テレメーター法による長距離走トレーニング強度の研究

In order to predict the training intensity in long distance running, the percent of maximum oxygen uptake in daily training was estimated from heart rate response which was measured by means of telemetering. Four male distance runners participated in this experiment. These results were summarized as follows ; 1) In order to clarify the difference between directly measured VO_2 max and that predicted from heart rate, oxygen uptake and heart rate were measured simultaneously in treadmill running which produced the same pattern as the daily training program. The differences of % of VO_2 max predicted from heart rate and measured directly were about 10% 2) The training intensity was evaluated by % of VO_2max which was predicted from the variation of heart rate in long distance running. The training intensity in 6, 000m continuous running was equivalent to 70～85% of VO_2max. In intermittent run ning, which consisted of 1, 000m run seven times and 3, 000m run five times, it indicated 90～100% of VO_2max. 3) There were rectilinear relationships between running speed and percent of maximum oxygen uptake. The regretion equation was different for each athlete. At a given running speed the large difference of % of VO_2max btween individuals was observed

Kansai University Library 100th anniversary

目次 【序文】記念誌の刊行にあたって（図書館長　内田慶市）図書館創設100周年によせて（学長　楠見晴重）記念誌の編集について【第1部　この20年を振り返って】高槻図書室開館（広瀬雅子）…3阪神・淡路大震災（高橋真澄）…8図書館システムの変遷（徳岡久実・濱生快彦）…12図書館ビジョン7項目の制定（濱生快彦）…20図書館におけるアウトソーシング（高橋真澄）…26電子展示（濱生快彦）…36市民利用開始（広瀬雅子）…41図書館ウェブサイト（濱生快彦）…442010プロジェクトによる新図書館（高橋真澄・田中恵美）…48図書館リニューアル工事（新谷大二郎）…60図書館の現在と未来（堀口和弘）…68【第2部　図書館に想う】関西大学図書館創設100周年に寄せて（市川訓敏）…79図書館の思い出、図書館への思い（北川勝彦）…85図書館在職時の思い出（柴田真一）…91数々の貴重書（田中登）…95関西大学図書館100周年にあたって : 私の夢想する図書館（内田慶市）…100【第3部　図書館の文庫・コレクション】文庫・コレクションの紹介（鵜飼香織）…111【第4部　資料編】図書館年譜（明治19.3 ～平成26.7）…119サービスに係る統計（総合図書館）…146サービスに係る統計（高槻図書室・ミューズ大学図書館・堺キャンパス図書館）…148蔵書数の推移…149図書費執行額の推移…150展示一覧…152他大学図書館との協定一覧…160【「図書館コラム」】新人時代の思い出（高松和美）…11エレベーターにまつわる話（吉田有輝）…19泣き別れたり、親子になったり（嶋田有理香）…35貴重なのは本だけ？貴重書担当のつぶやき（大上良樹）…40会長校のころ（金東瀅）…46『コアラ博士』にまつわるあれこれ（松本和剛）…57広報誌『KULione 』誕生秘話（白髪友賀）…59本と夢を運んだテレリフト（芝谷秀司）…66LOUIS VUITTON（加藤博之）…7

A Gammaherpesvirus Cooperates with Interferon-alpha/beta-Induced IRF2 to Halt Viral Replication, Control Reactivation, and Minimize Host Lethality

The gammaherpesviruses, including Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), establish latency in memory B lymphocytes and promote lymphoproliferative disease in immunocompromised individuals. The precise immune mechanisms that prevent gammaherpesvirus reactivation and tumorigenesis are poorly defined. Murine gammaherpesvirus 68 (MHV68) is closely related to EBV and KSHV, and type I (alpha/beta) interferons (IFNαβ) regulate MHV68 reactivation from both B cells and macrophages by unknown mechanisms. Here we demonstrate that IFNβ is highly upregulated during latent infection, in the absence of detectable MHV68 replication. We identify an interferon-stimulated response element (ISRE) in the MHV68 M2 gene promoter that is bound by the IFNαβ-induced transcriptional repressor IRF2 during latency in vivo. The M2 protein regulates B cell signaling to promote establishment of latency and reactivation. Virus lacking the M2 ISRE (ISREΔ) overexpresses M2 mRNA and displays uncontrolled acute replication in vivo, higher latent viral load, and aberrantly high reactivation from latency. These phenotypes of the ISREΔ mutant are B-cell-specific, require IRF2, and correlate with a significant increase in virulence in a model of acute viral pneumonia. We therefore identify a mechanism by which a gammaherpesvirus subverts host IFNαβ signaling in a surprisingly cooperative manner, to directly repress viral replication and reactivation and enforce latency, thereby minimizing acute host disease. Since we find ISREs 5′ to the major lymphocyte latency genes of multiple rodent, primate, and human gammaherpesviruses, we propose that cooperative subversion of IFNαβ-induced IRFs to promote latent infection is an ancient strategy that ensures a stable, minimally-pathogenic virus-host relationship

