Microsoft Word - 第13回国際学生セミナー募集用考案延期後.docx
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1 第 13 回国際学生セミナー (ISS) 演題募集要項 本年度は Knocking on life science's door: おっしゃ let's do science! をスローガンとし 研究活動に関わる参加者すべてが 国や言葉だけでなく 異なる研究分野を超えて活発に交流することを目指したセミナーを行います (1) 開催日程 日時 3 月 3 日 ( 火 ) 4 日 ( 水 ) 口頭発表 (Long Talk, Short Talk) ポスター発表 場所 京都大学芝蘭会館 (2) 発表形式 使用言語 英語 口頭発表 Long Talk 発表 20 分 討論 5 分計 25 分 Short Talk 発表 12 分 討論 3 分計 15 分 ポスター発表 ポスターサイズ A0 サイズ : 841 mm 1189 mm 発表形式 1 時間 2 部制口頭発表参加の方はこちらも参加していただくことになります 注記 口頭発表の方には ポスター発表も併せて行っていただきます 詳細なプログラムは決定次第 順次お伝えします
2 (3) 応募について生命科学研究科 ウイルス研究所 薬学研究科に所属する大学院生 および博士研究員を対象にし 以下のように募集いたします Long Talk ある程度の研究実績 成果があり 英語でのプレゼンテーションやディスカッションに挑戦しようとする意欲のある方を募集いたします Short Talk 研究実績 成果や学年に関わらず 英語でのプレゼンテーションやディス カッションに挑戦しようとする意欲のある方を幅広く募集いたします ポスター発表 上記に所属する大学院生 博士研究員を対象とし ポスターを通じて情報 交換したい方を募集いたします (4) 審査 表彰について 口頭発表 招待審査員と 京都大学に所属する教員より選出された審査員による審査表彰 奨学金あり ポスター発表 参加者全員による投票による審査表彰 奨学金あり 注記 口頭発表については Long Talk Short Talk ともに 審査員からのコメントを得ることができます これにより 自身の発表に対する評価を知ることができ 改善点を今後の活動にフィードバックすることが可能になります 本セミナーでは 生命科学研究科の James Hejna 教授に指導をお願いし 口頭発表に関わる要旨作成の指導やプレゼンテーションの練習など 皆さんの活動を全面的にサポートする環境を整えております ( 詳細は次項の第 13 回国際学生セミナーのホームページをご参照ください )
3 (5) 応募方法下記の第 13 回国際学生セミナーのホームページ内のオンラインフォームから登録して下さい なお 要旨は当委員会の作成した次項のフォーマットに必要事項を記入し 件名を 13th ISS Abstract (your name) としたメールにファイルを添付し 下記 E-メールアドレスまでご提出下さい Website 演題募集期間 2014 年 12 月 2 日 ( 火 ) 2014 年 12 月 27 日 ( 土 ) 抄録提出締め切り 2015 年 1 月 10 日 ( 金 ) まで 注記 注意事項をよくご確認の上 必要事項にご記入下さい 口頭発表希望者は応募の際に Long Talk Short Talk のいずれかの発表形式をお選び下さい ただし Long Talk に関しては 発表演題の数に応じて実行委員会で選考し ご登録いただいた演題の中から改めて採択いたします 選考については実行委員会にご一任下さいますようお願いいたします (6) お問い合わせご不明な点がありましたら 件名に Inquiries about registration of the 13th ISS (your name) とご記名の上 下記の E-メールアドレスまでご連絡下さい 13th.iss.registration@lif.kyoto-u.ac.jp 2014 年 12 月 16 日
4 Title (letters font: Times New Roman, 12 point, boldface, left adjust) Author(s) (Times New Roman, 10.5 point, left justification; please write * before the presenter) Example: *Daisuke Kizawa 1, Kazuhisa Fukue 2, Shuhei Ueda 3 (First name / Family name running numbers ) Affiliation(s) (Times New Roman, 10.5 point, left justification; your lab s school or institute and university) Example: 1; Igaki Lab., Graduate School of Biostudies, Kyoto University, 2; Nagao Lab., Graduate School of Biostudies, Kyoto University, 3; Koyanagi Lab., Institute for Virus Research, Kyoto University Abstract Body of text (Times New Roman, 10.5 point, right and left justification; maximum 250 words) Keywords: (Times New Roman, 10.5 point, left justification; 6 words or less, separated by commas) *Note Please read the following instructions carefully before filling out the text. 1. Language: English 2. File format: XXXX.doc (Please do not use XXXX.docx) 3. Please do not change any formats of this text. 4. Please use one-byte characters only. 5. Please fill in all necessary information within a single page (A4). 6. Please fill in your name in the file title before submission. e.g. 13thISS(your name) format.doc 13thISS(Tarou Kyoudai) format.doc 13thISS(Homer Jay Simpson) format.doc The next page is the sample abstract.
5 Mutations in the zinc transporter ZnT2 gene result in zinc deficiency in a breast-fed infant *Naoya Itsumura, Yusaku Miyamae, Masaya Nagao, Taiho Kambe Graduate School of Biostudies, Kyoto University Zinc is an essential mineral and has extensive roles in developmental processes. Therefore, zinc deficiency in infants can result in various disorders including growth restriction, skin lesions, alopecia and immune system dysfunctions. Zinc concentrations in breast milk are considerably higher than those of the maternal serum to meet infant s requirements. Thus, effective mechanisms ensuring secretion of large amounts of zinc into the milk operate during lactation in mammary epithelial cells. The zinc transporter ZnT2 and ZnT4 are thought to be involved in transporting zinc into the milk. Recently we found a Japanese mother with low milk zinc concentrations (>90% reduction) whose infant developed severe zinc deficiency. To investigate the cause of the milk zinc deficiency, we isolated the genomic DNA from the mother s blood and sequenced the ZnT2 and ZnT4 genes. We found no mutations in the ZnT4 gene, but identified two novel missense mutations, causing W152R and S296L substitution, on different alleles in the ZnT2 gene. Next, we characterized these ZnT2 mutants biochemically using zinc-sensitive DT40 cells. The W152R mutant abolished the activity to transport zinc and to form dimer complex, which is required for the ZnT2 to transport zinc. These results indicated the W152R mutant is a loss-of-function. The S296L mutant retained both abilities but was extremely destabilized. Taken together, the compound heterozygous mutations in the ZnT2 gene of the mother caused low milk zinc concentrations and resulted in severe zinc deficiency in the breast-fed infant. Our results show that ZnT2 doubtlessly plays an essential role in zinc secretion into milk. Keywords: zinc transporter, ZnT2, mutation, human disease
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