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• Let's（ ＾ω＾）study - Apache/2.設定ファイル(httpd.conf)

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  ヘッダ Section 1 Global EnvironmentServer HTTP応答ヘッダの設定 サーバ設定ファイルのルートディレクトリの指定 PIDファイルのパス タイムアウト時間 キープアライブ 最大キープアライブリクエスト数 キープアライブタイムアウト時間 (調査・編集中)先行してforkを行うWEBサーバの設定 (調査・編集中) 待ち受けポート番号 モジュール読み込み 外部設定ファイルの読み込み 拡張ステータス情報保存の有無 実行ユーザ・グループ Section 2 'Main' server configurationサーバ管理者メールアドレス サーバ名 (サーバが自分自身の名前とポートを決定する方法の設定 ドキュメントルートの定義 (調査・編集中) ドキュメントルート配下に適用される設定 ユーザディレクトリモジュールの設定 ユーザディレクトリ配下に適用される設定 ディレクトリインデックスの設定 分散設定ファイルの設定 (調査・編集中) MIMEタイプ設定ファイル デフォルトのMIMEタイプの設定 MIME MAGICモジュールの設定 DNSルックアップの設定 メモリマッピングの有無 sendfileサポートの有無 エラーログの設定 ログレベルの設定 ログフォーマットの設定 (調査・編集中) カスタムログの設定 カスタムログファイルの設定 カスタムログファイルの設定 サーバ生成ドキュメントのフッタの設定 アイコン画像ディレクトリの設定 アイコン画像ディレクトリに適用される設定 Web DAVモジュールの設定 (調査・編集中) CGIディレクトリの設定 ディレクトリインデックスの設定 (調査・編集中) アイコン画像の設定（設定ごとの関連付け） アイコン画像の設定（拡張子ごとの関連付け） デフォルトのアイコン画像の設定 (調査・編集中) (調査・編集中) インデックス対象外の設定 言語の設定 言語優先順位の設定 (調査・編集中) デフォルトの文字セットの設定 (調査・編集中) (調査・編集中) (調査・編集中) (調査・編集中) (調査・編集中) (調査・編集中) (調査・編集中) (調査・編集中) (調査・編集中) (調査・編集中) エラードキュメントの設定 (調査・編集中) サーバステータス表示設定 サーバ情報表示設定 プロキシモジュールの設定 プロキシ経由アクセス時のViaヘッダの有効・無効の設定 コンテンツキャッシュストレージ管理モジュールの設定 Section 3 Virtual Hosts TOPへ編集 ヘッダ # # This is the main Apache server configuration file. It contains the # configuration directives that give the server its instructions. # See URL http //httpd.apache.org/docs/2.2/ for detailed information. # In particular, see # URL http //httpd.apache.org/docs/2.2/mod/directives.html # for a discussion of each configuration directive. # # # Do NOT simply read the instructions in here without understanding # what they do. They re here only as hints or reminders. If you are unsure # consult the online docs. You have been warned. # # The configuration directives are grouped into three basic sections # 1. Directives that control the operation of the Apache server process as a # whole (the global environment ). # 2. Directives that define the parameters of the main or default server, # which responds to requests that aren t handled by a virtual host. # These directives also provide default values for the settings # of all virtual hosts. # 3. Settings for virtual hosts, which allow Web requests to be sent to # different IP addresses or hostnames and have them handled by the # same Apache server process. # # Configuration and logfile names If the filenames you specify for many # of the server s control files begin with "/" (or "drive /" for Win32), the # server will use that explicit path. If the filenames do *not* begin # with "/", the value of ServerRoot is prepended -- so "logs/foo.log" # with ServerRoot set to "/etc/httpd" will be interpreted by the # server as "/etc/httpd/logs/foo.log". # TOPへ編集 Section 1 Global Environment ### Section 1 Global Environment # # The directives in this section affect the overall operation of Apache, # such as the number of concurrent requests it can handle or where it # can find its configuration files. # Server HTTP応答ヘッダの設定 # # Don t give away too much information about all the subcomponents # we are running. Comment out this line if you don t mind remote sites # finding out what major optional modules you are running ServerTokens OS HTTP応答ヘッダの出力が「Server Apache/2.0.41 (Unix)」のように、OSの情報を含む形式で出力される。 参考 http //www.apache.jp/manual/mod/core.html#servertokens サーバ設定ファイルのルートディレクトリの指定 # # ServerRoot The top of the directory tree under which the server s # configuration, error, and log files are kept. # # NOTE! If you intend to place this on an NFS (or otherwise network) # mounted filesystem then please read the LockFile documentation # (available at URL http //httpd.apache.org/docs/2.2/mod/mpm_common.html#lockfile ); # you will save yourself a lot of trouble. # # Do NOT add a slash at the end of the directory path. # ServerRoot "/etc/httpd" 通常RHEL系OSの設定では、/etc/httpdを指定する。 設定ファイル中の相対パスは、このベースディレクトリからの相対パスになる。 PIDファイルのパス # # PidFile The file in which the server should record its process # identification number when it starts. # PidFile run/httpd.pid タイムアウト時間 # # Timeout The number of seconds before receives and sends time out. # Timeout 120 それぞれの処理（イベント）について、リクエストを失敗させるまでにサーバが待つ時間。 GETリクエストを受け取るのにかかる総時間 POSTやPUTリクエストにて、TCPパケットが届くまでの待ち時間 レスポンスを返す際、TCPのACKが帰ってくるまでの時間 参考 http //www.apache.jp/manual/mod/core.html#timeout参考 http //www.apache.jp/manual/mod/core.html#timeout キープアライブ # # KeepAlive Whether or not to allow persistent connections (more than # one request per connection). Set to "Off" to deactivate. # KeepAlive Off １回のページのリクエストで、沢山のHTTPリクエストを発行する必要がある場合、キープアライブはOnに設定した方がパフォーマンスは向上する。 参考 http //www.apache.jp/manual/mod/core.html#keepalive 最大キープアライブリクエスト数 # # MaxKeepAliveRequests The maximum number of requests to allow # during a persistent connection. Set to 0 to allow an unlimited amount. # We recommend you leave this number high, for maximum performance. # MaxKeepAliveRequests 100 参考 http //www.apache.jp/manual/mod/core.html#maxkeepaliverequests キープアライブタイムアウト時間 # # KeepAliveTimeout Number of seconds to wait for the next request from the # same client on the same connection. # KeepAliveTimeout 15 (調査・編集中) ## ## Server-Pool Size Regulation (MPM specific) ## 先行してforkを行うWEBサーバの設定 # prefork MPM # StartServers number of server processes to start # MinSpareServers minimum number of server processes which are kept spare # MaxSpareServers maximum number of server processes which are kept spare # ServerLimit maximum value for MaxClients for the lifetime of the server # MaxClients maximum number of server processes allowed to start # MaxRequestsPerChild maximum number of requests a server process serves IfModule prefork.c StartServers 8 MinSpareServers 5 MaxSpareServers 20 ServerLimit 256 MaxClients 256 MaxRequestsPerChild 4000 /IfModule 参考 http //httpd.apache.org/docs/2.2/ja/mod/prefork.html (調査・編集中) # worker MPM # StartServers initial number of server processes to start # MaxClients maximum number of simultaneous client connections # MinSpareThreads minimum number of worker threads which are kept spare # MaxSpareThreads maximum number of worker threads which are kept spare # ThreadsPerChild constant number of worker threads in each server process # MaxRequestsPerChild maximum number of requests a server process serves IfModule worker.c StartServers 2 MaxClients 150 MinSpareThreads 25 MaxSpareThreads 75 ThreadsPerChild 25 MaxRequestsPerChild 0 /IfModule 参考 http //httpd.apache.org/docs/2.2/ja/mod/worker.html 待ち受けポート番号 # # Listen Allows you to bind Apache to specific IP addresses and/or # ports, in addition to the default. See also the VirtualHost # directive. # # Change this to Listen on specific IP addresses as shown below to # prevent Apache from glomming onto all bound IP addresses (0.0.0.0) # #Listen 12.34.56.78 80 Listen 80 モジュール読み込み # # Dynamic Shared Object (DSO) Support # # To be able to use the functionality of a module which was built as a DSO you # have to place corresponding `LoadModule lines at this location so the # directives contained in it are actually available _before_ they are used. # Statically compiled modules (those listed by `httpd -l ) do not need # to be loaded here. # # Example # LoadModule foo_module modules/mod_foo.so # LoadModule auth_basic_module modules/mod_auth_basic.so LoadModule auth_digest_module modules/mod_auth_digest.so LoadModule authn_file_module modules/mod_authn_file.so #LoadModule authn_alias_module modules/mod_authn_alias.so LoadModule authn_anon_module modules/mod_authn_anon.so LoadModule authn_dbm_module modules/mod_authn_dbm.so LoadModule authn_default_module modules/mod_authn_default.so LoadModule authz_host_module modules/mod_authz_host.so LoadModule authz_user_module modules/mod_authz_user.so LoadModule authz_owner_module modules/mod_authz_owner.so LoadModule authz_groupfile_module modules/mod_authz_groupfile.so LoadModule authz_dbm_module modules/mod_authz_dbm.so LoadModule authz_default_module modules/mod_authz_default.so LoadModule ldap_module modules/mod_ldap.so LoadModule authnz_ldap_module modules/mod_authnz_ldap.so LoadModule include_module modules/mod_include.so LoadModule log_config_module modules/mod_log_config.so LoadModule logio_module modules/mod_logio.so LoadModule env_module modules/mod_env.so LoadModule ext_filter_module modules/mod_ext_filter.so LoadModule mime_magic_module modules/mod_mime_magic.so LoadModule expires_module modules/mod_expires.so LoadModule deflate_module modules/mod_deflate.so LoadModule headers_module modules/mod_headers.so LoadModule usertrack_module modules/mod_usertrack.so LoadModule setenvif_module modules/mod_setenvif.so LoadModule mime_module modules/mod_mime.so LoadModule dav_module modules/mod_dav.so LoadModule status_module modules/mod_status.so LoadModule autoindex_module modules/mod_autoindex.so LoadModule info_module modules/mod_info.so LoadModule dav_fs_module modules/mod_dav_fs.so LoadModule vhost_alias_module modules/mod_vhost_alias.so LoadModule negotiation_module modules/mod_negotiation.so LoadModule dir_module modules/mod_dir.so LoadModule actions_module modules/mod_actions.so LoadModule speling_module modules/mod_speling.so LoadModule userdir_module modules/mod_userdir.so LoadModule alias_module modules/mod_alias.so LoadModule rewrite_module modules/mod_rewrite.so LoadModule proxy_module modules/mod_proxy.so LoadModule proxy_balancer_module modules/mod_proxy_balancer.so LoadModule proxy_ftp_module modules/mod_proxy_ftp.so LoadModule proxy_http_module modules/mod_proxy_http.so LoadModule proxy_connect_module modules/mod_proxy_connect.so LoadModule cache_module modules/mod_cache.so LoadModule suexec_module modules/mod_suexec.so LoadModule disk_cache_module modules/mod_disk_cache.so LoadModule file_cache_module modules/mod_file_cache.so LoadModule mem_cache_module modules/mod_mem_cache.so LoadModule cgi_module modules/mod_cgi.so LoadModule version_module modules/mod_version.so # # The following modules are not loaded by default # #LoadModule cern_meta_module modules/mod_cern_meta.so #LoadModule asis_module modules/mod_asis.so 外部設定ファイルの読み込み # # Load config files from the config directory "/etc/httpd/conf.d". # Include conf.d/*.conf 拡張ステータス情報保存の有無 # # ExtendedStatus controls whether Apache will generate "full" status # information (ExtendedStatus On) or just basic information (ExtendedStatus # Off) when the "server-status" handler is called. The default is Off. # #ExtendedStatus On 実行ユーザ・グループ # # If you wish httpd to run as a different user or group, you must run # httpd as root initially and it will switch. # # User/Group The name (or #number) of the user/group to run httpd as. # . On SCO (ODT 3) use "User nouser" and "Group nogroup". # . On HPUX you may not be able to use shared memory as nobody, and the # suggested workaround is to create a user www and use that user. # NOTE that some kernels refuse to setgid(Group) or semctl(IPC_SET) # when the value of (unsigned)Group is above 60000; # don t use Group #-1 on these systems! # User apache Group apache TOPへ編集 Section 2 Main server configuration ### Section 2 Main server configuration # # The directives in this section set up the values used by the main # server, which responds to any requests that aren t handled by a # VirtualHost definition. These values also provide defaults for # any VirtualHost containers you may define later in the file. # # All of these directives may appear inside VirtualHost containers, # in which case these default settings will be overridden for the # virtual host being defined. # サーバ管理者メールアドレス # # ServerAdmin Your address, where problems with the server should be # e-mailed. This address appears on some server-generated pages, such # as error documents. e.g. admin@your-domain.com # ServerAdmin root@localhost サーバ名 # # ServerName gives the name and port that the server uses to identify itself. # This can often be determined automatically, but we recommend you specify # it explicitly to prevent problems during startup. # # If this is not set to valid DNS name for your host, server-generated # redirections will not work. See also the UseCanonicalName directive. # # If your host doesn t have a registered DNS name, enter its IP address here. # You will have to access it by its address anyway, and this will make # redirections work in a sensible way. # #ServerName www.example.com 80 ServerName www.sapporobeer.co.jp 80 (サーバが自分自身の名前とポートを決定する方法の設定 # # UseCanonicalName Determines how Apache constructs self-referencing # URLs and the SERVER_NAME and SERVER_PORT variables. # When set "Off", Apache will use the Hostname and Port supplied # by the client. When set "On", Apache will use the value of the # ServerName directive. # UseCanonicalName Off ドキュメントルートの定義 # # DocumentRoot The directory out of which you will serve your # documents. By default, all requests are taken from this directory, but # symbolic links and aliases may be used to point to other locations. # DocumentRoot "/var/www/html" (調査・編集中) # # Each directory to which Apache has access can be configured with respect # to which services and features are allowed and/or disabled in that # directory (and its subdirectories). # # First, we configure the "default" to be a very restrictive set of # features. # Directory / Options FollowSymLinks AllowOverride None /Directory # # Note that from this point forward you must specifically allow # particular features to be enabled - so if something s not working as # you might expect, make sure that you have specifically enabled it # below. # ドキュメントルート配下に適用される設定 # # This should be changed to whatever you set DocumentRoot to. # Directory "/var/www/html" # # Possible values for the Options directive are "None", "All", # or any combination of # Indexes Includes FollowSymLinks SymLinksifOwnerMatch ExecCGI MultiViews # # Note that "MultiViews" must be named *explicitly* --- "Options All" # doesn t give it to you. # # The Options directive is both complicated and important. Please see # http //httpd.apache.org/docs/2.2/mod/core.html#options # for more information. # Options Indexes FollowSymLinks ディレクトリインデックス作成の許可と、シンボリックリンクを辿ることの許可設定 # # AllowOverride controls what directives may be placed in .htaccess files. # It can be "All", "None", or any combination of the keywords # Options FileInfo AuthConfig Limit # AllowOverride None 分散設定ファイル（.htaccess）で許可するディレクティヴの種類の設定。 この場合はなし。 # # Controls who can get stuff from this server. # Order allow,deny Allow from all /Directory ユーザディレクトリモジュールの設定 # # UserDir The name of the directory that is appended onto a user s home # directory if a ~user request is received. # # The path to the end user account public_html directory must be # accessible to the webserver userid. This usually means that ~userid # must have permissions of 711, ~userid/public_html must have permissions # of 755, and documents contained therein must be world-readable. # Otherwise, the client will only receive a "403 Forbidden" message. # # See also http //httpd.apache.org/docs/misc/FAQ.html#forbidden # IfModule mod_userdir.c # # UserDir is disabled by default since it can confirm the presence # of a username on the system (depending on home directory # permissions). # UserDir disable ユーザディレクトリ機能は無効 # # To enable requests to /~user/ to serve the user s public_html # directory, remove the "UserDir disable" line above, and uncomment # the following line instead # #UserDir public_html /IfModule ユーザディレクトリ配下に適用される設定 # # Control access to UserDir directories. The following is an example # for a site where these directories are restricted to read-only. # # Directory /home/*/public_html # AllowOverride FileInfo AuthConfig Limit # Options MultiViews Indexes SymLinksIfOwnerMatch IncludesNoExec # Limit GET POST OPTIONS # Order allow,deny # Allow from all # /Limit # LimitExcept GET POST OPTIONS # Order deny,allow # Deny from all # /LimitExcept # /Directory ディレクトリインデックスの設定 # # DirectoryIndex sets the file that Apache will serve if a directory # is requested. # # The index.html.var file (a type-map) is used to deliver content- # negotiated documents. The MultiViews Option can be used for the # same purpose, but it is much slower. # DirectoryIndex index.html index.html.var 分散設定ファイルの設定 # # AccessFileName The name of the file to look for in each directory # for additional configuration directives. See also the AllowOverride # directive. # AccessFileName .htaccess (調査・編集中) # # The following lines prevent .htaccess and .htpasswd files from being # viewed by Web clients. # Files ~ "^\.ht" Order allow,deny Deny from all /Files MIMEタイプ設定ファイル # # TypesConfig describes where the mime.types file (or equivalent) is # to be found. # TypesConfig /etc/mime.types デフォルトのMIMEタイプの設定 # # DefaultType is the default MIME type the server will use for a document # if it cannot otherwise determine one, such as from filename extensions. # If your server contains mostly text or HTML documents, "text/plain" is # a good value. If most of your content is binary, such as applications # or images, you may want to use "application/octet-stream" instead to # keep browsers from trying to display binary files as though they are # text. # DefaultType text/plain MIME MAGICモジュールの設定 # # The mod_mime_magic module allows the server to use various hints from the # contents of the file itself to determine its type. The MIMEMagicFile # directive tells the module where the hint definitions are located. # IfModule mod_mime_magic.c # MIMEMagicFile /usr/share/magic.mime MIMEMagicFile conf/magic /IfModule DNSルックアップの設定 # # HostnameLookups Log the names of clients or just their IP addresses # e.g., www.apache.org (on) or 204.62.129.132 (off). # The default is off because it d be overall better for the net if people # had to knowingly turn this feature on, since enabling it means that # each client request will result in AT LEAST one lookup request to the # nameserver. # HostnameLookups Off メモリマッピングの有無 # # EnableMMAP Control whether memory-mapping is used to deliver # files (assuming that the underlying OS supports it). # The default is on; turn this off if you serve from NFS-mounted # filesystems. On some systems, turning it off (regardless of # filesystem) can improve performance; for details, please see # http //httpd.apache.org/docs/2.2/mod/core.html#enablemmap # #EnableMMAP off sendfileサポートの有無 # # EnableSendfile Control whether the sendfile kernel support is # used to deliver files (assuming that the OS supports it). # The default is on; turn this off if you serve from NFS-mounted # filesystems. Please see # http //httpd.apache.org/docs/2.2/mod/core.html#enablesendfile # #EnableSendfile off エラーログの設定 # # ErrorLog The location of the error log file. # If you do not specify an ErrorLog directive within a VirtualHost # container, error messages relating to that virtual host will be # logged here. If you *do* define an error logfile for a VirtualHost # container, that host s errors will be logged there and not here. # ErrorLog logs/error_log ログレベルの設定 # # LogLevel Control the number of messages logged to the error_log. # Possible values include debug, info, notice, warn, error, crit, # alert, emerg. # LogLevel warn ログフォーマットの設定 # # The following directives define some format nicknames for use with # a CustomLog directive (see below). # LogFormat "%h %l %u %t \"%r\" % s %b \"%{Referer}i\" \"%{User-Agent}i\"" combined LogFormat "%h %l %u %t \"%r\" % s %b" common LogFormat "%{Referer}i - %U" referer LogFormat "%{User-agent}i" agent (調査・編集中) # "combinedio" includes actual counts of actual bytes received (%I) and sent (%O); this # requires the mod_logio module to be loaded. #LogFormat "%h %l %u %t \"%r\" % s %b \"%{Referer}i\" \"%{User-Agent}i\" %I %O" combinedio カスタムログの設定 # # The location and format of the access logfile (Common Logfile Format). # If you do not define any access logfiles within a VirtualHost # container, they will be logged here. Contrariwise, if you *do* # define per- VirtualHost access logfiles, transactions will be # logged therein and *not* in this file. # #CustomLog logs/access_log common カスタムログファイルの設定 # # If you would like to have separate agent and referer logfiles, uncomment # the following directives. # #CustomLog logs/referer_log referer #CustomLog logs/agent_log agent カスタムログファイルの設定 # # For a single logfile with access, agent, and referer information # (Combined Logfile Format), use the following directive # CustomLog logs/access_log combined サーバ生成ドキュメントのフッタの設定 # # Optionally add a line containing the server version and virtual host # name to server-generated pages (internal error documents, FTP directory # listings, mod_status and mod_info output etc., but not CGI generated # documents or custom error documents). # Set to "EMail" to also include a mailto link to the ServerAdmin. # Set to one of On | Off | EMail # ServerSignature On アイコン画像ディレクトリの設定 # # Aliases Add here as many aliases as you need (with no limit). The format is # Alias fakename realname # # Note that if you include a trailing / on fakename then the server will # require it to be present in the URL. So "/icons" isn t aliased in this # example, only "/icons/". If the fakename is slash-terminated, then the # realname must also be slash terminated, and if the fakename omits the # trailing slash, the realname must also omit it. # # We include the /icons/ alias for FancyIndexed directory listings. If you # do not use FancyIndexing, you may comment this out. # Alias /icons/ "/var/www/icons/" アイコン画像ディレクトリに適用される設定 Directory "/var/www/icons" Options Indexes MultiViews AllowOverride None Order allow,deny Allow from all /Directory Web DAVモジュールの設定 # # WebDAV module configuration section. # IfModule mod_dav_fs.c # Location of the WebDAV lock database. DAVLockDB /var/lib/dav/lockdb /IfModule (調査・編集中) # # ScriptAlias This controls which directories contain server scripts. # ScriptAliases are essentially the same as Aliases, except that # documents in the realname directory are treated as applications and # run by the server when requested rather than as documents sent to the client. # The same rules about trailing "/" apply to ScriptAlias directives as to # Alias. # ScriptAlias /cgi-bin/ "/var/www/cgi-bin/" CGIディレクトリの設定 # # "/var/www/cgi-bin" should be changed to whatever your ScriptAliased # CGI directory exists, if you have that configured. # Directory "/var/www/cgi-bin" AllowOverride None Options None Order allow,deny Allow from all /Directory # # Redirect allows you to tell clients about documents which used to exist in # your server s namespace, but do not anymore. This allows you to tell the # clients where to look for the relocated document. # Example # Redirect permanent /foo http //www.example.com/bar # # Directives controlling the display of server-generated directory listings. # ディレクトリインデックスの設定 # # IndexOptions Controls the appearance of server-generated directory # listings. # IndexOptions FancyIndexing VersionSort NameWidth=* HTMLTable (調査・編集中) # # AddIcon* directives tell the server which icon to show for different # files or filename extensions. These are only displayed for # FancyIndexed directories. # AddIconByEncoding (CMP,/icons/compressed.gif) x-compress x-gzip アイコン画像の設定（設定ごとの関連付け） AddIconByType (TXT,/icons/text.gif) text/* AddIconByType (IMG,/icons/image2.gif) image/* AddIconByType (SND,/icons/sound2.gif) audio/* AddIconByType (VID,/icons/movie.gif) video/* アイコン画像の設定（拡張子ごとの関連付け） AddIcon /icons/binary.gif .bin .exe AddIcon /icons/binhex.gif .hqx AddIcon /icons/tar.gif .tar AddIcon /icons/world2.gif .wrl .wrl.gz .vrml .vrm .iv AddIcon /icons/compressed.gif .Z .z .tgz .gz .zip AddIcon /icons/a.gif .ps .ai .eps AddIcon /icons/layout.gif .html .shtml .htm .pdf AddIcon /icons/text.gif .txt AddIcon /icons/c.gif .c AddIcon /icons/p.gif .pl .py AddIcon /icons/f.gif .for AddIcon /icons/dvi.gif .dvi AddIcon /icons/uuencoded.gif .uu AddIcon /icons/script.gif .conf .sh .shar .csh .ksh .tcl AddIcon /icons/tex.gif .tex AddIcon /icons/bomb.gif core AddIcon /icons/back.gif .. AddIcon /icons/hand.right.gif README AddIcon /icons/folder.gif ^^DIRECTORY^^ AddIcon /icons/blank.gif ^^BLANKICON^^ デフォルトのアイコン画像の設定 # # DefaultIcon is which icon to show for files which do not have an icon # explicitly set. # DefaultIcon /icons/unknown.gif (調査・編集中) # # AddDescription allows you to place a short description after a file in # server-generated indexes. These are only displayed for FancyIndexed # directories. # Format AddDescription "description" filename # #AddDescription "GZIP compressed document" .gz #AddDescription "tar archive" .tar #AddDescription "GZIP compressed tar archive" .tgz (調査・編集中) # # ReadmeName is the name of the README file the server will look for by # default, and append to directory listings. # # HeaderName is the name of a file which should be prepended to # directory indexes. ReadmeName README.html HeaderName HEADER.html インデックス対象外の設定 # # IndexIgnore is a set of filenames which directory indexing should ignore # and not include in the listing. Shell-style wildcarding is permitted. # IndexIgnore .??* *~ *# HEADER* README* RCS CVS *,v *,t 言語の設定 # # DefaultLanguage and AddLanguage allows you to specify the language of # a document. You can then use content negotiation to give a browser a # file in a language the user can understand. # # Specify a default language. This means that all data # going out without a specific language tag (see below) will # be marked with this one. You probably do NOT want to set # this unless you are sure it is correct for all cases. # # * It is generally better to not mark a page as # * being a certain language than marking it with the wrong # * language! # # DefaultLanguage nl # # Note 1 The suffix does not have to be the same as the language # keyword --- those with documents in Polish (whose net-standard # language code is pl) may wish to use "AddLanguage pl .po" to # avoid the ambiguity with the common suffix for perl scripts. # # Note 2 The example entries below illustrate that in some cases # the two character Language abbreviation is not identical to # the two character Country code for its country, # E.g. Danmark/dk versus Danish/da . # # Note 3 In the case of ltz we violate the RFC by using a three char # specifier. There is work in progress to fix this and get # the reference data for rfc1766 cleaned up. # # Catalan (ca) - Croatian (hr) - Czech (cs) - Danish (da) - Dutch (nl) # English (en) - Esperanto (eo) - Estonian (et) - French (fr) - German (de) # Greek-Modern (el) - Hebrew (he) - Italian (it) - Japanese (ja) # Korean (ko) - Luxembourgeois* (ltz) - Norwegian Nynorsk (nn) # Norwegian (no) - Polish (pl) - Portugese (pt) # Brazilian Portuguese (pt-BR) - Russian (ru) - Swedish (sv) # Simplified Chinese (zh-CN) - Spanish (es) - Traditional Chinese (zh-TW) # AddLanguage ca .ca AddLanguage cs .cz .cs AddLanguage da .dk AddLanguage de .de AddLanguage el .el AddLanguage en .en AddLanguage eo .eo AddLanguage es .es AddLanguage et .et AddLanguage fr .fr AddLanguage he .he AddLanguage hr .hr AddLanguage it .it AddLanguage ja .ja AddLanguage ko .ko AddLanguage ltz .ltz AddLanguage nl .nl AddLanguage nn .nn AddLanguage no .no AddLanguage pl .po AddLanguage pt .pt AddLanguage pt-BR .pt-br AddLanguage ru .ru AddLanguage sv .sv AddLanguage zh-CN .zh-cn AddLanguage zh-TW .zh-tw 言語優先順位の設定 # # LanguagePriority allows you to give precedence to some languages # in case of a tie during content negotiation. # # Just list the languages in decreasing order of preference. We have # more or less alphabetized them here. You probably want to change this. # LanguagePriority en ca cs da de el eo es et fr he hr it ja ko ltz nl nn no pl pt pt-BR ru sv zh-CN zh-TW (調査・編集中) # # ForceLanguagePriority allows you to serve a result page rather than # MULTIPLE CHOICES (Prefer) [in case of a tie] or NOT ACCEPTABLE (Fallback) # [in case no accepted languages matched the available variants] # ForceLanguagePriority Prefer Fallback デフォルトの文字セットの設定 # # Specify a default charset for all content served; this enables # interpretation of all content as UTF-8 by default. To use the # default browser choice (ISO-8859-1), or to allow the META tags # in HTML content to override this choice, comment out this # directive # AddDefaultCharset UTF-8 (調査・編集中) # # AddType allows you to add to or override the MIME configuration # file mime.types for specific file types. # #AddType application/x-tar .tgz (調査・編集中) # # AddEncoding allows you to have certain browsers uncompress # information on the fly. Note Not all browsers support this. # Despite the name similarity, the following Add* directives have nothing # to do with the FancyIndexing customization directives above. # #AddEncoding x-compress .Z #AddEncoding x-gzip .gz .tgz (調査・編集中) # If the AddEncoding directives above are commented-out, then you # probably should define those extensions to indicate media types # AddType application/x-compress .Z AddType application/x-gzip .gz .tgz (調査・編集中) # # AddHandler allows you to map certain file extensions to "handlers" # actions unrelated to filetype. These can be either built into the server # or added with the Action directive (see below) # # To use CGI scripts outside of ScriptAliased directories # (You will also need to add "ExecCGI" to the "Options" directive.) # #AddHandler cgi-script .cgi (調査・編集中) # # For files that include their own HTTP headers # #AddHandler send-as-is asis (調査・編集中) # # For type maps (negotiated resources) # (This is enabled by default to allow the Apache "It Worked" page # to be distributed in multiple languages.) # AddHandler type-map var (調査・編集中) # # Filters allow you to process content before it is sent to the client. # # To parse .shtml files for server-side includes (SSI) # (You will also need to add "Includes" to the "Options" directive.) # AddType text/html .shtml AddOutputFilter INCLUDES .shtml (調査・編集中) # # Action lets you define media types that will execute a script whenever # a matching file is called. This eliminates the need for repeated URL # pathnames for oft-used CGI file processors. # Format Action media/type /cgi-script/location # Format Action handler-name /cgi-script/location # (調査・編集中) # # Customizable error responses come in three flavors # 1) plain text 2) local redirects 3) external redirects # # Some examples #ErrorDocument 500 "The server made a boo boo." #ErrorDocument 404 /missing.html #ErrorDocument 404 "/cgi-bin/missing_handler.pl" #ErrorDocument 402 http //www.example.com/subscription_info.html # # # Putting this all together, we can internationalize error responses. # # We use Alias to redirect any /error/HTTP_ error .html.var response to # our collection of by-error message multi-language collections. We use # includes to substitute the appropriate text. # # You can modify the messages appearance without changing any of the # default HTTP_ error .html.var files by adding the line # # Alias /error/include/ "/your/include/path/" # # which allows you to create your own set of files by starting with the # /var/www/error/include/ files and # copying them to /your/include/path/, even on a per-VirtualHost basis. # (調査・編集中) Alias /error/ "/var/www/error/" エラードキュメントの設定 IfModule mod_negotiation.c IfModule mod_include.c Directory "/var/www/error" AllowOverride None Options IncludesNoExec AddOutputFilter Includes html AddHandler type-map var Order allow,deny Allow from all LanguagePriority en es de fr ForceLanguagePriority Prefer Fallback /Directory # ErrorDocument 400 /error/HTTP_BAD_REQUEST.html.var # ErrorDocument 401 /error/HTTP_UNAUTHORIZED.html.var # ErrorDocument 403 /error/HTTP_FORBIDDEN.html.var # ErrorDocument 404 /error/HTTP_NOT_FOUND.html.var # ErrorDocument 405 /error/HTTP_METHOD_NOT_ALLOWED.html.var # ErrorDocument 408 /error/HTTP_REQUEST_TIME_OUT.html.var # ErrorDocument 410 /error/HTTP_GONE.html.var # ErrorDocument 411 /error/HTTP_LENGTH_REQUIRED.html.var # ErrorDocument 412 /error/HTTP_PRECONDITION_FAILED.html.var # ErrorDocument 413 /error/HTTP_REQUEST_ENTITY_TOO_LARGE.html.var # ErrorDocument 414 /error/HTTP_REQUEST_URI_TOO_LARGE.html.var # ErrorDocument 415 /error/HTTP_UNSUPPORTED_MEDIA_TYPE.html.var # ErrorDocument 500 /error/HTTP_INTERNAL_SERVER_ERROR.html.var # ErrorDocument 501 /error/HTTP_NOT_IMPLEMENTED.html.var # ErrorDocument 502 /error/HTTP_BAD_GATEWAY.html.var # ErrorDocument 503 /error/HTTP_SERVICE_UNAVAILABLE.html.var # ErrorDocument 506 /error/HTTP_VARIANT_ALSO_VARIES.html.var /IfModule /IfModule (調査・編集中) # # The following directives modify normal HTTP response behavior to # handle known problems with browser implementations. # BrowserMatch "Mozilla/2" nokeepalive BrowserMatch "MSIE 4\.0b2;" nokeepalive downgrade-1.0 force-response-1.0 BrowserMatch "RealPlayer 4\.0" force-response-1.0 BrowserMatch "Java/1\.0" force-response-1.0 BrowserMatch "JDK/1\.0" force-response-1.0 # # The following directive disables redirects on non-GET requests for # a directory that does not include the trailing slash. This fixes a # problem with Microsoft WebFolders which does not appropriately handle # redirects for folders with DAV methods. # Same deal with Apple s DAV filesystem and Gnome VFS support for DAV. # BrowserMatch "Microsoft Data Access Internet Publishing Provider" redirect-carefully BrowserMatch "MS FrontPage" redirect-carefully BrowserMatch "^WebDrive" redirect-carefully BrowserMatch "^WebDAVFS/1.[0123]" redirect-carefully BrowserMatch "^gnome-vfs/1.0" redirect-carefully BrowserMatch "^XML Spy" redirect-carefully BrowserMatch "^Dreamweaver-WebDAV-SCM1" redirect-carefully サーバステータス表示設定 # # Allow server status reports generated by mod_status, # with the URL of http //servername/server-status # Change the ".example.com" to match your domain to enable. # # Location /server-status # SetHandler server-status # Order deny,allow # Deny from all # Allow from .example.com # /Location サーバ情報表示設定 # # Allow remote server configuration reports, with the URL of # http //servername/server-info (requires that mod_info.c be loaded). # Change the ".example.com" to match your domain to enable. # # Location /server-info # SetHandler server-info # Order deny,allow # Deny from all # Allow from .example.com # /Location プロキシモジュールの設定 # # Proxy Server directives. Uncomment the following lines to # enable the proxy server # # IfModule mod_proxy.c #ProxyRequests On # # Proxy * # Order deny,allow # Deny from all # Allow from .example.com # /Proxy プロキシ経由アクセス時のViaヘッダの有効・無効の設定 # # Enable/disable the handling of HTTP/1.1 "Via " headers. # ("Full" adds the server version; "Block" removes all outgoing Via headers) # Set to one of Off | On | Full | Block # #ProxyVia On コンテンツキャッシュストレージ管理モジュールの設定 # # To enable a cache of proxied content, uncomment the following lines. # See http //httpd.apache.org/docs/2.2/mod/mod_cache.html for more details. # # IfModule mod_disk_cache.c # CacheEnable disk / # CacheRoot "/var/cache/mod_proxy" # /IfModule # # /IfModule # End of proxy directives. TOPへ編集 Section 3 Virtual Hosts ### Section 3 Virtual Hosts # # VirtualHost If you want to maintain multiple domains/hostnames on your # machine you can setup VirtualHost containers for them. Most configurations # use only name-based virtual hosts so the server doesn t need to worry about # IP addresses. This is indicated by the asterisks in the directives below. # # Please see the documentation at # URL http //httpd.apache.org/docs/2.2/vhosts/ # for further details before you try to setup virtual hosts. # # You may use the command line option -S to verify your virtual host # configuration. # # Use name-based virtual hosting. # #NameVirtualHost * 80 # # NOTE NameVirtualHost cannot be used without a port specifier # (e.g. 80) if mod_ssl is being used, due to the nature of the # SSL protocol. # # # VirtualHost example # Almost any Apache directive may go into a VirtualHost container. # The first VirtualHost section is used for requests without a known # server name. # # VirtualHost * 80 # ServerAdmin webmaster@dummy-host.example.com # DocumentRoot /www/docs/dummy-host.example.com # ServerName dummy-host.example.com # ErrorLog logs/dummy-host.example.com-error_log # CustomLog logs/dummy-host.example.com-access_log common # /VirtualHost 最終更新日 [2011-04-15]

