ゲーム攻略・無料ウィキレンタルのアットウィキ (@WIKI)

Cocoaリファレンス日本語化計画 - Foundation Data Types Reference

https://w.atwiki.jp/cocoareferencejp/pages/103.html

Tags Core Services Layer Foundation リファレンス未完 Cocoa トップリファレンス Core Services階層 Foundation Foundationのデータ型 Foundation データタイプリファレンス翻訳元このページの最終更新：2010-02-08 ADCの最終更新：2009-12-02 フレームワーク Foundation?/Foundation.h 宣言ファイル NSAppleEventManager.hNSByteOrder.hNSDate.hNSDecimal.hNSException.hNSGeometry.hNSHashTable.hNSMapTable.hNSObjCRuntime.hNSPathUtilities.hNSPort.hNSRange.hNSString.hNSZone.h 概観(Overview) 　このドキュメントはFoundationフレームワーク中のデータ型や定数について記述しています。データ型(Data Types) NSAppleEventManagerSuspensionID NSByteOrder NSComparator NSComparisonResult NSDecimal NSEnumerationOptions NSHashEnumerator NSHashTable NSHashTableCallBacks NSHashTableOptions NSInteger 　整数値の記述に使われます。 #if __LP64__ || TARGET_OS_EMBEDDED || TARGET_OS_IPHONE || TARGET_OS_WIN32 || NS_BUILD_32_LIKE_64typedef long NSInteger;#elsetypedef int NSInteger;#endif 解説 32ビットアプリケーションでは、NSIntegerは32ビット整数値です。64ビットアプリケーションではNSIntegerを64ビット整数値のように扱います。使用可能な環境 Max OS X v10.5以降宣言ファイル NSObjCRuntime.h NSMapEnumerator NSMapTable NSMapTableKeyCallBacks NSMapTableOptions NSMapTableValueCallBacks NSPoint 　デカルト座標系の座標を表します。 typedef struct _NSPoint { CGFloat x; CGFloat y; } NSPoint;   フィールド x x座標です。 y y座標です。特に気をつけること Mac OS v10.5以前では座標はCGFloat型ではなくfloat型です。 64ビットシステム向けに開発するか、32ビットマシンで64ビットのように開発している時は、NSPointはCGPointの型定義です。使用可能な環境 Mac OS X v10.0以降宣言ファイル NSGeometry.h NSPointArray NSPointPointer NSRange 　文字列やNSArrayオブジェクト等一つの連続した値の一部を表すのに使われる構造体です。 typedef struct _NSRange { NSUInteger location; NSUInteger length; } NSRange;   フィールド location 最初のインデックスです(Cの配列のように0から始まります)。 length 範囲の中のアイテムの数です(0にもなります)。解説 Foundationのレンジを操作する関数には以下のものがあります。 link_anchor plugin error idが指定されていないか、存在しないページを指定しています。 link_anchor plugin error idが指定されていないか、存在しないページを指定しています。 link_anchor plugin error idが指定されていないか、存在しないページを指定しています。 link_anchor plugin error idが指定されていないか、存在しないページを指定しています。 link_anchor plugin error idが指定されていないか、存在しないページを指定しています。 link_anchor plugin error idが指定されていないか、存在しないページを指定しています。 link_anchor plugin error idが指定されていないか、存在しないページを指定しています。 link_anchor plugin error idが指定されていないか、存在しないページを指定しています。使用可能な環境 Mac OS X v10.0 以降宣言ファイル NSRange.h NSRangePointer NSRect 　四角形を表します。 typedef struct _NSRect { NSPoint origin; NSSize size; } NSRect;   フィールド origin 四角形の原点です(x座標とy座標をとります)。 size 原点からはかった四角形の幅と高さです。特に気をつけること 64ビットシステム向けに開発しているか、32ビットマシンで64ビットのように開発している時は、NSRectはCGRectの型定義です。使用可能な環境 Mac OS X v10.0以降宣言ファイル NSGeometry.h NSRectArray NSRectEdge NSRectPointer NSSearchPathDirectory NSSearchPathDomainMask NSSize 　二次元の大きさを表します typedef struct _NSSize { CGFloat width; CGFloat height; } NSSize;   フィールド width 幅です。 height 高さです。解説通常、widthとheightの値は常に聖です。しかし、NSSize構造体を生成する関数群ではこれらの属性に負の値を入れることもできます。ですが、widthやheightが負の値を持つ時の動作が未定義なメソッドもあります。特に気をつけること Mac OS v10.5以前では幅と高さはCGFloat型ではなくfloat型です。 64ビットシステム向けに開発しているか、32ビットマシンで64ビットのように開発している時は、NSSizeはCGSizeの型定義です。使用可能な条件 Mac OS X v10.0以降宣言ファイル NSGeometry.h NSSizeArray NSSizePointer NSSocketNativeHandle NSSortOptions NSStringEncoding NSSwappedDouble NSSwappedFloat NSTimeInterval NSUncaughtExceptionHandler NSUInteger 　符号なし整数を表すのに使われます。 #if __LP64__ || TARGET_OS_EMBEDDED || TARGET_OS_IPHONE || TARGET_OS_WIN32 || NS_BUILD_32_LIKE_64typedef long NSInteger;#elsetypedef int NSInteger;#endif 解説 32ビットアプリケーションでは、NSUIntegerは32ビット符号なし整数値です。64ビットアプリケーションではNSUIntegerを64ビット符号なし整数値のように扱います。使用可能な環境 Max OS X v10.5以降宣言ファイル NSObjCRuntime.h NSZone 　メモリゾーンの識別、管理に使われます。 typedef struct _NSZone NSZone; 使用可能な環境 Mac OS X v10.0以降宣言ファイル NSZone.h

