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https://w.atwiki.jp/sainenotona/pages/15.html
【幹事】 ぐっさん 【日時】 2008/04/29 14 00-18 00 【場所】 秋葉原ラオックス Aスタジオ （地図） 【参加者】 ※第４回セッション準備スレに参加表明した順に表示しています。 No 名前 名前の読み パート 参加可能性 1 ぐっさん ベース ○ 2 鯖ノ介 ドラム ○ 3 yama3 ベース ○ 4 ユースケ ドラム × 5 Ｇａｂ ベース ○ 6 けいいち ギター ○ 7 20 ドラム △ 8 真理男 ボーカル △ 9 てつや ボーカル △ 10 はる ギター ○ 11 ポテチン ドラム △ 12 ろく ドラム ○ 【希望曲リスト】 タイトル アーチスト 提案者 コメント Rock n Roll Led Zeppelin ぐっさん 提示辞退 - 鯖ノ介 Blitzkrieg Bop Ramones yama3 提示辞退 - ユースケ Omens Of Love The Square Gab 提示辞退 - けいいち Move Over Janis Joplin 20 提示辞退 - 真理男 Goodbye Elenore TOTO てつや Rock n Roll Star Oasis はる My Sharona The Knack ポテチン 提示辞退 - ろく 【課題曲】 No 曲名 アーティスト ﾎﾞｰｶﾙ ギター ベース ドラム 鍵 盤 1 Rock n Roll Led Zeppelin （てつや） ぐっさん Gab 2 Blitzkrieg Bop Ramones てつや yama3 3 Omens Of Love The Square ぐっさん(EWI) Gab 4 Move Over Janis Joplin Gab 20 5 Goodbye Elenore TOTO てつや Gab 6 Rock n Roll Star Oasis ハル yama3 7 My Sharona The Knack てつや yama3 ポテチン
https://w.atwiki.jp/satoschi/pages/8303.html
Gabi-Gabi【gbw】 ガビガビ語 00 Australian 01 Pama-Nyungan 02 Waka-Kabic 《現》living language オーストラリア【AU】 言語名別称 alternate names Cabee Carby Carby-carbery Dhapil Dhipil Dippil Dipple Doondoora Doon-dooburra Dowarburra Dundu ra Dundubara Dunduura Gabi Gabigabi Kabbi Kabi Kabikabi Kahby Karabi Karbi Maiba 方言名 dialect names 参考文献 references WEB ISO 639-3 Registration Authority - SIL International Ethnologue Wikipedia
https://w.atwiki.jp/hctechnowiki/pages/20.html
Gabber(Gabba,Gabberhouse)（ガバ／同／ガバハウス） オランダ、ドイツ、イタリア、ベルギーでは最も人気があるジャンル。ディストーションをかけた強く歪んだバスドラム（キックドラムとも）が用いられ、一般的に１５０～２２０BPMである。Gabber、Gabba（オランダではガーバ、またはガーバーと発音）はハードコアテクノのサブジャンルであり、１９９０年代初期にオランダのロッテルダムにて誕生した。 ガバを語る上で欠かせないのが、前述の歪んだキックである。ガバキックとも呼ばれており、音程が認識可能な程度の重低音であり、はっきりとした矩形波（スクエアウェーヴ）になるまでディストーションをかけるのが特徴。ガバはメロディラインや多くのサンプルを使い、一般的なテンポの範囲は１６０～２２０BPMである。 ガバの特徴の一つにキックがある。バスドラムを合成してさらにそれをオーバードライブさせるのが普通である。ガバキックの最初におおよそ正弦波の波形サンプルをピッチを下げながら矩形波にクリップさせていく。これにより、周波数スペクトルが拡大し、よりけたたましく、アグレッシブなサウンドとなる。それによりサスティーンがより長引き、エンベロープも変化する。ディストーションをかけることにより判別しがたいピッチのドラム音もメロディックなトーンとなる。バスドラムのパターンをベースラインになぞらえてピッチを変えることも珍しくない。 そしてもう一つによく挙げられる構成要素がRoland Alpha Junoシンセサイザーによる”hoover（フーバー）”である。粗く歪んだサウンドで、低いキーで奏でることにより暗く陰気な雰囲気のベースラインを作り出すことができる。一方高いキーで奏でれば甲高くアグレッシブなリードを作り出すことができる。テンポの速いガバは極端に速いフーバーパターンを繰り返していたり、ギャッピング（Gapping、最大音量部と静音部の間の音量を急速に変えること）を多用する。ギターのリフ（ガバのパーティのライブでよく生演奏される）やMC（大抵ディストーションをかけている）もガバに共通して用いられる。 主流のガバのリリックやテーマは通常、好き勝手な内容であったり、性的、暴力的、反体制的である。しかしながら、ガバは通常それらのテーマに込められた皮肉をほのめかしているだけ（もっとも、一部にはシリアスに受け止められるような曲もあり、決して当時のトレンドというわけではない）ということも留意すべきだ。通常、陰謀説に基づく精神病的なものであったり、終末論的啓示や社会批判的なリリックであるが、それらのテーマの大部分は映画や楽曲からのサンプルである。
https://w.atwiki.jp/metachkanri/pages/33.html
スレッドフロート式掲示板群サイトmegabbsは2008年11月4日をもって閉鎖させていただきます。 http //www.megabbs.com/fin.html ねとらぼ：2ちゃんねる型掲示板「megabbs」閉鎖 8年半、「無法化」のため - ITmedia NEWS http //www.itmedia.co.jp/news/articles/0811/05/news114.html MEGA BBS2 ～広がるコミュニティ掲示板～ http //megabbs.net/ megabbs掲示板(megabbsっぽい掲示板。) http //megabbs.info/ megabbs掲示板避難所 http //jbbs.shitaraba.net/internet/6922/
https://w.atwiki.jp/tiger/pages/9.html
