エンティティ・リンキングのための候補検索とランキング方法に関する研究

Tohoku University乾健太郎課

Environmental ethics support for eco city construction

The modern city based on the principle of anthropocentrism has caused many urban environmental problems, resulting in the contradiction between man and nature gradually developing into a state of binary opposition, and promoting the urban ecosystem to be on the verge of danger. On the basis of deep reflection on modern urban environmental problems, eco city construction came into being and developed rapidly. Eco city is an urban development model to solve the current urban environmental crisis and realize the harmonious coexistence between man and nature, man and man, man and societyeco city has internal consistency with environmental ethics, which contains the environmental ethics of non anthropocentrism, sustainable development and environmental justiceenvironmental ethics guides the construction of ecological city and is an important support for the construction of ecological city. First of all, environmental ethical values such as environmental ethical values, environmental ethical codes of ethics and environmental ethical beliefs provide theoretical support for the construction of ecological citysecondly, environmental ethical practices such as ecological ethical culture, ecological moral education, low-carbon economic model and ecological ethical legal system provide practical support for the construction of ecological cities

Predicting adsorbed gas capacity of deep shales under high temperature and pressure: Experiments and modeling

Temperature and pressure conditions of deep shale are beyond experiment range, and the amount of adsorbed gas is difficult to determine. To predict the adsorbed gas content of deep shales under formation conditions, isothermal adsorption experiments and model building were conducted on shale samples from Longmaxi Formation in China. A temperature-dependent adsorption model based on the Langmuir equation is proposed, which can be well-fitted by observed isotherms with a high correlation coefficient. Based on the fitted parameters at 303.15 K, the isothermal adsorption curves at 333.15 K, 363.15 K, and 393.15 K are predicted, showing a good agreement with experimental curves available. Compared with previous prediction methods, the biggest advantage of the proposed method is that it can be carried out only based on one-time isothermal adsorption experiment. Based on the predictions, the downward trend of the excess adsorption curves will slow down under high temperature and pressure conditions, and when the pressure reaches a certain level (> 80 MPa), the temperature has little effect on the excess adsorption capacity. While for absolute adsorption, the gas adsorption reaches saturation much slowly at high temperature, it can also reach saturation under formation pressure. Under the burial depth of marine shale, temperature plays a major role in controlling the adsorbed gas, resulting in the decrease of adsorbed gas content in deep shale, and its ratio will further decrease as the depth increases.Cited as: Zhou, S., Wang, H., Li, B., Li, S., Sepehrnoori, K., Cai, J. Predicting adsorbed gas capacity of deep shales under high temperature and pressure: Experiments and modeling. Advances in Geo-Energy Research, 2022, 6(6): 482-491. https://doi.org/10.46690/ager.2022.06.0

Epithelial Neoplasia Coincides with Exacerbated Injury and Fibrotic Response in the Lungs of \u3cem\u3eGprc5a\u3c/em\u3e-Knockout Mice Following Silica Exposure

Exposure to crystalline silica is suggested to increase the risk for a variety of lung diseases, including fibrosis and lung cancer. However, epidemiological evidences for the exposure-risk relationship are ambiguous and conflicting, and experimental study from a reliable animal model to explore the relationship is lacking. We reasoned that a mouse model that is sensitive to both lung injury and tumorigenesis would be appropriate to evaluate the exposure-risk relationship. Previously, we showed that, Gprc5a-/- mice are susceptible to both lung tumorigenesis and endotoxin-induced acute lung injury. In this study, we investigated the biological consequences in Gprc5a-/- mouse model following silica exposure. Intra-tracheal administration of fine silica particles in Gprc5a-/- mice resulted in more severe lung injury and pulmonary inflammation than in wild-type mice. Moreover, an enhanced fibrogenic response, including EMT-like characteristics, was induced in the lungs of Gprc5a-/- mice compared to those from wild-type ones. Importantly, increased hyperplasia or neoplasia coincided with silica-induced tissue injury and fibrogenic response in lungs from Gprc5a-/- mice. Consistently, expression of MMP9, TGFβ1 and EGFR was significantly increased in lungs from silica-treated Gprc5a-/- mice compared to those untreated or wild-type ones. These results suggest that, the process of tissue repair coincides with tissue damages; whereas persistent tissue damages leads to abnormal repair or neoplasia. Thus, silica-induced pulmonary inflammation and injury contribute to increased neoplasia development in lungs from Gprc5a-/- mouse model

Mediator subunit MED31 is required for radial patterning of Arabidopsis roots

Stem cell specification in multicellular organisms relies on the precise spatiotemporal control of RNA polymerase II (Pol II)-dependent gene transcription, in which the evolutionarily conserved Mediator coactivator complex plays an essential role. In Arabidopsis thaliana, SHORTROOT (SHR) and SCARECROW (SCR) orchestrate a transcriptional program that determines the fate and asymmetrical divisions of stem cells generating the root ground tissue. The mechanism by which SHR/SCR relays context-specific regulatory signals to the Pol II general transcription machinery is unknown. Here, we report the role of Mediator in controlling the spatiotemporal transcriptional output of SHR/SCR during asymmetrical division of stem cells and ground tissue patterning. The Mediator subunit MED31 interacted with SCR but not SHR. Reduction of MED31 disrupted the spatiotemporal activation of CYCLIND6;1 (CYCD6;1), leading to defective asymmetrical division of stem cells generating ground tissue. MED31 was recruited to the promoter of CYCD6;1 in an SCR-dependent manner. MED31 was involved in the formation of a dynamic MED31/SCR/SHR ternary complex through the interface protein SCR. We demonstrate that the relative protein abundance of MED31 and SHR in different cell types regulates the dynamic formation of the ternary complex, which provides a tunable switch to strictly control the spatiotemporal transcriptional output. This study provides valuable clues to understand the mechanism by which master transcriptional regulators control organ patterning

