Minimum Supersymmetric Standard Model on the Noncommutative Geometry

We have obtained the supersymmetric extension of spectral triple which specify a noncommutative geometry(NCG). We assume that the functional space H constitutes of wave functions of matter fields and their superpartners included in the minimum supersymmetric standard model(MSSM). We introduce the internal fluctuations to the Dirac operator on the manifold as well as on the finite space by elements of the algebra A in the triple. So, we obtain not only the vector supermultiplets which meditate SU(3)xSU(2)xU(1)_Y gauge degrees of freedom but also Higgs supermultiplets which appear in MSSM on the same standpoint. Accoding to the supersymmetric version of the spectral action principle, we calculate the square of the fluctuated total Dirac operator and verify that the Seeley-DeWitt coeffients give the correct action of MSSM. We also verify that the relation between coupling constants of $SU(3)$,$SU(2)$ and $U(1)_Y$ is same as that of SU(5) unification theory

Supersymmetric Yang-Mills Theory on the Noncommutative Geometry

Recently, we found the supersymmetric counterpart of the spectral triple. When we restrict the representation space to the fermionic functions of matter fields, the counterpart which we name "the triple" reduces to the original spectral triple which defines noncommutative geometry. We see that the fluctuation to the supersymmetric Dirac operator induced by algebra in the triple generates vector supermultiplet which mediates gauge interaction. Following the supersymmetric version of spectral action principle, we calculate the heat kernel expansion of the square of fluctuated Dirac operator and obtain the correct supersymmetric Yang-Mills action with U(N) gauge symmetry.Comment: arXiv admin note: text overlap with arXiv:1201.344

Neuregulin 1 Type II-ErbB Signaling Promotes Cell Divisions Generating Neurons from Neural Progenitor Cells in the Developing Zebrafish Brain.

Post-mitotic neurons are generated from neural progenitor cells (NPCs) at the expense of their proliferation. Molecular and cellular mechanisms that regulate neuron production temporally and spatially should impact on the size and shape of the brain. While transcription factors such as neurogenin1 (neurog1) and neurod govern progression of neurogenesis as cell-intrinsic mechanisms, recent studies show regulatory roles of several cell-extrinsic or intercellular signaling molecules including Notch, FGF and Wnt in production of neurons/neural progenitor cells from neural stem cells/radial glial cells (NSCs/RGCs) in the ventricular zone (VZ). However, it remains elusive how production of post-mitotic neurons from neural progenitor cells is regulated in the sub-ventricular zone (SVZ). Here we show that newborn neurons accumulate in the basal-to-apical direction in the optic tectum (OT) of zebrafish embryos. While neural progenitor cells are amplified by mitoses in the apical ventricular zone, neurons are exclusively produced through mitoses of neural progenitor cells in the sub-basal zone, later in the sub-ventricular zone, and accumulate apically onto older neurons. This neurogenesis depends on Neuregulin 1 type II (NRG1-II)-ErbB signaling. Treatment with an ErbB inhibitor, AG1478 impairs mitoses in the sub-ventricular zone of the optic tectum. Removal of AG1478 resumes sub-ventricular mitoses without precedent mitoses in the apical ventricular zone prior to basal-to-apical accumulation of neurons, suggesting critical roles of ErbB signaling in mitoses for post-mitotic neuron production. Knockdown of NRG1-II impairs both mitoses in the sub-basal/sub-ventricular zone and the ventricular zone. Injection of soluble human NRG1 into the developing brain ameliorates neurogenesis of NRG1-II-knockdown embryos, suggesting a conserved role of NRG1 as a cell-extrinsic signal. From these results, we propose that NRG1-ErbB signaling stimulates cell divisions generating neurons from neural progenitor cells in the developing vertebrate brain

〈学術論文〉特別支援学校(聴覚障害)幼稚部における交流保育の現状と課題

Keyword: integrated childcare program preschools hearing-impaired childre

クラスリン被覆小孔の構成分子との会合がμオピオイド受容体下流のβアレスチンを介したMAPK経路のシグナル伝達を制御する

京都大学新制・課程博士博士(医学)甲第24525号医博第4967号新制||医||1065(附属図書館)京都大学大学院医学研究科医学専攻(主査)教授 渡邊 直樹, 教授 中川 一路, 教授 秋山 芳展学位規則第4条第1項該当Doctor of Medical ScienceKyoto UniversityDFA

