https://scholars.lib.ntu.edu.tw/handle/123456789/568039
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | YIN-HSIU CHIEN | en_US |
dc.contributor.author | Chang K.-W. | en_US |
dc.contributor.author | YAO-HSU YANG | en_US |
dc.contributor.author | MENG-YAO LU | en_US |
dc.contributor.author | YU-TSAN LIN | en_US |
dc.contributor.author | BOR-LUEN CHIANG | en_US |
dc.date.accessioned | 2021-07-02T03:42:38Z | - |
dc.date.available | 2021-07-02T03:42:38Z | - |
dc.date.issued | 2003 | - |
dc.identifier.issn | 0929-6646 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-0043011446&partnerID=40&md5=149a81987260ac489277b3e7c55da2f7 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/568039 | - |
dc.description.abstract | Background and Purpose: Tumor necrosis factor-alpha (TNF-α) has been shown to play a central role in the pathogenesis of vasculitis in Kawasaki disease (KD). We investigated the serum levels of TNF-α and soluble TNF receptor 1 (STNFR1) levels, and genetic polymorphisms of the TNF-α promoter gene in children with KD to delineate the genetic basis of KD. Methods: A total of 18 children (12 boys and 6 girls) with KD were studied, 9 of whom had the complication of coronary artery lesion (CAL) within 30 days after the onset of symptoms. Serum levels of TNF-α and STNFR1 were assayed by enzyme-linked immnosorbent assay, and DNA polymorphisms of the 5′ flanking region of TNF-α promoter gene at position -308 [guanine (G) to adenine (A)] and -238 (G to A) were studied by direct nucleotide sequencing. Results: The serum TNF-α level in KD patients was 113 ± 209.9 pg/mL (range, 2.0 to 756.9 pg/mL; median, 24.7 pg/mL; normal, < 10 pg/mL). The serum levels of STNFR1 in KD (4255 ± 2425 pg/mL) were higher than those of the control group (160 ± 116 pg/mL). Allele frequencies of -308A and -238A were 11.1% and 0% in the KD patients, and 0% and 3.1% in the control group. Neither TNF-α promoter polymorphism nor any significant risk factor for CAL was identified in KD patients. One patient, who was homozygous for -308A, showed the highest TNF-α level and elevated STNFR1 level but had no evidence of CAL. Positive correlations were found between serum levels of STNFR1 and C-reactive protein (r = 0.731, p = 0.007), and between STNFR1 and leukocyte counts at admission (r = 0.620, p = 0.008). Conclusions: Increased serum levels of TNF-α and STNFR1 were found in KD patients but there was no correlation between these levels. The relationship between the pathogenesis of KD and TNF-α gene promoter -308G to A mutation towards cytokine production remains to be clarified. | en_US |
dc.relation.ispartof | Journal of the Formosan Medical Association | en_US |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | adenine; C reactive protein; cytokine; DNA; guanine; tumor necrosis factor alpha; tumor necrosis factor receptor 1; article; child; clinical article; controlled study; coronary artery disease; correlation analysis; cytokine production; DNA flanking region; DNA polymorphism; enzyme linked immunosorbent assay; female; gene frequency; gene mutation; genetic analysis; genetic polymorphism; homozygosity; hospital admission; human; infant; leukocyte count; male; mucocutaneous lymph node syndrome; nucleotide sequence; pathogenesis; promoter region; risk factor; symptom; Case-Control Studies; Child; Child, Preschool; Female; Gene Frequency; Humans; Infant; Male; Mucocutaneous Lymph Node Syndrome; Polymorphism, Genetic; Promoter Regions (Genetics); Receptors, Tumor Necrosis Factor; Tumor Necrosis Factor-alpha | - |
dc.title | Association between levels of TNF-α and TNF-α promoter - 308 A/A polymorphism in children with kawasaki disease | en_US |
dc.type | journal article | en |
dc.identifier.pmid | 12783130 | - |
dc.identifier.scopus | 2-s2.0-0043011446 | - |
dc.relation.pages | 147-150 | en_US |
dc.relation.journalvolume | 102 | en_US |
dc.relation.journalissue | 3 | en_US |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
item.grantfulltext | none | - |
crisitem.author.dept | Pediatrics | - |
crisitem.author.dept | Pediatrics-NTUH | - |
crisitem.author.dept | Medical Genetics-NTUH | - |
crisitem.author.dept | Pediatrics | - |
crisitem.author.dept | Pediatrics-NTUH | - |
crisitem.author.dept | Pediatrics-NTUH | - |
crisitem.author.dept | Pediatrics | - |
crisitem.author.dept | Pediatrics | - |
crisitem.author.dept | Pediatrics-NTUH | - |
crisitem.author.dept | Pediatrics | - |
crisitem.author.dept | Pediatrics-NTUH | - |
crisitem.author.dept | Clinical Medicine | - |
crisitem.author.dept | Oral Biology | - |
crisitem.author.dept | College of Life Science | - |
crisitem.author.dept | Immunology | - |
crisitem.author.orcid | 0000-0001-8802-5728 | - |
crisitem.author.orcid | 0000-0002-6266-9864 | - |
crisitem.author.orcid | 0000-0003-4461-9967 | - |
crisitem.author.orcid | 0000-0002-4192-3165 | - |
crisitem.author.orcid | 0000-0002-6705-0286 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 醫學系 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。