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  • Oxford University Press (OUP)  (14)
  • Li, Yang  (14)
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  • Oxford University Press (OUP)  (14)
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  • 1
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2022
    In:  Military Medicine Vol. 187, No. 3-4 ( 2022-03-28), p. e343-e350
    In: Military Medicine, Oxford University Press (OUP), Vol. 187, No. 3-4 ( 2022-03-28), p. e343-e350
    Abstract: External hemorrhage control devices (EHCDs) are effective in reducing the death risk of noncompressible torso hemorrhage (NCTH), but the pressurized area is too large to prevent serious organ damage. This study aims to establish the surface localization strategy of EHCDs based on the anatomical features of NCTH-related arteries through CT images to facilitate the optimal design and application of EHCDs. Methods Two hundred patients who underwent abdominal CT were enrolled. Anatomical parameters such as the length of the common iliac artery (CIA), the external iliac artery (EIA), and the common femoral artery were measured; positional relationships among the EHCD-targeted arteries, umbilicus, anterior superior iliac spine (ASIS), and pubic tubercle (PT) were determined. The accuracy of surface localization was verified by the 3D-printed mannequins of 20 real patients. Results Aortic bifurcation (AB) was 7.5 ± 8.6 mm to the left of the umbilicus. The left CIA (left: 46.6 ± 16.0 mm vs. right: 43.3 ± 15.5 mm, P = .038) and the right EIA (left: 102.6 ± 16.3 mm vs. right: 111.5 ± 18.8 mm, P  & lt; .001) were longer than their counterparts, respectively. The vertical distance between the CIA terminus and the ipsilateral AB–ASIS line was 19.6 ± 8.2 mm, and the left and right perpendicular intersections were located at the upper one-third and one-fourth of the AB–ASIS line, respectively. The length ratio of EIA–ASIS to ASIS–PT was 0.6:1. The predicted point and its actual subpoint were significantly correlated (P ≤ .002), and the vertical distance between the two points was ≤5.5 mm. Conclusion The arterial localization strategy established via anatomical investigation was consistent with the actual situation. The data are necessary for improving EHCD design, precise hemostasis, and EHCD-related collateral injuries. Trial registration: Ratification no. 2019092. Registered November 4, 2020—retrospectively registered, www.chictr.org.cn.
    Type of Medium: Online Resource
    ISSN: 0026-4075 , 1930-613X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2130577-8
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  • 2
    In: Protein & Cell, Oxford University Press (OUP), Vol. 9, No. 12 ( 2018-12-01), p. 1013-1026
    Abstract: Lysosomes are degradation and signaling centers within the cell, and their dysfunction impairs a wide variety of cellular processes. To understand the cellular effect of lysosome damage, we screened natural small-molecule compounds that induce lysosomal abnormality using Caenorhabditis elegans (C. elegans) as a model system. A group of vobasinyl-ibogan type bisindole alkaloids (ervachinines A–D) were identified that caused lysosome enlargement in C. elegans macrophage-like cells. Intriguingly, these compounds triggered cell death in the germ line independently of the canonical apoptosis pathway. In mammalian cells, ervachinines A–D induced lysosomal enlargement and damage, leading to leakage of cathepsin proteases, inhibition of autophagosome degradation and necrotic cell death. Further analysis revealed that this ervachinine-induced lysosome damage and lysosomal cell death depended on STAT3 signaling, but not RIP1 or RIP3 signaling. These findings suggest that lysosome-damaging compounds are promising reagents for dissecting signaling mechanisms underlying lysosome homeostasis and lysosome-related human disorders.
    Type of Medium: Online Resource
    ISSN: 1674-800X , 1674-8018
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 2543451-2
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  • 3
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2015
    In:  Japanese Journal of Clinical Oncology Vol. 45, No. 8 ( 2015-08), p. 738-744
    In: Japanese Journal of Clinical Oncology, Oxford University Press (OUP), Vol. 45, No. 8 ( 2015-08), p. 738-744
    Type of Medium: Online Resource
    ISSN: 0368-2811 , 1465-3621
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2015
    detail.hit.zdb_id: 1494610-5
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  • 4
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2023
    In:  Journal of Experimental Botany Vol. 74, No. 3 ( 2023-02-05), p. 976-990
    In: Journal of Experimental Botany, Oxford University Press (OUP), Vol. 74, No. 3 ( 2023-02-05), p. 976-990
    Abstract: Plants have evolved a two-layer immune system comprising pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) that is activated in response to pathogen invasion. Microbial patterns and pathogen effectors can be recognized by surface-localized pattern-recognition receptors (PRRs) and intracellularly localized nucleotide-binding leucine-rich repeat receptors (NLRs) to trigger PTI and ETI responses, respectively. At present, the metabolites activated by PTI and ETI and their roles and signalling pathways in plant immunity are not well understood. In this study, metabolomic analysis showed that ETI and PTI induced various flavonoids and amino acids and their derivatives in plants. Interestingly, both glutathione and neodiosmin content were specifically up-regulated by ETI and PTI, respectively, which significantly enhanced plant immunity. Further studies showed that glutathione and neodiosmin failed to induce a plant immune response in which PRRs/co-receptors were mutated. In addition, glutathione-reduced mutant gsh1 analysis showed that GSH1 is also required for PTI and ETI. Finally, we propose a model in which glutathione and neodiosmin are considered signature metabolites induced in the process of ETI and PTI activation in plants and further continuous enhancement of plant immunity in which PRRs/co-receptors are needed. This model is beneficial for an in-depth understanding of the closed-loop mode of the positive feedback regulation of PTI and ETI signals at the metabolic level.
