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https://w.atwiki.jp/vocaloidenglishlyric/pages/669.html
【Tags Ienourademanbougashinderu-P M tM Gumi】 Original Music title My Colorful Confuse Romaji music title My Colorful Confuse Music Lyrics written, Voice edited by タカハシヨウ (Takahashi You) / 家の裏でマンボウが死んでるP (Ienourademanbougashinderu-P) Music arranged by タカハシヨウ (Takahashi You) / 家の裏でマンボウが死んでるP (Ienourademanbougashinderu-P) Singer(s) Gumi (Megpoid) Click here for the original Japanese Lyrics English Lyrics (translated by vgboy / vgperson)： My graduation day had arrived, And I was to arrive at 8 30 But according to the clock by the bed, It s already 8 20... I figured I had just enough time to make it, But despite my precidament, someone appeared... It s an old man rubbing students with white noodles! Those half-boiled noodles were making them all slippery! But in my first year, judo instructor Shudo taught me... THE COLLARBONE CRACK! After surmounting a tight situation, next up, There were crows dripping miso on students necks! But in my first year, science teacher Mokuhara taught me... THE SULPHIRIC ACID SPLASH! After putting an end to a crow s life, next, I saw a road paved with marbles made of mucus! But in my first year, club leader Kawata taught me... PERSONAL ANTI-GRAVITY! After ignoring the entire purpose of a road, There were lizards rubbing their eggs on people s necks! But in my second year, classmate Kandagawa taught me... THE CERBERUS RENTAL! Thank you - the things you ve all given me Live on within me - and so I have five minutes left... After rendering a lizard unable to breed, An old lady was flattening the town since she didn t know her way! But in my second year, geology teacher Okaguchi taught me... THE JUNGLE GROWER! After leading an old lady into disaster, next, I bumped into air that would vaporize a human body in seconds! But in my third year, biology teacher Mitsui taught me... THE MECHANICAL MOLT! After slipping past an atmospheric assault, I saw a demon king who stopped time when his butt clenched! But in my third year, hygiene teacher Shimatsu taught me... THE FALLING ANGEL! [A POWERFUL LAXATIVE!] After utterly humiliating a demon king, next, I saw a railway crossing that closed for five minutes, and no other routes! If this it how it is, then I m finished! No matter who it was... No one could get out of this situation! The time was 8 40, And I was trudging back home But my defeated eyes Saw seven figures... "Congratulations!" Everyone had waited for me, And spoke to me so tenderly I didn t want to cry, In fact, I wanted to smile, But neverending tears fell where I stood And I wanted to tell the people I had met here how I felt, but... I m sorry - you taught me how to street fight, But you never taught me how to say thank you very well As I bawled out, I was consoled By all of your gentle hands... Romaji lyrics (transliterated by vgboy / vgperson)： Sotsugyoushiki no hi ga otozureta Hachi-ji-han ni toukou suru hazu ga Makura moto no tokei ga sashiteiru no wa Mou hachi-ji ni-juu-fun Girigiri ma ni au ka douka no jikan Sonna pinchi no naka yatsu ga arawareta Gakusei no waki o soumen de migaku kei ojisan da! Yudetate no soumen de shikotama tsurutsuru sareru! Demo sonna toki wa ichi-nensei no koro ni juudou no Shudo-sensei ni osowatta Hissatsu - Sakotsu Kudaki! Hitotsu no