SYK deficient mice show defective in phagocytosis of macrophages and in generaction of reactive oxygen intermediates of neutrophils. ZAP-70 deficient mice impair the developmnt of NK1.1+ alpha beta T cells. ITK-/- mice reduce mast cell degranulation and acute allergic responses. Vav-2,3(-/-) neurons exhibit impaired axon guidance. Vav-1(-/-) NK cells are dramactically diminished 2B4 PLCG2-deficient mice exhibit a loss of collagen-induced platelet aggregation, mast cell FcepsilonR function, and NK cell FcgammaRIII and 2B4 function. GAB3 has no effect for phenotype. GAB2 deficient mast cells in mice result in impaired response of Fc epsilon RI. GAB2 deficient macrophages in mice result impaired phagocytosis. SYK deficient mice show defective in phagocytosis of macrophages and in generaction of reactive oxygen intermediates of neutrophils. 1 J Exp Med. 1997 Oct 6;186(7) 1027-39. A critical role for Syk in signal transduction and phagocytosis mediated by Fcgamma receptors on macrophages. Crowley MT, Costello PS, Fitzer-Attas CJ, Turner M, Meng F, Lowell C, Tybulewicz VL, DeFranco AL. G.W. Hooper Foundation, University of California, San Francisco, California 94143-0552, USA. mtcrow@scripps.edu Receptors on macrophages for the Fc region of IgG (FcgammaR) mediate a number of responses important for host immunity. Signaling events necessary for these responses are likely initiated by the activation of Src-family and Syk-family tyrosine kinases after FcgammaR cross-linking. Macrophages derived from Syk-deficient (Syk-) mice were defective in phagocytosis of particles bound by FcgammaRs, as well as in many FcgammaR-induced signaling events, including tyrosine phosphorylation of a number of cellular substrates and activation of MAP kinases. In contrast, Syk- macrophages exhibited normal responses to another potent macrophage stimulus, lipopolysaccharide. Phagocytosis of latex beads and Escherichia coli bacteria was also not affected. Syk- macrophages exhibited formation of polymerized actin structures opposing particles bound to the cells by FcgammaRs (actin cups), but failed to proceed to internalization. Interestingly, inhibitors of phosphatidylinositol 3-kinase also blocked FcgammaR-mediated phagocytosis at this stage. Thus, PI 3-kinase may participate in a Syk-dependent signaling pathway critical for FcgammaR-mediated phagocytosis. Macrophages derived from mice deficient for the three members of the Src-family of kinases expressed in these cells, Hck, Fgr, and Lyn, exhibited poor Syk activation upon FcgammaR engagement, accompanied by a delay in FcgammaR-mediated phagocytosis. These observations demonstrate that Syk is critical for FcgammaR-mediated phagocytosis, as well as for signal transduction in macrophages. Additionally, our findings provide evidence to support a model of sequential tyrosine kinase activation by FcgammaR s analogous to models of signaling by the B and T cell antigen receptors. Publication Types Research Support, Non-U.S. Gov t Research Support, U.S. Gov t, P.H.S. PMID 9314552 [PubMed - indexed for MEDLINE] 1 Mol Cell Biol. 1998 Jul;18(7) 4209-20. The Syk protein tyrosine kinase is essential for Fcgamma receptor signaling in macrophages and neutrophils. Kiefer F, Brumell J, Al-Alawi N, Latour S, Cheng A, Veillette A, Grinstein S, Pawson T. Programme in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5. The cytoplasmic protein tyrosine kinase Syk has two amino-terminal SH2 domains that engage phosphorylated immunoreceptor tyrosine-based activation motifs in the signaling subunits of immunoreceptors. Syk, in conjunction with Src family kinases, has been implicated in immunoreceptor signaling in both lymphoid and myeloid cells. We have investigated the role of Syk in Fcgamma receptor (FcgammaR)-dependent and -independent responses in bone marrow-derived macrophages and neutrophils by using mouse radiation