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Quality Control Protocol for Zebrafish Developmental Toxicity Studies
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A novel orexin antagonist from a natural plant was discovered using zebrafish behavioural analysis
Matsumoto Y, Oshida T, Obayashi I, Imai Y, Matsui K, Yoshida NL, Nagata N, OgawaK, Obayashi M, Kashiwabara T, Gu nji S, Nagasu T, Sugita Y, Tanaka T, Tsujimoto G, Katsunuma T, Akasawa A, Saito H.
Int Arch Allergy Immunol 129(4):327-40 2002
Abstract
BACKGROUND:
Analysis of genes that are differentially expressed in patients with atopic dermatitis (AD) and normal individuals will provide important information on the underlying molecular pathogenetic mechanisms of AD.
METHODS:
Transcript of freshly isolated peripheral blood T cells from 59 individuals were analyzed with a fluorescent differential display (FDD) method. Ninety-two differentially expressed genes were identified in this manner. Additionally, real-time quantitative RT-PCR was employed to investigate the expression of the FDD-selected genes and also genes related to T cell function.
RESULTS:
A number of genes, including CC chemokine receptor 4, T cell-specific tyrosine kinase (Emt/Itk), integrin beta1, integrin alpha6, IQGAP1 and MAR/SAR DNA-binding protein (SATB1), were shown to be more highly expressed in patients with moderate and/or severe AD than in controls or patients with mild AD. Because the products of these upregulated genes influence chemotaxis, adhesion, migration and Th2 polarization, it is suggested that in more severe AD, circulating T cells may function differently in this regard. Several other genes, the role of which in T cell function is currently unknown, were also found to be differentially expressed in AD. These included the heat shock protein 40 and vasopressin-activated calcium-mobilizing receptor 1.
CONCLUSION:
The upregulated genes identified in this work may serve as useful markers for moderate to severe AD as opposed to normal or mild AD and also as markers indicating progression to more severe AD. Further functional characterization will provide a better understanding of the pathophysiology of circulating T cells in AD.
Copyright 2002 S. Karger AG, Basel