Podcasts about cnvs

Thank you Liz "Smarty Pants" Mouw, OMS IV developing this podcast. This podcast is focused describing how the growing understanding of genetics has led to changes in how developmental disorders might be addressed. This podcast looks at neurodevelopmental disorders and syndromic disorders. There is a focus on CNVs in particular. This podcast has a great deal of descriptive language to introduce the topic to those that may be less familiar with the content. We enjoyed our discussion and hope you do too! Thank you to the immortal Jordan Turner for creating the perfect bumper music!

🟧チャンネル登録・高評価、よろしくお願いします！ ✅番組時間：40分13秒 ✅出演： ジャーマネ・tsZ・さゆ・Bros.・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： フリートーク ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦OP MUSIC ardent by aqua Celsius https://soundcloud.com/team-amx/ardent 🟦ED MUSIC my eternal love -オワラナイアイノウタ- by marshmallow pink https://www.youtube.com/watch?v=aLyHgPE8rL8 🟦CLOSING MUSIC 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年07月27日配信 #ラジオ #webラジオ #IOSYS #イオシス

2024/11/17 ぬるぽ放送局20周年記念トークライブ 来場予約受付中！ https://www.loft-prj.co.jp/schedule/naked/288081 ぬるぽ放送局投稿フォーム https://docs.google.com/forms/d/e/1FAIpQLScwYSAEyRhDCHd-JRk9dLA05JKnGINgvnDhY3Xmkw2lwwDjQw/viewform 2024年7月パワープレイ 「Garnet」 作編曲：CANVAS feat.Quimar 音楽ジャンル：Latin House 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 番組時間：53分14秒 出演者：夕野ヨシミ、たくや VOICEVOX:ずんだもん VOICEVOX:四国めたん ---- 2024/7/25に公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・世界まる見え！テレビ特捜部 ・めっちゃ噛んだ ・懐かしのテレビ番組 ・お中元スパチャありがとうございます ・本日は2本撮りです ・お盆は何をするんですか？ ＜Aパート＞ ・ふつおたです ・ヒメウズラの話 ・育てるときの注意点 ・ヒメウズラの配信楽しみです ・名前は決まりましたか？ ・隔離用の籠が必要？ ・ダンゴムシの名前を半角英数字6文字以内で募集してたことある ・MOCさん最近卵産んだんだよね ・昨日は土用の丑の日 ・意外と喉に詰まる麺類 ・越後屋さんの本業は何？ ・子育てがんばってください ・我が家もオイシックス始めました ・この番組、新規流入あるんだ… ・「プロモーションを含む」ボタンを押す準備はできてます ・ピーマンをジュワっとしたもの ・ピーマンは大事 ・ご飯がおいしくて太っちゃった ・アバターはスリムです ・忙しい指数は93です ・足の攣りの痛みが2日も続くってことあります？ ＜Bパート＞ ・男は黙って六甲のおいしい水 ・山形は雨が降ってます ・コミケ塩 ・醤油も飲んでもらって ・醤油に塩を入れてグイっと ・みつをたです ・Wi-Fiも夏バテ ・24日にウナギを食べる余裕はない ・ウグイス嬢のルックスもほどほどです ・満点はマンボです ・2000年のコントCDでしたか ・2本撮りなのでこの辺で ＜エンディング＞ ・スピニングバードキック・・・ ・ブルアカの曲3曲出てます ・夕野ヨシミ仕事してるね ・​​伊原木(いばらぎ)ヨシミ ・ネギの輪っか ・チルノのパーフェクトさんすう教室（YouTube版）⑨００万再生超えたー！！ ・900万踏んだ人はteacup掲示板に書きこんどいてください ・シンガポール行ける人は行ってください ・いかがでしょうか？ ・ドライTシャツの色は何色がいいですか？ ・高いからミックスカラーは無しだな ・全部混ぜてどどめ色にします

出演者： miko、quim 配信ペース： 隔週水曜日 番組時間：98分35秒 ♯本番組はリモート収録です。 ♯収録時環境の影響により、全体的に聴き取り辛くなっております。 　申し訳ございません。 mikoラジ、第351回です。 火曜夜収録！　お待たせしてごめんなさい！ 相変わらず忙しそうなおふたり、と思いきや……？ 最近のチーム我等の日常、そして突如始まるお勉強？ 話題はあちらからこちらへ、老舗のお家ラジオをご堪能くださいませ！ ♯途中で色々とノイズ等入りますが、収録時のものです。 　ご安心ください、お手持ちの機器は正常です。 //////////////////// VOICEVOX:ずんだもん VOICEVOX:四国めたん //////////////////// -------------------- ●お便り募集中！ mikoラジでは以下の内容でお便りを募集中です！ ・ふつおた 　／普通のお便り、お待ちしています！ ・mikoは大変な絵を描いていきました 　／miko画伯に描いて欲しいお題をお待ちしています！ ・メシヲコエテ 　／料理人・mikoに教えて欲しいレシピをお待ちしています！ https://bit.ly/2GAWjyv 投稿フォームからラジオに投稿が出来ます！ コーナー名を選び、メッセージ・ラジオネーム・お所を入力して、 どんどん送ってください！　お待ちしています！！ ------------ 本ラジオのメインパーソナリティーである「チーム我等(miko/quim)」、 それぞれ以下個人サークルにて活動中です。 ・miko：miko ・quim：SHIGANAI RECORDS（ https://shiganai.com/ ） 活動詳細については、上記HPの他 各人のブログ/twitter等にて随時告知しておりますので、チェックしてみてください！ ・みころぐ。(mikoのブログ)（ https://ameblo.jp/miko-nyu/ ） ・@ mikonyu(mikoのtwitter)（ https://twitter.com/mikonyu ） ・@ quim(quimのtwitter)（ https://twitter.com/quim ） --- その他の活動については、以下のとおりです！ -- チーム我等がメインクルーとして活動していた「アルバトロシクス（ albatrosicks.com/ ）」、 これまでリリースしたCDは、イオシスショップ（ https://iosys.booth.pm/ ）にて頒布しております。ご興味ある方は是非！ ---------- ☆2024年7月IOSYSはいてない.comパワープレイ楽曲 M03. Garnet 作編曲：CANVAS feat.Quimär 音楽ジャンル：Latin House 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003

🟧チャンネル登録・高評価、よろしくお願いします！ ✅番組時間：83分26秒 ✅出演： ジャーマネ・tsZ・さゆ・Bros.・ぴぃ・アサミ閣下 ✅ゲスト：キールさん・蛇草千尋さん 🟧キールさん Twitch 　　https://www.twitch.tv/lycee637 🟧蛇草千尋さん YouTube 　　https://www.youtube.com/channel/UCHW49xuPgxEtTVKob5Hefqw 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： クイズコーナー ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦OP MUSIC ardent by aqua Celsius https://soundcloud.com/team-amx/ardent 🟦ED MUSIC my eternal love -オワラナイアイノウタ- by marshmallow pink https://www.youtube.com/watch?v=aLyHgPE8rL8 🟦CLOSING MUSIC 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年07月20日配信 #ラジオ #webラジオ #IOSYS #イオシス

2024/11/17 ぬるぽ放送局20周年記念トークライブ 来場予約受付中！ https://www.loft-prj.co.jp/schedule/naked/288081 ぬるぽ放送局投稿フォーム https://docs.google.com/forms/d/e/1FAIpQLScwYSAEyRhDCHd-JRk9dLA05JKnGINgvnDhY3Xmkw2lwwDjQw/viewform 2024年7月パワープレイ 「Garnet」 作編曲：CANVAS feat.Quimar 音楽ジャンル：Latin House 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 番組時間：96分49秒 出演者：夕野ヨシミ、たくや VOICEVOX:ずんだもん VOICEVOX:四国めたん ---- 2024/7/18に公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・開運なんでも鑑定団イオシス ・なんで開運するんですか？ ・閉運 ・この世のすべてを鑑定し終わったのでは？ ・お大事になすってください ＜Aパート＞ ・ふつおたです ・デレステに「あの子が街に来なサンタ」実装 ・真夏ですけどサンタ来ちゃったね ・デレステやっといてください ・バグと魔法使い ・もちろん18禁とは ・背景は津田沼です ・飲食店無くなっちゃったね… ・駐車で戸惑うスバルさん ・飲酒運転ですか？ ・子供をディズニーに連れていきたい ・３歳までなら入園料がいらない ・シーはお酒飲める ・香港ディズニー ・金はめちゃくちゃかかる ・セブンの味付けに近い ・市中引き回しのほうの市中 ・ちょっと高いいい調味料がいい ・安い納豆がおいしくなかった ・びしゃびしゃならなんでもいい ・納豆農家さん食べていけるのかな？ ・パック農家さんも ・昔のイオシスのコントCDみたい ・初老の飲み会の話 ・ホテルの値上げがひどい ・平岸はそこまで下じゃない ・趣味トークライブはヤバい ・はかせ「ランサムウェアですー」 ・平岸は家賃が安くていい ・東京に家を借りた方がコスパがいい ・自宅をチェックアウト ・百合子さんどうっすか？ ・QUOカード付きプランの話はやめなさい ・​​わーい、パワープレーだーたのしみー ＜Bパート＞ ・ギターが弾けたらいいな ・だいたい挫折しますよね ・雲丹屋の動画をご覧ください ・ドラムも大変 ・雲丹屋（2009年） ・ハンバーグ師匠こども生まれたってよ ・みつをたです ・あと1.2万プレミアムポイント ・しっかり飛行機乗りに ・日本ヘリコプター輸送 ・プレミアムクラスの空席待ちは負けがち ・審査だけのつもりがアメックスのカードが届きます ・しどろもどろの同意 ・残念な生き物辞典の人間編 ・都知事が誰でもいいじゃない　住む予定ないんだから　みつを ・オセロを１人二役は悲しい ・五目並べRTA ・ちょうどいい下手さがいい ・マッドアイランドで人気になりとうなかった… ・ネコミミ生やしたおじさんだもの ・なんでドナルド関西弁なの ・すぐTシャツになってたね ・アイムシック ・ゲーム１日１時間 ・明けない梅雨はない　そもそも梅雨がない ・これ、縦読みになってる？ ・モックロスとは ・そろそろバブル来ちゃうのでは？ ・CDMA1 ・あんなとこに来るんだなバドガール ・菊陽町の土地いかがですか？ ・オオタニサンの家にヒカキンさんが住まないかな？ ・​​帰ってきたWinamp ・午後のこ～だもどこかで生きている ・謎うなぎ丼 ・カップめしでやんなくても ・うなぎのいとこ ・焼くのに40分かかるポークチャップ ・日本３大松原 ・ショート動画が誕生する前のショート動画があるイオシス ・時代の先に行き過ぎるイオシス ・はじまらずにおわるチルノのパーフェクトさんすう教室 ・ヒメウズラの話 ・たまご購入しました ・予定孵化日は7/29 ・新しいチャンネルを作ろうかと ・横浜に連れてきちゃう？ ・特別メニューってこと？ ・たまごかけごはん作っちゃう？ ・ネーミングライツしますか ・そんなわけでヒメウズラはじめました ＜エンディング＞ ・お知らせです ・七海Nana7miさんに楽曲提供しました！ ・john=hive(IOSYS) ・なんでジョンなのか ・ブルーアーカイブ中国語版の1周年記念曲の作詞を担当させて頂きました！8月3日に公開予定です！ ・きみ中国語うまいね ・明日コバヤシ会あります ・チルパの900万再生がもうすぐ ・1日1万再生されてるの？ ・ドラクエ１は3回でおわっちゃう ・あの人シンガポール好きだよね ・ケツがもげそうでもげない7時間 ・アメリカは取れます

🟧チャンネル登録・高評価、よろしくお願いします！ ✅番組時間：43分44秒 ✅出演： ジャーマネ・tsZ・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： 脳内グランドスラム「残念ながら連れていけなかったポケモンを教えてください」 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦OP MUSIC ardent by aqua Celsius https://soundcloud.com/team-amx/ardent 🟦ED MUSIC my eternal love -オワラナイアイノウタ- by marshmallow pink https://www.youtube.com/watch?v=aLyHgPE8rL8 🟦CLOSING MUSIC 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年07月13日配信 #ラジオ #webラジオ #IOSYS #イオシス

2024/11/17 ぬるぽ放送局20周年記念トークライブ 来場予約受付中！ https://www.loft-prj.co.jp/schedule/naked/288081 ぬるぽ放送局投稿フォーム https://docs.google.com/forms/d/e/1FAIpQLScwYSAEyRhDCHd-JRk9dLA05JKnGINgvnDhY3Xmkw2lwwDjQw/viewform 2024年7月パワープレイ 「Garnet」 作編曲：CANVAS feat.Quimar 音楽ジャンル：Latin House 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 番組時間：96分1秒 出演者：夕野ヨシミ、たくや VOICEVOX:ずんだもん VOICEVOX:四国めたん ---- 2024/7/11に公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・象印クイズ ヒントでピント ・素数回ですね ・983は166番目の素数 ・魔法瓶をプレゼント ・素数も割ろうと思えば割れるのでは？ ・なんだよ素数かよ ・数字も文字も大好き ・脳の稼働の10％は使ってますからね ＜Aパート＞ ・ふつおたです ・新しいCM流れましたね ・忙しいアピールは大事 ・関係者に監視されている ・忙しい指数は85 ・来週100になっちゃう？？？？ ・農家は暇でアルバイトに行ってます ・5万箱の切り花 ・ゲームを１日１時間くらいやりてーな ・ソウルでライブあるよー ・花き市場の朝ははやい ・花卉(かき) ・夕野シキミ ・ただのうざいおじさんになってる ・モッコク科 ・パクリじゃなくてアンサーソング ・逃げ上手の若君 ・時行くんのメス顔 ・たくや旅行記の感想 ・チキン南蛮発祥の地問題 ・おぐらのチキン南蛮美味しかった ・兀突骨 ・呂布vsテリーマン ・すみぺが言うなら間違いない ・ラテンにハウスがあるんですね ＜Bパート＞ ・みつをたです ・梅雨ってなんだっけ？ ・落ち着きがない梅雨前線 ・地理が弱すぎるヨシミだった ・パーフェクト地理教室 ・匿名みつをた流行ってるね ・憲兵さんもショタいかがですか？ ・キャラの名前が覚えられない ・ゆりこなんで関西弁なんだよ ・１２億の豪邸売ったったわ ・安全な場所がない ・例の豪邸になっちゃう ・さっきのところカットで ・もうすぐパリオリンピック ・逃げる場所が東京湾しかない ・百葉箱の置いてるところが涼しい ・n葉箱 ・頭につける日傘 ・イオシスショップ送料一律500円ありがとう ・ご相談がある雰囲気 ・キャラバンという言葉は高橋名人のためにあった ・北は手稲区から南は南口まで ・写真を見ますか ・できたてほかほかのあやしいところ ・ンーキそば ・白いマグロ ・沖縄から南大東へ ・クレーンで上陸 ・星野洞 ・わぁーマイクラみたい ・おすすめなので是非行ってください ・シュガートレイン ・大東そばと大東寿司 ・お土産屋さんがない ・詳しくはwikiをご覧ください ・途中からサインペンになってない？ ・サビサビぐっちゃぐちゃ ・拷問器具ではない ・マッドアイランド感 ・タイムカプセルの開封が来年 ・途中で折れちゃう風力発電 ・上に北大東が… ・儲ける人はがんばるんだねぇ ＜エンディング＞ ・お知らせです ・高橋名人伝説 - 魂の16連射 -完売しました ・超天体ぴろりろりんオリジナルソングの作詞提供しました！ ・19日コバヤシ会あります ・酔っぱらって世界記録出しましょう ・だいたいそんな感じです ・23時なるからおわろう

🟧チャンネル登録・高評価、よろしくお願いします！ ✅番組時間：49分47秒 ✅出演： ジャーマネ・tsZ・あくる・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： おたよりCLIMAX 新紙幣の話 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦OP MUSIC ardent by aqua Celsius https://soundcloud.com/team-amx/ardent 🟦ED MUSIC my eternal love -オワラナイアイノウタ- by marshmallow pink https://www.youtube.com/watch?v=aLyHgPE8rL8 🟦CLOSING MUSIC 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年07月06日配信 #ラジオ #webラジオ #IOSYS #イオシス

2024/11/17 ぬるぽ放送局20周年記念トークライブ 来場予約受付中！ https://www.loft-prj.co.jp/schedule/naked/288081 ぬるぽ放送局投稿フォーム https://docs.google.com/forms/d/e/1FAIpQLScwYSAEyRhDCHd-JRk9dLA05JKnGINgvnDhY3Xmkw2lwwDjQw/viewform 2024年7月パワープレイ 「Garnet」 作編曲：CANVAS feat.Quimar 音楽ジャンル：Latin House 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 番組時間：101分23秒 出演者：夕野ヨシミ、たくや VOICEVOX:ずんだもん VOICEVOX:四国めたん ---- 2024/7/4に公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・新婚さんいらっしゃーい！ ・いまなら99％OFF ・１週間があっという間 ・先週のぬるぽ面白かったなー ・あんなにいっぱいみつをたを読んではいけない ・マッドアイランド2400再生 ・子づくりしたい人がたくさん見てくれてる ・今週の伏線回収しちゃったね ・やっぱりえっちなのがいいのかね ・今月は地味なゲーム月間 ＜Aパート＞ ・ぬるぽ放送局20周年記念トークライブのチケットの予約が始まりました https://www.loft-prj.co.jp/schedule/naked/288081 ・場所は横浜です阿佐ヶ谷ではありません ・KOTOKOさんのラジオと同じくらい ・and more… はいない予定です ・MOCさんの写真をちゃんと撮ろう ・男子は写真撮らない ・犬が遺影なのはありなのか ・遺影だけにダブルピース ・アー写は2500ピクセル欲しい ・夕野ヨシミのアバターが新しくなりました ・ぬるぽ老人会カルタ ・できれば予約お願いします ・ロトの子孫も安心 ・ふつおたです ・サティスファクトリー買いました ・セール中にみんなに買ってほしい ・農家の人が暇な時期にやろうと思います ・サクナヒメで見たよ ・アスパラは別のものを植えない ・結局暇だから何か畑で育てがち ・余った畑で作った3Dモデル ・はかせの「ちょっと待てぃ!!ボタン」 ・当時のはかせはサラリーマン ・４人いるから麻雀できる ・第１回出演者は女性比率が多い ・恥ずかしいくらいでちょうどいい ・最近のアズレン ・ロリとかメスガキが多いのでは？ ・眼帯付けてみるか ・アズレンはだいたいロリか巨乳 ・１月にいただいたお便りです ・ホロメン紹介 ・ウーバーござる ・ピンクコヨーテ ・スイコパス ・最近マリオ1流行ってる ・下手過ぎるとハラハラしない ・無限１UPのために3-1に行ってるわけではない ・当時の女子はゲームをやってなかった ・女子はなにをやってたのか ・やっぱ麻雀か ・回り将棋は何が面白いのか ・令和に回り将棋 ・おねだり将棋を近々やります ・将棋の駒のカスタマイズ ・将、エキサイティン！ ・擦れた大人になっちゃった ・ディスクが擦り切れるくらいイース ・また、昔の話をやってしまったね ・メモのコピペを忘れちゃったね ・FDをピンセットで引き抜かなきゃいけないのはHB-F1XDの特性 ＜Bパート＞ ・それは製造上の問題なのでは？ ・みつをたです ・イオシス還暦放送局 ・可愛い子なら誰でもいいんだよな　モブみつを ・押収されちまったオデッセイ ・課金騎兵モバマス ・身代金は払うわけにはいかないからね ・デフラグじゃなかったのかー ・キズナアイさんが稼働中 ・５秒でおわるデフラグ ・デフラグの動画をテレビで流している老人ホーム ・OSが立ち上がる前のデフラグ ・作曲にも機材がいるよ ・写真の続きを見ていきます ・JALの傘を見飽きる ・奄美空港から与論空港へ ・自由な感じでターミナルに ・ズッ友荘 ・飛行機が欠航になったメールが ・JALのベテランの安心感 ・フェリーなら40分後に出ます ・地図に書いてあるフェリーターミナルはなんだったのか ・フェリー搭乗の見た目が密入国 ・脱出出来てよかった ・貨物の方がデカい顔してる ・隣と距離近くない？ ・客はついでです ・天気がいい方が旅は楽しい ・withアブラアゲ ・自販機スペースの両脇 ・売店が開いてない ・学校の購買みたいな売店 ・仮眠くらいいいじゃない ・本眠とは ・西（北） ・ポンできるの？ ・レンタル DVD ジャンプ ・色落ちゴーストバスターズ ・4000円儲かったけど30分の移動時間が5時間に ・ビックリするくらいおわらないのでここまで ＜エンディング＞ ・取れ高を求めていないので順調に乗れた方がいい ・お知らせです ・もうすぐ完売アイテムがありますのでイオシスショップご利用ください ・無理やりおわらせたイースⅢ ・イースⅤが見つからない ・イースⅤの情報お待ちしてます ・リミックス提供のお知らせ 「REWIND PLUS」 AQUAPLUS MUSIC REMIX 「夢想歌 (D.watt Remix) / Suara」TVアニメ 「うたわれるもの」 オープニングテーマ ・YouTube IOSYS musicチャンネル 登録者20000人になりました！めでたい！ ・いま！若い海外ネキに人気のMV 【東方MV】メイドやめますか？人間やめますか？【IOSYS】 ・あの狂気のMV ・13年前のMVがなんで流行るねん ・高橋名人伝説のこり２連射 ・MOGRAも15周年 ・韓国からフェリーで帰ってくるのかな ・チルパMVもうすぐ900万再生 ・ウイングベイ小樽行ったことあります？ ・あっという間の2時間でしたね ・すごく有意義でしたね ・今回はまあまあです ・前回は変なテンションでした

出演者： miko、quim 配信ペース： 隔週水曜日 番組時間：110分57秒 ♯本番組はリモート収録です。 ♯収録時環境の影響により、全体的に聴き取り辛くなっております。 　申し訳ございません。 mikoラジ、第350回です。 mikoお（350）回！ RADIO ARIMAXの1コーナーだったmikoラジも、気が付けば350（+いっぱい）回。 そんな記念すべき今回は「大変な絵」と「メシヲコエテ」の豪華二本立て！ 象さんの鼻やキリンさんの首もびっくりな長尺。 最後までごゆるりとお楽しみいただければ幸いです。 ♯途中で色々とノイズ等入りますが、収録時のものです。 　ご安心ください、お手持ちの機器は正常です。 //////////////////// VOICEVOX:ずんだもん VOICEVOX:四国めたん //////////////////// -------------------- ●お便り募集中！ mikoラジでは以下の内容でお便りを募集中です！ ・ふつおた 　／普通のお便り、お待ちしています！ ・mikoは大変な絵を描いていきました 　／miko画伯に描いて欲しいお題をお待ちしています！ ・メシヲコエテ 　／料理人・mikoに教えて欲しいレシピをお待ちしています！ https://bit.ly/2GAWjyv 投稿フォームからラジオに投稿が出来ます！ コーナー名を選び、メッセージ・ラジオネーム・お所を入力して、 どんどん送ってください！　お待ちしています！！ ------------ 本ラジオのメインパーソナリティーである「チーム我等(miko/quim)」、 それぞれ以下個人サークルにて活動中です。 ・miko：miko ・quim：SHIGANAI RECORDS（ https://shiganai.com/ ） 活動詳細については、上記HPの他 各人のブログ/twitter等にて随時告知しておりますので、チェックしてみてください！ ・みころぐ。(mikoのブログ)（ https://ameblo.jp/miko-nyu/ ） ・@ mikonyu(mikoのtwitter)（ https://twitter.com/mikonyu ） ・@ quim(quimのtwitter)（ https://twitter.com/quim ） --- その他の活動については、以下のとおりです！ -- チーム我等がメインクルーとして活動していた「アルバトロシクス（ albatrosicks.com/ ）」、 これまでリリースしたCDは、イオシスショップ（ https://iosys.booth.pm/ ）にて頒布しております。ご興味ある方は是非！ ---------- ☆2024年7月IOSYSはいてない.comパワープレイ楽曲 M03. Garnet 作編曲：CANVAS feat.Quimär 音楽ジャンル：Latin House 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003

🟧アリキラではおしゃべりメンバーを募集しています！ 詳しくはこちら。 https://ja-mane.com/menbo/ ✅番組時間：53分19秒 ✅出演： ジャーマネ・tsZ・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： おたよりネットワーク北海道 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦OP MUSIC ardent by aqua Celsius https://soundcloud.com/team-amx/ardent 🟦ED MUSIC my eternal love -オワラナイアイノウタ- by marshmallow pink https://www.youtube.com/watch?v=aLyHgPE8rL8 🟦CLOSING MUSIC 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年06月29日配信 #ラジオ #webラジオ #IOSYS #イオシス

🟧アリキラではおしゃべりメンバーを募集しています！ 詳しくはこちら。 https://ja-mane.com/menbo/ ✅番組時間：58分11秒 ✅出演： ジャーマネ・tsZ・Bros.・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： 脳内グランドスラム「セクシーアリキラあるある」 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦OP MUSIC ardent by aqua Celsius https://soundcloud.com/team-amx/ardent 🟦ED MUSIC my eternal love -オワラナイアイノウタ- by marshmallow pink https://www.youtube.com/watch?v=aLyHgPE8rL8 🟦CLOSING MUSIC 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年06月22日配信 #ラジオ #webラジオ #IOSYS #イオシス

🟧アリキラではおしゃべりメンバーを募集しています！ 詳しくはこちら。 https://ja-mane.com/menbo/ ✅番組時間：53分26秒 ✅出演： ジャーマネ・tsZ・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： おたよりソリューション 　たれワングランプリ 　アリキラ食堂 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦OP MUSIC ardent by aqua Celsius https://soundcloud.com/team-amx/ardent 🟦ED MUSIC my eternal love -オワラナイアイノウタ- by marshmallow pink https://www.youtube.com/watch?v=aLyHgPE8rL8 🟦CLOSING MUSIC 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年06月15日配信 #ラジオ #webラジオ #IOSYS #イオシス

🟧アリキラではおしゃべりメンバーを募集しています！ 詳しくはこちら。 https://ja-mane.com/menbo/ ✅番組時間：61分24秒 ✅出演： ジャーマネ・tsZ・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： おたよりプラーザ 　モックロスリスナーチャレンジおたより 　エビフライ何かける？ 　ゲームボーイの話 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦OP MUSIC ardent by aqua Celsius https://soundcloud.com/team-amx/ardent 🟦ED MUSIC my eternal love -オワラナイアイノウタ- by marshmallow pink https://www.youtube.com/watch?v=aLyHgPE8rL8 🟦CLOSING MUSIC 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年06月08日配信 #ラジオ #webラジオ #IOSYS #イオシス

🟧アリキラではおしゃべりメンバーを募集しています！ 詳しくはこちら。 https://ja-mane.com/menbo/ ✅番組時間：65分28秒 ✅出演： ジャーマネ・tsZ・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： 脳内グランドスラム「アリキラ運転免許試験2024」 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦OP MUSIC ardent by aqua Celsius https://soundcloud.com/team-amx/ardent 🟦ED MUSIC my eternal love -オワラナイアイノウタ- by marshmallow pink https://www.youtube.com/watch?v=aLyHgPE8rL8 🟦CLOSING MUSIC 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年06月01日配信 #ラジオ #webラジオ #IOSYS #イオシス

