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https://w.atwiki.jp/kelvy/pages/4.html
Ryota Matsumoto (松本良多) is a famous Philosopher, Artist, Japanese Author, and Instagram star from Japan. He is the founder of an award-winning interdisciplinary design office, Ryota Matsumoto Studio based in Tokyo and New York. As a video producer, he has worked with Peter Christopherson for Japanese Nike commercials. He is a renowned architect and one of the most prominent theorists of postdigital art in Japan and the United States. He has served as the MFA advisor of Transart institute, University of Plymouth and teaches at Asagaya Institute of Art and Design as a professor of practice. He is a man with a proactive approach and has painted the canvas of his dream with the colors of his consistent and persistent efforts. Bеіng passionate аbоut his work аnd аlwауѕ wanted tо carve а niche fоr himself іn life, wаѕ thе spark thаt ignited him to pursue his dreams and passion. We will walk you through all about him. BIOGRAPHY/Wiki He hails from Tokyo. He is 49 years old as of 2021. He is American by Nationality. His Zodiac sign is Pisces. His date of birth is March 9th 1972. He is a follower of Atheists. He attended Architectural Association in London and Mackintosh School of Architecture, Glasgow School of Art in the early ’90s. He has a degree Master of Architecture from the University of Pennsylvania, which he received in 2007. He has won various laurels for his amazing work. He is the recipient of Visual Art Open First Prize, Florence Biennale Mixed Media 2nd Place Award, Premio Ora Prize Italy 5th Edition, Premio Ora Prize Spain 1st Edition, Donkey Art Prize III Edition Finalist, Art Kudos Best of Show Award, Lynx International Prize Be Art Builder Award, Lumen Prize Finalist and many more. He specializes in building a positive brand image with the help of social media campaigns and digital marketing strategies. He collaborates with various renowned influencers including a cofounder of the Metabolist Movement, Kisho Kurokawa, and with Arata Isozaki, Peter Christopherson of Coil, Cesar Pelli, and MIT Media Lab before establishing his office. He has worked on high-profile projects including Kyushu University Ito Campus masterplan (2003-2005), Shinjuku redevelopment project in Tokyo (2009-2012), Bach Mai hospital in Hanoi (2000), and Qingdao mixed-use development in China (2011). He strongly believes “One of the best ways to grow a business and garner more success is by growing your own personal brand” Several of his paintings have been exhibited in various art galleries. Several articles have been published about him. He shares various quotes and articles to inspire the youth and helping them to build a better future. His Instagram is full of his paintings. He has helped various artists grow by polishing their talent and help them find the correct lane. He is passionate about making dreams come true and hopes to inspire a lot of passionate minds Physical Appearance He is Smart and Cute. He is hugely popular among the youth. He is approximately 175 cm tall and weighs around 70Kg. He has an Average Build. He has black hair and both of his eyes have different colors Left Grey Right Dark Green. Family Religion Not Much is known about his family and his personal Relationship. Facts His Instagram id is ryt.matsumoto His Instagram has 1K+ followers. He is a very talented person who enjoys Painting, Sculpturing, and Writing music in his leisure time. His pursuit for excellence has led him down various avenues His magnetic personality has gained him friends across the globe and the growing respect of ears in the industry. He is a Social media Influencer. He loves to explore new places He also had solo exhibitions at Transylvania University (2015), Los Angeles Center of Digital Art (2016) and Alviani ArtSpace, Pescara (2017). His work, writings, and interviews has been published in Kalubrt Magazine, University of North Carolina Wilmington Journal Palaver, Furtherfield.org, The Journal of Wild Culture, Studio Visit Magazine, Fresh Paint Magazine and many more
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準備 ツールのインストール先 httpd c \Opt\Apache openssl C \OpenSSL-Win64 証明書を作成するのでopensslをインストールする http //slproweb.com/products/Win32OpenSSL.html Win64OpenSSL-1_0_1h.exe 環境変数の設定 変数名 変数値 追記 Path C \Opt\Apache\bin;C \OpenSSL-Win64\bin; 新規 OPENSSL_CONF C \Opt\Apache\conf\openssl.cnf レジストリを修正 regedit(管理者権限有)の起動し、以下の内容を変更する HKEY_LOCAL_MACHINE\SYSTEM\CurrentControlSet\Services\Apache2.2\ImagePath C \Opt\apache\bin\httpd.exe -k runservice を C \Opt\apache\bin\httpd.exe -D SSL -k runservice 設定確認 コマンドプロンプトを起動する openssl version OpenSSL 0.9.8y 5 Feb 2013 httpd -v Server version Apache/2.2.25 (Win32) Server built Jul 10 2013 01 52 12 サーバ証明書を作成する コマンドプロンプト(管理者有)を起動する オレオレ証明書の場合は-des3を消して実行 手順１ C \ cd C \Opt\Apache\conf C \Opt\apache\conf openssl genrsa -des3 -out server.key 2048 Loading screen into random state - done Generating RSA private key, 2048 bit long modulus ...........+++ ..........................................................