約 5,198,061 件
https://w.atwiki.jp/cadencii_en/pages/39.html
English 日本語 Release Note Release Date 9 Sep., 2009 Notes Cadencii requires ".NET Framework Runtime(version 2.0 or later)". Installer of this rumtime is available from the link below. .NET Framework Runtime Download .NET Framework 3.5 SP1 Cadencii can be launched with the latest version of mono. This enable you to use Cadencii with many platforms supported by mono. (Note Several functions using VOCALOID2 VSTi are not available in this case.) Mono is available from the link mono download Download Cadencii version 2.3.4 (641KB) How to get source codes Source code is available on SourceForege.JP. Please follow the instruction below for checking out the SourceForge.JP s SVN repository. svn checkout -r 450 http //svn.sourceforge.jp/svnroot/cadencii/branches/2.3 ./ These svn command is for checiking out "THIS" version of Cadencii. In order to get the latest source codes, please remove "-r" option.
https://w.atwiki.jp/tiger/pages/8.html
RhoB null mice have retarded vascular development in the retina. SOS1-/- mice impair placental development. The interaction between DOC and CSW is needed for normal eye development. Gab1 and Gab2 are phosphorylated by EPO signal. Overexpression of Gab1 in kidney epithelial cells of a mouce results in constitutive and ligand-independent cell scattering and branching morphogenesis. RhoB null mice have retarded vascular development in the retina. 1 Genes Dev. 2003 Nov 1;17(21) 2721-32. RhoB controls Akt trafficking and stage-specific survival of endothelial cells during vascular development. Adini I, Rabinovitz I, Sun JF, Prendergast GC, Benjamin LE. Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. Blood vessel formation is a complex morphological process that is only beginning to be understood at the molecular level. In this study, we demonstrate a novel and critical role for the small GTPase, RhoB, in vascular development. RhoB null mice have retarded vascular development in the retina characterized by altered sprout morphology. Moreover, pharmaceutical means to deplete RhoB in neonatal rats is associated with apoptosis in the sprouting endothelial cells of newly forming vessels. Similarly, acute depletion of RhoB by antisense or dominant-negative strategies in primary endothelial cell culture models led to apoptosis and failures in tube formation. We identified a novel link between RhoB and the Akt survival signaling pathway to explain these changes. Confocal microscopy revealed that RhoB is highly localized to the nuclear margin with a small percentage found inside the nucleus. Similarly, total Akt is throughout the cell but has increased accumulation at the nuclear margin, and active phosphorylated Akt is found primarily inside the nucleoplasm, where it partially colocalizes with the RhoB therein. We show that this colocalization is functionally relevant, because when RhoB was depleted, Akt was excluded from the nucleus and total cellular Akt protein was decreased in a proteosome-dependent manner. Because the function of RhoB in vivo appears to only be rate limiting for endothelial cell sprouting, we propose that RhoB has a novel stage-specific function to regulate endothelial cell survival during vascular development. RhoB may offer a therapeutic target in diseases such as cancer, diabetic retinopathy, and macular degeneration, where the disruption of sprouting angiogenesis would be desirable. Publication Types Research Support, Non-U.S. Gov t Research Support, U.S. Gov t, P.H.S. PMID 14597666 [PubMed - indexed for MEDLINE] SOS1-/- mice impair placental development. 1 EMBO J. 2000 Feb 15;19(4) 642-54. The Sos1 and Sos2 Ras-specific exchange factors differences in placental expression and signaling properties. Qian X, Esteban L, Vass WC, Upadhyaya C, Papageorge AG, Yienger K, Ward JM, Lowy DR, Santos E. Laboratory of, National Cancer Institute, Bethesda, MD 20892, USA. Targeted disruption of both alleles of mouse sos1, which encodes a Ras-specific exchange factor, conferred mid-gestational embryonic lethality that was secondary to impaired placental development and was associated with very low placental ERK activity. The trophoblastic layers of sos1(-/-) embryos were poorly developed, correlating with high sos1 expression in wild-type trophoblasts. A sos1(-/-) cell line, which expressed readily detectable levels of the closely related Sos2 protein, formed complexes between Sos2, epidermal growth factor receptor (EGFR) and Shc efficiently, gave normal Ras.GTP and ERK responses when treated with EGF for or =10 min and was transformed readily by activated Ras. However, the sos1(-/-) cells were resistant to transformation by v-Src or by overexpressed EGFR and continuous EGF treatment, unlike sos1(+/-) or wild-type cells. This correlated with Sos2 binding less efficiently than Sos1 to EGFR and Shc in cells treated with EGF for or =90 min or to v-Src and Shc in v-Src-expressing cells, and with less ERK activity. We conclude that Sos1 participates in both short- and long-term signaling, while Sos2-dependent signals are predominantly short-term. PMID 10675333 [PubMed - indexed for MEDLINE] The interaction between DOC and CSW is needed for normal eye development. 