論理的思考の方略化を図る国語科の学習デザイン : アクティブ・ラーニングを視点とした高学年説明的文章の指導の在り方

　育成すべき資質・能力の中核「深く考える（思考力）」の構成要素として，「論理的思考力」及び「メタ認知・学び方の学び」が挙げられている。これを受け，これまでも重視されてきた論理的思考をさらに自覚的なものにすること，つまり「論理的思考の方略化」を図ることが必要であり，そのための学習デザインを検討することが求められると考える。本研究は，国語科の説明的文章を教材とした学習指導において，アクティブ・ラーニングを視点として学習デザインの要件を措定，実践を通して具体化し，その有効性を検証するものである。小学校第５学年児童を対象に実践を行い，論理的思考を促す課題に取り組む学習場面において，学習者の行為である「認知プロセスの外化」の様相から「論理的思考の方略化」の実際を分析・考察した。その結果，「論理的思考の方略化」を図る学習デザインの要件として，探究的な課題（単元レベル）と論理的思考を促す課題（１時間レベル）の設定，対話の重視，パターンや原理を含む教材の選択，思考ツールとしての教具の工夫，学習の振り返りの取り組みの６点が有効であることを明らかにした

Nuclear Hormone Receptor Expression in Mouse Kidney and Renal Cell Lines

Nuclear hormone receptors (NHRs) are transcription factors that regulate carbohydrate and lipid metabolism, immune responses, and inflammation. Although several NHRs, including peroxisome proliferator-activated receptor-γ (PPARγ) and PPARα, demonstrate a renoprotective effect in the context of diabetic nephropathy (DN), the expression and role of other NHRs in the kidney are still unrecognized. To investigate potential roles of NHRs in the biology of the kidney, we used quantitative real-time polymerase chain reaction to profile the expression of all 49 members of the mouse NHR superfamily in mouse kidney tissue (C57BL/6 and db/m), and cell lines of mesangial (MES13), podocyte (MPC), proximal tubular epithelial (mProx24) and collecting duct (mIMCD3) origins in both normal and high-glucose conditions. In C57BL/6 mouse kidney cells, hepatocyte nuclear factor 4α, chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) and COUP-TFIII were highly expressed. During hyperglycemia, the expression of the NHR 4A subgroup including neuron-derived clone 77 (Nur77), nuclear receptor-related factor 1, and neuron-derived orphan receptor 1 significantly increased in diabetic C57BL/6 and db/db mice. In renal cell lines, PPARδ was highly expressed in mesangial and proximal tubular epithelial cells, while COUP-TFs were highly expressed in podocytes, proximal tubular epithelial cells, and collecting duct cells. High-glucose conditions increased the expression of Nur77 in mesangial and collecting duct cells, and liver x receptor α in podocytes. These data demonstrate NHR expression in mouse kidney cells and cultured renal cell lines and suggest potential therapeutic targets in the kidney for the treatment of DN

<資料> ベトナムホーチミン市における聴覚障害児に対する早期介入の現状と課題

departmental bulletin pape

Properdin has an ascendancy over factor H regulation in complement-mediated renal tubular damage

BACKGROUND: Urinary (U)-complement components have been detected in patients with proteinuric renal diseases, and complement activation via the alternative pathway (AP) is believed to play a role in renal tubular damage. The present study aimed to examine the regulation of complement AP activation in patients with renal tubular damage by focusing on the balance between properdin (P) and factor H (fH). METHODS: In the in vivo studies, U concentrations of P, fH and membrane attack complex (MAC) were measured in patients with renal diseases using an enzyme-linked immunosorbent assay (ELISA), and their relationships with the clinical data were evaluated. In the in vitro studies, human proximal tubular epithelial cells (PTECs) were incubated with normal human serum (NHS), P-depleted serum (PDS), purified P and/or fH. Changes in cell morphology and phenotype were assessed by microscopy, real-time polymerase chain reaction (PCR), immunostaining and a cell viability assay. RESULTS: The U-P, fH and MAC concentrations were significantly higher in patients with renal disease than in normal controls and correlated with the U-protein and tubular damage markers. Furthermore, multivariate analysis revealed a relationship between P levels and tubular damage markers. There were no significant changes in morphology and mRNA expression in the AP components (P, fH, fB, C3, C5 and C9) after the addition of up to 25% NHS. Dose-dependent depositions of P or fH were observed after the addition of P or fH on PTECs. Depositions of P were not inhibited by fH in a mixture of a fixed concentration of P and a variable concentration of fH, and vice versa. Preincubation with the fixed concentration of P before the addition of NHS or PDS increased the depositions of P, C3 and MAC compared with incubation with intact NHS or intact PDS only; the depositions of C3 and MAC showed a serum-dependent trend. Preincubation with P before NHS addition significantly suppressed cell viability without causing morphological changes. CONCLUSIONS: In the pathogenesis of renal tubular damage, P can directly bind to PTECs and may accelerate AP activation by surpassing fH regulation