ぬるぽ放送局投稿フォーム https://docs.google.com/forms/d/e/1FAIpQLScwYSAEyRhDCHd-JRk9dLA05JKnGINgvnDhY3Xmkw2lwwDjQw/viewform 2024年5月パワープレイ M2. Crystal Breath feat. Sennzai 歌唱：Sennzai 作詞：DD”ナカタ”Metal 作編曲：CANVAS, Quimär Guitar：Quimär 音楽ジャンル：J-POP / Rock 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 番組時間：67分18秒 出演者：夕野ヨシミ、たくや VOICEVOX:ずんだもん VOICEVOX:四国めたん ---- 2024/5/30 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・やってこう！ ・ふぅ… ・前枠の苫小牧dis ＜Aパート＞ ・ふつおたです ・はかせって人いたじゃん ・千葉ロッテの話 ・ファン獲得の冠試合 ・人口が減ってる苫小牧 ・ホッキとか…ホッキとか…ホッキとかあるじゃん ・ドッグスレッド ・苫小牧新名物ラッコ鍋 ・岩倉市長がんばってください ・イオシスは苫小牧市を応援してます ・苫小牧何にもないから来ても楽しくないよ ・DV彼氏みたい ・アマプラに天使にラブソング ・ゆかりんのロリ神レクイエム ・最近The Planet Crafterにハマってるのでオデッセイを ・イオシスロードショーご覧ください ・ICQやっとなくなる ・オイシックスの話 ・料理教室よりお安い ・子犬はとてもきれいです ・オイシックスからお金貰ってるのかな？ ・ロコモコとは ・最近ごはんがおいしい ・年を取ると真人間になっちゃう ・最近起きて朝ごはん食べてる ・早く真人間になりたーい ・忙しくて出かける暇がない ・ヒメウズラは今年買うから ・結果は１週間後 ・北海道の感想 ・ザンギ入りドーナツ ・来年は旭川に行きたい ・東千歳駐屯地には鈴木宗男 ・札幌の観光名物きくお兄ちゃん ・ドラクエの日 ・ドラクエ全部やる ・FFならPCで全部やれる ・９は無理だな ・死ぬまでゲームをするのです ・すぐにけせ ・まだ５月です ＜Bパート＞ ・ういビーム！！ ・みつをたです ・手作業で田植えで農家を目指す人はいるのか ・俺は嫌だ ・残業になるのは陰謀論のせいだ ・ノルベサによるべさ ・それ、白樺の木ですよ ・ジュヒ！！ ・イルミナティの陰謀 ・な、なんだって！？　その他 ・大洗フェリー経由？ ・学マスくん初手でスモックは早いよ ・あさりよしとお先生のあんきら ・S木 ・負けないで欲しいな ・みんな電マ大好きだな ・みつをたは１時間前に集まってくる ・すき家のお冷は水なのかお茶なのか ・スケボーかスケベでしか言わない ・12億の豪邸が安く見えちゃう ・ショムニは復活しない ・都知事選はなんでいつもああなの？ ・カベおたになってるよ ・こうやって１週間をふりかえってるんだな　みつを ・各種お便りお待ちしてます ＜エンディング＞ ・ヨシ！ ・イオシスくんがんばってるねのコーナーです ・「ゆんゆん電波シンドローム」イオシスの東方アレンジ曲が収録されるのよ ・令和６年だぞ！ ・平成のしぼり汁 ・ロリ神レクイエムがDDRに ・「ポラリスコード」に「むしみこうにゃーのハッピッピー」が5/30に収録されました～ ・神01 ・岩手に全員来てください ・ゆっくりK - 最高やんK【オリジナル曲】200万再生突破しました！！！最高やんK～！！！ ・6/9イオパあります ・チルパがいろんなゲームに入り切った ・パンツの流れ ・母乳の海いい曲なんですよ ・５月おわっちゃう ・毎月結婚します

🟧アリキラではおしゃべりメンバーを募集しています！ 詳しくはこちら。 https://ja-mane.com/menbo/ ✅番組時間：60分38秒 ✅出演： ジャーマネ・tsZ・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： リモック生誕祭振り返り2024 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦CLOSING BGM 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年05月26日配信 #ラジオ #webラジオ #IOSYS #イオシス

出演者： miko、quim 配信ペース： 隔週水曜日（収録・編集都合により遅延しております） 番組時間：110分20秒 ♯本番組はリモート収録です。 ♯収録時環境の影響により、全体的に聴き取り辛くなっております。 　申し訳ございません。 ♯収録・編集都合により配信遅延となりました。 　申し訳ございません。 mikoラジ、第347回です。 コスプレカラオケMC会社員……？ 自分達の肩書きって、何だろう？　そんな雑談から現代の読書事情（？）まで。 普通の人はこんなに喋ることが出来るのか？？ 喋り続けて、気が付けば300回オーバーのWebラジオのパーソナリティー。 そんなふたりの自己紹介の悩みから始まるご長寿番組。 今回も最後までごゆるりとお楽しみくださいませ！ ♯途中で色々とノイズ等入りますが、収録時のものです。 　ご安心ください、お手持ちの機器は正常です。 //////////////////// VOICEVOX:ずんだもん VOICEVOX:四国めたん //////////////////// -------------------- ●お便り募集中！ mikoラジでは以下の内容でお便りを募集中です！ ・ふつおた 　／普通のお便り、お待ちしています！ ・mikoは大変な絵を描いていきました 　／miko画伯に描いて欲しいお題をお待ちしています！ ・メシヲコエテ 　／料理人・mikoに教えて欲しいレシピをお待ちしています！ https://bit.ly/2GAWjyv 投稿フォームからラジオに投稿が出来ます！ コーナー名を選び、メッセージ・ラジオネーム・お所を入力して、 どんどん送ってください！　お待ちしています！！ ------------ 本ラジオのメインパーソナリティーである「チーム我等(miko/quim)」、 それぞれ以下個人サークルにて活動中です。 ・miko：miko ・quim：SHIGANAI RECORDS（ https://shiganai.com/ ） 活動詳細については、上記HPの他 各人のブログ/twitter等にて随時告知しておりますので、チェックしてみてください！ ・みころぐ。(mikoのブログ)（ https://ameblo.jp/miko-nyu/ ） ・@ mikonyu(mikoのtwitter)（ https://twitter.com/mikonyu ） ・@ quim(quimのtwitter)（ https://twitter.com/quim ） --- その他の活動については、以下のとおりです！ -- チーム我等がメインクルーとして活動していた「アルバトロシクス（ albatrosicks.com/ ）」、 これまでリリースしたCDは、イオシスショップ（ https://iosys.booth.pm/ ）にて頒布しております。ご興味ある方は是非！ ---------- ☆2024年5月IOSYSはいてない.comパワープレイ楽曲 M2. Crystal Breath feat. Sennzai 歌唱：Sennzai 作詞：DD”ナカタ”Metal 作編曲：CANVAS, Quimar Guitar：Quimar 音楽ジャンル：J-POP / Rock 収録アルバム：CANVAS feat.Quimar / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003

ぬるぽ放送局投稿フォーム https://docs.google.com/forms/d/e/1FAIpQLScwYSAEyRhDCHd-JRk9dLA05JKnGINgvnDhY3Xmkw2lwwDjQw/viewform 2024年5月パワープレイ M2. Crystal Breath feat. Sennzai 歌唱：Sennzai 作詞：DD”ナカタ”Metal 作編曲：CANVAS, Quimär Guitar：Quimär 音楽ジャンル：J-POP / Rock 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 番組時間：80分11秒 出演者：夕野ヨシミ、たくや VOICEVOX:ずんだもん VOICEVOX:四国めたん ---- 2024/5/23 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・何も言ってないのに正解した ・その効果音は何？ ・税率1000％ ・アフターのときに取られたの？ ・シフトレバーにブロッコリー ・ブロッコリーの花蕾 ・揚げ具合でスープカレー屋のやる気がわかる ・オイシックス３年使ったら自炊できるようになる ・ぬるぽ1000回記念のイベントやりますよ ・農家基準のスケジュール ・週3でぬるぽやれば早まるよ！ ・流行りのえっちな服はお嫌いですか？ ・部下もロリコンなのか？ ＜Aパート＞ ・ｵﾜｰ ・ふつおたです ・田植えおわりました ・​​ビギニングオブ田植え ・流行りの田植えお疲れさまでした ・たうえら ・たほいや ・ゴールドジムに行くか行かないか ・家の中でゴミを燃やそう ・まさか焼却炉が出てこないとは ・作詞家が使わない単語ランキング ・幼好炉 ・農機具のGPSがズレた ・磁場が吹いたら休みにしてほしい ・健康診断が無事におわりました ・追加が気になるお年頃 ・ぼくも片玉に欲しい ・いじめてあげてください ・次回、ぬるぽに投稿される腫瘍マーカーの話、乞うご期待 ・あとは弁護士さんがほしい ・和尚元気にしてるかな？ ・バリウムおいしい ・胃カメラが好きかもしれない ・ToHeartの発売日 ・お兄ちゃん ・メイドロボに何をしてほしいか ・ダンボールを片付けるのがめんどくさい ・社員全員メイドロボなら会社行ってもいい ・何でも屋さんは何をしてくれるの？ ・陰謀論を吹き込むのは別料金になります ・準１級陰謀論者 ・はやくメイドロボできないかな ・初音ミクコラボモデルでちゃうな ・北海道旅行の話 ・２人合わせて80年北海道にいますからね ・最近だとエスコン ・布袋のザンギ ・山岡家はどうですか？ ・東千歳バーベキユー ・セコマでかつ丼買って大通公園で食べてください ・美味しくなかったら陰謀論のせいにしてください ＜Bパート＞ ・みつをたです ・フリスビーし放題 ・沖縄ではコンビニ飯 ・親の愚痴を言って許されるのか　みつを ・外が暑くてもいいじゃない　冷たいビールがあるから　みつを ・みすちゃさんかーが早いんだよ！ ・みすちゃさんだったかー ・なんで原液を試したんですか？ ・学マスの子たちは細い子が多い ・砂漠にラクダに逃げられて ・ニュータイプは伊達じゃないな ・​​勝俣州和は漢字で書けない ・アッコさんでも書けない説 ・今日はあぶおた寄り ・あぶなくなったらそくおわり ＜エンディング＞ ・最近はイオシスくんはゲームばっかりやってますね ・D.wattはほとんど家にいないのでは？ ・夕野ヨシミの逆だったかー ・バニーガーデンはsteam版もやった方がいいのかな？ ・雑魚資源 ・気が付いたら朝8時 ・お仕事しながらThe Planet Crafterやってます ・マイクラ以来のドハマリゲー ・えっ？ ・流行るよって言っといたからね ・不便さを楽しむゲーム ・どっちのマルチなのか ・面白いゲームばかりだとお仕事しなくて困っちゃうから ・仕事してる暇がない ・どっちが片手間なのか？

ぬるぽ放送局投稿フォーム https://docs.google.com/forms/d/e/1FAIpQLScwYSAEyRhDCHd-JRk9dLA05JKnGINgvnDhY3Xmkw2lwwDjQw/viewform 2024年5月パワープレイ M2. Crystal Breath feat. Sennzai 歌唱：Sennzai 作詞：DD”ナカタ”Metal 作編曲：CANVAS, Quimär Guitar：Quimär 音楽ジャンル：J-POP / Rock 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 番組時間：92分5秒 出演者：夕野ヨシミ、たくや VOICEVOX:ずんだもん VOICEVOX:四国めたん ---- 2024/5/16 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・今週はAIの発表がすごい ・GPT-4o ・もう、人間の負けです ・再来週にはぬるぽ放送局が生成できる ・余生をすごしたい ・メイドさんロボください ・初期状態にも"っ・・・ ・料理はまだ無理か ・一番成長が遅いチャンネルRTA ・どうやったらチャンネル登録者増えるんですかね？ ・えっちなショート増やしても結局登録者は増えない ・普通のチャンネルは2000本も動画ないもの ・7,8年前にやったゲーム実況を覚えてない ・検索したら自分の動画が出てきちゃう ・音楽の話はあんまりしません ・ただゲームをやりたいだけ ・イオシスはやめない ・再現しようにもICCはもうないんだよな ・ズリ山のぼる？ ・収録始まってましたっけ ・世間に媚びないでやってこう ＜Aパート＞ ・尿管結石を出すRTA ・ふつおたです ・トップガンの日 ・いかがでしたか？ ・知ってたってことにしましょう ・トップガンってどんな映画なの？ ・のりは出ますか？ ・世界三大トム ・気を抜くと毎月トムクルーズ ・イオシスロードショーご覧ください ・AIが作る映画 ・田植えが始まります　ぜひー ・田植えも自動運転 ・今年は伏線回収していくから ・アプリゲームの話 ・ミニ四駆超速グランプリ ・ミニ八駆 ・ブラウザ三国志は15周年 ・学マス ・満を持して小学生を投入 ・ブルアカで忙しい ・ニコニコ御三家とは ・ウマ娘はデータフルダウンロードすると26GBくらい ・日本にあるフロッピーディスク在庫全部 ・ドラクエやりたいなー ・とんでもないネタバレしちゃった ・曜日が足りないから動画にしよう ・まずはイースから ＜Bパート＞ ・フルでかけてみました ・岡山の写真の続きです ・岡山空港の成れの果て ・鳥人幸吉 ・追加製造してくれ ・ののちゃんの町 ・バグってる宇野駅 ・有害図書のみ入れてください ・おやORひな ・手づかみでみそ汁をﾌﾞｼｬｰ ・訴えられないバランス ・美味しいけどすぐなくなっちゃうの ・えびめしとは ・岡山の写真お疲れさまでした ・みつをたです ・みつを数え歌 ・いいですか王国民はしにました ・今はみんなおじさんです ・ラモスになりたかった人はアルシンドになってる ・新しい家が建ちました ・写真集をググっちゃった ・映画のジョジョでは誰も結婚しなかったね ・ワンチャン狙いに行く所ではない ・ないこともない ・​​あるのはフィリピンパブだけだよ ・１週間分のニュースをまとめるみつをた ・ワロス数えうたをかけます ＜エンディング＞ ・小腹がすいたらどうしたらいいの ・そんなときはしこたま食べます ・炭酸水がいい ・これが小浜ルートか ・新幹線は早くていい ・お知らせです ・アルバのベスト盤売り切れました ・ラストライブから７年 ・放棄したドメインは誰かがすぐ持ってちゃう ・チャンネル登録お願いします ・最近、テラフォーミングしたくてしょうがない ・はかせのLINEスタンプ使ってますか？ ・お堅いところは許可が下りてない ・薬を５倍飲もう ・なくなってた病院 ・診療がおざなり ・医者「どうします？」 ・お祓いに行きましょう ・日本が衰退していってる始まりを見ているのでは？ ・さあ、お時間です

🟧アリキラではおしゃべりメンバーを募集しています！ 詳しくはこちら。 https://ja-mane.com/menbo/ ✅番組時間：61分34秒 ✅出演： ジャーマネ・tsZ・あくる・トウカ・とおる・アサミ閣下・MOC 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： 名人によるモックロス2024解答 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦CLOSING BGM 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年05月11日配信 #ラジオ #webラジオ #IOSYS #イオシス

ぬるぽ放送局投稿フォーム https://docs.google.com/forms/d/e/1FAIpQLScwYSAEyRhDCHd-JRk9dLA05JKnGINgvnDhY3Xmkw2lwwDjQw/viewform 2024年5月パワープレイ M2. Crystal Breath feat. Sennzai 歌唱：Sennzai 作詞：DD”ナカタ”Metal 作編曲：CANVAS, Quimär Guitar：Quimär 音楽ジャンル：J-POP / Rock 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 番組時間：98分32秒 出演者：夕野ヨシミ、たくや VOICEVOX:ずんだもん VOICEVOX:四国めたん ---- 2024/5/9 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・NLP　イオシスぬるぽ放送局（紙パンツを履いた気持ちで） ・定着してないNLP ・HVC　ファミコン放送局 ・ゲーム実況の先駆け(2番目 ・ビックカメラの紙袋 ・switchの後継機 ・飛ばし記事ってなんなの？ ・オープニングで大喜利始まった ・木村拓哉の匂い ・象が踏んでも壊れない ・Dummyさんじゃないですか ・虚構ファンボックス ・9インチのでぇ画面 ​​ ＜Aパート＞ ・スパチャありがとうございます ・石原さとみが出てくる夢が見れる ・ふつおたです ・GWの話 ・大洗に行ってきました ・ドラクエⅢの後期ロム ・イースやってるのにドラクエまで？ ・ジーコサッカー全部やる ・バニーガーデンをやってる場合じゃない ・岩おじ ・プロのゲーム実況者におじさんは感心 ・配慮した言い回し ・偏見のコーナー ・日本人のトークのスキルは上がってる？ ・ステラーブレイドの動画が伸びてる ・パンチラがいいわけ？ ・控えめのチラリズムがいい ・その100万人はどこにいたの？ ・ヒカキンさんはパンチラしてないよな ・GWは金ビキニ ・ゴールデンみくにゃん ・シルバーウイークは銀ビキニ ・それなら透明なら ・詳しくはパンティをご覧ください ・明日は透明の日なの？ ・透明の水着とは ・通販に透明ビキニあるってよ ・投稿!特ホウ王国 ・薄毛と白髪が気になる ・スキンヘッドは維持が大変 ・紫色と緑色で乗りなさいシンジくん ・イオシスロードショーの感想 ・寝ずの番 ・特攻大作戦 ・マヤノトップガン？ ・マヤノって何？ ＜Bパート＞ ・アルバム聞いてほしいですよね ・夕野ヨシミの分まで聞いてください ・後ろのクリスタルを壊したくて仕方ない ・ポスター入稿係 ・M3と例大祭の話 ・東横イン水 ・前日設営 ・ラーメン平和家 ・やってなかったので☆１つです ・平日に流通センターに行かない ・有明ガーデン ・がんばれば一口で食べれるくらいのごはん ・東京ってこわいなー ・これはD.wattです ・ずーと英傑大戦の話してた ・D.wattに会いにインドネシアから ・どうなったら草野華余子さんに歌唱してもらえるの？ ・みそ汁こぼしたけど全然大丈夫 ・みつをたです ・暴飲暴食してもいいじゃないGWだもの ・ドリクラでもいいじゃない ・技術的には可能です ・屋内ゴルフ練習場ですか？ ・阿佐ヶ谷ですぐできそう ・健康診断の季節ですね ・いいスコアが出る気がしない ・全部ショタじゃねーか！ ・卒業したのに出てくる木久扇師匠 ・笑点で見るサンドウィッチマンの漫才 ・一番長くやってる山田くん ・聞こえてきたのはデレステですか？ブルアカですか？ ・昔覚えたキャラを忘れちゃう ・年を取ったらウサミンの本名忘れちゃう ・ええんですよじゃないんだよ ・ネコ娘じゃなくてエロ娘じゃないですか ・水色でうさだといえば… ＜エンディング＞ ・お知らせです ・ぬるぽ詰め合わせ16出てます ・新アイテム出てますのでイオシスショップご利用ください ・終売アイテムもありますのでチェックよろしくお願いします ・全部買ってください ・明日はコバヤシ会あります ・沖縄は梅雨の走りかな？ ・カッパの２，３匹捕まえてきます ・河童だからねマーヴェリック ・10月に即売会集まってきたね ・1000回はなんか作れたら作ります ・バニーガーデンRTA ・ミリオン貸し切り ・女の子の飲み物は別料金です ・謎のタックス

出演者： miko、quim 配信ペース： 隔週水曜日 番組時間：77分25秒 ♯本番組はリモート収録です。 ♯収録時環境の影響により、全体的に聴き取り辛くなっております。 　申し訳ございません。 mikoラジ、第346回です。 GW、終わっちゃいましたね……皆さんはどんな連休をお過ごしでしたか？ パーソナリティのふたりも、それぞれの連休を過ごした様子。 そんなふたりの、連休が終わろうとするタイミングでの会話。 どうぞ最後までごゆるりとお楽しみくださいませ。 ♯途中で色々とノイズ等入りますが、収録時のものです。 　ご安心ください、お手持ちの機器は正常です。 //////////////////// VOICEVOX:ずんだもん VOICEVOX:四国めたん //////////////////// -------------------- ●お便り募集中！ mikoラジでは以下の内容でお便りを募集中です！ ・ふつおた 　／普通のお便り、お待ちしています！ ・mikoは大変な絵を描いていきました 　／miko画伯に描いて欲しいお題をお待ちしています！ ・メシヲコエテ 　／料理人・mikoに教えて欲しいレシピをお待ちしています！ https://bit.ly/2GAWjyv 投稿フォームからラジオに投稿が出来ます！ コーナー名を選び、メッセージ・ラジオネーム・お所を入力して、 どんどん送ってください！　お待ちしています！！ ------------ 本ラジオのメインパーソナリティーである「チーム我等(miko/quim)」、 それぞれ以下個人サークルにて活動中です。 ・miko：miko ・quim：SHIGANAI RECORDS（ https://shiganai.com/ ） 活動詳細については、上記HPの他 各人のブログ/twitter等にて随時告知しておりますので、チェックしてみてください！ ・みころぐ。(mikoのブログ)（ https://ameblo.jp/miko-nyu/ ） ・@ mikonyu(mikoのtwitter)（ https://twitter.com/mikonyu ） ・@ quim(quimのtwitter)（ https://twitter.com/quim ） --- その他の活動については、以下のとおりです！ -- チーム我等がメインクルーとして活動していた「アルバトロシクス（ albatrosicks.com/ ）」、 これまでリリースしたCDは、イオシスショップ（ https://iosys.booth.pm/ ）にて頒布しております。ご興味ある方は是非！ ---------- ☆2024年5月IOSYSはいてない.comパワープレイ楽曲 M2. Crystal Breath feat. Sennzai 歌唱：Sennzai 作詞：DD”ナカタ”Metal 作編曲：CANVAS, Quimar Guitar：Quimar 音楽ジャンル：J-POP / Rock 収録アルバム：CANVAS feat.Quimar / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003

🟧アリキラではおしゃべりメンバーを募集しています！ 詳しくはこちら。 https://ja-mane.com/menbo/ ✅番組時間：64分10秒 ✅出演： ジャーマネ・tsZ・トウカ・とおる・さゆ・Bros.・アサミ閣下 2005年にスタートして、ついに700回。 みなさんのおたよりだけが頼りなこの番組。 回替わりレギュラー陣がお送りします。 　 ✅コーナー： フリートーク モックロス2024 出題 ✅パワープレイ： Crystal Breath feat. Sennzai CANVAS feat.Quimär / CRYSTAL BREATH https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 🟧投稿フォームはこちら。 → https://ja-mane.com/form/ ← 🟧投稿テーマや締切など、番組情報はジャーマネ.comからどうぞ。 → https://ja-mane.com ← 🟦音声ソフトウェア VOICEVOX: ずんだもん VOICEVOX: 四国めたん VOICEVOX: WhiteCUL https://voicevox.hiroshiba.jp/ 🟦CLOSING BGM 極東の羊、テレキャスターと踊る by しゃろう https://www.youtube.com/watch?v=qy05MFjNZbE ■2024年05月04日配信 #ラジオ #webラジオ #IOSYS #イオシス

ぬるぽ放送局投稿フォーム https://docs.google.com/forms/d/e/1FAIpQLScwYSAEyRhDCHd-JRk9dLA05JKnGINgvnDhY3Xmkw2lwwDjQw/viewform 2024年5月パワープレイ M2. Crystal Breath feat. Sennzai 歌唱：Sennzai 作詞：DD”ナカタ”Metal 作編曲：CANVAS, Quimär Guitar：Quimär 音楽ジャンル：J-POP / Rock 収録アルバム：CANVAS feat.Quimär / CRYSTAL BREATH Release　2024.4.28 https://notebookrecords.net/discographyportal.php?cdno=CNVS-003 番組時間：37分22秒 出演者：夕野ヨシミ、たくや VOICEVOX:ずんだもん VOICEVOX:四国めたん ---- 2024/4/25 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・2本録りの2本目だよ ・なんとか素数 ・GWですね ・1000回が見えてきちゃってる ・1ドル2500円 ・和製iPhone ・今のうちにドルを買うんじゃー ・​​ちょっと端子ぃ～ ・ヨシミちゃんの端子は何を使ってるんだい？ ・おじさんの端子が入んないのかい？ ＜Aパート＞ ・ふつおたです ・もやしこーひーさんお誕生日おめでとうございます ・初老の話 ・飲みやすくした結果、人を◯す酒に ・夕月Pは初老でもおじさんでもない ・スペシャルカクテル「残尿」 ・参加者の半分が寝てる ・ピアスの穴を開けたら金属アレルギー発覚 ・毎回気になるサザエ家の年齢 ・行けたら行く枠 ・夫婦ともに声優オタク ・ブルアカのアニメ見てください ・2本目なのでパワープレイに行こう ＜Bパート＞ ・いい曲ですね ・みつをたです ・思いついたことは誰かが思いついてる ・喜久子お姉ちゃんは娘が年上になったもんな ・センシティブ過ぎて没にしました ・マジカル頭脳パワーのときはいい人に見えたんだよな ・シャケのベイベー ・このネタが読まれる頃は職場が変わってるんだよな ・宝くじで3等でいいから当たらないかなー ・競馬がよくわからない ・シード固定値でやってたら大変 ＜エンディング＞ ・M3と例大祭委お疲れさまでした ・100万枚持って行っててよかった ・1億グラムってどのくらい？ ・100ｔ？もっこりじゃん ・ブルアカのCDは受注生産やってます ・子作り旅行に行こう

Shop Lunautics festival accessories (discount code EMMAK) - https://bit.ly/3Rf6vQA In this episode, I'm joined by Eric Fuller, the Founder of BLNK CNVS, a prominent event & production company based in South Florida. Eric has had a colorful career in dance music from founding & operating Life in Color (the world's largest paint party) expanding to work with SFX Entertainment to starting multiple companies in the event production space to co-owning Club Space. Today we're diving into what it's like launching live event brands, the behind-the-scenes of preparing for Miami Music Week and tips for networking in our industry! Follow BLNK CNVS: https://www.instagram.com/blnkcnvspresents BLNK CNVS MMW events: https://www.blnkcnvs.com/mmw24 Connect with Rave Culture Cast ➡️ https://beacons.ai/raveculturecast Timestamps: 0:00 Intro 0:46 Lunautics Ad 1:30 Episode introduction 3:30 Eric Fuller's early career 8:48 The expansion of Life in Color 11:45 SFX Entertainment transition 14:30 Miami's music scene 16:50 Eric's involvement in Space Miami 21:36 Miami Music Week planning 25:42 What inspired BLNK CNVS + relationship building 29:50 Networking during MMW 32:29 How to market events during MMW 37:14 Behind-the-scenes of event production 42:05 Influencer marketing in dance music 45:54 How Eric unwinds after MMW 48:28 The future of BLNK CNVS --- Send in a voice message: https://podcasters.spotify.com/pod/show/raveculturepodcast/message Support this podcast: https://podcasters.spotify.com/pod/show/raveculturepodcast/support

In this Papers Podcast, Dr. Sam Chawner discusses his JCPP Advances paper ‘Neurodevelopmental dimensional assessment of young children at high genomic risk of neuropsychiatric conditions' (doi.org/10.1002/jcv2.12162). Sam is the first author of the paper. There is an overview of the paper, methodology, key findings, and implications for practice. Discussion points include: - What are copy-number variants (CNVs) and how they impact child development. - Insight into what 22q11.2 deletion syndrome is, how it is typically diagnosed, and how it is associated with psychiatric risk. - Implications for clinicians and CAMH professionals. - Whether there are adequate interventions targeted at early age groups. - Recommendations for prevention, detection, and the targeting of interventions.