pinchi o norikoeta sono saki ni ita no wa Gakusei no unaji ni miso o tarashite kuru kei karasu! Demo sonna toki wa ichi-nensei no koro ni kagaku no Mokuhara-sensei ni osowatta Hissatsu - Ryuusan Houchiku! Ichiwa no karasu no inochi o owaraseta sono ato ni mita no wa Naniraka no neneki biidama o shiki tsumete aru kei douro! Demo sonna toki wa ichi-nensei no koro ni bukatsu no Kawata-senpai ni osowatta Hissatsu - Jiriki Hanjuuryoku! Ippon no douro ni sono imi o ushinawaseta ato ita no wa Ouryoku no tamago o eri no ura kosuritsukeru kei hachuurui! Demo sonna toki wa ni-nensei no koro ni kurasu no Kandagawa-kun ni osowatta Hissatsu - Keruberosu Rentaru! Arigatou minna kara moratta mono ga Watashi no naka de ikiteru wa nokori jikan wa ato go-fun Ichishu no hachuurui no hanshoku o samatageta ato mita no wa Michi ga wakaranai kara machi o taira ni shiteru kei obasan! Demo sonna toki ni-nensei no koro ni chigaku no Okaguchi-sensei ni osowatta Hissatsu - Janguru Hatsumou! Hitori no obasan o sounan ni michibiita ato butsukatta no wa Jintai teido nara wazuka suubyou de oshaka ni dekiru kei taiki! Demo sonna toki san-nensei no koro ni seibutsu no Mitsui-sensei ni osowatta Hissatsu - Kikaika Dappi! Hitotsu no taiki no moukou o surinuketa ato mita no wa Shiri-suji o hikishimeteru aida dake toki o tomerareru kei maou! Demo sonna toki wa san-nensei no koro ni hoken no Shimatsu-sensei ni osowatta Hissatsu - Kyouryoku na Gezai! Ichi-maou ni kyoudai no kutsujoku o ataeta ato mita no wa Shimaru to go-fun kurai akanai hoka no ruuto mo nai kei fumikiri! Kou natte shimattara oshimai da! Dare hitori kono joukyou o Daha suru koto nado dekinai! Jikoku wa hachi-ji yon-juu-fun Tobotobo aruku kaeri no michi Mou akirameta hitomi ni utsutta Shichi-jin no hitokage "Sotsugyou omedetou" Matte ite kureta minna no Koe wa totemo yawarakakute Nakitaku nante nai no ni Waratteitai no ni Tomaranai namida no ochiru saki kono basho ni Koko de deatta hito-tachi ni tsutaetai koto ga aru no ni Gomennasai sutoriito faito wa osowatta kedo Jouzu ni arigatou o tsutaeru houhou wa osowattenai no Tada nakijakuru watashi no atama o nadeta Atatakai minna no te no hira [Ienourademanbougashinderu-P, IenourademanbougashinderuP, Ie no Ura de Manbou ga Shinderu-P]
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/brainwiki/pages/58.html
用意するもの MioPocket4.0・・・http //www.gpspassion.com/forumsen/topic.asp?TOPIC_ID=136798 (MioPocket2.0などに入っているものだと無理な場合があります) Flashのダウンロード方法(Firefoxを使用する場合) 1. 欲しいFlashのページに行く 2. Firefoxの上部にある「ツール」より「ページ情報」を出す。 3. 「メディア」の中から.swfのものを選択。 4. 名前を付けて保存する。 Flashの起動方法 1. ceOpenerなどでエクスプローラーを開く 2. [MioAutoRun]→[System]からaygshel3.dllを 3. [MioAutoRun]→[Programs]→[Skyfire]からcellcore.dllを 4. [MioAutoRun]→[Program]→[Flash]のフォルダに加える 5. swFlash32を起動 6. 一度閉じる 7. swfファイル本体を選択する（エクスプローラーでダブルクリック） 8.Flashのゲームがはみでたりする場合は Viewの Show AllやFull Screenを押せば改善されます｡ SHARP BrainのWindows CEを活用する Part11より 105 ：Otakan ◆NsDd.YjbjM ：2016/02/08(月) 23 34 14 ID sSC7/sA0 SmallTweakとかを使ってファイルの関連付けをすれば、swFlash32を一度起動しなくてもflashが起動できるようになる。 107 ：名無しさん＠Brain：2016/02/09(火) 21 49 51 ID Bke/McsW Mioのフラッシュはフルパス入力でも起動できるぞ ※Flashの起動が確認できたものをリスト化しているので起動ができたものはBrain掲示板か2ch Brainで報告して下さい。お願いします 名 前 ＤＬリンク 説 明 さかなへん https //drive.google.com/file/d/0B_3HzqiqLYp7Y0xERGJEdFF3TU0/view?usp=sharing クイズゲーム。さかなへんの漢字を当てる。全10問。 スケート天国 https //drive.google.com/file/d/0B_3HzqiqLYp7cHNVV2EybFFKNkE/view?usp=sharing 屋外のコースで前方から来る人を避けながら進むスケートゲーム。