+++ e is 65537 (0x10001) Enter pass phrase for server.key パスワード Verifying - Enter pass phrase for server.key パスワード 手順２ C \Opt\apache\conf openssl req -new -key server.key -out server.csr Enter pass phrase for server.key パスワード Loading screen into random state - done You are about to be asked to enter information that will be incorporated into your certificate request. What you are about to enter is what is called a Distinguished Name or a DN. There are quite a few fields but you can leave some blank For some fields there will be a default value, If you enter . , the field will be left blank. ----- Country Name (2 letter code) [AU] State or Province Name (full name) [Some-State] Locality Name (eg, city) [] Organization Name (eg, company) [Internet Widgits Pty Ltd] Organizational Unit Name (eg, section) [] Common Name (e.g. server FQDN or YOUR name) [] ホスト名 Email Address [] Please enter the following extra attributes to be sent with your certificate request A challenge password [] An optional company name [] 以下は説明 Country Name※ 国を示す2文字のISO略語です。 JP State or Province Name※ 組織が置かれている都道府県です。 Osaka Locality Name※ 組織が置かれている市区町村です。 Osaka-shi Organization Name※ 組織の名称です。 GlobalSign K.K. Organization Unit Name "組織での部署名です。※指定がない場合は - （ハイフン）を入力してください。 Sales Common Name※ ウェブサーバのFQDNです。 ssl.globalsign.com Email Address 入力不要です。 - A challenge password 入力不要です。 - An optional company name 入力不要です。 - 手順３ 正式の証明書の場合は、ベルサインなどに依頼するらしいが、オレオレの場合は以下を実行する C \Opt\apache\conf openssl x509 -days 3650 -req -signkey server.key server.csr server.crt Loading screen into random state - done Signature ok subject=/C=AU/ST=Some-State/O=Internet Widgits Pty Ltd/CN=ホスト名 Getting Private key Enter pass phrase for server.key パスワード httpd.confの編集 C \Opt\Apache\conf\httpd.conf #LoadModule ssl_module modules/mod_ssl.so ↓ LoadModule ssl_module modules/mod_ssl.so #Include conf/extra/httpd-ssl.conf ↓ Include conf/extra/httpd-ssl.conf C \Opt\apache\conf\extra\httpd-ssl.conf #SSLCertificateFile "C /Opt/apache/conf/server.crt" ↓ SSLCertificateFile "C /Opt/apache/conf/server.crt" #SSLCertificateKeyFile "C /Opt/apache/conf/server.key" ↓ SSLCertificateKeyFile "C /Opt/apache/conf/server.key" SSLPassPhraseDialog builtin ↓ SSLPassPhraseDialog exec conf/passphrase.bat C \Opt\apache\conf\passphrase.bat(なければ作成する。中身はopensslで設定したパスワード) echo パスワード 設定が完了後、ApacheのConfigurationをテスト すべてのプログラム Apache HTTP Server 2.x.x Configure Apache Server Test Configuration エラーがある場合は設定ファイルの該当箇所を修正します SSLMutexのエラーが出る場合は、該当箇所をコメントアウト（行頭に#を記載）します # SSLMutex "file C /Program Files/Apache Software Foundation/Apache2.2/logs/ssl_mutex" 設定後サーバを再起動し、ブラウザで「https //localhost」に接続してみる このサイトのセキュリティ証明書は信頼できません と表示されればOKで「このまま続行」ボタンをクリックして、「It works!」と出れば完了 2014/7/22
https://w.atwiki.jp/freedo/pages/32.html
公式サイトAndroid版 概要 推奨環境 更新履歴 公式サイト http //www.arts-union.ru/node/23 Android版 https //play.google.com/store/apps/details?id=ru.vastness.altmer.real3doplayer 概要 FreeDOをベースにバグ修正されたエミュレータで市販ソフトが動作する。 メニューがすべてロシア語のキリル文字。 Windows版、Linux版、Android版がある。 Compatibility 3DO 100%?! Compatibility ColecoVision ~ 98%. Sega Master System compatibility ~ 99%. Compatibility Atari Jaguar ~ 95%. 推奨環境 pixel shader 2.0、1.6GHz以上のCPU 更新履歴 Google翻訳にてロシア語から英語に翻訳 Version 2.8.JAG (Changes concern only Atari Jaguar) Fixes in the object processor (earned by Rebooteroids) Fixed a blitter in the inner loop part (a number of hangs was removed) RISC processors reproduced a hardware error with writing to the flag register (compatibility is improved) Fixed prefetching of commands in DSP Added support for increased horizontal screen resolution The scan is corrected (unnecessary parts of the screen are removed) Alignment adjusted so that Protector SE works Added options for emulating RISC processors in separate streams General optimization performed Version 2.8.J Not very fast, not very high quality, but emulated by Atari Jaguar! Support for PAL BIOS with disabled RSA in 3DO Conversion (option via File menu) Jaguar ROM without title and incorrect 3DO ISO Profiling access to CD-ROM in 3DO Version 2.8 Highly refined emulation SMS (99% compatibility) Optimized original software renderer 3DO Improved MARIA mode CEL-Engine (D, Samurai Shawdow, ...?) Fixed an order of operations over the second source in the pixel processor 3DO (Crash n Burn) Fixed loading workers CEL registers (Wiked 18 other golf) Option drawing CCB-list at the end of the allotted time (helps in Phoenix 3) A more accurate picture peg to Scanline in 3DO Fixed interception SPORT in the hardware renderer 3DO (BC Racers) Implemented a more efficient multi-threading for CEL Improved accounting CEL-Engine cycles (for Jurasic Park, select "100% + is the frame") AngelScript updated to the latest version, the standard scaler textures improved, but requires optimization Generate a list of compatibility on the basis of the annotation Reduced latency management In the context of the library menu allows you to massively delete duplicates Call for abstracts editor Ctrl + A (in the screenshot will be automatically inserted into the game) Locked logging (left only in the debug build, as affect performance on slower machines) Added the option of accelerated emulation (for the test run, so you can evaluate the performance of your system in terms of emulation) Fixed a memory access error in the memory mapping structures (could cause a random crash when 3DO