and HD groups.Compared with LPS and LD groups,W/D ratio,pathological scores,and the concentrations of IL-6 and TNF-α in plasma and BALF were significantly decreased,and the expression of TLR4 mRNA was down-regulated in MD and HD groups.There was no significant difference in the parameters mentioned above between LPS and LD groups,and between MD and HD groups.Conclusion Dexmedetomidine postconditioning can alleviate ALI induced by LPS in rats,and up-regulated TLR4 mRNA expression and reduced inflammatory responses may be involved in the mechanism.

Objective To investigate the preventive effects of aspirin on liver metastases of colorectal cancer in mice and study the mechanisms.Methods Twenty BALB/c mice were divided into the control group and the experimental group according to the random number table with 10 mice in each group.Mice in the control group were fed with saline each day at a concentration of 0.2 mL/d for 60 days,while mice in the aspirin group were fed with aspirin each day at a concentration of 30 μg/(g · d) for 60 days.Then C26 colon cancer cells were injected into the spleen and then the spleen was cut to establish mice model of colon cancer liver metastasis.The C26 colon cancer cells were divided into 2 groups.C26 colon cancer cells in the control group remained untreated,and C26 colon cancer cells in the experimental group were treated with aspirin at a concentration of 10 mmol/L for 24 hours.The scratches and transwell assays were conducted to observe the effects of aspirin on the invasion and metastasis of C26 colon cancer cells.The expressions of epithelial-mesenchymal transition (EMT)-related genes were detected using RT-PCR and Western blot.All data were analyzed using the Student t test.The survival curve was drawn by Kaplan-Meier method,and the survival analysis was done by Log-rank test.Results The numbers and weights of hepatic metastatic tumors were 4.8 ± 1.9 and (504 ± 107) mg in the control group and 2.6 ± 1.6 and (362 ± 67) mg in the experimental group,with significant difference between the 2 groups (t =2.840,3.584,P ＜ 0.05).The 1-month survival rate was 80％ in the experimental group,which was significantly higher than 40％ of the control group (x2=4.418,P ＜ 0.05).The results of pathological examination showed that tumor cell heteromorphism was reduced by aspirin.The results of scratches experiment showed an obvious migration of C26 colon cancer cells in the control group at 24 hours later,while no C26 colon cancer cells migrated in the experimental group.The numbers of C26 colon cancer cells penetrated the Watrige were 253 ± 21 in the control group and 148 ± 13 in the experimental group,with significant difference between the 2 groups (t =5.101,P ＜0.05).The relative mRNA expression of the E-cadherin and the Vimentin were 0.002 ±0.001 and 1.005 ±0.286 in the control group and 0.005 ± 0.001 and 0.270 ± 0.168 in the experimental group,with significant difference between the 2 groups (t =-4.606,4.942,P ＜ 0.05).The relative protein expressions of the E-cadherin and the Vimentin were 0.473 ±0.179 and 0.787 ± 0.118 in the control group and 1.585 ± 0.410 and 0.280 ± 0.133 in the experimental group,with significant difference between the 2 groups (t =-5.542,6.355,P ＜ 0.05).Conclusion Aspirin inhibits liver metastasis of colon cancer and promote the survival ratio of mice.Aspirin can up-regulate the expression of E-cadherin and down-regulate the expression of Vimentin,which inhibits EMT and reduces the invasion and metastasis of tumor cells.