迫り来る人たちを華麗にかわそう！ スピード https //drive.google.com/file/d/0B_3HzqiqLYp7NDBhanBFRUtWR2M/view?usp=sharing トランプの「スピード」。コンピューターと対戦。 タイピング測定 https //drive.google.com/file/d/0B_3HzqiqLYp7OFFQakt3eXdEb2s/view?usp=sharing タイピング速度を測定できるタイピングゲーム。60秒以内に20単語をタイピング。画面上に表示される単語をなるべく速く、そして正確にタイピングしていこう。最終的に入力文字数、ミスした数、クリア時間をもとにスコア表示と段位が認定されるよ。 テニスゲーム https //drive.google.com/file/d/0B_3HzqiqLYp7aFppTHlXZXFtZUk/view?usp=sharing 矢印キーとスペースバーを使う本格？テニスゲームです。結構はまります。 ドミノプレッシャー https //drive.google.com/file/d/0B_3HzqiqLYp7eTdIaU5wa2JTMDQ/view?usp=sharing ドミノ倒しのパズルゲーム。一回のクリックで全てのドミノを倒す。 クロスワード https //drive.google.com/file/d/0B_3HzqiqLYp7RUZDaHgtSUZUREU/view?usp=sharing(日本語版) https //drive.google.com/file/d/0B_3HzqiqLYp7SXYtckZvUk5Xd00/view?usp=sharing(英語版) ヒント無しのクロスワードです。ギブアップ機能もあり、とても面白いものです。 国クイズ https //drive.google.com/file/d/0B_3HzqiqLYp7cnZMcEI5LVdwSzg/view?usp=sharing 人口や国旗などからどの国なのか答えるクイズです。難問もあるので自信のある人は全問正解目指してください。 四字熟語 https //drive.google.com/file/d/0B_3HzqiqLYp7ZkxFQXh1OGlLZWM/view?usp=sharing https //drive.google.com/file/d/0B_3HzqiqLYp7SklTYk1qenYyVGM/view?usp=sharing(こちらは三字熟語) 日本人ならできて…当然？並べ替えて熟語を作るゲームです。できて当然のはず…。 神経衰弱 https //drive.google.com/file/d/0B_3HzqiqLYp7bFZ4VlN0VmJFT2M/view?usp=sharing 3段階のレベルから選べる神経衰弱です。試しにしたらフルボッコにされました。 数独 https //drive.google.com/file/d/0B_3HzqiqLYp7Zkw4YTF0cmVBX0U/view?usp=sharing あの「ニコリの数独」です。数独好きにはたまらないものです。 脳が⑨になるチルノの算数トレーニング https //drive.google.com/file/d/0B_3HzqiqLYp7Vm1HaEJJSVBMaEk/view?usp=sharing はい、⑨生産機です。はい、東方です。１、２、⑨－－－－－。 文字認識による足し算 https //drive.google.com/file/d/0B_3HzqiqLYp7SEw1d09HMmFVWkE/view?usp=sharing 「文字認識機能がオレの８を０と認識するぞ。つまりオレの８は０だったのか」という文字が正しく書けない人の敵となるゲームです 迷路 https //drive.google.com/file/d/0B_3HzqiqLYp7cHoySkFkbjhfOFE/view?usp=sharing 時間制限ありの迷路ゲームです。これは人を操作して鍵を見つけてゴールするタイプのものです。
https://w.atwiki.jp/brainwiki/pages/51.html
Brainとは？やQ&Aでも書いてある通りほとんどのPocketPCやHandheldPC用のアプリは作動しません。 しかし、少数ながら動くアプリもあるので、このページではそのやりかたを書いて行きます。 また、XTBook等容量を圧迫するアプリもあるので、SDカードの使用を推奨します。 ※ファイルは「」、フォルダは『』、プログラム名は【】で囲ってあります。 はじめのいっぽ まず最初にBrainの[追加アプリ/動画]にアプリを表示させるための下準備をする。 1,Brainの[パソコン接続]で本体メモリに接続orSDカードに接続を選択し、PCに接続する。 2,PCに接続するとソフトドライバのインストールが始まるので、しばらく待つ。正常に終了すれば右下に通知もしくは自動再生が来る。 3,リムーバブル ディスクとして接続されるのでそこを開く。 4,右クリック→新規作成→フォルダーをクリック。『アプリ』というフォルダを作る。 これで下準備は終了。 アプリの追加 基本的にはフォルダの中身のアプリ本体の名前を[AppMain(.exe)]にしてダミーファイルの[index(.din)]を作るだけでOK。 [index(.din)]の作り方 1,PCでメモ帳を開く 2,何も書き込まずに[index]と名前を付けて保存 3,拡張子を[.txt]から[.din]に変更 稀にSDカードのルートディレクトリに入れなきゃ動かないアプリがあったりするので注意。 最初にはBrain用のタスク管理アプリを入れるのがオススメ。 TestCE（NexHawks氏作成） https //dl.dropboxusercontent.com/u/37804131/TestCE-1.62.zip ceOpener（Knatech氏作成） https //bitbucket.org/knatech/brain-ceopener/downloads/ceopener-0.22-arm.zip TaskSwicher（川本 優氏作成） http //kawamoto.no-ip.org/henteko/myapp/tswbrain18.zip Selector（NexHawks氏作成） https //dl.dropboxusercontent.com/u/37804131/Selector-0.32.zip http //ux.getuploader.com/brainup2ch/download/15/AppMain.exe (第三世代用) 有志による解説動画 また、最近はダミーDLL等の登場で動くアプリの数が増えてきています。 もし動いたアプリがあれば現行スレ、もしくは初心者スレで報告してくださると助かります。
https://w.atwiki.jp/mrfrtech/pages/128.html