emulation and debug all platforms) Mass undetected removal of dumps from the list ZEXALL test runs without errors (possibly corrected all errors Z80 emulation) Fixed an error in weight due TMS9918A VDPTEST (left some timings for HClock, but judging by the testing, no matter what they do not affect) 3D games through SMS displayed frame Made mapper for Pack 4 All Actions Support rooms and SG-1000 Sega Game Gear within SMS Implemented Korean mappers SMS Added support for SMS-dump up to 4 megabytes Emulating the Start button in the SMS (yes, I forgot the whole button! =) The SMS added support Codemasters mapper and mapper without page register Added option to bypass restrictions on TMS9918A rendering sprites Support modes 224 and 240 lines, as well as scan for PAL SMS Formed games base to bind to the mapper to SMS Mass of small changes Version 2.7 emulating ARM Processor Optimization (decreased requirements for emulation 3DO) Fixed a crash when using the emulator 3DO-DSP in a separate thread Added autosave and resave in the top slot to F4 Fixed bug emulation Z80 (instruction halt, earned many games ColecoVision) Fixed 2 TMS99XXA mode (graphical errors corrected in a number of ColecoVision games) Improved input settings (now you can play together in the arms of interactive shooting ranges) Added preliminary support for Sega Master System (terribly buggy 99% do not work =) Many minor fixes Version 2.6 Added emulation of consoles ColecoVision Videos passes (you can boot from the frame rewrite the record end - rewind and continue recording) Setting the video compression is done through the period of the keyframe (more often - the more space is required) Fixed a bug in kvikseyvah leads to incorrect determination of 3DO-disk size after recovery Redesigned main application cycle (should improve the synchronization of audio and video series) Improved sight (sight on the game screen, instead of the cursor, and for the sights from the input setting is disabled skipping frames) Expansion of the background color beyond the frame (can be disabled) Curbs according sweep (can be disabled) Version 2.5 Involved AngleScript for texture filtering (you can make your own filters) Added logging of errors for scripts and shaders (near samismi scripts will appear LOG-files) Settings are made more intuitive, non-active elements are blocked Now you can customize the interface style (skin folder, remove it, if you do not like it) Added support for the emulator interface transfers (file translation.xml) Setting the emulated CD-drive speed Checks for OpenGL (if falls emulator at startup - watch opengl.log) Setting per cent is accounted for traffic CEL-Engine in the quota of time Improved auto-commit axes when setting the joystick Fixed addition management (now possible to easily assign multiple controls on the console control, and vice versa) Removed binding assignable keyboard keys to the current layout (in some cases, management may need to reconfigure) Fixed loading saves with disabled optional rumami Update content when resizing windows and other events of context damage Interrupt Handling during operation CEL-Engine Many improvements to the debugger, which will further improve the emulator (debug version) Made reversinzhenerig gun and its support is implemented protocol (including machines with games) Made reversinzhenerig protocol service fee OrbAtak and implemented its support Made reversinzhenerig Flightstick Pro protocol Added the option of hiding the cursor in full screen mode Version 2.4 Multithreading (DSP and CEL in separate threads) Fixed a graphical bug in Alone in the Dark II A large-scale code optimization Added random seed for Random Shaders are now available for editing - you can mock picture =) Version 2.3.4 Fixed work with files in Unicode (Windows) Fixed problem with compressed images (Linux) Version 2.3.1 Fixed record attributes in the XML-configuration file Version 2.3 Support for images with exotic sector size (2353, 2368, 2448, 2449, etc.) Copy to Clipboard information about the selected titles (+ layout control information) Check the original signatures for integrity monitoring images 64-bit assembly It changes the composition of the subsidiary libraries to be less dependent on Qt Caching in the CD-ROM drive (not stutters Sailor Moon) Shortcuts in Full Screen mode Fixed pixel processor (palette Crash n Burn) Version 2.2 Fixed record is in the original frame rendering software Prohibited tessellation kvadropoligonov mono color (add speed in the same Wolfe) Fixed a bug with loading saves (no longer necessary to rename the exchange saves) Integrated converter for images of curves Highlighting contours textures (debug version) Implemented dostur to map graphics (debug version) Deleted LibJIT (buggy and prevents porting later compensate static patterns) Undo / Redo and tracking conversions in the debugger (debug version) The mass memory dump and resources (debug version) Image operations are performed as a background task Scaling CEL (the similarity 2xSAI) Version 2.1 The ability to set the frequency multiplier ARM Incrementing the position corrected in the original rendering software Fixed PBUS Added support exploding textures (only software