kiwakiri @ ウィキ - MenuBar

https://w.atwiki.jp/kiwakiri/pages/134.html

Done List 住宅購入住宅条件映画音楽本食事人々 FrontPage 取得中です。 Plug-in help MenuBar edit #counter2

TEST - Simple Implementation of DOM Events in JavaScript

https://w.atwiki.jp/eriax/pages/118.html

制限 DOM Events のシンプル(?)な実装試案。名前空間ありの旧仕様。ソースコード if ( undefined === typeof Array.prototype.indexOf) { Array.prototype.indexOf = function (ceil, floor) { return function (searchElement) { var fromIndex = arguments[1]; var count = this.length; var i = Number(fromIndex) || 0; i = (i 0) ? ceil(i) floor(i); if (i 0) { i += count; } for (; i count; i++) { if (i in this) { if (this[i] === searchElement) { return i; } } } return -1; }; }(Math.ceil, Math.floor); } //////////////////////////////////////////////////////////////////////// function DOMObject(arg) { if (arguments.length 0) { var name; for (name in arg) { if (arg.hasOwnProperty(name)) { this[name] = arg[name]; } } } } (function () { this.constructor = DOMObject; }).call(DOMObject.prototype); //////////////////////////////////////////////////////////////////////// (function () { // EventPhase this.CAPTURING_PHASE = 1; this.AT_TARGET = 2; this.BUBBLING_PHASE = 3; }).call(DOMEvent); function DOMEvent(arg) { if (arguments.length 0) { if (arg) { DOMObject.apply(this, arguments); } } } DOMEvent.prototype = new DOMObject; (function () { this.constructor = DOMEvent; // Level 2 this.type = null; this.target = null; this.currentTarget = null; this.eventPhase = null; this.bubbles = null; this.cancelable = null; this.timeStamp = null; // Level 3 this.namespaceURI = null; this.defaultPrevented = false; this.trusted = false; // extension this.ownerDocument = null; this.propagationStopped = false; this.immediatePropagationStopped = false; }).call(DOMEvent.prototype); (function () { this.stopPropagation = function () { this.propagationStopped = true; }; this.preventDefault = function () { if (this.cancelable) { this.defaultPrevented = true; } }; this.initEvent = function (eventTypeArg, canBubbleArg, cancelableArg) { this.initEventNS(null, eventTypeArg, canBubbleArg, cancelableArg); }; this.stopImmediatePropagation = function () { this.immediatePropagationStopped = true; }; this.toString = function () { return [object Event] ; }; this.initEventNS = function (namespaceURI, eventTypeArg, canBubbleArg, cancelableArg) { this.namespaceURI = namespaceURI; this.type = eventTypeArg; this.bubbles = canBubbleArg; this.cancelable = cancelableArg; }; }).call(DOMEvent.prototype); //////////////////////////////////////////////////////////////////////// function DOMEventTarget(arg) { if (arguments.length 0) { if (arg) { DOMObject.apply(this, arguments); } var name = [EventRegistry] ; if (!this.hasOwnProperty(name)) { var memo = this[name] = []; memo[DOMEvent.CAPTURING_PHASE] = { [] }; memo[DOMEvent.BUBBLING_PHASE] = { [] }; } } } DOMEventTarget.prototype = new DOMObject; (function () { this.constructor = DOMEventTarget; this[ [EventRegistry] ] = null; }).call(DOMEventTarget.prototype); (function () { this[ [IsValidEventListener] ] = function (listener) { return ( function === typeof listener) || ( object === typeof listener function === typeof listener.handleEvent); }; this.addEventListener = function (type, listener, useCapture) { return this.addEventListenerNS(null, type, listener, useCapture); }; this.removeEventListener = function (type, listener, useCapture) { return this.removeEventListenerNS(null, type, listener, useCapture); }; this.dispatchEvent = function (evt) { evt.target = this; evt.timeStamp = new Date; PROPAGATION { var targets = this[ [TraceRoute] ](); var targetCount = targets.length; var i; // capture evt.eventPhase = DOMEvent.CAPTURING_PHASE; for (i = targetCount - 1; 0 = i; i -= 1) { if (!targets[i][ [CallEventListener] ](evt)) { break PROPAGATION; // stop (Immediate)Propagation () called } } // target evt.eventPhase = DOMEvent.AT_TARGET; if (!this[ [CallEventListener] ](evt)) { break PROPAGATION; // stop (Immediate)Propagation () called } // bubble if (evt.bubbles) { evt.eventPhase = DOMEvent.BUBBLING_PHASE; for (i = 0; i targetCount; i++) { if (!targets[i][ [CallEventListener] ](evt)) { break PROPAGATION; // stop (Immediate)Propagation () called } } } } return evt.defaultPrevented; // preventDefault () called? }; this[ [TraceRoute] ] = function () { var result = []; var node = this; if (node.nodeType 0) { while ((node = node.parentNode)) { result[result.length] = node; } } return result; }; this[ [GetEventListener] ] = function (evt) { var type = evt.type; var eventPhase = evt.eventPhase; var namespaceURI = evt.namespaceURI; if (namespaceURI == null) { namespaceURI = ; } switch (eventPhase) { case DOMEvent.CAPTURING_PHASE case DOMEvent.BUBBLING_PHASE var registry = this[ [EventRegistry] ][eventPhase]; var listeners = registry[namespaceURI]; if (listeners instanceof Object) { var handlers = listeners[type]; if (handlers instanceof Array) { return handlers; } return listeners[type] = []; } listeners = registry[namespaceURI] = {}; return listeners[type] = []; case DOMEvent.AT_TARGET var listeners1 = this[ [GetEventListener] ]({ namespaceURI namespaceURI, type type, eventPhase DOMEvent.CAPTURING_PHASE }); var listeners2 = this[ [GetEventListener] ]({ namespaceURI namespaceURI, type type, eventPhase DOMEvent.BUBBLING_PHASE }); return listeners1.concat(listeners2); default return []; } }; this[ [CallEventListener] ] = function (evt) { var listeners = this[ [GetEventListener] ](evt); var listenerCount = listeners.length; var listener; var i; for (i = 0; i listenerCount; i++) { listener = listeners[i]; try { evt.currentTarget = this; if ( function === typeof listener) { listener.call(this, evt); } else if ( function === typeof listener.handleEvent) { listener.handleEvent(evt); } } catch (err) { ; } finally { if (evt.immediatePropagationStopped) { // stopImmediatePropagation () called return false; } } } return !evt.propagationStopped; // stopPropagation () called }; this.toString = function () { return [object EventTarget] ; }; this.addEventListenerNS = function (namespaceURI, type, listener, useCapture) { if (this[ [IsValidEventListener] ](listener)) { var listeners = this[ [GetEventListener] ]({ namespaceURI namespaceURI, type type, eventPhase useCapture ? DOMEvent.CAPTURING_PHASE DOMEvent.BUBBLING_PHASE }); listeners.push(listener); } }; this.removeEventListenerNS = function (namespaceURI, type, listener, useCapture) { if (this[ [IsValidEventListener] ](listener)) { var listeners = this[ [GetEventListener] ]({ namespaceURI namespaceURI, type type, eventPhase useCapture ? DOMEvent.CAPTURING_PHASE DOMEvent.BUBBLING_PHASE }); if (listeners.length 0) { var index = listeners.indexOf(listener); if (index = 0) { listeners.splice(index, 1); } } } }; }).call(DOMEventTarget.prototype); テスト。 !DOCTYPE HTML title TEST /title script type= text/javascript /script script type= text/javascript function TestController(controls) { var Log1 = []; // T1 を要素ノードとして作る var T1 = new DOMEventTarget({ nodeType 1, parentNode null, childNodes [] }); // T1 をイベントリスナで監視（キャプチャ） T1.addEventListener( click , function (e) { var log = []; log.push( T1 capturing_listener[0] ); // デフォルトアクションを取り消す if (controls[ preventDefault ].checked) { e.preventDefault(); log.push( preventDefault() was called ); } // イベント伝播を抑止する if (controls[ stopPropagation ].checked) { e.stopPropagation(); log.push( stopPropagation() was called ); } // イベント伝播を直ちに抑止する if (controls[ stopImmediatePropagation ].checked) { e.stopImmediatePropagation(); log.push( stopImmediatePropagation() was called ); } Log1.push(log.join( | )); }, true); T1.addEventListener( click , function (e) { Log1.push( T1 capturing_listener[1] ); }, true); T1.addEventListener( click , function (e) { Log1.push( T1 capturing_listener[2] ); }, true); // T1 をイベントリスナで監視（バブル） T1.addEventListener( click , function (e) { Log1.push( T1 bubbling_listener[0] ); }, false); T1.addEventListener( click , function (e) { Log1.push( T1 bubbling_listener[1] ); }, false); T1.addEventListener( click , function (e) { Log1.push( T1 bubbling_listener[2] ); }, false); //////////////////////////////////////////////////////////////////////// // T2 を要素ノード（T1 の子）として作る var T2 = new DOMEventTarget({ nodeType 1, parentNode T1, childNodes [] }); T1.childNodes.push(T2); // T2 をイベントリスナで監視（キャプチャ） T2.addEventListener( click , function (e) { Log1.push( T2 capturing_listener[0] ); }, true); T2.addEventListener( click , function (e) { Log1.push( T2 capturing_listener[1] ); }, true); T2.addEventListener( click , function (e) { Log1.push( T2 capturing_listener[2] ); }, true); // T2 をイベントリスナで監視（バブル） var T2_listener0 = { handleEvent function (e) { Log1.push( T2 bubbling_listener[0], this= + this); }, toString function () { return [object DOMEventListener] ; } }; T2.addEventListener( click , T2_listener0, false); T2.addEventListener( click , function (e) { Log1.push( T2 bubbling_listener[1], this= + this); }, false); T2.addEventListener( click , function (e) { Log1.push( T2 bubbling_listener[2] ); }, false); // T2 を監視している T2_listener0 を除去する（バブル） // T2.removeEventListener ( click , T2_listener0, false); //////////////////////////////////////////////////////////////////////// // T3 を要素ノード（T2 の子）として作る var T3 = new DOMEventTarget({ nodeType 1, parentNode T2, childNodes [] }); T2.childNodes.push(T3); // T3 をイベントリスナで監視（キャプチャ） T3.addEventListener( click , function (e) { Log1.push( T3 capturing_listener[0] ); }, true); T3.addEventListener( click , function (e) { Log1.push( T3 capturing_listener[1] ); }, true); T3.addEventListener( click , function (e) { Log1.push( T3 capturing_listener[2] ); }, true); // T3 をイベントリスナで監視（バブル） T3.addEventListener( click , function (e) { Log1.push( T3 bubbling_listener[0] ); }, false); T3.addEventListener( click , function (e) { Log1.push( T3 bubbling_listener[1] ); }, false); T3.addEventListener( click , function (e) { Log1.push( T3 bubbling_listener[2] ); }, false); //////////////////////////////////////////////////////////////////////// // イベント生成 var e = new DOMEvent({ ownerDocument document }); // イベント初期化 e.initEvent( click , controls[ bubbles ].checked, controls[ cancelable ].checked); Log1.push( bubbles + e.bubbles); Log1.push( cancelable + e.cancelable); // イベント通知 var defaultPrevented = T3.dispatchEvent(e); // デフォルトアクションが取り消されたか Log1.push( defaultPrevented + defaultPrevented); //////////////////////////////////////////////////////////////////////// controls[ OUTPUT-1 ].value = Log1.join( .\n ); } /script !-- ここから -- p id= D1 T1 と、その子 T2 と、その子 T3 を作り、それぞれにイベントリスナを取り付けた後、T3 にイベントを送る。 /p pre role= img aria-describedby= D1 + T1 | + T2 | + T3 --- click! /pre form action= # id= FORM-1 p input type= button value= 試す aria-describedby= D1 onclick= TestController(this.form.elements) label input type= checkbox name= bubbles checked= checked bubbles /label label input type= checkbox name= cancelable checked= checked cancelable /label label input type= checkbox name= preventDefault preventDefault /label label input type= checkbox name= stopPropagation stopPropagation /label label input type= checkbox name= stopImmediatePropagation stopImmediatePropagation /label /p p textarea rows= 20 cols= 100 name= OUTPUT-1 /textarea /p /form 初出 2011-08-23/25

