No abstract

Combined modality treatment consisting of aromatherapy, footsoak, and reflexology appears to be effective for alleviating fatigue in terminally ill cancer patients. To confirm safety and effectiveness of this combined modality treatment, further investigation including randomized treatment assignment is warranted.

a b s t r a c tMast cell activation by immunoglobulin E (IgE)-mediated stimuli is a central event in the pathogenesis of allergic disorders. The present report shows that treatment with pentagalloylglucose (PGG) resulted in a down-regulation of FceRI surface expression on mucosal-type murine bone marrowderived mast cells (mBMMCs), which correlated with a reduction in IgE-mediated activation of mBMMCs. Furthermore, PGG prevented development of allergic diarrhea in a food-allergy mouse model and suppressed the up-regulated FceRI surface expression on mast cells derived from the food-allergy mouse colon. These findings on PGG suggest its therapeutic potential for allergic diseases through suppressing the FceRI surface expression.

Here, we report a case of Cronkhite-Canada

Surface expression levels of high-affinity immunoglobulin E (IgE) receptors (Fce eRI) on mast cells are regulated by constitutive internalization from the plasma membrane, which is thought to be an important determinant of Fce eRI-mediated signaling potential. However, molecular mechanism of Fce eRI trafficking has remained poorly understood. Rab proteins are small guanosine 5 -triphosphatases (GTPases) involved in the regulation of membrane traffic. In particular, Rab5 has been shown to regulate transport in the early endocytic pathway, whereas it is not known whether the Fce eRI surface expression levels are regulated by Rab5. In this study, we investigated the role of individual Rab5 isoforms in mast cells by small interfering RNA knockdown method. Our results demonstrate that Rab5a knockdown enhanced Fce eRI-dependent mast cell activation and upregulated Fce eRI surface expression in its steady state. In contrast, Rab5c knockdown caused suppression of the activation. These findings revealed modulatory and individual roles of Rab5 isoforms in mast cell functions.