47 research outputs found

    Fine-scale behavioral analysis of the Greenland shark using 3-axis accelerometers

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    The Tenth Symposium on Polar Science/Ordinary sessions : [OB] Polar Biology, Wed. 4 Dec. / Entrance Hall (1st floor) , National Institute of Polar Researc

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

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    「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

    Metabolic engineering of E. coli for improving mevalonate production to promote NADPH regeneration and enhance acetyl-CoA supply

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    Microbial production of mevalonate from renewable feedstock is a promising and sustainable approach for the production of value-added chemicals. We describe the metabolic engineering of Escherichia coli to enhance mevalonate production from glucose and cellobiose. First, the mevalonate-producing pathway was introduced into E. coli and the expression of the gene atoB, which encodes the gene for acetoacetyl-CoA synthetase, was increased. Then, the deletion of the pgi gene, which encodes phosphoglucose isomerase, increased the NADPH/NADP+ ratio in the cells but did not improve mevalonate production. Alternatively, to reduce flux toward the tricarboxylic acid cycle, gltA, which encodes citrate synthetase, was disrupted. The resultant strain, MGΔgltA‐MV, increased levels of intracellular acetyl-CoA up to sevenfold higher than the wild-type strain. This strain produced 8.0 g/L of mevalonate from 20 g/L of glucose. We also engineered the sugar supply by displaying β-glucosidase (BGL) on the cell surface. When cellobiose was used as carbon source, the strain lacking gnd displaying BGL efficiently consumed cellobiose and produced mevalonate at 5.7 g/L. The yield of mevalonate was 0.25 g/g glucose (1 g of cellobiose corresponds to 1.1 g of glucose). These results demonstrate the feasibility of producing mevalonate from cellobiose or cellooligosaccharides using an engineered E. coli strain

    ブレンディッド・ラーニングによる英語学習意欲について ― ビデオプロジェクトを通して ―

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    研究論

    Improved spillover correction model to quantify myocardial blood flow by C-11-acetate PET : comparison with O-15-H2O PET

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    C-11-acetate has been applied for evaluation of myocardial oxidative metabolism and can simultaneously estimate myocardial blood flow (MBF). We developed a new method using two-parameter spillover correction to estimate regional MBF (rMBF) with C-11-acetate PET in reference to MBF derived from O-15-H2O PET. The usefulness of our new approach was evaluated compared to the conventional method using one-parameter spillover correction. Sixty-three subjects were examined with C-11-acetate and O-15-H2O dynamic PET at rest. Inflow rate of C-11-acetate (K1) was compared with MBF derived from O-15-H2O PET. For the derivation, the relationship between K1 and MBF from O-15-H2O was linked by the Renkin-Crone model in 20 subjects as a pilot group. One-parameter and two-parameter corrections were applied to suppress the spillover between left ventricular (LV) wall and LV cavity. Validation was set using the other 43 subjects' data. Finally, rMBFs were calculated using relational expression derived from the pilot-group data. The relationship between K1 and MBF derived from O-15-H2O PET was approximated as K1 = [1-0.764 x exp(-1.001/MBF)] MBF from the pilot data using the two-parameter method. In the validation set, the correlation coefficient between rMBF from C-11-acetate and O-15-H2O demonstrated a significantly higher relationship with the two-parameter spillover correction method than the one-parameter spillover correction method (r = 0.730, 0.592, respectively, p < 0.05). In C-11-acetate PET study, the new two-parameter spillover correction method dedicated more accurate and robust myocardial blood flow than the conventional one-parameter method
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