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プレイヤーキャラクター格納庫 ここは各プレイヤーが自分のキャラクターを公開、保存する格納庫です。 使用は強制ではなく自由なので、気が向いたら使ってください。 こちらは各自のプレイヤーが管理する項目です Index プレイヤーキャラクター格納庫a～zaoinu asd vza A～ZDEE GAB JAM RF11 あ～んせい たらら ア～ンアシタ スナオ シメサバ セントラル越前 漢字ＨＮ白石 楽斎 船橋 鋼 廣川 宗也 露木 雨の人 永楽 その他（記号等）￥600 295 a～z aoinu 【アート・ス・コーシ】? asd 【永源寺 港】? vza 【アサヅキコハク】? 【オジジ・モテーナイ】? A～Z DEE 【ディー・エール】? GAB 【六波羅入道】? JAM 【ジャ・ムール】? 【エーム・ジェイ】? RF11 【レイン＝フォレスト】? あ～ん せい 【セリア・リフィード】? たらら 【ラーラ・アリア】? ア～ン アシタ スナオ 【アシタスナオ】? シメサバ 【シメサバ】? セントラル越前 【セントラル越前】? 漢字ＨＮ 白石 【シロ・イシーラ】? 【白波 キッカ】? 楽斎 【大友流星】? 【レニー・Ｓ・ライン】? 船橋 【船橋ナガト】? 【橘 梓】? 鋼 【高原 錫】? 廣川 【廣野諒】? 宗也 【綾里 明人】? 露木 【リン・カーリー】? 雨の人 【ムム・ラーラ】? 永楽 【永楽】? 【エイミ・フジサワ】? 『野良デーモンの森』で死亡 その他（記号等） ￥600 【チュリー】? 【ロク】? 『VSヘカトンケイル』で死亡 295 【ジィ＝エイス】? -
https://w.atwiki.jp/buy-doujin/pages/101.html
サークル名：GABALL SCREEN 作家名：ゆきうさぎ ホームページ：GABALL SCREEN
https://w.atwiki.jp/daigakunext/pages/14.html
慶應義塾大学大学湘南藤沢キャンパス（SFC） 基本情報 学校公式web http //www.sfc.keio.ac.jp/ 無線LAN環境 全教室、屋外もほぼカバー 授業中のPC利用率 95% Twitter普及率 40% 学内メディア SFC CLIP その他特徴 iPhone所有率も高い プロジェクト概要 学校非公認プロジェクト#sfcnoteプロジェクト 授業中にtwitterで #sfc_(教室名) タグを付けてつぶやく。 09/10/19に開始された 関連リンク SFCのーたー ポストのあった授業のポストをまとめたノートが見られます。 フォローすると、ノートが生成された際にお知らせしてくれます。 作成者 @kakuit #sfcnote wiki #sfcnote へのポスト（意見、アイデア、技術情報、メディア掲載情報）や、利用に関するユーザーサポートサイト 管理者 @n0mzk #sfcnoteプロジェクト 観察・考察記 言い出しっぺによるブログ 管理者 @gab_ken 関わっている人々 言い出しっぺ：@gab_ken プロジェクトの状況 プロジェクト開始１ヶ月を経て利用者の伸び悩みや 様々な問題への対応のため、オープンプロジェクトからプロジェクトチーム化を検討中 検討中のスライドは、こちらを参照 その他、授業での教員公認利用なども活発 SFC CLIP（学内メディア）による、 授業での公式利用状況や教員のTwitterアカウントまとめ このページの編集にご協力下さい。 コメント欄へは、編集の報告や追加情報や内容についての注意等をお願いします。 授業での公式利用状況や〜のリンクが切れてマース -- saori (2009-11-19 12 53 26) 名前 コメント
https://w.atwiki.jp/ptm_bn0201/pages/383.html
Biography-Peter Gabriel Discography-Peter Gabriel
https://w.atwiki.jp/hctechnowiki/pages/21.html
Happy Gabber（ハッピーガバ） 工事中。
https://w.atwiki.jp/secretd/pages/23.html
チベットSOGABE 所属：裏番長グループ 性別：男 所持武器：足を引っ張る腕力 攻：12 防：10 体：5 精：3 FS「悟り」：0 元ネタ：初恋限定 特殊能力『所詮は曽我部』 効果：？？？ 範囲：同マス 0 対象：味方1名 0 時間・回数：1ターン 1倍 効果付属：？？？ 補正１：なし ボーナス：？？？ 秘匿される項目：効果、効果付属、ボーナス ★能力公開 効果：発動率半減 30 範囲：同マス 0 対象：味方１名 0 時間：１ターン １倍 効果付属：なし 補正：なし ボーナス：なし 【発動率：70％ 成功率：100％】 能力説明 持前の足手まとい力で、同マス1名（味方）の邪魔をする能力。 能力発動しようとする味方に「うまい棒が一本足りない」とか訴えて邪魔するんだと思います。 キャラ説明： 仏門を志すも、何が何だかよく分からんうちにお笑い芸人になってしまった25 歳。「チベットSOGABE」などといういかにも中途半端で個性の無い芸名が示すと おり、痛々しさがウリの面白くない系。そのあまりに痛々しい姿は物理的な破壊 力を持つ。思いのほか図太い。
https://w.atwiki.jp/seihou/pages/571.html
東京音頭 （2012：名言：とうきょうおんど） 2012年合宿テーマソング候補曲。 GAB♭A。 梅が島殺人事件の被害者『MI☆NA☆TO』の鎮魂曲 イントロから先に進めない
https://w.atwiki.jp/tiger/pages/7.html
SOS1-/- mice impair Cdc42 activation in PC12 cells. SOS-/- fly impair the development of eyes. Overexpression of GAB1 exhibit neurite outgrowth, DNA synthesis and survival in PC12 cells. SHCB-deficient animals exhibit a loss of peptidergic and nonpeptidergic nociceptive sensory neurons, Hippocampal long-term potentiation in ShcC mutant mice is significantly enhanced. SHCA controls the size of brain. Cbl-b null mice exhibit the enhancement of long-term memory. SOS1-/- mice impair Cdc42 activation in PC12 cells. 