rendering) Adjusted comparison shots in VDLP Added traffic profiling CLIO A more accurate calculation cycles ARM (ceased to rattle videos in WC3, and perhaps in other games) Improved noise generator (hang Daedalus Encounter) Version 2.0 Separate settings for dynamic recompilation ARM and PPROC Protection against accidental deletion of annotations Automatic snap axis joysticks Fixed DMA-Channels Fixed the random number generator Refined interrupt XBUS Exhibited the correct order of the stereo channels by default Restored support font ROM Annotations are changed after the current element in the collection Version 1.9 Restored Crash n Burn Fixed race thread Improved texture mapping with respect to the memory (texture RAM size of most console led to crash when hardware rendering) Remove restrictions on the size of the list draw Fixed interrupt XBUS Annotations Editor Fixed a bug in the hardware renderer by SPORT (falling Alone in the dark) Added memory bus load records from the CEL-Engine Fictitious FPS added to the profiler Version 1.8 Fixed static tools (error with the flag of the transfer) An refactoring Added the ability to search the list of dumps Optimization of constant calculations in recompiler ARM Fixed a reset CPU Adjusted emulation CD-ROM for the future support of Audio-CD or Play-sheet Picked up a white noise generator Added annotations editor Version 1.7 Optimized Triangulation quad texture Control aspect ratio of the screen in the hardware rendering mode Added zoom feature Restored Crush n Burn Texture caching LR-Cel non bitmaps Fixed duplication when adding images to the "#" symbol in the title Changes in the library dumps the status bar shows the checksums and the real size, duplicates are highlighted, you can delete the dumps with the file The DSP recompile two new tools Dynamic recompilation Version 1.6.3 Full support chip Anvil Implemented support for PAL consoles and custom screen resolutions (for launch in PAL mode needs an appropriate system BIOS) Optimized generation and loading textures Version 1.6 Optional bitmap optimization shipments (adds speed Virtuoso, ShockWawe 2 and other games due to a small loss of accuracy) Monitoring palette VDLP (in game Casper figures were dark-savers instead of gradually appear and disappear) SPORT Rewrote implementation in hardware rendering for better compatibility Fixed clipping (glitch with the panel in Return Fire in the hardware rendering) Adjusted for working with the list of CCB (background Samurai Shodown) Changed cycle DSP to avoid deadlocks with endless tools (As for Sailor Moon) The DSP-decompiler tool adds support for multiple entry points (improves performance) Fixed decompilation conditional jumps in DSP-tools (heals scratches at the start of video) Refactor code emulator core classes Version 1.5 Change active dumps by changing the current archive preserving and maintaining the current game An issue of backward compatibility and load the saved state when juggling supply Disassembler Command list VDLP Fixed DSP-decompilation tools in local procedure call commands Implemented hardware rendering (to control texture filtering has a setting - auto, forced to turn on or off, the resolution of the hardware renderer is adjusted scale factor FBO) Fixed size bitmaps decoder (DinoPark Tycoon) Profiler added to the Control Panel and is divided into two parts - general and the extended Version 1.4 Introduced video modes (for this 3DO 320x240 - for weak machines, 640x480 - is more correct, especially when mixing different frames) Written shader for rendering software interpolation (acts like 2xSAI and other filters to improve resolution) Framed tab video settings (all settings are transferred to the image) Added option to display an image without filtering (good old pixels) Fixed a bug with the measures in the DSP (zavisonam led to hex in specific areas and possibly some other problems) Static recompilation DSP-tools (significantly reduced requirements for emulation) The profiler added information about current DSP-tools Dobavlno sound settings menu Enter 3 emulation DSP (fast (statically recompiled tools), and normal instruction cycle (the slowest and most accurate)) Disassembler memory DSP Version 1.3 The system display Unicode fonts (for subtitles and other messages over the screen) Integrated profiler The new software to render caching (50-200% smarter than the old one, but DOOM 50% slower - in this game software rendering to texture, and therefore they are constantly rekeshiruyutsya) Control aspect ratio of the screen Fixed auto-update position sprites when rendering fonts Fixed handling of CCB-list Fixed loading PIP-words in the table PLUT Version 1.2 Improved mouse support It has a function to save and load states (delta encoding saves for further implementation of the debugger functions reverse step in the instructions) Resource Manager now supports navigating the file system ROMs The manager added a new type of BIOS (FMV - video BIOS module for 3DO, while you can only delve into its contents) Ability to take screenshots Full screen mode Version 1.1 Added support for image compression (integrated data logger) Improved support for joysticks (analog input) Added