Kac-Moody Lie algebras and associated groups

筑波大学University of Tsukuba博士（理学）Doctor of Philosophy in Science複素半単純リー環およびそれに対応する半単純リー群の研究は19世紀末に、Cartan,Killingによる分類が完成して以来、理論の再構成や一般化などの多くの研究がなされてきている。1968年、KacとMoodyは、カルタン行列から複素半単純リー環を構成するSerreの方法を拡張して、一般化されたカルタン行列からリー環を構成した。これらは、現在Kac-Moodyリー環と呼ばれ、有限次元とは限らないリー環であるが、整教論、微分方程式など広い分野への応用が発見され、数年来、活発に研究されている。一方、1955年Cheralleyは複素半単純リー環に対応して、半単純代数群を構成したが、これらはアフィン群スキームの概念に発展し、特種線形群、直交群などを含む可換環上の群として、整教論、代数幾何学などと関連して重要な研究対象となっている。森田氏は本論文で、Kac-Moodyリー環の構造を研究するとともに、複素半単純リー環に対応するChevalley群と類似の群をKac-Moodyリー環に対して考察し、次の結果を得ている。･･･1981この博士論文は内容の要約のみ公表していますdoctoral thesi

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Measurement of the Lifetime Difference in D0 Meson Decays

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Architecting a Reliable System

video/mp4Relentless scaling of silicon fabrication technology coupled with lower design tolerances are making ICs increasing susceptible to wear-out related permanent faults as well as transient faults (soft errors). A well known technique for tackling both transient and permanent faults is redundant execution, specifically space redundancy, wherein a program is executed redundantly on different processors, pipelines or functional units and the results are compared to detect faults.講演日: 平成25年6月26日講演場所: 情報科学研究科大講義室L1講演者所属: Indian Institute of Technology Bombayvide

1920 年代における地方財政問題の再検討―地方団体からみた両税委譲問題の一側面―

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Effect of principal strain directions on shear deformation characteristics of sand

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Image_3_Phagocytosis of Apoptotic Cells Is Specifically Upregulated in ApoE4 Expressing Microglia in vitro.TIF

Alzheimer’s disease (AD) is characterized by intracellular tau aggregates and extracellular deposition of amyloid-β (Aβ). The major genetic risk factor to develop AD is the Apolipoprotein E isoform 4 (ApoE4). ApoE4 may directly affect Aβ pathology, yet the exact role of ApoE4 in the progression of AD remains unclear. Although astrocytes are the main source of ApoE in brain tissue, other cell types might contribute to ApoE isotype-dependent effects. While ApoE expression does not play a relevant role in homeostatic microglia, we and others could recently show that ApoE expression is significant upregulated in disease-associated microglia including AD-mouse models and human AD. ApoE has been supposed to have an anti-inflammatory effect, with ApoE4 being less effective than ApoE3. However, ApoE-isotype specific effects on microglia function in disease have not been thoroughly investigated to date. In contrast to this, the role of ApoE2, the third most common major ApoE isoform, in neurodegeneration has not been characterized in detail, but it has been shown to delay the onset of disease in familial AD. To elucidate the differential roles of the three-major human ApoE isoforms on microglia function we each expressed the human ApoE isoforms in murine N9 microglia cells. We could show that ApoE4 specifically influences actin cytoskeleton rearrangement and morphology. In migration assays, ApoE4 significantly promotes cell motility. To quantify phagocytosis by microglia we established an uptake assay based on imaging flow cytometry. Although expression of ApoE4 led to significantly reduced uptake of Aβ in contrast to the other isoforms, we could show that ApoE4 specifically increased phagocytosis of apoptotic neuronal cells. Our findings show that ApoE4 intrinsically affects microglia physiology by upregulating motility and phagocytic behavior in vitro and may therefore specifically contribute to microglia dysregulation in AD.</p