1 EMBO J. 1999 Dec 15;18(24) 6950-61. Recruitment of the protein tyrosine phosphatase CSW by DOS is an essential step during signaling by the sevenless receptor tyrosine kinase. Herbst R, Zhang X, Qin J, Simon MA. Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020, USA. The pleckstrin homology (PH) domain-containing protein Daughter of Sevenless (DOS) is an essential component of the Sevenless receptor tyrosine kinase (SEV) signaling cascade, which specifies R7 photoreceptor development in the Drosophila eye. Previous results have suggested that DOS becomes tyrosine phosphorylated during SEV signaling and collaborates with the protein tyrosine phosphatase CSW. We have investigated this possibility by identifying tyrosine residues 801 and 854 of DOS as the phosphorylated binding sites for the CSW SH2 domains. We show that these sites become phosphorylated in response to SEV activation and that phosphorylation of both sites is required to allow CSW to bind DOS. Mutant DOS proteins in which either Y801 or Y854 of DOS has been changed to phenylalanine are unable to function during signaling by SEV and other receptor tyrosine kinases. In contrast, we find that a mutant DOS protein in which all tyrosine phosphorylation sites except Y801 and Y854 have been removed is able effectively to provide DOS function during SEV signaling and to rescue the lethality associated with dos loss-of-function mutations. These results indicate that a primary role for DOS during signaling by SEV and other receptor tyrosine kinases is to become phosphorylated at Y801 and Y854 and then recruit CSW. PMID 10601017 [PubMed - indexed for MEDLINE] Gab1 and Gab2 are phosphorylated by EPO signal. 1 Blood. 2004 Jun 15;103(12) 4457-65. Epub 2004 Feb 24. Tyrosine kinase receptor RON functions downstream of the erythropoietin receptor to induce expansion of erythroid progenitors. van den Akker E, van Dijk T, Parren-van Amelsvoort M, Grossmann KS, Schaeper U, Toney-Earley K, Waltz SE, Lowenberg B, von Lindern M. Department of Hematology, Erasmus MC, PO Box 1738, 3000 DR Rotterdam, the Netherlands. Erythropoietin (EPO) is required for cell survival during differentiation and for progenitor expansion during stress erythropoiesis. Although signaling pathways may couple directly to docking sites on the EPO receptor (EpoR), additional docking molecules expand the signaling platform of the receptor. We studied the roles of the docking molecules Grb2-associated binder-1 (Gab1) and Gab2 in EPO-induced signal transduction and erythropoiesis. Inhibitors of phosphatidylinositide 3-kinase and Src kinases suppressed EPO-dependent phosphorylation of Gab2. In contrast, Gab1 activation depends on recruitment and phosphorylation by the tyrosine kinase receptor RON, with which it is constitutively associated. RON activation induces the phosphorylation of Gab1, mitogen-activated protein kinase (MAPK), and protein kinase B (PKB) but not of signal transducer and activator of transcription 5 (Stat5). RON activation was sufficient to replace EPO in progenitor expansion but not in differentiation. In conclusion, we elucidated a novel mechanism specifically involved in the expansion of erythroblasts involving RON as a downstream target of the EpoR. PMID 14982882 [PubMed - indexed for MEDLINE] Overexpression of Gab1 in kidney epithelial cells of a mouce results in constitutive and ligand-independent cell scattering and branching morphogenesis. 1 Nature. 1996 Nov 14;384(6605) 173-6. Interaction between Gab1 and the c-Met receptor tyrosine kinase is responsible for epithelial morphogenesis. Weidner KM, Di Cesare S, Sachs M, Brinkmann V, Behrens J, Birchmeier W. Max Delbruck Center for Molecular Medicine, Berlin, Germany. The proteins Gab1 and the related DOS (for daughter of sevenless ) each bind to substrates of tyrosine kinases like Grb2 or Corkscrew, and act in signalling pathways downstream of tyrosine kinase receptors. Here we show that Gab1 interacts directly with the c-met-encoded receptor tyrosine kinase but not with a number of other tyrosine kinases from different subfamilies. A newly identified proline-rich domain of Gab1 is responsible for the binding of this protein to the tyrosine-phosphorylated bidentate docking site in c-Met. Expression of Gab1 in epithelial cells is sufficient to induce the c-Met-specific activities, including branching morphogenesis. Thus we have discovered a new phosphotyrosine interaction domain in Gab1 and shown that Gab1 is the substrate of the c-Met receptor tyrosine kinase that mediates epithelial morphogenesis. PMID 8906793 [PubMed - indexed for MEDLINE]