chimeras reconstituted with fetal liver cells from Syk-/- embryos. Chimeric mice developed an abdominal hemorrhage starting 2 to 3 months after transplantation that was ultimately lethal. Syk-deficient neutrophils derived from the bone marrow were incapable of generating reactive oxygen intermediates in response to FcgammaR engagement but responded normally to tetradecanoyl phorbol acetate stimulation. Syk-deficient macrophages were defective in phagocytosis induced by FcgammaR but showed normal phagocytosis in response to complement. The tyrosine phosphorylation of multiple cellular polypeptides, including the FcgammaR gamma chain, as well as Erk2 activation, was compromised in Syk-/- macrophages after FcgammaR stimulation. In contrast, the induction of nitric oxide synthase in macrophages stimulated with lipopolysaccharide and gamma interferon was not dependent on Syk. Surprisingly, Syk-deficient macrophages were impaired in the ability to survive or proliferate on plastic petri dishes. Taken together, these results suggest that Syk has specific physiological roles in signaling from FcgammaRs in neutrophils and macrophages and raise the possibility that in vivo, Syk is involved in signaling events other than those mediated by immunoreceptors. Publication Types Research Support, Non-U.S. Gov t PMID 9632805 [PubMed - indexed for MEDLINE] ZAP-70 deficient mice impair the developmnt of NK1.1+ alpha beta T cells. 1 Immunol Lett. 2000 Jul 3;73(1) 65-9. Induction of NK1.1(+) alpha beta TCR(+) T cells by bypassing TCR signals in ZAP-70 deficient mice. Tone S, Iwabuchi K, Iwabuchi C, Negishi I, Onoe K. Division of Immunobiology, Section of Pathophysiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-Ku, Sapporo 060-0815, Japan. The mechanism of development of a unique subset of T cells, thymic NK1.1(+) alpha beta T cells, has been poorly understood. We found that the development of thymic NK1.1(+) alpha beta T cells was defective in mice deficient in ZAP-70. Instead, an accumulation of NK1.1(+) TCR beta(-) NK-like population was detected in the thymus and spleen of the ZAP-70 deficient (ZAP -/-) mouse. In the present report, we examined whether biochemical treatments that replace TCR-mediated positive selection signals could restore the generation of thymic NK1.1(+) alpha beta T cells in ZAP -/- mice using the thymus organ culture. We found that a higher concentration of phorbol ester (PMA) than that required for CD4(+) T cell generation and ionomycin induced the generation of NK1.1(+) alpha beta T cells. Phenotypic analysis of the induced NK1.1(+) alpha beta T cell population suggested that these cells expressed CD8 but not CD4 molecules, which is a different characteristic from ordinary thymic NK1.1(+) alpha beta T cells. These results suggest that differential signaling is required for the generation of mainstream T cells and thymic NK1.1(+) alpha beta T cells. PMID 10963813 [PubMed - indexed for MEDLINE] ITK-/- mice reduce mast cell degranulation and acute allergic responses. 