1 Mol Biol Cell. 2005 May;16(5) 2207-17. Epub 2005 Feb 23. Local phosphatidylinositol 3,4,5-trisphosphate accumulation recruits Vav2 and Vav3 to activate Rac1/Cdc42 and initiate neurite outgrowth in nerve growth factor-stimulated PC12 cells. Aoki K, Nakamura T, Fujikawa K, Matsuda M. Department of Tumor Virology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan. Neurite outgrowth is an important process in the formation of neuronal networks. Rac1 and Cdc42, members of the Rho-family GTPases, positively regulate neurite extension through reorganization of the actin cytoskeleton. Here, we examine the dynamic linkage between Rac1/Cdc42 and phosphatidylinositol 3-kinase (PI3-kinase) during nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells. Activity imaging using fluorescence resonance energy transfer probes showed that PI3-kinase as well as Rac1/Cdc42 was transiently activated in broad areas of the cell periphery immediately after NGF addition. Subsequently, local and repetitive activation of PI3-kinase and Rac1/Cdc42 was observed at the protruding sites. Depletion of Vav2 and Vav3 by RNA interference significantly inhibited both Rac1/Cdc42 activation and the formation of short processes leading to neurite outgrowth. At the NGF-induced protrusions, local phosphatidylinositol 3,4,5-trisphosphate accumulation recruited Vav2 and Vav3 to activate Rac1 and Cdc42, and conversely, Vav2 and Vav3 were required for the local activation of PI3-kinase. These observations demonstrated for the first time that Vav2 and Vav3 are essential constituents of the positive feedback loop that is comprised of PI3-kinase and Rac1/Cdc42 and cycles locally with morphological changes. Publication Types Research Support, Non-U.S. Gov t PMID 15728722 [PubMed - indexed for MEDLINE] SOS-/- fly impair the development of eyes. 1 Cell. 1991 Jan 11;64(1) 39-48. Genetic dissection of a neurodevelopmental pathway Son of sevenless functions downstream of the sevenless and EGF receptor tyrosine kinases. Rogge RD, Karlovich CA, Banerjee U. Department of Biology, University of California, Los Angeles 90024. We have isolated a dominant mutation in a gene called Son of sevenless (Sos) that is an allele-specific suppressor of the sevenless phenotype. This suppressor function is autonomously required in R7 and is sensitive to the dosage of the Sos and bride of sevenless genes. Loss-of-function alleles of Sos are recessive lethals, but in the eye Sos has a role in R cell development. Mutations in Sos also interact with the Ellipse allele of the Drosophila EGF receptor. We propose a model suggesting that the Sos product is downstream of sevenless and the EGF receptor, and that the dominant suppression results from the overexpression or increased activity of the gene product. Publication Types Research Support, Non-U.S. Gov t Research Support, U.S. Gov t, P.H.S. PMID 1846090 [PubMed - indexed for MEDLINE] Overexpression of GAB1 exhibit neurite outgrowth, DNA synthesis and survival in PC12 cells. 