support for the mouse (not tested) Version 1.0 New frontend New core architecture emulator Integrated Resource Manager Temporarily do not support hardware rendering Version 0.8.6 Fixed Lost Iden Minor changes in the registers CLIO Added profiling cycle emulation (possible to learn - some emulation subsystem consumes the greatest amount of resources) Changes in DSP (should pay attention to the sound - I m not entirely sure of the changes) Added the ability to dump code and DSP (menu Debug) Version 0.8.5 Fixed custom error refresh in the optimized software rendering Fixed a bug with palette in Lucienne s Quest Improved interception SPORT (hle) Fixed-version Crush n Burn Version 0.8.4 Added control of the proportions of the screen in the hardware rendering Fixed twitching image after optimization otrisoki software (version 0.8.2 and 0.8.3) The window title adds information about the selected game To change the status bar The status bar is aligned Expanded Format VTR = percentage of video traffic (the ratio of the transmitted video card to the raster of frame). It is very indicative figure, in most cases it determines the speed of the emulation of a game (less - better). Progressive optimization software output buffer Version 0.8.3 Introduced Election rendering FBO considering modification of their content (extra team 3DO Graphics Folio ignored) Optimization software rendering and interpolator Version 0.8.2 Support for bios Anvil and original dump Japanese 2-megabyte bios Emulation is reduced to a single stream Optimized hardware rendering function Optimized software rendering Fixed interpolation at the edges of the framebuffer Fixed order of scanning lines VDLP Version 0.8.1 Change the way that the joints between the textures Fixed pixel decoder (level health Po ed) Small fixes pixel processor Version 0.8.0 Corrections emulate ARM, instruction STR Small code optimization ARM emulation Fixed emulation DSP (Killing Time saver and Blade Force) Improved interlocking functions of software and hardware rendering. Optimized cycle emulation Added files display debug messages and kprint Added saving the settings window Version 0.7.9 Fixed delete multiple textures (version 0.7.8 - is falling in a number of games are not recommended for use) The mechanism of monitoring the number of textures with the relevant (is fixed - texture 1024) Version 0.7.8 Added output in the status bar. Format Rendering mode - SW (software) or HW (hardware) TEX [number of texture RAM] FBO [number of frames, RAM] FPS = frames per second SND = percentage load sound buffer Added dropped frames Fixed color decoding operations SPORT (HLE) Adjusted contrast palette (HLE) Improved Intercept textures Version 0.7.7 Improvements menu (informative, autostart, lock, lock directory) A report on the possibilities of the system user (frontend.log) Error messages from the OpenGL (frontend.log) Controlling the volume scroll wheel mouse Version 0.7.6 (relative to the first beta 0.7.5) Fixed disappearing sprites DOOM Removed the limit on the size of the FBO (* 1024 was 512, affects the resolution of the frame) Improved clipping nelitsevyh faces (in HLE mode) Emulation project - "Phoenix" Top Licensing party information source [18+] All rights to published materials belong to these authors, or otherwise to authors site. 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https://w.atwiki.jp/conlang_arka/pages/68.html
Arka is good at literary and artistic expressions. Here is a sample from xistina, a picture book on Mel calendar. Every day in a year has its own color. The color of the day on the sample page is white. The name of the color is honoka which means snow in the language of Altia (Altian). Every day in a year has its own word. The word of the day on the sample page is honesty. It tells us snow is a symbol of honesty. There is a poem in the middle of the sample page. There is a picture which is related to the color. Next, read this article on Melidia . "Melidia" is a novel written in Arka. In this novel, a college student is murdered and the heroine named Sae become a suspect. A girl named Miina (it means a flower) thinks Sae is the murderer and makes the following remark el rens honoka til diasex. fien la fenvlen nekt tuuno enfrex, tyu klos xal laas til diasex i fiona yundi. They say snow doesn t tell a lie. But snow hides dirt on the ground. Do you really think the snow is still "intact"? Miina is a college student from the art department, so she knows xistina well. She knows snow is a symbol of honesty but says snow can hide dark secrets. What is the intention of her remark? There are three words which mean snow in her remark. Honoka is an Altian word for snow. "La fenvlen" is a Lutian word for something white and means snow in this case. Where is the third snow, then? It lies between lines. It is Sae whose name means snow in Arka. Yes, her remark implies that Sae told lies and is the murderer. She tells her idea without saying the suspect s name. It is a sophisticated euphemism. "La" of "la fenvlen" is a definite article of Lutian (the language of Lutia). Fenvl itself is just white. In Arka, la means that the following word is an animate noun, so "la fenvlen" also means "that white fellow". Who is the "fellow", then? It is Sae again. Remember what her name means. Miina s remark implies the suspected girl with a pale face. Thus Arka is good at literary and artistic expressions.