A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, “Copy number variation as a tool for implementing pregnancy as an aging model.” Copy number variations (CNV) are a major contributor to genome variability. CNVs have been linked to aging and other degradable phenotypes such as pregnancy physiology. In this new study, researchers Mariana Andrawus, Lital Sharvit, Noga Touitou, Batia Lerrer, Haim Y. Cohen, and Gil Atzmon from University of Haifa and Bar-Ilan University used CNVs from pregnant mice to demonstrate how pregnancy can be used as a model of aging. “We hypothesize that pregnancy can serve as a model for aging by demonstrating similar biomarkers, pathologies, and genetic and epigenetic effects [3]. To test this hypothesis, we designed a study that assesses CNVs associated with human longevity (unpublished results) in pregnancy.” Candidate CNVs were selected by applying case-control analysis in human centenarians compared with control groups. These CNVs were aligned with the mouse genome and their copy variation was assessed using qRT-PCR in liver and blood tissue samples from pregnant mice throughout pregnancy (baseline; first, second, and third trimester; post-partum). Eight of the ten selected CNVs demonstrated a significant decline/increase trend throughout the pregnancy followed by opposite direction soon after delivery in the liver and blood of the mouse tissues. Furthermore, significant differential expression was detected among the candidate CNVs' close vicinity genes (APA2A, LSS, RBDHF1, PLAAT1, and SCL17A2), but not in the WSCD2 gene. Establishing a genetic link between longevity and pregnancy is a significant step toward implementing the pregnancy process as a model for aging. These results in pregnant mice highlight the mechanism and similarities between pregnancy and aging. “Investigating the mechanisms that cause such rejuvenation after labor could change our aging treatment paradigm.” DOI - https://doi.org/10.18632/aging.204936 Corresponding author - Gil Atzmon - gatzmon@univ.haifa.ac.il Video short - https://www.youtube.com/watch?v=82466m-S-tU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204936 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, pregnancy, copy number variation, gene expression About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.04.547622v1?rss=1 Authors: Hao, Y., Li, C., Ming, C. Abstract: Alzheimer's disease (AD), particularly late-onset Alzheimer's disease (LOAD), is a prevalent form of dementia that significantly affects patients' cognitive and behavioral capacities and longevity. Although approximately 70 genetic risk factors linked with AD have been identified, their influence on patient longevity remains unclear. Further, recent studies have associated copy number variations (CNVs) with the longevity of healthy individuals and immune-related pathways in AD patients. This study aims to investigate the role of CNVs on the longevity of AD patients by integrating multi-omics data from the Religious Orders Study/Memory and Aging Project (ROSMAP) cohort through causality network inference. Our comprehensive analysis led to the construction of a CNV-gene-age of death (AOD) causality network. We successfully identified three key CNVs (DEL5006, mCNV14192, and DUP42180) and seven AD-longevity causal genes (PLGRKT, TLR1, PLAU, CALB2, SYTL2, OTOF, and NT5DC1) impacting AD patient longevity, independent of disease severity. This outcome emphasizes the potential role of plasminogen activation and chemotaxis in longevity. We propose several hypotheses regarding the role of identified CNVs and the plasminogen system on patient longevity. However, experimental validation is required to further corroborate these findings and uncover precise mechanisms. Despite these limitations, our study offers promising insights into the genetic influence on AD patient longevity and contributes to paving the way for potential therapeutic interventions. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.17.537199v1?rss=1 Authors: Kopal, J., Kumar, K., Shafighi, K., Saltoun, K., Modenato, C., Moreau, C. A., Huguet, G., Jean-Louis, M., Martin, C.-O., Saci, Z., Younis, N., Douard, E., Jizi, K., Beauchamp-Chatel, A., Kushan, L., Silva, A. I., van den Bree, M. B. M., Linden, D. E. J., Owen, M. J., Hall, J., Lippe, S., Draganski, B., Sonderby, I. E., Andreassen, O. A., Glahn, D. C., Thompson, P. M., Bearden, C. E., Zatorre, R., Jacquemont, S., Bzdok, D. Abstract: Asymmetry between the left and right brain is a key feature of brain organization. Hemispheric functional specialization underlies some of the most advanced human-defining cognitive operations, such as articulated language, perspective taking, or rapid detection of facial cues. Yet, genetic investigations into brain asymmetry have mostly relied on common variant studies, which typically exert small effects on brain phenotypes. Here, we leverage rare genomic deletions and duplications to study how genetic alterations reverberate in human brain and behavior. We quantitatively dissected the impact of eight high-effect-size copy number variations (CNVs) on brain asymmetry in a multi-site cohort of 552 CNV carriers and 290 non-carriers. Isolated multivariate brain asymmetry patterns spotlighted regions typically thought to subserve lateralized functions, including language, hearing, as well as visual, face and word recognition. Planum temporale asymmetry emerged as especially susceptible to deletions and duplications of specific gene sets. Targeted analysis of common variants through genome-wide association study (GWAS) consolidated partly diverging genetic influences on the right versus left planum temporale structure. In conclusion, our gene-brain-behavior mapping highlights the consequences of genetically controlled brain lateralization on human-defining cognitive traits. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.07.531594v1?rss=1 Authors: Sun, C., Kathuria, K., Emery, S. B., Kim, B., Burbulis, I. E., Shin, J., Brain Somatic Mosaicism Network,, Weinberger, D. R., Moran, J. V., Kidd, J. M., Mills, R. E., McConnell, M. J. Abstract: When somatic cells acquire complex karyotypes, they are removed by the immune system. Mutant somatic cells that evade immune surveillance can lead to cancer. Neurons with complex karyotypes arise during neurotypical brain development, but neurons are almost never the origin of brain cancers. Instead, somatic mutations in neurons can bring about neurodevelopmental disorders, and contribute to the polygenic landscape of neuropsychiatric and neurodegenerative disease. A subset of human neurons harbors idiosyncratic copy number variants (CNVs, ''CNV neurons''), but previous analyses of CNV neurons have been limited by relatively small sample sizes. Here, we developed an allele-based validation approach, SCOVAL, to corroborate or reject read-depth based CNV calls in single human neurons. We applied this approach to 2,125 frontal cortical neurons from a neurotypical human brain. This approach identified 226 CNV neurons, as well as a class of CNV neurons with complex karyotypes containing whole or substantial losses on multiple chromosomes. Moreover, we found that CNV location appears to be nonrandom. Recurrent regions of neuronal genome rearrangement contained fewer, but longer, genes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this episode, we had a special guest from the industry side of things, Paul Reed. He's one of the co-founders of BLNK CNVS, one of the biggest promoters in Florida. We chatted about what it's like to plan dozens of shows for Miami Music Week March 22-26, 2023. 

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.09.527866v1?rss=1 Authors: Kim, J., Vanrobaeys, Y., Peterson, Z., Kelvington, B., Gaine, M. E., Nickl-Jockschat, T., Abel, T. Abstract: Neurodevelopmental disorders (NDDs) are polygenic in nature and copy number variants (CNVs) are ideal candidates to study the nature of this polygenic risk. The disruption of striatal circuits is considered a central mechanism in NDDs. The 16p11.2 hemi-deletion (16p11.2 del) is one of the most common CNVs associated with NDD, and 16p11.2 del/+ mice show sex-specific striatum-related behavioral phenotypes. However, the critical genes among the 27 genes in the 16p11.2 region that underlie these phenotypes remain unknown. Previously, we applied a novel strategy to identify candidate genes associated with the sex-specific phenotypes of 16p11.2 del/+ mice and identified 3 genes of particular importance within the deleted region: thousand and one amino acid protein kinase 2 (Taok2), seizure-related 6 homolog-like 2 (Sez6l2), and major vault protein (Mvp). Using the CRISPR/Cas9 technique, we generated 3 gene hemi-deletion (3g del/+) mice carrying null mutations inTaok2, Sez6l2, and Mvp. We assessed striatum-dependent phenotypes of these 3g del/+ mice in behavioral, molecular, and imaging studies. Hemi-deletion of Taok2, Sez6l2, and Mvp induces sex-specific behavioral alterations in striatum-dependent behavioral tasks, specifically male-specific hyperactivity and impaired motivation for reward seeking, resembling behavioral phenotypes of 16p11.2 del/+ mice. Moreover, RNAseq analysis revealed that 3g del/+ mice exhibit gene expression changes in the striatum similar to 16p11.2 del/+ mice, but only in males. Pathway analysis identified ribosomal dysfunction and translation dysregulation as molecular mechanisms underlying male-specific, striatum-dependent behavioral alterations. Together, the mutation of 3 genes within the 16p11.2 region phenocopies striatal sex-specific phenotypes of 16p11.2 del/+ mice, unlike single gene mutation studies. These results support the importance of a polygenic approach to study NDDs and our novel strategy to identify genes of interest using gene expression patterns in brain regions, such as the striatum, which are impacted in these disorders. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In individuals with Down syndrome, there is an aging-like phenotype known as senescence. Hiruy Meharena, Ph.D., UC San Diego, discusses how this impacts neurodevelopment. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Show ID: 38388]

In individuals with Down syndrome, there is an aging-like phenotype known as senescence. Hiruy Meharena, Ph.D., UC San Diego, discusses how this impacts neurodevelopment. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Show ID: 38388]

In individuals with Down syndrome, there is an aging-like phenotype known as senescence. Hiruy Meharena, Ph.D., UC San Diego, discusses how this impacts neurodevelopment. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Show ID: 38388]

In individuals with Down syndrome, there is an aging-like phenotype known as senescence. Hiruy Meharena, Ph.D., UC San Diego, discusses how this impacts neurodevelopment. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Show ID: 38388]

In individuals with Down syndrome, there is an aging-like phenotype known as senescence. Hiruy Meharena, Ph.D., UC San Diego, discusses how this impacts neurodevelopment. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Show ID: 38388]

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.09.515866v1?rss=1 Authors: Forrest, M. P., Dos Santos, M., Piguel, N. H., Wang, Y. Z., Yoon, S., Bagchi, V. A., Hawkins, N. A., Dionisio, L. E., Simkin, D., Martin-de-Saavedra, M. D., Gao, R., Horan, K. E., George, A. L., LeDoux, M., Kearney, J. A., Savas, J., Penzes, P. Abstract: Neuropsychiatric disorders (NPDs) share genetic etiology and are frequently co-morbid with epilepsy, but the biological basis of this shared risk remains poorly understood. The 16p11.2 microduplication (16p11.2dup/+) is a highly pleiotropic copy number variant (CNV) conferring risk for multiple NPDs including autism spectrum disorder, schizophrenia and intellectual disability, and is associated with a high prevalence of seizures. We used a mouse model of the 16p11.2 duplication (16p11.2dup/+) to uncover molecular and circuit properties associated with this broad phenotypic spectrum, and examined genes within the locus capable of phenotype reversal. Quantitative proteomics of cortical membranes revealed alterations to synaptic protein networks and products of diverse NPD risk genes in 16p11.2dup/+ mice. Network analysis identified an epilepsy-associated protein subnetwork, which was dysregulated in 16p11.2dup/+ mice and proteomic datasets from human NPDs. We investigated circuit properties in 16p11.2dup/+ mice and found they exhibited hypersynchronous activity and enhanced network glutamate release, which increased susceptibility to seizures. We hypothesized that a regulator of the synaptic and epilepsy-associated protein network could have an important impact on pathophysiology. Human brain co-expression and interactome analysis revealed PRRT2 as a major hub in the dysregulated epilepsy subnetwork. Remarkably, restoring Prrt2 copy number to wild-type levels rescued aberrant circuit properties, seizure susceptibility and social interaction deficits in 16p11.2dup/+ mice. We show that proteomics and network biology can identify important disease hubs in multigenic CNVs, and reveal molecular and circuit phenotypes which may be relevant to the complex symptomatology of 16p11.2 duplication carriers. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.10.511483v1?rss=1 Authors: Mihailovich, M., Germain, P.-L., Shyti, R., Pozzi, D., Noberini, R., Liu, Y., Aprile, D., Tenderini, E., Troglio, F., Trattaro, S., Fabris, S., Ciptasari, U., Rigoli, M. T., Caporale, N., D Agostino, G., Vitriolo, A., Capocefalo, D., Skaros, A., Franchini, A., Ricciardi, S., Biunno, I., Neri, A., Kasri, N. N., Bonaldi, T., Aebersold, R., Matteoli, M., Testa, G. Abstract: Copy number variations (CNVs) at 7q11.23 cause Williams-Beuren (WBS) and 7q microduplication syndromes (7Dup), two neurodevelopmental disorders with shared and opposite cognitive-behavioral phenotypes. Using patient-derived and isogenic neurons, we integrated transcriptomics, translatomics and proteomics to elucidate the molecular underpinnings of this dosage effect. We found that 7q11.23 CNVs cause opposite alterations in neuronal differentiation and excitability. Genes related to neuronal transmission chiefly followed 7q11.23 dosage and appeared transcriptionally controlled, while translation and ribosomal protein genes followed the opposite trend and were post-transcriptionally buffered. Mechanistically, we uncovered REST regulon as a key mediator of observed phenotypes and rescued transcriptional and excitability alterations through REST inhibition. We identified downregulation of global protein synthesis, mGLUR5 and ERK-mTOR pathways activity in steady-state in both WBS and 7Dup, whereas BDNF stimulation rescued them specifically in 7Dup. Overall, we show that 7q11.23 CNVs alter protein synthesis and neuronal firing-established molecular and cellular phenotypes of neurodevelopmental disorders. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.08.24.505165v1?rss=1 Authors: Pak, C., Sebastian, R., Jin, K., Pavon, N., Bansal, R., Potter, A., Song, Y., Babu, J., Gabriel, R., Sun, Y., Aronow, B. J. Abstract: De novo mutations and copy number variations (CNVs) in NRXN1 (2p16.3) pose a significant risk for schizophrenia (SCZ). How NRXN1 CNVs impact cortical development in a cell type-specific manner and how disease genetic background modulates these phenotypes are unclear. Here, we leveraged human pluripotent stem cell-derived brain organoid models carrying NRXN1 heterozygous deletions in isogenic and SCZ patient genetic backgrounds and conducted single cell transcriptomic analysis over the course of cortical brain organoid development from 3 weeks to 3.5 months. We identified maturing glutamatergic and GABAergic neurons as being consistently impacted due to NRXN1 CNVs irrespective of genetic background, contributed in part by altered gene modules in ubiquitin-mediated pathways, splicing, and synaptic signaling. Moreover, while isogenic NRXN1 CNVs impact differentiation and maturation of neurons and astroglia, cell composition and developmental trajectories of early neural progenitors are affected in SCZ-NRXN1 CNVs. Our study reveals developmental timing dependent NRXN1 CNV-induced cellular mechanisms in SCZ at single cell resolution and highlights the emergence of disease-specific transcriptomic signatures and cellular vulnerabilities, which can arise from interaction between genetic variants and disease background. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

2022年4月パワープレイ アルバム：CNVS-002 FAIRY TAIL 曲名：M6. Fairy Tail (2min Edit) アーティスト：CANVAS feat. Quimär 2021/12/31 Release https://notebookrecords.net/discographyportal.php?cdno=CNVS-002 番組時間：109分0秒 出演者：夕野ヨシミ、たくや ---- 2022/4/28 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・あのー ・旅行に行って来まして ・壱岐に行きまして ・昭和の頃からある様な商店 ・しんでるのかのんびりしてるのか ・自販機の飲み物の賞味期限が4ヶ月ほど切れてまして ・これこれ～↑ ・最近のイオシス君の話 ・M3がありました ・「警察ください」 ・1000円で売り渡す警察 ・これでサーバー代が払えます ・会場に無事に遅刻してきたD.watt ・3000円の寿司です ・M3はコロナの谷間 ・この日のために筋肉を鍛えてきたんだ ・筋肉はすべてを解決する ・台車の方がコスパいいのでは ・チルノの曲ばっかり ・足技もやってましたね ・見れたら見るー ・知った顔がスパチャしてた ・えとたまの原作者さんです ・DDRにうどんげいん ・ウサテイもどうなってるのかな？ ・お前はいつ馬主になるんだい？ ・スカ警のナビゲーターが入ります ・関西弁のチルノ ・新録あります ・そんなグルコスワイワイパーティーは現在セール中！ ・ドット絵も作ってくれましたよ ・ノリノリの花形さん ・このあと土産話です ＜Ａパート＞ ・ふつおたです ・M3の話 ・車と一緒に盗まれたイオシスCD ・狙われやすい車にはGPSをつけるんだぞ ・スカ警は何もやってくれないですね ・3000円はちゃんといただきました ・盗難時のためのスカ警 ・スカ警、1万枚くらい買えますよ ・詳細は阿佐ヶ谷で？ ・暗号8ビットか･･･ ・即売会で酒を飲みながら売りたい ・ポスタースタンドがぐさー ・俺は不死身のヨシミだー！ ・夕野フジミ ・冬コミの時は人がいなかった ・熱燗はむずかしいな ・M3のあと旅行に行きました ・東急のワンデーパスは安い ・こどもの国 ・報酬石600個は元が取れる ・ガチャはクソなのでやりません ・また今度でいいですー ・これがスパチャだ ・M3から福岡空港へ ・日本全国サンパレェス巡礼の旅 ・らーめんにいれるやーつ ・ふにゃふにゃの固麺 ・タマゴの殻がいいアクセント ・夢みたいな場所 ・エレベーターの色いいでしょ ・つまりそれは築40年 ・夏目漱石のK？ ・知り合いいた ・C＆A ・1文字で検索のトップに出ちゃう ・株式会社MOC ・謎のサンパレスタワー ・真珠ガチャ1000円 ・島界玄 ・ビーナス２ ・売店サイコー ・旅情代いただきました ・知らない島 ・これ、メンテしてなくない？ ・ほんわかわんわん ・サルじゃん ・リンクが飛ぶための台 ・イオンあったよ ・ドムドムバーガーがあった可能性 ・こういうの求めてやってきたんだな ・めしうまランチ ・料理は素材がいのち　みつを ・ワンオペのモス ・壱岐牛のシャブ漬け牛丼 ・壱岐｜K｜ ・さて、ここで問題です ・モスに行くしかない ・泳ぎますか ・桃鉄なら繋がってるんだけどな ・「レンタカー、港に置いといてください」 ・これ、今日の脚本家大丈夫？ ・ぬるぽに構成作家はいませんよ ・大人　正規 ・正岡子規だ ・どうしてここに3店舗？ ・壱岐99％ ・離島の離島はやめてほしいな ・ん？なんだ今の？ ・国立競技場が見えました ・ゴーアラはめちゃ揺れる ・出費は2200円 ・耳にタコが生えたのだ ・離島の欠航はしんどい ・壱岐空港のターミナルに入ってない ・ちょっとがんばれば滑走路入れますから ・滑走路にベッドを置いて寝る ・道内の空港は利用するのがむずかしい ・三沢には用事がないよね ・丘珠空港行ってください ・夢かな？ ・漁船塗り ・拿捕塗り ・銃撃塗り ・こっそりなんだ ・イーロンマスクさんが買い取ってくれれば ・ここでガチャの話 ・課金塗りあるじゃん ・だいたい300億円 ・課金で塗れば、でーじょうぶだ ＜Ｂパート＞ ・イーロンマスクはー！お金持ちー！ ・錦鯉のコーナーでした ・CMのあとはエンディングです ＜エンディング＞ ・ふかわりょうはー！キス80万ー！ ・残りは再来週です ・土曜日の夜は何かやります ・グルコスのあれ買ってください ・初老はどうなっちゃうんだろうね ・インターネット長老のD.watt ・GW中は配信が変則的になります ・おもち ・例大祭は警察をお持ちします ・注目すべきはアスパラ ・何升お米を炊くか決められません ・お便りお待ちしてます ・SOUL STOREは移転したので行きやすくなりました ・イオパは6/5でしたっけ？ ・6/5のゲストはまろんくんです ・壱岐に行くより簡単なので、みなさん札幌に来てください ・次回の生放送はお休みです

出演者： miko、quim 配信ペース： 隔週水曜日 番組時間：84分05秒 ♯本番組はリモート収録です。 ♯収録時環境の影響により、聴き取り辛い部分があります。 　申し訳ございません。 終身系インターネットラジオこと、mikoラジ第294回です。 食べ物の話で盛り上がる（一方はドン引きですが……）チーム我等。 300回を目前にしても変わらないふたりのやり取りをお楽しみくださいませ。 ♯途中で色々とノイズ等入りますが、収録時のものです。 　ご安心ください、お手持ちの機器は正常です。 -------------------- ●お便り募集中！ mikoラジでは以下の内容でお便りを募集中です！ ・ふつおた 　／普通のお便り、お待ちしています！ ・mikoは大変な絵を描いていきました 　／miko画伯に描いて欲しいお題をお待ちしています！ ・メシヲコエテ 　／料理人・mikoに教えて欲しいレシピをお待ちしています！ https://bit.ly/2GAWjyv 投稿フォームからラジオに投稿が出来ます！ コーナー名を選び、メッセージ・ラジオネーム・お所を入力して、 どんどん送ってください！　お待ちしています！！ ------------ 本ラジオのメインパーソナリティーである「チーム我等(miko/quim)」、 それぞれ以下個人サークルにて活動中です。 ・miko：miko ・quim：SHIGANAI RECORDS（ https://shiganai.com/ ） 活動詳細については、上記HPの他 各人のブログ/twitter等にて随時告知しておりますので、チェックしてみてください！ ・みころぐ。(mikoのブログ)（ https://ameblo.jp/miko-nyu/ ） ・@ mikonyu(mikoのtwitter)（ https://twitter.com/mikonyu ） ・@ quim(quimのtwitter)（ https://twitter.com/quim ） --- その他の活動については、以下のとおりです！ -- チーム我等がメインクルーとして活動していた「アルバトロシクス（ albatrosicks.com/ ）」、 これまでリリースしたCDは、イオシスショップ（ https://iosys.booth.pm/ ）にて頒布しております。ご興味ある方は是非！ ---------- ◯2022年4月IOSYSはいてない.comパワープレイ楽曲 アルバム：CNVS-002 FAIRY TAIL 曲名：M6. Fairy Tail (2min Edit) アーティスト：CANVAS feat. Quimär 2021/12/31 Release

2022年4月パワープレイ アルバム：CNVS-002 FAIRY TAIL 曲名：M6. Fairy Tail (2min Edit) アーティスト：CANVAS feat. Quimär 2021/12/31 Release https://notebookrecords.net/discographyportal.php?cdno=CNVS-002 番組時間：69分30秒 出演者：夕野ヨシミ、たくや ---- 2022/4/21 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・あのー ・ドライブに行って来まして ・行ったことのない温泉に行こう ・厚沢部町の蛾虫温泉 ・あ、上には上があるんだな ・ずっと工事中？ ・廃墟と老舗旅館のハイブリットやー ・心霊スポットと言って集まるのはやめてほしい ・札幌市の人口がもうすぐピークアウトする ・致命傷で済んでよかった ・ABCDE ・ラフィラ２に引っ越しちゃう？ ・意味不明な水道料金 ・こんな綺麗じゃないよね ・今日は告知があります ・イオパありました ・イオパはリアタイで ・コバヤシ会のアーカイブは明日まで ・お寿司RTA ・早食いは太るんだな ・あの親方黙っちゃって指示ださない ・M3と例大祭の話 ・ぬるぽ詰め合わせ出ます ・コ-16abは入口は入ってすぐ ・ふつおたはやっとこう ・生放送始めて1時間経過してます ・先っちょだけCMです ＜Ａパート＞ ・ふつおたです ・初老の話 ・客がちゃんと入ってる ・初老イベントに誰もちゃんと怒ってくれない ・「月曜のたわわ」と「試験に落ちた」 ・地獄に落ちろの笑い ・イマジナリー息子 ・阿佐ヶ谷の床はQRコード ・昔のAVを見れるようにする財団 ・唐突のシャンパン ・あの目で見るからバイト辞めるんですよ ・赤霧島という名のシャンパン ・みんな外で飲みたくてしょうがないんですね ・ゆっくりしていってね ・みんな生きててえらい ・ラフさんの映像はオープニングで流れます ・ファンボックスの333円に1カ月だけ入れば167円お得です ・100人分とは？ ・捨て人間 ・捨て垢を 集めてはやし 阿佐ヶ谷ロフトA ・クイズに正解でドリンク1杯 ・クイズに参加するにはスマホが必須です ・肉の姿 ・久しぶりのイベントなのでよろしくお願いします ・スーパー稲の種まきタイム無事に完了しました ・農家さんは夜の配信はこの時期見れない ・夜農家 ・泥棒と間違えられます ・最近は電気代が高い ・ぬるぽ放送局は農家が多いな ・今期のアニメの話 ・SPY×FAMILY ・種崎敦美さん ・アーニャちゃん ・別名義の話はチャット欄が荒れますから ＜Ｂパート＞ ・みつをたのコーナー ・艦娘のシャブ漬け戦略 ・男の乳首は何のためにあるのか ・あれ？みつをは？？？ ・魚肉ホモソーセージ ・元NHKアナがスカ警音読しててよく分からない ・イースターはいつなのか分からない ・なんだかどうでもイースター ・可愛い女の子だと思った？川尻こだまでした ・キン肉マンはシャブ漬けってことですか！ ・「ぬるぽでも言わない」はよっぽど ・KKさんね ・ちんちんしゃぶしゃぶなんて言ってませんよ ・シャブ漬けはー、役職泥棒ー ＜エンディング＞ ・お知らせでーす ・全員ぬるぽ詰め合わせ買ってください ・光回線実装 ・5/5のぬるぽはお休みです ・新譜の話 ・スカーレット警察・総集編 春の特別警戒スペシャル ・みんな薄々コント集団と気付いてましてけどね ・アレのヤツ ・トラック名は合ってます ・D.wattがんばって生きてます ・増産はたぶんしないので早めに買ってください ・裏で糸を引いてました ・M3のお品書き用意しました ・現金持ってきてください ・高橋名人とCD作るなんて人生のピークだと思ってましたよ ・羽生名人CD ・名人コンピアルバム ・こんなアルバム作ってほしいをふつおたまで送ってください

2022年4月パワープレイ アルバム：CNVS-002 FAIRY TAIL 曲名：M6. Fairy Tail (2min Edit) アーティスト：CANVAS feat. Quimär 2021/12/31 Release https://notebookrecords.net/discographyportal.php?cdno=CNVS-002 番組時間：70分55秒 出演者：夕野ヨシミ、たくや ---- 2022/4/14 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・ワクチンの3回目を打ったんですけど ・網戸の所にカマキリ ・コアラが来まして ・コアラってカマキリ食べるんだ ・果たしてどこまでが夢だったんだろうか ・クマはいっぱいいますからね ・ドアラはドアラって生き物ですから ・世界は自分で作る ・少年ジャンプの最後から2ページ目のやつだ ・ブルーワーカーは理にかなっていたのでは？ ・レベル300だと楽勝でした ・この世は筋肉だ ・ブルーワーカーはAmazonにあります ・イオシスくんがんばってるねのコーナー ・シアターにも金を落とすイベントもしたい ・金を落としたい気持ち ・東方スペルバブルにスカ警24時入りました ・貴重なﾃｰﾝ ・極秘情報　ﾃｰﾝの入りが違う ・知的情報バラエティーだなー ・ラフスケッチ夫妻が夢中のBPL ・CHUNITHMにENDYMION ・解禁が大変らしいですよ ・まろんくんのオフィシャル稲川淳二のMAD動画 ・KOTOKOさんのアルバムにD.wattが参加しました ・インターネット老人会もニッコリ ・イオシスの電波ソングはどこから？ ・全日本電波ソング認定協会を我々で作りましょう ・しぐれういさんの話 ・すごく反応がいい ・曲ができてないのに予約とは？ ・あとしっぽだけだから ・イオシスショップ新アイテムのお知らせ ・宣伝するのを忘れてました ・出てるー出てるー ・大河ラジオとは ・例大祭に新譜出ます ・何警察かな～？ ・IOSYS23年半やってるんですよ ・平成からやってます ＜Ａパート＞ ・-1円の特典 ・ふつおたです ・明日からスーパー稲の種まきタイムです ・積雪０ ・よさこいやるんだ ・地下歩行空間に雪を隠しましょう ・小麦粉の代わりに米粉 ・獺祭で削ったあとの米粉 ・米粉アレンジCD ・同人作物 ・食べられるCD ・桜もうすぐ咲きます ・​米粉ローション ・山形は桜が満開 ・一生お酒が飲めなくなりました ・高い酒を飲んだ方がいいな ・酒の瓶缶のゴミが増えましたね ・すい臓には詳しくない ・母乳はすい臓に効く ・お酒を飲むイベントやります ・2022/5/8　IOSYSトークライブイベントを阿佐ヶ谷ロフトAでやります ・要3オーダー ・内さまみたいなタイトル ・ブラウザ三国志の話はやりません ・内容がないので詐欺ではありません ・ハンドルネームでもOK ＜Ｂパート＞ ・毎週金曜日はフライデー！！ ・油は継ぎ足し ・みつをたです ・ぬるぽで聞いたことは覚えているんだよなー ・AIくんもまだまだなんだな ・年下の姉ちゃんに甘えたいなー ・おおきなパイオツをください ・ツルツルシコシコ麺はショタだと思う ・すみぺも一緒にご参パイしてくれないかなー ・みつをたはすべてを包み込む ＜エンディング＞ ・ゲーム実況いろいろやってます ・YouTube IOSYS Gamingのチャンネル登録お願いします ・無修正ナイツ ・月曜日くま牧、コバヤシ会（はかせあり）あります ・M3-2022春 ■IOSYSブース コ16-AB ・ぬるぽ詰めのポスター作らなきゃ ・例大祭は、イ17-AB ・夕野氏からアッピル ・まろんくんも遊びに来る予定です ・超売れっ子まろんくん ・いかがだったでしょうかぬるぽ放送局 ・なんなら全部聞いてください ・ジョイマンのコーナーなかった ・来週は錦鯉のコーナーあります

出演者： miko、quim 配信ペース： 隔週水曜日 番組時間：64分00秒 ♯本番組はリモート収録です。 ♯収録時環境の影響により、聴き取り辛い部分があります。 　申し訳ございません。 甥っ子より会ってるよ……そんなmikoラジ第293回です。 最近リアルでよく会っているというチーム我等さん。 水面下でのあれやこれや、ワクワクワクチソチソチソのお話等々。 ふたりの近況をお楽しみくださいませ。 ♯途中で色々とノイズ等入りますが、収録時のものです。 　ご安心ください、お手持ちの機器は正常です。 -------------------- ●お便り募集中！ mikoラジでは以下の内容でお便りを募集中です！ ・ふつおた 　／普通のお便り、お待ちしています！ ・mikoは大変な絵を描いていきました 　／miko画伯に描いて欲しいお題をお待ちしています！ ・メシヲコエテ 　／料理人・mikoに教えて欲しいレシピをお待ちしています！ https://bit.ly/2GAWjyv 投稿フォームからラジオに投稿が出来ます！ コーナー名を選び、メッセージ・ラジオネーム・お所を入力して、 どんどん送ってください！　お待ちしています！！ ------------ 本ラジオのメインパーソナリティーである「チーム我等(miko/quim)」、 それぞれ以下個人サークルにて活動中です。 ・miko：miko ・quim：SHIGANAI RECORDS（ https://shiganai.com/ ） 活動詳細については、上記HPの他 各人のブログ/twitter等にて随時告知しておりますので、チェックしてみてください！ ・みころぐ。(mikoのブログ)（ https://ameblo.jp/miko-nyu/ ） ・@ mikonyu(mikoのtwitter)（ https://twitter.com/mikonyu ） ・@ quim(quimのtwitter)（ https://twitter.com/quim ） --- その他の活動については、以下のとおりです！ -- チーム我等がメインクルーとして活動していた「アルバトロシクス（ albatrosicks.com/ ）」、 これまでリリースしたCDは、イオシスショップ（ https://iosys.booth.pm/ ）にて頒布しております。ご興味ある方は是非！ ---------- ◯2022年4月IOSYSはいてない.comパワープレイ楽曲 アルバム：CNVS-002 FAIRY TAIL 曲名：M6. Fairy Tail (2min Edit) アーティスト：CANVAS feat. Quimär 2021/12/31 Release