ここに何かをWiki - MenuBar

https://w.atwiki.jp/justin/pages/2.html

メニュー FrontPage MenuBar 取得中です。

東方同人CDの歌詞＠Wiki - 04 4-dimension

https://w.atwiki.jp/touhoukashi/pages/3655.html

【登録タグ 4 False＆Trues YUKI/藤宮ゆき technological ネクロファンタジア曲】【注意】現在、このページはJavaScriptの利用が一時制限されています。この表示状態ではトラック情報が正しく表示されません。この問題は、以下のいずれかが原因となっています。ページがAMP表示となっているウィキ内検索からページを表示しているこれを解決するには、こちらをクリックし、ページを通常表示にしてください。 /** General styling **/ @font-face { font-family Noto Sans JP ; font-display swap; font-style normal; font-weight 350; src url(https //img.atwikiimg.com/www31.atwiki.jp/touhoukashi/attach/2972/10/NotoSansCJKjp-DemiLight.woff2) format( woff2 ), url(https //img.atwikiimg.com/www31.atwiki.jp/touhoukashi/attach/2972/9/NotoSansCJKjp-DemiLight.woff) format( woff ), url(https //img.atwikiimg.com/www31.atwiki.jp/touhoukashi/attach/2972/8/NotoSansCJKjp-DemiLight.ttf) format( truetype ); } @font-face { font-family Noto Sans JP ; font-display swap; font-style normal; font-weight bold; src url(https //img.atwikiimg.com/www31.atwiki.jp/touhoukashi/attach/2972/13/NotoSansCJKjp-Medium.woff2) format( woff2 ), url(https //img.atwikiimg.com/www31.atwiki.jp/touhoukashi/attach/2972/12/NotoSansCJKjp-Medium.woff) format( woff ), url(https //img.atwikiimg.com/www31.atwiki.jp/touhoukashi/attach/2972/11/NotoSansCJKjp-Medium.ttf) format( truetype ); } rt { font-family Arial, Verdana, Helvetica, sans-serif; } /** Main table styling **/ #trackinfo, #lyrics { font-family Noto Sans JP , sans-serif; font-weight 350; } .track_number { font-family Rockwell; font-weight bold; } .track_number after { content . ; } #track_args, .amp_text { display none; } #trackinfo { position relative; float right; margin 0 0 1em 1em; padding 0.3em; width 320px; border-collapse separate; border-radius 5px; border-spacing 0; background-color #F9F9F9; font-size 90%; line-height 1.4em; } #trackinfo th { white-space nowrap; } #trackinfo th, #trackinfo td { border none !important; } #trackinfo thead th { background-color #D8D8D8; box-shadow 0 -3px #F9F9F9 inset; padding 4px 2.5em 7px; white-space normal; font-size 120%; text-align center; } .trackrow { background-color #F0F0F0; box-shadow 0 2px #F9F9F9 inset, 0 -2px #F9F9F9 inset; } #trackinfo td ul { margin 0; padding 0; list-style none; } #trackinfo li { line-height 16px; } #trackinfo li nth-of-type(n+2) { margin-top 6px; } #trackinfo dl { margin 0; } #trackinfo dt { font-size small; font-weight bold; } #trackinfo dd { margin-left 1.2em; } #trackinfo dd + dt { margin-top .5em; } #trackinfo_help { position absolute; top 3px; right 8px; font-size 80%; } /** Media styling **/ #trackinfo .media th { background-color #D8D8D8; padding 4px 0; font-size 95%; text-align center; } .media td { padding 0 2px; } .media iframe nth-of-type(n+2) { margin-top 0.3em; } .youtube + .nicovideo, .youtube + .soundcloud, .nicovideo + .soundcloud { margin-top 0.75em; } .media_section { display flex; align-items center; text-align center; } .media_section before, .media_section after { display block; flex-grow 1; content ; height 1px; } .media_section before { margin-right 0.5em; background linear-gradient(-90deg, #888, transparent); } .media_section after { margin-left 0.5em; background linear-gradient(90deg, #888, transparent); } .media_notice { color firebrick; font-size 77.5%; } /** Around track styling **/ .next-track { float right; } /** Infomation styling **/ #trackinfo .info_header th { padding .3em .5em; background-color #D8D8D8; font-size 95%; } #trackinfo .infomation_show_btn_wrapper { float right; font-size 12px; user-select none; } #trackinfo .infomation_show_btn { cursor pointer; } #trackinfo .info_content td { padding 0 0 0 5px; height 0; transition .3s; } #trackinfo .info_content ul { padding 0; margin 0; max-height 0; list-style initial; transition .3s; } #trackinfo .info_content li { opacity 0; visibility hidden; margin 0 0 0 1.5em; transition .3s, opacity .2s; } #trackinfo .info_content.infomation_show td { padding 5px; height 100%; } #trackinfo .info_content.infomation_show ul { padding 5px 0; max-height 50em; } #trackinfo .info_content.infomation_show li { opacity 1; visibility visible; } #trackinfo .info_content.infomation_show li nth-of-type(n+2) { margin-top 10px; } /** Lyrics styling **/ #lyrics { font-size 1.06em; line-height 1.6em; } .not_in_card, .inaudible { display inline; position relative; } .not_in_card { border-bottom dashed 1px #D0D0D0; } .tooltip { display flex; visibility hidden; position absolute; top -42.5px; left 0; width 275px; min-height 20px; max-height 100px; padding 10px; border-radius 5px; background-color #555; align-items center; color #FFF; font-size 85%; line-height 20px; text-align center; white-space nowrap; opacity 0; transition 0.7s; -webkit-user-select none; -moz-user-select none; -ms-user-select none; user-select none; } .inaudible .tooltip { top -68.5px; } span hover + .tooltip { visibility visible; top -47.5px; opacity 0.8; transition 0.3s; } .inaudible span hover + .tooltip { top -73.5px; } .not_in_card span.hide { top -42.5px; opacity 0; transition 0.7s; } .inaudible .img { display inline-block; width 3.45em; height 1.25em; margin-right 4px; margin-bottom -3.5px; margin-left 4px; background-image url(https //img.atwikiimg.com/www31.atwiki.jp/touhoukashi/attach/2971/7/Inaudible.png); background-size contain; background-repeat no-repeat; } .not_in_card after, .inaudible .img after { content ; visibility hidden; position absolute; top -8.5px; left 42.5%; border-width 5px; border-style solid; border-color #555 transparent transparent transparent; opacity 0; transition 0.7s; } .not_in_card hover after, .inaudible .img hover after { content ; visibility visible; top -13.5px; left 42.5%; opacity 0.8; transition 0.3s; } .not_in_card after { top -2.5px; left 50%; } .not_in_card hover after { top -7.5px; left 50%; } .not_in_card.hide after { visibility hidden; top -2.5px; opacity 0; transition 0.7s; } /** For mobile device styling **/ .uk-overflow-container { display inline; } #trackinfo.mobile { display table; float none; width 100%; margin auto; margin-bottom 1em; } #trackinfo.mobile th { text-transform none; } #trackinfo.mobile tbody tr not(.media) th { text-align left; background-color unset; } #trackinfo.mobile td { white-space normal; } document.addEventListener( DOMContentLoaded , function() { use strict ; const headers = { title アルバム別曲名 , album アルバム , circle サークル , vocal Vocal , lyric Lyric , chorus Chorus , narrator Narration , rap Rap , voice Voice , whistle Whistle (口笛) , translate Translation (翻訳) , arrange Arrange , artist Artist , bass Bass , cajon Cajon (カホン) , drum Drum , guitar Guitar , keyboard Keyboard , mc MC , mix Mix , piano Piano , sax Sax , strings Strings , synthesizer Synthesizer , trumpet Trumpet , violin Violin , original 原曲 , image_song イメージ曲 }; const rPagename = /(?=^|.*

