約 2,076,098 件
https://w.atwiki.jp/jailbreakapps/pages/13.html
JailBreakアプリ対応表 アプリ名 対応iOS 機能 備考 Activator 4.2.1 コピペ等の機能を追加。PlusPackでもっと便利 AskToCall 電話前に確認 AskToSend メール前に確認 BrowserChanger 標準ブラウザ変更 SBSettings 多機能メニュー追加 Action Menu コピペ等の機能を追加。PlusPackでもっと便利 Backgrounder バックグラウンド動作。純正マルチタスクとの違いが分かる人には便利 Clock Hide ロック画面の時計非表示 FastNotesJ 日本語対応メモ FakeClockUp 動作毎のアニメーションを短縮する Five Icon Dock Dockアイコンを５つに FolderEnhancer 有料。フォルダ機能拡張 Gridlock アイコン配置自由自在 Iconoclasm ホームのアイコンの行、列カスタム iFile ファイル操作。 Infinidock 有料。Dockにページ追加、Dockアイコン数変更 $0.99 Infinifolders 有料。フォルダ内スクロール可能に。FolderEnhancerとの共存不可 LiveClock 時計アイコンが動くようになる MarkThatMessage MMSの全部に日時 MMSReq センター問い合わせ MultiCleaner 有料。アプリを全て終了したり、タスクバーの機能を追加したり WallpaperAutoChanger ホーム画面壁紙の自動切り替え WeatherIcon 天気アイコンが天気を教えてくれるようになる MobileTerminal Terminal NoLockScreen ロック画面を無くす NoSpot スポットライト検索を無くす No Screenshot Flash スクリーンショットの光を無くす No Page Dots Dockの上にある点を無くす Notified Push通知のログ OfflineMaps Googleマップをキャッシュしてくれたり PasteboardStacker コピペ履歴 PreventSleep 画面消してもWifi動いたままにする qTweeter 投稿専用Twitterクライアント QuickReply for SMS メッセージ受信時に返信ボタン追加 SMSアプリ起動せず返信 QuickScrollPlus スクロールバーをドラッグして移動できる SilentPatcher カメラ音消し StealthCam 有料。ボリュームボタンでシャッター、画面消しても撮影 SpringFlash ライトを付ける Shrink 有料。アイコンサイズ自由自在 TetherMe 純正テザリングON。パケ死しても自己責任。 User Agent Faker UA変更
https://w.atwiki.jp/freetrain-exav/pages/120.html
最終更新日時：2010年04月19日 (月) 16時47分48秒 RailStationaryContrib 鉄道アクセサリコントリビューションとは アクセサリとして設置できる建築物を追加するコントリビューションです。 追加したアクセサリは、アクセサリコマンドで建築することができます。 コンクリート高架橋や盛土高架、詰所などがプラグイン化されています。 書式 鉄道アクセサリの定義 contribution type="railStationary" id="コントリビューションID" group グループ名 /group name アクセサリの名前 /name price 建築費用 /price size 横幅,縦幅 /size height 高さ /height sprite スプライト定義 /sprite /contribution 説明 グループ名を指定すると、複数のアクセサリをまとめて１つのグループに配置します。 アクセサリの名前とグループ名は、どちらか１つを必ず指定しなければなりません。 横幅は、X軸方向（下端から右端）のボクセルの幅を、縦幅は、Y軸方向（下端から左端）のボクセルの幅をそれぞれ指定します。 高さは、アクセサリの高さを指定します。 sprite /sprite 内でスプライトの定義を行います。スプライトの定義については、スプライトタグを参照してください。 アクセサリの画像の作成方法は、建物と同じです。建物を作るを参照してください。 画像の定義の例については、建築物定義の例を参照してください。
https://w.atwiki.jp/rbxjptrain/pages/297.html