1 Am J Respir Cell Mol Biol. 2005 Jun;32(6) 511-20. Epub 2005 Mar 18. Interleukin-2-inducible T cell kinase regulates mast cell degranulation and acute allergic responses. Forssell J, Sideras P, Eriksson C, Malm-Erjefalt M, Rydell-Tormanen K, Ericsson PO, Erjefalt JS. Transplantation Center, Foundation for Biomedical Research, Academy of Athens, Athens, Greece. Bruton s tyrosine kinase (Btk) is thought to positively regulate mast cell activation, implying a role in allergic responses. We have compared acute and late phase allergic airway reactions in mice lacking either Btk or interleukin-2-inducible T cell kinase (Itk), another Tec kinase expressed in mast cells. Btk(-/-) mice showed minor protection against allergic symptoms when challenged with allergen via the airways. In sharp contrast, both acute and late phase inflammatory allergic responses were markedly reduced in Itk(-/-) mice. Notably, airway mast cell degranulation in Itk(-/-) mice was severely impaired, despite wild-type levels of allergen-specific IgE and IgG1. The degranulation defect was confirmed in DNP-conjugated human serum albumin-challenged mice passively sensitized with anti-DNP IgE antibodies, and was also observed after direct G-protein stimulation with the mast cell secretagogue c48/80. Moreover, late phase inflammatory changes, including eosinophilia, lymphocyte infiltration, and Th2 cytokine production in the lungs, was eliminated in Itk(-/-) mice. Collectively, our data suggest a critical role of Itk in airway mast cell degranulation in vivo that together with an impaired T cell response prevents the development of both acute and late phase inflammatory allergic reactions. Publication Types Research Support, Non-U.S. Gov t PMID 15778496 [PubMed - indexed for MEDLINE] Vav-2,3(-/-) neurons exhibit impaired axon guidance. 1 Neuron. 2005 Apr 21;46(2) 205-17. Comment in Vav family GEFs link activated Ephs to endocytosis and axon guidance. Cowan CW, Shao YR, Sahin M, Shamah SM, Lin MZ, Greer PL, Gao S, Griffith EC, Brugge JS, Greenberg ME. Neurobiology Program, Children s Hospital, Boston, Massachusetts 02115, USA. Ephrin signaling through Eph receptor tyrosine kinases can promote attraction or repulsion of axonal growth cones during development. However, the mechanisms that determine whether Eph signaling promotes attraction or repulsion are not known. We show here that the Rho family GEF Vav2 plays a key role in this process. We find that, during axon guidance, ephrin binding to Ephs triggers Vav-dependent endocytosis of the ligand-receptor complex, thus converting an initially adhesive interaction into a repulsive event. In the absence of Vav proteins, ephrin-Eph endocytosis is blocked, leading to defects in growth cone collapse in vitro and significant defects in the ipsilateral retinogeniculate projections in vivo. These findings suggest an important role for Vav family GEFs as regulators of ligand-receptor endocytosis and determinants of repulsive signaling during axon guidance. Publication Types PMID 15848800 [PubMed - indexed for MEDLINE] Vav-1(-/-) NK cells are dramactically diminished 1 Eur J Immunol. 2001 Aug;31(8) 2403-10. Vav-1 regulates NK T cell development and NK cell cytotoxicity. Chan G, Hanke T, Fischer KD. Abteilung Physiologische Chemie, Universitat Ulm, Ulm, Germany. The hematopoietic-specific Rho-family GTP exchange factor Vav-1 is a regulator of lymphocyte antigen receptor signaling and mediates normal maturation and activation of B and T cells.Recent findings suggest that Vav-1 also forms part of signaling pathways required for natural and antibody dependent cellular cytotoxicity (ADCC) of human NK cells. In this study, we show that Vav-1 is also expressed in murine NK cells. Vav-1(-/-) mice had normal numbers of splenic NK cells, and these displayed a similar expression profile of NK cell