• @wiki(あっとうぃき) テストページ - iPod Camera Connector

  https://w.atwiki.jp/wiki1_test/pages/2078.html

  iPod Camera Connector 本日の参照数： - 昨日の参照数： - これ以上情報が集められないので、誰が追記して。(^^;;; 互換リスト （ユーザ報告分） Nikon COOPIX5200 D2X D70s D100 D50 Canon EOS Kiss Digital N Olympus E-300 CAMEDIA C-8080WideZoom コニカミノルタ A200 Sanyo MZ-3 Sony F828 Ricoh GR DIGITAL Kyocera M410R Panasonic DMC-FX2 DMC-FZ5 Pentax Optio S4 Optio S4i カードリーダー バッファロー MCR-8U/U2 バッファロー MCR-C8/U2 メルコ MCR-6U メルコ MCR-C12/U2 Digio ロアス CRW-7M23 非互換リスト （ユーザ報告分） Ricoh Caplio GX Caplio GX8 SONY CyberShot U60 カードリーダー ロアス CRW-11M21SL I.O DATA USB2-7inRW 玄人志向 CRU2MSD 日本トラストテクノロジー SKY WALKER KINGMAX KCR2(SD/MMC) 互換リスト （Apple 発表分） http //www.apple.com/ipod/compatibility/cameraconnector.html Canon Digital Rebel XT (PTP) EOS Kiss Digital X EOS 5D EOS 20D IXUS V IXUS V2 IXY Digital 30 IXY Digital 40 IXY Digital 400 IXY Digital A300 PowerShot A400 PowerShot A410 PowerShot A510 PowerShot A520 PowerShot A610 PowerShot A85 PowerShot A95 Powershot Pro1 PowerShot S1 IS PowerShot S410 Elph PowerShot S500 Elph PowerShot S70 PowerShot SD110 Elph PowerShot SD20 PowerShot SD200 PowerShot SD30 PowerShot SD300 Elph PowerShot SD400 PowerShot SD450 PowerShot SD500 PowerShot SD550 Casio Exilim Zoom EX-S500 Exilim EX-Z750 Exilim QV-R51 Epson L-500v FujiFilm FinePix 2650 FinePix 2800 Zoom FinePix 3800z FinePix A101 HP Photosmart 315 Photosmart 320 Photosmart M22 Photosmart M23 Photosmart M407 Photosmart M417 Photosmart R507 Photosmart R607 Photosmart R707 Photosmart R717 Minolta DiMAGE 7i Dimage A2 Dimage X DiMage X50 DiMAGE Xg DiMAGE Xt DiMage Z2 DiMage Z3 Maxxum 7D Nikon Coolpix 3200 CoolPix 4100 CoolPix 4200 CoolPix 8400 Coolpix 8800 CoolPix S1 D70 Outfit Olympus C4040 D-380 D-40 D-520 M-10 Sanyo VPC-C5 Xacti E6 Sony Cyber-shot DSC-L1 Cyber-shot DSC-P200 Cyber-Shot DSC-T1 Cyber-Shot DSC-T7 DSC -P73

• 東方同人CDの歌詞＠Wiki - 03 active emotion

  https://w.atwiki.jp/touhoukashi/pages/4256.html

  【登録タグ A Silver Forest Silver Forest 2006-2012 BESTⅠ さゆり 天空のグリニッジ 曲 東方秘封魔術】 【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 = /(?=^|.*