都葉鉄道 とは、ゆう氏(yuu_557)が社長を務める、社員制(運行制)の鉄道である。 最近は運行をあまりしていない。 また、列車が脱線しやすかったり、独自のドア開閉機能が運行中に故障したり、軽量化出来ておらずスマホでのプレイには適しないなどの問題がある。 だが、現時点ではまだ正式リリースしていないので、今後の発展に期待できる。 車両 3000系、1500系、2000系（作成中） 路線図 現状都葉鉄道では、本線 都葉～桜井、支線 都葉～新飯塚が営業されている。 グループリンク https //www.roblox.com/groups/32713024/Japanese-toyo-rail-way ゲームリンク https //www.roblox.com/games/14016409599/Japanese-toyo-rail-way discordサーバーリンク https //discord.gg/GuZdWhDxMz
https://w.atwiki.jp/ficrailworld/pages/14.html
ここからよくある質問をまとめます。 私は他の会社が他の同盟に加盟しております。その場合はFicrail Worldに加盟してよいのでしょうか？ 加盟できます。 私が作った会社はすでにほかの同盟に加盟しています。その場合はFicrail Worldに加盟してよいのでしょうか？ 加盟できますが、一方の同盟のルールに抵触する場合は申し訳ありませんがお断りさせていただきます。 (こちらは開設当初より決められていましたが、従来の概要には記載されていませんでした。加盟ユーザーの方におかれましては、ご容赦いただけますようお願いいたします。) 私はすでにFicrail Worldに加盟していますが、複数社加盟してもよいのですか？ 構いません。
https://w.atwiki.jp/mahjlocal/pages/643.html
読み ドラゴンズテイル 正式名称 別名 龍尾 竜の尾 和了り飜 1飜 牌例 123456789南南発発発 解説 一気通貫、発の刻子、風牌の雀頭で成立。 成分分析 Dragon's Tailの半分は見栄で出来ています。Dragon's Tailの21%は砂糖で出来ています。Dragon's Tailの11%は呪詛で出来ています。Dragon's Tailの8%は宇宙の意思で出来ています。Dragon's Tailの4%は海水で出来ています。Dragon's Tailの2%は心の壁で出来ています。Dragon's Tailの1%は気の迷いで出来ています。Dragon's Tailの1%は歌で出来ています。Dragon's Tailの1%は嘘で出来ています。Dragon's Tailの1%はお菓子で出来ています。 下位役 上位役 複合の制限 この役は一気通貫の付加役である。 採用状況
https://w.atwiki.jp/nezumi3/pages/17.html
Kaillera導入までの流れ まずKailleraの入手！ すでに目的Emu等に入っている場合は次項目に移ってください。 Kaillera ClientとServerもしくは導入されたEmuを本家より入手してください。 Kaillera 本家HPはこちらをクリック願います 環境の準備について モデム直PCの場合、セキュリティがない場合は設定は不要な可能性があります。 ルータが存在する場合、セキュリティで通信がうまくいかない場合があります。 それぞれルータやセキュリティの設定を行ってください。 使用するポートは27888（先のkaillera設定で変更可能）です。 ポート設定：TCP 27888、UDP 27888を解放してください。 稼動出来ない時は、UDP 1000-6000も追加開放願います。 ルータ、セキュリティのポート開放手順についてはyamikageさんのHP ポート開放方法にて詳しく紹介されていますので確認お願いします。
https://w.atwiki.jp/railsimpiwiki/pages/55.html
利用規約等は各掲載先で必ずご確認ください。 ホーム照明(pasuko) ホーム照明(pasuko) PI名 paホーム照明 作者 pasuko PI画像 公開先URL プラグイン(メタセコイア素材)置き場（by pasuko) 最終更新日 2015年6月7日 利用規約 こちらに掲載 その他
https://w.atwiki.jp/railsimpiwiki/pages/25.html
利用規約等は各掲載先で必ずご確認ください。
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]
https://w.atwiki.jp/railsimpiwiki/pages/39.html
利用規約等は各掲載先で必ずご確認ください。 トヨタ エスティマルシーダ(?!?!?Aya) トヨタ エスティマルシーダ(?!?!?Aya) PI名 トヨタ エスティマルシーダ 作者 ?!?!?Aya PI画像 公開先URL NITROUS DRIVE 最終更新日 2015年11月16日 利用規約 その他