光化学反応に対する一酸化炭素の影響 : プロピレン-窒素酸化物-一酸化炭素系の反応

application/pdfIt has been considered that carbon monoxide has smalle effect on photochemical reactions. But, because of the large amount of CO in the urban atmosphere, its role to photochemical smog formation was regarded to be interesting. In the present paper, the authors have revealed the influence of carbon monoxide on photochemical reactions of propylene-nitric oxides-carbon monoxide-air mixtures. The oxidation of NO and the formation of HCHO and CH₃CHO are accelerated by CO. However, the consumption of C₃H₆ and the formation of HCOOH and CH₃COOH are controled to the contrary. It was eonfirmed that the competition occurred between C₃H₆ and CO for OH radical.departmental bulletin pape

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

Additional file 6: of Efficient identification of CRISPR/Cas9-induced insertions/deletions by direct germline screening in zebrafish

Amplicon screening data used for Fig. 5. (TXT 3213 kb

Additional file 8: of Efficient identification of CRISPR/Cas9-induced insertions/deletions by direct germline screening in zebrafish

Sample accession numbers. (TSV 80 kb

Additional file 1: of Efficient identification of CRISPR/Cas9-induced insertions/deletions by direct germline screening in zebrafish

Table of CRISPR target sequences. (TXT 7 kb

Additional file 4: of Efficient identification of CRISPR/Cas9-induced insertions/deletions by direct germline screening in zebrafish

Amplicon screening data used for Fig. 4a-c. (TXT 142 kb

Additional file 5: of Efficient identification of CRISPR/Cas9-induced insertions/deletions by direct germline screening in zebrafish

Results from KASP genotyping used for Fig. 4d. (TXT 910 bytes

Additional file 2: of Efficient identification of CRISPR/Cas9-induced insertions/deletions by direct germline screening in zebrafish

Tutorial for the bioinformatics including sgRNA/primer deisgn and MiSeq analysis. (PDF 7778 kb

Additional file 3: Figure S1 and Figure S2. of Efficient identification of CRISPR/Cas9-induced insertions/deletions by direct germline screening in zebrafish

Comparison of induced indels between germline and somatic tissues. (a) Plot shows the same data as Fig. 4a, split into separate plots for each sgRNA. (b) Plot of frequencies for individual variants in sperm versus fin clip (same data as in Fig. 4b with full axes). (PDF 374 kb

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