ゲンチョ ゼンソクジ ト ケンコウジ ノ シンタイナイ ブイ ノ ガイネン キノウ ノ リカイ オ チュウシン トシタ ケントウ

健康障害児の｢病気｣に関する教育の基礎資料を得るために､喘息児48名､健康児152名(小学校3年~6年)を｣対象に､身体内部位の機能に関する質問紙調査を実施した｡この結果は､2段階にわたり採点され､健康児の方が､身体内部位の機能に関する知識に関しては高得点をとり､その差も有意なものであった｡筆者の先行研究では､身体内部位､特に｢肺｣に関してのイメージは喘息児の方が健康児より早く出現するという傾向が報告されている｡この矛盾点を考察する中で､｢病気｣やそれに関する様々な情報の処理方法が異なることが示唆された｡つまり喘息児は､｢病気｣やそれに関わる情報について拡散的思考を用いて処理し､健康児は収束的思考を用いて処理しているように推測された｡過去､多くの研究は子どものパフォーマンスをもって｢病気｣や関連概念の研究を行ってきたが､この点については見直しが必要であろう

LRRK2 directly phosphorylates Akt1 as a possible physiological substrate: Impairment of the kinase activity by Parkinson’s disease-associated mutations

AbstractLRRK2 is the causal molecule for autosomal-dominant familial Parkinson’s disease, although its true function, including its physiological substrates, remains unknown. Here, using in vitro kinase assay with recombinant proteins, we demonstrated for the first time that LRRK2 directly phosphorylates Akt1, a central molecule involved in signal transduction for cell survival and prevention of apoptosis. Ser473, one of two amino acids essential for Akt1 activation, was the target site for LRRK2. A knockdown experiment using intact cells also demonstrated LRRK2-mediated phosphorylation of Akt1 (Ser473), suggesting that Akt1 is a convincing candidate for the physiological substrate of LRRK2. The disease-associated mutations, R1441C, G2019S, and I2020T, exhibited reduced interaction with, and phosphorylation of, Akt1, suggesting one possible mechanism for the neurodegeneration caused by LRRK2 mutations.Structured summary of protein interactionsLRRK2phosphorylates Akt1 by protein kinase assay (View Interaction 1, 2, 3).LRRK2 phosphorylates MBP by protein kinase assay (View Interaction 1, 2).LRRK2 binds to Akt1 by pull down (View Interaction 1, 2, 3)

LRRK2 Phosphorylates Tubulin-Associated Tau but Not the Free Molecule: LRRK2-Mediated Regulation of the Tau-Tubulin Association and Neurite Outgrowth

Leucine-rich repeat kinase 2 (LRRK2), a large protein kinase containing multi-functional domains, has been identified as the causal molecule for autosomal-dominant Parkinson's disease (PD). In the present study, we demonstrated for the first time that (i) LRRK2 interacts with tau in a tubulin-dependent manner; (ii) LRRK2 directly phosphorylates tubulin-associated tau, but not free tau; (iii) LRRK2 phosphorylates tau at Thr181 as one of the target sites; and (iv) The PD-associated LRRK2 mutations, G2019S and I2020T, elevated the degree of tau-phosphorylation. These results provide direct proof that tau is a physiological substrate for LRRK2. Furthermore, we revealed that LRRK2-mediated phosphorylation of tau reduces its tubulin-binding ability. Our results suggest that LRRK2 plays an important role as a physiological regulator for phosphorylation-mediated dissociation of tau from microtubules, which is an integral aspect of microtubule dynamics essential for neurite outgrowth and axonal transport

病弱児の「病気」の概念 : そのカテゴリー化の発達的変化と健康児との比較

病気に関する知識や概念を子どもに与える際の基礎資料として、カテゴリーとしての「病気」の概念を取りあげ、自由想起法による調査を行った。対象は小学校3年から6年の腎ネフ児74名、喘息児82名、健康児154名の計310名であった。分析の結果、病弱児、健康児共、病名外反応が5年生で増加し、その後減少するという共通の傾向を示し、先行研究の結果とあわせて「病気」に関する概念の発達にとって11歳前後がキーエイジとなることが示唆された。また「病気」の概念の広がりに関しては病弱児と健康児とでは違いはないものの、その内的構造には差異があり、特に腎ネフ児の概念構造が特徴的であることが明らかとなった。しかしながら「病気」の概念の発達も他の諸概念と同じく多元的なものであり、これらの差異は発達的な遅速を示すものではないと考えられる。This study investigated the development of children\u27s concepts of illness. A total of 310 children (74 with renal disease, 82 with asthma, and 154 with no special health problems), aged 8 to 12 years, were examined by the method of free recall. Children were asked to write the names of illnesses as many as possible. A comparison across age groups showed that a developmental change in concepts of illness occurred at about 11 years of age. Although the expansion of illness concepts and the developmental tendency were similar, the inner structure of illness concepts was different in the children with chronic illnesses and in those with no special health problems. Because, like other concepts, illness concepts are multi-dimensional, their differences would not be developmental differences