Business Analytics Industry, Segments Of The Tech World Reports, Recent Trends, Size, Was the Largest Region During Forecast Period 2027 Market Overview The Business Analytics Industry is projected to grow at a substantial CAGR during the forecast period. As per the business analytics market research report, the global market for business analytics is projected to grow swiftly. According to analysts, the enormous volumes of digital data as well as continuous developments in business analytics tools will drive the market growth during the forecast period. The business analytics market research report offers a comprehensive analysis of the global business analytics market and its application, end-user, industry, service, software, deployment, and region segments. The lack of awareness along with reluctance in adoption are the elements that could influence the business analytics market advancement throughout the forecast period. The business analytics market research report by expert analysts is developed to assist organizations in the business analytics market. Request a Free Sample @ https //www.marketresearchfuture.com/sample_request/6698 Competitive Analysis Availability of active marketplaces and lucrative offerings by platforms are presumed to drive the business analytics market growth worldwide. The global business analytics market could be challenged by the high cost of storage solutions, nevertheless, organizations in the business analytics market will carry the growth rate forward. The business analytics market research report presents company profiles of major companies active in the business analytics market globally. Furthermore, the global business analytics market report offers an all-inclusive analysis of the market collected from the business analytics market’s primary and secondary sources covering both decision makers and thought leaders. The business analytics market research report highlights such key areas assisting businesses operating in the business analytics market to build better growth strategies. Segmental Overview The global business analytics market has been segmented based on application, end-user, industry, service, software, deployment, and region. Based on deployment, the market for business analytics is segmented based on on-cloud and on-premises. Additionally, the market based on end-user, is segmented into BFSI, education, energy and power, government, healthcare, manufacturing, media and entertainment, retail, telecom, and IT, and other. The global market for business analytics is also covered based on industry segments which is further split into data mining, marketing analytics, supply chain analytics, finance analytics, and others. Based on software, the market for business analytics is segmented based on content analytics, corporate performance management suites, data discovery and visualization software, data warehousing platform, location intelligence, advanced and predictive analytics, and others. Major elements such as continued storage of data could obstruct the business analytics market growth. However, according to the business analytics market research report, the rise of smart data discovery capabilities along with an increase in investments across different industry areas will propel growth throughout the forecast period. The business analytics market is set to register growth at a high CAGR owing to these key factors. The exploration of application, end-user, industry, service, software, deployment, and region segments along with regional markets has been given in the global business analytics market research report. The research analysts