Basin scale evaluation of the groundwater recharge and nitrogen contamination processes in an intermountain basin of Himalayan region

University of Yamanashi (山梨大学)博士(工学)application/pdf医工農博甲第31号thesi

隣接椎間障害を防止する新たな脊椎固定具の開発

application/pdf三重大学大学院 工学研究科 機械工学専攻 生体システム工学研究室71thesi

How research institutions can foster innovation

Carrying out research—if done right—inherently means being innovative. We use ‘innovation’ in a broad sense, that is, as the creation of something new: an idea, a concept, way of looking at things, method or approach. We specifically do not use the term solely—as it often is— as the development of new technologies with practical applications, which can be marketed for commercial purposes. Naturally, in this sense, being innovative is intimately linked to being creative or imaginative. No-one wants to discover what others have already found. Innovation, by definition, requires novelty. Novelty is an important source of scientific breakthroughs and has great technological impact.[1] Such breakthroughs often come about when scientists combine disciplines, ideas, approaches, or tools in novel and unexpected ways. While clearly only very few scientific breakthroughs result in Nobel Prizes, we can all increase our impact by taking a more innovative approach. Importantly, research institutions stand to benefit from fostering innovation within their walls. A reputation for truly ground-breaking work attracts better scientists, students and more funding—all key success factors. But how can institutions promote innovative research? Various initiatives have been implemented to encourage researchers to collaborate across disciplines and embrace the ‘Third Mission’ of universities to promote relationships between public sector research and business.[2,3 ] However, dedicated institutional strategies aimed at fostering innovation at the level of their research units are still comparatively rare. Here, we try to briefly outline what, in our experience, academic research institutions can do to help their scientists become more innovative, followed by a brief example of a programme that implements these practices and approaches

平面配線可能性検証アルゴリズムの実現 (<特集>電子システムの設計技術と設計自動化)

配線可能性検証とは, 与えられた概略配線が詳細配線へ変換できるかどうかを判定することである. 本論文では, まず, 先に筆者らが提案した平面配線可能性検証アルゴリズムを計算機上に実現し, プリント配線板設計に適用した場合の性能について報告する. 次に, 使用する記憶量を削減するための方法を提案し, その性能について報告する.Routability checking is to decide whether the global wires can be transformed into the detailed ones or not. We proposed an efficient algorithm for routability checking. In this paper, we implement our algorithm and apply it to actual layout design. Furthermore, we modify our algorithm so that it use only linear space and give experimental results of its performance.journal articl

How research institutions can foster innovation

Carrying out research—if done right—inherently means being innovative. We use ‘innovation’ in a broad sense, that is, as the creation of something new: an idea, a concept, way of looking at things, method or approach. We specifically do not use the term solely—as it often is— as the development of new technologies with practical applications, which can be marketed for commercial purposes. Naturally, in this sense, being innovative is intimately linked to being creative or imaginative. No-one wants to discover what others have already found. Innovation, by definition, requires novelty. Novelty is an important source of scientific breakthroughs and has great technological impact.[1] Such breakthroughs often come about when scientists combine disciplines, ideas, approaches, or tools in novel and unexpected ways. While clearly only very few scientific breakthroughs result in Nobel Prizes, we can all increase our impact by taking a more innovative approach. Importantly, research institutions stand to benefit from fostering innovation within their walls. A reputation for truly ground-breaking work attracts better scientists, students and more funding—all key success factors. But how can institutions promote innovative research? Various initiatives have been implemented to encourage researchers to collaborate across disciplines and embrace the ‘Third Mission’ of universities to promote relationships between public sector research and business.[2,3 ] However, dedicated institutional strategies aimed at fostering innovation at the level of their research units are still comparatively rare. Here, we try to briefly outline what, in our experience, academic research institutions can do to help their scientists become more innovative, followed by a brief example of a programme that implements these practices and approaches

Autosomal-Dominant Corneal Endothelial Dystrophies CHED1 and PPCD1 Are Allelic Disorders Caused by Non-coding Mutations in the Promoter of OVOL2

Congenital hereditary endothelial dystrophy 1 (CHED1) and posterior polymorphous corneal dystrophy 1 (PPCD1) are autosomal-dominant corneal endothelial dystrophies that have been genetically mapped to overlapping loci on the short arm of chromosome 20. We combined genetic and genomic approaches to identify the cause of disease in extensive pedigrees comprising over 100 affected individuals. After exclusion of pathogenic coding, splice-site, and copy-number variations, a parallel approach using targeted and whole-genome sequencing facilitated the identification of pathogenic variants in a conserved region of the OVOL2 proximal promoter sequence in the index families (c.?339_361dup for CHED1 and c.?370T>C for PPCD1). Direct sequencing of the OVOL2 promoter in other unrelated affected individuals identified two additional mutations within the conserved proximal promoter sequence (c.?274T>G and c.?307T>C). OVOL2 encodes ovo-like zinc finger 2, a C2H2 zinc-finger transcription factor that regulates mesenchymal-to-epithelial transition and acts as a direct transcriptional repressor of the established PPCD-associated gene ZEB1. Interestingly, we did not detect OVOL2 expression in the normal corneal endothelium. Our in vitro data demonstrate that all four mutated OVOL2 promoters exhibited more transcriptional activity than the corresponding wild-type promoter, and we postulate that the mutations identified create cryptic cis-acting regulatory sequence binding sites that drive aberrant OVOL2 expression during endothelial cell development. Our data establish CHED1 and PPCD1 as allelic conditions and show that CHED1 represents the extreme of what can be considered a disease spectrum. They also implicate transcriptional dysregulation of OVOL2 as a common cause of dominantly inherited corneal endothelial dystrophies.journal articl

テレビの児童に及ぼす影響(第1報) : 1.総論(19.テレビ)

rights: 日本教育心理学会 rights: 本文データは学協会の許諾に基づきCiNiiから複製したものである relation: IsVersionOf: http://ci.nii.ac.jp/naid/110001894261/textapplication/pdfjournal articl