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Gene Polymorphisms And Familial Aggregation Of The Angiotensin Converting Enzyme (ACE) And The Effects Of Angiotensin Ⅱ(AⅡ) In Children Asthma

Posted on:2005-03-13Degree:MasterType:Thesis
Country:ChinaCandidate:H WangFull Text:PDF
GTID:2144360155967653Subject:Academy of Pediatrics
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Objective To observe the polymorphisms and familial aggregation of ACE and the expressions angiotensin â…¡ of asthmatic children and effects of Aâ…¡ on expressions of monocyte chemoattractant protein-1(MCP-1) and intercellular adhesion molecule-1(ICAM-1) of peripheral blood mononuclear(PBMC) in healthy children.Methods PCR was used to detect I/D polymorphisms of ACE in 149 children of asthma, 108 children of pneumonia with wheezing and 121 children of pneumonia. TIgE was detected in 36 asthmatic children. Aâ…¡ and MCP-1 and ICAM-1 of PBMC stimulated by Aâ…¡ were detected in 21 exacerbation of asthmatic children and 11 healthy children.Results The expressions of II, ID, DD genotype were 42(28.19%), 36(24.16%), 71(47.65%) in asthmatic group,34(31.48%) , 26(24.07%), 48(44.44%) in pneumonia with wheezing group,61(50.41%), 30(24.79%), 30(24.79%) in pneumonia group. I, D allelic gene frequency were 152 (62.81%) , 90 (37.19%) ; 94 (43.52%) , 122 (56.48%) ; 120 (40.27%) , 178 (59.73%) in three groups respectively.D, I allelic gene frequency odd ratio were 2.51 , 2.19 in asthma group compared to pneumonia, pneumonia with wheezing group compared to pneumonia respectively. There were significance. There were 83 asthmatic children with asthma history of primary, secondary relatives. The expressions of II, ID, DD genotype were 16(19.28%), 23(27.71%), 44(53.01%).They were26(39.39%) > 13(19.70%), 27(40.91%) in 66 asthmatic children without asthma history. There were significance. There were 46 pneumonia children with asthma history of primary, secondary relatives in pneumonia with wheezing group. The expressions of II > ID ^ DD genotype were 12(26.09%) â– , 12(26.09%) > 22(47.83%).They were 22(35.48%) , 14(22.58%^ 26(41.94%) in 62 pneumonia children without asthma history. There was no significance. TIgE were 849.08 + 350.65 KU/I^ 644.09 + 440.62 KU/L> 863.67 + 647.46 KU/L in 12 (II) > 11 (ID) , 13 (DD) asthmatic children respectively. There was no significance. The expressions of All in 21 exacerbation of asthmatic children were increased than that in 11 healthy children(P<0.05). The expressions of PBMC were cultured with All (10"\ 10"\ 10"7 ^ 10"6 mol/L) .After 24 hours , the expressions of MCP-1 and ICAM-1 in AII stimulating group were more than that in control. It was the most in 10"6 mol/L of A II group (PO.0001 ) . After A II stimulating 2^ 24^ 48 hours, the expression of MCP-1 and ICAM-1 were increased in 24n 48 hours groups. They were the most in 24 hours in the 10"6 mol/L of AII condition (PO.0001) .Conclusion There are the polymorphisms and familial aggregation y of ACE. The DD genotype is obvious. The expressions of AII in exacerbation of asthmatic children were increased. AII can stimulate PBMC to express MCP-1 and ICAM-1 and involve the inflammation of asthma.
Keywords/Search Tags:Asthma, Angiotensin converting enzyme, Polymorphism, Angiotensin Ⅱ, MCP-1, ICAM-1
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