studying the business analytics market have put out market forecasts in the business analytics market research report in order to support business analytics market-based companies. The business analytics market research report provides an extensive understanding of the business analytics market based on the information and forecasts till 2023. Regional Analysis North America, Europe, Asia Pacific and the rest of the world regional market for business analytics are predominantly covered in the global business analytics market research report. Country-level business analytics markets spread across North America – the United States, Canada, and Mexico are also covered in the report. In South America – Brazil and other country-level business analytics markets are covered in the report. In Asia-Pacific (APAC) region, the country-level business analytics markets covered are Japan, India, China, and others. The business analytics market research report also explores the regional market for business analytics present in Europe in the United Kingdom, France, Italy, Spain, and Germany, etc. The business analytics market research report also covers regional markets from the rest of the world alongside business analytics markets of Africa and the Middle East. Industry News The flagship Viya artificial intelligence, analytical and data processing platform is now available as a cloud-based, cloud-based carrier, which runs on Azure Cloud Platform, integrated with Azure S services. SAS is the provider of large-scale data analysis applications. Tuesday, SAS said that the latest containerized version of Viya is immediately available for Azure and supports other cloud platforms, such as AWS, Google Cloud Platform and Red Hat OpenShift. Browse Full Report Details @ https //www.marketresearchfuture.com/reports/business-analytics-market-6698 Table of Contents 1Executive Summary 2Scope of the Report 2.1Market Definition 2.2Scope of the Study 2.2.1Research objectives 2.2.2Assumptions Limitations 2.3Markets Structure 3Market Research Methodology 3.1Research Process 3.2Secondary Research 3.3Primary Research 3.4Forecast Model Continued…. Similar Report B2B Telecommunication Market Information by Solution (Unified Communication and Collaboration), Deployment (Fixed, Mobile), Organization Size (Large, Enterprise), Application (Industrial, Commercial) and regions Trending #MRFR Report** https //ictmrfr.blogspot.com/2022/04/geofencing-market-companies-growth-with.html https //blogfreely.net/pranali004/telecom-expense-management-market-size-impressive-cagr-changing-business-scope https //postheaven.net/pranali004/financial-app-industry-impressive-cagr-changing-business-needs-scope-of https //market-research-future.tribe.so/post/openstack-service-market-research-impressive-cagr-changing-scope-of-current--6263de46791566c10c79891e https //www.scutify.com/articles/2022-04-24-infrastructure-as-a-service-industry-cagr-changing-business-scope-of-current-and-future-industry- About Market Research Future At Market Research Future (MRFR), we enable our customers to unravel the complexity of various industries through our Cooked Research Report (CRR), Half-Cooked Research Reports (HCRR), Raw Research Reports (3R), Continuous-Feed Research (CFR), and Market Research Consulting Services. 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