receptors as wild-type mice. Unexpectedly, IL-2-activated Vav-1(-/-) NK cells retained normal ADCC. Fc-receptor mediated activation of ERK, JNK, and p38 was also normal. In contrast, Vav-1(-/-) NK cells exhibited reduced natural cytotoxicity against EL4, C4.4.25, RMA and RMA/S. Together, the results demonstrate that Vav-1 is dispensable for mainstream NK cell development, but is required for NK natural cytotoxicity. Unlike the findings for NK cells, NK T cells were dramatically diminished in Vav-1(-/-) mice and splenocytes from Vav-1 mutant mice failed to produce IL-4 in response to in vivo CD3 stimulation. These data highlight the important role of Vav-1 in NK T cell development and NK cell function. Publication Types Research Support, Non-U.S. Gov t PMID 11500824 [PubMed - indexed for MEDLINE] 2B4 2B4 is a cell-surface glycoprotein related to CD2 and implicated in the regulation of natural killer and T-lymphocyte function. It appears that the primary function of 2B4 is to modulate other receptor-ligand interactions to enhance leukocyte activation. PLCG2-deficient mice exhibit a loss of collagen-induced platelet aggregation, mast cell FcepsilonR function, and NK cell FcgammaRIII and 2B4 function. 1 Immunity. 2000 Jul;13(1) 25-35. Phospholipase Cgamma2 is essential in the functions of B cell and several Fc receptors. Wang D, Feng J, Wen R, Marine JC, Sangster MY, Parganas E, Hoffmeyer A, Jackson CW, Cleveland JL, Murray PJ, Ihle JN. Department of Biochemistry, St. Jude Children s Research Hospital, Memphis, Tennessee 38105, USA. Many receptors activate phospholipase Cgamma1 or -gamma2. To assess the role of PLCgamma2, we derived enzyme-deficient mice. The mice are viable but have decreased mature B cells, a block in pro-B cell differentiation, and B1 B cell deficiency. IgM receptor-induced Ca2+ flux and proliferation to B cell mitogens are absent. IgM, IgG2a, and IgG3 levels are reduced, and T cell-independent antibody production is absent. The similarity to Btk- or Blnk-deficient mice demonstrates that PLCgamma2 is downstream in Btk/Blnk signaling. FcRgamma signaling is also defective, resulting in a loss of collagen-induced platelet aggregation, mast cell FcepsilonR function, and NK cell FcgammaRIII and 2B4 function. The results define a signal transduction pathway broadly utilized by immunoglobulin superfamily receptors. Publication Types PMID 10933392 [PubMed - indexed for MEDLINE] GAB3 has no effect for phenotype. 1 Mol Cell Biol. 2003 Apr;23(7) 2415-24. Gab3-deficient mice exhibit normal development and hematopoiesis and are immunocompetent. Seiffert M, Custodio JM, Wolf I, Harkey M, Liu Y, Blattman JN, Greenberg PD, Rohrschneider LR. Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA. Gab proteins are intracellular scaffolding and docking molecules involved in signaling pathways mediated by various growth factor, cytokine, or antigen receptors. Gab3 has been shown to act downstream of the macrophage colony-stimulating factor receptor, c-Fms, and to be important for macrophage differentiation. To analyze the physiological role of Gab3, we used homologous recombination to generate mice deficient in Gab3. Gab3(-/-) mice develop normally, are visually indistinguishable from their wild-type littermates, and are healthy and fertile. To obtain a detailed expression pattern of Gab3, we generated Gab3-specific monoclonal antibodies. Immunoblotting revealed a predominant expression of