1 J Biol Chem. 1999 Dec 24;274(52) 37307-14. Gab1 mediates neurite outgrowth, DNA synthesis, and survival in PC12 cells. Korhonen JM, Said FA, Wong AJ, Kaplan DR. Montreal Neurological Institute, Brain Tumor Research Centre, Montreal, Quebec H3A 2B4, Canada. The Gab1-docking protein has been shown to regulate phosphatidylinositol 3-kinase PI3K activity and potentiate nerve growth factor (NGF)-induced survival in PC12 cells. Here, we investigated the potential of Gab1 to induce neurite outgrowth and DNA synthesis, two other important aspects of NGF-induced neuronal differentiation of PC12 cells and NGF-independent survival. We generated a recombinant adenovirus encoding hemagglutinin (HA)-epitope-tagged Gab1 and expressed this protein in PC12 cells. HA-Gab1 was constitutively tyrosine-phosphorylated in PC12 cells and induced the phosphorylation of Akt/protein kinase B and p44/42 mitogen-activated protein kinase. HA-Gab1-stimulated a 10-fold increase in neurite outgrowth in the absence of NGF and a 5-fold increase in NGF-induced neurite outgrowth. HA-Gab1 also stimulated DNA synthesis and caused NGF-independent survival in PC12 cells. Finally, we found that HA-Gab1-induced neuritogenesis was completely suppressed by pharmacological inhibition of mitogen-activated protein kinase kinase (MEK) activity and 50% suppressed by inhibition of PI3K activity. In contrast, HA-Gab1-stimulated cell survival was efficiently suppressed only by inhibition of both PI3K and MEK activities. These results indicate that Gab1 is capable of mediating differentiation, DNA synthesis, and cell survival and uses both PI3K and MEK signaling pathways to achieve its effects. Publication Types Research Support, Non-U.S. Gov t PMID 10601297 [PubMed - indexed for MEDLINE] SHCB-deficient animals exhibit a loss of peptidergic and nonpeptidergic nociceptive sensory neurons, 1 Neuron. 2000 Dec;28(3) 819-33. The mammalian ShcB and ShcC phosphotyrosine docking proteins function in the maturation of sensory and sympathetic neurons. Sakai R, Henderson JT, O Bryan JP, Elia AJ, Saxton TM, Pawson T. Program in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue, M5G 1X5, Toronto, Ontario, Canada. Shc proteins possess SH2 and PTB domains and serve a scaffolding function in signaling by a variety of receptor tyrosine kinases. There are three known mammalian Shc genes, of which ShcB and ShcC are primarily expressed in the nervous system. We have generated null mutations in ShcB and ShcC and have obtained mice lacking either ShcB or ShcC or both gene products. ShcB-deficient animals exhibit a loss of peptidergic and nonpeptidergic nociceptive sensory neurons, which is not enhanced by additional loss of ShcC. Mice lacking both ShcB and ShcC exhibit a significant loss of neurons within the superior cervical ganglia, which is not observed in either mutant alone. The results indicate that these Shc family members possess both unique and overlapping functions in regulating neural development and suggest physiological roles for ShcB/ShcC in TrkA signaling. PMID 11163269 [PubMed - indexed for MEDLINE] Hippocampal long-term potentiation in ShcC mutant mice is significantly enhanced. 1 J Neurosci. 