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1.
Chinese Journal of Rheumatology ; (12): 724-728, 2013.
Artículo en Chino | WPRIM | ID: wpr-442007

RESUMEN

Objective To investigate the association of TLR4 gene polymorphisms with susceptibility to primary gouty arthritis (GA) in Chinese Han population.Methods A total of 459 patients with GA and 459 healthy control subjects were enrolled into this study.All the genotyping assays of TLR4 gene polymorphisms loci [rs4986790 (Asp299Gly),rs4986791 (Thr399Ile),rs2 1 49356T>G] were measured using TaqMan probes that specifically target the alternate alleles.Results All the subjects were found to be homozygous for the wild-type TLR4 alleles (Asp/Asp,Thr/Thr) on TLR4 Asp299Gly and Thr399Ile genotyping.There was no significant deviation from HWE both in GA and controlsin the rs2149356 (x2=0.778,1.295; P>0.05,respectively).Significant differences were observed between the GA and control groups with respect to genotype and allele frequencies of TLR4 gene rs2149356 (x2=16.23,17.08; P<0.01,respectively),and TT genotype was the risk factor for gout (adjusted OR=2.09).Conclusion The TLR4 gene rs2149356 SNP may be associated with GA susceptibility,and TT genotype may be the risk factor for developing gout.

2.
Chinese Journal of Medical Education Research ; (12): 780-782, 2011.
Artículo en Chino | WPRIM | ID: wpr-421377

RESUMEN

Aiming at status of training the rural order directed free medical educational talents, we should improve the understanding of training the free medical students, perfect the relevant management system, strengthen medical ethics education of students, pay attention to humanistic care of students,strengthen the continuing education of students, standardize the access system of students, reform the medical distribution system, to ensure the quality of training free medical students.

3.
Chinese Journal of Clinical Pharmacology and Therapeutics ; (12)2004.
Artículo en Chino | WPRIM | ID: wpr-564108

RESUMEN

AIM: To explore the protective effects and mechanism of astragalus injection on asthmatic rats. METHODS: OVA was injected intraperitoneally and inhaled to produce the asthmatic rat models. Forty rats were randomly divided into five groups: control group, asthma group and astragalus groups of high, medium and low dose. The concentration of IL-5 in BALF and the expression of IL-5 mRNA, phospho-p38 MAPK in lung tissue were respectively measured by ELISA, in situ hybridization staining and Western blot. The number of inflammatory cell in BALF was calculated and histopathology changes were observed. RESULTS: The number of inflammatory cell and the concentration of IL-5 in BALF and the expression of IL-5 mRNA, phospho-p38 MAPK in lung tissue were higher in asthmatic rat group than those in normal control(P

4.
Chinese Pharmacological Bulletin ; (12)2003.
Artículo en Chino | WPRIM | ID: wpr-557592

RESUMEN

Aim To explore the effects of SB203580,a special inhibitor of p38 mitogen-activated protein kinase(p38 MAPK),on the airway inflammation and Th2 cytokines,interleukin 4(IL-4) and IL-5,in asthmatic mice.Methods Thirty mice were randomly divided into 3 groups: normal control,asthmatic group and SB203580 group.The expression of IL-4 mRNA and IL-5 mRNA in lung tissue and IL-4 and IL-5 protein in bronchial alveolar lavage fluid(BALF) were detected using in situ hybridization and ELISA,respectively.The number of inflammatory cells in BALF and histopathological changes were observed.Results The number of inflammatory cells and the concentrations of IL-4 and IL-5 in BALF,and the expression of IL-4 mRNA and IL-5 mRNA in lung tissue were higher in the asthmatic mice than in the normal control mice(P

5.
Chinese Journal of Pathophysiology ; (12)1989.
Artículo en Chino | WPRIM | ID: wpr-520790

RESUMEN

AIM: To investigate the role of p38 protein kinase in the activation of rat alveolar macrophages(AMs) induced by lipopolysaccharide(LPS). METHODS: Nuclear protein was extracted, p38 protein kinase in nuclear extracts was analyzed by Western blot. The concentrations of TNF-? and IL-8 in supernatant were measured by radioimmunoassay. RESULTS: The concentrations of TNF-?, IL-8 in supernatant and p38 protein kinase in nuclear extracts were increased significantly induced by LPS and blocked by SB203580, a selective inhibitor of p38 protein kinase. CONCLUSION: The inductoin of TNF-? and IL-8 in alveolar macrophages by LPS may be mediated through the activation of p38 protein kinase.

6.
Chinese Journal of Pathophysiology ; (12)1986.
Artículo en Chino | WPRIM | ID: wpr-526872

RESUMEN

AIM: To explore the role of p38 mitogen-activated protein kinase (p38 MAPK) in the regulation of IL-4 and IL-5 expression in asthmatic rats. METHODS: T lymphocytes were isolated and purified from blood of normal or asthmatic rats. p38MAPK in nuclear extracts, mRNA and protein of IL-4 and IL-5 in supernatants were measured by Western blotting, in situ hybridization and ELISA, respectively. RESULTS: The expression of p38MAPK, the percentage of IL-4 and IL-5 mRNA positive cells, IL-4 and IL-5 protein in supernatants were significantly increased in asthmatic T lymphocytes and was blocked by SB203580, a selective inhibitor of p38MAPK. There were good positive correlation between the expression of p38MAPK and either the percentage of positive cells of IL-4 and IL-5 mRNA (r=0.71, 0.63, P

7.
Chinese Pharmacological Bulletin ; (12)1986.
Artículo en Chino | WPRIM | ID: wpr-678277

RESUMEN

AIM To investigate the activation of p38 protein kinase in alveolar macrophages(AMs) stimulated with lipopolysaccharide(LPS) and the effects of dexamethasone(DEX) and N acetylcysteine(NAC) on the process. METHODS AMs isolated and purified from normal rats were divided into four groups:Control group, LPS stimulated group ,DEX group and NAC group. The activation of p38 protein kinase in nuclear protein extract from the AMs and the concentration of TNF ? and IL 8 in supernatant were measured by Western blot and radioimmunoassay, respectively. RESULTS The activation of p38 protein kinase and the concentration of TNF ?, and IL 8 in LPS stimulated group were significantly higher than those in control group( P

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