Effect of Simulated Patient Practice on the Self-Efficacy of Japanese Undergraduate Dietitians in Nutrition Care Process Skills.

OBJECTIVE: To examine the effect of an adapted simulated patient (SP) intervention on self-efficacy in nutrition care process skills. DESIGN: A repeated-measures design using a 25-item survey divided into 7 nutrition professional practice competencies (PPCs) employing a 5-point self-efficacy scale (1 = lowest to 5 = highest) administered immediately before and after the intervention. SETTING: A private Japanese university. PARTICIPANTS: Ninety Japanese third-year dietetics undergraduates aged 20-38 years. INTERVENTION: An adapted SP activity practicing nutrition care process skills for the infirm elderly population. MAIN OUTCOME MEASURES: Pre- to postintervention self-efficacy response scores and feedback. ANALYSIS: Mean preintervention survey scores were used to divide participants into statistical quartiles (Q1 indicated lowest mean scores and Q3, highest mean scores). Wilcoxon signed-rank tests compared each PPC's pre- and postintervention means. Kruskal-Wallis tests examined changes in quartiles' scores within each PPC. RESULTS: Self-efficacy improved significantly in PPCs relating to application of appropriate medical ethics and interpersonal skills (P = .02), appropriate nutrition assessment (P = .04), and creation of a nutrition management plan and nutrition intervention (P = .03). Self-efficacy of Q1 and Q2 rose significantly in most PPCs, although not for acting as a dietitian within a medical care team, whereas that of Q3 decreased for all PPCs. CONCLUSIONS AND IMPLICATIONS: Among initially low self-efficacy dietetics undergraduates, the SP intervention enhanced self-efficacy in 3 of the 6 PPCs practiced directly and may facilitate more realistic self-views among initially high self-efficacy students. However, further research in the design, implementation, and efficacy of this type of training is recommended to gauge its effects on the quality of related professional practice.

JNK1 controls mast cell degranulation and IL-1{beta} production in inflammatory arthritis.

Rheumatoid arthritis (RA) is a chronic inflammatory disease marked by bone and cartilage destruction. Current biologic therapies are beneficial in only a portion of patients; hence small molecules targeting key pathogenic signaling cascades represent alternative therapeutic strategies. Here we show that c-Jun N-terminal kinase (JNK) 1, but not JNK2, is critical for joint swelling and destruction in a serum transfer model of arthritis. The proinflammatory function of JNK1 requires bone marrow-derived cells, particularly mast cells. Without JNK1, mast cells fail to degranulate efficiently and release less IL-1ß after stimulation via Fcγ receptors (FcγRs). Pharmacologic JNK inhibition effectively prevents arthritis onset and abrogates joint swelling in established disease. Hence, JNK1 controls mast cell degranulation and FcγR-triggered IL-1ß production, in addition to regulating cytokine and matrix metalloproteinase biosynthesis, and is an attractive therapeutic target in inflammatory arthritis.

Dietary intake, neutrophil fatty acid profile, serum antioxidant vitamins and oxygen radical absorbance capacity in patients with ulcerative colitis.

Nutrition may play an important role in the pathogenesis and treatment of ulcerative colitis. Several studies suggest an association between dietary factors and the onset of ulcerative colitis; however, only few studies have examined the relationship between dietary intake and relapse of ulcerative colitis. The aim of this study was to assess the dietary intake and antioxidative capacity of ulcerative colitis patients and to elucidate the efficacy of dietary therapy for ulcerative colitis. Dietary intake, fatty acid composition of phospholipids in plasma and neutrophils, serum fat-soluble vitamin levels, and oxygen radical absorbance capacity were analyzed in 29 ulcerative colitis patients (7 males and 22 females), who were treated at the Department of Gastroenterology, Okayama University Hospital. Total fat intake, fat energy ratio and linoleic acid intake were significantly lower, while protein and carbohydrate intakes were significantly higher, in the patients than age- and sex-matched controls. In the neutrophil phospholipids of ulcerative colitis patients, significantly higher levels of linoleic aicd and arachidonic acid and a lower level of eicosapentaenoic acid were observed. The concentrations of serum retinol and beta-carotene but not alpha-tocopherol were significantly lower and serum oxygen radical absorbance capacity was also lower than in the controls. Significant correlations between serum oxygen radical absorbance capacity and retinol (r = 0.567, p = 0.0031), alpha-tocopherol (r = 0.560, p = 0.0036) and beta-carotene (r = 0.440, p = 0.0279) concentrations were observed in the ulcerative colitis patients. A diet restricting the intake of linoleic acid and supplemented with eicosapentaenoic acid and antioxidative vitamins may be recommendable for the nutritional management of ulcerative colitis patients.

O-methylated catechins from tea leaves inhibit multiple protein kinases in mast cells.

Tea contains a variety of bioactive compounds. In this study, we show that two O-methylated catechins, (-)-epigallocatechin-3-O-(3-O-methyl) gallate and (-)-epigallocatechin-3-O-(4-O-methyl) gallate, inhibit in vivo mast cell-dependent allergic reactions more potently than their nonmethylated form, (-)-epigallocatechin-3-O-gallate. Consistent with this, these O-methylated catechins inhibit IgE/Ag-induced activation of mouse mast cells: histamine release, leukotriene release, and cytokine production and secretion were all inhibited. As a molecular basis for the catechin-mediated inhibition of mast cell activation, Lyn, Syk, and Bruton's tyrosine kinase, the protein tyrosine kinases, known to be critical for early activation events, are shown to be inhibited by the O-methylated catechins. In vitro kinase assays using purified proteins show that the O-methylated catechins can directly inhibit the above protein tyrosine kinases. These catechins inhibit IgE/Ag-induced calcium response as well as the activation of downstream serine/threonine kinases such as Akt and c-Jun N-terminal kinase. These observations for the first time have revealed the molecular mechanisms of antiallergic effects of tea-derived catechins.