2022年4月パワープレイ アルバム：CNVS-002 FAIRY TAIL 曲名：M6. Fairy Tail (2min Edit) アーティスト：CANVAS feat. Quimär 2021/12/31 Release 番組時間：73分55秒 出演者：夕野ヨシミ、たくや ---- 2022/3/31 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・お葬式の時にね ・2倍くらいの木魚 ・完全にテクノ ・ホケキョテクノ ・2人体制 ・息子はシンバル ・シンバルがかっこよかったです ・さぞかしドリンクが出たでしょう ・遺影もデジタルサイネージ ・背景も変わっちゃう ・シンバル＝妙鉢 ・MOCさんのアルバム ・あーくたびれたなー ・明日はワクチン ・イオシスくんがんばってるねのコーナー ・銚子市長が踊っちゃう ・これ、30分後の話 ・スカ警1000万再生 ・スカ警完売しました ・新潟に行く前に売り切れてました ・スカ警は新潟にギリギリ持って行ってました ＜Ａパート＞ ・出し惜しみできるものはどんどん出し惜しみしましょう ・プレゼント当選のコーナー ・ピンクパイナップル ・ピートモス（園芸用の土） ・これで今日の仕事は半分おわりましたから ・うそおたのコーナー ・ホントにTOKIOさんが踊りそう ・かずという魚のタマゴ ・信じられるのはMOCさんだけ ・スペインの方にあいさつ ・AVに出演しました ・YouTubeが半分持ってちゃうんだっけ？ ・人間でいえば18歳 ・カレー1皿100円 ・ウナギの肝を多めに ・カレーに入ってたのはイワシでした ・真夜中のカレー ・レビューの星２つもカレーに入れて煮込んじゃえ ・ついでに･･･って何？ ・こんばんわ大統領です ・9000回目指してがんばってください ・プエルトリコにFANZAはあるのかな？ ・あぶおたじゃねーか！ ・どこまでがホント？ ・今年はイオシスはエイプリルフールネタがあるぞ ・こんばんヴァリス ・初老の話 ・2階席ー！ ・初老バンドの半分は副社長 ・PS4でAVを買う ・雲丹屋は金にならない ・トリプルアンコール ・みんな楽しそうでいいね ・誰がどのパートでもクオリティに差がないのね ・今知りたいのは阿佐ヶ谷ロフトAのフードメニュー ・マイクラ指示厨おじさん ・繁殖が女の子同士 ・ネザー地鶏 ・ガストの直火 ・もっぱら焼かれてるのは夕野さん ＜Ｂパート＞ ・ギターってすごいな ・みつをたです ・私も海自になって駆逐艦の味見がしたいな ・物価が上がるなら給料も上げてくれませんかね ・苦痛に耐えれないときはラーメン二郎を完飲すればいい ・これ、みつをって書いてないんだよな ・週７あべなな ・科捜研　バター犬 ・どうします？　え？ ・今後のみつをたについて会議したらいいのかな？ ・quimさんからスパチャいただきました ・もっと決算混乱したいな ・夢のコーナーです ・夢の話詰め合わせ ・鳥たちを洗濯ばさみで干す ・猫たちがキャッチボールしてました ・5度寝 ・チキン50ピース ・古ぼけた稚内駅 ・アナログモデムをノートPCに繋ぐ方法 ・USB規格ができてないことに気付き目が覚めました ・ａｕの３Ｇが終了します ・電話加入権50件分 ・ジョイマンのコーナーなど各種お便りお待ちしてます ＜エンディング＞ ・また昔の話か ・昔のデスクトップPCにはねこちゃんが入るスペースが無かったかも ・お知らせです ・つまぽんのＰＣはねこちゃんの毛だらけです ・東方アルカディアレコードにイオシス参加してます ・事前登録キャンペーン中です ・D.wattはＤＪやりすぎでは ・今週土曜日から踊りを始めます ・ジャンプがヴァリス並み ・大・東方Project展　4/2から ・スコブルブルさんの足技 ・mikoさんの足技 ・ベース版が売り切れてキック版だけになっちゃった ・K.K.K.K.K.K.K. ・ドンとカッ ・あと2時間くらいで、エイプリルフールですね ・M3と例大祭出ます ・阿佐ヶ谷ロフトの店員さんが驚くくらい発注したい ・お釜破壊RTA ・ライス大お願いします ・初手カレー ・農家ならいますよ

Pavlog se clavó en las entrañas del Vive Latino 2022, tomó el micrófono y capturó entrevistas, anécdotas, canciones y lo que el audio del festival permitió. Con cameos de Miguel Solis, Ricardo O'Farril, Jiots, Elsa y elmar, CNVS, Daniel Quién, Victor Zenteno, ElArturo, este no es un episodio cualquiera. Te acercamos a la edición que marca el regreso de los festivales después de una pandemia.

Estamos saliendo (por fin) a las calles, conciertos y festivales. Estos son los 6 grupos mexicanos que no se pueden perder en vivo los próximos meses...

Programa transmitido en vivo en radio digital. Entrevista con Pedro Ferriz. Conversación con CNVS. Colaboración de Alberto Lujambio

Durante nuestra emisión #13 contamos con la visita de CNVS, quienes nos contaron cómo se están preparando para su presentación en #VL22, además de darnos un panorama de la actual escena de Querétaro. Además, Marion Raw, Pahua, Silvana Estrada y DeSaloon nos contaron todos los detalles detrás de sus más recientes lanzamientos. A 50 días del festival, Señal VL te mantiene al día.

Programa transmitido el 11 de junio del 2021. Entrevistas con el Dr. Eduardo Márquez, CNVS y la sección de Rodrigo Arpón desde Holbox. Porque la Radio abierta no está en la radio al aire

2021年5月パワープレイ アルバム：CANVAS feat.Quimar / CARMINA M04. Whitebird 2021/4/25 M3-2021春リリース https://notebookrecords.net/discographyportal.php?cdno=CNVS-001 番組時間：72分30秒 出演者：夕野ヨシミ、たくや ---- 2020/5/27 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・発表されましたね ・アイマスとぶくぶ先生のコラボ ・まったく違和感がない ・TOHO EDMは名盤です ・イイハナシデスネー ・2842年 ・ドラクエも5までしかやってない ・老後の心配をしてます ・ちゃんとゲームしてから死にたい ・ホットプレートがあれば大丈夫 ・老後の趣味を早めに始めましょう ・最後のツイートが3日前 ・8時間前にいいねしてたから大丈夫 ・ダイイングいいね ・チキンナゲットそんなに好きですか？ ・それ、調味料の味を食べてますね ・豆腐をチンして揚げ玉入れてめんつゆ ・燻製マヨネーズ ・豆腐を溶鉱炉に ・ちょっとお腹がすいてきましたね ・昌苑行きたいですね ・札幌、お酒飲めるとこないんですよね ・定山渓も札幌市ですよ ・養命酒を持ち込んで飲む ・いよいよ1日中家でお酒飲んでますよ ＜Ａパート＞ ・ふつおたです ・うさぎさん情報ですよ ・たらこは無事です ・そろそろ性に目覚めそうです ・続報来てますよ ・タオル子さんにのっかりました ・7カ月で大人になりました ・たらこと言うか白子 ・七海ちゃん優勝おめでとうございます ・フリルドスクエア ・もう10年ですからね ・ウサミン優勝から3年 ・続々と農家さんが増えてますよ ・日本一農業の話をしてるポットキャスト ・スコアが出たらいいのにね ・ファーミング99 ・野菜ピックアップガチャ ・サンシャイン牧場の話してます？ ・実際の農業は大変 ・我々もいつか農業しますからね ・晴れて正社員になる見込みです ・明らかな躁状態 ・つづけ！ ・お大事にしてください ・人生なんとかなる ・ソロモンの鍵 ・毎月7日はルーミアの日 ・１と２はだいぶ違う ・もどかしい ・ファミコン末期のゲーム ・クマちゃんと雀魂 ・コアッちゃんは七対子以外で上がってほしくない ・麻雀やるご当地キャラ ・アックマ様おじさんじゃん ・ダマで高めの手をはるコアッちゃん ・アソビ対戦買うか ・アックマ様と花札 ・夕野さんそろそろswitch買ってください ・リングフィットアドベンチャーご検討ください ・今売れてます！ ＜Ｂパート＞ ・ナースタスカルのコーナーです ・ロリナースです ・それ放送できるやつ？ ・みんなこのコーナー好きですね ・間違えたことに安堵 ・母親似の美少年でした ・いけるかいけないか ・お薬どんどん出しときます ・性癖の話その３ ・大きいことはいいことだ ・ビルより大きい娘 ・巨大娘と巨大娘の戦い ・5万トンの女の子 ・ファンタジーですからね ・おにでか ・矢寺圭太先生 ・マウントレディー ・私も巨女ですからね ・強めの生理食塩水出しときますね ・各種お便りお待ちしてます ＜エンディング＞ ・出たー ・なんだこれ ・お知らせです ・電音部さんのお知らせです ・40週連続リリース ・東方アレンジは15年 ・初音ミクを描く前のKEIさん ・3万再生の動画じゃありません ・トニさんのMV是非ご覧ください ・スカ警そろそろ400万再生 ・スカ警のファンアート ・パイオニア過ぎた ・土曜日じゃんたまやります ・日曜日はクールミン島 ・なんだかんだいろいろありますね ・mikoラジと何やるの？ ・麻雀やるんじゃない？ ・リモートでゲスト呼びたい ・麻雀しかないのか ・３つチャンネルがあるので全部登録してください ・今なら古参になれますよ ・収益化前から観てました！

出演者： miko、quim 配信ペース： 隔週水曜日 番組時間：87分12秒 ♯本番組はリモート収録です。 ♯収録時環境の影響により、聴き取り辛い部分があります。 　申し訳ございません。 mikoラジ第270回です。 動画配信がメジャーな現代において、インターネットラジオのスタイルを維持し続けるmikoラジ。 話していることもおじさんとおば……おね゛えさんな話題にシフトしつつも、昔と変わらず。 胡散臭いビジネスモデルを思いついている場合なのでしょうか……？？ そんな平常運行のmikoラジ、最後までごゆるりとお楽しみくださいませ。 ♯途中でノイズ等入りますが、お手持ちの機器は正常です。 -------------------- ●お便り募集中！ mikoラジでは以下の内容でお便りを募集中です！ ・ふつおた 　／普通のお便り、お待ちしています！ ・mikoは大変な絵を描いていきました 　／miko画伯に描いて欲しいお題をお待ちしています！ ・メシヲコエテ 　／料理人・mikoに教えて欲しいレシピをお待ちしています！ https://bit.ly/2GAWjyv 投稿フォームからラジオに投稿が出来ます！ コーナー名を選び、メッセージ・ラジオネーム・お所を入力して、 どんどん送ってください！　お待ちしています！！ ------------ 本ラジオのメインパーソナリティーである「チーム我等(miko/quim)」、 それぞれ以下個人サークルにて活動中です。 ・miko：miko ・quim：SHIGANAI RECORDS（ https://shiganai.com/ ） 活動詳細については、上記HPの他 各人のブログ/twitter等にて随時告知しておりますので、チェックしてみてください！ ・みころぐ。(mikoのブログ)（ https://ameblo.jp/miko-nyu/ ） ・@ mikonyu(mikoのtwitter)（ https://twitter.com/mikonyu ） ・@ quim(quimのtwitter)（ https://twitter.com/quim ） --- その他の活動については、以下のとおりです！ -- チーム我等がメインクルーとして活動していた「アルバトロシクス（ albatrosicks.com/ ）」、 これまでリリースしたCDは、イオシスショップ（ https://www.iosysshop.com/SHOP/141643/50223/list.htmll ）にてダウンロード頒布しております。ご興味ある方は是非！ ---------- ◯2021年5月パワープレイ アルバム：CANVAS feat.Quimar / CARMINA M04. Whitebird 2021/4/25 M3-2021春リリース https://notebookrecords.net/discographyportal.php?cdno=CNVS-001

2021年5月パワープレイ アルバム：CANVAS feat.Quimar / CARMINA M04. Whitebird 2021/4/25 M3-2021春リリース https://notebookrecords.net/discographyportal.php?cdno=CNVS-001 番組時間：79分55秒 出演者：夕野ヨシミ、たくや ---- 2020/5/20 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・夢を見たんですけど ・ちゃんとしたラジオ番組のゲストに出ることになったんですよ ・はかせがいたのかなー？ ・演者しかいない ・放送事故になっちゃうじゃん ・「いやダメですね」 ・リモートでございます ・自宅楽でいいですね ・帰らなくていいのは楽 ・コロナなかったらリモート収録やってない ・テレワークし放題 ・完全在家 ・５Gホームルーター ・クソデカ生放送 ・のぼりが異常に遅い ＜Ａパート＞ ・ふつおたです ・PS3がいかれました ・頭がいかれた気がします ・靴を買いに行くのがめんどくさい ・そもそも靴を履いてない ・靴をはいてない.com ・うっかりwebカメラがオンに ・スーパー田植えウイーク終了！ ・ドローン直播 ・案外安いのかもしれません ・是非！ ・早苗ロリータ？ ・尺貫法 ・一反で500㎏ ・イオシス米 ・農業機械の中古はヤフオクで買うんだな ・コイン精米機が近くにない ・イオシスぬか ・Suica精米機 ・楽天精米マン ・今日はリアルな方の病院に来てます ・攻めと受けはどっちが母乳出すんですかね？ ・あ、コーナーが違いました ・ハンターハンターは大丈夫か ・ガッキーショックだったのね ・まろんくんは誰が結婚してもショック受けるよね ・古畑任三郎のマネしてましたね ・ジャーマネさんは最終イニングに放送やってます ・ロリの体になってみました ・今の時代新幹線で謝罪に行く異物混入発生 ・子猫1匹が混入 ・山形は平和とは言えなくなってきました ・ネコポスなのにネコは入らない ・ネコの箱はまだあります ・イオシスショップやってますよ ・箱が欲しいなら箱を買った方が早い ＜Ｂパート＞ ・お薬のコーナーです ・性癖の話その２ ・マイルドに言うと男性受けです ・怪力娘 ・ザ・ガッツ ・さらなる道が開けるとは･･･つづく ・これ、お薬出ます？ ・強めのプラセボ出しときますねー ・強めのプロテインとは ・ぬるぽ俳句のコーナー ・みくにゃんの　ファン辞めないでね　星野源 ・4次元の嫁 ・ほどほどのお薬出しときます ・Amazonでも買えますんで ＜エンディング＞ ・​おいでよpixivの森 ・アリスギアマガジンにコメント載ってます ・生放送はYouTube LIVEに移動しました ・YouTube IOSYS musicチャンネルは2000トラック聞けます ・次回は10月更新です ・YouTube IOSYS Gamingは早くチャンネル登録者1000人いってほしい ・東方スペルバブルに「はたてのバッコイ殺人事件」が収録されています ・IOSYS OSで歌詞が見れたりもします ・どうみてもケフィアです ・一番便利だな思ってるのは俺だからね ・海外ライブ履歴もある ・3334番組？ ・土曜日は雀魂配信があります ・あのMCMOCさん ・部屋を作っても1人でプレイはさみしい ・スカ警がもうすぐ400万再生に ・D.watt選手権 ・不名誉な1 ・ワタナベダイスケさんは1000円OFF ・もう、5月終わっちゃう ・もうすぐオリンピックですよ ・みなさん安全第一で ・米はまだ買って来てる ・そんなあなたにオンラインクレーンゲーム ・強めのワクチン打っときますねー

2021年5月パワープレイ アルバム：CANVAS feat.Quimar / CARMINA M04. Whitebird 2021/4/25 M3-2021春リリース https://notebookrecords.net/discographyportal.php?cdno=CNVS-001 番組時間：62分10秒 出演者：夕野ヨシミ、たくや ---- 2020/5/13 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・あのー ・４年おきにドラクエをやりたくなるんですよ ・スマホ版のドラクエIIIを買いまして ・戦士　コナミちゃん ・僧侶　バンナムちゃん ・魔法使い　タイトーちゃん ・武闘家　セガちゃん ・商人　サイゲちゃん ・遊び人　アニプレちゃん ・盗賊がいないんですよ ・さっきお風呂に入ってたんですか？ ・お風呂モードに？ ・コメントは読めません ・恥ずかしながら帰ってまいりました！ ・１年ぶりくらいにYouTube LIVEです ＜Ａパート＞ ・どっか旅行に行きたい ・早く脱北したいよー ・札幌市内もウロウロできない ・出家できない ・ふつおたです ・デレマス総選挙 ・最後のお願い ・新キャラが強い ・杏ちゃんは仕事が増えない程度で ・なんでも３５周年 ・プリティーダービーすごいなー ・じゃんたま始めました ・麻雀の役の覚え方 ・ゲームボーイ版 ・緑も赤もついてない ・MSX版やりましたよ ・野田ゲー売れてますよ ・勝ったら１枚脱ぐ ・完全にダメなヤツ ・脱北麻雀 ・北は捨てる ・緑色なら大丈夫 ・役満でテポドン発射 ・臨時賞与中止になりました ・野良猫は幸せになっているでしょう ・ダーマ工場 ・９秒でクリアー ・ホットプレートを余熱していたのでは？ ・また帯域幅が ・マンションの住人がzoom呑みやってるのかね？ ・田植えの時期ですね ・４反歩 ・端っこは祖母の暇つぶしにとっておきます ・ガイル農法 ・素人に植えさせるのが一番楽 ・うさぎさんニュースの時間です ・タオルを落とす遊び ・うさぎさんの明太子 ・ウサミンではない ・シーマン懐かしいですねー ・modのバッチファイルを作りました ・プレゼント応募者が２万人になると破たんします ・脱いだ衣装とは ・ＮＦＴの話してます？ ・新手のブルセラ ・セクシー女優 ・脱ぎたてのスクール水着データファイル.exe ＜Ｂパート＞ ・強めのお薬のコーナー ・アヘ顔ダブルピースナースさん ・あのスギちゃんね ・この単語は成人男性を表します ・お薬手帳のアプリ便利ですよ ・患者さん帰っちゃった？ ・ぬるぽ俳句のコーナーです ・入園式　隣のママに　欲情し ・ニッチな性癖の入口 ・数字を見て興奮 ・続きが気になる ＜エンディング＞ ・イオシスくん最近がんばってるねのコーナー ・もう、３年前かー ・タイトルが思い出せない ・アリス・ギア・アイリス遊んでください ・駿河屋使う前に新品買ってください ・イベントはどうなるか分かりませんのでTwitterなりをご覧ください ・いろいろやってますねー ・ヨシ！

出演者： miko、quim 配信ペース： 隔週水曜日 番組時間：101分13秒 ♯本番組はリモート収録です。 ♯収録時環境の影響により、聴き取り辛い部分があります。 　申し訳ございません。 mikoラジ第269回です。 GWも終わり、「何してた？」という話題。 話題は転がり続け、最終的に「高齢者のトレンドとは？」という話題に。 チーム我等、GW後も平常運転でお送りいたします。 最後までごゆるりとお楽しみくださいませ。 ♯ボカロPの話題になった際に、お名前を盛大に間違えております。 　正しくは、「Chinozo（ちのぞー）」様です。大変失礼いたしました。 ♯途中でノイズ等入りますが、お手持ちの機器は正常です。 -------------------- ●お便り募集中！ mikoラジでは以下の内容でお便りを募集中です！ ・ふつおた 　／普通のお便り、お待ちしています！ ・mikoは大変な絵を描いていきました 　／miko画伯に描いて欲しいお題をお待ちしています！ ・メシヲコエテ 　／料理人・mikoに教えて欲しいレシピをお待ちしています！ https://bit.ly/2GAWjyv 投稿フォームからラジオに投稿が出来ます！ コーナー名を選び、メッセージ・ラジオネーム・お所を入力して、 どんどん送ってください！　お待ちしています！！ ------------ 本ラジオのメインパーソナリティーである「チーム我等(miko/quim)」、 それぞれ以下個人サークルにて活動中です。 ・miko：miko ・quim：SHIGANAI RECORDS（ https://shiganai.com/ ） 活動詳細については、上記HPの他 各人のブログ/twitter等にて随時告知しておりますので、チェックしてみてください！ ・みころぐ。(mikoのブログ)（ https://ameblo.jp/miko-nyu/ ） ・@ mikonyu(mikoのtwitter)（ https://twitter.com/mikonyu ） ・@ quim(quimのtwitter)（ https://twitter.com/quim ） --- その他の活動については、以下のとおりです！ -- チーム我等がメインクルーとして活動していた「アルバトロシクス（ albatrosicks.com/ ）」、 これまでリリースしたCDは、イオシスショップ（ https://www.iosysshop.com/SHOP/141643/50223/list.htmll ）にてダウンロード頒布しております。ご興味ある方は是非！ ---------- ◯2021年5月パワープレイ アルバム：CANVAS feat.Quimar / CARMINA M04. Whitebird 2021/4/25 M3-2021春リリース https://notebookrecords.net/discographyportal.php?cdno=CNVS-001

2021年5月パワープレイ アルバム：CANVAS feat.Quimar / CARMINA M04. Whitebird 2021/4/25 M3-2021春リリース https://notebookrecords.net/discographyportal.php?cdno=CNVS-001 番組時間：73分20秒 出演者：夕野ヨシミ、たくや ---- 2020/5/6 公開録音したものを配信いたします。 ラジオ記事はリスナーのEEチャンピオンさんが書いてくれているので楽してます。 ＜オープニング＞ ・皆さんご存知ないかもしれませんが･･･ ・知ってます ・イース６オンライン ・文字がガビガビに ・イース６から15年 ・FCのイースは微妙だった思い出が ・なぜ今オンラインをやるのか？ ・イース６の現地妻 ・わたくしはイース6オンラインをやるのか ・今日はリモートでやってます ・あ、上の階の人 イオシスだ！ ＜Ａパート＞ ・あっちのイオシスさんの可能性 ・はちゃめちゃですね ・ショベルカー操縦体験に変更しました ・GW何してました？ ・あの黄色ジム、どさんこワイドで特集されてましたよ ・どさんこってダサイな ・みんな無の境地になってる ・え？ダサい方に？ ・ポンチオーレにしよう ・レバンガ北海道のグッズ買ってください ・寝GW ・ふつおたです ・自分でマイルドって言ってる人はマイルドじゃないよね ・ノートPCのバッテリーが死にかけてます ・chromeBookはどんな感じですか？ ・バッテリーはヘタるよね ・リモートになったらまったく意味がありませんね ・全固体電池 ・あぁ〜水素の音ォ＾〜 ・水素水飲み放題やってますよ ・5G受信したい ・東方すいすいそーすい ・往年のイオシスなら ・オプションがたくさん契約されてました ・いつの間にか悪徳商法になってました ・携帯は別のイオシスからのお求めがおすすめですよ ・違約金おかしくないですか？ ・2年に1回チャンスがありますよ ・d って言っちゃった ・今日は夕野さんがジャギジャギです ＜Ｂパート＞ ・CARMINA売れてます ・マルコの知らない世界 ・CARMINAのアルコールは40%かもしれない ・ウマ娘みんなやってるね ・プリメやろうかなー ・マイクロビキニをくれ！ ・広告が全部マイクロビキニになっちゃう ・誰か切り取り動画作ってくれないかな？ ・テロップって楽になってませんか？ ・字幕は編集しやすい ・1000人越えたいんですよね ・強めのお薬出しときますねのコーナー ・艦これ8周年 ・ハイエースででかけたい ・二次元普通免許 ・手術にします？ ・見た目が幼い田村ゆかりは最高 ・課金をしても　推しがこず ・それ幻覚ですか？ ・ｶﾚﾝﾁｬﾝを出すんじゃない ・天井ならいいか ・MMOとそのショップに強いお薬が必要です ・ぬるぽ俳句のコーナー ・連休は　気づいた時には　最終日 ・メリハリがない ・祝日のメリットがない ・路上飲みSPOT ・今日は具体名がでますね ＜エンディング＞ ・お知らせのコーナー ・今週末初老配信あります ・ダンマクカグラのライブやってましたね ・リリースが今夏 ・イオパがありました ・南区推し ・FC2かな？ ・イオシスくんと言うかD.wattくんとunoくんがんばってるね ・懐メロじゃん ・新しい曲も作ってもますよ ・夢の印税生活送りてーなー ・イエローMOCエビフライ ・江藤田中チャー ・夢の自転車生活

Here is a quick introduction to Blck Cnvs Podcast. It was low key a spur of the moment type segment where I just wanted to talk about why I'm starting Blck Cnvs. There is so much in store for this podcast and I want you all to get ready to join me as I open up the black canvas and create a space for everyday people like you and myself to talk a little bit about an array of different topics. So without further ado...Welcome to Blck Cnvs!! Intro track by Yung Kartz. --- Support this podcast: https://podcasters.spotify.com/pod/show/theblckcnvs/support

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.28.316372v1?rss=1 Authors: Lavrichenko, K., Helgeland, O., Njolstad, P. R., Jonassen, I., Johansson, S. Abstract: Motivation: Single nucleotide polymorphism (SNP) genotyping arrays remain an attractive platform for assaying copy number variants (CNVs) in large population-wide cohorts. However current tools for calling CNVs are still prone to extensive false positive calls when applied to biobank scale arrays. Moreover, there is a lack of methods exploiting cohorts with trios available (e.g. nuclear family) to assist in quality control and downstream analyses following the calling. Results: We developed SeeCiTe (Seeing Cnvs in Trios), a novel CNV quality control tool that post-processes output from current CNV calling tools exploiting child-parent trio data to classify calls in quality categories and provide a set of visualizations for each putative CNV call in the offspring. We apply it to the Norwegian Mother, Father, and Child Cohort Study (MoBa) and show that SeeCiTe improves the specificity and sensitivity compared to the common empiric filtering strategies. To our knowledge it is the first tool that utilizes probe-level CNV data in trios to systematically highlight potential artefacts and visualize signal intensities in a streamlined fashion suitable for biobank scale studies. Availability and Implementation: The software is implemented in R with the source code freely available at https://github.com/aksenia/SeeCiTe. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.17.301259v1?rss=1 Authors: Funk, M., Schuelert, N., Jaeger, S., Dorner-Ciossek, C., Rosenbrock, H., Mack, V. Abstract: Animal models reflecting human risk for schizophrenia are essential research tools for gaining further insight into the convergence of CNS pathology and clinical biomarkers. Amongst the variety of animal models that display schizophrenia-related neuronal network deficits, transgenic mice for rare and highly penetrant copy number variants (CNVs) provide a unique opportunity to study pathological correlates in models with strong construct validity. The Df(h15q13)/+ mouse model of the human 15q13.3 microdeletion CNV has been shown to mimic deficits in parvalbumin positive (PV+) interneuron and cortical network function. However, the corresponding changes in synapse density and activity within the medial prefrontal cortex (mPFC) have not been described. Using high-content immunofluorescence imaging, we have shown a reduced density of PV+ neurons and inhibitory synapses in the mPFC of Df(h15q13)/+ mice. We found that the reduced detection of PV+ synapses were accompanied by changes in spontaneous inhibitory and excitatory synaptic activity onto layer 2/3 pyramidal neurons. The aberrant cortical function was also evident in awake animals by a reduced high frequency auditory steady-state responses (ASSR), reliably monitored by EEG. Importantly, the imbalance of excitatory to inhibitory function could be attenuated on a cellular and cortical network level by activation of mGlu2/3 receptors, indicating the relevance of excessive excitatory transmission to the cortical network deficit in the Df(15q13)/+ mouse model. Our findings highlight the preclinical value of genetic risk and in particular CNV models such as the Df(15q13)/+ mice to investigate pathological network correlates of schizophrenia risk and to probe therapeutic opportunities based on clinically relevant biomarkers. Copy rights belong to original authors. Visit the link for more info

