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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. · 1.59 Impact Factor
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Tatsuji Nishioka,
Kazuhiko Uchida,
Kohji Meno,
Takashi Ishii, Takeshi Aoki,
Yoshiko Imada,
Yuka Makino,
Kenji Hirata,
Yuri Matsumoto,
Tadao Arinami,
Emiko Noguchi
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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. · 1.97 Impact Factor
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Pediatrics International 09/2007; 49(4):522-5. · 0.63 Impact Factor
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Hisako Enomoto,
Emiko Noguchi,
Shigeruko Iijima,
Takenori Takahashi,
Kazuhito Hayakawa,
Mikako Ito,
Toshiyuki Kano, Takeshi Aoki,
Yoichi Suzuki,
Minori Koga,
Mayumi Tamari,
Tetsuo Shiohara,
Fujio Otsuka,
Tadao Arinami
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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.
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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. · 2.57 Impact Factor
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ABSTRACT: Critical illness polyneuropathy (CIP) is a sensorimotor polyneuropathy recognized in adult intensive care patients with sepsis and multiple organ dysfunction and only a few cases have been reported in children. Here we report a 13-year-old Japanese boy with CIP that developed during the course of encephalopathy. Two months after the onset of encephalopathy, he developed tetraplegia although consciousness had already recovered. Deep tendon reflex was absent. MRI of the brain and spinal cord was normal and no abnormality in the cerebrospinal fluid was detected. Motor and sensory nerve conduction velocities of the lower limbs and somatosensory evoked potential could not be detected. The motor activity subsequently showed gradual recovery, although standing and walking could not be achieved. Sural nerve biopsy performed 3 years after the onset showed severe reduction of the number of myelinated large-diameter fibers, thin myelin in almost all fibers and cluster formation of myelinated small-diameter fibers, indicating primary axonal degeneration with regeneration. We report here for the first time the neuropathological changes in peripheral nerves during the chronic stage of CIP in children.
Brain and Development 11/2005; 27(7):535-8. · 2.12 Impact Factor
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Hisako Enomoto,
Emiko Noguchi,
Shigeruko Iijima,
Takenori Takahashi,
Kazuhito Hayakawa,
Mikako Ito,
Toshiyuki Kano, Takeshi Aoki,
Yoichi Suzuki,
Minori Koga,
Mayumi Tamari,
Tetsuo Shiohara,
Fujio Otsuka,
Tadao Arinami,
惠美子 野口,
毅法 高橋,
藤男 大塚,
忠雄 有波
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ABSTRACT: Background 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. Methods 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. Results 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). Conclusion 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.
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Junko Nakayama,
Kenzo Hamano,
Nobuaki Iwasaki,
Satoko Nakahara,
Yumi Horigome,
Hisako Saitoh, Takeshi Aoki,
Takako Maki,
Masahiro Kikuchi,
Takuo Migita,
Tatsuyuki Ohto,
Yukako Yokouchi,
Ryuta Tanaka,
Makoto Hasegawa,
Akira Matsui,
Hideo Hamaguchi,
Tadao Arinami
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ABSTRACT: Febrile seizures (FSs) represent the most common form of childhood seizure. In the Japanese population, the incidence rate is as high as 7%. It has been recognized that there is a significant genetic component for susceptibility to this type of seizure. Two putative FS loci, FEB1 (chromosome 8q13–q21) and FEB2 (chromosome 19p), have been mapped. Furthermore, a mutation in the voltage-gated sodium (Na+)-channel &bgr;1 subunit gene ( SCN1B ) at chromosome 19q13.1 was identified in a family with a clinical subset, termed generalized epilepsy with febrile seizures plus (GEFS+). These loci are linked to some large families. In this study, we conducted a genome-wide linkage search for FS in one large family with subsequent linkage confirmation in 39 nuclear families. Significant linkage was found at D5S644 by multipoint non-parametric analysis using GENEHUNTER ( P = 5.4 × 10–6). Estimated &lgr; s at D5S644 was 2.5 according to maximum likelihood analysis. Significant linkage disequilibria with FS were observed at the markers D5S644 , D5S652 and D5S2079 in 47 families by transmission disequilibrium tests. These findings indicate that there is a gene on chromosome 5q14 – q15 that confers susceptibility to FSs and we call this gene FEB4 .
