Effect of Air Pressure on Moisture Transfer inside Porous Building Materials Three-dimensional Behavior of Moisture and Air

The effect of air pressure on moisture transfer inside porous building materials cannot be ignored in cases in which air cannot escape through the surfaces of the materials; in such cases, the air is compressed by the movement of the moisture. Therefore, in a situation in which most surfaces of a specimen are sealed or treated with surface-protecting materials (a situation that is often encountered in typical water-absorption tests), the experimental results may differ from those without sealed or treated surfaces. In the present study, the influence of air pressure on moisture transfer was investigated quantitatively. First, the following water-absorption test was conducted. Water infiltrated into a brick through its top surface, whereas the side surfaces were sealed to prevent the transfer of moisture and air. The bottom surface was exposed to the ambient air. The water content was measured twodimensionally during the experiment using gamma-ray attenuation. Next, to investigate how air pressure affects water infiltration, another experiment was conducted after sealing the bottom surface. The air inside the brick was expected to be compressed by the infiltrating water when the bottom surface was sealed. A water-absorption test was then performed after a small hole was made in a side surface of the bottom-sealed brick to reduce the interior air pressure. Finally, we analyzed the experiments numerically using a three-dimensional calculation model for simultaneous air and moisture transfer, assessing the validity of the model by comparing the calculated and measured water contents. The experimental and numerical results show that water infiltration is slowed by higher air pressure inside the specimen when it is difficult for air to escape. It is also shown that the hole in the side surface helped limit the rise in air pressure to some extent

Timing jitter removers of photon detectors

Among various performances of photon detectors, the timing jitter is difficult to improve because of its trade-offs with other important performances such as detection efficiency. Such trade-offs have been an issue in applications, especially for high-purity non-Gaussian-state generation necessary in optical quantum computation. Here, we introduce a method using an external fast optical switch -- Timing Jitter Remover (TJR) -- whose time window limits the photon-detectable time of photon detectors and improve the timing jitter without sacrificing other performances. By using a TJR, we experimentally improve the timing jitter of a photon-number-resolving detector based on a transition edge sensor, from 50 ns to 10 ns. Using this improved detector, we generate one of important non-Gaussian states, a Schr\"{o}dinger cat state with Wigner negativity of -0.01, which cannot be observed without TJRs. TJRs would be the key technology for the realization of ultra-fast, fault-tolerant, universal optical quantum computer.Comment: 26 pages, 6 figure

DOCK2 is involved in the host genetics and biology of severe COVID-19

「コロナ制圧タスクフォース」COVID-19疾患感受性遺伝子DOCK2の重症化機序を解明 --アジア最大のバイオレポジトリーでCOVID-19の治療標的を発見--. 京都大学プレスリリース. 2022-08-10.Identifying the host genetic factors underlying severe COVID-19 is an emerging challenge. Here we conducted a genome-wide association study (GWAS) involving 2, 393 cases of COVID-19 in a cohort of Japanese individuals collected during the initial waves of the pandemic, with 3, 289 unaffected controls. We identified a variant on chromosome 5 at 5q35 (rs60200309-A), close to the dedicator of cytokinesis 2 gene (DOCK2), which was associated with severe COVID-19 in patients less than 65 years of age. This risk allele was prevalent in East Asian individuals but rare in Europeans, highlighting the value of genome-wide association studies in non-European populations. RNA-sequencing analysis of 473 bulk peripheral blood samples identified decreased expression of DOCK2 associated with the risk allele in these younger patients. DOCK2 expression was suppressed in patients with severe cases of COVID-19. Single-cell RNA-sequencing analysis (n = 61 individuals) identified cell-type-specific downregulation of DOCK2 and a COVID-19-specific decreasing effect of the risk allele on DOCK2 expression in non-classical monocytes. Immunohistochemistry of lung specimens from patients with severe COVID-19 pneumonia showed suppressed DOCK2 expression. Moreover, inhibition of DOCK2 function with CPYPP increased the severity of pneumonia in a Syrian hamster model of SARS-CoV-2 infection, characterized by weight loss, lung oedema, enhanced viral loads, impaired macrophage recruitment and dysregulated type I interferon responses. We conclude that DOCK2 has an important role in the host immune response to SARS-CoV-2 infection and the development of severe COVID-19, and could be further explored as a potential biomarker and/or therapeutic target

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

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