• The War of Eustrath ファンサイト - Episode 24 - A Partial Rejoice

  https://w.atwiki.jp/eustrath/pages/36.html

  Episode 24 - A Partial Rejoice

• Signal Transduction シグナル伝達 - Lymphnode

  https://w.atwiki.jp/tiger/pages/4.html

  TEC-/- BTK-/- double mutant T cells exhibit severely impaired T cell activitity. RLK-/-ITK-/- double mutant celles exhibit severely imparired Th2 responses. Grb2(+/-) mice disrupt T cell signaling networks and development. Dendric cells and macrophages of MEK3 deficient mice have impaired IL12 production. Bam32(-/-) B cell develop normally but have impaired T-independent antibody responses in vivo. T-cell and B-cell of RAP1A deficient mice impair integrin-mediated cell adhesion. T-cell of WASP deficient mice impair the proliferaction and antigen receptor cap formation in response to anti-CD3zeta stimulation. T-cell of SHB defective mice impair the phosphorylation of LAT and consequently the activation of MAP kinase pathways. B-cell of 3BP2 (-/-) deficient mice have defective in proliferation, cell cycle progression, PLC-gamma2 phosphorylation, calcium mobilization, NF-ATp dephosphorylation, and Erk and Jnk activation in response to BCR ligation. B-cell of Vav2(-/-) deficient mice are defective in the ability to switch immunoglobulin class. T-cell of Vav1(-/-) deficient mice exhibit impaired antigen receptor signaling. Vav1(-/-)Vav2(-/-) mice exhibit greatly reduced the mature B-cells. Vav-1-/-Vav-2-/- B cells were unresponsive to BCR-driven proliferation in vitro and to thymus-indepen-dent antigen in vivo. Fyn-deficient mice exhibit a remarkably specific lymphoid defect thymocytes are refractile to stimulation through the TCR with mitogen or antigen. Lck-deficient mice show a pronounced thymic atrophy, with a dramatic reduction in the double-positive (CD4+CD8+) thymocyte population. T cell from mice deficient in LCK is required for normal signal transduction through the TCR. T cells from mice deficient in SLAP-130/Fyb show markedly impaired proliferation. B cell of chicken deficient ITK reduce IP3 generation and phospholipase C gamma 2 tyrosine phosphorylation. T cell of mice deficient ITK reduce IP3 generation and phospholipase C gamma 1 tyrosine phosphorylation. T cell of mice deficient ITK have failure of Th2 development. Mice deficient in ITK have reduced proliferative responses to MHC stimulation and to anti-TCR cross-linking Mutations in Btk cause X-linked immunodeficiency. Gads(GRAP2) has a role in thymocyte proliferaction for maturation of T-cells. Gads(GRAP2) has a role for homeostatic proliferaction in B cells. Grap negatively regulates T-cell proliferation. Gab2 is a substrate of ZAP-70 and functions as a switch molecule toward inhibition of TCR signal transuduction. B cell signaling causes tyrosine phosphorylation of Gab1, and in turn SHP2 bind to Gab1 Gab1 phosophorylation potentiate the phosphorylation of Akt, PI3K-dependent response. RasGRP1 mediates Ras activation following TCR stimulatioin. RasGRP1 and RasGRP3 induces RAS activation in B-cell to response to T-cell stimulation. Grb2-hSos1-PLCgamma1-p36/p38-ZAP70 complexes localize in the vicinity of TCR-zeta Gads(Grap2) plays an important role in T-cell signaling via its association with SLP-76 and LAT. Lck is required for normal signal transduction through the TCR. ZAP-70 plays crucial roles in T-cell activation and development. Syk triggers cellular activation in T-cell. TEC-/- BTK-/- double mutant T cells exhibit severely impaired T cell activitity. 1 J Exp Med. 2000 Dec 4;192(11) 1611-24. Severe B cell deficiency in mice lacking the tec kinase family members Tec and Btk. Ellmeier W, Jung S, Sunshine MJ, Hatam F, Xu Y, Baltimore D, Mano H, Littman DR. Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine. wilfried.ellmeier@univie.ac.at The cytoplasmic protein tyrosine kinase Tec has been proposed to have important functions in hematopoiesis and lymphocyte signal transduction. Here we show that Tec-deficient mice developed normally and had no major phenotypic alterations of the immune system. To reveal potential compensatory roles of other Tec kinases such as Bruton s tyrosine kinase (Btk), Tec/Btk double-deficient mice were generated. These mice exhibited a block at the B220(+)CD43(+) stage of B cell development and displayed a severe reduction of peripheral B cell numbers, particularly immunoglobulin (Ig)M(lo)IgD(hi) B cells. Although Tec/Btk(null) mice were able to form germinal centers, the response to T cell-dependent antigens was impaired. Thus, Tec and Btk together have an important role both during B cell development and in the generation and/or function of the peripheral B cell pool. The ability of Tec to compensate for Btk may also explain phenotypic differences in X-linked immunodeficiency (xid) mice compared with human X-linked agammaglobulinemia (XLA) patients. Publication Types Research Support, Non-U.S. Gov t PMID 11104803 [PubMed - indexed for MEDLINE] RLK-/-ITK-/- double mutant celles exhibit severely imparired Th2 responses. 1 Nat Immunol. 2001 Dec;2(12) 1183-8. Mutation of Tec family kinases alters T helper cell differentiation. Schaeffer EM, Yap GS, Lewis CM, Czar MJ, McVicar DW, Cheever AW, Sher A, Schwartzberg PL. National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. The Tec kinases Rlk and Itk are critical for full T cell receptor (TCR)-induced activation of phospholipase C-gamma and mitogen-activated protein kinase. We show here that the mutation of Rlk and Itk impaired activation of the transcription factors NFAT and AP-1 and production of both T helper type 1 (TH1) and TH2 cytokines. Consistent with these biochemical defects, Itk-/- mice did not generate effective TH2 responses when challenged with Schistosoma mansoni eggs. Paradoxically, the more severely impaired Rlk-/-Itk-/- mice were able to mount a TH2 response and produced TH2 cytokines in response to this challenge. In addition, Rlk-/-Itk-/- cells showed impaired TCR-induced repression of the TH2-inducing transcription factor GATA-3, suggesting a potential mechanism for TH2 development in these hyporesponsive cells. Thus, mutations that affect Tec kinases lead to complex alterations in CD4+ TH cell differentiation. Publication Types Research Support, Non-U.S. Gov t Research Support, U.S. Gov t, P.H.S. PMID 11702066 [PubMed - indexed for MEDLINE] Grb2(+/-) mice disrupt T cell signaling networks and development. 1 Nat Immunol. 2001 Jan;2(1) 29-36. Disruption of T cell signaling networks and development by Grb2 haploid insufficiency. Gong Q, Cheng AM, Akk AM, Alberola-Ila J, Gong G, Pawson T, Chan AC. Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, USA. The developmental processes of positive and negative selection in the thymus shape the T cell antigen receptor (TCR) repertoire and require the integration of multiple signaling networks. These networks involve the efficient assembly of macromolecular complexes and are mediated by multimodular adaptor proteins that permit the functional integration of distinct signaling molecules. We show here that decreased expression of the adaptor protein Grb2 in Grb2+/- mice weakens TCR-induced c-Jun N-terminal kinase (JNK) and p38, but not extracellular signal-regulated kinase (ERK), activation. In turn, this selective effect decreases the ability of thymocytes to undergo negative, but not positive, selection. We also show that there are differences in the signaling thresholds of the three mitogen-activated protein kinase (MAPK) families. These differences may provide a mechanism by which quantitative differences in signal strength can alter the balance of downstream signaling pathways to induce the qualitatively distinct biological outcomes of proliferation, differentiation or apoptosis. PMID 11135575 [PubMed - indexed for MEDLINE] Dendric cells and macrophages of MEK3 deficient mice have impaired IL12 production. 1 EMBO J. 1999 Apr 1;18(7) 1845-57. Defective IL-12 production in mitogen-activated protein (MAP) kinase kinase 3 (Mkk3)-deficient mice. Lu HT, Yang DD, Wysk M, Gatti E, Mellman I, Davis RJ, Flavell RA. Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. The p38 mitogen-activated protein kinase (MAPK) pathway, like the c-Jun N-terminal kinase (JNK) MAPK pathway, is activated in response to cellular stress and inflammation and is involved in many fundamental biological processes. To study the role of the p38 MAPK pathway in vivo, we have used homologous recombination in mice to inactivate the Mkk3 gene, one of the two specific MAPK kinases (MAPKKs) that activate p38 MAPK. Mkk3(-/-) mice were viable and fertile; however, they were defective in interleukin-12 (IL-12) production by macrophages and dendritic cells. Interferon-gamma production following immunization with protein antigens and in vitro differentiation of naive T cells is greatly reduced, suggesting an impaired type I cytokine immune response. The effect of the p38 MAPK pathway on IL-12 expression is at least partly transcriptional, since inhibition of this pathway blocks IL-12 p40 promoter activity in macrophage cell lines and IL-12 p40 mRNA is reduced in MKK3-deficient mice. We conclude that the p38 MAP kinase, activated through MKK3, is required for the production of inflammatory cytokines by both antigen-presenting cells and CD4(+) T cells. PMID 10202148 [PubMed - indexed for MEDLINE] Bam32(-/-) B cell develop normally but have impaired T-independent antibody responses in vivo. 1 Immunity. 2003 Oct;19(4) 621-32. Bam32 links the B cell receptor to ERK and JNK and mediates B cell proliferation but not survival. Han A, Saijo K, Mecklenbrauker I, Tarakhovsky A, Nussenzweig MC. Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10021, USA. Bam32 is an adaptor protein recruited to the plasma membrane upon B cell receptor (BCR) crosslinking in a phosphoinositol 3-kinase (PI3K)-dependent manner; however, its physiologic function is unclear. To determine its physiologic function, we produced Bam32-deficient mice. Bam32(-/-) B cells develop normally but have impaired T-independent antibody responses in vivo and diminished responses to BCR crosslinking in vitro. Biochemical analysis revealed that Bam32 acts in a novel pathway leading from the BCR to MAPK/ERK Kinases (MEK1/2), MAPK/ERK Kinase Kinase-1 (MEKK1), extracellular signal-regulated kinase (ERK), and c-jun NH2-terminal kinase (JNK), but not p38 mitogen-activated protein kinase (p38). This pathway appears to be initiated by hematopoietic progenitor kinase-1 (HPK1), which interacts directly with Bam32, and differs from all previously characterized BCR signaling pathways in that it is required for normal BCR-mediated proliferation but not for B cell survival. PMID 14563325 [PubMed - indexed for MEDLINE] T-cell and B-cell of RAP1A deficient mice impair integrin-mediated cell adhesion. 1 Mol Cell Biol. 2006 Jan;26(2) 643-53. Rap1A-deficient T and B cells show impaired integrin-mediated cell adhesion. Duchniewicz M, Zemojtel T, Kolanczyk M, Grossmann S, Scheele JS, Zwartkruis FJ. Department of Computational Molecular Biology, Max Planck Institute for Molecular Genetics, Ihnestrasse 73, D-14195 Berlin, Germany. Studies in tissue culture cells have demonstrated a role for the Ras-like GTPase Rap1 in the regulation of integrin-mediated cell-matrix and cadherin-mediated cell-cell contacts. To analyze the function of Rap1 in vivo, we have disrupted the Rap1A gene by homologous recombination. Mice homozygous for the deletion allele are viable and fertile. However, primary hematopoietic cells isolated from spleen or thymus have a diminished adhesive capacity on ICAM and fibronectin substrates. In addition, polarization of T cells from Rap1-/- cells after CD3 stimulation was impaired compared to that of wild-type cells. Despite this, these defects did not result in hematopoietic or cell homing abnormalities. Although it is possible that the relatively mild phenotype is a consequence of functional complementation by the Rap1B gene, our genetic studies confirm a role for Rap1A in the regulation of integrins. PMID 16382154 [PubMed - indexed for MEDLINE] T-cell of WASP deficient mice impair the proliferaction and antigen receptor cap formation in response to anti-CD3zeta stimulation. 1 Immunity. 1998 Jul;9(1) 81-91. Wiskott-Aldrich syndrome protein-deficient mice reveal a role for WASP in T but not B cell activation. Snapper SB, Rosen FS, Mizoguchi E, Cohen P, Khan W, Liu CH, Hagemann TL, Kwan SP, Ferrini R, Davidson L, Bhan AK, Alt FW. Howard Hughes Medical Institute, Children s Hospital, Boston, Massachusetts 02115, USA. The Wiskott-Aldrich syndrome (WAS) is a human X-linked immunodeficiency resulting from mutations in a gene (WASP) encoding a cytoplasmic protein implicated in regulating the actin cytoskeleton. To elucidate WASP function, we disrupted the WASP gene in mice by gene-targeted mutation. WASP-deficient mice showed apparently normal lymphocyte development, normal serum immunoglobulin levels, and the capacity to respond to both T-dependent and T-independent type II antigens. However, these mice did have decreased peripheral blood lymphocyte and platelet numbers and developed chronic colitis. Moreover, purified WASP-deficient T cells showed markedly impaired proliferation and antigen receptor cap formation in response to anti-CD3epsilon stimulation. Yet, purified WASP-deficient B cells showed normal responses to anti-Ig stimulation. We discuss the implications of our findings regarding WASP function in receptor signaling and cytoskeletal reorganization in T and B cells and compare the effects of WASP deficiency in mice and humans. PMID 9697838 [PubMed - indexed for MEDLINE] T-cell of SHB defective mice impair the phosphorylation of LAT and consequently the activation of MAP kinase pathways. 9 Sep 24;274(39) 28050-7. Requirement of the Src homology 2 domain protein Shb for T cell receptor-dependent activation of the interleukin-2 gene nuclear factor for activation of T cells element in Jurkat T cells. Lindholm CK, Gylfe E, Zhang W, Samelson LE, Welsh M. Department of Medical Cell Biology, Box 571, Biomedicum, Uppsala University, S-75123 Uppsala, Sweden. Stimulation of the T cell antigen receptor (TCR) induces tyrosine phosphorylation of numerous intracellular proteins. We have recently investigated the role of the adaptor protein Shb in the early events of T cell signaling and observed that Shb associates with Grb2, linker for activation of T cells (LAT) and the TCR zeta-chain in Jurkat cells. We now report that Shb also associates with phospholipase C-gamma1 (PLC-gamma1) in these cells. Overexpression of Src homology 2 domain defective Shb caused diminished phosphorylation of LAT and consequently the activation of mitogen-activated protein kinases was decreased upon TCR stimulation. In addition, the Shb mutant also blocked phosphorylation of PLC-gamma1 and the increase in cytoplasmic Ca(2+) following TCR stimulation. Nuclear factor for activation of T cells is a major target for Ras and calcium signaling pathways in T cells following TCR stimulation, and the overexpression of the mutant Shb prevented TCR-dependent activation of the nuclear factor for activation of T cells. Consequently, endogenous interleukin-2 production was decreased under these conditions. The results indicate a role for Shb as a link between the TCR and downstream signaling events involving LAT and PLC-gamma1 and resulting in the activation of transcription of the interleukin-2 gene. PMID 10488157 [PubMed - indexed for MEDLINE] B-cell of 3BP2 (-/-) deficient mice have defective in proliferation, cell cycle progression, PLC-gamma2 phosphorylation, calcium mobilization, NF-ATp dephosphorylation, and Erk and Jnk activation in response to BCR ligation. 1 Mol Cell Biol. 2006 Jul;26(14) 5214-25. 