Takeshi Aoki

Tsukuba Medical Center Hospital, Tsukuba, Ibaraki, Japan

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Publications (9)10.07 Total impact

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    ABSTRACT: A 6-year-old boy was referred for evaluation because he had several vomiting episodes, from the age of 2 years, following short-neck clam ingestion. He tested negative for short-neck clam-specific IgE just before visiting our hospital, and he was not allergic to other foods or shellfish. The patient had low levels of short-neck clam-specific IgE (1.04 UA/ml), and the skin prick test was positive for short-neck clam (4 mm). The lymphocyte stimulation test was positive (5305 counts per min (cpm), stimulation index (SI) =1211%) and the patch test was positive for short-neck clam ingestion. An oral challenge test with boiled short-neck clam induced abdominal pain and vomiting 2 h after ingestion, and the patient presented with increased peripheral leukocytes after 6 h. He was therefore diagnosed with food protein-induced enterocolitis syndrome (FPIES) due to short-neck clam ingestion. To our knowledge, this is the first case report of FPIES induced by the intake of shellfish.
    Arerugī = [Allergy] 12/2010; 59(12):1628-33.
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    ABSTRACT: Human resistin is expressed strongly in monocytes or macrophages rather than in adipocytes and may play a pivotal role in inflammation. We hypothesize that resistin levels are elevated in patients with Kawasaki disease (KD) in the acute phase and may be associated with the disease severity. Serum resistin concentrations were measured in 44 Japanese children with KD and 17 age-matched healthy children. All the KD patients were given both aspirin and a single dose of intravenous immunoglobulin (IVIG). The serum resistin levels at baseline in KD children were significantly higher than those in controls [33.0 (21.6-45.3) vs. 14.8 (12.4-18.6) ng/mL, P < 0.001]. After IVIG therapy, serum resistin levels were significantly decreased to normal control levels. No significant difference in baseline resistin levels was found between the high-risk group and the low-risk group of coronary artery aneurysms. We confirmed that resistin was an acute inflammatory protein, but its concentrations were unlikely to predict the prognosis of disease in acute KD patients.
    Agents and Actions 11/2010; 59(11):915-20. DOI:10.1007/s00011-010-0202-8 · 2.14 Impact Factor
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    ABSTRACT: Asthma is the most common chronic disorder in childhood and asthma exacerbation is an important cause of childhood morbidity and hospitalization. Allergic responses are known to be biased toward T-helper type 2 in asthmatics; however, the pathogenesis of asthma is not simple, and our understanding of the disease mechanism remains incomplete. The aim of the present study was to identify protein expression signatures that reflect acute exacerbation of asthma. Plasma was taken twice from pediatric asthmatic patients, once during asthma exacerbation and once during a stable period. Plasma was also taken from healthy children as a control. The protein profiles of plasma during asthma exacerbation were analyzed by 2-DE and 49 spots were differentially expressed during asthma exacerbation. Thirty-eight of the spots were successfully identified by MALDI-TOF MS. Proteins up- or down-regulated during asthma exacerbation were involved in responses to stress and pathogens, in the complement and coagulation cascades, and in acute-phase responses. Among the differentially expressed proteins, up-regulation of alpha-1-antitrypsin and complement component C7 was confirmed by nephelometry and ELISA. Our present results suggest that protease inhibitors and complement components may be involved in asthma exacerbation, and plasma level of alpha-1-antitrypsin may be a potential biomarker for asthma.
    Proteomics. Clinical applications 01/2008; 2(1):46-54. DOI:10.1002/prca.200780065 · 2.68 Impact Factor
  • Pediatrics International 09/2007; 49(4):522-5. DOI:10.1111/j.1442-200X.2007.02417.x · 0.73 Impact Factor
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    ABSTRACT: Atopic dermatitis develops as a result of complex interactions between several genetic and environmental factors. To date, 4 genome-wide linkage studies of atopic dermatitis have been performed in Caucasian populations, however, similar studies have not been done in Asian populations. The aim of this study was to identify chromosome regions linked to atopic dermatitis in a Japanese population. We used a high-density, single nucleotide polymorphism genotyping assay, the Illumina BeadArray Linkage Mapping Panel (version 4) comprising 5,861 single nucleotide polymorphisms, to perform a genome-wide linkage analysis of 77 Japanese families with 111 affected sib-pairs with atopic dermatitis. We found suggestive evidence for linkage with 15q21 (LOD = 2.01, NPL = 2.87, P = .0012) and weak linkage to 1q24 (LOD = 1.26, NPL = 2.44, P = .008). We report the first genome-wide linkage study of atopic dermatitis in an Asian population, and novel loci on chromosomes 15q21 and 1q24 linked to atopic dermatitis. Identification of novel causative genes for atopic dermatitis will advance our understanding of the pathogenesis of atopic dermatitis.
