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  • Oxford University Press (OUP)  (495)
  • 1
    In: National Science Review, Oxford University Press (OUP), Vol. 10, No. 6 ( 2023-05-10)
    Abstract: With the aid of the newly developed ‘Sunway’ heterogeneous-architecture supercomputer, which has world-leading HPC (high-performance computer) capability, a series of high-resolution coupled Earth system models (SW-HRESMs) with up to 5 km of atmosphere and 3 km of ocean have been developed. These models can meet the needs of multiscale interaction studies with different computational costs. Here we describe the progress of SW-HRESMs development, with an overview of the major advancements made by the international Earth science community in HR-ESMs. We also show the preliminary results of SW-HRESMs with regard to capturing major weather-climate extremes in the atmosphere and ocean, stressing the importance of permitted clouds and ocean submesoscale eddies in modeling tropical cyclones and eddy-mean flow interactions, and paving the way for further model development to resolve finer scales with even higher resolution and more realistic physics. Finally, in addition to increasing model resolution, the development procedure for a non-hydrostatic cloud and ocean submesoscale resolved ESM is discussed, laying out the major scientific directions of such a huge modeling advancement.
    Type of Medium: Online Resource
    ISSN: 2095-5138 , 2053-714X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 2745465-4
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  • 2
    In: Clinical Infectious Diseases, Oxford University Press (OUP), Vol. 75, No. 1 ( 2022-08-24), p. e1054-e1062
    Abstract: To combat the coronavirus disease 2019 (COVID-19) pandemic, nonpharmaceutical interventions (NPIs) were implemented worldwide, which impacted a broad spectrum of acute respiratory infections (ARIs). Methods Etiologically diagnostic data from 142 559 cases with ARIs, who were tested for 8 viral pathogens (influenza virus [IFV], respiratory syncytial virus [RSV] , human parainfluenza virus [HPIV], human adenovirus [HAdV] , human metapneumovirus [HMPV], human coronavirus [HCoV] , human bocavirus [HBoV], and human rhinovirus [HRV] ) between 2012 and 2021, were analyzed to assess the changes in respiratory infections in China during the first COVID-19 pandemic year compared with pre-pandemic years. Results Test-positive rates of all respiratory viruses decreased during 2020, compared to the average levels during 2012–2019, with changes ranging from −17.2% for RSV to −87.6% for IFV. Sharp decreases mostly occurred between February and August when massive NPIs remained active, although HRV rebounded to the historical level during the summer. While IFV and HMPV were consistently suppressed year-round, RSV, HPIV, HCoV, HRV, and HBoV resurged and went beyond historical levels during September 2020–January 2021, after NPIs were largely relaxed and schools reopened. Resurgence was more prominent among children & lt;18 years and in northern China. These observations remain valid after accounting for seasonality and long-term trend of each virus. Conclusions Activities of respiratory viral infections were reduced substantially in the early phases of the COVID-19 pandemic, and massive NPIs were likely the main driver. Lifting of NPIs can lead to resurgence of viral infections, particularly in children.
    Type of Medium: Online Resource
    ISSN: 1058-4838 , 1537-6591
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2002229-3
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  • 3
    In: Plant Physiology, Oxford University Press (OUP), Vol. 190, No. 2 ( 2022-09-28), p. 1182-1198
    Abstract: Cell wall lignification is a key step in forming functional endodermis and protoxylem (PX) in plant roots. Lignified casparian strips (CS) in endodermis and tracheary elements of PX are essential for selective absorption and transport of water and nutrients. Although multiple key regulators of CS and PX have been identified, the spatial information that drives the developmental shift to root lignification remains unknown. Here, we found that brassinosteroid (BR) signaling plays a key role in inhibiting root lignification in the root elongation zone. The inhibitory activity of BR signaling occurs partially through the direct binding of BRASSINAZOLE-RESISTANT 1 (BZR1) to SHORT-ROOT (SHR), repressing the SHR-mediated activation of downstream genes that are involved in root lignification. Upon entering the mature root zone, BR signaling declines rapidly, which releases SHR activity and initiates root lignification. Our results provide a mechanistic view of the developmental transition to cell wall lignification in Arabidopsis thaliana roots.