3BP2 deficiency impairs the response of B cells, but not T cells, to antigen receptor ligation. de la Fuente MA, Kumar L, Lu B, Geha RS. Division of Immunology, Children s Hospital, 300 Longwood Ave., Boston, MA 02115, USA. The adapter protein 3BP2 is expressed in lymphocytes; binds to Syk/ZAP-70, Vav, and phospholipase C-gamma (PLC-gamma); and is thought to be important for interleukin-2 gene transcription in T cells. To define the role of 3BP2 in lymphocyte development and function, we generated 3BP2-deficient mice. T-cell development, proliferation, cytokine secretion, and signaling in response to T-cell receptor (TCR) ligation were all normal in 3BP2(-/-) mice. 3BP2(-/-) mice had increased accumulation of pre-B cells in the bone marrow and a block in the progression of transitional B cells in the spleen from the T1 to the T2 stage, but normal numbers of mature B cells. B-cell proliferation, cell cycle progression, PLC-gamma2 phosphorylation, calcium mobilization, NF-ATp dephosphorylation, and Erk and Jnk activation in response to B-cell receptor (BCR) ligation were all impaired. These results suggest that 3BP2 is important for BCR, but not for TCR signaling. PMID 16809760 [PubMed - indexed for MEDLINE] B-cell of Vav2(-/-) deficient mice are defective in the ability to switch immunoglobulin class. 1 Nat Immunol. 2001 Jun;2(6) 542-7. Comment in Nat Immunol. 2001 Jun;2(6) 482-4. Signal transduction through Vav-2 participates in humoral immune responses and B cell maturation. Doody GM, Bell SE, Vigorito E, Clayton E, McAdam S, Tooze R, Fernandez C, Lee IJ, Turner M. Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, UK. B and T lymphocytes develop normally in mice lacking the guanine nucleotide exchange factor Vav-2. However, the immune responses to type II thymus-independent antigen as well as the primary response to thymus-dependent (TD) antigen are defective. Vav-2-deficient mice are also defective in their ability to switch immunoglobulin class, form germinal centers and generate secondary immune responses to TD antigens. Mice lacking both Vav-1 and Vav-2 contain reduced numbers of B lymphocytes and display a maturational block in the development of mature B cells. B cells from Vav-1(-/-)Vav-2(-/-) mice respond poorly to antigen receptor triggering, both in terms of proliferation and calcium release. These studies show the importance of Vav-2 in humoral immune responses and B cell maturation. PMID 11376342 [PubMed - indexed for MEDLINE] T-cell of Vav1(-/-) deficient mice exhibit impaired antigen receptor signaling. 1 Nature. 1995 Mar 30;374(6521) 474-7. Defective T-cell receptor signalling and positive selection of Vav-deficient CD4+ CD8+ thymocytes. Fischer KD, Zmuldzinas A, Gardner S, Barbacid M, Bernstein A, Guidos C. Program in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada. During lymphocyte development, cellular proliferation and positive and negative selection events ensure the production of T and B lymphocytes bearing highly diverse, but self-tolerant, repertoires of antigen receptors. These processes are initiated when engagement of growth-factor receptors, or the T and B lymphocyte antigen receptors, induces tyrosine phosphorylation of specific SH2- and SH3-domain-containing cytoplasmic proteins, including Vav. Here we show that vav-/- embryonic stem cells generate only limited numbers of immature and mature T and B lymphocytes in the RAG-2 blastocyst complementation assay. Furthermore, Vav-deficient T lymphocytes showed severely impaired antigen receptor signalling. Finally, we demonstrate that Vav-dependent signalling pathways regulate maturation, but not CD4/CD8 lineage commitment, during T-cell-receptor-mediated positive selection of immature CD4+ CD8+ precursors into mature CD4+ CD8- or CD4- CD8+ T cells. PMID 7700360 [PubMed - indexed for MEDLINE] Vav1(-/-)Vav2(-/-) mice exhibit greatly reduced the mature B-cells. Vav-1-/-Vav-2-/- B cells were unresponsive to BCR-driven proliferation in vitro and to thymus-indepen-dent antigen in vivo. 1 Nat Immunol. 2001 Jun;2(6) 548-55. Comment in Nat Immunol. 2001 Jun;2(6) 482-4. Compensation between Vav-1 and Vav-2 in B cell development and antigen receptor signaling. Tedford K, Nitschke L, Girkontaite I, Charlesworth A, Chan G, Sakk V, Barbacid M, Fischer KD. Abteilung Physiologische Chemie, Universitat Ulm, Albert-Einstein-Allee 11, D-89069 Ulm, Germany. Vav-1 and Vav-2 are closely related Dbl-homology GTP exchange factors (GEFs) for Rho GTPases. Mutation of Vav-1 disrupts T cell development and T cell antigen receptor-induced activation, but has comparatively little effect on B cells. We found that combined deletion of both Vav-1 and Vav-2 in mice resulted in a marked reduction in mature B lymphocyte numbers. Vav-1(-/-)Vav-2(-/-) B cells were unresponsive to B cell antigen receptor (BCR)-driven proliferation in vitro and to thymus-independent antigen in vivo. BCR-stimulated intracellular calcium mobilization was greatly impaired in Vav-1(-/-)Vav-2(-/-) B cells. These findings establish a role for Vav-2 in BCR calcium signaling and reveal that the Vav family of GEFs is critical to B cell development and function. PMID 11376343 [PubMed - indexed for MEDLINE] Fyn-deficient mice exhibit a remarkably specific lymphoid defect thymocytes are refractile to stimulation through the TCR with mitogen or antigen. 1 Cell. 1992 Sep 4;70(5) 751-63. Defective T cell receptor signaling in mice lacking the thymic isoform of p59fyn. Appleby MW, Gross JA, Cooke MP, Levin SD, Qian X, Perlmutter RM. Howard Hughes Medical Institute, Department of Immunology, University of Washington, Seattle 98195. Considerable evidence supports the hypothesis that the nonreceptor protein tyrosine kinase p59fyn participates in signal transduction from the T cell receptor (TCR). To examine this hypothesis in detail, we have produced mice that lack the thymic isoform of p59fyn but retain expression of the brain isoform of the protein. fynTnull mice exhibit a remarkably specific lymphoid defect thymocytes are refractile to stimulation through the TCR with mitogen or antigen, while peripheral T cells, following what appears to be a normal maturation sequence, reacquire significant signaling capabilities. These data confirm that p59fynT plays a pivotal role in TCR signal transduction and demonstrate that additional developmentally regulated signaling components also contribute to TCR-induced lymphocyte activation. PMID 1516132 [PubMed - indexed for MEDLINE] Lck-deficient mice show a pronounced thymic atrophy, with a dramatic reduction in the double-positive (CD4+CD8+) thymocyte population. 1 Nature. 1992 May 14;357(6374) 161-4. Comment in Nature. 1993 Jan 21;361(6409) 213. Profound block in thymocyte development in mice lacking p56lck. Molina TJ, Kishihara K, Siderovski DP, van Ewijk W, Narendran A, Timms E, Wakeham A, Paige CJ, Hartmann KU, Veillette A, et al. Ontario Cancer Institute, University of Toronto, Canada. The protein Lck (p56lck) has a relative molecular mass of 56,000 and belongs to the Src family of tyrosine kinases. It is expressed exclusively in lymphoid cells, predominantly in thymocytes and peripheral T cells. Lck associates specifically with the cytoplasmic domains of both CD4 and CD8 T-cell surface glycoproteins and interacts with the beta-chain of the interleukin-2 receptor, which implicates Lck activity in signal transduction during thymocyte ontogeny and activation of mature T cells. Here we generate an lck null mutation by homologous recombination in embryonic stem cells to evaluate the role of p56lck in T-cell development and activation. Lck-deficient mice show a pronounced thymic atrophy, with a dramatic reduction in the double-positive (CD4+CD8+) thymocyte population. Mature, single-positive thymocytes are not detectable in these mice and there are only very few peripheral T cells. These results illustrate the crucial role of this T-cell-specific tyrosine kinase in the thymocyte development. PMID 1579166 [PubMed - indexed for MEDLINE] T cell from mice deficient in LCK is required for normal signal transduction through the TCR. 1 Cell. 1992 Aug 21;70(4) 585-93. Genetic evidence for the involvement of the lck tyrosine kinase in signal transduction through the T cell antigen receptor. Straus DB, Weiss A. Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco 94143. Signaling through the T cell antigen receptor (TCR) results both in rapid increases in tyrosine phosphorylation on a number of proteins and in the activation of the phosphatidylinositol pathway. It is not clear how stimulation of the TCR leads to these signaling events. Mutants of the Jurkat T cell line have been previously isolated that fail to show increases in calcium following receptor stimulation. Analysis of one of these mutants, JCaM1, which is defective in the induction of tyrosine phosphorylation, revealed a defect in the expression of functional lck tyrosine kinase. The lack of lck activity was caused in part by a splicing defect. Expression of the lck cDNA in JCaM1 restores the ability of the cell to respond to TCR stimulation. These results indicate that lck is required for normal signal transduction through the TCR. PMID 1505025 [PubMed - indexed for MEDLINE] T cells from mice deficient in SLAP-130/Fyb show markedly impaired proliferation. 1 Science. 2001 Sep 21;293(5538) 2263-5. Coupling of the TCR to integrin activation by Slap-130/Fyb. Peterson EJ, Woods ML, Dmowski SA, Derimanov G, Jordan MS, Wu JN, Myung PS, Liu QH, Pribila JT, Freedman BD, Shimizu Y, Koretzky GA. The Abramson Family Cancer Research Institute, Department of Medicine, School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA. SLAP-130/Fyb (SLP-76-associated phosphoprotein or Fyn-binding protein; also known as Fyb/Slap) is a hematopoietic-specific adapter, which associates with and modulates function of SH2-containing leukocyte phosphoprotein of 76 kilodaltons (SLP-76). T cells from mice lacking SLAP-130/Fyb show markedly impaired proliferation following CD3 engagement. In addition, the T cell receptor (TCR) in SLAP-130/Fyb mutant cells fails to enhance integrin-dependent adhesion. Although TCR-induced actin polymerization is normal, TCR-stimulated clustering of the integrin LFA-1 is defective in SLAP-130/Fyb-deficient cells. These data indicate that SLAP-130/Fyb is important for coupling TCR-mediated actin cytoskeletal rearrangement with activation of integrin function, and for T cells to respond fully to activating signals. PMID 11567141 [PubMed - indexed for MEDLINE] B cell of chicken deficient ITK reduce IP3 generation and phospholipase C gamma 2 tyrosine phosphorylation. 1 J Exp Med. 1996 Jul 1;184(1) 31-40. A role for Bruton s tyrosine kinase in B cell antigen receptor-mediated activation of phospholipase C-gamma 2. Takata M, Kurosaki T. Department of Oncology and Immunology, Wyeth-Ayerst Research, Pearl River, New York 10965, USA. Defects in the gene encoding Bruton s tyrosine kinase (Btk) result in a disease called X-linked agammaglobulinemia, in which there is a profound decrease of mature B cells due to a block in B cell development. Recent studies have shown that Btk is tyrosine phosphorylated and activated upon B cell antigen receptor (BCR) stimulation. To elucidate the functions of this kinase, we examined BCR signaling of DT40 B cells deficient in Btk. Tyrosine phosphorylation of phospholipase C (PLC)-gamma 2 upon receptor stimulation was significantly reduced in the mutant cells, leading to the loss of both BCR-coupled phosphatidylinositol hydrolysis and calcium mobilization. Pleckstrin homology and Src-homology 2 domains of Btk were required for PLC-gamma 2 activation. Since Syk is also required for the BCR-induced PLC-gamma 2 activation, our findings indicate that PLC-gamma 2 activation is regulated by Btk and Syk through their concerted actions. PMID 8691147 [PubMed - indexed for MEDLINE] T cell of mice deficient ITK reduce IP3 generation and phospholipase C gamma 1 tyrosine phosphorylation. 1 J Exp Med. 1998 May 18;187(10) 1721-7. T cell receptor-initiated calcium release is uncoupled from capacitative calcium entry in Itk-deficient T cells. Liu KQ, Bunnell SC, Gurniak CB, Berg LJ. Program of Immunology, Division of Medical Sciences, Harvard University, Boston, Massachusetts 02115, USA. Itk, a Tec family tyrosine kinase, plays an important but as yet undefined role in T cell receptor (TCR) signaling. Here we show that T cells from Itk-deficient mice have a TCR-proximal signaling defect, resulting in defective interleukin 2 secretion. Upon TCR stimulation, Itk-/- T cells release normal amounts of calcium from intracellular stores, but fail to open plasma membrane calcium channels. Since thapsigargin-induced store depletion triggers normal calcium entry in Itk-/- T cells, an impaired biochemical link between store depletion and channel opening is unlikely to be responsible for this defect. Biochemical studies indicate that TCR-induced inositol 1,4,5 tris-phosphate (IP3) generation and phospholipase C gamma1 tyrosine phosphorylation are substantially reduced in Itk-/- T cells. In contrast, TCR-zeta and ZAP-70 are phosphorylated normally, suggesting that Itk functions downstream of, or in parallel to, ZAP-70 to facilitate TCR-induced IP3 production. These findings support a model in which quantitative differences in cytosolic IP3 trigger distinct responses, and in which only high concentrations of IP3 trigger the influx of extracellular calcium. PMID 9584150 [PubMed - indexed for MEDLINE] T cell of mice deficient ITK have failure of Th2 development. 1 Immunity. 1999 Oct;11(4) 399-409. Impaired NFATc translocation and failure of Th2 development in Itk-deficient CD4+ T cells. Fowell DJ, Shinkai K, Liao XC, Beebe AM, Coffman RL, Littman DR, Locksley RM. Department of Medicine, University of California San Francisco 94143, USA. Naive Itk-deficient CD4+ T cells were unable to establish stable IL-4 production, even when primed in Th2-inducing conditions. In contrast, IFNgamma production was little affected. Failure to express IL-4 occurred even among cells that had gone through multiple cell divisions and was associated with a delay in the kinetics and magnitude of NFATc nuclear localization. IL-4 production was restored genetically by retroviral reconstitution of Itk or biochemically by augmenting the calcium flux with ionomycin. In vivo, Itk-deficient mice were unable to establish functional Th2 cells. Development of protective Th1 cells was unimpeded. These data define a nonredundant role for Itk in modulating signals from the TCR/CD28 pathways that are specific for the establishment of stable IL-4 but not IFNgamma expression. PMID 10549622 [PubMed - indexed for MEDLINE] Mice deficient in ITK have reduced proliferative responses to MHC stimulation and to anti-TCR cross-linking 1 Immunity. 1995 Dec;3(6) 757-69. Altered T cell receptor signaling and disrupted T cell development in mice lacking Itk. Liao XC, Littman DR. Department of Microbiology and Immunology, University of California, San Francisco 94143-0414, USA. Itk is a T cell protein tyrosine kinase (PTK) that, along with Btk and Tec, belongs to a family of cytoplasmic PTKs with N-terminal pleckstrin homology domains. Btk plays a critical role in B lymphocyte development. To determine whether Itk has an analogous role in T lymphocytes, we used gene targeting to prepare mice lacking expression of Itk. Such animals had decreased numbers of mature thymocytes, an effect most clearly observed in mice expressing T cell receptor (TCR) transgenes. Mature T cells from Itk-deficient mice had reduced proliferative responses to allogeneic MHC stimulation and to anti-TCR cross-linking, but responded normally to stimulation with phorbol ester plus ionomycin or with IL-2. These results provide genetic evidence that Itk is involved in T cell development and also suggest that Itk has an important role in proximal events in TCR-mediated signaling pathways. PMID 8777721 [PubMed - indexed for MEDLINE] Mutations in Btk cause X-linked immunodeficiency. 1 Semin Immunol. 1998 Aug;10(4) 309-16. Btk function in B cell development and response. Satterthwaite AB, Li Z, Witte ON. Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90095-1662, USA. Mutations in Bruton s tyrosine kinase (Btk) result in the B cell immunodeficiencies XLA in humans and Xid in mice. Both the maintenance of peripheral B cell numbers and their response to B cell antigen receptor (BCR) crosslinking depend on Btk. Btk integrates signals from multiple cell surface receptors, including BCR and G-protein coupled receptors. These Btk dependent signals control B cell proliferation and survival by mediating Ca2+ flux, activating JNK and p38 and inducing cell cycle regulatory genes. Publication Types Review PMID 9695187 [PubMed - indexed for MEDLINE] Gads(GRAP2) has a role in thymocyte proliferaction for maturation of T-cells. 1 Science. 