    BMC Dermatology 02/2007; 7:5. DOI:10.1186/1471-5945-7-5
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    ABSTRACT: Tumor necrosis factor (TNF) is a potent inflammatory cytokine that contributes to airway inflammation in asthma. Previous studies have reported that a G-to-A transition at position -308 (-308G/A, also referred to as TNF-alpha-308*1 and 308*2 respectively), is associated with asthma, but other studies have shown conflicting results. To investigate a possible association between the TNF-308G/A polymorphism and asthma, we performed transmission disequilibrium tests and a case-control study (family samples: 495 members in 165 Japanese trio families with one asthmatic child and both parents; case-control samples: 461 Japanese asthmatic children and 465 healthy controls). To increase the sample size and power, we performed a meta-analysis of all available relevant studies, including 2,477 asthmatics and 3,217 controls. We did not find a significant association between the TNF-308G/A polymorphism and childhood atopic asthma in two independent Japanese populations (P>0.05); however, meta-analysis revealed that the TNF-308G/A polymorphism was statistically significantly associated with asthma. The combined odds ratio with a fixed effects model and with a random effects for TNF-308A was 1.46 (95% confidence interval [CI], 1.27-1.68, P=0.0000001) and 1.46 (95% CI, 1.20-1.77, P=0.00014) respectively. Our data further support the importance of the TNF region in the development of asthma.
    Journal of Human Genetics 02/2006; 51(8):677-85. DOI:10.1007/s10038-006-0007-3 · 2.53 Impact Factor
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    ABSTRACT: The levels of naturally occurring IgG, IgGl and lgG2 antibodies against polyvalent pneumococcal capsular polysaccharide antigen (Pneumovax®) were compared between atopic and nonatopic children with different ages, 6-12 months and 1, 2, 3, 4, 5-9 and 10-15 years, by enzyme-linked immunosorbent assay. Children with asthma, atopic dermatitis, food allergy or a combination of these, and those having serum IgE levels exceeding 50 IU/mL at 6-12 months old and 100 IU/mL at more than 1-year-old were included as atopic groups. Asymptomatic children whose serum IgE levels were less than these atopic standards and those not having detectable IgE antibodies to Dermatophagoides farinae comprised the nonatopic groups. Geometric mean levels of IgG and IgG1 antibodies against pneumococcal antigen increased steadily with age, and that of IgG2 antibodies was low until 3 years of age and then gradually increased age-dependently up to 15 years of age. The levels of IgG antibody as well as IgG1 and IgG2 antibodies were not significantly different between atopic and nonatopic children in any age group. This suggests that the immune response to the most common bacterial pathogen in the respiratory tract does not influence atopic status.
    Allergology International 01/1998; 47(3):183-186. DOI:10.2332/allergolint.47.183
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    ABSTRACT: A 15-year-old girl with common variable immunodeficiency contracted hepatitis C, which progressed to liver cirrhosis and finally to hepatic failure 5 years later. Since she was agammaglobulinaemic, hepatitis C virus (HCV) infection was diagnosed on the basis of HCV-RNA detection. Quantification of her sera showed high levels of HCV-RNA (more than 10(7) copies of RNA/mL), which implied active viral replication. There were no other hepatotoxic factors except HCV infection. The initial liver biopsy at 16 years of age and the autopsy confirmed a rapid progression in liver histopathological change over 4 years. Conclusion: Contrary to the widely held view of a benign short-term prognosis in paediatric hepatitis C, progressive fatal liver disease can develop in some patients with HCV infection. Such a rapid progression of liver injury provides the rationale for antiviral therapy in at least certain high risk groups of these children. Hepatitis C may progress rapidly in an immune deficiency condition.
    European Journal of Pediatrics 08/1996; 155(7):532-4. DOI:10.1007/BF01957899 · 1.98 Impact Factor
  • Clinical Pediatric Endocrinology 01/1996; 5(1):31-36. DOI:10.1297/cpe.5.31