関西JAGA - MenuBar

https://w.atwiki.jp/wjaga/pages/17.html

MenuBar FrontPage 最新の１０件取得中です。

Signal Transduction シグナル伝達 - Hematopoiesis

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Hematopoietic cell regulation by Rac1 and Rac2 BTK-/- mice show impaired responsiveness to Epo. BTK-/-/TEC-/- plateles fail to undergo an inccrease in Ca2+ , aggregation, secretion, and spreading in response to collagen or CRP. PLCG2 -/- mice impair vasculogenesis and erythropoiesis. Jak2 -/- mice show defective erythropoiesis. RasGRP2 -/- mice have a platelet aggregation defect. Hematopoietic cell regulation by Rac1 and Rac2 1 Science. 2003 Oct 17;302(5644) 445-9. Hematopoietic cell regulation by Rac1 and Rac2 guanosine triphosphatases. Gu Y, Filippi MD, Cancelas JA, Siefring JE, Williams EP, Jasti AC, Harris CE, Lee AW, Prabhakar R, Atkinson SJ, Kwiatkowski DJ, Williams DA. Division of Experimental Hematology, Cincinnati Children s Hospital Medical Center, Cincinnati, OH 45229, USA. The Rho guanosine triphosphatases (GTPases) Rac1 and Rac2 are critical signaling regulators in mammalian cells. The deletion of both Rac1 and Rac2 murine alleles leads to a massive egress of hematopoietic stem/progenitor cells (HSC/Ps) into the blood from the marrow, whereas Rac1-/- but not Rac2-/- HSC/Ps fail to engraft in the bone marrow of irradiated recipient mice. In contrast, Rac2, but not Rac1, regulates superoxide production and directed migration in neutrophils, and in each cell type, the two GTPases play distinct roles in actin organization, cell survival, and proliferation. Thus, Rac1 and Rac2 regulate unique aspects of hematopoietic development and function. Publication Types Research Support, U.S. Gov t, P.H.S. PMID 14564009 [PubMed - indexed for MEDLINE] BTK-/- mice show impaired responsiveness to Epo. 1 J Exp Med. 2004 Mar 15;199(6) 785-95. Epub 2004 Mar 8. Btk is required for an efficient response to erythropoietin and for SCF-controlled protection against TRAIL in erythroid progenitors. Schmidt U, van den Akker E, Parren-van Amelsvoort M, Litos G, de Bruijn M, Gutierrez L, Hendriks RW, Ellmeier W, Lowenberg B, Beug H, von Lindern M. Institute of Molecular Pathology, Vienna, Austria. Regulation of survival, expansion, and differentiation of erythroid progenitors requires the well-controlled activity of signaling pathways induced by erythropoietin (Epo) and stem cell factor (SCF). In addition to qualitative regulation of signaling pathways, quantitative control may be essential to control appropriate cell numbers in peripheral blood. We demonstrate that Bruton s tyrosine kinase (Btk) is able to associate with the Epo receptor (EpoR) and Jak2, and is a substrate of Jak2. Deficiency of Btk results in reduced and delayed phosphorylation of the EpoR, Jak2, and downstream signaling molecules such as Stat5 and PLCgamma1 as well as in decreased responsiveness to Epo. As a result, expansion of erythroid progenitors lacking Btk is impaired at limiting concentrations of Epo and SCF. In addition, we show that SCF induces Btk to interact with TNF-related apoptosis-inducing ligand (TRAIL)-receptor 1 and that lack of Btk results in increased sensitivity to TRAIL-induced apoptosis. Together, our results indicate that Btk is a novel, quantitative regulator of Epo/SCF-dependent expansion and survival in erythropoiesis. Publication Types Comparative Study Research Support, Non-U.S. Gov t PMID 15007095 [PubMed - indexed for MEDLINE] BTK-/-/TEC-/- plateles fail to undergo an inccrease in Ca2+ , aggregation, secretion, and spreading in response to collagen or CRP. 1 Blood. 2003 Nov 15;102(10) 3592-9. Epub 2003 Jul 3. Tec regulates platelet activation by GPVI in the absence of Btk. Atkinson BT, Ellmeier W, Watson SP. Department of Pharmacology, University of Oxford, Mansfield Rd, Oxford, OX1 3QT, United Kingdom. ben.atkinson@pharm.ox.ac.uk The Tec family kinase Btk plays an important role in the regulation of phospholipase C gamma 2 (PLC gamma 2) downstream of the collagen receptor glycoprotein VI (GPVI) in human platelets. Platelets also express a second member of this family, Tec; however, its function has not been analyzed. To address the role of Tec, we analyzed Btk-/-, Tec-/-, and Btk/Tec double-deficient (Btk-/-/Tec-/-) platelets. Tec-/- platelets exhibit a minor reduction in aggregation to threshold concentrations of collagen or the GPVI-specific agonist collagen-related peptide (CRP), whereas responses to higher concentrations are normal. Tyrosine phosphorylation of PLC gamma 2 by collagen and CRP is not altered in Tec-/- platelets. However, Btk-/-/Tec-/- platelets exhibit a greater reduction in PLC gamma 2 phosphorylation than is seen in the absence of Btk, thus revealing an important role for Tec in this situation. Furthermore, Btk-/-/Tec-/- platelets fail to undergo an increase in Ca2+, aggregation, secretion, and spreading in response to collagen or CRP, whereas they aggregate normally to adenosine diphosphate (ADP) and spread on fibrinogen. A residual GPVI signal exists in the Btk-/-/Tec-/- platelets as CRP synergizes with ADP to mediate aggregation. These results demonstrate an essential requirement for Tec and Btk in platelet activation by GPVI and reveal a functional role for Tec in the regulation of PLC gamma 2 in the absence of Btk. Publication Types Research Support, Non-U.S. Gov t PMID 12842985 [PubMed - indexed for MEDLINE] PLCG2 -/- mice impair vasculogenesis and erythropoiesis. 