2001 Mar 9;291(5510) 1987-91. Requirement for the SLP-76 adaptor GADS in T cell development. Yoder J, Pham C, Iizuka YM, Kanagawa O, Liu SK, McGlade J, Cheng AM. Medical Scientist Training Program, Washington University School of Medicine, St. Louis, MO 63110, USA. GADS is an adaptor protein implicated in CD3 signaling because of its ability to link SLP-76 to LAT. A GADS-deficient mouse was generated by gene targeting, and the function of GADS in T cell development and activation was examined. GADS- CD4-CD8- thymocytes exhibited a severe block in proliferation but still differentiated into mature T cells. GADS- thymocytes failed to respond to CD3 cross-linking in vivo and were impaired in positive and negative selection. Immunoprecipitation experiments revealed that the association between SLP-76 and LAT was uncoupled in GADS- thymocytes. These observations indicate that GADS is a critical adaptor for CD3 signaling. PMID 11239162 [PubMed - indexed for MEDLINE] Gads(GRAP2) has a role for homeostatic proliferaction in B cells. 1 Eur J Immunol. 2005 Apr;35(4) 1184-92. Expression and function of the adaptor protein Gads in murine B cells. Yankee TM, Draves KE, Clark EA. Department of Immunology, University of Washington, Seattle, USA. tyankee@kumc.edu Nearly all hematopoietic receptors are dependent on adaptor proteins for the activation of downstream signaling pathways. The Gads adaptor protein is expressed in many hematopoietic tissues, including bone marrow, lymph node, and spleen. Using intracellular staining, we detected Gads protein in a number cells, including B cells, T cells, NK cells, monocytes, and plasmacytoid DC, but not in macrophages, neutrophils, or monocyte-derived DC. In the B cell compartment, Gads was first expressed after immature B cells leave the bone marrow and was down-regulated after B cell antigen receptor (BCR) ligation. Female Gads(-/-) mice had increased numbers of splenic B cells, as compared to female Gads(+/+) mice, suggesting a role for Gads in B cell homeostasis. Although B cell production and turnover of splenic B cell subsets appeared normal in Gads(-/-) mice, homeostatic proliferation was significantly impaired in Gads(-/-) B cells. Whereas BCR ligation can induce apoptosis in wild-type transitional stage 1 (T1) B cells, Gads(-/-) T1 B cells were resistant to BCR-induced apoptosis. Gads(-/-) B cells also showed increased BCR-mediated calcium mobilization. We conclude that Gads may have a negative regulatory role in signaling through survival pathways, and is necessary for normal homeostatic proliferation in B cells. PMID 15761845 [PubMed - indexed for MEDLINE] Grap negatively regulates T-cell proliferation. 1 Mol Cell Biol. 2002 May;22(10) 3230-6. Grap negatively regulates T-cell receptor-elicited lymphocyte proliferation and interleukin-2 induction. Shen R, Ouyang YB, Qu CK, Alonso A, Sperzel L, Mustelin T, Kaplan MH, Feng GS. Program in Signal Transduction Research, The Burnham Institute, La Jolla, California 92037, USA. Grb-2-related adaptor protein (Grap) is a Grb2-like SH3-SH2-SH3 adaptor protein with expression restricted to lymphoid tissues. Grap(-/-) lymphocytes isolated from targeted Grap-deficient mice exhibited enhanced proliferation, interleukin-2 production, and c-fos induction in response to mitogenic T-cell receptor (TCR) stimulation, compared to wild-type cells. Ectopic expression of Grap led to a suppression of Elk-1-directed transcription induced by the Ras/Erk pathway, without having effects on gene expression mediated by Jnk and p38 mitogen-activated protein kinases. Together, these data suggest that Grap, unlike Grb2, acts as a negative regulator of TCR-stimulated intracellular signaling by downregulating signal relay through the Ras/Erk pathway. PMID 11971956 [PubMed - indexed for MEDLINE] Gab2 is a substrate of ZAP-70 and functions as a switch molecule toward inhibition of TCR signal transuduction. 1 J Biol Chem. 2001 Nov 30;276(48) 45175-83. Epub 2001 Sep 25. Docking protein Gab2 is phosphorylated by ZAP-70 and negatively regulates T cell receptor signaling by recruitment of inhibitory molecules. Yamasaki S, Nishida K, Hibi M, Sakuma M, Shiina R, Takeuchi A, Ohnishi H, Hirano T, Saito T. Molecular Genetics, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan. To maintain various T cell responses and immune equilibrium, activation signals triggered by T cell antigen receptor (TCR) must be regulated by inhibitory signals. Gab2, an adaptor protein of the insulin receptor substrate-1 family, has been shown to be involved in the downstream signaling from cytokine receptors. We investigated the functional role of Gab2 in TCR-mediated signal transduction. Gab2 was phosphorylated by ZAP-70 and co-precipitated with phosphoproteins, such as ZAP-70, LAT, and CD3zeta, upon TCR stimulation. Overexpression of Gab2 in Jurkat cells or antigen-specific T cell hybridomas resulted in the inhibition of NF-AT activation, interleukin-2 production, and tyrosine phosphorylation. The structure-function relationship of Gab2 was analyzed by mutants of Gab2. The Gab2 mutants lacking SHP-2-binding sites mostly abrogated the inhibitory activity of Gab2, but its inhibitory function was restored by fusing to active SHP-2 as a chimeric protein. A mutant with defective phosphatidylinositol 3-kinase binding capacity also impaired the inhibitory activity, and the pleckstrin homology domain-deletion mutant revealed a crucial function of the pleckstrin homology domain for localization to the plasma membrane. These results suggest that Gab2 is a substrate of ZAP-70 and functions as a switch molecule toward inhibition of TCR signal transduction by mediating the recruitment of inhibitory molecules to the TCR signaling complex. PMID 11572860 [PubMed - indexed for MEDLINE] B cell signaling causes tyrosine phosphorylation of Gab1, and in turn SHP2 bind to Gab1 Gab1 phosophorylation potentiate the phosphorylation of Akt, PI3K-dependent response. 1 J Biol Chem. 2001 Apr 13;276(15) 12257-65. Epub 2001 Jan 22. The Gab1 docking protein links the b cell antigen receptor to the phosphatidylinositol 3-kinase/Akt signaling pathway and to the SHP2 tyrosine phosphatase. Ingham RJ, Santos L, Dang-Lawson M, Holgado-Madruga M, Dudek P, Maroun CR, Wong AJ, Matsuuchi L, Gold MR. Departments of Microbiology and Immunology and Zoology, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada. B cell antigen receptor (BCR) signaling causes tyrosine phosphorylation of the Gab1 docking protein. This allows phosphatidylinositol 3-kinase (PI3K) and the SHP2 tyrosine phosphatase to bind to Gab1. In this report, we tested the hypothesis that Gab1 acts as an amplifier of PI3K- and SHP2-dependent signaling in B lymphocytes. By overexpressing Gab1 in the WEHI-231 B cell line, we found that Gab1 can potentiate BCR-induced phosphorylation of Akt, a PI3K-dependent response. Gab1 expression also increased BCR-induced tyrosine phosphorylation of SHP2 as well as the binding of Grb2 to SHP2. We show that the pleckstrin homology (PH) domain of Gab1 is required for BCR-induced phosphorylation of Gab1 and for Gab1 participation in BCR signaling. Moreover, using confocal microscopy, we show that BCR ligation can induce the translocation of Gab1 from the cytosol to the plasma membrane and that this requires the Gab1 PH domain as well as PI3K activity. These findings are consistent with a model in which the binding of the Gab1 PH domain to PI3K-derived lipids brings Gab1 to the plasma membrane, where it can be tyrosine-phosphorylated and then act as an amplifier of BCR signaling. PMID 11278704 [PubMed - indexed for MEDLINE] RasGRP1 mediates Ras activation following TCR stimulatioin. RasGRP1 and RasGRP3 induces RAS activation in B-cell to response to T-cell stimulation. 1 Immunol Lett. 2006 May 15;105(1) 77-82. Epub 2006 Feb 20. The role of RasGRPs in regulation of lymphocyte proliferation. Coughlin JJ, Stang SL, Dower NA, Stone JC. Department of Biochemistry, University of Alberta, Edmonton, Alta., Canada T6G 2H7. RasGRP1 links TCR signaling to Ras in T cells, while both RasGRP1 and RasGRP3 link BCR signaling to Ras in B cells. T cells deficient in RasGRP1 have defective proliferative responses as do B cells deficient in both RasGRP1 and RasGRP3, confirming the importance of Ras activation in lymphocyte proliferation. While aged Rasgrp1-/- mice develop late-onset autoimmunity characterized by splenomegaly and the presence of anti-nuclear antibodies (ANA), the additional loss of RasGRP3 expression inhibits this phenotype. We show here that the autoimmunity in Rasgrp1-/- mice is T cell dependent. Compared to wildtype, Rasgrp1-/- T cells induce greater in vitro B cell proliferation that is due, at least in part, to increased production of interleukin-4 (IL-4). Rasgrp1 Rasgrp3 double mutant B cells are less responsive to this T cell stimulation. The reduced double mutant B cell proliferative response was paralleled by decreased induction of cyclin D2 upon stimulation with IL-4 and anti-IgM. Taken together these results suggest that double mutant mice fail to generate autoimmunity due to their decreased B cell cyclin D2 accumulation, and thus proliferation, in response to the elevated levels of IL-4 produced by mutant T cells. PMID 16530850 [PubMed - indexed for MEDLINE] Grb2-hSos1-PLCgamma1-p36/p38-ZAP70 complexes localize in the vicinity of TCR-zeta 1 J Biol Chem. 1995 Aug 4;270(31) 18428-36. Ligation of the T-cell antigen receptor (TCR) induces association of hSos1, ZAP-70, phospholipase C-gamma 1, and other phosphoproteins with Grb2 and the zeta-chain of the TCR. Nel AE, Gupta S, Lee L, Ledbetter JA, Kanner SB. Department of Medicine, UCLA School of Medicine 90024, USA. Signaling by the T-cell antigen receptor (TCR) involves both phospholipase C (PLC)-gamma 1 and p21ras activation. While failing to induce Shc/Grb2 association, ligation of the TCR/CD3 receptor in Jurkat T-cells induced hSos1-Grb2 complexes. In addition to hSos1, Grb2 participates in the formation of a tyrosine phosphoprotein complex that includes 145-, 95-, 70-, 54-, and 36-38-kDa proteins. p145 was identified as PLC-gamma 1 and p70 as the protein tyrosine kinase, ZAP-70. Although of the same molecular weight, p95 was not recognized by an anti-serum to p95 Vav. The SH2 domains of Grb2 and PLC-gamma 1 were required for the formation of this protein complex. In anti-CD3-treated cells, Grb2 redistributed from the cytosol to a particulate cell compartment along with p36/p38, ZAP-70, and PLC-gamma 1. Part of the Grb2 complex associated with the particulate compartment could be extracted with Nonidet P-40, while the rest was Nonidet P-40 insoluble. In both the detergent-soluble and -insoluble fractions, Grb2 coimmunoprecipitated with the zeta-chain of the TCR. Taken together, these results indicate that anti-CD3 induces Grb2-hSos1-PLC-gamma 1-p36/p38-ZAP70 complexes, which localize in the vicinity of TCR-zeta. PMID 7629168 [PubMed - indexed for MEDLINE] Gads(Grap2) plays an important role in T-cell signaling via its association with SLP-76 and LAT. 1 Curr Biol. 1999 Jan 28;9(2) 67-75. The hematopoietic-specific adaptor protein gads functions in T-cell signaling via interactions with the SLP-76 and LAT adaptors. Liu SK, Fang N, Koretzky GA, McGlade CJ. Department of Medical Biophysics, University of Toronto, The Arthur and Sonia Labatt Brain Tumour Research Centre, Hospital for Sick Children, Research Institute, 555 University Ave, Toronto, Ontario M5G 1X8, Canada. BACKGROUND The adaptor protein Gads is a Grb2-related protein originally identified on the basis of its interaction with the tyrosine-phosphorylated form of the docking protein Shc. Gads protein expression is restricted to hematopoietic tissues and cell lines. Gads contains a Src homology 2 (SH2) domain, which has previously been shown to have a similar binding specificity to that of Grb2. Gads also possesses two SH3 domains, but these have a distinct binding specificity to those of Grb2, as Gads does not bind to known Grb2 SH3 domain targets. Here, we investigated whether Gads is involved in T-cell signaling. RESULTS We found that Gads is highly expressed in T cells and that the SLP-76 adaptor protein is a major Gads-associated protein in vivo. The constitutive interaction between Gads and SLP-76 was mediated by the carboxy-terminal SH3 domain of Gads and a 20 amino-acid proline-rich region in SLP-76. Gads also coimmunoprecipitated the tyrosine-phosphorylated form of the linker for activated T cells (LAT) adaptor protein following cross-linking of the T-cell receptor; this interaction was mediated by the Gads SH2 domain. Overexpression of Gads and SLP-76 resulted in a synergistic augmentation of T-cell signaling, as measured by activation of nuclear factor of activated T cells (NFAT), and this cooperation required a functional Gads SH2 domain. CONCLUSIONS These results demonstrate that Gads plays an important role in T-cell signaling via its association with SLP-76 and LAT. Gads may promote cross-talk between the LAT and SLP-76 signaling complexes, thereby coupling membrane-proximal events to downstream signaling pathways. PMID 10021361 [PubMed - indexed for MEDLINE] Lck is required for normal signal transduction through the TCR. 1 Cell. 1992 Aug 21;70(4) 585-93. Genetic evidence for the involvement of the lck tyrosine kinase in signal transduction through the T cell antigen receptor. Straus DB, Weiss A. Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco 94143. Signaling through the T cell antigen receptor (TCR) results both in rapid increases in tyrosine phosphorylation on a number of proteins and in the activation of the phosphatidylinositol pathway. It is not clear how stimulation of the TCR leads to these signaling events. Mutants of the Jurkat T cell line have been previously isolated that fail to show increases in calcium following receptor stimulation. Analysis of one of these mutants, JCaM1, which is defective in the induction of tyrosine phosphorylation, revealed a defect in the expression of functional lck tyrosine kinase. The lack of lck activity was caused in part by a splicing defect. Expression of the lck cDNA in JCaM1 restores the ability of the cell to respond to TCR stimulation. These results indicate that lck is required for normal signal transduction through the TCR. PMID 1505025 [PubMed - indexed for MEDLINE] ZAP-70 plays crucial roles in T-cell activation and development. Syk triggers cellular activation in T-cell. 1 Mol Cell Biol. 1998 Mar;18(3) 1388-99. Genetic evidence for differential coupling of Syk family kinases to the T-cell receptor reconstitution studies in a ZAP-70-deficient Jurkat T-cell line. Williams BL, Schreiber KL, Zhang W, Wange RL, Samelson LE, Leibson PJ, Abraham RT. Department of Immunology, Mayo Clinic, Rochester, Minnesota 55905, USA. T-cell antigen receptor (TCR) engagement activates multiple protein tyrosine kinases (PTKs), including the Src family member, Lck, and the Syk-related PTK, ZAP-70. Studies in ZAP-70-deficient humans have demonstrated that ZAP-70 plays crucial roles in T-cell activation and development. However, progress toward a detailed understanding of the regulation and function of ZAP-70 during TCR signaling has been hampered by the lack of a suitable T-cell model for biochemical and genetic analyses. In this report, we describe the isolation and phenotypic characterization of a Syk- and ZAP-70-negative somatic mutant derived from the Jurkat T-cell line. The P116 cell line displays severe defects in TCR-induced signaling functions, including protein tyrosine phosphorylation, intracellular Ca2+ mobilization, and interleukin-2 promoter-driven transcription. These signaling defects were fully reversed by reintroduction of catalytically active versions of either Syk or ZAP-70 into the P116 cells. However, in contrast to ZAP-70 expression, Syk expression triggered a significant degree of cellular activation in the absence of TCR ligation. Transfection experiments with ZAP-70-Syk chimeric proteins indicated that both the amino-terminal regulatory regions and the carboxy-terminal catalytic domains of Syk and ZAP-70 contribute to the distinctive functional properties of these PTKs. These studies underscore the crucial role of ZAP-70 in TCR signaling and offer a powerful genetic model for further analyses of ZAP-70 regulation and function in T cells. PMID 9488454 [PubMed - indexed for MEDLINE]