    Type of Medium: Online Resource
    ISSN: 0022-0957 , 1460-2431
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1466717-4
    SSG: 12
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  • 5
    In: Horticulture Research, Oxford University Press (OUP), Vol. 10, No. 7 ( 2023-07-04)
    Abstract: Great progress has been made in our understanding of floral organ identity determination and its regulatory network in many species; however, the quantitative genetic basis of floral organ number variation is far less well understood for species-specific traits from the perspective of population variation. Here, using a tree peony (Paeonia suffruticosa Andrews, Paeoniaceae) cultivar population as a model, the phenotypic polymorphism and genetic variation based on genome-wide association studies (GWAS) and expression quantitative trait locus (eQTL) analysis were analyzed. Based on 24 phenotypic traits of 271 representative cultivars, the transcript profiles of 119 cultivars were obtained, which indicated abundant genetic variation in tree peony. In total, 86 GWAS-related cis-eQTLs and 3188 trans-eQTL gene pairs were found to be associated with the numbers of petals, stamens, and carpels. In addition, 19 floral organ number-related hub genes with 121 cis-eQTLs were obtained by weighted gene co-expression network analysis, among which five hub genes belonging to the ABCE genes of the MADS-box family and their spatial–temporal co-expression and regulatory network were constructed. These results not only help our understanding of the genetic basis of floral organ number variation during domestication, but also pave the way to studying the quantitative genetics and evolution of flower organ number and their regulatory network within populations.
    Type of Medium: Online Resource
    ISSN: 2052-7276
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 2781828-7
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  • 6
    In: Human Reproduction, Oxford University Press (OUP), Vol. 37, No. 7 ( 2022-06-30), p. 1664-1677
    Abstract: Do variants in helicase for meiosis 1 (HFM1) account for male infertility in humans? SUMMARY ANSWER Biallelic variants in HFM1 cause human male infertility owing to non-obstructive azoospermia (NOA) with impaired crossover formation and meiotic metaphase I (MMI) arrest. WHAT IS KNOWN ALREADY HFM1 encodes an evolutionarily conserved DNA helicase that is essential for crossover formation and completion of meiosis. The null mutants of Hfm1 or its ortholog in multiple organisms displayed spermatogenic arrest at the MMI owing to deficiencies in synapsis and severe defects in crossover formation. Although HFM1 variants were found in infertile men with azoospermia or oligozoospermia, the causal relationship has not yet been established with functional evidence. STUDY DESIGN, SIZE, DURATION A Pakistani family, having two infertile brothers born to consanguineous parents, and three unrelated Chinese men diagnosed with NOA were recruited for pathogenic variants screening. PARTICIPANTS/MATERIALS, SETTING, METHODS All the patients were diagnosed with idiopathic NOA and, for the Chinese patients, meiotic defects were confirmed by histological analyses and/or immunofluorescence staining on testicular sections. Exome sequencing and subsequent bioinformatic analyses were performed to screen for candidate pathogenic variants. The pathogenicity of identified variants was assessed and studied in vivo in mice carrying the equivalent mutations. MAIN RESULTS AND THE ROLE OF CHANCE Six variants (homozygous or compound heterozygous) in HFM1 were identified in the three Chinese patients with NOA and two brothers with NOA from the Pakistani family. Testicular histological analysis revealed that spermatogenesis is arrested at MMI in patients carrying the variants. Mice modeling the HFM1 variants identified in patients recapitulated the meiotic defects of patients, confirming the pathogenicity of the identified variants. These Hfm1 variants led to various reductions of HFM1 foci on chromosome axes and resulted in varying degrees of synapsis and crossover formation defects in the mutant male mice. In addition, Hfm1 mutant female mice displayed infertility or subfertility with oogenesis variously affected. LIMITATIONS, REASONS FOR CAUTION A limitation of the current study is the small sample size. Owing to the unavailability of fresh testicular samples, the defects of synapsis and crossover formation could not be detected in spermatocytes of patients. Owing to the unavailability of antibodies, we could not quantify the impact of these variants on HFM1 protein levels. WIDER IMPLICATIONS OF THE FINDINGS Our findings provide direct clinical and in vivo functional evidence that HFM1 variants cause male infertility in humans and also suggest that HFM1 may regulate meiotic crossover formation in a dose-dependent manner. Noticeably, our findings from mouse models showed that HFM1 variants could impair spermatogenesis and oogenesis with a varying degree of severity and might also be compatible with the production of a few spermatozoa in men and subfertility in women, extending the phenotypic spectrum of patients with HFM1 variants. STUDY FUNDING/COMPETING INTEREST(S) This work was supported by the National Natural Science Foundation of China (31890780, 32070850, 32061143006, 32000587 and 31900398) and the Fundamental Research Funds for the Central Universities (YD2070002007 and YD2070002012). The authors declare no potential conflicts of interest. TRIAL REGISTRATION NUMBER N/A.