#036 - Eric Fuller is a passionate executive, entrepreneur and investor that found his love for hospitality and live entertainment, where he fused his interest in business and music, by starting a promotional company that brought national talent to perform at local venues. Eric pursued an event concept he helped create while attending college , Life In Color, formerly known as Dayglo. Eric helped develop the concepts expansion and touring model, eventually serving as the company’s Chief Operating Officer. In late June of 2020, Eric announced his new venture as the Head of MRG Live South East and a strategic partnership with is promotional company BLNK CNVS Presents and MRG Live. The MRG Group has grown into one of the leading entertainment and hospitality companies in Canada.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.30.228601v1?rss=1 Authors: Gaziova, M., Pos, O., Krampl, W., Kubiritova, Z., Kucharik, M., Radvanszky, J., Budis, J., Szemes, T. Abstract: Copy number variants (CNVs) play important roles in many biological processes, including the development of genetic diseases, making them attractive targets for genetic analysis. This led to the demand for interpretation tools that would relieve researchers, laboratory diagnosticians, genetic counselors and clinical geneticists from the laborious process of annotation and classification of CNVs. Here we demonstrate that the prediction of the clinical impact of CNVs can be automated using modern machine learning methods applied to publicly available genomic annotations, requiring only basic input information about the genomic location and structural type (duplication/deletion) of the analyzed CNV. The presented approach achieved 0.95 prediction accuracy on deletions and 0.96 on duplications from the ClinVar dataset and therefore have a great potential to guide users to more precise conclusions. Copy rights belong to original authors. Visit the link for more info

Isaac, guitarrista y encargado de las atmósferas en Cnvs, nos cuenta un poco de su vida, pasiones y pasatiempos, así como del estreno de Cámara Lenta, último sencillo de la banda. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/tiqfun/message Support this podcast: https://anchor.fm/tiqfun/support

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.23.217976v1?rss=1 Authors: Bigio, B., Seeleuthner, Y., Kerner, G., Migaud, M., Rosain, J., Boisson, B., Nasca, C., Puel, A., Bustamante, J., Casanova, J.-L., Abel, L., Cobat, A. Abstract: The detection of copy number variations (CNVs) in whole-exome sequencing (WES) data is important, as CNVs may underlie a number of human genetic disorders. The recently developed HMZDelFinder algorithm can detect rare homozygous and hemizygous (HMZ) deletions in WES data more effectively than other widely used tools. Here, we present HMZDelFinder_opt, an approach that outperforms HMZDelFinder for the detection of HMZ deletions, including partial exon deletions in particular, in typical laboratory cohorts that are generated over time under different experimental conditions. We show that using an optimized reference control set of WES data, based on a PCA-derived Euclidean distance for coverage, strongly improves the detection of HMZ deletions both in real patients carrying validated disease-causing deletions and in simulated data. Furthermore, we develop a sliding window approach enabling HMZDelFinder-opt to identify HMZ partial deletions of exons that are otherwise undiscovered by HMZDelFinder. HMZDelFinder_opt is a timely and powerful approach for detecting HMZ deletions, particularly partial exon deletions, in laboratory cohorts, which are typically heterogeneous. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.16.087395v1?rss=1 Authors: Asgari, Y., Heng, J. I.-T., Lovell, N., Forrest, A., Alinejad-Rokny, H. Abstract: Noncoding RNAs (ncRNAs) comprise a significant proportion of the mammalian genome, but their biological significance in neurodevelopment and in diseases is poorly understood. In this study, we have performed a genome-wide investigation of human noncoding RNAs for cell regulatory functions in brain tissue. By analysing ENCODE regulatory features, associations with FANTOM5 tissue-specific enhancers, as well as tissue-specific expression profiles, we have identified 17,743 noncoding RNAs comprising at least one nervous system-related expression Quantitative Trait Loci (eQTL) polymorphism that is associated with protein coding genes. Of these, 908 brain-enriched noncoding RNAs (comprising 907 long noncoding RNAs and 1 pseudogene) also overlap with chromatin states characterised as enhancers. Based on these criteria, we referred to such noncoding RNAs with putative enhancer activity as brain "enhancer-ncRNAs". To investigate their impact in neurodevelopmental disorders, we integrated GWAS SNPs and Copy Number Variation (CNV) data and found that 265 enhancer-ncRNAs were either mutated (CNV deletion or duplication) or contain at least one GWAS SNPs in the context of such conditions. Of these, the eQTL-associated gene for 82 enhancer-ncRNAs did not overlap with either GWAS SNPs or CNVs. However, in 23 of these 82 enhancer-ncRNAs, eQTL interaction was explained solely by the presence of each of these noncoding RNAs, suggesting in such contexts that mutations to neurodevelopment gene enhancers disrupt ncRNA interaction. We also cross-referenced our data with the DECIPHER database of clinical phenotypes to find that mutations to 34 of the 82 enhancer-ncRNAs are significantly associated with phenotypes including behavioural abnormality, and cognitive impairment. Taken together, we provide evidence for a distinct set of brain-enriched ncRNAs that influence genomic enhancers during neurodevelopment, suggesting enhancer mutations may be relevant to the functions for such ncRNAs in neurodevelopmental disorders. Copy rights belong to original authors. Visit the link for more info