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]
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Market Scenario The growing demand for data protection and securement is increasing day today. This rising demand for protecting and safeguarding data will continue in future generations. These factors lead to the growth of various advanced data security center services. The rise in urbanization and industrialization leads to the development of big companies and e-commerce services. All these sectors are highly demanding for advanced data security systems. Therefore, to meet the public s ongoing requirement, different data centers are emerging in the market. The Hyper-Scale Data Center Market is one of the data securities markets that provides excellent data protection services. The Hyper-Scale Data Center Market is known for distributing and sharing huge data to a place where the required information can be easily accessed later through the internet. The hyper-scale data centers are used by cloud service providers and house cloud-based resources. These data centers even allow digital platforms for storing and effectively transferring data. The rise in awareness for cyber threats and privacy breaches accelerates the market. The business and IT professionals, those who are always worried about managing the huge amount of data, started investing in this market, which is propelling its growth. In the pandemic period, the markets that belonged to the IT sectors had mixed impacts, and the Hyper-Scale Data Center Market has shown a stable growth during the period because the requirement of data protection, management, and transferring has increased at a high rate. The use of cloud-based services even increased during the lockdown time. These factors had shown a positive impact on the market s growth rate. Due to the rise of widespread opportunities, the market is estimated to grow at a significate rate in the future years. The Hyper-Scale Data Center Market is estimated to reach a CAGR of 27 %, worth USD 96 Billion during the forecast period. Request a Free Sample @ https //www.marketresearchfuture.com/sample_request/3086 Competitive Outlook Prominent leaders in the market are Cavium (US), Intel Corporation (US), Dell Inc. (US), Hewlett Packard Enterprise Development LP (US), Cisco Systems Inc. (US), Broadcom Ltd. (US), Lenovo Group Ltd (China), IBM Corporation (US), Huawei Technologies Co. Ltd (China), Ericsson (Sweden), Quanta Computer Inc. (Taiwan), and more. Segmentation The Hyper-Scale Data Center Market is segmented based on type, solutions, and vertical. The type segment of the market is fragmented into enterprises, cloud providers, and colocation providers. The company needs to store and secure its data; therefore, a hyper-scale data center plays a major role in this process. The cloud providers include public clouds, manage private clouds, and offer on-demand computing components. The equipment, space, and bandwidth are provided under the collocation provider, and the solution segment includes software, storage, server, service, and others. The market is classified into energy utilities, government and defense, IT telecommunication, retail, BFSI, manufacturing, media and entertainment, healthcare, and others in the vertical segment. Regional Analysis According to the geographical status, the Hyper-Scale Data Center Market is distributed into different regions such as North America, Europe, and the Asia Pacific. Among these, North America holds the highest market share of the global market. This region is emerging due to the increase in investment in technological solutions; meanwhile, the Asia Pacific region to growing at a consistent rate during the forecast period. The market regions to propel the growth in the global level, especially due to the increased growth of IT infrastructure. Industry News According to the recent update, Extra by Airtel is all set to launch New 38 MW Hyperscale Data Center in Chennai, India. Browse Full Report Details @ https //www.marketresearchfuture.com/reports/hyper-scale-data-centers-market-3086 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 Continued…. View Similar Report Mixed Reality Market Research Report https //writeonwall.com/mixed-reality-market-by-development-size-share-and-demand-opportunity-size-share-trend-intel-corporation-u-s-sony-corporation-japan/ Smart Glass Market https //writeonwall.com/smart-glass-market-by-development-size-share-and-demand-opportunity-size-share-key-manufacturers-drivers-value-and-foreseen-2027/ Passport Reader Market https //writeonwall.com/passport-reader-market-by-development-size-share-and-demand-opportunity-it-security-and-data-protection-analysis-forecast-to-2030/Antivirus Software Market By Type (PC and Phones/Pad), By Application (Enterprises, Individual and Government) 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. Contact Market Research Future (Part of Wantstats Research and Media Private Limited) 99 Hudson Street, 5Th Floor New York, NY 10013 United States of America 1 628 258 0071 (US) 44 2035 002 764 (UK) Email sales@marketresearchfuture.com Website https //www.marketresearchfuture.com