https://w.atwiki.jp/blueskyblue/pages/20.html
BLCD－た行 た なし ち なし つ 月に狼 遊佐浩二×福山潤/三木眞一郎×鈴村健一/大川透×宮田幸季/伊藤健太郎×下野紘 て DEADLOCK(2枚組) 安元洋貴×中村悠一 DEADSHOT(2枚組) DEADHEAT(2枚組)
https://w.atwiki.jp/cadencii_en/pages/41.html
English 日本語 Release Note Release Date 15 Aug, 2009 Notes Cadencii requires ".NET Framework Runtime(version 2.0 or later)". Installer of this rumtime is available from the link below. .NET Framework Runtime Download .NET Framework 3.5 SP1 Cadencii can be launched with the latest version of mono. This enable you to use Cadencii with many platforms supported by mono. (Note Several functions using VOCALOID2 VSTi are not available in this case.) Mono is available from the link mono download Download Cadencii version 2.3.2 (639KB) How to get source codes Source code is available on SourceForege.JP. Please follow the instruction below for checking out the SourceForge.JP s SVN repository. svn checkout -r 416 http //svn.sourceforge.jp/svnroot/cadencii/branches/2.3 ./ These svn command is for checiking out "THIS" version of Cadencii. In order to get the latest source codes, please remove "-r" option.
https://w.atwiki.jp/cadencii_en/pages/52.html
English 日本語 Release Note Release Date 1 Jun, 2009 Notes Cadencii requires ".NET Framework Runtime(version 2.0 or later)" and "Visual C++ Library DLLs". Installers of these rumtimes are available from the links below. .NET Framework Runtime Download .NET Framework 3.5 SP1 Visual C++ Library DLL Microsoft Visual C++ 2008 Redistributable Package (x86) Cadencii can be launched with the latest version of mono. This enable you to use Cadencii with many platforms supported by mono. (Note Several functions using VOCALOID2 VSTi are not available in this case.) Mono is available from the link mono download Download Cadencii version 2.0.1 (565KB) CadenciiSDK version 2.0 (455KB) How to get source codes Source code is available on SourceForege.JP. Please follow the instruction below for checking out the SourceForge.JP s SVN repository. svn checkout -r 216 http //svn.sourceforge.jp/svnroot/cadencii/branches/2.0 ./ These svn command is for checiking out "THIS" version of Cadencii. In order to get the latest source codes, please remove "-r" option.
https://w.atwiki.jp/nicoratch/pages/887.html
概要 33,45回転、±10%のピッチコントロール可能な標準スペックのタンテ。トーンアームがストレートアームになっている。 SA-600 2002年 - 2005年まで販売 +スペック表・SA-600 Features feature Straight arm with angled headshell feature Pitch control range +/- 10% feature Electronic break feature Strobo illuminator feature Soft touch Start/Stop button feature Speed 33 1/3 and 45 RPM Specifications feature Direct Drive full manual feature Brushless DC motor feature Wow flutter 0.02% WRMS feature Rumble 56 dB feature Starting Torque 1.2kg feature Power Supply 115V~60Hz/230V~50Hz feature Power Consumption 15 Watts feature Dimensions 444 x 152 x 352 mm feature Weight 10 kg SA-600取扱説明書（英語） https //www.manualslib.com/manual/60377/Gemini-Sa-600.html SA-600Ⅱ 2003年発売。 +スペック表・ MakerGemini Brand Function Turntable Form FactorTabletop Signal PathAnalog Hardware Made InChina Dimensions450 x 152 x 352 mm Weight10 kg Additional Specifications Speed Select33⅓ rpm Speed Select45 rpm Speed Adjust (Pitch)±10% Drive TypeDirect Drive 取扱説明書（英語） https //www.manualslib.com/manual/60378/Gemini-Sa-600ii.html SA-600ⅡC 2003年発売。ハンピン製DJ-1160のOEMと思われる。こちらは普通のS字アーム。 +スペック表・SA-600ⅡC ※詳細情報なし Gemini http //geminisound.com
https://w.atwiki.jp/boare/pages/121.html
Release Note Release Date 16 Jun, 2009 Notes Cadencii requires ".NET Framework Runtime(version 2.0 or later)". Installer of this rumtime is available from the link below. .NET Framework Runtime Download .NET Framework 3.5 SP1 Cadencii can be launched with the latest version of mono. This enable you to use Cadencii with many platforms supported by mono. (Note Several functions using VOCALOID2 VSTi are not available in this case.) Mono is available from the link mono download Download Cadencii version 2.1.1 (603KB) CadenciiSDK version 2.0 (455KB) How to get source codes Source code is available on SourceForege.JP. Please follow the instruction below for checking out the SourceForge.JP s SVN repository. svn checkout -r 257 http //svn.sourceforge.jp/svnroot/cadencii/branches/2.0 ./ These svn command is for checiking out "THIS" version of Cadencii. In order to get the latest source codes, please remove "-r" option.
