Observation of the Color-Suppressed Decay B̅ 0→D0π0

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Annual Report of “Kanagawa University Space Rocket Club” in 2021

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Annual Report of “Kanagawa University Space Rocket Club” in 2022

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《資料論文》話すことに抵抗感のある児童に関する研究 ―支援方法としての自学教材の提案―

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研究速報 : 非軸対称クラッド棒・線材の引抜き加工・7 : 芯材のネッキングの予測

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Three-Dimensional Shape Modeling of Diamond Abrasive Grains Measured by Scanning Laser Microscope

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PMA synergistically enhances TLR-dependent MUC5AC induction by NTHi via TRAF6.

<p>(<b>A</b>) PMA synergistically enhanced NTHi-induced polyubiquitination of TRAF6 in human epithelial cells. Cells were transfected with TRAF6, and were treated with NTHi and PMA as indicated. Whole cell extracts were subjected to co-immunoprecipitation (IP) with either control IgG or anti-TRAF6 antibodies and immunoblotting with anti-ubiquitin antibody. The same blots were re-probed with anti-TRAF6. (<b>B</b>) Overexpression of a DN mutant form of TRAF6 blocked the synergistic phosphorylation of p38 MAPK and MKK3/6 induced by NTHi and PMA. Cells were transfected with 0.8 µg of DN-TRAF6 or control vector, and treated with NTHi with or without PMA. Cell lysate was blotted with antibodies as indicated in the figure. (<b>C</b>) The synergistic enhancement of NTHi-induced MUC5AC transcription by PMA was inhibited by overexpression of DN-TRAF6 in human epithelial cells, as assessed by MUC5AC-dependent promoter Luciferase assay. Cells were transfected with 0.8 µg of DN-TRAF6 or control vector, and treated with NTHi with or without PMA. Relative luciferase activity of MUC5AC was measured from the cell lysate. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. control; <i>**p<0.05</i> vs. NTHi alone; ***<i>p<0.05</i> vs. NTHi with PMA in control vector transfected cells. The data shown are representative of three independent experiments. −, absence of; +, presence of; NTHi, nontypeable <i>Haemophilus influenzae</i>; DN, dominant negative; Ubn, ubiquitin.</p

PMA synergistically enhances up-regulation of MUC5AC induced by activation of TLR signaling.

<p>(<b>A</b>) PMA synergistically enhanced MUC5AC expression induced only by NTHi, <i>S.p.</i> and PGN, but not by TNF-α and IL-6, as assessed by MUC5AC-dependent promoter Luciferase assay. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. NTHi, <i>S.p.</i>, or PGN alone; <i>^#p>0.05</i> vs. TNF-α or IL-6 alone. (<b>B</b>) PMA synergized with either NTHi or <i>S.p.</i>, but not with TNF-α to enhance MUC5AC expression in a dose-dependent manner. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. PMA alone; <i>^#p>0.05</i> vs. PMA alone. (<b>C</b>) PGN-induced MUC5AC transcription was synergistically enhanced by PMA in HEK293-TLR2 cells, but not in HEK293-pcDNA cells. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. PGN alone. (<b>D</b>) Synergistic enhancement of MUC5AC expression by PMA was also observed in the cells treated with TLR ligands, such as PGN, Zymosan, Poly(I:C) and LPS, respectively. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. PGN, Zymosan, Poly(I:C), or LPS alone. The data shown are representative of three independent experiments. −, absence of; +, presence of; <i>S.p.</i>, <i>Streptococcus pneumoniae</i>; NTHi, nontypeable <i>Haemophilus influenzae</i>.</p

PMA synergistically enhances NTHi-induced MUC5AC expression via MKK3/6-p38 MAPK pathway.

<p>(<b>A</b>) PMA synergistically enhanced NTHi-induced phosphorylation of p38 MAPK and MKK3/6, but not ERK and MEK1. (<b>B</b>) The synergistic induction of MUC5AC transcription by NTHi and PMA was inhibited by overexpressing DN mutant forms of p38α and p38β in human epithelial cells, as assessed by MUC5AC-dependent promoter Luciferase assay. Cells were transfected with 0.8 µg of DN p38α, DN p38β, or control vector, and treated with NTHi with or without PMA. Relative luciferase activity of MUC5AC was measured from the cell lysate. (<b>C</b>) SB203580, a specific inhibitor for p38 MAPK signaling, attenuated the synergistic induction of MUC5AC expression by NTHi and PMA at the mRNA level as assessed by Q-PCR. Cells were pre-treated with 10 µM of SB203580 or vehicle control, and treated with NTHi with or without PMA. mRNA expression level of MUC5AC was measured by Q-PCR. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. control; <i>**p<0.05</i> vs. NTHi alone; <i>***p<0.05</i> vs NTHi with PMA in control vector transfected (<b>B</b>) or vehicle treated (<b>C</b>) cells. The data shown are representative of three independent experiments. −, absence of; +, presence of; DN, dominant negative; NTHi, nontypeable <i>Haemophilus influenzae</i>.</p

TLR-TRAF6-dependent synergistic MUC5AC induction by NTHi and PMA is mediated by PKCθ.

<p>(<b>A</b>) Rottlerin, a specific PKC™/θ inhibitor, blocked the synergistic induction of MUC5AC transcription by NTHi and PMA in human epithelial cells, as assessed by MUC5AC-dependent promoter Luciferase assay. Cells were pre-treated with 20 µM of Rottlerin or vehicle control, and treated with NTHi with or without PMA. Relative luciferase activity of MUC5AC was measured from the cell lysate. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. control; <i>**p<0.05</i> vs. NTHi alone; ***<i>p<0.05</i> vs. NTHi with PMA in vehicle treated cells. (<b>B</b>) The synergistic induction of MUC5AC expression was also attenuated by Rottlerin at the mRNA level, as assessed by performing Q-PCR. Cells were pre-treated with 20 µM of Rottlerin or vehicle control, and treated with NTHi with or without PMA. mRNA expression level of MUC5AC was measured by Q-PCR. (<b>C</b>) Co-expressing WT-PKCθ enhanced, whereas DN-PKCθ inhibited, the synergistic induction of MUC5AC transcription by NTHi and PMA. Cells were transfected with 0.3 µg of WT- PKCθ, 0.6 µg of DN PKCθ, or control vector, and treated with NTHi with or without PMA. Relative luciferase activity of MUC5AC was measured from the cell lysate. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. control; <i>**p<0.05</i> vs. NTHi alone; ***<i>p<0.05</i> vs. NTHi with PMA in control vector transfected cells. (<b>D</b>) C/A-PKC-induced MUC5AC expression was synergistically enhanced by NTHi in human epithelial cells. Cells were transfeced with 0.3 µg of C/A PKCθ or control vecttor, and treated with NTHi. Relative luciferase activity of MUC5AC was measured from the cell lysate. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. NTHi alone. (<b>E</b>) C/A-PKCθ synergized with WT-TRAF6 to induce MUC5AC expression in a dose-dependent manner. Cells were transfected with 0.1, 0.3, or 0.6 µg of C/A PKCθ with or without 0.3 µg of WT-TRAF6. mRNA expression level of MUC5AC was measured by Q-PCR. Values are the means ± S.D. (n = 3). <i>*p<0.05</i> vs. control; <i>**p<0.05</i> vs. C/A PKCθ transfected cells. The data shown are representative of three independent experiments. −, absence of; +, presence of; NTHi, nontypeable <i>Haemophilus influenzae</i>; WT, wild-type; DN, dominant negative; C/A, constitutively active form.</p