2005 Feb 16;25(7) 1826-35. Hippocampal synaptic modulation by the phosphotyrosine adapter protein ShcC/N-Shc via interaction with the NMDA receptor. Miyamoto Y, Chen L, Sato M, Sokabe M, Nabeshima T, Pawson T, Sakai R, Mori N. Department of Molecular Genetics, National Institute for Longevity Sciences, Oobu 474-8522, Japan. N-Shc (neural Shc) (also ShcC), an adapter protein possessing two phosphotyrosine binding motifs [PTB (phosphotyrosine binding) and SH2 (Src homology 2) domains], is predominantly expressed in mature neurons of the CNS and transmits neurotrophin signals from the TrkB receptor to the Ras/mitogen-activated protein kinase (MAPK) pathway, leading to cellular growth, differentiation, or survival. Here, we demonstrate a novel role of ShcC, the modulation of NMDA receptor function in the hippocampus, using ShcC gene-deficient mice. In behavioral analyses such as the Morris water maze, contextual fear conditioning, and novel object recognition tasks, ShcC mutant mice exhibited superior ability in hippocampus-dependent spatial and nonspatial learning and memory. Consistent with this finding, electrophysiological analyses revealed that hippocampal long-term potentiation in ShcC mutant mice was significantly enhanced, with no alteration of presynaptic function, and the effect of an NMDA receptor antagonist on its expression in the mutant mice was notably attenuated. The tyrosine phosphorylation of NMDA receptor subunits NR2A and NR2B was also increased, suggesting that ShcC mutant mice have enhanced NMDA receptor function in the hippocampus. These results indicate that ShcC not only mediates TrkB-Ras/MAPK signaling but also is involved in the regulation of NMDA receptor function in the hippocampus via interaction with phosphotyrosine residues on the receptor subunits and serves as a modulator of hippocampal synaptic plasticity underlying learning and memory. PMID 15716419 [PubMed - indexed for MEDLINE] SHCA controls the size of brain. 1 J Neurosci. 2006 Jul 26;26(30) 7885-97. Neural-specific inactivation of ShcA results in increased embryonic neural progenitor apoptosis and microencephaly. McFarland KN, Wilkes SR, Koss SE, Ravichandran KS, Mandell JW. Department of Pathology (Neuropathology), Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia 22908, USA. Brain size is precisely regulated during development and involves coordination of neural progenitor cell proliferation, differentiation, and survival. The adapter protein ShcA transmits signals from receptor tyrosine kinases via MAPK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) and PI3K (phosphatidylinositol 3-kinase)/Akt signaling pathways. In the CNS, ShcA expression is high during embryonic development but diminishes as cells differentiate and switches to ShcB/Sck/Sli and ShcC/N-Shc/Rai. To directly test ShcA function in brain development, we used Cre/lox technology to express a dominant-negative form of ShcA (ShcFFF) in nestin-expressing neural progenitors. ShcFFF-expressing mice display microencephaly with brain weights reduced to 50% of littermate controls throughout postnatal and adult life. The cerebrum appeared most severely affected, but the gross architecture of the brain is normal. Body weight was mildly affected with a delay in reaching mature weight. At a mechanistic level, the ShcFFF microencephaly phenotype appears to be primarily attributable to elevated apoptosis levels throughout the brain from embryonic day 10.5 (E10.5) to E12, which declined by E14.5. Apoptosis remained at normal basal levels throughout postnatal development. Proliferation indices were not significantly altered in the embryonic neuroepithelium or within the postnatal subventricular zone. In another approach with the same nestin-Cre transgene, conditional deletion of ShcA in mice with a homozygous floxed shc1 locus also showed a similar microencephaly phenotype. Together, these data suggest a critical role for ShcA in neural progenitor survival signaling and in regulating brain size. PMID 16870734 [PubMed - indexed for MEDLINE] Cbl-b null mice exhibit the enhancement of long-term memory. 