• Community Tool Box Japan@Wiki - CTBまちづくりマニュアル

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

  メニュー wikiの説明：はじめにお読み下さい? CTBまちづくりマニュアル Part A. コミュニティ保健と開発を促進するためのモデル：道具箱の入口 　　Models for Promoting Community Health and Development Gateways to the Tools (Chapters 1 - 2) Chapter 1. Our Model for Community Change and Improvement Chapter 2. Some Other Models for Promoting Community Health and Development Contains an overview of the CTB (Chapter 1, Section 1) and frameworks for guiding, supporting and evaluating the works of community and systems change. Part B. Community Assessment, Agenda Setting, and Choice of Broad Strategies (Chapters 3 - 5) Chapter 3. Assessing Community Needs and Resources Chapter 4. Getting Issues on the Public Agenda Chapter 5. Choosing Strategies to Promote Community Health and Development Contains information about how to assess community needs and resources (e.g. conducting listening sessions, analyzing problems) how to get issues on the public agenda (e.g., gaining public support), and how to choose broad strategies to promote community health and development (e.g., building coalitions). Part C. Promoting Interest and Participation in Initiatives (Chapters 6 - 7) Chapter 6. Promoting Interest in Community Issues Chapter 7. Encouraging Involvement in Community Work Contains information about how to promote interest in an issue (e.g., persuasion, press releases, and newsletters) and how to encourage involvement (e.g., among diverse groups). Part D. Developing a Strategic Plan, Organizational Structure, and Training System (Chapters 8 - 12) Chapter 8. Developing a Strategic Plan Chapter 9. Developing an Organizational Structure for the Initiative Chapter 10. Hiring and Training Key Staff of Community Organizations Chapter 11. Recruiting and Training Volunteers Chapter 12. Providing Training and Technical Assistance Contains information about developing a strategic plan (e.g., vision, mission, action plan) and organizational structure (e.g., bylaws, board of directors) and hiring and training staff, recruiting and training volunteers, and providing technical assistance. Part E. Leadership, Management, and Group Facilitation (Chapters 13 - 16) Chapter 13. Orienting Ideas in Leadership Chapter 14. Core Functions in Leadership Chapter 15. Becoming an Effective Manager Chapter 16. Group Facilitation and Problem-Solving Contains information about the core functions of leadership (e.g., building relationships, influencing people), management (e.g., providing supervision and support), and group facilitation (e.g., leading meetings). Part F. Analyzing Community Problems and Designing and Adapting Community Interventions (Chapters 17 - 19) Chapter 17. Analyzing Community Problems and Solutions Chapter 18. Deciding Where to Start Chapter 19. Choosing and Adapting Community Interventions Contains information about analyzing community problems (e.g. thinking critically), designing an intervention (e.g. identifying those who can benefit and help), and choosing and adapting interventions for different cultures and communities. Part G. Implementing Promising Community Interventions (Chapters 20 - 26) Chapter 20. Providing Information and Enhancing Skills Chapter 21. Enhancing Support, Incentives, and Resources Chapter 22. Youth Mentoring Programs Chapter 23. Modifying Access, Barriers, and Opportunties Chapter 24. Improving Services Chapter 25. Changing Policies Chapter 26. Changing the Physical and Social Environment Contains information on illustrative interventions using the strategies of providing information and enhancing skills, enhancing support and resources, youth mentoring, modifying access and barriers, improving services, changing policies, and changing the physical and social environment. Part H. Cultural Competence, Spirituality, and the Arts and Community Building (Chapters 27 - 29) Chapter 27. Cultural Competence in a Multicultural World Chapter 28. Spirituality and Social Action Chapter 29. The Arts and Community Building Celebrating, Preserving, and Transforming Community Life Contains information on building cultural competence in a multicultural world, spirituality and community action, and the arts and community building. Part I. Organizing for Effective Advocacy (Chapters 30 - 35) Chapter 30. Principles of Advocacy Chapter 31. Conducting Advocacy Research Chapter 32. Providing Encouragement and Education Chapter 33. Conducting a Direct Action Campaign Chapter 34. Media Advocacy Chapter 35. Responding to Counterattacks Contains information on principles of advocacy (e.g., recognizing allies and opponents), conducting advocacy research, providing encouragement and education, conducting a direct action campaign (e.g., personal testimony letters), media advocacy, and responding to opposition. Part J. Evaluating Community Programs and Initiatives (Chapters 36 - 39) Chapter 36. Introduction to Evaluation Chapter 37. Some Operations in Evaluating Community Intervention Chapter 38. Some Methods for Evaluating Comprehensive Community Initiatives Chapter 39. Using Evaluation to Understand and Improve the Initiative Contains information on developing a plan for evaluation, methods for evaluation, and using evaluation to understand and improve the initiative. Part K. Maintaining Quality and Rewarding Accomplishments (Chapters 40 - 41) Chapter 40. Maintaining Quality Performance Chapter 41. Rewarding Accomplishments Contains information on achieving and maintaining quality performance, obtaining and using feedback from clients, arranging celebrations, providing incentives to staff and volunteers, holding awards ceremonies, and honoring colleagues and community champions. Part L. Generating, Managing and Sustaining Financial Resources (Chapters 42 - 44) Chapter 42. Getting Grants and Financial Resources Chapter 43. Managing Finances Chapter 44. Investing in Community Resources Contains information on writing a grant application, planning for financial sustainability, preparing an annual budget, accounting basics, contracting for service and establishing a micro-grants program for your community. Part M. Social Marketing and Institutionalization of the Initiative (Chapters 45 - 46) Chapter 45. Social Marketing of Successful Components of the Initiative Chapter 46. Planning for Long-Term Institutionalization Contains information on conducting a social marketing effort (e.g., promoting awareness, interest and behavior change), and planning for the long-term sustainability of the effort (e.g., becoming a line item in an existing budget). まちづくり参考資料 -

• 雨が降ったら休みたい @ ウィキ - C＃.NET：Linqで配列やリストを簡単に並べ替えor抽出

  https://w.atwiki.jp/kimikage/pages/109.html

  配列やリストの並べ替えや抽出はLinqを使えばお手軽に行えます。 使い方 from [変数名] in [対象のリスト] where [抽出条件] group [変数名] by [グループ条件] into [変数名] orderby [並べ替え条件] [descending/ascending] select [取得する項目] 例：並べ替え using System.Collections.Generic; using System.Linq; using System.Windows.Forms; namespace WindowsFormsApplication4 { public partial class Form1 Form { /// summary /// データ格納用 /// /summary private class CustomST { public int Para1 { get; set; } public string Para2 { get; set; } } /// summary /// コンストラクタ /// /summary public Form1() { InitializeComponent(); // 並べ替え string[] ary = (from st in GetTestData() orderby st.Para1 descending, st.Para2 descending select string.Format("{0} {1}", st.Para1, st.Para2)).ToArray(); MessageBox.Show(string.Join("\n", ary)); } /// summary /// テストデータ作成 /// /summary /// returns テストデータ /returns private List CustomST GetTestData() { List CustomST list = new List CustomST (); list.Add(new CustomST() { Para1 = 1, Para2 = "い" }); list.Add(new CustomST() { Para1 = 3, Para2 = "あ" }); list.Add(new CustomST() { Para1 = 3, Para2 = "う" }); return list; } } } 並べ替え② string[] ary = (from st in GetTestData() orderby st.Para1 descending, st.Para2 descending select string.Format("{0} {1}", st.Para1, st.Para2)).ToArray(); OrderByDescending、ThenByDescendingメソッドとラムダ式を使って下記のようにも書けます。 string[] ary = GetTestData().OrderByDescending(st = st.Para1) .ThenByDescending(st = st.Para2) .Select(st = string.Format("{0} {1}", st.Para1, st.Para2)) .ToArray(); 抽出 string[] ary = (from st in GetTestData() where st.Para1 == 1 select string.Format("{0} {1}", st.Para1, st.Para2)).ToArray(); Whereメソッドとラムダ式を使って下記のようにも書けます。 string[] ary = GetTestData().Where(st = st.Para1 == 1) .Select(st = string.Format("{0} {1}", st.Para1, st.Para2)) .ToArray(); group by string[] ary = (from st1 in GetTestData() group st1 by st1.Para1 into g select (from st2 in g orderby st2.Para2 select string.Format("{0} {1}", st2.Para1, st2.Para2)).First()) .ToArray(); GroupByメソッドとラムダ式を使って下記のようにも書けます。 string[] ary = GetTestData().GroupBy(st = st.Para1) .Select(g = g.OrderBy(st = st.Para2).First()) .Select(st = string.Format("{0} {1}", st.Para1, st.Para2)) .ToArray(); 複数の条件でgroupby string[] ary = GetTestData().GroupBy(st = new { st.Para1, st.Para2 }) .Select(g = g.OrderBy(st = st.Para2).First()) .Select(st = string.Format("{0} {1}", st.Para1, st.Para2)) .ToArray(); SelectMany IEnumerable T に対して、GroupByを行うとIEnumerableの入れ子IEnumerable IEnumerable T の状態になります。 この入れ子の中から必要なレコードを取り出して、IEnumerable T の型に格納したりするときなどに使用します。 using System.Collections.Generic; using System.Linq; using System.Windows.Forms; namespace WindowsFormsApplication4 { public partial class Form1 Form { /// summary /// データ格納用 /// /summary private class CustomST { public int Para1 { get; set; } public int Para2 { get; set; } public string Para3 { get; set; } } /// summary /// コンストラクタ /// /summary public Form1() { InitializeComponent(); string[] ary = GetTestData().GroupBy(st = st.Para1) .SelectMany(g = g.Where(st1 = st1.Para2 == g.Max(st2 = st2.Para2)).ToList()) .Select(st = string.Format("{0} {1} {2}", st.Para1, st.Para2, st.Para3)) .ToArray(); MessageBox.Show(string.Join("\n", ary)); } /// summary /// テストデータ作成 /// /summary /// returns テストデータ /returns private List CustomST GetTestData() { List CustomST list = new List CustomST (); list.Add(new CustomST() { Para1 = 1, Para2 = 1, Para3 = "あ" }); list.Add(new CustomST() { Para1 = 3, Para2 = 2, Para3 = "い" }); list.Add(new CustomST() { Para1 = 3, Para2 = 2, Para3 = "う" }); list.Add(new CustomST() { Para1 = 3, Para2 = 1, Para3 = "え" }); return list; } } } Take 先頭N件だけを取得したい時に使用します。 SqlのTopの機能です。 string[] ary = GetTestData().OrderBy(st = st.Para1) .Take(2) .Select(st = string.Format("{0} {1}", st.Para1, st.Para2)) .ToArray(); Max int maxValue = GetTestData().Max(st = st.Para1) Sum int sumValue = GetTestData().Sum(st = st.Para1); INNER JOIN Table1 Para1 Para2 1 い 3 あ 4 う INNER JOIN Table2 Para1 Para2 1 A 3 B ON Table1.Para1 = Table2.Para1 ↓ Table1 Table2 Para1 Para2 Para1 Para2 1 い 1 A 3 あ 3 B using System.Collections.Generic; using System.Linq; using System.Windows.Forms; namespace WindowsFormsApplication4 { public partial class Form1 Form { /// summary /// データ格納用 /// /summary private class CustomST { public int Para1 { get; set; } public string Para2 { get; set; } } /// summary /// コンストラクタ /// /summary public Form1() { InitializeComponent(); // INNER JOIN string[] ary = (from st1 in GetTestData() join st2 in GetTestData2() on st1.Para1 equals st2.Para1 select string.Format("{0} {1} {2}", st1.Para1, st1.Para2, st2.Para2)) .ToArray(); MessageBox.Show(string.Join("\n", ary)); } /// summary /// テストデータ作成 /// /summary /// returns テストデータ /returns private List CustomST GetTestData() { List CustomST list = new List CustomST (); list.Add(new CustomST() { Para1 = 1, Para2 = "い" }); list.Add(new CustomST() { Para1 = 3, Para2 = "あ" }); list.Add(new CustomST() { Para1 = 4, Para2 = "う" }); return list; } /// summary /// テストデータ作成 /// /summary /// returns テストデータ /returns private List CustomST GetTestData2() { List CustomST list = new List CustomST (); list.Add(new CustomST() { Para1 = 1, Para2 = "A" }); list.Add(new CustomST() { Para1 = 3, Para2 = "B" }); return list; } } } string[] ary = GetTestData().Join(GetTestData2(), st1 = st1.Para1, st2 = st2.Para1, (st1, st2) = new { Para1 = st1.Para1, Para2 = st1.Para2, Para3 = st2.Para2 }) .Select(st = string.Format("{0} {1} {2}", st.Para1, st.Para2, st.Para3)) .ToArray(); GROUP JOIN Table1 Para1 Para2 1 い 3 あ 4 う GROUP JOIN Table2 Para1 Para2 1 A 3 B 3 C ON Table1.Para1 = Table2.Para1 ↓ Table1 Table2 Para1 Para2 Para1 Para2 1 い 1 A 3 あ 3 B 3 C 4 う NULL NULL using System.Collections.Generic; using System.Linq; using System.Windows.Forms; namespace WindowsFormsApplication4 { public partial class Form1 Form { /// summary /// データ格納用 /// /summary private class CustomST { public int Para1 { get; set; } public string Para2 { get; set; } } /// summary /// コンストラクタ /// /summary public Form1() { InitializeComponent(); // GROUP JOIN string[] ary = (from st1 in GetTestData() join st2 in GetTestData2() on st1.Para1 equals st2.Para1 into g select string.Format("{0} {1} {2}", st1.Para1, st1.Para2, string.Join(",", (from st3 in g select st3.Para2) .ToArray()))) .ToArray(); MessageBox.Show(string.Join("\n", ary)); } /// summary /// テストデータ作成 /// /summary /// returns テストデータ /returns private List CustomST GetTestData() { List CustomST list = new List CustomST (); list.Add(new CustomST() { Para1 = 1, Para2 = "い" }); list.Add(new CustomST() { Para1 = 3, Para2 = "あ" }); list.Add(new CustomST() { Para1 = 4, Para2 = "う" }); return list; } /// summary /// テストデータ作成 /// /summary /// returns テストデータ /returns private List CustomST GetTestData2() { List CustomST list = new List CustomST (); list.Add(new CustomST() { Para1 = 1, Para2 = "A" }); list.Add(new CustomST() { Para1 = 3, Para2 = "B" }); list.Add(new CustomST() { Para1 = 3, Para2 = "C" }); return list; } } } string[] ary = GetTestData().GroupJoin(GetTestData2(), st1 = st1.Para1, st2 = st2.Para1, (st1, g) = new { Para1 = st1.Para1, Para2 = st1.Para2, Para3 = string.Join(",", g.Select(st3 = st3.Para2).ToArray()) }) .Select(st = string.Format("{0} {1} {2}", st.Para1, st.Para2, st.Para3)) .ToArray();

