Signal amplification in electrochemical detection of buckwheat allergenic protein using field effect transistor biosensor by introduction of anionic surfactant

AbstractFood allergens, especially buckwheat proteins, sometimes induce anaphylactic shock in patients after ingestion. Development of a simple and rapid screening method based on a field effect transistor (FET) biosensor for food allergens in food facilities or products is in demand. In this study, we achieved the FET detection of a buckwheat allergenic protein (BWp16), which is not charged enough to be electrically detected by FET biosensors, by introducing additional negative charges from anionic surfactants to the target proteins. A change in the FET characteristics reflecting surface potential caused by the adsorption of target charged proteins was observed when the target sample was coupled with the anionic surfactant (sodium dodecyl sulfate; SDS), while no significant response was detected without any surfactant treatment. It was suggested that the surfactant conjugated with the protein could be useful for the charge amplification of the target proteins. The surface plasmon resonance analysis revealed that the SDS-coupled proteins were successfully captured by the receptors immobilized on the sensing surface. Additionally, we obtained the FET responses at various concentrations of BWp16 ranging from 1ng/mL to 10μg/mL. These results suggest that a signal amplification method for FET biosensing is useful for allergen detection in the food industry

A Study of Control of Social Responsibility Strategy : Possibility of Enterprise Disk Management

1.はじめに 2.ERMの可能性 3.伝統的なコントロール理論 4.革新的な社会的責任戦略のコントロール理論 5.むす

フランスの社会的責任戦略コントロールの研究 : ダノン社とラファージュ社の二つの事例をめぐって

1.はじめに / ２.企業の社会的責任（CSR）戦略コントロールの生成とその起源 / ３.フランスにおけるCSR戦略コントロールの事例研究 / ４.むす

Familial immune‐mediated aplastic anaemia in six different families

Abstract We studied the pathophysiology of aplastic anaemia (AA) in six different pairs of relatives without a family history of hematologic disorders or congenital AA. Five and four of the six pairs shared the HLA‐DRB1*15:01 and B*40:02 alleles, respectively. Glycosylphosphatidylinositol‐anchored protein‐deficient blood cells were detected in eight of the 10 patients evaluated. In a mother‐daughter pair from one family, flow cytometry detected leukocytes lacking HLA‐A2 due to loss of heterogeneity in chromosome 6p. Whole‐exome sequencing of the family pair revealed a missense mutation in MYSM1. These results suggest that genetic inheritance of immune traits might underlie familial AA in some patients