1 Proc Natl Acad Sci U S A. 2006 Mar 28;103(13) 5125-30. Epub 2006 Mar 20. Enhancement of long-term memory retention and short-term synaptic plasticity in cbl-b null mice. Tan DP, Liu QY, Koshiya N, Gu H, Alkon D. Blanchette Rockefeller Neurosciences Institute, Rockville, MD 20850, USA. dptan@brni-jhu.org The cbl-b gene is a member of the cbl protooncogene family. It encodes a protein with multiple domains, which can interact with other proteins in a variety of signaling pathways. The functions of cbl family genes in the brain are unknown. In this report, we used genetic, immunohistochemical, behavioral, and electrophysiological approaches to study the role of cbl-b in learning and memory. Cbl-b null mice developed normally and had no abnormalities in their locomotor performance. In spatial learning and memory studies, cbl-b null and WT mice performed similarly during training. To test memory retention, two probe trials were used. cbl-b null mice performed slightly better 1 day after training. However, in the probe trial 45 days after training, the cbl-b null group showed significantly higher memory retention than WT mice, suggesting an enhancement of long-term memory. Using electrophysiological approaches, we found there was enhanced paired-pulse facilitation in the Schaffer Collateral-CA1 glutamatergic synapses of the cbl-b null mice. On the other hand, there was no difference in long-term potentiation between the two groups of mice. In summary, we provide evidence that (i) cbl-b protein is concentrated in the synaptic regions of CA1, CA3, and the dentate gyrus of the hippocampus; (ii) cbl-b null mice have enhanced long-term memory; and (iii) cbl-b null mice show an enhancement in short-term plasticity. These results indicate that cbl-b is a negative regulator of long-term memory, and its neuronal mechanism regulates synaptic transmission in the hippocampus. PMID 16549761 [PubMed - indexed for MEDLINE]
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Gabriella（ガブリエッラ） 害虫の魔女。その性質は恐怖。 あらゆる物体に対し過度なまでに怯える。そして、同じ恐怖を侵入者にも味わわせようとする魔女。 非常にグロテスクな外観をしているが、それと相反するように内面は脆い。 特に黒く小さいものが苦手で、常に結界の中から出たいと思っている。 使い魔 Gisela（ギーゼラ） 害虫の魔女の使い魔。その性質は悪魔。 黒くて小さくて大量にいる存在。魔女が最も恐れるもののひとつだ。 結界の中には彼らが敷き詰めてあると言ってよく、正直勘弁してください。 魔法少女時代 五輪吹 舞（ごりぶき まい）
https://w.atwiki.jp/vidcrown/pages/12.html