    Type of Medium: Online Resource
    ISSN: 0032-0889 , 1532-2548
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2004346-6
    detail.hit.zdb_id: 208914-2
    SSG: 12
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  • 4
    In: Gastroenterology Report, Oxford University Press (OUP), Vol. 9, No. 3 ( 2021-07-24), p. 257-268
    Abstract: p50-associated cyclooxygenase-2 extragenic RNA (PACER) is a recently identified antisense long non-coding RNA (lncRNA) located on the upstream of the promoter region of cyclooxygenase-2 (COX-2). Preliminary studies have suggested that PACER is involved in the regulation of COX-2 expression in macrophagocyte and osteosarcoma cells. However, the role of this lncRNA in colorectal cancer (CRC) remains elusive. Here, we investigated the expression of PACER and its effect on cell proliferation and invasion to explore the role of PACER in CRC. Methods Real-time quantitative PCR (RT-qPCR) analysis was used to evaluate the expression of PACER in CRC tissues and cells. Methyl thiazolyl tetrazolium (MTT) analysis was then used to investigate the inhibition effect of PACER knock-down in cell proliferation. The promoting role of this lncRNA on invasion by CRC cells was analysed by wound-healing assays, colony-formation assay, and transwell assays. We then used fluorescence in situ hybridization (FISH) to establish the subcellular localization of PACER. COX-2 protein levels were quantified by Western blot analysis and grayscale scanning analysis following the knock-down of PACER. Luciferase assay was carried out to monitor the modulation of the COX-2 promoter region by PACER. Tumor xenografts models were used to investigate the impact of PACER on the tumorigenesis of CRC cells in vivo. Enzyme-linked immunosorbent assay (ELISA) was then used to quantify prostaglandin E2 (PGE2) production upon knock-down of PACER. Results RT-qPCR analysis revealed that PACER was highly expressed in CRC tissues and cells, and a high PACER-expression level was associated with poor prognosis. MTT assay, wound-healing assay, colony-formation assay, and transwell assay revealed that PACER enhanced CRC-cell proliferation, invasion, and metastasis in vitro. Analysis of lncRNA localization by FISH showed that it mainly resided in the nucleus. RT-qPCR showed that PACER increased mRNA levels of COX-2. Western blot analysis demonstrated, under normal circumstances, that knock-down of PACER decreased the COX-2 protein level. In the case of p50 absence, COX-2 protein increased rapidly and remained highly expressed after knocking down PACER. Luciferase assay revealed that PACER modulated the COX-2 promoter region. Mouse xenograft models of CRC revealed that PACER promoted colorectal tumorigenesis in vivo. ELISA revealed that PACER knock-down inhibited PGE2 production. Conclusions PACER modulates COX-2 expression through the nuclear factor kappa B (NF-κB) pathway in CRC. An increased level of PACER enhances proliferation, migration, and invasion of tumor cells by increasing COX-2 and PGE2 synthesis.
    Type of Medium: Online Resource
    ISSN: 2052-0034
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2710871-5
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  • 5
    In: Briefings in Bioinformatics, Oxford University Press (OUP), Vol. 22, No. 5 ( 2021-09-02)
    Abstract: Transcriptional regulation is associated with complicated mechanisms including multiple molecular interactions and collaborative drive. Long noncoding RNAs (lncRNAs) have highly structured characteristics and play vital roles in the regulation of transcription in organisms. However, the specific contributions of conformation feature and underlying molecular mechanisms are still unclear. In the present paper, a hypothesis regarding molecular structure effect is presented, which proposes that lncRNAs fold into a complex spatial architecture and act as a skeleton to recruit transcription factors (TF) targeted binding, and which is involved in cooperative regulation. A candidate set of TF-lncRNA coregulation was constructed, and it was found that structural accessibility affected molecular binding force. In addition, transcription factor binding site (TFBS) regions of myopia-related lncRNA transcripts were disturbed, and it was discovered that base mutations affected the occurrence of significant molecular allosteric changes in important elements and variable splicing regions, mediating the onset and development of myopia. The results originated from structureomics and interactionomics and created conditions for systematic research on the mechanisms of structure-mediated TF-lncRNA coregulation in transcriptional regulation. Finally, these findings will help further the understanding of key regulatory roles of molecular allostery in cell physiological and pathological processes.