1 J Biol Chem. 2002 Mar 15;277(11) 9335-41. Epub 2001 Dec 13. Absence of erythrogenesis and vasculogenesis in Plcg1-deficient mice. Liao HJ, Kume T, McKay C, Xu MJ, Ihle JN, Carpenter G. Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, Tennessee 37232,USA. Mice nullizygous for Plcg1 cease growing at early to mid-gestation. An examination of carefully preserved wild-type embryos shows clear evidence of erythropoiesis, but erythropoiesis is not evident in Plcg1 nullizygous embryos at the same stage. The analyses of embryonic materials demonstrate that in the absence of Plcg1, erythroid progenitors cannot be detected in the yolk sac or embryo body by three different assays, burst-forming units, colony-forming units, and analysis for the developmental marker Ter119. However, non-erythroid granulocyte/macrophage colonies are produced by Plcg1 null embryos. Further analysis of these embryos demonstrates significantly diminished vasculogenesis in Plcg1 nullizygous embryos based on the lack of expression of the endothelial marker platelet endothelial cell adhesion molecule-1. In addition, Plcg1 nullizygous embryos express a greatly reduced level of vascular endothelial growth factor receptor-2/Flk-1, consistent with significantly impaired vasculogenesis and erythropoiesis. Interestingly, these early embryos do express phospholipase C-gamma2, however, it is unable to substitute for the absence of phospholipase C-gamma1, which can be detected in its tyrosine-phosphorylated state. Publication Types Research Support, U.S. Gov t, P.H.S. PMID 11744703 [PubMed - indexed for MEDLINE] Jak2 -/- mice show defective erythropoiesis. 1 Cell. 1998 May 1;93(3) 397-409. Jak2 deficiency defines an essential developmental checkpoint in definitive hematopoiesis. Neubauer H, Cumano A, Muller M, Wu H, Huffstadt U, Pfeffer K. Institute of Medical Microbiology, Immunology, and Hygiene, Technical University of Munich, Germany. Janus kinases (Jaks) play an important role in signal transduction via cytokine and growth factor receptors. A targeted inactivation of Jak2 was performed. Jak2-/- embryos are anemic and die around day 12.5 postcoitum. Primitive erythrocytes are found, but definitive erythropoiesis is absent. Compared to erythropoietin receptor-deficient mice, the phenotype of Jak2 deficiency is more severe. Fetal liver BFU-E and CFU-E colonies are completely absent. However, multilineage hematopoietic stem cells (CD34low, c-kit(pos)) can be found, and B lymphopoiesis appears intact. In contrast to IFNalpha stimulation, Jak2-/- cells do not respond to IFNgamma. Jak2-/- embryonic stem cells are competent for LIF signaling. The data provided demonstrate that Jak2 has pivotal functions for signal transduction of a set of cytokine receptors required in definitive erythropoiesis. Publication Types PMID 9590174 [PubMed - indexed for MEDLINE] RasGRP2 -/- mice have a platelet aggregation defect. 1 Nat Med. 2004 Sep;10(9) 982-6. Epub 2004 Aug 29. CalDAG-GEFI integrates signaling for platelet aggregation and thrombus formation. Crittenden JR, Bergmeier W, Zhang Y, Piffath CL, Liang Y, Wagner DD, Housman DE, Graybiel AM. Department of Brain and Cognitive Sciences, and McGovern Institute for Brain Research, Massachusetts Institute of Technology, 45 Carleton Street, E25-618, Cambridge, Massachusetts 02139, USA. Signaling through the second messengers calcium and diacylglycerol (DAG) is a critical element in many biological systems. Integration of calcium and DAG signals has been suggested to occur primarily through protein kinase C family members, which bind both calcium and DAG. However, an alternative pathway may involve members of the CalDAG-GEF/RasGRP protein family, which have structural features (calcium-binding EF hands and DAG-binding C1 domains) that suggest they can function in calcium and DAG signal integration. To gain insight into the signaling systems that may be regulated by CalDAG-GEF/RasGRP family members, we have focused on CalDAG-GEFI, which is expressed preferentially in the brain and blood. Through genetic ablation in the mouse, we have found that CalDAG-GEFI is crucial for signal integration in platelets. Mouse platelets that lack CalDAG-GEFI are severely compromised in integrin-dependent aggregation as a consequence of their inability to signal through CalDAG-GEFI to its target, the small GTPase Rap1. These results suggest that analogous signaling defects are likely to occur in the central nervous system when CalDAG-GEFI is absent or compromised in function. Publication Types PMID 15334074 [PubMed - indexed for MEDLINE]

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