• 東方同人CDの歌詞＠Wiki - 12 Red Deception

  https://w.atwiki.jp/touhoukashi/pages/4741.html

  【登録タグ BlazeOut EastNewSound R びびあん ほおずきみたいに紅い魂 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 ); 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• mrfrtech @ ウィキ - Digital Payment In Healthcare Market

  https://w.atwiki.jp/mrfrtech/pages/13.html

  Market Scenario According to Market Research Future, the global digital payment in healthcare market has been segmented based on component, deployment mode, organization size, and region/country. The major factors boosting market growth are increasing internet penetration and the digitalization in the healthcare vertical. Furthermore, there has been a significant increase in the adoption of smartphones, which is driving market growth as smartphone users prefer payment via digital modes. A large number of health insurance providers also prefer digital payments over hard cash payments. This fuels the growth of digital payments in healthcare market. However, concerns regarding data security and dominance of paper-based billing are expected to restrain market growth. Also, the rising number of cyber-attacks is a challenge for the digital payments solution providers. The global Digital Payment in Healthcare Market size will touch USD 9.62 billion at a 22.6% CAGR during the forecast period 2020- 2027, states the latest Market Research Future (MRFR) analysis. Digital payment solutions in healthcare provide an online payment platform which connects payers, providers, and consumers for every healthcare payment transaction. Such solutions are accessible as on the cloud and on-premise. The payee and the payer use electronic modes for sending and receiving money. The payment is done through digital wallets, bank cards, net banking, digital currencies, digital currencies, and contactless and contact payment methods. Request a Free Sample @ https //www.marketresearchfuture.com/sample_request/7977 Competitive Outlook The key players in the global digital payment in healthcare market are Aurus Inc. (US), Aliant Payments (US), Stripe (US), ACI Worldwide, Inc. (US), Global Payments Direct, Inc. (US), First Data Corporation (US), PayPal (US), Worldpay, LLC (UK), Wirecard AG (Germany), Fiserv, Inc. (US), InstaMed (US), BillingTree (US), Change Healthcare (US), Elavon Inc. (US), and Zelis Payments (US) Segmentation By component, the global digital payment in healthcare market has been divided into solutions and services. The solutions segment is expected to have a larger market share while the services segment is projected to register the higher CAGR during the forecast period. Based on deployment mode, the market has been segmented into cloud-based and on-premise. The cloud-based segment is expected to exhibit the higher CAGR during the forecast period due to the increasing adoption of cloud technology globally and technological advancements that offer security and privacy over the cloud. Based on organization size, the market has been segmented into large enterprises and small and medium enterprises (SME). The large enterprises segment is expected to have a greater market size during the review period. Large organizations deploy digital payment methods in healthcare solutions extensively to meet the considerable demand for fast and hassle-free transaction services. Large enterprises adopt on-premise or cloud-based solutions, while SMEs prefer only cloud-based solutions. By region, the global digital payment in healthcare market has been segmented into North America, Europe, Asia-Pacific, and the rest of the world. Regional Analysis The global digital payment in healthcare market has been segmented, by region, into North America, Europe, Asia-Pacific, and the rest of the world. North America was the largest market in 2018 as the US has the maximum number of leading market players. The market in Asia-Pacific is expected to be the fastest-growing during the forecast period of 2019 to 2024. Browse Full Report Details @ https //www.marketresearchfuture.com/reports/digital-payment-healthcare-market-7977 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…. Similar Report** Application Management Services Market By Service-Type (System Integration, Consulting Services, Modernization Services, And Others), By Organization Size, By Deployment, And By End-Users Biometric-as-a-Service Market https //blog.daum.net/mrfr/707 5G Industrial IoT Market https //telegra.ph/5G-Industrial-IoT-Market-Size-Growing-at-Market-Report-Analysis-Share-Revenue-Growth-Rate-Forecast-Overview-2027-Opportunity-Ass-04-01 About Market Research Future Market Research Future (MRFR) has created a niche in the world of market research. It is counted among the top market research companies that offer well-researched and updated market research reports and insights to businesses of all sizes. What sets us apart is our super-responsive team that offers quality work keeping clients abridged of the prospective challenges and opportunities in various markets. Our team is adept in their space as well as patiently listens to every client. The best part is they know their work inside out and possess the expertise to guide the client in the right direction and achieve results on a tight deadline. We are a one-stop solution for all your data research needs. Our team does not believe in the “one size fits all” approach to creating a report that is detailed and concise. We handle 13 industry verticals including Healthcare, Chemicals and Materials, Information and Communications Technology, Semiconductor and Electronics, Energy and Power, Food, Beverages Nutrition, Automobile, Consumer and Retail, Aerospace and Defense, Industrial Automation and Equipment, Packaging Transport, Construction, and Agriculture. With our unique approach for every market report, we aim to reach the zenith in qualitative business intelligence and syndicated market research. 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 #market #research #industry #data #growth #trend #report #analyis #share #marketing #forecast #digital #geographic #demographic #gnews Plugin Error キーワードを入力してください。 #tech #researchreport #marketreport #futrue

• Star Wars Galaxies 日本語化 wiki - expertise_d.stf

  https://w.atwiki.jp/swgstring/pages/126.html

  タグ　翻訳待ち 1 empty_description Click on an expertise icon to get started. Left-click to add points, right-click to remove them. Click Train when done. 2 expertise_bh_absorbtion_1 Increase Kinetic protection. 3 expertise_bh_absorbtion_2 Increase Kinetic protection. 4 expertise_bh_absorbtion_3 Increase Kinetic protection. 5 expertise_bh_absorbtion_4 Increase Kinetic protection. 6 expertise_bh_agility_1 Increased Agility 7 expertise_bh_agility_2 Increased Agility 8 expertise_bh_agility_3 Increased Agility 9 expertise_bh_agility_4 Increased Agility 10 expertise_bh_amb_act_1 Reduce action cost of Ambush special attacks. 11 expertise_bh_amb_act_2 Reduce action cost of Ambush special attacks. 12 expertise_bh_amb_act_3 Reduce action cost of Ambush special attacks. 13 expertise_bh_amb_act_4 Reduce action cost of Ambush special attacks. 14 expertise_bh_amb_cool_1 Reduce cooldown time of Ambush specials. 15 expertise_bh_amb_cool_2 Reduce cooldown time of Ambush specials. 16 expertise_bh_amb_cool_3 Reduce cooldown time of Ambush specials. 17 expertise_bh_amb_cool_4 Reduce cooldown time of Ambush specials. 18 expertise_bh_amb_dam_1 Increase damage of Ambush specials. 19 expertise_bh_amb_dam_2 Increase damage of Ambush specials. 20 expertise_bh_amb_dam_3 Increase damage of Ambush specials. 21 expertise_bh_armor_duelist_1 Energy protection and defense versus ranged attacks increased while active. 22 expertise_bh_armor_eng_1 Increased Energy protection when all vulnerable areas are equipped with Assault Armor. 23 expertise_bh_armor_eng_2 Increased Energy protection when all vulnerable areas are equipped with Assault Armor. 24 expertise_bh_armor_eng_3 Increased Energy protection when all vulnerable areas are equipped with Assault Armor. 25 expertise_bh_armor_eng_4 Increased Energy protection when all vulnerable areas are equipped with Assault Armor. 26 expertise_bh_armor_kin_1 Increased Kinetic protection when all vulnerable areas are equipped with Assault Armor. 27 expertise_bh_armor_kin_2 Increased Kinetic protection when all vulnerable areas are equipped with Assault Armor. 28 expertise_bh_armor_kin_3 Increased Kinetic protection when all vulnerable areas are equipped with Assault Armor. 29 expertise_bh_armor_kin_4 Increased Kinetic protection when all vulnerable areas are equipped with Assault Armor. 30 expertise_bh_armor_mgb_1 Increased defense against melee attack when all vulnerable areas are equipped with Assault Armor. 31 expertise_bh_armor_mgb_2 Increased defense against melee attack when all vulnerable areas are equipped with Assault Armor. 32 expertise_bh_armor_mgb_3 Increased defense against melee attack when all vulnerable areas are equipped with Assault Armor. 33 expertise_bh_armor_mgb_4 Increased defense against melee attack when all vulnerable areas are equipped with Assault Armor. 34 expertise_bh_armor_rgb_1 Increased defense against ranged attack when all vulnerable areas are equipped with Assault Armor. 35 expertise_bh_armor_rgb_2 Increased defense against ranged attack when all vulnerable areas are equipped with Assault Armor. 36 expertise_bh_armor_rgb_3 Increased defense against ranged attack when all vulnerable areas are equipped with Assault Armor. 37 expertise_bh_armor_rgb_4 Increased defense against ranged attack when all vulnerable areas are equipped with Assault Armor. 38 expertise_bh_armor_sprint_1 Increase run speed. Requires that all vulnerable areas are equipped with Assault Armor. 39 expertise_bh_ass_act_1 Reduce action cost of Assault special attacks. 40 expertise_bh_ass_act_2 Reduce action cost of Assault special attacks. 41 expertise_bh_ass_act_3 Reduce action cost of Assault special attacks. 42 expertise_bh_ass_act_4 Reduce action cost of Assault special attacks. 43 expertise_bh_ass_cool_1 Reduce cooldown time of Assault specials. 44 expertise_bh_ass_cool_2 Reduce cooldown time of Assault specials. 45 expertise_bh_ass_cool_3 Reduce cooldown time of Assault specials. 46 expertise_bh_ass_cool_4 Reduce cooldown time of Assault specials. 47 expertise_bh_ass_dam_1 Increase damage of Assault specials. 48 expertise_bh_ass_dam_2 Increase damage of Assault specials. 49 expertise_bh_ass_dam_3 Increase damage of Assault specials. 50 expertise_bh_carbine_act_1 Reduced action cost while using Carbines. 51 expertise_bh_carbine_act_2 Reduced action cost while using Carbines. 52 expertise_bh_carbine_act_3 Reduced action cost while using Carbines. 53 expertise_bh_carbine_act_4 Reduced action cost while using Carbines. 54 expertise_bh_carbine_crit_1 Critical hit bonus while using Carbines. 55 expertise_bh_carbine_dam_1 Increase damage while using Carbines. 56 expertise_bh_carbine_dam_2 Increase damage while using Carbines. 57 expertise_bh_carbine_dam_3 Increase damage while using Carbines. 58 expertise_bh_carbine_dam_4 Increase damage while using Carbines. 59 expertise_bh_constitution_1 Increased Constitution 60 expertise_bh_constitution_2 Increased Constitution 61 expertise_bh_constitution_3 Increased Constitution 62 expertise_bh_constitution_4 Increased Constitution 63 expertise_bh_cover_1 Substantial increase in defense versus ranged attacks. Requires the prone position. 64 expertise_bh_deflection_1 Increase Energy protection. 65 expertise_bh_deflection_2 Increase Energy protection. 66 expertise_bh_deflection_3 Increase Energy protection. 67 expertise_bh_deflection_4 Increase Energy protection. 68 expertise_bh_dread_strike_1 Reduces opponents damage output. 69 expertise_bh_fumble_1 Causes opponents to be more likely to make ineffective attacks but also more likely to attack you rather then others. 70 expertise_bh_innate_1 Chance for a Free Shot, reducing Assault special action cost to zero. 71 expertise_bh_intimidate_1 Attack against opponent s action pool. 72 expertise_bh_man_crit_1 Critical hit bonus versus humanoids. 73 expertise_bh_man_crit_2 Critical hit bonus versus humanoids. 74 expertise_bh_man_crit_3 Critical hit bonus versus humanoids. 75 expertise_bh_man_crit_4 Critical hit bonus versus humanoids. 76 expertise_bh_precision_1 Increased Precision 77 expertise_bh_precision_2 Increased Precision 78 expertise_bh_precision_3 Increased Precision 79 expertise_bh_precision_4 Increased Precision 80 expertise_bh_relentless_1 All action costs are dramatically reduced or eliminated while active. 81 expertise_bh_return_fire_1 Automatically retaliate against attacks made against you while Return Fire is active. 82 expertise_bh_rifle_act_1 Reduced action cost while using rifles. 83 expertise_bh_rifle_act_2 Reduced action cost while using rifles. 84 expertise_bh_rifle_act_3 Reduced action cost while using rifles. 85 expertise_bh_rifle_act_4 Reduced action cost while using rifles. 86 expertise_bh_rifle_dam_1 Increase damage while using Rifles. 87 expertise_bh_rifle_dam_2 Increase damage while using Rifles. 88 expertise_bh_rifle_dam_3 Increase damage while using Rifles. 89 expertise_bh_rifle_dam_4 Increase damage while using Rifles. 90 expertise_bh_shields_1 Dramatically increase Kinetic and Energy protection and chance to avoid incoming attacks. 91 expertise_bh_sniper_1 High damage attack made from the prone position. 92 expertise_bh_stamina_1 Increased Stamina. 93 expertise_bh_stamina_2 Increased Stamina. 94 expertise_bh_stamina_3 Increased Stamina. 95 expertise_bh_stamina_4 Increased Stamina. 96 expertise_bh_stun_1 Briefly knocks opponent senseless, leaving them unable to move or attack effectively. 97 expertise_bh_surprise_1 Extended line of Ambush special attacks. 98 expertise_bh_taunt_1 An attack intended to goad your opponent into attacking you while leaving others alone. 99 expertise_bh_trap_dam_1 Increase damage of Maim, Razor Net and Tangle Bomb special attacks. 100 expertise_bh_trap_dam_2 Increase damage of Maim, Razor Net and Tangle Bomb special attacks. 101 expertise_bh_trap_dam_3 Increase damage of Maim, Razor Net and Tangle Bomb special attacks. 102 expertise_bh_trap_dam_4 Increase damage of Maim, Razor Net and Tangle Bomb special attacks. 103 expertise_bh_trap_duration_1 Increase snare duration of Maim, Razor Net and Tangle Bomb effects. 104 expertise_bh_trap_duration_2 Increase snare duration of Maim, Razor Net and Tangle Bomb effects. 105 expertise_bh_trap_duration_3 Increase snare duration of Maim, Razor Net and Tangle Bomb effects. 106 expertise_bh_trap_duration_4 Increase snare duration of Maim, Razor Net and Tangle Bomb effects. 107 expertise_bh_trap_rng_1 Increase radius Razor Net and Tangle Bomb effects. 108 expertise_bh_trap_rng_2 Increase radius Razor Net and Tangle Bomb effects. 109 expertise_bh_trap_rng_3 Increase radius Razor Net and Tangle Bomb effects. 110 expertise_bh_trap_rng_4 Increase radius Razor Net and Tangle Bomb effects. 135 expertise_tree_beastmaster Beast Mastery 134 expertise_tree_beastmastery Beast Mastery 111 expertise_tree_bh_general Bounty Specialization 112 expertise_tree_bh_path Bounty Hunting 113 expertise_tree_co_general Commando assault expertise trees 114 expertise_tree_co_path Commando expertise trees 132 expertise_tree_en_general Drama Specialization 133 expertise_tree_en_path Artiste Specialization 115 expertise_tree_fs_general Force Sensitive trees for acquiring general abilities. 116 expertise_tree_fs_path Light and Dark side paths and their respective abilities. 126 expertise_tree_me_general Field Survival 125 expertise_tree_me_path Medic Specialization 117 expertise_tree_of_general Officer Specialization 118 expertise_tree_of_path Squad Command 119 expertise_tree_sm_general 120 expertise_tree_sm_path 123 expertise_tree_sp_general Spy Specialization 124 expertise_tree_sp_path Covert Operative Specialization 127 expertise_tree_trader_domestic A Domestic Trader crafts with the two sub-professions Chef and Tailor. 130 expertise_tree_trader_engineer An Engineer Trader crafts with the two sub-professions Droids and Weaponsmith. 131 expertise_tree_trader_general The general tree applies expertise to collection and manufacturing of goods for all trade skills. 128 expertise_tree_trader_munition A Munition Trader crafts with the two sub-professions Weaponsmith and Armorsmith. 129 expertise_tree_trader_structure A Structure Trader crafts with the two sub-professions Architect and Shipwright. 121 sui_expertise_introduction_body Expertise points are spent to customize your character and allow specialization in a number of areas. One expertise point is gained every two levels (after level 10). You may spend these points at any time or save them as you like. Click on the Expertise button in the Main Menu to spend your Expertise points. Once you have allocated your points into desired Expertise, click on the Train button to purchase those expertise abilities and skills. Be very sure that these are expertise you want as the only way to un-train expertise is to visit a Profession Counselor to reset your expertise. 122 sui_expertise_introduction_title You ve Earned Expertise Points!