    Type of Medium: Online Resource
    ISSN: 1467-5463 , 1477-4054
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2036055-1
    SSG: 12
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  • 6
    In: Plant Physiology, Oxford University Press (OUP), Vol. 175, No. 2 ( 2017-10), p. 774-785
    Type of Medium: Online Resource
    ISSN: 0032-0889 , 1532-2548
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
    detail.hit.zdb_id: 2004346-6
    detail.hit.zdb_id: 208914-2
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2016
    In:  Protein & Cell Vol. 7, No. 12 ( 2016-12), p. 878-887
    In: Protein & Cell, Oxford University Press (OUP), Vol. 7, No. 12 ( 2016-12), p. 878-887
    Type of Medium: Online Resource
    ISSN: 1674-800X , 1674-8018
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2016
    detail.hit.zdb_id: 2543451-2
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  • 8
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 164, No. 2 ( 2011-02), p. 263-268
    Abstract: Maternal thyroid disorders during early pregnancy can influence pregnancy outcome and fetal development. The recent Endocrine Society Clinical Practice Guideline recommends a case-finding approach in which pregnant women who are at high risk for developing thyroid disease are tested. Objective The purpose of this study was to use the first trimester-specific reference intervals of thyroid-related hormones to explore the prevalence of thyroid dysfunction during early pregnancy and to analyze effectiveness of different screening strategies. Design A multicenter cohort study. Method A total of 2899 pregnant women were enrolled in this study during their first trimester of gestation. Levels of TSH, free thyroxine, free triiodothyronine, and thyroid peroxidase antibodies (TPOAb) were measured and thyroid disorders of pregnant women were diagnosed based on the first trimester-specific reference intervals. Results The prevalence of hypothyroidism was significantly higher in the high-risk group than in the non-high-risk group (10.9 vs 7.0%, χ 2 =7.1, P =0.008). The prevalence of hyperthyroidism was not significantly different between the high-risk group and the non-high-risk group (2.7 vs 1.6%, χ 2 =2.27, P =0.13). Elevated levels of TPOAb and a personal history of thyroid disease increased the risk of thyroid dysfunction. Conclusions A case-finding strategy for screening thyroid function in the high-risk group would miss about 81.6% pregnant women with hypothyroidism and 80.4% pregnant women with hyperthyroidism.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    RVK:
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2011
    detail.hit.zdb_id: 1485160-X
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  • 9
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 110, No. 6 ( 2021-11-29), p. 1131-1142
    Abstract: Traumatic spinal cord injury (SCI) is a devastating condition marked by permanent motor, sensory, and autonomic dysfunction, in which the inflammatory response serves an important and preventable role. High mobility group box-1 (HMGB1) is a potent regulator of inflammation in numerous acute and chronic inflammatory conditions.; however, the role of HMGB1 in SCI remains unclear. The present study aimed to characterize the temporal dynamics of HMGB1 release after SCI, to investigate the role of spinal microglia activation in mediating the effects of HMGB1 on SCI, and to explore the therapeutic potential of intrathecal anti-HMGB1 polyclonal antibody on alleviating SCI. The present study demonstrated that HMGB1 expression was increased immediately after traumatic injury of a primary spinal neuron culture. It was found that neutralizing HMGB1 significantly ameliorated SCI pathogenesis and hind limb paralysis. Moreover, the levels of a number of pro-inflammatory cytokines in the SCI lesion were reduced when local HMGB1 was blocked by anti-HMGB1 antibody. In addition, the injured neuron-derived conditioned medium increased TNF-α secretion and the NF-κB pathway in the BV2 microglia cell line via HMGB1. Collectively, these results indicated that HMGB1 served an important role in SCI inflammation and suggested the therapeutic potential of an anti-HMGB1 antibody for SCI.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 10
    In: Human Molecular Genetics, Oxford University Press (OUP), Vol. 32, No. 13 ( 2023-06-19), p. 2229-2240
    Abstract: The susceptibility single nucleotide polymorphisms (SNPs) obtained by genome-wide association studies leave some thorny questions, such as prioritization, false positives and unknown pathogenesis. Previous studies suggested that genetic variation may perturb the RNA secondary structure, influence protein recruitment and binding and ultimately affect splicing processes. Therefore, exploring the perturbation of SNPs to structure–function correlations may provide an effective bridge toward understanding the genetic contribution to diseases. Here, aiming to decipher the regulatory mechanism of myopia susceptibility variants, we systematically evaluated the roles of SNP-induced structural changes during splicing. In addition, 7.53% of myopia-related SNPs exhibited significant global structural changes, 19.53% presented noteworthy local structural disturbance and there were wide-ranging structural perturbations in the splice-related motifs. We established a comprehensive evaluation system for structural disturbance in the splicing-related motifs and gave the priority ranking for the SNPs at RNA structural level. These high-priority SNPs were revealed to widely disturb the molecular interaction properties between splicing-related proteins and pre-mRNAs by HDOCK. Moreover, mini-gene assays confirmed that structural perturbation could influence splicing efficiency through structural remodelling. This study deepens our understanding of the potential molecular regulatory mechanisms of susceptible SNPs in myopia and contributes to personalized diagnosis, personalized medicine, disease-risk prediction and functional verification study by guiding the prioritization of the susceptibility SNPs.
    Type of Medium: Online Resource
    ISSN: 0964-6906 , 1460-2083
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1474816-2
    SSG: 12
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