Dr. Mohammed is the Founder and President of ManaGene considered one of the most innovative leaders in the emerging personalized medicine and lifestyle genomics space.   In August 2018, ManaGene merged with Youtrients (www.youtrients.me) to form a new company known as The DNA Company. The DNA Company represents the evolution of functional genomics and is focused solely on the optimization of human health and performance.   Dr. Mohammed is widely regarded as a pioneer in medical genomics and has been the recipient of multiple academic and industry awards. He is the holder of several patents in the general fields of molecular diagnostics and genomics research and is one of the most sought-after national and international conference speakers in the genre of personalized medical genomics. In this interview, Lisa and Dr. Mansoor dive deep into the power that lies in understanding your unique genes to change the outcome of your health.   Some take the fatalistic view that if you have a bad gene or combination of genes you are powerless against them so it's best not to know but nothing could be further from the truth. Understanding your genes through DNA testing is like getting the user manual to your body and learning how best to care and treat it. The granularity with which you can start to understand processes and how these affect you and how you impact these is astounding.   This s actionable knowledge that will help you make informed decisions regarding your health in such areas as your hormones, your cardiovascular risk factors, your methylation, your detoxification processes and even your mood and behavior, why for example some have a tendency to more problems around depression or PTSD than others.    Never before in the history of the human species have we had such deep insides into the way our intricate and complex bodies work.    This episode is set to blow your mind and the work of Dr. Mohammed and his team is set to change the future of the world's health. We have the opportunity for the first time to take control of our own destinies rather than falling victim to our genes through a lack of knowledge.   Once you start to see and understand the power of functional genomics you won't be able to go back to the way you understood yourself and your body before. Your level of self-acceptance and the ability to help yourself heal and be healthy and whole will be taken to a whole new level.   If you would like to get your hormones or your whole genomic profile tested you can find out more at www.thednacompany.com    We would like to thank our sponsors for this show:   www.vielight.com   Makers of Photobiomodulation devices that stimulate the brains mitocondria, the power houses of your brains energy, through infrared light to optimise your brain function.  To get 10% off your order use the code: TAMATI at www.vielight.com   For Lisa's New Book Relentless visit the website below to order https://shop.lisatamati.com/products/relentless   When extreme endurance athlete, Lisa Tamati, was confronted with the hardest challenge of her life, she fought with everything she had. Her beloved mother, Isobel, had suffered a huge aneurysm and stroke and was left with massive brain damage; she was like a baby in a woman's body. The prognosis was dire. There was very little hope that she would ever have any quality of life again. But Lisa is a fighter and stubborn. She absolutely refused to accept the words of the medical fraternity and instead decided that she was going to get her mother back or die trying.   For more information on Lisa Tamati's programs, books and documentaries please visit www.lisatamati.com    For Lisa's online run training coaching go to https://www.lisatamati.com/page/runningpage/ Join hundreds of athletes from all over the world and all levels smashing their running goals while staying healthy in mind and body.   Lisa's Epigenetics Testing Program https://www.lisatamati.com/page/epigenetics/ Get The User Manual For Your Specific Genes Which foods should you eat, and which ones should you avoid? When, and how often should you be eating? What type of exercise does your body respond best to, and when is it best to exercise? Discover the social interactions that will energize you and uncover your natural gifts and talents. These are just some of the questions you'll uncover the answers to in the Lisa Tamati Epigenetics Testing Program along with many others. There's a good reason why epigenetics is being hailed as the "future of personalized health", as it unlocks the user manual you'll wish you'd been born with!  No more guesswork. The program, developed by an international team of independent doctors, researchers, and technology programmers for over 15 years, uses a powerful epigenetics analysis platform informed by 100% evidenced-based medical research. The platform uses over 500 algorithms and 10,000 data points per user, to analyze body measurement and lifestyle stress data, that can all be captured from the comfort of your own home   For Lisa's Mental Toughness online course visit:  https://www.lisatamati.com/page/mindsetuniversity/ Developmental strength, emotional resilience, leadership skills and a never quit mentality - Helping you to reach your full potential and break free of those limiting beliefs.    For Lisa's free weekly Podcast "Pushing the Limits" subscribe on iTunes or your favorite podcast app or visit the website  https://www.lisatamati.com/page/podcast/     Transcript of the Podcast   Speaker 1: (00:01) Welcome to pushing the limits, the show that helps you reach your full potential with your host, Lisa Tamati, brought to you by Lisatamati.com Speaker 2: (00:13) Hey team. We're this week I have an absolutely superstar, the world's number one leading functional genomic specialists, Dr. Mohammed from Toronto and Canada. Dr Mansoor, Mohammed has two guests now. He is a scientist and entrepreneur in the field of genomics and is regarded as one of the most innovative leaders in the emerging personalized medicine and lifestyle genomic space. Dr Mohammed is a PhD and president and scientific officer at the DNA company and is really considered to be a pioneer medical genomics. He's a classically trained molecular immunologist who has received academic and industry awards, published numerous papers and holds patients in the general fields of molecular diagnostics in genomics. Now functional genomics is about understanding the DNA and how it behaves in every definition and this Dr. Mentor was very different than many of the other DNA companies that I've looked at recently and that he doesn't just look at the single litters, if you like, of the DNA, but it looks in combinations of genes. Speaker 2: (01:22) And how they're playing out. And this makes him very, very different. This, he sees DNA like a language rather than a vocabulary and language that has grammar, sentence structure, Syntex and nuances. And you've got to be able to read genetic structure at the holistic level. Now I'm super excited about document's all his work and I'm studying functional genomics at the moment and it is the next level in personalized health. I'm really, really excited to bring this interview to you. It's taken me months to get documents or on this podcast and I'm hoping later on the year to get Dr. Mansoor Down to New Zealand for a lecture tour to speak to functional medicine practitioners down here as well as the public. So if you'd like to know more about that, please reach out to me and let me know. I'm just like to remind you before I hand over to Dr. Mansoor that my book launch is happening just next week over the time of this recording is the 6th of March and on the 11th of March. Speaker 2: (02:26) So by the time this recording actually comes out, my book will be live. It's called relentless and it tells the story of bringing my mum back after a major aneurism myth. You're fighting for a life and lift her in and basically not much over a vegetative state. Massive brain damage at the age of 64 and what I did to beat all the odds and bringing my mum back to health, all of the CRPS I used, the protocols, the attitude, the mindset, the obstacles that we had to overcome, the problems that I've discovered in our medical system in on it goes. So this book is really, I'm, I'm so pleased to be able to bring it out. It's taken me two years to get this together and to bring it to the public, but I really want to pay it forward and I want to help thousands and thousands of other people facing difficult challenges to take them are hit on with the right mindset to overcome great obstacles. Speaker 2: (03:18) So if you'd like to check that out, we can head over to my website. I have Lisatamati.com Hit the shop button and you'll see all of my books there and my jewelry collections. But make sure you check out the neatness. It's really going to be worth a read for anyone who has major medical problems at the moment. Or of course anyone who has a stroke aneurysm Alzheimer's dementia, and wants to know about brain rehabilitation or optimizing your brain function and who isn't interested in that as well as the whole mental attitude and mindset that it takes to do all this. So without further ado, over to Dr. Mansoor Mohammed. Well, hi everybody. Lisa Tamati here at pushing the limits. It's fantastic to have you back again. Now I am just grinning from ear to ear. I can't stop smiling because I've been waiting for this interview for weeks. I have a very, very special guest, Dr. Mansoor Mohammed, all the way from Toronto in Canada. Dr. Mansoor How are you going? Speaker 3: (04:17) I am great, Lisa. And likewise, it's been something that I've been looking forward to, to the audience. Please forgive me. I'm a little bit sleepy from Jeff blog from last night, but Lisa has been pumping me up and so we're going to have some fun of this Speaker 2: (04:31) Now. I know what it's like when you're a little bit jetlagged and you have a main very much in demand. So I'm just so excited to have a little bit of time with you now. Dr Mansoor, I do the whole introduction on a separate recording, but dr Mansoor, can you give us a little bit of background about your what you did your PhD in your, your, a little bit of a brief history of your back. Speaker 3: (04:55) Sure. genes. Genetics has always have always been my love. The study of how this operating manual, just just thinking, just, just dialing it back and thinking that the human being, we've got this operating manual that by every definition of the word it behaves like an operating manual. And to think that it's there and to think that one date might be accessible and that we could read this and we could read it intelligently and just simply understand myself much less, much less. Anyone else has always been my love. And so I started, my PhD is in applied molecular genetics and immunology. So I was looking at the genetics of the immune system. I was very, very fortunate to have an awesome mentor. She was then the chair of molecular biology at UCLA invited me to UCLA. So I had an awesome couple of postdocs there where I got deeper and deeper involved in eugenics. Speaker 3: (05:47) But a real pivotal point happened when I was done, invited to come to Baylor college of medicine and Houston, Texas. And it was that heavy time just about the human genome project, its, you know, sort of pinnacle. And I was asked because of the work that I had been doing with UCLA to come over to Baylor and start a company, the goal of this company was to begin looking at multiplex genomics. In other words, to really do the, you know, the barrage searches into the human genome. Not one gene at a time, but looking at the entire genome in pathway type manners. Now initially we applied this knowledge to cancers. We apply this knowledge to developmental disorders syndromes, Prader, Willi syndrome, autistic spectrum disorders and so on and so forth. And about 15 years ago, after many years of doing what I call disease genomics, looking at the operating manual, looking at when the operating money was broken out of what happens from a disease perspective. Speaker 3: (06:45) Then I sort of thought, okay, well that was fun. That was good. That was, but why should I not look at the operating manual? But nothing is purportedly broken, but just the operating manual. So then still we can tell presumptively healthy individuals how to stay healthy or how to get over the type of chronic illnesses. So this is what I've been doing for the last 15 years, studying, researching and applying the knowledge of the human genomic operating manual. So we've been, we can just simply understand it. How does the body work, which clearly there's an individuality to that, obviously. I mean, we are human beings. We all, our cells, our organs, our bodies, all have to accomplish the same jobs that we do. These jobs with nuance differences, some of us less optimal, more optimal, more efficient, less efficient. And when we can zone into that, when we can read this operating manual from that perspective, really Lisa miracles happened with the sort of insights that you get, the nuances that you can tease out. It really has transformed the clinicians. We train the patients, we work with the transforms, it empowers the individual to understand how their body works and what they might do to obtain that optimal health. Speaker 2: (07:59) This is, and this is a super exciting and I can feel your passion coming through despite the jet lag for this area and it's now mind you, passion is of the last maybe two months or six weeks or however long it is now that I've been diving into this world and just going, Oh my gosh. Oh my gosh, this is just, this is just the next level and the information that I've been searching for to try to understand because everything seems so generic. And this a personalized house and yeah, doctor man saw you the president and founder of the DNA company, which is offering direct to public and in conjunction with conditions. A couple of reports. So our full genomic report in a hormone report and I want to tease apart a little bit today, why should people even consider having a look at these, the sort of testing what benefits they can get out of it. Speaker 2: (08:58) And I'd like to also tease a little bit about looking at other, like I've, I've looked at a lot of gene companies and that do gene DNA testing. And you had an analogy on a Bulletproof radio that I heard you on the same show who's amazing Dave and his work that was about the most people are looking at it DNA as a vocabulary and not a language. And that just seems them light bulb up in my head where I realized, okay, so it's not the siloed genes looking at them individually, but looking at cascades and pathways and combinations of genes as we are then interpretation has been missing today. Speaker 3: (09:43) Oh, 100%. So I always say, you know, Lisa, anyone that is in the data business, regardless of whatever data you're collecting, data is really quite dumb. Data in and of itself doesn't mean anything unless you know what to ask of the data unless you know how to triage, how to approach the data. So when we use the analogy as DNA, the operating manual, the genome, it really meets all the classifications and descriptions of a language. Thus far we've been looking at DNA and genetics from a language perspective purely as a vocabulary exercise. The more words we know, the better we presume to think we know the language. And as much as that is important as per the analogy that I drew with on Dave, show a person simply knowing more vocabulary by no means mean they understand the language. And so when it comes to DNA, when it comes to genetics, when it comes to how this awesome operating manual, the architecture of it, it's not just about vocabulary, it's not just about the individual genes. Speaker 3: (10:51) So here are the two layers implicit in your question that we do a bit differently and why we need to do that differently and why it's important that it's done this way. The first is this. When you're looking at the DNA, if the person are either genetic makeup, the vast, vast majority of companies right now, they're looking at things called snips, single nucleotide polymorphisms. In other words, they're looking at places which is absolutely important. They're looking at spelling variations in this operating manual. And of course these spelling variations, these single nucleotide polymorphisms will impart to you mean Jane, Paul, Peter, the same cellular job that we all want to do. These spelling differences can impact the efficiency with which we do that job and that is important to know, but while we're at that point of spelling, you see per any language, if I wrote a paragraph, I might have spelling errors in that paragraph, but there are examples where I may have inadvertently deleted a sentence or deleted a couple of sentences in that paragraph. Speaker 3: (12:00) Now, if the analogy here is that the gene is the paragraph, so your operating manual are these 23 volumes. Think of it. Think of a 23 volume and psychopathic set these awesome, huge volumes. Now we're going to inherit two of these 23 volumes. One from mom, one from dad, and these volumes are properly arranged and when we open up any page, let's say we go to volume three from mum volume three from dad, we open up page four on each of those volumes and we look at paragraph five page four, volume three we, I see the same paragraph. We're going to see the same information from dad's gene paragraphs of genes and mom's gene. We're going to see the same information, but when we look really carefully, when we look at those paragraphs, really collect carefully, we might find that there's some spelling differences. Those are the snips. Speaker 3: (12:57) We may also find that on either dad or mom's paragraph, a sentence was missing and I just taught this over the weekend. So I was in the auditorium and I said, okay, here's an instruction that was waiting for me coming to this auditorium to give this lecture, Dr Mansoor, go to auditorium B and to the left door approach to podium from the right side, press the enter button, begin your lecture. That's an instruction. That's a paragraph. That's an instruction and that's the equivalent of a gene. Now in that paragraph they make has been a few spelling errors or changes that may have confused me a little as to what the instructions are. But when I look at it carefully, I could sort of still figure it out. Okay. But if in that paragraph, the sentence that says go to auditorium B was missing at, of course there are multiple auditoriums, all of the other parts of the instructions are there. Speaker 3: (14:03) But I can really be confused as to what is the ultimate thing that I'm supposed to do. It's called an indel. So in our genes, not only do our genes have slips, many important genes actually have places within them that I'm missing. So until we test for those type of changes, we're by no means getting the full picture of what is happening. The third thing is this, not only do we have slips, not only do we have in Dells, there are occasions where the entire gene is missing is show I'm supposed to show up. I got to the hotel where the conferences are and the instruction just telling me what it's just not even there. So here I'm in the lobby going, I don't know what I'm supposed to do. This example is a genetic phenomenon keeping the analogy, this is called this C and V copy number variation. Speaker 3: (15:03) We see because we were supposed to have two copies of that. Paragraph five page four, volume three. Sometimes believe it or not, when we go to page four we've opened up mum's volume three dad's volume three. There they are. We're going to read both of the instructions cause that's what yourself has to do at any given moment. When there's a job to be done, your cell goes and pulls the volume that has that instruction, takes down a mum's copy, takes down, dad's copy, opens up and reads the instruction. Now in the case of a CMV copying of the variation, we can open up mum's volume three page four there is paragraph one, paragraph two, paragraph three paragraph four paragraph six. Oops, wait a minute. Where's part of our five? It's gone. There's part of four. There's part of six. I look over a dad. He's got all of the paragraphs or vice versa. Speaker 3: (16:02) Sometimes Lisa, both paragraph fives are gone. Okay. So the point of the first answer to your question, why we do things a bit differently is we're not just in the business of collecting data for data's sake. We're collecting data. Are you were doing gene testing to understand a process. When we designed genetic tests, we don't begin with genes. We begin in a whiteboard saying, what is the thing in the human body that we want to study? What is the thing that we want to study? Genetics, just good old fashioned medical textbook, human physiology. Do we want to study the way the newer chemicals are produced and bonding and response? Do we want to study how the human body makes sex hormones? Something we should talk about when it comes to human performance. So how does the male and female body makes progesterones androgens Astros? And then we mapped that out. Speaker 3: (16:56) Forget genetics, which is not about how does the human body do that? No, of course, if the human body's having to do something, then it means there are genetic instructions for that film. So only when we map out the cellular, the cellular biology, the cascade, only when we met that out, then we come in and we pencil it. This gene is responsible for here. This gene is responsible for there such that at the end of the exercise, we've got a genetic test that already tells a story. The result from that genetic test is telling you the entire cascade. Step one, step two. We look at each of those genes that are telling us the story and we ask are these snips that are important? Are there entails that are important? Are the CNVs that are important because all three make a wow. And so the first part to the answer to your question is if you've been looking at genetic tests that are only reporting snips, you are dramatically limiting the variations that you and I and every other person have within our genome. So you're missing the nuances that are in your language to clarify the job to be done. Does that make sense? Speaker 2: (18:16) Absolutely. So that actually puts them together in my head because I've been starting this, I don't know, like for example, the GSTT one gene and the detox and antioxidant pathway, one of those types of genes that can be completely done. Speaker 3: (18:31) Completely. Totally said, absolutely. And of course it belongs to super family. So there are multiple G S T genes, but two minutes on that. If you're going to design the human body and you're going to say, listen, one day we're going to make this thing called human being and we're going to put him or her in this wonderful world, but mind you, he or she is going to have to deal with some toxic insults, both from without and from within. Where would you, and you know that, where would you put your detox defenses? Well, they're about four places. If you're an intelligent designer, you would put your detox, different defenses at least in four places. You would say, how and where do things get into the human body, dermal skin, the nose, nasal Bronxville lung, the GI track. Okay. So those are how things get it. Speaker 3: (19:23) And unsurprisingly you would want to make sure your detox genes and the things that you'd want to make sure there's super active in those places. And then you, you'd also say, well look, at the end of the day, things are always going to get past borders inside of the body, their waste products. So then I'm also going to put a detox organ. The liver, when we go to the human body, this is where we find these detox genes expressing themselves. And each of the GST is have sub specialties. Some of them are more important in the nasal bronchial track, some of them more important in the GI track and so on and so forth. So when you know the story that you want to read about the body, you know how to read the manual and interpret, is the GST T one gene deleted or not? This is a massive implication to the human body. Speaker 3: (20:16) Can you imagine the GSTT one gene is one of, if not the most important bio transforming antioxidizing enzymes in the body per its name and its gene and its enzyme. And if a person doesn't have it, literally it's not in mere manual. The GSTT one gene is on volume 22 and if that paragraph you have not inherited it from either mum or dad, you are missing an enzyme in your body. That is one of the most important detox. Now doesn't mean that you're not compatible with life, but it most certainly means you could not be the person who says, well you know what do you have a metals mean after all they're not that bad. Oh you know what, my uncle smoked until he was 80 years old. I'm going to smoke as well. Well you can't compare yourself to that person cause you don't have one of the most awesome detox genes. Speaker 2: (21:13) You don't have a good defense mechanism. And so like the detox is actually the first port of call before the immune system even does this job. So I'm, I'm excited to get my tests back cause I haven't gotten gotten through the reports yet. I'm, I'm suspecting that I have a problem in my GC jeans because I'm a very young age. For example, I've been the next medic as a, as a severe asthmatic, as a child, and I'm very hypersensitive to smells and anything. So I'm like a Canary one C one, which is theta. Yes, Speaker 3: (21:54) Very important in the liver. Key one PI GSTP one is the one that's really important in your nasal bronchiolar lung cavity. Individuals with a suboptimal P one are at extreme risk of early ectopic asthmas. They're the ones that if they go into the shopping mall, you know, the perfume resection, they've got to avoid the perfume resection. Right? Those are the GSTP ones. Speaker 2: (22:21) Wow. I'm obey. Fascinating to see if that's what comes back. And so if you want it deleted into them, we'll get onto hormones next because I really want to dive into there, but just to, to to look at the GST genes. If you don't have, you either have only one inherited GST, one gene, your mother or your father and you're missing the other ones or you're missing both altogether, are you more likely to have you're more likely to have toxins coming in that you can't deal with as well. And then your immune system is this way or auto-immune or part of the Speaker 3: (22:57) Brilliant, brilliant question. Just before we answer that, I had mentioned there were two layers to differentiate yourself, so just so that we close the chapter on what we do differently. So I'm going to come back and, and so now we will take it forward. We just mentioned that there you have to be mindful of the three different layers of variations, snips in Dalles with pieces of the genome missing and CNVs where the whole gene may be missing. The other quick differentiator, bringing back the analogy of a language, bringing back the story of the human body, it's this, and I told the audience this, there was an audience of clinicians in Phoenix this weekend. I said, have you ever read a really good, you know, suspense novel and not suspense novel, the novel that the author's painting the character and you're thinking he's the bad guy, you know, and he's falling around the heroin and he knows he looks a bit shady. Speaker 3: (23:51) And then until or unless you've read the entire book, you only find out that he was a protector or he was something. He was a guardian and words. He wasn't about that guy. Now what the heck does this have to do with genes? The second player, when we mentioned that we do things differently, we said that DNA is really a language by all of its definitions, with its nuances is this, there are many genes, Lisa, where if you were to look at that gene as a standalone and if you was to look at the genotype of that gene, in other words, what version do you have? You think you have either the best version or the worst version depending, and you may think you have the best version for example, but it is not until you look at a completely independent gene that has nothing to do with this gene, that the version of that independent gene wow colors, whether your actual optimal version of gene a will stay optimal or not. Speaker 3: (24:52) Or conversely, whether you thought you had the suboptimal version of a bad guy, you read the full story, something else tells you what you fought was the bad guy was not the bad guy. Wow. And this is what it's called at peace basis. You see we're all concerned about epigenetics, which is important. FP genetics. How are we reading? Are we actually going to read that paragraph on the page or are we not going to read? That's at the genetics, but nobody's talking about epi. Stacy, this is Stacy. This is often, we've read the page after we've read the paragraph. We cannot yet make a conclusion until we read 10 pages later, 15 pages later, something there. We'll bring it to life. We'll color what we read on page three. Speaker 2: (25:48) Yeah, so, so for example, if you're, if you're looking at a specific gene and it has an, that is say the faster for the sip, 79A1 gene and the hormone a kiss guide. If it's a fast one that's not in and of itself a good or a bad thing. It depends on the other things. It depends on the, so that's what you're meaning. So one of Speaker 3: (26:14) The best examples of that is this, the BDNF gene, the BDNF gene, brain derived neurotrophic factor. What are the most important genes in the brain? Well, in the whole human genome that tells the brain how to secrete this awesome thing that heals the brain. You and I were having a conversation about a loved one, so that loved ones B, D and F was going to be hugely important. And how that loved one recuperated from the challenge that she had met BDNF. Now the beating of gene has an important variation. A snip this time, which is either a G version or a version. Okay. TheG version, Jews and George as in guanine is the optimal version of BDNF, the optimal version. So if you're a GG blessed, that's good. You are naturally predisposed. You have the in Harrods, the innate ability to make more BDNF. Speaker 3: (27:13) And let me tell you that's a good thing. Any which way you slice it. Wow. An independent gene, the TPH to gene the trip to five hydroxylase gene to TPH, two gene, which is involved in how the body deals with serotonin. K two has a sip. It comes in a G version and a T version G as in George T as in Thomas. The G version is considered optimal but hold on. If you happen to be GG fatigue, pH two and GG for BDNF ostensively both those genotypes for each affair genes are optimal, but if you were GG for both, it creates a haplotype. It creates a combination that is an act risk combination and it is, it is the negative combination. It is the, it is the deleterious combination when it comes to certain aspects of human behavior. These individuals, when you're GGGG, they exhibit poor inhibition of negative emotional stimuli. Speaker 3: (28:28) In other words, when something negatively emotionally affects them, their ability to kinship, the ability to say, you know what, I'm not going to focus. I'm not going to hamster wheel constantly play that over and over over again. They haven't, they have a hard time giving up that when something gets under their skin. So to speak emotionally, they have a really hard time getting over it so they have a strong imprint. The memory imprint, very strong EMI, emotional memory imprint and of course the stronger you EMI emotionally memory imprints, the easier you emotional memory recall EMR is because the deeper something is imprinted then the smallest cue. You have a love, you have a partner and you know you love each other to bits, but like human beings, you're going to have your ups and downs. I mean it's where human beings after all, and on one particular evening you were both getting on each other's nerves and she was wearing that beautiful red dress and that was the evening that you both said things you shouldn't have said and it hurts the person who has this phenomena. Speaker 3: (29:36) Whenever he sees his wife, would that red dress down the road, everything's perfect. You, you're going up for a birthday party, you're both happy, it rises back up. He remembers that evening more than he should. It brings back to the surface and vice versa. This is that Paul, inhibition of negative emotional stimuli that lead to profound memory imprinting and therefore profound memory. Recall. The point of all of this and the reason I mentioned this is, and we're going to come back to the GSTT one, was to clarify, you see Lisa, it's not just about even the type of things you're looking for. What matters is the interpretation we sell the combination, we are reading the manual, not just flipping, picking words out. Speaker 2: (30:24) This is we have a calmer is well we are the, the apostrophes are this is someone that is what they would be more prone to PTSD Speaker 3: (30:36) 100 that's the point actually and that is further exacerbated based on the no adrenergic pathway which dramatically increases the risk of PTSD. It is exacerbated based on how quickly they are removing their dopamine and noradrenaline via content. So what happens is you begin to pixelate a picture and you've got a low resolution picture and then the more intelligence information you put in, you start to increase the resolution of that picture. You start to get a clearer picture of the person that you're looking at. But to do so, you've got to know where to pick slate. If I'm trying to get a better look at what Lisa's face look like, I don't really be pixelating your toes. I need to pick slick your face and this, this ability to read intelligently. Lisa, I stress intelligently. Riyadh, human genome. Yeah, that's what we do. We do Speaker 2: (31:35) That is absolutely insane. And they've vacations because yeah, I would have seen, Oh, you've got a G G G is good, but I've just understood that nuance, that combination of things. And now I can't wait to get my reports and my family reports so I could because this helps us also understand like the speed in which you are dopamine is processed and gotten rid off or the speed of which we're saratonin tone and all of these things have a fixed on your personality and that we're not 100% to blame for some of our differences. Speaker 3: (32:12) Oh gosh, no. Gosh, no. In fact, what this needs to do on the one hand, it creates the empathy of appreciating, look, this is how some of this is their predisposition. Now, on the other hand, it is not to create a sense of fatalism. While that's the way I am, I know I have found and I have done. The only thing that I've done, probably somewhat unique and special Lisa, is I have reviewed thousands upon thousands of profiles. In terms of my in the world, most of my peers that work at the level I do would say Dr. Mansoor Probably reviewed the most genomic profiles in the world. I don't know if that's true or not, but I certainly have reviewed several thousand meaning meeting the patient, speaking with their doctor, looking at their health profiles and looking at underlining genetic phenomena to see if we can understand what's going on. Speaker 3: (33:00) You know what I found, at least as a fellow, when you empower a person to understand a predisposition, you, you might think that leads to fatalism, but when you explain the functional reality, it actually does the opposite. It gives the person a sense of ownership and then they can finally say, you know, I have dumped with my entire life, I've been this way and I just, I didn't even know why it was that way. Now that I can even understand what's going on, it gives me some closure. Yes, but it now gives me something to appreciate. I can, I can envision how this is working, how my emotions are working. I can now go, you know what? As soon as I see that stimulus that would have got me on that slippery slope, I'm going to stop. I'm not going to go down that slippery slope because I know if I do, there's no coming back for the next two weeks. Speaker 3: (33:52) So what we've found is that this crew all around it just creates empowerment. Which brings me now to the question that you asked about GSTT one and you are, your connections are on point, Lisa, the connection between the detox mechanism of the body. Here's the threefold, and of course it's a bit more complicated, but it's also remarkable. You can take complex systems, break them down to building blocks and keep the acuity. So there are three building blocks we need to look at when we connect detoxification pathways in the body and the immune system. And the, the only thing missing is the inflammatory system. So the triangulation between toxins and immune responses goes like this. The human body's insulted with whatever. It's insulted with the intentional, the unintentional of our daily lives, those toxins enter the body or they try to enter the body. Step number one, how individually efficient is that person at negating bio transforming, neutralizing those toxins either before they can enter the body, such as in the mucosa of the lung, the alveoli lumen, the the lining of the lung, such as the GI mucosa and so on. Speaker 3: (35:16) And so what can we, can we neutralize it so the toxin doesn't even get into the bloodstream? And of course to the degree that it gets into the bloodstream, can we live a hepatic re detoxified so that at least it does not by you accumulate in the body so that at least it does not reach levels that are unsafe. First step number one now too, there are genes, there are whole gene families, their whole cellular processes, GSTs, glutathione, ionization, UGI, Ts, glucuronidation, methylation, self, phonation and acetylation. These are the major enzymatic steps linked to genetic genes that are responsible for bio transforming neutralizing things in our body, okay? So what we need to do is we say, what is the lifestyle environmental context of the person? What are they getting exposed to? I'll be living in a home that has written with mold, are they living and so on and so forth. Speaker 3: (36:17) Okay, step number one, step number two, how good are they at individually neutralizing those toxins so as to not bio accumulate them to the degree that those, whatever. The answer to that question is we're going to have an individualization and with some individuals are better at getting rid of toxins and others are not. If a person is not genetically, innately efficient, optimal at getting rid of their toxins, then what happens? Well, what do toxins do? Toxins cause cellular inflammation, okay? And they cause inflammation via any number of methodologies. They can inflame cell surface receptors, they can get into the cell and create overproduction of oxidants as they can hamper the energy modules, the mitochondria. That's one of the places you'd never want toxins getting to. And of course they can get into the nuclear eye. They can get into the libraries of the operating manual and they can start to change gene expression. Speaker 3: (37:23) So toxins do all of these things. Ultimately, you see Lisa 15 not even 15 years ago, 10 years ago, if you told that a medical conference, there's this concept of inflammation. You'd have a lot of professionals. Well, come on, you gotta be more specific than that. We actually now know that there is a phenomena called chronic inflammation, and regardless of what stimulated that inflammation, bat bacterial toxin B, it's an inorganic chemical. It be it a physical inflammation. It does not matter the way the sun looks, the way the cell begins to behave when it has been insulted with toxins, with exposures, remarkably is the same regardless of the stimulus. Because chronic inflammation has hallmarks that are similar regardless of the stimulus. Now at that juncture, when the cell is inflamed, when the machinery in the cell isn't doing the job that it's meant to do properly, that cell now starts to be like this pulsing red thing just by analogy. Speaker 3: (38:35) In other words, the body is looking at it going, something's happening in there. It's not behaving the way it should. Okay, so now we're going to have two steps. The body now has an anti inflammatory set of steps to quiet us, to bring the cell back into line cause they Whoa, Whoa, hold on. You're starting to misbehave. There's too much inflammation. This is where it's selling the process known as methylation comes in. Cellular methylation can be viewed. It's a detox reaction by the way, but it is a cellular cascade that is radically responsible for bringing your soul from that humming, inflamed, you know, ticking bomb type of modality back down to acquire essence behavior. That's cellular methylation. Now, to the degree that you're able to do that, because suddenly methylation is a multigene cascade, multiple places where things could be not as optimal as we would like. Speaker 3: (39:36) So to the degree that we then triage, we stratify the patients based on their detox potential. We then stratify them based on their anti inflammatory potential. Now, to the degree that we are not quite yessing that chronic inflammation, this is where the immune system can be activated. Immune system was meant to be activated in acute episodes, not chronic episodes. The more you ask the cell to produce antibodies, IgG, IGA is IGMs, particularly IgGs. The more you keep telling that the body pump out IgG, something's not working right, something is there, which is why chronic infections are now very well understood to be linked to autoimmune diseases. The infection did, did not go away, constantly demanded of the body to produce antibodies. And somewhere along the line those antibodies begin to forget what was the bacteria or what and what was the self. And now we just start shooting friend and foe alike. Wow. This is the triangulation that has become now a focal point of so many diseases. Some diseases being more relevant to the whole, you know, things like lying disease. Do you guys have lung disease down in New Zealand? Speaker 2: (41:05) I think, yes, we do. And I think you know we have a massive problem with like thyroid, Hashimoto's sort of autoimmune diseases, crones, IVs. So this is, this is where the body is actually going in overdrive. So the, the original detox genes haven't been able to do their job because combination. Speaker 3: (41:26) There's that one. Exactly. There's inflammation. Yup. Speaker 2: (41:33) Yes. Speaker 3: (41:33) Methylation didn't do the job that was supposed to do and now we're triggering. So there are meta-analyses meta-analyses that show the deletion of the GSTT one gene or overall poor Ghouta finalization has been strongly linked with ulcerative colitis, Crohn's disease, IBD, strongly linked with ectopic asthma, particularly GSTP one in early childhood asthma. Then of course, if you, if you double down on poor math on poor detoxification with poor methylation, you really start seeing Speaker 2: (42:10) Clinical outcome. Yes. Yeah. So, so if we then we, we, we find out all this about ourselves. We find out we've got either the good or the bad and the ugly. And these combinations are not ideal. Then how, you know, we've got this information now, now we want to know what the heck do I do about this? I can't change my DNA. Of course, all things that these reports that your company does, for example, where it can actually lead to some successful outcomes. Obviously avoiding cigarette smoke or exhaust folk tunes and things your GPS deleted. But, but beyond that, nutraceuticals, new nutrients what can be done to help people. Speaker 3: (42:52) So it starts with, so the first thing I would have to say is we take our reports only so far. So the actual report, we take it to the point of explanation of what's happening. And there are certain recommendations, but the real magic must still come from a trained population, you know? So what, so what we do is through also training a certain class of healthcare providers. We might call them the, the new modern day biohackers. The healthcare providers who are really sniff, they're no longer just, you know, pill pushers. They're looking. So I just wanted to clarify. We take the reports, we explain the systems, we explain what's happening, but we also have to be careful so that people aren't jumping to conclusions and self-treating based. So you still want to have someone who understands the bigger picture. And by the way, that's the second part of what our company does. Speaker 3: (43:47) As per my travel schedule, I'm constantly traveling, teaching people, teaching auditoriums full of doctors who are now saying, listen, if I keep practicing medicine the way that I'm practicing, I'm just dealing with a disease population. I'm not healing people. Okay, so with that minor clarification, now we come to, let me paint a picture, paints a thousand words not to be, you know, blahzay here's what I like people to picture and here's what you would want to picture for yourself. Lisa. Picture slide. Okay, so there's a slide your screen, okay, and a circle. And then picture a circle on that screen somewhere on your screen. There's a circle. Now because you're a human being, your circle is going be on the screen. In other words, this is the screen of all human beings and your circle, you, your circle is somewhere on the screen or what does the circle represents? It represents your genetic makeup, which represents a part of your genetic makeup for whatever biochemical process we were studying. So this circle is Lisa's genomic pathway. Okay. Speaker 3: (44:56) I want you to then think of an equilateral triangle that equal three sided triangle that just perfectly encompasses your circle just perfectly. Your circle is perfectly encompassed just right in that triangle. And the emphases of this triangle are labeled environment, lifestyle and nutrition. Yes. What we're learning and what we're recognizing more and more is other than extreme cases, other than extreme cases, and there are mind you extreme cases where a particular genetic combination was really just a real doozy. And in other words, we're going to see some, you know, with the best of efforts, we're going to see some probably deleterious outcomes. Fair enough. But other than those extreme cases, for the vast majority of us, the spite, any inefficiencies we might have if we find the right triangulation of lifestyle, nutrition and lifestyle, nutrition and environment. If we could figure that out and it perfectly matches, I would circle. Speaker 3: (46:08) This is optimal health. So image, the image of optimal health is when you can find your genomic makeup, your circle for whatever you're studying and contextualize it perfectly within the right for you. For Lisa Laughlin, sir, not for Joanne Felisa. What is leases? Optimal lifestyle, nutrition and environment. Now the problem is, Lisa, when we begin working with a patient, obviously and clinicians with their patients, the vast majority of individuals, they do not know their circle. They don't know what's the economic influence. So they don't, and if you don't know your circle, your triangulation, choices of lifestyle choices, nutrition choices, and environmental choices offers skewed and they are not synergistic with your circle. So first objective of this, did you get that picture? Do you know when people say, well, it depends on your genes, your genes. It depends on how you're using your body. If you are, if you took, if you took five identical individuals, they were, you know, quintuplets identical, contemplative. Speaker 3: (47:27) If such a thing exists in today, the same genes and you give those five people at 35 years old, the exact diet. But if those five, one of them was an ultra marathon runner and extreme sports enthusiasts, the other was a couch potato, I don't know, doing whatever the other was a, you know, an accountant who had a nine to five job. We can exercise worrier, but from Monday through Friday really just goes to work, comes home, eats, goes to that and so on and so forth. Even with the same jeans, you can put the nutrition and an obviously not expect the same outcome because they got to know the genomic legacy. You've got to know what is the lifestyle context, what is the nutritional context, what is the environment or context? If one of the things quintuplets moved from your gorgeous country and move to massive metropolis with, you know, air quality, that breathing for one day is the equivalent of smoking a pack of cigarettes in your beautiful country. Speaker 3: (48:36) He or she may have gotten away with a GSTT one or GSTP, one suboptimal ability. He's living in those, you know, that wonderful country views. He's practicing otherwise good, not eating foods with pesticides and herbicides and so on and so forth. And he was going about life actually, not really realizing there was any suboptimal ability until one day his job took him to a big metropolis somewhere. He lost track of the quality of his foods. He's just so busy. He's day in, day out breathing the equivalent of a pack of cigarettes and then six months into this, all things ELLs as equal, his jeans are equal, but he now starts to show symptomologies that he would never have had any different environment and a nice clean environment. Right? So this triangulation is so important. Now coming back to the specifics, once we understand the pathways, we begin first with the dose. Speaker 3: (49:31) It may seem simple, but it actually enters Lisa into, it's not just about the obvious things that you might imagine. I give the example, Lisa, and by the way, it's relevant to the GSTT one gene. Now, juice, TT. Let's focus on the T one. It's the big sister in the glue, the fine fabric. So GSTT one no, it's what's called a phase two detox pathway. Phase two detox. Because when it talks and enters the human body, we typically go through two steps. We take toxin a, we converted into an intermediate B. Yup. We take B further, convert that to C. C is what leaves the body, the B to C part of the transformation. That's where the GSTs come in. The a to B. This is where your cytochrome P four 50s come in. That's the phase one. Bio transforming enzymes. Now if I were to ask you something, when you say fiber to say, would it be a good practice for person to start drinking a nice cup of green juice? Speaker 3: (50:38) You know, like some juice, juice, broccoli and some maybe put a little bit of a baby spinach in there. A bit of ginger, maybe some cute, cute curcumin at the end of it. Would that be a really healthy drink? Yes. Something I do every day. Beautiful, beautiful. And it is healthy generally speaking. So now someone puts a blog together giving this recipe of something that's ostensibly so healthy and there's this mechanic who works in a shop all day with fuse and so on and so forth. He read this blog, she read this blog and she decides that before she goes to work, she's going to have this beautiful juice. This green juice that they read was so healthy and it was a detox juice and they feel good about themselves. Hold on, hold on. Many of the ingredients and not green juice. Many of the ingredients in that green shoes turn on certain phase one sip four 50 enzymes so as to accelerate the conversion of a to B. Speaker 3: (51:54) Now some of the toxins a that this mechanic was facing in her shop, in the, in the, in the mechanic shop that she was working at, when she converts a to B, we know that the B, the intermediate is truly more toxic than wow. And by the way, she did not know she was a GST one deleted individual. Oh, so what did we do to this young woman? We encourage the things that is that we're getting into her body. When she drove that beautiful healthy green juice, she more rapidly converted her A's into B and then ups B's and to CS very well. Wow. Even something that would ostensibly be really healthy by normal standards. Do you see that's a healthy nutrition on the triangle, but we did not ask what was the environment on the triangle and so now we have skewed her triangle away because her genetics circle, she does not have the GSTT one. Do you get that picture? This is a little bit frightening for people who are listening to this or who might be going well, what's the point being? Speaker 3: (53:16) This is weird. The reports have the super value, isn't it? That's the point. It's, it's actually not discouraging. It's, it's finally, and this is all gold. It's finally meant to unravel those nuances that there is such a thing. Have you been? How many of us, you know, we do something that 20 or the coworkers swore was the best thing since sliced bread and then we tried it and not only did it not work, we actually felt like crap or less healthy, and we, we're all aware of this until it's what is it led? It's led for most of us to become numb. We're just kind of get to that point where we're like, well, I don't know what's right for me or run for me. Plus today it says one thing tomorrow it says another thing. So creating some sanity from this confusion is what this goal is about and it can be done. Speaker 3: (54:11) Lisa, when you take your time to read things, intelligent meals, explain things. That's why we've got these epiphany moments that constantly, I like my consults with patients because I feed off of the energy. When a patient just, you see that epiphany admission and they light up and they go, Oh, that's why this hasn't been working with. That's why that was better for me. That's why I took methyl B12 because everyone's telling me methyl B12 is the best version. But every time I take methyl B is it just in my head. I get a headache every time I take micro B12 I get a, and then I go, no, actually I got one too. I can't take methyl before. That's an actual thing. I can't take methyl B12 because my methylation cascade is inconsistent with me taking methyl Beto when I take a dental Sobe 12. Oh, completely different. Speaker 2: (55:07) Wow. So this is getting really granular for each individual. And this is what makes me so excited. And, but before we go on, we have to go and cover off the hormone report. This is something that I and, and this is, you know, for me and any woman, but I wanted to focus a little bit more in on the woman. We've got very complicated hormones, households, but this was the cascade for men and women is very, very similar, isn't it? Yes Speaker 3: (55:33) It is. It's just remarkably, this is what we taught at the cost on the weekend after introducing genomics, it was the first open to eyes that the cascade, the circadian rhythm with which the human body converts progesterones into androgens, androgens to estrogens, men, we do not have a monopoly over androgens. Women, you do not have a monopoly over estrogens. In fact, your estrogens come from androgens. Men, we have estrogens. It's just a matter of the circadian rhythm. When is it happening? How quickly is it happening? And of course, ultimately how much of any of these hormones are produced. And then the final component is how responsive are you, the the woman's body, all things equal. She's designed with the estrogen receptors to be more responsive to estrogen. She responds to androgens as well. Conversely, for men. Now keep in mind something as simple as, I can't believe how many clinicians do not realize how an androgen or estrogen receptors. Speaker 3: (56:32) Now let's stop there for this cascade. We can talk about all of the things about how hormones are produced and how they're metabolized and so on and so forth. But ultimately, how is estrogen affecting your body? Lisa, you're a young woman. You're making estrogen as if you're menstruating or if you want hormone replacement, there's likely some estrogens in your body, one way or the other when estrogen binds to your estrogen receptor. And to the degree that that can happen, mind you, because there are variations to that fidelity, this complex estrogen. So the estrogen receptor androgen to Stastrom, DHT to the androgen receptor. These complexes are some of the most potent DNA transcribing complex. They go into the nucleus and the churn on genes. This is how estrogen and testosterone impacts the human body. They live. They're not just, I don't know, causing breast development or, or, or, or Andrew demise in the book. Speaker 3: (57:39) They do that by churning on the genes that cause the cells to behave in a more underutilized manner or more estrogen. So the first thing I want, our audience needs, our clinicians, we need to re re climatize reacquaint ourselves with that. These hormones potently DNA transcribing, they go into the nucleus and they turn on and off genes. That is why they are not to be dealt with trivially. Number one. Number two, in a menstruating woman. Now I just told you when estrogen enters a cell, I did binds its receptor. It's not just staying in the, in the Maloo of the South, it's going in to the volts, the nuclear volts and churning on and turning off genes. Wow. When you look at the ministerial cycle of, of a, of a relatively normal, repeatable menstrual cycle, you will notice something radically important over the course of 28 days. Speaker 3: (58:43) The human female body isn't exposed to estrogen at the same amount every day, not at all. The human female body in 20 days only has about a six day or so window in which your estrogens that are really elevated and then it comes down. In other words, what is this telling us from a human biology perspective? It's saying that the type of gene expression changes the epigenetic phenomena that estrogens cause on your operating manual. You don't want that to be consistent and constant across the month, and this is very frightening when you look at contraceptive pill or hormone replacement therapy. So it's most certainly very frightening. That is not, let me be clear. That is not to say that there isn't a place or a time for these things. You know they are absolutely a young woman has to have the right to how she treats her body and what she does. Speaker 3: (59:47) But there is a place in time you at least be equipped, at least be empowered before you make this decision as to a knowing what it's doing for you. Say, okay, look for these few months of my life, for these couple of years of my life, this is going to be a bit more important that I take these precautions, for example, but you should know that to do so indefinitely, month after month, year after year. Now they've got clinicians encouraging young woman not to even have a bleed through. There's no point for even the bleed. So just stay on the, you know, constant level, 24 seven three 65 15 years. How is this compatible with normal human physiology? When you understood what I just said? Yep. Now let's go a step further than that. You see estrogens do what we just said. They bind their receptors, they go into the cell so they go into the nucleus. Speaker 3: (01:00:47) They change gene expression as they're meant to for brief periods during the month. Fair enough. Now, once those estrogens have done what they've done for those days, then the point of it is there's a circadian rhythm. The body breaks down those estrogens metabolizes them by a transforms them so that they're no longer active. They've been neutralized, and then we hit repeat, rinse and repeat, and we start a new cycle. But here's the point. Every a woman, Lisa, every a woman, a man for that matter, but let's focus on the ladies when she made her estrogens or she took her estrogens, because even whether you take it or whether you make it innately or you take it, it doesn't matter. You've got to metabolize the estrogen. Now, every young woman can metabolize estrogens into three byproducts. I estrogen 400 Z estrogen, 16 hours for hydroxy estrogen. Every human being does this, and this is a crucial point. Speaker 3: (01:01:49) Absolutely. But these three metabolites do not impact yourselves in the same way you say. If you thought of it, you've made the estrogen small window. Now you want to neutralize it so that the body isn't under its constant influence. So you want this metabolite, this estrogen, this hub light to have lost bind to the receptor. You want it to last. It's estrogen Ising properties. Lo and behold, four estrogen, one of those three metabolites retains the ability to bind the estrogen receptor. In fact, some studies show it might be an even more potent comm when it, when it binds and it creates this, this common, a tutorial, Leiden and receptor, it's DNA. Transcribing effects are even more potent, much like the analogy between DHT and the androgen receptor versus testosterone. DHT dihydrotestosterone, which is a metabolite of testosterone, has a higher potency binding affinity to the androgen receptor. Speaker 3: (01:03:00) Four hydroxy estrogen is to the estrogen receptor as DHT is to the androgen receptor. Wow. The ability innate tendency of a young woman when she's faced with estrogens to make either the two hydroxy which is considered protective because has lost or the four hydroxy that inmate differentiation is radically genetically determinable. Now, if something as simple as that, Lisa, when you stitch these things together, when you understand, look, estrogen should be my body needs security and rhythm. I do not want estrogen is constant. When I break down those estrogens, I want my body to have had a break from them. And you did not know whether you were four hydroxy dominant or not. If you had a tendency to make more of the four hydroxy than the two and why is four hydroxy so naughty? Three reasons. A, it binds the estrogen receptor, not giving your body a break from the estrogen ization one to four hydroxy estrogen if you are not flushing it out of the body and how do you flush out for drugs, the estrogen through methylation, the comp gene, which is catechal methyl transfers an oops. Speaker 3: (01:04:29) Can you imagine if you were innately genetic info, hydroxy dominant and have the slow comps because now you're making too much four hydroxyestrone you have a tendency to do so. You do not have the enzymatic ability to get rid of it. Now you buy your stagnate, your four hydroxy Astrid. Do you know what full hydroxy estrogen does other than binding the estrogen receptor and Quinones? Quinones? Listen, my God, you're speaking more than some of the best medical biologists that I've spoken to. So the, the decompose into Quinones and do you know what Quinones do? They get into your DNA. They stick to, they are mutagens. They stick to your DNA, causing the DNA to not be able to unravel and repair itself and by the Quinones then cause accidents. So here's what you don't want to be. You don't want to be the young woman who is genetically predisposed to overly produce four hydroxy estrogen simultaneously, have a poor comp, simultaneously, have a low GSTT one GSTP one, which was the thing, Quinones, and then have a poor mitochondrial superoxide dismutase or antioxidation to get rid of the oxidants Speaker 2: (01:05:52) And add to that. You're in your forties or your 50s and you're making more EstroZen, Speaker 3: (01:05:57) Which is a breast tissue because it's not in the liver anymore. The liver organ, at least it was designed for that type of metabolism. You're doing this in the breasts, you know, God forbid. Okay, Speaker 2: (01:06:10) This is where the cancers can come in Speaker 3: (01:06:13) This is weird and just why we have the the epidemiologic rise during that shift where the woman's body shifts from doing that grunt work in her liver, which was designed for it to doing that grunt work in such as breast tissue, cervical tissue, an ovarian tissue and so on and so forth. Which of course the human body, the female body does not express estrogen receptors, the same level for every cell type. You know, when you were, we lobby at nine years old and you could have gone outside, you know, flat chested like any other boy and you know, and then when, when men awe kits and the body changed your elbows and forms didn't change, it was suitable zone. Those are the zones that have more estrogen receptors. Speaker 2: (01:07:03) And this is so this is how we can see like when you're looking at the phenotype, if we can go look like the the the hormone cascade just for people that are listening, it's going from producer owns and pregnenolone's into testosterone's which can sometimes go into DHT and which then go into the estrogen. Is thrown in your estradiol if you're pregnant when you're older you have more strokes coming in which are, that's coming from the the other top of testosterone isn't it? One on one and then it's means a lighter than these three path rates into the two hydroxy four h

John 1:1     —AMU— AMU   —AR— ERV-AR NAV   —AWA— ERV-AWA   —BG— BG1940 BULG ERV-BG CBT BOB BPB   —CCO— CCO   —CEB— APSD-CEB   —CHR— CHR   —CKB— KSS   —CKW— CKW   —CS— B21 SNC   —CY— BWM   —DA— BPH DN1933   —DE— HOF LUTH1545 NGU-DE SCH1951 SCH2000   —EN— KJ21 ASV AMP AMPC BRG CSB CEB CJB CEV DARBY DLNT DRA ERV EHV ESV ESVUK EXB GNV GW GNT HCSB ICB ISV PHILLIPS JUB KJV AKJV LEB TLB MSG MEV MOUNCE NOG NABRE NASB NCV NET NIRV NIV NIVUK NKJV NLV NLT NMB NRSV NRSVA NRSVACE NRSVCE NTE OJB TPT RGT RSV RSVCE TLV VOICE WEB WE WYC YLT   —ES— LBLA DHH JBS NBLA NBV NTV NVI CST PDT BLP BLPH RVA-2015 RVC RVR1960 RVR1977 RVR1995 RVA SRV-BRG TLA   —FI— R1933   —FR— BDS LSG NEG1979 SG21   —GRC— TR1550 WHNU TR1894 SBLGNT THGNT   —HE— HHH WLC   —HI— ERV-HI SHB   —HIL— HLGN   —HNE— NCA   —HR— HNZ-RI CRO   —HT— HCV   —HU— KAR ERV-HU NT-HU   —HWC— HWP   —IS— ICELAND   —IT— BDG CEI LND NR1994 NR2006   —JA— JLB   —JAC— JAC   —KEK— KEK   —KO— KLB   —LA— VULGATE   —LG— LCB   —MI— MAORI   —MK— MNT   —MR— ERV-MR   —MVC— MVC   —MVJ— MVJ   —NDS— REIMER   —NE— ERV-NE   —NGU— NGU   —NL— BB HTB   —NO— DNB1930 LB   —NY— CCL   —OR— ERV-OR   —PA— ERV-PA   —PL— NP SZ-PL UBG   —PPL— NBTN   —PT— ARC NTLH NVT NVI-PT OL VFL   —QU— MTDS   —QUT— QUT   —RO— RMNN NTLR   —RU— NRT CARS CARST CARSA ERV-RU RUSV   —SK— NPK   —SO— SOM   —SQ— ALB   —SR— NSP ERV-SR   —SV— NUB SV1917 SFB SFB15 SVL   —SW— SNT   —TA— ERV-TA   —TH— TNCV ERV-TH   —TL— FSV ABTAG1978 ABTAG2001 ADB1905 SND MBBTAG MBBTAG-DC   —TWI— NA-TWI   —UK— UKR ERV-UK   —UR— ERV-UR   —USP— USP   —VI— VIET BD2011 NVB BPT   —YO— BYO   —ZH— CCB CCBT ERV-ZH CNVS CNVT CSBS CSBT CUVS CUV CUVMPS CUVMPT RCU17SS RCU17TS  —Amuzgo de Guerrero (AMU)— Amuzgo de Guerrero (AMU)   —العربية (AR)— Arabic Bible: Easy-to-Read Version (ERV-AR) Ketab El Hayat (NAV)   —अवधी (AWA)— Awadhi Bible: Easy-to-Read Version (ERV-AWA)   —Български (BG)— 1940 Bulgarian Bible (BG1940) Bulgarian Bible (BULG) Bulgarian New Testament: Easy-to-Read Version (ERV-BG) Библия, нов превод от оригиналните езици (с неканоничните книги) (CBT) Библия, синодално издание (BOB) Библия, ревизирано издание (BPB)   —Chinanteco de Comaltepec (CCO)— Chinanteco de […] The post God Became Man appeared first on Luxomni Baptist Church.