NMP4 regulates the innate immune response to influenza A virus infection

Severe influenza A virus infection typically triggers excessive and detrimental lung inflammation with massive cell infiltration and hyper-production of cytokines and chemokines. We identified a novel function for nuclear matrix protein 4 (NMP4), a zinc-finger-containing transcription factor playing roles in bone formation and spermatogenesis, in regulating antiviral immune response and immunopathology. Nmp4-deficient mice are protected from H1N1 influenza infection, losing only 5% body weight compared to a 20% weight loss in wild type mice. While having no effects on viral clearance or CD8/CD4 T cell or humoral responses, deficiency of Nmp4 in either lung structural cells or hematopoietic cells significantly reduces the recruitment of monocytes and neutrophils to the lungs. Consistent with fewer innate cells in the airways, influenza-infected Nmp4-deficient mice have significantly decreased expression of chemokine genes Ccl2, Ccl7 and Cxcl1 as well as pro-inflammatory cytokine genes Il1b and Il6. Furthermore, NMP4 binds to the promoters and/or conserved non-coding sequences of the chemokine genes and regulates their expression in mouse lung epithelial cells and macrophages. Our data suggest that NMP4 functions to promote monocyte- and neutrophil-attracting chemokine expression upon influenza A infection, resulting in exaggerated innate inflammation and lung tissue damage

H2AK121ub in Arabidopsis associates with a less accessible chromatin state at transcriptional regulation hotspots

Although it is well established that the Polycomb Group (PcG) complexes maintain gene repression through the incorporation of H2AK121ub and H3K27me3, little is known about the effect of these modifications on chromatin accessibility, which is fundamental to understand PcG function. Here, by integrating chromatin accessibility, histone marks and expression analyses in different Arabidopsis PcG mutants, we show that PcG function regulates chromatin accessibility. We find that H2AK121ub is associated with a less accessible but still permissive chromatin at transcriptional regulation hotspots. Accessibility is further reduced by EMF1 acting in collaboration with PRC2 activity. Consequently, H2AK121ub/H3K27me3 marks are linked to inaccessible although responsive chromatin. In contrast, only-H3K27me3-marked chromatin is less responsive, indicating that H2AK121ub-marked hotspots are required for transcriptional responses. Nevertheless, despite the loss of PcG activities leads to increased chromatin accessibility, this is not necessarily accompanied by transcriptional activation, indicating that accessible chromatin is not always predictive of gene expression.National Natural Science Foundation of China 31970532Ministerio de Ciencia e Innovación BIO2016-76457-P, PID2019-106664GB-I00, BIO2017-84066-

Genomic Variations in Pancreatic Cancer and Potential Opportunities for Development of New Approaches for Diagnosis and Treatment

This research was supported by Nature Sciences Foundation of China (31301007 and 81272525), Pancreatic Cancer Research Fund and The MRC (MR/M015696/1)

Causal associations between gut microbiota and Cholestatic liver diseases: a Mendelian randomization study

BackgroundThe etiological factors of Cholestatic Liver Diseases especially primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) are not fully illustrated. It has been reported in previous observational studies that gut microbiota are associated with cholestatic liver diseases. However, there is uncertainty regarding the causality of this association. By using Mendelian randomization, this study aimed to examine the causal impact of gut microbiota on cholestatic liver diseases.MethodsFrom large-scale genome-wide association studies, genetic instruments for each gut microbiota taxa as well as primary biliary cholangitis and primary sclerosing cholangitis were developed. Subsequently, we conducted a two-sample Mendelian randomization analysis, supplemented by multiple post hoc sensitivity analyses. Additionally, we performed reverse MR analyses to investigate the possibility of the reverse causal association.ResultThis two-sample MR study indicated that the order Bacillales, family Peptostreptococcaceae, family Ruminococcaceae, genus Anaerotruncu was associated with a decreased risk of developing PBC, and that order Selenomonadales, family Bifidobacteriaceae may be factors that increase the risk of PBC. On the other hand, we also identified order Selenomonadales, family Rhodospirillaceae, and genus RuminococcaceaeUCG013 were positively associated with PSC. The order Actinomycetales, family Actinomycetaceae, genus Actinomyces, genus Alloprevotella, genus Barnesiella, and genus Peptococcus were found negative associations with the risk of PSC. The reverse MR analysis demonstrated no statistically significant relationship between PBC, PSC and these specific gut microbial taxa.ConclusionOur findings offered novel evidence that the abundance of particular bacteria contributes to the risk of PBC and PSC, which may contribute to more effective approaches to PBC and PSC therapy and prevention