Interferon-alpha-induced mTOR activation is an anti-hepatitis C virus signal via the phosphatidylinositol 3-kinase-Akt-independent pathway.

OBJECT: The interferon-induced Jak-STAT signal alone is not sufficient to explain all the biological effects of IFN. The PI3-K pathways have emerged as a critical additional component of IFN-induced signaling. This study attempted to clarify that relationship between IFN-induced PI3-K-Akt-mTOR activity and anti-viral action. RESULT: When the human normal hepatocyte derived cell line was treated with rapamycin (rapa) before accretion of IFN-alpha, tyrosine phosphorylation of STAT-1 was diminished. Pretreatment of rapa had an inhibitory effect on the IFN-alpha-induced expression of PKR and p48 in a dose dependent manner. Rapa inhibited the IFN-alpha inducible IFN-stimulated regulatory element luciferase activity in a dose-dependent manner. However, wortmannin, LY294002 and Akt inhibitor did not influence IFN-alpha inducible luciferase activity. To examine the effect of PI3-K-Akt-mTOR on the anti-HCV action of IFN-alpha, the full-length HCV replication system, OR6 cells were used. The pretreatment of rapa attenuated its anti-HCV replication effect in comparison to IFN-alpha alone, whereas the pretreatment with PI3-K inhibitors, wortmannin and LY294002 and Akt inhibitor did not influence IFN-induced anti-HCV replication. CONCLUSION: IFN-induced mTOR activity, independent of PI3K and Akt, is the critical factor for its anti-HCV activity. Jak independent mTOR activity involved STAT-1 phosphorylation and nuclear location, and then PKR is expressed in hepatocytes

The whole blood transcriptional regulation landscape in 465 COVID-19 infected samples from Japan COVID-19 Task Force

「コロナ制圧タスクフォース」COVID-19患者由来の血液細胞における遺伝子発現の網羅的解析 --重症度に応じた遺伝子発現の変化には、ヒトゲノム配列の個人差が影響する--. 京都大学プレスリリース. 2022-08-23.Coronavirus disease 2019 (COVID-19) is a recently-emerged infectious disease that has caused millions of deaths, where comprehensive understanding of disease mechanisms is still unestablished. In particular, studies of gene expression dynamics and regulation landscape in COVID-19 infected individuals are limited. Here, we report on a thorough analysis of whole blood RNA-seq data from 465 genotyped samples from the Japan COVID-19 Task Force, including 359 severe and 106 non-severe COVID-19 cases. We discover 1169 putative causal expression quantitative trait loci (eQTLs) including 34 possible colocalizations with biobank fine-mapping results of hematopoietic traits in a Japanese population, 1549 putative causal splice QTLs (sQTLs; e.g. two independent sQTLs at TOR1AIP1), as well as biologically interpretable trans-eQTL examples (e.g., REST and STING1), all fine-mapped at single variant resolution. We perform differential gene expression analysis to elucidate 198 genes with increased expression in severe COVID-19 cases and enriched for innate immune-related functions. Finally, we evaluate the limited but non-zero effect of COVID-19 phenotype on eQTL discovery, and highlight the presence of COVID-19 severity-interaction eQTLs (ieQTLs; e.g., CLEC4C and MYBL2). Our study provides a comprehensive catalog of whole blood regulatory variants in Japanese, as well as a reference for transcriptional landscapes in response to COVID-19 infection