My guest this week is Derrick Williams aka Black Canvas. Derrick and I have been friends for awhile and have seen each other venture into different avenues within the music scene, from me booking shows and doing this podcast to Derrick getting into taking the time to become an MC, and how his life experiences have shaped his art over the years. We get into some discussions about the politics of Grand Rapids, as well as some conversations about our current social issues, and how Derrick conveys these thoughts into his music. We also go through the evolution of Derricks rap personas and what they meant on the way to becoming Black Canvas and much more. Had a lot of fun having a chat with an old friend. Hope you enjoy. Intro Music: "Ambition" and "Chin Ups" by Chae Hawk Outro Music: "Don't Follow Me" by BLK CNVS feat tryggs Links: Facebook: @blkcnvs, @moshpitnationwestMI, @jonsuntitledpodcast Instagram: @dreads_and_threads, @moshpitnation, @jonsuntitledpodcast Twitter: @moshpitnation, @jonsuntitledpod Soundcloud: Soundcloud.com/blkgr Website: Moshpitnation.com Email: jonsuntitledpod@gmail.com

This month, Deputy Editor Susan K. Schultz, M.D., discusses clinical genetic testing in psychiatry, binge drinking as a possible risk factor for alcohol use disorder, lithium versus divalproex for bipolar disorder in the elderly, the course of schizophrenia over the first 20 years, as well as trajectories of social functioning over 20 years. Articles may be viewed online at ajp.psychiatryonline.org. Also visit the online edition of this month’s Journal to watch a video of Deputy Editor Daniel S. Pine, M.D., present highlights from the issue (ajp.psychiatryonline.org/toc/ajp/174/11). We are conducting a listener survey. Please go to ajp.psychiatryonline.org/audio and select the link to the survey. It won’t take more than a few minutes to complete, and your feedback will remain anonymous. We appreciate your responses. Thank you.

Dr. Paul Wang:                  Welcome to the monthly podcast "On The Beat" for Circulation, Arrhythmia, and Electrophysiology. I'm Dr. Paul Wang, editor-in-chief, with some of the key highlights from this month's issue. We'll also hear from Dr. Suraj Kapa reporting on new research from the latest journal articles in the field.                                                 In our first manuscript this month, Cho and Associates investigate the need for readmission for Dofetilide reloading. The FDA labeling for Dofetilide loading states that Dofetilide must be initiated or reinitiated in hospital with continuous electrocardiographic monitoring.                                                 In this article, the authors retrospectively examine the hospital records for 138 patients admitted for Dofetilide reloading for atrial arrhythmias. Of these 138 patients, 102 were reloaded at a previously-tolerated dose, 30 with a dose higher than a previously tolerated dose, and 2 at a lower dose, with the prior dosage unknown in 4 patients.                                                 In 44 patients, or 31.9%, dose adjustment or discontinuation of Dofetilide was performed, although, torsades de pointes occurred in two patients admitted to increased Dofetilide dosage, no torsades de pointes was observed in patients loaded with the same dose of Dofetilide.                                                 This is 0 versus 6.7% or P = 0.05. In 30 out of 102 patients, 29.4% reloaded at a previously tolerated dose. Dofetilide dose adjustment was required. In 11 out of 30 patients or 36.7% admitted for an increase in dose, a dose adjustment or discontinuation was required.                                                 The authors therefore concluded that dosage adjustments or discontinuation were frequent, and that their observations support the need for hospitalization for Dofetilide reloading. In the next manuscript Tilman Maurer and Associates report a novel superolateral approach to creating a mitral isthmus ablation line.                                                 Because the creation of an endocardial mitral isthmus line with the end point of bidirectional block maybe challenging, the authors examine 114 patients with perimitral annular flutter without a prior mitral isthmus ablation line.                                                 The authors compared the initial group of 57 patients, group A, who underwent catheter ablation using a novel superolateral mitral isthmus ablation line connecting the left sided pulmonary veins with the mitral annulus along the base of the left atrial appendage visualized by selective angiography to another group of patients, 57 patients in groups B undergoing ablation using a conventional mitral isthmus ablation line connecting the left inferior pulmonary vein to the mitral annulus.                                                 The authors found that bidirectional block was achieved in 56 out 57 patients in group A, or 98.2%, and 50 patients in group B, or 87.7%, P=0.06. Ablation from within the coronary sinus was required significantly less for creation of a superolateral mitral isthmus ablation line compared to a conventional mitral isthmus ablation line, 7.0% versus 71.9%, P is less than 0.01.                                                 The need for epicardial ablation from within the coronary sinus in the total length of the mitral isthmus line, 29.3 versus 40.8 millimeters were predictors for unsuccessful bidirectional mitral isthmus blockade. Pericardial tamponade was observed in group A, but not in group B, 5.2% versus 0%, P=0.24.                                                 The authors, therefore, concluded that superolateral mitral isthmus ablation line has a higher acute success rate compared with conventional mitral isthmus ablation line with a low likelihood of needing ablation from within the coronary sinus.                                                 In our next paper, Cronin and Associates examine the relationship between right ventricular pacing frequency, and the incidence of ventricular arrhythmias leading to ICD shock.                                                 Using the altitude database, the authors examined 389 appropriate shocks, and 425,625 transmissions received from 8,435 patients over a mean follow-up of 15.0 months.                                                 Transmissions with 80 to 98% right ventricular pacing were associated with a hazard ratio of 1.56 for an appropriate shock in the subsequent week compared to less than 1% right ventricular pacing, P=0.04 using a time dependent Cox proportional hazard model, however, the authors found that greater than or equal to 98% right ventricular pacing trended towards a lower risk of appropriate shock. Hazard ratio 0.61.                                                 Lifetime cumulative percentage right ventricular pacing was similarly associated with an increased risk of appropriate shocks at 80 to 98% right ventricular pacing, but not greater than or equal to 98% right ventricular pacing.                                                 The authors, therefore, concluded that an increased frequency of right ventricular pacing is associated with an increased risk of appropriate ICD shocks until the right ventricular pacing is greater than or equal to 98%.                                                 In the next manuscript, Wesley O'Neal and Associates examined 12,241 patients from The Atherosclerosis Risk in Communities Study, ARIC study, the association of individual QT components, that is R-wave onset to R-wave peak, R-peak to R-wave end, ST-segment, T-wave onset to T-wave peak, and T-peak to T-wave end with the occurrence of sudden cardiac death.                                                 The authors identified a total of 346 cases of sudden cardiac death identified over a median followup of 23.6 years. The prolongation of the QT interval was associated with a 49% risk of sudden cardiac death. Of the components of the QT interval only the T-wave onset to T-peak component was associated with sudden cardiac death with each standard deviation increase, hazard ratio of 1.19.                                                 The authors found similar results when the QT interval components were included in the same model, thus the authors conclude that the risk of a sudden cardiac death is driven by prolongation of the T-wave onset to T-peak component.                                                 In the next article by Kalliopi Pilichou and Associates, the authors examined copy number variations or CNVs in arrhythmogenic cardiomyopathy patients. The author studied 160 arrhythmogenic cardiomyopathy proband genotype negative for 5 arrhythmogenic cardiomyopathy desmosome genes using conventional mutation screening.                                                 Using multiplex ligation dependent probe amplification, MLPA, 9 heterozygous copy number variations were identified in 11 or 6.9% of the 160 probands. Of these, the authors found that 5 had the least of the entire plakophilin-2 gene to a deletion of only the PRP2 [exon 00:08:45], 1 a deletion of the PRP2 exon 6211, and 1 a PRP2 duplication of the 5 UTR to exon 1. One the desmocollin 2 duplication of exon 7 to 9, and one large lesion of chromosome 18 comprising both DSC2 and desmoglein 2 genes.                                                 All probands were affected by moderate severe forms of disease and 10 or 32% of the 31 family members carrying one of these deletions met the diagnostic criteria for arrhythmogenic cardiomyopathy.                                                 The authors concluded that identifying the copy number variations may increase the yield of genetic testing. In family members carrying the copy number variations, but not displaying the phenotype other factors are likely involved.                                                 In the article by Rahul Samanta and Associates, the authors examined in 7 sheep a mean of 84 weeks post MI, the influence of intramyocardial adipose tissue on scar tissue identification during endocardial contact mapping, the authors found that endocardial electrogram amplitude correlated significantly with intramyocardial adipose tissue.                                                 Unipolar, Right = negative 0.48, bipolar R = negative 0.45, but not correlated with collagen. Unipolar, R = negative 0.36, bipolar, R = negative 0.43. Intramyocardial adipose tissue, dense regions of myocardium were reliably identified using endocardial mapping with thresholds of less than 3.7 millivolts and less than 0.6 millivolts respectively for unipolar, bipolar, and combined modalities.                                                 Unipolar mapping using optimal thresholding remained significantly reliable, an AUC of 0.76. During mapping of intramyocardial adipose tissue confined to punitive scar border zone regions. Bipolar amplitude range of 0.5 to 1.5 millivolts.                                                 The authors concluded that combined bipolar and unipolar voltage mapping with optimal thresholds may permit delineation of intramyocardial adipose dense regions of myocardium following infarction.                                                 In the next article by Kevin Leong and Associates, the authors examined the substraight in electrophysiologic mechanisms that contribute to the characteristic ECG of Brugada syndrome. The authors studied 11 patients with concealed type 1 Brugada syndrome and 2 healthy controls by performing noninvasive electrocardiographic imaging, or ECGI, and ECG recordings during an Ajmaline infusion.                                                 Following Ajmaline infusion the right ventricular outflow tract had the greatest increase in conduction delay and activation recovery interval prolongation compared to the right ventricle or the left ventricle. In controls there was minimal change in the JST point elevation, the conduction delay, or activation recovery intervals at all sites with Ajmaline.                                                 In Brugada syndrome patients, conduction delay in right ventricular outflow tract, but right ventricle or left ventricle correlated with a degree of JST point elevation. Pearson R 0.81.                                                 No correlation was found between the JST point elevation and activation recovery interval prolongation in the right ventricular outflow tract the right ventricle or the left ventricle.                                                  The authors, therefore, concluded that the degree of conduction delay in the right ventricular outflow tract and not prolongation or re-polarization time accounts for the ST or J-point elevation seen in type 1 Brugada syndrome pattern.                                                 In the next article by Jonas Diness and Associates, the authors investigate the role of inhibition with small conductance calcium activated potassium channels in atrial fibrillation termination.                                                 Since these channels are predominately expressed in the atria compared to ventricles, they are a particularly attractive drug target. With a total of 43 pigs atrial tachy pacing was performed until they developed sustained atrial fibrillation that could not be reverted by vernakalant administration.                                                 After the SK channel inhibitor AP14145 was administered, vernakalant resistant AF reverted to sinus rhythm and could not be re-induced by burst pacing. In open chest pigs both vernakalant and AP14145 significantly prolonged atrial refractory of this and reduced AF duration without affecting the ventricular refractory in this or blood pressure.                                                 The authors concluded that SK currents played a role in porcine atrial repolarization and their inhibition by AP14145 demonstrates an arrhythmic affects in a vernakalant resistant porcine model of atrial fibrillation.                                                 In our final article by Padmini Sirish and Associates, the authors examined the role of several ion transporters in action potential duration in cardiac function. The solute carrier SIC26A6, which is highly expressed in cardiomyocytes plays an important role in cardiac intracellular pH regulation.                                                 Using the SIC26A6 knockout mice, the authors found that ablation of SIC26A6 results in action potential shortening, reduced calcium transients, reduced sarcoplasmic reticulum calcium load, and decreased sarcomere shortening in the SIC26A6 knockout cardiomyocytes.                                                 Ablation of the SIC26A6 reduced fractual shortening and cardiac contractility in vivo. Intracelluar pH regulation is elevated in the SIC26A6 knockout cardiomyocytes consistent with the chloride bicarbonate exchange activities of SIC26A6.                                                 The SIC26A6 knockout mice exhibited bradycardia and fragmented QRS complexes supporting the role of SIC26A6 in the cardiac conduction system, therefore, the authors provided evidence that the role of SIC26A6 cardiac electrogenic chloride bicarbonate transporter in ventricular myocytes as well as intracellular pH regulation, excitability, and contractility.                                                 That's it for this month, but keep listening.  Suraj Kapa will be surveying all journals for the latest topics of interest in our field. Remember to download the podcast "On The Beat." Take it away Suraj. Suraj Kapa:                          Thank you very much Paul and welcome everybody back to "On The Beat," where we'll review hard hitting articles across the electrophysiologic literature. It is my pleasure to introduce you to 15 different articles published in the past month of September across all the journals in cardiovascular medicine.                                                 The first area that we will be focusing on is atrial fibrillation with a specific focus within the realm of anticoagulation, and we refer you to a paper published by [Kurshida Doll 00:16:55], entitled "Factors Associated With Anticoagulation Delay Following New-Onset Atrial Fibrillation," published in The American Journal Of Cardiology on October 15, 2017.                                                 In this publication Kurshida Doll, reviewed the frequency with which there is a delay in introduction of oral anticoagulation after a new diagnosis of atrial fibrillation, and the impact on overall outcomes. In a large electronic medical record they identify incident episodes of atrial fibrillation between 2006 and 2014.                                                 They used the CHADS2 score rather than the CHADS-VASc score to estimate overall risk, and then after this they reviewekud the outcomes of the patients. They found for those patients in whom oral anticoagulation would have been recommended, the median time to initiation was around five days, with an interquartile range of 1 to 43, with by far most patients receiving Warfarin with about 86%.                                                 Interestingly, about 98 strokes occurred between the time of new atrial fibrillation diagnosis, and the actual initiation of oral anticoagulation. Several factors led to this delay in oral anticoagulation including female gender, absence of hypertension, prior falls, and the presence of chronic kidney disease.                                                 However, ultimately, by 6 months over 90% of patients were on oral anticoagulants appropriately, though still a slightly higher proportion appropriately in men than woman.                                                 They noted that most patients with new diagnosis of atrial fibrillation and noted to have an elevated stroke risk started on oral anticoagulation within 1 week. Given these findings it is important to consider how we wait to introduce oral anticoagulation into patients after initial diagnosis given many initial diagnoses may be made by internists, or even in some cases by the patient themselves on a remote monitor or an ambulatory monitor it is important to consider how they are tied into the individual, who would feel most comfortable and who's most apt to prescribe oral anticoagulation.                                                 Changing gears within atrial fibrillation we next move on to cardiac mapping and ablation, and specifically focus on a paper published by Black-Maier et al, in the September edition of "Heart Rhythm" entitled "Risk Of Atrioesophageal Fistula Formation With Contact Force-Sensing Catheters."                                                 While atrioesophageal fistula formation is a relatively rare complication of atrial fibrillation ablation it can be life threatening, contact force catheters for ablation of atrial fibrillation have come into vogue as they are felt to improve procedural effectiveness and potentially reduce complications by improving individual understanding of contact with the myocardium and when contact is excessive.                                                 However, there's been little exploration of the actual risk of atrioesophageal fistula. An [inaudible 00:19:50] from the association they refused the mod database or the manufacturer and user facility device experience database for adverse event reports.                                                 Amongst almost 27,000 device reports they identified a total of 78 atrioesophageal fistula cases. About 1,200 of the reports were related to contact force-sensing catheters and about almost 1,500 were related to non contact force sensing catheters.                                                 Of the 78 atrioesophageal fistula cases reported the vast majority were the contact force-sensing catheters with a total number of 65, or about 5 times more than with non contact force-sensing catheters.                                                 Unfortunately, esophageal temperature increases were only mentioned in about 2.5% of cases in contact force and power settings were not consistently reported in order to come to any conclusions. They noted the overall mortality with atrioesophageal fistula in this population was around 56%, with really the vast majority surviving as a result of surgical repair as apposed to stenting or no intervention.                                                 While this data is somewhat skewed because it's based on self reported data by proceduralists, who are reporting back to the mod database, it is important to consider whether or not there is actually an increase complication rate associated with contact force-sensing catheters as these catheters do reflect a fundamentally different catheter than the non contact force-sensing catheters routinely used due to changes in the stiffness, and the mechanics of the catheter itself.                                                 It is important to consider when using any new catheter with any new options for monitoring, or that might alter the stiffness, or other mechanical properties of the catheter, whether or not application of similar power settings are relevant.                                                 While the data is potentially skewed in the status set it will be important to consider it going forward as to whether or not there are implications of some increased risk of complications, and how to mitigate these by altering our contact force and power setting decision making.                                                 Further study will be required in order to better understand these data and the implications. I would refer the readers also to an article published by [inaudible 00:22:02] in circulation where they reviewed the mechanism of atrioesophageal injury and also to another publication published in The Journal Of Cardiovascular Electrophysiology this past month by [inaudible 00:22:11], where they did a meta analysis of the overall benefit of contact force related catheters over non contact force related catheters.                                                 In that paper they demonstrated that based on this meta analysis there seems to be an overall benefit in terms of outcomes in contact force-sensing catheters without a difference in procedural complications. However, I would refer the reader to the fact that there are very limited randomized studies comparing contact force versus non contact force catheters.                                                 Next, also within the realm of cardiac mapping and ablation we reviewed a publication by Haldar, et al., entitled Resolving Bipolar Electrogram Voltages During Atrial Fibrillation Using Omnipolar Mapping, published in the last edition of Circulation Arrhythmia Electrophysiology. Also, reviewed by Dr. Wang in last months podcast.                                                 The importance of this article lays in an improved understanding of what we mean when we talk about voltage or substraight mapping. In his paper, Haldar, et al., tried to understand better what the bipolar electrogram might actually refer to when comparing traditional bipolar mapping versus omnipolar mapping.                                                 This becomes important as we consider a low voltage guided substraight modification for not just atrial fibrillation ablation, but also potentially for ventricular arrhythmia ablation. They sought to compare the use of peak-to-peak voltage for assessment of bipolar voltage with omnipolar peak-to-peak voltages in both sinus rhythm and atrial fibrillation.                                                 They demonstrated that in canines vertical orientation of a catheter relative to the underlying tissue consistently resulted in a higher bipolar voltage in both sinus rhythm and atrial fibrillation. Furthermore, they show that the max obtained ominipolar voltage were consistently larger than multi-horizontal and vertical voltages in both rhythms.                                                 Vector field analysis of these wave fronts during atrial fibrillation in particular, demonstrated the omnipolar electrograms can account for a collision in fractionation, and required an electrogram of voltages independent of these effects. Thus, they suggested that the omnipolar electrograms can use maximum voltages, and can separate the influence from directional factors, collision, or fractionation especially when compared with contemporary bipolar techniques.                                                 The implications of the study are several. First off, when performing substraight mapping we traditionally use what we can in terms of trying to get appropriate bipolar signal analysis. However, catheters have significantly evolved since the early studies of bipolar voltage mapping in terms of establishing voltage cutoffs.                                                 There are many different multipolar catheters with varying interelectrode spacing, but sometimes prefer parallel orientation to the underlying myocardium as opposed to vertical orientation. The fact that bipolar voltage can significantly vary based on both orientation of the catheter as well as the rhythm is important when considering whether a substraight actually exists in a specific location or not, and what "Normal voltage cutoffs," where specific patients should be."                                                 When we consider novel catheters with increasing complex design including introduction of mini electrodes as well as omnipolar electrodes, it is important to consider whether an assessment of "Normal voltage," should be the same. Further study will be required to better understand how to best analyze these results.                                                 Moving to a different form of management in atrial fibrillation we will next refer you to a paper by Borris [Madal 00:25:44] published in this last month's edition of Heart Rhythm, entitled Efficacy and safety of left atrial appendage closure with WATCHMAN in patients with or without contraindication to oral anticoagulation, 1-Year follow-up outcome data of the EWOLUTION  trial.                                                 The EWOLUTION trial was a prospective multi center registry looking at the outcomes of WATCHMAN patients, who had indication for closure based on European society of cardiology guidelines. They sought to evaluate a 1 year followup of these patients.                                                 The baseline CHADS-VASc score was on average about 4-1/2 with a mean age of over 73 years. Almost a third of the patients had prior transient ischemic attach or ischemic stroke. They noted that the vast majority of the patients had a successful WATCHMAN implantation with a 1,005 out of 1,025 patients having successful implantation, with only 3 of these 1,005 patients having any leak greater than 5 millimeters.                                                 The majority up to 87% had T-followup at least once after initial implantation. Interestingly, the vast majority only used antiplatelet therapy with only 8% having vitamin K antagonist used in the post WATCHMAN implantation period.                                                 There was a reasonably high mortality of 10% in the first year after implantation, though this was felt to typically reflect advanced age and other comorbidities. Also, interestingly almost 4% of patients had thrombus on their device, which was independent of the drug regimen used. In other words whether antiplatelet therapy or vitamin K antagonists.                                                 Overall, the ischemic stroke rate was relatively low at 1.1%, with a relative risk of 84% versus estimated historical data, and also with a relatively low major bleeding rate of only 2.6% and this predominately being non-procedure of device related.                                                 Thus, they concluded that LA closure with the WATCHMAN device had a high implant and sealing success, and it appeared to be safe and affective in reducing ischemic stroke risk given that the relative incidence was only 1.1%, despite the fact that the vast majority were not actually even using oral anticoagulation.                                                 There are trial ongoing in the United States to evaluate whether or not patients can be safely kept off of oral anticoagulation in the peri-implant period as in some countries standard of care is to place them on anticoagulants in the immediate post implantation period.                                                 However, two other things need to be noted in this real world analysis of outcomes with WATCHMAN. Almost 10% or 1 out of 10 patients died within 1 year of followup, thus whether or not better patient selection is required to understand those patients will receive maximal benefit from this invasive procedure might be considered.                                                 Further, more almost 4% had device related thrombus. What this means in terms of stroke risk especially over longterm followup needs to also be considered. I think overtime we'll get better understanding of what those risks might be for an endocardial system for a left atrial appendage occlusion.                                                 But, staying within the realm of stroke risk in atrial fibrillation, we next review the article by King, et al., published in The Journal Of American College Of Cardiology, in the September 2017 edition entitled, Left Atrial Fibrosis and Risk of Cerebrovascular and Cardiovascular Events in Patients With Atrial Fibrillation.                                                 Cardiac MRI to evaluate late gadolinium enhancements suggesting regional cardiac fibrosis and atrial fibrillation is slowly taking steam, but primarily as a method of assessing potential efficacy of atrial fibrillation ablation with greater amounts of delayed enhancement potentially suggesting an overall lower risk, or a lower likelihood of success of atrial fibrillation ablation.                                                 King, et al., sought to evaluate in a retrospective cohort study regarding the risk of cerebrovascular and cardiovascular major events associated with a degree of delayed enhancement in MRI. They reviewed 1,228 patients undergoing cardiac MRI to assess left atrial fibrosis between 2007 and 2015.                                                 They then staged these patients and stratified them according their [Utah 00:29:45] stage, which had been previously recorded for the degree of fibrosis seen. They demonstrated on followup that there was a significantly higher incidence of major cardiovascular and cerebrovascular events associated with higher degrees of late gadolinium enhancement with a relative risk ratio of about 1.67.                                                 However, the only individual component of these outcomes that remains significantly associated with advanced gadolinium enhancement was actually stroke or TIA, with a hazard ratio of 3.94, thus they concluded that severe LA late enhancement is associated with increased cerebrovascular events principally.                                                 This study is important in that it highlights another potential risk factor that may need to be considered when risk stratifying patients for their risk of stroke. We recognize that even some paroxysmal patients can have extensive left atrial fibrosis, and some persistent patients might not have a ton of atrial fibrosis.                                                 Whether this can further help risk stratified patients in terms of overall stroke risk, and might identify and help characterize low risk patients further needs to be considered.                                                 One of the key features of this evaluation needs to be also the mechanism. In theory patients with greater endocardial injury of the atrium might be more prone to clot formation, and thus it may seem reasonable to expect indeed when we have more left atrial fibrosis as suggested by delayed enhancement on MRI. There may in fact be a higher greater cerebrovascular event rate.                                                 Finally, changing gears a little bit within the realm of risk stratification and management for atrial fibrillation we focused on autonomics and specifically a publication by Stavrakis et al., in the last month edition of Jack Clinical Electrophysiology, entitled Low Level Vagus Nerve Stimulation Suppresses Postoperative Atrial fibrillation And Inflammation In A Randomized Study.                                                 The group, headed up by Sonny [Poe 00:31:42] have previously published on both tragus stimulation as well as low level of vagus nerve stimulation in patients undergoing atrial fibrillation ablation. In this particular study they sought to evaluate whether or not implantation of a low level of vagus nerve stimulator during cardiac surgery could reduce the risk of postoperative atrial fibrillation.                                                 They sutured a bipolar wire to the vagus nerve preganglionic fibers along the lateral aspect of the superior vena cava at the time of surgery. They then performed high frequency stimulation of 50% below the threshold for slowing the heart rate for 72 hours, and those randomized to the vagus nerve stimulation group.                                                 The secondary group was a sham cohort. They demonstrated amongst the 54 patients randomized to either group that the frequency of postoperative atrial fibrillation was almost a third in the low level of vagus stimulation group when compared with the control group.                                                 Interestingly, their frequency of atrial fibrillation was not only lower, but the level of inflammatory markers also decreased with both serum tumor necrose factor alpha and interleukin 6 levels being significantly lower in the low level vagus nerve stimulation cohorts.                                                 In line with prior data from atrial fibrillation ablation these data were suggesting that low level of vagus nerve stimulation can suppress postoperative atrial fibrillation and attenuate the inflammatory response.                                                 Also, in this past month there was a paper by [Yoo 00:33:09] et al., in The Journal Of The American Heart Association, specifically looking at the use of vagus nerve stimulation at the level of the tragus in patients with obstructive sleep apnea associated atrial fibrillation.                                                 Similar to prior work form the Oklahoma group, they demonstrated that in fact there is a beneficial effect on reduction of atrial fibrillation, and this is primarily mediated through attenuation of autonomic factors that mediate obstructive sleep apnea related atrial fibrillation.                                                 Moving away from atrial fibrillation, we next delve in cellular physiology first starting with an article published in Nature Scientific Report this past month, on very low density lipoprotein in metabolic syndrome, and how it modulates gap junctions and slows cardiac conduction.                                                 In the past year there have been multiple studies regarding specific cell types and how they might interplay with cardiac fibrosis, and risk of conduction slowing. In this publication we had all reviewed the effect of very low density lipoproteins, and their effect on cardiac conduction in, in vitro models.                                                 They demonstrated that primarily through down regulation of [conexion 00:34:21] 40 and conexion 43, very low density lipoproteins have significant impact on cardiac conduction with increased prolongation of the P-wave, PR-intervals, QR restoration, and QTC intervals.                                                 Thus, they concluded that very low density lipoproteins may contribute to the path of physiology of both atrial fibrillation and ventricular arrhythmias that can be seen in metabolic syndrome. This report is important because it highlights the fact that we can actually see other cell types including LDL causing a significant reduction in cardiac conduction and thus mediating arrhythmogenesis.                                                 In fact there was one other paper published just a couple weeks prior also in The Nature Of Scientific Reports by [Lee 00:35:04] et al., entitled Human Electronegative Low-Density Lipoprotein Modulates Cardiac Repolarization Via LOX-1-Mediated Alteration Of Sarcolemmal Ion Channels.                                                 They showed that LDL can actually result in QTC prolongation in patients with ischemic heart disease by specific mechanisms involving LOX-1. Recognition of the mechanisms behind which less traditional factors such as VLDL or LDL may mediate alterations in cardiac conduction are important when we consider our potential novel targets for treatment of arrhythmias in patients whether for prevention or for treatments.                                                 In light of this attempt to identify novel targets we next move on to another paper in the realm of cellular electrophysiology published by [Toib 00:35:52] et al., in The American Journal of Physiology, Heart and Circulatory Physiology, entitled Remodeling Of Repolarization And Arrhythmia Susceptibility In A Myosin-Binding Protein C Knockout Mouse Model.                                                 In hypertrophic cardiomyopathy there might be multiple mechanisms that might lead to increased risk of ventricular arrhythmias. These might be scar related due to the fact that patients can burn out from the hypertrophic cardiomyopathy overtime and get both endocardial, epicardial, and mid myocardial fibrosis, but what are the mechanisms that might mediate the development of ventricular arrhythmias and hypertrophic cardiomyopathy remain to be elucidated, and there's been very limited evaluation of the effect of repolarizing potassium currents on this risk.                                                 Thus, Toib, et al., studied myosin-binding protein C knockout mice to look at what happens with repolarizing potassium currents in his cohorts. They demonstrated that in these knockout mice there was a prolongation in the corrected QT interval when compared to the wild type mice with overt ventricular arrhythmias.                                                 They also demonstrated that there is action potential prolongation associated with a decrease for polarizing potassium currents, and a decreased MRNA levels of several key potassium channels subunits, thus, they concluded that in this specific subtype of hypertrophic cardiomyopathy needed by myocin combining protein C mutations that part of the ventricular arrhythmia risk might be due to a decrease in polarizing potassium currents in turn leading to increase in action potential and QT interval.                                                 The reason that this particular finding is important is in my highlight drug selection in specific types of hypertrophic cardiomyopathy. In my postulate for example the class 3 antiarrythmics drugs might actually increase risk in some subtypes of hypertrophic cardiomyopathy due to down regulation of potassium channel subunits.                                                 Consideration of this is critical when best evaluating how to mange and treat these patients. Changing gears to another method of channelopathy we focus within the realm of genetic channelopathies and specifically on Brugada syndrome.                                                 In this last month's edition of Heart Rhythm, Sierra, et al., published their series of longterm prognosis of drug induced Brugada syndrome. They reviewed a consecutive cord of 343 patients with drug induced Brugada syndrome, and compared their outcomes with 78 patients with a spontaneous type 1 pattern.                                                 The mean age of patients was around 41 years. Interestingly, about 4% of the patients had a clinical presentation of 7 cardiac deaths, and 25% had a clinical presentation of syncope. However, the majority of the patients were asymptomatic, around 71%.                                                 Most of the patients were female amongst the drug induced Brugada syndrome cohort. They demonstrated that there were less ventricular arrhythmias both induced string and electrophysiology study, and seen over followup of up to 62 months in the drug induced Brugada syndrome cohort as compared with the spontaneous type 1 cohort.                                                 Overall, the event rate in drug induced Brugada syndrome was 1.1% of [person year 00:38:54] versus 2.3% of person year in patients with spontaneous type 1 pattern.                                                 They suggested that presentation of sudden cardiac death or inducable ventricular arrhythmias at the time of VP study were independent risk factors associated with arrhythmic events in drug induced Brugada syndrome. However, if a patient was asymptomatic and had no inducible ventricular arrhythmias they had a significantly better prognosis with drug induced Brugada syndrome over a spontaneous type 1 pattern.                                                 Thus, they concluded that even in drug induced Brugada syndrome sudden cardiac death is possible. However, in asymptomatic patients without a prior clinical presentation of sudden cardiac death or inducible ventricular arrhythmias during electrophysiology study, they may be relatively safer than their spontaneous type 1 counterparts.                                                 This study highlights the importance of stratification of patients into the mechanism of how their genetic channelopathy presents whether as a spontaneous finding or as a finding in the setting of other events. Further prospective analysis, however, is needed to best guide how to manage these patients and in whom to put a defibrillator as I would note that almost 37% of these patients actually had an ICD placed with the vast majority without incident events.                                                 Speaking of implantable devices we next move to the realm of ICD pacemaker and CRT, and specifically we review the publication by Samar, et al., published in Jack Clinical Electrophysiology this past month on the diagnostic value of MRI in patients with implanted pacemakers and implanted cardiover defibrillators across the population.                                                 Does the benefit justify the risk of proof of concept study? Increasingly, MRIs are being done in patients with even Legacy defibrillators and permanent pacemakers. However, when assessing the benefit versus the risk it's important to understand did the MRI actually change outcomes, and this was a specific question that the authors tried to answer.                                                 They took patients with conventional or Legacy pacemakers or ICDs, and tried to evaluate what the actual benefit was on those patients in whom an MRI was done. They specifically asked four questions, one, did the primary diagnosis change, two, did the MRI provide additional information to the existing diagnosis, three, was the pre-MRI or tentative diagnosis confirmed, and four, did the patient management change?                                                 They noted there were no safety issues encountered in any of the 136 patients an MRI was performed. In 97% it was felt that MR added value to the patient diagnosis and managements, with 49% of investigators feeling that MR added additional valuable information to the primary diagnosis, and in nearly a third the MR actually changing the principle diagnosis and subsequent management of the patient.                                                 Increasing evidence suggesting that MRI can be safely performed even in Legacy pacemakers and ICDs, and the fact the MRI can wield important evidence related to diagnostics needs to be taken into consideration as investigators and other centers try to identify methodologies for safely performing MRIs in these patient cohorts.                                                 It seems thus far like MRI might justify risk of these procedures under controlled settings. Next, we move also within the realm of implantable cardioverted defibrillators, but to a different assessment published by Kawada et al., in this past months issue of Heart Rhythm where they sought to evaluate the comparison of longevity in clinical outcomes of implantable cardioverted defibrillator leads among manufacturers.                                                 They specifically sought to assess the longevity of [Lynox 00:42:35] SSD by [Atronic 00:42:36] leads compared with Sprint Fidelis by Matronic, Sprint Quattro by Matronic, and Endotac Reliance by Boston Scientific Leads. The reasoning for this was early failure of some of the biotronic Lynox leads has been reported. Thus, they retrospectively reviewed patients undergoing implantation with these different lead approaches between 2000 and 2013.                                                 They noted failure rates of the Lynox versus Spring Fidelis versus Endotac leads where 3.2% for a year, versus 3.4% for a year, versus 0.61% for a year respectively. No lead failure was notable with a followup [inaudible 00:43:13] in Sprint Quattro leads, thus, they felt that the survival probability of Lynox leads was comparable to Sprint Fidelis leads, and lower than that of Endotac or Sprint Quattro leads.                                                 They found that age was the primary predictor of Lynox lead failures with the patients less than 58 years old had significantly increased risk of lead failure compared with those greater than 58 years old, thus, they concluded that this was a first description of a lower survival rate for Lynox leads in an aging population.                                                 Early identification of leads that might be at risk of failure is critical in patient risk stratification. The finding that there might be other leads that might be at risk of failure highlights the importance of close monitoring of these leads in contribution to register data.                                                 I would note that within this study that it was primarily done at one center and the vast majority of patients actually received Lynox leads. Thus, further evidence was clinically required for more centers to understand what the mechanism of this risk is, and also whether the risk is born out consistently across multiple centers particularly because the vast minority got the one lead, but didn't have any lead failure encountered for.                                                 Further, speaking about defibrillators we focus on the different mechanism of failure, and specifically the publication by [Thogersen 00:44:38] et al., published in last months' edition of Circulation And Arrhythmia Electrophysiology entitled Failure To Treat Life Threatening Ventricular Tachy Arrhythmias In Temporary Implantable Cardioverted Defibrillators Implications For Strategic Programming.                                                 In this publication they did not so much focus on lead failure, but the failure the ICD due to potential strategic programming decision making on appropriately treating ventricular tachy arrhythmias. Their current consensus recommendations as far as using a generic rate threshold between 185 and 200 beats per minutes in primary prevention ICD patients, thus, they sought to determine in the case series what the relationship between program parameters and failure of modernizing ICDs to treat for VF actually worked.                                                 Between 2015 and 2017 at four institutions they reviewed cases where normally functioning ICDs failed to deliver timely therapy for VF. There were a small number of patients noted fitting this criteria with only 10 ambulatory patients. Five actually died from their untreated VF, whereas four had cardiac arrests through a witness requiring external shocks, and one was ultimately rescued by a delayed ICD shock.                                                 The main reason that they were not appropriately treated were that the ventricular fibrillation event did not satisfy the programmed detection criteria in nine out of ten patients. Seven of the patients had the slowest detection rates consistent with generic recommendations, but were never tested in the peer review trial for the manufacturers ICDs.                                                 Namely, the decision making on the appropriated generic rate threshold was tested on specific manufacturers ICDs, but didn't apply the decision making on programming on other manufactures ICDs. In some cases manufacturers specific factors were interacting with fast detection rates to withhold therapy such as enhancement in MIC wave oversensing.                                                 Thus, they demonstrated that in this population untreated VF despite recommendation programming, accounted overall for 56% of sudden deaths and 11% of all deaths in the overall cord of patients during the study period.                                                 Thus, over half of the cases where sudden death occurs in patients with ICDs appears to be due to untreated VF despite recommended programming. Thus, they concluded that these unanticipated interactions or complex decision making regrading generic program of parameters might in part lead to withholding of therapy inappropriately in ventricular fibrillation.                                                 This publication highlights the importance of thoughtful decision making when translating evidence based detection parameters both between manufacturers and applying them across individual patients.                                                 While the overall number of patients is quite low, mainly only ten patients who were affected by this event, the number of patients dying as a result of it is fairly high in terms of a percentage with 56% of sudden deaths occurring as a result of untreated VF from variation from recommended programming.                                                 Closer attention needs to be paid to understanding how to better assess which patients would benefit from the current generic rate thresholds as opposed to who will be harmed by it. It is possible that one size fits all approach will always result in some harm to some, while benefit to others as potentially cutting down the lower rate cutoff in some patients might lead to inappropriate therapies, which might be as life altering as untreated VF in many patients.                                                 Finally, keeping within the realm of defibrillation we review an article by [Layva 00:48:24] et al., published in last month's edition of The Journal of American College of Cardiology entitled Outcomes of Cardiac Resynchronization Therapy With or Without Defibrillation in Patients With Nonischemic Cardiomyopathy.                                                 There are several recent studies that have started to cast doubt on what the incremental benefit of defibrillation adage cardiac resynchronization therapy actually is in nonischemic cardiomyopathy.                                                 However, we also know that in patients with scar noted on MRI that there can be an increased risk of ICD therapy, thus, part of the difficulty that some individuals have is how we define the nonischemic cardiomyopathy cohorts. Namely, is all nonischemic cardiomyopathy crated equal and we can better risk stratify this population to subtypes some of whom might benefit from primary correction defibrillators and some of whom might not?                                                 Thus, in this study they aimed to determine whether CRTD is superior to CRTP in patients with nonischemic cardiomyopathy based on the presence or absence of left ventricular midwall fibrosis detected by cardiac magnetic resonance.                                                 There were a total of 68 patients who had midwall fibrosis, and 184 patients who had not, and all of them underwent the evaluation prior to CRT implantation. They noted that the presence of midwall fibrosis was an independent predictor of total mortality with a hazard ratio of 2.31 as well as total mortality or heart failure hospitalization.                                                 This sudden cardiac hazard ratio was about 3.75 with an increased risk attributable to the presence of midwall fibrosis. They also noted that total mortality or heart failure hospitalization, and total mortality or hospitalization for major adverse cardiac events was significantly lower in patients with CRT defibrillator than with CRT pacemaker in those with midwall fibrosis, but not in those without midwall fibrosis.                                                 These findings highlight that in some patients with nonischemic cardiomyopathy CRTD may be superior to CRTP, though these might be guided by the presence of abnormal substraights. The evaluation of what nonischemic cardiomyopathy means in an individual patient needs to be closely considered.                                                 Nonischemic cardiomyopathy is a blanket term for all those patients who do not have an ischemic cardiomyopathy and who may or may not have been fully evaluated for discrimination of another type of myopathy such as infiltrated myopathies for example sarcoidosis.                                                 The value of cardiac magnetic resonance imaging is being increasingly understood as it applies to both risk stratification, nonischemic cardiomyopathy, as well as the value in decision making as far as treatment of these patients. In a recent publication published this past month as well in Jack Electrophysiology, by [inaudible 00:51:13], et al., they reviewed the efficacy of implantable cardioverted defibrillator therapy in patients with nonischemic cardiomyopathy based on a meta analysis of existing trials.                                                 They demonstrated in a meta analysis of randomized controlled trials that compared to medical therapy ICD has significantly improved survival among patients with nonischemic cardiomyopathy with an injection fraction of less and equal to 35%. However, CRT defibrillator overall was not associated with statistically significant mortality death when compared to CRT pacemaker.                                                 These findings are actually complimentary to each other, but need to be considered in context. One of the indications for the recently published Danish study was the fact that not only is CRT being increasingly utilized appropriately in patients with nonischemic cardiomyopathies, but also guideline directed medical therapy has improved over the course of the last several years since the initial trials of defibrillator therapy as primary prevention.                                                 Furthermore, the trial was actually powered based on a 25% reduction in overall events. Thus, even if there's a smaller benefit it would not necessarily be powered to identify if this is statistically significant. One issue as stated is the fact that nonischemic cardiomyopathy might be a milieu of different causes in individual patients. Some of whom might be at high risk for sudden cardiac death and some of whom might not.                                                 The publication by Levya, et al., highlights that better attempts at risk stratification on the basis of either MRI or other modalities might be important in helping us further assess who actually benefits from ICD, however, when mixing in prior trials with more recent trials that existed at different areas of medical therapy, and different areas of appropriate use of devices such as CRT it is critical to consider whether or not the same cutoffs, the same power calculations still apply.                                                 It is doubtless that defibrillator therapy is needed in many patients with both ischemic and nonischemic cardiomyopathy even with improved therapies for these patients otherwise. However, this multitude of publications coming out to improve our assessment of the utility of ICDs should not necessarily call into question of whether or not ICDs are merited at all, but should call into question whether we understand and have come to the best form of risk stratification for those patients who would most benefit, and thus this is an opportunity for us to identify those patients better.                                                 Next, we will move to the realm of supraventricular tachycardia's and specifically an article published by [Yang 00:53:41], et al., in the last month's edition of Heart Rhythm, entitled Focal Atrial Tachycardia's From The Parahisian Region, Strategies From Mapping And Cather ablation.                                                 With focal atrial tachycardia's from the parahisian region can potentially be targeted from multiple different regions, the right atrial septum, the noncoronary cusp, and the right middle septum. However, the optical mapping and ablation strategy for these arrhythmias remains unclear, and thus they sought to investigate electrophysiology characteristics in optimal ablation sites for parahisian [inaudible 00:54:10] from these different areas.                                                 They reviewed 362 patients with atrial tachycardia's undergoing catheter ablation. They did DCG analysis and electrophysiology studies extensively on these patients. Overall, 91 patients had a parahistian origin. An ablation was successful in a majority of these up to 94.5%.                                                 The majority of these patients had their AT successfully eliminated from the noncoronary cusp with about 44 of the 91 having it targeted from this region, with the remaining 23 from the right atrial septum, and 19 from the right middle septum. They noted those who had an earliest potential at the distal HIS catheter tended to have their site of origin more successfully ablated from the noncoronary cusp.                                                 However, those with a greater [inaudible 00:54:55] in the proximal HIS catheter tended to more likely have successful ablation from the right atrial septum or right middle septum. The mean timing of the A potential in differentiating right and middle septum ATs from right atrial septum ATs, was that they attended to be later in right middle septum ATs, than right atrial septum ATs, or noncoronary cusp ATs.                                                 They noted that for atrial tachycardia's arising from the right atrial septum and right middle septum, an A to V ratio less than 1.22 predicted safe and successful ablation with a sensitivity of 88.4% and the specificity of 91.7%. Thus, they concluded that activation sequence and timing of the A and HIS catheter could provide clues for where the most likely successful site of ablation would occur for parahisian tachycardia's.                                       

