音声認識アプリケーション開発支援技術に関する研究

制度:新 ; 報告番号:甲2790号 ; 学位の種類:博士(工学) ; 授与年月日:2009/3/15 ; 早大学位記番号:新5010textthesi

Experimental study on the dynamic properties of rigid polyurethane foam in stress-controlled cyclic uniaxial tests

application/pdfFrequent major earthquakes in Japan necessitate earthquake-resistant infrastructure. The dynamic deformation characteristics of rigid polyurethane foam, used as a lightweight embankment material, is examined in this study. The effect of the initial static stress on the shear modulus of single-layer samples was small, while the shear modulus of two-layer samples increased with increasing initial static stress. The damping ratio of single-layer samples converged to 4–5%, but decreased with increasing initial static stress up to 30 kPa in two-layer samples before increasing above 40 kPa. Results from cyclic uniaxial and triaxial tests were compared. The dynamic properties depended on restriction conditions and the deformation direction

分子軌道法による原子炉用ジルコニウム合金の耐食機能設計

現在の主要な発電用原子炉において、その炉心部分にはジルコニウム合金が使われている。このジルコニウム合金の表面には、局部腐食(いわゆるノジュラ-腐食)が起こり問題となっている。さらに、ウラン資源の有効利用を目的として進められている核燃料の高燃焼度化の要請とあいまって、腐食ジルコニウム合金の開発が強く望まれている。本研究はこのような背景のもとに計画されたものであり、分子軌道法による電子状態の計算とX線光電子分光(XPS)などの実験を併用して、高耐食ジルコニウム合金の設計と開発の指針を得ることを目標にしている。ジルコニウム合金の表面にできる腐食生成物であるZrO_2(ジルコニア)については、これまでいろいろな方法で調べられてきたが、XPSによる表面皮膜の解析は新しく、その化学成分や電子状態について興味ある情報を得ることができた。例えば、 XPSスペクトルは耐食性の良い合金と悪い合金とでは違っていることがわかった。合金元素の周期表の位置に従って耐食性が変わることも明らかになった。さらに、ジルコニウア皮膜自体、決して均一なものではなく、膜厚方向に合金元素の濃度勾配があることもわかった。また、DV-Xα分子軌道計算からによるジルコニウムおよびジルコニア中の合金元素の振舞いを明らかにした。そして電子論に基づくジルコニウム合金の腐食メカニズムを初めて提案した。本研究を通し、ジルコニウムの腐食を新しい視点から捉えることができた。その結果、新しい高耐食性ジルコニウム合金を開発するときに有用な指針が得られた。科学研究費補助金 研究種目:研究(A)(1) 課題番号:07555500 研究代表者:森永 正彦 研究期間:1995-1996年度research repor

Observation of the ηc(2S) in Exclusive B→KKSK-π+ Decays

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AICAR-activation of AMPK mediates apoptosis in ALL cells via the mitochondrial pathway

<p><b>Copyright information:</b></p><p>Taken from "Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL) cells: implication for targeted therapy"</p><p>http://www.molecular-cancer.com/content/6/1/46</p><p>Molecular Cancer 2007;6():46-46.</p><p>Published online 10 Jul 2007</p><p>PMCID:PMC1948012.</p><p></p> () DNA fragmentation assay. CCRF-CEM, NALM6, REH, and SupB15 cells were treated for 48 h with increased concentrations of AICAR (0 – 2 mM), and nuclear DNA was analyzed by electrophoresis on a 1.6% Tris-Borate-EDTA agarose gel. () Western blot analysis of cytochrome C and caspase 9 expression in CCRF-CEM and NALM6 cells treated for 48 h with 0.5 mM AICAR alone, 0.1 μM iodotubericidin alone (Iodo), or both agents together (Iodo + AICAR). Equal amount of loaded protein (50 μg) was confirmed by immunoblotting with anti-β-actin antibody. The data shown are representative of 3 experiments

AICAR induces upregulation of the p53 and the cyclin dependent kinase inhibitor p27 in ALL cells

<p><b>Copyright information:</b></p><p>Taken from "Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL) cells: implication for targeted therapy"</p><p>http://www.molecular-cancer.com/content/6/1/46</p><p>Molecular Cancer 2007;6():46-46.</p><p>Published online 10 Jul 2007</p><p>PMCID:PMC1948012.</p><p></p> Western blot analyses of p53, p27, and p21 were done using cell extracts from CCRF-CEM, NALM6, REH, and SupB15 cells treated with the indicated concentrations of AICAR (0 – 2 mM) for 48 h. Equivalent amount of proteins (50 μg) were separated by SDS-PAGE and immunodetected with antibodies against p53, p27, and p21. Membranes were stripped and reprobed with anti-β-actin antibody to confirm equal amount of proteins loaded in all lanes. Density value of each band was normalized to their respective β-actin level and expressed relative to control (untreated). The data shown are representative of 3 experiments producing similar results

