行政で働く新人保健師の新任期現任教育におけるプリセプターによる取り組みの現状

行政で働く新人保健師の新任期現任教育におけるプリセプターによる取り組みの現状を明らかにすることを目的に、A県の行政機関で働く過去5年以内にプリセプターを経験した保健師を対象に質問紙調査を行い、75名より有効回答を得た。その結果、プリセプターを担っている保健師の多くは経験年数11年目以上の主任レベル以上で、半数以上は研修の受講、事前打ち合わせ、サポートがなく、64%が困った経験を有していた。また、研修責任者、教育担当者との事前打ち合わせは新人保健師の理解と、教育担当者との事前打ち合わせは新人保健師との良好な関係と、それぞれ有意な関連が認められた

A novel indole compound MA-35 attenuates renal fibrosis by inhibiting both TNF-α and TGF-β1 pathways

Renal fibrosis is closely related to chronic inflammation and is under the control of epigenetic regulations. Because the signaling of transforming growth factor-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α) play key roles in progression of renal fibrosis, dual blockade of TGF-β1 and TNF-α is desired as its therapeutic approach. Here we screened small molecules showing anti-TNF-α activity in the compound library of indole derivatives. 11 out of 41 indole derivatives inhibited the TNF-α effect. Among them, Mitochonic Acid 35 (MA-35), 5-(3, 5-dimethoxybenzyloxy)-3-indoleacetic acid, showed the potent effect. The anti-TNF-α activity was mediated by inhibiting IκB kinase phosphorylation, which attenuated the LPS/GaIN-induced hepatic inflammation in the mice. Additionally, MA-35 concurrently showed an anti-TGF-β1 effect by inhibiting Smad3 phosphorylation, resulting in the downregulation of TGF-β1-induced fibrotic gene expression. In unilateral ureter obstructed mouse kidney, which is a renal fibrosis model, MA-35 attenuated renal inflammation and fibrosis with the downregulation of inflammatory cytokines and fibrotic gene expressions. Furthermore, MA-35 inhibited TGF-β1-induced H3K4me1 histone modification of the fibrotic gene promoter, leading to a decrease in the fibrotic gene expression. MA-35 affects multiple signaling pathways involved in the fibrosis and may recover epigenetic modification; therefore, it could possibly be a novel therapeutic drug for fibrosis

A市市民の健康習慣とはつらつ感の実態 2016年の調査から(第3報)

　A市市民の健康習慣とはつらつ感の実態を明らかにするため，年齢階級別かつ性別で市民3000 人を無作為に抽出し，郵送による自記式質問紙調査を行った．その結果，1248 件（回収率41.6%）を回収し，性別，年齢，はつらつ感の記載のないものを除外し，1207 件を分析対象とした（有効回答率96.7%）．はつらつ感は「毎日はつらつ」155 人（12.8%），「まあまあはつらつ」727 人（60.2%），「あまりはつらつとしていない」261人（21.6%），「はつらつとしていない」64 人（5.3%）であった．はつらつ群と非はつらつ群の2 群間で有意差がみられたのは，「心や精神の病気」，「主観的健康観」と，健康習慣では，「30 分以上の早歩き」「エスカレーター・エレベーターの使用」「運動不足の自覚」「運動する仲間」「主食・主菜・副菜のそろった食事」「家族や仲間との楽しい食事」「よく噛むことの心がけ」「食生活の問題意識」「地元の食材の利用」「定期的な体重測定」「自分のBMI の認識」「年1 回の健康診査の受診」「身近に相談できる人・環境」「睡眠による休養」「近所の人のお互いに助け合う気持ち」「近所の人との会話」等の30 項目であった．　A市市民がはつらつと生活するためには，適切な運動や栄養バランスの良い食事等を啓蒙するとともに，健康管理では体重管理や健康診査の受診の勧奨が重要であり，また，はつらつ感は心の状態が反映されていることが推察され，近所の人との会話やつながり等ソーシャル・キャピタルの醸成や心の健康支援の取り組みの充実が示唆された

Mitochonic Acid 5 (MA-5) Facilitates ATP Synthase Oligomerization and Cell Survival in Various Mitochondrial Diseases

Mitochondrial dysfunction increases oxidative stress and depletes ATP in a variety of disorders. Several antioxidant therapies and drugs affecting mitochondrial biogenesis are undergoing investigation, although not all of them have demonstrated favorable effects in the clinic. We recently reported a therapeutic mitochondrial drug mitochonic acid MA-5 (Tohoku J. Exp. Med., 2015). MA-5 increased ATP, rescued mitochondrial disease fibroblasts and prolonged the life span of the disease model “Mitomouse” (JASN, 2016). To investigate the potential of MA-5 on various mitochondrial diseases, we collected 25 cases of fibroblasts from various genetic mutations and cell protective effect of MA-5 and the ATP producing mechanism was examined. 24 out of the 25 patient fibroblasts (96%) were responded to MA-5. Under oxidative stress condition, the GDF-15 was increased and this increase was significantly abrogated by MA-5. The serum GDF-15 elevated in Mitomouse was likewise reduced by MA-5. MA-5 facilitates mitochondrial ATP production and reduces ROS independent of ETC by facilitating ATP synthase oligomerization and supercomplex formation with mitofilin/Mic60. MA-5 reduced mitochondria fragmentation, restores crista shape and dynamics. MA-5 has potential as a drug for the treatment of various mitochondrial diseases. The diagnostic use of GDF-15 will be also useful in a forthcoming MA-5 clinical trial

CE-MS-Based Identification of Uremic Solutes Specific to Hemodialysis Patients

Uremic toxins are suggested to be involved in the pathophysiology of hemodialysis (HD) patients. However, the profile of uremic solutes in HD patients has not been fully elucidated. In this study using capillary electrophoresis mass spectrometry (CE-MS), we comprehensively quantified the serum concentrations of 122 ionic solutes before and after HD in 11 patients. In addition, we compared the results with those in non-HD patients with chronic kidney disease (CKD) to identify HD patient-specific solutes. We identified 38 solutes whose concentrations were higher in pre-HD than in CKD stage G5. Ten solutes among them did not significantly accumulate in non-HD CKD patients, suggesting that these solutes accumulate specifically in HD patients. We also identified 23 solutes whose concentrations were lower in both pre- and post-HD than in CKD stage G5. The serum levels of 14 solutes among them were not affected by renal function in non-HD patients, suggesting that these solutes tend to be lost specifically in HD patients. Our data demonstrate that HD patients have a markedly different profile of serum uremic solute levels compared to that in non-HD CKD patients. The solutes identified in our study may contribute to the pathophysiology of HD patients