    Type of Medium: Online Resource
    ISSN: 0268-1161 , 1460-2350
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1484864-8
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  • 7
    In: The Plant Cell, Oxford University Press (OUP), Vol. 33, No. 8 ( 2021-08-31), p. 2736-2752
    Abstract: Cotton, one of the most important crops in the world, produces natural fiber materials for the textile industry. WRKY transcription factors play important roles in plant development and stress responses. However, little is known about whether and how WRKY transcription factors regulate fiber development of cotton so far. In this study, we show that a fiber-preferential WRKY transcription factor, GhWRKY16, positively regulates fiber initiation and elongation. GhWRKY16-silenced transgenic cotton displayed a remarkably reduced number of fiber protrusions on the ovule and shorter fibers compared to the wild-type. During early fiber development, GhWRKY16 directly binds to the promoters of GhHOX3, GhMYB109, GhCesA6D-D11, and GhMYB25 to induce their expression, thereby promoting fiber initiation and elongation. Moreover, GhWRKY16 is phosphorylated by the mitogen-activated protein kinase GhMPK3-1 at residues T-130 and S-260. Phosphorylated GhWRKY16 directly activates the transcription of GhMYB25, GhHOX3, GhMYB109, and GhCesA6D-D11 for early fiber development. Thus, our data demonstrate that GhWRKY16 plays a crucial role in fiber initiation and elongation, and that GhWRKY16 phosphorylation by GhMPK3-1 is essential for the transcriptional activation on downstream genes during the fiber development of cotton.
    Type of Medium: Online Resource
    ISSN: 1040-4651 , 1532-298X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 623171-8
    detail.hit.zdb_id: 2004373-9
    SSG: 12
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  • 8
    In: Protein & Cell, Oxford University Press (OUP), Vol. 1, No. 5 ( 2010-5), p. 453-458
    Type of Medium: Online Resource
    ISSN: 1674-800X , 1674-8018
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2010
    detail.hit.zdb_id: 2543451-2
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  • 9
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2022
    In:  Journal of the Royal Statistical Society Series C: Applied Statistics Vol. 71, No. 5 ( 2022-11-01), p. 1623-1647
    In: Journal of the Royal Statistical Society Series C: Applied Statistics, Oxford University Press (OUP), Vol. 71, No. 5 ( 2022-11-01), p. 1623-1647
    Abstract: Length of stay (LOS) is an essential metric for the quality of hospital care. Published works on LOS analysis have primarily focused on skewed LOS distributions and the influences of patient diagnostic characteristics. Few authors have considered the events that terminate a hospital stay: Both successful discharge and death could end a hospital stay but with completely different implications. Modelling the time to the first occurrence of discharge or death obscures the true nature of LOS. In this research, we propose a structure that simultaneously models the probabilities of discharge and death. The model has a flexible formulation that accounts for both additive and multiplicative effects of factors influencing the occurrence of death and discharge. We present asymptotic properties of the parameter estimates so that valid inference can be performed for the parametric as well as nonparametric model components. Simulation studies confirmed the good finite-sample performance of the proposed method. As the research is motivated by practical issues encountered in LOS analysis, we analysed data from two real clinical studies to showcase the general applicability of the proposed model.
    Type of Medium: Online Resource
    ISSN: 0035-9254 , 1467-9876
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 204797-4
    detail.hit.zdb_id: 1482300-7
    detail.hit.zdb_id: 1476894-X
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  • 10
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2022
    In:  National Science Review Vol. 9, No. 8 ( 2022-09-03)
    In: National Science Review, Oxford University Press (OUP), Vol. 9, No. 8 ( 2022-09-03)
    Abstract: Allostery is a fundamental element during channel gating in response to an appropriate stimulus by which events occurring at one site are transmitted to distal sites to regulate activity. To address how binding of the first Ca2+ ion at one of the eight chemically identical subunits facilitates the other Ca2+-binding events in MthK, a Ca2+-gated K+ channel containing a conserved ligand-binding RCK domain, we analysed a large collection of MthK structures and performed the corresponding thermodynamic and electrophysiological measurements. These structural and functional studies led us to conclude that the conformations of the Ca2+-binding sites alternate between two quaternary states and exhibit significant differences in Ca2+ affinity. We further propose an allosteric model of the MthK-gating mechanism by which a cascade of structural events connect the initial Ca2+-binding to the final changes of the ring structure that open the ion-conduction pore. This mechanical model reveals the exquisite design that achieves the allosteric gating and could be of general relevance for the action of other ligand-gated ion channels containing the RCK domain.
    Type of Medium: Online Resource
    ISSN: 2095-5138 , 2053-714X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2745465-4
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