Activation of AMPK is required for phosphorylation of p38-MAPK in AICAR-treated ALL cells

<p><b>Copyright information:</b></p><p>Taken from "Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL) cells: implication for targeted therapy"</p><p>http://www.molecular-cancer.com/content/6/1/46</p><p>Molecular Cancer 2007;6():46-46.</p><p>Published online 10 Jul 2007</p><p>PMCID:PMC1948012.</p><p></p> () Immunoblot of p38-MAPK phosphorylation (P-p38-MAPK, Thr180/Tyr182) and β-actin (loading control) expressed in CCRF-CEM and NALM6 cells treated with 0.1% DMSO (Control), 0.5 mM AICAR alone, 0.1 mM iodotubericidin alone (Iodo), or both agents together (Iodo + AICAR). () Phosphorylation status of AMPK (P-AMPK, Thr172) from CCRF-CEM and NALM6 cells incubated with either 0.5 mM AICAR alone, 10 μM SB 202190 alone (SB) or both inhibitors together (SB + AICAR). Level of β-actin was used as loading controls. Density value of each band was normalized to their respective β-actin level and expressed relative to control. The immunoblots shown are representative of 3 independent experiments, which produced similar results

The anti-proliferative effect of AICAR on ALL cells is mediated via activation of AMPK

<p><b>Copyright information:</b></p><p>Taken from "Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL) cells: implication for targeted therapy"</p><p>http://www.molecular-cancer.com/content/6/1/46</p><p>Molecular Cancer 2007;6():46-46.</p><p>Published online 10 Jul 2007</p><p>PMCID:PMC1948012.</p><p></p> () Western blot analysis of phosphorylated AMPK (P-AMPK, Thr172) expression in CCRF-CEM, NALM6, REH, and SupB15 cells treated with various concentrations of AICAR (0 – 2.0 mM). Total protein was extracted from AICAR-treated cells and AMPK and P-AMPK were immunodetected using specific antibodies. Equal amounts of protein (50 μg) were loaded per lane as confirmed by β-actin level. Density value of P-AMPK bands were normalized to level of AMPK and expressed relative to control. () Cell proliferation assays of ALL cells treated for 18 h with AICAR alone (0.25 mM for CCRF-CEM, NALM6, REH, and 1.0 mM for SupB15), the adenosine kinase inhibitor iodotubericidin alone (Iodo, 0.1 μM), or both agents together (Iodo + AICAR). Growth inhibition was determined using the tetrazolium (MTS) reduction assay. Values are expressed as a percentage relative to those obtained with untreated control cells (mean ± SEM). Data are representative of at least three independent experiments. #, < 0.001 for AICAR Iodo + AICAR

Anti-proliferative action of AICAR on ALL cells is associated with downstream AMPK-dependent activation of p38-MAPK

<p><b>Copyright information:</b></p><p>Taken from "Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL) cells: implication for targeted therapy"</p><p>http://www.molecular-cancer.com/content/6/1/46</p><p>Molecular Cancer 2007;6():46-46.</p><p>Published online 10 Jul 2007</p><p>PMCID:PMC1948012.</p><p></p> () CCRF-CEM, NALM6, REH, and SupB15 ALL cells treated with 0.25 mM AICAR for the indicated times (0 – 24 h) were analyzed by Western blot for phosphorylated p38-MAPK protein (P-p38-MAPK, Thr180/Tyr182). β-actin was used as a loading control. Density value of each band was normalized to their respective β-actin level and expressed relative to control (untreated). () Cell proliferation assays of CCRF-CEM, NALM6, REH, and SupB15 cells treated with 0.25 mM AICAR alone, 10 μM of the p38-MAPK inhibitor SB 202190 alone (SB), or both agents together (SB + AICAR). The cell proliferation values are expressed as a percentage relative to those obtained with untreated control cells (mean ± SEM, n = 3). Data are representative of at least three independent experiments. *, < 0.01 for AICAR SB + AICAR; #, < 0.05 for AICAR SB + AICAR

AICAR treatment inhibits proliferation of human childhood leukemia ALL cells

<p><b>Copyright information:</b></p><p>Taken from "Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL) cells: implication for targeted therapy"</p><p>http://www.molecular-cancer.com/content/6/1/46</p><p>Molecular Cancer 2007;6():46-46.</p><p>Published online 10 Jul 2007</p><p>PMCID:PMC1948012.</p><p></p> The ALL cell lines CCRF-CEM (T-lineage), NALM6 (Bp-lineage), REH (Bp-ALL expressing the TEL/AML1 fusion protein), and SupB15 (Bp-ALL expressing the BCR/ABL fusion protein) were treated for 24 h with various concentrations of AICAR (0.25 – 2 mM), and cell growth analyzed by thymidine ribotide ([H]TdR) incorporation into DNA. The results are expressed as percentage of [H]thymidine uptake (%) relative to control values (mean ± SEM, n = 3). #, < 0.001 for AICAR-treated cells control