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Aim: Normal individuals are risk averse for decisions framed as gains but risk taking for decisions framed as losses. This framing effect is supposed to be attenuated in Alzheimer's disease (AD) patients. We investigated the effects of highlighting rewards versus highlighting punishments on the risky decision-making of AD patients. Method: Fourteen mild to moderate AD patients (Mini-Mental Status Examination score, 11–23; Clinical Dementia Rating, 1–2) and 16 healthy volunteers were recruited for the study. Subjects completed a computerized task on risky decision-making in which mathematically equivalent dilemmas were presented in terms of opportunities to gain monetary rewards (‘positive frame’) or avoid suffering losses (‘negative frame’). Results: As expected, AD patients chose more risky options under the positive frame than the negative frame, contrary to the control group (Z =−2.671, P= 0.007). The normal difference in the distribution of risky choices between positively and negatively framed dilemmas was significantly reduced in the AD group after we adjusted for years of education, mean age and depression (F= 5.321, P= 0.030). Deliberation time did not differ significantly between the two groups. Conclusion: These results suggest that AD patients making high-risk choices is associated with attenuated sensitivity to the emotional frames that highlight rewards or punishments, possibly reflecting altered evaluations of prospective gains and losses.

Mast cells are the principal effector cells involved in the allergic response, through the release of histamine. We investigated the effect of eriodictyol, derived from the painted maple and yerba santa, on mast cell degranulation and on an allergic response in an animal model. We also investigated its effect on the expression of the ceramide kinase (CERK) involved in calcium-dependent degranulation, and on ceramide activation by multiple cytokines. Eriodictyol suppressed the release of beta-hexosaminidase, a marker of degranulation, and the expression of interleukin (IL)-4 mRNA. It inhibited the expression of CERK mRNA, reduced the ceramide concentration in antigen-stimulated mast cells, and suppressed the passive cutaneous anaphylaxis (PCA) reaction in mice in a dose-dependent manner. These results suggest that eriodictyol can inhibit mast cell degranulation through inhibition of ceramide kinase, and that it might potentially serve as an anti-allergic agent.

Mast cells, the central effector cells involved in the allergic response, release histamine, arachidonic acid, and proinflammatory cytokines. We investigated the effect of the ethyl acetate fraction (EA), derived from Korean rice wine lees, on RBL-2H3 cell degranulation and passive cutaneous anaphylaxis in an animal model. The EA fraction suppressed the release of beta-hexosaminidase, a marker of degranulation, and the mRNA expression of interleukin-3 (IL-3) and IL-13. EA also successfully suppressed the passive cutaneous anaphylaxis (PCA) reaction in mice in a dose-dependent manner. These results suggest that EA can inhibit mast cell degranulation through the inhibition of IL-3 and IL-13 mRNA expression, and that EA may potentially serve as an anti-allergic agent.

Muscle disorders, such as muscular dystrophy, are associated with an increase in oxidative stress. Proposed treatments for muscular dystrophy, some in clinical trials, include gene therapy and muscle cell transplantation. In this study, we investigated the effects of idesolide, isolated from the fruits of Idesia polycarpa, on changes that occur in muscle disuse atrophy. We noted protective effects on oxidative stress response and HSP70 regulation. Pre-treatment with idesolide for 24 h maintained cell viability and decreased apoptosis in H(2)O(2)-treated C(2)C(12) muscle cells. The idesolide pretreatment also increased intracellular HSP70 protein. Our results suggest that idesolide inhibits cell death through induction of HSP70 in C(2)C(12) muscle cells. This work is the first to report that idesolide can regulate the decrease in HSP70 that occurs during skeletal muscle atrophy.