https://w.atwiki.jp/boare/pages/124.html
Release Note Release Date 20 Jun, 2009 Notes Cadencii requires ".NET Framework Runtime(version 2.0 or later)". Installer of this rumtime is available from the link below. .NET Framework Runtime Download .NET Framework 3.5 SP1 Cadencii can be launched with the latest version of mono. This enable you to use Cadencii with many platforms supported by mono. (Note Several functions using VOCALOID2 VSTi are not available in this case.) Mono is available from the link mono download Download Cadencii version 2.1.2 (604KB) CadenciiSDK version 2.0 (455KB) How to get source codes Source code is available on SourceForege.JP. Please follow the instruction below for checking out the SourceForge.JP s SVN repository. svn checkout -r 273 http //svn.sourceforge.jp/svnroot/cadencii/branches/2.0 ./ These svn command is for checiking out "THIS" version of Cadencii. In order to get the latest source codes, please remove "-r" option.
https://w.atwiki.jp/ayayo1990/pages/11.html
メニュー リンク名 半角 で始めると引用文になります。 半角 で始めると引用文になります。 半角 で始めると引用文になります。 更新履歴 トップページ プラグイン メニュー メニュー2 表組み | インライン要素 | インライン要素 |行頭から | でインライン要素を区切ることで表組みになります。 インライン要素のはじめに以下の記述をすることで、表組みのセルの表示を変えることができます。 BGCOLOR(色指定) COLOR(色指定) SIZE(サイズ指定) LEFT CENTER RIGHT @ウィキ ガイド @wiki 便利ツール @wiki めんどくせえ 更新履歴 取得中です。 名前 コメント すべてのコメントを見る これでいいのか -- (てすてす) 2007-10-06 22 46 12 arere -- (てすてす) 2007-10-06 22 45 06 あれ -- (てすてす) 2007-10-06 22 43 24 こめんと -- (てすてす) 2007-10-06 22 41 50
https://w.atwiki.jp/hmiku/pages/48526.html
【検索用 Identity 登録タグ I VOCALOID picco 初音ミク 曲】 + 目次 目次 曲紹介 歌詞 コメント 作詞：picco 作曲：picco 編曲：picco 唄：初音ミク 曲紹介 ─何度も泣いたって世界は変わらない─ Artwork ヘレミア アルバム『NX FUTURE HOUSE』、『光芒パラノイア』収録楽曲。 歌詞 （YouTubeの概要欄より転載） 眩しい街の明かり 真夜中 路地を歩く すれ違う人影は 何を思うの もう期待通りにできない 気づいて欲しくないけど いつもかわいくなんてできない 自分らしく生きろなんて 無責任な呪文みたいだ 何度も泣いたって世界は変わらない でも どっかに光があると信じているよ Identity 普通が正義なんて 誰が決めつけたのか？ みんなと違うことは おかしくないよ ねえ嘘ついて生きたって 誰も見抜けないでしょう あたしのこと何も見えてないの 気づいてなんて思ってないし 騙し騙される平行線 何度も笑ったって世界は変わらない でも どっかに光があると信じているよ Identity コメント 名前 コメント