This week on On Your Mind: It’s an OYM blast from the past with this week’s special-release, archived episode!   This episode starts out with a well-deserved congratulation to our very own Liam, for acing his PhD candidacy exam.  Now he’s formally allowed to do more work for no change in pay!  We also talk about how frustrating it can be when your experiments don’t work and how nerve wracking it is waiting for a funding decision.  This is the first (and hopefully last) episode where the “Kath-eter of science” makes an appearance and then it’s onto this week’s paper.   It’s called “Detection of Clinically Relevant Genetic Variants in Autism Spectrum Disorder by Whole-Genome Sequencing” by Jiang et al. doi:10.1016/j.ajhg.2013.06.012 This paper brings up some nostalgic flash-backs from Kat, who used to work in ASD research before taking the leap into grad school.  Autism spectrum disorders affect 1 in 88 children and are defined by deficits in social skills, communication and repetitive and restrictive interests.  Genome-wide association studies (GWAS) have identified genetic polymorphisms that contribute to the risk of ASD but these are common mutations that can’t explain the whole genetic landscape of the disease.  This week’s paper uses whole genome sequencing (for a video tutorial: http://www.youtube.com/watch?v=Rzmm57udYdk  ) to identify new, rare mutations that are found in 32 children with ASD.  These include single nucleotide changes (SNP or SNV), and larger alterations to the genetic sequence (indels and CNVs).  The authors attempt to prioritize future medical interventions and follow up for children based on their genetic findings.  Of course, this leads us to a rather epistemological discussion on personalized genomics and the pros and cons of putting disorders on a spectrum in the first place. Finally, this week wraps up with a debate about predicting the impact of your research inspired by this article in Science. (http://www.sciencemag.org/content/340/6138/1265.full.pdf)

With the advances in genome wide screening arrays and sequencing techniques scientists were enabled to examine genetic variations and their effects on behavioral phenotypes. While single nucleotide polymorphisms (SNPs) are the most widely studied form of genomic variations to date, another type of variants has become increasingly important in recent research, the copy number variants (CNVs). These large segments of DNA that can comprise up to several megabasepairs and differ in copy number with respect to a reference genome have been associated with several disorders and behavioral phenotypes before. This study investigated the influence of CNVs on anxiety related behavior. The detection of these variants turned out to be a major challenge since all methods available are biased by limitations of the design of the approach and the subsequent computational analyses. Therefore, three different techniques (next generation sequencing and two distinct whole genome genotyping arrays) were employed to identify CNVs in a CD 1 derived mouse model consisting of two mouse strains showing high (HAB) and low (LAB) anxiety related behavior, respectively. By comparing CNVs in HAB vs. LAB mice with expression data of four distinct brain regions of high relevance to the limbic system (central and basolateral amygdala, cingulate cortex and the hypothalamic paraventricular nucleus), it was shown that CNVs can influence the expression of protein coding genes by the alteration of the genes’ copy number per se. Therefore, the genes mapping into regions where CNVs were detected in HAB vs. LAB mice (by all three detection methods) were suggested to be possible effectors of anxiety related behavior. Amongst these candidate genes those were considered to be the most interesting ones that were additionally found to map into regions of CNVs associated with anxiety related behavior in CD 1 mice. CNVs in these mice were detected by means of a whole genome genotyping array and subsequent processing of the raw data with a novel computational approach that was adapted from existing analysis methods. Furthermore, to test the effect of a specific CNV on anxiety related behavior in vivo, a breeding approach was used to generate animals with a full genetic background of HAB mice except for one LAB derived locus harboring a CNV that included the Glo1 gene. No direct effect on the phenotype could be observed, however, the respective CNV might be involved in the manipulation of anxiety related behavior taken into account the interaction with other factors. Taken together, this study provides not only a comprehensive catalogue of CNVs in HAB/LAB mice but also the evidence that these variants can influence anxiety related behavior. Furthermore, it gives a first insight into the functionality of CNVs with respect to anxiety related behavior. Therefore, this thesis provides a profound basis for multiple advanced studies.

Background: Genome-wide association studies (GWAS) based on single nucleotide polymorphisms (SNPs) revolutionized our perception of the genetic regulation of complex traits and diseases. Copy number variations (CNVs) promise to shed additional light on the genetic basis of monogenic as well as complex diseases and phenotypes. Indeed, the number of detected associations between CNVs and certain phenotypes are constantly increasing. However, while several software packages support the determination of CNVs from SNP chip data, the downstream statistical inference of CNV-phenotype associations is still subject to complicated and inefficient in-house solutions, thus strongly limiting the performance of GWAS based on CNVs. Results: CONAN is a freely available client-server software solution which provides an intuitive graphical user interface for categorizing, analyzing and associating CNVs with phenotypes. Moreover, CONAN assists the evaluation process by visualizing detected associations via Manhattan plots in order to enable a rapid identification of genome-wide significant CNV regions. Various file formats including the information on CNVs in population samples are supported as input data. Conclusions: CONAN facilitates the performance of GWAS based on CNVs and the visual analysis of calculated results. CONAN provides a rapid, valid and straightforward software solution to identify genetic variation underlying the `missing' heritability for complex traits that remains unexplained by recent GWAS. The freely available software can be downloaded at http://genepi-conan.i-med.ac.at.

We report a genome-wide assessment of single nucleotide polymorphisms (SNPs) and copy number variants (CNVs) in schizophrenia. We investigated SNPs using 871 patients and 863 controls, following up the top hits in four independent cohorts comprising 1,460 patients and 12,995 controls, all of European origin. We found no genome-wide significant associations, nor could we provide support for any previously reported candidate gene or genome-wide associations. We went on to examine CNVs using a subset of 1,013 cases and 1,084 controls of European ancestry, and a further set of 60 cases and 64 controls of African ancestry. We found that eight cases and zero controls carried deletions greater than 2 Mb, of which two, at 8p22 and 16p13.11-p12.4, are newly reported here. A further evaluation of 1,378 controls identified no deletions greater than 2 Mb, suggesting a high prior probability of disease involvement when such deletions are observed in cases. We also provide further evidence for some smaller, previously reported, schizophrenia-associated CNVs, such as those in NRXN1 and APBA2. We could not provide strong support for the hypothesis that schizophrenia patients have a significantly greater ''load'' of large (> 100 kb), rare CNVs, nor could we find common CNVs that associate with schizophrenia. Finally, we did not provide support for the suggestion that schizophrenia-associated CNVs may preferentially disrupt genes in neurodevelopmental pathways. Collectively, these analyses provide the first integrated study of SNPs and CNVs in schizophrenia and support the emerging view that rare deleterious variants may be more important in schizophrenia predisposition than common polymorphisms. While our analyses do not suggest that implicated CNVs impinge on particular key pathways, we do support the contribution of specific genomic regions in schizophrenia, presumably due to recurrent mutation. On balance, these data suggest that very few schizophrenia patients share identical genomic causation, potentially complicating efforts to personalize treatment regimens.

Einleitung: Die altersbedingte Makuladegeneration (AMD) ist der führende Grund für Blindheit im Sinne des Gesetzes in den westlichen Industrienationen mit stark steigender Inzidenz und Prävalenz. Es gibt verschiedene Formen der AMD. Besonders die so genannte „feuchte Form“, die durch die Entstehung von chorioidalen Neovaskularisationsmembranen (CNV) am Ort des schärfsten Sehens gekennzeichnet ist, führt oft zu einem rasch progredienten Abfall des Visus. Für die Diagnostik solcher Neovaskularisationsmembranen dient neben der klinischen Untersuchung vor allem die Darstellung mittels Fluoreszenzangiographie (FLA), anhand derer auch eine weitere Einteilung von CNVs in verschiedene Typen (z.B. „klassische“ oder „okkulte“ Membranen) vorgenommen wird. Auch Defekte im retinalen Pigmentepithel, das topographisch der Netzhaut benachbart liegt, lassen sich diagnostisch mittels der FLA darstellen und quantifizieren. Bis dato stand als einzige aktive Therapieoption für diese Membranen die Verödung mittels Argon-Laser zur Verfügung, die allerdings auch unweigerlich mit einer Zerstörung der darüber liegenden neurosensorischen Netzhaut einhergeht. Daher wurde an der Augenklinik der Ludwig-Maximilians-Universität der Weg der chirurgischen Intervention beschritten, bei dem nach einer Pars-Plana-Vitrektomie und Retinotomie die entsprechende subfoveal gelegene Membran oder Blutung aus dem Subretinalraum extrahiert wird. Zwangsweise kommt es – wie sich herausstellte – dabei durch die Membranstruktur bedingt jedoch auch immer zu einer Mitentfernung von retinalem Pigmentepithel (RPE), das für die Netzhaut eine trophische Funktion besitzt. Methodik: Bei der Nachbeobachtung der Patienten fiel auf, dass es zu Rezidiven von CNVs kam. Ausgangspunkt dieser Studie war die Fragestellung, ob ein Zusammenhang zwischen Größe der RPE-Defekte und Rezidivwahrscheinlichkeit besteht. Hierzu wurden retrospektiv die Krankenakten und Fluoreszenzangiographien von 51 operierten Patienten ausgewertet, die Größe der RPE-Defekte auf postoperativ angefertigten Angiographien ausgemessen und zum Auftreten eines Rezidives bzw. zum Rezidivzeitpunkt in Relation gesetzt. Ergebnisse: Dabei konnte festgestellt werden, dass kleinere RPE-Defekte mit einer erhöhten Wahrscheinlichkeit sowohl für ein Auftreten eines Rezidives, als auch mit der für einen früheren Rezidivzeitpunkt einhergehen. Des weiteren ergab sich eine negative Korrelation zwischen der Größe des RPE-Defektes und dem bestkorrigierten Visus zu verschiedenen postoperativen Zeitpunkten während des ersten Jahres nach der Operation (bei einer Nachbeobachtungszeit von bis zu vier Jahren). Dementsprechend ergab sich auch eine positive Korrelation mit dem benötigten Vergrößerungsfaktor einiger Patienten. Zudem lässt sich eine Funktionsdiagnostik der Netzhaut, v.a. der Makula, mit Hilfe der Mikroperimetrie betreiben. Bei den mit dieser Diagnostikmöglichkeit untersuchten Patienten zeigten sich statistisch signifikante positive Korrelationen zwischen den RPE-Defekten und den gemessenen absoluten und relativen Skotomen. Ein statistischer Zusammenhang zwischen der Größe des RPE-Defektes und einer Visusverbesserung oder –verschlechterung konnte dabei nicht festgestellt werden, jedoch eine positive Korrelation zwischen präoperativen und dem besten postoperativ erreichten Visus. Diskussion: Mit Hilfe der chirurgischen Membranektomie lässt sich zwar eine Stabilisierung der Sehschärfe erreichen, die entstandenen RPE-Defekte sind aber Ursache des fehlenden Anstiegs des Visus. Andere Faktoren wie Vorschädigungen der Strukturen von Aderhaut, Bruch’scher Membran, RPE und Netzhaut durch den Krankheitsprozess spielen eine zusätzliche Rolle. Auch Lokalisation und Wachstumsmuster von Neovaskularisationen können einen Einfluss auf die postoperativ erreichten Sehschärfen haben. Dies zeigt sich insbesondere im Vergleich mit in der Literatur angegebenen Ergebnissen nach subfovealer Membranektomie bei anderen Erkrankungen, die mit der Bildung chorioidaler Neovaskularisationen einherge-hen. Die Beobachtung, dass kleinere RPE-Defekte mit einer erhöhten Rezidivrate einhergehen, lässt Rückschlüsse auf die mögliche Rolle des RPE bei der primären Krankheitsentstehung zu. Insbesondere unterstützt sie die These, dass zwischen zentralem und mittelperipherem retina-len Pigmentepithel Unterschiede bestehen z.B. in Bezug auf die Synthese von Wachstumsfak-toren, die bei der Entstehung solcher Membranen eine entscheidende Rolle spielen oder al-tersbedingte Unterschiede bezüglich der regenerativen Kapazität der RPE-Zellen. Für künfti-ge Therapieoptionen mit dem Resultat einer verbesserten Sehschärfe müssten Wege gefunden werden, den geschädigten Komplex von Bruch’scher Membran und RPE wiederherzustellen.

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Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.22.055731v1?rss=1 Authors: Roth, J. G., Muench, K. L., Asokan, A., Mallett, V. M., Gai, H., Verma, Y., Weber, S., Charlton, C., Fowler, J. L., Loh, K. M., Dolmetsch, R. E., Palmer, T. D. Abstract: Microdeletions and microduplications of the 16p11.2 chromosomal locus are associated with syndromic neurodevelopmental disorders and reciprocal physiological conditions such as macro/microcephaly and high/low body mass index. To facilitate cellular and molecular investigations of these phenotypes, 65 clones of human induced pluripotent stem cells (hiPSCs) were generated from 13 individuals with 16p11.2 copy number variations (CNVs). Cortical neural progenitor cells derived from these hiPSCs were profiled using RNA-Seq, which identified alterations in radial glial gene expression that precede morphological abnormalities reported at later neurodevelopmental stages. Moreover, a customizable bioinformatic strategy for the detection of random integration and expression of reprogramming vectors was developed and leveraged towards identifying a subset of footprint-free hiPSC clones that are available by request from the Simons Foundation Autism Research Initiative. This publicly available resource of 65 human hiPSC clones can serve as a powerful medium for probing the etiology of developmental disorders associated with 16p11.2 CNVs Copy rights belong to original authors. Visit the link for more info