Luxemburg, 6. Mai 2015 ein unbekannter Angriff mit einem laserpointer kaufen Air Rettungshubschrauber im Flug über Vianden. Die Piloten versuchen, Kontakt mit dem gefährlichen Lichtstrahl zu vermeiden. Der Vorfall ist genug, ernst, dass es eine Untersuchung durch die Polizei Luxemburg auslöst. Was die Zahl der Angriffe auf Flugzeuge oder Hubschrauber, stagnierte der Umsatz im Großherzogtum. Dies wurde in einer Antwort auf eine parlamentarische Anfrage, die, dass im Jahr 2013 gab es 33 gemeldete Angriffe Behörden von Luxemburg zu, darunter 13 im Großherzogtum gibt hervorgehoben. Im laserpointer grün Jahr 2014 gab es 32, elf in Luxemburg. In den ersten fünf Monaten dieses Jahres gab es 13 Angriffe, von denen sechs sollen Ort im Großherzogtum genommen haben. Klassifizierung von Lasereinrichtungen (gemäß den Normen NF EN 60825-1, IEC 825-1 und der Index C 43-805). © Universität Bordeaux 1 Die Mannschaften sind verpflichtet, jeden Angriff von Laser-Pointer zu melden. Wenn die Täter ermittelt werden, könnten sie eine Gefängnisstrafe von bis zu zehn Jahren konfrontiert, unter anderem für Angriff und Batterie, da dies kann dazu führen. Allerdings ist es sehr schwierig, den Schützen laserpointer 500mw zu bestimmen. Ein Augenarzt von Luxemburg, der anonym bleiben möchte, hat eine junge Patientin, die nach dem Spiel ein Spiel, wo Sie musste die längste mit einem Laser in das Auge zu halten Teil der sein Augenlicht verloren hatte, behandelt. "Es gab eine burn, die die Netzhaut durchbohrt hat," sagte der Arzt. Die junge Frau wird nie seine Vision zurück auf 100%. Es ist selten, mit diesen Geräten erblinden. Aber dieses System, zum ersten Mal auf dem Boden getestet, ist entworfen, um in der Zukunft bei einer Vielzahl von militärischen Fahrzeugen integriert werden. "Dieser Test stellt den nächsten Schritt in der Entwicklung von laserpointer shop und bei Helikoptern, Schiffen und Militärlastwagen geheilt", sagt Lockheed Martin in einer Erklärung. Neben der hohen Genauigkeit und niedrige Letalität im Vergleich zu konventioneller Munition, hat diese Waffen viele andere Vorteile. Sie überwindet die Beschränkungen des Transports und der Laserpointer 10000mw Laserpointer 10000mw der Munition (Geschosse, Flugkörper) und die Gefahr einer Explosion, die durch den letzteren im Brandfall gestellt. Und solange es mit Strom versorgt wird, kann dieser Laser eine Reihe von unbegrenzter Bursts zu ziehen. Jeder Schuss wird einen Dollar kosten. Ein Bericht des US Congressional Research Service beliefen sich Ende 2014 zwischen dem Preis einer einzigen Rakete Interception "Standard" 800.000 und 1,4 Millionen Dollar. Im Gebrauch werden die Kosten für die Entwicklung dieser neuen Waffe (von der Marine $ 32.000.000 geschätzt) schnell amortisieren. laserpointer 5000mw FRANKREICH. In Frankreich wie in vielen Ländern nur Laser, dessen Leistung nicht überschreiten 1 mW (dh, die der Klassen 1 und 2) sind zum Vertrieb zugelassen. Aber über das Internet, ist es sehr einfach, leistungsfähigere Modelle, Kategorien 3 und 4, in der Regel für den professionellen Einsatz reserviert zu bekommen. Nach Ansicht von Experten, die gefährlichste sind die laserpointer 2000mw , die in der grünen emittieren, mit einer Leistung von bis zu 1500 mW (Kategorie 4 gehört). Diese Art von Laser, um kurz die Augen für ein paar Minuten kann die Netzhaut brennen und ermöglichen irreversible Schäden. Weil der Grad der Schädigung hängt von der Laserleistung und der Belichtungszeit."Wenn der Zeiger über einmal die Augen, ist es egal", sagte der Augenarzt. Die Gefahr, mit den Fahrern ist, dass sie ihre Aufmerksamkeit zu verlieren, indem sie noch eine kurze Zeit geblendet.