Image_2_Phagocytosis of Apoptotic Cells Is Specifically Upregulated in ApoE4 Expressing Microglia in vitro.TIF

Alzheimer’s disease (AD) is characterized by intracellular tau aggregates and extracellular deposition of amyloid-β (Aβ). The major genetic risk factor to develop AD is the Apolipoprotein E isoform 4 (ApoE4). ApoE4 may directly affect Aβ pathology, yet the exact role of ApoE4 in the progression of AD remains unclear. Although astrocytes are the main source of ApoE in brain tissue, other cell types might contribute to ApoE isotype-dependent effects. While ApoE expression does not play a relevant role in homeostatic microglia, we and others could recently show that ApoE expression is significant upregulated in disease-associated microglia including AD-mouse models and human AD. ApoE has been supposed to have an anti-inflammatory effect, with ApoE4 being less effective than ApoE3. However, ApoE-isotype specific effects on microglia function in disease have not been thoroughly investigated to date. In contrast to this, the role of ApoE2, the third most common major ApoE isoform, in neurodegeneration has not been characterized in detail, but it has been shown to delay the onset of disease in familial AD. To elucidate the differential roles of the three-major human ApoE isoforms on microglia function we each expressed the human ApoE isoforms in murine N9 microglia cells. We could show that ApoE4 specifically influences actin cytoskeleton rearrangement and morphology. In migration assays, ApoE4 significantly promotes cell motility. To quantify phagocytosis by microglia we established an uptake assay based on imaging flow cytometry. Although expression of ApoE4 led to significantly reduced uptake of Aβ in contrast to the other isoforms, we could show that ApoE4 specifically increased phagocytosis of apoptotic neuronal cells. Our findings show that ApoE4 intrinsically affects microglia physiology by upregulating motility and phagocytic behavior in vitro and may therefore specifically contribute to microglia dysregulation in AD.</p

Table_1_Phagocytosis of Apoptotic Cells Is Specifically Upregulated in ApoE4 Expressing Microglia in vitro.DOCX

Alzheimer’s disease (AD) is characterized by intracellular tau aggregates and extracellular deposition of amyloid-β (Aβ). The major genetic risk factor to develop AD is the Apolipoprotein E isoform 4 (ApoE4). ApoE4 may directly affect Aβ pathology, yet the exact role of ApoE4 in the progression of AD remains unclear. Although astrocytes are the main source of ApoE in brain tissue, other cell types might contribute to ApoE isotype-dependent effects. While ApoE expression does not play a relevant role in homeostatic microglia, we and others could recently show that ApoE expression is significant upregulated in disease-associated microglia including AD-mouse models and human AD. ApoE has been supposed to have an anti-inflammatory effect, with ApoE4 being less effective than ApoE3. However, ApoE-isotype specific effects on microglia function in disease have not been thoroughly investigated to date. In contrast to this, the role of ApoE2, the third most common major ApoE isoform, in neurodegeneration has not been characterized in detail, but it has been shown to delay the onset of disease in familial AD. To elucidate the differential roles of the three-major human ApoE isoforms on microglia function we each expressed the human ApoE isoforms in murine N9 microglia cells. We could show that ApoE4 specifically influences actin cytoskeleton rearrangement and morphology. In migration assays, ApoE4 significantly promotes cell motility. To quantify phagocytosis by microglia we established an uptake assay based on imaging flow cytometry. Although expression of ApoE4 led to significantly reduced uptake of Aβ in contrast to the other isoforms, we could show that ApoE4 specifically increased phagocytosis of apoptotic neuronal cells. Our findings show that ApoE4 intrinsically affects microglia physiology by upregulating motility and phagocytic behavior in vitro and may therefore specifically contribute to microglia dysregulation in AD.</p

Additional file 1: of Patient-perceived barriers and facilitators to the implementation of a medication review in primary care: a qualitative thematic analysis

Interview guide for telephone interviews and focus groups. (DOCX 22 kb