Gab3 in lymphocytes and bone marrow-derived macrophages. However, detailed analysis demonstrated that hematopoiesis in mice lacking Gab3 is not impaired and that macrophages develop in normal numbers and exhibit normal function. The lack of Gab3 expression during macrophage differentiation is not compensated for by increased levels of Gab1 or Gab2 mRNA. Furthermore, Gab3-deficient mice have no major immune deficiency in T- and B-lymphocyte responses to protein antigens or during viral infection. In addition, allergic responses in Gab3-deficient mice appeared to be normal. Together, these data demonstrate that loss of Gab3 does not result in detectable defects in normal mouse development, hematopoiesis, or immune system function. PMID 12640125 [PubMed - indexed for MEDLINE] GAB2 deficient mast cells in mice result in impaired response of Fc epsilon RI. 1 Nature. 2001 Jul 12;412(6843) 186-90. Essential role for Gab2 in the allergic response. Gu H, Saito K, Klaman LD, Shen J, Fleming T, Wang Y, Pratt JC, Lin G, Lim B, Kinet JP, Neel BG. Cancer Biology Program, Division of Hematology and Oncology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA hgu@caregroup.harvard.edu. Dos/Gab family scaffolding adapters (Dos, Gab1, Gab2) bind several signal relay molecules, including the protein-tyrosine phosphatase Shp-2 and phosphatidylinositol-3-OH kinase (PI(3)K); they are also implicated in growth factor, cytokine and antigen receptor signal transduction. Mice lacking Gab1 die during embryogenesis and show defective responses to several stimuli. Here we report that Gab2-/- mice are viable and generally healthy; however, the response (for example, degranulation and cytokine gene expression) of Gab2-/- mast cells to stimulation of the high affinity immunoglobulin-epsilon (IgE) receptor Fc(epsilon)RI is defective. Accordingly, allergic reactions such as passive cutaneous and systemic anaphylaxis are markedly impaired in Gab2-/- mice. Biochemical analyses reveal that signalling pathways dependent on PI(3)K, a critical component of Fc(epsilon)RI signalling, are defective in Gab2-/- mast cells. Our data identify Gab2 as the principal activator of PI(3)K in response to Fc(epsilon)RI activation, thereby providing genetic evidence that Dos/Gab family scaffolds regulate the PI(3)K pathway in vivo. Gab2 and/or its associated signalling molecules may be new targets for developing drugs to treat allergy. PMID 11449275 [PubMed - indexed for MEDLINE] GAB2 deficient macrophages in mice result impaired phagocytosis. 1 J Cell Biol. 2003 Jun 23;161(6) 1151-61. Critical role for scaffolding adapter Gab2 in Fc gamma R-mediated phagocytosis. Gu H, Botelho RJ, Yu M, Grinstein S, Neel BG. Harvard Institutes of Medicine, 77 Ave. Louis Pasteur, HIM 1047 Boston, MA 02115, USA. hgu@caregroup.harvard.edu Grb2-associated binder 2 (Gab2), a member of the Dos/Gab subfamily scaffolding molecules, plays important roles in regulating the growth, differentiation, and function of many hematopoietic cell types. In this paper, we reveal a novel function of Gab2 in Fcgamma receptor (FcgammaR)-initiated phagocytosis in macrophages. Upon FcgammaR activation, Gab2 becomes tyrosyl phosphorylated and associated with p85, the regulatory subunit of phosphoinositide 3-kinase (PI3K), and the protein-tyrosine phosphatidylinositol Shp-2. FcgammaR-mediated phagocytosis is severely impaired in bone marrow-derived macrophages from Gab2-/- mice. The