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Market Analysis The market for Augmented Analytics (AR) Market Growth is estimated to grow at a significant rate during the forecast period 2020 to 2027. Augmented analytics tools are utilized for analyzing automated data with the support of natural language processing technology and machine learning techniques. It helps in streamlining the process of data modeling and data profiling thus supporting reuse and data governance. The Augmented Analytics (AR) Market Growth is predicted to touch USD 13 billion at a stellar 24% CAGR between 2020- 2027, states the recent Market Research Future (MRFR) analysis. Various factors are fuelling the global augmented analytics market share. As per the recent MRFR market estimates, such factors include the increasing volume of complex data, growing adoption of analytical tools for business intelligence, development of artificial intelligence technology, development in blockchain and modernization of digital technology, increasing need for intelligent business tools in data analysis, growing need for increased productivity of business processes, and increasing implementation of natural language processing tools, machine learning, and artificial intelligence. On the contrary, lack of skilled workforce, high cost of analytical tools, impact of the COVID-19 pandemic on the global economy, and analyzing the huge generated data by maintaining safety and quality may impede the global augmented analytics market growth over the forecast period. Request a Free Sample @ https //www.marketresearchfuture.com/sample_request/7464 Market Segmentation The MRFR report throws light on an inclusive segmental analysis of the global augmented analytics market based on vertical, organization size, deployment mode, and component. By component, the global augmented analytics market is segmented into services and software. The services segment is again bifurcated into managed services and professional services. Of these, the service segment will lead the market over the forecast period. By deployment, the global augmented analytics market is segmented into hybrid, on-cloud, and on-premise. Of these, the on-cloud segment will dominate the market over the forecast period. By organization size, the global augmented analytics market is segmented into large enterprises and SMEs. Of these, the SMEs will spearhead the market over the forecast period. By vertical, the global augmented analytics market is segmented into healthcare, media and entertainment, transportation, energy and utilities, manufacturing, retail, IT and telecommunication, government and defense, BFSI, and others. Of these, BFSI will have the lions share over the forecast period. Regional Analysis By region, the global augmented analytics market covers the recent trends and growth opportunity across North America, Europe, the Asia Pacific (APAC), and Rest of the World (RoW). Of these, North America will rule the market over the forecast period. Presence of key players in the US, technically advanced infrastructure, high technical expertise in technology like machine learning and natural language processing, widespread customer base in various industry verticals, adoption of advanced analytics to improve business operations, rapid adoption of technologies, and focus by companies to improve their data analysis capabilities are adding to the global augmented analytics market growth in the region. In Europe, the global augmented analytics market is predicted to hold the second-largest share over the forecast period. Developing digital technology, increasing need for augmented analytics solutions for business intelligence, and high growth in retail and consumer goods industry are adding to the global augmented analytics market growth in the region. In the APAC region, the global augmented analytics market is predicted to have promising growth over the forecast period. Development in digital technology, increasing expertise in machine learning and natural language processing techniques, development in big data analytics and artificial technology, increasing implementation of data discovery, self-service business intelligence tools, and visualization across business organizations are adding to the global augmented analytics market growth in the region. Japan, China, and India hold the utmost market share. Key Players The leading players profiled in the global augmented analytics market report include Birst, Pyramid Analytics, Logi Analytics, Board International, Yellowfin, Looker, MicroStrategy, Qlik, Sisense, Tibco Software, SAS, Tableau Software, Oracle, Microsoft Corporation, IBM Corporation, SAP SE, and Salesforce. Industry Updates April 2021- Subex has launched hypersense, an end-to-end augmented analytics platform. Browse Complete Report @ https //www.marketresearchfuture.com/reports/augmented-analytics-market-7464 Table of Contents 1 Executive Summary 2 Scope of The Report 2.1 Market Definition 2.2 Scope of The Study 2.2.1 Research Objectives 2.2.2 Assumptions Limitations 2.3 Market Structure 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. Contact Market Research Future (Part of Wantstats Research and Media Private Limited) 99 Hudson Street, 5Th Floor New York, NY 10013 United States of America 1 628 258 0071 (US) 44 2035 002 764 (UK) Email sales@marketresearchfuture.com Website https //www.marketresearchfuture.com