defect in phagocytosis correlates with decreased FcgammaR-evoked activation of Akt, a downstream target of PI3K. Using confocal fluorescence microscopy, we find that Gab2 is recruited to the nascent phagosome, where de novo PI3K lipid production occurs. Gab2 recruitment requires the pleckstrin homology domain of Gab2 and is sensitive to treatment with the PI3K inhibitor wortmannin. The Grb2 binding site on Gab2 also plays an auxiliary role in recruitment to the phagosome. Because PI3K activity is required for FcgammaR-mediated phagocytosis, our results indicate that Gab2 acts as a key component of FcgammaR-mediated phagocytosis, most likely by amplifying PI3K signaling in the nascent phagosome. PMID 12821647 [PubMed - indexed for MEDLINE]
https://w.atwiki.jp/sikoku/pages/150.html
筆記本番 筆記の大多数がSPI2である。それにSPI亜種、その他の筆記となる。すべてを把握したければ最初にバイブルとして紹介した この業界・企業でこの「採用テスト」が使われている! 2013年度版を読めばいいわけだが個別に紹介しておく。 まずSPI2 2014年度版 NEW! [テストセンター対応] これが本当のSPI2だ! (2014年度版) これが本当のテストセンターだ! 2014年度版 NEW! 直前でもOK! [パソコン版SPI2] これが本当のテストセンターだ! (2014年度版) CAB・GAB完全対策 2014年度版 NEW! CAB・GAB完全突破法! (2014年度版) [Web-CAB・GAB Compact・IMAGES対応] つづき就活関連書籍３ 文句・苦情・感想があればどうぞ 名前 コメント すべてのコメントを見る テスト１ -- (名無しさん) 2006-01-24 05 20 55
https://w.atwiki.jp/dollabo/pages/84.html
プレイヤー名 アンドリュー デッキ名 gabu結界 デッキコード[デッキコード] 1074y5z4q5F6u6B6H6T6W747D7K7N7S86898n8D8Maeatbr [ユニット] × 7 No003 アサシン × 2 No095 ガーゴイル × 1 No116 戦女神ヴァルキリー × 1 No092 熾天使ガブリエル × 2 No118 山の神パールヴァティー × 1 [マジック] × 33 No135 精神の秘箱 × 1 No137 心削りの石 × 2 No139 補充の緑泡 × 2 No143 未完のキューブ × 2 No144 封魔石の欠片 × 2 No147 生命の滅亡 × 1 No158 ソーマの烙印 × 3 No161 生体転送 × 1 No162 魔道転送 × 1 No163 生命吸収 × 3 No168 魔力の石 × 2 No169 契約の石 × 2 No174 支援要請の紅玉 × 1 No179 恐怖公の召喚 × 2 No182 降魔の蓮華門 × 2 No212 絶対防御 × 2 No217 闘神の結界 × 2 No237 LP抽出の力 × 2 解説 光を使わない結界デッキ。 恐怖公の召喚で出すアスタはユニット扱いなので 誰が何を言おうとユニット軸。 結界デッキは受けを前提として作られることが多いが このデッキは魔力の石と恐怖公の召喚を 展開上必要としているため 使う時にはLP管理を求められる。 基本的なメインユニットはガブリエルを仕様していくが デッキの構想ではあくまでもサブ。 メインは召喚で出されるアスタロスで あわよくばガブと並べて無双したい。 LP抽出を個人的にはうまく使っていて 例えば結界下のLP３０００以下で恐怖公の召喚をした時に 結界を割られれば降魔で結界を持って来ても発動できないので 困るが場のユニットにLP抽出をつけて回収すれば 必要分のLPはある程度確保出来るので 切り返し手として仕様することが出来る。 ただ使ってみて結界なのにLP管理を適当にできないのが 本当に辛いので難しいところ。 （LP３０００以下になると半分の機能しか使えなくなる） このデッキを使っていた動画がSTAGEAさんのやつであるので 詳しい展開の仕方はそっちを見るのが早いかも →Road to Legend #16 【デュエルオブレジェンド】 （STAGEA・ゲンダ vs ぽけ民・アクア） デッキ名の「gabu結界」の「gabu」が ローマ字になっているのは打ち間違いをそのまま残しているだけなので 深い意味はない。 このデッキに関してのコメントは以下のテキストボックスから 名前 コメント アンドリューのデッキリスト プレイヤーリストへ
https://w.atwiki.jp/tribalrug/pages/41.html
Gabeh ギャッベ、ギャベ【技法】 元々はルル語で「粗い」という意味だったが、最近では毛足の長いラグ全般を指す代名詞となっている。 中央ザクロス山脈の遊牧民がテントの外などで使用するために作ったものである。夏の山頂付近でのキャンプでは敷きふとん代わりに使われることもあるようだ。 技法的には、タテ方向に打ち込みが粗く、ヨコ糸が数本入っている物が多い。そのために粗くても毛足が抜けてこないようだ。 1950年代にスイス人のG.Bornet氏がその面白さを発見し欧州に紹介し、それが世界に広まっていった。 ギャッベの持つ奔放でアブストラクト(抽象的)パターンやナイーブなデザイン装飾が当時のクラシックな装飾にインパクトを与え大ブレイクしたようだ。 当初多くのイラン人ディーラーはあまりにも粗すぎて、交易には値しないとしていたが、最近ではアーティスティクな価値が認められて来ている。
https://w.atwiki.jp/hmiku/pages/59325.html
【検索用 gaburyu 登録タグ 作G 作GA-D 作り手 作曲家 作詞家】 + 目次 目次 特徴 リンク 曲 CD 動画 関連タグ内の更新履歴 コメント 特徴 作り手名：『gaburyu』 ハイパーポップ風の曲を制作している。 nyankobrq氏との合作『sweety glitch』は音楽イベント「HATSUNE MIKU Digital Stars 2021」の公式テーマソングになっている。 最近は『メイドサントウィッチシリーズ』を展開している。 使用VOCALOIDは初音ミク、可不、IA。 リンク YouTube 公式サイト Twitter 曲 sweety glitch ホロウ CD 絶景魔法 動画 関連タグ内の更新履歴 + 関連タグ内の更新履歴 関連タグ内の更新履歴 ※「gaburyu」「gaburyuCD」タグ内で最近編集やコメントのあった記事を新しい方から10件表示しています。 まだ曲、CDが登録されていません。 コメント 名前 コメント
https://w.atwiki.jp/kakis/pages/5777.html
jagabe /// / 絆創膏、ばんそうこう、バンドエイド、キズテープ jag\abe \ 14 seren klel 粘着布 \ [ ova ] \ 傷口に絆創膏を貼る \ 大きな絆創膏 \