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"We need to transcend the de facto dichotomy of empiricism and rationalism that is immanent in embedded and embodied entities. Hybrid media is one trajectory to make a rapture for becoming or to draw a line of flight that breaks the mold of the preconceived hylomorphic notion of existentialism, but there are still uncharted territories and new areas for creative exploration, particularly in terms of the affect-driven epistemology of perception." Ryota Matsumoto As an artist, designer, and architect, Ryota Matsumoto is internationally recognized as one of the progenitors of the postdigital art movement. Born in Tokyo, he was raised in Hong Kong and Japan. He received a Master of Architecture degree from University of Pennsylvania in 2007 after his studies at Architectural Association in London and Mackintosh School of Architecture, Glasgow School of Art in early 90’s. Over the years, he has studied with Manuel DeLanda, Vincent Joseph Scully Jr., Cecil Balmond, and Giancarlo De Carlo, among others. Matsumoto has previously collaborated with a cofounder of the Metabolist Movement, Kisho Kurokawa, and with Arata Isozaki, Peter Christopherson, and MIT Media Lab. Matsumoto's multidisciplinary projects have been exhibited recently at Meadows Gallery University of Texas at Tyler, S. Tucker Cooke Gallery University of North Carolina Asheville, Sebastopol Center for the Arts, National Museum of Korea, Czong Institute for Contemporary Art, Van Der Plas Gallery, ArtHelix Gallery, Caelum Gallery, Limner Gallery, the Cello Factory, University of the District of Columbia, Lux Art Gallery, Studio Montclair, Manifest Gallery, Tenerife Espacio de las Artes, Art Basel Miami, ISEA International, FILE Sao Paulo, Nook Gallery, and Arts and Heritage Centre Altrincham. He had solo exhibitions at BYTE Gallery Transylvania University (2015), Los Angeles Center of Digital Art (2016) and Alviani ArtSpace, Pescara (2017). https //www.ryotamatsumotostudio.com 美術 デザイン アーバニズム
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Meet! 2011 15. Oktober - 05. November 2011 Kulturetage im SofaLoft Jordanstrasse 26, 30173 Hannover Three most important things "Food" "Clothing" " Shelter" Our basic needs - they are real. We are exploring their existence, asking ourselves how contemporary art discusses and realizes the essential issues. We are going to present answers to our question in this year s art project "Meet!2011", an international exhibition including several related events. We are looking for interesting contributions from all forms and genres art may offer, including literature and music. Participation An art group from Hanover, Germany, has brought "Meet!" into being but other artists are invited to join the project and participate in the exhibition and accompanying events. The Meet! hosts will view tendered art works and/or concepts and chose further contributions. Application Form Meet! is an art project brought into life by an art group from Hanover. Other artists are, however, invited to participate in the project as well. The hosts will carefully view handed-in works concepts and chose further contributions. Conditions of participation Artists from all over the world are invited to hand in their concepts or works from any genre or form art may offer - including music and literature. The delivery of a complete application form in due time(deadline is the 1st August 2011) is a prerequisite for the participation. Until the 15th August 2011 the hosts will chose and inform the participating contributors. Please e-mail or mail us your applications, containing the application form, including personal data and up to three works/concepts visual material of the work(s) in the form of photos (not exceeding the A4 format, limited to ten photos) or a DVD (not exceeding ten minutes) a short description of the work/concept (not exceeding half a page) including some explanations of the original idea or intention behind it. Incomplete applications cannot be regarded. Application Form #ref(Aplicationformmeet2011.pdf) Mail to Meet! 2011 Kesselstraße 17 30453 Hannover Germany E-Mail to meet.artproject@gmail.com (JPG, PDF, TIFF or GIF not exceeding 5 MB) Organization Meet!2011 takes the responsibility and covers the costs to print invitation cards and posters and promote the project. Meet!2011assures that an insurance covers all participating works for the duration of the exhibition. The artists will cover the costs of – and take full responsibility for – the transport of his/her works. The artist will make sure that his/her work(s) arrive(s) in due time before the beginning of the exhibition and is picked up afterward (precise dates will be announced along with the confirmation of participation). Copyright (c) Meet! 2011 All Right Reserved